Policy Assessment for the Review of the Lead 

National Ambient Air Quality Standards 

External Review Draft 
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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 Carolina 
DISCLAIMER

This draft document has been reviewed by the Office of Air Quality Planning and 

Standards (OAQPS), U.S. Environmental Protection Agency (EPA), and approved for 

publication. This OAQPS Policy Assessment contains preliminary conclusions of the staff of the 

OAQPS and does not necessarily reflect the views of the Agency. Mention of trade names or 

commercial products is not intended to constitute 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 ambient air quality standards (NAAQS) for lead (Pb). The Pb 

NAAQS review team has been led by Dr. Deirdre Murphy. Dr. Karen Martin has managed the 

project. For the chapter on the health effects evidence and exposure/risk information, the 

principal authors include Dr. Deirdre 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 secondary Pb standard, the principal author is 

Ms. Ginger Tennant. The principal author on the 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 the Office of General 

Counsel, also provided valuable comments and contributions. 
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January 2013 Draft – Do Not Quote or Cite i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: FATE 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 ............................................................ 2-32
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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 Included 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 Reflecting 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 STANDARD 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 .......................................................................................................... 4-36 
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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 CONCLUSIONS 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 Sources, 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 Ecological Screening Assessment ........................ 5A-1 

 
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LIST OF FIGURES 

Figure 1-1. Pathways of human and ecosystem exposure 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 estimated to emit at least 0.50 tpy in 2008. ... 2-11

Figure 2-3. Map of Pb-TSP Monitoring Sites in Current Pb NAAQS Monitoring 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-PM10 monitoring sites. ....................................................................................... 2-17

Figure 2-6. Pb-PM2.5 monitoring sites in CSN and IMPROVE networks (2012). .................... 2-18

Figure 2-7. Temporal trend in Pb -TSP concentrations: 1980-2010 (31 sites). ......................... 2-24

Figure 2-8. Temporal trend in Pb-TSP concentrations: 2000-2010 (92 sites). .......................... 2-24 

Figure 2-9. Airborne Pb -TSP concentrations (3-month average) at five sites near 

 roadways: 1979-2010. ............................................................................................ 2-25

Figure 2-10. Pb-TSP maximum 3-month means (215 sites), 2009-2011. ................................. 2-27

Figure 2-11. Distribution of maximum 3-month mean concentrations of Pb-TSP, Pb-PM10 

 and Pb-PM2.5 at different site types, 2009-2011. .................................................... 2-29

Figure 2-12. Distribution of annual mean concentrations of Pb-TSP, Pb-PM10 and Pb-PM2.5 

 at different site types, 2009-2011. .......................................................................... 2-30

Figure 2-13. Distribution of maximum monthly mean concentrations of Pb-TSP, Pb-PM10 

 and Pb-PM2.5 at different site types, 2009-2011. .................................................... 2-31

Figure 2-14. Temporal trend in sediment concentration from core samples in 12 lakes at 

 eight National Parks or Preserves. .......................................................................... 2-41

Figure 3-1. Temporal trend in mean blood Pb levels for NHANES cohorts. .............................. 3-4

Figure 3-2. Human exposure pathways for air-related lead. ...................................................... 3-38

Figure 3-3. Overview of analysis approach. .............................................................................. 3-42

Figure 3-4. Comparison of four concentration-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. ............................ 6-4 

 
January 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 metropolitan areas and in a smelter town. ............. 2-36

Table 3-1. Empirically derived air-to-blood ratios for populations inclusive of children. ....... 3-12

Table 3-2. Associations with neurocognitive function measures in analyses with child study 

 group blood lead levels <5 μg/dL. .......................................................................... 3-21

Table 3-3. Summary of quantitative relationships of IQ and blood Pb for analyses with 

 blood Pb levels closest to those of young children in the U.S. today. .................... 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 sources of lead emissions. ........................................... 3-35

Table 3-6. Types of population exposures assessed. ................................................................ 3-40

Table 3-7. Summary of approaches used to estimate 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 concentration-response functions. .............................. 3-50

Table 3-10.Estimates of air-related risk from 2007 risk assessment. ........................................ 3-57

Table 3-11.Estimates of air-related risk for the generalized (local) urban case study, 

 including interpolated estimates for current standard. ............................................ 3-58
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1 EXECUTIVE SUMMARY 

2 

3 This draft Policy Assessment (PA) has been prepared by staff in the Environmental 

4 Protection Agency’s (EPA) Office of Air Quality Planning and Standards (OAQPS) as part of 

5 the Agency’s ongoing review of the primary (health-based) and secondary (welfare-based) 

6 national ambient air quality standards (NAAQS) for lead (Pb). It presents analyses and 

7 preliminary staff conclusions regarding the policy implications of the key scientific and technical 

8 information that informs this review. The final PA is intended to “bridge the gap” between the 

9 relevant scientific evidence and technical information and the judgments required of the EPA 

10 Administrator in determining whether to retain or revise the current standards. Development of 

11 the PA is also intended to facilitate advice and recommendations on the standards to the 

12 Administrator from an independent scientific review committee, the Clean Air Scientific 

13 Advisory Committee (CASAC), as provided for in the Clean Air Act (CAA). 

14 Staff analyses in this draft PA are based on the scientific assessment presented in the 

15 third draft Integrated Science Assessment for Pb (ISA) prepared for this review by the EPA’s 

16 Office of Research and Development (ORD) as well as scientific and technical assessments from 

17 prior Pb NAAQS reviews. Such assessments include quantitative human health and ecological 

18 risk and exposure assessments (REAs) developed in the last review as new health and ecological 

19 REAs were not warranted based on staff’s and CASAC’s consideration of the evidence newly 

20 available in this review with regard to risk and exposure assessment. In considering the 

21 scientific evidence and other technical information available in this review, emphasis is given to 

22 consideration of the extent to which the evidence newly available since the last review alters 

23 conclusions drawn in the last review with regard to health and welfare effects of Pb, the exposure 

24 levels at which they occur and the associated at-risk populations and ecological receptors or 

25 ecosystems. 

26 The overarching questions in this review, as in all NAAQS reviews, regard the support 

27 provided by the currently available scientific evidence and exposure/risk-based information for 

28 the adequacy of the current standards and the extent to which the scientific evidence and 

29 technical information provides support for concluding that consideration of alternative standards 

30 may be appropriate. The analyses presented in this draft PA to address such questions lead to 

31 preliminary staff conclusions that it is appropriate to consider retaining the current primary and 

32 secondary standards without revision; accordingly, no potential alternative standards have been 

33 identified by staff for consideration in this review. Comments and recommendations from 

34 CASAC, and public comments, based on review of this draft PA, will inform final staff 

35 conclusions and the presentation of information in the final PA. 
January 2013 ES-2 Draft - Do Not Quote or Cite

1 Current Lead NAAQS and Scope of Review

2 The NAAQS for Pb was initially set in 1978. Review of the 1978 NAAQS for Pb, 

3 completed in October 2008, resulted in substantial revision based on the large body of evidence 

4 accumulated over the intervening three decades. In terms of the basic elements of the NAAQS, 

the level of the primary standard was lowered by an order of magnitude from 1.5 μg/m3 5 to 0.15 

μg/m3 6 and the averaging time was revised to a rolling three-month period (from a period based 

7 on calendar quarters) with a maximum (not-to-be exceeded) form, evaluated over a 3-year 

8 period. The indicator of Pb in total suspended particles (Pb-TSP) was retained, reflecting the 

9 evidence that Pb particles of all sizes pose health risks. The secondary standard was revised to 

10 be identical in all respects to the revised primary standard. 

11 The multimedia and persistent nature of Pb contributes complexities to the review of the 

12 Pb NAAQS unlike issues addressed in other NAAQS reviews. Air-related Pb distributes from 

13 air to other media, including indoor and outdoor dusts, soil, food, drinking water, as well as 

14 surface water and sediments. As a result, review of the Pb NAAQS considers the protection 

15 provided against the health and environmental effects of air-related Pb associated both with 

16 exposures to Pb in ambient air and with exposures to Pb that makes its way from ambient air into 

17 other media. Additional complexity derives from the recognition that exposure to Pb also results 

18 from nonair sources, including Pb in paint, tap water affected by plumbing containing Pb, lead19 tainted products, as well as surface water discharges and runoff from industrial sites. Such 

20 nonair sources contribute to the total burden of Pb in the human body and in the environment, 

21 making it much more difficult to assess independently the health and welfare effects attributable 

22 to air-related Pb that are the focus of the NAAQS. Further, the persistence of Pb in the human 

23 body and the environment is another important consideration in assessing the adequacy of the 

24 current Pb standards. In so doing, staff is mindful of the history of the greater and more 

25 widespread atmospheric emissions that occurred in previous years (e.g., under the previous Pb 

26 standard, and prior to establishment of any Pb NAAQS) and that contributed to the Pb that exists 

27 in human populations and ecosystems today. Likewise, staff also recognizes the role of nonair 

28 sources of Pb, now and in the past, that also contribute to the Pb that exists in human populations 

29 and ecosystems today. As in the last Pb NAAQS review, this backdrop of environmental Pb 

30 exposure, and its impact on the populations and ecosystems which may be the subjects of the 

31 currently available scientific evidence, complicates our consideration of the health and welfare 

32 protection afforded by the current NAAQS. 
January 2013 ES-3 Draft - Do Not Quote or Cite

1 Characterization of Ambient Air Lead 

2 Emissions to ambient air and associated air Pb concentrations have declined substantially 

3 over the past several decades. The most dramatic reductions in Pb emissions occurred prior to 

4 1990 in the transportation sector due to the removal of Pb from gasoline. Lead emissions were 

5 further reduced substantially between 1990 and 2008, with significant reductions occurring in the 

6 metals industries at least in part as a result of national emissions standards for hazardous air 

7 pollutants. Additional reductions in stationary source emissions are also anticipated from 

8 regulations which have been promulgated since 2008 under Section 112 of the CAA. 

9 As at the time of the last review, the majority of Pb emissions nationally is associated 

10 with combustion of leaded aviation gasoline by piston-driven aircraft. The largest sources on a 

11 local scale are generally associated with metals industries. As a result of revisions to monitoring 

12 regulations stemming from the last Pb NAAQS review, Pb NAAQS monitors are required near 

13 the largest Pb emissions sources, as well as in sites distant from such sources in large population 

14 areas. Ambient air Pb monitoring data available thus far from this expanded network continue to 

15 illustrate the source-related aspect of airborne Pb, with highest concentrations near large sources 

16 and lowest in areas removed from sources. In addition, Pb monitoring data are also being 

17 collected over at least a one-year period near a set of airports identified as most likely to have 

18 elevated Pb concentrations due to leaded aviation gasoline usage. These data will inform future 

19 airport monitoring activities, as well as an ongoing investigation into Pb emissions from piston20 engine aircraft under Section 231 of the Clean Air Act, separate from this Pb NAAQS review. 

21 Lead occurs in ambient air in particulate form and, with characteristics and spatial 

22 patterns influenced by a number of factors, deposits from air to surfaces in natural and human23 made environments. By this deposition process and subsequent transfer processes, ambient air 

24 Pb is distributed into multiple human exposure pathways and environmental media in aquatic 

25 and terrestrial ecosystems. In areas removed from large air emissions sources, currently 

26 available information on Pb concentrations in nonair media includes numerous examples of 

27 declines in surface concentrations reflective of the reductions in deposition over the past several 

28 decades. In areas near large air sources where emissions reductions have occurred, only very 

29 limited information is available, such as for reductions in air and surface dust concentrations, 

30 with even less information available on trends for other media such as surface soils. 

31 Health Effects and Review of the Primary Standard

32 Lead has long been recognized to exert a broad array of deleterious effects on multiple 

33 organ systems as described in the ISA for this review and consistent with conclusions of prior 

34 scientific assessments. Over the three decades from the time the standard was initially set in 

35 1978 through its revision with the NAAQS review completed in 2008, the evidence base 
January 2013 ES-4 Draft - Do Not Quote or Cite

1 expanded considerably in a number of areas, including with regard to effects on neurocognitive 

2 function in young children at increasingly lower blood Pb levels. These effects formed the 

3 primary basis for the 2008 revisions to the primary standard. The current standard was set most 

4 specifically to provide appropriate public health protection from the effects of air-related Pb on 

5 cognitive function (e.g., IQ loss) in young children. In so doing, the standard was judged to 

6 provide the requisite public health protection from the full array of health effects of Pb, 

7 consistent with the CAA requirement that the primary standard, in the judgment of the 

8 Administrator, based on the latest scientific knowledge, is requisite to protect public health with 

9 an adequate margin of safety. 

10 The health effects evidence newly available in this review, as critically assessed in the 

11 ISA in conjunction with the full body of evidence, reaffirms conclusions on the broad array of 

12 effects recognized for Pb in the last review. Further, staff observes the general consistency of the 

13 current evidence with the evidence available in the last review, particularly with regard to key 

14 aspects of the evidence on which the current standard is based. These key aspects include those 

15 regarding the relationships between air Pb concentrations and the associated Pb in the blood of 

16 young children (i.e., air-to-blood ratios) as well as between total blood Pb levels and effects on 

17 neurocognitive function (i.e., concentration-response (C-R) functions for IQ loss). Factors 

18 characterizing these two relationships are the key inputs to the framework developed in the last 

19 review to translate the available evidence into a basis for considering a primary Pb standard that 

20 would be requisite to protect against this and other Pb-related health endpoints. This framework 

21 is again considered in light of the current available evidence. This Pb NAAQS review, like any 

22 NAAQS review, requires public health policy judgments. The public health policy judgments 

23 for this review include the public health significance of a given magnitude of IQ loss in a small 

24 subset of highly exposed children (i.e., those likely to experience air-related Pb exposures at the 

25 level of the standard), as well as how to consider the nature and magnitude of the array of 

26 uncertainties that are inherent in the evidence and in the application of this specific framework. 

27 In also considering the quantitative risk estimates associated with the current standard, 

28 based on the risk assessment conducted in the last review, staff observes that these estimates 

29 indicate a level of risk that is roughly consistent with and generally supportive of conclusions 

30 drawn from the evidence using the evidence-based air-related IQ loss framework. Staff 

31 additionally recognizes the complexity of the modeling done as part of that assessment and the 

32 substantial limitations and uncertainties in the resulting risk estimates. 

33 Based on the above considerations, staff preliminarily concludes that the currently 

34 available information supports a primary standard as protective as the current standard and that it 

35 is appropriate to consider retaining the current standard without revision. In so doing, staff 

36 additionally notes that the final decision on the adequacy of the current standard is largely a 
January 2013 ES-5 Draft - Do Not Quote or Cite

1 public health policy judgment to be made by the Administrator, drawing upon the scientific 

2 information as well as judgments about how to consider the range and magnitude of uncertainties 

3 that are inherent in the scientific evidence and technical analyses. In this context, staff 

4 recognizes that the uncertainties and limitations associated with the many aspects of the 

5 relationship between air Pb concentrations and blood Pb levels and associated health effects are 

6 amplified with consideration of increasingly lower air concentrations. In staff’s view, based on 

7 the current evidence there is appreciable uncertainty associated with drawing conclusions 

8 regarding whether there would be reductions in risk to public health from alternative lower levels 

9 as compared to the level of the current standard. Thus, staff concludes that the basis for any 

10 consideration of alternative lower standard levels would reflect different public health policy 

11 judgments as to the appropriate approach for weighing uncertainties in the evidence and for 

12 providing requisite protection of public health with an adequate margin of safety. Accordingly, 

13 and in light of the preliminary staff conclusion that it is appropriate to consider the current 

14 standard to be adequate, this document does not identify potential alternative standards for 

15 consideration in this review. 

16 Welfare Effects and Review of the Secondary Standard

17 Consideration of the welfare effects evidence and screening-level risk information in the 

18 last review (completed in 2008) led to the conclusion that there was a potential for adverse 

19 welfare effects occurring under the then-current Pb standard (set in 1978), although there were 

20 insufficient data to provide a quantitative basis for setting a secondary standard different from 

21 the primary standard. Accordingly, the secondary standard was substantially revised to be 

22 identical in all respects to the newly revised primary standard. 

23 In assessing the currently available scientific evidence and the exposure/risk information 

24 with regard to support for the adequacy of the protection afforded by the current standard, staff 

25 observes the general consistency of the current evidence with that available in the last review, 

26 including the substantial limitations in the current evidence that complicate conclusions 

27 regarding the potential for Pb emissions under the current, much lower standard to contribute to 

28 welfare effects. Thus, based on the staff analysis, framed by key policy-relevant questions for 

29 the review, staff preliminarily concludes that consideration should be given to retaining the 

30 current standard, without revision, and this document does not identify potential alternative 

31 standards for consideration in this review. 

32 
January 2013 Draft – Do Not Quote or Cite 1-1

1 1 INTRODUCTION 

2 1.1 PURPOSE 

3 The U.S. Environmental Protection Agency (EPA) is presently conducting a review of 

4 the primary (health-based) and secondary (welfare-based) national ambient air quality standards 

5 (NAAQS) for lead (Pb). The overall plan and schedule for this review were presented in the 

6 Integrated Review Plan for the National Ambient Air Quality Standards for Lead (IRP; USEPA, 

7 2011a). The IRP also identified key policy-relevant issues to be addressed in this review and 

8 discussed the key documents that generally inform NAAQS reviews, including an Integrated 

9 Science Assessment (ISA), Risk and Exposure Assessments (REAs), and a Policy Assessment 

10 (PA). The PA presents a staff evaluation of the policy implications of the key scientific and 

technical information in the ISA and REAs for EPA’s consideration.1 11 The PA generally 

12 provides a transparent evaluation and staff conclusions regarding policy considerations related to 

13 reaching judgments about the adequacy of the current standards, and, if revision is considered, 

14 what revisions may be appropriate to consider. 

15 When final, the PA is intended to help “bridge the gap” between the Agency’s scientific 

16 assessments presented in the ISA and REAs, and the judgments required of the EPA 

17 Administrator in determining whether it is appropriate to retain or revise the NAAQS. In 

18 evaluating the adequacy of the current standard and whether it is appropriate to consider 

19 alternative standards, the PA focuses on information that is most pertinent to evaluating the basic 

elements of the NAAQS: indicator,2 averaging time, form,3 20 and level. These elements, which 

21 together serve to define each standard, must be considered collectively in evaluating the health 

22 and welfare protection afforded by the Pb standards. The PA integrates and interprets the 

23 information from the ISA and REAs to frame policy options for consideration by the 

24 Administrator. In so doing, the PA recognizes that the selection of a specific approach to 

25 reaching final decisions on primary and secondary NAAQS will reflect the judgments of the 

26 Administrator. 

 

1

 The terms “staff” and “we” throughout this document refer to staff in the EPA’s Office of Air Quality 

Planning and Standards (OAQPS). In past NAAQS reviews, this document was referred to as the OAQPS Staff 

Paper. 

2

 The “indicator” of a standard defines the chemical species or mixture that is to be measured in 

determining whether an area attains the standard. The indicator for the Pb NAAQS is lead in total suspended 

particles. 

3

 The “form” of a standard defines the air quality statistic that is to be compared to the level of the standard 

in determining whether an area attains the standard. For example, the form of the annual PM2.5 NAAQS is the 3-

year average of the weighted annual mean PM2.5 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

1 The development of the PA is also intended to facilitate advice to the Agency and 

2 recommendations to the Administrator from an independent scientific review committee, the 

3 Clean Air Scientific Advisory Committee (CASAC), as provided for in the Clean Air Act. As 

4 discussed below in section 1.2.1, the CASAC is to advise not only on the Agency’s assessment 

5 of the relevant scientific information, but also on the adequacy of the existing standards, and to 

6 make recommendations as to any revisions of the standards that may be appropriate. The EPA 

7 facilitates CASAC advice and recommendations, as well as public input and comment, by 

8 requesting CASAC review and public comment on one or more drafts of the PA. 

9 The decision whether to prepare one or more drafts of the PA is influenced by 

10 preliminary staff conclusions and associated CASAC advice and public comment, among other 

11 factors. Typically, a second draft PA has been prepared in cases where the available information 

12 calls into question the adequacy of the current standard and analyses of potential alternative 

13 standards are developed taking into consideration CASAC advice and public comment. In such 

14 cases, a second draft PA includes preliminary staff conclusions regarding potential alternative 

15 standards and undergoes CASAC review and public comment prior to preparation of the final 

16 PA. When such analyses are not undertaken, a second draft PA may not be warranted. 

17 In this draft PA for this review of the Pb NAAQS, we consider the scientific and 

18 technical information available in this review as assessed in the third draft Integrated Science 

19 Assessment for Lead (henceforth referred to as the ISA [USEPA, 2012a]), prepared by EPA’s 

20 National Center for Environmental Assessment (NCEA), and the quantitative human exposure 

21 and health risk and screening-level ecological risk assessments performed in the last review. As 

22 discussed below in section 1.2.3, upon consideration of the evidence newly available in this 

23 review with regard to risk and exposure assessment, staff concluded that new health and welfare 

24 REAs were not warranted. Accordingly, the quantitative risk information considered in this PA 

25 is drawn from the quantitative human exposure and health risk and screening-level ecological 

26 risk assessments performed in the last review (the 2007 Health Risk Assessment Report or 2007 

27 REA [USEPA, 2007a] and the 2006 screening-level Ecological Risk Assessment or 2006 REA 

28 [ICF, 2006]), and is interpreted in the context of newly available evidence in this review. 

29 The evaluation and preliminary staff conclusions presented in this draft PA for the Pb 

30 NAAQS have been informed by comments and advice received from CASAC in their reviews of 

31 the other draft Agency documents prepared thus far in this NAAQS review. Review and 

32 comments from CASAC, and public comment, on this draft PA will inform the final evaluation 

33 and staff conclusions in the final PA. 

34 Beyond informing the EPA Administrator and facilitating the advice and 

35 recommendations of CASAC and the public, the PA is also intended to be a useful reference to 

36 all parties interested in the Pb NAAQS review. In these roles, it is intended to serve as a single 
January 2013 Draft – Do Not Quote or Cite 1-3

1 source of the most policy-relevant information that informs the Agency’s review of the lead 

2 NAAQS, and it is written to be understandable to a broad audience. 

3 1.2 BACKGROUND 

4 1.2.1 Legislative Requirements 

5 Two sections of the Clean Air Act (CAA or the Act) govern the establishment and 

6 revision of the NAAQS. Section 108 (42 U.S.C. section 7408) directs the Administrator to 

7 identify and list certain air pollutants and then to issue air quality criteria for those pollutants. 

8 The Administrator is to list those air pollutants that in her “judgment, cause or contribute to air 

9 pollution which may reasonably be anticipated to endanger public health or welfare;” “the 

10 presence of which in the ambient air results from numerous or diverse mobile or stationary 

11 sources;” and “for which . . . [the Administrator] plans to issue air quality criteria...” Air quality 

12 criteria are intended to “accurately reflect the latest scientific knowledge useful in indicating the 

13 kind and extent of all identifiable effects on public health or welfare which may be expected 

14 from the presence of [a] pollutant in the ambient air . . .” 42 U.S.C. § 7408(b). Section 109 (42 

15 U.S.C. 7409) directs the Administrator to propose and promulgate “primary” and “secondary” 

16 NAAQS for pollutants for which air quality criteria are issued. Section 109(b)(1) defines a 

17 primary standard as one “the attainment and maintenance of which in the judgment of the 

18 Administrator, based on such criteria and allowing an adequate margin of safety, are requisite to 

protect the public health.”4 19 A secondary standard, as defined in section 109(b)(2), must “specify 

20 a level of air quality the attainment and maintenance of which, in the judgment of the 

21 Administrator, based on such criteria, is requisite to protect the public welfare from any known 

or anticipated adverse effects associated with the presence of [the] pollutant in the ambient air.”5 22 

23 The requirement that primary standards provide an adequate margin of safety was 

24 intended to address uncertainties associated with inconclusive scientific and technical 

25 information available at the time of standard setting. It was also intended to provide a reasonable 

26 degree of protection against hazards that research has not yet identified. See Lead Industries 

27 Association v. EPA, 647 F.2d 1130, 1154 (D.C. Cir 1980), cert. denied, 449 U.S. 1042 (1980); 

28 American Petroleum Institute v. Costle, 665 F.2d 1176, 1186 (D.C. Cir. 1981), cert. denied, 455 

 

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 representative 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, animals, wildlife, weather, visibility and climate, damage to 

and deterioration of property, and hazards to transportation, as well as effects on economic values and on personal 

comfort and well-being.” 
January 2013 Draft – Do Not Quote or Cite 1-4

1 U.S. 1034 (1982); American Farm Bureau Federation v. EPA, 559 F. 3d 512, 533 (D.C. Cir. 

2 2009); Association of Battery Recyclers v. EPA, 604 F. 3d 613, 617-18 (D.C. Cir. 2010). Both 

3 kinds of uncertainties are components of the risk associated with pollution at levels below those 

4 at which human health effects can be said to occur with reasonable scientific certainty. Thus, in 

5 selecting primary standards that provide an adequate margin of safety, the Administrator is 

6 seeking not only to prevent pollution levels that have been demonstrated to be harmful but also 

7 to prevent lower pollutant levels that may pose an unacceptable risk of harm, even if the risk is 

8 not precisely identified as to nature or degree. The CAA does not require the Administrator to 

9 establish a primary NAAQS at a zero-risk level or at background concentration levels, see Lead

10 Industries v. EPA, 647 F.2d at 1156 n.51, but rather at a level that reduces risk sufficiently so as 

11 to protect public health with an adequate margin of safety. 

12 In addressing the requirement for an adequate margin of safety, the EPA considers such 

13 factors as the nature and severity of the health effects involved, the size of sensitive population(s) 

14 at risk, and the kind and degree of the uncertainties that must be addressed. The selection of any 

15 particular approach to providing an adequate margin of safety is a policy choice left specifically 

16 to the Administrator’s judgment. See Lead Industries Association v. EPA, 647 F.2d at 1161-62; 

17 Whitman v. American Trucking Associations, 531 U.S. 457, 495 (2001). 

18 In setting primary and secondary standards that are “requisite” to protect public health 

19 and welfare, respectively, as provided in section 109(b), EPA’s task is to establish standards that 

20 are neither more nor less stringent than necessary for these purposes. In so doing, the EPA may 

21 not consider the costs of implementing the standards. See generally, Whitman v. American 

22 Trucking Associations, 531 U.S. 457, 465-472, 475-76 (2001). Likewise, “[a]ttainability and 

23 technological feasibility are not relevant considerations in the promulgation of national ambient 

24 air quality standards.” American Petroleum Institute v. Costle, 665 F. 2d at 1185. 

25 Section 109(d)(1) requires that “not later than December 31, 1980, and at 5-year 

26 intervals thereafter, the Administrator shall complete a thorough review of the criteria 

27 published under section 108 and the national ambient air quality standards . . . and shall make 

28 such revisions in such criteria and standards and promulgate such new standards as may be 

29 appropriate . . . .” Section 109(d)(2) requires that an independent scientific review committee 

30 “shall complete a review of the criteria . . . and the national primary and secondary ambient air 

31 quality standards . . . and shall recommend to the Administrator any new . . . standards and 

32 revisions of existing criteria and standards as may be appropriate . . . .” Since the early 1980's, 
January 2013 Draft – Do Not Quote or Cite 1-5

1 this independent review function has been performed by the Clean Air Scientific Advisory 

Committee (CASAC).6 2 

3 1.2.2 History of Lead NAAQS Reviews 

4 Unlike pollutants such as particulate matter and carbon monoxide, air quality criteria had 

5 not been issued for Pb as of the enactment of the Clean Air Act of 1970, which first set forth the 

6 requirement to set national ambient air quality standards based on air quality criteria. In the 

7 years just after enactment of the CAA, the EPA did not intend to issue air quality criteria for Pb, 

8 and accordingly had not listed Pb under Section 108 of the Act. The EPA had determined to 

9 control Pb air pollution through regulations to phase-out use of Pb additives in gasoline and the 

10 EPA viewed those controls, and possibly additional federal controls, as the best approach to 

11 controlling Pb emissions (See 41 FR 14921 (April 8, 1976). However, the decision not to list Pb 

12 under Section 108 was challenged by environmental and public health groups and the U.S. 

13 District Court for the Southern District of New York concluded that the EPA was required to list 

14 Pb under Section 108. (Natural Resources Defense Council v. EPA, 411 F. Supp. 864 21 [S.D. 

15 N.Y. 1976], aff’d, 545 F.2d 320 [2d Cir. 1978]). 

16 Accordingly, on April 8, 1976, the EPA published a notice in the Federal Register that 

17 Pb had been listed under Section 108 as a criteria pollutant (41 FR 14921) and on October 5, 

18 1978, the EPA promulgated primary and secondary NAAQS for Pb under Section 109 of the Act 

19 (43 FR 46246). Both primary and secondary standards were set at a level of 1.5 micrograms per 

cubic meter (μg/m3 20 ), measured as Pb in totalsuspended particles (Pb-TSP), not to be exceeded 

21 by the maximum arithmetic mean concentration averaged over a calendar quarter. These 

22 standards were based on the 1977 Air Quality Criteria for Lead (USEPA, 1977). 

23 The first review of the Pb standards was initiated in the mid-1980s. The scientific 

24 assessment for that review is described in the 1986 Air Quality Criteria for Lead (USEPA, 

25 1986a), the associated Addendum (USEPA, 1986b) and the 1990 Supplement (USEPA, 1990a). 

26 As part of the review, the Agency designed and performed human exposure and health risk 

27 analyses (USEPA, 1989), the results of which were presented in a 1990 Staff Paper (USEPA, 

28 1990b). Based on the scientific assessment and the human exposure and health risk analyses, the 

29 1990 Staff Paper presented recommendations for consideration by the Administrator (USEPA, 

30 1990b). After consideration of the documents developed during the review and the significantly 

31 changed circumstances since Pb was listed in 1976, the Agency did not propose any revisions to 

32 the 1978 Pb NAAQS. In a parallel effort, the Agency developed the broad, multi-program, 

33 multimedia, integrated U.S. Strategy for Reducing Lead Exposure (USEPA, 1991). As part of 

 

6 Lists of CASAC members and of members of the CASAC Pb Review Panel are available at: 

http://yosemite.epa.gov/sab/sabproduct.nsf/WebCASAC/CommitteesandMembership?OpenDocument. 
January 2013 Draft – Do Not Quote or Cite 1-6

1 implementing this strategy, the Agency focused efforts primarily on regulatory and remedial 

2 clean-up actions aimed at reducing Pb exposures from a variety of nonair sources judged to pose 

3 more extensive public health risks to U.S. populations, as well as on actions to reduce Pb 

4 emissions to air, such as bringing more areas into compliance with the existing Pb NAAQS 

5 (USEPA, 1991). 

6 The most recent review of the Pb air quality criteria and standards was initiated in 

7 November 2004 (69 FR 64926) and the Agency’s plans for preparation of the Air Quality 

8 Criteria Document and conduct of the NAAQS review were presented in documents completed 

in 2005 and early 2006 (USEPA, 2005; USEPA 2006a).7 9 The schedule for completion of the 

10 review was governed by a judicial order in Missouri Coalition for the Environment v. EPA (No. 

11 4:04CV00660 ERW, Sept. 14, 2005; and amended on April 29, 2008 and July 1, 2008), which 

12 specified a schedule for the review of duration substantially shorter than five years. 

13 The scientific assessment for the review is described in the 2006 Air Quality Criteria for 

14 Lead (USEPA, 2006b; henceforth referred to as the 2006 CD), multiple drafts of which received 

15 review by CASAC and the public. The EPA also conducted human exposure and health risk 

16 assessments and a pilot ecological risk assessment for the review, after consultation with 

17 CASAC and receiving public comment on a draft analysis plan (USEPA, 2006c). Drafts of these 

18 quantitative assessments were reviewed by CASAC and the public. The pilot ecological risk 

19 assessment was released in December 2006 (ICF, 2006) and the final health risk assessment 

20 report was released in November 2007 (USEPA, 2007a). The policy assessment based on both 

21 of these assessments, air quality analyses and key evidence from the AQCD was presented in the 

22 Staff Paper (USEPA, 2007b), a draft of which also received CASAC and public review. The 

23 final Staff Paper presented OAQPS staff’s evaluation of the public health and welfare policy 

24 implications of the key studies and scientific information contained in the Criteria Document and 

25 presented and interpreted results from the quantitative risk/exposure analyses conducted for this 

26 review. Based on this evaluation, the Staff Paper presented OAQPS staff recommendations that 

27 the Administrator give consideration to substantially revising the primary and secondary 

standards to a range of levels at or below 0.2 μg/m3 28 . 

29 Immediately subsequent to completion of the Staff Paper, the EPA issued an advance 

30 notice of proposed rulemaking (ANPR) that was signed by the Administrator on December 5, 

2007 (72 FR 71488).8 31 CASAC provided advice and recommendations to the Administrator with 

32 regard to the Pb NAAQS based on its review of the ANPR and the previously released final Staff 

 

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 NAAQS 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

1 Paper and risk assessment reports. The proposed decision on revisions to the Pb NAAQS was 

2 signed on May 1, 2008 and published in the Federal Register on May 20, 2008 (73 FR 29184). 

3 Members of the public provided both written and, at two public hearings, oral comments and the 

4 CASAC Pb Panel also provided advice and recommendations to the Administrator based on its 

5 review of the proposal notice. The final decision on revisions to the Pb NAAQS was signed on 

6 October 15, 2008 and published in the Federal Register on November 12, 2008 (73 FR 66964). 

7 The November 2008 notice described EPA’s decision to revise the primary and 

8 secondary NAAQS for Pb, as discussed more fully in section 4.1.1 below. In consideration of 

9 the much-expanded health effects evidence on neurocognitive effects of Pb in children, the EPA 

substantially revised the primary standard from a level of 1.5 μg/m3 to a level of 0.15 μg/m3 10 . 

11 The averaging time was revised to a rolling three-month period with a maximum (not-to-be12 exceeded) form, evaluated over a three-year period. The indicator of Pb-TSP was retained, 

13 reflecting the evidence that Pb particles of all sizes pose health risks. The secondary standard 

was revised to be identical in all respects to the revised primary standards.9 14 Revisions to the 

15 NAAQS were accompanied by revisions to the data handling procedures, the treatment of 

16 exceptional events and the ambient air monitoring and reporting requirements, as well as 

emissions inventory reporting requirements.10 17 One aspect of the new data handling requirements 

18 is the allowance for the use of Pb-PM10 monitoring for Pb NAAQS attainment purposes in 

19 certain limited circumstances at non-source-oriented sites. Subsequent to the 2008 rulemaking, 

20 additional revisions were made to the monitoring network requirements as described in chapter 2 

21 below. 

22 1.2.3 Current Lead NAAQS Review 

23 On February 26, 2010, the EPA formally initiated its current review of the air quality 

24 criteria and standards for Pb, requesting the submission of recent scientific information on 

25 specified topics (75 FR 8934). Soon after this, the EPA held a science policy workshop to 

26 discuss the policy-relevant science, which informed identification of key policy issues and 

27 questions to frame the review of the Pb NAAQS (75 FR 20843). Drawing from the workshop 

28 discussions, the EPA developed the draft IRP (USEPA, 2011c). The draft IRP was made 

29 available in late March 2011 for consultation with the CASAC Pb Review Panel and for public 

30 comment (76 FR 20347). This document was discussed by the Panel via a publicly accessible 

 

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

1 teleconference consultation on May 5, 2011 (76 FR 21346; Frey, 2011a). The final IRP, 

2 developed in consideration of CASAC advice and public comment, was released in November, 

3 2011 (USEPA, 2011a; 76 FR 76972). 

4 In developing the ISA for this review, the EPA held a workshop in December 2010 to 

5 discuss with invited scientific experts preliminary draft materials and released the first external 

6 review draft of the document for CASAC review and public comment on May 6, 2011 (USEPA, 

7 2011d; 76 FR 26284; 76 FR 36120). The CASAC Pb Review Panel met at a public meeting on 

8 July 20, 2011 to review the draft ISA (76 FR 36120). The CASAC provided comments in a 

9 December 9, 2011 letter to the EPA Administrator (Frey and Samet, 2011). The second external 

10 review draft ISA was released for CASAC review and public comment in February 2012 

11 (USEPA, 2012b, 77 FR 5247) and was the subject of a public meeting on April 10-11, 2012 (77 

12 FR 14783). The CASAC provided comments in a July 20, 2012 letter (Samet and Frey, 2012). 

13 The third external review draft was released for CASAC review and public comment in 

14 November 2012 (USEPA, 2012a, 77 FR 70776). That document, together with this draft Policy 

15 Assessment, will be the subject of a public meeting on February 5-6, 2013 (78 FR 938). The 

16 final ISA is targeted for release in late spring 2013. 

17 As described in the IRP, the EPA developed and released for CASAC review and public 

18 comment in June 2011 an REA Planning Document (USEPA, 2011b; 76 FR 58509). This 

19 document presented a critical evaluation of the information related to Pb human and ecological 

20 exposure and risk (e.g., data, modeling approaches) newly available in this review, with a focus 

21 on consideration of the extent to which new or substantially revised REAs for health and 

22 ecological risk are warranted by the newly available evidence. Evaluation of the newly available 

23 information with regard to designing and implementing health and ecological REAs for this 

24 review led us to conclude that the currently available information did not provide a basis for 

25 developing new quantitative risk and exposure assessments that would have substantially 

26 improved utility for informing the Agency’s consideration of health and welfare effects and 

27 evaluation of the adequacy of the current primary and secondary standards, respectively (REA 

28 Planning Document, sections 2.3 and 3.3, respectively). The CASAC Pb Panel provided 

29 consultative advice on that document and its conclusions at a public meeting on July 21, 2011 

30 (76 FR 36120; Frey, 2011b). Based on their consideration of the REA Planning Document 

31 analysis, the CASAC Pb Review Panel generally concurred with the conclusion that a new REA 

32 was not warranted in this review (Frey, 2011b). In consideration of the conclusions reached in 

33 the REA Planning Document and CASAC’s consultative advice, the EPA has not developed 

34 REAs for health and ecological risk for this review. Accordingly, this Policy Assessment 

35 considers the risk assessment findings from the last review with regard to any appropriate further 

36 interpretation in light of the evidence newly available in this review. 
January 2013 Draft – Do Not Quote or Cite 1-9

1 This draft Policy Assessment is being released for public comment and review by 

2 CASAC. Advice from CASAC and public comments received on this draft will be considered in 

3 preparing the final PA.

4 1.3 SCOPE OF CURRENT REVIEW: FATE AND MULTIMEDIA PATHWAYS OF 

5 AMBIENT AIR LEAD 

6 The multimedia and persistent nature of Pb contributes complexities to the review of the 

Pb NAAQS unlike issues addressed in other NAAQS reviews.11 7 As described in section 1.1, 

8 NAAQS are established to protect public health with an adequate margin of safety, and public 

9 welfare from known or anticipated adverse effects, from air pollutants (substances emitted to 

10 ambient air). Since Pb distributes from air to other media and is persistent, our review of the 

11 NAAQS for Pb considers the protection provided against such effects associated both with 

12 exposures to Pb in ambient air and with exposures to Pb that makes its way into other media 

13 from ambient air. Additionally, in assessing the adequacy of protection afforded by the current 

14 NAAQS, we are mindful of the history of the greater and more widespread atmospheric 

15 emissions that occurred in previous years (e.g., under 1978 NAAQS, and prior to establishment 

16 of any Pb NAAQS) and that contributed to the Pb that exists in human populations and 

17 ecosystems today. Likewise, we also recognize the role of other, nonair sources of Pb now and 

18 in the past that also contribute to the Pb that exists in human populations and ecosystems today. 

19 As in the last Pb NAAQS review, this backdrop of environmental Pb exposure, and its impact on 

20 the populations and ecosystems which may be the subjects of the currently available scientific 

21 evidence, complicates our consideration of the health and welfare protection afforded by the 

22 current NAAQS. In the first section below, we summarize the environmental pathways of 

23 human and ecosystem exposures to Pb emitted to ambient air and associated complexities. The 

24 subsequent section briefly discusses the role of historically emitted Pb in our consideration of the 

25 adequacy of the current NAAQS for Pb. 

26 1.3.1 Environmental Distribution and Exposure Pathways 

27 Lead emitted to ambient air is transported through the air and is also distributed to other 

28 media through the process of deposition, which may occur in dry conditions or in association 

29 with precipitation, as summarized further in section 2.3 below (ISA, section 3.7.2). Once 

30 deposited, the fate of Pb is influenced by the type of surface onto which the particles deposit and 

31 by the type and activity level of transport processes in that location. Precipitation and other 

 

11 Some aspects of the review of the secondary standard for oxides of nitrogen and sulfur, which involved 

consideration of pollutant transport 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

1 natural, as well as human-influenced, processes contribute to the fate of such particles, which 

2 affects the likelihood of subsequent human and ecological exposures, e.g., tracking into nearby 

3 houses or transport with surface runoff into nearby water bodies (ISA, sections 3.3 and 4.1). For 

4 example, Pb particles deposited onto impervious surfaces, such as roadway, sidewalk or other 

5 urban surfaces, may be more available for human contact while they remain on such surfaces or 

6 are transferred to other human environments, such as on clothing or through resuspension and 

7 infiltration (ISA, section 4.1.1.1). Deposited Pb can also be transported (by direct deposition or 

8 stormwater runoff) to water bodies and into associated sediments, which may provide a storage 

9 function for Pb in aquatic ecosystems (ISA, sections 3.3.2 and 7.2.1). Lead deposited in 

10 terrestrial ecosystems can also be incorporated into soil matrices (ISA, sections 3.3.3 and 7.2.1). 

11 Figure 1-1 illustrates, in summary fashion, the pathways by which Pb emitted into 

12 ambient air can be distributed in the environment and contribute to human and ecosystem 

13 exposures. As shown in this figure, the multimedia distribution of Pb emitted into ambient air 

14 (air-related Pb) contributes to multiple air-related pathways of human and ecosystem exposure 

(ISA, sections 4.1.1 and 4.7.1).12 15 As illustrated in Figure 1-1, air-related pathways may involve 

16 media other than air. Additionally, as recognized by the figure and discussed more completely in 

17 the subsections below, Pb that has not passed through ambient air (nonair Pb) may complicate 

18 our consideration of ambient air Pb exposures. Further, the persistence of Pb poses an additional 

19 complication, also discussed below, with regard to consideration of exposures associated with 

20 current Pb emissions. 

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 

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

3 

4 1.3.1.1 Human Exposure Pathways 

5 Air-related Pb exposure pathways for humans include inhalation of ambient air or 

6 ingestion of food, water or other materials, including dust and soil, that have been contaminated 

7 through a pathway involving Pb deposition from ambient air (ISA, section 4.1.1.1). Ambient air 

8 inhalation pathways include both inhalation of air outdoors and inhalation of ambient air that has 

9 infiltrated into indoor environments. The air-related ingestion pathways occur as a result of Pb 

10 passing through the ambient air, being distributed to other environmental media and contributing 

11 to human exposures via contact with and ingestion of indoor and outdoor dusts, outdoor soil, 

12 food and drinking water. 

13 Lead currently occurring in nonair media may also derive from sources other than 

14 ambient air (nonair Pb sources), as summarized further in section 2.3 below (ISA, section 4.7.1). 

15 For example, Pb in dust inside some houses or outdoors in some urban areas may derive from the 

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 distribution or food processing/packaging.

‐‐‐‐‐‐‐deposition ‐‐‐‐‐‐‐

resuspension‐

‐‐‐deposition‐‐‐

Note: Arrows indicate general pathways by which Pb distributes in environment and human populations. Individual 

pathway significance varies with location- and receptor-specific factors.

*

*

*

*

Human * Exposures

(Inhalation and Ingestion)
January 2013 Draft – Do Not Quote or Cite 1-12

1 common past usage of leaded paint, while Pb in drinking water may derive from the use of 

2 leaded pipe or solder in drinking water distribution systems (ISA, section 4.1.3.3). We also 

3 recognize the history of much greater air emissions of Pb in the past, such as that associated with 

4 leaded gasoline usage and higher industrial emissions (as summarized in section 2.1.1 below) 

5 which have also contributed to Pb currently occurring in other (nonair) media. 

6 The relative importance of different pathways of human exposure to Pb, as well as the 

7 relative contributions from Pb resulting from recent and historic air emissions and from nonair 

8 sources, vary across the U.S. population as a result of both extrinsic factors, such as a home’s 

9 proximity to industrial Pb sources or its history of leaded paint usage, and intrinsic factors, such 

10 as a person’s age and nutritional status (ISA, sections 6.1, 6.2, 6.2.1, 6.2.5 and 6.2.6). For 

11 example, a predominant Pb exposure pathway for very young children is the incidental ingestion 

12 of indoor dust by hand-to-mouth activity (ISA, section 4.1.1.1). For adults, diet may be the 

13 primary Pb exposure pathway (2006 CD, section 3.4). Similarly, the relative importance of air14 related and nonair-related Pb also varies with the relative magnitudes of exposure by those 

15 pathways, which may vary with different circumstances. For example, relative contributions to a 

16 child’s total Pb exposure from air-related exposure pathways compared to other (nonair) Pb 

17 exposures depend on many factors, including ambient air concentrations and air deposition in the 

18 area where the child resides (as well as in the area from which the child’s food derives), as well 

19 as access to other sources of Pb exposure such as Pb paint, tap water affected by plumbing 

20 containing Pb, and lead-tainted products. Studies indicate that in the absence of paint-related 

21 exposures, Pb from other sources such as nearby stationary sources of Pb emissions may 

22 dominate a child’s Pb exposures (ISA, sections 4.1 and 4.1.3.2; 2006 CD, section 3.2.3). In 

23 other cases, such as children living in older housing with peeling paint or where renovations have 

24 occurred, the dominant source of Pb exposure may be dust from lead paint used in the house in 

25 the past. Depending on Pb levels in a home’s tap water, drinking water can sometimes be a 

26 significant source. Lead exposure may also be the result of a mixture of contributions from 

27 multiple sources, with no one source dominating. Our understanding of the relative contribution 

28 of air-related Pb to ingestion exposure pathways is limited by the paucity of studies that parse 

29 ingestion exposure pathways with regard to air-related and nonair Pb. Our understanding of the 

30 relative contribution of air-related Pb associated with historical emissions and that from recent 

31 emissions is similarly limited. 

32 1.3.1.2 Ecosystem Exposure Pathways 

33 The distribution of Pb from ambient air to other environmental media also influences the 

34 exposure pathways in terrestrial and aquatic ecosystems. Exposure of terrestrial animals and 

35 vegetation to air-related Pb can occur by contact with ambient air or by contact with soil, water 
January 2013 Draft – Do Not Quote or Cite 1-13

1 or food items that have been contaminated by Pb from ambient air (ISA, section 7.2). Transport 

2 of Pb into aquatic systems similarly provides for exposure of biota in those systems, and 

3 exposures may vary among systems as a result of differences in sources and levels of 

4 contamination, as well as characteristics of the systems themselves. In addition to Pb contributed 

5 by current atmospheric deposition, Pb may occur in aquatic systems as a result of nonair sources 

6 such as industrial discharges or mine-related drainage, of historical air Pb emissions (e.g., 

7 contributing to deposition to a water body or via runoff from soils near historical air sources) or 

8 combinations of different types of sources (e.g., resuspension of sediments contaminated by 

9 urban runoff and surface water discharges). 

10 The persistence of Pb contributes an important temporal aspect to lead’s environmental 

11 pathways, and the time (or lag) associated with realization of the impact of air Pb concentrations 

12 on concentrations in other media can vary with the media (e.g., ISA, section 7.2.2). For example, 

13 human exposure pathways most directly involving Pb in ambient air and exchanges of ambient 

14 air with indoor air can respond more quickly while pathways involving exposure to Pb deposited 

15 from ambient air into the environment (e.g., diet) generally respond more slowly. An additional 

16 influence on the response time for nonair media is the environmental presence of Pb associated 

17 with past, generally higher, air concentrations. For example, after a reduction in air Pb 

18 concentrations, the time needed for sediment or surface soil concentrations to indicate a response 

19 to reduced air Pb concentrations might be expected to be longer in areas of more substantial past 

20 contamination than in areas with lesser past contamination. Thus, considering the Pb 

21 concentrations occurring in nonair media as a result of air quality conditions that meet the 

22 current NAAQS is a complexity of this review, as it also was, although to a lesser degree, with 

23 regard to the prior standard in the last review. 

24 1.3.2 Considerations Related to Historically Emitted Lead 

25 In reviews of NAAQS, the overarching consideration of each review is first focused on 

26 the general question as to whether the currently available information supports or calls into 

27 question the adequacy of the current standard(s). In addressing that consideration for the 

28 NAAQS for Pb, our focus is on Pb emitted to ambient air under conditions meeting the current 

29 standard and its potential to cause health or welfare effects as a result of exposures to Pb in air or 

30 in other media. We frame the focus in this way, which differs from that for NAAQS reviews 

31 involving other pollutants, in consideration of the persistence of Pb in the environment over time, 

32 a characteristic which does not affect reviews of other NAAQS. In considering the case for Pb, 

33 however, we recognize that, because of its persistence, both recent and past Pb emissions to 

34 ambient air contribute to current Pb exposures (via multiple exposure pathways, as summarized 

35 in section 1.4.1 above). And we recognize that past Pb emissions in many situations were well in 
January 2013 Draft – Do Not Quote or Cite 1-14

1 excess of the current Pb standard. Yet our task in this and every NAAQS review is focused on 

2 assessing the adequacy of the current standard. 

3 Lead emissions, and air concentrations, were higher in the past, and most substantially so 

4 during the time of leaded gasoline usage, as summarized in sections 2.1 and 2.2 below. Nonair 

5 sources of Pb to human exposure and the environment, an additional complicating feature of Pb 

6 NAAQS reviews, were also much higher in the past. These air and nonair sources contributed 

7 to historical human and environmental exposures. Because of the persistence of Pb, historical 

8 exposures associated both with air-related and nonair-related sources, have contributed Pb that is 

9 now stored within older humans and ecosystems. For example, concentrations of Pb in the bone 

10 and blood of older members of the U.S. population, who lived during the time of widespread air 

11 emissions associated with leaded gasoline usage (as well as higher industrial emissions) under 

12 the previous Pb NAAQS or prior to establishment of any Pb NAAQS, are greater than what 

13 would result from air quality conditions allowed by the current, more restrictive NAAQS. 

14 Epidemiological studies of these populations, in which this exposure history is represented by 

15 current bone or blood Pb concentrations, contribute to the overall evidence base regarding lead16 related health effects (as discussed in chapter 3 below). Such studies of these historically 

17 exposed populations, however, are generally less informative in judging the adequacy of the 

18 current primary standard (as discussed in chapter 3 below). This is in contrast to epidemiological 

19 studies of very young populations with much shorter and more recent exposure histories (also 

20 discussed in chapter 3). 

21 The current distribution of Pb in U.S. ecosystems also reflects the widespread and greater 

22 air emissions that occurred in the past, under the prior Pb NAAQS and prior to establishment of 

any Pb NAAQS.13 23 We lack information on whether adverse effects could be anticipated from 

24 the Pb in terrestrial and aquatic ecosystems that results from air quality conditions allowed by the 

25 current, more restrictive NAAQS. As is discussed in section 2.3 below, media in ecosystems 

26 across the U.S. are still recovering from the past period of higher atmospheric emissions, and 

27 their responses (e.g., in terms of temporal change in media concentrations) differ with the extent 

28 of contamination in individual systems as well as with ecosystem-specific characteristics. Thus, 

29 the time required for these ecosystem media to “equilibrate” or come to a “steady-state” that 

30 reflects the influence of the current NAAQS (established in 2008) will also vary, and the 

31 resulting “steady-state” media concentrations for the range of U.S. ecosystems are unknown. 

32 Evidence of effects pertaining to the concentrations associated with the past, higher emissions (as 

33 well as from nonair sources), while informative to our understanding of welfare effects 

34 associated with environmental Pb generally, does not directly inform our consideration of 

 

13 The current distribution of Pb in U.S. ecosystems also reflects historical nonair releases. 
January 2013 Draft – Do Not Quote or Cite 1-15

1 welfare effects that might be anticipated under the current secondary standard and thus may be 

2 generally less informative in judging the adequacy of the current standard. 

3 1.4 GENERAL ORGANIZATION OF THE DOCUMENT 

4 Following this introductory chapter, this document is organized into three main parts: the 

5 characterization of ambient Pb; lead-related health effects and the primary Pb NAAQS; and lead6 related welfare effects and the secondary Pb NAAQS. The characterization of ambient Pb is 

7 presented in Chapter 2 and includes information on Pb properties in ambient air, current Pb 

8 emissions and air quality patterns, historic trends, and background levels. Chapter 2 also 

9 describes the Pb NAAQS surveillance and other Pb monitoring networks. In recognition of the 

10 multimedia nature of Pb and the distribution into other media of Pb emitted into the air, Chapter 

11 2 also includes information on Pb in media other than air including outdoor dust, soil, surface 

12 water and sediment. This chapter provides a frame of reference for exposure and risk-related 

13 considerations and subsequent discussion of the Pb NAAQS. 

14 Chapters 3 and 4 comprise the second main part of this document, dealing with human 

15 health and the primary standard. These chapters are organized around a series of questions, 

16 drawn from the IRP, that address the key policy-relevant issues related to the primary standard. 

17 Chapter 3 presents an overview of key policy-relevant health effects evidence and major health18 related conclusions from the ISA; an examination of issues related to the quantitative assessment 

19 of health risks; key results from quantitative assessments together with a discussion of 

20 uncertainty and variability in the results; and discussion of the public health implications of the 

21 evidence and exposure/risk information. In this draft PA, chapter 4 includes staff’s preliminary 

22 consideration of the scientific evidence and exposure/risk information related to the primary 

23 standard and associated preliminary conclusions on the adequacy of the current primary 

24 standard. 

25 Chapters 5 and 6 comprise the third main part of this document. These chapters are 

26 similarly organized around a series of questions, drawn from the IRP, that address the key 

27 policy-relevant issues related to the secondary standard. Chapter 5 presents an overview of 

28 welfare effects evidence related to these key policy-relevant issues and major welfare effects 

29 related conclusions from the ISA; an examination of issues related to the screening level 

30 ecological risk assessment; and key results from the risk assessment together with a discussion of 

31 uncertainty and variability in the results; and discussion of the public welfare implications of the 

32 quantitative assessment with regard to the current standard. The final chapter, chapter 6, 

33 includes staff’s preliminary conclusions related to the adequacy of the current secondary 

34 standard. 
January 2013 Draft – Do Not Quote or Cite 1-16

1 1.5 REFERENCES 

2 Frey, H.C. (2011a) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee Lead 

3 Review Panel, to Administrator Lisa P. Jackson. Re: Consultation on EPA’s Draft Integrated Review Plan 

4 for the National Ambient Air Quality Standards for Lead. May 25, 2011. 

5 Frey, H.C. (2011b) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee Lead 

6 Review Panel, to Administrator Lisa P. Jackson. Re: Consultation on EPA’s Review of the National 

7 Ambient Air Quality Standards for Lead: Risk and Exposure Assessment Planning Document. October 14, 

8 2011. 

9 Frey, H.C. and Samet, J.M. (2011) Letter from Drs. H. Christopher Frey, Chair, Clean Air Scientific Advisory 

10 Committee Lead Review Panel, and Jonathan M. Samet, Chair, Clean Air Scientific Advisory Committee, 

11 to Administrator Lisa P. Jackson. Re: CASAC Review of the EPA’s Integrated Science Assessment for 

12 Lead (First External Review Draft – May 2011). December 9, 2011. 

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

14 Selected Areas. Pilot Phase. Draft Technical Report. Prepared for the U.S. EPA's Office of Air Quality 

15 Planning and Standards, Research Triangle Park, NC. December. 

16 Jackson, L. (2009) Memorandum from Administrator Lisa Jackson, Subject: Development of regulations and 

17 policies. September 11, 2009. Available at: 

18 http://www.epa.gov/ttn/naaqs/pdfs/NAAQSReviewProcessMemo52109.pdf 

19 Samet, J.M. and Frey, H.C. (2012) Letter from Drs. Jonathan M. Samet, Chair, Clean Air Scientific Advisory 

20 Committee and H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee Lead Review Panel, 

21 to Administrator Lisa P. Jackson. Re: CASAC Review of the EPA’s Integrated Science Assessment for 

22 Lead (Second External Review Draft – February 2012). July 20, 2012. 

23 U.S. Environmental Protection Agency. (1977) Air quality criteria for lead. Research Triangle Park, NC: Health 

24 Effects Research Laboratory, Criteria and Special Studies Office; EPA report no. EPA-600/8-77-017. 

25 Available from: NTIS, Springfield, VA; PB-280411. 

26 U.S. Environmental Protection Agency. (1986a) Air quality criteria for lead. Research Triangle Park, NC: Office of 

27 Health and Environmental Assessment, Environmental Criteria and Assessment Office; EPA report no. 

28 EPA-600/8-83/028aF-dF. 4v. Available from: NTIS, Springfield, VA; PB87-142378. 

29 U.S. Environmental Protection Agency. (1986b) Lead effects on cardiovascular function, early development, and 

30 stature: an addendum to U.S. EPA Air Quality Criteria for Lead (1986). In: Air quality criteria for lead, v. 

31 1. Research Triangle Park, NC: Office of Health and Environmental Assessment, Environmental Criteria 

32 and Assessment Office; pp. A1-A67; EPA report no. EPA-600/8-83/028aF. Available from: NTIS, 

33 Springfield, VA; PB87-142378. 

34 U.S. Environmental Protection Agency. (1989) Review of the national ambient air quality standards for lead: 

35 Exposure analysis methodology and validation: OAQPS staff report. Research Triangle Park, NC: Office of 

36 Air Quality Planning and Standards; report no. EPA-450/2-89/011. Available on the web: 

37 http://www.epa.gov/ttn/naaqs/standards/pb/data/rnaaqsl_eamv.pdf

38 U.S. Environmental Protection Agency. (1990a) Air quality criteria for lead: supplement to the 1986 addendum. 

39 Research Triangle Park, NC: Office of Health and Environmental Assessment, Environmental Criteria and 

40 Assessment Office; report no. EPA/600/8-89/049F. Available from: NTIS, Springfield, VA; PB91-138420. 

41 U.S. Environmental Protection Agency. (1990b) Review of the national ambient air quality standards for lead: 

42 assessment of scientific and technical information: OAQPS staff paper. Research Triangle Park, NC: Office 
January 2013 Draft – Do Not Quote or Cite 1-17

1 of Air Quality Planning and Standards; report no. EPA-450/2-89/022. Available from: NTIS, Springfield, 

2 VA; PB91-206185. Available on the web: http://www.epa.gov/ttn/naaqs/standards/pb/data/rnaaqsl_asti.pdf

3 U.S. Environmental Protection Agency. (1991) U.S. EPA Strategy for Reducing Lead Exposure. Available from 

4 U.S. EPA Headquarters Library/Washington, D.C. (Library Code EJBD; Item Call Number: EAP 

5 100/1991.6; OCLC Number 2346675). http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_pr.html 

6 U.S. Environmental Protection Agency. (2005) Project Work Plan for Revised Air Quality Criteria for Lead. 

7 CASAC Review Draft. National Center for Environmental Assessment, Research Triangle Park, NC. 

8 NCEA-R-1465. Available at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html 

9 U.S. Environmental Protection Agency. (2006a) Plan for Review of the National Ambient Air Quality Standards for 

10 Lead. Office of Air Quality Planning and Standards, Research Triangle Park, NC. Available at: 

11 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html 

12 U.S. Environmental Protection Agency. (2006b) Air Quality Criteria for Lead. Washington, DC, EPA/600/R13 5/144aF. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html 

14 U.S. Environmental Protection Agency. (2006c) Analysis Plan for Human Health and Ecological Risk Assessment 

15 for the Review of the Lead National Ambient Air Quality Standards. Office of Air Quality Planning and 

16 Standards, Research Triangle Park, NC. Available at: 

17 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html 

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

19 Case Studies, Volume I. Human Exposure and Health Risk Assessments – Full-Scale and Volume II. 

20 Appendices. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA-452/R-07-

21 014a and EPA-452/R-07-014b. http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_td.html 

22 U.S. Environmental Protection Agency. (2007b) Review of the National Ambient Air Quality Standards for Lead: 

23 Policy Assessment of Scientific and Technical Information, OAQPS Staff Paper. Office of Air Quality 

24 Planning and Standards, Research Triangle Park, NC. EPA-452/R-07-013. Available at: 

25 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_sp.html 

26 U.S. Environmental Protection Agency. (2011a) Integrated Review Plan for the National Ambient Air Quality 

27 Standards for Lead. Research Triangle, NC. EPA-452/R-11-008. Available online at: 

28 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html 

29 U.S. Environmental Protection Agency. (2011b) Review of the National Ambient Air Quality Standards for Lead: 

30 Risk and Exposure Assessment Planning Document. Office of Air Quality Planning and Standards, 

31 Research Triangle Park, NC. EPA/452/P-11-003. Available at: 

32 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pd.html 

33 U.S. Environmental Protection Agency. (2011c) Integrated Review Plan for the National Ambient Air Quality 

34 Standards for Lead. External Review Draft. Research Triangle, NC. EPA-452/D-11-001. Available online 

35 at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html 

36 U.S. Environmental Protection Agency. (2011d) Integrated Science Assessment for Lead (First External Review 

37 Draft). Washington, DC, EPA/600/R-10/075A. Available online at: 

38 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html 

39 U.S. Environmental Protection Agency. (2012a) Integrated Science Assessment for Lead (Third External Review 

40 Draft). Washington, DC, EPA/600/R-10/075C. Available online at: 

41 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html 
January 2013 Draft – Do Not Quote or Cite 1-18

1 U.S. Environmental Protection Agency. (2012b) Integrated Science Assessment for Lead (Second External Review 

2 Draft). Washington, DC, EPA/600/R-10/075B. Available online at: 

3 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html 
January 2013 Draft – Do Not Quote or Cite 2-1

1 2 AMBIENT AIR LEAD 

2 The focus for this Pb NAAQS review is on Pb derived from those sources emitting Pb to 

3 ambient air. As noted in section 1.3, air emissions contribute to concentrations in multiple 

4 environmental media and the role of the nonair media is enhanced by the persistent nature of Pb. 

5 Consequently this chapter discusses our current understanding of Pb in ambient air and of 

6 ambient air-related Pb in other media. 

