TOXICOLOGICAL PROFILE FOR 

RADON 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
 

Public Health Service 

Agency for Toxic Substances and Disease Registry 

May 2012 
RADON ii 

DISCLAIMER 

Use of trade names is for identification only and does not imply endorsement by the Agency for Toxic 

Substances and Disease Registry, the Public Health Service, or the U.S. Department of Health and Human 

Services. 

 


 

RADON iii 

UPDATE STATEMENT 

A Toxicological Profile for Radon, Draft for Public Comment was released in September 2008. This 

edition supersedes any previously released draft or final profile. 

Toxicological profiles are revised and republished as necessary. For information regarding the update 

status of previously released profiles, contact ATSDR at: 

Agency for Toxic Substances and Disease Registry 

Division of Toxicology and Human Health Sciences (proposed)/
 

Environmental Toxicology Branch (proposed) 

1600 Clifton Road NE 

Mailstop F-62 

Atlanta, Georgia 30333
 
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RADON v 

FOREWORD
 

This toxicological profile is prepared in accordance with guidelines* developed by the Agency for Toxic 

Substances and Disease Registry (ATSDR) and the Environmental Protection Agency (EPA). The 

original guidelines were published in the Federal Register on April 17, 1987. Each profile will be revised 

and republished as necessary. 

The ATSDR toxicological profile succinctly characterizes the toxicologic and adverse health effects 

information for the toxic substances each profile describes. Each peer-reviewed profile identifies and 

reviews the key literature that describes a substance's toxicologic properties. Other pertinent literature is 

also presented but is described in less detail than the key studies. The profile is not intended to be an 

exhaustive document; however, more comprehensive sources of specialty information are referenced. 

The profiles focus on health and toxicologic information; therefore, each toxicological profile begins with 

a public health statement that describes, in nontechnical language, a substance's relevant toxicological 

properties. Following the public health statement is information concerning levels of significant human 

exposure and, where known, significant health effects. A health effects summary describes the adequacy 

of information to determine a substance's health effects. ATSDR identifies data needs that are significant 

to protection of public health. 

Each profile: 

(A) Examines, summarizes, and interprets available toxicologic information and 

epidemiologic evaluations on a toxic substance to ascertain the levels of significant human 

exposure for the substance and the associated acute, subacute, and chronic health effects; 

(B) Determines whether adequate information on the health effects of each substance is 

available or being developed to determine levels of exposure that present a significant risk to 

human health of acute, subacute, and chronic health effects; and 

(C) Where appropriate, identifies toxicologic testing needed to identify the types or levels of 

exposure that may present significant risk of adverse health effects in humans. 

The principal audiences for the toxicological profiles are federal, state, and local health professionals; 

interested private sector organizations and groups; and members of the public. 

This profile reflects ATSDR’s assessment of all relevant toxicologic testing and information that has been 

peer-reviewed. Staff of the Centers for Disease Control and Prevention and other federal scientists also 

have reviewed the profile. In addition, this profile has been peer-reviewed by a nongovernmental panel 

and was made available for public review. Final responsibility for the contents and views expressed in 

this toxicological profile resides with ATSDR. 

Christopher J. Portier, Ph.D. 

Assistant Administrator
	

Agency for Toxic Substances and Disease Registry
	
 

 

 

 

 

RADON vi 

*Legislative Background 

The toxicological profiles are developed under the Comprehensive Environmental Response, 

Compensation, and Liability Act of 1980, as amended (CERCLA or Superfund). CERCLA section 

104(i)(1) directs the Administrator of ATSDR to “...effectuate and implement the health related 

authorities” of the statute. This includes the preparation of toxicological profiles for hazardous 

substances most commonly found at facilities on the CERCLA National Priorities List and that pose the 

most significant potential threat to human health, as determined by ATSDR and the EPA. Section 

104(i)(3) of CERCLA, as amended, directs the Administrator of ATSDR to prepare a toxicological profile 

for each substance on the list. In addition, ATSDR has the authority to prepare toxicological profiles for 

substances not found at sites on the National Priorities List, in an effort to “...establish and maintain 

inventory of literature, research, and studies on the health effects of toxic substances” under CERCLA 

Section 104(i)(1)(B), to respond to requests for consultation under section 104(i)(4), and as otherwise 

necessary to support the site-specific response actions conducted by ATSDR. 
 


 

RADON vii 

QUICK REFERENCE FOR HEALTH CARE PROVIDERS 

Toxicological Profiles are a unique compilation of toxicological information on a given hazardous 

substance. Each profile reflects a comprehensive and extensive evaluation, summary, and interpretation 

of available toxicologic and epidemiologic information on a substance. Health care providers treating 

patients potentially exposed to hazardous substances will find the following information helpful for fast 

answers to often-asked questions. 

Primary Chapters/Sections of Interest 

Chapter 1: Public Health Statement: The Public Health Statement can be a useful tool for educating 

patients about possible exposure to a hazardous substance. It explains a substance’s relevant 

toxicologic properties in a nontechnical, question-and-answer format, and it includes a review of 

the general health effects observed following exposure. 

Chapter 2: Relevance to Public Health: The Relevance to Public Health Section evaluates, interprets, 

and assesses the significance of toxicity data to human health. 

Chapter 3: Health Effects: Specific health effects of a given hazardous compound are reported by type 

of health effect (death, systemic, immunologic, reproductive), by route of exposure, and by length 

of exposure (acute, intermediate, and chronic). In addition, both human and animal studies are 

reported in this section. 

NOTE: Not all health effects reported in this section are necessarily observed in the clinical 

setting. Please refer to the Public Health Statement to identify general health effects observed 

following exposure. 

Pediatrics: Four new sections have been added to each Toxicological Profile to address child health 

issues: 

Section 1.6 How Can (Chemical X) Affect Children? 

Section 1.7 How Can Families Reduce the Risk of Exposure to (Chemical X)? 

Section 3.7 Children’s Susceptibility 

Section 6.6 Exposures of Children
 

Other Sections of Interest: 

Section 3.8 Biomarkers of Exposure and Effect 

Section 3.11 Methods for Reducing Toxic Effects 

ATSDR Information Center 

Phone: 1-800-CDC-INFO (800-232-4636) or 1-888-232-6348 (TTY) Fax: (770) 488-4178

 E-mail: cdcinfo@cdc.gov Internet: http://www.atsdr.cdc.gov 

The following additional material can be ordered through the ATSDR Information Center: 

Case Studies in Environmental Medicine: Taking an Exposure History—The importance of taking an 

exposure history and how to conduct one are described, and an example of a thorough exposure 

history is provided. Other case studies of interest include Reproductive and Developmental 

Hazards; Skin Lesions and Environmental Exposures; Cholinesterase-Inhibiting Pesticide 

Toxicity; and numerous chemical-specific case studies. 
RADON viii 

Managing Hazardous Materials Incidents is a three-volume set of recommendations for on-scene 

(prehospital) and hospital medical management of patients exposed during a hazardous materials 

incident. Volumes I and II are planning guides to assist first responders and hospital emergency 

department personnel in planning for incidents that involve hazardous materials. Volume III— 

Medical Management Guidelines for Acute Chemical Exposures—is a guide for health care 

professionals treating patients exposed to hazardous materials. 

Fact Sheets (ToxFAQs) provide answers to frequently asked questions about toxic substances. 

Other Agencies and Organizations 

The National Center for Environmental Health (NCEH) focuses on preventing or controlling disease, 

injury, and disability related to the interactions between people and their environment outside the 

workplace. Contact: NCEH, Mailstop F-29, 4770 Buford Highway, NE, Atlanta, 

GA 30341-3724 • Phone: 770-488-7000 • FAX: 770-488-7015. 

The National Institute for Occupational Safety and Health (NIOSH) conducts research on occupational 

diseases and injuries, responds to requests for assistance by investigating problems of health and 

safety in the workplace, recommends standards to the Occupational Safety and Health 

Administration (OSHA) and the Mine Safety and Health Administration (MSHA), and trains 

professionals in occupational safety and health. Contact: NIOSH, 200 Independence Avenue, 

SW, Washington, DC 20201 • Phone: 800-CDC-INFO (800-232-4636) or NIOSH Technical 

Information Branch, Robert A. Taft Laboratory, Mailstop C-19, 4676 Columbia Parkway, 

Cincinnati, OH 45226-1998 • Phone: 800-35-NIOSH. 

The National Institute of Environmental Health Sciences (NIEHS) is the principal federal agency for 

biomedical research on the effects of chemical, physical, and biologic environmental agents on 

human health and well-being. Contact: NIEHS, PO Box 12233, 104 T.W. Alexander Drive, 

Research Triangle Park, NC 27709 • Phone: 919-541-3212. 

Radiation Emergency Assistance Center/Training Site (REAC/TS) provides support to the U.S. 

Department of Energy, the World Health Organization, and the International Atomic Energy 

Agency in the medical management of radiation accidents. A 24-hour emergency response 

program at the Oak Ridge Institute for Science and Education (ORISE), REAC/TS trains, 

consults, or assists in the response to all kinds of radiation accidents. Contact: Oak Ridge 

Institute for Science and Education, REAC/TS, PO Box 117, MS 39, Oak Ridge, TN 37831-0117 

• Phone 865-576-3131 • FAX 865-576-9522 • 24-Hour Emergency Phone 865-576-1005 (ask for 

REAC/TS) • e-mail: cooleyp@orau.gov • website (including emergency medical guidance): 

http://www.orau.gov/reacts/default.htm 

Referrals 

The Association of Occupational and Environmental Clinics (AOEC) has developed a network of clinics 

in the United States to provide expertise in occupational and environmental issues. Contact: 

AOEC, 1010 Vermont Avenue, NW, #513, Washington, DC 20005 • Phone: 202-347-4976 

• FAX: 202-347-4950 • e-mail: AOEC@AOEC.ORG • Web Page: http://www.aoec.org/. 

The American College of Occupational and Environmental Medicine (ACOEM) is an association of 

physicians and other health care providers specializing in the field of occupational and 
RADON ix 

environmental medicine. Contact: ACOEM, 25 Northwest Point Boulevard, Suite 700, Elk 

Grove Village, IL 60007-1030 • Phone: 847-818-1800 • FAX: 847-818-9266. 
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CONTRIBUTORS 

CHEMICAL MANAGER(S)/AUTHOR(S): 

Sam Keith, M.S., C.H.P.
 

John R. Doyle, M.P.A. 

Carolyn Harper, Ph.D. 

Moiz Mumtaz, Ph.D. 

Oscar Tarrago, M.D., M.P.H., C.H.E.S. 

ATSDR, Division of Toxicology and Human Health Sciences (proposed), Atlanta, GA 

David W. Wohlers, Ph.D. 

Gary L. Diamond, Ph.D.
 

Mario Citra, Ph.D. 

Lynn E. Barber, M.S. 

SRC, Inc., North Syracuse, NY 

THE PROFILE HAS UNDERGONE THE FOLLOWING ATSDR INTERNAL REVIEWS: 

1. Health Effects Review. The Health Effects Review Committee examines the health effects 

chapter of each profile for consistency and accuracy in interpreting health effects and classifying 

end points. 

2.	 Minimal Risk Level Review. The Minimal Risk Level Workgroup considers issues relevant to 

substance-specific Minimal Risk Levels (MRLs), reviews the health effects database of each 

profile, and makes recommendations for derivation of MRLs. 

3.	 Data Needs Review. The Environmental Toxicology Branch (proposed) reviews data needs 

sections to assure consistency across profiles and adherence to instructions in the Guidance. 

4. Green Border Review. Green Border review assures the consistency with ATSDR policy. 
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RADON	 	 xiii 

PEER REVIEW 

A peer review panel was assembled in 2008 for radon. The panel consisted of the following members: 

1. R. William Field, Ph.D., M.S., Professor, College of Public Health, Department of Occupational and 

Environmental Health and Department of Epidemiology, University of Iowa, Iowa City, Iowa; 

2. Naomi H. Harley, Ph.D., Research Professor, Department of Environmental Medicine, New York 

University School of Medicine, New York, New York; and 

3. Jonathan Samet, M.D., Professor and Chairman, Department of Epidemiology, Bloomberg School 

of Public Health, The Johns Hopkins University, Baltimore, Maryland. 

These experts collectively have knowledge of radon’s physical and chemical properties, toxicokinetics, 

key health end points, mechanisms of action, human and animal exposure, and quantification of risk to 

humans. All reviewers were selected in conformity with the conditions for peer review specified in 

Section 104(I)(13) of the Comprehensive Environmental Response, Compensation, and Liability Act, as 

amended. 

Scientists from the Agency for Toxic Substances and Disease Registry (ATSDR) have reviewed the peer 

reviewers' comments and determined which comments will be included in the profile. A listing of the 

peer reviewers' comments not incorporated in the profile, with a brief explanation of the rationale for their 

exclusion, exists as part of the administrative record for this compound. 

The citation of the peer review panel should not be understood to imply its approval of the profile's final 

content. The responsibility for the content of this profile lies with the ATSDR. 
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RADON	 xv 

CONTENTS 

DISCLAIMER .............................................................................................................................................. ii
 

UPDATE STATEMENT ............................................................................................................................. iii
 

FOREWORD ................................................................................................................................................ v
 

QUICK REFERENCE FOR HEALTH CARE PROVIDERS....................................................................vii
 

CONTRIBUTORS ....................................................................................................................................... xi
 

PEER REVIEW ......................................................................................................................................... xiii
 

CONTENTS ................................................................................................................................................ xv
 

LIST OF FIGURES ................................................................................................................................... xix
 

LIST OF TABLES ..................................................................................................................................... xxi
 

1. PUBLIC HEALTH STATEMENT.......................................................................................................... 1
 

1.1 WHAT IS RADON? ...................................................................................................................... 2
 

1.2 WHAT HAPPENS TO RADON WHEN IT ENTERS THE ENVIRONMENT? ......................... 3
 

1.3 HOW MIGHT I BE EXPOSED TO RADON AND RADON PROGENY? ................................. 3
 

1.4 HOW CAN RADON AND RADON PROGENY ENTER AND LEAVE MY BODY? .............. 4
 

1.5 HOW CAN RADON AND RADON PROGENY AFFECT MY HEALTH? ............................... 5
 

1.6 HOW CAN RADON AND RADON PROGENY AFFECT CHILDREN? .................................. 5
 

1.7 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO RADON AND RADON 

PROGENY? ................................................................................................................................... 6
 

1.8 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN EXPOSED TO 

RADON AND RADON PROGENY? ........................................................................................... 6
 

1.9 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH? ................................................................................................... 6
 

1.10 WHERE CAN I GET MORE INFORMATION? .......................................................................... 8
 

2. RELEVANCE TO PUBLIC HEALTH ................................................................................................... 9
 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO RADON IN THE UNITED 

STATES ......................................................................................................................................... 9
 

2.2 SUMMARY OF HEALTH EFFECTS ......................................................................................... 10
 

2.3 MINIMAL RISK LEVELS (MRLs) ............................................................................................ 12
 

3. HEALTH EFFECTS.............................................................................................................................. 15
 

3.1 INTRODUCTION........................................................................................................................ 15
 

3.2 DISCUSSION OF HEALTH EFFECTS OF RADON BY ROUTE OF EXPOSURE................ 18
 

3.2.1 Inhalation Exposure .............................................................................................................. 20
 

3.2.1.1 Death .................................................................................................................................. 31
 

3.2.1.2 Systemic Effects ................................................................................................................ 32
 

3.2.1.3 Immunological and Lymphoreticular Effects .................................................................... 34
 

3.2.1.4 Neurological Effects..........................................................................................................34
 

3.2.1.5 Reproductive Effects ......................................................................................................... 34
 

3.2.1.6 Developmental Effects ...................................................................................................... 35
 

3.2.1.7 Cancer................................................................................................................................ 35
 

3.2.2 Oral Exposure........................................................................................................................ 42
 

3.2.2.1 Death .................................................................................................................................. 42
 

3.2.2.2 Systemic Effects ................................................................................................................ 42
 

3.2.2.3 Immunological and Lymphoreticular Effects .................................................................... 42
 

3.2.2.4 Neurological Effects..........................................................................................................42
 

3.2.2.5 Reproductive Effects ......................................................................................................... 42
 

3.2.2.6 Developmental Effects ...................................................................................................... 42
 

 


 


 


 


 


 


 


 


 
 


 
 


 
 

 
 
 


 
 


 
 


 
 

 
 
 


 
 


 
 


 
 

 
 
 

 
 
 


 
 


 
 


 
 


 
 

 
 
 


 
 

 
 
 

 
 
 

 
 
 


 
 


 
 


 

 
 

 
 


 
 


 
 


 
 


 
 


 
 


 


 
 


 
 


 
 


 
 


 
 


 
 


 
 

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3.2.2.7 Cancer................................................................................................................................ 42
 

3.2.3 Dermal Exposure................................................................................................................... 43
 

3.2.3.1 Death .................................................................................................................................. 43
 

3.2.3.2 Systemic Effects ................................................................................................................ 43
 

3.2.3.3 Immunological and Lymphoreticular Effects .................................................................... 43
 

3.2.3.4 Neurological Effects..........................................................................................................43
 

3.2.3.5 Reproductive Effects ......................................................................................................... 43
 

3.2.3.6 Developmental Effects ...................................................................................................... 43
 

3.2.3.7 Cancer................................................................................................................................ 43
 

3.3 GENOTOXICITY ........................................................................................................................ 45
 

3.4 TOXICOKINETICS..................................................................................................................... 49
 

3.4.1 Absorption............................................................................................................................. 51
 

3.4.1.1 Inhalation Exposure ....................................................................................................... 51
 

3.4.1.2 Oral Exposure ................................................................................................................ 54
 

3.4.1.3 Dermal Exposure ........................................................................................................... 55
 

3.4.2 Distribution ........................................................................................................................... 56
 

3.4.2.1 Inhalation Exposure ....................................................................................................... 56
 

3.4.2.2 Oral Exposure ................................................................................................................ 57
 

3.4.2.3 Dermal Exposure ........................................................................................................... 58
 

3.4.3 Metabolism............................................................................................................................ 58
 

3.4.4 Elimination and Excretion ..................................................................................................... 58
 

3.4.4.1 Inhalation Exposure ....................................................................................................... 58
 

3.4.4.2 Oral Exposure ................................................................................................................ 59
 

3.4.4.3 Dermal Exposure ........................................................................................................... 60
 

3.4.4.4 Other Routes of Exposure.............................................................................................. 60
 

3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models ............. 60
 

3.5 MECHANISMS OF ACTION ..................................................................................................... 82
 

3.5.1 Pharmacokinetic Mechanisms ............................................................................................... 82
 

3.5.2 Mechanisms of Toxicity........................................................................................................ 84
 

3.5.3 Animal-to-Human Extrapolations ......................................................................................... 88
 

3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS............................. 88
 

3.7 CHILDREN’S SUSCEPTIBILITY .............................................................................................. 89
 

3.8 BIOMARKERS OF EXPOSURE AND EFFECT ....................................................................... 91
 

3.8.1 Biomarkers Used to Identify or Quantify Exposure to Radon and Radon Progeny .............. 92
 

3.8.2 Biomarkers Used to Characterize Effects Caused by Radon and Radon Progeny ................ 92
 

3.9 INTERACTIONS WITH OTHER CHEMICALS ....................................................................... 93
 

3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE .................................................. 96
 

3.11 METHODS FOR REDUCING TOXIC EFFECTS ...................................................................... 96
 

3.11.1 Reducing Peak Absorption Following Exposure ............................................................... 97
 

3.11.2 Reducing Body Burden ..................................................................................................... 97
 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects ............................................ 97
 

3.12 ADEQUACY OF THE DATABASE .......................................................................................... 98
 

3.12.1 Existing Information on Health Effects of Radon ............................................................. 98
 

3.12.2 Identification of Data Needs ............................................................................................ 100
 

3.12.3 Ongoing Studies .............................................................................................................. 105
 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION ............................................. 107
 

4.1 CHEMICAL IDENTITY............................................................................................................ 107
 

4.2 PHYSICAL, CHEMICAL, AND RADIOLOGICAL PROPERTIES ....................................... 107
 

 


 


 


 


 


 
 


 


 

 
 

 
 

 
 


 

 
 

 
 


 
 


 
 


 
 


 
 


 
 

 
 
 

 
 
 

 
 
 

 
 
 


 
 


 
 


 
 


 
 

 
 
 

 
 
 


 
 


 
 


 
 


 
 

 
 

 
 


 


 
 


 
 

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5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL.......................................................... 115
 

5.1 PRODUCTION .......................................................................................................................... 115
 

5.2 IMPORT/EXPORT .................................................................................................................... 117
 

5.3 USE ............................................................................................................................................ 117
 

5.4 DISPOSAL ................................................................................................................................. 118
 

6. POTENTIAL FOR HUMAN EXPOSURE ......................................................................................... 121
 

6.1 OVERVIEW ............................................................................................................................... 121
 

6.2 RELEASES TO THE ENVIRONMENT................................................................................... 124
 

6.2.1 Air ....................................................................................................................................... 124
 

6.2.2 Water................................................................................................................................... 126
 

6.2.3 Soil ...................................................................................................................................... 127
 

6.3 ENVIRONMENTAL FATE ...................................................................................................... 127
 

6.3.1 Transport and Partitioning................................................................................................... 127
 

6.3.2 Transformation and Degradation ........................................................................................ 130
 

6.3.2.1 Air ................................................................................................................................ 130
 

6.3.2.2 Water............................................................................................................................ 131
 

6.3.2.3 Sediment and Soil ........................................................................................................ 131
 

6.3.2.4 Other Media ................................................................................................................. 131
 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT .................................. 131
 

6.4.1 Air ....................................................................................................................................... 131
 

6.4.2 Water................................................................................................................................... 133
 

6.4.3 Sediment and Soil ............................................................................................................... 135
 

6.4.4 Other Environmental Media................................................................................................ 136
 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE ........................................ 137
 

6.6 EXPOSURES OF CHILDREN .................................................................................................. 141
 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES .............................................. 142
 

6.8 ADEQUACY OF THE DATABASE ........................................................................................ 143
 

6.8.1 Identification of Data Needs ............................................................................................... 143
 

6.8.2 Ongoing Studies .................................................................................................................. 146
 

7. ANALYTICAL METHODS ............................................................................................................... 147
 

7.1 BIOLOGICAL MATERIALS.................................................................................................... 147
 

7.2 ENVIRONMENTAL SAMPLES .............................................................................................. 149
 

7.3 ADEQUACY OF THE DATABASE ........................................................................................ 157
 

7.3.1 Identification of Data Needs ............................................................................................... 158
 

7.3.2 Ongoing Studies .................................................................................................................. 158
 

8. REGULATIONS, ADVISORIES, AND GUIDELINES ..................................................................... 159
 

9. REFERENCES .................................................................................................................................... 165
 

10. GLOSSARY ...................................................................................................................................... 205
 

APPENDICES 

A. ATSDR MINIMAL RISK LEVELS AND WORKSHEETS .............................................................A-1 

B. USER’S GUIDE.................................................................................................................................. B-1 

C. ACRONYMS, ABBREVIATIONS, AND SYMBOLS ...................................................................... C-1 

D. OVERVIEW OF BASIC RADIATION PHYSICS, CHEMISTRY, AND BIOLOGY ..................... D-1 

E. INDEX................................................................................................................................................. E-1 
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LIST OF FIGURES 

3-1. Cumulative Absolute Risk of Death from Lung Cancer by Age 75 Years Versus Long-Term 

Average Radon Concentration at Home for Continuing Smokers, Ex-Smokers, and Lifelong 

Nonsmokers in the United Kingdom .................................................................................................. 40
 

3-2. Conceptual Representation of a Physiologically Based Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance ...................................................................................................... 62
 

3-3. Compartment Model to Represent Particle Deposition and Time-Dependent Particle Transport 

in the Respiratory Tract ...................................................................................................................... 66
 

3-4. Reaction of Gases or Vapors at Various Levels of the Gas-Blood Interface ...................................... 68
 

3-5. The Human Respiratory Tract Model: Absorption into Blood .......................................................... 74
 

3-6. Simplified Version of the Human Respiratory Tract Model (HRTM) ............................................... 76
 

3-7. Schematic Diagram of the NAS (1999b) PBPK Model Developed to Describe the Fate of 

Radon within Systemic Tissues .......................................................................................................... 78
 

3-8. Khursheed (2000) PBPK Model for Inhalation and Ingestion of Radon Gas ..................................... 81
 

3-9. Conceptual Model of the Biology Leading From Alpha Irradiation of Cells by Radon and 

Radon Progeny to Tumor Development ............................................................................................. 86
 

3-10. Existing Information on Health Effects of Radon ............................................................................ 99
 

4-1. 238U Decay Series Showing Sources and Decay Products ................................................................ 112
 

4-2. 232Th Decay Series Showing Sources and Decay Products .............................................................. 113
 

4-3. 235U Decay Series Showing Sources and Decay Products ................................................................ 114
 
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RADON xxi 

LIST OF TABLES 

3-1. Selected Characteristics and Exposure Data for Individual Miner Cohort Studies Included in the 

Analysis of Pooled Data from the Individual Studies, and Lung Cancer Mortality Rates and 

Relative Risks by Cumulative WLM for Pooled Data ....................................................................... 24
 

3-2. Selected Results from Analysis of Pooled Data from 11 Mining Cohorts, Based on Deciles of 

Case Exposures That Were Each Under 100 WLM ........................................................................... 25
 

3-3. ORs for Lung Cancer from Combined Analysis of Two China Residential Case-Control Studies 

(Using a 5–30-Year Exposure Time Window).................................................................................. 27
 

3-4. Selected Characteristics of Study Subjects, Exposure Estimates, and ORs for Lung Cancer 

from Combined Analysis of Seven North American Residential Case-Control Studies (Using a 

5–30-Year Exposure Time Window) ................................................................................................. 29
 

3-5. Relative Risk and Excess Relative Risk of Lung Cancer by Radon Level in Homes 5–34 Years 

Previously, Estimated from the Pooled Data for 13 European Residential Case-Control Studies ..... 30
 

3-6. Genotoxicity of Radon and Radon Progeny In Vivo........................................................................... 46
 

3-7. Genotoxicity of Radon and Radon Progeny In Vitro.......................................................................... 47
 

3-8. Reference Respiratory Values for a General Caucasian Population at Different Levels of 

Activity............................................................................................................................................... 67
 

3-9. Reference Values of Parameters for the Compartment Model to Represent Time-Dependent 

Particle Transport from the Human Respiratory Tract....................................................................... 70
 

3-10. Parameters in the NAS (1999b) PBPK Model .................................................................................. 80
 

3-11. Parameters in Khursheed (2000) PBPK Model for Radon Gas ........................................................ 83
 

4-1. Chemical Identity of Radon .............................................................................................................. 108
 

4-2. Physical, Chemical, and Radiological Properties of Radon ............................................................. 109
 

4-3. Radioactive Properties of 222Rn and Its Short-lived Progeny ........................................................... 111
 

7-1. Analytical Methods for Determining Radon Progeny in Biological Samples .................................. 148
 

7-2. Analytical Methods for Determining Radon and Progeny in Environmental Samples .................... 154
 

8-1. Regulations, Advisories, and Guidelines Applicable to Radon ........................................................ 161
 
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RADON 1

1. PUBLIC HEALTH STATEMENT 

This public health statement tells you about radon and the effects of exposure to it. 

The Environmental Protection Agency (EPA) identifies the most serious hazardous waste sites in 

the nation. These sites are then placed on the National Priorities List (NPL) and are targeted for 

long-term federal clean-up activities. The presence of radon at any site could be a consequence 

of its natural occurrence in the environment; its production from substances in anthropogenic 

hazardous waste; or both. These sites may be sources of exposure and exposure to this substance 

may be harmful. 

When a substance is released from a large area, such as an industrial plant, or from a container, 

such as a drum or bottle, it enters the environment. This release does not always lead to 

exposure. You are exposed to a substance when you come in contact with it. You may be 

exposed by breathing, eating, or drinking the substance, or by skin contact. External exposure to 

radiation may occur from natural or man-made sources. Radon is a naturally-occurring 

radioactive gas that changes into other radioactive substances, called progeny. Since radon and 

its progeny are present together in rock, soil, water, air, and construction materials, you will be 

exposed to the low-level radiation they give off just by being near them. Naturally occurring 

sources of radiation include radon and other radioactive elements in air, water, soil, or building 

materials, as well as cosmic radiation from space. Man-made radioactive materials are found in 

consumer products, industrial equipment, nuclear medicine patients, and to a smaller extent from 

atomic bomb fallout, hospital waste, and nuclear reactors. 

The results of the 1992 EPA National Residential Radon Survey estimated that 1 in 15 homes 

had an elevated radon level (i.e., a level at or above the EPA action level of 4 picocuries per liter 

of air). At the time, an estimated 5.8 million homes had an elevated radon level. The source of 

radon in homes is from naturally occurring (geologic) sources. 

When you are exposed to radon many factors will determine whether you will be harmed. These 

factors include the dose (how much), the duration (how long), and how you come in contact with 
RADON 2

1. PUBLIC HEALTH STATEMENT 

it. You must also consider any other chemicals you are exposed to and your age, sex, diet, 

family traits, lifestyle, and state of health. 

1.1 WHAT IS RADON? 

Radioactive gas Radon (Rn) is a naturally occurring colorless, odorless, tasteless radioactive 

gas that occurs in differing atomic structure with the same atomic number 

but different atomic mass, called isotopes. 

As radon undergoes radioactive decay, it gives off radiation and becomes 

another radioactive element. This is repeated several times until it becomes 

stable lead. The elements that radon changes into are called radon 

daughters or radon progeny. The radiation given off is alpha particles, beta 

particles, and gamma rays. This radiation gives a radiation dose to people 

when they are exposed to radon. 

Radon is measured in terms of its activity (curies or becquerels). Both the 

curie (Ci) and the becquerel (Bq) tell us how much a radioactive material 

decays every second (1 Ci = 37 billion Bq = 37 billion decays per second). 

The radiation dose from radon and its progeny is measured in terms of the 

energy that they impart to tissue (in units called gray or rem for public 

exposure, or working levels for occupational exposure). 

Natural product 

of the 

environment 

Radon isotopes are formed naturally through the radioactive decay of 

uranium or thorium. 

Uranium and thorium (solids) are found in rocks, soil, air, and water. 

Uranium and thorium decay to other elements such as radium (a solid), 

which in turn decays into radon (a gas). 

Uranium and thorium have been present since the earth was formed and 

have very long half-lives (4.5 billion years for uranium and 14 billion years for 

thorium). The half-life is the time it takes for half of the atoms of a 

radionuclide (radioactive element) to undergo radioactive decay and change 

it into a different element, some of which are radioactive and some are 

stable. Because of the long half-lives of uranium, thorium, and radium, and 

since they constantly decay into radon, all of these elements will continue to 

exist indefinitely at about the same levels as they do now. 

Radon has no commercial uses other than as a radiation standard for 

calibrating radon monitoring equipment in support of environmental surveys 

of homes and other buildings. 
 

 

RADON 3 

1. PUBLIC HEALTH STATEMENT 

Exists in various 

forms called 

isotopes and 

decays to other 

radioactive 

isotopes 

The most common radon isotope is radon-222 (222Rn). 

An atom of 222Rn gives off an alpha particle (which is the size of a helium 

atom without electrons), transforming into an atom of polonium-218 (218Po), 

which later gives off an alpha particle of its own, transforming into an atom of 

radioactive lead (214Pb). The final step in the radioactive decay of radon 

progeny results in the formation of an atom of stable lead which is not 

radioactive. 

The half-life of 222Rn is 3.82 days. Some of the radon decay products have 

the following half-lives: 218Po is 3.05 minutes; 214Pb is 26.8 minutes; and 

210Pb is 22.2 years. 

More information about the properties of radon can be found in Chapters 4, 5, and 6. 

1.2 WHAT HAPPENS TO RADON WHEN IT ENTERS THE ENVIRONMENT? 

Moves to air, 

groundwater, 

and surface 

water 

Radon gas in rocks and soil can move to air, groundwater, and surface water. 

Decay products of 222Rn, such as 218Po and 214Pb, are solids that can attach 

to particles in the air and be transported this way in the atmosphere. They 

can be deposited on land or water by settling or by rain. 

Radon will undergo radioactive decay in the environment. 

For more information on radon in the environment, see Chapter 6 (Potential for Human 

Exposure). 

1.3 HOW MIGHT I BE EXPOSED TO RADON AND RADON PROGENY? 

Air Since radon progeny are often attached to dust, you are exposed to them 

primarily by breathing them in. They are present in nearly all air. Depending 

on the size of the particles, the radioactive particulates can deposit in your 

lungs and impart a radiation dose to the lung tissue. 

Background levels of radon in outdoor air are generally quite low 

(0.4 picocuries/L average activity of radon in outdoor air in the United 

States), but can vary based on time of day, location, and the underlying soil 

geology. Background levels also vary as a result of meteorological 

conditions, such as precipitation and temperature inversions. Temperature 

inversions occur when the air temperature increases with elevation above 

the ground. 

In indoor locations, such as homes, schools, or office buildings, levels of 

radon and radon progeny are generally higher than outdoor levels. House 

construction can affect radon levels; however, radon levels can be elevated 

in homes of all types: old homes, new homes, drafty homes, insulated 
RADON 4

1. PUBLIC HEALTH STATEMENT 

homes, homes with basements, and homes without basements. Local 

geology, construction materials, and how the home was built are among the 

factors that can affect radon levels in homes. 

Radon typically moves up through the ground to the air above and into the 

home through cracks and other holes in the foundation, in part due to 

convective flow. Your home traps radon inside, where it can build up. Any 

home may have elevated radon levels. The only way to know if you are 

exposed to elevated household radon levels is to have your home tested. 

Water You may be exposed to radon and radon progeny by coming into contact 

with surfacewater or groundwater that contains radon or by drinking water 

from wells that contain radon. 

Radon in water can become airborne. In general, domestic water from a 

well with a concentration of 10,000 pCi/L of radon is estimated to contribute 

about 1 pCi/L of radon to the indoor air. 

Further information on how you might be exposed to radon and radon progeny is given in 

Chapter 6. 

1.4 HOW CAN RADON AND RADON PROGENY ENTER AND LEAVE MY BODY? 

When they are 

inhaled or 

swallowed 

Radon and its radioactive progeny can enter your body when you breathe 

them in or swallow them. 

Most of the inhaled radon gas is breathed out again. 

Some of the radon progeny, both unattached and attached to dust, may 

remain in your lungs and undergo radioactive decay. The radiation 

released during this process passes into lung tissue and can cause lung 

damage. 

Some of the radon that you swallow with drinking water passes through the 

walls of your stomach and intestine. 

After radon enters your blood stream most of the radon quickly moves to 

the lungs where you breathe most of it out. 

Radon that is not breathed out goes to other organs and fat tissue where it 

may remain and undergo decay. 

Further information on how radon and radon progeny enter and leave the body is given in 

Chapter 3. 
RADON 5

1. PUBLIC HEALTH STATEMENT 

1.5 HOW CAN RADON AND RADON PROGENY AFFECT MY HEALTH? 

This section looks at studies concerning potential health effects in animal and human studies. 

Lung cancer Lung cancer is essentially the only health effect associated with exposure 

to radon and radon progeny. Many scientists believe that long-term 

exposure to elevated levels of radon and radon progeny in air increases 

your chance of getting lung cancer. 

Smoking cigarettes greatly increases your chance of developing lung 

cancer if you are exposed to radon and radon progeny at the same levels 

as people who do not smoke. 

The greater your exposure to radon, especially if you smoke cigarettes, the 

greater your chance of developing lung cancer. 

More information on the health effects of radon and radon progeny is presented in Chapters 2 

and 3. 

1.6 HOW CAN RADON AND RADON PROGENY AFFECT CHILDREN? 

This section discusses potential health effects in humans from exposures during the period from 

conception to maturity at 18 years of age. 

Differences 

between children 

and adults 

Smaller lungs and faster breathing rates in children may result in higher 

estimated radiation doses to the lungs of children relative to adults. 

However, limited information from children employed as miners in China do 

not provide evidence of increased susceptibility to the effects of exposure to 

radon and radon progeny. 
RADON 6

1. PUBLIC HEALTH STATEMENT 

1.7 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO RADON AND RADON 

PROGENY? 

Reduce indoor 

exposure levels 

Indoor radon levels can be reduced by the installation of a sub-slab suction 

(depressurization) system, also known as an active soil depressurization 

system (ASD). A radon vent fan connected to the suction pipe(s) draws the 

radon gas from below the house and releases it into the outdoor air, while 

simultaneously creating a negative pressure (vacuum) beneath the slab. 

Sealing of openings to the soil can improve the operation and efficiency of the 

ASD system. Certified radon mitigation experts can be located by contacting 

your state health or environmental program. If the ASD does not reduce 

levels sufficiently, consider reversing the fan direction to pressurize the 

subslab, and then compare the results and use the more effective method. 

Measures to prevent high radon levels in new home construction are 

expected to be effective at reducing radon-related lung cancer deaths, but 

remediating old homes with high radon levels may be less effective. 

If you smoke in your home, stopping will reduce the radiation dose from radon 

since smoke particles help increase the radiation dose. 

1.8 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN EXPOSED TO 

RADON AND RADON PROGENY? 

Radon progeny in 

urine and in lung 

and bone tissues 

Radon in human tissues is not detectable by routine medical testing. 

Some radon progeny can be detected in urine and in lung and bone tissue. 

Tests for these products are not generally available to the public and are of 

limited value since they cannot be used to accurately determine how much 

radon you were exposed to, nor can they be used to predict whether you 

will develop harmful health effects. 

Further information on how radon and radon progeny can be measured in exposed humans is 

presented in Chapters 3 and 7. 

1.9 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH? 

The federal government develops regulations and recommendations to protect public health. 

Regulations can be enforced by law. Federal agencies that develop regulations for toxic 

substances include the Environmental Protection Agency (EPA), the Occupational Safety and 

Health Administration (OSHA), the Food and Drug Administration (FDA), and the U.S. Nuclear 

Regulatory Commission (USNRC). 
RADON 7

1. PUBLIC HEALTH STATEMENT 

Recommendations provide valuable guidelines to protect public health but cannot be enforced by 

law. Federal organizations that develop recommendations for toxic substances include the 

Agency for Toxic Substances and Disease Registry (ATSDR), the National Institute for 

Occupational Safety and Health (NIOSH), and the FDA. 

Regulations and recommendations can be expressed as “not-to-exceed” levels, that is, levels of a 

toxic substance in air, water, soil, or food that do not exceed a critical value that is usually based 

on levels that affect animals; they are then adjusted to levels that will help protect humans. 

Sometimes these not-to-exceed levels differ among federal organizations because they used 

different exposure times (an 8-hour workday, a 24-hour day, or a work-year), different animal 

studies, or other factors. 

Recommendations and regulations are also updated periodically as more information becomes 

available. For the most current information, check with the federal agency or organization that 

provides it. 

Air EPA recommends actions that can be taken to reduce radon levels if 

measured indoor levels of radon are 4 or more pCi per liter (pCi/L) of air. 

This is the same as 148 Becquerels per cubic meter [Bq/m3

] of air in the 

international system. EPA also notes that radon levels less than 4 pCi/L still 

pose a health risk and can be reduced in many cases, and that smoking 

increases the risk from radon. The EPA recommends using a certified 

radon mitigation specialist if indoor radon levels need to be reduced to 

ensure that appropriate methods are used to reduce radon levels. 

The Mine Safety and Health Administration (MSHA) has adopted an 

exposure limit of 4 Working Level Months (WLM) per year for people who 

work in underground mines (WLMs basically combine the concentration of 

radon progeny in mine air with the portion that is attached to dust in the air 

and the length of exposure inside the mine). 

The Nuclear Regulatory Commission published a table of allowable 

exposure to radon by workers and allowable releases of radon to the 

environment by its licensees. 

Water EPA does not have a drinking water limit for radon. 
 

 

 

 

 

RADON 8 

1. PUBLIC HEALTH STATEMENT 

EPA maintains a website (http://www.epa.gov/radon) that provides extensive information on 

radon for the general public. Additional information on governmental regulations regarding 

radon and radon progeny can be found in Chapter 8. 

1.10 WHERE CAN I GET MORE INFORMATION? 

If you have any more questions or concerns, please contact your community or state health or 

environmental quality department, or contact ATSDR at the address and phone number below. 

ATSDR can also tell you the location of occupational and environmental health clinics. These 

clinics specialize in recognizing, evaluating, and treating illnesses that result from exposure to 

hazardous substances. 

Toxicological profiles are also available on-line at www.atsdr.cdc.gov and on CD-ROM. You 

may request a copy of the ATSDR ToxProfilesTM CD-ROM by calling the toll-free information 

and technical assistance number at 1-800-CDCINFO (1-800-232-4636), by e-mail at 

cdcinfo@cdc.gov, or by writing to: 

Agency for Toxic Substances and Disease Registry

 Division of Toxicology and Human Health Sciences (proposed) 

1600 Clifton Road NE 

Mailstop F-62 

Atlanta, GA 30333 

Fax: 1-770-488-4178 

Organizations for-profit may request copies of final Toxicological Profiles from the following: 

National Technical Information Service (NTIS) 

5285 Port Royal Road 

Springfield, VA 22161 

Phone: 1-800-553-6847 or 1-703-605-6000 

W eb site: http://www.ntis.gov/ 
 

 

 

 

 


 

 

 

 

 

 

 

 

RADON 9 

2. RELEVANCE TO PUBLIC HEALTH
 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO RADON IN THE UNITED 

STATES 

Radon is a noble gas formed from the natural radioactive decay of uranium (U) and thorium (Th), natural 

components of the earth’s crust, which decay to radium (Ra) and then to radon (Rn). Decay chains 

include 226Ra and 222Rn for 238U; 223Ra and 219Rn for 235U; and 224Ra and 220Rn for 232Th. As radium 

decays, radon is formed and released into pores in the soil. Fissures and pores in the substrate allow the 

radon to migrate to the surface, where it can be released to the air. Radon may also be released into 

surface and groundwater from the surrounding soil. Though radon is chemically inert, it decays by 

normal radioactive processes to other radon progeny. The alpha emitting progeny of radon (primarily 

polonium isotopes 218Po and 214Po) are the ones that can damage the lungs and potentially cause cancer. 

Radon may be useful in helping to detect seismic activity, for radiation therapy (as a decay product of 

223Ra), as a tracer for leak detection, for flow rate measurements, in radiography, and is used in some 

chemical laboratory research. It can also be used in the exploration of petroleum or uranium, as a tracer 

in the identification of NAPL (non-aqueous phase liquid) contamination of the subsurface, in atmospheric 

transport studies, and as a radiation standard for calibrating radon monitoring equipment in support of 

environmental surveys of homes and other buildings. 

The primary source of radon is its precursors in soil where it is formed and released. On a global scale, it 

is estimated that 2,400 million curies of radon are released from soil annually. Groundwater provides a 

secondary source of radon, with an estimated 500 million curies released globally per year. Additional 

sources of radon include surface water, metal mines (uranium, phosphorus, tin, silver, gold, etc.), coal 

residues and combustion products, natural gas, and building materials. Global radon releases from 

oceans, phosphate residues, uranium mill tailings, coal residues, natural gas emissions, coal combustion, 

and human exhalation are estimated at 34, 3, 2, 0.02, 0.01, 0.009, and 0.00001 millions of curies per year, 

respectively. Geology, soil moisture conditions, and meteorological conditions can affect the amount of 

radon released from soil. 

The primary pathway for human exposure to radon is inhalation, both indoors and outdoors. Ambient 

outdoor levels are the result of radon emanating from soil or released from coal, oil, or gas power plants, 

which can vary temporally and spatially. Outdoor radon levels are typically much lower than indoor 

radon levels. Soil gas intrusion into buildings accounts for the majority of indoor radon. However, 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 10 

2. RELEVANCE TO PUBLIC HEALTH 

indoor radon also can originate from water used for domestic purposes, outdoor air, and building 

materials. 

Exposure to high concentrations can occur in any location with geologic radon sources. Relatively highlevel occupational exposure can occur through employment at underground mines (uranium, phosphorus, 

tin, silver, gold, hard rock, and vanadium), sites contaminated with radon precursors (radium, uranium, or 

thorium), natural caverns, phosphate fertilizer plants, oil refineries, utility and subway tunnels, excavators, 

power plants, natural gas and oil piping facilities, “health” mines and spas, fish hatcheries, and, 

historically, hospitals that used radium needles for therapy. 

2.2 SUMMARY OF HEALTH EFFECTS 

The most compelling evidence of radon-induced health effects in humans derives from numerous studies 

of underground miners, particularly uranium miners exposed in the middle part of the twentieth century in 

the United States and several European countries. These cohort mortality studies typically involved longterm estimates of exposure to high levels of radon based on available measurements in the working 

environment and contained inherent uncertainty due to confounding factors such as smoking status and 

coexposure to known or suspected carcinogens (diesel exhaust, arsenic, and silica dust). Nevertheless, the 

results consistently demonstrate increased risk of lung cancer with increasing exposure to radon in the 

working environment. The mining cohorts have been followed for several decades or more. Continued 

follow-up and refined assessments of the most widely-studied mining cohorts have resulted in improved 

exposure estimates (except for silica dust, which was not considered) and more complete categorization 

of individuals according to cause of death, mining history, and smoking status. Assessments did not 

account for actual confounding due to exposure to silica dust (which has since been identified as a known 

human carcinogen), nor did they necessarily include adjustments for potential confounding exposures to 

arsenic and diesel exhaust, although considerations for arsenic were made in several studies. One indepth analysis included assessment of results pooled from 11 of the most widely-studied mining cohorts 

using the most recent and comprehensive follow-up results available at the time for each individual 

cohort. The results provide evidence for increasing risk of lung cancer mortality with increasing 

cumulative exposure to radon and its progeny, and the risk is significantly increased when there is 

coexposure to cigarette smoke, arsenic, or silica dust. 

Reported associations between radon and lung cancer in the mining cohorts raised concern regarding 

the potential health effects of radon in homes, particularly at levels lower than those experienced in 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 11 

2. RELEVANCE TO PUBLIC HEALTH 

mining cohorts. Numerous residential case-control studies of lung cancer have been performed in the 

United States and in many other countries, including Canada, China, Finland, Germany, Sweden, and 

the United Kingdom. Some of these studies reported positive or weakly positive associations between 

lung cancer risk and residential indoor radon concentrations, whereas significant associations were not 

observed in others. One recent residential case-control study reported a borderline statistically significant 

negative association between lung cancer risk and exposure to radon at levels in the range of 25– 

150 Bq/m3

 (1.4–4.1 pCi/L), which are near or below the 4.0 pCi/L EPA action limit. Numbers of cases 

and controls in the individual residential case-control studies limited the statistical power to identify a 

significant association between radon exposure and an adverse health outcome such as lung cancer. In 

order to increase the statistical power, investigators involved in most of the studies pooled the results in 

three separate assessments that included: (1) a combined analysis of 2 China case-control studies, (2) a 

combined analysis of 7 North American case-control studies, and (3) a combined analysis of 13 European 

case-control studies. In addition, an overall assessment of the China, North American, and European 

analyses was conducted by the United Kingdom. Independent results of the pooled analyses provide 

convincing evidence of an association between residential radon and lung cancer risk in cigarette smokers 

and recent ex-smokers as demonstrated by increased lung cancer risk with increasing cumulative 

exposure. The risk to nonsmokers was found to be 25-fold lower. Thus, the risk of radon-induced lung 

cancer decreases more by reducing or stopping smoking than by reducing residential radon concentration, 

and both can be used in conjunction for further risk reduction. Collectively, these studies show 

appreciable health hazard from residential radon, particularly for smokers and recent ex-smokers. An 

overall pooling of the China, North American, and European case-control studies is in progress. 

Associations between radon and health effects other than lung cancer have been made by some 

investigators. Excess mortality from noncancer diseases reported in some of the mining cohorts include 

all noncancer respiratory diseases, pneumoconioses, emphysema, interstitial pneumonitis, other 

(unspecified) chronic obstructive respiratory diseases, and tuberculosis. However, confounding factors 

such as exposure to crystalline silica dust and other respiratory toxicants, smoking history, and work 

experience were likely major contributors to mortalities from noncancer respiratory diseases. Alterations 

in respiratory function in U.S. uranium miners have been reported. Analyses among U.S. uranium miners 

indicated a loss of pulmonary function associated with increasing cumulative exposure to radon and radon 

progeny and with the duration of underground mining. Evaluations of these respiratory end points did not 

include adjustment for effects other mine pollutants, such as ore crystalline silica and diesel engine 

exhaust particles, which were not recognized as human carcinogens at the time the studies were 

conducted. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 12 

2. RELEVANCE TO PUBLIC HEALTH 

Some information is available regarding lung cancer in animals exposed to radon and its progeny at 

concentrations considered relevant to human health. Significantly increased incidences of lung tumors 

were reported in rats repeatedly exposed to radon and its progeny at cumulative exposures as low as 20– 

50 Working Level Months (WLM). These results are consistent with the demonstrated associations 

between lung cancer risk and exposure to radon and radon progeny in occupationally-exposed miners and 

residentially-exposed individuals. 

2.3 MINIMAL RISK LEVELS (MRLs) 

Inhalation MRLs 

No acute-, intermediate-, or chronic-duration inhalation MRLs were derived for radon due to a lack of 

suitable human or animal data regarding health effects following inhalation exposure to radon and its 

progeny. The strongest evidence for radon exposure-response and radiation dose-response relationships 

in humans is for lung cancer; however, cancer is not an appropriate end point for MRL derivation. 

Nonneoplastic lesions have been reported in animals exposed to radon and its progeny for acute, 

intermediate, and chronic exposure durations; however, these effects were consistently observed only at 

lethal or near lethal exposure levels, which were several orders of magnitude higher than those associated 

with lung cancer in chronically-exposed humans. 

Oral MRLs 

No acute-, intermediate-, or chronic-duration oral MRLs were derived for radon due to a lack of suitable 

human or animal data regarding health effects following oral exposure to radon and its progeny. 

Available human data are limited. In an ecological study, radon levels were measured in 2,000 public and 

private wells in 14 counties in Maine (Hess et al. 1983). The county averages were compared to cancer 

rate by county to determine any degree of correlation. Significant correlation was reported for all lung 

cancer and all cancers combined, when both sexes were combined, and for lung tumors in females. 

Confounding factors (e.g., smoking) were not considered in this analysis. In addition, exposure to radon 

in these water supplies could have been by the inhalation route as well as the oral route. No significant 

associations were observed between cases of bladder or kidney cancer, relative to controls, where mean 

concentrations of radon in the drinking water were 170, 140, and 130 Bq/L in bladder cancer cases, 

kidney cancer cases, and controls, respectively (Kurttio et al. 2006). The U.K. Health Protection Agency 
 

 

 

 

 

 

RADON 13 

2. RELEVANCE TO PUBLIC HEALTH 

(HPA 2009) reviewed available studies that assessed possible associations between radon and cancer end 

points and concluded that there is insufficient evidence to suggest that radon is associated with increased 

risk of cancer at sites other than the lung. 

 

 

RADON 14
 

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RADON 15 

3. HEALTH EFFECTS 

3.1 INTRODUCTION 

The primary purpose of this chapter is to provide public health officials, physicians, toxicologists, and 

other interested individuals and groups with an overall perspective on the toxicology of radon. It contains 

descriptions and evaluations of toxicological studies and epidemiological investigations and provides 

conclusions, where possible, on the relevance of toxicity and toxicokinetic data to public health. 

A glossary and list of acronyms, abbreviations, and symbols can be found at the end of this profile. 

Radon (Rn) is an inert noble gas that does not interact chemically with other elements. All of the isotopes 

of radon are radioactive and evaluation of the adverse health effects due to exposure to radon requires 

additional consideration of the effects of radiation. Radioactive elements are those that undergo 

spontaneous transformation (decay) in which energy is released (emitted) either in the form of particles, 

such as alpha and beta particles, or photons, such as gamma or x-rays. This disintegration, or decay, 

results in the formation of new elements, some of which may themselves be radioactive, in which case, 

they will also decay. The process continues until a stable (nonradioactive) state is reached. The isotopes 

of radon encountered in nature (219Rn, 220Rn, and 222Rn) are part of long decay chains starting with 

isotopes of uranium (U) or thorium (Th), more precisely 235U, 232Th, and 238U, respectively, and ending 

with stable lead (Pb). The intermediates between radon and stable lead are termed radon daughters or 

radon progeny (see Chapter 4, Figures 4-1, 4-2, and 4-3 for radioactive decay schemes of 235U, 232Th, and 

238U, respectively). The isotope 222Rn is a direct decay product of radium-226 (226Ra), which is part of the 

decay series that begins with uranium-238 (238U). Thorium-230 and -234 (230Th and 234Th) are also part 

of this decay series. Other isotopes of radon, such as 219Rn and 220Rn, are formed in other radioactive 

decay series. However, 219Rn usually is not considered in the evaluation of radon-induced health effects 

because it is not abundant in the environment (219Rn is part of the decay chain of 235U, a relatively rare 

isotope) and has an extremely short half-life (4 seconds). The isotope 220Rn has usually not been 

considered when evaluating radon-related health effects, although many recent assessments have 

attempted to include measurements of 220Rn as well as 222Rn. While the average rate of production of 

220Rn is about the same as 222Rn, the amount of 220Rn entering the environment is much less than that of 

222Rn because 220Rn is a noble gas with a short half-life (56 seconds). As a noble gas, it diffuses slowly 

from the ground but decays so rapidly into polonium (a particle that bonds with the soil) that most radon 

does not reach the atmosphere. The soil characteristics that enhance or retard radon migration from the 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 16 

3. HEALTH EFFECTS 

soil indirectly affect air concentrations of radon and radon progeny. All discussions of radon in the text 

refer to 222Rn unless otherwise indicated. 

The decay rate or activity of radioactive elements has traditionally been specified in curies (Ci). The 

activity defines the number of radioactive transformations (disintegrations) of a radionuclide over unit 

time. The curie is the amount of radioactive material in which 37 billion disintegrations (decay events) 

occur each second (3.7x1010 transformations per second). In discussing radon, a smaller unit, the 

picocurie (pCi), is used, where 1 pCi=1x10-12 Ci. In international usage, the S.I. unit (the International 

System of Units) for activity is the becquerel (Bq), which is the amount of material in which one atom 

disintegrates each second (1 Bq is approximately 27 pCi). The activity concentration of radon or any 

radionuclide in air is typically expressed in units of pCi/L or Bq/m3 of air. One pCi/L is equivalent to 

37 Bq/m3

. The activity concentration is typically a description of the concentration of radioactive 

material in air or water. The product of concentration and exposure time equals exposure; models are 

used to estimate a radiation dose to tissue from exposure. Since the isotopes continue to decay for some 

time, and some excretion occurs, the term dose refers specifically to the amount of radiant energy 

absorbed per mass in a particular tissue or organ and is expressed in rad (or gray). 

As radon and its progeny decay, they cumulatively emit alpha and beta particles as well as gamma- and 

x-rays. The health hazard from radon does not come primarily from radon itself, but rather from its 

radioactive progeny (see Chapter 4 for more information on the chemical and physical properties of 

radon). When an atom of radium transforms to radon, the alpha particle it emits slows down by the 

attraction of nearby electrons until it captures two electrons and becomes a stable atom of helium (He). 

The transformed radon and subsequent decay product atoms are charged and tend to attach to aerosol 

particles. Radon progeny are similarly charged, readily aggregate, form clusters, and attach to dust 

particles in air. The main health problems arise when primarily those radon progeny that are attached to 

dust particles (termed the attached fraction) are inhaled, deposit in the airway (particularly the 

tracheobronchial tree), and irradiate nearby cells repetitively with alpha particles as each atom transforms 

through the decay chain. These alpha particles can deliver a large localized radiation dose. The attached 

fraction is much higher in homes with smokers relative to those with nonsmokers, and in dusty mines 

relative to those that are well ventilated. Exposures to radon gas are accompanied by exposure to radon 

progeny, although the exact mix of radon and progeny are determined by several physical-chemical and 

environmental factors. In this toxicological profile, unless indicated otherwise, exposure to radon refers 

to exposure to the mixture of radon and progeny. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 17 

3. HEALTH EFFECTS 

Because it is not feasible to measure the activities of individual radon progeny in the environment and 

while they decay inside the body, a unit termed the “Working Level (WL)” is used for the purpose of 

quantifying the cumulative radiation dose from inhaled radon progeny, which may not be in secular 

equilibrium. The WL unit is a measure of the amount of alpha radiation emitted from the short-lived 

progeny of radon. As applied to exposures to 222Rn, this encompasses the decay series, 222Rn(α)→

218Po(α)→ 214Pb→ 214Bi→214Po(α) →210Pb, and represents any combination of the short-lived progeny of 

radon. Working Level (WL) means the concentration of short-lived radon progeny in 1 L of air that will 

release 1.3x105 million electron volts (MeV) of alpha energy during decay. One WL is equivalent to the 

potential alpha energy of 2.08x10-5 joules in 1 cubic meter of air (J/m3

). 

To convert between units of 222Rn concentration (pCi/m3

 or Bq/m3) and the potential alpha energy that 

can be released by its progeny as they fully decay (WL or J/m3

), the equilibrium between radon gas and 

its progeny at the time of exposure must be known or assumed (see Chapter 10 for conversion formula). 

When radon is in secular equilibrium with its progeny (i.e., when each of the short-lived radon progeny is 

present at the same activity concentration in air as 222Rn), each pCi of radon in air will give rise to (almost 

precisely) 0.01WL (EPA 2003). By definition, 1 WL is equal to 100 pCi of radon gas. However, when 

removal processes other than radioactive decay are operative, such as with room air ventilation or air 

filtration, the concentration of short-lived progeny will be less than the equilibrium amount. In such 

cases, an equilibrium factor (F) is applied. The National Research Council Committee on Health Risks of 

Exposure to Radon (BEIR VI) assumes 40% equilibrium (F=0.4) between radon and radon progeny in the 

home (NAS 1999a), in which case, 1 pCi/L (37 Bq/m3

) of 222Rn in the air is approximately equivalent to 

0.004 WL. 

The unit of measurement used to describe cumulative human exposure to radon progeny in mines is the 

Working Level Month (WLM). It is the product of the average concentration in WL and the exposure 

time in months. One WLM is defined as exposure at a concentration of 1 WL for a period of 1 working 

month (WM). A working month is assumed to be 170 hours. The S.I. unit for WLM is J-hour/m3

; 

1 WLM=3.6x10-3 J-hours/m3

. 

Measurements in WLM can be made using special equipment that measures the total alpha emission of 

short-lived radon progeny. However, measurements in homes are typically made for radon gas and are 

expressed in Bq/m3 or pCi/L. To convert from residential exposures expressed in pCi/L, it is considered 

that 70% of a person’s time is spent indoors and that 1 pCi/L of radon in the indoor air is equivalent to 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 18 

3. HEALTH EFFECTS 

0.004 WL of radon progeny (EPA 2003; NAS 1999a). These conditions result in the following 

relationship: 

1 pCi/L x 0.004 WL/pCi/L x 0.7 x (8,760 hours/WL-year ÷ 170 hours/WL-M) = 0.144 WLM/year 

Because 1 pCi/L is equivalent to 37 Bq/m3

, a residential exposure scenario using equivalent assumptions 

to those described above results in the same cumulative exposure to radon progeny (0.144 WLM/year). 

As discussed in detail in Section 3.2.1 (Inhalation Exposure), lung cancer is the toxicity concern 

following long-term exposure to radon and radon progeny. The high-energy alpha emissions from radon 

progeny, deposited predominantly in the tracheobronchial tree, and to a lesser extent in the lung, are the 

major source of toxicity concern. As shown in Figure 4-1, the radiological half-life for radon (222Rn) is 

3.8 days. The radioactive decay of radon to 218Po (radiological half-life=3.05 minutes) is accompanied by 

the release of high-energy (5.5 MeV) alpha particles; decay of 218Po to lead-214 (214Pb; radiological halflife=26.8 minutes) also releases high-energy (6.0 MeV) alpha particles. Subsequent radioactive decay to 

bismuth-214 (214Bi; radiological half-life=19.7 minutes) and 214Po involve release of beta and gamma 

radiation, which are of sufficiently low energy and long range as to be considered of little relative toxicity 

concern to nearby cells. The decay of 214Po via release of high-energy (7.69 MeV) alpha particles occurs 

so rapidly (radiological half-life=1.6x10-4 seconds) that, in radiation dose modeling, these alpha emissions 

are generally attributed to 214Bi decay (i.e., the rate of decay of 214Bi is essentially equal to the rate of 

formation of 210Pb due to the essentially instantaneous decay of 214Po from 214Bi). The subsequentlyformed radioactive radon progeny (210Pb, 210Bi, and 210Po in respective order of decay) are not considered 

to make significant contributions to respiratory tract toxicity (relative to the short-lived progeny). This is, 

in large part, because the radiological half-life associated with the decay of 210Pb is 22.2 years, which is 

sufficiently long that biological clearance mechanisms limit the radiation dose attributed to it and the 

other progeny. Therefore, the radon progeny of primary toxicity concern are 218Po and 214Po (due to the 

rapid decay of these alpha emitters, especially when part of the attached fraction). 

3.2 DISCUSSION OF HEALTH EFFECTS OF RADON BY ROUTE OF EXPOSURE 

To help public health professionals and others address the needs of persons living or working near 

hazardous waste sites, the information in this section is organized first by route of exposure (inhalation, 

oral, and dermal) and then by health effect (death, systemic, immunological, neurological, reproductive, 
 

 

	 

 

	 

	 

	 

	 

RADON	 19 

3. HEALTH EFFECTS 

developmental, genotoxic, and carcinogenic effects). These data are discussed in terms of three exposure 

periods: acute (14 days or less), intermediate (15–364 days), and chronic (365 days or more). 

ATSDR Toxicological Profiles typically include tables and figures for each route and duration in which 

levels of significant effects (LSEs) are presented. Points in the figures show no-observed-adverse-effect 

levels (NOAELs) or lowest-observed-adverse-effect levels (LOAELs) and reflect the actual doses (levels 

of exposure) used in each study for which adequate information is available regarding exposure level and 

a particular effect. LOAELs are classified into "less serious" or "serious" effects. "Serious" effects are 

those that evoke failure in a biological system and can lead to morbidity or mortality (e.g., acute 

respiratory distress or death). "Less serious" effects are those that are not expected to cause significant 

dysfunction or death, or those whose significance to the organism is not entirely clear. 

