TOXICOLOGICAL PROFILE FOR 

STRONTIUM 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES 

Public Health Service 

Agency for Toxic Substances and Disease Registry
 

April 2004 
STRONTIUM ii 

DISCLAIMER 

The use of company or product name(s) is for identification only and does not imply endorsement by the 

Agency for Toxic Substances and Disease Registry. 
STRONTIUM iii 

UPDATE STATEMENT 

A Toxicological Profile for strontium, Draft for Public Comment was released in July 2001. 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/Toxicology Information Branch 

1600 Clifton Road NE, 

Mailstop F-32 

Atlanta, Georgia 30333 


vi 

Background Information 

The toxicological profiles are developed by ATSDR pursuant to Section 104(i) (3) and (5) of the 

Comprehensive Environmental Response, Compensation, and Liability Act of 1980 (CERCLA or 

Superfund) for hazardous substances found at Department of Energy (DOE) waste sites. CERCLA 

directs ATSDR to prepare toxicological profiles for hazardous substances most commonly found at 

facilities on the CERCLA National Priorities List (NPL) and that pose the most significant potential threat 

to human health, as determined by ATSDR and the EPA. ATSDR and DOE entered into a Memorandum 

of Understanding on November 4, 1992 which provided that ATSDR would prepare toxicological profiles 

for hazardous substances based upon ATSDR=s or DOE=s identification of need. The current ATSDR 

priority list of hazardous substances at DOE NPL sites was announced in the Federal Register on July 24, 

1996 (61 FR 38451). 
STRONTIUM 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 3.9 Biomarkers of Exposure and Effect 

Section 3.12 Methods for Reducing Toxic Effects 

ATSDR Information Center 

Phone: 1-888-42-ATSDR or (404) 498-0110 Fax: (770) 488-4178 

E-mail: atsdric@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. 
STRONTIUM 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: 800-356-4674 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/. 
STRONTIUM ix 

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 

environmental medicine. Contact: ACOEM, 55 West Seegers Road, Arlington Heights, IL 

60005 • Phone: 847-818-1800 • FAX: 847-818-9266. 

STRONTIUM xi 

CONTRIBUTORS 

CHEMICAL MANAGER(S)/AUTHOR(S): 

Alfred F. Dorsey, D.V.M 

ATSDR, Division of Toxicology, Atlanta, GA 

Margaret E. Fransen, Ph.D. 

Syracuse Research Corporation, North Syracuse, NY 

Gary L. Diamond, Ph.D. 

Syracuse Research Corporation, North Syracuse, NY 

Richard J. Amata, Ph.D. 

Syracuse Research Corporation, 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 Research Implementation Branch reviews data needs sections to assure 

consistency across profiles and adherence to instructions in the Guidance. 

STRONTIUM xiii 

PEER REVIEW 

A peer review panel was assembled for strontium. The panel consisted of the following members: 

1.	 Adele L. Boskey, Ph.D., Professor of Biochemistry, Starr Chair in Mineralized Tissues, Hospital for 

Special Surgery, Weill Medical College of Cornell University, New York, New York, 

2.	 Marvin Goldman, Ph.D., Emeritus Professor of Radiation Biology, Department of Surgical and 

Radiological Sciences, University of California, Davis, California, 

3.	 Richard Leggett, Ph.D., Life Sciences Division, Oak Ridge National Laboratory, Knoxville, 

Tennessee, and 

4.	 Bruce Muggenburg, D.V.M., Ph.D., Senior Scientist and Veterinary Physiologist, Toxicology 

Division, Lovelace Respiratory Research Institute, Albuquerque, New Mexico. 

These experts collectively have knowledge of strontium'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. A list of databases reviewed and 

a list of unpublished documents cited are also included in the administrative record. 

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. 

STRONTIUM 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 STRONTIUM?...........................................................................................................1 

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

1.3 HOW MIGHT I BE EXPOSED TO STRONTIUM?..................................................................4 

1.4 HOW CAN STRONTIUM ENTER AND LEAVE MY BODY?...............................................5 

1.5 HOW CAN STRONTIUM AFFECT MY HEALTH? ................................................................6 

1.6 HOW CAN STRONTIUM AFFECT CHILDREN? ...................................................................8 

1.7 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO STRONTIUM? ...............9 

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

TO STRONTIUM? ...................................................................................................................10 

1.9 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH? ..............................................................................................11 

1.10 WHERE CAN I GET MORE INFORMATION? .....................................................................12 

2. RELEVANCE TO PUBLIC HEALTH .................................................................................................15 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO STRONTIUM IN THE 

UNITED STATES....................................................................................................................15 

2.2 SUMMARY OF HEALTH EFFECTS......................................................................................16 

2.3 MINIMAL RISK LEVELS .......................................................................................................23 

3. HEALTH EFFECTS..............................................................................................................................27 

3.1 INTRODUCTION.....................................................................................................................27 

3.2 DISCUSSION OF HEALTH EFFECTS OF STABLE STRONTIUM BY ROUTE OF 

EXPOSURE..............................................................................................................................31 

3.2.1 Inhalation Exposure ..........................................................................................................33 

3.2.1.1 Death ........................................................................................................................33 

3.2.1.2 Systemic Effects.......................................................................................................33 

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.............................................................................................34 

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

3.2.2 Oral Exposure ...................................................................................................................35 

3.2.2.1 Death ........................................................................................................................36 

3.2.2.2 Systemic Effects.......................................................................................................36 

3.2.2.3 Immunological and Lymphoreticular Effects ..........................................................58 

3.2.2.4 Neurological Effects.................................................................................................58 

3.2.2.5 Reproductive Effects................................................................................................58 
STRONTIUM	 xvi 

3.2.2.6 Developmental Effects.............................................................................................58 

3.2.2.7 Cancer ......................................................................................................................59 

3.2.3 Dermal Exposure ..............................................................................................................59 

3.2.3.1 Death ........................................................................................................................60 

3.2.3.2 Systemic Effects.......................................................................................................60 

3.2.3.3 Immunological and Lymphoreticular Effects ..........................................................60 

3.2.3.4 Neurological Effects.................................................................................................60 

3.2.3.5 Reproductive Effects................................................................................................60 

3.2.3.6 Developmental Effects.............................................................................................60 

3.2.3.7 Cancer ......................................................................................................................60 

3.2.4 Other Routes of Exposure.................................................................................................60 

3.3 DISCUSSION OF HEALTH EFFECTS OF RADIOACTIVE STRONTIUM BY ROUTE OF 

EXPOSURE..............................................................................................................................62 

3.3.1 Inhalation Exposure ..........................................................................................................63 

3.3.1.1 Death ........................................................................................................................64 

3.3.1.2 Systemic Effects.......................................................................................................65 

3.3.1.3 Immunological and Lymphoreticular Effects ..........................................................73 

3.3.1.4 Neurological Effects.................................................................................................74 

3.3.1.5 Reproductive Effects.........................................................................................................74 

3.3.1.6 Developmental Effects......................................................................................................74 

3.3.1.7 Cancer ......................................................................................................................74 

3.3.2 Oral Exposure ...................................................................................................................76 

3.3.2.1 Death ........................................................................................................................77 

3.3.2.2 Systemic Effects.......................................................................................................80 

3.3.2.3 Immunological and Lymphoreticular Effects ..........................................................93 

3.3.2.4 Neurological Effects.................................................................................................94 

3.3.2.5 Reproductive Effects................................................................................................94 

3.3.2.6 Developmental Effects.............................................................................................95 

3.3.2.7 Cancer ......................................................................................................................97 

3.3.3 External Exposure...........................................................................................................100 

3.3.3.1 Death ......................................................................................................................101 

3.3.3.2 Systemic Effects.....................................................................................................101 

3.3.3.3 Immunological and Lymphoreticular Effects ........................................................108 

3.3.3.4 Neurological Effects...............................................................................................108 

3.3.3.5 Reproductive Effects..............................................................................................108
 

3.3.3.6 Developmental Effects...........................................................................................108 

3.3.3.7 Cancer ....................................................................................................................108 

3.3.4 Other Routes of Exposure...............................................................................................110 

3.4 GENOTOXICITY ...................................................................................................................113 

3.5 TOXICOKINETICS................................................................................................................118 

3.5.1 Absorption ......................................................................................................................118 

3.5.1.1 Inhalation Exposure ...............................................................................................118
 

3.5.1.2 Oral Exposure.........................................................................................................120 

3.5.1.3 Dermal Exposure....................................................................................................123 

3.5.2 Distribution .....................................................................................................................125 

3.5.2.1 Inhalation Exposure ...............................................................................................125
 

3.5.2.2 Oral Exposure.........................................................................................................126 

3.5.2.3 Dermal Exposure....................................................................................................129 

3.5.3 Metabolism .....................................................................................................................129 

3.5.3.1 Inhalation Exposure ...............................................................................................130
 

3.5.3.2 Oral Exposure.........................................................................................................130 
STRONTIUM xvii 

3.5.3.3 Dermal Exposure....................................................................................................130 

3.5.4 Elimination and Excretion ..............................................................................................130 

3.5.4.1 Inhalation Exposure ...............................................................................................130
 

3.5.4.2 Oral Exposure.........................................................................................................131 

3.5.4.3 Dermal Exposure....................................................................................................132 

3.5.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models.......132 

3.6 MECHANISMS OF ACTION ................................................................................................147 

3.6.1 Pharmacokinetic Mechanisms ........................................................................................147 

3.6.2 Mechanisms of Toxicity .................................................................................................150 

3.6.3 Animal-to-Human Extrapolations...................................................................................154 

3.7 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS ........................155 

3.8 CHILDREN’S SUSCEPTIBILITY.........................................................................................156 

3.9 BIOMARKERS OF EXPOSURE AND EFFECT ..................................................................162 

3.9.1 Biomarkers Used to Identify or Quantify Exposure to Strontium ..................................163 

3.9.2 Biomarkers Used to Characterize Effects Caused by Strontium ....................................164 

3.10 INTERACTIONS WITH OTHER CHEMICALS ..................................................................164 

3.11 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE.............................................165 

3.12 METHODS FOR REDUCING TOXIC EFFECTS.................................................................167 

3.12.1 Reducing Peak Absorption Following Exposure........................................................168 

3.12.2 Reducing Body Burden ..............................................................................................170 

3.12.3 Interfering with the Mechanism of Action for Toxic Effects.....................................173 

3.13 ADEQUACY OF THE DATABASE......................................................................................173 

3.13.1 Existing Information on Health Effects of Strontium.................................................173 

3.13.2 Identification of Data Needs.......................................................................................176
 

3.13.3 Ongoing Studies .........................................................................................................187 

4. CHEMICAL, PHYSICAL, and RADIOLOGICAL INFORMATION ...............................................189 

4.1 CHEMICAL IDENTITY.........................................................................................................189 

4.2 PHYSICAL, CHEMICAL, AND RADIOLOGICAL PROPERTIES.....................................189 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL..........................................................199 

5.1 PRODUCTION .......................................................................................................................199 

5.2 IMPORT/EXPORT .................................................................................................................200 

5.3 USE..........................................................................................................................................200 

5.4 DISPOSAL..............................................................................................................................201 

6. POTENTIAL FOR HUMAN EXPOSURE .........................................................................................205 

6.1 OVERVIEW............................................................................................................................205 

6.2 RELEASES TO THE ENVIRONMENT................................................................................208 

6.2.1 Air...................................................................................................................................208 

6.2.2 Water...............................................................................................................................213 

6.2.3 Soil..................................................................................................................................213 

6.3 ENVIRONMENTAL FATE....................................................................................................214
 

6.3.1 Transport and Partitioning ..............................................................................................214 

6.3.2 Transformation and Degradation ....................................................................................217 

6.3.2.1 Air...............................................................................................................................219 

6.3.2.2 Water......................................................................................................................219 

6.3.2.3 Sediment and Soil ..................................................................................................219 

6.3.2.4 Other Media ...........................................................................................................220 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT...............................220 

6.4.1 Air...................................................................................................................................220 
STRONTIUM xviii 

6.4.2 Water...............................................................................................................................222 

6.4.3 Sediment and Soil ...........................................................................................................228 

6.4.4 Other Environmental Media ...........................................................................................229
 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE .....................................236 

6.6 EXPOSURES OF CHILDREN...............................................................................................239 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES ...........................................241 

6.8 ADEQUACY OF THE DATABASE......................................................................................241 

6.8.1 Identification of Data Needs ...........................................................................................242 

6.8.2 Ongoing Studies..............................................................................................................246 

7. ANALYTICAL METHODS ...............................................................................................................249 

7.1 BIOLOGICAL MATERIALS.................................................................................................249 

7.1.1 Internal Strontium Measurements...................................................................................249 

7.1.2 In Vivo and In Vitro Radiostrontium Measurements ......................................................251 

7.2 ENVIRONMENTAL SAMPLES............................................................................................251 

7.2.1 Field Measurements of Radiostrontium..........................................................................252 

7.2.2 Laboratory Analysis of Environmental Samples............................................................252 

7.3 ADEQUACY OF THE DATABASE......................................................................................254 

7.3.1 Identification of Data Needs ...........................................................................................255 

7.3.2 Ongoing Studies..............................................................................................................255 

8. REGULATIONS AND ADVISORIES ...............................................................................................257 

9. REFERENCES ....................................................................................................................................277 

10. GLOSSARY ......................................................................................................................................367 

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

APPENDIX B. USER'S GUIDE..............................................................................................................B-1 

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

APPENDIX D. OVERVIEW OF BASIC RADIATION PHYSICS, CHEMISTRY, 

 AND BIOLOGY.......................................................................................................................D-1 

APPENDIX E. INDEX............................................................................................................................ E-1 
STRONTIUM xix 

LIST OF FIGURES 

3-1. Levels of Significant Exposure to Strontium—Chemical Toxicity—Oral ...................................45 

3-2. Levels of Significant Exposure to Strontium—Radiation Toxicity—Inhalation..........................69 

3-3. Levels of Significant Exposure to Strontium—Radiation Toxicity—Oral...................................86 

3-4. Conceptual Representation of a Physiologically Based Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance ............................................................................................... 134
 

3-5. Compartment Model to Represent Particle Deposition and Time-Dependent Particle Transport in 

the Respiratory Tract.................................................................................................................... 136
 

3-6. Reaction of Gases or Vapors at Various Levels of the Gas-Blood Interface............................... 138
 

3-7. The Human Respiratory Tract Model: Absorption into Blood .................................................... 140
 

3-8. ICRP (1993) Model of Strontium Biokinetics ............................................................................. 145
 

3-9. Existing Information on Health Effects of Stable Strontium....................................................... 174
 

3-10. Existing Information on Health Effects of Radioactive Strontium.............................................. 175
 

6-1. Frequency of NPL Sites with Strontium Contamination ............................................................. 206
 

6-2. Frequency of NPL Sites with Strontium-90 Contamination........................................................ 207
 

6-3. U.S. Daily Dietary Intake of 90Sr, 1961–1992 ............................................................................. 235
 

STRONTIUM xxi 

LIST OF TABLES 

3-1. Levels of Significant Exposure to Strontium—Chemical Toxicity—Oral..................................... 37 

3-2. Levels of Significant Exposure to Strontium—Radiation Toxicity—Inhalation ........................... 66 

3-3. Levels of Significant Exposure to Strontium—Radiation Toxicity—Oral .................................... 81 

3-4. Levels of Significant Exposure to Strontium—Radiation Toxicity—External............................ 102 

3-5. Genotoxicity of Stable and Radioactive Strontium In Vivo .......................................................... 114
 

3-6. Genotoxicity of Stable and Radioactive Strontium In Vitro ......................................................... 115
 

3-7. Summary of Estimates of Absorption of Ingested Strontium in Humans .................................... 121
 

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

 Activity ........................................................................................................................................... 137
 

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

Particle Transport from the Human Respiratory Tract.................................................................. 141
 

4-1. Chemical Identity of Strontium and Strontium Compounds......................................................... 190
 

4-2. Physical and Chemical Properties of Strontium and Strontium Compounds............................... 193
 

4-3. Percent Natural Occurrence and Radioactive Properties of Isotopes of Strontium...................... 196
 

6-1. Radiostrontium Releases from Nuclear Power Plants for 1993.................................................... 210
 

6-2. Selected Bioconcentration Factors for 90Sr in Aquatic, Wetland, and Terrestrial Ecosystems at the 

Savannah River Site ....................................................................................................................... 218
 

6-3. Average or Ranges of Concentration of Strontium in Earth Materials......................................... 221
 

6-4. 90Sr in Drinking Water (Composites) for January–December 1995 ............................................. 224
 

6-5. Quarterly and Annual Deposition of 90Sr in Selected U.S. Cites for the Year 1990.................... 227
 

6-6. Concentration of Strontium in Fruit Juices and Produce .............................................................. 230
 

6-7. 90Sr in the Human Diets During 1982............................................................................................ 232
 

6-8. 90Sr in Pasteurized Milk in July 1997 ............................................................................................ 233
 

6-9. Strontium Concentrations in Human Body Fluids and Tissues .................................................... 238
 

6-10. Ongoing Studies on the Environmental Effects of Strontium....................................................... 247
 
STRONTIUM xxii 

7-1. Analytical Methods for Determining Strontium in Biological Samples...................................... 250
 

7-2. Analytical Methods for Determining Strontium in Environmental Samples............................... 253
 

8-1. Regulations and Guidelines Applicable to Stable Strontium....................................................... 258
 

8-2. Regulations and Guidelines Applicable to Radioactive Strontium.............................................. 260
 

8-3. Effective Dose Coefficients (e(50)) and Annual Limits on Intake (ALI) for Occupational 

Exposures to Radioactive Strontium Isotopes ............................................................................. 273
 
STRONTIUM 1 

1. PUBLIC HEALTH STATEMENT 

This public health statement tells you about strontium and the effects of exposure. 

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

the nation. These sites make up the National Priorities List (NPL) and are the sites targeted for 

long-term federal cleanup activities. Strontium and strontium-90 have been found in at least 

102 and 12 of the 1,636 current or former NPL sites, respectively. However, the total number of 

NPL sites evaluated for strontium and strontium-90 are not known. As more sites are evaluated, 

the sites at which strontium and strontium-90 are found may increase. This information is 

important because exposure to strontium and strontium-90 may harm you and because these sites 

may be sources of exposure. 

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 only 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. Naturally occurring sources of radiation 

are cosmic radiation from space or radioactive materials in soil or building materials. Man-made 

sources of radioactive materials are found in consumer products, industrial equipment, atom 

bomb fallout, and to a smaller extent from hospital waste and nuclear reactors. 

If you are exposed to strontium, many factors determine whether you’ll be harmed. These 

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

it. You must also consider the other chemicals you’re exposed to and your age, sex, diet, family 

traits, lifestyle, and state of health. 

1.1 WHAT IS STRONTIUM? 

Strontium is a natural and commonly occurring element. Strontium can exist in two oxidation 

states: 0 and +2. Under normal environmental conditions, only the +2 oxidation state is stable 
STRONTIUM 2 

1. PUBLIC HEALTH STATEMENT 

enough to be important. Pure strontium is a hard, white-colored metal, but this form is not found 

in the environment. Rather, strontium is usually found in nature in the form of minerals. 

Strontium can form a variety of compounds. Strontium compounds do not have any particular 

smell. There are two types of strontium compounds, those that dissolve in water and those that 

do not. Natural strontium is not radioactive and exists in four stable types (or isotopes), each of 

which can be written as 84Sr, 86Sr, 87Sr, and 88Sr, and read as strontium eighty-four, strontium 

eighty-six, etc. All four isotopes behave the same chemically, so any combination of the four 

would have the same chemical effect on your body. 

Rocks, soil, dust, coal, oil, surface and underground water, air, plants, and animals all contain 

varying amounts of strontium. Typical concentrations in most materials are a few parts per 

million (ppm). Strontium ore is found in nature as the minerals celestite (SrSO4) and strontianite 

(SrCO3). After the strontium is extracted from strontium ore, it is concentrated into strontium 

carbonate or other chemical forms by a series of chemical processes. Strontium compounds, 

such as strontium carbonate, are used in making ceramics and glass products, pyrotechnics, paint 

pigments, fluorescent lights, medicines, and other products. For more information, see 

Chapter 5. 

Strontium can also exist as radioactive isotopes (see Chapter 4). 90Sr, or strontium ninety, is the 

most hazardous of the radioactive isotopes of the chemical element strontium. 90Sr is formed in 

nuclear reactors or during the explosion of nuclear weapons. Each radioactive element, 

including strontium, constantly gives off radiation, and this process changes it into an isotope of 

another element or a different isotope of the same element. This process is called radioactive 

decay. 90Sr gives off beta particles (sometimes referred to as beta radiation) and turns into 

yttrium ninety (90Y); 90Y is also radioactive and gives off radiation to form zirconium ninety 

(

90Zr), which is a stable isotope. The radioactive half-life is the time that it takes for half of a 

radioactive strontium isotope to give off its radiation and change into a different element. 90Sr 

has a half-life of 29 years. 
STRONTIUM 3 

1. PUBLIC HEALTH STATEMENT 

90Sr has limited use and is considered a waste product. The radioactive isotope 89Sr is used as a 

cancer therapeutic to alleviate bone pain. 85Sr has also been used in medical applications. For 

more information about the properties and use of radioactive strontium, see Chapters 4 and 5. 

Quantities of radioactive strontium, as well as other radioactive elements, are measured in units 

of mass (grams) or radioactivity (curies or becquerels). Both the curie (Ci) and the becquerel 

(Bq) tell us how much a radioactive material decays every second. The becquerel is a new 

international unit known as the SI unit, and the curie is an older unit; both are used currently. A 

becquerel is the amount of radioactive material in which 1 atom transforms every second. 

One curie is the amount of radioactive material in which 37 billion atoms transform every 

second; this is approximately the radioactivity of 1 gram of radium. For more information on 

radiation, see Appendix D and the glossary, Chapter 10, at the end of this profile or the ATSDR 

Toxicological Profile for Ionizing Radiation. 

1.2 WHAT HAPPENS TO STRONTIUM WHEN IT ENTERS THE ENVIRONMENT? 

Stable and radioactive strontium compounds in the air are present as dust. Emissions from 

burning coal and oil increase stable strontium levels in air. The average amount of strontium that 

has been measured in air from different parts of the United States is 20 nanograms per cubic 

meter (a nanogram is a trillion times smaller than a gram). Most of the strontium in air is in the 

form of stable strontium. Very small dust particles of stable and radioactive strontium in the air 

fall out of the air onto surface water, plant surfaces, and soil either by themselves or when rain or 

snow falls. These particles of strontium eventually end up back in the soil or in the bottoms of 

lakes, rivers, and ponds, where they stay and mix with stable and radioactive strontium that is 

already there. 

In water, most forms of stable and radioactive strontium are dissolved. Stable strontium that is 

dissolved in water comes from strontium in rocks and soil that water runs over and through. 

Only a very small part of the strontium found in water is from the settling of strontium dust out 

of the air. Some strontium is suspended in water. Typically, the amount of strontium that has 

been measured in drinking water in different parts of the United States by the EPA is less than 
STRONTIUM 4 

1. PUBLIC HEALTH STATEMENT 

1 milligram for every liter of water (1 mg/L). 90Sr in water comes primarily from the settling of 

90Sr dust out of the air. Some 90Sr is suspended in water. In general, the amount of 90Sr that has 

been measured in drinking water in different parts of the United States by EPA is less than 

one-tenth of a picocurie for every liter of water (0.1 pCi/L or 0.004 Bq/L). 

Strontium is found naturally in soil in amounts that vary over a wide range, but the typical 

concentration is 0.2 milligrams per kilogram (kg) of soil (or 0.2 mg/kg). The disposal of coal 

ash, incinerator ash, and industrial wastes may increase the concentration of strontium in soil. 

Generally, the amount of 90Sr in soil is very small and is only a fraction of the total concentration 

of strontium in soil. Higher concentrations of 90Sr in soil may be found near hazardous waste 

sites, radioactive waste sites, and Department of Energy facilities located around the United 

States. A major portion of stable and radioactive strontium in soil dissolves in water, so it is 

likely to move deeper into the ground and enter groundwater. However, strontium compounds 

may stay in the soil for years without moving downward into groundwater. In the environment, 

chemical reactions can change the water-soluble stable and radioactive strontium compounds 

into insoluble forms. In some cases, water-insoluble strontium compounds can change to soluble 

forms. For more information about the transport properties of stable and radioactive strontium in 

the environment, see Chapter 6. 

1.3 HOW MIGHT I BE EXPOSED TO STRONTIUM? 

Strontium is found nearly everywhere in small amounts, and you can be exposed to low levels of 

strontium by breathing air, eating food, drinking water, or accidentally eating soil or dust that 

contains strontium. Food and drinking water are the largest sources of exposure to strontium. 

