Policy Assessment for the Review of the Lead 

National Ambient Air Quality Standards 
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EPA-452/R-14-001 

May 2014 

Policy Assessment 

for the Review of the Lead 

National Ambient Air Quality Standards 

U.S. Environmental Protection Agency 

Office of Air Quality Planning and Standards 

Health and Environmental Impacts Division 

Research Triangle Park, North Carolina 
DISCLAIMER

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

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

OAQPS Policy Assessment contains conclusions of the staff of the OAQPS and does not 

necessarily reflect the views of the Agency. Mention of trade names or commercial products is 

not intended to constitute endorsement or recommendation for use. 
ACKNOWLEDGMENTS

This Policy Assessment is the product of the Office of Air Quality Planning and 

Standards. It has been developed as part of the Environmental Protection Agency’s (EPA) 

ongoing review of the national ambient air quality standards (NAAQS) for lead (Pb). The Pb 

NAAQS review team has been led by Dr. Deirdre Murphy. 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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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 

1.2.4 Related Lead Control Programs ........................................................................... 1-9 

1.3 SCOPE OF CURRENT REVIEW: FATE AND MULTIMEDIA PATHWAYS 

 OF AMBIENT AIR LEAD ........................................................................................ 1-14

1.3.1 Environmental Distribution and Exposure Pathways......................................... 1-14

1.3.1.1 Human Exposure Pathways ....................................................................... 1-16

1.3.1.2 Ecosystem Exposure Pathways ................................................................. 1-18

1.3.2 Considerations Related to Historically Emitted Lead ........................................ 1-18

1.4 GENERAL ORGANIZATION OF THE DOCUMENT ........................................... 1-20 

1.5 REFERENCES .......................................................................................................... 1-21 

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

2.1 SOURCES AND EMISSIONS TO AMBIENT AIR .................................................. 2-1

2.1.1 Temporal Trends on a National Scale .................................................................. 2-2

2.1.2 Sources and Emissions on National Scale - 2008 ................................................ 2-3

2.1.2.1 Stationary Sources ....................................................................................... 2-5

2.1.2.2 Mobile Sources ............................................................................................ 2-6

2.1.2.3 Natural Sources and Long-range Transport ................................................ 2-7

2.1.2.4 Previously Deposited Lead.......................................................................... 2-7

2.1.3 Sources and Emissions on Local Scale ................................................................ 2-9

2.2 AMBIENT AIR QUALITY ....................................................................................... 2-12

2.2.1 Air Monitoring ................................................................................................... 2-12

2.2.1.1 Lead NAAQS Surveillance Network ........................................................ 2-12

2.2.1.2 Other Lead Monitoring Networks ............................................................. 2-16

2.2.1.3 NAAQS Surveillance Monitoring Considerations .................................... 2-19

 2.2.1.3.1 Sampling Considerations .................................................................... 2-19

 2.2.1.3.2 Analysis Considerations ..................................................................... 2-21

 2.2.1.3.3 Network Design Considerations ......................................................... 2-21

2.2.2 Ambient Concentrations ..................................................................................... 2-24

2.2.2.1 Temporal Trends ....................................................................................... 2-24

2.2.2.2 Current Concentrations ............................................................................. 2-26

2.3 AMBIENT AIR LEAD IN OTHER MEDIA ............................................................ 2-32

2.3.1 Atmospheric Deposition ..................................................................................... 2-32
ii

2.3.2 Terrestrial Media ................................................................................................ 2-34

2.3.2.1 Indoor Household Dust ............................................................................. 2-34

2.3.2.2 Outdoor Dust in Areas of Human Activity ............................................... 2-35

2.3.2.3 Soil ............................................................................................................ 2-36

2.3.2.4 Biota .......................................................................................................... 2-38

2.3.3 Aquatic Media .................................................................................................... 2-39

2.3.3.1 Surface Waters .......................................................................................... 2-39 

2.3.3.2 Sediments .................................................................................................. 2-40 

 2.3.3.3 Biota .......................................................................................................... 2-42 

2.4 REFERENCES .......................................................................................................... 2-42 

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

3.1 INTERNAL DISPOSITION AND BIOMARKERS OF EXPOSURE AND DOSE .. 3-1

3.2 NATURE OF EFFECTS............................................................................................ 3-15

3.3 PUBLIC HEALTH IMPLICATIONS AND AT-RISK POPULATIONS ................ 3-29

3.4 EXPOSURE AND RISK ........................................................................................... 3-38

3.4.1 Conceptual Model for Air-Related Lead Exposure and Risk ............................ 3-39

3.4.2 Case Studies ....................................................................................................... 3-42

3.4.3 Analysis Approach ............................................................................................. 3-43

3.4.3.1 Estimating Exposure ................................................................................. 3-46

3.4.3.2 Air Quality Scenarios Included in 2007 Assessment ................................ 3-49

3.4.3.3 Methods for Deriving Risk Estimates ....................................................... 3-51

 3.4.3.3.1 Full Risk Model in 2007 REA .............................................................. 3-52

 3.4.3.3.2 Air Quality Scenarios Reflecting the Current Standard ........................ 3-55

3.4.4 Challenges in Characterizing Air-related Exposure and Risk ............................ 3-56

3.4.5 Risk Estimates .................................................................................................... 3-58

3.4.6 Treatment of Variability ..................................................................................... 3-63

3.4.7 Characterizing Uncertainty ................................................................................ 3-64

3.4.8 Updated Interpretation of Risk Estimates .......................................................... 3-67

3.5 REFERENCES .......................................................................................................... 3-68 

4 REVIEW OF THE PRIMARY 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 Approach Regarding the Need for Revision ............................................... 4-3

4.1.1.2 Approach Regarding Elements of Revised Standard .................................. 4-5

4.1.2 Approach for the Current Review ...................................................................... 4-11

4.2 ADEQUACY OF THE CURRENT STANDARD .................................................... 4-14

4.2.1 Evidence-based Considerations .......................................................................... 4-14

4.2.2 Exposure/Risk-based Considerations ................................................................. 4-22 

4.2.3 CASAC Advice .................................................................................................. 4-26 

4.3 STAFF CONCLUSIONS ON THE PRIMARY STANDARD ................................. 4-28

4.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND 

 DATA COLLECTION .............................................................................................. 4-36

4.5 REFERENCES .......................................................................................................... 4-39 
iii

5 WELFARE EFFECTS AND EXPOSURE/RISK INFORMATION ............................. 5-1

5.1 WELFARE EFFECTS INFORMATION ................................................................... 5-1

5.2 EXPOSURE AND RISK INFORMATION ............................................................. 5-16

5.2.1 Screening Assessment from Last Review ......................................................... 5-17

5.2.2 Screening Assessment Results and Interpretation ............................................. 5-20

5.3 REFERENCES .......................................................................................................... 5-25 

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

6.1 APPROACH ............................................................................................................... 6-1

6.1.1 Approach Used in the Last Review ..................................................................... 6-2

6.1.2 Approach for the Current Review ....................................................................... 6-3

6.2 ADEQUACY OF THE CURRENT STANDARD ..................................................... 6-5

6.2.1 Evidence-based Considerations ........................................................................... 6-5

6.2.2 Exposure/Risk-based Considerations .................................................................. 6-9 

6.2.3 CASAC Advice ................................................................................................. 6-11 

6.3 STAFF CONCLUSIONS ON THE SECONDARY 

 STANDARD ............................................................................................................. 6-12

6.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND 

 DATA COLLECTION ............................................................................................. 6-13

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

CHAPTER APPENDICES 

 Appendix 2A. The 2008 NEI: Data 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 

ATTACHMENT 

Clean Air Scientific Advisory Committee Letter (June 4, 2013) 
iv

LIST OF FIGURES 

Figure 1-1.    Pathways of human and ecosystem exposure to lead from ambient air. .............. 1-16 

Figure 2-1.    Temporal trend in U.S. air emissions of Pb: 1970-2008. ....................................... 2-3

Figure 2-2. Geographic distribution of facilities and airports estimated to emit at least 

 0.50 tpy of Pb in 2008. ......................................................................................... 2-11

Figure 2-3.    Map of Pb-TSP monitoring sites in current Pb NAAQS monitoring network. .... 2-15

Figure 2-4.    Sites near airports for which one year of Pb-TSP 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). ................. 2-19

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

Figure 2-8.    Temporal trend in Pb-TSP concentrations: 2000-2012 (50 sites). ....................... 2-25 

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

 roadways: 1979-2010. ......................................................................................... 2-26

Figure 2-10. Pb-TSP maximum 3-month means (215 sites), 2010-2012. ................................ 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, 2010-2012. ................................................. 2-29

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

 at different site types, 2010-2012. ........................................................................ 2-30

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

 and Pb-PM2.5 at different site types, 2010-2012. ................................................. 2-31

Figure 2-14. Temporal trend in sediment Pb 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 Pb. ..................................................... 3-40

Figure 3-3.    Overview of analysis approach. ........................................................................... 3-45

Figure 3-4.    Comparison of four concentration-response functions used in risk assessment. . 3-53

Figure 3-5.    Parsing of air-related risk estimates. .................................................................... 3-57 

Figure 4-1.    Overview of approach for review of current primary standard. ........................... 4-13 

Figure 5-1. Analytical approach for screening-level ecological risk assessment in the last 

 review (2006 REA, Exhibit 2-6) .......................................................................... 5-19 

Figure 6-1.    Overview of approach for review of current secondary standard. ......................... 6-4 

 
v

LIST OF TABLES 

Table 2-1.    U.S. Pb 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 of Pb in 2008. .................................. 2-10

Table 2-3.    Dry deposition of Pb in large metropolitan areas. ................................................. 2-36

Table 3-1.    Empirically derived air-to-blood ratios for populations inclusive of children. ..... 3-13

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

 study group blood Pb levels <5 μg/dL. ................................................................. 3-23

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

 blood Pb levels closest to those of young children in the U.S. today. ................... 3-29 

Table 3-4.    Number of children aged 5 and under in areas of elevated ambient air Pb 

 concentrations relative to the NAAQS. ................................................................. 3-37

Table 3-5.    Population size near larger sources of Pb emissions. ............................................ 3-38

Table 3-6.    Types of population exposures assessed. .............................................................. 3-43

Table 3-7.    Summary of approaches used to estimate case study media concentrations. ........ 3-47

Table 3-8.    Air quality scenarios assessed. .............................................................................. 3-51

Table 3-9.    Comparison of total and incremental IQ loss estimates for blood Pb below 

 10 μg/dL based on the four concentration-response functions. ............................. 3-53

Table 3-10. Estimates of air-related risk from 2007 risk assessment. ...................................... 3-60

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

 including interpolated estimates for current standard. .......................................... 3-61
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 ES-1 

EXECUTIVE SUMMARY 

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

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

ongoing review of the primary (health-based) and secondary (welfare-based) national ambient air 

quality standards (NAAQS) for lead (Pb). It presents analyses and staff conclusions regarding 

the policy implications of the key scientific and technical information that informs this review. 

The PA is intended to “bridge the gap” between the relevant scientific evidence and technical 

information and the judgments required of the EPA Administrator in determining whether to 

retain or revise the current standards. Development of the PA is also intended to facilitate advice 

and recommendations on the standards to the Administrator from an independent scientific 

review committee, the Clean Air Scientific Advisory Committee (CASAC), as provided for in 

the Clean Air Act (CAA). 

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

Integrated Science Assessment for Lead (ISA) prepared for this review by the EPA’s Office of 

Research and Development (ORD) as well as scientific and technical assessments from prior Pb 

NAAQS reviews. Such assessments include quantitative human health and ecological risk and 

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

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

in this review with regard to risk and exposure assessment. For the purpose of review of the 

NAAQS in considering the scientific evidence and other technical information available in this 

review, emphasis is given to consideration of the extent to which the evidence newly available 

since the last review alters conclusions drawn in the last review with regard to health and welfare 

effects of Pb, the exposure levels at which they occur and the associated at-risk populations and 

ecological receptors or ecosystems. 

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

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

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

technical information provides support for concluding that consideration of alternative standards 

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

conclusions that it is appropriate to consider retaining the current primary and secondary 

standards without revision; accordingly, no potential alternative standards have been identified 

by staff for consideration in this review. Comments and recommendations from CASAC, and 

public comments, based on review of the draft PA, have informed staff conclusions and the 

presentation of information in this final document. 
 ES-2 

Current Lead NAAQS and Scope of Review 

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

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

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

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

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

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

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

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

be identical in all respects to the revised primary standard. 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

protection afforded by the current NAAQS. 
 ES-3 

Characterization of Ambient Air Lead 

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

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

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

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

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

pollutants issued under Section 112 of the CAA. Additional reductions in stationary source 

emissions are also anticipated from further regulations which have been promulgated since 2008 

under Section 112 of the CAA. 

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

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

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

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

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

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

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

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

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

elevated Pb concentrations due to leaded aviation gasoline usage. These data will improve our 

understanding of Pb concentrations in ambient air near airports and conditions influencing these 

concentrations. These data will also inform EPA’s ongoing investigation into Pb emissions from 

piston-engine aircraft under Section 231 of the CAA, separate from this Pb NAAQS review. 

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

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

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

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

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

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

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

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

with even less information available on trends for other media such as surface soils. 
 ES-4 

Health Effects and Review of the Primary Standard 

Lead has long been recognized to exert an array of deleterious effects on multiple organ 

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

assessments. Over the three decades from the time the standard was initially set in 1978 through 

its revision with the NAAQS review completed in 2008, the evidence base expanded 

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

young children at increasingly lower blood Pb levels. These effects formed the primary basis for 

the 2008 revisions to the primary standard. The current standard was set most specifically to 

provide appropriate public health protection from the effects of air-related Pb on cognitive 

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

requisite public health protection from the full array of health effects of Pb, consistent with the 

CAA requirement that the primary standard, in the judgment of the Administrator, based on the 

latest scientific knowledge, be requisite to protect public health with an adequate margin of 

safety. 

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

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

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

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

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

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

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

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

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

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

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

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

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

judgments for this review include the public health significance of a given magnitude of IQ loss 

in a small subset of highly exposed children (i.e., those likely to experience air-related Pb 

exposures at the level of the standard), as well as how to consider the nature and magnitude of 

the array of uncertainties that are inherent in the evidence and in the application of this specific 

framework. 

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

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

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

drawn from the evidence using the evidence-based air-related IQ loss framework. Staff 
 ES-5 

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

substantial limitations and uncertainties in the resulting risk estimates. 

Based on the above considerations, staff concludes that the currently available 

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

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

additionally notes that the final decision on the adequacy of the current standard is largely a 

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

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

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

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

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

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

the current evidence there is appreciable uncertainty associated with drawing conclusions 

regarding whether there would be reductions in blood Pb levels and risk to public health from 

alternative lower levels as compared to the level of the current standard. Thus, staff concludes 

that the basis for any consideration of alternative lower standard levels would reflect different 

public health policy judgments as to the appropriate approach for weighing uncertainties in the 

evidence and for providing requisite protection of public health with an adequate margin of 

safety. Accordingly, and in light of the staff conclusion that it is appropriate to consider the 

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

for consideration in this review. 

Welfare Effects and Review of the Secondary Standard 

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

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

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

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

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

identical in all respects to the newly revised primary standard. 

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

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

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

including that with regard to ecological effects associated with Pb exposure and the substantial 

limitations in the current evidence that complicate conclusions regarding the potential for Pb 

emissions under the current, much lower standard to contribute to welfare effects. Such 

complications include the significant difficulties in interpreting effects evidence from laboratory 
 ES-6 

studies to the natural environment and linking those effects to ambient air Pb concentrations. 

Based on staff analysis, including the above considerations, staff concludes that the currently 

available evidence and exposure/risk information do not call into question the adequacy of the 

current standard to provide the requisite protection for public welfare. Thus, staff concludes that 

consideration should be given to retaining the current standard, without revision, and this 

document does not identify potential alternative standards for consideration in this review. 
 1-1

1 INTRODUCTION 

1.1 PURPOSE 

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

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

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

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

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

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

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

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

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

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

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

what revisions may be appropriate to consider. 

The PA is intended to help “bridge the gap” between the Agency’s scientific assessments 

presented in the ISA and REAs and the judgments required of the EPA Administrator in 

determining whether it is appropriate to retain or revise the NAAQS. In evaluating the adequacy 

of current standards and whether it is appropriate to consider 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 and level. These elements, which together serve to define each 

standard, must be considered collectively in evaluating the health and welfare protection 

afforded by the Pb standards. The PA integrates and interprets the information from the ISA and 

REAs to frame policy options for consideration by the Administrator. In so doing, the PA 

recognizes that the selection of a specific approach to reaching final decisions on primary and 

secondary NAAQS will reflect the judgments of the Administrator. 

 

1

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

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

Paper. 

2

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

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

particles. 

3

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

in determining whether an area attains the standard. For example, the form of the annual NAAQS for fine 

particulate matter (PM2.5) is the average of annual mean PM2.5 concentrations for three consecutive years, while the 

form of the 8-hour NAAQS for carbon monoxide is the second-highest 8-hour average in a year. 
 1-2

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

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

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

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

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

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

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

requesting CASAC review and public comment on one or more drafts of the PA.4 In this PA for 

this review of the Pb NAAQS, we consider the scientific and technical information available in 

this review as assessed in the Integrated Science Assessment for Lead (henceforth referred to as 

the ISA [USEPA, 2013a]), prepared by EPA’s National Center for Environmental Assessment 

(NCEA), and the quantitative human exposure and health risk and screening-level ecological risk 

assessments performed in the last review. As discussed below in section 1.2.3, upon 

consideration of the evidence newly available in this review with regard to risk and exposure 

assessment, staff concluded that new health and welfare REAs were not warranted. Accordingly, 

the quantitative risk information considered in this PA is based on the quantitative human 

exposure and health risk and screening-level ecological risk assessments performed in the last 

review (the 2007 Health Risk Assessment Report or 2007 REA [USEPA, 2007a] and the 2006 

screening-level Ecological Risk Assessment or 2006 REA [ICF, 2006]) and is interpreted in the 

context of newly available evidence in this review. The evaluation and staff conclusions 

presented in this PA for the Pb NAAQS have been informed by comments and advice received 

from CASAC in their reviews of the draft PA and of other draft Agency documents prepared in 

this NAAQS review. 

Beyond informing the EPA Administrator and facilitating the advice and 

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

all parties interested in the Pb NAAQS review. In these roles, it is intended to serve as a single 

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

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

 

4

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

conclusions and associated CASAC advice and public comment, among other factors. Typically, a second draft PA 

has been prepared in cases where the available information calls into question the adequacy of the current standard 

and analyses of potential alternative standards are developed taking into consideration CASAC advice and public 

comment. In such cases, a second draft PA includes preliminary staff conclusions regarding potential alternative 

standards and undergoes CASAC review and public comment prior to preparation of the final PA. When such 

analyses are not undertaken, a second draft PA may not be warranted. 
 1-3

1.2 BACKGROUND 

1.2.1 Legislative Requirements 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

protect the public health.”5

 A secondary standard, as defined in section 109(b)(2), must “specify 

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

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

or anticipated adverse effects associated with the presence of [the] pollutant in the ambient air.”6

The requirement that primary standards provide 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. See Lead Industries 

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

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

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

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

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

 

5

 The legislative history of section 109 indicates that a primary standard is to be set at “the maximum 

permissible ambient air level . . . which will protect the health of any [sensitive] group of the population,” and that 

for this purpose “reference should be made to a 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). 

6

 Welfare effects as defined in section 302(h) (42 U.S.C. § 7602(h)) include, but are not limited to, “effects 

on soils, water, crops, vegetation, man-made materials, 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.” 
 1-4

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

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

seeking not only to prevent pollution 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 the Administrator to 

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

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

to protect public health with an adequate margin of safety. 

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

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

at risk,7

 and the kind and degree of the uncertainties that must be addressed. The selection of any 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

revisions of existing criteria and standards as may be appropriate . . . .” Since the early 1980s, 

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

Committee (CASAC).8

 

7

 As used here and similarly throughout this document, the term population (or group) refers to persons 

having a quality or characteristic in common, such as a specific pre-existing illness or a specific age or life stage. As 

discussed more fully in section 3.3 below, the identification of sensitive groups (called at-risk groups or at-risk 

populations) involves consideration of susceptibility and vulnerability. 

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

http://yosemite.epa.gov/sab/sabproduct.nsf/WebCASAC/CommitteesandMembership?OpenDocument. 
 1-5

1.2.2 History of Lead NAAQS Reviews 

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

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

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

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

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

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

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

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

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

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

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

N.Y. 1976), aff’d, 545 F.2d 320 (2d Cir. 1978). 

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

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

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

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

cubic meter (μg/m3

), measured as Pb in totalsuspended particles (Pb-TSP), not to be exceeded 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

emissions to air, such as bringing more areas into compliance with the existing Pb NAAQS 
 1-6

(USEPA, 1991). EPA continues this broad, multi-program, multimedia approach to reducing Pb 

exposures today, as described in section 1.2.4 below. 

The last review of the Pb air quality criteria and standards was initiated in November 

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

Document and conduct of the NAAQS review were presented in documents completed in 2005 

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

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

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

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

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

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

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

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

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

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

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

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

of these assessments, air quality analyses and key evidence from the 2006 CD, was presented in 

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

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

implications of the key studies and scientific information contained in the 2006 CD and 

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

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

the Administrator give consideration to substantially revising the primary and secondary 

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

. 

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

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

2007 (72 FR 71488).10 CASAC provided advice and recommendations to the Administrator with 

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

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

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

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

 

9

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

10 The ANPR was one of the features of the revised NAAQS review process that EPA instituted in 2006. In 

2009 (Jackson, 2009), this component of the process was replaced by reinstatement of a policy assessment prepared 

by OAQPS staff (previously termed the OAQPS Staff Paper). 
 1-7

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

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

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

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

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

the much-expanded health effects evidence on 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. 

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

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

was revised to be identical in all respects to the revised primary standards.11 Revisions to the 

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

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

emissions inventory reporting requirements.12 One aspect of the new data handling requirements 

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

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

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

below. 

1.2.3 Current Lead NAAQS Review 

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

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

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

discuss the policy-relevant scientific information, which informed identification of key policy 

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

workshop discussions, the EPA developed the draft IRP (USEPA, 2011b). The draft IRP was 

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

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

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

IRP, developed in consideration of the CASAC consultation and public comment, was released 

in November, 2011 (USEPA, 2011a; 76 FR 76972). 

 

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

12 The current federal regulatory measurement methods for Pb are specified in 40 CFR 50, Appendix G and 

40 CFR part 53. Consideration of ambient air measurements with regard to judging attainment of the standards is 

specified in 40 CFR 50, Appendix R. The Pb monitoring network requirements are specified in 40 CFR 58, 

Appendix D, section 4.5. Guidance on the approach for implementation of the new standards was described in the 

Federal Register notices for the proposed and final rules (73 FR 29184; 73 FR 66964). 
 1-8

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

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

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

2011c; 76 FR 26284). The CASAC Pb Review Panel met at a public meeting on July 20, 2011 

to review the draft ISA (76 FR 36120). The CASAC provided comments in a December 9, 2011 

letter to the EPA Administrator (Frey and Samet, 2011). The second external review draft ISA 

was released for CASAC review and public comment in February 2012 (USEPA, 2012b; 77 FR 

5247) and was the subject of a public meeting on April 10-11, 2012 (77 FR 14783). The 

CASAC provided comments in a July 20, 2012 letter (Samet and Frey, 2012). The third external 

review draft was released for CASAC review and public comment in November 2012 (USEPA, 

2012a; 77 FR 70776) and was the subject of a public meeting on February 5-6, 2013 (78 FR 

938). The CASAC provided comments in a June 4, 2013 letter (Frey, 2013a). The final ISA was 

released in late June 2013 (USEPA, 2013a; 78 FR 38318). 

In June 2011, the EPA developed and released the REA Planning Document for 

consultation with CASAC and public comment (USEPA, 2011d; 76 FR 58509). This document 

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

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

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

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

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

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

developing new quantitative risk and exposure assessments that would have substantially 

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

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

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

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

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

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

was not warranted in this review (Frey, 2011b; Frey, 2013b). In consideration of the conclusions 

reached in the REA Planning Document and CASAC’s consultative advice, the EPA has not 

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

Assessment considers the risk assessment findings from the last review with regard to any 

appropriate further interpretation in light of the evidence newly available in this review. 

A draft of this Policy Assessment was released for public comment and review by 

CASAC in January 2013 (USEPA, 2013b; 77 FR 70776) and was the subject of a public meeting 

on February 5-6, 2013 (78 FR 938). Comments provided by the CASAC in a June 4, 2013 letter 
 1-9

(Frey, 2013b), as well as public comments received on the draft PA were considered in preparing 

the final PA. 

1.2.4 Related Lead Control Programs 

States are primarily responsible for ensuring attainment and maintenance of the NAAQS. 

Under section 110 of the Act (42 U.S.C. 7410) and related provisions, states are to submit, for 

EPA approval, state implementation plans (SIPs) that provide for the attainment and 

maintenance of such standards through control programs directed to sources of the pollutants 

involved. The states, in conjunction with EPA, also administer the prevention of significant 

deterioration program (42 U.S.C. 7470–7479) for these pollutants. In addition, federal programs 

provide for nationwide reductions in emissions of these and other air pollutants through the 

Federal Motor Vehicle Control Program under Title II of the Act (42 U.S.C. 7521–7574), which 

involves controls for automobile, truck, bus, motorcycle, nonroad engine, and aircraft emissions; 

the new source performance standards under section 111 of the Act (42 U.S.C. 7411); and the 

national emission standards for hazardous air pollutants under section 112 of the Act (42 U.S.C. 

7412). 

As noted in section 1.2.2 above, the NAAQS is only one component of EPA’s programs 

to address Pb in the environment. Some recent actions expected to result in air Pb emissions 

reductions that are associated with other EPA programs, such as those recognized above, are 

more specifically recognized in section 2.1. The presentation below briefly summarizes 

additional ongoing activities that, although not directly pertinent to the review of the NAAQS, 

are associated with controlling environmental Pb levels and human Pb exposures more broadly. 

Among those identified are EPA programs intended to encourage exposure reduction programs 

in other countries. 

Reducing Pb exposures has been recognized as a federal priority as environmental and 

public health agencies continue to grapple with soil and dust Pb levels from the historical use of 

Pb in paint and gasoline and from other sources.13 A broad range of federal programs beyond 

those that focus on air pollution control provide for nationwide reductions in environmental 

releases and human exposures. For example, pursuant to Section 1412 of the Safe Drinking 

Water Act (SDWA), EPA regulates lead in public drinking water systems through corrosion 

 

13 In 1991, the Secretary of the Health and Human Services (HHS) characterized Pb poisoning as the 

“number one environmental threat to the health of children in the United States” (Alliance to End Childhood Lead 

Poisoning. 1991). In 1997, President Clinton created, by Executive Order 13045, the President’s Task Force on 

Environmental Health Risks and Safety Risks to Children in response to increased awareness that children face 

disproportionate risks from environmental health and safety hazards (62 FR 19885). By Executive Orders issued in 

October 2001 and April 2003, President Bush extended the work for the Task Force beyond its original charter (66 

FR 52013 and 68 FR 19931). Reducing Pb poisoning in children was identified as the Task Force’s top priority. 
 1-10

control and other utility actions which work together to minimize lead levels at the tap. (40 CFR 

141.80-141.91). In addition, under Section 1417 of the Safe Drinking Water Act, pipes, fittings 

and fixtures for potable water applications may not be used or introduced into commerce unless 

they are considered “lead free” as defined by that Act (40 CFR 141.43).14 Additionally, federal 

Pb abatement programs provide for the reduction in human exposures and environmental 

releases from in-place materials containing Pb (e.g., Pb-based paint, urban soil and dust, and 

contaminated waste sites). Federal regulations on disposal of Pb-based paint waste help facilitate 

the removal of Pb-based paint from residences (68 FR 36487). 

Federal programs to reduce exposure to Pb in paint, dust, and soil are specified under the 

comprehensive federal regulatory framework developed under the Residential Lead-Based Paint 

Hazard Reduction Act (Title X). Under Title X (codified as Title IV of the Toxic Substances 

Control Act [TSCA]), EPA has established regulations and associated programs in the following 

six categories: (1) training, certification and work practice requirements for persons engaged in 

lead-based paint activities (abatement, inspection and risk assessment); accreditation of training 

providers; and authorization of state and tribal lead-based paint programs; (2) training, 

certification, and work practice requirements for persons engaged in home renovation, repair and 

painting (RRP) activities; accreditation of RRP training providers; and authorization of state and 

tribal RRP programs; (3) ensuring that, for most housing constructed before 1978, information 

about lead-based paint and lead-based paint hazards flows from sellers to purchasers, from 

landlords to tenants, and from renovators to owners and occupants; (4) establishing standards for 

identifying dangerous levels of Pb in paint, dust and soil; (5) providing grant funding to establish 

and maintain state and tribal lead-based paint programs; and, (6) providing information on Pb 

hazards to the public, including steps that people can take to protect themselves and their 

families from lead-based paint hazards. 

Under Title IV of TSCA, EPA established standards identifying hazardous levels of Pb in 

residential paint, dust, and soil in 2001. This regulation supports the implementation of other 

regulations which deal with worker training and certification, Pb hazard disclosure in real estate 

transactions, Pb hazard evaluation and control in federally-owned housing prior to sale and 

housing receiving federal assistance, and U.S. Department of Housing and Urban Development 

grants to local jurisdictions to perform Pb hazard control. The TSCA Title IV term "lead-based 

paint hazard" implemented through this regulation identifies lead-based paint and all residential 

lead-containing dust and soil regardless of the source of Pb, which, due to their condition and 

 

14 In 2011, revisions to this section of the Safe Drinking Water Act lowered the amount of Pb permitted in 

pipes, fittings, and fixtures; the changes became effective in January 2014. More information is provided in 

“Summary of the Reduction of Lead in Drinking Water Act and Frequently Asked Questions” at 

http://water.epa.gov/drink/info/lead/index.cfm) 
 1-11

location, would result in adverse human health effects. One of the underlying principles of Title 

X is to move the focus of public and private decision makers away from the mere presence of 

lead-based paint to the presence of lead-based paint hazards, for which more substantive action 

should be undertaken to control exposures, especially to young children. In addition, the success 

of the program relies on the voluntary participation of states and tribes as well as counties and 

cities to implement the programs and on property owners to follow the standards and EPA's 

requirements. 

On March 31, 2008, the EPA issued a new rule (Lead: Renovation, Repair and Painting 

[RRP] Program, 73 FR 21692) to protect children from lead-based paint hazards. This rule 

applies to compensated renovators and maintenance professionals who perform renovation, 

repair, or painting in housing and child-care facilities built prior to 1978. Among its 

requirements is one that requires that firms that conduct RRP activities be certified; that their 

employees be trained; and that they follow protective work practice standards. These standards 

prohibit certain dangerous work practices, such as open flame burning or torching of lead-based 

paint. The required work practices also include posting warning signs, restricting occupants 

from work areas, containing work areas to prevent dust and debris from spreading, conducting a 

thorough cleanup, and verifying that cleanup was effective. The rule became fully effective in 

April 2010. The rule also specifies procedures for the authorization of states, territories, and 

tribes to administer and enforce these standards and regulations in lieu of a federal program. In 

announcing this rule, EPA noted that approximately 37 million homes in the United States 

contain some lead-based paint, and that this rule’s requirements are key components of a 

comprehensive effort to eliminate childhood Pb poisoning. To foster adoption of the rule’s 

measures, EPA has been conducting an extensive education and outreach campaign to promote 

awareness of these new requirements among both the regulated entities and the consumers who 

hire them. In addition, the EPA is investigating whether lead hazards are also created by RRP 

activities in public and commercial buildings, and if appropriate, to issue RRP requirements for 

this class of buildings. 

Programs associated with the Comprehensive Environmental Response, Compensation, 

and Liability Act (CERCLA or Superfund) and Resource Conservation Recovery Act (RCRA) 

also implement abatement programs, reducing exposures to Pb and other pollutants. For 

example, EPA determines and implements protective levels for Pb in soil at Superfund sites and 

RCRA corrective action facilities. Federal programs, including those implementing RCRA, 

provide for management of hazardous substances in hazardous and municipal solid waste (see, 

e.g., 66 FR 58258). Federal regulations concerning batteries in municipal solid waste facilitate 
 1-12

the collection and recycling or proper disposal of batteries containing Pb.15 Similarly, federal 

programs provide for the reduction in environmental releases of hazardous substances such as Pb 

in the management of wastewater (http://www.epa.gov/owm/). 

A variety of federal nonregulatory programs also provide for reduced environmental 

release of Pb-containing materials by encouraging pollution prevention, promotion of reuse and 

recycling, reduction of priority and toxic chemicals in products and waste, and conservation of 

energy and materials. These include the Resource Conservation Challenge 

(http://www.epa.gov/epaoswer/osw/conserve/index.htm), the National Waste Minimization 

Program (http://www.epa.gov/epaoswer/hazwaste/minimize/leadtire.htm), “Plug in to eCycling” 

(a partnership between EPA and consumer electronics manufacturers and retailers; 

http://www.epa.gov/epaoswer/hazwaste/recycle/electron/crt.htm#crts), and activities to reduce 

the practice of backyard trash burning (http://www.epa.gov/msw/backyard/pubs.htm). 

In addition to the Pb control programs summarized above, EPA’s research program 

identifies, encourages and conducts research needed to locate and assess serious risks and to 

develop methods and tools to characterize and help reduce risks. For example, EPA’s Integrated 

Exposure Uptake Biokinetic Model for Lead in Children (IEUBK model) is widely used and 

accepted as a tool that informs the evaluation of site-specific data. More recently, in recognition 

of the need for a single model that predicts Pb concentrations in tissues for children and adults, 

EPA has been developing the All Ages Lead Model (AALM) to provide researchers and risk 

assessors with a pharmacokinetic model capable of estimating blood, tissue, and bone 

concentrations of Pb based on estimates of exposure over the lifetime of the individual (ISA, 

section 3.6). EPA research activities on substances including Pb, such as those identified here, 

focus on improving our characterization of health and environmental effects, exposure, and 

control or management of environmental releases (see http://www.epa.gov/research/). 

Other federal agencies also participate in programs intended to reduce Pb exposures. For 

examples programs of the Centers for Disease Control and Prevention (CDC) provide for the 

tracking of children’s blood Pb levels in the U.S. and provide guidance on levels at which 

medical and environmental case management activities should be implemented (CDC, 2012; 

ACCLPP, 2012).16 As a result of coordinated, intensive efforts at the national, state and local 

levels, including those programs described above, blood Pb levels in all segments of the 

population have continued to decline from levels observed in the past. For example, blood Pb 

 

15 See, e.g., “Implementation of the Mercury-Containing and Rechargeable Battery Management Act” 

http://www.epa.gov/epaoswer/hazwaste/recycle/battery.pdf and “Municipal Solid Waste Generation, Recycling, and 

Disposal in the United States: Facts and Figures for 2005” 

http://www.epa.gov/epaoswer/osw/conserve/resources/msw-2005.pdf. 

16 The CDC guidance on blood Pb levels is described further in section 3.1 below. 
 1-13

levels for the general population of children 1 to 5 years of age have dropped to a geometric 

mean level of 1.17 μg/dL in the 2009-2010 National Health and Nutrition Examination Survey 

(NHANES) as compared to the geometric mean in 1999-2000 of 2.23 μg/dL and in 1988-1991 of 

3.6 μg/dL (ISA, section 3.4.1; CD, AX4-2). Similarly, blood Pb levels in non-hispanic black, 

Mexican American and lower socioeconomic groups, which are generally higher than those for 

the general population, have also declined (ISA, section 3.4.1; Jones et al, 2009). 

The EPA also participates in a broad range of international programs focused on reducing 

environmental releases and human exposures in other countries. For example, the Partnership 

for Clean Fuels and Vehicles program engages governments and stakeholders in developing 

countries to eliminate Pb in gasoline globally.17 From 2007 to 2011, the number of countries 

known to still be using leaded gasoline was reduced from just over 20 to six, with three of the six 

also offering unleaded fuel. All six were expected to eliminate Pb from fuel in the subsequent 

few years (USEPA, 2011e). The U.S. EPA is a contributor to the Global Alliance to Eliminate 

Lead Paint, which is a cooperative initiative jointly led by the World Health Organization and 

the United Nations Environment Programme (UNEP) to focus and catalyze the efforts to achieve 

international goals to prevent children’s Pb exposure from paints containing Pb and to minimize 

occupational exposures to Pb paint. This alliance has the broad objective of promoting a phaseout of the manufacture and sale of paints containing Pb and eventually to eliminate the risks that 

such paints pose. The UNEP is also engaged on the problem of managing wastes containing Pb, 

including lead-containing batteries. The Governing Council of the UNEP, of which the U.S. is a 

member, has adopted decisions focused on promoting the environmentally sound management of 

products, wastes and contaminated sites containing Pb and reducing risks to human health and 

the environment from Pb and cadmium throughout the life cycles of those substances (UNEP 

Governing Council, 2011, 2013). EPA is also engaged in the issue of environmental impacts of 

spent lead-acid batteries internationally through the Commission for Environmental Cooperation 

(CEC), where the EPA Administrator along with the cabinet-level or equivalent representatives 

of Mexico and Canada comprise the CEC’s senior governing body (CEC Council).18

 

17 International programs in which the U.S. participates, including those identified here, are described at 

several web sites: http://epa.gov/international/air/pcfv.html, http://www.unep.org/transport/pcfv/, 

http://www.unep.org/hazardoussubstances/Home/tabid/197/hazardoussubstances/LeadCadmium/PrioritiesforAction/

GAELP/tabid/6176/Default.aspx 

18 The CEC was established to support cooperation among the North American Free Trade Agreement 

partners to address environmental issues of continental concern, including the environmental challenges and 

opportunities presented by continent-wide free trade. 
 1-14

1.3 SCOPE OF CURRENT REVIEW: FATE AND MULTIMEDIA PATHWAYS OF 

AMBIENT AIR LEAD 

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

Pb NAAQS unlike issues addressed in other NAAQS reviews.19 As described in section 1.1, 

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

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

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

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

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

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

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

emissions that occurred in previous years (both before and after establishment of the 1978 

NAAQS) and that contributed to the Pb that exists in human populations and ecosystems today. 

Likewise, we also recognize the role of other, nonair sources of Pb now and in the past that also 

contribute to the Pb that exists in human populations and ecosystems today. As in the last Pb 

NAAQS review, this backdrop of environmental Pb exposure, and its impact on the populations 

and ecosystems which may be the subjects of the currently available scientific evidence, 

complicates our consideration of the health and welfare protection afforded by the current 

NAAQS. In the first section below, we summarize the environmental pathways of human and 

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

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

of the current NAAQS for Pb. 

1.3.1 Environmental Distribution and Exposure Pathways 

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

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

with precipitation, as summarized further in section 2.3 below (ISA, section 2.7.2). Once 

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

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

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

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

houses or transport with surface runoff into nearby water bodies (ISA, sections 2.3 and 3.1). For 

 

19 Some aspects of the review of the secondary standard for oxides of nitrogen and sulfur (completed in 

2012), 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. 
 1-15

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

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

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

infiltration (ISA, section 3.1.1.1). Deposited Pb can also be transported (by direct deposition or 

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

function for Pb in aquatic ecosystems (ISA, sections 2.3.2 and 6.2.1). Lead deposited in 

terrestrial ecosystems can also be incorporated into vegetation and soil matrices (ISA, sections 

2.3.3 and 6.2.1). 

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

ambient air can be distributed in the environment, contributing to human and ecosystem 

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

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

(ISA, sections 3.1.1 and 3.7.1).20 Figure 1-1 additionally illustrates that air-related pathways 

may involve media other than air, including indoor and outdoor dust, soil, surface water and 

sediments, vegetation and biota. As recognized by the figure and discussed more completely in 

the subsections below, Pb occurring in indoor and outdoor environments that has not passed 

through ambient air (nonair Pb) may complicate our consideration of ambient air related Pb 

exposures. Further, the persistence of Pb and the associated environmental legacy of historical 

releases pose an additional complication, also discussed below, with regard to consideration of 

exposures associated with current Pb emissions. 

 

20 The exposure assessment for children performed for the review completed in 2008 employed available 

data and methods to develop estimates intended to inform a characterization of these pathways, as described in the 

rulemaking notices for that review (73 FR 29184; 73 FR 66964) and the associated health risk assessment report 

(USEPA, 2007). 
 1-16

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

1.3.1.1 Human Exposure Pathways 

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

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

through a pathway involving Pb deposition from ambient air (ISA, section 3.1.1.1). Ambient air 

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

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

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

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

food and drinking water. The various inhalation and ingestion air-related pathways may vary 

with regard to the time in which they respond to changes in air Pb concentrations. For example, 

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

air with indoor air (e.g., inhalation) can respond most quickly, while pathways involving 

Ecosystem

Exposures

Ambient  Air

Outdoor Dust

and Soil

Indoor Air,

Indoor Dust

Surface Waters

and Sediments

Wildlife, Livestock, Crops

Current Pb Emissions

to Ambient Air

Human Population

(body burden)

* Compartments marked by asterisk may also include Pb emitted to air in the past 

and Pb from nonair sources (released now and in the past). Depending on the 

compartment, nonair sources may include wastewater releases to surface water or 

Pb usage in paint, drinking water 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)
 1-17

exposure to Pb deposited from ambient air into the environment (e.g., diet) may be expected to 

respond more slowly. The extent of this will be influenced by the magnitude of change, as well 

as – for deposition-related pathways - the extent of prior deposition and environment 

characteristics influencing availability of prior deposited Pb (section 1.3.1.2 below). 

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

ambient air (nonair Pb sources), as summarized further in section 2.3 below (ISA, section 3.7.1). 

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

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

leaded pipe or solder in drinking water distribution systems (ISA, section 3.1.3.3). We also 

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

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

which have left a legacy of Pb in other (nonair) media. 

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

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

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

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

as a person’s age and nutritional status (ISA, sections 5.1, 5.2, 5.2.1, 5.2.5 and 5.2.6). Thus, the 

relative contributions from specific pathways is situation specific (ISA, p. 1-11), although a 

predominant Pb exposure pathway for very young children is the incidental ingestion of indoor 

dust by hand-to-mouth activity (ISA, section 3.1.1.1). For adults, however, diet may be the 

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

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

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

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

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

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

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

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

dominate a child’s Pb exposures (ISA, sections 3.1 and 3.1.3.2; 2006 CD, section 3.2.3). In 

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

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

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

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

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

of air-related Pb to ingestion exposure pathways is limited by the paucity of studies that parse 
 1-18

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

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

emissions is similarly limited, as discussed further in section 1.3.2 below. 

1.3.1.2 Ecosystem Exposure Pathways 

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

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

vegetation to air-related Pb can occur by contact with ambient air or by contact with soil, water 

or food items that have been contaminated by Pb from ambient air (ISA, section 6.2). Transport 

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

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

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

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

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

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

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

urban runoff and surface water discharges). 

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

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

on concentrations in other media can vary with the media (e.g., ISA, section 6.2.2). For example, 

exposure pathways most directly involving Pb in ambient air or surface waters can respond more 

quickly to changes in ambient air Pb concentrations while pathways involving exposure to Pb in 

soil or sediments generally respond more slowly. An additional influence on the response time 

for nonair media is the environmental presence of Pb associated with past, generally higher, air 

concentrations. For example, after a reduction in air Pb concentrations, the time needed for 

sediment or surface soil concentrations to indicate a response to reduced air Pb concentrations 

might be expected to be longer in areas of more substantial past contamination than in areas with 

lesser past contamination. Thus, considering the Pb concentrations occurring in nonair media as 

a result of air quality conditions that meet the current NAAQS is a complexity of this review, as 

it also was, although to a lesser degree, with regard to the prior standard in the last review. 

1.3.2 Considerations Related to Historically Emitted Lead 

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

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

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

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

standard and its potential to cause health or welfare effects as a result of exposures to Pb in air or 
 1-19

in other media. Our framing of the focus in this way differs from that for NAAQS reviews 

involving other pollutants. We frame the focus in this way in consideration of the multiple 

exposure pathways for Pb currently being emitted and in consideration of the persistence of Pb in 

the environment over time, a characteristic which does not affect reviews of other NAAQS. In 

considering the case for Pb, however, we recognize that, because of its persistence, both recent 

emissions to ambient air and the substantial emissions of the past contribute to current Pb 

exposures (via multiple exposure pathways, as summarized in section 1.4.1 above). And we 

recognize that past Pb emissions contributed to many situations where air concentrations were 

well in excess of the current Pb standard, and may continue to contribute to exposures even 

where air concentrations are below the current standard. Yet our task in this and every NAAQS 

review is focused on assessing the adequacy of the current standard. 

The substantial historical emissions to air and releases to nonair media contributed to 

human and environmental exposures in the past (e.g., 1978 CD, 1986 CD, 2006 CD, ISA). 

Because of the persistence of Pb, historical exposures associated with both air-related and 

nonair-related sources have contributed a legacy of Pb that is now stored within older humans 

and ecosystems. For example, concentrations of Pb in the bone and blood of older members of 

the U.S. population, who lived during the time of widespread air emissions associated with 

leaded gasoline usage (as well as higher industrial emissions) under the previous Pb NAAQS or 

prior to establishment of any Pb NAAQS, are greater than what would result from air quality 

conditions allowed by the current, more restrictive NAAQS. Epidemiological studies of these 

populations, in which this exposure history is represented by current bone or blood Pb 

concentrations, contribute to the overall evidence base regarding lead-related health effects (as 

discussed in chapter 3 below). Such studies of these historically exposed populations, however, 

are generally less informative in judging the adequacy of the current primary standard (as 

discussed in chapter 3 below). This is in contrast to epidemiological studies of very young 

populations with much shorter and more recent exposure histories (also discussed in chapter 3). 

Substantial and widespread atmospheric emissions of Pb in the U.S. (as well as releases 

to other media) extend back through the 19th century (Yohn et al, 2004; Jackson et al., 2004; 

Graney et al., 1995). These historical emissions contributed to the distribution of Pb within and 

well beyond the U.S. (ISA, section 2.5.5; Reuer and Weiss, 2002; McConnell and Edwards, 

2008). Although it has not been completely and totally characterized, multiple aspects of the 

legacy of this widespread distribution have been documented and described. The current 

concentrations of Pb in U.S. ecosystems thus reflect the influence of greater air emissions that 

occurred in the past, under the prior Pb NAAQS and prior to establishment of any Pb NAAQS.21 

 

21 The current distribution of Pb in U.S. ecosystems also reflects historical nonair releases. 
 1-20

As described further in section 2.3 below, media in ecosystems across the U.S. are still 

recovering from the past period of greater atmospheric emissions and deposition that is 

documented in media such as soil, aquatic sediments and peat bogs (2006 CD, section 2.3.1; 

ISA, section 2.6.2). Core samples of these media show a pattern of Pb concentrations in 

deposited material that peaks around the 1970s followed by marked decline in more recent years 

(2006 CD, section 2.3.1; ISA section 2.6.2). Individual ecosystem responses differ with regard 

to their rates of change in media concentrations due to the extent of contamination in individual 

systems as well as the influence of ecosystem-specific characteristics (further described in 

section 2.3 below). Thus, the time required for these ecosystem media to come to a condition 

that is relatively stable with time (i.e., “steady-state”) will also vary, and the resulting range of 

“steady-state” media concentrations in U.S. ecosystems under ambient air concentrations 

consistent with the current NAAQS are unknown. Future research may better inform our 

understanding in this area. 

In considering the array of ecological effects evidence in this review, we recognize that 

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

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

associated with environmental Pb, does not directly inform our consideration of welfare effects 

that might be anticipated under the current secondary standard and thus may be generally less 

informative in judging the adequacy of the current standard. The availability of information on 

whether adverse effects could be anticipated from the Pb in terrestrial and aquatic ecosystems 

that results from air quality conditions allowed by the current, more restrictive NAAQS is 

discussed in chapter 5, with consideration of the current NAAQS discussed in chapter 6. 

1.4 GENERAL ORGANIZATION OF THE DOCUMENT 

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

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

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

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

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

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

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

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

considerations and subsequent discussion of the Pb NAAQS. 

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

health and the primary standard. These chapters are organized around a series of questions, 
 1-21

building on those identified in the IRP, that address the key policy-relevant issues related to the 

primary standard. Chapter 3 presents an overview of key policy-relevant health effects evidence 

and major health-related conclusions from the ISA; an examination of issues related to the 

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

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

implications of the evidence and exposure/risk information. Chapter 4 includes staff’s 

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

standard and associated conclusions related to the adequacy of the current primary standard. 

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

similarly organized around a series of questions, building on those identified in the IRP, that 

address the key policy-relevant issues related to the secondary standard. Chapter 5 presents an 

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

welfare effects-related conclusions from the ISA; an examination of issues related to the 

screening-level ecological risk assessment; and key results from the risk assessment together 

with a discussion of uncertainty and variability in the results; and discussion of the public 

welfare implications of the quantitative assessment with regard to the current standard. The final 

chapter, chapter 6, includes staff’s conclusions related to the adequacy of the current secondary 

standard. 

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and Implementation of the Lead Campaign. Final Report. Document number EPA-100-R-11-008. Office of 

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

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

http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html 

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

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

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

U.S. Environmental Protection Agency. (2013a) Integrated Science Assessment for Lead. Washington, DC, 

EPA/600/R-10/075F. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html 

U.S. Environmental Protection Agency. (2013b) Policy Assessment for for the National Ambient Air Quality 

Standards for Lead. External Review Draft. Research Triangle, NC. EPA-452/P-13-001. Available online 

at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_pa.html. 
2-1 

2 AMBIENT AIR LEAD 

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

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

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

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

ambient air-related Pb in other media. 

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

in various sizes (ISA, section 2.3).1 Once emitted, particle-bound Pb can be transported long or 

short distances depending on particle size, which influences the amount of time spent in the 

aerosol phase. Consistent with previous evidence, recent research on particulate matter with 

mass median diameter of 2.5 and of 10 micrometers (PM2.5 and PM10) confirms the transport of 

airborne Pb in smaller particles appreciable distances from its sources. For example, samples 

collected at altitude over the Pacific Ocean, as well as the seasonal pattern of Pb-PM2.5 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 to western U.S. Pb concentrations (ISA, 

sections 2.3.1 and 2.5.5; Murphy et al., 2007). In general, larger particles tend to deposit more 

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

phase and travel longer distances before depositing (ISA, section 1.2.1). As summarized in 

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

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

sources. 

In this chapter, we discuss the current information on on sources and emissions of Pb to 

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

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

2.3). 

2.1 SOURCES AND EMISSIONS TO AMBIENT AIR 

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

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

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

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

 

1

 While in some circumstances Pb can be emitted in gaseous form, the Pb compounds that may be produced 

initially in vapor phase can be expected to condense into particles upon cooling to ambient temperature and/or upon 

oxidizing with mixing into the atmosphere (ISA, section 2.2.2.1; Gidney et al., 2010). 
2-2 

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

U.S. 

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

20082

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

hazardous air pollutants from air emissions sources. The NEI is generally prepared at three-year 

intervals, such that the next NEI, for 2011, is currently under development. The NEI is prepared 

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

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

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

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

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

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

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

the ISA) are drawn from the 2008 NEI version 3.3

 As a result of various Clean Air Act 

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

categories represented in the NEI are projected to result in considerably lower emissions at the 

current time or in the near future. (Appendix 2A) 

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

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

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

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

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

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

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

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

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

summarized here is described in Appendix 2B. 

2.1.1 Temporal Trends on a National Scale 

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

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

in the transportation sector due to the removal of Pb from gasoline used in on-road vehicles. 

Lead emissions were further reduced substantially between 1990 and 2008, with significant 

 

2 http://www.epa.gov/ttn/chief/net/2008inventory.html 3

 With regard to Pb emissions, the 2008 NEI, version 3 (January 2013) has been augmented with sources 

not included in the 2008 NEI, version 2. 
2-3 

reductions occurring in the metals industries at least in part as a result of national emissions 

standards for hazardous air pollutants. 

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

2.1.2 Sources and Emissions on National Scale - 2008 

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

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

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

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

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

combustion). The latter individually are generally small sources, which comprise a large 

category when aggregated nationally (Table 2-1). The next largest categories are various metals 

industries, including lead-specific industries (Table 2-1). Together these and other sources were 

estimated to emit just under a thousand tpy of Pb in the U.S. in 2008. 
2-4 

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

Source Category Description 2008 

Emissions (tons) 

ALL CATEGORIES A 950 

Aircraft operating on leaded fuel B 550 

Industrial/Commercial/Institutional Boilers & Process Heaters 63 

Utility Boilers 51 

Iron and Steel Foundries 30 

Integrated Iron and Steel Manufacturing 27 

Steel Manufacturing: Electric Arc Furnaces 22 

Secondary Lead Smelting 20 

Primary Lead Smelting 19 C

Primary Copper Smelting 17 

Mining 15 

Military Base 13 

Cement Production 8 

Glass Manufacturing 8 

Battery Manufacturing 8 

Secondary Non-ferrous Metals (other) 7 

Primary Non-ferrous Metals (other) 7 

Carbon Manufacturing 6 

Pulp and Paper Production 6 

Secondary Copper Smelting 5 

Commercial Marine Vessels 5 

Fabricated Metal Products Manufacturing 5 

Residential Heating 5 

Municipal Waste Incineration 4 

Sewage Sludge Incineration 4 

Mineral Products Manufacturing 4 

A - Emissions estimate totals from 2008 National 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 Pb 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 ceased smelter operations at this site at the end of 2013 (USEPA, 2012). 
2-5 

2.1.2.1 Stationary Sources 

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

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

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

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

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

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

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

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

category (a 68% reduction). Also, the NESHAPs for Primary and Secondary Lead Smelting 

were revised in 2011 and 2012, respectively (76 FR 70834, 77 FR 555), as well as more than a 

dozen additional EPA actions taken in the past 5 years, which would not be reflected in the 2008 

NEI estimates, will result in Pb emissions reductions (Appendix 2A). 

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

Facilities have numerous processes that can fall into 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. 
2-6 

2.1.2.2 Mobile Sources 

Forty years ago, combustion of leaded gasoline was the main contributor of Pb to the air. 

In the early 1970s, the EPA set national regulations to gradually reduce the Pb content in 

gasoline. In 1975, unleaded gasoline was introduced for motor vehicles equipped with catalytic 

converters. The EPA banned the use of leaded gasoline in highway vehicles after December 

1995. 

Lead emissions from piston-engine aircraft operating on leaded fuel are currently the 

largest source of Pb air emissions on a national scale. Lead is added to aviation gasoline 

(commonly referred to as “avgas”) used in most piston-engine aircraft in order to boost octane 

and prevent engine knock.4

 The most commonly used avgas, 100 Octane Low Lead, contains up 

to 2.12 grams Pb per gallon (ASTM D 910). The Federal Aviation Administration estimates that 

in 2008, 248 million gallons of avgas were consumed in the U.S.5

 contributing an estimated 550 

tons of Pb to the air that comprise 58% of the national Pb inventory.6

 Leaded avgas is used at 

approximately 20,000 airport facilities in the United States. 

The EPA is currently collecting and evaluating information regarding emissions and air 

concentrations of Pb resulting from avgas combustion by piston-engine aircraft (including 

monitoring data described in section 2.2.1.1 below). This is part of an ongoing investigation 

under section 231 of the Clean Air Act into the potential for these emissions to cause or 

contribute to air pollution that may reasonably be anticipated to endanger public health or 

welfare. This evaluation by the EPA is occurring separate from the NAAQS review. The EPA’s 

investigation includes substantial analytical work. The timeline for completion of this 

investigation and possible issuance of a final endangerment determination includes completion 

of necessary modeling and monitoring information and other data, development of a proposal 

which will be published for public comment, review and analysis of comments received and 

issuance of the final determination. If the EPA issues a positive determination that Pb emissions 

from aircraft engines cause or contribute to air pollution that may reasonably be anticipated to 

endanger public health or welfare, the EPA would then be required to propose and promulgate 

emissions standards to control aircraft engine Pb emissions, and the Federal Aviation 

 

4

 Lead is not added to jet fuel used in commercial aircraft, military aircraft, or other turbine engine aircraft. 5 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. 6

 EPA (2010) Calculating Piston-Engine Aircraft Airport Inventories for Lead for the 2008 National 

Emissions Inventory. EPA-420-B-10-044. Available at: 

http://www.epa.gov/otaq/regs/nonroad/aviation/420b10044.pdf 
2-7 

Administration would be required to promulgate regulations addressing the fuel used by those 

aircraft. More information about EPA’s actions is available at www.epa.gov/otaq/aviation.htm. 

Vehicles used in racing are not regulated by the EPA under the Clean Air Act and can 

therefore use alkyl-Pb additives to boost octane. The National Association for Stock Car Auto 

Racing (NASCAR) formed a voluntary partnership with the EPA with the goal of permanently 

removing alkyl-Pb from racing fuels used in the racing series now known as the Sprint Cup, the 

Nationwide Series and the Camping World Truck Series. The major NASCAR race series now 

use unleaded fuels. 

Due to the presence of Pb as a trace contaminant in gasoline, diesel fuel and lubricating 

oil, cars, trucks, and engines operating in nonroad equipment, marine engines and jet aircraft 

emit small amounts of Pb (ISA, Section 2.2.2.6). Additional mobile sources of Pb include brake 

wear, tire wear, and loss of Pb wheel weights (ISA, Section 2.2.2.6). 

2.1.2.3 Natural Sources and Long-range Transport 

Some amount of Pb in the air in the U.S. derives from natural sources, such as volcanoes, 

sea salt, and windborne soil particles from areas free of anthropogenic activity and some may 

also derive from anthropogenic sources of airborne Pb located outside of the U.S. (ISA, section 

2.5.5). Emissions estimates for these sources, as well as forest wildfires and biogenic sources, 

have not been developed for the NEI. Quantitative estimates for these processes remain an area 

of significant uncertainty. Based on several different approaches, the ISA identifies several 

estimates of the concentration of airborne Pb derived from natural sources. The estimates extend 

no higher than 1 nanogram per cubic meter (ng/m3

), and extend down as low as 0.02 ng/m3 (ISA, 

section 2.5.5). The data available to derive such an estimate are limited and such a value might 

be expected to vary geographically with the natural distribution of Pb. 

Another contribution to U.S. airborne Pb concentrations is long-range transport such as 

that associated with air masses carrying Pb from sources in Asia, where controls on Pb emissions 

have lagged those in the U.S. and Canada (ISA, section 2.5.5; Osterberg et al., 2008). The most 

recent estimates of contributions from Asia, however, conclude that the Asian contribution to 

U.S. airborne Pb concentrations is generally less than 1 ng/m3

 (ISA, section 2.5.5; Murphy, 

2007; Ewing et al., 2010). 

2.1.2.4 Previously Deposited Lead 

Lead-bearing particles that occur in outdoor dust on soil or built surfaces (e.g., streets and 

sidewalks) can be a source of airborne Pb as a result of particle resuspension (ISA, section 

2.3.1.3). Proximity to major sources of Pb emissions, the extent of previous or historic 

deposition, and the effectiveness of natural and human removal processes dictate how important 

resuspension may be as a contribution to air Pb concentrations. In addition to resuspension and 
2-8 

subsequent dispersion, surface water runoff (e.g., associated with rainfall) also plays a role in the 

movement of Pb-bearing particles from outdoor surfaces to human-made or natural stormwater 

sediment catchments (ISA, sections 1.2.1, 2.3.1.3, 2.3.2 and 2.3.2.4; Wong et al., 2006). Mean 

residence time of street dust has been estimated for a low-traffic street (approximately 30 

vehicles/hour) to be several months but less than a year (ISA, section 2.3.1.3; Allott et al 1990). 

Outdoor dust may be resuspended into the air by wind or human-induced mechanical 

forces, such that the main drivers of particle resuspension are typically mechanical stressors such 

as vehicular traffic, construction and agricultural operations, and, generally to a lesser extent, the 

wind (ISA, section 2.3.1.3; 2006 CD, section 2.3.3). Wind resuspension, often defined in terms 

of a resuspension rate (the fraction of a surface contaminant released per unit time) is dependent 

on many factors, including wind speed, soil/surface moisture, particle size, presence of saltating 

particles and presence of vegetation; typical values range over several orders of magnitude (ISA, 

section 3.3.1.3; 2006 CD, section 2.3.3). Vehicular resuspension results from shearing stress of 

tires or turbulence generated by a passing vehicle and can be affected by a number of factors 

including vehicle size, vehicle speed, soil or surface moisture, and particle size (ISA, section 

2.3.1.3; 2006 CD, section 2.3.3). Variability and 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).7

The relative importance of resuspension of previously deposited dust particles as an 

influence on airborne Pb concentrations will depend on site-specific circumstances, such as the 

magnitude of Pb concentrations in the surface dust and air Pb contributions from nearby sources 

of new Pb emissions, as well as with variation in the forces that influence particle resuspension. 

For example, the highest air Pb concentrations associated with resuspension appear to occur in 

areas of highly contaminated surface dust associated with historically active industrial sites, 

which may or may not be currently active (ISA, sections 2.3.1.3). Air concentrations near such 

sites with currently active facilities (e.g., metals industries) will reflect the impact of emissions 

from the current industrial activity in addition to that from resuspension of any previously 

deposited material (often a component of “fugitive” emissions estimates8

). Accordingly, as 

might be expected, the limited data available for comparison indicate the relative magnitude of 

 

7

 Quantitative estimates of resuspension-related emissions associated with many active industrial sources 

(particularly metals sources) are included within the NEI, although such emissions associated with previously and 

no longer active Pb sources are not as generally included in the NEI. 8

 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). 
2-9 

air Pb concentrations associated with no-longer-active industrial sites to be generally lower than 

that for active sites yet greater than that in locations somewhat removed from industrial sources 

(section 2.2.2.2 below). 

Lead-bearing particulate matter in other, non-industrial, locations of appreciable historic 

Pb contamination, such as in soils or on surfaces in older urban areas or near older transportation 

corridors may, if disturbed, also become suspended into the air and contribute to air Pb 

concentrations, although the availability of such material for resuspension might be expected to 

decline over time in most locations due to transport and removal processes. In older 

transportation corridors or other locations not influenced by active industries, the significance of 

resuspension (e.g., in terms of resultant air Pb concentrations) appears to be much less than that 

associated with active industries or now-closed industries with substantial emissions in the past.9

 

For example, the available data indicate that current Pb concentrations near roadways are 

substantially lower than those near large, currently active industrial sources (see ISA, sections 

2.3.1.3 and 2.5.1.2 and Figures 2-9 and 2-11 below). In general, air Pb concentrations at sites 

described as not influenced by an active industry are much lower than those near active sources 

(see ISA, section 2.5.1.2 and Figure 2-11 below). 

2.1.3 Sources and Emissions on Local Scale 

Based on the 2008 estimates, the highest emissions in specific situations locally are from 

different types of metals industries, 23 of which had 2008 estimates greater than or equal to 1.0 

tpy Pb (Table 2-2). The geographic distribution of the facilities summarized in Table 2-2 is 

presented in Figure 2-2. 

 

9

 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). 
2-10 

Table 2-2. Facilities estimated to emit at least 0.50 tpy of Pb 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 4 3 2.3 - 8.8 

Military Base 4 3 1.4 - 7.2 3 3 

Secondary Lead Smelting Plant 5 5 1.4 - 7.1 3 2 

Carbon or Graphite Plant 1 1 6.3 

Primary Non-ferrous Metal Smelting/Refining Plant (not 

Lead, Gold, Aluminum, or Copper) 1 1 5.4 

Mines/Quarries 5 2 1.6 - 3.8 

Ethanol Biorefineries 2 2 1.5 - 3.8 

Portland Cement Manufacturing 1 1 3.3 

Pulp and Paper Plant 2 2 2.5 - 3.0 2 2 

Calcined Pet Coke Plant 1 1 2.5 

Battery Plant 3 3 1.5 - 2.5 1 1 

Wood Board Manufacturing Plant 1 1 2.3 

Foundries, Iron and Steel 3 3 1.1 - 2.3 10 8 

Foundries, Non-ferrous 3 2 1.2 - 2.0 2 2 

Secondary Non-ferrous Metal Smelting/Refining Plant 

(not Lead, Aluminum, or Copper) 2 2 1.2 - 2.0 1 1 

Coke Battery 2 2 1.0 - 1.8 

Electricity Generation via Combustion 2 2 1.0 - 1.7 7 5 

Chemical Plant 1 1 1.7 2 2 

Airport 6 4 1.0 - 1.3 52 17 

Automobile/Truck or Parts Plant 1 1 1.2 3 2 

Wastewater Treatment Facility 1 1 1.0 2 2 

Munition or Explosives Plant 1 1 1.0 2 2 

Glass Plant 2 2 

Fabricated Metal Products Plant 5 4 

Municipal Waste Combustor 3 3 

Lumber/Sawmill 2 1 

Plastic, Resin, or Rubber Products Plant 1 1 

Taconite Processing Plant 1 1 

Petroleum Storage Facility (Bulk Station) 1 1 

A - Emissions totals from 2008 National Emissions Inventory, version 3 (January 2013), except in the case of airports for which 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 additional uncertainty regarding this total emissions estimate for this facility, the only remaining operational primary Pb smelter in 

the U.S., which ceased smelter operations at this site at the end of 2013 (USEPA, 2012).
2-11

Figure 2-2. Geographic distribution of facilities and airports estimated to emit at least 0.50 tpy of Pb in 2
2-12 

2.2 AMBIENT AIR QUALITY 

The EPA and state and local agencies have been measuring Pb in the atmosphere since 

the 1970s. In response to reduced emissions (see section 2.1), Pb concentrations have decreased 

dramatically over that period. Currently, the highest concentrations occur near some metals 

industries where some individual locations have concentrations that exceed the NAAQS. This 

section describes the ambient Pb measurement methods, the sites and networks where these 

measurements are made, and how the ambient Pb concentrations vary geographically and 

temporally. 

2.2.1 Air Monitoring 

Ambient air Pb concentrations are measured by five national monitoring networks. The 

networks include the State and Local Air Monitoring Sites (SLAMS) intended for Pb NAAQS 

surveillance, the PM2.5 Chemical Speciation Network (CSN), the Interagency Monitoring of 

Protected Visual Environments (IMPROVE) network, the National Air Toxics Trends Stations 

(NATTS) network, and the Urban Air Toxics Monitoring program. All of the data from these 

networks are accessible via EPA’s Air Quality System (AQS): 

http://www.epa.gov/ttn/airs/airsaqs/. In addition to these networks, various environmental 

organizations have operated other sampling sites yielding data (which may or may not be 

accessible via AQS) on ambient air concentrations of Pb, often for limited periods and/or for 

primary purposes other than quantification of Pb itself. The subsections below describe each 

network and the Pb measurements made at these sites. 

2.2.1.1 Lead NAAQS Surveillance Network 

This section describes sample collection, analysis and network aspects for the Pb SLAMS 

network, the main purpose of which is surveillance for the Pb NAAQS. As such, the EPA 

regulates how this monitoring is conducted in order to ensure accurate and comparable data for 

determining compliance with the NAAQS. The code of federal regulations (CFR) at parts 50, 53 

and 58 specifies required aspects of the ambient monitoring program for NAAQS pollutants.10 

In order to be used in NAAQS attainment designations, ambient Pb concentration data must be 

obtained using either the federal reference method (FRM) or a federal equivalent method (FEM). 

The indicator for the current Pb NAAQS is Pb-TSP. However, in some situations,11 ambient Pb-

 

10 The FRMs for sample collection and analysis are specified in 40 CFR part 50, the procedures for 

approval of FRMs and federal equivalent methods are specified in 40 CFR part 53 and the rules specifying 

requirements for the planning and operations of the ambient monitoring network are specified in 40 CFR part 58. 11 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 C, section 2.10.1.2. These conditions 

include where Pb concentrations are not expected to equal or exceed 0.10 micrograms per cubic meter as an 
2-13 

PM10 concentrations may be used in judging nonattainment. Accordingly, FRMs have been 

established for Pb-TSP and for Pb-PM10. The current FRM for the measurement of Pb-TSP is 

provided in 40 CFR part 50 Appendix G. This FRM includes sampling using a high-volume 

TSP sampler that meets the design criteria identified in 40 CFR part 50 Appendix B and sample 

analysis for Pb content using flame atomic absorption. There are 24 FEMs currently approved 

for Pb-TSP.12 All 24 FEMs are based on the use of high-volume TSP samplers and a variety of 

approved equivalent analysis methods. 

A new FRM for Pb-PM10 was promulgated as part of the 2008 review (40 CFR part 50 

Appendix Q). This FRM is based on the PM10 sampler defined in 40 CFR part 50 Appendix J 

coupled with x-ray fluorescence (XRF) analysis. In addition, one FEM for Pb-PM10 has been 

finalized for the analysis of Pb-PM10 based on inductively coupled plasma mass spectroscopy 

(ICP-MS). 

The current Pb monitoring network design requirements for NAAQS compliance 

purposes (40 CFR part 58, Appendix D, paragraph 4.5) include two types of monitoring sites – 

source-oriented monitoring sites and non-source-oriented monitoring sites. Source-oriented 

monitoring sites are required near sources of air Pb emissions which are expected to or have been 

shown to contribute to ambient air Pb concentrations in excess of the NAAQS. At a minimum, 

there must be one source-oriented site located to measure the maximum Pb concentration in 

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.13 The EPA 

Regional Administrators may require additional monitoring beyond the minimum requirements 

where the likelihood of Pb air quality violations is significant. Such locations may include those 

near additional industrial Pb sources, recently closed industrial sources and other sources of 

resuspended Pb dust, as well as airports where piston-engine aircraft emit Pb (40 CFR, part 58, 

Appendix D, section 4.5(c)). 

Monitoring agencies are also required, under 40 CFR, part 58, Appendix D, to conduct 

non-source-oriented Pb monitoring at the NCore sites required in metropolitan areas with a 

population of 500,000 or more.14 NCore is a network of multipollutant monitoring stations 

 

arithmetic three-month mean and where the source of Pb emissions is expected to emit a substantial majority of its 

Pb in the size fraction captured by PM10 monitors. 12 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 13 The Regional Administrator may waive the requirement in paragraph 4.5(a) for monitoring near Pb 

sources if the State or, where appropriate, local agency can demonstrate the Pb source will not contribute to a 

maximum three-month average Pb 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)). 14 Defined by the US Census Bureau - http://www.census.gov/population/www/metroareas/metroarea.html 
2-14 

intended to meet multiple monitoring objectives that formally began in January 2011. The NCore 

stations are a subset of the state and local air monitoring stations network and are intended to 

support long-term trends analysis, model evaluation, health and ecosystem studies, as well as 

NAAQS compliance. The complete NCore network consists of approximately 60 urban and 20 

rural stations, including some existing SLAMS sites that have been modified for additional 

measurements. Each state will contain at least one NCore station, and 46 of the states plus 

Washington, DC, will have at least one urban station. 

Either Pb-TSP or Pb-PM10 monitoring may be performed at these sites. Of 50 NCore 

sites measuring Pb concentrations as of April 2014, 28 are measuring Pb in TSP and 24 are 

measuring Pb in PM10 (two sites are measuring both Pb in TSP and Pb in PM10). While nonsource-oriented monitoring data can be used for purposes of NAAQS attainment designations, a 

main objective for non-source-oriented monitoring is to gather information on neighborhoodscale Pb concentrations that are typical in urban areas in order to better understand ambient airrelated Pb exposures for populations in these areas. 

Source-oriented monitors near sources estimated to emit 1.0 tpy Pb were required to be 

operational by January 1, 2010, and the remainder of the newly required source-oriented 

monitors were required to be operational by December 27, 2011 (75 FR 81126). Currently, 

approximately 260 Pb-TSP monitors are in operation; these are a mixture of source- and nonsource-oriented monitors. Figure 2-3 shows the geographic distribution of these monitors (in 

addition to the airport study monitors described below) in the Pb NAAQS surveillance 

network,15 with the Pb-TSP monitors existing at the time of the 2008 rulemaking indicated 

separately from the newly sited Pb-TSP monitors. 

 

15 This figure reflects Pb-TSP monitors in AQS as of September 2012. 
2-15 

Figure 2-3. Map of Pb-TSP monitoring sites in current Pb NAAQS monitoring network. 

The current regulations also required one year of Pb-TSP monitoring (using FRM or 

FEM methods) near 15 specific airports in order to gather additional information on the 

likelihood of NAAQS exceedances near airports due to the combustion of leaded aviation 

gasoline (75 FR 81126). These airports were selected based on three criteria: annual Pb 

inventory between 0.5 ton/year and 1.0 ton/year, ambient air within 150 meters of the location of 

maximum emissions (e.g., the end of the runway or run-up location), and airport configuration 

and meteorological scenario that leads to a greater frequency of operations from one runway. 

