UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

 WASHINGTON D.C. 20460 

 OFFICE OF THE ADMINISTRATOR 

 SCIENCE ADVISORY BOARD

 

January 5, 2010 

EPA-SAB-10-001 

The Honorable Lisa P. Jackson 

Administrator 

U.S. Environmental Protection Agency 

1200 Pennsylvania Avenue, N.W. 

Washington, D.C. 20460 

Subject: SAB Review of Draft “EPA Radiogenic Cancer Risk Models and Projections for the 

 U.S. Population” 

 

Dear Administrator Jackson: 

 

The Radiation Advisory Committee (RAC) of the Science Advisory Board (SAB) reviewed the 

draft “EPA Radiogenic Cancer Risk Models and Projections for the U.S. Population, December 2008,” 

also known as the draft revised “Blue Book,” which was prepared by the EPA’s Office of Radiation and 

Indoor Air (ORIA). It describes proposed changes in methods for estimating radiogenic cancer risk, and 

gives examples of risk estimates for individual radiogenic cancers that it derived mostly from advice and 

methods based on the 2006 National Research Council Biological Effects of Ionizing Radiation (BEIR 

VII) Report, which was sponsored by EPA and other federal agencies. The revised Blue Book will then 

be used to obtain values of radionuclide risk coefficients for over 800 radionuclides in the revised Federal 

Guidance Report 13 (FGR 13). 

The SAB Committee, augmented with consultants for this specific review, found that the EPA’s 

draft revised Blue Book is impressively researched, based on carefully considered concepts, and well 

written. We recommend the following in response to the three charge questions posed by EPA: 

1) Appropriateness of models not taken directly from BEIR VII: The SAB agrees with the approaches 

proposed by the EPA except for the following: (a) The discussion of a revised relative biological 

effectiveness (RBE) value for low-energy beta particles, gamma rays, and x rays is unsuitably vague. 

We recommend that the EPA select a value of the RBE after compiling and evaluating the pertinent 

information and submitting it to peer review; the revised Blue Book publication need not be delayed 

as long as the value of the RBE is decided before the revised FGR 13 is published; (b) We 

recommend, in contrast to BEIR VII, using the arithmetic mean for combining information from each 

pair of excess absolute risk value and excess relative risk value for transferring lifetime attributable 

risk from the Japanese lifespan study to the U.S. population; use of the geometric mean recommended 

by BEIR VII and accepted by the EPA has no preferred theoretical basis, can present difficulties in 

further data processing, and results in unjustified lower mean values; and (c) We recommend that for 

bone cancer, the EPA reconsider modeling the data base for the radium dial painter cohort with 

consideration of the recently published data analyses. We compliment the EPA on developing an 
improved model that considers the survival rate of breast cancer patients. In the future, the EPA 

should consider applying this model to other cancers with high rates of survival. 

 

2) Adequacy and reasonableness of the uncertainty analysis by the EPA: The risk uncertainty analysis 

in the draft revised Blue Book is reasonable and comprehensive for deriving overall estimate 

uncertainty from sampling variation, model parameters, and data transfer to the U.S. population. We 

recommend these improvements: (a) Increase the clarity and transparency in quantifying the sources 

of uncertainty, notably in the selection of distributions chosen for the sources of uncertainty; (b) 

Verify the uncertainty analysis by determining uncertainty intervals by a perturbation approach, i.e., 

varying the value of each major contributor to uncertainty over a reasonable range to calculate the 

corresponding range of point estimates; and (c) Make Bayesian uncertainty analysis of confidence 

intervals as consistent as possible with the point estimate of risk and justify use of these two distinct 

approaches. 

 

3) Presentation of overall information and application of BEIR VII: The draft revised Blue Book is 

scientifically defensible and appropriate. We recommend that the EPA expand the presented 

information by including: (a) studies of noncancer mortality; (b) brain cancer studies; (c) recent 

reviews by the International Commission on Radiological Protection (ICRP) and United Nations 

Scientific Committee on the Effects of Atomic Radiation (UNSCEAR); and (d) conclusions from the 

National Council on Radiation Protection and Measurements (NCRP) Report #159 on the risks of 

radiation-induced thyroid cancer.

The calculations and results in the draft revised Blue Book are readily understood. However, we 

recommend that EPA clarify the purpose and application of the draft revised Blue Book contents in its 

first Section by presenting in sufficient detail the path toward a revised FGR 13, and in its last Section by 

listing sufficient FGR 13 values of radionuclide risk coefficients to demonstrate the impact – if any – on 

them by the revised methods and updated data for estimated cancer risks proposed in the draft revised 

Blue Book. The draft revised Blue Book has commendable accuracy and balance. We recommend that 

the EPA enhance the level of detail by (a) reporting risk estimates associated with cohorts exposed to 

protracted low doses of ionizing radiation, and (b) considering distinguishable types of cancer within a 

given organ. 

The SAB appreciates the opportunity to review this draft document and hopes that its 

recommendations will support the EPA in implementing modifications in the current methods for 

estimating radiogenic cancer risks and updating the Blue Book accordingly. We look forward to your 

response to the recommendations contained in this review. 

 Sincerely, 

 /Signed/ /Signed/ 

Dr. Deborah L. Swackhamer, Chair, Dr. Bernd Kahn, Chair, 

Science Advisory Board SAB Radiation Advisory Committee 

ii 
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NOTICE 

 This report has been written as part of the activities of the Environmental Protection 

Agency (EPA) Science Advisory Board (SAB), a public advisory group providing extramural 

scientific information and advice to the Administrator and other officials of the EPA. The SAB 

is structured to provide balanced, expert assessment of scientific matters related to problems 

facing the Agency. This report has not been reviewed for approval by the Agency and, hence, 

the contents of this report do not necessarily represent the views and policies of the EPA, nor of 

other agencies in the Executive Branch of the Federal government, nor does mention of trade 

names of commercial products constitute a recommendation for use. Reports and advisories of 

the SAB are posted on the EPA website at http://www.epa.gov/sab.
U.S. Environmental Protection Agency 

Science Advisory Board (SAB) 

Radiation Advisory Committee (RAC) 

Augmented for the Review of EPA’s Radiogenic 

Cancer Risk Assessment 

CHAIR

Dr. Bernd Kahn, Professor Emeritus, Nuclear and Radiological Engineering Program, and 

Director, Environmental Radiation Center, Georgia Tech. Research Institute, Georgia Institute of 

Technology, Atlanta, GA 

MEMBERS

Dr. Susan M. Bailey, Associate Professor, Department of Environmental and Radiological 

Health Sciences, Colorado State University, Fort Collins, CO 

Dr. Thomas B. Borak, Professor, Department of Environmental and Radiological Health 

Sciences, Colorado State University, Fort Collins, CO 

Dr. Faith G. Davis, Senior Associate Dean and Director of Graduate Studies, Professor of 

Epidemiology, Division of Epidemiology and Biostatistics, School of Public Health, University 

of Illinois at Chicago, Chicago, IL 

Dr. Brian Dodd, Independent Consultant, Las Vegas, NV 

Dr. R. William Field, Professor, Department of Occupational and Environmental Health, 

College of Public Health, University of Iowa, Iowa City, IA 

Dr. Shirley A. Fry, Independent Consultant, Indianapolis, IN 

Dr. William C. Griffith, Associate Director, Institute for Risk Analysis and Risk 

Communication, Department of Environmental and Occupational Health Sciences, University of 

Washington, Seattle, WA 

Dr. Jonathan M. Links, Professor and Deputy Chair, Department of Environmental Health 

Sciences, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 

Dr. William F. Morgan, Director of Radiation Biology and Biophysics, Biological Sciences 

Division, Fundamental & Computational Sciences Directorate, Pacific Northwest National 

Laboratory, Richland, WA 

Mr. Bruce A. Napier, Staff Scientist, Radiological Science & Engineering Group, Pacific 

Northwest National Laboratory, Richland, WA 

iv 
v 

Dr. Daniel O. Stram, Professor, Department of Preventive Medicine, Division of Biostatistics 

and Genetic Epidemiology, Keck School of Medicine, University of Southern California, Los 

Angeles, CA 

CONSULTANTS

Dr. Ethel S. Gilbert, Staff Scientist, U.S. National Institutes of Health, National Cancer 

Institute, Rockville, MD 

Dr. Peter G. Groer, Professor Emeritus, University of Tennessee, Dept. of Nuclear 

Engineering, Tampa, FL 

Dr. David G. Hoel, Distinguished University Professor, Medical University of So. Carolina, 

Department of Biometry & Epidemiology, Charleston, SC 

Dr. Richard W. Hornung, Director of Biostatistics and Data Management, Division of General 

& Community Pediatrics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 

Dr. Genevieve Matanoski, Professor, Department of Epidemiology, Johns Hopkins University, 

Baltimore, MD 

Dr. Dale L. Preston, Principal Scientist, Hirosoft International, Eureka, CA 

Dr. Genevieve S. Roessler, Professor Emerita and Radiation Consultant, Department of Nuclear 

and Radiological Engineering, University of Florida, Elysian, MN 

SCIENCE ADVISORY BOARD STAFF 

Dr. K. Jack Kooyoomjian, Designated Federal Officer, US EPA, Science Advisory Board 

(1400F), 1200 Pennsylvania Avenue, NW, Washington, DC, 20460 
U.S. Environmental Protection Agency 

Science Advisory Board 

FY 2009 

CHAIR 

Dr. Deborah L. Swackhamer, Professor and Co-Director, Environmental Health Sciences and 

Water Resources Center, University of Minnesota, St. Paul, MN 

MEMBERS 

Dr. David T. Allen, Professor, Department of Chemical Engineering, University of Texas, 

Austin, TX 

Dr. John Balbus, Adjunct Associate Professor, George Washington University, School of 

Public Health and Health Services, Washington, DC 

Dr. Gregory Biddinger, Coordinator, Natural Land Management Programs, Toxicology and 

Environmental Sciences, ExxonMobil Biomedical Sciences, Inc., Houston, TX 

Dr. Timothy Buckley, Associate Professor and Chair, Division of Environmental Health 

Sciences, College of Public Health, The Ohio State University, Columbus, OH 

Dr. Thomas Burke, Professor, Department of Health Policy and Management, Johns Hopkins 

Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD 

Dr. James Bus, Director of External Technology, Toxicology and Environmental Research and 

Consulting, The Dow Chemical Company, Midland, MI 

Dr. Deborah Cory-Slechta, Professor, Department of Environmental Medicine, School of 

Medicine and Dentistry, University of Rochester, Rochester, NY 

Dr. Terry Daniel, Professor of Psychology and Natural Resources, Department of Psychology, 

School of Natural Resources, University of Arizona, Tucson, AZ 

Dr. Otto C. Doering III, Professor, Department of Agricultural Economics, Purdue University, 

W. Lafayette, IN 

Dr. David A. Dzombak, Walter J. Blenko Sr. Professor of Environmental Engineering, 

Department of Civil and Environmental Engineering, College of Engineering, Carnegie Mellon 

University, Pittsburgh, PA 

Dr. T. Taylor Eighmy, Vice President for Research, Office of the Vice President for Research, 

Texas Tech University, Lubbock, TX 

vi 
Dr. Baruch Fischhoff, Howard Heinz University Professor, Department of Social and Decision 

Sciences, Department of Engineering and Public Policy, Carnegie Mellon University, Pittsburgh, 

PA 

Dr. James Galloway, Sidman P. Poole Professor of Environmental Sciences 

Associate Dean for the Sciences, College and Graduate School of Arts and Sciences, University 

of Virginia, Charlottesville, VA 

Dr. John P. Giesy, Professor and Canada Research Chair, Veterinary Biomedical Sciences and 

Toxicology Centre, University of Saskatchewan, Saskatoon, Saskatchewan, Canada 

Dr. James K. Hammitt, Professor, Center for Risk Analysis, Harvard University, Boston, MA 

 

Dr. Rogene Henderson, Senior Scientist Emeritus, Lovelace Respiratory Research Institute, 

Albuquerque, NM 

Dr. James H. Johnson, Professor and Dean, College of Engineering, Architecture & Computer 

Sciences, Howard University, Washington, DC 

Dr. Bernd Kahn, Professor Emeritus, Nuclear and Radiological Engineering Program and 

Director, Environmental Radiation Center, GTRI, Georgia Institute of Technology, Atlanta, GA 

Dr. Agnes Kane, Professor and Chair, Department of Pathology and Laboratory Medicine, 

Brown University, Providence, RI 

Dr. Meryl Karol, Professor Emerita, Graduate School of Public Health, University of 

Pittsburgh, Pittsburgh, PA 

Dr. Catherine Kling, Professor, Department of Economics, Iowa State University, Ames, IA 