Because of the nature of strontium, some of it gets into fish, vegetables, and livestock. Grain, 

leafy vegetables, and dairy products contribute the greatest percentage of dietary strontium to 

humans. The concentration of strontium in leafy vegetables, such as cabbage, grown in the 

United States is less than 64 mg in a kg of the fresh vegetables (i.e., 64 ppm). For most people, 

the intake of strontium will be moderate. More information about strontium exposure can be 

found in Chapter 6. 
STRONTIUM 5 

1. PUBLIC HEALTH STATEMENT 

90Sr is found nearly everywhere in small amounts from past nuclear accidents and fallout from 

nuclear explosions. You can be exposed to low levels of 90Sr by eating food, drinking water, or 

accidentally eating soil or dust that contains 90Sr. Food and drinking water are the largest 

sources of exposure to 90Sr. Because of the nature of 90Sr, some of it gets into fish, vegetables, 

and livestock. Grain, leafy vegetables, and dairy products contribute the greatest percentage of 

dietary 90Sr to humans. The concentration of 90Sr in fresh vegetables grown in the United States 

is less than 9 pCi (or 0.3 Bq) in 1 kg of dried vegetables (in a hot oven). The intake of 

radioactive strontium for most people will be small. You can take in more 90Sr if you eat food 

that was grown on a radioactive strontium-contaminated hazardous waste site. More information 

about radioactive strontium exposure can be found in Chapter 6. 

1.4 HOW CAN STRONTIUM ENTER AND LEAVE MY BODY? 

Both stable strontium and radioactive strontium enter and leave the body in the same way. 

If a person breathes in vapors or dust containing a chemical form of strontium that is soluble in 

water, then the chemical will dissolve in the moist surface inside the lungs and strontium will 

enter the bloodstream relatively quickly. If the chemical form of strontium does not dissolve in 

water easily, then particles may remain in the lung for a time. When you eat food or drink water 

that contains strontium, only a small portion leaves the intestines and enters the bloodstream. 

Studies in animals suggest that infants may absorb more strontium from the intestines than 

adults. If a fluid mixture of a strontium salt is placed on the skin, the strontium will pass through 

the skin very slowly and then enter the bloodstream. If the skin has scratches or cuts, strontium 

will pass through the skin much more quickly. 

Once strontium enters the bloodstream, it is distributed throughout the body, where it can enter 

and leave cells quite easily. In the body, strontium behaves very much like calcium. A large 

portion of the strontium will accumulate in bone. In adults, strontium mostly attaches to the 

surfaces of bones. In children, whose bones are still growing, strontium may be used by the 

body to create the hard bone mineral itself. As a result the strontium will be stored in the bone 

for a long time (years). Because of the way bone grows, strontium will be locally dissolved from 
STRONTIUM 6 

1. PUBLIC HEALTH STATEMENT 

bone and recirculate through the bloodstream, where it may be reused by growing bone, or be 

eliminated. This process accounts for the slow removal of strontium from the body. 

Strontium is eliminated from the body through urine, feces, and sweat. Elimination through 

urine may occur over long periods, when small amounts of strontium are released from bone and 

do not get recaptured by bone. When strontium is taken in by mouth, the portion that does not 

pass through the intestinal wall to enter the bloodstream is eliminated through feces during the 

first day or so after exposure. 

See Chapter 3 for further information. 

1.5 HOW CAN STRONTIUM AFFECT MY HEALTH? 

To protect the public from the harmful effects of toxic chemicals and to find ways to treat people 

who have been harmed, scientists use many tests. 

One way to see if a chemical will hurt people is to learn how the chemical is absorbed, used, and 

released by the body. In the case of a radioactive chemical, it is also important to gather 

information concerning the radiation dose and dose rate to the body. For some chemicals, 

animal testing may be necessary. Animal testing may also be used to identify health effects such 

as cancer or birth defects. Without laboratory animals, scientists would lose a basic method to 

get information needed to make wise decisions to protect public health. Scientists have the 

responsibility to treat research animals with care and compassion. Laws today protect the 

welfare of research animals, and scientists must comply with strict animal care guidelines. 

There are no harmful effects of stable strontium in humans at the levels typically found in the 

environment. The only chemical form of stable strontium that is very harmful by inhalation is 

strontium chromate, but this is because of toxic chromium and not strontium itself. Problems 

with bone growth may occur in children eating or drinking unusually high levels of strontium, 

especially if the diet is low in calcium and protein. Ordinary strontium salts are not harmful 

when inhaled or placed on the skin. 
STRONTIUM 7 

1. PUBLIC HEALTH STATEMENT 

Animal studies showed that eating or drinking very large amounts of stable strontium can be 

lethal, but the public is not likely to encounter such high levels of strontium. In these unusually 

high amounts, so much strontium was taken into bone instead of calcium that growing bones 

were weakened. Strontium had more severe effects on bone growth in young animals than in 

adults. 

It is not known whether stable strontium affects reproduction in people. The effect of stable 

strontium on reproduction in animals is not known. The Department of Health and Human 

Services has determined that strontium chromate is expected to be a carcinogen, but this is 

because of chromium. There is no information that any other form of stable strontium causes 

cancer in humans or animals. 

The harmful effects of radioactive strontium are caused by the high energy effects of radiation. 

Since radioactive strontium is taken up into bone, bone itself and the soft tissues nearby may be 

damaged by radiation released over time. Because bone marrow is the essential source of blood 

cells, blood cell counts may be reduced if the dose is too high. This has been seen in humans 

who received injections of radioactive strontium (89Sr) to destroy cancer tissue that had spread to 

the bone marrow. Lowered blood cell counts were also seen in animals that breathed or 

swallowed radioactive strontium. Numerous problems occur when the number of blood cells is 

too low. A loss of red blood cells, anemia, prevents the body from getting sufficient oxygen, 

resulting in tiredness. A loss of platelets may prevent the blood from clotting properly, and may 

result in abnormal bleeding, especially in the intestines. A loss in white blood cells harms the 

body’s ability to fight infectious disease. 

Radiation damage may also occur from exposure to the skin. Medically, radioactive strontium 

probes have been used intentionally to destroy unwanted tissue on the surface of the eye or skin. 

The eye tissues sometimes become inflamed or abnormally thin after a long time. Thinning of 

the lower layer of the skin (dermis) has also been reported in animal studies as a delayed effect. 
STRONTIUM 8 

1. PUBLIC HEALTH STATEMENT 

It is not known whether exposure to radioactive strontium would affect human reproduction. 

Harmful effects on animal reproduction occurred at doses that were more than a million times 

higher than typical exposure levels for the general population. 

Radioactive strontium may cause cancer as a result of damage to the genetic material (DNA) in 

cells. An increase in leukemia over time was reported in individuals in one foreign population 

who swallowed relatively large amounts of 90Sr (and other radioactive materials) in river water 

contaminated by a nuclear weapons plant. Cancers of the bone, nose, and lung (in the case of a 

breathing exposure), and leukemia were reported in animal studies. In addition, skin and bone 

cancer were reported in animals that received radiation at high doses to the skin. The 

International Agency for Research on Cancer (IARC) has determined that radioactive strontium 

is carcinogenic to humans, because it is deposited inside the body and emits beta radiation. The 

EPA has determined that radioactive strontium is a human carcinogen. 

To learn more about the health effects of exposure to stable or radioactive strontium, see 

Chapter 3. 

1.6 HOW CAN STRONTIUM AFFECT CHILDREN? 

This section discusses potential health effects from exposures during the period from conception 

to maturity at 18 years of age in humans. 

Children are exposed to stable strontium in the same manner as adults: usually in small amounts 

in drinking water and food. Young children who have more hand-to-mouth activity or who eat 

soil may accidentally eat more strontium. Infants and children with active bone growth absorb 

more strontium from the gut than adults. 

Excess stable strontium causes problems with growing bone. For this reason, children are more 

susceptible to the effects of stable strontium than adults who have mature bone. Children who 

eat or drink unusually high levels of stable strontium may have problems with bone growth, but 

only if the diet is low in calcium and protein. Children who drink milk, especially milk fortified 
STRONTIUM 9 

1. PUBLIC HEALTH STATEMENT 

with vitamin D, are not likely to have bone problems from exposure to excess stable strontium. 

The amount of stable strontium that is usually taken in from food or water or by breathing is too 

low to cause bone problems in children. No developmental studies in humans or animals 

examined the effect on the fetus when the mother takes in excess strontium. However, no 

problems are expected with fetal bone growth because only small amounts of strontium are 

transferred from the mother across the placenta to the fetus. Evidence suggests that stable 

strontium can be transferred from the mother to nursing infants through breast milk, but the 

presence of calcium and protein in milk protects against bone problems during nursing. 

Children take in, use, and get rid of radioactive strontium in the same ways as stable strontium. 

Children are likely to be more vulnerable than adults to the effects of radioactive strontium 

because relatively more goes into bone when it is growing. Also, children are potentially more 

vulnerable than adults to radiation damage because they keep radioactive strontium in bone for a 

longer time. 

Children would be expected to have the same types of effects from exposure to radioactive 

strontium as exposed adults. Children can be exposed to radioactive strontium at levels higher 

than background without showing increases in cancer rates. Evidence from one foreign 

population showed that children who drank water containing unusually high levels of radioactive 

strontium for 7 years showed an increase in leukemia. High levels of radioactive strontium cause 

more bone damage and higher bone cancer rates when animals are exposed before birth or as 

juveniles rather than as adults. In humans and animals, radioactive strontium can be transferred 

into milk or across the placenta into the fetus. 

1.7 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO STRONTIUM? 

If your doctor finds that you have been exposed to significant amounts of strontium, ask whether 

your children might also be exposed. Your doctor might need to ask your state health 

department to investigate. Public health officials may publish guidelines for reducing exposure 

to strontium when necessary. 
STRONTIUM 10 

1. PUBLIC HEALTH STATEMENT 

It is possible that higher-than-normal levels of stable strontium may occur naturally in soil in 

some places or that higher levels of radioactive strontium may be found in soil near hazardous 

waste sites. Some children eat a lot of dirt. You should prevent your children from eating dirt. 

Make sure they wash their hands frequently, and before eating. If you live near a hazardous 

waste site, discourage your children from putting their hands in their mouths or from engaging in 

other hand-to-mouth activities. 

Since strontium is so common in the environment, and is naturally present in food and water, we 

cannot avoid being exposed to it. For several reasons, having a balanced diet with sufficient 

vitamin D, calcium, and protein will be protective by reducing the amount of ingested strontium 

that is absorbed. 

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

EXPOSED TO STRONTIUM? 

All people have small amounts of stable strontium in their bodies, mostly in bone. It can be 

measured in the blood, hair, feces, or urine. The amount is usually measured by its mass 

(grams). Measurements in urine can show whether you have been exposed recently to largerthan-normal amounts of strontium. Measurements in hair can reveal whether you were exposed 

to high amounts of strontium in the past. Most physicians do not test for strontium in their 

offices, but can collect samples and send them to a special laboratory. X-rays can show changes 

in bone that may occur from exposure to high amounts of strontium, but these changes may have 

other causes (a diet low in vitamin D or a high exposure to some other trace metal). 

If a person has been exposed to radioactive strontium, special tests can be used to measure 

radioactive strontium in blood, feces, or urine. These tests are most useful when done soon after 

exposure, since radioactive strontium quickly enters into bone and takes many years to be 

completely removed from bone. Radioactive strontium can be measured by its mass (in grams) 

or by its radiation emissions. These emissions, which differ for the various isotopes of 

strontium, are used to tell the amount of radioactive strontium (in curies or bequerels) and the 

radiation dose that it gives to your body (in sieverts or rem). In a procedure that is similar to 
STRONTIUM 11 

1. PUBLIC HEALTH STATEMENT 

being x-rayed, specialized equipment can measure radioactive strontium that has been 

incorporated into bone. 

For more information, please read 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). 

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 in not-to-exceed levels in air, water, soil, or 

food that are usually based on levels that affect animals; they are then adjusted to help protect 

people. Sometimes these not-to-exceed levels differ among federal organizations because of 

different exposure times (an 8-hour workday or a 24-hour day), the use of different animal 

studies, or other factors. 

Recommendations and regulations are also periodically updated as more information becomes 

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

provides it. Some regulations and recommendations for strontium include the following: 

EPA recommends that drinking water levels of stable strontium should not be more than 

4 milligrams per liter of water (4 mg/L). 
STRONTIUM 12 

1. PUBLIC HEALTH STATEMENT 

The Department of Energy (DOE) established derived air concentrations (DAC) for workplace 

exposure to radiation at DOE facilities. The DAC ranges from 0.000000002 microcuries per 

milliliter (μCi/mL) (2x10-9 μCi/mL of air = 70 μBq/mL of air) for radioactive particles remaining 

in the lung for 100 days to 0.000000008 μCi/mL (8x10-9 μCi/mL of air = 300 μBq/mL of air) for 

radioactive particles remaining in the lung for less than 10 days. The USNRC established an 

annual intake limit of 20 μCi (7 MBq) for on-the-job exposure to 90Sr in air. 

EPA set standards for the concentration of 90Sr in community water supplies. The average 

annual concentration of 90Sr in water supplies should not exceed 8 pCi/L (0.3 Bq/L). EPA also 

established maximum contaminant levels (MCLs) in drinking water for radionuclide activities to 

protect against harmful effects of 90Sr. For beta particles like strontium, the MCL is 4 mrem per 

year (4x10-5 Sv per year). The USNRC set a workplace value of 31 μCi (1.1 MBq) for the 

amount of 90Sr that can be taken in by mouth in a year without any harmful effects. 

More information on regulations and guidelines is available 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, your regional Nuclear Regulatory Commission office, 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 resulting 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 ToxProfiles CD-ROM by calling the information and 

technical assistance toll-free number at 1-888-42ATSDR (1-888-422-8737), by email at 

atsdric@cdc.gov, or by writing to: 
STRONTIUM 13 

1. PUBLIC HEALTH STATEMENT 

Agency for Toxic Substances and Disease Registry 

Division of Toxicology 

1600 Clifton Road NE 

Mailstop F-32 

Atlanta, GA 30333 

Fax: 1-770-488-4178 

For-profit organizations may request a copy of final 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 

Web site: http://www.ntis.gov/ 

STRONTIUM 15 

2. RELEVANCE TO PUBLIC HEALTH 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO STRONTIUM IN THE 

UNITED STATES 

Stable Strontium. Elemental strontium (atomic number 38) occurs naturally in the earth's mantle as a 

mixture of four stable isotopes, 88Sr, 86Sr, 87Sr, and 84Sr, and is present everywhere in very dilute 

concentrations. It is very similar to calcium in its environmental and physiological behavior. Strontium 

is generally found in molecular compounds with other elements. Commercially important strontium 

minerals include celestite (SrSO4) and strontianite (SrCO3). Strontium is used in the manufacture of 

ceramics and glass products, primarily in the faceplate glass of televisions and other cathode-ray-tube 

devices, where it serves to block x-ray emissions. 

The general population is exposed to stable strontium primarily by ingestion of food and water, and to a 

lesser degree, by inhalation. The strontium content in air averages 20 ng/m3

, with higher concentrations 

resulting from stack emissions from coal-burning plants. Strontium is present in nearly all fresh waters in 

amounts generally ranging between 0.5 and 1.5 mg/L, with higher levels occurring where there are 

celestite-rich limestone deposits. The average concentration of stable strontium in soil is approximately 

240 mg Sr/kg, but agricultural soils may be treated with phosphate fertilizer or limestone, which contain 

~610 mg Sr/kg. Because strontium is chemically similar to calcium, it is taken up from the soil by fruits 

and vegetables. The average concentration of strontium in fruit produce ranged from 0.0416 to 

2.232 μg/L. The total estimated daily exposure to stable strontium is approximately 3.3 mg/day 

(0.046 mg/kg/day): 400 ng/day from inhalation, 2 mg/day from drinking water, and 1.3 mg/day from the 

diet (see Chapter 6). Assuming a reference body weight of 70 kg, the typical daily strontium exposure is 

46 μg/kg body weight. The strontium content of the human body is approximately 4.6 ppm by weight, 

99% of which is localized in bones and teeth. Blood concentrations of strontium are in the range of 

20–31 μg/L. 

Radioactive Strontium. The radioactive isotopes of strontium do not occur naturally but are produced as 

a by-product of nuclear fission of 235U, 238U, or 239Pu. The most significant isotopes are 90Sr (half-life of 

29 years), 89Sr (half-life of 51 days), and 85Sr (half-life of 65 days), which decay by the emission of beta 

particles. 90Sr is currently found in spent fuel rods in nuclear reactors and is considered a waste product. 

Other radioactive strontium isotopes have been employed for medical uses: 89Sr (as MetastronTM) as a 

cancer therapeutic for the relief of bone pain and 85Sr in the radiologic imaging of bone. 85Sr also has 
STRONTIUM 16 

2. RELEVANCE TO PUBLIC HEALTH 

minor commercial applications in thermoelectric power generation, as a beta particle standard source, and 

in instruments that measure the thickness and density of materials. Disposal and handling of radioactive 

strontium isotopes are regulated by the U.S. Nuclear Regulatory Commission. 

The general population is exposed to very small amounts of radioactive strontium from the ingestion of 

contaminated water and food; inhalation exposure is negligible. The average concentration of 90Sr in 

drinking water in 1994 was estimated as 0.1 pCi/L; after 1994, estimates were based on gross beta activity 

and not reported by individual elements since the amounts were so small. Fresh vegetables contribute 

more than one third of the yearly dietary intake of 90Sr, followed by grains and dairy products. The 

current total daily exposure levels to radioactive strontium are estimated to be approximately 5.2 pCi/day 

(0.16 Bq/day; 0.074 pCi/kg/day): 5 pCi/day from food and 0.2 pCi/day from drinking water. 

See Chapter 6 for more detailed information regarding concentrations of stable and radioactive strontium 

in environmental media. 

2.2 SUMMARY OF HEALTH EFFECTS 

Stable Strontium. There is no direct evidence that stable strontium is toxic to humans under normal 

environmental exposures. The primary toxicological effect of absorbed excess strontium in laboratory 

animals is abnormal skeletal development (rickets), which occurs only at relatively high oral doses. The 

inhalation toxicity of pure stable strontium has not been evaluated. At levels normally encountered in the 

environment, strontium appears to have low toxicity to adults or to juveniles with adequate nutrition. 

Juveniles, especially those with poor nutrition, are vulnerable because strontium, as an imperfect 

surrogate for calcium, interferes with bone mineralization in the developing skeleton. The data for 

adverse health effects of stable strontium in humans are sparse, but indicate a possibility of skeletal 

effects under special circumstances: an epidemiological study of strontium-related rickets in Turkish 

children and a few studies of hemodialysis patients who developed osteomalacia because of strontium in 

dialysis water. Numerous animal studies demonstrated adverse effects on skeletal development in 

juveniles following ingestion of excess stable strontium (discussed below under Skeletal Effects). No 

developmental or reproductive studies have been conducted involving exposure to stable strontium during 

gestation. No studies examined whether stable strontium is carcinogenic to humans or animals. One 

strontium compound, strontium chromate, is a genotoxic human carcinogen by the inhalation route, but 

the hazard is caused by hexavalent chromium and not strontium. 
STRONTIUM 17 

2. RELEVANCE TO PUBLIC HEALTH 

Other effects have been observed sporadically and are of unclear physiological significance. Paralysis of 

the hindlimbs was observed in orally-exposed rats, but it is uncertain whether the cause was 

neurophysiological or the result of local neuronal damage secondary to deformation of the femora. Minor 

unspecified changes in hepatic histology and glycogen content were observed in orally-exposed rats. The 

following section discusses effects in the primary target of stable strontium, the skeleton, in greater detail. 

Skeletal Effects. Although strontium, as a molecular surrogate for calcium, can be distributed 

throughout the body, its main target for deposition is the skeleton. One suggestive epidemiological study 

found that increased strontium ingestion contributed to an increase in the prevalence of signs of rickets 

(craniomalacia, rachitic rosary, bulging at the wrist, bony deformities of the leg, and delayed closure of 

the fontanelles) in children in a region of Turkey. A significantly increased incidence of rickets was 

associated with a diet restricted to water and cereals grown locally in soils with strontium concentrations 

in excess of 350 mg/kg. Other contributing factors included probable deficiencies in vitamin D, protein, 

and calcium after weaning; breast feeding for >2 years appeared to be a protective factor against the 

development of rickets in this population. The only reports of strontium-related skeletal problems in 

adults concerned osteomalacia in hemodialysis patients exposed to strontium in dialysis water. Dialysis 

patients may be unusually susceptible because of their impaired handling of strontium. Stable strontium 

compounds have been used for the treatment of osteoporosis (see Section 2.3). 

Animal studies strongly support the identification of bone as the most sensitive target of strontium 

toxicity. Relatively high doses of strontium (≥500 mg/kg/day) caused a reduction in bone mineralization 

(ash weight) and an alteration in the chemical composition of organic bone matrix. In addition, the 

hypertrophic zones of the epiphyseal growth plates of long bones became abnormally deep and wide, as 

calcification failed to occur. Severe weakening of the bones resulted from rickets, in which the skeleton 

could not support the body adequately; deformity of the head of the femur may have contributed to 

paralysis of the hind limbs in some cases. Young animals were more sensitive to the effect of excess 

strontium than older animals, possibly because the absorption and retention of strontium were higher in 

the young. In addition, inadequate calcium and vitamin D in the diet increased the severity of skeletal 

effects. The chemical form of strontium may influence toxicity by affecting gastrointestinal absorption. 

One intermediate oral animal study that tested strontium phosphate reported a much higher no-effect level 

than studies that tested strontium chloride or carbonate. However, cation effects on strontium toxicity 

have not been studied systematically. 
STRONTIUM 18 

2. RELEVANCE TO PUBLIC HEALTH 

Evidence from the few human studies and numerous animal toxicity studies suggest that healthy adults 

living near hazardous waste sites are unlikely to be exposed to levels of stable strontium sufficiently high 

to cause adverse skeletal effects. Children living in areas where the soil and drinking water contain 

relatively high amounts of strontium may be vulnerable to skeletal effects if their nutritional status is poor 

(deficient in calcium, vitamin D, and/or protein) and if the diet is restricted to foods grown locally. All 

these conditions are not likely to be common in the United States, since the food supply generally comes 

from a wide geographic area. 

Radioactive Strontium. Exposure to radioactive strontium can result in health consequences that vary 

depending on the dose, the route of exposure, and the chemical form. Both 90Sr and 89Sr emit beta 

particles, which, in tissue, may ionize cellular molecules within a range of 1 cm, resulting in tissue 

damage and disruption of cellular function if the capacity of natural repair mechanisms is exceeded. 

Adverse health effects occur at high levels of exposure that significantly exceed background levels 

encountered by the general population. It should be noted that no discernable adverse health effects were 

detected in the general population from chronic low-level exposure to 90Sr in fallout during the period of 

aboveground weapons testing. 

90Sr represents the most significant isotope of concern because of its relatively long half-life (29 years) 

and because of the bone-seeking properties of strontium. The most serious effects of oral exposure to 

absorbed radioactive strontium are necrotic lesions and cancers of bone and the adjacent tissues. High 

level acute exposures can destroy hematopoietic bone marrow, leading to acute radiation syndrome (see 

below), the primary cause of mortality in the short term. At lower doses, irradiation of bone marrow may 

lead to chronic suppression of immune function. 

The consequences of inhalation exposures in animals vary depending on the solubility of the form of 

radiostrontium. Insoluble particles tend to be retained in the lung, resulting in pneumonitis; necrosis of 

the pulmonary, vascular, and adjacent myocardial tissues; pulmonary fibrosis; and, later, pulmonary and 

vascular cancers. Inhalation of soluble radiostrontium does not have these local effects because the 

material is absorbed and distributed in the skeleton. The effects of inhalation of soluble strontium are, 

therefore, similar to those described for the oral route: acute radiation syndrome and other hematopoietic 

effects, osteosarcoma, and immunosuppression. 

External exposure to solid strontium sources placed near the skin or eye can cause local lesions when 

doses are significantly higher than background. Effects observed in clinical studies on the eye included 
STRONTIUM 19 

2. RELEVANCE TO PUBLIC HEALTH 

keratitis or scarring of the cornea, telangiectasis or scarring of the conjunctiva, iritis, conjunctivitis, mild 

irritation, and scleral thinning. Dermal effects in clinical studies range from erythema and pigmentation 

changes, dry and moist desquamation (which involves destruction of the basal epithelial cells), and 

telangiectasis and increased vascular permeability, to long-term responses such as epithelial and dermal 

hyperplasia, chronic fibrosis, and dermal atrophy. 