These characteristics were selected because they are expected, collectively, to identify airports 

with the highest potential to have ambient Pb concentrations approaching or exceeding the Pb 

NAAQS. Data from this monitoring study will be used to assess the need for additional Pb 

monitoring at airports. These 15 sites (Figure 2-4) were intended to be operational no later than 

December 27, 2011, although delays in monitor siting extended the installation of some of these 

monitors into late 2012. 
2-16 

Figure 2-4. Sites near airports at which one year of Pb-TSP monitoring is required.16

2.2.1.2 Other Lead Monitoring Networks 

The NATTS network, designed to monitor concentrations of hazardous air pollutants 

including Pb compounds, included 25 sites measuring Pb-PM10 as of 2012. Most of these sites 

(20) are in urban areas (Figure 2-5). In addition to the NATTS network, as of 2012, states were 

collecting Pb-PM10 at an additional 22 sites (most as part of the Urban Air Toxics Monitoring 

program). All collect particulate matter as PM10 for toxic metals analysis using either a highvolume PM10 sampler or a low volume PM10 sampler, typically on a 1 in 6 day sampling 

schedule. Most of these monitoring locations are not measuring using FRM/FEM methods at 

this time. Lead in the collected sample is generally quantified via an ICP/MS method. The 

standard operating procedure for metals by ICP/MS is available at: 

 

16 The 15 Airports are: Merrill Field (Anchorage, AK), Pryor Field Regional (Limestone, AL), Palo Alto 

Airport of Santa Clara County and Reid-Hillview (both in Santa Clara, CA), McClellan-Palomar and Gillespie Field 

(both in San Diego, CA), San Carlos (San Mateo, CA), Nantucket Memorial (Nantucket, MA), Oakland County 

International (Oakland, MI), Republic and Brookhaven (both in Suffolk, NY), Stinson Municipal (Bexar, TX), 

Northwest Regional (Denton, TX), Harvey Field (Snohomish, WA), and Auburn Municipal (King, WA). 
2-17 

http://www.epa.gov/ttn/amtic/airtox.html . As noted in section 2.2.1.1 above, non-sourceoriented Pb monitoring using FRM/FEMs that is required at the 51 NCore sites with a population 

of 500,000 or more (shown in Figure 2-5) may be Pb-PM10. As shown in Figure 2-5, there are 

some cases where states have addressed their NATTS and NCore Pb monitoring needs with the 

use of a single monitoring site or may have nearby sites. 

Figure 2-5. Pb-PM10 monitoring sites.17 

 

 

17 Presented on this map are all NCore sites where FRM/FEM Pb monitoring is required along with other 

sites actively monitoring Pb-PM10 (by any method) based on having 2012 data in AQS as of September 2012. 
2-18 

Two networks measure Pb in PM2.5, the EPA CSN and the IMPROVE network. The 

CSN consists of 53 long-term trends sites (commonly referred to as the Speciation Trends 

Network or STN sites) and approximately 150 supplemental sites, all operated by state and local 

monitoring agencies. Most STN sites operate on a 1 in 3 day sampling schedule, while most 

supplemental sites operate on a 1 in 6 day sampling schedule. All sites in the CSN network 

determine Pb concentrations in PM2.5 samples. Lead is quantified via the XRF method.18 Data 

are accessible through AQS. The locations of the CSN are shown in Figure 2-6. Nearly all of the 

CSN sites are in urban areas, often at the location of highest known PM2.5 concentrations. The 

first CSN sites began operation around 2000. 

The IMPROVE network is administered by the National Park Service, largely with 

funding by the EPA, on behalf of federal land management agencies and state air agencies that 

use the data to track trends in rural visibility. Lead in PM2.5 is quantified via the XRF method, as 

in the CSN. Data are managed and made accessible mainly through the VIEWS website 

(http://vista.cira.colostate.edu/views/) but are also available via AQS. Samplers are operated by 

several different federal, state, and tribal host agencies on the same 1 in 3 day schedule as the 

STN. In the IMPROVE network, PM2.5 monitors are placed in “Class I” areas (including 

National Parks and wilderness areas) and are mostly in rural locations (Figure 2-6). The oldest 

of these sites began operation in 1988, while many others began in the mid 1990s. There are 110 

formally designated IMPROVE sites, which are located in or near national parks and other Class 

I visibility areas, virtually all of these being rural. Approximately 80 additional sites at various 

urban and rural locations, requested and funded by various parties, are also informally treated as 

part of the network. 

 

18 The standard operating procedure for metals by XRF is available at: 

http://www.epa.gov/ttnamti1/files/ambient/pm25/spec/xrfsop.pdf . 
2-19 

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

2.2.1.3 NAAQS Surveillance Monitoring Considerations 

In this section, aspects of the methods for sampling and analysis of the Pb are reviewed, 

and the current NAAQS surveillance network of monitoring locations are considered. The 

methods for sampling and analysis are considered in light of the indicator for the Pb NAAQS, 

and conclusions regarding the current NAAQS and associated indicator appear in chapter 4. 

Consideration of the ambient air monitoring network generally informs the interpretation of 

current data on ambient air concentrations and helps identify whether the monitoring network is 

adequate to determine compliance with the NAAQS. This section discusses considerations 

related to these aspects of the ambient air monitoring program for Pb.19

2.2.1.3.1 Sampling Considerations 

As described in section 2.2.1.1 above, consistent with the Pb NAAQS indicator being PbTSP, the FRM for Pb, which is required at all source-oriented sites, is measurement of Pb-TSP 

using a high-volume TSP sampler meeting the design criteria specified in 40 CFR part 50 

 

19 The code of federal regulations (CFR) at parts 50, 53 and 58 specifies required aspects of the ambient 

monitoring program for NAAQS pollutants. The FRMs for sample collection and analysis are specified in 40 CFR 

part 50, the procedures for approval of FRMs and FEMs are specified in 40 CFR part 53 and the rules specifying 

requirements for the planning and operations of the ambient monitoring network are specified in 40 CFR part 58. 
2-20 

Appendix B. During the review of the Pb NAAQS completed in 2008, CASAC noted the 

variability in high-volume TSP sample measurements associated with the effects of wind speed 

and wind direction on collection efficiency in their comments regarding the indicator. However, 

at the time of the 2008 review, no alternative TSP sampler designs were identified that had an 

adequate characterization of their collection efficiency over a wide range of particle sizes. The 

existing high-volume sampler was retained as the sampling approach for the Pb-TSP FRM and 

FEMs. 

Since promulgation of the 2008 Pb NAAQS, the EPA has initiated an effort to review 

alternative sampler designs in an effort to develop a new sampler to replace the current highvolume Pb-TSP sampler. Efficient collection of particles much larger than 10 μm is 

considerably more challenging because the greater inertia and higher settling velocities of Pb 

particles hinder their efficient intake by samplers. The sampling difficulties and the long history 

of research to develop adequate sampling technology for large particles have been thoroughly 

reviewed (Garland and Nicholson, 1991). Some existing commercially available sampler inlets 

are designed to collect particles larger than 10 μm with greater than 50% efficiency (Kenny et 

al., 2005), and these inlets can be tested as potential replacements for TSP sampling. However, 

no alternatives to the FRM TSP sampler have been identified that have been adequately 

characterized. 

The EPA has initiated efforts to characterize the collection efficiency of alternative 

sampler designs through wind tunnel testing as a necessary step towards the development of a 

new sampler capable of sampling particles larger than PM10 without the noted wind speed and 

wind direction biases. Important considerations in specifying a sampler design with these 

desired features include the feasibility and challenges to collection of particles much larger than 

10 μm; some existing alternative sample collection methods are discussed in ISA (ISA, section 

2.4.1.1). Also important to consider are physical limitations in the ability to generate and 

transport ultra-coarse particles that affect the ability to adequately characterize the new sampler. 

Although all sizes of airborne Pb particles are of interest, the factors identified above are 

expected to ultimately limit the upper cut-point of potential samplers to the range of 18-20 

micrometers. Following characterization in a wind tunnel, field testing of promising candidates 

would be required to evaluate performance and to make comparisons to the existing Pb-TSP 

samplers. This effort is expected to take several years to complete, and, as such, it is unlikely 

that this new sampler will be available in time for consideration during this NAAQS review due 

to the activities which will need to be completed to adequately characterize its performance both 

in the laboratory and the field. We expect the new sampler to be available for consideration in a 

future review and consequently do not expect to consider new alternatives for sampling methods 

for Pb-TSP as part of this review. 
2-21 

In addition to the FRM for Pb-TSP, there is also, as noted in section 2.2.1.1 above, a 

FRM for Pb-PM10 (40 CFR part 50 Appendix Q), based on the PM10 sampler defined in 40 CFR 

part 50 Appendix J coupled with XRF analysis. The Pb-PM10 measurements may be used as an 

alternative to Pb-TSP measurements in certain conditions defined in 40 CFR part 58 Appendix C 

paragraph 2.10. These conditions include where Pb concentrations are not expected to equal or 

exceed 0.10 micrograms per cubic meter on an arithmetic 3-month mean and where the source of 

Pb emissions is expected to emit a substantial majority of its Pb in the PM10 size fraction. At this 

time, we believe the low-volume FRM sampler for Pb-PM10 to be adequate for this application. 

Hence, we do not expect to consider new sampling methods for Pb-PM10 as part of this review. 

2.2.1.3.2 Analysis Considerations 

Due to reduced availability of laboratories capable of performing flame atomic 

absorption analyses and general advances in analysis methods, the EPA has initiated an effort to 

expand FRM analysis methods beyond atomic absorption to include the more modern analysis 

method, ICP-MS. A consultation with the CASAC Ambient Air Monitoring and Methods 

Subcommittee was held on September 15, 2010 (Russell and Samet, 2010), and the EPA plans to 

propose a new FRM for Pb-TSP based on this more modern analysis method in 2013. In 

addition, the EPA has approved several new FEMs (for ICP-MS and other analysis methods) 

since the last Pb NAAQS review was completed in 2008. 

With regard to Pb-PM10 samples, in addition to the FRM analysis method (XRF), two 

FEMs have been accepted for Pb-PM10 analysis since the 2008 Pb NAAQS rulemaking. These 

methods are based on ICP-MS and are consistent with analysis methods used for the NATTS 

network. The EPA will continue to consider new FEMs for analysis of Pb-PM10 and Pb-TSP as 

applications are received, although no new FRMs (beyond the Pb-TSP FRM for ICP-MS 

discussed above) are expected during this NAAQS review. 

2.2.1.3.3 Network Design Considerations 

Significant revisions to the Pb network design requirements (40 CFR part 58, Appendix 

D) were made as part of the 2008 Pb NAAQS review and an associated revision to the 

requirements in 2010. As summarized in section 2.1.1.1 above, the current Pb monitoring 

network design requirements (40 CFR part 58, Appendix D, paragraph 4.5) include two types of 

monitoring sites – source-oriented monitoring sites and non-source-oriented monitoring sites - as 

well as the collection of a year of Pb-TSP measurements at 15 specific airports. This section 

describes the design considerations for the Pb NAAQS surveillance network. 

Source-Oriented Monitoring. Since the phase out of Pb in on-road gasoline, Pb is 

widely recognized as a source-oriented air pollutant. As summarized in the ISA, variability in 

air Pb concentrations is highest in areas including a Pb source, “with high concentrations 
2-22 

downwind of the sources and low concentration at areas far from sources” (ISA, p. 2-92). 

Recent data summarized in section 2.2.2.2 below indicates that the highest ambient Pb 

concentrations are found near large Pb sources, usually metals industries (see, for example, 

Figures 2-11 through 2-13 below). Analysis of the monitoring network during the last Pb 

NAAQS review with regard to adequacy of monitoring near such sources found that monitors 

were lacking near many of the larger Pb emissions sources, leading the EPA to conclude that the 

monitoring network existing at that time was inadequate to determine compliance with the 

revised Pb NAAQS (73 FR 29262). Findings and conclusions of that analysis led to revisions of 

network design requirements for source-oriented monitoring, begun with the 2008 Pb NAAQS 

rulemaking (73 FR 66964). Additional revisions were completed as part of a reconsideration of 

the monitoring requirements in December 2010 (75 FR 81126). 

The current requirements for source-oriented monitoring include placement of monitor 

sites near sources of air Pb emissions which are expected to or have been shown to contribute to 

ambient air Pb concentrations in excess of the NAAQS. At a minimum, there must be one 

source-oriented site located to measure the maximum Pb concentration in ambient air resulting 

from each non-airport Pb source which emits 0.50 or more tons of Pb per year and from each 

airport which emits 1.0 or more tons of Pb per year.20 The expansion of the network, including 

these source-oriented sites, is shown in Figure 2-3. Comparison of Figure 2-3 (monitors) with 

Figure 2-2 (sources) illustrates the coverage which the monitoring network provides, as of 2012, 

of large Pb emissions sources. 

The emissions threshold for source-oriented monitoring sites, 0.50 tpy, was developed 

based on an analysis intended to estimate the lowest emission rate that under reasonable worstcase conditions (e.g., meteorological and emission release conditions that lead to poor dispersion 

and associated elevations in Pb concentrations) could lead to Pb concentrations exceeding the Pb 

NAAQS (Cavender, 2008). This analysis included three approaches. The first two of the three 

approaches included a simple scaling of the historic 5 tpy emission threshold applied to the old 

1.5 μg/m3

 Pb NAAQS, and a simplified modeling effort using a screening model. The third 

approach relied on design values based on Pb monitoring data surrounding large sources (1 tpy 

or greater) of Pb. At the time of the 2008 review, complete 3-year design values were only 

available for seven source-monitor pairs. 

As more recent data become available, analysis of the updated and expanded dataset will 

inform evaluation of the appropriateness of the current requirements. Since the analysis 

 

20 The Regional Administrator may waive the requirement in paragraph 4.5(a) for monitoring near Pb 

sources if the State or, where appropriate, local agency can demonstrate the Pb source will not contribute to a 

maximum Pb concentration in ambient air in excess of 50 percent of the NAAQS (based on historical monitoring 

data, modeling, or other means). 
2-23 

performed during the 2008 review, over 150 additional source-oriented monitors have been 

installed. At this time, the full set of these new monitors have not collected a complete 3-year 

dataset, which is needed for the development of complete design values for the new sourceoriented monitors. For monitors installed in response to the 2008 revisions (near sources 

estimated to emit 1.0 tpy or more of Pb), 3-years of certified data would be expected to have 

been available in spring 2013. Three-years of certified data for the monitors required in the 2010 

regulations will be available in spring 2015. As is seen from Figures 2-11 through 2-13 below, 

Pb concentrations very widely across the source oriented monitors. This variation is not 

unexpected given potential for appreciable differences in source characteristics beyond 

estimated annual Pb emissions that would be expected to affect airborne Pb concentrations. 

Such characteristics include source or industry type and associated processes and work practices, 

proximity of emissions points to source boundaries, extent of fugitive emissions. 

One-year Airport Monitoring. In addition to the above source-oriented monitoring 

requirement for airports estimated to emit more than 1 tpy of Pb (40 CFR part 58, Appendix D, 

4.5(a)) and the Regional authority to require monitoring near airports where piston-engine 

aircraft emit Pb (40 CFR part 58, Appendix D, 4.5(c)), one year of monitoring was required near 

15 specific airports in order to gather additional information on the likelihood of NAAQS 

exceedances due to the combustion of leaded aviation gasoline (75 FR 81126; 40 CFR part 58, 

Appendix D, 4.5(a)(iii)). Given delays in monitor siting, monitor installation at some of these 

sites extended into late 2012. Accordingly, the timing for completion of the year of monitoring 

has varied across the 15 locations. As described further in section 2.1.2.2 above, these airport 

monitoring data along with other data gathering and analyses will inform EPA’s ongoing 

investigation into the potential for Pb emissions from piston-engine aircraft to cause or 

contribute to air pollution that may reasonably be anticipated to endanger public health or 

welfare. This investigation is occurring under Section 231 of the Clean Air Act (CAA), separate 

from the Pb NAAQS review. As a whole, the various data gathering and analyses are expected to 

improve our understanding of Pb concentrations in ambient air near airports and conditions 

influencing these concentrations. 

Non-Source-Oriented Monitoring. Monitoring agencies are also required to conduct 

non-source-oriented monitoring NCore sites with a population of 500,000 or more, as noted 

above.21 Currently, all 50 NCore sites are operational and measuring Pb concentrations, with 28 

measuring Pb in TSP and 24 measuring Pb in PM10 (2 sites are measuring both Pb in TSP and Pb 

in PM10). While non-source-oriented monitoring data can be used for designation purposes, an 

alternative objective stated for these sites is the collection of data on neighborhood-scale Pb 

 

21 Defined by the US Census Bureau - http://www.census.gov/population/www/metroareas/metroarea.html 
2-24 

concentrations that are typical in urban areas to inform our understanding of ambient air-related 

Pb exposures for the general population. The data available as of April 2014 for these sites 

indicate little variation in concentrations, with a range from less than 0.01 to 0.06 μg/m3

 in terms 

of maximum 3-month average concentration (of Pb-PM10 or Pb-TSP), with the vast majority of 

sites showing concentrations less than 0.03 μg/m3

. In recognition of the limited extent of this 

data analysis, we have not drawn conclusions here on the usefulness of these data for purposes of 

characterizing neighborhood-scale concentrations. We additionally note the existence of other 

monitoring networks that, although not required by regulation, provide data on Pb in PM10, and 

also in PM2.5, at non-source-oriented urban sites. These include the NATTS for PM10 and the 

CSN for PM2.5, as described in section 2.2.1.2 above.

2.2.2 Ambient Concentrations 

2.2.2.1 Temporal Trends 

Ambient air concentrations of Pb in the U.S. have declined substantially over the past 30 

years. Figure 2-7 illustrates this decline in terms of site-specific maximum 3-month average 

concentrations at the set of 31 monitoring sites that have been operating across this period. The 

median of this dataset has declined by more than 90% over the 30-year period, and the average 

by 89%. Over the past 12 years, a larger dataset of 50 sites operating across that period also 

indicates a decline, which is on the order of 50% for the average of that dataset (Figure 2-8).22 

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

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

 

22 In Figures 2-7 and 2-8, the top of the blue band is the 90th percentile among sites, the bottom is the 10th

percentile, and the white line is the average. http://www.epa.gov/air/airtrends/lead.html
2-25 

Note: Based on annual maximum 3-month average at 50 sites. 

Figure 2-8. Temporal trend in Pb-TSP concentrations: 2000-2012 (50 sites). 

The role of the phase-out of leaded gasoline for on-road vehicles on declining 

concentrations is evident from temporal trends in air Pb concentrations near roadways, as 

illustrated in Figure 2-9 which presents data for five monitors sited near roadways during the 

years 1979 through 2010.23 These sites additionally indicate the concentrations currently 

common at such sites, with the maximum 3-month average concentrations at all five sites falling 

below 0.03 μg/m3 in the most recent years. 

 

 

23 In selecting these sites, the objective was to identify sites near roadways that do not appear to be near 

other (stationary) sources of Pb emissions. In addition to consideration of information in national emissions 

inventories, the areas around the sites were examined using satellite pictures (in Google Maps) for signs of current 

or historical industrial activity. 
2-26 

Monitor locations: Los Angeles, CA (06-037-4002), Riverside, CA (06-065-1003), Cook, IL (17-031-0052, 17-031-6003), Suffolk, MA (25-025-0002). 

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

roadways: 1979-2010. 

2.2.2.2 Current Concentrations 

As a result of revisions to the Pb NAAQS surveillance monitoring requirements 

(described in section 2.2.1 above), Pb monitoring sites have been in transition over the last few 

years as indicated by Figure 2-3. For presentation in this document, we have focused on the 

most recent period for which adequately complete data are available, 2010-2012, recognizing 

that the dataset developed for this period includes many but not all of the monitors newly 

required by the December 2010 regulations described in section 2.2.1.1 above. 

Lead concentrations, in terms of maximum 3-month average Pb-TSP concentration, at 

monitoring sites active across the U.S. during the period 2010-2012, and for which sufficient 

data are available to meet completeness criteria described in Appendix 2C, are presented in 

Figure 2-10.24 Highest concentrations occur in the vicinity of large metals industries, as 

discussed in section 2.1.2.1.25 Note that due to differences in data completeness criteria which 

reflect the different purposes of the analyses (characterization of air quality at different types of 

monitoring sites vs identification of sites exceeding the NAAQS), Figure 2-10 (and Figures 2-11 

through 2-13) do not include some sites which may have been reported elsewhere (e.g., with 

“design values” which are used for comparison to the NAAQS level).26 

 

24 Criteria for development of the 2010-2012 air Pb-TSP, Pb-PM10 and Pb-PM2.5 datasets discussed in this 

section are described in Appendix 2C. Data summaries are included in Appendix 2D. 25 Information regarding areas of U.S. designated nonattainment with the Pb NAAQS is available at: 

http://www.epa.gov/air/oaqps/greenbk/mindex.html . 26 Design values for the 2010-2012 period are available at: http://www.epa.gov/airtrends/values.html 

0

0.2

0.4

0.6

0.8

1

1.2

1.4

1.6

1.8

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
2-27

Figure 2-10. Pb-TSP maximum 3-month means (215 sites), 2010-2012. 
2-28 

Figures 2-11 through 2-13 illustrate differences in Pb-TSP concentrations, in terms of 

three different metrics (maximum 3-month mean, annual mean, and maximum monthly mean), 

among sites near and more distant from emissions sources.27 The Pb-TSP sites indicate the much 

greater site and temporal variability in concentrations at source-oriented and previous sourceoriented sites as compared to non-source-oriented sites. Across the Pb-TSP sites, as would be 

expected, the highest concentrations are observed at the source-oriented sites, followed by the 

previous source-oriented sites. This is the case for all three metrics analyzed (maximum 3-

month mean, maximum monthly mean and annual mean). 

Figures 2-11 through 2-13 additionally present distributions of Pb-PM10 and Pb-PM2.5

concentrations in urban and rural locations where they are monitored. The Pb-PM10 and PbPM2.5 networks are described in section 2.2.1.2 and shown in Figures 2-5 and 2-6, respectively. It 

is important to note that there are few sites in these recent datasets with colocated monitors for 

the different size fractions. As described in the ISA, at 18 urban sites (without specification as to 

proximity to Pb sources) with at least 30 co-located Pb-TSP and Pb-PM10 samples collected 

during various time periods (nearly all between 1990 and 2000), approximately 80% of the Pb 

mass, on average, is captured by the Pb-PM10 measurements (ISA, sections 2.5.3.1 and 2.8.4). 

The data distributions in Figures 2-11 through 2-13 indicate reduced variability in concentration 

for non-source-oriented sites and for particulate Pb of smaller size fractions.28

 

27 In the Figures 2-11 through 2-13, the whiskers indicate the 5th and 95th percentiles, the box indicates the 

25th 50th and 75th percentiles and the star indicates the arithmetic mean. 28 The number of observations for some categories of monitoring site varies among the three figures due to 

the impact of data completeness criteria used for the three different concentration metrics (see Appendix 2C). 
2-29

Figure 2-11. Distribution of maximum 3-month mean concentrations of Pb-TSP, Pb-PM10 and Pb-PM2.5 a

2010-2012. 

0.00.10.20.30.40.50.60.70.80.91.01.11.21.3

Concentration (μg/m

3

)

Pb-TSP 

all sites

(n=236)

Pb-TSP

source-oriented 

(non-airport) sites 

(n=119)

Pb-TSP 

not source-oriented 

sites (n=93)

Pb-TSP 

previous sourceoriented sites 

(n=11)

Pb-PM10

urban sites 

(n=45)

Pb-PM2.5

urban CSN 

sites (n=193)

Pb-TSP 

source-oriented 

(airport) sites 

(n=13)
2-30

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

0.00.10.20.30.40.50.6

Pb-TSP 

all sites

(n=242)

Pb-TSP

source-oriented 

(non-airport) sites 

(n=121)

Pb-TSP 

not source-oriented 

sites (n=96)

Pb-TSP 

previous sourceoriented sites 

(n=11)

Pb-PM10

urban sites 

(n=54)

Pb-PM2.5

urban CSN 

sites (n=195)

Concentration (μg/m

3

)

Pb-TSP 

source-oriented 

(airport) sites 

(n=15)
2-31

Figure 2-13. Distribution of maximum monthly mean concentrations of Pb-TSP, Pb-PM10 and Pb-PM2.5 a

2010-2012. 

0.00.10.20.30.40.50.60.70.80.91.01.11.21.31.41.51.61.71.8

Concentration (μg/m

3

)

Pb-TSP 

all sites

(n=243)

Pb-TSP 

source-oriented 

(non-airport) sites 

(n=121)

Pb-TSP 

not source-oriented 

sites (n=96)

Pb-TSP 

previous sourceoriented sites 

(n=11)

Pb-PM10

urban sites 

(n=54)

Pb-PM

urban C

sites (n=

Pb-TSP

source-oriented 

(airport) sites 

(n=15)
2-32 

2.3 AMBIENT AIR LEAD IN OTHER MEDIA 

Lead emitted into the ambient air, depending on its chemical and physical characteristics, 

deposits out of air onto surfaces in the environment. The environmental fate of atmospherically 

emitted Pb, once deposited, is influenced by the type of surface onto which the particles deposit 

and by the type and activity level of transport forces in that location. Deposited Pb can be 

incorporated into soil matrices in terrestrial ecosystems or transported (by direct deposition or 

stormwater runoff) to water bodies and into aquatic sediments, which may serve as aquatic 

ecosystem sinks. Particles deposited onto impervious surfaces, such as urban surfaces or 

roadways, are more available for human contact while they remain on such surfaces. For 

example, particles on urban surfaces may be available for adherence onto skin or they may be 

resuspended into the air and inhaled. Precipitation and other natural, as well as humaninfluenced, processes contribute to the fate of such particles and their potential transport to areas 

or environments of lesser or greater likelihood for human contact, e.g., transport with surface 

runoff into nearby water bodies or tracking into nearby houses (ISA, section 2.3). 

Lead from current and historical air emissions sources, in addition to a range of nonair 

sources (e.g., land disposal of wastes as well as surface runoff and releases to surface waters), 

contribute to Pb in outdoor dust, soil and aquatic systems. Because of its persistence, Pb from all 

of these sources can contribute to media concentrations into the future. The pattern of resulting 

Pb concentrations changes over time in response to changes in new Pb contributions to the 

systems (e.g., in types and rates of addition), as well as environmental processes (chemical, 

biological and physical) particular to each type of media and ecosystem. Accordingly, media 

and ecosystems differ with regard to Pb concentrations and the changes in those concentrations 

in response to airborne Pb. These differences relate to ecosystem processes as well as Pb source 

or emissions characteristics and proximity. 

The initial section below (section 2.3.1) summarizes salient information regarding 

atmospheric deposition and how it is monitored. Subsequent sections describe the current 

information related to the presence of ambient air Pb in nonair media and what it indicates 

regarding impacts of current patterns of Pb in and being emitted to ambient air, including 

relationships to impacts in the past and to other Pb sources. Section 2.3.2 focuses on terrestrial 

media, while section 2.3.3 discusses aquatic media. 

2.3.1 Atmospheric Deposition 

Deposition is the pathway by which Pb particles are removed from the atmosphere and 

transferred to other environmental media. There are several approaches by which atmospheric 

deposition, or the transfer of Pb from the atmosphere to soil or water bodies, can be assessed. 

These include measurements of Pb in rainfall (wet deposition) and on collection surfaces during 
2-33 

dry periods (dry deposition); dry deposition is also estimated from measurements of airborne Pb 

particles coupled with estimates of deposition velocity (see 2006 CD, Section 2.3.2). Less direct 

approaches include monitoring changes in Pb concentration in various biological or physical 

media such as lichen or mosses, snowpack, soil and aquatic sediments (ISA, sections 2.6.2, 2.6.4 

and 2.6.6). Approaches for the latter three media may involve repeated measurements of surface 

samples over time or core samples coupled with isotope dating. To gain information on 

atmospheric deposition unaffected by contributions from direct nonair environmental releases, 

such studies are generally conducted in somewhat remote areas. As there are currently no 

nationwide Pb atmospheric deposition monitoring programs, the discussion of atmospheric 

deposition in this and subsequent sections is drawn from this range of approaches (2006 CD, 

sections 2.3, 8.2.2 and AX7.1.2.3; ISA, sections 2.3.1.2 and 2.6 ). Geographic differences in 

deposition generally relate to differences in the amount and size distribution of airborne Pb 

particles in that location, as well as meteorology and other site-specific factors. For example, the 

size of particles, as well as solubility in rainwater, can also influence wet deposition rates (ISA, 

section 2.3.1.2; 2006 CD, p. 2-59). Factors that particularly influence dry deposition are the 

level of atmospheric turbulence, especially in the layer nearest the ground, particle size 

distributions and density, and the nature of the surface itself, such as smooth or rough (2006 CD, 

pp. 2-55 to 2-57). 

Evidence for the temporal pattern of U.S. Pb deposition generally indicates a peak during 

the middle twentieth century (e.g., 1940s through 1970s) followed by substantial declines in the 

latter part of the century (ISA, section 2.3.1; 2006 CD section 2.3.1; Jackson et al., 2004). This 

pattern reflects the increased use of Pb in the industrial age (including its use in gasoline in the 

twentieth century) and declines in response to environmental controls on gasoline and metals 

industries in the latter part of the twentieth century. Studies continue to document declines in 

atmospheric deposition since the 1980s in locations remote from industrial areas (e.g., 

Watmough and Dillon, 2007). As would be expected, stationary sources of Pb continue to 

contribute to relatively higher deposition rates in industrial areas as compared to other areas, 

although rates in those areas appear to have also declined since the 1970s-80s (ISA, section 

2.3.1.2; Sabin and Schiff, 2008). 

In addition to records of atmospheric deposition in the U.S., evidence also documents the 

long-range atmospheric transport and distribution of the substantial emissions of Pb from the 

U.S. and other developed countries to regions well beyond those source countries. For example, 

evidence provided by isotopic analyses of rainwater and surface water in the North Atlantic and 

ice cores in Greenland have documented the long-range transport and distribution of Pb from 

North American and European sources (ISA, section 2.5.5; 2006 CD, p. AX7-141; 1977 CD, 

section 6.3.1; Veron et al., 1998). The historical record provided by those cores indicate the 
2-34 

period of most substantial deposition to that remote region during the 1960s and 1970s followed 

by a dramatic decline (ISA, section 2.5.5; McConnell and Edwards, 2008). These and other 

records of long-range transport indicate the widespread distribution of historically emitted Pb 

(e.g., 2006 CD, section 2.3.1). 

2.3.2 Terrestrial Media 

Lead in the terrestrial media discussed here may originate from current or historical air 

emissions or other sources. Other sources to these media include historical use of indoor and 

outdoor leaded paint, more prevalent in areas with older buildings, and the processing of leadcontaining materials. Further, the concentrations of Pb in each media, as well as the relative 

contributions from various types of sources to those concentrations, vary among media and 

among locations for any one media. Differences among locations in media concentrations of airrelated Pb are generally related to the current and historical magnitude of Pb emissions and 

deposition at that location, as well as location- and media-specific removal factors. 

2.3.2.1 Indoor Household Dust 

Household dust arises from particulate matter generated indoors and outdoors, and Pb in 

household dust can reflect a combination of these sources.29 Airborne particles can be 

transported indoors with ambient air, while particles deposited outdoors from ambient air may be 

carried in on humans and their clothing or other items transported indoors. Depending on factors 

such as the proximity of the residence to current or historical metals industries, leaded paint 

usage, and age of the residence (which informs consideration of potential for presence of leaded 

paint), Pb in indoor residential dust can reflect current or historical atmospheric Pb or nonairrelated sources, such as leaded paint. Another indoor source is tobacco smoking (ISA, section 

3.1.3.2; Gaitens et al., 2009; 2006 CD, p. 3-15; Mannino et al., 2003). The age of the residence 

may be an indicator of the potential for the presence of leaded paint and, in areas of significant 

levels of airborne Pb in the past, such as near mining or smelting industries, may also indicate 

the potential for the residual presence of historically emitted Pb (ISA, sections 3.1.1 and 3.1.3.2; 

2006 CD section 3.2.3). A study of households in the Baltimore metropolitan area (in which 

there are no areas designated non-attainment for the current Pb NAAQS)30 indicated indoor air 

Pb concentrations to be significantly associated with outdoor air Pb concentrations but did not 

show a statistically significant relationship of outdoor air Pb with indoor dust Pb (ISA, 3.1.3.2; 

Egeghy et al., 2005). Rather, indoor dust Pb was associated with Pb concentration in soil and 

 

29 As discussed in chapter 4 below, indoor dust is a major pathway for air-related Pb exposure for preschool children, largely related to prevalent hand-to-mouth behavior at that age. 30 http://www.epa.gov/air/oaqps/greenbk/mnc.html 
2-35 

several factors related to housing age, perhaps indicating the greater role of sources other than air 

Pb for those households (Egeghy et al., 2005). 

2.3.2.2 Outdoor Dust in Areas of Human Activity 

Lead in particulate matter occurring on outdoor surfaces (outdoor dust) may reflect 

current or historical Pb emissions, as well as the historical uses of Pb in products on buildings 

and infrastructure in surrounding areas. The concentrations of air-related Pb in outdoor dust and 

the relative contribution of air-related Pb to the total Pb concentrations in outdoor dust vary 

depending on the location-specific characteristics of air–related (and other) Pb sources. The role 

of air-related sources in outdoor dust Pb has been documented in areas near industrial sources, 

such as smelters, where Pb concentrations in outdoor dust have been documented to decline in 

response to reduced emissions. For example, outdoor dust Pb concentrations in a long-time 

Canadian smelter town were found to track smelter Pb emissions, as a new smelting technology 

which reduced airborne Pb concentrations by 75% resulted in a 50% reduction in outdoor dust 

Pb loading rate and concentrations (2006 CD, p. 3-23; Hilts, 2003). The residence time of settled 

dust Pb (e.g., on sidewalks and other public surfaces) and thus the response of settled dust Pb 

concentrations to changes in emissions and associated atmospheric deposition of Pb particles are 

expected to reflect site-specific rates of transport or removal processes, such as stormwater 

runoff and atmospheric resuspension and transport (ISA, sections 2.3.1.3 and 2.3.2.4; Allott et 

al., 1990; Wong et al., 2006). 

Rates of dry deposition of Pb in large metropolitan areas during the past decade are much 

lower than those reported for the 1970s (ISA, sections 2.3.1 and 2.6.1; Table 2-4, below). For 

example, dry deposition of Pb into Los Angeles harbor during 2002-2006 was more than an 

order of magnitude lower than rates reported for the same location in 1975 (ISA section 2.3.1.2; 

Sabin and Schiff, 2008; Lim et al., 2006). Across the Los Angeles metropolitan area, average 

rates generally ranged from 10 to 32 micrograms per square meter per day (μg/m2

/day) and down 

to 0.3 μg/m2/day for the non-urban site of Malibu during 2002-2003 (Lim et al., 2006). Rates 

within this range are reported from studies in Manhattan and a non-industrial area of New Jersey, 

with a somewhat higher rate reported for a major industrial location within the New York City 

metropolitan area (Yi et al., 2006; Caravanos et al., 2006a). Although rates have not been 

reported recently for smelter locations in the U.S., the outdoor dustfall deposition rate reported in 

a smelter town in British Columbia, Canada, after the 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) was several orders of magnitude higher than those 

reported for New York, Los Angeles and Chicago urban areas (Hilts, 2003; Lim et al., 2006; 

Sabin et al., 2006; Yi et al., 2006; Caravanos et al., 2006a). 
2-36 

From the few studies reporting levels of Pb loading or concentration in outdoor dust 

within the past decade or so, loading to surfaces of pedestrian traffic signals in New York City 

was on average approximately 15% of the loading reported on sidewalks in older, residential 

areas of downtown Baltimore (e.g., approximately 250 ug/ft2

 as compared to 1500 ug/ft2) and an 

order of magnitude or more below that reported in the long-time Canadian smelter town 

(Caravanos et al., 2006b; Farfel et al 2005; Hilts, 2003). 

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

Description 

Average (or 

Median*) Dry 

Deposition Rate 

(μg Pb/m2/day) A

Study 

Los Angeles Harbor, June-Nov 2006 14*B Sabin and Schiff, 2008 

Los Angeles Harbor, 2002-2003C 15 Lim et al., 2006 

Los Angeles Harbor, 1975 300* Sabin and Schiff, 2008 

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

Los Angeles, metropolitan area, non-urban site Malibu, 2002- 2003 C 0.3 “ 

Los Angeles, I-405, near Westwood (downwind side), spring 2003 D 24 Sabin et al., 2006 

Los Angeles, I-405, near Westwood (upwind side), spring 2003 D 7.3 “ 

Jersey City, NJ, 2001- 2002 50 Yi et al., 2006 

New Brunswick, NJ, 2001- 2002 8 “ 

Manhattan, NYC, 2nd story rooftop (unprotected), 2003-2005 27 Caravanos et al., 2006a

Chicago, 1993-95E 38-71 Yi et al 2001; Paode et al., 1998 

A – Methods generally involved collection and analysis of samples of deposited particulate matter; details provided in references cited.

B - Rates for rest of off-shore transact from Santa Barbara to San Diego Bay ranged from 0.52 (Oxnard) – 3.3 (San Diego Bay) μg/m3. 

C - Average Pb-TSP range= 0.0056-0.017 μg/m3 for urban sites; 0.0022 at Malibu site. 

D - Average Pb-TSP at downwind site over sampling period ~0.02 μg/m3. 

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

2.3.2.3 Soil 

As is the case for Pb in outdoor dust, Pb occurring in surface soils can be derived from 

current or historical emissions, as well as leaded paint usage on older buildings and other 

structures. The relative role of these sources may vary with the type of environment and 

proximity to industry and population centers.

In forested areas away from old urban areas, the role of leaded gasoline in soil 

contamination is illustrated by the documented reductions in Pb in surface soils subsequent to the 

phase-out of leaded gasoline for on-road vehicles. For example, forest surface soil (litter) 

concentrations in a transect from Vermont through Maine and up to Gaspe in Quebec, which in 

1979 exhibited a significant spatial trend ranging from 200 milligrams per kilogram, dry weight 
2-37 

(mg/kg dw) at its southernmost point down to 60 mg/kg dw at its northernmost and most remote 

point in Quebec, declined to 32-66 mg/kg dw (with no spatial trend) by 1996 (ISA, section 2.6.1; 

Evans, 2005). In forests from the mid-Atlantic to southern New England, a reduction in litter Pb 

concentration was observed between 1978 and 2004-05 (ISA, section 2.6.1; Johnson and Richter, 

2010). In the latter study, the authors observed less change in concentration in the more northern 

sampling sites, which they attribute to reduced rates of organic matter decomposition in those 

colder temperature areas. Similarly, an additional New England study by Kaste et al (2006) also 

documented a pattern in temporal reductions in soil Pb (O-horizon) related to decomposition 

activity. These recent findings are generally consistent with findings reported in the last review 

which indicated the gradual migration of deposited Pb into mineral soils (e.g., Miller and 

Friedland, 1994; Kaste et al., 2003; Wang and Benoit, 1997; Johnson et al., 1995; Zhang, 2003). 

Few studies have investigated temporal trends of surface soil Pb concentrations in more 

populated areas in relation to reductions in usage of leaded gasoline and paint. Current 

concentrations in areas of past heavy traffic powered by leaded gasoline are generally elevated 

above areas more distant from these areas (ISA, section 2.6.1). Current roadway-related sources 

of Pb (e.g., wear of vehicle parts), while substantially less significant than the historic use of 

leaded gasoline, may continue to provide some contribution to surface dust/soil in these areas 

(ISA, section 2.2.2.6). Surface soil and dust concentrations are much higher in such areas in 

large, older cities than surrounding suburban areas (ISA, section 2.6.1). In older residential 

areas, the presence of leaded house paint is another contributor to surface soil concentrations 

(ISA, sections 2.6.1; Yesilonis et al., 2008; Brown et al., 2008; Clark et al., 2006). 

Areas of long-term Pb emissions from point sources appear to be the areas of highest 

surface soil Pb concentrations (ISA, sections 2.6 and 2.6.1). For example, Pb surface soil 

concentrations within approximately 100-250 meters of long-established Pb smelters have been 

five to ten times higher than those at 3-5 km distance (ISA, section 2.6.1; 2006 CD, Table 3-4). 

Surface soil concentrations of Pb near U.S. mines that are no longer active have also been found 

to be elevated above more distant areas (2006 CD, Table 3-6). Information described in the 2006 

CD for areas surrounding smelters after implementation of pollution controls, although showing 

declines in Pb concentrations in outdoor dustfall, street dust and indoor dustfall, has not indicated 

a noticeable decline in soil Pb concentrations (2006 CD, pp. 3-23 to 3-24). The continued Pb 

emissions in such industrial areas likely influence the dynamics of Pb concentrations in the soil, 

affecting any response to emissions reductions. Estimates of associated steady-state surface soil 

Pb concentrations or the expected longer-term temporal pattern for this situation have not been 

made. 

In summary, findings to date indicate that many of those systems less influenced by 

current point sources have and may still be responding to reduced Pb deposition rates associated 
2-38 

with reduced atmospheric emissions of Pb, including those associated with the phase-out of 

leaded gasoline for on-road vehicles, while potential responses of soils near point sources and 

those involving historically deposited Pb near roadways are less well characterized, but might be 

expected to have longer time horizons. 

2.3.2.4 Biota 

Terrestrial plants can take up Pb from soils into roots and then transport it to other plant 

tissues, as well as absorb deposited Pb into above-ground plant tissues (ISA, section 3.1.3.3; 

2006 CD, section 2.3.7; 1986 CD, sections 6.5.3 and 7.2.2.2.1). The relative contributions of 

these pathways to the different plant tissues differ with the physiology of different plants, the 

chemical and physical characteristics of the soil, and the relative levels of Pb in soil and 

atmospheric deposition (ISA, section 3.1.3.3). Terrestrial animals may take in Pb through 

ingestion of vegetation, vegetation-consuming animals or soil, as well as directly from air. The 

relative contributions from these terrestrial animal exposure pathways vary with contamination 

level of the different items, as well as with species-specific factors, including intake rates. 

The availability of data to document temporal trends in Pb concentrations in terrestrial 

biota is somewhat limited. Measurements of Pb in some biota indicate reductions in biologically 

available Pb over the past 30 years in some remote locations. For example, measurements of Pb 

in lichen from Golden Lake in Mount Ranier National Park (2005) and Emerald Lake basin in 

Sequoia/Kings Canyon National Parks (2004) indicate significant reductions (approximately 3-5-

fold) since samples were previously collected in those locations in 1984 (ISA, section 2.6.6; 

Landers et al., 2008). Further, Pb in teeth of juvenile and adult moose in Isle Royale National 

Park in northern Michigan have also declined substantially (ISA, section 2.6.8; Vucetich et al., 

2009). 

Few recent data are available to characterize terrestrial biota Pb contamination levels 

associated with current air Pb deposition. In one example, however, Pb deposition associated 

with hauling mining materials has substantially increased Pb concentrations in moss within 10 

meters of a road in the remote wilderness areas of Cape Krusenstern National Monument, 

Alaska.31 In this example, the median Pb concentration measured within 10 meters of the haul 

road in summer 2001 was more than 20 times higher than at sites at greater distance from the 

road and nearly three orders of magnitude greater than those reported for this moss in other 

Alaska locations in 1990-1992 ( ISA, section 2.3.1.2; Hasselbach et al., 2005). 

The composition of human and wildlife diets (and associated contamination levels) 

influences the relative magnitude of dietary Pb intake, which may derive from currently existing 

 

31 Red Dog mine is a zinc and Pb mine initiated in 1987. The materials are transported from the mine to a 

port on the Chukchi Sea via a 52-mile long haul road. 
2-39 

or historic air sources in the U.S. or in countries that export food to the U.S. As noted in section 

1.3.1.1 above, U.S. dietary Pb may also derive from nonair sources, such as through processing 

steps. 

2.3.3 Aquatic Media 

2.3.3.1 Surface Waters 

In addition to delivery by atmospheric deposition directly to surface waters, Pb is also 

carried into surface waters via wastewater effluent from municipalities and industry, stormwater 

runoff, erosion, and accidental discharges (2006 CD, p. AX7-142; ISA section 2.3.2). As a result 

of the phasing out of leaded gasoline for use in on-road vehicles, reductions in Pb concentrations 

have been documented in surface waters of the North Atlantic Ocean, as well as the relatively 

less remote areas of the Great Lakes (2006 CD, p. 7-23). The availability of studies investigating 

historical trends in surface waters is limited, in part due to analytical issues that challenged many 

monitoring programs in the past (2006 CD, AX7.2.2.2). Thus, temporal trends reported in many 

aquatic systems are based on sediment analyses (see section 2.3.3.2 below). 

Most Pb occurring in aquatic systems is associated with particles, with the distribution 

between particle-bound and dissolved form being influenced by water chemistry as well as 

suspended sediment levels (ISA, 2.3.2; 2006 CD, pp. AX7-117 to AX7-118, Section AX7.2.2). 

Water columns have been described as “transient reservoirs” for pollutants (2006 CD, p. 2-75). 

Once deposited to sediments, whether Pb is available for resuspension back into the water 

column with potential transport further down a watershed versus being buried into deeper 

sediments depends on the aquatic system (ISA, section 2.7.2). In open ocean waters (generally 

characterized by depth and distance from continental sources), resuspension to surface waters is 

unlikely. In more shallow systems, and those influenced by land sources (e.g., stormwater runoff 

as well as point sources), resuspension may play a role in water column concentrations. For 

example, studies in San Francisco Bay, the southern arm of which has an average depth of 2 m, 

have indicated that Pb particles may be remobilized from surface sediments into the water 

column (2006 CD, AX7-141). 

The distribution of Pb dissolved in many U.S. surface waters has been reported by the 

United States Geological Survey (USGS) National Water-Quality Assessment (NAWQA) 

program. The NAWQA data set referenced in the ISA (ISA, section 2.6) encompasses data 

collected from 1991-2003 on Pb concentrations in flowing surface waters for more than 50 river 

basins and aquifers throughout the country (2006 CD, Section AX7.2.2.3). These data indicate a 

mean dissolved Pb concentration in U.S. surface waters of 0.66 μg/L (range 0.04 to 30 μg/L) in 

waters affected by a combined contribution of natural and anthropogenic sources, as compared to 

a mean of 0.52 μg/L (range 0.04 to 8.4 μg/L) for waters in “forest”, “rangeland”, and “reference” 
2-40 

sites (2006 CD, Section AX7.2.2.3). The highest surface water Pb concentrations were observed 

in sites impacted by land uses such as mining (2006 CD, p. AX7-131). The role of surface 

runoff in delivering contamination to waters near such land uses, as well as near metals 

industries, presents a challenge to the task of disentangling the relative contributions from 

atmospheric deposition as compared to those associated with surface runoff. 

2.3.3.2 Sediments 

Many studies have investigated temporal trends in sediment Pb concentrations, using 

sediment cores or surface sediment Pb concentration, with declines documented in many systems 

and usually attributed to the phasing out of leaded gasoline for on-road vehicles and industrial 

emissions reductions (ISA, sections 2.6.2 and 2.7.5; 2006 CD, section AX7.2.2). Several studies 

documenting the increased Pb deposition of the industrial age, including specifically leaded 

gasoline usage, and the subsequent declines associated with on-road leaded gasoline phase-out 

were reported in the 2006 CD. They include investigations involving sediment cores from the 

Okefenokee Swamp in Georgia as well as from 35 reservoirs and lakes in urban and reference 

locations (ISA, section 2.6.2; 2006 CD, p. AX7-141). In the latter, the median reduction in Pb 

mass accumulation rate in the cores, adjusted for background concentrations, was 246%, with the 

largest decreases in lakes located in dense urban watersheds (ISA, section 2.6.2; 2006 CD, p. 

AX7-141; Mahler et al, 2006). A third study of sediment cores in 12 lakes in the Great Lakes 

area also documented a peak in Pb concentrations consistent with peak use of leaded gasoline in 

the U.S. in the mid 1970s and declining concentrations in most lake sediments through the mid 

1990s (2006 CD, p. 2-55; Yohn et al., 2004). Sediment surveys by the USGS NAWQA have 

reported the highest Pb concentrations in Idaho, Utah, and Colorado, with seven of the highest 

concentrations at sites classified as mining land use (2006 CD, p. AX7-133). 

Among the more recent investigation of temporal trends in aquatic sediments described in 

the ISA is that associated with the Western Airborne Contaminants Assessment Project which 

documented Pb in sediment cores from 14 lakes in eight U.S. national parks in western states, 

including three in Alaska (ISA, section 2.6.2; Landers et al., 2010). Among the Alaska cores, in 

which concentrations were generally on the order of 20 μg/kg dw, there was little variation in Pb 

concentration, flux or enrichment factor. The other park cores, with few exceptions, generally 

exhibited an increase in concentration commencing in the mid-nineteenth century, which 

transitioned to declining trends in the past few decades, with lower concentrations in more 

recent, surface material. The highest concentration was recorded at core depth corresponding to 
2-41 

the mid-1970s, in one of the Sequoia/Kings Canyon lake cores (Figure 2-16; ISA, section 2.6.2; 

Landers et al., 201032). 

Figure 2-14. Temporal trend in sediment Pb concentration from core samples in twelve 

lakes at eight National Parks or Preserves. 

Analyses of cores taken in several lakes and reservoirs along the Apalachicola, 

Chattahoochee, and Flint River Basin from north of the Atlanta, GA metropolitan area to the 

Gulf of Mexico indicate changes in sediment concentration both with time and in relation to 

influence of the large metropolitan area of Atlanta (ISA, section 2.6.2; Callender and Rice, 

2000). Highest concentrations were documented just downstream from Atlanta at the core depth 

corresponding to the 1975-1980 time period; the corresponding concentration for the most 

recent time period (1990-1995) at that location was approximately 50% lower (ISA, section 

2.6.2; Callender and Rice, 2000). These data may reflect changes in surface water discharges of 

Pb in the Atlanta area, during this time period, as well as changes in air deposition. The smaller 

 

32 Figure created from database for Landers et al (1980); 

http://www.nature.nps.gov/air/Studies/air_toxics/wacap.cfm . 

0

25

50

75

100

125

1800 1830 1860 1890 1920 1950 1980 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)
2-42 

reduction (on the order of 20%) observed across the 20-year time period at the upstream site is 

likely more generally reflective of changes in air deposition. 

2.3.3.3 Biota 

Aquatic biota can contain Pb that may be derived from historic or current atmospheric 

deposition in the watershed, from historic or current direct water discharges or from natural 

sources (ISA, section 6.2.1). In near-shore systems and populated watersheds, all of these 

sources may play a role in observed Pb concentrations, complicating consideration of the role of 

ambient air Pb deposition. Additional challenges are presented by available data for mobile 

species such as fish (e.g., ISA, section 2.6.8; 2006 CD, section AX7.2.2.2). A 20-year record of 

Pb concentrations in blue and zebra mussels and oysters in U.S. coastal waters provides varying 

evidence on temporal trends that may reflect patterns in site-specific environmental releases as 

well as other ecosystem impacts on Pb fate and transport over that period (ISA, section 2.6.7; 

Kimbrough et al., 2008). 

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Brown, RW; Gonzales, C; Hooper, MJ; Bayat, AC; Fornerette, AM; McBride, TJ; Longoria, T; Mielke, HW. 

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Evans, GC; Norton, SA; Fernandez, IJ; Kahl, JS; Hanson, D. (2005). Changes in concentrations of major elements 

and trace metals in northeastern US-Canadian sub-alpine forest floors. Water Air Soil Pollut 163: 245-267. 

Farfel, MR; Orlova, AO; Lees, PSJ; Rohde, C; Ashley, PJ; Chisolm, JJ, Jr. (2005). A study of urban housing 

demolition as a source of lead in ambient dust on sidewalks, streets, and alleys. Environ Res 99: 204-213. 

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children to residential dust lead, 1999-2004: I. Housing and demographic factors. Environ Health Perspect 

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radioactivity. J. Aerosol Sci. Vol.22 (4):479-499. 

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gasoline passenger car. Environ Sci Technol 44: 2562-2569. 

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patterns of cadmium and lead deposition on and adjacent to National Park Service lands in the vicinity of 

Red Dog Mine, Alaska. Sci Total Environ 348: 211-230. http://dx.doi.org/10.1016/j.scitotenv.2004.12.084 . 

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

58. 

Jackson, B.P., P.V. Winger, P.J. Lasier (2004) Atmospheric lead deposition to Okefenokee Swamp, Georgia, USA. 

Environ Poll. 130: 445-451. 

Johnson, C. E.; Siccama, T. G.; Driscoll, C. T.; Likens, G. E.; Moeller, R. E. (1995) Changes in lead 

biogeochemistry in response to decreasing atmospheric inputs. Ecol. Appl. 5: 813-822. 

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1978-2004. Soil Sci Soc Am J 74: 1001-1009. http://dx.doi.org/10.2136/sssaj2008.0337. 

Kaste, JM; Bostick, BC; Friedland, AJ; Schroth, AW; Siccama, TG. (2006). Fate and speciation of gasoline-derived 

lead in organic horizons of the northeastern USA. Soil Sci Soc Am J 70: 1688-1698. 

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Kaste, J.; Friedland, A.; Stürup, S. (2003) Using stable and radioactive isotopes to trace atmospherically deposited 

Pb in montane forest soils. Environ. Sci. Technol. 37: 3560-3567. 

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TSP and louvered particulate matter inlets. J Environ Monit. May 2005. 7 481-487. 

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contaminant monitoring in the nation's coastal zone. Silver Spring, MD: National Centers for Coastal 

Ocean Science. http://aquaticcommons.org/2232/ 

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Western Ecology Division. http://www.nature.nps.gov/air/studies/air_toxics/WACAPreport.cfm . 

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Taylor, HE; Hageman, K; Usenko, S; Ackerman, L; Schrlau, J; Rose, N; Blett, T; Erway, MM. (2010). The 
2-44 

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of particle-associated metals in the Los Angeles region. Atmos Environ 40: 7810-7823. 

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Pollut. 146: 197-210. 
3-1 

3 HEALTH EFFECTS AND EXPOSURE/RISK INFORMATION 

This chapter presents key aspects of the current evidence of lead-related health effects 

and presents exposure/risk information from the quantitative assessment performed in the last 

review in the context of the currently available evidence. Staff has drawn from EPA’s synthesis 

of the scientific evidence presented in the Integrated Science Assessment for Lead (USEPA, 

2013; henceforth referred to as the ISA) and 2006 Air Quality Criteria Document for Lead

(USEPA, 2006; henceforth referred to as the 2006 CD), and from the documentation of the 2007 

human exposure and health risk assessment (documented in USEPA, 2007a; henceforth referred 

to as the 2007 REA). The chapter is organized into sections considering the information on 

blood Pb as a biomarker (section 3.1), the nature of Pb effects on health (section 3.2), public 

health implications and at-risk populations (section 3.3), and exposure and risk information 

(section 3.4). Presentation within these sections is organized to address key policy-relevant 

questions for this review concerning the evidence and exposure/risk information, building upon 

the questions included in the IRP (IRP, section 3.1). 

3.1 INTERNAL DISPOSITION AND BIOMARKERS OF EXPOSURE AND DOSE 

The health effects of Pb, discussed in detail in the ISA and summarized in section 3.2 

below, are remote from the portals of entry to the body (i.e., the respiratory system and 

gastrointestinal tract). Consequently, the internal disposition and distribution of Pb is an integral 

aspect of the relationship between exposure and effect. As discussed below, blood Pb has 

traditionally been used as a biomarker of Pb exposure and of internal dose, with relationships 

between air Pb concentrations and blood Pb concentrations informing consideration of the 

NAAQS for Pb. Information available in this review continues to support conclusions in the last 

review with regard to these relationships. 

Lead associated with inhaled particles may, depending on particle size and Pb solubility, 

be absorbed into the systemic circulation or transported with particles to the gastrointestinal tract 

(ISA, section 3.2.1.1). The absorption efficiency of Pb from the gastrointestinal (GI) tract varies 

with characteristics associated with the ingested Pb (e.g., particle size and chemical form or 

matrix), as well as with an individual’s physiology (e.g., maturity of the GI tract), nutritional 

status (e.g., iron, calcium, and zinc deficiencies increase absorption), and the presence of food in 

the GI tract (ISA, section 3.2.1.2). Once in the blood stream, where approximately 99% of the 

Pb is associated with red blood cells (mostly bound to aminolevulinic acid dehydratase, the 

predominant ligand), Pb is quickly distributed throughout the body (e.g., within days) and is 

available for exchange with the soft and skeletal tissues, conceptually viewed as the fast and 

slow turnover pools, respectively (ISA, section 3.2.2). Skeletal tissue serves as the largest 
3-2 

storage compartment, with much less Pb stored in soft tissues (e.g., kidney, liver, brain, etc.) 

(ISA, section 3.2.2.2). 

The role of the bone as the main storage compartment is related to the ability of Pb to 

form stable complexes with phosphate and replace calcium in the salt comprising the primary 

crystalline matrix of bone (ISA, section 3.2.2.2). In infants less than a year old, the bone is 

estimated to contain approximately 60% of the total body burden of Pb (ISA, section 3.2.2.2; 

Barry, 1975). Circulating Pb is taken up into the bone regions of active calcification. 

Accordingly, during early childhood there is rapid uptake of Pb into mineralizing bone, with 

somewhat more than 70% of total body burden Pb estimated to reside in bone of children aged 2 

to 16, increasing up to more than 90% by adulthood (ISA, section 3.2.2.2; Barry, 1975). The net 

accumulation of Pb in bone over a person’s lifetime results in bone lead concentrations generally 

increasing with age (ISA, section 3.2.2.2). 

The distribution of Pb in the body is dynamic. Throughout life, Pb in the body is 

exchanged between blood and bone and between blood and soft tissues (ISA, sections 3.3.5 and 

3.2.2; 2006 CD, section 4.3.2). The rates of these exchanges vary with age, exposure and 

various physiological variables. For example, resorption of bone, which results in the 

mobilization of Pb from bone into the blood, is a somewhat rapid and ongoing process during 

childhood and a more gradual process in later adulthood (ISA, sections 3.2.2.2, 3.3.5 and 3.7.2). 

Resorption rate is appreciably increased in pregnant or nursing women and in association with 

osteoporosis in postmenopausal women or, to a lesser magnitude, in older men (ISA, sections 

3.3.5.2). Changes in Pb exposure circumstances can also influence these exchanges, e.g., when 

exposure levels are substantially reduced, the relative contribution of Pb from bone to blood Pb 

concentration increases (ISA, section 3.3.5). The studies that address the relative contributions 

of bone Pb and current Pb exposure to blood Pb are limited to a few human studies during the 

1980s and early 1990s, when leaded gasoline usage was common, and a study in non-human 

primates. These studies indicate an appreciable contribution from bone Pb stores to Pb in blood, 

on the order of 40-70% of blood Pb contributed from bone, under circumstances with higher 

concurrent exposure than exposures common today (ISA, section 3.3.5; Smith et al., 1996; 

Gulson et al., 1995; Manton, 1985; Franklin et al., 1997). 

During bone resorption that occurs in pregnancy, Pb is released from bone, increasing the 

bone contribution to maternal blood Pb levels, and maternal Pb circulates across the placenta, 

posing risk to the developing fetus and providing the fetal body burden (ISA, sections 3.2.2.4, 

3.3.5, 3.7.2 and 3.7.3; 2006 CD, 6.6.2; Chuang et al., 2001). The relative size of contributions of 

maternal bone Pb and current maternal exposure to maternal blood Pb and fetal body burden are 

influenced by the relative magnitude of current and historical exposures. In various study 

populations with mean maternal blood Pb levels ranging from 1.7 to 8.6 μg/dL, average blood Pb 
3-3 

concentration in the umbilical cord (as representative of newborn blood) has been reported to 

range from 70% to 100% of average maternal blood Pb (ISA, section 3.2.2.4); the range is 

similar for four study populations with mean maternal blood Pb level below 4 μg/dL (Amaral et 

al., 2010; Patel and Prabhu, 2009; Lagerkvist et al., 1996; Jedrychowski et al., 2011). The 

relationship between cord blood Pb and maternal blood Pb concentrations is more variable for 

individual mother-child pairs. In a low-income population with mean maternal blood Pb of 1.9 

μg/dL, factors associated with occurrences of relatively higher cord-to-maternal blood Pb ratios 

included higher maternal blood pressure and alcohol consumption, while factors associated with 

relatively lower cord-to-maternal blood Pb ratios included higher maternal hemoglobin and 

sickle cell trait presence (Harville et al., 2005). As a result of the contributions of maternal bone 

Pb to maternal blood Pb during pregnancy, the contribution to fetal body burden from maternal 

bone Pb relative to maternal concurrent exposure can be appreciable. This maternal bone Pb 

contribution to fetal body burden is likely to vary, however, in response to differences between 

maternal historical exposures and those during pregnancy, among other factors (2006 CD, 

sections 4.3.1.5 and 4.3.2.5; ISA, section 5.1; Chuang et al., 2001; Gulson et al., 1999; Gulson et 

al., 2003; Gulson et al., 2004a; Rothenberg et al., 2000). 

Limited data indicate that blood Pb levels in some newborns may decline during the 

period extending through the first few months of life; the extent to which this may occur may be 

influenced by the magnitude of blood Pb level at birth and of subsequent exposure during early 

infancy (ISA, section 3.4.1; Carbone et al., 1998; Simon et al., 2007; Gulson et al., 1999, 2001). 

As infants become more mobile and engage in hand-to-mouth behavior, blood Pb levels then 

commonly increase to a peak around one to two years of age (ISA, sections 3.4.1 and 5.2.1.1). 

 Does the current evidence continue to support blood Pb level as a useful indicator 

of Pb exposure and dose for purposes of characterizing Pb health effects, with 

well-recognized strengths and limitations? To what extent does the evidence 

suggest alternatives? 

As discussed in past CDs and in the ISA, blood Pb is the most commonly used indicator 

of human Pb exposure. Given the association with exposure and the relative ease of collection, 

blood Pb levels are extensively used as an index or biomarker of exposure by national and 

international health agencies, as well as in epidemiological and toxicological studies of Pb health 

effects and dose-response relationships (ISA, sections 3.3.2, 3.4.1, 4.3, 4.4, 4.5, 4.6, 4.7, and 

4.8). While bone Pb measurements are also used in epidemiological studies as an indicator of 

cumulative Pb exposure, blood Pb measurements remain the predominant, well-established and 

well-characterized exposure approach. 
3-4 

Since 1976, the U.S. Centers for Disease Control and Prevention (CDC) has been 

monitoring blood Pb levels nationally through the National Health and Nutrition Examination 

Survey (NHANES). This survey has documented the dramatic decline in mean blood Pb levels 

in all ages of the U.S. population that has occurred since the 1970s, as shown in Figure 3-1, and 

that coincides with actions on leaded fuels, leaded paint, lead in food packaging, and leadcontaining plumbing materials that have reduced Pb exposure in the U.S. (ISA, section 3.4.1; 

Pirkle et al., 1994; Schwemberger et al., 2005). This decline has continued over the more recent 

past. For example, the 2009-2010 geometric mean blood Pb level in U.S. children aged 1-5 

years is 1.17 μg/dL, as compared to 1.51 μg/dL in 2007-2008 (ISA, section 3.4.1) and 1.8 μg/dL 

in 2003-2004, the most recent data available at the time of the last review (73 FR 67002). 

Somewhat less dramatic declines have been reported in the upper tails of the distribution and in 

different groups with higher blood Pb levels than the general child population (ISA, Figures 3-17 

and 3-19). 

Source: Adapted from data from the NHANES (NCHS, 2010) 

Note: The means of log blood Pb were weighted to represent national averages. Data were from the publically available NHANES II, NHANES 

III (1988-1991 and 1992-1994), and the continuous NHANES (1999-2000, 2003-2004, 2005-2006, 2007-2008). Continuous NHANES data from 

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 

exam year was the reported exam year for NHANES II, the middle year of each of the phases of NHANES III, and the second year of each of 

the continuous NHANES.

Figure 3-1. Temporal trend in mean blood Pb levels for NHANES cohorts (ISA, Figure 3-

18). 
3-5 

The CDC, and its predecessor agencies, have for many years used blood Pb level as a 

metric for identifying highly exposed children at risk of adverse health effects for whom 

recommendations might be made for their protection (e.g., CDC, 1991; CDC, 2005). In 1978, 

when the Pb NAAQS was initially established, the CDC recognized a blood Pb level of 30 μg/dL 

as a level warranting individual intervention (CDC, 1991). In 1985, the CDC recognized a level 

of 25 μg/dL for intervention, and in 1991, they adopted a multi-tier approach that recommended 

individual intervention actions at a level of 15 μg/dL and implementation of more general 

community-wide prevention activities if many children in a community have blood Pb at or 

above 10 μg/dL (CDC, 1991; CDC, 2005). In 2005, CDC revised their statement on Preventing 

Lead Poisoning in Young Children, specifically 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

 Consistent with this statement, the CDC revised their 

approach in 2012 to one that relies on the 97.5th percentile of blood Pb concentrations in U.S. 

children aged one to five years of age (currently 5 μg/dL)2

 as a reference level for identifying 

young children for whom they recommend particular follow-up actions (CDC, 2012). 

Unless influenced by a recent elevation in exposure, blood Pb measurements are a 

reflection of total body burden. Accordingly, Figure 3-1 illustrates the reduction in Pb body 

burden in the U.S. population over the past 40 years. Associations of health effects with blood 

Pb measurements indicate relationships with body burden and may, in some cases, indicate 

relationships with recent exposures. The extent to which blood Pb measurements represent 

current or recent exposure circumstances, however, may be uncertain, particularly where 

histories include exposures largely different from those occurring more recently (ISA, sections 

3.3 and 3.3.2). This uncertainty may be greater for blood Pb measurements taken in older 

children3

 and adults than those for young children as a result of their longer exposure histories. 

For example, the Pb in bone of adults may have accumulated over decades of Pb exposure (with 

past exposures often greater than current ones for current U.S. populations) such that the bone 

may be a significant source of Pb in blood in later years of life, after exposure has ended or been 

appreciably reduced. Thus, in adult and older child populations with past exposures that were 

 

1

 With the 2005 statement, CDC identified a variety of reasons, reflecting both scientific and practical 

considerations, for not lowering the 1991 level of concern, including a lack of effective clinical or public health 

interventions to reliably and consistently reduce blood Pb levels that are already below 10 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). 

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 3.3). 
3-6 

appreciably elevated in comparison to more recent exposures, current blood Pb levels may 

predominantly reflect their exposure history rather than their current exposures (ISA, sections 

3.3.5, 3.3.5.2 and 3.4.1). Accordingly, the extent to which studies using cross-sectional blood Pb 

measurements as the exposure biomarker inform our understanding of relationships between 

recent Pb exposures and various health effects can differ across age groups and is greatest for 

very young children, as discussed in section 3.3 below. 

The relationship of children’s blood Pb to recent exposure may reflect their labile bone 

pool, with their rapid bone turnover in response to rapid childhood growth rates (ISA, section 

3.3.5). The relatively smaller skeletal compartment of Pb in children (particularly very young 

children) compared to adults is subject to more rapid turnover. As a result the blood Pb 

concentration of children can more quickly reflect changes in their total body burden (associated 

with their shorter exposure history) and can also reflect changes in recent exposures (ISA, 

section 3.3.5). 

Multiple studies of the relationship between Pb exposure and blood Pb in children (e.g., 

Lanphear and Roghmann 1997; Lanphear et al., 1998) have shown young children’s blood Pb 

levels to reflect Pb exposures, including exposures to Pb in surface dust. These and studies of 

child populations near sources of air Pb emissions, such as metal smelters, further demonstrate 

the effect of airborne Pb on interior dust and on blood Pb (ISA, sections 3.4.1, 3.5.1 and 3.5.3; 

Hilts, 2003; Gulson et al., 2004b). Accordingly, blood Pb level was the index of exposure for 

children in the risk assessment performed in the last Pb NAAQS review (described in section 3.4 

below). 

A well-recognized strength of using children’s blood Pb to investigate relationships 

between Pb exposure and health effects is the relatively lesser uncertainty in the causality aspects 

of such relationships than might be associated with such relationships based, for example, on 

media concentration. Blood Pb is an integrated marker of aggregate Pb exposure across all 

pathways. The blood Pb concentration-response relationships described in epidemiological 

studies of lead-exposed populations do not distinguish among different sources of Pb or 

pathways of Pb exposure (e.g., inhalation, ingestion of indoor dust, ingestion of dust containing 

leaded paint). Given our focus on ambient air contributions to Pb exposures, discussion in 

response to the question below considers the available information regarding relationships 

between Pb in ambient air and the associated Pb in blood. Additionally, the exposure component 

of the risk assessment performed for the last Pb NAAQS review (and described in section 3.4 

below) employed biokinetic modeling to estimate blood Pb levels associated with aggregate Pb 

exposure to inform our estimates of contributions to blood Pb arising from ambient air-related 

Pb. 
3-7 

Alternative biomarkers of Pb exposure include bone Pb, teeth Pb, and hair Pb (ISA, 

section 3.3.1, 3.3.3 and 3.3.4). Given the role of bone as the repository of more than 90% of an 

adult body’s Pb burden, bone Pb levels are recognized as indicators of body burden and 

cumulative lifetime exposure (ISA, sections 3.2.2.2, 3.3 and 3.3.5). The currently available 

evidence does not, however, indicate these or any other alternatives to be superior to blood Pb in 

young children or as commonly used for the purposes of tracking recent Pb exposures and for 

assessing potential health risk for this age group (ISA, section 3.7.3). In summary, the current 

evidence continues to support our conclusions from the last review regarding the use of blood Pb 

levels as an internal biomarker of Pb exposure and dose informative to characterize Pb health 

effects in young children. 

 To what extent has new information altered scientific conclusions regarding the 

relationships between Pb in ambient air and Pb in children’s blood? 

As described above, blood Pb is an integrated marker of aggregate exposure across all 

pathways and a reflection of exposure history. Thus, our interpretation of the health effects 

evidence for purposes of this review necessitates characterization of the relationships between Pb 

from those sources and pathways of interest in this review (i.e., those related to Pb emitted into 

the air) and blood Pb. The evidence in this regard derives from analyses of datasets for 

populations residing in areas with differing air Pb concentrations, including datasets for 

circumstances in which blood Pb levels have changed in response to changes in air Pb. The 

control for variables other than air Pb that can affect blood Pb varies across these analyses. 

Lead in ambient air contributes to Pb in blood by multiple exposure pathways by both 

inhalation and ingestion exposure routes (ISA, section 3.1.1). The quantitative relationship 

between ambient air Pb and blood Pb, which is often termed a slope or ratio, describes the 

increase in blood Pb (in μg/dL) estimated to be associated with each unit increase of air Pb (in 

μg/m3

). Ratios are presented in the form of 1:x, with the 1 representing air Pb (in μg/m3) and x 

representing blood Pb (in μg/dL). Description of ratios as higher or lower refers to the values for 

x (i.e., the change in blood Pb per unit of air Pb). Slopes are presented as simply the value of x. 

At the conclusion of the last review in 2008, the EPA interpreted the evidence as 

providing support for use (in informing the Administrator’s decision on standard level) of a 

range “inclusive at the upper end of estimates on the order of 1:10 and at the lower end on the 

order of 1:5” (73 FR 67002). This conclusion reflected consideration of the air-to-blood ratios 

presented in the 1986 CD4

 and associated observations regarding factors contributing to variation 

in such ratios, ratios reported subsequently and ratios estimated based on modeling performed in 

the REA, as well as advice from CASAC (73 FR 66973-66975, 67001-67002). The information 

 

4

 The 2006 CD did not include an assessment of then-current evidence on air-to-blood ratios. 
3-8 

available in this review, which is assessed in the ISA and largely, although not completely, 

comprises studies that were available in the last review, does not alter the primary scientific 

conclusions drawn in the last review regarding the relationships between Pb in ambient air and 

Pb in children’s blood. The ratios summarized in the ISA in this review span a range generally 

consistent with the range concluded in 2008 (ISA, section 3.5.1). 

The air-to-blood ratios for children, or for populations inclusive of children, discussed in 

the ISA for this review are summarized in Table 3-1. The evidence pertaining to this 

quantitative relationship between air Pb and children’s blood Pb is now, as in the past, limited by 

the circumstances in which the data are collected. These estimates are generally developed from 

studies of populations in a variety of Pb exposure circumstances. Accordingly, there is 

significant variability in air-to-blood ratios among the different study populations exposed to Pb 

through different air-related exposure pathways and at different exposure levels. This variability 

in air-to-blood estimates can relate to the representation of air-related pathways and study 

populations, including, for example, relatively narrow age ranges for the population in order to 

reduce age-related variability in blood Pb, or including populations with narrowly specified 

dietary sources. It can relate to the study population exposure and blood Pb levels (ISA, section 

3.7.4). It can also relate to the precision of air and blood measurements and of the study 

circumstances, such as with regard to spatial and temporal aspects. Additionally, in situations 

where exposure to nonair sources covaries with air-related exposures that are not accounted for 

in deriving ratio estimates, uncertainties may relate to the potential for confounding by nonair 

exposure covariance (ISA, section 3.5). Most studies have reported the relationship as either 

log-log or linear (Table 3-1; ISA, section 3.7.4). 

As was noted in the last review, age is an important influence on the magnitude of air-toblood ratio estimates derived. Ratios for children are generally higher than those for adults, and 

higher for young children than older children, perhaps due to behavioral differences between the 

age groups, as well as their shorter exposure history. Similarly, given the common pattern of 

higher blood Pb levels in pre-school aged children than during the rest of childhood, related to 

behaviors that increase environmental exposures (e.g., hand-to-mouth activity), ratios would be 

expected to be highest in earlier childhood. Additionally, estimates of air-to-blood ratios that 

include air-related ingestion pathways in addition to the inhalation pathway are “necessarily 

higher,” in terms of blood Pb response, than those estimates based on inhalation alone (USEPA 

1986, p. 11-106). Thus, the extent to which studies account for the full set of air-related 

inhalation and ingestion exposure pathways affects the magnitude of the resultant air-to-blood 

estimates, such that including fewer pathways as “air-related” yields lower ratios. Estimates of 

air-to-blood ratios can also be influenced by population characteristics that may influence blood 
3-9 

Pb; accordingly, some analyses include adjustments. Most of the studies in Table 3-1 include 

ratios derived from linear analyses, while a subset are derived from nonlinear models. 