Dr. George Lambert, Associate Professor of Pediatrics, Director, Center for Childhood 

Neurotoxicology, Robert Wood Johnson Medical School-UMDNJ, Belle Mead, NJ 

Dr. Jill Lipoti, Director, Division of Environmental Safety and Health, New Jersey Department 

of Environmental Protection, Trenton, NJ 

Dr. Lee D. McMullen, Water Resources Practice Leader, Snyder & Associates, Inc., Ankeny, 

IA 

Dr. Judith L. Meyer, Distinguished Research Professor Emeritus, University of Georgia, Lopez 

Island, WA 

Dr. Jana Milford, Professor, Department of Mechanical Engineering, University of Colorado, 

Boulder, CO 

vii 
Dr. Christine Moe, Eugene J. Gangarosa Professor, Hubert Department of Global Health, 

Rollins School of Public Health, Emory University, Atlanta, GA 

Dr. M. Granger Morgan, Lord Chair Professor in Engineering, Department of Engineering and 

Public Policy, Carnegie Mellon University, Pittsburgh, PA 

Dr. Duncan Patten, Research Professor , Department of Land Resources and Environmental 

Sciences, Montana State University, Bozeman, MT 

Mr. David Rejeski, Director, Foresight and Governance Project , Woodrow Wilson 

International Center for Scholars, Washington, DC 

Dr. Stephen M. Roberts, Professor, Department of Physiological Sciences, Director, Center for 

Environmental and Human Toxicology, University of Florida, Gainesville, FL 

Dr. Joan B. Rose, Professor and Homer Nowlin Chair for Water Research, Department of 

Fisheries and Wildlife, Michigan State University, East Lansing, MI 

Dr. Jonathan M. Samet, Professor and Chair, Department of Preventive Medicine, University 

of Southern California, Los Angeles, CA 

 

Dr. James Sanders, Director and Professor, Skidaway Institute of Oceanography, Savannah, 

GA 

Dr. Jerald Schnoor, Allen S. Henry Chair Professor, Department of Civil and Environmental 

Engineering, Co-Director, Center for Global and Regional Environmental Research, University 

of Iowa, Iowa City, IA 

Dr. Kathleen Segerson, Professor, Department of Economics, University of Connecticut, Storrs, 

CT 

Dr. Kristin Shrader-Frechette, O'Neil Professor of Philosophy, Department of Biological 

Sciences and Philosophy Department, University of Notre Dame, Notre Dame, IN 

Dr. V. Kerry Smith, W.P. Carey Professor of Economics , Department of Economics , W.P 

Carey School of Business , Arizona State University, Tempe, AZ 

Dr. Thomas L. Theis, Director, Institute for Environmental Science and Policy, University of 

Illinois at Chicago, Chicago, IL 

Dr. Valerie Thomas, Anderson Interface Associate Professor, School of Industrial and Systems 

Engineering, Georgia Institute of Technology, Atlanta, GA 

viii 
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Dr. Barton H. (Buzz) Thompson, Jr., Robert E. Paradise Professor of Natural Resources Law 

at the Stanford Law School and Perry L. McCarty Director, Woods Institute for the 

Environment, Stanford University, Stanford, CA 

Dr. Robert Twiss, Professor Emeritus, University of California-Berkeley, Ross, CA 

Dr. Thomas S. Wallsten, Professor and Chair, Department of Psychology, University of 

Maryland, College Park, MD 

Dr. Lauren Zeise, Chief, Reproductive and Cancer Hazard Assessment Branch, Office of 

Environmental Health Hazard Assessment, California Environmental Protection Agency, 

Oakland, CA 

SCIENCE ADVISORY BOARD STAFF 

Mr. Thomas Miller, Designated Federal Officer, US EPA, Science Advisory Board (1400F), 

1200 Pennsylvania Avenue, NW, Washington, DC, 20460 
TABLE OF CONTENTS 

 

1. EXECUTIVE SUMMARY ...................................................................................................................................1 

2. INTRODUCTION .................................................................................................................................................4 

2.1 BACKGROUND..................................................................................................................................................4 

2.2 REVIEW PROCESS AND ACKNOWLEDGEMENT..................................................................................................5

2.3 OVERVIEW OF EPA'S DRAFT BLUE BOOK........................................................................................................5 

3. RESPONSE TO CHARGE QUESTION 1: APPLICATION OF THE EXTENSIONS AND 

MODIFICATIONS TO THE BEIR VII APPROACH IN THE DRAFT BLUE BOOK..........8 

3.1 CHARGE QUESTION # 1 ....................................................................................................................................8 

3.2 RESPONSE TO CHARGE QUESTION # 1A............................................................................................................8 

 3.2.1 ALPHA PARTICLE RADIATION ...........................................................................................................8

 3.2.2 LOW-ENERGY ELECTRON AND PHOTON RADIATIONS.......................................................................9 

3.3 RESPONSE TO CHARGE QUESTION # 1B..........................................................................................................10

3.4 RESPONSE TO CHARGE QUESTION # 1C..........................................................................................................11 

 3.4.1 KIDNEY...........................................................................................................................................11

 3.4.2 BONE ..............................................................................................................................................11

 3.4.3 SKIN (FATAL AND NONFATAL NONMELANOMA CANCERS).............................................................11

 3.4.4 LIVER..............................................................................................................................................12

 3.4.5 LUNG ..............................................................................................................................................12

 3.4.6 LEUKEMIA.......................................................................................................................................13

3.5 RESPONSE TO CHARGE QUESTION # 1D..........................................................................................................13

3.6 RESPONSE TO CHARGE QUESTION # 1E..........................................................................................................14

 3.6.1 NONFATAL SKIN CANCER ..............................................................................................................14

 3.6.2 PRENATAL EXPOSURE CANCER RISK ..............................................................................................14

4. RESPONSE TO CHARGE QUESTION 2: UNCERTAINTY ANALYSIS ..................................................16 

4.1 CHARGE QUESTION # 2 ..................................................................................................................................16 

4.2 RESPONSE TO CHARGE QUESTION # 2A..........................................................................................................16 

 4.2.1 GENERAL COMMENTS.....................................................................................................................16

 4.2.2 SPECIFIC COMMENTS ......................................................................................................................17

 4.2.3 ADDITIONAL COMMENTS ON RISK TRANSFER ................................................................................19

4.3 RESPONSE TO CHARGE QUESTION # 2B..........................................................................................................20 

5. RESPONSE TO CHARGE QUESTION 3: COMMENTS ON PRESENTATION OF OVERALL 

INFORMATION AND APPLICATION OF BEIR VII IN THE DRAFT BLUE BOOK ......21 

5.1 CHARGE QUESTION # 3 ..................................................................................................................................21 

5.2 RESPONSE TO CHARGE QUESTION # 3A..........................................................................................................21 

 5.2.1 NONCANCER MORTALITY ...............................................................................................................21

 5.2.2 INFORMATION FROM ICRP AND UNSCEAR REPORTS ...................................................................22

 5.2.3 RADIOGENIC THYROID CANCER......................................................................................................22 

 5.2.4 RADIOGENIC BRAIN CANCER..........................................................................................................22 

5.3 RESPONSE TO CHARGE QUESTION # 3B..........................................................................................................22 

 5.3.1 TABULAR PRESENTATIONS .............................................................................................................23

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 5.3.2 TOPICAL ORGANIZATION AND CONTENT ........................................................................................23

 5.3.3 RELATION OF INPUT INFORMATION TO PRESENTED RESULTS.........................................................23

 5.3.4 APPLICATION OF DDREF................................................................................................................24

5.4 RESPONSE TO CHARGE QUESTION # 3C..........................................................................................................24 

 5.4.1 LOW-DOSE PROTRACTED EXPOSURE..............................................................................................24

 5.4.2 CANCER SITES WITH LIMITED DATA ..............................................................................................24

 5.4.3 CANCER SUBTYPES .........................................................................................................................24

 5.4.4 PRESENTATION OF STEPWISE EPA DEVELOPMENT OF REVISED FGR 13........................................25 

REFERENCES CITED.............................................................................................................................................26 

APPENDIX A – EDITORIAL COMMENTS .........................................................................................................36

APPENDIX B –ACRONYMS .................................................................................................................................38 
1. EXECUTIVE SUMMARY 

The Radiation Advisory Committee (RAC) of the Science Advisory Board (SAB) has 

completed its review of the Agency’s draft titled “EPA Radiogenic Cancer Risk Models and 

Projections for the U.S. Population” dated December 2008 (U.S. EPA/ORIA 2008). In this 

draft “Blue Book”, the EPA Office of Radiation and Indoor Air (ORIA) outlines proposed 

changes in the Agency’s methods for estimating radiogenic cancer risks and gives risk estimates 

for individual radiogenic cancers that it derived by the proposed methods. The EPA sought the 

RAC’s advice on its draft Blue Book to assure reliable application of radiogenic cancer risk 

assessment in EPA programs, notably updating Federal Guidance Report (FGR) 13, Health Risks 

from Low-level Environmental Exposure to Radionuclides (U.S.EPA/ORIA 1999). 

 The RAC responded as follows to the EPA’s itemized charge questions: 

Charge Question 1 on appropriateness of models not directly taken from the National Research 

Council BEIR VII Report:

1a. The RAC agrees with the methods proposed by the EPA to estimate the cancer risks of alpha 

particles that have greater linear energy transfer (LET) and relative biological effect (RBE) 

values than beta particles, gamma rays and x rays. For low-energy beta particles (notably 

tritium) and low-energy photons, on the other hand, the RAC finds that while the EPA review of 

information is sufficient to conclude that the RBE exceeds 1, it is insufficient for selecting 

appropriate RBE values. The RAC recommends that EPA staff publish, for review by the 

scientific community, a compilation and evaluation of pertinent studies in a peer-reviewed 

journal and then select an RBE value based on this document and professional responses to it. 

This effort should not delay publication of the Blue Book, but its results should be available 

before the EPA issues the revised FGR 13. 

1b. The RAC recommends – in contrast to BEIR VII -- use of an arithmetic mean for each 

pair of excess absolute risk (EAR) value and excess relative risk (ERR) value in transferring 

lifetime attributable risk (LAR) to the U.S. population from the Japanese life span study (LSS) 

population. The most important reason, in the absence of a theoretical basis for using either the 

arithmetic or the geometric mean, is that the arithmetic mean results from a linear addition and 

averaging of excess risk data, with equal emphasis on higher and lower values. The subsequent 

choice of weighting factor then explicitly captures judgments about the relative importance of 

the ERR- and EAR-based risk estimates. This approach has other benefits as well, such as 

consistency with uncertainty estimates. Neither the EPA approach to calculating the geometric 

mean (although supported in the RAC review of the EPA White Paper because of its 

calculational consistency) nor the BEIR VII approach provides any calculational advantage 

relative to the arithmetic mean. 

1c. The RAC agrees with the approaches proposed by the EPA to derive risk estimates not 

specified in BEIR VII for solid cancers (kidney, skin) and for cancers associated with exposure 

to alpha-particle emitters (lung, liver). With regard to the liver, the RAC cautions that the organ 

1 
is subject to tumors with diverse histopathologies and possibly different outcomes. The RAC 

recommends for bone cancer that the EPA reconsider utilizing the radium data for the dial 

painter cohort (as asserted in the Blue Book, p.64, but not done), and, most importantly, apply 

recently published analyses of the data. For leukemia, the RAC notes the uncertainty related to 

the EPA changing the RBE for alpha-particle radiation from 1 to 2 and suggests that the EPA 

review the extent of these uncertainties before committing to the change. 

1d. The RAC compliments the EPA on developing an improved model that considers the 

survival rate of breast cancer patients. It suggests that the EPA consider in the future applying 

this approach to derive risk estimates as sufficient data become available for other cancers (e.g., 

colon cancer) for which current survival rates are higher than previously observed. 

1e. The RAC agrees with the EPA approach for separating from its overall risk estimates the 

nonfatal skin cancer risk estimates because of the dominance of spontaneous (nonradiogenic) 

nonmelanoma skin cancers and the associated experience that most respond to treatment and are 

not fatal. Their inclusion with cancers that result in a much higher mortality rate would greatly 

distort the overall cancer morbidity and mortality risk estimates. 

The RAC also agrees with the EPA that it is appropriate to use the same model to 

estimate radiogenic cancer risk in adults whether the exposure occurs in utero or in childhood. 

Differences in risk estimates between the two groups were not statistically significant. 

Charge Question 2 on the adequacy of the uncertainty analysis:

2a. The RAC considers the approach to uncertainty analysis in the draft Blue Book to be 

reasonable and comprehensive in deriving (1) overall risk estimate uncertainty from sampling 

variation, (2) the various model parameters, and (3) transfer of data to the U.S. population. The 

RAC recommends greater specificity, clarity, and transparency in identifying and quantifying 

each source of uncertainty. One effective technique is to discuss each contributing uncertainty 

to the LAR in the text and to summarize it in a table (in greater detail than is now in the Blue 

Book) with emphasis on the major sources of uncertainty and how each is quantified. 