The December 1990 ATSDR Toxicological Profile for Radon included an LSE table and figure for 

exposure via the inhalation route in which levels of significant exposure were presented for noncancer 

effects in radon-exposed animals and cancer effect levels (CELs) were presented for lung cancer in 

humans exposed in the workplace, with the exception of one study of residential exposure. However, the 

LSE table and figure in the 1990 version of the Toxicological Profile for Radon were not retained in this 

update Toxicological Profile for Radon for the following reasons: 

	 LSEs for noncancer end points in the animal studies occurred at exposure levels that were several 

orders of magnitude higher than exposure levels expected to be of toxicological consequence in 

humans and are thus not reliable indicators of expected LSEs for noncancer end points in humans. 

	 Most occupational and residential studies of cancer end points (mainly lung cancer) include 

uncertain estimations of historical exposure levels for radon and radon progeny, and occupational 

studies are limited by confounding exposure to other substances including known human 

carcinogens. 

	 Assessment of individual epidemiological studies leads to uncertainty regarding human health 

effects associated with exposure to radon and radon progeny because individual studies may 

provide conflicting results. 

	 Recent emphasis has focused on pooled results from multiple human studies to provide more 

comprehensive evaluation that increases statistical power and decreases uncertainty, and it is not 

appropriate to assign LSEs from pooled analyses of individual epidemiological studies. 

Presentation of epidemiological data for radon and radon progeny in this updated Toxicological Profile 

for Radon is focused on results of pooled data from individual studies of occupationally-exposed cohorts 
 

 

RADON 20 

3. HEALTH EFFECTS 

and pooled data from individual studies that assessed residential exposure. Refer to the introductory 

statement of Section 3.2.1 for additional information regarding presentation of epidemiological data for 

radon and radon progeny. 

A User's Guide has been provided at the end of this profile (see Appendix B). 

3.2.1 Inhalation Exposure 

Epidemiological studies designed to assess human health risks from exposure to radon mainly consist of: 

(1) cohort mortality studies of underground miners that investigated possible associations between lung 

cancer and individual exposure to radon or radon progeny, (2) residential case-control studies that 

investigated possible associations between lung cancer cases and residential radon levels using estimates 

of individual exposure for lung cancer cases as well as controls, and (3) ecological studies that 

investigated possible associations between rates of selected diseases within a geographic population and 

some measure of average radon levels within the same defined geographic region. It should be noted that 

there is no known threshold dose for exposure to alpha radiation from sources including radon and radon 

progeny, and there is evidence of an inverse exposure rate response at low dose rates (i.e., for a given 

total exposure, the effect might be greater if delivered at a lower rate over a longer time period). The 

response relative to increased radon progeny exposure was 25 times larger for nonsmokers (HPA 2009) 

and tended to decrease with time since the exposure ended, attained age since exposure ended, and 

exposure duration or exposure rate effect. This apparent inverse dose rate effect may not be real since it 

was predicated on effects observed for the most highly exposed individuals (early miners in highly dusty 

environments) for which radon progeny were not measured and equilibrium factors had to be assumed, 

making dose assignments more uncertain (Lubin et al. 1995b). Also, the portion of the estimated radon 

cancer risk that is due to silica dust is yet to be evaluated in mining studies before 2000 since crystalline 

silica was not recognized by the International Agency for Research on Cancer (IARC) as a known human 

carcinogen until 1997 (IARC 1997). Studies since then have found a high correlation between radon and 

silica regarding lung cancer and concluded that exposure to quartz can be an important confounder 

(Bergdahl et al. 2010). 

Compelling evidence of radon-induced health effects in humans derives from numerous studies of 

underground miners, particularly uranium miners exposed beginning in the middle part of the twentieth 

century in the United States and several European countries. Although these cohort mortality studies 

typically involved rather crude estimates of exposure to high levels of radon in the working environment 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 21 

3. HEALTH EFFECTS 

and inherent uncertainty due to confounding factors such as smoking status and coexposure to known or 

suspected human carcinogens (diesel exhaust and arsenic), the results nevertheless consistently 

demonstrate increased risk of lung cancer with increasing exposure to radon in the working environment. 

These results are consistent across the various individual studies of mining cohorts and with analyses of 

pooled data from multiple cohorts. However, the miner studies were completed prior to crystalline silica 

and diesel exhaust being designated as known and suspected human carcinogens, respectively. The 

highest exposure groups in those studies tended to receive most of their dose before adequate ventilation 

was established to reduce mine air dust. An assessment of a cohort of iron ore miners with exposure 

information for radon, diesel exhaust, and silica found excess lung cancers (relative risk [RR] 5.65; 95% 

confidence interval [CI] 3.15–10.14) in a group of workers at the Malmberget mine with radon exposure 

>80 mBq-year/m3 (Bergdahl et al. 2010). After accounting for silica exposure, the RR was only 

3.90 (95% CI 1.21–12.55). The study authors concluded that accounting for silica exposure in 

epidemiological studies involving exposure to both radon and silica is important to prevent 

overestimating the cancer risk from radon. This high correlation between radon, inorganic arsenic, and 

silica was also reported for a cohort of German uranium miners (Taeger et al. 2008, 2009). 

Reported associations between radon and lung cancer in the mining cohorts raised concern regarding the 

potential health effects of radon in homes, where levels are usually lower than those experienced in 

mining cohorts and do not include confounding by arsenic and silica dust. Numerous residential casecontrol studies of lung cancer have been performed in the United States and in many other countries, 

including Canada, China, Finland, Germany, Sweden, and the United Kingdom. Some of these studies 

reported positive or weakly positive associations between lung cancer risk and residential radon 

concentrations, and others suggested that radon reduced the cancer risk, whereas no consistent 

associations were observed in others. None of the residential case-control studies available for the 

pooling reported a statistically significant negative association (i.e., decreasing cancer risk in association 

with increasing radon exposure). Limitations of these studies include: (1) uncertainty in estimating longterm radon levels from relatively few prospective and/or retrospective periodic measurements of radon 

levels in a particular location; (2) uncertainty in assumptions regarding radon levels in homes where 

measurements were not made, length of residence and history of prior residences; and (3) accuracy of 

reported data on confounding factors such as smoking history or active smoker in the home, or including 

different percentages of smokers in the control and exposed groups. The individual residential casecontrol studies typically employed relatively low numbers of cases and matched controls, which limits the 

statistical power of an individual study to identify a statistically significant association between radon 

exposure and an adverse health outcome such as lung cancer. The statistical power is further reduced by 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 22 

3. HEALTH EFFECTS 

measurement error, and residential mobility. In order to more precisely estimate risk, most of the 

residential study investigators have pooled data from their studies. The pooled analyses have found 

statistically significant, positive associations between lung cancer and residential radon levels among 

smokers, but not among lifelong nonsmokers (Darby et al. 2005). 

Several ecological studies have been performed to assess possible relationships between selected cancers 

and estimated radon levels within particular geographic regions where environmental radon levels appear 

to be higher than other geographic regions. Typically, estimates of mean radon levels for the geographic 

regions were significantly elevated, but were based on relatively few actual measurements of radon levels 

in homes in the region and were not matched to individuals. This is problematic because radon 

(particularly indoor) levels can vary greatly between residences in a particular geographic region. 

Additional sources of uncertainty in methodology used to estimate radon levels in ecological studies 

include use of current exposure to represent past exposure, inherent error in measuring devices, use of 

indirect measures of indoor concentrations as an index of indoor radon exposure, use of sample 

measurements rather than total-population data, and estimation of individual exposure from group data 

(Greenland et al. 1989; Morgenstern 1995; Stidley and Samet 1993). Other factors that can lead to 

inaccurate results regarding associations between exposure to radon and lung cancer include inadequate 

control of confounding, model misspecification, and misclassification of factors such as health end points, 

job classifications, and exposure. Results of available ecological studies assessing possible associations 

between environmental radon levels and lung cancer incidence are mixed; reports include positive and 

negative associations, as well as no significant associations. Several ecological studies have indicated 

positive associations between radon levels and selected types of leukemia. Statistically significant 

associations between radon levels and leukemia were also reported in a miner cohort study (Řeřicha et al. 

2006), but not in residential case-control studies from which outcomes and exposures were more 

accurately matched to individuals. 

The health effects chapter of this toxicological profile for radon focuses, primarily, on health effects 

observed in studies of occupationally-exposed miners and results of pooled analyses of residential casecontrol studies. Results of animal studies provide additional support to the compelling evidence of radoninduced lung cancer in the miner cohorts and to the evidence of radon-induced lung tumors from results 

of pooled analyses of residential case-control studies, especially among cigarette smokers. Since these 

studies are discussed in various sections of the profile, the general design features, attributes, limitations 

and major findings of the studies that form the bases for conclusions regarding the epidemiological 

evidence of health effects of radon exposures in humans are provided here. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 23 

3. HEALTH EFFECTS 

Mining cohorts have been followed for several decades or more. Continued follow-up and refined 

assessments of the most widely-studied mining cohorts have resulted in improved exposure estimates and 

more complete categorization of individuals according to cause of death, mining history, and smoking 

status. However, until recently, studies of mining cohorts did not address confounding by silica exposure 

since crystalline silica was not recognized as a known human carcinogen before most of these studies 

were published. Assessments also did not necessarily include adjustments for confounding exposures to 

arsenic and/or diesel exhaust. The bulk of health effects information for the mining cohorts reported in 

this toxicological profile for radon derives from the most recent analyses of pooled data from 11 mining 

cohorts (Lubin et al. 1997; NAS 1999a; NIH 1994) using the most recent and comprehensive follow-up 

results from available studies of individual mining cohorts. Requirements for inclusion of a particular 

cohort in the analysis of pooled results included: (1) a minimum of 40 lung cancer deaths and 

(2) estimates of radon progeny exposure in units of WLM for each member of the cohort based on 

historical measurements of either radon or radon progeny. All 11 studies reported positive associations 

between lung cancer mortality and radon progeny exposure. For all subjects in each study cohort, personyears were accumulated from the date of entry (based on a minimum time of employment or the 

occurrence of a medical examination in some studies). A latency period of 5 years was incorporated to 

represent the expected minimum time necessary for a transformed cell to result in death from lung cancer. 

Although the accuracy of exposure estimates varied widely among the individual study cohorts, no 

attempt was made to restrict or limit the role of any particular cohort in the combined analysis. Relative 

risk for lung cancer was calculated as a function of cumulative WLM after adjustments for cohort, age, 

other occupational exposures (except silica dust), and ethnicity (NIH 1994). Selected characteristics of 

the individual cohorts and pooled data are presented in Table 3-1, as well as relative risks of lung cancer 

mortality for selected categories of cumulative WLM. The results provide evidence for increasing risk of 

lung cancer mortality with increasing cumulative WLM. Updated analysis of the 11 mining cohorts that 

contributed to the pooled data of NIH (1994) was particularly focused on relative risk of lung cancer in 

the miners exposed to relatively low cumulative WLM (Lubin et al. 1997); results demonstrate significant 

risk of lung cancer mortality at well below 100 WLM (Table 3-2). Excess relative risks (ERRs) for lung 

cancer mortality (excess risk per WLM) were estimated to be 0.0117/WLM (95% CI 0.002–0.025) for 

exposures <50 WLM and 0.0080/WLM (95% CI 0.003–0.014) for exposures <100 WLM. 
 

 

 

 


 


 


 
 


 


 


 


 


 
 


 


 


 


 


 
 


 


 

RADON 24 

3. HEALTH EFFECTS 

Table 3-1. Selected Characteristics and Exposure Data for Individual Miner
 

Cohort Studies Included in the Analysis of Pooled Data from the Individual
 

Studies, and Lung Cancer Mortality Rates and Relative Risks by
 

Cumulative WLM for Pooled Dataa
 

Non-exposed Exposed workers and mean 

Follow-up workers cumulative WLM 

Mine Length Person- PersonStudy cohort type Period (years) Number years Number years WLM 

China Tin 1976–1987 10.2 3,494 39,985 13,649 135,357 277.4 

Czech Uranium 1952–1990 25.2 0 4,216 4,284 103,652 198.7 

Republic 

Colorado Uranium 1950–1987 24.6 0 7,403 3,347 75,032 807.2 

Ontario Uranium 1955–1986 17.8 0 61,017 21,346 319,701 30.8 

Newfoundland Fluorspar 1950–1984 23.3 337 13,713 1,751 35,029 367.3 

Sweden Iron 1951–1991 25.7 0 841 1,294 32,452 80.6 

New Mexico Uranium 1943–1985 17.0 12 12,152 3,457 46,797 110.3 

Beaverlodge Uranium 1950–1980 14.0 1,591 50,345 6,895 68,040 17.2 

Port Radium Uranium 1950–1980 25.2 683 22,222 1,420 30,454 242.8 

Radium Hill Uranium 1948–1987 21.9 1,059 26,301 1,457 25,549 7.6 

France Uranium 1948–1986 24.7 16 4,556 1,769 39,487 68.7 

Totalsb 7,176 242,332 60,570 908,983 

Averages 17.2 161.6 

Cumulative Relative riskd 

WLM Lung cancer cases Person-years Mean WLM (95% CI) 

0 107 214,089 0.0 1.00 

1–49 367 502,585 14.8 1.03 (0.8–1.4) 

50–99 212 118,196 73.0 1.30 (1.0–1.7) 

100–199 462 132,207 144.8 1.74 (1.3–2.3) 

200–399 511 91,429 280.4 2.24 (1.7–3.0) 

400–799 612 65,105 551.7 2.97 (2.2–3.9) 

800–1,599 294 27,204 1105.1 4.06 (3.0–5.4) 

≥1,600 140 10,336 2408.4 10.2 (7.4–14.0) 

Totals 2,705 1,161,150 130.6c 

a

Table entries include 5-year lag interval for radon progeny exposure. b

Totals adjusted for 115 workers (including 12 lung cancer cases) who were included in both New Mexico and 

Colorado cohorts.
 c

Mean WLM among exposed miners is 160.2.

d

Adjusted for cohort, age, other occupational exposures, and ethnicity.
 

CI = confidence interval; WLM = working level months 

Source: NIH 1994 
 

 

 

 

 

 

 


 


 
 


 


 


 


 


 


 


 


 


 
 


 


 


 


 


 


 


 


 


 
 


 


 


 


 


 


 


 

RADON 25 

3. HEALTH EFFECTS 

Table 3-2. Selected Results from Analysis of Pooled Data from 11 Mining
 

Cohortsa, Based on Deciles of Case Exposures That Were Each
 

Under 100 WLMb
 

Cumulative WLM Lung cancer casesc Person-years Mean WLM Relative riskd (95% CI) 

0 115 274,161 0.0 1.00 

0.1–3.5 56 111,424 2.4 1.37 (1.0–2.0) 

3.6–6.9 56 95,727 5.3 1.14 (0.8–1.7) 

7.0–15.1 56 72,914 12.4 1.16 (0.8–1.7) 

15.2–21.2 57 67,149 17.3 1.45 (1.0–2.2) 

21.3–35.4 56 57,890 33.1 1.50 (1.0–2.2) 

35.5–43.5 57 42,068 38.6 1.53 (1.0–2.2) 

43.6–59.4 56 25,622 53.2 1.69 (1.1–2.5) 

59.5–70.3 56 40,220 63.3 1.78 (1.2–2.6) 

70.4–86.5 56 28,076 81.1 1.68 (1.1–2.5) 

86.6–99.9 56 23,682 91.4 1.86 (1.2–2.8) 

a

The 11 mining cohorts and reports used for the pooled analysis included China (Xuan et al. 1993), Sweden 

(Radford and Renard 1984), Newfoundland (Morrison et al. 1988), Czech Republic (Ševc et al. 1988; Tomášek et al.
 

1994b), Colorado (Hornung and Meinhardt 1987; Hornung et al. 1995), Ontario (Kusiak et al. 1993), New Mexico 

(Samet et al. 1991), Beaverlodge (Howe et al. 1986), Port Radium (Howe et al. 1987), Radium Hill (Woodward et al.
 

1991), and France (Tirmarche et al. 1993).

b

Table entries include 5-year lag interval for radon progeny exposure.
 c

Totals adjusted for 115 workers (including 12 lung cancer cases) who were included in both New Mexico and 

Colorado cohorts.
 d

Adjusted for cohort, age, other occupational exposures, and ethnicity; excess relative risks for lung cancer mortality
 

were 0.0117 per WLM (95% CI: 0.002–0.025) for exposures <50 WLM and 0.0080 per WLM (95% CI: 0.003–0.014)
 

for exposures <100 WLM.
 

CI = confidence interval; WLM = working level months 

Source: Lubin et al. 1997 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 26 

3. HEALTH EFFECTS 

Assessments of pooled data from major residential case-control studies include a combined analysis of 

2 China case-control studies (Lubin et al. 2004), a combined analysis of 7 North American case-control 

studies (Krewski et al. 2005, 2006), and a combined analysis of 13 European case-control studies (Darby 

et al. 2005, 2006). 

The combined analysis of the residential case-control studies in China included a study that assessed all 

incident lung cancer cases recorded with the Shenyang Cancer Registry and diagnosed between 

September 1985 and September 1987 (Blot et al. 1990; Xu et al. 1989) and all incident lung cancer cases 

occurring in two rural prefectures of Gansu Province between June 1994 and April 1998 (Wang et al. 

2002). The combined analysis included 1,050 lung cancer cases and 1,996 controls (Lubin et al. 2004). 

As shown in Table 3-3, odds ratios (ORs) increased significantly with increasing radon concentration. 

For subjects residing in the current home for ≥30 years, the OR at 100 Bq/m3

 was 1.32 (95% CI 1.07– 

1.91). 

The individual case-control studies that contributed to the combined analysis of North American casecontrol studies (Krewski et al. 2005, 2006) were performed in regions of New Jersey, the Canadian 

Province of Winnipeg, Missouri, Iowa, Connecticut, and Utah-South Idaho. Requirements for inclusion 

in the combined analysis of North American case-control studies included: (1) ascertainment of at least 

200 lung cancer cases (histologically or cytologically confirmed); (2) radon exposure estimates based 

primarily on long-term α-track detectors located in living areas of homes; and (3) in-person or telephone 

interviews with subjects or next of kin to obtain data on a variety of demographic, socioeconomic, and 

smoking-related factors. Of 10,127 total subjects in the 7 North American case-control studies, 

765 subjects were excluded from the pooled analysis due to no radon measurements, no residence data 

within a 5–30-year time exposure window prior to the index date, or insufficient smoking data. The 5– 

30-year time exposure window presumes that neither radon exposure within 5 years of lung cancer 

occurrence nor 30 years prior to the index date contributes to lung cancer, although the window is 

presumed to be generally reflective of a biologically relevant exposure. Thus, the combined analysis 

included 4,081 lung cancer cases and 5,281 matched controls (Krewski et al. 2006). Selected 

characteristics of the study subjects and exposure estimates are presented in Table 3-4, along with ORs 

for lung cancer from pooled data without restriction and ORs resulting from restriction to subjects 

residing in one or two houses with ≥20 years of the residence time covered by α-track monitors. All 

analyses of the data were conducted using conditional likelihood regression for matched or stratified data 

and included covariates for sex, age at index date, number of cigarettes smoked per day, duration of 

smoking, and an indicator variable for each study. An excess odds ratio (EOR) was 0.10 per 100 Bq/m3 
 

 

 

 


 


 


 

 

 


 


 


 

 

 


 


 


 

 

 

RADON 27 

3. HEALTH EFFECTS 

Table 3-3. ORs for Lung Cancer from Combined Analysis of Two China
 

Residential Case-Control Studies (Using a 5–30-Year
 

Exposure Time Window)
 

ORs for lung cancer 

Radon concentration Number of subjects ORa 

Bq/m3 pCi/L Cases Controls (95% CI) 

<100 <2.70 164 298 1.00 

100–149 2.70–4.01 223 387 1.13 (0.94–1.31) 

150–199 4.05–5.38 198 354 1.05 (0.86–1.27) 

200–249 5.41–6.73 181 372 1.14 (0.90–1.45) 

250–299 6.76–8.08 114 256 1.22 (0.95–1.56) 

≥300 ≥8.11 148 307 1.29 (0.93–1.80) 

Excess OR (β)=0.133 per 100 Bq/m3 (95% CI 0.01–0.36)b 

Excess ORs by years covered by radon detectors and residential mobility within the 5–30-year 

exposure time window prior to enrollment 

Years in exposure time window 25 20–24 <20 

Excess OR 0.319 -0.134 -0.072 

Number of homes 1 2 ≥3

Excess OR 0.332 -0.071 0.099 

a

ORs adjusted for sex, age, smoking risk, years in exposure time window, and number of homes inhabited in the 

exposure time window.

b

Based on linear model: OR(x)=1+βx, where x is the radon concentration in the exposure time window.

CI = confidence interval; OR = odds ratio 

Source: Lubin et al. 2004 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 28 

3. HEALTH EFFECTS 

(95% CI -0.1–0.28) for the unrestricted dataset, indicating that radon was not associated with residential 

lung cancer, but the EOR increased to 0.18 per 100 Bq/m3

 (95% CI 0.02–0.43) when restricting to 

subjects residing in one or two houses with ≥20 years of the residence time covered by α-track monitors. 

This combined analysis provides evidence of an association between residential radon and lung cancer 

risk (Table 3-4). Histologically, no effect of radon concentration was found for any specific lung cancer 

type. 

The analysis of pooled data from residential case-control studies in 13 European studies (Darby et al. 

2005, 2006) included Austria, the Czech Republic, nationwide Finland, south Finland, France, eastern 

Germany, western Germany, Italy, Spain, nationwide Sweden, never smokers in Sweden, Stockholm 

Sweden, and the United Kingdom. The pooled data included 7,148 lung cancer cases and 

14,208 controls. Inclusion in the analysis required detailed residential histories for at least 15 years, at 

least 2 months of measurements of radon gas concentrations that were likely to be representative of levels 

experienced by the study subjects during their tenure in the residences, and details regarding smoking 

habits. Each study in the pooled analysis included at least 150 lung cancer cases and 150 control subjects. 

Results of this analysis provide additional evidence of an association between residential radon and lung 

cancer risk, but mostly among smokers and recent ex-smokers for which the risk was as much as 25 times 

higher than for never smokers. The evidence for smokers includes statistically significant relative risks at 

exposure concentrations ≥400 Bq/m3

 (10.8 pCi/L), an ERR of 0.084 per 100 Bq/m3 (95% CI 0.03–0.158) 

for the full range of observed radon concentrations, and ERRs of 0.140 per 100 Bq/m3

 (95% CI 0.004– 

0.309) for exposure concentrations <200 Bq/m3

 (<5.4 pCi/L), 0.095 per 100 Bq/m3 (95% CI 0.005–0.206) 

for exposure concentrations <400 Bq/m3

 (<10.8 pCi/L), and 0.078 per 100 Bq/m3 (95% CI 0.012–0.164) 

for exposure concentrations <800 Bq/m3

 (<21.6 pCi/L) (Table 3-5). For lifelong nonsmokers, an ERR of 

0.106 per 100 Bq/m3 (95% CI 0.003–0.280) was observed for the full range of observed radon 

concentrations. 

Although the dose-response coefficients from the mining studies and residential studies are expressed in 

different units of exposure (i.e., WLM vs. Bq-year/m3

), they can be compared by applying the 

relationship described above, namely that 1 pCi/L (37 Bq/m3

) of continuous exposure throughout the year 

(i.e., 37 Bq-year/m3

) is equivalent to 0.144 WLM for that year. Thus, a 25-year exposure at 200 Bq/m3 

(5.4 pCi/L) would be equivalent to a cumulative exposure of 19.5 WLM. Using this conversion factor, an 

estimated excess relative risk of 0.0117/WLM at occupational exposures <50 WLM (Lubin et al. 1997) 

would be roughly equivalent to an ERR of 0.114 per 100 Bq/m3

, assuming that the miners were not 

exposed to silica dust since accounting has not yet been conducted for confounding by this carcinogen. 
 

 

 

 

 

 

 


 


 


 

 

 

 


 


 

 
 

 
 


 


 


 


 


 

 

 

 


 


 

 
 

 
 


 


 


 


 


 

 

 

 


 


 

 
 

 
 


 


 

RADON 29 

3. HEALTH EFFECTS 

Table 3-4. Selected Characteristics of Study Subjects, Exposure Estimates, and
 

ORs for Lung Cancer from Combined Analysis of Seven North American 

Residential Case-Control Studies (Using a 5–30-Year
 

Exposure Time Window)
 

Number of subjectsa Time-weighted average radon concentration in Bq/m3 

Region Lung cancer cases Controls Lung cancer cases Controls All subjects 

New Jersey 480 442 26.5 24.9 25.7 

Winnipeg 708 722 137.4 146.9 142.2 

Missouri-I 530 1,177 62.2 62.9 62.7 

Missouri-II 477 516 55.3 56.1 55.7 

Iowa 412 613 136.2 121.3 127.3 

Connecticut 963 949 32.2 32.8 32.5 

Utah-Idaho 511 862 55.4 58.1 57.1 

ORs for lung cancer 

Radon concentration Number of subjects ORb 

Bq/m3 pCi/L Cases Controls (95% CI) 

<25 <0.68 994 1,055 1.00 

25–49 0.68–1.32 1,169 1,549 1.13 (0.94–1.31) 

50–74 1.35–2.00 704 1,087 1.05 (0.86–1.27) 

75–99 2.03–2.68 356 507 1.14 (0.90–1.45) 

100–149 2.70–4.03 513 602 1.22 (0.95–1.56) 

150–199 4.05–5.38 166 229 1.19 (0.86–1.66) 

≥200 ≥5.45 179 252 1.29 (0.93–1.80) 

Excess OR (β)=0.10 per 100 Bq/m3 (95% CI -0.01–0.28)c 

ORs for lung cancer with data restricted to subjects residing in one or two houses in the exposure 

window with ≥20 years covered by α-track air monitors 

Radon concentration Number of subjects ORb 

Bq/m3 pCi/L Cases Controls (95% CI) 

<25 <0.68 503 596 1.00 

25–49 0.68–1.32 481 717 1.01 (0.80–1.28) 

50–74 1.35–2.00 295 418 1.29 (0.98–1.70) 

75–99 2.03–2.68 181 293 1.22 (0.88–1.69) 

100–149 2.70–4.03 202 282 1.28 (0.91–1.78) 

150–199 4.05–5.38 115 160 1.41 (0.83–2.14) 

≥200 ≥5.45 133 185 1.29 (0.91–2.06) 

Excess OR (β)=0.18 per 100 Bq/m3 (95% CI 0.02–0.43)c 

a

For the combined analysis of the 7 North American residential case-control studies, 339 lung cancer cases and 426 control
 

subjects were excluded based on lack of smoking, radon, and/or residence data.

b

ORs stratified by sex and categories of age, duration of smoking, number of cigarettes smoked per day, number of
 

residences, and years with α-track measurements in the exposure time window.
 c

Based on linear model: OR(x)=1+βx, where x is the radon concentration in the exposure time window.
 

CI = confidence interval; OR = odds ratio
 

Source: Krewski et al. 2006
 
 

RADON 30 

3. HEALTH EFFECTS 

Table 3-5. Relative Risk and Excess Relative Risk of Lung Cancer by Radon 

Level in Homes 5–34 Years Previously, Estimated from the Pooled Data for 

13 European Residential Case-Control Studies 

Radon concentration Number of subjects 

Range 

(Bq/m3) 

Mean 

(Bq/m3) 

Mean 

(pCi/L) Lung cancer cases Controls RR (95% CI) 

<25 17 0.46 566 1,474 1.00 (0.87–1.15) 

25–49 39 1.05 1,999 3,905 1.06 (0.98–1.15) 

50–99 71 1.92 2,618 5,033 1.03 (0.96–1.10) 

100–199 136 3.68 1,296 2,247 1.20 (1.08–1.32) 

200–399 273 7.38 434 936 1.18 (0.99–1.42) 

400–799 542 14.65 169 498 1.43 (1.06–1.92) 

≥800 1,204 32.54 66 115 2.02 (1.24–3.31) 

Excess relative risk for lung cancer according to selected ranges of radon concentrations 

Range of radon concentrations Lung cancer cases Controls ERR per 100 Bq/m3 (95% CI) 

<800 Bq/m3 21.6 pCi/L 7,082 14,093 0.078 (0.012–0.164) 

<400 Bq/m3 10.8 pCi/L 6,913 13,595 0.095 (0.005–0.206) 

<200 Bq/m3 5.4 pCi/L 6,479 12,659 0.140 (0.004–0.309) 

<100 Bq/m3 2.7 pCi/L 5,183 10,412 0.025 (-0.192–0.306) 

All radon concentrations 7,148 14,208 0.084 (0.030–0.158) 

CI = confidence interval; ERR = excess relative risk; RR = relative risk 

Source: Darby et al. 2006 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 31 

3. HEALTH EFFECTS 

This value is similar to the estimates for excess relative risk (0.084/Bq/m3) estimated from the analysis of 

pooled data from the 13 European case-control studies (Darby et al. 2005, 2006) and EOR (0.18 per 

100 Bq/m3

) estimated from the pooled analysis of the North American residential case-control studies 

restricted to subjects residing in one or two houses with ≥20 years of the residence time covered by 

α-track monitors (Krewski et al. 2006). Based on this comparison, the studies of mining cohorts and the 

residential studies appear to converge on similar estimates for the relationship between exposure to radon 

(and its progeny) and risk of lung cancer mortality. However, since the miners were exposed to silica 

dust and those studies did not assess confounding by this substance (which was confirmed as a known 

human carcinogen after those studies were published), attempts to correlate radon risk from residential 

and mining studies may be premature. This is emphasized in the re-assessed results of Swedish mines in 

which strong correlation was found between radon and silica, and accounting for silica reduced the RR 

previously attributed to radon by approximately 30%, from 5.65 to 3.90 (Bergdahl et al. 2010). 

Available animal data consist mainly of inhalation studies performed at the University of Rochester (UR) 

in the 1950s and 1960s using rats, mice, and dogs (AEC 1961, 1964, 1966; Morken 1955, 1973); at the 

Pacific Northwest Laboratory (PNL, presently Pacific Northwest National Laboratory [PNNL]) between 

the 1960s and 1980s using rats, dogs, and hamsters (Cross 1988, 1994; Cross et al. 1981a, 1981b, 1984; 

Dagle et al. 1992; Gilbert et al. 1996; NIEHS 1978; Palmer et al. 1973); and at laboratories in France 

using rats (Chameaud et al. 1974, 1980, 1982a, 1982b, 1984; Monchaux 2004; Monchaux and Morlier 

2002; Monchaux et al. 1999; Morlier et al. 1992, 1994). Most of these studies employed exposure levels 

that were many orders of magnitude higher than those considered to be relevant to human health. 

Discussion of animal studies in Section 3.2.1 is limited to studies that employed exposure levels 

considered relevant to plausible human exposure scenarios (Chameaud et al. 1984; Morlier et al. 1994). 

3.2.1.1 Death 

Possible associations between exposure to radon and lung cancer mortality among underground miners 

are discussed in Section 3.2.1.7 (Cancer). 

Excess mortality from noncancer diseases reported in some of the mining cohorts include all noncancer 

respiratory diseases, pneumoconioses, emphysema, interstitial pneumonitis, other (unspecified) chronic 

obstructive respiratory diseases, and tuberculosis (Lundin et al. 1971; Muller et al. 1985; Roscoe 1997; 

Roscoe et al. 1989, 1995; Samet et al. 1991; Tirmarche et al. 1993; Waxweiler et al. 1981). However, 

confounding factors such as exposure to other respiratory toxicants (most notably arsenic and silica dust), 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 32 

3. HEALTH EFFECTS 

ethnicity, smoking history, and work experience were likely major contributors to mortalities from 

noncancer respiratory diseases. A statistically significant excess of mortality due to chronic nephritis and 

renal sclerosis was also reported in the U.S. uranium miner cohort, although it is unclear whether this was 

related to exposure to radon, uranium ore, or other mining conditions or to nonmining factors (Waxweiler 

et al. 1981). 

No significant association was observed between cumulative exposure to radon progeny and death from 

cardiovascular diseases in cohorts of German uranium miners (Kreuzer et al. 2010) or Newfoundland 

fluorspar miners (Villeneueve et al. 2007a). 

Limited information is available regarding exposure to radon and death in animals. No significant effects 

on longevity were observed in male Sprague-Dawley rats exposed to atmospheres of radon and radon 

progeny for 6 hours/day, 5 days/week during 18 months to obtain a cumulative exposure of 25 WLM 

(Morlier et al. 1994) or in rats exposed to a cumulative exposure of 20 WLM (1 hour exposures twice 

weekly for 42 total exposures) or 40 WLM (1-hour exposures twice weekly for 82 total exposures) 

(Chameaud et al. 1984). It should be noted that these studies employed relatively low dose rates. 

3.2.1.2 Systemic Effects 

No studies were located regarding gastrointestinal, musculoskeletal, hepatic, dermal, or body weight 

effects after inhalation exposure to radon and its progeny at exposure levels considered relevant to human 

health. 

Respiratory Effects. Possible associations between exposure to radon and lung cancer are discussed in 

Section 3.2.1.7. Adverse noncancer respiratory effects have been observed in humans under occupational 

conditions and in laboratory animals exposed to radon and its progeny. Some studies of miner cohorts 

identified excess cases of nonmalignant respiratory diseases such as asthma, bronchitis, pneumoconioses, 

emphysema, interstitial pneumonitis, pulmonary fibrosis, and tuberculosis (Boice et al. 2008; Fox et al. 

1981; Lundin et al. 1971; Muller et al. 1985; Roscoe 1997; Roscoe et al. 1989, 1995; Samet et al. 1991; 

Tirmarche et al. 1993; Waxweiler et al. 1981). However, potential confounding by smoking and 

respirable dust, especially crystalline silica dust, were likely major contributors to mortalities from 

noncancer respiratory diseases. Excess mortality associated with exposure to silica dust was reported in 

California diatomaceous earth miners for which the standard mortality ratio (SMR) was 2.01 (95% CI 

1.56–2.55). The mortality rate increased sharply with exposure using a 15-year latency, which is longer 
 

 

 

 

 

RADON 33 

3. HEALTH EFFECTS 

than the 5-year latency used for most miner and residential radon studies (Checkoway et al. 1997). 

Chronic lung disease was reported to increase with increasing cumulative exposure to radiation and with 

cigarette smoking (Archer 1980). In addition, nonsmoking uranium miners were also reported to have 

increased deaths from nonmalignant respiratory disease compared to a nonsmoking U.S. veteran cohort 

(Roscoe et al. 1989). For non-miners, the rate of chronic obstructive pulmonary disease (COPD) was 

reported to increase with increasing radon exposure (Turner et al. 2012). 

Alterations in respiratory function have been reported in studies of U.S. uranium miners (Archer et al. 

1964; Samet et al. 1984a; Trapp et al. 1970). Archer et al. (1964) reported decrements in pulmonary 

function with increasing cumulative exposure; however, the study also noted that pulmonary disability 

was affected by age and smoking more than by radiation exposure. Samet at al. (1984a) reported 

significantly increased prevalence of dyspnea with increasing duration of underground mining. 

Evaluations of these respiratory end points did not include assessment of the effects of each of the other 

possible mine pollutants, such as ore dust, silica, or diesel engine exhaust. 

No information was located regarding respiratory effects in animals following exposure to radon and its 

progeny at concentrations considered relevant to human health. 

Cardiovascular Effects. No significant association was observed between cumulative exposure to 

radon progeny and death from cardiovascular diseases in cohorts of German uranium miners (Kreuzer et 

al. 2010) or Newfoundland fluorspar miners (Villeneueve et al. 2007a). A significant relationship was 

noted between cumulative radon exposure and prevalence of mortality from cerebrovascular disease 

(excess relative risk of 0.49 [95% CI 0.07–1.23] per 100 WLM) in a French cohort study of uranium 

miners between 1946 and 1999 (Nusinovici et al. 2010). However, the study authors cautioned that a lack 

of data limited the ability to assess possible confounding by cardiovascular risk factors. 

No information was located regarding cardiovascular effects in animals following exposure to radon and 

its progeny at concentrations considered relevant to human health. 

Hematological Effects. No studies were located regarding hematological effects after inhalation 

exposure to radon at concentrations considered relevant to human health. 

Renal Effects. Although a statistically significant increase in mortality due to kidney disease, 

characterized by chronic nephritis and renal sclerosis, was reported among U.S. uranium miners 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 34 

3. HEALTH EFFECTS 

(Waxweiler et al. 1981) and in Canadian miners at the Eldorado mines (Muller et al. 1985), this finding is 

not generally considered to be related to radon exposure per se. 

No information was located regarding renal effects in animals following exposure to radon and its 

progeny. 

Ocular Effects. Abdelkawi et al. (2008) reported significantly increased refractory index, decreased 

protein concentration, and increased protein molecular weight after 6 weeks of exposure in the lens and 

cornea of mice exposed to radon at a mean concentration of 55.8 kBq/m3

 (attached fraction of 0.62) for 

6 hours/day, 5 days/week for up to 8 weeks. Effective radon lung doses ranged from 20.92 to 83.68 mSv. 

The study investigators considered the effects on the lens and cornea to have resulted from systemic 

distribution of inhaled radioactivity. Although the dermal route of exposure was not considered, the 

permeability of corneal epithelium to atmospheric gases could allow radon at the high concentrations used 

in the study to diffuse toward and expose both the cornea and lens to alpha radiation. 

3.2.1.3 Immunological and Lymphoreticular Effects 

No information was located regarding immunological effects after inhalation exposure to radon at 

concentrations considered relevant to human health. 

3.2.1.4 Neurological Effects 

No studies were located regarding neurological effects after inhalation exposure to radon at 

concentrations considered relevant to human health. 

3.2.1.5 Reproductive Effects 

No maternal or fetal reproductive effects in humans have been attributed to exposure to radon and its 

progeny. However, a decrease in the secondary sex ratio (males:females) of the children of male 

underground miners may be related to exposure to radon and its progeny (Dean 1981; Muller et al. 1967; 

Wiese and Skipper 1986). Ismail and Jaafar (2010) assessed possible relationships between radiation 

dose to the lungs from radon and radon progeny and rates of infertility within various locations in Iraqi 

Kurdistan. Radon levels were measured in homes; annual effective lung doses by inhalation of radon and 

radon progeny were estimated to range from approximately 2 to 6 mSv/yr. The dose to the gonads was 

not estimated, but would have been lower than that for the lungs and orders of magnitude lower than the 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 35 

3. HEALTH EFFECTS 

protracted external radiation doses stated to induce temporary sterility (400 mSv/yr) or permanent sterility 

(2000 mSv/year). The study authors reported an exponential relationship between annual effective lung 

dose and the rate of male infertility that is not supported by the reported low estimates of radiation dose. 

The authors also stated that there were increases in blood and prostate cancers (which influence male 

fertility), but did not provide quantitative data. Overall, the scientific value of this study is questionable. 

No information was located regarding reproductive effects in animals following exposure to radon and its 

progeny at concentrations considered relevant to human health. 

3.2.1.6 Developmental Effects 

No studies were located regarding developmental effects in humans following inhalation exposure to 

radon and its progeny. 

No information was located regarding developmental effects in animals following exposure to radon and 

its progeny at concentrations considered relevant to human health. 

3.2.1.7 Cancer 

Associations between exposure to radon and lung cancer mortality have been examined in studies of 

underground miners at facilities in the United States (Archer et al. 1973, 1976, 1979; Boice et al. 2008; 

Checkoway et al. 1985; Gottlieb and Husen 1982; Hornung and Meinhardt 1987; Hornung et al. 1998; 

Lane et al. 2010; Lubin et al. 1995a, 1995b; Luebeck et al. 1999; Lundin et al. 1971; Moolgavkar et al. 

1993; NIH 1994; Roscoe 1997; Roscoe et al. 1989, 1995; Samet et al. 1984b, 1989, 1991, 1994; 

Schubauer-Berigan et al. 2009; Stayner et al. 1985; Stram et al. 1999; Thomas et al. 1994; Wagoner et al. 

1963, 1964; Waxweiler et al. 1981), Australia (Woodward et al. 1991); Brazil (Veiga et al. 2006), Canada 

(Howe and Stager 1996; Howe et al. 1986, 1987; Kusiak et al. 1993; L’Abbé et al. 1991; Morrison et al. 

1985, 1998; Muller et al. 1985), China (Qiao et al. 1989, 1997; Yao et al. 1994), the Czech Republic 

(Kulich et al. 2011; Ševc et al. 1988, 1993; Tomášek 2002, 2011; Tomášek and Darby 1995; Tomášek 

and Plaček 1999; Tomášek and Žárská 2004; Tomášek et al. 1993, 1994a, 1994b, 2008), England (Fox et 

al. 1981; Hodgson and Jones 1990b), France (Amabile et al. 2009; Laurier et al. 2004; Leuraud et al. 

2007; Rogel et al. 2002; Tirmarche et al. 1993; Vacquier et al. 2007, 2009), Germany (Brüske-Hohlfeld et 

al. 2006; Kreuzer et al. 2000, 2010; Schnelzer et al. 2010; Taeger et al. 2006, 2008, 2009; Walsh et al. 

2010), Italy (Carta et al. 1994), Norway (Solli et al. 1985), and Sweden (Axelson and Sundell 1978; 

Bergdahl et al. 2010; Damber and Larsson 1982; Edling and Axelson 1983; Jonsson et al. 2010; 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 36 

3. HEALTH EFFECTS 

Jorgensen 1984; Radford and Renard 1984; Snihs 1974). The mining cohorts were primarily uranium 

miners, but included some cohorts mining other metals, hard rock, or coal. 

Lubin et al. (1997) provide combined results from eleven of these cohorts; the results demonstrate 

increased risk of mortality from lung cancer with increasing WLM (see Table 3-2). The combined data 

included 115 lung cancer deaths among workers without known occupational exposure to radon and 

2,674 lung cancer deaths among exposed miners. Some of these miners had been exposed to more than 

10,000 WLM; the mean exposure among the pooled miner data was 162 WLM. In order to make more 

meaningful comparisons between radon exposure among mining cohorts and residential radon exposure, 

Lubin et al. (1997) assessed mortality from lung cancer among two groups of workers with the lowest 

exposure levels (<50 and <100 WLM, respectively). Even in these groups of miners with relatively lowlevel exposure, relative risk of lung cancer mortality exhibited an apparent linear and statistically 

significant increasing trend with WLM (in decile categories). RRs for the two highest exposure 

categories (142.3–250.8 and >250.8 Bq/m3

; equivalent to 3.84–6.77 and >6.77 pCi/L, respectively) were 

1.28 (95% CI 1.0–1.6) and 1.20 (95% CI 1.0–1.5), respectively. ERRs per WLM were estimated to be 

0.0117/WLM (95% CI 0.002–0.025) for exposures <50 WLM and 0.0080/WLM (95% CI 0.003–0.014) 

for exposures <100 WLM. General patterns of declining excess relative risk per WLM with attained age, 

time since exposure, and exposure rate were observed in both the unrestricted pooled data and in those 

restricted to <50 and <100 WLM. Lubin et al. (1997) noted an apparent inadequacy in the fit of the ERR 

model, but this was not improved using nonlinear or linear threshold models. Lubin et al. (1997) also 

noted that results for the mining cohorts with relative low-level exposure might not be applicable to 

residential radon exposure due to uncertainties in estimating miner exposure to radon, radon progeny, and 

other carcinogens (e.g., silica dust) during the earliest years of mining when ventilation was poor. 

Leuraud et al. (2011) assessed the effects of exposure to radon and radon decay products and smoking 

status on the risk of lung cancer in a combined analysis of 1,046 lung cancer cases and 2,492 controls 

with detailed radon exposure data and smoking status selected from three major minor cohorts in the 

Czech Republic (Tomášek et al. 2003), France (Laurier et al. 2004), and Germany (Kreuzer et al. 2010). 

The combined analysis resulted in an ERR/WLM of 0.010 (95% CI 0.006–0.018) unadjusted for smoking 

and an ERR/WLM of 0.008 (95% CI 0.004–0.014) after adjustment for smoking, which was based on 

four categories: never smoker, ex-smoker for ≥10 years, ex-smoker for <10 years, and current smoker. 

The results of Leuraud et al. (2011) suggest a sub-multiplicative interaction between radon exposure and 

smoking. 
RADON 37 

3. HEALTH EFFECTS 

The results of the miner studies consistently demonstrate significant positive associations between lung 

cancer and exposure to radon. However, most miner studies were performed prior to the identification of 

other substances as known human carcinogens (silica dust and arsenic; NTP 2011) or probable human 

carcinogens (diesel exhaust particulates; Attfield et al. 2012; NTP 2011) in the mining air. Accounting 

for these carcinogens would likely reduce the calculated impact of radon on lung cancer mortality in the 

mining cohorts. For example, Xuan et al. (1993) estimated a 75% reduction in the lung cancer risk to a 

cohort of Chinese tin miners after adjusting for arsenic exposure. Bergdahl et al. (2010) reported 

decreased lung cancer risk from radon after adjusting for silica exposure within the highest exposure 

group from a cohort of Swedish iron ore miners. Statistically significant excess lung cancer mortality has 

been associated with average cumulative exposures to radon progeny as low as 36–39 WLM in Czech and 

French cohorts of uranium miners (Ševc et al. 1988; Vacquier et al. 2007); exposure levels were higher 

among many of the other uranium miner cohorts. Vacquier et al. (2009) reported an ERR per 100 WLM 

of 0.58 (p<0.01) for lung cancer within a cohort of 5,086 French uranium miners (4,133 with positive 

radon exposure; mean cumulative exposure of 36.6 WLM) and 159 lung cancer cases during 30 years of 

follow up and noted that higher risk persisted when the effects of hard labor and period of exposure were 

taken into account. An inverse exposure rate effect (i.e., lower exposure rates for long periods are more 

hazardous than equivalent cumulative exposure received at higher exposure rates over a shorter time) was 

evident at relatively high exposure levels (WL) (Hornung et al. 1998; Lubin et al. 1995a, 1997; Luebeck 

et al. 1999; Moolgavkar et al. 1993; NIH 1994); however, this effect appeared to be attenuated or absent 

at relatively low exposure levels (Lubin et al. 1995a; NIH 1994; Tomášek et al. 2008). The apparent 

inverse exposure rate effect could have been associated with using no-threshold models, a restriction that 

was not required in the European residential assessment (HPA 2009). 

Among smoking and nonsmoking uranium miners, the most frequently reported type of lung cancer was 

small cell lung carcinoma (SCLC) in the early phase of follow-up (Archer et al. 1974; Auerbach et al. 

1978; Butler et al. 1986; Gottlieb and Husen 1982; Saccomanno et al. 1971, 1988; Samet 1989). Archer et 

al. (1974) also noted relatively high rates of epidermoid and adenocarcinomas, while large-cell 

undifferentiated and other morphological types of lung cancer were seen less frequently. A report on the 

German uranium mining cohort identified squamous cell carcinoma as the predominant lung tumor cell 

type, followed by adenocarcinoma and SCLC (Kreuzer et al. 2000). Jonsson et al. (2010) reported lung 

cancer risk in a cohort of 5,449 male iron ore miners in Sweden; the follow-up period spanned the years 

1958–2000. A total of 3,597 of the miners had been exposed to radon; the average cumulative radon 

exposure was 65 WLM over an average of 14.6 years of employment. For all lung cancers, the ERR per 

kBq-year/m3

 was 0.046 (95% CI 0.015–0.077), which equals an ERR/WLM of 0.022WLM (95% CI 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 38 

3. HEALTH EFFECTS 

0.007–0.038). For small cell cancer (55 cases), squamous cell cancer (51 cases), and adenocarcinoma 

(12 cases), ERRs per kBq-year/m3

 were 0.072 (95% CI -0.003–0.147), 0.049 (95% CI -0.003–0.102), and 

0.000 (95% CI 0.017–0.017), respectively. After adjusting for cumulative quartz (silica) together with 

attained age and calendar period, the ERR for all lung cancers was 0.031 per kBq-year/m3

 (95% CI 0.009– 

0.070), which equals an ERR of 0.015 per WLM (95% CI 0.04–0.034). 

In a subcohort of 516 white nonsmoking uranium miners (drawn from a larger cohort of U.S. uranium 

miners), mean exposure was reported as 720 WLM. For this cohort, the mortality risk for lung cancer 

was found to be 12-fold greater than that of nonsmoking, nonmining U.S. veterans; the SMR was 

12.7 (95% CI 8.0–20.1) for lung cancer in nonsmoking mining cohort. No lung cancer deaths were found 

in nonsmoking miners (Colorado Plateau cohort) who had exposure <465 WLM (Roscoe et al. 1989); 

continued follow-up of this cohort (1960–2005) revealed SMRs of 2.9 (95% CI 1.8–4.4) for never 

smokers with cumulative exposure to radon progeny in the range of 400–1,000 WLM and 6.3 (95% CI 

4.6–8.5) for never smokers with cumulative exposure to radon progeny ≥1,000 WLM (Schubauer-Berigan 

et al. (2009). These results for nonsmokers follow a dose rate rather than an inverse dose rate response 

curve. 

Some studies of mining cohorts included assessments of mortality from cancers other than lung cancer. 

Kreuzer et al. (2010) reported a slight, but statistically significant excess of cancers of the extrathoracic 

airways and trachea (ERR/WLM = 0.062%; 95%CI 0.002–0.121%) within a cohort of 58,987 male 

uranium miners at the Wismut mine in Germany with follow-up from 1946 to 2003. Řeřicha et al. (2006) 

reported significant positive associations between cumulative radon exposures and incidences of leukemia 

(RR=1.75; 95% CI 1.10–2.78) and incidences of chronic lymphocytic leukemia (CLL) (RR=1.98; 95% CI 

1.10–3.59) in a cohort of Czech uranium miners at 110 WLM. In apparent contrast, this same group did 

not find this relationship to hold in a longer-term follow-up of the same population (Kulich et al. 2011). 

Möhner et al. (2006, 2010) observed no significant associations between leukemia risk (from acute 

myeloid leukemia [AML], CLL, or all types) and exposure to radon progeny (from <50 to >1,500 WLM) 

among 377 leukemia cases and 980 individually matched controls from a cohort of 360,000 uranium 

miners at the Wismut mine in the former East Germany that supported the Soviet nuclear weapons 

program. However, the leukemia risk became significant (OR 2.64, 95% CI 1.60–2.35) in the highest 

dose category when doses were lagged 20 years (Möhner et al. 2010), the same period used by Pelucchi et 

al. (2006) for the silica dust study, but much longer than 5 years used in other studies in this section. This 

indicates that the 5-year lag period might be too short. Results of a few other studies indicate statistically 

significant excessive mortalities from laryngeal, liver, kidney, stomach, and/or gall bladder cancers 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 39 

3. HEALTH EFFECTS 

(Kreuzer et al. 2004, 2008; Tirmarche et al. 1992; Tomášek et al. 1993; Vacquier et al. 2007); however, 

the excess mortalities from these cancers did not appear to be related to cumulative exposure to radon and 

were not supported by results from other studies of mining cohorts (Kreuzer et al. 2010; Kulich et al. 

2011; Laurier et al. 2004; Möhner et al. 2008). 

Numerous residential case-control studies of lung cancer have been performed in the United States and 

other countries, including Brazil, Canada, China, Croatia, the Czech Republic, Finland, France, Germany, 

Israel, Italy, Japan, Romania, Spain, Sweden, and the United Kingdom. Some of these studies reported 

positive or weakly positive associations between lung cancer risk and residential radon concentrations, 

whereas no significant associations were observed in others. As discussed earlier, recent assessment of 

available residential case-control studies includes analyses of pooled data from 2 China case-control 

studies (Lubin et al. 2004), a combined analysis of 7 North American case-control studies (Krewski et al. 

2005, 2006), a combined analysis of 13 European case-control studies (Darby et al. 2005, 2006), and a 

comparative assessment of the three combined analyses (HPA 2009). Pooling resulted in much larger 

numbers of lung cancer cases and controls than were achieved in individual case-control studies. The 

results of these analyses of pooled data provide evidence of increased risk for lung cancer with increasing 

residential levels of radon (Tables 3-3, 3-4, and 3-5) for cigarette smokers, including a statistically 

significant relative risk of lung cancer at mean radon concentrations ≥542 Bq/m3

 (14.65 pCi/L) reported 

by Darby et al. (2006) (Table 3-5). The HPA (2009) assessment identified flaws that resulted in the 

China and North American studies overestimating the radon cancer risk. According the HPA (2009), the 

European study properly assessed radon risk by using more accurate dosimetry and including more 

homes, and the resulting radon risk estimate paralleled that of the whole China and North American 

database. However, the China and North American studies selected only a portion of the database, 

limiting inclusion to those living in one or two homes with more complete dosimetry, but the manner in 

which homes were selected would have introduced socioeconomic bias, which in addition to lower 

dosimetry approach, caused the China and North American studies to overestimate the radon risk. 

Nevertheless, all three combined analyses support the conclusion that residential radon is carcinogenic. 

HPA (2009) estimated that the cumulative (absolute) radon-induced lung cancer risk to age 75 for longterm exposure to radon at 0, 100, 200, 400, and 800 Bq/m3

 (0, 2.7, 5.41, 10.81, and 21.62 pCi/L) is 15, 

17, 19, 23, and 30%, respectively, for lifetime smokers, and 0.4, 0.5, 0.5, 0.7, and 0.9%, respectively, for 

lifetime nonsmokers. Overall, the risk for the lifetime nonsmokers was 25 times lower than for the 

lifetime smokers (Darby et al. 2006; HPA 2009). Figure 3-1 shows the cumulative absolute risk of death 

from lung cancer by age 75 years relative to long-term average in-home radon concentration for 
 

 

 

 


 


 


 


 

RADON 40 

3. HEALTH EFFECTS 

Figure 3-1. Cumulative Absolute Risk of Death from Lung Cancer by Age 

75 Years Versus Long-Term Average Radon Concentration at Home for 

Continuing Smokers, Ex-Smokers, and Lifelong Nonsmokers in the 

United Kingdom 

35
 

30
 

25
 

20 

15 

10 

5 

0 

Long-term average radon concentration, Bq m-3 

Source: adapted from HPA 2009 Cumulative lung cancer mortality by age 75 years, % 

Continuing cigarette smoker 

Cigarette smoker until age 50 years 

Cigarette smoker until age 30 years 

Lifelong nonsmoker 

0 200 400 600 800
 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 41 

3. HEALTH EFFECTS 

continuing smokers, ex-smokers, and lifelong nonsmokers in the United Kingdom, as reported by Darby 

et al. (2006) and HPA (2009). 

Assessment of the results of residential case-control studies and comparisons between the presentlyavailable pooled results of the China case-control studies (Lubin et al. 2004), North American casecontrol studies (Krewski et al. 2005, 2006), and European case-control studies (Darby et al. 2005, 2006) 

must take into account the effects of exposure measurement error and methodological differences in final 

analyses. Estimates based on measured radon concentrations will likely underestimate the true risks 

associated with residential radon, due to misclassification of exposure from detector measurement error, 

spatial radon variations within a home, temporal radon variation, missing data from previously occupied 

homes that currently are inaccessible, failure to link radon concentrations with subject mobility, and 

measuring radon gas concentration as a surrogate for radon progeny exposure (Field et al. 1996, 2002). 

Generally, if exposure misclassification does not differ systematically between cases and controls, the 

observed results tend to be biased toward the null (for example, the true effect is actually underestimated). 

In fact, Field et al. (2002) demonstrated that empirical models with improved retrospective radon 

exposure estimates were more likely to detect an association between prolonged residential radon 

exposure and lung cancer. Direct comparisons between the pooled results of the China case-control 

studies (Lubin et al. 2004), North American case-control studies (Krewski et al. 2005, 2006), and those of 

the European case-control studies (Darby et al. 2005, 2006) are problematic because only the pooled 

results of the European case-control studies included regression calibration in an attempt to adjust for 

some of the measurement error. 

Turner et al. (2011) recently reported the results of a large prospective study that found positive 

associations between ecological indicators of residential radon and lung cancer. The study included a 

cohort of 811,961 individuals from nearly 1.2 million participants recruited in 1982 for the American 

Cancer Society Cancer Prevention Study-II. The cohort encompasses 2,754 U.S. counties and 

3,493 observed lung cancer deaths as of 1988. Ecological estimates of residential radon concentrations 

were obtained from the Lawrence Berkeley National Laboratory and were intended to represent the 

average annual radon concentrations in the main living areas of homes by primary county of residence. 

The study authors reported a significant positive trend between categories of radon concentrations and 

lung cancer mortality (p=0.02), a 15% (95% CI 1–31) increase in risk of lung cancer mortality per 

100 Bq/m3

 (2.7 pCi/L) increase in radon, and a 34% (95% CI 7–68) increase in risk of lung cancer 

mortality among residents with estimated radon concentrations above the EPA guideline value of 

148 Bq/m3

 (4 pCi/L). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 42 

3. HEALTH EFFECTS 

Information regarding radon-induced lung cancer in animals exposed to radon and its progeny at 

concentrations considered relevant to human health includes significantly increased incidences of lung 

tumors in rats repeatedly exposed to radon and its progeny at cumulative exposures as low as 20– 

50 WLM (Chameaud et al. 1984; Morlier et al. 1994). These results are consistent with the demonstrated 

associations between lung cancer risk and exposure to radon and radon progeny in occupationallyexposed miners and residentially-exposed individuals. 

3.2.2 Oral Exposure 

No studies were located regarding the following health effects, other than cancer, in humans or animals 

after oral exposure to radon or its progeny: 

3.2.2.1 Death 

3.2.2.2 Systemic Effects 

3.2.2.3 Immunological and Lymphoreticular Effects 

3.2.2.4 Neurological Effects 

3.2.2.5 Reproductive Effects 

3.2.2.6 Developmental Effects 

3.2.2.7 Cancer 

Information regarding cancer in humans after exposure to radon and its progeny in water is limited to 

ecological studies. As noted earlier, ecological studies are limited by several factors that may include bias 

in estimated indoor radon levels, inadequate control of confounding, model misspecification, and 

misclassification. Radon levels were measured in 2,000 public and private wells in 14 counties in Maine 

(Hess et al. 1983). The county averages were compared to cancer rate by county to determine any degree 

of correlation. Significant correlation was reported for all lung cancer and all cancers combined, when 

both sexes were combined, and for lung tumors in females. Confounding factors (e.g., smoking) were not 

considered in this analysis. In addition, exposure from radon in these water supplies could have been by 

the inhalation route as well as the oral route. Results of some ecological studies suggest positive 

associations between radon levels in ground water sources and incidences of cancers, including lung 

cancer (Hess et al. 1983), all cancers combined (Mose et al. 1990), and childhood cancer (leukemias and 

all cancers combined) (Collman et al. 1990). In another study, Collman et al. (1988) found no consistent 

associations between radon concentrations in ground water and cancer mortality. More recent case-cohort 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 43 

3. HEALTH EFFECTS 

studies in Finland found no significant associations between mean concentrations of radon in well water 

and cases of stomach cancer (Auvinen et al. 2005) or bladder or kidney cancer (Kurttio et al. 2006). 

No studies were located regarding cancer in animals after oral exposure to radon and its progeny. 

3.2.3 Dermal Exposure 

3.2.3.1 Death 

3.2.3.2 Systemic Effects 

No studies were located regarding respiratory, cardiovascular, gastrointestinal, musculoskeletal, hepatic, 

renal, endocrine, dermal, body weight, or metabolic effects in humans or animals following exposure to 

radon and radon progeny. 

Ocular Effects. Abdelkawi et al. (2008) reported increased refractory index, increased molecular 

weight, and decreased concentration of soluble proteins in the cornea and lens of mice exposed to radon at 

a mean concentration of 55.8 kBq/m3 for 6 hours/day, 5 days/week for up to 8 weeks. Effective radon 

lung doses ranged from 20.92 to 83.68 mSv for combined dermal contact and inhaled radioactivity. 

Corneal effects were observed after 2 weeks, followed by lenticular effects (after 6 weeks). The study 

authors suggested that the corneal effects resulted from direct radon exposure and plating out of radon 

progeny on the cornea; thus, effects on both the cornea and lens might be the result of combined external 

and internal exposures. 

No studies were located regarding the following health effects in humans or animals after dermal 

exposure to radon and radon progeny: 

3.2.3.3 Immunological and Lymphoreticular Effects 

3.2.3.4 Neurological Effects 

3.2.3.5 Reproductive Effects 

3.2.3.6 Developmental Effects 

3.2.3.7 Cancer 

A statistically significant increase in the incidence of basal cell skin cancers (103.8 observed vs. 

13.0 expected) was observed in uranium miners in the Czech Republic who were exposed to radon and 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 44 

3. HEALTH EFFECTS 

radon progeny for >10 years (Ševcová et al. 1978). The study authors used the permissible concentration 

of radon progeny in the workplace air (41,000 MeV/L; approximately equal to 31.9 pCi/L) at the time of 

the study to calculate a skin contamination of 2.3±0.7 kBq/m2

 (6.22 pCi/cm2), based on total alpha 

activity per unit area from the radon progeny, for an experimental group of the miners. Assuming 

1,700 working hours per year and using a quality factor of 10 for alpha radiation, the study authors 

calculated a mean dose equivalent to the basal layer of the epidermis of 60 rem/year. The standard 

quality factor (now termed radiation weighting factor) for alpha particles is 20, which would yield an 

equivalent dose of 120 rem/year. Additionally, the study authors noted that during earlier times, 

concentrations of radon progeny in the uranium mines were up to 10 times higher than the permissible 

concentration in the late 1970s. Exposure to other agents (such as arsenic, a known dermal carcinogen 

(see Agency for Toxic Substances and Disease Registry [2007a])) in the uranium mining environment, as 

well as minor traumas of the skin, may also have contributed to the observed incidence of skin cancer. 

Increased incidences of skin cancer have not been reported in other uranium miner cohorts or for workers 

in other types of mining, such as metal or coal mines; these end points were not examined in most of 

these studies. 

Eatough and coworkers performed a series of studies designed to estimate the average dose of alpha 

radiation from radon and radon progeny to the skin under normal environmental exposure conditions in 

which airborne particles containing radon and radon progeny make dermal contact (Eatough 1997; 

Eatough and Henshaw 1992; Eatough et al. 1999). In the study of Eatough et al. (1999), results of 

personnel monitoring of airborne radon progeny 218Po and 214Po in which individuals were immersed 

under normal environmental conditions in the United Kingdom indicated that at the average radon 

concentration of 20 Bq/m3

 (0.54 pCi/L) to continuously exposed skin would result in 3,500– 

28,000 decays/cm2

/year from 218Po and 7,000–21,000 decays/cm2/year from 214Po. The results of Eatough 

and coworkers indicate a potential for radon and radon progeny to elicit skin cancer under normal 

environmental conditions. Few of the alpha particles from those decays would actually reach and expose 

the dermis since fewer than half would be released toward the body (reducing the values by more than 

50%) and most of their energy would transfer to the nonliving epidermis, leaving little to expose the 

underlying dermis. 

