UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

WASHINGTON D.C. 20460

OFFICE OF THE ADMINISTRATOR
SCIENCE ADVISORY BOARD

March 27, 2007

EPA-CASAC-07-003

Honorable Stephen L. Johnson

Administrator U.S. Environmental Protection Agency 1200 Pennsylvania Avenue, NW Washington, DC 20460

Subject: Clean Air Scientific Advisory Committee’s (CASAC) Review of the 1 st Draft Lead Staff Paper and Draft Lead Exposure and Risk Assessments

Dear Administrator Johnson:

The Clean Air Scientific Advisory Comm ittee (CASAC or Committee), augmented by subject-matter-expert Panelists — collectively referred to as the CASAC Lead Review Panel (Lead Panel) — completed its review of the Agency’s 1 st Draft Lead Air Quality Criteria Document (AQCD) in September 2006 (EPA -CASAC-06-010). On December 7, 2006, Mr. Marcus Peacock, the EPA Deputy Administrato r, issued a memorandum providing his final decisions on revisions to the process by whic h the National Ambient Air Quality Standards (NAAQS) are reviewed. In this memo, Deputy Admi nistrator Peacock directed that this revised NAAQS review process should begin with the cu rrent, ongoing review of the NAAQS for lead. (See URLs: http://www.epa.gov/ttnnaaqs/memo_process_for_reviewing_naaqs.pdf and http://www.epa.gov/ttnnaaqs/naaqs_pr ocess_report_march2006_attachments.pdf ).

On February 6–7, 2007, the CASAC’s Lead Pa nel conducted a peer review of EPA’s Draft Review of the National Ambient Air Quality Standards for Lead: Policy Assessment of Scientific and Tec hnical Information (1 st Draft Lead Staff Paper, December 2006) and a related draft technical support document, Lead Human Exposure and Health Risk Assessments and Ecological Risk Assessment fo r Selected Areas: Pilot P hase, Draft Technical Report (Draft Lead Exposure and Risk Assessments, December 2006). In addition, on March 9, 2007, the Lead Panel held a public teleconferen ce to review the CASAC’s draft letter to the Administrator resulting from its February meeting. The CASAC roster is found in Appendix A of this report, and the Lead Panel roster is attached as Appendi x B. The charge questions provided to the Lead Panel by EPA staff are contained in Appendix C to this report, and examples of population-based approaches to lead risk assessments for the primary Lead NAAQS are found in Appendix D. A discussion of issues related to setting of the secondary Lead NAAQS is attached as Appendix E,

and Panelists’ individual review co mments are provided in Appendix F.2 At the February 6–7 public meeting, the Lead Panel expressed serious concerns both about the EPA documents to be reviewed and the Agency’s proposed rulemaking schedule for the Lead NAAQS, as follows:

• 1 st Draft Lead Staff Paper had no staff-derived options for keeping or altering the current Lead NAAQS.

• The Draft Lead Exposure and Risk Assessmen ts document did not have a full discussion of the risk associated with different opti ons for keeping or alte ring the Lead NAAQS. The Lead Panel judges that, while the latter document represented a good first effort, it was nowhere near completion.

• Under the Agency’s new NAAQS review pro cess, EPA’s Staff Paper for lead will no longer be prepared but will be replaced by a Policy Assessment (PA) for lead, to be

issued in the form of an Advance Notice of Proposed rulemaking (ANPR). However, the Agency’s proposed schedule for the Lead NAA QS review calls for completion of the Lead Exposure and Risk Assessments document after the PA for lead is issued via the ANPR. Thus, it was not planned for the CASA C to be given an opportunity to review a more fully-developed, second-draft version of the Risk/Exposure Assessment (RA) prior to the ANPR, so that the PA would not be informed by the science assessments of the

Lead Panel.

Subsequent to the February 6–7 meeting of the CASAC Lead Review Panel, Agency officials, managers and staff held administrativ e discussions with the chartered members of the CASAC to learn directly from these seven member s their specific concerns with the schedule for review of the lead standards and the revised NAAQS review process in general. The Lead Panel is pleased to have been briefed by Agency sta ff during the Panel’s Marc h 9 teleconference that EPA has modified its timeline both for the gene ric NAAQS review process and the current Lead NAAQS review in particular, such that the Lead Panel will now review the 2 nd draft of the Agency’s Lead Risk/Exposure Assessment this summer, prior to the issuance of the associated

PA document in the ANPR.

The CASAC Lead Review Panel used the sc ientific information found in the Agency’s Final Lead AQCD, which was also reviewed by the Lead Panel, in its review of EPA’s 1 st Draft Lead Staff Paper and the Draft Lead Exposure and Risk Assessments document. The Lead

Panel’s recommendations and the associated sc ientific basis for these recommendations are presented below. The unanimous judgment of the Lead Panel is that lead should not be de-listed as a criteria air pollutant, as defined by the Clean Air Act, for which primary (public-health based) and secondary (public-welfare based) NAAQS are established, and that both the primary and secondary NAAQS should be substantially lowered. It is also recommended that future monitoring of lead exposure be conducted with low-volume PM 10 samplers rather than with total suspended particulate (TSP) samplers, and that th e averaging time be decreased from quarterly to monthly.

The reasons for these recomme ndations are given below.3 Introduction

Over the past three decades, blood lead (PbB) concentrations in the U.S. population have plummeted (1). This decline was largely due to the elimination of leaded gasoline (2). In 1976, the Consumer Products Safety Comm ission restricted the allowable am ount of lead in residential paints to 0.06 percent (600 ppm) (3). Lead solder used in canned foods was also decreased — from over 90% in 1978 to less than 5% in 1988 (4 ). Finally, there was a decrease in the abundance of residential housing in which lead-bas ed paints had been us ed (5). Although it is difficult to quantify the extent of decrease in bloo d lead concentrations attributable to specific sources, the 1978 NAAQS for lead were undoubtedly among the major reasons for the rapid and widespread decrease in PbB leve ls in the U.S. population (6).

Despite the dramatic decrease in environmental lead exposur e, lead toxicity remains a major public health problem. Environmental lead exposure in children has been associated with increased risks for reading problems, school failu re, Attention Deficit Hyperactivity Disorder (ADHD), delinquency, and criminal behavior (6–10). Among U.S. children, eight to fifteen years old, those in the highest quint ile (> 2 μg/dl) of lead exposure were four times more likely to have doctor-diagnosed ADHD (11). Moreover, there is no evidence of a threshold for the adverse consequences of lead exposure; studies show that th e decrements in intellectual (cognitive) functions in children are proportionately greater at Pb B concentrations < 10 μg/dl,

the concentration considered acceptable by the Centers for Disease Control (11–14).

Lead’s effects extend beyond childhood. In adults, lead exposure is a ri sk factor for some of the most prevalent diseases or conditions of industrialized society, including cardiovascular disease and renal disease (16–20). There is also compelling evidence that the risks for mortality from stroke and myocardial infarction are incr eased at PbB concentrations below 10 μg/dl, which is considerably lower than those considered acceptable for adults (19). Finally, although less definitive, there is also evidence that lead exposure during pregnancy is a risk factor for spontaneous abortion or miscarriag e at PbB concentrations < 10 μg /dl (21). (It should be noted

that references 11 and 19 above were not cited in EPA’s Final Ozone AQCD.)

Scientific Basis for Continuing or De-listing the Lead NAAQS

The CASAC Lead Review Panel considered the implications of present scientific understanding regarding the need for protecti on of public health and public welfare from exposure to lead in the environment. One of thes e implications relates to the question of whether the current science continues to support the need for lead to be listed as a criteria air pollutant for which a NAAQS is established, or might warrant th e de-listing of lead, as presented as a policy option in the 1 st Draft Lead Staff Paper. In addressi ng this question, the L ead Panel examined

several scientific issues and rela ted public health and public welfar e issues that are essential in determining whether or not a pollutant such as lead should be de-listed or maintained as a criteria air pollutant.

1. Does new scientific information accumulate d since EPA’s promulgation of the current primary Lead NAAQS of 1.5 μg/m 3 in 1978 suggest that science previously overstated the toxicity of lead ? Here, the Lead Panel’s answer clea rly is No. The data accumulated over the past three decades make it apparent that adverse health effects on both humans and4 other species appear at blood lead concentr ations and environmental exposures well below those previously thought to pose impor tant risks. Indee d, if anything, this improved scientific understand ing indicates that scien tific studies previously underestimated the toxicity of lead.

2. Have past regulatory and other controls on le ad decreased PbB concentrations in human populations so far below levels of concern as to suggest there is now an adequate margin of safety inherent in those PbB levels ? Again, the Panel’s answer here is No. The Nation can take great pride in the extent to which e xposures to lead have been decreased, leading

to laudable decreases in PbB concentrations to an average approaching 2 μg/dl. However, there remains a significant se gment of the populati on with blood-lead concentrations above 5 μg/dl — and some ev en above 10 μg/dl — and scientific evidence supports the contention that these PbB concentr ations do not provide an adequate margin of safety. In fact, this ev idence suggests these blood lead concentrations below 5 μg/dl are associated with unacceptable adverse effects.

3. Have the activities that produced emissions and atmospheric redistribut ion of lead in the past changed to such an extent that society can have confid ence that emissions will remain low even in the absence of NAAQS controls ? Here, the Lead Panel concludes that the answer, once again, is No. While there ha ve been major decreases in emissions of lead from use of leaded gasoline, industrial and other activities, even the current air emissions from some lead mining and re processing facilities produce considerable environmental exposures once the concentra tions of lead in environmental media equilibrate. The Lead Panel conclude s that past success in decreasing PbB concentrations in human populati ons are due in part to NAAQS controls, and that in the absence of such controls, there will be a significant possibility that blood-lead concentrations would begin to rise again.

4. Are airborne concentrations and amounts of le ad sufficiently low throughout the United States that future regulati on of lead exposures can be effectively accomplished by regulation of lead-based products and allow able amounts of lead in soil and/or water?

Lead Panel concludes that th e answer to this question is No. While airborne lead concentrations have been decreased throughout much of the United States, airborne lead remains a primary vehicle for movement of lead between different environmental compartments. While control of airborne lead is not sufficient by itself to control exposure to lead, it is an essential co mponent of a successful control strategy. Maintaining appropriate Lead NAAQS is consid ered by the Lead Panel to be an essential component of a national program to decrea se the ongoing adverse effects of lead in children, adults, and in both terrestrial and aquatic ecosystems.

5. If lead were de-listed as a criteria air pollutant, would it be appropriately regulated under the Agency’s Hazardous Air Pollutants (HAP) program? The Panel’s answer is again No. The HAP program, which regulates according to use of maximum achievable control technology (MACT), followed by an analys is of residual risk, is appropriate for point sources. However, the most widesp read source of airborne lead throughout the5 nation is the historically-depos ited lead along roadways. Thus, this source of airborne lead could not be regulated under the HAP program.

As a result of the CASAC Lead Review Panel’ s own answers to these scientific and public
health issues, the Panel concludes that the existin g state of science is c onsistent with continuing to list ambient lead as a criteria air pollutant for which fully-protective NAAQS are required.

Additional Analyses to In form Decisions About a Prim ary (Health-Based) NAAQS for

Lead

Despite the dramatic decreases in amounts of airborne lead exposures and humanpopulation blood-lead concentrations following the pha se-out of leaded gasoline, lead toxicity remains a major public health problem. As discu ssed above, there is incr easing evidence of leadinduced toxicity at the lowest contemporary expo sures to lead — resul ting in significant IQ deficits in children (11–14), and increased freque ncy of ADHD (11) and cardiovascular disease (16–19). Although less definitive, there is eviden ce that lead exposure is a risk factor for spontaneous abortion and renal disease (20–21).

Although relatively few counties in the United St ates are out of compliance, the greatest benefit to public health will be realized by broad decreases in airborne lead concentrations across the U.S. population because:

1. The adverse consequences are proportionately greater at the lowest increments of lead

exposure;

2. Lead exposure is cumulative; and

3. Airborne lead exposure, in c ontrast with exposure to lead-b ased paint, is more widely dispersed. Thus, reducing exposure from ai r lead will broadly reduce population blood

lead levels.

In 1978, EPA established a primary Lead NAAQS of 1.5 μg/m 3 to ensure that 99.5% of the public did not exceed a blood-lead concentrati on of 30 μg/dl, with the 99.5% figure being the Agency’s risk management ( i.e. , policy) choice at that time. In addition to the separate Federal regulations that had been adopt ed in 1973 that requiring the phas e-out of leaded gasoline, the 1978 Lead NAAQS was instrumental in helping to produce the dramatic decreases in air lead

and blood-lead concentrations ove r the last 30 years. However, these primary and secondary Lead NAAQS are totally inadequate for assuring the necessary decreases of lead exposures in sensitive U.S. populations below those current he alth hazard markers iden tified by a wealth of new epidemiological, experiment al and mechanistic studies.

Consequently, it is the CASAC Lead Review Panel’ s considered judgment that the NAAQS for Lead must be decreased to fully-pr otect both the health of children and adult populations.

The EPA pilot-phase human health risk a ssessment focused on three case study locations ( i.e. , primary lead smelter, secondary lead smelte r, and near-roadway urban). While the case study approach undertaken in the risk assessmen t is enlightening and provides a potentially6 useful framework for understanding lead exposure for some discrete populations within the U.S.,

there are some additional considerations and anal yses that the Lead Panel strongly feels could help inform a scientific ally-defensible NAAQS for lead. In part icular, the Panel believes that the

risk assessment would be better informed with a “population-based“ risk assessment to supplement the current case study approach. A population-based risk assessment would typically include two key components:

1. A quantitative description of the relationship between concentrations of lead in national

ambient air and distributions of resu lting blood lead concentrations; and

2. A quantitative description of the relationship between blood lead concentrations and impacts on IQ.

There are multiple ways in which EPA could conduct a population-based analysis, and the Panel illustrates some possibili ties in Appendix D attached to th is letter. Please note that this work does not represent a complete analysis on the part of the Lead Panel; rather, it is meant to illustrate the Panel’s thinking in this area. It will be important for EPA to consider these approaches and to fully evaluate their pros, cons , and associated uncertainties. An adequately comprehensive analysis should characterize the un certainty, preferably in a quantitative manner, in two key areas: (1) the rela tionship between a change in the NAAQS for lead and the distribution of population blood lead concentrations; and (2) the relationship between blood lead

concentrations and the risk of adverse health eff ects. This type of review by the Agency will be necessary to highlight the streng ths and weaknesses of the ava ilable approaches and help to elucidate a primary Lead NAAQS that is scientif ically-defensible and ad equately-protective of public health.

As described in Appendix D, the Lead Pane l considered three separate, but related, population-based analytical approaches as examples to be considered in deriving an acceptable range of alternative levels, on the basis of the sc ientific evidence, for setting a new level for the primary Lead NAAQS, as follows: Approach A relate s air lead levels to blood lead levels using the approach used in previous lead NAAQS cal culations; Approach B uses an epidemiologic approach to derive an adjusted slope factor relating air lead leve ls to blood levels taking into account all exposure pathways between air lead a nd blood lead; and Approach C relates air lead

levels to blood lead levels and then to IQ loss in children. In addition, the CASAC Lead Review Panel considers that a population lo ss of 1-2 IQ points is highly si gnificant from a public health perspective (22). Therefore, the primary lead st andard should be set so as to protect 99.5% of the population from exceeding that IQ loss.

The three approaches provide comparable results. Given the Panel’s assumptions and preliminary analysis conducted for the three approaches, the resulting analyses indicate to the CASAC that there is a need for a substan tial reduction in the primary Lead NAAQS

, to a level of about 0.2 μg/m 3 or less . CASAC recognizes that these prel iminary calculations are dependent upon the results of EPA’s forthcoming uncertainty analyses and the current risk management choice for the percentage of the population left at risk, as well as acceptable blood levels, IQ loss and slope factor — the appropriate ness of which all depend on certa in scientific assumptions and the risk management criteria that are chosen. Imposing more stringent cr iteria would result in a lower (that is, more stringent) range of prim ary Lead NAAQS levels, whereas less stringent7 criteria would result in th e calculation of a higher ( i.e. , less stringent) range of primary lead

standards.

Possible Revision to Lead Indicator from TSP to Low-Volume PM 10

As revisions to the level, form, and averag ing time of the Lead NAAQS are considered,

CASAC also recommends that EP A revise the indicator. Curren tly, Lead NAAQS monitoring is predominantly based on atomic absorption analysis of fiberglass filters run on hi-volume total suspended particulate (TSP) samplers. Most other TSP sampling was discontinued after PM 10 standards were promulgated in 1987. TSP sample rs capture particles w ith an imprecise and variable upper particle cut si ze in the range of approximate ly 30 to 50 microns on fiberglass filters which are not well-suited for analysis by inexpensive, multi-elemental surface beam techniques like particle-induced X-ray emi ssion (PIXE) or X-ray fluorescence (XRF). Consequently TSP sampling by imprecise samplers is primarily conducted onl y for lead analysis and these filters are rarely analyzed for other species.

If Lead NAAQS monitoring wa s based on (low-volume) PM 10 sampling on Teflon filters, the resulting data would be correlated with TSP lead, as suggested by limited data in the 1 st Draft Lead Staff Paper, but would have substantia lly improved sampling precision. The Lead Panel recognizes that either monitoring system woul d be subject to variab ility based on location, particularly near sources. Ot her advantages of low-volume PM 10 sampling include:

1. Focus on those biologic ally-relevant particles that, when inhaled, are deposited in the thoracic region;

2. Larger spatial-scale represen tativeness for populati on exposures to m onitored particles which remain airborne longer;

3. Could utilize more widespread PM 10 and “air toxics“ metals sampling networks, leading to collection of more data at lower costs;

4. Potential for inexpensive multi-elemental anal ysis by XRF or PIXE would provide useful supplemental metals information for health effects studies and source apportionment;

5. Potential for automated sequential PM 10 samplers (not available for TSP) would be especially useful if sampling frequency is increased from once every six days; and

6. Weighing filters would provide useful information on PM 10 mass; and, if collocated with

PM 2.5 Federal Reference Methods (FRM), c ould provide needed information on PM 10–2.5 mass and speciation.

Reasons for retaining the current TSP lead in dicator include: preser vation of a long-term historical record at some sites; and inclusion of very coarse (> 10 micron particle) lead which may deposit in upper regions of the respiratory tr act and ultimately be ingested, or which may deposit on surfaces and be ingested via hand-to-m outh activity of children. Some such coarse particles might be missed by PM10 samplers. Pres umably a downward scaling of the level of the Lead NAAQS could accommodate the loss of very large coarse-mode lead particles, and some short period of concurrent PM 10 and TSP lead sampling could help develop site-specific scaling factors at sites with highest concentrations wh ere long-term historical records are important.8 Given the advantages of using PM 10 , the CASAC Lead Review Panel recommends that the Agency revise the lead indicator to utilize low-volume PM 10 sampling, and also develop equivalent analytical met hods to allow use of XRF and Inductively-Coupled Plasma Mass Spectrometry (ICP-MS) analysis

.

Possible Revision to Averaging Time Used for the Lead NAAQS

A second change that should be considered wi th a change in the Lead NAAQS is possible use of a different averaging time. Currently, qua rterly averaging is used. However, studies suggest that blood lead concentra tions respond at shorter time s cales than would be captured completely by quarterly values. Here, the L ead Panel recommends that the Agency conduct monthly averaging instead of quarterly.

One consideration involved in using a shorte r averaging period is sampling frequency. Currently, many of the samplers operate with sampling frequencies less than once per day, and as infrequently as every sixth day. In the most extreme case, as few as four samples may be involved in determining a monthly average (assumi ng no samples are considered invalid). This may make the average susceptible to anomalous ly-high events. On the other hand, this may motivate more frequent sampling in those areas whos e air concentrations are near the level of the Lead NAAQS, which would increase the protecti on of public health and significantly decrease the impact of a single high lead exposure even t. One could also c onsider having the lead standards based on the second highest monthly aver age, a form that appears to correlate well with using the maximum quarterly value.

The CASAC Lead Review Panel recommends adop ting monthly averaging as being more protective of human health in light of the res ponse of blood lead concentrations that occur at sub-quarterly time scales, and further recommends t hat the most protective form would be the highest monthly average in a year . An area could choose to in crease sampling frequency to make the monthly average less susceptible to more extreme events. Such a change is consistent with either using TSP or PM 10 sampling.

Secondary (Welfare-Based) NAAQS for Lead

An extended discussion of issues related to setting the secondary Lead NAAQS can be found in Appendix E. Chapter 6 of the 1 st Draft Lead Staff Paper a nd Chapter 7 of the “Pilot Phase“ Draft Lead Exposure and Risk Asse ssments technical support document present compelling scientific evidence that current atmo spheric lead concentrations and deposition — combined with a large reservoir of historically-deposited lead in soils, sediments and surface

waters — continue to cause a dverse environmental effects in aquatic and/or terrestrial ecosystems, especially in the vici nity of large emission sources. These effects persist in some

cases at locations where current airborne lead co ncentrations are below the levels of the current primary and secondary lead standards.

Thus, from an environmental pe rspective, there are convinci ng reasons to both retain lead as a regulated criteria air pollutant and to lower the level of the current secondary

standard.9 Since concentrations of histor ically deposited lead in soil s throughout the U.S. (averaging 0.5 to 4 g/m 2 of land area) are changing only slowly — with a half-life exceeding a century — these concentrated deposits of lead are expected to remain accessible for exchange with the atmosphere and the rest of the biosphere into the foreseeable future. Fires, changes in land use, or climatic events such as regional dust storms could mobilize significant quantities of lead that

would be harmful both to human health and ecos ystems downwind. This potential for harm is not adequately recognized in the 1 st Draft Lead Staff Paper and the Draft Lead Exposure and Risk Assessments technical suppor t document, but is a concern th at warrants careful continued monitoring in the future.

In addition, while neither the 1 st Draft Lead Staff Paper nor the Draft Lead Risk/Exposure Assessments document provide a cl ear quantitative basis for identifying a specific lower level at which a more protective secondary (welfare- or environmental-based) Lead NAAQS should be set, there are no reasons to expect that humans are uniquely sensitive to lead pollution among the millions of animal and plant species.

Therefore, at a minimum, the level of the secondary Lead NAAQS should be at least as low as the lowest-recommended primary lead st andard. The EPA is also encouraged to identify the necessary funds to support needed continuing research on the ecologica l effects of airborne lead pollution and to consider developing al ternative secondary standards such as critical loads for lead, which may be different from primary st andards in indicator, averaging time, level or form

.

The CASAC continues to be pleased to provi de advice to you concer ning the scientific basis for the setting of the primary and seconda ry Lead NAAQS. In addition, the CASAC looks forward to continued dialog with Agency offi cials and staff aimed at improving EPA’s NAAQS review process in a manner that enhances the e fficiency of the process while maintaining its integrity and adherence to the stipulations of the Clean Air Act. Finally, the Committee also looks forward to reviewing the 2 nd draft of the Agency’s Lead Risk/Exposure Assessment this summer. As always, we wish Agency staff well in this important task.

Sincerely,

Dr. Rogene Henderson, Chair Clean Air Scientific Advisory Committee

Appendix A – Roster of the Clean Air Scientific Advisory Committee

Appendix B – Roster of the CASAC Lead Review Panel

Appendix C – Agency Charge to the CASAC Lead Review Panel10 Appendix D – Population-Based Appr oaches to Risk Assessment An alyses for the Primary Lead NAAQS

Appendix E – Issues Related to the Setting of the Secondary Lead NAAQS

Appendix F – Review Comments from Indi vidual CASAC Lead Review Panel Members

References

1. Pirkle JL, Kaufmann RB, Brody DJ, Hickman T, Gunter EW, Paschal DC. Exposure of the U.S. population to lead, 1991–1994. Environ Health Perspect 1998;11:745–50.

2. Mahaffey KR, Annest JL, Roberts J, Murphy RS . National estimates of blood lead levels: United States, 1976–1980. Association with sele cted demographic and socioeconomic

factors. New Engl J Med 1982;307:573–579.

3. Committee on Toxicology, Assembly of life Sciences, National Research Council. Recommendations for the prevention of lead poisoning in children. Nutrition Rev 1976;34:321–327.

4. Bolger PM, Carrington CD, Capar SG, Adams MA . Reductions in dietary lead exposure in

the United States. Chem Spec Bioavail 1991;3:31–36.

5. Jacobs DR, Friedman W, Clickner RP, et al. Th e prevalence of lead-bas ed paint hazards in U.S. Housing. Env Health Perspect 2002;110:A599–A606.

6. Needleman HL, Gunnoe C, Leviton A, et al . Deficits in psychologic and classroom performance of children with el evated dentine lead levels. N Engl J Med 1979;300:689–95.

7. Needleman HL, Schell A, Bellinger D, Leviton A, Allred EN. The long-term effects of exposure to low doses of lead in childhood: An 11-year follow-up report. N Engl J Med 1990;322:83–88.

8. Denno D. Biology and Violence. New York: Cambridge University Press, 1990.

9. Needleman HL, Reiss JA, Tobin MJ, Biesecker GE, Greenhouse JB. Bone lead levels and delinquent behavior. JAMA . 1996;275:363–369.

10. Dietrich K, Ris M, Succop P, Berger O, Born shein R. Early exposure to lead and juvenile delinquency. Neurotox Teratol 2001;23:511–518.

11. Braun J, Kahn RS, Froehlich T, Auinger P, Lanphear BP. Exposures to environmental toxicants and attention deficit hypera ctivity disorder in U.S. children. Environ Health Perspect 2006;114:1904–1909.

12. Canfield RL, Henderson CR, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP. Intellectual impairment in children with blood lead con centrations below 10 micrograms per deciliter. N Engl J Med 2003;348:1517–1526.

13. Lanphear BP, Hornung R, Khoury J, et al. Lo w-level Environmental Lead Exposure and

Children’s Intellectual Function: An International Pooled Analysis. Environ Health Perspect 2005;113:894–899.

14. Kordas K, Canfield RL, Lopez P, et al. Defi cits in cognitive function and achievement in Mexican first-graders with lo w blood lead concentrations. Environ Res. 2006;100:371–386.11 15. Tellez-Rojo MM, Bellinger DC, Arroyo-Quiroz C, et al. Long itudinal associations between blood lead concentrations lower than 10 μg /dl and neurobehavioral development in environmentally exposed ch ildren in Mexico City. Pediatrics. 2006;118:e323–330.

16. Schwartz J. Lead, blood pressure, and cardiovascular disease in men. Arch Environ Health 1995;50:31–37.

17. Nash D, Magder L, Lustberg M, Sherwin RW, Rubin RJ, Kaufmann RB, Silbergeld EK. 2003. Blood lead, blood pressure, and hypertensi on in perimenopausal and postmenopausal

women. JAMA 289:1523–1532.

18. McDonald JA Potter NU. Lead’s legacy? Earl y and late mortality of 454 lead- poisoned

children. Arch Environ Health 1996;51:116–121.

19. Menke A, Muntner P, Batuman V, Silbergeld EK, Guallar E. Blood Lead Below 0.48

μ mol/L (10 μ g/dl) and mortality among U.S. Adults. Circulation 2006;114;1388–1394.

20. Lin JL, Lin-Tan DT, Hsu KH, Yu CC. 2003. En vironmental lead exposure and progression

of chronic renal diseases in patients without diabetes. N Engl J Med 348:277–286.

21. Borja-Aburto VH, Hertz-Picciotto I, Rojas Lopez M, Farias P, Ri os C, Blanco J. Blood lead levels measured prospectively a nd risk of spontaneous abortion. Am J Epidemiol 1999;150:590–597.

22. U.S. Centers for Disease Control. Preventing Lead Poisoning in Young Children. A Statement by the Centers for Disease Control (Ch. 1, Introduction), October 1991. Atlanta, GA: Department of Health and Human Services.A-1 

### Appendix A – Roster of the Clean Air Scientific Advisory Committee

U.S. Environmental Protection Agency Science Advisory Board (SAB) Staff Office

Clean Air Scientific Advi sory Committee (CASAC)

CHAIR

Dr. Rogene Henderson , Scientist Emeritus, Lovelace Re spiratory Research Institute, Albuquerque, NM

MEMBERS

Dr. Ellis Cowling , University Distinguished Professo r At-Large, North Carolina State University, Colleges of Natural Resources and Agriculture and Life Sciences, North Carolina State University, Raleigh, NC

Dr. James D. Crapo , Professor, Department of Medi cine, National Jewish Medical and Research Center, Denver, CO

Dr. Douglas Crawford-Brown , Director, Carolina Environmental Program; Professor,

Environmental Sciences and E ngineering; and Professor, P ublic Policy, Department of Environmental Sciences and Engineering, Univers ity of North Carolina at Chapel Hill, Chapel Hill, NC

Mr. Richard L. Poirot , Environmental Analyst, Air Pollutio n Control Division, Department of Environmental Conservation, Vermont Agency of Natural Resources, Waterbury, VT

Dr. Armistead (Ted) Russell , Georgia Power Distinguished Professor of Environmental Engineering, Environmental Engineering Group, School of Civil and Environmental Engineering, Georgia Institute of Technology, Atlanta, GA

Dr. Frank Speizer , Edward Kass Professor of Medici ne, Channing Laboratory, Harvard Medical School, Boston, MA

SCIENCE ADVISORY BOARD STAFF

Mr. Fred Butterfield , CASAC Designated Federal Officer , 1200 Pennsylvania Avenue, N.W., Washington, DC, 20460, Phone : 202-343-9994, Fax: 202-233-0643 ( butterfield.fred@epa.gov ) (Physical/Courier/FedEx Address: Fred A. Butterf ield, III, EPA Science Advisory Board Staff Office (Mail Code 1400F), Woodies Building, 1025 F Street, N.W., Room 3604, Washington, DC 20004, Telephone: 202-343-9994)B-1 

### Appendix B – Roster of the CASAC Lead Review Panel

U.S. Environmental Protection Agency Science Advisory Board (SAB) Staff Office

Clean Air Scientific Advi sory Committee (CASAC)

CASAC Lead Review Panel

CHAIR

Dr. Rogene Henderson *, Scientist Emeritus, Lovelace Respiratory Research Institute, Albuquerque, NM

MEMBERS

Dr. Joshua Cohen , Research Associate Professor of Me dicine, Tufts University School of Medicine, Institute for Clinical Research and Health Policy Studies, Center for the Evaluation of Value and Risk, Tufts New Engla nd Medical Center, Boston, MA

Dr. Deborah Cory-Slechta , Director, Environmental and Occupational Health Sciences Institute, a joint Institute of the Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, and Ru tgers University, Piscataway, NJ

Dr. Ellis Cowling *, University Distinguished Profe ssor At-Large, North Carolina State University, Colleges of Natural Resources and Agriculture and Life Sciences, North Carolina State University, Raleigh, NC

Dr. James D. Crapo [M.D.] *, Professor, Department of Medi cine, National Jewish Medical and Research Center, Denver, CO

Dr. Douglas Crawford-Brown *, Director, Carolina Environmental Program; Professor,

Environmental Sciences and E ngineering; and Professor, P ublic Policy, Department of Environmental Sciences and Engineering, Univers ity of North Carolina at Chapel Hill, Chapel Hill, NC

Dr. Bruce Fowler , Assistant Director for Science, Di vision of Toxicology and Environmental Medicine, Office of the Director, Agency for Toxic Substances and Disease Registry, U.S.

Centers for Disease Control and Pr evention (ATSDR/CDC), Chamblee, GA

Dr. Andrew Friedland , Professor and Chair, Environmen tal Studies Program, Dartmouth College, Hanover, NH

Dr. Robert Goyer [M.D.] , Emeritus Professor of Pathology, Facu lty of Medicine, University of Western Ontario (Canada), Chapel Hill, NC

Mr. Sean Hays , President, Summit Toxicology, Allenspark, COB-2 Dr. Bruce Lanphear [M.D.] , Sloan Professor of Children’s Environmental Health, and the

Director of the Cincinnati Ch ildren’s Environmental Health Ce nter at Cincinnati Children’s Hospital Medical Center and the Univer sity of Cincinnati, Cincinnati, OH

Dr. Samuel Luoma , Senior Research Hydrologist, U.S. Geological Survey (USGS), Menlo Park, CA

Dr. Frederick J. Miller , Consultant, Cary, NC

Dr. Paul Mushak , Principal, PB Associates, and Visiting Professor, Albert Einstein College of Medicine (New York, NY), Durham, NC

Dr. Michael Newman , Professor of Marine Science, Sc hool of Marine Sciences, Virginia Institute of Marine Science, College of William & Mary, Gloucester Point, VA

Mr. Richard L. Poirot *, Environmental Analyst, Air Pollut ion Control Division, Department of Environmental Conservation, Vermont Agency of Natural Resources, Waterbury, VT

Dr. Michael Rabinowitz , Geochemist, Marine Biological Laboratory, Woods Hole, MA

Dr. Armistead (Ted) Russell *, Georgia Power Distinguished Professor of Environmental Engineering, Environmental Engineering Group, School of Civil and Environmental Engineering, Georgia Institute of Technology, Atlanta, GA

Dr. Joel Schwartz , Professor, Environmental Health, Harvard University School of Public Health, Boston, MA

Dr. Frank Speizer [M.D.] *, Edward Kass Professor of Medicine, Channing Laboratory, Harvard Medical School, Boston, MA

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

Dr. Barbara Zielinska , Research Professor, Division of At mospheric Science, Desert Research Institute, Reno, NV

SCIENCE ADVISORY BOARD STAFF

Mr. Fred Butterfield , CASAC Designated Federal Officer , 1200 Pennsylvania Avenue, N.W., Washington, DC, 20460, Phone : 202-343-9994, Fax: 202-233-0643 ( butterfield.fred@epa.gov )

* Members of the statutory Clean Air Scientific Advisory Committee (CASAC) appointed by the EPA

AdministratorC-1 

### Appendix C – Agency Charge to the CASAC Lead Review Panel

Charge to the CASAC Pb Panel

Within each of the main sections of the firs t draft Staff Paper, questions that we ask the Panel to focus on in their review include the following:

Ambient Pb information and analyses (Chapter 2) :

1. To what extent are the emissions and air qua lity characterizations and analyses clearly communicated, appropriately char acterized, and relevant to the review of the primary and secondary Pb NAAQS?

2. Does the information in Chapter 2 provide a sufficient ambient Pb-related basis for the exposure, human health and environmental effects, health risk assessment, and environmental assessment presented in later chapters?

Pb-related health effects (Chapter 3):

1. To what extent is the presentation of eviden ce from the health studies assessed in the Pb AQCD and the integration of information from across the various health-related research areas drawn from the Pb AQCD technically sound, appropriately balanced, and clearly

communicated?

2. What are the views of the Panel on the appropr iateness of staff’s discussion and conclusions in Chapter 3 on key issues related to quantit ative interpretation of epidemiologic study results, including, particularly, the form of a blood Pb-response function for neurocognitive effects, and the form of the associated blood Pb metric?

3. What are the Panel’s views on the adequacy and clarity of the di scussion of potential thresholds in concentration-response re lationships presented in Chapter 3?

Human Exposure and Health Risk An alysis, Pilot-Phase (Chapter 4):

1. To what extent are the assessment, interpretation, and presentation of the results of the pilot exposure analysis, including char acterization of Pb concentrati ons in media, the modeling of multi-pathway Pb exposure and application of bi okinetic blood Pb models, as presented in Chapter 4 technically sound, appropriately balanced, and clearly communicated?

2. Are the methods used to conduct the pilot e xposure analysis, including the modeling of population-level distributions of total blood Pb levels and the path way-apportionment of those blood Pb levels ( e.g. , air-inhalation, versus soil-ingestion versus dust-ingestion, versusC-2 background) technically sound? Does the Pane l have any suggestions for improvements in

the methods used?

3. What are the Panel’s views on the staff in terpretation of the pe rformance evaluation completed for the pilot analysis (and descri bed in Chapter 4) with regard to the representativeness of indi vidual modeling steps comple ted for the analysis ( e.g. , characterization of ambient air and outdoor soil Pb levels and the estimation of blood Pb levels for specific case studies)?

4. In general, are the concentration-resp onse functions and blood Pb metrics ( i.e. , lifetime average, concurrent blood lead) used in the p ilot analysis appropriate for this review?

5. Are the methods used to conduct the pilot health risk assessment, including the application of the cutpoints in relation to the concentra tion-response functions employed, technically sound? Does the Panel have any suggesti ons for improvements in the methods used?

6. To what extent does the sensitiv ity analysis completed for the pilot analysis (and described in Chapter 4) identify key sources of uncertainty and provide an assessment of their impact on

risk results?

7. As part of the NAAQS review, there is interest in attempting to differentiate Pb exposure and health risk impacts for modeled populations between: (a) histori cally-deposited Pb ( e.g. , near-roadway dust/soil lead from leaded gasoline); and (b) newly-emitted Pb. Does the Panel have specific recommendations regarding appr oaches that might be employed in the fullscale assessment for this purpose?