The RAC recommends that the Blue Book make the Bayesian uncertainty analysis as 

consistent as possible with the point estimates of risk. The EPA should justify use of these two 

separate approaches to obtain best estimate values and confidence intervals. 

 

The RAC recommends that the EPA verify the uncertainty analysis by obtaining 

uncertainty intervals with a perturbation approach. The EPA should vary the value of each 

major contributor to uncertainty over a reasonable range to recalculate the corresponding range 

of the point estimate and demonstrate the validity of the recommended uncertainty. 

2b. The RAC recommends that the EPA expand the text to clarify the reasoning behind the 

selection of distributions chosen for the various sources of uncertainty. The discussion of 

subjective priors listed partially in Table 4-1 of the draft Blue Book should justify the assigned 

2 
3 

distributions so that the reader can trace the basis of each decision concerning central value, 

uncertainty, and distribution, and have confidence in these characteristics. 

Charge Question 3 on presentation of overall information and application of BEIR VII:

3a. The RAC recognizes the scientific defensibility and appropriateness of the Blue Book. 

However, the RAC recommends that EPA enhance Blue Book contents by reporting further 

information on radiogenic cancer at low radiation doses from (1) studies of noncancer 

mortality; (2) brain cancer studies; (3) recent ICRP and UNSCEAR reviews; and (4) NCRP 

Report #159 on the risk of radiation-induced thyroid cancer (NCRP 2009). 

3b. The RAC found that most of the calculations and results in the draft Blue Book are readily 

understandable. The RAC recommends that the EPA clarify the purpose and application of 

the Blue Book by presenting in detail, in its first Section, the contributions by Blue Book 

contents in preparing Federal Guidance Report (FGR) 13 and, in its last Section, FGR 13 

values of radionuclide risk coefficients. This information should be sufficient to permit the 

reader to attribute any significant changes in FGR 13 values to changes proposed in this Blue 

Book, or to changes in the physiological models with which they will be combined, or to both, so 

that such changes then can be examined in greater detail. 

3c. The RAC considers the draft Blue Book to have the accuracy and balance appropriate to its 

intended purpose, once the recommended revisions noted in this review are implemented. The 

RAC recommends that EPA enhance the level of detail by expanding its discussion of the 

following risk estimates: (1) those based on studies of cohorts exposed to low-dose protracted 

radiation, and (2) those for distinguishable types of cancer within a given organ.
2. INTRODUCTION 

2.1 Background 

In 1994, the U.S. Environmental Protection Agency (EPA) published the report 

“Estimating Radiogenic Cancer Risks,” (U.S. EPA 1994) often referred to as the “Blue Book,” 

because of the blue cover on the document (http://epa.gov/radiation/docs/assessment/402-r-93-

076.pdf). The Blue Book presents EPA’s current methodology for quantitatively estimating 

radiogenic cancer risks. This EPA estimation of cancer risks due to low linear energy transfer 

(LET) radiation exposures is based on information, mainly about the Japanese atomic bomb 

survivors, that had become available since the publication of “The Effects on Populations 

Exposed to Low Levels of Ionizing Radiation BEIR III” (NAS/NRC 1980) and the original Blue 

Book (U.S. EPA 1984) that followed it. The incidence of fatal cancer in specified organs and 

tissues per unit dose was estimated for a stationary U.S. population based on 1980 vital statistics. 

The effect of high-LET alpha particles in terms of their RBE also was considered. The 1994 

EPA report replaced the 1984 EPA report. 

In an addendum to the 1994 report, the EPA published minor adjustments to the previous 

values in terms of more recent vital statistics (U.S. EPA/ORIA 1999a). The addendum also 

presented a partial analysis of the uncertainties in the values to provide a confidence interval for 

the cancer risk per unit radiation dose (http://epa.gov/radiation/docs/assessment/402-r-99-

003.pdf). 

Also in 1999, the Agency applied the 1994 Blue Book contents, metabolic models, and 

usage patterns to publish Federal Guidance Report 13 (FGR 13), “Health Risks from Low-level 

Environmental Exposure to Radionuclides” (U.S. EPA/ORIA 1999), with cancer risk estimates 

for over 800 radionuclides by several exposure pathways, models, and U.S. usage patterns 

(http://epa.gov/radiation/docs/federal/402-r-99-001.pdf). The risk estimates were later updated 

(http://www.epa.gov/radiation/federal/techdocs.html#cd_supplement). Prior to their 

publications, both the 1994 Blue Book and the addendum were reviewed by the Radiation 

Advisory Committee (RAC) of the EPA Science Advisory Board (SAB) (U.S. EPA/SAB 1994, 

1999). 

In 2006, the National Research Council (NRC) of the National Academies of Sciences 

(NAS) released “Health Risks from Exposure to Low Levels of Ionizing Radiation, BEIR VII 

Phase 2” (NAS/NRC 2006) (available at http://nap.edu/catalog/11340.html#toc) which 

primarily addresses cancer and genetic risks from low doses of low energy transfer (LET) 

radiation. This report was co-sponsored by the EPA and several other Federal agencies. 

Also in 2006, the EPA prepared the draft “White Paper: Modifying EPA Radiation Risk 

Models Based on BEIR VII” (U.S. EPA/ORIA 2006) in anticipation of issuing a revised Blue 

Book (http://epa.gov/radiation/docs/assessment/white-paper8106.pdf). In the White Paper, the 

Agency proposed changes to the EPA’s methods for estimating radiogenic cancers, based on the 

contents of BEIR VII and some ancillary information. The Agency expected to adopt the models 

and methods recommended in BEIR VII, but believed that certain modifications and expansions 

4 
were desirable or necessary for the EPA’s purposes. The EPA Office of Radiation and Indoor 

Air (ORIA) requested the SAB to review the Agency’s draft White Paper and provide advice 

regarding the proposed approach to dose-response assessment of radionuclides. The SAB/RAC 

prepared an advisory, EPA-SAB-08-006 (U.S. EPA/SAB 2008) 

(http://yosemite.epa.gov/sab/sabproduct.nsf/FD9963E56C66E4FF852573E200493359/$File/EP

A-SAB-08-006-unsigned.pdf). The SAB reviews responding to the above-cited EPA documents 

can be found on the EPA SAB Web site at http://www.epa.gov/sab. 

In December 2008, the ORIA issued the draft of the revised Blue Book, “EPA 

Radiogenic Cancer Risk Models and Projections for the U.S. Population” (U.S. EPA/ORIA 

2008), and asked the SAB to review it. The draft document contains specific methods and their 

applications for estimating the risks of radiogenic cancer for many organs and tissues, with 

uncertainty estimates. It utilizes the advice contained in the BEIR VII Phase 2 report, as well as 

in the SAB’s advisory for the White Paper and the earlier Blue Book addendum, both described 

above. 

2.2 Review Process and Acknowledgement 

 The SAB RAC met in a public teleconference on February 27, 2009, and conducted a 

public meeting on March 23, 24, and 25, 2009, for this draft Blue Book review (see 74 Fed. 

Reg., 5935, February 3, 2009). Additional public teleconferences took place on June 18, 2009 

and July 22, 2009 (see 74 Fed. Reg., 25529, May 28, 2009). The notices, the charge to the RAC, 

and supplemental information may be found at the SAB’s Web site (http://www.epa.gov/sab). 

The draft quality review dated August 20, 2009, was forwarded to the Chartered SAB for its 

September 24, 2009, public teleconference (see 74 Fed. Reg., 42297, August 21, 2009). This 

final report reflects the suggested editorial changes from the Chartered SAB. 

 The draft document “EPA Radiogenic Cancer Risk Models and Projections for the U.S. 

Population,” December, 2008, is impressively researched, scientifically sound and well written. 

Presentations by the EPA staff and the public commentary in the course of the public meetings 

were helpful to the RAC in preparing this review. The EPA staff provided useful clarifications 

of its approach to preparing the draft Blue Book, and conveyed information in response to 

questions by the augmented RAC. The EPA/ORIA staff responded to all RAC requests and was 

forthcoming in explanations and clarifications. 

2.3 Overview of EPA’s Draft Blue Book 

The Agency is now requesting that the SAB review the draft document, “EPA 

Radiogenic Cancer Risk Models and Projections for the U.S. Population,” dated December 

2008, which was developed as a result of the previous White Paper advisory review. This draft 

document presents the scientific basis for new EPA estimates of cancer incidence and mortality 

risks due to low doses of ionizing radiation (IR) for the U.S. population. These estimates are 

based on available information, and for the most part, are calculated using models recommended 

in the NRC’s BEIR VII Report. The three specific charge questions that follow (U.S. EPA/ 

ORIA 2009) are presented in Sections 3.1, 4.1, and 5.1 of this review. The revised Blue Book 

will then serve as a basis for an updated version of FGR-13. 

5 
The introductory Section 1 cites the earlier Blue Book (U.S. EPA 1994) and the BEIR 

VII Report (NAS/NRC 2006). The BEIR VII Report is the major source of information, but 

more-recently published information has also been considered. Major sources of uncertainty are 

highlighted. 

Section 2 presents the scientific basis for cancer risk. It briefly discusses biological 

mechanisms that lead to radiogenic cancers. It describes a modified linear no-threshold 

hypothesis and the extrapolation of low–LET risks from the measured results at relatively high 

radiation doses to exposures at low doses and low dose rates. A Dose/Dose Rate Effectiveness 

Factor (DDREF) is described for calculating the risk due to chronic low-dose and low-dose-rate 

radiation exposure. Several effects that have been observed or proposed at low doses are 

discussed, but are not invoked in subsequent calculations of risk. The authors present a survey 

of the epidemiological evidence for radiogenic cancer risk, notably the LSS of atomic bomb 

survivors at Hiroshima and Nagasaki, but also patients exposed to medical radiation. 

Epidemiological studies of cohorts exposed to low levels of radiation over extended periods, 

such as radiologists and nuclear workers, are cited.

The draft Blue Book presents revised estimates of cancer incidence and mortality risks 

associated with low doses of ionizing radiation, defined as <0.1 Gray (Gy), for the U.S. 

population. The risk estimates for solid cancers and leukemia following exposure to low doses 

of low-LET radiations are derived exclusively from preferred models developed by the BEIR 

VII committee. These models are applied to stationary year 2000 population mortality based on 

survival rates in the U.S. to obtain an estimate of the LAR per person-Gy for the U.S. population. 

The process for obtaining the LAR is described in Section 3. It is based on the mean of 

each paired set of the ERR and EAR values derived from models in BEIR VII (Table 3-3). The 

EPA uses a weighted geometric mean to combine the results from the ERR and EAR models to 

obtain a point estimate of the excess risk, M (d,a,e), at an attained age a, following a single 

exposure to dose d, at age e. This value is applied to the stationary population to obtain the “best 

estimate” LAR. Section 3 also presents distinct approaches for breast cancer, leukemia, skin 

cancer, and residual cancer sites. Each of these cancer types is treated with a separate risk 

model. 

Uncertainties in projections of the LAR for low-LET radiations are described in Section 

4. The focus of the uncertainty analysis is on the calculation of LAR per person-Gy for the U.S. 

population, based on the data for the LSS. An independent Bayesian assessment of uncertainty 

is applied with a methodology quite different from that used to obtain point estimates in Section 

3. 

 

Risk of radiogenic cancer associated with the high-LET radiation of alpha particles is 

discussed in Section 5. Laboratory and epidemiological studies that provide data on RBEs for 

alpha-particle radiation are presented. The latter include bone cancer associated with internal 

exposure to radium isotopes by injection (224Ra) or ingestion (226Ra, 228Ra); liver cancer 

associated with administration of diagnostic doses of Thorotrast to patients, and plutonium 

intake by Russian nuclear workers; and lung cancer among underground miners exposed to alpha 

particles from inhalation of radon gas and radon-daughter particles, and among Russian nuclear 

6 
7 

workers at risk of inhaling plutonium particles. The risk is evaluated in terms of the RBE values 

based on contemporary data for alpha particles in specific organs or tissues. 

Section 6 addresses risk from prenatal exposure to radiation. Induction of childhood 

cancer due to fetal radiation has been shown in various case-control studies (Stewart et al. 1958; 

MacMahon 1962; and other references in Section 6, p.96). While a causal link between in utero

radiation exposure and childhood cancer is generally accepted (Doll and Wakeford 1997), some 

have termed the evidence for childhood cancers other than leukemia “equivocal” (Boice and 

Miller 1999). 