No studies were located regarding cancer in animals after dermal exposure to radon and its progeny. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 45 

3. HEALTH EFFECTS 

3.3 GENOTOXICITY 

Abundant information is available regarding the genotoxicity of ionizing radiation (refer to the 

Toxicological Profile for Ionizing Radiation for a detailed discussion of the genotoxic effects of various 

forms of ionizing radiation). The genotoxicity of alpha radiation from radon and its progeny has been 

investigated in underground miners, in individuals residing in homes with measured radon levels, in 

laboratory animals in vivo, and in a variety of in vitro test systems. Tables 3-6 and 3-7 present the results 

of in vivo and in vitro genotoxicity assessments, respectively. 

Increases in chromosomal aberrations have been reported in peripheral blood lymphocytes of 

underground miners exposed to relatively high levels of radon and radon progeny (Bilban and Jakopin 

2005; Brandom et al. 1978; Smerhovsky et al. 2001, 2002). Significantly increased frequency of 

micronuclei was also noted in peripheral blood lymphocytes of lead-zinc miners in the Czech Republic 

(Bilban and Jakopin 2005). Significantly increased frequency of mutations of glycophorin A was 

reported in the blood from a cohort of Radium Hill uranium miners in Australia (Shanahan et al. 1996). 

The mutation rate tended to increase with increasing radon exposure, with the exception of the most 

highly exposed group (>10 WLM); there was no clear relation between HPRT mutation rates and 

previous occupational exposure to radon. 

Several studies investigated possible associations between residential exposure to radon and radon 

progeny and genotoxic end points. Significantly increased frequency of chromosomal aberrations was 

noted in peripheral blood lymphocytes of a small group of individuals in Germany who resided in homes 

where radon concentrations were 4–60 times higher than the national average of 50 Bq/m2 (Bauchinger et 

al. 1994). The prevalence of DNA damage in peripheral blood lymphocytes was significantly associated 

with increased residential radon levels at airborne levels exceeding 200 Bq/m3

; no correlation was seen in 

comparisons of DNA damage to levels of radon in the drinking water for these same individuals, at levels 

drinking water ranging from 10 to 2,410 Bq/L (Hellman et al. 1999). Results of one small study of 

20 individuals indicated a positive association between HPRT mutations in peripheral blood lymphocytes 

and measured radon levels (Bridges et al. 1991). However, a subsequent assessment by the same 

investigators using a larger number of exposed subjects (n=66) found no significant positive or negative 

association between HPRT mutation rates and indoor radon levels (Cole et al. 1996). Radon did not 

induce increased HPRT mutation rates in another study of a small group (n=11) of residentially-exposed 

subjects (Albering et al. 1992). No significant increase in the frequency of chromosomal aberrations was 
 

 

 

 

 

	 

	 

	 

	 


 


 

	 


 


 


 

	 


 


 


 

	 
 


 

	 


 


 

	 

	 


 


 

	 


 


 


 


 


 


 


 

	 

	 

	 

	 

	 


 


 

	 


 


 


 

	 


 


 


 

	 
 


 

	 


 


 

	 

	 


 


 

	 


 


 


 


 


 


 


 

	 

	 

	 

	 

	 


 


 

	 


 


 


 

	 


 


 


 

	 
 


 

	 


 


 

	 

	 


 


 

	 


 


 


 


 


 


 


 

	 

RADON	 46 

3. HEALTH EFFECTS 

Table 3-6. Genotoxicity of Radon and Radon Progeny In Vivo 

Species (test system) End point	 Results Reference 

Mammalian systems: 

Human (peripheral Chromosomal aberrations +	 Bauchinger et al. 1994; Bilban and 

blood lymphocytes)	 Jakopin 2005; Brandom et al. 1978; 

Hellman et al. 1999; Pohl-Rüling and 

Fischer 1979, 1982; Pohl-Rüling et al. 

1976; Smerhovsky et al. 2001, 2002; 

Stenstrand et al. 1979 

Human (peripheral Chromosomal aberrations – Maes et al. 1996
 

blood lymphocytes)
 

Human (peripheral Micronuclei +	 Bilban and Jakopin 2005 

blood lymphocytes)
 

Human (peripheral Gene mutations (HPRT) – Shanahan et al. 1996
 

blood lymphocytes)
 

Human (peripheral Gene mutations (HPRT) –	 Cole et al. 1996 

blood lymphocytes)
 

Human (peripheral Gene mutations (HPRT) – Albering et al. 1992
 

blood lymphocytes)
 

Human (whole blood)	 Gene mutations + Shanahan et al. 1996
 

(glycophorin A)
 

Human (lymphocytes) DNA repair +	 Tuschl et al. 1980 

Rat (tracheal Chromosomal aberrations + Brooks et al. 1992
 

epithelial cells)
 

Rabbit (somatic cells) Chromosomal aberrations –	 Leonard et al. 1981 

Mouse (bone marrow) Chromosomal aberrations +	 Abo-Elmagd et al. 2008 

Rat (alveolar Micronuclei + Taya et al. 1994
 

macrophages)
 

Rat (lung fibroblasts) Micronuclei +	 Brooks et al. 1994; Khan et al. 1994, 

1995
 

Syrian hamster (lung Micronuclei + Khan et al. 1995
 

fibroblasts)
 

Chinese hamster Micronuclei + Khan et al. 1995
 

(lung fibroblasts)
 

Mouse (red blood Micronuclei + Abo-Elmagd et al. 2008
 

cells)
 

Rat (bone marrow) Sister chromatid exchanges +	 Poncy et al. 1980 

– = negative result; + = positive result 
 

	 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

RADON	 47 

3. HEALTH EFFECTS 

Table 3-7. Genotoxicity of Radon and Radon Progeny In Vitro 

Result 

Species (test With Without 

system) End point activation activation Reference 

Mammalian cells: 

Human 

(blood lymphocytes)
 

Human 

(blood lymphocytes)
 

Human 

(fibroblasts)
 

Chinese hamster
 

(ovary AA8 cells)
 

Chinese hamster
 

(ovary EM9 cells)
 

Chinese hamster
 

(ovary K-1 cells)
 

Chinese hamster
 

(ovary xrs-5 cells)
 

Chinese hamster
 

(ovary K-1 cells)
 

Chinese hamster
 

(ovary xrs-5 cells)
 

Chinese hamster
 

(ovary AA8 cells)
 

Chinese hamster
 

(ovary EM9 cells)
 

Chinese hamster
 

(ovary C18 cells)
 

Mouse 

(L5178Y cells)
 

Chromosomal aberrations 

Chromosomal aberrations 

Chromosomal aberrations 

Chromosomal aberrations 

Chromosomal aberrations 

Chromosomal aberrations 

Chromosomal aberrations 

Gene mutations 

Gene mutations 

Gene mutations 

Gene mutations 

Gene mutations 

Gene mutations 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

+	 Wolff et al. 1991 

+	 Hamza and Mohankumar 

2009 

+	 Loucas and Geard 1994 

+	 Schwartz et al. 1990 

+	 Schwartz et al. 1990 

+	 Shadley et al. 1991 

–	 Shadley et al. 1991 

+	 Shadley et al. 1991 

+	 Shadley et al. 1991 

+	 Schwartz et al. 1990 

+	 Schwartz et al. 1990 

+	 Jostes et al. 1994 

+	 Evans et al. 1993a, 1993b 

C = negative result; + = positive result 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 48 

3. HEALTH EFFECTS 

found in another small group (n=22) of subjects with residential exposure to radon at concentrations in 

the range of 50–800 Bq/m3

 (Maes et al. 1996). 

Increases in chromosomal aberrations were reported among spa-house personnel and in area residents in 

Badgastein, Austria, who were chronically exposed to radon and radon decay products present in the 

environment (Pohl-Rüling and Fischer 1979, 1982; Pohl-Rüling et al. 1976). A study by Tuschl et al. 

(1980) indicated a stimulating effect of repeated low-dose in vitro ultraviolet or beta irradiation on DNA 

repair in lymphocytes of persons occupationally exposed to radon (3,000 pCi/L of air [1.1x105 Bq/m3

]). 

The study authors suggested that this “stimulating” effect of either type of radiation might be attributable 

to induction of de novo synthesis of repair enzymes. They noted that an error-free repair pathway for 

DNA involving de novo synthesis of proteins had been reported in Escherichia coli, and that miners 

exposed to radon in Badgastein (a community with elevated levels of background radiation) had fewer 

chromosomal aberrations than the public despite being exposed to more radiation. 

An increase in chromosomal aberrations in lymphocytes was observed in 18 Finnish people of different 

ages chronically exposed to radon in household water at concentrations of 2.9x104

–1.2x106 pCi radon/L 

of water (1.1x103

–4.4x104 Bq/L) compared with people who did not have a history of exposure to high 

radon levels (Stenstrand et al. 1979). This study also indicated that the frequencies of chromosomal 

aberrations and multiple chromosomal breaks were more common in older people than in younger people 

exposed to radon. Although the radon was in household water, it is probable that much of this radon 

volatilized and was available to be inhaled. Therefore, this route of exposure includes both oral and 

inhalation routes. 

Available in vivo animal data generally support the human data. Significantly increased frequency of 

micronuclei was observed in lung fibroblasts of Wistar rats, Syrian hamsters, and Chinese hamsters that 

inhaled radon and radon progeny; cumulative exposures were 115–323 WLM for the rats, 126–278 WLM 

for the Syrian hamsters, and 496 WLM for the Chinese hamsters (Khan et al. 1994, 1995). The Chinese 

hamsters appeared to be 3 times more sensitive than rats. Significantly increased frequency of 

chromosomal aberrations was noted in tracheal epithelial cells of F-344/N rats that had inhaled radon and 

radon progeny at cumulative exposures of 900 or 1,000 WLM (Brooks et al. 1992). Abo-Elmagd et al. 

(2008) exposed Swiss albino mice to airborne radon from a pitchblende powder source for 5–25 weeks at 

concentrations resulting in accumulated radon doses in the range of 13.01–65.05 WLM and reported 

exposure-related increased structural chromosomal aberrations and decreased mitotic index in bone 

marrow cells and increased micronuclei in red blood cells. Brooks and coworkers (Brooks et al. 1994) 
 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 49 

3. HEALTH EFFECTS 

reported significantly increased frequency of micronuclei in lung fibroblasts of Wistar rats exposed to 

radon at levels resulting in cumulative exposures ranging from 115 to 320 WLM. Significantly increased 

frequency of alveolar macrophages with micronuclei was observed in rats exposed to radon and its 

progeny at levels designed to give cumulative exposures ranging from 120 to 990 WLM (Taya et al. 

1994). Evidence of chromosomal aberrations was equivocal in two rabbit studies. Rabbits exposed to 

high natural background levels of radon (12 WLM) for over 28 months displayed an increased frequency 

of chromosomal aberrations (Leonard et al. 1981). However, when a similar study was conducted under 

controlled conditions (10.66 WLM), chromosomal aberrations were not found. According to the authors, 

the increased chromosomal aberrations in somatic cells of rabbits exposed to natural radiation were 

mainly due to the gamma radiation from sources other than radon. Exposure of Sprague-Dawley male 

rats to radon at cumulative doses as low as 100 WLM resulted in an increase in sister chromatid 

exchanges (SCEs) in bone marrow by 600 days postexposure (Poncy et al. 1980). At 750 days 

postexposure, the number of SCEs reached 3.21 per cell. The SCEs in the 500 and 3,000 WLM groups 

reached constant values of 3.61 and 4.13 SCEs per cell. In the high-dose group (6,000 WLM), SCEs 

continued to increase from 100 to 200 days after exposure, reaching a mean value of 3.5 SCE per cell. In 

controls, SCEs were constant with age (2.4 per cell). 

The genotoxicity of radon and radon progeny has been assessed in a variety of mammalian cells in vitro. 

Chromosomal aberrations were reported in human blood lymphocytes (Hamza and Mohankumar 2009; 

Wolff et al. 1991) and human fibroblasts (Loucas and Geard 1994). Hamza and Mohankumar (2009) 

noted increasing frequency of chromosomal aberrations with increasing radon dose (range 0–0.127 Gy 

and dose rate (range 5.4x10-8–7.08x10-4 Gy/min) for 3-hour exposures. Exposure of Chinese hamster 

ovary (CHO) cells to the radon daughter, bismuth-212 (212Bi) caused chromosomal aberrations and gene 

mutations (Schwartz et al. 1990; Shadley et al. 1991). Gene mutations were induced by irradiation of 

CHO cells with radiation from radon (Jostes et al. 1994). Another study employed an isotope of helium 

(

4

He) to simulate alpha particles from radon progeny and found exposure-induced gene mutations (Jin et 

al. 1995). Gene mutations were also induced in mouse L5178Y lymphoblasts exposed to alpha radiation 

from radon (Evans et al. 1993a, 1993b). 

3.4 TOXICOKINETICS 

In radiation biology, the term dose has a specific meaning. Dose refers to the amount of radiation 

absorbed by the organ or tissue of interest and is expressed in rad (grays). Estimation of this radiation 

dose to lung tissue or specific cells in the lung from a given exposure to radon and radon progeny is 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 50 

3. HEALTH EFFECTS 

accomplished by modeling the sequence of events involved in the inhalation, deposition, clearance, and 

decay of radon progeny within the lung. While based on the current understanding of lung morphometry 

and experimental toxicokinetics data on radon and radon progeny, different models make different 

assumptions about these processes, thereby resulting in different estimates of dose and risk. These 

models are described in numerous reports including ICRP (1982), NEA/OECD (1983), NCRP (1984a), 

Bair (1985), James (1987), EPA (1988), and NAS (1988). 

The focus of this section is on describing the empirical basis for our understanding of the toxicokinetics of 

radon. Physiologically-based models of radon toxicokinetics used in radon radiation dosimetry are 

described in Section 3.4.5. A complete discussion of toxicokinetics of radon as it relates to the 

development of adverse health effects in exposed populations (e.g., respiratory tract cancer) must consider 

not only the physical trapping of the attached fraction of radon progeny in the respiratory tract, but also the 

toxicokinetics of radon progeny, both of which contribute to the internal radiation dose that occurs in 

association with exposures to radon. While radioactive decay of the short-lived radon progeny, contribute 

most of the radiation dose to the respiratory tract following exposures to radon, they are sufficiently longlived, relative to rates of toxicokinetics processes that govern transport and distribution, to exhibit 

radionuclide-specific toxicokinetics. Rather than providing a detailed review of the toxicokinetics of each 

element in the uranium and thorium decay chains leading to the production of radon and radon progeny 

elements (uranium, thorium, radium, astatine, polonium, bismuth, lead, and thallium) in this profile, the 

reader is referred to relevant literature on the toxicokinetics of the most widely-studied of these elements, 

including uranium (Agency for Toxic Substances and Disease Registry 2011; ICRP 1995a, 1995b); 

thorium (Agency for Toxic Substances and Disease Registry 1990b; ICRP 1995a, 1995b); radium (Agency 

for Toxic Substances and Disease Registry 1990a; ICRP 1992, 1995b); polonium (ICRP 1992, 1995b; 

NCRP 1980), lead (Agency for Toxic Substances and Disease Registry 2007b; ICRP 1992, 1995b), and 

thallium (Agency for Toxic Substances and Disease Registry 1992). The longer-term fate of radon 

progeny in the body will be reflected in the toxicokinetics of longer-lived progeny, which include 210Pb 

(radioactive half-life of approximately 22.2 years) and 206Pb (stable end product of the 222Rn decay chain). 

The reader is referred to the Toxicological Profile for Lead (Agency for Toxic Substances and Disease 

Registry 2007b) for a discussion of the toxicokinetics of lead. A further complication in relating radon 

toxicokinetics to adverse health effects associated with exposure to radon is that radon progeny are present 

with radon in the environment and are inhaled or ingested along with radon. Progeny formed in the 

environment contribute substantially to radiation dose associated with environments that contain radon gas 

(Kendall and Smith 2002). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 51 

3. HEALTH EFFECTS 

3.4.1 Absorption 

3.4.1.1 Inhalation Exposure 

Inhalation exposures to radon deliver the gas and its progeny (e.g., 214Bi, 214Pb, 210Pb, 218Po, and 210Po; 

some attached to atmospheric particles and the rest unattached) into the respiratory tract (Marsh and 

Birchall 2000). Longer-lived radon progeny (e.g., 210Pb and 210Po) contribute little to the radiation dose to 

lung tissue because they have a greater likelihood of being physically cleared from the lung by 

mucociliary or cellular transport mechanisms before they can decay and deliver a significant radiation 

dose. 

Progeny aerosol formation involves distinct physical-chemical processes (Butterweck et al. 2002; 

El-Hussein et al. 1998; Ishikawa et al. 2003b): (1) immediately after formation, progeny react with gases 

and vapors and form clusters, referred to as unattached particles, having diameters of approximately 0.5– 

3 nm or (2) unattached particles form complexes with other aerosols or particles in air to form attached 

particles, which can undergo hygroscopic growth to achieve diameters ranging from approximately 50 to 

1,500 nm. The magnitude of the unattached fraction in inhaled air depends on the concentration and size 

distribution of aerosols in the ambient environment, and will vary with the exposure conditions (e.g., 

indoor, outdoor) and activities of the individual (e.g., sleeping, activities that release particulates into the 

air) (Marsh and Birchall 2000). The sizes and size distributions of attached particles in smoker homes 

and mines can be approximately the same, while the particle sizes are smaller in nonsmoker residences 

(HPA 2009). The unattached fraction for typical indoor environments has been estimated to be 5–20% 

(Porstendörfer 1994, 2001), while EPA assumes 50%. Smoking and other aerosol-generating activities 

(e.g., vacuum cleaning, cooking, fireplace and circulating fan usage) will increase the attached fraction, 

which correspondingly increases the dose (Sun 2008). 

Deposition and the subsequent absorption of inhaled radon and radioactive decay progeny are influenced 

by physiological factors as well as chemical and physical characteristics of the radionuclides, carrier 

aerosols, and atmospheric particles. Radon is a nonreactive noble gas, and deposition and absorption will 

be determined by Brownian motion, its solubility in lung fluids, its permeability at the lung:circulating 

blood interface, and blood flow to the lungs. The blood:air partition coefficient for radon has been 

estimated to be approximately 0.4 (Nussbaum and Hursh 1957; Sharma et al. 1997); therefore, at steadystate, the blood concentration of radon will be approximately 0.4 times the concentration of radon in lung 

air. Assuming rapid (i.e., near-instantaneous) partitioning of radon between air and blood, the absorption 

clearance of radon gas from air in the lung will be governed by the blood flow to the lung (i.e., absorption 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 52 

3. HEALTH EFFECTS 

rate will be flow-limited). At a blood flow to the lung of 5.3 L/minute in an adult, and lung air volume of 

2.82 L, the t1/2 for absorption of radon from lung to blood would be approximately 0.4 min (rate 

constant=113 hours-1) (Peterman and Perkins 1988). A similar value was estimated for the t1/2 for 

clearance of radon gas from the lung air to external air (t1/2=0.4 minute; rate constant=115 hours-1) 

(Peterman and Perkins 1988). Rapid clearance of radon gas from the lung by absorption and exhalation 

will result in steady-state concentrations of radon in blood within 2–3 minutes of initiating exposure to 

radon gas. Clearance of radon from the blood following removal from exposure will be governed by 

blood flow rates to major tissue depots for radon (see Section 3.4.2). 

Exposures to radon in air occur along with exposures to aerosols of radon progeny, which will deposit on 

the lung epithelia. The amounts and location of deposition of radon progeny will be determined by 

factors that influence convection, diffusion, sedimentation, and interception of particles in the airways. 

These factors include air flow velocities, which are affected by breathing rate and tidal volume; airway 

geometry; and aerosol particle size (Cohen 1996; James et al. 1994; Kinsara et al. 1995; Marsh and 

Birchall 2000; Yu et al. 2006). Radon progeny consist of a mixed distribution of unattached and attached 

particles. Assuming activity median aerodynamic diameters (AMAD) of approximately 1–3 nm for the 

unattached fraction and 100–200 nm for attached particles (Butterweck et al. 2002; Ishikawa et al. 

2003b), deposition fractions of inhaled radon progeny can be estimated from models of particle 

deposition in the human respiratory tract (ICRP 1994b). The deposition fraction (i.e., percent of total 

number of inhaled particles that deposit) for unattached particles is predicted to be approximately 97– 

99%, with most of the deposition (70–80%) occurring in the extrathoracic region of the respiratory tract. 

The deposition fraction for attached particles is predicted to be approximately 20–40% with most of the 

deposition occurring in the alveolar region. Deposition will occur more predominantly in the nasal 

airways when breathing occurs through the nose. These predictions are based on the ICRP (1994b) 

human respiratory tract model assuming recommended values for deposition fractions for adult members 

of the general public exposed to homogeneous aerosols, and will vary with different assumptions for 

breathing rate and ratio of nose-to-mouth breathing (ICRP 2001). Predictions that deposition will be 

higher for the unattached fraction compared to the attached fraction and higher for nose-breathing 

exposures are in reasonable agreement with experiments conducted in humans exposed to heterogeneous 

distributions of aerosols of radon progeny (Booker et al. 1969; George and Breslin 1967, 1969; Holleman 

et al. 1969; Hursh and Mercer 1970; Hursh et al. 1969a; Ishikawa et al. 2003b; Pillai et al. 1994; Swift 

and Strong 1996) and with experiments conducted using casts of the human respiratory tract 

(Chamberlain and Dyson 1956; Cohen 1996; Kinsara et al. 1995; Martin and Jacobi 1972). The 

deposition fraction in subjects who inhaled (nose-only) 0.5–0.6-nm particles of 218Po was estimated to be 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 53 

3. HEALTH EFFECTS 

approximately 94–99% (Swift and Strong 1996). Near complete deposition (>99%) was observed in an 

adult subject who inhaled (mouth-only) unattached particles of 212Pb formed from decay of 220Rn in a low 

ambient aerosol environment, whereas the deposition fraction was 34–60% when the exposure was to 

aerosols formed in room air and having a particle size range of 50–500 nm, more typical of attached 

particles (Booker et al. 1969). Deposition fractions for radon progeny have been measured during 

exposures to aerosols in underground uranium mines (George and Breslin 1969; Holleman et al. 1969). 

Deposition fractions increased with increasing tidal volume, and decreased with increasing aerosol 

aerodynamic diameter, from 50–70% for diameters <10 nm to 30–40% for diameters >70 nm. Hursh and 

Mercer (1970) estimated thoracic deposition (i.e., total of bronchi, bronchioles, and alveolar region) based 

on external gamma counting of the chest area of 212Pb produced from decay of 220Rn and inhaled (mouthonly) as aerosols having AMADs of 20–25 or 200–230 nm. The deposition fractions in adult subjects 

were approximately 50–62% for the smaller particles and 27–38% for the larger particles. When adult 

subjects inhaled (mouth-only) natural 212Pb aerosols generated from 220Rn decay in room air, the 

measured deposition fractions ranged from 14–45% (Hursh et al. 1969a). Pillai et al. (1994) made chest 

gamma measurements on four subjects who were exposed to 212Pb aerosols for 10–60 minutes in a 

thorium hydroxide storage facility. The particle size of the 212Pb aerosol was approximately 90 nm. 

Deposition fraction was estimated to have been 55–76%. 

Particles containing radon progeny that deposit in the respiratory tract are subject to three general 

clearance processes: (1) mucociliary transport to the gastrointestinal tract for progeny deposited in the 

ciliated airways (i.e., trachea, bronchi, and bronchioles); (2) phagocytosis by lung macrophages and 

cellular transport to lymph nodes (e.g., lung, tracheobronchial, mediastinal); or (3) absorption and transfer 

by blood and/or lymph to other tissues. The above processes apply to all forms of deposited radon 

progeny, although the relative contributions of each pathway and rates associated with each pathway may 

vary with the physical characteristics (e.g., particle size), chemical form (degree of water solubility), and 

radiological characteristics (e.g., specific activity). 

Absorption half-times (t1/2) have been estimated for radon decay progeny in adults who inhaled aerosols 

of lead and bismuth isotopes generated from decay of 220Rn or 222Rn. Values for 212Pb and 212Bi in an 

aerosol having an activity median particle diameter of approximately 160 nm (range 50–500 nm), a value 

typical of attached radon progeny particles, were estimated to be approximately 10 and 13 hours, 

respectively (Marsh and Birchall 1999). The latter estimates were based on an analysis of data from 

human inhalation exposures to 212Pb and 212Bi progeny of 220Rn (Booker et al. 1969; Hursh and Mercer 

1970; Hursh et al. 1969a; Jacobi 1964; Pillai et al. 1994). However, absorption of unattached radon 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 54 

3. HEALTH EFFECTS 

progeny may be faster than that of attached progeny. Butterweck et al. (2002) exposed nose- or mouthbreathing human subjects to 222Rn-derived aerosols that had diameters of approximately 0.3–3 nm, typical 

of unattached progeny particles. Absorption half-times were estimated to be approximately 68 minutes 

(range 56–86) for 218Po/214Pb and 18 minutes (range 17–21) for 214Bi. Binding of unattached radon 

progeny in the respiratory tract may result in slower absorption kinetics. Butterweck et al. (2002) 

proposed that a 10-hour t1/2 would apply to the unattached fraction after binding in the respiratory tract, 

and that the unbound fraction may have an absorption t1/2<10 minutes. This behavior would be consistent 

with dissolution of deposited particles being the rate-limiting step in absorption and smaller particles 

dissolving faster than larger particles. 

3.4.1.2 Oral Exposure 

Exposure to radon by the oral route can occur as a result of radon gas dissolving in water. At equilibrium, 

the concentration of radon dissolved in water will be approximately 0.25 of that in air (i.e., Henry’s law 

constant=4.08 at 20 °C) (NAS 1999b). Radioactive decay of radon in water produces radon progeny; 

therefore, ingestion of water containing dissolved radon will also result in ingestion of radon progeny. 

Absorption of radon is thought to occur primarily in the stomach and small intestine, although some 

absorption may also occur in the large intestine (Ishikawa et al. 2003a; Khursheed 2000; NAS 1999b). 

Radon is relatively nonreactive and its absorption from the stomach will be determined largely by rates of 

diffusion of radon from stomach contents to vascularized mucosa; its solubility in the stomach tissues and 

blood; blood flow to the stomach; and rates of transfer of stomach contents into the intestine (Ishikawa et 

al. 2003a; NAS 1999b). Diffusion of radon from stomach contents to stomach tissues may be ratelimiting in absorption (NAS 1999b). However, assuming rapid (i.e., near-instantaneous) partitioning of 

radon from vascularized mucosa to blood, the absorption clearance of radon from stomach mucosa will be 

governed by the blood flow rate to the stomach (i.e., absorption rate will be flow-limited). At a stomach 

blood flow of 1% of cardiac output (1% of 6.5 L/minute in an adult), and stomach wall volume of 

approximately 0.15 L (NAS 1999b), the t1/2 for absorption of radon from the stomach wall to blood would 

be approximately 1.6 minutes (rate constant=0.43 minute-1). An absorption t1/2 of 1–2 minutes is 

consistent with observations of peak blood radon concentrations and peak radon concentrations in exhaled 

air within 5 minutes following ingestion of radon in water by adults (Brown and Hess 1992; Hursh et al. 

1965; Sharma et al. 1997). 

Kinetics of absorption of radon progeny are more complex, reflecting different mechanisms (e.g., 

membrane cation transport proteins and channels) and sites of absorption for radon and progeny. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 55 

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Absorption of radon progeny following oral exposure is thought to occur largely in the small intestine 

(Agency for Toxic Substances and Disease Registry 2007b; ICRP 1994c). As a result, absorption of 

ingested progeny, and progeny formed from radon after ingestion, will be influenced by rates of transfer 

of stomach contents into the small intestine, as well as rates of absorption of progeny from the small 

intestine. Ishikawa et al. (2003a) used external gamma counting to measure the kinetics of elimination of 

214Pb and 214Bi from the stomach following ingestion of water containing radon. Elimination kinetics 

from the stomach exhibited multiple components, with a fast phase (40–50% of ingested activity) having 

a t1/2 value of approximately 10 minutes and two slower phases having t1/2 values of 150 and 240 minutes. 

The presence of food in the stomach delays stomach emptying and may alter the absorption kinetics of 

radon and progeny (Brown and Hess 1992; Hursh et al. 1965; Suomela and Kahlos 1972). ICRP (1995c, 

2001) recommends values of 0.05 and 0.1 as gastrointestinal absorption fractions for bismuth and 

polonium, respectively. The absorption fraction for ingested inorganic lead varies with age; from 40 to 

50% in infants and children to approximately 8–15% in adults (Agency for Toxic Substances and Disease 

Registry 2007b; Leggett 1993; O’Flaherty 1993). 

3.4.1.3 Dermal Exposure 

Data regarding the absorption of radon following dermal exposure are very limited. Dermal absorption of 

radon has been measured in subjects after bathing in a radon-water spa (Furuno 1979; Pohl 1965) or after 

application of a radon-containing ointment to the intact skin (Lange and Evans 1947). After bathing for 

5–15 minutes, radon concentrations in expired air reached approximately 0.9% of that in the water and 

ranged from 17.9 to 49.1 pCi/L of air (662–1,817 Bq/m3

) compared to pre-bath levels of <1 pCi/L of air 

(37 Bq/m3

). Radon concentrations in the water were reported by the authors as 5,800 pCi (215 Bq)/kg. 

However, the relative contributions of the dermal and inhalation routes of absorption cannot be 

determined in these studies (Furuno 1979). Radon concentrations in blood reached 0.85–1% of the radon 

concentration in the bath water, which was 1.8x105

 pCi (4.9x106 Bq)/L of water after 30–40 minutes of 

bathing while breathing compressed air (Pohl 1965). Approximately 4.5% of the radon applied in 

ointment to intact skin was measured in expired air within 24 hours following application (Lange and 

Evans 1947). 

Peterman and Perkins (1988) proposed a model for simulating the absorption of radon, based on a model 

largely parameterized to simulate absorption of xenon gas through the skin. Although parameter values 

for radon were not reported and skin penetration of radon was not modeled, the general structure is 

potentially relevant to estimating radon absorption rates. In the Peterman and Perkins (1988) model, the 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 56 

3. HEALTH EFFECTS 

rate-limiting step in dermal absorption was considered to be the diffusion of xenon through the skin to the 

subcutaneous fat. Transfer from subcutaneous fat to blood was assumed to be flow-limited and 

determined by blood flow to subcutaneous fat. Peterman and Perkins (1988) estimated the dermal 

diffusion rate of xenon to be approximately 0.18 hour-1 . This rate would be equivalent to a t1/2 value of 

approximately 4 hours and is substantially slower than the t1/2 for absorption from lung (t1/2=0.4 minutes; 

rate constant=115 hours-1) (Peterman and Perkins 1988). The corresponding t1/2 value for absorption from 

subcutaneous fat was approximately 38 minutes (rate=0.018 minute-1), assuming a blood flow of 

0.16 L/minute and a tissue volume of 8.2 L. 

3.4.2 Distribution 

3.4.2.1 Inhalation Exposure 

Based on studies conducted in animals, the distribution of absorbed radon appears to reflect its solubility 

in water and fat. Nussbaum and Hursh (1957) exposed rats to radon gas in an enclosed exposure chamber 

(whole body) for periods of 30 minutes to 48 hours and measured tissue radon levels at the conclusion of 

the exposure. The highest radon concentrations were observed in fat. Tissue:air concentration ratios 

were as follows (mean±standard error [SE]): omental fat 4.83±0.07, venous blood 0.405±0.016, brain 

0.309±0.008, liver 0.306±0.004, kidney 0.285±0.012, heart 0.221±0.013, testis 0.184±0.007, and skeletal 

muscle 0.154±0.005. Tissue:air ratios for soft tissues reported by Nussbaum and Hursh (1957) are close 

to those expected for a Henry’s law constant of 4 (i.e., water:air=0.25) and a lipid:air partition coefficient 

of 6 (Nussbaum and Hursh 1957). For example, assuming fat and water contents of soft tissue of 5 and 

70%, respectively, in the rat (Davies and Morris 1993), the tissue:air ratio for soft tissue would be 

approximately 0.36 if solubility in water and fat were the only determinants of tissue radon levels. The 

corresponding fat:air ratio would be 5.85 for a lipid content of adipose tissue of 80% and water content of 

15%. The tissue:air ratios reported in Nussbaum and Hursh (1957) are the bases of tissue:blood partition 

coefficients that have been used in various biokinetics models (e.g., Khursheed 2000; NAS 1999b; 

Peterman and Perkins 1988; Sharma et al. 1997). 

Nussbaum and Hursh (1957) also reported information on the kinetics of uptake of inhaled radon in 

tissues. In all tissues studied, except fat, steady-state levels of radon were achieved within 1 hour of 

initiating a continuous inhalation exposure. Uptake into omental fat was slower and exhibited fast and 

slow components having t1/2 values of 21 and 138 minutes, respectively. The slower uptake kinetics of fat 

may reflect, in part, the relatively slower blood perfusion of adipose tissue (per unit mass of tissue) 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 57 

3. HEALTH EFFECTS 

compared to other soft tissues. Similarly, relatively slow perfusion of fat should contribute a slower 

component to total body elimination kinetics following cessation of exposure to radon (see Section 3.4.3). 

Information about the distribution of absorbed radon progeny, bismuth, lead, and polonium can be found 

in reviews of these subjects (Agency for Toxic Substances and Disease Registry 2007b; ICRP 1980, 

1994c, 1995c). A relatively large fraction of inhaled 212Pb (inhaled as natural 212Pb aerosols generated 

from 220Rn decay in room air) distributes to red blood cells (Booker et al. 1969; Hursh et al. 1969a). Red 

cell 212Pb burdens, expressed as percent of the lead initially deposited in the respiratory tract, increased 

from approximately 5% within 1–2 hours following exposure to approximately 50% at times >24 hours 

following exposure (Hursh et al. 1969a). Long-lived (210Pb) and stable progeny (206Pb, 207Pb, and 208Pb), 

can be expected to deposit and be retained in bone, where approximately 90% of the total lead body 

burden resides (Agency for Toxic Substances and Disease Registry 2007b). Following chronic exposure 

in humans, 210Pb has been found in bone (Black et al. 1968; Blanchard et al. 1969; Cohen et al. 1973; Fry 

et al. 1983) and teeth (Clemente et al. 1982, 1984). ICRP (1980, 2001) recommends, for the purpose of 

modeling bismuth-derived radiation doses, that 40% of absorbed bismuth distributes to kidneys and 30% 

to other tissues; the remaining 30% is assumed to be excreted rapidly and does not contribute to 

distribution beyond the central compartment. Retention in kidneys and other tissues are assumed to be 

the same (elimination t1/2 values of 0.6 and 5 days for fast and slow phases); therefore, approximately 

40% of the body burden of bismuth would be in the kidneys. ICRP (1994c, 2001) recommends the 

following values for percentages of absorbed polonium distributed to tissues: 30% liver, 10% kidney, 

10% red marrow, 5% spleen, and 45% other tissues. Retention in all tissues is assumed to be the same 

(elimination t1/2=50 days); therefore, the latter percent distributions will reflect the distribution of the 

body burden of polonium (e.g., 30% in liver). 

3.4.2.2 Oral Exposure 

Measurements of the tissue distribution of radon or progeny following ingestion of radon have not been 

reported. However, as discussed in Section 3.4.2.1, the distribution of absorbed radon appears to reflect 

its solubility in water and fat; therefore, steady-state distribution following absorption from the 

gastrointestinal tract would be determined by tissue:blood partition coefficients and the rate of approach 

to steady state would be determined by tissue blood flows. Based on tissue:air ratios reported by 

Nussbaum and Hursh (1957) during inhalation exposures of rats (see Section 3.4.2.1 for further 

discussion), the following tissue:blood ratios (i.e., tissue:blood=tissue:air/blood:air) can be estimated for 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 58 

3. HEALTH EFFECTS 

radon in the rat: omental fat 12, brain 0.76, liver 0.76, kidney 0.70, heart 0.55, testes 0.45, and skeletal 

muscle 0.38. Therefore, the highest concentrations of radon would be predicted for adipose tissues. 

Distribution of absorbed radon progeny would be expected to be similar to the distribution following 

inhalation exposures, although, first-pass delivery to the liver from the gastrointestinal tract may influence 

the tissue distribution. As discussed in Section 3.4.2.1, the largest fractions of the body burdens for radon 

progeny would be expected to be found in bone for lead, kidney for bismuth, and liver for polonium 

(Agency for Toxic Substances and Disease Registry 2007b; ICRP 1980, 1994c, 2001). 

3.4.2.3 Dermal Exposure 

No studies were located regarding distribution in humans or laboratory animals after dermal exposure to 

radon or its progeny. However, as discussed in Sections 3.4.2.1 and 3.4.2.2, the distribution of absorbed 

radon appears to reflect its solubility in water and fat; therefore, steady-state distribution following 

absorption from the skin would be determined by tissue:blood partition coefficients and the rate of 

approach to steady state would be determined by tissue blood flows. 

3.4.3 Metabolism 

Radon is an inert noble gas that does not interact chemically with cellular macromolecules. Radon does 

not undergo metabolism in biological systems. 

3.4.4 Elimination and Excretion 

3.4.4.1 Inhalation Exposure 

Measurements of exhaled radon following ingestion of radon dissolved in water indicate that absorbed 

radon is rapidly excreted in exhaled air (see Section 3.4.4.2). Inhaled 212Pb is excreted in urine and feces. 

Hursh et al. (1969a) estimated that, following inhalation of natural 212Pb aerosols generated from 220Rn 

decay in room air, 3% of the amount initially deposited in the respiratory tract was excreted in urine per 

day and approximately 3%/day was excreted in feces. Longer-term kinetics of excretion of 210Pb 

following chronic exposures to radon progeny may be contributed from slow release of 210Pb accumulated 

in bone (Black et al. 1968). Additional information on the elimination of inhaled radon progeny can be 

found in reviews of the biokinetics of bismuth, lead, and polonium (Agency for Toxic Substances and 

Disease Registry 2007b; ICRP 1980, 1994c, 2001). ICRP (1995c, 2001) recommends the following 

values for the purpose of modeling bismuth-derived radiation doses: a urine:fecal excretion ratio of 1:1 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 59 

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and elimination t1/2 values of 0.6 (60% of issue burden) and 5 days (40% of tissue burden) for fast and 

slow phases, respectively. ICRP (1995c, 2001) recommends the following values for elimination of 

polonium from tissues into urine and feces: a urine:fecal excretion ratio of 1:2 and an elimination t1/2 

value of 50 days. 

3.4.4.2 Oral Exposure 

Measurements of exhaled radon following ingestion of radon dissolved in water indicate that exhaled air 

is the dominant route of excretion of ingested radon (Brown and Hess 1992; Gosink et al. 1990; Hursh et 

al. 1965). Biological elimination kinetics of absorbed radon in exhaled air exhibit multiple phases, with 

the first half-time ranging from 15 to 80 minutes (Brown and Hess 1992; Gosink et al. 1990; Hursh et al. 

1965). Hursh et al. (1965) estimated the following t1/2 values for fast, moderate and slow phases of 

biological elimination: approximately 13 minutes (61% of body burden), 19 minutes (34%), and 

207 minutes (5%), respectively; 95% of the dose was eliminated within 100 minutes. The slow phase of 

elimination is consistent with observations made in rats of relatively slow accumulation of radon in 

adipose tissue during continuous inhalation exposures to radon (Nussbaum and Hursh 1957). The latter 

t1/2 values were estimated for subjects who ingested radon in water during fasting. In a subject who 

ingested radon in water with a meal, moderate and slow phases of elimination appeared to be delayed, 

with approximate t1/2 values of 12 minutes (39% of body burden), 60 minutes (51%), and 300 minutes 

(10%), respectively. Slowing of elimination when radon is ingested with a meal or with lipid has been 

observed in several studies and may be related to a delay in stomach emptying that alters the absorption 

kinetics of radon and progeny (Brown and Hess 1992; Hursh et al. 1965; Meyer 1937; Suomela and 

Kahlos 1972; Vaternahm 1922). 

Suomela and Kahlos (1972) estimated radon elimination kinetics in adults who ingested radon in water by 

monitoring external gamma-radiation from 214Bi (i.e., assuming 214Bi:222Rn disequilibrium ratios ranging 

from 0.4 to 1). Biological elimination t1/2 values ranged from 30 to 50 minutes; these are consistent with 

estimates based on exhaled radon as described above. Out of 10 subjects, 214Bi was detected in urine in 

two subjects (0.4 and 1.8% of ingested 214Bi dose; duration of urine collection was not reported). 

Additional information on the elimination of ingested radon progeny can be found in reviews of the 

biokinetics of bismuth, lead, and polonium (Agency for Toxic Substances and Disease Registry 2007b; 

ICRP 1980, 1994c, 2001). In general, the rates and routes of elimination of each progeny absorbed from 

the gastrointestinal and respiratory tracts are likely to be similar. Information on elimination of inhaled 

radon progeny is discussed in Section 3.4.4.1. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 60 

3. HEALTH EFFECTS 

3.4.4.3 Dermal Exposure 

Information on the excretion of radon and its progeny following dermal exposure is very limited. Within 

24 hours, 4.5% of the radon, which was applied as a salve to intact human skin, was eliminated by 

exhalation, while 10% was exhaled after application of the radon to an open wound (Lange and Evans 

1947). Bathers breathing compressed air while immersed in radon-containing water had exhaled 

approximately one-third of radon measured in blood immediately after bathing (Pohl 1965). By 6– 

8 minutes after bathing, these persons were exhaling one-half of the amounts exhaled immediately after 

bathing. The author stated that the remaining radon which distributed to fatty tissue was excreted more 

slowly. 

3.4.4.4 Other Routes of Exposure 

Experiments in animals have reported the retention of radon after exposure by the intraperitoneal and 

intravenous routes. Following intravenous administration, 1.6–5.0% of the administered activity was 

retained in the animals after 120 minutes (Hollcroft and Lorenz 1949). Retention was greatest at 

120 minutes following intraperitoneal administration, but by 240 minutes, it was nearly the same for both 

routes of administration. These authors also reported that the amount of radon retained in tissues was 

greater in obese mice than in normal mice, especially after intraperitoneal administration (Hollcroft and 

Lorenz 1949). Radon retention has also been studied in dogs following intravenous administration of 

226Ra. The amount of radon in bone was found to increase with increasing time after injection (Mays et 

al. 1975). 

3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models 

Physiologically based pharmacokinetic (PBPK) models use mathematical descriptions of the uptake and 

disposition of chemical substances to quantitatively describe the relationships among critical biological 

processes (Krishnan et al. 1994). PBPK models are also called biologically based tissue dosimetry 

models. PBPK models are increasingly used in risk assessments, primarily to predict the concentration of 

potentially toxic moieties of a chemical that will be delivered to any given target tissue following various 

combinations of route, dose level, and test species (Clewell and Andersen 1985). Physiologically based 

pharmacodynamic (PBPD) models use mathematical descriptions of the dose-response function to 

quantitatively describe the relationship between target tissue dose and toxic end points. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 61 

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PBPK/PD models refine our understanding of complex quantitative dose behaviors by helping to 

delineate and characterize the relationships between: (1) the external/exposure concentration and target 

tissue dose of the toxic moiety, and (2) the target tissue dose and observed responses (Andersen and 

Krishnan 1994; Andersen et al. 1987). These models are biologically and mechanistically based and can 

be used to extrapolate the pharmacokinetic behavior of chemical substances from high to low dose, from 

route to route, between species, and between subpopulations within a species. The biological basis of 

PBPK models results in more meaningful extrapolations than those generated with the more conventional 

use of uncertainty factors. 

The PBPK model for a chemical substance is developed in four interconnected steps: (1) model 

representation, (2) model parameterization, (3) model simulation, and (4) model validation (Krishnan and 

Andersen 1994). In the early 1990s, validated PBPK models were developed for a number of 

toxicologically important chemical substances, both volatile and nonvolatile (Krishnan and Andersen 

1994; Leung 1993). PBPK models for a particular substance require estimates of the chemical substancespecific physicochemical parameters, and species-specific physiological and biological parameters. The 

numerical estimates of these model parameters are incorporated within a set of differential and algebraic 

equations that describe the pharmacokinetic processes. Solving these differential and algebraic equations 

provides the predictions of tissue dose. Computers then provide process simulations based on these 

solutions. 

The structure and mathematical expressions used in PBPK models significantly simplify the true 

complexities of biological systems. If the uptake and disposition of the chemical substance(s) are 

adequately described, however, this simplification is desirable because data are often unavailable for 

many biological processes. A simplified scheme reduces the magnitude of cumulative uncertainty. The 

adequacy of the model is, therefore, of great importance, and model validation is essential to the use of 

PBPK models in risk assessment. 

PBPK models improve the pharmacokinetic extrapolations used in risk assessments that identify the 

maximal (i.e., the safe) levels for human exposure to chemical substances (Andersen and Krishnan 1994). 

PBPK models provide a scientifically sound means to predict the target tissue dose of chemicals in 

humans who are exposed to environmental levels (for example, levels that might occur at hazardous waste 

sites) based on the results of studies where doses were higher or were administered in different species. 

Figure 3-2 shows a conceptualized representation of a PBPK model. 
 

Inhaled chemical Exhaled chemical 

Ingestion 

Lungs 

Liver 

Fat 

Slowly 

perfused 

tissues 

Richly 

perfused 

tissues 

Kidney 

Skin 

A 

R 

T 

E 

R 

I 

A 

L 

B 

L 

O 

O 

D 

Vmax 

Km GI 

Tract 

Feces 

Urine

V 

E 

N 

O 

U 

S 

B 

L 

O 

O 

D 

Chemicals 

contacting skin 


 


 

RADON 62 

3. HEALTH EFFECTS 

Figure 3-2. Conceptual Representation of a Physiologically Based
 

Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance
 

Note: This is a conceptual representation of a physiologically based pharmacokinetic (PBPK) model for a 

hypothetical chemical substance. The chemical substance is shown to be absorbed via the skin, by inhalation, or by 

ingestion, metabolized in the liver, and excreted in the urine or by exhalation. 

Source: adapted from Krishnan and Andersen 1994 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 63 

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PBPK models for radon are discussed in this section in terms of their use in risk assessment, tissue 

dosimetry, and dose, route, and species extrapolations. For radionuclides, the PBPK model depicted in 

Figure 3-2 is replaced with a set of physiologically based biokinetic (PBBK) models for inhalation, 

ingestion, and submersion. These were developed to accomplish virtually the same end as the PBPK 

models above, while integrating additional parameters (for radioactive decay, particle and photon 

transport, and compound-specific factors). Goals are to facilitate interpreting chest monitoring and 

bioassay data, assessing risk, and calculating radiation doses to a variety of tissues throughout the body. 

The standard for these models has been set by the ICRP, and their models receive international support 

and acceptance. ICRP periodically considers newer science in a type of weight of evidence approach 

toward improving the state of knowledge and reducing uncertainties associated with applying the model 

to any given radionuclide. ICRP publications also allow for the use of situation- and individual-specific 

data to reduce the overall uncertainty in the results. Even though there may be conflicting data for some 

parameters, such as absorption factors, one can use conservative values and still reach conclusions on 

whether the dose is below recommended limits. One of the strengths of the ICRP model is that it permits 

the use of experimentally determined material-specific absorption parameter values rather than requiring 

the use of those provided for default types. If the material of interest does not include absorption 

parameter values that correspond to those in the model (e.g., Type F, M, or S), the difference can have a 

profound effect on the assessment of intake and dose from bioassay measurements. This has been 

discussed in National Radiological Protection Board (NRPB) published reports on uranium (NRPB 2002). 

The ICRP (1994b, 1996a) developed a Human Respiratory Tract Model for Radiological Protection, 

which contains respiratory tract deposition and clearance compartmental models for inhalation exposure 

that may be applied to particulate aerosols and gases. The National Council on Radiation Protection and 

Measurements (NCRP) has also developed a respiratory tract model for inhaled radionuclides (NCRP 

1997). At this time, the NCRP recommends the use of the ICRP model for calculating exposures for 

radiation workers and the general public. Readers interested in this topic are referred to NCRP Report 

No. 125; Deposition, Retention and Dosimetry of Inhaled Radioactive Substances (NCRP 1997). 

Models to estimate radiation doses from inhalation exposures to radon account for the deposition and 

clearance of radon gas as well as aerosols of radon progeny (Yu et al. 2006). Several radiation dose 

models for inhaled and/or ingested radon gas and progeny in humans have been reported (Birchall and 

James 1994; Crawford-Brown 1989; El-Hussein et al. 1998; Harley and Robbins 1994; Ishikawa et al. 

2003a, 2003b; James et al. 2004; Khursheed 2000; Marsh and Birchall 2000; NAS 1999b; Peterman and 

Perkins 1988; Porstendörfer, 2001; Sharma et al. 1997). Some of these are extensions or modifications of 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 64 

3. HEALTH EFFECTS 

the ICRP (1994b) model that simulates deposition, clearance, and absorption of inhaled gaseous and 

particulate radionuclides in the human respiratory tract. An example of the latter is the Radon Dose 

Evaluation Program (RADEP), which has been used extensively in risk assessment of exposures to radon 

and radon progeny (Birchall and James 1994; Marsh and Birchall 2000). Two other extensions of the 

ICRP (1994b) model that have been widely applied to radon radiation risk assessment are those of 

Porstendörfer (2001) and James et al. (2004), which implement different approaches to the simulation of 

attached and unattached particles (e.g., fractional distributions in inhaled air and hygroscopic growth) 

and/or effective radiation dose calculations (e.g., tissue weighting factors for radon progeny in respiratory 

tract tissues). The structure of the biokinetics portion of the generic ICRP human respiratory tract model 

is described below, along with modifications that have been reported for applications to radon (e.g., 

RADEP). Systemic distribution and excretion of radon progeny are simulated with models specific for 

the progeny radionuclides. Descriptions of ICRP models for bismuth, lead, and polonium are reported 

elsewhere (Agency for Toxic Substances and Disease Registry 2007b; ICRP 1979, 1994c, 1995c; Leggett 

1993). 

Most physiologically based models of radon biokinetics simulate radon transfers between tissues and 

blood as flow-limited processes in which clearance is determined by tissue blood flow and tissue 

concentrations are defined by tissue:blood partition coefficients (Crawford-Brown 1989; Harley and 

Robbins 1994; Khursheed 2000; NAS 1999b; Peterman and Perkins 1988; Sharma et al. 1997). The 

model proposed by Peterman and Perkins (1988) was actually developed to simulate noble gases (e.g., 

xenon); however, it has been applied to radon biokinetics (Peterman and Perkins 1988; Sharma et al. 

1997). A unique feature of the model is that it included parameters for simulating absorption of xenon 

gas through the skin, although parameter values for radon were not reported and skin penetration of radon 

was not modeled (see Section 3.4.1.3 for discussion of possible implications of this model for dermal 

absorption of radon). The NAS (1999b) and Khursheed (2000) models are described below as examples 

of flow-limited models that simulate absorption, distribution, and excretion of inhaled or ingested radon 

gas. Both were developed to be used in conjunction with ICRP models of progeny to simulate radiation 

doses from inhalation or ingestion of radon gas in drinking water. 

Human Respiratory Tract Model for Radiological Protection (ICRP 1994b) 

Deposition. The ICRP (1994b) has developed a deposition model for behavior of aerosols and vapors in 

the respiratory tract. It was developed to estimate the fractions of radioactivity in breathing air that are 

deposited in each anatomical region of the respiratory tract. ICRP (1994b) provides information used in 
 

 

 

 

 

 

 

 

 

 

 

 

	 

 

	 

 

 

 

 

 

 

 

 

 

 

	 

 

 

RADON	 65 

3. HEALTH EFFECTS 

calculating effective doses of radiation to organs and tissues throughout the body based on a unit intake of 

radioactive material. The model applies to three levels of particle solubility, a wide range of particle sizes 

(approximately 0.0005–100 μm in diameter), and parameter values that can be adjusted for various 

segments of the population (e.g., sex, age, and level of physical exertion). This model also allows one to 

evaluate the bounds of uncertainty in deposition estimates. Uncertainties arise from natural biological 

variability among individuals and the need to interpret some experimental evidence that remains 

inconclusive. The model has been used for estimating radiation doses from inhalation of radon gas and 

aerosols of radon progeny; however, it was developed to be applied to a wide variety of radionuclides and 

their chemical and physical forms. 

The ICRP deposition model estimates the fraction of inhaled material initially retained in each 

compartment (see Figure 3-3). The model was developed with five compartments: (1) the anterior nasal 

passages (ET1); (2) all other extrathoracic airways (ET2) (posterior nasal passages, the naso- and 

oropharynx, and the larynx); (3) the bronchi (BB); (4) the bronchioles (bb); and (5) the alveolar 

interstitium (AI). Particles deposited in each of the regions may be removed and redistributed either 

upward into the respiratory tree or to the lymphatic system and blood by different particle removal 

mechanisms. 

For extrathoracic deposition of particles, the model uses measured airway diameters and experimental 

data, where deposition is related to particle size and airflow parameters, and scales deposition for women 

and children from adult male data. Similar to the extrathoracic region, experimental data served as the 

basis for lung (bronchi, bronchioles, and alveoli) aerosol transport and deposition. A theoretical model of 

gas transport and particle deposition was used to interpret data and to predict deposition for compartments 

and subpopulations other than adult males. Table 3-8 provides reference respiratory values for the 

general Caucasian population during various intensities of physical exertion. 

Deposition of inhaled gases and vapors is modeled as a partitioning process that depends on the 

physiological parameters noted above as well as the solubility and reactivity of a compound in the 

respiratory tract (see Figure 3-4). The ICRP (1994b) model defines three categories of solubility and 

reactivity: SR-0, SR-1, and SR-2: 

•	 Type SR-0 compounds include insoluble and nonreactive gases (e.g., inert gases such as H2, He). 

These compounds do not significantly interact with the respiratory tract tissues, and essentially all 

compound inhaled is exhaled. Radiation doses from inhalation exposure of SR-0 compounds are 

assumed to result from the irradiation of the respiratory tract from the air spaces. 
 


 


 

Sequestered in Tissue Surface Transport 

Anterior
 

Nasal
 Extrathoracic 

Naso-oropharynx 

Larynx 

Environment

16

ET1

14

1

Environment 

16 

ET1

14

1 

14 

1 

ETSEQ

12

LNET

13

2

11 15

ETSEQ

12 

LNET 

13 

2

11

2 

11 15 

Bronchi

bb2

BB2

LNTH bbSEQ

0.03 2

0.01

0.01

8

BBSEQ

9

Thoracic

6 5

10

Al3

0.0001

BB1

bb1

7

4

Al Al2 1

0.001 0.02

3 2 1

Bronchioles

Alveolar

Interstitium

0.03 10

0.00002

Bronchi 

bb2 

BB2 

LNTH bbSEQ

0.03 2 

0.01 

0.01 

8 

BBSEQ

9

SEQ 

9 

Thoracic 

6 5

10 

Al3 

0.0001 

BB1 

bb1 

7 

4 

Al Al2 1

0.001 0.02 

3 2 1

Bronchioles 

Alveolar 

Interstitium 

0.03 10 

0.00002 

0.001 ET GI Tract 0.001 100

 

 


 

RADON 66 

3. HEALTH EFFECTS 

Figure 3-3. Compartment Model to Represent Particle Deposition and 

Time-Dependent Particle Transport in the Respiratory Tract*
 

*Compartment numbers shown in lower right corners are used to define clearance pathways. The clearance rates, 

half-lives, and fractions by compartment, as well as the compartment abbreviations are presented in Table 3-9. 

Source: ICRP 1994b 
 

 

 


 


 


 


 


 

RADON 67 

3. HEALTH EFFECTS 

Table 3-8. Reference Respiratory Values for a General Caucasian Population at
 

Different Levels of Activity
 

Breathing 10 Years 15 Years Adult 

parameters: 3 Months 1 Year 5 Years Male Female Both Male Female Male Female
 

Resting (sleeping); maximal workload 8%
 

Breathing parameters:
 

VT(L) 0.04 0.07 0.17 — — 0.3 0.500 0.417 0.625 0.444 

B(m3hour-1) 0.09 0.15 0.24 — — 0.31 0.42 0.35 0.45 0.32 

fR(minute-1) 38 34 23 — — 17 14 14 12 12 

Sitting awake; maximal workload 12% 

Breathing parameters: 

VT(L) NA 0.1 0.21 — — 0.33 0.533 0.417 0.750 0.464 

B(m3hour-1) NA 0.22 0.32 — — 0.38 0.48 0.40 0.54 0.39 

fR(minute-1) NA 36 25 — — 19 15 16 12 14 

Light exercise; maximal workload 32% 

Breathing parameters: 

VT(L) 0.07 0.13 0.24 — — 0.58 1.0 0.903 1.25 0.992 

B(m3hour-1) 0.19 0.35 0.57 — — 1.12 1.38 1.30 1.5 1.25 

fR(minute-1) 48 46 39 — — 32 23 24 20 21 

Heavy exercise; maximal workload 64% 

Breathing parameters: 

VT(L) NA NA NA 0.841 0.667 — 1.352 1.127 1.923 1.364 

B(m3hour-1) NA NA NA 2.22 1.84 — 2.92 2.57 3.0 2.7 

fR(minute-1) NA NA NA 44 46 — 36 38 26 33 

B = ventilation rate; fR = respiration frequency; NA = not applicable; VT = tidal volume 

Source: See Annex B (ICRP 1994b) for data from which these reference values were derived. 
 

Airway Uptake Gas or Vapor 

Lumen 

Airway 

Fluid 

Tissue 

Blood Blood 

Sb 

Reaction 

Product 

Reaction 

Product 

Bound 

Product 

Material 

Gas/Vapor 

Gas/Vapor 

Reaction Gas/Vapor 

Convection 

Diffusion 

Diffusion 

Reaction 

Metabolism 


 

RADON 68 

3. HEALTH EFFECTS 

Figure 3-4. Reaction of Gases or Vapors at Various Levels of the Gas-Blood 

Interface
 

Source: ICRP 1994b 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

	 

	 

	 

 

 

 

	 

 

 

 

 

 

 

 

 

 

 

 

 

RADON	 69 

3. HEALTH EFFECTS 

•	 Type SR-1 compounds include soluble or reactive gases and vapors which are expected to be 

taken up by the respiratory tract tissues and may deposit in any or all of the regions of the 

respiratory tract, depending on the dynamics of the airways and properties of the surface mucous 

and airway tissues, as well as the solubility and reactivity of the compound. 

•	 Type SR-2 compounds include soluble and reactive gases and vapors which are completely 

retained in the extrathoracic regions of the respiratory tract. SR-2 compounds include sulfur 

dioxide (SO2) and hydrogen fluoride (HF). 

Radon gas is categorized by ICRP (1994b) as SR-1, because, even though it has a low reactivity, it is 

sufficiently soluble to be taken up in the alveolar region where it can be absorbed into blood. ICRP 

(1994b) recommended default values for regional distribution of inhaled gases (except for those having 

low solubility) as follows: 10% ET1, 20% ET2, 10% BB, 20% bb, and 40% AI. Radon progeny, such as 

218Po, 214Pb, and 214Bi are sufficiently reactive to attach to aerosols in the respiratory tract (and external 

air) and deposit in the respiratory tract according to factors that determine particulate deposition (e.g., 

sedimentation, inertial impaction, diffusion, and interception). Radon progeny are represented in the 

ICRP (1994b) model and in extensions of the model (e.g., RADEP) as a mixed distribution of unattached 

particles (i.e., products of the initial reactions between progeny with gases and vapors) and attached 

particles (i.e., products of hygroscopic growth of complexes between unattached particles and aerosols in 

air). AMADs for the two fractions are typically represented in the ICRP model as 1 nm for unattached 

particles and 200 nm for attached particles (Butterweck et al. 2002; Ishikawa et al. 2003b), although the 

use of more complex mixed distributions for attached particles has also been used (Marsh and Birchall 

2000; Porstendörfer 1994, 2001). 

The magnitude of the unattached fraction in inhaled air depends on the concentration and size distribution 

of aerosols in the ambient environment, and will vary with the exposure conditions (e.g., indoor, outdoor) 

and activities of the individual (e.g., sleeping, activities that release particulates into the air such as 

smoking) (Marsh and Birchall 2000). The unattached fraction for typical indoor environments has been 

estimated to be 5–20% (Porstendörfer 1994, 2001). NRC (1991) recommended a default value of 3% for 

modeling exposures in homes where smoking occurs and 5% for exposures during cooking or vacuum 

cleaning activities. The Commission of European Communities recommended a default value of 8% 

(Monchaux et al. 1999). 

Respiratory Tract Clearance. This portion of the model identifies the principal clearance pathways 

within the respiratory tract. The model was developed to predict the retention of various radioactive 

materials. The compartmental model represents particle deposition and time-dependent particle transport 

in the respiratory tract (see Figure 3-3) with reference values presented in Table 3-9. This table provides 
 


 


 


 


 

RADON 70 

3. HEALTH EFFECTS 

Table 3-9. Reference Values of Parameters for the Compartment Model to
 

Represent Time-Dependent Particle Transport
 

from the Human Respiratory Tract
 

Part A
 

Clearance rates for insoluble particles 

Pathway From To Rate (d-1) Half-lifea 

m1,4 AI1 bb1 0.02 35 days 

m2,4 AI2 bb1 0.001 700 days 

m3,4 AI3 bb1 1x10-4 7,000 days 

m3,10 AI3 LNTH 2x10-5 No data 

m4,7 bb1 BB1 2 8 hours 

m5,7 bb2 BB1 0.03 23 days 

m6,10 bbseq LNTH 0.01 70 days 

m7,11 BB1 ET2 10 100 minutes 

m8,11 BB2 ET2 0.03 23 days 

m9,10 BBseq LNTH 0.01 70 days 

m11,15 ET2 GI tract 100 10 minutes 

m12,13 ETseq LNET 0.001 700 days 

m14,16 ET1 Environment 1 17 hours 

See next page for Part B 
 

 

 

 

 

 

 

 

 

 

 

	 


 


 


 

	 

	 

	 

	 


 


 


 

 	 

 

	 


 


 


 

	 


 


 


 

	 


 


 


 

	 


 


 


 

RADON	 71 

3. HEALTH EFFECTS 

Table 3-9. Reference Values of Parameters for the Compartment Model to 

Represent Time-dependent Particle Transport
 

from the Human Respiratory Tract
 

Part B
 

Partition of deposit in each region between compartmentsb 

Fraction of deposit in region 

Region or deposition site Compartment assigned to compartmentc 

ET2 ET2 0.9995 

ETseq 0.0005 

BB BB1 0.993-fs 

BB2 fs 

BBseq 0.007 

bb bb1 0.993-fs 

bb2 fs 

bbseq 0.007 

AI	 AI1 0.3 

AI2 0.6 

AI3 0.1 

a

The half-lives are approximate since the reference values are specified for the particle transport rates and are 

rounded in units of days-1 . A half-life is not given for the transport rate from Al3 to LNTH, since this rate was chosen to 

direct the required amount of material to the lymph nodes. The clearance half-life of compartment Al3 is determined
 

by the sum of the clearance rates.

b

See paragraph 181, Chapter 5 (ICRP 1994b) for default values used for relating fs to dae.
 c

It is assumed that fs is size-dependent. For modeling purposes, fs is taken to be:
 

f s = 05 . for d ae ≤ 2 5 . ρ / χ μm and 

0 . 63 (d ρ χ −2 5 . ) ae f s = 05 . e / for d ae > 2 5 . ρ / χ μm 

where 

fs = fraction subject to slow clearance 

dae = aerodynamic particle diameter/(μm)

ρ = particle density (g/cm3

) 

χ = particle shape factor 

AI = alveolar-interstitial region; BB = bronchial region; bb = bronchiolar region; BBseq = compartment representing 

prolonged retention in airway walls of small fraction of particles deposited in the bronchial region; 

bbseq = compartment representing prolonged retention in airway walls of small fraction of particles deposited in the 

bronchiolar region; ET = extrathoracic region; ETseq = compartment representing prolonged retention in airway tissue 

of small fraction of particles deposited in the nasal passages; GI = gastrointestinal; LNET = lymphatics and lymph 

nodes that drain the extrathoracic region; LNTH = lymphatics and lymph nodes that drain the thoracic region 

Source: ICRP 1994b 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 72 

3. HEALTH EFFECTS 

clearance rates, expressed as a fraction per day and also as half-time (Part A), and deposition fractions 

(Part B) for each compartment for insoluble particles. ICRP (1994b) also developed modifying factors 

for some of the parameters, such as age, smoking, and disease status. Parameters of the clearance model 

are based on human evidence for the most part, although particle retention in airway walls is based on 

experimental data from animal experiments. 