8. What are the Panel‘s views on the most important issues to be addressed in the subsequent full-scale human exposure and health assessment that will be presented in the revised

documents?

The Primary Pb NAAQS (Chapter 5)

1. What are the Panel’s views on the adequacy and clarity of the presentation of the basis for the existing standard and conclusi ons reached in the last review?

2. Based on the information contained in the first draft Staff Paper, as well as the AQCD, does the Panel have recommendations with regard to specific aspects of the standard to be considered in developing policy alternatives? For example, considering the prominence of the soil and dust pathways for ambient Pb exposures, and the evidence regarding environmental response times, is there reason to give more emphasis to consideration of an alternative (shorter or longer) averaging time; an d, how might this be considered in the fullscale risk assessment give n current capabilities?C-3 Pb-related welfare effects and screening le vel ecological risk a ssessment (Chapter 6) :

1. To what extent is the presentation of evidence from the ecological studies assessed in the Pb AQCD and the integration of information from across the various ecologically-related research areas drawn from the Pb AQCD t echnically sound, appropriately balanced, and clearly communicated?

2. Given the lack of quantitative information on Pb-related ecosystem effects, what are the Panel’s views on the presentation of this topic in chapter 6?

3. What are the Panel’s views of the data sources and models used to estim ate current levels of Pb in soil, freshwater, and sedime nt for the case study locations?

4. To what extent are the methods used to conduct the exposure assessment and the interpretation and presentation of the results technically sound, appropriately balanced, and clearly communicated?

5. What are the Panel’s views of the approach for addressing uncertainty in apportionment of

Pb contributions in the national-scale screen by factoring out those locations with known non-air sources ( e.g. , mining, point discharges)?

6. To what extent are the assessment, interpreta tion, and presentation of the results of the screening-level risk analysis, including characterization of lead concentrations in media and the comparisons to ecological screening values , as presented in Chapter 6 and the risk assessment report technically sound, appropriate ly balanced, and clearly communicated?

7. Does the Panel feel that ade quate screening criteria (ecot oxicity screeni ng values) were

selected for each of the media?

8. What are the Panel’s views on the derivation of the soil screening values for birds and mammals ( i.e. , using the Eco-SSL methodology)? Do the resultant values adequately reflect current information on exposure characteristics of these organisms?

9. To what extent are the uncertainties associ ated with the exposure analysis clearly and appropriately characterized in Chapte r 6 and the risk as sessment report?D-1 

### Appendix D – Population-Based Approaches to Risk Assessment on Analyses for the Primary Lead NAAQS

The CASAC Lead Review Panel considered three separate, but re lated, population-based analytical approaches as examples to be consider ed in deriving an acceptable range of alternative levels, on the basis of the scientific evidence, for setting a new level for the primary Lead NAAQS, as follows:

• Approach A relates air lead levels to blood lead le vels using the approach established in previous lead NAAQS calculations;

• Approach B uses an epidemiologic approach to de rive an adjusted sl ope factor relating air lead levels to blood levels taking into account all pathways be tween air lead and blood lead; and

• Approach C relates air lead levels to blood lead leve ls and then to IQ loss in children.

These approaches consider existing info rmation and the following assumptions:

 the population to be protected (99.5 % of the population of children);

 the maximal acceptable blood concentration (up to 5.0 μg/dl);

 an appropriate geometric standard deviation (GSD) for the blood lead levels in children exposed to a given level of air lead (range 1.3–2.0);

 the non-air background (1.0–1.4 μg/dl or lower range should be considered);

 the slope factor for the relation between air lead and blood lead for levels of blood lead below 10 μg/dl, with the candidate values considered being 2.0 μg/dl per μg/m 3
(m 3 /dl) used in 1978, 5.0 m 3 /dl used by the World Hea lth Organization (WHO) in 2000, 10.0 m 3 /dl noted in recent studies (see th e discussion in Approach B below), and assuming 20.0 m 3 /dl as a maximum; and

 the most sensitive toxicity endpoint ( i.e. , IQ loss in children).

In addition, the CASAC Lead Review Panel c onsiders that a popula tion loss of 1-2 IQ points is highly significant from a public hea lth perspective (22). Therefore, the primary lead standard should be set so as to protect 99.5% of the population from exceeding that IQ loss.

The three approaches provide comparable results. Given the Panel’s assumptions and preliminary analysis conducted for the three approaches, the resulting analyses indicate to the CASAC that there is a need for a substan tial reduction in the primary Lead NAAQS

, to a level of about 0.2 μg/m 3 or less . CASAC recognizes that these prel iminary calculations are dependent upon the results of the Agency’s forthcoming uncerta inty analyses and: the values chosen for the percent of the population left at risk; acceptable bl ood levels and IQ loss; and slope factor — the appropriateness of which all depend on certain scie ntific assumptions and the risk management criteria that are chosen. Imposi ng more stringent criteria would result in a lower (that is, moreD-2 stringent) range of primary Lead NAAQS levels, wh ereas less stringent cr iteria would result in the calculation of a higher ( i.e. , less stringent) range of pr imary lead standards.



### Approach A

The first approach (A) relates air lead levels to blood lead (PbB) levels using a simplified and modified empirical-determinis tic approach that is essentially the same approach used in previous EPA NAAQS (1978) and World H ealth Organization (WHO, 2000) guidance documents. This approach begins with selection of a “not-to-be-exceeded” PbB value or values

based on scientific evidence. These “not-t o-be-exceeded” PbB values for beginning the 1978 NAAQS and the 2000 WHO uses of the approach were 30 and 10 μg/dl respectively. The

current scientific evidence revi ewed by the Panel, per the Agency’s Final Lead AQCD indicates

that the concentration of lead in blood shown to be harmful ha s declined substantially below those levels, to around 5 μg/dl or less.

For example, based on current evidence, one might consider two “not-to-be-exceeded” PbB values, such as 5.0 and 2.5 μg/dl. These ar e not to be exceeded at the 99.5 percentile and, for an illustrative GSD of 1.3, produce geometric mean values of 2.5 and 1.3 μg/dl, respectively. The non-air portion of these two means must be subt racted to give the air Pb-based contributions to PbB. Panel member Dr. Paul Mushak (Append ix F) calculated the non -air portion using the Integrated Exposure Uptake Biokinetic M odel for Lead in Children (IEUBK).

The use of a “not-to-be-exceeded” PbB value of 5 μg/dl in Approach A and slope factors of 5, 10, or 20 produce corresponding suggest ed NAAQS values of 0.22, 0.11, or 0.06 μg/m 3

. Use of a “not-to-be-exceeded” value of 2.5 μg/d l and the same slope factors produce air lead values half as high, i.e. , 0.11, 06 and 0.03 μg/m 3 , respectively. (Note that, for the 1.25 mean PbB scenario, the non-air PbB contribution is the dom inant source and modeling does not provide an exact value; see Dr. Paul Mushak’s detail ed derivation comments in Appendix F, pp. F-55 through F-57.) Based on these values alone , the current primary Lead NAAQS set in 1978 should be lowered by at least a factor of seven and by as much as 50, depending on the slope factor used (see, in particular , the individual comments of Lead Panel members Dr. Mushak and Dr. Ian von Lindern found in Appendix F).



### Approach B

Approach B is a “top-down” approach. That is, instead of estimating the effect of inhalation alone, the effect of air lead on deposition into dust, food, etc. and the uptakes from those pathways, an epidemiologic approach should be used to derive an adjusted slope factor taking into account all pathways between air lead and blood lead. This is based on the changes in blood lead observed when lead began to be phased -out of gasoline. This analysis relies on the results of Schwartz and Pitcher (23).

The Schwartz and Pitcher analysis showed that in 1978, the midpoint of the National Health and Nutrition Examination Survey (NHANE S) II, gasoline lead was responsible for 9.1 μg/dl of blood lead in children. Their estimate is based on their coefficient of 2.14 μg/dl per 100 metric tons (MT) per day of gasoline lead us e, and usage of 426 MT/day in 1976. Between 1976 and when the phase-out of lead from gasoline wa s completed, air lead concentrations in U.S.D-3 cities fell a little less than 1 μg/m 3 (24). These two facts imply a ratio of 9–10 μg/dl per μg/m 3
reduction in air lead, taking a ll pathways into account.

Under this scenario, a de crease of mean air lead concentrations of 0.1 μg/m 3 could be expected to produce a further d ecrease in average bl ood lead concentrations of 0.9–1.0 μg/dl. Assuming a slope of three IQ poi nts per μg/dl reduction in blood l ead, which is indicated by the pooled analysis of low concentration lead exposur e (13), this further decr ease would be expected to raise the average IQ of children in U.S. cities by approximately three IQ points — a significant positive health impact. Put another way, the derivation a bove empirically justifies the use of the slope factor of 10 in Approach C, and the resulting estimates that an air quality standard of 0.11 μg/m 3 (that is, a 13-fold reduction) would be required to keep 99.5% of the children below a blood lead of 5 μg/dl.



### Approach C

Approach C is more sophisticated, starting with an air lead level and a blood lead level produced only by airborne lead, a nd relates that air level to IQ point loss (see Table 2). A linear model between the ranges of 1-7.5 μg/dL PbB for both concurrent and lifetime exposures suggests a three-point decrement in IQ for each unit change in PbB (13). Approach A and C are in agreement on the relationship be tween air lead levels associat ed with PbB, dependent on the slope factor used. (Approach A does not consid er IQ loss or any othe r health effect.)

These considerations are summarized in Tables 1 and 2, and are al so contained in the

individual review comments from various L ead Panel members attached as Appendix F. Depending on the slope factor selected between 5 and 20 m 3 /dl, the estimate of blood lead

concentrations from various air lead concentratio ns varies by a factor of four (Table 1). For example, using the linear estimate of IQ loss a ssociated with PbB below 7.5 μg/dl (13), the Lead Panel estimated that, over the range of PbB from 0.5–4.0 μg/dl ( i.e. , an eight-fold range), the loss of IQ would similarly increase from 1.5 to 12 IQ points (Table 2).

Since the Lead Panel considers a population lo ss of 1-2 IQ points to be highly significant from a public health perspective, the Lead Panel ther efore considers this extent of loss in IQ as a “change in IQ not to be exceeded.” Depending upon the slope factor se lected, this results in a range of 0.025–0.200 μg/m 3 ( i.e. , about a 7.5- to 60-fold decrease from the current primary Lead NAAQS) as the estimated air lead concentr ation to consider under Approach A.

References

23. Schwartz J, Pitcher H. The relationship betw een gasoline lead and blood lead in the United

States. 1989 J. Official Stat. 5: 421-431.

24. U.S. Environmental Protection Agency. (1986) Air Quality Criteria for Lead . Research Triangle Park, NC: Office of Health and Envi ronmental Assessment, Environmental Criteria and Assessment Office; EPA report no. EPA/ 600/8-83/028aF-dF. 4v. Available from: NTIS, Springfield, VA; PB87-142378, p. 1-21.D-4 TABLE 1. Relationship of Blood Lead (PbB) to Air Lead (Pb-Air) by Differing Slope

Factors

PbB ( μ g/dl) Pb-Air ( μ g/m 3)

S.F.* = 5 S.F.* = 10 S.F.* = 20

0.010 0.05 0.10 0.20

0.025 0.13 0.25 0.50

0.050 0.25 0.50 1.00

0.100 0.50 1.00 2.00

0.200 1.00 2.00 4.00

*S.F. = slope factor (m 3 /dl) = PbB/Pb-Air; S.F. value varies with increasing impact of indirect Pb-Air pathway (Dust Pb + Soil Pb)D-5TABLE 2.Relationship of IQ Point Losses toIncreases in Pb-Air and Pb-Air-BasedBlood Lead (PbB) Values Above Zeroa,b,cS.F. = 5S.F. = 10S.F. = 20Pb-Air(μg/m3)PbBdIQ Losse,fPbBIQ LossPbBIQ Loss00000000.0100.05< 10.10< 10.20< 10.0250.13< 10.25< 10.501.50.0500.25< 10.501.51.003.00.1000.501.51.003.02.006.00.200 1.00 3.0 2.00 6.0 4.00 12.0a Pb-Air-related increases affecting IQpoint loss through calculated PbB values using 3 slope factors per Table 1b IQ vs. PbB dose-response relationships based on Lanphearet al., 2005 (13): sub-7.5μg/dl linear segment, average slope = 3.0,combining slopes of 2.9 and 3.1 for concurrent and lifetime average dosemetrics, respectivelyc Slope factors as defined in Table 1 and textd PbB as derived in Table 1e Rounding for values < 1 IQ pointf Population, not individual, IQloss/gain projections; U.S. CDC 2007 estimates 23,380,860 U.S. children 0-71 months of age.Source: U.S. Centers for Disease Control, 2007. CDC Surveillance Data. (Last updated 2/16/2007). URL:http://www.cdc.gov/nceh/surv/stats.htm[accessed 3/8/2007]E-1 

### Appendix E – Issues Related to the Se tting of the Secondary Lead NAAQS

Chapters 6 of the Agency’s 1 st Draft Lead Staff Paper a nd Chapter 7 of EPA’s Draft (Pilot-Phase) Lead Exposure and Risk Assessments document summarize a very large body of scientific knowledge about envi ronmental and ecological effects of atmospherically deposited lead on the biota, soils, sediments, and surf ace and ground waters of terrestrial and aquatic ecosystems in various parts of the U.S. and near by parts of the world. This significant body of scientific knowledge includes environmental eff ects of both historically -deposited lead and continuing air dispersal or reen trainment of lead compounds from primary and secondary lead smelters, along roadsides, and in ecologi cally-sensitive areas such the Hubbard Brook Experimental Forest as descri bed in Chapter 7 of the pilot- phase technical support document.

Although lead is recognized in these two chapters as one among a longer list of heavy metals in the environment (including cadmium, zinc, and mercury), thes e two chapters do not contain adequate discussion of the special character istics of lead or its ecological effects in the

context of these other metals — or other air-dispersed criteria pollutants. Also, little of the information about specific environm ental effects of lead is presen ted in a way that is directly

relevant to the issue of whethe r the EPA Administrator should retain, increase, or decrease the present primary and secondary National Ambien t Air Quality Standard (NAAQS) for lead.

These identical standards were established in 19 78 and have been maintained ever since at a level of 1.5μg/m 3 as a quarterly average (maximum ar ithmetic mean averaged over a calendar quarter).

The Lead Panel believes that especially Ch apter 6 of the draft Lead Staff Paper (and perhaps also at least parts of Chapter 7 of the pilot-phase risk-exposure assessment document) would be much improved in their intended purpose s if they were to contain a concise summary

of:

1. The knowledge available and (as best they can discern) the rationale used by the Administrator in promulgating the or iginal NAAQS for Lead in 1978;

2. The knowledge available and rationale used in the decisions made in 1989 and 1990 to retain unchanged the identical primary and s econdary Lead NAAQS established in 1978;

and

3. The knowledge available and rationale used by the Administrator in establishing and maintaining identical primary and secondary standards for criteria air pollutant — not only for lead — but also for most of the other criteria pollutant s for NAAQS since 1970.

Despite the limitations mentioned in the la st two preceding paragraphs, the Lead Panel believes that the body of scientific knowledge summarized in the Agency’s Final Air Quality Criteria Document (AQCD) for lea d, and further presented in the aforementioned chapters in the

1 st

Draft Lead Staff Paper and the Draft (Pilot- Phase) Lead Exposure and Risk Assessments documents, provide compelling scien tific justification for both:E-2 1. The original (1978) decision by EPA to regulate lead as a Criteria Air Pollutant and to

establish what was then considered to be an appropriately-des igned primary (publichealth based) NAAQS for lead, with a secondary (public-welfare based) standard set at the same level and form, and

2. Maintaining for the foreseeable future si milarly well designed (but contemporarily scientifically well-informed) primary and secondary NAAQS for lead — standards with levels and forms that may be different fr om, rather than identical to each other.

There are several features of the environmen tal and ecological effects of lead, and both the chemical and physical properties of lead in the environment, that make lead distinct from the other four criteria pollutants for which NAAQS have been developed by the EPA. These distinctive properties include:

1. The widespread use of lead as an ingredient in decorative paints, lead -acid batteries, as an additive for gasoline used in motor vehicles, and even in some pest icides used earlier to protect some horticultural crops from plant pathogens;

2. The persistence of lead in soils, surface and ground waters, sediments, and in both the structural- and some biologically-active ti ssues of plants, animals, insects, and microorganisms;

3. The well-known toxicity and interference in development of cognitive functional capacity in humans (especially children) and the mu ch less well-known toxicological and other

effects of lead on all the other different types of animals, plants, insects, and microorganisms in managed and natural terres trial and aquatic ecosy stems of the Earth — some of which are undoubtedly even more sensitive to lead than human infants;

4. The very substantial decreases in current ai r concentrations and atmospheric deposition

of lead into the environment that were achieved in recent decades through:

(a) The Phase-out of lead additives in gasoline during the 1970s, ‘80s, and ‘90s;

(b) Severe limits on air emissions from lead smelters during earlier decades; and

(c) Decreases in air emissions from lead batte ry processing facilities in more recent

years.

Thus, most current exposures of living organisms in natura l and managed terrestrial and aquatic ecosystems are caused primarily by re distribution of envir onmentally persistent airborne lead compounds deposited in soils , sediments, and surface waters during the

latter earlier decades of the 20 th century.

5. The continuing airborne resuspension and dispersa l of lead that persists in soils, fugitive dusts, sediments, and surface waters and are transported and deposited once again from air in both fine and coarse particulate ma tter and aerosols — especially along roadways.

These distinctive properties of lead suggest to some polic y makers that ecological and environmental effects of lead might be manage d by other means than maintaining both primary and secondary Lead NAAQS. In the Lead Panel’ s considered judgment, the limitations of the other methods of management now available to th e EPA are such that none of these alternativeE-3 methods would be anywhere near as effective in protecting p ublic health or welfare as maintaining for the foreseeable future as appropriately well-des igned (and contemporarily scientifically well-grounded) prim ary and secondary NAAQS for lead.

As indicated in the body of the letter to the EPA Administrator, the members of the CASAC Lead Review Panel have provided a consen sus scientific judgment that the present level (1.5μg/m 3 ) of the primary Lead NAAQS should be decr eased substantially and that appropriate adjustments probably also should be made in the indicator, averagi ng time, and statistical form of the primary NAAQS for lead.

The scientific evidence on ecological and e nvironmental effects of lead summarized in the Draft Lead Staff Paper and the Draft L ead Exposure and Risk Assessments documents indicate that any significant de crease in the present level of the primary Lead NAAQS will very likely have similarly significant beneficial effects on the magnit ude of lead exposures in the environment and lead toxicity impacts on natural and managed terrestrial and aquatic ecosystems in various regions of the U.S., Canada, Mexic o, the Great Lakes, and also in the open-water regions of the Atlantic Ocean.

Since concentrations of historically deposit ed lead in soils throughout the United States (averaging 0.5 to 4 grams/m 2 of land area) are changing onl y slowly — with a half-time exceeding a century — these concentrated deposits of lead are expected to remain accessible for exchange with the atmosphere and the rest of th e biosphere into the foreseeable future. Fires, changes in land use, or climatic events such as regional dust storms c ould mobilize significant quantities of lead that would be harmful both to human health and ecosystems downwind. This potential for harm is not adequately recognized in the present Draft Lead Staff Paper and the Draft Lead Exposure and Risk Assessments documents.

Considering the magnitude of important ecologica l effects of lead in the environment, as described in these document, it is very disappoi nting to note that the EP A apparently lacks (or chooses not to expend) funds for any additional ec ological risk assessment work for this current (2006–2008) review of the NAAQS for lead. This di sappointment also is increased by the very welcome attention given in the Final Lead AQCD to the alternative concepts of critical loads, critical limits, target loads, and target times th at have been developed in Europe and Canada to guide the processes of decision making regarding both environmental and public health effects of

airborne chemicals.

Although these alternative concepts and pro cesses of analysis of multiple pollutant/ multiple effects have not been carefully considered for use in the U. S., the CASAC Lead Review Panel — together with the authors of the National Research Council (NRC)/National Academy of Sciences (NAS) 2004 report on “Air Quality Management in the United States” —

believes that these alternatives should be consider ed very carefully in th e future as air quality management tools for use in this country as well as in other countries around the world.F-1 

### Appendix F – Review Comments from

Individual CASAC Lead Re view Panel Members

This appendix contains the preliminary a nd/or final written review comments of

the individual members of the Clean Air Sc ientific Advisory Committee (CASAC) Lead

Review Panel who submitted such comments electronically. The co mments are included here to provide both a full perspective a nd a range of individual views expressed by Panel members during the review process. These comments do not represent the views of the CASAC Lead Review Panel, the CA SAC, the EPA Science Advisory Board, or

the EPA itself. The views of the CASAC Lead Review Panel and the CASAC as a

whole are contained in the text of the report to which this a ppendix is attached. Panelists providing review comments are listed on the next page, and their individual comments

follow.F-2 Panelist Page #

Dr. Ellis Cowling......................................................................................... F-3

Dr. Douglas Crawford-Brown.......................................................................... F-9

Dr. Andrew Friedland ................................................................................... F-17

Dr. Robert Goyer .......................................................................................... F-18

Mr. Sean Hays............................................................................................ F-21

Dr. Bruce Lanphear....................................................................................... F-25

Dr. Samuel Luoma ...................................................................................... F-30

Dr. Frederick J. Miller .................................................................................. F-32

Dr. Paul Mushak ........................................................................................... F-33

Dr. Michael Newman........................................................................................F-65

Mr. Rich Poirot .......................................................................................... F-69

Dr. Michael Rabinowitz .................................................................................F-75

Dr. Armistead (Ted) Russell.............................................................................F-79

Dr. Joel Schwartz ........................................................................................F-83

Dr. Frank Speizer ........................................................................................F-86

Dr. Ian von Lindern ....................................................................................... F-89

Dr. Barbara Zielinska ................................................................................... F-111F-3 

### Dr. Ellis Cowling

Dr. Ellis Cowling North Carolina State University January 29, 2007

Individual Comments prepared in advance of the February 6-7, 2007 Peer Review of the Ecological Risk Assessment chapter (Chapter 7) within the Pilot Phase External Review Draft Technical Report titled “Lead Human Exposure a nd Health Risk Assessments and Ecological

Risk Assessments for Selected Areas”

This “Pilot Phase” techni cal support document is inte nded to provide background scientific information for possible revision of the existing primary and secondary National Ambient Air Quality Standards for lead. After re view by CASAC, this document will be used to develop a “Full Scale” technical support document that will be used as further background for what traditionally has been called the “EPA Staff Paper” on lead and in the future will be called a “Policy Assessment of Scientific and Tec hnical Information” document for lead.

This Pilot Phase document is based on a series of case studies that have been selected to provide further information that will be summar ized in the “Policy Assessment” document which in turn will be used by the Administrator of EPA in making final decisions about whether to retain or change one or the ot her, or both, of the presently ex isting (since 1978) id entical primary (public-health based) and secondary (public-w elfare based) National Ambient Air Quality

Standards for lead.

The “case studies” chosen for inclusion in this Pilot Phase report are intended to illuminate the lead-exposure and lead public-health effects and lead eco-system effects relationships in a variety of locations and situations where both current and historical air emissions of lead have resulted in significant gradients in both human exposures and ecosystem exposures to lead. The case st udies included in this Pilot Ph ase report were developed on the basis of studies at the following locations:

1) A primary lead smelter near Herculeaneum, MO where lead ores has been mined and smelted for most of the past 100 years — and where recent measurements have been made of lead concentrations in air, soil, indoor dust, surface water, and sediment. This

location was used for both the human health risk assessment and the ecological risk assessment studies in the Pilot Phase report.

2) A secondary lead smelter near Troy, AL was selected as representative of 15 secondary smelters in the US where scrap metal and le ad-acid motor vehicle batteries are processed to recover molten lead metal, spent acid, and slag waste materials. At the Troy, AL site,

recent measurements of lead air concentra tions were available. Estimates of air emissions were used to provide mathemati cal-modeling estimates of various types of human and ecosystem exposures and effects.F-4 3) A near-roadway urban site in Houston, TX was used for the human health risk assessment. A single air-quality monitoring instrument about 115 meters from this roadway was used to measure lead air concentrations but no direct measurements of human exposures or records of health impa cts were available. Thus, mathematical models were used to estimate the probable human exposures and health effects at this near road-roadway urban locat ion and in another case study near Corpus Christi, TX.

4) Two different non-urban near-roadway locatio ns were selected for analysis in the ecological risk assessment part of this Pilot Phase study: one site wa s along Interstate 37 near an oil refinery in the vici nity of Corpus Christi, TX a nd the other site was near exist

86 on Interstate 95 north of Richmond, VA. At both of these locations, soil lead

measurements were made at various distances from the roadway. These data were then used to estimate expected uptake rates which th en were used to calculate expected effects of soil lead on growth, development, reproductio n, etc of various species of trees, aquatic plants, invertebrates, and birds.

5) The Hubbard Brock Experimental Forest in the White Mountains of New Hampshire was selected to serve as an “ecological ly vulnerable case st udy.” Although a few

measurements of soil lead concentrations at various depth in the soil on different

watershed areas within the H ubbard Brook Experimental Forest have been made, very few analyses have yet been made to determin e probable effects of hi storically deposited lead or current lead deposition rates on the health, productivity, reproduction, or other characteristics of the trees and other sp ecies of plants within the Hubbard Brook Experimental forest.

6) Using the National Water Quality Assessmen t (NAWQA) Database developed by the US Geological Survey, a National-Scale Surface Wa ter and Sediment Screening Assessment was made using lead concentrations measur ements in water columns within 47 river

basins and sediments with 12 river basins at various locations across the United States.

This data base was used to develop a rough screening assessmen t that is relevant mainly

to the current concentration of lead in water columns and sediments which appears mainly to be the result of redistribution of l ead from soils, sediments, and other reservoirs that were contaminated by atmospheric deposit ion of lead in the later decades of the 20 th

Century.

As I completed this very short description of the case studies used in the Pilot Phase study, my intention was to go on to consider the lim itations of both the available data and the conceptual frame of reference for evaluating the results of each case study by making some recommendations for what might be included in the “Full Scale” techni cal support document. But as I contemplated these recommendations, I could not help but remember [and be inspired by] the following four assertions made in the transmittal letter and attachments to our July 26, 2006 CASAC report to Ad ministrator Johnson:

1) Many of us in CASAC continue to believe that:

“The principal goal of the NAAQS review pr ocess is to answer the following policy question: ‘What scientific evidence is there sinc e the last review to indicate if the currentF-5 NAAQS standards are satisfactory or need to be revised or if addi tional standards needs to be implemented to protect public health and public welfare and the environment.’”

2) The most impressive general conclusions in the First and Second External Review Drafts of the Lead Criteria Document are the very s ubstantial decreases in air concentrations and atmospheric deposition of lead into the envi ronment that were achieved in recent decades– especially as the result of the phase-out and al most complete discontinued use of lead as a

motor fuel additive. The amounts of lead that were emitted into the air by human activities, transported through the atmosphere, and deposited onto vegetation, surface waters, soils, and accumulated into sediments during earlier decades of the past century were very substantial

indeed.

Total lead cumulative deposition in the United States during the 20 th Century is estimated to be 0.5-4 grams per square meter of land and water surface area – depending on elevation and proximity to urba n areas and lead smelting and processing

facilities.

Contemporary loadings to terrestrial ecosystems are now about 1-2 milligrams per square meter per year – about three orders of magnitude smaller than the cumulative loading from all atmospheri c sources during th e past century.

Thus, with rare exceptions in the imme diate vicinity of some lead processing facilities, most contemporary exposures of living organisms (and consequent risks to the health and productivity of natural a nd managed ecosystems in the United States) are not caused by contemporary air concentrat ions and exposures to airborne lead compounds, but rather are caused primarily by redistribution of environmentally persistent lead compounds deposited in soil s, sediments, and surface waters during the

past century.

3) Multi-Media Nature of Lead

More than any other of the five Criteria Po llutants which CASAC has been charged to review in recent years, lead cr osses more if not all of the “m edia of concern” to USEPA. These multi-media aspects include: 1) air emissions and deposition of lead from transportation vehicles, metal sm elters, and battery production and recycling facilities, 2) lead content of drinking water, 3) lead containing paints, 4) lead containing pesticides involved in food production, 5) soil contamination with lead, 6) lead in municipal and solid waste management, 7) lead contamination of su perfund sites, etc. The multi-media nature of this pollutant is touched upon in several different parts of this the First External Review Draft [of the lead Criteria Document]. It may be wo rthwhile to draw these multi-media aspects of lead together in a single part of the Criteria Document, probably in Chapter 1 [and also in the Pilot Phase study and the soon-to-be-completed Final Phase technical support documents for the 2007 Policy Assessment document].F-6 4) ... it was very encouraging to see the fo llowing statements pr epared by my CASAC colleagues Jim Crapo and Paul Mushak, in their individual comme nts after the CASAC meeting on the lead Criteria Document and Staff Paper.

Jim Crapo’s very brief statement was as follows: “It is recommended that the

introduction include a more detailed disc ussion of the history of EPA Lead NAAQS revisions including recommendations of previo us CASAC groups. It is recommended that

this section also include th e chronology of inte rnational policies on lead air quality

standards.”

Paul Mushak’s more detailed statemen t was as follows: “CASAC member Dr. Cowling recommended acceptance of the document but only so long as the history of past efforts by EPA and others, post-1978, to evalua te and make recommendations on air lead standards or guidelines be includ ed. Similar sentiment was expr essed by others. I agree. I particularly agree with the need for inclusi on of discussion of past CASAC actions, post1978, as part of the review record.

Members of the current CASAC Panel may or may not be aware that, in the 1989-90 timeframe, a former CASAC Panel presented a set of quite clear recommendations to Administrator William K. Reilly regarding that Panel’s review, conclusions and recommendations for the EPA/OAQPS Staff Paper on NAAQS evaluation dated March, 1989. I was a member of the CASAC Panel prepar ing the 1/90 report (a nd also a member of the two WHO-Europe panels noted below w ho presented WHO-Europe air lead guidance values in 1987 and again in 2000).

The 1990 CASAC Report on the NAAQS . The most significant parts of EPA’s former SAB/CASAC Committee on NAAQS re view for Pb, in its January 3, 1990 transmittals to EPA Administrator Reilly, were specific conclusions and recommendations deriving from its review of the OAQPS March, 1989 Staff Paper. I would urge that the current CASAC Chair include, in any near-f uture transmittals to Administrator Johnson, complete copies of both the January 3, 1990 transmittals and the March, 1989 OAQPS/EPA Staff Paper as part of the Administrative Record. The subject 1/90 CASAC transmittal to Administrator Reilly included two paragraphs among the conclusions and recommendations that captured the essence of the CASAC Panel’ s efforts. I strongly recommend that these two paragraphs be quoted in the cu rrent AQCD and any new OAQPS St aff Paper so as to provide important context. These two paragra phs are presented verbatim below:

[1990 CASAC Report, p. 1, 2nd Par.] “In discus sing blood lead levels used to assess alternative standards, it is the consensus of CASAC that blood lead levels above 10 μ g/dl clearly warrant avoidance, especially for development of advers e health effects in sensitive populations. The value of 10 μ g/dl refers to the ma ximum blood-lead level permissible for all members of these sensit ive groups, and not mean or median values. The Committee concluded that the Agency should seek to establish an air quality

standard which minimizes the number of childre n with blood lead le vels above a target

value of 10 μ g/dl. In reaching this conclusion, the Committee recognizes there is no

discernible threshold for severa l lead effects and that biologi cal effects can occur at lowerF-7 levels. In setting a target valu e for blood lead (matched ultimately to air lead level) the Committee emphasized the importance of always being mindful that blood lead levels

and health outcome measures are best charact erized as a distribution of values about mean or median values. The importance of c onsidering the distribution of values about the mean or median is apparent from consid eration of the influence of lead exposure on I.Q. A seemingly modest decrease in the m ean or median I.Q. may result in significant changes at the outer limits of the distributi on with both a reduction in the number of bright children (I.Q. > 125) and an increase in the number of children with I.Q. < 80.”

[1990 CASAC Report, p. 3, 1st Par.] “The EPA Staff recommended in the Staff Position Paper that the lead NAAQS be expresse d as a monthly standard in the range of

0.5 to 1.5 μ g/m 3 not to be exceeded more than once in three years. The Committee

concurs with the EPA Staff recommendation to express the lead NAAQS as a monthly

standard not to be exceeded more than once in three years. The Committee strongly recommends that in selecting the level of the standard you take into account, the significance and persistence of the effects associ ated with lead as well as those sensitive population groups for which valid quantitative exposure/risk estimates could not be made at this time. The Committee believes you should consider a revised st andard with a wide margin of safety, because of the risk posed by lead exposures, particularly to the very young whose developing nervous system ma y be compromised by even low level exposures. At the upper level of the staff paper range (1.0-1.5 μ g/m 3 ) there is relatively little, if any, margin of safety. Therefore, the Committee recommends that in reaching a decision on the level of the standard, greater consideration be given to air lead values

below 1.0 μ g/ m 3 . To provide perspective in setti ng the NAAQS for lead it would be appropriate to have the EPA St aff compute the distribution of blood- lead levels resulting from a monthly standard of 0.25 μ g/ m 3 for comparison with the values already computed for higher levels. In setting the NAAQS for lead it is important to recognize that airborne lead serves not only as a source of inhalation exposures, but that lead in air deposits on soil and plants becoming a potential source for intake into the body.”

The WHO-Europe Air Lead Guidelines . The 1987 (first edition) WHO-Europe “Air Quality Guidelines for Europe” developed an ai r lead guideline for Europe consisting of a level in the range of 0.5 to 1.0 μ g/m 3. The process for development of the 1987 air Pb guideline is contained in Chapter 23. The ke y elements in that development included, but were not limited to, the fact that both adults and very young children are affected; children are affected at lower exposure s than adults; and air lead en ters the body directly through inhalation but also subsequently via ingesti on of dusts and soils pr oduced from air lead

fallout.

World Health Organization. 1987. Air Qualit y Guidelines for Europe. Lead. Ch. 23.WHO Regional Bureau for Europe, Copenhagen, pp. 242-261.

In Conclusion:

In light of these four asse rtions — all of them made in the context of our earlier CASAC reports to Administrator Johnson — I recommen d that our CASAC discussions on February 6,F-8 2007 regarding at least th e Ecological Risk Assessment chapte r (Chapter 7) — if not the whole

of the Pilot Phase External Re view Draft technical support doc ument — begin with a careful reexamination of these four (and perhaps ot her) already existing CASAC conclusions and

recommendations.

I say this because I believe it is important that CASAC be very clear about: 1) the scientific and policy purpose of thes e periodic reviews of National Ambient Air Quality Standards, 2) our Congressionally mandated role in the (now recently revised) NAAQS review processes and procedures, and 3) many of the unique multi-media features of lead as a Criteria Air Pollutant,

before discussing: A) the details of the case studies in this Pilo t Phase technical support document, and/or B) the special features of these case studies – a nd both their relevance to and adequacy (or inadequacy) – as a foundation for current de cisions about management of both publichealth risks and ecological risks associated with both current and historical atmospheric deposition of lead in various parts of these United States.F-9 

### Dr. Douglas Crawford-Brown

Comments on Chapter 4: Charac terization of Health Risks

Doug Crawford-Brown, January, 2007

The following comments apply to Chapter 4 as a self-contained document. I provide related comments in my review of Chapter 5. I end with bulleted comments summarizing my main points.

Overall, I am impressed with the analysis perf ormed, especially the general structure of the analysis. I begin here, however, with consider ation of the reason for conducting the assessment in the first place. As I understand it, the goal was to determine whethe r Pb should still be considered under the NAAQS program, or might be “de-listed” becau se it is no longer a significant component of environmen tal risk. Given this goal, I am not fully convinced that the three case studies fully answer that question.

In saying this, I am assuming that there are times when the ubiquity of an issue requires a national approach such as NAAQS , and other times when the probl em is so isolated (in space and/or time) as to suggest a more targeted risk management strategy. The fact that one can find an example where residual risks are high despit e existing regulations, such as at the primary smelter, is not in itself evidence that a NAAQS a pproach remains valid. It simply means there is continued need to apply risk management strategi es in some parts of the country. As a result, I am not sure whether I buy into the idea that this assessment allows the EPA to determine whether continuation of Pb within the NAAQS progr am is justified. But ha ving said that, I still believe the assessment that was conducted provid es a reasonable picture of the risks in the population living within the three case study areas. What is missing is a clear statement of the relationship between these three cases and the more general national picture.