The atomic bomb survivors provide the only data on radiation effects of adult-onset 

cancer risks among persons exposed in utero (Preston et al. 2008). The survivor data exhibit a 

statistically significant radiation dose response for adult-onset cancers with levels of risk that are 

considerably less than those reported for childhood cancers. There is also a weak suggestion that 

the radiation effect for those exposed in utero may be less than what has been seen for atomic 

bomb survivors exposed as children. The EPA decided to base risk estimates for childhood 

cancers following in utero exposure on the summary risk estimates presented in Doll and 

Wakeford (1997) and recommended by the International Commission on Radiological Protection 

(ICRP 2000), and risk estimates for adult-onset cancers on the corresponding risk estimates for 

childhood exposure. 

In the very brief Section 7, application to calculating radionuclide risk coefficients is 

considered. The EPA will combine the revised excess cancer morbidity and mortality risk per 

person-Gy from this Blue Book with the latest available ICRP dose models to revise the risk for 

each radionuclide per Bq intake or per unit exposure by external radiation. This information will 

be reported in a revision of FGR 13. The ORIA expects some increases and some decreases, 

depending on the radionuclide and target organ. 
3. RESPONSE TO CHARGE QUESTION 1: APPLICATION OF THE 

EXTENSIONS AND MODIFICATIONS TO THE BEIR VII APPROACH IN 

THE DRAFT BLUE BOOK 

3.1 Charge Question # 1: As in BEIR VII, models are provided in the draft document for 

estimating risk as a function of age at exposure, age at risk, gender, and cancer site, but a 

number of extensions and modifications to the BEIR VII approach have been implemented. 

First, BEIR VII focused on the risk from low-LET radiation only, whereas risks from higher LET 

radiations are also addressed here. Second, this document presents a slightly modified 

approach for combining BEIR VII models for projecting risks from Japanese A-bomb survivors 

to the U.S. population. Third, this document goes beyond BEIR VII in providing estimates of risk 

for certain other cancers. Fourth, a modified method is employed for estimating breast cancer 

mortality risk, which corrects for temporal changes in breast cancer incidence and survival. 

Finally, quantitative estimates of risks for skin cancers and from prenatal exposures are 

included. Please comment on the appropriateness of the following either not specified in BEIR 

VII or else otherwise modified by EPA from BEIR VII: 

a. Approaches described for extending risk estimates to radiations of different LETs 

- in particular, deriving site-specific risk estimates for alpha or low energy 

electron and photon radiations based on models derived from the A-bomb 

survivors, who were primarily exposed to higher energy gamma rays (see Section 

5). 

b. EPA’s adaptation of the BEIR VII weighted geometric mean approach for 

combining the EAR and ERR models for projecting risk from the LSS to the U.S. 

population (see Section 3.9). 

c. Estimation of risks not specified in BEIR VII, including kidney, bone, and skin 

cancers, as well as for alpha particle irradiation of the liver (see Sections 3.3 and 

5.1). 

a. Method for calculating breast cancer mortality risk, accounting for the relatively 

long time from detection until death (see Section 3.10) 

b. Approach for separating out nonfatal skin cancers and risks from prenatal 

exposures from the overall risk estimates (see Sections 3.3 and 6). 

3.2 Response to Charge Question # 1a 

3.2.1 Alpha Particle Radiation 

To derive risk estimates for site-specific alpha-particle induced cancers, the EPA 

proposes to use the BEIR VII gamma-ray risk estimates, directly or with proposed modifications 

as necessary, after applying an RBE of 20. Exceptions to this general approach are proposed for: 

(1) Leukemia, for which an RBE of 2 will be applied to the BEIR VII-based gamma-ray 

estimate; 

8 
(2) Liver cancer with an RBE of 40; 

(3) Lung cancer, for which the EPA proposes continuing to use models derived from BEIR VI 

(NAS/NRC 1994) to estimate the lung cancer risk from inhaled radon progeny; and 

(4) Bone cancer, for which the EPA obtains the alpha-particle exposure risk per Gy from patients 

injected with 224Ra. This value is divided by an RBE of 10 to obtain the low-LET risk. 

The RAC considers reasonable and generally acceptable the approach proposed by the 

EPA for obtaining cancer risk estimates from alpha-particle emitters with the RBE values that 

the EPA proposes. Specific advice is given in response to question #1c in Section 3.4 below.

3.2.2 Low-Energy Electron and Photon Radiations 

Extensive discussion by RAC members regarding proposed changes by the EPA to the 

RBE for low-energy electron and photon radiations identified the following questions that should 

be addressed before a revised RBE is selected: 

• Was this change recommended/suggested/implied in BEIR VII? 

• Does ICRP, NCRP, or UNSCEAR have similar recommendations? 

• Does the NIOSH Interactive Radioepidemiological Program (IREP) use an RBE > 1? 

• Is the scientific rationale for this change suitably mature at present (Hunter and Muirhead 

2009)? 

• What will be the reference source (1 MeV electrons and/or 60Co)? 

• Will this change be restricted only to radionuclides with beta-particle energies similar to 

3

H? 

• How will “estimations” of “low energies” be determined in the case of mixed exposures 

(e.g., photons and beta particles)? 

• What is the rationale for using cutoffs at specific energies, i.e., 1, 3 or 5 keV? 

• Which radionuclides will be included and/or excluded? 

In previous comments (U.S. EPA/SAB 2008) on the EPA White Paper (U.S. EPA/ORIA 

2006), the RAC supported EPA use of an RBE of 2 – 2.5 for photons of energies less than 30 

keV and for 3

H beta particles (0 to 18.6 keV). In light of this White Paper review and the current 

discussion, the RAC recommends that the EPA prepare detailed justification to support a 

proposed change in the RBE values for low-energy low-LET ionizing radiation. The EPA 

should encourage preparation of a peer-reviewed publication that addresses these issues, consider 

the responses by the scientific community, and then, before publishing the revised FGR 13, 

decide the RBE value. 

An important concern is the validity for diagnostic medical x rays of the proposed change 

in the RBE (to ~ 1.4). The draft Blue Book notes (on pages 72 and 95) that risk coefficients 

derived from studies of cohorts medically treated with x rays (at high but fractionated doses) in 

some cases differ from those observed for A-bomb survivors (Hunter and Muirhead 2009; Little 

2001). Given that medical radiation exposures make up the majority of the average U.S. 

individual annual radiation dose (NCRP 2009a), the implications of a change in the RBE on the 

reported dose for individuals can be significant in the long term. 

9 
3.3 Response to Charge Question # 1b 

 The site-specific risk estimates in BEIR VII were computed as a weighted geometric 

mean of ERR- and EAR-based LAR estimates for the year 2000 US population. The EPA has 

proposed a method to compute an LAR as a weighted geometric mean of age- (and age-atexposure-) specific excess rates for the ERR and EAR models and then to apply this mean excess 

rate function to a stationary US population. The EPA specifically asked the RAC about its 

decision to use an average excess rate function rather than averaging the ERR- and EAR-based 

LAR estimates. The EPA staff explained during the meeting that the primary motivation for 

developing the average rate method was to insure additivity of age-specific risks. 

The RAC recommends that the LAR computation makes use of the arithmetic mean 

instead of the choice described by the EPA. The RAC considers the arithmetic mean preferable 

even though this is a departure from the BEIR VII approach and even though the RAC endorsed 

the average rate method in its Advisory on the White Paper (U.S. EPA/SAB 2008). The primary 

reason for this current RAC recommendation is that the geometric mean results in a lower risk 

estimate whereas the arithmetic mean equally balances the low and high risk estimates. It is the 

selection of weights that explicitly captures judgments about the relative importance of the ERRand EAR-based risk estimates for weighted arithmetic means. Furthermore, use of arithmetic 

means for risk estimates insures additivity of the age-specific risk estimates. The RAC 

recommends that the Blue Book present both ERR- and EAR-based LAR estimates and then 

compute the suggested risk estimate as a weighted arithmetic mean of the two estimates. 

 

The BEIR VII report does not discuss these issues; geometric means may have been used 

primarily because they simplified the analytical uncertainty assessment carried out for BEIR VII. 

Because the EPA uses Bayesian Monte-Carlo methods to assess uncertainty, the complexity of 

the uncertainty evaluation is not affected by how the risks are combined. 

Arithmetic means have been used for the current (and earlier) ICRP recommendations. 

The IREP also uses arithmetic means to combine relative-risk and absolute-risk based estimates 

when computing probability of causation. Recent UNSCEAR reports (UNSCEAR 2000, 2008) 

present ERR- and EAR-based estimates, but do not combine them. 

Concerning the key issue of weighting results by the two models, the sense of the RAC is 

that weighting should emphasize ERR models more than EAR models except for outcomes with 

enough relevant data outside the LSS population (e.g., breast cancer) to indicate that EAR 

models transfer risk information more accurately. This emphasis appears in the point estimation 

process which, to the extent that it follows BEIR VII, places a weight of 0.7 on the ERR and 0.3 

on the EAR results. Observations of tumor sites with different frequency of background 

occurrence, and sometimes also over different strains of experimental animals, show that ERR 

parameters tend to be more similar than EAR parameters (Storer et al. 1988). The RAC 

recommends that the Blue Book include a brief discussion concerning the greater weight given to 

the ERR-based risks than to the EAR-based risks in most cases, but not all (for example, lung 

and breast cancer). 

10 
Use of arithmetic instead of geometric means for averaging results based on ERR and 

EAR models should improve consistency between the recommended point estimates and central 

estimates from the uncertainty analysis. To resolve remaining discrepancies, the RAC suggests 

that EPA make the prior distributions of weight parameters for the ERR and EAR models used in 

the uncertainty analysis more compatible with the provided point estimates. 

The question arises that if weighted arithmetic means are used in place of weighted 

geometric means, do the site-specific ERR/EAR weights recommended by BEIR VII require 

change? The RAC does not believe so because BEIR VII members apparently were thinking in 

terms of linear (arithmetic) weights when they defined the weights used in their computations. 

The RAC agrees with the EPA decision to use a stationary population rather than a 

census-based population in LAR computations. The reasons for this change were cogently 

described in the EPA staff presentation to the RAC. The RAC recommends that this discussion 

(including presentation of gender-specific population pyramids or age-adjusted rates for selected 

cancers) be included in the Blue Book to show the effect on solid cancer risk estimates of the 

switch from a census based population to a stationary population. 

3.4 Response to Charge Question # 1c 

3.4.1 Kidney 

In the absence of adequate epidemiological data for deriving a separate estimate for the 

risk of radiogenic kidney cancer following exposure to low-LET radiation, the proposed EPA 

kidney cancer risk calculation reasonably uses the BEIR VII residual cancers ERR model and the 

EAR model with an adjustment factor. 

3.4.2 Bone 

The RAC notes that its Advisory on the Agency Draft White Paper (U.S. EPA/SAB 

2008) (Section 5.7, page 19) supported the use of human data to derive estimates of the bone 

cancer risk from 224Ra. The data from the study of radium dial painters who were exposed to 

226Ra and 228Ra were recommended to derive directly the bone cancer risk from these 

radionuclides. These approaches are outlined in the draft Blue Book (Section 4.2.2, page 64), 

but radium dial painter data apparently were not used. The more detailed approach considered in 

Section 5.1.2, pages 84-85, does not reflect attention to the Advisory’s recommendation. The 

RAC now reiterates this recommendation because the nature of the exposures (chronic, lifetime) 

and the biokinetics of 226Ra and 228Ra are different from those of 224Ra. 

When reconsidering the use of the radium dial painter data, the RAC recommends that 

the EPA include the more recent analyses of the data for this population (Carnes et al. 1997; 

Hoel and Carnes 2004). 

3.4.3 Skin (Fatal and Nonfatal Nonmelanoma Cancers) 

The EPA proposes, in draft Blue Book pages 31-32, to deviate from its previous approach 

(U.S. EPA 1994) based on ICRP recommendations (ICRP 1991) for estimating the risk of 

11 
radiation-induced nonmelanoma skin cancer (NMSC). This change reflects the findings of more 

recent epidemiological analyses, changing disease patterns, and the conclusion that essentially all 

NMSCs induced by low-to moderate doses of ionizing radiation are of the basal cell carcinoma 

(BCC) type and nonfatal (Shore 2001, 2002; Preston et al. 2007; Karagas et al. 1999; Ron et al. 

1991), as stated in the draft Blue Book (see also Section 3.6.1). 

The RAC considers the proposed updated approach for deriving risk estimates for fatal 

and nonfatal NMSC to be reasonable and acceptable. This EPA approach applies its new model 

described in the Blue Book with age-specific baseline incidence rates to derive the ERR for the 

nonfatal incidence of radiation-induced NMSC. More recent estimates of mortality due to BCC 

in the general population (Lewis and Weinstock 2004) will be used as baseline data in estimating 

the risk of fatal radiogenic NMSC. The NMSC risks for both incidence and mortality will be 

estimated for males and females separately and in combination (sex-averaged). The EPA also 

will use the revised DDREF value of 1.5 from BEIR VII to derive NMSC risk estimates in the 

low-dose range in place of the value 2 used previously. 