Given the recognition of young children as a key at-risk population in section 3.3 below, 

as well as the influence of age on blood Pb levels, the studies presented in Table 3-1 are grouped 

with regard to the extent of their inclusion of children younger than or barely school age (less 

than or equal to five years of age). Among the first group of studies, focused exclusively on 

young children, only one study dates from the end of or after the phase-out of leaded gasoline 

usage (namely, Hilts, 2003). This study reports changes in children’s blood Pb levels associated 

with reduced Pb emissions and associated air concentrations near a Pb smelter in Canada (for 

children through age five). Given the timing of this study, after the leaded gasoline phase-out, 

and its setting near a smelter, the ambient air Pb in this study may be somewhat more 

comparable to that near sources in the U.S. today than other studies discussed herein. The study 

authors report an air-to-blood ratio of 1:6.5

 An EPA analysis of the air and blood data reported 

for 1996, 1999 and 2001 results in a ratio of 1:6.5, and the analysis focused only on the 1996 and 

1999 data (pre- and post- the new technology) yields a ratio of 1:7 (ISA, section 3.5.1; Hilts, 

2003).6 The two other studies that focused on children of age 5 or younger analyzed variations 

in air Pb as a result of variations in leaded gasoline usage in Chicago, Illinois. The study by 

Hayes et al. (1994) compared patterns of ambient air Pb reductions and blood Pb reductions for 

large numbers of children, aged 6 months to 5 years, in Chicago between 1974 and 1988, a 

period when significant reductions occurred in both measures. The study reported a better fit for 

the log-log model which describes a pattern of higher ratios with lower ambient air Pb and blood 

Pb levels (Hayes et al., 1994). Based on the log-log model, the ratio derived for the relationship 

of quarterly mean air concentration with blood Pb during the period is 1:8 (Table 3-1). Another 

analysis for a Chicago dataset, performed by Schwartz and Pitcher (1989) focused on the 

 

5

 Sources of uncertainty include the role of factors other than ambient air Pb reduction in influencing 

decreases in blood Pb (ISA, section 3.5.1). The author cited remedial programs (e.g., community and home-based 

dust control and education) as potentially responsible for some of the blood Pb reduction seen during the study 

period (1997 to 2001), although the author notes that these programs were in place in 1992, suggesting they are 

unlikely to have contributed to the sudden drop in blood Pb levels occurring after 1997 (Hilts, 2003). Other aspects 

with potential implications for ratios include the potential for children with lower blood Pb levels not to return for 

subsequent testing, and the age range of 6 to 36 months in the 2001 blood screening compared to ages up to 60 

months in earlier years of the study (Hilts, 2003). 

6

 This study considered changes in ambient air Pb levels and associated blood Pb levels over a five-year 

period which included closure of an older Pb smelter and subsequent opening of a newer facility in 1997 and 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 3.5.1). 
3-10 

association of blood Pb in black children (aged < 5 years) with the use of leaded gasoline from 

1976 through 1980. Given that leaded gasoline exposure occurs by air-related pathways, 

additional analyses have related the leaded gasoline usage for this period to air concentrations. 

The resulting relationship of blood Pb with air Pb (adjusted for age and a number of other 

covariates) yields a ratio of 1:8.6 (ISA, table 3-12, section 3.5.1). The blood Pb concentrations 

in the two leaded gasoline studies are appreciably higher (a factor of two or more) than those in 

the study near the smelter (Hilts, 2003). 

The second group of studies in Table 3-1 (comprising studies including but not limited to 

children less than or equal to five years of age) includes a complex statistical analysis and 

associated dataset for a cohort of children born in Mexico City from 1987 through 1992 (Schnaas 

et al., 2004). This study, which was not assessed in the last review, encompasses the period of 

leaded gasoline usage and further informs our understanding of factors influencing the 

quantitative relationship between air Pb and children’s blood Pb. Air-to-blood ratios developed 

from this study are influenced by a number of factors and appear to range from roughly 2 to 6, in 

addition to an estimate of 9 (ISA, section 3.5.1), although the latter is derived from a data set 

restricted to the latter years of the study when little change in air Pb concentration occurred, such 

that the role of air Pb may be more uncertain. Estimates associated with the developmental 

period of highest exposure (e.g., age 2 years) range up to approximately 6, illustrating the 

influence of age on the ratio (ISA, section 3.5.1). Also in the second group in Table 3-1 are two 

much older studies of populations with age ranges extending well beyond 6 years. The first is 

the review and meta-analysis by Brunekreef (1984) using datasets available at the time for 

variously aged children as old as 18 years with identified air monitoring methods and reliable 

blood Pb data for 18 locations in the U.S. and internationally.7

 The author discusses potential 

confounders of the relationship between air Pb and blood Pb, recognizing the desirability of 

taking them into account when deriving an air-to-blood relationship from a community study but 

noting that was not feasible in such an 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 values were 0.692 and 0.331, respectively). From these two logn-logn models, airto-blood ratio estimates were derived for air concentrations corresponding to the geometric 

means of the two sets of data pairs. At those concentrations (1.5 and 0.54 μg/m3

, respectively), 

the resultant ratios both round to 5. The study by Schwartz and Pitcher (1989) described above 

also analyzed the relationship between U.S. NHANES II blood Pb levels for white subjects, aged 

 

7

 In the dataset reviewed by Brunekreef (1984), air-to-blood ratios from the subset of those studies that 

used quality control protocols and presented adjusted slopes include values of 3.6 (Zielhuis et al., 1979), 5.2 (Billick 

et al., 1979, 1980); 2.9 (Billick et al., 1983), and 8.5 (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 (1984) used multiple regression to control for several confounders (73 FR 66974). 
3-11 

<74 years, and national usage of leaded gasoline. A separate, less specifically described, air Pb 

dataset was used to convert the relationship of blood Pb with gas Pb to one for blood Pb with air 

Pb, with a resultant ratio on the order of 9, adjusted for age and other covariates (Henderson, 

2007a, pp. D-2 to D-3; ISA, Table 3-12). 

The last two studies included in Table 3-1 are focused on older children (ages 6-11). The 

methods for characterization of air Pb concentrations (and soil Pb for Ranft et al., 2008) also 

differ from other studies in Table 3-1. The first study regressed average blood Pb concentrations 

for multiple locations around Mumbai, India on average air Pb concentrations at those locations 

(Tripathi et al., 2001). The values in the linear regression were 13 pairs of location-specific 

geometric means of all the data collected over the 13-year period from 1984 to 1996; the 

reported slope was 3.6 (Tripathi et al., 2001). The location-specific geometric mean blood Pb 

levels in this study (8.6-14.4 μg/dL) indicate blood Pb distributions in this age group much 

higher than those pertinent to similarly aged children in the U.S. today. The second study 

analyzed air, soil and children’s blood Pb concentrations in Duisburg, Germany, during the 

leaded gasoline phase-out (Ranft et al., 2008). Average blood Pb levels declined over the nearly 

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

to 0.06 μg/m3 over the same period, with the largest reduction occurring between the first study 

year (derived from two monitoring sites for full study area) and the second study year, 1991, for 

which air concentrations were derived from a combination of dispersion modeling and the two 

monitoring sites.9

 For a mean air Pb concentration of 0.1 μg/m3, the study’s multivariate loglinear regression model predicted air-to-blood ratios of 3.2 and 6.4 for “background” blood Pb 

concentrations of 1.5 and 3 μg/dL, respectively. In this study, background referred to Pb in 

blood from other sources; the blood Pb distribution over the study period, including levels when 

air Pb concentrations are lowest, indicates 3 μg/dL may be the better estimate of background for 

this study population. Inclusion of soil Pb as a variable in the model may have contributed to an 

underestimation of the these blood Pb-air Pb ratios for this study because some of the Pb in soil 

likely originated in air and the blood Pb-air Pb slope does not include the portion of the soil/dust 

Pb ingestion pathway that derives from air Pb. Using univariate linear, log-log and log-linear 

models on the median air and blood Pb concentrations reported for the five years included in this 

study, the ISA also derived air-to-blood ratio estimates ranging from 9 to 17 (ISA, p. 3-126; 

 

8

 Blood Pb measurements were available on a total of 843 children across five time periods, in the first of 

which the average child age was 9 years while it was 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). 
3-12 

Ranft et al., 2008, Table 2). Uncertainties related to this study’s estimates include those related 

to the bulk of air concentration reduction occurring between the first two time points (1983 and 

1991) and the difference among the year’s air datasets (e.g., two data sources [air monitors] in 

1983 and multiple geographical points from a combination of the monitors and modeling in 

subsequent years). 
3-13 

Table 3-1. Empirically derived air-to-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 median PbB and quarterly 

mean PbA 

[unadjusted] 

PbB: 10-28 μg/dL (quarterly median) 

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 (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 

Average age increased over study period: <3yrs (1987-1992), 

and increased by a year each year after that 

Urban area during/after leaded gasoline usage 

 Schnaas et al. (2004) 

Linear , 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); average: ~9.5 yr (1983), ~6.5 (others) 

Duisburg, Germany–5 areas: 1983, 1991, 1994, 1997, 2000 

Industrial urban area during/after leaded gasoline usage 

 Ranft et al. (2008) 

Linear, 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, Table 3-12; Hayes et al., 1994)

C - See discussion in text and ISA, section 3.5.1. 

D - Based on data for U.S. (1986 CD). See ISA, section 3.5.1. Log-lin = log-linear model. 

E - ln(PbB) = ln(PbA) x 0.3485 +2.853 

F - ln(PbB) = ln(PbA) x 0.2159 + 2.620 

G -Derived from regressions with separate soil Pb variable, contributing to underestimation of contribution from air Pb (see text and ISA, section 3.5.1).

GM, geometric mean; AM, arithmetic mean; GSD, geometric standard deviation; PbB, blood Pb concentration, μg/dL; PbA, air Pb concentration, μg/m3
3-14 

In the 2008 Pb NAAQS review, in addition to considering the evidence presented in the 

published literature and that reviewed in the 1986 CD, we also considered air-to-blood ratios 

derived from the exposure assessment (73 FR 66974; 2007 REA, section 5.2.5.2). In the 

exposure assessment (summarized in section 3.4 below), current modeling tools and information 

on children’s activity patterns, behavior and physiology were used to estimate blood Pb levels 

associated with multimedia and multipathway Pb exposure. The results from the various case 

studies assessed, with consideration of the context in which they were derived (e.g., the extent to 

which the range of air-related pathways was simulated, and the limitations associated with those 

simulations), and the multiple sources of uncertainty (see section 3.4.7 below) are also 

informative to our understanding of air-to-blood ratios. Estimates of air-to-blood ratios for the 

two REA case studies that represent localized population exposures exhibited an increasing trend 

across air 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

down to a monthly average of 0.02 μg/m3

, the ratios ranged from 1:2 to 1:9 for the general urban 

case study, with a similar trend although of generally higher ratio for the primary smelter case 

study subarea. This pattern of model-derived ratios is generally consistent with the range of 

ratios obtained from the literature. We continue to recognize a number of sources of uncertainty 

associated with these model-derived ratios which may contribute to high or low biases.10 

The evidence on the quantitative relationship between air Pb and air-related Pb in blood 

is now, as in the past, limited by the circumstances (such as those related to Pb exposure) in 

which the data were collected. Previous reviews have recognized the significant variability in 

air-to-blood ratios for different populations exposed to Pb through different air-related exposure 

pathways and at different air and blood levels, with the 1986 CD noting that ratios derived from 

studies involving the higher blood and air Pb levels pertaining to occupationally exposed 

workers are generally smaller than ratios from studies involving lower blood and air Pb levels 

(ISA, p. 3-132; 1986 CD, p. 11–99). Consistent with this observation, slopes in the range of 3 to 

 

10 For example, the limited number of air-related pathways (inhalation and indoor dust ingestion) simulated 

to change in response to changes in ambient air Pb reductions in these case studies could have implications for the 

air-to-blood ratios. Additionally, with regard to the 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 2007 REA, 

Volume II, Appendix G, Attachment G-1). The use of leaded paint in some housing constructed before 1980 

contributes some uncertainty due to the potential role of indoor Pb paint (compared to ambient air Pb) in the 

relationship. The empirically-based ambient air Pb – dust Pb relationships used in the primary Pb smelter (subarea) 

case study may contribute to a potential for the ratios from this case study to more fully capture the impact of 

changes in ambient air Pb on indoor dust Pb, and consequently on blood Pb. Some have suggested, however, that 

the regression used may not accurately reflect the 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. 
3-15 

5 were estimated for child population datasets assessed in the 1986 CD (ISA, p. 3-132; 1986 CD 

p. 11–100; Brunekreef, 1984; Tripathi et al., 2004). Additional studies considered in the last 

review and those assessed in the ISA provide evidence of ratios above this older range (ISA, p. 

3-133). For example a ratio of 6.5-7 is indicated by the study by Hilts (2003), one of the few 

studies that evaluate the air Pb-blood Pb relationship in conditions that are closer to the current 

state in the U.S. ( ISA, p. 3-132). We additionally note the variety of factors identified in the 

ISA that may potentially affect estimates of various ratios (including potentially coincident 

reductions in nonair Pb sources during the course of the studies), and for which a lack of 

complete information may preclude any adjustment of estimates to account for their role (ISA, 

section 3.5). 

In summary, as at the time of the last review of the NAAQS for Pb, the currently 

available evidence includes estimates of air-to-blood ratios, both empirically- and model-derived, 

with associated limitations and related uncertainties. These limitations and uncertainties, which 

are summarized here and also noted in the ISA, usually include uncertainty associated with 

reductions in other Pb sources during the study period. The limited amount of new information 

available in this review has not appreciably altered the scientific conclusions reached in the last 

review regarding relationships between Pb in ambient air and Pb in children’s blood or with 

regard to the range of ratios. The currently available evidence continues to indicate ratios 

relevant to the population of young children in the U.S. today, reflecting multiple air-related 

pathways in addition to inhalation, to be generally consistent with the approximate range of 1:5 

to 1:10 given particular attention in the 2008 NAAQS decision, including the “generally central 

estimate” of 1:7 (73 FR 67002, 67004; ISA, pp. 3-132 to 3-133). 

3.2 NATURE OF EFFECTS 

Lead has been demonstrated to exert a broad array of deleterious effects on multiple 

organ systems as described in the assessment of the evidence available in this review and 

consistent with conclusions of past CDs (ISA, section 1.6; 2006 CD, section 8.4.1). A sizeable 

number of studies on Pb health effects are newly available in this review and are critically 

assessed in the ISA as part of the full body of evidence. The newly available evidence reaffirms 

conclusions on the broad array of effects recognized for Pb in the last review (see ISA, section 

1.10).11 Consistent with those conclusions, in the context of pollutant exposures considered 

 

11 Since the last Pb NAAQS review, the ISAs which have replaced CDs in documenting each review of the 

scientific evidence (or air quality 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). 
3-16 

relevant to the Pb NAAQS review,12 the ISA determines that causal relationships13 exist for 

Pbwith effects on the nervous system in children (cognitive function decrements and the group of 

externalizing behaviors comprising attention, impulsivity and hyperactivity), the hematological 

system (altered heme synthesis and decreased red blood cell survival and function), and the 

cardiovascular system (hypertension and coronary heart disease), and on reproduction and 

development (postnatal development and male reproductive function) (ISA, table 1-2). 

Additionally, the ISA describes relationships between Pb and effects on the nervous system in 

adults, on immune system function and with cancer14 as likely to be causal15 (ISA, table 1-2, 

sections 1.6.4 and 1.6.7). 

In some categories of health effects, there is newly available evidence regarding some 

aspects of the effects described in the last review or that strengthens our conclusions regarding 

aspects of Pb toxicity on a particular physiological system. Among the nervous system effects of 

Pb, the newly available evidence is consistent with conclusions in the previous review which 

recognized that “[t]he neurotoxic effects of Pb exposure are among those most studied and most 

extensively documented among human population groups” (2006 CD, p. 8-25). Nervous system 

effects that receive prominence in the current review, as in previous reviews, include those 

 

12 With regard to consideration of pollutant exposures for studies included in the ISA, the ISA states the 

following (ISA, pp. lx-lxi). 

In drawing judgments regarding causality for the criteria air pollutants, the ISA focuses on 

evidence of effects in the range of relevant pollutant exposures or doses, and not on determination 

of causality at any dose. Emphasis is placed on evidence of effects at doses (e.g., blood Pb 

concentration) or exposures (e.g., air concentrations) that are relevant to, or somewhat above, 

those currently experienced by the population. The extent to which studies of higher 

concentrations are considered varies by pollutant and major outcome category, but generally 

includes those with doses or exposures in the range of one to two orders of magnitude above 

current or ambient conditions. Studies that use higher doses or exposures may also be considered 

to the extent that they provide useful information to inform understanding of mode of action, 

interspecies differences, or factors that may increase risk of effects for a population. Thus, a 

causality determination is based on weight of evidence evaluation for health, ecological or 

welfare effects, focusing on the evidence from exposures or doses generally ranging from current 

levels to one or two orders of magnitude above current levels. 

13 In determining there to be a causal relationship for Pb with specific health effects, EPA has concluded 

that “[e]vidence is sufficient to conclude that there is a causal relationship with relevant pollutant exposures (i.e., 

doses or exposures generally within one to two orders of magnitude of current levels)” (ISA, p. lxii) 

14 Lead has been classified as a probable human 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 4.10). In this assessment, EPA concludes that a causal relationship 

is likely to exist between Pb exposure and cancer, based primarily on consistent, strong evidence from experimental 

animal studies, but inconsistent epidemiological evidence (ISA, section 4.10.5). 

15 In determining that there is likely to be a causal relationship for Pb with specific health effects, EPA has 

concluded that “[e]vidence is sufficient to conclude that a causal relationship is likely to exist with relevant pollutant 

exposures, but important uncertainties remain” (ISA, p. lxii). 
3-17 

affecting cognitive function and behavior in children (ISA, section 4.3), with conclusions that are 

consistent with findings of the last review. 

Across the broad array of Pb effects for systems and processes other than the nervous 

system, the evidence base has been augmented with additional epidemiological investigations in 

a number of areas, including developmental outcomes, such as puberty onset, and adult outcomes 

related to cardiovascular function, for which several large cohorts have been analyzed (ISA, 

Table 1-8 and sections 4.4 and 4.8). Conclusions on these other systems and processes are 

consistent with conclusions reached in the last review, while also extending our conclusions on 

some aspects of these effects. For example, evidence in this review for the cardiovascular 

system includes information on the role of interactions of cumulative Pb exposure with other 

factors, such as stress in contributing to hypertension, and on a role for Pb in contributing to 

coronary heart disease (ISA, section 4.4 and Table 1-8). 

Based on the extensive assessment of the full body of evidence available in this review, 

the major conclusions drawn by the ISA regarding health effects of Pb in children include the 

following (ISA, p. lxxxvii). 

Multiple epidemiologic studies conducted in diverse populations of children 

consistently demonstrate the harmful effects of Pb exposure on cognitive function 

(as measured by IQ decrements, decreased academic performance and poorer 

performance on tests of executive function).... Evidence suggests that some Pbrelated cognitive effects may be irreversible and that the neurodevelopmental 

effects of Pb exposure may persist into adulthood (Section 1.9.4). Epidemiologic 

studies also demonstrate that Pb exposure is associated with decreased attention, 

and increased impulsivity and hyperactivity in children (externalizing behaviors). 

This is supported by findings in animal studies demonstrating both analogous 

effects and biological plausibility at relevant exposure levels. Pb exposure can 

also exert harmful effects on blood cells and blood producing organs, and is likely 

to cause an increased risk of symptoms of depression and anxiety and withdrawn 

behavior (internalizing behaviors),decreases in auditory and motor function, 

asthma and allergy, as well as conduct disorders in children and young adults. 

There is some uncertainty about the Pb exposures contributing to the effects and 

blood Pb levels observed in epidemiologic studies; however, these uncertainties 

are greater in studies of older children and adults than in studies of young 

children (Section 1.9.5). 

Based on the extensive assessment of the full body of evidence available in this review, 

the major conclusions drawn by the ISA regarding health effects of Pb in adults include the 

following (ISA, p. lxxxviii). 

A large body of evidence from both epidemiologic studies of adults and 

experimental studies in animals demonstrates the effect of long-term Pb exposure 

on increased blood pressure (BP) and hypertension (Section 1.6.2). In addition to 

its effect on BP, Pb exposure can also lead to coronary heart disease and death 
3-18 

from cardiovascular causes and is associated with cognitive function decrements, 

symptoms of depression and anxiety, and immune effects in adult humans. The 

extent to which the effects of Pb on the cardiovascular system are reversible is not 

well-characterized. Additionally, the frequency, timing, level, and duration of Pb 

exposure causing the effects observed in adults has not been pinpointed, and 

higher past exposures may contribute to the development of health effects 

measured later in life. 

As in prior reviews of the Pb NAAQS, this review is focused on those effects most 

pertinent to ambient air Pb exposures. Given the reductions in ambient air Pb levels over the 

past decades, these effects are generally those associated with the lowest levels of Pb exposure 

that have been evaluated. Additionally, we recognize the limitations on our ability to draw 

conclusions regarding the exposure conditions contributing to the findings from epidemiological 

analyses of blood Pb levels in populations of older children and adults, particularly in light of 

their history of higher Pb exposures. In the last review, while recognizing the range of health 

effects in variously aged populations related to Pb exposure, we focused on the health effects for 

which the evidence was strongest with regard to relationships with the lowest exposure levels, 

neurocognitive effects in young children. The policy-relevant questions on health effects for this 

review (identified in the IRP) were framed in recognition of the conclusions of the last review. 

Our consideration of the health effects evidence in this review is framed by policy-relevant 

questions building on those identified in the IRP. 

 To what extent is there new scientific evidence available to improve our 

understanding of the health effects associated with various time periods of Pb 

exposures at various stages of life? 

As in the last review, we base our current understanding of health effects associated with 

different Pb exposure circumstances at various stages of life on the full body of available 

evidence which includes epidemiological studies of health effects associated with population Pb 

biomarker levels as well as laboratory animal studies in which the effects of different exposures 

on different lifestages are assessed under controlled conditions. The epidemiological evidence is 

overwhelmingly comprised of studies that rely on blood Pb for the exposure metric, with the 

remainder largely including a focus on bone Pb. Because these metrics reflect Pb in the body 

(e.g., as compared to Pb exposure concentrations) and, in the case of blood Pb, reflect Pb 

available for distribution to target sites, they strengthen the evidence base for purposes of 

drawing causal conclusions with regard to Pb generally. The complexity of Pb exposure 

pathways and internal dosimetry tends to limit the extent to which these types of studies inform 

our more specific understanding of the Pb exposure circumstances (e.g., timing, duration, 

frequency and magnitude) eliciting the various effects. 
3-19 

The specific exposure circumstances, including timing during the lifetime, that contribute 

to the blood Pb (or bone Pb) measurements with which associations have been analyzed in 

epidemiological studies are unknown. This is particularly the case with regard to the 

contributing role of recent exposures for which uncertainty is greater in adults and older children 

than in younger children (ISA, sections 1.9.4). For example, a critical aspect of much of the 

epidemiological evidence, particularly that focused on older adults in the U.S. today, is the 

backdrop of generally declining environmental Pb exposure (from higher exposures during their 

younger years) that is common across many study populations (ISA, p. 4-2). An additional 

factor complicating the interpretation of health effect associations with blood Pb measurements 

in older children and younger adults is the common behaviors of younger children (e.g., hand-tomouth contact) which generally contribute to relatively greater environmental exposures earlier 

in life (ISA, sections 3.1.1, 4.2.1). Such exposure histories complicate our ability to draw 

conclusions regarding critical time periods and lifestages for Pb exposures eliciting the effects 

with which associations with Pb biomarkers have been observed in populations of adults and 

older children (e.g., ISA, section 1.9.6).16

As at the time of the last review, assessment of the full evidence base, including evidence 

newly available in this review, demonstrates that Pb exposure prenatally and also in early 

childhood can contribute to neurocognitive impacts in childhood, with evidence also indicating 

the potential for effects persisting into adulthood (ISA, sections 1.9.5, 1.9.6, and 1.10). In 

addition to the observed associations of prenatal and childhood blood Pb with effects at various 

ages in childhood, there is also evidence of lead-related cognitive function effects in nonoccupationally exposed adults (ISA, section 4.3.11). This includes evidence of associations of 

such effects in adulthood with childhood blood Pb levels and, in other cohorts, with concurrent 

(adult) blood Pb levels (ISA, sections 4.3.2.1, 4.3.2.7 and 4.3.11). As the studies finding 

associations of adult effects with childhood blood Pb levels did not examine adult blood Pb 

levels, the relative influence of adult Pb exposure cannot be ascertained, and a corresponding 

lack of early life exposure or biomarker measurements for the latter studies limit our ability to 

draw conclusions regarding specific Pb exposure circumstances eliciting the observed effects 

(4.3.11). Findings of stronger associations for adult neurocognitive effects with bone Pb, 

 

16 The evidence from experimental animal studies can be informative with regard to key aspects of 

exposure circumstances in eliciting specific effects which can inform our interpretation of the epidemiological 

evidence. For example, the animal evidence base with regard to Pb effects on blood pressure demonstrates the 

etiologically-relevant role of long-term (as compared to short-term) exposure (ISA, section 4.4.1). 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 4.4.1). For other health effects, the animal evidence base may or may not be informative with regard to the 

role of specific exposure circumstances in eliciting those effects. 
3-20 

however, indicate the role of historical or cumulative exposures for those effects (ISA, section 

4.3). 

Given the relatively short exposure histories of young children, there is relatively reduced 

uncertainty regarding the lifestages in which exposures contribute to effects for associations of 

early childhood effects with early childhood blood Pb levels (ISA, sections 1.9.4, 1.9.6 and 

4.3.11). In considering our understanding of the relative impact on neurocognitive function of 

additional Pb exposure of children by school age or later we recognize increasing uncertainty 

associated with limitations of the currently available evidence, including epidemiological cohorts 

with generally similar temporal patterns of exposure. We take note, additionally, of evidence 

from experimental animal studies and a small body of epidemiological studies that indicates that 

Pb exposures during different lifestages can induce cognitive impairments. The limited 

epidemiological evidence is of populations with blood Pb levels that are not strongly correlated 

over time and that can, accordingly, address the issue of the role of exposure subsequent to the 

earliest lifestages (ISA, section 4.3.11; Hornung et al., 2009). Some animal evidence 

demonstrates impaired learning with infancy only, from infancy into adulthood, and postinfancy 

only Pb exposure (Rice, 1990; Rice and Gilbert 1990; Rice, 1992). Further, evidence that Pb 

exposure presents a risk during different lifestages is also consistent with our broader 

understanding that nervous system development continues throughout childhood. The limited 

analyses of this issue that are newly available in this review do not appreciably change our 

understanding or conclusions on this from those of the prior review (ISA, section 4.3.11). 

As in the last review, there is also substantial evidence of other neurobehavioral effects in 

children, such as reduced attention span, increased impulsivity, hyperactivity, conduct disorders 

and effects on internalizing behaviors. The evidence for many of these endpoints, as with 

neurocognitive effects, also includes associations of effects at various ages in childhood and, for 

some effects, into adulthood, with blood Pb levels reflective of several different lifestages (e.g., 

prenatal and several different ages in childhood) (ISA, sections 4.3.3 and 4.3.4). There is similar 

or relatively less extensive evidence to inform our understanding of such effects associated with 

specific time periods of exposure at specific lifestages than is the case for effects on cognitive 

function. 

Across the range of Pb effects on physiological systems and processes other than the 

nervous system, the full body of evidence on etiologically relevant circumstances of Pb exposure 

eliciting increases in blood pressure and hypertension is somewhat more informative than is the 

case with regard to many other effects. In the case of lead-induced increases in blood pressure, 

the evidence indicates an importance of long-term exposure (ISA, sections 1.6.2 and 4.4.7.1). 

In summary, as in the last review, we continue to recognize a number of uncertainties 

regarding the circumstances of Pb exposure, including timing or lifestages, eliciting specific 
3-21 

health effects. Consideration of the evidence newly available in this review has not appreciably 

changed our understanding on this topic. The relationship of long-term exposure to Pb with 

hypertension and increased blood pressure in adults is substantiated despite some uncertainty 

regarding the exposures circumstances (e.g., magnitude and timing) contributing to blood Pb 

levels measured in epidemiological studies. Across the full evidence base, the effects for which 

our understanding of relevant exposure circumstances is greatest are neurocognitive effects in 

young children. Thus, we continue to recognize and give particular attention to the role of Pb 

exposures relatively early in childhood in contributing to neurocognitive effects which may 

persist into adulthood. 

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

evidence of effects at exposure levels lower than previously observed and what 

are important uncertainties in that evidence? 

In considering the question posed here, we recognize, as discussed in section 3.1 above, 

that the epidemiological evidence base for our consideration in this review, as in the past, 

includes substantial focus on internal biomarkers of exposure, such as blood Pb, with relatively 

less information specific to exposure levels, including those derived from air-related pathways. 

Given that blood and bone Pb are integrated markers of aggregate exposure across all sources 

and exposure pathways, our interpretation of studies relying on them is informed by what is 

known regarding the historical context and exposure circumstances of the study populations. For 

example, a critical aspect of much of the epidemiological evidence is the backdrop of generally 

declining Pb exposure over the past several decades. Thus as a generality, recent 

epidemiological studies of populations with similar characteristics as those studied in the past 

tend to involve lower overall Pb exposures and accordingly lower blood Pb levels (e.g., ISA, 

sections 2.5 and 3.4.1; 2006 CD, section 3.4). This has been of particular note in the evidence of 

blood Pb associations with nervous system effects, particularly impacts on cognitive function in 

children, for which we have seen associations with progressively lower childhood blood Pb 

levels across past reviews (ISA, section 4.3.12; 1986 CD; USEPA, 1990; 2006 CD; 73 FR 

66976). 

The evidence currently available with regard to the magnitude of blood Pb levels 

associated with neurocognitive effects in children is generally consistent with that available in 

the review completed in 2008. Nervous system effects in children, specifically effects on 

cognitive function, continue to be the effects that are best substantiated as occurring at the lowest 

blood Pb concentrations (ISA, pp. lxxxvii-lxxxviii). Associations of blood Pb with effects on 

cognitive function measures in children have been reported in many studies across a range of 
3-22 

childhood blood Pb levels, including study group (mean/median) levels ranging down to 2 μg/dL 

(e.g., ISA, p. lxxxvii and section 4.3.2).17 

Studies in which such findings were reported for childhood study group blood Pb levels 

below 5 μg/dL are summarized in Table 3-2.18 In recognition of the influence of age on blood 

Pb levels, the analyses in Table 3-2 are listed in order of age at which the blood Pb 

measurements were taken. Findings for studies newly available in this review are indicated in 

bold text. Although the analyses from Lanphear et al (2005) listed in Table 3-2 were available in 

the last review, the information presented in Table 3-2 for sample size and mean blood Pb 

concentration has been updated to reflect recalculations using data corrected for recently 

identified errors, as described further in the next section below (Kirrane and Patel, 2014). 

 

17 The value of 2 μg/dL refers to the regression analysis of blood Pb and end-of-grade test scores, in which 

blood Pb was represented by categories for integer values of blood Pb from 1 μg/dL to 9 and >10 μg/dL from large 

statewide database. A significant effect estimate was 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). 

18 Two additional studies (both newly available) that report such associations with blood Pb levels for 

which the mean is equal to 5.0 μg/dL. The first is a study of 506 children in Detroit, MI (born, 1982-1984) at age 7 

years which observed a significant 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 4.3.2.1 and 4.3.3.1; Chiodo et 

al., 2007). The second study focuses on 174 of the Rochester cohort children at age 6 years, reporting significant 

negative associations with FSIQ for four different blood Pb metrics: concurrent (mean = 5.0 μg/dL), lifetime 

average (mean=7.2 μg/dL), infancy average (mean = 7.1 μg/dL) and peak (mean = 11.4 μg/dL) (Jusko et al., 2008). 
3-23 

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 4.3.2) 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/dL

Bellinger 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 3.3 0.9 – 7.4 118 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; statisticaassociation 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; Kirrane and P

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 24.6% age 5 (Boston, Cleveland), 58.5% age 6 (Rochester), 16.9% 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 
3-24 

Among the analyses of lowest study group blood Pb levels at the youngest ages in Table 

3-2 are analyses available in the last review of Pb associations with neurocognitive decrement in 

study groups with mean levels on the order of 3-4 μg/dL in children aged 24 months or ranging 

from 5 to 7 years (73 FR 66978-66969; ISA, sections 4.3.2.1 and 4.3.2.2; Bellinger and 

Needleman, 2003; Canfield et al., 2003; Lanphear et al., 2005; Tellez-Rojo et al., 2006; 

Bellinger, 2008; Canfield, 2008; Tellez-Rojo, 2008; Kirrane and Patel, 2014).19 Newly available 

in this review are two studies reporting association of blood Pb levels prior to three years of age 

with academic performance on standardized tests in primary school; mean blood Pb levels in 

these studies were 4.2 and 4.8 μg/dL (ISA, section 4.3.2.5; Chandramouli et al., 2009; Miranda 

et al., 2009). One of these two studies, which represented integer blood Pb levels as categorical 

variables, indicated a small effect on end-of-grade reading score of blood Pb levels as low as 2 

μg/dL, after adjustment for age of measurement, race, sex, enrollment in free or reduced lunch 

program, parental education, and school type (Miranda et al., 2009). 

In a newly available study of blood Pb levels at primary school age, a significant 

association of blood Pb in children aged 8-11 years and concurrently measured full scale IQ 

(FSIQ) was reported for a cross-sectional cohort in Korea with a mean blood Pb level of 1.7 

μg/dL and range of 0.43-4.91 μg/dL (Kim et al., 2009).20 In considering the blood Pb levels in 

this study, we note that blood Pb levels in children aged 8-11 are generally lower than those in 

pre-school children, for reasons related to behavioral and other factors (ISA, sections 3.3.5, 3.4.1 

and 5.2.1.1).21 It is likely that the blood Pb levels of this study group at earlier ages, e.g., prior to 

school entry, were higher and the available information does not provide a basis to judge whether 

the blood Pb levels in this study represent lower exposure levels than those experienced by the 

younger study groups. In still older children, a large cross-sectional investigation of blood Pb 

association with effects on memory and learning that was available in the last review was 

focused on children aged 6-16 years, born during 1972-1988, with a mean blood Pb of 1.9 

μg/dL. A study newly available in this review, focused on a subset of the earlier study cohort 

 

19 The tests for cognitive function in these studies include age-appropriate Wechsler intelligence tests 

(Lanphear et al., 2005; Bellinger and Needleman, 2003), the Stanford-Binet intelligence test (Canfield et al., 2003), 

and the Bayley Scales of Infant Development (Tellez-Rojo et al., 2006). The Wechsler and Stanford-Binet tests are 

widely used to assess neurocognitive function in children and adults. These tests,however, are not appropriate for 

children under age three. For such children, studies generally use the age-appropriate Bayley Scales of Infant 

Development as a measure of cognitive development. 

20 Limitations of this study included a lack of consideration of potential confounding by parental caregiving 

quality or IQ (ISA, Table 4-3). 

21 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 4.3.2). Separate analysis of the full study group found a 

significant negative association of IQ with blood Mn (Kim et al., 2009). 
3-25 

(ages 12-16, born during 1975-1982), also reports a significant negative association of blood Pb 

with learning and memory test results with mean blood Pb levels of approximately 2 μg/dL (ISA, 

section 4.3.2.3; Lanphear et al., 2000; Krieg et al., 2010). In considering these study findings 

with regard to the question of exposure levels eliciting effects, we recognize, however, that blood 

Pb levels are, in general, lower among teenagers than young children and also that, for these 

subjects specifically, the magnitude of blood Pb levels during the earlier childhood (e.g., preschool ages) was much higher. For example, the mean blood Pb levels for the 1-5 year old age 

group in the NHANES 1976-80 sample was 15 μg/dL, declining to 3.6 μg/dL in the NHANES 

1988-1991 sample (Pirkle et al., 1994; ISA, section 3.4.1). 

With regard to other nervous system effects in children, the evidence base at lower blood 

Pb levels is somewhat extended since the last review with regard to the evidence on Pb and 

effects on externalizing behaviors, such as attention, impulsivity, hyperactivity and conduct 

disorders (ISA, section 4.3.3 and table 4-17). Several newly available studies investigating the 

role of blood Pb levels in older children (primary school age and older) have reported significant 

associations for these effects with concurrent blood Pb levels, with mean levels generally on the 

order of 5 μg/dL or higher (ISA, section 4.3.3). One exception is the newly available crosssectional, categorical analysis of the NHANES 2001-2004 sample of children aged 8-15 years, 

which found higher prevalence of conduct disorder in the subgroup with concurrent blood Pb 

levels of 0.8-1.0 μg/dL as compared to the <0.8 μg/dL group (ISA, section 4.3.4 and Table 4-

12). As noted above, we recognize that many of these children, born between 1986 and 1996, 

are likely to have had much higher Pb exposures (and associated blood Pb levels) in their earlier 

years than those commonly experienced by young children today, thus precluding a conclusion 

regarding evidence of effects associated with lower exposure levels than provided by evidence 

previously available. 

As summarized earlier in this section, blood Pb has been associated with a range of health 

effects on multiple organ systems or processes. As is the case for studies of nervous system 

effects in children, newly available studies of other effects in child and adult cohorts include 

cohorts with similar or somewhat lower mean blood levels than in previously available studies. 

Categories of effects for which a causal relationship has been concluded in the ISA and for 

which there are a few newly available epidemiological studies indicating blood Pb associations 

with effects in study groups with somewhat lower blood Pb levels than previously available for 

these effects include effects on development (delayed puberty onset) and reproduction (male 

reproductive function) and on the cardiovascular system (hypertension) (ISA, sections 4.4 and 

4.8; 2006 CD, sections 6.5 and 6.6). With regard to the former category, study groups in the 

newly available studies include groups comprised of older children ranging up to age 18 years, 

for which there is increased uncertainty regarding historical exposures and their role in the 
3-26 

observed effects. 22 An additional factor that handicaps our consideration of exposure levels 

associated with these findings is the appreciable uncertainty associated with our understanding of 

Pb biokinetics during this lifestage (ISA, sections 3.2, 3.3, and 4.8.6). The evidence newly 

available for Pb relationships with cardiovascular effects in adults include some studies with 

somewhat lower blood Pb levels than in the last review. The long exposure histories of these 

cohorts, as well as the generally higher Pb exposures of the past complicate conclusions 

regarding exposure levels that may be eliciting observed effects (ISA, sections 4.4.2.4 and 

4.4.7).23

In summary, our conclusions regarding exposure levels at which Pb health effects occur, 

particularly with regard to such levels that might be common in the U.S. today, are complicated 

now, as in the last review, by several factors. These factors include the scarcity of information in 

epidemiological studies on cohort exposure histories, as well as by the backdrop of higher past 

exposure levels which frame the history of some study cohorts. Recognizing the complexity, as 

well as the potential role of higher exposure levels in the past, we continue to focus our 

consideration of this question on the evidence of effects in young children for which our 

understanding of exposure history is less uncertain.24 Within this evidence base, we recognize 

the lowest study group blood Pb levels to be associated with effects on cognitive function 

measures, indicating that to be the most sensitive endpoint. As described above, and 

summarized in Table 3-2, the evidence available in this review is generally consistent with that 

available in the last review with regard to blood Pb levels at which such effects had been 

reported (ISA, section 4.3.2; 2006 CD, section 8.4.2.1; 73 FR 66976-66979). As blood Pb levels 

are a reflection of exposure history, particularly in early childhood (ISA, section 3.3.2), we 

conclude, by extension, that the currently available evidence does not indicate Pb effects at 

exposure levels appreciably lower than recognized in the last review. 

We additionally note that, as in the last review, a threshold blood Pb level with which 

nervous system effects, and specifically neurocognitive effects, occur in young children cannot 

be discerned from the currently available studies (ISA, sections 1.9.3 and 4.3.12). 

Epidemiological analyses have reported blood Pb associations with neurocognitive effects (FSIQ 

 

22 Several of these studies involve NHANES III cohorts for which early childhood exposures were 

generally much higher than those common in the U.S. today (ISA, section 4.8.5). 

23 Studies from the late 1960s and 1970s suggest that adult blood Pb levels during that period ranged from 

roughly 13 to 16 μg/m3

 and from 15 to 30 μg/dL in children aged six and younger (ISA, section 4.4.1). 

24 In focusing on effects associated with blood Pb levels in early childhood, however, we additionally 

recognize the evidence across 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 4.3, 4.4, 4.5, 4.6, 4.7, 4.8). 
3-27 

or BSID MDI25) for young child population subgroups (age five years or younger) with 

individual blood Pb measurements as low as approximately 1 μg/dL and mean concentrations as 

low as 2.9 to 3.8 μg/dL (ISA, section 4.3.12; Bellinger and Needleman, 2003; Bellinger, 2008; 

Canfield el al., 2003; Canfield, 2008; Tellez-Rojo et al., 2006; Tellez-Rojo et al., 2008). As 

concluded in the ISA, however, “the current evidence does not preclude the possibility of a 

threshold for neurodevelopmental effects in children existing with lower blood levels than those 

currently examined” (ISA, section 4.3.13). 

Important uncertainties associated with the evidence of effects at low exposure levels are 

similar to those recognized in the last review, including the shape of the concentration-response 

relationship for effects on neurocognitive function at low blood Pb levels in today’s young 

children. Also of note is our interpretation of associations between blood Pb levels and effects in 

epidemiological studies, with which we recognize uncertainty with regard to the specific 

exposure circumstances (timing, duration, magnitude and frequency) that have elicited the 

observed effects, as well as uncertainties in relating ambient air concentrations (and associated 

air-related exposures) to blood Pb levels in early childhood, as discussed in section 3.1 above. 

We additionally recognize uncertainties associated with conclusions drawn with regard to the 

nature of the epidemiological associations with blood Pb (e.g., ISA, section 4.3.13), but note that, 

based on consideration of the full body of evidence for neurocognitive effects, the EPA has 

determined a causal relationship to exist between relevant blood Pb levels and neurocognitive 

impacts in children (ISA, section 4.3.15.1). 

 To what extent does the newly available evidence alter our understanding of the 

concentration-response relationship for neurocognitive effects (IQ) with blood Pb 

levels in young children? 

Based primarily on studies of FSIQ, the assessment of the currently available studies, as 

was the case in the last review, continues to recognize a nonlinear relationship between blood Pb 

and effects on cognitive function, with a greater incremental effect (greater slope) at lower 

relative to higher blood Pb levels within the range thus far studied, extending from well above 10 

μg/dL to below 5 μg/dL (ISA, section 4.3.12). This was supported by the evidence available in 

the last review, including the analysis of the large pooled international dataset comprised of 

blood Pb measurements and IQ test results from seven prospective cohorts (Lanphear et al., 

2005; Rothenberg and Rothenberg, 2005; ISA, section 4.3.12). The blood Pb measurements in 

this pooled dataset that were concurrent with the IQ tests ranged from 2.5 μg/dL to 33.2 μg/dL. 

The study by Lanphear et al (2005) additionally presented analyses that stratified the dataset 

 

25 Bayley Scales of Infant Development, Mental Development Index. The Bayley MDI is a wellstandardized and widely used assessment measure of infant cognitive development. Scores earlier than 24 months 

are not necessarily correlated with later FSIQ scores in children with normal development (ISA, section 4.3.15.1). 
3-28 

based on peak blood Pb levels (e.g., with cutpoints of 7.5 μg/dL and 10 μg/dL peak blood Pb) 

and found that the coefficients from linear models of the association for IQ with concurrent 

blood Pb were higher in the lower peak blood Pb level subsets than the higher groups (ISA, 

section 4.3.12; Lanphear et al., 2005). 

We note that since the completion of the ISA, two errors have been identified with the 

pooled dataset analyzed by Lanphear et al (2005) (Kirrane and Patel, 2014). A recent 

publication and EPA have separately recalculated the statistics and mathematical models of 

Lanphear et al (2005) using the corrected pooled dataset (Kirrane and Patel, 2014). While the 

magnitude of the loglinear and linear regression coefficients are modified slightly based on the 

corrections, the conclusions drawn from these coefficients, including the finding of a steeper 

slope at lower (as compared to higher) blood Pb concentrations are not affected (Kirrane and 

Patel, 2014). 

In other publications, stratified analyses of several individual cohorts also observed 

higher coefficients for blood Pb relationships with measures of neurocognitive function in lower 

as compared to higher blood Pb subgroups (ISA, section 4.3.12; Canfield et al., 2003; Bellinger 

and Needleman, 2003; Kordas et al., 2006; Tellez-Rojo et al., 2006). Of these subgroup 

analyses, those involving the lowest mean blood Pb levels and closest to the current mean for 

U.S. preschool children are listed in Table 3-3 below (drawn from Table 3 of the 2008 final 

rulemaking notice [73 FR 67003], and Kirrane and Patel, 2014). These analyses were important 

inputs for the evidence-based, air-related IQ loss framework which informed decisions on a 

revised standard in the last review (73 FR 67005), discussed in section 4.1.1 below. As the 

framework focused on the median of the four slopes in Table 3-3, the change to the one from 

Lanphear et al (2005) based on the recent recalculation described above has no impact.
3-29 

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

blood Pb levels closest to those of young children in the U.S. today. 

Blood Pb Levels 

(μg/dL) 

Study/Analysis 

Average 

Linear 

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 

3.3 0.9 – 7.4 Lanphear et al (2005)C, subgroup with peak blood Pb <7.5 μg/dL -2.53 

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 to 7 years. 

The blood Pb levels and coefficient presented here reflect the recalculation using the corrected pooled dataset (Kirrane and Patel, 2014). 

Several studies newly available in the current review have, in all but one instance, also 

found a nonlinear blood Pb-cognitive function relationship in nonparametric regression analyses 

of the cohort blood Pb levels analyzed (ISA, section 4.3.12). These studies, however, used 

statistical approaches that did not produce quantitative results for each blood Pb group (ISA, 

section 4.3.12). Thus, newly available studies have not extended the range of observation for 

quantitative estimates of this relationship to lower blood Pb levels than those of the previous 

review. The ISA further notes that the potential for nonlinearity has not been examined in detail 

within a lower, narrower range of blood Pb levels than those of the full cohorts thus far studied 

in the currently available evidence base (ISA, section 4.3.12). Such an observation in the last 

review supported the consideration of linear slopes with regard to blood Pb levels at and below 

those represented in Table 3-3. In summary, the newly available evidence does not substantively 

alter our understanding of the concentration-response relationship (including quantitative 

aspects) for neurocognitive impact, such as IQ with blood Pb in young children. 

3.3 PUBLIC HEALTH IMPLICATIONS AND AT-RISK POPULATIONS 

There are several potential public health impacts associated with Pb exposure. In 

recognition of effects causally related to blood Pb levels somewhat near those most recently 

reported for today’s population and for which the weight of the evidence is greatest, the potential 

public health impacts most prominently recognized in the ISA are population IQ impacts 

associated with childhood Pb exposure and prevalence of cardiovascular effects in adults (ISA, 
3-30 

section 1.9.1). With regard to the latter category, as discussed above, the full body of evidence 

indicates a role of long-term cumulative exposure, with uncertainty regarding the specific 

exposure circumstances contributing to the effects in the epidemiological studies of adult 

populations, for whom historical Pb exposures were likely much higher than exposures that 

commonly occur today (ISA, section 4.4). There is less uncertainty regarding the exposure 

patterns contributing to the blood Pb levels reported in studies of younger populations (ISA, 

sections 1.9.4, 1.10). Accordingly, we focus the discussion of public health implications relevant 

to this review predominantly on nervous system effects, including IQ decrements, in children. 

We focus this discussion on IQ in 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 4.3.2; 2006 CD, sections 

6.2.2 and 8.4.2). We recognize, however, that IQ is one of several measures of cognitive 

function negatively associated with Pb exposure. Other examples include other tests of 

intelligence and cognitive development and tests of other cognitive abilities, such as learning, 

memory, and executive functions, as well as academic performance and achievement (ISA, 

section 4.3.2). In considering the public health significance of neurocognitive effects of Pb in 

children, we recognize that, although some may be transient, some effects may persist into 

adulthood (ISA, section 1.9.5).26 We also note that deficits in neurodevelopment early in life 

may have lifetime consequences as “[n]eurodevelopmental deficits measured in childhood may 

set affected children on trajectories more prone toward lower educational attainment and 

financial well-being” (ISA, section 4.3.14). Thus, population groups for which 

neurodevelopment is affected by Pb exposure in early childhood are at risk of related impacts on 

their success later in life. 

There are important distinctions between population and individual risk such that 

“[s]mall shifts in the population mean IQ can be highly significant from a public health 

perspective” (ISA, p. xciii). For example, if lead-related decrements are manifested uniformly 

across the range of IQ scores in a population, “a small shift in the population mean IQ may be 

significant from a public health perspective because such a shift could yield a larger proportion 

of individuals functioning in the low range of the IQ distribution, which is associated with 

increased risk of educational, vocational, and social failure” as well as a decrease in the 

proportion with high IQ scores (ISA, section 1.9.1). 

 

26 The ISA states that the “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, p. 1-77; Bellinger et al., 1990). 
3-31 

In the discussion below, we use the term at-risk populations27 to recognize populations 

that have a greater likelihood of experiencing lead-related health effects, i.e., groups with 

characteristics that contribute to an increased risk of Pb-related health effects. These populations 

are also sometimes referred to as sensitive groups, as in section 1.2.1 above. This increased 

likelihood of lead-related effects can result from many factors, including lifestage or age, sex, 

race or ethnicity, diet, pre-existing disease state, or increased exposure (ISA, chapter 5). 

Accordingly, in identifying factors that increase risk of lead-related health effects, there has been 

consideration of evidence regarding factors contributing to increased susceptibility (i.e., 

physiological or intrinsic factors contributing to a greater response for the same exposure), and 

those contributing to increased exposure (including that resulting from behavior leading to 

increased contact with contaminated media). As noted in the ISA, “definitions of susceptibility 

and vulnerability vary across studies, but in most instances ‘susceptibility’ refers to biological or 

intrinsic factors (e.g., age, sex) while ‘vulnerability’ refers to nonbiological or extrinsic factors 

(e.g., socioeconomic status [SES])” and the terms “at-risk” and “sensitive” populations have in 

various instances been used to encompass these concepts more generally (ISA, p. 5-1). Although 

we emphasize the term “at-risk”, we rely on the other terms in particular instances below; in so 

doing, our usage is consistent with these definitions. 

Factors that increase risk of lead-related effects include, among others, behavioral and 

physiological factors. A behavioral factor of great impact on Pb exposure is the incidence of 

hand-to-mouth activity that is prevalent in very young children and by which they transfer Pb in 

settled particles to their mouths (ISA, sections 3.7.1 and 5.2.1.1). Physiological factors include 

both conditions contributing to a group’s increased risk of effects at a given blood Pb level, and 

those that contribute to blood Pb levels higher than those otherwise associated with a given Pb 

exposure (ISA, sections 5.3 and 5.1, respectively). We also considered evidence encompassing 

situations of elevated exposure, such as residing in old housing with Pb-containing paint or near 

sources of ambient Pb, as well as socioeconomic factors, such as reduced access to health care or 

low socioeconomic status (SES) that can contribute to increased risk of adverse health effects 

from Pb (ISA, sections 1.9.7, 5.2, and 5.4).

 Has new information altered our understanding of human populations that are 

particularly at risk of health effects from Pb exposures? 

The information newly available in this review has not substantially altered our 

understanding of at-risk populations. As in the last review, the factor most prominently 

 

27 In the context of “at-risk populations”, the term population refers to persons having one or more qualities 

or characteristics including, for example, a specific pre-existing illness or a specific age or lifestage, with lifestage 

referring to a distinguishable time frame in an individual’s life characterized by unique and relatively stable 

behavioral and/or physiological characteristics that are associated with development and growth. 
3-32 

recognized to contribute to increased risk of Pb effects is age (ISA, section 1.9.6). As noted in 

section 3.2 above, although the specific ages or lifestages of greatest susceptibility or risk have 

not been established (e.g., ISA, section 4.3.11), the at-risk status of young children to the 

neurodevelopmental effects of Pb is well recognized (e.g., ISA, sections 1.9.6, 4.3, 5.2.1, 5.3.1, 

and 5.4). The evidence indicates that prenatal blood Pb levels are associated with nervous 

system effects, including mental development in very young children and can also be associated 

with cognitive decrements in older children (ISA, section 4.3). The coincidence during early 

childhood of behaviors that increase exposure, such as hand-to-mouth contact, and the 

development of the nervous system contributes increased risk during this time (ISA, sections 

4.3.2.6, 5.2.1.1, and 5.3.1.1). The evidence also indicates a relationship of postnatal blood Pb 

levels (through early childhood to school age) with cognitive function decrement in older 

children and adolescents (ISA, section 4.3). In epidemiological studies, associations have been 

observed of neurocognitive, and some other nervous system effects, at various ages from early 

childhood to school age with prenatal, early-childhood, lifetime average, and concurrent blood 

Pb levels as well as with childhood tooth Pb levels (ISA, section 4.3). Consideration of 

epidemiological study results for different lifestages of exposure, particularly later in childhood, 

is complicated by the fact that blood Pb levels in children, although highly affected by recent 

exposure, are also influenced by their history of Pb exposure due to rapid growth-related bone 

turnover in children (ISA, section 3.3.5). Thus, blood Pb level in children also may reflect past 

Pb exposures and, to some extent, maternal Pb, with relative contributions varying with child and 

maternal exposure history (ISA, section 3.2.2.4, 3.4.1 and 4.3.15; 2006 CD, section 6.6.2). 

Collectively, however, the evidence indicates both the susceptibility of the developing fetus and 

early postnatal years, as well as the potential for continued susceptibility through childhood as 

the human central nervous system continues to mature and be vulnerable to neurotoxicants (ISA, 

sections 1.9.5 and 4.3.15; 2006 CD, section 6.2.12). 

In the collective body of evidence of nervous system effects in children, it is difficult to 

distinguish exposure in later lifestages (e.g., school age) and its associated risk from risks 

resulting from exposure in prenatal and early childhood (ISA, section 4.3.11). While early 

childhood is recognized as a time of increased susceptibility, a difficulty in identifying a discrete 

period of susceptibility from epidemiological studies has been that the period of peak exposure, 

reflected in peak blood Pb levels, is around 18-27 months when hand-to-mouth activity is at its 

maximum (ISA, section 3.4.1 and 5.2.1.1; 2006 CD, p. 6-60). The task is additionally 

complicated by the role of maternal exposure history in contributing Pb to the developing fetus 

(ISA, section 3.2.2.4.). Epidemiological analyses evaluating risk of neurocognitive impacts (e.g., 

reduced IQ) associated with different blood Pb metrics in cohorts with differing exposure 

patterns (including those for which blood Pb levels at different ages were not highly correlated) 
3-33 

indicate associations with blood Pb measurements concurrent with FSIQ tests at ages of 

approximately 6-7 years, although the analyses did not conclusively demonstrate stronger 

findings for early (e.g., age 2 years) or concurrent blood Pb (ISA, section 4.3.11). The 

experimental animal evidence additionally indicates early life susceptibility (ISA, section 4.3.15 

and p. 5-21). Thus, the full evidence base continues to indicate prenatal and early childhood 

lifestages as periods of increased lead-related risk. In summary, while uncertainties remain with 

regard to the role of Pb exposures during a particular age of life in eliciting nervous system 

effects, such as cognitive function decrements, the evidence continues to indicate the at-risk 

status of pre- and postnatal childhood lifestages (ISA, sections 4.3.11 and 4.3.15). 

Several physiological factors increase risk of lead-related health effects by contributing to 

increased blood Pb levels over those otherwise associated with a given Pb exposure (ISA, 

sections 3.2, 3.3 and 5.1). These include nutritional status, which plays a role in Pb absorption 

from the GI tract (ISA, section 3.2.1.2). For example, diets deficient in iron, calcium or zinc can 

contribute to increased Pb absorption and associated higher blood Pb levels (ISA, sections 

3.2.1.2, and 5.1). Evidence is suggestive of some genetic characteristics as potential risk factors, 

such as presence of the δ-aminolevulinic acid dehydratase-2 (ALAD-2) allele which has been 

indicated to increase blood Pb levels or lead-related risk (ISA, sections 3.3.2 and 5.1). 

Risk factors based on increased exposure include spending time in proximity to sources 

of Pb to ambient air or other environmental media (e.g., large active metals industries or 

locations of historical Pb contamination) (ISA, sections 3.7.1 and 5.2.5). Residential factors 

associated with other sources of Pb exposure (e.g., leaded paint or plumbing with Pb pipes or 

solder) are another exposure-related risk factor (ISA, sections 3.7.1 and 5.2.6). The role of 

socioeconomic status (SES) with regard to lead-related risk is somewhat complicated. SES often 

serves as a marker term for one or a combination of unspecified or unknown environmental or 

behavioral variables. Lower SES has been associated with higher Pb exposure and higher blood 

Pb concentration (ISA, sections 5.3.16, 6.2.4 and 6.4). Further, it is independently associated 

with an adverse impact on neurocognitive development, and a few studies have examined SES as 

a potential modifier of the association of childhood Pb exposure with cognitive function with 

inconsistent findings regarding low SES as a potential risk factor. Although the differences in 

blood Pb levels among children of lower as compared to higher income levels have lessened, 

blood Pb levels continue to be higher among lower-income children indicating higher exposure 

and/or greater influence of factors independent of exposure, such as nutritional factors (ISA, 

sections 1.9.6, 5.2.1.1 and 5.4). 

In considering risk factors associated with increased Pb exposure or increased blood Pb 

levels, we note that the currently available evidence continues to support a nonlinear relationship 

between neurocognitive effects and blood Pb that indicates incrementally greater impacts at 
3-34 

lower as compared to higher blood Pb levels (ISA, section 4.3.12), as described in section 3.2 

above. An important implication of this finding is that while children with higher blood Pb 

levels are at greater risk of lead-related effects than children with lower blood Pb levels, on an 

incremental basis (e.g., per μg/dL), the risk is greater for children at lower blood Pb levels. This 

was given particular attention in the last review of the Pb NAAQS, in which the standard was 

revised with consideration of the incremental impact of air-related Pb on young children in the 

U.S and the recognition of greater impact for those children with lower absolute blood Pb levels 

(73 FR 67002). Such consideration included a focus on those C-R studies involving the lowest 

blood Pb levels, as described in section 4.1.1 below. 

Some racial or ethnic backgrounds have been identified as factors that may increase risk 

of lead-related health effects (ISA, sections 1.9.6, 5.2.3 and 5.3.7). For example, although blood 

Pb levels in the U.S. general population (e.g., geometric mean level in children aged 1-5) have 

declined, mean levels reported in recent NHANES samples continue to differ among children of 

different ethnic backgrounds, with higher levels in non-white persons as compared to whites 

(ISA, sections 3.4.1, 5.2.1.1 and 5.2.3). Additionally, a study of lead-related risk of hypertension 

among adults reported greater risk associated with blood Pb levels above 1 μg/dL among 

Mexican Americans and non-Hispanic blacks than among non-Hispanic whites (ISA, section 

5.3.7; Muntner et al., 2005). The evidence available in the current review, consistent with that in 

the last, also suggests that health status or pre-existing disease is potentially a physiological risk 

factor for lead-related effects (ISA, section 1.9.6). Populations with pre-existing health 

conditions, such as hypertension, may be more susceptible than those without such conditions for 

particular Pb-associated effects (ISA, section 5.3.4). For example, increased risks of lead-related 

renal effects and heart rate variability have been reported among hypertensive individuals 

compared to those that are normotensive (ISA, section 1.9.6). Additionally, African Americans, 

as a group, have a higher frequency of hypertension than the larger U.S. population as a whole 

and than other ethnic groups (NCHS, 2011) and, as a result, may face a greater risk of adverse 

health impact from Pb-associated cardiovascular effects. 

Older adulthood has been identified as a lifestage of potentially greater risk of leadrelated health effects based primarily on the evidence of increases in blood Pb levels during this 

lifestage (ISA, sections 5.2.1.2, 5.3.1.2, and 5.4). Contributing to blood Pb levels in the studied 

populations of older adults are likely to be their exposure histories, which included younger 

years during the time of leaded gasoline usage and other sources of Pb exposures which were 

more prevalent in the past than today (e.g., ISA, Figure 2-1 and section 2.5.2). Exposure history 

has a contributing role to blood Pb levels throughout life, and the increased rate of bone 

remodeling during later adulthood increases contributions of Pb from bone stores into the 

systemic circulation during that lifestage (ISA, sections 3.3.5 and 5.2.1.2). Additionally, limited 
3-35 

animal evidence has indicated specific brain pathology in older animals that had substantial Pb 

exposures earlier in life (ISA, sections 4.3.9.1 and 5.3.1). Further, the full body of evidence 

includes observed associations of some cardiovascular and neurological effects with bone and 

blood Pb in older populations, with biological plausibility for the role of Pb provided by 

experimental animal studies (ISA, sections 4.3.5, 4.3.7 and 4.4). 

 In summary, the information newly available in this review has not appreciably altered 

our understanding of human populations that are particularly sensitive to Pb exposures. In the 

current review, as at the time of the last review of the Pb NAAQS, we recognize young children 

as an important at-risk population, with sensitivity extending to prenatal exposures and into 

childhood development. Additional risk factors include deficiencies in dietary minerals (iron, 

calcium and zinc), some racial or ethnic backgrounds, and spending time in proximity to 

environmental sources of Pb or residing in older houses. The evidence for SES continues to 

indicate increased blood Pb levels in lower income children, although its role with regard to an 

increased health risk for same blood Pb level is unclear. Additionally, the currently available 

evidence continues to suggest a potential for increased risk associated with several other factors, 

including older adulthood, pre-existing disease (e.g., hypertension), variants for certain genes 

and increased stress. 

 Is there new evidence on health effects beyond neurocognitive endpoints in 

children that suggest additional at-risk populations should be given increased 

focus in this review? 

The evidence newly available in this review supports or strengthens our previous 

conclusions regarding the broad array of health effects of Pb (see ISA, section 1.10 which 

compares key conclusions drawn in the last review with conclusions drawn in the current 

assessment). Additionally, in some categories of health effects, the newly available studies 

extend the evidence for some aspects of the health effects described in the last review. For 

example, among the nervous system effects, the newly available evidence continues to support 

the conclusions from the last review regarding Pb and neurocognitive and behavioral effects 

(ISA, section 4.3). Across the array of neurocognitive and behavioral effects, we recognize the 

sensitivity of the prenatal period and several lifestages of childhood, and we particularly 

recognize young children as an important at-risk population in light of current environmental 

exposure levels. 

As discussed in section 3.2 above, the blood Pb levels of populations studied in newly 

available epidemiological studies that report associations of blood Pb with effects for systems 

and processes other than the nervous system (e.g., cardiovascular, developmental and 

reproductive) are similar to or, in a few cases, somewhat lower than those assessed in the last 

review (ISA, sections 4.4, 4.6, 4.7, and 4.8). The greater uncertainties regarding the time, 
3-36 

duration and magnitude of exposure contributing to these observed health effects complicate 

identification of sensitive lifestages and associated exposure patterns that might be compared 

with our understanding of the sensitivity of young children to neurocognitive impacts of Pb. 

Thus, while augmenting the evidence base on these additional endpoints, the newly available 

evidence does not lead us to identify a health endpoint expected to be more sensitive to Pb 

exposure than neurocognitive endpoints in children, leading us to continue to conclude that the 

appropriate primary focus for our review is on neurocognitive endpoints in children. 

In summary, there are a variety of ways in which lead-exposed populations might be 

characterized and stratified for consideration of public health impacts. Age or lifestage was used 

to distinguish potential groups on which to focus in the last review in recognition of its role in 

exposure and susceptibility, and young children were selected as the priority population for the 

risk assessment (see section 3.4 below) in consideration of the health effects evidence regarding 

endpoints of greatest public health concern and in recognition of effects on the developing 

nervous system as a sentinel endpoint for public health impacts of Pb. This identification 

continues to be supported by the evidence available in the current review. 

 What does the information about air Pb concentrations available in this review 

indicate with regard to the size of at-risk populations and their distribution 

across the U.S.? 

The magnitude of a public health impact is dependent upon the size of populations 

affected, as well as type or severity of the effect. As summarized above, the population group 

that may be most at risk of health effects associated with exposure to Pb is young children. The 

2010 census indicates nearly 310 million people residing in the U.S., approximately 74 million 

of whom are children under the age of 18, with some 20 million under the age of five years. 

Children at greatest risk from air-related Pb are those children with highest air-related Pb 

exposure which are considered to be those living in areas of higher ambient air Pb 

concentrations. The discussion below considers the information available to inform our 

understanding of areas of children potentially at risk from air-related Pb. 

In considering the extent of this at-risk population, we turn first to consideration of those 

areas in the U.S. with air Pb concentrations above the current standard (e.g., section 2.2.2.2 

above). Using the available monitoring data and U.S. census information, Table 3-4 summarizes 

the size of populations within 0.5 km of monitors in our current Pb NAAQS surveillance 

network at which Pb concentrations were higher than the current standard during the recent 

period from 2009-2011. The distance to which concentrations exceeding the standard might 

extend will vary with the magnitude of the Pb concentrations and particle size, among other 

factors; a half-kilometer distance was selected for purposes of illustration here. This analysis 

indicates that approximately 2,400 children aged 5 or under reside within 0.5 km of monitors 
3-37 

exceeding the current standard. To also account for the population in areas with air 

concentrations just at (or very near) the current standard, we have also identified an additional 

nine Pb-TSP monitors with 3-month average concentrations within 10% of, but not exceeding, 

the current standard (Appendix 2D). Based on the 2010 U.S. census, 265 children aged 5 or 

under reside within 0.5 km of these additional sites. 

Table 3-4. Number of children aged 5 and under in areas of elevated ambient air Pb 

concentrations relative to the NAAQS. 

Population within 0.5 km of monitors 

with maximum 3-month Pb concentration greater than 0.15 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 and recent Pb-TSP dataset 

presented in Figure 2-10 above (dataset criteria and summaries included Appendices 2C and 2D, respectively). 

Section 2.2.1.1 above describes the surveillance monitoring network required for identifying locations with the 

potential to exceed the NAAQS. 

As the air quality data set analyzed in section 2.2.2 above may not be inclusive of all of 

the newly sited monitors, as discussed in section 2.2.1 above, we recognize there may be other 

areas of the country where concentrations are above or just meet the current standard but for 

which such data are not yet available. To consider the potential for there to be additional, not yet 

identified, areas with elevated Pb concentrations, we have separately quantified the size of young 

child populations residing in areas near large Pb sources in Table 3-5. In so doing, we recognize 

uncertainties and potential limitations associated with these emissions estimates for these 

purposes, uncertainties both with regard to the accuracy of such estimates and also with regard to 

the role of specific source characteristics and meteorology, not explicitly considered here, in 

influencing ambient air Pb concentrations and contributing to substantial variation in air Pb 

concentrations at source locations (e.g., Figure 2-11 above). Accordingly, while the summary in 

Table 3-5 is informative in considering the potential prevalence of airborne Pb emissions and 

potential exposure of human populations, it is limited with regard to its ability to identify 

populations living in areas of elevated ambient air Pb concentrations. We interpret this analysis 

to indicate that fewer than about 7,800 young children (aged 5 or younger) live in areas with air 

Pb concentrations near or above the current standard, with the current monitoring data indicating 

the size of this population to be approximately 2,700. 
3-38 

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

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

Facilities (other than airports) Airports All 

Number of 

Locations 

Population, 

all ages 

Population, 

aged 5 and 

younger 

Number of 

Locations 

Population, 

all ages 

Population, 

aged 5 and 

younger 

Population, 

aged 5 and 

younger 

Facilities/Airports 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.

3.4 EXPOSURE AND RISK 

The risk information available for this review and described here is based primarily on 

the exposure and risk assessment developed in the last review of the Pb NAAQS (henceforth 

referred to as the 2007 REA [USEPA, 2007a]), as considered in the context of the evidence 

newly available in this review (as presented in the ISA). As described in the REA Planning 

Document, careful consideration of the information newly available in this review, with regard to 

designing and implementing a full REA for this review, led us to conclude that performance of a 

new REA for this review was not warranted. We did not find the information newly available in 

this review to provide the means by which to develop an updated or enhanced risk model that 

would substantially improve the utility of risk estimates in informing the current Pb NAAQS 

review (REA Planning Document, section 2.3). Based on their consideration of the REA 

Planning Document analysis, the CASAC Pb Review Panel generally concurred with the 

conclusion that a new REA was not warranted in this review (Frey, 2011).28 Accordingly, the 

information described here is drawn primarily from the 2007 REA, augmented by a limited new 

case study-specific analysis focused on risk associated with the current standard, as described in 

section 3.4.3.3 below. 

 

28 In our evaluation presented in the REA Planning Document and in consultation with CASAC, we 

indicated our conclusion that the information newly 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. In their review of the draft PA, the CASAC Pb Review Panel reenforced 

their concurrence with EPA’s decision not to develop a new REA (Frey, 2013). 
3-39 

The focus for the risk assessment and associated estimates presented here is on Pb 

derived from sources emitting Pb to ambient air. As discussed in section 1.3 above (and 

conceptually illustrated in Figure 1-1), the multimedia and persistent nature of Pb, the role of 

multiple exposure pathways, and the contributions of nonair sources of Pb to human exposure 

media all present challenges and contribute significant additional complexity to the health risk 

assessment that goes far beyond the situation for similar assessments typically performed for 

other NAAQS pollutants (e.g., that focus only on the inhalation pathway). Limitations in the 

available data and models affected our characterization of the various complexities associated 

with exposure to ambient air Pb. As a result, the assessment includes a number of simplifying 

assumptions in a number of areas and, as described in section 3.4.4 below, our estimates of airrelated Pb risk are approximate and are characterized by upper and lower bounds. 

The conceptual model developed to inform planning for the 2007 REA, including 

identification of key exposure media, target population, health endpoint and risk metric is 

described in section 3.4.1. The 2007 REA relied on a case study approach to provide estimates 

that inform our understanding of air-related exposure and risk in different types of air Pb 

exposure situations; the case studies included are described in section 3.4.2. In section 3.4.3, the 

analysis approach and general aspects of exposure and risk assessment methods are summarized, 

and the air quality scenarios simulated are described. In section 3.4.3, we also summarize the 

2007 REA risk model and the interpolation approach used in the limited new analyses performed 

for purposes of this review. Section 3.4.4 identifies key aspects of the exposure assessment and 

risk estimates are presented in section 3.4.5. Treatment of key sources of variability in exposure 

and risk estimates is described in section 3.4.6 and the characterization of uncertainty is 

summarized in 3.4.7. An updated interpretation of the risk estimates for our purposes in this Pb 

NAAQS review section is presented in section 3.4.8. 

3.4.1 Conceptual Model for Air-Related Lead Exposure and Risk 

In considering public health risks associated with Pb from ambient air, the focus is on Pb 

derived from those sources emitting Pb to ambient air. The multimedia and persistent nature of 

Pb, illustrated in Figure 1-1 above, as well as the existence of many nonair sources of Pb to the 

environment, contribute multiple complexities to the consideration of exposure and risk for 

ambient air-related Pb. The conceptual model that informed planning for the 2007 REA 

identified sources, pathways, routes, exposed populations, and health endpoints, focusing on 

those aspects of Pb exposure most relevant to the review, while also recognizing the role of Pb 

exposure pathways unrelated to Pb in ambient air (2007 REA, section 2.1). 
3-40 

As recognized in section 1.3 above, sources of human Pb exposure include current and 

historical air emissions sources, as well as miscellaneous nonair sources, which can contribute to 

multiple exposure media and associated pathways (e.g., inhalation of ambient air, ingestion of 

indoor dust, outdoor soil/dust and diet or drinking water).29 Figure 3-2 illustrates these human 

exposure pathways from an analytical perspective, drawing on the conceptual model for the 

assessment (2007 REA, Figure 2-1).30 As shown in Figure 3-2, in addition to airborne emissions 

(recent or those in the past), sources of Pb to these pathways also include old leaded paint, 

including Pb mobilized indoors during renovation/repair activities, and contaminated soils. Lead 

in diet and drinking water may have air pathway-related contributions as well as contributions 

from nonair sources (e.g., Pb solder on water distribution pipes and Pb in materials used in food 

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.31 

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

 

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

the 2007 REA. 

30 We additionally note that Pb in children at birth is from maternal exposures, recent or historical, as 

recognized in section 3.1 above, and that ingestion of maternal breast milk may be a Pb exposure pathway for 

infants in some cases (ISA, section 3.1.3.3). 

31 The assessment grouped the exposure and risk estimates for Pb in diet and drinking water together and 

combined them with the other pathways in estimates 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. 

Pb in ambient air

Indoor air

Indoor dust

Outdoor 

soil/dust

Food (crops/

livestock)

Drinking water

Paint 

Pb

Historic

Pb

Deposition 

outdoors

Deposition 

indoors

Pb from 

distribution

/processing

*Green ovals indicate nonair or historic sources. 

Sources unrelated to environmental pathways (e.g., jewelry, mini-blinds) not shown.

Infiltration

Inhalation of 

ambient air Pb

(outdoors or 

indoors) 

Ingestion of 

indoor dust Pb

Ingestion of outdoor 

soil/dust Pb

Ingestion of Pb in 

diet/drinking water

Resuspension

Resuspension

Water 

discharges

Land

releases

*
3-41 

Identification of exposure populations, exposure/dose metric, health effects endpoint and 

risk metric to be included in the 2007 REA were based on consideration of the then-currently 

available evidence as assessed in detail in the 2006 CD. As discussed in the REA Planning 

Document (USEPA, 2011), these selections continue to be supported by the evidence now 

available in this review as described in the ISA. 