The structure of the assessments performed, both in terms of the treatment of spatial variation and the modeling of exposure routes, seems to me to be sound, or at leas t in keeping with best scientific practice. The EPA a nd its contractors have establis hed these methods over the past decade, and so they have become fairly routin e and accepted as a reasonable approximation to the intersubject variability dist ribution for risk. I might quibble with specific parameter values (and this would be only a quibble, since my preferences wouldn’t ch ange the assessment significantly), but the gene ral approach is sound.

I am comfortable with the decision to use mode ling approaches for the smelters and monitoring

data for the road scenario. I am not that well ve rsed in the monitoring programs, and so I can’t attest to their ability to yield results that are suitable for a spatially-gridded risk assessment. But

it seems to me the authors have used the re sults correctly. And the choice to focus on a geographic area where the data are plentiful was wise, with one caveat: plentiful data at times mean an area was monitored more extensively because of a finding that it is unusually high in some sense. This would call into question whet her it is a representative case study. I can see noF-10 discussion of this issue in the document, and will look for some clarification in the upcoming meeting.

I cannot follow the reasoning at the top of Page 4-11 justifying the focus on a particular roadway

location. I can think of a number of reasons why monitoring might ex ceed predicted ambient concentrations, such as incorrect monitori ng results, poor modeling assumptions, incorrect alignment of modeling predictions (which tend to be spatially averag ed) with particular monitoring locations, etc. The f act that this ratio is above one does not seem to me strong evidence that re-entrainment is important there.

As I mention in my review of Chapter 5, I am comfortable with the treatment of inter-subject variability as a post-processing step using a l ognormal distribution of adjustment factors. I remain unconvinced that the particular characteris tics of this distribution, such as the GSD, can

be determined from data such as measurements in NHANES because I believe the data cited by the authors are produced by BOTH inter-subjec t variability of expos ure and inter-subject exposure and pharmacokinetic properties. As a re sult, the dispersion in the measured blood Pb levels will overstate the dispersion in th e intake-to blood Pb level distribution.

At several points in the document, it would have been useful to have a picture showing the spatial template for the dispersion calculations fo r both the smelter and road scenarios. A reader familiar with the modeling process can guess what these must have been, but a picture would

have been better. This would also have been a good place to show how the census blocks/tracts

were overlain. I assume the centroid of a block or tract was used as the point of exposure, but can’t be sure given the discussion.

On Page 4-20, I cannot follow the justification fo r what seem to me thresholds in blood Pb

levels. I know the authors state that these ar e “cut-points” below whic h calculations are not performed, but they function as thresholds if a read er then interprets later tables of results as indicating no risk at the lower percentiles. We can discuss this at the mee ting, as there is a need

to be clear in the document as to the interpretation of a dash (rather than an IQ loss value) in the summary tables.

On Page 4-22, the authors state that the sensi tivity (elasticity) result s can provide a “semiqualitative feel” for the magnitude of uncertainty . “Semi-qualitative feel” strikes me as about the softest statement one can make about the quality of an uncertainty analysis. I am not even sure I

know what it means. I remain unconvinced that a ny of the sensitivity results presented give much in the way of information on the degree of un certainty. I doubt a more rigorous uncertainty analysis is justified, especially since this is a series of case studies and not a representative sample of locations throughout the country, so I may not push this issue too strongly.

On Page 4-24, the authors say that a block group wa s included in the study area if “the majority

of their air concentration would come from the study area”. I have no idea what this means. I assume the authors included a block group if more than 50% of the geographic area of the block group fell within the study area. It makes no se nse to speak of the “majority of the air

concentration”.F-11 I am comfortable that the partic ular models chosen throughout ar e appropriate for the purpose of this assessment, and so won’t comment on these fu rther here. The one issue I would raise is that

the authors have assumed that the ratio of the exposure concentration to the ambient

concentration can be obtained from NATA. This is valid if the part icle size distribution is about the same, but invalid if this is not true. Some assurance that the assumption is valid seems

warranted here.

On Page 4-34, the authors state that their justif ication for particular regression equations was based on goodness-of-fit and “other considerations”. Th e latter crite ria are much too vague and need to be specified to provide reasonable c onfidence in the regressions. But I do believe the regressions they developed are reasonable approx imations to the data. They simply need to display this goodness-of-fit in exposure-response figures showing the data and model fits.

I commented in Chapter 5 on the issue of the va lidation and verification of the Leggett model, and so won’t repeat that here. Again, I am surprised that the Leggett model is now predicting

blood Pb concentration below that of the IEUBK m odel, and so it would be useful for the authors to explain why this change has appeared. But itis clear from the va lidation/verification study conducted in this chapter that the models are predicting reasonable values when compared against the NHANES data (see Table 4-12).

Once the assessment methods are set up, the auth ors have done a good job of summarizing the results in the remaining tables, including the one on sensitivity. So, I have no qualms about these tables or that they accurately represent the resu lts from the model runs. And I find the tables to include precisely the information n eeded to draw policy conclusions.

As a final comment, section 4.4.3.3.2 on Qualitative Discussion of Uncertainty contains very

little useful information. I left this chapter with little apprec iation for what the magnitude of uncertainties might be. As I said before, I am not convinced that any more rigorous analysis of uncertainty would be warranted given the non-rando m nature of the three case study sites and the inability to do a full nested vari ability-uncertainty analysis. But th e authors should try to give at least some subjective estimate of the uncertainty (accurate to within a f actor of 2, factor of 4, etc).

Overall, an impressive study that is probably as informative as one can find for these case

studies.

Summary Comments:

• Even after several readings, I am unclear as to how the case studies will be used to decide any particular issue related to delisting or an appropriate regulatory limit. There must be a discussion in the report of th e rationale behind application of the results to specific risk questions that will inform policy. Absent this discussion, it is impossi ble to judge whether a policy decision is warranted by the scientific analysis.

• The case studies themselves are well developed in terms of the computational steps. There are a number of key points in estimating exposur es, however, where data are scarce, and thisF-12 affects the reliability of the risk estimates. I am particularly concerne d that exposures due to contact with surfaces may be underestimated, a nd that exposures due to re-entrainment in indoor and outdoor air may be underestimated.

• The EPA should consider looking at all three ways of estim ating blood Pb levels from exposure, and weight these equally in a form of uncertainty or sensitivity analysis.

• Overall, the analysis of uncertainty in the docum ent is too qualitative and fails to adequately characterize that uncertainty. Variability is handl ed better. I especially like the use of the post-processing approach to generating variab ility distributions from central tendency

estimates.

Comments on Chapter 5: The Primary Lead NAAQS

Doug Crawford-Brown

My comments here apply primarily to the issue of Statistical Form, as I will be the one guiding that discussion. Before providing those comments, I do have several other minor issues to raise with the current chapter. I end with bulle ted comments summarizing my main points.

1. On Page 5-2, I don’t understand the distinctio n being drawn between “evidence-based” and “quantitative exposure – and risk-based consider ations”. The last time I looked, evidence was being used in “quantitative e xposure – and risk-based” assessme nts. I suppose the authors have some further distinction in mind, such as a distinction between (i) direct epidemiological studies of the impact of a policy and (ii) predictions of this impact ba sed on separate exposure estimates and exposure-response relationships. But to call one evidence-based in distinction with the other

isn’t correct.

2. On Page 5-5, there is a discussion of the ta rget level (99.5%) of th e population to be brought

below a maximum safe blood lead level. While I agree with the sentimen t here, the ability to reliably estimate the upper tail of this distribution, especi ally a value (99.5%) so far into that tail, is severely limited at present. I haven’t done a fo rmal uncertainty analysis of this estimate, but my guess is that the confidence in terval would be quite large.

Now to the issue of Statistical Form. The current form is to use a strict average over a calendar quarter. The Agency appears to have consider ed a variety of alternatives, ranging from a

violation if ANY measurement is above the limit (1.5 μg/L), to monthly, to even annual averages. In the end, the quarterly average was se lected based in part on the larger number of samples that would be averaged (reducing statistical variability due to sma ll sample size) and the fact that the human body in a se nse “integrates” or “smoothes” exposures through storage in body tissue.F-13 The quarterly average appears to me a reason able compromise scientifically. Given the possibility of windows of vulnerabi lity during development, it woul d not have been wise to use an annual average, as these windows probably co ntain developmental processes that are on a scale closer to months than years. And I agree with the authors that both the issues of sample size and storage in tissue make any statistical form on the scale of individual measurements or even weeks subject to too many false negatives and false positives.

There is some ambiguity in at least the curren t chapter as to what is meant by a “maximum arithmetic mean”. Consider a single year, with weekly measurements (and, hence, 52 measurements). I could imagine that the meas urements for January, February and March are averaged to yield the first quarterly result. Then the same is done for April, May and June. And so on to yield four quarterly values . The rule then might be that th e site is in violation if ANY of these four values exceeds 1.5 μg/L.

But we could also imagine a “rolling” quart erly average. One would use the first 13 measurements and compute an average. Then one would use measurements 2 through 14 and compute an average. Then one would use measurements 3 through 15, and so on. This would yield about 52 such “quarterly averages” in the year. These are sorted and the highest examined. If THAT one is above 1.5 μg/L, there is a vi olation. I simply am not sure which of these approaches the authors intend. I believe the latter is the more justified approach.

On a related note, there is also the issue of th e sampling schedule. I am completely comfortable

with the Statistical Fo rm selected if the samples are on a fixed schedule, or are randomly scheduled throughout the year. We just need to be sure there is no chance that the monitoring includes deliberate over-sampling dur ing periods of high concentra tion. I realize that such oversampling is not supposed to be part of a samp ling program for compliance monitoring, but there is always the possibility that a manager some where will want to de viate from the sampling schedule when problems are suspected. I just want to be sure this issue is built into the sampling used for the compliance monitoring.

Other than these points, I am comfortable with the Statistical Form selected by the EPA.

Summary Comments:

• I am not confident that the 99.5 percentile of th e variability distributi on for blood Pb levels can be estimated reliably, and so don’t believe it is appropriate to use such a percentile in establishing any sort of limits on exposure.

• On Statistical Form, this issue must be disc ussed by the EPA after the Averaging Period is established. The appropriate form to be used depends on the averaging period, the frequency of sampling needed for such a period, and on the monitoring methods appropriate to such a frequency. It is clear that, what ever Statistical Form is used, it must be chosen based on the rates of false positives and false negatives fo r the particular monitoring methods, sample frequency and averaging time.F-14 • I doubt there is a biological ju stification for going to a monthly rather than quarterly averaging time, as this would presume a ra ther narrow developmental window. And I would be particularly concerned about an attempt to choose a short averaging time simply as a way to get more stringent contro ls on exposures. The averaging time needs to be based on biological considerations (e.g., developmental windows) and not on broader policy goals at this stage of the NAAQS process.

Comments on Chapter 5: Human Exposure Assessment and Blood Pb Estimation

Doug Crawford-Brown

As a general comment, I am supportive of the overa ll approach being taken in this assessment, which has several aspects:

1. Modeling of the variability of health risk from Pb exposures in a series of case studies that include primary and secondary sme lters and exposures near roads.

2. Use of the biokinetics models as the basis for converting exposur e information to estimates of blood burden. I also support the idea of examining the variation between the two models proposed to provide a sort of sensitivity analysis examining the robustness of the results.

3. Use of inter-subject variabil ity distributions to be applie d in post-processing to central tendency values generated by the exposure and biokinetics models.

4. Performing the variability analysis in part by modeling the exposures in individual blocks within the geographic area, and sampling indivi duals from these blocks (followed by the postprocessing treatment of inter-s ubject variability in the relati onship between exposure and blood lead levels).

Having said this, I have some specific issues to raise:

1. On Page 5-2, I can’t begin to unpack that fi rst paragraph. Two dose metrics are mentioned: a lifetime average, which is said to be between ag e 6 to 84 months, and a concurrent concentration, defined as the average over ages 73 to 84 months. What is the difference here? Both seem to focus on one year immediately starting at age 6. We aren’t given the code, so I can’t determine

whether there is an actual difference between th ese two metrics, perhaps with poor wording here.

We can discuss this.

2. In that same paragraph, the claim is made that these models yield central tendency estimates of

blood lead. I am not sure that this is strictly true, given that th e parameter values used don’t seem to me to be all central tendency values, if by th is the authors mean median values. And in any event, the model is so complex th at I doubt the use of a ll central tendency values yields a finalF-15 estimate of burden that is itself the central tend ency. But perhaps I am being too picky on this point, as the science isn’t good enough to develop fu lly probabilistic versions of the models yet,

In any event, this issue is important because the post-processing approach of multiplying the central tendency estimate by a randomly select ed value from a lognormal distribution with geometric mean (median) of 1 depends critica lly on the model result being interpreted as a median (and not only the looser conc ept of a central tendency value).

3. On Page 5-3, I am not sure I would agree that the Leggett model is wide ly used and subject to

a lot of validation and verification. At least in th e original versi on of the All Ages Lead Model I reviewed for the EPA, there was a signifi cant difference between the Leggett and IEUBK models, with the former predicting higher concentra tions than the latter. This is even mentioned on Page 5-7 of the current document. I am interested in the fact that in this new assessment, the pattern is reversed, with Legge tt predicting under the IEUBK model. Perhaps this indicates some error in the original use of the Leggett model was uncovered and corrected (the authors of the current document suggest the Leggett model was “tai lored” for the current application – I am not sure what they mean by “tailored”), but I suggest the CASAC determine whet her this is the case.

The authors of the current document state in th e footnote that they ar e doing additional model evaluations, and it will be interesting to see how these turn out. In any event, the current agreement between the IEUBK, Leggett and NHANES results, shown later in the chapter, seems reasonably good at present, and certainly within the error bounds of both the models and the

data.

4. On Page 5-12, second paragraph, the author s say that they have “added” a lognormally distributed term. I hope by “added” they mean “inc luded” in the calculat ion. My understanding is that the randomly sampled term should be multiplied by the calculated median blood

concentration to obtain an individu al-specific blood concentration.

5. I am generally uncomfortable with the us e of a generic water concentration and food concentration, rather than a distri bution. But part of my discomfort comes from the fact that I am not clear from the document whether the post-pr ocessing inter-subject va riability distribution correction was applied only to the component fromair/soil, followed by addition of the nonair/soil contributions, or whethe r all pathways were first summ ed and THEN the post-processing adjustment applied. If it is the latter, I am less concerned, but I can’t be sure from the document

The reason this issue arose in my mind is Ta ble 5-15, which shows the average proportion of exposure from policy-relevant sources increasing from about 50% at the median of the intersubject variability distribution to 98% at the upper tails of the distribution. To get to 98%, it must

be the case that there is a MUCH wider variati on in blood Pb levels from policy-relevant sources than from the other sources (such as water). But that may be because everyone who is sampled is given the same water con centration. I worry that there may be significant under-dispersion of the variability distribution for the non-policy-relevant sour ces than for the po licy-relevant ones, which would be increasingly apparent out in the tails of the aggregate exposure distribution. This

would tend to over-state the case th at the policy-relevant sources are the primary ways to control exposures and risks.F-16 Having said this, I understand the large problems with incorporating inter-subject variability in the non-policy-relevant sources. It would require developing co rrelations between the sources, since I doubt that the sources are fully independen t. For example, someone living in an old home with lead paint is probably more likely to live ne ar a smelter, and also more likely to have elevated lead in the water due to aging pipes an d fixtures. So, this issue isn’t trivial to fix.

6. Finally, I believe the authors ha ve used measured inter-subject variability in blood Pb levels within a study population to deve lop the lognormal distribution I mentioned previously (used in post-processing). The authors argue that the sample population c onsisted of individuals with equal exposures, and so the variation in blood Pb le vel is also the variatio n in the ratio of blood Pb over exposure. But I am not convinced this assu mption is completely true. To the extent it is not, it will produce over-dispersion in the inter-subject variability adjustment factor used in the

current assessment.

Summary Comments:

• There remains significant work to validate a nd verify any of the biokinetics models, but particularly that of Leggett.

• There is difficulty comparing any specific bl ood Pb level predictions in the current study against NHANES values due to significant diffe rences in the composition of the populations and the levels of exposure. I am unconvinced, therefore, by the model-data comparisons in

the document.

• The contribution of water and soil and food to the variability in exposure is underestimated since the same values are applied to all indi viduals in the region. Ho wever, I don’t think it will be possible to obtain data needed to improve this situation significantly.F-17 

### Dr. Andrew Friedland

Andy Friedland, Dartmouth College 1 February 2007

Preliminary Individual Review Comments on OAQPS “Staff Paper” First Draft Chapter 6 “Policy Relevant Assessment of We lfare Effects” and TSD Chapter 7 “Ecological

Risk Assessment”

In general, the staff paper Chapter 6 is a reas onable condensation and in terpretation of the Air Quality Criteria Document for Pb (the “CD”).

I think the most important information that needs to be taken away from this chapter that will

inform both health and welfare di scussions is the material on the legacy of the leaded gasoline era preserved in soils both near roadways and urban areas and in remote locations.

Page 6-8: “The deposition of gaso line-derived Pb into forest soils has produced a legacy of slow moving Pb that remains bound to organic materials despite the removal of Pb from most fuels and the resulting dramatic reduc tions in overall deposition rates.”

Page 6-2 discusses mobilization of previously stored Pb. However, the fullest discussion in the Staff Paper occurs on page 2-7 which points out th e lack of estimates for Pb emissions from resuspension of Pb residing in roadway dust and so il and from burning of biomass materials. The Staff Paper describes that the eff ects of emissions from forest fire s or mechanical disturbance of soils are unknown. Finally, it states: “As describe d in the CD (Section 8.2.2), re-suspension of soil bound Pb and contaminated road dust may be a significant source of airborne Pb....”

These and other sections establish tha t: (1) soils are an important potential source of Pb for the foreseeable future and; (2) this is anthropogeni c Pb stored in a natural substrate. Although it appears that this source is not particularly mobile at present, it still merits short- and long-term monitoring due to its potentia l to contaminate other compon ents of ecosystems and human systems long after more typical sources such as the atmosphere are no longer monitored due to

lack of need.

Because the Pb is moving very slowly (i.e., ha rdly at all), it is actually present as a very concentrated deposit of Pb. Fires, changes in land use, or climatic events such as regional dust storms could mobilize significant quantities of Pb which would be harmful to humans and biological organisms downwind. This potential for harm needs to be kept in mind throughout various aspects of the Staff Paper and the Risk Assessment document.F-18 

### Dr. Robert Goyer

Comments by Robert Goyer on QAQPS Staff Paper – First draft and HRT-pilot phase January 29, 2007

Chapter 5: The Primary Lead NAAQS

This Chapter addresses the general approach used to derive the current Pb NAAQS. An objective is to determine the adequacy of the current standard and to provide background for revision of the standard. The chapter systematically reviews the basis for the standard as established in 1978. and provides a number of charge questions that will assist in making the policy decision. My comments are in response to charge questions.

There is considerable new information that reinfo rces the association of exposure to lead with various effects supporting the 1978 standard. The critical effects then were neurocognitive effects on the developing nervous system particul arly in children ages 1 to 6 years. The new evidence, both experimental and from human st udies strengthen this association and reduces uncertainty regarding the quantit ative relationship. Much more is known about the mechanisms responsible for these effects and thei r persistence with continued exposure

In terms of new information about exposure a nd effects, risk of ne urological effects from exposure to the fetus in utero due to transplacenta l transfer to fetus from the mother and possible developmental effects during the neonatal period from lead in maternal milk have been identified. The quantitative relationships of the ea rly in life exposure <1 yr have a high degree of uncertainty. Nevertheless the evidence identifying children in early ch ildhood as the most sensitive population has been strengthened.

What extent does new inform ation affect uncertainties?

New information does provide greater uncertainti es regarding factors that influence host responsiveness. These include ro le of nutrition, (dietary iron, calcium) and polymorphisms, (e.g. alleles for ALAD, and vitamin D metabolism).

Are there questions regarding basic elements of current standard?

The new evidence suggests that the maximum safe level blood lead is below the level of 10-15 μg/dl on which the current standard is based. Agai n, in terms of uncertainty, the lower the level of the dose- effect relationship, th e greater the risk if uncertainty. The new information reinforces the nature of the exposure-effects relationships and provides additional information about the quantitative aspects of these relationships.

There is no reason for questioning or calling in to question the nature of the lead-exposure relationships considered at the last review (effects on the CNS, hematological and cardiovascular systems and kidneys) but the association of these effects with lead exposure has beenF-19 strengthened and newer studies provide addi tional information about their quantitative relationships particul arly at lower levels.

New information about lead effects on other orga n systems since the last review such as the immune system, skeletal system and reproducti ve system provide stre ngth to the potential toxicity of exposure to lead particularly

The new information cited above and presented in detail in the 2006 AQCD does suggest that it is appropriate to consider revi sion of the current standard at least in terms of maximum safe

levels of blood lead.

Are exposures of concern and health risks estimat ed to occur in areas that meet the current

standard?

Cannot comment

Do causal associations extend to air quality levels that are as low or lower than had previously

been observed?

I do not know

Does the new evidence provide suppor t for a different lead indicator?

No, lead in blood is in close proximity (equilibrium) to target organs and cells.

Averaging Times?

I am not aware of any evidence to suggest any other time is better than the calendar quarter.

Suggestions for alternative standards?

Only that the standard for blood lead levels sh ould be lower but do not have any comments for changing the air standard.

Comments on Lead human Exposure and He alth Risk Assessment — Pilot Phase

Chapter 2. Overview of Risk assessment

The basis for the risk assessment is an estimat e of neurological effects on young children from exposures to lead emitted into ambient air fo r three case studies, a primary Pb smelter, a secondary Pb smelter and a near roadway urba n location. A question might be whether these three examples are appropriate basis for risk assessment but they do represent real world

situations.F-20 The pathways shown in the conceptual model E xhibit 2-1 seem appropriate. The model correctly

includes contribution of air lead to pathways resulting in inge stion as well as inhalation. Blood lead levels were predicted for a child populat ion at each case study using the IEUBK and Leggett models. The cutpoints of 2.4 and 6.1 μ/dl are based on results of the models as blood lead levels below which IQ loss was not to be predicted. Thes e cutpoints are dependent on the validity of the models. I cannot comment on application and interpretation of the models.F-21 

### Mr. Sean HaysF-22F-23F-24F-25 

### Dr. Bruce Lanphear

Characterization of Health Ri sks (Chapter 4) – Lanphear

1. To what extent are the assessm ent, interpretation and presen tation of the results of the pilot exposure analysis technically sound, appropriately balanced and clearly

communicated?

The case studies and scenarios used by US EP A were based on extremely limited data and therefore they were not technically sound. Nor was it obvious how the assumptions and modeling led to the results; thus, it was not clearly communicated.

It was not clear why there were only two scenarios; estimated IQ deficits at current ambient air lead levels and estimated IQ de ficits if NAAQ standards were achieved. It is essential to thoroughly estimate the impact of lowering the l ead NAAQS to various intervals, such as 0.5

μ g/m 3 , 0.25 μ g/m 3 and 0.01 μ g/m 3 , depending on the distribution of ambient lead exposure in the United States. What percent of the population is exposed to air lead levels below each of these cut-offs? What is the estimated reduction in IQ deficits (or IQ benefits) from reductions in the lead NAAQS for each of these cut-off values?

Why didn’t The Report consider wh at air lead standard would be required to achieve >99.5% of

children to have a blood lead concentration < 2.4 μ g/dL, < 1.0 μ g/dL (and lower), analogous to the approach that was used in the 1987 document?

2. Are the methods used to conduct the pilot exposure analysis ... sound? Does the Panel have any suggestions for impr ovements in the methods used?

The methods are not sound. This absence of any da ta ultimately raises ques tions about the ability to define this Report as having a ny basis in science. The modeling relies on data that was largely “made-up”.

On page 4-7, line 32: The Report provides a ra tionale for selection of case studies, including availability of site-specific monitoring data. Ye t it was troubling how little data existed for any

of the case studies. In the vast majority of cases, there was inad equate data on blood lead levels, soil lead concentrations, dust lead levels or wa ter lead levels. As such, there is no evidence presented to allow the Committee to have any c onfidence that the estimated benefit of reducing (or not reducing) are reasonable; indeed, as noted in the report Page 4-80, line 14-16), the risk

estimates for the 90 th to 99.9 th percentile could vary by up to several hundred percent.

Page 4-8: The Report indicates that they were unable to a satisfactory location for examining a multiple-source case study for inclusion as a case study. This is incorrect and unsatisfactory for a public health standard. In the last CASAC advisory meeting, I recommended that The Report provide parallel evid ence that any data generated using bi okinetic models was consistent with epidemiologic data. This is essential given the pauc ity of empiric data used in the Case Studies.F-26 I also indicated that there were two data sets available from Rochester, NY with extensive measures of environmental lead exposure (paint , dust, soil and water) and children’s blood lead levels. In the first study, which was a random sample, there were 204 children 1who were 2 to 31 months of age with extensive me asures of dust lead (troughs, sills and floors), paint lead, soil lead and water lead. Air monitoring data are available from the local health authority.

In the second study, a prospectiv e cohort involving 248 representa tive children followed from 6 months to 24 months of age, blood lead levels and dust lead le vels were availa ble at 6-month intervals. Soil lead, paint lead and water lead we re available at baseline or if children moved to a different housing unit. Alt hough there are the usual caveats th at the results may not be generalizable, there are at least actual data to te st the numerous assumptions inherent in the case studies. This latter study has th e added value of having IQ results linked with the exposure data.

3. What are the Panel’s views on the performance evaluation?

Once again, given the lack of any da ta, it was of limited value.

4. In general, are the concentration-response functions and blood lead metrics (i.e., lifetime average and concurrent blood lead ) used in the pilot analysis appropriate for this

review?

They are reasonable metrics to select based on the existing evidence, which generally indicates that chronic measures of exposure are stronger predictors of lead-asso ciated deficits than peak or early childhood.

However, on page 4-20, the Report relied on 2.4 μ g/dL (concurrent blood l ead concentration) as the lower cut-point for estimated decrements in QI scores. This cut-off, which was reported in the pooled analysis to ensure that we didn’t overestimate the adverse consequences of lead exposure, doesn’t provide any margin of safe ty. A lower cut-off — including levels below 1

μ g/dL — should be examined for additional benef its because the NAAQ standard is intended to provide a margin of safety.

5. Are the methods used to conduct the pilo t health risk assessment, including the application of the cutpoints in relation to the concentration-respon se functions employed technically sound? Does the Panel have sugge stions for improvement in the methods used?

As noted above, a lower cut-off, such as blood lead levels below 1 μ g/dL, should be examined for additional benefits because the NAAQ standard is intended to provide a margin of safety.

It is also important to essential to estimate the impact of lowering th e lead NAAQS to various intervals (e.g., 0.5 μ g/m 3 , 0.25 μ g/m 3 and 0.01 μ g/m 3 ). What percent of the population is exposed to air lead levels below each of these cu t-offs? What is the estimated reduction in IQ deficits (or IQ benefits) from reductions in th e lead NAAQS for each of these cut-off values?

6. To what extent does the sensitivity analysis completed for the pilot analysis identify key sources of uncertainty and provide an assessme nt of their impact on risk results.F-27 It does provide some evidence of the uncertainties and their impacts. In pa rticular, on page 4-80, line 14-16, the Report indicates that the risk estimates for the 90 th to 99.9 th percentile could vary by up to several hundred percent. This conclusion, along with the fact that the vast majority of the blood lead and exposure variables were co ntrived, confirms that parallel epidemiologic

studies are critical to ha ve any confidence in the re vised NAAQ lead standard.

7. Does the Panel have specific recomme ndations about approaches that might be employed in the full-scale assessment for this purpose?

Yes. Use epidemiologic data.

8. What are the Panel’s views on the most important issues toi be addressed in the subsequent full-scale human exposure and health assessment?

It is essential to examine additional case stud ies and additional air qual ity scenarios. These additional case studies and air quality standards must use empiric data; additional case studies that rely on populations without adequate blood lead or exposu re variables are inadequate.

Page 4-13, line 6: The Report indicated that CASAC requested recognitio n of “the importance of dust lead loading”. But there was no recognition or estimates fo r dust lead loading; instead all modeling appeared to rely on dust lead concentrat ion. It is widely recognized that dust lead loading is a significantly stronger predictor of children’s bl ood lead concentration. Moreover, dust lead loading is the metric used to estimate de position of airborne lead and subsequent risk to

childhood lead intake.

4-34: The inverse relationship of soil lead levels with interior dust lead levels only makes sense if remediation had occurred, which is indeed the case in the prim ary smelter site. This finding, while casually brushed aside (soil was subsequent ly excluded from the model), raises serious questions about the extremely limited data sets used in the Case Studies in the Report. Why weren’t more of the existing data considered ? Why did the Report fail to examine existing epidemiologic studies — as previously reco mmended by this Committee — to test results

obtained from the case studi es that lack any data?

Page 4-18, line 32: The Report indicated that, to predict ambient lead in indoor dust, they used empirical (regression) models that relate indoor dust to outdoor air lead and/or outdoor soil lead. It would be helpful, as repeatedly requested by Paul Mushak, to have these data tabulated. If they are tabulated elsewhere in the Report, it w ould be useful to describe where it can be found in this paragraph.

Page 4-12: It is disturbing, to say the least, that the vast majority the blood lead and environmental blood lead data were “made up.” This makes the performance evaluation of

limited value.

Page 4-37: The Report indicates that modeling of blood lead levels is required for the pilot analysis for a number of reasons (e.g., measured blood lead levels were only available for a smallF-28 fraction of the study population in the primary sme lter study and entirely ab sent for the other two case studies; exposure needs to be apportio ned between policy-rele vant and background exposures and; potential changes in existing blood lead levels dist ributions need to be predicted given reductions in ambient air lead levels). Bu t these blood lead levels ar e available for at least two epidemiologic studies — along with other exposures and ambien t air lead levels. Moreover, the effect of lowering the air lead standard can be quantified and the various policy and background exposures apportioned.

The failure to use existing epidemiologic studies to test the reality of the biokinetic models is unacceptable, especially given the lack of any obj ective exposure data and blood lead levels for

the case studies.

Page 4-37: The Report indicates that it is unacce ptable to use regression models for populations and exposure scenarios other than th ose used in their derivation. This is a false argument. First,

the authors used contrived data from three case st udies to “quantify” the effects of lowering the air lead standard to populations and exposure sc enarios that will ultimat ely affect populations

other than those used in their derivations. The only ot her rationale is that mechanistic models have greater flexibility in their app lication. This may be tr ue. It is also true that it is easier to make up data than to use actual data, but that doesn’t justify making up data to promulgate

standards that are essent ial to protect the public ’s health. Conducting good science is rarely

easy.

Page 4-39: The Report indicates that “a number of input parameters for both models have been adjusted to reflect the latest data on behavior, bi okinetic models and lead exposure. This sounds reassuring, but it is not; ther e is no exposure data.

4-42, line 24: and 4.45, line 5-22: It would be quite important to understand the impact of using a GSD=2.0-2.2 (which is found in the NHANES data) versus the GSD=1.6, used in the exercises. On the surface, it would seem more relevant to use the GSD=2.1 for a national air quality standard.

Page 4-49, line 19-24: The Report is incomplete. It is essential to thoroughly estimate the impact of lowering the lead NAAQS to various intervals, such as 0.5 μ g/m 3 , 0.25 μ g/m 3 and 0.01

μ g/m 3 , depending on the distribution of ambient l ead exposure in the United States. What percent of the population is exposed to air lead le vels below each of these cut-offs? What is the estimated reduction in IQ deficits (or IQ benef its) from reductions in the lead NAAQS for each

of these cut-off values?

Page 4-59, line 22-25: It is difficu lt to believe that there wouldn’t be additional IQ benefits with

further reductions in ambient l ead exposure. This conclusion — which is in conflict with the prevention principle — and the fact that most of th e data used in the simulated models were also simulated, raises serious questi ons about the entire Report.

Page 4-61, lines 1-9: It is im plausible, from my recollection of participating in an ATSDR workshop on Herculaneum that included extensive measures of children’s blood lead, that only 1% to 10% of children in this primary lead smel ter case study would experi ence IQ point lossesF-29 at current or proposed attainment of 1.5 μ g/m 3 from ambient air lead exposure. The only way this makes sense is if you limit the range of expos ure to such a small increment that any change is inconsequential.

Page 4-72, footnote: The footnote “it was necessary to convert dust lead concentrations derived for each study site into dust lead loading” is in accurate. Many of the dust lead measures were measured only as dust lead loading. Moreover, the investigators of th e pooled dust lead study, which included many of the national experts in l ead exposure, unanimously concluded that it was

not useful to convert dust l ead loading into a dust lead concentration (o r vice versa).

4-77, lines 20-40: The report indicates that th e Performance Evaluation involved comparison of

modeled results with available em piric data to characterize poten tial uncertainty. There was not, however, sufficient comparison of the mechanistic models with empiric (i.e., epidemiologic)

data.F-30 

### Dr. Samuel Luoma

Comments on Lead Staff paper and Risk Assessment February 2007

Samuel N. Luoma

The staff paper must meet the challenge of linki ng atmospheric inputs to water, sediments and soils to ecological risks. The measures required are concentrations in air, concentrations in water, sediment and soils and the effects conc entration (measures of ecological risk) in each media. The greatest uncertainty lies in the m easures of risk. The in-depth evaluation and synthesis is insufficient for the reader to get a grasp of the very great uncertainties in all the standards. For example,

1. the Eco-SSLs can only be described as wildly incoherent; 11 mg/Kg for birds (probably below most background Pb concentrations) and 1700 mg/Kg (typical of the worst minecontaminated soils – i.e. “slickens”) for i nvertebrates simply do not make biological or ecological sense. The agency must be co mmended for using good pr ofessional judgment in choosing more a more coherent set of Ec o-SSL’s in the risk assessments. But those

choices do eliminate correction factors built in to correct for the great uncertainty in toxicity tests relative to the environment. More science is needed to make these

standards more defensible. On the other hand, the very large HQs that occur in some instances in the case study sugge st the high end tail of the eff ects distribution is not being eliminated by implementation of the current standard.

2. The agency must also be commended for choosing the NOAA/MacDonald statistical approach in evaluating risks from sediment contamination. This approach has many limitations, but its great advantages are simp licity and the way it constrains different levels of uncertainty about effects from Pb contamination in sediment. These are the most informative analyses in the risk assessment and the case study. Using these risk levels with the NAWQA data set was a way to address the question of risks from widely

distributed lead concentrations. The se veral very HQs relative to the PEC in the NAWQA data were somewhat surprising, again raising questions about existing standard as implemented. However, it was noted that most of these effects were not from modern atmospheric inputs (historically deposited atmo spheric Pb was not eliminated, however). The core data presented from the Great La kes does allow an analysis (Fig 2-22 from Yohn et al 2004). It suggests that there were substantial ecological risks from at least

some sediments in the Great Lakes when i nputs were at their highest, even though the 90th percentile of atmospheric concentr ations at that time were ~1 μg/m 3 . This suggests that if a standard were set at 1 μg/m 3 and atmospheric concentra tions were allowed to go

back to that level then it is likely that there would be risk for ecological damage in many aquatic environments (HQ>>1 based upon PEC). This logic suggests th at a regression of historical, dated lake sediments against atmo spheric lead might be a way to address the question of how atmosphere links to ecosyst ems. The TEC and PEC approach might be used to estimate risks based upon that curve. It is also notable that at the ~1 μg/m 3 90 th
percentile atmospheric Pb, dissolved concentr ations in the open oceans rose to >30XF-31 undisturbed Pb concentrations in the ocean. It is not possible to relate this to ecological risk to open ocean ecosystems (the toxicity te sting data is probably irrelevant for this pristine environment); but from a common sense point of view one must ask if we want a standard that would allow us to go back to this condition?

3. The HQs developed from NA WQA data and the AWQC, un fortunately, do not take sufficient account of the predominance of bad analytical data (for dissolved Pb) in the

literature and the limited value of standardized dissolved toxic ity tests in establishing risk limits. One solution would be to limit NAWQA data to recent years. In any case the analytical uncertainties rais e questions about the credibil ity of both high and low HQs. The report should be commended for using a mu lti-media approach (sediment and water) to evaluate situations where HQ>1; but shoul d add a similar analysis for HQ<1 for water and/or HQ>TEC for sediment.

For the future, modeling efforts are needed to link any proposed standard to the eventual Pb concentrations in water, sediments and soils. This could go on after a st andard is promulgated and monitoring data begin to come in. “Critical loading models” are being used in Europe to great effect in understanding trajec tories in soil contamination in response to existing or forecast atmospheric concentrations of metals. The re gulatory process and use of indicators would benefit from exploring us e of these models.

An analytical, weight of eviden ce synthesis is not avai lable of the existing literature (toxicology, geochemistry, processes and observations of na ture) relevant to water, sediment and soil standards. This could be another way to reduc e uncertainties in the standards against which atmospheric inputs are compared. Contradictions among such lines of evidence should be used to point toward needs for greater understandi ng. The sensitivity of different ecosystems subjected to atmospheric lead i nputs might also be systematica lly recognized in such a review (e.g. are pristine systems like the open ocean and large lakes sensit ive to atmospheric Pb inputs?