There is inconclusive evidence in humans and definitive evidence in laboratory animals that exposure to 

radioactive strontium at very high doses in utero can lead to adverse developmental effects. Slight 

increases in developmental effects were noted in a population of the former Soviet Union whose drinking 

water (the Techa River) was contaminated with multiple radioactive elements released from a plutonium 

production plant between 1949 and 1956. These effects included slight increases in child mortality from 

chromosomal defects and from congenital anomalies of the nervous system, circulatory system, and other 

unspecified anomalies in the progeny of exposed individuals. However, the specific contribution of 

radiostrontium to these effects is not known. Developmental effects in laboratory animals were noted at 

extremely high doses, as if, on a kilogram body weight basis, individual pregnant females were receiving 

daily the entire amount of 90Sr currently released from one nuclear power plant into the environment 

during a year (see Table 6-1). There is evidence that maternal oral exposure to radioactive strontium can 

lead to reduced fetal and postnatal survival in the offspring, but there is no evidence for birth defects. At 

the very highest doses of radioactive strontium injected into pregnant females, the offpsring exhibit 

increases in birth defects (skeletal anomalies and partial atelectasis of the lungs), and cancers of soft 

tissues near bone (meningeal and pituitary tumors), as well as hyperplasia of lymph nodes and spleen and 

deficient hematopoiesis. Exposure to radioactive strontium in milk from dams injected at very high doses 

reduces the numbers of early-stage oocytes in the ovary of neonatal mice, but the effect is less severe than 

when offspring are exposed only in utero. 

There is no evidence in humans that radioactive strontium leads to reproductive effects, but there is some 

evidence in laboratory animals. Although the Techa River populations received the highest known 

extended oral exposure to radioactive strontium (and other radionuclides) of any human group, there were 

no significant effects on reproductive parameters (birth rate, fertility, incidence of spontaneous abortion).

An increase in fetal deaths was noted in some studies in rats, but no reproductive effects were noted in 

larger laboratory animals at equivalent oral doses. This difference appears to be related to the fact that in 

small animals, the bone marrow cavity diameters are not wide enough to leave the central hematopoetic 

tissues untouched by beta-irradiation emitted by radioactive strontium bound to bone. Exposure to high 
STRONTIUM 20 

2. RELEVANCE TO PUBLIC HEALTH 

doses of radioactive strontium by injection led to significant reproductive effects (reduced fertility, 

reduced gonadal cellularity, suppressed spermatocyte maturation) in mice. 

Other effects of radioactive strontium have been observed sporadically in animal studies and are of 

unclear physiological significance. Anorexia, reduced body weight, and liver effects that were possibly 

secondary to radiation pneumonitis (chronic passive congestion of the liver and mild centrilobular hepatic 

fibrosis) were observed in beagles following a single inhalation exposure of insoluble 90Sr particles at an 

initial lung burden of 25 :Ci/kg. 

The populations potentially most sensitive to radiostrontium exposure include the young and individuals 

that have poor nutrition or deficiencies in vitamin D. Infants and children are more vulnerable than adults 

because they absorb strontium through the gastrointestinal tract at slightly higher rates and because they 

have actively growing bones that incorporate more strontium than mature bones. Very high prenatal 

exposure levels may cause major developmental anomalies in the skeleton and adjacent areas if critical 

tissues are destroyed. In addition, since children have a higher proportion of mitotic cells than adults, 

their rates of genotoxic damage are higher. This is because genetic lesions become fixed mutations when 

mitosis occurs before genetic damage is repaired. Genetic lesions in genes controlling the cell cycle can 

lead to the development of cancer and may be the basis of excess cancer cases attributed to exposure to 

radioactive strontium. Individuals with poor nutrition or deficiencies in vitamin D, such as those with 

osteomalacia, are theoretically more vulnerable to radioactive strontium because their lower absorption of 

calcium results in relatively higher rates of strontium incorporation into bone during the remodeling 

process that continues throughout life. The level of incorporation of radiostrontium into bone can be 

somewhat reduced by ingestion of alginates soon after exposure. Removal from bone after incorporation 

is not feasible. 

The major adverse effects of exposure to radioactive strontium, non-cancerous lesions of hematopoietic 

bone marrow tissue, cancer, and dystrophic lesions of the skeleton, are discussed below in greater detail. 

It should be noted that the large animal studies are more relevant than rodent studies to humans because 

the severity of bone marrow effects is inversely proportional to the diameter of the bone marrow cavity. 

Non-Cancerous Bone Marrow Effects (Including Acute Radiation Syndrome). Bone 

marrow effects are the most serious immediate consequences of exposure to high levels of radioactive 

strontium by either the inhalation or oral route. When absorbed radioactive strontium incorporates into 

bone, irradiation of the bone marrow results in hypoplasia of the hemopoietic tissue and pancytopenia, 
STRONTIUM 21 

2. RELEVANCE TO PUBLIC HEALTH 

with the severity depending on the dose. At the highest doses, acute radiation syndrome (anorexia, 

bloody diarrhea) would be expected because of the virtual destruction of the bone marrow. Acute 

radiation syndrome was not observed in the orally-exposed Techa River population, but was observed in 

dogs several weeks after receiving long-term retained body burdens of ≥47 :Ci 90Sr/kg (≥1.74 MBq/kg) 

following a single exposure to soluble 90SrCl2 by inhalation. Hemorrhaging is caused by the drastic 

depression in platelet counts; a severe drop in neutrophil counts precedes death. At lower exposure 

levels, pancytopenia is detectable, but is not immediately life-threatening. This was observed in dogs that 

received long-term retained burdens >10 :Ci 90Sr/kg (>0.37 MBq/kg) following a single inhalation 

exposure of soluble 90SrCl2

At lower levels of exposure, not all types of hematopoietic cells within bone marrow are affected, 

possibly because of differences in intrinsic rates of replacement. In the orally-exposed Techa River 

populations, milder chronic effects of bone marrow irradiation were reported in a small percentage of 

exposed individuals: leukopenia, thrombocytopenia, and granulocytopenia, as well as lymphopenia 

involving T lymphocytes and large granulocytic lymphocytes. Reduced lymphocyte counts, indicators of 

weakened immune function, in some individuals who received radiation to the bone marrow in excess of 

30 rem (0.3 Sv) per year, were implicated as the cause of the higher incidences of infectious disease in 

those who developed radiation-induced cancers. Suppression of the immune system is also supported by 

studies in pigs exposed to 625 :Ci 90Sr/day (23.13 MBq/day) in feed for 4–9 months or in dogs receiving 

single inhalation exposures of soluble (long-term retained burden >10 :Ci 90Sr/kg [>370 kBq/kg]) or 

insoluble (initial lung burden ≥5 :Ci 90Sr/kg [≥185 kBq/kg]) radioactive strontium. 

mice indicate that natural killer cells were preferentially eliminated. Chronic myeloid metaplasia, 

possibly related to genotoxicity, was another effect of bone marrow irradiation in orally-exposed pigs that 

received cumulative doses in excess of 40 rad (0.4 Gy) and in a small percentage of dogs that received 

≥0.4 :Ci 90Sr/kg/day (44.4 kBq/kg/day) from mid-gestation to 1.5 years. 

Injection studies in 

Cancer. Radioactive strontium, like other radionuclides, is a genotoxic carcinogen. Mutations in 

genes controlling the cell cycle can lead to cancer if the damage is not repaired before the next cell 

division; rapidly dividing cells, such as the hematopoietic cells in bone marrow, are especially vulnerable. 

Incorporation of radioactive strontium into bone places bone and the adjacent soft tissues at risk for 

cancer. Chronic consumption of radioactive strontium (and other radionuclides), leading to estimated 

doses to bone marrow in excess of 10 rem (0.1 Sv), significantly increased the incidence of leukemia in 

the Techa River population, but this effect was not observed in offspring exposed in utero who received 

lower doses. Leukemia has also been observed in animals exposed orally or by inhalation to soluble 
STRONTIUM 22 

2. RELEVANCE TO PUBLIC HEALTH 

radioactive strontium. Other cancers observed in animal studies include osteosarcomas, 

hemangiosarcomas, cancers of other soft tissues near bone, and, in feeding studies, nasal, oral, and 

periodontal carcinomas. In dogs that inhaled insoluble 90Sr, the particles lodged in the respiratory tract, 

causing cancers of the immediately surrounding tissues: hemangiosarcomas of the lung and heart and 

carcinomas of the respiratory tract. External exposure to 90Sr (solid source) in mice induced skin cancers 

(squamous cell carcinoma, basal cell carcinoma, fibrosarcoma) and, in one study, osteosarcomas. 

Immature organisms are potentially more vulnerable than adults to radioactive strontium partly because 

they have a higher proportion of cells in mitotic phase and partly because they incorporate relatively more 

radiostrontium into bone. In a multigenerational swine study, doses that were not carcinogenic in the 

females exposed as adults induced osteosarcomas in the F1 or F2 generations exposed from conception.

National Council on Radiation Protection and Measurements concluded that uncertainties remain 

regarding extrapolation from the high doses of 90Sr known to cause cancer in animals to the lower doses 

that might increase the incidence of leukemia in humans. The Council suggested that more basic 

knowledge on the mechanism of cancer induction by ionizing radiation would be required to understand 

the risk of internal exposure to 90Sr. EPA has determined that radioactive strontium is a known human 

carcinogen (Group A). EPA estimated that the risk of developing cancer following exposure to 8 pCi/L in 

drinking water is 1 in 100,000. The International Agency for Research on Cancer has determined that 

internally deposited radionuclides, such as radioactive strontium, are carcinogenic to humans (Group 1). 

Skeletal Effects. Dystrophic lesions of the skeleton occur when the level of oral exposure of soluble 

radioactive strontium is high enough that the amount incorporated into bone results in irradiation of the 

bone at levels exceeding natural repair mechanisms. The effect could occur by acute exposure to a very 

high dose, by intermediate-duration exposure at a moderate dose, or by chronic-duration exposure at a 

lower dose. Such lesions, primarily affecting articular and periarticular tissues, were reported in the 

Techa River populations that received mean radiation doses to the surface of bone in excess of 200 rem 

(2 Sv) following chronic oral exposure to radiostrontium, but not at the lower doses. 

Animal oral exposure studies support the findings in humans. Skeletal or dental effects in adults are less 

severe than in developing animals because in adults, incorporation of radioactive strontium is mainly 

restricted to the surfaces of bone or teeth. Incorporation throughout the developing bone renders it 

vulnerable to weakening as a result of focal necrosis from long-term irradiation. Intermediate-exposure at 

6 μCi/kg/day for 1–10 months reduced numbers of osteocytes and damaged blood vessels in the bone of 

adult rabbits. More severe effects damaging the bone structure (necrosis of vasculature, impaired 

transformation into cortical bone, and fracturing) were observed in dogs exposed in utero and chronically 
STRONTIUM 23 

2. RELEVANCE TO PUBLIC HEALTH 

into adulthood at 0.4 μCi/kg/day. Damage to developing teeth (disordered tooth structure and increased 

cell death of differentiating odontoblasts and pulp cells) has been reported in rabbits following injection 

of a very high dose (600 μCi 90Sr/kg), but effects were less severe in mature teeth. 

2.3 MINIMAL RISK LEVELS 

Inhalation MRLs 

Stable Strontium. Data on the toxicity of inhaled stable strontium are not suitable for derivation of an 

inhalation MRL: one case report of a woman exposed to an undetermined concentration of strontium 

mixed with other chemicals in smoke from an ignited flare (Federman and Sachter 1997). 

Radioactive Strontium. The main sources on the toxicity of inhaled radioactive strontium are two acuteduration studies in dogs reporting severe hematological and immunological effects following a single 

nose-only exposure to 90Sr as fused clay particles for several minutes (Jones et al. 1976) or strontium 

chloride (Gillett et al. 1987a). Inhalation of 90Sr fused-clay particles leading to initial lung burdens of 

5 μCi 90Sr/kg (185 kBq/kg) resulted in chronic significant depression of lymphocyte counts and 

suppression of immune function (Jones et al. 1976). Chronic thrombocytopenia and neutropenia, which 

persisted for 1,000 days in dogs at all tested exposure levels (long-term retained burdens at or above 

1 μCi 90Sr/kg; 0.04 MBq/kg), was observed in dogs exposed to soluble 90SrCl2 (Gillett et al. 1987a). 

These data were not considered adequate for derivation of an acute-duration inhalation MRL because the 

observed hematological and immunological effects were considered severe adverse effects. 

Oral MRLs 

Stable Strontium. 

•	 An MRL of 2.0 mg/kg/day has been derived for intermediate-duration oral exposure 

(15–364 days) to stable strontium and its compounds.
 

The most consistent effects of oral exposure to excess stable strontium are rickets (impaired cartilage 

calcification) and osteomalacia (impaired bone mineralization), especially in the young. One Turkish 

epidemiological study provided indirect evidence that excess oral exposure to strontium (in the presence 

of other predisposing factors) may contribute to the development of rickets in children (Ögzür et al. 

1996). Overall, animal studies on strontium have concentrated on the evaluation of skeletal effects, with 
STRONTIUM 24 

2. RELEVANCE TO PUBLIC HEALTH 

occasional consideration to body weight and serum chemistry. In young rodents, typical effects of excess 

strontium included an abnormal widening of the cartilaginous epiphyseal plates of the long bones, a lack 

of bone calcification, and abnormal deposition of unmineralized bone matrix or osteoid (Johnson et al. 

1968; Kshirsagar 1976; Marie and Hott 1986; Morohashi et al. 1994; Neufeld and Boskey 1994; Storey 

1962). The skeletal effects of strontium are known to be related to its chemical similarity to calcium and 

its suppression of vitamin D metabolism and intestinal calcium absorption (Armbrecht et al. 1998). 

Effects are more severe in young rats than in adults because the rate of skeletal incorporation of strontium 

is higher in young animals (see Section 3.5.2.2). 

A lowest-observed-adverse-effect level (LOAEL) of 550 mg strontium/kg/day is identified for bone 

mineralization abnormalities in weanling rats that were exposed to dietary strontium carbonate for 

20 days (Storey 1961). The epiphyseal plates of long bones were irregular and abnormally thick. 

Furthermore, areas of uncalcified bone matrix were deposited in the distal ends of the metaphyseal 

trabeculae and proximal end of the diaphyses. Irregularities in the organization of the cells of the 

hypertrophic zone, in the pattern of calcification, and in the deposition of osteoid were more conspicuous 

with increasing dose. In tibias, the dry weight, ash weight, ash percentage, and calcium in ash were 

significantly reduced with increased strontium intake. No effects on bone mineralization occurred in 

weanling rats ingesting 140 mg strontium/kg/day, the NOAEL for intemediate-duration exposure. In 

adult rats examined in this study, the effects of strontium ingestion were less severe in that higher doses 

were required to produce the same effect. The no-effect level in adults was 690 mg strontium/kg/day, 

which was higher than the LOAEL for weanlings. In adults, changes in tibial histology, such as abnormal 

thickening of the epiphyseal cartilages and abnormally widened metaphyseal osteoid seams, were noted at 

or above 1,370 mg strontium/kg/day. At 2,750 mg strontium/kg/day, osteoid tissue was deposited near 

vascular canals and the areas of bone resorption were reduced. In adult rat tibias, the dry weight, ash 

weight, ash percentage, and calcium in ash were only significantly affected at the highest dose. This 

study demonstrates the difference in sensitivity to strontium between young and old animals, which is 

caused by the higher rate of strontium incorporation into the developing skeleton in young animals. 

The critical dose levels identified in the Storey (1961) study are supported by other studies in rodents. 

Similar LOAELs (500–565 mg strontium/kg/day) for abnormal bone mineralization are identified in 

several studies on weanling rats exposed to strontium carbonate (Morohashi et al. 1994; Neufeld and 

Boskey 1994) or an unspecified form of strontium (Johnson et al. 1968). Slight skeletal effects were 

noted in mice exposed to 350 mg strontium/kg/day as strontium chloride (Marie and Hott 1986). In 

addition, similar no-observed-adverse-effect levels (NOAELs) in the range of 110–168 mg 
STRONTIUM 25 

2. RELEVANCE TO PUBLIC HEALTH 

strontium/kg/day for skeletal effects were identified from studies in weanling rats exposed to an 

unspecified form of strontium (Grynpas et al. 1996), strontium chloride hexahydrate (Kroes et al. 1977), 

or strontium carbonate (Morohashi et al. 1994). The study by Storey (1961) is preferred as the basis for 

the intermediate MRL because both young and adult animals were tested, the administered doses included 

NOAELs and LOAELs for both age groups, and the evaluation of skeletal effects included 

histopathological analysis. Some of the other studies have serious deficiencies that render them 

unsuitable for deriving an MRL. Two studies administered single doses of 166–168 mg/kg, but reported 

no adverse effects (Grynpas et al. 1996; Kroes et al. 1977); although the results support the NOAEL by 

Storey (1961), the lack of higher doses causing positive results raises uncertainty about the experiments. 

The study by Johnson et al. (1968) administered a single dose of 565 mg/kg that was a serious LOAEL 

for increased mortality. Three of the other studies had deficiencies that rendered them less suitable than 

Storey (1961). The study by Morohashi et al. (1994) did not analyze bone histopathology. Studies by 

Marie and Hott (1986) and Neufield and Boskey (1994) administered single doses of 350 and 500 mg/kg, 

respectively, which were LOAELs for skeletal effects, but the studies provided no information on noeffect levels or effects at higher doses. Therefore, the NOAEL of 140 mg strontium/kg/day for skeletal 

effects in weanling rats (Storey 1961) would appear to be the most appropriate basis for calculating an 

intermediate MRL. The NOAEL of 140 mg strontium/kg/day was divided by an uncertainty factor of 

30 (10 for extrapolation from animal to human and 3 for human variability) and a modifying factor of 

3 (for short study duration and limited end point examination). A partial uncertainty factor was used to 

account for human variability because the selected NOAEL was based on the response of juveniles, which 

is also the most sensitive human group. The resulting MRL is calculated to be 2.0 mg strontium/kg/day, 

which is approximately 40 times higher than the total estimated daily exposure to stable strontium of 

0.047 mg/kg/day. The MRL represents an estimate of daily human exposure that is likely to be without 

an appreciable risk of adverse health effects. Since the MRL is based on effects in young rats, it is 

considered to be protective of children, who are similar with respect to immaturity of the skeleton and 

high intestinal rates of strontium absorption. 

MRLs were not derived for acute- or chronic-duration oral exposures to stable strontium. The relevant 

acute data are limited to two lethality studies in mice (Ghosh et al. 1990; Llobet et al. 1991a) and two 

toxicity studies in rats (Kshirsagar 1976; Kroes et al. 1977). The rat studies were not considered suitable 

for MRL derivation. In the Kshirsagar (1976) study, the only administered dose, 3,000 mg strontium per 

kg/day as strontium phosphate, resulted in severe body weight effects (62% reduction in body weight 

gain) and was higher than the LD50 values reported for mice (Ghosh et al. 1990; Llobet et al. 1991a). The 

Kroes et al. (1977) study did not identify an adverse effect level. Limited data on the chronic toxicity of 
STRONTIUM 26 

2. RELEVANCE TO PUBLIC HEALTH 

stable strontium are available for humans and no data are available for animals. The available data 

involve patients with osteoporosis or other disorders of bone mineralization who were treated for several 

years with low doses of strontium in the form of strontium salts: strontium lactate (Shorr and Carter 

1952), strontium gluconate or strontium carbonate (Skoryna 1981a, 1984), and strontium ranelate 

(Meunier et al. 2002, 2004; Reginster 2002, 2003, Reginster et al. 2002). None of the studies reported 

adverse effects on bone or significant increases in side-effects related to treatment, but reporting was poor 

in some of the studies (Shorr and Carter 1952; Skoryna 1981a, 1984). These data are not suitable for 

MRL derivation for several reasons. All subjects in these studies were co-administered calcium and some 

were given vitamin D, both of which are known to interfere with strontium toxicity. In addition, all of the 

subjects were adults, the majority being postmenopausal women with osteoporosis. Considering that the 

intermediate oral MRL is based upon bone effects in juvenile rats, there is reason to suspect that a chronic 

oral MRL based on these data would not be protective of the most sensitive population (juveniles). 

Radioactive Strontium. No MRLs were derived for oral exposure to radioactive strontium, although the 

database includes chronic-duration human studies and acute-, intermediate-, and chronic-duration animal 

studies in several species. Strontium dosimetry information is available for the populations affected by 

contamination of the Techa River, but these exposures included simultaneous external gamma radiation 

from 137Cs, 106Ru, and 95Z and internal radiation from 137Cs, in addition to 89Sr and 90Sr (Kossenko et al. 

1994). The combined exposure studies are not suitable for the derivation of MRLs. An increase in the 

incidence of leukemia was reported for Techa River individuals receiving estimated bone marrow doses, 

attributed to radioactive strontium, in excess of 10 rem (0.1 Sv) (Kossenko 1996; Kossenko et al. 1997, 

2000, 2002). Dystrophic lesions of the skeleton were observed in individuals with mean radiation doses 

to the surface of bone in excess of 200 rem (2 Sv) (Akleyev et al. 1995). Studies on rodents are not 

suitable models for establishing MRL levels for human exposure to radioactive strontium because of their 

relatively smaller bone diameter which places their bone marrow tissues at greater risk of radiation 

damage. Most of the large animal studies reported serious hematological effects at all dose levels. 

Immunosuppression was observed in pigs fed 625 :Ci 90Sr/day (23.13 MBq/day) for 4–9 months 

(Howard 1970; Howard and Clarke 1970). Chronic myeloid metaplasia was another effect of bone 

marrow irradiation in orally-exposed pigs that received cumulative doses in excess of 40 rad (0.4 Gy) and 

a small percentage of dogs that received ≥0.4 :Ci 90Sr/kg/day (44.4 kBq/kg/day) from mid-gestation to 

1.5 years (Dungworth et al. 1969; Howard 1970; Howard and Clarke 1970). These serious effects are not 

suitable bases for determining MRL levels. 
STRONTIUM 27 

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 strontium. 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. 

Appendix D contains background information on radiation physics, chemistry, and biology. 

Naturally occurring strontium is a mixture of four stable (nonradioactive) isotopes, 84Sr, 86Sr, 87Sr, and 

88Sr, the last being the most abundant. Section 3.2 contains a discussion of the chemical toxicity of stable 

strontium; radiation toxicity associated with exposure to radiostrontium (primarily 90Sr and 89Sr) is 

discussed in Section 3.3. The chemical properties of stable and radioactive strontium isotopes are 

identical and are described in Chapter 4. 

Strontium is fairly reactive and therefore is rarely found in its pure form in the earth’s crust. Examples of 

common strontium compounds include strontium carbonate, strontium chloride, strontium hydroxide, 

strontium nitrate, strontium oxide, and strontium titanate. The most toxic strontium compound is 

strontium chromate, which is used in the production of pigments and can cause cancer by the inhalation 

route. Strontium chromate is not included in the Levels of Significant Exposure (LSE) tables for 

strontium since the carcinogenic effects of the compound are a function of the concentration of 

hexavalent chromium, and strontium only contributes to solubility. The Toxicological Profile for 

Chromium (Agency for Toxic Substances and Disease Registry 2000) should be consulted for additional 

information on the health effects of strontium chromate. 

There is no direct evidence that strontium is toxic to humans, but there is suggestive epidemiological 

evidence that the oral toxicity observed at high doses in juvenile laboratory animals may pertain to 

humans under special circumstances. Stable strontium is of relatively low toxicity. It comprises about 

4.6 ppm by weight of the human body, but does not have any recognized essential biological role. 

Human exposure to strontium is primarily by the oral route (via fruits, vegetables, and drinking water), 
STRONTIUM 28 

3. HEALTH EFFECTS 

although inhalation exposures are also possible. No toxic effects of stable strontium have been reported 

for the exposure levels normally encountered in the environment. Strontium is not readily absorbed 

through intact skin, but is absorbed through abraded skin and through puncture wounds. The biological 

effects of strontium are related to its chemical similarity to calcium, with both elements being found in 

Group 2 of the periodic table and forming divalent cations. However, since strontium is not the same size 

as calcium, it does not substitute precisely for calcium in biological processes. At different stages of the 

life cycle, organisms vary in their ability to discriminate between strontium and calcium, which may 

cause age-related differences in gastrointestinal absorption, and therefore in health effects. Because of its 

similarity to calcium, strontium accumulates to a high degree in bone, and, in high concentrations, may 

seriously interfere with the normal process of bone development. The young are particularly vulnerable 

because a lack of discrimination between calcium and strontium occurs during a dynamic period of bone 

formation and growth. For this reason, body burdens of strontium will be higher in children than in 

adults, and the health effects associated with high exposure levels would be more severe. As suggested in 

one human study and demonstrated in several animal studies, strontium ‘rickets’ is one potential 

consequence of childhood exposure to excess stable strontium. 