7 Lead emitted to the air is predominantly in particulate form, with the particles occurring 

8 in various sizes (ISA, section 3.3.1). While in some limited circumstances associated with 

9 incomplete combustion of leaded gasoline, Pb may be emitted in gaseous form, atmospheric 

10 conditions readily contribute to condensation into particles (ISA, section 3.2). Once emitted, Pb 

11 can be transported long or short distances depending on their size, which influences the amount 

12 of time spent in the aerosol phase. Consistent with previous evidence, recent research on 

13 particulate matter with mass median diameter of 2.5 and of 10 micrometers (PM2.5 and PM10) 

14 confirms the transport of airborne Pb appreciable distances from its sources. For example, 

15 samples collected at altitude over the Pacific Ocean, as well as the seasonal pattern of Pb-PM2.5

16 at rural sites in the western U.S. indicate transport of Pb from sources in Asia, although such 

sources have been estimated to contribute less than 1 ng/m3 17 to western U.S. Pb concentrations 

18 (ISA, section 3.3.1; Murphy et al., 2007). As a generality, larger particles tend to deposit more 

19 quickly, within shorter distances from emissions points, while smaller particles remain in aerosol 

20 phase and travel longer distances before depositing (ISA, section 2.2.1). As summarized in 

21 section 2.2.2 below, airborne concentrations of Pb near sources are much higher, and the 

22 representation of larger particles generally greater, than at sites not directly influenced by 

23 sources. 

24 In this chapter, we discuss the current information on ambient Pb regarding sources and 

25 emissions (section 2.1), current ambient air monitoring methods and networks and associated 

26 measurements (section 2.2) and the contribution of ambient air Pb to Pb in other media (section 

27 2.3). 

28 2.1 SOURCES AND EMISSIONS TO AMBIENT AIR 

29 In this section we describe the most recently available information on sources and 

30 emissions of Pb into the ambient air. The section does not provide a comprehensive list of all 

31 sources of Pb, nor does it provide estimates of emission rates or emission factors for all source 

32 categories. Rather, the discussion here is intended to identify the larger source categories, either 

33 on a national or local scale, and generally describe their emissions and distribution within the 

34 U.S. 
January 2013 Draft – Do Not Quote or Cite 2-2

1 The primary data source for this discussion is the National Emissions Inventory (NEI) for 

20081 2 . The NEI is a comprehensive and detailed estimate of air emissions of both criteria and 

3 hazardous air pollutants from air emissions sources. The NEI is generally prepared every three 

4 years by the EPA based primarily upon emission estimates and emission model inputs provided 

5 by state, local, and tribal air agencies for sources in their jurisdictions, and supplemented by data 

6 developed by the EPA. Some of these estimates are required by regulation while some are 

7 voluntarily reported. For example, states are required to report Pb emissions from facilities 

8 emitting more than 5 tons of Pb per year (tpy) and from facilities emitting greater than threshold 

9 amounts for other criteria pollutants (e.g., 100 tpy of particulate matter or volatile organic 

10 compounds; CFR 51, subpart A). Estimates of Pb emissions presented in this document (and in 

the ISA) are drawn from the 2008 NEI version 3.2 11 As a result of various Clean Air Act 

12 requirements, emissions standards implemented since 2008 for a number of source categories 

13 represented in the NEI are projected to result in considerably lower emissions at the current time 

14 or in the near future. 

15 The following sections present information relative to 2008 Pb emissions on a national 

16 and local scale. Lead is emitted from a wide variety of source types, some of which are small 

17 individually but for which the cumulative emissions are large, and some for which the opposite is 

18 true. For example, a source category may be composed of many small (i.e., low-emitting) 

19 sources or of just a few very large (high-emitting) sources. Temporal trends in the national totals 

20 of Pb emissions are presented in Section 2.1.1. Information about the emissions source types or 

21 categories that are large on a national scale as of 2008 is presented in Section 2.1.2, while 

22 information on the sources that are large at the local scale is presented in Section 2.1.3. 

23 Additional information on data sources for, limitations of and our confidence in the information 

24 summarized here is described in Appendix 2A. 

25 2.1.1 Temporal Trends on a National Scale 

26 Figure 2-1 shows the substantial downward trend in Pb emissions that has occurred over 

27 the past several decades. The most dramatic reductions in Pb emissions occurred prior to 1990 

28 in the transportation sector due to the removal of Pb from gasoline. Lead emissions were further 

29 reduced substantially between 1990 and 2008, with significant reductions occurring in the metals 

30 industries at least in part as a result of national emissions standards for hazardous air pollutants. 

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 

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

10 

11 2.1.2 Sources and Emissions on National Scale - 2008 

12 As indicated in Figure 2-1, the largest source sector emitting Pb into the atmosphere on a 

13 national scale is aviation gasoline usage by piston engine driven aircraft. The next largest 

14 nationally is metal working and mining. Considering the national estimates at a more detailed 

15 scale, the largest source categories emitting Pb into the atmosphere on a national scale, after 

16 emissions from aircraft operating on leaded fuel, are boilers and process heaters (fuel 

17 combustion) which, while individually are generally small sources, are large when aggregated 

18 nationally (Table 2-1). The next largest categories are various metals industries, including lead19 specific industries (Table 2-1). Together these and other sources were estimated to emit just 

20 under a thousand tpy of Pb in the U.S. in 2008. 
January 2013 Draft – Do Not Quote or Cite 2-4

1 Table 2-1. U.S. lead emissions by source categories estimated to emit at least 4 tpy. 

Source Category Description 2008 

Emissions (tons) 

ALL CATEGORIES A 950 

Aircraft operating on leaded fuel B 550 

Industrial/Commercial/Institutional Boilers & Process Heaters 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 Emissions 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 emissions 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 2.1.2.1 Stationary Sources 

3 Since the last review of the Pb NAAQS, the EPA has completed a number of regulations 

4 which will result in reduced Pb emissions from stationary sources regulated under the Clean Air 

5 Act sections 112 and 129. For example, in January 2012, the EPA updated the National 

6 Emission Standards for Hazardous Air Pollutants (NESHAP) for Secondary Lead Smelting (77 

7 FR 555). These amendments to the original maximum achievable control technology standards 

8 apply to facilities nationwide that use furnaces to recover lead from lead-bearing scrap, mainly 

9 from automobile batteries (15 existing facilities, one under construction). By the effective date 

10 in 2014, this action is estimated to result in a lead emissions reduction of 13.6 tpy across the 

11 category (a 68% reduction). Also, the NESHAP for Primary Lead Smelting was revised in 2011 

12 (76 FR 70834) and more than a dozen additional EPA actions taken in the past 5 years, which 

13 would not be reflected in the 2008 NEI estimates, will result in Pb emissions reductions 

14 (Appendix 2B). 

15 

Explanation of aggregation approaches used for Tables 2-1 and 2-2: 

Facilities have numerous processes that can fall into different source categories and the NEI includes process-specific 

emissions estimates. Source categories are groups of facilities that can be considered as the same type of emissions 

source. In order to present the emissions for source categories (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. The source categories used were assigned using a three-tiered 

approach. First, processes known to be affected by sector-specific rules were set to the source categories. This was done 

for Utility Boilers, Portland Cement plants, Electric Arc Furnaces, Municipal Waste Combustors, and Taconite Ore facilities 

(mapped to Integrated Iron and Steel Manufacturing). Other source categories did not use this first tier because the 

processes in the inventory have not yet been mapped to other rules. Second, for processes that clearly map to source 

categories, the inventory process descriptions (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 source 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 identified for the facility, which usually confirmed the NAICS code. 

A facility only has a single Facility Type but can have multiple 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 Secondary 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, the emissions for these facilities are split across multiple 

processes as summed in Table 2-1. To prevent double counting 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

1 2.1.2.2 Mobile Sources 

2 Forty years ago, combustion of leaded gasoline was the main contributor of Pb to the air. 

3 In the early 1970s, the EPA set national regulations to gradually reduce the Pb content in 

4 gasoline. In 1975, unleaded gasoline was introduced for motor vehicles equipped with catalytic 

5 converters. The EPA banned the use of leaded gasoline in highway vehicles after December 

6 1995. 

7 Lead emissions from piston-engine aircraft operating on leaded fuel are currently the 

8 largest source of Pb air emissions on a national scale. Lead is added to aviation gasoline 

9 (commonly referred to as “avgas”) used in most piston-engine aircraft in order to boost octane 

and prevent engine knock.3 10 The most commonly used avgas, 100 Octane Low Lead, contains up 

11 to 2.12 grams Pb per gallon (ASTM D 910). The Federal Aviation Administration estimates that 

in 2008, 248 million gallons of avgas were consumed in the U.S.4 12 contributing an estimated 550 

tons of Pb to the air that comprise 57% of the national Pb inventory.5 13 Leaded avgas is used at 

14 approximately 20,000 airport facilities in the U.S. 

15 The EPA is currently collecting and evaluating information regarding emissions and air 

16 concentrations of lead resulting from avgas combustion by piston-engine aircraft. This is part of 

17 an ongoing investigation under section 231 of the Clean Air Act into the potential for these 

18 emissions to cause or contribute to air pollution that may reasonably be anticipated to endanger 

19 public health or welfare. This evaluation by the EPA is occurring separate from the NAAQS 

20 review. The EPA’s investigation includes substantial analytical work. The timeline for 

21 completion of this investigation and possible issuance of a final endangerment determination 

22 includes completion of necessary modeling and monitoring information and other data, 

23 development of a proposal which will be published for public comment, review and analysis of 

24 comments received and issuance of the final determination. If the EPA issues a positive 

25 determination that Pb emissions from aircraft engines cause or contribute to air pollution that 

26 may reasonably be anticipated to endanger public health or welfare, the EPA would then be 

27 required to propose and promulgate emissions standards to control aircraft engine Pb emissions, 

28 and the Federal Aviation Administration would be required to promulgate regulations addressing 

 

3

 Lead is not added to jet fuel used in commercial aircraft, military aircraft, or other turbine engine aircraft. 4 U.S. Department of Transportation Federal Aviation Administration Aviation Policy and Plans. FAA

Aerospace Forecast Fiscal Years 2010-2030. p.99. Available at: 

http://www.faa.gov/about/office_org/headquarters_offices/apl/aviation_forecasts/aerospace_forecasts/2010-

2030/media/2010%20Forecast%20Doc.pdf This document provides historical 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.pdf 
January 2013 Draft – Do Not Quote or Cite 2-7

1 the fuel used by those aircraft. More information about EPA’s actions is available at 

2 www.epa.gov/otaq/aviation.htm. 

3 Vehicles used in racing are not regulated by the EPA under the Clean Air Act and can 

4 therefore use alkyl-Pb additives to boost octane. The National Association for Stock Car Auto 

5 Racing (NASCAR) formed a voluntary partnership with the EPA with the goal of permanently 

6 removing alkyl-Pb from racing fuels used in the racing series now known as the Sprint Cup, the 

7 Nationwide Series and the Camping World Truck Series. The major NASCAR race series now 

8 use unleaded fuels. 

9 Due to the presence of Pb as a trace contaminant in gasoline, diesel fuel and lubricating 

10 oil, cars, trucks, and engines operating in nonroad equipment, marine engines and jet aircraft 

11 emit small amounts of Pb (ISA, Section 3.2.2.6). Additional mobile sources of Pb include brake 

12 wear, tire wear, and loss of Pb wheel weights (ISA, Section 3.2.2.6). 

13 2.1.2.3 Natural Sources and Long-range Transport 

14 Some amount of Pb in the air derives from natural sources, such as volcanoes, sea salt, 

15 and windborne soil particles from areas free of anthropogenic activity and some may also derive 

16 from anthropogenic sources of airborne Pb located outside of the U.S. (ISA, section 3.5.5). 

17 Emissions estimates for these sources, as well as wild forest fires and biogenic sources have not 

18 been developed for the NEI and quantitative estimates for these processes remain an area of 

19 significant uncertainty. Based on several different approaches, the ISA identifies several 

20 estimates of the concentration of airborne Pb derived from natural sources. All of the estimates 

are no higher than 1 nanogram per cubic meter (ng/m3

), and range down as low as 0.02 ng/m3 21 

22 (ISA, section 3.5.5). The data available to derive such an estimate are limited and such a value 

23 might be expected to vary geographically with the natural distribution of Pb. 

24 Another contribution to U.S. airborne Pb concentrations is long-range transport such as 

25 that associated with air masses carrying Pb from sources in Asia, where controls on Pb emissions 

26 have lagged those in the U.S. and Canada (ISA, section 3.5.5; Osterberg et al., 2008). The most 

27 recent estimates of contributions from Asia, however, conclude that the Asian contribution to 

U.S. airborne Pb concentrations is generally less than 1 ng/m3 28 (ISA, section 3.5.5; Murphy, 

29 2007; Ewing et al., 2010). 

30 2.1.2.4 Previously Deposited or Released Lead 

31 Lead-bearing particles that occur on surface soils or built surfaces as a result of previous 

32 or historic deposition can be a source of airborne Pb as a result of particle resuspension and may 

33 be a significant source of airborne Pb in areas near major sources of Pb emissions. Outdoor dust 

34 may be resuspended into the air by wind or human-induced mechanical forces, such that the 

35 main drivers of particle resuspension are typically mechanical stressors such as vehicular traffic, 
January 2013 Draft – Do Not Quote or Cite 2-8

1 construction and agricultural operations, and, generally to a lesser extent, the wind (ISA, section 

2 3.3.1.3; 2006 CD, section 2.3.3). Wind resuspension is often defined in terms of a resuspension 

3 rate, which is the fraction of a surface contaminant released per unit time. Resuspension rates 

4 are dependent on many factors, including wind speed, soil/surface moisture, particle sizes, 

5 presence of saltating particles and presence of vegetation; typical values range over several 

6 orders of magnitude (ISA, section 3.3.1.3; 2006 CD, section 2.3.3). Vehicular resuspension 

7 results from shearing stress of tires or turbulence generated by a passing vehicle and can be 

8 affected by a number of factors including vehicle size, vehicle speed, moisture and particle size 

9 (ISA, section 3.3.1.3; 2006 CD, section 2.3.3). Additionally, the amount of material available 

10 for resuspension can be influenced by removal processes such as surface runoff associated with 

11 rainfall (ISA, sections 2.2.1, 3.3.2 and 3.3.2.4). Rather than a continuous process, resuspension 

12 may occur as a series of events. Short episodes of conditions or factors conducive to 

13 resuspension may dominate annual averages of upward flux (2006 CD, p. 2-65). Variability and 

14 uncertainty in these factors, and with regard to surface soil/dust composition, affect quantitative 

emissions estimates for these processes (2006 CD, section 2.3.3).6 15 

16 Consideration of Pb concentrations in air and surface soil/dust in different types of 

17 locations also informs our understanding of the relative importance of resuspension of previously 

18 deposited dust particles as an influence on airborne Pb concentrations. The relative importance 

19 would be expected to vary with site-specific circumstances, such as the magnitude of Pb 

20 concentrations in the surface dust and air Pb contributions from nearby sources of new Pb 

21 emissions, as well as with variation in the forces that influence particle resuspension. For 

22 example, the contribution of resuspension to airborne concentrations appears to be greatest in 

23 areas of highly contaminated surface dust such as at historically active industrial sites, which 

24 may or may not be currently active (ISA, sections 3.3.1.3 and 3.5.3). 

25 Emissions from currently active metals industries include those related to current 

26 industrial activity and to resuspension of previously deposited material (often a component of 

“fugitive” emissions estimates7 27 ). Accordingly, the relative magnitude of air Pb concentrations 

28 associated with no longer active industries would be expected to generally be lower than that for 

 

6

 Quantitative estimates of resuspension-related emissions associated with many active industrial sources 

(particularly metals sources) are included within the NEI, although such emissions associated with previously and 

no longer active Pb sources are not as generally included in the NEI. 7

 For example, emissions factors have been established to estimate fugitive emissions from resuspension of 

previously deposited material as a result of vehicular traffic on facility roadways (USEPA, 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 facility. Accordingly, control of resuspension resulting from 

facility roadways, buildings or other property may be part of a strategy to meet regulatory 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

1 active industries yet greater than that in locations somewhat removed from industrial sources. 

2 The limited available data for comparison generally confirms this (section 2.2.2.2 below). 

3 Lead-bearing particulate matter in other, non-industrial, locations of appreciable historic 

4 lead contamination, such as in soils or on surfaces in older urban areas or near older 

5 transportation corridors may, if disturbed, also become suspended into the air and contribute to 

6 air Pb concentrations. In older transportation corridors or other locations not influenced by 

7 active industries, the significance of resuspension (e.g., in terms of resultant air Pb 

8 concentrations) appears to be much less that that associated with active industries or now closed 

industries with substantial emissions in the past.8 9 For example, the available data indicate that 

10 current Pb concentrations near roadways are substantially lower than those near large, currently 

11 active industrial sources (see ISA, section 3.3.1.3 and Figures 2-9 and 2-11 below). In general, 

12 air Pb concentrations at sites described as not influenced by an active industry are much lower 

13 than those near active sources (see ISA, section 3.5.1.2 and Figure 2-11 below). 

14 2.1.3 Sources and Emissions on Local Scale 

15 Based on the 2008 estimates, the highest emissions in specific (local) situations are 

16 different types of metals industries, 23 of which had 2008 estimates greater than or equal to 1.0 

17 tpy Pb (Table 2-2). The geographic distribution of the facilities summarized in Table 2-2 is 

18 presented in Figure 2-2. 

19 

 

8

 Mass-balance analyses of emissions in southern California 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

1 Table 2-2. Facilities estimated to emit at least 0.50 tpy in 2008. 

Facility Type 

Facilities emitting ≥ 1.0 tpyA,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 19.2D 

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 

Primary Non-ferrous Metal Smelting/Refining Plant

(not Lead, Aluminum, or Copper) 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 operations at this site by April, 2014 (DRRC, 2010).
January 2013 Draft – Do Not Quote or Cite 2-11

1 2 Figure 2-2. Geographic distribution of facilities estimated to emit at least 0.50 tpy in 2008. 

* 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

1 2.2 AMBIENT AIR QUALITY 

2 The EPA and state and local agencies have been measuring Pb in the atmosphere since 

3 the 1970s. In response to reduced emissions (see section 2.1), Pb concentrations have decreased 

4 dramatically over that period. Currently, the highest concentrations occur near some metals 

5 industries where some individual locations have concentrations that exceed the NAAQS. This 

6 section describes the ambient Pb measurement methods, the sites and networks where these 

7 measurements are made, and how the ambient Pb concentrations vary geographically and 

8 temporally. 

9 2.2.1 Air Monitoring 

10 Ambient air Pb concentrations are measured by five national monitoring networks. The 

11 networks include the State and Local Air Monitoring Sites (SLAMS) intended for Pb NAAQS 

12 surveillance, the PM2.5 Chemical Speciation Network (CSN), the Interagency Monitoring of 

13 Protected Visual Environments (IMPROVE) network, the National Air Toxics Trends Stations 

14 (NATTS) network, and the Urban Air Toxics Monitoring program. All of the data from these 

15 networks are accessible via EPA’s Air Quality System (AQS): 

16 http://www.epa.gov/ttn/airs/airsaqs/. In addition to these networks, various environmental 

17 organizations have operated other sampling sites yielding data (which may or may not be 

18 accessible via AQS) on ambient air concentrations of Pb, often for limited periods and/or for 

19 primary purposes other than quantification of Pb itself. The subsections below describe each 

20 network and the Pb measurements made at these sites. 

21 2.2.1.1 Lead NAAQS Surveillance Network 

22 This section describes sample collection, analysis and network aspects for the Pb SLAMS 

23 network, the main purpose of which is surveillance of the Pb NAAQS. As such, the EPA 

24 regulates how this monitoring is conducted in order to ensure accurate and comparable data for 

25 determining compliance with the NAAQS. The code of federal regulations (CFR) at parts 50, 53 

and 58 specifies required aspects of the ambient monitoring program for NAAQS pollutants.9 26 In 

27 order to be used in NAAQS attainment designations, ambient Pb concentration data must be 

28 obtained using either the federal reference method (FRM) or a federal equivalent method (FEM). 

The indicator for the current Pb NAAQS is Pb-TSP. However, in some situations,10 29 ambient Pb-

 

9

 The federal 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 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-PM10 measurements may be used for NAAQS monitoring as an alternative to Pb-TSP 

measurements in certain conditions defined in 40 CFR part 58 Appendix D paragraph 2.10.1.2. These conditions 
January 2013 Draft – Do Not Quote or Cite 2-13

1 PM10 concentrations may be used in judging nonattainment. Accordingly, FRMs have been 

2 established for Pb-TSP and for Pb-PM10. The current FRM for the measurement of Pb-TSP is 

3 provided in 40 CFR part 50 Appendix G. This FRM includes sampling using a high-volume 

4 TSP sampler that meets the design criteria identified in 40 CFR part 50 Appendix B and sample 

5 analysis for Pb content using flame atomic absorption. There are 24 FEMs currently approved 

for Pb-TSP.11 6 All 24 FEMs are based on the use of high-volume TSP samplers and a variety of 

7 approved equivalent analysis methods. 

8 A new FRM for Pb-PM10 was promulgated as part of the 2008 review. This FRM is 

9 based on the PM10 sampler defined in 40 CFR part 50 Appendix J coupled with x-ray 

10 fluorescence (XRF) analysis. In addition, one FEM for Pb-PM10 has been finalized for the 

11 analysis of Pb-PM10 based on inductively coupled plasma mass spectroscopy (ICP-MS). 

12 The current Pb monitoring network design requirements for NAAQS compliance 

13 purposes (40 CFR part 58, Appendix D, paragraph 4.5) include two types of monitoring sites – 

14 source-oriented monitoring sites and non-source-oriented monitoring sites. Source-oriented 

15 monitoring sites are required near sources of air Pb emissions which are expected to or have been 

16 shown to contribute to ambient air Pb concentrations in excess of the NAAQS. At a minimum, 

17 there must be one source-oriented site located to measure the maximum Pb concentration in 

18 ambient air resulting from each non-airport Pb source estimated to emit 0.50 or more tons of Pb 

per year and from each airport estimated to emit 1.0 or more tons of Pb per year.12 19 The EPA 

20 Regional Administrators may require additional monitoring beyond the minimum requirements 

21 where the likelihood of Pb air quality violations is significant. Such locations may include those 

22 near additional industrial Pb sources, recently closed industrial sources and other sources of 

23 resuspended Pb dust, as well as airports where piston-engine aircraft emit Pb (40 CFR, part 58, 

24 Appendix D, section 4.5(c)). 

25 Monitoring agencies are also required, under 40 CFR, part 58, Appendix D, to conduct 

26 non-source-oriented Pb monitoring at the NCore sites required in Core metropolitan with a 

population of 500,000 or more.13 27 NCore is a new network of multipollutant monitoring stations 

 

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 PM10 monitors. 11 A complete list of FEM can be found at the following webpage - 

http://www.epa.gov/ttn/amtic/files/ambient/criteria/reference-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 concentration 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.census.gov/population/www/metroareas/metroarea.html 
January 2013 Draft – Do Not Quote or Cite 2-14

1 intended to meet multiple monitoring objectives. The NCore stations are a subset of the state and 

2 local air monitoring stations network and are intended to support long-term trends analysis, 

3 model evaluation, health and ecosystem studies, as well as NAAQS compliance. The complete 

4 NCore network consists of approximately 60 urban and 20 rural stations, including some existing 

5 SLAMS sites that have been modified for additional measurements. Each state will contain at 

6 least one NCore station, and 46 of the states plus Washington, DC, will have at least one urban 

7 station. 

8 Either Pb-TSP or Pb-PM10 monitoring may be performed at these sites. Of 24 NCore 

9 sites measuring Pb concentrations, 17 are measuring Pb in TSP and 7 are measuring Pb in PM10. 

10 While non-source-oriented monitoring data can be used for purposes of NAAQS attainment 

11 designations, a main objective for non-source-oriented monitoring is to gather information on 

12 neighborhood-scale lead concentrations that are typical in urban areas in order to better 

13 understand ambient air-related Pb exposures for populations in these areas. 

14 Source-oriented monitors near sources estimated to emit 1.0 tpy Pb were required to be 

15 operational by January 1, 2010, and the remainder of the newly required source-oriented 

16 monitors were required to be operational by December 27, 2011 (75 FR 81126). Currently, 

17 approximately 260 Pb-TSP monitors are in operation; these are a mixture of source- and non18 source-oriented monitors. Figure 2-3 shows the geographic distribution of these monitors (in 

addition to the airport study monitors described below) in the current14 19 Pb NAAQS surveillance 

20 network, with the Pb-TSP monitors existing at the time of the 2008 rulemaking indicated 

21 separately from the newly sited Pb-TSP monitors. 

 

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

1 

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

Network.15 3 

4 The current regulations also required one year of Pb-TSP monitoring (using FRM or 

5 FEM methods) near 15 specific airports in order to gather additional information on the 

6 likelihood of NAAQS exceedances near airports due to the combustion of leaded aviation 

7 gasoline (75 FR 81126). These airports were selected based on three criteria: annual Pb 

8 inventory between 0.5 ton/year and 1.0 ton/year, ambient air within 150 meters of the location of 

9 maximum emissions (e.g., the end of the runway or run-up location), and airport configuration 

10 and meteorological scenario that leads to a greater frequency of operations from one runway. 

11 These characteristics were selected because they are expected, collectively, to identify airports 

12 with the highest potential to have ambient Pb concentrations approaching or exceeding the Pb 

13 NAAQS. Data from this monitoring study will be used to assess the need for additional Pb 

 

15 Estimates for source-oriented monitors are based on Pb emissions estimates in the 2008 National 

Emissions Inventory. 
January 2013 Draft – Do Not Quote or Cite 2-16

1 monitoring at airports. These 15 sites (Figure 2-4) were intended to be operational no later than 

2 December 27, 2011, although delays in monitor siting extended the installation of some of these 

3 monitors into late 2012. 

4 

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

6 

7 2.2.1.2 Other Lead Monitoring Networks 

8 The NATTS network, designed to monitor concentrations of hazardous air pollutants 

9 including lead compounds, included 25 sites measuring Pb-PM10 as of June 2012. Most of these 

10 sites (20) are in urban areas (Figure 2-5). In addition to the NATTS network, states collect Pb11 PM10 at an additional 28 sites (most as part of the Urban Air Toxics Monitoring program). All 

12 collect particulate matter as PM10 for toxic metals analysis using either a high-volume PM10

13 sampler or a low volume PM10 sampler, typically on a 1 in 6 day sampling schedule. Most of 

14 these monitoring locations are not measuring using FRM/FEM methods at this time. Lead in the 

 

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 2-17

1 collected sample is generally quantified via an ICP/MS method. The standard operating 

2 procedure for metals by ICP/MS is available at: http://www.epa.gov/ttn/amtic/airtox.html. 

3 

4 Figure 2-5. Pb-PM10 monitoring sites. 

5 Two networks measure Pb in PM2.5, the EPA CSN and the IMPROVE network. The 

6 CSN consists of 53 long-term trends sites (commonly referred to as the Speciation Trends 

7 Network or STN sites) and approximately 150 supplemental sites, all operated by state and local 

8 monitoring agencies. Most STN sites operate on a 1 in 3 day sampling schedule, while most 

9 supplemental sites operate on a 1 in 6 day sampling schedule. All sites in the CSN network 

determine Pb concentrations in PM2.5 samples. Lead is quantified via the XRF method.17 10 Data 

11 are accessible through AQS. The locations of the CSN are shown in Figure 2-6. Nearly all of the 

12 CSN sites are in urban areas, often at the location of highest known PM2.5 concentrations. The 

13 first CSN sites began operation around 2000. 

 

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

1 The IMPROVE network is administered by the National Park Service, largely with 

2 funding by the EPA, on behalf of federal land management agencies and state air agencies that 

3 use the data to track trends in rural visibility. Lead in PM2.5 is quantified via the XRF method, as 

4 in the CSN. Data are managed and made accessible mainly through the VIEWS website 

5 (http://vista.cira.colostate.edu/views/) but are also available via AQS. Samplers are operated by 

6 several different federal, state, and tribal host agencies on the same 1 in 3 day schedule as the 

7 STN. In the IMPROVE network, PM2.5 monitors are placed in “Class I” areas (including 

8 National Parks and wilderness areas) and are mostly in rural locations (Figure 2-6). The oldest 

9 of these sites began operation in 1988, while many others began in the mid 1990s. There are 110 

10 formally designated IMPROVE sites, which are located in or near national parks and other Class 

11 I visibility areas, virtually all of these being rural. Approximately 80 additional sites at various 

12 urban and rural locations, requested and funded by various parties, are also informally treated as 

13 part of the network. 

14 

15 Figure 2-6. Pb-PM2.5 monitoring sites in CSN and IMPROVE networks (2012). 

16 
January 2013 Draft – Do Not Quote or Cite 2-19

1 2.2.1.3 NAAQS Surveillance Monitoring Considerations 

2 In this section aspects of the methods for sampling and analysis of the Pb are reviewed, 

3 and the current NAAQS surveillance network of monitoring locations is considered. The 

4 methods for sampling and analysis are considered in light of the indicator for the Pb NAAQS, 

5 and conclusions regarding the current NAAQS and associated indicator appear in chapter 4. 

6 Consideration of the ambient air monitoring network generally informs the interpretation of 

7 current data on ambient air concentrations and helps identify whether the monitoring network is 

8 adequate to determine compliance with the NAAQS. This section discusses considerations 

related to these aspects of the ambient air monitoring program for Pb.18 9 

10 2.2.1.3.1 Sampling Considerations 

11 As described in section 2.2.1.1 above, consistent with the Pb NAAQS indicator being Pb12 TSP, the FRM for Pb, which is required at all source-oriented sites, is measurement of Pb-TSP 

13 using a high-volume TSP sampler meeting the design criteria specified in 40 CFR part 50 

14 Appendix B. During the review of the Pb NAAQS completed in 2008, CASAC noted the 

15 variability in high-volume TSP sample measurements associated with the effects of wind speed 

16 and wind direction on collection efficiency in their comments regarding the indicator. However, 

17 at the time of the 2008 review, no alternative TSP sampler designs were identified that had an 

18 adequate characterization of their collection efficiency over a wide range of particle sizes. The 

19 existing high-volume sampler was retained as the sampling approach for the Pb-TSP FRM and 

20 FEMs. 

21 Since promulgation of the 2008 Pb NAAQS, the EPA has initiated an effort to review 

22 alternative sampler designs in an effort to develop a new sampler to replace the current high23 volume Pb-TSP sampler. Efficient collection of particles much larger than 10 μm is 

24 considerably more challenging because the greater inertia and higher settling velocities of Pb 

25 particles hinder their efficient intake by samplers. The sampling difficulties and the long history 

26 of research to develop adequate sampling technology for large particles have been thoroughly 

27 reviewed (Garland and Nicholson, 1991). Some existing commercially available sampler inlets 

28 are designed to collect particles larger than 10 μm with greater than 50% efficiency (Kenny et 

29 al., 2005), and these inlets can be tested as potential replacements for TSP sampling. However, 

30 no alternatives to the FRM TSP sampler have been identified that have been adequately 

31 characterized. 

 

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 federal 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

1 The EPA has initiated efforts to characterize the collection efficiency of alternative 

2 sampler designs through wind tunnel testing as a necessary step towards the development of a 

3 new sampler capable of sampling particles larger than PM10 without the noted wind speed and 

4 wind direction biases. In addition to the difficulties in collection of particles much larger than 10 

5 μm, physical limitations in the ability to generate and transport ultra-coarse particles limit the 

6 ability to adequately characterize the new sampler. These limitations ultimately limit the upper 

7 cut-point of potential samplers to the range of 18-20 micrometers. Following characterization in 

8 a wind tunnel, field testing of promising candidates would be required to evaluate performance 

9 and to make comparisons to the existing Pb-TSP samplers. This effort is expected to take 

10 several years to complete, and, as such, it is unlikely that this new sampler will be available in 

11 time for consideration during this NAAQS review due to the activities which will need to be 

12 completed to adequately characterize its performance both in the laboratory and the field. We 

13 expect the new sampler to be available for consideration in a future review and consequently do 

14 not expect to consider new alternatives for sampling methods for Pb-TSP as part of this review. 

15 In addition to the FRM for Pb-TSP, there is also, as noted in section 2.2.1.1 above, a 

16 FRM for Pb-PM10, based on the PM10 sampler defined in 40 CFR part 50 Appendix J coupled 

17 with XRF analysis. The Pb-PM10 measurements may be used as an alternative to Pb-TSP 

18 measurements in certain conditions defined in 40 CFR part 58 Appendix D paragraph 2.10.1.2. 

19 These conditions include where Pb concentrations are not expected to equal or exceed 0.10 

20 micrograms per cubic meter on an arithmetic 3-month mean and where the source of Pb 

21 emissions is expected to emit a substantial majority of its Pb in the PM10 size fraction. At this 

22 time, we believe the low-volume FRM sampler for Pb-PM10 to be adequate for this application. 

23 Hence, we do not expect to consider new sampling methods for Pb-PM10 as part of this review. 

24 2.2.1.3.2 Analysis Considerations 

25 Due to reduced availability of laboratories capable of performing flame atomic 

26 adsorption analyses and general advances in analysis methods, the EPA has initiated an effort to 

27 expand FRM analysis methods beyond atomic adsorption to include the more modern analysis 

28 method, ICP-MS. A consultation with the CASAC Ambient Air Monitoring and Methods 

29 Subcommittee was held on September 15, 2010 (Russell and Samet, 2010), and the EPA plans to 

30 propose a new FRM for Pb-TSP based on this more modern analysis method in 2013. In 

31 addition, the EPA has approved several new FEMs (for ICP-MS and other analysis methods) 

32 since the last Pb NAAQS review was completed in 2008. 

33 With regard to Pb-PM10 samples, in addition to the FRM analysis method (XRF), two 

34 FEMs have been accepted for Pb-PM10 analysis since the 2008 Pb NAAQS rulemaking. These 

35 methods are based on ICP-MS and are consistent with analysis methods used for the NATTS 
January 2013 Draft – Do Not Quote or Cite 2-21

1 network. The EPA will continue to consider new FEMs for analysis of Pb-PM10 and Pb-TSP as 

2 applications are received, although no new FRMs (beyond the Pb-TSP FRM for ICP-MS 

3 discussed above) are expected during this NAAQS review. 

4 2.2.1.3.3 Network Design Considerations 

5 Significant revisions to the Pb network design requirements (40 CFR part 58, Appendix 

6 D) were made as part of the 2008 Pb NAAQS review and an associated revision to the 

7 requirements in 2010. As summarized in section 2.1.1.1 above, the current Pb monitoring 

8 network design requirements (40 CFR part 58, Appendix D, paragraph 4.5) include two types of 

9 monitoring sites – source-oriented monitoring sites and non-source-oriented monitoring sites - as 

10 well as the collection of a year of Pb-TSP measurements at 15 specific airports. This section 

11 describes the design considerations for the Pb NAAQS surveillance network. 

12 Source-Oriented Monitoring. Since the phase out of Pb in on-road gasoline, Pb is 

13 widely recognized as a source-oriented air pollutant. As summarized in the ISA, variability in 

14 air Pb concentrations is highest in areas including a Pb source, “with high concentrations 

15 downwind of the sources and low concentration at areas far from sources” (ISA, p. 3-88). 

16 Recent data summarized in section 2.2.2.2 below indicates that the highest ambient Pb 

17 concentrations are found near large Pb sources, usually metals industries (see, for example, 

18 Figures 2-11 through 2-13 below). Analysis of the monitoring network during the last Pb 

19 NAAQS review with regard to adequacy of monitoring near such sources found that monitors 

20 were lacking near many of the larger Pb emissions sources, leading the EPA to conclude that the 

21 monitoring network existing at that time was inadequate to determine compliance with the 

22 revised Pb NAAQS (73 FR 29262). Findings and conclusions of that analysis led to revisions of 

23 network design requirements for source-oriented monitoring, begun with the 2008 Pb NAAQS 

24 rulemaking (73 FR 66964). Additional revisions were completed as part of a reconsideration of 

25 the monitoring requirements in December 2010 (75 FR 81126). 

26 The current requirements for source-oriented monitoring include placement of monitor 

27 sites near sources of air Pb emissions which are expected to or have been shown to contribute to 

28 ambient air Pb concentrations in excess of the NAAQS. At a minimum, there must be one 

29 source-oriented site located to measure the maximum Pb concentration in ambient air resulting 

30 from each non-airport Pb source which emits 0.50 or more tons of Pb per year and from each 

airport which emits 1.0 or more tons of Pb per year.19 31 The expansion of the network, including 

32 these source-oriented sites, is shown in Figure 2-3. Comparison of Figure 2-3 (monitors) with 

 

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

1 Figure 2-2 (sources) illustrates the coverage which the current monitoring network now provides 

2 of large Pb emissions sources. 

3 The emissions threshold for source-oriented monitoring sites, 0.50 tpy, was developed 

4 based on an analysis intended to estimate the lowest emission rate that under reasonable worst5 case conditions (e.g., meteorological and emission release conditions that lead to poor dispersion 

6 and associated elevations in Pb concentrations) could lead to Pb concentrations exceeding the Pb 

7 NAAQS (Cavender, 2008). This analysis included three approaches. The first two of the three 

8 approaches included a simple scaling of the historic 5 tpy emission threshold applied to the old 

1.5 μg/m3 9 Pb NAAQS, and a simplified modeling effort using a screening model. The third 

10 approach relied on design values based on Pb monitoring data surrounding large sources (1 tpy 

11 or greater) of Pb. At the time of the 2008 review, complete 3-year design values were only 

12 available for 7 source-monitor pairs 

13 As more recent data become available, analysis of the updated and expanded dataset will 

14 inform evaluation of the appropriateness of the current threshold. Since the analysis performed 

15 during the 2008 review, over 150 additional source-oriented monitors have been installed that 

16 may be useful in such an evaluation. At this time, the new monitors have not collected a 

17 complete 3-year dataset, which is needed for the development of complete design values for the 

18 new source-oriented monitors. For monitors installed in response to the 2008 revisions (near 

19 sources estimated to emit 1.0 tpy or more of Pb), 3-years of certified data will be available in 

20 spring 2013. Three-years of certified data for the monitors required in the 2010 reconsideration 

21 will be available in spring 2015. Accordingly, analysis of the emissions threshold for source22 oriented monitors may be an appropriate issue for consideration in future reviews. 

23 One-year Airport Monitoring. In addition to the above source-oriented monitoring 

24 requirement, one year of monitoring was required near 15 specific airports in order to gather 

25 additional information on the likelihood of NAAQS exceedances near airports due to the 

26 combustion of leaded aviation gasoline (75 FR 81126). This airport monitoring study may 

27 provide useful information to assess the need for additional Pb monitoring at airports, and 

28 appropriate requirements, such as consideration of the 1.0 tpy emissions threshold and regional 

29 administrator authority for siting of source-oriented monitors at airports (75 FR 81131-81132). 

30 This airport monitoring study is currently underway. Given delays in monitor siting, monitor 

31 installation at some of these sites extended into late 2012. Accordingly, the timing for 

32 completion of the year of monitoring will vary across the 15 locations, with all of them projected 

33 to finish by late 2013. The completed datasets, when available and certified, will inform EPA’s 

34 considerations on next steps with regard to monitoring at airports using leaded aviation gasoline. 

35 Also, as described further in section 2.1.2.2above, the airport monitoring data will also inform 

36 EPA’s ongoing investigation into the potential for lead emissions from piston-engine aircraft to 
January 2013 Draft – Do Not Quote or Cite 2-23

1 cause or contribute to air pollution that may reasonably be anticipated to endanger public health 

2 or welfare. This investigation is occurring under Section 231 of the Clean Air Act (CAA), 

3 separate from the lead NAAQS review. 

4 Non-Source-Oriented Monitoring. Monitoring agencies are also required to conduct 

5 non-source-oriented monitoring at NCore sites with a population of 500,000 or more, as noted 

above.20 6 Currently, there are 24 NCore sites measuring Pb concentrations, with 17 measuring Pb 

7 in TSP and 7 measuring Pb in PM10. While non-source-oriented monitoring data can be used for 

8 designation purposes, an alternative objective stated for these sites is the collection of data on 

9 neighborhood-scale Pb concentrations that are typical in urban areas to inform our understanding 

10 of ambient air-related Pb exposures for the general population. At this still early stage in data 

11 collection at these sites, we have not identified specific gaps or inadequacies. Thus, at this stage, 

12 the current requirement for non-source-oriented Pb monitoring appears to be adequate for these 

13 purposes. 

14 

 

20 Defined by the US Census Bureau - http://www.census.gov/population/www/metroareas/metroarea.html 
January 2013 Draft – Do Not Quote or Cite 2-24

1 2.2.2 Ambient Concentrations 

2 2.2.2.1 Temporal Trends 

3 Ambient air concentrations of Pb in the U.S. have declined substantially over the past 30 

4 years. Figure 2-7 illustrates this decline in terms of site-specific maximum 3-month average 

5 concentrations at the set of 31 monitoring sites that have been operating across this period. The 

6 median of this dataset has declined by more than 90% over the 30-year period, and the average 

7 by 89%. Over the past 10 years, a larger dataset of 92 sites operating across that period also 

indicates a decline, which is on the order of 60% for the average of that dataset (Figure 2-8).21 8 

9 

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

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

12 

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

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

 

21 http://www.epa.gov/air/airtrends/lead.html
January 2013 Draft – Do Not Quote or Cite 2-25

1 The role of the phase-out of leaded gasoline on declining concentrations is evident from 

2 temporal trends in air Pb concentrations near roadways, as illustrated in Figure 2-9 which 

presents data for five monitors sited near roadways.22 3 These sites additionally indicate the 

4 concentrations currently common at such sites, with the maximum 3-month average 

concentrations at all five sites falling below 0.03 μg/m3 5 in the most recent years. 

6 

7 Monitor locations: Los Angeles, CA (06-037-4002), Riverside, CA (06-065-1003), Cook, IL (17-031-0052, 17-031-6003), Suffolk, MA (25-025-0002). 

8 Figure 2-9. Airborne Pb -TSP concentrations (3-month average) at five sites near 

9 roadways: 1979-2010. 

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 using 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

1.8

January‐79

October‐79

July‐80

April‐81

January‐82

October‐82

July‐83

April‐84

January‐85

October‐85

July‐86

April‐87

January‐88

October‐88

July‐89

April‐90

January‐91

October‐91

July‐92

April‐93

January‐94

October‐94

July‐95

April‐96

January‐97

October‐97

July‐98

April‐99

January‐00

October‐00

July‐01

April‐02

January‐03

October‐03

July‐04

April‐05

January‐06

October‐06

July‐07

April‐08

January‐09

October‐09

July‐10

Concentration (μg/m3

)

060374002

060651003

170310052

170316003

250250002
January 2013 Draft – Do Not Quote or Cite 2-26

1 2.2.2.2 Current Concentrations 

2 As a result of revisions to the Pb NAAQS surveillance monitoring requirements 

3 (described in section 2.2.1 above), Pb monitoring sites have been in transition over the last few 

4 years as indicated by Figure 2-3. For presentation in this document, we have focused on the 

5 most recent period for which adequately complete data are available, 2009-2011, recognizing 

6 that the dataset developed for this period includes many but not all of the monitors newly 

7 required by the December 2010 regulations. 

8 Lead concentrations, in terms of maximum 3-month average Pb-TSP concentration, at 

9 monitoring sites active across the U.S. during the period 2009-2011, and for which sufficient 

10 data are available to meet completeness criteria described in Appendix 2C, are presented in 

Figure 2-10.23 11 Highest concentrations occur in the vicinity of large metals industries, as 

discussed in section 2.1.2.1.24 12 As can be seen through comparison of Figure 2-10 with Figure 2-

13 3, only limited data (not meeting completeness criteria for the data analysis) are available to date 

14 for some of the monitors newly required by the Pb NAAQS monitoring network revisions 

15 completed in 2010 (see section 2.2.1.1). 

 

23 Criteria for development of the 2009-2011 air Pb-TSP, Pb-PM10 and Pb-PM2.5 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 nonattainment with the Pb NAAQS is available at: 

http://www.epa.gov/air/oaqps/greenbk/mindex.html. 
January 2013 Draft – Do Not Quote or Cite 2-2

7

1 2 Figure 2-10. Pb-TSP maximum 3-month means (215 sites), 2009-2011. 
January 2013 Draft – Do Not Quote or Cite 2-28

1 Figures 2-11 through 2-13 illustrate differences in Pb-TSP concentrations, in terms of 

2 three different metrics (maximum 3-month mean, annual mean, and maximum monthly mean), 

3 among sites near and more distant from emissions sources. The Pb-TSP sites indicate the much 

4 greater site and temporal variability in concentrations at source-oriented and previous source5 oriented sites as compared to non-source-oriented sites. Across the Pb-TSP sites, as would be 

6 expected, highest concentrations are observed at the source-oriented sites, followed by the 

7 previous source-oriented sites. This is the case for all three metrics analyzed (maximum 3-

8 month mean, maximum monthly mean and annual mean). 

9 Figures 2-11 through 2-13 additional indicate distributions of Pb-PM10 and Pb-PM2.5

10 concentrations in urban and rural locations where they are monitored. The Pb-PM10 and Pb11 PM2.5 networks are described in section 2.2.1.2 and shown in Figures 2-5 and 2-6, respectively. It 

12 is important to note that there are few sites in these recent datasets with colocated monitors for 

13 the different size fractions. As described in the ISA, at 18 urban sites (without specification as to 

14 proximity to Pb sources) with at least 30 co-located Pb-TSP and Pb-PM10 samples collected 

15 during various time periods (nearly all between 1990 and 2000), approximately 80% of the Pb 

16 mass, on average, is captured by the Pb-PM10 measurements (ISA, sections 3.5.3.1 and 3.8.6). 

17 The data distributions in Figures 2-11 through 2-13 indicate reduced variability in concentration 

18 for non-source-oriented sites and for particulate Pb of smaller size fractions. 
January 2013 Draft – Do Not Quote or Cite 2-29

1 

2 Figure 2-11. Distribution of maximum 3-month mean concentrations of Pb-TSP, Pb-PM10 and Pb-PM2.5 a3 2009-2011. 

Concentration (μg/m3)

0.00.10.20.30.40.50.60.70.80.91.01.11.2

All Pb-TSP 

sites

(n=215)

Pb-TSP 

sourceoriented 

sites 

(n=112)

Pb-TSP 

not sourceoriented sites 

(n=91)

Pb-TSP 

previous 

sourceoriented sites 

(n=12)

Pb-PM10

urban 

sites 

(n=35)

Pb-PM2.5

urban 

CSN sites 

(n=198)
January 2013 Draft – Do Not Quote or Cite 2-30

1 2 Figure 2-12. Distribution of annual mean concentrations of Pb-TSP, Pb-PM10 and Pb-PM2.5 at different si

0.00.10.20.30.40.50.60.7

Concentration (μg/m3)

All Pb-TSP 

sites

(n=215)

Pb-TSP 

sourceoriented 

sites 

(n=112)

Pb-TSP 

not sourceoriented sites 

(n=91)

Pb-TSP 

previous 

sourceoriented sites 

(n=12)

Pb-PM10

urban 

sites 

(n=35)

Pb-PM2.5

urban 

CSN sites 

(n=198)
January 2013 Draft – Do Not Quote or Cite 2-31

1 

2 Figure 2-13. Distribution of maximum monthly mean concentrations of Pb-TSP, Pb-PM10 and Pb-PM2.5 a3 2009-2011. 

0.00.10.20.30.40.50.60.70.80.91.01.11.21.31.41.51.61.71.8

All Pb-TSP 

sites

(n=215)

Pb-TSP 

sourceoriented 

sites 

(n=112)

Pb-TSP 

not sourceoriented sites 

(n=91)

Pb-TSP 

previous 

sourceoriented sites 

(n=12)

Pb-PM10

urban 

sites 

(n=35)

Pb-PM

urban 

CSN sit

(n=198

Concentration (μg/m3)
January 2013 Draft – Do Not Quote or Cite 2-32

1 2.3 AMBIENT AIR LEAD IN OTHER MEDIA 

2 Lead emitted into the ambient air, depending on its chemical and physical characteristics, 

3 deposits out of air onto surfaces in the environment. The environmental fate of atmospherically 

4 emitted Pb once deposited, is influenced by the type of surface onto which the particles deposit 

5 and by the type and activity level of transport forces in that location. Deposited Pb can be 

6 incorporated into soil matrices in terrestrial ecosystems or transported (by direct deposition or 

7 stormwater runoff) to water bodies and into aquatic sediments, which may serve as aquatic 

8 ecosystem sinks. Particles deposited onto impervious surfaces, such as roadway or urban 

9 surfaces, are more available for human contact while they remain on such surfaces. For 

10 example, they may be available for adherence onto skin or they may be resuspended into the air 

11 and inhaled. Precipitation and other natural, as well as human-influenced, processes contribute 

12 to the fate of such particles and their potential transport to areas or environments of lesser or 

13 greater likelihood for human contact, e.g., transport with surface runoff into nearby water bodies 

14 or tracking into nearby houses (ISA, section 3.3). 

15 Lead from current and historical air emissions sources, in addition to a range of nonair 

16 sources (e.g., land disposal of wastes as well as surface runoff and releases to surface waters), 

17 contribute to Pb in outdoor dust, soil and aquatic systems. Because of its persistence, Pb from all 

18 of these sources can contribute to media concentrations into the future. The pattern of resulting 

19 Pb concentrations changes over time in response to changes in new Pb contributions to the 

20 systems (e.g., in types and rates of addition), as well as environmental processes (chemical, 

21 biological and physical) particular to each type of media and ecosystem. Accordingly, media 

22 and ecosystems differ with regard to Pb concentrations and changes in those concentrations in 

23 response to airborne Pb. These differences relate to ecosystem processes as well as Pb source or 

24 emissions characteristics and proximity. 

25 The initial section below (section 2.3.1) summarizes salient information regarding 

26 atmospheric deposition and how it is monitored. Subsequent sections describe the current 

27 information related to the presence of ambient air Pb in nonair media and what it indicates 

28 regarding impacts of current patterns of Pb in and being emitted to ambient air, including 

29 relationships to impacts in the past and to other Pb sources. Section 2.3.2 focuses on terrestrial 

30 media, while section 2.3.3 discusses aquatic media. 

31 2.3.1 Atmospheric Deposition 

32 Deposition is the pathway by which Pb particles are removed from the atmosphere and 

33 transferred to other environmental media. There are several approaches by which atmospheric 

34 deposition, or the transfer of Pb from the atmosphere to soil or water bodies, can be assessed. 

35 These include measurements of Pb in rainfall (wet deposition) and on collection surfaces during 
January 2013 Draft – Do Not Quote or Cite 2-33

1 dry periods (dry deposition); dry deposition is also estimated from measurements of airborne Pb 

2 particles coupled with estimates of deposition velocity (see 2006 CD, Section 2.3.2). Less direct 

3 approaches include monitoring changes in Pb concentration in various biological or physical 

4 media such as lichen or mosses, snowpack, soil and aquatic sediments (ISA, sections 3.6.2, 3.6.4 

5 and 3.6.6). Approaches for the latter three media may involve repeated measurements of surface 

6 samples over time or core samples coupled with isotope dating. To gain information on 

7 atmospheric deposition, unaffected by contributions from direct nonair environmental releases, 

8 such studies are generally conducted in somewhat remote areas. As there are currently no 

9 nationwide Pb atmospheric deposition monitoring programs, the discussion of atmospheric 

10 deposition in this and subsequent sections is drawn from this range of approaches (2006 CD, 

11 sections 2.3, 8.2.2 and AX7.1.2.3; ISA, sections 3.3.1.2 and 3.6 ). Geographic differences in 

12 deposition generally relate to differences in the amount and size distribution of airborne Pb 

13 particles in that location, as well as meteorology and other site-specific factors. For example, the 

14 size of particles, as well as solubility in rainwater, can also influence wet deposition rates (ISA, 

15 section 3.3.1.2; 2006 CD, p. 2-59). Factors that particularly influence dry deposition are the 

16 level of atmospheric turbulence, especially in the layer nearest the ground, particle size 

17 distributions and density, and the nature of the surface itself, such as smooth or rough (2006 CD, 

18 pp. 2-55 to 2-57). 

19 Evidence for the temporal pattern of U.S. lead deposition generally indicates a peak 

20 during the middle twentieth century (e.g., 1940s through 1970s) followed by substantial declines 

21 in the latter part of the century (ISA, section 3.3.1; 2006 CD section 2.3.1; Jackson et al., 2004). 

22 This pattern reflects the increased use of Pb in the industrial age (including its use in gasoline in 

23 the twentieth century) and declines in response to environmental controls on gasoline and metals 

24 industries in the latter part of the twentieth century. Studies continue to document declines in 

25 atmospheric deposition since the 1980s in areas remote from industrial areas (e.g., Watmough 

26 and Dillon, 2007). As would be expected, stationary sources of Pb continue to contribute to 

27 relatively higher deposition rates in industrial areas as compared to other areas, although rates in 

28 those areas appear to have also declined since the 1970s-80s (ISA, section 3.3.1.2; Sabin and 

29 Schiff, 2008). 

30 2.3.2 Terrestrial Media 

31 Lead in the terrestrial media discussed here may originate from current or historical air or 

32 other sources. Other sources to these media include historical use of indoor and outdoor leaded 

33 paint, more prevalent in areas with older buildings, and the processing of lead-containing 

34 materials. Further, the concentrations of Pb in each media, as well as the relative contributions 

35 from various types of sources to those concentrations, vary among media and among locations 
January 2013 Draft – Do Not Quote or Cite 2-34

1 for any one media. Differences among locations in 0air-related Pb are generally related to the 

2 current and historical magnitude of Pb emissions and deposition at that location, as well as 

3 location- and media-specific removal factors. 

4 2.3.2.1 Indoor Household Dust 

5 Household dust arises from particulate matter generated indoors and outdoors and Pb in 

6 household dust can reflect a combination of these sources. Airborne particles can be transported 

7 indoors with ambient air, while particles deposited outdoors from ambient air may be carried in 

8 on humans and their clothing or other items transported indoors. Depending on factors such as 

9 the proximity of the residence to current or historical metals industries, leaded paint usage, and 

10 age of the residence, Pb in indoor residential dust can reflect current or historical atmospheric Pb 

11 or nonair-related sources, such as leaded paint. Another indoor source is tobacco smoking (ISA, 

12 section 4.1.3.2; Gaitens et al., 2009; 2006 CD, p. 3-15; Mannino et al., 2003). The age of the 

13 residence may be an indicator of the potential for the presence of leaded paint and, in areas of 

14 significant levels of airborne Pb in the past, such as near mining or smelting industries, may also 

15 indicate the potential for the residual presence of historically emitted Pb (ISA, sections 4.1.1 and 

16 4.1.3.2; 2006 CD section 3.2.3). A study of households in the Baltimore metropolitan area (in 

which there are no areas designated non-attainment for the current Pb NAAQS)25 17 indicated 

18 indoor air Pb concentrations to be significantly associated with outdoor air Pb concentrations but 

19 did not show a statistically significant relationship of outdoor air Pb with indoor dust Pb, perhaps 

20 indicating the greater role of sources other than current airborne concentrations in those 

21 households (ISA, 4.1.3.2; Egeghy et al., 2005). 

22 As discussed in chapter 4 below, indoor dust is a major pathway for air-related Pb 

23 exposure for pre-school children, largely related to prevalent hand-to-mouth behavior at that age. 

24 2.3.2.2 Outdoor Dust in Areas of Human Activity 

25 Lead in particulate matter occurring on outdoor surfaces (outdoor dust) may reflect 

26 current or historical Pb emissions, as well as the historical uses of lead in products on buildings 

27 and infrastructure in surrounding area. The concentrations of air-related Pb in outdoor dust and 

28 the relative contribution of air-related Pb to the total Pb concentrations in outdoor dust varies 

29 depending on the location-specific characteristics of air–related (and other) Pb sources. The role 

30 of air-related sources in outdoor dust Pb has been documented in areas near industrial sources, 

31 such as smelters, where Pb concentrations in outdoor dust have been documented to decline in 

32 response to reduced emissions. For example, outdoor dust Pb concentrations in a long-time 

33 Canadian smelter town were found to track smelter Pb emissions, as a new smelting technology 

 

25 http://www.epa.gov/air/oaqps/greenbk/mnc.html 
January 2013 Draft – Do Not Quote or Cite 2-35

1 which reduced airborne Pb concentrations by 75% resulted in a 50% reduction in outdoor dust 

2 Pb loading rate and concentrations (2006 CD, p. 3-23; Hilts, 2003). 

3 Rates of dry deposition of Pb in large metropolitan areas during the past decade are much 

4 lower than those reported for the 1970s (ISA, sections 3.3.1 and 3.6.1; Table 2-4, below). For 

5 example, dry deposition of Pb into Los Angeles harbor during 2002-2006 was more than an 

6 order of magnitude lower than rates reported for the same location in 1975 (ISA section 3.3.1.2; 

7 Sabin and Schiff, 2008; Lim et al., 2006). Across the Los Angeles metropolitan area, average 

rates generally ranged from 10 to 32 micrograms per square meter per day (μg/m2 8 /day) and down 

to 0.3 μg/m2 9 /day for the non-urban site of Malibu during 2002-2003 (Lim et al., 2006). Rates 

10 within this range are reported from studies in Manhattan and a non-industrial area of New Jersey, 

11 with a somewhat higher rate reported for a major industrial location within the New York City 

12 metropolitan area. Although rates have not been reported recently for smelter locations in the 

13 U.S., the outdoor dustfall deposition rate reported in a Canadian smelter town after the 

14 installation of new technology that reduced average airborne Pb-TSP concentrations to a level 

still at least twice the current U.S. NAAQS (0.3 μg/m3 from prior average of 1.1 μg/m3 15 ) was 

16 several orders of magnitude higher than those reported for New York, Los Angeles and Chicago 

17 urban areas (Table 2-4). 

18 From the few studies reporting levels of Pb loading or concentration in outdoor dust 

19 within the past decade or so, loading to surfaces of pedestrian traffic signals in New York City 

20 was on average approximately 15% the loading reported on sidewalks in older, residential areas 

of downtown Baltimore (e.g., approximately 250 ug/ft2

 as compared to 1500 ug/ft2 21 ), an order of 

22 magnitude or more below that reported in the long-time Canadian smelter town (Caravanos et al., 

23 2006b; Farfel et al 2005; Hilts, 2003). 
January 2013 Draft – Do Not Quote or Cite 2-36

1 Table 2-3. Dry deposition of lead in large metropolitan areas and in a smelter town. 

Description 

Dry Deposition 

Rate 

(μg Pb/m2/day)

Study 

Los Angeles Harbor, June-Nov 2006 14A Sabin and Schiff, 2008 

Los Angeles Harbor, 2002-2003b 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, 2nd 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 San Diego Bay ranged from 0.52 (Oxnard) – 3.3 (San Diego Bay) μg/m3. 

B - Average Pb-TSP range= 0.0056-0.017 μg/m3 for urban sites; 0.0022 at Malibu site. 

C - Average Pb-TSP at downwind site over sampling period ~0.02 μg/m3.

D - Average Pb-TSP = 0.3 μg/m3, this reflects new technology (previously 1.1 μg/m3) for smelter that existed in this town for past 95 years.

2 

3 2.3.2.3 Soil 

4 As is the case for Pb in outdoor dust, occurring in surface soils can be derived from 

5 current or historical Pb emissions, as well as leaded paint usage in older residential areas. The 

6 relative role of these sources may vary with the type of environment and proximity to industry 

7 and population centers. 

8 In forested areas away from old urban areas, the role of leaded gasoline in soil 

9 contamination is illustrated by the documented reductions in Pb in surface soils subsequent to the 

10 leaded gasoline phasout. For example, forest surface soil (litter) concentrations in a transect 

11 from Vermont, through Maine and up to Gaspe in Quebec, which in 1979 exhibited a significant 

12 spatial trend, ranging from 200 milligrams per kilogram, dry weight (mg/kg dw) at its 

13 southernmost point down to 60 mg/kg dw at its northernmost and most remote point in Quebec, 

14 declined to 32-66 mg/kg dw (with no spatial trend) in 1996 (ISA, section 3.6.1; Evans, 2005). In 

15 forests from the mid-Atlantic to southern New England, a reduction in litter Pb concentration 

16 was observed between 1978 and 2004-05 (ISA, section 3.6.1; Johnson and Richter, 2010). In the 

17 latter study, the authors observed less change in concentration in the more northern sampling 

18 sites, which they attribute to reduced rates of organic matter decomposition in those colder 

19 temperature areas. Similarly, an additional New England study by Kaste et al (2006) also 
January 2013 Draft – Do Not Quote or Cite 2-37

1 documented a pattern in temporal reductions in soil Pb (o-horizon) related to decomposition 

2 activity. These recent findings are generally consistent with findings reported in the last review 

3 which indicated the gradual migration of deposited Pb into mineral soils (e.g., Miller and 

4 Friedland, 1994; Kaste et al., 2003; Wang and Benoit, 1997; Johnson et al., 1995; Zhang, 2003). 

5 Few studies have investigated temporal trends of surface soil Pb concentrations in more 

6 populated areas in relation to reductions in usage of leaded gasoline and paint. Current 

7 concentrations in areas of past heavy traffic powered by leaded gasoline are generally elevated 

8 above areas more distant from these areas (ISA, section 3.6.1). Current roadway-related sources 

9 of Pb, while substantially less significant than leaded gasoline, continue to provide some 

10 contribution to surface dust/soil in these areas (ISA, section 3.2.2.6). Surface soil and dust 

11 concentrations are much higher in such areas in large, older cities than surrounding suburban 

12 areas (ISA, section 3.6.1). In older residential areas, the use of leaded house paint is another 

13 contributor to surface soil concentrations (ISA, sections 3.6.1 and 3.7.7.2; Yesilonis et al., 2008; 

14 Brown et al., 2008; Clark et al., 2006). 

15 Areas of long-term Pb emissions from point sources appear to be the areas of highest 

16 surface soil Pb concentrations (ISA, sections 3.6 and 3.6.1). For example, Pb surface soil 

17 concentrations within approximately 100-250 meters of long-established lead smelters have been 

18 five to ten times higher than those at 3-5 km distance (ISA, section 3.6.1; 2006 CD, Table 3-4). 