Can the historic data be used to evaluate such questions?). Again, l ooking toward the future, approaches like Europe’s water framework directive might lead us toward a more a unified view of atmosphere, soils, water and sediments with regard to inputs, concen trations and ecological risk. Unification could guide a research agenda that could vastly improve the justification for future atmospheric Pb standards.F-32 

### Dr. Frederick J. Miller

Fred J. Miller, Ph.D. February 16, 2007

Chapter 3 Policy-Relevant Assessme nt of Health Effects Evidence

General Comments Overall, staff has done an excellent job of summarizing th e health effects of Pb most relevant for policy and NAAQS standards issues. The chapter is well written and staff clearly describes the key studies from the CD that support the point s they discuss. Organi zationally, the chapter

structure assists the reader in following the basis for which endpoints and subpopulations should be focused upon in the risk assessment that will be done later, as well as the Pb dose metrics that

should be used.

CASAC’s discussion at the Feb. 5-6 meeting was very useful relative to staff including a “hypothetical threshold or cutpoint” in the pilot quantitative risk assessment that is subsequently described in the document (i.e., a blood Pb valu e of 2.4 μg/dL for concurrent blood Pb level and 6.1 μg/dL for lifetime average blood Pb). The net effect of the selection of a threshold is to reduce resulting risk estimates for whatever bi ological endpoint is being examined. While the epidemiology studies conducted at low levels provide no clear cut evidence of a threshold, neither do they demonstrate that there is no threshold.

In view of the long-range public health impor tance of CNS cognitive effects in children, an endpoint that staff has sel ected for quantitative risk analyses, th is reviewer is now of the of the opinion that the risk analyses s hould be done without incorporati on of a threshold. The additional new studies circulated during th e Feb. 5-6 meeting show effect s on attention deficit below 2 μg/dL, effects on cardiovascular mortality and str oke below 10 μg/dL, etc. The importance of the level for a standard can be approached from a ri sk viewpoint by looking at the percentage of the population that would be at risk rather than by assuming there is some exposure level below

which there is no risk.

Specific Comments

Page & line Comment 3-2, 17 The use of “upper resp iratory tract” is not corr ect here. Suggest replacing with ‘head and in the conducting airways”. 3-11, 13 Staff in this paragraph quote the CD for implying that Pb may play a role in the epigenesist of behavioral pr oblems in inner-city children. This contention is very poorly supported by a ny data and this paragraph is too speculative. Suggest dele ting this paragraph. 3-15, 14 The statement about the change of 1 millimeter mercury increase in systolic pressure per doubling of blood Pb is confusing. Suggest a specific example be included (e.g., a blood level increase from X to Y results in a systolic pr essure increase of Z).F-33 

### Dr. Paul Mushak

PRE-MEETING COMMENTS ON:

REVIEW OF THE NATIONAL AMBIENT AIR QUALIT Y STANDARDS FOR LEAD (Pb): POLICY ASSESSMENT OF SCIENT IFIC AND TECHNICAL INFORMATION OAQPS STAFF PAPER - FIRST DRAFT

Reviewer: Paul Mushak, Ph.D.

I have both general and specific comments a bout the referenced document. I confine comments to the first five Chapters, and defe r comments on the welfare/ecological effects Chapter (6) to the Panel’s ecotox experts. My overall critique of this draft document addresses clarity, organization, quality of analys is, validity of conclusions, etc.

Specific comments are offered across Chapte rs in addition to comments within the framework requested by OAQPS staff.

I. GENERAL COMMENTS ON THE DRAFT STAFF PAPER

This draft represents an enormous amount of work by OAQPS staff and contractors and they are to be commended for the effort. I do have general comments about the case study procedures and the results. My comments cover both scientific aspects and the editorial/organizational status of the draft.

This body of work suffers from some unclear writing and some verbosity. It can be tightened and clarified.

It is quite difficult to follow the writing in parts and there is considerable imprecision in what may be intended. These are complex topics and unclear writing makes them more complex.

It’s far easier to see all the devi ls in the details of these drafts when the details are clearly presented.

An example of seemingly garbled writing is data contained in Table 4.3, which deals with IEUBK input parameters for Pb-B modeli ng. The numbers and the text for Table 4.3, and

the associated Table 5-11 in the Pilot risk asse ssment, need to be double-checked. Be sure that the bioavailability values give n in the Table section for soil and dust Pb inputs are clear and

correct for all three case scenarios. The bioavailability (uptak e fraction) of Pb for the secondary smelter and roadway dust cases are the defaults typically used with the IEUBK model for dusts and soils, i.e., 0.3. However, the authors state for the secondary and near roadway values that the “USEPA (1989) reflects ev idence that Pb in dust and soil is as accessible as dietary lead...” If the authors mean to use dietary uptake for the seco ndary smelter and roadway dust and soil uptakes, then the value is 0.5, not 0.3.F-34 The discussion of values stated for the pr imary smelter soil and dust uptake seems even more confusing. Are the values of 0.48 for soil a nd 0.26 for dust relative bioavailability (RBA), i.e., “bioaccessibility” (which is system-specific solubility) or absolute bioavailability? Relative bioavailability is reduced by half to get absolute bioavailability (ABA), i.e.,

ABA = RBA x 0.5 (maximum uptake from th e child’s gut for fully soluble lead)

Check the original data for the dust versus soil Pb values. The dust versus soil values seem to be

reversed.

There are some problems with the organiza tion of the draft. Why is the Chapter on welfare and ecological effects pl aced after Chapter 5, the latter a sort of general schematic for how EPA regulates criteria pollutants such as lead to come up with a de-facto history of the current NAAQS. The same sequencing problem ar ose with the original AQCD draft. The NAAQS for lead has both primary and secondary ra tionales for the standards. One needs to have the material for both types before laun ching into discussions of NAAQS.

Should a chapter on NAAQS development appear in this first draf t at all, since no proposed NAAQS options are presented? Is this simply a placeholder draft chapter? The NAAQS development chapter in general says lit tle about the proposed “transitioning” process and little about the logic behind the proposed process. If it’s historic ally useful for the draft, why have it as Chapter 5 instead of a Chapter 1 or 2, “History”? Past usually goes before present.

Might not the subject matter of Chapter 5 be expanded to cl early set forth the various regulatory schemes for lead, such as control of ai r lead through various pa rts of Sec. 112 of the 1970 CAA and 1990 CAA Amendments dealing w ith hazardous air po llutants (HAPs)?

General Comments on Chapter 4

This draft’s functional innards for huma n population impacts of (generally) current condition ambient air lead impacts are to be f ound in Chapter 4, but preceding Chapters are important as well. Chapter 3 mainly presents the important adverse effects and dose-response data for the risk evaluation and quantifica tion methodologies. The exposure approaches are summarized in Chapter 4 and more is provided in the supporting Pilot Study draft. Chapter 3 was generally well done.

Exposure Modeling

Utility of the biokinetic models described in the Pilot draft and summarized in Sec. 4.3 of the staff paper draft is of major importance, the models providing th e exposure link between environmental lead inputs and resu lting neurotoxic risks expressed as IQ point losses. I believe, however, that the authors shoul d summarize the interim findings of the SAB Panel that is reviewing the all ages lead m odel (AALM) and various other bi okinetic models for EPA lead regulatory use, especially how the supporti ng IEUBK, the Leggett (Pounds Leggett) and O’Flaherty models perform relative to each othe r. A number of members of this CASAC Panel

are also on that AALM Panel.F-35 The authors should summarize the typical perf ormance of the models and the principal biokinetic and exposure inputs that drive the models. For example, those of us who routinely use

the IEUBK model know that it can either overestimate or underest imate validly and accurately

measured Pb-B levels depending on such factors as the site-specific and site segment-specific uptake fraction (bioavailability) and the daily in take quantities of environmental lead media (dusts, soils).

IEUBK models can both underest imate and overestimate measur ed Pb-B at a given locale depending on the spatial segment of the risk study area being examined. Panel member Ian von

Lindern has shown this for the reaches of the B unker Hill lead Superfund site impacted along the lower Coeur d’ Alene River Basin. The manual for the AALM and the background document provided to the models Panel by EPA’s NCEA can be consulted for details on how the different models perform.

The O’Flaherty model will either underestimate or overestimate measured Pb-Bs depending on where along the dosing-Pb-B curve th e comparison is done. Relative to each other, the input parameters for Pb-B output differ. Legge tt uses different gut uptake fractions than does

the IEUBK.

I think it’s important to k eep a quantitative pers pective on the models vis-à-vis other elements of variability or uncer tainty in these case- study scenarios. For th ese case studies, the greatest source of variability and uncertainty are the environmental measures, especially the

modeled air Pb levels.

The draft notes that consider ation will be given to bot h biokinetic lead exposure modeling and ad-hoc lead exposure statistical mode ling, but this draft only appears to directly use regression relationships for inter-media estimating of lead content. The Lanphear et al. statistical model for Pb exposures was only used in the sensitivity analysis.

Summary of General Conclusions:

A. The Precise, and Only, Purpose of the Case St udy Approach is to Provide the Administrator With a Range of NAAQS-Relevant Exposures and Risks Versus Ai r Lead Levels for Illustrative

Point Sources and Selected Conditions.

• The authors need to be absolutely clear and precise about what is the actual utility of results from these three case study assessments so that any reviewer or other interested reader will not misinterpret the results, ge t ambiguous and erroneous messages, or misuse the results. The data from the three studies pr ovide a three-part illustrative tableau of the range of current Pb exposures and associated health risk (IQ point loss) for ranges of

environmental media Pb that would and do va ry across the three illustrative cases.

• For example, as I read the point of the Pilot and eventually the Full Assessment exercises, the Administrator may conclude that he/she mu st regulate air Pb to the lowest air Pb (in whatever averaging and statisti cal air lead form) that even tually produces <1 IQ pointF-36 loss in 99.9% of U.S. children < 6 years of age. These three sets of results theoretically would provide the wherewithal for making this determination via selection(s) among the three options presented. That selection may be a single air Pb that springs from the Chapter 4 Tables or it may be a set of air Pb levels from the three study areas that give

the same risk criterion of th ere being < 1 point IQ loss.

• If one misinterpreted the exer cises here to mean they se rve for source characterization globally or historically, then this would imply that one of the toxicologically safest places in America for families to raise young ch ildren is in the general proximity of an operating primary lead smelter which has very rarely been in regulatory compliance — over almost 30 years — with a relatively high, 29 -year old air lead standard, and that has had a long recorded history of adverse impacts on the adjacent community in such forms as high frequencies of elevated Pb-Bs in young children living in the Herculaneum, MO community.

• It would also be erroneous to conclude th at the illustrative resu lts for the secondary operating smelter in this draft in any way characterize the operating history of this particular secondary smelter, secondary smelte rs historically or cu rrently globally. That would mean that another safe place toxicologi cally for families to raise young children is in the proximity of a secondary lead smelter that (1) has the third highest lead emissions of 15 U.S. secondary smelters, (2) has actual air m onitoring data that place air lead from this secondary smelter within the highest 15% of secondary smelter air lead monitoring results nationwide, and (3) is located in a county (Pike County, AL) which CDC in 2003 found has 8% of children with Pb-B >10 μg/dl, a fraction four times higher than national results and over three times the Alabama-wide figure.

B. “New” Lead Inputs for Defining Health Risk are not Trivial Compared to Historical Levels

• Finally, there are technical reas ons for why “current condition” results cannot be used to support any policy conclusion that new inputs of Pb in any of the three case studies are minor compared to levels already accumulated. First, there are limitations I note that are rooted in the three-case methodology. There ar e other important reasons as well.

• First, as I noted in Tables of dust Pb loadings at different very low air Pb levels in my earlier AQCD comments provided last year, hazardous dust Pb loadings for interior and exterior will rapidly accumulate on hard su rfaces encountered by children. Refer to those tables for details, especially health risks for children at an air Pb of 0.1 μ g/m 3 . Any air Pb above or around the very low levels employe d in those calculations will pose a risk.

• Secondly, the “current conditions” scenario for dust and soil Pb do not provide a temporal estimate of how quickly air Pb at “current conditions” will result in soil and

dust Pb that become hazardous in the fullne ss of time. Equally troublesome, dust and soil leads used in the environmental Pb Tables gi ve soil and dust Pb leve ls that are greatly

underestimated when based on modeled air P b. Table 4-11, Performance Evaluation, says the secondary smelter case s hows modeled soil Pb is three times lower than a reference

measured Pb data set.F-37 • The authors also state in Table 4-11 , “Performance Evaluation...” for the primary smelter case that Pb in soils were calculated directly from measured data for the remediation zone and extrapolation results for the site remainde r. But the remediation zone soil Pb data are difficult to link to current air Pb. They re present rapid recontamination in terms of

average lead content for recontamination from the smelter (arguably from fugitive dust movement). They cannot be explained by the actual dispersion-mode led ambient air lead levels provided even though dispersion modelin g of the 266 tons of facility Pb included fugitive dusts (Pilot draft, Appendix B). The median air Pb level in [Table 4-4] appears along with a “measured” soil Pb median value of 84 ppm [Table 4-5].

• Could the authors clarify and specify the extentto which the listed median and other air Pb values for the primary and secondary smelter air Pb values reliably predict the

indicated soil Pb distributions in the Tables? If they cannot do that, then it is pointless to talk about distinguishing “new” air, soil and dust Pb from “histori cal” air, soil and dust Pb in terms of relative ranking for adve rse impacts on lead-exposed populations.

• Current air Pb cannot be considered trivia l in terms of producing the main exposure drivers, soil and dust Pb. S econdly, soil Pb and undisturbed dust Pb are never in equilibrium, i.e., never in “steady state” with air Pb. The relationship of the former to the latter is time-contingent and th e longer air Pb deposits onto soils, the higher the soil Pb will be. The primary smelter community recont amination data for soils appears to say that air Pb (as direct stack and fugitive dus t inputs) has to be much greater than the

modeled values.

C. Design and Results of the Ca se Study Approach, Selected Areas

• The conceptual approach and its associated methodological rationales for the case-study approach in this draft staff paper remain to be laid out clearly and adequately up front, as does a comparative discussion of other approaches one might us e. I urged this be done in my previous comments for the Panel consul tation done last year but I still don’t see a

clear discussion. The closest to this is bur ied back in Chapter 2 (p. 2-46, Findings and Limitations).

• The authors, in 4.1, lay out a nice and clear c ontrast as to the con ceptual distinctions between the 1989-1990 Staff Paper assessmen t for NAAQS selection and the current approach. As the authors note, modeling of risk was done here, versus modeling of exposure indexed as Pb-B elevations and fr equencies in the 1990 assessment. Modeling toxicodynamics (effects), as opposed to m odeling of conventional toxicokinetics (exposures), is something new for the Agency ’s approach to lead risk assessment.

• The Staff Paper analyses and the suppor ting pilot study draft consist of (1) a computational marathon of sequential modeling data mixed to some extent with measurement data but mainly modeled data, and (2) modeling data sequentially fed as inputs into one or more downstream mode ls to get even more modeling data.F-38 • All of these methodological elements are for three case-study scenar ios, each of which contains within themselves a raft of ques tions about suitabilit y, problems complicating reliable use of the study scenarios for nati onal projections, and serious data gaps.

• Tandem use of (1) case studies with their pecu liarities and their problematic utility for national scenarios and (2) compounded mode ling methodologies have produced results that raise a number of questions.

• The sequential modelings with the acco mpanying intra-model and inter-model compounding of variability and uncertainty m ean that a high potenti al for mis-estimation exists and that even limited parameter se lection and assumption biasing well upstream can eventually produce large errors in the downstream risk assessments – child neurotoxicity (IQ loss) risk.

• For example, the secondary smelter scenario for current conditions produces (1) modeled risks of IQ loss in young children from (2) bi okinetically-modeled Pb -B levels that are based on the combination of (3) modeled dus t and partially modeled soil lead from

measurements done for other than the location of the smelter, which in turn were based on (4) dispersion-modeled ambient air lead leve ls that in turn are based on (5) only three

stack test results done 7 to 10 years ago at the facili ty. A further concern for this case study is that air monitor data near the sme lter indicates that 2003 ambient air lead, not used in the modeling, is likely much highe r than the air leads found 1997-2000 (see Table 2-6 of the draft Staff Paper).

• This draft paper describes methodologies whic h operate in the dimensions of time and space. The dispersion modeling used a spatial re ach of 10 km for the air Pb distributional statistics. However, their calculations indica te that 50% of bac kground, from the primary smelter, is not reached closer than 50 km. Restriction to 10 km was dictated by run times.

• The authors indicate in Table 1 the cumulativ e time periods for testing air, soil and dust Pb as 2000 to 2005 for the primary smelter, 1997 to 2000, and circa 2001 for the roadway dust Pb scenario. At the same time, the author s for the primary smelter case make use of

dust and soil Pb data that had accumulated for decades for the no remediation zone. Similarly, the secondary smelter “hybrid” scen ario uses long-impacted soil Pb values.

• Assumptions and parameter selections used in this draft for the above evaluations frequently serve to underestimate exposure a nd associated risks in affected populations. For example, the soil lead results presented in Table 4-5 for the projected soil Pb around the operating primary lead smelter represent “current condition” Pb that may or may not capture the significant role of fugitive dust Pb contributions in the remediation zone and to some distance beyond that.

• The combined impact of stack Pb and on-site fugitive dust sources for off-site Pb levels must be sizeable. I am not sure that one can ge t a stable soil Pb level near this smelter.

The soil was remediated out to 1.5 km but th e MO DNR has reported that there is rapid recontamination. EPA in follow-up has also shown serious recontamination for the 1.5F-39 km distance corresponding to th e remediation zone. Areas th at were remediated with

removal and use of low-lead soils were s hown by the MO DNR to have recontamination with an average of 600 ppm lead. The highe st recontamination level was 2400 ppm.

Ref:

Missouri Department of Natural Resour ces. 2002. Doe Run Herculaneum Smelter –

Residential Yard Data on Historic Recontamination. February. Internet: www.dnr.state.mo.us/deq/herc.htm

Equally troubling is that remediated soil surfaces appear to have continued being recontaminated through May, 2006.

Ref:

U.S. EPA. 2006. Lead soil trend analysis through May 2006. Eval uation by individual quadrant. Herculaneum lead smelter site, He rculaneum, MO. Kansas City, KS: Region 7, US Environmental Protection Agency.

• One can readily calculate that to recontaminate from “clean” replacement soil at a low background Pb content (

  50 ppm Pb) to the above reported r econtamination levels in a few years would require quite high direct stack and fugitive dust emissions. See USEPA 1996

for the calculations.

Ref: U.S. EPA. Urban Soil Lead Abatement Demo nstration Project. Vol. I: Integrated Report. Report No. EPA/600/P-93/001aF Washington, DC: Office of Research and Development.

1996.

• Equation 2-3 in that document can be used to calculate that for a 1.0 μ g/m 3 air Pb level, and an ultra-conservative deposition rate of 0.2 cm/sec, receiving soils collect lead at the rate of 3 ppm/year. The very rapid reaccumulatio n of lead in soils to an average of 600 ppm Pb over, say, four years or so, using th e above indicates an annual recontamination rate of ca. 140 ppm (600 - 50 background) and an annual air Pb level of ca. 40-50 μ g/m 3
from combined stack and fugitive dust releases.

• This air Pb figure can be compared to findings of air Pb levels proximate to the smelter ranging up to 85 μ g/m 3 (noted in Ref. 4 of the ATSDR Consultation, Jan. 15, 2004, and discussed in that Consultation). A house with remediated soil showe d, after two years, a soil lead level of 300 ppm, indicating 250 ppm of contamination (300 - 50 ppm low-Pb fill soil), at a rate of 125 ppm/year. This jib es with the above estimate from calculations. This corresponds to about 40 μ g/m 3 air Pb as an average.

Performance Evaluations, Uncertainty Analyses, Etc.

• The authors need to use reality checks to do a full conceptual and me thodological audit of

their results at both the macr o level of collective scientific conclusions and weight-of-F-40 published-evidence and the more micro level of, for example, performance evaluations and sensitivity analyses. It is not useful to know one has a valid and reliable way to get to Union Square in New York if one actually has to be at Union Square in San Francisco.

• A critical point to keep in mind is that the exposure assessment and health risk determinations in the form of IQ losses laid out in Chapter 4 Tables in the draft Staff Paper are only for current c onditions (see related discussi on above) and the associated

dust and soil lead increases reflect this curre nt state. Percent frequency of measured

children’s Pb-Bs ≥ 10 in the Herculaneum area, especially for areas closer to the smelter, accord with exposures that appear much higher than what is modeled in the upper tails of

Pb-B here.

• The 2002 screening of Herculaneum ch ildren’s Pb-Bs by ATSDR showed 14% ≥ 10 μg/dl.

Refs:

ATSDR Health Consultation.2002. Herculaneu m Lead Smelter Site, Herculaneum, Jefferson County, MO. Blood Lead Results for 2001 Calendar Year.

ATSDR Health Consultation.2003. Herculaneu m Lead Smelter Site, Herculaneum, Jefferson County, MO. Blood Lead Results for 2002 Calendar Year.

• A second critical point is that the exposure and risk assessments are for the spatial reach of 10 km, while much of the Pb-B historical data have been gathered for child exposures close to the smelter, within a mile or so (1.5 km).

• The 2003 CDC sampling of Pb-B levels for ch ildren in the secondary smelter (Troy, AL)

area needs to be evaluated for those results li kely being driven by lead emissions from the smelter. Presumably, this secondary smelter community was selected in the first place because there were no other significant lead emitting point sources voiding the case study entry criterion that there be one principal lead source.

• The 2003 CDC Pb-B data for the secondary sm elter community needs to be broken out via such devices as zip code exceedence frequencies and name-redacted Pb-B measurements for group-stratified Pb-B fr equency dependence on proximity to the facility.

• The authors don’t seem to connect with the fact that if a count ywide Pb-B elevation frequency is 8%, 1-in-12, as determined by the 2003 CDC sampling, and this overall frequency occurs from and is driven by th e secondary smelter emissions, the reported frequency is very likely a dilution of the highe r frequency of Pb-B elevations closer to the facility, i.e., the latter is >8%.

• Overall, the Herculaneum projected soil Pb levels as medians are quite low [Table 4-5]

, and approach typical background soil lead levels at many locales. The background soilF-41 lead value for comparison with Herculaneum would be that of unimpacted agricultural soils distant from the primary smelter. This background is on the or der of 50 ppm Pb or so. Soil recontamination and the likely elevat ed soil Pb levels for unremediated properties in the 8.5 km spatial interval from 1.5 to 10 km would clearly produce much higher soil Pb due to more than 100 years of lead deposit ions. A problem at this site is the relative absence of measured soil (and dust) lead levels beyond the immediate impact zone.

• This draft remains unclear about the flexib ility of multi-layer se quential modeling to permit differentiation between current c onditions, i.e., new air Pb inputs to compartments, versus the historical Pb levels already in place give n the complexity and unwieldy nature of a multi-layered, multi- case study methodology. Results from this approach show sequential points of questi on in any differentiation of current from historical Pb impacts at the locales chosen. Pediatric blood lead levels were modeled as very low at these two smelter sites despite Pb-B screening data: ATSDR results for Herculaneum, CDC results for Pike County, AL [Tables 4-7, 4-8: Leggett and IEUBK outputs] . In some cases the modeled Pb-B valu es are actually approaching detection limits and typical laboratory meas urement variability of Pb-B (

 1-2 μg/dl). There are the median Pb-B levels ranging from 0.7 to 1.8 μg/dl for the primary smelter case [Table 4- 7, current conditions and NAAQS attainment s cenarios, both biokinetic models used in both modes] and a primary smelter 95t h percentile value of 2.0 μ g/dl [Table 4-7; concurrent Leggett, both current conditi ons exposures and NAAQS attainment exposures].

• There are the median Pb-B levels in a range of 0.5 to 1.5 μg/dl for the secondary smelter

case [Table 4-8; model-only and hybrid ca ses, both models, both Pb-B metrics] and a secondary smelter 99th percentile value as low as 1.4 μg/dl [Table 4-8; model only, Leggett concurrent].

• These very low Pb-Bs will give rise to IQ decrements that would be minimal or

nonexistent [Table 4-13, primary smelter, cu rrent exposures; Table 4-14, primary smelter, NAAQS attainment; Table 4-15, s econdary lead smelter, modeled only; Table 4-16, hybrid] . The primary smelter case results [Tables 4-13, 4-14] would have us believe that children in proximity to an ope rating primary lead smelter would have no more than a 1-in-100 chance (99t h percentile) of having an IQ loss of as much as 3 points [Tables 4-13 & 4-14] and a loss of as little as <1 IQ point [Tables 4-13 & 4-14, Leggett lifetime Pb-B metric, both current and NAAQS attainment scenarios]

.

• The secondary smelter case results [Tables 4-15 & 4-16] are equally lower than expected, given the weight of the empirical evidence. In particular, the modeling shows an operating secondary lead smelter has no likelihood of producing any IQ point loss in virtually all combinations of risk modeling depicted in these two Tables. In fact the highest modeled loss of IQ points is 2, for wh ich there is only a 1-in-1000 chance (99.9th percentile) [ Table 4-16, hybrid scenario, concurrent IEUBK ]. The modeled soil approach for the secondary smelter shows [Table 4-15, IEUBK concurrent Pb-B] IQ point losses of 1, 1, and <1 for the 99.9, the 99.5 and 99th percentiles re spectively.F-42 • The authors would have the Panel believe th at the authors could legitimately create a hypothetical threshold of either 2.4 or 6.0 μg/dl for whatever arcane purpose in Pb-B in the absence of any biological or toxico logical evidence suppor ting this step. The literature and expert consensus documents support a conclusion of no thresholds to effects so far. The authors cannot simply ar gue that there’s uncertainty below the range 2.4 - 6.0 μg/dl. Uncertainty cuts both ways. There is no more argument for setting a threshold for IQ decrements in this region th an there is for not setting one. Setting a hypothetical threshold is not simply an arbitr ary computational step. A threshold to lead toxicity indexed as blood lead has implications for multi-endpoint toxicity in children and implies a toxicological mechanism of action th at has not been accepted for low-level lead neurotoxicity by the scientific and health communities.

• Besides scientific objections, an arbitrary setting of a Pb-B threshold for adverse effects would appear to violate the statutory language in Section 109 of the CAA. That section mandates use of an “adequate margin of sa fety” for those effects (or accompanying doseresponse relationships) not fully amenable to quantification. Use of a purely arbitrary “hypothetical” threshold clearly violates the “adequate margin of safety” mandate in Sec. 109 while avoidance of any threshold accords with an adequate margin of safety and is

therefore in accord with 109.

• Have the authors characterized the air Pb emi ssions for this primary smelter in terms of expected correlations with Pb production ra tes, and are NAAQS attainment achievements or failures artifacts of the lower or higher ope rating levels of the smelter in response to variable demands in the prevailing metal markets? The instability of smelter lead production rates due to market fluctuations means that “current conditions” have an economic component as well as environmental ones.

• The projected operating secondary lead smelter air lead levels are also low, but much lower than the primary smelter results. This relative ranking is expected, being five-fold

lower at the median and 33-fold lower at the 95th percentile. Ho wever, the absolute levels seem lower than the bulk of the globa l literature on such facilities indicates and that the two site monitors would suggest.

• The Pilot support draft implies that this secondary smelter is not a particularly clean one, having lead emissions over 1997 to 2000 (three stack tests) that rank it as the third highest lead emitter of 15 remaining U.S. sec ondary smelters. Further evidence of a dirty facility are the two lead mon itor results, which indicate ambien t air levels that lie within the top 15% of air lead levels for secondary smelter re leases nationally. Furthermore,

information in the Pilot draft indicates that 2003 air lead monitori ng data off-site may indicate this operation is ge tting dirtier via higher producti on rates or equipment aging

and failures.

• There are other complications as well. The primary smelter owners in 2002 and before bought 160 of the homes closer to the facilit y. This block of purchased homes would not represent a typical hou sehold occupant distribution for purpose of census tract modelingF-43 and would not fall within modeled dust and soil lead values. How have the authors dealt with these 160 smelter-owned properties?

• Herculaneum is also a community with a long history of exterior a nd interior dust lead levels and loadings. Dust lead levels in Herculaneum homes measured in 1992 were as high as 6000 ppm in children’s bedrooms. An ear lier set of interior du st Pb tests showed an average of ca. 1900 ppm and a maximum of 8,300 ppm. Exterior street and curb dusts measured in August 2001 showed lead conten t as high as 300,000 ppm on roads used to

haul lead concentrate. The authors used m easurement data for 17 homes to capture this

accumulation.

• It is unlikely that the above interior dust, wh atever the soil lead abatement efforts, would have ceased being released from interior reservoirs. It is also unlikely that road surfaces having 30,000 to 300,000 ppm would have been remediated enough by washing to void

this as an exterior dust Pb reservoir. It is likely high external dust reservoirs as well as

interior dust reservoirs rema in. Also relevant to exterior dust levels, a March 2002 testing

of a Thurwell St. address closer to the sm elter showed a porch eave lead loading of 24,400 μ g/ft 2 with associated high cadmium and ar senic levels. Co-occurrence of high

arsenic and cadmium levels rule s out porch lead paint and ru les in a geochemical source.

NHANES National Pb-B Data are no Validation of the Modeling Results for Pb-B in Three Specific Locales

The authors seem to take comfort in noting th at the modeling results are sort of in line with the latest NHANES survey data. The main probl em with this is that one cannot disaggregate the statistical design and nationa l snapshot numbers from an NHANES survey for the nation as a whole into site-specific Pb-B distributions . The 1988 ATSDR report to Congress on childhood lead poisoning in America makes clear that one cannot use data for the nation as a whole for comparisons to geographic areas smaller than the nation. The Executive Summary in this Congressional report no tes on p. 4, top, that:

“Valid estimates of the total number of lead-exposed children according to SMSAs [Standard Metropolitan Statistical Areas] or some other appropriate geographic unit smaller than the Nation as a whole cannot be made, given the available data. The only national data set for Pb-B levels in children comes from

the National Health and Nutrition Exam ination Survey II (NHANES II) of CDC’s

National Center for Health Statistics. The NHANES II statis tical sampling plan, however, does not permit valid estimates to be made for geographic subsets of the

total database [Italics added for emphasis].”

This caveat to localized use of national NHANES II da ta was provided to me as the senior author of the Congressional report from the contributin g authors representing th e National Center for

Health Statistics.F-44 Alternative Approaches

• Given all the problems inherent or demonstrab le in the case-study approaches in this draft, why is this approach atthe end of the risk assessment day any more useful than any alternative that begins with use of actual environmental lead levels derived from measurement data at source-oriented monitoring sites. Specifically, the data for the 59 air Pb monitoring sites for nationwid e industrial source ai r lead levels depicted in Figure 2- 12 and text, p. 2-31??

• The driver for modeled lead exposure distribu tions (Pb-B) and modele d risk distributions (IQ loss) in any approach, and for this Pilot assessment, is simply the environmental lead inputs to the exposure models and the resulti ng Pb-B outputs being used for inputs to the IQ loss modeling. The exposure and risk result s in the Chapter 4 Tables for the case studies are what they are mainly because the environmental lead inputs, especially air, dust and soil Pb, are what they are modeled to be.

• Based on these 59 source-oriented sites describe d in Fig. 2-12, measured air Pb levels for source-oriented monitors give air Pb distributions that are well above the air lead

measurements and distributions for areas w ithout lead source-oriented monitors. For example, medians for the former are 16X highe r than for the latter. A key component of looking at Pb NAAQS for revision or other di sposition is to first look at where the air lead is. Approaches that maximize use of m easured data to show where air lead is do

have merit.

• These 59 air lead monitor sites are known, thei r distances from the major lead sources are known for purposes of modeling soil and dust lead, their census unit child populations and demographics can be determined, etc., so statistical analyses and media Pb modeling

from air lead can be done. It is not clear that policy-relevant partitioning of air lead levels from the 59 monitors pose any greater probl ems than do the assumptions and limitations in the case-study approach.

• Comparison of air Pb distributions for all th e lead source-depicting air lead monitoring data on p. 2-31 with modeled data tabulated in Chapter 4 (Table 4-4) is done in my

Comments Table 1 at the end of this comme ntary. The measured air Pb values greatly exceed the dispersion-modeled air Pb values, as seen with the median and 95th percentile values for the secondary smelter case study modeled air Pb levels given in Table 4-4

. The ratio of measured vs. dispersion modeled ai r Pb for the secondary smelter scenario at the 95th percentile (where th e Pb-exposed individuals woul d be those nearer to the secondary smelter), is 107, giving two full or ders of magnitude underestimate when using modeling.F-45 II. SPECIFIC COMMENTS

Chapter 1, Intro

pp. 1-3, 1-4 The discussion here of “adequate margin of safety” indica tes that one cannot arbitrarily set a threshold (to effects) that actu ally voids an “adequate margin of safety.”

Chapter 2, Characterization of Ambient Lead

p. 2-24, Figure 2-6. It is troubling that only 2 of 26 f acilities (both lead smelters) having emissions of more than 5 tons/year have a NAAQS compliance monitor within one mile. This would appear to limit the reliability of the data depicted in Table 2-4 a nd Figures 2-2 and 2-3 for areas closer (<1 mile) to the emission sources. The actual amount of air lead measurement data

for ambient air lead in the NEI 2002 must be a ssumed to be significant underestimates for the national air lead picture.

p. 2-28, Figure 2-10. It is also troubling that the air lead monitoring trend data were gathered for monitors that were principally set up as a f unction of (urban) population density, presumably areas with high vehicular densities and associated mobile lead source relationships. They were not set up for depicting point sour ce-impacted air lead levels. While the trend curves in 2-10 say

a lot about mobile source lead d eclines, it’s problematic what they could say about the major source emissions depicted in Table 2-4.

p. 2-30, Figure 2-11 and text This discussion and the figure are important for comparisons with earlier text (p. 2-24, Figure 2-6). The discussion also offers some peculiar reasoning in terms of significance of air monitoring data that do and don’t reflect capture of industrial emissions. The earlier text noted that only two ai r lead monitors were set up to more reliably capture air lead releases and these were for smelters. This Figur e 2-11 says that data from 224 monitoring sites

were used.

p. 2-31, Figure 2-12 and text Figure 2-12 requires further discu ssion in appropriate context. The

median air lead value for the 59 source-oriented sites is 0.252 μ g/m 3 and for the 95th percentile

is 1.923 μ g/m 3 . These values greatly exceed the correspond ing scenario modeling of air Pb given in Table 4-4 of Chapter 4. Comment Table 1 gives ratios of measured to dispersion-modeled air Pb. In the Comment Table, the rati o of the 95th percentile of record ings of air Pb levels for the 59 sites is over 100X higher th an the corresponding modeled fi gure for the secondary smelter

scenario.

Table 2-7, p. 2-37 This is an important Table in that it shows the impact of averaging times or

forms for determination of fractional exceedence of standard levels and shows why expressions of the form and averaging time ar e as important a consideration as the level of the NAAQS itself. The maximum monthly average, as mathematica lly expected, always shows more exceedences than the other averaging and form combinations. As the reference air Pb levels increase, the ratio of maximum monthly average to 3-year annual average in creases greatly.F-46 p. 2-46, Findings and Limitations This is an important discus sion, since it states the major limitations of this approach of using case studies.

p. 2-47, Air Quality Summary This summary correctly notes that the 30-day maximum average will capture more instances of elevated air lead excursions than the present quarterly maximum average. The reason for a 30-day average should al so be expanded to include the fact that we know that air lead changes produc ing children’s Pb-B changes are better captured over 30 days than a quarter. The authors should check the Pb AQCD for information on this.

p. 2-49, Sec. 2.6 The authors need to include exterior dusts on outside play surfaces, which can be a significant source of dust l ead ingestion during play activities outside in warmer months and in warmer areas of the country.

p. 3-1, dose-response Authors need to point out that low-dose lead effects occur with no

definable threshold indexed as Pb-B so far.

p. 3-14, Discussion of threshold cut points I have already stated criticisms of any use of threshold cut points in my general comments earlier.

pp. 4-1, 4-2 Ch. 4 Intro There is too little regard ing the criteria for selecti on of case study locales. Also, there are no discussions on alternative gene ral approaches to the case study approach. The primary operating smelter is necessarily confin ed to one choice, but there are 15 secondary

smelters to choose from and an almost infinite set of road stretches wi th reentrained roadside

dust lead.