Beta emissions from 90Sr have a limited ability to penetrate through tissue (see Appendix D 

Section D.2.3). For that reason, radiostrontium must be internalized or placed in close contact with skin 

before adverse health effects will occur. The ‘bone-seeking’ behavior of strontium is the basis for 

concern regarding oral or inhalation exposures to the radioactive isotopes, particularly 90Sr, with its long 

half-life of 29 years and highly energetic 0.546 MeV beta particles, plus the 2.2 MeV beta particles of its 

short-lived 90Y decay product isotope. Radioactive strontium isotopes incorporate into bone and irradiate 

the bone cells, the hemopoietic bone marrow, and potentially, the soft tissues surrounding bone, 

especially in the skull. Human populations accidentally exposed to high levels of radiation from 

radiostrontium (and other radionuclides and external radiation) experienced chronic radiation sickness 

(postirradiation changes in hematological parameters) and increased leukemia and cancer mortality in the 

decades following exposure. In animal studies, high-level exposures to 90Sr led to death within weeks 

because of radiation damage to hemopoietic tissues. Longer-term lower level exposures that overcome 

genetic repair mechanisms may lead to myeloid leukemia, osteosarcoma, and lymphoma (only observed 

in some rodent studies). It should be understood that because strontium is retained for a long time in the 

skeleton, acute- or intermediate-duration uptakes (i.e., absorption events occurring within a period of 

<2 weeks or <1 year, respectively) can result in decade-long (i.e., chronic) effects from internal exposure 

to the radiation emitted from the retained isotopes. Children would appear to have a higher lifetime risk 

for cancer effects per unit uptake, because of their relatively higher rate of skeletal incorporation of 
STRONTIUM 29 

3. HEALTH EFFECTS 

strontium and potentially longer radiation exposure period. Immediately nonlethal exposures to high 

levels of radioactive strontium may contribute to suppression of the immune system. 

Limited human data are available regarding health effects that can be exclusively associated with 

exposure to radioactive strontium sources such as 90Sr and 89Sr. These radionuclides are products of 

nuclear fission and may, therefore, be released from sites where nuclear fission occurs, from radioactive 

material removed from such sites, or from leakage of radioactive strontium sources. Both 90Sr and 89Sr 

emit beta radiation that travels short distances and can penetrate the skin and superficial body tissues. 

The radiation dose from these radionuclides can be classified as either external (if the source is outside 

the body) or internal (if the source is inside the body). 

The external dose from strontium radionuclides emitting beta radiation outside the body is normally of 

little health concern unless the radioactive material contacts the skin. Skin contact can allow the beta 

radiation to pass through the epidermis to live dermal tissue where it becomes a major contributor to a 

radiostrontium-generated radiation dose to the skin. At very high doses, the beta radiation can cause such 

adverse effects as erythema, ulceration, or even tissue necrosis. 

Once radioactive strontium is internalized, it is absorbed, distributed, and excreted in the same manner as 

stable strontium; the chemical similarity of strontium to calcium results in deposition of radioactive 

strontium in bone. The internal radiation dose from strontium is actually a measure of the amount of 

energy that the beta emissions deposit in tissue. The short-range beta radiation produces a localized dose, 

generally to bone and the soft tissues adjacent to bone; hemopoietic bone marrow is the most biologically 

significant target of radioactive strontium emissions. Molecular damage results from the direct ionization 

of atoms that are encountered by beta radiation and by interactions of resulting free radicals with nearby 

atoms. Tissue damage results when the molecular damage is extensive and exceeds the capacity of 

natural repair mechanisms. 

In radiation biology, the term absorbed dose is the amount of energy deposited by radiation over time per 

unit mass of tissue, expressed in units of rad or gray (Gy) (see Appendix D for a detailed description of 

principles of ionizing radiation). The term dose equivalent refers to the biologically significant dose, 

which is determined by multiplying the absorbed dose by a quality factor for the type and energy of the 

radiations involved. Dose equivalent is expressed in units of rem or sievert (Sv). The quality factor is 

considered to be unity for the beta radiation emitted from 90Sr and 89Sr, so for these radionuclides, the 

absorbed dose (in rad or gray) is numerically identical to the dose equivalent (in rem or sievert). The dose 
STRONTIUM 30 

3. HEALTH EFFECTS 

equivalent from internalized strontium radionuclides is estimated using the quantity of material entering 

the body (via ingestion or inhalation), the biokinetic parameters for strontium (retention, distribution, and 

excretion), the energies and intensities of the beta radiation emitted, and the parameters describing the 

profile of absorbed radiation energy within the body. If, for example, a person ingests a given activity of 

radiostrontium (measured in curies [Ci] or becquerels [Bq]), the tissues of the body will absorb some of 

the energy of the emitted beta radiation in a pattern reflecting the kinetics of distribution and elimination 

of the ingested radiostrontium, the rate at which the radioactive isotope decays to a stable form, and the 

age of the person at the time of ingestion (which affects both the biokinetics of the radiostrontium and the 

potential length of time over which the tissues can be exposed to the radiation). Each tissue, therefore, 

can receive a different dose equivalent. The total dose equivalent for the body will reflect the integration 

of the dose equivalents for the various tissues using a weighting scheme for the relative sensitivities of 

tissues and organs. 

The EPA has published a set of internal dose conversion factors for standard persons of various ages 

(newborn; 1, 5, 10, or 15 years of age; and adult) in its Federal Guidance Report No. 13 supplemental CD 

(EPA 2000e). For example, the EPA has estimated that the dose equivalents following ingestion of 1 Bq 

of 90Sr are 2.77x10-8 and 2.77x10-7 Sv, respectively, for the adult and infant (assuming an integration time 

of 50 years for an adult following the initial exposure). For 89Sr, these values are 2.57x10-9 Sv and 

3.59x10-8 Sv, respectively. Age-specific dose coefficients for inhalation and ingestion of any of the 

radioactive isotopes of strontium by the general public can be found in ICRP publications 71 (ICRP 1995) 

and 72 (ICRP 1996), respectively. Dose coefficients for inhalation and ingestion of strontium 

radionuclides can be found in U.S. EPA Federal Guidance Report No. 11 (EPA 1988). Dose coefficients 

for external exposure to radioisotopes of strontium in air, surface water, or soil contaminated to various 

depths can be found in U.S. EPA Federal Guidance Report No. 12 (EPA 1993b). 

Unless otherwise stated, exposure levels in the text are presented per kg of body weight. In Appendix D, 

standard and SI units of radiation activity (curies, becquerels) and absorbed dose (rad, gray) are compared 

in Table D-5 and are discussed in Sections D.2.2 Half-Life and Activity and D.3.1.2 Absorbed Dose and 

Absorbed Dose-Rate. 
STRONTIUM 31 

3. HEALTH EFFECTS 

3.2 DISCUSSION OF HEALTH EFFECTS OF STABLE STRONTIUM BY ROUTE OF 

EXPOSURE 

Section 3.2 discusses the chemical toxicity of strontium. Radiation toxicity resulting from exposure to 

radiostrontium is discussed in Section 3.3. 

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, 

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). 

Levels of significant exposure for each route and duration are presented in tables and illustrated in 

figures. The points in the figures showing no-observed-adverse-effect levels (NOAELs) or lowestobserved-adverse-effect levels (LOAELs) reflect the actual doses (levels of exposure) used in the studies. 

LOAELs have been 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. ATSDR acknowledges that a 

considerable amount of judgment may be required in establishing whether an end point should be 

classified as a NOAEL, "less serious" LOAEL, or "serious" LOAEL, and that in some cases, there will be 

insufficient data to decide whether the effect is indicative of significant dysfunction. However, the 

Agency has established guidelines and policies that are used to classify these end points. ATSDR 

believes that there is sufficient merit in this approach to warrant an attempt at distinguishing between 

"less serious" and "serious" effects. The distinction between "less serious" effects and "serious" effects is 

considered to be important because it helps the users of the profiles to identify levels of exposure at which 

major health effects start to appear. LOAELs or NOAELs should also help in determining whether or not 

the effects vary with dose and/or duration, and place into perspective the possible significance of these 

effects to human health. 

The significance of the exposure levels shown in the Levels of Significant Exposure (LSE) tables and 

figures may differ depending on the user's perspective. Public health officials and others concerned with 

appropriate actions to take at hazardous waste sites may want information on levels of exposure 

associated with more subtle effects in humans or animals (LOAELs) or exposure levels below which no 
STRONTIUM 32 

3. HEALTH EFFECTS 

adverse effects (NOAELs) have been observed. Estimates of levels posing minimal risk to humans 

(Minimal Risk Levels or MRLs) may be of interest to health professionals and citizens alike. 

Levels of exposure associated with carcinogenic effects (Cancer Effect Levels, CELs) of strontium are 

indicated in Tables 3-2, 3-3, and 3-4 and Figures 3-2 and 3-3. Because cancer effects could occur at 

lower exposure levels, Figures 3-2 and 3-3 also show a range for the upper bound of estimated excess 

risks, ranging from a risk of 1 in 10,000 to 1 in 10,000,000 (10-4 to 10-7), as developed by EPA. 

Estimates of exposure levels posing minimal risk to humans (Minimal Risk Levels or MRLs) have been 

made for strontium. An MRL is defined as an estimate of daily human exposure to a substance that is 

likely to be without an appreciable risk of adverse effects (noncarcinogenic) over a specified duration of 

exposure. 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 within a given route of exposure. 

MRLs are based on noncancerous health effects only and do not consider carcinogenic effects. MRLs can 

be derived for acute, intermediate, and chronic duration exposures for inhalation and oral routes. 

Appropriate methodology does not exist to develop MRLs for dermal exposure. 

Although methods have been established to derive these levels (Barnes and Dourson 1988; EPA 1990), 

uncertainties are associated with these techniques. Furthermore, ATSDR acknowledges additional 

uncertainties inherent in the application of the procedures to derive less than lifetime MRLs. As an 

example, acute inhalation MRLs may not be protective for health effects that are delayed in development 

or are acquired following repeated acute insults, such as hypersensitivity reactions, asthma, or chronic 

bronchitis. As these kinds of health effects data become available and methods to assess levels of 

significant human exposure improve, these MRLs will be revised. 

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

the interpretation of the tables and figures for Levels of Significant Exposure and the MRLs. 
STRONTIUM 33 

3. HEALTH EFFECTS 

3.2.1 Inhalation Exposure 

3.2.1.1 Death 

The only studies located regarding death in humans following inhalation exposure to stable strontium are 

related to strontium chromate. Strontium chromate has been implicated as a cause of increased deaths 

from lung cancer in occupational studies (Davies 1979, 1984) (see Section 3.2.1.7). The toxicity of 

strontium chromate is attributed to hexavalent chromium ion, which enters lung cells and is metabolized 

to a genotoxic agent. Strontium itself contributes to solubility of strontium chromate, but any associated 

health effect is expected to be masked by that of the chromate. No studies were located regarding death 

in animals following inhalation exposure to stable strontium. 

3.2.1.2 Systemic Effects 

No data are available regarding systemic effects following inhalation exposure to stable strontium for 

which the exposure levels are known. For that reason, no LSE table has been created for stable strontium. 

No studies were located that described gastrointestinal, hematological, hepatic, renal, body weight, 

metabolic, endocrine, dermal, or ocular effects in humans or animals following inhalation exposure to 

stable strontium. 

Respiratory Effects. The only report of adverse respiratory effects in humans resulting from the 

inhalation of stable strontium is a case report of an anaphylactic reaction to smoke from an ignited 

roadside flare (Federman and Sachter 1997). The flare contained approximately 75% strontium nitrate 

(31% strontium), among other known irritating ingredients, and the exact contribution of strontium to the 

effect is uncertain. The anaphylactic reaction to the smoke included coughing, wheezing, and severe 

respiratory difficulties. This case report is discussed in Section 3.2.1.3 Immunological and 

Lymphoreticular Effects. No other reports were located describing longer-term respiratory effects 

following inhalation of stable strontium compounds by humans or animals. 

Cardiovascular Effects. A single study documented adverse cardiovascular effects in humans 

resulting from the inhalation of stable strontium in smoke from an ignited roadside flare (Federman and 

Sachter 1997). Extreme tachycardia resulted as part of an anaphylactic reaction to the smoke, which 

contained ~31% strontium as strontium nitrate, in addition to other known irritants. The role of strontium 
STRONTIUM 34 

3. HEALTH EFFECTS 

in this reaction is not established. No other reports were located describing longer-term cardiovascular 

effects following inhalation of stable strontium compounds by humans or animals. 

3.2.1.3 Immunological and Lymphoreticular Effects 

The single located study of immunological effects in humans following inhalation exposure to stable 

strontium is a case report of an anaphylactic reaction to smoke from an emergency roadside flare 

(Federman and Sachter 1997). A 35-year-old female paramedic developed a sudden, severe reaction upon 

inhaling fumes from a flare that contained approximately 31% strontium as strontium nitrate. Initial 

symptoms included coughing, wheezing, and shortness of breath that was not responsive to albuterol, 

epinephrine, or steroids; recovery ultimately required sedation, intubation, and intensive care for several 

days. Although the paramedic had been unsymptomatic before the incident, her medical history included 

several significant contributory factors: rheumatic fever requiring penicillin prophylaxis until age 12, a 

severe anaphylactic reaction to a bee sting at age 23, and adult-onset asthma at age 32. The ingredients of 

the flare (Road Fusee®; Standard Fusee Corporation, Easton, Maryland) included ±75% strontium nitrate 

(~31% strontium), ±10% potassium perchlorate, ±10% sulfur, and ±10% sawdust/oil binder. Upon 

combustion, each of these would yield products known to be irritating to the respiratory tract: strontium 

oxide, nitrous oxide, potassium oxide, chlorine gas, sulfur dioxide, and particulates. Thus, the exact 

contribution of strontium to the development of anaphylaxis in this case is uncertain. However, see 

Section 3.6.2 for a possible mechanism by which strontium could contribute to an immunological effect. 

No studies were located regarding immunological effects in animals following inhalation exposure to 

stable forms of strontium. 

No studies were located regarding the following effects in humans or animals following inhalation 

exposure to stable strontium: 

3.2.1.4 Neurological Effects 

3.2.1.5 Reproductive Effects 

3.2.1.6 Developmental Effects 
STRONTIUM 35 

3. HEALTH EFFECTS 

3.2.1.7 Cancer 

There were no reports regarding cancer in humans or animals resulting from inhalation exposure to stable 

strontium compounds except for strontium chromate. In an epidemiological study, no excess risk for lung 

cancer was found among workers in two Japanese factories who were involved in the production of 

strontium chromate pigment (Kano et al. 1993). However, exposures to strontium chromate in the 

factories may have been low because of suitable industrial hygiene procedures. Another epidemiological 

study examined workers in British chromate pigment manufacturing plants (Davies 1979, 1984). In one 

factory, both lead and zinc chromate were produced until 1976, and strontium chromate was produced 

from 1950 to 1968. For lung cancer deaths in workers exposed to ‘high’ and ‘medium’ levels of 

chromates before 1961, when industrial hygiene improvements were introduced, the observed/expected 

ratio (O/E) was 6/1.61, with a standard mortality ratio (SMR) of 373 (p<0.01). For workers exposed to 

‘high’ and medium’ levels from 1961 to 1967, the values were O/E=5/089, SMR=562 (p<0.01). The 

contribution of strontium to toxicity in these studies was not addressed. 

No standard inhalation study of strontium chromate in animals was located. However, Levy et al. (1986) 

used an intrabronchial pellet implantation technique to evaluate the carcinogenicity of 23 different 

commercially available chromates, including two batches of strontium chromate. Metal pellets were 

coated with a mixture of cholesterol and strontium chromate and implanted into the left bronchus of male 

and female young rats (100 per group). Of 198 lungs treated with strontium chromate, 105 (53%) had a 

primary keratinizing squamous carcinoma of the bronchial epithelium. The authors indicated that 

carcinogenicity was associated with sparingly soluble hexavalent chromium compounds such as 

strontium, calcium, or zinc chromates. 

3.2.2 Oral Exposure 

There are no direct dose-response data for adverse effects of exposure to stable strontium in humans, but 

one epidemiological study suggests that the skeletal toxicity observed at high oral doses in juvenile 

animals may be relevant to humans (see Musculoskeletal Effects). At low exposure levels, ingestion of 

stable strontium poses no harm to organisms with access to adequate calcium, phosphorus, and vitamin D. 

At higher exposure levels, especially under conditions of inadequate calcium, phosphorus, and vitamin D, 

stable strontium will interfere with normal bone development, causing ‘strontium rickets’ of variable 

severity. 
STRONTIUM 36 

3. HEALTH EFFECTS 

3.2.2.1 Death 

No deaths in healthy humans have been reported after oral exposure to stable strontium. Stable strontium 

caused death in laboratory animals only at doses that are very high compared to normal human exposure. 

In acute exposure studies in mice, the oral LD50 for strontium nitrate was reported to be 2,350 mg 

strontium/kg in males (Llobet et al. 1991a). For strontium chloride administered by gavage, the acute oral 

LD50 in albino mice was reported to be 2,900 mg strontium/kg for males and 2,700 mg strontium/kg for 

females (Ghosh et al. 1990). 

In intermediate-duration animal studies, ingestion of excess stable strontium resulted in increased 

mortality. The premature death rate was 40% among weanling male Sprague-Dawley rats fed stable 

strontium (form not specified) at a dose level of 565 mg strontium/kg/day for 43 days (Johnson et al. 

1968). Weanling male Wistar rats exposed to strontium phosphate in the diet at a dose level of 2,820 mg 

strontium/kg/day for 4–6 weeks had a mortality rate of 30%, but no mortality occurred at 580 or 1,270 mg 

strontium/kg/day (Kshirsagar 1976). From an analysis of a pair-fed group (food intake matched to the 

high-dose group), the author concluded that the increased mortality in the high-dose group was not related 

to reduced food intake, but rather to the ingestion of strontium. No studies were located regarding death 

in animals following chronic-duration oral administration of stable strontium. 

All reliable LOAEL values for death from stable strontium in each species and duration category are 

recorded in Table 3-1 and plotted in Figure 3-1. 

3.2.2.2 Systemic Effects 

No studies were located regarding dermal or ocular effects in humans or animals following oral exposure 

to stable strontium. The highest reliable NOAEL and all LOAEL values for the systemic effects from 

oral exposure to stable strontium in each species and duration category are shown in Table 3-1 and plotted 

in Figure 3-1. 

Respiratory Effects. No studies were located regarding respiratory effects in humans following oral 

exposure to stable strontium. No studies were located regarding acute or chronic respiratory effects in 

animals following exposure to stable forms of strontium. In one intermediate-duration study, respiratory 

difficulties were noted in rats following lethal ingestion of 565 mg strontium/kg/day of stable strontium 
Table 3-1 Levels of Significant Exposure to Strontium - Chemical Toxicity - Oral 

Exposure/ LOAEL
 

Duration/

a

Key to Species Frequency NOAEL Less Serious Serious 

(Specific Route) figure (Strain) System (mg/kg/day) (mg/kg/day) (mg/kg/day) 

ACUTE EXPOSURE Death 

1 Mouse once 

2900 M (LD50)
 (albino) (GW) 

c

2700 F (LD50) 

2 Mouse NR 

2350 M (LD50)
 (NS) (NS) 

Systemic 

3 Rat 2 wks 

ad lib Hemato 110 (Wistar) 

(F) 

Musc/skel 110 

Hepatic 110 Renal 110 Bd Wt 110 
Table 3-1 Levels of Significant Exposure to Strontium - Chemical Toxicity - Oral (continued) 

a

Key to Species 

figure (Strain) 

Exposure/ 

Duration/

Frequency 

(Specific Route) System 

NOAEL 

(mg/kg/day) 

LOAEL
 

Less Serious 

(mg/kg/day) 

Serious 

(mg/kg/day) 

4 5 6 

Rat 2 wks 

ad lib (Wistar) 

(F) 

INTERMEDIATE EXPOSURE Death 

Rat PND 21-64 

ad lib (SpragueDawley) (F)

Rat 4-6 wks 

ad lib (Wistar) 

(F) 


 

Gastro Musc/skel Hepatic Bd Wt 

3000 M (small intestine: decr acid & 

alkaline phosphatase; reversible) 

3000 M (bone: incr alkaline

phosphatase; reversible)

3000 M (incr alk phosphatase, decr acid 

phosphatase; reversible) 


 


 

3000 M (bd wt gain decr 62%) 

565 M (40% mortality) 

2820 M (30% mortality) 
a

Key to 

figure 

Species 

(Strain) 

LOAEL 

NOAEL Less Serious

System 

Table 3-1 Levels of Significant Exposure to Strontium - Chemical Toxicity -

(mg/kg/day) (mg/kg/day) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) 

Oral 

Serious 

(mg/kg/day) 

(continued) 

7 

Systemic 

(SpragueDawley) Rat 8 wks 

ad lib (W) 

Musc/skel 168 M Bd Wt 168 M Metab 168 M 

8 

(SpragueDawley) Rat PND 21-64 

ad lib (F) 

Resp 565 M (unspecified difficulties) 

Musc/skel 565 M (rickets) 

9 

(Wistar) Rat 90 d 

ad lib (F) 

Hemato 166 F 

Musc/skel 166 F Hepatic 166 F Renal 166 F Bd Wt 166 F Metab 166 F 
a

Key to 

figure 

Species 

(Strain) 

LOAEL 

NOAEL Less Serious

System 

Table 3-1 Levels of Significant Exposure to Strontium - Chemical Toxicity - Oral 

(mg/kg/day) (mg/kg/day) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) 

Serious 

(mg/kg/day) 

(continued) 

10 

(Wistar) Rat 4-6 wks 

ad lib (F) 

Cardio 2820 M (hemorrhage) 

Gastro 580 M 1270 M (small intestine: reversible decr 

alkaline phosphatase) 

Musc/skel 580 M 1270 M (bone: incr alkaline 

phosphatase, reversible) 

Hepatic 1270 M 2820 M (reversible decr alkaline 

phosphatase) 

Bd Wt 580 M 1270 M (reversible decr in wt gain) 

11 

(SpragueDawley) Rat 9 wks 

ad lib (W) 

Musc/skel 524 M 633 M (bone calcification rate decr by 

17%) 

Bd Wt 633 M Metab 633 M 
Table 3-1 Levels of Significant Exposure to Strontium - Chemical Toxicity - Oral (continued) 

Exposure/ LOAEL

Duration/ a Frequency 

Key to Species NOAEL Less Serious Serious (Specific Route) figure (Strain) System (mg/kg/day) (mg/kg/day) (mg/kg/day) 

12 Rat 4 wk 

Musc/skel 1970 M (tibiae: length decr 33%, ad lib (Wistar) epiphyseal plates 5 x wider, 

(F) decr mineralization) 

Bd Wt 1970 M (bd wt gain decr by 60%) 

13 Rat 27 d 

Gastro ad lib 102 510 F (20% decr net intestinal Ca2+ (Wistar) 

absorption) (F) 

Musc/skel 102 510 F (decr bone formation, 

resorption, Ca2+ content of 

	 

bone) 


 

Bd Wt 510 F Metab 102 F 510 F (hypocalcemia) 

14 Rat 3 wk 

Musc/skel ad lib 500 M (abnormal bone mineralization) (Sprague- 

Dawley) (F)

Bd Wt 500 M Metab 500 M 

	 

	 


 

	 	 	 

	 	 	 
a

Key to 

figure 

Species 

(Strain) 

LOAEL 

NOAEL Less Serious

System 

Table 3-1 Levels of Significant Exposure to Strontium - Chemical Toxicity - Oral 

(mg/kg/day) (mg/kg/day) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) 

Serious 

(mg/kg/day) 

(continued) 

15 

(England Wright Y) Rat PND 21-41 

ad lib (F) 

Musc/skel 1850 M (epiphyseal cartilage 

histopathology) 

Bd Wt Metab 1850 M 

1850 M (28% decr bd wt gain) 

16 

(NS) Rat 20 d 

ad lib (F) 

Musc/skel 140 F 

b

550 F (tibial epiphyseal cartilage 

abnormally wide) 

Bd Wt Metab 

1460 F 4975 F 

2220 F (24% decr bd wt gain) 

17 

(NS) Rat 20 d 

ad lib (F) 

Musc/skel 690 F 1370 F (tibial epiphyseal cartilage 

abnormally wide; incr metaphyseal osteoid) 

Bd Wt 2750 F Metab 2750 F 
a

Key to 

figure 

Species 

(Strain) 

LOAEL 

NOAEL Less Serious

System 

Table 3-1 Levels of Significant Exposure to Strontium - Chemical Toxicity - Oral 

(mg/kg/day) (mg/kg/day) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) 

Serious 

(mg/kg/day) 

(continued) 

18 

(NS) Rat up to 7 months 

ad lib (F) 

Musc/skel 2160 (rickets) 

Bd Wt 2160 (30% decr bd wt gain) 

19 

(NS) Rat >7 mo 

ad lib (F) 

Musc/skel 1570 (rickets: abnormal bone 

mineralization) 

20 

(SpragueDawley) Rat 26 d 

ad lib (F) 

Musc/skel 1520 M (rickets) 

Endocr 1520 M Bd Wt 1520 M (16% decr bd wt gain) Metab 1520 M 

21 

(C57BL/6J) Mouse 29 d 

ad lib (W) 

Musc/skel 350 M (11% decr number of 

osteoclasts; decr bone resorption; 10% incr osteoid surface) 

Bd Wt 350 M Metab 350 M 
Table 3-1 Levels of Significant Exposure to Strontium - Chemical Toxicity - Oral (continued) 

a

Key to 

figure 

Species 

(Strain) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(mg/kg/day) 

Less Serious 

(mg/kg/day) 

LOAEL 

Serious 

(mg/kg/day) 

22 

Neurological 

PND 21-64 

(Sprague- (F)Dawley) Rat 565 M (paralysis of hindlimbs) 

a The number corresponds to entries in Figure 3-1. b Used to derive an intermediate oral MRL of 2.0 mg/kg/day. The MRL was derived by dividing the NOAEL by an uncertainty factor of 30(10 for extrapolation 

humans, and 3 for human variability), and by a modifying factor of 3(for limited endpoint examination and short duration). 

c Differences in levels of health effects and cancer effects between males and females are not indicated in Figure 3-2. Where such differences exist, only the l

most sensitive gender are presented. 