In the REA, we focused on IQ loss in children exposed up to age 7 years. This focus 

reflected the evidence for young children with regard to air-related exposure pathways and 

susceptibility to Pb health impacts (e.g., ISA, sections 3.1.1, 4.3, 5.2.1.1, 5.3.1.1, and 5.4). For 

example, the hand-to-mouth activity of young children contributes to their Pb exposure (i.e., 

incidental soil and indoor dust ingestion) and ambient air-related Pb has been shown to 

contribute to Pb in outdoor soil and indoor house dust (ISA, sections 3.1.1 and 3.4.1; 2006 CD, 

section 3.2.3). 

Blood Pb is commonly used as an integrated index or biomarker of exposure due to both 

its association with exposure, particularly recent exposure in young children, and the relative 

ease of the measurements, as discussed in section 3.1 above. Although bone Pb measurements 

have become easier to collect and consequently, their use has been more widespread, 

epidemiological and toxicological studies of Pb health effects and dose-response relationships 

(particularly for neurodevelopmental effects in children) tend to be dominated by blood Pb as the 

exposure metric. Therefore, we focused on modeling blood Pb in young children, developing 

estimates for two blood Pb metrics: “concurrent” and “lifetime average”. For the former we 

estimated blood Pb at age 7 years, while lifetime average was estimated as the average across the 

7-year period.32 

In addition, our focus on young children reflects the evidence that the developing nervous 

system in children is among, if not, the most sensitive of the endpoints associated with Pb 

exposure (ISA, sections 1.6 and 1.10). At the time of the last review, we noted that limitations 

precluded prediction of changes in adult blood Pb levels (or bone Pb levels) given changes in 

ambient Pb levels. This reflects the fact that the presence of substantial historic Pb stores in most 

adults introduces uncertainty into the prediction of changes in blood or bone Pb in these adult 

populations resulting from changes in ambient air Pb exposure. Additionally, in considering 

concentration-response relationships for adult blood Pb and adult health outcomes, we 

recognized the uncertainty with regard to the role of historic compared to recent exposures in 

eliciting the observed outcomes. Based on conclusions regarding the scientific evidence 

available in the last review (presented in the 2006 CD), the assessment focused on risk to the 

 

32 The pathways represented in this modeling included childhood inhalation and ingestion pathways, as 

well as maternal contributions to newborn body burden (2007 REA, Appendix H, Exhibit H-6). 
3-42 

central nervous system in childhood as the most sensitive effect that could be quantitatively 

assessed, with decrement in IQ used as the risk metric.

3.4.2 Case Studies 

Lead exposure and associated risk were estimated for multiple case studies that generally 

represent two types of residential population exposures to air-related Pb (see Table 3-6): (1) 

location-specific urban populations of children with a broad range of air-related exposures, 

reflecting existence of urban concentration gradients; and, (2) children residing in localized areas 

with air-related exposures representing air concentrations specifically reflecting the standard 

level being evaluated. Thus, the two types of case studies differed with regard to the extent to 

which they represented population variability in air-related Pb exposure (as discussed further in 

section 3.4.7 below). Three location-specific urban case studies focused on residential areas 

within Cleveland, Chicago, and Los Angeles, providing representations of urban populations 

with a broad range of air-related exposures due to spatial gradients in both ambient air Pb levels 

and population density. For example, the highest air concentrations in these case studies (i.e., 

those closest to the standard being assessed) were found in very small parts of the study areas, 

while a large majority of the case study populations resided in areas with much lower air 

concentrations. The case studies representing the children most highly exposed via air-related 

pathways were the generalized (local) urban case study (also referred to as general urban case 

study) and the primary Pb smelter case study subarea. The generalized (local) urban case study 

was not based on a specific geographic location and reflected several simplifying assumptions in 

representing exposure including uniform ambient air Pb levels associated with the standard of 

interest across the hypothetical study area and a uniform study population. The primary Pb 

smelter case study provides risk estimates for children living in a specific area within which 

some locations, at the time of the 2007 REA, were not meeting the then-current standard. In 

addition to characterizing risks within a 10 km radius area surrounding the smelter (full area), we 

focused particularly on a subarea within 1.5 km of the facility, where airborne Pb concentrations 

were closest to the then-current standard (a maximum calendar quarter average concentration of 

1.5 μg/m3

 Pb-TSP) and where children’s air-related exposures are most impacted by emissions 

associated with the Pb smelter from which air Pb concentrations were estimated. Based on the 

nature of the population exposures represented by the two categories of case study, the 

generalized (local) urban and primary Pb smelter case study subarea include populations that are 

relatively more highly exposed by way of air pathways to air Pb concentrations near the standard 
3-43 

level evaluated, compared with the populations in the three cities or the full area of the primary 

smelter case study.33,34 

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)

3.4.3 Analysis Approach 

The approach to assessing exposure and risk for the two categories of case studies was 

comprised of four main analytical steps: (a) estimation of ambient air Pb concentrations, (b) 

estimation of Pb concentrations in other key exposure media, including outdoor soil and indoor 

dust, (c) use of exposure media Pb concentrations, with other pathway Pb intake rates (e.g., diet), 

to estimate blood Pb levels in children using biokinetic modeling, and (d) use of concentrationresponse functions derived from epidemiology studies to estimate IQ loss associated with the 

blood Pb levels. In implementing these steps for the primary smelter case study, air 

concentrations were estimated using dispersion modeling; indoor dust concentrations were 

estimated for the case study subarea using a site-specific regression model. The approach for the 

generalized (local) urban case study and location-specific urban case studies was somewhat 

 

33 An additional case study (the secondary Pb smelter case study) was also developed in the 2007 REA, 

however, significant limitations associated with the use of dispersion modeling to predict ambient air, dust and soil 

Pb levels near the facility contributed to large uncertainties in the risk estimates (2007 REA, section 4.3.1). 

34 In addition to the case studies included in the 2007 REA, the pilot phase of the 2007 REA also included a 

near-roadway case study, focused on subset of urban population exposed immediately near roadways (ICF 

International, 2006). Based on the pilot results and 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. 
3-44 

simpler, since it did not involve fate and transport modeling for air concentration estimates and, 

instead, used ambient monitor levels to characterize the gradient in air Pb levels across the study 

area. All steps are somewhat simpler in the generalized (local) urban case study which included 

a single exposure zone. Figure 3-3 identifies the key input data sets, modeling steps and 

intermediate model output in each of the four analytical steps. The first three steps were 

employed in the exposure assessment (discussed in section 3.4.3.1), while the fourth is the risk 

assessment step (discussed in section 3.4.3.3).
3-45 

Drawn from 2007 REA, Figure 3-3 (USEPA, 2007). 

Figure 3-3. Overview of analysis approach. 

Characterizing ambient air levels and 

deposition to soil

Air dispersion modeling

(primary Pb smelter)

Ambient monitoring data 

(general urban and location-specific urban)

Stack and 

fugitive 

emissions data

Ambient air 

concentrations 

for study areas

Characterizing soil and indoor 

dust concentrations

Outdoor residential 

soil concentrations

Site-specific soil 

monitoring data 

combined with 

statistical 

extrapolation 

(primary Pb 

smelter)

Nationally-representative 

residential soil Pb value selected 

from literature

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

(regression) and/or (b) mechanistic 

(compartmental) indoor dust prediction 

models 

(all case studies)

Indoor residential dust 

concentrations

Biokinetic blood Pb 

modeling 

(all case studies)

Background Pb exposure levels

• diet

• drinking water

• indoor paint (actually reflected in 

dust modeling)

Probabilistic modeling of blood Pb 

levels for children within each case 

study location

(all case studies)

GSD reflecting interindividual variability 

in behavior related to 

Pb exposure and 

biokinetics

Characterizing blood Pb levels

Concentration-response functions 

based on log-normal functions 

(Lanphear pooled analysis), or on data 

from that study

Demographics (distribution of 

children within study areas)

(primary Pb smelter and locationspecific urban)

Distribution of IQ loss for 

study populations 

(partitioned between policyrelevant exposures and 

policy-relevant background)

Characterizing risk (IQ loss)

Ambient air 

concentrations 

(see above)

Risk estimation - IQ 

change estimation

(all case studies)

EXPOSURE ASSESSMENT RISK CHARACTERIZATION
3-46 

3.4.3.1 Estimating Exposure 

Concentrations of Pb were estimated in ambient media and indoor dust using a 

combination of empirical data and modeling projections. The use of empirical data brings with it 

uncertainty related to the potential inclusion of nonair source signals in these measurements (e.g., 

house paint contributions to indoor dust and outdoor soil Pb). Conversely, the use of modeling 

tools introduces other uncertainties (e.g., model and parameter uncertainties). The 

characterization of uncertainty associated with the risk assessment is discussed in section 3.4.7. 

Table 3-7 summarizes the exposure modeling approaches and data used to characterize Pb 

concentrations or input associated with each exposure pathway for each of the case studies. 

Characterization of Pb in ambient air relied on (a) dispersion modeling of facility-related 

(including fugitive) Pb emissions for the primary Pb smelter case study, (b) the use of ambient 

monitor data for the location-specific urban case studies, and (c) an assumption of uniform 

ambient air Pb levels (matching the standard level being considered) for the generalized (local) 

urban case study. The use of dispersion modeling for the primary Pb smelter case study allowed 

us to capture more spatially refined patterns of ambient air Pb over residential areas in the 

vicinity of the facility, where ambient Pb levels were dominated by Pb released from the facility. 

For the location-specific urban case studies, we used Pb monitors within each of the urban study 

areas to characterize spatial gradients. By contrast, the generalized (local) urban case study is 

designed to assess exposure and risk for a smaller group of residents (e.g., neighborhood) 

exposed at the level of the standard and therefore, did not rely on monitor data in characterizing 

levels, since ambient air Pb was fixed at the standard being assessed. While ambient air Pb 

concentrations in the primary Pb smelter case study reflected only contributions from direct and 

fugitive emissions associated with the facility, concentrations in the location-specific urban study 

areas, which relied on empirical (monitor-based) data to define ambient air Pb concentrations, 

reflected contributions from all contributing sources, be they currently active stationary or 

mobile sources, resuspension of previously deposited Pb or other. Additional detail on 

estimation of ambient (outdoor) and indoor air concentrations is presented in section 5.2.2 and 

Appendices A through D of the 2007 REA. 

Characterization of Pb concentrations in outdoor surface soil/dust resulting from 

deposition of airborne Pb was based on the use of (a) existing site-specific measurements 

(primary Pb smelter case study) and (b) nationally representative residential soil measurements 

obtained from the literature (general and location-specific urban case studies). In the case of the 

primary Pb smelter case study, soil Pb concentration data were available for a zone close to the 

facility and statistical extrapolation from these data was used to predict soil levels for portions of 

the study area beyond this zone. Additional detail on estimation of Pb concentrations in outdoor 

surface soil or dust is presented in sections 3.1.3 and 5.2.2.2 and Appendix F of 2007 REA. 
3-47 

To predict concentrations of ambient Pb in indoor dust, we relied on a combination of (a) 

regression-based models that relate indoor dust to outdoor air Pb and/or outdoor soil Pb and (b) 

mechanistic models that predict indoor dust Pb based on key mechanisms (e.g., infiltration of 

outdoor air indoors, deposition rates of Pb from indoor air to indoor surfaces, house cleaning 

rates). For the point source case study, we used a combination of regression-based models 

obtained from the literature and developed based on site-specific data and we developed a 

customized hybrid empirical-mechanistic model for the general and location-specific urban case 

studies. This reflected the fact that available regression-based models had been developed 

largely based on residential exposures near large point sources and were not considered 

representative of more general urban exposures. Consequently, a mechanistic model, augmented 

with empirical data, was developed for the generalized (local) urban case study. Additional 

detail on estimation of Pb concentrations in indoor dust is presented in sections 3.1.4 and 5.2.2.2 

and Appendix G of 2007 REA. 

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 

Blood Pb levels were predicted from estimates of Pb contained in various media (e.g., 

ambient air, diet, water, indoor dust) and estimates of Pb intake from dietary and drinking water 

pathways, using the Integrated Exposure and Uptake Biokinetic (IEUBK) model (2007 REA, 
3-48 

sections 3.2.1.1 and 5.2.4).35 Diet and drinking water intake and concentrations, as well as other 

model inputs, were based on the most current information (2007 REA, Appendix H). Detail on 

methods used to characterize media Pb concentrations and all IEUBK inputs for each case study 

are in the 2007 REA, sections 3.1, 3.2, 5.2.3 and 5.2.4 and appendices C through H. As the 

shortest temporal scale accepted for inputs to the IEUBK is a year, all model inputs, developed 

for each exposure zone in each case study, were annual average values. For media concentration 

inputs, the same values were used for each year of the seven-year simulation. Other model 

inputs varied as appropriate with the age of the simulated child (2007 REA, Appendix H). 

To simulate population variability in Pb intake and uptake, we used the IEUBK model to 

first generate a central-tendency estimate of the blood Pb levels for the group of children within a 

given exposure zone of a study area.36 Outside the IEUBK model, we then combined this centraltendency estimate with a geometric standard deviation (GSD) reflecting variability in blood Pb 

levels for groups of children to generate a distribution of blood Pb levels for a study area. The 

procedure for combining the IEUBK-based central tendency blood Pb estimate with a GSD to 

generate a population distribution of blood Pb levels differs somewhat for the categories of case 

studies. The approach for the general urban case study is fairly simple in that we have a single 

IEUBK-based estimate of blood Pb levels, and this is, in turn, combined with the GSD selected 

for this study area to produce a population distribution of blood Pb levels. For both the primary 

Pb smelter and the location-specific urban study areas, multiple polygons within the larger study 

area (e.g., U.S. Census blocks for the location specific urban study areas) are used as the basis 

for generating distributions of blood Pb levels for the child population in each study area. These 

distributions are generated using a Monte Carlo-based population-weighted sampling method 

with U.S. Census child counts for each polygon and an adjustment factor distribution based on 

the chosen GSD (see 2007 REA, sections 3.2.2 and 5.2.2.3). 

The GSD reflects a number of factors which operate together to produce interindividual 

variability in blood Pb levels, including: (a) biokinetic variability (differences in the uptake, 

distribution or clearance of Pb), (b) differences in behavior related to Pb exposure (e.g., varying 

hand-to-mouth activity, tap water ingestion rates, and time spent playing indoors) and (c) 

 

35 In predicting PbB levels, we assumed that Pb concentrations in exposure media remained constant 

throughout the 7 year simulation period. 

36 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. 
3-49 

differences in environmental Pb exposure concentrations (e.g., spatial gradients in ambient Pb 

levels of a resolution beyond that simulated in each case study, differences in 

cleaning/vacuuming rates and air exchanges rates).37 For all of the study areas, we assumed that 

pathway apportionment of blood Pb levels based on the modeling of the central-tendency blood 

Pb level (using IEUBK) holds for all percentiles of blood Pb levels derived by combining that 

central tendency estimate with the GSD. Blood Pb modeling completed for all case studies 

included estimates of both concurrent and lifetime-average blood Pb metrics, although ultimately 

we focused on the concurrent blood Pb metric in estimating risk (2007 REA, section 2.1.5).38

3.4.3.2 Air Quality Scenarios Included in 2007 Assessment 

The air quality scenarios assessed in the 2007 REA for the case studies identified in 

Table 3-6 above included conditions just meeting the NAAQS that was current at the time of the 

last review (1.5 μg/m3, maximum calendar quarter average) and conditions meeting several 

alternative, lower standards. Additionally, scenarios for current conditions (2003-2005) were 

also included for the three location-specific urban case studies.39 These air quality scenarios are 

characterized by quarterly or monthly averaging times and a not-to-be-exceeded form. Once the 

air quality dataset representing each scenario was developed, the associated annual average 

concentrations for each exposure zone were derived for input to the IEUBK model, which does 

not accept air quality inputs of a temporal scale shorter than a year (2007 REA, Appendix H). 40

As a result of the differing air quality conditions of the location-specific case studies, 

there were differences among them with regard to the scenarios assessing the then-existing or 

alternative standards (see Table 3-8). To simulate the previous (1978) standard at the primary Pb 

 

37 We specified GSDs for each of the case studies 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). 

38 As discussed in section 2.1.5 of the 2007 REA, the concurrent PbB measurement (i.e., PbB 

measurements at the time of IQ test) and the lifetime-average blood level (i.e., average of measurements taken over 

child’s first 6-7 years) were considered stronger predictors of lead’s effect on IQ than were peak and early childhood 

levels. 

39 For the location-specific urban 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). 

40 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. 
3-50 

smelter location, at which then-current monitoring data indicated exceedance of that standard, a 

proportional roll-down was performed across the area to achieve conditions that just met that 

standard. Additionally, although it was considered an extremely unlikely scenario that air 

concentrations in urban areas across the U.S. that were well below the previous NAAQS would 

increase to just meet that standard (e.g., by way of expansion of existing sources or congregation 

of multiple sources in adjacent locations), we simulated this scenario in all case studies. In so 

doing, the air Pb concentrations were rolled up proportionally across the location-specific urban 

study areas to conditions just meeting the standard. No other scenario simulations involved 

rolling concentrations up. For the primary Pb smelter case study, air Pb concentrations were 

proportionally rolled down to conditions just meeting each of the potential alternative standards 

assessed. In the three location-specific urban case studies, the temporally and spatially varying 

concentrations were rolled down to conditions just meeting each of the potential alternative 

standards that they exceeded (2007 REA, section 5.2.2.1).41 

For the generalized (local) urban case study, which has a single exposure zone in which 

air Pb concentrations do not vary spatially, we derived a single air Pb concentration estimate to 

meet the standard assessed (e.g., specified maximum monthly or quarterly average). To reflect 

the variability in air Pb concentrations that occur over time scales less than a year as a result of 

temporal changes in meteorology and source and emission characteristics, the annual average air 

concentration (input for IEUBK and dust model) was derived for the maximum monthly and 

quarterly average metrics assessed using relationships based on the available Pb-TSP monitoring 

data for large U.S. urban areas (2007 REA, Appendix A). 

 

41 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”. 
3-51 

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. 

The approaches for estimating Pb concentrations in other media varied depending on the 

type of case study (see section 3.4.3.1 above). Limitations in the available data and modeling 

tools precluded simulation of linkages between some media and air Pb, such that the full impact 

of changes in air Pb conditions associated with attainment of lower standards was not simulated. 

For example, dietary and drinking water Pb concentrations, as well as soil Pb concentrations, 

were not varied across the air quality scenarios in any case study (see Table 3-7). For all case 

studies, however, indoor dust Pb concentrations were simulated to change with the different air 

quality scenarios that also provided differing ambient air Pb concentrations (outdoors and 

indoors). 

3.4.3.3 Methods for Deriving Risk Estimates 

In this section, we first summarize the full risk model employed in the 2007 REA for 

estimating risk for a broad range of air quality scenarios (section 3.4.3.3.1). Then, in section 

3.4.3.3.2, we summarize approaches by which we have identified risk estimates pertaining to the 

current standard, the second of which involves an analysis newly completed in this review in 

which risk estimates are interpolated for the current standard based on the 2007 REA risk 

estimates. 
3-52 

3.4.3.3.1 Full Risk Model in 2007 REA 

The risk characterization step employed in the 2007 REA involved generating a 

distribution of IQ loss estimates for the set of children simulated in the exposure assessment. 

Specifically, estimated blood Pb levels for the concurrent blood Pb metric42 were combined with 

four blood Pb concentration-response (C-R) functions for IQ loss based on the analysis by 

Lanphear et al (2005) of a pooled international dataset of blood Pb and IQ (see 2007 REA, 

section 5.3.1.1). Four different C-R functions were selected to provide different 

characterizations of behavior at low exposures. The decision to use four different functions is in 

recognition of uncertainty related to modeling this endpoint, particularly at lower blood Pb levels 

for which there is limited representation in the Lanphear et al (2005) pooled dataset; the 5th 

percentile for the concurrent blood Pb measurements in that dataset is 2.5 μg/dL, and the mean is 

9.7 μg/dL (73 FR 66978). The four different functions are either based directly on the lognormal 

model described in Lanphear et al (2005), or they are derived from data presented in that study.43 

The four functions are presented in Figure 3-4 and compared in Table 3-9 with regard to total IQ 

loss and incremental IQ loss (IQ loss per μg/dL blood Pb) across a range of concurrent blood Pb 

levels. A brief description of each of the functions is also here: 

 Log-linear with cutpoint: log-linear function derived from the pooled analysis applied 

down to 1 μg/dL (concurrent blood Pb metric) with no IQ loss projected below that 

exposure level. 

 Log-linear with low-exposure linearization: log-linear function applied down to 1 μg/dL 

(concurrent blood Pb metric) with linearization of the slope at that point which is used to 

project IQ loss down to the origin. 

 Dual linear – stratified at 10 μg/dL: function developed by fitting a two-piece linear 

function stratified at 10 μg/dL (peak blood Pb concentration) to the log-linear function 

developed from the pooled analysis. 

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

function at 7.5 μg/dL (peak blood Pb concentration). 

 

42 Risk estimates were also developed for lifetime average PbB levels using concentration-response 

functions derived from the Lanphear et al (2005) analysis for lifetime average PbB levels. Estimates based on the 

concurrent PbB metric are given primary emphasis, consistent with advice from CASAC (Henderson, 2007b). 

43 The two log-linear C-R functions rely on the loglinear model in Lanphear et al (2005). The two dual 

linear C-R functions rely on the linear models reported in Lanphear et al (2005) for concurrent blood Pb in four 

groupings of children based on whether peak blood Pb levels were below or at/above 10 or 7.5 μg/dL. In order to 

utilize the linear models in the REA, we considered the relationship between peak and concurrent blood Pb levels in 

the pooled dataset, as well as in the cohort comprising the bulk of the low blood Pb subsets. In both cases, the 

difference was approximately a factor of two (2007 REA, section 5.3.1.1). The “dual linear –stratified at 10 μg/dL” 

function applies the Lanphear et al (2005) linear coefficient for children with peak blood Pb below 10 μg/dL to REA 

concurrent blood Pb estimates below 5 ug/dL and the linear coefficient for children with peak blood Pb at or above 

10 μg/dL to REA concurrent blood Pb estimates at or above 5 μg/dL (Figure 3-4). The “dual linear –stratified at 7.5 

μg/dL” function applies the Lanphear et al (2005) linear coefficient for children with peak blood Pb below 7.5μg/dL 

to REA concurrent blood Pb estimates below 3.75 μg/dL and the linear coefficient for children with peak blood Pb 

at or above 7.5 μg/dL to REA concurrent blood Pb estimates at or above 3.75 μg/dL. 
3-53 

Figure 3-4. Comparison of four concentration-response functions used in risk assessment. 

Table 3-9. Comparison of total and incremental IQ loss estimates for blood Pb below 10 

μg/dL based on the four concentration-response functions. 

Performance Metric 

Concentration-Response Function 

Log-linear 

with cutpoint 

Log-linear with 

low-exposure 

linearization 

Dual linear - 

stratified at 10 

μg/dL peak 

Dual linear - 

stratified at 7.5 

μg/dL peak 

Points, IQ loss 

Total IQ loss 

at 2 μg/dL 1.9 4.6 1.6 5.9 

at 5 μg/dL 4.3 7.0 3.9 11.1 

at 7.5 μg/dL 5.4 8.1 4.3 11.5 

at 10 μg/dL 6.2 8.9 4.6 11.9 

Incremental IQ loss 

(average # points 

 per μg/dL) 

<2 μg/dL 0.94 2.29 0.80 2.94 

<5 μg/dL 0.87 1.41 0.80 2.24 

<7.5 μg/dL 0.73 1.09 0.58 1.55 

<10 μg/dL 0.62 0.89 0.47 1.20 

Of the four C-R functions provided above, we have the greatest overall confidence in risk 

estimates generated using the log-linear with low-exposure linearization (LLL) function because 

this function (a) is nonlinear, describing greater response per unit blood Pb at lower blood Pb 

levels consistent with multiple studies, (b) is based on fitting a function to the entire pooled 

dataset (and hence uses all of the data in describing response across the range of exposures), (c) 

is supported by sensitivity analyses showing the model coefficients to be robust (Lanphear et al., 

0

2

4

6

8

10

12

14

0 1 2 3 4 5 6 7 8 9 10

Concurrent blood Pb (ug/dL)

IQ loss

log-linear w ith cutpoint

dual linear - stratified at

10 ug/dL, peak

dual linear - stratified at

7.5 ug/dL, peak

log-linear w ith low -

exposure linearization
3-54 

2005), and (d) provides an approach for predicting IQ loss at the lowest exposures simulated in 

the assessment (which for some simulated children yield blood Pb levels below those studied). 

Risk estimates generated using the other three C-R functions are also presented to provide 

perspective on the impact of uncertainty in this key modeling step. For additional detail on the 

rationale for placing greater emphasis on the LLL function, see section 4.2.1 of the 2007 Pb Staff 

Paper (USEPA, 2007b). 

As noted in section 3.2 above, since the completion of the ISA in the current review, two 

errors have been identified with the pooled dataset analyzed by Lanphear et al (2005) (Kirrane 

and Patel, 2014). A recent publication and EPA have separately recalculated the statistics and 

mathematical models of Lanphear et al (2005) using the corrected pooled dataset (Kirrane and 

Patel, 2014). While the conclusions drawn from these coefficients, including the finding of a 

steeper slope at lower (as compared to higher) blood Pb concentrations are unaffected, the 

magnitude of the loglinear and linear regression coefficients are somewhat lower based on the 

corrections. For example, the loglinear model coefficient used for the LLL function, which we 

focused on in the last review and also focus on here, changed only negligibly from -2.7 to -2.65 

when recalculated using the corrected pooled dataset (Kirrane and Patel, 2014). As a result, the 

risk estimates for this function described below and presented in Tables 3-10 and 3-11 would be 

expected to be very similar although slightly lower if derived using the recalculated loglinear 

model coefficient for the corrected dataset.44, 45

Two categories of risk metrics were generated for each of the location-specific case 

studies: 

 Population risk percentiles: The IQ loss associated with policy-relevant exposure 

pathways for specific percentiles of the child population (e.g., the 50th, 90th and 95th

percentile modeled child). This category of metric provides perspective on the 

distribution of IQ loss resulting from policy-relevant exposure pathways, ranging from 

the typical or average child (50th percentile, mean) to children experiencing higher 

exposures (90th, 95th percentiles). Greater emphasis has been placed on the median IQ 

loss estimates due to increased confidence in these estimates relative to the higher 

percentile estimates, as noted in section 3.4.7. 

 

44 Since the loglinear model coefficient calculated from the corrected dataset is unchanged at two 

significant figures from that original reported, any change to the risk estimates would be very small and, particularly 

in light of other uncertainties in the analysis, does not materially affect staff’s consideration of the results. 

45 We also note that risk estimates for the other three C-R functions would also be expected to change as a 

result of corrections to two of the linear model coefficients (Kirrane and Patel, 2014), such that the upper end of the 

risk estimates range presented parenthetically in Tables 3-10 and 3-11 for all four functions would also be expected 

to be somewhat lower (the upper end is generally based on estimates from the dual linear-stratified at 7.5 μg/dL, 

peak, function). As was the case in the last review, the ranges reflecting all four functions are not a focus in this 

review. 
3-55 

 Child frequency counts associated with specific risk percentiles: Number of children 

associated with each of the population percentiles (e.g., the number of children predicted 

to have risk levels at or above the 95th percentile). This risk metric provides a perspective 

on the number of children associated with various levels of IQ loss for a particular case 

study. 

For the generalized (local) urban case study, only the first type of risk metric, population 

risk percentiles, was developed because a specific location with associated demographic data 

was not modeled. In summarizing risk estimates from the 2007 REA in this document, we have 

focused on the first category of risk metric and,specifically, on the median IQ loss estimates. 

3.4.3.3.2 Air Quality Scenarios Reflecting the Current Standard 

As the 2007 REA did not include an air quality scenario simulated to just meet the 

standard selected by the 2008 decision,46 we have considered two approaches for identifying risk 

estimates pertaining to conditions just meeting the current Pb standard (set in 2008) for our 

purposes in this review. We first reviewed all the scenarios analyzed in the 2007 REA and 

recognize the similarity to the current standard of the then-current conditions scenario for the 

Chicago case study. Accordingly, we consider the risk estimates for that scenario for our 

purposes in this review of considering risk associated with the current standard (see section 3.4.5 

below). Additionally, in recognition of the variation among specific locations and urban areas 

with regard to air quality patterns and exposed population, we have also newly developed 

estimates for an air quality scenario just meeting the current Pb NAAQS in the context of the 

generalized (local) urban case study to augment the risk information available in this current 

review. The newly developed estimates were derived based on interpolation from the risk 

estimates available for scenarios previously assessed for the generalized (local) urban case study. 

Such interpolated estimates were only developed for the generalized urban case study due to its 

use of a single exposure zone which greatly simplified the method employed, thus contributing 

relatively lesser uncertainty from the interpolation step.47

In newly developing estimates for the current standard in the generalized (local) urban 

case study, the general approach we followed was to identify the two alternative standard 

 

46 The 2008 decision on the level for the revised NAAQS was based primarily on consideration of the 

evidence-based air-related IQ loss 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). 

47 We did not complete interpolation of risk estimates for the current standard for the other case studies 

(i.e., the primary Pb smelter and location-specific 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. 
3-56 

scenarios simulated in the 2007 REA which represented air quality conditions bracketing those 

for the current standard and then linearly interpolate an estimate of risk for the current standard 

based on the slope created from the two bracketing estimates. In representing air quality 

conditions for these purposes, we focused on the annual average air Pb concentration estimates 

used as IEUBK model inputs for the various air quality scenarios. An annual average 

concentration estimate to represent the current standard was identified in a manner consistent 

with that employed in the 2007 REA for this case study (see section 3.4.3.2 above) with the use 

of currently available monitoring data for relationships between air quality metrics for 

representation of the current standard. By this method, the air quality scenario for the current 

standard (0.15 μg/m3

, 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

 (maximum calendar quarter average) and 

0.20 μg/m3 (maximum monthly average). A risk estimate for the current standard was then 

derived using the slope relating general urban case study IQ loss to annual average Pb 

concentration used for those two air quality scenarios. We used this interpolation approach to 

develop median risk estimates for the current standard based on each of the four C-R functions. 

Details on the method for the interpolation approach are provided in Appendix 3A. The 

interpolated median estimates of risk for the current standard for the generalized (local) urban 

case study are provided below in Table 3-9. 

3.4.4 Challenges in Characterizing Air-related Exposure and Risk 

In estimating the portion of total (all-pathway) blood Pb and IQ loss attributable to airrelated pathways, we faced a variety of challenges. Although we parsed total estimates into 

those for diet/drinking water and two air-related categories, referred to as “recent air” and “past 

air”, significant limitations in our modeling tools and data resulted in an inability to parse 

specific risk estimates into specific pathways. Although Pb in diet and drinking water sources 

may include Pb derived from Pb in the ambient air (as well as Pb from nonair sources), 

limitations precluded explicit modeling of the contribution from air pathways to these exposure 

pathways, such that the air-related component of these exposures was not estimated.48 As a result 

we utilized the estimates from recent and past air categories to create bounds within which we 

consider air-related risk to fall, as illustrated in Figure 3-5 and described further below.

 

48 Further, although paint is not an air-related source of Pb exposure, for this analysis, may be reflected 

somewhat in estimates developed for the “past air” category, due to modeling 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. 
3-57 

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

Those Pb exposure pathways tied most directly to ambient air, which consequently have 

the potential to respond relatively more quickly to changes in air Pb (i.e., inhalation and 

ingestion of indoor dust Pb derived from the infiltration of ambient air Pb indoors), were placed 

into the "recent air" category. The other air-related Pb exposure pathways, all of which are 

associated with atmospheric deposition, were placed into the “past air” category. These include 

ingestion of Pb in outdoor dust/soil and ingestion of the portion of Pb in indoor dust that after 

deposition from ambient air outdoors is carried indoors with humans. Additionally, while we 

recognized the potential for these other air-related exposures to be affected (over some time 

frame) by an adjustment to the Pb NAAQS, limitations in our date and tools precluded our 

simulation of that relationship with air Pb levels. 

Among the limitations affecting our estimates for the air-related categories is the 

apportionment of nonair pathways. For example, while conceptually indoor Pb paint 

contributions to indoor dust Pb would be considered background and included in a “background” 

category for this assessment, due to technical limitations related to indoor dust Pb modeling, dust 

from Pb paint was included as part of "other" indoor dust Pb (i.e., as part of past air exposure). 

The inclusion of indoor paint Pb as a component of "other" indoor dust Pb (and consequently as 

a component of the “past air” category) represents a source of potential high bias in our 

prediction of exposure and risk associated with the “past air” category because indoor paint Pb is 

a nonair Pb source. At the same time, Pb in ambient air does contribute to the drinking water 

“Recent air”

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

• 2007 REA simulated just meeting alternative NAAQS by changing recent air exposures. 

• Although no changes were simulated for past air exposures or to diet and drinking water pathways, changes 

to the NAAQS were expected to also influence those exposure pathways to some extent.

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

Ambient air

• newly emitted lead

• resuspension of historically

emitted and deposited lead

• historically emitted Pb (still in home

and/or still available for contact in

external soil/dust)

• paint

• Diet

Indoor dust • Drinking water

“Past air”

Indoor dust (other)

Outdoorsoil

• newly emitted Pb

•historically emitted Pb

• nonair contributions
3-58 

and diet exposure pathways and is likely a substantial contribution to diet. We could not 

separate the air contribution from the nonair contributions in the drinking water and diet 

pathways. As a result, our risk estimate for the drinking water/diet category of pathways 

includes some air-related risk representing a source of potential low bias in our predictions of 

air-related risk. 

Further, we note that in simulating reductions in exposure associated with reducing 

ambient air Pb levels through alternative NAAQS (and increases in exposure if the current 

NAAQS was reached in certain case studies) only the exposure pathways categorized as “recent 

air” (inhalation and ingestion of that portion of indoor dust associated with outdoor ambient air) 

were varied with changes in air concentration. The assessment from the previous review did not 

simulate decreases in “past air” exposure pathways (e.g., reductions in outdoor soil Pb levels 

following reduction in ambient air Pb levels and a subsequent decrease in exposure through 

incidental soil ingestion and the contribution of outdoor soil to indoor dust). These exposures 

were held constant across all air quality scenarios. This modeling/data limitation, accordingly, 

precluded estimates for this category from reflecting any impact of changes in air quality 

conditions and thus any impacts of the alternative standard levels simulated. 

In summary, because of limitations in the assessment design, data and modeling tools, 

our risk estimates for the “past air” category in the last review include both risks that are truly 

air-related and potentially, some nonair risk. Because we could not sharply separate Pb linked to 

ambient air from Pb from other (nonair) sources, some of the three categories of risk are 

underestimated and others overestimated. On balance, we believe this limitation leads to a slight 

overestimate of the risks in the “past air” category. At the same time, as discussed above, the 

"recent air" category does not fully represent the risk associated with all air-related pathways. 

Thus, we considered the risk attributable to air-related exposure pathways to be bounded on the 

low end by the risk estimated for the “recent air” category and on the upper end by the risk 

estimated for the “recent air” plus “past air” categories. With regard to the latter, we are 

additionally cognizant of the modeling and data limitations which reduce the extent to which the 

upper end of these bounds reflects impacts of alternative air quality conditions simulated. 

3.4.5 Risk Estimates 

This section summarizes air-related risk estimates generated for the previous review and 

also risk estimates that have been newly derived in this review by interpolation from the previous 

review estimates for the current standard (see section 3.4.3.3.2 above). Included in this summary 

is consideration of the following question: 
3-59 

 What is the nature and magnitude of air-related risks remaining upon just 

meeting the current Pb standard? 

The air-related risk quantified in the 2007 REA is for IQ loss associated with Pb 

exposure. As discussed in section 3.2 above, the evidence in the last review, as well as in the 

current review, supports identification of neurocognitive effects in young children as a 

particularly sensitive endpoint for the exposure circumstances relevant to this review and which 

addresses the important at-risk population, young children. With this support in the evidence for 

quantification, the risk assessment quantified decrements in IQ, an established indicator of 

neurocognitive function. With regard to the nature of the risks, in addition to recognizing the 

role of IQ as an indicator of an array of neurocognitive function impacts, we additionally take 

note of the evidence regarding implications of neurocognitive impacts in young children with 

regard to potential future impacts as the children age, as recognized in section 3.2 above. 

In presenting risk estimates here, we focus on the median estimates of air-related IQ loss 

for each case study. Estimates of air-related risk are substantially more uncertain for extremes of 

the risk distribution, such as the 95th percentile. Those estimates and estimates for other risk 

metrics, including population incidence for IQ loss at those case studies with population 

enumeration, are available elsewhere (2007 REA, sections 4.2 and 5.3.2). In this section, Table 

3-10 presents air-related IQ loss estimates derived in the 2007 REA for the full set of case 

studies. Table 3-11 provides a subset of these risk estimates for the generalized (local) urban case 

study in addition to estimates for air quality conditions just meeting the current standard, derived 

by interpolation. A number of details, listed here, should be kept in mind when reviewing the 

estimates presented in Tables 3-9 and 3-10. 

 The risk estimates represent IQ loss associated with air-related Pb exposure for the 

median child (exposure is modeled through age seven years). 

 Our estimation of risk attributable to air-related exposure pathways is approximate, as 

described in sections 3.4.4 and 3.4.7. We consider the air-related risk to fall within the 

ranges presented, bounded on the low end by estimates for the pathways categorized as 

“recent air” and on the upper end by the sum of the estimates for both the “recent” and 

“past air” pathways. 49 

 The bolded range of risk estimates is derived using the C-R function in which we have 

the highest overall confidence (the log-linear with low-exposure linearization – see 

section 3.4.3.3.1). The wider range of risk estimates presented within the parentheses in 

both tables reflects the application of all four C-R functions (see discussion in section 

3.4.3.3.1) to exposure estimates for the “recent” and “recent” plus “past” air categories. 

 

49 The third category of pathways for which risk was estimated in the 2007 REA comprised diet and 

drinking water pathways. As other (nonair) sources of Pb can be appreciable contributors of Pb to these pathways, 

this category is referred to as “background” in the 2007 REA. 
3-60 

Consequently, this range of risk estimates reflects both uncertainty in estimation of airrelated exposures as well as uncertainty in the C-R function for IQ loss in children. 

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

Air Quality Scenario 

Just meeting specified 

maximum quarterly/monthly 

average (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 C-R function in which we have the highest 

overall confidence (the log-linear with low-exposure linearization). Values in parentheses reflect the range of estimates 

associated with all four concentration-response functions (see discussion in section 3.4.3.3.1). 

B – In the case of the primary Pb smelter case study, only recent plus past air estimates are available. 

C – Median air-related IQ loss estimates for the primary Pb 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. 
3-61 

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

including interpolated estimates for current standard. 

Air Quality Scenario 

Just meeting specified metric (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 estimates are generated using the C-R function in 

which we have the highest overall confidence (the log-linear with low-exposure 

linearization). Values in parentheses reflect the range of estimates associated with all 

four concentration-response functions (see discussion in section 3.4.3.3.1). Values in 

parentheses reflect the range of estimates associated with all four concentrationresponse functions. 

B – Risk estimates interpolated - see text. 

Key observations regarding these air-related risk estimates across the array of air 

quality scenarios include the following: 

All Case Studies 

 Relative to the previous Pb NAAQS, substantial reduction in estimates of air-related risk 

is demonstrated across the full set of potential alternative standards simulated (Table 3-

10). This is particularly the case for the lower bound (the recent air estimates) which 

reflects only the pathways simulated to respond to changes in air concentrations 

associated with different air quality scenarios. 

Generalized (local) Urban Case Study 

 As described above, the general urban case study provides risk estimates for a single 

group of children residing in a single area where air concentrations throughout area are 

near the level of the standard being simulated. In this case study, air-related median IQ 
3-62 

loss, based on the higher confidence C-R function (bold), ranged from roughly 2 to 4 IQ 

points for the 0.5 μg/m3

, maximum monthly average scenario, to <1 to roughly 3 IQ 

points for the 0.02 μg/m3, maximum monthly average scenario. These ranges are 

expanded somewhat with consideration of the full range of C-R functions considered in 

the analysis. 

Location-specific Case Studies 

 Compared to the other case studies, the air-related risk estimates for the location-specific 

urban case studies are lower because of the broader range of air-related exposures and the 

distribution of the population within the study areas. For example, the majority of the 

populations in each of the location-specific case studies reside in areas with ambient air 

Pb levels well below each standard assessed, particularly for standard levels above 0.05 

μg/m3

, as a maximum monthly average. Consequently, risk estimates for these case 

studies indicate little response to alternative standard levels above 0.05μg/m3

 maximum 

monthly average (as shown in Table 3-10). 

 For the primary Pb smelter subarea, only an upper bound on risk attributable to airrelated exposures is provided due to uncertainties associated with the dust Pb model used 

for this case study.50 For all air quality scenarios, the population median recent plus past

air risk estimate is generally similar to or slightly higher than those for the general urban 

case study, likely due to differences in the indoor dust models used for the two case 

studies (discussed in the 2007 REA, sections 3.1.4). 

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

the following: 

 The median air-related IQ loss estimate for then-current conditions in the Chicago study 

area, which just met a level of 0.14 μg/m3 as a maximum calendar quarter average, falls 

somewhere within the lower and upper bounds of 0.6 and 2.9 points IQ loss, respectively 

(Table 3-10). 

 The median air-related IQ loss estimate for the current standard in the Generalized (local) 

Urban Case Study, newly derived by interpolation from 2007 REA results, falls 

somewhere within the lower and upper bounds of 1.5 and 3.4 points IQ loss, respectively 

(Table 3-11). This estimate is derived by interpolation between the estimates for the 0.2 

μg/m3

 maximum quarterly and 0.2 μg/m3 maximum monthly average scenarios that were 

derived in 2007 REA. The newly interpolated estimate is essentially the same as the 

estimate for 0.2 μg/m3

 maximum quarterly average scenario for this case study. 

 Based on results from the last review for a location-specific urban study area and on 

those newly derived in this review based on interpolation from 2007 REA results, median 

air-related IQ loss for the current standard is estimated, with rounding, to generally fall 

above a rough lower bound of 1 point IQ loss and below a rough upper bound of 3 points 

IQ loss. 

 

50 The regression model used for estimating dust Pb concentrations in the primary Pb smelter case study 

does not lend itself to partitioning the recent air Pb from other contributions. Accordingly, this partitioning was not 

done for this case study (2007 REA, sections 2.4.3 and 3.1.4.2). 
3-63 

3.4.6 Treatment of Variability 

This section discusses the degree to which the design of the previous risk assessment 

reflected consideration for key sources of variability associated with the scenarios evaluated 

(e.g., IQ loss in children associated with ambient Pb in various residential settings). In so doing, 

we address the following question. 

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

Key sources of variability associated with the risk assessment include: 

 Variation in ambient air Pb levels among U.S. urban residential areas: The locationspecific urban study areas were chosen to provide coverage for diverse residential 

populations in U.S. urban areas with relatively elevated ambient air Pb levels (as 

characterized using monitoring). We believe that the three cities included in those case 

studies capture the variability in spatial patterns of ambient air Pb concentrations within 

and across such areas reasonably well. In addition, the generalized (local) urban case 

study provides coverage for a residential population exposed in a localized area with air 

concentrations somewhat near the standard being evaluated, providing coverage for a 

higher-end population risk scenario where a subset of urban children are exposed without 

any spatial gradient in ambient air Pb levels. 

 Variation in the spatial distribution of children within an urban area and assignment of 

ambient air Pb exposure: Exposure of populations within the three location-specific 

urban study areas was characterized to the U.S. Census block group level. Each block 

group was associated ambient air Pb exposure based on proximity to the monitor nearest 

to block group centroid (2007 REA, section 5.2.2). While there is uncertainty associated 

with these exposures (population weighted through use of census block groups) - for 

example, we did not consider time spent by children away from their residential block 

group - we believe that this approach provides reasonable coverage for the potential 

pattern of interaction between resident children located in these urban study areas and the 

associated spatial gradients of ambient air Pb levels. 

 Variation among children in factors other than media concentrations that influence 

Blood Pb levels: The inputs to the blood Pb model were central tendency estimates for 

each exposure zone within each study area (pathway-specific estimates for centraltendency child). The IEUBK model then generated blood Pb levels for that centraltendency child within each exposure zone. These central-tendency blood Pb levels were 

then combined with a GSD reflecting variability in blood Pb levels for young children 

(at/near age 7 years) to generate a distribution of total blood Pb for a group of children 

within each exposure zone in a given case study under the specific air quality scenario. 

We have reasonable confidence that this modeling approach captures variability in total 

Pb exposure (and consequently total blood Pb levels) for children modeled for a given 

study area. As noted in section 3.4.7 below, however, there is uncertainty associated with 

parsing individual pathway contributions to total blood Pb levels (and consequently to 
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total Pb-attributable risk). This is particularly true for high-end population percentile 

estimates of IQ loss. 

 Inter-individual variability in IQ loss related to Pb exposure: The use of C-R functions 

based on a pooled analysis (Lanphear et al., 2005) which combined study populations 

from a number of different epidemiological studies of IQ loss in children likely provides 

reasonable coverage for variation across children regarding IQ loss attributable to Pb 

exposure. Furthermore, our estimation of risk based on several C-R functions provides 

further coverage for that variability, as well as also addressing uncertainty in the 

specification of that C-R functional form (see section 3.4.7 below). 

3.4.7 Characterizing Uncertainty 

Although the risk assessment utilized a number of innovative modeling elements in order 

to generate representative estimates of risk for the various study area populations, like all risk 

models there was uncertainty associated with the model and its output. 

 What are the important uncertainties associated with any risk/exposure 

estimates? 

One overarching area of uncertainty concerns the precision of our estimation of the 

neurocognitive risk (as represented by IQ loss) associated with ambient air Pb. For example, 

because of the evidence for a nonlinear response of blood Pb to Pb exposure and also for 

nonlinearity in the C–R relationship for Pb-associated IQ loss, the assessment first estimated 

blood Pb levels and associated risk for total Pb exposure (i.e., including Pb from air-related and 

nonair exposure pathways) and then separated out estimates for pathways of interest. We 

separated out the estimates of total (all-pathway) blood Pb and IQ loss into three categories that 

included two air-related categories (“past” and “recent”), in addition to a third category for diet 

and drinking water. However, significant limitations in our modeling tools affected our ability to 

develop precise estimates for air-related exposure pathways. As recognized in section 3.4.4 

above, we believe these limitations led to a slight overestimation of the risks for the past air

category and to an under-representation of air-related pathways for the recent air category. 

Thus, we characterized the risk attributable to air-related exposure pathways to be bounded by 

the estimates developed for the past air category and the sum of estimates for the recent air and

past air categories. For air quality scenarios other than those for the previous NAAQS, this 

upper bound is recognized as having a potential upward bias with regard to its reflection of the 

simulated air quality conditions because modeling and data limitations precluded simulation of 

the influence of lower air Pb concentrations on the outdoor dust and soil exposure pathways, as 

noted in section 3.4.4 above. 

Additional limitations, assumptions and uncertainties, recognized in various ways in the 

assessment and presentation of results, along with a concise characterization of their expected 

impact on results, are listed below. The list begins with factors related to design of the 
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assessment or of the case studies, followed by those related to estimation of Pb concentrations in 

ambient air, indoor dust, outdoor soil/dust, and blood, and estimation of Pb-related IQ loss. 

 Temporal Aspects: During the 7-year exposure period, media concentrations remain 

fixed and the simulated child resides at the same residence (although exposure factors, 

including behavioral and physiological parameters, are adjusted to match the aging of the 

child). While these aspects of simulation introduce uncertainty into the risk estimates, it 

is not clear whether there is a directional bias. For example, failure to consider population 

mobility during the simulation period could bias the overall risk distribution upwards 

unless children move to or from a residential location with higher Pb exposure, in which 

case this would not be the case. 

 Generalized (local) Urban Case Study: The design for this case study employs 

assumptions regarding uniformity that are reasonable in the context of a general 

description of a small neighborhood population but would contribute significant 

uncertainty to extrapolation of these estimates to a specific urban location, particularly a 

relatively large one. Thus, the risk estimates for this case study, while generally 

representative of an urban residential population exposed to the specified ambient air Pb 

levels, cannot be readily related to a specific large urban population. As long as these 

important caveats are considered in interpreting the risk estimates (i.e., these risk 

estimates likely represent a relatively small portion of the resident child population in any 

given city just meeting specific air quality conditions), then the potential error of 

extrapolating these results to a larger child population can be avoided. An additional area 

of uncertainty is with regard to the representation of variability in air quality. Given the 

relatively greater variability common in areas of high Pb concentrations, the approach 

used to reflect variability may bias the estimates high, although there is uncertainty with 

regard to the representativeness of the monitoring dataset used to characterize this. 

 Location-specific Urban Case Studies: Limitations in the spatial density of ambient air 

monitors in the three metropolitan areas simulated limit our characterization of spatial 

gradients of ambient air Pb levels in these case studies. While this factor introduces 

uncertainty into the risk estimates for this category of case study, it is not clear whether 

there is a directional bias. 

 Air Quality Simulation: The proportional roll-up and roll-down procedures used in some 

case studies to simulate air quality conditions just meeting the previous NAAQS and 

alternative NAAQS, respectively, assume proportional changes in air concentrations 

across those case study areas to create those air quality scenarios. The EPA recognizes 

the uncertainty with our simulation of higher air Pb concentrations that would just meet 

the previous (1978) NAAQS in the urban location-specific case studies, as well as the 

uncertainty in simulation of conditions associated with the implementation of emissions 

reduction actions to meet a lower standard. There is the potential that the use of the 

proportional approach for adjusting monitor values introduced a degree of high bias into 

estimates of risk reduction. This could result if we find that urban areas can target 

specific Pb sources impacting individual monitors, thereby avoiding the need for more 

generalized reduction strategies resulting in a uniform pattern of reduction across all 

monitors in an urban area. It is important to point out, however, that the generalized 

urban case study is not affected by this potential bias, since, given the single exposure 
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zone involved, the single ambient air Pb level is fixed to reflect meeting the standard 

being considered (i.e., no spatial gradient is simulated in the small, localized residential 

area being modeled). 

 Outdoor Soil/Dust Pb Concentrations: Limitations in datasets on Pb levels in surface 

soil/dust Pb in urban areas and in our ability to simulate the impact of reduced air Pb 

levels related to lowering the NAAQS contribute uncertainty to air-related risk estimates. 

In this case, it is likely that we have low biased our estimates of risk reduction associated 

with alternative (lower) Pb NAAQS levels, since we have not simulated potential 

changes in soil Pb related to changes in ambient air Pb. 

 Indoor Dust Pb Concentrations: Limitations and uncertainty in modeling of indoor dust 

Pb levels, including the impact of reductions in ambient air Pb levels, contributes 

uncertainty to air-related risk estimates. Although our modeling of indoor dust does link 

changes in ambient air Pb to changes in indoor dust Pb (via air exchanges and indoor 

deposition onto surfaces), the modeling does not include a link between ambient air Pb, 

outdoor soil Pb and subsequent changes in the level of Pb carried (or “tracked”) into the 

house. This could introduce low bias into our total estimates of air-related Pb exposure 

and risk. 

 Interindividual Variability in Blood Pb Levels: Uncertainty related to population 

variability in blood Pb levels (i.e., interindividual variability in factors other than media 

concentration that influence blood Pb) and limitations in modeling of this introduces 

significant uncertainty into blood Pb and IQ loss estimates for the 95th percentile of the 

population. We are not aware of any systematic bias introduced into the analysis from 

this source of uncertainty. 

 Pathway Apportionment for Higher Percentile Blood Pb and risks: Limitations, 

primarily in data, prevented us from characterizing the degree of correlation among highend Pb exposures for the various pathways (e.g., the degree to which an individual 

experiencing high drinking water Pb exposure would also experience high Pb paint 

exposure and high ambient air-related Pb exposure). Our inability to characterize 

potential correlations between exposure pathways (particularly at the higher percentile 

exposure levels) limited our ability to (a) effectively model high-end Pb risk and (b) 

apportion that risk between different exposure pathways, including ambient air-related 

pathways. 

 IQ Loss Concentration-response Functions: Specification of the quantitative relationship 

between blood Pb level and IQ loss is subject to greater uncertainty at lower blood Pb 

levels (e.g., particularly below 2.5 μg/dL concurrent blood Pb). However, we believe that 

by considering four different models (which each treat the response at low blood Pb 

levels in a different manner), we have completed a reasonable characterization of this 

source of uncertainty and its impact on risk estimates. Given comparison of risk estimates 

generated using the four models, it would appear that this source of uncertainty has a 

potentially significant impact on risk. 
3-67 

3.4.8 Updated Interpretation of Risk Estimates 

As summarized in prior sections, a range of information gaps and areas of uncertainty 

were associated with the information available in the last review. In the REA Planning 

Document, staff considered the degree to which information newly available since the last Pb 

NAAQS review might address specific uncertainties associated with the 2007 REA, such that an 

updated risk model might be developed with the potential to provide new exposure and risk 

estimates substantially different51 from estimates generated in 2007 (USEPA, 2011). Staff 

concluded that the newly available information 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 Pb NAAQS review. Specifically it was concluded that none of the primary 

sources of uncertainty identified to have the greatest impact on risk estimates would be 

substantially reduced through the use of newly available information (USEPA, 2011). 

Our ongoing review of the newly available information leads us to conclude at this time, 

that the key observations regarding air-related Pb risk modeled for the set of standard levels 

covered in the 2007 REA, as well as the risk estimates interpolated for the current standard (as 

discussed in section 3.4.5) are not significantly affected by the new information. Our overall 

characterization of uncertainty and variability associated with those estimates (as described 

above in sections 3.4.6 and 3.4.7) is not appreciably affected by new information. As recognized 

at the time of the last review, exposure and risk modeling conducted for this analysis was 

complex and subject to significant uncertainties due to limitations in the data, and models, 

among other aspects. Further, limitations in the assessment design, data and modeling tools 

handicapped us from sharply separating Pb linked to ambient air from Pb that is not air related. 

In summary, the estimates of risk attributable to air-related exposures, with which we 

recognize a variety of sources of uncertainty, are considered to be approximate, falling within 

upper and lower bounds, roughly estimated as 3 and 1 IQ points, which over- and underestimate 

risk, respectively. In scenarios for more restrictive air quality conditions than those associated 

with the previous Pb standard, substantial reductions in air-related risk were demonstrated. 

Focusing on the results for the generalized (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

scenarios (maximum monthly and quarterly averages) simulated in the 2007 REA52 and are 

 

51 In this context, “substantially different” has been intended to mean that the degree of uncertainty is 

substantially reduced, or bias is addressed, such that the new risk estimates could convey a different message 

regarding the magnitude of public health impacts associated with the current or potential alternative standards. 

52 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. 
3-68 

appreciably lower than those associated with the previous standard. In characterizing the 

magnitude of air-related risk associated with the current standard, we focus on median estimates, 

for which we have appreciably greater confidence than estimates for outer ends of risk 

distribution (see section 3.4.7) and on risks derived using the C-R function in which we have 

greatest confidence (see sections 3.4.3.3.1 and 3.4.7). The risk results for the current standard 

estimated in the last review for one of the location-specific urban study area populations and 

those newly derived in this review using interpolation of the estimates from the last review for 

the generalized (local) urban case study, which is recognized to reflect a generalized high end of 

air-related exposure for localized populations, provide approximate bounds for air-related risk, 

with attendant uncertainties described above. 

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

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

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

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

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

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

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

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

014a and EPA-452/R-07-014b. 

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

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

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

http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_sp.html
3-73 

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

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

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

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

U.S. Environmental Protection Agency. (2013) Integrated Science Assessment for Lead. Washington, DC, 

EPA/600/R-10/075F. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html 

Zielhuis, R.L.; del Castilho, P.; Herber, R.F.M.; Wibowo, A.A.E.; Salle, H.J.A. (1979) Concentrations of lead and 

other metals in blood of two and three year-old children living near a secondary smelter. Int. Arch. Occup. 

Environ. Health 42: 231-239. 
4-1 

4 REVIEW OF THE PRIMARY STANDARD FOR LEAD 

This chapter presents staff conclusions regarding the primary Pb standard. These staff 

conclusions are guided by consideration of key policy-relevant questions and based on the 

assessment and integrative synthesis of information presented in the ISA and by staff analyses 

and evaluations presented in chapters 2 and 3 herein. The evaluations and staff conclusions 

presented in this chapter have also been developed with consideration of CASAC advice and 

public comment on the external review draft of this document. These evaluations and staff 

conclusions will inform the Administrator’s decisions on whether to retain or revise the existing 

primary standard for Pb. 

Following an introductory section on the general approach for reviewing the primary 

standard (section 4.1), including a summary of considerations in the last review, the discussion in 

this chapter focuses on the central issue of whether the information available in this review 

supports or calls into question the adequacy of the current primary standard. Building on the 

responses to specific policy-relevant questions on the scientific evidence and exposure-risk 

information in chapter 3 above, presentation in section 4.2 is also organized into consideration of 

key policy-relevant questions framing evidence-based and exposure/risk-based considerations. 

The policy-relevant questions in this document are based on those included in the IRP (IRP, 

section 3.1). In section 4.3, staff conclusions are developed. Section 4.4 presents a brief 

overview of key uncertainties and areas for future research. 

4.1 APPROACH 

Staff’s approach in this review of the current primary standard takes into consideration 

the approaches used in the last Pb NAAQS review addressing key policy-relevant questions in 

light of currently available scientific and technical information. The past and current approaches 

described below are both based, most fundamentally, on using EPA’s assessment of the current 

scientific evidence and associated quantitative analyses to inform the Administrator’s judgment 

regarding a primary standard for Pb that protects public health with an adequate margin of safety. 

In drawing conclusions for consideration with regard to the primary standard, we note that the 

final decision on the adequacy of the current standard is largely a public health policy judgment 

to be made by the Administrator. The Administrator’s final decision must draw upon scientific 

information and analyses about health effects, population exposure and risks, as well as 

judgments about how to consider the range and magnitude of uncertainties that are inherent in 

the scientific evidence and analyses. Our approach to informing these judgments, discussed 

more fully below, is based on the recognition that the available health effects evidence generally 

reflects a continuum, consisting of levels at which scientists generally agree that health effects 
4-2 

are likely to occur, through lower levels at which the likelihood and magnitude of the response 

become increasingly uncertain. This approach is consistent with the requirements of the 

NAAQS provisions of the Act and with how the EPA and the courts have historically interpreted 

the Act. These provisions require the Administrator to establish primary standards that, in the 

judgment of the Administrator, are requisite to protect public health with an adequate margin of 

safety. In so doing, the Administrator seeks to establish standards that are neither more nor less 

stringent than necessary for this purpose. The Act does not require that primary standards be set 

at a zero-risk level, but rather at a level that avoids unacceptable risks to public health including 

the health of sensitive groups.1

 The four basic elements of the NAAQS (indicator, averaging 

time, level, and form) are considered collectively in evaluating the health protection afforded by 

the current standard. 

The following subsections include background information on the approach used in the 

previous review of the standard (section 4.1.1) and a discussion of the approach for the current 

review (section 4.1.2). 

4.1.1 Approach Used in the Last Review 

The last review of the NAAQS for Pb was completed in 2008 (73 FR 66964). In 

consideration of the much-expanded health effects evidence on neurocognitive effects of Pb in 

children available at that time, the EPA substantially revised the primary standard from 1.5 

μg/m3, as a not-to-be exceeded average concentration over a calendar quarter, to a level of 0.15 

μg/m3

, as a not-to-be-exceeded rolling 3-month average concentration. The 2008 decision to 

revise the primary standard was based on the extensive body of scientific evidence published 

over almost three decades, from the time the standard was originally set in 1978 through 2005-

2006. The 2008 decision considered the body of evidence as assessed in the 2006 CD (USEPA, 

2006) as well as the 2007 Staff Paper assessment of the policy-relevant information contained in 

the CD and the quantitative risk/exposure assessment (USEPA, 2007a, 2007b), the advice and 

recommendations of CASAC (Henderson 2007a, 2007b, 2008a, 2008b), and public comment. 

While recognizing that Pb has been demonstrated to exert “a broad array of deleterious 

effects on multiple organ systems”, the review focused on the effects most pertinent to ambient 

air exposures, which given ambient air Pb reductions over the past 30 years are those associated 

with relatively lower exposures and associated blood Pb levels (73 FR 66975). In so doing, the 

 

1

 The at-risk population groups identified in a NAAQS review may include low income or minority groups. 

Where low income/minority groups are among the at-risk populations, the rulemaking decision will be based on 

providing protection for these and other at-risk populations and lifestages (e.g., children, older adults, persons with 

pre-existing heart and lung disease). To the extent that low income/minority groups are not among the at-risk 

populations identified in the ISA, a decision based on providing protection of the at-risk lifestages and populations 

would be expected to provide protection for the low income/minority groups. 
4-3 

EPA recognized the general consensus that the developing nervous system in children is among, 

if not the most sensitive health endpoint associated with Pb exposures. Thus, primary attention 

was given to consideration of nervous system effects, including neurocognitive and 

neurobehavioral effects, in children (73 FR 66976). The body of evidence included associations 

of such effects in study populations of variously-aged children with mean blood Pb levels below 

10 μg/dL, extending from 8 down to 2 μg/dL (73 FR 66976). The public health implications of 

effects of air-related Pb on cognitive function (e.g., IQ) in young children were given particular 

focus in the review. 

4.1.1.1 Approach Regarding the Need for Revision 

The conclusions reached by the Administrator in the last review were based primarily on 

the scientific evidence, with the risk- and exposure-based information providing support for 

various aspects of the decision. In reaching his conclusion on the adequacy of the then-current 

standard, which was set in 1978, the Administrator placed primary consideration on the large 

body of scientific evidence available in the review including significant new evidence 

concerning effects at blood Pb concentrations substantially below those identified when the 

standard was initially set (73 FR 66987; 43 FR 46246). Given particular attention was the robust 

evidence of neurotoxic effects of Pb exposure in children, recognizing: (1) that while blood Pb 

levels in U.S. children had decreased notably since the late 1970s, newer epidemiological studies 

had investigated and reported associations of effects on the neurodevelopment of children with 

those more recent lower blood Pb levels and (2) that the toxicological evidence included 

extensive experimental laboratory animal evidence substantiating well the plausibility of the 

epidemiological findings observed in human children and expanding our understanding of likely 

mechanisms underlying the neurotoxic effects (73 FR 66987). Additionally, within the range of 

blood Pb levels investigated in the available evidence base, a threshold level for neurocognitive 

effects was not identified (73 FR 66984; 2006 CD, p. 8-67). Further, the evidence indicated a 

steeper dose-response relationship for effects on cognitive function at those lower blood Pb 

levels than at higher blood Pb levels that were more common in the past, “indicating the 

potential for greater incremental impact associated with exposure at these lower levels” (73 FR 

66987). As at the time when the standard was initially set in 1978, the health effects evidence 

and exposure/risk assessment available in the last review supported the conclusion that airrelated Pb exposure pathways contribute to blood Pb levels in young children by inhalation and 

ingestion (73 FR 66987). The available information in the last review also indicated, however, 

that the air-to-blood ratio was likely larger than the air-to-blood ratio (of 2 μg/dL blood Pb to 1 

μg/m3

 air Pb) estimated when the standard was initially set (73 FR 66987). 
4-4 

In the Administrator’s decision on the adequacy of the 1978 standard, the Administrator 

considered the evidence using a very specifically defined framework, referred to as an air-related 

IQ loss evidence-based framework. This framework integrates evidence for the relationship 

between Pb in air and Pb in young children’s blood with evidence for the relationship between 

Pb in young children’s blood and IQ loss (73 FR 77987), as described in more detail in section 

4.1.1.2 below. This evidence-based approach considers air-related effects on neurocognitive 

function (using the quantitative metric of IQ loss) associated with exposure in those areas with 

elevated air concentrations equal to potential alternative levels for the Pb standard. Thus, the 

conceptual context for the framework is that it provides estimates of air-related IQ loss for a 

subset of the population of U.S. children (i.e., the subset living in close proximity to air Pb 

sources that contribute to elevated air Pb concentrations that equal the current level of the 

standard). This is the subset expected to experience air-related Pb exposures at the high end of 

the national distribution of such exposures, not at the average. This is the case since when a 

standard of a particular level is just met at a monitor sited to record the highest source-oriented 

concentration in an area, the large majority of children in the larger surrounding area would 

likely experience exposures to concentrations well below that level. 

The two primary inputs to the evidence-based air-related IQ loss framework are air-toblood ratios and C-R functions for the relationship between blood Pb and IQ response in young 

children. Additionally taken into consideration in applying and drawing conclusions from the 

framework were the uncertainties inherent in these inputs. Application of the framework also 

entailed consideration of an appropriate level of protection from air-related IQ loss to be used in 

conjunction with the framework. In simplest terms, the framework provides for estimation of a 

mean air-related IQ decrement for young children in the high end of the national distribution of 

air-related exposures by focusing on children exposed to air-related Pb in those areas with 

elevated air Pb concentrations equal to specific potential standard levels. The framework 

estimates of mean air-related IQ loss are 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 air concentration 

and slope for the C-R function in terms of points IQ decrement per μg/dL blood Pb. 

Based on the application of the air-related IQ loss framework to the evidence, the 

Administrator concluded that, for exposures projected for air Pb concentrations at the level of the 

1978 standard, the quantitative estimates of IQ loss associated with air-related Pb indicated risk 

of a magnitude that in his judgment was significant from a public health perspective, and that the 

evidence-based framework supported a conclusion that the 1978 standard did not protect public 

health with an adequate margin of safety (73 FR 77987). The Administrator further concluded 

that the evidence indicated the need for a substantially lower standard level to provide increased 

public health protection, especially for at-risk groups (most notably children), against an array of 
4-5 

effects, most importantly including effects on the developing nervous system (73 FR 77987). In 

addition to giving primary consideration to the much expanded evidence base since the standard 

was set, the Administrator also took into consideration the exposure/risk assessments. In so 

doing, he observed that, while taking into consideration their inherent uncertainties and 

limitations, the quantitative estimates of IQ loss associated with air-related Pb in air quality 

scenarios just meeting the then-current standard also indicated risk of a magnitude that in his 

judgment was significant from a public health perspective. Thus, the Administrator concluded 

the exposure/risk estimates provided additional support to the evidence-based conclusion that the 

standard needed revision (73 FR 66987). 

4.1.1.2 Approach Regarding Elements of Revised Standard 

In considering appropriate revisions to the prior standard in the review completed in 

2008, each of the four basic elements of the NAAQS (indicator, averaging time, form and level) 

was evaluated. The rationale for decisions on those elements is summarized below. 

With regard to indicator, consideration was given to replacing Pb-TSP with Pb-PM10. 

The EPA recognized, however, that Pb in all particle sizes contributes to Pb in blood and 

associated health effects, additionally noting that the difference in particulate Pb captured by 

TSP and PM10 monitors may be on the order of a factor of two in some areas (73 FR 66991). 

Further, the Administrator recognized uncertainty with regard to whether a Pb-PM10-based 

standard would also effectively control ultra-coarse2 Pb particles, which may have a greater 

presence in areas near sources where Pb concentrations are highest (73 FR 66991). The 

Administrator decided to retain Pb-TSP as the indicator to provide sufficient public health 

protection from the range of particle sizes of ambient air Pb, including ultra-coarse particles (73 

FR 66991). Additionally, a role was provided for Pb-PM10 in the monitoring required for a PbTSP standard (73 FR 66991) based on the conclusion that use of Pb-PM10 measurements at sites 

not influenced by sources of ultra-coarse Pb, and where Pb concentrations are well below the 

standard, would take advantage of the increased precision of these measurements and decreased 

spatial variation of Pb-PM10 concentrations, without raising the same concerns over a lack of 

protection against health risks from all particulate Pb emitted to the ambient air that support 

retention of Pb-TSP as the indicator (versus revision to Pb-PM10) (73 FR 66991). Accordingly, 

allowance was made for the use of Pb-PM10 monitoring for Pb NAAQS attainment purposes in 

certain limited circumstances, at non-source-oriented sites, where the Pb concentrations are 

 

2

 The term ultra-coarse is used to refer to particles collected by a TSP sampler but not by a 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. 
4-6 

expected to be substantially below the standard and ultra-coarse particles are not expected to be 

present (73 FR 66991). 

With regard to averaging time and form for the revised standard, consideration was given 

to a monthly averaging time, with a form of second maximum, and a 3-month calendar quarter 

averaging time, with not-to-be exceeded forms. While the Administrator recognized that there 

were some factors that might imply support for a period as short as a month for averaging time, 

he also noted other factors supporting use of a longer time. He additionally took note of the 

complexity inherent in this consideration for the primary Pb standard, which is greater than in the 

case of other criteria pollutants due to the multimedia nature of Pb and its multiple pathways of 

human exposure. 

In this situation for Pb, the Administrator emphasized the importance of considering all 

of the relevant factors, both those pertaining to the human physiological response to changes in 

Pb exposures and those pertaining to the response of air-related Pb exposure pathways to 

changes in airborne Pb, in an integrated manner. With regard to the human physiological 

response to changes in Pb exposures, the evidence discussed in the CD indicated that children’s 

blood Pb levels respond quickly to increased Pb exposures, such that an abrupt increase in Pb 

uptake results in increased blood Pb levels. Contributing to this response is the absorption 

through the lungs and the gastrointestinal tract and the rapid distribution, once absorbed, 

throughout the body. With regard to the relationship between airborne Pb and children’s blood 

Pb, evidence collected during the time of leaded gasoline usage when airborne Pb was a 

prominent Pb exposure pathway across the population indicated children’s blood Pb to respond 

to changes in airborne Pb over a month’s time lag. The phase-out of on-road leaded gasoline, 

however, has resulted in changed circumstances with regard to children’s exposure pathways, 

with accompanying temporal implications. Accordingly, EPA considered the limited evidence 

indicating the more numerous factors influencing ingestion (versus inhalation) pathways, which 

were considered likely to lessen the impact of month-to-month variations in airborne Pb 

concentrations on levels of air-related Pb in children’s blood. Such factors were considered 

likely to lead to response times (e.g., for the response of blood to air Pb via these pathways) 

extending longer than a month (73 FR 66996). The Administrator also recognized limitations 

and uncertainties in the evidence including the limited available evidence specific to the 

consideration of the particular duration of sustained airborne Pb levels having the potential to 

contribute to the adverse health effects identified as most relevant to this review, as well as 

variability in the response time of indoor dust Pb loading to ambient airborne Pb. Based on these 

various considerations, the Administrator concluded that the information provided support for an 

averaging time no longer than a 3-month period. 
4-7 

With regard to a three-month averaging time, the EPA recognized that a rolling threemonth averaging time can provide (e.g., compared to a block calendar quarter) control on monthto-month variability in air Pb concentrations and in associated exposures (73 FR 66996). The 

rolling three-month average eliminates the possibility for two consecutive “high” months falling 

in two separate calendar quarters to be considered independently (perhaps being mitigated by 

“low” months falling in each of the same calendar quarters). Rather, in the rolling 3-month 

approach, the same month would contribute to three different 3-month periods through separate 

combinations with three different pairs of months, thus providing a more complete consideration 

of air quality during that month and the 3-month periods in which it falls. The Administrator 

additionally concluded it appropriate to modify the method by which the 3-month average metric 

is derived, to be the average of three monthly average concentrations, as compared to the thencurrent practice by which the average was derived across the full dataset for a quarter without 

equally weighting each month within the quarter. Thus, in consideration of the uncertainty 

associated with the evidence pertinent to averaging time discussed above, the Administrator 

noted that the two changes in form for the standard (to a rolling 3-month average and to 

providing equal weighting to each month in deriving the 3-month average) both afford greater 

weight to each individual month than did the calendar quarter form of the 1978 standard, tending 

to control both the likelihood that any month will exceed the level of the standard and the 

magnitude of any such exceedance. 

Based on this integrated consideration of the range of relevant factors, the averaging time 

was revised to a rolling three-month period with a maximum (not-to-be-exceeded) form, 

evaluated over a three-year period. As compared to the previous averaging time and form of 

calendar quarter (not-to-be exceeded), this revision was considered to be more scientifically 

appropriate and more health protective (73 FR 77996). The rolling average gives equal weight to 

all three-month periods, and the new calculation method gives equal weight to each month 

within each three-month period (73 FR 77996). Further, the rolling average yields 12 threemonth averages each year to be compared to the NAAQS versus four averages in each year for 

the block calendar quarters pertaining to the previous standard (73 FR 77996). 

Lastly, based on the body of scientific evidence and information available, as well as 

CASAC recommendations and public comment, the Administrator decided on a standard level 

that, in combination with the specified choice of indicator, averaging time, and form, he judged 

requisite to protect public health, including the health of sensitive groups, with an adequate 

margin of safety (73 FR 67006). In reaching the decision on level for the revised standard, the 

Administrator considered as a useful guide the evidence-based framework developed in that 

review. As described in section 4.1.1.1 above, that framework integrates evidence for the 

relationship between Pb in air and Pb in children’s blood and the relationship between Pb in 
4-8 

children’s blood and IQ loss. Application of the air-related IQ loss evidence-based framework 

was recognized, however, to provide “no evidence- or risk-based bright line that indicates a 

single appropriate level” for the standard (73 FR 67006). Rather, the framework was seen as a 

useful guide for consideration of health risks from exposure to ambient levels of Pb in the air, in 

the context of a specified averaging time and form, with regard to the Administrator’s decision 

on a level for a revised NAAQS that provides public health protection that is sufficient but not 

more than necessary under the Act (73 FR 67004). 