On p. 4-1 , What exactly are “buffered” populations not ed in footnote 2 in terms of quantifying lead exposures?

p. 4-20, discussion of hypothetical threshold to Pb neurotoxicity See discussions on the topic in my general comments.

p. 4-38, IEUBK There seems to be some author conf usion on application of the IEUBK model for childhood exposure. The model cannot be used for just community-wide expressions of lead exposure, and this proscription is stated in the IEUBK manual (1994). The model applies to a typical child or set of children, e.g., siblings, at a given lead exposure unit. EPA considers the exposure unit for regulatory actions at, say, Supe rfund sites to be the residential property, house plus yard. One can of course derive batch mode statistical comparisons for modeled vs. measured Pb-Bs etc. using all the indivi dually modeled Pb-Bs derived for each residential exposure unit vs. their measured Pb-B. The broader the modeling ne t that’s cast, the highe r the required geometric standard deviation (GSD) and the higher the probability of more than one set of Pb-B distributions, for example a subset of child ren at lead “hot spots,” being missed.

Table 4-3. IEUBK input parameters See earlier comments. The soil/ dust bioavailability data are confusing. Dust Pb is stated to be about half th at of soil lead, 26% vs. 48 %. Typically dust Pb is

more bioavailable than soil Pb because of smaller particles in dust, dust Pb in more bioavailable chemical forms, e.g., lead oxide dusts from smelte r emission lead fallout from air, etc. The 48%F-47 for the primary smelter case is virtually the same as bioavailability of fully soluble simple lead salts, e.g., lead acetate, which are considered to be 50% bioavailabl e. That is, the most one ever encounters as an uptake fraction from the human gut, which is the case for very young children, is 50%, based on available data. The assumption of only 30% absolute lead bioavailability for secondary smelter and roadside soil scenar ios are the model default selections.

p. 4-45, GSD for Population. I follow the logic of Dale Hattis ’ estimates in the cited paper about use of a higher GSD nationally for current lead exposures compared to the national 1.3 to 1.4 used in the 1986 lead criteria document, Chap ter 11 (Table 11-9, p. 11- 30). I don’t quite follow the logic of why a smaller GSD than that given by Hattis for a national increase in GSD is used for the primary and secondary smelter scenario s when historically separate and cumulative fugitive dust emissions may behave as bei ng uncoupled from current stack emissions.

The Midvale case is not the only Western smelte r/milling site with Pb-B data. Bornschein and colleagues at the U. of Cinci nnati have done a number of these as have other groups such as local and state health departments. Some sites have produced GSDs greater than 1.6.

p. 4-46, Sec. 4.3.4 I would point out the need to disc uss a bit more the “NAAQS attainment” assumptions as part of the modeling for the primary smelter case study. The validity of the scenario is predicated on some high expectati ons that attainment is a good probability. However, nonattainment has typified monitoring results fro m this operation. The noncompliance is current, is significant as to level of ex ceedence, and is likely to get much worse if a 30-day averaging vs. quarter averaging time is selected.

p. 4-48, Table 4-6 footnote The footnote says that outdoor soil has less of an impact the further away one is from the facility. That may be ge nerally true, but unremediated soils outside the maximum impact zone would still have accumulate d soil leads and internal dust reservoirs that are under-represented by modeled soils in these more remote quadrants that don’t account for the 100-plus years of contamination.

Secondly, the authors need to keep in mind that soil lead remediation around the Herculaneum smelter was triggered by soil lead leve ls at or above the action level. Unremediated soil lead areas farther away from the smelter do not indicate that they were unaffected or not elevated above background, merely that they were below the selected action level.

The calculation I indicated earlier using EPA’ s own equations and data showed a soil lead accumulation rate of 3 ppm/year for each 1 μ g/m 3 air Pb. That would say that an average soil Pb at more remote quadrants from the smelter that would have, for example, only 1 μ g/m 3
would be 300-plus ppm for 100-plus years of lead emissions. The median projected soil Pb for the primary smelter in Table 4-5 is 84 ppm.

p. 4-59, 4.4.1.2, 4.4.1.3 There is no basis for running the pr ojections with the cut point, for

reasons noted earlier. Please also run without the cut point or, pr eferably, don’t use an arbitrary cut point that appears at odds with the CAA, S ec. 109 requirement for an “adequate margin of safety.”F-48 p. 4-62, Table 4-13 . It is not convincing that a group with a 99th percentile Pb -B of 6.8 (Leggett, lifetime average) would show no imp act at all on IQ (< 1 point) at the 99th percentil e in view of the dose-neurotoxic response statistics presented in Lanphear et al. 2005.

p. 4-78, top half . This is a typical example of the author s flagging or highlighting variability or uncertainty that overestimates the risk results, but not the many elements of underestimating.

III. RESPONSES TO CHARGE QUESTIONS FOR CHAPTER 4

1. To what extent are the various aspects of the exposure analysis technically sound, appropriately balanced, and clearly communicated?

This overall effort, for reasons given in th e above general and specific comments, has technically sound components and some problems. There is a mixed picture for balance. Clear communication is a challenge. See my general comments.

2. Are the methods used to conduct the pilo t exposure analysis...pathway apportionment...versus background technically sound?

Overall, the exposure analysis in the pilot draft is sound only to the extent that the biokinetic models used are crunching on s ound environmental Pb inputs to produce sound

results. The biokinetic construction of the models is generally O.K.

3. What are the Panel’s views on the staff inte rpretation of performan ce review...for the pilot analysis...with regard to representativene ss of the individual modeling steps?

See my general and specific comments. Macros copic reality checks and knowledge of the measured local and the measured global litera ture for these case st udy sites are needed.

4. Are the Pb-B metrics used in the pilot analy sis appropriate...?

Yes.

5. Are the methods used to conduct the pilot he alth risk assessment...technically sound? Does the Panel have any sugges tions for improvement?

The health risk dose-response functions for use later in th e draft are generally sound. The use of a purely arbitrary cut poi nt is not valid. See my general and specific comments. A recommended improvement is dispensing with the notion of using arbitrary cut points.

6. To what extent does the sensitivity analysis...i dentify key areas of uncertainty in this pilot analysis?

See my general and specific comments.F-49 7. As part of the NAAQS review...there is in terest in ...differentiating...historical and deposited...newly deposited...air lead? Does the Panel have ...recommendations...that might be employed...?

See my general and specific comments above. Firs t, it is critical to keep in mind that “new” lead inputs to soils and dus ts, the latter being th e main exposure drivers, are continuous so long as air Pb input is continuous. “New” Pb i nput simply becomes a rate by which one will get to historical accumulations over the long term. Th e short term is not the ultimate question, as I made clear earlier, referring to modeled data in Tables 4-4 and 4-5. Secondly, it is equally or even more important to recognize that all sources of lead bei ng ingested by children, i.e., the ingested sum of historical soil and dust lead pl us newly produced dust an d soil lead all contribute to absorbed lead. Toxicologica l dose-response relationships do not biologically differentiate between the two temporally different histories for the ingested lead.

Third, it is not necessary that newly emitted lead, inhaled directly or as lead newly entering as dust and soil lead for ingestion, is required to produce al l the dose (exposure) for

harmful effects. A minor amount of new lead can add enough to a large historical fraction of lead to push the dose metric into the ne xt category of toxic risk. I prep ared dust lead loading tables entered into the review record for the AQCD revi ew early last year show ing that dust lead on a

hard surface rises to a ha zardous level with an interi or air lead level of 0.1 μ g/m 3

.

The seemingly endless dissection of compone nts of this draft staff paper such as fractional or “policy-rele vant” lead sources and fractional ex posure contributions into regulatory

salami slices strikes me as a somewhat stat utorily Balkanized exer cise with no apparent redeeming feature, toxicologi cally or epidemiologically.

There is little scientific evidence to for ce disaggregation for some ranking purpose of what toxicologically is a con tinuum of exposure producing signif icant risk down to very low exposures. The impact of even modest new ai r Pb entering the dose-re sponse continuum to produce some risk impact argues for both air Pb as a criteria pollutant for regulation via the Pb NAAQS mechanism and revising the NAAQS to a much lower level than this current and

indefensible 1.5 μ g/m 3

.

8. What are the Panel’s views on the most important issues to be addressed...in the fullscale...assessment that will be presented in the revised documents?

One significant issue is that of a clea r presentation of the us es and limits of the methodology and results for the three selected sites. A second issue is to establish the overall validity of the collective approaches used in this pilot draft. Unless this pilot approach can be shown to be scientifically sound, there is little argument for doing much more of the same with more case studies. Thirdly, there is the issue of how the current approach accurately addresses the relative importance of “new” versus “historical” lead inputs and what this means over time.F-50 COMMENT TABLE 1. Measured a nd Modeled Air Lead Levels ( μ g/m 3 )

Pb-Air Metric Measured Air Pb

a Primary Smelter Dispersion Modeling b

Current

Condition Secondary

Smelter Dispersion Modeling b Ratio (rounding)

c

of Measured to

Modeled Data

5 th percentile 0.019 0.008 0.001 19/8

25 th percentile 0.081 — — —

Median 0.252 0.022 0.005 50/4

Mean 0.484 — — —

75 th percentile 0.695 — — —

95 th percentile 1.923 0.662 0.018 107/3

a = Air Pb distributions from data for 59 air Pb monitoring sites, p. 2-31.

b = Table 4-4, draft staff paper.

c = Ratio measured to secondary smelter cas e/ ratio measured to primary smelter case.

PRE-MEETING COMMENTS:

LEAD HUMAN EXPOSURE AND HEAL TH RISK ASSESSMENTS AND

ECOLOGICAL RISK ASSESSMENT FOR SELECTED AREAS

PILOT PHASE

EXTERNAL REVIEW DRAFT

Reviewer: Paul Mushak, Ph.D.

I comment on the human impact chapters and leave the welfare and ecotoxicity issues in Chapter 7 to others. Many general comments would be those already stated as to key points in the draft staff paper and are not repeated here. However, I have some additional ones. I mainly have specific comments across the Chapters.F-51 I. GENERAL COMMENTS

The overall clarity of the draft is good.

The pilot draft seems to lag in its informa tion relative to the staff paper draft. For example, discussions on determination of environm ental lead in relevant media seem somewhat disconnected in the pilot document from the parallel section in the staff paper.

Chapter 2 (draft Sec. 2.1) does not spell out in any detail why the particular case study sites were chosen. It particularly does not rank the criteria for se lection of the secondary smelter and roadway dust case studies. The primary smelte r selection, of necessity, was the only one operating.

For the secondary smelter case study, it appear s that the more important criterion was availability of more recent ai r Pb monitoring data and not neighboring population numbers. Both Herculaneum, MO, and Troy, AL are very sm all communities. I assume a second criterion ranking higher than impacted population size was th e presence of the one principal (e.g., smelter) point source. This would steer toward more remote sites with few other lead point sources. There are about 15 secondary smelters and potentially endless stretches of road ways with reentrained dusts with Pb (from former use of l eaded gasoline) as the point source.

I would add to this list, for purposes of performance evaluation, the availability of exposure data indexed as blood l ead (Pb-B). These include the ma ny reported Pb-B testings at Herculaneum done by ATSDR in 2001 and 2002 and earlier efforts, and the 2003 CDC Pb-B survey done for Pike County, AL, the site of the secondary smelter. For the latter, the authors need to do some spatial stratification of elev ated Pb-B frequency versus distance from the secondary smelter.

As I also noted in comments for the draft sta ff paper, the overall driver for the results from these case study analyses are the environmental lead levels, in terms of the relative levels of variability and uncertainty. Th e exposure modeling uses reasonably understood biokinetic models and the dose-response relationships for mode ling health risk, especi ally for IQ loss, are

also well understood.

II. SPECIFIC COMMENTS

Chapter 2, Overview of Risk Assessment

p. 2-10, Table 2-4. The information for the primary and secondary smelter environmental media determinations is a bit confusing. For soil P b, the secondary smelter case study used both modeled and “hybrid” data, the latte r entailing use of some measured soil Pb from another site, Corpus Christi, TX. Here, the entry noted “mod eled” soil Pb based on ai r deposition. Similarly, the indoor dust Pb at the secondary smelter site is referred to as being “estimated” from ambient air levels. My understanding is that the sec ondary smelter indoor dusts were modeled from

modeled air Pb via the three stack tests.F-52 The Table notes that indoor air levels were based on ambient air and soil levels. But the

authors did use interior dust valu es from 17 homes as part of a ll the calculations, correct?

p. 2-11, 2nd par. The soils at the remediation zone in Herculaneum will continue to rapidly accumulate Pb from recontamination. See my comments for the draft Staff Paper.

p. 2-12, Secondary Pb Smelter, top The text indicates only mode led soil and dust PB. However,

the actual soil lead values in the model arose from both “mod eled” and “hybrid” approaches. Footnote 3 notes that the regres sion-based Pb-B model of Lanphear et al., 1988, was only used in the sensitivity analysis.

Chapter 3, Case Study Descriptions

Chapter 3 deals with the measur ed data sets available for environmental lead for the three

selected sites. These data sets were used to ch aracterize what has been measured over the years

for lead in various media of interest to the documen ts: air, soil, dust, etc. These data sets were not the principal means for determining current condi tion lead levels in the media. The exercises used in the drafts to get these current levels entailed modeling, beginning with modeled air Pb using dispersion models crunching on stack emissi ons plus some level of fugitive dust burdens. Measurement data mainly appeared to se rve for checking modeling performance.

p. 3.1, Sec. 3.1 Intro This par. should be clarified to s how that both historical media lead

accumulations and remediation soil lead were elev ated and the rate of elevation of Pb in lowlead, post-remediation soils show ed a rapid rate of recontamin ation. Appendix A contains the various stages of soil Pb sampling: pre-remedi ation, post-remediation (s oon after clean-up) and

recontamination.

pp. 3-4, 3-5 The various rounds of Pb-B testings are plagued by factors that tend to underestimate exposures indexed as Pb-B eleva tions and exceedence fr equencies and both the authors and the readers should keep that in mind. First, the ATDSR samplings were not structured surveys of statistically valid design that would better reflect true distributions and exceedence frequencies. They i nvolved voluntary efforts by mainly the MO health department in which children showed up for testing in each of two years: 2001 and 2002. Some showed up for both years.

The Pb-B levels rise to a peak in young children during the Summ er, being at maximum around August. Collection of Pb-B samples throughout the year obscures the seasonal impact on the level of Pb-Bs, in that Pb-B testing in o ff-peak, colder months w ould yield lower results versus a structured survey done in, say, August.

The child data for 2001 and 2002 are only broke n out for ages <72 months. However, within that larger risk band, th ere is a highest risk band for infants and toddlers. One would expect that prevalences of Pb-Bs

 10 μg/dl for tested children 12-30/36 months would be higher.

This relative increase was in fact seen and is noted in the Ju ly 13, 2001 ATSDR Health consultation for the Herculaneum area (see below). Other sites show this child age stratification, e.g., the Human Health Risk Assessment (HHR A, 2001) done for the lower Coeur d’ AleneF-53 River Basin in Idaho by Idaho and EPA Region X. The ID HHRA showed significantly higher Pb-B exceedences, within the overall young child age band, for children 24 months or less.

Other factors may or would reduce exposures indexed as Pb-B. The distribution of people showing up for testing in the 2002 year as a func tion of distance is not noted. We don’t know if a lighter or heavier weighting is occurring by w ho shows up vs. where they live. That is, the participant selection bias is unknow n but potentially troublesome. If the relative testing of older children entails more than younge r children within the 71-month age band, the exposures for infants and toddlers are under-represented. Seco ndly, the smelter owners bought a number of

residences closest to the sme lter around the 2002 time frame. Where renting of these houses was permitted, the owners barred families with children. So, the newest data set versus older sets would have a reduced sampling popul ation for the high risk zone.

The 2000 Herculaneum Pb-B Study showed ther e still was a major blood lead elevation problem for 0-6 y. preschool childr en in Herculaneum, especially for children closest to the smelter. It is not clear that the data were gather ed in a way that they could be compared to past years in terms of past blood lead results. Each ad-hoc screening appe ars to have been done differently, which frustrates even simple or crude comparisons. We do not actually know how real or rapid the blood lead decline rate has been.

The August 2000 Pb-B survey results are tabul ated in the ATSDR Health Consultation dated July 13, 2001. Table 7 shows the age depende nce of Pb-B elevations for the Herculaneum community and Pb-B statistics for children when te sted in August. For chil dren 1 to 3 years of age, the highest risk subgroup, 4 of 13 children or 31%, had a Pb-B 10-20 μ g/dl and 1 child of the 4 had a Pb-B >20 μg/dl. Earlie r testings 1/95 to 6/99, recorded in Table 6 of this report also showed high frequency of elevated Pb-B. Tabl e 6 notes, for 100 children 5 to 21 months old,

43% had Pb-B

 10 μg/dl.

p. 3-6, Table 3-5 and Appendices A-6, A-7 Residential soil recontam ination rates are significant for the residences tested, showing recontamina tion from 2002, when the MO DNR released their own recontamination figures, to 2006 (see the re levant citation in my comments on the draft paper. Table A-7, Appendices, indi cates that many of the 31 remedi ated soil locations showed a

2 to 4-fold increase in lead 2002 to 2006.

p. 3-8, Pb deposition into soil boxes Soil lead in 10 boxes placed around the site indicated that over the course of one year, 2003 to 2004, mean Pb content doubled, from 49 to 97 ppm Pb, an increase approaching 50 ppm. At this rate, th e EPA child Pb hazard standard of 400 ppm for

contact soils would be achieved in about 8-9 years. It is not cl ear whether the ten soil test boxes were placed on any of the 31 prope rties also selected for testing total yard surface contamination.

It would have made sense to do so.

Ibid, Indoor Dust The problem, as recognized in the draf t, is that one has ongoing and variable dusting of residential interiors. Unless one is using undisturbed household surfaces or, better yet, dust plate deposition methods, the va riable cleaning factor is diffi cult to separate from dust fall rate variability. Lead loadings, in any case, are less sensitive to housekeeping than dustF-54 concentration, and this characte ristic was first tested by Milar and Mushak, 1982, who presented lead loading methodology versus use of lead concentrations.

Ref:

Milar CR, Mushak P. 1982. Lead-contamin ated house dust: Hazard, management, and decontamination. In: Proceedings of the C onference on Management of Increased Lead Absorption in Children: Management, Clini cal, and Environmental Aspects. JJ Chisolm Jr, DM O’Hara, Eds. Baltimore, MD: Urban and Schwarzenberg, pp. 143-152.

p. 3-14, Sec. 3.2.3 It is not quite true that there were no Pb-B data around the secondary smelter. There was a 2003 CDC survey for the county cont aining the smelter. It would have been inconceivable that the Pb-B sampling would have ignored areas close to the secondary smelter. As I noted elsewhere, the authors need to brea k out the results via various means. Presumably, the AL health department has these data. I would have to assume that CDC did a Pb-B testing in Pike County in the first place because of the s econdary smelter. The Pb-B elevation rate was over three times the AL rate, and was also likely due to the smelter.

Chapter 4, Estimates of Media Concentrations

p. 4-2, last par. Are these six census blocks mentione d those corresponding to blocks of properties purchased over the years by the smelter owner?

p. 4-5, Sec. 4.1.2.3 What exactly is the point of doing an “attainment” scenario for a case study involving an operating primary smelter which has ra rely been in attainme nt. It’s a hypothetical case. This strikes me as the triumph of EPA’ s modeling hopes over its regulatory experience with this particular site. Would it not be more realistic and protect ive of public health to assume

some level of non-attainment in term s of air Pb and go from there?

p. 4-9, Table 4-4 This is a significant Tabl e, in that it says that once one goes beyond 0.5 miles from the main stack using Region 7 HiVols data , for a total modeling re ach of 10 km (6.3 mi.), the dispersion modeling markedly underestimates air Pb, up to 5.4 times, monitored vs. modeled. Similarly, for “AirData” results, distances be yond 1.7 mi., for a total modeling reach of 6.3 mi,

the modeled air lead values underestimate the m easurement data, as much as 7-fold lower.

p. 4-21, Sec. 4.2.1 More to the point, the 2003 monitoring data showing the exceedence of the current NAAQS (1.9 units) indicate that the modeli ng of air Pb for the se condary smelter site would be underestimating actual air Pb.

p. 4-27, Sec. 4.2.2.4 The underestimation of the seconda ry monitoring results when using

modeled results is rationalized based on diffe rences in actual site meteorology versus meteorology used. This is puzzling, since the signif icant differences in the primary smelter case did not encounter meteorological disparities.F-55 p. 4-30, Sec. 4.2.3.1 The authors note that using just mode led soil levels, the results were threefold lower than a comparison secondary smelte r site, studied by Kimbrough and Suffet in a 1995 report. The smelter was in an urban area. We re other media levels measured as well?

Chapter 5. Human Exposure Assessment and Blood Lead Estimations.

p. 5-2, 1st full par. I have looked through both drafts (sta ff paper and pilot) and don’t see actual counts of children by census block groups or an y other Census Bureau metric. However, the authors have these numbers, since they say so on p. 5-2, and used such numbers in generating central tendency estimates from the models. Is th ere a place in one of these chapters to lay out child counts at least by distance from the smelters? Some of the other, earlier data sources in the

case of Herculaneum do break out total childr en’s representation inthe town population by

distance from the smelters. Counts of children are also useful for matching up areas of

underestimation and overestimation of modeled data with the child count a nd the fraction of total counts impacted.

p. 5-9 to 5-11, 5.1.3.3 I am astonished that the significan t changes in the construction of the original Leggett (Pounds Leggett) core (Fortran) constr uction, done for the specific needs of the pilot analyses, were done without any input from the SAB’s All Ages Lead Model review Panel,

who reviewed the various models and their useful ness for EPA’s regulatory use. I do not see, in Chapter 8: References, any reference to the va rious reports from the Panel to EPA pointing out the usefulness of Leggett and other biokinetic mode ls for modeling of risk. What validating steps were taken for these changes?

p. 5-21 to 5-22, Table 5-11 See also my comments for the draf t Staff Paper. Since submission of my comments on the draft Staff Paper for questio ns of bioavailability for IEUBK model use, I have been in touch with Dr. John Drexler, Univ ersity of Colorado-Boulde r, who did the in-vitro, bioaccessibility testings for Herculaneum environm ental samples. The in-vitro bioaccessibility testings were done in collabora tion with Drs. Casteel and Br attin, who did the young swine invivo studies for Herculaneum site samples. I have not yet contacted the la tter investigators, but Dr. Drexler’s results point to their results as well.

First, the dust Pb and soil Pb values as indicated —0.48 soil, 0.26 dust— are correct for

the indicated media and these fractions are abso lute bioavailability figures and not relative bioavailability. The term “accessibi lity” (or “bioaccessibility”) s hould be dropped in the present context, because it has a meaning different from bioavailability, the actual uptake rate of lead

from the GI tract.

The anomalous uptake fractions for dust vers us soil are rationalized from the Drexler speciation data, showing more oxidized (and more bioavailable) forms of the starting galenic (PbS) lead form in soils, but higher fractions of pe rsisting galenic Pb dusts in the interiors of the tested residences. However, bioaccessibility in th e Drexler in-vitro testi ng as indicated shows the small galena particles in these an alyses translated to absolute bioavailabilities of .29 for dusts and .41 for residential soils, not materially different from the in-vivo young swine results (0.26 and 0.48). The dust bioavailability for galena at 26% is not materially different from the default value of 0.3 (30%). I would take these findings to mean that the dusts in the tested homes aroseF-56 from high-lead-concentrate fugitive dusts in the general proximity of the haulage roads and from direct deposition from atmospheric emissions from the facility.

The roadside dusts tested for lead levels as high as 300,000 ppm in 2001 testings (see my Staff Paper comments).The Drexler report notes ro adside soils in that testing had Pb levels ranging from 16,085 to 132,218 ppm. The dust and soil Pb speciation results rule out lead paint.

Dr. Drexler, in his Final Report, indicated chemical speciation results showed interior dusts largely arose from atmosphe ric lead directly rather than via soil and subsequent tracking into the residences. The Report’s findings of quite similar air Pb vs. interior dust Pb speciation profiles is consistent with this . The report notes “...also suggest that the pathway for household dust is dominated by recent air infiltration [int o the residences] and not by foot-traffic from residential yards.”

The bulk Pb content for the 10 residential dust samples ranged from 1272 to 24,651 ppm. These bulk values, to the extent they are deri ved from recent air Pb infiltration into the residential interiors, indicate rapi d dust lead loadings and the Drex ler report is consistent with my earlier calculations that atmospheric air l ead entering residences can rapidly lead to hazardous depositional Pb loadings onto inte rior surfaces accessible to young children.

Ref:

Drexler JW. 2005. Final Report. The Speciation and Bioaccessibility of Anomalous Lead

Concentrations in Soils from the Herc ulaneum Community-Her culaneum, Missouri. Boulder, CO: Laboratory for Environmenta l and Geological Studies. University of

Colorado. Done for: U.S. Environmental Pr otection Agency Region VII, via Black and

Veatch .

Related Refs:

Mushak P. 1991. Gastrointestinal absorption of lead in children and adults: Overview of biological and biophysico-chemical aspects. Ch emical Speciation and Bioavailability 3:

87-104.

Drexler J, Mushak P. 1994. Health risks from extractive industry wastes: An approach to bioavailability of toxic me tal and metalloidal contaminants. Seattle, WA, 1994 Annual Meeting of the Geological Society of America, October 24-27.

Drexler J, Mushak P. 1995. Health risks from extractive industry wa stes: Characterization of heavy metal contaminants and quantif ication of their bioavailability and bioaccessibility. Paris, France, Third Internat ional Conference on the Biogeochemistry of Trace Elements, May 15-19.

Mushak P. 1998. Uses and limits of empirical data in measuring and modeling human lead exposure. Environ. Health Perspect.106 (Suppl 6) 1467-1484.F-57 p. 5-22, 5-23 Sec. 5.1.4.4, Table 5-12 I provided chapter and verse in discussions for the draft Staff Paper regarding the importance of having th e right GSD and the exis tence of various GSDs empirically generated from measured Pb-Bs.

p. 5-25, Sec. 5.2, Table 5-12. Again, one cannot use national NHANES data to compare with local geographical areas regardi ng Pb-B statistics. See the disc ussion in my comments on the draft Staff Paper.

Chapter 6: Risk Assessment

See my comments for this porti on of the draft Staff Paper.

SUMMARY COMMENTS: APPROACHES TO DEVELOPMENT OF CASAC PANEL-DERIVED LEAD NAAQS NUMERICAL VALUES

Paul Mushak, Ph.D. March 1, 2007

Below are bullet comments on preliminary deriva tions of numerical primary NAAQS values by

the CASAC Pb Panel.

• The lead NAAQS CASAC Panel is presentl y evaluating EPA's OA QPS staff paper and its supporting documentation for derivations of a lead primary NAAQS. CASAC Panels on criteria pollutants are manda ted by statute and qualified by scientific expertise to review any proposed EPA NAAQS and its scientif ic basis. It follows that this Panel is qualified to independently present a suggested range of NAAQS values for consideration by the EPA Administrator and information on other elements of a Pb NAAQS.

• The Panel has had a good opportunity to assim ilate OAQPS' current draft approaches to Pb NAAQS options and to put them in interpretive perspective.

• There are concerns that the methodological approaches presente d in the draft OAQPS documents for eventual generation of NAAQ S options may not fully reveal national childhood lead exposures.

• Given present advisory concerns and process uncertainties, it is appropriate for the Panel to offer input on ranges and options for th e Pb NAAQS at this time based upon CASAC's statutory mandate and scientific expertise

1. Status of the Current U.S. Pb NAAQS for Adequate Public Health Protection.

• Preservation of the current NAAQS for Pb of 1.5 μg/dl is indefensible in terms of the large amount of new health risk data for lead in the environment.F-58 • Any allowed increases in the current low air Pb levels to near or at the current Pb NAAQS for the U.S. would be catastrophic to public health in general and children's health in particular. It woul d also be devastating to th e ecological environment.

• Preservation of the current, obsolete air Pb NAAQS only because air Pb levels happen to be low at this time is logically as well as scientifically indefensible.

• Regulatory controls for lead or any other health hazards do not come or go based on single temporal snapshots but rather on the enduring need fo r the controls for protection of public and ecological health -- in this case, on the pers istence of robust dose-toxic response relationships for lead. New data from credible sources invariably show lead is more toxic than was assumed and virtually neve r that lead is less toxic than was assumed.

• Anyone familiar with the checkered history of lead's entry into commercial channels and human environments in the 20th Century or before would likely not reject the future possibility of some rapidly introduced technology or industrial activity producing

elevated air Pb levels.

2. Preliminary Approaches to Development of a Panel-derived Numerical Value for a Pb NAAQS

Three potential approaches have been considered by the Numerical NAAQS Value subgroup for Panel-recommended NAAQS air Pb con centrations. One or more of these can be hybrids. The various approaches are not mutually exclusive, but rather are complementary.

A. The Modified Empirical-Deter ministic/Slope Factor Approach

The Derived NAAQS Values

Based on the current health risk literature, this approach produces two sets of NAAQS

values based on two not-to-exceed child Pb-B values at the 99.5 percentile:

Not-to-exceed child Pb-B of 5.0 μ g/dl: 0.22, 0.11, 0.06 μg Pb/m 3 NAAQS values corresponding to slope factors of 5, 10, and 20, respectively.

Not-to-exceed child Pb-B of 2.5 μ g/dl: 0.11, 0.06, 0.03 μg Pb/m 3 NAAQS values corresponding to slope factors of 5, 10, and 20, respectively.

These two ranges are between se ven (rounding) and 50 (rounding) ti mes lower than the current NAAQS numerical value of 1.5 μ g/m 3

.

These suggested air lead values using Method A mi ght be viewed as protective in terms of the indicated reductions below the current NAAQS. Howe ver, the use of Approach C would indicate

that some of these estimated air lead values ma y not be fully protective in preventing IQ losses. For example, Table 2 in my Approach C indicates that the amounts of IQ point loss for 0.11 andF-59 0.22 air lead values are too high. Table 2 shows IQ point losses of 6 and 12 (rounding) for air

lead values of 0.100 and 0.200 μ g/m 3

.

Details for Derivation Rationale and Methods

• This approach is probably the most direct a nd simplified of the prel iminary options that have been considered. It is, however, one that arguably engenders no more overall uncertainty for a NAAQS than the many and compounded uncertainties attending the macro multi-modeling approach presented by OAQPS in its draft documents for three

case studies. Each of the case studies has multiple uncertainties that collectively pose added uncertainties in their translation to a NAAQS.

• This approach also allows accommodation of the contributions of air Pb to dusts and soils, a critical aspect in NAAQS derivations , by use of appropriate blood lead/air lead slope factors that derive from both direct and indirect pathways (air Pb deposited to dusts and soils).

• The conceptual premise of this approach is rooted in the valid use of a not-to-exceed blood lead value for any child in the upper tails of a dose -response distribution arising from the dose-risk response literature. The validity of this concept was essentially confirmed in the January 3, 1990 CASAC report to the EPA Administrator in its review of the 1986 and 1990 Pb AQCD and staff paper (p. 1, par. 2):

o "...it is the consensus of CASAC that bl ood levels above 10 μg/dl clearly warrant avoidance, especially for development of adverse health effects in sensitive populations. The value of 10 μg/dl refers to the maximum blood-lead level permissible for all members of these sensitive groups, and not mean or median

values " [italics added].

• This was the approach for both (1) the 1978 NAAQS promulgation and its survival after court challenges from regulated stak eholders, and (2) the WHO 1987 and 2000 guidelines, which were the ba sis for ministerial directives (standards) within the European Union and other in ternational jurisdictions.

• The 1978 EPA NAAQS and the more recent WHO 2000 derivations are methodologically the same, differing only in th e choice of input parameters. They began by setting, in the case of the 1978 EPA NAAQS, a not-to-be exceeded Pb-B as the thencurrent CDC guidance level of 30 μg/dl fo r 99.5% of U.S. young children, and, in WHO 2000, a not-to-exceed level of 10 μg/dl in 98% of young children.

• This produced a mean Pb-B value of 15 in the 1978 EPA case, and 5.4 in the WHO case. In the EPA NAAQS derivation, 12 μg/dl of the total came from diet and water. In the WHO 2000 approach, 3 μg/dl came from all non- air contributions. Non-air components of 12 μg/dl for the 1978 EPA standard and 3 μg/dl for the WHO 2000 case left 3 μg/dl for EPA's 1978 figure and 2.4 for the WHO deri vation process. These non-air selections

were based on non-air Pb cont ributions at those times.F-60 • A Pb-B/ air Pb slope factor was then use d, a factor of 2 for the EPA 1978 NAAQS and a

factor of 5 for the WHO 2000 case. The latter took into account a mo re valid impact of air Pb depositing as dusts or onto soils than did the EPA 1978 selection. This produced the 1978 NAAQS of 1.5 μ g/m 3 and the 2000 WHO value of 0.5 μ g/m 3 , respectively.

• For the present approach, we suggest use of the starting not-to-exc eed values of 5.0 and 2.5 μg/dl for avoidance of risk of IQ loss at the 99.5 percentile, th e percentile used by EPA 1978. The scientific logic of th is selection as to risk is th at the values are within the bounds of science-based protection of public and ecological health. While a percentile within the upper tail of a risk population distribution might be viewed as a policy parameter, there is no scientific basis for saying protection should be any lower in terms of that population fraction being protected.

• There are five supporting elements to the two choices as a boundi ng range for any child. They arise from (1) avoiding any significant IQ loss from Pb exposure in children; (2) the values represent the mid and lower portion of the linear segment, i.e., the sub-10 μg/dl segment, of the dose-response relationships in the Lanphear et al . (2005) report for IQ loss in Pb-exposed children; (3) the values are those for the sub-7.5 μg/dl linear segment having the steepest dose-response curve; (4) are one-fourth to one half the value the

CASAC recommended in 1990 as the maximum to occur in any child; and (5) are within the range indicated in various current consensus treatises as a sub-10 μg/dl value of concern (e.g., CDC, 2005).

• For keeping 99.5% of U.S. young children below 5.0 and 2.5 μg/dl, respectively, mean blood Pb values of 2.50 and 1.25 μg/dl are requi red. These mean values reflect air and non-air Pb. Adjustment for the air portion wo rking through direct and indirect pathways (soil, dust deposition) is needed.

• Modifications for any current use of this approach must recogni ze that the non-Air Pb levels contributing to current children's Pb -Bs are much lower than were the cases considered in 1978 and 2000. For example, the daily diet and tap water Pb intake estimates for the early 1970s used for th e EPA 1978 NAAQS non-air Pb estimation were on the order of 200 μg Pb/day, producing 12 μg/d l, i.e., 6 μg/dl Pb-B/100 μg Pb intake. OAQPS estimates of current diet Pb intakes by children are only about 2-3 μg Pb/day, which are two orders of magnitude lower.

• To provide the estimate for the background, non-ai r (no direct or indi rect, i.e., dust soil)

Pb levels from air Pb in the above 2.50 a nd 1.25 μg/dl mean Pb-B selections, the IEUBK model for lifetime child exposures 0-72 mos. was used, without air lead, and with only typical geochemical non-air input levels for dust and soil, 50 ppm, and the dust default of 35 ppm, respectively (dust Pb = soil Pb x 0.70). The exposure and biokinetic inputs for this non-air Pb exposure modeling were those for non-air sources in Ch. 4, Table 4-3, in the OAQPS draft staff paper, with uptake f actors of 0.3 for geochemical soil and dust

lead.F-61 • The modeling produces a background Pb-B of 1.4 μg/dl as a geometric mean, using all current non-air related and geochemical soil and dust inputs but no air Pb. For the mean of 2.5 μg/dl scenario, the non-air Pb-B for subt raction (1.4 μg/dl) produces an air-related contribution of 1.1 μg/dl. For the 1.25 mean Pb-B scenario, the modeling background was very close to the 1.25 μg/dl mean level. Modeling noise does not permit a non-air Pb calculation. Therefore, one-half the 2 .5 mean Pb-B scenario was used.

• To convert adjusted Pb-B values to air Pb va lues, three different slope factors were used: 5, 10 and 20. The 5 slope factor gives 0.22 and 0.11 μ g/m 3 respectively for the two risk

scenario mean Pb-Bs. Use of the WHO 2000 Pb -B/ air Pb slope factor of 5, which was acceptable for that time and set of circumstan ces (the 1980s/1990s European picture) is currently insufficient to capture the growi ng contribution to Pb-B of dust and soil Pb generated from both present and past air Pb. Us ing a slope factor of 10 appears consistent with the discussion for Approach B presente d by Panel member Joel Schwartz. A slope

factor of 20 was selected to address need fo r an adequate "margin of safety." One cannot realistically approach what NAAQS value is protective without accoun ting for all of the dust and soil Pb present.

• Slope factors of 10 or 20 best reflect the mi x of historical and ongoing input of air Pb. Using these slope factors, correspond ing Pb NAAQS values of 0.11 and 0.06 μ g/m 3 and

0.06 and 0.03 μ g/m 3 for the 2.5 and 1.25 μg/dl mean scenarios are derived.