The clearance of particles from the respiratory tract is a dynamic process. The rate of clearance generally 

changes with time from each region and by each route. Following deposition of large numbers of 

particles (acute exposure), transport rates change as particles are cleared from the various regions. 

Physical and chemical properties of deposited material determine the rate of dissolution and, as particles 

dissolve, absorption rates tend to change over time. By creating a model with compartments of different 

clearance rates within each region (e.g., BB1, BB2, BBseq), the ICRP model overcomes problems 

associated with time-dependent functions. Each compartment clears to other compartments by constant 

rates for each pathway. 

Particle transport from all regions is toward both the lymph nodes and the pharynx, and a majority of 

deposited particles end up being swallowed. In the front part of the nasal passages (ET1), nose blowing, 

sneezing, and wiping remove most of the deposited particles. Particles remain here for about a day. For 

particles with AMADs of a few micrometers or greater, the ET1 compartment is probably the largest 

deposition site. A majority of particles deposited at the back of the nasal passages and in the larynx (ET2) 

are removed quickly by the fluids that cover the airways. In this region, particle clearance is completed 

within 15 minutes. 

Ciliary action removes deposited particles from both the bronchi and bronchioles. Though it is generally 

thought that mucociliary action rapidly transports most particles deposited here toward the pharynx, a 

fraction of these particles is cleared more slowly. Evidence for this is found in human studies. For 

humans, retention of particles deposited in the lungs (BB and bb) is apparently biphasic. The “slow” 

action of the cilia may remove as much as half of the bronchi- and bronchiole-deposited particles. In 

human bronchi and bronchiole regions, mucus moves more slowly when it is closer to the alveoli. For the 

faster compartment, it has been estimated that it takes about 2 days for particles to travel from the 

bronchioles to the bronchi and 10 days from the bronchi to the pharynx. The second (slower) 

compartment is assumed to have approximately equal fractions deposited between BB2 and bb2, with both 

fractions having clearance half-times estimated at 20 days. Particle size is a primary determinant of the 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

	 

	 

	 

	 

	 

 

 

 

 

 

 

 

 

 

 

 

	 

	 

	 

	 

RADON	 73 

3. HEALTH EFFECTS 

fraction deposited in this slow thoracic compartment. A small fraction of particles deposited in the BB 

and bb regions is retained in the airway wall for even longer periods (BBseq and bbseq). 

If particles reach and become deposited in the alveoli, they tend to become imbedded in the fluid on the 

alveolar surface or move into the lymph nodes. Coughing is the one mechanism by which particles are 

physically resuspended and removed from the AI region. For modeling purposes, the AI region is divided 

into three subcompartments to represent different clearance rates, all of which are slow. 

In the alveolar-interstitial region, human lung clearance has been measured. The ICRP model uses 2 halftimes to represent clearance: about 30% of the particles have a 30-day half-time, and the remaining 

70% are assigned a half-time of several hundred days. Over time, AI particle transport falls, and some 

compounds have been found in lungs 10–50 years after exposure. 

Absorption into Blood. The ICRP model assumes that absorption into blood occurs at equivalent rates in 

all parts of the respiratory tract, except in the anterior nasal passages (ET1), where no absorption occurs. 

It is essentially a 2-stage process, as shown in Figure 3-5. First, there is a dissociation (dissolution) of 

particles; then the dissolved molecules or ions diffuse across capillary walls and are taken up by the 

blood. Immediately following dissolution, rapid absorption is observed. For some elements, rapid 

absorption does not occur because of binding to respiratory-tract components. In the absence of specific 

data for specific compounds, the model uses the following default absorption rate values for those specific 

compounds that are classified as Types F (fast), M (medium), S (slow), and V (instantaneous): 

•	 For Type F, there is rapid 100% absorption within 10 minutes of the material deposited in the BB, 

bb, and AI regions, and 50% of material deposited in ET2. Thus, for nose breathing, there is rapid 

absorption of approximately 25% of the deposit in ET; for mouth breathing, the value is 50%. 

•	 For Type M, about 70% of the deposit in AI reaches the blood eventually. There is rapid 

absorption of about 10% of the deposit in BB and bb, and 5% of material deposited in ET2. Thus, 

there is rapid absorption of approximately 2.5% of the deposit in ET for nose breathing, and 

5% for mouth breathing. 

•	 For Type S, 0.1% is absorbed within 10 minutes and 99.9% is absorbed within 7,000 days, so 

there is little absorption from ET, BB, or bb, and about 10% of the deposit in AI reaches the 

blood eventually. 

•	 For Type V, complete absorption (100%) is considered to occur instantaneously. 
 

 

Dissociated Material 

Bound Material 

Dissolutio

Uptake 

Blood 

Particulate Material 

n 

RADON 74 

3. HEALTH EFFECTS 

Figure 3-5. The Human Respiratory Tract Model: Absorption into Blood 

Source: ICRP 1994b 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 75 

3. HEALTH EFFECTS 

ICRP (1994b) assigned gases and vapors to Type F, unless alternative values for absorption rates are 

available. However, alternatives to this assumption have been explored, including instantaneous 

partitioning of radon gas into dissolved blood (Butterweck et al. 2002). Radiation doses from exposures 

to radon have been estimated assuming radon and its progeny behave as Type F or Type M (Kendall and 

Smith 2002). The difference between the two categories is important for estimating tissue specific 

radiation dose coefficients (e.g., Sv/Bq inhaled) because of the relatively fast decay of radon 

(t1/2=3.8 days) and its short-lived progeny (e.g., 218Po, t1/2=3.05 minutes; 214Pb, t1/2=26.8 minutes; 214Bi, 

t1/2=19.7 minutes). Type F materials (absorption t1/2=10 minutes) will have a smaller proportion of 

progeny formed in the respiratory tract (i.e., prior to clearance) and, as a result, will deliver a smaller 

internal radiation dose and smaller dose to the respiratory tract relative to systemic tissues. Type M 

materials (absorption t1/2=100 days for 90% of deposited material, t1/2=10 minutes for 10%) will have a 

larger portion of progeny formed in the respiratory tract, which will deliver a larger internal radiation 

dose and larger dose to the respiratory tract relative to systemic tissues (Kendall and Smith 2002). 

Absorption t1/2 values for 212Pb and 212Bi, in an aerosol having an activity median particle diameter of 

approximately 160 nm (range 50–500 nm), a value typical of attached radon progeny particles, were 

estimated to be approximately 10 and 13 hours, respectively (Marsh and Birchall 1999). Use of a 

t1/2 value of 10 hours for radon progeny in the ICRP (1994b) model results in predicted radiation dose 

coefficients that are similar in magnitude to the Type M assumption (Kendall and Smith 2002). However, 

absorption of unattached radon progeny may be faster than that of attached particles. Absorption halftimes for aerosols having approximately 0.3–3 nm in diameter, typical of unattached progeny particles, 

were estimated to be approximately 68 minutes (range 56–86) for 218Po and 214Pb and 18 minutes (range 

17–21) for 214Bi (Butterweck et al. 2002). Butterweck et al. (2002) proposed that binding of unattached 

radon progeny in the respiratory tract may result in slower absorption kinetics. They proposed that a 

10-hour t1/2 would apply to the unattached fraction after binding in the respiratory tract and that the 

unbound fraction may have an absorption t1/2<10 minutes (see Section 3.4.1.1 for further discussion of 

absorption estimates). 

The Radon Dose Evaluation Program (RADEP) implements a simplified version of the ICRP (1994b) 

model and is designed to simulate radon and radon progeny radiation dosimetry (Marsh and Birchall 

2000; Figure 3-6): (1) the alveolar interstitial compartment is represented as a single compartment that 

has a particle transport rate of 0.00661 d-1 to the fast bronchiolar compartment, bb1; (2) sequestered 

compartments, ETseq, BBseq, and bbseq are not considered; (3) radon progeny are assumed to not bind to the 

respiratory tract; and (4) hygroscopic growth of unattached particles is simulated. 
 

RADON 76 

3. HEALTH EFFECTS 

Figure 3-6. Simplified Version of the Human Respiratory Tract Model (HRTM) 

BB2 BB1 

bb2 bb1 

Al 

ET2 

ET2 

0.03 

0.03 

1 

.100 

10 

2 

0.00661 

Blood 

Environment 

GI tract 

Source: Marsh and Birchall 2000 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 77 

3. HEALTH EFFECTS 

Validation of the Model. ICRP (1994b) and RADEP have been evaluated with data on deposition and 

clearance of inhaled particulate aerosol and gases in humans and absorption of radon progeny (ICRP 

1994b; Ishikawa et al. 2003b; Marsh and Birchall 1999). Sensitivity and uncertainty analyses of model 

predictions have been reported (Marsh and Birchall 2000; Yu et al. 2006). 

Risk Assessment. The model has been used to establish the radiation dose (Sv) per unit of inhaled radon 

(Bq) for ages 3 months to 70 years (Kendall and Smith 2002). 

Target Tissues. The model is designed to calculate radiation dose coefficients (Sv/Bq) corresponding to 

specific inhalation exposures to radionuclides. Dose coefficients for radon and progeny have been 

estimated for all major organs, including the bone surfaces, bone marrow, and liver, and other tissues 

(Kendall and Smith 2002). 

Species Extrapolation. The model is based on both human and animal data. However, it is intended for 

applications to human dosimetry. Applications to other species would require consideration of speciesspecific adjustments in modal parameters. 

Interroute Extrapolation. The ICRP model is designed to simulate kinetics of inhaled radionuclides. 

(Note: ICRP/NCRP models are for normal lungs, not those of smokers.) 

National Research Council Radon PBPK Model (NAS 1999b) 

NAS (1999b) developed a PBPK model for simulating absorption and distribution of ingested or inhaled 

radioactive materials, including radon gas (Figure 3-7). NAS noted that statistically significant excesses 

of mortality from leukemia; esophagus, stomach, colon, liver, lung, breast, ovary, and urinary tract 

cancers; and multiple myeloma had been associated with atomic bomb survivors, but other 

epidemiological studies were used to establish risk models for thyroid and breast (based mainly on 

medical exposure data), bone (from radium exposures), and liver (from thoratrast) cancers, along with 

laboratory animal study data. The NAS cancer risk estimates were based on calculations with specific 

cancer site risk projection models using the computational method described in Federal Guidance Report 

No. 13 (EPA 1999a). The model simulates absorption of inhaled radon and distribution to tissues as 

flow-limited processes (i.e., tissue clearance equivalent to tissue blood flow) with parameters for tissue 

volumes, blood flow, and blood:tissue partition coefficients. Absorption of radon gas from the stomach 

and small intestine is simulated as diffusion-limited transfer from the lumen to the wall (i.e., vascularized 
 


 

RADON 78 

3. HEALTH EFFECTS 

Figure 3-7. Schematic Diagram of the NAS (1999b) PBPK Model Developed to 

Describe the Fate of Radon within Systemic Tissues
 

Intake 

L 

a 

r 

g 

e 

V 

e 

i 

n 

s 

LLI Cont ULI Cont Sl Cont St Cont 

LLI Wall ULI Wall Sl Wall St Wall 

Pancreas 

Spleen 

Perfused 

Tissues 

Lung Tissue 

Right Heart Left Heart 

Heart Wall 

Liver 

Alveolar 

Excreta 

Exhalation 

L 

a 

r 

g 

e 

A 

r 

t 

e 

r 

i 

e 

s 

Source: NAS 1999b 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 79 

3. HEALTH EFFECTS 

submucosa), and flow-limited exchange between blood and wall. A separate model is described in NAS 

(1999b) for estimating wall diffusion rate constants, which predicts a time-integrated radon concentration 

in the stomach wall of approximately 30% of that of the lumen. Parameter values for adults are presented 

in Table 3-10. Values for blood flows were derived from Leggett and Williams (1991, 1995); volumes 

and densities from ICRP (1990); and tissue:blood partition coefficients from Nussbaum and Hursh 

(1957). Parameter values for infants, children, and adolescents are also presented in NAS (1999b). 

Validation of the Model. The NRC model has been evaluated with data on deposition and clearance of 

inhaled particulate aerosols and gases in humans and absorption of radon progeny (Correia et al. 1988; 

Crawford-Brown 1989; Harley and Robbins 1994; Harley et al. 1994; Hursh et al. 1965; NAS 1999b). 

Risk Assessment. The model has been used to establish the radiation dose (Sv) per unit of inhaled or 

ingested radon (Bq) for ages 3 months to 70 years (NAS 1999b). 

Target Tissues. The model is designed to calculate radiation dose coefficients (Sv/Bq) corresponding to 

inhalation or ingestion exposures to radon. Dose coefficients for radon and progeny have been estimated 

for all major organs, including the bone surfaces, bone marrow, and liver, and other tissues (NAS 1999b). 

Species Extrapolation. The model is based on both human and animal data. However, it is intended for 

applications to human dosimetry. Applications to other species would require consideration of speciesspecific adjustments in modal parameters. 

Interroute Extrapolation. The model is designed to simulate kinetics of inhaled or ingested radon. 

Extrapolation to other routes of external exposure would require modifications of the model to simulate 

absorption from those routes. 

Khursheed (2000) Model 

Khursheed (2000) developed a PBPK model for simulating absorption and distribution of ingested or 

inhaled radon gas (Figure 3-8). The model is similar in structure to the NRC (NAS 1999b) model, with 

the addition of a tissue compartment representing breast. The model has not had widespread use in risk 

assessment, relative to that of ICRP (1994b), RADEP, or the NRC (NAS 1999b) models. Absorption of 

inhaled and ingested radon, and distribution to tissues, are simulated as flow-limited processes (i.e., tissue 

clearance equivalent to tissue blood flow) with parameters for tissue volumes, blood flow, and 
 

 

 

RADON 80 

3. HEALTH EFFECTS 

Table 3-10. Parameters in the NAS (1999b) PBPK Modela 

Flow (percent Tissue mass Tissue:blood 

Compartment cardiac output) (kg) Tissue density partition coefficient 

Stomach wall 1.0 0.15 1.05 0.7 

Small intestine wall 10.0 0.64 1.04 0.7 

Upper large 2.0 0.21 1.04 0.7 

intestine wall 

Lower large 2.0 0.16 1.04 0.7 

intestine wall 

Pancreas 1.0 0.10 1.05 0.4 

Spleen 3.0 0.18 1.05 0.7 

Adrenals 0.3 0.014 1.02 0.7 

Brain 12.0 1.4 1.03 0.7 

Heart wall 4.0 0.33 1.03 0.5 

Liver 6.5 1.8 1.04 0.7 

Lung tissue 2.5 0.47 1.05 0.7 

Kidneys 19.0 0.31 1.05 0.66 

Muscle 17.0 28.0 1.04 0.36 

Red marrow 3.0 1.5 1.03 8.2 

Yellow marrow 3.0 1.5 0.98 8.2 

Trabecular bone 0.9 1.0 1.92 0.36 

Cortical bone 0.6 4.0 1.99 0.36 

Adipose tissue 5.0 12.5 0.92 11.2 

Skin 5.0 2.6 1.05 0.36 

Thyroid 1.5 0.02 1.05 0.7 

Testes 0.05 0.035 1.04 0.43 

Other 3.2 3.2 1.04 0.7 

a

Values shown for physiological parameters (flows, masses, densities) are for adults. 

Source: NAS 1999b 
 

Liver 

GI tract 

GI contents 

Stomach contents 

Radon in environment 

Lung (air) 

Lung (blood) 

Venous Arterial 

blood blood 

Breast 

RBM 

Gonads 

Stomach 

RADON 81 

3. HEALTH EFFECTS 

Figure 3-8. Khursheed (2000) PBPK Model for Inhalation and Ingestion of Radon 

Gas 

Source: Khursheed 2000 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 82 

3. HEALTH EFFECTS 

blood:tissue partition coefficients (Table 3-11). Values for blood flows were derived from Leggett and 

Williams (1991, 1995); and tissue volumes were derived from ICRP (1990). Tissue:blood partition 

coefficients were derived from Nussbaum and Hursh (1957); however, a single value (0.36) was adopted 

for all soft tissues, with a higher value used for the gastrointestinal tract and stomach to account for higher 

fat content of these tissues. Values for partition coefficients for breast and red marrow assumed 30 and 

40% fat content, respectively. Although age-dependence of radon biokinetics is discussed in Khursheed 

(2000), age-specific parameter values for the model are not reported. 

Validation of the Model. The model has been evaluated with data on whole body retention kinetics of 

radon following ingestion of radon in water (Hursh et al. 1965; Khursheed 2000). 

Risk Assessment. The model has been used to predict tissue-specific annual radiation doses associated 

with continuous inhalation exposures to 20 Bq/m3

 of radon, or following ingestion of 1 Bq of radon 

(Khursheed 2000). 

Target Tissues. The model is designed to calculate radiation dose coefficients (Sv/Bq) corresponding to 

inhalation or ingestion exposures to radon. Dose coefficients for radon and progeny have been estimated 

for major organs, including the bone surfaces, bone marrow, and liver, and other tissues (Khursheed 

2000). 

Species Extrapolation. The model is based on both human and animal data (e.g., partition coefficients). 

However, it is intended for applications to human dosimetry. Applications to other species would require 

consideration of species-specific adjustments in modal parameters. 

Interroute Extrapolation. The model is designed to simulate kinetics of inhaled or ingested radon. 

Extrapolation to other routes of external exposure would require modifications of the model to simulate 

absorption from those routes. 

3.5 MECHANISMS OF ACTION 

3.5.1 Pharmacokinetic Mechanisms 

As discussed in Section 3.4 (Toxicokinetics), the radionuclide radon-222 (222Rn; radioactive half-life of 

3.82 days) is an inert noble gas found in air and some deep well water sources. Radon occurs in air and 

water along with its short-lived radioactive progeny (i.e., 214Bi, 214Pb, 218Po). Deposition and absorption 
 

 

 
 


 

RADON 83 

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Table 3-11. Parameters in Khursheed (2000) PBPK Model for Radon Gas 

Tissue:blood partition Tissue blood flow
 

Tissue coefficient (L/minute) Tissue volume (L)
 

Lung (blood) 6.5 0.52 

Lung (air) 2.33 2.82 

Breast 3.07 0.015 0.35 

Red bone marrow 4.70 0.195 1.46 

Gonads 0.360 0.00325 0.033 

Brain 0.411 0.78 1.25 

Kidneys 0.33 1.23 0.295 

Muscle 0.36 1.11 26.5 

Other 0.36 1.05 25.1 

Adipose 11.2 0.325 16.4 

Bone 0.21 0.13 2.27 

Liver 0.36 1.66 1.7 

Gastrointestinal 0.411 1.17 0.95 

(upper intestines) 

Stomach wall 0.411 0.065 0.14 

Arterial blood 6.5 0.556 

Venous blood 6.5 1.19 

Source: Khursheed 2000 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 84 

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of inhaled or ingested radon gas will be determined largely by its solubility in tissues and blood flow to 

the lungs or gastrointestinal tract (i.e., absorption rate will be flow-limited). Distribution of radon and its 

clearance from the blood following exposure will be governed by its solubility in water and fat and blood 

flow rates to major tissue depots for radon (i.e., fatty tissues). Absorbed radon is quickly eliminated from 

the blood by diffusion across the lung, followed by exhalation. Radon can be absorbed through the skin, 

as demonstrated by its appearance in the blood following dermal exposure; however, underlying 

mechanisms have not been elucidated. 

The pharmacokinetics of inhaled radon progeny will be determined by physiological and physicochemical characteristics (i.e., relative proportions of particular radon progeny and particle size 

(unattached particles with diameters of 0.5–3 nm to attached particles with diameters of 50–1,500 nm). 

The relative proportions vary with exposure conditions (i.e., indoor, outdoor), activities of the individual 

(e.g., sleeping, activities that release particulates into the air), smoking, and other aerosol-generating 

activities (i.e., vacuum cleaning, cooking, fireplace and circulating fan usage). Amounts and location of 

deposition of radon progeny will be determined by factors that influence convection, diffusion, 

sedimentation, and interception of particles in the airways. Absorption of ingested radon progeny, and 

progeny formed from radon after ingestion, will be influenced by rates of transfer of stomach contents 

into the small intestine, as well as rates of absorption of progeny from the small intestine. Specific 

mechanisms involved in absorption of radon progeny from the small intestine have not been completely 

elucidated; however, based on our understanding of lead absorption, it is likely that the mechanisms 

include those common to other divalent cations (e.g., membrane cation transporters and channels). 

Information regarding the distribution and elimination of radon progeny (bismuth, lead, and polonium) 

can be found in reviews of these subjects (Agency for Toxic Substances and Disease Registry 2007b; 

ICRP 1980, 1994c, 1995c). The largest fractions of the body burdens for radon progeny would be 

expected to be found in bone for lead, kidney for bismuth, and liver for polonium (Agency for Toxic 

Substances and Disease Registry 2007b; ICRP 1980, 1994c, 2001). 

3.5.2 Mechanisms of Toxicity 

Extensive efforts have been made to elucidate mechanisms responsible for ionizing radiation-induced 

adverse effects. The Toxicological Profile for Ionizing Radiation (Agency for Toxic Substances and 

Disease Registry 1999b) includes an in-depth discussion of mechanisms of biological effects of ionizing 

radiation in general. Summaries of available information regarding underlying mechanisms of radoninduced lung cancer include Evans (1991, 1992) and, more recently, Jostes (1996) and NAS (1999a, 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 85 

3. HEALTH EFFECTS 

1999b). The intent of this Toxicological Profile for Radon is to provide a brief overview of the present 

state of the science regarding mechanisms that may play roles in radon-induced lung cancer. The 

information in this section is summarized predominantly from Chapter 6 (Molecular and Cellular 

Mechanisms of Radon-Induced Carcinogenesis) of the Risk Assessment of Radon in Drinking Water 

produced for the National Academy of Sciences (NAS 1999b). The reader is referred to this source for 

more detailed information on mechanisms of radon-induced lung cancer. 

Toxicity of radon derives primarily from the biological effects of alpha radiation released during the 

radiological decay of radon progeny, particularly 218Po and 214Bi (attributed to essentially instantaneous 

decay of 214Po to 210Pb following its formation via beta and gamma decay of 214Bi). The sequence of 

events leading from irradiation of living cells involves ionization that causes cellular damage that includes 

DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and 

genetic instability (Kronenberg 1994; Ward 1988, 1990). Figure 3-9 depicts a general conceptual model 

of the biology leading from alpha irradiation of cells by radon and radon progeny to tumor development 

(NAS 1999b). The process includes a series of events by which radiation-induced molecular changes 

affect the normal functions of regulatory genes, leading to genomic instability, loss of normal cell and 

tissue homeostasis, and development of malignancy. 

One pathway leading to tumor formation begins with the induction of DNA damage to irradiated cells 

(Figure 3-9). The average track of alpha particles through a spherical cell nucleus can cross many 

individual strands of DNA, depositing energy in ion clusters and producing corresponding numbers of 

double-strand breaks, known as multiply locally damaged sites (MLDSs) (Ward 1990). Double-strand 

breaks are the most prominent form of DNA damage to cells irradiated by radon alpha particles. Such 

double-strand breaks can be repaired by homologous or nonhomologous (illegitimate) rejoining. In 

homologous repair, pairing proteins such as rad51 and associated modulatory proteins, pair a DNA 

terminus with the intact DNA homolog. A major signaling protein (p53) that regulates cell-cycle control, 

apoptosis, and the transcription of many downstream genes may interact with rad51 and suppress 

rad51-dependent DNA pairing. However, homologous repair of DNA is likely to be highly accurate 

because sequence information from the intact chromatid is used to repair the broken DNA. The 

nonhomologous recombination pathway involves end-to-end rejoining of broken DNA ends by 

supporting proteins including Ku70, Ku86, p450 kinase, and DNA ligase IV. The end result of DNA 

breakage and rejoining via this pathway may include some degree of deletion, insertion, or rearrangement 

of genetic material, which can persist over many cell generations. 
 

α

Cellular exposure to radon 

alpha particles 

α

DNA double strand breaks Reactive oxygen intermediates 

Homologous Base damage recombination 

(Rad51, Brca1, Brca2) Nonhomologous 

recombination 

Base excision 

repair Deletions, rearrangement, mutation (glycosylases, (Ku70, Ku86, p450K, etc.) pol β, ligases) 

protein-protein direct activation 

interactions p53 (signal-specific 

phosphorylation) 

Signal transduction, cycle delays 

apoptosis, altered gene expression 

Genomic instability, mutations, persistent changes 

in gene expression, suppression of apoptosis 

Tumor initiation, progression, invasive 

malignancy 


 


 

RADON 86 

3. HEALTH EFFECTS 

Figure 3-9. Conceptual Model of the Biology Leading From Alpha Irradiation of
 

Cells by Radon and Radon Progeny to Tumor Development
 

Source: NAS 1999b 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 87 

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Ionizing radiation that does not directly damage DNA can produce reactive oxygen intermediates that 

directly affect the stability of p53, resulting in downstream effects on cell regulation and activate cellular 

systems sensitive to the cellular redox states. Reactive oxygen intermediates can also produce oxidative 

damage to individual bases in DNA and point mutations by mispairing during DNA replication. Such 

damage can be repaired by the base-excision repair system which involves glycosylases, polymerase β, 

and ligases. 

The p53 protein plays a critical role in regulating responses that are elicited in damaged cells, particularly 

responses involving cell-cycle arrest and apoptosis. The p53 protein also interacts with other regulatory 

and repair proteins. In the presence of cellular damage via direct DNA damage or via reactive oxygen 

intermediates, the lifetime of p53 increases, which can result in cell cycle delays and apoptosis. 

Surviving cells may contain gene deletions, rearrangements, amplifications, and persistent genomic 

instability. Resultant mutations in oncogenes, loss of function in tumor suppressors, and loss of 

heterozygosity can lead to tumor initiation, progression, and invasive malignancy. 

The cells most likely involved in a carcinogenic response to ionizing radiation such as alpha irradiation of 

the lung by inhaled radon and radon progeny are the cells that incur genetic damage or altered genomic 

stability, not cells that receive lethal damage. At relatively low exposure levels, most irradiated cells 

would be expected to survive. The strong synergism between radon exposure and cigarette smoking may 

be the result of initial radon exposure that produces damaged, yet viable, cells that are further affected by 

carcinogens in cigarette smoke (Brenner and Ward 1992; Moolgavkar et al. 1993). 

Both tobacco smoke and ionizing radiation are known to induce oxidative stress via reactive oxygen 

species (ROS). Under the assumption that glutathione-S-transferase M1 (GSTM1) null homozygotes 

would exhibit decreased ability to neutralize ROS, Bonner et al. (2006) used a case-only design to assess 

the GSTM1 genotype of lung cancer cases for whom long-term α-track radon detectors had been used to 

measure residential radon concentrations. Second-hand smoke levels were also estimated. Radon 

concentrations in excess of 121 Bq/m3

 (3.27 pCi/L) were significantly associated with GSTM1 null 

homozygotes compared to GSTM1 carriers; an odds ratio for second-hand smoke and GSTM1 interaction 

among never smokers was elevated as well. The results provide suggestive evidence that radon and 

second-hand smoke might promote carcinogenic responses via a common pathway. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 88 

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A recent study reported a lack of expression of the p16Ink4a protein (Ink4a is a tumor suppressor gene) in 

50% of radon-induced lung tumors of rats, suggesting that deregulation of p16Ink4a may play a role in 

lung tumors induced by radon and radon progeny (Bastide et al. 2009). 

3.5.3 Animal-to-Human Extrapolations 

Epidemiological studies clearly identify lung cancer as the health effect of greatest concern, both from 

occupational and residential exposure to radon and its progeny. Results of studies assessing the health 

effects of exposure to radon in a variety of animal species indicate that rats and dogs are relatively 

sensitive to radon-induced lung tumor development, whereas hamsters and mice did not develop tumors, 

even at cumulative exposures >10,000 WLM. This species difference may represent a real difference in 

sensitivity to radon; however, other factors may also have contributed to the lack of tumors in mice and 

hamsters, including decreased longevity in some exposed groups (i.e., animals die before tumors could 

develop) and termination of exposure or observations prior to the development of lung tumors. The lack 

of demonstrated exposure-related lung cancer in the hamsters may reflect species-specific resistance to 

alpha radiation-induced lung tumors since similar negative results were observed in hamsters exposed to 

plutonium, another alpha-emitting radionuclide (Sanders 1977). Based on a wide range of species 

differences in susceptibility to radon-induced lung cancer and insufficient information regarding 

mechanisms of interspecies differences in susceptibility, animal-to-human extrapolations for purposes of 

risk assessment do not appear useful at this time, nor are they needed given the wealth of epidemiological 

data. 

3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS 

Recently, attention has focused on the potential hazardous effects of certain chemicals on the endocrine 

system because of the ability of these chemicals to mimic or block endogenous hormones. Chemicals 

with this type of activity are most commonly referred to as endocrine disruptors. However, appropriate 

terminology to describe such effects remains controversial. The terminology endocrine disruptors, 

initially used by Thomas and Colborn (1992), was also used in 1996 when Congress mandated the EPA to 

develop a screening program for “...certain substances [which] may have an effect produced by a 

naturally occurring estrogen, or other such endocrine effect[s]...”. To meet this mandate, EPA convened a 

panel called the Endocrine Disruptors Screening and Testing Advisory Committee (EDSTAC), and in 

1998, the EDSTAC completed its deliberations and made recommendations to EPA concerning endocrine 

disruptors. In 1999, the National Academy of Sciences released a report that referred to these same types 

of chemicals as hormonally active agents. The terminology endocrine modulators has also been used to 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 89 

3. HEALTH EFFECTS 

convey the fact that effects caused by such chemicals may not necessarily be adverse. Many scientists 

agree that chemicals with the ability to disrupt or modulate the endocrine system are a potential threat to 

the health of humans, aquatic animals, and wildlife. However, others think that endocrine-active 

chemicals do not pose a significant health risk, particularly in view of the fact that hormone mimics exist 

in the natural environment. Examples of natural hormone mimics are the isoflavinoid phytoestrogens 

(Adlercreutz 1995; Livingston 1978; Mayr et al. 1992). These chemicals are derived from plants and are 

similar in structure and action to endogenous estrogen. Although the public health significance and 

descriptive terminology of substances capable of affecting the endocrine system remains controversial, 

scientists agree that these chemicals may affect the synthesis, secretion, transport, binding, action, or 

elimination of natural hormones in the body responsible for maintaining homeostasis, reproduction, 

development, and/or behavior (EPA 1997). Stated differently, such compounds may cause toxicities that 

are mediated through the neuroendocrine axis. As a result, these chemicals may play a role in altering, 

for example, metabolic, sexual, immune, and neurobehavioral function. Such chemicals are also thought 

to be involved in inducing breast, testicular, and prostate cancers, as well as endometriosis (Berger 1994; 

Giwercman et al. 1993; Hoel et al. 1992). 

Radon itself is a noble gas and would not have hormonally active properties. In addition, no studies were 

located regarding endocrine disruption in humans and/or animals after exposure radon progeny. 

No in vitro studies were located regarding endocrine disruption associated with radon progeny. 

3.7 CHILDREN’S SUSCEPTIBILITY 

This section discusses potential health effects from exposures during the period from conception to 

maturity at 18 years of age in humans, when all biological systems will have fully developed. Potential 

effects on offspring resulting from exposures of parental germ cells are considered, as well as any indirect 

effects on the fetus and neonate resulting from maternal exposure during gestation and lactation. 

Relevant animal and in vitro models are also discussed. 

Children are not small adults. They differ from adults in their exposures and may differ in their 

susceptibility to hazardous substances. Children’s unique physiology and behavior can influence the 

extent of their exposure. Exposures of children are discussed in Section 6.6, Exposures of Children. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 90 

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Children sometimes differ from adults in their susceptibility to hazardous substances, but whether there is 

a difference depends on the substance (Guzelian et al. 1992; NRC 1993). Children may be more or less 

susceptible than adults to health effects, and the relationship may change with developmental age 

(Guzelian et al. 1992; NRC 1993). Vulnerability often depends on developmental stage. There are 

critical periods of structural and functional development during both prenatal and postnatal life, and a 

particular structure or function will be most sensitive to disruption during its critical period(s). Damage 

may not be evident until a later stage of development. There are often differences in pharmacokinetics 

and metabolism between children and adults. For example, absorption may be different in neonates 

because of the immaturity of their gastrointestinal tract and their larger skin surface area in proportion to 

body weight (Morselli et al. 1980; NRC 1993); the gastrointestinal absorption of lead is greatest in infants 

and young children (Ziegler et al. 1978). The infant also has an immature blood-brain barrier (Adinolfi 

1985; Johanson 1980) and probably an immature blood-testis barrier (Setchell and Waites 1975). There 

may also be differences in excretion, particularly in newborns who all have a low glomerular filtration 

rate and have not developed efficient tubular secretion and resorption capacities (Altman and Dittmer 

1974; NRC 1993; West et al. 1948). Children and adults may differ in their capacity to repair damage 

from substance insults. Children also have a longer remaining lifetime in which to express damage from 

substances; this potential is particularly relevant to cancer. 

Certain characteristics of the developing human may increase exposure or susceptibility, whereas others 

may decrease susceptibility to the same substance. For example, although infants breathe more air per 

kilogram of body weight than adults breathe, this difference might be somewhat counterbalanced by their 

alveoli being less developed, which results in a disproportionately smaller surface area for alveolar 

absorption (NRC 1993). 

Available information from children employed as miners in China does not provide evidence of increased 

susceptibility to the effects of exposure to radon (Lubin et al. 1990; NIH 1994). However, a child in a 

smoking household will receive a higher radiation dose from radon (and is therefore more susceptible) 

than one in a nonsmoking household based on exposures to the same concentration of radon because 

cigarette smoke increases the attached fraction (HPA 2009), which in turn increases the radiation dose. 

Age-related differences in susceptibility to the effects of exposure to radon and radon progeny have not 

been demonstrated. Differences in lung morphometry and breathing rates in children could result in 

higher estimated radiation doses relative to adults (NCRP 1984a; Samet et al. 1989). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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3.8 BIOMARKERS OF EXPOSURE AND EFFECT 

Biomarkers are broadly defined as indicators signaling events in biologic systems or samples. They have 

been classified as markers of exposure, markers of effect, and markers of susceptibility (NAS/NRC 

1989). 

Normally, a biomarker of exposure is defined as a xenobiotic substance or its metabolite(s) or the product 

of an interaction between a xenobiotic agent and some target molecule(s) or cell(s) that is measured 

within a compartment of an organism (NAS/NRC 1989). This does not apply to radon or its progeny 

since they are naturally present in individuals, and xenobiotics are not. The preferred biomarkers of 

exposure to radon and radon progeny are the substances themselves in readily obtainable body fluid(s), or 

excreta. However, several factors can confound the use and interpretation of biomarkers of exposure. 

The body burden of a substance may be the result of exposures from more than one source. Depending 

on the properties of the substance (e.g., biologic half-life) and environmental conditions (e.g., duration 

and route of exposure), radon and all of its progeny may have left the body by the time samples can be 

taken. It may be difficult to identify individuals exposed to hazardous substances that are commonly 

found in body tissues and fluids (e.g., essential mineral nutrients such as copper, zinc, and selenium). 

Biomarkers of exposure to radon and radon progeny are discussed in Section 3.9.1. 

Biomarkers of effect are defined as any measurable biochemical, physiologic, or other alteration within an 

organism that, depending on magnitude, can be recognized as an established or potential health 

impairment or disease (NAS/NRC 1989). This definition encompasses biochemical or cellular signals of 

tissue dysfunction (e.g., increased liver enzyme activity or pathologic changes in female genital epithelial 

cells), as well as physiologic signs of dysfunction such as increased blood pressure or decreased lung 

capacity. Note that these markers are not often substance specific. They also may not be directly 

adverse, but can indicate potential health impairment (e.g., DNA adducts). Biomarkers of effects caused 

by radon and radon progeny are discussed in Section 3.9.2. 

A biomarker of susceptibility is an indicator of an inherent or acquired limitation of an organism's ability 

to respond to the challenge of exposure to a specific substance. It can be an intrinsic genetic or other 

characteristic or a preexisting disease that results in an increase in absorbed dose, a decrease in the 

biologically effective dose, or a target tissue response. If biomarkers of susceptibility exist, they are 

discussed in Section 3.11, Populations That Are Unusually Susceptible. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 92 

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3.8.1 Biomarkers Used to Identify or Quantify Exposure to Radon and Radon Progeny 

Biomarkers of exposure to radon and its progeny include the presence of radon progeny in several human 

tissues and fluids, including bone, teeth, blood, hair, and whiskers; these progeny can be quantified by 

methods which are both specific and reliable (Blanchard et al. 1969; Clemente et al. 1984; Gotchy and 

Schiager 1969). Although the presence of radon progeny in these tissues and fluids indicates exposure to 

radon and radon progeny, particularly as a consequence of absorption of inhaled radon and radon progeny 

and ingestion of food or water containing radon-producing radionuclides such as uranium and thorium, 

exposure to uranium or radium may also result in the presence of these decay products. The isotope 210Po 

may also be found in tissues after exposure to cigarette smoke. Levels of 210Pb in teeth have been 

associated with levels of radon in the environment in an area with high natural background levels of radon 

and its progeny (Clemente et al. 1984). Black et al. (1968) reported a correlation between radiation 

exposure and 210Pb levels in bone from uranium miners. However, cumulative exposure to these 

individuals was estimated. Biomarkers of exposure to radon or its progeny may be present after any 

exposure duration (e.g., acute, intermediate, chronic). Because of the relatively short half-lives of most 

radon progeny, with respect to a human lifetime, the time at which the biological sample is taken related 

to time of exposure may be important. However, for the longer-lived progeny the time factor is less 

critical. 

Models are available which estimate exposure to radon and its progeny, 210Pb and 210Po, in bone, teeth, 

and blood (Blanchard et al. 1969; Clemente et al. 1982, 1984; Eisenbud et al. 1969; Gotchy and Schiager 

1969; Weissbuch et al. 1980). However, these models make numerous assumptions, and uncertainties 

inherent in all models are involved in these estimates. Therefore, at present, these estimated levels of 

biomarkers of exposure are not useful for quantifying exposure to radon and its progeny. 

3.8.2 Biomarkers Used to Characterize Effects Caused by Radon and Radon Progeny 

The principal target organ identified in both human and animal studies following exposure to radon and 

its progeny is the lung. Alterations in sputum cytology have been evaluated as an early indicator of 

radiation damage to lung tissue. The frequency of abnormalities in sputum cytology, which may indicate 

potential lung cancer development, increased with increasing cumulative exposures to radon and its 

progeny (Band et al. 1980; Saccomanno et al. 1974). Abnormal sputum cytology can be used in 

diagnosis of lung cancer (Rivera et al. 2003). Abnormal sputum cytology may be observed following 

radon exposure, as well as exposure to other carcinogens such as cigarette smoke; it is not recommended 

as a screening tool for radon exposure. In addition, even though increases in the frequency of abnormal 
 

 

RADON 93 

3. HEALTH EFFECTS 

sputum cytology parameters can be measured, they may not provide reliable information regarding 

predicted health effects in exposed individuals. 

Associations between chromosomal aberrations and environmental levels of radon have been reported 

(Pohl-Rüling and Fischer 1983; Pohl-Rüling et al. 1976, 1987). Signs of genotoxicity in underground 

miners exposed to radon and other potentially genotoxic substances include increased frequencies of 

chromosomal aberrations and micronuclei in lymphocytes (Bilban and Jakopin 2005; Brandom et al. 

1978; Smerhovsky et al. 2001, 2002) and increased frequency of mutations of glycophorin A in blood 

(Shanahan et al. 1996). However, these genotoxic effects cannot be exclusively attributed to exposure to 

radon and its progeny. 

3.9 INTERACTIONS WITH OTHER CHEMICALS 

Interactions of radon, cigarette smoke, arsenic, crystalline silica dust, and diesel exhaust particulates and 

the possible effects on radon-induced toxicity is an actively-researched complex issue. Cigarette smoke 

appears to interact with radon and its progeny to potentiate their effects. In general, epidemiological 

studies have reported synergistic, multiplicative, or additive effects of cigarette smoke in lung cancer 

induction among miners exposed to radon and its progeny (see NAS 1999a for an in-depth discussion of 

interactions between smoking and exposure to radon). 

Some studies of occupational exposure to radon and radon progeny provide information to indicate that 

lung cancer was more prevalent among exposed workers who smoked compared to nonsmoking workers. 

For example, studies by Lundin et al. (1969, 1971) reported 10 times more lung cancer among U.S. 

uranium miners who smoked. Modeling results of Thomas et al. (1994), using data on lung cancer 

mortality in a Colorado Plateau uranium mining cohort, indicated a multiplicative synergistic relationship 

between lung cancer mortality and exposure to radon among smokers. Modeling results of data from 

another mining cohort in China (Yao et al. 1994) suggested that the synergistic effect of radon exposure 

and smoking was greater than additive and less than multiplicative; furthermore, the risk of lung cancer 

was higher if smoking and exposure to radon progeny occurred together rather than if smoking was 

initiated following the cessation of occupational exposure to radon progeny. Leuraud et al. (2011) 

assessed the effects of exposure to radon and radon decay products and smoking status on the risk of lung 

cancer in a combined analysis of 1,046 lung cancer cases and 2,492 controls with detailed radon exposure 

data and smoking status selected from three major miner cohorts in the Czech Republic (Tomášek et al. 

2003), France (Laurier et al. 2004), and Germany (Kreuzer et al. 2010). The combined analysis resulted 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 94 

3. HEALTH EFFECTS 

in a significant excess risk of lung cancer with and without adjustment for smoking; the study authors 

indicated that the results of the combined analysis suggest a sub-multiplicative interaction between radon 

exposure and smoking. Analysis of pooled results from 13 European residential case-control studies 

resulted in findings that the absolute risk of death from lung cancer at age 75 years at usual residential 

radon concentrations of 0, 100, and 400 Bq/m3

 (0, 2.7, and 10.8 pCi/L) would be 25 times greater for 

cigarette smokers than lifelong nonsmokers (Darby et al. 2005, 2006). It should be noted that these 

studies were typically limited by lack of adjustment for concomitant exposure to other known or probable 

human carcinogens such as arsenic, crystalline silica dust, and diesel exhaust particulates. 

Interactions between radon and arsenic were evaluated in a cohort of Chinese tin miners (Xuan et al. 

1993). A 75% reduction in the lung cancer risk was indicated after adjusting for arsenic exposure. In 

another study (Bergdahl et al. 2010), decreased lung cancer risk from radon exposure was indicated after 

adjusting for silica exposure within the highest exposure group of a cohort of Swedish iron ore miners. In 

a multistate study of 12,315 non-metal underground and surface workers exposed to diesel exhaust 

particulates at facilities in Missouri, New Mexico, Ohio, and Wyoming (Attfield et al. 2012), an SMR of 

1.26 (95% CI 1.09–1.44) was calculated for mortality from lung cancer among the workers compared to 

state-based mortality rates. 

Some animal studies support the theory that cigarette smoke potentiates the effects of radon and its 

progeny alone or in conjunction with uranium ore dust. A study by Chameaud et al. (1982b) reported an 

increase in the incidence of lung cancer, as well as a decrease in the cancer latency period in rats exposed 

to radon and then to cigarette smoke, compared to rats exposed to radon and its progeny alone. This 

study did not include untreated controls. Alterations in normal blood parameters, including 

carboxyhemoglobin levels and leukocyte counts, were observed in dogs exposed to cigarette smoke 

followed by exposure to radon progeny plus uranium ore dust, compared to animals exposed to only 

radon progeny plus uranium ore (Filipy et al. 1974). In contrast, some studies suggest an antagonistic 

interaction between smoking and radon progeny-induced lung cancer. Dogs exposed daily to cigarette 

smoke followed immediately by exposure to radon and its progeny and uranium ore dust exhibited a 

decrease in the incidence of lung tumors, compared to dogs exposed to radon and its progeny plus 

uranium ore dust (Cross et al. 1982b). Cross (1988) reported that this was possibly due to a thickening of 

the mucus layer as a result of smoking and, to a lesser extent, a stimulatory effect of cigarette smoke on 

mucociliary clearance, although no empirical evidence was collected during the experiment to test these 

possibilities. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 95 

3. HEALTH EFFECTS 

In rats, administration of chemicals present in cigarette smoke after exposure to radon and its progeny 

resulted in a decrease in the lung cancer latency period when compared to the time-to-tumor induction in 

animals treated with radon alone. This effect was seen with 5,6-benzoflavon (Queval et al. 1979) and 

cerium hydroxide (Chameaud et al. 1974). 

Other airborne irritants, as well as ore dust and diesel exhaust, may act synergistically with radon and its 

progeny to increase the incidence of adverse health effects. Epidemiological and other studies report the 

presence of other airborne irritants in mining environments, including arsenic, hexavalent chromium, 

nickel, cobalt (Ševc et al. 1984), serpentine (Radford and Renard 1984), silica dust (Maciejewska 2008), 

iron ore dust (Damber and Larsson 1982; Edling and Axelson 1983; Radford and Renard 1984), and 

diesel exhaust (Damber and Larsson 1982; Ševc et al. 1984). 

Cross and colleagues at Pacific Northwest Laboratory have conducted extensive experiments involving 

exposure of dogs, mice, rats, and hamsters to radon and its progeny in conjunction with uranium ore dust 

and/or diesel exhaust (Cross 1988; Cross et al. 1981a, 1982b, 1984; NIEHS 1978; Palmer et al. 1973). 

Studies in hamsters, mice, and rats have shown that exposure to uranium ore dust and/or diesel exhaust 

increases the pulmonary effects of radon. Radon and combinations of uranium ore dust and/or diesel 

exhaust produced greater incidences of pulmonary emphysema and fibrosis in hamsters than radon and its 

progeny alone (Cross 1988). Exposure to uranium ore dust or diesel exhaust alone caused significant 

bronchial hyperplasia, but not as great an effect as combining either of these with radon and its progeny. 

The incidence of severe lesions of the upper respiratory tract (nasal passages and trachea) of mice and rats 

was increased following exposure to radon and uranium ore dust, compared to animals exposed to radon 

and its progeny alone (Palmer et al. 1973). An increased incidence of thoracic cancer (40%) was 

observed in rats treated with asbestos (mineral dust) after inhalation of radon and its progeny, compared 

with animals exposed to radon alone (Bignon et al. 1983). However, these tumors may have been due to 

asbestos rather than to an interaction between agents. This experiment did not include a group exposed 

only to mineral dusts. In a study of tin miners in China, radon was found to account for only around 25% 

of the age-adjusted ERR/WLM once arsenic was accounted for as a confounder (Xuan et al. 1993). 

Inhalation exposure to radon and its progeny in conjunction with silicon dioxide increased the incidence 

of nodular fibrosis of the lungs in rats (Kushneva 1959). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 96 

3. HEALTH EFFECTS 

3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE 

A susceptible population will exhibit a different or enhanced response to a substance than will most 

persons exposed to the same level in the environment. Reasons may include genetic makeup, age, health 

and nutritional status, and exposure to other toxic substances (e.g., cigarette smoke), arsenic, crystalline 

silica dust, or diesel exhaust particulates. These parameters result in reduced detoxification or excretion 

of the substance, or compromised function of organs affected by the substance. Populations who are at 

greater risk due to their unusually high exposure are discussed in Section 6.7, Populations with Potentially 

High Exposures. 

Smokers who are exposed to elevated levels of radon and radon progeny are at much higher risk of lung 

cancer than nonsmokers (Darby et al. 2005, 2006). Nonsmoking children in smoking households are 

more susceptible than nonsmoking children in nonsmoking households since smoke increases the 

attached fraction and therefore the radiation dose (HPA 2009). People who have chronic respiratory 

disease, such as asthma, emphysema, or fibrosis often have reduced expiration efficiency and increased 

residual volume (i.e., greater than normal amounts of air left in the lungs after normal expiration) (Guyton 

1977). Radon progeny can remain in the lungs for long periods of time, increasing the risk of damage to 

the lung tissue. Persons who have existing lung lesions may be more susceptible to the tumor-causing 

effects of radon progeny (Morken 1973). In an assessment of lung cancer cases pooled from three 

residential case-control studies, radon concentrations >121 Bq/m3

 (3.3 pCi/L) were associated with more 

than a 3-fold interaction odds ratio among glutathione-S-transferase M1 (GSTM1) null homozygotes 

compared to GSTM1 carriers (Bonner et al. 2006). In the study, it was hypothesized that GSTM1 null 

homozygotes would have decreased ability to neutralize reactive oxygen species induced by ionizing 

radiation and tobacco smoke. Thus, GSTM1 null homozygotes may exhibit increased susceptibility to the 

respiratory effects of radon progeny. 

3.11 METHODS FOR REDUCING TOXIC EFFECTS 

As discussed in detail in Section 3.2.1 (Inhalation Exposure), lung cancer is the primary toxicity concern 

following long-term exposure to radon and radon progeny. The high-energy alpha emissions from radon 

progeny deposited in the airways are the source of toxicity concern. The sequence of events leading from 

irradiation of living cells is generally believed to involve ionization that causes cellular damage including 

DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, chromosomal change, and 

genetic instability. Cigarette smoke appears to interact with radon and its progeny to potentiate their 

effects. 
 

 

RADON 97 

3. HEALTH EFFECTS 

There are no known methods for reducing the toxic effects of radon once exposure has occurred. Inhaled 

radon, as a noble gas, is rapidly absorbed from the lung and readily excreted in exhaled air. Inhaled radon 

progeny that are attached to dust particles and tobacco products may lodge in the lung. Most radon 

progeny decay via alpha or beta emission with half-lives so short that conventional methods for reducing 

toxicity would be ineffective. Although selected radon progeny (e.g., 210Po) have longer half lives, 

conventional medical interventions such as pulmonary lavage carry significant risk and are not 

recommended. Methods for reducing the potential exposure to radon (and therefore its toxic effects) 

consist of periodically testing for radon in indoor air and reducing radon concentrations to below the EPA 

recommended action level of 4 pCi/L, using active soil depressurization (ASD) in existing homes and 

radon-reducing features in new home construction. If ASD does not reduce levels sufficiently, reversing 

the fan direction to pressurize the subslab can be used to determine the more effective method (Kearney 

and Mason 2011). Measures to prevent high radon levels in new home construction are expected to be 

effective at reducing radon-related lung cancer deaths, while remediating old homes with high radon 

levels may be more expensive and less effective. An additional method to reduce toxic effects of radon is 

to stop smoking (EPA 2009a; Mendez et al. 1998, 2011) since the presence of smoke particles increases 

the radiation dose from radon progeny. Port-of-entry mitigation methods for reducing radon levels in 

drinking water are recommended over mitigation at the tap since the latter is not effective for radon (EPA 

2009a; 2012a). 

3.11.1 Reducing Peak Absorption Following Exposure 

There are no methods for reducing peak absorption of radon gas following exposure and radon progeny 

decay via alpha or beta emission so rapidly that efforts to remove inhaled radon progeny would be 

ineffective. 

3.11.2 Reducing Body Burden 

There are no known methods for reducing the body burden of absorbed radon and radon progeny. 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects 

There is an increasing amount of information regarding the possible efficacy of dietary micronutrients at 

reducing lung cancer risk in smokers. Alavanja (2002) published a review of tobacco smoke- and radoninduced damage and potential preventive interventions. Since smoking multiplies the risk of lung cancer 
 

 

RADON 98 

3. HEALTH EFFECTS 

from radon exposure, stopping smoking could significantly reduce the risk of radon induced lung cancer; 

however, reducing exposure to radon is a first consideration. It was noted that available data indicate that 

micronutrients associated with a reduction in lung cancer risk among smokers might also reduce the risk 

in nonsmokers, possibly via antioxidant properties. Thus, diets high in fruits and vegetables might be of 

benefit in neutralizing reactive oxygen species produced by cigarette smoke and radon. However, the 

American College of Chest Physicians does not recommend the use of supplements for the prevention of 

lung cancer as they have not been shown to be helpful, and beta-carotene has been associated with 

increases in lung cancer (Alberts 2007). 

3.12 ADEQUACY OF THE DATABASE 

Section 104(I)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of radon is available. Where adequate information is not 

available, ATSDR, in conjunction with the National Toxicology Program (NTP), is required to assure the 

initiation of a program of research designed to determine the health effects (and techniques for developing 

methods to determine such health effects) of radon. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 

3.12.1 Existing Information on Health Effects of Radon 

The existing data on health effects of inhalation, oral, and dermal exposure of humans and animals to 

radon are summarized in Figure 3-10. The purpose of this figure is to illustrate the existing information 

concerning the health effects of radon. Each dot in the figure indicates that one or more studies provide 

information associated with that particular effect. The dot does not necessarily imply anything about the 

quality of the study or studies, nor should missing information in this figure be interpreted as a “data 

need”. A data need, as defined in ATSDR’s Decision Guide for Identifying Substance-Specific Data 

Needs Related to Toxicological Profiles (Agency for Toxic Substances and Disease Registry 1989), is 

substance-specific information necessary to conduct comprehensive public health assessments. 
 

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RADON 99 

3. HEALTH EFFECTS 

Figure 3-10. Existing Information on Health Effects of Radon 

Existing Studies 
 

 

RADON 100 

3. HEALTH EFFECTS 

Generally, ATSDR defines a data gap more broadly as any substance-specific information missing from 

the scientific literature. 

Figure 3-10 graphically describes whether a particular health effect end point has been studied for a 

specific route and duration of exposure. Most of the information on health effects in humans caused by 

exposure to radon and radon progeny was obtained from epidemiological studies of uranium and other 

hard rock miners. These studies of chronic occupational exposure to radon via inhalation provide 

information on cancer and lethality, and limited insight into reproductive and genetic effects. Limited 

information is also available regarding cancer following dermal exposure to radon and its progeny. No 

information on the health effects of radon and its progeny in humans was available following acute or 

intermediate exposure by any route. No information on the health effects of radon and its progeny in 

animals following acute, intermediate, or chronic oral or dermal exposure was located. The only 

information available from animal studies was by the inhalation route of exposure, which provides data 

on systemic and genetic effects, as well as cancer. 

3.12.2 Identification of Data Needs 

Acute-Duration Exposure. No data were located regarding adverse health effects in humans 

following acute exposure to radon and its progeny by any route. Single dose studies are available for 

laboratory animals that have been exposed by the inhalation and parenteral routes. No information is 

available on acute oral exposure in laboratory animals. Information is available on lethality following 

acute inhalation exposure to high doses. However, this study did not provide information on target 

organs, sensitive tissues, or cause of death. No information is available on effects in humans or animals 

following relatively low-level acute exposure to radon and its progeny. However, the greatest health 

concern for radon and its progeny is lung cancer, which results from long-term exposure, not acuteduration exposure. Studies designed to assess the potential for adverse health effects in humans following 

acute-duration exposure to radon and its progeny do not appear necessary at this time. 

Intermediate-Duration Exposure. No data were located regarding adverse health effects associated 

with intermediate-duration exposure of humans to radon and its progeny by any exposure route. 

Epidemiological miner-based studies, in general, have focused on cohorts exposed to radon and its 

progeny for durations >1 year. Animal studies demonstrate that intermediate exposure to high levels of 

radon and its progeny can cause chronic respiratory toxicity and lung cancers and indicate that similar 

effects might occur following intermediate-duration exposure in humans. The relationship between the 
 

 

RADON 101 

3. HEALTH EFFECTS 

nature and severity of the respiratory toxicity and the amount of radon exposure is not clearly defined; nor 

is there any information regarding systemic toxicity following intermediate-duration exposure. 

Additional research on the dose-duration-response relationship between radon exposure and the type and 

permanence of resulting toxicity would provide pertinent information. If populations exposed to radon 

and its progeny for intermediate durations can be identified, such populations could be assessed for 

potential adverse health outcomes. 

Chronic-Duration Exposure and Cancer. Knowledge of the adverse health effects in 

occupationally-exposed humans following chronic-duration exposure to radon and its progeny is 

historically based on studies in adult male underground miners. These studies describe predominantly 

respiratory end points, such as pneumoconiosis, emphysema, interstitial pneumonitis, pulmonary fibrosis, 

tuberculosis, and cancer. Interactions of radon and known or probable human carcinogens in 

occupational and residential exposure scenarios need to be evaluated for the earlier study groups as well 

as more recent and current exposed populations. One study of a cohort of uranium miners in the Czech 

Republic included a finding of significant positive associations between cumulative radon exposures and 

incidences of chronic lymphocytic leukemia and all leukemias combined (Řeřicha et al. 2006). 

Additional studies of occupationally- and residentially-exposed individuals are needed to more 

completely assess the potential for radon-induced leukemias. To a large extent, other health effects have 

not been studied; additional studies assessing health effects other than cancer do not appear necessary. 

Numerous residential case-control studies are available for which possible associations between lung 

cancer and residential radon levels have been assessed. Collectively, these studies provide evidence of 

radon-induced lung cancer from long-term residential exposure. Continued assessment of residential 

radon exposure should include improved methods such as glass-based retrospective radon detectors (Field 

et al. 1999b; Steck et al. 2002; Sun 2008) and validation of such methods to more accurately estimate 

exposure scenarios. In addition, extensive data regarding radon exposure in non-residential and 

residential buildings that use radon-emitting building materials (e.g., natural stone counter tops, floors, 

and heat sinks) are needed. 

Although radon dissolved in drinking water is a source of human exposure, few studies have reported on 

the potential health implications associated with ingested radon and radon progeny. However, additional 

studies do not appear necessary at this time. 
RADON 102 

3. HEALTH EFFECTS 

Genotoxicity. The genotoxicity of alpha radiation from radon and radon progeny has been 

investigated in underground miners, in individuals residing in homes with measured radon levels, in 

laboratory animals in vivo, and in a variety of in vitro test systems. Increases in chromosomal 

abnormalities have been reported in peripheral blood lymphocytes of underground miners and occupants 

of residences where relatively high levels of radon were measured. Results of numerous in vivo and 

in vitro studies support the findings of radiation-induced chromosomal abnormalities associated with 

exposure to radon and radon progeny. Additional studies do not appear necessary at this time. 

Reproductive Toxicity. Results of a few epidemiological studies indicated that exposure to radon 

and its progeny during uranium mining may be associated with alterations in the secondary sex ratio 

among offspring (Dean 1981; Muller et al. 1967; Wiese and Skipper 1986). More recent assessments of 

mining cohorts did not focus on reproductive end points. Limited animal data are available regarding 

potential reproductive effects following exposure to radon and radon progeny. Available toxicokinetic 

data do not implicate reproductive tissues as particularly vulnerable tissues of concern following exposure 

to radon and radon progeny. 

Developmental Toxicity. Available information regarding the potential for radiation-induced 

developmental effects following exposure to radon and radon progeny is limited to negative findings in 

rats following inhalation exposure to 12 WLM of radon and radon progeny (absorbed onto ore dust) for 

18 hours/day at a rate of 124 WLM/day on gestation days 6–19 (Sikov et al. 1992). Additional animal 

studies could be designed to support or refute the results of Sikov et al. (1992). 

Immunotoxicity. No information was located regarding potential radon-induced effects on the 

immune system of humans or in animals exposed to radon and its progeny at concentrations considered 

relevant to human health. 

Neurotoxicity. Cells and tissues in the nervous system may be less radiosensitive, due to a lack of cell 

turnover or cellular regeneration, than faster regenerating cells of the gastrointestinal tract or pulmonary 

epithelium. Consequently, neuronal impairment as a result of radon alpha emissions is not expected. 

Therefore, studies that specifically or directly measure either pathological or functional damage to the 

nervous system following exposure to radon do not appear to be necessary at this time. 

Epidemiological and Human Dosimetry Studies. Knowledge of the adverse health effects in 

occupationally-exposed humans following chronic-duration exposure to radon and its progeny is based on 
 

 

RADON 103 

3. HEALTH EFFECTS 

studies in primarily adult male underground miners. These studies describe predominantly respiratory 

end points, such as pneumoconiosis, emphysema, interstitial pneumonitis, pulmonary fibrosis, 

tuberculosis, and cancer. However, lung cancer is the only respiratory effect that has been clearly 

associated with exposure to radon and radon progeny. One study of a cohort of uranium miners in the 

Czech Republic included a finding of significant positive associations between cumulative radon 

exposures and incidences of chronic lymphocytic leukemia and all leukemias combined (Řeřicha et al. 

2006). Additional studies of occupationally- and residentially-exposed individuals could be of benefit in 

assessing the potential for radon-induced leukemias; however, such studies would need to include large 

numbers of subjects given the low incidences of leukemias observed in available studies of radon. To a 

large extent, other health effects have not been either reported or studied; additional studies assessing 

health effects other than respiratory and cancer end points do not appear necessary. 

Numerous residential case-control studies are available for which possible associations between lung 

cancer and residential radon levels have been assessed. Collectively, these studies provide evidence of 

radon-induced lung cancer from long-term residential exposure. Continued monitoring of residential 

radon exposure is needed to more completely characterize exposure-response relationships. These 

assessments should include improved methods such as glass-based retrospective radon detectors (Field et 

al. 1999b; Steck et al. 2002; Sun 2008) and validation of such methods to more accurately estimate 

exposure scenarios. In addition, extensive data regarding radon exposure in non-residential buildings are 

needed. 