Ad lib - ad libitum; Bd Wt = body weight; Cardio = cardiovascular; d = day(s); decr = decreased; (F) = food; Gastro = gastrointestinal; (GW) = gavage in water; 

hematological; hr = hour(s); incr = increased; LD50 = lethal does, 50% kill; LOAEL = lowest-observed-adverse-effect level; Metab = metabolic; Musc/skel = m= no-observed-adverse-effect level; NR = not reported; (NS) = not specified; PND = post natal day; wk = week(s); x = time(s); yr = year(s) 
Gastrointestinal Hematological Musculoskeletal Hepatic Renal Body W

10000 

Death eight 

Figure 3-1 Levels of Significant Exposure to Strontium - Chemical Toxicity - Oral 

Acute (≤14 days) 

Systemic 

mg/kg/day 

4r 4r 4r 4r 

1m
 2m
 

1000 

3r 3r 3r 3r 3r 

100 

c-Cat -Humans f-Ferret n-Mink Cancer Effect Level-Animals Cancer Effect Level-Humans 

d-Dog k-Monkey j-Pigeon o-Other LOAEL, More Serious-Animals LOAEL, More Serious-Humans 

r-Rat m-Mouse e-Gerbil LOAEL, Less Serious-Animals LOAEL, Less Serious-Humans 

p-Pig h-Rabbit s-Hamster NOAEL - Animals NOAEL - Humans 

q-Cow a-Sheep g-Guinea Pig 
Respiratory Cardiovascular Gastrointestinal Hematological Musculoskeletal Hepatic Renal 

10000 

Death E

Figure 3-1 Levels of Significant Exposure to Strontium - Chemical Toxicity - Oral (Continue

Intermediate (15-364 days) 

Systemic 

mg/kg/day 

6r 10r 10r 

18r 12r 15r 19r 20r 2

10r 10r 17r 10r 

1000 

11r 17r 10r 5r 8r 8r 10r 11r 13r 16r 13r 14r

21m 

9r 7r 9r 9r 9r 

16r 

100 13r 13r

10 

1 

c-Cat -Humans f-Ferret n-Mink Cancer Effect Level-Animals Cancer Effect Level-Humans 

d-Dog k-Monkey j-Pigeon o-Other LOAEL, More Serious-Animals LOAEL, More Serious-Humans 

r-Rat m-Mouse e-Gerbil LOAEL, Less Serious-Animals LOAEL, Less Serious-Humans 

p-Pig h-Rabbit s-Hamster NOAEL - Animals NOAEL - Humans 

q-Cow a-Sheep g-Guinea Pig 
Metabolic Neurological 

10000 

Body Weight 

Figure 3-1 Levels of Significant Exposure to Strontium - Chemical Toxicity - Oral (Continue

Intermediate (15-364 days) 

Systemic 

mg/kg/day 

16r 

17r 17r 16r 18r 12r 15r 15r 

16r 20r 20r 10r 

1000 

11r 11r 10r 22r 13r 14r 13r 14r 

21m 21m 

7r 9r 7r 9r 

100 13r

10 

1 

c-Cat -Humans f-Ferret n-Mink Cancer Effect Level-Animals Cancer Effect Level-Humans 

d-Dog k-Monkey j-Pigeon o-Other LOAEL, More Serious-Animals LOAEL, More Serious-Humans 

r-Rat m-Mouse e-Gerbil LOAEL, Less Serious-Animals LOAEL, Less Serious-Humans 

p-Pig h-Rabbit s-Hamster NOAEL - Animals NOAEL - Humans 

q-Cow a-Sheep g-Guinea Pig 
STRONTIUM 48 

3. HEALTH EFFECTS 

(form unspecified) for 4–6 weeks (Johnson et al. 1968). No description of the respiratory effects or 

incidence data were reported. 

Cardiovascular Effects. No studies were located regarding cardiovascular effects in humans 

following acute- or intermediate-duration oral exposure to stable strontium. 

One epidemiological study examined the relationship between trace metals, including strontium, in 

drinking water and the rates of various kinds of vascular disease in 24 communities in the lowest quartile 

of the economic scale in Texas (Dawson et al. 1978). The concentration of strontium was measured in 

samples of drinking water and 2,187 urine samples from subjects (aged 5–97 years) in families that had 

resided within their respective communities for at least 10 years. There was a significant correlation 

between mean strontium levels in drinking water and in the urine. However, the only statistically 

significant product-moment correlationship for strontium (in urine and in drinking water) was for a 

decreased community mortality rate (in people over 45 years old) for hypertension with heart disease. 

There was no correlation found between strontium and mortality from arteriosclerotic and degenerative 

heart disease, other heart diseases, hypertension, general arteriosclerosis, or vascular diseases of the 

central nervous system. 

No studies were located regarding cardiovascular effects after acute- or chronic-duration oral exposure in 

animals. In male weanling Wistar rats (5–6 per group) given strontium as strontium phosphate in the diet 

for 4–6 weeks, hemorrhage (unspecified) occurred at 2,820 mg strontium/kg/day, possibly related to the 

increased mortality at this dose level, but not at or ≤1,270 mg strontium/kg/day (Kshirsagar 1976). 

Gastrointestinal Effects. No studies were located regarding gastrointestinal effects in humans 

following oral exposure to stable strontium. 

No studies were located regarding gastrointestinal effects in animals following chronic-duration oral 

exposure to various forms of stable strontium. Acute- and intermediate-duration oral studies in animals 

have examined gastrointestinal effects that would be likely to influence calcium and phosphorus 

metabolism. Decreases in acid and alkaline phosphatase activities were observed in the small intestine of 

5–6 male weanling (21 days old) Wistar rats given 3,000 mg strontium/kg/day as strontium phosphate for 

2 weeks (Kshirsagar 1976). These effects were reversed by giving the rats a normal low-strontium diet 

for 2 weeks. The biological significance of the decreased phosphatase activities is not known. Studies in 
STRONTIUM 49 

3. HEALTH EFFECTS 

chickens first demonstrated the relationship between strontium toxicity, calcium, and vitamin D. In male 

white Leghorn chickens raised on a diet deficient in vitamin D for the first 2 weeks of life, ingestion of 

>2,300 mg strontium/kg/day as strontium carbonate in a low-calcium, low-vitamin D diet for 11–14 days, 

affected calcium transport in the duodenum (Omdahl and DeLuca 1972). Strontium ingestion reduced the 

duodenal activation of vitamin D3 (conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol), reduced the activity of calcium binding protein, and reduced the absorption of calcium 

by the duodenum. Similar effects were observed in chickens given excess strontium in a diet with 

adequate vitamin D, but deficient in calcium (0.01%) (Corradino and Wasserman 1970; Corradino et al. 

1971a, 1971b). In addition, excess strontium ingestion significantly reduced the absorption of glucose, 

histidine, and alanine by the duodenum to levels typical of rachitic (vitamin D-deprived) chickens 

(Corradino et al. 1971b). The effects of strontium on calcium transport by the duodenum were reversed 

by transferring chickens to a normal low-strontium diet containing adequate amounts of vitamin D3 and 

calcium. The chicken data are not included in Table 3-2, because the physiological rates are likely to be 

very different from mammals, and also because health risk assessment methodology is currently limited 

to mammals. However, these phenomena were confirmed in a recent study in rats (Armbrecht et al. 

1998). Six days on a diet low in calcium, but containing 0.8% strontium, was sufficient to suppress the 

serum levels of activated vitamin D, the concentrations of calbindin D protein (two calcium-binding 

protein induced by vitamin D; see Sections 3.6.1 and 3.6.2), and the rates of calcium transport in the 

duodenum of young, adult, and old rats. 

In male weanling (3 weeks old) Wistar rats (5–6 per group) given strontium phosphate in the diet for 

6 weeks, a decrease in alkaline phosphatase activity in the small intestine occurred at 1,270 mg 

strontium/kg/day, but not at 580 mg strontium/kg/day (Kshirsagar 1976). This decrease in enzyme 

activity was partly reversed by feeding the rats a normal low-strontium diet for 2 weeks. As mentioned 

above, the biological significance of these changes in phosphatase activity is not known. In slightly older 

female juvenile Wistar rats (36 days old, 6–8 per group) that ingested 510 mg strontium/kg/day as 

strontium carbonate for 27 days, the net intestinal absorption of calcium was reduced by 20%, but no 

effects occurred at 100 mg strontium/kg/day (Morohashi et al. 1994). In male white Leghorn chickens 

fed 255 mg strontium/kg/day (probably as carbonate) in a diet low in vitamin D3 for the first 16 days after 

hatching, the conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol and the transport 

of calcium were suppressed in the duodenum (Omhdahl and DeLuca 1971). This study is omitted from 

Table 3-1 because of probable differences in physiology. 
STRONTIUM 50 

3. HEALTH EFFECTS 

Hematological Effects. No studies were located regarding hematological effects in humans 

following oral exposure to stable strontium. 

No studies were located regarding hematological effects in animals following chronic-duration oral 

exposure to stable strontium. In adult Wistar rats given up to 110 mg strontium/kg/day as strontium 

chloride in the diet for 2 weeks, the total number of erythrocytes was slightly elevated in both sexes, and 

the leucocyte count was slightly elevated in males at the highest dose level at termination (Kroes et al. 

1977). However, since the results were not reported quantitatively, the significance of this information is 

uncertain. No hematological changes were observed among weanling Wistar rats fed up to 166 mg 

strontium/kg/day as strontium chloride in the diet for 90 days (Kroes et al. 1977). However, the relatively 

high level of calcium (0.85%) in the diet given to these animals may have reduced absorption and 

therefore the effect of strontium. 

Musculoskeletal Effects. No studies were located regarding musculoskeletal effects in humans after 

acute-duration oral exposure to stable strontium. The only long-term human exposure study is an 

epidemiological study that was carried out in the Ulaş Health Region of Sivas, Turkey (Özgür et al. 

1996). This region has a high prevalence of childhood rickets, 32% compared to 4.4% nationally among 

children aged up to 5 years, and the study sought to determine whether higher levels of strontium in the 

soil might be a contributing factor. Soils surrounding 55 villages were characterized as to strontium 

concentration (Group 1, >350 ppm; Group 2, <350 ppm). A total of 2,140 children (ages 6–60 months) 

from these localities (613 in Group 1 and 1,527 in Group 2) were examined for one or more signs of 

rickets: craniotabes (localized craniomalacia or thinning of cranium), rachitic rosary (beadlike growths at 

the ends of ribs where they join cartilage), conspicuous bulging at the wrist, bony deformities of the legs 

(bowleg, knock-knee), and delayed closure of the fontanelles. A significantly higher proportion of 

Group 1 children had one or more rachitic signs than those in Group 2: 37.5 vs 19.5%. In addition, the 

severity of disease (number of rachitic signs per child) was proportionally higher in Group 1 (p<0.001). 

For each cohort, the incidence of rickets was higher in Group 1 than in Group 2 and the differences were 

statistically significant for ages 6–12, 13–18, 25–36, and 37–48 months (odds ratios 1.66–2.55). When 

the duration of breast feeding was considered, the incidence of rickets within the two groups did not differ 

for children breast fed for 24 months or longer. However, for shorter periods of breast feeding, between 0 

and 24 months, the incidence of rickets was significantly higher in Group 1 (odds ratios 1.79–3.14). The 

implication of this study is that breast feeding may be protective against strontium toxicity in nursing 

infants, probably by providing both calcium and protein, both of which tend to reduce the incorporation of 

strontium into bone (see Sections 3.10, 3.11, and 3.12.2). The authors attributed the higher incidence of 
STRONTIUM 51 

3. HEALTH EFFECTS 

rickets in Group 1 children to their diet, which, after weaning, is mainly based on grains grown in 

strontium-rich soil. 

No studies were located regarding musculoskeletal effects in animals after chronic-duration oral exposure 

to stable strontium. Acute- and intermediate-duration studies in animals documented significant adverse 

effects of strontium on bone that were especially severe in the young. In an acute-duration study, there 

was no effect on bone in groups of adult SPF Wistar rats that ingested up to 110 mg strontium/kg/day as 

strontium chloride in the diet for 2 weeks (Kroes et al. 1977). Strontium was detected in bone following 

ingestion of 11 or 110 mg/kg/day, but not at lower doses (0.1 or 1.0 mg/kg/day). Among male weanling 

(21 days old) Wistar rats that ingested 3,000 mg strontium/kg/day as strontium phosphate in the diet for 

2 weeks, alkaline phosphatase activity was significantly increased in bone compared to controls 

(Kshirsagar 1976). The author speculated that the observed increase in alkaline phosphatase activity may 

have been related to a stimulation of osteoblasts, which secrete osteoid and have a high alkaline 

phosphatase content. In acute studies on young chickens fed 2,300–2,400 mg/kg/day of strontium, and an 

inadequate level of calcium, severe defects in bone organization and decreased mineralization were 

observed within 1 or 2 weeks (Corradino and Wasserman 1970; Corradino et al. 1971a, 1971b; Omdahl 

and DeLuca 1972): abnormally wide hypertrophic cartilaginous zone and impaired endochondral 

ossification (the removal of hypertrophic cartilage and its replacement by bone). As noted above, the 

chicken data are omitted from Table 3-1. 

Numerous abnormalities of bone structure and bone mineralization were observed in weanling male 

Sprague-Dawley rats (100–125 g) that ingested 500 mg strontium/kg/day as strontium carbonate in the 

diet for 3 weeks (Neufeld and Boskey 1994). In strontium-fed rats, the ash weight (mineral content) of 

metaphyseal bone was reduced and the complexed acidic phospholipid content (lipid nucleator of bone 

mineral) was significantly higher than in controls. Large areas of nonmineralized bone (osteoid) were 

observed in epiphyseal bone and secondary spongiosa. The epiphyseal plates were abnormally wide and 

the metaphyses were abnormally long and dense. The diaphyses contained localized areas of decreased 

bone density. The primary spongiosa of the proximal tibia was longer and the trabeculae was 

disorganized and apparently disconnected from the overlying calcified cartilage. The authors suggested 

that since the levels of complexed acidic phospholipids were high and vitamin D deficiency is known to 

increase complexed acidic phospholipid levels, that the effect of strontium was probably not mediated 

through its effect on vitamin D. They suggested the binding of strontium to the surface of initial 

hydroxyapatite crystallites reduced their further proliferation, resulting in a smaller crystal size. 
STRONTIUM 52 

3. HEALTH EFFECTS 

Similarly, significant abnormalities of bone organization occurred in five weanling (21 days old) male 

England Wright Y rats that ingested 1,850 mg strontium/kg/day (form unspecified) for 20 days in a diet 

sufficient in calcium, phosphorus, and vitamin D (Reinholt et al. 1984). In treated rats, the mean 

thickness of the epiphyseal growth plate was 70% larger than normal. In the epiphyseal regions of long 

bones, the volume of each zone was larger than its normal counterpart, and in addition, the relative sizes 

were altered; the proportional volumes of the resting, proliferative, and calcifying zones were 

significantly smaller and that of the hypertrophic zone was significantly larger than normal. There was an 

increase in the volume of extracellular matrix in bone, suggested to be associated with a reduced rate of 

extracellular matrix vesicle degradation. Another study from this laboratory examined the biochemistry 

of epiphyseal cartilage in rats treated as above (Reinholt et al. 1985). In strontium-treated rats, alterations 

were observed in the proteoglycan composition (slightly higher galactosamine content), chondroitin 

sulfate chain lengths (larger), regional distributions of large and small chondroitin sulfate peptides, and 

regional distributions of both non-sulfated chondroitin sulfate disaccharides and hyaluronic aciddisaccharides. The authors suggested that these strontium-induced alterations in cartilage matrix might 

affect the process of mineralization. 

No effects on bone histology were observed in young female rats (40–60 g) that were fed 140 mg 

strontium/kg/day as strontium carbonate for 20 days, but histological abnormalities were detected at doses 

between 550 and 4,975 mg/kg/day (Storey 1961). Alterations in the appearance of the cartilage plate 

(irregular, thicker, with areas of uncalcified bone matrix in the distal ends of the metaphyseal trabeculae 

and proximal end of the diaphysis) were observed at 550 mg strontium/kg/day. Irregularities in the 

organization of the cells of hypertrophic zone (distorting the usual parallel arrangement of intercellular 

matrix columns), in the pattern of calcification, and in deposition of osteoid were more conspicuous with 

increasing dose. At higher doses, bands of uncalcified cartilage matrix were isolated between areas of 

osteoid tissue. In tibias, the dry weight, ash weight, ash percentage, and calcium in ash were significantly 

reduced with increased strontium intake. In the same study, adult female rats given doses of 170– 

2,750 mg strontium/kg/day exhibited milder effects in bone. Histological changes in the tibia (thicker 

epiphyseal cartilage, increased width of metaphyseal osteoid seams) were noted at 1,370 or 2,750 mg 

strontium/kg/day only. Other significant effects seen only at 2,750 mg strontium/kg/day included the 

deposition of osteoid tissue near vascular canals, a reduction in the area of bone resorption, and reductions 

in the dry weight, ash weight, ash percentage, and calcium in ash of bone (Storey 1961). 

A 24% reduction in bone formation rate, 28% reduction in bone resorption rate (based on 45Ca uptake), 

and a significantly reduced calcium content in ashed femurs, but no change in ash weight were observed 
STRONTIUM 53 

3. HEALTH EFFECTS 

after female juvenile Wistar rats (36 days old) ingested 510 mg strontium/kg/day as strontium carbonate 

in the diet for 27 days (Morohashi et al. 1994). These rats were also significantly hypocalcemic. No 

effects were observed at 50 or 100 mg strontium/kg/day other than an unexplained increase in calcium 

content of bone at 50 mg strontium/kg/day (Morohashi et al. 1994). Minor bone effects occurred in 

21-day-old male C57BL/6J mice after ingesting 350 mg strontium/kg/day as strontium chloride in the 

drinking water for 29 days (Marie and Hott 1986). Strontium had no significant effect on tibial length or 

bone mineral content (percent ash, calcium, or phosphorus). In vertebrae, strontium had no effect on the 

osteoblastic surface (percent endosteal surface showing plump osteoblasts), bone matrix apposition rate, 

osteoid seam thickness (average width of all endosteal osteoid seams), or calcified bone volume. 

However, exposure to strontium resulted in a 10% increase in osteoid surface (percent endosteal surface 

covered by an osteoid seam) and an 11% reduction in the number of active osteoclasts. 

There was radiographic evidence of abnormally thickened epiphyseal cartilage plates in the long bones of 

weanling male Wistar rats exposed to strontium phosphate in the diet at a dose level of 2,820 mg 

strontium/kg/day for 4–6 weeks, but no effect at 580 mg strontium/kg/day and little effect at 1,270 mg 

strontium/kg/day (Kshirsagar 1976). Ingestion of 565 mg strontium/kg/day for 43 days resulted in several 

bone abnormalities in young Sprague-Dawley rats (Johnson et al. 1968). The level of sodium in bone was 

significantly lowered, and the level of potassium was significantly increased, and the overall index of 

bone mineralization (percent bone ash) was decreased. Unmineralized osteoid was visible in histological 

sections of vertebrae. Rats became rachitic and osteomalacic and exhibited paralysis of the hindlimbs. 

Beneficial effects of a low dose of strontium were noted on bone mineralization, such as a 17% increase 

in mineral bone volume and a 70% increase in the number of bone forming sites, with no adverse effect 

on the hydroxyapatite mineral particle size in 28-day-old male Sprague-Dawley rats ingesting 168 mg 

strontium/kg/day in an unspecified form for 8 weeks (Grynpas et al. 1996) or in young SPF Wistar rats 

fed doses up to 166 mg strontium/kg/day as strontium chloride in the diet for 90 days (Kroes et al. 1977). 

Stimulation of calcified bone growth was noted among male weanling Sprague-Dawley rats ingesting 

between 316 and 524 mg strontium/kg/day as strontium chloride for 9 weeks, but reduced bone 

calcification was observed at 633 mg/kg/day (Marie et al. 1985). In male weanling Sprague-Dawley rats 

ingesting 1,520 mg strontium/kg/day for 26 days, epiphyseal growth plates had abnormally thick 

hypertrophic zones and impaired calcification and resorption at the metaphyseal side (Svensson et al. 

1985, 1987). In addition, cartilage from strontium-treated rats contained 75% less calcium and had a 60% 

lower rate of synthesis of glycosaminoglycans and collagen. When 4-week-old male Wistar rats (50– 

60 kg body weight) were fed 1,970 mg strontium/kg/day as strontium carbonate in a diet low in calcium 
STRONTIUM 54 

3. HEALTH EFFECTS 

(0.04%), bone mineralization was significantly affected (Matsumoto 1976). This study is presented in 

detail in Section 3.2.2.6 Developmental Effects, as an example of skeletal anomalies in young animals 

resulting from strontium ingestion. 

In another intermediate-duration animal study, young (50–70 g) rats ingested 2,160 mg strontium/kg/day 

and adult rats ingested 1,570 mg strontium/kg/day as strontium carbonate for 7 months (Storey 1962). At 

3 weeks, young rats developed a rachitic gait, and subsequently, some rats (numbers not specified) 

developed spinal kyphosis, bent tibiae, and irregular discolored enamel on anterior teeth. Histological 

abnormalities in long bone differentiation included reduced calcification, excess growth of epiphyseal 

cartilage, abnormal deposition of osteoid (unmineralized bone) in the metaphysis, fragmentation of the 

epiphyseal plates, and isolated nodules of cartilage. Osteoid accumulation was observed in the skull. 

Adult rats were affected by strontium ingestion in the same way, but to a lesser degree than young 

animals. Abnormal depositions of osteoid in long bones and skull were not as extensive as in young rats. 

The epiphyseal plate did not become fragmented. Tooth enamel was abnormally white and pitted. 

Hepatic Effects. No studies were located regarding hepatic effects in humans following oral exposure 

to stable strontium. 

No studies were located regarding hepatic effects in animals after chronic-duration oral exposure to stable 

strontium. In acute- and intermediate-duration studies, in which the diet contained adequate amounts of 

calcium and vitamin D, few hepatic effects were reported. No histological changes were observed in the 

livers of adult Wistar rats given up to 110 mg strontium/kg/day as strontium chloride in the diet for 

2 weeks (Kroes et al. 1977). Acid phosphatase activity decreased by about 8% in the livers of 5–6 male 

weanling (21 days old) Wistar rats given 3,000 mg strontium/kg/day as strontium phosphate for 2 weeks 

(Kshirsagar 1976). However, this effect was reversible by feeding the rats a normal, low-strontium diet 

for 2 weeks. In male weanling Wistar rats, ingestion of strontium phosphate in the diet for 4–6 weeks 

resulted in a >26% decrease in hepatic alkaline phosphatase activity at 2,820 mg strontium/kg/day, but no 

decrease at 1,270 mg strontium/kg/day (Kshirsagar 1976). The biological significance of these small, but 

statistically significant, changes in hepatic phosphatase activity is not known. Among weanling male and 

female Wistar rats fed strontium chloride in the diet for 90 days, the only hepatic effects were ‘slight 

histological changes’ (not described) and an ‘increase in peripheral glycogen’ in females at the highest 

dose (166 mg strontium/kg/day); no other hepatic effects were observed in either sex ≤146 mg 

strontium/kg/day (Kroes et al. 1977). 
STRONTIUM 55 

3. HEALTH EFFECTS 

Renal Effects. No studies were located regarding renal effects in humans after oral exposure to stable 

strontium. 