• The above computations and the IEUBK es timates of air-added and non-air "new" outputs indicate that very little additional or "new" Pb can be permitted in ambient air.

• Panel member Ian von Lindern has provided a mo re detailed version of this approach using different GSDs, non-air Pb backgr ounds, etc. His comments should also be

reviewed.

B. An Approach Using National Relationships Between Changes in National Child Pb-B Statistics and Changes in National Air Pb Values

The Derived NAAQS Value(s)

See the Approach described by Panel member Joel Schwartz.

Derivation

See the comments of Panel member Joel Schwartz for details of this suggested NAAQS value.

C. Modified Health Risk Estimation Approach

Derived Pb NAAQS Values

Relationships of a range of air Pb values to blood lead values are presented in Table 1. Relationships of a range of air Pb values to a ra nge of IQ point losses ar e contained in Table 2.F-62 Panel member Bruce Lanphear has also addre ssed dose-responses for air lead- IQ loss relationships. His comments should be reviewed.

Derivation

• This approach is a variation on the empirica l slope-factor approach with some use of directly measured dose-response relationships for the risk relationships. Panel member Bruce Lanphear and I discusse d this approach at some le ngth. It was agreed I would provide one approach and he would l ook at providing something further.

• A set of Pb-B levels and their associated IQ point loss values can be generated directly from Lanphear et al. 2005 without inclusion or assumptions of thresholds. OAQPS' use of thresholds to these data means the current IQ loss risk tables in Chapter 4 of the OAQPS draft staff paper are of limited use. In fact , the biasing downward of the otherwise robust dose-IQ loss response is quite significant fr om the Ch. 4 Tables because of these threshold interpositions.

• My approach first generates a set of Pb-B values from direct and indir ect air Pb inputs to

Pb-B. These estimates are in Table 1. The ai r Pb and air Pb-generated Pb-B values are then connected to IQ point changes in Ta ble 2. The IQ--Pb-B re lationship chosen from Lanphear et al. 2005 is that for the sub-7.5 μg/dl linear segment of the dose-response curves. The sub-7.5 segment was chosen becau se it depicts the most robust relationship and the Pb-B range is more relevant to national Pb-B figures seen in current NHANES

data.

• Table 2 estimates for IQ loss can be read bi -directionally. One can observe IQ point loss

as Pb-B rises from a zero value. Conversel y, one can observe estimates of avoided IQ point loss with reduction in air Pb-based Pb-B.

D. Caveats to the Approaches

In terms of the national childhood lead exposure picture embodied in NHANES IV data, one must consider relative impacts of lead sources on child Pb exposures.

• The subset of the U.S. child population im pacted by paint lead exposures may not respond as quantitatively to protective NAAQ S as those with air Pb-derived, non-paint sources. That has always been true. That subset would still require additional interventions. However, the need to impleme nt lead exposure cont rol X does not void the need to also implement lead exposure control Y.

• Subsets of U.S. children impacted by lead paint are simultaneously impacted, in many instances, by industrial and ot her air emissions in close proximity. These children would still benefit in aggregate exposure terms fr om the air emission control component, much

as this subset of children also benef ited from leaded gasoline removal.F-63 • One needs to keep in mind that the relationshi p of leaded gasoline removal to falling PbB statistics through the 1990s was expre ssed across all of the demographic and socioeconomic strata used in NHANES survey compilations, including those strata linked to old, deteriorated urban housing with re latively more deteriorating Pb paint. Consequently, the Nation colle ctively received a huge prev entive medical payoff across all strata from the phase-out of leaded gasoline in the 1980s and early 1990s.

• All subsets of U.S. children ar e impacted by interior and exte rior dust lead. The interior dust values are summed across pa int plus industrial inputs. It is atypical to have no air Pb input and only lead paint input to reside ntial dusts encountered by many urban child subsets of the population. Relativ e contributions of the above to Pb-B are teased out by such methods as the form of multiple regre ssion analysis known as structural equation modeling.

TABLE 1. Relationship of Pb-B to Pb-Air by Differing Slope Factors

Pb-B ( μ g/dl) Pb-Air ( μ g/m 3)

S.F.* = 5 S.F.* = 10 S.F.* = 20

0.010 0.05 0.10 0.20

0.025 0.13 0.25 0.50

0.050 0.25 0.50 1.00

0.100 0.50 1.00 2.00

0.200 1.00 2.00 4.00

*S.F. = slope factor (m 3 /dl) = Pb-B/Pb-Air; S.F. value va ries with increasing impact of indirect Pb-Air pathway (Dust Pb + Soil Pb)F-64TABLE 2. Relationship of IQ Point Losses to Increases in Air Pband Air Pb-Based Pb-B Above Zeroa,b,cS.F. = 5S.F. = 10S.F. = 20Air Pb(μg/m3)Pb-BdIQ LossePb-BIQ LossPb-BIQ Loss00000000.0100.05< 10.10< 10.20< 10.0250.13< 10.25< 10.501.50.0500.25< 10.501.51.002.90.1000.501.51.002.92.005.80.2001.002.92.005.84.0011.6a Air Pb-related increases affecting IQpoint loss through calculated Pb-B values using 3 slope factors per Table 1b IQ vs. Pb-B dose-response relationship based on Lanphear etal., 2005: sub- 7.5μg/dl linear segment, slope - 2.9c Slope factors as defined in Table 1 and textd Pb-B as derived in Table 1e Rounding valuesF-65 

### Dr. Michael Newman

6. Policy Relevant Assessmen t of Welfare Effects

General “This chapter presents information in support of the review of the secondary NAAQS for lead (Pb). Welfare effects addressed by the secondary NAAQS include, but are not limited to, effects on soils, water, crops, vegetation, man-made material s, animals, wildlife, we ather, visibility and climate, damage to or deteriora tion of property, and hazards to tr ansportation, as well as effects on economic values and on personal comfort and well-being.” In my opinion, this section is well written a nd presents a sound approach. As stated in the associated Ecological Risk Assessment review , the points made below are intended to further enhance the value of the document, not to high light significant shortcomings. Because the Ecological Risk Assessment (Section 7) details in formation also discussed in this section, the reader is referred to my review of that section for more comments.

Specific

1. In Section 6.2.5, Lines 2-5, Lines 25-30 and el sewhere. There does not appear to be any mention of exposure to dabbling ducks or swan s from Pb shot or other birds using such solid Pb materials as grit.

2. Page 6-11, Lines 6-7. It is ve ry helpful for the document to emphasize the importance of considering non-individual ecological entities. Unfortunately, the wording of this

sentence is confused. Lead effects ar e stated to potentially harm organisms at the individual, population, communit y, and ecosystem level. What is meant is clear but ecosystems are not only organisms to be impacted. Effects can occur to interactions among species or to biogeochemical processes. I suggest a slight rewording of this important sentence.

3. Page 6-16, Lines 1-11. The purpose of the thr ee cases studies is clear but that of the national-level screening assessment is not as clear. This was also the case in the Ecological Risk Assessment documen t. I suggest that the purpos e or goal be stated more clearly or prominently. The text in Secti on 6.4.3.1 does not seem to do this (Page 6-20, Lines 21-27).

4. Table 6-3 on Page 6-27 and Table 6-4 on Page 6-28. The division of the arithmetic mean Pb concentration by the CCC (which is a predicted geometric mean) results in a biased HQ. The reasons are outlined in my review of the related Ecological Risk Assessment document and references are provided to reinforce this statement.

5. On Page 6-29 (Lines 3-5), the statement is made that “Five of the PEC-based HQs exceeded 1.0, indicating probable adverse effects. Three of these exceeded a PEC-based HQ of 10, indicating a very high probability of adverse effects, and possibly higher severity of effects than at the locations with lower HQ values.” As much as I would tend to agree, the HQ values strictly indicate pr esence of potential danger/hazard, not the level of risk (probability of a specified adverse eff ect) or severity of the effect. (Elsewhere in this document, e.g., Page 6-35, Line 30, HQ-base d inferences are also used imprecisely to judge risk.) An example can be used to show one situati on (of many) in which this is true: risk is not reflected effectively with hazard quotie nts and a HQ only indicates the presence of aF-66 potential danger or hazard. Assume that two toxicants have an HQ=1 but each has a different shaped concentration-effect curve. A specified multiple of HQ for A will not result in the same probability of effect or ma gnitude of effect as that same HQ multiple

for B. Let both A and B have the same re ference concentration (i.e., NOEC for A = NOEC for B = 4 ppm). They will have identi cal HQ values at different concentrations, i.e., as concentration increases, HQ values for both A and B will change by the same amount (see X-axis concentration and HG units); however, the probability of an effect or magnitude of the effect (Y-axis) could be di fferent for the two toxicants at HQs > 1. The HQ is not a good measure of probability or magn itude of effect. It is a metric suggesting presence or absence of danger or hazard.

6. Page 6-36, Line 9. The authors may want to mention that th e scenarios being considered were not for hydrological or seasonal conditions that could generate the highest dissolved

Pb concentrations.

7. Page 6-36, Lines 10-15. What is the factual fo undation for the judgment of “might easily be at least ten times higher than what is represented in the NAWQA database.” What does “easily” mean in the context of these data ? What is the basis for the estimate of “at least ten times higher?”

8. Page 6-36, Lines 24-26. The hardness adjusted concentration predictions are biased (see details in Ecological Risk Assessment review please) and this should be acknowledged.

9. Page 6-36, Line 28-29. May wa nt to include a statement that hydrology- and seasonlinked variations were not considered direct ly although dissolved Pb concentrations often vary with season and hydraulic flow. 0.25 .50 .75 1 1.25 1.50 1.75 2.00 2.25 2.50 2.75 < HQ Probability of Effect or Effect Magnitude A

BF-67 7. Ecological Risk Assessment

General

This section is well written and reasoned. It provides detail for gauging the potential hazard

associated with each of the case studies. Ther efore, the comments provided below are intended as suggestions to further enhance its obvious value.

This section begins as follows:

“The ecological risk assessment for this NAAQS review consiste d of three case study screening assessments and a national-scale surface water and sediments screening assessment. The case study screening assessments were designed to estimate the potential for ecological risks associated with exposures to Pb emitted into am bient air for three case studies: primary Pb smelter, secondary Pb smelter, and near roadway non-urban locatio n. The national scale screening assessment evaluated the potential for eco logical risks associated with the atmospheric deposition of Pb released into ambient air at surface water and sediment monitoring locations

across the United States.”

Specific

10. The surface water and sediment screening involved culling of locations based on a series

of criteria: minimum number of exceedances of chronic dissolved Pb screening values, dissolved Pb not sufficiently elevated rela tive to WQ-related levels, and presence of likely sources of Pb. As stated in 7-28 (lines 23-26), the selected sites “represent a small

fraction if surface waters in the United States ...” Consequently, it is important to define clearly what the population this sample of s ites is thought to repr esent and how strong inferences are about that population based on this sample. Currently, the selection and results are clearly described but statements linking sample sites to population are not equally clear. Statements such as that on Page 7-28 (Lines 23-26) might be made more prominent or expanded.

11. The soil screening section also seems sound and appropriate.

12. Section 7.1.3.2 Water quality Criteria applies soon-to-be-released Pb AWQC that use a power model to adjust criteria for hardne ss, producing CCC or CMC values. Although the document does faithfully apply the Pb AW QC equations, it is an inconvenient truth that the equations are demonstrably biased. The downward bias becomes larger as the mean squared error increases for the regres sion technique/data set with which the model was generated. This fact has been docum ented in general by many authors (e.g., Koch and Smillie 1986, Miller 1984) and specifically for hardness corrections (i.e., Newman 1991). Minimally, this bias s hould be acknowledged as a so urce of uncertainty. Ideally, it should be adjusted for so that more accurate predictions result. Adjustment is easily

done as described in the referenc es above and other publications. An example of the confusion about what th e hardness models predict is evident in

Exhibit 7-10. The arithmetic mean dissolved Pb concentration is compared to the CCC. Strictly, the CCC derived from the model is th e geometric mean, not the arithmetic mean.F-68 Therefore, the HQ shown in the Exhibit 7-10 table and the other similar tables (Exhibit 7- 13) is inherently inaccurate. (See references for detail.)

13. Page 7-13, Lines 19-20, page 7-14, Line 1, Pa ge 7-17, Line 1, Page 7-23, Lines 12 and 16, Page 7-27, Line 19. The HQ is used to infer risk or even combined as the phrase, “risk HQs” here and in other places in the se ction. The Hazard Quotient (HQ) is a metric for hazard, not risk. Although the significance of the associated statements is clear, it would improve the presentation if the distin ction was clearer in some places. As an example of some resulting confusion, Page 7- 23, Lines 27 use HQ to infer probability of a specified type of effect, i.e ., to infer risk. Minimally, the use of HQ to infer risk should

be added to the list in “7.3. Limita tions and Uncertainties” on page 7-25.

14. Perhaps, “Using a single value approach instead of a probabilistic risk assessment” could

be added to “7.3 Limitations a nd Uncertainties” on page 7-25.

15. On Page 7-27 it is stated that “It is unlikel y that there is significant avian and mammalian use of habitats within 2 meters of heavily traveled roads; therefore, HQs above 1 at locations as 2 meters might not be associ ated with ecological impacts beyond those associated with traffic on the road.” Many sp ecies are drawn to edges (ecotones) so this statement could be questioned. Also some spec ies, such as birds seeking pebbles/large sand grit from the roadside, raptors attracted to meadow rodents, or reptiles seeking the

road’s warmth at certain seasons /times of day, might be drawn to road edges. It would be better to remove the opinion that the Atlee, Virginia might be an overestimate.

References Koch, R.W. and G.M. Smillie. 1986. Bias in hyd rologic prediction using log-transformed regression models. Water Res. 22: 717-723.

Miller, D.M. 1984. Reducing transformation bias in curve fitting, Am. Stat. 38(2): 124-126.

Newman, M. C. 1991. A statistical bias in the de rivation of hardness-dependent metals criteria.

Environ. Toxicol. Chem. 10:1295-1297.F-69 

### Mr. Rich Poirot

Review of the National Ambient Air Qualit y Standards for Lead: Policy Assessment of

Scientific and Technical Information

OAQPS Staff Paper – First Draft

CASAC Pre-meeting Review Co mments on Chapter 6, R. Poirot, January 30, 2007

Generally the authors of chapte r 6 and the supporting ecological risk assessment have made a commendable first attempt to assess environmen tal risks from atmospheric lead pollution

— considering that they have such limited quantitative information to work with. It is therefore disappointing to note up front th at the Agency lacks (chooses not to expend) funds for any additional ecological risk assessment work for th is review, especially considering that the 1978 decision to (simply and conveniently) set the secondary Pb standard equal to the primary

standard was “due to a lack of relevant data at that time”. Here we go again...

The information presented here is primarily fo cused on identifying the kinds of locations and

environmental media where adverse effects from historical and continuing atmospheric lead emissions are most likely. These “screening” anal yses do seem to indicate that there are adverse

environmental effects from lead contamination in relatively limited areas near large point sources or along roadways with high historical accumulation where, in some cases, the contributions from current atmospheric Pb emissions are adding to the severity of the problem or, at least adding to the time for which injurious levels of Pb will persist in various environmental media (soils, sediments, surface waters). The chapter indicates that these areas most susceptible to adverse environmental effects could be subject to additional future an alyses, although its not clear what the intended future analyses would entail or whether such analyses would support considering a revised secondary st andard equal to or different from the current standard(s).

Several key questions that are not directly addressed in the current document include the extent

to which current environmental effects would be remedied if current standards were attained everywhere, or whether there are environmental eff ects occurring in locations that currently meet the primary & secondary NAAQS. No information is provided to relate the current indicator (particulate Pb on TSP filters) to total (wet & dry) deposition a nd accumulation of airborne Pb to the environment, nor is there any discussion of other more environmentally relevant indicators

—such as deposition or exceedance of critical loads. Much of the staff paper chapter is a repetition of results from the (fairly brief) risk assessment. There is no discussion of alternative indicators, averaging times, forms and levels of possible secondary (or primary) standards - which typically form the central organizing concepts for NAAQS “sta ff papers,” and only minimal information is provided on the planned a pproach for the upcoming “policy assessment”.

This makes for an awkward and inef ficient science review process.

It would be useful to more closely consider the ways and locations where rates of current atmospheric Pb deposition are greater than or less than the rates at which historically deposited Pb is removed from the “biologically active la yers” of soils and sedi ments (or perhaps buried under newly deposited layers of clean er material). In remote deciduous forest soils, for example,F-70 its estimated that historically deposited Pb ma y be removed from the biologically active layer within 60 years. How does this removal rate slow or reverse as we move from remote areas to

suburban or urban areas or to th e vicinity of large point sources where lead concentrations in biologically active environmental media continue to accumulate.

1. To what extent is the presentation of evidence from the ecological studies assessed in the Pb AQCD and the integration of information from ac ross the various ecologically-related research areas drawn from the Pb AQCD technicall y sound, appropriately balanced, and clearly

communicated?

Given the relative absence of quantitative research data

—especially for relating ecological effects from accumulated lead pol lution to current airborne lead contributions, the presentation of “evidence” seems sufficiently sound, balanced and clearl y communicated. I thought the

discussion of “critical loads” a nd there potential applicability to Pb in the CD was especially useful, even though the concept did not seem to be quite ready to apply to Pb in the current review cycle. I think it would be useful to at least mention the concept in the staff paper and identify some of the research needed to ma ke the technique more applicable for Pb NAAQS

review.

2. Given the lack of quantitative information on Pb -related ecosystem effects, what are the Panel’s views on the presentation of this topic in chapter 6?

I don’t see how you could have done this much more effectively. An inherent difficulty is that in specific locations

—such as in the vicinity of large mining or smelting sources

—where adverse ecological effects are most evident, lead is typi cally only one of multiple metal, gaseous and/or acidic stressors, and its also often difficult to separate the contri butions from current and

historical airborne contaminants from past or present direct discharges to water or soil.

3. What are the Panel’s views of the data sources and models used to estimate current levels of Pb in soil, freshwater, and sedime nt for the case study locations?

The data sources and models generally seem a ppropriate. For the second ary smelter case study, the logic of increasing the soil Pb by a factor of 3 to better reflect measured soil Pb in the vicinity of “a similar source” would benefit from additional discussion (in the risk assessment or SP). Can you at least offer some explanation of why your atmospheric model calculations might be way too low? For the soil and sediment data, an important detail is the depth to which or at which the samples are taken. I couldn’t find any i ndication of the depth of the sediment samples. The soil lead at the Corpus Chri sti site shows large variation by depth, although it’s not clear if a sample depth of 10 cm means “averaged over th e top 10 cm” or “specifically at the 10 cm depth.” I assume it must be the latter since Pb concentration for 10 cm is >40x concentration for 20 cm. At the Virginia site, it ’s not clear whether the indicate d “sampling depths of 0 to 15 inches” (38 cm) represent the range of variability in the sampling or the total depth of sample. Neither seems right. The NAWQA water quality da ta are unfortunately very limited, although I

don’t know of alternate data th at would be more useful, a nd also think you do a good job pointing out the limitations of these data in your discussions of uncertainties.F-71 4. To what extent are the methods used to c onduct the exposure assessm ent & the interpretation and presentation of the resu lts technically sound, appropria tely balanced, and clearly

communicated?

As indicated above, some addi tional explanation for the di screpancy between modeled & measured soil lead for the sec ondary smelter seems warranted. Th e discussion of the national water quality screening methods is d ifficult to follow in the risk assessment. Is there a way you could provide a graphic plot of the equations used to calculate the CCC and CMC values to more clearly communicate the critical impor tance of water hardne ss as it affects lead bioavailability and toxicity?

5. What are the Panel’s views of the approach for addressing un certainty in apportionment of

Pb contributions in the national-scale screen by factoring out those locations with known non-air sources (e.g. mining, point discharges)?

I think you point out the uncertain ties associated with this ap proach reasonably clearly. Unfortunately, many of the large sources likes mi ning activities that have substantial non-air discharges also have substantial air discharg es, and over time with changing climates, waterdeposited contaminants or tailing piles can beco me important air emission sources. Furthermore these kinds of locations are likely to have very high accumulated levels of lead and other metals

—to which any additional atmospheric deposit ion exacerbates an existing adverse condition. It’s important to communicate that current air borne lead adds to the problem even though it may be difficult or impossible to quantify the incremen tal effect of current air emissions. We are least able to quantify air contribu tions in locations where we suspect total current and historical contributions are most injurious.

6. To what extent are the assessment, interpre tation, and presentation of the results of the screening-level risk analysis, in cluding characterization of lead concentrations in media and the comparisons to ecological screening values, as presented in Chapter 6 and the risk assessment report technically sound, appropriately balanced, and clearly communicated?

It’s important to indicate that these are screening results for a limited number of terrestrial & aquatic species at a limited number of locations where relatively recent environmental lead data are available. As such, I think you make and just ify reasonable adjustments to some of the most extreme eco-SSLs, develop reasonable estimates of lead concentrations in various media and clearly present the results with appropriate cavea ts. For the water quality criteria, I get the impression that the current CCC and CMC calculati ons may not work well for very soft water environments, and that these equations may be fu rther modified within the year. It might be useful to explore this more cl osely. Conversely, I note that the hardness of the selected surface waters near the Herculaneum smelter is excep tionally high and wonder if there may be lower alkalinities at other relatively ne arby locations – or in the vicin ity of secondary smelters or roadways.

7. Does the Panel feel that adequate screening criteria (ecotoxicity sc reening values) were selected for each of the media?F-72 I’m not aware of other options. The relativel y small upward adjustments you made to the ecoSSLs for birds and mammals seems reasonable. Su rely we expect some additional Pb burden to these terrestrial species from direct inhalation

— just as there is for humans

—especially at

locations near sources where at mospheric lead continues to ad d to soil contamination levels.

8. What are the Panel’s views on the derivation of the soil screening values for birds and mammals (i.e., using the Eco-SSL methodology)? Do the resultant values adequately reflect current information on exposure char acteristics of these organisms?

I don’t have sufficient expertise to comment

—other than to indicate that you present reasonable arguments for these modifications.

9. To what extent are the uncertainties associ ated with the exposure analysis clearly and appropriately characterized in Chapter 6 and the risk assessment report?

(Unfortunately) I think your discu ssion of uncertainties is one of the stronger sections of the chapter. As always it would be useful where possible to point out appr oaches for reducing these

uncertainties.

Minor Comments on other Chapters 1-5

P. 2-27 lines 16-20: It might be appropriate to indicate that absence of these road dust and soil emission factors likely results in underestimates of lead exposur es in the vicinity of these

sources.

P. 2-9, Table 2-3: After seeing several differe nt source categories listed as the predominant current Pb emitters, its interesting to se yet another new #1 category (aviation fuel) here in the staff paper. Does this suggest a need to consider possible curren t effects on health or environment near airports?

P. 2-18, Figure 2-3: There looks like an indication of applying diffe rent emissions factors in the clear step-functi on change along the PA/MD border.

P. 2-21, line 3: Delete “a” or “es” from “approach(es)”.

P. 2-21, lines 27-34 & page 2-22, li nes 1-4: Might be worth men tioning that while TSP samplers do collect larger particle sizes than PM-10, they are consequently extremely sensitive to distance from source, height above ground, wind condition, etc., have relatively poor precision and limited spatial representativeness. Also the fiberglass filters used for TSP sampling are generally elementally dirty, subject to artif acts for acidic gasses, not amenab le to surface beam analysis techniques, and poorly suited for analyses fo r anything but mass and Pb. Low-vol PM-10 samplers would capture somewhat less coarse Pb, but with much grea ter precision, and with much more useful application for other speciation analysis. They are increasingly being used for “air toxics” metals sampling a nd would provide needed information on coarse PM and its speciation. A Pb standard could always be tightened to account for the very coarse Pb missed by

PM-10 heads.F-73 P. 2-28, lines 14-16: Should be “decline...has” or “declines...have”.

P. 2-47, lines 25-26: Would like to see some additional discussion of “significant ‘undermonitoring’ near known Pb emission sources”. This certainly implies that the highest air exposures are not well-character ized at all – and with the Agency’s knowledge & approval.

P. 2-47, line 31: “15.” Should be “1.5.” Also th is might be a good place to mention numbers of sites that exceed other lower thresholds – like 1.0 0.5, 0.25

—despite significant ‘undermonitoring’ near known Pb emission sources.

P 2-51, lines 10-20: It’s not en tirely clear what these repo rted re-suspension rates (10 -11 per second) refer to. Is this the fr action of total soil Pb (within a ce rtain depth of wh at?) that’s resuspended? Need some explanation.

P. 2-55: lines 11-13: Its not at all clear what “as compared to a mean of 109 ug/g...” refers to.

P. 4-11, lines13-21: Does this ob servation that measured concentr ations are higher than modeled relatively near to a large airport indicate that aviation fuel emissions we re not included or were

underestimated? Also the later indication that air measurements were based on only 3 days in February 2001 doesn’t provide much confidence in the measurements (sounds like “significant under-monitoring near large Pb emission sources...”). I would imagine Pb emissions from roadside soils could be extremely episodic – high wind speeds, etc.

P. 4-27, lines 25-31: I’m not sure this adjustme nt of reducing only the above 1.5 concentrations to 1.5 ug/m3 is a reasonable way of evaluating bene fits of attaining curre nt standard. Emission

reductions to achieve this would shift the whol e distribution downward dow nwind of the source. Conversely, its sort of a silly paper exercise si nce the current (non-protective) standard has not

been attained near this source since 1978, so setting a standard at any level does not appear to reduce ambient concentrations to any predictabl e level (even at a sign ificantly under-monitored location). Possibly there would be some logic to setting a standard at lower levels since certain sources seem likely to chronically exceed standard s by X %. Since there are not PSD increments for Pb, would there be some logic to including additional modeled impacts from new utility, smelting or mining sources up to allowable emission limits?

P. 4-31, Footnote 13: First sentence needs a verb or something. Maybe “...soil Pb levels for this case study (were) modeled”.

P. 4-47, Table 4-4: As indicated previously, ju st attaining current st andard would obviously require reductions in emissions that will shift the whole distribution – not just the maximumdownward.

P. 4-51, Table4-7: This seems inconsistent with Table 4-4 (see previous comment) in that there are changes in blood Pb at all pe rcentiles from the attainment s cenario. Also how can blood Pb at some percentiles (for example 99 th & 50 th for IEUBK concurrent) increase with NAAQS

attainment?F-74 P. 4-54, Table 4-10, lower right box: Interesti ng that these very nearby monitors are not

downwind of the facili ty. What was their purpose, background?

P. 5-2, lines 30-32: Not quite stated correctl y. You could add something like “those at which

effects” between “than” and “had” in line 31.F-75 

### Dr. Michael Rabinowitz

Comments by Michael Rabinowitz January 2007



### 1 st 

### Draft Lead Staff Paper

Chapter 2: Characterization of Ambient Lead

Charge Questions:

1 . To what extent are the em issions and air quality characteri zations and analyses clearly communicated, appropriately characterized, and re levant to the review of the primary and secondary Pb NAAQS?

Generally, current ambient air borne lead has been presente d with sufficient clarity and

relevance to serve well. However, I would offer:

Lead is a multi-media pollutant. Airborne lead is only one source. Somewhere in the document,

it needs to be stressed that lead exposure is from not only the air, but is a combination or summation that also includes the diet, drinking wa ter, and any other sour ces in the household, neighborhood, or occupational environment. A small table, or pie chart, might be offered about the role of airborne lead, diet, water ... for one or just a few exam ples (typical urban adult, child, exposed person...). A portion of the diet could nece ssarily be assigned to having been airborne.

The reader could see airborne lead in the cont ext of these other sour ces, and would see the futility of regulating only airbor ne lead without addressing th ese other sources.

If such a pie chart were compared to a chart fr om the time of the first Lead Criteria Document, the Agency could show real succes s in terms of the magnitude of lead exposure (the size of the pie) but also changes in the relative importance of the remaining sources. This topic is touched on in Chapter 5, but could be introduced more in this chapter and even ex panded in Chapter 5. It is among the basic importan t aspects of lead exposure.

2. Does the information in Chapter 2 provide a sufficient ambient Pb-r elated basis for the exposure, human health, and environmental effect s, health risk assessm ent, and environmental assessment presented in the later chapters?

Yes, I suppose it does. Fortunately, now we ar e in a situation where generally, nationwide,

current air lead levels are much lower than most proposed standards, for example as offered in Chapter 5. Setting a standard at a level higher than current levels might result in increasing allowed emissions. Somehow we should guard against that.F-76 Other Comments on Chapter 2

2-5 L7 Consider adding here: The particle size of the re-suspended lead would be expected to strongly influence its environmental transport an d human uptake, with larger particles being less mobile and respirable.

2-50 L12 Suggest changing “low” to “slow” for a more active phrasing.

2-51 L20 Does this model involve this mech anism (re-suspension) only or does it include the other known mechanisms by wh ich soil lead concentrations de crease slowly over time?? If the former, maybe add at end of sentence...”..by this mechanism alone .”

I suppose that means we can’t wait for re-suspension to be of much assistance in remediation.

I mention this because often revisiting known ol d lead works yields new landscapes, including new land use patterns.

2-52 L20 Really <1 ppm as a background va lue? I might have expected a higher value, more like 25, like agricultural or suburban soils. Or is that peculiar to forests, because forest floor litter and the uppermost soils are so rich in organic matter?

A Few Comments on Chapter 4:

4-34 4.2 Would like to see a comparison of fugitive lead emissions with total factory through-put (annual pr oduction tonnage) for primary and secondary smelters. Which process is less contained? The on e that’s cleaner could be held up as an example for the other.

4-9 L 10 That’s a lot of ingots. 130+ lbs daily.

4-34 L 17 Using 5 significant figures I found jarring. Why put down more figures than the uncertainties permit. This format en shrines computer output suggesting a level of accuracy which it lacks. So I suggest 2 or 3 si gnificant figures and a statement of uncertainty such as 8.4± .8 and 0.74 ± 0.1 (I made up th ese standard errors, but trust that the Risk Assessment Report contains them.)

Comments by Michael Rabinowitz January 2007

On 

### Lead Exposure/Risk Assessmen t Technical Support Document

Comments on Chapter 5:

I found section 5.1 to be clearly written.F-77 Section 5.2, Exhibit 5-12. Is it possible to add to the Results Column values for the observed range and average values of blood lead for co mparison with the models, as was done for the Primary Pb Smelters as shown on the fo llowing page of the same Table?

In the Implications Column the Leggett Model’ s performance was described as underestimating “somewhat”. Could specific values be provided? Percentage or abso lute amount would be helpful.

On page 5-26, line 14-16 makes a general statem ent about the agreement between the 2 models

and the measured values. This is shown above in the Results Column. I was struck by how the 2 models differed. One gives a 95 th percentile as 20 to 29, but the other generated a value of 5. If other panel members, who are more comfortable with is sort of sta tistical comparison, see no reason for my concern, then I’ll go along. If this is as good an agreement as modeling can provide at this stage of their development, then we need to consider other means of setting a

standard.

Page 5-32. I was struck by the good agreement between the fraction of lead from PolicyRelevant Sources across the wide range of blood l ead levels for both the Current Conditions and the Attainment Exposure Scenarios. I concur wi th the observations expressed on lines 6 to 10.

Generally from Section 5.4 The predicted medi an blood lead between the two models differ by only about 0.3 μg/dL for the median values of lifetime average blood lead, and 0.6 for concurrent values. Compared to the distri bution of blood lead va lues, it appears that the models agree for lifetime average predictions much more closely th an for the concurrent values. This may be because the IEUBK model gives a broader distribution of lead values, so differences near the mean affect smaller fractions of the population. I take this general agr eement as support for the overall approach of using these models to pred ict blood lead levels sufficiently well for policy discussions, if their limita tions are presented.

Reflecting on these developments, I imagine that the two models could be forced to concur (at the median) by arbitrarily adjusting some of the ma in parameters. For example, values used for fractional gut absorption could be set to make the blood values aggr ess. At least the blood lead distribution would be scaled up or down, without changing its shape. Similarly, varying the

value for the fractional excretion of lead into urine from blood plasma would proportionately change the predicted blood lead level. I woul d predict that the amount by which the variable

would be tweaked is well within the range of our uncertainty for th is variable, based on clinical

measurements. The values used for those biokine tic parameters often are based on just a few subjects, with higher lead intake s and higher blood levels, closer to 20 μg/dL, than currently prevail. Adjusting these biokinetic coefficients to match the models’ blood value outputs would likely improve our estimates for these biokinetic vari ables. Try not to thi nk of this suggestion as cheating but as calibrating.

Comments on Chapter 6:

Overall I applaud the overall approach of taki ng a few “case studies” of contemporary American lead exposure. It should be usef ul for teaching and standard setting.F-78 P6-17, line 36. Last sentence is confusing for me. Does it mean: “The predicted IQ losses at difference ages for a given blood lead level might all be equivalent, but the blood lead for a given environmental lead is known to be age depende nt.” Or some permutation of that? It’s not clear to me how or why the persistency issue is required here. Or drop the whole sentence.

In Section 6.4, the graphs in Exhibits 3-3, 3-6, 3-8. I had difficulty in my copy matching the symbols with the lines. Perhaps la rger or more extreme symbols could be used or putting the order of th e symbols in the key box to same as the order they appear on the vertical axis. It might help those of us who were not able to attend the presentation.

Exhibit 6-24. I wish I was in RTP to sympathize with you over these findings: Both for blood and IQ, of the eight issues you explored, usi ng reasonable values for what we know, you found very often ranges of over 100% or 200% between the highest and lowest number of people in the highest risk category for a given environm ental lead load. For example, if I’m reading this right, our uncertainty in gut absorption factors impacts our ability to estimate IQ loss among the most

effected 10% of our children over an error range of -100 to +50%.

Looking at the many ranges in Exhibit 6-24, does it matter being zero-centered, and others have

a non-zero bias?

What to do to decrease these ranges of uncertain ties? We could identify research needs for next rounds decades from now? Maybe if we knew more, we could re fine our estimates. But I suspect that human variability is such that we will always have a wide blood lead GSD and a wide range in our responses to lead, hence we wi ll always be faced with a wide range of risk

estimates. But at least it is not a thousand or ten-thousand percent.

For now, we recognize this level of predicativ e imprecision, with some estimates being off by 100%. We can use the size of this range in setting appropriate safety factors in the setting of standards. The size of any safety factor needs to accommodate the magnitude of these unknowns.F-79 

### Dr. Armistead (Ted) Russell

Review of Chapter 2 of the Lead Staff Pa per: Characterization of Ambient Lead

Ted Russell

This chapter has a plethora of information about ambient lead concentrations, along with emissions, loss processes and physical characteri zation. If one reads though it, you can get a very good idea of what is out there, its physical why and where it is going. In that regard, the chapter succeeds. However, it does not do so ve ry efficiently, and does not seem to capture the real issues as well as it might. To me, given the general trend in lead, the real issue is best portraying the high end concentrat ions, providing trends at such locations, along with the more typical. I would also want a good concentration distribution plot (e.g., like a pdf), which I think provides much more information than the box and whisker plots, particularly when the box plots do not also show the high outliers. For exampl e, they could plot the maximum quarter average for each site on the distribution. They might comp are this with, say, a similar plot of the second highest monthly average.

I was also disappointed in the modeling estimates s ection. I started reading it, thinking that there would be some actual results represented. W ithout some results, the section raises more questions than it answers, and falls far short of the information that could be provided. First, as noted beforehand, a number of the larger sources do not have monitors nearby. Models can provide some idea of hot spot levels and locations . Second, it is noted that the modeling results generally are below the observations . They proffer some explanations. A key one is that the source strengths are underestimated. This feeds back to the prior sections of this chapter, and significantly impacts any uncertainty assessment. It would be good if they were to take the model results and also develop a concentration distribution for direct comparison to the one developed based on the observations (thus use the same metric in both cases). Again, specific attention should be paid to loca tions with higher concen trations. In doing this, they should look to adjust the modeled dist ribution to account for the lo w bias in the simulations.

At this point, the analysis should be able to pr ovide a good characterization of the likely levels of lead around the country, even where no monitoring is being conducted. From this, a much better view of the severity and extent of the problem is achieved. In the process of getting to this point,

uncertainties should be characterized.

Specific points.

2:21:6 (Chapter:page:line): Not all measurement approaches re quire chemical extraction (e.g., XRF).

2:23:14-16. These lines suggest (s omewhat repetitively) that the reduction in Pb monitoring was due to the need to fund PM2.5 and ozone monitoring. Given when PM2.5 monitoring was initiated over most of the US (early this d ecade), that PAMS came on line starting in about 1993F-80 and the trend in ozone monitoring, does this gel w ith what is shown in Figure 2-5? This should

be documented.