19 Surface soil concentrations near U.S. mines that are no longer active have also been found to be 

20 elevated above more distant areas (2006 CD, Table 3-6). Information described in the 2006 CD 

21 for areas surrounding smelters after implementation of pollution controls, although showing 

22 declines in Pb concentrations in outdoor dustfall, street dust and indoor dustfall, has not indicated 

23 a noticeable decline in soil Pb concentrations (2006 CD, pp. 3-23 to 3-24). The continued Pb 

24 emissions in such industrial areas likely influence the dynamics of Pb concentrations in the soil, 

25 affecting any response to emissions reductions. Estimates of associated steady-state surface soil 

26 Pb concentrations or the expected longer-term temporal pattern for this situation have not been 

27 made. 

28 In summary, findings to date indicate that many of those systems less influenced by 

29 current point sources have and may still be responding to reduced Pb deposition rates associated 

30 with reduced atmospheric emissions of Pb, including those associated with the phase-out of 

31 leaded gasoline, while potential responses of soils near point sources and those involving 

32 historically deposited Pb near roadways are less well characterized. 

33 2.3.2.4 Biota 

34 Measurements of Pb in some biota indicate reductions in biologically available Pb over 

35 the past 30 years in some remote locations. For example, measurements of Pb in lichen from 
January 2013 Draft – Do Not Quote or Cite 2-38

1 Golden Lake in Mount Ranier National Park (2005) and Emerald Lake basin in Sequoia/Kings 

2 Canyon National Parks (2004) indicate significant reductions (approximately 3-5-fold) since 

3 samples were previously collected in those locations in 1984 (ISA, section 3.6.6; Landers et al., 

4 2008). Further, Pb in teeth of juvenile and adult moose in Isle Royale National Park in northern 

5 Michigan have also declined substantially (ISA, section 3.6.8; Vucetich et al., 2009). 

6 Biota measurements have also documented sources of Pb deposition in mining areas 

7 including the transportation of materials along haul roads. Lead deposition from these mining8 related activities has been documented in remote wilderness areas in Alaska. For example, Pb 

9 concentration in moss in Cape Krusenstern National Monument declines with distance from the 

road on which product from Red Dog mine26 10 in northwest Alaska is transported (ISA, section 

11 3.3.1.2; Hasselbach et al., 2005). In summer 2001, the median Pb concentration measured within 

12 10 meters of the haul road was more then 20 times higher than sites at greater distance from the 

13 road and nearly three orders of magnitude greater than those reported for this moss in other 

14 Alaska locations in 1990-1992. Concentrations in moss within 10 meters of the haul road ranged 

15 from 271-912 mg/kg dw (Hasselbach et al., 2005). 

16 2.3.3 Aquatic Media 

17 2.3.3.1 Surface Waters 

18 In addition to delivery by atmospheric deposition, Pb is also carried into surface waters 

19 via wastewater effluent from municipalities and industry, stormwater runoff, erosion, and 

20 accidental discharges (2006 CD, p. AX7-142; ISA section 3.3.2). As a result of the phasing out 

21 of leaded gasoline, reductions in Pb concentrations have been documented in surface waters of 

22 the North Atlantic Ocean, as well as the relatively less remote areas of the Great Lakes (2006 

23 CD, p. 7-23). The availability of studies investigating historical trends in surface waters is 

24 limited, in part due to analytical issues that challenged many monitoring programs in the past 

25 (2006 CD, AX7.2.2.2). Thus, temporal trends reported in many aquatic systems are based on 

26 sediment analyses (see section 2.3.3.2 below). 

27 Most Pb occurring in aquatic systems is associated with particles, with the distribution 

28 between particle-bound and dissolved form being influenced by water chemistry as well as 

29 suspended sediment levels (ISA, 3.3.2; 2006 CD, pp. AX7-117 to AX7-118, Section AX7.2.2). 

30 Water columns have been described as “transient reservoirs” for pollutants (ISA, section 3.7.2; 

31 2006 CD, p. 2-75). Once deposited to sediments, whether Pb is available for resuspension back 

32 into the water column with potential transport further down a watershed versus being buried into 

33 deeper sediments depends on the aquatic system. In open ocean waters (generally characterized 

 

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

1 by depth and distance from continental sources), resuspension to surface waters is unlikely. In 

2 more shallow systems, and additionally those influenced by land sources (e.g., stormwater runoff 

3 as well as point sources), resuspension may play a role in water column concentrations. For 

4 example, studies in San Francisco Bay, the southern arm of which has an average depth of 2 m, 

5 have indicated that Pb particles may be remobilized from surface sediments into the water 

6 column (2006 CD, AX7-141). 

7 The distribution of Pb dissolved in many U.S. surface waters has been reported by the 

8 United States Geological Survey (USGS) National Water-Quality Assessment (NAWQA) 

9 program. The NAWQA data set encompasses data, collected from 1991-2003 on Pb 

10 concentrations in flowing surface waters for more than 50 river basins and aquifers throughout 

11 the country (2006 CD, Section AX7.2.2.3). These data indicate a mean dissolved Pb 

12 concentration in U.S. surface waters of 0.66 μg/L (range 0.04 to 30 μg/L) in waters affected by a 

13 combined contribution of natural and anthropogenic sources, as compared to a mean of 0.52 

14 μg/L (range 0.04 to 8.4 μg/L) for waters in “forest”, “rangeland”, and “reference” sites (2006 

15 CD, Section AX7.2.2.3). The highest surface water Pb concentrations were observed in sites 

16 impacted by land uses such as mining (2006 CD, p. AX7-131). The role of surface runoff in 

17 delivering contamination to waters near metals industries presents a challenge to the 

18 disentangling of atmospheric deposition contributions from those associated with surface runoff. 

19 2.3.3.2 Sediments 

20 Many studies have investigated temporal trends in sediment Pb concentrations, using 

21 sediment cores or surface sediment Pb concentration, with declines documented in many systems 

22 and usually attributed to the phasing out of leaded gasoline (ISA, section 3.6.2; 2006 CD, section 

23 AX7.2.2). Several studies documenting the increased Pb deposition of the industrial age, 

24 including specifically leaded gasoline usage, and the subsequent declines associated with leaded 

25 gasoline phase-out were reported in the 2006 CD. They include investigations involving 

26 sediment cores from the Okefenokee Swamp in Georgia as well as from 35 reservoirs and lakes 

27 in urban and reference locations (ISA, section 3.6.2; 2006 CD, p. AX7-141). In the latter, the 

28 median reduction in Pb mass accumulation rate in the cores, adjusted for background 

29 concentrations, was 246%, with the largest decreases in lakes located in dense urban watersheds 

30 (ISA, section 3.6.2; 2006 CD, p. AX7-141; Mahler et al, 2006). A third study of sediment cores 

31 in 12 lakes in the Great Lakes area also documented a peak in Pb concentrations consistent with 

32 peak use of leaded gasoline in the U.S. in the mid 1970’s and declining concentrations in most 

33 lake sediments through the mid 1990’s (2006 CD, p. 2-55; Yohn et al., 2004). Sediment surveys 

34 by the USGS NAWQA have reported the highest Pb concentrations in Idaho, Utah, and 
January 2013 Draft – Do Not Quote or Cite 2-40

1 Colorado, with seven of the highest concentrations at sites classified as mining land use (2006 

2 CD, p. AX7-133). 

3 Among the more recent investigation of temporal trends in aquatic sediments described in 

4 the ISA is that associated with the Western Airborne Contaminants Assessment Project which 

5 documented Pb in sediment cores from 14 lakes in eight U.S. national parks in western states, 

6 including three in Alaska (ISA, section 3.6.2; Landers et al., 2010). Among the Alaska cores, in 

7 which concentrations were generally on the order of 20 μg/kg, dw, there was little variation in Pb 

8 concentration, flux or enrichment factor. The other park cores, with few exceptions, generally 

9 exhibited an increase in concentration commencing in the mid-nineteenth century, which 

10 transitioned to declining trends in the past few decades, with lower concentrations in more 

11 recent, surface material. The highest concentration was recorded at core depth corresponding to 

12 the mid-1970s, in one of the Sequoia/Kings Canyon lake cores (Figure 2-16; ISA, section 3.6.2; 

Landers et al., 201027 13 ). 

14 

 

27 Figure created from database for Landers et al (1980); 

http://www.nature.nps.gov/air/Studies/air_toxics/wacap.cfm. 
January 2013 Draft – Do Not Quote or Cite 2-41

1 

2 Figure 2-14. Temporal trend in sediment concentration from core samples in 12 lakes at 

3 eight National Parks or Preserves. 

4 Analyses of cores taken in several lakes and reservoirs along the Apalachicola, 

5 Chattahoochee, and Flint River Basin from north of the Atlanta, GA metropolitan area to the 

6 Gulf of Mexico indicate changes in sediment concentration both with time and in relation to 

7 influence of the large metropolitan area of Atlanta (ISA, section 3.6.2; Callender and Rice, 

8 2000). Highest concentrations were documented just downstream from Atlanta at the core depth 

9 corresponding to the 1975-1980 time period; the corresponding concentration for the most 

10 recent time period (1990-1995) at that location was approximately 50% lower (ISA, section 

11 3.6.2; Callender and Rice, 2000). These data may reflect changes in surface water discharges of 

12 Pb in the Atlanta area, during this time period, as well as changes in air deposition. The smaller 

13 reduction (on the order of 20%) observed across the 20 year time period at the upstream site is 

14 likely more generally reflective of changes in air deposition. 

0

25

50

75

100

125

1800 1830 1860 1890 1920 1950 1980 2010

Pb Concentration (mg/kg, DW)

Year Material Deposited

Sequoia/Kings Canyon-Pear (mid California)

Sequoia/Kings Canyon-Emerald (mid California)

Mt Ranier-Golden (mid Washington)

Mt Ranier-LP19 (mid Washington)

Glacier-Snyder (Montana)

Glacier-Oldman (Montana)

Rocky Mnt-Lone Pine (Colorado)

Rocky Mtn-Mills (Colorado)

Olympic (Washington)

Denali (mid Alaska)

Gates of the Arctic (n. Alaska)

Noatak (n. Alaska)
January 2013 Draft – Do Not Quote or Cite 2-42

1 2.4 REFERENCES 

2 Brown, RW; Gonzales, C; Hooper, MJ; Bayat, AC; Fornerette, AM; McBride, TJ; Longoria, T; Mielke, HW. 

3 (2008). Soil lead (Pb) in residential transects through Lubbock, Texas: A preliminary assessment. Environ 

4 Geochem Health 30: 541-547. http://dx.doi.org/10.1007/s10653-008-9180-y. 

5 Callender, E; Rice, KC. (2000). The urban environmental gradient: Anthropogenic influences on the spatial and 

6 temporal distributions of lead and zinc in sediments. Environ Sci Technol 34: 232-238. 

7 http://dx.doi.org/10.1021/es990380s. 

8 Caravanos, J.; Weiss, A.L.; Jaeger, R.J. (2006a) An exterior and interior leaded dust deposition survey in New York 

9 City: results of a 2-year study. Environ. Res. 100: 159-164. 

10 Caravanos, J; Weiss, AL; Blaise, MJ; Jaeger, RJ. (2006b). A survey of spatially distributed exterior dust lead 

11 loadings in New York City. Environ Res 100: 165-172. http://dx.doi.org/10.1016/j.envres.2005.05.001. 

12 Cavender, K. (2008). Update of Analysis of Proposed Source-Oriented Monitoring Emission Threshold. 

13 Memorandum to Lead NAAQS Review Docket (OAQ-2006-0735) 

14 http://www.epa.gov/ttnnaaqs/standards/pb/data/20081015Cavender.pdf

15 Clark, HF; Brabander, DJ; Erdil, RM. (2006). Sources, sinks, and exposure pathways of lead in urban garden soil. J 

16 Environ Qual 35: 2066-2074. http://dx.doi.org/10.2134/jeq2005.0464. 

17 DRRC. (Doe Run Company). (2010). DRRC multi-media Consent Decree. Herculaneum, MO: Doe Run Resources 

18 Corporation. 

19 Egeghy, P. P.; Quackenboss, J. J.; Catlin, S.; Ryan, P. B. (2005) Determinants of temporal variability in 

20 NHEXASMaryland environmental concentrations, exposures, and biomarkers. J. Exposure Anal. Environ. 

21 Epidemiol. 15: 388-397. 

22 Evans, GC; Norton, SA; Fernandez, IJ; Kahl, JS; Hanson, D. (2005). Changes in concentrations of major elements 

23 and trace metals in northeastern US-Canadian sub-alpine forest floors. Water Air Soil Pollut 163: 245-267. 

24 Farfel, MR; Orlova, AO; Lees, PSJ; Rohde, C; Ashley, PJ; Chisolm, JJ, Jr. (2005). A study of urban housing 

25 demolition as a source of lead in ambient dust on sidewalks, streets, and alleys. Environ Res 99: 204-213. 

26 http://dx.doi.org/10.1016/j.envres.2004.10.005. 

27 Gaitens, JM; Dixon, SL; Jacobs, DE; Nagaraja, J; Strauss, W; Wilson, JW; Ashley, PJ. (2009). Exposure of US 

28 children to residential dust lead, 1999-2004: I. Housing and demographic factors. Environ Health Perspect 

29 117: 461-467. http://dx.doi.org/10.1289/ehp.11917. 

30 Garland, JA, Nicholson, KW 1991. A review of methods for sampling large airborne particles and associated 

31 radioactivity. J. Aerosol Sci. Vol.22 (4):479-499. 

32 Hasselbach, L; Ver Hoef, JM; Ford, J; Neitlich, P; Crecelius, E; Berryman, S; Wolk, B; Bohle, T. (2005). Spatial 

33 patterns of cadmium and lead deposition on and adjacent to National Park Service lands in the vicinity of 

34 Red Dog Mine, Alaska. Sci Total Environ 348: 211-230. http://dx.doi.org/10.1016/j.scitotenv.2004.12.084. 

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

36 58. 

37 Jackson, B.P., P.V. Winger, P.J. Lasier (2004) Atmospheric lead deposition to Okefenokee Swamp, Georgia, USA. 

38 Environ Poll. 130: 445-451. 
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1 Johnson, C. E.; Siccama, T. G.; Driscoll, C. T.; Likens, G. E.; Moeller, R. E. (1995) Changes in lead 

2 biogeochemistry in response to decreasing atmospheric inputs. Ecol. Appl. 5: 813-822. 

3 Johnson, AH; Richter, SL. (2010). Organic-horizon lead, copper, and zinc contents of Mid-Atlantic forest soils, 

4 1978-2004. Soil Sci Soc Am J 74: 1001-1009. http://dx.doi.org/10.2136/sssaj2008.0337. 

5 Kaste, JM; Bostick, BC; Friedland, AJ; Schroth, AW; Siccama, TG. (2006). Fate and speciation of gasoline-derived 

6 lead in organic horizons of the northeastern USA. Soil Sci Soc Am J 70: 1688-1698. 

7 http://dx.doi.org/10.2136/sssaj2005.0321. 

8 Kaste, J.; Friedland, A.; Stürup, S. (2003) Using stable and radioactive isotopes to trace atmospherically deposited 

9 Pb in montane forest soils. Environ. Sci. Technol. 37: 3560-3567. 

10 Kenny L; Beaumont G, Gudmundsson A, Thorpe A, Koch W. (2005) Aspiration and sampling efficiencies of the 

11 TSP and louvered particulate matter inlets. J Environ Monit. May 2005. 7 481-487. 

12 Landers, DH; Simonich, SL; Jaffe, DA; Geiser, LH; Campbell, DH; Schwindt, AR; Schreck, CB; Kent, ML; Hafner, 

13 WD; Taylor, HE; Hageman, KJ; Usenko, S; Ackerman, LK; Schrlau, JE; Rose, NL; Blett, TF; Erway, MM. 

14 (2008). The fate, transport, and ecological impacts of airborne contaminants in western national parks 

15 (USA). (EPA/600/R-07/138). Corvallis, Oregon: U.S. Environmental Protection Agency, NHEERL, 

16 Western Ecology Division. http://www.nature.nps.gov/air/studies/air_toxics/WACAPreport.cfm. 

17 Landers, DH; Simonich, SM; Jaffe, D; Geiser, L; Campbell, DH; Schwindt, A; Schreck, C; Kent, M; Hafner, W; 

18 Taylor, HE; Hageman, K; Usenko, S; Ackerman, L; Schrlau, J; Rose, N; Blett, T; Erway, MM. (2010). The 

19 Western Airborne Contaminant Assessment Project (WACAP): An interdisciplinary evaluation of the 

20 impacts of airborne contaminants in western U.S. National Parks. Environ Sci Technol 44: 855-859. 

21 http://dx.doi.org/10.1021/es901866e. 

22 Lim, JH; Sabin, LD; Schiff, KC; Stolzenbach, KD. (2006). Concentration, size distribution, and dry deposition rate 

23 of particle-associated metals in the Los Angeles region. Atmos Environ 40: 7810-7823. 

24 http://dx.doi.org/10.1016/j.atmosenv.2006.07.025. 

25 Mahler, B. J.; Van Metre, P. C.; Callender, E. (2006) Trends in metals in urban and reference lake sediments across 

26 the United States, 1970 to 2001. Environ. Toxicol. Chem. 25: 1698-1709. 

27 Mannino, D.M.; Albalak, R.; Grosse, S.; Repace, J. (2003) Second-hand smoke exposure and blood lead levels in 

28 U.S. children. Epidemiology 14(6): 719-727. 

29 Miller, E. K.; Friedland, A. J. (1994) Lead migration in forest soils: response to changing atmospheric inputs. 

30 Environ. Sci. Technol. 28: 662-669. 

31 Osterberg, E; Mayewski, P; Kreutz, K; Fisher, D; Handley, M; Sneed, S; Zdanowicz, C; Zheng, J; Demuth, M; 

32 Waskiewicz, M; Bourgeois, J. (2008). Ice core record of rising lead pollution in the North Pacific 

33 atmosphere. Geophys Res Lett 35: L05810. http://dx.doi.org/10.1029/2007gl032680 

34 Paode, RD; Sofuoglu, SC; Sivadechathep, J; Noll, KE; Holsen, TM; Keeler, GJ. (1998). Dry deposition fluxes and 

35 mass size distributions of Pb, Cu, and Zn measured in southern Lake Michigan during AEOLOS. Environ 

36 Sci Technol 32: 16291635. http://dx.doi.org/10.1021/es970892b. 

37 Russell A. and Samet, J.M. (2010) Letter from Dr. A. Russell, Chair, Clean Air Scientific Advisory Committee, 

38 Ambient Air Monitoring Methods Subcommittee and J.M. Samet, Chair, Clean Air Scientific Advisory 

39 Committee, to Administrator Lisa P. Jackson. Re: CASAC Review of EPA’s White Paper Approach for 

40 the Development of a new Federal Reference Method (FROM) for Lead in Total Suspended Particulates 

41 (Pb-TSP). November 30, 2010. 
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1 Sabin, LD; Schiff, KC. (2008). Dry atmospheric deposition rates of metals along a coastal transect in southern 

2 California. Atmos Environ 42: 6606-6613. http://dx.doi.org/10.1016/j.atmosenv.2008.04.042 

3 U.S. Environmental Protection Agency. (1996-2011) . AP-42, Compilation of Air Pollutant Emission Factors, 5th 

4 Edition. Volume 1: Stationary Point and Area Sources, Chapter 13: Miscellaneous Sources. Available at: 

5 http://www.epa.gov/ttn/chief/ap42/ch13/index.html 

6 U.S. Environmental Protection Agency. (2012) National Emissions Inventory for 2008, version 3. Office of Air 

7 Quality Planning and Standards, Research Triangle Park, NC. November 2012. 

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

9 Vucetich, JA; Outridge, PM; Peterson, RO; Eide, R; Isrenn, R. (2009). Mercury, lead and lead isotope ratios in the 

10 teeth of moose (Alces alces) from Isle Royale, U.S. Upper Midwest, from 1952 to 2002. J Environ Monit. 

11 Wang, E. X.; Benoit, G. (1997) Fate and transport of contaminant lead in spodosols: a simple box model analysis. 

12 Water Air Soil Pollut. 95: 381-397. 

13 Watmough, SA; Dillon, PJ. (2007). Lead biogeochemistry in a central Ontario forested watershed. Biogeochemistry 

14 84: 143-159. http://dx.doi.org/10.1007/s10533-007-9110-6 

15 Yesilonis, ID; Pouyat, RV; Neerchal, NK. (2008). Spatial distribution of metals in soils in Baltimore, Maryland: 

16 Role of native parent material, proximity to major roads, housing age and screening guidelines. Environ 

17 Pollut 156: 723-731. http://dx.doi.org/10.1016/j.envpol.2008.06.010. 

18 Yi, SM; Totten, LA; Thota, S; Yan, S; Offenberg, JH; Eisenreich, SJ; Graney, J; Holsen, TM. (2006). Atmospheric 

19 dry deposition of trace elements measured around the urban and industrially impacted NY-NJ harbor. 

20 Atmos Environ 40: 6626-6637. http://dx.doi.org/10.1016/j.atmosenv.2006.05.062. 

21 Yohn, S., Long, D., Fett, J., Patino, L. (2004) Regional versus local influences on lead and cadmium loading to the 

22 Great Lakes region. Appl. Geochem. 19: 1157-1175. 

23 Zhang, Y.-H. (2003) 100 years of Pb deposition and transport in soils in Champaign, Illinois, U.S.A. Water Air Soil 

24 Pollut. 146: 197-210. 
January 2013 3-1 Draft - Do Not Quote or Cite

1 3 HEALTH EFFECTS AND EXPOSURE/RISK INFORMATION 

2 This chapter presents key aspects of the current evidence of lead-related health effects 

3 and presents exposure/risk information from the quantitative assessment performed in the last 

4 review in the context of the currently available evidence. Staff has drawn from EPA’s synthesis 

5 of the scientific evidence presented in the draft Integrated Science Assessment for Lead (USEPA, 

6 2012; henceforth referred to as the ISA) and 2006 Air Quality Criteria Document for Lead

7 (USEPA, 2006; henceforth referred to as the 2006 CD), and from the documentation of the 2007 

8 human exposure and health risk assessment (documented in USEPA, 2007a; henceforth referred 

9 to as the 2007 REA). The chapter is organized into sections considering the information on 

10 blood Pb as a biomarker (section 3.1), the nature of Pb effects on health (section 3.2), public 

11 health implications and at-risk populations (section 3.3), and exposure and risk information 

12 (section 3.4). Presentation within these sections is organized to address key policy-relevant 

13 questions for this review concerning the evidence and exposure/risk information, building upon 

14 the questions included in the IRP (IRP, section 3.1). 

15 3.1 INTERNAL DISPOSITION AND BIOMARKERS OF EXPOSURE AND DOSE 

16 The health effects of Pb, discussed in detail in the ISA and summarized in Section 3.2 

17 below, are remote from the portals of entry to the body (i.e., the respiratory system and 

18 gastrointestinal tract). Consequently, the internal disposition and distribution of Pb is an integral 

19 aspect of the relationship between exposure and effect. Inhaled lead-bearing particles, depending 

20 on size and solubility, may be absorbed into the systemic circulation or transported to the 

21 gastrointestinal tract (ISA, section 4.2.1.1). The absorption efficiency of Pb from the 

22 gastrointestinal (GI) tract varies with characteristics associated with the ingested Pb (e.g., 

23 particle size and chemical form or matrix), as well as with an individual’s physiology (e.g., 

24 maturity of the GI tract), nutritional status (e.g., iron, calcium, and zinc deficiencies increase 

25 absorption), and the presence of food in the GI tract (ISA, section 4.2.1.2). Once in the blood 

26 stream, where approximately 99% of the Pb is associated with red blood cells (mostly bound to 

27 aminolevulinic acid dehydratase, the predominant ligand), Pb is quickly distributed throughout 

28 the body (e.g., within days) and is available for exchange with the soft and skeletal tissues, 

29 conceptually viewed as the fast and slow turnover pools, respectively (ISA, section 4.2.2). 

30 Skeletal tissue serves as the largest storage compartment, with much less Pb stored in soft tissues 

31 (e.g., kidney, liver, brain, etc) (ISA, section 4.2.2.2). 

32 The role of the bone as the main storage compartment is related to the ability of Pb to 

33 form stable complexes with phosphate and replace calcium in the salt comprising the primary 

34 crystalline matrix of bone (ISA, section 4.2.2.2). In infants less than a year old, the bone is 
January 2013 3-2 Draft - Do Not Quote or Cite

1 estimated to contain approximately 60% of the total body burden of Pb (ISA, section 4.2.2.2; 

2 Barry, 1975). Circulating Pb is taken up into the bone regions of active calcification. 

3 Accordingly, during early childhood there is rapid uptake of Pb into mineralizing bone, with 

4 somewhat more than 70% of total body burden Pb estimated to reside in bone of children aged 2 

5 to 16, increasing up to more than 90% by adulthood (ISA, section 4.2.2.2; Barry, 1975). The net 

6 accumulation of Pb in bone over a person’s lifetime results in bone lead concentrations generally 

7 increasing with age (ISA, section 4.2.2.2). 

8 The distribution of Pb in the body is dynamic. Throughout life, Pb in the body is 

9 exchanged between blood and bone, and between blood and soft tissues (ISA, sections 4.3.5 and 

10 4.2.2; 2006 CD, section 4.3.2). The rates of these exchanges vary with age, exposure and 

11 various physiological variables. For example, resorption of bone, which results in the 

12 mobilization of Pb from bone into the blood, is a gradual process in later adulthood. Resorption 

13 rate is appreciably increased in pregnant or nursing women, and in association with osteoporosis 

14 in postmenopausal women or, to a lesser magnitude, in older men (ISA, sections 4.3.5.2). 

15 Changes in Pb exposure circumstances can also influence these exchanges, e.g., substantial 

16 reductions in exposure levels contribute to increased release of Pb from the bone into the blood 

17 (ISA, section 4.3.5). The studies that address the relative contributions of bone Pb and current 

18 Pb exposure to blood Pb are limited to a few human studies during the 1980s and early 1990s, 

19 when leaded gasoline usage was common, and a primate study. These studies indicate an 

20 appreciable contribution from bone Pb stores to Pb in blood, on the order of 40-70% of blood Pb 

21 contributed from bone, under circumstances with higher concurrent exposure than exposures 

22 common today (ISA, section 4.3.5; Smith et al., 1996; Gulson et al., 1995; Manton, 1985; 

23 Franklin et al., 1997). 

24 During bone resorption that occurs in pregnancy, Pb is released from bone, increasing the 

25 bone contribution to maternal blood Pb levels, and maternal Pb circulates across the placenta, 

26 posing risk to the developing fetus and providing the fetal body burden (ISA, sections 4.2.2.4, 

27 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 

28 maternal bone Pb and current maternal exposure to maternal blood Pb and fetal body burden, are 

29 influenced by the relative magnitude of current and historical exposures. In various study 

30 populations with mean maternal blood Pb levels ranging from 1.7 to 8.6 μg/dL, average blood Pb 

31 concentration in the umbilical cord (as representative of newborn blood) has been reported to 

32 range from 70% to 100% of average maternal blood Pb (ISA, section 4.2.2.4); the range is 

33 similar for four study populations with mean maternal blood Pb level below 4 μg/dL (Amaral et 

34 al., 2010; Patel and Prabhu, 2009; Lagerkvist et al., 1996; Jedrychowski et al., 2011). The 

35 relationship for individual mother-child pairs is more variable. In a low income population with 

36 mean maternal blood Pb of 1.9 μg/dL, factors associated with occurrences of relatively higher 
January 2013 3-3 Draft - Do Not Quote or Cite

1 cord blood Pb level to maternal blood Pb level pairs included maternal blood pressure and 

2 alcohol consumption, while factors associated with relatively lower ratios of cord blood Pb to 

3 maternal blood Pb included maternal hemoglobin and sickle cell trait (Harville et al., 2005). As 

4 a result of the contributions of maternal bone Pb to maternal blood Pb during pregnancy, the 

5 contribution to fetal body burden from maternal bone Pb relative to maternal concurrent 

6 exposure is appreciable. This maternal bone Pb contribution to fetal body burden is likely to 

7 vary, however, in response to differences between maternal historical exposures and those during 

8 pregnancy, among other factors (2006 CD, sections 4.3.1.5 and 4.3.2.5; ISA, section 6.1; Chuang 

9 et al., 2001; Gulson et al., 1999; Gulson et al., 2003; Gulson et al., 2004a; Rothenberg et al., 

10 2000). 

11 Limited data indicate that blood Pb levels in some newborns may decline during the 

12 period extending through the first few months of life; the extent to which this may occur may be 

13 influenced by the magnitude of blood Pb level at birth and of subsequent exposure during early 

14 infancy (ISA, section 4.2.2.1; Carbone et al., 1998; Simon et al., 2007; Gulson et al., 1999, 

15 2001). As infants become more mobile and engage in hand-to-mouth behavior, blood Pb levels 

16 then commonly increase to a peak around two years of age (ISA, sections 4.4.1 and 6.2.1.1). 

17  Does the current evidence continue to support blood Pb level as a useful indicator 

18 of Pb exposure and dose for purposes of characterizing Pb health effects, with 

19 well recognized strengths and limitations? To what extent does the evidence 

20 suggest alternatives? 

21 As discussed in past CDs and in the ISA, blood Pb is the most commonly used indicator 

22 of human Pb exposure. For example, given the association with exposure and the relative ease of 

23 collection, blood Pb levels are extensively used as an index or biomarker of exposure by national 

24 and international health agencies, as well as in epidemiological and toxicological studies of Pb 

25 health effects and dose-response relationships (ISA, sections 4.3.2, 4.4.1, 5.3, 5.4, 5.5, 5.6, 5.7, 

26 and 5.8). Since 1976, the U.S. Centers for Disease Control and Prevention (CDC) has been 

27 monitoring blood Pb levels nationally through the National Health and Nutrition Examination 

28 Survey (NHANES). This survey has documented the dramatic decline in mean blood Pb levels 

29 in all ages of the U.S. population that has occurred since the 1970s, as shown in Figure 3-1, and 

30 that coincides with actions on leaded fuels, leaded paint, lead in food packaging, and lead31 containing plumbing materials that have reduced Pb exposure in the U.S. (ISA, section 4.4.1; 

32 Pirkle et al., 1994; Schwemberger et al., 2005). This decline has continued over the more recent 

33 past. For example, the 2009-2010 geometric mean blood Pb level in U.S. children aged 1-5 

34 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 

35 in 2003-2004, the most recent data available at the time of the last review (73 FR 67002); 
January 2013 3-4 Draft - Do Not Quote or Cite

1 somewhat less dramatic declines have also been reported in the upper tails of the distribution and 

2 in different groups with higher levels than the general child population (ISA, Figure 4-19). 

3 

4 Source: Adapted from data from the NHANES (NCHS, 2010) 

5 Note: The means of logged blood Pb were weighted to represent national averages. Data were from the publically NHANES II, NHANES III for 

6 1988 1991 and 1992 1994, and the continuous NHANES in 1999 2000, 2003 2004, 2005 2006, 2007 2008. Continuous NHANES data from 

7 2001 2002 and 2009 2010 are not included because there were only 551 blood Pb samples in each of those data sets. The year plotted for 

8 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 

9 the continuous NHANES.

10 Figure 3-1. Temporal trend in mean blood Pb levels for NHANES cohorts. 

11 The CDC, and its predecessor agencies, have for many years used blood Pb level as a 

12 metric for identifying highly exposed children at risk of adverse health effects for whom 

13 recommendations might be made for their protection (e.g., CDC, 1991; CDC, 2005). In 1978, 

14 when the current Pb NAAQS was established, the CDC recognized a blood Pb level of 30 μg/dL 

15 as a level warranting individual intervention (CDC, 1991). In 1985, the CDC recognized a level 

16 of 25 μg/dL for individual child intervention, and in 1991, they recognized a level of 15 μg/dL at 

17 which individual intervention actions were recommended, and a level of 10 μg/dL at which more 

18 general community-wide prevention activities were to be implemented (CDC, 1991; CDC, 

19 2005). In 2005, with consideration of a review of the evidence by their advisory committee, 
January 2013 3-5 Draft - Do Not Quote or Cite

1 CDC revised their statement on Preventing Lead Poisoning in Young Children, specifically 

2 recognizing the evidence of adverse health effects in children with blood Pb levels below 10 

μg/dL and emphasizing the importance of preventive measures (CDC, 2005).1 3 Consistent with 

this statement, the CDC revised their approach in 2012 to one that relies on the 97.5th 4 percentile 

of blood Pb concentrations in U.S. children (currently 5 μg/dL)2 5 as a reference level for 

6 identifying children for whom they recommend particular follow-up actions (CDC, 2012). 

7 Multiple studies of the relationship between Pb exposure and blood Pb in children (e.g., 

8 Lanphear and Roghmann 1997; Lanphear et al., 1998), have shown blood Pb levels to reflect Pb 

9 exposures, including exposures to Pb in surface dust. These and studies of child populations 

10 near active sources of air emissions (e.g., metal smelters), further demonstrate the effect of 

11 airborne Pb on interior dust and on blood Pb (ISA, sections 4.4.1, 4.5.1 and 4.5.3; Hilts, 2003; 

12 Gulson et al., 2004b). Accordingly, blood Pb level was the index of exposure in the assessment 

13 of young children’s risk performed in the last Pb NAAQS review (described in section 3.4 

14 below). 

15 A well recognized strength of using children’s blood Pb to investigate relationships 

16 between Pb exposure and health effects is the relatively lesser uncertainty in the causality 

17 aspects of such relationships than might be associated with such relationships based, for 

18 example, on media concentration. Blood Pb is an integrated marker of aggregate exposure 

19 across all pathways. For example, the blood Pb-response relationships described in 

20 epidemiological studies of lead-exposed populations do not distinguish among different sources 

21 of Pb or pathways of Pb exposure (e.g., inhalation, ingestion of indoor dust, ingestion of dust 

22 containing leaded paint). Given our focus on ambient air contributions to Pb exposures, 

23 discussion in response to the question below considers the available information regarding 

24 relationships between Pb in ambient air and the associated Pb in blood. Additionally, the 

25 exposure assessment performed for the last review of the Pb NAAQS (and described in section 

26 3.4 below), employed biokinetic modeling to estimate blood Pb levels associated with aggregate 

27 Pb exposure to inform our estimates of contributions to blood Pb arising from ambient air related 

28 Pb. 

29 The response of adult blood Pb levels to appreciable changes in exposure circumstances 

30 is generally slower than that of blood Pb levels in young children. For example, simulations 

31 using biokinetic models indicate that blood Pb levels in adults achieve a new quasi-steady state 

 

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 μg/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

1 within 75-100 days (approximately 3-4 times the blood elimination half-life) subsequent to 

2 abrupt increases in Pb intake (ISA, section 4.3.5.2); similar models indicate a much quicker 

3 response of blood Pb levels in children both with regard to abrupt increases and reductions in Pb 

4 exposure (ISA, section 4.3.5.1). The response in young children may reflect their much more 

5 labile bone pool associated with the rapid turnover of bone mineral in response to their rapid 

6 growth rates (ISA, section 4.3.5). As a result of these physiological processes in young children, 

7 their blood Pb levels tend to more quickly reflect changes in their total body burden (associated 

8 with their shorter exposure history), and can also reflect changes in recent exposures (ISA, 

9 section 4.3.5). 

10 The extent to which blood Pb measurements represent current exposure circumstances 

11 may be uncertain, particularly where histories include exposures largely different from those 

12 occurring more recently (ISA, section 4.3.2). This uncertainty may be greater for blood Pb 

measurements taken in older children3 13 and adults that those for young children as a result of their 

14 longer exposure histories. For example, the bone of adults has accumulated decades of Pb 

15 exposures (with past exposures often greater than current ones for current U.S. populations) such 

16 that the bone may be a significant source of Pb in blood in later years, after exposure has ended. 

17 Thus, in populations with past exposures that were appreciably elevated in comparison to more 

18 recent exposures, current blood Pb levels may predominantly reflect their exposure history rather 

19 than current exposures (ISA, sections 4.3.5.2 and 4.4.1). Accordingly, the extent to which 

20 studies using cross-sectional blood Pb measurements as the exposure biomarker inform our 

21 understanding of relationships between recent Pb exposures and various health effects, can differ 

22 across age groups, and is greatest for very young children, as discussed in section 3.3 below. 

23 Alternative biomarkers of Pb exposure include bone Pb, teeth Pb, and hair Pb (ISA, 

24 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 

25 adult body’s Pb burden, bone Pb levels are recognized as indicators of body burden and 

26 cumulative exposure history (ISA, sections 4.2.2.2 and 4.3). The currently available evidence 

27 does not, however, indicate these or any other alternatives to be superior to blood Pb in young 

28 children or as commonly used for the purposes of tracking recent Pb exposures and for assessing 

29 potential health risk for this age group (ISA, section 4.7.3). In summary, the current evidence 

30 continues to support our conclusions from the last review regarding the use of blood Pb levels as 

31 an internal biomarker of Pb exposure and dose informative to characterizing Pb health effects in 

32 young children. 

 

3

 There is a paucity of experimental measurements of Pb biomarkers during adolescence to inform our 

characterization of Pb biokinetics (and relative roles of recent 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

1  To what extent has new information altered scientific conclusions regarding the 

2 relationships between Pb in ambient air and Pb in children’s blood? 

3 As described above, blood Pb is an integrated marker of aggregate exposure across all 

4 pathways and a reflection of exposure history. Thus, our interpretation of the health effects 

5 evidence for purposes of this review necessitates characterization of the relationships between Pb 

6 from those sources and pathways of interest in this review (i.e., those related to Pb emitted into 

7 the air) and blood Pb. The evidence in this regard derives from analyses of datasets for 

8 populations residing in areas with differing air Pb concentrations, including datasets for 

9 circumstances in which blood Pb levels have changed in response to changes in air Pb. The 

10 control for variables other than air Pb that can affect blood Pb varies across these analyses. 

11 Lead in ambient air contributes to Pb in blood by multiple exposure pathways by both 

12 inhalation and ingestion exposure routes (ISA, section 4.1.1). The quantitative relationship 

13 between ambient air Pb and blood Pb, which is often termed a slope or ratio, describes the 

14 increase in blood Pb (in μg/dL) estimated to be associated with each unit increase of air Pb (in 

μg/m3 15 ). Ratios are presented in the form of 1:x, with the 1 representing air Pb (in μg/m3) and x 

16 representing blood Pb (in μg/dL). Description of ratios as higher or lower refers to the values for 

17 x (i.e., the change in blood Pb per unit of air Pb). Slopes are presented as simply the value of x. 

18 At the conclusion of the last review in 2008, the EPA interpreted the evidence as 

19 providing support for use (in informing the Administrator’s decision on standard level) of a 

20 range “inclusive at upper end of estimates on the order of 1:10 and at the lower end on the order 

21 of 1:5” (73 FR 67002). This conclusion reflected consideration of the air-to-blood ratios 

presented in the 1986 CD4 22 and associated observations regarding factors contributing to variation 

23 in such ratios, ratios reported subsequently and ratios estimated based on modeling performed in 

24 the REA, as well as advice from CASAC (73 FR 66973-66975, 67001-67002). The information 

25 available in this review, which is assessed in the ISA and is largely, although not completely, 

26 comprised of studies that were available in the last review, does not alter the primary scientific 

27 conclusions drawn in the last review regarding the relationships between Pb in ambient air and 

28 Pb in children’s blood. The ratios summarized in the ISA in this review span a range generally 

29 consistent with the range concluded in 2008 (ISA, section 4.5.1). 

30 The air-to-blood ratios for children, or for populations inclusive of children, discussed in 

31 the ISA for this review are summarized in Table 3-1. The evidence pertaining to this 

32 quantitative relationship between air Pb and children’s blood Pb is now, as in the past, limited by 

33 the circumstances in which the data are collected. These estimates are generally developed from 

34 studies of populations in a variety of Pb exposure circumstances. Accordingly, there is 

 

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

1 significant variability in air-to-blood ratios among the different study populations exposed to Pb 

2 through different air-related exposure pathways and at different exposure levels. This variability 

3 in air-to-blood estimates can relate to the representation of air-related pathways and study 

4 populations, including, for example, relatively narrow age ranges for the population, to reduce 

5 age-related variability in blood Pb or including populations with narrowly specified dietary 

6 sources. It can also relate to the precision of air and blood measurements and of the study 

7 circumstances, such as with regard to spatial and temporal aspects. Additionally, in situations 

8 where exposure to nonair sources covaries with air-related exposures that are not accounted for 

9 in deriving ratio estimates, uncertainties may relate to the potential for confounding by nonair 

10 exposure covariance (ISA, section 4.5). 

11 As was noted in the last review, population age is an important influence on the 

12 magnitude of air-to-blood ratio estimates derived. Ratios for children are generally higher than 

13 those for adults, and higher for young children than older children, perhaps due to behavioral 

14 differences between the age groups, as well as the more rapid response of children’s blood Pb to 

15 exposure and body burden changes (as discussed above) and shorter exposure history. Similarly, 

16 given the common pattern of higher blood Pb levels in pre-school aged children than during the 

17 rest of childhood, related to behaviors that increase environmental exposures, ratios would be 

18 expected to be highest in earlier childhood. Additionally, estimates of air-to-blood ratios that 

19 include air-related ingestion pathways in addition to the inhalation pathway are “necessarily 

20 higher”, in terms of blood Pb response, than those estimates based on inhalation alone (USEPA 

21 1986, p. 11-106). Thus, the extent to which studies account for the full set of air-related 

22 inhalation and ingestion exposure pathways affects the magnitude of the resultant air-to-blood 

23 estimates, such that including fewer pathways as “air-related” yields lower ratios. Estimates of 

24 air-to-blood ratios can also be influenced by population characteristics that may influence blood 

25 Pb; accordingly, some analyses include adjustments. 

26 Given the recognition of young children as a key at-risk population in section 3.3 below, 

27 as well as the influence of age on blood Pb levels, the studies presented in Table 3-1 are grouped 

28 with regard to the extent of their inclusion of young children (e.g., children barely school age). 

29 Among the first group of studies, focused exclusively on young children, is the only study that 

30 dates from the end of or after the phase-out of leaded gasoline usage (Hilts, 2003). This study 

31 reports changes in children’s blood Pb levels associated with reduced Pb emissions and 

32 associated air concentrations near a Pb smelter in Canada (for children through age five). Given 

33 the timing of this study, after the leaded gasoline phase-out, and its setting near a smelter, the 

34 ambient air Pb in this study may be somewhat more comparable to that near sources in the U.S. 
January 2013 3-9 Draft - Do Not Quote or Cite

today than other studies discussed here. The study authors report an air-to-blood ratio of 1:6.5 1 

2 An EPA analysis of the air and blood data reported for 1996, 1999 and 2001 results in a ratio of 

3 1:6.5, and the analysis focused only on the 1996 and 1999 data (pre- and post- the new 

technology) yields a ratio of 1:7 (ISA, section 4.5.1; Hilts, 2003).6 4 The two other studies that 

5 focused on children of age 5 or younger analyze variations in air Pb as a result of variations in 

6 leaded gasoline usage in Chicago, Illinois. The study by Hayes et al. (1994) compared patterns 

7 of ambient air Pb reductions and blood Pb reductions for large numbers of children, aged 6 

8 months - 5 years, in Chicago between 1974 and 1988, a period when significant reductions 

9 occurred in both measures. The study reports a better fit for the log-log model which describes a 

10 pattern of higher ratios with lower ambient air Pb and blood Pb levels (Hayes et al., 1994). 

11 Based on the log-log model, the ratio derived for the relationship of quarterly mean air 

12 concentration with blood Pb during the period is 1:8 (Table 3-1). Another analysis for a Chicago 

13 dataset, performed by Schwartz and Pitcher (1989) focused on the association of blood Pb in 

14 black children (aged < 5 years) with the use of leaded gasoline from 1978 through 1980. Given 

15 that leaded gasoline exposure occurs by air-related pathways, additional analyses have related 

16 the leaded gasoline usage for this period to air concentrations. Using the resulting relationship of 

17 blood Pb with air Pb (adjusted for age and a number of other covariates) yields a ratio of 1:8.6 

18 (ISA, table 4-12, section 4.5.2). The blood Pb concentrations in the two leaded gasoline studies 

19 are appreciably higher (a factor of two or more) than those in the study near the smelter (Hilts, 

20 2003). 

21 The second group of studies in Table 3-1 (comprised of studies including but not limited 

22 to children less than or equal to five years of age) includes a complex statistical analysis and 

23 associated dataset for a cohort of children born in Mexico City from 1987 through 1992 (Schnaas 

24 et al., 2004). This study, which was not assessed in the last review, encompasses the period of 

 

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 programs were in place in 1992, suggesting they are unlikely to 

have contributed to the sudden drop in blood Pb levels occurring after 1997 (Hilts, 2003). Other aspects with 

potential implications for ratios include the potential for children with lower blood Pb levels not to return for 

subsequent testing, and the age range of 6 to 36 months in the 2001 blood screening compared to ages up to 60 

months in 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 a 

temporary (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 period, 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 first 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

1 leaded gasoline usage and further informs our understanding of factors influencing the 

2 quantitative relationship between air Pb and children’s blood Pb. Air-to-blood ratios developed 

3 from this study are influenced by a number of factors and appear to range from roughly 2 to 6, in 

4 addition to an estimate of 9 (ISA, section 4.5.1), although this is derived from data set restricted 

5 to the latter years of the study when little change in air Pb concentration occurred, such that the 

6 role of air Pb may be more uncertain. Estimates associated with the developmental period of 

7 highest exposure – e.g., age 2 years - range up to approximately 6, illustrating the influence of 

8 age on the ratio (ISA, section 4.5.1). Also in the Table 3-1 second group are two much older 

9 studies of populations comprising age ranges extending well beyond 6 years. The first is the 

10 review and meta-analysis by Brunekreef (1984) using datasets available at the time for variously 

11 aged children as old as 18 years with identified air monitoring methods and reliable blood Pb 

data for 18 locations in the U.S. and internationally.7 12 The author discusses potential confounders 

13 of the relationship between air Pb and blood Pb, recognizing the desirability of taking them into 

14 account when deriving an air-to-blood relationship from a community study, but noting that was 

15 not feasible in such an analysis. Two models were produced, one based on the full pooled dataset 

and a second limited to blood Pb-air Pb data pairs with blood Pb levels below 20 μg/dL (r2 16 

17 values were 0.692 and 0.331, respectively). From these two logn-logn models, air-to-blood ratio 

18 estimates were derived for air concentrations corresponding to the geometric means of the two 

sets of data pairs. At those concentrations (1.5 and 0.54 μg/m3 19 , respectively), the resultant ratios 

20 both round to 5. The study by Schwartz and Pitcher (1989) described above also analyzed the 

21 relationship between U.S. NHANES II blood Pb levels for white subjects, aged <74 years, and 

22 national usage of leaded gasoline. A separate, less specifically described, air Pb dataset was used 

23 to convert the relationship of blood Pb with gas Pb to one for blood Pb with air Pb, with a 

24 resultant ratio on the order of 9, adjusted for age and other covariates (Henderson, 2007, pp. D-2 

25 to D-3; ISA, Table 4-12). 

26 The last two studies included in Table 3-1 are focused on older children (ages 6-11). The 

27 methods for characterization of air Pb concentrations (and soil Pb for latter study) also differ 

28 from other studies in Table 3-1. The first study regressed average blood Pb concentrations for 

29 multiple locations around Mumbai, India on average air Pb concentrations at those locations 

30 (Tripathi et al., 2001). The values in the linear regression were 13 pairs of location-specific 

31 geometric means of all the data collected over the 13-year period from 1984 to 1996; the 

32 reported slope was 3.6 (Tripathi et al., 2001). The location-specific geometric mean blood Pb 

 

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 (Brunekreef et al, 1983). The studies cited here adjusted for 

parental education (Zielhuis 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

1 levels in this study (8.6-14.4 μg/dL) indicate blood Pb distributions in this age group much 

2 higher than those pertinent to similarly aged children in the U.S. today. The second study 

3 analyzed air, soil and children’s blood Pb concentrations in Duisburg, Germany during the 

4 leaded gasoline phase-out (Ranft et al., 2008). Average blood Pb levels declined over the nearly 

5 20-year study period from 9 μg/dL in 1983 (345 children average age of 9 years) to 3 μg/dL in 

2000 (162 children average of 6 years).8

 Average air Pb concentration declined from 0.45 μg/m3 6 

to 0.06 μg/m3 7 over the same period, with the largest reduction occurring between the first study 

8 year (derived from two monitoring sites for full study area) and the second study year, 1991, for 

9 which air concentrations were derived from a combination of dispersion modeling and the two 

monitoring sites.9 For a mean air Pb concentration of 0.1 μg/m3 10 , the study’s multivariate log11 linear regression model predicted air to blood ratios of 3.2 and 6.4 for “background” blood Pb 

12 concentrations of 1.5 and 3 μg/dL, respectively. In this study, background referred to Pb in 

13 blood from other sources; the blood Pb distribution over the study period, including levels when 

14 air Pb concentrations are lowest, indicates 3 μg/dL may be the better estimate of background for 

15 this study population. Inclusion of soil Pb as a variable in the model may have contributed to an 

16 underestimation of the these blood Pb-air Pb ratios for this study because some of the Pb in soil 

17 likely originated in air and the blood Pb-air Pb slope does not include the portion of the soil/dust 

18 Pb ingestion pathway that derives from air Pb. The ISA also presents somewhat higher air-to19 blood ratio estimates derived using univariate linear, log-log and log-linear models on the 

20 median air and blood Pb concentrations reported for the five years included in this study (ISA, 

21 section 4.5.1; Ranft et al., 2008, Table 2). Uncertainties related to this study’s estimates include 

22 those related to the bulk of air concentration reduction occurring between the first two time 

23 points (1983 and 1991) and the difference among the year’s air datasets (e.g., two data sources 

24 [air monitors] in 1983 and multiple geographical points from a combination of the monitors and 

25 modeling in subsequent years). 

 

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 approximately 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 years. Surface soil Pb measurements 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

1 Table 3-1. Empirically derived air-to-blood ratios for populations inclusive of children. 

Study Information Quantitative Analysis Air-to-Blood 

Ratio A

Focused on children < 5 years old 

Children, 0.5-5 yr (n = 9,604), average age 2.5 yr 

Chicago, IL, 1974-1988 

Urban area with lead-emitting industries, leaded gasoline usage 

 Hayes et al. (1994) 

logn-logn regression: quarterly mean PbB and PbA 

[unadjusted] 

PbB: 10-28 μg/dL (quarterly mean) 

PbA: 0.05-1.2 μg/m3 (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/m3 (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 and 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/m3) 

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 (logn-logn 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/m3 (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 , logn-logn 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/m3 (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 and 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/m3) 

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/m3 (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, logn-logn, 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/m3 (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/m3 from study’s central air Pb, which is provided in μg/m3 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 ISA, 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, contributing to underestimation of contribution from air Pb (see text and ISA, section 4.5.1).

GM, geometric mean; AM, arithmetic mean; GSD, geometric standard deviation; PbB, blood Pb concentration, μg/dL; PbA, air Pb concentration, μg/m3

2 
January 2013 3-13 Draft - Do Not Quote or Cite

1 In the 2008 review, in addition to considering the evidence presented in the published 

2 literature and that reviewed in the 1986 CD, we also considered air-to-blood ratios derived from 

3 the exposure assessment (73 FR 66974; 2007 REA, section 5.2.5.2). In the exposure assessment 

4 (summarized in section 3.4 below), current modeling tools and information on children’s activity 

5 patterns, behavior and physiology were used to estimate blood Pb levels associated with 

6 multimedia and multipathway Pb exposure. The results from the various case studies assessed, 

7 with consideration of the context in which they were derived (e.g., the extent to which the range 

8 of air-related pathways were simulated, and limitations associated with those simulations), and 

9 the multiple sources of uncertainty (see section 3.4.7 below) are also informative to our 

10 understanding of air-to-blood ratios. Estimates of air-to-blood ratios for the two REA case 

11 studies that represent localized population exposures exhibited an increasing trend across air 

12 quality scenarios representing decreasing air concentrations. For example, across the alternative 

standard levels assessed, which ranged from a calendar quarter average of 1.5 μg/m3 13 down to a 

monthly average of 0.02 μg/m3 14 , the ratios ranged from 1:2 to 1:9 for the general urban case 

15 study, with a similar trend although of generally higher ratio for the primary smelter case study 

16 subarea. This pattern of model-derived ratios is generally consistent with the range of ratios 

17 obtained from the literature. We continue to recognize a number of sources of uncertainty 

associated with these model-derived ratios which may contribute to high or low biases.10 18 

19 The evidence on the quantitative relationship between air Pb and air-related Pb in blood 

20 is now, as in the past, limited by the circumstances (such as those related to Pb exposure) in 

21 which the data were collected. Previous reviews have recognized the significant variability in 

22 air-to-blood ratios for different populations exposed to Pb through different air-related exposure 

23 pathways and at different air and blood levels, with the 1986 CD noting that ratios derived from 

24 studies involving the higher blood and air Pb levels pertaining to workers in lead-related 

25 occupations are generally smaller than ratios from studies involving lower blood and air Pb 

26 levels (ISA, p. 4-129; 1986 CD, p. 11–99). Consistent with this observation, slopes in the range 

27 of 3 to 5 were estimated for child population datasets assessed in the 1986 CD (ISA, p. 4-129; 

 

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 urban 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 ratios from this case study to more fully capture the impact 

of changes in ambient air Pb on indoor dust Pb, and consequently on blood Pb. Some have suggested, however, that 

the regression used may not accurately reflect the temporal relationship between reductions 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

1 1986 CD p. 11–100; Brunekreef, 1984; Tripathi et al., 2004). Additional studies considered in 

2 the last review and those assessed in the ISA provide evidence of ratios above this older range 

3 (ISA, p. 4-130). For example a ratio of 6.5-7 is indicated by the study by Hilts (2003), one of the 

4 few studies that evaluate the air Pb-blood Pb relationship in conditions that are closer to the 

5 current state in the U.S. ( ISA, p. 4-130). We additionally note the variety of factors identified in 

6 the ISA that may potentially affect estimates of various ratios (including potentially coincident 

7 reductions in nonair Pb sources during the course of the studies), and for which a lack of 

8 complete information may preclude any adjustment of estimates to account for their role (ISA, 

9 section 4.5). 

10 In summary, as at the time of the last review of the NAAQS for Pb, the currently 

11 available evidence includes estimates of air-to-blood ratios, both empirically- and model-derived, 

12 with associated limitations and related uncertainties. These limitations and uncertainties, which 

13 are summarized here and also noted in the ISA, usually include uncertainty associated with 

14 reductions in other Pb sources during study period. The limited amount of new information 

15 available in this review has not appreciably altered the scientific conclusions reached in the last 

16 review regarding relationships between Pb in ambient air and Pb in children’s blood or with 

17 regard to the range of ratios. The currently available evidence continues to indicate ratios 

18 relevant to the population of young children in the U.S. today, reflecting multiple air-related 

19 pathways in addition to inhalation, to be generally consistent with the approximate range of 1:5 

20 to 1:10 given particular attention in the 2008 NAAQS decision, including the “generally central 

21 estimate” of 1:7 (73 FR 67002, 67004; ISA, pp. 4-129 to 4-130). 

22 3.2 NATURE OF EFFECTS 

23 Lead has been demonstrated to exert a broad array of deleterious effects on multiple 

24 organ systems as described in the assessment of the evidence available in this review and 

25 consistent with conclusions of past CDs (ISA, section 2.6; 2006 CD, section 8.4.1). A sizeable 

26 number of studies on Pb health effects are newly available in this review and are critically 

27 assessed in the ISA as part of the full body of evidence. The newly available evidence reaffirms 

28 conclusions on the broad array of effects recognized for Pb in the last review (see ISA, section 

2.10). Consistent with those conclusions, the ISA determines that causal relationships11 29 exist for 

 

11 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 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

Pb12 1 with effects on the nervous system (cognitive function decrements and attention-related 

2 behavioral problems in children), hematological system (altered heme synthesis and decreased 

3 red blood cell survival and function), and cardiovascular system (hypertension and coronary 

4 heart disease), and on reproduction and development (postnatal development and male 

5 reproductive function) (ISA, table 2-2). Additionally, the ISA describes relationships between 

Pb and effects on kidney and immune system function, and with cancer13 as likely causal14 6 (ISA, 

7 table 2-2, sections 2.6.3, 2.6.4 and 2.6.7). 

8 In some categories of health effects, there is newly available evidence regarding some 

9 aspects of the effects described in the last review or that strengthens our conclusions regarding 

10 aspects of Pb toxicity on a particular physiological system. Among the nervous system effects of 

11 Pb, the newly available evidence is consistent with conclusions in the previous review which 

12 recognized that “[t]he neurotoxic effects of Pb exposure are among those most studied and most 

13 extensively documented among human population groups” (2006 CD, p. 8-25). Nervous system 

14 effects that receive prominence in the current review, as in previous reviews, include those 

15 affecting cognitive function and behavior in children (ISA, section 5.3), with conclusions that are 

16 consistent with findings of the last review. 

17 Across the broad array of Pb effects for systems and processes other than the nervous 

18 system, the evidence base has been augmented with additional epidemiological investigations in 

19 a number of areas, including developmental outcomes, such as puberty onset, and adult outcomes 

20 related to cardiovascular function, for which several large cohorts have been analyzed (ISA, 

21 Table 2-8 and sections 5.4 and 5.8). Conclusions on these other systems and processes are 

22 consistent with conclusions reached in the last review, while also extending our conclusions on 

23 some aspects of these effects. For example, evidence in this review for the cardiovascular 

24 system includes information on the role of interactions of cumulative Pb exposure with other 

25 factors such as stress in contributing to hypertension, and on a role for Pb in contributing to 

26 coronary heart disease (ISA, section 5.4 and Table 2-8). 

 

12 In determining that a causal relationship exists for Pb with specific health effects, EPA has concluded 

that “[e]vidence is sufficient to conclude that there is a causal relationship with relevant pollutant exposures (i.e., 

doses or exposures generally within one to two orders of magnitude of current levels)” (ISA, p. lxiv) 13 Lead has been classified as a probable human carcinogen by the International Agency for Research on 

Cancer, based mainly on sufficient animal evidence, and as reasonably anticipated 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 for Pb with specific health effects, EPA has concluded 

that “[e]vidence is sufficient to conclude that a causal relationship is likely to exist with relevant pollutant 

exposures, but important uncertainties remain” (ISA, p. lxiv). 
January 2013 3-16 Draft - Do Not Quote or Cite

1 Based on the extensive assessment of the full body of evidence available in this review, 

2 the major conclusions drawn by the ISA regarding health effects of Pb in children include the 

3 following (ISA, section 1.3.1). 

4 Multiple epidemiologic studies conducted in diverse populations of children 

5 consistently demonstrate the harmful effects of Pb exposure on IQ, academic 

6 performance, learning and memory. Epidemiologic studies also demonstrate the 

7 effect of Pb exposure on inattention, impulsivity, and hyperactivity in children. 

8 The evidence in children is supported by findings in animal studies demonstrating 

9 analogous effects and biological plausibility at relevant exposure levels. Evidence 

10 suggests that some Pb-related cognitive effects may not be reversible and that 

11 neurodevelopmental effects of Pb may persist into adulthood (section 2.9.4). 

12 Lead exposure also causes hematologic effects (such as effects on blood cells or 

13 blood producing organs) in children and is associated with an increased risk of 

14 internalizing behaviors (e.g., withdrawn behavior and depressive symptoms), 

15 sensory and motor function decrements, atopic and inflammatory conditions (e.g., 

16 asthma and allergy) in children, as well as misconduct in older children and 

17 young adults. Uncertainties arising from the lack of information about the specific 

18 Pb-exposure histories which contribute to observed blood Pb levels are greater in 

19 adults and older children than in young children (section 2.9.5). 

20 

21 Based on the extensive assessment of the full body of evidence available in this review, 

22 the major conclusions drawn by the ISA regarding health effects of Pb in adults include the 

23 following (ISA, section 1.3.1). 

24 A large body of evidence from both epidemiologic studies of adults and 

25 experimental studies in animals demonstrates the effect of long-term Pb exposure 

26 on increased blood pressure (BP) and hypertension (Section 2.6.2). In addition to 

27 its effect on BP, Pb exposure leads to coronary heart disease and death from 

28 cardiovascular causes and is likely to cause cognitive function decrements, 

29 symptoms of depression and anxiety, reduced kidney function, and immune effects 

30 in adults. The extent to which the effects of Pb on the cardiovascular system are 

31 reversible is not well characterized. It is also important to note that the 

32 frequency, timing, level and duration of Pb exposure causing the effects observed 

33 in adults has not been pinpointed, and higher past exposures may well have 

34 contributed to the development of health effects measured later in life. 

35 

36 As in prior reviews of the Pb NAAQS, this review is focused on those effects most 

37 pertinent to ambient air Pb exposures. Given the reductions in ambient air Pb levels over the 

38 past decades, these effects are generally those associated with the lowest levels of Pb exposure 

39 that have been evaluated. Additionally, we recognize the limitations on our ability to draw 

40 conclusions regarding the exposure conditions contributing to the findings from epidemiological 

41 analyses of blood Pb levels in populations of older children and adults, particularly in light of 

42 their history of higher Pb exposures. In the last review, while recognizing the range of health 
January 2013 3-17 Draft - Do Not Quote or Cite

1 effects in variously aged populations related to Pb exposure, we focused on the health effects for 

2 which the evidence was strongest with regard to relationships with the lowest exposure levels, 

3 neurocognitive effects in young children. The policy-relevant questions on health effects for this 

4 review (identified in the IRP) were framed in recognition of the conclusions of the last review. 

5 Our consideration of the health effects evidence in this review is framed by policy-relevant 

6 questions building on those identified in the IRP. 

7  To what extent is there new scientific evidence available to improve our 

8 understanding of the health effects associated with various time periods of Pb 

9 exposures at various stages of life? 

10 As in the last review, we base our current understanding of health effects associated with 

11 different Pb exposure circumstances at various stages of life on the full body of available 

12 evidence which includes epidemiological studies of health effects associated with population Pb 

13 biomarker levels as well as laboratory animal studies in which the effects of different exposures 

14 on different lifestages are assessed under controlled conditions. The epidemiological evidence is 

15 overwhelmingly comprised of studies that rely on blood Pb for the exposure metric, with the 

16 remainder largely including a focus on bone Pb. Because these metrics reflect Pb in the body 

17 (e.g., as compared to Pb exposure concentrations) and, in the case of blood Pb, reflect Pb 

18 available for distribution to target sites, they strengthen the evidence base for purposes of 

19 drawing causal conclusions with regard to Pb generally. The complexity of Pb exposure 

20 pathways and internal dosimetry tends to limit the extent to which these types of studies inform 

21 our more specific understanding of the Pb exposure circumstances (e.g., timing, duration, 

22 frequency and magnitude) eliciting the various effects. 