As noted above, use of the evidence-based air-related IQ loss framework to inform 

selection of a standard level involved consideration of the evidence with regard to two input 

parameters. The two input parameters are an air-to-blood ratio and a C-R function for population 

IQ response associated with blood Pb level (73 FR 67004). The evidence at the time of the last 

review indicated a broad range of air-to-blood ratio estimates, each with limitations and 

associated uncertainties. Based on the then-available evidence, the Administrator concluded that 

1:5 to 1:10 represented a reasonable range to consider and identified 1:7 as a generally central 

value on which to focus (73 FR 67004). With regard to C-R functions, in light of the evidence of 

nonlinearity and of steeper slopes at lower blood Pb levels, the Administrator concluded it was 

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.,3

 recognizing EPA’s identification of four such 

analyses and giving weight to the central estimate or median of the resultant C-R functions (73 

FR 67003, Table 3; 73 FR 67004). The four study groups from which C-R functions were drawn 

in 2008, and the associated C-R slopes, are summarized in Table 3-3 above.4

 The median 

estimate of -1.75 IQ points decrement per μg/dL was selected for use with the framework. With 

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 air Pb) and 

the median slope for the C-R function (points IQ decrement per μg/dL blood Pb), yielding 

estimates of a mean air-related IQ decrement for a specific subset of young children (i.e., those 

children exposed to air-related Pb in areas with elevated air Pb concentrations equal to specified 

alternative levels). As such, the application of the framework yields estimates for the mean airrelated IQ decrements of the subset of children expected to experience air-related Pb exposures 

 

3

 The geometric mean blood Pb level for U.S. children aged five years and below, reported for NHANES in 

2003-04 (the most recent years for which such an estimate was available at the time of the 2008 decision) was 1.8 

μg/dL and the 5th and 95th percentiles were 0.7 μg/dL and 5.1 μg/dL, respectively (73 FR 67002). 4

 One of these four is from the analysis of the lowest blood Pb subset of the pooled international study by 

Lanphear et al., (2005). The nonlinear model developed from the full pooled dataset is the basis of the C-R 

functions used in the 2007 REA (see section 3.4.3.3 above), in which risk was estimated over a large range of blood 

Pb levels. Given the narrower focus of the evidence-based framework on IQ response at the end of studied blood Pb 

levels (closer to U.S. mean level), the C-R functions in Table 3-3 are from linear analyses (each from separate 

publications) for the study group subsets with blood Pb levels closest to mean for children in the U.S. today. 
4-9 

at the high end of the distribution of such exposures. The associated mean IQ loss estimate is the 

average for this highly exposed subset and is not the average air-related IQ loss projected for the 

entire U.S. population of children. Uncertainties and limitations were recognized in the use of 

the framework and in the resultant estimates (73 FR 67000). 

In considering the use of the evidence-based air-related IQ loss framework to inform his 

judgment as to the appropriate degree of public health protection that should be afforded by the 

NAAQS to provide requisite protection against risk of neurocognitive effects in sensitive 

populations, such as IQ loss in children, the Administrator recognized in the 2008 review that 

there were no commonly accepted guidelines or criteria within the public health community that 

would provide a clear basis for such a judgment. During the 2008 review, CASAC commented 

regarding the significance from a public health perspective of a 1-2 point IQ loss in the entire 

population of children and, along with some commenters, emphasized that the NAAQS should 

prevent air-related IQ loss of a significant magnitude, such as on the order of 1-2 IQ points, in all 

but a small percentile of the population. Similarly, the Administrator stated that “ideally airrelated (as well as other) exposures to environmental Pb would be reduced to the point that no IQ 

impact in children would occur” (73 FR 66998). The Administrator further recognized that, in 

the case of setting a NAAQS, he was required to make a judgment as to what degree of 

protection is requisite to protect public health with an adequate margin of safety (73 FR66998). 

The NAAQS must be sufficient but not more stringent than necessary to achieve that result, and 

the Act does not require a zero-risk standard (73 FR 66998). The Administrator additionally 

recognized that the evidence-based air-related IQ loss framework did not provide estimates 

pertaining to the U.S. population of children as a whole. Rather, the framework provides 

estimates (with associated uncertainties and limitations) for the mean of a subset of that 

population, the subset of children assumed to be exposed to the level of the standard. As 

described in the final decision “[t]he framework in effect focuses on the sensitive subpopulation 

that is the group of children living near sources and more likely to be exposed at the level of the 

standard” (73 FR 67000). As further noted in the final decision (73 FR 67000): 

EPA is unable to quantify the percentile of the U.S. population of children that 

corresponds to the mean of this sensitive subpopulation. Nor is EPA confident in 

its ability to develop quantified estimates of air-related IQ loss for higher 

percentiles than the mean of this subpopulation. EPA expects that the mean of 

this subpopulation represents a high, but not quantifiable, percentile of the U.S. 

population of children. As a result, EPA expects that a standard based on 

consideration of this framework would provide the same or greater protection 

from estimated air-related IQ loss for a high, albeit unquantifiable, percentage of 

the entire population of U.S. children. 

In reaching a judgment as to the appropriate degree of protection, the Administrator 

considered advice and recommendations from CASAC and public comments and recognized the 
4-10 

uncertainties in the health effects evidence and related information as well as the role of, and 

context for, a selected air-related IQ loss in the application of the framework, as described above. 

Based on these considerations, the Administrator identified an air-related IQ loss of 2 points for 

use with the framework, as a tool for considering the evidence with regard to the level for the 

standard (73 FR 67005). In so doing, the Administrator was not determining that such an IQ 

decrement value was appropriate in other contexts (73 FR 67005). Given the various 

uncertainties associated with the framework and the scientific evidence base, and the focus of the 

framework on the sensitive subpopulation of children that are more highly exposed to air-related 

Pb, a standard level selected in this way, in combination with the selected averaging time and 

form, was expected to significantly reduce and limit for a high percentage of 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

, with the combination of the generally central estimate of air-to-blood ratio 

of 1:7 and the median of the four C-R functions (-1.75 IQ point decrement per μg/dL blood Pb), 

the framework estimates of air-related IQ loss were below 2 IQ points (73 FR 67005, Table 4). 

In reaching the decision in 2008 on level for the revised standard, the Administrator also 

considered the results of the quantitative risk assessment to provide a useful perspective on risk 

from air-related Pb. In light of important uncertainties and limitations for purposes of evaluating 

potential standard levels, however, the Administrator placed less weight on the risk estimates 

than on the evidence-based assessment. Nevertheless, in recognition of the general 

comparability of quantitative risk estimates for the case studies considered most conceptually 

similar to the scenario represented by the evidence-based framework, he judged the quantitative 

risk estimates to be “roughly consistent with and generally supportive” of the evidence-based 

framework estimates (73 FR 67006). 

Based on consideration of the entire body of evidence and information available in the 

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

, in combination with the specified 

choice of indicator, averaging time and form was requisite to protect public health, including the 

health of sensitive groups, with an adequate margin of safety (73 FR 67006). In reaching 

decisions on level as well as the other elements of the revised standard, the Administrator took 

note of the complexity associated with consideration of health effects caused by different 

ambient air concentrations of Pb and with uncertainties with regard to the relationships between 

air concentrations, exposures, and health effects For example, selection of a maximum, not to 

be exceeded, form in conjunction with a rolling 3-month averaging time over a 3-year span was 

expected to have the effect that the at-risk population of children would be exposed below the 

standard most of the time (73 FR 67005). The Administrator additionally considered the 

provision of an adequate margin of safety in making decisions on each of the elements of the 
4-11 

standard, including, for example “selection of TSP as the indicator and the rejection of the use of 

PM10 scaling factors; selection of a maximum, not to be exceeded form, in conjunction with a 3-

month averaging time that employs a rolling average, with the requirement that each month in 

the 3-month period be weighted equally (rather than being averaged by individual data) and that 

a 3-year span be used for comparison to the standard; and the use of a range of inputs for the 

evidence-based framework, that includes a focus on higher air-to-blood ratios than the lowest 

ratio considered to be supportable, and steeper rather than shallower C-R functions, and the 

consideration of these inputs in selection of 0.15 μg/m3 as the level of the standard” (73 FR 

67007). 

He additionally noted that a standard with this level would reduce the risk of a variety of 

health effects associated with exposure to Pb, including effects indicated in the epidemiological 

studies at lower blood Pb levels, particularly including neurological effects in children, and the 

potential for cardiovascular and renal effects in adults (73 FR 67006). The Administrator 

additionally considered higher and lower levels for the standard, concluding that a level of 0.15 

μg/m3 provides for a standard that is neither more or less stringent than necessary for this 

purpose, recognizing that the Clean Air Act does not require that primary standards be set at a 

zero-risk level, but rather at a level that reduces risk sufficiently so as to protect public health 

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

, 

which he concluded were insufficient to protect public health with an adequate margin of safety. 

The Administrator also noted that in light of all of the evidence, including the evidence-based 

framework, the degree of public health protection likely afforded by standard levels below 0.15 

μg/m3

 would be greater than what is necessary to protect public safety with an adequate margin 

of safety. 

The Administrator concluded, based on review of all of the evidence (including the 

evidence-based framework), that when taken as a whole the selected standard, including the 

indicator, averaging time, form, and level, would be “sufficient but not more than necessary to 

protect public health, including the health of sensitive subpopulations, with an adequate margin 

of safety” (73 FR 67007). 

4.1.2 Approach for the Current Review 

To evaluate whether it is appropriate to consider retaining the current primary Pb 

standard, or whether consideration of revision is appropriate, we have adopted an approach in 

this review that builds upon the general approach used in the last review and reflects the broader 

body of evidence and information now available. As summarized above, the Administrator’s 

decisions in the prior review were based on an integration of information on health effects 
4-12 

associated with exposure to Pb, relationships between ambient air Pb and blood Pb; expert 

judgments on the adversity and public health significance of key health effects; and policy 

judgments as to when the standard is requisite to protect public health with an adequate margin 

of safety. These considerations were informed by air quality and related analyses, quantitative 

exposure and risk assessments, and qualitative assessment of impacts that could not be 

quantified. 

In conducting this assessment, we draw on the current evidence and quantitative 

assessments of exposure pertaining to the public health risk of Pb in ambient air. In considering 

the scientific and technical information, we consider both the information available at the time of 

the last review and information newly available since the last review, including the current ISA 

(USEPA, 2012), as well as the quantitative exposure/risk assessments from the last review that 

estimated Pb-related IQ decrements associated with different air quality conditions in simulated 

at-risk populations in multiple case studies (USEPA, 2007a). Figure 4-1 illustrates the basic 

construct of our two part approach in developing conclusions regarding options appropriate for 

the Administrator to consider in this review with regard to the adequacy of the current standard 

and, as appropriate, potential alternate standards. In the boxes of Figure 4-1, the range of 

questions considered in chapter 3 above and section 4.2 below is represented by a summary of 

policy-relevant questions that frame our consideration of the scientific evidence and 

exposure/risk information. 
4-13 

Figure 4-1. Overview of approach for review of current primary standard. 

Evidence-based Considerations

 Does currently available evidence and related 

uncertainties strengthen or call into question prior 

conclusions?

 Evidence of health 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
4-14 

4.2 ADEQUACY OF THE CURRENT STANDARD 

 In considering the adequacy of the current Pb standard, the overarching question we 

consider is:

 Does the currently available scientific evidence- and exposure/risk-based 

information, as reflected in the ISA and REA, support or call into question the 

adequacy of the protection afforded by the current Pb standard? 

In considering the scientific and technical information, we give our attention to both the 

information available at the time of the last review and information newly available since the last 

review, including most particularly that which has been critically analyzed and characterized in 

the ISA. In chapter 3 above, attention was given to addressing specific questions on key aspects 

of this information. To assist us in interpreting the currently available scientific evidence and 

results of quantitative exposure/risk analyses to address the overarching question here, we draw 

on discussions in chapter 3 above in our consideration of broader or more policy-related 

questions, posed within sections 4.2.1 and 4.2.2 below. 

For the purposes of this PA, staff has drawn from EPA’s assessment and integrated 

synthesis of the scientific evidence presented in the ISA and on the quantitative exposure and 

risk information, based on the 2007 REA (USEPA, 2007a), described in section 3.4 above. The 

evidence-based discussions presented in this chapter draw upon evidence from epidemiological 

studies and experimental animal studies evaluating health effects related to exposures to Pb, as 

discussed in the ISA. The exposure/risk-based discussions have drawn from the quantitative 

health risk analyses for Pb performed in the last Pb NAAQS review in light of the currently 

available evidence (2007 REA, REA Planning Document). Together the evidence-based and 

risk-based considerations inform our conclusions related to the adequacy of the current primary 

standard for Pb. 

4.2.1 Evidence-based Considerations 

In considering the evidence with regard to the issue of adequacy of the current standard, 

we address several questions that build on the information summarized in chapter 3 to more 

broadly address the extent to which the current evidence base supports the adequacy of the 

public health protection afforded by the current primary standard. The first question addresses 

our integrated consideration of the health effects evidence, in light of aspects described in 

chapter 3. The second question focuses on our consideration of associated areas of uncertainty. 

The third question then integrates our consideration of the prior two questions with a focus on 

the standard, including each of the four elements. 
4-15 

 To what extent has new information altered the scientific support for the 

occurrence of health effects as a result of multimedia exposure associated with 

levels of Pb occurring in the ambient air? 

The current evidence continues to support our conclusions from the previous review 

regarding key aspects of the health effects evidence for Pb and the health effects of multimedia 

exposure associated with levels of Pb occurring in ambient air in the U.S. Our conclusions in 

this regard are based on consideration of the assessment of the currently available evidence in the 

ISA, particularly with regard to key aspects summarized in chapter 3 of this PA, in light of the 

assessment of the evidence in the last review as described in the 2006 CD and summarized in the 

notice of final rulemaking (73 FR 66964). Key aspects of these conclusions are summarized 

below. 

As at the time of the last review, blood Pb continues to be the predominant biomarker 

employed to assess exposure and health risk of Pb (ISA, chapters 3 and 4), as discussed in 

section 3.1 above. This widely accepted role of blood Pb in assessing exposure and risk is 

illustrated by its established use in programs to prevent both occupational Pb poisoning and 

childhood Pb poisoning, with the latter program, implemented by the CDC, recently issuing 

updated guidance on blood Pb measurement interpretation (CDC, 2012). As in the past, the 

current evidence continues to indicate the close linkage of blood Pb levels in young children to 

their body burden; this linkage is associated with the ongoing bone remodeling during that 

lifestage (ISA, section 3.3.5). This tight linkage plays a role in the somewhat rapid response of 

children’s blood Pb to changes in exposure (particularly to exposure increases), which 

contributes to its usefulness as an exposure biomarker (ISA, sections 3.2.2, 3.3.5, and 3.3.5.1). 

Additionally, the weight of evidence documenting relationships between children’s blood Pb and 

health effects, most particularly those on the nervous and hematological systems (e.g., ISA, 

sections 4.3 and 4.7), speaks to its usefulness in assessing health risk. 

As in the last review, the evidence on air-to-blood relationships available today continues 

to be comprised of studies based on an array of circumstances and population groups (of 

different age ranges), analyzed by a variety of techniques, which together contribute to 

appreciable variability in the associated quantitative estimates and uncertainty with regard to the 

relationships existing in the U.S. today. Accordingly, our interpretation of this evidence base, as 

discussed in section 3.1 above, also includes consideration of factors that may be influencing 

various study estimates, both with regard to their usefulness for our general purpose of 

quantitatively characterizing relationships between Pb in ambient air and air-related Pb in 

children’s blood and with regard to their pertinence more specifically to conditions and 

populations in the U.S. today. In so doing, we note that the current evidence, while including 

two additional studies not available at the time of the last review, is not much changed from that 
4-16 

available in the last review. The range of estimates that can be derived from the full dataset is 

broad and not changed by the inclusion of the newly available estimates. Further, we recognize 

significant uncertainties regarding the air Pb to air-related blood Pb relationship for the current 

conditions where concentrations of Pb in both ambient air and children’s blood are substantially 

lower than they have been in the past. In considering the strengths, limitations and uncertainties 

associated with the full dataset, the currently available evidence appears to continue to support a 

range of estimates for our purposes that is generally consistent with the range given weight in the 

last review, 1:5 to 1:10 (ISA, section 3.7.4 and Table 3-12; 73 FR 67001-2, 67004). We 

additionally note that the generally central estimate of 1:7 identified for this range in the last 

review is consistent with the study involving blood Pb for pre-school children and air Pb 

conditions near a large source of Pb to ambient air with concentrations near (and/or previously 

above) the level of the current Pb standard (ISA, section 3.5.1; Hilts, 2003).5

 In so noting, we 

also recognize the general overlap of such circumstances with those represented by the evidencebased, air-related IQ loss framework,6

 for which air-to-blood ratio is a key input. In 

characterizing the range of air-to-blood ratio estimates, we recognize uncertainty inherent in such 

estimates as well as the variation in currently available estimates resulting from a variety of 

factors, including differences in the populations examined, as well as in the Pb sources or 

exposure pathways addressed in those study analyses (ISA, section 3.7.4). 

The scientific evidence continues to recognize a broad array of health effects on multiple 

organ systems or biological processes related to blood Pb, including Pb in blood prenatally (ISA, 

section 1.6). The currently available evidence continues to support identification of 

neurocognitive effects in young children as the most sensitive endpoint associated with blood Pb 

concentrations (ISA, section 1.6.1), which as an integrated index of exposure reflects the 

aggregate exposure to all sources of Pb through multiple pathways (inhalation and ingestion). 

Evidence continues to indicate that neurocognitive effects in young children may not be 

reversible and may have effects that persist into adulthood (ISA, section 1.9.6). Thus, as 

discussed in section 3.2 above, we continue to consider the evidence of Pb effects at the low end 

of the studied blood Pb levels (closest to those common in the U.S. today) to be strongest and of 

greatest concern for effects on the nervous system, most particularly those on cognitive function 

in children. 

As in the last review, evidence on risk factors continues to support the identification of 

young children as an important at-risk population for Pb health effects (ISA, section 5.4). The 

 

5

 The older study by Hayes et al (1994) during time of leaded gasoline indicated a generally similar ratio of 

1:8, although the blood Pb levels in 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. 
4-17 

current evidence also continues to indicate important roles as factors that increase risk of leadrelated health effects for the following: nutritional factors, such as iron and calcium intake; 

elevated blood Pb levels; and proximity to sources of Pb exposure, such as industrial releases or 

buildings with old, deteriorating, leaded paint. Further, some races or ethnic groups continue to 

demonstrate increased blood Pb levels relative to others, which may be related to these and other 

factors (ISA, sections 5.1, 5.2 and 5.4). 

With regard to our understanding of the relationship between exposure or blood Pb levels 

in young children and neurocognitive effects, the evidence in this review, as in the last, does not 

establish a threshold blood Pb level for neurocognitive effects in young children (ISA, sections 

1.9.4 and 4.3.12). The lowest blood Pb levels at which associations with neurocognitive impacts 

have been observed in pre-school and school age children continue to range down below 5 

μg/dL, with the lowest group levels that have been associated with such effects ranging down to 

2 μg/dL (ISA, sections 1.6.1 and 4.3.15.1). Additionally, as in the last review, there is evidence 

that the relationship of young children’s blood Pb with neurocognitive impacts, such as IQ, is 

nonlinear across a wide range of blood Pb, with greater incremental impacts at lower vs. higher 

blood Pb levels (ISA, sections 1.9.4 and 4.3.12). Accordingly, as in the last review, we continue 

to focus our interest on C-R relationships from study groups with blood Pb levels closest to those 

in children in the U.S. today, which are generally lower than epidemiological study groups. The 

currently available evidence does not identify additional C-R slopes for study groups of young 

children (e.g., < 7 years) with mean blood Pb levels below that of groups identified in the last 

review, 2.9 – 3.8 μg/dL, as discussed in section 3.2 above (ISA, section 4.3.12). Thus, the blood 

Pb concentration - IQ response functions or slopes identified in this review for epidemiological 

study groups of young children with mean blood Pb levels closest to that of children in the U.S. 

today include the same set recognized at the time of the last review (see Table 3-3 above), the 

median of which is 1.75 points decrement per μg/dL blood Pb (73 FR, 67003). 

 To what extent have important uncertainties identified in the last review been 

reduced and/or have new uncertainties emerged? 

In our consideration of the evidence, as summarized in discussing the previous question 

and in chapter 3 above, we have not identified any new uncertainties as emerging since the last 

review. However, we continue to recognize important uncertainties identified in the last review 

that remain today. Importantly, given our focus in this review, as in the last review, on 

neurocognitive impacts associated with Pb exposure in early childhood, we recognize remaining 

uncertainties in our understanding of the C-R relationship of neurocognitive impacts, such as IQ 

decrements, with blood Pb level in young children, particularly across the range of blood Pb 

levels common in the U.S. today. With regard to C-R relationships for IQ, the evidence 

available in this review does not include studies that appreciably extend the range of blood Pb 
4-18 

levels studied beyond those available in the last review. As in the last review, the early 

childhood (e.g., 2 to 6 or 7 years of age) blood Pb levels for which associations with IQ response 

have been reported continue to extend at the low end of the range to study group mean blood Pb 

levels of 2.9 to 3.8 μg/dL (e.g., 73 FR 67003, Table 3). The lack of studies considering 

concentration-response relationships for Pb effects on IQ at lower blood Pb levels contributes to 

uncertainty regarding the quantitative relationship between blood Pb and IQ response in 

populations with mean blood Pb levels closer to the most recently available mean for children 

aged one to five years of age (e.g., 1.17 μg/dL in 2009-2010 [ISA, p. 3-85]). The studies at the 

blood Pb levels studied, as summarized in section 3.2 above, continue to indicate higher C-R 

slopes in these groups with lower blood Pb levels than in study groups with higher blood Pb 

levels (ISA, section 4.3.12). 

Further, we recognize important uncertainties in our understanding of the relationship 

between ambient air Pb concentrations and air-related Pb in children’s blood. The evidence 

newly available in this review has not reduced such key uncertainties. As in the last review, airto-blood ratios based on the available evidence continue to vary, with our conclusions based on 

the current evidence generally consistent with the range of 1:5 to 1:10 given emphasis in the last 

review (73 FR 67002; ISA, section 3.7.4). There continues to be uncertainty regarding the extent 

to which this range represents the relationship between ambient air Pb and Pb in children’s blood 

(derived from the full set of air-related exposure pathways) and with regard to its reflection of 

exposures associated with ambient air Pb levels common in the U.S. today and to circumstances 

reflecting just meeting the current Pb standard (ISA, section 3.7.4). We note additionally the 

significant uncertainty remaining with regard to the temporal relationships of ambient Pb levels 

and associated exposure with occurrence of a health effect (73 FR 67005). 

 To what extent does newly available information support or call into question any 

of the basic elements of the current Pb standard? 

We address this question for each of the elements of the standard in light of the health 

effects evidence and other relevant information available in this review. As an initial matter, 

however, we recognize the weight of the scientific evidence available in this review that 

continues to support our focus on effects on the nervous system of young children, specifically 

neurocognitive decrements, as the most sensitive endpoint. Consistent with the evidence 

available in the last review, the currently available evidence continues to indicate that a standard 

that provides requisite public health protection against the occurrence of such effects in at-risk 

populations would also provide the requisite public health protection against the full array of 

health effects of Pb. Accordingly, the discussion of the elements below is framed by that 

background. 
4-19 

Indicator 

The indicator for the current Pb standard is Pb-TSP. Key considerations in retaining this 

indicator in the last review are summarized in section 4.1.1.2 above. Exposure to Pb in all sizes 

of particles passing through ambient air can contribute to Pb in blood and associated health 

effects by a wide array of exposure pathways (ISA, section 3.1). These pathways include the 

ingestion route, as well as inhalation (ISA, section 3.1), and a wide array of particle sizes play a 

role in these pathways (ISA, section 3.1.1.1). As at the time of the last review, we continue to 

recognize the variability of the Pb-TSP FRM in its capture of airborne Pb particles (see section 

2.2.1.3.1 above). As in the last review, we also note that an alternative approach for collection of 

a conceptually comparable range of particle sizes, including ultra-coarse particles, is not yet 

available, although we take note of activities underway that may remedy that situation in the 

future, as referenced in section 2.2.1.3.1 above. Additionally, the limited available information 

regarding relationships between Pb-TSP and Pb in other size fractions indicates appreciable 

variation in this relationship, particularly near sources of Pb emissions where concentrations and 

potential exposures are greatest. Thus, the information available in this review does not address 

previously identified limitations and uncertainties for the current indicator. Nor does the newly 

available information identify additional limitations or uncertainties. 

The evidence available in this review continues to indicate the role of a range of air Pb 

particle sizes in contributing to Pb exposure (e.g., ISA, section 3.1.1.1) that contributes to Pb in 

blood and associated health effects. For example, the evidence indicates larger particle sizes for 

Pb that occurs in soil and house dust and may be ingested as compared to Pb particles commonly 

occurring in the atmosphere and the size fraction of the latter that may be inhaled (ISA, section 

3.1.1.1). Taken together the evidence currently available reinforces the appropriateness of an 

indicator for the Pb standard that reflects a wide range of airborne Pb particles. 

Averaging time and form 

The averaging time and form of the standard were revised in the last Pb NAAQS review, 

based on considerations summarized in section 4.1.1.2 above. The current standard is a not-tobe-exceeded rolling three-month average (CFR 50.16), derived from three monthly averages 

calculated in accordance with the current data handling procedures (CFR, Appendix R to Part 

50). The form is a maximum, evaluated within a three-year period (CFR 50.16). As at the time 

of the last review, evidence continues to support the importance of periods on the order of three 

months and the prominent role of deposition-related exposure pathways, with uncertainty 

associated with characterization of precise time periods associating ambient air Pb with airrelated health effects. Relevant factors continue to be those pertaining to the human 

physiological response to changes in Pb exposures and those pertaining to the response of airrelated Pb exposure pathways to changes in airborne Pb. The newly available evidence in this 
4-20 

review does not appreciably improve our understanding of the period of time in which air Pb 

concentrations would lead to the health effects most at issue in this review. Thus, there continue 

to be limitations in the evidence to inform our consideration of these elements of the standard 

and associated uncertainty. However, there is no newly available information that calls into 

question this element of the current Pb standard. 

Level 

The level of the current standard is 0.15 μg/m3

 (CFR 50.16). As described in section 

4.1.1 above, this level was selected in 2008 with consideration of, among other factors, an 

evidence-based air-related IQ loss framework, for which there are two primary inputs: air-toblood ratios and C-R functions for blood Pb – IQ response in young children. Additionally taken 

into consideration were the uncertainties inherent in these inputs. Application of the framework 

also entailed consideration of a magnitude of air-related IQ loss, which as further described in 

section 4.1.1.2 above, is used in conjunction with this specific framework in light of the 

framework context, limitations and uncertainties. Additionally, selection of a level for the 

standard in 2008 was made in conjunction with decisions on indicator, averaging time and form. 

As an initial matter, we consider the extent to which the evidence-based, air-related IQ 

loss framework which informed the Administrator’s decision in the last review is supported by 

the currently available evidence and information. In so doing, we recognize the support provided 

by the currently available evidence for the key conclusions drawn in the last review with regard 

to health effects of greatest concern, at-risk populations, the influence of Pb in ambient air on Pb 

in children’s blood and the association between children’s blood Pb and decrements in 

neurocognitive function (e.g., IQ). We additionally note the complexity associated with 

interpreting the scientific evidence with regard to specific levels of Pb in ambient air, given the 

focus of the evidence on blood Pb as the key biomarker of children’s aggregate exposure. The 

need to make such interpretations in the face of the associated complexity supported use of the 

evidence-based framework in the last review. In considering the currently available evidence for 

the same purposes in this review, we conclude that the evidence-based framework continues to 

provide a useful tool for consideration of the evidence with regard to the level of the standard. 

We next turn to consideration of the primary inputs to the framework: air-to-blood ratios 

and C-R functions for blood Pb – IQ response in young children. With regard to the former, the 

limited newly available information assessed in the ISA and discussed in section 3.1 above, is 

generally consistent with the information in this area that was available at the time of the last 

review. We additionally recognize the variability and uncertainty associated with quantitative 

air-to-blood ratios based on this information, as also existed in the last review. As in the last 

review, we recognize that factors contributing to the variability and uncertainty of these 

estimates are varied and include aspects of the study populations (e.g., age and Pb exposure 
4-21 

pathways) and the study circumstances (e.g., length of study period and variations in sources of 

Pb exposure during the study period). We note that the full range of estimates associated with 

the available evidence is wide and consider it appropriate to give emphasis to estimates 

pertaining to circumstances closest to those in the U.S. today with regard to ambient air Pb and 

children’s blood Pb concentrations, while recognizing the limitations associated with the 

available information with regard to this emphasis. With that in mind, we consider the currently 

available evidence to continue to support the range of estimates concluded in the last review to 

be most appropriate for the current population of young children in the U.S., in light of the 

multiple air-related exposure pathways by which children are exposed, in addition to inhalation 

of ambient air, and of the levels of air and blood Pb common today. Identification of this range 

also included consideration of the limitations associated with the available information and 

inherent uncertainties. This range of air-to-blood ratios included 1:10 at the upper end and 1:5 at 

the lower end. We further recognize that the limited evidence for air Pb and children’s blood Pb 

concentrations closest to those in U.S. today continues to provide support for the Administrator’s 

emphasis in the 2008 decision on the relatively central estimate of 1:7. 

With regard to the second input to the evidence-based framework, C-R functions for the 

relationship of young children’s blood Pb with neurocognitive impacts (e.g., IQ decrements), we 

consider several aspects of the evidence. First, as discussed in section 3.2 above, the currently 

available information continues to provide evidence that this C-R relationship is nonlinear across 

the range of blood Pb levels from the higher concentrations more prevalent in the past to lower 

concentrations more common today. Thus, we continue to consider it particularly appropriate to 

focus on the evidence from studies with blood Pb levels closest to those of today’s population, 

which in the last review included studies with study group mean blood Pb levels ranging roughly 

from 3 to 4 μg/dL in children aged 24 months to 7 years (Table 3-3 above). As discussed in 

sections 3.2 above, this is also consistent with the evidence currently available for this age group 

of young children, and the currently available evidence does not include additional C-R slopes 

for incremental neurocognitive decrement with blood Pb levels at or below this range. In 

considering whether this set of functions continues to be well supported by the evidence, as 

assessed in the ISA (ISA, section 4.3.2), we note the somewhat wide range in slopes 

encompassed by these study groups, while also noting the stability of the median. For example, 

omission of any of the four slopes considered in the last review does not appreciably change the 

median (e.g., the median would change from -1.75 IQ points per μg/dL blood Pb to -1.71 or -

1.79). Thus, we conclude that while differing judgments might be made with regard to inclusion 

of each of the four study groups, these estimates are generally supported by the current review of 

the evidence in the ISA. Further, the stability of the median to modifications to this limited 

dataset lead us to conclude that the currently available evidence continues to support 
4-22 

consideration of -1.75 IQ points per μg/dL blood Pb as a well-founded and stable estimate for 

purposes of describing the neurocognitive impact quantitatively on this age group of U.S. 

children. 

In summary, in considering the evidence and information available in this review 

pertaining to the level of the current Pb standard, we note that the evidence available in this 

review, as summarized in the ISA, continues to support the air-related IQ loss evidence-based 

framework, with the inputs that were used in the last review. These include estimates of air-toblood ratios ranging from 1:5 to 1:10, with a generally central estimate of 1:7. Additionally, the 

C-R functions most relevant to blood Pb levels in U.S. children today continue to be provided by 

the set of four analyses considered in the last review for which the median estimate is -1.75 IQ 

points per μg/dL Pb in young children’s blood. Thus, we observe that the evidence available in 

this review has changed little if at all with regard to the aspects given weight in the conclusion on 

level for the new standard in the last review and would not appear to call into question any of the 

basic elements of the standard. In so doing, we additionally recognize that the overall decision 

on adequacy of the current standard is a public health policy judgment by the Administrator; we 

discuss considerations that inform such judgments in section 4.3 below. 

4.2.2 Exposure/Risk-based Considerations 

Our consideration of the issue of adequacy of public health protection provided by the 

current standard is also informed by the quantitative exposure/risk assessment completed in the 

last review, augmented as described in section 3.4 above. We have organized the discussion that 

follows around two questions to assist us in interpreting the results of the assessment of case 

studies simulated to meet several different air quality conditions, including those just meeting the 

current standard. 

 What is the level of confidence associated with estimates of air-related risk 

generated for simulations just meeting the current Pb standard? 

As an initial matter, we recognize the significant limitations and complexity associated 

with the risk/exposure assessment for Pb that are far beyond those associated with similar 

assessments typically performed for other criteria pollutants. In completing the assessment we 

were constrained by significant limitations with regard to data and tools particular to the problem 

at hand. Further, the multimedia and persistent nature of Pb and the role of multiple exposure 

pathways contribute significant additional complexity to the assessment as compared to other 

assessments that focus only on the inhalation pathway. As a result, our estimates of air-related 

exposure and risk are approximate, presented as upper and lower bounds within which we 

consider air-related risk likely to fall. We base our description of overall confidence in this 

characterization of air-related risk on our consideration of the overall design of the analysis (as 
4-23 

described in section 3.4 above), the degree to which key sources of variability are reflected in the 

design of the analysis, and our characterization of key sources of uncertainty. 

In considering the degree to which key sources of variability (discussed in section 3.4.6 

above) are reflected in the design of the analysis, we note the following aspects addressed by the 

risk assessment. 

 Variation in distributions of potential urban residential exposure and risk across U.S. 

urban residential areas. This is addressed by the inclusion of three different (locationspecific) urban study areas that reflect a diverse set of urban areas in the U.S. 

 Representation of a more highly exposed subset of urban residents potentially exposed at 

the level of the standard. This is addressed by the inclusion of the generalized (local) 

urban study area. 

 Variation in residential exposure to ambient air Pb within an urban area. This is 

addressed through the partitioning of the location-specific study areas into exposure 

zones to provide some representation of spatial gradients in ambient air Pb and their 

interaction with population distribution and demographics. This was done in a somewhat 

more precise manner in the primary Pb smelter case study, which relied on dispersion 

modeling to describe gradients, as compared with the manual assignment of gradients 

related to air concentration differences among monitors in an area. 

 Inter-individual variability in blood Pb levels. This is addressed though the use of 

empirically-derived GSDs to develop blood Pb distribution for the child population in 

each exposure zone, with GSDs selected particular to each case study population. 

 Inter-individual variability in IQ response to blood Pb. This is addressed through the use 

of C-R functions for IQ loss based on a pooled analysis reflecting studies of diverse 

populations. 

We also considered key sources of uncertainty (discussed in section 3.4.7 above), in 

particular those affecting the precision of the air-related risk estimates, as mentioned above. 

Associated sources of uncertainty include our inability to simulate changes in air-related Pb as a 

function of changes in ambient air Pb in exposure pathways other than those involving inhalation 

of ambient air and ingestion of indoor dust. This contributes to the positive bias of the upper 

bound for the air-related risk estimates. We additionally recognize the significant uncertainty 

associated with estimating upper percentiles of the distribution of air-related blood Pb 

concentration estimates (and associated IQ loss estimates) due to limitations in available 

information. Lastly, we recognize the uncertainty associated with application of the C-R 

function at the lower blood Pb levels in the distribution; this relates to the limited representation 

of blood Pb levels of this magnitude in the dataset from which the C-R function is derived. 

In the quantitative risk information available in this review, we have air-related risk 

estimates for simulations just meeting the current standard from one of the location-specific 

urban case studies (Chicago) and from the generalized (local) urban case study. With regard to 
4-24 

the latter, we note its simplified design that does not include multiple exposure zones, thus 

reducing the dimensions simulated. We have a reasonable degree of confidence in aspects of the 

generalized (local) urban case study for the specific situation we consider it to represent (i.e., a 

temporal pattern of air Pb concentrations that just meets the level of the standard), and when the 

associated estimates are characterized as approximate, within upper and lower bounds (as 

described in section 3.4.4 above), while also recognizing considerable associated uncertainty. 

 To what extent are the air-related risks remaining upon just meeting the current 

Pb standard important from a public health perspective? 

In considering public health importance of estimated air-related risks, we consider here 

the nature and magnitude of such estimated risks (and attendant uncertainties), including such 

impacts on the affected population, and we additionally consider the size of the affected 

population. Based on the evidence available in the last review and consistent with that available 

today, the quantitative risk estimates developed in the 2007 REA and augmented slightly in this 

review are for decrements in IQ, an established indicator of neurocognitive function. In 

considering these estimates, we recognize that although some neurocognitive effects may be 

transient, some effects may persist into adulthood, affecting success later in life (ISA, sections 

1.9.5 and 4.3.14). We additionally recognize the potential population impacts of small changes 

in population mean values of metrics such as IQ, presuming a uniform manifestation of leadrelated decrement across the range of population IQ (ISA, section 1.9.1), as noted in section 3.3 

above. 

Exposures and risks associated with air-related Pb under several different air quality 

conditions were estimated in the 2007 REA. As summarized in section 3.4 above, limitations in 

our modeling tools and data affected our ability to develop precise estimates for air-related 

exposure pathways and contributed uncertainties. The results are approximate estimates which 

we describe through the use of rough upper and lower bounds within which we estimate airrelated risk to fall. We have recognized a number of uncertainties in the underlying risk 

estimates from the 2007 REA and in the interpolation approach employed in the new analyses 

for this review. We have characterized the magnitude of air-related risk associated with the 

current standard with a focus on median estimates, for which we have appreciably greater 

confidence than estimates for outer ends of risk distribution (see section 3.4.7) and on risks 

derived using the C-R function in which we have greatest confidence (see sections 3.4.3.3.1 and 

3.4.7). These risk estimates include estimates from the last review for one of the locationspecific urban study area populations as well as estimates newly derived in this review based on 

interpolation from 2007 REA results for the generalized (local) urban case study, which is 

recognized to reflect a generalized high end of air-related exposure for localized populations. 

Taken together, these results for just meeting the current standard include a high-end localized 
4-25 

risk estimate for air-related Pb of a magnitude generally bounded by roughly 1 and 3 points IQ 

loss, with attendant uncertainties, and with appreciably lower risks with increasing distance from 

the highest exposure locations 

In considering the importance of such risk from a public health perspective, we also 

consider the size of at-risk populations represented by the REA case studies. As discussed in 

section 3.4 above, the generalized (local) urban case study is considered to represent a localized 

urban population exposed near the level of the standard, such as a very small, compact 

neighborhood near a source contributing to air Pb concentrations just meeting the standard. This 

case study provides representation in the risk assessment for such small populations at the upper 

end of the gradient in ambient air concentrations expected to occur near sources; thus estimates 

for this case study reflect exposures nearest the standard being evaluated. While we do not have 

precise estimates of the number of young children living in such areas of the U.S. today, we have 

information that informs our understanding of their magnitude. For example, as discussed in 

section 3.3 above (Table 3-4), we estimate there to be approximately 2,400 children, aged 5 

years and younger, residing within 0.5 km of a monitor with air Pb concentrations above the 

current standard. We further observe several additional monitors with maximum 3-month Pb 

concentrations that fall below but within 10% of the current standard level (as noted in section 

3.3 above); an estimated 265 young children reside near these monitors. Thus, together we 

estimate some 2700 children, aged 5 years and younger, living in localized areas with elevated 

air Pb concentrations that are above or near the current standard. Based on the 2010 census 

estimates of approximately 24.3 million children in the U.S. aged five years or younger, this 

represents approximately one hundredth of one percent of this age group in the U.S.7

 This 

indicates the size of the population of young children of this age living in areas in close 

proximity to areas where air Pb concentrations may be above or near the current standard 

approximately a hundredth of one percent of the full population of correspondingly aged 

children.8

 

 

7

 While these estimates pertain to the age group of children aged 5 years and younger, we additionally note 

that a focus on an alternative age range, such as inclusive of slightly older children (e.g., through age 7), while 

increasing the number for children living in such locations, would not be expected to appreciably change the 

percentage of the full U.S. age group that the subset represents. Further, to the extent some of the source-oriented 

monitors required by the 2010 monitoring regulation summarized in section 2.2.1.1 above were not yet represented 

in the analysis of monitoring data summarized in Table 3-4 above and might report such elevated concentrations, 

consideration of the analysis summarized in Table 3-5 indicates the potential for only small changes in the 

percentage of the full age group represented by the subset (e.g., potential for less than an additional 0.01%). 8

 This estimate includes children in areas where recent information indicates the standard is exceeded 

because areas not in attainment 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 standard. 
4-26 

In summary, we recognize substantial uncertainty inherent in the REA estimates of airrelated risk associated with localized conditions just meeting the current standard, which we have 

characterized as approximate and falling near or somewhat above the rough lower bound of 1 

and below the rough upper bound of 3 IQ points.9

 This approximate estimate of risk for children 

living in such areas is generally overlapping with and consistent with the evidence-based airrelated IQ loss estimates summarized in section 4.2.1 above. With regard to the importance of 

the estimated risks from a public health perspective, we note, based on the currently available 

monitoring and census data, the estimated size of the population at risk in such areas to be 

approximately 2700 young children, representing slightly more than one one hundredth of a 

percent of the full population of similarly aged children. In considering the exposure/risk 

estimates during the last review, the Administrator took note of the important uncertainties and 

limitations associated with these assessments and, while placing less weight on the assessment 

estimates, he recognized the quantitative risk estimates to be “roughly consistent with and 

generally supportive” of those estimated by the evidence-based framework. In our consideration 

of the risk estimates considered in the last review, as well as the estimates for the current 

standard that have been newly developed in this review for the generalized (local) urban case 

study (see section 3.4.3.3.2), we agree with the previous characterization. As would be expected 

by the use of interpolation, the newly derived estimates are consistent with the estimates for 

similar air quality scenarios that were available in the last review. 

4.2.3 CASAC Advice 

In our consideration of the adequacy of the current standard, in addition to the evidenceand risk/exposure-based information discussed above, we have also considered the advice and 

recommendations of CASAC, based on their review of the ISA, the REA Planning Document, 

and the earlier draft of this document, as well as comments from the public on the earlier draft of 

this document. 

A limited number of public comments have been received on this review to date, 

including comments focused on the draft IRP, the draft REA Planning Document or the draft PA. 

Of the three commenters that addressed adequacy of the current primary Pb standard, two are in 

agreement with staff conclusions in the draft PA. A third expressed the view that the standard 

 

9

 We note that the value of the upper bound is influenced by risk associated with exposure pathways that 

were not varied with alternative standard levels, a modeling limitation with the potential to contribute to 

overestimation of the upper bound with air quality scenarios involving air Pb levels below current conditions for the 

study area (see sections 3.4.4 and 3.4.7 above). 
4-27 

should be revised to be more restrictive given the evidence of Pb effects in populations with 

mean blood Pb levels below 10 μg/dL.10 

In their comments on the draft PA, the CASAC Pb Panel concurred with staff’s overall 

preliminary conclusions that it is appropriate to consider retaining the current primary standard 

without revision, stating that “the current scientific literature does not support a revision to the 

Primary Lead (Pb) National Ambient Air Quality Standard (NAAQS)” (Frey, 2013). They 

further noted that “[a]lthough the current review incorporates a substantial body of new scientific 

literature, the new literature does not justify a revision to the standards because it does not 

significantly reduce substantial data gaps and uncertainties (e.g., air-blood Pb relationship at low 

levels; sources contributing to current population blood Pb levels, especially in children; the 

relationship between Pb and childhood neurocognitive function at current population exposure 

levels; the relationship between ambient air Pb and outdoor dust and surface soil Pb 

concentrations)”. In recognition of these limitations in the available information, the CASAC 

provided recommendations on research to address these data gaps and uncertainties so as to 

inform future Pb NAAQS reviews (Frey, 2013). 

The CASAC comments indicated agreements with key aspects of staff’s consideration of 

the exposure/risk information and currently available evidence in this review (Frey, 2013, 

Consensus Response to Charge Questions, p. 7). 

The use of exposure/risk information from the previous Pb NAAQS review 

appears appropriate given the absence of significant new information that could 

fundamentally change the interpretation of the exposure/risk information. This 

interpretation is reasonable given that information supporting the current 

standard is largely unchanged since the current standard was issued. 

The CASAC agrees that the adverse impact of low levels of Pb exposure on 

neurocognitive function and development in children remains the most sensitive 

health endpoint, and that a primary Pb NAAQS designed to protect against that 

effect will offer satisfactory protection against the many other health impacts 

associated with Pb exposure. 

The CASAC concurs with the draft PA that the scientific findings pertaining to 

air-to-blood Pb ratios and the C-R relationships between blood Pb and childhood 

IQ decrements that formed the basis of the current Pb NAAQS remain valid and 

are consistent with current data. 

The CASAC concurred with the appropriateness of the application of the evidence-based 

framework from the last Pb NAAQS review. With regard to the key inputs to that framework, 

CASAC concluded that “[t]he new literature published since the previous review provides 

 

10 All written comments submitted to the Agency will be available in the docket for this rulemaking, as will 

be transcripts of the public meetings held in conjunction with CASAC’s review of the earlier draft of this document, 

of the REA Planning Document and of drafts of the ISA. 
4-28 

further support for the health effect conclusions presented in that review” and that the studies 

newly available in this review “do not fundamentally alter the uncertainties for air-to-blood 

ratios or C-R functions for IQ decrements in young children (Frey, 2013, Consensus Response to 

Charge Questions, p. 6). 

The comments from CASAC took note of the uncertainties that remain in this review, 

which contribute to the uncertainties associated with drawing conclusions regarding air-related 

exposures and associated health risk at or below the level of the current standard (Frey, 2013, 

Consensus Response to Charge Questions, p. 6). 

This draft PA is constrained by the absence of new observational and 

experimental data that address, at least in part, limitations and uncertainties in 

the evidence that was present at the time of the last update of the Pb NAAQS. 

Until evidence is available to assess Pb exposure and health risks related to air 

Pb levels reflecting the current standard, a substantive refinement and update of 

the PA will not be possible. The obvious uncertainty underlying evaluation of this 

PA is whether lowering the standard would (or would not) impact exposure and 

thus risk. The CASAC agrees with the EPA conclusion that “there is appreciable 

uncertainty associated with drawing conclusions regarding whether there would 

be reductions in blood Pb levels from alternative lower levels as compared to the 

level of the current standard.” 

4.3 STAFF CONCLUSIONS ON THE PRIMARY STANDARD 

This section describes staff conclusions regarding adequacy of the current primary Pb 

standard. These conclusions are based on considerations described above and in the discussion 

below regarding the currently available scientific evidence summarized in the ISA and prior CDs 

and the risk and exposure information drawn from the 2007 REA. Further, these staff 

conclusions have taken into account advice from CASAC and public comment on the draft PA 

and preliminary staff conclusions. 

Taking into consideration the discussions responding to specific questions above in this 

and the prior chapter, this section addresses the following overarching policy question. 

 Does the currently available scientific evidence- and exposure/risk-based 

information, as reflected in the ISA and REA, support or call into question the 

adequacy of the protection afforded by the current Pb standard? 

Our response to this question takes into consideration the discussions responding to the 

specific policy-relevant questions in prior sections of this document (see sections 3.1-3.4, 4.2.1, 

and 4.2.2). In so doing, we focus first on consideration of the evidence, including that newly 

available in this review, and the extent to which it alters key conclusions supporting the current 

standard. We then turn to consideration of the quantitative risk estimates drawn from the 2007 

REA and associated limitations and uncertainties. We additionally consider the public health 

policy judgments and judgments about the uncertainties inherent in the scientific evidence and 
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quantitative analyses that are inherent in decisions on the adequacy of the current primary Pb 

standard. 

We first recognize the complexity involved in considering the adequacy of protection in 

the case of the primary Pb standard, which differs substantially from that involved in 

consideration of the NAAQS for other pollutants. Unlike the case for Pb, the other pollutants for 

which NAAQS are set involve only inhalation exposure pathways, a relatively simpler context.11 

In addition, generally an important component of the scientific evidence base considered in 

reviewing the adequacy of NAAQS for other pollutants is the availability of studies that have 

investigated associations between current concentrations of the pollutant in ambient air 

(including in circumstances where the current standard is met) and the occurrence of health 

effects judged plausibly related to ambient air exposure to the NAAQS pollutant. While such 

studies, targeting locations near air Pb sources such as smelters, were available at the time the Pb 

NAAQS was initially set in 1978, and to a much more limited degree at the time of the last 

review, such studies of health effects under air quality conditions near those reflecting the 

current standard are not available in this review. Rather, the evidence base that supports our 

conclusions in this review includes most prominently epidemiological studies reporting 

associations of blood Pb levels in U.S. populations, including the particularly at-risk population 

of young children with health effects judged plausibly related to Pb exposures. Support for our 

conclusions regarding the plausibility for ambient air Pb to play a role in such findings derives, 

in part, from studies linking Pb in ambient air with the occurrence of health effects. However, 

such studies (dating from the past or from other countries) involve ambient air Pb concentrations 

many times greater than those that would meet the current standard. Thus, in considering the 

adequacy of the current Pb standard, rather than considering studies that have investigated 

current concentrations of Pb in ambient air (including in locations where the current standard is 

met) and the occurrence of health effects, we primarily consider the evidence for, and risk 

estimated from, models based upon key relationships, such as those between ambient air Pb, Pb 

exposure, blood Pb and health effects. This evidence, with its associated limitations and 

uncertainties, contributes to our conclusions regarding a relationship between ambient air Pb 

conditions under the current standard and health effects. 

In considering the currently available evidence, staff gives great weight to the longstanding body of evidence on the health effects of Pb, augmented in some aspects since the last 

review, which continues to support identification of neurocognitive effects in young children as 

 

11 As described in sections 1.3 and 3.1 above, exposure to Pb from ambient air, unlike exposures for other 

NAAQS pollutants, involves both ingestion and inhalation 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). 
4-30 

the most sensitive endpoint associated with Pb exposure, as discussed in sections 3.2 and 3.3 

above. The evidence continues to indicate that a standard that provides protection from 

neurocognitive effects in young children additionally provides protection for other health effects 

of Pb, such as cardiovascular effects later in life. Application of the evidence-based, air-related 

IQ loss framework, developed in the last review, continues to provide a useful approach for 

considering and integrating the evidence on relationships between Pb in ambient air and Pb in 

children’s blood and risks of neurocognitive effects (IQ loss). The currently available evidence 

base, while somewhat expanded since the last review, is not appreciably expanded or supportive 

of appreciably different conclusions with regard to air-to-blood ratios (section 3.1 above) or C-R 

functions for neurocognitive decrements (section 3.2 above) in young children. 

As in the last review, uncertainties remain in our understanding of important aspects of 

ambient air Pb exposure and associated health effects. For example, important uncertainties 

remain, both with regard to air-to-blood ratios that reflect the relationship between 

concentrations of Pb in ambient air and air-related Pb in children’s blood, and with regard to 

estimates of the slope of the C-R function for neurocognitive impacts (IQ loss) at lower blood Pb 

levels. With regard to the former, we note particularly the limitations associated with the 

available studies and gaps in the evidence base with regard to studies that have investigated such 

quantitative relationships under conditions pertaining to the current standard (e.g., in localized 

areas near air Pb sources where the standard is met in the U.S. today). Further, in considering 

our reliance on the evidence in performing quantitative modeling of exposure and risk we 

additionally note important uncertainties associated with relationships between ambient air Pb 

and outdoor soil/dust Pb and indoor dust Pb that particularly affect our quantitative estimates of 

air-related risk under conditions of lower ambient air Pb concentrations and lower blood Pb 

levels (73 FR 66981). These critical exposure pathways are also inherent in the evidence-based 

air-related IQ loss framework, encompassed within the estimates of air-to-blood ratios. Thus, we 

recognize uncertainties related to our understanding of these and other processes that also 

contribute uncertainty to our application of the evidence-based framework. We consider this 

uncertainty to be greater with application of the framework for levels below the current standard 

given the weaker linkage with existing evidence, as noted below. 

We additionally take note of the role of public health policy judgments in considering the 

evidence-based framework and the exposure/risk information to inform the Administrator’s 

decision in 2008 to set the current standard, as summarized in section 4.1.1.2 above. We 

recognize that public health policy judgments always play an important role in each NAAQS 

review for each pollutant. One type of public health policy judgment focuses on how to consider 

the nature and magnitude of the array of uncertainties that are inherent in the scientific evidence 

and analyses. These judgments are traditionally made with a recognition that our understanding 
4-31 

of the relationships between the presence of a pollutant in ambient air and associated health 

effects is based on a broad body of information encompassing not only more established aspects 

of the evidence but also aspects in which there may be substantial uncertainty. In the case of the 

Pb NAAQS review, we recognize increased uncertainty in characterizing the relationship of 

effects on IQ with blood Pb levels below those represented in the evidence base. We also 

recognize increased uncertainty in projecting the magnitude of blood Pb response to ambient air 

Pb concentrations at and below the level of the current standard. We recognize this increased 

uncertainty particularly in light of the multiple factors that play a role in such a projection (e.g., 

meteorology, atmospheric dispersion and deposition, human physiology and behavior), for each 

of which we recognize attendant uncertainties. Collectively, these aspects of the evidence and 

associated uncertainties contribute to a recognition that for Pb, as for other pollutants, the 

available health effects evidence generally reflects a continuum, consisting of levels at which 

scientists generally agree that health effects are likely to occur, through lower levels at which the 

likelihood and magnitude of the response become increasingly uncertain. 

Reviews may also require judgments as to the point at which health effects become 

important from a public health perspective. In the case of Pb, such a judgment includes 

consideration of the public health significance of one to two points IQ loss in at-risk populations, 

such as young children, in light of associated uncertainties. This type of judgment also includes 

consideration of the IQ loss estimates yielded by the air-related IQ loss evidence-based 

framework for specific combinations of standard level, air-to-blood ratio and C-R function. 

With regard to public health significance of one to two points IQ loss in young children, staff 

gives weight to the comments of CASAC and some public commenters in the last review which 

recognized such a magnitude of IQ loss to be of public health significance and recommended 

that a very high percentage of the population be protected from such a magnitude of IQ loss (73 

FR 67000).12 With this objective in mind, we consider the extent to which the air-related IQ loss 

evidence-based framework informs consideration of standards that might be concluded to 

provide such a level of protection. In so doing, we first recognize that the IQ loss estimates 

produced with the evidence-based framework do not correspond to a specific quantitative public 

health policy goal for air-related IQ loss that would be acceptable or unacceptable for the entire 

population of children in the U.S. Rather, the conceptual context for the evidence-based 

framework is that it provides estimates for the mean air-related IQ loss of a subset of the 

population of U.S. children (i.e., the subset living in close proximity to air Pb sources that 

 

12 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 4.3.2; 2006 CD, sections 6.2.2 and 8.4.2). Use of IQ in this 

framework is thus considered to appropriately also reflect neurocognitive effects more generally. 
4-32 

contributed to elevated air Pb concentrations that equal the current level of the standard). This is 

the subset expected to experience air-related Pb exposures at the high end of the national 

distribution of such exposures. The associated mean IQ loss estimate is the average for this 

highly exposed subset and is not the average air-related IQ loss projected for the entire U.S. 

population of children. Further, we recognize uncertainties associated with those estimates, 

which increase with estimates associated with successively lower standard levels. 

For the current standard level of 0.15 μg/m3

, an air-to-blood ratio estimate of 7 μg/dL per 

μg/m3 (which we note as reasonably representative of the range supported by the evidence) and a 

C-R slope of -1.75 IQ points per μg/dL, the IQ loss estimate using the evidence-based 

framework is 1.8 points.13 As noted above, this value is considered to be an estimate, with 

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.14 As noted in section 4.2.2 above, 

our current information on numbers of young children living near monitors above or within 10% 

of the current Pb standard indicates the size of this population subset to be on the order of 2700 

children aged 5 years or younger, which would correspond to approximately one hundredth of 

one percent of the U.S. population of children of this age (estimated at approximately 24 million 

in 2010 census). A primary objective of the monitoring network for Pb is to identify and monitor 

sites of maximum concentration in areas anticipated to be at risk of exceeding the NAAQS. 

While we acknowledge the possibility that the monitoring data thus far available may not 

identify every occurrence of elevated Pb concentrations, the size of such a population subset can 

still be concluded to fall well below one tenth of one percent of the full population of children 

aged 5 years or younger in the U.S. today. Thus, we conclude that the current evidence, as 

considered within the conceptual and quantitative context of the evidence-based framework, and 

current air monitoring information indicates that the current standard would be expected to 

achieve the public health policy goal recommended by CASAC in the last Pb NAAQS review 

that IQ loss on the order of one to two IQ points be “prevented in all but a small percentile of the 

population” (73 FR 67000). 

In drawing conclusions from application of the evidence-based framework with regard to 

adequacy of the current standard, we further recognize the degree to which IQ loss estimates 

 

13 Using an air-to-blood ratio estimate of 8 μg/dL per μg/m3

 yields a similar, but just slightly higher IQ loss 

estimate (of approximately 2 IQ points). 14 In giving weight to consideration of the evidence within the context of the air-related IQ loss evidencebased framework, we note that the air-related IQ loss 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. 
4-33 

drawn from the air-related IQ loss evidence-based framework reflect mean blood Pb levels 

below those represented in the currently available evidence for young children. For example, in 

the case of the current standard level of 0.15 μg/m3

, multiplication by the air-to-blood ratio of 7 

yields a mean air-related blood Pb level of 1.05 μg/dL, which is half the level of the lowest blood 

Pb subgroup of pre-school children in which neurocognitive effects have been observed (Table 

3-2 above; Miranda et al., 2009) and well below the means of subgroups for which continuous CR functions have been estimated (Table 3-3 above).15 Such an extension below the lowest 

studied levels may be viewed as appropriate given the lack of identified blood Pb level threshold 

in the current evidence base for neurocognitive effects and the need for the NAAQS to provide a 

margin of safety.16 We note, however, that the framework IQ loss estimates for still lower 

potential standard levels represent still greater extrapolations from the current evidence base with 

corresponding increased uncertainty. 

In recognition of the role of public health policy judgments in drawing conclusions as to 

adequacy of the Pb NAAQS, we consider the availability of new information or new commonly 

accepted guidelines or criteria within the public health community with regard to the public 

health significance of specific IQ decrements in exposed, at-risk populations that might inform 

public health policy judgments on the appropriate degree of public health protection that should 

be afforded to protect against risk of such neurocognitive effects in at-risk populations,17 such as 

children living near air Pb sources. As an initial matter, we note that no such new information, 

guidelines or criteria are described in the ISA. In further considering the occurrence of any new 

actions by public health agencies that might indicate the availability of new information, 

 

15 We recognize that children also have Pb in their blood derived from other (nonair) sources. The 

evidence-based air-related IQ loss 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 neurocognitive risk per increment of 

blood Pb is greater for children with the lowest blood Pb levels, as noted in section 3.2 above. Since the evidence 

indicates Pb exposure to pose the greatest risk on an incremental basis at lower blood Pb levels, the focus on 

estimating IQ loss attributable solely to air-related lead (i.e., assuming the presence of no other blood Pb) is a 

conservative approach, the use of which contributes to the margin of safety provided by the standard. 16 As noted in section 1.2.1 above, the requirement 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. 17The 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. 
4-34 

guidelines or criteria for interpreting public health significance of such effects, we note that the 

CDC has revised the blood Pb level used to prioritize young children for whom they recommend 

particular follow-up health-protective actions, as summarized in section 3.1 above.18 The CDC 

decision, while emphasizing the critical importance of primary prevention of Pb exposure, 

provides no new guidelines or criteria with regard to the significance of specific IQ decrements 

or judgments on appropriate public health protection from risk of neurocognitive effects, and 

their consideration of the evidence base at the time of their decision does not substantively differ 

from that presented in the ISA (CDC, 2012). Thus, we are aware of no new information or new 

commonly accepted guidelines or criteria within the public health community for interpreting 

public health significance of neurocognitive effects in the context of a decision on adequacy of 

the current Pb standard. 

With respect to exposure/risk-based considerations, we recognize the complexity of the 

REA modeling analyses and the associated limitations and uncertainties. We additionally note 

the differences among the case studies included in the REA and the extent to which they inform 

our understanding of different aspects of the risk associated with air-related Pb in the U.S. For 

example, the location-specific case studies indicate the distribution of population risk in urban 

areas with differing types of Pb sources and gradients in air Pb concentrations as well as in 

population density, while the generalized urban (local) case study indicates the magnitude of airrelated risk associated with those specific localized circumstances where air concentrations just 

meet the Pb standard (regardless of source type). We agree with conclusions drawn in the 2008 

review that the quantitative risk estimates, with a focus on those for the generalized (local) urban 

case study, are “roughly consistent with and generally supportive” of estimates from the 

evidence-based air-related IQ loss framework (73 FR 67006). We further take note of the 

increasing uncertainty recognized for air quality scenarios involving air Pb concentrations 

increasingly below the current conditions for each case study, recognizing that such uncertainty 

is due in part to modeling limitations deriving from uncertainty regarding relationships between 

ambient air Pb and outdoor soil/dust Pb and indoor dust Pb (as noted in section 3.4 above). 

Based on the above considerations and with consideration of advice from CASAC, we 

reach the conclusion that the current body of evidence, in combination with the exposure/risk 

information, supports a primary standard as protective as the current standard. Further 

consideration of the evidence and exposure/risk information available in this review and its 

attendant uncertainties and limitations, advice from CASAC and consideration of the availability 

of other information that might also inform public health policy judgments by the Administrator, 

leads us to reach the additional conclusion that it is appropriate to consider retaining the current 

 

18 Uses identified for the CDC reference level include is the identification of “ high-risk childhood 

populations and geographic areas most in need of primary prevention” (CDC, 2012). 
4-35 

standard without revision. We base these conclusions on consideration of the health effects 

evidence, including consideration of this evidence in the context of the evidence-based, airrelated IQ loss framework, and in combination with the exposure/risk information (chapter 3 and 

sections 4.2.1 and 4.2.2 above) and the uncertainties attendant with both. In so doing, we 

recognize the complexities and limitations in the evidence base in reaching conclusions 

regarding the magnitude of risk associated with the current standard, as well as the increasing 

uncertainty of risk estimates for lower air Pb concentrations. Based on these considerations, 

these conclusions also recognize what may be considered reasonable judgments on the public 

health implications of the blood Pb levels and risk estimated for air-related Pb under the current 

standard, including the public health significance of the Pb effects being considered, as well as 

aspects of the use of the evidence-based framework that may be considered to contribute to the 

margin of safety. 

In reaching these conclusions, we additionally note that different public health policy 

judgments could lead to different conclusions regarding the extent to which the current standard 

provides protection of public health with an adequate margin of safety. Such public health 

policy judgments include those related to the appropriate degree of public health protection that 

should be afforded to protect against risk of neurocognitive effects in at-risk populations, such as 

IQ loss in young children, as well as with regard to the appropriate weight to be given to 

differing aspects of the evidence and exposure/risk information, and how to consider their 

associated uncertainties. For example, different judgments might give greater weight to more 

uncertain aspects of the evidence or reflect a differing view with regard to margin of safety. As 

noted in section 4.1 above, in establishing primary standards under the Act that, in the 

Administrator’s judgment, are requisite to protect public health with an adequate margin of 

safety, the Administrator seeks to establish standards that are neither more nor less stringent than 

necessary for this purpose. The Act does not require that primary standards be set at a zero-risk 

level, but rather at a level that avoids unacceptable risks to public health, even if the risk is not 

precisely identified as to nature or degree. The requirement that primary standards provide an 

adequate margin of safety was intended to 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 from hazards that research has not yet identified. 

In this context, we recognize that the uncertainties and limitations associated with the 

many aspects of the estimated relationships between air Pb concentrations and blood Pb levels 

and associated health effects are amplified with consideration of increasingly lower air 

concentrations. We believe the current evidence supports the conclusion that the current 

standard is requisite to protect public health with an adequate margin of safety. In staff’s view, 

with which CASAC has agreed (Frey, 2013, p. 6) based on the current evidence, there is 
4-36 

appreciable uncertainty associated with drawing conclusions regarding whether there would be 

reductions in blood Pb levels and risk to public health from alternative lower levels of the 

standard as compared to the level of the current standard. Thus, we conclude that the basis for 

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

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

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

In summary, the newly available health effects evidence, critically assessed in the ISA as 

part of the full body of evidence, reaffirms conclusions on the broad array of effects recognized 

for Pb in the last review. Further, we observe the general consistency of the current evidence 

with the evidence available in the last review with regard to key aspects on which the current 

standard is based, including those particular to the evidence-based framework developed in the 

last review. We additionally observe that quantitative risk estimates associated with the current 

standard, based on the risk assessment performed in the last review, indicate a level of risk 

generally consistent with conclusions drawn from the evidence using the evidence-based 

framework. In so doing, we also recognize the limitations and uncertainties associated with the 

currently available information. These considerations and the advice from CASAC provide the 

basis for the staff conclusion that consideration should be given to retaining the current standard, 

without revision. In light of this conclusion, we have not identified any potential alternative 

standards for consideration in this review. 

4.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA 

COLLECTION 

In this section, we highlight key uncertainties associated with reviewing and establishing 

NAAQS for Pb. Such key uncertainties and areas for future health-related research, model 

development, and data gathering are outlined below. In some cases, research in these areas can 

go beyond aiding standard setting to aiding in the development of more efficient and effective 

control strategies. We note, however, that a full set of research recommendations to meet 

standards implementation and strategy development needs is beyond the scope of this discussion. 

Rather, listed below are key uncertainties and research questions and data gaps that have been 

thus far highlighted in this review of the health-based primary standard. 

 A critical aspect of our consideration of the evidence and the quantitative risk assessment 

in this review is our understanding of the C-R relationship between blood Pb levels in 

young children and neurodevelopmental effects, specifically IQ decrement. An important 

area of uncertainty in the Pb NAAQS review concerns interpretation of neurocognitive 

impact risks and the shape of the C-R relationship at blood Pb levels similar to and below 

those common in today’s U.S. young child population. Accordingly, additional 

epidemiological research involving substantially sized populations with mean blood Pb 

levels closer to those common in today’s population of young children, particularly those 
4-37 

less affected by higher Pb exposures earlier in childhood, would help to reduce 

uncertainty in our estimates of IQ decrement associated with these lower blood Pb levels 

and, accordingly, in characterizing Pb health effects. 

 Key uncertainties with regard to other aspects of the health effects evidence include the 

following. 

 There remains uncertainty in the evidence base with regard to the exposure 

circumstances (pre- and postnatal timing, duration, magnitude and frequency) 

eliciting effects in older children and adults. Effects of particular focus include 

effects on the nervous system later in life, cardiovascular function, and delayed 

onset of puberty. 

 Alzheimer’s-like pathology has been reported in aged laboratory animals (nonhuman primates and rodents) exposed to Pb early in life. Uncertainty remains, 

however, regarding the relationships of such pathology with altered function or 

behavior. 

 Epidemiological studies indicate detrimental effects of Pb on sperm production 

and quality, often in occupational cohorts. Uncertainty remains regarding these 

effects in otherwise healthy cohorts without occupational Pb exposure or other 

underlying medical conditions. 

 An additional area of uncertainty is that related to the inverse association 

observed in some studies between low blood Pb and renal function. 

 A key consideration in the Pb NAAQS review concerns the relationship between air Pb 

concentrations and blood Pb levels, most particularly those in young children. Our 

quantitative estimation of blood Pb levels in response to various exposure circumstances, 

including air-related exposure pathways associated with current ambient air Pb 

concentrations, would benefit from research into this relationship. 

 Information is limited with regard to the temporal aspects of the relationship 

between ambient air Pb and levels of air-related Pb in blood in young children, 

and our understanding of the factors influencing this relationship is incomplete, 

particularly in the Pb exposure circumstances common in the U.S. today. 

 Important aspects of (or influence on) the air-to-blood relationship include the 

relationships (1) between ambient air Pb and outdoor dust and surface soil Pb 

concentrations and (2) between ambient air Pb and indoor dust Pb. Additional 

information would help to reduce uncertainty in our understanding of these 

relationships and in models and methods used to characterize these pathways in 

future reviews. Specific mechanistic aspects for indoor dust modeling include air 

exchange rates, home cleaning frequency and efficiency, among other factors. 

The impact of changes in ambient air Pb on Pb in indoor dust, outdoor dust and 

soil, including the temporal dynamics of these relationships, and variations for 

different environments, are important aspects of the Pb NAAQS review, yet 

current information on multiple aspects of these pathways is limited. 

 There is appreciable uncertainty regarding the magnitude of the contribution of 

air-related Pb to diet. Additional information is needed regarding sources of Pb to 
4-38 

the diet of different age groups of the U.S. population, including particularly those 

sources that relate to current ambient air Pb, as well as those related to the legacy 

of historic ambient air Pb emissions. 

 Information is lacking on toxicokinetics of Pb during adolescence which could 

inform interpretation of epidemiological studies of relationships between blood 

Pb and health effects in this lifestage. 

 Future quantitative blood Pb modeling would benefit from additional research into 

several aspects of population blood Pb levels, including contributing exposure pathways. 

Examples include: 

 Interindividual variability in blood Pb levels and methods for characterizing 

interindividual variability, including consideration of both empirical and 

mechanistic methods; 

 Apportionment of blood Pb levels with regard to exposure pathway contributions, 

with particular focus on understanding exposure pathways and sources that cause 

the more elevated blood Pb levels among children today, as well as those related 

to ambient air Pb; and 

 Blood Pb model performance evaluations, with emphasis on applications 

pertaining to blood Pb response to ambient air-related pathways and responses to 

changes in exposures for those pathways. 

 An understanding of the spatial gradient of ambient air Pb concentrations and associated 

particle sizes in urban residential areas, as well as near Pb sources, is an important aspect 

to our implementation of the NAAQS for Pb and a key element in assessing exposure and 

risk. Additional research in this area is needed. Current limitations in this area 

additionally contribute uncertainty to characterization of ambient air Pb levels in the risk 

assessment and the resulting exposure and risk estimates. Research in the 

characterization of spatial variation in ambient air Pb concentrations in different 

environments and related to different air sources would help to reduce this uncertainty. 

The potential for systematic trends in the relationship between ambient air Pb 

concentrations and distribution of urban residential populations is of interest. Example 

locations of interest include neighborhoods downwind of airports with substantial leaded 

aviation gasoline usage, as well as those in the vicinity of older roads with a substantial 

historical use of leaded gasoline, including inner city neighborhoods (with and without 

substantial reconstruction). 

 Another area of uncertainty relates to our understanding of concentrations of relatively 

larger airborne particles carrying Pb that occur in areas near sources and where exposure 

may occur. 
4-39 

4.5 REFERENCES 

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

349: 500. 

Canfield, R. L.; Henderson, C. R., Jr.; Cory-Slechta, D. A.; Cox, C.; Jusko, T. A.; Lanphear, B. P. (2003) 

Intellectual impairment in children with blood lead concentrations below 10 μg per deciliter. N. Engl. J. 

Med. 348: 1517-1526. 

Centers for Disease Control and Prevention (2012) CDC Response to Advisory Committee on Childhood Lead 

Poisoning Prevention Recommendations in “Low Level Lead Exposure Harms Children: A Renewed Call 

of Primary Prevention”. Atlanta, GA: U.S. Department of Health and Human Services, Public Health 

Service. June 7. 

Frey, H.C. (2013) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee and Clean 

Air Scientific Advisory Committee Lead Review Panel, to Acting Administrator Bob Perciasepe. Re: 

CASAC Review of the EPA’s Policy Assessment for Lead (External Review Draft – January 2013). June 4, 

2013. 

Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

the 1st Draft Lead Staff Paper and Draft Lead Exposure and Risk Assessments. March 27, 2007. 

Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

the 2nd Draft Lead Human Exposure and Health Risk Assessments. September 27, 2007. 

Henderson, R. (2008a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

the Advance Notice of Proposed Rulemaking (ANPR) for the NAAQS for lead. January 22, 2008. 

Henderson, R. (2008b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

the Notice of Proposed Rulemaking for the NAAQS for lead. July 18, 2008. 

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

58. 

Lanphear, B. P.; Hornung, R.; Khoury, J.; Yolton, K.; Baghurst, P.; Bellinger, D. C.; Canfield, R. L.; Dietrich, K. 

N.; Bornschein, R.; Greene, T.; Rothenberg, S. J.; Needleman, H. L.; Schnaas, L.; Wasserman, G.; 

Graziano, J.; Roberts, R. (2005) Low-level environmental lead exposure and children's intellectual 

function: an international pooled analysis. Environ. Health Perspect. 113: 894-899. 

Téllez-Rojo, M. M.; Bellinger, D. C.; Arroyo-Quiroz, C.; Lamadrid-Figueroa, H.; Mercado-García, A.; SchnaasArrieta, L.; Wright, R. O.; Hernández-Avila, M.; Hu, H. (2006) Longitudinal associations between blood 

lead concentrations < 10 μg/dL and neurobehavioral development in environmentally-exposed children in 

Mexico City. Pediatrics 118: e323-e330. 

U.S. Environmental Protection Agency. (2006) Air Quality Criteria for Lead. Washington, DC, EPA/600/R5/144aF. Available online at: www.epa.gov/ncea/

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

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

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

014a and EPA-452/R-07-014b. 
4-40 

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

Policy Assessment of Scientific and Technical Information, OAQPS Staff Paper. EPA-452/R-07-013. 

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

U.S. Environmental Protection Agency. (2013) Integrated Science Assessment for Lead. Washington, DC, 

EPA/600/R-10/075F. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_2010_isa.html 
5-1 

5 WELFARE EFFECTS AND EXPOSURE/RISK INFORMATION 

This chapter presents key aspects of the current evidence of Pb-related welfare effects 

and presents exposure and risk information from the last review in the context of the currently 

available information. Staff has drawn from the EPA’s synthesis of the scientific evidence 

presented in the Integrated Science Assessment for Lead (USEPA, 2013; henceforth referred to 

as the ISA) and the 2006 Air Quality Criteria Document for Lead (USEPA, 2006a; henceforth 

referred to as the 2006 CD) and from the screening level risk assessment performed in the last 

review and described in Lead Human Exposure and Health Risk Assessments and Ecological 

Risk Assessment for Selected Areas. Pilot Phase (documented in ICF International, 2006; 

henceforth referred to as the 2006 REA). This chapter is organized into two sections regarding 

the currently available welfare effects evidence (section 5.1) and the exposure and risk 

information (section 5.2) interpreted in light of currently available evidence. Presentation within 

these sections is organized to address key policy-relevant questions for this review concerning 

the evidence and exposure/risk information, building upon the questions included in the 

Integrated Review Plan (IRP, section 3.2). 