No studies were located regarding renal effects in animals after chronic-duration oral exposure to stable 

strontium. In acute- and intermediate-duration studies, in which the diet contained adequate amounts of 

calcium and vitamin D, no renal effects were reported. No organ weight or histological changes were 

observed in the kidneys of adult Wistar rats given up to 110 mg strontium/kg/day as strontium chloride in 

the diet for 2 weeks (Kroes et al. 1977). Similarly, no such changes were observed among weanling 

Wistar rats fed up to 166 mg strontium/kg/day as strontium chloride in the diet for 90 days (Kroes et al. 

1977). In male white Leghorn chickens raised on a diet deficient in vitamin D for the first 2 weeks of life, 

ingestion of 2,350 mg strontium/kg/day in a low-calcium, low-vitamin D diet for 7 additional days, 

reduced the activation of vitamin D3 in mitochondria of the kidney (Omdahl and DeLuca 1972). Because 

of physiological differences between birds and mammals, this study is omitted from Table 3-1. 

Endocrine Effects. Few studies were located regarding endocrine effects in humans after oral 

exposure to stable strontium. Vezzoli et al. (1998) reported that strontium absorption was inversely 

correlated with parathyroid hormone levels. 

No studies were located regarding endocrine effects in animals of acute- or chronic-duration oral 

exposure to stable forms of strontium. There were no histological changes in the parathyroid gland or 

alterations in parathyroid hormone levels observed in male weanling Sprague-Dawley rats given 

1,520 mg strontium/kg/day in the diet for 26 days (Svensson et al. 1987). The authors cautioned that their 

biochemical methods could not distinguish between active and inactive forms of the hormone. A few 

organ weight changes were observed among weanling Wistar rats fed up to 166 mg strontium/kg/day as 

strontium chloride in the diet for 90 days (Kroes et al. 1977). The relative thyroid weight was 

significantly heavier in males at 36 and 146 mg strontium/kg/day and the relative pituitary weight was 

significantly decreased in females at 10 and 166 mg strontium/kg/day, but in neither case was there a 

clear dose-response. Slight histological changes in the thyroid were reported. 

Body Weight Effects. No studies were located regarding body weight effects in humans after oral 

exposure to stable strontium. 

No studies were located regarding body weight effects in animals after chronic-duration oral exposure to 

stable strontium. In acute- and intermediate-duration animal studies, the effective dose levels for body 
STRONTIUM 56 

3. HEALTH EFFECTS 

weight effects were relatively high and young animals were more sensitive than adults. In an acuteduration study, there was no effect on body weight in groups of adult SPF Wistar rats that ingested up to 

110 mg strontium/kg/day as strontium chloride in the diet for 2 weeks (Kroes et al. 1977). Body weight 

gain was reduced by 62% among male weanling (21-day-old) Wistar rats that ingested 2,820 mg 

strontium/kg/day as strontium phosphate in the diet for 2 weeks, but this effect was reversible by feeding 

rats a diet low in strontium for 2 weeks (Kshirsagar 1976). From an analysis of a pair-fed control group 

(food intake matched to this high-dose group), the author concluded that the severe effects were a result 

of excess strontium, and not the reduced diet. Ingestion of 1,090 or 1,630 mg strontium/kg/day as 

strontium lactate reduced body weight gain in 5-week-old albino rats within several days (Teree et al. 

1965). However, it seems likely that the reduced body weight gains resulted from an observed (but not 

measured) reduction in food intake, possibly because of reduced palatibility at the higher dose levels. 

Since the reduction appears not to be a systemic effect of strontium ingestion, this study is omitted from 

Table 3-1. 

Most of the intermediate-duration oral exposure studies in weanling rodents have reported no effect on 

body weight for exposures <633 mg strontium/kg/day (rats: Grynpas et al. 1996; Kroes et al. 1977; Marie 

et al. 1985; Morohashi et al. 1994; Neufeld and Boskey 1994; Skoryna 1981a; and mice: Marie and Hott 

1986). Intermediate-duration exposures to stable strontium at levels above 1,000 mg/kg/day adversely 

affected body weight. A 15% reduction in body weight gain was observed among weanling (21-day-old) 

male Wistar rats that ingested 1,270 mg strontium/kg/day as strontium phosphate for 4–6 weeks, but no 

reduction was observed at 580 mg strontium/kg/day (Kshirsagar 1976). The body weight gain was 28% 

lower than controls in weanling (21-day-old) male England Wright Y rats that ingested 1,850 mg 

strontium/kg/day (form unspecified) for 20 days (Reinholt et al. 1985). The terminal body weight was 

16% lower than normal in male weanling Sprague-Dawley rats that ingested 1,520 mg strontium/kg/day 

(form not specified in this paper, but other publications from this lab used strontium chloride) for 26 days 

(Svensson et al. 1987). 

A >30% loss in body weight occurred in young female rats (40–60 g) that were fed 4,975 mg 

strontium/kg/day as strontium carbonate for 20 days (Storey 1961); body weight gain was reduced by 

24% at 2,220 mg, but was unaffected at 1,460 mg strontium/kg/day. Food intake was not reported, so it is 

uncertain to what extent these results are attributable to unpalatability. Similarly treated adult female rats 

exhibited no significant body weight changes at 2,750 mg strontium/kg/day (Storey 1961). Body weight 

gain was about a third lower than controls in young (50–70 g) rats that ingested 2,160 mg 
STRONTIUM 57 

3. HEALTH EFFECTS 

strontium/kg/day as strontium carbonate for 7 months (Storey 1962); no quantitative body weight data 

were reported for young or adult animals. 

In acute- and intermediate-duration studies, strontium effects on body weight were more severe in 

animals on diets low in calcium. Reduced body weight gain was reported in young white Leghorn chicks 

following ingestion of a high strontium/low calcium diet for 1 or 2 weeks (Corradino and Wasserman 

1970; Corradino et al. 1971a, 1971b). The body weight gain of male weanling Wistar rats was reduced 

by 60% after ingestion of strontium carbonate (1,960 mg strontium/kg/day) in a diet low in calcium 

(0.04%) for 4 weeks (Matsumoto 1976). 

Metabolic Effects. No studies were located regarding metabolic effects in humans after oral exposure 

to stable strontium. 

No studies were located regarding metabolic effects in animals after chronic-duration oral exposure to 

stable strontium. In animal studies, few metabolic effects resulted from acute- or intermediate-duration 

oral exposure to stable strontium. In chicks given a normal Vitamin D3-containing diet for 2 weeks after 

hatching, ingestion of a diet containing excess strontium reduced the plasma concentration of calcium, 

probably a consequence of reduced calcium absorption by the duodenum (Corradino et al. 1971a). 

Intermediate-duration exposures to 150–1,850 mg strontium/kg/day as strontium carbonate or strontium 

chloride had no effects on the serum levels of calcium, phosphorus, or magnesium in young or adult 

rodents given adequate dietary calcium, phosphorus, and vitamin D (rats: Grynpas et al. 1996; Kroes et al. 

1977; Marie et al. 1985; Neufeld and Boskey 1994; Svensson et al. 1985, 1987; Reinholt et al. 1984; 

Skoryna 1981a; and mice: Marie and Hott 1986). No effects on serum calcium levels were observed in 

young female rats (40–60 g) that were fed 4,975 mg strontium/kg/day as strontium carbonate for 20 days 

or in adult female rats similarly fed 2,750 mg strontium/kg/day (Storey 1961). At 4,975 mg 

strontium/kg/day in the young rats, the calcium/strontium ratio was 1, whereas the ratio at 2,750 mg 

strontium/kg/day in adult rats was 1.4. A 13% reduction in serum calcium was observed in female 

juvenile Wistar rats (36-day-old, 6–8 per group) that ingested 510 mg strontium/kg/day as strontium 

carbonate in the diet for 27 days, but no effect was observed at 100 mg strontium/kg/day (Morohashi et al. 

1994). 
STRONTIUM 58 

3. HEALTH EFFECTS 

3.2.2.3 Immunological and Lymphoreticular Effects 

No studies were located that reported immunological or lymphoreticular effects in humans or animals 

following oral exposure to stable strontium. 

3.2.2.4 Neurological Effects 

No studies were located that reported neurological effects in humans following oral exposure to stable 

strontium. No behavioral effects were observed in rats that ingested strontium chloride at levels up to 

110 mg strontium/kg/day for 2 weeks or 166 mg strontium/kg/day for 90 days (Kroes et al. 1977). 

Johnson et al. (1968) reported paralysis of the hindlimbs in weanling male Sprague-Dawley rats that were 

fed 565 mg/kg/day of stable strontium (form not specified) for 43 days. It is not clear whether the 

observed paralysis was neurological or muscular, but it could have been related to abnormal calcium 

signaling in muscle or nerve. It is unlikely that the paralysis was due to the deformation of the femora as 

severely rachitic and osteomalacic rodents are not generally paralyzed. The NOAEL and LOAEL are 

recorded in Table 3-1 and plotted in Figure 3-1. 

3.2.2.5 Reproductive Effects 

No studies were located regarding reproductive effects in humans or animals following oral exposure to 

stable strontium. 

3.2.2.6 Developmental Effects 

No studies were located regarding developmental effects in humans following acute- or intermediateduration oral exposure to stable forms of strontium. The only chronic-duration study is the Turkish 

epidemiological analysis that found a relationship between the concentration of strontium in the local soil 

and the prevalence of rickets in children between the ages of 6 months and 5 years (Ögzur et al. 1996). A 

relatively short period of breast feeding, which presumably affected calcium intake, and soil levels of 

strontium higher than 350 ppm, which probably determined the level of strontium in dietary grains 

consumed after weaning, were associated with an increase in the prevalence and severity of rickets. This 

study is discussed above in Section 3.2.2.2 Musculoskeletal Effects. 
STRONTIUM 59 

3. HEALTH EFFECTS 

No studies were located that examined the effect of exposure to stable strontium in utero following oral 

maternal exposure in animals. However, the studies discussed in Section 3.2.2.2 Musculoskeletal Effects 

address the effects of strontium on bone organogenesis, in particular, endochondral ossification, a 

developmental process that continues long after birth. For example, in a study in which 4-week-old male 

Wistar rats (50–60 g body weight) were fed 1,970 mg strontium/kg/day as strontium carbonate in a diet 

low in calcium (0.04%), bone mineralization was significantly affected (Matsumoto 1976). Tibial length 

was reduced by 33% and the tibial proximal and distal epiphyseal plates were both about 5 times wider 

than normal. Microradiographic and histological analyses of tibial proximal heads revealed that no 

mineralization was detectable, that the organization of chondroblasts was irregular, and that osteoid rather 

than mineralized bone was deposited. Other studies on weanlings were conducted for acute durations 

(rat: Kshirsagar 1976) and intermediate durations (rat: Grynpas et al. 1996; Kroes et al. 1977; Morohashi 

et al. 1994; Neufeld and Boskey 1994; Reinholt et al. 1984, 1985; Svensson et al. 1985, 1987; and mice: 

Marie and Hott 1986). Intermediate-duration studies on rats demonstrated that ingestion of strontium 

resulted in more severe skeletal effects in young animals than in adults (Storey 1961, 1962). These 

studies are described in Section 3.2.2.2 Musculoskeletal Effects and are listed in Table 3-1 and Figure 3-1 

under that category. 

3.2.2.7 Cancer 

No studies were located that demonstrated cancer effects of stable strontium following oral exposure in 

humans or animals. In one case-control study, no association was found between the incidence of liver 

cancer in 1984 on Chongming Island in China and the levels of stable strontium detected in hair (Wang et 

al. 1990). 

3.2.3 Dermal Exposure 

No studies were located regarding the following health effects in humans or animals after dermal 

exposure to stable strontium: 
STRONTIUM 60 

3. HEALTH EFFECTS 

3.2.3.1 Death 

3.2.3.2 Systemic Effects 

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 

3.2.4 Other Routes of Exposure 

This section includes injection and in vitro studies that provide evidence for the biological basis of 

toxicity of stable strontium in humans and animals. Since these studies are not directly relevant to general 

population exposure conditions, no LSE tables have been created for this section. 

Cardiovascular Effects. Cardiovascular effects of strontium have been investigated by intravenous 

infusion studies in dogs. Infusions of strontium (as chloride or gluconate) averaging 172 mg strontium/kg 

under conditions of lowered potassium induced accelerated ventricular escape beats, ventricular 

tachycardia, or atrial fibrillation (Foster et al. 1977). High levels of strontium also induced oscillatory 

potentials and prolonged depolarization (precursors to arrhythmia) in Purkinje fibers of isolated sheep 

hearts (Gonzalez and Vassalle 1990). Whereas intravenous infusions at 4 mg strontium/kg had no effect 

on cardiac physiology, infusions at ~15 mg strontium/kg that brought the strontium/Ca ratio above 1 had 

a temporary negative chronotropic effect, reduced cardiac output, increased pulmonary vascular 

resistance, and systemic vascular resistance, but had no effect on pulmonary or systemic arterial pressure 

or pulmonary wedge pressure (Barry et al. 1972; Skoryna et al. 1986). The concentrations of strontium 

used in these studies are very high relative to the mean concentration of strontium in human blood, 27 μg 

strontium/L (see Table 6-9). 

Hematological Effects. Because of its molecular similarity to calcium, the association of stable 

strontium with several kinds of blood cells has been investigated in a number of in vitro experiments. 

Strontium ions were found to be transported across the cell membrane of human erythrocytes by means of 

an ATP-dependent calcium pump (de la Sierra et al. 1990; Olson 1979; Olson and Cazort 1969; Porzig 

1973). In washed platelets from human and rabbit, strontium stimulated the secretion of 
STRONTIUM 61 

3. HEALTH EFFECTS 

5-hydroxytryptamine (Best et al. 1981; Bone et al. 1980; Togna et al. 1989). Best et al. (1981) concluded 

that strontium activates the release of arachidonate from platelet membrane phospholipid, with the 

subsequent synthesis of thromboxane A2, a reaction that was antagonized by aspirin. These authors also 

suggested that strontium, because of its smaller hydrated ionic radius compared to calcium, is able to 

enter the platelet and mimic the rise in cytosolic calcium concentration that normally serves to activate 

secretion of 5-hydroxytryptamine (Best et al. 1981). Strontium was also found to stimulate degranulation 

of human large granular lymphocytes, which resulted in the inhibition of natural killer (NK) cells 

(Neighbour et al. 1982). The content of strontium (and calcium) was found to be significantly elevated 

above healthy control levels in granulocytes isolated from Swedish patients with active rheumatoid 

arthritis or seronegative spondarthritis (Hällgren et al. 1984). The strontium overload was thought to be 

linked to the degree of inflammation, and was positively related to serum levels of the acute-phase protein 

haptoglobin; corticosteroid therapy differentially reduced the strontium content of granulocytes compared 

to calcium. The authors suggested that leukocyte endogenous mediator (LEM) regulated the 

accumulation of strontium in granulocytes. 

Immunological and Lymphoreticular Effects. Several in vitro experiments have demonstrated 

that strontium, although less efficient than calcium, is able to stimulate histamine release from rat mast 

cells (Alm and Bloom 1981a, 1981b; Atkinson et al. 1979; Foreman 1977; Foreman and Mongar 1972a, 

1972b; Foreman et al. 1977). This is probably relevant to humans, since strontium has been shown to 

degranulate human lymphocytes (Neighbor et al. 1982) and stimulate the release of 5-hydroxytryptamine 

by human platelets (Best et al. 1981) (see Hematological Effects above). In rabbit blood treated with 

strontium chloride in vitro, the bacterocidal properties of serum were reduced (Toshioka et al. 1974); this 

effect was attributed to the inhibition of complement. 

Neurological Effects. In vitro studies have demonstrated subtle differences between strontium and 

calcium with respect to neurological function at the cellular level. In a calcium-free medium, strontium 

ion weakly supported the generation of excitatory postsynaptic potentials following stimulation of guinea 

pig superior cervical ganglia (i.e., the release of acetylcholine was less efficient than when calcium was 

present) (McLachlan 1977). Calcium is sequestered in mitochondria and smooth endoplasmic reticulum 

of isolated presynaptic nerve terminals in preference to strontium (Rasgado-Flores et al. 1987). Strontium 

ion inhibits the uptake of calcium by synaptic vesicles in vitro, thereby blocking the antiport-regulated 

release of H+ (Gonçalves et al. 1999). Strontium ion was slightly more efficient than calcium ion in 

supporting the release of neurotransmitter from synaptosomes induced by leptinotoxin-h (Madeddu et al. 

1985). Strontium ion was found to support the asynchronous mode of transmitter release in isolated layer 
STRONTIUM 62 

3. HEALTH EFFECTS 

V pyramidal cells of the prefrontal cortex (Aghajanian and Marek 1999). This is apparently mediated 

through calcium-binding protein synaptotagmin III, as strontium does not support the function of 

calcium-binding synaptotagmins I and II (Li et al. 1995). 

Reproductive Effects. The results of one in vitro study suggest that stable strontium is not directly 

harmful to human spermatozoa. In developing an improved method to be used by fertility clinics for 

testing the functional capacity of human spermatozoa, it was found that inclusion of strontium chloride in 

the testing medium improved the rate of penetration compared to calcium chloride (Mortimer 1986; 

Mortimer et al. 1986). 

Developmental Effects. Subcutaneous injection of up to 82 mg strontium/kg/day as strontium 

nitrate into female Wistar rats between days 9 and 19 of gestation had no teratogenic effect, no adverse 

effect on the ossification of the skeleton, and no effect on the number of resorptions (Lansdown et al. 

1972). 

3.3 DISCUSSION OF HEALTH EFFECTS OF RADIOACTIVE STRONTIUM BY ROUTE OF 

EXPOSURE 

Section 3.3 discusses radiation toxicity associated with exposure to radionuclides of strontium and is 

organized in the same manner as that of Section 3.2, first by route of exposure (inhalation, oral, and 

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

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). 

Levels of significant exposure for each route and duration are presented in tables and illustrated in 

figures. The points in the figures showing NOAELs or LOAELs reflect the actual dose (levels of 

exposure) used in the studies. Refer to Section 3.2 for detailed discussion of the classification of 

endpoints as a NOAEL, less serious LOAEL, or serious LOAEL. 

Levels of exposure associated with carcinogenic effects (Cancer Effect Levels, CELs) of radiostrontium 

are indicated in Tables 3-2, 3-3, and 3-4 and Figures 3-2 and 3-3. Because cancer effects could occur at 

lower exposure levels, Figures 3-2 and 3-3 also show a range for the upper bound of estimated excess 

risks, ranging from a risk of 1 in 10,000 to 1 in 10,000,000 (10-4 to 10-7), as developed by EPA. 
STRONTIUM 63 

3. HEALTH EFFECTS 

Refer to Appendix B for a User's Guide, which should aid in the interpretation of the tables and figures 

for Levels of Significant Exposure. 

3.3.1 Inhalation Exposure 

The two major sources of data regarding health effects of inhaled radioactive strontium are long-term 

studies using beagles at the Lovelace Foundation, Albuquerque, New Mexico (now known as the 

Lovelace Respiratory Research Institute). One study examined the acute inhalation effects of a relatively 

soluble aerosol of 90SrCl2, and the other examined the acute inhalation effects of relatively insoluble 

particles of 90Sr fused to aluminum silicate (‘90Sr fused-clay particles’). 

In the soluble aerosol study, beagles were exposed by nose breathing for varying exposure durations 

(2–22 minutes) to graded concentrations (2.16–419 μCi 90Sr/L; 0.08–15.5 MBq/L) of 90SrCl2 to produce 

graded levels of initial body burdens. Individual variations in the degree to which aerosol was cleared 

from the respiratory tract and swallowed contributed to variability in the initial rapid rate of clearance 

during the first few days. Therefore, exposures were expressed in terms of the long-term retained burden 

(LTRB), which ranged from 1.08 to 119 μCi (0.04–4.4 MBq) 90Sr/kg of body weight. Radiostrontium 

quickly passed through the lungs and was overwhelmingly retained in the skeleton, where initial skeletal 

dose rates were calculated to be 0.43–55 rad/day (0.0043–0.55 Gy/day). Clearance of radiostrontium 

from the skeleton was gradual. For that reason, the initial and long-term health effects were primarily 

related to hemopoietic bone marrow and osteogenic tissues. Reports relating to the 90SrCl2 aerosol study 

include Benjamin et al. (1974b, 1975, 1976a, 1976c, 1979), Boecker et al. (1969, 1991), Fission Product 

Inhalation Project (1967a), Gillett et al. (1987a, 1987b), Hahn et al. (1991), McClellan et al. (1973, 

1983a), and Muggenburg et al. (1977, 1978, 1979). 

In the other study, beagles were exposed by nose-only inhalation to 90Sr fused-clay particles for initial 

lung burdens ranging from 0.21 to 94 μCi 90Sr/kg (0.008–3.5 MBq/kg) of body weight. Control animals 

were exposed to similar aluminosilicate clay particles fused to stable strontium. Early and late-occurring 

health effects of inhaled particulate radiostrontium were primarily associated with the lung. Some 

particles were cleared into the lung-associated lymph nodes, where radiation damage led to their entry 

into the circulatory system, leading to distribution to spleen, liver, and possibly other tissues. Trapping of 

radioactive particles by these tissues created possible sites for radiation damage and tumor development. 

The biological retention half-time for 90Sr in fused-clay particles was approximately 490 (±320 days 

standard deviation). Reports relating to 90Sr fused clay particles include Benjamin et al. (1974a, 1975), 
STRONTIUM 64 

3. HEALTH EFFECTS 

Griffith et al. (1992), Hahn et al. (1983a), Hobbs et al. (1972), Jones et al. (1972, 1976), Scott (1980), and 

Snipes et al. (1974a, 1974b, 1976, 1977, 1978, 1979). A similar study with a smaller group of dogs was 

carried out by Benjamin et al. (1976c). 

3.3.1.1 Death 

No studies were located regarding death in humans following inhalation exposure to radioactive 

strontium. Information on the lethality of inhaled radioactive strontium is limited to acute exposure 

studies. Because of the bone-seeking behavior of strontium, an acute exposure to airborne 90Sr results in 

chronic exposure to radiation from 90Sr incorporated into bone. If insoluble radiostrontium compounds 

are inhaled, there could be long-term lung exposure (see discussion of the study by Willard and Snyder 

(1966) in Section 3.5.1.1). 

In two different experiments briefly described in a report by the Lovelace Foundation (now known as the 

Lovelace Respiratory Research Institute), young male and female Holtzman rats were exposed once to 

90Sr by whole body inhalation for initial body burdens ranging from 170 to 1,660 μCi 90Sr/kg (0.63– 

61.4 MBq/kg) of body weight and average skeletal radiation doses ranging from 12,600 to 19,000 rad 

(126–190 Gy) (Fission Product Inhalation Project 1967b). Survival was inversely proportional to dose, 

with rats receiving the lowest dose living for more than 700 days, and those receiving the highest dose 

living less than 200 days. In the two experiments, 77% of the rats that died and 47% of the rats that were 

killed in a moribund state were found to have osteosarcoma. Among rats dying with tumors, the average 

skeletal dose was 81 rad/day, compared to 62 rad/day for rats without tumors (0.81 vs 0.62 Gy/day). The 

small sample sizes in this study do not permit its inclusion in the LSE Table 3-2. 

In acute inhalation studies in beagle dogs, high-dose radiation effects of inhaled 90SrCl2 on bone marrow 

resulted in death within days or weeks of exposure, whereas lower doses reduced long-term survival 

through carcinogenetic effects. For all exposed dogs, the mean survival time was 3,000 days, compared 

to 4,500 days for the controls (Gillett et al. 1987b). Among dogs receiving high or medium doses (longterm retained body burdens between 47 and 120 μCi 90Sr/kg (1.74 and 4.44 MBq/kg), 6/22 died within 

32 days from severe hypoplasia of the bone marrow (Gillett et al. 1987a; Muggenburg et al. 1979). 