3.4.4 Liver 

The liver is recognized as a target organ for certain alpha-particle emitters. The 

relevance of the colloidal nature of Thorotrast should be considered and how this might impact 

the radiogenic risks of liver cancer. Comparison of the liver cancer risk estimate for gamma 

radiation derived by BEIR VII from the LSS data with that obtained from the follow-up study of 

Danish Thorotrast patients suggested an RBE of 20 for alpha-particle radiation (Andersson et al. 

1994). While recognizing the uncertainties inherent in both studies with respect to liver cancer 

and the value of this RBE, the EPA initially proposed use of an RBE of 20 with the BEIR VII 

liver cancer risk estimate to derive an estimate for alpha-particle-induced liver cancer (U.S. 

EPA/ORIA 2006). The RAC supported this approach for liver and certain other cancers that 

have been associated with alpha particle radiation (U.S. EPA/SAB 2008) with the 

recommendation that any additional epidemiological data be taken into consideration. 

Based on additional data from the follow-up study of German Thorotrast patients (Van 

Kaick et al. 1999) and a reanalysis of the Danish patient data (Leenhouts et al. 2002) with an 

empirical model and a lifetime risk projection, the EPA has revised its proposal to use a scaled 

version of the BEIR VII model. The EPA now will use the BEIR VII low-LET age and genderspecific liver cancer risk estimates and an RBE of 40 to provide risk estimates for alpha-particleinduced liver cancer at environmental low doses. The RAC considers this approach reasonable, 

and the use of an RBE of 40 as appropriate. However, because in the context of this report, 

‘liver cancer’ (like ‘cancer’ in most other organs) is an all-embracing term that includes a diverse 

number of histopathologies, the RAC cautions that the uncertainties associated with grouping 

these different tumor histopathologies may outweigh any benefits gained by changing the RBE 

to 40, and suggests that the EPA address this uncertainty before confirming this change to 40. 

3.4.5 Lung 

The draft Blue Book adopts an RBE of 20 for lung cancer by alpha-particle emitters other 

than radon, baesd on BEIR VI (NAS/NRC 1994) models. A separate risk model for radon is the 

suitable approach outlined in the draft Blue Book. The epidemiological evidence for other 

12 
inhaled alpha-particle emitters comes primarily from the Mayak worker studies, because other 

studies do not have sufficient power (i.e., precision) to estimate risks. As noted in the draft Blue 

Book, the Mayak worker studies are in an early stage, but several reports are available. The lung 

cancer risk estimates reported by the two most recent Mayak reports (Jacob et al. 2007; 

Sokolnikov et al. 2008) were consistent with an RBE of 20. The EPA proposes to use an RBE of 

20 which the RAC considers reasonable. The same value of 20 was recommended recently by 

the ICRP (2003, 2005). 

Animal studies show RBE values at, above, and below 20. Some animal studies of 

radionuclides deposited in the lung obtained an RBE value of 20 or above (Gilbert et al. 1998; 

Hahn et al. 1999; Lundgren et al. 1995, 1996, 1997; Muggenburg et al. 1996, 2006) by 

comparing the effects of radionuclides that emit alpha particles with those that emit beta particles 

and gamma rays. Other animal studies obtained a much lower RBE (Priest et al. 2006). The 

RAC suggests caution in applying these values derived from animals that in many of these 

groups were exposed to doses above 1 Gy, well above the low-dose range. Such elevated doses 

can have a strong influence on the shape of the dose response curve and the calculated RBE. 

3.4.6 Leukemia 

The draft Blue Book recommends an RBE of 2 for alpha-particle-induced leukemia based 

on epidemiological studies at low doses of 224Ra. This is a change from the value of 1 used in 

past EPA reports. The RAC considers that the RBE of 2 may be reasonable, but recommends 

that the EPA discuss in the Blue Book the uncertainties in this value that derive from estimating 

doses from alpha-particle emitters and from different temporal patterns between the LSS and the 

224Ra group for the appearance of leukemia. Animal studies have not been helpful in 

understanding the RBE for alpha particles because of the variability in leukemia induction 

among strains (Storer et al. 1990); moreover, they have not had sufficient power to estimate 

leukemia risks from radiation (NAS-NRC 1990). 

 3.5 Response to Charge Question # 1d 

BEIR VII computed breast cancer mortality risk estimates by scaling age-specific 

incidence risks for the ratio of the (age-specific) mortality-to-incidence rate ratios. The EPA 

proposes replacing this simple ratio by a factor that allows for the relative survival of breast 

cancer patients. The data presented to the RAC by EPA staff suggest that the modified method 

leads to more realistic breast cancer mortality risk estimates. The RAC believes that the EPA 

method is an improvement over that used by BEIR VII because the relative survival of breast 

cancer patients is high and the excess risk estimates, including those derived by application of 

ERR estimates used in the LAR computations, increase with attained age. The EPA should 

consider in the future using a similar approach in computing mortality risks as sufficient data 

become available for other types of cancer with relatively high survival rates, such as colon 

cancer. 

13 
 3.6 Response to Charge Question # 1e 

3.6.1 Nonfatal Skin Cancer 

As noted in the response to Question #1c with regard to Skin (Fatal and Nonfatal 

Nonmelanoma Cancers) in Section 3.4.3, the RAC supports the EPA proposal to update its 

approach by deriving risk estimates for incidence and mortality associated with radiationinduced NMSC from data for BCC in the light of more recent epidemiological data. In 

particular, the RAC supports Shore’s conclusion that essentially all NMSC induced by ionizing 

radiation in the low to moderate dose range are of the BCC type with a very low mortality rate 

(Shore 2001). 

The RAC supports the EPA decision not to include NMSC risk estimates in estimating 

total radiogenic cancer risk (see Tables in the draft Blue Book, Sections 3 and 4). The 

dominance of NMSC incidence at the very low NMSC mortality would seriously distort the 

summed incidence and mortality rates used for estimatng total radiogenic cancer rates. 

3.6.2 Prenatal Exposure Cancer Risk 

The RAC considers that estimation of cancer risks from prenatal radiation in the draft 

Blue Book is appropriately based on the literature. Prenatal radiation exposure has been shown 

in some studies to be causally associated with increases in childhood cancers and, in the LSS, 

with increases in adult cancers. The recent ICRP Report 103 (ICRP 2007), however, concluded 

that the DDREF value should remain at 2 and not be reduced to 1.5 as recommended by BEIR 

VII. The EPA should justify its decision to disagree with the ICRP conclusion and follow BEIR 

VII’s recommendation. 

In the draft Blue Book, the EPA accepts the absolute risk estimate of 0.06 Gy-1 of 

prenatal exposure for death from cancer prior to age 16 that was suggested by Doll and 

Wakeford (1997) and adopted by the ICRP (2000). Based on a review of the same studies 

considered by Doll and Wakeford, Boice and Miller (1999) expressed some skepticism about this 

estimate. However, the RAC considers it is reasonable to use the 0.06 Gy-1 risk estimate at this 

time. This evidence is largely derived from exposure to 80 kVp medical x rays; hence, the risk 

coefficient should be adjusted to 0.04 Gy-1 if the EPA adopts an RBE of 1.4 for diagnostic 

medical x rays. 

For estimating the risks of adult cancers among populations exposed in utero, EPA 

proposes adopting the cancer risk models in draft Blue Book Section 3 with age set to zero. 

Although an analysis of A-bomb survivors exposed in utero found a lower risk than those who 

were irradiated as young children, the difference is not statistically significant (Preston et al. 

2008). The RAC considers this a reasonable approach. 

Caution should be expressed because some spontaneous abortions in women who received 

the higher doses may have occurred in the periods immediately after the A-bombs. These 

14 
possible abortions were unaccounted for in the LSS, would lower the risk estimates, and should 

be mentioned by the EPA as an additional source of uncertainty for prenatal exposure effects. 

15 
4. RESPONSE TO CHARGE QUESTION 2: UNCERTAINTY ANALYSIS 

4.1 Charge Question # 2: BEIR VII’s approach to uncertainty is primarily based on data 

from the Life Span Study (LSS). The LSS provides a great deal of information on risks for 

many cancer sites; however precision is limited by errors in dosimetry and sampling errors. 

The sampling errors are often quite large for specific cancer types, and the uncertainties are 

even larger if one focuses on a specific gender, age at exposure, or time after exposure. 

Another important uncertainty is the transfer of site-specific cancer risk estimates to the U.S. 

population, based on results obtained on the LSS population, for sites with substantially 

different baseline incidence rate. Compared to BEIR VII, this document provides a 

somewhat altered and expanded analysis of the uncertainties in the cancer risk estimates.

Regarding the uncertainty analysis contained in Section 4, 

a Please comment on the adequacy of the approach to uncertainty analysis. 

b Are the distributions chosen for the various sources of uncertainty reasonable? 

4.2 Response to Charge Question # 2a 

The approach to obtaining quantitative estimates of uncertainty is reasonable and 

comprehensive. The RAC has identified the specific issues, described below, related to the 

uncertainty analysis that the EPA should address to clarify assumptions and processes. 

4.2.1 General Comments 

The methods used for the full uncertainty analysis of stomach, colon, liver, lung, and 

bladder cancer are based on analysis of the data for the LSS. The LAR is a complex function of 

parameters that can be classified into three types: 

• Type I are the risk estimates obtained from models with parameters derived from the 

LSS data. 

• Type II are other parameters, such as RBE, DDREF, and population transfer, about which 

little or no direct information comes from the LSS data. 

• Type III is the age distribution obtained from a hypothetical (stationary) population that 

mimics the US population. 

The goal of the uncertainty analysis in the draft Blue Book is to combine sampling variation in 

the estimates for Type I parameters with uncertainties in Type II parameters in order to provide 

an overall uncertainty estimate for the LAR that is calculated either separately for individual 

tumor types or for groupings of tumors (e.g. all solid tumors, leukemia). 

A Bayesian analysis has been adopted by the EPA. It provides a consistent framework 

for the treatment of unknown parameters as random variables and a formal method for updating 

initial prior distributions for these random parameters with the information contained in the LSS 

data about the parameters of Type I. The Bayesian nature of the uncertainty analysis rests on a 

somewhat different statistical basis than a “frequentist” approach that yields the “best estimates” 

of LAR for these cancers. It is not surprising that the LAR uncertainty bounds from the 

Bayesian analysis are not symmetric around the best estimate. 

16 
The Bayesian analysis for stomach and colon actually is a joint analysis of these cancers 

and combines information about the linear ERR parameters across these cancer types. It 

estimates a common mean (but separately by gender) and a common variance in the distribution 

of these risk parameters. Doing this should have the useful property of reducing the uncertainty 

in the posterior distribution of these risk estimates, especially for rarer cancers where the 

information in the LSS is not large. 

Because all Type I and Type II parameters are regarded as random variables, the LAR 

itself is treated as a random variable that is a function of the other random variables in the 

uncertainty analysis. While this general framework is sound, it is complicated, especially given 

the need to provide prior distributions for all Type I and Type II parameters. Because of the 

large amount of direct data from the LSS related to incidence and survival, the selection of prior 

distributions for Type I parameters does not have a very strong effect on the final “posterior” 

estimates of these parameters. However, prior distributions specified for Type II parameters tend 

to dominate their posterior distributions because little or no information about these latter 

parameters is in the LSS data. 

4.2.2 Specific Comments 

The Blue Book should clearly state and justify why one method is used to obtain a point 

estimate of LAR and another method based on different assumptions is used for the uncertainty 

analysis. The Bayesian approach provides a posterior density function for LAR that could be 

used to obtain a “best estimate” (i.e., mean or median) as well as confidence limits for a 

quantitative description of uncertainty. Thus, a Bayesian approach could provide a consistent 

value for both the best estimate and uncertainty interval, to replace the existing frequentist 

approach for the best estimate, accompanied by Bayesian methods to estimate the confidence 

interval. 

Presumably, the EPA used separate approaches to obtain a best estimate and confidence 

intervals partly because the best estimate of a LAR for a specific cancer site does not impose the 

constraint that the risk estimates for each cancer be similar. Thus, because such risk estimates 

are not known a priori to be similar, it may be scientifically more sensible to use completely 

different analyses of each cancer subtype to give the best estimate, even if an assumption of 

commonality is necessary and reasonable to impose when evaluating uncertainty, especially for 

relatively rare cancers. 