5.1 WELFARE EFFECTS INFORMATION 

Lead has been demonstrated to have harmful effects on reproduction and development, 

growth, and survival in many species as described in the assessment of the evidence available in 

this review and consistent with the conclusions drawn in the last review (ISA, section 1.7; 2006 

CD). A number of studies on ecological effects of Pb are newly available in this review and are 

critically assessed in the ISA as part of the full body of evidence. The full body of currently 

available evidence reaffirms conclusions on the array of effects recognized for Pb in the last 

review (ISA, section 1.7). In so doing, in the context of pollutant exposures considered 

relevant,1

 the ISA determines2 that causal3 or likely causal4 relationships exist in both freshwater 

 

1

 With regard to consideration of pollutant exposures for studies included in the ISA, the ISA states the 

following (ISA, pp. lx-lxi). 

In drawing judgments regarding causality for the criteria air pollutants, the ISA focuses on evidence of 

effects in the range of relevant pollutant exposures or doses, and not on determination of causality at 

any dose. Emphasis is placed on evidence of effects at doses (e.g., blood Pb concentration) or 

exposures (e.g., air concentrations) that are relevant to, or somewhat above, those currently 

experienced by the population. The extent to which studies of higher concentrations are considered 

varies by pollutant and major outcome category, but generally includes those with doses or exposures 

in the range of one to two orders of magnitude above current or ambient conditions. Studies that use 

higher doses or exposures may also be considered to the extent that they provide useful information to 

inform understanding of mode of action, interspecies differences, or factors that may increase risk of 

effects for a population. Thus, a causality determination is based on weight of evidence evaluation for 

health, ecological or welfare effects, focusing on the evidence from exposures or doses generally 

ranging from current levels to one or two orders of magnitude above current levels.
5-2 

and terrestrial ecosystems for Pb with effects on reproduction and development in vertebrates 

and invertebrates; growth in plants and invertebrates; and survival in vertebrates and 

invertebrates (ISA, table 1-3). Although considerable uncertainties are recognized in 

generalizing effects observed under particular, small-scale conditions, up to the ecosystem level 

of biological organization, the ISA determines that the cumulative evidence reported for Pb 

effects at higher levels of biological organization and for the above described population-level 

endpoints is sufficient to conclude that a causal relationship is likely to exist between Pb 

exposures and community and ecosystem-level effects in freshwater and terrestrial systems (ISA, 

section 1.7.3.7). The ISA also presents evidence for saltwater ecosystems, concluding that 

current evidence is inadequate to make causality determinations for most population-level 

responses, as well as community and ecosystem effects, while finding the evidence to be 

suggestive linking Pb and effects on reproduction and development in marine invertebrates (ISA, 

Table 1-3, section 6.3.12 and section 6.4.21). 

Based on the extensive assessment of the full body of evidence available in this review, 

the major conclusions drawn by the ISA regarding ecological effects of Pb include the following 

(ISA, Executive Summary, p. xcvi). 

With regard to the ecological effects of Pb, uptake of Pb into fauna and 

subsequent effects on reproduction, growth and survival are established and are 

further supported by more recent evidence. These may lead to effects at the 

population, community, and ecosystem level of biological organization. In both 

terrestrial and aquatic organisms, gradients in response are observed with 

increasing concentration of Pb and some studies report effects within the range of 

Pb detected in environmental media over the last several decades. Specifically, 

observations from controlled studies on reproduction, growth, and survival in 

sensitive freshwater invertebrates are well-characterized at concentrations at or 

near Pb concentrations occasionally encountered in U.S. fresh surface waters.... 

However, in natural environments, modifying factors affect Pb bioavailability and 

toxicity and there are considerable uncertainties associated with generalizing 

effects observed in controlled studies to effects at higher levels of biological 

organization. Furthermore, available studies on community and ecosystem-level 

 

2

 Since the last Pb NAAQS review, the ISAs which have replaced CDs in documenting each review of the 

scientific evidence (or air quality criteria) employ a systematic framework for weighing the evidence and describing 

associated conclusions with regard to causality, using established descriptors (“causal” relationship with relevant 

exposure, “likely” to be causal, evidence is “suggestive” of causality, “inadequate” evidence to infer causality, “not 

likely”) (ISA, Preamble). 3

 In determining that a causal relationship exists for Pb with specific ecological effects, EPA has concluded 

that “[e]vidence is sufficient to conclude that there is a causal relationship with relevant pollutant exposures (i.e., 

doses or exposures generally within one to two orders of magnitude of current levels)” (ISA, p. lxii) 4

 In determining a likely causal relationship exists for Pb with specific ecological effects, EPA has 

concluded that “[e]vidence is sufficient to conclude that there is a likely causal relationship with relevant pollutant 

exposures ... important uncertainties remain” (ISA, p. lxii). 
5-3 

effects are usually from contaminated areas where Pb concentrations are much 

higher than typically encountered in the environment. The contribution of 

atmospheric Pb to specific sites is not clear and the connection between air 

concentration of Pb and ecosystem exposure continues to be poorly 

characterized. Furthermore, the level at which Pb elicits a specific effect is 

difficult to establish in terrestrial and aquatic systems, due to the influence of 

other environmental variables (e.g., pH, organic matter) on both Pb 

bioavailability and toxicity, and also to substantial species differences in Pb 

sensitivity.

As in prior reviews of the Pb NAAQS, this review is focused on those effects most 

pertinent to ambient air Pb exposures. Given the reductions in ambient air Pb concentrations 

over the past decades, these effects are generally those associated with the lowest levels of Pb 

exposure that have been evaluated. Additionally, we recognize the limitations on our ability to 

draw conclusions about environmental exposures from ecological studies of organism-level 

effects, as most studies were conducted in laboratory settings which may not accurately represent 

field conditions or the multiple variables that govern exposure. 

Our consideration of welfare effects evidence in this review is framed by key policyrelevant questions drawn from those included in the IRP. In the following sections, we discuss 

the pathways by which Pb exposure occurs in ecosystems, the mechanisms that distribute Pb in 

the environment and the bioavailability of Pb in different ecosystems. Understanding the 

movement of Pb in the environment is important to understanding exposure and bioavailability 

and, thus, informs the subsequent discussion of the effects of Pb on terrestrial and aquatic 

ecosystems. Finally, we discuss the association of ambient air Pb with effects and the important 

role a “critical loads” approach5

 might play in assessing the overall ability of ecosystems to 

recover from past Pb exposures and the degree to which newly deposited Pb may affect 

ecosystem function and recovery. 

 To what extent has the newly available evidence altered our understanding of the 

movement and accumulation of air-deposited Pb through ecosystems over time? 

The extensive history of Pb uses in developed countries coupled with atmospheric 

transport processes has left a legacy of Pb in ecosystems globally (e.g., 1977 CD, section 6.3.1). 

Records of U.S. atmospheric emissions of Pb in the twentieth and late nineteenth centuries have 

been documented in sediment cores, as noted in section 2.3 above (ISA, section 2.6.2; Landers et 

 

5

 As discussed further in subsequent text of this section, the phrase “critical loads” is generally used to 

describe loading (i.e. addition of a pollutant) to a system that can occur without causing a critical impact, e.g., 

deposition rates of air pollutants that current knowledge indicates will not cause long-term adverse effects to 

ecosystem structure and function. A critical loads analysis approach takes into account what is known about the 

release of a specific chemical into the environment, its distribution and cycling within and across ecosystems and 

each ecosystem's sensitivity to the chemical (ISA, section 6.1.3). 
5-4 

al., 2010). Once deposited, Pb can be transported by stormwater runoff or resuspension to 

catchments and nearby waterbodies or stored in soil layers in forested areas, its further 

movement influenced by soil or sediment composition and chemistry and physical processes. 

Some new studies are available that provide additional information, briefly summarized below, 

on Pb cycling, flux and retention within terrestrial and aquatic systems. This new information 

does not fundamentally change our understanding from the last review of Pb movement through 

or accumulation in ecosystems over time but rather improves our understanding of some of the 

underlying processes and mechanisms in soil, water and sediment. There is little new 

information, however, on fate and transport in ecosystems specifically related to air-derived Pb 

(ISA, section 2.3). There is limited newly available information with regard to the timing of 

ecosystem recovery from historic atmospheric deposition of Pb. 

Overall, recent studies in terrestrial ecosystems provide deposition data consistent with 

deposition fluxes reported in the 2006 CD, and demonstrate consistently that atmospheric 

deposition of Pb has decreased since the phase-out of leaded on-road gasoline, as described in 

section 2.3.2.2 above (ISA, section 2.3.3). Follow-up studies in several locations at high 

elevation sites indicate little change in soil Pb concentrations since the phase-out of leaded onroad gasoline in surface soils, consistent with the high retention reportedly associated with 

reduced microbial activity at lower temperatures associated with high elevation sites. However, 

amounts of Pb in the surface soils at some lower altitude sites were reduced over the same time 

period in the same study (ISA, section 2.3.3). New studies in the ISA also enhance our 

understanding of Pb sequestration in forest soils by providing additional information on the role 

of leaf litter as a Pb reservoir in some situations and the effect of litter decomposition on Pb 

distribution (ISA, section 2.3.3). 

Recent research on Pb transport in aquatic systems has provided a large body of 

observations confirming that such transport is dominated by colloids rich in iron and organic 

material (ISA, section 2.3.2). Recent research on Pb flux in sediments provides greater detail on 

resuspension processes than was available in the 2006 CD, including research on resuspended Pb 

largely associated with organic material or iron and manganese particles and research on the 

important role played by anoxic or depleted oxygen environments in Pb cycling in aquatic 

systems. This newer research is consistent with prior evidence in indicating that appreciable 

resuspension and release from sediments largely occurs during discrete events related to storms. 

It has also confirmed that resuspension is an important process that strongly influences the 

lifetime of Pb in bodies of water. Finally, there have been advances in understanding and 

modeling of Pb partitioning between organic material and sediment in aquatic environments 

(ISA, section 2.7.2). 
5-5 

 In summary, the newly available evidence builds on our understanding of some specific 

aspects of processes involved in the movement and accumulation of Pb through ecosystems over 

time. The new information, however, does not substantially alter our overall understanding of 

the fate and transport of Pb in ecosystems or provide a broad quantitative understanding of U.S. 

ecosystem responses to atmospheric Pb deposition. 

 Does the newly available evidence further inform our understanding of the 

bioavailability of Pb in different types of ecosystems and organisms? 

As discussed in the ISA, bioavailability of Pb is an important component of 

understanding the effects Pb is likely to have on organisms and ecosystems (ISA, section 6.3.3). 

It is the amount of Pb that can interact within the organism that leads to toxicity, and there are 

many factors which govern this interaction (ISA, sections 6.2.1 and 6.3.3; USEPA, 2007a). The 

bioavailability of metals varies widely depending on the physical, chemical, and biological 

conditions under which an organism is exposed (USEPA, 2007a). In both aquatic and terrestrial 

systems, a primary factor influencing the bioavailability of Pb, as well as its fate and tranport is 

solubility (ISA, p. 6-63). Additionally important characteristics that affect bioavailability are 

(1) chemical form or species, (2) particle size, (3) lability, and (4) source. The bioavailability of a 

metal is also dependent upon the fraction of metal that is bioaccessible. The bioaccessible 

fraction of a metal is the portion (fraction or percentage) of environmentally available metal that 

actually interacts at the organism’s contact surface and is potentially available for absorption or 

adsorption by the organism (USEPA, 2007a; ISA, section 6.3.3). 

Studies newly available since the last Pb NAAQS review provide additional insight into 

factors that influence the bioavailability of Pb to specific organisms (ISA, section 6.3.3). In 

general, this evidence, briefly summarized below, is supportive of previous conclusions and does 

not identify significant new variables from those identified previously. Section 6.3.3 of the ISA 

provides a detailed discussion of bioavailability in terrestrial systems. With regard to aquatic 

systems, a detailed discussion of bioavailability in freshwater systems is provided in sections 

6.4.3 and 6.4.4 of the ISA, and section 6.4.14 of the ISA discusses bioavailability in saltwater 

systems. 

In terrestrial systems, the amount of bioavailable Pb present determines the impact of soil 

Pb to a much greater extent than does the total amount present (ISA, section 6.3.11). In such 

ecosystems, Pb is deposited either directly onto plant surfaces or onto soil where it can bind with 

organic matter or dissolve in pore water.6

 The Pb dissolved in pore water is particularly 

bioavailable to organisms in the soil and thereby influences the impact of soil Pb on terrestrial 

ecosystems to a much greater extent than the total amount of Pb present (ISA, section 6.3.11). 

 

6

 The term “pore water” refers to the water occupying the spaces among the grains of sediment or soil. 
5-6 

Several soil characteristics control the amount of Pb that is dissolved in pore water, and the ISA 

presents evidence that has advanced scientific understanding of some of these variables (ISA, 

section 6.4.21). Studies have shown that the two most important determinants of both Pb 

solubility and toxicity in soils are pH and cation exchange capacity (ISA, section 2.6.1). Also, 

evidence newly available in this review has confirmed the important influence of organic matter 

on Pb sequestration, leading to relatively longer retention in soils with higher organic matter 

content (ISA, section 2.6.1). When soils are amended with soluble metals, aging, both under 

natural conditions and simulated through leaching, reduces the bioavailability of Pb to plants and 

soil organisms (ISA, sections 6.3.2, 6.3.9 and 6.3.11; USEPA, 2007a). In general, soils with 

higher organic matter content have the capacity for greater retention of Pb in the soil matrix and 

lesser availability of Pb for release into pore water. Reduction in soil organic material, such as 

through decomposition, can contribute to subsequent increased availability of Pb (ISA, section 

6.3.9; 2006 CD, section 6.1.5). 

In aquatic systems as in terrestrial systems, the amount of Pb bioavailable to organisms is 

a better predictor of effect on organisms than the overall amount of Pb in the system. Once 

atmospherically derived Pb enters surface water bodies through deposition or runoff, its fate and 

bioavailability are influenced by many water quality characteristics, such as pH, suspended 

solids levels and organic content (ISA, section 6.4.2). In sediments, bioavailability of Pb to 

sediment-dwelling organisms may be influenced by the presence of other metals, sulfides, iron 

oxides and manganese oxides and also by physical disturbance (ISA, section 2.6.2). For many 

aquatic organisms Pb dissolved in the water column can be the primary exposure route, while for 

others sediment ingestion is significant (ISA, section 2.6.2). As recognized in the 2006 CD and 

further supported in the ISA, there is a body of evidence showing that uptake and elimination of 

Pb vary widely among aquatic species. 

Although in freshwater systems the presence of humic acid in dissolved organic material 

(DOM) is considered to reduce the bioavailable fraction of metals in the water column, there is 

evidence presented in the ISA that DOM does not have the same effect on free Pb ion 

concentration and toxicity in seawater (ISA, section 6.4.2). For example, the ISA discusses two 

new studies, performed in artificial seawater systems, that suggest that in saltwater, the presence 

of DOM increases (rather than decreases) uptake of Pb by mussel gill structures, potentially 

through the alteration of membrane permeability (ISA, section 6.4.2.4). These studies also 

investigated the individual roles of some DOM components. This recent evidence supports the 

conclusion from the last review that factors that modify bioavailability of Pb in saltwater 

environments are not identical to those in freshwater systems (ISA, section 6.4.14). 

The newly available evidence about bioavailability from experimental systems, briefly 

summarized above, builds on our fundamental understanding of Pb bioavailability in aquatic and 
5-7 

terrestrial systems and species from the last review. Bioavailability remains an important 

consideration in Pb toxicity and a significant source of uncertainty in relating ambient Pb and 

adverse effects. 

 Does the current evidence alter our conclusions from the previous review 

regarding the ecological effects associated with exposure to Pb? Does the newly 

available evidence indicate new exposure levels at which ecological systems or 

receptors are expected to experience effects? 

There is a substantial amount of new evidence in this review regarding the ecological 

effects of Pb on individual terrestrial and aquatic species. On the whole, this evidence supports 

previous conclusions that Pb has effects on growth, reproduction and survival, and that under 

some conditions these effects can be adverse to organisms and ecosystems. The ISA provides 

evidence of effects in additional species, and in a few cases, at lower exposures than reported in 

the previous review, but does not substantially alter our understanding of the ecological 

endpoints affected by Pb from the previous review. Looking beyond organism-level evidence, 

the evidence of adversity in natural systems remains sparse due to the difficulty in determining 

the effects of confounding factors such as co-occurring metals or system characteristics that 

influence bioavailability of Pb in field studies. The following is a brief comparison of the newly 

available evidence to evidence considered in the 2006 review. 

Terrestrial Ecosystems 

 The evidence available in the last review indicated a range of biological effects of Pb on 

terrestrial organisms that varied with type of organism and life stage, duration of exposure, form 

of Pb, and soil characteristics. New research since the 2006 CD has broadened our 

understanding of the evidence of damage to photosynthetic ability in plants exposed to Pb and 

provided additional evidence of oxidative stress in response to Pb exposure (ISA, section 6.3.4). 

For example, reactive oxygen species have been found to increase in plant tissue grown in Pbcontaminated soil, and, with increasing Pb exposure, the plant tissue responded with increased 

antioxidant activity (ISA, section 6.3.4). In addition, recent studies have reported reduced 

growth of plants with increased Pb concentration in soil in some experiments, as well as 

evidence of genotoxicity, decreased germination, and pollen sterility (ISA, section 6.3.4). 

 In terrestrial invertebrates, previous CDs have reported adverse effects of Pb on 

neurological and reproductive endpoints. Recently published studies have further explored the 

potential for neurotoxic action of Pb, albeit under artificial liquid media conditions (ISA, 

section 6.3.4.2). Increased mortality was found in recent studies of earthworms at 

concentrations similar to those in studies reviewed previously, with additional evidence 

indicating the strong dependence of effects on soil characteristics including pH, cation exchange 

capacity, and aging (ISA, section 6.3.4.2). There is also newly available evidence for adverse 
5-8 

effects in terrestrial snails and arthropods exposed through soil or diet (ISA, section 6.3.4.2). 

The effects vary with species and exposure conditions, and they include diminished growth and 

fecundity, endocrine and reproductive anomalies, and body deformities. Increasing 

concentration of Pb in the exposure medium generally resulted in increased effects within each 

study, but the relationship between concentration and effects is highly variable between studies, 

even when the same medium, e.g. soil, was used. Current evidence suggests that soil aging and 

pH are important modifiers of Pb toxicity in these studies (ISA, section 6.3.11). 

In terrestrial vertebrates, some new evidence is available for effects of Pb on amphibians 

and reptiles as well as birds.7

 Effects reported in reptiles and amphibians include decreased white 

blood cell counts, decreased testis weight, and behavioral anomalies (ISA, section 6.3.4.3). 

However, depending on various factors, studies report large differences in effects in different 

species at the same concentration of Pb in soil, and effects were generally smaller when fieldcollected soils were used. In some birds, recent studies have found maternal elevated blood Pb 

level to be associated with decreased hatching success, smaller clutch size, high corticosteroid 

level, and abnormal behavior in offspring. Studies on some species show little or no effect of 

elevated blood Pb level. Effects of dietary exposure have been studied in several mammalian 

species, with cognitive, endocrine, immunological, and growth effects observed (ISA, section 

6.3.11) in some studies. 

 Experimental evidence of organism-level effects presented in the ISA demonstrates that 

increased exposure to Pb is generally associated with increases in observed effects in terrestrial 

species (ISA, section 6.3.11). It also demonstrates that many factors, including the form of Pb 

and various soil physiochemical properties, influence the Pb concentration-response relationship 

(ISA, section 6.3.11). Further, results from amended soil exposures generally do not reflect the 

important effect of environmental aging on bioavailability and associated toxicity of such soil 

Pb amendments and therefore make interpretation of the results in an ecosystem context 

difficult. Given that in natural settings, these modifying factors are highly variable, the ISA 

notes that without quantitatively accounting for these factors, laboratory-derived 

“characterizations of exposure-response relationships would likely not be transferable outside of 

experimental settings” (ISA, section 1.7.1). Newly available soil invertebrate studies of 

multiple Pb concentrations in different soil systems also provide inconsistent results with 

respect to exposure-response relationships (ISA, sections 1.7.1 and 6.3.5). In consideration of 

these results, the ISA notes that “laboratory-amended artificial soils provide a poor model for 

predicting the toxicity of Pb-contaminated field soils, because aging and leaching processes, 

 

7

 Elevated blood and tissue concentrations of Pb reported in avian species in some areas have been 

indicated to be a result of nonair pathways, including ingestion of lead-containing materials such as paint chips in 

urban areas and Pb ammunition fragments in other areas (ISA, sections 6.3.3.3 and 6.3.4.3). 
5-9 

along with variations in physiochemical proterties ... influence metal bioavailability” (ISA, 

section 6.3.5) 

As reported in both the ISA and the 2006 CD, direct evidence for community- and 

ecosystem-level effects comes from locations near sources of Pb to the environment, where Pb 

concentrations are much higher than typically observed environmental concentrations and often 

derive from multiple sources to multiple media (e.g. soil, water, air). Impacts of Pb on terrestrial 

ecosystems near smelters, mines, and other industrial sources have been studied for several 

decades (ISA, section 6.3.12.7). Atmospheric emissions of Pb from smelting and other 

industrial activities are commonly accompanied by other trace metals (e.g., Zn, Cu, Cd) and 

SO2 that may cause toxic effects independently or in concert with Pb. Those impacts have been 

shown to include decreases in species diversity and changes in floral and faunal community 

composition in locations with histories of substantial Pb emissions affecting air concentrations 

that were likely well in exceedance of the current NAAQS, (e.g., 1977 CD, section 8.8; 1986 

CD, section 8.1.1.3; 2006 CD, p. 7-15). Interpretation of ecosystem-level field studies with 

regard to ambient Pb levels associated with ecosystem and community effects is complicated by 

these confounding factors and the inherent variability in natural systems (ISA, section 6.3.12.7). 

Limited new evidence of effects of Pb at the community scale has been reported. This 

evidence includes several studies of the ameliorative effects of mycorrhizal fungi on plant 

growth with Pb exposure as well as recently published research on soil microbial communities, 

which have been shown to be impacted by Pb in both composition and activity (ISA, sections 

1.7.1 and 6.3.6). Many recent studies have been conducted using mixtures of metals, which 

have attempted to separate the effects of individual metals when possible. In studies that 

included only Pb, or where effects of Pb could be separated, soil microbial activity was 

generally diminished with increased Pb concentration and was shown in some of those cases to 

recover with time (ISA, section 6.3.6). In studies involving heavily contaminated soils from 

historic smelters, mining sites, or natural Pb deposits, microbial species and genotype 

composition were consistently altered after Pb exposure, and findings indicate that those 

alterations were long-lasting or permanent (ISA, section 6.3.6, pg 6-120). 

A recent review has examined differences in species sensitivity, using blood Pb level in 

birds and mammals as an exposure index rather than external dose (ISA, section 6.3.9.1; 

Buekers et al., 2009). In this analysis, variation across organisms was lower with the blood Pb 

index compared to use of media concentration, and variation of Pb absorption from the diet of 

the organism largely accounted for the variation seen in the blood Pb. The analysis also suggests 

a larger variation in sensitivity across avian species tested compared to mammalian species with 

regard to the association between blood Pb concentration and toxicity (ISA, section 6.3.9.1). 
5-10 

 Overall, recent studies cited in this review support previous conclusions about the effects 

of Pb on terrestrial ecosystems, namely that increasing soil Pb concentrations in areas of Pb 

contamination (e.g. mining sites and industrial sites) can cause decreases in microorganism 

abundance, diversity, and function. Previous reviews have also reported on effects on bird and 

plant communities (2006 CD, section AX7.1.3). The shifts in bacterial species and fungal 

diversity have been observed near long-established sources of Pb contamination (ISA, section 

6.3.12.7). Most recent evidence for Pb toxicity to terrestrial plants, invertebrates and vertebrates 

is from single-species assays in laboratory studies which do not capture the complexity of 

bioavailability and other modifiers of effect in natural systems (ISA, section 6.3.12.7). Further, 

models that might account for modifiers of bioavailability have proven difficult to develop 

(ISA, p. 6-16). 

Freshwater Ecosystems 

 Studies newly available in this review address trophic transfer of Pb in freshwater 

ecosystems (ISA, section 6.4.4.4). Evidence summarized in the 2006 CD indicated that 

measured concentrations of Pb in the tissues of aquatic organisms were generally higher in 

algae and benthic organisms than in higher trophic-level consumers, indicating that Pb was 

bioconcentrated but not biomagnified (ISA, section 1.7.2). Some recent studies indicate transfer 

of Pb in aquatic food webs; while other recent studies that have traced Pb in freshwater aquatic 

food webs have found, similar to the 2006 CD findings, that Pb concentration decreases with 

increasing trophic level (biodilution) (ISA, sections 1.7.2 and 6.4.4.4). 

 Evidence presented in the ISA further supports the findings of past CDs that Pb in 

freshwater can be highly toxic to aquatic organisms, with toxicity varying with species and life 

stage, duration of exposure, form of Pb, and water quality characteristics. The 2006 CD 

identified evidence of adverse growth effects on several species of freshwater algae from Pb 

exposure (2006 CD, Section 7.2.4). The ISA describes several new studies which expand the 

list of algal species for which these adverse effects have been identified (ISA, section 6.4.5.1). 

For vascular plants, the ISA describes additional evidence that oxidative damage, decreased 

photosynthesis and reduced growth occur with elevated Pb exposure (ISA, section 6.4.5.2). 

 Since the 2006 CD, there is some additional evidence for Pb effects on cellular processes 

in aquatic invertebrates. Recent studies of reproductive and developmental effects of Pb 

augment similar findings in the 2006 CD and add additional species information on 

reproductive endpoints for rotifers and freshwater snails as well as multigenerational effects of 

Pb in mosquito larvae (ISA, section 6.4.5.2). In the 2006 CD, study concentrations cited at 

which effects were observed in various aquatic invertebrates reflected an expansive range from 

5μg/L (for acute toxicity to Pb nitrate in a test system at a hardness of 18 mg/L calcium 

carbonate) to greater than 8000 μg/L (for acute toxicity to Pb chloride at a hardness of 280-300 
5-11 

mg/L calcium carbonate) (ISA, p.1-45; 2006 CD, Table AX7-2.4.1). Recent studies cited in the 

ISA provide additional evidence of effects from chronic exposures. These findings are 

generally consistent with those of the previous review and reflect the variability of Pb toxicity 

under different environmental conditions and in species with varying sensitivity. 

 Evidence of effects in aquatic vertebrates presented in the ISA reiterates the findings of 

reproductive, behavioral, and growth effects stated in previous CDs. Some additional 

mechanisms of Pb toxicity in the gill and the renal system of fish have been elucidated since the 

2006 CD as well as the identification of potential new molecular targets for Pb neurotoxicity 

(ISA, section 1.7.2). 

 As in terrestrial organisms, evidence presented in the ISA and prior CDs demonstrates the 

toxicity of Pb in aquatic ecosystems and the role of many factors, including Pb speciation and 

various water chemistry properties, in modifying toxicity (ISA, section 1.7.2). Since the 2006 

CD, additional evidence for community and ecosystem level effects of Pb is available, primarily 

in microcosm studies or field studies with other metals present (ISA, section 6.4.11). Such 

evidence described in previous CDs includes alteration of predator-prey dynamics, species 

richness, species composition, and biodiversity. New studies available in this review provide 

evidence in additional habitats for these community and ecological-scale effects, specifically in 

aquatic plant communities and sediment-associated communities at both acute and chronic 

exposures involving concentrations similar to those previously reported (ISA, section 6.4.7). In 

many cases it is difficult to characterize the nature and magnitude of effects and to quantify 

relationships between ambient concentrations of Pb and ecosystem response due to existence of 

multiple ecosystem-level stressors, variability in field conditions, and differences in Pb 

bioavailability (ISA, sections 1.7.3.7 and 6.4.7). Additionally, the degree to which air 

concentrations have contributed to such effects in freshwater ecosystems is largely unknown. 

Saltwater Ecosystems 

As assessed in the ISA, the evidence for saltwater species and ecosystems is generally 

inadequate to draw conclusions regarding the effect of Pb (ISA, Tables 1-3 and II). The extent 

of newly available evidence in the context of prior available evidence is summarized here. 

With regard to evidence in marine plants, recently available evidence on the toxicity of 

Pb to marine algae augments the 2006 CD findings of variation in sensitivity across marine 

species. Recent studies on Pb exposure include reports of growth inhibition and oxidative stress 

in a few additional species of marine algae (ISA, section 6.4.15). 

 Recent literature provides little new evidence of endpoints or effects in marine 

invertebrates beyond those reported in the 2006 CD. For example, some recent studies 

strengthen the evidence of Pb effects on enzymes and antioxidant activity in marine 

invertebrates and have identified an additional behavioral endpoint (i.e., valve closing speed in 
5-12 

juveniles of a marine scallop affected by 20 days exposure to 40-400 μg/L Pb nitrate) from 

those discussed previously (ISA, section 6.4.15.2). Also, as noted in the 2006 CD and supported 

by new studies reviewed in the ISA, Pb exposure negatively affects the growth of marine 

invertebrates (ISA, section 6.4.15.2). Recent studies also identify several species exhibiting 

particularly low sensitivity to high acute exposures (ISA, section 6.4.15.2). 

 Little new evidence is available of Pb effects on marine fish and mammals for 

reproductive, growth and survival endpoints that are particularly relevant to the population level 

of biological organization and higher (ISA, section 6.4.15). Evidence for effects at higher levels 

of biological organization in saltwater habitats is primarily supported by observations in a small 

number of microcosm and field studies where shifts in nematode community structure are the 

most commonly observed effects of Pb in experimentally contaminated sediments (ISA, 

sections 6.4.17 and Table 6-6). These types of studies were presented in the 2006 CD, and 

while there are new studies presented in the ISA, they primarily expand the types of 

communities (seagrass and amphipods) for which data exist but reach similar conclusions about 

community structure as the 2006 CD. However, there is no evidence of adverse effects in 

saltwater environments associated with current ambient air Pb concentrations, and linkages 

between any level of ambient air deposition and effects are unknown in all but a few organisms. 

New studies on organism-level effects from Pb in saltwater ecosystems (ISA, section 

6.4.15) provide little evidence to inform our understanding of linkages between atmospheric 

concentrations, ambient exposures in saltwater systems and such effects or our conclusions 

regarding the likelihood of adverse effects under conditions associated with the current NAAQS 

for Pb. Nor does the currently available evidence indicate significantly different exposure 

levels from the previous review at which ecological systems or receptors are expected to 

experience effects. 

 To what extent is there new information that informs our understanding of 

critical loads of Pb, including critical loads in sensitive ecosystems? 

Critical loads analyses are a method that facilitates the assessment of ecosystem impacts 

as a result of pollutant loading which may arise from multiple pathways. A critical loads 

analysis approach can take into account what is known about the release of a specific chemical 

into the environment, its distribution and cycling within (and, as appropriate, across) ecosystems 

and each ecosystem's sensitivity to the chemical (ISA, section 6.1.3). Thus, this approach 

provides a conceptual framework for linking atmospheric deposition to environmental media 

concentration target values related to ecological endpoints associated with impairment (termed 

“critical limits”). Given the potential relevance to consideration of the secondary NAAQS for 

Pb, research in this area has been assessed in the current ISA and the 2006 CD. 
5-13 

The following generally accepted definition for a critical load of atmospheric pollutant 

deposition was developed from a pair of international workshops in the late 1980s (USEPA, 

2008). 

A quantitative estimate of an exposure to one or more pollutants below which 

significant harmful effects on specified sensitive elements of the environment do 

not occur according to present knowledge. 

As critical loads estimates reflect the current state of knowledge and policy priorities, as 

well as scientific and science policy judgments pertaining to the context for their use, there is no 

single “definitive” critical load for a natural resource. The state of scientific knowledge in this 

area can change in reflection of new information in various areas including, for example, new 

information about dose-response relationships; more comprehensive and detailed 

characterization of ecosystem resources (e.g., improved maps, inventories and survey datasets); 

more detailed information on pollutant concentrations (e.g., continuing time-series monitoring); 

and improved numerical models of pollutant fate and transport and ecosystem response. Science 

policy judgments reflect their context (e.g., goal for protection) as well as the state of scientific 

knowledge and consideration of its attendant strengths, limitations and uncertainties. 

Additionally inherent in critical loads analyses, due to their predictive nature, are a variety of 

assumptions, which may be relatively more or less numerous depending on the extent of 

knowledge on environmental processes for a particular application. 

Some of the earliest uses of critical loads analyses date to consideration of the evidence 

for air pollutant deposition impacts on acidification of sensitive lake systems (2006 CD, section 

7.3.2). Accordingly, the integrated science assessment of the evidence for the air pollutants 

nitrogen oxides (NOx) and sulfur oxides (SOx) described in detail the critical loads concept and 

the substantial evidence base pertaining to its application in consideration of acidification and 

eutrophication of aquatic ecosystems (USEPA, 2008). In this case, the substantial evidence of 

these ecosystem effects and the role of NOx/SOx atmospheric deposition was assessed (USEPA, 

2008), and multiple alternative biological indicators, critical biological responses, chemical 

indicators, and critical chemical limits were presented that could be used to determine 

appropriate critical loads for aquatic and terrestrial ecosystems with regard to acidification and 

eutrophication (e.g., USEPA, 2008, Table 3-1, sections 3.2 and 3.3 and Annexes B, C and D). 

A comparable evidence base does not exist with regard to impacts of air deposition of Pb 

on ecosystems. Nonetheless, the potential exists for critical loads to be an especially powerful 

tool allowing us to assess Pb atmospheric input into an ecosystem (e.g., deposition) and the 

potential ecological impairment resulting from that input. Critical load analyses are dependent on 

data relating pollutant release into an ecosystem (or multiple connected systems) from various 

sources with an understanding of the ecosystem concentrations likely to result in significant 
5-14 

harmful effects. In the context of Pb, a persistent, naturally occurring material, the 

bioavailability and mobility are influenced by multiple ecosystem characteristics; the data types 

for such analysis are numerous and may include information in the following areas: 

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

 Current Pb presence within and among ecosystems,8

 including spatial distribution, 

bioavailability and mobility; 

 Fate and transport processes, within and among ecosystem components, as well as 

associated rates and factors influencing them; 

 Forms and concentrations of Pb in ecosystem exposure media that likely result in 

critical ecosystem effects (e.g., concentrations that might relate to critical limits). 

 Additional information pertaining to the consideration of critical loads analyses in the 

context of ambient air standard setting for Pb includes factors that influence the transport and 

spatial pattern of deposition of airborne Pb, such as particle size (ISA, section 2.3.1). 

During the last review, the 2006 CD assessed the available information on critical loads 

for Pb (2006 CD, section 7.3). This information included publications on methods and example 

applications, primarily in Europe, specific to the bedrock geology, soil types, vegetation, and 

historical deposition trends in each European country (2006 CD, p. E-24), with no analyses 

available for U.S. locations (2006 CD, sections 7.3.4-7.3.6).9

 As a result, the 2006 CD 

concluded that “[c]onsiderable research is necessary before critical load estimates can be 

formulated for ecosystems extant in the United States” (2006 CD, p. E-24). More generally, the 

2006 CD identified the largest sources of uncertainty to include: derivation of the critical limit, 

Pb speciation, and soil runoff as an input to aquatic ecosystems (2006 CD, p. 7-45). Overarching 

conclusions reached included the following (2006 CD, p. 7-46). 

... At this time, the methods and models commonly used for the calculation of 

critical loads have not been validated for Pb. Many of the methods neglect the 

speciation of Pb when estimating critical limits, the uptake of Pb into plants, and 

out flux of Pb in drainage water, limiting the utility of current models. Future 

efforts should focus on fully incorporating the role of Pb speciation into critical 

load models, and validating the assumptions used by the models. 

 

8

 In the case of Pb, in addition to the role of current air-related pathways, its presence in the ecosystem 

results from larger historical air emissions as well as contributions from nonair pathways which may be appreciable 

in some areas (e.g., industrial discharges to surface waters, contaminated waste disposal, drainage from metals 

mining sites, Pb ammunition near outdoor shooting areas). 9

 The work in Europe is largely responsive to developments, beginning in the late 1980s, associated with 

the consideration of the critical-load concept for a range of air pollutants in future international agreements limiting 

air pollutant emissions (2006 CD, section 7.3.2). A key impetus for such international cooperation efforts was 

research in the 1960s and 1970s indicating the role of long-range trans-boundary transport on ecosystems (e.g., 

sulfur emissions on the European continent contributing to acidification of Scandinavian lakes). Since about 1990, 

research has been exploring the use of critical loads in Europe for other air pollutants, including metals (2006 CD, 

section 7.3.2). 
5-15 

Accordingly, the quantitative assessment for the last Pb NAAQS review (ICF, 2006) did not 

involve critical load analyses. 

Newly available evidence pertaining to critical loads analysis in this review includes 

limited recent research on consideration of bioavailability in characterizing Pb effect 

concentrations or indices and on modeling approaches to incorporate chemistry effects on Pb 

speciation and bioavailability (ISA, sections 6.3.7 and 6.4.8). With consideration of this 

information and the four critical load analysis studies newly available in this review (none of 

which are for U.S. ecosystems), the ISA does not modify the conclusions noted above from the 

2006 CD (ISA, sections 6.1.3, 6.3.7 and 6.4.8). In summary, the new information in this review 

does not appreciably change our evidence base or further inform our understanding of critical 

loads of Pb, including critical loads in sensitive ecosystems. 

 To what extent is there information that improves our understanding of the 

portion of environmental Pb derived from ambient air and the associated effects 

on sensitive ecosystems? 

There is no new evidence since the last review that substantially improves our 

understanding of the relationship between ambient air Pb and measurable ecological effects. As 

stated in the last review, the role of ambient air Pb in contributing to ecosystem Pb has been 

declining over the past several decades. It remains difficult to apportion exposure between air 

and other sources to better inform our understanding of the potential for ecosystem effects that 

might be associated with air emissions. As noted in the ISA, “[t]he amount of Pb in ecosystems 

is a result of a number of inputs and it is not currently possible to determine the contribution of 

atmospherically-derived Pb from total Pb in terrestrial, freshwater or saltwater systems” (ISA, 

section 6.5). Further, considerable uncertainties also remain in drawing conclusions from 

evidence of effects observed under laboratory conditions with regard to effects expected at the 

ecosystem level in the environment. In many cases it is difficult to characterize the nature and 

magnitude of effects and to quantify relationships between ambient concentrations of Pb and 

ecosystem response due to the existence of multiple stressors, variability in field conditions, and 

differences in Pb bioavailability at that level of organization (ISA, section 6.5). In summary, the 

ISA concludes that “[r]ecent information available since the 2006 Pb AQCD, includes additional 

field studies in both terrestrial and aquatic ecosystems, but the connection between air 

concentration and ecosystem exposure continues to be poorly characterized for Pb and the 

contribution of atmospheric Pb to specific sites is not clear” (ISA, section 6.5). 
5-16 

5.2 EXPOSURE AND RISK INFORMATION 

The risk information available for this review and described here is based primarily on 

the pilot ecological risk assessment developed in the last review of the Pb NAAQS (henceforth 

referred to as the 2006 REA [ICF, 2006]). This information is described within the context of 

the evidence presented in the ISA that is newly available for this review. As described in the 

IRP, careful consideration of newly available information in this review led us to conclude that 

developing a new REA for this review was not warranted. In light of critical limitations and 

uncertainties that are still unresolved in the current evidence, staff concluded that currently 

available information does not provide the basis for developing a new quantitative risk and 

exposure assessment with substantially improved utility for informing the Agency’s 

consideration of welfare effects and evaluation of the adequacy of the current secondary standard 

or alternatives (REA Planning Document, section 3.3). More specificallly, we also indicated our 

conclusion that the information newly available in this review did not provide the means by 

which to develop an updated or enhanced risk model that would substantially improve the utility 

of risk estimates in informing the current Pb NAAQS review (REA Planning Document, section 

3.3). Based on their consideration of the REA Planning Document, the CASAC Pb Review 

Panel generally concurred with the conclusion that a new REA was not warranted in this review 

(Frey, 2011; Frey, 2013). Accordingly, the information described here is drawn primarily from 

the 2006 REA. 

The focus for the risk assessment and associated estimates presented here is on Pb 

derived from sources emitting Pb to ambient air. While there is some new evidence that 

improves our understanding of some of the environmental variability affecting the disposition 

and toxicity of Pb in the environment, the information and methods to support a quantitative 

assessment of the role of atmospheric Pb in the U.S are limited. Specific constraints include the 

limited availability of location-specific data describing a range of U.S. ecosystems and their 

pertinent environmental characteristics as well as a more complete understanding of 

bioavailability and its modifiers and data and methods to inform the apportionment of Pb 

allowed by the current standard and of lead-related effects between air and non air sources. 

These data gaps and areas of uncertainty in the current evidence restrict our ability to assess 

quantitatively the relationship between concentrations of Pb in ambient air and terrestrial and/or 

aquatic systems, and their effect on welfare. 

As discussed in section 1.3 above, the multimedia and persistent nature of Pb, the role of 

multiple exposure pathways (illustrated in Figure 1-1 above), and the contributions of nonair 

sources of Pb to exposure media all present challenges and contribute significant additional 

complexity to the ecological risk assessment that goes far beyond the situation for similar 

assessments typically performed for other NAAQS pollutants (e.g., that focus only on a single 
5-17 

media pathway or for which air is the only significant source). Limitations in the available data 

and models affected our characterization of the various complexities associated with exposure to 

ambient air Pb. As a result, the 2006 assessment was conducted as a pilot study with a number 

of simplifying assumptions with regard to the representativeness of the case studies for 

ecological exposures and our ability to isolate case studies where air-derived Pb was the only or 

most significant source. Therefore, this section presents a brief summary of the screening-level 

ecological risk assessment conducted in 2006 for the Pb NAAQS review completed in 2008 and 

addresses several questions relating to the current evidence and understanding that may inform 

our view of the results of that assessment. The discussion here also takes into consideration 

CASAC recommendations in the last review with regard to interpretation of the screening-level 

assessment (Henderson, 2007a, b), as well as comments received from the CASAC Pb Panel in 

the current review, as part of the consultation on the REA Planning Document (Frey, 2011). 

5.2.1 Screening Assessment from Last Review 

The screening-level risk assessment performed for the last review was focused on 

estimating the potential for ecological risks associated with ecosystem exposures to Pb emitted 

into ambient air (2006 REA, section 7). A national-scale screen was used to evaluate surface 

water and sediment monitoring locations across the United States for the potential for ecological 

impacts that might be associated with atmospheric deposition of Pb (described in detail in 2006 

REA, section 7.1.2). In addition to the national-scale screen (2006 REA, section 3.6), the 

assessment involved a case study approach, with case studies for areas surrounding a primary Pb 

smelter (2006 REA, section 3.1) and a secondary Pb smelter (2006 REA, section 3.2), as well as 

a location near a non-urban roadway (2006 REA, section 3.4). An additional case study, focused 

on consideration of atmospherically derived Pb effects on an ecologically vulnerable ecosystem 

(Hubbard Brook Experimental Forest), was identified (2006 REA, section 3.5). The Hubbard 

Brook Experimental Forest (HBEF), in the White Mountain National Forest, near North 

Woodstock, New Hampshire, was selected as a fourth case study because of its location and its 

long record of available data on concentration trends of Pb in three media (air or deposition from 

air, soil, and surface water). While no quantitative analyses were performed, summary review of 

the literature search was included in the assessment report (2006 REA, Appendix E). For the 

other three case studies, exposure concentrations of Pb in soil, surface water, and/or sediment 

concentrations were estimated from available monitoring data or modeling analysis and then 

compared to ecological screening benchmarks (2006 REA, section 7.1). 

All three case studies and the national-scale assessment generally considered then-current 

or recent environmental conditions. In all cases but the primary Pb smelter case study, current 

air quality conditions were below the then-current NAAQS. Air Pb concentrations in the 
5-18 

primary Pb smelter case study exceeded the then-current NAAQS. A complete discussion of air 

quality in each of the case studies can be found in section 4 of the 2006 REA. 

 An overview of the approach developed to implement the selected elements of the 

conceptual model for the ecological risk assessment is provided in Figure 5-1. This figure shows 

the key types of information and models involved in each part of the assessment and how they 

are related to each other and to the other parts of the analysis. Appendix 5A gives the locations 

and spatial resolution for each of the case studies and the national scale screen while 

summarizing the source of the screening values used or each location and media type. As 

indicated in Figure 5-1 and Appendix 5A, the specific approach for each case study differed 

based on the nature of the case study (e.g., type of source, locations of populations) and the sitespecific measurements available. 

 
5-19 

Figure 5-1. Analytical approach for screening-level ecological risk assessment in the last 

review (2006 REA, Exhibit 2-6). 
5-20 

To estimate the potential for ecological risk, modified ecological soil screening levels 

(Eco-SSLs) derived from those developed by EPA’s Superfund program (USEPA, 2005a,b), 

EPA’s recommended ambient water quality criteria (2006 REA, section 7.1) and sediment 

screening values developed by MacDonald and others (2000, 2003) were used, as described in 

detail in section 7.1.3 of the 2006 REA. A hazard quotient (HQ) was calculated for adverse 

effects on the survival, growth, and reproduction of exposed ecological receptors to determine 

the potential for risk to that receptor. Ecological receptors used in the pilot are discussed in detail 

in section 7.1 of the 2006 REA. The HQ was calculated as the ratio of the media concentration to 

the ecotoxicity screening value. In each case study, HQ values were calculated for each location 

where either modeled or measured media concentrations were available. Separate soil HQ 

values were calculated for each ecological receptor group for which an ecotoxicity screening 

value has been developed (i.e., birds, mammals, soil invertebrates, and plants), as described in 

detail in section 7.1.2 of the 2006 REA. HQ values less than or equal to 1.0 were concluded to 

suggest that Pb concentrations in a specific medium were unlikely to pose significant risks to 

ecological receptors, while HQ values greater than 1.0 indicated a potential for adverse effects. 

5.2.2 Screening Assessment Results and Interpretation 

The results for the ecological screening assessment for the three case studies and the 

national-scale screen for surface water and for sediment indicated a potential for adverse effect 

from ambient Pb to multiple ecological receptor groups in terrestrial and aquatic locations. 10 

Below are descriptions of the location-specific case studies and the national screening 

assessment, key findings of the risk assessment for each, and an interpretation of the results with 

regard to past air conditions as well as the current standard (USEPA, 2007b). 

 What do the key findings of the 2006 screening-level assessment indicate 

regarding the likelihood that adverse welfare effects would result from levels of 

air-related Pb that would meet the current standard? 

In addressing this question, the findings of the 2006 REA are summarized below. 

Primary Pb Smelter Case Study 

 The primary Pb smelter case study location is at one of the largest and longestoperating primary Pb smelters in the world (since 1892), the only one currently 

operating in the U. S. (ICF, 2006).11 

 Concentrations of total Pb in several of the soil and sediment locations within the case 

study were measured in 2000 and exceeded screening values, indicating a potential for 

adverse effects to terrestrial and sediment-dwelling organisms. 

 

10 It is important to note that the screening values available and used in the assessment lacked adjustment 

for some critical measures of bioavailability. See uncertainty discussion below. 11 As noted in section 2.1.2 above, this smelter ceased smelting operations at this facility at the end of 2013. 
5-21 

 While the contribution to these Pb concentrations from air as compared to nonair 

sources is not quantified, air emissions from this facility are substantial (ICF, 2006). In 

addition, this facility that has been emitting Pb for many decades, including some 

seven decades prior to establishment of any Pb NAAQS, such that it is likely air 

concentrations associated with the facility were substantial relative to the 1978 

NAAQS, which it exceeded at the time of the last review. At the time of the previous 

review (2006) and also since the adoption of the current standard, concentrations 

monitored near this facility exceeded the level of the applicable NAAQS (USEPA 

2007b, Appendix 5A and Appendix 2D of this document). Accordingly, this case 

study is not informative for considering the likelihood of adverse welfare effects 

related to Pb from air sources under air quality conditions associated with meeting the 

current Pb standard. 

Secondary Pb Smelter Case Study 

 The secondary Pb smelter location falls within the Alabama Coastal Plain in Pike 

County, Alabama, in an area of disturbed forests. The industrial facility in this case 

study is much younger than the primary Pb smelter, becoming active less than ten years 

prior to the establishment of the 1978 Pb standard. 

 Estimates of total Pb concentration in soils (based on fate and transport modeling using 

1997-2000 emissions data and data for similar locations measured in a 1995 study) 

exceeded screening values for plants, birds and mammals, indicating the potential for 

adverse effects to these groups. 

 While the contributions from air-related Pb to the total Pb concentrations modeled in 

soils at this location are unclear, the facility continues to emit Pb, and the county where 

this facility is located does not meet the current Pb standard (Appendix 2D and 5A). 

Given the exceedances of the current standard, which likely extend back over 4 to 5 

decades, this case study also is not informative for considering the likelihood of 

adverse welfare effects related to Pb from air sources under air quality conditions 

associated with meeting the current Pb standard. 

Near-Roadway Non-urban Case Study 

 This case study comprises two non-urban sites adjacent to established highways for 

which soil Pb data were available: (1) in Corpus Christi, Texas (ICF, 2006), and (2) in 

Atlee, Virginia (ICF, 2006). Measured soil concentration data were used to develop 

estimates of Pb in soils for each location. 

 Estimates of total Pb concentrations taken in 1994 and 1998 in soils in this case study 

exceeded screening values for plants, birds and mammals, indicating the potential for 

adverse effect to these groups. 

These case study locations are highly impacted by past deposition of gasoline Pb. It is 

unknown whether current conditions at these sites exceed the current Pb standard, but 

given evidence from the past of Pb concentrations near highways that ranged above the 

previous (1978) Pb standard (1986 CD, section 7.2.1), conditions at these locations 

during the time of leaded gasoline very likely exceeded the current standard. Similarly, 

those conditions likely resulted in Pb deposition associated with leaded gasoline that 

exceeds that being deposited under air quality conditions that would meet the current 
5-22 

Pb standard. Given this legacy, consideration of the potential for environmental risks 

from levels of air–related Pb associated with meeting the current Pb standard in these 

locations is highly uncertain. 

Vulnerable Ecosystem Case Study 

 This case study was focused on consideration of information available for the Hubbard 

Brook Experimental Forest (HBEF) in the White Mountain National Forest near North 

Woodstock, New Hampshire, which included a long record (from 1976 through 2000) 

of available data on concentration trends of Pb in three media (air or deposition from 

air, soil, and surface water). 

 While no quantitative analyses were performed, a summary review of literature 

published on HBEF was developed. This literature indicated: (1) atmospheric Pb 

inputs do not directly affect stream Pb levels at HBEF because deposited Pb is almost 

entirely retained in the soil profile; and (2) soil horizon analysis results showed Pb to 

have become more concentrated at lower soil depths over time, with the soil serving as 

a Pb sink, appreciably reducing Pb in pore water as it moves through the soil layers to 

streams (dissolved Pb concentrations were reduced from 5 μg/L to about 5 ng/L from 

surface soil to streams). Further, the available studies concluded insignificant 

contribution of dissolved Pb from soils to streams (ICF, 2006, Appendix E). It is 

unlikely that conditions have changed from the previous conclusions made based on 

soil data through 2000, and, therefore, current ambient air concentrations likely do not 

directly impact stream Pb levels under air quality conditions associated with meeting 

the current standard.

National-scale Surface Water and Sediment Screen 

 The national-scale screen was performed using a national database of surface water and 

sediment monitoring data (see Appendix 5A; ICF, 2006). 

 The screen identified 15 non-mining sites at which at least one surface water 

dissolved Pb concentration taken between 1994 and 2004 exceeded the chronic 

screening value, indicating a potential for adverse effect if concentrations were 

persistent over long time periods. The acute screening value was not exceeded 

at any of these locations. 

 Analysis of the sediment concentrations for the 15 sites taken from 1991 to 

2000 analyzed in the surface water screen identified a subset for which 

concentrations exceeded the screening value, indicating a potential for adverse 

effects to sediment dwelling organisms. 

 The extent to which past air emissions of Pb have contributed to surface water or 

sediment Pb concentrations at the locations identified in the screen is unclear. For 

some of the surface water locations, nonair sources likely contributed significantly to 

the surface water Pb concentrations. For other locations, a lack of nearby nonair 

sources indicated a potential role for air sources to contribute to observed surface water 

Pb concentrations. Additionally, these concentrations may have been influenced by Pb 

in resuspended sediments and may reflect contribution of Pb from erosion of soils with 

Pb derived from historic as well as current air emissions. 
5-23 

 There are multiple sources of uncertainty associated with different aspects of this 

assessment (discussed in detail in 2006 REA, section 7.4). For example, there are significant 

limitations and uncertainties associated with conclusions that can be drawn from the primary Pb 

smelter case study regarding the impact of atmospheric deposition under conditions associated 

with meeting the Pb NAAQS (past or present). Additionally, while case study locations were 

chosen with the objective of including locations for which recent Pb data were available and for 

which Pb exposures might be influenced by air-related Pb and not be dominated by nonair 

sources, there is significant uncertainty regarding the extent to which nonair sources and 

conditions associated with historic emissions (e.g., prior to establishment of past or present Pb 

NAAQS) have likely contributed to the Pb exposure estimates in some locations. The screening 

values available and used in the assessment (e.g., ambient water quality criteria, Eco-SSLs, 

sediment criteria) lacked adjustment for some critical measures of bioavailability and were 

sources of uncertainty with regard to potential for ecological risk. There is also uncertainty 

regarding the extent to which the screening values could identify potential hazards of Pb for 

some threatened or endangered species or unusually sensitive aquatic ecosystems (ICF 2006). 

Thus, while the assessment results are generally consistent with evidence-based observations of 

the potential influence of Pb on ecological systems, they are limited with regard to quantitative 

conclusions and potential hazard or risk associated with the Pb NAAQS, most particularly with 

regard to the current standard. The Hubbard Brook case study represents the most applicable 

case study for current conditions, and based on the previous analysis undertaken in the last 

review, current ambient air concentrations likely do not directly impact stream Pb levels under 

air quality conditions associated with meeting the current standard. With data limitations and the 

difficulties in apportioning Pb in ecosystems, there are no additional known locations in the U.S. 

that would likely provide additional insight into the effects of ambient Pb under the current 

standard, therefore no additional case study analyses were undertaken in this review. 

 What are the important uncertainties associated with interpreting the prior 

assessment in light of newly available evidence in this review? 

In interpreting the results from the 2006 REA, we consider newly available evidence that 

may inform our interpretation of risk under the current standard. Factors necessary to alter our 

interpretation of risk would include new evidence of harm at lower concentrations of Pb, new 

linkages that enable us to draw more explicit conclusions as to the air contribution of 

environmental exposures, and/or new methods of interpreting confounding factors that were 

largely uncontrolled in the previous risk assessment. In general, however, the key uncertainties 

identified in the last review remain today, as described below. 

With regard to new evidence of harm at lower concentrations, it is necessary to consider 

that the evidence of adversity due specifically to Pb in natural systems is limited, in no small part 
5-24 

because of the difficulty in determining the effects of confounding factors such as multiple 

metals and modifying factors influencing bioavailability in field studies. Modeling of Pb-related 

exposure and risk to ecological receptors is subject to a wide array of sources of both variability 

and uncertainty. Variability is associated with geographic location, habitat types, physical and 

chemical characteristics of soils and water that influence Pb bioavailability, terrestrial and 

aquatic community composition. Furthermore Pb uptake rates by invertebrates, fish, and plants 

may vary by species and season. For wildlife, variability also is associated with food ingestion 

rates by species and season, prey selection, and locations of home ranges for foraging relative to 

the Pb contamination levels (USEPA, 2005b). 

There are significant difficulties in quantifying the role of air emissions under the current 

standard, which is significantly lower than the previous standard. As recognized in section 1.3.2 

above, Pb deposited before the standard was enacted remains in soils and sediments, 

complicating interpretations regarding the impact of the current standard; historic Pb emitted 

from leaded gasoline usage continues to move slowly through systems along with more recently 

deposited Pb and Pb derived from non air sources. The results from the location-specific case 

studies and the surface and sediment screen performed in the last review are difficult to interpret 

in light of the current standard and are not largely useful in informing our judgments of the 

potential for adverse effects at levels of deposition meeting the current standard. Under such 

constraints it is difficult to assess the merit of the risk findings from the previous review. 
5-25 

5.3 REFERENCES 

Buekers, J; Redeker, ES; Smolders, E. (2009). Lead toxicity to wildlife: Derivation of a critical blood concentration 

for wildlife monitoring based on literature data [Review]. Sci Total Environ 407: 3431-3438. 

http://dx.doi.org/10.1016/j.scitotenv.2009.01.044 

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

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

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

2011. 

Frey, H.C. (2013) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee Lead 

Review Panel, to Acting Administrator Bob Perciasepe. Re: Review of EPA’s Policy Assessment for the 

Review of the National Ambient Air Quality Standards for Lead. June 4, 2013. 

Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

the 1st Draft Lead Staff Paper and Draft Lead Exposure and Risk Assessments. March 27, 2007. 

Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

the 2nd Draft Lead Human Exposure and Health Risk Assessments. September 27, 2007. 

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

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

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

Landers, DH; Simonich, SM; Jaffe, D; Geiser, L; Campbell, DH; Schwindt, A; Schreck, C; Kent, M; Hafner, W; 

Taylor, HE; Hageman, K; Usenko, S; Ackerman, L; Schrlau, J; Rose, N; Blett, T; Erway, MM. (2010). The 

Western Airborne Contaminant Assessment Project (WACAP): An interdisciplinary evaluation of the 

impacts of airborne contaminants in western U.S. National Parks. Environ Sci Technol 44: 855-859. 

MacDonald, D.D., Ingersoll, C.G., and Berger, T.A. (2000) Development and evaluation of consensus-based 

sediment quality guidelines for freshwater ecosystems. Archives of Environmental Contamination and 

Toxicology. 39:20-31. 

MacDonald, D.D., Ingersoll, C.G., Smorong, D.E., Lindskoog, R.A., Sloane, G., and Biernacki, T. (2003) 

Development and Evaluation of Numerical Sediment Quality Assessment Guidelines for Florida Inland 

Waters. British Columbia: MacDonald Environmental Sciences, Lt. Columbia, MO: U.S. Geological 

Survey. Prepared for: Florida Department of Environmental Protection, Tallahassee, FL. January. 

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

Washington, DC: Office of Solid Waste and Emergency Response.OSWER Directive 9285.7-55. 

November 2003; revised (chapter 4) February 2005. 

U.S. Environmental Protection Agency. (2005b) Ecological Soil Screening Levels forLead, Interim Final. 

Washington, DC: Office of Solid Waste and Emergency Response. OSWER Directive 9285.7-70. 

Available at http://www.epa.gov/ecotox/ecossl/pdf/eco-ssl_lead.pdf . 

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

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

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

Standards, Research Triangle Park, NC. Available at: 

http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr_pd.html 
5-26 

U.S. Environmental Protection Agency. (2007a). Framework for metals risk assessment [EPA Report]. (EPA 120/R07/001). Washington, D.C. Available online at: http://www.epa.gov/raf/metalsframework/index.htm 

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

Policy Assessment of Scientific and Technical Information OAQPS Staff Paper. Washington, DC, EPA452/R-07-013. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html

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

and Sulfur–Ecological Criteria (Final Report). EPA/600/R-08/082F. U.S. Environmental Protection 

Agency, National Center for Environmental Assessment–RTP Division, Office of Research and 

Development, Research Triangle Park, NC. Available at 

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=201485. 

U.S. Environmental Protection Agency. (2013) Integrated Science Assessment for Lead. Washington, DC, 

EPA/600/R-10/075F. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_index.html 
 6-1 

6 REVIEW OF THE SECONDARY STANDARD FOR LEAD 

This chapter presents staff conclusions regarding the secondary Pb standard. These staff 

conclusions are guided by consideration of key policy-relevant questions and based on the 

assessment and integrative synthesis of information presented in the ISA and by staff analyses 

and evaluations presented in chapters 2 and 5 herein. These evaluations and staff conclusions 

have also taken into consideration CASAC advice and public comment on the draft PA and will 

inform the Administrator’s decisions on whether to retain or revise the existing secondary 

standard for Pb. 

Following an introductory section on the general approach for reviewing the secondary 

standard (section 6.1), including a summary of considerations in the last review, the discussion in 

this chapter focuses on whether the information available in this review supports or calls into 

question the adequacy of the current secondary standard. Building on the responses to specific 

policy-relevant questions on the scientific evidence and exposure-risk information in chapter 5, 

presentation in section 6.2 is also organized into consideration of key policy-relevant questions 

framing evidence-based and exposure/risk-based considerations. The policy-relevant questions 

in this document are based on those included in the IRP (IRP, section 3.2). Staff conclusions are 

reported in Section 6.3. Section 6.4 presents a brief overview of key uncertainties and areas for 

future research. 

6.1 APPROACH 

Staff’s approach for reviewing the current secondary standard takes into consideration the 

approaches used in the last Pb NAAQS review and involves addressing key policy-relevant 

questions in light of currently available scientific and technical information. The past and 

current approaches described below are all based most fundamentally on using EPA’s 

assessment of the current scientific evidence and previous quantitative analyses to inform the 

Administrator’s judgment with regard to the secondary standard for Pb. In drawing conclusions 

for the Administrator’s consideration with regard to the secondary standard, we note that the 

final decision on the adequacy of the current secondary Pb standard is largely a public welfare 

policy judgment to be made by the Administrator. The Administrator’s final decision must draw 

upon scientific information and analyses about welfare effects, exposure and risks, as well as 

judgments about the appropriate response to the range of uncertainties that are inherent in the 

scientific evidence and analyses. This approach is consistent with the requirements of the 

NAAQS provisions of the Clean Air Act. These provisions require the Administrator to 

establish a secondary standard that, in the judgment of the Administrator, is “requisite to protect 

the public welfare from any known or anticipated adverse effects associated with the presence of 
 6-2 

the pollutant in the ambient air”. In so doing, the Administrator seeks to establish standards that 

are neither more nor less stringent than necessary for this purpose. 

6.1.1 Approach Used in the Last Review 

In the last review, completed in 2008, the current secondary standard for Pb was set equal 

to the primary standard (73 FR 66964). As summarized in section 1.2.2 and described in more 

detail in section 4.1.1, the primary standard was substantially revised in the last review based on 

the much-expanded health effects evidence of neurocognitive effects of Pb in children. The level 

of the revised NAAQS is 0.15 μg/m3

. The averaging time was also revised to a rolling threemonth period with a maximum (not-to-be-exceeded) form, evaluated over a three-year period. 

Compared to the previous averaging time of one calendar quarter, this revision was considered to 

be more scientifically appropriate and more protective for human health. The indicator of PbTSP was retained, reflecting the evidence that Pb particles of all sizes pose health risks (73 FR 

67007). The 2008 decision considered the body of evidence as assessed in the 2006 CD 

(USEPA, 2006) as well as the 2007 Staff Paper assessment of the policy-relevant information 

contained in the 2006 CD and the screening-level ecological risk assessment (ICF, 2006; 

USEPA, 2007), the advice and recommendations of CASAC (Henderson 2007a, 2007b, 2008a, 

2008b), and public comment. 

In the 2008 review, the Staff Paper concluded, based on laboratory studies and current 

media concentrations in a wide range of locations, that it seemed likely that adverse effects were 

occurring, particularly near point sources, under the then-current standard (73 FR 67010). Given 

the limited data on Pb effects in ecosystems, and associated uncertainties, such as those with 

regard to factors such as the presence of multiple metals and historic environmental burdens, it 

was at the time, as it is now, necessary to look at evidence of Pb effects on organisms and 

extrapolate to ecosystem effects. Taking into account the available evidence and current media 

concentrations in a wide range of locations, the Administrator concluded that there was potential 

for adverse effects occurring under the then-current standard; however there were insufficient 

data to provide a quantitative basis for setting a secondary standard different than the primary 

(73 FR 67011). Therefore, citing a general lack of data that would indicate the appropriate level 

of Pb in environmental media that may be associated with adverse effects, as well as the 

comments of the CASAC Pb panel that a significant change to current air concentrations (e.g., 

via a significant change to the standard) was likely to have significant beneficial effects on the 

magnitude of Pb exposures in the environment, the secondary standard was revised to be 

consistent with the revised primary standard (73 FR 67011). 
 6-3 

6.1.2 Approach for the Current Review 

In evaluating whether it is appropriate to consider retaining the current secondary Pb 

standard, or whether consideration of revision is appropriate, we have adopted an approach in 

this review that builds on the general approach from the last review and reflects the body of 

evidence and information now available. As summarized above, the Administrator’s decisions in 

the previous review were based on the conclusion that there was the potential for adverse 

ecological effects under the previous standard. In our approach here, we intend to focus on 

consideration of the extent to which a broader body of scientific evidence is now available that 

would inform decisions on either the potential for adverse effects to ecosystems under the current 

standard or the ability to set a more ecologically relevant secondary standard than was feasible in 

the previous review. In conducting this assessment, we draw on the ecological effects evidence 

presented in detail in the ISA and aspects summarized above in chapter 5, along with the 

information associated with the screening-level risk assessment also summarized above. Figure 

6-1 illustrates the basic construct of our approach in developing conclusions regarding options 

appropriate for the Administrator to consider in this review with regard to the adequacy of the 

current secondary NAAQS standard and, as appropriate, potential alternate standards. 

In developing conclusions in this review, we have taken into account both evidencebased and risk-based considerations framed by a series of policy-relevant questions. These 

questions are outlined in the sections below and generally discuss the extent to which we are able 

to better characterize effects and the likelihood of adverse effects in the environment under the 

current standard. Our approach to considering these questions recognizes that the available 

welfare effects evidence generally reflects laboratory-based evidence of toxicological effects on 

specific organisms exposed to concentrations of Pb. It is widely recognized, however, that 

environmental exposures from atmospherically derived Pb are likely to be lower and/or 

accompanied by significant confounding and modifying factors (e.g., other metals, acidification), 

which increases our uncertainty about the likelihood and magnitude of organism and ecosystem 

responses. 
 6-4 

Figure 6-1. Overview of approach for review of current secondary standard. 

Evidence-based Considerations

 Does currently available evidence and related 

uncertainties strengthen or call into question prior 

conclusions?

 Evidence of welfare effects not previously identified 

or at lower exposures?

 Newly identified at-risk ecosystems?

Changed understanding of lead bioavailability and 

movement of through ecosystems?

Effects at lower air-related exposures than 

previously understood or in conditions that would 

have likely met current standard? 

Risk-based Considerations 

 Nature, magnitude and importance of 

screening level risk information?

Uncertainties in the screening level risk 

assessment?

Consideration of Potential Alternative Standards

Consider 

Retaining 

Current Standard

YES

NO

Adequacy of Current Standard

Does information call into 

question the adequacy of 

current standard?

Elements of Potential Alternative Standards

Indicator

 Averaging Time

Form

Level

Potential Alternative Standards for Consideration
 6-5 

6.2 ADEQUACY OF THE CURRENT STANDARD 

 In considering the adequacy of the current Pb standard, the overarching question we 

consider is:

 Does the currently available scientific evidence- and exposure/risk-based 

information, as reflected in the ISA and REA, support or call into question the 

adequacy of the protection afforded by the current Pb standard? 

To assist us in interpreting the currently available scientific evidence and screening-level 

risk information to address this question, we have focused on a series of more specific questions, 

posed within sections 6.2.1 and 6.2.2 below. In so doing, we consider both the information 

available at the time of the last review and information newly available since the last review 

which has been critically analyzed and characterized in the ISA. 

6.2.1 Evidence-based Considerations 

In considering the welfare effects evidence with respect to the adequacy of the current 

standard, we consider the array of evidence newly assessed in the ISA with regard to the degree 

to which this evidence supports conclusions about the effects of Pb in the environment that were 

drawn in the last review and the extent to which it reduces previously recognized areas of 

uncertainty. Further, we consider the current evidence and associated conclusions about the 

potential for effects to occur as a result of the much lower ambient Pb concentrations allowed by 

the current secondary standard (set in 2008) than those allowed by the prior standard, which was 

the focus of the last review. These considerations, discussed in the context of the specific 

questions below, inform our conclusions regarding the extent to which the evidence supports or 

calls into question the adequacy of protection afforded by the current standard. 

 To what extent does the available information indicate that Pb-related effects are 

occurring as a result of multimedia pathways associated with ambient air 

conditions that would meet the current standard? 

The current evidence continues to support our conclusions from the previous review 

regarding key aspects of the ecological effects evidence for Pb and the effects of exposure 

associated with levels of Pb occurring in ecological media in the U.S. Our conclusions in this 

regard are based on consideration of the assessment of the currently available evidence in the 

ISA, particularly with regard to key aspects summarized in chapter 5 of this PA, in light of the 

assessment of the evidence in the last review as described in the 2006 CD and summarized in the 

notice of final rulemaking (73 FR 67008). Key aspects of conclusions drawn in the last review 

(73 FR 67010) are summarized below. 

 There are several difficulties to quantifying the role of recent air emissions of Pb in the 

environment: 
 6-6 

 While the removal of Pb from on-road gasoline and reductions in industrial 

emissions have resulted in dramatic reductions in overall deposition rates (2006 

CD, pp. AX7-34 and AX7-103), Pb deposited before the 1978 standard, and the 

relatively lesser amount deposited since, is still present in soils and sediments. 

 Historic Pb from gasoline-derived and other air emissions as well as nonair sources 

has produced a legacy of Pb in forest soils that continues to move slowly through 

these systems (2006 CD, section AX7.1.4.3). 

 The evidence of adversity in natural systems is very sparse due in no small part to the 

difficulty in determining the effects of confounding factors such as multiple metals or 

factors influencing bioavailability of Pb in field studies (2006 CD, E-19). 

 For areas influenced by stationary sources of air Pb that met the standard considered in 

the last review at the time of the last review (although they likely did not throughout 

their active period), concentrations of Pb in soil may exceed by many orders of 

magnitude the concentrations which are considered harmful to laboratory organisms 

(2006 CD, sections 3.2 and AX7.1.2.3). 

 Environmental conditions exist in which Pb-associated adverse effects to aquatic 

organisms and thereby ecosystems may be anticipated given experimental results. 

While the evidence does not indicate that dissolved Pb in surface water constitutes a 

threat to those ecosystems that are not directly influenced by point sources, the 

evidence regarding Pb in sediment is less clear. Some areas with long term historical 

deposition of Pb to sediment from a variety of sources as well as areas influenced by 

point sources have the potential for adverse effects to aquatic communities (2006 CD, 

sections AX7.2.2.2 and AX7.2.4). 

The range of effects that Pb can exert on terrestrial and aquatic organisms indicated by 

information available in the current review is summarized in the ISA (ISA, sections 1.7, 6.3 and 

6.4) and largely mirror the findings of from the previous review (summarized above). The 

integrated synthesis contained in the ISA conveys how effects of Pb can vary with species and 

life stage, duration of exposure, form of Pb, and media characteristics such as soil and water 

chemistry. A wide range of organism effects are recognized, including effects on growth, 

development (particularly of the neurological system) and reproductive success (ISA, section 6.3 

and 6.4). Lead is recognized to distribute from the air into multiple environmental media, as 

summarized in section 1.3 above, contributing to multiple exposure pathways for ecological 

receptors. As discussed in section 5.1 above, many factors affect the bioavailability of Pb to 

receptors in terrestrial and aquatic ecosystems, contributing to differences between laboratory-
 6-7 

assessed toxicity and Pb toxicity in these ecosystems, challenging our consideration of 

environmental impacts of Pb emitted to ambient air. 

In studies in a variety of ecosystems, adverse ecosystem-level effects (including 

decreases in species diversity, loss of vegetation, changes to community composition, primarily 

in soil microbes and plants, decreased growth of vegetation, and increased number of invasive 

species) have been demonstrated near smelters, mines and other industries that have released 

substantial amounts of Pb, among other materials, to the environment (ISA, sections 6.3.12 and 

6.4.12). As noted in section 5.1 above, however, our ability to characterize the role of air 

emissions of Pb in contributing to these effects is complicated because of coincident releases to 

other media and of other pollutants. Co-released pollutants include a variety of other heavy 

metals, in addition to sulfur dioxide, which may cause toxic effects in themselves and may 

interact with Pb in the environment, contributing uncertainty to characterization of the role of Pb 

from ambient air with regard to the reported effects. These uncertainties limit our ability to draw 

conclusions regarding the extent to which Pb-related effects may be associated with ambient air 

conditions that would meet the current standard. 