23 The specific exposure circumstances, including timing during the lifetime, that contribute 

24 to the blood Pb (or bone Pb) measurements with which associations have been analyzed in 

25 epidemiological studies are unknown. This is particularly the case with regard to the 

26 contributing role of recent exposures for which uncertainty is greater in adults and older children 

27 than in younger children (ISA, section 1.4). For example, a critical aspect of much of the 

28 epidemiological evidence, particularly that focused on older adults in the U.S. today, is the 

29 backdrop of generally declining environmental Pb exposure that is common across many study 

30 populations. An additional complication pertaining to older children and younger adults is the 

31 common behaviors of younger children (e.g., hand to mouth contact) which generally contribute 

32 to relatively greater environmental exposures earlier in life (ISA, sections 4.1.1, 6.2.1). Such 

33 exposure histories complicate our ability to draw conclusions regarding critical time periods and 
January 2013 3-18 Draft - Do Not Quote or Cite

1 lifestages for Pb exposures eliciting the effects with which associations with Pb biomarkers have 

been observed in populations of adults and older children (e.g., ISA, section 2.9.5).15 2 

3 As at the time of the last review, assessment of the full evidence base, including evidence 

4 newly available in this review, demonstrates that Pb exposure prenatally and also in early 

5 childhood can contribute to neurocognitive impacts in childhood, with evidence also indicating 

6 the potential for effects persisting into adulthood (ISA, sections 2.9.5, 2.9.6, and 2.10). In 

7 addition to the observed associations of prenatal and childhood blood Pb with effects at various 

8 ages in childhood, there is also evidence of lead-related cognitive function effects in non9 occupationally exposed adults (ISA, section 5.3.12). This includes evidence of associations of 

10 such effects in adulthood with childhood blood Pb levels and, in other cohorts, with concurrent 

11 (adult) blood Pb levels (ISA, sections 5.3.2.1, 5.3.2.7 and 5.3.12). As the studies finding 

12 associations of adult effects with childhood blood Pb levels did not examine adult blood Pb 

13 levels, the relative influence of adult Pb exposure cannot be ascertained, and a corresponding 

14 lack of early life exposure or biomarker measurements for the latter studies limit our ability to 

15 draw conclusions regarding specific Pb exposure circumstances eliciting the observed effects 

16 (5.3.12). Findings of stronger associations for adult neurocognitive effects with bone Pb, 

17 however, indicate the role of historical or cumulative exposures for those effects (ISA, section 

18 5.3). 

19 Given the relatively short exposure histories of young children, there is relatively 

20 reduced uncertainty regarding the lifestages in which exposures contribute to effects for 

21 associations of early childhood effects with early childhood blood Pb levels (ISA, sections 2.9.5 

22 and 5.3.12). In considering our understanding of the relative impact on neurocognitive function 

23 of additional Pb exposure of children by school age or later we recognize increasing uncertainty 

24 associated with limitations of the currently available evidence, including epidemiological cohorts 

25 with generally similar temporal patterns of exposure. We take note, additionally, of evidence 

26 from experimental animal studies and a small body of epidemiologic studies that indicates that 

27 Pb exposures during different lifestages can induce cognitive impairments. The limited 

28 epidemiological evidence is of populations with blood Pb levels that are not strongly correlated 

29 over time and that can, accordingly, address the issue of the role of exposure subsequent to the 

 

15 The evidence from experimental animal studies can be informative with regard to key aspects of 

exposure circumstances in eliciting specific effects. Accordingly, for health effects where 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 particularly 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 studies of adult populations for whom historical exposures 

were likely more substantial than concurrent ones to suggest that the observed effects may be related to the past 

exposure (ISA, section 5.4.1). For other health effects, the animal 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

1 earliest lifestages (ISA, section 5.3.12; Hornung et al., 2009). Some animal evidence 

2 demonstrates impaired learning with infancy only, from infancy into adulthood, and postinfancy 

3 only Pb exposure (Rice, 1990; Rice and Gilbert 1990; Rice, 1992). Further, evidence that Pb 

4 exposure presents a risk during different lifestages is also consistent with our broader 

5 understanding that nervous system development continues throughout childhood. The limited 

6 analyses of this issue that are newly available in this review do not appreciably change our 

7 understanding or conclusions on this from those of the prior review (ISA, section 5.3.12). 

8 As in the last review, there is also substantial evidence of other neurobehavioral effects in 

9 children, such as attention-related behavioral problems, conduct problems or internalizing 

10 behaviors. The evidence for many of these endpoints, as with neurocognitive effects, also 

11 includes associations of effects at various ages in childhood and, for some effects, into 

12 adulthood, with blood Pb levels reflective of several different lifestages (e.g., prenatal and 

13 several different ages in childhood) (ISA, sections 5.3.3 and 5.3.4). There is similar or relatively 

14 less extensive evidence to inform our understanding of such effects associated with specific time 

15 periods of exposure at specific lifestages than is the case for effects on cognitive function. 

16 Across the range of Pb effects on physiological systems and processes other than the 

17 nervous system, the full body of evidence on etiologically relevant circumstances of Pb exposure 

18 eliciting increases in blood pressure and hypertension is somewhat more informative than is the 

19 case with regard to many other effects. In the case of lead-induced increases in blood pressure, 

20 the evidence indicates an importance of long-term exposure (ISA, sections 2.6.2 and 5.4.7.1). 

21 In summary, as in the last review, we continue to recognize a number of uncertainties 

22 regarding the circumstances of Pb exposure, including timing or lifestages, eliciting specific 

23 health effects. Consideration of the evidence newly available in this review has not appreciably 

24 changed our understanding on this topic. Across the full evidence base, the effects for which our 

25 understanding of relevant exposure circumstances is greatest are neurocognitive effects in 

26 children, and to a lesser degree, hypertension and increased blood pressure. Thus, we continue 

27 to recognize and give particular attention to the role of Pb exposures relatively early in childhood 

28 in contributing to neurocognitive effects which may persist into adulthood. 

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

30  Is there evidence of effects at exposure levels lower than previously observed and 

31 what are important uncertainties in that evidence? 

32 In considering the question posed here, we recognize, as discussed in section 3.1 above, 

33 that the epidemiological evidence base for our consideration in this review, as in the past, 

34 includes substantial focus on internal biomarkers of exposure, such as blood Pb, with relatively 

35 less information specific to exposure levels, including those derived from air-related pathways. 
January 2013 3-20 Draft - Do Not Quote or Cite

1 Given that blood and bone Pb are integrated markers of aggregate exposure across all sources 

2 and exposure pathways, our interpretation of studies relying on them is informed by what is 

3 known regarding the historical context and exposure circumstances of the study populations. For 

4 example, a critical aspect of much of the epidemiological evidence is the backdrop of generally 

5 declining Pb exposure over the past several decades. Thus as a generality, recent 

6 epidemiological studies of populations with similar characteristics as those studied in the past 

7 tend to involve lower overall Pb exposures and accordingly lower blood Pb levels (e.g., ISA, 

8 sections 3.5 and 4.4.1; 2006 CD, section 3.4). This has been of particular note in the evidence of 

9 blood Pb associations with nervous system effects, particularly impacts on cognitive function in 

10 children, for which we have seen associations with progressively lower childhood blood Pb 

11 levels across past reviews (ISA, section 5.3.13; 1986 CD; USEPA, 1990; 2006 CD; 73 FR 

12 66976). 

13 The evidence currently available with regard to the magnitude of blood Pb levels 

14 associated with neurocognitive effects in children is generally consistent with that available in 

15 the review completed in 2008. Nervous system effects in children, specifically effects on 

16 cognitive function, continue to be the effects that are best substantiated as occurring at the lowest 

17 blood Pb concentrations (ISA, sect 1.5). Associations of blood Pb with effects on cognitive 

18 function measures in children have been reported in many studies across a range of childhood 

19 blood Pb levels, including study group (mean/median) levels ranging down to 2 μg/dL (e.g., ISA, 

sections 1.5 and 5.3.2).16 20 Studies in which such findings were reported for childhood study 

group blood Pb levels below 5 μg/dL are summarized in Table 3-2.17 21 In recognition of the 

22 influence of age on blood Pb levels, the analyses in Table 3-2 are listed in order of age at which 

23 the blood Pb measurements were taken. Findings for studies newly available in this review are 

24 indicated in bold text.

 

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 reported for test scores with all blood Pb categories in 

comparison to the reference category (1 μg/dL), which included 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 negative 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 average (mean = 7.1 μg/dL) and peak (mean = 11.4 μg/dL) (Jusko et al., 2008). 
January 2013 3-21 Draft - Do Not Quote or Cite

1 Table 3-2. Associations with neurocognitive function measures in analyses with child study group blood 

MeasureA Study Group Dataset Description 

Blood Pb Levels 

Additional Information on Analyses Age MeanB (μg/dL) RangeB (μg/dL) N 

CStudies discussed in ISA (section 5.3.2) with findings of effects on neurocognitive measures reported for childhood study group PbB < 5 μg/dL(ordered by age of blood Pb measurements)FSIQ Boston, prospective, age 5 yr 

Subgroup with peak PbB <10 μg/dLBellinger and Needleman 2003 

24 mo 3.8 1 - 9.3 48 Regression, PbB as continuous variable; statistical

association 

BSID/MDI Mexico City, age 24 mo,Tellez-Rojo et al., 2006

Subgroup with PbB<5 μg/dL

Full dataset

24 mo  “ “ 

2.9 4.3 

0.8 – 4.9 0.8 - 9.8 

193 294 

Regression, PbB as continuous variable; statisticalassociation 

AcadPerf North Carolina, 4th graders 

4th grade reading scores, Full dataset 

Miranda et al., 2009 

9-36 mo 4.8 1-16 57,678 Linear and quantal regressions with integer PbB as 

=reference category, includes LOD). Linear analysfor all comparison categories. Quantal analysis: stareading score quantiles for PbB categories greater effect in lower quantiles. Means not reported for Pb

AcadPerf Avon, United Kingdom, age 7-8 yr 

standard assessment scores, Full dataset, Chandramouli et al., 2009

30 mo 4.22 21% < 2

52% 2-5 21% 5-10 

488 D Regressions with PbB as continuous and categoric

analysis (statistically significant negative associatioreduced scores for 5-10 μg/dL vs reference group 

FSIQ Rochester, prospective cohort, age 5 yr

Subgroup with peak PbB <10 μg/dL Canfield et al., 2003 

5 yr 3.32 0.5 – 8.4

(LOD=1) 

71 Regression, PbB as continuous variable; statistical

association 

FSIQ Pooled International, age 6-10 yr 

Subgroup with peak PbB <7.5 μg/dL Lanphear et al 2005 E

5-7 yr 3.24 0.9 – 7.4 103 Regression, PbB as continuous variable; statistical

association 

FSIQ LM, EF AcadPerf

New England, 2 areas, age 6-10, , Full dataset, Surkan et al., 2007 

6-10 yr 2.3 1 – 10 389 Regression, PbB grouped into categories; statistica

association for high subgroup (5-10 μg/dL, n=32) csubgroup (1-2 μg/dL, n=286). 

FSIQ Korea, 4 areas, age 8-11 yr 

Full dataset Kim et al., 2009 

8-11 yr 1.73 0.4 – 4.9 261 Regression, PbB analyzed as quartiles; statistically 

quartiles; statistically significant negative associatiodataset and high blood manganese group 

LM AcadPerf 

NHANES III (1988-1994) Lanphear et al., 2000 

6-16 yr 1.9 4,853 Continuous (unadjusted) and categorical (adjusted) 

among PbB quartiles (< 1, 1.1-1.9, 2.0-3.0, >3.0 μg

LM AcadPerf

NHANES III (1991-1994) Krieg et al., 2010 

12-16 yr 1.95 766-80 Regression analysis; PbB as continuous variable; s

association. 

A - FSIQ = Full Scale Intelligence Quotient; BSID = Bayley Scales of Development; MDI= Mental Development Index; LM=Learning and Memory; EF= Executive Function; AcadPerf= AcadB - Blood Pb level (PbB) information provided here is in some cases augmented by study 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 <7.5 μg/dL comprised of 13.6% age 5 (Boston, Cleveland), 67.0% age 6 (Rochester), 19.4% age 7 (Yugoslavia, Mexico, Cincinna

single member of this subgroup from Cleveland cohort. This analysis includes blood Pb data from Rochester and Boston cohorts, although for different ages (6 and 5 years, respectively) t

et 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 
January 2013 3-22 Draft - Do Not Quote or Cite

1 Among the analyses of lowest study group blood Pb levels at the youngest ages in Table 

2 3-2 are analyses available in the last review of Pb associations with neurocognitive decrement in 

3 study groups with mean levels on the order of 3-4 μg/dL in children aged 24 months, or ranging 

4 from 5 to 7 years (73 FR 66978-66969; ISA, section 5.3.2.2; Bellinger and Needlemann, 2003; 

5 Canfield et al., 2003; Lanphear et al., 2005; Tellez-Rojo et al., 2006; Bellinger, 2008; Canfield, 

2008; Hornung, 2008; Tellez-Rojo, 2008).18 6 Newly available in this review are two studies 

7 reporting association of blood Pb levels prior to three years of age with academic performance 

8 on standardized tests in primary school; mean blood Pb levels in these studies were 4.2 and 4.8 

9 μg/dL (ISA, section 5.3.2.5; Chandramouli et al., 2009; Miranda et al., 2009). One of these two 

10 studies, which represented integer blood Pb levels as categorical variables, indicated a small 

11 effect on end-of-grade reading score of blood Pb levels as low as 2 μg/dL, after adjustment for 

12 age of measurement, race, sex, enrolled in free or reduced lunch program, parental education, 

13 and school type (Miranda et al., 2009). 

14 In a newly available study of blood Pb levels at primary school age, a significant 

15 association of blood Pb in children aged 8-11 years and concurrently measured full scale IQ 

16 (FSIQ) was reported for a cross-sectional cohort in Korea with a mean blood Pb level of 1.7 

μg/dL and range of 0.43-4.91 μg/dL (Kim et al., 2009).19 17 In considering the blood Pb levels in 

18 this study, we note that blood Pb levels in children aged 8-11 are generally lower than those in 

19 pre-school children, for reasons related to behavioral and other factors (ISA, sections 4.3.5, 4.4.1 

and 6.2.1.1).20 20 It is likely that the blood Pb levels of this study group at earlier ages, e.g., prior to 

21 school entry, were higher and the available information does not provide a basis to judge whether 

22 the blood Pb levels in this study represent lower exposure levels than those experienced by the 

23 younger study groups. In still older children, a large cross-sectional investigation of blood Pb 

24 association with effects on memory and learning, that was available in the last review was 

25 focused on children aged 6-16 years, born during 1972-1988, with a mean blood Pb of 1.9 

26 μg/dL. A study newly available in this review, focused on a subset of the earlier study cohort 

27 (ages 12-16, born during 1975-1982), also reports a significant negative association of blood Pb 

 

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 Development (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 generally use the age-appropriate Bayley Scales of Infant 

Development as a measure of cognitive development. 19 Limitations of this study included a lack of consideration of potential confounding by parental caregiving 

quality or IQ (ISA, Table 5-3). 20 This study also investigated the potential role of manganese (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 (IQ) 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

1 with learning and memory test results with mean blood Pb levels of approximately 2 μg/dL (ISA, 

2 section 5.3.2.3; Lanphear et al., 2000; Krieg et al., 2010). In considering these study findings 

3 with regard to the question of exposure levels eliciting effects, we recognize, however, that blood 

4 Pb levels are, in general, lower among teenagers than young children and also that, for these 

5 subjects specifically, the magnitude of blood Pb levels during the earlier childhood (e.g., pre6 school ages) was much higher. For example, the mean blood Pb levels for the 1-5 year old age 

7 group in the NHANES 1976-80 sample was 15 μg/dL, declining to 3.6 μg/dL in the NHANES 

8 1988-1991 sample (Pirkle et al., 1994; ISA, section 4.4.1). 

9 With regard to other nervous system effects in children, the evidence base at lower blood 

10 Pb levels is somewhat extended since the last review with regard to the evidence on Pb and 

11 attention-related behavioral problems, such as inattention, impulsivity, hyperactivity and 

12 attention deficit hyperactivity disorder (ISA, section 5.3.3 and table 5-17). Several newly 

13 available studies investigating the role of blood Pb levels in older children (primary school age 

14 and older) have reported significant associations of attention-related behavior or conduct 

15 problem measures with concurrent blood Pb levels, with mean levels generally on the order of 5 

16 μg/dL or higher (ISA, section 5.3.3). One exception is the newly available cross-sectional, 

17 categorical analysis of the NHANES 2001-2004 sample of children aged 8-15 years, which 

18 found higher prevalence of conduct disorder in the subgroup with concurrent blood Pb levels of 

19 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 

20 noted above, we recognize that many of these children, born between 1986 and 1996, are likely 

21 to have had much higher Pb exposures (and associated blood Pb levels) in their earlier years than 

22 those commonly experienced by young children today, thus precluding a conclusion regarding 

23 evidence of effects associated with lower exposure levels than provided by evidence previously 

24 available. 

25 As summarized earlier in this section, blood Pb has been associated with a range of health 

26 effects on multiple organ systems or processes. As is the case for studies of nervous system 

27 effects in children, newly available studies of other effects in child and adult cohorts include 

28 cohorts with similar or somewhat lower mean blood levels than in previously available studies. 

29 Categories of effects for which a causal relationship has been concluded in the ISA and for 

30 which there are a few newly available epidemiological studies indicating blood Pb associations 

31 with effects in study groups with somewhat lower blood Pb levels than previously available for 

32 these effects include effects on development (delayed puberty onset) and reproduction (male 

33 reproductive function) and on the cardiovascular system (hypertension) (ISA, sections 5.4 and 

34 5.8; 2006 CD, sections 6.5 and 6.6). With regard to the former category, study groups in the 

35 newly available studies include groups comprised of older children ranging up to age 18 years, 

36 for which there is increased uncertainty regarding historical exposures and their role in the 
January 2013 3-24 Draft - Do Not Quote or Cite

observed effects. 21 1 An additional factor that handicaps our consideration of exposure levels 

2 associated with these findings is the appreciable uncertainty associated with our understanding of 

3 Pb biokinetics during this lifestage (ISA, sections 4.3, 5.8.6). The evidence newly available for 

4 Pb relationships with cardiovascular effects in adults include some studies with somewhat lower 

5 blood Pb levels than in the last review. The long exposure histories of these cohorts, as well as 

6 the generally higher Pb exposures of the past complicate conclusions regarding exposure levels 

that may be eliciting observed effects (ISA, sections 5.4.2.4 and 5.4.7).22 7 

8 In summary, our conclusions regarding exposure levels at which Pb health effects occur, 

9 and particularly with regard to such levels that might be common in the U.S. today, are 

10 complicated now, as in the last review, by several factors. These factors include the scarcity of 

11 information in epidemiological studies on cohort exposure histories, as well as by the backdrop 

12 of higher past exposure levels which frame the history of some study cohorts. Recognizing the 

13 complexity, as well as the potential role of higher exposure levels in the past, we continue to 

14 focus our consideration of this question on the evidence of effects in young children for which 

our understanding of exposure history is less uncertain.23 15 Within this evidence base, we 

16 recognize the lowest study group blood Pb levels to be associated with effects on cognitive 

17 function measures, indicating that to be the most sensitive endpoint. As described above, and 

18 summarized in Table 3-2, the evidence available in this review is generally consistent with that 

19 available in the last review with regard to blood Pb levels at which such effects had been 

20 reported (ISA, section 5.3.2; 2006 CD, section 8.4.2.1; 73 FR 66976-66979). As blood Pb levels 

21 are a reflection of exposure history, particularly in early childhood (ISA, section 4.3.2), we 

22 conclude, by extension, that the currently available evidence does not indicate Pb effects at 

23 exposure levels appreciably lower than recognized in the last review. 

24 We additionally note that, as in the last review, a threshold blood Pb level with which 

25 nervous system effects, and specifically neurodevelopmental effects, occur in young children 

26 cannot be discerned from the currently available studies (ISA, sections 2.9.4 and 5.3.13). 

27 Epidemiological analyses have reported blood Pb associations with neurocognitive effects (FSIQ 

or BSID MDI24 28 ) in young child population subgroups, which included individual blood Pb 

 

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 μg/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 categories 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

1 measurements as low as approximately 1 μg/dL and mean concentrations as low as 2.9 to 3.8 

2 μg/dL (ISA, section 5.3.13; Bellinger and Needleman, 2003; Bellinger, 2008; Canfield el al., 

3 2003; Canfield, 2008; Tellez-Rojo et al., 2006; Tellez-Rojo et al., 2008). As concluded in the 

4 ISA, however, “the current evidence does not preclude the possibility of a threshold for 

5 neurodevelopmental effects in children existing with lower blood levels than those currently 

6 examined” (ISA, section 5.3.13). 

7 Important uncertainties associated with the evidence of effects at low exposure levels are 

8 similar to those recognized in the last review, including the shape of the concentration-response 

9 relationship for effects on neurocognitive function at low blood Pb levels in today’s young 

10 children. Also of note is our interpretation of associations between blood Pb levels and effects in 

11 epidemiological studies, with which we recognize uncertainty with regard to the specific 

12 exposure circumstances (timing, duration, magnitude and frequency) that have elicited the 

13 observed effects, as well as uncertainties in relating ambient air concentrations (and associated 

14 air-related exposures) to blood Pb levels in early childhood, as discussed in section 3.1 above. 

15 We additionally recognize uncertainties associated with conclusions drawn with regard to the 

16 nature of the epidemiological associations with blood Pb (e.g., ISA, section 5.3.14), but note that 

17 based on consideration of the full body of evidence for neurocognitive effects, the EPA has 

18 determined a causal relationship to exist between relevant blood Pb levels and neurocognitive 

19 impacts in children (ISA, section 5.3.16.1). 

20  To what extent does the newly available evidence alter our understanding of the 

21 concentration-response relationship for neurocognitive effects (IQ) with blood Pb 

22 levels in young children? 

23 Based primarily on studies of FSIQ, the assessment of the currently available studies, as 

24 was the case in the last review, continues to recognize a nonlinear relationship between blood Pb 

25 and effects on cognitive function, with a greater incremental effect (greater slope) at lower 

26 relative to higher blood Pb levels within the range thus far studied, extending from well above 10 

27 μg/dL to below 5 μg/dL (ISA, section 5.3.13). This was supported by the evidence available in 

28 the last review, including the analysis of the large pooled international dataset comprised of 

29 blood Pb measurements concurrent with the IQ tests that ranged from 2.5 μg/dL to 33.2 μg/dL 

30 (Lanphear et al., 2005; Rothenberg and Rothenberg, 2005; ISA, section 5.3.13). The study by 

31 Lanphear et al (2005) additionally presented analyses that stratified the dataset based on peak 

32 blood Pb levels (e.g., with cutpoints of 7.5 μg/dL and 10 μg/dL peak blood Pb) and found that 

33 the coefficients from linear models of the association for IQ with concurrent blood Pb were 

34 higher in the lower peak blood Pb level subsets than the higher groups (ISA, section 5.3.13; 

35 Lanphear et al., 2005). Stratified analyses of several individual cohorts also observed higher 

36 coefficients for blood Pb relationships with measures of neurocognitive function in lower as 
January 2013 3-26 Draft - Do Not Quote or Cite

1 compared to higher blood Pb subgroups (ISA, section 5.3.13; Canfield et al., 2003; Bellinger and 

2 Needleman, 2003; Kordas et al., 2006; Tellez-Rojo et al., 2006). Of these subgroup analyses, 

3 those involving the lowest mean blood Pb levels and closest to the current mean for U.S. 

4 preschool children are listed in Table 3-3 below (drawn from Table 3 of the 2008 final 

5 rulemaking notice [73 FR 67003]). These analyses were important inputs for the evidence6 based, air-related IQ loss framework which informed decisions on a revised standard in the last 

7 review (73 FR 67005), discussed in section 4.1.1 below. 

8 Table 3-3. Summary of quantitative relationships of IQ and blood Pb for analyses with 

9 blood Pb levels closest to those of young children in the U.S. today. 

Blood Pb Levels 

(μg/dL) 

Study/Analysis 

Average 

Linear 

SlopeA

(IQB 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 μg/dL -1.71 

3.24 0.9 – 7.4 Lanphear et al (2005)C, subgroup with peak blood Pb <7.5 μg/dL -2.94 

3.32 0.5 – 8.4 Canfield et al (2003) C, subgroup with peak blood Pb <10 μg/dL -1.79 

3.8 1 - 9.3 Bellinger and Needleman (2003)C, subgroup with peak blood Pb <10 μg/dL -1.56 

Median value -1.75 

A - Average 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 data 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 age (24-mos). 

C - The Lanphear et al. (2005) pooled International study also includes blood Pb data from the Rochester and Boston cohorts, although 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 

11 Several studies newly available in the current review have, in all but one instance, also 

12 found a nonlinear blood Pb-cognitive function relationship in nonparametric regression analyses 

13 of the cohort blood Pb levels analyzed (ISA, section 5.3.13). These studies, however, used 

14 statistical approaches that did not produce quantitative results for each blood Pb group (ISA, 

15 section 5.3.13). Thus, newly available studies have not extended the range of observation for 

16 quantitative estimates of this relationship to lower blood Pb levels than those of the previous 

17 review. The ISA further notes that the potential for nonlinearity has not been examined in detail 

18 within a lower more narrow range of blood Pb levels than those of the full cohorts thus far 

19 studied in the currently available evidence base (ISA, section 5.3.13). Such an observation in the 

20 last review supported the consideration of linear slopes with regard to blood Pb levels at and 

21 below those represented in Table 3-3. In summary, the newly available evidence does not 

22 substantively alter our understanding of the concentration-response relationship (including 

23 quantitative aspects) for neurocognitive impact, such as IQ with blood Pb in young children. 
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1 3.3 PUBLIC HEALTH IMPLICATIONS AND AT-RISK POPULATIONS 

2 There are several potential public health impacts associated with Pb exposure. In 

3 recognition of effects causally related to blood Pb levels somewhat near those most recently 

4 reported for today’s population and for which the weight of the evidence is greatest, the potential 

5 public health impacts most prominently recognized in the ISA are population IQ impacts 

6 associated with childhood Pb exposure and prevalence of cardiovascular effects in adults (ISA, 

7 section 2.9.1). With regard to the latter category, as discussed above, the full body of evidence 

8 indicates a role of long-term cumulative exposure, with uncertainty regarding the specific 

9 exposure circumstances contributing to the effects in the epidemiological studies which focused 

10 largely on adult populations for whom historical Pb exposures were likely much higher than 

11 exposures that commonly occur today (ISA, section 5.4). There is less uncertainty regarding the 

12 exposure patterns contributing to the blood Pb levels reported in studies of younger populations 

13 (ISA, section 2.10). Accordingly, we focus the discussion of public health implications relevant 

14 to this review predominantly on nervous system effects, including IQ decrements, in children. 

15 We focus this discussion on IQ in recognition of IQ being a well established, widely 

16 recognized and rigorously standardized measure of neurocognitive function, as well as a global 

17 measure reflecting the integration of numerous processes (ISA, section 5.3.2; 2006 CD, sections 

18 6.2.2 and 8.4.2). We recognize, however, that IQ is one of several measures of cognitive 

19 function negatively associated with Pb exposure. Other examples include other tests of 

20 intelligence and cognitive development, and tests of other cognitive abilities, such as learning, 

21 memory, and executive functions, as well as academic performance and achievement (ISA, 

22 section 5.3.2). In considering the public health significance of neurocognitive effects of Pb in 

23 children, we recognize that, although some may be transient, some effects may persist into 

adulthood (ISA, section 2.9.5).25 24 We also note that deficits in neurodevelopment early in life 

25 may have lifetime consequences as “[n]eurodevelopmental deficits measured in childhood may 

26 set affected children on trajectories more prone toward lower educational attainment and 

27 financial well-being” (ISA, section 5.3.15). Thus, population groups for which 

28 neurodevelopment is affected by Pb exposure in early childhood are at risk of related impacts on 

29 their success later in life. 

30 There are important distinctions between population and individual risk such that “small 

31 shifts in population means are often significant from a public health perspective” (ISA, p. 2-63). 

32 For example, if lead-related decrements are manifested uniformly across the range of IQ scores 

 

25 The ISA states that the “persistence 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

1 in a population, “a small shift in the population mean IQ may result in a substantial increase in 

2 the number of individuals functioning in the low range of the IQ distribution, which is associated 

3 with increased risk of educational, vocational, and social failure” as well as a decrease in the size 

4 of the subgroup achieving very high scores (ISA, section 2.9.1). 

5 In the discussion below, we use the term at-risk populations to recognize populations that 

6 have a greater likelihood of experiencing lead-related health effects, i.e., groups with 

7 characteristics that contribute to an increased risk of Pb-related health effects. These populations 

8 are also sometimes referred to as sensitive groups, as in section 1.2.1 above. This increased 

9 likelihood of lead-related effects can result from many factors, including lifestage or age, gender, 

10 race or ethnicity, diet, pre-existing disease state, or increased exposure (ISA, chapter 6). 

11 Accordingly, in identifying factors that increase risk of lead-related health effects, there has been 

12 consideration of evidence regarding factors contributing to increased susceptibility (i.e., 

13 physiological or intrinsic factors contributing to a greater response for the same exposure), and 

14 those contributing to increased exposure (including that resulting from behavior leading to 

15 increased contact with contaminated media). As noted in the ISA, “definitions of susceptibility 

16 and vulnerability vary across studies, but in most instances ‘susceptibility’ refers to biological or 

17 intrinsic factors (e.g., age, sex) while ‘vulnerability’ refers to nonbiological or extrinsic factors 

18 (e.g., socioeconomic status [SES])” and the terms “at-risk” and “sensitive” populations have in 

19 various instances been used to encompass these concepts more generally (ISA, p. 6-1). Although 

20 we emphasize the term “at-risk”, we rely on the other terms in particular instances below; in so 

21 doing, our usage is consistent with these definitions. 

22 Factors that increase risk of lead-related effects include, among others, behavioral 

23 physiological factors. A behavioral factor of great impact on Pb exposure is the incidence of 

24 hand-to-mouth activity that is prevalent in very young children and by which they transfer Pb in 

25 settled particles to their mouths (ISA, sections 4.7.1 and 6.2.1.1). Physiological factors include 

26 both conditions contributing to a group’s increased risk of effects at a given blood Pb level, and 

27 those that contribute to blood Pb levels higher than those otherwise associated with a given Pb 

28 exposure (ISA, sections 6.3 and 6.1, respectively). We also considered evidence encompassing 

29 situations of elevated exposure, such as residing in old housing with Pb-containing paint or near 

30 sources of ambient Pb, as well as socioeconomic factors, such as reduced access to health care or 

31 low socioeconomic status (SES) that can contribute to increased risk of adverse health effects 

32 from Pb (ISA, sections 2.9.7, 6.2, and 6.4). 

33 
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1  Has new information altered our understanding of human populations that are 

2 particularly at risk of health effects from Pb exposures? 

3 The information newly available in this review has not substantially altered our 

4 understanding of at-risk populations. As in the last review, the factor most prominently 

5 recognized to contribute to increased risk of Pb effects is age (ISA, section 2.9.7). As noted in 

6 section 3.2 above, although the specific ages or lifestages of greatest susceptibility have not been 

7 established (e.g., ISA, section 5.3.12), the susceptibility of young children to the 

8 neurodevelopmental effects of Pb is well recognized (e.g., ISA, sections 2.9.7, 5.3, 6.2.1, 6.3.1, 

9 and 6.4). The evidence indicates that prenatal blood Pb levels are causally associated with 

10 nervous system effects, including mental development in very young children and can also be 

11 associated with cognitive decrements in older children (ISA, section 5.3). The coincidence 

12 during early childhood of behaviors that increase exposure, such as hand-to-mouth contact, and 

13 the development of the nervous system contributes increased risk during this time (ISA, sections 

14 5.3.2.6, 6.2.1.1, and 6.3.1.1). The evidence also indicates a causal relationship of postnatal blood 

15 Pb levels (through early childhood to school age) with cognitive function decrement in older 

16 children and adolescence (ISA, section 5.3). In epidemiological studies, associations have been 

17 observed of neurocognitive, and some other nervous system effects, at various ages from early 

18 childhood to school age with prenatal, early-childhood, lifetime average, and concurrent blood 

19 Pb levels as well as with childhood tooth Pb levels (ISA, section 5.3). Consideration of 

20 epidemiological study results for different lifestages of exposure, particularly later in childhood, 

21 is complicated by the fact that blood Pb levels in children, although highly affected by recent 

22 exposure, are also influenced by their history of Pb exposure due to rapid growth-related bone 

23 turnover in children (ISA, section 4.3.5). Thus, blood Pb level in children also may reflect past 

24 Pb exposures and, to some extent, maternal Pb, with relative contributions varying with child and 

25 maternal exposure history (ISA, section 4.2.2.4, 4.4.1 and 5.3.16; 2006 CD, section 6.6.2). 

26 Collectively, however, the evidence indicates both the susceptibility of the developing fetus and 

27 early postnatal years, as well as the potential for continued susceptibility through childhood as 

28 the human central nervous system continues to mature and be vulnerable to neurotoxicants (ISA, 

29 sections 2.9.5 and 5.3.16; 2006 CD, section 6.2.12). 

30 In the collective body of evidence of nervous system effects in children, it is difficult to 

31 distinguish exposure in later lifestages (e.g., school age), and its associated risk, from prenatal 

32 and early childhood (ISA, section 5.3.12). While early childhood is recognized as a time of 

33 increased susceptibility, a difficulty in identifying a discrete period of susceptibility from 

34 epidemiological studies has been that the period of peak exposure, reflected in peak blood Pb 

35 levels, is around 18-27 months when hand-to-mouth activity is at its maximum (ISA, section 

36 4.4.1 and 6.2.1.1; 2006 CD, p. 6-60). The task is additionally complicated by the role of 
January 2013 3-30 Draft - Do Not Quote or Cite

1 maternal exposure history in contributing Pb to the developing fetus (ISA, section 4.2.2.4.). 

2 Epidemiological analyses evaluating risk of neurocognitive impacts (e.g., reduced IQ) associated 

3 with different blood Pb metrics in cohorts with differing exposure patterns (including those for 

4 which blood Pb levels at different ages were not highly correlated) indicate associations with 

5 blood Pb measurements concurrent with FSIQ tests at ages of approximately 6-7 years, although 

6 the analyses did not conclusively demonstrate stronger findings for early (e.g., age 2 years) or 

7 concurrent blood Pb (ISA, section 5.3.12). The experimental animal evidence additionally 

8 indicates early life susceptibility (ISA, section 5.3.16). Thus, the full evidence base continues to 

9 indicate prenatal and early childhood lifestages as periods of increased lead-related risk. In 

10 summary, while uncertainties remain with regard to the role of Pb exposures during a particular 

11 age of life in eliciting nervous system effects, such as cognitive function decrements, the 

12 evidence continues to indicate the at-risk status of pre- and postnatal childhood lifestages (ISA, 

13 sections 5.3.12 and 5.3.16). 

14 Several physiological factors increase risk of lead-related health effects by contributing to 

15 increased blood Pb levels over those otherwise associated with a given Pb exposure (ISA, 

16 sections 4.2, 4.3 and 6.1). These include nutritional status, which plays a role in Pb absorption 

17 from the GI tract (ISA, section 4.2.1.2). For example, diets deficient in iron, calcium or zinc can 

18 contribute to increased Pb absorption and associated higher blood Pb levels (ISA, sections 

19 4.2.1.2, and 6.1). Evidence is suggestive of some genetic characteristics as potential risk factors, 

20 such as presence of the δ-aminolevulinic acid dehydratase-2 (ALAD-2) allele which has been 

21 indicated to increase blood Pb levels and or lead-related risk (ISA, sections 4.3.2 and 6.1). 

22 Risk factors based on increased exposure include spending time in proximity to sources 

23 of Pb to ambient air or other environmental media (e.g., large active metals industries or 

24 locations of historical Pb contamination) (ISA, section 2.9.7, 6.2.5). Residential factors 

25 associated with other sources of Pb exposure (e.g., leaded paint or plumbing with Pb pipes or 

26 solder) are another exposure-related risk factor (ISA, section 2.9.7, 6.2.6). The role of 

27 socioeconomic status (SES) with regard to lead-related risk is somewhat complicated. SES often 

28 serves as a marker term for one or a combination of unspecified or unknown environmental or 

29 behavioral variables. Lower SES has been associated with higher Pb exposure and higher blood 

30 Pb concentration (ISA, sections 5.3.16, 6.2.4 and 6.4). Further, it is independently associated 

31 with an adverse impact on neurocognitive development and a few studies have examined SES as 

32 a potential modifier of the association of childhood Pb exposure with cognitive function with 

33 inconsistent findings regarding low SES as a potential risk factor. Although the differences in 

34 blood Pb levels among children of lower as compared to higher income levels have lessened, 

35 blood Pb levels continue to be higher among lower income children indicating higher exposure 
January 2013 3-31 Draft - Do Not Quote or Cite

1 and/or greater influence of factors independent of exposure, such as nutritional factors (ISA, 

2 sections 2.9.7, 6.2.1.1 and 6.4). 

3 In considering risk factors associated with increased Pb exposure or increased blood Pb 

4 levels, we note that the currently available evidence continues to support a nonlinear relationship 

5 between neurocognitive effects and blood Pb that indicates incrementally greater impacts at 

6 lower as compared to higher blood Pb levels (ISA, section 5.3.13), as described in section 3.2 

7 above. An important implication of this finding is that while children with higher blood Pb 

8 levels are at greater risk of lead-related effects than children with lower blood Pb levels, on an 

9 incremental basis (e.g., per μg/dL), the risk is greater for children at lower blood Pb levels. This 

10 was given particular attention in the last review of the Pb NAAQS, in which the standard was 

11 revised with consideration of the incremental impact of air-related Pb on young children in the 

12 U.S and the recognition of greater impact for those children with lower absolute blood Pb levels 

13 (73 FR 67002). Such consideration included a focus on those C-R studies involving the lowest 

14 blood Pb levels, as described in section 4.1.1 below. 

15 Some racial or ethnic backgrounds have been identified as factors that may increase risk 

16 of lead-related health effects (ISA, sections 2.9.7, 6.2.3 and 6.3.7). For example, although blood 

17 Pb levels in the U.S. general population (e.g., geometric mean level in children aged 1-5) have 

18 declined, mean levels reported in recent NHANES samples continue to differ among children of 

19 different ethnic backgrounds, with higher levels in non-white persons as compared to whites 

20 (ISA, sections 4.4.1, 6.2.1.1 and 6.2.3). Additionally, a study of lead-related risk of hypertension 

21 among adults reported greater risk associated with blood Pb levels above 1 μg/dL among 

22 Mexican Americans and non-Hispanic blacks than among non-Hispanic whites (ISA, section 

23 6.3.7; Muntner et al., 2005). The evidence available in the current review, consistent with that in 

24 the last, also suggests that health status or pre-existing disease is potentially a physiological risk 

25 factor for lead-related effects (ISA, section 2.9.7). Populations with pre-existing health 

26 conditions, such as hypertension, may be more susceptible (as compared to the general 

27 population) for particular Pb-associated effects (ISA, section 6.3.4). For example, increased risk 

28 of lead-related renal effects and heart rate variability have been reported among hypertensive 

29 individuals compared to those that are normotensive (ISA, section 2.9.7). Additionally, African 

30 Americans, as a group, have a higher frequency of hypertension than the general population or 

31 other ethnic groups (NCHS, 2011), and as a result may face a greater risk of adverse health 

32 impact from Pb-associated cardiovascular effects. 

33 Older adulthood has been identified as a lifestage of potentially greater risk of lead34 related health effects based primarily on the evidence of increases in blood Pb levels during this 

35 lifestage, and of potential for effects, such as (ISA, sections 6.2.1.2, 6.3.1.2, and 6.4). 

36 Contributing to blood Pb levels in the studied populations of older adults are likely to be their 
January 2013 3-32 Draft - Do Not Quote or Cite

1 exposure histories, which included younger years during the time of leaded gasoline usage and 

2 other sources of Pb exposures which were more prevalent in the past than today (e.g., ISA, 

3 Figure 3-1 and section 3.4.3.2). Exposure history has a contributing role to blood Pb levels 

4 throughout life, and the increased rate of bone remodeling during later adulthood increases 

5 contributions of Pb from bone stores into the systemic circulation during that lifestage (ISA, 

6 sections 4.3.5 and 6.2.1.2). Additionally, limited animal evidence has indicated specific brain 

7 pathology in older animals that had substantial Pb exposures earlier in life (ISA, sections 

8 5.3.10.1 and 6.3.1). Further, the full body of evidence includes observed associations of various 

9 health effects, such cardiovascular and neurological effects with bone and blood Pb in older 

10 populations, with biological plausibility for the role of Pb provided by experimental animal 

11 studies (ISA, sections 5.3.6, 5.3.8, 5.3.10 and 5.4). 

12 In summary, the information newly available in this review has not appreciably altered 

13 our understanding of human populations that are particularly sensitive to Pb exposures. In the 

14 current review, as at the time of the last review of the Pb NAAQS, we recognize young children 

15 as an important at-risk population, with sensitivity extending to prenatal exposures and into 

16 childhood development. Additional risk factors include deficiencies in dietary minerals (iron, 

17 calcium and zinc), some racial or ethnic backgrounds, and spending time in proximity to 

18 environmental sources of Pb or residing in older houses. The evidence for SES continues to 

19 indicate increased blood Pb levels in lower income children, although its role with regard to an 

20 increased risk for same blood Pb level is unclear. Additionally, the currently available evidence 

21 continues to indicate a potential for increased risk associated with several other factors, including 

22 older adulthood, pre-existing disease (e.g., hypertension), variants for certain genes and 

23 increased stress. 

24  Is there new evidence on health effects beyond neurocognitive endpoints in 

25 children that suggest additional at-risk populations should be given increased 

26 focus in this review? 

27 The evidence newly available in this review supports or strengthens our previous 

28 conclusions regarding the broad array of health effects of Pb (see ISA, section 2.10 which 

29 compares key conclusions drawn in the last review with conclusions drawn in the current 

30 assessment). Additionally, in some categories of health effects, the newly available studies 

31 extend the evidence for some aspects of the health effects described in the last review. For 

32 example, among the nervous system effects, the newly available evidence continues to support 

33 the conclusions from the last review regarding Pb and neurocognitive and neurobehavioral 

34 effects (ISA, section 5.3). Across the array of neurocognitive and behavioral effects, we 

35 recognize the sensitivity of the prenatal period and several lifestages of childhood, and 
January 2013 3-33 Draft - Do Not Quote or Cite

1 particularly recognize young children as an important at-risk population in light of current 

2 environmental exposure levels. 

3 As discussed in section 3.2 above, the blood Pb levels of populations studied in newly 

4 available epidemiological studies that report associations of blood Pb with effects for systems 

5 and processes other than the nervous system (e.g., cardiovascular, developmental and 

6 reproductive) are similar, or in a few cases, somewhat lower than those assessed in the last 

7 review (ISA, sections 5.4, 5.6, 5.7, and 5.8). The greater uncertainties regarding the time, 

8 duration and magnitude of exposure contributing to these observed health effects complicate 

9 identification of sensitive lifestages and associated exposure patterns that might be compared 

10 with our understanding of the sensitivity of young children to neurocognitive impacts of Pb. 

11 Thus, while augmenting the evidence base on these additional endpoints, the newly available 

12 evidence does not lead us to identify a health endpoint expected to be more sensitive to Pb 

13 exposure than neurocognitive endpoints in children, leading us to continue to conclude that the 

14 appropriate primary focus for our review is on neurocognitive endpoints in children. 

15 In summary, there are a variety of ways in which lead-exposed populations might be 

16 characterized and stratified for consideration of public health impacts. Age or lifestage was used 

17 to distinguish potential groups on which to focus in the last review in recognition of its role in 

18 exposure and susceptibility, and young children were selected as the priority population for the 

19 risk assessment (see section 3.4 below) in consideration of the health effects evidence regarding 

20 endpoints of greatest public health concern and in recognition of effects on the developing 

21 nervous system as a sentinel endpoint for public health impacts of Pb. This identification 

22 continues to be supported by the evidence available in the current review. 

23  What does the information about air Pb concentrations available in this review 

24 indicate with regard to the size of at-risk populations and their distribution 

25 across the U.S.? 

26 The magnitude of a public health impact is dependent upon the size of populations 

27 affected, as well as type or severity of the effect. As summarized above, the population group 

28 that may be most at risk of health effects associated with exposure to Pb is young children. The 

29 2010 census indicates nearly 310 million people residing in the U.S., 74 million of which 

30 approximately are children under the age of 18, with some 20 million under the age of five years. 

31 Children at greatest risk from air-related Pb are considered to be those children living in areas of 

32 higher air Pb exposures. Accordingly, the discussion below considers the information available 

33 to inform our understanding of areas of children potentially at risk from air-related Pb. 

34 In considering the extent of this at-risk population, we turn first to consideration of those 

35 areas in the U.S. with air Pb concentrations above the current standard (e.g., section 2.2.2.2 

36 above). Using the available monitoring data and U.S. census information, Table 3-4 summarizes 
January 2013 3-34 Draft - Do Not Quote or Cite

1 the size of populations within 0.5 km of monitors in our current Pb NAAQS surveillance 

2 network at which Pb concentrations were higher than the current standard during the recent 

3 period from 2009-2011. The distance to which concentrations exceeding the standard might 

4 extend will vary with the magnitude of the Pb concentrations and particle size, among other 

5 factors; a half kilometer distance was selected for purposes of illustration here. This analysis 

6 indicates approximately 2,400 children aged 5 or under to reside within 0.5 km of monitors 

7 exceeding the current standard. To also account for the population in areas with air 

8 concentrations just at (or very near) the current standard, we have also identified an additional 

9 nine Pb-TSP monitors with 3-month average concentrations within 10% of the current standard 

10 (Appendix 2D). Based on the 2010 U.S. census, 265 children aged 5 or under reside within 0.5 

11 km of these additional sites. 

12 Table 3-4. Number of children aged 5 and under in areas of elevated ambient Pb 

13 concentrations relative to the NAAQS. 

Population within 0.5 km of monitors 

with maximum 3-month Pb concentration greater than 0.15 μg/m3

(2009-2011)

Number of 

Counties 

Number of States 

or Territories 

Total 

population 

Children, 

5 and under 

All sites >0.15 μg/m3 29 20 25,344 2,416 

Subset of sites >0.5 μg/m3 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 

15 As the current air quality data set (analyzed in section 2.2.2 above) may not be inclusive 

16 of all of the newly sited monitors, as discussed in section 2.2.1 above, we recognize there may be 

17 other areas of the country where concentrations are above or just meet the current standard but 

18 for which such data are not yet available. To consider the potential for there to be additional, not 

19 yet identified, areas with elevated Pb concentrations, we have separately quantified the size of 

20 young child populations residing in areas near large Pb sources in Table 3-5. In so doing, we 

21 recognize uncertainties and potential limitations associated with these emissions estimates for 

22 these purposes, uncertainties both with regard to the accuracy of such estimates and also with 

23 regard to the role of specific source characteristics and meteorology, not explicitly considered 

24 here, in influencing ambient air Pb concentrations and contributing to substantial variation in air 

25 Pb concentrations at source locations (e.g., Figure 2-11 above). Accordingly, while the summary 

26 in Table 3-5 is informative to considering the potential prevalence of airborne Pb emissions and 

27 potential exposure of human populations, it is limited with regard to its ability to identify 
January 2013 3-35 Draft - Do Not Quote or Cite

1 populations living in areas of elevated ambient air Pb concentrations. We interpret this analysis 

2 to indicate that fewer than about 7,800 young children (aged 5 or younger) live in areas with air 

3 Pb concentrations near or above the current standard, with the current monitoring data indicating 

4 the size of this population to be approximately 2,700. 

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

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

Facilities (other than airports) Airports All 

Number of 

Locations 

Population, 

all ages 

Population, 

aged 5 and 

younger 

Number of 

Locations 

Population, 

all ages 

Population, 

aged 5 and 

younger 

Population, 

aged 5 and 

younger 

Facilities/Airports estimated to emit > 5.0 tpy 

8 484 61 0 0 0 61 

Facilities/Airports estimated to emit 1.0 - 4.9 tpy A

53 12,143 731 6 6,261 266 997 

Facilities/Airports estimated 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 decimal 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 decimal 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 (December 2012); estimates for airports reflect EPA’s best estimates of piston-engine aircraft 

emissions. Piston-engine aircraft emissions inventory is available at: http://www.epa.gov/ttn/chief/net/2008neiv2/2008_neiv2_tsd_draft.pdf.

6 

7 
January 2013 3-36 Draft - Do Not Quote or Cite

1 3.4 EXPOSURE AND RISK 

2 This risk information available for this review and described here is based primarily on 

3 the exposure and risk assessment developed in the last review of the Pb NAAQS (henceforth 

4 referred to as the 2007 REA [USEPA, 2007a]), in the context of the evidence newly available in 

5 this review, as presented in the ISA. As described in the REA Planning Document, careful 

6 consideration of the information newly available in this review, with regard to designing and 

7 implementing a full REA for this review, led us to conclude that performance of a new REA for 

8 the review was not warranted. We did not find the information newly available in this review to 

9 provide the means by which to develop an updated or enhanced risk model that would 

10 substantially improve the utility of risk estimates in informing the current Pb NAAQS review 

11 (REA Planning Document, section 2.3). Based on their consideration of the REA Planning 

12 Document analysis, the CASAC Pb Review Panel generally concurred with the conclusion that a 

new REA was not warranted in this review (Frey, 2011).26 13 Accordingly, the information 

14 described here is drawn primarily from the 2007 REA, augmented by a limited new case study15 specific analysis focused on risk associated with the current standard, as described in section 

16 3.4.3.3 below. 

17 The focus for the risk assessment and associated estimates presented here is on Pb 

18 derived from sources emitting Pb to ambient air. As discussed in section 1.3 above (and 

19 conceptually illustrated in Figure 1-1), the multimedia and persistent nature of Pb, the role of 

20 multiple exposure pathways, and the contributions of nonair sources of Pb to human exposure 

21 media all present challenges and contribute significant additional complexity to the health risk 

22 assessment that goes far beyond the situation for similar assessments typically performed for 

23 other NAAQS pollutants (e.g., that focus only on the inhalation pathway). Limitations in the 

24 available data and models affected our characterization of the various complexities associated 

25 with exposure to ambient air Pb. As a result, the assessment includes a number of simplifying 

26 assumptions in a number of areas and, as described in section 3.4.4 below, our estimates of air27 related Pb risk are approximate and are characterized by upper and lower bounds. 

28 The conceptual model developed to inform planning for the 2007 REA, including 

29 identification of key exposure media, target population, health endpoint and risk metric is 

30 described in section 3.4.1. The 2007 REA relied on a case study approach to provide estimates 

31 that inform our understanding of air-related exposure and risk in different types of air Pb 

32 exposure situations; the case studies included are described in section 3.4.2. In section 3.4.3, the 

 

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

1 analysis approach and general aspects of exposure and risk assessment methods are summarized, 

2 and the air quality scenarios simulated are described. In section 3.4.3, we also summarize the 

3 2007 REA risk model and the interpolation approach used in the limited new analyses performed 

4 for purposes of this review. Section 3.4.4 identifies key aspects in exposure assessment and risk 

5 estimates are presented in section 3.4.5. Treatment of key sources of variability in exposure and 

6 risk estimates is described in section 3.4.6 and the characterization of uncertainty is summarized 

7 in 3.4.7. An updated interpretation of the risk estimates for our purposes in this Pb NAAQS 

8 review section is presented in section 3.4.8. 

9 3.4.1 Conceptual Model for Air-Related Lead Exposure and Risk 

10 The focus in consideration of public health risks associated with Pb from ambient air is 

11 on Pb derived from those sources emitting Pb to ambient air. The multimedia and persistent 

12 nature of Pb, illustrated in Figure 1-1 above, as well as the existence of many nonair sources of 

13 Pb to the environment, contribute multiple complexities to the consideration of exposure and risk 

14 for ambient air-related Pb. The conceptual model that informed planning for the 2007 REA 

15 identified sources, pathways, routes, exposed populations, and health endpoints, focusing on 

16 those aspects of Pb exposure most relevant to the review, while also recognizing the role of Pb 

17 exposure pathways unrelated to Pb in ambient air (2007 REA, section 2.1). 

18 As recognized in section 1.3 above, sources of human Pb exposure include current and 

19 historical air emissions sources, as well as miscellaneous nonair sources, which can contribute to 

20 multiple exposure media and associated pathways (e.g., inhalation of ambient air, ingestion of 

indoor dust, outdoor soil/dust and diet or drinking water).27 21 Figure 3-2 illustrates these human 

22 exposure pathways from an analytical perspective, drawing on the conceptual model for the 

23 assessment (2007 REA, Figure 2-1). As shown in Figure 3-2, in addition to airborne emissions 

24 (recent or those in the past), sources of Pb to these pathways also include old leaded paint, 

25 including Pb mobilized indoors during renovation/repair activities, and contaminated soils. Lead 

26 in diet and drinking water may have air pathway related contributions as well as contributions 

27 from nonair sources (e.g., Pb solder on water distribution pipes and Pb in materials used in food 

28 processing). Limitations in our data and modeling tools handicapped our ability to separate the 

nonair contributions to Pb exposure from estimates 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 presented for “total Pb exposure”. Characterization of the risk 

assessment results in the rulemaking recognized the contribution, albeit unquantified, from air-related pathways 

within this category. 
January 2013 3-38 Draft - Do Not Quote or Cite

1 

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

3 Identification of exposure populations, exposure/dose metric, health effects endpoint and 

4 risk metric to be included in the 2007 REA were based on consideration of the then-currently 

5 available evidence as assessed in detail in the 2006 CD. As discussed in the REA Planning 

6 Document (USEPA, 2011), these selections continue to be supported by the evidence now 

7 available in this review as described in the ISA. 

8 In the REA, we focused on IQ loss in children exposed up to age 7 years. This focus 

9 reflected the evidence for young children with regard to air-related exposure pathways and 

10 susceptibility to Pb health impacts (e.g., ISA, sections 4.1.1, 5.3, 6.2.1, 6.3.1, and 6.4). For 

11 example, the hand-to-mouth activity of young children contributes to their Pb exposure (i.e., 

12 incidental soil and indoor dust ingestion) and ambient air-related Pb has been shown to 

13 contribute to Pb in outdoor soil and indoor house dust. Accordingly, the Agency maintains a 

14 biokinetic blood Pb model for estimating blood Pb levels in young children (through age 7), 

which was used in this risk assessment.29 15 In addition, our focus on young children reflects the 

16 evidence that the developing nervous system in children is among, if not, the most sensitive of 

17 the endpoints associated with Pb exposure (ISA, sections 2.6 and 2.10). 

18 In terms of internal disposition and the biometrics used to assess Pb exposure, blood Pb 

19 (PbB) levels continue to be extensively used as an index or biomarker of exposure by national 

 

29 The pathways represented in this modeling includeing 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

1 and international health agencies. This reflects the association of PbB with exposure, particularly 

2 recent exposure in young children, and the relative ease of collecting PbB measurement. 

3 Although bone Pb measurements have become easier to collect and consequently, their use has 

4 been more widespread, epidemiological and toxicological studies of Pb health effects and dose5 response relationships (particularly for neurodevelopmental effects in children) tend to be 

6 dominated by PbB as the exposure metric. Therefore, we focused on modeling PbB in young 

7 children, developing estimates for two PbB metrics: “concurrent” and “lifetime average”. For 

8 the former we estimated PbB at age 7 years, while lifetime average was estimated as the average 

9 of PbB levels across the 7 year period. 

10 At the time of the last review, we noted that limitations precluded prediction of changes 

11 in adult PbB levels (or bone Pb levels) given changes in ambient Pb levels. This reflects the fact 

12 that the presence of substantial historic Pb stores in most adults introduces uncertainty into the 

13 prediction of changes in blood or bone Pb in these adult populations resulting from changes in 

14 ambient air Pb exposure. Additionally, in considering concentration-response relationships for 

15 adult PbB and adult health outcomes, we recognized the uncertainty with regard to the role of 

16 historic compared to recent exposures in eliciting the observed outcomes. 

17 Based on conclusions regarding the scientific evidence available in the last review 

18 (presented in the 2006 CD), the assessment focused on risk to the central nervous system in 

19 childhood as the most sensitive effect that could be quantitatively assessed, with decrement in IQ 

20 used as the risk metric.

21 3.4.2 Case Studies 

22 Lead exposure and associated risk was estimated for multiple case studies that generally 

23 represent two types of residential population exposures to air-related Pb (see Table 3-6): (1) 

24 location-specific urban populations of children with a broad range of air-related exposures, 

25 reflecting existence of urban concentration gradients; and, (2) children residing in localized areas 

26 with air-related exposures representing air concentrations specifically reflecting the standard 

27 level being evaluated. Thus, the two types of case studies differed with regard to the extent to 

28 which they represented population variability in air-related Pb exposure (as discussed further in 

29 section 3.4.7 below). Three location-specific urban case studies focused on residential areas 

30 within Cleveland, Chicago, and Los Angeles, providing representations of urban populations 

31 with a broad range of air-related exposures due to spatial gradients in both ambient air Pb levels 

32 and population density. For example, the highest air concentrations in these case studies (i.e., 

33 those closest to the standard being assessed) were found in very small parts of the study areas, 

34 while a large majority of the case study populations resided in areas with much lower air 

35 concentrations. The case studies representing the children most highly exposed via air-related 
January 2013 3-40 Draft - Do Not Quote or Cite

1 pathways were the generalized (local) urban case study (also referred to as general urban case 

2 study) and the primary Pb smelter case study subarea. The generalized (local) urban case study 

3 was not based on a specific geographic location and reflected several simplifying assumptions in 

4 representing exposure including uniform ambient air Pb levels associated with the standard of 

5 interest across the hypothetical study area and a uniform study population. The primary Pb 

6 smelter case study provides risk estimates for children living in a specific area that, at the time of 

7 the 2007 REA, was not meeting the then current NAAQS. In addition to characterizing risks 

8 within a 10 km radius area surrounding the smelter (full area), we focused particularly on a 

9 subarea within 1.5 km of the facility, where airborne Pb concentrations were closest to the 

10 current standard and where children’s air-related exposures are most impacted by emissions 

11 associated with the Pb smelter from which air Pb concentrations were estimated. Based on the 

12 nature of the population exposures represented by the two categories of case study, the 

13 generalized (local) urban and primary Pb smelter case study subarea include populations that are 

14 relatively more highly exposed by way of air pathways to air Pb concentrations near the standard 

15 level evaluated, compared with the populations in the three cities or the full area of the primary 

smelter case study.30,31 16 

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

Type of Population Exposure Case Study1

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 uncertainties 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-related Pb associated with the standard being assessed. 
January 2013 3-41 Draft - Do Not Quote or Cite

1 3.4.3 Analysis Approach 

2 The approach to assessing exposure and risk for the two categories of case studies was 

3 comprised of four main analytical steps: (a) estimation of ambient air Pb concentrations, (b) 

4 estimation of Pb concentrations in other key exposure media, including outdoor soil and indoor 

5 dust, (c) use of exposure media Pb concentrations, with other pathway Pb intake rates (e.g., diet), 

6 to estimate PbB levels in children using biokinetic modeling, and (d) use of concentration7 response functions derived from epidemiology studies to estimate IQ loss associated with the 

8 PbB levels. In implementing these steps for the primary smelter case study, air concentrations 

9 were estimated using dispersion modeling; indoor dust concentrations were estimated for the 

10 case study subarea using a site-specific regression model. The approach for the generalized 

11 (local) urban case study and location-specific urban case studies is somewhat simpler, since it 

12 does not involve fate and transport modeling for air concentration estimates and, instead, uses 

13 ambient monitor levels to characterize the gradient in air Pb levels across the study area. All 

14 steps are somewhat simpler in the generalized (local) urban case study which includes a single 

15 exposure zone. Figure 3-3 identifies the key input data sets, modeling steps and intermediate 

16 model output in each of the four analytical steps. The first three steps were employed in the 

17 exposure assessment (discussed in section 3.4.3.1), while the fourth is the risk assessment step 

18 (discussed in section 3.4.3.3).
January 2013 3-42 Draft - Do Not Quote or Cite

1 

2 Drawn from 2007 REA, Figure 3-3 (USEPA, 2007). 

3 Figure 3-3. Overview of analysis approach. 

Characterizing ambient air levels and 

deposition to soil

Air dispersion modeling

(primary Pb smelter)

Ambient monitoring data 

(general urban and location-specific urban)

Stack and 

fugitive 

emissions data

Ambient air 

concentrations 

for study areas

Characterizing soil and indoor 

dust concentrations

Outdoor residential 

soil concentrations

Site-specific soil 

monitoring data 

combined with 

statistical 

extrapolation 

(primary Pb 

smelter)

Nationally-representative 

residential soil Pb value selected 

from literature

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

(regression) and/or (b) mechanistic 

(compartmental) indoor dust prediction 

models 

(all case studies)

Indoor residential dust 

concentrations

Biokinetic blood Pb 

modeling 

(all case studies)

Background Pb exposure levels

• diet

• drinking water

• indoor paint (actually reflected in 

dust modeling)

Probabilistic modeling of blood Pb 

levels for children within each case 

study location

(all case studies)

GSD reflecting interindividual variability 

in behavior related to 

Pb exposure and 

biokinetics

Characterizing blood Pb levels

Concentration-response functions 

based on log-normal functions 

(Lanphear pooled analysis), or on data 

from that study

Demographics (distribution of 

children within study areas)

(primary Pb smelter and locationspecific urban)

Distribution of IQ loss for 

study populations 

(partitioned between policyrelevant exposures and 

policy-relevant background)

Characterizing risk (IQ loss)

Ambient air 

concentrations 

(see above)

Risk estimation - IQ 

change estimation

(all case studies)

EXPOSURE ASSESSMENT RISK CHARACTERIZATION
January 2013 3-43 Draft - Do Not Quote or Cite

1 3.4.3.1 Estimating Exposure 

2 Concentrations of Pb were estimated in ambient media and indoor dust using a 

3 combination of empirical data and modeling projections. The use of empirical data brings with it 

4 uncertainty related to the potential inclusion of nonair source signals in these measurements (e.g., 

5 house paint contributions to indoor dust and outdoor soil Pb). Conversely, the use of modeling 

6 tools introduces other uncertainties (e.g., model and parameter uncertainties). The 

7 characterization of uncertainty associated with the risk assessment is discussed in section 3.4.7. 