An additional reason why Bayesian analysis might not be applied to generating the point 

estimates is that Bayesian estimates depend greatly on the details of the priors used for Type II 

parameters, which are inherently subjective. One also needs to utilize inherently subjective 

choices to develop the point estimate, but the technical details and software (WinBUGS) used for 

the Bayesian analysis are quite delicate. Although WinBUGS (Lunn et al. 2000) is preferred for 

many Bayesian applications, convergence issues often arise. The Monte Carlo Markov Chain 

(MCMC) methodology can be demanding. For example, minor changes in starting values used 

in the simulations can have a large effect on the results. The RAC is sympathetic to the process 

of using specific assumptions for Type II parameters to produce the point estimates, but then 

allowing these to range widely when the uncertainty intervals are computed. 

17 
In addition to concerns relating to prior distributions, the RAC notes an overall lack of 

clarity concerning the likelihood function for the LSS data. The likelihood function for Poisson 

regression analysis of grouped survival data may not be very familiar even to readers relatively 

knowledgeable in statistics and should be described carefully. Moreover, because for the cancers 

listed above (stomach, colon), a joint analysis is being performed (where tables of person years 

and events are given for more than one outcome), the legitimacy of multiplying the likelihoods 

for each outcome together should be affirmed, even though the same “denominator” values 

(person years) are being used in each table. 

The current description of LARs and corresponding uncertainty intervals are not 

sufficiently detailed. No indication is given which parameters, either Type I or Type II, are the 

most influential in controlling the uncertainty intervals for LAR. The RAC suggests that the 

EPA create a table depicting the relative contribution of each source of uncertainty to the total 

uncertainty for each LAR (i.e., site-specific and overall). The sources of uncertainty include (1) 

incidence data (where ‘incidence’ includes both background and radiogenic incidence), (2) 

DDREF, (3) risk transport model, and (4) other EPA data sources, including age and time 

dependence, errors in dosimetry, and diagnostic misclassification. The relative contribution 

could be expressed as a percent or as the squared correlation between LAR uncertainty and each 

source of uncertainty, i.e. the correlations between the random parameters and the LAR in the 

Monte-Carlo simulations used to evaluate the posterior distributions of these quantities. 

Given the delicate nature of the MCMC calculations, verification of the uncertainty 

intervals so obtained by a perturbation approach would be beneficial as a means of extending the 

analysis. The RAC suggests the following: use the results of the current approach to the 

uncertainty analysis to identify one or two key parameters for each point estimate (where ‘key’ 

means most contributory to overall uncertainty). Then, in the model used to generate the point 

estimate, vary the key parameters over their range in a parametric sensitivity analysis 

(perturbation analysis) to generate a range of resulting risk estimates. This process should 

indicate the operational range of the point estimate. In this way, one can verify whether the 

results of the current uncertainty analyses are appropriate for a given point estimate, and observe 

the width of the confidence interval for that point estimate. 

As a general methodological comment on the usefulness of the posterior densities 

resulting from a Bayesian approach, the RAC suggests considering in future risk predictions the 

concept of the predictive density. It is well established in other applications of survival analysis, 

e.g. reliability analysis, and takes all remaining parameter uncertainty into account for the 

calculation of predicted quantities. Increased computing power and advances in numerical 

integration (e.g., Quasi Monte Carlo Methods) make this feasible if the dimensionality of the 

integrand is not too high (e.g. < 10) (c.f., Bolstad 2007). 

When comparing the results of the draft Blue Book to previous estimates published in 

FGR 13, the EPA stated that “The overall increase in LAR is not due to changes in the basic risk 

models,” but that “...the increase in results is largely attributable to the use of the more recent 

Surveillance, Epidemiology and End Results (SEER) incidence data as a primary basis for 

18 
calculating incidence rates.” The EPA should clarify how this information is reflected in the 

distributions for sources of uncertainty in Table 4-2. 

The prior distributions for Type I parameters in the ERR and EAR risk models are 

formed by directly assigning probability density functions to each parameter as shown in Table 

4-1. Uncertainty of the Type II parameters is based on a different methodology. For these, a 

parameter is assumed to have a constant value (i.e., DDREF =1.5) and the uncertainty in the 

parameter is quantified by a multiplicative factor that is assigned a probability density such as 

LN (GM=1, GSD=1.35). The EPA should explain the reason for the two different approaches. 

A multiplicative factor that is log-normally distributed would lead to a bias unless the mean 

value for this multiplicative factor is equal to 1.0. This is not the case in Table 4-2 when LN 

(0.95, 1.1) is used for systematic errors in dosimetry or LN (1.1, 1.1) is used for uncertainty in 

selection bias. 

4.2.3 Additional Comments on Risk Transfer

Risk due to radiation exposure may differ between populations for many reasons. The 

EPA should consider commenting on the following topics in the Blue Book. 

Important issues such as population differences in genetic susceptibility to cancer and 

how such genetic differences would interact with radiation are only now beginning to be 

understood. Risk assessments by UNSCEAR, ICRP, BEIR VII and the draft Blue Book make 

the implicit assumption that, if the background rate of a particular cancer is similar in two 

populations, then the excess radiogenic cancer risk also will be similar. In reality, this 

assumption may be a simplification and as more is learned about genes (or environmental 

exposures other than radiation) that interact with radiation, other differences in gene or exposure 

frequency may be found between Japanese and U.S. populations. Nevertheless, a reasonable 

assumption, given today’s lack of knowledge, is that cancers with similar baseline rates will have 

similar response to radiation exposure in the two populations. This forms the basis for risk 

transfer models and the associated LAR calculations from the Japanese to U.S. populations. 

For cancers with widely different baseline risks (e.g., stomach and prostate cancer) 

between the Japan and U.S. populations, the choice of an ERR or EAR model can make a large 

difference in the LAR when applying the Japanese risk estimates to the U.S. data. One key Type 

II parameter is the weighting parameter that interpolates between the EAR and ERR models. 

The LSS data provide no direct information about whether EAR or ERR models are more 

reasonable because both models provide equivalent descriptions of the LSS data. 

The uncertainty analysis gives only slight overall bias in favor of ERR compared to EAR 

models in the MCMC calculations. The tendency for the EAR models to be stressed more in the 

uncertainty analysis than in the point estimation may be the reason why in Table 3-11 the point 

estimates for stomach cancer (31 cases per 10,000 person Gy) are so far from the midpoint of the 

uncertainty interval (9-280 cases per 10,000 person Gy). 

19 
4.3 Response to Charge Question # 2b 

The RAC did not identify any specific issue with the selection of distributions to 

characterize uncertainty in parameters used in the models to obtain LAR, but recommends that 

the EPA clarify the reasoning for selecting the subjective priors used in the analysis (e.g., in 

Table 4-1). This information would increase transparency in the draft Blue Book and facilitate 

future scrutiny and verification of the assumptions used in the uncertainty analysis. 

20 
5. RESPONSE TO CHARGE QUESTION 3: COMMENTS ON 

PRESENTATION OF OVERALL INFORMATION AND APPLICATION 

OF BEIR VII IN THE DRAFT BLUE BOOK 

5.1 Charge Question # 3: Please comment on the presentation of the following overall 

information and application of BEIR VII contained in the draft document: 

a. Scientific defensibility and appropriateness of the models and assumptions employed 

for estimating risk. 

b. Presentations of the calculations and results. 

c. Regarding the document’s intended purpose, the accuracy, balance, and level of 

detail of the scientific background material presented. 

5.2 Response to Charge Question # 3a 

The RAC finds that the models and assumptions for estimating risk presented in the draft 

Blue Book are broadly applicable and scientifically defensible. The EPA effort in the draft Blue 

Book to apply BEIR VII models is commendable. The draft Blue Book is one in a sequence of 

EPA publications that apply various methods and models – especially those by BEIR VII for 

low-dose, low-LET, radiation – and lead to FGR 13 as a basis for radiation protection programs. 

The RAC suggests the following topics for additional consideration in the Blue Book. 

 

5.2.1 Noncancer Mortality 

The draft Blue Book focuses on cancer mortality and incidence, and does not address the 

possibility of radiation-related noncancer mortality. Noncancer mortality, particularly mortality 

from cardiovascular disease, has been linked with exposure to high therapeutic radiation doses 

(NAS-NRC 2006), but it is not clear whether such effects are found at lower doses. Mortality 

from most broad noncancer disease categories has been found to be related to radiation dose in 

the LSS cohort (Preston et al. 2003). Because the identified radiation risks were small compared 

to baseline risks, the shape of the dose-response function or age effects could not be evaluated 

with any precision. For example, it was not possible to distinguish a linear dose response from a 

dose response with a threshold as high as 0.5 Gy. Indications also exist of radiation-associated 

increases in diseases of the circulatory system among nuclear workers in the United Kingdom 

(McGeoghegan et al. 2008). 

Lifetime risk estimates for radiation-related non-cancer mortality in the LSS cohort are 

uncertain and range from zero to levels that approach those for cancer mortality estimates 

(Preston et al. 2003). Due to the large uncertainties in the possible magnitude, or even existence, 

of increased noncancer disease risk at low doses, the EPA decision not to provide lifetime risk 

estimates for noncancer mortality is reasonable. The RAC recommends that noncancer mortality 

be mentioned as a possible effect of radiation exposure even at low doses, and that the reasons be 

stated for not providing risk estimates for this endpoint at the present time. 

21 
5.2.2 Information from ICRP and UNSCEAR Reports 

Since the publication of BEIR VII, both ICRP (2007) and UNSCEAR (2008) have 

published reports that include lifetime risk estimates for radiation-related cancers. The ICRP 

developed estimates for a world population defined as an average of risks for hypothetical EuroAmerican and Asian populations, whereas UNSCEAR developed estimates for several different 

countries, including the United States. The RAC recommends that the EPA add a brief 

description of the methods used in the ICRP and UNSCEAR reports and a comparison with 

those that are being used by the EPA. Tables showing comparisons of the EPA estimates not 

only with BEIR VII but also with relevant estimates from ICRP and from UNSCEAR would be a 

desirable addition to the Blue Book. 

5.2.3 Radiogenic Thyroid Cancer

 The draft Blue Book provides limited information regarding the risk of radiogenic thyroid 

cancer as estimated by BEIR VII, although the EPA discussed this issue extensively in its draft 

White Paper (U.S. EPA/ORIA 2006), where the EPA noted that “we now favor adoption of the 

NCRP thyroid cancer model, assuming that we would have a proper reference that can be cited.” 

This reference is now available in National Council on Radiation Protection and 

Measurements Report #159 (NCRP 2009). The RAC recommends that the EPA follow the 

NCRP approach, but also consider in its modeling the latest epidemiological data on exposures 

to the thyroid, published since the NCRP report was written in 2006, such as recent Chernobyl 

thyroid studies (Zablotska et al. 2008). 

5.2.4 Radiogenic Brain Cancer 

 Information on an association between ionizing radiation and brain cancer has been 

generated from radiation-exposed cohorts that provide quantitative dose data and allow 

estimation of radiogenic risks. Based on data from multiple cohorts including A- bomb 

survivors, tinea capitus, hemangiomas, and childhood cancer survivors, the brain-tumor 

epidemiology literature has reached consensus that ionizing radiation is an established risk factor 

for brain tumor development (Ohgaki 2009, Bondy et al. 2008, Davis 2007). While brain tumors 

are complex histologically, radiation risk estimates for gliomas (the most common malignant 

brain tumor) are available from several of these cohorts. The RAC recommends that the EPA 

include the radiogenic risk to the brain in the context of the other cancer sites discussed in the 

draft Blue Book. If the EPA does not wish to do so, it should present the rationale for excluding 

radiogenic risks to the brain. 

 

5.3 Response to Charge Question # 3b 

The RAC found the presentation of calculations and results in the draft Blue Book to be 

competent and comprehensible; it suggests the following for greater clarity and readability: 

22 
5.3.1 Tabular Presentations 

The RAC recommends that, in Table 4-2 on sources of uncertainty, a column listing 

references for the source of the distribution parameters be added, and that these be discussed in 

the text. It also recommends eliminating repetition in several tables of the same values of 

lifetime risk estimates of cancer incidence or mortality. 

5.3.2 Topical Organization and Content 

The RAC recommends that the EPA clearly state the purpose and application of the Blue 

Book in Section 1, notably the intended contributions of Blue Book cancer incidence and 

mortality values to the contents of Federal Guidance Report 13. 

The organization of the Blue Book can be improved by pulling together some scattered 

topics. For example, in Section 3.3, pages 29-32 (U.S. EPA/ORIA 2008), risk models for 

cancers not specified by BEIR VII (kidney, bone, NMSC, etc.) are discussed and conclusions 

presented, but estimating cancer risks for these organs is discussed in detail in Section 5, pages 

84-88.   