The role of historically emitted Pb, as discussed in section 1.3.2 above, poses additional 

complications in addressing this question. The vast majority of Pb in the U.S. environment 

today, particularly in terrestrial ecosystems, was deposited in the past during the use of Pb 

additives in gasoline (2006 CD, pp. 2-82, AX7-36 to AX7-38, AX7-98; Johnson et al., 2004), 

although contributions from industrial activities, including metals industries have also been 

documented ( ISA, section 2.2.2.3, Jackson et al., 2004). The gasoline-derived Pb was emitted in 

very large quantities (2006 CD, p. AX7-98 and ISA, Figure 2-8) and predominantly in small 

sized particles which were widely dispersed and transported across large distances, within and 

beyond the U.S. (ISA, section 2.2). As recognized in sections 2.3.1 and 2.3.3.2 above, historical 

records provided by sediment cores in various environments document the substantially reduced 

Pb deposition (associated with reduced Pb emissions) in many locations (ISA, section 2.2.1). As 

Pb is persistent in the environment, these substantial past environmental releases are expected to 

generally dominate current nonair media concentrations. There is limited evidence to relate 

specific ecosystem effects with current ambient air concentrations of Pb through deposition to 

terrestrial and aquatic ecosystems and subsequent movement of deposited Pb through the 

environment (e.g., soil, sediment, water, organisms). The potential for ecosystem effects of Pb 

from atmospheric sources under conditions meeting the current standard is difficult to assess due 

to limitations on the availability of information to fully characterize the distribution of Pb from 

the atmosphere into ecosystems over the long term, as well as limitations on information on the 

bioavailability of atmospherically deposited Pb (as affected by the specific characteristics of the 

receiving ecosystem). Therefore, while information available since the 2006 CD includes 
 6-8 

additional terrestrial and aquatic field studies, “the connection between air concentration and 

ecosystem exposure and associated potential for welfare effects continues to be poorly 

characterized for Pb” (ISA, section 6.5). Such a connection is even harder to characterize with 

respect to the current standard than it was in the last review with respect to the previous, much 

higher, standard. 

 To what extent have important uncertainties identified in the last review been 

reduced and/or have new uncertainties emerged? 

In the characterization of effects associated with Pb in ambient air for the last review, the 

areas of largest uncertainty were identified to be associated with our abilities to determine the 

extent of lead-related effects in the natural environment and to apportion effects between air and 

nonair sources, and with the relationship between effects and environmental conditions 

associated with the standard. While we have some new evidence with regard to bioavailability 

and its role in influencing the potential for effects in the environment, overall these remain the 

major sources of uncertainty in our evaluation of effects and exposure evidence for Pb in 

ecosystems. Moreover, the impact of these uncertainties is larger in this review given our 

current focus on a secondary standard much lower than that which was the focus of the last 

review. 

With regard to the extent of lead-related effects in the natural environment, it remains 

difficult to assess the concentrations at which Pb elicits specific effects in terrestrial and aquatic 

systems, due to the influence of other environmental variables on both Pb bioavailability and 

toxicity and also due to substantial species differences in Pb susceptibility (ISA, sections 6.3.2-

6.3.4 and 6.4.2 -6.4.5). There is little new information that would facilitate extrapolation of 

evidence on individual species, generally from controlled laboratory studies, to conclusions 

regarding adversity to populations or ecosystems within the natural environment. For example, in 

terrestrial systems, evidence reviewed in the ISA (ISA, sections 6.2.3 and 6.2.4) demonstrates 

that exposure to Pb is generally associated with negative effects on growth, reproduction and 

survival in terrestrial ecosystems. Many factors, including species composition and various soil 

physiochemical properties, interact strongly with Pb concentration to modify effects. Also, the 

changes associated with environmental aging of lead-contaminated material is a particularly 

important factor in terrestrial systems, where soil is the main route of exposure, however, aging 

of lead-contaminated soil is difficult to reproduce experimentally (ISA, sections 6.3.9.3 and 

6.3.11). Without quantitatively accounting for these factors, laboratory-derived 

“characterizations of exposure-response relationships would likely not be transferable outside of 

experimental settings” (ISA, p. 1-42). 

With regard to the role of air-related Pb, as discussed above and noted in the ISA, “the 

connection between air concentration and ecosystem exposures continues to be poorly 
 6-9 

characterized for Pb and the contribution of atmospheric Pb to specific sites is not clear” (ISA, p. 

6-264). Thus, the limited evidence and associated uncertainties connecting air concentrations to 

ecosystem exposures and possible effects, in combination with those that influence Pb 

bioavailability and ecosystem mobility, are areas particularly limiting the extent to which critical 

loads analyses might otherwise be useful to our assessment in this review, as discussed in section 

5.1. Thus, the evidence is lacking in quantitative relationships between Pb in ambient air and 

welfare effects, including identification of a specific exposure metric or index (e.g., 

mathematical formulation of averaging time and concentration) by which to consider ambient air 

Pb concentrations with regard to the potential for adverse effects to public welfare. In the 

decision in the last review to set the secondary standard equal to the primary standard, EPA 

similarly recognized a lack of evidence that related welfare effects to Pb in ambient air and from 

which differing standard elements (e.g., averaging time and concentration) might be derived for 

the secondary standard.1

 These limitations in the evidence base remain in the current review. 

As in the last review, consideration of the environmental risks and potential welfare 

effects associated with the current standard is complicated by the environmental burden 

associated with air Pb concentrations, predominantly in the past, that exceeded both the 

previously existing standard and the current standard (USEPA, 2007, section 6.4.4.2). For 

example, a large portion of Pb deposited before the current standard was enacted is likely still 

present in soils and sediments, and historic Pb from gasoline (and other historic sources) 

continues to move slowly through systems as does Pb derived from current air and nonair 

sources. As a general matter, the currently available evidence, as assessed in the ISA, does not 

significantly reduce any of the areas of uncertainty described here which, given the standard 

considered in the present review (with its much lower level than the previous standard), weigh 

heavily in our consideration of the adequacy of the current standard. 

6.2.2 Exposure/Risk-based Considerations 

 To what extent does risk or exposure information indicate that air-related 

ecosystem exposures important from a public welfare perspective are likely to 

occur with air Pb levels that just meet the current standard? 

The current evidence continues to support our conclusions with regard to interpreting the 

risk and exposure results from the previous review. Our conclusions in this regard are based on 

 

1

 As described in section 6.1.1 above, the EPA concluded in the last review that the then-current secondary 

standard did not provide requisite protection from effects adverse to public welfare. In considering the appropriate 

revision, EPA recognized that the Agency lacked the relevant data to provide a clear quantitative basis for setting a 

secondary Pb NAAQS that differs from the primary standard, yet recognized that significant beneficial effects were 

likely to result in terms of reduced magnitude of Pb exposures in the environment and associated toxicity impacts on 

ecosystems from a significant change to the level for the secondary standard, such as the order-of-magnitude change 

which was achieved by setting the secondary standard identical to the revised primary standard (73 FR 67012). 
 6-10 

consideration of the screening-level ecological risk assessment results from the previous review 

as described in the 2006 REA and summarized in the notice of final rulemaking (73 FR 67009) 

and in light of the currently available evidence in the ISA. Key aspects of these results in the 

context of the current standard are summarized below, drawing from the discussion of the 2006 

REA results in section 5.2.2 above, which is based on the information in the 2006 REA (ICF, 

2006). 

Primary Pb Smelter Case Study 

 While the contribution to Pb concentrations from air as compared to nonair sources is 

not quantified, air emissions from this facility are substantial (ICF, 2006). Currently, 

the county where this facility is located exceeds the now-current Pb NAAQS. 

Secondary Pb Smelter Case Study 

 While the contribution from air deposited Pb to the overall Pb concentrations modeled 

in soils at this location is unclear, the facility continues to emit Pb and the county 

where this facility is located exceeds the now-current Pb NAAQS (Appendices 2D and 

5A). 

Near Roadway Non-urban Case Study 

 These case study locations are highly impacted by past deposition of gasoline Pb. It is 

unknown whether current conditions at these sites exceed the now-current Pb standard, 

but given evidence from the past of Pb concentrations near highways that ranged above 

the previous (1978) Pb standard (1986 CD, section 7.2.1), conditions at these locations 

during the time of leaded gasoline very likely exceeded the 1978 standard. 

Vulnerable Ecosystem Case Study 

 The previous review concluded that atmospheric Pb inputs do not directly affect stream 

Pb levels at Hubbard Brook Experimental Forest because deposited Pb is almost 

entirely retained in the soil profile and that there was “little evidence that sites affected 

primarily by long-range Pb transport [such as this one] have experienced significant 

effects on ecosystem structure or function” (2006 CD, p. AX-98). Further, it is 

unlikely that conditions have changed from the data through 2000 on which the 

previous conclusions were based, and, therefore, current ambient air concentrations 

likely do not directly impact stream Pb levels under air quality conditions associated 

with meeting the now-current standard. 

National-scale Surface Water and Sediment Screen 

 The extent to which past air emissions of Pb have contributed to surface water or 

sediment Pb concentrations at the locations identified in the screen is unclear. For 

some of the surface water locations, nonair sources likely contributed significantly to 

the surface water Pb concentrations. For other locations, a lack of nearby nonair 

sources indicated a potential role for air sources to contribute to observed surface water 

Pb concentrations. Additionally, these concentrations may have been influenced by Pb 
 6-11 

in resuspended sediments and/or reflect contribution of Pb from erosion of soils with 

Pb derived from historic as well as current air emissions. 

Although the available risk and exposure information continues to be sufficient to 

conclude that the 1978 standard was not providing adequate protection to ecosystems, that 

information, when considered with regard to air-related ecosystem exposures likely to occur with 

air Pb levels that just meet the now-current standard, does not provide evidence that the current 

secondary standard (set in 2008) is inadequate. 

6.2.3 CASAC Advice 

In our consideration of the adequacy of the current standards, in addition to the evidenceand risk/exposure-based information discussed above, we have also considered the advice and 

recommendations of CASAC, based on their review of the ISA and the earlier draft of this 

document. Comments from the public on earlier drafts of this document did not address the 

adequacy of the current secondary standard.2

 

In their advice and comments conveyed in the context of their review of the draft PA, the 

CASAC agreed with staff’s preliminary conclusions that the available information since the last 

review is not sufficient to warrant revision to the secondary standard (Frey, 2013). On this 

subject, the CASAC letter said the following. 

Overall, the CASAC concurs with the EPA that the current scientific literature 

does not support a revision to the Primary Lead (Pb) National Ambient Air 

quality Standard (NAAQS) nor the Secondary Pb NAAQS. 

The CASAC also recognized the many uncertainties and data gaps in the new scientific literature 

and recommended that research be performed in the future to address these limitations. 

Given the existing scientific data, the CASAC concurs with retaining the current 

secondary standard without revision. However, the CASAC also notes that 

important research gaps remain. For example questions remain regarding the 

relevance of the primary standard’s indicator, level, averaging time, and form for 

the secondary standard. Other areas for additional research to address data gaps 

and uncertainty include developing a critical loads approach for U.S. conditions 

and a multi-media approach to account for legacy Pb and contributions from 

different sources. Addressing these gaps may require reconsideration of the 

secondary standard in future assessments.

 

2

 All written comments submitted to the Agency will be available in the docket for this rulemaking, as will 

be transcripts of the public meetings held in conjunction with CASAC’s review of the earlier draft of this document, 

of the REA Planning Document and of drafts of the ISA. 
 6-12 

6.3 STAFF CONCLUSIONS ON THE SECONDARY STANDARD 

This section describes staff conclusions regarding adequacy of the current secondary Pb 

standard. These conclusions are based on considerations described above and in the discussion 

below regarding the currently available scientific evidence summarized in the ISA and prior CDs 

and the risk and exposure information drawn from the 2006 REA. These conclusions also take 

into account advice from CASAC and public comment on the draft PA and preliminary 

conclusions. 

Taking into consideration the discussions responding to specific questions above in this 

and the prior chapter, this section addresses the following overarching policy question: 

 Does the currently available scientific evidence- and exposure/risk-based 

information, as reflected in the ISA and REA, support or call into question the 

adequacy of the protection afforded by the current secondary Pb standard? 

With respect to evidence-based considerations, the body of evidence on the ecological 

effects of Pb, expanded in some aspects since the last review, continues to support identification 

of ecological effects in organisms relating to growth, reproduction, and survival as the most 

relevant endpoints associated with Pb exposure. In consideration of the appreciable influence of 

site-specific environmental characteristics on the bioavailability and toxicity of environmental Pb 

in our assessment here, we give greater weight to studies conducted under conditions most 

closely reflecting the natural environment as compared to laboratory-based exposures. The 

currently available evidence, while somewhat expanded since the last review, does not include 

evidence of significant effects at lower concentrations or evidence of higher level ecosystem 

effects beyond those reported in the last review. There continue to be significant difficulties in 

interpreting effects evidence from laboratory studies to the natural environment and linking those 

effects to ambient air Pb concentrations. Further, we are aware of no new critical loads 

information that would inform our interpretation of the public welfare significance of the effects 

of Pb in various ecosystems (as discussed in section 5.1). In summary, while new research has 

added to the understanding of Pb biogeochemistry and expanded the list of organisms for which 

Pb effects have been described, there remains a significant lack of knowledge about the potential 

for adverse effects on public welfare from ambient air Pb in the environment and the exposures 

that occur from such air-derived Pb, particularly under the current standard. 

With respect to exposure/risk-based considerations, we recognize the complexity of 

interpreting the previous risk assessment with regard to the ecological risk of ambient air Pb 

associated with conditions meeting the current standard and the associated limitations and 

uncertainties of such assessments. For example, the location-specific case studies as well as the 

national screen conducted in the last review reflect both current air Pb deposition as well as past 

air and nonair source contributions. We conclude that while the previous assessment is 
 6-13 

consistent with and generally supportive of the evidence-based conclusions about Pb in the 

environment, the limitations of apportioning Pb between past and present air contributions and 

between air and nonair sources remain significant. 

In now considering the adequacy of the current standard in this review, we have 

considered the ecological and welfare effects evidence assessed in the ISA and discussed in 

sections 5.1, 2.3 and 6.2.1 above, as well screening-level exposure;/risk information gained from 

the 2006 REA discussed in sections 5.2 and 6.2.2 above, and staff judgments on associated 

implications with regard to public welfare. As summarized, in section 6.2.1 above, the scientific 

evidence presented in detail in the ISA, inclusive of that newly available in this review, is not 

substantively changed, most particularly with regard to our needs in reviewing the current 

standard, from the information that was available in the last review. The evidence base does not 

indicate that the current standard is inadequate. Further, our updated consideration of the 

screening-level risk information from the 2006 REA, as summarized in section 6.2.2 above, 

additionally does not provide evidence that the current secondary standard is inadequate. Thus, 

we conclude that the currently available evidence and exposure/risk information do not call into 

question the adequacy of the current standard to provide the requisite protection for public 

welfare. Accordingly, we reach the conclusion that it is appropriate to consider retaining the 

current secondary standard without revision. 

6.4 KEY UNCERTAINTIES AND AREAS FOR FUTURE RESEARCH AND DATA 

COLLECTION 

In this section, we highlight key uncertainties associated with reviewing the secondary 

NAAQS for Pb. Such key uncertainties and recommendations for ecosystem-related research, 

model development, and data gathering are outlined below. In some cases, research in these 

areas can go beyond supporting standard setting to aiding in the development of more efficient 

and effective control strategies. We note, however, that a full set of research recommendations 

to meet standards implementation and strategy development needs is beyond the scope of this 

discussion. Rather, listed below are key uncertainties and research questions and data gaps that 

have been thus far highlighted in this review of the welfare-based secondary standard for Pb. 

 Our understanding of the extent and degree of adverse impact occurring in the 

environment due to Pb (from atmospheric and other sources) is incomplete and leads to 

uncertainty in characterizing environmental effects of Pb, which is necessary to assess 

potential associated effects on public welfare. 

 The available studies on community and ecosystem-level effects are sparse and 

usually from contaminated areas where Pb concentrations are much higher than 

typically encountered in the environment as a result of atmospheric input and are 

usually co-occurring with elevated concentrations of other pollutants.
 6-14 

 Many ecosystem-specific characteristics affect bioavailability and associated 

toxicity, contributing uncertainty to our interpretation of study results from 

laboratory test-systems. For example, the role of modifying factors such as soil and 

water chemistry on Pb toxicity continues to be a source of uncertainty when 

determining the degree of adverse impact from Pb. 3

 Evidence regarding relationships between organism-level effects of Pb (e.g., 

reproduction, growth, and survival) and effects at the population level and higher is 

lacking especially in natural systems. 

 A better understanding of the potential for adverse effects from Pb in estuarine and 

marine systems is needed. 

 There is appreciable uncertainty in our understanding of the current dynamics of Pb in 

U.S. ecosystems. 

 In general, the connection between air concentration of Pb and ecosystem exposure 

continues to be poorly characterized and is complicated by the legacy of historical 

inputs both from air and, in some systems, also from other sources.

 There is uncertainty in characterizing the fate and transport of Pb in the 

environment through air, water, and soil media. This limits our ability to account 

for the role of past Pb releases in current media concentrations and to link effects to 

current air contributions. 

 An important source of uncertainty in characterizing the effects of air-related Pb in 

some U.S. ecosystems is that associated with distinguishing air-related Pb from 

other sources of Pb. It is difficult to determine the portion of Pb occurring in some 

ecosystems that derives from the atmosphere as compared to that from other 

sources. 

 Development of critical loads information for U.S. ecosystems would allow for a 

much improved understanding of the significance of air contributions to ecosystems 

and ecological receptor exposures, as well as that of contributions from other sources. 

Development of a critical loads approach, with sensitivity analysis, would inform 

identification of processes critical to ecological receptor exposures and toxicity. 

 Such critical loads analyses could inform characterization of the variability of 

response across ecosystems to determine which ecosystems are most sensitive. 

 Additional research is needed to provide inputs for development of critical loads, 

particularly for a broader range of ecosystem-level endpoints. 

 Information is currently lacking to inform identification of standard elements, such as 

averaging time and form, specifically reflecting a ecological and public welfare 

context for ambient air Pb. 

 

3

 Further uncertainty accompanies the interpretation of toxicity data from test systems involving artificial 

media such as hydroponic systems, agar or culture media. 
 6-15 

6.5 REFERENCES 

Frey, H.C. (2013) Letter from Dr. H. Christopher Frey, Chair, Clean Air Scientific Advisory Committee and Clean 

Air Scientific Advisory Committee Lead Review Panel, to Acting Administrator Bob Perciasepe. Re: 

CASAC Review of the EPA’s Policy Assessment for Lead (External Review Draft – January 2013). June 4, 

2013. 

Henderson, R. (2007a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

the 1st Draft Lead Staff Paper and Draft Lead Exposure and Risk Assessments. March 27, 2007. 

Henderson, R. (2007b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

the 2nd Draft Lead Human Exposure and Health Risk Assessments. September 27, 2007. 

Henderson, R. (2008a) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

the Advance Notice of Proposed Rulemaking (ANPR) for the NAAQS for lead. January 22, 2008. 

Henderson, R. (2008b) Letter from Dr. Rogene Henderson, Chair, Clean Air Scientific Advisory Committee, to 

Administrator Stephen L. Johnson. Re: Clean Air Scientific Advisory Committee’s (CASAC) Review of 

the Notice of Proposed Rulemaking for the NAAQS for lead. July 18, 2008. 

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

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

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

Jackson, B. P.; Winger, P. V.; Lasier, P. J. (2004) Atmospheric lead deposition to Okefenokee Swamp, Georgia, 

USA. Environ. Pollut. 130: 445-451. 

Johnson, C. E.; Petras, R. J.; April, R. H.; Siccama, T. G. (2004) Post-glacial lead dynamics in a forest soil. Water 

Air Soil Pollut. 4: 579-590. 

U.S. Environmental Protection Agency. (2006) Air Quality Criteria for Lead. Referred to as 2006 CD. Washington, 

DC, EPA/600/R-5/144aF. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html 

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

Policy Assessment of Scientific and Technical Information OAQPS Staff Paper. Washington, DC, EPA452/R-07-013. Available online at: http://www.epa.gov/ttn/naaqs/standards/pb/s_pb_cr.html 

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

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

 Appendix 2A. Recent Regulatory Actions on Stationary Sources of Lead ............................ 2A-1 

 Appendix 2B. The 2008 NEI: Data Sources, Limitations and Confidence ........................... 2B-1 

 Appendix 2C. Criteria for Air Quality Data Analysis ............................................................ 2C-1 

 Appendix 2D. Air Quality Data Analysis Summary .............................................................. 2D-1 

 Appendix 3A. Interpolated Risk Estimates for the Generalized (Local) Urban Case Study .. 3A-1 

 Appendix 5A. Additional Detail on 2006 Ecological Screening Assessment ........................ 5A-1 
2A-1 

APPENDIX 2A 

RECENT REGULATORY ACTIONS ON STATIONARY SOURCES OF LEAD 

The table below identifies recent actions projected to result in reductions in Pb emissions 

from stationary sources. 

Action Source Categories Affected Citation 

Estimated Pb 

Emissions 

Reduction 

(tons per 

year)

Year of 

Compliance 

(year in which 

reductions 

estimated to 

begin)

NESHAP Secondary Lead Smelting 77 FR 555 

(1/5/2012) 13.6 2014 

NESHAP Primary Lead Smelting 76 FR 70834 

(11/15/2011) 10 2013 

NESHAP Area Sources: Clay Ceramics Manufacturing, Glass 

Manufacturing, and Secondary Nonferrous Metals 

Processing 

72 FR 73179 

(12/26/2007) Unquantified* 2007, 2009, 2007 

NESHAP Area Sources: Electric Arc Furnace Steelmaking Facilities 72 FR 74088 

(12/28/2007) Unquantified* 2008 or 2010 

NESHAP Iron and Steel Foundries Area Sources 73 FR 225 

(1/2/2008) Unquantified* 2010 

NESHAP Area Source Standards for Aluminum, Copper, and Other 

Nonferrous Foundries 

74 FR 30366 

(6/25/2009) Unquantified* 2011 

NESHAP, 

NSPS Portland Cement Manufacturing Industry 78 FR 10006 

(2/12/2013) 6.72 2015 

EGES, 

NSPS Commercial and Industrial Solid Waste Incineration Units 76 FR 9112 

(02/07/2013) 2.51 2018 

EGES, 

NSPS 

Standards of Performance for New Stationary Sources and 

Emission Guidelines for Existing Sources: Sewage Sludge 

Incineration Units 

76 FR 15372 

(3/21/2011) 1.2-1.5 2016 

NESHAP Major Sources: Industrial, Commercial, and Institutional 

Boilers, and Process Heaters 

78 FR 7138 

(1/31/2013) Unquantified* 2016 

EGES, 

NSPS 

Standards of Performance for New Stationary Sources and 

Emissions Guidelines for Existing Sources: 

Hospital/Medical/Infectious Waste Incinerators 

74 FR 51367 

(10/6/2009) 0.16 2014 

EGES = Emissions Guidelines for Existing Sources 

NESHAP = National Emission Standards for Hazardous Air Pollutants 

NSPS = New Source Performance Standards 

*Unquantified = Reductions in Pb emissions expected from controls in response to regulatory action have not been quantified. 
2B-1 

APPENDIX 2B 

THE 2008 NEI: DATA SOURCES, LIMITATIONS AND 

CONFIDENCE 

The process of identifying sources that emit Pb into the air has been ongoing since before 

the Clean Air Act of 1970. The comprehensiveness of emission inventories generally, and the 

NEI, specifically, depends upon knowledge of source types emit Pb, their locations and their 

operating characteristics, as well as the reporting of this information to the inventory. As noted 

above, the NEI relies on information that is available from a variety of sources for this 

information. There are numerous steps, each with its own uncertainties, associated with the 

development of this information for use in the emissions inventory. First, the categories emitting 

Pb must be identified. Second, the sources’ processes and control devices must be known. 

Third, the activity throughputs and operating schedules of these sources must be known. Finally, 

we must have emission factors to relate emissions to the operating throughputs, process 

conditions and control devices. The process, control device, throughputs and operating 

schedules are generally available for each source. However, the emission factors represent 

average emissions for a source type and average emissions may differ significantly from source 

to source. In some cases, emissions testing provides source-specific information. In others, 

emissions factors must be estimated from similar sources or source categories, or from other 

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

 

The Pb emissions information presented in chapter 2 is drawn largely from EPA’s NEI 

for 2008. The NEI is based on information submitted from State, Tribal and local air pollution 

agencies and data obtained during the preparation of technical support information for EPA’s 

hazardous air pollutant regulatory programs. Data in the 2008 NEI for Pb emissions from the 

use of leaded aviation gasoline were developed by EPA using the Federal Aviation 

Administration’s operations activity data, where available.2

 The data were then reviewed by 

State, Tribal, and local air pollution agencies. With some additions, the information presented in 

this document is primarily based on version 3 of the NEI for 2008, available on the EPA’s 

CHIEF website at (http://www.epa.gov/ttn/chief/net/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. 
2B-2 

with regard to Pb emissions estimates for some sources. For example, we have not yet 

developed estimates for the NEI of Pb emissions for the miscellaneous categories of on-road 

emissions (e.g., combustion of fuel with Pb traces, lubricating oil, mechanical wear of vehicle 

components, etc.) and Pb that may be emitted from wildfires, or for emissions associated with 

resuspension of Pb residing in roadway dust and nearby surface soil in areas not otherwise 

associated with industrial facilities (see section 2.1.2). 

The 2008 NEI underwent extensive external review, including a review of the process for 

developing the inventory which includes extensive quality assurance and quality control steps 

(QA/QC). We provided feedback reports to point source data providers and we posted several 

versions of the inventory on our website. We also conducted additional QA targeted at facilities 

with appreciable Pb emissions in previous years to ensure that 2008 Pb emissions were reported, 

and we augmented with TRI where facilities with annual emissions greater than 0.5 tpy in 2005 

were not reported to NEI in 2008 due to Pb emissions reporting thresholds 

(ftp://ftp.epa.gov/EmisInventory/20008v2/doc/2008neiv2_issues.xlsx). Further, there was 

additional QA/QC conducted for emission inventory information for facilities that are included 

in Risk and Technology Review source categories.3

 As a result we have strong confidence in the 

quality of the data for these facilities. In summary, generic limitations to the 2008 NEI include 

the following. 

 Consistency: The 2008 NEI for Pb is a composite of emissions estimates generated by 

state and local regulatory agencies, industry, and EPA. Because the estimates 

originated from a variety of sources, as well as for differing purposes, they will in turn 

vary in quality, whether Pb is reported for particular source types, method of reporting 

compound classes, level of detail, and geographic coverage. 

 Variability in Quality and Accuracy of Emission Estimation Methods: The accuracy of 

emission estimation techniques varies with pollutants and source categories. In some 

cases, an estimate may be based on a few or only one emission measurement at a 

similar source. The techniques used and quality of the estimates will vary between 

source categories and between area, major, and mobile source sectors. Generally, the 

more review and scrutiny given to emissions data by states and other agencies, the 

more certainty and accuracy there is in those estimates. 

 

3

 The Risk and Technology Review is a combined effort to evaluate both risk and technology as required 

by the Clean Air Act (CAA) after the application of maximum achievable control technology (MACT) standards. 

Section 112(f)(2) of the CAA directs EPA to conduct 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 . 
2C-1 

APPENDIX 2C 

CRITERIA FOR AIR QUALITY DATA ANALYSIS 

Criteria for the 2010-2012 data analysis presented in Figures 2-10 through 2-13 are as 

listed below, with abbreviations defined following this list. 

 Years utilized were 2010-2012. November and December 2009 data were also used for 

the rolling 3-month average analysis. 

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

 Data for parameter 14129 (Pb-TSP FRM/FEM LC) were used for Pb-TSP analysis; 

data for parameters 84128 (Pb-PM2.5 STP) and 88128 (Pb-PM2.5 LC) were used for PbPM2.5 analysis; and data for parameters 82128 (Pb-PM10 STP), 85128 (Pb-PM10 LC), 

and 85129 (Pb-PM10 FRM/FEM LC) were used for Pb-PM10 analysis. No adjustment 

was made to the STP or LC data to make them more comparable to each other; based 

on previous analysis, the LC and STP versions of same-site-day samples are extremely 

similar. Collocated data – for same size cut- were combined to a site basis by using the 

following hierarchy, evaluated each site-day: LC FRM/FEM parameter data takes 

precedence over LC (non-FRM/FEM) parameter data, and those data take precedence 

overSTP parameter data; also, within those categories, lower POC numbers take 

precedence over higher POC numbers. 

 For maximum rolling 3-month average analysis, the 2010-2012 databases also 

encompassed the prior 2 months (i.e., November and December 2009 data): 3 or more 

observations were needed to make a valid monthly; 3 valid consecutive months were 

required to make a valid rolling 3-month period; 6 valid rolling 3-month periods were 

required to make a valid year; and 1, 2, or 3 valid years were required to make a valid 

3-year metric. Thus, the shortest duration that could potentially meet these criteria for 

the maximum 3-month average analysis is 8 months. The 3-year maximum rolling 3-

month average metric (by size cut for 2010-2012) was identified as the highest valid 3-

month average across the valid (1, 2, or 3) years. 

 For maximum monthly analysis: 3 or more observations were needed to make a valid 

monthly; 6 valid months were required to make a valid year; and 1, 2, or 3 valid years 

were required to make a valid 3-year metric. Thus, the shortest duration that could 

potentially meet these criteria for the maximum monthly analysis is 6 months. The 3-

year maximum monthly metric (by size cut for 2010-2012) was identified as the 

highest valid monthly average across the valid (1, 2, or 3) years. 

 For annual average analysis: monthly averages were used to construct annual 

averages,3 or more observations were required to make a valid; 6 valid months were 

required to make a valid year (i.e., annual average) and 1, 2, or 3 valid years were 

required to make a valid annual metric. Thus, the shortest duration that could 

potentially meet these criteria for the annual average analysis is 6 months. The 3-year 

annual mean metric (by size cut for 2010-2012) was identified as the average of the 1, 

2, or 3 (2010, 2011, and/or 2012) valid annual means. 
2C-2 

Definitions for Abbreviations 

FEM – Federal equivalent method 

FRM – Federal reference method 

LC – Local conditions 

POC – Parameter occurrence code 

STP – Standard temperature and pressure 

The process for classifying monitors as “source oriented” or “non-source-oriented” began 

with the application of these criteria: (a) a minimum of 0.5 cumulative tons per year of Pb 

emissions within 1 mile of the monitoring site based on 2008 NEI and/or (b) monitors identified 

as “source-oriented” within AQS based on the same-name Monitoring Objective tag. Next, the 

Regional monitoring leads reviewed the listings and provided local, and often monitor-specific 

information and lastly Google Earth and more focused queries were applied. 

The 14 monitors sited for the airport monitoring study, along with the 3 monitors sited at 

airports estimated to emit at least 1 tpy were classified as source-oriented (airport) sites and the 

remaining source-oriented sites were classified as source-oriented (non-airport) sites. 

Among the remaining sites that were not classified as “source-oriented”, previous sourceoriented sites were those that had previously been active source sites but for which current 

information indicated the impacting facility had closed. The particular circumstances related to 

the emission sources associated with these nine monitoring sites vary considerably. In some 

instances the emission sources have been closed for more than a decade and the facility locations 

have undergone remediation. For other sources, production and clean-up status was not fully 

ascertained. 

Non-source sites were what was left after making the airport source-oriented, non-airport 

source-oriented, and previous source-oriented designations. 
APPENDIX 2D

State County Site

Maximum 3-

month 

mean 

(μg/m3)

Annual 

average 

(μg/m3

)

Maximum 

monthly 

mean 

(μg/m3

)

Non-airport

sourceoriented 

(during 

2010-

2012)

Airport 

sourceoriented

Previous 

sourceoriented 

Alabama Limestone 010830005 0.009 0.007 0.012 0 1 0

Alabama Pike 011090003 1.296 0.613 2.262 1 0 0

Alaska Anchorage Municipali 020200051 0.067 0.054 0.073 0 1 0

Arizona Gila 040071002 0.267 0.131 0.306 1 0 0

Arizona Gila 040078000 0.061 0.030 0.077 1 0 0

Arizona Maricopa 040134018 0.038 0.031 0.049 0 1 0

Arizona Pima 040191028 0.002 0.002 0.003 0 0 0

California Fresno 060190011 0.005 0.004 0.005 0 0 0

California Imperial 060250005 0.026 0.017 0.031 0 0 0

California Los Angeles 060371103 0.013 0.009 0.014 0 0 0

California Los Angeles 060371302 0.015 0.007 0.014 0 0 0

California Los Angeles 060371402 0.061 0.033 0.092 0 1 0

California Los Angeles 060371403 0.110 0.055 0.124 1 0 0

California Los Angeles 060371404 0.108 0.042 0.140 1 0 0

California Los Angeles 060371405 0.450 0.241 0.523 1 0 0

California Los Angeles 060371406 0.072 0.035 0.085 1 0 0

California Los Angeles 060371602 0.013 0.008 0.017 0 0 0

California Los Angeles 060374002 0.009 0.005 0.010 0 0 0

California Los Angeles 060374004 0.010 0.006 0.010 0 0 0

California Los Angeles 060375005 0.006 0.003 0.008 0 0 0

California Riverside 060651003 0.008 0.005 0.010 0 0 0

California Riverside 060658001 0.008 0.006 0.010 0 0 0

California San Bernardino 060711004 0.010 0.006 0.012 0 0 0

California San Bernardino 060719004 0.011 0.007 0.013 0 0 0

California San Diego 060730003 0.006 0.005 0.007 0 0 0

California San Diego 060731020 0.127 0.234 0 1 0

California San Diego 060731021 0.058 0.074 0 1 0

California San Mateo 060812002 0.331 0.255 0.401 0 1 0

California Santa Clara 060852010 0.119 0.090 0.151 0 1 0

California Santa Clara 060852011 0.093 0.070 0.102 0 1 0

Colorado Arapahoe 080050007 0.023 0.014 0.035 0 1 0

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

 2D - 1
APPENDIX 2D

State County Site

Maximum 3-

month 

mean 

(μg/m3)

Annual 

average 

(μg/m3

)

Maximum 

monthly 

mean 

(μg/m3

)

Non-airport

sourceoriented 

(during 

2010-

2012)

Airport 

sourceoriented

Previous 

sourceoriented 

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

Colorado Denver 080310025 0.010 0.006 0.013 0 0 0

District of ColumbDistrict of Columbia 110010043 0.004 0.003 0.005 0 0 0

Florida Hillsborough 120570100 0.044 0.025 0.100 1 0 0

Florida Hillsborough 120571066 0.984 0.374 1.959 1 0 0

Florida Hillsborough 120571073 0.423 0.151 0.977 1 0 0

Georgia Bartow 130150003 0.027 0.015 0.039 1 0 0

Georgia DeKalb 130890003 0.004 0.003 0.006 0 0 0

Georgia Muscogee 132150009 0.230 0.128 0.424 1 0 0

Georgia Muscogee 132150010 0.170 0.114 0.234 1 0 0

Georgia Muscogee 132150011 0.071 0.023 0.140 0 0 1

Hawaii Honolulu 150030010 0.001 0.001 0.001 0 0 0

Illinois Cook 170310001 0.024 0.018 0.028 0 0 0

Illinois Cook 170310022 0.047 0.034 0.064 0 0 0

Illinois Cook 170310026 0.034 0.023 0.038 0 0 0

Illinois Cook 170310052 0.024 0.017 0.032 0 0 0

Illinois Cook 170310110 0.294 0.077 0.580 1 0 0

Illinois Cook 170310210 0.053 0.032 0.092 1 0 0

Illinois Cook 170313103 0.041 0.014 0.103 0 0 0

Illinois Cook 170313301 0.027 0.019 0.028 0 0 0

Illinois Cook 170314201 0.011 0.010 0.012 0 0 0

Illinois Cook 170316003 0.042 0.024 0.080 0 0 0

Illinois Macon 171150110 0.199 0.073 0.386 1 0 0

Illinois Madison 171190010 0.416 0.140 0.848 1 0 0

Illinois Madison 171193007 0.036 0.020 0.053 0 0 0

Illinois Peoria 171430037 0.011 0.010 0.013 0 0 0

Illinois Peoria 171430110 0.016 0.012 0.024 1 0 0

Illinois Peoria 171430210 0.015 0.011 0.026 1 0 0

Illinois St. Clair 171630010 0.029 0.020 0.038 0 0 1

Illinois Whiteside 171950110 0.028 0.020 0.040 1 0 0

Illinois Winnebago 172010110 0.063 0.028 0.118 1 0 0

Indiana Delaware 180350009 0.338 0.159 0.476 1 0 0

 2D - 2
APPENDIX 2D

State County Site

Maximum 3-

month 

mean 

(μg/m3)

Annual 

average 

(μg/m3

)

Maximum 

monthly 

mean 

(μg/m3

)

Non-airport

sourceoriented 

(during 

2010-

2012)

Airport 

sourceoriented

Previous 

sourceoriented 

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

Indiana Lake 180890023 0.077 0.031 0.087 1 0 0

Indiana Lake 180890032 0.060 0.023 0.144 1 0 0

Indiana Lake 180890033 0.139 0.055 0.298 1 0 0

Indiana Lake 180892008 0.046 0.020 0.103 0 0 0

Indiana Marion 180970063 0.079 0.028 0.125 1 0 0

Indiana Marion 180970076 0.020 0.010 0.029 1 0 0

Indiana Marion 180970078 0.011 0.006 0.021 0 0 0

Indiana Porter 181270023 0.022 0.013 0.032 1 0 0

Indiana Porter 181270027 0.041 0.027 0.085 1 0 0

Indiana Vanderburgh 181630020 0.006 0.004 0.008 0 0 0

Iowa Pottawattamie 191550011 0.263 0.123 0.282 1 0 0

Iowa Scott 191630015 0.012 0.010 0.024 0 0 0

Kansas Saline 201690004 0.421 0.164 0.488 1 0 0

Kansas Wyandotte 202090021 0.011 0.008 0.012 0 0 0

Kentucky Boyd 210190016 0.004 0.003 0.007 1 0 0

Kentucky Madison 211510003 0.248 0.057 0.281 1 0 0

Kentucky Madison 211510005 1.584 0.703 2.244 1 0 0

Kentucky Russell 212070001 0.063 0.027 0.109 1 0 0

Louisiana East Baton Rouge Pa 220330009 0.002 0.002 0.003 0 0 0

Louisiana East Baton Rouge Pa 220330014 0.011 0.004 0.027 1 0 0

Louisiana St. John the Baptist P 220950003 0.053 0.025 0.066 1 0 0

Massachusetts Nantucket County 250190001 0.010 0.009 0.020 0 1 0

Michigan Charlevoix 260290011 0.006 0.005 0.010 1 0 0

Michigan Ionia 260670002 0.049 0.071 0.298 1 0 0

Michigan Ionia 260670003 0.284 0.096 0.414 1 0 0

Michigan Kent 260810020 0.008 0.005 0.010 0 0 0

Michigan Oakland 261250013 0.022 0.019 0.027 0 1 0

Michigan Tuscola 261570001 0.034 0.021 0.063 1 0 0

Michigan Wayne 261630001 0.006 0.005 0.007 0 0 0

Michigan Wayne 261630033 0.023 0.012 0.034 0 0 0

Minnesota Anoka 270031002 0.011 0.006 0.012 0 0 0

 2D - 3
APPENDIX 2D

State County Site

Maximum 3-

month 

mean 

(μg/m3)

Annual 

average 

(μg/m3

)

Maximum 

monthly 

mean 

(μg/m3

)

Non-airport

sourceoriented 

(during 

2010-

2012)

Airport 

sourceoriented

Previous 

sourceoriented 

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

Minnesota Anoka 270036020 0.038 0.017 0.078 1 0 0

Minnesota Beltrami 270072303 0.001 0.002 0 0 0

Minnesota Cass 270210001 0.001 0.002 0 0 0

Minnesota Dakota 270370020 0.004 0.004 0.018 0 0 0

Minnesota Dakota 270370465 0.259 0.096 0.568 1 0 0

Minnesota Dakota 270370470 0.002 0.001 0.004 0 0 0

Minnesota Hennepin 270530963 0.004 0.003 0.006 0 0 0

Minnesota Hennepin 270530966 0.005 0.004 0.008 0 0 0

Minnesota Hennepin 270531007 0.004 0.003 0.007 0 0 0

Minnesota Mille Lacs 270953051 0.001 0.000 0.002 0 0 0

Minnesota Ramsey 271230871 0.007 0.005 0.010 0 0 0

Minnesota St. Louis 271377001 0.008 0.002 0.022 0 0 0

Minnesota St. Louis 271377555 0.004 0.003 0.008 0 0 0

Minnesota Stearns 271453053 0.008 0.004 0.012 1 0 0

Minnesota Washington 271630438 0.005 0.003 0.008 0 0 0

Minnesota Washington 271630446 0.001 0.000 0.003 0 0 0

Missouri Iron 290930016 0.882 0.484 1.436 1 0 0

Missouri Iron 290930021 1.147 0.522 1.698 1 0 0

Missouri Iron 290930027 0.083 0.033 0.107 0 0 1

Missouri Iron 290930029 0.115 0.038 0.271 0 0 1

Missouri Iron 290930032 0.354 0.987 1 0 0

Missouri Iron 290930033 0.057 0.026 0.105 1 0 0

Missouri Iron 290930034 0.402 0.241 0.615 1 0 0

Missouri Iron 290939007 0.581 0.392 0.844 1 0 0

Missouri Iron 290939008 0.387 0.209 0.538 1 0 0

Missouri Jasper 290970005 0.019 0.014 0.024 0 0 0

Missouri Jefferson 290990004 1.122 0.888 1.576 1 0 0

Missouri Jefferson 290990005 0.396 0.223 0.498 1 0 0

Missouri Jefferson 290990009 0.191 0.055 0.280 1 0 0

Missouri Jefferson 290990013 0.305 0.135 0.418 1 0 0

Missouri Jefferson 290990020 0.865 0.546 1.233 1 0 0

 2D - 4
APPENDIX 2D

State County Site

Maximum 3-

month 

mean 

(μg/m3)

Annual 

average 

(μg/m3

)

Maximum 

monthly 

mean 

(μg/m3

)

Non-airport

sourceoriented 

(during 

2010-

2012)

Airport 

sourceoriented

Previous 

sourceoriented 

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

Missouri Jefferson 290990022 0.630 0.469 0.861 1 0 0

Missouri Jefferson 290990023 0.563 0.386 0.700 1 0 0

Missouri Jefferson 290990024 0.659 0.340 0.862 1 0 0

Missouri Jefferson 290990025 0.085 0.042 0.134 1 0 0

Missouri Jefferson 290990026 0.080 0.036 0.138 1 0 0

Missouri Jefferson 290990027 0.592 0.454 0.857 1 0 0

Missouri Jefferson 290999001 1.100 0.812 1.558 1 0 0

Missouri Jefferson 290999002 0.431 0.228 0.593 1 0 0

Missouri Jefferson 290999003 0.327 0.175 0.551 1 0 0

Missouri Jefferson 290999004 0.442 0.156 0.545 1 0 0

Missouri Jefferson 290999005 1.432 0.913 2.185 1 0 0

Missouri Jefferson 290999006 0.103 0.049 0.136 1 0 0

Missouri Reynolds 291790001 0.059 0.031 0.087 1 0 0

Missouri Reynolds 291790002 0.068 0.034 0.172 1 0 0

Missouri Reynolds 291790003 0.100 0.027 0.268 1 0 0

Missouri Reynolds 291790034 0.161 0.078 0.297 1 0 0

Missouri St. Francois 291870006 0.132 0.043 0.302 0 0 0

Missouri St. Francois 291870007 0.134 0.053 0.364 0 0 0

Missouri St. Louis 291892003 0.008 0.007 0.009 0 0 0

Missouri St. Louis city 295100085 0.028 0.026 0.045 0 0 0

Nebraska Dodge 310530005 0.139 0.055 0.197 1 0 0

Nebraska Douglas 310550019 0.006 0.005 0.008 0 0 0

Nebraska Nemaha 311270002 0.115 0.034 0.206 1 0 0

Nevada Clark 320030540 0.003 0.004 0 0 0

New Mexico Bernalillo 350010023 0.006 0.003 0.012 0 0 0

New York Orange 360713001 0.101 0.025 0.134 1 0 0

New York Orange 360713002 1.027 0.123 2.821 1 0 0

New York Orange 360713004 0.007 0.005 0.011 1 0 0

New York Suffolk 361030024 0.027 0.017 0.031 0 1 0

Ohio Butler 390170015 0.009 0.006 0.013 0 0 0

Ohio Columbiana 390290019 0.057 0.020 0.136 0 0 0

 2D - 5
APPENDIX 2D

State County Site

Maximum 3-

month 

mean 

(μg/m3)

Annual 

average 

(μg/m3

)

Maximum 

monthly 

mean 

(μg/m3

)

Non-airport

sourceoriented 

(during 

2010-

2012)

Airport 

sourceoriented

Previous 

sourceoriented 

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

Ohio Columbiana 390290020 0.025 0.015 0.035 0 0 0

Ohio Columbiana 390290022 0.044 0.019 0.065 0 0 0

Ohio Cuyahoga 390350038 0.021 0.013 0.026 0 0 0

Ohio Cuyahoga 390350042 0.030 0.013 0.044 0 0 0

Ohio Cuyahoga 390350049 0.531 0.136 0.719 1 0 0

Ohio Cuyahoga 390350060 0.030 0.020 0.035 0 0 0

Ohio Cuyahoga 390350061 0.023 0.015 0.030 0 0 1

Ohio Cuyahoga 390350072 0.035 0.014 0.054 1 0 0

Ohio Franklin 390490025 0.011 0.009 0.016 0 0 0

Ohio Fulton 390510001 0.178 0.070 0.210 1 0 0

Ohio Logan 390910006 0.006 0.004 0.008 0 0 1

Ohio Marion 391010003 0.088 0.041 0.155 1 0 0

Ohio Marion 391010004 0.017 0.013 0.028 1 0 0

Ohio Montgomery 391137001 0.008 0.007 0.012 0 0 0

Ohio Stark 391510017 0.023 0.015 0.032 1 0 0

Ohio Trumbull 391550012 0.011 0.007 0.017 1 0 0

Ohio Washington 391670008 0.007 0.005 0.010 0 0 0

Ohio Washington 391670010 0.008 0.005 0.010 0 0 0

Oklahoma Ottawa 401159006 0.022 0.012 0.049 0 0 0

Oklahoma Ottawa 401159007 0.034 0.018 0.056 0 0 0

Oklahoma Pittsburg 401210416 0.004 0.003 0.006 1 0 0

Oklahoma Tulsa 401431127 0.008 0.006 0.009 0 0 0

Oregon Yamhill 410711702 0.045 0.021 0.078 1 0 0

Pennsylvania Allegheny 420030002 0.016 0.014 0.024 0 0 0

Pennsylvania Allegheny 420030008 0.014 0.008 0.020 0 0 0

Pennsylvania Allegheny 420030070 0.056 0.018 0.110 1 0 0

Pennsylvania Allegheny 420031009 0.138 0.035 0.149 1 0 0

Pennsylvania Beaver 420070006 0.085 0.051 0.198 1 0 0

Pennsylvania Beaver 420070007 0.253 0.166 0.393 1 0 0

Pennsylvania Beaver 420070505 0.151 0.089 0.291 1 0 0

Pennsylvania Berks 420110020 0.509 0.158 1.064 1 0 0

 2D - 6
APPENDIX 2D

State County Site

Maximum 3-

month 

mean 

(μg/m3)

Annual 

average 

(μg/m3

)

Maximum 

monthly 

mean 

(μg/m3

)

Non-airport

sourceoriented 

(during 

2010-

2012)

Airport 

sourceoriented

Previous 

sourceoriented 

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

Pennsylvania Berks 420110021 0.139 0.044 0.319 1 0 0

Pennsylvania Berks 420110022 0.118 0.035 0.261 1 0 0

Pennsylvania Berks 420111717 0.217 0.146 0.285 1 0 0

Pennsylvania Carbon 420250214 0.104 0.321 1 0 0

Pennsylvania Delaware 420450002 0.047 0.028 0.048 0 0 0

Pennsylvania Delaware 420450004 0.047 0.028 0.048 1 0 0

Pennsylvania Franklin 420550002 0.046 0.028 0.047 1 0 0

Pennsylvania Indiana 420630005 0.049 0.025 0.058 1 0 0

Pennsylvania Lancaster 420710009 0.068 0.039 0.093 1 0 0

Pennsylvania Lawrence 420730011 0.023 0.026 0.046 1 0 0

Pennsylvania Luzerne 420790036 0.137 0.054 0.268 1 0 0

Pennsylvania Philadelphia 421010449 0.029 0.021 0.029 0 0 1

Pennsylvania Philadelphia 421011002 0.051 0.030 0.069 0 0 0

Pennsylvania Westmoreland 421290009 0.046 0.023 0.047 1 0 0

South Carolina Charleston 450190003 0.007 0.005 0.013 0 0 0

South Carolina Florence 450418001 0.044 0.013 0.101 1 0 0

South Carolina Florence 450418002 0.015 0.006 0.024 1 0 0

South Carolina Florence 450418003 0.011 0.005 0.013 0 0 0

South Carolina Greenville 450450015 0.006 0.005 0.008 0 0 0

South Carolina Richland 450790007 0.005 0.004 0.007 0 0 0

South Carolina Richland 450790019 0.024 0.011 0.061 0 0 0

Tennessee Knox 470930023 0.165 0.108 0.214 1 0 0

Tennessee Knox 470930027 0.042 0.020 0.078 1 0 0

Tennessee Knox 470931017 0.037 0.018 0.058 1 0 0

Tennessee Shelby 471570075 0.005 0.004 0.005 0 0 0

Tennessee Sullivan 471633001 0.076 0.056 0.107 0 0 1

Tennessee Sullivan 471633002 0.044 0.036 0.052 0 0 1

Tennessee Sullivan 471633003 0.053 0.038 0.056 0 0 1

Tennessee Sullivan 471633004 0.080 0.044 0.124 0 0 1

Texas Cameron 480610006 0.008 0.004 0.018 0 0 0

Texas Collin 480850003 0.371 0.136 0.625 1 0 0

 2D - 7
APPENDIX 2D

State County Site

Maximum 3-

month 

mean 

(μg/m3)

Annual 

average 

(μg/m3

)

Maximum 

monthly 

mean 

(μg/m3

)

Non-airport

sourceoriented 

(during 

2010-

2012)

Airport 

sourceoriented

Previous 

sourceoriented 

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

Texas Collin 480850007 0.199 0.093 0.240 1 0 0

Texas Collin 480850009 0.774 0.388 1.178 1 0 0

Texas Collin 480850029 0.180 0.052 0.335 1 0 0

Texas Dallas 481130069 0.013 0.009 0.022 0 0 0

Texas El Paso 481410002 0.040 0.022 0.087 0 0 0

Texas El Paso 481410033 0.019 0.017 0.023 0 0 0

Texas El Paso 481410037 0.025 0.022 0.032 1 0 0

Texas El Paso 481410055 0.019 0.010 0.032 0 0 0

Texas El Paso 481410058 0.022 0.016 0.022 0 0 0

Texas Harris 482011034 0.008 0.005 0.009 0 0 0

Texas Harris 482011039 0.004 0.003 0.008 0 0 0

Texas Kaufman 482570020 0.104 0.044 0.110 1 0 0

Texas Potter 483750024 0.020 0.007 0.029 1 0 0

Texas Webb 484790016 0.026 0.018 0.035 0 0 0

Utah Salt Lake 490351001 0.057 0.024 0.086 1 0 0

Virginia Amherst 510090007 0.018 0.006 0.016 1 0 0

Virginia Buchanan 510270006 0.014 0.012 0.021 1 0 0

Virginia Henrico 510870014 0.005 0.005 0.024 0 0 0

Virginia Roanoke city 517700011 0.109 0.033 0.272 1 0 0

Washington King 530330029 0.055 0.036 0.087 0 1 0

Washington Snohomish 530610013 0.023 0.013 0.032 0 1 0

West Virginia Cabell 540110006 0.012 0.010 0.013 0 0 0

Wisconsin Sheboygan 551170008 0.152 0.056 0.225 1 0 0

Puerto Rico Arecibo Municipio, Pu 720130001 0.339 0.171 0.416 1 0 0

Puerto Rico Bayamón Municipio, P 720210010 0.011 0.004 0.027 0 0 0

Puerto Rico Salinas Municipio, Pu 721230002 0.017 0.008 0.042 0 0 0

counts → 236 243 243 121 15 11

 2D - 8
APPENDIX 2D

State County Site

Maximum 

3-month 

mean 

(μg/m3)

Annual 

average 

(μg/m3

)

Maximum 

monthly 

mean 

(μg/m3

)

North CarolinaWake 371830014 0.002 0.002

Georgia DeKalb 130890002 0.002 0.001 0.003

MassachusettsSuffolk 250250002 0.002 0.002 0.003

New HampshiRockingham 330150018 0.002 0.002 0.003

North CarolinaMecklenburg 371190041 0.002 0.003

Oregon Jackson 410290133 0.003 0.002 0.003

Oregon Jackson 410292129 0.002 0.003

Oregon Lane 410390060 0.002 0.001 0.003

Oregon Lane 410390062 0.002 0.002 0.003

Vermont Chittenden 500070007 0.002 0.001 0.003

Florida Hillsborough 120573002 0.003 0.002 0.004

Florida Pinellas 121030018 0.003 0.002 0.004

Kentucky Henderson 211010014 0.003 0.003 0.004

Nevada Clark 320030540 0.003 0.004

New York Monroe 360551007 0.003 0.003 0.004

Arkansas Pulaski 051190007 0.004 0.003 0.005

California Sacramento 060670006 0.003 0.002 0.005

Delaware New Castle 100032004 0.004 0.003 0.005

District of ColDistrict of Columb 110010043 0.004 0.003 0.005

Florida Orange 120951004 0.002 0.005

Idaho Ada 160010010 0.002 0.002 0.005

MassachusettsSuffolk 250250042 0.005 0.003 0.005

Rhode Island Providence 440070022 0.003 0.003 0.005

Washington King 530330080 0.004 0.003 0.005

California Santa Clara 060850005 0.006 0.002 0.006

Florida Pinellas 121030026 0.004 0.002 0.006

Kentucky Fayette 210670012 0.004 0.003 0.006

Kentucky Fayette 210670014 0.005 0.004 0.006

Michigan Wayne 261630001 0.006 0.004 0.006

New Jersey Essex 340130003 0.005 0.003 0.006

Arizona Maricopa 040139997 0.006 0.004 0.007

Ohio Hamilton 390610040 0.005 0.005 0.007

Texas Harris 482011039 0.004 0.002 0.007

Arizona Maricopa 040134009 0.005 0.008

Kentucky Jefferson 211110067 0.006 0.005 0.008

MassachusettsHampden 250132009 0.006 0.004 0.008

New York Bronx 360050110 0.006 0.006 0.008

Utah Davis 490110004 0.006 0.003 0.009

Table 2D-2. Pb-PM10 concentrations at urban Pb-PM10 sites, 2010-2012.

 2D - 9
APPENDIX 2D

State County Site

Maximum 

3-month 

mean 

(μg/m3)

Annual 

average 

(μg/m3

)

Maximum 

monthly 

mean 

(μg/m3

)

Table 2D-2. Pb-PM10 concentrations at urban Pb-PM10 sites, 2010-2012.

Illinois Cook 170314201 0.006 0.004 0.010

Wisconsin Milwaukee 550790010 0.006 0.010

New York Bronx 360050080 0.008 0.006 0.012

Oregon Multnomah 410510246 0.006 0.004 0.012

Connecticut New Haven 090090027 0.008 0.004 0.013

Maryland Prince George's 240330030 0.008 0.004 0.016

Texas Harris 482011035 0.008 0.005 0.016

Virginia Henrico 510870014 0.007 0.003 0.016

California Los Angeles 060371103 0.013 0.007 0.026

Kentucky Boyd 210190002 0.020 0.013 0.029

California Riverside 060658001 0.013 0.006 0.030

Illinois St. Clair 171639010 0.015 0.031

Missouri St. Louis city 295100085 0.017 0.012 0.032

Michigan Wayne 261630033 0.023 0.011 0.035

Alabama Jefferson 010730023 0.029 0.019 0.040

Mississippi Hinds 280490019 0.074 0.082

counts → 45 54 54

 2D - 10
APPENDIX 2D

state_name county_name SITE

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3)

Maximum 

monthly 

mean 

(μg/m3

)

California Kern 060299001 0.001 0.001 0.001

Hawaii Honolulu 150030010 0.001 0.000 0.001

Wyoming Laramie 560210100 0.000 0.000 0.001

California Butte 060070008 0.002 0.002

Colorado Adams 080010006 0.002 0.001 0.002

Florida Broward 120111002 0.001 0.001 0.002

Idaho Ada 160010010 0.001 0.001 0.002

North Carolina Buncombe 370210034 0.001 0.001 0.002

North Carolina Wake 371830014 0.002 0.001 0.002

Oklahoma Oklahoma 401091037 0.001 0.001 0.002

Rhode Island Providence 440071010 0.002 0.002 0.002

South Carolina Charleston 450190049 0.002 0.001 0.002

South Carolina Richland 450790007 0.002 0.001 0.002

Texas Harris 482011039 0.001 0.001 0.002

Vermont Chittenden 500070012 0.002 0.001 0.002

Wisconsin Brown 550090005 0.001 0.001 0.002

Alabama Madison 010890014 0.002 0.001 0.003

Arizona Pima 040191028 0.002 0.001 0.003

California Butte 060070002 0.003 0.002 0.003

California Fresno 060190008 0.002 0.001 0.003

California Ventura 061112002 0.002 0.001 0.003

Colorado Weld 081230008 0.002 0.001 0.003

District of ColumbDistrict of Columbia 110010043 0.002 0.001 0.003

Florida Hillsborough 120573002 0.002 0.001 0.003

Florida Pinellas 121030026 0.002 0.001 0.003

Georgia Clarke 130590001 0.002 0.001 0.003

Georgia DeKalb 130890002 0.002 0.001 0.003

Iowa Linn 191130037 0.002 0.002 0.003

Iowa Polk 191530030 0.002 0.001 0.003

Louisiana East Baton Rouge Parish 220330009 0.003 0.002 0.003

Minnesota Hennepin 270530963 0.002 0.002 0.003

Mississippi Hinds 280490019 0.003 0.001 0.003

Missouri Clay 290470005 0.002 0.001 0.003

Nevada Washoe 320310016 0.002 0.001 0.003

New Jersey Morris 340273001 0.002 0.001 0.003

New York Monroe 360551007 0.002 0.002 0.003

North Carolina Catawba 370350004 0.002 0.002 0.003

Table 2D-3. Pb-PM2.5 concentrations at urban CSN PM2.5 sites, 2010-2012.

 2D - 11
APPENDIX 2D

state_name county_name SITE

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3)

Maximum 

monthly 

mean 

(μg/m3

)

Table 2D-3. Pb-PM2.5 concentrations at urban CSN PM2.5 sites, 2010-2012.

North Carolina Mecklenburg 371190041 0.002 0.001 0.003

North Carolina Rowan 371590021 0.006 0.001 0.003

Oregon Lane 410392013 0.002 0.001 0.003

Pennsylvania Centre 420270100 0.002 0.001 0.003

South Dakota Minnehaha 460990008 0.002 0.001 0.003

Tennessee Roane 471451001 0.002 0.002 0.003

Texas Cameron 480612004 0.002 0.001 0.003

Texas Jefferson 482450021 0.002 0.002 0.003

Texas Travis 484530020 0.002 0.001 0.003

Washington Yakima 530770009 0.002 0.001 0.003

California Fresno 060190011 0.002 0.001 0.004

California Santa Clara 060850005 0.003 0.001 0.004

Colorado Denver 080310025 0.002 0.001 0.004

Georgia Bibb 130210007 0.003 0.001 0.004

Illinois Madison 171199010 0.002 0.004

Indiana Elkhart 180390008 0.003 0.002 0.004

Indiana Vanderburgh 181630021 0.003 0.002 0.004

Maryland Prince George's 240330030 0.002 0.001 0.004

Massachusetts Hampden 250130008 0.003 0.002 0.004

Michigan Wayne 261630001 0.003 0.002 0.004

Nevada Clark 320030540 0.003 0.001 0.004

New Jersey Middlesex 340230006 0.003 0.002 0.004

New Jersey Union 340390004 0.004 0.002 0.004

New Mexico Bernalillo 350010023 0.002 0.001 0.004

New York New York 360610134 0.003 0.002 0.004

North Dakota Cass 380171004 0.002 0.001 0.004

Ohio Franklin 390490081 0.003 0.002 0.004

Ohio Lucas 390950026 0.003 0.002 0.004

Oklahoma Tulsa 401431127 0.003 0.001 0.004

Pennsylvania Adams 420010001 0.002 0.001 0.004

Tennessee Shelby 471570024 0.003 0.002 0.004

Washington Clark 530110013 0.003 0.001 0.004

Arizona Maricopa 040134009 0.004 0.003 0.005

Arizona Maricopa 040139997 0.003 0.002 0.005

California Kern 060290014 0.004 0.001 0.005

California Riverside 060658001 0.003 0.002 0.005

California Sacramento 060670010 0.003 0.002 0.005

 2D - 12
APPENDIX 2D

state_name county_name SITE

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3)

Maximum 

monthly 

mean 

(μg/m3

)

Table 2D-3. Pb-PM2.5 concentrations at urban CSN PM2.5 sites, 2010-2012.

California San Diego 060730003 0.004 0.002 0.005

California San Diego 060731002 0.004 0.002 0.005

California Tulare 061072002 0.004 0.002 0.005

Delaware New Castle 100032004 0.004 0.002 0.005

Illinois Cook 170314201 0.003 0.002 0.005

Indiana Clark 180190006 0.003 0.002 0.005

Minnesota Olmsted 271095008 0.003 0.001 0.005

New Jersey Essex 340130003 0.003 0.002 0.005

New York Bronx 360050110 0.004 0.003 0.005

North Carolina Davidson 370570002 0.003 0.001 0.005

Pennsylvania Chester 420290100 0.004 0.002 0.005

Pennsylvania Philadelphia 421010055 0.003 0.002 0.005

Tennessee Davidson 470370023 0.003 0.002 0.005

Tennessee Hamilton 470654002 0.003 0.002 0.005

Tennessee Montgomery 471251009 0.003 0.001 0.005

Texas Nueces 483550034 0.003 0.002 0.005

Virginia Henrico 510870014 0.002 0.001 0.005

Washington Snohomish 530611007 0.004 0.001 0.005

West Virginia Kanawha 540390011 0.003 0.002 0.005

California Alameda 060010007 0.005 0.002 0.006

Delaware Kent 100010003 0.003 0.001 0.006

Illinois Cook 170310076 0.004 0.003 0.006

Illinois St. Clair 171630900 0.005 0.003 0.006

Iowa Linn 191130040 0.003 0.002 0.006

Michigan Kent 260810020 0.004 0.002 0.006

Nebraska Douglas 310550019 0.004 0.001 0.006

New York Albany 360010005 0.004 0.002 0.006

Pennsylvania Westmoreland 421290008 0.004 0.003 0.006

Rhode Island Providence 440070022 0.004 0.003 0.006

Tennessee Shelby 471570075 0.003 0.002 0.006

Wisconsin Milwaukee 550790026 0.004 0.003 0.006

Connecticut New Haven 090090027 0.004 0.002 0.007

Indiana Marion 180970078 0.004 0.003 0.007

Kentucky Boyd 210190017 0.005 0.003 0.007

Maryland Baltimore 240053001 0.006 0.002 0.007

Michigan Monroe 261150005 0.005 0.002 0.007

Ohio Summit 391530023 0.005 0.004 0.007

 2D - 13
APPENDIX 2D

state_name county_name SITE

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3)

Maximum 

monthly 

mean 

(μg/m3

)

Table 2D-3. Pb-PM2.5 concentrations at urban CSN PM2.5 sites, 2010-2012.

Pennsylvania Erie 420490003 0.004 0.002 0.007

Tennessee Knox 470931020 0.006 0.003 0.007

Texas Dallas 481130050 0.005 0.003 0.007

Utah Davis 490110004 0.003 0.002 0.007

Washington King 530330080 0.003 0.001 0.007

West Virginia Kanawha 540391005 0.005 0.002 0.007

West Virginia Marshall 540511002 0.007 0.004 0.007

Alaska Fairbanks North Star Borough 020900010 0.005 0.002 0.008

California Solano 060950004 0.006 0.003 0.008

Florida Leon 120730012 0.004 0.002 0.008

Georgia Richmond 132450091 0.004 0.001 0.008

Georgia Walker 132950002 0.005 0.002 0.008

Illinois DuPage 170434002 0.004 0.002 0.008

Kansas Sedgwick 201730010 0.004 0.002 0.008

Kansas Wyandotte 202090021 0.006 0.004 0.008

Oregon Multnomah 410510080 0.005 0.003 0.008

Pennsylvania Washington 421255001 0.005 0.003 0.008

South Carolina Greenville 450450015 0.006 0.002 0.008

Texas Ellis 481390016 0.006 0.003 0.008

Texas El Paso 481410044 0.006 0.003 0.008

Texas Harris 482010024 0.006 0.003 0.008

Washington Pierce 530530029 0.005 0.003 0.008

California Sacramento 060670006 0.004 0.001 0.009

California Stanislaus 060990005 0.005 0.003 0.009

Georgia Floyd 131150003 0.005 0.002 0.009

Louisiana Bossier Parish 220150008 0.006 0.003 0.009

Ohio Hamilton 390610040 0.005 0.002 0.009

Pennsylvania Lancaster 420710007 0.007 0.003 0.009

Pennsylvania York 421330008 0.006 0.002 0.009

New York Queens 360810124 0.005 0.002 0.010

Pennsylvania Lackawanna 420692006 0.006 0.003 0.010

West Virginia Ohio 540690010 0.008 0.005 0.010

Kentucky Fayette 210670012 0.006 0.002 0.011

North Carolina Forsyth 370670022 0.006 0.002 0.011

Ohio Cuyahoga 390350060 0.009 0.006 0.011

Pennsylvania Dauphin 420430401 0.007 0.003 0.011

Pennsylvania Philadelphia 421010004 0.006 0.003 0.011

 2D - 14
APPENDIX 2D

state_name county_name SITE

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3)

Maximum 

monthly 

mean 

(μg/m3

)

Table 2D-3. Pb-PM2.5 concentrations at urban CSN PM2.5 sites, 2010-2012.

Kentucky Jefferson 211110067 0.007 0.004 0.012

Massachusetts Suffolk 250250042 0.005 0.002 0.012

Ohio Cuyahoga 390350038 0.008 0.004 0.012

Ohio Jefferson 390811001 0.009 0.005 0.012

Ohio Lawrence 390870012 0.009 0.005 0.012

Texas Dallas 481130069 0.007 0.003 0.012

Utah Utah 490494001 0.006 0.002 0.012

Washington King 530330057 0.008 0.004 0.013

Wisconsin Waukesha 551330027 0.010 0.005 0.013

Alabama Montgomery 011011002 0.008 0.003 0.014

Arkansas Pulaski 051190007 0.006 0.002 0.014

California Los Angeles 060371103 0.015 0.002 0.015

Missouri St. Louis city 295100085 0.010 0.006 0.016

New York Erie 360290005 0.012 0.007 0.016

Pennsylvania Berks 420110011 0.013 0.007 0.016

Utah Salt Lake 490353006 0.007 0.002 0.016

Iowa Scott 191630015 0.010 0.005 0.017

Missouri Jefferson 290990019 0.009 0.004 0.017

Ohio Mahoning 390990014 0.012 0.007 0.017

Texas Lubbock 483030325 0.007 0.003 0.017

Indiana Lake 180890022 0.011 0.005 0.018

Pennsylvania Northampton 420950025 0.008 0.003 0.018

Texas El Paso 481410053 0.017 0.006 0.018

Illinois St. Clair 171639010 0.014 0.010 0.019

Minnesota Anoka 270031002 0.012 0.006 0.019

Ohio Stark 391510017 0.012 0.007 0.019

Pennsylvania Philadelphia 421011002 0.012 0.006 0.020

California Alameda 060010011 0.011 0.004 0.021

Pennsylvania Allegheny 420030008 0.016 0.008 0.022

Alabama Jefferson 010732003 0.018 0.006 0.023

Ohio Lorain 390933002 0.012 0.006 0.023

Pennsylvania Cambria 420210011 0.013 0.007 0.023

California Imperial 060250005 0.018 0.012 0.025

Michigan Wayne 261630015 0.012 0.006 0.027

Alabama Russell 011130001 0.016 0.004 0.028

Michigan Wayne 261630033 0.017 0.006 0.028

Georgia Muscogee 132150011 0.014 0.004 0.029

 2D - 15
APPENDIX 2D

state_name county_name SITE

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3)

Maximum 

monthly 

mean 

(μg/m3

)

Table 2D-3. Pb-PM2.5 concentrations at urban CSN PM2.5 sites, 2010-2012.

Michigan St. Clair 261470005 0.015 0.004 0.030

Illinois Madison 171190024 0.020 0.010 0.032

Washington Pierce 530530031 0.015 0.004 0.032

Ohio Montgomery 391130032 0.014 0.003 0.033

California San Bernardino 060712002 0.037 0.017 0.037

Indiana Lake 180892004 0.022 0.010 0.037

California Orange 060590007 0.042 0.013 0.043

Pennsylvania Allegheny 420030064 0.038 0.018 0.051

Alabama Jefferson 010730023 0.041 0.020 0.063

Illinois Cook 170310057 0.069 0.011 0.199

counts → 193 195 195

 2D - 16
APPENDIX 2D

state_name county_name SITE

Maximum 

3-month 

mean 

(μg/m3)

Annual 

average 

(μg/m3)

Maximum 

monthly 

mean 

(μg/m3)

Alaska Aleutians East Borough 020130002 0.002 0.001 0.002

Alaska Denali Borough 020680003 0.001 0.000 0.001

Alaska Kenai Peninsula Borough 021220009 0.001 0.000 0.002

Alaska Northwest Arctic Borough 021889000

Alaska Yukon-Koyukuk Census Area 022909000 0.001 0.000 0.001

Arizona Apache 040018001 0.001 0.001 0.002

Arizona Gila 040070010 0.005 0.003 0.008

Arizona Gila 040078100 0.001 0.001 0.002

Arizona Navajo 040170119 0.001 0.001 0.002

Arkansas Newton 051019000 0.002 0.001 0.003

Arkansas Polk 051130003 0.002 0.001 0.003

California Del Norte 060150002 0.001 0.000 0.001

California Inyo 060270101 0.001 0.001 0.002

California Mariposa 060430003 0.001 0.001 0.002

California Mono 060519000 0.001 0.000 0.001

California Siskiyou 060930005 0.001 0.000 0.001

California Trinity 061059000 0.001 0.001 0.001

Colorado Alamosa 080039000 0.001 0.000 0.002

Colorado Garfield 080450015 0.001 0.002

Colorado Jackson 080579000 0.001 0.000 0.001

Colorado La Plata 080679000 0.001 0.001 0.001

Colorado Montezuma 080839000 0.001 0.001 0.001

Colorado Pitkin 080979000 0.001 0.000 0.001

Colorado Rio Blanco 081039000

Colorado San Juan 081119000 0.001 0.001 0.001

Connecticut Litchfield 090050005 0.002 0.001 0.002

Georgia Charlton 130499000 0.002 0.001 0.002

Hawaii Hawaii 150019000

Hawaii Hawaii 150019001

Hawaii Hawaii 150019002 0.005 0.001 0.010

Idaho Custer 160370002 0.001 0.000 0.001

Idaho Lemhi 160590007

Iowa Montgomery 191370002 0.002 0.002 0.003

Iowa Van Buren 191770006 0.003 0.002 0.004

Iowa Van Buren 191779000

Kansas Brown 200139000 0.003 0.002 0.003

Kansas Chase 200170001 0.002 0.001 0.003

Table 2D-4. Pb-PM2.5 concentrations at non-urban IMPROVE PM2.5 sites, 2010-2012.

 2D - 17
APPENDIX 2D

state_name county_name SITE

Maximum 

3-month 

mean 

(μg/m3)

Annual 

average 

(μg/m3)

Maximum 

monthly 

mean 

(μg/m3)

Table 2D-4. Pb-PM2.5 concentrations at non-urban IMPROVE PM2.5 sites, 2010-2012.

Kansas Trego 201950001 0.001 0.001 0.001

Louisiana Winn Parish 221279000 0.001 0.001 0.002

Maine Aroostook 230031020 0.002 0.001 0.004

Maine Hancock 230090103 0.001 0.001 0.002

Maine Washington 230291004 0.001 0.001 0.002

Maryland Garrett 240239000 0.002 0.002 0.003

Massachusetts Dukes 250070001 0.001 0.001 0.002

Michigan Keweenaw 260839000 0.001 0.001 0.002

Michigan Keweenaw 260839001

Michigan Schoolcraft 261539000 0.002 0.001 0.002

Minnesota Lake 270759000 0.001 0.001 0.002

Minnesota Rock 271339000 0.002 0.002 0.003

Minnesota Winona 271699000 0.002 0.002 0.002

Missouri Cedar 290390001 0.002 0.002 0.003

Missouri Stoddard 292070001 0.004 0.003 0.005

Missouri Taney 292130003 0.002 0.002 0.003

Montana Fergus 300279000 0.001 0.001 0.001

Montana Flathead 300299001 0.001 0.000 0.001

Montana Lake 300479000 0.001 0.000 0.001

Montana Lewis and Clark 300499000 0.001 0.000 0.001

Montana Powell 300779000 0.001 0.000 0.001

Montana Ravalli 300819000 0.001 0.000 0.001

Montana Roosevelt 300859000 0.001 0.001 0.001

Montana Rosebud 300870762 0.001 0.000 0.001

Montana Sanders 300899000 0.001 0.000 0.001

Montana Sheridan 300919000 0.001 0.001 0.001

Nebraska Garden 310699000 0.001 0.001 0.001

Nebraska Thomas 311719000 0.001 0.001 0.001

Nebraska Thurston 311739000

Nevada Elko 320079000 0.001 0.000 0.002

Nevada Mineral 320219000

Nevada White Pine 320339000 0.001 0.000 0.001

New Hampshire Coos 330074002 0.001 0.001 0.001

New Mexico Catron 350039000 0.001 0.001 0.001

New Mexico Chaves 350059000 0.001 0.001 0.002

New Mexico Lincoln 350279000 0.001 0.001 0.002

New Mexico Los Alamos 350281002 0.001 0.001 0.002

 2D - 18
APPENDIX 2D

state_name county_name SITE

Maximum 

3-month 

mean 

(μg/m3)

Annual 

average 

(μg/m3)

Maximum 

monthly 

mean 

(μg/m3)

Table 2D-4. Pb-PM2.5 concentrations at non-urban IMPROVE PM2.5 sites, 2010-2012.