Individual neutrophil counts were the most reliable predictors of lethality. Death from primary bone 

tumors occurred from 2 to 10 years after exposure to inhaled 90SrCl2 (Gillett et al. 1987b). Fibrosarcomas 

and metastasizing hemangiosarcomas occurred somewhat earlier than osteosarcomas and were the major 
STRONTIUM 65 

3. HEALTH EFFECTS 

contributors to shortened mean survival times for the dogs exposed to inhaled 90SrCl2 (Gillett et al. 

1987b). Deaths from myelomonocytic leukemia and from bone-associated soft tissues of the skull were 

also concluded to be associated with radiostrontium; the long-term retained burdens were 9.2–27 μCi 

90Sr/kg (0.34–1.0 MBq/kg) and 21–35 μCi 90Sr/kg (0.081–1.3 MBq/kg), respectively. These are extreme 

doses. 

In beagle dogs exposed by acute inhalation to 90Sr fused-clay particles, the pattern of mortality was 

different since the radioactive particles were initially embedded in the lung. No deaths occurred until the 

5th month postexposure. Of 36 dogs with initial lung burdens ≥25 μCi 90Sr/kg (925 kBq/kg) of body 

weight, 35 died within the first 2 years, primarily of radiation pneumonitis and/or pulmonary fibrosis 

(Snipes et al. 1979). Subsequently, within the 2nd to 7th years after exposure, deaths from 

hemangiosarcoma and carcinoma of the lung were common. None of the control dogs died during the 

9 years following exposure (Snipes et al. 1979), indicating that the observed mortality was not caused by 

inhalation of nonradioactive aluminum silicate particles alone. Among dogs dying prematurely from 

neoplasms of the lung, the initial lung burdens were between 3.7 and 94 μCi/kg (0.14–3.5 MBq/kg) and 

the doses to the lungs ranged from 43,000 to 67,000 rad (430–670 Gy) (Benjamin et al. 1975). 

The percent mortality values for dogs from exposure to radioactive strontium by the inhalation route are 

presented in Table 3-2 and plotted in Figure 3-2. 

3.3.1.2 Systemic Effects 

No studies were located that described endocrine, dermal, or ocular effects in humans or animals 

following inhalation exposure to radioactive strontium. The highest NOAEL values and all reliable 

LOAEL values in each species and duration category for systemic effects from radiation exposure to 

strontium by the inhalation route are presented in Table 3-2 and plotted in Figure 3-2. 

Respiratory Effects. The only respiratory effects reported for the study in which beagle dogs were 

exposed to soluble aerosols of 90SrCl2 (Boecker et al. 1969; Gillett et al. 1987b) were late primary cancers 

of the respiratory tract or tumors metastasizing to the lung. These effects are discussed in Section 3.2.1.7 

Cancer. 
Table 3-2 Levels of Significant Exposure to Strontium - Radiation Toxicity - Inhalation 

Exposure/ LOAEL 

Duration/ a Frequency 

Key to Species NOAEL Less Serious Serious (Specific Route) figure (Strain) System (μCi/kg) (μCi/kg) (μCi/kg) 

ACUTE EXPOSURE Death 

1 Dog 2-22 min 

47 [LTRB] (6/24 died from bone once (Beagle) marrow hypoplasia) 

Systemic 

2 Dog once 

Cardio 25 [ILB] (damaged pulmonary (Beagle) vasculature; hypertrophic right 

ventricle; congestive heart failure) 

Hepatic 25	 	 	 [ILB] (all with chronic passive 

	 	 

congestion; one with mild centrilobular fibrosis) 

Bd Wt 25 [ILB] (emaciation) 

3 Dog 2-22 min 

Gastro 47 [LTRB] (anorexia, bloody once (Beagle) diarrhea from acute radiation 

syndrome) 

	 

Hemato 1.5 [LTRB] (60% decr platelet 

count) 

Renal 47 [LTRB] (incr blood urea 

nitrogen, decr urine output from acute radiation syndrome) 

	 

	 

	 	 
Table 3-2 Levels of Significant Exposure to Strontium - Radiation Toxicity - Inhalation (continued) 

Exposure/ LOAEL

Duration/ a Frequency 

Key to Species NOAEL Less Serious Serious (Specific Route) figure (Strain) System (μCi/kg) (μCi/kg) (μCi/kg) 

4 Dog 2-22 min 

Gastro 1.9 [LTRB] (malabsorption once (Beagle) syndrome at age >11 yrs) 

Bd Wt 1.9 [LTRB] (decr bd wt) 

5 Dog once 

Resp 25 [ILB] (pulmonary pneumonitis, (Beagle) fibrosis) 

	 

Gastro 4.1	 [ILB] (ulcerating lesion of 

	 

pharynx; anorexia) 

Immuno/ Lymphoret 

once 


 

6 Dog 25 [ILB] (50% decr lymphocytes (Beagle) for 28 weeks) 

7 Dog 2-22 min 

10 [LTRB] (22% decr lymphocyte once (Beagle) count lasting 3 years) 

	 

8 Dog once 

5 [ILB] (lymphocyte counts decr (Beagle) 40% for two years) 

	 

	 	 

	 	 

	 	 
Table 3-2 Levels of Significant Exposure to Strontium - Radiation Toxicity - Inhalation (continued) 

Exposure/ LOAEL

Duration/ a Frequency 

Key to Species NOAEL Less Serious Serious (Specific Route) figure (Strain) System (μCi/kg) (μCi/kg) (μCi/kg) 

Cancer 

9 Rat once 

210 (CEL: osteosarcoma) (Holtzman) 

10 Dog once 

3.7 [ILB] (CEL: hemangiosarcoma (Beagle) of lung, heart) 

11 Dog 2-22 min 

7 [LTRB] (CEL: osteosarcoma) once (Beagle) 

	 

9 [LTRB] (CEL: leukemia) 

	 

27 [LTRB] (one premature death 

after 585 days from leukemia) 


 

2 [LTRB] (CEL: nasal carcinoma) 

a The number corresponds to entries in Figure 3-2. 

	 

Bd Wt = body weight; Cardio = cardiovascular; CEL = cancer effect level; decr = decreased; Gastro = gastrointestinal; (GW) = gavage in water; Hemato = hem[ILB] = initial lung burden; incr = increased; LOAEL = lowest-observed-adverse-effect level; [LTRB] = long-term retained burden; min = minute(s); NOAEL = no-observed-adverse-effect level; Resp = respiratory 

	 

	 

	 
Death Respiratory Cardiovascular Gastrointestinal Hematological Hepatic Renal Body W Immuno/L Cancer * 

1000 

eight ymphor 

Figure 3-2 Levels of Significant Exposure to Strontium - Radiation Toxicity - Inhalation 

Acute (≤14 days) 

Systemic 

uCi/kg 

9r 

100 

1d 3d 3d 

11d 5d 2d 2d 2d 6d 

10 7d 11d 

11d 

8d 

5d 10d 

11d 

3d 

4d 4d 

1 

*Doses represent the lowest dose tested per study that produced a tumorigenic response and do not imply the existence of a threshold for the cancer endpoint. 

0.1 

c-Cat -Humans f-Ferret n-Mink Cancer Effect Level-Animals Cancer Effect Level-Humans 

d-Dog k-Monkey j-Pigeon o-Other LOAEL, More Serious-Animals LOAEL, More Serious-Humans 

r-Rat m-Mouse e-Gerbil LOAEL, Less Serious-Animals LOAEL, Less Serious-Humans 

p-Pig h-Rabbit s-Hamster NOAEL - Animals NOAEL - Humans 

q-Cow a-Sheep g-Guinea Pig 
STRONTIUM 70 

3. HEALTH EFFECTS 

Respiratory effects were more pronounced in beagle dogs that were exposed to 90Sr fused-clay particles 

by inhalation (Benjamin et al. 1976c; Snipes et al. 1979). The primary cause of early death among dogs 

exposed to initial lung burdens ≥25 μCi 90Sr/kg (925 kBq/kg) was radiation pneumonitis and/or 

pulmonary fibrosis (Snipes et al. 1979). No such effects were reported in control dogs exposed to 

nonradioactive aluminosilicate-fused clay particles (Snipes et al. 1979). Clinical signs included an 

increased respiratory rate, dyspnea, cyanosis, and dry and moist rales (Benjamin et al. 1976c). 

Radiographically, the dogs showed increased focal or diffuse lung-field densities. The pneumonitis was 

characterized by acute and chronic inflammation with increased numbers of alveolar macrophages, 

hypertrophy and hyperplasia of alveolar lining cells, degeneration of the bronchiolar epithelium and 

alveolar ducts, focal emphysema, and edema. The fibrosis involved the alveolar septa, pleura, and 

perivascular regions, with substantial scarring. Vascular damage in the lungs was characterized by 

congestion, hemorrhage (possibly related to thrombocytopenia), fibrin exudation, and occasional vessels 

with fibrinoid necrosis or intimal proliferation. 

Cardiovascular Effects. Acute inhalation of radiostrontium was reported to lead to adverse 

cardiovascular effects in dogs. Among beagles that died within 5–15 months following inhalation 

exposure to 90Sr fused-clay particles, most exhibited myocardial necrosis or degeneration, and fibrosis, 

primarily of the right atrium (Hobbs et al. 1972); these animals had initial lung burdens between 33 and 

100 μCi/kg (1.2–3.7 MBq/kg) and cumulative beta radiation doses to the lung of 34,000 to 82,000 rad 

(340–820 Gy). In a later report of the same study, acute and chronic vascular lesions, characterized as 

inflammatory or degenerative, affected the elastic and muscular pulmonary arteries in dogs with initial 

lung burdens between 16 and 94 μCi/kg (0.6–3.5 MBq/kg) and doses to the lung between 40,000 and 

96,000 rad (400–960 Gy) at the time of death (Snipes et al. 1977). Vascular damage in the lungs was 

characterized by congestion, hemorrhage, fibrin exudation, and occasional vessels with fibrinoid necrosis 

or intimal proliferation (Benjamin et al. 1976c). These effects were attributed to the direct effect of beta 

radiation (from radiostrontium particles embedded in the lung) on adjacent tissue. In addition, 

presumably as a consequence of radiation damage to the pulmonary vasculature, the right ventricle 

became dilated and hypertrophic with congestive heart failure. Hemangiosarcomas resulting from 

radiostrontium exposure in this study are discussed in Section 3.3.1.7 Cancer. 

Gastrointestinal Effects. Gastrointestinal effects were observed in beagle dogs receiving single 

high doses (long-term retained body burdens between 47 and 83 μCi/kg; 1.74 and 3.07 MBq/kg) of 

soluble aerosols containing 90SrCl2 (Gillett et al. 1987a). Anorexia and, 2 days before death, bloody 

diarrhea, developed in six dogs that died between 18 and 32 days after the extreme radiation dose rate 
STRONTIUM 71 

3. HEALTH EFFECTS 

induced acute radiation syndrome (Gillett et al. 1987a). It is likely that severe thrombopenia, one of the 

features of radiation-induced bone marrow hypoplasia, contributed to hemorrhage in the gastrointestinal 

tract as elsewhere in the body. In addition, some effects could have been due to inhaled 90SrCl2 droplets 

being transported from the mucoid, ciliated nasopharyngeal and tracheobronchial epithelia to the pharynx 

and then swallowed. The gastrointestinal epithelium then would have been exposed directly to beta 

emissions from radiostrontium for a day or two. Another report of the same study described three 

exposed dogs that died at age >11 years with a malabsorption syndrome (Muggenburg et al. 1977). All of 

the dogs exhibited chronic diarrhea with anorexia, and at necropsy, contained chronic degenerative and 

inflammatory lesions of the small intestines. Their long-term retained burdens were 1.9–9.6 μCi/kg 

(70.3–355.2 kBq/kg) and the absorbed doses to the skeleton were calculated to be 530–5,600 rad (5.3– 

56 Gy). Although the authors could not firmly establish whether the syndrome was a consequence of 

exposure or of age, the cumulative radiation dose to the digestive tract was likely to have been very low 

and this argues against 90Sr as the cause. 

One beagle dog that was exposed to 90Sr fused-clay particles and had an initial lung burden of 4.1 μCi/kg 

(151.7 kBq/kg) and a cumulative radiation dose to the lung of 20,000 rad (200 Gy) died 9 years after 

exposure with anorexia and an ulcerative lesion to the pharynx (Snipes et al. 1979). Whether the 

pharyngeal lesion was related to exposure is uncertain, since the report was preliminary and no other 

response to radiation had been observed in this animal. 

Hematological Effects. Profound hematological effects were observed in beagle dogs that were 

exposed once by inhalation either to soluble aerosols containing 90SrCl2, or to 90Sr fused to 

aluminosilicate particles that produced extremely large radiation dose rates and doses in the affected 

tissues sufficient to induce acute radiation syndrome. 

Significant dose-related pancytopenia developed in dogs that were exposed to 90SrCl2 aerosols and had 

long-term retained burdens >10 μCi (370 kBq) 90Sr/kg (Gillett et al. 1987a). Profound decreases in 

platelet numbers were evident by 7 days and were maximal by 28 days. Drastic thrombocytopenia 

(platelets reduced >90%) probably contributed to widespread hemorrhaging and premature death in dogs 

with long-term retained burdens ≥47 μCi/kg (≥1.7 MBq/kg). Significant immediate reductions in platelet 

counts (>60%) occurred in surviving dogs with long-term retained burdens of ≥1.5 μCi/kg 

(≥0.56 MBq/kg). However, even dogs with the lowest long-term retained burdens (1–10 μCi/kg; 0.04– 

0.36 MBq/kg), which otherwise showed little immediate effect, exhibited long-term (>3 years) depression 

in platelet counts compared to controls. The pattern of neutropenia followed a similar exposure-response, 
STRONTIUM 72 

3. HEALTH EFFECTS 

and profound neutropenia was the most accurate predictor of death. In surviving dogs that were 

immediately affected by exposure, neutrophil counts recovered, but in these dogs, as well as those 

immediately unaffected, significant long-term (>3 years) suppression was observed compared to controls. 

Similarly, lymphocyte counts were drastically reduced (by 75%) in dogs dying within weeks of exposure 

with long-term retained burdens ≥47 μCi/kg (≥1.7 MBq/kg). Surviving dogs with long-term retained 

burdens >10 μCi (370 kBq) 90Sr/kg exhibited a long-term (>3 years) suppression of lymphocyte counts 

(>30%). Dogs with long-term retained burdens between 6 and 10 μCi/kg (0.26–0.36 MBq/kg) exhibited 

normal lymphocyte counts that were normal over 1,400 days except for periods of significant depression 

at 60–120 and 900–1,000 days. Dogs with long-term retained burdens between 1 and 3 μCi/kg (0.04– 

0.12 MBq/kg) had lymphocyte counts that were not significantly different from controls. Reduced 

erythrocyte mass, as exemplified by decreases in hematocrit, red blood cell counts, and hemoglobin 

levels, occurred between 2 and 3 weeks after exposure (slightly later than the depression in platelet and 

white cell counts). In the most severely affected dogs, red blood cell counts fell to 70–80% of preexposure values, with maximal depression at 32 days. Prolonged depression of erythrocyte counts was 

observed in surviving dogs with long-term retained burdens ≥27 μCi/kg (≥1 MBq/kg). 

Significant suppression of peripheral lymphocyte counts was observed in beagle dogs that were exposed 

by inhalation to 90Sr fused-clay particles (Jones et al. 1976). Lymphocytes declined gradually over time 

in all exposed groups (initial lung burdens ≥5 μCi/kg; ≥185 kBq/kg), and remained more than 50% lower 

than controls after 2 years. 

Hepatic Effects. No studies were located that described hepatic effects in humans following 

inhalation exposure to radioactive strontium. All beagle dogs that died from radiation pneumonitis 

following a single inhalation exposure to high concentrations of 90Sr fused-clay particles (25 μCi 90Sr/kg 

of body weight; 925 kBq/kg) exhibited chronic passive congestion of the liver, and one had mild 

centrilobular fibrosis (Benjamin et al. 1976c). 

Renal Effects. No studies were located that described renal effects in humans following inhalation 

exposure to radioactive strontium isotopes. Some beagle dogs in the terminal stages of acute radiation 

syndrome following inhalation exposure to aerosols of 90SrCl2 (long-term retained burden 

47–83 μCi 90Sr/kg; 1.74–3.07 MBq/kg) had low urine output and elevated blood urea nitrogen (Gillett et 

al. 1987a). 
STRONTIUM 73 

3. HEALTH EFFECTS 

Body Weight Effects No studies were located that described body weight effects in humans 

following inhalation of radiostrontium. Anorexia and reduced body weight were observed among beagle 

dogs with long-term retained burdens between 45 and 119 μCi/kg (1.7–4.4 MBq/kg) following inhalation 

of 90SrCl2 aerosols (Gillett et al. 1987a; Muggenburg et al. 1977) or initial lung burdens between 25 and 

32 μCi/kg (0.93–1.2 MBq/kg) following inhalation of 90Sr fused-clay particles (Benjamin et al. 1976c). 

3.3.1.3 Immunological and Lymphoreticular Effects 

No studies were located regarding immunological effects in humans following inhalation exposure to 

radioactive strontium isotopes. However, profound effects on the immune system were a consequence of 

acute inhalation exposure to radiostrontium in dog studies. Effects in dogs exposed to soluble aerosols of 

90SrCl2 were sequelae of general irradiation of the bone marrow from 90Sr incorporated into bone. 

Significant dose-related lymphopenia was observed in young adult beagle dogs (12–14 months old) after 

a single inhalation exposure to 90SrCl2 at long-term retained burdens >10 μCi 90Sr/kg (370 kBq/kg; Gillett 

et al. 1987a). Furthermore, there was some evidence of immunosuppression in dogs with average initial 

body burdens of 35 μCi 90Sr/kg (1.3 MBq/kg) (Fission Product Inhalation Project 1967a); titers for 

infectious canine hepatitis and leptospira vaccines were depressed more than 30% following exposure to 

90SrCl2 aerosols. Effects in dogs exposed to relatively insoluble 90Sr fused-clay particles were primarily a 

consequence of irradiation of the blood as it circulated through the lungs, although some damage to 

thoracic lymph nodes was observed. Among beagle dogs (17–20 months old) exposed by nose-only 

inhalation to 90Sr fused clay particles (initial lung burdens 25–32 μCi 90Sr/kg; 0.925–1.18 MBq/kg), the 

numbers of peripheral lymphocytes were depressed by more than 50% during the 12th through 28th weeks 

after exposure, although recovery was observed by week 44 (Benjamin et al. 1976c). The cumulative 

radiation dose to the lungs ranged from 35,000 to 43,000 rad (350–430 Gy). During the period of 

lymphocyte suppression, the immune response to phytohemagglutinin antigen tested in vitro was 

depressed 10-fold in the dog that had the highest initial lung burden (32 μCi/kg; 1.18 MBq/kg) and was 

the first to die. In this animal, the tracheobronchial and sternal lymph nodes, which received a significant 

radiation dose from 90Sr, were depleted of lymphocytes, although peripheral nodes, which received much 

lower doses, were nearly normal. In the main study that employed 1-year-old beagles, the highest initial 

lung burdens of 90Sr fused-clay particles resulted in severe atrophy and fibrosis of the tracheobronchial 

lymph nodes (Snipes et al. 1977). In other dogs, which had initial lung burdens averaging between 5 and 

19 μCi/kg (185 and 703 kBq/kg), fluctuations in the peripheral lymphocyte numbers were observed, but 

the values remained depressed by 40% for 2 years following inhalation exposure (Jones et al. 1976). 
STRONTIUM 74 

3. HEALTH EFFECTS 

Cumulative doses in these dogs ranged from 1,055 to 4,005 rad (10.5–40 Gy). None of the dog studies 

reported whether there was a NOAEL identified for immunological effects. Significant chronic 

suppression of the immune system is considered a serious effect because of the impaired resistance to 

infectious disease. 

3.3.1.4 Neurological Effects 

No studies were located that described neurological effects in humans following inhalation exposure to 

radioactive strontium. A beagle dog that was exposed to the highest concentration of 90SrCl2 aerosol 

(long-term retained burden of 119 μCi/kg or 4.4 MBq/kg) succumbed with epileptic seizures, but the 

authors deemed these to be unrelated to exposure (Gillett et al. 1987b). Serious neurological effects 

(convulsions, paralysis) were observed in several dogs that were in the terminal stages of cancer 

following inhalation of 90Sr fused clay particles (Snipes et al. 1977, 1978). No other studies addressed 

neurological effects in animals following inhalation exposure to radioactive strontium isotopes. 

The highest NOAEL values and all reliable LOAEL values in each species and duration category for 

neurological effects from exposure to radioactive strontium by the inhalation route are presented in 

Table 3-2 and plotted in Figure 3-2. 

No studies were located regarding the following effects in humans or animals following inhalation 

exposure to radioactive strontium: 

3.3.1.5 Reproductive Effects 

3.3.1.6 Developmental Effects 

3.3.1.7 Cancer 

No studies were located regarding cancer in humans following inhalation exposure to radioactive 

strontium isotopes, but several studies reported carcinogenetic effects in animals. The types of cancers 

produced varied with the form of strontium administered. In studies using soluble forms of radioactive 

strontium, (e.g., 90SrCl2), bone-associated cancers were the predominant types, because absorbed 

strontium primarily incorporates into bone. Studies using relatively insoluble 90Sr fused-clay particles 
STRONTIUM 75 

3. HEALTH EFFECTS 

reported lung-related cancers as the major initial types, since the particles were initially embedded in the 

lungs. As particles slowly dissolved (releasing 90Sr) or were cleared from the lungs, tumors were induced 

in other tissues. 

In two different experiments described in a report by the Lovelace Foundation (now known as the 

Lovelace Respiratory Research Institute), young male and female Holtzman rats were exposed once to an 

aerosol of 90Sr in cesium chloride by whole body inhalation for initial body burdens ranging from 170 to 

1,660 μCi 90Sr/kg (6.3–61.4 MBq/kg) of body weight (Fission Product Inhalation Project 1967b). The 

average skeletal radiation doses over their remaining lifespans averaged from 12,600 to 25,900 rad (126– 

259 Gy). In the two experiments, 77 or 47% of the rats that died or were euthanized in a moribund state 

were found to have bone tumors (osteosarcomas). Among rats dying with tumors, the average skeletal 

dose rate was 81 rad/day, compared to 62 rad/day for rats without tumors (0.81 vs 0.62 Gy/day). 

Primary bone cancer was the most frequent cause of death in beagle dogs (30/66) given a single 

inhalation exposure to 90SrCl2 aerosol and then observed for their lifespans (Benjamin et al. 1974a, 1976a, 

1979; Gillett et al. 1987b; McClellan et al. 1973; Muggenburg et al. 1977, 1978, 1979). The cumulative 

absorbed doses of beta radiation to bone ranged from 12 to 1,200 rad (0.012–12 Gy) at 30 days and from 

200 to 170,000 rad (2–1,700 Gy) at 1,000 days after exposure. In dogs with bone-related tumors, the 

long-term retained burdens ranged from 2 to 119 μCi 90Sr/kg (0.081–4.4 MBq/kg ) of body weight. 

Bone-tumor-related deaths occurred 759–3,472 days after exposure (median survival time of 1,702 days, 

compared to 4,500 days for controls). Twenty-seven tumors were classified as different subtypes of 

osteosarcoma, 14 as hemangiosarcomas, 3 as fibrosarcomas, and 1 as a myxosarcoma. Four additional 

animals developed carcinomas in soft tissues adjacent to the bones of the skull: invasive baso-squamous 

carcinoma, transitional carcinomas of the nasal cavity, and an adenocarcinoma in the maxilloturbinate 

region (Benjamin et al. 1979). In addition, two dogs died from myelomonocytic leukemia resulting from 

irradiation of bone marrow. Metastasis occurred from 21 tumors, in particular the hemangiosarcomas, 

with the lungs being the most frequent site of metastasis (76%). 

Among 127 beagle dogs exposed by inhalation to 90Sr fused-clay particles, deaths from primary 

pulmonary tumors were common: 19 dogs with hemangiosarcomas (one each also with bronchioalveolar 

carcinoma, nasal squamous cell carcinoma, or pulmonary epidermoid carcinoma), and one with 

pulmonary squamous cell carcinoma (Snipes et al. 1979). All 34 dogs exposed to 90Sr fused clay particles 

with cumulative exposures of >29,000 rad (290 Gy) developed pulmonary hemangiosarcoma. The heart 

wall was the other primary location of hemangiosarcoma (11 dogs), the others being the mediastinum, 
STRONTIUM 76 

3. HEALTH EFFECTS 

spleen, rib, lung-associated lymph nodes, and liver (Snipes et al. 1979). Hemangiosarcomas were 

metastatic in all but one affected dog. Among dogs dying prematurely from neoplasms of the lung, the 

initial lung burdens were 3.7–94 μCi/kg (0.14–3.5 MBq/kg) and the estimated cumulative doses to the 

lungs ranged from 43,000 to 67,000 rad (430–670 Gy) (Benjamin et al. 1975). Considering all dogs with 

tumors, pulmonary carcinomas or sarcomas occurred in 3/12 dogs that received cumulative radiation 

doses of 17,000–25,000 rad (170–250 Gy), but no pulmonary tumors were reported for three dogs with 

cumulative exposure levels of 11,000–15,000 rad (110–150 Gy; Hahn et al. 1983a). 