8 Table 3-7 summarizes the exposure modeling approaches and data used to characterize Pb 

9 concentrations or input associated with each exposure pathway for each of the case studies. 

10 Characterization of Pb in ambient air relied on (a) dispersion modeling of facility-related 

11 (including fugitive) Pb emissions for the primary Pb smelter case study, (b) the use of ambient 

12 monitor data for the location-specific urban case studies, and (c) an assumption of uniform 

13 ambient air Pb levels (matching the standard level being considered) for the generalized (local) 

14 urban case study. The use of dispersion modeling for the primary Pb smelter case study allowed 

15 us to capture more spatially refined patterns of ambient air Pb over residential areas in the 

16 vicinity of the facility, where ambient Pb levels were dominated by Pb released from the facility. 

17 For the location-specific urban case studies, we used Pb monitors within each of the urban study 

18 areas to characterize spatial gradients. By contrast, the generalized (local) urban case study is 

19 designed to assess exposure and risk for a smaller group of residents (e.g., neighborhood) 

20 exposed at the level of the standard and therefore, did not rely on monitor data in characterizing 

21 levels, since ambient air Pb was fixed at the standard being assessed. While ambient air Pb 

22 concentrations in the primary Pb smelter case study reflected only contributions from direct and 

23 fugitive emissions associated with the facility, concentrations in the location-specific urban study 

24 areas, which relied on empirical (monitor-based) data to define ambient air Pb concentrations, 

25 reflected contributions from all contributing sources, be they currently active stationary or 

26 mobile sources, resuspension of previously deposited Pb or other. Additional detail on 

27 estimation of ambient (outdoor) and indoor air concentrations is presented in section 5.2.2 and 

28 Appendices A through D of the 2007 REA. 

29 Characterization of Pb concentrations in outdoor surface soil/dust, resulting from 

30 deposition of airborne Pb was based on the use of (a) existing site-specific measurements 

31 (primary Pb smelter case study), and (b) nationally representative residential soil measurements 

32 obtained from the literature (general and location-specific urban case studies). In the case of the 

33 primary Pb smelter case study, soil Pb concentration data were available for a zone close to the 

34 facility and statistical extrapolation from these data was used to predict soil levels for portions of 

35 the study area beyond this zone. Additional detail on estimation of Pb concentrations in outdoor 

36 surface soil or dust is presented in sections 3.1.3 and 5.2.2.2 and Appendix F of 2007 REA. 
January 2013 3-44 Draft - Do Not Quote or Cite

1 To predict concentrations of ambient Pb in indoor dust, we relied on a combination of (a) 

2 regression-based models that relate indoor dust to outdoor air Pb and/or outdoor soil Pb and (b) 

3 mechanistic models that predict indoor dust Pb based on key mechanisms (e.g., infiltration of 

4 outdoor air indoors, deposition rates of Pb from indoor air to indoor surfaces, house cleaning 

5 rates). For the point source case study, a combination of regression-based models obtained from 

6 the literature and developed based on site-specific data were used, and a customized hybrid 

7 empirical-mechanistic model was developed for the general and location-specific urban case 

8 studies. This reflected the fact that available regression-based models had been developed 

9 largely based on residential exposures near large point sources and were not considered 

10 representative of more general urban exposures. Consequently, a mechanistic model, augmented 

11 with empirical data, was developed for the generalized (local) urban case study. Additional 

12 detail on estimation of Pb concentrations in indoor dust is presented in sections 3.1.4 and 5.2.2.2 

13 and Appendix G of 2007 REA. 

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

Simulation of 

air quality 

impacts 

Media 

category 

Generalized (local) 

urban case study 

Location-specific 

urban case study 

Primary Pb smelter case 

study (1.5 km subarea 

and 10 km full area) 

Concentrations 

for these 

media were

varied across 

air quality 

scenarios 

(see section 

3.4.3.2). 

Ambient air 

Pb levels 

Single ambient air Pb 

level assumed across 

entire study area 

(single exposure zone) 

Source and non-source 

monitors describe 

concentration gradient (6 

to 11 exposure zones 

per case study) 

 Dispersion modeling of 

smelter-related emissions ( 

22 census block groups 

and 115 blocks) 

Indoor dust 

Pb levels 

Hybrid model: dynamic aspect relates ambient air 

Pb concentrations to indoor dust Pb; empirical 

aspect represents Pb from other sources (e.g., 

paint, historical air, Pb carried indoors with people) 

For subarea - regression of 

site-specific air, dust data. 

For full area - regression of 

air, dust, soil data from 

other, historical locations. 

Concentrations 

were constant

across air 

quality 

scenarios 

(data/modeling 

limitations)

Outdoor soil 

Pb levels 

National dataset (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 

16 Blood Pb levels were predicted from estimates of Pb contained in various media (e.g., 

17 ambient air, diet, water, indoor dust), and estimates of Pb intake from dietary and drinking water 

18 pathways, using the Integrated Exposure and Uptake Biokinetic (IEUBK) model (2007 REA, 
January 2013 3-45 Draft - Do Not Quote or Cite

sections 3.2.1.1 and 5.2.4).32 1 Diet and drinking water intake and concentrations, as well as other 

2 model inputs, were based on the most current information (2007 REA, Appendix H). Detail on 

3 methods used to characterize media Pb concentrations and all IEUBK inputs for each case study 

4 are in the 2007 REA, sections 3.1, 3.2, 5.2.3 and 5.2.4 and Appendices C through H. As the 

5 shortest temporal scale accepted for inputs to the IEUBK is a year, all model inputs, developed 

6 for each exposure zone in each case study, were annual average values. For media concentration 

7 inputs, the same values were used for each year of the seven-year simulation. Other model 

8 inputs varied as appropriate with the age of the simulated child (2007 REA, Appendix H). 

9 To simulate population variability in Pb intake and uptake, we used the IEUBK model to 

10 first generate a central-tendency estimate of the PbB levels for the group of children within a 

given exposure zone of a study area.33 11 Outside the IEUBK model, we then combined this central12 tendency estimate with a geometric standard deviation (GSD) reflecting variability in PbB levels 

13 for groups of children to generate a distribution of PbB levels for a study area. The procedure 

14 for combining the IEUBK-based central tendency blood Pb estimate with a GSD to generate a 

15 population distribution of PbB levels differs somewhat for the categories of case studies. The 

16 approach for the general urban case study is fairly simple in that we have a single IEUBK-based 

17 estimate of PbB levels and this is in turn, combined with the GSD selected for this study area to 

18 produce a population-distribution of PbB levels. For both the primary Pb smelter and the 

19 location-specific urban study areas, multiple polygons within the larger study area (e.g., US 

20 Census blocks for the location specific urban study areas) are used as the basis for generating 

21 distributions of PbB levels for the child population in each study area. These distributions are 

22 generated using a MonteCarlo-based population-weighted sampling method with U.S. Census 

23 child counts for each polygon and an adjustment factor distribution based on the chosen GSD 

24 (see 2007 REA, sections 3.2.2 and 5.2.2.3). 

25 The GSD reflects a number of factors which operate together to produce interindividual 

26 variability in blood Pb levels, including: (a) biokinetic variability (differences in the uptake, 

27 distribution or clearance of Pb), (b) differences in behavior related to Pb exposure (e.g., varying 

28 hand-to-mouth activity, tap water ingestion rates, and time spent playing indoors) and (c) 

 

32 In predicting PbB levels, we assumed that Pb concentrations in exposure media remained constant 

throughout the 7 year simulation period. 33 In typical IEUBK applications, the 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 outside 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 population-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

1 differences in environmental Pb exposure concentrations (e.g., spatial gradients in ambient Pb 

2 levels of a resolution beyond that simulated in each case study, differences in 

cleaning/vacuuming rates and air exchanges rates).34 3 Note, that for all of the study areas, we 

4 assumed that pathway apportionment of PbB levels based on the modeling of the central5 tendency PbB level (using IEUBK) holds for all percentiles of PbB levels derived by combining 

6 that central-tendency with the GSD. Blood Pb modeling completed for all case studies included 

7 estimates of both concurrent and lifetime-average PbB metrics, although ultimately, we focused 

on the concurrent PbB metric in estimating risk.35 8 

9 3.4.3.2 Air Quality Scenarios Included in 2007 Assessment 

10 The air quality scenarios assessed in the 2007 REA for the case studies identified in 

11 Table 3-6 above included conditions just meeting the NAAQS that was current at the time of the 

last review (1.5 μg/m3 12 , maximum calendar quarter average) and conditions meeting several 

13 alternative, lower standards. Additionally, for the three location-specific urban case studies, 

scenarios were included for then-current conditions (2003-2005) in each location.36 14 These air 

15 quality scenarios are characterized by quarterly or monthly averaging times and a not-to-be16 exceeded form. Once the air quality dataset representing each scenario was developed, the 

17 associated annual average concentrations for each exposure zone were derived for input to the 

18 IEUBK model, which does not accept air quality inputs of a temporal scale shorter than a year 

(2007 REA, Appendix H). 37 19 

20 As a result of the differing then-current conditions of the location-specific case studies, 

21 the specific alternative standards assessed for each differed (see Table 3-8). To simulate the 

 

34 We specified GSDs for each of the case studies that 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 case studies of Cleveland, Chicago and Los Angeles, the maximum 

monthly average concentration was 0.56, 0.31 and 0.17 μg/m3

, respectively, and the maximum calendar quarter 

average concentration was 0.36, 0.14 and 0.09 μg/m3

, respectively, (2003-2005 data; 2007 REA, Appendix O). 37 Although many different patterns of temporally varying air concentration will just meet a given potential 

alternative standard, the shortest time step accommodated by the blood Pb model is a year. Thus, the air Pb 

concentration inputs to the blood Pb model for each air quality scenario are annual average air Pb concentrations. 

For the generalized (local) urban case study, the national Pb-TSP monitoring dataset was 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 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, 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

1 previous NAAQS scenario at the primary Pb smelter location, at which then-current monitoring 

2 data indicated exceedance of that standard, a proportional roll-down was performed across the 

3 area to achieve conditions that just met that standard. Additionally, although it was considered 

4 an extremely unlikely scenario that air concentrations in urban areas across the U.S. that were 

5 well below the previous NAAQS would increase to just meet that standard (e.g., by way of 

6 expansion of existing sources or congregation of multiple sources in adjacent locations), we 

7 simulated this scenario in all case studies. In so doing, the air Pb concentrations were rolled up 

8 proportionally across the location-specific urban study areas to conditions just meeting the 

9 standard. No other scenario simulations involved rolling concentrations up. For the primary Pb 

10 smelter case study, air Pb concentrations were proportionally rolled down to conditions just 

11 meeting each of the potential alternative standards assessed. In the three location-specific urban 

12 case studies, the temporally and spatially varying concentrations were rolled down to conditions 

13 just meeting each of the potential alternative standards that they exceeded (2007 REA, section 

5.2.2.1).38 14 

15 For the generalized (local) urban case study, which has a single exposure zone in which 

16 air Pb concentrations do not vary spatially, we derived a single air Pb concentration estimate to 

17 meet the standard assessed (e.g., specified maximum monthly or quarterly average). To reflect 

18 the variability in air Pb concentrations that occur over time scales less than a year as a result of 

19 temporal changes in meteorology and source and emission characteristics, the annual average air 

20 concentration (input for IEUBK and dust model) was derived for the maximum monthly and 

21 quarterly average metrics assessed using relationships based on the available Pb-TSP monitoring 

22 data for large U.S. urban areas (2007 REA, Appendix A). 

23 

 

38 When concentrations in the exposure zone (within the 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

1 Table 3-8. Air quality scenarios assessed. 

Air Quality Conditions Just Meeting ... 

Case Studies Where Simulated 

Generalized 

(local) 

UrbanA

Location Specific 

Maximum 

Quarterly Average 

(μg/m3)

Maximum 

Monthly Average 

(μg/m3)

Primary 

Smelter Cleveland Chicago Los 

Angeles 

1.5B √ √ √ √ √

0.2C √ √ 

 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 

3 The approaches for estimating Pb concentrations in other media varied depending on the 

4 type of case study (see section 3.4.3.1 above). Limitations in the available data and modeling 

5 tools precluded simulation of linkages between some media and air Pb, such that the full impact 

6 of changes in air Pb conditions associated with attainment of lower standards was not simulated. 

7 For example, dietary and drinking water Pb concentrations, as well as soil Pb concentrations, 

8 were not varied across the air quality scenarios in any case study (see Table 3-7). For all case 

9 studies, however, indoor dust Pb concentrations were simulated to change with the different air 

10 quality scenarios that also provided differing ambient air Pb concentrations (outdoors and 

11 indoors). 

12 3.4.3.3 Methods for Deriving Risk Estimates 

13 In this section, we first summarize the full risk model employed in the 2007 REA for 

14 estimating risk for a broad range of air quality scenarios (section 3.4.3.3.1). Then, in section 

15 3.4.3.3.2, we summarize approaches by which we have identified risk estimates pertaining to the 

16 current standard, the second of which involves an analysis newly completed in this review in 

17 which risk estimates are interpolated for the current standard based on the 2007 REA risk 

18 estimates. 

19 
January 2013 3-49 Draft - Do Not Quote or Cite

1 3.4.3.3.1 Full Risk Model in 2007 REA 

2 The risk characterization step employed in the 2007 REA involved generating a 

3 distribution of IQ loss estimates for the set of children simulated in the exposure assessment. 

Specifically, estimated PbB levels (for the concurrent PbB metric)39 4 were combined with four 

5 PbB concentration-response (C-R) functions for IQ loss based on the analysis by Lanphear et al 

6 (2005) of a pooled international dataset of blood Pb and IQ (see 2007 REA, section 5.3.1.1). 

7 Four different C-R functions were selected to provide different characterizations of behavior at 

8 low exposures. The decision to use four different functions is in recognition of uncertainty 

9 related to modeling this endpoint, particularly at lower PbB levels for which there is limited 

10 representation in the Lanphear et al (2005) pooled dataset; the 5th percentile for the concurrent 

11 PbB measurements in that dataset is 2.5 μg/dL, and the mean is 9.7 μg/dL (73 FR 66978). The 

12 four different functions are either based directly on the lognormal model described in Lanphear 

13 et al (2005), or they are derived from data presented in that study. The four functions are 

14 presented in Figure 3-4 and compared in Table 3-9 with regard to total IQ loss and incremental 

15 IQ loss (IQ loss per μg/dL blood Pb) across a range of concurrent PbB levels. A brief 

16 description of each of the functions is also here: 

17  Log-linear with cutpoint: log-linear function derived from the pooled analysis applied 

18 down to 1 μg/dL (concurrent PbB metric) with no IQ loss projected below that 

19 exposure level. 

20  Log-linear with low-exposure linearization: log-linear function applied down to 1 

21 μg/dL (concurrent PbB metric) with linearization of the slope at that point which is 

22 used to project IQ loss down to the origin. 

23  Dual linear – stratified at 10 μg/dL: function developed by fitting a two-piece linear 

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

25 from the pooled analysis. 

26  Dual linear-stratified at 7.5 μg/dL: as above, but based on stratification of the two27 piece function at 7.5 μg/dL (peak PbB metric). 

 

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 levels. 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 

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

3 

4 Table 3-9. Comparison of total and incremental IQ loss estimates for blood Pb below 10 

5 μg/dL based on the four concentration-response functions. 

Performance Metric 

Concentration-Response Function 

Log-linear 

with cutpoint 

Log-linear with 

low-exposure 

linearization 

Dual linear - 

stratified at 10 

μg/dL peak 

Dual linear - 

stratified at 7.5 

μg/dL peak 

Points, IQ loss 

Total IQ loss 

at 2 μg/dL 1.9 4.6 1.6 5.9 

at 5 μg/dL 4.3 7.0 3.9 11.1 

at 7.5 μg/dL 5.4 8.1 4.3 11.5 

at 10 μg/dL 6.2 8.9 4.6 11.9 

Incremental IQ loss 

(average # points 

 per μg/dL) 

<2 μg/dL 0.94 2.29 0.80 2.94 

<5 μg/dL 0.87 1.41 0.80 2.24 

<7.5 μg/dL 0.73 1.09 0.58 1.55 

<10 μg/dL 0.62 0.89 0.47 1.20 

6 

7 Of the four C-R functions provided above, we have the greatest overall confidence in risk 

8 estimates generated using the log-linear with low-exposure linearization (LLL) function because 

9 this function is (a) nonlinear, describing greater response per unit blood Pb at lower blood Pb 

10 levels consistent with multiple studies, (b) is based on fitting a function to the entire pooled 

11 dataset (and hence uses all of the data in describing response across the range of exposures), (c) 

12 is supported by sensitivity analyses showing the model coefficients to be robust (Lanphear et al., 

0

2

4

6

8

10

12

14

0 1 2 3 4 5 6 7 8 9 10

Concurrent blood Pb (ug/dL)

IQ loss

log-linear w ith cutpoint

dual linear - stratified at

10 ug/dL, peak

dual linear - stratified at

7.5 ug/dL, peak

log-linear w ith low -

exposure linearization
January 2013 3-51 Draft - Do Not Quote or Cite

1 2005), and (d) provides an approach for predicting IQ loss at the lowest exposures simulated in 

2 the assessment (which for some simulated children yield blood Pb levels below those studied). 

3 Risk estimates generated using the other three C-R functions are also presented to provide 

4 perspective on the impact of uncertainty in this key modeling step. For additional detail on the 

5 rationale for placing greater emphasis on the LLL function, see section 4.2.1 of the 2007 Pb Staff 

6 Paper (USEPA, 2007b). 

7 Two categories of risk metrics were generated for each of the location-specific case 

8 studies: 

9  Population risk percentiles: The IQ loss associated with policy-relevant exposure 

pathways for specific percentiles of the child population (e.g., the 50th, 90th and 95th 10 

11 percentile modeled child). This category of metric provides perspective on the 

12 distribution of IQ loss resulting from policy-relevant exposure pathways, ranging 

from the typical or average child (50th 13 percentile, mean) to children experiencing 

higher exposures (90th, 95th 14 percentiles). Greater emphasis has been placed on the 

15 median IQ loss estimates due to increased confidence in these estimates relative to the 

16 higher percentile estimates, as noted in section 3.4.7. 

17  Child frequency counts associated with specific risk percentiles: Number of children 

18 associated with each of the population percentiles (e.g., the number of children 

predicted to have risk levels at or above the 95th 19 percentile). This risk metric provides 

20 a perspective on the number of children associated with various levels of IQ loss for a 

21 particular case study. 

22 For the generalized (local) urban case study, only the first type of risk metric, population 

23 risk percentiles, was developed because a specific location with associated demographic data 

24 was not modeled. In summarizing risk estimates from the 2007 REA in this document, we have 

25 focused on the first category of risk metric, and specifically, on the median IQ loss estimates. 

26 3.4.3.3.2 Air Quality Scenarios Reflecting the Current Standard 

27 As the 2007 REA did not include an air quality scenario simulated to just meet the 

standard selected by the 2008 decision,40 28 we have considered two approaches for identifying risk 

29 estimates pertaining to conditions just meeting the now-current Pb standard for our purposes in 

30 this review. We first reviewed all the scenarios analyzed in the 2007 REA and recognize the 

31 similarity to the current standard of the then-current conditions scenario for the Chicago case 

32 study. Accordingly, we consider the risk estimates for that scenario for our purposes in this 

33 review of considering risk associated with the current standard (see section 3.4.5 below). 

34 Additionally, in recognition of the variation among specific locations and urban areas with 

 

40 The 2008 decision on the level for the revised NAAQS was based primarily on consideration of the 

evidence-based air-related IQ loss framework. Although the specific level, averaging 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 estimates (73 FR 67006; see section 4.1.1 below). 
January 2013 3-52 Draft - Do Not Quote or Cite

1 regard to air quality patterns and exposed population, we have also newly developed estimates 

2 for an air quality scenario just meeting the current Pb NAAQS in the context of the generalized 

3 (local) urban case study to augment the risk information available in this current review. The 

4 newly developed estimates were derived based on interpolation from the risk estimates available 

5 for scenarios previously assessed for the generalized (local) urban case study. Such interpolated 

6 estimates were only developed for the generalized urban case study due to its use of a single 

7 exposure zone which greatly simplified the method employed, thus contributing relatively lesser 

uncertainty from the interpolation step.41 8 

9 In newly developing estimates for the current standard in the generalized (local) urban 

10 case study, the general approach we followed was to identify the two alternative standard 

11 scenarios simulated in the 2007 REA which represented air quality conditions bracketing those 

12 for the current standard and then linearly interpolate an estimate of risk for the current standard 

13 based on the slope created from the two bracketing estimates. In representing air quality 

14 conditions for these purposes, we focused on the annual average air Pb concentration estimates 

15 used as IEUBK model inputs for the various air quality scenarios. An annual average 

16 concentration estimate to represent the current standard was identified in a manner consistent 

17 with that employed in the 2007 REA for this case study (see section 3.4.3.2 above) with the use 

18 of currently available monitoring data for relationships between air quality metrics for 

19 representation of the current standard. By this method, the air quality scenario for the current 

standard (0.15 μg/m3 20 , as a not-to-be-exceeded 3-month average) was found to be bracketed by 

the scenarios for alternative standards of 0.20 μg/m3 21 (maximum calendar quarter average) and 

0.20 μg/m3 22 (maximum monthly average). A risk estimate for the current standard was then 

23 derived using the slope relating general urban case study IQ loss to annual average Pb 

24 concentration used for those two air quality scenarios. We used this interpolation approach to 

25 develop median risk estimates for the current standard based on each of the four C-R functions. 

26 Details on the method for the interpolation approach are provided in Appendix 3A. The 

27 interpolated median estimates of risk for the current standard for the generalized (local) urban 

28 case study are provided below in Table 3-9. 

 

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 urban case studies) because those case studies utilized a more 

complex, spatially-differentiated and population-based approach 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

1 3.4.4 Challenges in Characterizing Air-related Exposure and Risk 

2 In estimating the portion of total (all-pathway) PbB and IQ loss attributable to air-related 

3 pathways, we faced a variety of challenges. Although we parsed total estimates into those for 

4 diet/drinking water and two air-related categories, referred to as “recent air” and “past air”, 

5 significant limitations in our modeling tools and data resulted in an inability to parse specific risk 

6 estimates into specific pathways. Although Pb in diet and drinking water sources may include 

7 Pb derived from Pb in the ambient air (as well as Pb from nonair sources), limitations precluded 

8 explicit modeling of the contribution from air pathways to these exposure pathways, such that 

the air-related component of these exposures was not estimated.42 9 As a result we utilized the 

10 estimates from recent and past air categories to create bounds within which we consider air11 related risk to fall, as illustrated in Figure 3-5 and described further below.

12 

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

14 Those Pb exposure pathways tied most directly to ambient air, which consequently have 

15 the potential to respond relatively more quickly to changes in air Pb (i.e., inhalation and 

16 ingestion of indoor dust Pb derived from the infiltration of ambient air Pb indoors), were placed 

17 into the "recent air" category. The other air-related Pb exposure pathways, all of which are 

18 associated with atmospheric deposition, were placed into the “past air” category. These include 

 

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 constraints. 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

Indoor dust • Drinking water

“Past air”

Indoor dust (other)

Outdoorsoil

• newly emitted Pb

•historically emitted Pb

• nonair contributions
January 2013 3-54 Draft - Do Not Quote or Cite

1 ingestion of Pb in outdoor dust/soil and ingestion of the portion of Pb in indoor dust that after 

2 deposition from ambient air outdoors is carried indoors with humans. Additionally, while we 

3 recognized the potential for these other air-related exposures to be affected (over some time 

4 frame) by an adjustment to the Pb NAAQS, limitations in our date and tools precluded our 

5 simulation of that relationship with air Pb levels. 

6 Among the limitations affecting our estimates for the air-related categories is the 

7 apportionment of nonair pathways. For example, while conceptually indoor Pb paint 

8 contributions to indoor dust Pb would be considered background and included in a “background” 

9 category for this assessment, due to technical limitations related to indoor dust Pb modeling, dust 

10 from Pb paint was included as part of "other" indoor dust Pb (i.e., as part of past air exposure). 

11 The inclusion of indoor paint Pb as a component of "other" indoor dust Pb (and consequently as 

12 a component of the “past air” category) represents a source of potential high bias in our 

13 prediction of exposure and risk associated with the “past air” category because, indoor paint Pb 

14 is a nonair Pb source. At the same time, Pb in ambient air does contribute to the drinking water 

15 and diet exposure pathways, and is likely a substantial contribution to diet. We could not 

16 separate the air contribution from the nonair contributions in the drinking water and diet 

17 pathways. As a result, our risk estimate for the drinking water/diet category of pathways 

18 includes some air-related risk representing a source of potential low bias in our predictions of 

19 air-related risk. 

20 Further, we note that in simulating reductions in exposure associated with reducing 

21 ambient air Pb levels through alternative NAAQS (and increases in exposure if the current 

22 NAAQS was reached in certain case studies) only the exposure pathways categorized as “recent 

23 air” (inhalation and ingestion of that portion of indoor dust associated with outdoor ambient air) 

24 were varied with changes in air concentration. The assessment from the previous review did not 

25 simulate decreases in “past air” exposure pathways (e.g., reductions in outdoor soil Pb levels 

26 following reduction in ambient air Pb levels and a subsequent decrease in exposure through 

27 incidental soil ingestion and the contribution of outdoor soil to indoor dust). These exposures 

28 were held constant across all air quality scenarios. This modeling/data limitation, accordingly, 

29 precluded estimates for this category from reflecting any impact of alternative standard levels 

30 simulated. 

31 In summary, because of limitations in the assessment design, data and modeling tools, 

32 our risk estimates for the “past air” category in the last review include both risks that are truly 

33 air-related and potentially, some nonair risk. Because we could not sharply separate Pb linked to 

34 ambient air from Pb from other (nonair) sources, some of the three categories of risk are 

35 underestimated and others overestimated. On balance, we believe this limitation leads to a slight 

36 overestimate of the risks in the “past air” category. At the same time, as discussed above, the 
January 2013 3-55 Draft - Do Not Quote or Cite

1 "recent air" category does not fully represent the risk associated with all air-related pathways. 

2 Thus, we considered the risk attributable to air-related exposure pathways to be bounded on the 

3 low end by the risk estimated for the “recent air” category and on the upper end by the risk 

4 estimated for the “recent air” plus “past air” categories. With regard to the latter, we are 

5 additionally cognizant of the modeling and data limitations which reduce the extent to which the 

6 upper end of these bounds reflects impacts of alternative air quality conditions simulated. 

7 3.4.5 Risk Estimates 

8 This section summarizes air-related risk estimates generated for the previous review and 

9 also risk estimates that have been newly derived in this review by interpolation from the previous 

10 review estimates for the current standard (see section 3.4.3.3.2 above). Included in this summary 

11 is consideration of the following question: 

12  What is the nature and magnitude of air-related risks remaining upon just 

13 meeting the current Pb standard? 

14 The air-related risk quantified in the 2007 REA is for IQ loss associated with Pb 

15 exposure. As discussed in section 3.2 above, the evidence in the last review, as well as in the 

16 current review, supports identification of neurocognitive effects in young children as a 

17 particularly sensitive endpoint for the exposure circumstances relevant to this review and which 

18 addresses the important at-risk population, young children. With this support in the evidence for 

19 quantification, the risk assessment quantified decrements in IQ, an established indicator of 

20 neurocognitive function. With regard to the nature of the risks, in addition to recognizing the 

21 role of IQ as an indicator of an array of neurocognitive function impacts, we additionally take 

22 note of the evidence regarding implications of neurocognitive impacts in young children with 

23 regard to potential future impacts as the children age, as recognized in section 3.2 above. 

24 In presenting risk estimates here, we focus on the median estimates of air-related IQ loss 

25 for each case study. Estimates of air-related risk are substantially more uncertain for extremes of 

the risk distribution, such as the 95th 26 percentile. Those estimates and estimates for other risk 

27 metrics, including population incidence for IQ loss at those case studies with population 

28 enumeration, are available elsewhere (2007 REA, sections 4.2 and 5.3.2). In this section, Table 

29 3-10 presents air-related IQ loss estimates derived in the 2007 REA for the full set of case 

30 studies. Table 3-11 provides a subset of these risk estimates for the generalized (local) urban case 

31 study in addition to estimates for air quality conditions just meeting the current standard, derived 

32 by interpolation. A number of details, listed here, should be kept in mind when reviewing the 

33 estimates presented in Tables 3-9 and 3-10. 

34  The risk estimates represent IQ loss associated with air-related lead exposure for the 

35 median child (exposure is modeled through age seven years). 
January 2013 3-56 Draft - Do Not Quote or Cite

1  Our estimation of risk attributable to air-related exposure pathways is approximate, as 

2 described in sections 3.4.4 and 3.4.7. We consider the air-related risk to fall within 

3 the ranges presented, bounded on the low end by estimates for the pathways 

4 categorized as “recent air” and on the upper end by the sum of the estimates for both 

the “recent” and “past air” pathways. 43 5 

6  The bolded range of risk estimates are derived using the C-R function in which we 

7 have the highest overall confidence (the log-linear with low-exposure linearization – 

8 see section 3.4.3.3.1). The wider range of risk estimates presented within the 

9 parentheses in both tables reflects the application of all four C-R functions (see 

10 section 3.4.3.3.1) to exposure estimates for the recent and recent plus past air

11 categories. Consequently, this range of risk estimates reflects both uncertainty in 

12 estimation of air-related exposures as well as uncertainty in the C-R function for IQ 

13 loss in children. 

14 

 

43 The third category of pathways for which risk was estimated 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

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

Air Quality Scenario 

Just meeting specified 

maximum quarterly/monthly 

average (μg/m3)

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 of 

presented range) (see section 3.4.4). Boldface estimates are 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 – 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 smelter (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 standard 

levels (see section 4.2 of the Risk Assessment, Volume 1). 

D – This corresponds to roughly 0.7 - 1.0 μg/m3 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 estimates 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 

5 
January 2013 3-58 Draft - Do Not Quote or Cite

1 Table 3-11. Estimates of air-related risk for the generalized (local) urban case study, 

2 including interpolated estimates for current standard. 

Air Quality Scenario 

Just meeting specified metric (μg/m3) 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 presented 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 

4 Key observations regarding these air-related risk estimates across the array of air quality 

5 scenarios: 

6 All Case Studies 

7  Relative to the previous Pb NAAQS, substantial reduction in estimates of air- related 

8 risk is demonstrated across the full set of potential alternative standards simulated 

9 (Table 3-10). This is particularly the case for the lower bound (the recent air 

10 estimates) which reflects only the pathways simulated to respond to changes in air 

11 concentrations associated with different air quality scenarios. 

12 Generalized (local) Urban Case Study 

13  As described above, the general urban case study provides risk estimates for a single 

14 group of children residing in a single area where air concentrations throughout area 

15 are near the level of the standard being simulated. In this case study, air-related 

16 median IQ loss, based on the higher confidence C-R function (bold), ranged from 

roughly 2 to 4 IQ points for the 0.5 μg/m3 17 , maximum monthly average scenario, to <1 

to roughly 3 IQ points for the 0.02 μg/m3 18 , maximum monthly average scenario. 

19 These ranges are expanded somewhat with consideration of the full range of C-R 

20 functions considered in the analysis. . 
January 2013 3-59 Draft - Do Not Quote or Cite

1 Location-specific Case Studies 

2  Compared to the other case studies, the air-related risk estimates for the location3 specific urban case studies are lower because of the broader range of air-related 

4 exposures and the distribution of the population within the study areas. For example, 

5 the majority of the populations in each of the location-specific case studies reside in 

areas with ambient air Pb levels well 6 below each standard assessed, particularly for 

standard levels above 0.05 μg/m3 7 , as a maximum monthly average. Consequently, 

risk estimates for these case studies indicat 8 e little response to alternative standard 

levels above 0.05μg/m3 9 maximum monthly average (as shown in Table 3-10). 

10  For the primary Pb smelter subarea, only an upper bound on risk attributable to air11 related exposures is provided due to uncertainties associated with dust Pb model used 

for this case study.44 12 For all air quality scenarios, the population median recent plus 

13 past air risk estimate is generally similar to or slightly higher than those for the 

14 general urban case study, likely due to differences in the indoor dust models used for 

15 the two case studies (discussed in Risk Assessment Report, sections 3.1.4). 

16 

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

18  The median air-related IQ loss estimate for then current conditions in Chicago study 

19 area, which just met a level of 0.14 μg/m3 as a maximum calendar quarter average, 

20 falls somewhere within the lower and upper bounds of 0.6 and 2.9 points IQ loss, 

21 respectively (Table 3-10). 

22  The median air-related IQ loss estimate for the current standard in the Generalized 

23 (local) Urban Case Study, newly derived by interpolation from 2007 REA results, 

24 falls somewhere within the lower and upper bounds of 1.5 and 3.4 points IQ loss, 

25 respectively (Table 3-11). This estimate is derived by interpolation between the 

estimates for the 0.2 μg/m3

 maximum quarterly and 0.2 μg/m3 26 maximum monthly 

27 average scenarios that were derived in 2007 REA. The newly interpolated estimate is 

essentially the same as the estimate for 0.2 μg/m3 28 maximum quarterly average 

29 scenario for this case study. 

30  Based on results from the last review for a location-specific urban study area and on 

31 those newly derived in this review based on interpolation from 2007 REA results, 

32 median air-related IQ loss for the current standard is estimated, with rounding, to 

33 generally fall above a rough lower bound of 1 point IQ loss and below a rough upper 

34 bound of 3 points IQ loss. 

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

1 3.4.6 Treatment of Variability 

2 This section discusses the degree to which the design of the previous risk assessment 

3 reflected consideration for key sources of variability associated with the scenarios evaluated 

4 (e.g., IQ loss in children associated with ambient Pb in various residential settings). In so doing, 

5 the following question is address. 

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

7 

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

9  Variation in ambient air Pb levels among U.S. urban residential areas: The location10 specific urban study areas were chosen to provide coverage for diverse residential 

11 populations in U.S. urban areas with relatively elevated ambient air Pb levels (as 

12 characterized using monitoring). We believe that the three cities included in those 

13 case studies capture the variability in spatial patterns of ambient air Pb concentrations 

14 within and across such areas reasonably well. In addition, the generalized (local) 

15 urban case study provides coverage for a residential population exposed in a localized 

16 area with air concentrations somewhat near the standard being evaluated, providing 

17 coverage for a higher-end population risk scenario where a subset of urban children 

18 are exposed without any spatial gradient in ambient air Pb levels. 

19  Variation in the spatial distribution of children within an urban area and assignment 

20 of ambient air Pb exposure: Exposure of populations within the three location21 specific urban study areas was characterized to the US Census block group-level 

22 characterization. Each block group was associated ambient air Pb exposure based on 

23 proximity to monitor nearest to block group centroid (Risk Assessment Report, 

24 section 5.2.2). While there is uncertainty associated with these exposures 

25 (population-weighted through use of census block groups) - for example, we did not 

26 consider time spent by children away from their residential block group - we believe 

27 that this approach provides reasonable coverage for the potential pattern of interaction 

28 between resident children located in these urban study areas and the associated spatial 

29 gradients of ambient air Pb levels. 

30  Variation among children in factors other than media concentrations that influence 

31 PbB levels: The inputs to the blood Pb model were central tendency estimates for 

32 each exposure zone within each study area (pathway-specific estimates for central33 tendency child). The IEUBK model then generated PbB levels for that central34 tendency child within each exposure zone. These central-tendency PbB levels were 

35 then combined with a GSD reflecting variability in PbB levels for young children 

36 (at/near age 7 years) to generate a distribution of total PbB for a group of children 

37 within each exposure zone in a given case study under the specific air quality 

38 scenario. We have reasonable confidence that this modeling approach captures 

39 variability in total Pb exposure (and consequently total PbB levels) for children 

40 modeled for a given study area. As noted in section 3.4.7 below, however, there is 

41 uncertainty associated with parsing individual pathway contributions to total PbB 
January 2013 3-61 Draft - Do Not Quote or Cite

1 levels (and consequently to total Pb-attributable risk). This is particularly true for 

2 high-end population percentile estimates of IQ loss. 

3  Inter-individual variability in IQ loss related to Pb exposure: The use of C-R 

4 functions based on a pooled analysis (Lanphear et al., 2005) which combined study 

5 populations from a number of different epidemiological studies of IQ loss in children 

6 likely provides reasonable coverage for variation across children regarding IQ loss 

7 attributable to Pb exposure. Furthermore, our estimation of risk based on several C-R 

8 functions provides further coverage for that variability, as well as also addressing 

9 uncertainty in the specification of that C-R functional form (see section 3.4.7 below). 

10 3.4.7 Characterizing Uncertainty 

11 Although the risk assessment utilized a number of innovative modeling elements in order 

12 to generate representative estimates of risk for the various study area populations, like all risk 

13 models there was uncertainty associated with the model and its output. 

14  What are the important uncertainties associated with any risk/exposure 

15 estimates? 

16 One overarching area of uncertainty concerns the precision of our estimation of the 

17 neurocognitive risk (as represented by IQ loss) associated with ambient air Pb. For example, 

18 because of the evidence for a nonlinear response of PbB to Pb exposure and also for nonlinearity 

19 in the C–R relationship for Pb-associated IQ loss, the assessment first estimated PbB levels and 

20 associated risk for total Pb exposure (i.e., including Pb from air-related and nonair exposure 

21 pathways), and then separated out estimates for pathways of interest. We separated out the 

22 estimates of total (all-pathway) PbB and IQ loss into three categories that included two air23 related categories (“past” and “recent”), in addition to a third category for diet and drinking 

24 water. However, significant limitations in our modeling tools affected our ability to develop 

25 precise estimates for air-related exposure pathways. As recognized in section 3.4.4 above, we 

26 believe these limitations led to a slight overestimation of the risks for the past air category and to 

27 an under representation of air-related pathways for the recent air category. Thus, we 

28 characterized the risk attributable to air-related exposure pathways to be bounded by the 

29 estimates developed for the past air category and the sum of estimates for the recent air and past 

30 air categories. For air quality scenarios other than those for the previous NAAQS, this upper 

31 bound is recognized as having a potential upward bias with regard to its reflection of the 

32 simulated air quality conditions because modeling and data limitations precluded simulation of 

33 the influence of lower air Pb concentrations on the outdoor dust and soil exposure pathways, as 

34 noted in section 3.4.4 above. 

35 Additional limitations, assumptions and uncertainties, recognized in various ways in the 

36 assessment and presentation of results, along with a concise characterization of their expected 

37 impact on results, are listed below. The list begins with factors related to design of the 
January 2013 3-62 Draft - Do Not Quote or Cite

1 assessment or of the case studies, followed by those related to estimation of Pb concentrations in 

2 ambient air, indoor dust, outdoor soil/dust, and blood, and estimation of Pb-related IQ loss. 

3  Temporal Aspects: During the 7-year exposure period, media concentrations remain 

4 fixed and the simulated child resides at the same residence (although exposure 

5 factors, including behavioral and physiological parameters, are adjusted to match the 

6 aging of the child). While these aspects of simulation introduce uncertainty into the 

7 risk estimates, it is not clear if there is a directional bias. For example, failure to 

8 consider population mobility during the simulation period could bias the overall 

9 distribution upwards unless children move to, or from a residential location with 

10 higher Pb exposure, in which case this would not be the case. 

11  Generalized (local) Urban Case Study: The design for this case study employs 

12 assumptions regarding uniformity that are reasonable in the context of a general 

13 description of a small neighborhood population, but would contribute significant 

14 uncertainty to extrapolation of these estimates to a specific urban location, 

15 particularly a relatively large one. Thus, the risk estimates for this case study, while 

16 generally representative of an urban residential population exposed to the specified 

17 ambient air Pb levels, cannot be readily related to a specific large urban population. 

18 As long as these important caveats are considered in interpreting the risk estimates 

19 (i.e., these risk estimates are likely represent a relatively small portion of the resident 

20 child population in any given city just meeting specific air quality conditions) then 

21 the potential error of extrapolating these results to a larger child population can be 

22 avoided. An additional area of uncertainty is with regard to the representation of 

23 variability in air quality. Given the relatively greater variability common in areas of 

24 high Pb concentrations, the approach used to reflect variability may bias the estimates 

25 high, although there is uncertainty with regard to the representativeness of the 

26 monitoring dataset used to characterize this. 

27  Location-specific Urban Case Studies: Limitations in the spatial density of ambient 

28 air monitors in the three metropolitan areas simulated limit our characterization of 

29 spatial gradients of ambient air Pb levels in these case studies. While this factor 

30 introduces uncertainty into the risk estimates for this category of case study, it is not 

31 clear if there is a directional bias. 

32  Air Quality Simulation: The proportional roll-up and roll-down procedures used in 

33 some case studies to simulate air quality conditions just meeting the previous 

34 NAAQS and alternative NAAQS, respectively, assume proportional changes in air 

35 concentrations across those case study areas to create those air quality scenarios. The 

36 EPA recognizes the uncertainty with our simulation of higher air Pb concentrations 

37 that would just meet the previous NAAQS in the urban location-specific case studies, 

38 as well as the uncertainty in simulation of conditions associated with the 

39 implementation of emissions reduction actions to meet a lower standard. There is the 

40 potential that the use of the proportional approach for adjusting monitor values 

41 introduced a degree of high-bias into estimates of risk reduction. This could result if 

42 we find that urban areas can target specific Pb sources impacting individual monitors, 

43 thereby avoiding the need for more generalized reduction strategies resulting in a 

44 uniform pattern of reduction across all monitors in an urban area. It is important to 
January 2013 3-63 Draft - Do Not Quote or Cite

1 point out however, that the generalized urban case study is not effected by this 

2 potential bias, since, given the single exposure zone involved, the single ambient air 

3 Pb level is fixed to reflect meeting the standard being considered (i.e., no spatial 

4 gradient is simulated in the small, localized residential area being modeled). 

5  Outdoor Soil/Dust Pb Concentrations: Limitations in datasets on Pb levels in surface 

6 soil/dust Pb in urban areas and in our ability to simulate the impact of reduced air Pb 

7 levels related to lowering the NAAQS contributes uncertainty to air-related risk 

8 estimates. In this case, it is likely that we have low-biased our estimates of risk 

9 reduction associated with alternative (lower) Pb NAAQS levels, since we have not 

10 simulated potential changes in soil Pb related to changes in ambient air Pb. 

11  Indoor Dust Pb Concentrations: Limitations and uncertainty in modeling of indoor 

12 dust Pb levels, including the impact of reductions in ambient air Pb levels, contributes 

13 uncertainty to air-related risk estimates. Although our modeling of indoor dust does 

14 link changes in ambient air Pb to changes in indoor dust Pb (via air exchanges and 

15 indoor deposition onto surfaces), the modeling does not include a link between 

16 ambient air Pb, outdoor soil Pb and subsequent changes in the level of Pb carried (or 

17 “tracked”) into the house. This could introduce low-bias into our total estimates of 

18 air-related Pb exposure and risk. 

19  Interindividual Variability in PbB Levels: Uncertainty related to population 

20 variability in PbB levels (i.e., interindividual variability in factors other than media 

21 concentration that influence PbB) and limitations in modeling of this introduces 

22 significant uncertainty into PbB and IQ loss estimates for the 95th percentile of the 

23 population. We are not aware of any systematic bias introduced into the analysis from 

24 this source of uncertainty. 

25  Pathway Apportionment for Higher Percentile PbB and risks: Limitations, primarily 

26 in data, prevented us from characterizing the degree of correlation among high-end 

27 Pb exposures for the various pathways (e.g., the degree to which an individual 

28 experiencing high drinking water Pb exposure would also experience high Pb paint 

29 exposure and high ambient air-related Pb exposure). Our inability to characterize 

30 potential correlations between exposure pathways (particularly at the higher 

31 percentile exposure levels) limited our ability to (a) effectively model high-end Pb 

32 risk and (b) apportion that risk between different exposure pathways, including 

33 ambient air-related pathways. 

34  IQ Loss Concentration-response Functions: Specification of the quantitative 

35 relationship between PbB level and IQ loss is subject to greater uncertainty at lower 

36 PbB levels (e.g., particularly below 2.5 μg/dL concurrent PbB). However, we believe 

37 that by considering four different models (which each treat the response at low PbB 

38 levels in a different manner), we have completed a reasonable characterization of this 

39 source of uncertainty and its impact on risk estimates. Given comparison of risk 

40 estimates generated using the four models, it would appear that this source of 

41 uncertainty has a potentially significant impact on risk. 
January 2013 3-64 Draft - Do Not Quote or Cite

1 3.4.8 Updated Interpretation of Risk Estimates 

2 As summarized in prior sections, a range of information gaps and areas of uncertainty 

3 were associated with the information available in the last review. In the REA Planning 

4 document, staff considered the degree to which information newly available since the last Pb 

5 NAAQS review, as summarized in the draft ISA, might address specific uncertainties associated 

6 with the 2007 REA, such that an updated risk model might be developed with the potential to 

provide new exposure and risk estimates substantially different45 7 from estimates generated in 

8 2007 (USEPA, 2011). Staff concluded that the newly available information did not provide the 

9 means by which to develop an updated or enhanced risk model that would substantially improve 

10 the utility of risk estimates in informing the Pb NAAQS review. Specifically it was concluded 

11 that none of the primary sources of uncertainty indentified to have the greatest impact on risk 

12 estimates would be substantially reduced through the use of newly available information 

13 (USEPA, 2011). 

14 Our ongoing review of the newly available information leads us to conclude at this time, 

15 that the key observations regarding air-related Pb risk modeled for the set of standard levels 

16 covered in the 2007 REA, as well as the risk estimates interpolated for the current standard (as 

17 discussed in Section 3.4.5) are not significantly affected by the new information. Our overall 

18 characterization of uncertainty and variability associated with those estimates (as described 

19 above in sections 3.4.6 and 3.4.7) is not appreciably affected by new information. As recognized 

20 at the time of the last review, exposure and risk modeling conducted for this analysis was 

21 complex and subject to significant uncertainties due to limitations, data, and models, among 

22 other aspects. Further, limitations in the assessment design, data and modeling tools 

23 handicapped us from sharply separating Pb linked to ambient air from Pb that is not air-related. 

24 In summary, the estimates of risk attributable to air-related exposures, with which we 

25 recognize a variety of sources of uncertainty, are considered to be approximate, falling within 

26 upper and lower bounds which over- and underestimate, respectively. In scenarios for more 

27 restrictive air quality conditions than those associated with the previous Pb standard, substantial 

28 reductions in air-related risk were demonstrated. Focusing on the results for the generalized 

29 (local) urban case study, the interpolated estimates for the scenario representing the current 

standard are very similar to estimates for the two 0.2 μg/m3 30 scenarios (maximum monthly and 

quarterly averages) simulated in the 2007 REA,46 31 and are appreciably lower than those 

 

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 associated with the current or potential alternative standards. 46 There is uncertainty associated with judging differences between the current standard and these potential 

alternative standards due to the difference in air quality datasets 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

1 associated with the previous standard. In characterizing the magnitude of air-related risk 

2 associated with the current standard, we focusing on median estimates, for which we have 

3 appreciably greater confidence than estimates for outer ends of risk distribution (see section 

4 3.4.7) and on risks derived using the C-R function in which we have greatest confidence (see 

5 sections 3.4.3.3.1 and 3.4.7). The risk results for the current standard from the last review for 

6 one of the location-specific urban study area populations and those newly derived in this review 

7 based on interpolation from 2007 REA results for the generalized (local) urban case study, which 

8 is recognized to reflect a generalized high end of air-related exposure for localized populations, 

9 indicate air-related risk for the current standard of a magnitude generally within the bounds of 

10 roughly 1 and 3 points IQ loss. 
January 2013 3-66 Draft - Do Not Quote or Cite

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16 Teratol 32: 262-272. http://dx.doi.org/10.1016/j.ntt.2009.12.004

17 Lagerkvist, BJ; Ekesrydh, S; Englyst, V; Nordberg, GF; Soderberg, HA; Wiklund, DE. (1996). Increased blood lead 

18 and decreased calcium levels during pregnancy: A prospective study of Swedish women living near a 

19 smelter. Am J Public Health 86: 1247-1252. 

20 Lanphear, BP; Roghmann, KJ. (1997). Pathways of lead exposure in urban children. Environ Res 74: 67-73. 

21 Lanphear, BP; Matte, TD; Rogers, J; Clickner, RP; Dietz, B; Bornschein, RL; Succop, P; Mahaffey, KR; Dixon, S; 

22 Galke, W; Rabinowitz, M; Farfel, M; Rohde, C; Schwartz, J; Ashley, P; Jacobs, DE. (1998). The 

23 contribution of lead-contaminated house dust and residential soil to children's blood lead levels: A pooled 

24 analysis of 12 epidemiologic studies. Environ Res 79: 51-68. http://dx.doi.org/10.1006/enrs.1998.3859

25 Lanphear, BP; Dietrich, K; Auinger, P; Cox, C. (2000). Cognitive deficits associated with blood lead concentrations 

26 <10 microg/dL in US children and adolescents. Public Health Rep 115: 521-529.Lanphear, B. P.; Hornung, 

27 R.; Khoury, J.; Yolton, K.; Baghurst, P.; Bellinger, D. C.; Canfield, R. L.; Dietrich, K. N.; Bornschein, R.; 

28 Greene, T.; Rothenberg, S. J.; Needleman, H. L.; Schnaas, L.; Wasserman, G.; Graziano, J.; Roberts, R. 

29 (2005) Low-level environmental lead exposure and children's intellectual function: an international pooled 

30 analysis. Environ. Health Perspect. 113: 894-899.Manton, WI. (1985). Total contribution of airborne lead 

31 to blood lead. Occup Environ Med 42: 168-172. http://dx.doi.org/10.1136/oem.42.3.168 

32 Miranda, ML; Kim, D; Reiter, J; Overstreet Galeano, MA; Maxson, P. (2009). Environmental contributors to the 

33 achievement gap. Neurotoxicology 30: 1019-1024. http://dx.doi.org/10.1016/j.neuro.2009.07.012

34 National Center for Health Statistics. (2010) National Center for Health Statistics. (2011) Health, United States, 

35 2011: With Special Feature on Socioeconomic Status and Health. Hyattsville, MD. 

36 2012http://www.cdc.gov/nchs/data/hus/hus11.pdf 

37 Patel, AB; Prabhu, AS. (2009). Determinants of lead level in umbilical cord blood. Indian Pediatr 46: 791-

38 793.Pirkle, JL; Brody, DJ; Gunter, EW; Kramer, RA; Paschal, DC; Flegal, KM; Matte, TD. (1994). The 

39 decline in blood lead levels in the United States: The National Health and Nutrition Examination Surveys 

40 (NHANES). JAMA 272: 284-291. http://dx.doi.org/10.1001/jama.1994.03520040046039 
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1 Ranft, U; Delschen, T; Machtolf, M; Sugiri, D; Wilhelm, M. (2008). Lead concentration in the blood of children and 

2 its association with lead in soil and ambient air: Trends between 1983 and 2000 in Duisburg. J Toxicol 

3 Environ Health A 71: 710-715. http://dx.doi.org/10.1080/15287390801985117

4 Rice, DC. (1990). Lead-induced behavioral impairment on a spatial discrimination reversal task in monkeys exposed 

5 during different periods of development. Toxicol Appl Pharmacol 106: 327-333. 

6 http://dx.doi.org/10.1016/0041-008X(90)90251-O 

7 Rice, DC. (1992). Lead exposure during different developmental periods produces different effects on FI 

8 performance in monkeys tested as juveniles and adults. Neurotoxicology 13: 757-770. 

9 Rice, DC; Gilbert, SG. (1990). Sensitive periods for lead-induced behavioral impairment (nonspatial discrimination 

10 reversal) in monkeys. Toxicol Appl Pharmacol 102: 101-109. http://dx.doi.org/10.1016/0041-

11 008X(90)90087-BRothenberg, S. J.; Khan, F.; Manalo, M.; Jian, J.; Cuellar, R.; Reyes, S.; Acosta, S.; 

12 Jauregui, M.; Diaz, M.; Sanchez, M.; Todd, A. C.; Johnson, C. (2000) Maternal bone lead contribution to 

13 blood lead during and after pregnancy. Environ. Res. 82: 81-90. 

14 Schnaas, L; Rothenberg, SJ; Flores, MF; Martinez, S; Hernandez, C; Osorio, E; Perroni, E. (2004). Blood lead 

15 secular trend in a cohort of children in Mexico City (1987-2002). Environ Health Perspect 112: 1110-1115. 

16 http://dx.doi.org/10.1289/ehp.6636 

17 Schwartz, J., and Pitcher, H. (1989) The relationship between gasoline lead and blood lead in the United States. J 

18 Official Statistics 5(4):421-431. 

19 Schwemberger, MS, JE Mosby, MJ Doa, DE Jacobs, PJ Ashley, DJ Brody, MJ Brown, RL Jones, D Homa. (2005) 

20 Mortality and Morbidity Weekly Report 54(20):513-516. May 27, 2005 

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22 living near a smelter. J Expo Sci Environ Epidemiol 17: 248-259. http://dx.doi.org/10.1038/sj.jes.7500512 

23 Smith, D. R.; Osterloh, J. D.; Flegal, A. R. (1996) Use of endogenous, stable lead isotopes to determine release of 

24 lead from the skeleton. Environ. Health Perspect. 104: 60-66. 

25 Surkan, PJ; Zhang, A; Trachtenberg, F; Daniel, DB; McKinlay, S; Bellinger, DC. (2007). Neuropsychological 

26 function in children with blood lead levels <10 μg/dL. Neurotoxicology 28: 1170-1177. 

27 http://dx.doi.org/10.1016/j.neuro.2007.07.007 

28 Téllez-Rojo, M. M.; Bellinger, D. C.; Arroyo-Quiroz, C.; Lamadrid-Figueroa, H.; Mercado-García, A.; Schnaas29 Arrieta, L.; Wright, R. O.; Hernández-Avila, M.; Hu, H. (2006) Longitudinal associations between blood 

30 lead concentrations < 10 μg/dL and neurobehavioral development in environmentally-exposed children in 

31 Mexico City. Pediatrics 118: e323-e330. 

32 Tellez-Rojo, M. 2008. Email message to Jee-Young Kim, U.S. EPA. February 11, 2008. Docket number EPA-HQ33 OAR-2006-0735. 

34 Tripathi, R.M.; Raghunath, R.; A.V. Kumar; V.N. Sastry; S. Sadasivan. (2001) Atmospheric and children’s blood 

35 lead as indicators of vehicular traffic and other emission sources in Mumbai, India. Sci Total Enviro 267: 

36 101-108. 

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41 Exposure analysis methodology and validation: OAQPS staff report. Research Triangle Park, NC: Office of 
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9 Case Studies, Volume I. Human Exposure and Health Risk Assessments – Full-Scale and Volume II. 

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11 014a and EPA-452/R-07-014b. 

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14 Planning and Standards, Research Triangle Park, NC. EPA-452/R-07-013. Available at: 

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17 Risk and Exposure Assessment Planning Document. Office of Air Quality Planning and Standards, 

18 Research Triangle Park, NC. EPA/452/P-11-003. Available at: 

19 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pd.html 

20 U.S. Environmental Protection Agency. (2012) Integrated Science Assessment for Lead (Third External Review 

21 Draft). Washington, DC, EPA/600/R-10/075C. Available online at: 

22 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html 

23 Zielhuis, R.L.; del Castilho, P.; Herber, R.F.M.; Wibowo, A.A.E.; Salle, H.J.A. (1979) Concentrations of lead and 

24 other metals in blood of two and three year-old children living near a secondary smelter. Int. Arch. Occup. 

25 Environ. Health 42: 231-239. 
January 2013 4-1 Draft - Do Not Quote or Cite

1 4 REVIEW OF THE PRIMARY STANDARD FOR LEAD 

2 This chapter presents preliminary staff conclusions regarding the primary Pb standard. 

3 These preliminary staff conclusions are guided by consideration of key policy-relevant questions 

4 and based on the assessment and integrative synthesis of information presented in the ISA and by 

5 staff analyses and evaluations presented in chapters 2 and 3 herein. Final evaluations and staff 

6 conclusions, to be developed taking into consideration CASAC advice and public comment on 

7 this draft document, will be presented in the final PA. The final evaluations and staff 

8 conclusions will inform the Administrator’s decisions on whether to retain or revise the existing 

9 primary standard for Pb. 

10 Following an introductory section on the general approach for reviewing the primary 

11 standard (section 4.1), including a summary of considerations in the last review, the discussion in 

12 this chapter focuses on the central issue of whether the information available in this review 

13 supports or calls into question the adequacy of the current primary standard. Building on the 

14 responses to specific policy-relevant questions on the scientific evidence and exposure-risk 

15 information in chapter 3 above, presentation in section 4.2 is also organized into consideration of 

16 key policy-relevant questions framing evidence-based and exposure/risk-based considerations. 

17 The policy-relevant questions in this document are based on those included in the IRP (IRP, 

18 section 3.1). In section 4.3, preliminary staff conclusions are developed. Section 4.4 presents a 

19 brief overview of key uncertainties and areas for future research. 

20 4.1 APPROACH 

21 Staff’s approach in this review of the current primary standard takes into consideration 

22 the approaches used in the previous Pb NAAQS review. The past and current approaches 

23 described below are both based, most fundamentally, on using EPA’s assessment of the current 

24 scientific evidence and associated quantitative analyses to inform the Administrator’s judgment 

25 regarding a primary standard for Pb that protects public health with an adequate margin of safety. 

26 We note that the final decision on the adequacy of the current standard is largely a public health 

27 policy judgment to be made by the Administrator. The Administrator’s final decision must draw 

28 upon scientific information and analyses about health effects, population exposure and risks, as 

29 well as judgments about how to consider the range and magnitude of uncertainties that are 

30 inherent in the scientific evidence and analyses. Our approach to informing these judgments, 

31 discussed more fully below, is based on the recognition that the available health effects evidence 

32 generally reflects a continuum, consisting of ambient levels at which scientists generally agree 

33 that health effects are likely to occur, through lower levels at which the likelihood and magnitude 

34 of the response become increasingly uncertain. This approach is consistent with the 
January 2013 4-2 Draft - Do Not Quote or Cite

1 requirements of the NAAQS provisions of the Act and with how the EPA and the courts have 

2 historically interpreted the Act. These provisions require the Administrator to establish primary 

3 standards that, in the Administrator’s judgment, are requisite to protect public health with an 

4 adequate margin of safety. In so doing, the Administrator seeks to establish standards that are 

5 neither more nor less stringent than necessary for this purpose. The Act does not require that 

6 primary standards be set at a zero-risk level, but rather at a level that avoids unacceptable risks to 

7 public health. The four basic elements of the NAAQS (indicator, averaging time, level, and 

8 form) are considered collectively in evaluating the health protection afforded by the current 

9 standard. 

10 The following subsections include background information on the approach used in the 

11 previous review of the standard (section 4.1.1) and a discussion of the approach for the current 

12 review (section 4.1.2). 

13 4.1.1 Approach Used in the Last Review 

14 The last review of the NAAQS for Pb was completed in 2008 (73 FR 66964). In 

15 consideration of the much-expanded health effects evidence on neurocognitive effects of Pb in 

16 children available at that time, the EPA substantially revised the primary standard from 1.5 

μg/m3 17 , as a not-to-be exceeded average concentration over a calendar quarter, to a level of 0.15 

μg/m3 18 , as a not-to-be-exceeded rolling 3-month average concentration. The 2008 decision to 

19 revise the primary standard was based on the extensive body of scientific evidence published 

20 over almost three decades, from the time the standard was originally set in 1978 through 2005-

21 2006. The 2008 decision considered the body of evidence as assessed in the 2006 CD (USEPA, 

22 2006) as well as the 2007 Staff Paper assessment of the policy-relevant information contained in 

23 the CD and the quantitative risk/exposure assessment (USEPA, 2007a, 2007b), the advice and 

24 recommendations of CASAC (Henderson 2007a, 2007b, 2008a, 2008b), and public comment. 

25 While recognizing that Pb has been demonstrated to exert “a broad array of deleterious 

26 effects on multiple organ systems”, the review focused on the effects most pertinent to ambient 

27 air exposures, which given ambient air Pb reductions over the past 30 years are those associated 

28 with relatively lower exposures and associated blood Pb levels (73 FR 66975). In so doing, the 

29 EPA recognized the general consensus that the developing nervous system in children is among, 

30 if not the most sensitive health endpoint associated with Pb exposures. Thus, primary attention 

31 was given to consideration of nervous system effects, including neurocognitive and 

32 neurobehavioral effects, in children (73 FR 66976). The body of evidence included associations 

33 of such effects in study populations of variously-aged children with mean blood Pb levels below 

34 10 μg/dL, extending from 8 down to 2 μg/dL (73 FR 66976). The public health implications of 
January 2013 4-3 Draft - Do Not Quote or Cite

1 effects of air-related Pb on cognitive function (e.g., IQ) in young children were given particular 

2 focus in the review. 