Biomarkers of Exposure and Effect. 

Exposure. Potential biomarkers of exposure may include the presence of radon progeny in urine, blood, 

bone, teeth, or hair. Although the detection of radon progeny in these media is not a direct measurement 

of an exposure level, estimates may be derived from mathematical models. Quantification of exposure to 

radon is further complicated by the fact that radon is a ubiquitous substance and background levels of 

radon and radon progeny are needed to quantify higher than “average” exposures. 

Effect. It has been reported that chromosome aberrations in the peripheral blood lymphocytes may be a 

biological dose-response indicator of radiation exposure (Bilban and Jakopin 2005; Brandom et al. 1978; 

Pohl-Rüling et al. 1976; Smerkovsky et al. 2001, 2002). In addition, the frequency of abnormalities in 

sputum cytology has been utilized as an early indicator of radiation damage to lung tissue (Band et al. 

1980); this has not been recommended regarding exposure to radon. However, more extensive research is 
RADON 104 

3. HEALTH EFFECTS 

needed in order to correlate these effects with radon exposure levels and subsequent development of lung 

cancer or other adverse effects. 

Absorption, Distribution, Metabolism, and Excretion. The toxicokinetics of inhaled and 

ingested radon and radon progeny has been fairly well studied, but information regarding the 

toxicokinetics of radon and radon progeny following dermal exposure is limited. Additional information 

on the deposition patterns in airways for radon progeny and the relationship of these deposition patterns to 

the onset of respiratory disease could help to enhance understanding of the disease process and delineate 

health protective measures to reduce deposition. 

Comparative Toxicokinetics. Similar target organs have been identified in both humans and 

laboratory animals exposed to radon and radon progeny. More information on respiratory physiology, 

target cells, lung deposition, and absorption of radon and its progeny in different animal species is needed 

to clarify observed differences in species-sensitivity and tumor types. For example, rats generally 

develop lung tumors in the bronchioalveolar region of the lung while humans develop lung tumors in 

higher regions (tracheobronchial area). These studies could identify the appropriate animal model for 

further study of radon-induced adverse effects, although differences in anatomy and physiology of the 

respiratory system between animals and humans require careful consideration. Most of the information 

available on the toxicokinetics of radon and progeny has been obtained from studies of inhalation 

exposure. Studies on the transport of radon and progeny following oral and dermal exposures would be 

of use for comparing different routes of exposure, although oral and dermal exposure routes do not appear 

to be of particular toxicity concern. 

Methods for Reducing Toxic Effects. Lung cancer is generally considered to be the only toxicity 

concern following long-term exposure to radon and radon progeny. The high-energy alpha emissions 

from radon progeny deposited in the lung are the source of toxicity concern. The sequence of events 

leading from irradiation of living cells is generally believed to involve ionization that causes cellular 

damage that includes DNA breakage, accurate or inaccurate repair, apoptosis, gene mutations, 

chromosomal change, and genetic instability. Cigarette smoke, crystalline silica dust, and arsenic have 

been reported to interact with radon and its progeny to potentiate their effects. The quality of breathing 

air in mines was addressed decades ago and the concentrations of radon, its progeny, silica dust, arsenic, 

and other mine pollutants that contribute to lung cancer were effectively reduced. 
RADON 105 

3. HEALTH EFFECTS 

Methods for reducing the potential for radon-induced toxic effects consist of reducing or eliminating 

smoking, as well as periodically testing for radon in indoor air and reducing radon concentrations to 

below the EPA recommended action level of 4 pCi/L, using active soil depressurization (ASD) in existing 

homes and radon-reducing features in new home construction. In some cases, an active soil 

pressurization system (ASP) may be necessary (see Section 6.5 for explanatory information regarding 

ASD and ASP systems. Laws are being enacted to eliminate or limit smoking in public areas and 

business locations. Continued research is needed to develop effective smoking reduction and stop 

smoking campaigns and to develop and implement additional techniques for reducing radon levels in 

homes and public buildings. 

Children’s Susceptibility. If data needs, relating to both prenatal and childhood exposures, and 

developmental effects expressed either prenatally or during childhood, are identified, they are discussed 

in detail in the Developmental Toxicity subsection above. 

Age-related differences in susceptibility to the effects of exposure to radon and radon progeny have not 

been demonstrated. Differences in lung morphometry and breathing rates in children may result in higher 

estimated radiation doses relative to adults (NCRP 1984a; Samet et al. 1989). However, available 

information from children employed as miners in China does not provide evidence of increased 

susceptibility to the effects of exposure to radon (Lubin et al. 1990; NIH 1994). 

Child health data needs relating to exposure are discussed in Section 6.8.1, Identification of Data Needs: 

Exposures of Children. 

3.12.3 Ongoing Studies 

Additional research known to be underway includes pooling of results from Iowa and Missouri residential 

radon studies using glass-based detectors that are undergoing final calibration (Field, personal 

communication) and pooling of results from the residential radon studies that contributed to the results of 

Lubin et al. (2004; China studies), Krewski et al. (2005, 2006; North American studies) and Darby et al. 

(2005, 2006; European studies). 
 

RADON 106
 

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RADON 107 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

4.1 CHEMICAL IDENTITY 

Radon is a naturally occurring radionuclide. The largest source of radon in the environment is due to the 

ambient levels produced by the widespread distribution of uranium, thorium, and their decay products in 

the soil (Buttafuoco et al. 2007; Weast 1980). Radon is a decay product of radium and part of the 

uranium and thorium decay chains (see Figure 4-1) (Buttafuoco et al. 2007; O’Neil et al. 2006). The 

chemical identity of radon isotopes and identification numbers for several of the radon isotopes (218Rn, 

219Rn, 220Rn, 222Rn, 226Rn, 229Rn, and 230Rn) are listed in Table 4-1. 

4.2 PHYSICAL, CHEMICAL, AND RADIOLOGICAL PROPERTIES 

Radon is the densest of all the gases. Important physical and chemical properties of radon are listed in 

Table 4-2. The radioactive properties of the important, short-lived daughters of 222Rn are listed in 

Table 4-3. Figure 4-1 depicts the 238U decay series containing 222Rn. Figure 4-2 depicts the 232Th decay 

series containing 220Rn (thoron). Figure 4-3 depicts the 235U decay series containing 219Rn (actinon). 
 

 

RADON 108 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-1. Chemical Identity of Radon 

Characteristic Radon Reference 

Isotope(s) Recognized isotopes:

195Rn through 228Rn 

DOE 2008 

Naturally-occurring isotopes:

222Rn (radon)

220Rn (thoron)

219Rn (actinon) 

Registered trade name(s) No data 

Chemical formula Rn 

Chemical structure Monatomic 

Identification numbers: 

CAS Registry 10043-92-2 Radon 

51712-92-6 (230Rn) 

51712-91-5 (229Rn) 

16369-95-2 (226Rn) 

14859-67-7 (222Rn) 

22481-48-7 (220Rn) 

14835-02-0 (219Rn) 

15411-71-9 (218Rn) 

ChemIDPlus 2012 

NIOSH RTECS No data 

EPA Hazardous Waste No data 

OHM/TADS No data 

DOT/UN/NA/IMDG No data 

HSDB 6369 (radon radioactive) HSDB 2008 

NCI No data 

CAS = Chemical Abstracts Services; DOT/UN/NA/IMDG = Department of Transportation/United Nations/North 

America/International Maritime Dangerous Goods Code; DOE = Department of Energy; Environmental Protection 

Agency; HSDB = Hazardous Substance Data Bank; NCI = National Cancer Institute; NIOSH = National Institute for 

Occupational Safety and Health; OHM/TADS = Oil and Hazardous Materials/Technical Assistance Data System; 

RTECS = Registry of Toxic Effects of Chemical Substances 
 

 

 

RADON 109 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-2. Physical, Chemical, and Radiological Properties of Radon 

Property Radon Reference 

Molecular weight 222 (radon), 220 (thoron), 219 (actinon) Cothern 1987a 

Color Colorless Lewis 2001 

Physical state Gas at 0 °C and 760 mm Hg Lewis 2001 

Melting point -71 °C Lide 2005 

Boiling point -61.8 °C Lewis 2001 

Density at -20 °C 9.96x10-3

 g/cm3 Cothern 1987a 

Odorb Odorless O’Neil et al. 2006 

Odor threshold: 

 Water Odorless 

Air Odorless 

Solubility: 

Water at 20 °C 230 cm3

/L O’Neil et al. 2006 

Organic solvents Organic liquid, slightly soluble in alcohol Weast 1980 

Vapor pressure at 25 °Ca 395.2 mm Hg Cothern 1987a 

Henry’s Law constant No data 

Autoignition temperature Noble gas; does not autoignite 

Flash point Noble gas; does not burn 

Flammability limits Noble gas; is not flammable 

Half-life: 

222Rn 3.8235 days DOE 2008 

220Rn 55.6 seconds DOE 2008 

219Rn 3.96 seconds DOE 2008 

Decay energies (MeV), and 

intensities (%) 

222Rn Alpha particles: DOE 2008 

4.826 (0.0005%) 

4.986 (0.078%) 

5.48948 (99.920%) 

Gamma rays: 

0.510 (0.076%) 

220Rn Alpha particles: DOE 2008 

5.747 (0.114%) 

6.288 (99.886%) 

Gamma rays:

 0.5497 (0.114%) 
 

RADON 110 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-2. Physical, Chemical, and Radiological Properties of Radon 

Property Radon Reference 

219Rn Alpha particles (15 reported): U.S. DHEW 1970 

6.425 (7.5%) 

6.530 (0.12%) 

6.553 (12.9%) 

6.819 (79.4%) 

Gamma rays (dozens reported): 

0.0111 (9.6% 

0.0769 (5.0%) 

0.0793 (8.4%) 

0.2712 (10.8%) 

Specific activity, nλ/mass (Ci/g): 

222Rn 1.538x105 Based on DOE 2008 

220Rn 9.135x108 Based on DOE 2008 

219Rn 1.301x1010 Based on DOE 2008 

Decay products: Radon progeny (daughters) 

222Rn (see Figure 4-1) 218Po DOE 2008 

214Pb 

214Bi 

214Po 

210Tl 

210Pb 

210Bi 

210Po 

206Tl 

206Pb 

220Rn (see Figure 4-2) 216Po DOE 2008 

212Pb 

212Bi 

212Po 

208Tl 

208Pb 

219Rn (see Figure 4-3) 215

Po DOE 2008 

215At 

211Pb 

211Bi 

211Po 

207Tl 

207Pb 

MeV = million electron volts 
 

RADON 111 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-3. Radioactive Properties of 222Rn and Its Short-lived Progeny 

Q-Value of 

Historical Principal principal decay Specific activity 

Isotope symbol radiation(s) mode (MeV) Half-life (Ci/g) 

222Rn Rn α 5.5903 3.8235 days 1.54x105 

218Poa RaA α 6.1147 3.098 minutes 2.78x108 

218At At α 6.874 1.5 seconds 3.45x1010 

214Pb RaB β,γ 1.023 26.8 minutes 3.28x107 

214Bi RaC β,γ 5.6168 19.9 minutes 4.41x107 

214Poa RaC’ α 7.8335 164.3 μseconds 3.21x1014 

210Tl RaC” β 5.489 1.30 minutes 6.89x108 

a

Isotopes of primary radiological interest due to the potential for retention in the lung and subsequent alpha decay. 

MeV = million electron volts 

Source: DOE 2008 
 

 

 

 

 

 

 

 

 

 

RADON 112 

4. CHEMICAL AND PHYSICAL INFORMATION 

Figure 4-1. 238U Decay Series Showing Sources and Decay Products* 

238U Series 

U 

238U 

4.468x109 

years 

234U 

2.455x105 

years 

Pa ↓

234mPa 

1.159 minutes 234Pa 

6.70 hours 

↓

Th 

234Th 

24.10 days 

230Th 

7.54x104 

years 

Ac ↓

Ra 

226Ra 

1,600 years 

Fr ↓

Rn 

222Rn 

3.8235 days 0.1% 218Rn 

0.035 

seconds 

At ↓ 0.02% 218At 

1.5 

seconds ↓

Po 

218Po 

3.098 

minutes 

↓99.90% 99.98% 214Po 

1.643x10-4 

seconds 99.9999% 

210Po 

138.4376 

days 

Bi ↓99.98% 

214Bi 

19.9 

minutes 

↓ 210Bi 

5.012 days ↓

Pb 

214Pb 

26.8 

minutes ↓0.02% 

210Pb 

22.20 

years ↓1.3x10-4% 

206Pb 

stable 

Tl 

210Tl 

1.30 

minutes 

206Tl 

4.202 

minutes 

*All of the single transitions are 100%; other branching ratios are shown in the decay series. 

↓ alpha (α) decay; beta (β-) decay or internal transition (IT) 

Source: NNDC 2012b 
 

 

 

 

 

 

RADON 113 

4. CHEMICAL AND PHYSICAL INFORMATION 

Figure 4-2. 232Th Decay Series Showing Sources and Decay Products 

232Th Series 

U 

Pa 

Th 

232Th 

1.40x1010 years 

228Th 

1.9116 years 

Ac ↓ 228Ac 

6.15 hours ↓

Ra 

228Ra 

5.75 years 

224Ra 

3.6319 days 

Fr ↓

Rn 

220Rn 

55.6 seconds 

At ↓

Po 

216Po 

0.145 

seconds 98.62% 

212Po 

2.99x10-7 

seconds 

Bi ↓ 212Bi 60.55 

minutes ↓

Pb 

212Pb 

10.64 hours ↓35.94% 

208Pb 

stable 

Tl 

208Tl 

3.053 minutes 

*All of the single transitions are 100%; other branching ratios are shown in the decay series. 

↓ alpha (α) decay; beta (β-) decay or internal transition (IT) 

Source: NNDC 2012b 
 

 

 

 

 

 

 

 

 

 

RADON 114 

4. CHEMICAL AND PHYSICAL INFORMATION 

Figure 4-3. 235U Decay Series Showing Sources and Decay Products 

235U Series 

U 

235U 

7.04x108 

years 

Pa ↓ 231Pa 3.276x104 

years 

Th 

231Th 

25.52 hours ↓ 98.62% 

227Th 

18.68 days 

Ac 

227Ac 

21.772 years ↓

Ra ↓1.38% 

99.994% 

223Ra 

11.43 days 

Fr 

223Fr 

22.00 minutes ↓

Rn ↓6.03x10-3% 

3.00% 

219Rn 

3.96 seconds 

At 

219At 

56 seconds ↓

2.3x10-4 

215At 

1.0x10-4 

second 

Po ↓97.00% 

215Po 

1.781x10-3 

second ↓ 0.28% 

211Po 

0.516 second 

Bi 

215Bi 

7.6 minutes ↓99.99977% 

211Bi 

2.14 

minutes ↓

Pb 

211Pb 

36.1 minutes ↓99.72% 

207Pb 

stable 

Tl 

207Tl 

4.77 minutes 

*All of the single transitions are 100%; other branching ratios are shown in the decay series. 

↓ alpha (α) decay; beta (β-) decay or internal transition (IT) 

Source: NNDC 2012b 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 115 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

5.1 PRODUCTION 

No information is available in the TRI database on facilities that manufacture or process radon because 

this chemical is not required to be reported under Section 313 of the Emergency Planning and Community 

Right-to-Know Act (Title III of the Superfund Amendments and Reauthorization Act of 1986) (EPA 

1998). 

Radon is a naturally occurring element; the isotope of primary health concern is 222Rn. The largest source 

of radon in the environment is widely distributed uranium and its decay products in the soil (Buttafuoco et 

al. 2007; UNSCEAR 2000; Weast 1980). Radon is a decay product of radium and part of the uranium 

decay chain (see Figure 4-1) (Buttafuoco et al. 2007; O’Neil et al. 2006; UNSCEAR 2000). Every square 

mile of surface soil, to a depth of 6 inches, contains approximately 1 gram of radium, which slowly 

releases radon to the atmosphere (Weast 1980) when conditions of secular equilibrium exist. 

The total production rate of radon in soil equates to the decay rate or concentration of radium present, 

which can range from 10 to 100 Bq/kg (270–2,700 pCi/kg) in the surface soil and from ~15 to ~50 Bq/kg 

(~400–~1,350 pCi/kg) in rock (Buttafuoco et al. 2007). The release of radon from the soil-gas or water to 

ambient air is affected by the soil porosity, meteorological factors, variations in atmospheric pressure, and 

concentration of radon in the soil-gas or water (WHO 1983). The concentration of radon in soil gas is 

affected by grain size, mineralogy, porosity, density permeability, and moisture, radium, and uranium 

content of the soil (Ericson and Pham 2001; Price et al. 1994; USNRC 1981). Meteorological factors, 

such as temperature and precipitation, may both enhance and inhibit transport of radon from the soil into 

other media. Radon progeny in the air can be removed by rainfall, soil moisture, and snow (UNSCEAR 

2000). Alternatively, radon and its progeny may be temporarily increased at ground level after being 

brought to the surface by precipitation. If this is by rainfall, then the radon itself is rapidly released back 

into the atmosphere causing a spike in near-surface levels but leaving the particulate progeny behind in 

the water or on the surface. If this is by snowfall, then the progeny decay quickly, and any trapped radon 

builds up progeny toward equilibrium until snowmelt releases the remaining radon. Surface freezing can 

retard the radon emanation rate (Bunzl et al. 1998; Fujiyoshi et al. 2002). Vertical temperature gradients 

in which temperature decreases with elevation above the ground can help release radon from the soil, 

while temperature inversions inhibit this movement. The mechanism of radon transport in soil is 

described more fully in Section 6.3.1. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 116 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

Outdoor radon levels vary significantly with geographic location. The ambient outdoor radon level goes 

through a daily cycle of concentrations ranging from approximately 0.03 to 3.50 pCi/L (Martin and Mills 

1973) with the average level in the United States, based on a natural residential radon survey, being about 

0.4 pCi L of outdoor air (EPA 2008b). Radon levels can be highly elevated in indoor spaces (UNSCEAR 

2000). Indoor radon levels in the United States were found to range from approximately 0 to >80 pCi/L 

(3,000 Bq/m3

) (Fleischer 1986; Steck et a. 1999; White et al. 1992). EPA estimates that the average 

indoor radon level is 1.25 pCi/L in the United States (EPA 2003; Marcinowski et al. 1994). 

The amount of naturally occurring radon released to the atmosphere is increased in areas with uranium 

and thorium ore deposits and granite formations, which have a high concentration of natural uranium. It 

is the presence of granite formations that has greatly increased radon concentrations in eastern 

Pennsylvania and parts of New York and New Jersey (EPA 2003; NAS 1999b; NCRP 1984a; Nero 1987), 

although elevated radon levels were also found in other parts of the country (map available at 

http://www.epa.gov/radon/zonemap.html) (EPA 2011a). Large granite outcroppings, such as the 

mountain in Stone Mountain, Georgia, are sources of additional airborne radon in that region. Sources of 

radon in the global atmosphere include natural emissions from radium in soil and water, tailings from 

metal mines (uranium, thorium, silver, tin, and phosphorus), agricultural lands utilizing phosphate 

fertilizers, and from construction materials and the burning of coal (EPA 2003; NAS 1999b; NCRP 

1984a; Nero 1987). In a few locations, tailings have been used for yard fill, garden soil, sand for masonry 

work, or landfills and were subsequently built on, resulting in possible increased exposure to radon 

(Eichholz 1987). There is also an increased radon concentration in spring water due to the deposition of 

radium isotopes in the sinter areas around hot springs, where it is coprecipitated with calcium carbonate 

or silica (NCRP 1975). In groundwater, radon is present due to migration from rock and soil into 

surrounding groundwater (Hess et al. 1985; Lam et al. 1994). 

Radon is not distributed commercially (Hwang et al. 2005). It has been produced commercially for use in 

radiation therapy, but for the most part, it has been replaced by radionuclides made in accelerators and 

nuclear reactors. Although no longer used, radiopharmaceutical companies and a few hospitals had 

pumped the radon from a radium source into tubes called “seeds” or “needles”, which may be implanted 

in patients (Cohen 1979). Due to the short half-life, research laboratories and universities typically 

produce radon in the laboratory for experimental studies (Hwang et al. 2005). Radon gas is collected by 

bubbling air through a radium salt solution (Hwang et al. 2005; Lewis 2001). The evolved gas containing 

radon, hydrogen, and oxygen is cooled to condense the radon and the gaseous hydrogen and oxygen are 

removed (Hwang et al. 2005). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 117 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

5.2 IMPORT/EXPORT 

Radon is not imported into or exported from the United States. 

5.3 USE 

While there are currently few significant technical uses for radon (Hwang et al. 2005), it does have 

several potentially useful applications. Medical uses of radon in the United States began as early as 1914. 

Treatments were primarily for malignant tumors. The radon was encapsulated in gold seeds and then 

implanted into the site of malignancy. During the period of 1930–1950, radon seeds were used for 

dermatological disorders, including acne. Radon therapy was still being studied and applied as recent as 

1980 (Morken 1980). 

Radium-223 (223Ra), an isotope of radium that is a calcium surrogate and bone seeker, and which decays 

to 219Rn, is being studied for possible use as a radiopharmaceutical in the treatment of skeletal metastases 

(NIST 2010). 223Ra decays into 219Rn, making this isotope a significant contributor to the radiation dose 

delivered to the tumor. 

Water or air containing naturally high levels of 222Rn has been used for therapeutic treatment of various 

diseases, such as arthritis (Becker 2003; Dobbin 1987; Pohl-Rüling and Fischer 1982). Small “radon 

mines” (caves with a high radon concentration in the air, such as abandoned mines) have been used as a 

health treatment (Cohen 1979). People would seek medical cures through exposure to radon gas for 

ailments ranging from arthritis, asthma, and allergies to diabetes and ulcers (Dobbin 1987), as well as for 

cancer treatment (Dobbin 1987; Lewis 2001). Radon “spas,” with their commensurately high radon 

levels, have been used in Europe for the treatment of hypertension and a number of other disorders. In 

the former Soviet Union., for example, radon baths were often prescribed by the National Health System 

(Uzunov et al. 1981). 

Radon may be utilized in the prediction of earthquakes (Cothern 1987b). Large quantities of radon have 

been found to migrate to the atmosphere from the earth from active fault zones, varying with atmospheric 

conditions and potentially with seismic activity (Buttafuoco et al. 2007). The emission of radon from soil 

and the concentration measured in groundwater appear to be good indicators of crustal activity. Other 

uses of radon include the study of atmospheric transport, the exploration for petroleum or uranium 

(Cothern 1987b), as a tracer in leak detection, for flow-rate measurement, and in radiography. Radon is 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 118 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

also used in chemical research (Lewis 2001) to initiate and influence reactions, as a label in surface study 

reactions, for radium and thorium determination, and in determining the behavior of filters (O’Neil et al. 

2006). 

As a tracer, radon can also be used in the identification and quantification of non-aqueous phase liquid 

(NAPL) contamination of the subsurface (Semprini et al. 2000). In the subsurface, naturally occurring 

222Rn exists as a dissolved gas in the saturated zone. While groundwater radon concentrations vary with 

the mineral composition of the substrate, they rapidly equilibrate in the absence of NAPL. The 

groundwater radon concentration, however, may be much less when NAPL is present due to its affinity 

for partitioning into NAPL. Reduced radon concentration correlates to the amount of NAPL in the 

subsurface pores. Scientists may then predict the location and saturation levels of NAPL by examining 

the distribution of radon in the subsurface (Semprini et al. 2000). 

5.4 DISPOSAL 

Disposal of radon would only be applicable to those facilities producing and/or using it for medical or 

experimental purposes where its release may be controlled. Regulations regarding the land disposal of 

radionuclides, as set forth in 10 CFR 61 (USNRC 2008), do not apply to radium, radon, or its daughters. 

Since radon is naturally occurring, it is not regulated by the U.S. Nuclear Regulatory Commission 

(USNRC) with the exception of emissions from uranium mill tailings. Uranium mill tailings contain 

radium, the precursor to radon. The Uranium Mill Tailings Radiation Control Act of 1978 (UMTRCA) 

established programs to control the disposal and stabilization of uranium mill tailings to minimize public 

health hazards associated with the decay of radium within the tailings (EPA 1995). Any other regulation 

of radon is up to the individual states. The allowable release rate of radon from the surface is 20 pCi/m2

/ 

second. See Chapter 8 for a listing of regulations concerning radon. 

Radon emanation is not regulated under 10CFR20 for facilities operating under a USNRC license, but its 

flux or emanation rate is restricted by EPA regulation to 20 pCi/m2

/second (EPA 2011c). The two 

primary isotopes from natural sources have short half-lives and typically slow diffusion rates, so most 

ambient radon is produced in the top 30 cm or 1 foot of soil. Radon emanation rates from typical soil can 

be on the order of several pCi/m2

/second (Cember and Johnson 2009), but some mill tailings sites exceed 

the 20 pCi/m2

/second limit. In such cases, disposal involves moving the tailings or reducing the levels by 

adding a retarding layer over the tailings, such as a several foot thick layer of clay or shale soil (EPA 

2008a). In small use facilities, radon may be compressed and stored in tanks until it decays or, if the 
 

 

 

 

 

 

 

 

 

RADON 119 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

quantity is small, it may be adsorbed on activated charcoal (Cember 1983). Particulate matter may be 

removed from the gas by a variety of different devices including detention chambers, adsorbent beds, and 

liquefaction columns. After filtration, the remaining radioactive particulates are discharged into the 

atmosphere for dispersion of the nonfilterable low levels of activity (Cember 1983). 

Discharge via combustion stream from a natural gas incinerator power plant may contain high levels of 

radon when the natural gas is retrieved from an area with high concentrations of radium. Radon can be 

released to the environment from fossil-fueled power plants since radon cannot be scrubbed from the 

combustion stream by standard methods. The average concentration of radon in the combustion stream of 

a plant reported by Ericson and Pham (2001) was 370 pCi /L (13,700 Bq/m3

). Federal and State of 

California regulations do not control radioactive emissions such as these, which are considered to be 

“natural” emissions (Ericson and Pham 2001). 
 

RADON 120
 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

This page is intentionally blank. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 121 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.1 OVERVIEW 

The presence of radon at any site can be a consequence of its natural occurrence in the environment plus 

any releases from anthropogenic hazardous waste. 

The results of the 1992 EPA National Residential Radon Survey (EPA 1992b) estimated that 1 in 

15 homes had an elevated radon level (i.e., a level at or above the EPA action level of 4 pCi/L). At the 

time, an estimated 5.8 million homes had an elevated radon level. The source of radon in homes is from 

naturally occurring (geologic) sources. For more information, refer to EPA’s A Citizen’s Guide to Radon 

(EPA 2009a). 

222Rn is a naturally occurring radioactive noble gas that is part of the 238U decay chain, and is the daughter 

of 226Ra. Similarly, 219Rn and 220Rn are in the 235U and 232Th decay chains and immediate daughters of 

223Ra and 224Ra. 218Rn is in the 238U decay chain and the immediate daughter of 218At. As radium decays, 

radon is formed and is released into small air or water-containing pores between soil and rock particles. 

If this occurs within radon’s diffusion length of the soil surface, the radon may be released to ambient air 

(EPA 2003). Similarly, radon may migrate into groundwater. If this groundwater reaches the surface, 

some of the radon gas will release into the ambient air, but small amounts remain dissolved in the water. 

By far, the major sources of radon are its formation in and release from soil and groundwater, with soil 

contributing the greater amount (EPA 2003; Planinić et al. 1994). Radon is also released from the near 

surface water of oceans, tailings from mines (particularly uranium, phosphate, silver, and tin mines), coal 

residues, the combustion of fossil fuels (coal, oil, and natural gas), and building products (concrete, 

drywall, and brick) (Ericson and Pham 2001; Nero 1987). Global radon emissions from soil are estimated 

to be 2,400 million Ci 222Rn (8,880x1016 Bq), followed by release from groundwater (500 million Ci), 

oceans (34 million Ci), phosphate residues (3 million Ci), uranium mill tailings (2 million Ci), coal 

residues (0.02 million Ci), natural gas emissions (0.01 million Ci), coal combustion (0.009 million Ci), 

and human exhalation (1x10-5 million Ci) annually (Fishbein 1992). Monitoring data in this chapter are 

reported for 222Rn unless otherwise specified. The two other naturally occurring radioactive isotopes of 

radon, 219Rn and 220Rn, are not discussed due to their short half-lives (3.96 and 55.6 seconds, respectively; 

see Figures 4-2 and 4-3) (DOE 2008). 

The ultimate fate of radon is transformation through radioactive decay. Radon decays only by normal 

radioactive processes (i.e., an atom of radon emits an alpha particle resulting in an atom of polonium, 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 122 

6. POTENTIAL FOR HUMAN EXPOSURE 

which itself undergoes radioactive decay to other radon daughters or progeny) (EPA 2003). There are no 

sinks for radon, since its radioactive half-life is so short (3.8 days) (O’Neil et al. 2006). 

In soil, radium atoms decay to radon, which can be released from the soil mineral matrix and transported 

through the soil column, ultimately being released to air. Alpha recoil is the process by which radon, 

when it is formed by radium emitting an alpha particle, actually recoils in the opposite direction from the 

path of particle ejection. Alpha recoil is important because this process dislodges radon from the edge of 

the soil mineral matrix and allows it to enter pore space between the soil grains. After radon is released 

into the pore spaces, its ultimate release to ambient air is a function of the soil porosity, soil moisture 

content, and meteorological factors, such as precipitation, atmospheric pressure, and the temperature 

versus altitude profile. Once radon is released to ambient air, its dispersion is primarily determined by 

atmospheric stability, including vertical temperature gradients and effects of wind. Transport of radon in 

indoor air is almost entirely controlled by the ventilation flow path and rate. Generally, the indoor radon 

concentrations increase as ventilation rates decrease. These transport processes are discussed in more 

detail in Section 6.3.1. 

In groundwater, radon moves by diffusion and, primarily, by the mechanical flow of the water. Radon 

solubility in water is relatively low and, with its short radioactive half-life of 3.825 days (O’Neil et al. 

2006), much of it will decay before it can be released from groundwater. Groundwater supplies in the 

United States have been surveyed for radon levels. In larger aquifers, average radon concentrations were 

reported to be 240 pCi (8.8 Bq)/L of water, while in smaller aquifers and wells, average levels were 

considerably higher (780 pCi/L of water; 28.9 Bq/L) (Cothern et al. 1986). These differences in radon 

levels between large and small groundwater supplies are a reflection of the types of rock and soil, as well 

as their uranium concentrations, through which the groundwater flows (Agency for Toxic Substances 

and Disease Registry 2011). Granitic rock, which is associated with high radon levels, does support 

large aquifers, although small aquifers may be present (Field and Kross 1998). For public groundwaterderived water supplies, the average radon concentration is estimated at 540 pCi/L (20 Bq/L), although 

some wells have been found to have radon concentrations up to 400 times the average concentration (up 

to 1x107 Bq/m3

; 270,000 pCi/L). Surface water tends to have the lowest radon concentrations (NAS 

1999b). Additional detail on radon in water is provided in Section 6.4.2. 

Radon levels in ambient air vary with the type of soil and underlying bedrock of the area. The average 

outdoor radon concentration in the United States is about 0.4 pCi/L (14.8 Bq/m3

) (NAS 1999b). 

Measurements in Iowa and Minnesota show higher levels, with average outdoor concentrations of 0.60– 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 123 

6. POTENTIAL FOR HUMAN EXPOSURE 

0.82 pCi/L (22.2–30.3 Bq/m3) (Steck et al. 1999). Indoor concentrations as high as 2,000 pCi/L 

(74,000 Bq/m3

) have been observed in certain locations in the United States (EPA 2008b). Based on the 

National Residential Radon Survey, EPA estimates that the average indoor radon level is 1.25 pCi/L 

(46.25 Bq/m3

) in the United States (EPA 2003; Marcinowski et al. 1994); however, several locations in 

the country have been documented where the average indoor air levels are several times greater than the 

national average (Field 2005; Steck et al. 1999). The 1992 National Residential Radon Survey indicated 

that radon levels above the EPA recommended action level of 4 pCi/L could be present in 1 in 15 homes. 

At the time of the survey (1990), it was estimated that about 5.8 million homes had a higher radon level. 

For more information, refer to EPA’s A Citizen’s Guide to Radon (EPA 2009a). 

Measurements of radon in soil are expressed in terms of levels in soil-gas. However, these measurements 

do not directly relate to rates of radon released to the atmosphere. Factors that affect radon soil-gas levels 

include soil properties such as radium content, mineral composition, moisture content, density, and soil 

porosity. Radon concentrations in soil may also be affected by meteorological conditions on the surface, 

such as snow (Fujiyoshi et al. 2002). 

The primary pathway for human exposure to radon is inhalation from soil gas intrusion to dwellings and 

buildings; however, indoor radon levels can also originate from water usage, outdoor air infiltration, and 

the presence of building materials containing radium (EPA 2003). The committed dose from radon and 

its progeny is estimated by complex mathematical models and simplified tables have been published by 

EPA as Federal Guidance Report No. 13 (EPA 1999a). Exposure, both occupational and environmental, 

will be discussed primarily in terms of radon or radon progeny levels in the air. However, some estimates 

of daily intake can be made. For example, using an average indoor air radon concentration of 1.25 pCi/L 

(EPA 2003; Marcinowski et al. 1994) and an assumed breathing rate of 20 m3

/day, the radon daily intake 

from indoor air is 25,000 pCi/day. Using an estimated outdoor concentration of 0.4 pCi/L (NAS 1999b) 

and the same inhalation rate, the radon daily intake from outdoor air is 8,000 pCi/day. 

Radon releases from groundwater also contribute to exposure. The daily intake of radon originating from 

drinking water only is estimated at 100–600 pCi (3.7–22.2 Bq)/day both from ingestion of drinking water 

and inhalation of radon released from drinking water (Cothern et al. 1986). 

The highest occupational exposures to radon typically result from employment in underground uranium 

and other hard rock mining, or in phosphate mining due to the high airborne levels of radon and its 

progeny (NIOSH 2006). For example, an abandoned uranium mine located in Hungary had an average 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 124 

6. POTENTIAL FOR HUMAN EXPOSURE 

radon concentration of 410 kBq/m3 (11,100 pCi/L) at a depth of 15–55 m below the surface (Somlai et al. 

2006). Although persons engaged in uranium mining are believed to receive the greatest exposures, the 

number of persons employed in uranium mining has greatly decreased. Furthermore, continuous 

improvements in engineering controls have lessened radon exposure in underground mines (NIOSH 

1987). Measurements of radon progeny in U.S. mines from 1976 to 1985 showed annual mean 

concentrations of 0.11–0.36 working level (WL). A working level is “any combination of short-lived 

radon progeny in 1 liter of air that will ultimately release 1.3x105

 million electron volts of alpha energy 

during decay to lead-210” (NIOSH 1987). However, levels in phosphate mines measured during the 

same period showed a larger range of mean levels (0.12–1.20 WL) (NIOSH 1987). In 2006, assessments 

of radon exposure during phosphate plant operations resulted in an estimated mean concentration of 

0.003 WL, based on limited data (NIOSH 2006). 

While certain professions pose a higher risk of occupational exposure to radon (employment at 

underground mines for instance), exposure to high concentrations can occur in any location with geologic 

radon sources (Field 1999). A list of common occupations that have the potential for high radon and 

progeny exposure was developed by Field (1999). These occupations include mine workers (uranium, 

hard rock, and vanadium mines) and employees of water treatment plants, and radioactively contaminated 

sites can include uranium mill sites and associated mill tailing piles, phosphate fertilizer plants, oil 

refineries, power plants, and natural gas and oil piping facilities. Locations that are not contaminated, but 

at which elevated natural radon levels exist, can include natural caverns, utility and subway tunnels, 

excavation sites, health mines and spas, and fish hatcheries (EPA 2003; Field 1999; Fisher et al. 1996). 

Higher exposures can occur to farmers, radon mitigation professionals, and scientists studying radon or 

other radionuclides, although exposure to local radon sources occurs to everyone present, and elevated 

exposures can occur in any occupation (Field 1999). 

6.2 RELEASES TO THE ENVIRONMENT 

Manufacturing and processing facilities are required to report Toxics Release Inventory (TRI) to the EPA 

if specific criteria are met (EPA 2005). The TRI requirements do not apply to radon. 

6.2.1 Air 

There is no information on releases of radon to the atmosphere from manufacturing and processing 

facilities because these releases are not required to be reported (EPA 1998). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

Because of the extended half-lives of uranium and radium and their abundance in the earth's surface, 

radon is continually being formed in soil and released to air. This normal emission of radon from 226Ra in 

soils is the largest single source of radon in the global atmosphere (NAS 1999b; NCRP 1984a; Planinić et 

al. 1994). Using an average soil emanation rate of 1,600 pCi/cm2

-year and an estimated global surface 

area of 1.5x1018 cm2

, Harley (1973) estimated soil emanation of radon to be on the order of 2.4x109 Ci 

(8.9x1019 Bq)/year. Some solubilized radon is removed from the soil by plants through 

evapotranspiration where it is subsequently released to the atmosphere by diffusion through the leaf 

(Kozak et al. 2003; Taskayev et al. 1986). 

Radon levels in outdoor air are affected by the composition of the substrate in the region. A monitoring 

study of radon in outdoor air conducted at 50 sites with varying geological characteristics in the state of 

Nevada indicated that the median statewide concentration of radon was essentially that of the nationwide 

average level of 0.4 pCi/L (Price et al. 1994). However, concentrations as large as 1.4 pCi/L were 

observed and these high levels usually correlated with silica rich igneous rocks (rhyolite and granite). 

Groundwater radon concentrations are also affected by the type of substrate. According to a study of 

North Carolina groundwater from private wells, areas with soil comprised on sand, silt, sandstones, and 

shales tend to have lower groundwater radon concentrations (67–1,700 pCi/L [2.5–63 Bq/L]) than 

groundwater in areas with metamorphic and granitic rocks (21–59,000 pCi/L [0.8–2,200 Bq/L]) (Watson 

et al. 1993). 

Groundwater that is in contact with radium-containing rock and soil will be a receptor of radon emanating 

from the surroundings. When the groundwater reaches the surface by natural or mechanical means, this 

radon will start to be released to air. Although most of the radon present in groundwater will decay 

before reaching the surface, groundwater is considered to be the second largest source of environmental 

radon and is estimated to contribute 5x108 Ci (1.85x1019 Bq)/year to the global atmosphere (Fishbein 

1992; NCRP 1984a). Radon is also released from oceans, but only from the near surface water, and in 

amounts that are an order of magnitude less than that from groundwater. As radium in oceans is largely 

restricted to bottom sediments, most radon would decay before water could carry it to the surface. Radon 

emissions from oceans were estimated as 3.4x107 Ci/year (Fishbein 1992). 

Radon in indoor air may also originate from volatilization of radon gas from water supplies used within 

homes for drinking, bathing, cooking, etc. Approximately 1–5% of the radon in indoor air was estimated 

to originate from water (Lam et al. 1994). Radon can also be released from water during the aeration and 

backwashing portions of the water treatment process. In a study of the water treatment process, exposure 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

to 222Rn was measured at 31 Iowa water treatment plants found to have the largest decrease in 222Rn water 

concentrations between raw and finished water. Workers were estimated to be exposed to an average 

annual air concentration of 3.4 pCi/L (126 Bq/m3

) ranging from 0.4 to 133 pCi/L (15–4,921 Bq/m3). 

Facilities with the highest 222Rn air concentrations treated groundwater containing moderate 226Ra 

concentrations using aeration and iron filters. The estimated worker exposures were below the OSHA 

limit of 4 WLM/year based on short exposure intervals, even though exposures were overestimated by 

assuming radon-progeny equilibrium (Fisher et al. 1996) 

Tailings from uranium mines and residues from phosphate mines each contribute to global radon in the 

approximate amount of 2–3x106

 Ci (7.4x1016–1.11x1017 Bq)/year, or a combined total of approximately 

5x106 Ci (1.85x1017 Bq)/year. An abandoned mine in Hungary, with a subsurface radon concentration of 

410 kBq/m3

 (11,100 pCi/L), was thought to have a significant effect on the air concentration of radon in 

houses above the mine. Indoor air concentrations, which averaged 667 Bq/m3

 (18.0 pCi/L), were likely 

elevated due to gas concentration within fissures reaching from the mine to the surface (Somlai et al. 

2006). Fishbein (1992) reported that 3x106 Ci of 222Rn is emitted from phosphate residues and 2x106 Ci 

of 222Rn originates from uranium mill tailings each year. 

Coal residues and fossil fuel (coal, oil, and natural gas) combustion products each contribute to 

atmospheric radon levels to a minor extent (NCRP 1984a). The portion from coal residues, such as fly 

ash, is very small. As natural gas retrieved from an area with concentrations of radium may contain high 

levels of radon, discharge via a combustion stream from a natural gas incinerator power plant may also 

have high radon levels. Emissions from one plant were measured as having an average concentration of 

370 pCi/L (13,700 Bq/m3

). Radon is a noble gas, so it is not feasible to scrub it from any combustion 

stream. As of 2001, federal and State of California regulations did not control radioactive emissions such 

as these, which are considered to be “natural” emissions. Liquefied natural gas products from these sites 

may contain radon and progeny (Ericson and Pham 2001). Fishbein (1992) reported that coal residue and 

natural gas emissions release 20,000 and 10,000 Ci of 222Rn each year, respectively, while coal 

combustion results in 900 Ci of 222Rn production annually. 

6.2.2 Water 

There is no information on releases of radon to the water from manufacturing and processing facilities 

because these releases are not required to be reported (EPA 1998). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

The amount of radon released to groundwater is a function of the chemical concentration of 226Ra in the 

surrounding soil or rock and in the water itself (Hess et al. 1985). Radon can dissolve in groundwater 

following radioactive decay of the radium. High radon concentrations are associated with groundwater 

running over granitic rock or through alluvial soils originating from granite (Hess et al. 1985; Lam et al. 

1994). The physical characteristics of the rock matrix are also important since it is believed that much of 

the radon released diffuses along microcrystalline imperfections in the rock matrix (Hess et al. 1985). 

Radon can also enter surface water through decay of radium. 

6.2.3 Soil 

There is no information on releases of radon to the soil from manufacturing and processing facilities 

because these releases are not required to be reported (EPA 1998). 

As stated in Section 6.2.1, soil is the primary source of radon (NCRP 1984a; Planinić et al. 1994). As 

such, radon is not released to soil but is the result of radioactive decay of 226Rn within the soil. Hopke 

(1987) states that normal soil-gas radon measurements are in the range of 270–675 pCi/L of air (10,000– 

25,000 Bq/m3

). However, levels exceeding 10,000 pCi/L of air (370,000 Bq/m3) have been documented. 

6.3 ENVIRONMENTAL FATE 

6.3.1 Transport and Partitioning 

The transport of radon from subsurface soil to air is a complex process that is dependent upon 

characteristics of the soil and meteorological conditions. 

Emanation is the process by which radon is transported from the edge of a solid soil matrix to a gas or 

liquid pore space between the soil grains (Michel 1987). The mechanism by which this process occurs is 

primarily through alpha recoil. When a 226Ra atom decays, it emits either a 4.6 or 4.8 MeV alpha particle, 

which results in the formation of a radon atom. The alpha particle takes a virtually straight line path in 

one direction, heavily ionizing the matrix in one direction and temporarily weakening the local mineral 

structure. At the same time, the radon atom experiences a 4.6 or 4.8 MeV equal, yet opposite reaction 

push, called a recoil, that physically moves the atom away from its original location. This recoil aids in 

moving a radon atom near the surface of a grain to a soil pore. The rate of emanation is typically slower 

in very dry soils since alpha recoil may also result in moving the recoiled atoms into an adjacent wall of 

another soil particle rather than an open pore space. On the other hand, if there is a small amount of water 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 128 

6. POTENTIAL FOR HUMAN EXPOSURE 

in the pore space, the kinetic energy of the recoiling atom can be dissipated and radon atoms can be 

slowed sufficiently before becoming embedded into an adjacent soil particle. In a model developed to 

calculate radon emanation in soil, Sasaki et al. (2004) estimated that the alpha recoil range for radon was 

0.02–0.07 μm in common minerals, 0.1 μm in water, and 63 μm in air. Once held within the pore space, 

radon may be transported by diffusion and convection to the surface where it is ultimately released to air. 

The actual release of radon from the pore space or soil-gas to ambient air is called exhalation, while its 

release from water is called evaporation. The rates of these processes are functions of many variables 

including the concentration of radon in the soil-gas or water, soil porosity and moisture, meteorological 

factors (such as temperature and precipitation), and variations in atmospheric pressure (NAS 1999b; 

WHO 1983). Soil moisture has an important but varying effect on radon release to the air. While lower 

levels of soil moisture greatly increase emanation by preventing recoil atoms from embedding into 

adjacent walls of soil particles as described above, saturated soil conditions in which the pores are filled 

with water tend to slow the rate of diffusion to the surface since the diffusion coefficient of radon is about 

3 orders of magnitude lower in water as compared to air (Markkanen and Arvela 1992; Michel 1987; 

WHO 1983). The influence of moisture and temperature on the radon exhalation rate in concrete, alum 

shale, and alum shale bearing soil was studied in laboratory experiments (Stranden et al. 1984). The 

results indicated that for each material, increasing the rate of moisture up to a certain point increased the 

radon exhalation rate from the material due to enhanced emanation. For concrete samples, the maximum 

exhalation rate occurred at a moisture content of 4.5–5.5%, for the alum shale, the maximum rate 

occurred at 10–15%, and for the soil samples, the maximum exhalation rate occurred at 20–30% moisture 

content (Stranden et al. 1984). As the moisture content increased beyond these levels, a dramatic 

decrease in the exhalation rate was observed. The authors concluded that when the pores were 

completely filled with water, the reduced rate of diffusion significantly attenuated the exhalation rate of 

radon from the material. If the porosity of the samples is high as in the case of the soil, more water can be 

absorbed by the sample before the pores are filled and the maximum rate of radon exhalation will occur at 

a higher moisture content than for low porosity materials. 

Vertical temperature gradients in the atmosphere can create slight vacuum conditions that pull radon from 

the soil, or temperature inversions that inhibit this movement. Therefore, meteorological events may both 

enhance and inhibit transport of radon from the soil into other media. For instance, radon may be released 

from the soil surface into water from melting snow (Fujiyoshi et al. 2002). Alternatively, winter 

conditions may cause radon-containing soil-gas to become trapped in frozen soil, thus decreasing 

transmission of radon to the atmosphere (Bunzl et al. 1998). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 129 

6. POTENTIAL FOR HUMAN EXPOSURE 

Diurnal and seasonal changes affect the behavior of radon at the interface between soil and ambient air by 

impacting temperature and atmospheric mixing (NAS 1999b; UNSCEAR 2000). Once radon reaches a 

height of approximately 1 meter above the soil surface, its dispersion is predominantly determined by 

atmospheric stability (Cohen 1979). This stability is a function of vertical temperature gradient, direction 

and force of the wind, and turbulence. Temperature inversions in the early morning act to produce a 

stable atmosphere which keeps radon in the soil or near the ground or water surface. Solar radiation 

breaks up the inversion, leading to upward dispersion of radon which reverses with radiant cooling in late 

afternoon (Gesell 1983; NAS 1999b; UNSCEAR 2000). In general, radon levels in air typically decrease 

exponentially with altitude (Cohen 1979). In a study by Chandrashekara et al. (2006), outdoor radon 

concentrations at 1 meter above the ground were found to increase during the night, peak in the very early 

morning, and decrease during the day. In the United States, radon concentrations typically reach their 

maximum in the summer to early winter, whereas from late winter to spring, concentrations are usually at 

a minimum as a result of meteorological changes and soil moisture conditions (NAS 1999b). 

Sources of indoor radon include entry of amounts released beneath the structure, entry in utilities such as 

water and natural gas, and release from building materials. Normally, the greatest contribution is that 

from radon released from soil or rock (Nero 1987; Planinić et al. 1994). Entry occurs primarily by bulk 

flow of soil-gas driven by small pressure differences between the lower and upper parts of the house 

interior and the outdoors. The pressure differences are primarily due to differences in indoor/outdoor 

temperature and the effects of wind (Nero 1987). 

In cases where uranium or other metal mine or mill tailings are used for construction purposes, the 

primary source of indoor radon can be from these materials (Agency for Toxic Substances and Disease 

Registry 2006). Mill tailings are a rather uniform sand that may be superior to local supplies in quality 

and price. They have been used for under slab foundations, for concrete and mortar mix (used in laying 

foundations, block, brick, and stone work), and even as a supplement for vegetable gardens. Radon 

buildup in such homes, along with direct gamma emissions from radium and radon progeny, contribute to 

elevated radiation exposure. 

Transport of radon in indoor air is primarily a function of the outflow ventilation rate of the enclosure. 

Most residential heating and air conditioning systems operate in a total recirculation mode, which doesn’t 

contribute to a ventilation rate. Under most conditions, the indoor radon concentration increases in direct 

proportion to the decrease in ventilation rates (WHO 1983). However, in some indoor radon studies, 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 130 

6. POTENTIAL FOR HUMAN EXPOSURE 

radon concentrations showed greater variability than could be accounted for by ventilation rates. This 

was said to suggest that the strength of the radon source was the main cause of the wide range in observed 

indoor radon levels (Nero 1987). Behavior of radon in enclosed areas has also been extensively studied 

and predicted by modeling (Bowring 1992; Eichholz 1987; Kitto 2003). 

Transport is primarily a function of the fraction of attachment of radon daughters to dust and dirt particles 

in the air, the concentration and size of the particles, and the rate of deposition. A major complication of 

modeling both radon and radon daughter transport indoors is that the outflow ventilation rate acts both to 

increase flow of radon into the structure and to remove radon and radon daughters from the structure 

through cracks and openings (Nero 1987). Air circulation rate also acts on the movement of air indoors 

causing variations in radon concentrations from room to room, as well as within a room. 

Mechanisms for transport of radon in groundwater are complex. Just as transport in air is primarily 

governed by air flow patterns, the transport of radon in groundwater is accomplished by diffusion and, 

primarily, by the mechanical flow patterns of groundwater (Watson et al. 1993). As previously stated, the 

diffusion coefficient of radon in water is sufficiently low so that diffusion is only important for movement 

in very small and poorly ventilated spaces (such as pore spaces). The solubility of radon in water is 

relatively low (230 cm3

/L of water at 20 °C) and, due to radon's relatively short half-life, much of it will 

have decayed to polonium and other non-volatile progeny before the groundwater reaches the surface. 

However, that remaining in solution can be released to ambient air once it is encountered. In areas where 

groundwater has high levels of radon, release from groundwater may significantly affect ambient air 

levels. 

6.3.2 Transformation and Degradation 

6.3.2.1 Air 

Regardless of the surrounding media, radon is a noble gas that transforms only by radioactive decay. 

There are no sinks for radon, and it is estimated that only negligible amounts escape to the stratosphere 

(Harley 1973). Therefore, the transformation of 222Rn proceeds by alpha-emission with a half-life of 

3.8235 days (NNDC 2012b). The half-lives of its first four progeny are much shorter, ranging from 

164.3 μsec for 214Po to 26.8 minutes for 214Pb. The half-lives and progeny for 219Rn, 220Rn, and 222Rn (as 

well as for all known radionuclides) are internationally maintained by DOE (NNDC 2012a) and are 

shown in Figures 4-1 through 4-3. NIST has developed and provides precise radon emanation rate 

standards in encapsulated solution form (currently, SRMs 4971, 4972, 4973, and 4974) for use in 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 131 

6. POTENTIAL FOR HUMAN EXPOSURE 

calibrating radon monitors. Since 222Rn standards are required for home radon testing, NIST has worked 

to transfer the U.S. national standards to secondary calibration laboratories (Kotrappa et al. 2005; NIST 

2010). 

6.3.2.2 Water 

Radon undergoes natural radioactive decay in water by the mechanisms described in Chapter 4. 

6.3.2.3 Sediment and Soil 

Radon undergoes natural radioactive decay in soil by the mechanisms described in Chapter 4. 

6.3.2.4 Other Media 

Though radon is inert, it can react with highly electronegative elements, such as oxygen, fluorine, and 

chlorine, to form relatively stable compounds (Hwang et al. 2005; O’Neil et al. 2006). For example, 

radon reacts with fluorine to form radon fluoride, which has a fairly low volatility (Chernick et al. 1962). 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 

Reliable evaluation of the potential for human exposure to radon depends in part on the reliability of 

supporting analytical data from environmental samples and biological specimens. Concentrations of 

radon in unpolluted atmospheres and in pristine surface waters are typically within the limits of current 

analytical methods. In reviewing data on radon levels monitored or estimated in the environment, it 

should also be noted that the amount of chemical identified analytically is not necessarily equivalent to 

the amount that is available. The analytical methods available for monitoring radon in a variety of 

environmental media are detailed in Chapter 7. 

6.4.1 Air 

Outdoor radon levels vary with geographic location and their proximity to radon sources in rocks and soil, 

water bodies, mines or mill tailings, and fossil-fuel combustion facilities (NAS 1999b). Gesell (1983) 

provided a compilation of data on radon levels in outdoor air. Measurements were taken over the 

continental United States, Hawaii, and Alaska. The highest concentrations were found in the Colorado 

Plateau, which is a region containing high levels of uranium as well as mines and uranium tailings. 

Measurements in this region ranged from 0.5 to 0.75 pCi/L of air (18.5–30 Bq/m3

). Average values from 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 132 

6. POTENTIAL FOR HUMAN EXPOSURE 

the continental United States ranged from 0.12 to 0.3 pCi/L of air (4.4–11 Bq/m3). More recent estimates 

based on an analysis of the available data of radon concentrations outdoors and on the transfer from water 

to air approximate the average outdoor air concentration over the entire United States as approximately 

0.4 pCi/L (14.8 Bq/m3

) (NAS 1999b). 

Price et al. (1994) reported the statewide median outdoor air concentration in Nevada to be 0.4 pCi/L 

(15 Bq/m3

), with a range of 0.07–1.40 pCi/L (2.6–52 Bq/m3) for 50 sites. The ranges correlated to 

various concentrations of radon in soil as well as uranium and progeny in rocks. In Iowa and Minnesota, 

Steck et al. (1999) reported average outdoor radon concentrations of 0.82 pCi/L (30 Bq/m3

) and 

0.60 pCi/L (22 Bq/m3

), respectively. Values in Iowa ranged from 0.2 to 1.5 pCi/L (7–55 Bq/m3), while 

those in Minnesota ranged from 0.1 to 1.5 pCi/L (4–55 Bq/m3

). 

Radon concentrations in air decrease with height from the soil surface (NAS 1999b). Several 

investigators have measured radon levels in the troposphere. Machta and Lucas (1962) measured 

0.007 pCi/L of air (0.26 Bq/m3

) at 25,000 feet. Comparable measurements have been taken over Alaska 

and the southwestern United States (Harley 1973). Radon concentrations measured at a few centimeters 

above the ground surface may be a factor of 10 higher than measurements from 1 meter above the 

surface, although this factor would vary with atmospheric conditions (UNSCEAR 2000). The changes in 

radon concentration with height are thought to be the result of atmospheric conditions (mixing and 

turbulence) (NAS 1999b). 

Numerous studies have been conducted to measure the radon concentrations of indoor air. Nero et al. 

(1986) reanalyzed up to 38 small data sets, of which 22 were considered unbiased. Biased data were 

those collected from areas where high radon concentrations were expected. On the basis of the unbiased 

data, the geometric mean of indoor radon levels was reported to be approximately 0.9 pCi/L of air 

(33 Bq/m3

). The arithmetic mean concentration was 1.5 pCi/L of air (56 Bq/m3). Distribution studies of 

household levels indicated that from 1 to 3% of single-family houses may exceed 8 pCi/L of air 

(296 Bq/m3

). In this study, many of the measurements were made in main-floor living rooms or average 

living areas (Nero et al. 1986). On average the relative air concentrations of radon in residential 

dwellings are 1.8, 1.0, 0.9, and 0.5 pCi/L (66.6, 37, 33.3, and 18.5 Bq/m3

) for the basement, first, second, 

and third floors, respectively (Planinić et al. 1994), indicating that radon concentrations decrease with 

distance from the earth’s surface. The National Residential Radon Survey conducted in 1989 and 1990 

(published in 1992) determined that the indoor average concentration of radon for U.S. homes was 

approximately 1.25 pCi/L (46.3 Bq/m3

) (Marcinowski et al. 1994). Approximately 6% of homes studied 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 133 

6. POTENTIAL FOR HUMAN EXPOSURE 

(5.8 million homes in 1990) had radon levels exceeding the EPA’s recommended action level of 4 pCi/L 

(148 Bq/m3

) (Marcinowski et al. 1994). 

A screening assessment conducted by the EPA of 55,000 homes located in 38 different states indicated 

that six counties in the Three Mile Island vicinity of Pennsylvania (Cumberland, Dauphin, Lancaster, 

Lebanon, Perry, and York) had the highest regional average indoor air levels of radon (17.8 pCi/L) (Field 

2005). The author suggested that these high radon levels are the main source of radiation exposure to 

residents in this area and have not often been accounted for in epidemiological studies of residents in this 

area. Homes built in contact with bedrock may have a higher likelihood of elevated radon concentrations 

in indoor air. Brookins (1991) reported high indoor radon levels in residential dwellings of Albuquerque, 

New Mexico. These values correspond to high soil radon levels in the area, although they may have also 

been affected by the type of building materials used in the homes. Four of five adobe buildings showed 

radon levels >4 pCi/L (ranging from 2.0 to 10.7 pCi/L), while smaller percentages of homes utilizing 

other construction methods had elevated levels. 

In an EPA assisted survey of indoor radon concentrations within 30 states, concentrations were found to 

vary widely between states. Additionally, houses with livable basements had higher radon concentrations 

than houses without basements. The mean concentration for those with basements ranged from 1.8 pCi/L 

(67 Bq/m3

) in Arizona and California to 9.4 pCi/L (348 Bq/m3) in Iowa. Those without basements had 

mean concentrations ranging from 0.5 pCi/L (19 Bq/m3

) in Louisiana to 5.5 pCi/L (204 Bq/m3) in Iowa 

(White et al. 1992). 

Indoor radon levels were measured in homes located in the Reading Prong area of Pennsylvania. This 

area has an unusual abundance of homes with high radon concentrations that is presumed to be from 

geologically produced emanation of radon. Indoor levels of radon in this area ranged from 4–20 pCi/L 

(150–740 Bq/m3

) in 29% of the homes to >80 pCi/L (3,000 Bq/m3) in 1% of the homes (Fleischer 1986). 

During a hot spot survey, indoor residential radon levels, also in the Reading Prong area, ranged from 

0.2 to 360 pCi/L (Lewis 1996). 

6.4.2 Water 

In a nationwide survey by the EPA, almost 2,500 public drinking water supplies were sampled 

(nonrandom) with most of these serving greater than 1,000 people (Cothern et al. 1986). Average 

concentrations for U.S. groundwater were estimated to be 240 pCi/L of water (8.8 Bq/L) for larger 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 134 

6. POTENTIAL FOR HUMAN EXPOSURE 

systems (>1,000 persons served) and 780 pCi/L of water (28.9 Bq/L) for smaller systems. The 

nationwide average for all groundwater samples tested in this study was 351 pCi/L (13 Bq/L). The 

highest levels reported were in smaller groundwater systems in Maine that averaged 10,000 pCi/L 

(370 Bq/L); lowest average levels were found in larger systems in Tennessee with levels of 24 pCi/L 

(0.9 Bq/L). Small, private groundwater systems appear to have higher radon concentrations than larger 

systems (Swistock et al. 1993; Watson et al. 1993). The average radon concentration in groundwaterderived public water supplies is approximately 540 pCi/L (20 Bq/L), although some public water supplies 

have been found to have radon concentrations up to 1x107 Bq/m3

 (270,000 pCi/L) (NAS 1999b). Longtin 

(1988, 1990) has compiled the results of a comprehensive monitoring study (1984–1986) regarding the 

levels of radon, radium, and uranium in public drinking water supplies in the United States. The results 

indicated that over 72% of the sites sampled had radon concentrations greater than the minimum reporting 

limit of 100 pCi/L (3.7 Bq/L), and a maximum concentration of 25,700 pCi/L (951 Bq/L) was observed. 

The USGS conducted a comprehensive groundwater monitoring study (1992–2003) of aquifers across the 

United States for the presence of radon and various trace elements (USGS 2011). The median 

concentration of radon (n=3,877) was 430 pCi/L (15.8 Bq/L), with a maximum level of 220,000 pCi/L 

(8,140 Bq/L). 

The relationship between radon concentrations in groundwater and system size (concentrations tend to 

increase with decreasing system size) was previously reported by Hess et al. (1985). This correlation may 

reflect a relationship between system size and aquifer composition. Those rock types that are associated 

with high radon levels (granitic rock) do not form aquifers large enough to support large systems. 

However, smaller systems may tap into such aquifers. Additionally, radon concentrations tend to 

decrease as the well depth increases, which may be attributed to the substrate composition at the various 

depths (Field and Kross 1998). 

Crystalline aquifers of igneous and metamorphic rocks generally have higher radon levels than other 

aquifer types. Aquifers comprised of granites or alluvial soils derived from granite consistently show the 

highest levels (Lam et al. 1994; Michel 1987), though sandstone and feldspar substrates are also 

correlated to high radon levels (Lam et al. 1994). Average radon levels in water from granite aquifers are 

usually ≥2,703 pCi/L of water (100 Bq/L) (Michel 1987). This is indicated in the data of Cothern et al. 

(1986) which report the following trends in groundwater radon levels: in New England and the Piedmont 

and Appalachian Mountain Provinces, where igneous and metamorphic rocks form the aquifers, 

concentrations are in the range of 1,000–10,000 pCi/L of water (37–370 Bq/L); in the sandstone and sand 

aquifers that extend from the Appalachian Mountains west to the Plains, concentrations are generally 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 135 

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<1,000 pCi/L of water (37 Bq/L). NAS (1999b) also reported high radon concentrations in public water 

supplies for New England, the Appalachian states, and the Rocky Mountain states, as well as areas of the 

Southwest and Great Plains. A granitic substrate in the San Joaquin Valley of California contributes to 

high radon concentration in groundwater. The groundwater of several California counties contains levels 

of radon as high as 1,000–10,000 pCi/L (Lam et al. 1994). 