2-28 Figure 2-10. This figure coul d be greatly improved. First, why just 42 sites? Second, go back before 1983 (n.b., the figure caption mistaken ly says 1980). Why is it flat from 83-84. Seems unlikely at best. This should also show th e outliers at the upper end, e.g., all sites that had levels above the NAAQS. It also brings up an interesting question: why did the average Pb go up by about 2x in 2001? Bottom line: Can this fi gure be extended back in time and also show the sites over the NAAQS?

2-30 Figure 2-11: A better fi gure caption is warranted.

2-31 Figure 2-12: The table in this figure appear s inconsistent with the same information in Figure 2-11. It looks like the table is summarizing Max quarterly average.

2:34:4. It would be of interest to note Pb leve ls for East Helena as they are not given in the

tables below. What do the Pb levels look like in such an area that is out of compliance, but would appear to have dropped to the point that the site would now be in compliance (with an explanation of why).

2:37:2 I very much agree with th e statement that shorte r term averaging than quarterly, and that monthly would appear to provide a balance between the weight given any one observation and the need to assess variations in [Pb].

In direct respons e to the Charge:

To what extent are the emissions and air qua lity characterizations and analyses clearly communicated, appropriately characterized a nd relevant to the review of the primary and secondary lead NAAQS?

As noted above, there is a plethora of information on these topics in this chapter. However, I view it as inefficiently presented for the charge at hand. More concentration and details should be provided relating to the areas that continue to have Pb leve ls near or above the current, and somewhat tighter NAAQS. To adequately assess what will be the populati on risks and decreases in those risks, associated with various standards, the high end is where the action is. Further, as noted, there are many areas near major sources th at are not well monitored. Modeling results are required in such a case, and the level of inform ation provided from the modeling is inadequate.

If there are but one or two areas that might even be affected by a change in the standard, this is important to know.F-81 Does the information in Chapter 2 provide a sufficient ambient Pb-related basis for the exposure, human health and environmental effects, health risk assessment and environmental assessment pres ented in later chapters?

Similar to above, it is lacking in terms of providing a more co mprehensive characterization of lead levels nationally and the hi gh-end concentrations. This may be particul arly true if other health endpoints are examined besides IQ loss, e.g., more acute impacts.

A further limitation is that one needs to look in to the future as to what various standards will do to risks associated with Pb expos ure, particularly given the incr eased evidence of risks below 10 ug/dl. I was hoping to see some more concrete an alysis of how future Pb levels and exposures across media will evolve, and how those relate to different standards. While such data may be scarce, the current SP could provide some more quantitative information. Along these lines, they provide a graph for resuspension rates, and say that for SoCal conditions, this will lead to little change in soil Pb for quite a while. How about other areas?

Review of Chapter 2 of the Lead Human Exposure and Health Risk Assessments and Ecological Risk Assessme nt for Selected Area

This chapter presents an overview of the wa y the Risk Assessment will be conducted, in particular identification of select ed case studies and models to be used. The first section notes that they will present the huma n and ecological associated with two scenarios: current conditions and attainment of the NAAQS. This is a very good start on providing th e type of information needed, but is insufficient to provide the inform ation necessary for CASAC or the administrator to do the job at hand. What is also required is information on ri sks associated with levels, and forms, averaging times, etc., other than the cu rrent NAAQS. Further, it took a bit to find the results of those two cases later on in the chapte rs, in part because only one of the cases had a non-attainment vs. attainment comparison. Th is document could benefit from a two page summary of the key approaches and results. In particular, they should provide the change in

each of the cases considered.

In setting up how they plan to assess the reductions in risk asso ciated with meeting the current standard, they make a mistake in the approach. Unlike the ozone SP, to simulate attainment, they essentially cap ambient levels at the standa rd, leaving all other conc entrations unchanged. This is not what will happen in real life. C ontrols implemented to meet the standard will

decrease Pb at other times as well (or else they should c onsider tighter standards). Thus, a more

real life attainment scenario would be to decrea se Pb concentrations at all times, rolling the levels back towards the background.

While I like the idea of case studies, they do not replace an assessment for the population as a whole. While there are always uncertainties asso ciated with scaling thin gs up (or down), they are instructive and provide the type of informati on needed to set a national standard. For one, it is important to know what are the risks and estima ted impacts, nationally, at the curren t level of exposure. While this may be viewed as be ing provided by the NATA assessments, they areF-82 insufficient for the reasons spelled out in the SP, and also they do not go far enough, e.g., considering alternative standards. A more co mprehensive national-level analysis should be added. Further, this lays the groundwork for asse ssing the change in risks, nationally, associated

with different standards.

I am somewhat perplexed by Exhibits 6-1 a nd 6-2. Looking at the column IQ Loss under IEUBK in 6-1 and 6-2, the first thing that struck me was that in 6-1, a value of <1 is used, and in 6-2, a value of 0.5 is reported. Why the differenc e in how the values are reported? Are they different? Second, given how the attainment scenar io is run, i.e., that air concentrations are truncated, how can the impacts be greater in the a ttainment scenario for any of the %’iles? The results from this case study also reveals a pr oblem when only taking a sn apshot in time: given that the inhalation pathway is so small, there wi ll be virtually no immediat e impact from meeting (or tightening) the standard as only the inhalation and how dus t exposures respond, and the dust response is muted as it does not ha ve a factor that inte grates over time and is dominated by other terms in the functional representa tion. It would be useful in Chapter 4 (e.g., around page 4-16)

to show the fraction of dust from air. While I ca n only ball park this at present, it would appear that significant reductions in le ad in the air, using the H6 mode l, would lead to very significant reductions in dust-Pb, and hence a major reduction in the highest IQ loss individuals. True? I would like to see this case run, e.g., tightening the standa rd to, say, 0.5 ug/m 3 . Would this push all of the blood lead levels to below 10 ug/dl?F-83 

### Dr. Joel Schwartz

Comments on Lead Staff Paper

Joel Schwartz

First I would like to address the issue of whether there is anything to be gained by a national (i.e. Ambient Air Quality Standard) approach Vs a site by site (Air Toxics) approach to controlling lead. The argument for dropping a NAA QS is that there is little to be gained, except in a few places that could be addressed by MACT. To examine this, I took the data from the STN network, took the average by locatio n, and plotted a histogram of th e distribution below. What is

clear is that about 60% of the locations have levels below 0.005, but that the remaining locations have concentrations that range up to five times as much. Clearly then, there is a range of exposures that our urban citizen s suffer from, and that a good third of them have exposures considerably higher than the leas t exposed half of the urban US . This suggests that there is exposure above what is typical in a large number of US cities, and that a national approach to get those cities to identify what needs to be done to reduce exposure is appropriate.

Figure 1. Distribution of Long Term M ean Pb from the STN urban sites

The following figure shows the locati ons of the sites, by long term average concentration. It is

noticeable that one of the four highest urban locations is close enough to Herculaneum to potentially be impacted by long range transport. This raises the questi on of whether the risk assessment, by not including exposure outside a de fined radius around the sites, is missing some health impacts. Certainly, if one assessed the im pacts of coal-burning power plants within 100km of the plant, one would miss most of the particle health effects. 0.000 0.005 0.010 0.015 0.020 0.025 1 0 50 100 150F-84 While I recognize that th ere are limits to what OAQPS can do with its modeling, I am concerned that the re-suspension of road dust issue is not being quantitati vely addressed. In some source apportionment models we have done of elementals on PM2.5 filters, we have seen Pb load on a factor that seems to be traffic related, a combina tion of road dust, brake lining, etc. That means, at our monitor on the roof top of the Countway Libr ary, a major source of lead is road dust. This is likely to be true for many children in Boston as well.

While the tables present sources in order of emissions this does not include the important concept of intake fraction. For example, recent PM related studies have shown that roadside emissions are much more likely to make it into a lung than emissions from distant power plants or factories. Are we missing im portant exposures by ignoring this ? One suspects that the traffic related sources, including re-suspension, are under appreciated when ranked simply by

emissions.

Specific Comments:

3.3 While bone resorption is higher in women, this is an issue for older men as well.

3.13-14 I agree that th e evidence points to a higher slope at lower doses, and that a log-linear

curve is a reasonable choice. I am therefore mystified by the latter choice of several thresholds to examine. Yes, it is true that there is little data below 2.5 ug/dL. But the available data suggests the slope is steepening, not get ting less steep, so why is it reas onable to argue the uncertaintyF-85 suggests a sensitivity analysis with a slope of zero? A more reasonable sensitivity analysis would have the slope double below 2.5 ug/dL. Why was this not tried? Given asymmetric evidence in favor of steeper slopes, sensitivity analyses that are only asymmetric in going in the contradictory direction seem unjustif iable. Do the sensitivity in bot h directions, or not at all.

4.7 While cognitive health benefits in children may be the most sensitive endpoint, we are talking about an ambient standard, not setting a reference dose. That is, we can quantify health benefits for multiple outcomes, and not just choo se one. While there is a finite amount of time (and labor) available, the health benefit analys es for both the lead pha se-down and the drinking

water lead standard included other outcomes . So did the CDC benefit analysis for housing abatement. This would be a minor point except th at in those analyses, the adult benefits were

about the same size as the ones fo r children, so this could well imp act the choice of the standard.

TSD Comments

1: Uncertainty. The TSD assumes a GSD of 1.5. This is considerably smaller than that seen in NHANES IV. The authors argue that since they are look ing at small areas, their GSD should be smaller. While directionally true, it is not clear that this justifies the drop from 2.2 to 1.5, which is a great deal. The use of localized site data from the 1990’s to justify 1.5 is unsatisfying, since as the authors note, as the mean blood lead fall s, the GSD increases. The mean blood lead in the locations they are examining is lower than was seen in the sites from the 1990’s which provided

a GSD of 1.5. I think this is t oo low, and should be increased.

Secondly, the authors are somewhat schizophrenic in their modeling. They reject epidemiologic studies relating dust and soil lead to blood lead, and insist on onl y using the biokinetic model to estimate means. They then reject the biokine tic model and only use epidemiologic data to estimate variances. The reason everyone does not have the same blood lead in the same block group is, in part, that intake varies, absorption varies, etc. Hence, a Monte Carlo simulation varying parameters for the IEUBK model should produce estimates of variance. These could be compared to the variance estimates from the ep idemiology studies. Large differences from the empirical data would suggest changing the range of some of the parameters. Deviations between means estimated from the epidemiology and IEUBK model could likewise be useful. I think both approaches need to be used for both mean and variance.

2. The assumption that no improvement in IQ will be seen if blood lead levels fall below the 5 th
percentile of the Lanphear distribution is unjus tified. Recent data from NHANES show effects below levels of 2.4 to 6 ug/dL, and there is no data that supports a threshold. The baseline approach should assume no threshold in the range of exposure seen in the population, and sensitivity analyses should be done around that baseline. To argue that uncertainty in an association justifies assuming it is zero is bad science and bad risk assessment. The expected value of uncertainty is not zero.

There is no need to include the intercept in the an alysis; the risk assessment is predicting IQ loss, not IQ. Hence that issue need not be dealt with.F-86 

### Dr. Frank Speizer

Pre-meeting Comments on Lead Staff Paper dated Dec. 4, 2006

Submitted by Frank Speizer, MD

1/29/07

I have reviewed Paul Mushak’s comments and in large part I agree with much of what he has done in a thoughtful outline of the details with which I believe Staff needs to promptly consider. Many of my comments simple express frustrations as to where I see inconsistencies and concerns about lack of completeness to this point. I am sure much will be handled in subsequent drafts, but those drafts will be under time pressures an d I would predict will lead to frustration by CASAC as well as the public in have adequate time for review. (I may be wrong, but past history does not offer much hope).

From Chapter 1, I note in the footnote on page 1- 5 that the agency indicates that it does not anticipate having funding to perform additional quan titative ecological risk assessment work for this review. This seems inappropriate since we indicated at the last review that the progress on information to inform the secondary standard ha d not progressed in the la st 10 years. Why are

we still in this same state and seem to not be able to move forward on it?

Chapter 2

Section 2.3.2, page 7. Sources other than air not yet evaluated. Will this be done? Seems like an important source would otherwise be overlook ed. Page 2.52 section 2.6.2.2 suggests that soils can contain up to 50-100x background and somehow this needs to be at least discussed as to how this might alter policy relevant background.

Chapter relevant questions: It w ould appear that at least for l ead the decline in monitoring of TSP to PM10 and PM2.5 results in an uncertainty as to the trends and less capacity to follow trends. Although TSP and PM10 are highly corr elated this breaks down for PM2.5. Although this is described in this chapter it seems not to ha ve been resolved as to how it will be dealt with. Unless this comes up later I think a “policy relevant statement” is required.

Chapter 3

Section 3.2 leads to a conclusion th at seems appropriate but incomple te. If we were only worried about “acute” exposure then blood lead seems appropr iate but this certainly is not the case.

Therefore need to at least the discuss the role of other biomarkers of lead that might be

considered as alternatives or in addition to bl ood lead for more chronic exposures. These would

include both other markers measured in blood as well as bone lead (that can be measured noninvasively.

Table 3.1 and 3.2 I will need to go back and check but I would have thought if not updated this figure would have been reproduced in the current CD and reference to it rather than the 1986 CD would have been more appropriate. Ditto table 3.2.F-87 Summary of staff questions: The presentation seems to have integrated the material from the CD reasonably well. There seems however, presumably for reasons of simplicity to have ignored the potential importance of chronic vs. acute exposure as expressed by focusing on blood lead as the parameter of interest. With regard to the conc lusions I find it hard to focus on the form of the blood Pb metric as the only value to consider. This clearly is important for the children but does not do well for adult effects. With regard to the threshold argument, it seems inappropriate to have focused on it. Clearly both human and an imal toxicology do not justify any threshold and although this is stated it is muddled in the discussion by suggesting a hypothetical level for

individuals when in fact this would be the specific case where no threshold would exist and if

there is a “threshold” it would be for a subgroup.

Chapter 4

Page4.5 and 4.6, Figure 4.1 I am concerned about putting all exposures other than ambient as “Background” for Pathways . As indicated in Routes the ingestion route is likely to be considerably higher than ambient and thus will make Background overwhelm other sources. This may all be semantic but may have important relevance to what might be c onsidered policy relevant. Clearly this is more complicated and cannot be simply managed as ba ckground. (I suggest a separate term in the modeling will be necessary.)

Page 4.9-10:The fact that this area is in non co mpliance for Pb NAAQS and this is based on 9

TSP monitors it is not clear how this might relate to standards going forward, particularly as we have moved away from TSP for particles. This s hould be discussed in great er detail (even if it is only to say we are staying with (or changing from) a TSP standard.

The three selected sites will each have to be considered separately as each has measures which do not overlap. Eg. No measure of alte rnative sources, PM10 vs. TSP measures.

Page 4-24, section 4.3.1.3: Further discussion or documentation is needed on the difference in particle size distribution for lead from presumed mobile sources vs. diesel particle distribution.

Page 4.26, Table 4.2: For ambient concentrati on estimates may need a footnote fact that dispersion model based on TSP (if it is ) and Monitoring data based on PM10.

Page 4.27, line 29: Should this be “l ess than” rather than greater!!!!

Table 4.10: This seems unacceptable. Caveats ar e given for the above two models that suggest potential biases in estimates. Performance eval uation for perhaps the most relevant component to the general population must be completed (a long with what ever cav eats are necessary).

Page 4.78: Must keep in mind: “Consequently, the risk results as sociated with th e pilot are not

intended to reflect our best estimates of risk a ssociated with these case studies. Rather, they reflect preliminary estimates, limited by the in itial application of our modeling tools and information. We intend to build on our experien ce and findings associated with the pilot assessment in designing and implementing the full-s cale risk assessment, the purpose of which isF-88 to inform the Agency’s development of and cons ideration of NAAQS polic y options with regard to policy relevant sources of ambient Pb.”

4.81 comment on summary of plans: It is not clea r which of the suggested additional activities to be carried out will, in fact, be done . It would have been better to have seen these bullets as a list of work scope factors. The past experience has been that the agency will run out of time and the work will not be completed. Worse would be to do partial work on each topic that to have set out a set of priorities of what woul d be accomplished and in what order.

General comments on questions:

There seems to be incompleteness in this chapte r that permeates througho ut. Consideration of the sites, seem to have been selected as a matter of convenience. Suggestions in the final analyses that other sights will be added are ma de yet no details are provided and one wonders where these will be, how they will be selected, how much less or more the completeness of data

will be and how useful the additional results will be . Although uncertainty is considered, it is not

clear how much is a statistical exercise vs. real lack of data used or av ailable to make a more objective assessment of uncertainty. Given that most of the population does not live near primary or secondary smelter sources, it seems to me that more work needs to be devoted to finding data that might be used to do better mode ling of roadway or urban exposure and analyses devoted to this segment of the risk assessment.

Chapter 5

Page 5.9: The current data would suggest that this figur e would need to be reduced by a factor of 3 (5ug/dl).

General comments on questions:

The entire chapter reads like a promissory note with out much e xpectation that the promise will be met. By simply discussing what was done in the past the authors have not told us much of what they plan to do. In addition, the “facts” that lead to the previous conclusions, though stated do not appear to take into account current knowle dge. For example the indication that 30ug/dl is the 99.5% level to shoot at may have been ok in 1 977 but is clearly irreleva nt today (as indicated by various footnotes that bring the level down to 10ug/dl). So mewhere it might be indicated that the all these level may be as much as three time higher than the science today would indicate, and therefore NEW CA LCULATIONS WILL BE PERFORMED

Chapter 6

General comment: This chapter seems to be as incomplete as the preceding one. Will Staff have time to do the additional analyses suggest that must be done and will CASAC see them before the work goes to the administra tor? If not than the purpose of CASAC being in the loop is clearly inappropria tely relegated to an after thought. Even in light of a cha nge in the approach being used to the setting of NAAQS this seems to be violation of de facto if not de jure . I for one will not be part of it a nd will not sign off in any way on draft without the work being

reviewed.F-89 

### Dr. Ian von Lindern

CASAC Review of First Draft Lead Staff Paper and Related Analyses

Pre-Meeting Comments of Ian von Lindern

My comments address both the OAQPS Staf f Paper and the Pilot Analyses and are arranged in three main sections – i) Intr oductory Comments that provides general observations and policy related comments; ii) Answers to the Charge Questions: and iii)

Technical Comments that follow the structure of the analyses.



### Introductory Comments

Overall Strategy and Presentation: The Staff Paper and the unde rlying Pilot Risk Assessment Methodology represents a substan tial and comprehensive effort to quantify the pathway-specific effects of childhood lead exposure in typical scenarios that might be considered under a revised NAAQS. The logic and seque ncing of the modules that have b een combined to characterize lead

from source to adverse health risk represents a thorough understa nding of important factors and

mechanisms that influence childhood lead poisoning and the consequent effects.

It is a commendable effort and appropriately captures both th e knowledge and advancement in assessing environmental mechanisms and lead health risks that have occurred in the last twenty years. It also is indicative of th e level of sophistication in the sc ience of risk assessment that has been accomplished; and the data presented and used largely captures the environmental improvements and consequent benefits of l ead regulation strategies employed since 1991.

In producing these documents the staff has done an excellent job of asse mbling and developing a series of empirical and mechanistic models to assist in quantifying lead health risk. However, the emphasis to this point reflects an understanda ble bias toward development of the methodology that comes at the expense of critiquing how it ca n assist in developing effective policy, and in performing such analyses. There is some confusion, at least for th is reviewer, as to how these analyses will be used in po licy recommendations. The corollary risk and exposure assessment analyses conducted for the last review in 1990 were presented to CASA C members as a prototype methodology for assessing risk to lead in multi-pathway environments that could then be used to assist in developing remedial and co mpliance strategies for the agency programs. Notably, that methodology was subsequently used and constantly upgraded in several Agency programs that ultimately led to the successes in multi-media exposure reductions noted in this Staff Paper. The 1990 Committee reviewed those anal yses in the context of its scientific and technical appropriateness for a ssessing risk, specifically for the Air Programs, but also was charged by then Administrator Riley to assess lead risk assessment protocols across several Agency programs.

NAAQS Policy Implications: However, there is in this draft report a seeming, but less understandable, bias toward supporting a revocati on of the NAAQS. This seems premature, asF-90 there is little in the analyses, to this point, suggesting what mi ght be a “safe” or, at least, an acceptable ambient air lead level. There also seem s to be no obvious route laid out to make such a determination. More skeptical reviewers mi ght view the document as tending toward a conclusion that because we see no problem, there is no problem and no need to regulate. This conclusion, it seems, could only be supported if we were sure that that we had adequately monitored for potential problems and there are sufficient guara ntees and safeguards that no problems could occur in the future. In this regard , the monitoring record is shallow, at best, and, as yet no determination of what is an acceptable am bient level, if there were a record to compare to it. And most importantly, what mechanisms are in place to ensure that any new source developed would not produce emissions that would exceed this critical threshold, whatever that “ safe or acceptable” level might be.

A clear and transparent understandi ng of the policy questions that th ese analyses will assist in answering is of critical importance to entire procedure. This is im portant to any reviewer to help focus comments and to any stakeholder to criti que and weigh in on the decisions. However, for this case it is paramount that th e hypotheses be clearly stated. The inherent nature of the structure of the models and the lack of precise input da ta regarding the sources of pollution, the receptor populations, and the specification of parameters and co-factors require that the problem be clearly stated and the uncertainty and sensit ivity analyses addre ss that hypothesis.



### Charge Questions to the CASAC Pb Panel

Ambient Pb information an d analyses (Chapter 2):

1. To what extent are the emissions and air quality characterizations and analyses clearly communicated, appropriately characterized, and re levant to the review of the primary and secondary Pb NAAQS?

It is a commendable effort and appropriately captures both th e knowledge and advancement in assessing environmental mechanisms and lead health risks that have occurred in the last twenty years. It also is indicative of th e level of sophistication in the sc ience of risk assessment that has been accomplished; and the data presented and used largely captures the environmental improvements and consequent benefits of l ead regulation strategies employed since 1991. However, little in the analyses, to this point, suggesting what might be a “safe” or, at least, an acceptable ambient air lead level. There also seem s to be no obvious route laid out to make such

a determination. A clear and tran sparent understanding of the policy questions that these analyses will assist in answering is of cr itical importance to entire proce dure. This is important to any reviewer to help focus comments and to a ny stakeholder to critique and weigh in on the

decisions.

2. Does the information in Chapter 2 provide a sufficient ambient Pb-r elated basis for the exposure, human health and environmental effects, health risk assessment, and environmental assessment presented in later chapters?

The Staff Paper provides significantl y more information in this regard than was presented in the AQCD and the information seems to be a good and fair representation of the state of knowledgeF-91 in the U.S. at this time. It does indicate, however , that the database is a poor representation of

true emissions and ambient air lead levels in the U.S. today. This lack of appropriate data should be dealt with in a more comprehensive sens itivity analyses and un certainty discussions.

Pb-related health effects (Chapter 3):

1. To what extent is the presen tation of evidence from the heal th studies assessed in the Pb AQCD and the integration of information from ac ross the various health-r elated research areas drawn from the Pb AQCD technically sound, appropriately balanced, and clearly

communicated?

These analyses seem to suggest the risk metric is whether there is significant potential for IQ loss among children exposed to the policy relevant so urces? This, however, doesn’t seem to be explicitly stated and it is unclear whether the Agency considers IQ loss an unacceptable

outcome. There is little in the current documents regarding what the Agency considers regarding the significance of IQ loss and whether there is a threshold of concern that will be a benchmark in setting a new standard or developing an alte rnate protective risk management strategy. This discussion needs to be clearly laid out in future drafts.

2. What are the views of the P anel on the appropriateness of staff’s discussion and conclusions in Chapter 3 on key issues related to quantitative in terpretation of epidemiologic study results, including, particularly, the form of a blood Pb -response function for neurocognitive effects, and the form of the associated blood Pb metric?

The discussions are well devel oped and clearly presented. The appropriateness of the blood lead metrics seem to be in question b ecause the use of lifetime value and the concurrent (6-7 year old)

blood lead level tends to modera te the observation that both the maximum blood lead tends to occur at the most vulnerable age. Presumably, th is is accounted for in the structure of the empirical relationship used, but I must defer other committee members more familiar with these results regarding the appropriateness of the quantit ative estimations associ ated with the health

effects.

3. What are the Panel’s views on the adequacy a nd clarity of the discussion of potential thresholds in concentration-response relationships presented in Chapter 3?

There is some concern with the treatment of th e “cut points” in these analyses. Assuming that there is no effect below the cut point eliminates the possibility of a Type I error as no false positive is possible below the cut point. The only possible error result is a false negative. This should be pointed out in the discussions and cons idered in determining an acceptable level of risk or margin of safety in recommending a standard.

Human Exposure and Health Risk An alysis, pilot phase (Chapter 4):

1. To what extent are the assessment, interpreta tion, and presentation of the results of the pilot exposure analysis, including char acterization of Pb concentrati ons in media, the modeling ofF-92 multi-pathway Pb exposure and application of biokinetic blood Pb models, as presented in Chapter 4 technically sound, appropriate ly balanced, and clearly communicated?

The Staff Paper and the underlying Pilot Risk A ssessment Methodology repr esents a substantial and comprehensive effort to quantify the pathwa y-specific effects of childhood lead exposure in typical scenarios that might be considered unde r a revised NAAQS. The l ogic and sequencing of

the modules that have been combined to character ize lead from source to adverse health risk represents a thorough understand ing of important factors and mechanisms that influence childhood lead poisoning and the consequent effect s. The report recognizes that there are several difficulties inherent in both estimating and quantifying outcomes within each step and in utilizing those results in subse quent steps. However, the report fails to recognize the effects are often multiplicative, meaning that, although uncerta inty increases, the consequences of underestimation or over-estimation can be dissimilar, and are dependent on the status of other

variables in the formulations.

2. Are the methods used to conduct the pilot exposure analysis, includi ng the modeling of population-level distributions of total blood Pb levels and the pathway-apportionment of those blood Pb levels (e.g., air-inhalation, versus soil-ingestion versus dust-ingestion, versus background) technically sound? Does the Panel ha ve any suggestions for improvements in the

methods used?

Several assumptions made in individual steps in the methodology tend to possibly underestimate of the policy relevant background contributions to intake, ignore the potential impacts of aggregate soils in the community, and underestimate dust lead concentrations . This likely results in minimally low intake estimates for soil and du st that translate to low blood lead predictions and health impacts in the primary and secondary sm elter situations. These in turn can result in false negative findings for children near the th reshold concentrations. A dditionally, the lack of air quality data may dictate that determining an appropriate standard will likely rely on modeled concentrations, emphasizing the importance of conducting appropriate sensitivity analyses.

3. What are the Panel’s views on the staff in terpretation of the performance evaluation completed for the pilot analysis (and desc ribed in Chapter 4) with regard to the representativeness of indi vidual modeling steps completed for the analysis (e.g., characterization of ambient air and outdoor soil Pb levels and the es timation of blood Pb levels for specific case studies)?

See the response to the previous question and the expanded discussion in the text of the

comments.

4. In general, are the concen tration-response functions and bl ood Pb metrics (i.e., lifetime average, concurrent blood lead) used in the pilot analysis appropria te for this review?

The discussions are well devel oped and clearly presented. The appropriateness of the blood lead metrics seem to be in question b ecause the use of lifetime value and the concurrent (6-7 year old)

blood lead level tends to modera te the observation that both the maximum blood lead tends to occur at the most vulnerable age. Presumably, th is is accounted for in the structure of theF-93 empirical relationship used, but I must defer other committee members more familiar with these results regarding the appropriateness of the quantit ative estimations associ ated with the health

effects.

5. Are the methods used to conduct the pilot health risk assessment, including the application of the cut points in relation to the concentratio n-response functions empl oyed, technically sound? Does the Panel have any suggestions fo r improvements in the methods used?

There is some concern with the treatment of th e “cut points” in these analyses. Assuming that there is no effect below the cut point eliminates the possibility of a Type I error as no false positive is possible below the cut point. The only possible error result is a false negative. This should be pointed out in the discussions and c onsidered in determining an acceptable level of risk or margin of safety in recommending a standard.

6. To what extent does the sensi tivity analysis completed for the pilot analysis (and described in Chapter 4) identify key sources of uncertainty an d provide an assessment of their impact on risk

results?

The inherent nature of the structure of the models and the lack of precise input data regarding the sources of pollution, the receptor populations, and th e specification of para meters and co-factors require that the problem be clearly stated and co mprehensive uncertainty and sensitivity analyses address that hypothesis. Extensive sensitivity anal yses should be conducted by first (as indicated in the reports) identifying an appropriate baseli ne or typical model r un, and then varying key components while holding others constant. However, the sensitivity runs should be accomplished using both lower and upper limit analyses. It woul d enhance the uncertainty analyses by framing the discussions in terms of Type I (false positive) and Type II (fal se negative) errors for the final

risk assessment.

7. As part of the NAAQS review, th ere is interest in attempting to differentiate Pb exposure and health risk impacts for modeled populations be tween (a) historically deposited Pb (e.g., near roadway dust/soil lead from leaded gasoline) and (b) newly emitted Pb. Does the Panel have specific recommendations regarding approaches that might be employed in the full-scale assessment for this purpose?

The document fails to recognize that there is significant variance in the background levels and certain populations and individual members of all popula tions will be at greater risk as a result of these background sources. It is as important to identify these at-risk populations and assess the possibility for Type II er ror (false negative) with these gr oups as it is to assess uncertainties based on statistical extrapolations of mean or baseline characterizations.

8. What are the Panel’s views on the most import ant issues to be addressed in the subsequent full-scale human exposure and health assessmen t that will be presented in the revised

documents?

The intended use of the exposure and risk analyses as these relate to standard setting or alternate risk management strategies should be clearly, ex plicitly and transparently stated. The baselineF-94 concentrations used in the initial model runs should reflect typical levels and corresponding reasonable maximum and likely minimum valu es should be identified and supported by references, if available. Sensitivity analyses shou ld be structured to specifically address the likelihood of false negative or false positive conclu sions in the uncertainty analysis. Values in

the current draft for soils and dust estimates are likely low and should either be adjusted higher in the baseline runs, or higher values should be specifically addressed in sensitivity analyses and subsequent uncertainty discussions.

The Primary Pb NAAQS (Chapter 5)

1. What are the Panel’s views on the adequacy and cl arity of the presentation of the basis for the existing standard and conclusions reached in the last review?

The document accurately captures the history of the NAAQS process for lead, but does little to indicate any policy implicatio ns or conclusions for today.

2. Based on the information contained in the first draft Staff Paper, as well as the AQCD, does the Panel have recommendations with regard to speci fic aspects of the standard to be considered in developing policy alternativ es? For example, considering th e prominence of the soil and dust pathways for ambient Pb exposures, and the ev idence regarding environmental response times, is there reason to give more emphasis to consid eration of an alternativ e (shorter or longer) averaging time; and, how might this be considered in the full-scale risk assessment given current capabilities?

The report needs to comprehensively consider an d address the relationshi p between ambient air

lead concentrations and result ant soil and, particular ly, dust lead concentrations. There then

needs to be a best effort made to determine an acceptable air lead con centration. Once that is determined the Agency could assess whether ther e are significant national exposures that require an NAAQS to address. There is in this draf t report a suggestive bias toward supporting a revocation of the NAAQS. This seems premature, as there is little in the analyses, to this point, suggesting what might be a “safe” or, at l east, an acceptable ambient air lead level.

Pb-related welfare effects an d screening level ecological ri sk assessment (Chapter 6):

I defer to other Committee members comments regarding Chapter 6.



### Technical Comments

Consideration of Uncertainty: The basic elements of the risk assessment methodology presented can be described by the breakdown of the proc edures employed in the documents. Those generally include i) identifyi ng and quantifying the sources, ii ) using empirical models to estimate media concentrations, iii) estimating ex posures via intake calculations, iv) predicting typical blood lead levels, v) estimating outcome blood lead distributions, vi ) predicting the health effect, and vii) partitioning the effect betw een “policy relevant and background” sources.F-95 The report recognizes that ther e are several difficulties inhe rent in both estimating and quantifying outcomes within each st ep and in utilizing those results in subsequent steps. These models also encompass a combination of non-lin ear relationships that provide input to the following steps. As a result, errors can propagate and this must be recognized in the uncertainty analyses. However, the effects are often mu ltiplicative, meaning that, although uncertainty increases, the consequences of under-estimation or over-estimation can be dissimilar, and are dependent on the status of othe r variables in the formulations.

As a result, it is important to thoroughly exam ine and discuss uncertainty and the potential for error in developing and assessing these models. It could enhance the unc ertainty analyses by framing the discussions in terms of Type I (false positive) and Type II (false negative) errors for the final risk assessment. Uncertainty in the risk assessment process basically produces the potential for two types of errors. Type I error is the identification of a specific chemical, area, or activity as a health concern, when in fact it is no t (false positive). Type II error is the elimination of a chemical, area or activity from further cons ideration, when in fact, it is a potential health hazard (false negative). In risk assessment, uncertainties are generally handled conservatively (i.e., health protective choices are preferentially made) to avoid Type II errors.

For these analyses, it seems the question is whether there is significant potential for IQ loss among children exposed to the policy relevant sources? This presupposes that the Agency considers IQ loss an unacceptable outcome. There is little in the current documents regarding what the Agency considers regarding the signifi cance of IQ loss and whethe r there is a threshold

of concern. This discussion needs to be clearly laid out in future drafts. The Type I error (false positive) would be predicting IQ loss for children that in fact suffer no such loss. The Type II error (false negative) would be predicting no loss for children that do indeed suffer a decrement. The consequences of the Type I error is requ iring unnecessary regulati on for the source(s) and damaged children is the outcome for the Type II error.

Each step in the risk assessment process can be evaluated in the context of the Type I/Type II error format and the sensitivity analysis conducted should be specified to provide insight into the likelihood of each error occurring. As a result my comments are provided by examining the main steps used and noted above:

i) identifying and quantif ying the sources,

The Staff Paper provides significantl y more information in this regard than was presented in the AQCD and the information seems to be a good and fair representation of the state of knowledge in the U.S. at this time. It does indicate, however, that the state of knowledge is a poor representation of true emissions and ambient ai r lead levels in the U.S. today. This seems particularly true around the majority of smaller source types that constitute a significant segment of overall emissions. This shortage of representa tive emissions data becomes acutely evident in the Pilot Risk analyses, where in several instance s there are no site-specific data and there is reliance on surrogate data, which also seems in short supply. As a result, it seems inherent on the Agency to develop as complete an evaluati on of the range of potentia l emissions associated with the types of facilities assessed in the Pilot. In the absence of real data, the Agency couldF-96 draw on its experience with regulating and evaluating emissions in similar facilities over the past thirty years.

Once this determination is made, an appropriate baseline emission rate should be identified. It may be that the current document does provide th e best baseline values that can be developed. The sensitivity analysis, howev er, should then be conducted using some reasonable maximum estimates and a similar reduced rate, while holding all other inputs consta nt as was accomplished in the draft. However, it is important that bo th upper and lower limits be accomplished as the effects may differ in each direction due to the non-linear relationships in the models. It is important to remember that these multiplicative effects can be real and are not artifacts of the

mathematical structure of the models. In the abse nce of “better” emissions estimates, a factor of 2 analysis might be appropriate, i.e., 1⁄2 and 2 times the baseline.

ii) using empirical models/observed data to estimate media concentrations,

There are two model efforts that are ultimately most important in estimating risk outcome and subsequently relating outcomes to a critical ambien t air lead level. Those are the ambient air lead

estimates and dust lead concentra tion models. There is a lack of air quality data, at least, in comparison to the previous NAAQS reviews and the monitors indicated in the Pilot analyses seem to be disadvantageously located. As a result, determining an appropriate standard will likely rely on modeled concentrations. The doc ument does indicate that current models are thought to be accurate to factor of 2. This might be an appropriate ratio to use for the sensitivity analysis, by substituting increase d and decreased air lead estima tes into the subsequent risk assessment steps and relating the outcomes to t hose levels. This is as opposed to doubling and halving the dispersion model inputs. Again it is important to conduct sensitivity runs using both upper and lower limits as the outcome must be related to this input parameter.