The RAC found that the more detailed explanations and examples provided in the 

materials orally presented by ORIA staff on March 23, 2009, and referred to above, clarified 

draft Blue Book contents and suggests that they be included in the Blue Book. 

 5.3.3 Relation of Input Information to Presented Results 

The RAC suggests that clarification of the changes based on updated SEER would be 

helpful. The statement on page 55 that increased LAR estimates (compared to those of FGR 13) 

are “largely attributable to the use of more recent SEER incidence [rates]” is confusing. 

Similarly, on page 55 is a statement that “the LAR for all cancers combined is increased by about 

20%” because of the new SEER incidence data, followed by a statement that the models 

themselves would yield lower estimates of LAR than those published in FGR13 if the new 

models were applied to comparable mortality and incidence rates. The EPA appears to be 

making the point that for FGR 13 it uses poorly approximated incidence rates computed as 

lethality-adjusted mortality risks but that the new estimates are based on actual age-specific 

incidence rates. 

The interplay between mathematical models and compiled incidence rates should be 

explained clearly and simply in the Blue Book to address suspicion expressed by members of the 

public at the meetings that the EPA will distort results to present falsely low risk values for 

implementation in the revised FGR 13. The rationale and implications of calculating LAR based 

on a life table for a hypothetical stationary population rather than the existing life tables for the 

current US population also should be further explained to eliminate this approach as a cause of 

distrust by the general reader. 

23 
5.3.4 Application of DDREF

The recent ICRP Report 103 (ICRP 2007) concluded that the DDREF value should 

remain at 2 and not be reduced to 1.5 as recommended by BEIR VII (U.S. NAS/NRC 2006). 

The EPA should justify the decision to disagree with the ICRP conclusion and follow the BEIR 

VII recommendation. 

The RAC recommends that tables with LAR estimates indicate whether the estimates 

include a DDREF adjustment. 

5.4 Response to Charge Question # 3c 

The RAC finds that the draft Blue Book presents the scientific background material with 

appropriate accuracy and balance, but recommends that the scientific background can be 

enhanced by including the following topics:

5.4.1 Low-Dose Protracted Exposure

The RAC realizes that much of the draft Blue Book relies on BEIR VII risk estimates 

based primarily on LSS data, but suggests that the EPA compare the revised EPA estimates with 

risk estimates from studies of persons exposed to low-level, protracted radiation exposure. 

These include nuclear workers in the 15-country radiation worker study (Cardis et al. 2007) and 

the study of United Kingdom National Registry of Radiation Workers (Muirhead et al. 2009). 

The EPA is primarily interested in the health effects of low-dose protracted radiation exposure, 

and acknowledges that risk estimates based on an acute exposure in a Japanese population carry 

with them considerable uncertainty when applied to low-dose exposure of the U.S. population. 

5.4.2 Cancer Sites with Limited Data 

 The RAC recommends that the EPA, in support for its rationale for estimating risk for 

specific cancer sites, look to the expected summary of cancer sites that have limited or 

inadequate data in the soon-to-be-published updated report by the International Agency for 

Research on Cancer (IARC) on the cancer risks of ionizing radiation. Specifically, justification 

should be given for estimating cancer risk for sites in which IARC concluded that the 

epidemiological data are inadequate or limited. Conversely, the EPA needs to justify having 

omitted any cancer sites for which IARC concluded that sufficient epidemiological evidence 

exists. 

5.4.3 Cancer Subtypes 

The RAC encourages expanding the discussion of issues related to lympho-hematopoietic 

cancers. For example, comment on: (1) recent discussions of whether chronic lymphocytic 

leukemia (CLL) is radiogenic (Linet et al. 2007; Schubauer-Berigan 2007a, 2007b; Vrijhead et 

24 
al. 2008; Silver et al. 2007), and appropriate references contained within; (2) absence of risk 

estimates for leukemia subtypes; and (3) absence of risk estimates for non-Hodgkin’s lymphoma 

or multiple myeloma. 

5.4.4 Presentation of Stepwise EPA Development of Revised FGR 13 

The RAC recommends that the EPA include in Section 7 of the Blue Book specific 

information concerning the anticipated radionuclide risk coefficient values in the revised FGR 

13, based on currently available dosimetric models. Tables A4a and A4b in the 1994 Blue Book 

can be taken as models. This information will enable the public and professionals to attribute 

reasponsibility for changes in FGR 13 to revised cancer risk projections in the Blue Book or to 

revised dosimetric models, or to both. 

 

25 
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2007. 

Sokolnikov, M.E., E.S. Gilbert, D.L. Preston, N.S. Shilnikova, V.V. Khokhryakov, E.K. 

Vasilenko, N.A. Koshurnikova 2008. Lung, liver, and bone cancer mortality in Mayak workers. 

Int J Cancer 123: 905-911. 2008.

Stewart, A., J. Webb, D. Hewitt 1958. A survey of childhood malignancies. Br. Med J. 1(5086): 

1495-1508. 1958. 

Storer, J.B., T.J. Mitchell, and R.J.M. Fry 1988. Extrapolation of the relative risk of radiogenic 

neoplasms across mouse species and to man. Radiat.Res. 114: 331-353. 1988. 

UNSCEAR. 2008. United Nations Scientific Committee on the Effects of Atomic Radiation, 

Effects of Ionizing Radiation - - UNSCEAR 2006 Report to the General Assembly with Scientific 

Annexes. Volume I. Effects of Ionizing Radiation. United Nations, New York. 2008. 

UNSCEAR. 2000. United Nations Scientific Committee on the Effects of Atomic Radiation, 

Sources, Effects, and Risks of Ionizing Radiation with Annexes, Volume II: Effects. United 

Nations, New York. 2000.

. 

U.S. EPA 1994. Estimating Radiogenic Cancer Risks (“Blue Book”), Washington, DC (EPA 

402-R-93-076), June 1994: http://epa.gov/radiation/docs/assessment/402-r-93-076.pdf

U.S. EPA. 1984. Radionuclides: Background Information Document for Final Rules, Vol. 1,

Washington, DC, EPA/1-84-022-1. 1984. 

30 
U.S. EPA/ORIA 2009. Memorandum entitled “Advisory Review of the Draft Document: EPA 

Radiogenic Cancer Risk Models and Projections for the U.S. Population,” from Elizabeth A. 

Cotsworth, Director, Office of Radiation and Indoor Air to Vanessa Vu, Director, Science 

Advisory Board Staff Office, January 26, 2009. 

U.S. EPA/ORIA 2008. “EPA Radiogenic Cancer Risk Models and Projections for the U.S. 

Population,” U.S. Environmental Protection Agency (EPA), Office of Radiation and Indoor Air 

(ORIA), Draft December 2008, 116 pages (“The Blue Book”) 

http://epa.gov/radiation/assessment/pubs.html

U.S. EPA/ORIA 2006. “Modifying EPA Radiation Risk Models Based on BEIR VII,” Draft 

White Paper, Prepared by Office of Radiation and Indoor Air, U.S. Environmental Protection 

Agency, August 1, 2006, 36 pages 

http://yosemite.epa.gov/sab/sabproduct.nsf/8097D8CE7070C1E4852571DA0005C605/$File/rac

_oria_white_paper_08-01-06.pdf 

U.S. EPA/ORIA 1999. “Cancer Risk Coefficients for Environmental Exposure to 

Radionuclides,” Federal Guidance Report No. 13, EPA 402-R-99-001, September 1999, 335 

pages http://epa.gov/radiation/docs/federal/402-r-99-001.pdf

U.S. EPA/ORIA 1999a. “Estimating Cancer Risks Addendum: Uncertainty Analysis,” U.S. 

Envrionmental Protection Agency, Office of Radiation and Indoor Air (6608J), Washington, DC, 

May 1999, EPA 402-R-99-003. http://epa.gov/radiation/docs/assessment/402-r-99-003.pdf

U.S. EPA/SAB 2008. Advisory on Agency Draft White Paper Entitled “Modifying EPA 

Radiation Risk Models Based on BEIR VII,” EPA-SAB-08-006. January 31, 2008. 

http://yosemite.epa.gov/sab/sabproduct.nsf/FD9963E56C66E4FF852573E200493359/$File/EPA

-SAB-08-006-unsigned.pdf

U.S. EPA/SAB 1999. “An SAB Report: Estimating Uncertainties in Radiogenic Cancer Risk,”

EPA-SAB-RAC-99-008, February 18, 1999. 

http://yosemite.epa.gov/sab/sabproduct.nsf/D3511CC996FB97098525718F0064DD44/$File/rac

9908.pdf

U.S. EPA/SAB 1994. “Evaluation of EPA’s Proposed Methodology for Estimating Radiogenic 

Cancer Risks,” EPA-SAB-RAC-LTR-93-004, December 9, 1992.

http://yosemite.epa.gov/sab/sabproduct.nsf/0A0E72B3E05BC8928525731C007830F3/$File/RA

DIOGENIC+CANCER+RAC-LTR-93-004_93004_5-8-1995_68.pdf

Van Kaick, G., A. Dalheimer, S. Hornik, A. Kaul, D. Liebermann, H. Luhrs, A. Spiethoff, K. 

Wegener, H. Welch 1999. The German Thorotrast study: Recent results and assessment of risks. 

Radiation Research 152(6): S64-S71. 1999. 

31 
Vrijhead, M., E. Cardis, P. Ashmore, A. Auvinen, E. Gilbert, R.R. Habib, H. Malker, C.R. 

Muirhead, D.B. Richardson, A. Rogel, M. Schubauer-Berigan, H. Tardy, M. Telle-Lamberton 

2008. Ionizing radiation and risk of chronic lymphocytic leukemia in the 15-country study of 

nuclear industry workers. 15-Country Study Group. Radiat. Res. 170(5): 661-5. 2008. 

Zablotska LB, Bogdanova TI, Ron E, Epstein OV, Robbins J, Likhtarev IA, Hatch M, Markov 

VV, Bouville AC, Olijnyk VA, McConnell RJ, Shpak VM, Brenner A, Terekhova GN, 

Greenebaum E, Tereshchenko VP, Fink DJ, Brill AB, Zamotayeva GA, Masnyk IJ, Howe GR, 

Tronko MD. A cohort study of thyroid cancer and other thyroid diseases after the Chornobyl 

accident: dose of thyroid follicular adenomas detected during first screening in Ukraine (1998-

2000). Am J Epidemiol. 2008 Feb 1; 167(3):305-12. 

32 
WEB-BASED CITATIONS AND HOTLINKS

NAS/NRC. 2006. BEIR VII. Health Risks from Exposure to Low levels of Ionizing Radiation 

BEIR VII Phase 2, National Academies of Sciences (NAS), National Research Council, 

Committee to Assess Health Risks from Exposure to Low levels of Ionizing Radiation, 

http://nap.edu/catalog/11340.html#toc

U. S. EPA/ORIA. 1994. Estimating Radiogenic Cancer Risks (“Blue Book”), Washington, DC 

(EPA 402-R-93-076), June, 1994: http://epa.gov/radiation/docs/assessment/402-r-93-076.pdf

U.S. EPA /ORIA. 1999. Federal Guidance Report (FGR)-13. Federal Guidance Report 13: 

Cancer Risk Coefficients for Environmental Exposure to Radionuclides, Washington, DC (EPA 

402-R-99-001), September, 1999 http://epa.gov/radiation/docs/federal/402-r-99-001.pdf

U. S. EPA/ORIA. 1999a. Estimating Radiogenic Cancer Risks Addendum: Uncertainty Analysis, 

Washington, DC (EPA 402-R-99-003), May, 1999: 

http://epa.gov/radiation/docs/assessment/402-r-99-003.pdf

U.S. EPA/ORIA. 1999b. Update to the Federal Guidance Report No. 13 and CD Supplement: 

http://epa.gov/radiation/assessment/pubs.html (can also view pubs site for the April 2002 update: 

CD Supplement) 

U.S. EPA/ORIA. 2006. Office of Radiation and Indoor Air (ORIA), Draft White Paper: 

Modifying EPA Radiation Risk Models Based on BEIR VII, August 1, 2006 

http://yosemite.epa.gov/sab/sabproduct.nsf/8097D8CE7070C1E4852571DA0005C605/$File/rac

_oria_white_paper_08-01-06.pdf

U.S. EPA/ORIA. 2008. “EPA Radiogenic Cancer Risk Models and Projections for the U.S. 