A study of groundwater from 48 Pennsylvania counties indicated a median radon concentration of 

1,100 pCi/L for all samples, with a maximum concentration of 141,270 pCi/L. The highest 

concentrations were present in samples obtained from Southeastern Pennsylvania, which includes 

geologic formations typical of high radon emission (Swistock et al. 1993). In North Carolina, the 

arithmetic mean radon concentration tested in groundwater supplies of 400 homes was 1,800 pCi/L 

(67 Bq/L) (Watson et al. 1993). 

It has been reported that the radon concentration in surface waters is usually <4,000 Bq/m3

 (108 pCi/L) 

NAS (1999b). 

6.4.3 Sediment and Soil 

Because radon is a gas, its occurrence in soil is most appropriately referred to as its occurrence in “soilgas,” which is the gas or water-filled space between individual particles of soil. Factors that affect radon 

soil-gas levels include radium content and distribution, soil porosity, moisture, and density. However, 

soil as a source of radon is seldom characterized by radon levels in soil-gas, but is usually characterized 

directly by emanation measurements or indirectly by measurements of members of the 238U series (NRC 

1981). Radon content is not a direct function of the radium concentration of the soil, but radium 

concentration is an important indicator of the potential for radon production in soils and bedrock. 

However, Michel (1987) stated that average radium content cannot be used to estimate radon soil-gas 

levels, primarily due to differences in soil porosity. Similarly, Fujiyoshi et al. (2002) found that radium 

content may not control radon concentration in soil. In the study, radium concentrations were fairly 

consistent across various sites though the radon concentrations varied. 

Despite such caveats, theoretical rates of radon formation in soil have been estimated as demonstrated by 

the following (Nevissi and Bodansky 1987): 

Consider a cube which is 1 meter in each dimension. Using rounded numbers, if the 

average density of the soil is 2.0 grams per cubic-centimeter and the average radium-226 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

concentration is 1.0 pCi/g (0.037 Bq/g), the cube will contain 2 million grams of soil and 

2x10-6 Ci (7.4x104 Bq) of radium-226. This corresponds to the production of 

7.4x104

 radon atoms per cubic-meter per second and the escape of 7,400 atoms per 

square-meter per second, in rough correspondence to the average measured value. In 

alternative units, the figure of 0.5 pCi per square-meter per second corresponds to the 

emission of 16 Ci of radon per square-kilometer per year. 

For a discussion of 238U and 226Ra levels in soil, see the ATSDR Toxicological Profiles for uranium and 

radium (Agency for Toxic Substances and Disease Registry 1999a, 2011). 

Brookins (1991) reported the average concentration of radon in soil-gas in the United States is 

approximately 100 pCi/L. However, this value does not compare well with two soil-gas measurements 

for U.S. locations found in the literature: one from Spokane, Washington, with soil-gas radon levels of 

189–1,000 pCi/L (7,000–37,000 Bq/m3

) in soils formed from coarse glacial outwash deposits with 

2.3 ppm uranium, and the other from Reading Prong, New Jersey, with soil-gas radon levels of 1,081– 

27,027 pCi/L of air (40,000–1,000,000 Bq/m3

) (Michel 1987). Hopke (1987) states that normal soil-gas 

radon measurements are in the range of 270–675 pCi/L (10,000–25,000 Bq/m3

). 

Radon levels in soil-gas can fluctuate greatly, both temporally and spatially (Bunzl et al. 1998). A 

Bavarian study found that the concentration of radon in soil-gas of a high gravel content soil was higher at 

a depth of 0.5 m than at 1.0 m during the winter months, whereas in the summer, concentrations at the 

1.0-m depth were higher. Bunzl et al. (1998) reasoned that high levels exhibited during the winter months 

were most likely the result of frozen soil conditions, whereby transmission of radon to the atmosphere is 

decreased and thus, levels in soil-gas are increased. The annual mean concentration at a depth of 0.5 m 

was observed to be 17.1 kBq/m3

 (462 pCi/L) while the mean level at a depth of 1.0 m was 15.2 kBq/m3 

(411 pCi/L) (Bunzl et al. 1998). At a depth of 38 cm, radon levels were found to range from 40 to 

890 pCi/L in Albuquerque, New Mexico. The average summer value was 360 pCi/L, while the average 

winter levels were 200 pCi/L (Brookins 1991). 

6.4.4 Other Environmental Media 

Limited information exists to indicate that plants absorb both 226Ra and 222Rn from the soil layer and that 

these compounds are translocated to above ground plant parts (Taskayev et al. 1986). However, there is 

little information on the quantitative contribution of this process to exposure from ingestion of plant crops 

or of emanation rates from these plants. A measurement of the emission rates of radon from field corn 

was located in the literature. 222Rn flux from leaves was reported to be 2.47x10-4 pCi 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

(9.15x10-6 Bq)/cm2/second. This rate was 1.8 times greater than the exhalation rate from local soil 

(Pearson 1967). Solubilized radon can be removed from the soil by plants through evapotranspiration, 

where it is subsequently released to the atmosphere by diffusion through the leaf. Kozak et al. (2003) 

designed a flow and transport model to describe the transport or radon and radium through soil and 

vegetation. 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE 

In the following section, exposure to radon is discussed in terms of environmental levels rather than in 

terms of actual or estimated dose. The estimation of whole body or target tissue dose of radionuclides is 

extremely complex and must be accomplished by mathematical models for the specific radionuclide. 

Although such models are available to estimate whole body and target tissue dose for radon, discussion of 

these lies outside the scope of this document. For a discussion of these models, the reader is referred to 

NCRP (1984a) or NAS (1999a). 

The general population is exposed to radon by inhalation, both outdoors and indoors, as well as by 

ingestion. Radon concentrations in outdoor air often correspond to soil gas levels (Price et al. 1994), 

although concentrations vary widely with geographical location, depending on factors such as the radium 

content, soil porosity, and moisture content. Comparing data from multiple studies, NAS (1999b) reports 

that the mean radon concentrations range from 1 to 63 Bq/m3

 (0.027–1.7 pCi/L) with the highest values 

reported in Iowa and Maine, with an overall average radon concentration of 0.32 pCi/L (12 Bq/L). 

Measurements in Iowa and Minnesota show average outdoor concentrations of 0.60–0.82 pCi/L (Steck et 

al. 1999). The average outdoor air concentration of radon over the entire United States is approximately 

0.4 pCi/L (NAS 1999b). Due to the gaseous nature of radon, radon levels will decrease with increasing 

height from the soil surface; however, Price et al. (1994) reported that radon concentrations in Nevada 

obtained at heights of 0.5, 1.0, and 2.0 m from the surface were not statistically different from each other. 

This indicates that adults and children sitting or standing in the same location are exposed to similar 

concentrations. 

Average radon levels indoors are found to be higher than ambient outdoor levels (Steck et al. 1999). 

When the general population encounters elevated concentrations of radon, it generally is while indoors, 

such as at home, school, or work where concentrations exceed the EPA-recommended action level of 

4 pCi/L (CDC 1999). The National Residential Radon Survey conducted in 1989 and 1990 (published in 

1992) determined that the indoor average annual concentration for U.S. homes was approximately 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

1.25 pCi/L (EPA 2003; Marcinowski et al. 1994). Approximately 6% of homes studied (5.8 million 

homes in 1990) had radon levels exceeding the EPA’s action level of 4 pCi/L (Marcinowski et al. 1994). 

Two large indoor monitoring efforts in the United States reported arithmetic mean levels ranging from 

1.5 to 4.2 pCi/L of air (55–157 Bq/m3

) (Alter and Oswald 1987; Nero et al. 1986). The data from Alter 

and Oswald (1987) are limited in that the dwellings do not represent a random sample and individual 

measurement values were reported rather than average concentrations from a residence. 

The composition and physical properties of concrete, such as porosity, can affect the rate by which radon 

moves through an intact concrete slab and enters a home. Renken and Rosenberg (1995) estimated that a 

typical basement with a 1,500 ft2 (140 m2

) concrete slab would have approximately 7.1 Bq/hour of radon 

diffusing through the concrete slab. Decreasing the porosity, permeability, and diffusion coefficient of 

the concrete mix can result in less radon gas diffusing through the slab and into the home. 

Although the primary source of indoor radon is from soil, release of radon from water may contribute to 

indoor levels (Fishbein 1992; Lam et al. 1994). Nazaroff et al. (1987) performed an analysis that 

combined information on water use, efficiency of radon release from water, house volumes, and 

ventilation rates to determine the impact on indoor radon levels. Their analysis estimated that use of 

groundwater contributes an average of 2% to the mean indoor radon concentration in houses. Lam et al. 

(1994) concluded that groundwater may contribute 1–5% of indoor radon. As with levels in other media, 

levels of radon in groundwater vary greatly. In areas with high groundwater levels, the relative 

contribution to indoor radon levels will increase accordingly. Cothern et al. (1986) report a daily intake 

of radon originating from drinking water of 100–600 pCi (3.7–22.2 Bq)/day, assuming that consumption 

was 2 L/day of groundwater. Additionally, small groundwater systems appear to have higher radon 

concentrations than larger systems (Swistock et al. 1993). 

The contribution of building materials to indoor radon (other than homes where metal mine or mill 

tailings have been used in construction) is estimated to be low in comparison with amounts which 

originate from soil and rock. In general, among common building materials, concrete and gypsum board 

release more radon than other materials. 

The type of concrete used in a house slab can affect the rate at which radon diffuses from the ground 

through a basement slab and into the home. Renken and Rosenberg (1995) assessed porosity, 

permeability, and diffusion constants through three mix types. Diffusion constants in increasing order 

were 4.96x10-4 cm2

second-1 for a typical basement slab concrete mix, 9.09x10-4 cm2second-1 for concrete 
 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

with an increased water:cement ratio, and 1.43x10-3 cm2second-1 for concrete with substituted fly ash. 

The respective porosities for these slabs were 0.12, 0.17, and 0.20. It was concluded that controlling the 

porosity of a concrete slab can reduce the rate of radon transmission into a house. 

Active soil depressurization (ASD) was assessed for its effectiveness in mitigating radon in a home with 

basement concentrations averaging 7,580 Bq/m3

 (205 pCi/L). The system reduced levels to 520 Bq/m3 

(14 pCi/L). After a more powerful fan was installed to increase vacuum, radon levels in the basement 

unexpectedly increased to 1,070 Bq/m3

 (29 pCi/L). Upon reversal of the fan direction to produce an 

active soil pressurization system (ASP), the large fan reduced levels to 63 Bq/m3

 (1.7 pCi/L). 

Reinstallation of the small fan into the ASP system further reduced the radon level to 44 Bq/m3 

(1.2 pCi/L). The indications are that an overly forceful ASD vacuum can break the ground seal, reducing 

its effectiveness, and that ASP might be more effective than ASD in some cases (Kearney and Mason 

2011). 

Persons who are occupationally exposed to radon typically are those employed in mining and milling, 

primarily underground mining of uranium and hard rock (NIOSH 1987), but which also include silver, 

tin, bertrandite and beryl ores, and other mines (Kaczynski 2011; Lubin et al. 1994). Exposure to radon in 

underground mines has been shown by numerous studies to be a high risk factor for developing lung 

cancer (EPA 2003), particularly for miners in China, the Czech Republic, the United States, and Canada 

(Lubin et al. 1994). Exposures in above-ground mines and in mills are typically lower. 

NIOSH reports that in 2005, 22,838 workers were employed in underground metal and nonmetal mines in 

the United States, with 29,705 workers employed at all underground mines (including metal, nonmetal, 

coal, and stone mines) (NIOSH 2008a). In 2005, 263 metal mines and 739 nonmetal mines were reported 

(NIOSH 2008b). The number of underground uranium mines has decreased from 300 in 1980 to 16 in 

1984 (NIOSH 1987) to 17 in 1992 (EPA 1995), although the number may have increased to <100 in 2003 

(IAEA 2004). The number of employees in underground uranium mines has decreased from 9,000 in 

1979 to 448 in 1986 (NIOSH 1987), although figures were not available for later years. Measurements of 

radon progeny concentrations in these mines from 1976 to 1985 showed annual geometric mean 

concentrations in uranium mines of 0.11–0.36 WL (equivalent to 22–72 pCi/L of air [800–2,664 Bq/m3

] 

assuming an equilibrium factor of 0.5), with 95th percentile levels ranging up to 2.73 WL (546 pCi/L of 

air; 20,202 Bq/m3

). Annual geometric mean levels in phosphate mines for the same period were 0.12– 

1.20 WL (24–240 pCi/L of air [888–8,880 Bq/m3

]) with 95th percentile levels as high as 1.69 WL 

(338 pCi/L of air; 12,506 Bq/m3

). Measurements in uranium/vanadium mines showed annual geometric 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 140 

6. POTENTIAL FOR HUMAN EXPOSURE 

mean concentrations similar to those in uranium mines. However, 95th percentile levels ranged up to 

4.80 WL (960 pCi/L of air [3.6x104 Bq/m3

]), which was the highest annual concentration reported among 

the different types of mines (NIOSH 1987). Estimates of annual cumulative radon progeny exposures 

indicated that of the 1,405 underground uranium miners working in 1984, 28% had exposures >1 WL 

(200 pCi/L of air; 7,400 Bq/m3

). As uranium is a minor impurity in bertrandite and beryl ores, radon may 

be present above ambient levels where these ores are processed, such as at a beryllium extraction facility 

located in Delta, Utah (Kaczynski 2011). 

Radon exposure in underground mines has been vastly reduced by installation of improved engineering 

controls. In New Mexico mines, the median annual exposure in 1967 of 5.4 WLM was reduced to 

0.5 WLM by 1980 due to these improvements (Eichholz 1987). For 1982, Samet et al. (1986) reported a 

mean WLM of 0.7. A WLM expresses both intensity and duration of exposure (see Chapter 3 for further 

discussion). 

MSHA regulates safety practices and worker protection in the mining industry. OSHA has established air 

monitoring requirements for underground mines and exposure limits for mine workers. These involve 

monitoring mine exhaust air for radon daughters, with values >0.1 WL for areas where uranium is mined 

(or between 0.1 and 0.3 WL for areas where uranium is not mined) requiring periodic monitoring of air 

representative of the workers’ breathing zones (MSHA 2011c). Workers are not to be exposed to 

concentrations exceeding 1.0 WL in any active mine area (MSHA 2011b). In cases where accepted 

engineering control measures have not been implemented or when work conditions require, higher-level 

exposure is permitted under an appropriate respiratory protection program (MSHA 2001d). The goal is to 

ensure that no underground mine worker receives >4 WLM in any calendar year (MSHA 2011a). 

Occupational exposure to radon can extend beyond mining. Water-plant operators may be exposed to 

high levels of radon gas created during the water treatment process. This occurs when radon emanates 

from water to air during the aeration process or when filter material to strip out uranium or radium is 

removed for disposal as radioactive waste. The geometric annual mean air concentration of radon in 

31 water plants was 3.4 pCi/L (126 Bq/m3

), with a maximum value of 133 pCi/L (4,921 Bq/m3) (Fisher et 

al. 1996). A high exposure risk is also present for employees at radioactive contaminated sites, nuclear 

waste repositories, natural caverns, phosphate fertilizer plants, oil refineries, utility and subway tunnels, 

excavators, power plants, natural gas and oil piping facilities, health mines and spas, fish hatcheries, and 

hospitals (EPA 2003; Field 1999; Fisher et al. 1996). Higher exposure risks are also present for farmers, 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

radon mitigation professionals, and scientists, although exposure to local radon sources can occur in any 

occupation (Field 1999). 

6.6 EXPOSURES OF CHILDREN 

This section focuses on exposures from conception to maturity at 18 years in humans. Differences from 

adults in susceptibility to hazardous substances are discussed in Section 3.7, Children’s Susceptibility. 

Children are not small adults. A child’s exposure may differ from an adult’s exposure in many ways. 

Children drink more fluids, eat more food, breathe more air per kilogram of body weight, and have a 

larger skin surface in proportion to their body volume. A child’s diet often differs from that of adults. 

The developing human’s source of nutrition changes with age: from placental nourishment to breast milk 

or formula to the diet of older children who eat more of certain types of foods than adults. A child’s 

behavior and lifestyle also influence exposure. Children crawl on the floor, put things in their mouths, 

sometimes eat inappropriate things (such as dirt or paint chips), and spend more time outdoors. Children 

also are closer to the ground, and they do not use the judgment of adults to avoid hazards (NRC 1993). 

Exposure levels at schools were utilized to provide an estimate of radon levels to which children may be 

exposed during the school day. However, limited U.S. data were available to address radon exposure of 

children. 

The EPA recommends that all schools test for radon and mitigate areas with elevated concentrations. 

EPA’s 1990 National School Radon Survey obtained radon measurements from 927 randomly selected 

schools across the United States. Based on these measurements, it is estimated that approximately 

15,000 U.S. schools have at least one room with a potential for long-term elevation of radon levels. 

Radon is often unevenly distributed within a building. Overall, short-term radon concentrations in 

roughly 2.7% of all ground contact schoolrooms were >4 pCi/L, indicating 73,000 schoolrooms with a 

potential radon problem (EPA 1993c). 

Additionally, higher respiration rates of children may influence the extent of radon and radon progeny 

inhaled. MacDonald and Laverock (1998) studied the exposure levels of soil-dwelling mammals in a 

radon-rich environment, concluding that larger mammals with higher lung capacities were least affected 

by radon. Most affected were smaller mammals with higher respiration rates. Using this logic, small 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

children with high respiration rates, as compared to adults, may receive relatively higher radiation doses 

from inhaled radon and radon progeny. 

Kendall and Smith (2005) examined the doses of radon and its decay products inhaled or ingested by 

1-year-old infants and 10-year-old children in the United Kingdom. The largest internal doses were found 

to be associated with the organ of intake (the respiratory tract and stomach). Dose coefficients (or the 

dose per unit intake factors) were found to be higher for children than for adults, although the overall 

annual doses were fairly consistent between children and adults (likely due to the smaller amount of air 

and water consumed by children). 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 

Populations with potentially high exposures include those occupationally exposed. Those who use 

excavation equipment or are employed at underground mines (uranium, hard rock, and vanadium), water 

treatment plants, radioactively contaminated sites, natural caverns, phosphate fertilizer plants, oil 

refineries, utility and subway tunnels, fossil fueled power plants, natural gas and oil piping facilities, 

health mines and spas, and fish hatcheries have the potential to be more highly exposed to radon (EPA 

2003; Field 1999; Fisher et al. 1996). Higher exposures are also possible for farmers, radon mitigation 

professionals, and scientists (Field 1999). 

High radon exposure can occur in any location with geologic radon sources (see 

http://www.epa.gov/radon/zonemap.html) (EPA 2011a; Field 1999). High outdoor air radon 

concentrations were reported in Iowa, Main, and Minnesota NAS (1999b). NAS (1999b) also reported 

high radon concentrations in public water supplies for New England, the Appalachian states, and the 

Rocky Mountain states, as well as areas of the Southwest and Great Plains. Though the average radon 

concentration in groundwater-derived public water supplies is approximately 540 pCi/L (20 Bq/L), some 

public water supplies have been found to have radon concentrations up to 1x107 Bq/m3

 (270,000 pCi/L) 

(NAS 1999b). 

Communities that are very near uranium or phosphate mill tailing piles may have increased environmental 

radon levels. In addition, in some areas, mill tailings have been used as fill dirt, garden soil, sub-base for 

concrete slabs, and sand mix for brick mortar in home construction (for example, in Monticello, Utah) 

(Agency for Toxic Substances and Disease Registry 1997). Persons in these communities could be 

exposed to levels of radon exceeding typical indoor background levels. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 143 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.8 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of radon is available. Where adequate information is not 

available, ATSDR, in conjunction with NTP, is required to assure the initiation of a program of research 

designed to determine the health effects (and techniques for developing methods to determine such health 

effects) of radon. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 

6.8.1 Identification of Data Needs 

Physical and Chemical Properties. Information is available on the physical and chemical 

properties of radon, and parameters that influence the behavior of radon in the environment have been 

determined. Therefore, no data needs are identified concerning physical and chemical properties of 

radon. 

Production, Import/Export, Use, Release, and Disposal. According to the Emergency 

Planning and Community Right-to-Know Act of 1986, 42 U.S.C. Section 11023, industries are required 

to submit substance release and off-site transfer information to the EPA. The TRI, which contains this 

information for 2006, became available in March of 2008. This database is updated yearly and should 

provide a list of industrial production facilities and emissions. 

The production of radon occurs directly from a radium source either in the environment or in a laboratory 

environment. The disposal of gaseous radioactive effluents has been documented. Increased radon 

concentrations have been detected in waste generated by uranium and phosphate mining; therefore, these 

sites should be monitored on a continual basis. Although there are regulations for disposal of 

radionuclides in general, there are none that specifically address disposal of materials due to their radon 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 144 

6. POTENTIAL FOR HUMAN EXPOSURE 

content. If such regulations were promulgated, they would be developed by states since the Federal 

government has no authority in this area. 

Environmental Fate. Information is available on the environmental fate of radon in air and water and 

on the transport of radon in environmental media. Factors that affect the partitioning of radon from soil 

or water to air have been identified. Movement of radon into and within homes and the influence of 

meteorological conditions and other parameters on this movement should continue to be investigated. 

Transformation of radon has been adequately characterized. There is limited information on the uptake 

and release of radon by plants. Additional research of this phenomenon is needed in order to determine 

the relative contribution plants provide to atmospheric levels. Exposure from smoking tobacco should be 

explored. 

Bioavailability from Environmental Media. Radon and radon progeny are known to be released 

from air and water and information is available, which characterizes the relative contribution of various 

media to levels of radon in air and water. 

Food Chain Bioaccumulation. Since radon is a noble gas, it will not bioaccumulate. However, 

bioaccumulation has been reported for radon progeny such as 210Pb in cephalopods (Khan and Wesley 

2011) and 210Po in marine birds (Skwarzec and Fabisiak 2007), mushrooms (Skwarzec and Jakusik 2003), 

cephalopods (Khan and Wesley 2011), and coastal sand dune wild legumes (Bhat et al. 2005). 

Exposure from Environmental Media. Reliable monitoring data for the levels of radon in 

contaminated media at hazardous waste sites might be helpful, particularly if uranium mine tailings have 

been disposed of at these sites. 

Information is available regarding the levels of radon in indoor air, outdoor air, and water. Continued 

comprehensive data on levels of radon in ambient air are needed in order to assess potential human 

exposure. The measurement of indoor and ambient radon levels are not mandated, and EPA has found 

that most homeowners do not choose to spend the money to have these measurements made. 

Exposure Levels in Humans. EPA maintains information on those states and jurisdictions that 

have enacted Radon-Resistant New Construction building codes (EPA 2011g). Large-scale monitoring of 

radon in public buildings (e.g., schools) was conducted in the 1990s. Limited information for the United 

States in general is available on remediation activities conducted in response to those measurements and 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

the resulting radon levels, or on radon levels in building constructed since that time. Radon is a naturally 

occurring gas and is ubiquitous in the environment; therefore, humans are constantly exposed to some 

level of radon. The primary pathway for human exposure to radon is inhalation from soil gas intrusion to 

dwellings and buildings. Outdoor radon levels vary with geographic location and their proximity to radon 

sources in rocks and soil, water bodies, mines or mill tailings, and fossil-fuel combustion facilities. Since 

the half-life of radon is short, its measurement in biological samples, such as serum, urine, blood, etc., is 

not practical. Concentrations of radon progeny are measurable in urine, blood, bone, teeth, and hair, and 

these levels can be used to provide some indication of exposure; however, they are not direct 

measurements of levels of exposure. These estimates may be derived through use of mathematical 

models. 

This information is necessary for assessing the need to conduct health studies on these populations. 

Exposures of Children. Limited information is available to address radon exposure of children, 

particularly within the United States. Some communities require testing of schools for radon and 

abatement if levels are ≥4 pCi/L (NJDEP 2004). Available data were not always in agreement, and thus, 

conclusions were difficult to assess. Studies are needed to better characterize exposure levels specific to 

children in the United States. 

Child health data needs relating to susceptibility are discussed in Section 3.12.2, Identification of Data 

Needs: Children’s Susceptibility. 

Exposure Registries. No exposure registries for radon were located. This substance is not currently 

one of the compounds for which a sub-registry has been established in the National Exposure Registry. 

The substance will be considered in the future when chemical selection is made for sub-registries to be 

established. The information that is amassed in the National Exposure Registry facilitates the 

epidemiological research needed to assess adverse health outcomes that may be related to exposure to this 

substance. 

The Hanford Environmental Foundation in Richland, Washington, maintains a registry of United States 

uranium miners and millers. The data in the registry are derived from autopsy material and include 

exposure information. Since uranium decays to radon, this exposure registry on miners and millers may 

provide information on radon exposure. The NIOSH dose reconstruction and worker compensation 

programs should also be addressed. 
 

 

 

RADON 146 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.8.2 Ongoing Studies 

No ongoing studies were identified. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 147 

7. ANALYTICAL METHODS 

The purpose of this chapter is to describe the analytical methods that are available for detecting, 

measuring, and/or monitoring radon and its progeny. The intent is not to provide an exhaustive list of 

analytical methods. Rather, the intention is to identify well-established methods that are used as the 

standard methods of analysis. Many of the analytical methods used for environmental samples are the 

methods approved by federal agencies and organizations such as EPA and the National Institute for 

Occupational Safety and Health (NIOSH). Other methods presented in this chapter are those that are 

approved by groups such as the Association of Official Analytical Chemists (AOAC), the American 

Public Health Association (APHA), the National Radon Safety Board (NRSB), and the National Radon 

Proficiency Program (NRPP), which is operated jointly by the National Environmental Health 

Association (NEHA) and the American Association of Radon Scientists and Technologists (AARST). 

Additionally, analytical methods are included that modify previously used methods to obtain lower 

detection limits and/or to improve accuracy and precision. 

7.1 BIOLOGICAL MATERIALS 

Table 7-1 lists various methods used to detect radon progeny in biological samples. Since the half-life of 

radon is short, its measurement in biological samples, such as serum, urine, blood, etc., is not practical. 

Measurements of the longer lived radon progeny 210Pb and 210Po in biological samples may be used as an 

indication of radon exposure; however, ingestion of these isotopes from food and drinking water or direct 

exposure from other environmental media are considered the primary sources of exposure for these 

isotopes. Therefore, while this chapter discusses the analysis of 210Pb and 210Po in biological media, their 

presence in the body arises from a variety of sources, not just direct inhalation of radon, and should not be 

considered unique biomarkers of radon exposure. 

A method of estimating individual, chronic human exposure to natural waterborne radionuclides using 

in vivo skull measurements and in vitro urine measurements of 210Pb and natural uranium (234,235,238U) is 

described by Muikku et al. (2003). Four, high-purity broad energy Ge detectors, situated near the top and 

back of the head, measure the activity of the 186 keV 235U and 46 keV 210Pb gamma rays. Urine samples 

were analyzed with inductively coupled plasma mass spectrometry (ICP-MS) for uranium content 

(Muikku et al. 2003). A similar technique was used by Eisenbud et al. (1969), who concluded that in vivo 

skull measurements of 210Pb allow cumulative exposure to radon daughters to be estimated in uranium 

miners. In vivo measurements of 210Pb in the knee have also been reported (by measuring the 46 keV 
 

 

 

 

 

 

	 


 


 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 


 


 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 


 


 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

RADON	 148 

7. ANALYTICAL METHODS 

Table 7-1. Analytical Methods for Determining Radon Progeny in Biological
 

Samples
 

Sample Sample 

matrix Preparation method Analytical method detection limit Reference 

Tooth	 Clean and dry tooth; dry overnight 

and grind to fine powder; separate 

enamel from dentin and compress 

into pellets; coat with titanium 

nitride 

Urine, Wet ash in HNO3-NaClO4, 

blood, electrostatic precipitation 

hair, feces 

Urine,	 Wet ashing with concentrated nitric 

blood, hair acid and hydrogen peroxide, 

followed by drying and dissolution 

in hydrochloric acid solution 

Blood	 Wet ash and plate on disk 

Bone	 Wash with acetone, hydrogen 

peroxide and isopropanol followed 

by drying and homogenization to a 

grain size of 1–3 mm 

Bone	 Extract fat with anhydrous 

benzene; wet ash using nitric acid 

and perchloric acid 

Bone	 In vivo 

Tissue	 Immediate measurement of 

dissected tissue samples following 

inhalation exposure 

Tissue Homogenize tissue in 

(Brain)	 trichloroacetic acid solution 

followed by centrifugation 

PIXE for total lead content 

in teeth 

Alpha spectometry 

Alpha particle counting of

209Po (4.866 MeV) and 210Po (5.305 MeV) using 

silicon surface barrier 

detectors 

Autoradio-graphy of alpha 

tracks, using nuclear 

emulsion 

Gamma ray spectrometry 

(46.5 keV 210Pb) using 

HPGe detector 

Alpha particle counting 

210Po using a ZnS(Ag) 

scintillation counter 

Whole body gamma ray 

spectroscopy (46 keV 

210Pb) 

Gamma ray activity using a 

NaI(Tl) scintillation counter 

Alpha particle counting of

210Po and beta particle 

counting of 210Bi 

0.5 ppm	 Anttila 1987 

0.1 pCi	 Gotchy and 

(3.7x10-3 Bq) Schiager 

1969 

1.1–1.5 mBq/L Al-Arifi et al. 

(24-hour (2006) 

counting time) 

No data Weissbuch 

et al. 1980 

0.4–0.7 mBq Johnston et 

per gram of al. 2005 

sample 

No data	 Blanchard et 

al. 1969 

No data	 Eisenbud et 

al. 1969 

No data	 Nussbaum 

and Hursh 

1957 

1x10-5 Bq per Momčilović

gram tissue et al. 1999 

HPGe = High purity germanium; PIXE = proton induced X-ray emission analysis 
 

 

 

 

 

 

 

 

 

 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

 
 


 

 
 


 

 
 


 


 


 

 

 

 

 

 

 

RADON 149 

7. ANALYTICAL METHODS 

gamma ray); however, calibration for the skull is generally simpler than for the knee (Johnston et al.
	

2005).
	

Urine analysis and whole body counting have been used to measure levels of radon progeny in humans. 

It is generally known that 210Pb is deposited primarily in bone with a relatively long biological half-life,
	

which enables it to reach transient radioactive equilibrium conditions with its descendant, 210Po (Clemente 

et al. 1984). The short half-lives of radon and the daughters, 218Po through 214Po, preclude their detection 

through normal bioassay techniques that typically require a day or more after the sample has been 

collected before counting can commence (Gotchy and Schiager 1969).
	

Al-Arifi et al. (2006) discussed an analytical method for measuring levels of 210Po in samples of blood,
	

urine, and hair for various populations using a high resolution alpha spectrometer. Although the main 

route of 210Po intake by the human body is the ingestion of food, smoking, ingestion of drinking water, 

and inhalation of radon may also contribute to the body burden.
	

Radon exposure in humans is typically assessed by monitoring air levels indoors, outdoors, and under
	

occupational settings as discussed in Section 7.2.
	

7.2 ENVIRONMENTAL SAMPLES 

Most methods of measuring radon and its decay products in environmental samples are based on the 

detection of alpha particles emitted during the radioactive decay process, although some methods are 

based on the detection of emitted gamma rays. Detailed reviews of the measurement of radon and its 

progeny in environmental samples can be found in NCRP (1988), George (1988), and European 

Commission (1995). EPA issued updates regarding radon measurement techniques in 1992 and provided 

general guidelines for optimal measurement conditions, device placement, and documentation of results 

(EPA 1992a). EPA has also issued technical guidance for measuring radon concentrations in residences 

(EPA 1993b). 

There are several generalizations about the measurement of radon that apply regardless of the specific 

measurement technique used. Radon concentrations in the same location may differ by a factor of 2 over 

a period of 1 hour. Also, the concentration in one room of a building may be significantly different than 

the concentration in an adjoining room. Therefore, improvements in sampling methodology would be 

helpful. Since the accuracy and level of uncertainty of individual measurements are important, especially 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 150 

7. ANALYTICAL METHODS 

when assessing the implications of elevated readings, the measurement uncertainty should be reported for 

each sample analysis result. 

Air radon and radon progeny measurement devices fall broadly into two categories: passive devices and 

continuous monitor devices (AARST 2006). Passive radon monitors allow air to diffuse into a sensor 

chamber and do not require any power to operate. However, passive monitors only provide average 

concentrations for the entire sampling time period (usually at least 48 hours) and typically require 

laboratory analysis to determine radon concentrations. Continuous radon monitors (CRMs) measure 

radon gas and continuous working level monitors (CWMs) measure radon progeny. These continuous 

monitoring devices can record and review radon concentrations in time increments of ≤1 hour, but may 

require a power source. CRMs are commercially available to home inspectors or radon testing 

professionals. The principles by which radon detectors operate are described in the following paragraphs. 

Activated charcoal adsorption devices are inexpensive, passive detectors used for monitoring radon in air 

samples. Commercially available devices are often sold at hardware or home improvement stores for 

estimating radon levels in households or buildings. A typical detector consists of a circular, 6–10 cm 

diameter container that is approximately 2.5 cm deep and filled with 25–100 g of activated charcoal (EPA 

1992a). One side of the container is fitted with a screen that encloses the charcoal sample and allows air 

to diffuse in. The passive nature of these detectors allows for the continuous adsorption and desorption of 

radon, and the adsorbed radon undergoes radioactive decay during the measurement period. Following a 

brief exposure period (2–7 days), the charcoal detectors are returned to a laboratory and analyzed directly 

by counting gamma rays emitted by the radon decay products on the charcoal using a sodium iodide 

gamma detector. The detector may be used in conjunction with a multi-channel gamma spectrometer or 

with a single-channel analyzer with the window set to include the appropriate gamma energy window. 

The detector system and detector geometry must be the same used to derive the calibration factors for the 

device (EPA 1992a). Alternatively, the sample may be desorbed by an aromatic solvent (typically 

toluene or benzene) and analyzed using liquid scintillation counting using an appropriate fluor solution. 

Indoor radon levels are also frequently measured using alpha track detection devices (EPA 1992a). The 

detector consists of a small piece of plastic or film enclosed in a container with a filter-covered opening or 

similar design to allow radon, but not its progeny, to enter. Some common materials used in this capacity 

for radon detection are the cellulose nitrate film (LR-115), the thermoset polymer plastic (CR-39), and the 

polycarbonate plastic (Makrofol) (European Commission 1995). Radon gas diffuses into the container 

and alpha particles emitted by the radon and its subsequently-produced progeny strike the detector and 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 151 

7. ANALYTICAL METHODS 

produce submicroscopic damage tracks to the enclosed plastic material. Following the analysis period, 

the plastic detectors are placed in a caustic solution that accentuates the damage tracks so they can be 

counted using a microscope or an automated counting system. The number of tracks per unit area is 

correlated to the radon concentration in air, using a conversion factor derived from data generated at a 

laboratory. The number of tracks per unit of analyzed detector area produced per unit of time (minus the 

background) is proportional to the radon concentration. When compared to charcoal adsorption detectors, 

alpha track detectors have the advantage that they can be used for measurements over long time frames 

and thus, they measure true time-integrated average concentrations (EPA 1992a). Inexpensive alpha track 

radon detection kits are commercially available to the general public to estimate radon exposure in a 

dwelling. Unlike the activated charcoal test kits that have a brief exposure period, the alpha track 

monitors are typically used for 90 days to 1 year and provide a better estimate of the annual radon 

exposure. 

Electret ion chamber (EC) radon detectors are passive detectors that use an electrostatically charged disk 

to collect ions formed in the chamber by radiation generated from radon and radon progeny (EPA 1992a). 

Radon diffuses into the chamber through filtered openings and ions that are generated continuously by the 

decay of radon, and its progeny are drawn to the surface of the electret, which subsequently reduces its 

surface voltage. The change of voltage measured by an electrostatic voltmeter is related to the average 

radon concentration based on the duration of the exposure period. 

Flow through alpha scintillation cells (Lucas type cells) are frequently used to measure radon 

concentrations in air for field measurements and in occupational settings (NCRP 1988). The cell consists 

of a silver activated zinc sulfide (ZnS) phosphor screen that emits photons of visible light when impacted 

by alpha particles (Lucas 1957). Air is drawn continuously through the cell by an air pump and the cell is 

coupled to a photomultiplier tube for continuous analysis. The scintillations or flashes of light caused by 

the alpha particles from radon and its progeny, which strike the ZnS screen, are recorded by the 

photomultiplier tube. Using appropriate calibration and decay scheme factors, the radon gas 

concentration may be determined from the rate at which the pulses are recorded (European Commission 

1995). 

Personal and occupational exposure to radon is frequently assessed using personal dosimeters. An early 

personal radon dosimeter used in occupational settings by miners, called a radon film badge, was 

described by Geiger (1967). It consisted of a plastic holder, which encompassed a nuclear track film to 

detect emitted alpha particles. Radon gas diffused through the central opening of the badge and into the 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 152 

7. ANALYTICAL METHODS 

film emulsion. The number of alpha particles was determined by counting the tracks in the processed 

film emulsion. Another example of a passive radon dosimeter based on alpha particle etched track 

detection used to assess personal exposure is described by Taheri et al. (2006). This particular dosimeter 

employs a polycarbonate detector and a porous fiberglass filter to collect the radon progeny, 218Po and 

214Po. A thin aluminum foil is placed between the filter and the detector in order to attenuate the energy 

of the emitted alpha particles. 

Retrospective radon detection methods using surface traps or volume traps provide a means of estimating 

long-term radon exposure at a building or residence. By determining the historical average concentration, 

the methodology provides an estimate of the indoor radon level to which a person was exposed over a 

period of time. For surface trap methods, the activity is measured at the surface of objects, such as glass, 

that were present in the location of interest during the exposure assessment period. The average radon 

concentration over several decades is related to the surface activity of the glass. This results from the 

radon progeny 210Pb, which has a long half-life (22.26 years) and is found implanted within the glass (or 

other hard surface) due to the kinetic energy transferred by alpha decay to the radon progeny atoms 

plating out on the surface (Lagarde et al. 2002; Mahaffey et al. 1993; Samuelsson 1988; Steck and Field 

1999). A field study conducted from 2005 to 2007 in 38 homes in Iowa occupied by either smokers or 

nonsmokers using surface trap CR-39 chip retrospective radon detectors indicated that radon progeny 

(

214Po and 218Po) deposited on the surface of these detectors was effective for predicting the airborne 

radon progeny dose rate for individuals and estimating long-term exposure in nonsmoking environments. 

The operation of ceiling fans or fireplaces in monitoring areas adversely affected the measurements (Sun 

2008). 

Pressyanov et al. (2003) explored the use of compact disks as retrospective radon detectors. After 

exposure, a surface layer was removed and electrochemically etched marks were counted. The study 

results indicated that compact disks may be useful for retrospectively obtaining radon measurements for 

levels above 3 Bq/m3 (0.08 pCi/L). 

Radon volume trap detectors also provide a convenient method to estimate average radon concentrations 

in dwellings over several years in time (Oberstedt and Vanmarcke 1996). Sponge-like materials, such as 

mattresses and cushions, build-up 210Pb, which reaches an equilibrium with the alpha emitter 210Po, which 

is used to estimate the average radon concentration over the exposure period. Laboratory tests employing 

polyester foam samples to simulate mattress material of differing densities and rigidity were exposed to a 

radon source (Oberstedt and Vanmarcke 1996). Following the initial exposure period, the materials were 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 153 

7. ANALYTICAL METHODS 

stored in a radon-free environment for at least one half-life of 210Po (138 days). The 210Po was separated 

from the polyester materials in a series of extraction steps and the activity was analyzed by alpha 

spectrometry. The results indicated that home dwelling materials, such as cushions and mattress material, 

could be used as an accurate and sensitive retrospective radon monitor. Wooden furniture material has 

also been tested as a volume trap; however, the natural varying background concentrations of 210Po in 

different wood types make these materials a less attractive retrospective detection system. 

A standard test method for the detection of radon in drinking water has been developed by the American 

Society for Testing and Materials (ASTM) based on scintillation counting of radon and its progeny 

(ASTM 1999). A sample of unaerated water is injected into a vial containing toluene or a scintillation 

cocktail mix and analyzed using a commercially available liquid scintillation spectrometer. This method 

has a reported detection limit of 0.040 Bq/L (1.1 pCi/L). 

A method for measuring radon in soil gas that utilizes liquid scintillation counting for determining 

concentration is given by Wadach and Hess (1985). A description of this method may be found in 

Table 7-2. A detection system for continuous soil radon concentration measurements was developed 

using a continuous monitor RM-3. The system detects radon based on an airflow ionization chamber. 

Details are available in Fronka et al. (2008). 

The accuracy of any measurement will depend upon the calibration of the instrument used. The 

calibration of an instrument determines its response to a known amount or concentration of radioactivity. 

This allows a correlation to be made between the instrument reading and the actual amount or 

concentration present. A range of activities of 226Ra standard reference materials (SRM) is available from 

the National Institute of Standards and Technology (NIST) polyethylene-encapsulated 226Ra/222Rn 

emanation standards (PERE). These are used to produce an accurate concentration of 222Rn in air, such as 

for calibrating passive radon detection systems. Ionization pulse chambers are often used for instrumental 

calibration and measurement systems in interlaboratory comparisons (NCRP 1988). NIST developed a 

226Ra222Rn generator for use as a transfer standard for radon-in-water measurement calibrations 

(Hutchinson et al. 1984, 1986). Modifications to this standard generator and its long-term performance 

have been evaluated and described using 4π-αβ liquid scintillation spectrometry of gravimetrically 

determined aliquants dispensed from the generator (Collé and Kishore 1997). Analytical methods for 

measuring radon in environmental samples are given in Table 7-2. To quantify the sensitivity of a 

particular analytical method, the lower limits of detection (LLD) are given when possible. The LLD is 

typically defined as the minimum activity that would result in a quantifiable signal on some analytical 
 

 

 

 

 

 

 

 


 

RADON 154 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining Radon and Progeny in 

Environmental Samples
 

Sample 

matrix Preparation method 

Analytical 

method 

Sample 

detection limit 

Percent 

recovery Reference 

Radon 

Air Adsorb onto activated charcoal; Gamma No data No data Cohen and 

2–7 days spectroscopy Nason 1986 

Air Adsorb onto activated charcoal Gamma No data 94% of true Prichard and 

followed by direct analysis; 

extract with toluene add 1–2 mL 

counting of 

0.295 and 

concentration Marlen 1983 

fluor 0.352 γ MeV 

lines of 214Pb; 

liquid 

scinilation 

analysis of 

desorbed 

sample 

Air Scintillation cell method; allow air 

to enter detection chamber 

through millipore filter until 

equlibrated, or collect sample in 

bag (Mylar or Tedlar); transer to 

chamber as soon as possible 

ZnS(Ag) 

scintillation/ 

photomultiplier 

tube 

No data No data CrawfordBrown and 

Michel 1987 

Air Two-filter method: draw air into 

fixed length tube with entry and 

exit filters; monitor exit filter 

activity 

ZnS(Ag) 

scintillation/ 

photomultiplier 

tube 

No data 90% Schery et al. 

1980 

Air Diffuse through a filter into a cup 

containing alpha track material 

(cellulose nitrate film) for up to 

1 year; etch in acidic or basic 

solution operated upon an 

alternating electric field 

Solid state 

nuclear track 

detector 

Microscopic 

examination of 

damaged 

material 

14 pCi/m3 

(0.519 Bq/m3) 

No data NCRP 1988 

Air Adsorb onto compact disks; 

remove surface layer at 25 °C 

with aqueous 45% KOH and 

40% methanol; apply 

electrochemical etching 

Marks counted 

using video 

camera 

No data No data Pressyanov 

et al. 2003 

Air Dissolve material in nitric acid 

followed by additional digestion 

in hydrochloric acid. Auto 

deposit polonium on a silver 

plate during drying with an 

infrared source 

Volume trap 

detector using 

alpha 

spectrometer 

54 pCi/L Oberstedt 

and 

Vanmarcke 

1996 
 

 

 

 

 

 

 


 

RADON 155 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining Radon and Progeny in 

Environmental Samples
 

Sample 

matrix Preparation method 

Analytical 

method 

Sample 

detection limit 

Percent 

recovery Reference 

Glass Attach dosimetry-grade track 

registration material (CR-39 and 

LANTRAK®) to ordinary smooth 

glass without visible coatings or 

colorings that has been in an 

unobstructed location without 

strong air currents; leave in 

place for long periods (several 

weeks to a year) 

Chemically 

etch the 

dosimeter, 

read 210Po 

tracks 

manually with 

microscope, 

determine 

cumulative 

radon gas 

~0.3 kym-1 NA Steck et al. 

2002 

exposure as 

kym-1 (i.e., 

kBqym-1/Bqm-2)

a 

Soil Dry in 55 °C oven for 24 hours; 

place 5 g in 20 mL borosilicate 

glass scintillation; cover with 

10 mL distilled water; allow soil 

Scintillation 

counter 

No data No data Rangarajan 

and Eapen 

1987; 

Wadach and 

to become wet; add 5 mL highefficiency mineral oil; allow to 

age 30 days 

Hess 1985 

Soil None Track etch 

detector buried 

30 cm deep 

No data No data Rangarajan 

and Eapen 

1987 

Drinking 

Water 

Draw an aliquot of unaerated 

water into a syringe and inject in 

a scintillation vial containing the 

liquid scintillation cocktail 

solution 

ASTM Method 

D5072 

(Scintillation 

counter) 

0.04 Bq/L 

(1.1 pCi/L) 

94–96% ASTM 1999 

Water Pass carrier gas through 

samples in a bubbler flask to 

purge out dissolved radon; 

transfer radon to evacuated 

Scintillation 

counter 

1.4 pCi/L 

(52 Bq/m3) 

90% CrawfordBrown and 

Michel 1987 

scintillation cell 
RADON 156 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining Radon and Progeny in 

Environmental Samples 

Sample 

matrix Preparation method 

Analytical 

method 

Sample 

detection limit 

Percent 

recovery Reference 

Water Inject into glass vial containing 

liquid scintillation solution; shake 

vigorously 

Liquid 

scintillation 

counter 

10 pCi/L 

(370 Bq/m3

) 

No data CrawfordBrown and 

Michel 1987 

Water Direct measurement Gamma ray 

spectroscopy 

10 pCi/L for 1-L 

sample 

(370 Bq/m3

) 

No data Yang 1987 

Air CR-39 chip bathed in 6.25N 

sodium hydroxide at 75 °C oven 

for 6 hours 

Alpha track 

density 

determined by 

microscopy 

No data No data Sun 2008 

a

Unit of measure (kym-1) equals radon gas exposure in kiloBecquerel-years per m3 (kBqym-3) divided by surface 

activity in Becquerels per m2

 (Bqm-2). 

TLD = thermoluminescent dosimeter 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 157 

7. ANALYTICAL METHODS 

instrument that would yield a net count for which there is confidence at a predetermined level (usually the 

95th percentile confidence limit) that activity is present (Harley and Pasternack 1982; NCRP 1988). In 

order to calculate the LLD, the measurement system characteristics, detection system efficiency, 

background count rate, sampling volume, and sampling period must be known. 

The EPA Radiation and Indoor Environments National Laboratory (RIENL) provides radon measurement 

technical support for the radon monitoring proficiency testing programs in the United States (as supported 

by NIST) and for tribal, state, and local governments, federal agencies, and private industry (EPA 2011b). 

The National Environmental Health Association-National Radon Proficiency Program (NEHA-NRPP) 

operates a radon proficiency test (PT) and contractor certification program for those who want to become 

a Certified Radon Professional (NEHA-NRPP 2008). NIST has developed and provides precise radon 

emanation rate standards (currently, SRMs 4971, 4972, and 4973) for use in calibrating radon monitors. 

Since 222Rn standards are required for home radon testing, NIST has worked to transfer the U.S. national 

standards (which are still based on the international standards produced by Marie Curie in 1912) to 

secondary calibration laboratories (NIST 2011). 

7.3 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of radon is available. Where adequate information is not 

available, ATSDR, in conjunction with NTP, is required to assure the initiation of a program of research 

designed to determine the health effects (and techniques for developing methods to determine such health 

effects) of radon. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 158 

7. ANALYTICAL METHODS 

7.3.1 Identification of Data Needs 

Methods for Determining Biomarkers of Exposure and Effect. 

Exposure. Methods are available to measure the presence of radon progeny in urine, blood, bone, teeth, 

and hair. However, these radon progeny detected in biological systems arise from ingestion of these 

progeny from food and drinking water as well as from the inhalation of radon. Therefore, these methods 

cannot be considered as specific biomarkers for radon inhalation. 

Effect. The frequency of abnormalities in sputum cytology has been utilized as a possible early indicator 

of radiation damage to lung tissue (Band et al. 1980; Brandom et al. 1978; Saccomanno et al. 1974). The 

accuracy and precision of this measurement is not known. 

Methods for Determining Parent Compounds and Degradation Products in Environmental 

Media. Analytical methods are available that allow for the quantification of radon in air, water, and 

soil. However, methods for the measurement of radon concentrations in soil-gas are limited. The ability 

to accurately measure soil-gas is needed to provide a better understanding of the emanation rate of radon 

gas from soil. 

7.3.2 Ongoing Studies 

Researchers at the University of Iowa are involved in ongoing studies that include pooling results from 

Iowa and Missouri residential radon studies using glass-based detectors that are undergoing final 

calibration (field, personal communication) and pooling results from the residential radon studies that 

contributed to the results of Krewski et al. (2005, 2006; North American studies) and Darby et al. (2005, 

2006; European studies). 
 

 

 

 

 

 

 

 

 

 


 

 

 

 

 

 

 

 

 

 

RADON 159 

8. REGULATIONS, ADVISORIES, AND GUIDELINES
 

Recommendations for radiation protection for people in the general population as a result of exposure to 

radon in the environment are found in the International Commission on Radiological Protection (ICRP) 

Publication 65 (ICRP 1994a). National guidelines for occupational radiation protection are found in the 

“Federal Radiation Protection Guidance for Occupational Exposure” (EPA 1987b). The guidance 

presents general principles for the radiation protection of workers and specifies the numerical primary 

guides for limiting occupational exposure. These recommendations are consistent with the ICRP (ICRP 

1994a). 

The basic philosophy of radiation protection is the concept of ALARA (As Low As Reasonably 

Achievable). As a rule, all exposure should be kept as low as reasonably achievable and the regulations 

and guidelines are meant to give an upper limit to exposure. Based on the primary guides, guides for 

Annual Limits on Intake (ALIs) have been calculated (USNRC 2011). The ALI is defined as “that 

activity of a radionuclide which, if inhaled or ingested by Reference Man (ICRP 1975), will result in a 

dose equal to the most limiting primary guide for committed dose” (EPA 1988). 

MRLs are substance specific estimates, which are intended to serve as screening levels, are used by 

ATSDR health assessors and other responders to identify contaminants and potential health effects that 

may be of concern at hazardous waste sites. 

No inhalation or oral MRLs were derived for radon. 

The international and national regulations, advisories, and guidelines regarding radon in air, water, and 

other media are summarized in Table 8-1. 

The EPA IRIS database (IRIS 2012) has withdrawn its cancer classification for radionuclides, but the 

EPA Office of Air and Radiation believes that all radionuclides, including radon and its radioactive 

progeny, should be considered to be known carcinogens, and has assigned them to Group A (EPA 2012b). 

The EPA has not derived reference concentrations (RfCs) or reference doses (RfDs) for radon (IRIS 

2012). EPA has not promulgated a maximum contaminant level (MCL) for radon in drinking water. In 

1991, EPA proposed an MCL, but was directed in 1996 to withdraw it and did so in 1997. In 1999, EPA 

again proposed an MCL (EPA 1999b), but finalized the current radionuclides in drinking water rule in 

2000 without a value for radon (EPA 2000) and this status has not changed. The EPA website contains a 
 

 

 

 

 

 

 

 

 

RADON 160 

8. REGULATIONS, ADVISORIES, AND GUIDELINES 

wealth of information, including a publication entitled A Citizen’s Guide to Radon (EPA 2009a). This 

guide includes information on the health risk from inhaling radon and its progeny, methods for radon 

testing in homes, methods and techniques for reducing the radon level, and a recommendation to use a 

certified radon mitigation specialist to ensure that appropriate methods are used to reduce radon levels. 

EPA recommends actions to take if the measured radon indoor level is ≥4 pCi/L and notes that radon 

levels <4 pCi/L still pose a health risk and can be reduced in many cases, and recommends not smoking 

as an additional way to reduce radon risk. 
 

 

 

	 

	 

RADON	 161 

8. REGULATIONS, ADVISORIES, AND GUIDELINES 

Table 8-1. Regulations, Advisories, and Guidelines Applicable to Radon 

Agency Description	 Information Reference 

INTERNATIONAL 

Guidelines: 

IARC Carcinogenicity classification IARC 2008 

222Rn and its decay products Group 1a 

ICRP Summary of values recommended 

Nominal probability coefficient for 5x10-4 per WLM (0.14 per ICRP 2010 

radon- and radon-progeny- J h m-3) 

induced lung cancer 

Dose conversion convention, ICRP 1994a 

effective dose per unit of exposure 

At home 1.1 mSv (mJ h m-3) 

At work 1.4 mSv (mJ h m-3) 

Action level (dwellings) 

Radon concentration 200–600 (Bq m-3)

b 

Annual effective dose 3–10 mSv 

Action level (workplace) 

Radon concentration 500–1,500 (Bq m-3)

b 

Annual effective dose 3–10 mSv 

Occupational annual limit on 

exposure 

Per year, averaged over 14 (mJ h m-3) 

5 years 

In a single year 35 (mJ h m-3) 

WHO Air quality guidelines WHO 2000 

Risk estimates and recommended 

action level for radon progeny for 

exposure to 1 Bq/m3 

Lung cancer excess lifetime 3–6x10-5 

risk estimate 

Recommended level for ≥100 Bq/m3 (2.7 pCi/L); 

remedial action in buildings annual average 

Drinking water quality guidelines WHO 2004 

Radon 100 Bq/L (2,700 pCi/L) 

NATIONAL 

Regulations and 

Guidelines: 

a. Air 

ACGIH Guidelines for exposure to ionizing ACGIH 2007 

radiation 

Radon daughters 4 WLM/year 
 

 

 

 

	 

	 

	 


 


 


 

	 

	 

	 


 


 


 

	 

	 

	 


 


 


 

RADON	 162 

8. REGULATIONS, ADVISORIES, AND GUIDELINES 

Table 8-1. Regulations, Advisories, and Guidelines Applicable to Radon 

Agency Description	 Information Reference 

NATIONAL (cont.) 

EPA AEGL-1, -2, and -3 No data EPA 2011e 

Hazardous air pollutant EPA 2010b 

Radon Yes 42 USC 7412 

Effective dose equivalent to public From operating uranium EPA 2011i 

from 222Rn not to exceed mine (40CFR61.22) 

10 mrem/year From a DOE facility EPA 2011j 

(40CFR61.92) 

222Rn emissions rate from soil not From a DOE facility EPA 2011k 

to exceed 20 pCi/m2-second (40CFR61.192) 

average for entire source 

From an inactive EPA 2011l 

phosphogypsum stack (40CFR61.202) 

From a non-operational EPA 2011m 

uranium mill tailings pile (40CFR61.222) 

From an existing uranium EPA 2011n 

mill tailings pile (40CFR61.252) 

Standards for uranium byproduct Provisions from soil for EPA 2011h 

materials shall apply to thorium 222Rn from uranium (40CFR192.41) 

byproduct materials byproduct materials are 

applicable to 220Rn from 

thorium byproduct 

materials 

210Po (222Rn progeny)	 Emissions from elemental EPA 2011o 

phosphorus plant (40CFR61.122) 

<2 Ci/year, or 4.5 Ci/year 

with scrubbers 

Monitoring of radon in homes EPA 2009a 

No action necessary <4 pCi/L, 0.02 WL 

Take necessary action to ≥4 pCi/L

decrease indoor radon levels 

MSHA Annual exposure limits MSHA 2011a 

Radon daughters 4 WLM in any calendar 30 CFR 57.5038 

year underground 

MSHA 2011b Maximum permissible concentration 30CFR57.5039 Radon daughters 1 WL in active workings
 

underground
 

NIOSH REL (10-hour TWA) No data
 
 

 

 

 

	 

	 

	 

RADON	 163 

8. REGULATIONS, ADVISORIES, AND GUIDELINES 

Table 8-1. Regulations, Advisories, and Guidelines Applicable to Radon 

Agency Description	 Information Reference 

NATIONAL (cont.) 

OSHA OSHA adopted the 1971 version of 

USNRC regulatory limits in 10CFR20 

Appendix B for exposure to radon in 

air. Applies to employers. OSHA 

states that following the current 

10CFR20 App B is a de minimis 

violation. 

USNRC	 ALI for occupational exposure 

(values for oral ingestion) 

220Rn (with daughters removed) 

220Rn (with daughters present) 

222Rn (with daughters removed) 

222Rn (with daughters present) 

ALI for occupational exposure 

(values for inhalation) 

220Rn (with daughters removed) 

220Rn (with daughters present) 

222Rn (with daughters removed) 

222Rn (with daughters present) 

Derived air concentrations for 

occupational exposure (values for 

inhalation) 

220Rn (with daughters removed) 

220Rn (with daughters present) 

222Rn (with daughters removed) 

222Rn (with daughters present) 

Annual average effluent air 

concentration (no values provided for 

effluent water) 

220Rn (with daughters removed) 

Adult workers: 

1x10-7 μCi/mL (100 pCi/L) 

averaged over 40-hour 

work week of 7 consecutive 

days 

Workers under 18 years of 

age: 3x10-9 μCi/mL 

(3 pCi/L) averaged over 

40-hour work week of 

7 consecutive days 

Surveys are required in 

order to comply 

Post airborne radioactivity 

area signs when weekly 

average exceeds 25% of 

limit (i.e., 25 pCi/L adults, 

0.75 pCi/L child workers) 

Not listed 

Not listed 

Not listed 

Not listed 

20,000 μCi 

20 μCi (or 12 WLM) 

10,000 μCi 

100 μCi (or 4 WLM) 

7x10-6 μCi/mL 

9x10-9 μCi/mL (or 1.0 WL) 

4x10-6 μCi/mL 

3x10-8 μCi/mL (or 0.33 WL) 

2x10-8 μCi/mL 

OSHA 2011 

29 CFR 

1910.1096; OSHA 

1971; 

OSHA 2002 

OSHA 2011 

29CFR1910.1096 

(c)(2); OSHA 1971, 

OSHA 2002 

OSHA 2011, 

29CFR1910.1096 

(e)(4)ii 

OSHA 2011, 

29CFR1910.1096 

(e)(4)(i)(b) 

USNRC 2011 

10 CFR 20, 

Appendix B 
 

 

 

 

 

 

 

 

 

	 

	 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

	 

	 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

	 

	 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

RADON	 164 

8. REGULATIONS, ADVISORIES, AND GUIDELINES 

Table 8-1. Regulations, Advisories, and Guidelines Applicable to Radon 

Agency Description	 Information Reference 

NATIONAL (cont.) 

220Rn (with daughters present) 3x10-11 μCi/mL 

222Rn (with daughters removed) 1x10-8 μCi/mL 

222Rn (with daughters present) 1x10-10 μCi/mL 

b. Water 

EPA Drinking water standards and health None; EPA proposed an EPA 2011d, EPA 

advisories for radon activity MCL for radon in 1991, 1997 

withdrew it in 1997, and 

published the final rule in 

2000 without a radon MCL 

National recommended water quality No data
 

criteria
 

c. Food No data 

d. Other 

ACGIH Carcinogenicity classification No data ACGIH 2007 

EPA Carcinogenicity classification IRIS 2012 

222Rn Withdrawn in 1993 

RfC
 

222Rn
 Not established 

RfD
 

222Rn
 Not established 

Superfund, emergency planning, and EPA 2011f 

community right-to-know 40 CFR 302.4 App 

Designated CERCLA hazardous B 

substance 

220Rnc 0.1 Ci 

222Rnc 0.1 Ci
 

NTP Carcinogenicity classification NTP 2011
 

Ionizing radiation (includes 220Rn Known to be a human 

and 222Rn) carcinogen 

a

Group 1: carcinogenic to humans. b

Assuming 7,000 hours/year indoors or 2,000 hours/year at work and an equilibrium factor of 0.4.
 c

Designated CERCLA hazardous substance pursuant to Section 112 of the Clean Air Act.
 

ACGIH = American Conference of Governmental Industrial Hygienists; AEGL = Acute Exposure Guideline Levels;
 

ALI = annual limit on intake; CERCLA = Comprehensive Environmental Response, Compensation, and Liability Act;
 

CFR = Code of Federal Regulations; EPA = Environmental Protection Agency; IARC = International Agency for
 

Research on Cancer; ICRP = International Commission on Radiological Protection; MCL = maximum contaminant
 

level; MSHA = Mine Safety and Health Administration; NAS = National Academy of Sciences; NIOSH = National
 

Institute for Occupational Safety and Health; NTP = National Toxicology Program; OSHA = Occupational Safety and 

Health Administration; REL = recommended exposure limit; RfC = inhalation reference concentration; RfD = oral
 

reference dose; TWA = time-weighted average; USC = United States Code; USNRC = U.S. Nuclear Regulatory
 

Commission; WHO = World Health Organization; WL = working level; WLM = working level months
 
 

 

 

 

 

 

_______________________ 


 

 

 

 

 

 

 

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RADON 205 

10. GLOSSARY 

Some terms in this glossary are generic and may not be used in this profile. 

Absorbed Dose, Chemical—The amount of a substance that is either absorbed into the body or placed in 

contact with the skin. For oral or inhalation routes, this is normally the product of the intake quantity and 

the uptake fraction divided by the body weight and, if appropriate, the time, expressed as mg/kg for a 

single intake or mg/kg/day for multiple intakes. For dermal exposure, this is the amount of material 

applied to the skin, and is normally divided by the body mass and expressed as mg/kg. 

Absorbed Dose, Radiation—The mean energy imparted to the irradiated medium, per unit mass, by 

ionizing radiation. Units: rad (rad), gray (Gy). 

Absorbed Fraction—A term used in internal dosimetry. It is that fraction of the photon energy (emitted 

within a specified volume of material) which is absorbed by the volume. The absorbed fraction depends 

on the source distribution, the photon energy, and the size, shape and composition of the volume. 

Absorption—The process by which a chemical penetrates the exchange boundaries of an organism after 

contact, or the process by which radiation imparts some or all of its energy to any material through which 

it passes. 

Self-Absorption—Absorption of radiation (emitted by radioactive atoms) by the material in which 

the atoms are located; in particular, the absorption of radiation within a sample being assayed. 

Absorption Coefficient—Fractional absorption of the energy of an unscattered beam of x- or gammaradiation per unit thickness (linear absorption coefficient), per unit mass (mass absorption coefficient), or 

per atom (atomic absorption coefficient) of absorber, due to transfer of energy to the absorber. The total 

absorption coefficient is the sum of individual energy absorption processes (see Compton Effect, 

Photoelectric Effect, and Pair Production). 