3 4.1.1.1 Conclusion Regarding the Need for Revision 

4 The conclusions reached by the Administrator in the last review were based primarily on 

5 the scientific evidence, with the risk- and exposure-based information providing support for 

6 various aspects of the decision. In reaching his conclusion on the adequacy of the prior standard, 

7 the Administrator placed primary consideration on the large body of scientific evidence available 

8 in the review including significant new evidence concerning effects at blood Pb concentrations 

9 substantially below those identified when the NAAQS for Pb was initially set in 1978 (73 FR 

10 66987; 43 FR 46246). Given particular attention was the robust evidence of neurotoxic effects 

11 of Pb exposure in children, recognizing: (1) that while blood Pb levels in U.S. children had 

12 decreased notably since the late 1970s, newer epidemiologic studies had investigated and 

13 reported associations of effects on the neurodevelopment of children with those more recent 

14 lower blood Pb levels and (2) that the toxicological evidence included extensive experimental 

15 laboratory animal evidence substantiating well the plausibility of the epidemiologic findings 

16 observed in human children and expanding our understanding of likely mechanisms underlying 

17 the neurotoxic effects (73 FR 66987). Additionally, within the range of blood Pb levels 

18 investigated in the available evidence base, a threshold level for neurocognitive effects was not 

19 identified (73 FR 66984; 2006 CD, p. 8-67). Further, the evidence indicated a steeper dose20 response relationship for effects on cognitive function at those lower blood Pb levels than at 

21 higher blood Pb levels that were more common in the past, “indicating the potential for greater 

22 incremental impact associated with exposure at these lower levels” (73 FR 66987). As at the 

23 time when the standard was set, the health effects evidence and exposure/risk assessment 

24 supported the conclusion that air-related Pb exposure pathways contribute to blood Pb levels in 

25 young children by inhalation and ingestion (73 FR 66987). The available information also 

26 suggested that the air-to-blood ratio was likely larger, when all inhalation and ingestion pathways 

for air-related Pb are considered, than the air-to-blood ratio (of 2 μg/dL blood Pb to 1 μg/m3 27 air 

28 Pb) estimated when the standard was initially set in 1978 (73 FR 66987). 

29 In the Administrator’s decision on the adequacy of the 1978 standard, the Administrator 

30 considered the evidence using a very specifically defined framework, referred to as an air-related 

31 IQ loss evidence-based framework. This framework integrates evidence for the relationship 

32 between Pb in air and Pb in young children’s blood with evidence for the relationship between 

33 Pb in young children’s blood and IQ loss (73 FR 77987), as described in more detail in section 

34 4.1.1.2 below. This evidence-based approach considers air-related effects on neurocognitive 

35 function (using the quantitative metric of IQ loss) associated with exposure in those areas with 
January 2013 4-4 Draft - Do Not Quote or Cite

1 elevated air concentrations equal to potential alternative levels for the Pb standard. Thus, the 

2 conceptual context for the framework is that it provides estimates of air-related IQ loss for a 

3 subset of the population of U.S. children (i.e., the subset living in close proximity to air Pb 

4 sources that contribute to elevated air Pb concentrations that equal the current level of the 

5 standard). This is the subset expected to experience air-related Pb exposures at the high end of 

6 the national distribution of such exposures, not at the average. This is the case since when a 

7 standard of a particular level is just met at a monitor sited to record the highest source-oriented 

8 concentration in an area, the large majority of children in the larger surrounding area would 

9 likely experience exposures to concentrations well below that level. 

10 The two primary inputs to the evidence-based air-related IQ loss framework are air-to11 blood ratios and C-R functions for the relationship between blood Pb and IQ response in young 

12 children. Additionally taken into consideration in applying and drawing conclusions from the 

13 framework were the uncertainties inherent in these inputs. Application of the framework also 

14 entailed consideration of an appropriate level of protection from air-related IQ loss to be used in 

15 conjunction with the framework. In simplest terms, the framework provides for estimation of a 

16 mean air-related IQ decrement for young children in the high end of the national distribution of 

17 air-related exposures by focusing on children exposed to air-related Pb in those areas with 

18 elevated air Pb concentrations equal to specific potential standard levels. The framework 

19 estimates of mean air-related IQ loss are derived through multiplication of the following factors: 

standard level (μg/m3

), air-to-blood ratio in terms of μg/dL blood Pb per μg/m3 20 air concentration 

21 and slope for the C-R function in terms of points IQ decrement per μg/dL blood Pb. 

22 Based on the application of the air-related IQ loss framework to the evidence, the 

23 Administrator concluded that, for exposures projected for air Pb concentrations at the level of the 

24 1978 standard, the quantitative estimates of IQ loss associated with air-related Pb indicated risk 

25 of a magnitude that in his judgment was significant from a public health perspective, and that the 

26 evidence-based framework supported a conclusion that the 1978 standard did not protect public 

27 health with an adequate margin of safety (73 FR 77987). The Administrator further concluded 

28 that the evidence indicated the need for a substantially lower standard level to provide increased 

29 public health protection, especially for at-risk groups (most notably children), against an array of 

30 effects, most importantly including effects on the developing nervous system (73 FR 77987). In 

31 addition to giving primary consideration to the much expanded evidence base since the standard 

32 was set, the Administrator also took into consideration the exposure/risk assessments. In so 

33 doing, he observed that, while taking into consideration their inherent uncertainties and 

34 limitations, the quantitative estimates of IQ loss associated with air-related Pb in air quality 

35 scenarios just meeting the then-current standard also indicated risk of a magnitude that in his 

36 judgment was significant from a public health perspective. Thus, the Administrator concluded 
January 2013 4-5 Draft - Do Not Quote or Cite

1 the exposure/risk estimates provided additional support to the evidence-based conclusion that the 

2 standard needed revision (73 FR 66987). 

3 4.1.1.2 Conclusions on Elements of Revised Standard 

4 In considering appropriate revisions to the prior standard in the review completed in 

5 2008, each of the four basic elements of the NAAQS (indicator, averaging time, level, and form) 

6 were evaluated. The rationale for decisions on those elements is summarized below. 

7 With regard to indicator, consideration was given to replacing Pb-TSP with Pb-PM10. 

8 The EPA recognized, however, that Pb in all particle sizes contributes to Pb in blood and 

9 associated health effects, additionally noting that the difference in particulate Pb captured by 

10 TSP and PM10 monitors may be on the order of a factor of two in some areas (73 FR 66991). 

11 Further, the Administrator recognized uncertainty with regard to whether a Pb-PM10-based 

standard would also effectively control ultra-coarse1 12 Pb particles, which may have a greater 

13 presence in areas near sources where Pb concentrations are highest (73 FR 66991). The 

14 Administrator decided to retain Pb-TSP as the indicator to provide sufficient public health 

15 protection from the range of particle sizes of ambient air Pb, including ultra-coarse particles (73 

16 FR 66991). Additionally, a role was provided for Pb-PM10 in the monitoring required for a Pb17 TSP standard (73 FR 66991) based on the conclusion that use of Pb-PM10 measurements at sites 

18 not influenced by sources of ultra-coarse Pb, and where Pb concentrations are well below the 

19 standard, would take advantage of the increased precision of these measurements and decreased 

20 spatial variation of Pb-PM10 concentrations, without raising the same concerns over a lack of 

21 protection against health risks from all particulate Pb emitted to the ambient air that support 

22 retention of Pb-TSP as the indicator (versus revision to Pb-PM10) (73 FR 66991). Accordingly, 

23 allowance was made for the use of Pb-PM10 monitoring for Pb NAAQS attainment purposes in 

24 certain limited circumstances, at non-source-oriented sites, where the Pb concentrations are 

25 expected to be substantially below the standard and ultra-coarse particles are not expected to be 

26 present (73 FR 66991). 

27 With regard to averaging time and form, consideraton was given to monthly and 3-month 

28 averaging times. The Administrator recognized the complexity related to the multimedia nature 

29 of Pb and its multiple pathways of human exposure, in addition to uncertainty remaining over the 

30 period of time needed for air Pb concentrations to lead to the health effects most at issue in this 

31 review (73 FR 77995). Relevant factors pertaining to the human physiological response to 

32 changes in Pb exposures and those pertaining to the response of air-related Pb exposure 

 

1

 The term ultra-coarse is used to refer to particles collected by a TSP sampler but not by a PM10 sampler. 

This terminology is consistent with the traditional usage of ‘‘fine’’ to refer to particles collected by a PM2.5 sampler, 

and ‘‘coarse’’ to refer to particles collected by a PM10 sampler but not by a PM2.5 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

1 pathways to changes in airborne Pb were considered in an integrated manner (73 FR 77996). 

2 Key considerations included the limited evidence indicating more numerous factors influencing 

3 ingestion (versus inhalation) pathways, which were considered likely to lessen the impact of 

4 month-to-month variations in airborne Pb concentrations on levels of air-related Pb in children’s 

5 blood. Such factors were considered likely to lead to response times (e.g., for the response of 

6 blood to air Pb via these pathways) extending longer than a month (73 FR 66996). The EPA 

7 additionally considered the control that a rolling 3-month averaging time can provide (e.g., 

8 compared to a block calendar quarter) on month-to-month variability in air Pb concentrations 

9 and in associated exposures (73 FR 66996). Based on this integrated consideration of the range 

10 of relevant factors, the averaging time was revised to a rolling three-month period with a 

11 maximum (not-to-be-exceeded) form, evaluated over a three-year period. As compared to the 

12 previous averaging time and form of calendar quarter (not-to-be exceeded), this revision was 

13 considered to be more scientifically appropriate and more health protective (73 FR 77996). The 

14 rolling average gives equal weight to all three-month periods, and the new calculation method 

15 gives equal weight to each month within each three-month period (73 FR 77996). Further, the 

16 rolling average yields 12 three-month averages each year to be compared to the NAAQS versus 

17 four averages in each year for the block calendar quarters pertaining to the previous standard (73 

18 FR 77996). 

19 Lastly, based on the body of scientific evidence and information available, as well as 

20 CASAC recommendations and public comment, the Administrator decided on a standard level 

21 that, in combination with the specified choice of indicator, averaging time, and form, he judged 

22 requisite to protect public health, including the health of sensitive groups, with an adequate 

23 margin of safety (73 FR 67006). In reaching the decision on level for the revised standard, the 

24 Administrator considered as a useful guide the evidence-based framework developed in that 

25 review. As described in section 4.1.1.1 above, that framework integrates evidence for the 

26 relationship between Pb in air and Pb in children’s blood and the relationship between Pb in 

27 children’s blood and IQ loss. Application of the air-related IQ loss evidence-based framework 

28 was recognized, however, to provide “no evidence- or risk-based bright line that indicates a 

29 single appropriate level” for the standard (73 FR 67006). Rather, the framework was seen as a 

30 useful guide for consideration of health risks from exposure to ambient levels of Pb in the air, in 

31 the context of a specified averaging time and form, with regard to the Administrator’s decision 

32 on a level for a revised NAAQS that provides public health protection that is sufficient but not 

33 more than necessary under the Act (73 FR 67004). 

34 As noted above, use of the evidence-based air-related IQ loss framework to inform 

35 selection of a standard level involved consideration of the evidence with regard to two input 

36 parameters. The two input parameters are an air-to-blood ratio and a C-R function for population 
January 2013 4-7 Draft - Do Not Quote or Cite

1 IQ response associated with blood Pb level (73 FR 67004). The evidence at the time of the last 

2 review indicated a broad range of air-to-blood ratio estimates, each with limitations and 

3 associated uncertainties. Based on the then-available evidence, the Administrator concluded that 

4 1:5 to 1:10 represented a reasonable range to consider and identified 1:7 as a generally central 

5 value on which to focus (73 FR 67004). With regard to C-R functions, in light of the evidence of 

6 nonlinearity and of steeper slopes at lower blood Pb levels, the Administrator concluded it was 

7 appropriate to focus on C-R analyses based on blood Pb levels that most closely reflected the 

then-current population of children in the U.S.,2 8 recognizing EPA’s identification of four such 

9 analyses and giving weight to the central estimate or median of the resultant C-R functions (73 

10 FR 67003, Table 3; 73 FR 67004). The four study groups from which C-R functions were drawn 

in 2008, and the associated C-R slopes, are summarized in Table 3-3 above.3 11 The median 

12 estimate of -1.75 IQ points decrement per μg/dL was selected for use with the framework. With 

13 the framework, as summarized in section 4.1.1.1 above, potential alternative standard levels 

(μg/m3) are multiplied by estimates of air-to-blood ratio (μg/dL blood Pb per μg/m3 14 air Pb) and 

15 the median slope for the C-R function (points IQ decrement per μg/dL blood Pb), yielding 

16 estimates of a mean air-related IQ decrement for a specific subset of young children (i.e., those 

17 children exposed to air-related Pb in areas with elevated air Pb concentrations equal to specified 

18 alternative levels). As such, the application of the framework yields estimates for the mean air19 related IQ decrements of the subset of children expected to experience air-related Pb exposures 

20 at the high end of the distribution of such exposures. The associated mean IQ loss estimate is the 

21 average for this highly exposed subset and is not the average air-related IQ loss projected for the 

22 entire U.S. population of children. Uncertainties and limitations were recognized in the use of 

23 the framework and in the resultant estimates (73 FR 67000). 

24 In considering the use of the evidence-based air-related IQ loss framework to inform his 

25 judgment as to the appropriate degree of public health protection that should be afforded by the 

26 NAAQS to provide requisite protection against risk of neurocognitive effects in sensitive 

27 populations, such as IQ loss in children, the Administrator recognized in the 2008 review that 

28 there were no commonly accepted guidelines or criteria within the public health community that 

29 would provide a clear basis for such a judgment. During the 2008 review, CASAC commented 

 

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 5th and 95th 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

1 regarding the significance from a public health perspective of a 1-2 point IQ loss in the entire 

2 population of children and, along with some commenters, emphasized that the NAAQS should 

3 prevent air-related IQ loss of a significant magnitude, such as on the order of 1-2 IQ points, in all 

4 but a small percentile of the population. Similarly, the Administrator stated that “ideally air5 related (as well as other) exposures to environmental Pb would be reduced to the point that no IQ 

6 impact in children would occur” (73 FR 66998). The Administrator further recognized that, in 

7 the case of setting a NAAQS, he was required to make a judgment as to what degree of 

8 protection is requisite to protect public health with an adequate margin of safety (73 FR66998). 

9 The NAAQS must be sufficient but not more stringent than necessary to achieve that result, and 

10 does not require a zero-risk standard (73 FR 66998). The Administrator additionally recognized 

11 that the evidence-based air-related IQ loss framework did not provide estimates pertaining to the 

12 U.S. population of children as a whole. Rather, the framework provides estimates (with 

13 associated uncertainties and limitations) for the mean of a subset of that population, the subset of 

14 children assumed to be exposed to the level of the standard. As described in the final decision 

15 “[t]he framework in effect focuses on the sensitive subpopulation that is the group of children 

16 living near sources and more likely to be exposed at the level of the standard” (73 FR 67000). 

17 As further noted in the final decision (73 FR 67000): 

18 EPA is unable to quantify the percentile of the U.S. population of children that 

19 corresponds to the mean of this sensitive subpopulation. Nor is EPA confident in 

20 its ability to develop quantified estimates of air-related IQ loss for higher 

21 percentiles than the mean of this subpopulation. EPA expects that the mean of 

22 this subpopulation represents a high, but not quantifiable, percentile of the U.S. 

23 population of children. As a result, EPA expects that a standard based on 

24 consideration of this framework would provide the same or greater protection 

25 from estimated air-related IQ loss for a high, albeit unquantifiable, percentage of 

26 the entire population of U.S. children. 

27 

28 In reaching a judgment as to the appropriate degree of protection, the Administrator 

29 considered advice and recommendations from CASAC and public comments and recognized the 

30 uncertainties in the health effects evidence and related information as well as the role of, and 

31 context for, a selected air-related IQ loss in the application of the framework. In so doing, the 

32 Administrator identified an air-related IQ loss of 2 points to be used in conjunction with the 

evidence-based framework in considering an appropriate level for the standard (73 FR 67005).4 33 

34 Given the various uncertainties associated with the framework and the scientific evidence base, 

35 and the focus of the framework on the sensitive subpopulation of more highly exposed children, 

 

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

1 a standard level selected using this air-related IQ loss, in combination with the selected 

2 averaging time and form, was expected to significantly reduce and limit for a high percentage of 

3 U.S. children the risk of experiencing an air-related IQ loss of that magnitude (73 FR 67005). At 

the standard level of 0.15 μg/m3 4 , with the combination of the generally central estimate of air-to5 blood ratio of 1:7 and the median of the four C-R functions (-1.75 IQ point decrement per μg/dL 

6 blood Pb), the framework estimates of air-related IQ loss were below 2 IQ points (73 FR 67005, 

7 Table 4). 

8 In reaching the decision in 2008 on level for the revised standard, the Administrator also 

9 considered the results of the quantitative risk assessment to provide a useful perspective on risk 

10 from air-related Pb. In light of important uncertainties and limitations for purposes of evaluating 

11 potential standard levels, however, the Administrator placed less weight on the risk estimates 

12 than on the evidence-based assessment. Nevertheless, in recognition of the general 

13 comparability of quantitative risk estimates for the case studies considered most conceptually 

14 similar to the scenario represented by the evidence-based framework, he judged the quantitative 

15 risk estimates to be “roughly consistent with and generally supportive” of the evidence-based 

16 framework estimates (73 FR 67006). 

17 Based on consideration of the entire body of evidence and information available in the 

18 review, as well as the recommendations of CASAC and public comments, the Administrator 

decided that a level for the primary Pb standard of 0.15 μg/m3 19 , in combination with the specified 

20 choice of indicator, averaging time and form was requisite to protect public health, including the 

21 health of sensitive groups, with an adequate margin of safety (73 FR 67006). In reaching 

22 decisions on level as well as the other elements of the revised standard, the Administrator took 

23 note of the complexity associated with consideration of health effects caused by different 

24 ambient air concentrations of Pb and with uncertainties with regard to the relationships between 

25 air concentrations, exposures, and health effects For example, selection of a maximum, not to 

26 be exceeded, form in conjunction with a rolling 3-month averaging time over a three year span 

27 was expected to have the effect that the at-risk subpopulation of children would be exposed 

28 below the standard most of the time (73 FR 67005). The Administrator additionally noted his 

29 consideration of the provision of an adequate margin of safety in making decisions on each of the 

30 elements of the standard, including, for example “selection of TSP as the indicator and the 

31 rejection of the use of PM10 scaling factors; selection of a maximum, not to be exceeded form, in 

32 conjunction with a 3-month averaging time that employs a rolling average, with the requirement 

33 that each month in the 3-month period be weighted equally (rather than being averaged by 

34 individual data) and that a 3-year span be used for comparison to the standard; and, the use of a 

35 range of inputs for the evidence-based framework, that includes a focus on higher air-to-blood 

36 ratios than the lowest ratio considered to be supportable, and steeper rather than shallower C-R 
January 2013 4-10 Draft - Do Not Quote or Cite

functions, and the consideration of these inputs in selection of 0.15 μg/m3 1 as the level of the 

2 standard” (73 FR 67007). 

3 He additionally noted that a standard with this level would reduce the risk of a variety of 

4 health effects associated with exposure to Pb, including effects indicated in the epidemiological 

5 studies at lower blood Pb levels, particularly including neurological effects in children, and the 

6 potential for cardiovascular and renal effects in adults (73 FR 67006). The Administrator 

7 additionally considered higher and lower levels for the standard, concluding that a level of 0.15 

μg/m3 8 provides for a standard that is neither more or less stringent than necessary for this 

9 purpose, recognizing that the Clean Air Act does not require that primary standards be set at a 

10 zero-risk level, but rather at a level that reduces risk sufficiently so as to protect public health 

11 with an adequate margin of safety (73 FR 67007). For example, the Administrator additionally 

considered potential public health protection provided by standard levels above 0.15 μg/m3 12 , 

13 which he concluded were insufficient to protect public health with an adequate margin of safety. 

14 The Administrator also noted that in light of all of the evidence, including the evidence-based 

15 framework, that the degree of public health protection likely afforded by standard levels below 

0.15 μg/m3 16 would be greater than what is necessary to protect public safety with an adequate 

17 margin of safety. 

18 The Administrator concluded, based on review of all of the evidence (including the 

19 evidence- based framework), that when taken as a whole the selected standard, including the 

20 indicator, averaging time, form, and level, would be “sufficient but not more than necessary to 

21 protect public health, including the health of sensitive subpopulations, with an adequate margin 

22 of safety” (73 FR 67007). 

23 4.1.2 Approach for the Current Review 

24 To evaluate whether it is appropriate to consider retaining the current primary Pb 

25 standard, or whether consideration of revision is appropriate, we have adopted an approach in 

26 this review that builds upon the general approach used in the last review and reflects the broader 

27 body of evidence and information now available. As summarized above, the Administrator’s 

28 decisions in the prior review were based on an integration of information on health effects 

29 associated with exposure to Pb, relationships between ambient air Pb and blood Pb; expert 

30 judgments on the adversity and public health significance of key health effects; and policy 

31 judgments as to when the standard is requisite to protect public health with an adequate margin 

32 of safety. These considerations were informed by air quality and related analyses, quantitative 

33 exposure and risk assessments, and qualitative assessment of impacts that could not be 

34 quantified. 
January 2013 4-11 Draft - Do Not Quote or Cite

1 In conducting this assessment, we draw on the current evidence and quantitative 

2 assessments of exposure pertaining to the public health risk of Pb in ambient air. In considering 

3 the scientific and technical information, we consider both the information available at the time of 

4 the last review and information newly available since the last review, including the current ISA 

5 (USEPA, 2012), as well as the quantitative exposure/risk assessments from the last review that 

6 estimated Pb-related IQ decrements associated with different air quality conditions in simulated 

7 at-risk populations in multiple case studies (USEPA, 2007a). Figure 4-1 illustrates the basic 

8 construct of our two part approach in developing conclusions regarding options appropriate for 

9 the Administrator to consider in this review with regard to the adequacy of the current standard 

10 and, as appropriate, potential alternate standards. In the boxes of Figure 4-1, the range of 

11 questions considered in chapter 3 above and section 4.2 below are represented by a summary of 

12 policy-relevant questions that frame our consideration of the scientific evidence and 

13 exposure/risk information. 
January 2013 4-12 Draft - Do Not Quote or Cite

1 

2 Figure 4-1. Overview of approach for review of current primary standard. 

Evidence-based Considerations

 Does currently available evidence and related 

uncertainties strengthen or call into question prior 

conclusions?

 Evidence of health effects 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 the 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 Consideration
January 2013 4-13 Draft - Do Not Quote or Cite

1 4.2 ADEQUACY OF THE CURRENT STANDARD 

2 In considering the adequacy of the current Pb standard, the overarching question we 

3 consider is:

4  Does the currently available scientific evidence- and exposure/risk-based 

5 information, as reflected in the ISA and REA, support or call into question the 

6 adequacy of the protection afforded by the current Pb standard? 

7 In considering the scientific and technical information, we give our attention to both the 

8 information available at the time of the last review and information newly available since the last 

9 review, including most particularly that which has been critically analyzed and characterized in 

10 the ISA. In chapter 3 above, attention was given to addressing specific questions on key aspects 

11 of this information. To assist us in interpreting the currently available scientific evidence and 

12 results of quantitative exposure/risk analyses to address the overarching question here, we draw 

13 on discussions in chapter 3 above in our consideration of broader or more policy related 

14 questions, posed within sections 4.2.1 and 4.2.2 below. 

15 For the purposes of this draft PA, staff has drawn from EPA’s assessment and integrated 

16 synthesis of the scientific evidence presented in the third draft ISA and on the quantitative 

17 exposure and risk information, based on the 2007 REA (USEPA, 2007a), described in section 3.4 

18 above. The evidence-based discussions presented in this chapter draw upon evidence from 

19 epidemiologic studies and experimental animal studies evaluating health effects related to 

20 exposures to Pb, as discussed in the ISA. The exposure/risk-based discussions have drawn from 

21 the quantitative health risk analyses for Pb performed in the last Pb NAAQS review in light of 

22 the currently available evidence (2007 REA, REA Planning Document). Together the evidence23 based and risk-based considerations inform our preliminary conclusions related to the adequacy 

24 of the current Pb standard. 

25 4.2.1 Evidence-based Considerations 

26 In considering the evidence with regard to the issue of adequacy of the current standard, 

27 we address several questions that build on the information summarized in chapter 3 to more 

28 broadly address the extent to which the current evidence base supports the adequacy of the 

29 public health protection afforded by the current primary standard. The first question addresses 

30 our integrated consideration of the health effects evidence, in light of aspects described in 

31 chapter 3. The second question focuses on our consideration of associated areas of uncertainty. 

32 The third question then integrates our consideration of the prior two questions with a focus on 

33 the standard, including each of the four elements. 
January 2013 4-14 Draft - Do Not Quote or Cite

1  To what extent has new information altered the scientific support for the 

2 occurrence of health effects as a result of multimedia exposure associated with 

3 levels of Pb occurring in the ambient air? 

4 The current evidence continues to support our conclusions from the previous review 

5 regarding key aspects of the health effects evidence for Pb and the health effects of multimedia 

6 exposure associated with levels of Pb occurring in ambient air in the U.S. Our conclusions in 

7 this regard are based on consideration of the assessment of the currently available evidence in the 

8 ISA, particularly with regard to key aspects summarized in chapter 3 of this PA, in light of the 

9 assessment of the evidence in the last review as described in the 2006 CD and summarized in the 

10 notice of final rulemaking (73 FR 66964). Key aspects of these conclusions are summarized 

11 below. 

12 As at the time of the last review, blood Pb continues to be the predominant biomarker 

13 employed to assess exposure and health risk of Pb (ISA, chapters 4 and 5), as discussed in 

14 section 3.1 above. This widely accepted role of blood Pb in assessing exposure and risk is 

15 illustrated by its established use in programs to prevent both occupational Pb poisoning and 

16 childhood Pb poisoning, with the latter program, implemented by the CDC, recently issuing 

17 updated guidance on blood Pb measurement interpretation (CDC, 2012). As in the past, the 

18 current evidence continues to indicate the close linkage of blood Pb levels in young children to 

19 their body burden; this linkage is associated with the ongoing bone remodeling during that 

20 lifestage (ISA, section 4.3.5). This tight linkage plays a role in the somewhat rapid response of 

21 children’s blood Pb to changes in exposure (particularly to exposure increases), which 

22 contributes to its usefulness as an exposure biomarker (ISA, sections 4.2.2, 4.3.5, and 4.3.5.1). 

23 Additionally, the weight of evidence documenting relationships between children’s blood Pb and 

24 health effects, most particularly those on the nervous and hematological systems (e.g., ISA, 

25 sections 5.3 and 5.7) speaks to its usefulness in assessing health risk. 

26 As in the last review, the evidence on air-to-blood relationships available today continues 

27 to be comprised of studies based on an array of circumstances and population groups (of 

28 different age ranges), analyzed by a variety of techniques, which together contribute to 

29 appreciable variability in the associated quantitative estimates and uncertainty with regard to the 

30 relationships existing in the U.S. today. Accordingly, our interpretation of this evidence base, as 

31 discussed in section 3.1 above, also includes consideration of factors that may be influencing 

32 various study estimates, both with regard to their usefulness for our general purpose of 

33 quantitatively characterizing relationships between Pb in ambient air and air-related Pb in 

34 children’s blood, and with regard to their pertinence more specifically to conditions and 

35 populations in the U.S. today. In so doing, we note that the current evidence, while including 

36 two additional studies not available at the time of the last review, is not much changed from that 
January 2013 4-15 Draft - Do Not Quote or Cite

1 available in the last review. The range of estimates that can be derived from the full dataset is 

2 broad and not changed by the inclusion of the newly available estimates. Further, we recognize 

3 significant uncertainties regarding the air Pb to air-related blood Pb relationship for the current 

4 conditions where concentrations of Pb in both ambient air and children’s blood are substantially 

5 lower than they have been in the past. In considering the strengths, limitations and uncertainties 

6 associated with the full dataset, the currently available evidence appears to continue to support a 

7 range of estimates for our purposes that is generally consistent with the range given weight in the 

8 last review, 1:5 to 1:10 (ISA, section 4.7.4 and Table 4-12; 73 FR 67001-2, 67004). We 

9 additionally note that the generally central estimate of 1:7 identified for this range in the last 

10 review is consistent with the study involving blood Pb for pre-school children and air Pb 

11 conditions near a large source of Pb to ambient air with concentrations near (and/or previously 

above) the level of the current Pb standard (ISA, section 4.5.1; Hilts, 2003).5 12 In so noting, we 

13 also recognize the general overlap of such circumstances with those represented by the evidencebased, air-related IQ loss framework,6 14 for which air-to-blood ratio is a key input. In 

15 characterizing the range of air-to-blood ratio estimates, we recognize uncertainty inherent in such 

16 estimates as well as the variation in currently available estimates resulting from a variety of 

17 factors, including differences in the populations examined, as well as in the Pb sources or 

18 exposure pathways addressed in those study analyses (ISA, section 4.7.4). 

19 The scientific evidence continues to recognize a broad array of health effects on multiple 

20 organ systems or biological processes related to blood Pb, including Pb in blood prenatally (ISA, 

21 section 2.6). The currently available evidence continues to support identification of 

22 neurocognitive effects in young children as the most sensitive endpoint associated with blood Pb 

23 concentrations (ISA, section 2.6.1), which as an integrated index of exposure reflect the 

24 aggregate exposure to all sources of Pb through multiple pathways (inhalation and ingestion). 

25 Evidence continues to indicate that neurocognitive effects in young children may not be 

26 reversible and may have effects that persist into adulthood (ISA, section 2.9.6). Thus, as 

27 discussed in section 3.2 above, we continue to consider the evidence of Pb effects at the low end 

28 of the studied blood Pb levels (closest to those common in the U.S. today) to be strongest and of 

29 greatest concern for effects on the nervous system, most particularly those on cognitive function 

30 in children. 

31 As in the last review, evidence on risk factors continues to support the identification of 

32 young children as an important at-risk population for Pb health effects (ISA, section 6.4). The 

 

5

 The older study by Hayes et al (1994) during time of leaded gasoline indicated a generally similar ratio of 

1:8, although the blood Pb levels in that 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

1 current evidence also continues to indicate important roles as factors that increase risk of lead2 related health effects for: nutritional factors, such as iron and calcium intake; elevated blood Pb 

3 levels; and proximity to sources of Pb exposure, such as industrial releases or buildings with old, 

4 deteriorating, leaded paint. Further, some races or ethnic groups continue to demonstrate 

5 increased blood Pb levels relative to others, which may be related to these and other factors (ISA, 

6 sections 6.1, 6.2 and 6.4). 

7 With regard to our understanding of the relationship between exposure or blood Pb levels 

8 in young children and neurocognitive effects, the evidence in this review, as in the last, does not 

9 establish threshold blood Pb level for neurocognitive effects in young children (ISA, sections 

10 2.9.4 and 5.3.13). The lowest blood Pb levels at which associations with neurocognitive impacts 

11 have been observed in pre-school and school age children continue to range down below 5 

12 μg/dL, with lowest group levels that have been associated with such effects ranging down to 2 

13 μg/dL (ISA, sections 2.6.1.1 and 5.3.16.1). Additionally, as in the last review, there is evidence 

14 that the relationship of young children’s blood Pb with neurocognitive impacts, such as IQ, is 

15 nonlinear across a wide range of blood Pb, with greater incremental impacts at lower vs. higher 

16 blood Pb levels (ISA, sections 2.9.4 and 5.3.13). Accordingly, as in the last review, we continue 

17 to focus our interest on C-R relationships from study groups with blood Pb levels closest to those 

18 in children in the U.S. today, which are generally lower than epidemiological study groups. The 

19 currently available evidence does not identify additional C-R slopes for study groups of young 

20 children (e.g., < 7 years) with mean blood Pb levels below that of groups identified in the last 

21 review, 2.9 – 3.8 μg/dL, as discussed in section 3.2 above (ISA, section 5.3.13). Thus, the blood 

22 Pb concentration - IQ response functions or slopes identified in this review for epidemiological 

23 study groups of young children with mean blood Pb levels closest to that of children in the U.S. 

24 today include the same set recognized at the time of the last review (see Table 3-3 above), the 

25 median of which is 1.75 points decrement per μg/dL blood Pb (73 FR, 67003). 

26  To what extent have important uncertainties identified in the last review been 

27 reduced and/or have new uncertainties emerged? 

28 In our consideration of the evidence, as summarized in discussing the previous question 

29 and in chapter 3 above, we have not identified any new uncertainties as emerging since the last 

30 review. However, we continue to recognize important uncertainties identified in the last review 

31 that remain today. Importantly, given our focus in this review, as in the last review, on 

32 neurocognitive impacts associated with Pb exposure in early childhood, we recognize remaining 

33 uncertainties in our understanding of the C-R relationship of neurocognitive impacts, such as IQ 

34 decrements, with blood Pb level in young children, particularly across the range of blood Pb 

35 levels common in the U.S. today. With regard to C-R relationships for IQ, the evidence 

36 available in this review does not include studies that appreciably extend the range of blood Pb 
January 2013 4-17 Draft - Do Not Quote or Cite

1 levels studied beyond those available in the last review. As in the last review, the early 

2 childhood (e.g., 2 to 6 or 7 years of age) blood Pb levels for which associations with IQ response 

3 have been reported continue to extend at the low end of the range to study group mean blood Pb 

4 levels of 2.9 to 3.8 μg/dL (e.g., 73 FR 67003, Table 3). The studies at these blood Pb levels do 

5 not provide evidence of a threshold level and, as summarized in section 3.2 above, continue to 

6 indicate higher C-R slopes in these groups with lower blood Pb levels than in study groups with 

7 higher blood Pb levels (ISA, section 5.3.13). 

8 Further, we recognize important uncertainties in our understanding of the relationship 

9 between ambient air Pb concentrations and air-related Pb in children’s blood. The evidence 

10 newly available in this review has not reduced such key uncertainties. As in the last review, air11 to-blood ratios based on the available evidence continue to vary, with our conclusions based on 

12 the current evidence generally consistent with the range of 1:5 to 1:10 given emphasis in the last 

13 review (73 FR 67002; ISA, section 4.7.4). There continues to be uncertainty regarding the extent 

14 to which this range represents the relationship between ambient air Pb and Pb in children’s blood 

15 (derived from the full set of air-related exposure pathways), and with regard to its reflection of 

16 exposures associated with ambient air Pb levels common in the U.S. today and to circumstances 

17 reflecting just meeting the current Pb standard (ISA, section 4.7.4). We note additionally the 

18 significant uncertainty remaining with regard to the temporal relationships of ambient Pb levels 

19 and associated exposure with occurrence of a health effect (73 FR 67005). 

20  To what extent does newly available information support or call into question any 

21 of the basic elements of the current Pb standard? 

22 We address this question for each of the elements of the standard in light of the health 

23 effects evidence and other relevant information available in this review. As an initial matter, 

24 however, we recognize the weight of the scientific evidence available in this review that 

25 continues to support our focus on effects on the nervous system of young children, and 

26 specifically neurocognitive decrements, as the most sensitive endpoint. Consistent with the 

27 evidence available in the last review, the currently available evidence continues to indicate that a 

28 standard that provides requisite public health protection against the occurrence of such effects in 

29 at-risk populations would also provide the requisite public health protection against the full array 

30 of health effects of Pb. Accordingly, the discussion of the elements below is framed by that 

31 background. 

32 Indicator 

33 The indicator for the current Pb standard is Pb-TSP. Exposure to Pb in all sizes of 

34 particles passing through ambient air can contribute to Pb in blood and associated health effects 

35 by a wide array of exposure pathways (ISA, section 4.1). These pathways include the ingestion 

36 route, as well as inhalation (ISA, section 4.1), and a wide array of particle sizes play a role in 
January 2013 4-18 Draft - Do Not Quote or Cite

1 these pathways (ISA, section 4.1.1.1). As at the time of the last review, we continue to recognize 

2 the variability of the Pb-TSP FRM in its capture of airborne Pb particles (see section 2.2.1.3.1 

3 above). As in the last review, we also note that an alternative approach for collection of a 

4 conceptually comparable range of particle sizes, including ultra-coarse particles, is not yet 

5 available, although we take note of activities underway to remedy that situation in the future, as 

6 referenced in section 2.2.1.3.1 above. Additionally, the limited available information regarding 

7 relationships between Pb-TSP and Pb in other size fractions indicates appreciable variation in 

8 this relationship, particularly near sources of Pb emissions where concentrations, and potential 

9 exposures, are greatest. Thus, the information available in this review does not address 

10 previously identified limitations and uncertainties for the current indicator. Nor does the newly 

11 available information identify additional limitations or uncertainties. The evidence available in 

12 this review continues to indicate the role of a range of air Pb particle sizes in contributing to Pb 

13 exposure (e.g., ISA, section 4.1.1.1), that contributes to Pb in blood and associated health effects, 

14 reinforcing the appropriateness of an indicator for the Pb standard that reflects a wide range of 

15 airborne Pb particles. 

16 Averaging time and form 

17 The averaging time and form of the current standard is a not-to-be-exceeded rolling 

18 three-month average (CFR 50.16), derived from three monthly averages calculated in accordance 

19 with the current data handling procedures (CFR, Appendix R to Part 50). As at the time of the 

20 last review, evidence continues to support the importance of periods on the order of 3 months 

21 and the prominent role of deposition-related exposure pathways, with uncertainty associated with 

22 characterization of precise time periods associating ambient air Pb with air-related health effects. 

23 Relevant factors continue to be those pertaining to the human physiological response to changes 

24 in Pb exposures and those pertaining to the response of air-related Pb exposure pathways to 

25 changes in airborne Pb. The newly available evidence in this review does not appreciably 

26 improve our understanding of the period of time in which air Pb concentrations would lead to the 

27 health effects most at issue in this review. Thus, there continue to be limitations in the evidence 

28 to inform our consideration of these elements of the standard and associated uncertainty. 

29 However, there is no newly available information that calls into question this element of the 

30 current Pb standard. 

31 Level 

The level of the current standard is 0.15 μg/m3 32 (CFR 50.16). As described in section 

33 4.1.1 above, this level was selected in 2008 with consideration of, among other factors, an 

34 evidence-based air-related IQ loss framework, for which there are two primary inputs: air-to35 blood ratios and C-R functions for blood Pb – IQ response in young children. Additionally taken 

36 into consideration were the uncertainties inherent in these inputs. Application of the framework 
January 2013 4-19 Draft - Do Not Quote or Cite

1 also entailed consideration of a magnitude of air-related IQ loss, which as further described in 

2 section 4.1.1.2 above, is used in conjunction with this specific framework in light of the 

3 framework context, limitations and uncertainties. Additionally, selection of a level for the 

4 standard in 2008 was made in conjunction with decisions on indicator, averaging time and form. 

5 As an initial matter, we consider the extent to which the evidence-based, air-related IQ 

6 loss framework which informed the Administrator’s decision in the last review is supported by 

7 the currently available evidence and information. In so doing, we recognize the support provided 

8 by the currently available evidence for the key conclusions drawn in the last review with regard 

9 to health effects of greatest concern, at-risk populations, the influence of Pb in ambient air on Pb 

10 in children’s blood and the association between children’s blood Pb and decrements in 

11 neurocognitive function (e.g., IQ). We additionally note the complexity associated with 

12 interpreting the scientific evidence with regard to specific levels of Pb in ambient air, given the 

13 focus of the evidence on blood Pb as the key biomarker of children’s aggregate exposure. The 

14 need to make such interpretations in the face of the associated complexity supported use of the 

15 evidence-based framework in the last review. In considering the currently available evidence for 

16 the same purposes in this review, we conclude that the evidence-based framework continues to 

17 provide a useful tool for consideration of the evidence with regard to the level of the standard. 

18 We next turn to consideration of the primary inputs to the framework: air-to-blood ratios 

19 and C-R functions for blood Pb – IQ response in young children. With regard to the former, the 

20 limited newly available information assessed in the ISA, and discussed in section 3.1 above, is 

21 generally consistent with the information in this area that was available at the time of the last 

22 review. We additionally recognize the variability and uncertainty associated with quantitative 

23 air-to-blood ratios based on this information, as also existed in the last review. As in the last 

24 review, we recognize that factors contributing to the variability and uncertainty of these 

25 estimates are varied, and include aspects of the study populations (e.g., age and Pb exposure 

26 pathways) and the study circumstances (e.g., length of study period and variations in sources of 

27 Pb exposure during the study period). We note that the full range of estimates associated with 

28 the available evidence is wide, and consider it appropriate to give emphasis to estimates 

29 pertaining to circumstances closest to those in the U.S. today with regard to ambient air Pb and 

30 children’s blood Pb concentrations, while recognizing the limitations associated with the 

31 available information with regard to this emphasis. With that in mind, we consider the currently 

32 available evidence to continue to support the range of estimates concluded in the last review to 

33 be most appropriate for the current population of young children in the U.S., in light of the 

34 multiple air-related exposure pathways by which children are exposed, in addition to inhalation 

35 of ambient air, and of the levels of air and blood Pb common today. Identification of this range 

36 also included consideration of the limitations associated with the available information and 
January 2013 4-20 Draft - Do Not Quote or Cite

1 inherent uncertainties. This range of air-to-blood ratios included 1:10 at the upper end and 1:5 at 

2 the lower end. We further recognize that the limited evidence for air Pb and children’s blood Pb 

3 concentrations closest to those in U.S. today continues to provide support for the Administrator’s 

4 emphasis in the 2008 decision on the relatively central estimate of 1:7. 

5 With regard to the second input to the evidence-based framework, C-R functions for the 

6 relationship of young children’s blood Pb with neurocognitive impacts (e.g., IQ decrements), we 

7 consider several aspects of the evidence. First, as discussed in section 3.2 above, the currently 

8 available information continues to provide evidence that this C-R relationship is nonlinear across 

9 the range of blood Pb levels from the higher concentrations more prevalent in the past to lower 

10 concentrations more common today. Thus, we continue to consider it particularly appropriate to 

11 focus on the evidence from studies with blood Pb levels closest to those of today’s population, 

12 which in the last review included studies with study group mean blood Pb levels ranging roughly 

13 from 3 to 4 μg/dL in children aged 24 months to 7 years (Table 3-3 above). As discussed in 

14 sections 3.2 above, this is also consistent with the evidence currently available for this age group 

15 of young children, and the currently available evidence does not include additional C-R slopes 

16 for incremental neurocognitive decrement with blood Pb levels at or below this range. In 

17 considering whether this set of functions continues to be well supported by the evidence, as 

18 assessed in the ISA (ISA, section 5.3.2), we note the somewhat wide range in slopes 

19 encompassed by these study groups, while also noting the stability of the median. For example, 

20 omission of any of the four slopes considered in the last review does not appreciably change the 

21 median (e.g., the median would change from -1.75 IQ points per μg/dL blood Pb to -1.71 or -

22 1.79). Thus, we conclude that while differing judgments might be made with regard to inclusion 

23 of each of the four study groups, these estimates are generally supported by the current review of 

24 the evidence in the ISA. Further, the stability of the median to modifications to this limited 

25 dataset lead us to conclude that the currently available evidence continues to support 

26 consideration of -1.75 IQ points per μg/dL blood Pb as a well founded and stable estimate for 

27 purposes of describing the neurocognitive impact quantitatively on this age group of U.S. 

28 children. 

29 In summary, in considering the evidence and information available in this review 

30 pertaining to the level of the current Pb standard, we note that the evidence available in this 

31 review, as summarized in the ISA, continues to support the air-related IQ loss evidence-based 

32 framework, with the inputs that were used in the last review. These include estimates of air-to33 blood ratios ranging from 1:5 to 1:10, with a generally central estimate of 1:7. Additionally, the 

34 C-R functions most relevant to blood Pb levels in U.S. children today continue to be provided by 

35 the set of four analyses considered in the last review for which the median estimate is -1.75 IQ 

36 points per μg/dL Pb in young children’s blood. Thus, we observe that the evidence available in 
January 2013 4-21 Draft - Do Not Quote or Cite

1 this review has changed little if at all with regard to the aspects given weight in the conclusion on 

2 level for the new standard in the last review and would not appear to call into question any of the 

3 basic elements of the standard. In so doing, we additionally recognize that the overall decision 

4 on adequacy of the current standard is a public health policy judgment by the Administrator; we 

5 discuss considerations that inform such judgments in section 4.3 below. 

6 4.2.2 Exposure/Risk-based Considerations 

7 Our consideration of the issue of adequacy of public health protection provided by the 

8 current standard is also informed by the quantitative exposure/risk assessment completed in the 

9 last review, augmented as described in section 3.4 above. We have organized the discussion that 

10 follows around two questions to assist us in interpreting the results of the assessment of case 

11 studies simulated to meet several different air quality conditions, including those just meeting the 

12 current standard. 

13  What is the level of confidence associated with estimates of air-related risk 

14 generated for simulations just meeting the current Pb standard? 

15 As an initial matter, we recognize the significant limitations and complexity associated 

16 with the risk/exposure assessment for Pb that are far beyond those associated with similar 

17 assessments typically performed for other criteria pollutants. In completing the assessment we 

18 were constrained by significant limitations with regard to data and tools particular to the problem 

19 at hand. Further, the multimedia and persistent nature of Pb and the role of multiple exposure 

20 pathways contribute significant additional complexity to the assessment as compared to other 

21 assessments that focus only on the inhalation pathway. As a result, our estimates of air-related 

22 exposure and risk are approximate, presented as upper and lower bounds within which we 

23 consider air-related risk likely to fall. We base our description of overall confidence in this 

24 characterization of air-related risk on our consideration of the overall design of the analysis (as 

25 described in section 3.4 above), the degree to which key sources of variability are reflected in the 

26 design of the analysis, and our characterization of key sources of uncertainty. 

27 In considering the degree to which key sources of variability (discussed in section 3.4.6 

28 above) are reflected in the design of the analysis, we note the following aspects addressed by the 

29 risk assessment. 

30  Variation in distributions of potential urban residential exposure and risk across U.S. 

31 urban residential areas. This is addressed by the inclusion of three different (location32 specific) urban study areas that reflect a diverse set of urban areas in the U.S. 

33  Representation of a more highly-exposed subset of urban residents potentially exposed at 

34 the level of the standard. This is addressed by the inclusion of the generalized (local) 

35 urban study area. 
January 2013 4-22 Draft - Do Not Quote or Cite

1  Variation in residential exposure to ambient air Pb within an urban area. This is 

2 addressed through the partitioning of the location-specific study areas into exposure 

3 zones to provide some representation of spatial gradients in ambient air Pb and their 

4 interaction with population distribution and demographics. This was done in a somewhat 

5 more precise manner in the primary Pb smelter case study, which relied on dispersion 

6 modeling to describe gradients, as compared with the manual assignment of gradients 

7 related to air concentration differences among monitors in an area. 

8  Inter-individual variability in blood Pb levels. This is addressed though the use of 

9 empirically-derived GSDs to develop blood Pb distribution for the child population in 

10 each exposure zone, with GSDs selected particular to each case study populations. 

11  Inter-individual variability in IQ response to blood Pb. This is addressed through the use 

12 of C-R functions for IQ loss based on a pooled analysis reflecting studies of diverse 

13 populations. 

14 We also considered key sources of uncertainty (discussed in section 3.4.7 above), in 

15 particular the overarching area concerning the precision of the air-related risk estimates, as 

16 mentioned above. Associated sources of uncertainty include our inability to simulate changes in 

17 air-related Pb as a function of changes in ambient air Pb in exposure pathways other than those 

18 involving inhalation of ambient air and ingestion of indoor dust. This contributes to the positive 

19 bias of the upper bound for the air-related risk estimates. We additionally recognize the 

20 significant uncertainty associated with estimating upper percentiles of the distribution of air21 related blood Pb concentration estimates (and associated IQ loss estimates) due to limitations in 

22 available information. Lastly, we recognize the uncertainty associated with application of the C23 R function at the lower blood Pb levels in the distribution; this relates to the limited 

24 representation of blood Pb levels of this magnitude in the dataset from which the C-R function is 

25 derived. 

26 In the quantitative risk information available in this review, we have air-related risk 

27 estimates for simulations just meeting the current standard from one of the location-specific 

28 urban case studies (Chicago) and from the generalized (local) urban case study. With regard to 

29 the latter, we note its simplified design that does not include multiple exposure zones, thus 

30 reducing the dimensions simulated. We have a reasonable degree of confidence in aspects of the 

31 generalized (local) urban case study for the specific situation we consider it to represent (i.e., a 

32 temporal pattern of air Pb concentrations that just meets the level of the standard), and when the 

33 associated estimates are characterized as approximate, within upper and lower bounds (as 

34 described in section 3.4.4 above), while also recognizing considerable associated uncertainty. 
January 2013 4-23 Draft - Do Not Quote or Cite

1  To what extent are the air-related risks remaining upon just meeting the current 

2 Pb standard important from a public health perspective? 

3 In considering public health importance of estimated air-related risks, we consider here 

4 the nature and magnitude of such estimated risks (and attendant uncertainties), including such 

5 impacts on the affected population, and we additionally consider the size of the affected 

6 population. Based on the evidence available in the last review and consistent with that available 

7 today, the quantitative risk estimates developed in the 2007 REA and augmented slightly in this 

8 review are for decrements in IQ, an established indicator of neurocognitive function. In 

9 considering these estimates, we recognize that although some neurocognitive effects may be 

10 transient, some effects may persist into adulthood, affecting success later in life (ISA, sections 

11 2.9.5 and 5.3.15). We additionally recognize the potential population impacts of small changes 

12 in population mean values of metrics such as IQ, presuming a uniform manifestation of lead13 related decrement across the range of population IQ (ISA, section 2.9.1), as noted in section 3.3 

14 above. 

15 Exposures and risks associated with air-related Pb under several different air quality 

16 conditions were estimated in the 2007 REA. As summarized in section 3.4 above, limitations in 

17 our modeling tools and data affected our ability to develop precise estimates for air-related 

18 exposure pathways and contributed uncertainties. The results are approximate estimates which 

19 we describe through the use of rough upper and lower bounds within which we estimate air20 related risk to fall. We have recognized a number of uncertainties in the underlying risk 

21 estimates from the 2007 REA and in the interpolation approach employed in the new analyses 

22 for this review. We have characterized the magnitude of air-related risk associated with the 

23 current standard with a focus on median estimates, for which we have appreciably greater 

24 confidence than estimates for outer ends of risk distribution (see section 3.4.7) and on risks 

25 derived using the C-R function in which we have greatest confidence (see sections 3.4.3.3.1 and 

26 3.4.7). These risk estimates include estimates from the last review for one of the location27 specific urban study area populations as well as estimates newly derived in this review based on 

28 interpolation from 2007 REA results for the generalized (local) urban case study, which is 

29 recognized to reflect a generalized high end of air-related exposure for localized populations. 

30 Taken together, these estimates indicate air-related risk associated with just meeting the current 

31 standard of a magnitude generally within the bounds of roughly 1 and 3 points IQ loss. 

32 In considering the importance of such risk from a public health perspective, we also 

33 consider the size of at-risk populations represented by the REA case studies. As discussed in 

34 section 3.4 above, the generalized (local) urban case study is considered to represent a localized 

35 urban population exposed near the level of the standard, such as a very small, compact 

36 neighborhood near a source contributing to air Pb concentrations just meeting the standard. This 
January 2013 4-24 Draft - Do Not Quote or Cite

1 case study provides representation in the risk assessment for such small populations at the upper 

2 end of the gradient in ambient air concentrations expected to occur near sources; thus estimates 

3 for this case study reflect exposures nearest the standard being evaluated. While we do not have 

4 precise estimates of the number of young children living in such areas of the U.S. today, we have 

5 information that informs our understanding of their magnitude. For example, as discussed in 

6 section 3.3 above (Table 3-3), we estimate there to be approximately 2,400 children, aged 5 

7 years and younger, residing within 0.5 km of a monitor with air Pb concentrations above the 

8 current standard. We further observe several additional monitors with maximum 3-month Pb 

9 concentrations that fall below but within 10% of the current standard level (as noted in section 

10 3.3 above); an estimated 265 young children reside near these monitors. Thus, together we 

11 estimate some 2700 children, aged 5 years and younger, living in localized areas with elevated 

12 air Pb concentrations that are above or near the current standard. Based on the 2010 census 

13 estimates of approximately 24.3 million children in the U.S. aged five years or younger, this 

represents approximately one hundredth of one percent of this age group in the U.S.7 14 This 

15 indicates the size of the population of young children of this age living in areas in close 

16 proximity to areas where air Pb concentrations may be above or near the current standard to be 

17 approximately 2700, which is approximately a hundredth of one percent of the full population of 

correspondingly aged children.8 18 

19 In summary, we recognize substantial uncertainty inherent in the REA estimates of air20 related risk associated with conditions just meeting the current standard, which we characterize 

21 as approximate and falling somewhat above the rough lower bound of 1 and below the rough 

upper bound of 3 IQ points.9 22 This approximate estimate of risk for children living in such areas 

23 is generally overlapping with and consistent with the evidence-based air-related IQ loss estimates 

24 summarized in section 4.2.1 above. With regard to the the importance of the estimated risks 

25 from a public health perspective, we note, based on the currently available monitoring and 

26 census data, the estimated size of the affected population to be approximately 2700 young 

27 children, representing slightly more than one one hundredth of a percent of the full population of 

 

7

 While these estimates pertain to the age group of children aged 5 years and younger, we additionally note 

that a focus on an alternative age range, such as inclusive of slightly older children (e.g., through age 7), while 

increasing the number for children living in such locations, would not be expected to appreciably change the 

percentage of the full U.S. age group that the subset represents. 8

 This estimate includes children in areas where recent information indicates the standard is exceeded 

because areas not in atttainment with the standard are required to attain the standard as expeditiously as practicable, 

but no later than five years after designation. Accordingly, these areas are for present purposes treated as areas with 

air Pb concentrations just meeting the current standard and are included for purposes of identifying the size of the atrisk population residing in areas likely to have air Pb concentrations near the current 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

1 similarly aged children. In considering the exposure/risk estimates during the last review, the 

2 Administrator took note of the important uncertainties and limitations associated with these 

3 assessments and, while placing less weight on the assessment estimates, he recognized the 

4 quantitative risk estimates to be “roughly consistent with and generally supportive” of those 

5 estimated by the evidence-based framework. In our consideration of the risk estimates 

6 considered in the last review, as well as the estimates for the current standard that have been 

7 newly developed in this review for the generalized (local) urban case study (see section 

8 3.4.3.3.2), we agree with the previous characterization. As would be expected by the use of 

9 interpolation, the newly derived estimates are consistent with the estimates for similar air quality 

10 scenarios that were available in the last review.

11 4.3 PRELIMINARY STAFF CONCLUSIONS ON THE PRIMARY STANDARD 

12 This section describes preliminary staff conclusions regarding adequacy of the current 

13 primary Pb standard. These conclusions are based on considerations described above and in the 

14 discussion below regarding the currently available scientific evidence summarized in the third 

15 draft ISA and prior CDs and the risk and exposure information drawn from the 2007 REA. The 

16 final PA will draw upon the final ISA, developed after CASAC review and public comment on 

17 the third draft ISA. Further, staff conclusions presented in the final PA will take into account 

18 advice from CASAC and public comment on the draft PA and the preliminary conclusions. 

19 Taking into consideration the discussions responding to specific questions above in this 

20 and the prior chapter, this section addresses the following overarching policy question. 

21  Does the currently available scientific evidence- and exposure/risk-based 

22 information, as reflected in the ISA and REA, support or call into question the 

23 adequacy of the protection afforded by the current Pb standard? 

24 Our response to this question takes into consideration the discussions responding to the 

25 specific policy-relevant questions in prior sections of this document (see sections 3.1-3.4, 4.2.1, 

26 and 4.2.2). In so doing, we focus first on consideration of the evidence, including that newly 

27 available in this review, and the extent to which it alters key conclusions supporting the current 

28 standard. We then turn to consideration of the quantitative risk estimates drawn from the 2007 

29 REA, and associated limitations and uncertainties. We additionally consider the public health 

30 policy judgments and judgments about the uncertainties inherent in the scientific evidence and 

31 quantitative analyses that are inherent in decisions on the adequacy of the current primary Pb 

32 standard. 

33 We first recognize the complexity involved in considering the adequacy of protection in 

34 the case of the primary Pb standard, which differs substantially from that involved in 

35 consideration of the NAAQS for other pollutants. Unlike the case for Pb, the other pollutants for 
January 2013 4-26 Draft - Do Not Quote or Cite

which NAAQS are set involve only inhalation exposure pathways, a relatively simpler context.10 1 

2 In addition, generally an important component of the scientific evidence base considered in 

3 reviewing the adequacy of NAAQS for other pollutants is the availability of studies that have 

4 investigated associations between current concentrations of the pollutant in ambient air 

5 (including in circumstances where the current standard is met) and the occurrence of health 

6 effects judged plausibly related to ambient air exposure to the NAAQS pollutant. While such 

7 studies, targeting locations near air Pb sources such as smelters, were available at the time the Pb 

8 NAAQS was initially set in 1978, and to a much more limited degree at the time of the last 

9 review, such studies of health effects under air quality conditions near those reflecting the 

10 current standard are not available in this review. Rather, the evidence base that supports our 

11 conclusions in this review includes most prominently epidemiological studies reporting 

12 associations of blood Pb levels in U.S. populations, including the particularly at-risk population 

13 of young children with health effects judged plausibly related to Pb exposures. Support for our 

14 conclusions regarding the plausibility for ambient air Pb to play a role in such findings derives, 

15 in part, from studies linking Pb in ambient air with the occurrence of health effects. However, 

16 such studies (dating from the past or from other countries) involve ambient air Pb concentrations 

17 many times greater than those that would meet the current standard. Thus, in considering the 

18 adequacy of the current Pb standard, rather than considering studies that have investigated 

19 current concentrations of Pb in ambient air (including in locations where the current standard is 

20 met) and the occurrence of health effects, we primarily consider the evidence for, and risk 

21 estimated from, models based upon key relationships, such as those between ambient air Pb, Pb 

22 exposure, blood Pb and health effects. This evidence, with its associated limitations and 

23 uncertainties, contributes to our conclusions regarding a relationship between ambient air Pb 

24 conditions under the current standard and health effects. 

25 In considering the currently available evidence, staff gives great weight to the long26 standing body of evidence on the health effects of Pb, augmented in some aspects since the last 

27 review, which continues to support identification of neurocognitive effects in young children as 

28 the most sensitive endpoint associated with Pb exposure, as discussed in sections 3.2 and 3.3 

29 above. The evidence continues to indicate that a standard that provides protection from 

30 neurocognitive effects in young children additionally provides protection for other health effects 

31 of Pb, such as cardiovascular effects later in life. Application of the evidence-based, air-related 

32 IQ loss framework, developed in the last review, continues to provide a useful approach for 

 

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 exposure pathways. As an additional complication, other 

(nonair) sources of Pb also contribute to these pathways, particularly 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

1 considering and integrating the evidence on relationships between Pb in ambient air and Pb in 

2 children’s blood and risks of neurocognitive effects (IQ loss). The currently available evidence 

3 base, while somewhat expanded since the last review, is not appreciably expanded or supportive 

4 of appreciably different conclusions with regard to air-to-blood ratios (section 3.1 above) or C-R 

5 functions for neurocognitive decrements (section 3.2 above) in young children. 

6 As in the last review, uncertainties remain in our understanding of important aspects of 

7 ambient air Pb exposure and associated health effects. For example, important uncertainties 

8 remain, both with regard to air-to-blood ratios that reflect the relationship between 

9 concentrations of Pb in ambient air and air-related Pb in children’s blood, and to estimates of the 

10 slope of the C-R function for neurocognitive impacts (IQ loss) at lower blood Pb levels. With 

11 regard to the former, we note particularly the limitations associated with the available studies and 

12 gaps in the evidence base with regard to studies that have investigated such quantitative 

13 relationships under conditions pertaining to the current standard (e.g., in localized areas near air 

14 Pb sources where the standard is met in the U.S. today). Further, in considering our reliance on 

15 the evidence in performing quantitative modeling of exposure and risk we additionally note 

16 important uncertainties associated with relationships between ambient air Pb and outdoor 

17 soil/dust Pb and indoor dust Pb that particularly affect our quantitative estimates of air-related 

18 risk under conditions of lower ambient air Pb levels and lower blood Pb levels (73 FR 66981). 

19 These critical exposure pathways are also inherent in the evidence-based air-related IQ loss 

20 framework, encompassed within the estimates of air-to-blood ratios. Thus, we recognize 

21 uncertainties related to our understanding of these and other processes that also contribute 

22 uncertainty to our application of the evidence-based framework. We consider this uncertainty to 

23 be increased with application of the framework for levels below the current standard given the 

24 weaker linkage with existing evidence, as noted below. 

25 We additionally take note of the role of public health policy judgments in the 

26 Administrator’s setting of the current standard in 2008, as summarized in section 4.1.1.2 above. 

27 Such judgments are inherent in setting the standard, and particularly in using the evidence-based 

28 framework to inform the decision on level for the standard, and in considering the exposure/risk 

29 information. We recognize that public health policy judgments always play an important role in 

30 each NAAQS review for each pollutant. One type of public health policy judgments focuses on 

31 how to consider the nature and magnitude of the array of uncertainties that are inherent in the 

32 scientific evidence and analyses. These judgments are traditionally made with a recognition that 

33 our understanding of the relationships between the presence of a pollutant in ambient air and 

34 associated health effects is based on a broad body of information encompassing not only more 

35 established aspects of the evidence but also aspects in which there may be substantial 

36 uncertainty. In the case of the Pb NAAQS review, we recognize increased uncertainty in 
January 2013 4-28 Draft - Do Not Quote or Cite

1 characterizing the IQ response to blood Pb levels below those represented in the evidence base. 

2 We also recognize increased uncertainty in projecting the magnitude of blood Pb response to 

3 ambient air Pb concentrations at and below the level of the current standard. We recognize this 

4 increased uncertainty particularly in light of the multiple factors that play a role in such a 

5 projection (e.g., meteorology, atmospheric dispersion and deposition, human physiology and 

6 behavior), for each of which we recognize attendant uncertainties. Collectively, these aspects of 

7 the evidence and associated uncertainties contribute to a recognition that for Pb, as for other 

8 pollutants, the available health effects evidence generally reflects a continuum, consisting of 

9 ambient levels at which scientists generally agree that health effects are likely to occur, through 

10 lower levels at which the likelihood and magnitude of the response become increasingly 

11 uncertain. 