Population,” U.S. Environmental Protection Agency (EPA), Office of Radiation and Indoor Air 

(ORIA), Draft December 2008, 116 pages (“The Blue Book”) 

http://epa.gov/radiation/assessment/pubs.html

FEDERAL REGISTER SOLICITING NOMINATIONS TO AUGMENT EXPERTISE ON 

THE RADIATION ADVISORY COMMITTEE (RAC): 

Federal Register, Vol. 73, No. 76, Friday, April 18, 2008, pp. 21129-21130 

http://www.epa.gov/fedrgstr/EPA-SAB/2008/April/Day-18/sab8400.htm

33 
FEDERAL REGISTER ANNOUNCING MEETINGS OF THE AUGMENTED 

RADIATION ADVISORY COMMITTEE (RAC): 

Federal Register, 74, Tuesday, February 3, 2009, pp. 5935-5936

http://www.epa.gov/fedrgstr/EPA-SAB/2009/February/Day-03/sab2249.htm

Federal Register, 74, Thursday, May 28, 2009, pp. 25529-25530 

http://www.epa.gov/fedrgstr/EPA-SAB/2009/May/Day-28/sab12480.htm

FEDERAL REGISTER ANNOUNCING MEETING OF THE CHARTER SCIENCE 

ADVISORY BOARD TO CONDUCT THE QUALITY REVIEW OF THE RAC’S 

AUGUST 20, 2009 DRAFT REPORT

Federal Register, Volume 74, No. 161, Friday, August 21, 2009, pp. 42297-42298 

http://www.epa.gov/fedrgstr/EPA-SAB/2009/August/Day-21/sab20171.htm

BACKGROUND SAB REPORTS AND ADVISORIES:

U.S. EPA/SAB. 1992. “Evaluation of EPA’s Proposed Methodology for Estimating Radiogenic 

Cancer Risks,” EPA-SAB-RAC-LTR-93-004, December 9, 1992.

http://yosemite.epa.gov/sab/sabproduct.nsf/0A0E72B3E05BC8928525731C007830F3/$File/RA

DIOGENIC+CANCER+RAC-LTR-93-004_93004_5-8-1995_68.pdf

U.S. EPA/SAB. 1998. “An SAB Report: Review of Health Risks from Low-Level Environmental 

Exposures to Radionuclides (FRG-13 Report),” EPA-SAB-RAC-99-009, December 23, 1998 

http://yosemite.epa.gov/sab/sabproduct.nsf/2EF0698AA08A29098525718F006532D8/$File/rac9

909.pdf

U.S. EPA/SAB. 1999. “An SAB Report: Estimating Uncertainties in Radiogenic Cancer Risk,”

EPA-SAB-RAC-99-008, February 18, 1999. 

http://yosemite.epa.gov/sab/sabproduct.nsf/D3511CC996FB97098525718F0064DD44/$File/rac

9908.pdf

U.S. EPA/SAB. 2008. Advisory on Agency Draft With Paper Entitled “Modifying EPA 

Radiation Risk Models Based on BEIR VII,” EPA-SAB-08-006. January 31, 2008. 

http://yosemite.epa.gov/sab/sabproduct.nsf/FD9963E56C66E4FF852573E200493359/$File/EPA

-SAB-08-006-unsigned.pdf

AGENCY AND OTHER DOCUMENTS (AND HOTLINKS) RELATED TO 

ESTIMATING RADIOGENIC CANCER RISKS:

U.S. EPA/ORIA. 1994. Blue Book: Estimating Radiogenic Cancer Risks, EPA 402-R-93-076, 

June 1994 http://www.epa.gov/radiation/docs/assessment/402-r-93-076.pdf

34 
U.S. EPA/ORIA. 1999. Uncertainty Addendum: Estimating Radiogenic Cancer Risks 

Addendum: Uncertainty Analysis, EPA 402-R-99-003, May 1999. 

http://www.epa.gov/radiation/docs/assessment/402-r-99-003.pdf

The basis for the Blue Book SAB peer review is at: 

U.S. EPA/SAB. 1992. “Evaluation of EPA’s Proposed Methodology for Estimating Radiogenic 

Cancer Risks,” EPA-SAB-RAC-LTR-93-004, December 9, 1992.

http://yosemite.epa.gov/sab%5Csabproduct.nsf/0A0E72B3E05BC8928525731C007830F3/$File/

RADIOGENIC+CANCER+RAC-LTR-93-004_93004_5-8-1995_68.pdf

The Uncertainty Addendum SAB peer review is at: 

U.S. EPA/SAB. 1999. “An SAB Report: Estimating Uncertainties in Radiogenic Cancer Risk,”

EPA-SAB-RAC-99-008, February 18, 1999. 

http://yosemite.epa.gov/sab%5Csabproduct.nsf/D3511CC996FB97098525718F0064DD44/$File

/rac9908.pdf

 

FEDERAL GUIDANCE REPORT 13:

U.S. EPA/OAR. 1999. “Cancer Risk Coefficients for Environmental Exposure to 

Radionuclides,” Federal Guidance Report No. 13, EPA 402-R-99-001, September 1999, 335 

pages http://epa.gov/radiation/docs/federal/402-r-99-001.pdf

NATIONAL ACADEMY OF SCIENCES BEIR VII REPORT:

NAS/NRC, 2006. Health Risks from Exposure to Low Levels of Ionizing Radiation, BEIR VII 

Phase 2, National Academies of Sciences (NAS), National Research Council, Committee to 

Assess Health Risks from Exposure to Low levels of Ionizing Radiation, 2006, 416 pages 

http://nap.edu/catalog/11340.html#toc

AGENCY UPDATED DRAFT WHITE PAPER:

U.S. EPA/ORIA. 2006. Modifying EPA Radiation Risk Models Based on BEIR VII, Draft 

White Paper, Prepared by Office of Radiation and Indoor Air, U.S. Environmental Protection 

Agency, August 1, 2006, 36 pages 

http://yosemite.epa.gov/sab/sabproduct.nsf/8097D8CE7070C1E4852571DA0005C605/$File/rac

_oria_white_paper_08-01-06.pdf 

35 
APPENDIX A – EDITORIAL COMMENTS 

Minor (editorial) comments on the draft EPA document on Radiogenic Cancer Risk. 

p.6: Insert acronyms: 

 UI Uncertainty interval 

 ICD ? (used on p.23) 

p. 7, paragraph 2: This should mention the provision of estimates for alpha-emitters, X-rays etc. 

Also, kidney cancer should be added to the list in the 3rd sentence. 

p. 7, paragraph 4: Sentence “Nevertheless ... time after exposure.” This is true, but for most 

cancers the estimates are more precise than those from any other study. This point might be 

worked into the paragraph. Another limitation that might be mentioned is the relevance for low 

dose rate exposure. 

p.16, Section 2.1.5, line 2: Replace ‘new’ by ‘recently observed’. 

p. 20, 1st full paragraph: The study of British radiologists by Berrington et al. (Br. J. of 

Radiology 2001) might also be cited. 

p. 20, 2nd full paragraph: An important paper on workers that needs to be cited is the recent 

update of the study of NRRW British nuclear workers (Muirhead et al. Brit. J. Cancer, 2009). 

The most important limitations (in my opinion) are not mentioned. These are lack of statistical 

power (imprecise risk estimates) and vulnerability to confounding when studying small risks. 

There are also more recent Chernobyl papers that might be cited including 2 papers on thyroid 

cancer (Cardis et al. JNCI 2005; Tronko et al. JNCI 2006) and 2 papers on leukemia incidence 

(Romanenko et al. Radiat. Res. 2008; Kesminiene et al. Radiat. Res. 2008). 

p. 21, line 1: Kidney cancer should be added here. 

p. 23, last 2 lines: Suggest revising as following: “... the BEIR VII committee found that the 

ERR per Gy decreased by about 25% per decade of age at exposure (for ages under 30) in the 

model ... 

p. 25, Table 3-2: For thyroid cancer, attained age (a) id not an effect modifier. The Ron et al. 

pooled analysis should also be cited. For leukemia, the ERR and EAR were linear-quadratic 

functions of dose. 

p. 27, “Breast” paragraph: It would be helpful to indicate briefly the rationale for using only an 

EAR model for this site. 

p.27, Table 3-3: Last letter in heading should be Greek eta, not ‘H’. 

36 
p.28, Fig.3-2 and others: Always show units along axes. 

p.41, Section 3.9.2: insert period after ‘9’. 

p. 43: Line just below equation 3-21. The inequality is incorrect. When one multiplies the 

expression in 3-21 by M(A) –M(R), the direction of the inequality will change when M(A) –M(R) is 

negative. 

p. 43, last paragraph: The wording here is confusing. Equation (3-20) seems to assume the 

M(true) that is between the EAR and ERR estimates. 

p. 55, 3rd sentence: BEIR VII accounted for uncertainty in the age parameters for the all solid 

cancer estimate. 

p.57, Table 3-13: Do the 90% UI values refer to Kidney or to combined Residual + kidney as in 

Table 3-11? 

p. 59, paragraph 2: Another important difference is the approach to transport. 

p. 62 ff: If there is sharing of the main effect parameters, there should be sharing of the age 

parameters as well. Also, there should probably be allowance for correlation of the age at 

exposure and attained age parameters. (I have no idea what the impact of the changes might be.) 

p.63, Table 4-1: Replace 2nd parameter heading (it is the same as the 1st). 

p.77, Table 4-4b: Insert ‘age’ in heading before ‘15’. 

p.83, Table 4-5: Although heading says ‘95% uncertainty intervals’, the values are similar to the 

90% uncertainty intervals of Table 3-11. Check. 

 

 p. 88, 1st full paragraph: The more recent Sokolnikov et al. paper should also be cited here. 

p. 90, 1st full paragraph: Provide confidence intervals for these estimates to remind readers of the 

considerable uncertainty. This comment also applies to many other estimates presented in the 

report. 

p. 90, 2nd full paragraph: The Gilbert et al. 2004 paper argued that the estimates of the ERR per 

Gy from plutonium and from radon were fairly comparable. You might want to check this paper 

(beginning 2nd column on p. 514). 

37 
APPENDIX B –ACRONYMS 

A Atomic 

AM Arithmetic Mean 

BCC Basal Cell Carcinoma 

BEIR Biological Effects of Ionizing Radiation (Pertains to committees of the Board of 

Radiation Effects, National Research Council of the National Academy (now the 

National Academies’), charged with assessing the Biological Effects of Ionizing 

Radiation 

BEIR VII The report entitled “Health Risks from Exposure to Low Levels of Ionizing 

Radiation BEIR VII – Phase 2” published (2006) by the Committee to Assess 

Health Risks from Exposure to Low levels of Ionizing Radiation of the Board on 

Radiation Effects Research, National Research Council of the National 

Academies 

Bq Becquerel 

CLL Chronic Lymphocytic Leukemia 

Co Chemical symbol for Cobalt (60Co isotope) 

CT scan Computed tomography scan 

DDREF Dose and Dose-Rate Effectiveness Factor 

EAR Excess Absolute Risk 

EPA Environmental Protection Agency (U.S. EPA) 

ERR Excess Relative Risk 

eV Electron Volts 

FGR Federal Guidance Report 

FY Fiscal Year 

GM Geometric Mean 

GSD Geometric Standard Deviation 

Gy Gray, SI unit of radiation absorbed dose (1 Gy is equivalent to 100 rad in 

traditional units) 

H Chemical symbol for Hydrogen (3H isotope) 

IARC International Agency for Research on Cancer 

ICRP International Commission on Radiological Protection 

I Chemical Symbol for Iodine (131I isotope) 

IR Ionizing Radiation 

IREP Interactive Radio-epidemiology Program 

k Kilo (thousands) 

kVp Kilo Volt potential 

LAR Lifetime Attributable Risk 

LET Linear Energy Transfer 

LN Linear Non-Threshold (also LNT) 

LSS Life-Span Study 

mGY Milli (one Thousandth) Gray 

M Point estimate of the excess risk (d, a, e) [at an attained age, a, following a single 

exposure to a dose, d, at age, e] 

MCMC Markov Chain Monte Carlo methods 

38 
39 

NAS National Academy of Sciences 

NCRP National Council on Radiation Protection and Measurements 

NIOSH National Institute for Occupational Safety and Health 

NMSC Non-Melanoma Skin Cancer 

NRC National Research Council 

OAR Office of Air and Radiation (U.S. EPA/OAR) 

ORIA Office of Radiation and Indoor Air (U.S. EPA/OAR/ORIA) 

Ra Chemical symbol for Radium (Isotopes include 224Ra, 226 Ra, 228Ra, and 236Ra) 

RAC Radiation Advisory Committee ((U.S. EPA/SAB/RAC) 

RBE Relative Biological Effectiveness 

SAB Science Advisory Board (U.S. EPA/SAB) 

SEER Surveillance, Epidemiology and End Results 

UNSCEAR United Nations Scientific Committee on the Effects of Atomic Radiation 

US United States of America – used interchangeably with USA 

WinBUGS Windows (for Microsoft windows programs) for Bayesian inference Using Gibbs 

Sampling analysis software