Absorption Coefficient, Linear—A factor expressing the fraction of a beam of x- or gamma radiation 

absorbed in a unit thickness of material. In the expression I=Ioe

-μx, Io is the initial intensity, I the intensity 

of the beam after passage through a thickness of the material x, and μ is the linear absorption coefficient. 

Absorption Coefficient, Mass—The linear absorption coefficient per cm divided by the density of the 

absorber in grams per cubic centimeter. It is frequently expressed as μ/ρ, where μ is the linear absorption 

coefficient and ρ the absorber density. 

Absorption Ratio, Differential—Ratio of concentration of a nuclide in a given organ or tissue to the 

concentration that would be obtained if the same administered quantity of this nuclide were uniformly 

distributed throughout the body. 

Activation—The process of making a material radioactive by bombardment with neutrons or protons. 

Activity—The number of radioactive nuclear transformations occurring in a material per unit time (see 

Curie, Becquerel). The term for activity per unit mass is specific activity. 

Activity Median Aerodynamic Diameter (AMAD)—The diameter of a unit-density sphere with the 

same terminal settling velocity in air as that of the aerosol particle whose activity is the median for the 

entire size distribution of the aerosol. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 206 

10. GLOSSARY 

Acute Exposure, Chemical—Exposure to a chemical for a duration of 14 days or less, as specified in the 

Toxicological Profiles. 

Acute Exposure, Radiation—The absorption of a relatively large amount of radiation (or intake of a 

radioactive material) over a short period of time. 

Acute Radiation Syndrome—The symptoms which taken together characterize a person suffering from 

the effects of intense radiation. The effects occur within hours or days. 

Ad libitum—Available in excess and freely accessible. 

Adsorption Coefficient (Koc)—The ratio of the amount of a chemical adsorbed per unit surface area or 

per unit weight of organic carbon of a specific particle size in the soil or sediment to the concentration of 

the chemical in solution at equilibrium. 

Adsorption Ratio (Kd)—See Distribution Coefficient 

Alpha Particle—A positively charged particle ejected spontaneously from the nuclei of some radioactive 

elements. It is identical to a helium nucleus, i.e., 2 neutrons and two protons, with a mass number of 4 

and an electrostatic charge of +2. 

Alpha Track—The track of ionized atoms (pattern of ionization) left in a medium by an alpha particle 

that has traveled through the medium. 

Annihilation (Positron-Electron)—An interaction between a positive and a negative electron in which 

they both disappear; their rest mass, being converted into electromagnetic radiation (called annihilation 

radiation) with two 0.51 MeV gamma photons emitted at an angle of 180 to each other. 

Annual Limit on Intake (ALI)—The derived limit for the amount of radioactive material taken into the 

body of an adult worker by inhalation or ingestion in a year. It is the smaller value of intake of a given 

radionuclide in a year by the reference man that would result in a committed effective dose equivalent of 

5 rem or a committed dose equivalent of 50 rem to any organ or tissue. 

Atom—The smallest particle of an element that cannot be divided or broken up by chemical means. It 

consists of a central core called the nucleus, which contains protons and neutrons and an outer shell of 

electrons. 

Atomic Mass (u)—The mass of a neutral atom of a nuclide, usually expressed in terms of “atomic mass 

units.” The “atomic mass unit” is one-twelfth the mass of one neutral atom of carbon-12; equivalent to 

1.6604x10-24 g. 

Atomic Mass Number—See Mass Number. 

Atomic Number—The number of protons in the nucleus of an atom. The “effective atomic number” is 

calculated from the composition and atomic numbers of a compound or mixture. An element of this 

atomic number would interact with photons in the same way as the compound or mixture. (Symbol: Z). 

Atomic Weight—The weighted mean of the masses of the neutral isotopes of an element expressed in 

atomic mass units. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 207 

10. GLOSSARY 

Attenuation—A process by which a beam from a source of radiation is reduced in intensity by 

absorption and scattering when passing through some material. 

Attenuation Coefficient—The fractional reduction in the intensity of a beam of radiation as it passes 

through an absorbing medium. It may be expressed as reduction per unit distance, per unit mass 

thickness, or per atom, and is called the linear, mass, or atomic attenuation coefficient, respectively. 

Auger Effect—The emission of an electron from the extranuclear portion of an excited atom when the 

atom undergoes a transition to a less excited state. 

Background Radiation—The amount of radiation to which a member of the general population is 

exposed from natural sources, such as terrestrial radiation from naturally occurring radionuclides in the 

soil, cosmic radiation originating from outer space, and naturally occurring radionuclides deposited in the 

human body. 

Becquerel (Bq)—International System of Units unit of activity and equals that quantity of radioactive 

material in which one transformation (disintegration) occurs per second (see Units). 

Terabecquerel (TBq)—One trillion becquerel. 

Gigabecquerel (GBq)—One billion becquerel. 

Megabecquerel (MBq)—One million becquerel. 

Kilobecquerel (kBq))—One thousand becquerel. 

Millibecquerel (mBq)—One-thousandth of a becquerel. 

Microbecquerel (μBq)—One-millionth of a becquerel. 

Benchmark Dose (BMD)—Usually defined as the lower confidence limit on the dose that produces a 

specified magnitude of changes in a specified adverse response. For example, a BMD10 would be the 

dose at the 95% lower confidence limit on a 10% response, and the benchmark response (BMR) would be 

10%. The BMD is determined by modeling the dose response curve in the region of the dose response 

relationship where biologically observable data are feasible. 

Benchmark Dose Model—A statistical dose-response model applied to either experimental toxicological 

or epidemiological data to calculate a BMD. 

Beta Particle—An electron that is emitted from the nucleus of an atom during one type of radioactive 

transformation. A beta particle has a mass and charge equal in magnitude to that of the electron. The 

charge may be either +1 or -1. Beta particles with +1 charges are called positrons (symbolized β+

), and 

beta particles with -1 charges are called negatrons (symbolized β-

). 

Bioconcentration Factor (BCF)—The quotient of the concentration of a chemical in aquatic organisms 

at a specific time or during a discrete time period of exposure divided by the concentration in the 

surrounding water at the same time or during the same period. 

Biologic Effectiveness of Radiation—See Relative Biological Effectiveness. 

Biological Half-time—The time required for a biological system, such as that of a human, to eliminate by 

natural process half of the amount of a substance (such as a chemical substance, either stable or 

radioactive) that has entered it. 

Biomagnification—The progressive increase in the concentration of a bioaccumulated chemical in 

organisms as that chemical is passed from the bottom to the top of the food web. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 208 

10. GLOSSARY 

Biomarkers—Broadly defined as indicators signaling events in biologic systems or samples. They have 

been classified as markers of exposure, markers of effect, and markers of susceptibility. 

Body Burden, Chemical—The total amount of a chemical found in an animal or human body. 

Body Burden, Radioactivity—The amount of radioactive material found in an animal or human body. 

Bone Seeker—Any compound or ion which migrates in the body and preferentially deposits into bone. 

Branching—The occurrence of two or more modes by which a radionuclide can undergo radioactive 

decay. For example, 214Bi can undergo alpha or beta minus decay, 64Cu can undergo beta minus, beta 

plus, or electron capture decay. An individual atom of a nuclide exhibiting branching disintegrates by one 

mode only. The fraction disintegrating by a particular mode is the “branching fraction” for that mode. 

The “branching ratio” is the ratio of two specified branching fractions (also called multiple 

disintegration). 

Bremsstrahlung—X rays that are produced when a charged particle accelerates (speeds up, slows down, 

or changes direction) in the strong field of a nucleus. 

Buildup Factor—The ratio of the radiation intensity, including both primary and scattered radiation, to 

the intensity of the primary (unscattered) radiation. 

Cancer Effect Level (CEL)—The lowest dose of chemical or radiation in a study, or group of studies, 

that produces significant increases in the incidence of cancer (or tumors) between the exposed population 

and its appropriate control. 

Capture, Electron—A mode of radioactive decay involving the capture of an orbital electron by its 

nucleus. Capture from a particular electron shell, e.g., K or L shells, is designated as “K-electron 

capture” or “L-electron capture.” 

Capture, K-Electron—Electron capture from the K shell by the nucleus of the atom. Also loosely used 

to designate any orbital electron capture process. 

Carcinogen—A chemical or radiation that is capable of inducing cancer. 

Carcinoma—Malignant neoplasm composed of epithelial cells, regardless of their derivation. 

Case-Control Study—A type of epidemiological study which examines the relationship between a 

particular outcome (disease or condition) and a variety of potential causative agents (such as toxic 

chemicals). In a case-controlled study, a group of people with a specified and well-defined outcome is 

identified and compared to a similar group of people without outcome. 

Case Report—Describes a single individual with a particular disease or exposure. These may suggest 

some potential topics for scientific research but are not actual research studies. 

Case Series—Describes the experience of a small number of individuals with the same disease or 

exposure. These may suggest potential topics for scientific research, but are not actual research studies. 

Cataract—A clouding of the crystalline lens of the eye which obstructs the passage of light. 

Ceiling Value—A concentration of a substance that should not be exceeded, even temporarily. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 209 

10. GLOSSARY 

Charged Particle—A nuclear particle, atom, or molecule carrying a positive or negative charge. 

Chronic Exposure—A long-term, continuous exposure to a chemical or radioactive material. For 

example, exposure to a chemical for 365 days or more, as specified in the Toxicological Profiles. 

Cohort Study—A type of epidemiological study of a specific group or groups of people who have had a 

common insult (e.g., exposure to an agent suspected of causing disease or a common disease) and are 

followed forward from exposure to outcome. At least one exposed group is compared to one unexposed 

group. 

Collective Dose—The sum of the individual doses received in a given period of time by a specified 

population from exposure to a specified source of radiation. Collective dose is expressed in units such as 

man-rem and person-sievert. 

Compton Effect—An attenuation process observed for x- or gamma radiation in which an incident 

photon interacts with an orbital electron of an atom to produce a recoil electron and a scattered photon 

whose energy is less than the incident photon. 

Containment—The confinement of a chemical or radioactive substance in such a way that it is prevented 

from being dispersed from its container or into the environment, or is released only at a specified rate. 

Contamination—Deposition of a stable or radioactive substance in any place where it is not desired. 

Cosmic Rays—High-energy particulate and electromagnetic radiations that originate outside the earth's 

atmosphere and interact with the atmosphere to produce a shower of secondary cosmic rays. 

Count (Radiation Measurements)—The external indication of a radiation-measuring device designed to 

enumerate ionizing events. It refers to a single detected event. The term “count rate” refers to the total 

number registered in a given period of time. The term is sometimes erroneously used to designate a 

disintegration, ionizing event, or voltage pulse. 

Counter, Gas-flow Proportional (GPC)—An instrument for detecting beta particle radiation. Beta 

particles are detected by ionization of the counter gas which results in an electrical impulse at an anode 

wire. 

Counter, Geiger-Mueller (GM counter)—Highly sensitive, gas-filled radiation-measuring device that 

detects (counts) individual photons or particulate radiation. 

Counter, Scintillation—The combination of a crystal or phosphor, photomultiplier tube, and associated 

circuits for counting light emissions produced in the phosphors by ionizing radiation. Scintillation 

counters generally are more sensitive than GM counters for gamma radiation. 

Counting, Cerenkov—Relatively energetic β-particles pass through a transparent medium of high 

refractive index and a highly-directional, bluish-white light (“Cerenkov” light) is emitted. This light is 

detected using liquid scintillation counting equipment. 

Cross-sectional Study—A type of epidemiological study of a group or groups which examines the 

relationship between exposure and outcome to a chemical or to chemicals at one point in time. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 210 

10. GLOSSARY 

Curie (Ci)—A unit of radioactivity. One curie equals that quantity of radioactive material in which there 

are 3.7x1010 nuclear transformations per second. The activity of 1 gram of radium is approximately 1 Ci. 

Attocurie (aCi)—One-thousandth of a femtocurie (3.7x10-8 disintegrations per second). 

Femtocurie (fCi)—One-billionth of a microcurie (3.7x10-5 disintegrations per second). 

Megacurie (MCi)—One million curies (3.7x1016 disintegrations per second). 

Microcurie (μCi)—One-millionth of a curie (3.7x104 disintegrations per second). 

Millicurie (mCi)—One-thousandth of a curie (3.7x107 disintegrations per second). 

Nanocurie (nCi)—One-billionth of a curie (3.7x101 disintegrations per second). 

Picocurie (pCi)—One-millionth of a microcurie (3.7x10-2 disintegrations per second). 

Data Needs—Substance-specific informational needs that if met would reduce the uncertainties of human 

health assessment. 

Daughter Products—See Progeny and Decay Product 

Decay Chain or Decay Series—A sequence of radioactive decays (transformations) beginning with one 

nucleus. The initial nucleus, the parent, decays into a daughter or progeny nucleus that differs from the 

first by whatever particles were emitted during the decay. If further decays take place, the subsequent 

nuclei are also usually called daughters or progeny. Sometimes, to distinguish the sequence, the daughter 

of the first daughter is called the granddaughter, etc. 

Decay Constant (λ)—The fraction of the number of atoms of a radioactive nuclide which decay in unit 

time (see Disintegration Constant). 

Decay Product, Daughter Product, Progeny—A new nuclide formed as a result of radioactive decay. 

A nuclide resulting from the radioactive transformation of a radionuclide, formed either directly or as the 

result of successive transformations in a radioactive series. A decay product (daughter product or 

progeny) may be either radioactive or stable. 

Decay, Radioactive—Transformation of the nucleus of an unstable nuclide by spontaneous emission of 

radiation, such as charged particles and/or photons (see Disintegration). 

Decile—A method of splitting up a set of ranked data into 10 equally large subsections. 

Delta Ray—An electron removed from an atom of a medium that is irradiated, or through which 

radiation passes, during the process of ionization (also called secondary electron). Delta rays cause a 

track of ionizations along their path. 

Derived Air Concentration (DAC)—The concentration of radioactive material in air that, if breathed by 

the reference man for a working year of 2000 hours under conditions of light work (at a rate of 1.2 liters 

of air per hour), would result in an intake of one ALI (see Annual Limit on Intake). 

Deterministic Effect—A health effect, the severity of which varies with the dose and for which a 

threshold is believed to exist (also called a non-stochastic effect). 

Developmental Toxicity—The occurrence of adverse effects on the developing organism that may result 

from exposure to a chemical or radiation prior to conception (either parent), during prenatal development, 

or postnatally to the time of sexual maturation. Adverse developmental effects may be detected at any 

point in the life span of the organism. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 211 

10. GLOSSARY 

Disintegration Constant—Synonymous with decay constant. The fraction of the number of atoms of a 

radioactive material that decays per unit time (see Decay Constant.) 

Disintegration, Nuclear—A spontaneous nuclear transformation (radioactivity) characterized by the 

emission of energy and mass from the nucleus. When large numbers of nuclei are involved, the process is 

characterized by a definite half-life (see Transformation, Nuclear). 

Distribution Coefficient (Kd)—Describes the distribution of a chemical between the solid and aqueous 

phase at thermodynamic equilibrium, is given as follows: 

[C] s Kd = [C] w , Units = (L solution)/(kg solid), 

where [C]s is the concentration of the chemical associated with the solid phase in units of (mg)/(kg solid), 

and [C]w is the concentration of the chemical in the aqueous phase in units of (mg)/(L solution). As the 

magnitude of Kd decreases, the potential mobility of the chemical to groundwater systems increases and 

vice versa. 

Dose—A general term denoting the quantity of a substance, radiation, or energy absorbed. For special 

purposes it must be appropriately qualified. If unqualified, it refers to radiation absorbed dose. 

Absorbed Dose—The energy imparted to matter by ionizing radiation per unit mass of irradiated 

material at the place of interest. The unit of absorbed dose is the rad. One rad equals 100 ergs 

per gram. In SI units, the absorbed dose is the gray which is 1 J/kg (see Rad). 

Cumulative Dose (Radiation)—The total dose resulting from repeated or continuous exposures 

to radiation. 

Dose Assessment—An estimate of the radiation dose to an individual or a population group usually by 

means of predictive modeling techniques, sometimes supplemented by the results of measurement. 

Dose Equivalent (DE)—A quantity used in radiation safety practice to account for the relative biological 

effectiveness of the several types of radiation. It expresses all radiations on a common scale for 

calculating the effective absorbed dose. The NRC defines it as the product of the absorbed dose, the 

quality factor, and all other modifying factors at the location of interest. ICRP has changed its definition 

to be the product of the absorbed dose and the radiation weighting factor. (The unit of dose equivalent is 

the rem. In SI units, the dose equivalent is the sievert, which equals 100 rem.) 

Dose, Fractionation—A method of administering therapeutic radiation in which relatively small doses 

are given daily or at longer intervals. 

Dose, Protraction—A method of administering therapeutic radiation by delivering it continuously over a 

relatively long period at a low dose rate. 

Dose, Radiation—The amount of energy imparted to matter by ionizing radiation per unit mass of the 

matter, usually expressed as the unit rad, or in SI units, the gray. 100 rad1 gray (Gy) (see Absorbed 

Dose). 

Committed Dose Equivalent (HT,50)—The dose equivalent to organs or tissues of reference (T) 

that will be received from an intake of radioactive material by an individual during the 50 years 

following the intake. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 212 

10. GLOSSARY 

Committed Effective Dose Equivalent (HE,50)—The sum of the products of the weighting 

factors applicable to each of the body organs or tissues that are irradiated and the committed dose 

equivalent to those organs or tissues. 

Effective Dose —A dose value that attempts to normalize the detriment to the body (for cancer 

mortality and morbidity, hereditary effects, and years of life lost) from a non-uniform exposure to 

that of a uniform whole body exposure. Effective dose is calculated as the sum of products of the 

equivalent dose and the tissue weighting factor (wT) for each tissue exposed. (E = ∑DT,R wR wT)). 

Effective Dose Equivalent (HE)—This dose type is limited to internal exposures and is the sum 

of the products of the dose equivalent to the organ or tissue (HT) and the weighting factors (wT) 

applicable to each of the body organs or tissues that are irradiated. (HE = ∑wT HT). 

Equivalent Dose—A dose quantity that places the biological effect of all radiation types on a 

common scale for calculating tissue damage. Alpha particles, for example, are considered to 

cause 20 times more damage than gamma rays. Equivalent dose is calculated as the sum of 

products of the average absorbed dose (in gray) in an organ or tissue (DT,R) from each type of 

radiation and the radiation weighting factor (wR) for that radiation (∑DT,R wR). 

External Dose—That portion of the dose equivalent received from radiation sources outside the 

body. 

Internal Dose—That portion of the dose equivalent received from radioactive material taken into 

the body. 

Limit—A permissible upper bound on the radiation dose. 

Maximum Permissible Dose (MPD)—The greatest dose equivalent that a person or specified 

part thereof shall be allowed to receive in a given period of time. 

Median Lethal Dose (MLD)—Dose of radiation required to kill, within a specified period 

(usually 30 days), 50% of the individuals in a large group of animals or organisms. Also called 

the LD50, or LD50/30 if for 30 days. 

Threshold Dose—The minimum absorbed dose that will produce a detectable degree of any 

given effect. 

Tissue Dose—Absorbed dose received by tissue in the region of interest, expressed in rad (see 

Dose, Gray, and Rad). 

Dose Rate—The amount of radiation dose delivered per unit time. Generically, the rate at which 

radiation dose is delivered to any material or tissue. 

Dose-Response Relationship—The quantitative relationship between the amount of exposure to a 

toxicant and the incidence of the adverse effects. 

Dosimetry—Quantification of radiation doses to cells, tissues, organs, individuals or populations 

resulting from radiation exposures. 

Early Effects (of radiation exposure)—Effects that appear within 60 days of an acute exposure. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 213 

10. GLOSSARY 

Electron—A stable elementary particle having an electric charge equal to ±1.60210x10-19 C (Coulombs) 

and a rest mass equal to 9.1091x10-31 kg. A positron is a positively charged “electron” (see Positron). 

Electron Volt—A unit of energy equivalent to the energy gained by an electron in passing through a 

potential difference of one volt. Larger multiple units of the electron volt are frequently used: keV for 

thousand or kilo electron volts; MeV for million or mega electron volts (eV). 1 eV=1.6x10-12 erg. 

Embryotoxicity and Fetotoxicity—Any toxic effect on the conceptus as a result of prenatal exposure to 

a chemical; the distinguishing feature between the two terms is the stage of development during which the 

insult occurred. The terms, as used here, include malformations and variations, altered growth, and in 

utero death. 

Energy—Capacity for doing work. Gravitationally, “potential energy” is the energy inherent in a mass 

because of its spatial relation to other masses. Chemically or radiologically, “potential energy” is the 

energy released when a chemical reaction or radiological transformation goes to completion. “Kinetic 

energy” is the energy possessed by a mass because of its motion (SI unit: joules): 

Binding Energy (Electron)—The amount of energy that must be expended to remove an 

electron from an atom. 

Binding Energy (Nuclear)—The energy represented by the difference in mass between the sum 

of the component parts and the actual mass of the nucleus. It represents the amount of energy 

that must be expended to break a nucleus into its component neutrons and protons. 

Excitation Energy—The energy required to change a system from its ground state to an excited 

state. Each different excited state has a different excitation energy. 

Ionizing Energy—The energy required to knock an electron out of an atom. The average energy 

lost by electrons or beta particles in producing an ion pair in air or in soft tissue is about 34 eV. 

Radiant Energy—The energy of electromagnetic radiation, such as radio waves, visible light, x 

and gamma rays. 

Enrichment, Isotopic—An isotopic separation process by which the relative abundances of the isotopes 

of a given element are altered, thus producing a form of the element that has been enriched in one or more 

isotopes and depleted in others. In uranium enrichment, the percentage of uranium-235 in natural 

uranium can be increased from 0.7% to >90% in a gaseous diffusion process based on the different 

thermal velocities of the constituents of natural uranium (234U, 235U, 238U) in the molecular form UF6. 

EPA Health Advisory—An estimate of acceptable drinking water levels for a chemical substance based 

on health effects information. A health advisory is not a legally enforceable federal standard, but serves 

as technical guidance to assist federal, state, and local officials. 

Epidemiology—Refers to the investigation of factors that determine the frequency and distribution of 

disease or other health-related conditions within a defined human population during a specified period. 

Equilibrium, Radioactive—In a radioactive series, the state which prevails when the ratios between the 

activities of two or more successive members of the series remains constant. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 214 

10. GLOSSARY 

Secular Equilibrium—If a parent element has a very much longer half-life than the daughters 

(so there is not appreciable change in its amount in the time interval required for later products to 

attain equilibrium) then, after equilibrium is reached, equal numbers of atoms of all members of 

the series disintegrate in unit time. This condition is never exactly attained, but is essentially 

established in such a case as 226Ra and its transformation series to stable 206Pb. The half-life of 

226Ra is about 1,600 years; of 222Rn, approximately 3.82 days, and of each of the subsequent 

members, a few minutes. After about a month, essentially the equilibrium amount of radon is 

present; then (and for a long time) all members of the series disintegrate the same number of 

atoms per unit time. At this time, the activity of the daughter is equal to the activity of the parent. 

Transient Equilibrium—If the half-life of the parent is short enough so the quantity present 

decreases appreciably during the period under consideration, but is still longer than that of 

successive members of the series, a stage of equilibrium will be reached after which all members 

of the series decrease in activity exponentially with the period of the parent. At this time, the 

ratio of the parent activity to the daughter activity is constant. 

Equilibrium, Electron—The condition in a radiation field where the energy of the electrons entering a 

volume equals the energy of the electrons leaving that volume. 

Excitation—The addition of energy to a system, thereby transferring it from its ground state to an excited 

state. Excitation of a nucleus, an atom, or a molecule can result from absorption of photons or from 

inelastic collisions with other particles. The excited state of an atom is an unstable or metastable state and 

will return to ground state by radiation of the excess energy. 

Exposure (Chemical)—Contact of an organism with a chemical or physical agent. Exposure is 

quantified as the amount of the agent available at the exchange boundaries of the organism (e.g., skin, 

lungs, gut) and available for absorption. 

Exposure (Radiation)—Subjection to ionizing radiation or to a radioactive material. For example, 

exposure in air is a measure of the ionization produced in air by x or gamma radiation; the sum of the 

electric charges on all ions of one sign produced in air when all electrons liberated by photons in a 

volume of air are completely stopped in air (dQ), divided by the mass of the air in the volume (dm). The 

unit of exposure in air is the roentgen, or coulomb per kilogram (SI units). One roentgen is equal to 

2.58x10-4 coulomb per kilogram (C/kg). 

Fission, Nuclear—A nuclear transformation characterized by the splitting of a nucleus into at least two 

other nuclei with emission of several neutrons, accompanied by the release of a relatively large amount of 

energy. 

Gamma Ray, Penetrating—Short wavelength electromagnetic radiation of nuclear origin. 

Genetic Effect of Radiation—Inheritable change, chiefly mutations, produced by the absorption of 

ionizing radiation by germ cells. Genetic effects have not been observed in any human population 

exposed at any dose level. 

Genotoxicity—A specific adverse effect on the genome of living cells that, upon the duplication of 

affected cells, can be expressed as a mutagenic, clastogenic or carcinogenic event because of specific 

alteration of the molecular structure of the genome. 

Gray (Gy)—SI unit of absorbed dose, 1 J/kg. One gray equals 100 rad (see Units). 
 

 

 

 

 

 

 

 

 

 

 

 

 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

 

 

 

 

 

 


 

 
 


 


 


 


 

 


 

 
 


 


 

 
 


 

 
 

 
 


 

 
 

 
 

RADON 215 

10. GLOSSARY 

Half-life, Effective—See Half-Time, Effective. 

Half-life, Radioactive—Time required for a radioactive substance to lose 50% of its activity by decay. 

Each radio-nuclide has a unique physical half-life. Known also as physical half-time and symbolized as 

Tr or Trad. 

Half-time, Biological—Time required for an organ, tissue, or the whole body to eliminate one-half of any 

absorbed substance by regular processes of elimination. This is the same for both stable and radioactive 

isotopes of a particular element, and is sometimes referred to as half-time, symbolized as tbiol or Tb. 

Half-time, Effective—Time required for a radioactive element in an organ, tissue, or the whole body to 

be diminished 50% as a result of the combined action of radioactive decay and biological elimination, 

symbolized as Te or Teff. 

Biological half-time × Radioactive half-life Effective half-time = Biological half-time + Radioactive half-life 

Immediately Dangerous to Life or Health (IDLH)—The maximum environmental concentration of a 

contaminant from which one could escape within 30 minutes without any escape-impairing symptoms or 

irreversible health effects. 

Immunologic Toxicity—The occurrence of adverse effects on the immune system that may result from 

exposure to environmental agents such as chemicals.
	

Immunological Effects—Functional changes in the immune response.
	

Incidence—The ratio of individuals in a population who develop a specified condition to the total
	

number of individuals in that population who could have developed that condition in a specified time
	

period. 

Intensity—Amount of energy per unit time passing through a unit area perpendicular to the line of
	

propagation at the point in question.
	

Intermediate Exposure—Exposure to a chemical for a duration of 15–364 days, as specified in the 

Toxicological Profiles.
	

Internal Conversion—Process in which a gamma ray knocks an electron out of the same atom from
	

which the gamma ray was emitted. The ratio of the number of internal conversion electrons to the
	

number of gamma quanta emitted in the de-excitation of the nucleus is called the “conversion ratio.”
	

In Vitro—Isolated from the living organism and artificially maintained, as in a test tube. Literally, “in
	

glass.”
	

In Vivo—Occurring within the living organism. Literally, “in life.”
	

Ion—Atomic particle, atom or chemical radical bearing a net electrical charge, either negative or positive.
	

Ion Pair—Two particles of opposite charge, usually referring to the electron and positive atomic or
	

molecular residue resulting after the interaction of ionizing radiation with the orbital electrons of atoms.
	

Ionization—The process by which a neutral atom or molecule acquires a positive or negative charge.
	
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 216 

10. GLOSSARY 

Primary Ionization—(1) In collision theory: the ionization produced by the primary particles as 

contrasted to the “total ionization” which includes the “secondary ionization” produced by delta 

rays. (2) In counter tubes: the total ionization produced by incident radiation without gas 

amplification. 

Specific Ionization—Number of ion pairs per unit length of path of ionizing radiation in a 

medium; e.g., per centimeter of air or per micrometer of tissue. 

Total Ionization—The total electric charge of one sign on the ions produced by radiation in the 

process of losing its kinetic energy. For a given gas, the total ionization is closely proportional to 

the initial ionization and is nearly independent of the nature of the ionizing radiation. It is 

frequently used as a measure of absorption of radiation energy. 

Ionization Density—Number of ion pairs per unit volume. 

Ionization Path (Track)—The trail of ion pairs produced by an ionizing particle in its passage through 

matter. 

Ionizing Radiation—Any radiation capable of knocking electrons out of atoms and producing ions. 

Examples: alpha, beta, gamma and x rays, and neutrons. 

Isobars—Nuclides having the same mass number but different atomic numbers. 

Isomers—Nuclides having the same number of neutrons and protons but capable of existing, for a 

measurable time, in different quantum states with different energies and radioactive properties. 

Commonly the isomer of higher energy decays to one with lower energy by the process of isomeric 

transition. 

Isotopes—Nuclides having the same number of protons in their nuclei, and hence the same atomic 

number, but differing in the number of neutrons, and therefore in the mass number. Identical chemical 

properties exist in isotopes of a particular element. The term should not be used as a synonym for nuclide 

because isotopes refer specifically to different nuclei of the same element. 

Stable Isotope—A nonradioactive isotope of an element. 

Joule—The S.I. unit for work and energy. It is equal to the work done by raising a mass of one newton 

through a distance of one meter (J = Nm), which corresponds to about 0.7 ft-pound. 

Kerma (k)—A measure of the kinetic energy transferred from gamma rays or neutrons to a unit mass of 

absorbing medium in the initial collision between the radiation and the absorber atoms. The SI unit is 

J/kg. The special name of this unit is the rad (traditional system of units) or Gray (SI). 

Labeled Compound—A compound containing one or more radioactive atoms intentionally added to its 

structure. By observations of radioactivity or isotopic composition, this compound or its fragments may 

be followed through physical, chemical, or biological processes. 

Late Effects (of radiation exposure)—Effects which appear 60 days or more following an acute 

exposure. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 217 

10. GLOSSARY 

LD50/30—The dose of a chemical or radiation expected to cause 50% mortality in those exposed within 

30 days. For radiation, this is about 350 rad (3.5 gray) received by humans over a short period of time. 

Lethal Concentration(Lo) (LCLo)—The lowest concentration of a chemical in air that has been reported 

to have caused death in humans or animals. 

Lethal Concentration(50) (LC50)—A calculated concentration of a chemical in air to which exposure for 

a specific length of time is expected to cause death in 50% of a defined experimental animal population 

within a specified time, usually 30 days. 

Lethal Dose(Lo) (LDLo)—The lowest dose of a chemical introduced by a route other than inhalation that is 

expected to have caused death in humans or animals within a specified time, usually 30 days. 

Lethal Dose(50) (LD50)—The dose of a chemical which has been calculated to cause death in 50% of a 

defined experimental animal population. 

Lethal Time(50) (LT50)—A calculated period of time within which a specific concentration of a chemical 

is expected to cause death in 50% of a defined experimental animal population. 

Linear Energy Transfer (LET)—A measure of the energy that a charged particle transfers to a material 

per unit path length. 

Average LET—The energy of a charged particle divided by the length of the path over which it 

deposits all its energy in a material. This is averaged over a number of particles. 

High-LET—Energy transfer characteristic of heavy charged particles such as protons and alpha 

particles where the distance between ionizing events is small on the scale of a cellular nucleus. 

Low-LET—Energy transfer characteristic of light charged particles such as electrons produced 

by x and gamma rays where the distance between ionizing events is large on the scale of a 

cellular nucleus. 

Lowest-Observed-Adverse-Effect Level (LOAEL)—The lowest dose of chemical in a study, or group 

of studies, that produces statistically or biologically significant increases in frequency or severity of 

adverse effects between the exposed population and its appropriate control. 

Lung Clearance Class (fast, F; medium, M; slow, S)—A classification scheme for inhaled material 

according to its rate of clearance from the pulmonary region of the lungs to the blood and the 

gastrointestinal tract. 

Lymphoreticular Effects—Represent morphological effects involving lymphatic tissues such as the 

lymph nodes, spleen, and thymus. 

Malformations—Permanent structural changes that may adversely affect survival, development, or 

function. 

Mass Numbers (A)—The number of nucleons (protons and neutrons) in the nucleus of an atom. 

Minimal Risk Level—An estimate of daily human exposure to a substance that is likely to be without an 

appreciable risk of adverse noncancerous effects over a specified duration of exposure. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 218 

10. GLOSSARY 

Modifying Factor (MF)—A value (greater than zero) that is applied to the derivation of a Minimal Risk 

Level (MRL) to reflect additional concerns about the database that are not covered by the uncertainty 

factors. The default value for a MF is 1. 

Morbidity—State of being diseased; morbidity rate is the incidence or prevalence of disease in a specific 

population. 

Mortality—Death; mortality rate is a measure of the number of deaths in a population during a specified 

interval of time. 

Mutagen—A substance that causes changes (mutations) in the genetic material in a cell. Mutations can 

lead to birth defects, miscarriages, or cancer. 

Necropsy—The gross examination of the organs and tissues of a dead body to determine the cause of 

death or pathological conditions. 

Neurotoxicity—The occurrence of adverse effects on the nervous system following exposure to a 

substance. 

Neutrino (ν)—A neutral particle of infinitesimally small rest mass emitted during beta plus or beta minus 

decay. This particle accounts for conservation of energy in beta plus and beta minus decays. It plays no 

role in damage from radiation. 

Noble Gas—Any of a group of rare gases that include helium, neon, argon, krypton, xenon, and radon. 

Because the outermost electron shell of atoms of these gases is full, they do not react chemically with 

other substances except under certain special conditions. Also called inert gas. 

No-Observed-Adverse-Effect Level (NOAEL)—The dose of a substance at which there were no 

statistically or biologically significant increases in frequency or severity of adverse effects seen between 

the exposed population and its appropriate control. Effects may be produced at this dose, but they are not 

considered to be adverse. 

Nuclear Reactor—A power plant that heats the medium (typically water) by using the energy released 

from the nuclear fission of uranium or plutonium isotopes instead of burning coal, oil, or natural gas. All 

of these sources of energy simply heat water and use the steam which is produced to turn turbines that 

make electricity or propel a ship. 

Nucleon—Common name for a constituent particle of the nucleus. Applied to a proton or neutron. 

Nuclide—A species of atom characterized by the constitution of its nucleus. The nuclear constitution is 

specified by the number of protons (Z), number of neutrons (N), and energy content; or, alternatively, by 

the atomic number (Z), mass number A(N+Z), and atomic mass. To be regarded as a distinct nuclide, the 

atom must be capable of existing for a measurable time. Thus, nuclear isomers are separate nuclides, 

whereas promptly decaying excited nuclear states and unstable intermediates in nuclear reactions are not 

so considered. 

Octanol-Water Partition Coefficient (Kow)—The equilibrium ratio of the concentrations of a chemical 

in n-octanol and water, in dilute solution. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 219 

10. GLOSSARY 

Odds Ratio (OR)—The ratio of the odds of an event (e.g., lung cancer) occurring in one group (e.g., a 

group exposed to a particular substance) to the odds of the same event (e.g., lung cancer) occurring in 

another group (e.g., a group not exposed to the same substance). An odds ratio of greater than 1 is 

considered to indicate greater risk of disease in the exposed group compared to the unexposed. 

Excess Odds Ratio—The ‘extra’ or ‘additional’ odds of an effect due to exposure to some 

stressor above and beyond the odds of that effect occurring in the absence of the stressor, 

expressed as excess odds per some unit increase in the stressor. 

Organophosphate or Organophosphorus Compound—A phosphorus-containing organic compound 

and especially a pesticide that acts by inhibiting cholinesterase. 

Pair Production—An absorption process for x- and gamma radiation in which the incident photon is 

absorbed in the vicinity of the nucleus of the absorbing atom, with subsequent production of an electron 

and positron pair (see annihilation). This reaction can only occur for incident photon energies exceeding 

1.02 MeV. 

Parent—Any radionuclide nuclide which, upon disintegration, yields a new nuclide (termed the progeny 

or daughter), either directly or as a later member of a radioactive series. 

Permissible Exposure Limit (PEL)—A maximum allowable atmospheric level of a substance in 

workplace air averaged over an 8-hour shift. 

Pesticide—General classification of chemicals specifically developed and produced for use in the control 

of agricultural and public health pests. 

Pharmacokinetic Model—A set of equations that can be used to describe the time course of a parent 

chemical or metabolite in an animal system. There are two types of pharmacokinetic models: data-based 

and physiologically-based. A data-based model divides the animal system into a series of compartments 

which, in general, do not represent real, identifiable anatomic regions of the body whereas the 

physiologically-based model compartments represent real anatomic regions of the body. 

Pharmacokinetics—The dynamic behavior of a material in the body, used to predict the fate 

(disposition) of an exogenous substance in an organism. Utilizing computational techniques, it provides 

the means of studying the absorption, distribution, metabolism and excretion of chemicals by the body. 

Physiologically Based Pharmacodynamic (PBPD) Model—A type of physiologically-based doseresponse model which quantitatively describes the relationship between target tissue dose and toxic end 

points. These models advance the importance of physiologically based models in that they clearly 

describe the biological effect (response) produced by the system following exposure to an exogenous 

substance. 

Physiologically Based Pharmacokinetic (PBPK) Model—A model comprising a series of 

compartments representing organs or tissue groups with realistic weights and blood flows. These models 

require a variety of physiological information: tissue volumes, blood flow rates to tissues, cardiac output, 

alveolar ventilation rates and, possibly membrane permeabilities. The models also utilize biochemical 

information such as air/blood partition coefficients, and metabolic parameters. PBPK models are also 

called biologically based tissue dosimetry models. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 220 

10. GLOSSARY 

Photoelectric Effect—An attenuation process observed for x and gamma radiation in which an incident 

photon interacts with a tightly bound inner orbital electron of an atom delivering all of its energy to knock 

the electron out of the atom. The incident photon disappears in the process. 

Photon—A quantum of electromagnetic energy (E) whose value is the product of its frequency (ν) in 

hertz and Planck's constant (h). The equation is: E = hν. 

Population dose—See Collective dose. 

Positron—A positively charged electron. 

Potential, Ionization—The energy expressed as electron volts (eV) necessary to separate one electron 

from an atom, resulting in the formation of an ion pair. 

Power, Stopping—A measure of the ability of a material to absorb energy from an ionizing particle 

passing through it; the greater the stopping power, the greater the energy absorbing ability (see Linear 

Energy Transfer). 

Prevalence—The number of cases of a disease or condition in a population at one point in time. 

Progeny—The decay product or daughter products resulting after a radioactive decay or a series of 

radioactive decays. The progeny can also be radioactive, and the chain continues until a stable nuclide is 

formed. 

Prospective Study—A type of cohort study in which the pertinent observations are made on events 

occurring after the start of the study. A group is followed over time. 

Proton—Elementary nuclear particle with a positive electric charge equal numerically to the charge of 

the electron and a rest mass of 1.007 mass units. 

q1*—The upper-bound estimate of the low-dose slope of the dose-response curve as determined by the 

multistage procedure. The q1* can be used to calculate an estimate of carcinogenic potency, the 

incremental excess cancer risk per unit of exposure (usually μg/L for water, mg/kg/day for food, and 

μg/m3 for air). 

Quality—A term describing the distribution of the energy deposited by a particle along its track; 

radiations that produce different densities of ionization per unit intensity are said to have different 

“qualities.” 

Quality Factor (Q)—The linear-energy-transfer-dependent factor by which absorbed doses are 

multiplied to obtain (for radiation protection purposes) a quantity that expresses - on a common scale for 

all ionizing radiation - the approximate biological effectiveness of the absorbed dose. 

Type of radiation Quality Factor 

X, gamma, or beta 1 

Alpha particles 20 

Neutrons of unknown energy 10 

High energy protons 10 

Rad—The traditional unit of absorbed dose equal to 100 ergs per gram, or 0.01 joule per kilogram 

(0.01 Gy) in any medium (see Absorbed Dose). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 221 

10. GLOSSARY 

Radiation—The emission and propagation of energy through space or through a material medium in the 

form of waves (e.g., the emission and propagation of electromagnetic waves, or of sound and elastic 

waves). The term radiation or radiant energy, when unqualified, usually refers to electromagnetic 

radiation. Such radiation commonly is classified according to frequency, as microwaves, infrared, visible 

(light), ultraviolet, and x and gamma rays (see Photon.) and, by extension, corpuscular emission, such as 

alpha and beta radiation, neutrons, or rays of mixed or unknown type, as cosmic radiation. 

Radiation, Annihilation—Photons produced when an electron and a positron unite and cease to 

exist. The annihilation of a positron-electron pair results in the production of two photons, each 

of 0.51 MeV energy. 

Radiation, Background—See Background Radiation. 

Radiation, Characteristic (Discrete)—Radiation originating from an excited atom after removal 

of an electron from an atom. The wavelength of the emitted radiation is specific, depending only 

on the element and particular energy levels involved. 

Radiation, External—Radiation from a source outside the body. 

Radiation, Internal—Radiation from a source within the body (as a result of deposition of 

radionuclides in body tissues). 

Radiation, Ionizing—Any electromagnetic or particulate radiation capable of producing ions, 

directly or indirectly, in its passage through matter (see Radiation). 

Radiation, Monoenergetic—Radiation of a given type in which all particles or photons originate 

with and have the same energy. 

Radiation, Scattered—Radiation which during its passage through a substance, has been 

deviated in direction. It may also have been modified by a decrease in energy. 

Radiation, Secondary—A particle or ray that is produced when the primary radiation interacts 

with a material, and which has sufficient energy to produce its own ionization, such as 

bremsstrahlung or electrons knocked from atomic orbitals with enough energy to then produce 

ionization (see Delta Rays). 

Radiation Weighting Factor (also called Quality Factor)—In radiation protection, a factor (1 for xrays, gamma rays, beta particles; 20 for alpha particles) weighting the absorbed dose of radiation of a 

specific type and energy for its effect on tissue. 

Radioactive Material—Material containing radioactive atoms. 

Radioactivity—Spontaneous nuclear transformations that result in the formation of new elements. These 

transformations are accomplished by emission of alpha or beta particles from the nucleus or by the 

capture of an orbital electron. Each of these reactions may or may not be accompanied by a gamma 

photon. 

Radioactivity, Artificial—Man-made radioactivity produced by particle bombardment or 

nuclear fission, as opposed to naturally occurring radioactivity. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 222 

10. GLOSSARY 

Radioactivity, Induced—Radioactivity produced in a substance after bombardment with 

neutrons or other particles. The resulting activity is “natural radioactivity” if formed by nuclear 

reactions occurring in nature and “artificial radioactivity” if the reactions are caused by man. 

Radioactivity, Natural—The property of radioactivity exhibited by more than 50 naturally 

occurring radionuclides. 

Radioisotope—An unstable or radioactive isotope of an element that decays or disintegrates 

spontaneously, emitting radiation. 

Radionuclide—Any radioactive isotope of any element. Approximately 5,000 natural and artificial 

radioisotopes have been identified. 

Radiosensitivity—Relative susceptibility of cells, tissues, organs, organisms, or any living substance to 

the injurious action of radiation. Radiosensitivity and its antonym, radioresistance, are used 

comparatively, rather than absolutely. 

Recommended Exposure Limit (REL)—A National Institute for Occupational Safety and Health 

(NIOSH) time-weighted average (TWA) concentration for up to a 10-hour workday during a 40-hour 

workweek. 

Reference Concentration (RfC)—An estimate (with uncertainty spanning perhaps an order of 

magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) 

that is likely to be without an appreciable risk of deleterious noncancer health effects during a lifetime. 

The inhalation reference concentration is for continuous inhalation exposures and is appropriately 

expressed in units of mg/m3 or ppm. 

Reference Dose (RfD)—An estimate of the daily exposure of the human population to a potential hazard 

that is likely to be without risk of deleterious effects during a lifetime. The RfD is operationally derived 

from the NOAEL (from animal and human studies) by a consistent application of uncertainty factors that 

reflect various types of data used to estimate RfDs and an additional modifying factor, which is based on 

a professional judgment of the entire database on the chemical. The RfDs are not applicable to nonthreshold effects such as cancer. 

Relative Biological Effectiveness (RBE)—The RBE is a factor used to compare the biological 

effectiveness of absorbed radiation doses (i.e., rad) due to different types of ionizing radiation. More 

specifically, it is the experimentally determined ratio of an absorbed dose of a radiation in question to the 

absorbed dose of a reference radiation (typically 60Co gamma rays or 200 kVp x rays) required to produce 

an identical biological effect in a particular experimental organism or tissue (see Quality Factor). 

Relative Risk (RR)— Risk as a ratio of the incidence among subjects exposed to a particular risk factor 

divided by the incidence among subjects who were not exposed to the risk factor. 

Excess Relative Risk (ERR)— In epidemiology typically defined to be the difference between 

the proportion of subjects in a population with a particular disease who were exposed to a 

specified risk factor and the proportion of subjects with that same disease who were not exposed. 

Rem—The traditional unit of dose equivalent that is used in the regulatory, administrative, and 

engineering design aspects of radiation safety practice. The dose equivalent in rem is numerically equal 

to the absorbed dose in rad multiplied by the quality factor (1 rem is equal to 0.01 sievert). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 223 

10. GLOSSARY 

Reportable Quantity (RQ)—The quantity of a hazardous substance that is considered reportable under 

CERCLA. Reportable quantities are (1) 1 pound or greater or (2) for selected substances, an amount 

established by regulation either under CERCLA or under Sect. 311 of the Clean Water Act. Quantities 

are measured over a 24-hour period. 

Reproductive Toxicity—The occurrence of adverse effects on the reproductive system that may result 

from exposure to a chemical. The toxicity may be directed to the reproductive organs and/or the related 

endocrine system. The manifestation of such toxicity may be noted as alterations in sexual behavior, 

fertility, pregnancy outcomes, or modifications in other functions that are dependent on the integrity of 

this system. 

Roentgen (R)—A unit of exposure (in air) to ionizing radiation. It is the amount of x or gamma rays 

required to produce ions carrying 1 electrostatic unit of electrical charge in 1 cubic centimeter of dry air 

under standard conditions. Named after William Roentgen, a German scientist who discovered x rays in 

1895. 

Retrospective Study—A type of cohort study based on a group of persons known to have been exposed 

at some time in the past. Data are collected from routinely recorded events, up to the time the study is 

undertaken. Retrospective studies are limited to causal factors that can be ascertained from existing 

records and/or examining survivors of the cohort. 

Risk—The possibility or chance that some adverse effect will result from a given exposure to a chemical. 

Risk Factor—An aspect of personal behavior or lifestyle, an environmental exposure, or an inborn or 

inherited characteristic that is associated with an increased occurrence of disease or other health-related 

event or condition. 

Risk Ratio—The ratio of the risk among persons with specific risk factors compared to the risk among 

persons without risk factors. A risk ratio greater than 1 indicates greater risk of disease in the exposed 

group compared to the unexposed group. 

Self-Absorption—Absorption of radiation (emitted by radioactive atoms) by the material in which the 

atoms are located; in particular, the absorption of radiation within a sample being assayed. 

Short-Term Exposure Limit (STEL)—The maximum concentration to which workers can be exposed 

for up to 15 minutes continually. No more than four excursions are allowed per day, and there must be at 

least 60 minutes between exposure periods. The daily TLV-TWA may not be exceeded. 

SI Units—The International System of Units as defined by the General Conference of Weights and 

Measures in 1960. These units are generally based on the meter/kilogram/second units, with special 

quantities for radiation including the becquerel, gray, and sievert. 

Sickness, Acute Radiation (Syndrome)—The complex symptoms and signs characterizing the condition 

resulting from excessive exposure of the whole body (or large part) to ionizing radiation. The earliest of 

these symptoms are nausea, fatigue, vomiting, and diarrhea, and may be followed by loss of hair 

(epilation), hemorrhage, inflammation of the mouth and throat, and general loss of energy. In severe 

cases, where the radiation dose is relatively high (over several hundred rad or several gray), death may 

occur within two to four weeks. Those who survive six weeks after exposure of a single high dose of 

radiation may generally be expected to recover. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 224 

10. GLOSSARY 

Sievert (Sv)—The SI unit of any of the quantities expressed as dose equivalent. The dose equivalent in 

sieverts is equal to the absorbed dose, in gray, multiplied by the quality factor (1 sievert equals 100 rem). 

The sievert is also the SI unit for effective dose equivalent, which is the sum of the products of the dose 

equivalent to each organ or tissue and its corresponding tissue weighting factor. 

Specific-Activity—Radioactivity per unit mass of a radionuclide, expressed, for example, as Ci/gram or 

Bq/kilogram. 

Specific Energy—The actual energy per unit mass deposited per unit volume in a small target, such as 

the cell or cell nucleus, as the result of one or more energy-depositing events. This is a stochastic 

quantity as opposed to the average value over a large number of instance (i.e., the absorbed dose). 

Standardized Mortality Ratio (SMR)—A ratio of the observed number of deaths and the expected 

number of deaths in a specific standard population. 

Stochastic Effect—A health effect that occurs randomly and for which the probability of the effect 

occurring, rather than its severity, is assumed to be a linear function of dose without a threshold (also 

called a nondeterministic effect). 

Stopping Power—The average rate of energy loss of a charged particle per unit thickness of a material or 

per unit mass of material traversed. 

Surface-seeking Radionuclide—A bone-seeking internal emitter that deposits and remains on the bone 

surface for a long period of time, although it may eventually diffuse into the bone mineral. This contrasts 

with a volume seeker, which deposits more uniformly throughout the bone volume. 

Target Organ Toxicity—This term covers a broad range of adverse effects on target organs or 

physiological systems (e.g., renal, cardiovascular) extending from those arising through a single limited 

exposure to those assumed over a lifetime of exposure to a chemical. 

Target Theory (Hit Theory)—A theory explaining some biological effects of radiation on the basis that 

ionization, occurring in a discrete volume (the target) within the cell, directly causes a lesion which 

subsequently results in a physiological response to the damage at that location. One, two, or more “hits” 

(ionizing events within the target) may be necessary to elicit the response. 

Teratogen—A chemical that causes birth defects. 

Threshold Limit Value (TLV)—The maximum concentration of a substance to which most workers can 

be exposed without adverse effect. TLV is a term used exclusively by the ACGIH. Other terms used to 

express similar concepts are the MAC (Maximum Allowable Concentration) and PEL (Permissible 

Exposure Limits). 

Time-Weighted Average (TWA)—An allowable exposure concentration averaged over a normal 8-hour 

workday or 40-hour workweek. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 225 

10. GLOSSARY 

Tissue Weighting Factor (Wt)—Organ- or tissue-specific factor by which the equivalent dose is 

multiplied to give the portion of the effective dose for that organ or tissue. Recommended values of 

tissue weighting factors are: 

Tissue/Organ Tissue Weighting Factor 

Gonads 0.70 

Bone marrow (red) 0.12 

Colon 0.12 

Lung 0.12 

Stomach 0.12 

Bladder 0.05 

Breast 0.05 

Liver 0.05 

Esophagus 0.05 

Thyroid 0.05 

Skin 0.01 

Bone surface 0.01 

Remainder (adrenals, brain, upper large 0.05 

intestine, small intestine, pancreas, spleen, 

thymus, and uterus) 

Toxic Dose (TD50)—A calculated dose of a chemical, introduced by a route other than inhalation, which 

is expected to cause a specific toxic effect in 50% of a defined experimental animal population. 

Toxicokinetic—The absorption, distribution and elimination of toxic compounds in the living organism. 

Toxicosis—A diseased condition resulting from poisoning. 

Transformation, Nuclear—The process of radioactive decay by which a nuclide is transformed into a 

different nuclide by absorbing or emitting particulate or electromagnetic radiation. 

Transition, Isomeric—The process by which a nuclide decays to an isomeric nuclide (i.e., one of the 

same mass number and atomic number) of lower quantum energy. Isomeric transitions (often abbreviated 

I.T.) proceed by gamma ray and internal conversion electron emission. 

Tritium—The hydrogen isotope with one proton and two neutrons in the nucleus (Symbol: 3

H). It is 

radioactive and has a physical half-life of 12.3 years. 

Unattached Fraction—That fraction of the radon daughters, usually 218Po and 214Po, which has not yet 

attached to a dust particle or to water vapor. As a free atom, it has a high probability of being exhaled and 

not retained within the lung. It is the attached fraction which is primarily retained. 

Uncertainty Factor (UF)—A factor used in operationally deriving the RfD from experimental data. UFs 

are intended to account for (1) the variation in sensitivity among the members of the human population, 

(2) the uncertainty in extrapolating animal data to the case of human, (3) the uncertainty in extrapolating 

from data obtained in a study that is of less than lifetime exposure, and (4) the uncertainty in using 

LOAEL data rather than NOAEL data. Usually each of these factors is set equal to 10. 
 

 

 

 

 

 

 

 

 

 

 

 

 

RADON 226 

10. GLOSSARY 

Units, Prefixes—Many units of measure are expressed as submultiples or multiples of the primary unit 

(e.g., 10-3 curie is 1 mCi and 103 becquerel is 1 kBq). 

Factor Prefix Symbol Factor Prefix Symbol 

10-18 atto a 103 kilo k 

10-15 femto f 106 mega M 

10-12 pico p 109 giga G 

10-9 nano n 1012 tera T 

10-6 micro μ 1015 peta P 

10-3 milli m 1018 exa E 

10-2 centi c 

Units, Radiological— 

Units Equivalents 

Becquerel* (Bq) 1 disintegration per second = 2.7x10-11 Ci 

Curie (Ci) 3.7x1010 disintegrations per second = 3.7x1010 Bq 

Gray* (Gy) 1 J/kg = 100 rad 

Rad (rad) 100 erg/g = 0.01 Gy 

Rem (rem) 0.01 sievert 

Sievert* (Sv) 100 rem 

*International Units, designated (SI) 

Working Level (WL)—Any combination of short-lived radon daughters in 1 liter of air that will result in 

the ultimate emission of 1.3x105 MeV of potential alpha energy. 

Working Level Month (WLM)—A unit of exposure to radon daughters corresponding to the product of 

the radon daughter concentration in Working Level (WL) and the exposure time in nominal months 

(1 nominal month = 170 hours). Inhalation of air with a concentration of 1 WL of radon daughters for 

170 working hours results in an exposure of 1 WLM. 

Xenobiotic—Any chemical that is foreign to the biological system. 

X rays—Penetrating electromagnetic radiations whose wave lengths are very much shorter than those of 

visible light. They are usually produced by bombarding a metallic target with fast electrons in a high 

vacuum. X rays (called characteristic x rays) are also produced when an orbital electron falls from a high 

energy level to a low energy level. 

Zero-Threshold Linear Hypothesis (or No-Threshold Linear Hypothesis)—The assumption that a 

dose-response curve derived from data in the high dose and high dose-rate ranges may be extrapolated 

through the low dose and low dose range to zero, implying that, theoretically, any amount of radiation 

will cause some damage. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON A-1 

APPENDIX A. ATSDR MINIMAL RISK LEVELS AND WORKSHEETS 

The Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) [42 U.S.C. 

9601 et seq.], as amended by the Superfund Amendments and Reauthorization Act (SARA) [Pub. L. 99– 

499], requires that the Agency for Toxic Substances and Disease Registry (ATSDR) develop jointly with 

the U.S. Environmental Protection Agency (EPA), in order of priority, a list of hazardous substances most 

commonly found at facilities on the CERCLA National Priorities List (NPL); prepare toxicological 

profiles for each substance included on the priority list of hazardous substances; and assure the initiation 

of a research program to fill identified data needs associated with the substances. 

The toxicological profiles include an examination, summary, and interpretation of available toxicological 

information and epidemiologic evaluations of a hazardous substance. During the development of 

toxicological profiles, Minimal Risk Levels (MRLs) are derived when reliable and sufficient data exist to 

identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration for a 

given route of exposure. An MRL is an estimate of the daily human exposure to a hazardous substance 

that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration 

of exposure. MRLs are based on noncancer health effects only and are not based on a consideration of 

cancer effects. These substance-specific estimates, which are intended to serve as screening levels, are 

used by ATSDR health assessors to identify contaminants and potential health effects that may be of 

concern at hazardous waste sites. It is important to note that MRLs are not intended to define clean-up or 

action levels. 

MRLs are derived for hazardous substances using the no-observed-adverse-effect level/uncertainty factor 

approach. They are below levels that might cause adverse health effects in the people most sensitive to 

such chemical-induced effects. MRLs are derived for acute (1–14 days), intermediate (15–364 days), and 

chronic (365 days and longer) durations and for the oral and inhalation routes of exposure. Currently, 

MRLs for the dermal route of exposure are not derived because ATSDR has not yet identified a method 

suitable for this route of exposure. MRLs are generally based on the most sensitive chemical-induced end 

point considered to be of relevance to humans. Serious health effects (such as irreparable damage to the 

liver or kidneys, or birth defects) are not used as a basis for establishing MRLs. Exposure to a level 

above the MRL does not mean that adverse health effects will occur. 

MRLs are intended only to serve as a screening tool to help public health professionals decide where to 

look more closely. They may also be viewed as a mechanism to identify those hazardous waste sites that 
 

 

RADON A-2 

APPENDIX A 

are not expected to cause adverse health effects. Most MRLs contain a degree of uncertainty because of 

the lack of precise toxicological information on the people who might be most sensitive (e.g., infants, 

elderly, nutritionally or immunologically compromised) to the effects of hazardous substances. ATSDR 

uses a conservative (i.e., protective) approach to address this uncertainty consistent with the public health 

principle of prevention. Although human data are preferred, MRLs often must be based on animal studies 

because relevant human studies are lacking. In the absence of evidence to the contrary, ATSDR assumes 

that humans are more sensitive to the effects of hazardous substance than animals and that certain persons 

may be particularly sensitive. Thus, the resulting MRL may be as much as 100-fold below levels that 

have been shown to be nontoxic in laboratory animals. 

Proposed MRLs undergo a rigorous review process: Health Effects/MRL Workgroup reviews within the 

Division of Toxicology and Human Health Sciences (proposed), expert panel peer reviews, and agencywide MRL Workgroup reviews, with participation from other federal agencies and comments from the 

public. They are subject to change as new information becomes available concomitant with updating the 

toxicological profiles. Thus, MRLs in the most recent toxicological profiles supersede previously 

published levels. For additional information regarding MRLs, please contact the Division of Toxicology 

and Human Health Sciences (proposed), Agency for Toxic Substances and Disease Registry, 1600 Clifton 

Road NE, Mailstop F-62, Atlanta, Georgia 30333. 

For reasons discussed in Section 2.3, MRLs were not derived for radon. 
 

 

 

 

 

 

 

 

 

 

 

	 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON	 B-1 

APPENDIX B. USER'S GUIDE 

Chapter 1 

Public Health Statement 

This chapter of the profile is a health effects summary written in non-technical language. Its intended 

audience is the general public, especially people living in the vicinity of a hazardous waste site or 

chemical release. If the Public Health Statement were removed from the rest of the document, it would 

still communicate to the lay public essential information about the chemical. 

The major headings in the Public Health Statement are useful to find specific topics of concern. The 

topics are written in a question and answer format. The answer to each question includes a sentence that 

will direct the reader to chapters in the profile that will provide more information on the given topic. 

Chapter 2 

Relevance to Public Health 

This chapter provides a health effects summary based on evaluations of existing toxicologic, 

epidemiologic, and toxicokinetic information. This summary is designed to present interpretive, weightof-evidence discussions for human health end points by addressing the following questions: 

1. What effects are known to occur in humans? 

2. What effects observed in animals are likely to be of concern to humans? 

3. What exposure conditions are likely to be of concern to humans, especially around hazardous 

waste sites? 

The chapter covers end points in the same order that they appear within the Discussion of Health Effects 

by Route of Exposure section, by route (inhalation, oral, and dermal) and within route by effect. Human 

data are presented first, then animal data. Both are organized by duration (acute, intermediate, chronic). 

In vitro data and data from parenteral routes (intramuscular, intravenous, subcutaneous, etc.) are also 

considered in this chapter. 

The carcinogenic potential of the profiled substance is qualitatively evaluated, when appropriate, using 

existing toxicokinetic, genotoxic, and carcinogenic data. ATSDR does not currently assess cancer 

potency or perform cancer risk assessments. Minimal Risk Levels (MRLs) for noncancer end points (if 

derived) and the end points from which they were derived are indicated and discussed. 

Limitations to existing scientific literature that prevent a satisfactory evaluation of the relevance to public 

health are identified in the Chapter 3 Data Needs section. 

Interpretation of Minimal Risk Levels 

Where sufficient toxicologic information is available, ATSDR has derived MRLs for inhalation and oral 

routes of entry at each duration of exposure (acute, intermediate, and chronic). These MRLs are not 

meant to support regulatory action, but to acquaint health professionals with exposure levels at which 

adverse health effects are not expected to occur in humans. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON B-2 

APPENDIX B 

MRLs should help physicians and public health officials determine the safety of a community living near 

a chemical emission, given the concentration of a contaminant in air or the estimated daily dose in water. 

MRLs are based largely on toxicological studies in animals and on reports of human occupational 

exposure. 

MRL users should be familiar with the toxicologic information on which the number is based. Chapter 2, 

"Relevance to Public Health," contains basic information known about the substance. Other sections such 

as Chapter 3 Section 3.9, "Interactions with Other Substances,” and Section 3.10, "Populations that are 

Unusually Susceptible" provide important supplemental information. 

MRL users should also understand the MRL derivation methodology. MRLs are derived using a 

modified version of the risk assessment methodology that the Environmental Protection Agency (EPA) 

provides (Barnes and Dourson 1988) to determine reference doses (RfDs) for lifetime exposure. 

To derive an MRL, ATSDR generally selects the most sensitive end point which, in its best judgement, 

represents the most sensitive human health effect for a given exposure route and duration. ATSDR 

cannot make this judgement or derive an MRL unless information (quantitative or qualitative) is available 

for all potential systemic, neurological, and developmental effects. If this information and reliable 

quantitative data on the chosen end point are available, ATSDR derives an MRL using the most sensitive 

species (when information from multiple species is available) with the highest no-observed-adverse-effect 

level (NOAEL) that does not exceed any adverse effect levels. When a NOAEL is not available, a 

lowest-observed-adverse-effect level (LOAEL) can be used to derive an MRL, and an uncertainty factor 

(UF) of 10 must be employed. Additional uncertainty factors of 10 must be used both for human 

variability to protect sensitive subpopulations (people who are most susceptible to the health effects 

caused by the substance) and for interspecies variability (extrapolation from animals to humans). In 

deriving an MRL, these individual uncertainty factors are multiplied together. The product is then 

divided into the inhalation concentration or oral dosage selected from the study. Uncertainty factors used 

in developing a substance-specific MRL are provided in the footnotes of the levels of significant exposure 

(LSE) tables. 