12 Reviews may also require judgments as to the point at which health effects become 

13 important from a public health perspective. In the case of Pb, such a judgment is explicitly made 

14 in considering the public health significance of one to two points IQ loss in at-risk populations, 

15 such as young children. This type of judgment also includes consideration of the IQ loss 

16 estimates yielded by the air-related IQ loss evidence-based framework for specific combinations 

17 of standard level, air-to-blood ratio and C-R function. With regard to public health significance 

18 of one to two points IQ loss in young children, staff gives weight to the comments of CASAC 

19 and some public commenters in the last review which recognized such a magnitude of IQ loss to 

20 be of public health significance and recommended that a very high percentage of the population 

be protected from such a magnitude of IQ loss (73 FR 67000).11 21 With this objective in mind, we 

22 consider the extent to which the air-related IQ loss evidence-based framework informs 

23 consideration of standards that might be concluded to provide such a level of protection. In so 

24 doing, we first recognize that the IQ loss estimates produced with the evidence-based framework 

25 do not correspond to a specific quantitative public health policy goal for air-related IQ loss that 

26 would be acceptable or unacceptable for the entire population of children in the U.S. Rather, the 

27 conceptual context for the evidence-based framework is that it provides estimates for the mean 

28 air-related IQ loss of a subset of the population of U.S. children (i.e., the subset living in close 

29 proximity to air Pb sources that contributed to elevated air Pb concentrations that equal the 

30 current level of the standard). This is the subset expected to experience air-related Pb exposures 

31 at the high end of the national distribution of such exposures. The associated mean IQ loss 

32 estimate is the average for this highly exposed subset and is not the average air-related IQ loss 

 

11 Our focus on IQ, as noted in section 3.3 above, reflects recognition of IQ being a well established, widely 

recognized and rigorously standardized measure of neurocognitive 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

1 projected for the entire U.S. population of children. Further, we recognize uncertainties 

2 associated with those estimates, which increase with estimates associated with successively 

3 lower standard levels. 

For the current standard level of 0.15 μg/m3 4 , an air-to-blood ratio estimate of 7 μg/dL per 

μg/m3 5 (which we note as reasonably representative of the range supported by the evidence) and a 

6 C-R slope of -1.75 IQ points per μg/dL, the IQ loss estimate using the evidence-based 

framework is 1.8 points.12 7 As noted above, this value is considered to be an estimate, with 

8 attendant uncertainties, of mean air-related IQ loss of a subset of the population of U.S. children 

in the high end of the exposure distribution for air-related Pb.13 9 As noted in section 4.2.2 above, 

10 our current information on numbers of young children living near monitors above or within 10% 

11 of the current Pb standard indicates the size of this population subset to be on the order of 2700 

12 children aged 5 years or younger, which would correspond to approximately one hundredth of 

13 one percent of the U.S. population of this age children (estimated at approximately 24 million in 

14 2010 census). A primary objective of the monitoring network for Pb is to identify and monitor 

15 sites of maximum concentration in areas anticipated to be at risk of exceeding the NAAQS. 

16 While we acknowledge the possibility that the monitoring data thus far available may not 

17 identify every occurrence of elevated Pb concentrations, the size of such a population subset can 

18 still be concluded to fall well below one tenth of one percent of the full population of children 

19 aged 5 years or younger in the U.S. today. Thus, we conclude that the current evidence, as 

20 considered within the conceptual and quantitative context of the evidence-based framework, and 

21 current air monitoring information indicates that the current standard would be expected to 

22 achieve the public health policy goal recommended by CASAC in the last Pb NAAQS review 

23 that IQ loss on the order of one to two IQ points be “prevented in all but a small percentile of the 

24 population” (73 FR 67000). 

25 In drawing conclusions from application of the evidence based framework with regard to 

26 adequacy of the current standard, we further recognize the degree to which IQ loss estimates 

27 drawn from the air-related IQ loss evidence-based framework reflect mean blood Pb levels 

28 below those represented in the currently available evidence for young children. For example, in 

the case of the current standard level of 0.15 μg/m3 29 , multiplication by the air-to-blood ratio of 7 

 

12 Using an air-to-blood ratio estimate of 8 μg/dL per μg/m3

 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 estimated 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 pathways, estimates are not available 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

1 yields a mean air-related blood Pb level of 1.05 μg/dL, which is half the level of the lowest blood 

2 Pb subgroup of pre-school children in which neurocognitive effects have been observed (Table 

3 3-2 above; Miranda et al., 2009) and well below the means of subgroups for which continuous CR functions have been estimated (Table 3-3 above).14 4 Such an extension below the lowest 

5 studied levels may be viewed as appropriate given the lack of identified blood Pb level threshold 

6 in the current evidence base for neurocognitive effects and the need for the NAAQS to provide a 

margin of safety.15 7 We note, however, that the framework IQ loss estimates for still lower 

8 potential standard levels represent still greater extrapolations from the current evidence base with 

9 corresponding increased uncertainty. 

10 In recognition of the role of public health policy judgments in drawing conclusions as to 

11 adequacy of the Pb NAAQS, we consider the availability of new information or new commonly 

12 accepted guidelines or criteria within the public health community with regard to the public 

13 health significance of specific IQ decrements in exposed, at-risk populations that might inform 

14 public health policy judgments on the appropriate degree of public health protection that should 

be afforded to protect against risk of such neurocognitive effects in at-risk populations,16 15 such as 

16 children living near air Pb sources. As an initial matter, we note that no such new information, 

17 guidelines or criteria are described in the ISA. In further considering the occurrence of any new 

18 actions by public health agencies that might indicate the availability of new information, 

19 guidelines or criteria for interpreting public health significance of such effects, we note that the 

20 CDC has revised the blood Pb level used to prioritize young children for whom they recommend 

 

14 We recognize that children also have Pb in their blood derived from other (nonair) sources. The 

evidence- based air-related IQ loss framework is used, however, to estimate IQ loss attributable to air-related Pb 

because the NAAQS is intended to protect against risks from ambient air-related 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 that primary standards include an adequate margin of 

safety was intended to address uncertainties associated with 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 identified. Both kinds of uncertainties are components of the risk associated with 

pollution at levels below those at which human health effects can be said to occur with reasonable scientific 

certainty. Thus, in selecting primary standards that includes 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, even 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-risk level or at background concentration 

levels, but rather at a level that reduces risk sufficiently so as to protect public health with an adequate margin of 

safety. 16The term at-risk populations is used here, rather then 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 discussion in section 1.2.1 above. 
January 2013 4-31 Draft - Do Not Quote or Cite

particular follow-up health protective actions, as summarized in section 3.1 above.17 1 The CDC 

2 decision, while emphasizing the critical importance of primary prevention of Pb exposure, 

3 provides no new guidelines or criteria with regard to the significance of specific IQ decrements 

4 or judgments on appropriate public health protection from risk of neurocognitive effects, and 

5 their consideration of the evidence base at the time of their decision does not substantively differ 

6 from that presented in the current draft ISA (CDC, 2012). Thus, we are aware of no new 

7 information or new commonly accepted guidelines or criteria within the public health 

8 community for interpreting public health significance of neurocognitive effects in the context of 

9 a decision on adequacy of the current Pb standard. 

10 With respect to exposure/risk-based considerations, we recognize the complexity of the 

11 REA modeling analyses and the associated limitations and uncertainties. We additionally note 

12 the differences among the case studies included in the REA and the extent to which they inform 

13 our understanding of different aspects of the risk associated with air-related Pb in the U.S. For 

14 example, the location-specific case studies indicate the distribution of population risk in urban 

15 areas with differing types of Pb sources and gradients in air Pb concentrations as well as in 

16 population density, while the generalized urban (local) case study indicates the magnitude of air17 related risk associated with those specific localized circumstances where air concentrations just 

18 meet the Pb standard (regardless of source type). We agree with conclusions drawn in the 2008 

19 review that the quantitative risk estimates, with a focus on those for the generalized (local) urban 

20 case study, are “roughly consistent with and generally supportive” of estimates from the 

21 evidence-based air-related IQ loss framework (73 FR 67006). We further take note of the 

22 increasing uncertainty recognized for air quality scenarios involving air Pb concentrations 

23 increasingly below the current conditions for each case study, recognizing that such uncertainty 

24 is due in part to modeling limitations deriving from uncertainty regarding relationships between 

25 ambient air Pb and outdoor soil/dust Pb and indoor dust Pb (as noted in section 3.4 above). 

26 Based on the above considerations, we reach the preliminary conclusion that the current 

27 body of evidence, in combination with the exposure/risk information, supports a primary 

28 standard as protective as the current standard. Further consideration of the evidence and 

29 exposure/risk information available in this review and its attendant uncertainties and limitations, 

30 as well as consideration of the availability of other information that might also inform public 

31 health policy judgments by the Administrator, leads us to reach the additional preliminary 

32 conclusion that it is appropriate to consider retaining the current standard without revision. 

33 These preliminary conclusions are based on consideration of the health effects evidence, 

34 including consideration of this evidence in the context of the evidence-based, air-related IQ loss 

 

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

1 framework, and in combination with the exposure/risk information (chapter 3 and sections 4.2.1 

2 and 4.2.2 above) and the uncertainties attendant with both, recognizing the complexities and 

3 limitations in the evidence base in reaching conclusions regarding the magnitude of risk 

4 associated with the current standard, as well as the increasing uncertainty of risk estimates for 

5 lower air Pb levels. Based on these considerations, these preliminary conclusions also recognize 

6 what may be considered reasonable judgments on the public health implications of the blood Pb 

7 levels and risk estimated for air-related Pb under the current standard, including the public health 

8 significance of the Pb effects being considered, as well as aspects of the use of the evidence9 based framework that may be considered to contribute to the margin of safety. 

10 In reaching these preliminary conclusions, we additionally note that different public 

11 health policy judgments could lead to different conclusions regarding the extent to which the 

12 current standard provides protection of public health with an adequate margin of safety. Such 

13 public health policy judgments include those related to the appropriate degree of public health 

14 protection that should be afforded to protect against risk of neurocognitive effects in at-risk 

15 populations, such as IQ loss in young children, as well as with regard to the appropriate weight 

16 to be given to differing aspects of the evidence and exposure/risk information, and how to 

17 consider their associated uncertainties. For example, different judgments might give greater 

18 weight to more uncertain aspects of the evidence or reflect a differing view with regard to margin 

19 of safety. As noted in section 4.1 above, in establishing primary standards under the Act that, in 

20 the Administrator’s judgment, are requisite to protect public health with an adequate margin of 

21 safety, the Administrator seeks to establish standards that are neither more nor less stringent than 

22 necessary for this purpose. The Act does not require that primary standards be set at a zero-risk 

23 level, but rather at a level that avoids unacceptable risks to public health, even if the risk is not 

24 precisely identified as to nature or degree. The requirement that primary standards provide an 

25 adequate margin of safety was intended to address uncertainties associated with inconclusive 

26 scientific and technical information available at the time of standard setting. It was also intended 

27 to provide a reasonable degree of protection from hazards that research has not yet identified. 

28 In this context, we recognize that the uncertainties and limitations associated with the 

29 many aspects of the estimated relationships between air Pb concentrations and blood Pb levels 

30 and associated health effects are amplified with consideration of increasingly lower air 

31 concentrations. We believe the current evidence supports the conclusion that the current 

32 standard is requisite to protect public health with an adequate margin of safety. In staff’s view, 

33 based on the current evidence there is appreciable uncertainty associated with drawing 

34 conclusions regarding whether there would be reductions in risk to public health from alternative 

35 lower levels as compared to the level of the current standard. Thus, we conclude that the basis 

36 for any consideration of alternative lower standard levels would reflect different public health 
January 2013 4-33 Draft - Do Not Quote or Cite

1 policy judgments as to the appropriate approach for weighing uncertainties in the evidence and 

2 for providing requisite protection of public health with an adequate margin of safety. 

3 In summary, the newly available health effects evidence, critically assessed in the ISA as 

4 part of the full body of evidence, reaffirms conclusions on the broad array of effects recognized 

5 for Pb in the last review. Further, staff observes the general consistency of the current evidence 

6 with the evidence available in the last review with regard to key aspects on which the current 

7 standard is based, including those particular to the evidence-based framework developed in the 

8 last review. Staff additionally observes that quantitative risk estimates associated with the 

9 current standard, based on the risk assessment performed in the last review, indicate a level of 

10 risk generally consistent with conclusions drawn from the evidence using the evidence-based 

11 framework. Staff additionally recognizes the limitations and uncertainties associated with the 

12 currently available information. These considerations provide the basis for the preliminary staff 

13 conclusion that consideration should be given to retaining the current standard, without revision. 

14 Accordingly, and in light of staff preliminary conclusions that it is appropriate to consider the 

15 current standard to be adequate, we have not identified any potential alternative standards for 

16 consideration in this review. 

17 4.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA 

18 COLLECTION 

19 In this section, we highlight key uncertainties associated with reviewing and establishing 

20 NAAQS for Pb. Such key uncertainties and areas for future health-related research, model 

21 development, and data gathering are outlined below. In some cases, research in these areas can 

22 go beyond aiding standard setting to aiding in the development of more efficient and effective 

23 control strategies. We note, however, that a full set of research recommendations to meet 

24 standards implementation and strategy development needs is beyond the scope of this discussion. 

25 Rather, listed below are key uncertainties and research questions and data gaps that have been 

26 thus far highlighted in this review of the health-based primary standard. 

27  A critical aspect of our consideration of the evidence and the quantitative risk assessment 

28 in this review is our understanding of the C-R relationship between blood Pb levels in 

29 young children and neurodevelopmental effects, specifically IQ decrement. Additional 

30 epidemiological research involving substantially-sized populations with mean blood Pb 

31 levels closer to those common in today’s population of young children, particularly those 

32 less affected by higher Pb exposures earlier in childhood, would help to reduce 

33 uncertainty in our estimates of IQ decrement associated with these lower blood Pb levels, 

34 and accordingly, in characterizing Pb health effects. 

35 

36  There remains uncertainty in the evidence base with regard to the exposure circumstances 

37 (timing, duration, magnitude and frequency) eliciting effects in older children and adults. 
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1 Effects of particular focus include effects on the nervous system later in life, 

2 cardiovascular function, and delayed onset of puberty. 

3  Alzheimer’s-like pathology has been reported in aged laboratory animals (non-human 

4 primates and rodents) exposed to Pb early in life, however uncertainty remains with 

5 regard to relationships of such pathology with altered function/behavior. 

6  Epidemiologic studies indicate detrimental effects of Pb on sperm production and quality, 

7 often in occupational cohorts. Uncertainty remains regarding these effects in otherwise 

8 healthy cohorts without occupational Pb exposure or other underlying medical 

9 conditions. 

10  Quantitative estimation of blood Pb levels in children and other at-risk subgroups in 

11 response to various exposure circumstances, including air-related exposure pathways, 

12 would benefit from research in a number of areas including: 

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

14 o Temporal aspects of changes in blood Pb levels associated with changes in 

15 ambient air Pb; 

16 o Interindividual variability in blood Pb levels and methods for characterizing 

17 interindividual variability, including consideration of both empirical and 

18 mechanistic methods; 

19 o Apportionment of blood Pb levels with regard to exposure pathway contributions, 

20 particular distinctions pertinent to policy-relevant exposures and background 

21 sources; and 

22 o Blood Pb model performance evaluations, with emphasis on applications 

23 pertaining to blood Pb response to ambient air-related pathways and responses to 

24 changes in exposures for those pathways. 

25  An important aspect of exposure and risk posed by ambient air Pb is the contribution of 

26 ambient air Pb to indoor dust Pb. Research on the relationship between Pb in these two 

27 media, both generally, as well as in specific environments, and also with regard to aspects 

28 associated with mechanistic modeling (e.g., air exchange rates, home cleaning frequency 

29 and efficiency) would reduce uncertainty in models and methods applied in consideration 

30 of this pathway in future reviews. 

31  An understanding of the spatial gradient of ambient air Pb concentrations, and associated 

32 particle sizes, in urban residential areas, as well as near Pb sources, is an important aspect 

33 to our implementation of the NAAQS for Pb and a key element in assessing exposure and 

34 risk. Additional research in this area is needed. 

35 o Current limitations in this area additionally contribute uncertainty to 

36 characterization of ambient air Pb levels in the risk assessment and associated 

37 exposure and risk estimates. Research in the area of characterizing spatial 

38 variation in air Pb concentrations in different environments and related to different 

39 air sources would help to reduce this uncertainty. Of particular interest is the 

40 potential for systematic trends in the relationship between ambient air Pb 

41 concentrations and distribution of urban residential populations. Examples of 
January 2013 4-35 Draft - Do Not Quote or Cite

1 locations of interest include neighborhoods downwind of airports with substantial 

2 leaded aviation gasoline usage or in the vicinity of older roads with substantial 

3 historical use of leaded gasoline, as well as inner city neighborhoods, both those in 

4 which substantial reconstruction has occurred and more static areas. 

5  An important aspect to this review is the relationship between ambient air Pb and outdoor 

6 dust and surface soil Pb concentrations, including the temporal dynamics of that 

7 relationship and variation in that for different environments. Research to improve our 

8 understanding of these areas would contribute to reducing associated uncertainty with 

9 regard to characterization of the relationship between air and soil Pb and the impact of 

10 changes in air Pb on outdoor soil Pb levels over time. 
January 2013 4-36 Draft - Do Not Quote or Cite

1 4.5 REFERENCES 

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

3 349: 500. 

4 Canfield, R. L.; Henderson, C. R., Jr.; Cory-Slechta, D. A.; Cox, C.; Jusko, T. A.; Lanphear, B. P. (2003) 

5 Intellectual impairment in children with blood lead concentrations below 10 μg per deciliter. N. Engl. J. 

6 Med. 348: 1517-1526. 

7 Centers for Disease Control and Prevention (2012) CDC Response to Advisory Committee on Childhood Lead 

8 Poisoning Prevention Recommendations in “Low Level Lead Exposure Harms Children: A Renewed Call 

9 of Primary Prevention”. Atlanta, GA: U.S. Department of Health and Human Services, Public Health 

10 Service. June 7. 

11 Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

12 Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

13 the 1st Draft Lead Staff Paper and Draft Lead Exposure and Risk Assessments. March 27, 2007. 

14 Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

15 Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

16 the 2nd Draft Lead Human Exposure and Health Risk Assessments. September 27, 2007. 

17 Henderson, R. (2008a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

18 Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

19 the Advance Notice of Proposed Rulemaking (ANPR) for the NAAQS for lead. January 22, 2008. 

20 Henderson, R. (2008b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

21 Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

22 the Notice of Proposed Rulemaking for the NAAQS for lead. July 18, 2008. 

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

24 58. 

25 Lanphear, B. P.; Hornung, R.; Khoury, J.; Yolton, K.; Baghurst, P.; Bellinger, D. C.; Canfield, R. L.; Dietrich, K. 

26 N.; Bornschein, R.; Greene, T.; Rothenberg, S. J.; Needleman, H. L.; Schnaas, L.; Wasserman, G.; 

27 Graziano, J.; Roberts, R. (2005) Low-level environmental lead exposure and children's intellectual 

28 function: an international pooled analysis. Environ. Health Perspect. 113: 894-899. 

29 Téllez-Rojo, M. M.; Bellinger, D. C.; Arroyo-Quiroz, C.; Lamadrid-Figueroa, H.; Mercado-García, A.; Schnaas30 Arrieta, L.; Wright, R. O.; Hernández-Avila, M.; Hu, H. (2006) Longitudinal associations between blood 

31 lead concentrations < 10 μg/dL and neurobehavioral development in environmentally-exposed children in 

32 Mexico City. Pediatrics 118: e323-e330. 

33 U.S. Environmental Protection Agency. (2006) Air Quality Criteria for Lead. Washington, DC, EPA/600/R34 5/144aF. Available online at: www.epa.gov/ncea/

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

36 Case Studies, Volume I. Human Exposure and Health Risk Assessments – Full-Scale and Volume II. 

37 Appendices. Office of Air Quality Planning and Standards, Research Triangle Park, NC. EPA-452/R-07-

38 014a and EPA-452/R-07-014b. 

39 U.S. Environmental Protection Agency. (2007b) Review of the National Ambient Air Quality Standards for Lead: 

40 Policy Assessment of Scientific and Technical Information, OAQPS Staff Paper. EPA-452/R-07-013. 

41 Office of Air Quality Planning and Standards, Research Triangle Park. 
January 2013 4-37 Draft - Do Not Quote or Cite

1 U.S. Environmental Protection Agency. (2012) Integrated Science Assessment for Lead (Third External Review 

2 Draft). Washington, DC, EPA/600/R-10/075C. Available online at: 

3 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html 
January 2013 5-1 Draft - Do Not Quote or Cite

1 5 WELFARE EFFECTS AND EXPOSURE/RISK INFORMATION 

2 This chapter presents key aspects of the current evidence of lead-related welfare effects, 

3 and presents exposure and risk information from the last review in the context of the currently 

4 available information. Staff has drawn from the EPA’s synthesis of the scientific evidence 

5 presented in the third draft Integrated Science Assessment for Lead (USEPA, 2012; henceforth 

6 referred to as the ISA) and the 2006 Air Quality Criteria Document for Lead (USEPA, 2006; 

7 henceforth referred to as the 2006 CD), and from the screening level risk assessment performed 

8 in the last review and described in Lead Human Exposure and Health Risk Assessments and 

9 Ecological Risk Assessment for Selected Areas. Pilot Phase (documented in ICF, 2006; 

10 henceforth referred to as the 2006 REA). This chapter is organized into two sections regarding 

11 the currently available welfare effects evidence (section 5.1) and the exposure and risk 

12 information (section 5.2) interpreted in light of currently available evidence. Presentation within 

13 these sections is organized to address key policy-relevant questions for this review concerning 

14 the evidence and exposure/risk information, building upon the questions included in the IRP 

15 (IRP, section 3.2). 

16 5.1 WELFARE EFFECTS INFORMATION 

17 Lead has been demonstrated to have harmful effects on reproduction and development, 

18 growth, and survival in many species as described in the assessment of the evidence available in 

19 this review and consistent with the conclusions drawn in past CDs (ISA, section 2.7; 2006 CD). 

20 A number of studies on Pb ecological effects are newly available in this review and are critically 

21 assessed in the ISA as part of the full body of evidence. The newly available evidence reaffirms 

22 conclusions on the array of effects recognized for Pb in the last review (ISA, section 2.7). The 

23 current ISA, unlike the 2006 CD, makes causal determinations for the effects of Pb on 

organisms. The ISA determines that causal or likely causal relationships1 24 exist in both 

freshwater and terrestrial ecosystems for Pb2 25 with effects on reproduction and development in 

26 vertebrates and invertebrates; growth in plants and invertebrates; and survival in vertebrates and 

27 invertebrates (ISA, table 2-3). Based on these determinations and a weight of evidence 

28 approach, the ISA concludes that higher level community and ecosystem effects in freshwater 

 

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 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). 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 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) 
January 2013 5-2 Draft - Do Not Quote or Cite

1 and terrestrial systems are likely to result from the above described population-level endpoints. 

2 The ISA also presents evidence for saltwater ecosystems but concludes that current evidence is 

3 inadequate to make causality determinations for most organisms and communities but finds the 

4 evidence to be suggestive linking Pb and effects on reproduction and development in marine 

5 invertebrates (ISA, section 1.5, Table 2-3, section 7.3.12 and section 7.4.21). 

6 Based on the extensive assessment of the full body of evidence available in this review, 

7 the major conclusions drawn by the ISA regarding ecological effects of Pb include the following 

8 (ISA, section 1.5). 

9 With regard to the ecological effects of Pb, uptake of Pb into fauna and 

10 subsequent effects on reproduction, growth and survival are established and are 

11 further supported by more recent evidence. These may lead to effects at the 

12 population, community, and ecosystem level of biological organization. In both 

13 terrestrial and aquatic organisms, gradients in response are observed with 

14 increasing concentration of Pb and some studies report effects within the range of 

15 Pb detected in environmental media. Specifically, observations from controlled 

16 studies on reproduction, growth, and survival in sensitive freshwater 

17 invertebrates are well-characterized at concentrations at or near Pb 

18 concentrations occasionally encountered in U.S. surface waters.... However, in 

19 natural environments, modifying factors affect Pb bioavailability and toxicity and 

20 there are considerable uncertainties associated with generalizing effects observed 

21 in controlled studies to effects at higher levels of biological organization. 

22 Furthermore, available studies on community and ecosystem-level effects are 

23 usually from contaminated areas where Pb concentrations are much higher than 

24 typically encountered in the environment. The contribution of atmospheric Pb to 

25 specific sites is not clear and the connection between air concentration of Pb and 

26 ecosystem exposure continues to be poorly characterized. Furthermore, the level 

27 at which Pb elicits a specific effect is difficult to establish in terrestrial and 

28 aquatic systems, due to the influence of other environmental variables (e.g., pH, 

29 organic matter) on both Pb bioavailability and toxicity, and also to substantial 

30 species differences in Pb sensitivity.

31 

32 As in prior reviews of the Pb NAAQS, this review is focused on those effects most 

33 pertinent to ambient air Pb exposures. Given the reductions in ambient air Pb levels over the 

34 past decades, these effects are generally those associated with the lowest levels of Pb exposure 

35 that have been evaluated. Additionally, we recognize the limitations on our ability to draw 

36 conclusions about environmental exposures from ecological studies of organism-level effects as 

37 most studies were conducted in laboratory settings which may not accurately represent field 

38 conditions or the multiple variables that govern exposure. 

39 Our consideration of welfare effects evidence in this review is framed by key policy40 relevant questions drawn from those included in the IRP. In the following sections, we discuss 

41 the pathways by which Pb exposure occurs in ecosystems, the mechanisms that distribute Pb in 
January 2013 5-3 Draft - Do Not Quote or Cite

1 the environment and the bioavailability of Pb in different ecosystems. Understanding the 

2 movement of Pb in the environment is important to understanding exposure and bioavailability 

3 and, thus, informs the subsequent discussion of the effects of Pb on terrestrial and aquatic 

4 ecosystems. Finally, we discuss the association of ambient air Pb with effects and the important 

5 role critical loads play in assessing the overall ability of ecosystems to recover from past Pb 

6 exposures and the degree to which newly deposited Pb may affect ecosystem function and 

7 recovery. 

8  To what extent has the newly available evidence altered our understanding of the 

9 movement and accumulation of air-deposited Pb through ecosystems over time? 

10 There is little new information on fate and transport in ecosystems specifically related to 

11 air-derived Pb. Nonetheless, some new studies are available that provide additional information, 

12 briefly summarized below, on Pb cycling, flux and retention. This new information does not 

13 fundamentally change our understanding from the last review of Pb movement or accumulation 

14 through ecosystems over time but rather improves our understanding of some of the underlying 

15 processes and mechanisms in soil, water and sediment. The newly available information also 

16 adds to the evidence base with regard to the timing of ecosystem recovery from historic 

17 atmospheric deposition of Pb. 

18 Overall, recent studies in terrestrial ecosystems provide deposition data consistent with 

19 deposition fluxes reported in the 2006 CD, and demonstrate consistently that Pb deposition to 

20 soils has decreased since the phase-out of leaded on-road gasoline (ISA, section 3.3.3.1). 

21 Although follow-up studies in several locations at high elevation sites indicate little change in 

22 soil Pb concentrations since the phase-out of leaded on-road gasoline in surface soils, consistent 

23 with the high retention reportedly associated with reduced microbial activity at lower 

24 temperatures associated with high elevation sites, amounts of Pb in the surface soils at some 

25 lower altitude sites were reduced over the same time period in the same study (ISA, section 

26 3.3.3.1). New studies in the ISA also enhance our understanding of Pb sequestration in forest 

27 soils by providing additional information on the role of leaf litter as a Pb reservoir and the effect 

28 of decomposition on Pb distribution and sequestration (ISA, section 3.3.3.2). 

29 Recent research on Pb transport in aquatic systems has provided a large body of 

30 observations confirming that Pb transport is dominated by colloids rich in iron and organic 

31 material (ISA, section 3.3.2.1). In sediments, recent research on Pb flux provides greater detail 

32 on resuspension processes than was available in the 2006 CD, including research on resuspended 

33 Pb largely associated with organic material or iron and manganese particles, and research on the 

34 important role played by anoxic or depleted oxygen environments in Pb cycling in aquatic 

35 systems. This newer research is consistent with prior evidence in indicating that appreciable 

36 resuspension and release from sediments largely occurs during discrete events related to storms. 
January 2013 5-4 Draft - Do Not Quote or Cite

1 It has also confirmed that resuspension is an important process that strongly influences the 

2 lifetime of Pb in bodies of water. Finally, there have been advances in understanding and 

3 modeling of Pb partitioning between organic material and sediment in complex aquatic 

4 environments (ISA, section 3.7.2). 

5 In summary, the newly available evidence builds on our understanding of some specific 

6 aspects of processes involved in the movement and accumulation of air-deposited Pb through 

7 ecosystems over time. This new information, however, does not substantially alter our overall 

8 understanding of fate and transport of Pb in ecosystems. 

9  Does the newly available evidence further inform our understanding of the 

10 bioavailability of Pb in different types of ecosystems and organisms? 

11 As discussed in the ISA, bioavailability of Pb is an important component of 

12 understanding the effects Pb is likely to have on organisms and ecosystems (ISA, section 7.3.3). 

13 It is the amount of Pb that can interact within the organism that leads to toxicity and there are 

14 many factors which govern this interaction. Bioavailability is defined in the Framework for 

15 Metals Risk Assessment (USEPA, 2007) as “the extent to which bioaccessible metals absorb 

16 onto, or into, and across biological membranes of organisms, expressed as a fraction of the total 

17 amount of metal the organism is proximately exposed to (at the sorption surface) during a given 

18 time and under defined conditions.” The bioavailability of metals varies widely depending on the 

19 physical, chemical, and biological conditions under which an organism is exposed (USEPA, 

20 2007). Characteristics of the toxicant itself that affect bioavailability are: (1) chemical form or 

21 species, (2) particle size, (3) lability, and (4) source. The bioavailability of a metal is also 

22 dependent upon the fraction of metal that is bioaccessible. The bioaccessible fraction of a metal

23 is the portion (fraction or percentage) of environmentally available metal that actually interacts at 

24 the organism’s contact surface and is potentially available for absorption or adsorption by the 

25 organism (USEPA, 2007; ISA, section 7.3.3). 

26 New studies provide additional insight into factors that influence the bioavailability of Pb 

27 to specific organisms (ISA, section 7.3.3). In general, this evidence, briefly summarized below, 

28 is supportive of previous conclusions and does not identify significant new variables from those 

29 identified previously. Section 7.3.3 of the ISA provides a detailed discussion of bioavailability in 

30 terrestrial systems. With regard to aquatic systems, a detailed discussion of bioavailability in 

31 freshwater systems is provided in sections 7.4.3 and 7.4.4 of the ISA and section 7.4.14 of the 

32 ISA discusses bioavailability in saltwater systems. 

33 In terrestrial systems, the bioavailability of Pb has a far greater impact on the adverse 

34 effects of Pb than does the total Pb burden (ISA, section 7.3.11). In such ecosystems, Pb is 

35 deposited either directly onto plant surfaces or onto soil where it can bind with organic matter or 
January 2013 5-5 Draft - Do Not Quote or Cite

dissolve in pore water.3 1 The Pb dissolved in pore water is particularly bioavailable to organisms 

2 in the soil and thereby influences the impact of soil Pb on terrestrial ecosystems to a much 

3 greater extent than the total amount of Pb present (ISA, section 7.3.11). Several soil variables 

4 control the amount of Pb that is dissolved in pore water, and the ISA presents new evidence that 

5 has advanced scientific understanding of some of these variables (ISA, section 7.4.21). Studies 

6 have shown that the two most important determinants of both Pb solubility and toxicity in soils 

7 are pH and cation exchange capacity (ISA, section 2.7.1). Also, evidence newly available in this 

8 review has confirmed the important influence of organic matter on Pb sequestration, leading to 

9 relatively longer retention in soils with higher organic matter content, with the potential for later 

10 release of deposited Pb (ISA, section 2.7.1). In general, soils with higher organic matter content 

11 have the capacity for greater retention of Pb in the soil matrix and lesser availability of Pb for 

12 release into pore water. Subsequent reduction in soil organic material, such as through 

13 decomposition, can contribute to subsequent increased availability. Aging of Pb in soils, both 

14 under natural conditions and simulated through leaching, has also been shown to reduce 

15 bioavailability to plants and soil organisms (ISA, sections 7.3.2.3 and 7.3.11). 

16 In aquatic systems as in terrestrial systems, the amount of Pb bioavailable to organisms is 

17 a better predictor of effect on organisms than the overall amount of Pb in the system. Once 

18 atmospherically-derived Pb enters surface water bodies through deposition or runoff, its fate and 

19 bioavailability are influenced by many water quality characteristics, such as pH, suspended 

20 solids loading and organic content (ISA, section 7.4.2). In sediments, bioavailability of Pb to 

21 sediment-dwelling organisms may be influenced by the presence of other metals, sulfides, iron 

22 oxides and manganese oxides and also by physical disturbance (ISA, section 2.7.2). For many 

23 aquatic organisms Pb dissolved in the water column can be the primary exposure route, while for 

24 others sediment ingestion is significant (ISA, section 2.7.2). As recognized in the 2006 CD and 

25 further supported in the ISA, there is a body of evidence showing that uptake and elimination of 

26 Pb varies widely between species. 

27 Although in freshwater systems the presence of humic acid in dissolved organic material 

28 (DOM) is considered to reduce the bioavailable fraction of metals in the water column, there is 

29 evidence presented in the ISA that dissolved organic carbon and DOM do not have the same 

30 effect on free Pb ion concentration in saltwater systems (ISA, section 7.4.24). Recent studies 

31 have broadened previous understandings of the role of DOM in Pb bioavailability and have 

32 shown that different components of DOM have different effects on Pb bioavailability in 

33 saltwater systems. For example, the ISA discusses two new studies that suggest that in saltwater 

34 aquatic systems, surface water DOM increases (rather than decreases) uptake of Pb by fish gill 

 

3

 The term “pore water” refers to the water occupying the spaces among the grains of sediment or soil. 
January 2013 5-6 Draft - Do Not Quote or Cite

1 structures, potentially through the alteration of membrane permeability. This recent evidence 

2 supports the conclusion from the last review that factors that modify bioavailability of Pb in 

3 saltwater environments are not identical to those in freshwater systems (ISA, section 7.4.14). 

4 There is new evidence about bioavailability in some ecosystems, briefly summarized 

5 above, which further informs our understanding of bioavailability of Pb in different ecosystems 

6 and organisms, building on our fundamental understanding in the last review. Bioavailability 

7 remains an important consideration in Pb toxicity and a significant source of uncertainty relating 

8 ambient Pb and adverse effects. 

9  Does the current evidence alter our conclusions from the previous review 

10 regarding the ecological effects associated with exposure to Pb? Does the newly 

11 available evidence indicate new exposure levels at which ecological systems or 

12 receptors are expected to experience effects? 

13 There is a substantial amount of new evidence in this review regarding the ecological 

14 effects of Pb on specific terrestrial and aquatic organisms. On the whole, this evidence supports 

15 previous conclusions that Pb has effects on growth, reproduction and survival, and that under 

16 some conditions these effects can be adverse to organisms and ecosystems. The ISA provides 

17 evidence of effects in additional species, and in a few cases, at lower exposures than reported in 

18 the previous review, but does not substantially alter the effects endpoints from the previous 

19 review. Looking beyond organism-level evidence, the evidence of adversity in natural systems 

20 remains sparse due to the difficulty in determining the effects of confounding factors such as 

21 multiple metals or factors influencing bioavailability in field studies. The following is a brief 

22 comparison of the newly available evidence to evidence considered in the 2006 review. 

23 Terrestrial Ecosystems 

24 The evidence available in the last review indicated a range of biological effects of Pb on 

25 terrestrial organisms that varied with type of organism and life stage, duration of exposure, form 

26 of Pb, and soil characteristics. New research since the 2006 CD has broadened our 

27 understanding of the evidence of damage to photosynthetic ability in plants exposed to Pb, and 

28 provided additional evidence of oxidative stress in response to Pb exposure (ISA, section 

29 7.3.4.1). Reactive oxygen species have been found to increase in plant tissue grown in Pb30 contaminated soil; with increasing Pb exposure, the plant tissue responded with increased 

31 antioxidant activity (ISA, section 7.3.4.1). In addition, reduced growth has been observed in 

32 some experiments, as well as evidence of genotoxicity, decreased germination, and pollen 

33 sterility (ISA, section 7.3.4.1). 

34 In terrestrial invertebrates, previous CDs have reported adverse effects of Pb on 

35 neurological and reproductive endpoints. Recently published studies have shown some 

36 additional evidence of neurological changes in nematodes at relatively low concentrations of 
January 2013 5-7 Draft - Do Not Quote or Cite

1 soil Pb (2.5 μM) but given the study design the relevance to environmental exposure is unclear 

2 (ISA, section 7.3.4.2). Increased mortality was found in recent studies of earthworms at 

3 concentrations similar to those in studies reviewed previously, but additional evidence indicated 

4 that effects were strongly dependent on soil characteristics including pH, cation exchange 

5 capacity, and aging (ISA, section 7.3.4.2). There is also newly available evidence for adverse 

6 effects in snails and arthropods exposed through soil or diet (ISA, section 7.3.4.2). The effects 

7 vary with species and exposure conditions, and include diminished growth and fecundity, 

8 endocrine and reproductive anomalies, and body deformities. Increasing concentration of Pb in 

9 the exposure medium generally resulted in increased effects within each study, but the 

10 relationship between concentration and effects is highly variable between studies, even when 

11 the same medium, e.g. soil, was used. Current evidence suggests that aging and pH are 

12 important modifiers of Pb toxicity (ISA, section 7.3.11). 

13 In terrestrial vertebrates, some new evidence is available for effects of Pb on amphibians 

14 and reptiles as well as birds. Effects reported in reptiles and amphibians include decreased white 

15 blood cell counts, decreased testis weight, and behavioral anomalies (ISA, section 7.3.4.3). 

16 However, depending on various factors, studies report large differences in effects in different 

17 species at the same concentration of Pb in soil, and effects were generally smaller when field18 collected soils were used. In some birds, recent studies have found maternal elevated blood Pb 

19 level to be associated with decreased hatching success, smaller clutch size, high corticosteroid 

20 level, and abnormal behavior. Studies on some species show little or no effect of elevated blood 

21 Pb level. Effects of dietary exposure have been studied in several mammalian species, with 

22 cognitive, endocrine, immunological, and growth effects observed (ISA, section 7.3.11) in some 

23 studies. 

24 Experimental evidence of organism-level effects presented in the ISA demonstrates that 

25 increased exposure to Pb is generally associated with increases in observed effects in terrestrial 

26 ecosystems (ISA, section 7.3.11). It also demonstrates that many factors, including species and 

27 various soil physiochemical properties, interact strongly with Pb concentration to modify those 

28 effects (ISA, section 7.3.11). In terrestrial ecosystems, where soil is generally the main 

29 component of the exposure route, Pb aging is a particularly important factor, and one that may 

30 be difficult to reproduce experimentally. Given that in natural settings, these modifying factors 

31 are highly variable, the ISA notes that “[w]ithout quantitative characterization of those 

32 interactions, characterizations of exposure-response relationships would likely not be 

33 transferable outside of experimental settings” (ISA, section 2.7.1). The results of the few 

34 exposure-response studies conducted since the 2006 CD have been inconsistent (ISA, section 

35 2.7.1). 
January 2013 5-8 Draft - Do Not Quote or Cite

1 As reported in both the ISA and the 2006 CD, most direct evidence of community- and 

2 ecosystem-level effects is from releases by near sources of Pb to the environment, where Pb 

3 concentrations are much higher than typically observed environmental concentrations and often 

4 derive from separate releases to multiple media. Impacts of Pb on terrestrial ecosystems near 

5 smelters, mines, and other industrial sources have been studied for several decades (ISA, section 

6 7.3.12.7). Emissions of Pb from smelting and other industrial activities are commonly 

7 accompanied by other trace metals (e.g., Zn, Cu, Cd) and SO2 that may cause toxic effects 

8 independently or in concert with Pb. Those impacts have been long shown to include decreases 

9 in species diversity and changes in floral and faunal community composition. Ecosystem-level 

10 field studies are complicated by these confounding exposures and the inherent variability in 

11 natural systems (ISA, section 7.3.12.7). 

12 New evidence of effects of Pb at the community and ecosystem scales has been 

13 reported. This evidence includes several studies of the ameliorative effects of mycorrhizal fungi 

14 on plant growth with Pb exposure as well as recently published research on soil microbial 

15 communities, which have been shown to be impacted by Pb in both composition and activity 

16 (ISA, sections 2.7.1 and 7.3.6). Many recent studies have been conducted using mixtures of 

17 metals, which have attempted to separate the effects of individual metals when possible. In 

18 studies that included only Pb, or where effects of Pb could be separated, soil microbial activity 

19 was generally diminished, and was shown in some of those cases to recover with time (ISA, 

20 section 7.3.6). Regardless of the recovery of such microbial communities, species and 

21 genotypical composition were consistently altered after Pb exposure, and findings indicate that 

22 those alterations were long-lasting or permanent (ISA, section 7.3.11). 

23 A recent review has examined differences in species sensitivity, using blood Pb level in 

24 birds and mammals as an exposure index rather than external dose (ISA, section 7.3.9.1; 

25 Buekers et al., 2009). In this analysis, variation across organisms was reduced with the blood 

26 Pb index and variation of Pb absorption from the diet of the organism largely accounted for the 

27 variation seen in the blood Pb. The analysis also suggests that the association between blood Pb 

28 concentration and toxicity is different between birds and mammals (ISA, section 7.3.9.1). 

29 Overall, new studies in this review support previous conclusions about the effects of Pb 

30 on terrestrial ecosystems, namely that increasing soil Pb concentrations in areas of Pb 

31 contamination (e.g. mining sites and industrial sites) can cause decreases in microorganism 

32 abundance, diversity, and function. Specifically, shifts in bacterial species and fungal diversity 

33 have been recently observed near long-established sources of Pb contamination (ISA, section 

34 7.3.12.7). Most evidence for Pb toxicity to terrestrial plants, invertebrates and vertebrates, 

35 however, is from single-species assays in laboratory studies which do not capture the 
January 2013 5-9 Draft - Do Not Quote or Cite

1 complexity of bioavailability and other modifiers of effect in natural systems (ISA, section 

2 7.3.12.7). 

3 Freshwater Ecosystems 

4 In fish, while there are species differences in the rate of Pb accumulation and distribution 

5 of Pb within the organism, the gills and diet are the primary routes of uptake. Recent studies 

6 have identified the anterior intestine as an additional site of uptake of Pb through dietary 

7 exposure (ISA, section 7.4.4.3). While there are few new studies on Pb uptake through 

8 freshwater exposure by amphibians and mammals, there are some new studies presented in the 

9 ISA which seem to provide new information on trophic transfer of Pb (ISA, section 7.4.4.4). 

10 Evidence summarized in the 2006 CD indicated that measured concentrations of Pb in the 

11 tissues of aquatic organisms were generally higher in algae and benthic organisms than in 

12 higher trophic-level consumers, indicating that Pb was bioconcentrated but not biomagnified 

13 (ISA, section 2.7.2). Some recent studies indicate transfer of Pb in aquatic food webs; recent 

14 studies that have traced Pb in freshwater aquatic food webs have found that Pb concentration 

15 decreases with increasing trophic level (biodilution) (ISA, sections 2.7.2 and 7.4.4.4). 

16 Evidence presented in the ISA further supports the findings of past CDs that Pb in 

17 freshwater can be highly toxic to aquatic organisms, with toxicity varying with species and life 

18 stage, duration of exposure, form of Pb, and water quality characteristics. The 2006 CD 

19 identified evidence of adverse growth effects on several species of freshwater algae from Pb 

20 exposure (2006 CD, Section 7.2.4). The ISA describes several new studies which expand the 

21 list of algal species for which these adverse effects have been identified (ISA, section 7.4.5.1). 

22 For vascular plants, the ISA describes additional evidence that oxidative damage, decreased 

23 photosynthesis and reduced growth occur with Pb exposure (ISA, section 7.4.5.2). 

24 Since the 2006 CD, there is some additional evidence for Pb effects on cellular processes 

25 in aquatic invertebrates. Recent studies of reproductive and developmental effects of Pb provide 

26 further support for findings in the 2006 CD and add additional species information on 

27 reproductive endpoints for rotifers and freshwater snails as well as multigenerational effects of 

28 Pb in mosquito larvae (ISA, section 7.4.5.2). In the 2006 CD, study concentrations cited at 

29 which effects were observed in aquatic invertebrates reflected an expansive range from 5μg/L 

30 (for acute toxicity to Pb nitrate in a test system at a hardness of 18 mg/L calcium carbonate) to 

31 greater than 8000 μg/L (for acute toxicity to Pb chloride at a hardness of 280-300 mg/L calcium 

32 carbonate) (ISA, p.2-38; 2006 CD, Table AX7-2.4.1). Recent studies cited in the ISA provide 

33 additional evidence of effects from chronic exposures. These findings are generally consistent 

34 with those of the previous review and reflect the variability of Pb toxicity under different 

35 environmental conditions and in species with varying sensitivity. 
January 2013 5-10 Draft - Do Not Quote or Cite

1 Evidence of effects in aquatic vertebrates presented in the ISA reiterates the findings of 

2 reproductive, behavioral, and growth effects stated in previous CDs. Some additional 

3 mechanisms of Pb toxicity in the gill and the renal system of fish have been elucidated since the 

4 2006 CD as well as the identification of potential new molecular targets for Pb neurotoxicity 

5 (ISA, section 2.7.2). Recent studies reported sublethal effects on tadpole growth, deformity, and 

6 swimming ability at concentrations within two orders of magnitude of environmental levels of 

7 Pb (ISA, section 7.4.5.3) based on nominal concentrations. 

8 As in terrestrial organisms, evidence presented in the ISA and prior CDs demonstrates the 

9 toxicity of Pb in aquatic ecosystems and the role of many factors, including Pb speciation and 

10 various water chemistry properties in modifying toxicity (ISA, section 2.7.2). Since the 2006 

11 CD, additional evidence for community and ecosystem level effects of Pb is available, primarily 

12 in microcosm studies or field studies with other metals present (ISA, section 7.4.11). Such 

13 evidence described in previous CDs includes alteration of predator-prey dynamics, species 

14 richness, species composition, and biodiversity. New studies available in this review provide 

15 evidence in additional habitats for these community and ecological-scale effects, specifically in 

16 aquatic plant communities and sediment-associated communities at both acute and chronic 

17 exposures involving concentrations similar to previously reported (ISA, section 7.4.4.1). In 

18 many cases it is difficult to characterize the nature and magnitude of effects and to quantify 

19 relationships between ambient concentrations of Pb and ecosystem response due to existence of 

20 multiple stressors, variability in field conditions, and to differences in Pb bioavailability at that 

21 level of organization (ISA, section 2.7.3.7). In these field studies, the degree to which air 

22 concentrations contribute to such effects is largely unknown. 

23 Saltwater Ecosystems 

24 Recently available evidence in the ISA on toxicity of Pb to marine algae augments the 

25 2006 CD findings of variation in sensitivity across marine species. Recent studies on Pb 

26 exposure include reports of growth inhibition and oxidative stress in a few additional species of 

27 marine algae (ISA, section 7.4.15). 

28 Recent literature provides little new evidence of endpoints or effects in marine 

29 invertebrates beyond those reported in the 2006 CD. For example, some recent studies 

30 strengthen the evidence of Pb effects on enzymes and antioxidant activity in marine 

31 invertebrates and have identified an additional behavioral endpoint (i.e., valve closing speed in 

32 juveniles of a marine scallop was affected by 20-day exposure to 40-400 μg/L Pb nitrate) from 

33 those discussed previously (ISA, section 7.4.15.2). Also, as noted in the 2006 CD and supported 

34 by new studies reviewed in the ISA, Pb exposure negatively affects the growth of marine 

35 invertebrates (ISA, section 7.4.15.2). Recent studies also identify several species exhibiting 

36 particularly low sensitivity to high acute exposures (ISA, section 7.4.15.2). 
January 2013 5-11 Draft - Do Not Quote or Cite

1 Little new evidence is available of Pb effects on marine fish and mammals for 

2 reproductive, growth and survival endpoints that are particularly relevant to population-level of 

3 biological organization and higher (ISA, section 7.4.15). Evidence for effects at higher levels of 

4 biological organization in saltwater habitats is primarily supported by observations in a small 

5 number of microcosm and field studies where shifts in community structure are the most 

6 commonly observed effects of Pb (ISA, section 7.4.20). These types of studies were presented 

7 in the 2006 CD and while there are new studies presented in the ISA, they primarily expand the 

8 types of communities for which data exist but reach similar conclusions about community 

9 structure as the 2006 CD. However, there is no evidence of adverse effects in saltwater 

10 environments from current ambient air concentrations and linkages between any level of 

11 ambient exposure and effects are unknown in all but a few organisms. 

12 New studies on organism-level effects from Pb in saltwater ecosystems provide little 

13 evidence to inform our understanding of linkages between atmospheric concentrations, ambient 

14 exposures in saltwater systems and such effects or our conclusions regarding the likelihood of 

15 adverse effects under conditions associated with the current NAAQS for Pb. Nor does the 

16 currently available evidence indicate significantly different exposure levels at which ecological 

17 systems or receptors are expected to experience effects. The new evidence, as outlined above, 

18 serves to support previous conclusions regarding effects evidence and provides information on 

19 additional species, but does not significantly improve our understanding of ecological effects 

20 levels of Pb. 

21  To what extent is there new information that informs our understanding of 

22 critical loads of Pb, including critical loads in sensitive ecosystems? 

23 Critical loads are an especially powerful tool that can link Pb input into an ecosystem, 

24 including atmospheric deposition, with ecological impairment. Critical load calculations are 

25 dependent on data relating Pb released into an ecosystem from various sources with an 

26 understanding of the level of Pb in an ecosystem that is likely to result in measurable effects. 

27 Importantly, with these data, critical loads can account for heterogeneity in ecosystem sensitivity 

28 and exposure which often results in critical load values that vary by ecosystem (e.g., aquatic29 water; aquatic-sediment; terrestrial), and differ by endpoint of concern (ISA, section 7.1.3). 

30 During the last review, the 2006 CD assessed the available information on critical loads for Pb 

31 which was drawn primarily from Europe. Analyses were not available for U.S. locations, and 

32 the European critical load values for Pb that had been developed were highly specific to the 

33 bedrock geology, soil types, vegetation, and historical deposition trends in each European 

34 country (2006 CD, p. E-24). As a result, the 2006 CD concluded that “[a]t this time, the methods 

35 and models commonly used for the calculation of critical loads have not been validated for Pb” 

36 and that “[m]any of the methods neglect the speciation of Pb when estimating critical limits, the 
January 2013 5-12 Draft - Do Not Quote or Cite

1 uptake of Pb into plants, and out flux of Pb in drainage water, limiting the utility of current 

2 models” (2006 CD, p. 7-46). Accordingly, the quantitative assessment for the last Pb NAAQS 

3 review did not involve critical load analyses. 

4 There are no critical loads for Pb reported in the ISA or 2006 CD for any ecosystems in 

5 the U.S.; however, as reported in the 2006 CD and further discussed in section 7.3.7 of the ISA, 

6 work has been conducted in terrestrial systems in Europe and aquatic ecosystems in Canada 

7 (ISA, section 7.3.7 and section 7.4.8). Given that local conditions (including historic loading, soil 

8 transport and transformation processes) are key elements to critical load calculation, the utility of 

9 critical loads that are developed from other countries for application to U.S. ecosystems is 

10 unclear. Given the heterogeneity of ecosystems affected by Pb, and the differences in 

11 expectations for ecosystem services attached to different land uses, it is expected that there 

12 would be a range of critical load values for Pb for soils and freshwaters within the U.S. 

13 In the short term, metal emissions generally have greater effects on biota in freshwater 

14 systems than in terrestrial systems because metals are more readily immobilized in soils than in 

15 sediment. However, over the longer term, terrestrial systems may be more affected by increasing 

16 concentrations, particularly by those metals with a long soil residence time, such as Pb (ISA, 

17 section 7.4.8). There is no new evidence regarding critical loads for Pb in saltwater ecosystems. 

18  To what extent is there information that improves our understanding of the 

19 portion of environmental Pb derived from ambient air and the associated effects 

20 on sensitive ecosystems? 

21 As stated in the last review, the role of ambient air Pb in contributing to ecosystem Pb 

22 has been declining over the past several decades. However, it remains difficult to apportion 

23 exposure between air and other sources to better inform our understanding of ecosystem effects 

24 that might be associated with air emissions. Considerable uncertainties also remain in drawing 

25 conclusions from evidence of effects observed under laboratory conditions with regard to effects 

26 expected at the ecosystem level in the environment. In many cases it is difficult to characterize 

27 the nature and magnitude of effects and to quantify relationships between ambient concentrations 

28 of Pb and ecosystem response due to the existence of multiple stressors, variability in field 

29 conditions, and to differences in Pb bioavailability at that level of organization (ISA, section 

30 7.5). There is no new evidence that substantially improves our understanding of the relationship 

31 between ambient air Pb and measurable ecological effects.

32 
January 2013 5-13 Draft - Do Not Quote or Cite

1 5.2 EXPOSURE AND RISK INFORMATION 

2 This risk information available for this review and described here is based primarily on 

3 the pilot ecological risk assessment developed in the last review of the Pb NAAQS (henceforth 

4 referred to as the 2006 REA [ICF, 2006]), which is described within the context of the evidence 

5 presented in the ISA that is newly available for this review. As described in the IRP, careful 

6 consideration of newly available information in this review led us to conclude that developing a 

7 new REA for this review was not warranted. In light of critical limitations and uncertainties that 

8 are still unresolved in the current evidence, staff concluded that currently available information 

9 does not provide the basis for developing a new quantitative risk and exposure assessment with 

10 substantially improved utility for informing the Agency’s consideration of welfare effects and 

11 evaluation of the adequacy of the current secondary standard or alternatives (IRP, section 3.3). 

12 Based on their consideration of the IRP, the CASAC Pb Review Panel generally concurred with 

the conclusion that a new REA was not warranted in this review (Frey, 2011).4 13 Accordingly, the 

14 information described here is drawn primarily from the 2006 REA. 

15 The focus for the risk assessment and associated estimates presented here is on Pb 

16 derived from sources emitting Pb to ambient air. While there is some new evidence that 

17 improves our understanding of some of the environmental variability affecting the disposition 

18 and toxicity of Pb in the environment, the information and methods to support a quantitative 

19 assessment of the role of atmospheric Pb in the U.S are limited. Specific constraints include the 

20 limited availability of location-specific data describing a range of U.S. ecosystems and their 

21 pertinent environmental characteristics as well as the ability to apportion effects between air and 

22 non air sources, and a more complete understanding of bioavailability and its modifiers. These 

23 data gaps and areas of uncertainty in the current evidence restrict our ability to assess 

24 quantitatively the relationship between concentrations of Pb in ambient air and terrestrial and/or 

25 aquatic systems, and their effect on welfare. 

26 As discussed in section 1.3 above, the multimedia and persistent nature of Pb, the role of 

27 multiple exposure pathways (illustrated in Figure 1-1 above), and the contributions of nonair 

28 sources of Pb to exposure media all present challenges and contribute significant additional 

29 complexity to the ecological risk assessment that goes far beyond the situation for similar 

30 assessments typically performed for other NAAQS pollutants (e.g., that focus only on a single 

31 media pathway or for which air is the only significant source). Limitations in the available data 

32 and models affected our characterization of the various complexities associated with exposure to 

 

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

1 ambient air Pb. As a result, the 2006 assessment was conducted as a pilot study with a number 

2 of simplifying assumptions with regard to the representativeness of the case studies for 

3 ecological exposures and our ability to isolate case studies where air-derived Pb was the only or 

4 most significant source. Therefore, this section presents a brief summary of the screening-level 

5 ecological risk assessment conducted in 2006 for the Pb NAAQS review completed in 2008 and 

6 addresses several questions relating to the current evidence and understanding that may inform 

7 our view of the results of that assessment. The discussion here also takes into consideration 

8 CASAC recommendations in the last review with regard to interpretation of the screening-level 

9 assessment (Henderson, 2007a, b), as well as comments received from the CASAC Pb Panel in 

10 the current review, as part of the consultation on the REA Planning Document (Frey, 2011). 

11 5.2.1 Screening Assessment from Last Review 

12 The screening-level risk assessment performed for the last review was focused on 

13 estimating the potential for ecological risks associated with ecosystem exposures to Pb emitted 

14 into ambient air (2006 REA, section 7). A national-scale screen was used to evaluate surface 

15 water and sediment monitoring locations across the United States for the potential for ecological 

16 impacts that might be associated with atmospheric deposition of Pb (described in detail in 2006 

17 REA, section 7.1.2). In addition to the national-scale screen (2006 REA, section 3.6), the 

18 assessment involved a case study approach, with case studies for areas surrounding a primary Pb 

19 smelter (2006 REA, section 3.1) and a secondary Pb smelter (2006 REA, section 3.2), as well as 

20 a location near a non-urban roadway (2006 REA, section 3.4). An additional case study, focused 

21 on consideration of gasoline-derived Pb effects on an ecologically vulnerable ecosystem 

22 (Hubbard Brook Experimental Forest), was identified (2006 REA, section 3.5). The Hubbard 

23 Brook Experimental Forest (HBEF), in the White Mountain National Forest, near North 

24 Woodstock, New Hampshire, was selected as a fourth case study because of its location and its 

25 long record of available data on concentration trends of Pb in three media (air or deposition from 

26 air), soil, and surface water). While no quantitative analyses were performed, summary review of 

27 the literature search was included in the assessment report (2006 REA, Appendix E). For the 

28 other three case studies, exposure concentrations in soil, surface water, and/or sediment 

29 concentrations were estimated from available monitoring data or modeling analysis, and then 

30 compared to ecological screening benchmarks (2006 REA, section 7.1). 

31 All three case studies and the national-scale assessment generally considered then-current 

32 or recent environmental conditions. In all cases but the primary Pb smelter case study, current 

33 air quality conditions were below the then-current NAAQS. Air Pb concentrations in the 

34 primary Pb smelter case study exceeded the then-current NAAQS. A complete discussion of air 

35 quality in each of the case studies can be found in section 4 of the 2006 REA. 
January 2013 5-15 Draft - Do Not Quote or Cite

1 An overview of the approach developed to implement the selected elements of the 

2 conceptual model for the ecological risk assessment is provided in Figure 5-1. This figure shows 

3 the key types of information and models involved in each part of the assessment and how they 

4 are related to each other and to the other parts of the analysis. Appendix 5A gives the locations 

5 and spatial resolution for each of the case studies and the national scale screen while summarizes 

6 the source of the screening values used or each location and media type. As indicated in Figure 

7 5-1 and Appendix 5A, the specific approach for each case study differed based on the nature of 

8 the case study (e.g., type of source, locations of populations) and the site-specific measurements 

9 available. 

10 
January 2013 5-16 Draft - Do Not Quote or Cite

1 Figure 5-1. Analytical approach for screening-level assessment in the last review (2006 

2 REA, Exhibit 2-6). 

3 

4 

5 

6 

7 
January 2013 5-17 Draft - Do Not Quote or Cite

1 To estimate the potential for ecological risk, ecological soil screening values (Eco-SSLs) 

2 developed by the EPA’s Superfund program (USEPA, 2003, 2005), the EPA’s recommended 

3 ambient water quality criteria (2006 REA, section 7.1) and sediment screening values developed 

4 by MacDonald and others (2000, 2003) were used, as described in detail in section 7.1.3 of the 

5 2006 REA. A hazard quotient (HQ) was calculated for adverse effects on the survival, growth, 

6 and reproduction of exposed ecological receptors to determine the potential for risk to that 

7 receptor. Ecological receptors used in the pilot are discussed in detail in section 7.1 of the 2006 

8 REA. The HQ was calculated as the ratio of the media concentration to the ecotoxicity screening 

9 value. In each case study, HQ values were calculated for each location where either modeled or 

10 measured media concentrations were available. Separate soil HQ values were calculated for 

11 each ecological receptor group for which an ecotoxicity screening value has been developed (i.e., 

12 birds, mammals, soil invertebrates, and plants), as described in detail in section 7.1.2 of the 2006 

13 REA. HQ values less than 1.0 were concluded to suggest that Pb concentrations in a specific 

14 medium were unlikely to pose significant risks to ecological receptors, while HQ values greater 

15 than 1.0 indicated a potential for adverse effects. 

16 5.2.2 Screening Assessment Results and Interpretation 

17 The results for the ecological screening assessment for the three case studies and the 

18 national-scale screen for surface water and for sediment indicated a potential for adverse effect 

19 from ambient Pb to multiple ecological receptor groups in terrestrial and aquatic locations. 

20 Below are descriptions of the location-specific case studies and the national screening 

21 assessment, key findings of the risk assessment for each, and an interpretation of the results with 

22 regard to past air conditions as well as the current standard (USEPA, 2007b). 

23  What do the key findings of the 2006 screening-level assessment indicate 

24 regarding the likelihood that adverse welfare effects would result from levels of 

25 air-related Pb that would meet the current standard? 

26 In addressing this question, the findings of the 2006 REA are summarized below. 

27 Primary Pb Smelter Case Study

28  The primary Pb smelter case study location is at one of the largest and longest29 operating primary Pb smelters in the world (since 1892), the only one currently 

operating in the U. S. (ICF, 2006).5 30 

31  Concentrations of total Pb in several of the soil and sediment locations within the case 

32 study were measured in 2000 and exceeded screening values, indicating a potential for 

33 adverse effects to terrestrial and sediment dwelling organisms. 

 

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

1  While the contribution to these Pb concentrations from air as compared to nonair 

2 sources is not quantified, air emissions from this facility are substantial (ICF, 2006). In 

3 addition, this facility that has been emitting Pb for many decades, including some 

4 seven decades prior to establishment of any Pb NAAQS, such that it is likely air 

5 concentrations associated with the facility were substantial relative to the 1978 

6 NAAQS, which it exceeded at the time of the last review. Currently, concentrations 

7 monitored near this facility exceed the level of the current standard. Accordingly, this 

8 case study is not informative for considering the likelihood of adverse welfare effects 

9 related to Pb from air sources under air quality conditions associated with meeting the 

10 current Pb standard. 

11 Secondary Pb Smelter Case Study

12  The secondary Pb smelter location falls within the Alabama Coastal Plain in Pike 

13 County, Alabama, in an area of disturbed forests. The industrial facility in this case 

14 study is much younger than the primary Pb smelter, becoming active less than ten years 

15 prior to the establishment of the 1978 Pb standard. 

16  Estimates of total Pb concentration in soils (based on fate and transport modeling using 

17 1997-2000 emissions data and data for similar locations measured in a 1995 study) 

18 exceeded screening values for plants, birds and mammals, indicating the potential for 

19 adverse effects to these groups. 

20  While the contributions from air-related Pb to the total Pb concentrations modeled in 

21 soils at this location is unclear, the facility continues to emit Pb and the county where 

22 this facility is located does not meet the current Pb standard (Appendix 5A). Given the 

23 exceedances of the current standard, which likely extends back over 4 to 5 decades, this 

24 case study also is not informative for considering the likelihood of adverse welfare 

25 effects related to Pb from air sources under air quality conditions associated with 

26 meeting the current Pb standard. 