New Mexico Rio Arriba 350399000 0.001 0.001 0.002

New Mexico Socorro 350539000 0.001 0.001 0.002

New Mexico Taos 350559000 0.001 0.000 0.001

New York Steuben 361019000 0.002 0.002

North Carolina Avery 370110002 0.001 0.001 0.002

North Carolina Hyde 370959000 0.002 0.001 0.002

North Dakota Billings 380070002 0.001 0.001 0.001

North Dakota Burke 380130004 0.001 0.001 0.001

Ohio Noble 391219000 0.005 0.003 0.008

Oklahoma Adair 400019009 0.002 0.002 0.003

Oklahoma Ellis 400450890 0.001 0.001 0.001

Oklahoma Kay 400719010 0.002 0.001 0.003

Oregon Klamath 410358001 0.001 0.000 0.001

Oregon Union 410610010 0.001 0.000 0.001

Oregon Wallowa 410630002 0.002 0.001 0.003

South Dakota Jackson 460710001 0.001 0.001 0.001

Texas Brewster 480430101 0.002 0.001 0.002

Texas Culberson 481099000 0.001 0.001 0.002

Utah Garfield 490170101 0.001 0.001 0.001

Utah San Juan 490379000 0.001 0.001 0.001

Utah Wayne 490559000 0.001 0.000 0.001

Vermont Bennington 500038001 0.001 0.001 0.002

Virginia Madison 511139000 0.002 0.001 0.002

Virginia Rockbridge 511639000 0.004 0.003 0.006

Washington Clallam 530090013 0.000 0.000 0.001

Washington Clallam 530090014

Washington Clallam 530090020 0.001 0.001 0.002

Washington Kittitas 530370004 0.001 0.001 0.001

Washington Klickitat 530390010 0.002 0.001 0.002

Washington Klickitat 530390011 0.001 0.001 0.001

Washington Lewis 530410007 0.001 0.000 0.001

Washington Okanogan 530470012 0.001 0.000 0.001

West Virginia Tucker 540939000 0.002 0.001 0.002

Wyoming Albany 560019000

Wyoming Campbell 560050123 0.000 0.000 0.001

Wyoming Johnson 560199000 0.001 0.000 0.001

Wyoming Park 560299002 0.001 0.000 0.001

 2D - 19
APPENDIX 2D

state_name county_name SITE

Maximum 

3-month 

mean 

(μg/m3)

Annual 

average 

(μg/m3)

Maximum 

monthly 

mean 

(μg/m3)

Table 2D-4. Pb-PM2.5 concentrations at non-urban IMPROVE PM2.5 sites, 2010-2012.

Wyoming Sublette 560359000 0.001 0.000 0.001

Wyoming Sublette 560359001 0.001 0.000 0.001

Wyoming Teton 560399000 0.001 0.000 0.001

Virgin Islands St John 780209000 0.001 0.001 0.001

counts → 102 104 104

 2D - 20
APPENDIX 2D

(units are μg/m3) n min Pct1 Pct5 Pct10 Pct25 mean Pct50 Pct75 Pct90 Pct95 Pct99 max

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

Pb-TSP non-airport source-oriented sites 119 0.004 0.004 0.011 0.017 0.045 0.2493 0.109 0.338 0.659 1.100 1.432 1.584

Pb-TSP airport source-oriented sites 13 0.010 0.010 0.010 0.010 0.020 0.0677 0.040 0.070 0.120 0.330 0.330 0.330

Pb-TSP previous source-oriented sites 11 0.006 0.006 0.006 0.023 0.029 0.0554 0.053 0.080 0.083 0.115 0.115 0.115

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

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

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

Pb-PM2.5 non-urban IMPROVE sites 102 0.000 0.000 0.001 0.001 0.001 0.0014 0.001 0.002 0.002 0.003 0.005 0.005

Table 2D-5. Distribution of maximum 3-month means, 2010-2012.

 2D - 21
APPENDIX 2D

(units are μg/m3) n min Pct1 Pct5 Pct10 Pct25 mean Pct50 Pct75 Pct90 Pct95 Pct99 max

All Pb-TSP sites 242 0.000 0.001 0.003 0.004 0.007 0.0718 0.021 0.055 0.166 0.386 0.812 0.913

Pb-TSP non-airport source-oriented sites 121 0.003 0.003 0.006 0.012 0.024 0.1261 0.044 0.140 0.386 0.522 0.888 0.913

Pb-TSP airport source-oriented sites 15 0.004 0.004 0.004 0.009 0.014 0.0557 0.033 0.071 0.128 0.254 0.254 0.254

Pb-TSP previous source-oriented sites 11 0.004 0.004 0.004 0.015 0.020 0.0298 0.033 0.038 0.044 0.056 0.056 0.056

Pb-TSP not source-oriented sites 96 0.000 0.000 0.001 0.003 0.004 0.0101 0.006 0.014 0.020 0.028 0.053 0.053

Pb-PM10 urban sites 54 0.001 0.001 0.001 0.002 0.002 0.0055 0.003 0.005 0.011 0.015 0.074 0.074

Pb-PM2.5 urban CSN sites 195 0.000 0.000 0.001 0.001 0.001 0.0029 0.002 0.003 0.006 0.008 0.018 0.020

Pb-PM2.5 non-urban IMPROVE sites 104 0.000 0.000 0.000 0.000 0.000 0.0009 0.001 0.001 0.002 0.002 0.003 0.003

Table 2D-6. Distribution of annual means, 2010-2012.

 2D - 22
APPENDIX 2D

(units are μg/m3) n min Pct1 Pct5 Pct10 Pct25 mean Pct50 Pct75 Pct90 Pct95 Pct99 max

All Pb-TSP sites 243 0.000 0.000 0.010 0.010 0.020 0.2213 0.060 0.230 0.580 0.990 2.240 2.820

Pb-TSP non-airport source-oriented sites 121 0.010 0.010 0.020 0.030 0.080 0.4012 0.210 0.500 0.990 1.580 2.260 2.820

Pb-TSP airport source-oriented sites 15 0.010 0.010 0.010 0.020 0.030 0.0933 0.070 0.100 0.230 0.400 0.400 0.400

Pb-TSP previous source-oriented sites 11 0.010 0.010 0.010 0.030 0.030 0.0882 0.060 0.120 0.140 0.270 0.270 0.270

Pb-TSP not source-oriented sites 96 0.000 0.000 0.000 0.010 0.010 0.0299 0.010 0.030 0.060 0.100 0.360 0.360

Pb-PM10 urban sites 54 0.000 0.000 0.000 0.000 0.000 0.0109 0.010 0.010 0.030 0.030 0.080 0.080

Pb-PM2.5 urban CSN sites 184 0.000 0.000 0.000 0.000 0.000 0.0098 0.010 0.010 0.020 0.030 0.050 0.200

Pb-PM2.5 non-urban IMPROVE sites 104 0.000 0.000 0.000 0.000 0.000 0.0005 0.000 0.000 0.000 0.000 0.010 0.010

Table 2D-7. Distribution of maximum monthly means, 2010-2012.

 2D - 23
APPENDIX 2D

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

State County Site

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3

)

Ratio of max 

3-month 

mean to 

annual mean

Ratio of max 3-

month mean to 

annual mean for 

CBSAs > 1M 

population

Alabama Limestone 010830005 0.009 0.007 1.2857

Alabama Pike 011090003 1.296 0.613 2.1142

Alaska Anchorage Municipality 020200051 0.067 0.054 1.2407

Arizona Gila 040071002 0.267 0.131 2.0382

Arizona Gila 040078000 0.061 0.030 2.0333

Arizona Maricopa e 040134018 0.038 0.031 1.2258 1.2258

Arizona Pima 040191028 0.002 0.002 1.0000

California Fresno 060190011 0.005 0.004 1.2500

California Imperial 060250005 0.026 0.017 1.5294

California Los Angeles e 060371103 0.013 0.009 1.4444 1.4444

California Los Angeles e 060371302 0.015 0.007 2.1429 2.1429

California Los Angeles e 060371402 0.061 0.033 1.8485 1.8485

California Los Angeles e 060371403 0.110 0.055 2.0000 2.0000

California Los Angeles e 060371404 0.108 0.042 2.5714 2.5714

California Los Angeles e 060371405 0.450 0.241 1.8672 1.8672

California Los Angeles e 060371406 0.072 0.035 2.0571 2.0571

California Los Angeles e 060371602 0.013 0.008 1.6250 1.6250

California Los Angeles e 060374002 0.009 0.005 1.8000 1.8000

California Los Angeles e 060374004 0.010 0.006 1.6667 1.6667

California Los Angeles e 060375005 0.006 0.003 2.0000 2.0000

California Riverside e 060651003 0.008 0.005 1.6000 1.6000

California Riverside e 060658001 0.008 0.006 1.3333 1.3333

California San Bernardino e 060711004 0.010 0.006 1.6667 1.6667

California San Bernardino e 060719004 0.011 0.007 1.5714 1.5714

California San Diego e 060730003 0.006 0.005 1.2000 1.2000

California San Diego e 060731020 0.127

California San Diego e 060731021 0.058

California San Mateo e 060812002 0.331 0.255 1.2980 1.2980

California Santa Clara e 060852010 0.119 0.090 1.3222 1.3222

California Santa Clara e 060852011 0.093 0.070 1.3286 1.3286

Colorado Arapahoe e 080050007 0.023 0.014 1.6429 1.6429

Colorado Denver e 080310025 0.010 0.006 1.6667 1.6667

District of Columbia District of Columbia e 110010043 0.004 0.003 1.3333 1.3333

Florida Hillsborough e 120570100 0.044 0.025 1.7600 1.7600

Florida Hillsborough e 120571066 0.984 0.374 2.6310 2.6310

 2D - 24
APPENDIX 2D

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

State County Site

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3

)

Ratio of max 

3-month 

mean to 

annual mean

Ratio of max 3-

month mean to 

annual mean for 

CBSAs > 1M 

population

Florida Hillsborough e 120571073 0.423 0.151 2.8013 2.8013

Georgia Bartow e 130150003 0.027 0.015 1.8000 1.8000

Georgia DeKalb e 130890003 0.004 0.003 1.3333 1.3333

Georgia Muscogee 132150009 0.230 0.128 1.7969

Georgia Muscogee 132150010 0.170 0.114 1.4912

Georgia Muscogee 132150011 0.071 0.023 3.0870

Hawaii Honolulu 150030010 0.001 0.001 1.0000

Illinois Cook e 170310001 0.024 0.018 1.3333 1.3333

Illinois Cook e 170310022 0.047 0.034 1.3824 1.3824

Illinois Cook e 170310026 0.034 0.023 1.4783 1.4783

Illinois Cook e 170310052 0.024 0.017 1.4118 1.4118

Illinois Cook e 170310110 0.294 0.077 3.8182 3.8182

Illinois Cook e 170310210 0.053 0.032 1.6563 1.6563

Illinois Cook e 170313103 0.041 0.014 2.9286 2.9286

Illinois Cook e 170313301 0.027 0.019 1.4211 1.4211

Illinois Cook e 170314201 0.011 0.010 1.1000 1.1000

Illinois Cook e 170316003 0.042 0.024 1.7500 1.7500

Illinois Macon 171150110 0.199 0.073 2.7260

Illinois Madison e 171190010 0.416 0.140 2.9714 2.9714

Illinois Madison e 171193007 0.036 0.020 1.8000 1.8000

Illinois Peoria 171430037 0.011 0.010 1.1000

Illinois Peoria 171430110 0.016 0.012 1.3333

Illinois Peoria 171430210 0.015 0.011 1.3636

Illinois St. Clair e 171630010 0.029 0.020 1.4500 1.4500

Illinois Whiteside 171950110 0.028 0.020 1.4000

Illinois Winnebago 172010110 0.063 0.028 2.2500

Indiana Delaware 180350009 0.338 0.159 2.1258

Indiana Lake e 180890023 0.077 0.031 2.4839 2.4839

Indiana Lake e 180890032 0.060 0.023 2.6087 2.6087

Indiana Lake e 180890033 0.139 0.055 2.5273 2.5273

Indiana Lake e 180892008 0.046 0.020 2.3000 2.3000

Indiana Marion e 180970063 0.079 0.028 2.8214 2.8214

Indiana Marion e 180970076 0.020 0.010 2.0000 2.0000

Indiana Marion e 180970078 0.011 0.006 1.8333 1.8333

Indiana Porter e 181270023 0.022 0.013 1.6923 1.6923

 2D - 25
APPENDIX 2D

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

State County Site

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3

)

Ratio of max 

3-month 

mean to 

annual mean

Ratio of max 3-

month mean to 

annual mean for 

CBSAs > 1M 

population

Indiana Porter e 181270027 0.041 0.027 1.5185 1.5185

Indiana Vanderburgh 181630020 0.006 0.004 1.5000

Iowa Pottawattamie 191550011 0.263 0.123 2.1382

Iowa Scott 191630015 0.012 0.010 1.2000

Kansas Saline 201690004 0.421 0.164 2.5671

Kansas Wyandotte e 202090021 0.011 0.008 1.3750 1.3750

Kentucky Boyd 210190016 0.004 0.003 1.3333

Kentucky Madison 211510003 0.248 0.057 4.3509

Kentucky Madison 211510005 1.584 0.703 2.2532

Kentucky Russell 212070001 0.063 0.027 2.3333

Louisiana East Baton Rouge Parish 220330009 0.002 0.002 1.0000

Louisiana East Baton Rouge Parish 220330014 0.011 0.004 2.7500

Louisiana St. John the Baptist Parish e 220950003 0.053 0.025 2.1200 2.1200

Massachusetts Nantucket County 250190001 0.010 0.009 1.1111

Michigan Charlevoix 260290011 0.006 0.005 1.2000

Michigan Ionia 260670002 0.049 0.071 0.6901

Michigan Ionia 260670003 0.284 0.096 2.9583

Michigan Kent 260810020 0.008 0.005 1.6000

Michigan Oakland e 261250013 0.022 0.019 1.1579 1.1579

Michigan Tuscola 261570001 0.034 0.021 1.6190

Michigan Wayne e 261630001 0.006 0.005 1.2000 1.2000

Michigan Wayne e 261630033 0.023 0.012 1.9167 1.9167

Minnesota Anoka e 270031002 0.011 0.006 1.8333 1.8333

Minnesota Anoka e 270036020 0.038 0.017 2.2353 2.2353

Minnesota Beltrami 270072303 0.001

Minnesota Cass 270210001 0.001

Minnesota Dakota e 270370020 0.004 0.004 1.0000 1.0000

Minnesota Dakota e 270370465 0.259 0.096 2.6979 2.6979

Minnesota Dakota e 270370470 0.002 0.001 2.0000 2.0000

Minnesota Hennepin e 270530963 0.004 0.003 1.3333 1.3333

Minnesota Hennepin e 270530966 0.005 0.004 1.2500 1.2500

Minnesota Hennepin e 270531007 0.004 0.003 1.3333 1.3333

Minnesota Mille Lacs e 270953051 0.001 0.000

Minnesota Ramsey e 271230871 0.007 0.005 1.4000 1.4000

Minnesota St. Louis 271377001 0.008 0.002 4.0000

 2D - 26
APPENDIX 2D

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

State County Site

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3

)

Ratio of max 

3-month 

mean to 

annual mean

Ratio of max 3-

month mean to 

annual mean for 

CBSAs > 1M 

population

Minnesota St. Louis 271377555 0.004 0.003 1.3333

Minnesota Stearns 271453053 0.008 0.004 2.0000

Minnesota Washington e 271630438 0.005 0.003 1.6667 1.6667

Minnesota Washington e 271630446 0.001 0.000

Missouri Iron 290930016 0.882 0.484 1.8223

Missouri Iron 290930021 1.147 0.522 2.1973

Missouri Iron 290930027 0.083 0.033 2.5152

Missouri Iron 290930029 0.115 0.038 3.0263

Missouri Iron 290930032 0.354

Missouri Iron 290930033 0.057 0.026 2.1923

Missouri Iron 290930034 0.402 0.241 1.6680

Missouri Iron 290939007 0.581 0.392 1.4821

Missouri Iron 290939008 0.387 0.209 1.8517

Missouri Jasper 290970005 0.019 0.014 1.3571

Missouri Jefferson e 290990004 1.122 0.888 1.2635 1.2635

Missouri Jefferson e 290990005 0.396 0.223 1.7758 1.7758

Missouri Jefferson e 290990009 0.191 0.055 3.4727 3.4727

Missouri Jefferson e 290990013 0.305 0.135 2.2593 2.2593

Missouri Jefferson e 290990020 0.865 0.546 1.5842 1.5842

Missouri Jefferson e 290990022 0.630 0.469 1.3433 1.3433

Missouri Jefferson e 290990023 0.563 0.386 1.4585 1.4585

Missouri Jefferson e 290990024 0.659 0.340 1.9382 1.9382

Missouri Jefferson e 290990025 0.085 0.042 2.0238 2.0238

Missouri Jefferson e 290990026 0.080 0.036 2.2222 2.2222

Missouri Jefferson e 290990027 0.592 0.454 1.3040 1.3040

Missouri Jefferson e 290999001 1.100 0.812 1.3547 1.3547

Missouri Jefferson e 290999002 0.431 0.228 1.8904 1.8904

Missouri Jefferson e 290999003 0.327 0.175 1.8686 1.8686

Missouri Jefferson e 290999004 0.442 0.156 2.8333 2.8333

Missouri Jefferson e 290999005 1.432 0.913 1.5685 1.5685

Missouri Jefferson e 290999006 0.103 0.049 2.1020 2.1020

Missouri Reynolds 291790001 0.059 0.031 1.9032

Missouri Reynolds 291790002 0.068 0.034 2.0000

Missouri Reynolds 291790003 0.100 0.027 3.7037

Missouri Reynolds 291790034 0.161 0.078 2.0641

 2D - 27
APPENDIX 2D

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

State County Site

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3

)

Ratio of max 

3-month 

mean to 

annual mean

Ratio of max 3-

month mean to 

annual mean for 

CBSAs > 1M 

population

Missouri St. Francois 291870006 0.132 0.043 3.0698

Missouri St. Francois 291870007 0.134 0.053 2.5283

Missouri St. Louis e 291892003 0.008 0.007 1.1429 1.1429

Missouri St. Louis city e 295100085 0.028 0.026 1.0769 1.0769

Nebraska Dodge 310530005 0.139 0.055 2.5273

Nebraska Douglas 310550019 0.006 0.005 1.2000

Nebraska Nemaha 311270002 0.115 0.034 3.3824

Nevada Clark e 320030540 0.003

New Mexico Bernalillo 350010023 0.006 0.003 2.0000

New York Orange e 360713001 0.101 0.025 4.0400 4.0400

New York Orange e 360713002 1.027 0.123 8.3496 8.3496

New York Orange e 360713004 0.007 0.005 1.4000 1.4000

New York Suffolk e 361030024 0.027 0.017 1.5882 1.5882

Ohio Butler e 390170015 0.009 0.006 1.5000 1.5000

Ohio Columbiana 390290019 0.057 0.020 2.8500

Ohio Columbiana 390290020 0.025 0.015 1.6667

Ohio Columbiana 390290022 0.044 0.019 2.3158

Ohio Cuyahoga e 390350038 0.021 0.013 1.6154 1.6154

Ohio Cuyahoga e 390350042 0.030 0.013 2.3077 2.3077

Ohio Cuyahoga e 390350049 0.531 0.136 3.9044 3.9044

Ohio Cuyahoga e 390350060 0.030 0.020 1.5000 1.5000

Ohio Cuyahoga e 390350061 0.023 0.015 1.5333 1.5333

Ohio Cuyahoga e 390350072 0.035 0.014 2.5000 2.5000

Ohio Franklin e 390490025 0.011 0.009 1.2222 1.2222

Ohio Fulton 390510001 0.178 0.070 2.5429

Ohio Logan 390910006 0.006 0.004 1.5000

Ohio Marion 391010003 0.088 0.041 2.1463

Ohio Marion 391010004 0.017 0.013 1.3077

Ohio Montgomery 391137001 0.008 0.007 1.1429

Ohio Stark 391510017 0.023 0.015 1.5333

Ohio Trumbull 391550012 0.011 0.007 1.5714

Ohio Washington 391670008 0.007 0.005 1.4000

Ohio Washington 391670010 0.008 0.005 1.6000

Oklahoma Ottawa 401159006 0.022 0.012 1.8333

Oklahoma Ottawa 401159007 0.034 0.018 1.8889

 2D - 28
APPENDIX 2D

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

State County Site

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3

)

Ratio of max 

3-month 

mean to 

annual mean

Ratio of max 3-

month mean to 

annual mean for 

CBSAs > 1M 

population

Oklahoma Pittsburg 401210416 0.004 0.003 1.3333

Oklahoma Tulsa 401431127 0.008 0.006 1.3333

Oregon Yamhill e 410711702 0.045 0.021 2.1429 2.1429

Pennsylvania Allegheny e 420030002 0.016 0.014 1.1429 1.1429

Pennsylvania Allegheny e 420030008 0.014 0.008 1.7500 1.7500

Pennsylvania Allegheny e 420030070 0.056 0.018 3.1111 3.1111

Pennsylvania Allegheny e 420031009 0.138 0.035 3.9429 3.9429

Pennsylvania Beaver e 420070006 0.085 0.051 1.6667 1.6667

Pennsylvania Beaver e 420070007 0.253 0.166 1.5241 1.5241

Pennsylvania Beaver e 420070505 0.151 0.089 1.6966 1.6966

Pennsylvania Berks 420110020 0.509 0.158 3.2215

Pennsylvania Berks 420110021 0.139 0.044 3.1591

Pennsylvania Berks 420110022 0.118 0.035 3.3714

Pennsylvania Berks 420111717 0.217 0.146 1.4863

Pennsylvania Carbon 420250214 0.104

Pennsylvania Delaware e 420450002 0.047 0.028 1.6786 1.6786

Pennsylvania Delaware e 420450004 0.047 0.028 1.6786 1.6786

Pennsylvania Franklin 420550002 0.046 0.028 1.6429

Pennsylvania Indiana 420630005 0.049 0.025 1.9600

Pennsylvania Lancaster 420710009 0.068 0.039 1.7436

Pennsylvania Lawrence 420730011 0.023 0.026 0.8846

Pennsylvania Luzerne 420790036 0.137 0.054 2.5370

Pennsylvania Philadelphia e 421010449 0.029 0.021 1.3810 1.3810

Pennsylvania Philadelphia e 421011002 0.051 0.030 1.7000 1.7000

Pennsylvania Westmoreland e 421290009 0.046 0.023 2.0000 2.0000

South Carolina Charleston 450190003 0.007 0.005 1.4000

South Carolina Florence 450418001 0.044 0.013 3.3846

South Carolina Florence 450418002 0.015 0.006 2.5000

South Carolina Florence 450418003 0.011 0.005 2.2000

South Carolina Greenville 450450015 0.006 0.005 1.2000

South Carolina Richland 450790007 0.005 0.004 1.2500

South Carolina Richland 450790019 0.024 0.011 2.1818

Tennessee Knox 470930023 0.165 0.108 1.5278

Tennessee Knox 470930027 0.042 0.020 2.1000

Tennessee Knox 470931017 0.037 0.018 2.0556

 2D - 29
APPENDIX 2D

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

State County Site

Maximum 

3-month 

mean 

(μg/m3

)

Annual 

average 

(μg/m3

)

Ratio of max 

3-month 

mean to 

annual mean

Ratio of max 3-

month mean to 

annual mean for 

CBSAs > 1M 

population

Tennessee Shelby e 471570075 0.005 0.004 1.2500 1.2500

Tennessee Sullivan 471633001 0.076 0.056 1.3571

Tennessee Sullivan 471633002 0.044 0.036 1.2222

Tennessee Sullivan 471633003 0.053 0.038 1.3947

Tennessee Sullivan 471633004 0.080 0.044 1.8182

Texas Cameron 480610006 0.008 0.004 2.0000

Texas Collin e 480850003 0.371 0.136 2.7279 2.7279

Texas Collin e 480850007 0.199 0.093 2.1398 2.1398

Texas Collin e 480850009 0.774 0.388 1.9948 1.9948

Texas Collin e 480850029 0.180 0.052 3.4615 3.4615

Texas Dallas e 481130069 0.013 0.009 1.4444 1.4444

Texas El Paso 481410002 0.040 0.022 1.8182

Texas El Paso 481410033 0.019 0.017 1.1176

Texas El Paso 481410037 0.025 0.022 1.1364

Texas El Paso 481410055 0.019 0.010 1.9000

Texas El Paso 481410058 0.022 0.016 1.3750

Texas Harris e 482011034 0.008 0.005 1.6000 1.6000

Texas Harris e 482011039 0.004 0.003 1.3333 1.3333

Texas Kaufman e 482570020 0.104 0.044 2.3636 2.3636

Texas Potter 483750024 0.020 0.007 2.8571

Texas Webb 484790016 0.026 0.018 1.4444

Utah Salt Lake e 490351001 0.057 0.024 2.3750 2.3750

Virginia Amherst 510090007 0.018 0.006 3.0000

Virginia Buchanan 510270006 0.014 0.012 1.1667

Virginia Henrico e 510870014 0.005 0.005 1.0000 1.0000

Virginia Roanoke city 517700011 0.109 0.033 3.3030

Washington King e 530330029 0.055 0.036 1.5278 1.5278

Washington Snohomish e 530610013 0.023 0.013 1.7692 1.7692

West Virginia Cabell 540110006 0.012 0.010 1.2000

Wisconsin Sheboygan 551170008 0.152 0.056 2.7143

Puerto Rico Arecibo Municipio, Puerto Rico 720130001 0.339 0.171 1.9825

Puerto Rico Bayamón Municipio, Puerto Rico e 720210010 0.011 0.004 2.7500 2.7500

Puerto Rico Salinas Municipio, Puerto Rico 721230002 0.017 0.008 2.1250

 2D - 30
3A-1 

APPENDIX 3A 

INTERPOLATED RISK ESTIMATES FOR THE GENERALIZED 

(LOCAL) URBAN CASE STUDY 

This Appendix describes the method used to develop risk estimates for conditions just 

meeting the current standard (0.15 μg/m3

, as a maximum 3-month average) for the generalized 

(local) urban case study. These risk estimates were developed by interpolation from the 2007 

REA results for this case study. The general approach was to identify the two alternative 

standard scenarios simulated in the 2007 REA which represented air quality conditions 

bracketing those for the current standard and then linearly interpolate an estimate of risk for the 

current standard based on the slope created from the two bracketing estimates. In representing 

air quality conditions for these purposes, we focused on the annual average air Pb concentration 

estimates 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 An 

annual average concentration estimate to represent the current standard was identified in a 

manner consistent with that employed in the 2007 REA for this case study (see section 3.4.3.2 

above, use of 2003-2005 data) with the use of currently available monitoring data (2010-2012) 

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, as a not-to-be-exceeded 3-

month average) was found to be bracketed by the scenarios for alternative standards of 0.5 and 

0.20 μg/m3 (maximum monthly averages). A risk estimate for the current standard was then 

derived using the slope relating generalized (local) urban case study IQ loss to the annual 

average Pb concentration used for those two air quality scenarios. We used this interpolation 

approach to develop median risk estimates for the current standard based on each of the four C-R 

functions. Details on the method for the interpolation approach are provided below. 

1. Identify an estimate of annual average air Pb concentration to represent each air quality 

scenario. For the alternative scenarios, this was done in the 2007 REA using the 2003-

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. 
3A-2 

of the current standard here, this uses the recent Pb-TSP dataset (2010-2012) for urban 

areas of population greater than one million. The concentration in terms of the metric 

being assessed (e.g., maximum 3-month or calendar quarter average) was derived per 

monitoring site, as was the annual average concentration and also the ratio of the two 

(2007 REA, Appendix A; Appendix 2D of this document). From the average of the 

monitor-specific ratios we derived the annual average estimate. [In the 2007 REA, this 

was the IEUBK air quality input for each AQ scenario.] With the 2010-2012 data, the 

average, across monitors in urban areas greater than 1 million population, of the ratio of 

maximum 3-month average to annual average is 1.92 (Appendix 2D in this document). 

- This ratio was used to derive an annual average air Pb-TSP concentration 

estimate to represent the current standard scenario (annual value = 0.15 μg/m3

* 1/1.92 = 0.078 μg/m3

). The annual average values for the scenarios 

included in the 2007 REA and also for the current standard scenario 

considered in this interpolation are shown in Table 3A-1 below. 

Table 3A-1. Annual average air Pb-TSP concentration estimates for different air quality 

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 2010-2012 air quality dataset. 

2. Identify the two “bounding” alternative standard levels that will be used to derive a 

slope for the risk interpolation for the current standard level. Based on comparison of 

the annual ambient air Pb estimates for each of the 2007 REA air quality scenarios and 

for the current standard we determine which scenarios “bound” the current standard (in 

terms of the annual average ambient Pb estimate). As Table 3A-1 above shows, the 

bounding scenarios are the scenarios for just meeting maximum monthly average 

concentrations of 0.5 and 0.2 μg/m3

. 

3. Calculate the slopes of generalized (local) urban case study IQ loss per unit annual 

average Pb estimate for each risk estimate of interest for the two bounding scenarios.

This calculation is (IQ LossScenario X – IQ LossScenario Y)/ (annual averageScenario X – annual 

averageScenario Y). The risk estimates for the 4 different C-R functions and two exposure 

pathway categories of interest (Recent Air and Recent + Past Air), with the derived 

slopes, are in Table 3A-2. 
3A-3 

Table 3A-2. Risk estimates for bounding air 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).

4. Derive interpolated risk estimates for the current standard scenario. Using the 

slopes presented in Table 3A-2 and the lower bounding air quality scenario risk 

estimates, derive corresponding risk estimates for the current standard scenario: 

Risk = lower bounding risk + (increment annual average Pb * slope) 

Where: 

 lower bounding risk = risk for the lower bound air quality scenario (i.e., 

for 0.2 μg/m3

 maximum monthly average) 

 increment annual average Pb is the difference between the annual average 

estimates for the current standard and the lower bounding scenario. 

 slope is the value described in Step 4, which differs across the 8 

combinations of C-R functions and exposure pathway categories. 

The resulting interpolated risk estimates are presented in Table 3A-3.

Table 3A-3. Interpolated risk estimates for the current NAAQS scenario for the 

generalized (local) urban case study. 

Risk Estimates 

for different C-R functions 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).
5A-1 

APPENDIX 5A 

ADDITIONAL DETAIL ON 2006 ECOLOGICAL SCREENING 

ASSESSMENT 

Setting and spatial 

extent of dataset or 

modeling analysis 

Media Screened and Screening Levels Used 

Soil Freshwater 

water column 

Freshwater 

Sediment 

Primary 

Smelter Case 

Study

Herculaneum, Missouri: 

soil and waterbody 

samples from study 

area 6 km diameter, 

centered on point 

source 

Soil 

screening 

values 

developed 

based on 

U.S. EPA 

Superfund 

methodology 

for 

developing 

ecological 

soil screening 

levels 

(USEPA, 

2005a,b) 

U.S. EPA 

freshwater AWQC 

for aquatic life 

adjusted for sitespecific water 

hardness 

Sediment screening 

values based on 

MacDonald et al. 

(2000) sediment quality 

assessment guidelines 

Seconday 

Smelter Case 

Study

Troy (Pike County), 

Alabama: soil 

concentrations in 

census blocks near 

facility predicted from 

dispersion and soil 

mixing model NA NA 

Near Roadway 

Non-Urban 

Case Study 

Two datasets: Corpus 

Christi, Texas (within 4 

m from road), and 

Atlee, Virginia (within 2 

to 30 m from road) 

Vulnerable 

Ecosystem 

Case Study 

Hubbard Brook 

Experimental Forest, 

New Hampshire: forest 

in oblong basin about 8 

km long by 5 km wide 

While no quantitative analyses were performed, summary 

review of literature search indicated: (1) atmospheric Pb inputs 

do not directly affect stream Pb levels at HBEF because 

deposited Pb is almost entirely retained in the soil profile; (2) 

soil horizon analysis results show Pb has become more 

concentrated at lower depths over time and that the soil profile 

serves as a Pb sink, appreciably reducing Pb in porewater as it 

moves through the soil layers to streams, (3) dissolved Pb 

concentrations were reduced (5 ppb to about 5 ppt) as Pb 

moves from the Oa horizon to streams. Studies concluded 

insignificant contribution of dissolved Pb from soils to streams 

(less than 0.2 g·ha ̄1·yr ̄1). (ICF, 2006, Appendix E) 

National 

Surface Water 

Screen 

Surface water bodies in 

the 47 basin study units 

from all regions of the 

United States, covering 

approx. 50% of U.S. 

land base 

NA 

U.S. EPA 

freshwater AWQC 

for aquatic life 

adjusted for 

hardness at site or 

nearby water body 

Sediment screening 

values based on 

MacDonald et al. 

(2000) sediment quality 

assessment 

guidelines 

AWQC= Ambient water quality criteria. NA = Not applicable; medium not part of case study. 

NOTE: Information here is drawn from ICF, 2006 and EPA, 2007b.
ATTACHMENT 

Clean Air Scientific Advisory Committee Letter (June 4, 2013) 
UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

WASHINGTON D.C. 20460

OFFICE OF THE ADMINISTRATOR

SCIENCE ADVISORY BOARD

June 4, 2013

EPA-CASAC-13-005

The Honorable Bob Perciasepe

Acting Administrator

U.S. Environmental Protection Agency

1200 Pennsylvania Avenue, N.W.

Washington, D.C. 20460

Subject: CASAC Review of the EPA’s Policy Assessment for the Review of the Lead National 

Ambient Air Quality Standards (External Review Draft – January 2013)

Dear Acting Administrator Perciasepe:

The Clean Air Scientific Advisory Committee (CASAC) Lead Review Panel met on February 5 - 6, 

2013, to peer review the EPA’s Policy Assessment for the Review of the Lead National Ambient Air 

Quality Standards (External Review Draft – January 2013), hereafter referred to as the PA. The 

CASAC’s consensus responses to the agency’s charge questions and the individual review comments 

from the CASAC Lead Review Panel are enclosed. The CASAC’s key points are highlighted below.

Overall, the CASAC concurs with the EPA that the current scientific literature does not support a 

revision to the Primary Lead (Pb) National Ambient Air Quality Standard (NAAQS) nor the Secondary 

Pb NAAQS. Although the current review incorporates a substantial body of new scientific literature, the 

new literature does not justify a revision to the standards because it does not significantly reduce 

substantial data gaps and uncertainties (e.g., air-blood Pb relationship at low levels; sources contributing 

to current population blood Pb levels, especially in children; the relationship between Pb and childhood 

neurocognitive function at current population exposure levels; the relationship between ambient air Pb 

and outdoor dust and surface soil Pb concentrations). Further details on these and other research needs 

are provided in the consensus responses. The CASAC recommends that research be performed to 

address these data gaps and uncertainties to inform future Pb NAAQS reviews.

The CASAC has additional comments and recommendations on improving the document. With the 

completion of the recommended revisions outlined below and in the consensus responses, the PA will 

serve its intended purpose. Another CASAC review of the document is not needed.

The PA should include a discussion that Pb is a unique pollutant in many ways. Unlike other criteria air 

pollutants, Pb is of concern from a multimedia perspective. Millions of tons of Pb are present in the 

environment from legacy sources. The distribution of this substantial reservoir of Pb is not known. Thus,

the extent of current human exposure from this legacy cannot be reliably estimated.

The PA generally captures the key aspects of the health effects evidence presented in the Integrated 

Science Assessment, but can be made more concise and clear by providing summary conclusions 
2

regarding the health effects evidence at the beginning of the sections. The risk and exposure information 

from the previous Pb NAAQS review is adequately presented. The CASAC concurs that a new risk and 

exposure assessment (REA) is not needed due the lack of sufficient new scientific information to 

warrant revision of the prior REA data and methods. 

The application of the evidence-based framework and the use of the health risk and exposure 

information from the previous Pb NAAQS review seem appropriate and provide a sufficient rationale to 

support retaining the current primary standard without revision. However, there should be more 

description in the PA of the data and rationale behind the averaging time and form of the current primary 

standard. Additionally, research is needed to address uncertainties and data gaps in the evidence-based 

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

Given the existing scientific data, the CASAC concurs with retaining the current secondary standard

without revision. However, the CASAC also notes that important research gaps remain. For example 

questions remain regarding the relevance of the primary standard’s indicator, level, averaging time, and 

form for the secondary standard. Other areas for additional research to address data gaps and uncertainty 

include developing a critical loads approach for U.S. conditions and a multi-media approach to account 

for legacy Pb and contributions from different sources. Addressing these gaps may require 

reconsideration of the secondary standard in future assessments. 

The CASAC also wishes to highlight the importance of a separate but related policy issue. The CASAC 

notes that it has not considered this separate policy issue in providing advice on the NAAQS. The 

decrease in childhood lead poisoning in the United States over the last three decades is a great public 

health success story. Concurrently, there is a trend of increased relocation of Pb production, recycling, 

and recovery to other nations. One example is the export of spent lead acid batteries (SLAB) to Mexico. 

As detailed in a report by the Secretariat of the Commission for Environmental Cooperation (CEC), 

environmental and health protections in the secondary lead industry in other countries are not 

functionally equivalent to those in the United States. The CEC offers recommendations to avoid 

development of pollution havens and for the United States to work with Mexico and Canada to foster 

adoption of best practices throughout North America. The CASAC recognizes the role of the EPA 

Administrator as a member of the CEC Council and strongly urges the EPA to carefully consider the 

recommendations of the CEC report, and to support decisive action that will enable the success of the Pb 

NAAQS in the United States to be a role model for development of best practices internationally that 

avoid adverse public health impacts abroad. For example, the considerable effort by the EPA to develop 

the ISA and the PA could be a valuable starting point for other countries to develop or revise their own 

ambient standards for lead.
3

The CASAC appreciates the opportunity to provide advice and looks forward to receiving the EPA’s 

response.

Sincerely,

/signed/

Dr. H. Christopher Frey, Chair

Clean Air Scientific Advisory Committee

Enclosures
i

NOTICE

This report has been written as part of the activities of the EPA's Clean Air Scientific Advisory 

Committee (CASAC), a federal advisory committee independently chartered to provide extramural 

scientific information and advice to the Administrator and other officials of the EPA. The CASAC 

provides balanced, expert assessment of scientific matters related to issues and problems facing the 

agency. This report has not been reviewed for approval by the agency and, hence, the contents of this 

report do not necessarily represent the views and policies of the EPA, nor of other agencies within the 

Executive Branch of the federal government. In addition, any mention of trade names or commercial 

products does not constitute a recommendation for use. The CASAC reports are posted on the EPA 

website at: http://www.epa.gov/casac.
ii

U.S. Environmental Protection Agency

Clean Air Scientific Advisory Committee

CASAC Lead Review Panel (2010-2013)

CHAIR

Dr. H. Christopher Frey, Distinguished University Professor, Department of Civil, Construction and 

Environmental Engineering, College of Engineering, North Carolina State University, Raleigh, NC

OTHER CASAC MEMBER

Mr. George A. Allen, Senior Scientist, Northeast States for Coordinated Air Use Management 

(NESCAUM), Boston, MA

CONSULTANTS

Dr. Herbert Allen, Professor Emeritus, Department of Civil and Environmental Engineering, 

University of Delaware, Newark, DE

Dr. Richard Canfield, Senior Research Associate, Division of Nutritional Sciences, Cornell University, 

Ithaca, NY

Dr. Deborah Cory-Slechta, Professor, Department of Environmental Medicine, School of Medicine 

and Dentistry, University of Rochester, Rochester, NY

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

NY

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

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

Dr. Philip Hopke, Bayard D. Clarkson Distinguished Professor, Department of Chemical and 

Biomolecular Engineering, Clarkson University, Potsdam, NY

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

University, Syracuse, NY

Dr. Susan Korrick, Assistant Professor of Medicine , Department of Medicine, Brigham and Women's 

Hospital, Channing Laboratory, Harvard Medical School, Boston, MA

Dr. Michael Kosnett, Associate Clinical Professor, Division of Clinical Pharmacology and Toxicology,

Department of Medicine, University of Colorado School of Medicine, Denver, CO
iii

Dr. Roman Lanno, Associate Professor and Associate Chair, Department of Evolution, Ecology, and 

Organismal Biology, Ohio State University, Columbus, OH

Mr. Richard L. Poirot, Environmental Analyst, Air Pollution Control Division, Department of 

Environmental Conservation, Vermont Agency of Natural Resources, Waterbury, VT

Dr. Joel G. Pounds, Laboratory Fellow, Cell Biology & Biochemistry, Biological Sciences Division, 

Pacific Northwest National Laboratory, Richland, WA

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

Dr. William Stubblefield, Senior Research Professor, Department of Molecular and Environmental 

Toxicology, Oregon State University, Corvallis, OR

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

Dr. Gail Wasserman, Professor of Clinical Psychology in Child Psychiatry, Division of Child and 

Adolescent Psychiatry, College of Physicians and Surgeons, Columbia University, New York, NY

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

New York, NY

SCIENCE ADVISORY BOARD STAFF

Mr. Aaron Yeow, Designated Federal Officer, U.S. Environmental Protection Agency, Science 

Advisory Board (1400R), 1200 Pennsylvania Avenue, NW, Washington, DC
iv

U.S. Environmental Protection Agency

Clean Air Scientific Advisory Committee

CASAC

CHAIR

Dr. H. Christopher Frey, Distinguished University Professor, Department of Civil, Construction and 

Environmental Engineering, College of Engineering, North Carolina State University, Raleigh, NC

MEMBERS

Mr. George A. Allen, Senior Scientist, Northeast States for Coordinated Air Use Management 

(NESCAUM), Boston, MA

Dr. Ana Diez-Roux, Professor of Epidemiology, School of Public Health, University of Michigan, Ann 

Arbor, MI

Dr. Jack Harkema, Professor, Department of Pathobiology, College of Veterinary Medicine, Michigan 

State University, East Lansing, MI

Dr. Helen Suh, Associate Professor, Bouve School of Health Sciences, Northeastern University, 

Boston, MA

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

Dr. Ronald Wyzga, Technical Executive, Air Quality Health and Risk, Electric Power Research 

Institute, Palo Alto, CA

SCIENCE ADVISORY BOARD STAFF

Dr. Holly Stallworth, Designated Federal Officer, U.S. Environmental Protection Agency, Science 

Advisory Board (1400R), 1200 Pennsylvania Avenue, NW, Washington, DC
1

Consensus Responses to Charge Questions on 

EPA’s Policy Assessment for the Review of the Lead National Ambient Air Quality Standards 

(External Review Draft – January 2013)

Chapter 1 – Introduction

This chapter provides context for the review, including the background of past reviews, as well as the 

scope for the current review. This includes discussion of fate and multimedia pathways of ambient air 

Pb and other nonair sources of Pb in the environment.

Does the Panel find the introductory and background material, including that pertaining to previous 

reviews of the Pb standard and the scope of the current review to be appropriately characterized and 

clearly communicated?

Chapter 1 of the Policy Assessment (PA) is reasonably well characterized and for the most part clearly 

communicated, although there are several improvements that should be made (see below). The CASAC

concurs with the EPA that the current scientific evidence does not justify a change to the current Lead 

(Pb) National Ambient Air Quality Standards (NAAQS), with the caveats stated below.

Chapter 1 should emphasize Pb as a unique pollutant in many ways. Historically, anthropogenic

emissions of Pb to the air around the globe exceeded natural emissions by a huge margin, more than any 

other trace metal. Natural emissions come from unpolluted soil, seaspray, and other natural sources. 

Removal of Pb from gasoline, paint, solder, and other anthropogenic sources constitutes what is 

arguably the biggest environmental success story for any pollutant to-date. Unlike other criteria air 

pollutants, Pb is of concern from a multimedia perspective; human exposure to Pb comes from 

inhalation of air and also from ingestion of food, water, and dust. In addition, Pb may be the pollutant 

with the biggest legacy problem: millions of tons of Pb are now present in the environment as a result of 

discharges from years ago. The distribution of this huge reservoir of Pb is not known, and thus current 

human exposure from this legacy cannot reliably be estimated. What is known, however, is that human 

activities have on average substantially elevated the Pb content of soil at numerous locations around the 

United States, more so than other trace metals processed in large quantities. Although air Pb levels are 

much lower because of reduced emissions, soil Pb can be expected to remain elevated for many years. 

These unique aspects of Pb, especially the problem of not knowing the distribution of legacy Pb, should 

be clearly discussed in the PA.

This chapter concludes that there is no information published in the last five years justifying 

reconsideration of the current NAAQS. Although that is true, this conclusion should be conveyed with 

an assessment of the adequacy of the old information. In particular, there were significant unknowns and 

uncertainties associated with a lack of information five years ago; those unknowns and uncertainties still 

remain.

There are no statements in the PA that the Integrated Science Assessment (ISA) is limited only to 

exposures and data sources considered currently relevant to the U.S. population, as opposed to 

populations outside of the United States. Furthermore, the literature is considered only to assess how 

new studies relate to conclusions drawn in the past review, and then only to studies in the peer-reviewed 

literature. This has resulted in an ISA that is dedicated predominately to toxicology, health effects, 
2

biokinetics, and causal determinations. These are areas that were data rich in the last review, and 

continue to produce volumes of new peer-reviewed information. In contrast, in areas where the least is 

known and EPA relies on past findings, uncertainty is becoming greater as the existing information 

becomes outdated. Additionally, the current assessment excludes consideration of impacts on 

populations outside of the United States. 

There is considerable discussion dedicated to the reduction of Pb in air and other media in the United 

States over the last four decades. Most of the reduction was achieved through the elimination of tetraethyl Pb gasoline additives. Another major component of the reduction was substantial decreases in 

emissions from primary and secondary smelters, and metals processing industries. In the case of motor 

vehicle gasoline-related emissions, these ceased and other non-Pb products were substituted in 

commerce. This resulted in decreased Pb emissions and health and environmental effects in both the 

United States and globally. Within the United States, Pb continues to be used as an octane boosting fuel 

additive for very high octane fuels used in general aviation for piston engine aircraft. In the case of Pb

production and secondary recovery, however, this production and recovery were exported overseas.

There is no mention of the impact of the “avoided emissions” in their new locales.

Thus, overall, there is no reason to change the current airborne Pb standard. However, although airborne 

Pb is far more limited as a problem within the United States, potential exposure to Pb in other 

environmental media in the United States is likely to be more significant. Furthermore, there may be 

increasing Pb exposures overseas (e.g., as described in CEC, 2013).

There are a few areas that need revision for clarity and accuracy. On page ES-1, line 25, the following 

sentence should be added to the end of the paragraph: “This approach was taken to aid in the decision to 

retain or revise the current standards.” On page 1-13 line 35, it states: “And we recognize that past Pb

emissions in many situations were well in excess of the current Pb standard.” One cannot compare 

emissions to an airborne standard. This sentence can be revised to state: “We recognize that past Pb

emissions in many situations caused airborne Pb concentrations far in excess of the current Pb standard.”

Chapter 2 – Ambient Air Lead

This chapter provides an overview of current information on air Pb emissions and monitoring data, 

consideration of the current air Pb monitoring requirements and an overview of current information on 

Pb in nonair media.

To what extent does the Panel agree that the most relevant information on emissions (section 2.1), air 

quality (section 2.2.2), and Pb concentrations in other media (section 2.3) is presented, and to what 

extent is the information presented appropriately characterized and clearly communicated?

With a few minor exceptions (see specific individual panel member comments), the information on Pb 

emissions, air quality and concentrations in other media is appropriately characterized and clearly 

presented. Historical and recent (2008) emissions data are summarized quantitatively in clear charts and 

tables, with additional detail on the 2008 National Emissions Inventory (NEI) data sources and 

limitations provided in Appendix 2A. There are also qualitative discussions and an informative 

Appendix 2B on recent regulatory actions, indicating that current emissions have declined since 2008, 

with additional reductions pending. However, quantitative estimates of emissions reductions would be
3

informative. To the extent that these or other historical controls of U.S. Pb source categories have 

shifted Pb emissions to other countries, it would be informative to include discussion of those displaced 

emissions.

The information on ambient air concentrations is clearly presented (for sites with 1 to 3 years of valid 

data for 2009 to 2011) in maps, charts and in a detailed appendix (Appendix 2D). More recent 

measurements from sites (including near airports) initiated since the previous Pb NAAQS review would 

help inform the current Pb NAAQS review, as well as the separate Section 231 aviation gasoline 

(“avgas”) review.

Given the “not to be exceeded” 3-month rolling average form of the Pb NAAQS, an exceedance could 

be determined with as few as 3 months of new data. Therefore, it would be useful if more recent data are

summarized in the next Pb PA, without being limited to sites with multiple years of valid data.

The information on Pb concentrations in other media is clearly presented. The sections (2.3.2.1 and 

2.3.2.2) on indoor and outdoor dust are highly relevant to exposure assessments and would benefit from 

some added discussion of how dust Pb concentration, loading, and loading rates are measured. In 

particular, information relating to the differences in particle sizes in dust samples and ambient air 

samples would be helpful. More information on changes, if any, over time in the availability of 

historically deposited soil Pb for resuspension to the air or for direct uptake through ingestion could help 

clarify the significance of this potentially important source category.

With regard to information on ambient Pb monitoring (section 2.2.1), to what extent is this information 

appropriately characterized and clearly communicated?

The information on ambient Pb monitoring is appropriately characterized and clearly communicated. It

is understood that the high-volume (Hi-Vol) Total Suspended Particulates (TSP) sampler is an imperfect 

historical artifact, and that there is not time for this review cycle of the Pb NAAQS to develop, fully test, 

and deploy alternative samplers that would consistently capture particles (less than and) greater than 10 

microns with appropriate collection efficiencies and size ranges under varying wind speeds and 

directions. The draft PA notes that the EPA expects a new, improved sampler to be “available for 

consideration in a future review.” Toward this goal, discussion is needed regarding the desirable cut size 

characteristics of, and practical constraints on, an alternative sampler. Information from the ISA could 

be cited here, such as material currently on page 3-67 of the 3rd external draft of the ISA that may be 

revised for the final ISA regarding discussion of the desirable cut size. 

If an alternative low-volume sampler could be developed with an upper 50% particle cut size in the 

range of 15 to 20 microns, and without the wind speed and direction biases of the Hi-Vol TSP sampler, 

it seems likely that such a sampler would typically capture as much (or occasionally more) Pb as the HiVol TSP sampler. The CASAC has previously recommended the development of a new air Pb sampler 

that collects larger particle sizes, that could improve the quality of sampling in the National Air Toxics 

Trends Station (NATTS) network, and that could serve as an Federal Reference Method (FRM) or 

Federal Equivalent Method (FEM) for Pb. Filters collected by this sampler also would be amenable to 

multi-elemental analyses by lower-cost analytical methods and could be useful for more accurate and 

precise assessments of other particulate pollutants with significant coarse mode concentrations, 

including chemical contaminants (like hexavalent chromium, silica, and cadmium) and biological 

components like pollen, fungi, and endotoxins.
4

Chapter 3 – Health Effects and Exposure/Risk Information

This chapter discusses key policy relevant aspects of the health effects evidence and exposure/risk 

information.

To what extent does the information in sections 3.1 (Internal Disposition and Biomarkers of Exposure 

and Dose), 3.2 (Nature of Effects) and 3.3 (Public Health Implications and At-Risk Populations) capture 

and appropriately characterize the key aspects of the evidence assessed and integrated in the ISA?

Chapter 3 of the draft PA generally captures the key aspects of the evidence presented in the ISA;

therefore, concerns about content stem from the content of the ISA and not its condensation in the PA.

Recognizing the degree of condensation needed to summarize the ISA in only a few pages, this format 

presents a great writing challenge, and the writing in the chapter lacks clarity. Wordiness should be 

reduced to directly and efficiently convey the meaning. For example, sentences such as the following 

could be shortened and recast in a more active voice: “The results from the various case studies 

assessed, with consideration of the context in which they were derived (e.g., the extent to which the 

range of air-related pathways were simulated, and limitations associated with those simulations), and the 

multiple sources of uncertainty (see section 3.4.7 below) are also informative to our understanding of 

air-to-blood ratios.” (Please refer to Dr. Canfield’s individual comments for details on the sentences in 

need of streamlining and clarification.)

In addition, there are a few places where legacy text from the previous PA remains, so extraneous words 

need to be deleted and tenses updated. What needs the most attention is the length and complexity of 

some sentences.

To what extent is the newly available evidence on air-to-blood ratios appropriately characterized and 

considered in light of information previously available in past reviews?

The new information on air-to-blood ratios is presented in context of previous information and no 

change in the estimate is justified at this time. 

When revising this section (3.1) it would be helpful to first read the last (summary paragraph) on page 3-

14. Those conclusions should be included in the first paragraph of the section and then restated at the 

end of the section when the reader will be in a position to understand the context.

To what extent is the newly available evidence on concentration-response functions for IQ decrements 

in young children appropriately characterized and considered in light of information previously 

available in past reviews?

The newly available evidence is appropriately characterized. Parametric information could be extracted 

from these data to produce quantitative results for blood Pb subgroups, but the quality of the data would

not likely provide a useful basis for altering the conclusions reached from the data available prior to 

2008.

There is a critical need for more information about effects of Pb at levels in the 0-5 μg/dL range. Studies 

about effects of Pb at these low levels are a future research need.
5

With regard to the exposure and risk information, to what extent is the information drawn from the 

human exposure and health risk assessment in the last review sufficiently characterized and clearly 

communicated? To what extent is the information appropriately interpreted in light of the currently 

available information and for the purpose of assessing the adequacy of the now current standard?

Information from the last review is well-characterized and appropriately interpreted, but the clarity of 

communication should be improved. Putting the conclusion in the first paragraph of the section was very 

helpful. The CASAC concurs that a new risk and exposure assessment (REA) is not warranted at this 

time.

Are the limitations and uncertainties in the exposure/risk information appropriately characterized and 

considered in our interpretation of the information in the context of this current review?

The limitations and uncertainties in the exposure/risk information are well characterized.

Epidemiological data are inherently limited; there is a lack of data on the effects of Pb exposure at the 

levels that are common today and thus concentration-response (C-R) estimates require extrapolation.

Parameter choices for biokinetic models typically require restrictive assumptions. No single air quality 

scenario is adequate.

There are specific areas of the chapter that should be revised for clarity:

• Page 3-2, Line 15, referring to distribution of Pb from bone to blood, includes the sentence: 

“Changes in Pb exposure circumstances also can influence these exchanges, e.g., substantial 

reductions in exposure levels contribute to increased release of Pb from the bone into the blood 

(ISA, section 4.3.5).” This sentence should be revised, as it appears to incorrectly characterize 

the information in section 4.3.5 of the ISA. A reduction in external Pb exposure does not, from a 

pharmacodynamic standpoint, induce an increase in the release of Pb from bone. In the context 

of the paragraph, the intended point could be expressed as follows: “When there are substantial 

reductions in external Pb exposure, the relative contribution of Pb from bone to the concentration 

of Pb in blood increases.”

• Page 3-5, line 29 to Page 3-6, line 9: The italicized sentence in this paragraph, reproduced 

below, should be revised to improve clarity:

“The response of adult blood Pb levels to appreciable changes in exposure circumstances is 

generally slower than that of blood Pb levels in young children. For example, simulations using 

biokinetic models indicate that blood Pb levels in adults achieve a new quasi-steady state within 

75-100 days (approximately 3-4 times the blood elimination half-life) subsequent to abrupt 

increases in Pb intake (ISA, section 4.3.5.2); similar models indicate a much quicker response of 

blood Pb levels in children both with regard to abrupt increases and reductions in Pb exposure 

(ISA, section 4.3.5.1). The response in young children may reflect their much more labile bone 

pool associated with the rapid turnover of bone mineral in response to their rapid growth rates 

(ISA, section 4.3.5). As a result of these physiological processes in young children, their blood 

Pb levels tend to more quickly reflect changes in their total body burden (associated with their 

shorter exposure history), and also can reflect changes in recent exposures (ISA, section 4.3.5).”
6

Instead of the italicized sentence above, substitution of a sentence such as the following might 

enhance clarity: “Because the skeletal compartment of Pb is relatively smaller and subject to 

more rapid turnover in children compared to adults, the blood Pb concentration of children is 

more reflective of their recent external exposure.” 

• Page 3-19 lines 23-24: It might be clearer to use the phrase “qualitatively change” rather than 

“appreciably change” to allow for appreciable strengthening of the previous conclusion but no 

change of consequence.

• Page 3-22 lines 17-23: This is a helpful discussion of the problem with unknown earlier 

exposures in adults and older children. The topic comes up multiple times throughout this 

document and becomes redundant. Maybe this should be covered fully (including this as a 

general critique of cross-sectional studies), early in the chapter and then simply referred back to 

when the context warrants.

Chapter 4 – Review of the Primary Standard for Lead

This chapter describes the basis for the current primary standard and consideration of the current 

evidence and exposure/risk-based information with regard to reaching preliminary staff conclusions 

about the adequacy of the current standard.

In this chapter, staff applies the same evidence-based air-related IQ loss framework as developed and 

used in the last review, which has fundamentally two key inputs: an air-to-blood ratio and the slope of a 

concentration-response (C-R) function for IQ decrements in young children.

This draft PA is constrained by the absence of new observational and experimental data that address, at 

least in part, limitations and uncertainties in the evidence that was present at the time of the last update 

of the Pb NAAQS. Until evidence is available to assess Pb exposure and health risks related to air Pb 

levels reflecting the current standard, a substantive refinement and update of the PA will not be possible. 

The obvious uncertainty underlying evaluation of this PA is whether lowering the standard would (or 

would not) impact exposure and thus risk. The CASAC agrees with the EPA conclusion that “there is 

appreciable uncertainty associated with drawing conclusions regarding whether there would be 

reductions in blood Pb levels from alternative lower levels as compared to the level of the current 

standard.” If lowering the primary standard would lower blood Pb levels amongst the U.S. population, 

then there would be potential public health benefits from a lower standard. Research priorities discussed 

below are designed to help inform these uncertainties.

To what extent does the Panel agree with application of the evidence-based framework from the last 

review, particularly with regard to consideration of the currently available information, and related 

limitations and uncertainties, for air-to-blood ratios and C-R functions for IQ decrements in young 

children?

The application of the evidence-based framework from the previous Pb NAAQS review seems 

appropriate. The new literature published since the previous review provides further support for the 

health effect conclusions presented in that review. Additionally, the new studies do not fundamentally 

alter the uncertainties for air-to-blood ratios or C-R functions for IQ decrements in young children.
7

As previously discussed with CASAC, staff concluded that the current information does not warrant 

development of a new REA in this review. Thus, exposure/risk information was drawn from the REA 

conducted in the last review.

What are the Panel’s views on staff’s interpretation of the exposure/risk information, and on staff’s 

conclusions that the information is generally supportive of conclusions drawn from the evidence-based 

framework as to the adequacy of the current standard?

The use of exposure/risk information from the previous Pb NAAQS review appears appropriate given 

the absence of significant new information that could fundamentally change the interpretation of the 

exposure/risk information. This interpretation is reasonable given that information supporting the current 

standard is largely unchanged since the current standard was issued.

The CASAC agrees that the adverse impact of low levels of Pb exposure on neurocognitive function and 

development in children remains the most sensitive health endpoint, and that a primary Pb NAAQS 

designed to protect against that effect will offer satisfactory protection against the many other health 

impacts associated with Pb exposure.

The CASAC concurs with the draft PA that the scientific findings pertaining to air-to-blood Pb ratios 

and the C-R relationships between blood Pb and childhood IQ decrements that formed the basis of the 

current Pb NAAQS remain valid and are consistent with current data.

In reaching preliminary staff conclusions, staff notes that, like any NAAQS review, this Pb NAAQS 

review requires public health policy judgments. The public health policy judgments for this review 

include the public health significance of a given magnitude of IQ loss in a small subset of highly exposed 

children (i.e., those likely to experience air-related Pb exposures at the level of the standard), as well as 

how to consider the nature and magnitude of the array of uncertainties that are inherent in the evidence 

and in the application of this specific framework.

What are the Panel’s views on public health policy judgments that inform staff’s preliminary

conclusions with regard to the adequacy of current standard and a lack of support for consideration of 

potential alternative standards?

The PA states repeatedly that no threshold for Pb effects on IQ can be identified. In some respects, the 

ability to define a threshold may already be a moot issue. Reductions in IQ in children are being 

reported at blood Pb values as low as 2 μg/dL. In essence, these effects are being reported at the lowest 

levels of Pb in blood that can be reliably measured by most laboratories doing such analyses. 

Child IQ is the Pb-sensitive health endpoint on which this PA (and the previous one) is based. Thus, the 

discussion of health policy judgment needs to be carefully considered in light of the far-reaching public 

health value of childhood cognitive and neurobehavioral health. For example, the 2012 Centers for 

Disease Control and Prevention (CDC) update of recommendations regarding childhood Pb poisoning 

acknowledges that there is no blood Pb level in childhood that has been shown to be without deleterious 

effects. In this context, defining the threshold for "unacceptable risks to public health" or "sufficient 

public health protection" is difficult. Indeed, such language - with its implicit use of a threshold 

approach to a process that presumably has no threshold - may no longer be appropriate. Although there 

is evidence that even very low Pb levels are related to measurable reductions in IQ in children, the 

extent to which the blood Pb levels observed in children are linked to ambient air Pb levels below the 
8

current standard (as opposed to other sources of Pb in the environment) has not been established. 

Therefore there is not justification for modifying the current standard based on these data at this point in 

time. However additional research on air to blood Pb at low levels may require reconsideration of this 

decision in the future.

In the Panel’s view, does the discussion in section 4.3 provide an appropriate and sufficient rationale to 

support staff’s preliminary conclusion that it is appropriate to consider retaining the current standard 

(including the indicator, level, averaging time, and form) without revision?

Given the evidence-based framework, the discussion in section 4.3 provides an appropriate and 

sufficient rationale to support retaining the current standard without revision. For example, there is 

discussion in the PA regarding the choice of indicator level. However, there should be more description 

of supporting data and rationale behind the recommendation for the averaging time and form of the 

current standard.

The CASAC concurs that the new science does not support lowering the Pb NAAQS from its current 

level (0.15 μg/m3

). Additionally, the CASAC concurs with the caveats provided about the uncertainty in 

the science behind the NAAQS for Pb. In particular it appreciates and affirms a key point on page 4-28, 

lines 2-3: “We also recognize increased uncertainty in projecting the magnitude of blood Pb response to 

ambient air Pb concentrations at and below the level of the current standard.” Likewise, the key idea on 

page 4-32, lines 32-35 is important, but a clarifying revision is recommended as follows:

Page 4-32, lines 32-35, current text: “In staff’s view, based on current evidence there is 

appreciable uncertainty associated with drawing conclusions regarding whether there would be 

reductions in risk to public health from alternative lower levels as compared to the level of the 

current standard.” This should be re-written to read “In staff’s view, based on current evidence 

there is appreciable uncertainty associated with drawing conclusions regarding whether there 

would be reductions in blood lead levels from alternative lower levels as compared to the level of 

the current standard.”

Does the Panel have any recommendations regarding additional interpretations and conclusions based 

on the available information that would be appropriate for consideration beyond those discussed in this 

chapter?

As noted above, repeated statements about a threshold do not seem warranted given that IQ reductions 

now occur at the lowest blood Pb levels that can be reliably measured in most laboratories. It is for this 

reason that the Advisory Committee on Childhood Lead Poisoning Prevention recommended to CDC a 

complete elimination of the phrase ‘level of concern’ and stated that no blood Pb level in children has 

been shown to be without deleterious effects.

The EPA should encourage development of research programs to address those limitations and 

uncertainties in currently available evidence (and exposure/risk information) that are critical to the 

identification of "sufficiently health protective" air Pb standards in the future.
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There are some areas that need revision for clarity:

• Page 4-34, line 13: The statement should be edited to: “Factors affecting relationships between 

Pb in ambient air and Pb in blood at low exposures experienced in the general population 

today”

• Page 4-34, lines 19-21: This research need is profound, but as written is too vague to be 

appreciated by the average reader. This research need should be revised to: “Apportionment of 

blood Pb levels with regard to exposure pathways, with particular focus on understanding 

exposure pathways and sources that cause the more elevated blood Pb levels among children 

today.”

Research Needs

Several areas of research that could assist in further refinement of the Pb NAAQS include:

1. For the purposes of policy and decision making, key research priorities should be studies that

elucidate: (1) the air-blood Pb relationship at low levels; (2) sources (exposure pathways) 

contributing to current population blood Pb levels, especially in children; (3) the relationship 

between Pb and childhood neurocognitive function at current population exposure levels; and (4) 

the relationship between ambient air Pb and outdoor dust and surface soil Pb concentrations, 

including the temporal dynamics of that relationship. These research priorities are of particular 

interest because of the prominent contribution of past (as opposed to recent) Pb emissions to Pb

in soil and dust, and the significant contribution of dust and soil matrices to the Pb exposure of 

children. 

2. For the typical American adult not subject to current or past point sources or occupational Pb

exposure, Pb in the diet is likely to constitute the largest fraction of daily Pb exposure. Therefore, 

another research need of considerable interest is to determine the source of contemporary dietary 

Pb, including the indirect contribution of historical air Pb emissions (i.e. “legacy Pb”). Further, 

there remains a need to determine how much of dietary Pb is from legacy and how much can be 

amenable to interventions. 

3. The shape of the C-R curve for IQ reductions at extremely low levels requires further 

clarification. In addition, studies on more sensitive endpoints in the domain of emotion and 

behavior regulation are warranted, given that they may yield specific and sensitive measures and 

thereby assist in defining appropriate intervention strategies for children. 

4. There has been a long-term reliance on the Integrated Exposure Uptake Biokinetic (IEUBK)

model. However, greater understanding of inter-individual variability, as quantified in the 

Geometric Standard Deviation (GSD) input parameter, is needed. Information about 

toxicokinetics during adolescence remains limited. The All Ages Lead Model could be utilized to 

improve this understanding. There is also the need to know more about gene-environment 

interactions, particularly in driving inter-individual susceptibility and vulnerability.

5. Characterization and better understanding of Pb exposure hotspots/sources will give better 

representation of significant exposure risks.
10

6. Understanding of the impacts of Pb exposures during critical developmental windows and their 

contribution to adverse outcomes; e.g., little is known about the specific effects of prenatal 

exposure.

7. The effect of contemporary Pb exposure (i.e., that resulting in blood Pb concentrations on the 

order of 5 μg/dL or lower) on the future risk of hypertension and cardiovascular morbidity and 

mortality, and on age-related neurodegeneration, as these could lead to additional information 

related to most sensitive health outcomes.

8. A further understanding of the role of “reverse causation” in the inverse association observed in 

some studies between low blood Pb concentration and renal function (e.g., glomerular filtration 

rate).

9. The extent to which product substitution, i.e., replacement of Pb with less hazardous alternative 

substances in contemporary commerce, may result in reduction of human Pb exposure. The EPA 

might consider supporting studies on Pb potentially undertaken by programs such as the Toxic 

Use Reduction Program in Massachusetts, and the Green Chemistry Initiative in California.

10. As yet, the extent to which global warming will influence exposure to Pb (e.g., through soil 

erosion, resuspension) has not been evaluated.

Chapter 5 – Welfare Effects and Exposure/Risk Information

This chapter discusses key policy relevant aspects of the environmental evidence and exposure/risk 

information.

Chapter 5 of the PA is a well-written synthesis of the findings related to ecological effects in the ISA. 

The ISA supports the conclusion that recent research has not changed our fundamental understanding of 

Pb fate, transport and toxicity in the environment.

To what extent does the information in section 5.1 (Welfare Effects Information) capture and 

appropriately characterize the key aspects of the evidence assessed and integrated in the ISA?

Section 5.1 does a good job of summarizing the evidence for ecological effects from the ISA. The 

general conclusion is that recent research has added depth and nuance to the understanding of the fate 

and transport of Pb in ecological systems, and to the understanding of effects on organisms in terrestrial 

and aquatic ecosystems, but has not changed the understanding in a way that merits reconsideration of 

the relationships used to assess risk. 

A persistent theme in the ecological effects sections of the ISA and this PA document is that it is 

difficult to isolate the effects of air Pb on ecosystems from other Pb sources, including “legacy” Pb 

accumulated in soils and sediments. The threat of release of legacy Pb in soils and sediments, whatever 

the original source, may necessitate a lower secondary air quality standard than would be warranted in 

the absence of the legacy Pb. With respect to critical loads, it is recommended that Chapter 5 

acknowledge the impact on raptors and water fowl of Pb in spent ammunition; these are the ecological 
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receptors most heavily exposed to Pb, and thus potentially the most susceptible to the incremental 

contribution of Pb in air.

With regard to the exposure and risk information in section 5.2 (Exposure and Risk Information), to 

what extent is the information drawn from the screening-level risk assessment in the last review 

sufficiently characterized and clearly communicated? To what extent is the information appropriately 

interpreted in light of the currently available information and for the purpose of assessing the adequacy 

of the current standard?

The results of the 2006 REA are summarized in section 5.2. The summary is concise and clear, both in 

the explanation of the model employed and in the descriptions of the case studies used in the assessment.

The interpretation of the results from the 2006 REA is appropriate insofar as it re-states the conclusions 

from that document, and there have been no fundamental changes to our understanding of key thresholds 

or ecological receptors in the intervening years. Of four terrestrial case studies employed, the results 

from two (the primary and secondary smelter cases) are judged to be “not informative.” The relevance 

of a third case study (non-urban near-roadway conditions) is deemed “highly uncertain” due to the 

presence of legacy Pb in roadside soils. The only terrestrial case study that is deemed relevant is the 

Hubbard Brook case, where ambient Pb concentrations are far below the current (and proposed) 

standard. Results from analysis of surface water and sediment data are judged to be inconclusive 

because of possible non-air sources to waters and legacy Pb in sediments. Therefore, overall, four of the 

five major efforts in the 2006 REA are judged to be of limited or no value for the purposes of this PA. 

Given that there is little field research underway on Pb in U.S. ecosystems that are not impacted by point 

sources, it would appear to be unlikely that data for new REA case studies is forthcoming. A robust 

critical loads approach, which is a research priority to support a future review, is needed to fill this gap.

Are the limitations and uncertainties in the exposure/risk information appropriately characterized and 

considered in our interpretation of the information in the context of this current review?

The discussion of limitations and uncertainties is generally good. Issues such as legacy Pb, multistressor effects, and lab-to-field applicability create considerable uncertainty. The use of conservative 

screening levels in the calculation of hazard quotients is particularly useful because the calculated risks 

are overstated.

Chapter 6 – Review of the Secondary Standard for Lead

This chapter describes the basis for the current secondary standard and consideration of the current 

evidence and exposure/risk-based information with regard to reaching preliminary staff conclusions 

about the adequacy of the current standard.

Does the Panel agree with preliminary staff conclusions about the evidence and previous risk

assessment in light of current standards as presented in section 6.2 (Adequacy of the Current 

Standard)?
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The preliminary staff conclusions provide a good assessment of the available evidence and the previous 

risk assessment in light of the current secondary standard. The CASAC notes, however, the concerns 

raised in the response to the chapter 5 charge questions regarding the previous risk assessment.

In the Panel’s view, does the discussion in this chapter provide an appropriate and sufficient rationale 

to support preliminary staff conclusions that it is appropriate to consider retaining the current standard 

(including the indicator, level, averaging time, and form) without revision?

The discussion provides appropriate and sufficient rationale to support retaining the current secondary 

standard without revision. A general lack of new data that would indicate the appropriate level of Pb in 

environmental media that may be associated with adverse effects suggests that the secondary standard 

should be retained. Questions remain regarding the relevance of the indicator, level, averaging time and 

form to the secondary standard (ecological context). A multi-media approach may be necessary to 

account for legacy Pb and contributions from different sources for a secondary standard. 

Does the Panel have any recommendations regarding additional interpretations and conclusions based 

on the available information that would be appropriate for consideration beyond those discussed in this

chapter?

The CASAC does not have any recommendations regarding additional interpretations and conclusions 

beyond what is contained in the chapter. Developing a critical loads approach for U.S. conditions would 

be an important area for additional research. The discussion of uncertainties at the end of the chapter is 

excellent. It should include mention of the use and/or relevance of toxicity data that are generated in test 

systems that deploy exposures to media other than soil or water for appropriate organisms (e.g., plants in 

hydroponic systems, soil nematodes in agar or culture medium).

Research Needs

Application of a critical loads approach with sensitivity analysis will help to determine which processes 

are most important in determining Pb exposure to ecological receptors. This would be an integrated, 

holistic, multi-media approach that could be used to examine the contributions of current aerial Pb 

deposition to historical aerial deposition as well as Pb from other sources. Current critical loads models 

are largely qualitative and empirical. Mechanistic sub-models need to be incorporated into the critical 

loads model to provide an adequate means to predict Pb bioavailability, exposure, and toxicity. This 

critical loads approach could be integrated to include other aerial pollutants such as oxides of nitrogen 

and oxides of sulfur.
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Reference

Secretariat of the Commission for Environmental Cooperation (CEC), (2013), Hazardous Trade? An 

Examination of US-generated Spent Lead-acid Battery Exports and Secondary Lead Recycling in 

Mexico, the United States and Canada, Final Report, 15 April.
Agency 

Environmental Protection United States 

Health and Environmental Impacts Division 

Office of Air Quality Planning and Standards 

Research Triangle Park, NC 

Publication No. EPA-452/R-14-001

May 2014