Chapter 3 

Health Effects 

Tables and Figures for Levels of Significant Exposure (LSE) 

Tables and figures are used to summarize health effects and illustrate graphically levels of exposure 

associated with those effects. These levels cover health effects observed at increasing dose 

concentrations and durations, differences in response by species, MRLs to humans for noncancer end 

points, and EPA's estimated range associated with an upper- bound individual lifetime cancer risk of 1 in 

10,000 to 1 in 10,000,000. Use the LSE tables and figures for a quick review of the health effects and to 

locate data for a specific exposure scenario. The LSE tables and figures should always be used in 

conjunction with the text. All entries in these tables and figures represent studies that provide reliable, 

quantitative estimates of NOAELs, LOAELs, or Cancer Effect Levels (CELs). 

The legends presented below demonstrate the application of these tables and figures. Representative 

examples of LSE Table 3-1 and Figure 3-1 are shown. The numbers in the left column of the legends 

correspond to the numbers in the example table and figure. 
 

 

 

 

 

 

 

 

 

 

 

 

 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

 

 

 

	 

 

 

	 

 

	 

 

	 

	 

 

 

	 

 

 

 

	 

 

RADON	 B-3 

APPENDIX B 

LEGEND 

See Sample LSE Table 3-1 (page B-6) 

(1)		 Route of Exposure. One of the first considerations when reviewing the toxicity of a substance 

using these tables and figures should be the relevant and appropriate route of exposure. Typically 

when sufficient data exist, three LSE tables and two LSE figures are presented in the document. 

The three LSE tables present data on the three principal routes of exposure, i.e., inhalation, oral, 

and dermal (LSE Tables 3-1, 3-2, and 3-3, respectively). LSE figures are limited to the inhalation 

(LSE Figure 3-1) and oral (LSE Figure 3-2) routes. Not all substances will have data on each 

route of exposure and will not, therefore, have all five of the tables and figures. 

(2)		 Exposure Period. Three exposure periods—acute (less than 15 days), intermediate (15– 

364 days), and chronic (365 days or more)—are presented within each relevant route of exposure. 

In this example, an inhalation study of intermediate exposure duration is reported. For quick 

reference to health effects occurring from a known length of exposure, locate the applicable 

exposure period within the LSE table and figure. 

(3)		 Health Effect. The major categories of health effects included in LSE tables and figures are 

death, systemic, immunological, neurological, developmental, reproductive, and cancer. 

NOAELs and LOAELs can be reported in the tables and figures for all effects but cancer. 

Systemic effects are further defined in the "System" column of the LSE table (see key number 

18). 

(4)		 Key to Figure. Each key number in the LSE table links study information to one or more data 

points using the same key number in the corresponding LSE figure. In this example, the study 

represented by key number 18 has been used to derive a NOAEL and a Less Serious LOAEL 

(also see the two "18r" data points in sample Figure 3-1). 

(5)		 Species. The test species, whether animal or human, are identified in this column. Chapter 2, 

"Relevance to Public Health," covers the relevance of animal data to human toxicity and 

Section 3.4, "Toxicokinetics," contains any available information on comparative toxicokinetics. 

Although NOAELs and LOAELs are species specific, the levels are extrapolated to equivalent 

human doses to derive an MRL. 

(6)		 Exposure Frequency/Duration. The duration of the study and the weekly and daily exposure 

regimens are provided in this column. This permits comparison of NOAELs and LOAELs from 

different studies. In this case (key number 18), rats were exposed to “Chemical x” via inhalation 

for 6 hours/day, 5 days/week, for 13 weeks. For a more complete review of the dosing regimen, 

refer to the appropriate sections of the text or the original reference paper (i.e., Nitschke et al. 

1981). 

(7)		 System. This column further defines the systemic effects. These systems include respiratory, 

cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, and 

dermal/ocular. "Other" refers to any systemic effect (e.g., a decrease in body weight) not covered 

in these systems. In the example of key number 18, one systemic effect (respiratory) was 

investigated. 

(8)		 NOAEL. A NOAEL is the highest exposure level at which no harmful effects were seen in the 

organ system studied. Key number 18 reports a NOAEL of 3 ppm for the respiratory system, 

which was used to derive an intermediate exposure, inhalation MRL of 0.005 ppm (see 

footnote "b"). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

 

 

 

 

 

	 

	 

	 

 

 

	 

 

	 

 

	 

	 

 

 

 

	 

RADON	 B-4 

APPENDIX B 

(9)		 LOAEL. A LOAEL is the lowest dose used in the study that caused a harmful health effect. 

LOAELs have been classified into "Less Serious" and "Serious" effects. These distinctions help 

readers identify the levels of exposure at which adverse health effects first appear and the 

gradation of effects with increasing dose. A brief description of the specific end point used to 

quantify the adverse effect accompanies the LOAEL. The respiratory effect reported in key 

number 18 (hyperplasia) is a Less Serious LOAEL of 10 ppm. MRLs are not derived from 

Serious LOAELs. 

(10)		 Reference. The complete reference citation is given in Chapter 9 of the profile. 

(11)		 CEL. A CEL is the lowest exposure level associated with the onset of carcinogenesis in 

experimental or epidemiologic studies. CELs are always considered serious effects. The LSE 

tables and figures do not contain NOAELs for cancer, but the text may report doses not causing 

measurable cancer increases. 

(12)		 Footnotes. Explanations of abbreviations or reference notes for data in the LSE tables are found 

in the footnotes. Footnote "b" indicates that the NOAEL of 3 ppm in key number 18 was used to 

derive an MRL of 0.005 ppm. 

LEGEND 

See Sample Figure 3-1 (page B-7) 

LSE figures graphically illustrate the data presented in the corresponding LSE tables. Figures help the 

reader quickly compare health effects according to exposure concentrations for particular exposure 

periods. 

(13)		 Exposure Period. The same exposure periods appear as in the LSE table. In this example, health 

effects observed within the acute and intermediate exposure periods are illustrated. 

(14)		 Health Effect. These are the categories of health effects for which reliable quantitative data 

exists. The same health effects appear in the LSE table. 

(15)		 Levels of Exposure. Concentrations or doses for each health effect in the LSE tables are 

graphically displayed in the LSE figures. Exposure concentration or dose is measured on the log 

scale "y" axis. Inhalation exposure is reported in mg/m3

 or ppm and oral exposure is reported in 

mg/kg/day. 

(16)		 NOAEL. In this example, the open circle designated 18r identifies a NOAEL critical end point in 

the rat upon which an intermediate inhalation exposure MRL is based. The key number 18 

corresponds to the entry in the LSE table. The dashed descending arrow indicates the 

extrapolation from the exposure level of 3 ppm (see entry 18 in the table) to the MRL of 

0.005 ppm (see footnote "b" in the LSE table). 

(17)		 CEL. Key number 38m is one of three studies for which CELs were derived. The diamond 

symbol refers to a CEL for the test species-mouse. The number 38 corresponds to the entry in the 

LSE table. 
 

 

 

	 

	 

	 

 

 

	 

RADON	 B-5 

APPENDIX B 

(18)		 Estimated Upper-Bound Human Cancer Risk Levels. This is the range associated with the upperbound for lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. These risk levels are derived 

from the EPA's Human Health Assessment Group's upper-bound estimates of the slope of the 

cancer dose response curve at low dose levels (q1*). 

(19)		 Key to LSE Figure. The Key explains the abbreviations and symbols used in the figure. 
1 

2 3 4 12 

→

SAMPLE 

Table 3-1. Levels of Significant Exposure to [Chemical x] – Inhalation 

→→

Exposure 

Key to frequency/ figurea Species duration 

INTERMEDIATE EXPOSURE 

5 6 

Systemic ↓ ↓

NOAEL 

System (ppm) 

7 8 ↓ ↓

LOAEL (effect) Less serious (ppm) 9 

↓

Serious (ppm) 

Re

10 

↓

→→

18 Rat 13 wk Resp 3b 10 (hyperplasia) 

5 d/wk Nit6 hr/d 

CHRONIC EXPOSURE Cancer 11 

↓

38 Rat 18 mo 20 (CEL, multiple Wo

5 d/wk organs) 7 hr/d 

39 Rat 89–104 wk 10 (CEL, lung tumors, NT

5 d/wk nasal tumors) 6 hr/d 

40 Mouse 79–103 wk 10 (CEL, lung tumors, NT

5 d/wk hemangiosarcomas) 6 hr/d 

a The number corresponds to entries in Figure 3-1. b Used to derive an intermediate inhalation Minimal Risk Level (MRL) of 5x10-3 ppm; dose adjusted for intermittent ex

by an uncertainty factor of 100 (10 for extrapolation from animal to humans, 10 for human variability). 

RADON B-8
 

APPENDIX B 

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RADON C-1 

APPENDIX C. ACRONYMS, ABBREVIATIONS, AND SYMBOLS 

AARST American Association of Radon Scientists and Technologists 

ACGIH American Conference of Governmental Industrial Hygienists 

ACOEM American College of Occupational and Environmental Medicine 

ADI acceptable daily intake 

ADME absorption, distribution, metabolism, and excretion 

AED atomic emission detection 

AFID alkali flame ionization detector 

AFOSH Air Force Office of Safety and Health 

ALT alanine aminotransferase 

AML acute myeloid leukemia 

AOAC Association of Official Analytical Chemists 

AOEC Association of Occupational and Environmental Clinics 

AP alkaline phosphatase 

APHA American Public Health Association 

ASD active soil depressurization 

AST aspartate aminotransferase 

atm atmosphere 

ATSDR Agency for Toxic Substances and Disease Registry 

AWQC Ambient Water Quality Criteria 

BAT best available technology 

BCF bioconcentration factor 

BEI Biological Exposure Index 

BMD benchmark dose 

BMD/C benchmark dose or benchmark concentration 

BMDX dose that produces a X% change in response rate of an adverse effect 

BMDLX 95% lower confidence limit on the BMDX 

BMDS Benchmark Dose Software 

BSC Board of Scientific Counselors 

C centigrade 

CAA Clean Air Act 

CAG Cancer Assessment Group of the U.S. Environmental Protection Agency 

CAS Chemical Abstract Services 

CDC Centers for Disease Control and Prevention 

CEL cancer effect level 

CELDS Computer-Environmental Legislative Data System 

CERCLA Comprehensive Environmental Response, Compensation, and Liability Act 

CFR Code of Federal Regulations 

Ci curie 

CI confidence interval 

CL ceiling limit value 

CLP Contract Laboratory Program 

cm centimeter 

CML chronic myeloid leukemia 

CPSC Consumer Products Safety Commission 

CRM continuous radon monitor 

CWA Clean Water Act 

CWM continuous working level monitor 

DHEW Department of Health, Education, and Welfare 

DHHS Department of Health and Human Services 
 

 

 

 

 

 

 

 

 

 

 

 

RADON C-2 

APPENDIX C 

DNA deoxyribonucleic acid 

DOD Department of Defense 

DOE Department of Energy 

DOL Department of Labor 

DOT Department of Transportation 

DOT/UN/ Department of Transportation/United Nations/ 

NA/IMDG North America/Intergovernmental Maritime Dangerous Goods Code 

DWEL drinking water exposure level 

ECD electron capture detection 

ECG/EKG electrocardiogram 

EEG electroencephalogram 

EEGL Emergency Exposure Guidance Level 

EPA Environmental Protection Agency 

ERR excess relative risk 

F Fahrenheit 

F1 first-filial generation 

FAO Food and Agricultural Organization of the United Nations 

FDA Food and Drug Administration 

FEMA Federal Emergency Management Agency 

FIFRA Federal Insecticide, Fungicide, and Rodenticide Act 

FPD flame photometric detection 

fpm feet per minute 

FR Federal Register 

FSH follicle stimulating hormone 

g gram 

GC gas chromatography 

gd gestational day 

GLC gas liquid chromatography 

GPC gel permeation chromatography 

HPLC high-performance liquid chromatography 

HRGC high resolution gas chromatography 

HSDB Hazardous Substance Data Bank 

IARC International Agency for Research on Cancer 

IDLH immediately dangerous to life and health 

ILO International Labor Organization 

IRIS Integrated Risk Information System 

Kd adsorption ratio 

kg kilogram 

kkg metric ton 

Koc organic carbon partition coefficient 

Kow octanol-water partition coefficient 

L liter 

LC liquid chromatography 

LC50 lethal concentration, 50% kill 

LCLo lethal concentration, low 

LD50 lethal dose, 50% kill 

LDLo lethal dose, low 

LDH lactic dehydrogenase 

LH luteinizing hormone 

LOAEL lowest-observed-adverse-effect level 

LSE Levels of Significant Exposure 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON C-3 

APPENDIX C 

LT50 lethal time, 50% kill 

m meter 

MA trans,trans-muconic acid 

MAL maximum allowable level 

mCi millicurie 

MCL maximum contaminant level 

MCLG maximum contaminant level goal 

MF modifying factor 

MFO mixed function oxidase 

mg milligram 

mL milliliter 

mm millimeter 

mmHg millimeters of mercury 

mmol millimole 

mppcf millions of particles per cubic foot 

MRL Minimal Risk Level 

MS mass spectrometry 

NAAQS National Ambient Air Quality Standard 

NAS National Academy of Science 

NATICH National Air Toxics Information Clearinghouse 

NATO North Atlantic Treaty Organization 

NCE normochromatic erythrocytes 

NCEH National Center for Environmental Health 

NCI National Cancer Institute 

ND not detected 

NFPA National Fire Protection Association 

ng nanogram 

NHANES National Health and Nutrition Examination Survey 

NIEHS National Institute of Environmental Health Sciences 

NIOSH National Institute for Occupational Safety and Health 

NIOSHTIC NIOSH's Computerized Information Retrieval System 

NLM National Library of Medicine 

nm nanometer 

nmol nanomole 

NOAEL no-observed-adverse-effect level 

NOES National Occupational Exposure Survey 

NOHS National Occupational Hazard Survey 

NPD nitrogen phosphorus detection 

NPDES National Pollutant Discharge Elimination System 

NPL National Priorities List 

NR not reported 

NRC National Research Council 

NRPP National Radon Proficiency Program 

NRSB National Radon Safety Board 

NS not specified 

NSPS New Source Performance Standards 

NTIS National Technical Information Service 

NTP National Toxicology Program 

ODW Office of Drinking Water, EPA 

OERR Office of Emergency and Remedial Response, EPA 

OHM/TADS Oil and Hazardous Materials/Technical Assistance Data System 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON C-4 

APPENDIX C 

OPP Office of Pesticide Programs, EPA 

OPPT Office of Pollution Prevention and Toxics, EPA 

OPPTS Office of Prevention, Pesticides and Toxic Substances, EPA 

OR odds ratio 

OSHA Occupational Safety and Health Administration 

OSW Office of Solid Waste, EPA 

OTS Office of Toxic Substances 

OW Office of Water 

OWRS Office of Water Regulations and Standards, EPA 

PAH polycyclic aromatic hydrocarbon 

PBPD physiologically based pharmacodynamic 

PBPK physiologically based pharmacokinetic 

PCE polychromatic erythrocytes 

PEL permissible exposure limit 

pg picogram 

PHS Public Health Service 

PID photo ionization detector 

pmol picomole 

PMR proportionate mortality ratio 

ppb parts per billion 

ppm parts per million 

ppt parts per trillion 

PSNS pretreatment standards for new sources 

RADEP RAdon Dose Evaluation Program 

RBC red blood cell 

REL recommended exposure level/limit 

RfC reference concentration 

RfD reference dose 

RNA ribonucleic acid 

RQ reportable quantity 

RR relative risk 

RTECS Registry of Toxic Effects of Chemical Substances 

SARA Superfund Amendments and Reauthorization Act 

SCE sister chromatid exchange 

SGOT serum glutamic oxaloacetic transaminase 

SGPT serum glutamic pyruvic transaminase 

SIC standard industrial classification 

SIM selected ion monitoring 

SMCL secondary maximum contaminant level 

SMR standardized mortality ratio 

SNARL suggested no adverse response level 

SPEGL Short-Term Public Emergency Guidance Level 

STEL short term exposure limit 

STORET Storage and Retrieval 

TD50 toxic dose, 50% specific toxic effect 

TLV threshold limit value 

TOC total organic carbon 

TPQ threshold planning quantity 

TRI Toxics Release Inventory 

TSCA Toxic Substances Control Act 

TWA time-weighted average 
 

 

 

RADON C-5 

APPENDIX C 

UF uncertainty factor 

U.S. United States 

USDA United States Department of Agriculture 

USGS United States Geological Survey 

VOC volatile organic compound 

WBC white blood cell 

WHO World Health Organization 

> greater than 

≥ greater than or equal to 

= equal to 

< less than 

≤ less than or equal to 

% percent 

α alpha 

β beta 

γ gamma 

δ delta 

μm micrometer 

μg microgram q1

* cancer slope factor 

– negative 

+ positive 

(+) weakly positive result 

(–) weakly negative result 
RADON C-6
 

APPENDIX C 

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RADON D-1 

APPENDIX D
 

OVERVIEW OF BASIC RADIATION PHYSICS, CHEMISTRY, AND BIOLOGY 

Understanding the basic concepts in radiation physics, chemistry, and biology is important to the evaluation and 

interpretation of radiation-induced adverse health effects and to the derivation of radiation protection principles. 

This appendix presents a brief overview of the areas of radiation physics, chemistry, and biology and is based to a 

large extent on the reviews of Mettler and Moseley (1985), Hobbs and McClellan (1986), Eichholz (1982), Hendee 

(1973), Cember (1996, 2009), and Early et al. (1979). 

D.1 RADIONUCLIDES AND RADIOACTIVITY 

The substances we call elements are composed of atoms. Atoms in turn are made up of neutrons, protons and 

electrons: neutrons and protons in the nucleus and electrons in a cloud of orbits around the nucleus. Nuclide is the 

general term referring to any nucleus along with its orbital electrons. The nuclide is characterized by the 

composition of its nucleus and hence by the number of protons and neutrons in the nucleus. All atoms of an element 

have the same number of protons (this is given by the atomic number) but may have different numbers of neutrons 

(this is reflected by the atomic mass numbers or atomic weight of the element). Atoms with different atomic mass 

but the same atomic numbers are referred to as isotopes of an element. 

The numerical combination of protons and neutrons in most nuclides is such that the nucleus is quantum 

mechanically stable and the atom is said to be stable, i.e., not radioactive; however, if there are too few or too many 

neutrons, the nucleus is unstable and the atom is said to be radioactive. Unstable nuclides undergo radioactive 

transformation, a process in which a neutron or proton converts into the other and a beta particle is emitted, or else 

an alpha particle is emitted. Each type of decay is typically accompanied by the emission of gamma rays. These 

unstable atoms are called radionuclides; their emissions are called ionizing radiation; and the whole property is 

called radioactivity. Transformation or decay results in the formation of new nuclides some of which may 

themselves be radionuclides, while others are stable nuclides. This series of transformations is called the decay 

chain of the radionuclide. The first radionuclide in the chain is called the parent; the subsequent products of the 

transformation are called progeny, daughters, or decay products. 

In general there are two classifications of radioactivity and radionuclides: natural and artificial (man-made). 

Naturally-occurring radioactive material (NORM) exists in nature and no additional energy is necessary to place 

them in an unstable state. Natural radioactivity is the property of some naturally occurring, usually heavy elements, 

that are heavier than lead. Radionuclides, such as radium and uranium, primarily emit alpha particles. Some lighter 

elements such as carbon-14 and tritium (hydrogen-3) primarily emit beta particles as they transform to a more stable 

atom. Natural radioactive atoms heavier than lead cannot attain a stable nucleus heavier than lead. Everyone is 

exposed to background radiation from naturally-occurring radionuclides throughout life. This background radiation 

is the major source of radiation exposure to man and arises from several sources. The natural background exposures 

are frequently used as a standard of comparison for exposures to various artificial sources of ionizing radiation. 

Artificial radioactive atoms are produced either as a by-product of fission of uranium or plutonium atoms in a 

nuclear reactor or by bombarding atoms with particles (such as neutrons, protons, or heavy nuclei) at high velocity 

via a particle accelerator. Goals of these efforts can include producing medical isotopes or new elements. These 

artificially produced radioactive elements usually decay by emission of particles, such as alpha particles, positive or 

negative beta particles, and one or more high energy photons (gamma rays). Unstable (radioactive) atoms of any 

element can be produced. 

Both naturally occurring and artificial radioisotopes find application in medicine, industrial products, and consumer 

products. Some specific radioisotopes, called fall-out, are still found in the environment as a result of nuclear 

weapons use or testing, or nuclear power plant accidents (e.g., Three Mile Island Unit 2, Chernobyl, and Fukushima 

Dai-ichi). 
 

 

 

 

 

 

 

 

 

 

 

 

	 


 


 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 
 


 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON	 D-2 

APPENDIX D 

D.2 RADIOACTIVE DECAY 

D.2.1 Principles of Radioactive Decay 

The stability of an atom is the result of the balance of the forces of the various components of the nucleus. An atom 

that is unstable (a radionuclide) will release energy (decay) in various ways and transform to stable atoms or to 

intermediate radioactive species called progeny or daughters, often with the release of ionizing radiation. If there 

are either too many or too few neutrons for a given number of protons, the resulting nucleus may undergo 

transformation. For some elements, a chain of progeny decay products may be produced until stable atoms are 

formed. Radionuclides can be characterized by the type and energy of the radiation emitted, the rate of decay, and 

the mode of decay. The mode of decay indicates how a parent compound undergoes transformation. Radiations 

considered here are primarily of nuclear origin, i.e., they arise from nuclear excitation, usually caused by the capture 

of charged or uncharged nucleons by a nucleus, or by the radioactive decay or transformation of an unstable nuclide. 

The type of radiation may be categorized as charged or uncharged particles, protons, and fission products) or 

electromagnetic radiation (gamma rays and x rays). Table D-1 summarizes the basic characteristics of the more 

common types of radiation encountered. 

D.2.2 Half-Life and Activity 

For any given radionuclide, the rate of decay is a first-order process that is constant, regardless of the radioactive 

atoms present and is characteristic for each radionuclide. The process of decay is a series of random events; 

temperature, pressure, or chemical combinations do not affect the rate of decay. While it may not be possible to 

predict exactly which atom is going to undergo transformation at any given time, it is possible to predict, on 

average, the fraction of the radioactive atoms that will transform during any interval of time. 

The activity is a measure of the quantity of radioactive material. For these radioactive materials it is customary to 

describe the activity as the number of disintegrations (transformations) per unit time. The unit of activity is the curie 

(Ci), which was originally related to the activity of one gram of radium, but is now defined as the disintegration or 

transformation rate occurring in a quantity of radioactive material. The definition is: 

1 curie (Ci) = 3.7x1010 disintegrations (transformations)/second (dps) or
	

= 2.22x1012 disintegrations (transformations)/minute (dpm).
	

The SI unit of activity is the becquerel (Bq); 1 Bq = that quantity of radioactive material in which there is 

1 transformation/second. Since activity is proportional to the number of atoms of the radioactive material, the 

quantity of any radioactive material is usually expressed in curies, regardless of its purity or concentration. The 

transformation of radioactive nuclei is a random process, and the number of transformations is directly proportional 

to the number of radioactive atoms present. For any pure radioactive substance, the rate of decay is usually 

described by its radiological half-life, t1⁄2, i.e., the time it takes for a specified source material to decay to half its 

initial activity. The specific activity is an indirect measure of the rate of decay, and is defined as the activity per unit 

mass or per unit volume. The higher the specific activity of a radioisotope, the faster it is decaying. 

The activity of a radionuclide at time t may be calculated by: 

-0.693t/t1⁄2 A = Aoe , 

where A = the activity in dps or curies or becquerels, 

Ao = the activity at time zero, 

t = the time at which measured, and 

t1⁄2 = the radiological half-life of the radionuclide (t1⁄2 and t must be in the same units of time). 

The time when the activity of a sample of radioactivity becomes one-half its original value is the radioactive halflife and is expressed in any suitable unit of time. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON D-3 

APPENDIX D 

Table D-1. Characteristics of Nuclear Radiations 

Radiation 

Alpha (α) 

Negatron (β–

) 

Positron (β+

) 

Neutron 

Rest massa 

4.00 amu 

5.48x10-4 amu; 

0.51 MeV 

5.48x10-4 amu; 

0.51 MeV 

1.00866 amu; 

939.565 MeV 

Charge 

+2 

–1 

+1 

0 

Typical 

energy range 

4–10 MeV 

0–4 MeV 

0-4 MeV 

0–15 MeV 

Path lengthb 

Air Solid 

5–10 cm 25–80 μm 

0–10 m 0–1 cm 

0–10 m 0–1 cm 

b b 

Comments 

Identical to ionized 

He nucleus 

Identical to electron 

Identical to electron 

except for sign of 

charge 

Half life: 10.183 min 

X ray (e.m. photon) – 0 5 keV–100 keV b b Photon from 

transition of an 

electron between 

atomic orbits 

Gamma () 

(e.m. photon) 

– 0 10 keV–3 MeV b b Photon from nuclear 

transformation 

a The rest mass (in amu) has an energy equivalent in MeV that is obtained using the equation E=mc2

, where 1 amu = 932 MeV. b Path lengths are not applicable to x- and gamma rays since their intensities decrease exponentially; path lengths in solid tissue 

are variable, depending on particle energy, electron density of material, and other factors. 

amu = atomic mass unit; e.m. = electromagnetic; MeV = MegaElectron Volts 

The specific activity is a measure of activity, and is defined as the activity per unit mass or per unit volume. This 

activity is usually expressed in curies per gram and may be calculated by 

curies/gram = 1.3x108 / (t1⁄2) (atomic weight) or 

[3.577 x 105 x mass(g)] / [t1⁄2 x atomic weight] 

where t1⁄2 = the radiological half-life in days. 

In the case of radioactive materials contained in living organisms, an additional consideration is made for the 

reduction in observed activity due to regular processes of elimination of the respective chemical or biochemical 

substance from the organism. This introduces a rate constant called the biological half-life (tb) which is the time 

required for biological processes to eliminate one-half of the activity. This time is virtually the same for both stable 

and radioactive isotopes of any given element. 

Under such conditions the time required for a radioactive element to be halved as a result of the combined action of 

radioactive decay and biological elimination is the effective clearance half-time: 

teff = (tb x t1⁄2) / (tb + t1⁄2). 

Table D-2 presents representative effective half-lives of particular interest. 
 

 

 

 

 

 

 

 


 

 

 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON D-4 

APPENDIX D 

Table D-2. Half-Lives of Some Radionuclides in Adult Body Organs 

Half-lifea 

Radionuclide 

Uranium 238 

Hydrogen 3b 

(Tritium) 

Iodine 131 

Strontium 90 

Plutonium 239 

Cobalt 60 

Iron 55 

Iron 59 

Manganese 54 

Cesium 137 

Critical organ 

Kidney 

Whole body 

Thyroid 

Bone 

Bone surface 

Lung 

Whole body 

Spleen 

Spleen 

Liver 

Whole body 

Physical 

4,460,000,000 y 

12.3 y 

8 d 

28 y 

24,400 y 

24,400 y 

5.3 y 

2.7 y 

45.1 d 

303 d 

30 y 

Biological 

4 d 

10 d 

80 d 

50 y 

50 y 

500 d 

99.5 d 

600 d 

600 d 

25 d 

70 d 

Effective 

4 d 

10 d 

7.3 d 

18 y 

50 y 

500 d 

95 d 

388 d 

42 d 

23 d 

70 d 

a

d = days, y = years

b

Mixed in body water as tritiated water
	

D.2.3 Interaction of Radiation with Matter 

Both ionizing and nonionizing radiation will interact with materials; that is, radiation will lose kinetic energy to any 

solid, liquid or gas through which it passes by a variety of mechanisms. The transfer of energy to a medium by 

either electromagnetic or particulate radiation may be sufficient to cause formation of ions. This process is called 

ionization. Compared to other types of radiation that may be absorbed, such as radio waves or microwave radiation, 

ionizing radiation deposits a relatively large amount of energy into a small volume. 

The method by which incident radiation interacts with the medium to cause ionization may be direct or indirect. 

Electromagnetic radiations (x rays and gamma photons) and neutral particles (neutrons) are indirectly ionizing; that 

is, they give up their energy in various interactions with cellular molecules, and the energy is then utilized to 

produce a fast-moving charged particle such as an electron. It is the electron that then may react with and transfer 

energy to a target molecule. This particle is called a “primary ionizing particle. Charged particles, in contrast, strike 

the tissue or medium and directly react with target molecules, such as oxygen or water. These particulate radiations 

are directly ionizing radiations. Examples of directly ionizing particles include alpha and beta particles. Indirectly 

ionizing radiations are always more penetrating than directly ionizing particulate radiations. 

Mass, charge, and velocity of a particle, as well as the electron density of the material with which it interacts, all 

affect the rate at which ionization occurs. The higher the charge of the particle and the lower the velocity, the 

greater the propensity to cause ionization. Heavy, highly charged particles, such as alpha particles, lose energy 

rapidly with distance and, therefore, do not penetrate deeply. The result of these interaction processes is a gradual 

slowing down of any incident particle until it is brought to rest or "stopped" at the end of its range. 

D.2.4 Characteristics of Emitted Radiation 

D.2.4.1 Alpha Emission. In alpha emission, an alpha particle consisting of two protons and two neutrons is 

emitted with a resulting decrease in the atomic mass number by four and reduction of the atomic number of two, 

thereby changing the parent to a different element. The alpha particle is identical to a helium nucleus consisting of 

two neutrons and two protons. It results from the radioactive decay of some heavy elements such as uranium, 

plutonium, radium, thorium, and radon. All alpha particles emitted by a given radioisotope have the same energy. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON D-5 

APPENDIX D 

Most of the alpha particles that are likely to be found have energies in the range of about 4 to 8 MeV, depending on 

the isotope from which they came. 

The alpha particle has an electrical charge of +2. Because of this double positive charge and their size, alpha 

particles have great ionizing power and, thus, lose their kinetic energy quickly. This results in very little penetrating 

power. In fact, an alpha particle cannot penetrate a sheet of paper. The range of an alpha particle (the distance the 

charged particle travels from the point of origin to its resting point) is about 4 cm in air, which decreases 

considerably to a few micrometers in tissue. These properties cause alpha emitters to be hazardous only if there is 

internal contamination (i.e., if the radionuclide is inside the body). 

D.2.4.2 Beta Emission. A beta particle (β) is a high-velocity electron ejected from a disintegrating nucleus. 

The particle may be either a negatively charged electron, termed a negatron (β

) or a positively charged electron, 

termed a positron (β

). Although the precise definition of "beta emission" refers to both β and β, common usage 

of the term generally applies only to the negative particle, as distinguished from the positron emission, which refers 

to the β particle. 

D.2.4.2.1 Beta Negative Emission. Beta particle (β) emission is another process by which a radionuclide, 

with a neutron excess achieves stability. Beta particle emission decreases the number of neutrons by one and 

increases the number of protons by one, while the atomic mass number remains unchanged.1 This transformation 

results in the formation of a different element. The energy spectrum of beta particle emission ranges from a certain 

maximum down to zero with the mean energy of the spectrum being about one-third of the maximum. The range in 

tissue is much less. Beta negative emitting radionuclides can cause injury to the skin and superficial body tissues, 

but mostly present an internal contamination hazard. 

D.2.4.2.2 Positron Emission. In cases in which there are too many protons in the nucleus, positron 

emission may occur. In this case a proton may be thought of as being converted into a neutron, and a positron (β

) 

is emitted.1 This increases the number of neutrons by one, decreases the number of protons by one, and again leaves 

the atomic mass number unchanged. The gamma radiation resulting from the annihilation (see glossary) of the 

positron makes all positron emitting isotopes more of an external radiation hazard than pure β emitters of equal 

energy. 

D.2.4.2.3 Gamma Emission. Radioactive decay by alpha, beta, or positron emission, or electron capture 

often leaves some of the energy resulting from these changes in the nucleus. As a result, the nucleus is raised to an 

excited level. None of these excited nuclei can remain in this high-energy state. Nuclei release this energy returning 

to ground state or to the lowest possible stable energy level. The energy released is in the form of gamma radiation 

(high energy photons) and has an energy equal to the change in the energy state of the nucleus. Gamma and x rays 

behave similarly but differ in their origin; gamma emissions originate in the nucleus while x rays originate in the 

orbital electron structure or from rapidly changing the velocity of an electron (e.g., as occurs when shielding high 

energy beta particles or stopping the electron beam in an x ray tube). 

D.3 ESTIMATION OF ENERGY DEPOSITION IN HUMAN TISSUES 

Two forms of potential radiation exposures can result: internal and external. The term exposure denotes physical 

interaction of the radiation emitted from the radioactive material with cells and tissues of the human body. An 

exposure can be "acute" or "chronic" depending on how long an individual or organ is exposed to the radiation. 

Internal exposures occur when radionuclides, which have entered the body (e.g., through the inhalation, ingestion, or 

dermal pathways), undergo radioactive decay resulting in the deposition of energy to internal organs. External 

exposures occur when radiation enters the body directly from sources located outside the body, such as radiation 

emitters from radionuclides on ground surfaces, dissolved in water, or dispersed in the air. In general, external 

exposures are from material emitting gamma radiation, which readily penetrate the skin and internal organs. Beta 

and alpha radiation from external sources are far less penetrating and deposit their energy primarily on the skin's 

outer layer. Consequently, their contribution to the absorbed dose of the total body dose, compared to that deposited 

by gamma rays, may be negligible. 

1 Neutrinos accompany negative beta particle emissions; anti-neutrinos accompany positron emissions 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON D-6 

APPENDIX D 

Characterizing the radiation dose to persons as a result of exposure to radiation is a complex issue. It is difficult to: 

(1) measure internally the amount of energy actually transferred to an organic material and to correlate any observed 

effects with this energy deposition; and (2) account for and predict secondary processes, such as collision effects or 

biologically triggered effects, that are an indirect consequence of the primary interaction event. Radiation exposure 

(a measure of ionization density in air) is sometimes used as a surrogate for radiation dose in tissue from external 

radiation. Both exposure and dose are described below. 

D.3.1 Exposure (Roentgen). The roentgen (R) is a unit of x or gamma-ray exposure and is a measured by 

the amount of ionization caused in air by gamma or x radiation. One roentgen produces 2.58x10-4 coulomb per 

kilogram of air. In the case of gamma radiation, over the commonly encountered range of photon energy, the energy 

deposition in tissue for an exposure of 1 R is about 0.0096 joules (J)/kg of tissue. Exposure is only defined for x and 

gamma radiation ionization in air, and is often incorrectly interchanged with the term dose. 

D.3.2 Absorbed Dose (Gy, rad) and Absorbed Dose Rate (Gy/hr, rad/hr). The absorbed dose 

is defined as the energy absorbed from the incident radiation by a unit mass of the tissue or organ (dm). The 

differential equation for absorbed dose is: 

D = de/dm 

where: D = absorbed dose 

e = mean energy deposited 

m = mass in which the energy was deposited. 

The SI unit of absorbed dose in any medium is the J/kg with the special name of Gray (Gy), where 1 J/kg = 10,000 

ergs/gram = 1 Gy. In the historical system, 0.01 J/kg = 100 ergs/g = 1 rad, so 1 Gy = 100 rad.. For neutrons, the 

absorbed dose may be estimated using the similar metric, kinetic energy released in matter (kerma). Kerma is the 

sum of initial kinetic energies of all charged ionizing particles liberated in a unit mass. 

Absorbed dose is a measurable quantity, so there are primary national and international standards for its 

determination. In practice, absorbed dose is averaged over organ or tissue volumes. This allows the absorbed dose 

from both external and internal sources of radiation to be added. For low doses, the acceptance of the linear no 

threshold (LNT) theory allows the correlation of dose with degree of adverse deterministic health effects. Radiation 

that does not penetrate tissue well (low energy x-rays, beta particles, and alpha particles) can produce a nonuniform 

distribution of absorbed dose resulting in differential health effects across an organ or tissue. An example is using 

shielding in radiation therapy so that a kidney tumor receives a lethal dose while sparing as much health tissue as 

practical, thus maximizing the remaining kidney function. 

Internal and external absorbed doses delivered by radiation sources are not usually instantaneous but are distributed 

over extended periods of time. The resulting rate of change of the absorbed dose to a small volume of mass is 

referred to as the absorbed dose rate, which has units of Gy/unit time or rad/unit time. 

As a rough conversion, an exposure of 1 R in air results in an absorbed dose to soft tissue of approximately 0.01 

J/kg. 

See text below on other units of measure. 

D.4 UNITS IN RADIATION PROTECTION AND REGULATION 

D.4.1 Equivalent Dose (or Dose Equivalent) 

Equivalent dose (international term) and dose equivalent (US term)are a radiation protection quantity used for 

setting limits that help ensure that deterministic effects (e.g. damage to a particular tissue) are kept within acceptable 

levels. The SI unit of equivalent dose is the J/kg, has the special name of Sievert (Sv) or rem, and is abbreviated HT. 

It is a special radiation protection quantity that is used, for administrative and radiation safety purposes only, to 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON D-7 

APPENDIX D 

express the absorbed dose in a manner which considers the difference in biological effectiveness of various kinds of 

ionizing radiation. The equivalent dose concept is applicable only to doses that are not great enough to produce 

biomedical effects. 

The equivalent dose in an organ or tissue (HT) is determined by multiplying the absorbed dose by a radiation 

weighting factor and any modifying factors at the location of interest. The absorbed dose in an organ or tissue from 

radiation of type R (DT,R) is a measurable or estimable quantity, while the radiation weighting factor (ωR) for each 

primary radiation type (ωR) has been studied and recommendations made for their values. The formula for 

calculating equivalent dose is: 

HT = or 

Where = radiation weighting factor, 

= absorbed dose to tissue T from radiation type R, and 

= quality factor. 

The radiation weighting factor (ω) or quality factor (Q) is a dimensionless quantity that depends in part on the 

stopping power for charged particles, and it accounts for the differences in biological effectiveness found among the 

types of radiation. Originally, relative biological effectiveness (RBE) was used rather than ω or Q to define the 

quantity, rem, which is of use in risk assessment. The NRC and DOE in the US, and the ICRU and ICRP in most of 

the remaining international community havepublished values for quality factors and radiation weighting factors 

provided in Tables D-3 and D-4. 

The equivalent dose rate (or dose equivalent rate in the US) is the time rate of change of the equivalent dose (or dose 

equivalent) to organs and tissues and is expressed as Sv/unit time (or rem/unit time). 

Table D-3. Recommended Values of Quality Factors and Radiation Weighting Factors 

Type of Radiation Quality Factor Radiation Weighting Factor (wR) 

(NRC 2011) (ICRP 2007) 

Photons (x and γ rays) 1 1 

Electrons 

1 

Electrons and muons 

1 

High energy protons 10 

Protons and charged pions 2 

Alpha particles, multiple-charged 

particles, fission fragments and heavy 20 

particles of unknown charge 

Alpha particles, fission fragments, 

heavy ions 20 

Neutrons of unknown energy 10 

Neutrons of known energy See Table D-4 A continuous function 

of neutron energy 

(range 2.4-21; see equation) 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

 
 


 


 

 
 


 

RADON D-8
 

APPENDIX D
 

Source:
	

USNRC. 2011. Standards for the protection against radiation, tables 1004(b).1 and 1004(b).2. 10 CFR 20.1004. U.S. Nuclear
	

Regulatory Commission, Washington, D.C.
	

ICRP
	

Radiation weighting factors for neutrons are based on particle energy according to the following formulas (ICRP
	

2007):
	

ωR = 

Table D-4 Mean Quality Factors, Q, and Fluence per Unit Dose Equivalent for Monoenergetic 

Neutrons 

Neutron energy (MeV) Quality factora(Q) Fluence per unit dose equivalentb(neutrons cm−2rem−1) 

(thermal) 2.5×10−8 2 980×106 

1×10−7 2 980×106 

1×10−6 2 810×106 

1×10−5 2 810×106 

1×10−4 2 840×106 

1×10−3 2 980×106 

1×10−2 2.5 1010×106 

1×10−1 7.5 170×106 

5×10−1 11 39×106 

1 11 27×106 

2.5 9 29×106 

5 8 23×106 

7 7 24×106 

10 6.5 24×106 

14 7.5 17×106 

20 8 16×106 

40 7 14×106 

60 5.5 16×106 

1×102 4 20×106 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 


 


 

	 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

	 

 

 

 

 

 

RADON D-9
 

APPENDIX D
 

2×102 3.5 19×106 

3×102 3.5 16×106 

4×102 3.5 14×106 

D.4.2 Relative Biological Effectiveness 

RBE is used to denote the experimentally determined ratio of the absorbed dose from one radiation type to the 

absorbed dose of a reference radiation required to produce an identical biological effect under the same conditions. 

Gamma rays from cobalt-60, cesium-137, and 200–250 keV x-rays have been used as reference standards. The term 

RBE has been widely used in experimental radiobiology, and the term radiation weighting factor used in 

calculations of dose equivalent for radiation safety purposes (ICRP 2007; NCRP 1971; UNSCEAR 1982). RBE 

applies only to a specific biological end point, in a specific exposure, under specific conditions to a specific species. 

There are no generally accepted values of RBE. 

D.4.3 Effective Dose or Effective Dose Equivalent 

In an attempt to compare stochastic (e.g., cancer) detriment from absorbed dose of radiation in a limited portion of 

the body with the detriment from total body dose, the ICRP (1977) derived a concept of effective dose equivalent. 

ICRP changed this term to effective dose in 1990 (ICRP 1990) and reintroduced the term “effective dose equivalent” 

in 2007 (ICRP 2007). The term “effective dose equivalent” allows for the addition or direct comparison of cancer 

and genetic risk from various partial or whole body doses. In the U.S., the term “effective dose equivalent” is 

presently used by the NRC (NRC 2011) and DOE. 

The effective dose (or effective dose equivalent) approach was developed to overcome limitations in using absorbed 

dose as a metric of the stochastic impact of ionizing radiation. The absorbed dose is usually defined as the mean 

absorbed dose within an organ or tissue. This represents a simplification of the actual problem. Normally when an 

individual ingests or inhales a radionuclide or is exposed to external radiation that enters the body (gamma), the dose 

is not uniform throughout the whole body. 

The simplifying assumption is that the detriment will be the same whether the body is uniformly or non-uniformly 

irradiated. This required the development of a tissue weighting factor, which represents the estimated proportion of 

the stochastic risk resulting from tissue, T, to the stochastic risk when the whole body is uniformly irradiated for 

occupational exposures under certain conditions (ICRP 1977). 

The effective dose (or effective dose equivalent) (HE) is weighted for both the type of radiation (R) and the type of 

tissue (T), and has the formula: 

HE = , 

where		 HE = the effective dose (or effective dose equivalent) in tissue T, 

ωT = the tissue weighting factor in tissue T, 

HT = the equivalent dose (or dose equivalent dose), 

ωR = the radiation weighting factor, and 

DT,R = the absorbed dose from radiation R to tissue T. 

Tissue weighting factors for selected tissues are listed in Table D-5. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON D-10 

APPENDIX D 

Table D-5. Tissue Weighting Factors for Calculating Effective Dose (or Effective Dose 

Equivalent) for Selected Tissues 

Tissue Weighting factor 

NRC (2011) NCRP115 ICRP103 Tissue /ICRP26 and ICRP60 

Bladder 0.05 0.04 

Bone marrow (red) 0.12 0.12 0.12 

Bone surface 0.03 0.01 0.01 

Brain 0.01 

Breast 0.15 0.05 0.12 

Colon – 0.12 0.12 

Esophagus – 0.05 0.04 

Gonads 0.25 0.20 0.08 

Liver – 0.05 0.04 

Lung 0.12 0.12 0.12 

Salivary glands 0.01 

Skin – 0.01 0.01 

Stomach – 0.12 0.12 

Thyroid 0.03 0.05 0.04 

Subtotal 0.70 0.95 0.88 

Remainder 0.30 0.05 0.12a 

Total 1.00 1.00 1.00 

ICRP60 = International Commission on Radiological Protection, 1990 Recommendations of the ICRP 

NCRP115 = National Council on Radiation Protection and Measurements. 1993. Risk Estimates for 

Radiation Protection, Report 115. Bethesda, Maryland 

NRC = Nuclear Regulatory Commission, Title 10, Code of Federal Regulations, Part 20 

a

ICRP Publication 103 remainder tissues include adrenals, extrathoracic (ET) region, gall bladder, 

heart, kidneys, lymphatic nodes, muscle, oral mucosa, pancreas, prostate, small intestine, spleen, 

thymus, uterus/cervix 

The ICRU (1980), ICRP (1984), and NCRP (1985) recommended that the terms rad, roentgen, curie, and 

rem be replaced by the SI units: gray (Gy), Coulomb per kilogram (C/kg), Becquerel (Bq), and sievert (Sv), 

respectively. The relationship between the historical units and the international system of units (SI) for 

radiological quantities is shown in Table D-6. 

Table D-6. Comparison of Common and SI Units for Radiation Quantities 

Quantity 

(Abbreviation) 

Historical 

Unit Historical 

Definition 

SI unit SI 

Definition 

Activity (A) curie (Ci) 3.7x1010 

transformations s-1 

becquerel (Bq) s

-1 

Absorbed dose (D) rad (rad) 10-2 Jkg-1 gray (Gy) Jkg-1 

Absorbed dose rate 

(Ď) rad per second 

(rad s-1) 

10-2 Jkg-1s

-1 gray per second 

(Gy s-1) 

Jkg-1 s

-1 

Equivalent Dose 

(or Dose rem 10-2 Jkg-1 sievert (Sv) Jkg-1 

equivalent) (HT) 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON D-11 

APPENDIX D 

Equivalent Dose -1 -1 rem per second 10-2 Jkg-1s sievert per second Jkg-1 s Rate (or Dose (rem s-1) (Sv s-1) equivalent rate) 

Effective dose (or rem 10-2 Jkg-1 sievert (Sv) Jkg-1 

Effective Dose 

Equivalent) (HE) 

Linear energy kiloelectron 1.602x10-10 Jm-1 kiloelectron volts per 1.602x10-10 Jm-1 

transfer (LET) volts per micrometer (keV μmmicrometer (keV 1

) 

μm-1) 

Jkg-1 = Joules per kilogram; Jkg-1s

-1 = Joules per kilogram per second; Jm-1 = Joules per meter; s-1 = per second 

D.4.4 Working Levels and Working Level Months (for Radon Dosimetry). Working level 

(WL) is a measure of the atmospheric concentration of radon and its short-lived progeny. One WL is defined as any 

combination of short-lived radon progeny (through polonium-214 [214Po]), per liter of air, that will result in the 

emission of 1.3x105 MeV of alpha energy. An activity concentration of 100 pCi 222Rn/L of air, in equilibrium with 

its progeny, corresponds approximately to a potential alpha-energy concentration of 1 WL. The WL unit can also be 

used for thoron or 220Rn. In this case, 1.3x105 MeV of alpha energy (1 WL) is released by 7.5 pCi 220Rn/L in 

equilibrium with its progeny. The potential alpha energy exposure of miners is commonly expressed in the unit 

Working Level Month (WLM). One WLM corresponds to inhalinga concentration of 1 WL for the reference period 

of 170 hours, or more generally 

WLM = concentration (WL) x exposure time (months) / (one “month” = 170 working hours). 

D.5 Dosimetry Models 

Dosimetry models are used to estimate the dose from internally deposited radioactive substances. The models for 

internal dosimetry consider the amount of radionuclides entering the body, the factors affecting their movement or 

transport through the body, distribution and retention of radionuclides in the body, and the energy deposited in 

organs and tissues from the radiation that is emitted during spontaneous decay processes. The dose pattern for 

radioactive materials in the body may be strongly influenced by the route of entry of the material. For industrial 

workers, inhalation of radioactive particles with pulmonary deposition and puncture wounds with subcutaneous 

deposition have been the most frequent. The general population has been exposed via ingestion, inhalation, and 

external exposure to low levels of naturally occurring radionuclides as well as artificial radionuclides used in nuclear 

medicine procedures and released from isotope generation facilities, nuclear weapons testing, and nuclear reactor 

operations and accidents. 

The models for external dosimetry consider only the photon doses (and neutron doses, where applicable) to organs 

of individuals who are immersed in air or are exposed to a contaminated object. 

D.5.1 Ingestion. Ingestion of radioactive materials is most likely to occur from eating food or drinking water 

containing naturally occurring radioactive material and possibly also contaminated with artificial radionuclides. 

Also, a portion of inhaled radionuclides initially deposited in the lung will relocate to the throat and be swallowed. 

Ingestion of a sufficient amount of radioactive material may result in toxic effects as a result of either absorption of 

the radionuclide or irradiation of the gastrointestinal tract during passage through the tract, or a combination of both. 

The fraction of a radioactive material absorbed from the gastrointestinal tract is variable, depending on the specific 

element, the physical and chemical form of the material ingested, and the diet, as well as some other metabolic and 

physiological factors. The absorption of some elements is influenced by age, usually with higher absorption in the 

very young. 

D.5.2 Inhalation. The nose and mouth have long been recognized as being a major portal of entry for both 

nonradioactive and radioactive materials. The deposition of particles within the lung is largely dependent upon the 

size and shape of the particles being inhaled (sometimes termed the atmospheric mean aerodynamic diameter or 

AMAD). After a particle is deposited, its retention will depend upon the physical and chemical properties of the 

dust and the physiological status of the lung. The retention of the particle in the lung depends on the location of 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON D-12 

APPENDIX D 

deposition, in addition to the physical and chemical properties of the particles. The converse of pulmonary retention 

is pulmonary clearance. There are three distinct mechanisms of clearance which operate simultaneously. Ciliary 

clearance acts only in the upper respiratory tract. The second and third mechanisms act mainly in the deep 

respiratory tract. These are phagocytosis and absorption. Phagocytosis is the engulfing of foreign bodies by 

alveolar macrophages and their subsequent removal either up the ciliary "escalator" or by entrance into the 

lymphatic system. Some inhaled soluble particles are absorbed into the blood and translocated to other organs and 

tissues. 

D.5.3 Internal Emitters 

An internal emitter is a radionuclide that is inside the body. The absorbed dose from internally deposited 

radioisotopes depends on the energy absorbed per unit tissue by the irradiated tissue. For a radioisotope distributed 

uniformly throughout an infinitely large medium, the concentration of absorbed energy must be equal to the 

concentration of energy emitted by the isotope. An infinitely large medium may be approximated by a tissue mass 

whose dimensions exceed the range of the particle. All alpha and most beta radiation will be absorbed in the organ 

(or tissue) of reference. Gamma-emitting isotope emissions are penetrating radiation, and a substantial fraction of 

gamma energy may not be absorbed in tissue. The dose to an organ or tissue is a function of the effective retention 

half-time, the energy released in the tissue, the amount of radioactivity initially introduced, and the mass of the 

organ or tissue. 

D.6 BIOLOGICAL EFFECTS OF RADIATION 

When biological material is exposed to ionizing radiation, a chain of cellular events occurs as the ionizing particle 

passes through the biological material. A number of theories have been proposed to describe the interaction of 

radiation with biologically important molecules in cells and to explain the resulting damage to biological systems 

from those interactions. Many factors may modify the response of a living organism to a given dose of radiation. 

Factors related to the exposure include the dose rate, the energy of the radiation, and the temporal pattern of the 

exposure (e.g., protracted or fractionated exposures). Biological considerations include factors such as species, age, 

sex, and the portion of the body exposed. Several excellent reviews of the biological effects of radiation have been 

published, and the reader is referred to these for a more in-depth discussion (Brodsky 1996; Klaassen 2001; Hobbs 

and McClellan 1986; ICRP 1984; Mettler and Moseley 1985; Rubin and Casarett 1968). 

D.6.1 Radiation Effects at the Cellular Level 

breaks in DNA may be produced. These single strand breaks may be repaired rapidly. With doses in the range of 

0.5-5 Gy (50–500 rad), irreparable double-stranded DNA breaks are likely, resulting in cellular reproductive death 

after one or more divisions of the irradiated parent cell. At large doses of radiation, usually greater than 5 Gy (500 

rad), direct cell death before division (interphase death) may occur from the direct interaction of free-radicals with 

essentially cellular macromolecules. Morphological changes at the cellular level, the severity of which are dosedependent, may also be observed. 

The sensitivity of various cell types varies. According to the Bergonie-Tribondeau law, the sensitivity of cell lines 

is directly proportional to their mitotic rate and inversely proportional to the degree of differentiation (Mettler and 

Moseley 1985). Rubin and Casarett (1968) devised a classification system that categorized cells according to type, 

function, and mitotic activity. The categories range from the most sensitive type, "vegetative intermitotic cells," 

found in the stem cells of the bone marrow and the gastrointestinal tract, to the least sensitive cell type, "fixed 

postmitotic cells," found in striated muscles or long-lived neural tissues. 

Cellular changes may result in cell death, which if extensive, may produce irreversible damage to an organ or tissue 

or may result in the death of the individual. If the cell recovers, altered metabolism and function may still occur, 

which may be repaired or may result in the manifestation of clinical symptoms. These changes may also be 

expressed at a later time as tumors, cellular mutations, or transformed tissue (scar tissue) which may result in 

abnormal tissue or compromised function. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

RADON D-13 

APPENDIX D 

D.6.2 Radiation Effects at the Organ Level 

In most organs and tissues the injury and the underlying mechanism for that injury are complex and may involve a 

combination of events. The extent and severity of this tissue injury are dependent upon the radiosensitivity of the 

various cell types in that organ system. Rubin and Casarett (1968) describe and schematically display the events 

following radiation in several organ system types. These include: a rapid renewal system, such as the 

gastrointestinal mucosa; a slow renewal system, such as the pulmonary epithelium; and a nonrenewal system, such 

as neural or muscle tissue. In the rapid renewal system, organ injury results from the direct destruction of highly 

radiosensitive cells, such as the stem cells in the bone marrow. Injury may also result from constriction of the 

microcirculation and from edema and inflammation of the basement membrane, designated as the histohematic 

barrier (HHB), which may progress to fibrosis. In slow renewal and nonrenewal systems, the radiation may have 

little effect on the parenchymal cells, but ultimate parenchymal atrophy and death over several months result from 

HHB fibrosis and occlusion of the microcirculation. 

D.6.3 Low Level Radiation Effects 

Cancer is the major latent harmful effect produced by ionizing radiation and the one that most people exposed to 

radiation are concerned about. The ability of alpha, beta, and gamma radiation to produce cancer in virtually every 

tissue and organ in laboratory animals has been well-demonstrated, while radiogenic cancer has not been observed 

in some human tissues and organs. The development of cancer is not an immediate effect. In humans, radiationinduced leukemia has the shortest latent period at 2 years, thyroid cancer after Chernobyl showed up in children 

about four years after the accident, while other radiation induced cancers have latent periods >20 years. For the nonradiogenic cancers, it has been hypothesized either that repair mechanisms effectively protect the individual or that 

the latency period exceeds the current human life span (Raabe 2010). The mechanism by which cancer is induced in 

living cells is complex and is a topic of intense study. Exposure to ionizing radiation can produce cancer; however, 

some sites appear to be more common than others, such as the breast, lung, stomach, and thyroid. 

DNA is a major target molecule during exposure to ionizing radiation. Other macromolecules, such as lipids and 

proteins, are also at risk of damage when exposed to ionizing radiation. The genotoxicity of ionizing radiation is an 

area of intense study, as damage to the DNA is ultimately responsible for many of the adverse toxicological effects 

ascribed to ionizing radiation, including cancer. Damage to genetic material is basic to developmental or teratogenic 

effects, as well. 

There is limited evidence of non-cancer human effects at low radiation doses. Non-cancer effects that have been 

reported are associated with the Japanese atomic bomb survivor population and include neurological and 

cardiovascular effects. Neurological effects were observed in fetuses exposed to prompt radiation during the 

detonations while they were in gestation weeks 8–15, less so for weeks 16–25, and were not observed for other 

developmental time frames. Cardiovascular effects have been reported for atomic bomb survivors following 

60 years of follow-up. These include a statistically significant increase in heart disease (% elevated relative risk per 

Gy with 95% confidence interval = 14 [6–23] %/Gy, p<0.001) and a non-statistically significant increase in stroke 

(9 [1–17]%/Gy, p=0.02) above a dose of 0.5 Gy. These radiation-induced circulatory effects may be increased by 

other factors such as smoking, microvascular damage in the kidney and associated hypertension, high serum 

cholerterol, diabetes, and infection. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 
 

 
 

 
 

 
 

 
 

 
 

 
 

 

 
 

 
 

 
 

 
 

 
 

 
 

 

 

 

RADON D-14 

APPENDIX D 

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APPENDIX D 

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APPENDIX D 

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Sources and biological effects. New York: United Nations. 

UNSCEAR. 1986. United Nations Scientific Committee on the Effects of Atomic Radiation. Genetic and somatic 

effects of ionizing radiation. New York: United Nations. 

UNSCEAR. 1988. United Nations Scientific Committee on the Effects of Atomic Radiation. Sources, effects and 

risks of ionization radiation. New York: United Nations. 

UNSCEAR. 1993. United Nations Scientific Committee on the Effects of Atomic Radiation. Sources and effects 

of ionizing radiation. New York: United Nations. 

USNRC. 2011a. Title 10, Code of Federal Regulations Part 20.1003, U.S. Nuclear Regulatory Commission, 

Washington, DC. http://ecfr.gpoaccess.gov/cgi/t/text/textidx?c=ecfr&sid=a0927f5dead51eb92d3892fad0f1ac42&rgn=div8&view=text&node=10:1.0.1.1.16.1.76.3&idno=10. 

(December 9, 2011) 

USNRC. 2011. Title 10 Code of Federal Regulations Part 20, Table 1004(b).1. U.S. Nuclear Regulatory 

Commission, Washington, D.C. http://ecfr.gpoaccess.gov/cgi/t/text/textidx?c=ecfr&sid=a0927f5dead51eb92d3892fad0f1ac42&rgn=div8&view=text&node=10:1.0.1.1.16.1.76.4&idno=10. 

(December 9, 2011) 
 

 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

RADON E-1 

APPENDIX E. INDEX 

absorbed dose.............................................................................................................................................. 91 

adenocarcinoma .......................................................................................................................................... 37 

adipose tissue .................................................................................................................................. 56, 58, 59
	

adsorbed............................................................................................................................................ 119, 150
	

adsorption.......................................................................................................................................... 150, 151
	

ambient air ................................................................................................ 115, 121, 122, 128, 129, 130, 144
	

bioaccumulation........................................................................................................................................ 144 

biokinetics..................................................................................................................... 56, 58, 59, 63, 64, 82
	

biomarkers..................................................................................................................... 91, 92, 103, 147, 158
	

body weight effects..................................................................................................................................... 32 

breast milk................................................................................................................................................. 141 

cancer................................................. 5, 9, 10, 11, 12, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 

32, 35, 36, 37, 38, 39, 41, 42, 43, 44, 50, 77, 84, 87, 88, 90, 92, 

93, 94, 95, 96, 97, 100, 101, 102, 103, 104, 117, 139, 159, 161
	

carcinogen............................................................................................................. 10, 20, 23, 28, 31, 44, 164
	

carcinogenic ............................................................................................................................ 19, 39, 87, 164
	

carcinoma .................................................................................................................................................... 37 

cardiovascular ................................................................................................................................. 32, 33, 43
	

cardiovascular effects.................................................................................................................................. 33 

chromosomal aberrations.......................................................................................................... 45, 48, 49, 93
	

clearance ..................................................... 18, 50, 51, 53, 54, 63, 64, 66, 69, 71, 72, 73, 75, 77, 79, 84, 94
	

death.......................................................................................................... 10, 18, 19, 23, 32, 33, 39, 94, 100
	

developmental effects ..................................................................................................... 35, 42, 43, 102, 105
	

DNA................................................................................................................ 45, 46, 48, 85, 87, 91, 96, 104 

endocrine......................................................................................................................................... 43, 88, 89
	

fetus............................................................................................................................................................. 89 

general population............................................................................................................................. 137, 159
	

genotoxic......................................................................................................................................... 19, 45, 93
	

genotoxicity............................................................................................................................. 45, 49, 93, 101
	

groundwater .................. 3, 4, 9, 116, 117, 118, 121, 122, 123, 125, 126, 127, 130, 133, 134, 135, 138, 142
	

half-life...................................................... 2, 15, 18, 50, 71, 82, 91, 116, 122, 130, 145, 147, 149, 152, 153
	

hematological effects .................................................................................................................................. 33 

immune system ......................................................................................................................................... 102 

immunological ...................................................................................................................................... 18, 34
	

immunological effects................................................................................................................................. 34 

leukemia.......................................................................................................................... 22, 38, 77, 101, 102
	

lymphatic .................................................................................................................................................... 65 

metabolic effects ......................................................................................................................................... 43 

micronuclei ..................................................................................................................................... 45, 48, 93
	

mucociliary ............................................................................................................................... 51, 53, 72, 94
	

neurobehavioral........................................................................................................................................... 89 

neurological effects......................................................................................................................... 34, 42, 43
	

nuclear............................................................................................................. 1, 38, 116, 140, 148, 151, 154 

ocular effects......................................................................................................................................... 34, 43
	

odds ratio............................................................................................................................. 26, 27, 29, 87, 96
	

partition coefficients ............................................................................................... 56, 57, 58, 64, 77, 79, 82
	

pharmacodynamic ....................................................................................................................................... 60 

pharmacokinetic.................................................................................................................. 60, 61, 62, 84, 90
	
 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

RADON E-2 

APPENDIX E 

pulmonary fibrosis ...................................................................................................................... 32, 101, 102
	

rate constant .............................................................................................................................. 52, 54, 56, 79
	

renal effects........................................................................................................................................... 33, 34
	

reproductive effects........................................................................................................... 34, 35, 42, 43, 102
	

respiratory effects............................................................................................................................ 32, 33, 96
	

retention ...................................................................................................................... 60, 69, 71, 72, 82, 111
	

sequestered.................................................................................................................................................. 75 

solubility ..................................................................................... 51, 53, 54, 56, 57, 58, 65, 69, 84, 122, 130
	

systemic effects............................................................................................................................... 32, 42, 43
	

thyroid......................................................................................................................................................... 77 

toxicokinetic.................................................................................................................. 15, 50, 102, 103, 104
	

tumors ........................................................................................................... 12, 22, 42, 88, 94, 95, 104, 117 

volatility.................................................................................................................................................... 131 

volatilization ............................................................................................................................................. 125