27 Near Roadway Non-urban Case Study

28  This case study comprises two nonurban sites adjacent to established highways for 

29 which soil Pb data were available: (1) in Corpus Christi, Texas (ICF, 2006) and (2) in 

30 Atlee, Virginia (ICF, 2006). Measured soil concentration data were used to develop 

31 estimates of Pb in soils for each location. 

32  Estimates of total Pb concentrations taken in 1994 and 1998 in soils in this case study 

33 exceeded screening values for plants, birds and mammals, indicating the potential for 

34 adverse effect to these groups. 

35 These case study locations are highly impacted by past deposition of gasoline Pb. It is 

36 unknown whether current conditions at these sites exceed the current Pb standard but 

37 given evidence from the past of Pb concentrations near highways that ranged above the 

38 previous (1978) Pb standard (1986 CD, section 7.2.1), conditions at these locations 

39 during the time of leaded gasoline very likely exceeded the current standard. Similarly, 

40 those conditions likely resulted in Pb deposition associated with leaded gasoline that 

41 exceeds that being deposited under current air quality conditions that likely meet the 

42 current Pb standard. Given this legacy, consideration of the potential for 
January 2013 5-19 Draft - Do Not Quote or Cite

1 environmental risks from levels of air–related Pb associated with meeting the current 

2 Pb standard in these locations is highly uncertain. 

3 Vulnerable Ecosystem Case Study 

4  This case study was focused on consideration of information available for the Hubbard 

5 Brook Experimental Forest (HBEF) in the White Mountain National Forest near North 

6 Woodstock, New Hampshire, which included a long record (from 1976 through 2000) 

7 of available data on concentration trends of Pb in three media (air or deposition from 

8 air, soil, and surface water). 

9  While no quantitative analyses were performed, summary review of literature search 

10 indicated: (1) atmospheric Pb inputs do not directly affect stream Pb levels at HBEF 

11 because deposited Pb is almost entirely retained in the soil profile; (2) soil horizon 

12 analysis results showed Pb to have become more concentrated at lower soil depths over 

13 time, with the soil serving as a Pb sink, appreciably reducing Pb in pore water as it 

14 moves through the soil layers to streams (dissolved Pb concentrations were reduced 

15 from 5 ppb to about 5 ppt from surface soil to streams). Further, the available studies 

16 concluded insignificant contribution of dissolved Pb from soils to streams (ICF, 2006, 

17 Appendix E). It is unlikely that conditions have changed from the previous 

18 conclusions made based on soil data through 2000 and therefore, current ambient air 

19 concentrations likely do not directly impact stream Pb levels under air quality 

20 conditions associated with meeting the current standard.

21 National-scale Surface Water and Sediment Screen

22  The national-scale screen was performed using a national database of surface water and 

23 sediment monitoring data (see Appendix 5A; ICF, 2006). 

24  The screen identified 15 non-mining sites at which at least one surface water 

25 dissolved Pb concentration taken between 1994 and 2004 exceeded the chronic 

26 screening value, indicating a potential for adverse effect if concentrations were 

27 persistent over long time periods. The acute screening value was not exceeded 

28 at any of these locations. 

29  Analysis of the sediment concentrations for the 15 sites taken from 1991 to 

30 2000 analyzed in the surface water screen identified a subset for which 

31 concentrations exceeded the screening value, indicating a potential for adverse 

32 effects to sediment dwelling organisms. 

33  The extent to which past air emissions of Pb have contributed to surface water or 

34 sediment Pb concentrations at the locations identified in the screen is unclear. For 

35 some of the surface water locations, nonair sources likely contributed significantly to 

36 the surface water Pb concentrations. For other locations, a lack of nearby nonair 

37 sources indicated a potential role for air sources to contribute to observed surface water 

38 Pb concentrations. Additionally, these concentrations may have been influenced by Pb 

39 in resuspended sediments and/or reflect contribution of Pb from erosion of soils with 

40 Pb derived from historic as well as current air emissions. 

41 
January 2013 5-20 Draft - Do Not Quote or Cite

1 There are multiple sources of uncertainty associated with different aspects of this 

2 assessment (discussed in detail in 2006 REA, section 7.4). For example, there are significant 

3 limitations and uncertainties associated with conclusions that can be drawn from the primary 

4 smelter case study regarding the impact of atmospheric deposition under conditions associated 

5 with meeting the Pb NAAQS (past or present). Additionally, while case study locations were 

6 chosen with the objective of including locations for which recent Pb data were available and for 

7 which Pb exposures might be influenced by air-related Pb and not be dominated by nonair 

8 sources, there is significant uncertainty regarding the extent to which nonair sources and 

9 conditions associated with historic emissions (e.g., prior to establishment of past or present Pb 

10 NAAQS) have likely contributed to the Pb exposure estimates in some locations. The screening 

11 values available and used in the assessment were also sources of uncertainty with regard to 

12 conclusions as to potential for ecological risk as the selected screening values (e.g., ambient 

13 water quality criteria, Eco-SSLs, sediment criteria) lacked adjustment for some critical measures 

14 of bioavailability. There is also uncertainty regarding the extent to which the screening values 

15 could identify potential hazard for some threatened or endangered species or unusually sensitive 

16 aquatic ecosystems (ICF 2006). Thus, while the assessment results are generally consistent with 

17 evidence-based observations of the potential influence of Pb on ecological systems, they are 

18 limited with regard to quantitative conclusions and potential hazard or risk associated with the Pb 

19 NAAQS, most particularly with regard to the current standard. 

20  What are the important uncertainties associated with interpreting the prior 

21 assessment in light of newly available evidence in this review? 

22 In interpreting the results from the 2006 REA, we consider newly available evidence that 

23 may inform our interpretation of risk under the current standard. Factors necessary to alter our 

24 interpretation of risk would include new evidence of harm at lower concentrations of Pb, new 

25 linkages that enable us to draw more explicit conclusions as to the air contribution of 

26 environmental exposures, and/or new methods of interpreting confounding factors that were 

27 largely uncontrolled in the previous risk assessment. 

28 With regard to new evidence of harm at lower concentrations, it is necessary to consider 

29 that the evidence of adversity due specifically to Pb in natural systems is limited, in no small part 

30 because of the difficulty in determining the effects of confounding factors such as multiple 

31 metals and modifying factors influencing bioavailability in field studies. Modeling of Pb related 

32 exposure and risk to ecological receptors is subject to a wide array of sources of both variability 

33 and uncertainty. Variability is associated with geographic location, habitat types, physical and 

34 chemical characteristics of soils and water that influence Pb bioavailability, terrestrial and 

35 aquatic community composition, Pb uptake rates by invertebrates, fish, and plants by species and 

36 season. For wildlife, variability also is associated with food ingestion rates by species and 
January 2013 5-21 Draft - Do Not Quote or Cite

1 season, prey selection, and locations of home ranges for foraging relative to the Pb 

2 contamination levels (USEPA, 2006b). 

3 There are significant difficulties in quantifying the role of air emissions under the current 

4 standard, which is significantly lower than the previous standard. As recognized in section 1.3.2 

5 above, lead deposited before the standard was enacted remains in soils and sediments, 

6 complicating interpretations regarding the impact of the current standard; historic Pb emitted 

7 from leaded gasoline usage continues to move slowly through systems along with more recently 

8 deposited Pb and Pb derived from non air sources. The results from the location-specific case 

9 studies and the surface and sediment screen performed in the last review are difficult to interpret 

10 in light of the current standard and are not largely useful in informing our judgments of the 

11 potential for adverse effects at levels of deposition meeting the current standard. Under such 

12 constraints it is difficult to assess the merit of the risk findings from the previous review. 
January 2013 5-22 Draft - Do Not Quote or Cite

1 5.3 REFERENCES 

2 Buekers, J; Redeker, ES; Smolders, E. (2009). Lead toxicity to wildlife: Derivation of a critical blood 

3 concentration for wildlife monitoring based on literature data [Review]. Sci Total Environ 

4 407: 3431-3438. http://dx.doi.org/10.1016/j.scitotenv.2009.01.044 

5 Frey, C; Samet, JM. (2011). CASAC review of the EPA's integrated science assessment for lead 

6 (first external review draft- May 2011). (EPA-CASAC-12-002). Washington, DC: U.S. 

7 Environmental Protection Agency, Clean Air Scientific Advisory Committee. 

8 Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory 

9 Committee, to Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory 

10 Committee’s (CASAC) Review of the 1st Draft Lead Staff Paper and Draft Lead Exposure 

11 and Risk Assessments. March 27, 2007. 

12 Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory 

13 Committee, to Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory 

14 Committee’s (CASAC) Review of the 2nd Draft Lead Human Exposure and Health Risk 

15 Assessments. September 27, 2007. 

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

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

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

19 December. 

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

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

22 Environmental Contamination and Toxicology. 39:20-31. 

23 

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

25 (2003) Development and Evaluation of Numerical Sediment Quality Assessment Guidelines 

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

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

28 Protection, Tallahassee, FL. January. 

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

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

31 9285.7-55. November. 

32 U.S. Environmental Protection Agency. (2005b) Ecological Soil Screening Levels forLead, Interim 

33 Final. Washington, DC: Office of Solid Waste and Emergency Response. OSWER Directive 

34 9285.7-70. Available at http://www.epa.gov/ecotox/ecossl/pdf/eco-ssl_lead.pdf. 

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

36 EPA/600/R-5/144aF. Available online at: 

37 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html

38 U.S. Environmental Protection Agency. (2006b) Analysis Plan for Human Health and Ecological 
January 2013 5-23 Draft - Do Not Quote or Cite

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

2 Office of Air Quality Planning and Standards, Research Triangle Park, NC. Available at: 

3 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html

4 U.S. Environmental Protection Agency. (2007a). Framework for metals risk assessment [EPA 

5 Report]. (EPA 120/R-07/001). Washington, D.C. Available online at: 

6 http://www.epa.gov/raf/metalsframework/index.htm

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

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

9 Paper. Washington, DC, EPA-452/R-07-013. Available online at: 

10 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html

11 U.S. Environmental Protection Agency. (2012) Integrated Science Assessment for Lead (Third 

12 External Review Draft). Washington, DC, EPA/600/R-10/075C. Available online at: 

13 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html 
January 2013 6-1 Draft – Do Not Quote or Cite

1 6 REVIEW OF THE SECONDARY STANDARD FOR LEAD 

2 This chapter presents preliminary staff conclusions regarding the secondary Pb standard. 

3 These preliminary staff conclusions are guided by consideration of key policy-relevant questions 

4 and based on the assessment and integrative synthesis of information presented in the ISA and by 

5 staff analyses and evaluations presented in chapters 2 and 5 herein. Final evaluations and staff 

6 conclusions, to be developed taking into consideration CASAC advice and public comment on 

7 this draft document, will be presented in the final PA. The final evaluations and staff 

8 conclusions will inform the Administrator’s decisions on whether to retain or revise the existing 

9 secondary standard for Pb. 

10 Following an introductory section on the general approach for reviewing the secondary 

11 standard (section 6.1), including a summary of considerations in the last review, the discussion in 

12 this chapter focuses on the central issue of whether the information available in this review 

13 supports or calls into question the adequacy of the current secondary standard. Building on the 

14 responses to specific policy-relevant questions on the scientific evidence and exposure-risk 

15 information in chapter 5 above, presentation in section 6.2 is also organized into consideration of 

16 key policy-relevant questions framing evidence-based and exposure/risk-based considerations. 

17 The policy-relevant questions in this document are based on those included in the IRP (IRP, 

18 section 3.2). In section 6.3, preliminary staff conclusions are developed. Section 6.4 presents a 

19 brief overview of key uncertainties and areas for future research. 

20 6.1 APPROACH 

21 Staff’s approach for reviewing the current secondary standard, which involves translating 

22 scientific and technical information into the basis for addressing key policy-relevant questions, 

23 takes into consideration the approaches used in the previous Pb NAAQS review. The past and 

24 current approaches described below are all based most fundamentally on using EPA’s 

25 assessment of the current scientific evidence and previous quantitative analyses to inform the 

26 Administrator’s judgment with regard to the secondary standard for Pb. 

27 Staff final conclusions will be developed for the next version of this document with 

28 consideration of CASAC advice and public comment. In drawing conclusions regarding the 

29 secondary standard for the Administrator’s consideration, we note that the final decision on the 

30 adequacy of the current secondary Pb standard is largely a public welfare policy judgment to be 

31 made by the Administrator. The Administrator’s final decision draws upon scientific 

32 information and analyses about welfare effects, exposure and risks, as well as judgments about 

33 the appropriate response to the range of uncertainties that are inherent in the scientific evidence 

34 and analyses. This approach is consistent with the requirements of the NAAQS provisions of the 
January 2013 6-2 Draft – Do Not Quote or Cite

1 Act. Section 109 of the Clean Air Act requires the Administrator to establish a secondary 

2 standard that, in the judgment of the Administrator, is “requisite to protect the public welfare 

3 from any known or anticipated adverse effects associated with the presence of the pollutant in 

4 the ambient air”. In so doing, the Administrator seeks to establish standards that are neither 

5 more nor less stringent than necessary for this purpose. 

6 6.1.1 Approach Used in the Last Review 

7 The current secondary standard for Pb is equal to the primary standard for human health. 

8 As summarized in section 1.2.2 and described in more detail in section 4.1.1, the primary 

9 standard was substantially revised in the last review based on the much-expanded health effects 

10 evidence of neurocognitive effects of Pb in children. The level of the revised NAAQS is 0.15 

μg/m3 11 . The averaging time was also revised to a rolling three-month period with a maximum 

12 (not-to-be-exceeded) form, evaluated over a three-year period. Compared to the previous 

13 averaging time of one calendar quarter, this revision was considered to be more scientifically 

14 appropriate and more protective for human health. The indicator of Pb-TSP was retained, 

15 reflecting the evidence that Pb particles of all sizes pose health risks (73 FR 67007). 

16 The scientific assessment for the last review is described in the 2006 Air Quality Criteria 

17 for Lead (AQCD; USEPA, 2006b), multiple drafts of which received review by CASAC and the 

18 public. EPA also conducted a pilot ecological risk assessment for the review, after consultation 

19 with CASAC and receiving public comment on a draft analysis plan (USEPA, 2006c). The pilot 

20 ecological risk assessment was released in December 2006 (ICF, 2006) and the policy 

21 assessment based on these assessments, air quality analyses and key evidence from the AQCD 

22 was presented in the Staff Paper (USEPA, 2007b), a draft of which also received CASAC and 

23 public review. The final Staff Paper presented OAQPS staff’s evaluation of the public health and 

24 welfare policy implications of the key studies and scientific information contained in the 2006 

25 CD and presented and interpreted results from the pilot risk/exposure analyses conducted for this 

26 review. Based on this evaluation, the Staff Paper presented OAQPS staff recommendations that 

27 the Administrator give consideration to substantially revising the primary and secondary 

28 standards to a range of levels at or below 0.2 μg/m3. 

29 In the previous review, the Administrator considered the evidence-based information 

30 presented in the CD and the risk-based information presented in the 2006 REA. It was his 

31 conclusion that the available data and evidence, while primarily qualitative, suggested that there 

32 was the potential for adverse environmental impacts under the then-current standard. Given the 

33 limited data on Pb effects in ecosystems, it was at the time, as it is now, necessary to look at 

34 evidence of Pb effects on organisms and extrapolate to ecosystem effects. Therefore, taking into 

35 account the available evidence and current media concentrations in a wide range of areas, the 
January 2013 6-3 Draft – Do Not Quote or Cite

1 Administrator concluded that there was potential for adverse effects occurring under the then2 current standard; however there was insufficient data to provide a quantitative basis for setting a 

3 secondary standard different than the primary (73 FR 67011). Therefore, citing a general lack of 

4 data that would indicate the appropriate level of Pb in environmental media that may be 

5 associated with adverse effects, as well as the comments of the CASAC Pb panel that a 

6 significant change to current air concentrations (e.g., via a significant change to the standard) 

7 was likely to have significant beneficial effects on the magnitude of Pb exposures in the 

8 environment, the secondary standard was revised to be consistent with the revised primary 

9 standard (73 FR 67011). 

10 6.1.2 Approach for the Current Review 

11 In evaluating whether it is appropriate to consider retaining the current secondary Pb 

12 standard, or whether consideration of revision is appropriate, we have adopted an approach in 

13 this review that builds on the general approach from the last review and reflects the body of 

14 evidence and information now available. As summarized above, the Administrator’s decisions in 

15 the previous review were based on the conclusion that there was the potential for adverse 

16 ecological effects under the previous standard. In our approach here, we intend to focus on 

17 consideration of the extent to which a broader body of scientific evidence is now available that 

18 would inform decisions on either the potential for adverse effects to ecosystems under the current 

19 standard or the ability to set a more ecologically relevant secondary standard than was feasible in 

20 the previous review. In conducting this assessment, we draw on the ecological effects evidence 

21 presented in detail in the ISA, and aspects summarized above in chapter 5, along with the 

22 information associated with the screening-level risk assessment also summarized above. Figure 

23 6-1 illustrates the basic construct of our approach in developing conclusions regarding options 

24 appropriate for the Administrator to consider in this review with regard to the adequacy of the 

25 current secondary NAAQS standard and, as appropriate, potential alternate standards. 

26 In developing preliminary conclusions in this review, we have taken into account both 

27 evidence-based and risk-based considerations framed by a series of policy-relevant questions. 

28 These questions are outlined in the sections below and generally discuss the extent to which we 

29 are able to better characterize effects and the likelihood of adverse effects in the environment 

30 under the current standard. Our approach to considering these questions recognizes that the 

31 available welfare effects evidence generally reflects laboratory-based evidence of toxicological 

32 effects on specific organisms exposed to concentrations of Pb at which scientists generally agree 

33 that adverse effects are likely to occur. It is widely recognized, however, that environmental 

34 exposures from atmospherically-derived Pb are likely to be lower and/or accompanied by 
January 2013 6-4 Draft – Do Not Quote or Cite

1 significant confounding and modifying factors (e.g., other metals, acidification), which increases 

2 our uncertainty about the likelihood and magnitude of organism and ecosystem responses. 

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

Evidence-based Considerations

 Does currently available evidence and related 

uncertainties strengthen or call into question prior 

conclusions?

 Evidence of welfare effects not previously identified 

or at lower exposures?

 Newly identified at-risk ecosystems?

Changed understanding of 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 Consideration
January 2013 6-5 Draft – Do Not Quote or Cite

1 6.2 ADEQUACY OF THE CURRENT STANDARD 

2 In considering the adequacy of the current Pb standard, the overarching question we 

3 consider is:

4  Does the currently available scientific evidence- and exposure/risk-based 

5 information, as reflected in the ISA and REA, support or call into question the 

6 adequacy of the protection afforded by the current Pb standard? 

7 To assist us in interpreting the currently available scientific evidence and screening-level 

8 risk information to address this question, we have focused on a series of more specific questions, 

9 posed within sections 6.2.1 and 6.2.2 below. In so doing, we consider both the information 

10 available at the time of the last review and information newly available since the last review 

11 which has been critically analyzed and characterized in the ISA. 

12 6.2.1 Evidence-based Considerations 

13 In considering the welfare effects evidence with respect to the adequacy of the current 

14 standard, we must consider the array of evidence newly assessed in the ISA and the degree to 

15 which the newly available evidence supports previous conclusions about the effects of Pb in the 

16 environment and the extent to which it reduces areas of uncertainty recognized in decisions on 

17 the secondary standard in the last review. Additionally, as the secondary standard set in 2008 is 

18 significantly lower than the previous standard, which was the focus of evaluation in the last 

19 review, we must consider the extent to which the current evidence supports conclusions about 

20 the effects of current ambient levels under the current standard and the extent to which the 

21 evidence supports or calls into question the adequacy of protection afforded by the current 

22 standard. 

23  To what extent does the available information indicate that Pb-related effects are 

24 occurring as a result of multimedia pathways associated with ambient air 

25 conditions that would meet the current standard? 

26 The current evidence continues to support our conclusions from the previous review 

27 regarding key aspects of the ecological effects evidence for Pb and the effects of exposure 

28 associated with levels of Pb occurring through ecological media in the U.S. Our conclusions in 

29 this regard are based on consideration of the assessment of the currently available evidence in the 

30 ISA, particularly with regard to key aspects summarized in chapter 5 of this PA, in light of the 

31 assessment of the evidence in the last review as described in the 2006 CD and summarized in the 

32 notice of final rulemaking (73 FR 67008). Key aspects of these previous conclusions are 

33 summarized below. 

34  Deposition of gasoline-derived Pb into forest soils has produced a legacy of slow 

35 moving Pb that remains bound to organic materials despite the removal of Pb from 
January 2013 6-6 Draft – Do Not Quote or Cite

1 most fuels and the resulting dramatic reductions in overall deposition rates (2006 CD, 

2 Section AX7.1.4.3). 

3  For areas influenced by point sources of air Pb that meet the standard considered in the 

4 previous review, concentrations of Pb in soil may exceed by many orders of magnitude 

5 the concentrations which are considered harmful to laboratory organisms (2006 CD, 

6 Section 3.2 and AX7.1.2.3). 

7  Some Pb deposited before the previous standard was enacted is still present in soils and 

8 sediments; historic Pb from gasoline continues to move slowly through systems as does 

9 current Pb derived from both air and nonair sources. 

10  The evidence of adversity in natural systems is very sparse due in no small part to the 

11 difficulty in determining the effects of confounding factors such as multiple metals or 

12 factors influencing bioavailability in field studies. 

13  Environmental conditions exist in which Pb-associated adverse effects to aquatic 

14 organisms and thereby ecosystems may be anticipated given experimental results. 

15  Some areas with long term historical deposition of Pb to sediment from a variety of 

16 sources as well as areas influenced by point sources have the potential for adverse 

17 effects to aquatic communities (2006 CD, Sections AX7.2.2.2.2 and AX7.2.4). 

18 The range of effects of Pb on terrestrial and aquatic organisms based on new information 

19 in the current review are summarized in the ISA (ISA, section 2.7 and section 7.3 and 7.4) and 

20 largely mirror the conclusions presented above from the previous review. 

21 The integrated synthesis contained in the ISA conveys how effects of Pb can vary with 

22 species and life stage, duration of exposure, form of Pb, and media characteristics such as soil 

23 and water chemistry. A wide range of organism effects are recognized, including effects on 

24 growth, development (particularly of the neurological system) and reproductive success (ISA, 

25 section 7.3 and section 7.4). Lead is recognized to distribute from the air into multiple 

26 environmental media, as summarized in section 1.3 above, contributing to multiple exposure 

27 pathways for ecological receptors. As discussed in section 5.1 above, many factors affect the 

28 bioavailability of Pb to receptors in terrestrial and aquatic ecosystems, contributing to differences 

29 between laboratory-assessed toxicity and Pb toxicity in these ecosystems, challenging our 

30 consideration of environmental impacts of Pb emitted to ambient air. 

31 In studies in a variety of ecosystems, adverse ecosystem-level effects (including 

32 decreases in species diversity, loss of vegetation, changes to community composition, decreased 

33 growth of vegetation, and increased number of invasive species) have been demonstrated near 

34 smelters, mines and other industries that have released Pb, among other materials (ISA, section 

35 7.3.12 and 7.4.12). As noted in section 5.1 above, however, our ability to characterize the role of 

36 air emissions of Pb in contributing to these effects is complicated because of coincident releases 

37 to other media and of other pollutants. Co-released pollutants include a variety of other heavy 

38 metals, in addition to sulfur dioxide, which may cause toxic effects in themselves and may 
January 2013 6-7 Draft – Do Not Quote or Cite

1 interact with Pb in the environment. There is also some uncertainty as to the extent to which Pb 

2 in ambient air is contributing to the exposure. These uncertainties limit our ability to draw 

3 conclusions regarding the extent to which Pb-related effects may be associated with ambient air 

4 conditions that would meet the current standard. 

5 The role of historically emitted Pb, as discussed in section 1.3.2 above, poses additional 

6 complications in addressing this question. The vast majority of Pb in the environment today, 

7 particularly in terrestrial ecosystems, was deposited in the past during the use of Pb additives in 

8 gasoline (USEPA 2007b, section 6.2.1) although industrial coal use has also been documented as 

9 a significant source as well (ISA, section 3.2.1). This gasoline-derived Pb was emitted in very 

10 large quantities (CD, pl AX7-98 and ISA, Figure 3-8) and predominantly in small sized particles 

11 which were widely dispersed and transported across large distances (ISA, section 3.2). As 

12 recognized in section 2.3.1 and 2.3.3.2 above, historical records provided by sediment cores in 

13 various environments document the substantially reduced Pb deposition (associated with reduced 

14 Pb emissions) in many locations (ISA, section 3.2.1). As Pb is extremely persistent in the 

15 environment, past environmental releases are expected to generally dominate current media 

16 concentrations. There is limited evidence to relate specific ecosystem effects with current 

17 ambient air concentrations of Pb through deposition to terrestrial and aquatic ecosystems and 

18 subsequent movement of deposited Pb through the environment (e.g., soil, sediment, water, 

19 organisms). The potential for ecosystem effects of Pb from atmospheric sources under conditions 

20 meeting the current standard is difficult to assess due to limitations on available information not 

21 only on bioavailability (as affected by the specific characteristics of the receiving ecosystem), 

22 but also information to fully characterize the distribution of Pb from the atmosphere into 

23 ecosystems in long-term exposure scenarios. Therefore, the connection between air concentration 

24 and ecosystem exposure and associated potential for welfare effects continues to be poorly 

25 characterized for Pb (ISA, Section 7.5), and is even harder to characterize with respect to the 

26 current standard than it was in last review with respect to the previous standard. 

27  To what extent have important uncertainties identified in the last review been 

28 reduced and/or have new uncertainties emerged? 

29 With regard to uncertainties in effects associated with Pb in the ambient air, the last 

30 review illustrated the largest of these uncertainties were the ability to determine the prevalence of 

31 effects in the natural environment, the ability to apportion effects between air and nonair sources, 

32 and the understanding of the effects in the context of the current standard (IRP, section 3.2). 

33 While we have some new evidence with regard to bioavailability and its role in determining 

34 effects, overall these remain the major sources of uncertainty in evaluating effects and exposure 

35 evidence for Pb in ecosystems. 
January 2013 6-8 Draft – Do Not Quote or Cite

1 With regard to the prevalence of effects in the natural environment, it remains difficult to 

2 assess the concentration at which Pb elicits a specific effect in terrestrial and aquatic systems, 

3 due to the influence of other environmental variables on both Pb bioavailability and toxicity, and 

4 also due to substantial species differences in Pb susceptibility. There is little new information 

5 that would facilitate extrapolation of evidence on individual species, generally from controlled 

6 laboratory studies, to conclusions regarding adversity to populations or ecosystems within the 

7 natural environment. For example, in terrestrial systems, evidence reviewed in the ISA (ISA, 

8 Sections 7.2.3 and 7.2.4) demonstrates that exposure to Pb is generally associated with negative 

9 effects on growth, reproduction and survival in terrestrial ecosystems. Many factors, including 

10 species composition and various soil physiochemical properties, interact strongly with Pb 

11 concentration to modify effects. Also, Pb aging is a particularly important factor in terrestrial 

12 systems, where soil is the main route of exposure, and it is difficult to reproduce experimentally. 

13 Without quantitative characterization of those interactions, characterizations of exposure14 response relationships would likely not be transferable outside of experimental settings (ISA, 

15 Section 2.7.1).

16 As reported in the ISA, there continues to be limited evidence linking current ambient 

17 air sources of Pb through deposition to environmental media (e.g., soil, sediment, water, and 

18 biota) and to ecological effects (ISA, section 7.3.11). The ability to apportion effects between air 

19 deposited Pb and nonair sources is difficult to assess due to a lack of information not only on the 

20 bioavailability of that Pb, which is greatly influenced by the specific characteristics of the 

21 receiving ecosystem, but also on Pb distribution in ecosystems in long-term exposure scenarios. 

22 Consideration of the environmental risks associated with the current standard is 

23 complicated by the environmental burden associated with air Pb concentrations, predominantly 

24 in the past, that exceeded the current standard (USEPA, 2007b, section 6.4.4.2). For example, a 

25 large portion of Pb deposited before the standard was enacted is likely still present in soils and 

26 sediments and historic Pb from gasoline continues to move slowly through systems as does 

27 current Pb derived from both air and nonair sources. As a general matter, the currently available 

28 evidence, as assessed in the ISA, does not significantly reduce any of these areas of uncertainty 

29 or inform our consideration of the adequacy of the current standard. 

30 
January 2013 6-9 Draft – Do Not Quote or Cite

1 6.2.2 Exposure/Risk-based Considerations 

2 

3  To what extent does risk or exposure information indicate that air-related 

4 ecosystem exposures important from a public welfare perspective are likely to 

5 occur with air Pb levels that just meet the current standard? 

6 The current evidence continues to support our conclusions with regard to interpreting the 

7 risk and exposure results from the previous review. Our conclusions in this regard are based on 

8 consideration of the screening-level ecological risk assessment results from the previous review 

9 in light of the currently available evidence in the ISA and as described in the 2006 REA and 

10 summarized in the notice of final rulemaking (73 FR 67009). Key aspects of these results in the 

11 context of the current standard are summarized below, drawing from the discussion of the 2006 

12 REA results in section 5.2.2 above, which is based on the information in the 2006 REA (ICF, 

13 2006). 

14 Primary Pb Smelter Case Study

15  While the contribution to Pb concentrations from air as compared to nonair sources is 

16 not quantified, air emissions from this facility are substantial (ICF 2006). Currently, 

17 the county where this facility is located exceeds the now current Pb NAAQS. 

18 Secondary Pb Smelter Case Study

19  While the contribution from air deposited Pb to the overall Pb concentrations modeled 

20 in soils at this location is unclear, the facility continues to emit Pb and the county 

21 where this facility is located exceeds the now current Pb NAAQS (Appendix 5-A). 

22 Near Roadway Non-urban Case Study

23  These case study locations are highly impacted by past deposition of gasoline Pb. It is 

24 unknown whether current conditions at these sites exceed the now current Pb standard 

25 but given evidence from the past of Pb concentrations near highways that ranged above 

26 the previous (1978) Pb standard (1986 CD, section 7.2.1), conditions at these locations 

27 during the time of leaded gasoline very likely exceeded the 1978 standard. 

28 Vulnerable Ecosystem Case Study 

29  The previous review concluded that atmospheric Pb inputs do not directly affect stream 

30 Pb levels at Hubbard Brook Experimental Forest because deposited Pb is almost 

31 entirely retained in the soil profile. It is unlikely that conditions have changed from the 

32 previous conclusions made based on soil data through 2000 and therefore, current 

33 ambient air concentrations likely do not directly impact stream Pb levels under air 

34 quality conditions associated with meeting the now current standard. 

35 National-scale Surface Water and Sediment Screen

36  The extent to which past air emissions of Pb have contributed to surface water or 

37 sediment Pb concentrations at the locations identified in the screen is unclear. For 

38 some of the surface water locations, nonair sources likely contributed significantly to 
January 2013 6-10 Draft – Do Not Quote or Cite

1 the surface water Pb concentrations. For other locations, a lack of nearby nonair 

2 sources indicated a potential role for air sources to contribute to observed surface water 

3 Pb concentrations. Additionally, these concentrations may have been influenced by Pb 

4 in resuspended sediments and/or reflect contribution of Pb from erosion of soils with 

5 Pb derived from historic as well as current air emissions. 

6 

7 Although the available risk and exposure information continues to be sufficient to 

8 conclude that the 1978 standard was not providing adequate protection to ecosystems, that 

9 information, when considered with regard to air-related ecosystem exposures likely to occur with 

10 air Pb levels that just meet the now current standard, does not provide evidence that the current 

11 secondary standard is inadequate. 

12 6.3 PRELIMINARY STAFF CONCLUSIONS ON THE SECONDARY STANDARD 

13 This section describes preliminary staff conclusions regarding adequacy of the current 

14 secondary Pb standard. These conclusions are based on considerations described above and in 

15 the discussion below regarding the currently available scientific evidence summarized in the 

16 third draft ISA and prior CDs and the risk and exposure information drawn from the 2006 REA. 

17 The final PA will draw upon the final ISA, developed after CASAC review and public comment 

18 on the third draft ISA. Staff conclusions presented in the final PA will take into account advice 

19 from CASAC and public comment on this document and these draft conclusions. 

20 Taking into consideration the discussions responding to specific questions above in this 

21 and the prior chapter, this section addresses the following overarching policy question: 

22  Does the currently available scientific evidence- and exposure/risk-based 

23 information, as reflected in the ISA and REA, support or call into question the 

24 adequacy of the protection afforded by the current secondary Pb standard? 

25 With respect to evidence-based considerations, staff gives weight to the body of evidence 

26 on the ecological effects of Pb in the natural environment, expanded in some aspects since the 

27 last review, which continues to support identification of ecological effects in organisms relating 

28 to growth, reproduction, and survival as the most relevant endpoints associated with Pb 

29 exposure. The currently available evidence, while somewhat expanded since the last review, 

30 does not include evidence of significant effects at lower concentrations or evidence of higher 

31 level ecosystem effects beyond those reported in the last review. There continues to be 

32 significant difficulties in interpreting effects evidence from laboratory studies to the natural 

33 environment and linking those effects to ambient air Pb concentrations. Further, we are aware of 

34 no new critical loads information that would inform our interpretation of the public welfare 

35 significance of the effects of Pb in various ecosystems. In summary, while new research has 

36 added to the understanding of Pb biogeochemistry and expanded the list of organisms for which 
January 2013 6-11 Draft – Do Not Quote or Cite

1 Pb effects have been described, there remains a significant lack of knowledge about the potential 

2 for adverse effects from ambient air Pb in the environment and the exposures that occur from 

3 such air-derived Pb, particularly under the current standard. 

4 With respect to exposure/risk-based considerations, we recognize the complexity of 

5 interpreting the previous risk assessment with respect to ambient air Pb under the current 

6 standard and the associated limitations and uncertainties of such assessments. For example, the 

7 location-specific case studies as well as the national screen reflect both current air Pb deposition 

8 as well as past air and nonair source contributions. We conclude that while the previous 

9 assessment is consistent with and generally supportive of the evidence-based conclusions about 

10 Pb in the environment the limitations of apportioning Pb between past and present air 

11 contributions and between air and nonair sources remain significant. 

12 In making the decision on revision of the secondary standard in the last review, the 

13 Administrator concurred with the conclusions by CASAC that we lack the relevant data to 

14 provide a clear quantitative basis for setting a secondary Pb NAAQS that differs from the 

15 primary in indicator, averaging time, level or form. As a result, the Administrator revised the 

16 secondary standard to be identical in all respects to the primary standard (73 FR 67012). 

17 In now considering the adequacy of the current standard in this review, we have 

18 considered evidence assessed in the ISA and discussed in sections 5.1, 2.3 and 6.2.1 above, as 

19 well as information gained from the 2006 REA discussed in sections 5.2 and 6.2.2 above. As 

20 summarized in section 6.2.1 above, the scientific evidence presented in detail in the ISA, 

21 inclusive of that newly available in this review, is not substantively changed, most particularly 

22 with regard to our needs in reviewing the current standard, from the information that was 

23 available in the last review. Further, our updated consideration of the screening-level risk 

24 information from the 2006 REA, as summarized in section 6.2.2 above, additionally does not 

25 provide alternative conclusions with regard to a basis for judging the adequacy of the current 

26 standard. Thus, while the current secondary standard is not expressed in elements derived from 

27 ecological effects evidence, we preliminarily conclude that the currently available information 

28 does not call into question the adequacy of the current standard to provide the requisite 

29 protection for public welfare. In addition, as in the last review, there continues to be insufficient 

30 data to provide a quantitative basis for setting a secondary standard different than the primary 

31 standard. Accordingly, we reach the preliminary conclusion that it is appropriate to consider 

32 retaining the current standard without revision. This preliminary conclusion is based on 

33 consideration of the welfare effects evidence in combination with the screening-level 

34 exposure/risk information (chapter 5 and sections 6.2.1 and 6.2.2 above) and staff judgments on 

35 the associated public welfare implications. 
January 2013 6-12 Draft – Do Not Quote or Cite

1 6.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA 

2 COLLECTION 

3 In this section, we highlight key uncertainties associated with reviewing the secondary 

4 NAAQS for Pb. Such key uncertainties and recommendations for ecosystem-related research, 

5 model development, and data gathering are outlined below. In some cases, research in these 

6 areas can go beyond aiding standard setting to aiding in the development of more efficient and 

7 effective control strategies. We note, however, that a full set of research recommendations to 

8 meet standards implementation and strategy development needs is beyond the scope of this 

9 discussion. Rather, listed below are key uncertainties and research questions and data gaps that 

10 have been thus far highlighted in this review of the health-based primary standard. 

11  An important source of uncertainty in characterizing the effects of air related Pb in the 

12 environment is the ability to apportion the sources of Pb to specific ecosystems. 

13  It is difficult to identify the atmospheric component of Pb deposited in ecosystems 

14 from other sources of Pb. Without such information, it is not possible to determine 

15 the appropriately protective air concentrations of Pb. 

16  Development of critical loads information for various ecosystems would allow for a 

17 much improved understanding of the significance of air contributions to 

18 ecosystems. 

19  There is significant uncertainty regarding the timeframes under which Pb currently in 

20 the environment was deposited. 

21  In general, the connection between air concentration of Pb and ecosystem exposure 

22 continues to be poorly characterized.

23  There is uncertainty in characterizing the fate and transport of Pb in the 

24 environment through air, water, and soil media, especially in ecosystems. This 

25 limits our ability to account for past Pb exposures in current media concentrations 

26 and to link effects to current air contributions. 

27  Our understanding of the degree of adverse impact that is occurring in the environment 

28 due to Pb is incomplete and leads to uncertainty in interpreting the significance of 

29 effects at specific endpoints. 

30  Critical loads are important to capture the variability of response across ecosystems 

31 to determine which ecosystems are most sensitive and additional research is needed 

32 to provide inputs for development of critical loads, particularly for a broader range 

33 of ecosystem level endpoints. 

34  The available studies on community and ecosystem-level effects are sparse and 

35 usually from contaminated areas where Pb concentrations are much higher than 

36 typically encountered in the environment.

37  The role of modifying factors on Pb toxicity continues to be a source of uncertainty 

38 when determining the degree of adverse impact from Pb.
January 2013 6-13 Draft – Do Not Quote or Cite

1  Evidence regarding relationships between organism-level effects of Pb (e.g., 

2 reproduction, growth, and survival) and effects at the population level and higher, 

3 is lacking especially in natural systems. 

4  Better indicators of Pb effects are needed in estuarine and marine systems to allow 

5 us to understand the potential for adverse effects from Pb in these environments. 

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

1 6.5 REFERENCES 

2 Frey, C; Samet, JM. (2011). CASAC review of the EPA's integrated science assessment for lead 

3 (first external review draft- May 2011). (EPA-CASAC-12-002). Washington, DC: U.S. 

4 Environmental Protection Agency, Clean Air Scientific Advisory Committee. 

5 Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory 

6 Committee, to Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory 

7 Committee’s (CASAC) Review of the 1st Draft Lead Staff Paper and Draft Lead 

8 Exposure and Risk Assessments. March 27, 2007. 

9 Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory 

10 Committee, to Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory 

11 Committee’s (CASAC) Review of the 2nd Draft Lead Human Exposure and Health Risk 

12 Assessments. September 27, 2007. 

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

14 Risk Assessment for Selected Areas. Pilot Phase. Draft Technical Report. Prepared for 

15 the U.S. EPA's Office of Air Quality Planning and Standards, Research Triangle Park, 

16 NC. December. 

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

18 EPA/600/R-5/144aF. Available online at: 

19 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html 

20 U.S. Environmental Protection Agency. (2012) Integrated Science Assessment for Lead (Third 

21 External Review Draft). Washington, DC, EPA/600/R-10/075C. Available online at: 

22 http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html 
January 2013 Draft – Do Not Quote or Cite 

APPENDICES 

 Appendix 2A. The 2008 NEI: Data Sources, 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 Ecological Screening Assessment ........................ 5A-1 
January 2013 2A-1 Draft - Do Not Quote or Cite

1 APPENDIX 2A 

2 THE 2008 NEI: DATA SOURCES, LIMITATIONS AND 

3 CONFIDENCE 

4 The process of identifying sources that emit Pb into the air has been ongoing since before 

5 the Clean Air Act of 1970. The comprehensiveness of emission inventories generally, and the 

6 NEI, specifically, depends upon knowledge of source types emit Pb, their locations and their 

7 operating characteristics, as well as the reporting of this information to the inventory. As noted 

8 above, the NEI relies on information that is available from a variety of sources for this 

9 information. There are numerous steps, each with its own uncertainties, associated with the 

10 development of this information for use in the emissions inventory. First, the categories emitting 

11 Pb must be identified. Second, the sources’ processes and control devices must be known. 

12 Third, the activity throughputs and operating schedules of these sources must be known. Finally, 

13 we must have emission factors to relate emissions to the operating throughputs, process 

14 conditions and control devices. The process, control device, throughputs and operating 

15 schedules are generally available for each source. However, the emission factors represent 

16 average emissions for a source type and average emissions may differ significantly from source 

17 to source. In some cases, emissions testing provides source-specific information. In others, 

18 emissions factors must be estimated from similar sources or source categories, or from other 

19 information. More information on emission factors and the estimation of emissions is found in 

the introduction to EPA’s Compilation of Air Pollutant Emissions Factors.1 20 

21 The Pb emissions information presented in chapter 2 is drawn largely from EPA’s NEI 

22 for 2008. The NEI is based on information submitted from State, Tribal and local air pollution 

23 agencies and data obtained during the preparation of technical support information for EPA’s 

24 hazardous air pollutant regulatory programs. Data in the 2008 NEI for Pb emissions from the 

25 use of leaded aviation gasoline were developed by EPA using the Federal Aviation 

Administration’s operations activity data, where available.2 26 The data were then reviewed by 

27 State, Tribal, and local air pollution agencies. With some additions, the information presented in 

28 this document is primarily based on version 3 of the NEI for 2008, available on the EPA’s 

29 CHIEF website at (http://www.epa.gov/ttn/chief/net/2008inventory.html). The NEI is limited 

 

1

 U.S. Environmental Protection Agency. (1996-2011) . AP-42, Compilation of Air Pollutant Emission 

Factors, 5th Edition. Volume 1: Stationary Point and Area Sources, Chapter 13: Miscellaneous Sources. Available 

at: http://www.epa.gov/ttn/chief/ap42/ch13/index.html. Further information on emission 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

1 with regard to Pb emissions estimates for some sources. For example, we have not yet 

2 developed estimates for the NEI of Pb emissions for the miscellaneous categories of on-road 

3 emissions (e.g., combustion of fuel with Pb traces, lubricating oil, mechanical wear of vehicle 

4 components, etc.) and Pb that may be emitted from wildfires, or for emissions associated with 

5 resuspension of Pb residing in roadway dust and nearby surface soil in areas not otherwise 

6 associated with industrial facilities (see section 2.1.2). 

7 The 2008 NEI underwent extensive external review, including a review of the process for 

8 developing the inventory which includes extensive quality assurance and quality control steps 

9 (QA/QC). We provided feedback reports to point source data providers and we posted several 

10 versions of the inventory on our website. We also conducted additional QA targeted at facilities 

11 with appreciable Pb emissions in previous years to ensure that 2008 Pb emissions were reported, 

12 and we augmented with TRI where facilities with annual emissions greater than 0.5 tpy in 2005 

13 were not reported to NEI in 2008 due to Pb emissions reporting thresholds 

14 (ftp://ftp.epa.gov/EmisInventory/20008v2/doc/2008neiv2_issues.xlsx). Further, there was 

15 additional QA/QC conducted for emission inventory information for facilities that are included 

in Risk and Technology Review source categories.3 16 As a result we have strong confidence in the 

17 quality of the data for these facilities. In summary, generic limitations to the 2008 NEI include 

18 the following. 

19  Consistency: The 2008 NEI for Pb is a composite of emissions estimates generated by 

20 state and local regulatory agencies, industry, and EPA. Because the estimates 

21 originated from a variety of sources, as well as for differing purposes, they will in turn 

22 vary in quality, whether Pb is reported for particular source types, method of reporting 

23 compound classes, level of detail, and geographic coverage. 

24  Variability in Quality and Accuracy of Emission Estimation Methods: The accuracy of 

25 emission estimation techniques varies with pollutants and source categories. In some 

26 cases, an estimate may be based on a few or only one emission measurement at a 

27 similar source. The techniques used and quality of the estimates will vary between 

28 source categories and between area, major, and mobile source sectors. Generally, the 

29 more review and scrutiny given to emissions data by states and other agencies, the 

30 more certainty and accuracy there is in those estimates. 

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 risk assessments on each source category subject to MACT 

standards, and to determine if additional standards are needed to reduce residual risks. Section 112(d)(6) of the CAA 

requires EPA to review and revise the MACT standards, as necessary, taking into 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

1 APPENDIX 2B 

2 RECENT REGULATORY ACTIONS ON STATIONARY SOURCES OF LEAD 

3 The table below identifies recent regulatory actions on stationary sources estimated to 

4 result in reductions in lead emissions. 

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 Manufacturing, 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 Standards for Aluminum, Copper, and Other 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

5 
January 2013 2C-1 Draft - Do Not Quote or Cite

1 APPENDIX 2C 

2 CRITERIA FOR AIR QUALITY DATA ANALYSIS 

3 Criteria for the 2009-2011 data analysis presented in Figures 2-10 through 2-13 are as 

4 listed below, with abbreviations defined following this list. 

5  Years utilized were 2009-2011. November and December 2008 data were also used for 

6 rolling 3-month average analysis. 

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

8  Data for parameters 12128 (STP) and 14129 (LC) were used for Pb-TSP analysis; data 

9 for parameters 84128 (STP) and 88128 (LC) were used for Pb-PM2.5 analysis; and data 

10 for parameters 82128 (STP) and 85128 (LC) were used for Pb-PM10 analysis. No 

11 adjustment was made to the STP or LC data to make them more comparable to each 

12 other; based on previous analysis, the LC and STP versions of same-site-day samples 

13 are extremely similar. Collocated data – for same size cut- were combined to a site 

14 basis by using the following hierarchy, evaluated each site-day: LC parameter data 

15 takes precedence over STP parameter data and lower POC numbers take precedence 

16 over higher POC numbers. 

17  For maximum rolling 3-month average analysis, the 2009-2011 databases also 

18 encompassed the prior 2 months (i.e., November and December 2008 data): 3 or more 

19 observations were needed to make a valid monthly average (for Pb-TSP, the daily data 

20 had to be collected/analyzed via an FRM or FEM); 3 valid consecutive months were 

21 required to make a valid rolling 3-month period; 6 valid rolling 3-month periods were 

22 required to make a valid year; and 1, 2, or 3 valid years were required to make a valid 

23 3-month metric. The rolling 3-month average metric (by size cut for 2009-2011) was 

24 identified as the highest valid 3-month average across the valid (1, 2, or 3) years. 

25  For maximum monthly analysis: 3or more observations were needed to make a valid 

26 monthly average (for Pb-TSP, the daily data had to be collected/analyzed via an FRM 

27 or FEM); 6 valid months were required to make a valid year; and 1, 2, or 3 valid years 

28 were required to make a valid monthly metric. The maximum monthly metric (by size 

29 cut for 2009-2011) was identified as the highest valid monthly average across the valid 

30 (1, 2, or 3) years. 

31  For annual average analysis: monthly averages were used to construct annual averages, 

32 3 or more observations were required to make a valid month (for Pb-TSP, the daily 

33 data had to be collected/analyzed via an FRM or FEM); 6 valid months were required 

34 to make a valid year (i.e., annual average) and 1, 2, or 3 valid years were required to 

35 make a valid annual metric. The annual metric (by size cut for 2009-2011) was 

36 identified as the average of the 1, 2, or 3 (2009, 2010, and/or 2011) valid annual means. 

37 
January 2013 2C-2 Draft - Do Not Quote or Cite

1 Definitions for Abbreviations

2 FEM – Federal equivalent method 

3 FRM – Federal reference method 

4 LC – Local conditions 

5 POC – Parameter occurrence code 

6 STP – Standard temperature and pressure 
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2009-2011.

Appendix 2D - Air Quality Data Analysis Summary

SITE

Max 3-month 

Mean (ug/m3

)

Annual Mean 

(ug/m3

)

Max Monthly 

Mean (ug/m3)

previous 

source

current 

source State County

011090003 1.035 0.564 2.069 0 1 Alabama Pike County

040071002 0.267 0.133 0.306 0 1 Arizona Gila County

040078000 0.061 0.033 0.077 0 1 Arizona Gila County

040134018 0.033 0.023 0.042 0 0 Arizona 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 Arapahoe 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 Cite
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2009-2011.

Appendix 2D - Air Quality Data Analysis Summary

SITE

Max 3-month 

Mean (ug/m3

)

Annual Mean 

(ug/m3

)

Max Monthly 

Mean (ug/m3)

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 Anoka 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 Cite
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2009-2011.

Appendix 2D - Air Quality Data Analysis Summary

SITE

Max 3-month 

Mean (ug/m3

)

Annual Mean 

(ug/m3

)

Max Monthly 

Mean (ug/m3)

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 Cite
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2009-2011.

Appendix 2D - Air Quality Data Analysis Summary

SITE

Max 3-month 

Mean (ug/m3

)

Annual Mean 

(ug/m3

)

Max Monthly 

Mean (ug/m3)

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 Allegheny County

420030008 0.014 0.01 0.02 0 0 Pennsylvania Allegheny County

420030070 0.056 0.022 0.11 0 1 Pennsylvania Allegheny County

420031009 0.138 0.043 0.149 0 1 Pennsylvania Allegheny 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 Cite
Table 2D-1. Pb-TSP concentrations at Pb-TSP sites, 2009-2011.

Appendix 2D - Air Quality Data Analysis Summary

SITE

Max 3-month 

Mean (ug/m3

)

Annual Mean 

(ug/m3

)

Max Monthly 

Mean (ug/m3)

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 Amherst 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 Arecibo Municipio

720210010 0.011 0.005 0.027 0 0 Puerto Rico Bayamón Municipio

January 2013 2D - 5 Draft - Do Not Quote or Cite
Table 2D-2. Pb-PM10 concentrations at urban PM10 sites, 2009-2011.

Appendix 2D - Air Quality Data Analysis Summary

SITE

Max 

3-month 

Mean 

(ug/m3

)

Annual Mean

(ug/m3)

Max 

Monthly 

Mean 

(ug/m3

) State County

040134009 0.005 0.008 Arizona Maricopa County

040139997 0.007 0.004 0.007 Arizona 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 quote
Table 2D-3. Pb-PM2.5 concentrations at urban CSN PM2.5 sites, 2009-2011.

Appendix 2D - Air Quality Data Analysis Summary

SITE

Max 

3-month 

Mean 

(ug/m3)

Annual 

Mean 

(ug/m3

)

Max 

Monthly 

Mean 

(ug/m3) State County

010730023 0.041 0.017 0.064 Alabama Jefferson County

010732003 0.032 0.008 0.078 Alabama Jefferson County

010890014 0.003 0.002 0.003 Alabama Madison County

011011002 0.007 0.003 0.011 Alabama Montgomery County

011130001 0.013 0.004 0.028 Alabama Russell County

020900010 0.006 0.003 0.008 Alaska Fairbanks North Star Borough

040134009 0.004 0.003 0.005 Arizona Maricopa County

040139997 0.004 0.002 0.004 Arizona Maricopa County

040191028 0.003 0.002 0.003 Arizona Pima County

051190007 0.004 0.002 0.006 Arkansas Pulaski County

060010007 0.005 0.004 0.005 California Alameda County

060010011 0.012 0.005 0.023 California Alameda 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 Adams 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 Columbia 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 quote
Table 2D-3. Pb-PM2.5 concentrations at urban CSN PM2.5 sites, 2009-2011.

Appendix 2D - Air Quality Data Analysis Summary

SITE

Max 

3-month 

Mean 

(ug/m3)

Annual 

Mean 

(ug/m3

)

Max 

Monthly 

Mean 

(ug/m3) 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 Ada 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 quote
Table 2D-3. Pb-PM2.5 concentrations at urban CSN PM2.5 sites, 2009-2011.

Appendix 2D - Air Quality Data Analysis Summary

SITE

Max 

3-month 

Mean 

(ug/m3)

Annual 

Mean 

(ug/m3

)

Max 

Monthly 

Mean 

(ug/m3) State County

261630033 0.017 0.007 0.029 Michigan Wayne County

270031002 0.009 0.006 0.013 Minnesota Anoka 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 Albany 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 quote
Table 2D-3. Pb-PM2.5 concentrations at urban CSN PM2.5 sites, 2009-2011.

Appendix 2D - Air Quality Data Analysis Summary

SITE

Max 

3-month 

Mean 

(ug/m3)

Annual 

Mean 

(ug/m3

)

Max 

Monthly 

Mean 

(ug/m3) 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 Allegheny County

420030064 0.03 0.017 0.052 Pennsylvania Allegheny 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 quote
Table 2D-3. Pb-PM2.5 concentrations at urban CSN PM2.5 sites, 2009-2011.

Appendix 2D - Air Quality Data Analysis Summary

SITE

Max 

3-month 

Mean 

(ug/m3)

Annual 

Mean 

(ug/m3

)

Max 

Monthly 

Mean 

(ug/m3) 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 quote
Table 2D-4. Pb-PM2.5 concentrations at non-urban PM2.5 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 Alaska Aleutians East Borough

020680003 0.001 0 0.001 Alaska Denali Borough

021220009 0.001 0 0.001 Alaska Kenai Peninsula Borough

040018001 0.001 0.001 0.001 Arizona Apache County

040038001 0.002 0.001 0.003 Arizona Cochise County

040039000 0.009 0.004 0.012 Arizona Cochise County

040070010 0.004 0.003 0.008 Arizona Gila County

040078100 0.001 0.001 0.002 Arizona Gila County

040170119 0.001 0.001 0.001 Arizona Navajo County

051019000 0.002 0.001 0.002 Arkansas Newton County

051130003 0.001 0.001 0.002 Arkansas 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 Alamosa 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 Aroostook 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 quote
Table 2D-4. Pb-PM2.5 concentrations at non-urban PM2.5 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 Avery 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 Adams 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 quote
Table 2D-4. Pb-PM2.5 concentrations at non-urban PM2.5 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 quote
Table 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 quote
Table 2D-6. Distribution of annual mean concentrations, 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 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 quote
Table 2D-7. Distribution of lead concentrations, 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 0.002 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 quote
Table 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 Cite
Table 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 Cite
Table 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 Cite
Table 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 Cite
Table 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 Cite
Table 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 Cite
January 2013 3A-1 Draft – Do Not Quote or Cite

1 APPENDIX 3A 

2 INTERPOLATED RISK ESTIMATES FOR THE GENERALIZED 

3 (LOCAL) URBAN CASE STUDY 

4 This Appendix describes the method used to develop risk estimates for conditions just 

meeting the current standard (0.15 μg/m3 5 , as a maximum 3-month average) for the generalized 

6 (local) urban case study. These risk estimates were developed by interpolation from the 2007 

7 REA results for this case study. The general approach was to identify the two alternative 

8 standard scenarios simulated in the 2007 REA which represented air quality conditions 

9 bracketing those for the current standard and then linearly interpolate an estimate of risk for the 

10 current standard based on the slope created from the two bracketing estimates. In representing 

11 air quality conditions for these purposes, we focused on the annual average air Pb concentration 

12 estimates as that is the metric which had been the IEUBK model inputs for the various air quality 

scenarios (IEUBK does not accept air quality inputs of a temporal scale shorter than a year).1 13 An 

14 annual average concentration estimate to represent the current standard was identified in a 

15 manner consistent with that employed in the 2007 REA for this case study (see section 3.4.3.2 

16 above, use of 2003-2005 data) with the use of currently available monitoring data (2009-2011) 

17 for relationships between air quality metrics for representation of the current standard. By this 

method, the air quality scenario for the current standard (0.15 μg/m3 18 , as a not-to-be-exceeded 3-

19 month average) was found to be bracketed by the scenarios for alternative standards of 0.5 and 

0.20 μg/m3 20 (maximum monthly averages). A risk estimate for the current standard was then 

21 derived using the slope relating generalized (local) urban case study IQ loss to the annual 

22 average Pb concentration used for those two air quality scenarios. We used this interpolation 

23 approach to develop median risk estimates for the current standard based on each of the four C-R 

24 functions. Details on the method for the interpolation approach are provided below. 

25 1. Identify an estimate of annual average air Pb concentration to represent each air quality 

26 scenario. For the alternative scenarios, this was done in the 2007 REA using the 2003-

27 2005 Pb-TSP dataset for urban areas of population greater than one million. For analysis 

 

1

 Although many different patterns of temporally varying air concentration will just meet a given potential 

alternative standard, the shortest time step accommodated by the blood Pb model is a year. Thus, the air Pb 

concentration inputs to the blood Pb model for each air quality scenario are annual average air Pb concentrations. 

For the generalized (local) urban case study, the national Pb-TSP monitoring dataset was 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 document) 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

1 of the current standard here, this uses the recent Pb-TSP dataset (2009-2011) for urban 

2 areas of population greater than one million. The concentration in terms of the metric 

3 being assessed (e.g., maximum 3-month or calendar quarter average) was derived per 

4 monitoring site, as was the annual average concentration and also the ratio of the two 

5 (2007 REA, Appendix A; Appendix 2D of this document). From the average of the 

6 monitor-specific ratios we derived the annual average estimate. [In the 2007 REA, this 

7 was the IEUBK air quality input for each AQ scenario.] With the 2009-2011 data, the 

8 average, across monitors in urban areas greater than 1 million population, of the ratio of 

9 maximum 3-month average to annual average is 1.92 (Appendix 2D in this document). 

10 - This ratio was used to derive an annual average air Pb-TSP concentration 

estimate to represent the current standard scenario (annual value = 0.15 μg/m3 11 

* 1/1.92 = 0.078 μg/m3 12 ). The annual average values for the scenarios 

13 included in the 2007 REA and also for the current standard scenario 

14 considered in this interpolation are shown in Table 3A-1 below. 

15 Table 3A-1. Annual average air Pb-TSP concentration estimates for different air quality 

16 scenarios. 

Air Quality Scenarios 

Annual Average Estimate 

(μg/m3)

Maximum 

Quarterly Average D 

(μg/m3)

Maximum 

Monthly Average 

(μg/m3)

Maximum 

3-month Average 

(μg/m3)

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 

18 2. Identify the two “bounding” alternative standard levels that will be used to derive a 

19 slope for the risk interpolation for the current standard level. Based on comparison of 

20 the annual ambient air Pb estimates for each of the 2007 REA air quality scenarios and 

21 for the current standard we determine which scenarios “bound” the current standard (in 

22 terms of the annual average ambient Pb estimate). As Table 3A-1 above shows, the 

23 bounding scenarios are the scenarios for just meeting maximum monthly average 

concentrations of 0.5 and 0.2 μg/m3 24 . 

25 

26 3. Calculate the slopes of generalized (local) urban case study IQ loss per unit annual 

27 average Pb estimate for each risk estimate of interest for the two bounding scenarios.

28 This calculation is (IQ LossScenario X – IQ LossScenario Y)/ (annual averageScenario X – annual 

29 averageScenario Y). The risk estimates for the 4 different C-R functions and two exposure 

30 pathway categories of interest (Recent Air and Recent + Past Air), with the derived 

31 slopes, are in Table 3A-2. 
January 2013 3A-3 Draft – Do Not Quote or Cite

1 Table 3A-2. Risk estimates for bounding air quality scenarios and associated slopes. 

Risk Estimates 

for different C-R functions and exposure pathway categories 

Log-linear with 

low-exposure 

linearization 

Dual linear – 

stratified 

at 10 μg/dL peak 

Log-linear with 

cutpoint 

Dual linear - 

stratified 

at 7.5 μg/dL peak 

Recent 

air 

Recent + 

past air 

Recent 

air 

Recent + 

past air 

Recent 

air 

Recent + 

past air 

Recent 

air 

Recent + 

past air 

0.2 μg/m3, max 

quarterly average 1.53 3.37 0.54 1.18 0.63 1.38 1.97 4.34 

0.2 μg/m3 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 

3 4. Derive interpolated risk estimates for the current standard scenario. Using the 

4 slopes presented in Table 3A-2 and the lower bounding air quality scenario risk 

5 estimates, derive corresponding risk estimates for the current standard scenario: 

6 Risk = lower bounding risk + (increment annual average Pb * slope) 

7 Where: 

8  lower bounding risk = risk for the lower bound air quality scenario (i.e., 

for 0.2 μg/m3 9 maximum monthly average) 

10  increment annual average Pb is the difference between the annual average 

11 estimates for the current standard and the lower bounding scenario. 

12  slope is the value described in Step 4, which differs across the 8 

13 combinations of C-R functions and exposure pathway categories. 

14 The resulting interpolated risk estimates are presented in Table 3A-3.

15 Table 3A-3. Interpolated risk estimates for the current NAAQS scenario for the 

16 generalized (local) urban case study. 

Risk Estimates 

for different C-R functions and exposure pathway categories 

Log-linear with 

low-exposure 

linearization 

Dual linear – 

stratified 

at 10 μg/dL peak 

Log-linear with 

cutpoint 

Dual linear - 

stratified 

at 7.5 μg/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).

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

1 APPENDIX 5A 

2 ADDITIONAL DETAIL ON 2006 ECOLOGICAL SCREENING 

3 ASSESSMENT 

Setting and spatial 

extent of dataset or 

modeling analysis 

Media Screened and Screening Levels Used 

Soil Freshwater 

water column 

Freshwater 

Sediment 

Primary 

Smelter Case 

Study

Herculaneum, 

Missouri: soil and 

waterbody samples 

from study area 6 km 

diameter, centered on 

point source 

Soil screening 

values 

developed 

based on U.S. 

EPA 

Superfund 

methodology 

for developing 

ecological soil 

screening 

levels 

(USEPA, 

2005a,b) 

U.S. EPA 

freshwater AWQC 

for aquatic life 

adjusted 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. 

4 
United States 

Environmental Protection Agency 

Office of Air Quality Planning and Standards 

Health and Environmental Impacts Division 

Research Triangle Park, NC 

Publication No. EPA-452/P-13-001

January 2013