Perhaps, most critical is the estimation of dust le ad concentrations. It is interesting that despite the immense amount of work accomplished with lead dust in the last sixteen years, the same relationships developed for the 1990 analyses are employed today. These models are likely appropriate in the absence of any data, as they relate to estimating the increases in dust lead concentrations associated with increasing air an d soil concentrations. These models however, at

least in this reviewers experience, tend to underestimate dust lead concentrati ons at the much lower air and soil levels seen today. The empirical relationships were de veloped from databases

in which the dust concentrations were overwhelmed by high air and soil l ead levels associated with the point sources. Although le ad associated with other sources , such as paint, was always present, it seldom showed up as si gnificant variable in these equations. This resulted in intercept terms that failed to reflect “policy-related b ackground sources” and under-prediction in dust lead

levels as soil and air lead a pproached background concentrations. At the primary smelter site in Idaho (Bunker Hill Site) that underwent a similar remediation to the Missouri site, dust lead levels reached a plateau at 300-350 μg/g after completion of soil cleanup ( mean soil concentrations were less than <200 μg/g post-re mediation with no significant air lead remaining after smelter demolition). Dust lead survey s conducted in socio-economically similar communities with no history of lead emissions show ed house dust lead levels of about 50 μg/g in homes built after 1978 and 200 μg/g in older homes. It is unlikely, at the Bunker Hill site that

mean dust lead levels will decrease to be low 200-300 μg/g due to residual soil and dustF-97 contamination and the age of the housing stock. Th e low dust lead levels estimated for both the active primary and secondary smelters seem low to use as the baseline, but might be appropriate for the lower limit sensitivity r un. The Agency should consider ad justing the baseline run to reflect higher dust concentrations and a backgr ound component indicative of older housing, and then performing sensitivity analyses at higher and lower concentrations based on a review of available data, or a “factor of 2” type analys is. If not, increasing and decreasing this background component should be one of the sensitivity analyses.

iii) estimating exposures via intake calculations,

Various intake estimates are developed as input to the bio-kinetic models. These intakes depend on the media concentrations developed above an d exposure variables that ultimately determine how much lead enters the body. It is clear that under typical c onditions in the U.S. today, the majority of that lead comes via the ingesti on of soils and dusts, a nd significant efforts are directed at determining these parameters for th e Pilot and Staff Paper, as discussed below. However, this should not discount the importance of other routes, i.e. diet, drinking water, maternal contribution, and other “policy relevant background” sour ces. In a direct corollary to how the current NAAQS was established in 1978, these sources set a foundation blood lead level. Any “policy relevant air sources” can only be accommodated between this baseline and whatever unacceptable threshold is determined fo r the NAAQS or other critical risk management criteria. Because typical baseline blood lead levels are of the same order of magnitude as the effect levels, (i.e., 1-3 μg/dl vs . 2-5 μg/dl) it is equally important to appropriately identify the typical values and variability in “background” levels as it is in the “policy relevant source”. This seems particularly important to accomplish in th e primary and secondary smelter pilot analyses,

as there are reasons to believe that blood lead levels would be elevated over “non-industrially” lead impacted communities. This could be due to the age of housing stock, residual lead from historic operations impacting “baseline dust and soil concentr ations”, increased dietary components due to contamination of local food s ources, preparation, and so on. For example, at the Bunker Hill site, desp ite remediation of 97% of homes in some communities, house dust and blood lead levels both remain somewhat greater than the typical “national” values reflected in the default input parameters used in these analys es. Although “post-remedia tion” blood lead testing and risk analyses conducted at this site show compliance with CDC criteri a at Bunker Hill, these communities could not safely accommodate significan t emissions from a “new” smelter, as most of the acceptable exposure is accommodated in the “ post-remedial baseline”. Similarly, at least the primary and, likely, the secondary smelter pi lot studies should consider that higher than “typical U.S.” background blood lead levels are pr evalent in the communities. This possibility should be addressed either by incr easing the default input values for the baseline analysis, or investigating the potential effects of this uncertainty in the sensitivity analyses.

The most critical intake estimates with respect to the “policy relevant sources” are related to the dust ingestion rates (as the uncertainty in concen tration was discussed above). The overall soil and dust ingestion rate is set in the IEUB K and comparable Leggett model inputs and are appropriate values. There is uncertainty however, in the partition factor to employ (default 55:45 dust:soil). The default is appropriate for the baseli ne, but the use of the B unker Hill Site partition values (von Lindern et al., Please note the lower case v) in the sensitivity analysis bears some discussion. The 40:30:30 dust:yard:community part ition at Bunker Hill was empirically derivedF-98 and most critically differs from the IEUBK defau lt assumption, in that it reflects a significant contribution from soils outside the home yard, (i .e. other soils in the community). Other yards, commercial properties, parks, playgrounds, roadside s, streets, etc. were found to contribute as much to soil ingestion and house dust lead content, as the home yard soil. This became a more obvious problem with the IEUBK default guidance as the soil remediation program advanced.

Use of the clean soil values established at the child’s home to describe the soil intake and soil contribution to house dust, ignored the more impo rtant (after remediati on) contribution by other soils in the community to both soil ingestion and dust lead. In the Pilot Analysis and Staff Report, there are two important omissions in the determination of soil and dust intake

calculations. The first omission is use of the reme diated home yard soil concentration as the only

soil contribution. This limits the soil contributio n to the lowest possible value in the site, and ignores potential contributions to soil ingestion from other un remediated soils throughout the community. Secondly, this has a double impact in reducing the dust contribution. This minimal concentration is used in estimating dust concentr ations and it is possibl e that the impact of community soils as portrayed in von Lindern et al. is manifested through house dust. The treatment in the pilot analysis limits this contribution to the absolute minimum.

Combined with low concentrations predicted a bove for dust, possible underestimation of the policy relevant background, ignoring the potential impacts of other soils in the community likely results in minimally low intake estimates for soil and dust to blood lead in the primary and secondary smelter situations.

iv) predicting typical blood lead levels,

There have reportedly been some difficulties encountered in the application of the Leggett model. As a result, any critique of the Le ggett methodology will be reserved for the following draft. With respect to the IEUBK estimates, mo st of the factors that influence outcome blood

lead levels are associated with the input variables discussed a bove. However, there are important considerations with resp ect to the absorption or bioavailability utilized. The baseline runs should use the default bioavailability unless there is co mpelling site-specific information to substitute.

The use of the Midvale results for the Missouri site is a professional judgment and is likely appropriate in that it is similar to the default values for dust. The 42% value for soil could be applicable for a smelter situati on, but perhaps high if mine wastes were predominant. It is curious, however, why dust bioavailability would be lower than soils if the sources of lead to

both media are similar. The use of 18% from von Li ndern et al. for the sensitivity analysis also

bears some discussion. The 18% value was also derived empirically from some 5000 paired

blood lead:soil/dust concentration observations over several years. It had long been noted at the site the overall dose-response relationship at Bunk er Hill was reduced from that indicated by the IEUBK default parameters. However, the underl ying reason for the reduced response was never clearly determined. The most plausible expl anations were either lower than default bioavailability and reduced inge stion rates associated with th e health intervention efforts aggressively pursued with community families. The analyses in the von Lindern et al. paper

attribute the full effect to redu ced bioavailability and acknowledge that decreased ingestion rates are also a likely explanation. As a result, the 18% absorption estimate is an absolute minimum value and should be regarded as the lower limit in the sensitivity analysis and uncertainty discussion. The upper limit for sensitivity analyses should likely be near 40%, reflecting theF-99 likely predominance of lead oxides and small par ticles associated with the smelters and paint

contributions.

v) estimating outcome blood lead distributions,

Estimating the blood lead distribution depends on the selection of the GSD value. The 1.6 selected is correctly described as appropriate for a group of ch ildren with uniform exposures. However, it is not likely that a ll of the variance should be ascrib ed to differences in individual response. The GSD reflects both individual vari ation and some degree of variation in the exposure variables, as well. The 1.6 value is reco gnized as being appropriate to situations where the degree of variation in exposure is typical of the types of scenarios being evaluated. It becomes important that in the discussion of uncer tainties pursuant to the sensitivity analyses, the variances typically associ ated with realities of individual response and distributions of exposures,

not be confused with uncertainties related to the lack of characterization data. That is, there are real variances associated with individual respon se and the source and exposure parameters that should be captured in the 1.6 GSD. There are unk nowns associated with using average emission

factors that should be addressed in the sensitivity analyses an d uncertainty discussions. Some alternate GSDs, perhaps, 1.5 and 1.7 should be test ed to assess the effect on outcome variables

due to this selection.

vi) predicting the health effect,

There is some concern with the treatment of th e “cut points” in these analyses. Assuming that there is no effect below the cut point eliminates the possibility of a Type I error as no false positive is possible. The only error result would then be a false negative. This should be pointed

out in the discussions and considered in determ ining an acceptable level of risk or margin of safety in recommending a standard.

vii) partitioning the effect between “poli cy relevant and background” sources.

The methodology developed does allow determinati on of the relative contributions to absorbed lead and will be useful in developing a new st andard or alternative ri sk management strategy. However, it must be recognized that there is significant variance in the background levels and certain populations and individual members of all popula tions will be at greater risk as a result of these background sources. It is as important to identify these at-risk populations and assess the possibility for Type II error with these groups as it is to assess uncertainties based on statistical extrapolations of mean or baseline characterizations.

Summary: A clear and transparent understa nding of the policy questions that these analyses will assist in answering is of critical importance to entire procedure. Th ere is little in the analyses, to this point, suggesting what might be a “safe” or, at least, an acceptable ambient air lead level.

There needs to be a best effort made to determ ine an acceptable air lead concentration. Once that is determined the Agency could assess whether there are significant na tional exposures that require an NAAQS to address. The report ne eds to acknowledge the poor state of knowledge with respect to emissions and am bient air data relative to the pot ential standard level, and the necessity of depending on modeling and surroga te data. The report needs to complete anF-100 evaluation of the range of potential emissions asso ciated with the types of facilities assessed in the Pilot. The report needs to comprehensively consider and address the relationship between

ambient air lead concentrations and resultant soil and, particular ly, dust lead concentrations. The current methodologies likely underestimate both background and policy related house dust

concentrations. All of these factors combine to ma ke the sensitivity and un certainty analyses an essential component of the pr ocedure. These analyses shou ld pay special attention to distinguishing between va riability and uncertainty and discu ssing the potential for false positive and false negative conclusions relative the policy decisions under consideration.



### Post-Meeting Comments of Ian von Lindern

Following the February 5-7 meetings, it seems that the OAQPS staff will continue to assess potential NAAQS revisions and present those in Advanced Notice of Proposed Rule (ANPR) process. The technical aspects of potential NAAQ S development and speci fication, or de-listing, will be supported by the Pilot Risk Assessment activ ities. This differs in several respects from the original NAAQS process. Although the ne w procedure is endeavoring to provide the safeguards and opportunity to provide scientif ic advice, there seems to be two notable shortcomings that are not addresse d in the current Pilot Studies.

Both of these shortcomings and the problems in troduced are traced to the lack of sufficient monitoring data for sources, emissions, ambient ai r levels and impacts. This lack of data has

evolved because EPA has failed to monitor lead in situations that were at levels considerably lower than the 1978 NAAQS. However, it seems that health impact studies conducted over the last two decades suggest that th is strategy may not have been h ealth protective. This may not have been the case had the Agency diligently monitored at the levels suggested in the 1990 proposed revision to the NAAQS. Nevertheless, the result is th at the risk assessments now requisite to establish a protective strategy must rely on modeling and substantial inputs of professional judgment, experience, and protective policies. It is ironic that EPA’s attempt to streamline the process may discourage, rath er than solicit, this type of input.

The first deficiency considers the lack of na tional perspective with respect to populations impacted by potentially significant air lead leve ls. The reliance on the three case studies does address examples of the country’s primary sm elter, major secondary point sources, and emissions from roadside re-entrainment. However, it seems likely that the new level of concern will extend to lead TSP values of .25 μg/m3, or be low. There are large urban areas and numerous smaller sources that are of pot ential significance, and poorly ch aracterized, at these levels. Moreover, there is little presen ted in the AQCD, Draft Staff Pa per or the Pilot Study regarding the source-receptor relationships between these s ources, ambient air lead levels and populations potentially impacted. This seems to be a major omission that, if addressed in the ANPR, will not receive CASAC critique prior to vetting by policy and management. That could be remedied by including such a “national view” risk assessment as an additional analysis, but at this point it seems this most important issue will not benefit from critical scientific review.F-101 The CASAC committee is addressing this situat ion by trying to provi de pro-active advice regarding a critical assessment of the current st andard and potential strate gies for determining a protective standard for implementation. My commen ts in this regard are included in the subcommittee recommendations.

The second critical shortcoming has to do with de veloping the risk assess ment with the current population residing in the Pilot S ite impact areas and extending t hose conclusions to a national standard protective of human health. This is because, although the P ilot studies, with some modifications, may be representative of current co nditions at those sites; these analyses may not reflect potential exposures that could apply at these or other locations in the future.

My comments in this regard are included belo w as recommendations as to how the Pilot Risk

Assessment could be modified.

Potential modifications to th e baseline characterizations:

Several assumptions made in individual steps in the methodology tend to underestimate background contributions to intake. The Agency should consider adjustin g the baseline run to reflect higher dust concentrations and a bac kground component indicat ive of older housing. Similarly, at least the primary (and possibly the s econdary) smelter pilot st udies should consider that higher than “typical U.S.” background blood lead levels are pr evalent in the communities, or

would be in the absence of active health intervention programs. In these cases, the draft analyses ignore the potential impacts of aggregate soils in the communiti es, and underestimate dust lead concentrations through the use of regression models that likely don’t extra polate appropriately to levels that are lower than the parent database.

Potential Sensitivity Analyses

Extensive sensitivity analyses should be conduc ted by (as indicated above) identifying an appropriate baseline or typical model run, and then varying key components while holding others constant. However, the sensitivity runs shoul d be accomplished using both lower and upper limit analyses. It would enhance the un certainty analyses by framing the discussions in terms of Type I (false positive) and Type II (false negativ e) errors for the final risk assessment.

Baseline Blood Lead Levels: It should be recognized that th ere is significant variance in the background levels and certain populations and indi vidual members of all populations will be at greater risk as a result of the background sources . It is as important to identify these at-risk populations and assess the possibility for Type II error with these groups as it is to assess

uncertainties based on statistical extrapolations of mean or baseline characterizations. The potential effects of increasing and decreasing the background components should be one of the sensitivity analyses.

Baseline Emission Rates: The current analyses rely on average emission rates that may be out of date. In several instances there are no site-speci fic data and there is re liance on surrogate data, which also seems in short supply. It may be th at the current document does provide the best

baseline values that can be deve loped. However, the range of poten tial emissions associated withF-102 the types of facilities assessed in the Pilot should be developed. The sensitivity analysis should then be conducted using some reasonable ma ximum estimates and similar reduced rates.

Soil Lead Levels: Possible underestimation of background soil levels for the point source communities, as discussed above, and ignoring th e potential impacts of other soils in these communities could result in minimally low intake estimates for soil. As a result, soil

concentrations should be varied as one of the sensitivity components.

Dust Lead Levels: Perhaps, most critical is the estimati on made in the entire methodology is dust

lead concentration from soil a nd air lead concentrations. Poss ible underestimation of background dust lead levels and ignoring the potential impacts of other soils in the community likely results in minimally low input variables for soil contribu tion to dust. Additionally, the air variable that

determines this route’s contribution to dust has particular uncertainties. As a result, it will be important not only to assess the effect of dust on outcome health indices, but the agency should also consider additional sensitivity analyses of the soil and air se lections on dust lead.

Bioavailability: The 18% absorption estimate is an ab solute minimum value and should be regarded as the lower limit in the sensitivity an alysis and uncertainty discussion. The upper limit for sensitivity analyses should lik ely be near 40%, reflecting th e likely predominance of lead oxides and small particles associated with the smelters and paint contributions.

GS D: Alternate GSDs, both higher and lower than th e baseline 1.6 should be tested to assess the

effect on outcome variables due to this selecti on. A substantially higher level, perhaps 2.0 should

also be considered.

Alternative Standard levels: The overall process envi sioned in the Pilot A ssessment suggests that the final runs will be accomplished at candidate NAAQS revision concentrations. This will be a convenient method to examine pros pective standard levels. Howeve r, due the lack of pertinent air quality data at critical exposure locations, these analyses ultimately rely on modeled data. Because the accuracy of model pred ictions is (at best) a factor of two this will pr esent “special” uncertainty questions. The predictions drive much of the internal concentr ations derived in the model will ultimately be used to determine ris k. However, those same model predictions will presumably be used to determine the protective concentration for the most exposed location and then at the property line. This va lue will, presumably be a driver with an appropriate margin of safety as the proposed NAAQS, if adopted. As a result, it may be advisable to conduct a “last” uncertainty discussion relative to the selection of the appropriate air concentration value.

TSP/PM10 Conversion: This problem is compounded by the possible need to convert from a TSP-based risk assessment analysis to a proposed PM-10 standard. If it is proposed to develop a PM10 standard, the sensitivity to the conversion equation assumptions should be tested in a sensitivity analysis.F-103 Prepare Intake and Uptake Tables and Partition those by Pathway

The risk assessment documents would be consider ably more convenient to review if summary tables were prepared for pathway specific inta ke and uptake for the various model runs. These could be provided as an appendi x for interested parties.

Property Line Implementation

The Standard, if and when modified, will be requir ed to apply at the facility property lines in relation to point sources. However, if the lowe st acceptable air concentration determined to protect the surrounding population, for example, is found to be .25 μg/m3 for highest exposed current resident, the air value at the property line would be considerably hi gher. According to the

manner in which the current standard should be en forced, the least protective level that would qualify as a result of the risk as sessment would apply at the propert y line. This would result in a margin of safety for those currently most expos ed after implementation. However, this analysis may not be protective because of the non-linear inter-dependencies of air soil and dust exposures accounted for in the risk assessments. This pres ents the basic question, of why don’t the Pilot assessments consider potentially exposed children at the property line, and use the existing population data to assess model performance. Th e agency should consider model runs with population blocks filled with a hypothetical childhood population.

Long-term Air-Soil-Dust Equilibrium

Determination of recontamination rates and equi librium media concentrations for active source areas remains a major shortcoming in the overall analysis.



### Comments of Ian von Lindern Regarding the Primary NAAQS

February 22, 2007

Standard Setting Considerations

Proposing a primary NAAQS for lead is a sophi sticated and complex undertaking that must reflect numerous scientific, societal, technica l and policy considerations. These must be integrated into comprehensive policy that reflects the best science available. In the past it has been CASAC’s job to i) identify the appropriate science and ii) provide advice to EPA as to how to interpret those findings in applying policy co nsiderations and developing a protective health strategy. It seems the CASAC’s f undamental problem is that the “new” process shortcuts and endangers the effectiveness of th e latter portion of this protoc ol. EPA managers and political appointees will now combine policy directives with their own inte rpretation and application of the science in a composite document that will be pr esented “after the fact” for scientific appraisal by CASAC concurrent with public review. This limits CASAC’s ro le to critiquing the AQCD to identify and describe the pertinent science, but diminishes the committee’s ability to judge whether the science is appropria tely applied in developing th e proposed NAAQS, or de-listing.F-104 CASAC’s immediate challenge, it seems, is to send a clear message to EPA regarding the perceived health significance of ambient air lead, the adequacy of the current standard, the need for revision, and how the availa ble scientific information can and should be used. The Chair’s proposal to take a pro-active stance and forw ard recommendations on a primary NAAQS is a positive strategy to achieve this end. This sub-gr oup has been assigned the task of undertaking the steps of developing and proposing a revised pr imary standard. In going through this exercise,

those issues that must be addressed in devel oping the standard, and the CASAC’s opinion of how the science identified in the AQCD can be applie d, will be illuminated for the Administrator.

There are some clear conclusions that the CASA C seems to have reached consensus on. Paul Mushak did a good job of identifying those in hi s earlier transmittal. A candidate list includes:

• The current NAAQS is not protective, allo wing these concentra tions would be poor public health policy and likely cause irreversible harm to children.

• This finding is not new. The NAAQS was re garded by CASAC in 1990 to be insufficient to protect public health. The EPA elected to pursue a policy of multi-media exposure reduction that was, given the understanding of po tential health effect s at that time, in large part successful in reducing chil dhood lead absorption throughout the country.

• Since 1990, new findings suggest that adverse effects, in partic ular those associated with neuro-cognitive deficits in young children, occur at lower blood lead levels than previously understood.

• Dose-response and exposure/bio- kinetic studies suggest that current ambient air lead levels in portions of the U.S. can result in elevated blood lead levels among children that

are of concern. Analyses conducted by this sub- group suggest that ambient air concentrations of .25 μg/m3 or lower could be of concern.

• Lead is a ubiquitous, multi-media contaminant that has been traditi onally regulated as a priority pollutant. Both am bient air and background concentrations in other media of sufficient magnitude to increase children’ s blood lead to levels of concern.

• Although air quality and emissions were appr opriately monitored for the current NAAQS over the last two decades, the existing national database is insufficient to identify those populations at-risk in the count ry today. Failure to lower the NAAQS in 1990 resulted in

abandonment of numerous monitors. As a resu lt, the extent of exposures exceeding likely revised NAAQS levels is unknown.

• OAQPS has elected to conduct a risk assessmen t analyses that focus on impacts around “pilot” point and area sources. This information will be useful in estimating specific impacts in such locations, and presumably in evaluating control strategies to reduce excess exposures. However, these analyses do not address the potentially large number of children in the U.S. exposed to air lead concen trations in the potenti al range of a revised NAAQS.F-105 • As a result, the CASAC is concerned that th e EPA does not have a sufficient database to evaluate the efficacy of regulat ing lead emissions as a hazardous air pollutant and should exercise great caution in considering delisting.

Paul Mushak has laid out th ree potential methods to develop a primary NAAQS. This is obviously a substantial unde rtaking and it is unlikely that the CASAC, in its limited capacity can fully develop a revised NAAQS, pa rticularly considering the need to integrate policy concerns. However, the exercise can illuminate those issues that require responsible consideration of the science and illustrate CASAC’s understanding and recommendations regarding the use of the science in resolving those issues.

Method A

As Paul Mushak points out, this is the met hod employed in 1978 to set the current NAAQS and the subsequent WHO standard. It is simplified a nd nearly 30 years old, but has the particular advantage of being in a familiar structure and ha ving addressed the several issues that must be considered in developing a standard. EPA’s c onsiderations were documented in the Federal Register, Vol. 43, No. 194 (46252) and the met hodology essentially condensed the procedure into the selection of five key parameters. Discus sing the scientific considerations that go into selecting these parameters provides a vehicle fo r CASAC to convey an opinion on the issues and the science that should be relied upon. Doing this in parallel to EPA’ s 1978 strategy, and in the context of new information developed in the AQCD, is an opportunity to convey scientific advances in each of these areas, and simultaneously provide, at le ast, a range of potential primary NAAQS values to support the above conclusions.

Selection of Key Parameters

In selecting values for the key parameters it is important to note that these are interrelated. Similar factors are considered in each parameter and the effects are multiplicative. The overall objective of the procedure is to accurately predict the “tail” of the population. As a result, failure to “balance” the selection, or choosing all cons ervative or protective pa rameters, will increase the probability of error.

The three attached Tables show various permut ations of parameter selections in the ranges indicated by Paul Mushak and Bruce Lanphear’s earlier transmittals. Their specific numbers, I believe, are highlighted in the first table along with EPA’s 1978 calculation.

Maximum Blood Lead Level – This is related to lowest obs ervable effects of concern, and previously cited CDC criteria that was 30 μg /dl in 1978 and has been 10 μg/dl since 1991. The weight of evidence in the AQCD seems to suggest that deleterious effects extend to 5 μg/dl, or below. CASAC will need to justify these values and address the applicability of CDC’s current

recommendations. Current candidate values are 2.5 and 5.0 μg/dl.

Protectiveness – This represents the percent of populat ion can be protected by a reasonable standard. In 1978 EPA selected 99.5% (and a GSD of 1.3) in order to accommodate “special high risk groups within the ove rall population,” that was larg e and estimated to exceed 20F-106 million children at that time. This parameter is likely the most “policy” driven selection in the process, but there is little scientific reason to advocate a lessening of the degree of protectiveness today. However, there are, at least two additiona l considerations that are both related to why

those children are observed in the “unprotected” portion of the tail of the blood lead distribution.

The first consideration relates to factors that can’t practi cably be addressed by the NAAQS strategy. These children may show high blood lead levels due to exposures and sources unrelated to the air lead input, or may be the result of extreme co-factor considerations (i.e., pica-type behavior or physiological pre-di sposition). With regard to the second consideration these children may be in extreme situations where seve ral factors multiply to result in excessive blood lead levels. This is the special population that EP A elected to protect with a combination of the 99.5 % /GSD=1.3 combination in 1978. These two para meters must be selected in concert in order to encompass those groups th at can be effectively addresse d with the control strategy. EPA

faced a similar decision in the last decade in other programs and elected to pursue a 95%/GSD=1.6 selection as a risk management goal in CERCLA programs. Based on this precedent, it seems the candidate values for prot ectiveness range from 95-99.5%, and include the

98%-tile WHO value.

GSD – This parameter, in concert with protectiven ess, is the most important to define. The selection of the GSD is the likely reason for the difference in values presented by Bruce Lanphear and Paul Mushak in their transmittals. Ther e are, at least, two particular problems in selecting an appropriate GSD. Those are firs t, defining what variance the GSD accommodates and second, the GSD for a similarly exposed popul ation likely increases at lower blood lead

levels. I find it convenient to consider the elem ents of variance that make up the GSD for the blood lead distribution. The GSD, as used by EP A, encompasses a basic individual response

variance for those with similar in ternal exposure, additional vari ance associated with absorption

and excretion that can be due to differences in pre-disposition such as nutritional status, etc.;

variance due to differences in in take associated with behavior ; and differences due exposure gradients. The GSD found in typical population surv eys includes to some degr ee all of these (and perhaps others), and uses this single parameter to account for several el ements of variance in blood lead response. The 1.3 value selected in 19 78 was reported for the epidemic at the Bunker Hill site in Idaho and likely represents the indi vidual response differences and lowest reasonable

value. This GSD is also reflective of the dos e-response relationship and the mechanisms of absorption. Exposure, pre-disposit ion, behavioral and absorption m echanisms in these severely exposed children were possibly saturated, masking out several potential cont ributors to variance, leaving individual response. Slig htly higher (1.4) GSDs were noted for highly (but no so severely) exposed children in urban environments (New York City) at that time. As these high exposures and blood lead levels decreased GSDs we re noted to increase, arriving at a consensus value of 1.6 for risk assessment in the 1990s, alth ough this value is often disputed. More recent surveys, notably NHANES, show GSDs of 2.0 and greater. These large surveys likely encompass several elements of overall varian ce and includes those “spe cial populations” that should be considered (in or out ) in selecting the le vel of protectiveness. GSDs are probably higher now than in 1978 (possibly excepting the individual variance), both because lower blood

lead levels can show more variance as means decrease and fluctuations are relatively more significant; and because the dose-response relations hip is “steeper” at lower blood leads. This becomes important in the selection of the slope fact or relating blood lead leve ls to air lead levels below. The selection of the slop e factor must consider the shap e of the dose response relationshipF-107 at current blood lead levels, as opposed to typical levels in 1978. As a result, the GSD must be

selected in concert with both th e level of protectiveness descri bed above and the slope factor discussed below. Candidate values likely range from 1.3 to 2.0.

These first three parameters are largely related to protectiveness and the distribution of at-risk

children in the “tail” of the population. The next two parameters are related to the mean blood lead response, and the dose-re sponse relationship at the mea n. However, the GSD must be

selected to accommodate those factors used in se lecting the other paramete rs in both categories.

Non-air Background – This parameter is most important to se lect as it represents the baseline or background component of lead exposure that is not amenable to reduction through the NAAQS. This value was selected as 12 μg/dl in 1978, and wa s believed to be based on blood lead levels in supposedly “non-air” exposed area s. It is important to note that this background level has decreased to near 1 μg/dl in the interim due to EPA and other agencies multi-media exposure reduction programs. It is also true that mu ch of what was consid ered non-air in 1978, subsequently decreased due to the air lead re ductions. These were likely related to secondary dust exposures resulting from what EPA ac knowledged as the poorly understood air-soil-dust relationship at that time. That relationship is no better understood at today’s media concentration levels. It is also important to note that the bl ood lead levels ascribed to background sources in 1978 were of similar or greater magnitude than th e air, and in some cases exceeded acceptable criteria in the absence of significant air l ead exposure. This was cited as a reason for implementing an NAAQS strategy that accounted for contributions from other sources in favor a technology-based or hazardous air pollutant standa rd. The same situation exists today at about

1/12 th the overall exposure level. This parameter s hould be carefully selected to include those typical background sources, but no t those “special exposure popul ations” considered in the protectiveness and GSD selection. Candidate va lues are 1.0, 1.2, and 1.4 μg/dl. A lower level

could be considered.

Blood/Air Slope – EPA selected a slope value of 2 μg/dl blood per 1 μg/m3 air lead in 1978. This was based on three studies, two contro lled adult inhalation st udies and one childhood epidemiologic study that was the sa me Bunker Hill site in Idaho st udy used in selecting the GSD. For reasons discussed above, both of these parameter values were derived from a severely exposed population that had absorbed almost all the lead it could accommoda te. It is likely that these values represent minimums today, as the blood lead levels are much lower and the doseresponse rate seems to increase as blood lead leve ls go below 10 μg/dl. However, in selecting the value to use in subsequent analyses, it should accommodate, and not “double count”, any effect of increased dose response accoun ted for in the GSD selection. Ca ndidate values are 2 used in 1978, 5 used by WHO, 10 noted in recent studies, and 20 as a maximum.

The attached Tables are my attempt to calcu late the range of a revised NAAQS using the 1978 methodology and the candidate values discussed above for the five parameters. This may be of use in identifying likely values for a health prot ective standard. I have not had the opportunity as yet to review Methods B and C in similar detail. I do, however endorse the approaches and believe we should develop those, as well. In that way we may a rrive at a consensus value (or range of values) from all three methods that we, as a committee, may consider protective ofF-108 public health. We can then, in our best scient ific judgment, convey to the Administrator the CASAC’s view of the application of science in developing this most important health protection.

Table 1: NAAQS Calculations Using the 1978 meth odology and a Non-air Background of 1.0 μg/dlF-109 Table 2: NAAQS Calculations Using the 1978 meth odology and a Non-air Background of 1.4 μg/dlF-110 Table 3: NAAQS Calculations Using the 1978 meth odology and a Non-air Background of 1.2 μg/dlF-111 

### Dr. Barbara Zielinska

Barbara Zielinska



### Comments on Chapter 4 of the Draft Technical Report : Estimates of Media

Concentrations

Overall, this is a very well written and info rmative chapter that describes the results of modeling of media concentrations at three locat ions and compares them with measurements. The question one may ask is if the selected locations do represen t the general population exposures. While the case of primary Pb smelted represents the upper leve l of exposure (as this is the only location exceeding the current Pb stan dard), the exposure near roadways is far more common in urban and suburban areas and perhap s it should be expanded further. Although TSP lead data are rather sparse, the general popula tion exposure is probably better characterized by

PM 10 lead (especially close to roadways) and I be lieve that there are data available (beside Houston) that can support such evaluation. It would be also de sirable to extend the analysis beyond attainment of the current NAAQS and include much lower levels, down to approximately 0.1 ug/m 3

.

Specific comments/questions:

1. Section 4.1.2.4 – Air Modeling Performance As sessment for Primary Smelter (p. 4-8 to 4-10).

a. It is evident from Table 4-4 that th e model overestimates the actual ambient

concentrations at close distances to the f acility and underestimates at more distant locations. However, in case of dry deposit ion, the data in Tabl e 4-5 indicate that the model overestimates deposition as co mpared to measurements (although text on page 4-8, line 28-29 says something opposite). Yet, the overall conclusion on page 4-9, line 1-2 is that “modeled concentrations a nd depositions are fairly representative of conditions over the la st 5 years based on comparison with the monitors”. This statement seems to be overly optimistic.

b. One of the possible reasons for the undere stimation of Pb ambi ent concentrations by the model could be a severe underestima tion of resuspension of deposited lead

c. The lack of a proper representation of Pb particle size distribution could be a reason for deposition differences between modeling and measurements

d. The footnote to Table 4-4 on p. 4-9 says that all non-detects were assigned half of the detection limit for averaging. The doc ument does not specify the MDL, but this may elevate artificially the averages.

2. In the case of secondary smelter (section 4-2, page 4-21) the m odeled period was from 1997 to 2000. For the primary Pb smelter, this was 2000-2005. Were emission data not available for a more recent period? Th e footnote on p 4-21 says that in 2003 the quarterly average Pb concentration at one monitor exceeded the current NAAQS, so the 1997 – 2000 period may not represent current conditions.F-112 3. Air modeling performance assessment for seco ndary smelters (section 4.2.2.4) indicates 3

times lower modeled concentrations than mon itored values at the monitor locations. The potential differences between actual meteorol ogical conditions and used in the model are cited as a possible explanation, but this e xplanation is not convincing. Again, was the resuspension properly accounted for in the model?

4. Incidentally, the modeled soil concentrations are also 3 times lower than measured soil concentrations at similar facility (page 4- 29). So, the modeled results were scaled up 3 times (this procedure was called “hybrid conc entrations”). But this scale-up was not

done for ambient concentr ations – this seems to be inconsistent.

5. Houston was selected as a representative s ite for the “near roadway” scenario. For

characterization of “zone of influence” for the near-roadway location the modeling results for diesel PM were used (page 4-33) . Since both diesel and gasoline vehicle (main source of lead) PM are very small (below 1 um) this seems to be a reasonable assumption.



### Comments on Chapter 2 of the OAQPS Le ad Staff Paper: Characterization of

Ambient Lead

Chapter 2 is very well written and provides ample information regarding Pb emissions, concentrations and fate. However, it seems to be a little disconnected from the Technical Report. While the Chapter 4 of the Technical Report deals mostly with modeling, Chapter 2 of the Staff Paper states flatly on pages 2-46 to 2-47 th at the Gaussian disper sion models generally

underestimate ambient concentrations and are not useful for national scale exposure assessments. However, due to the sparse monitoring data, th e modeling is a necessary tool to estimate the exposure of general population. What is the reason that the models are not good enough? Are the emission data inadequate? Or are there so me other reasons? No explanation is offered.

Answers to specific charge questions:

1. To what extent are the emissions and ai r quality characterizations and analyses clearly communicated, approp riately characterized and rel evant to the review of the primary and secondary lead NAAQS?

Chapter 2 relays primary on the EPA National Emission Inventory of 2002 in describing the major emission sources of lead. The Pb Crite ria Document expresse d the opinion that the inventory data are inadequate. Chapter 2 of SP does not comment on quality of these data. However, the authors mention on page 2-7 that ma ny Pb sources are not reflected in the national emission inventory, including resuspension of the road dust, Pb present in vehicle emissions from lubricating oil and from tr aces of Pb in gasoline, break wear, etc. These sources are the most relevant as far as general population is c oncerned. After all, the majority of population resides in cities, not in the vicinity of primary and secondary smelters.F-113 2. Does the information in Chapter 2 provide a sufficient ambient Pb-related basis for the exposure, human health and environmen tal effects, health risk assessment and environmental assessment pres ented in later chapters?

The information presented in this chapter emphasi zes that in general, ambient levels of Pb

are much lower than the current standard. Howeve r, due to the lack of information as to what might be a safe or, at least, an acceptable ambien t air lead level, the dist ribution of ambient lead levels across the country should be better charact erized. In this regar d, I find the histogram presented by Dr. Joel Schwartz in his comments more informative than the box and whisker plots in Chapter 2. Although the STN data used by Dr. Schwartz are for lead concentrations in PM 2.5 , thus they may represent the lower end of exposure, they seem to be rele vant to traffic-related sources. This Chapter needs to emphasize the p oor state of ambient air data relative to the potential standard level, which necessitate the dependence on modeli ng and surrogate data.

The TSP Pb measurement method is rather outdat ed and the data are sparse, thus the effort should be made to replace it with PM 10 . In this regard more info rmation about correlations between Pb concentrations in different par ticle sizes would be highly beneficial.

A few minor editorial comments :

1. Page 2-12, line 24. A period is missing after “metal”.

2. Page 2-21, line 6: Not all analytical tec hniques for Pb measurements require filter extraction (e.g., XRF).

3. Page 2-23, line 14-16. I’m not sure if the statem ent that the decline in the number of Pb NAAQS compliance sites was due to the need to fund PM 2.5 and ozone monitoring sites, is fully justified.

4. Page 2-29, line 15. What is a “composite” form?

5. Page 2-43. line 3: 2.4.2.3

6. Page 2-49, line 26: remove one of the “as well”

### NOTICE

This report has been written as part of the activities of the U.S. Environmental Protection Agency’s (EPA) Clean Air Scie ntific Advisory Committee (CASAC), a Federal advisory committee administra tively located under the EPA Science Advisory Board (SAB) Staff Office that is ch artered to provide ex tramural scientific

information and advice to the Administrato r and other officials of the EPA. The CASAC is structured to provi de balanced, expert assessm ent of scientific matters related to issue and problems facing the Agen cy. This report has not been reviewed for approval by the Agency and, hence, the co ntents of this report do not necessarily represent the views and policie s of the EPA, nor of other agencies in the Executive Branch of the Federal government, nor doe s mention of trade names or commercial products constitute a recommendation for us e. CASAC reports are posted on the SAB

Web site at: http://www.epa.gov/sab

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