The highest NOAEL values and all reliable LOAEL values in each species and duration category for 

cancer effects from exposure to radioactive strontium by the inhalation route are presented in Table 3-2 

and plotted in Figure 3-2. 

3.3.2 Oral Exposure 

Upon ingestion, radioactive strontium isotopes become incorporated into bone, and irradiate the 

surrounding hard and soft tissues, resulting in hypoplasia of the bone marrow or various forms of cancer 

(osteosarcoma, leukemia). Adverse effects are associated with higher skeletal burdens of radioactive 

strontium. Younger organisms are more vulnerable to adverse effects of both stable and radioactive 

strontium. Maternal oral exposure to sufficient radioactive strontium can adversely affect the fetus. 

The database for oral exposures to radioactive strontium is substantial. Human health effect data are 

derived primarily from long-term and ongoing studies of a population that was exposed to contaminated 

drinking water and food following the release of large quantities of radioactive materials into the Techa 

River from a Soviet nuclear weapons facility between 1949 and 1956. This population received a mixed 

exposure to external gamma radiation and to internal radiation from 89Sr, 90Sr, and 137Cs (Akleyev et al. 

1995; Kossenko et al. 2000). Animal data include several large, long-term studies in dogs, miniature 

pigs, and rodents. In addition to the papers cited below, interim reports and analyses for the beagle 

lifetime study (Laboratory for Energy-Related Health Research at the University of California at Davis) 

were published by Nilsson and Book (1987), Nilsson et al. (1985), Pool et al. (1972, 1973b), and Raabe et 

al. (1981a, 1981b, 1983, 1994). 
STRONTIUM 77 

3. HEALTH EFFECTS 

3.3.2.1 Death 

In the Techa River population that was exposed to radiostrontium and radiocesium in drinking water and 

food between 1949 and 1956, an increase in the number of deaths from leukemia and solid cancers was 

reported (Kossenko 1996). In the exposed group, the standardized mortality rate was 140 (95% CI: 131– 

150) per 100,000 compared to 105 (95% CI: 101–109) per 100,000 in the control group during the 

followup period (1950–1982). Absorbed doses to the red bone marrow in the study group were between 

17.6 and 164 rad (0.176 and 1.64 Gy). No increase in cancer mortality was observed among offspring of 

exposed individuals. These data are omitted from Table 3-3 because the exposures were to multiple 

sources of radiation. 

Oral exposure to radioactive strontium caused dose-related increases in mortality in animal studies. In 

general, younger animals were more sensitive to the effects of radiation than older animals. There was an 

increase in deaths in a small number (6 out of 7) of Rhesus monkeys given 100 μCi of 90Sr per day 

(3.7 MBq/day) by gavage for 5 or 10 days (Casarett et al. 1962). One monkey given 11 μCi/kg/day 

(0.42 MBq/kg/day) for 5 days died 4 years after treatment from leukemia with a total skeletal dose of 

4,300 rad (43 Gy). One monkey given a dose of 28 μCi/kg/day (1.0 MBq/kg/day) for 10 days died within 

4 months of treatment from pancytopenia with an estimated skeletal dose of 4,500 rad (45 Gy). Two 

others exposed to an average of 18 μCi/kg/day (0.67 MBq/kg/day) for 10 days died from bone associated 

cancers within 36 months of treatment, and with estimated skeletal doses of 4,700–9,500 rad (47–95 Gy). 

Because of the small sample size and the fact that the animals were of different ages, this study serves as 

an indicator, but not as proof of dose-response effects of ingested radiostrontium. 

In experiments in which weanling (30 days old) and adult Long-Evans rats were given 90Sr in drinking 

water for 10 days, survival at 5 months was reduced by 80% in the weanlings consuming at least 297– 

386 μCi 90Sr/kg/day (11 MBq/kg/day; total 464 μCi or 17 MBq), but was unaffected in adults consuming 

64–194 μCi 90Sr/kg/day (7.2 MBq/kg/day; total 650 μCi or 24.1 MBq; Casarett et al. 1962). The reduced 

survival of the weanlings was consistent with their higher skeletal burden at 5 months: >20 times higher 

than in the adults. In another acute study, six young female dairy cattle (three sets of twins from three 

different strains, ages 398 and 479 days and weighing 145–349 kg at the start of treatment) were given 

44 μCi 90Sr/kg/day (1.63 MBq/kg/day) ‘orally’ for 5 days (Cragle et al. 1969). The four youngest 

(398 days) and lightest heifers (145–212 kg), which were administered a total of 32–46 mCi (1.18– 

1.70 GBq), died of radiation sickness between 93 and 132 days after treatment was started, whereas the 

older and heavier animals (342–349 kg), which had received a total of 75–77 mCi of 90Sr (2.78– 
STRONTIUM 78 

3. HEALTH EFFECTS 

2.85 GBq), were still alive 3 years after treatment. In addition to age-related differences, strain 

differences may have contributed to the results; the older cows were Holsteins, which have more massive 

skeletons than the Brown Swiss and Jersey strains. The authors suggested that the larger animals 

survived because of the wider diameter of the marrow cavity, which possibly shielded the central marrow 

from beta radiation released from 90Sr (and its 90Y decay product) deposited at the periphery of the bone 

shaft. 

In an intermediate-duration experiment, young (87-day-old) Long-Evans rats were treated with up to 

104 μCi of 90Sr per kg of body weight per day (3.8 MBq/kg/day) for 30 days over a period of 37 days 

(Casarett et al. 1962; Hopkins et al. 1966); the total amount administered was 790 μCi (29.2 MBq). In 

these rats, the estimated skeletal activity of 90Sr at 5 months was 11 μCi (407 kBq) and survival was 

reduced by about 36%. In the young rats treated for 30 days, skeletal activity was higher and survival 

was reduced accordingly compared to the adult rats treated for 10 days (see previous paragraph), but the 

differences were out of proportion to the total amounts of 90Sr administered to the two sets of rats. The 

total amount given to adults was 18% less than to the juveniles, but the skeletal doses in the adults were 

82% less, suggesting age-related differences in incorporation. 

In a lifetime study, adult CF-1 mice that were exposed to 90Sr beginning at ages 110–250 days were less 

vulnerable to continuous exposure than mice that had been exposed since conception (Finkel et al. 1960). 

The adult lifespan was shortened by 17% in mice given 31 μCi 90Sr/kg/day (1.15 MBq/kg/day), but was 

unaffected by administration of up to 16 μCi 90Sr/kg/day (592 kBq/kg/day). In mice exposed from 

conception, the lifetime was shortened by 40% when given 36 μCi 90Sr/kg/day (1.33 MBq/kg/day), and 

by 26% when given between 4 and 19 μCi 90Sr/kg/day (148 and 703 kBq/kg/day), but was unaffected by 

0.05–0.4 μCi 90Sr/kg/day (1.85–14.8 kBq/kg/day). In albino rats that were fed 0.5 or 2 μCi 90Sr/kg/day 

(18.5 or 74 kBq/kg/day) for their postweaning lifetime, the lifespan was shortened, by about 18 or 30%, 

respectively, compared to controls (Zapol’skaya et al. 1974). The authors calculated that the lifespan was 

shortened by 0.09 day per rad. A plot of mortality against absorbed dose showed maximum mortality 

(40%) against a skeletal absorbed dose of 4,000 rad (40 Gy). In a study in which eight weanling Dutch 

rabbits were fed approximately 6 μCi/kg/day (218 kBq/kg/day) in pellets once a day for 31–280 days, 

some died within a few weeks with bone marrow that was slightly hypoplastic (Downie et al. 1959). The 

bone marrow was entirely atrophic in rabbits dying several months later with osteogenic sarcoma. 

Two related long-term oral exposure studies demonstrated dose-related effects of 90SrCl2 on survival in 

beagle dogs. In the main study, groups of pregnant beagles were fed 0.002–3.6 μCi 90Sr/kg/day (0.074– 
STRONTIUM 79 

3. HEALTH EFFECTS 

133.2 kBq/kg/day) from gestational day 21 through lactation to postnatal day 44, and the pups were fed 

the same doses from weaning at day 42 through day 540 (Raabe et al. 1983; White et al. 1993). Survival 

of the pups was reduced by 18, 64, and 85% at the three highest levels (0.4, 1.2, and 3.6 μCi/kg/day or 

14.8, 44.4, and 133.2 kBq/kg/day, respectively). Survival was not significantly different from the 

controls for exposures of 0.002–0.13 μCi/kg/day (0.074–4.8 kBq/kg/day). Mean absorbed skeletal 

absorbed doses at or below 2,250 rad (22.5 Gy) had no effect on mortality, whereas increased mortality 

was observed at or above 5,040 rad (50.4 Gy). The secondary study had a similar protocol, except that 

the dogs were given doses of 0.13–1.2 μCi/day (4.81–44.4 kBq/day) from gestational day 21 throughout 

their entire lifetime (Book et al. 1982). The mean lifetime absorbed skeletal doses were 2,840–11,190 rad 

(28.4–111.9 Gy). The median lifespans were reduced by 11–65%, which was similar to the results of the 

main study. This implies that irradiation after day 540 did not significantly change the survival rate and 

that survival was shortened because of exposure at a young age. The two main radiation-related causes of 

death in these studies were myeloproliferative syndrome and skeletal sarcomas (see Section 3.3.2.7 

Cancer). 

In a multigenerational study of female Pitman-Moore miniature swine, there were dose-related effects on 

mortality following chronic ingestion of 90Sr in the form of strontium chloride (Clarke et al. 1970; 

McClellan et al. 1963; Ragan et al. 1973). Sows ingesting 3,100 μCi 90Sr/day (114.7 MBq/day) from age 

9 months did not survive their first pregnancy, succumbing from the destruction of hemopoietic tissue in 

the bone marrow. The sows developed anemia, leukopenia, thrombocytopenia, and terminal hemorrhagic 

syndrome (Clarke et al. 1972). Exposure to 25, 125, or 625 μCi 90Sr/day (0.925, 4.625, or 

23.13 MBq/day) significantly increased mortality after 11, 5, and 1 year(s), respectively, whereas 

exposure to 1 or 5 μCi 90Sr/day (37 or 185 kBq/day) had no effect on survival. Effects on the F1 females 

exposed from the time of conception were more severe, even though, after weaning, their administered 

dose level was only a fraction of the maternal level until the age of 6 months. None of the F1 females 

exposed to 625 μCi 90Sr/day (23.13 MBq/day) survived to the age of 9 months, whereas that dose was not 

immediately fatal to the parental generation of sows. Furthermore, the F1 females receiving 25 μCi 

90Sr/day (925 kBq/day) showed a significant increase in cumulative mortality after 7 years, rather than 11. 

However, the 1 and 5 μCi 90Sr/day levels (37 and 185 kBq/day), as in the parental generation, had no 

effect on survival. In this study, the average attained body burden was 10, 50, 250, 1,250, and 4,700 μCi 

(0.37, 1.85, 9.25, 46.25, and 173.9 MBq) for the 1, 5, 25, 125, and 625 μCi 90Sr/day (0.037, 0.185, 0.925, 

4.625, and 23.13 MBq/day) levels, respectively. 
STRONTIUM 80 

3. HEALTH EFFECTS 

All reliable LOAEL values for death from oral exposure to radioactive strontium in each species and 

duration category are recorded in Table 3-3 and plotted in Figure 3-3. 

3.3.2.2 Systemic Effects 

No studies were located regarding endocrine, dermal, or metabolic effects in humans or animals after oral 

exposure to radioactive strontium. The highest reliable NOAEL and all LOAEL values for the systemic 

effects from oral exposure to radioactive strontium are shown in Table 3-3 and plotted in Figure 3-3. 

Respiratory Effects. No studies were located regarding respiratory effects in humans following oral 

exposure to radioactive strontium isotopes. No studies were located regarding respiratory effects in 

animals following acute- or intermediate-duration exposure to radioactive strontium. In a chronicduration beagle study, animals exposed to 0.4 or 1.2 μCi/kg/day (14.8 or 44.4 kBq/kg/day) of 90Sr in 

utero from gestational day 21, throughout lactation, and from weaning on day 42 to day 540 exhibited 

only secondary respiratory effects (Dungworth et al. 1969); lungs showed varying degrees of myeloid 

infiltration (see Section 3.3.2.7 Cancer). Since this effect is not the direct result of the action of 

radiostrontium on lung tissue, but rather a secondary effect of myeloid proliferation induced by irradiation 

of bone marrow, it is not categorized under Systemic: Respiratory Effects in Table 3-3. 

Cardiovascular Effects. No studies were located regarding cardiovascular effects in humans after 

oral exposure to radioactive strontium isotopes. No studies were located regarding cardiovascular effects 

in animals after acute- or intermediate-duration oral exposure to radioactive strontium isotopes. 

Petechiae, ecchymoses, and gastrointestinal bleeding were found postmortem in some beagles in a 

chronic-duration study, in which animals were exposed to 0.002–1.2 μCi 90Sr/kg/day (0.074– 

44.4 kBq/kg/day) in utero from gestational day 21, throughout lactation, and from weaning on day 42 to 

day 540 (Dungworth et al. 1969). These findings, observed in high dose animals (0.4 and 1.2 μCi/kg/day; 

14.8 and 44.4 kBq/kg/day), indicated the presence of a hemorrhagic disorder related to thrombocytopenia 

(see Hematological Effects below). 

The highest reliable NOAEL and all LOAEL values for cardiovascular effects from oral exposure to 

radioactive strontium in each species and duration category are shown in Table 3-3 and plotted in 

Figure 3-3. 
Table 3-3 Levels of Significant Exposure to Strontium - Radiation Toxicity - Oral 

Exposure/ LOAEL

Duration/

a Frequency 

Key to Species NOAEL Less Serious Serious (Specific Route) figure (Strain) System (uCi/kg/day) (uCi/kg/day) (uCi/kg/day) 

ACUTE EXPOSURE Death 

1 Monkey 5-10 d 

28 M (1/1 dead within 4 months (Rhesus) (GW) from pancytopenia; est 

skeletal dose at death =4,500 rad) 

2 Rat 10 d 

297 M (lifespan decr 80%) (Long- Evans) ad lib 

(W) 

3 Cow 5 d 

44 F (4/6 died within 5 months) 1 x/d 

	 

Systemic 

4 Rat 10 d 

Hemato 297 M (hypoplasia of bone marrow) (Long- Evans) ad lib 

(W) 


 

Musc/skel 297 M (failure of osteogenesis) 

5 Rat 10 d 

ad lib Hemato 64 M (slight hypoplasia of bone (Long- Evans) marrow) 

(W) 

6 Cow 5 d 

Gastro 44 F (intestinal hemorrhage) 1 x/d 

Hemato 44 F (severe leukopenia, 

thrombocytopenia) 

Reproductive 

7 Rat once 

0.15 F (20% fetal mortality) (G) 

	 	 	 


 

	 	 	 	 

	 	 	 	 
Table 3-3 Levels of Significant Exposure to Strontium - Radiation Toxicity - Oral (continued) 

a 

Key to 

figure 

Species 

(Strain)	 

Exposure/ 

Duration/

Frequency 

(Specific Route) System 

NOAEL 

(uCi/kg/day) 

LOAEL
 

Less Serious 

(uCi/kg/day) 

Serious 

(uCi/kg/day) 

8 9 

10 

11 

12 13 14 

Cancer Monkey 5-10 d 

1 x/d (Rhesus) 

(GW)

Rat 10 d

(Long- Evans) ad lib

(W) 

Rat 10 d

(Long- Evans) ad lib

(W) 

INTERMEDIATE EXPOSUREDeathRat 30 d

(Long- Evans) ad lib

(W) 

Rabbit 31-280 d

1 x/d (Dutch)

(F) 

Systemic Rat 30 d 

(Long- Evans) ad lib

(W) 

Rabbit 31-280 d

1 x/d (Dutch)

(F) 


 

	 	 


 	 	 	 

	 	 	 

	 	 
 Hemato Musc/skel Hemato

Musc/skel 

	 	 	 

11 (CEL: leukemia in 1/1)

300 M (CEL: osteosarcoma)135 M (CEL: 2 x incr in incidence of

malignancies) 

	 

74 M (35% decr survival)

6 (premature death from bone

marrow hypoplasia) 

74 M (moderate bone marrow

hypoplasia) 

74 M (damaged epiphyseal cartilage

6 (bone marrow hypoplasia;

anemia, reduced platelets) 

6 (decr osteocytes, decr blood 

vessels of bone) 
Table 3-3 Levels of Significant Exposure to Strontium - Radiation Toxicity - Oral (continued) 

a 

Key to 

figure 

Species 

(Strain) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(uCi/kg/day) 

Less Serious 

(uCi/kg/day) 

LOAEL 

(uCi/kg/day) 

Serious 

15 16 

Reproductive 

(CF-1) 

(F) 

600 d ad lib 

Mouse Cancer 

(Long- Evans) 

(W) 

30 d ad lib 

Rat 

31 F 

74 (CEL: 28% osteosarcoma, 

11% skin carcinoma, 6% leukemia compared to none in control group) 

M 

17 

(Long- Evans) 

37 d 1 x 30 d ad lib 

Rat 74 F (CEL: osteosarcoma) 

(W) 

18 19 

(Dutch) 

(F) 

31-280 d 1 x/d 

Rabbit 

CHRONIC EXPOSURE Death 

(albino) 

372-620 d daily ad lib 

Rat 

6 (CEL: osteosarcoma; 

multiple myeloma) 

0.5 (18% mortality) 

(F) 

20 

(CF-1) 

Mouse 

(F) 

600 d ad lib 31 F (survival decr 17%) 

21 

(CF-1) 

Mouse 

(F) 

GD0-PND 414 ad lib 4 F (survival decr 36%) 
Table 3-3 Levels of Significant Exposure to Strontium - Radiation Toxicity - Oral (continued) 

a 

Key to 

figure 

Species 

(Strain) 

Exposure/ 

Duration/

Frequency 

(Specific Route) System 

NOAEL 

(uCi/kg/day) 

LOAEL
 

Less Serious 

(uCi/kg/day) 

Serious 

(uCi/kg/day) 

22 

23 

24 

25 26 

Systemic Rat 

(albino) 

Mouse 

(CF-1) 

Dog 

(Beagle) 

Dog 

(Beagle) 

Dog 

(Beagle) 

372-620 d dailyad lib 

(F) 

GD0-PND 414 

ad lib

(F) 

GD40-death ad lib

(F) 

GD40-PND540ad lib 

(F) 

GD40-PND540ad lib 

(F) 

Hemato 

Bd Wt 

Musc/skel 

Cardio Hemato Hepatic Bd Wt Musc/skel 

36 F 

0.5 (~21% leukopenia lasting 2

yrs) 

0.4 M (osteodystrophy)

0.4 M (petechiae, ecchymoses,

gastrointestinal bleeding) 

0.4 M (leukopenia, anemia, 

thrombocytopenia; poikilocytosis, anisocytosis, hypochromasia of erythrocytes) 

0.4 M (periacinar lipidosis; 

terminal necrosis) 

0.4 M (progressive weight loss 

in anemic dogs) 

0.4 M (osteolytic lesions,

osteoporosis, cortical sclerosis and thickening,mottling) 
Table 3-3 Levels of Significant Exposure to Strontium - Radiation Toxicity - Oral (continued) 

a 

Key to 

figure 

Species 

(Strain) 

Exposure/ 

Duration/

Frequency 

(Specific Route) System 

NOAEL 

(uCi/kg/day) 

LOAEL
 

Less Serious 

(uCi/kg/day) 

Serious 

(uCi/kg/day) 

27 28 29 

30 

31 

32 

33 

Immuno/ Lymphoret Dog GD40-PND540 

ad lib (Beagle) 

(F) 

Developmental Mouse 600 d 

ad lib (CF-1) 

(F) 

Cancer Rat 372-620 d 

daily (albino) ad lib 

(F) 

Mouse 600 d 

ad lib (CF-1) 

(F) 

Mouse GD0-PND 414 

ad lib (CF-1) 

(F) 

Dog GD40-death 

ad lib (Beagle) 

(F) 

Dog GD40-

PND540 (Beagle) ad lib 

(F) 

0.4 M (splenic myeloid metaplasia)

3 F (decr postnatal survival

from cancer) 

2 (CEL: lymphosarcoma,

osteosarcoma) 

0.03 F (CEL: reticular tumors)

36 F (CEL: 4x incr reticulocyte

tumors; osteosarcoma) 

0.4 M (premature death from

cancer) 

1.3 M (CEL: osteosarcoma)0.4 M (incr death from cancer)

a The number corresponds to entries in Figure 3-3. 

Ad lib - ad libitum; Bd Wt = body weight; Cardio = cardiovascular; CEL = cancer effect level; d = day(s); decr = decreased; (F) = food; (G) = gavage; Gastro = g

gestational day; (GW) = gavage in water; Hemato = hematological; incr = increased; LOAEL = lowest-observed-adverse-effect level; min = minute(s); mo = momusculoskeletal; NOAEL = no-observed-adverse-effect level; PND = post natal day; (W) = water; wk = week(s); x = time(s); yr = year(s) 
Gastrointestinal Hematological Musculoskeletal Reproductive Cancer * 

1000 

Death 

Figure 3-3 Levels of Significant Exposure to Strontium - Radiation Toxicity - Oral 

Acute (≤14 days) 

Systemic 

uCi/kg 

9r 10r 

2r 4r 4r 

100 

5r
 

3q
 6q 6q
 

1k
 

8k 10 

1 

7r *Doses represent the lowest dose tested per study that 

response and do not imply the existence of a threshold 

0.1 

c-Cat -Humans f-Ferret n-Mink Cancer Effect Level-Animals Cancer Effect Level-Humans 

d-Dog k-Monkey j-Pigeon o-Other LOAEL, More Serious-Animals LOAEL, More Serious-Humans 

r-Rat m-Mouse e-Gerbil LOAEL, Less Serious-Animals LOAEL, Less Serious-Humans 

p-Pig h-Rabbit s-Hamster NOAEL - Animals NOAEL - Humans 

q-Cow a-Sheep g-Guinea Pig 
Hematological Musculoskeletal Reproductive Cancer * 

100 

Death 

Figure 3-3 Levels of Significant Exposure to Strontium - Radiation Toxicity - Oral (Continu

Intermediate (15-364 days) 

Systemic 

uCi/kg 

11r 13r 13r 16r 17r 

15m 

10 

12h 14h 14h 18h 

*Doses represent the lowest dose tested per study that produced a tumorigenic response and do not imply the existence of a threshold for the cancer endpoint. 

1 

c-Cat -Humans f-Ferret n-Mink Cancer Effect Level-Animals Cancer Effect Level-Humans 

d-Dog k-Monkey j-Pigeon o-Other LOAEL, More Serious-Animals LOAEL, More Serious-Humans 

r-Rat m-Mouse e-Gerbil LOAEL, Less Serious-Animals LOAEL, Less Serious-Humans 

p-Pig h-Rabbit s-Hamster NOAEL - Animals NOAEL - Humans 

q-Cow a-Sheep g-Guinea Pig 
Cardiovascular Hematological Musculoskeletal Hepatic Body W Immuno/L Developmental Cancer * 

100 

Death eight ymphor 

Figure 3-3 Levels of Significant Exposure to Strontium - Radiation Toxicity - Oral (Continued) 

Chronic (≥365 days) 

Systemic 

uCi/kg 

23m 31m 20m 

10 

21m 

28m 

29r 

33d 

1 

19r 22r 

25d 25d 24d 26d 25d 25d 27d 32d 33d 

0.1 

30m 

*Doses represent the lowest dose tested per study that produced a tumorigenic
 response and do not imply the existence of a threshold for the cancer endpoint.
 

0.01 

c-Cat -Humans f-Ferret n-Mink Cancer Effect Level-Animals Cancer Effect Level-Humans 

d-Dog k-Monkey j-Pigeon o-Other LOAEL, More Serious-Animals LOAEL, More Serious-Humans r-Rat m-Mouse e-Gerbil LOAEL, Less Serious-Animals LOAEL, Less Serious-Humans p-Pig h-Rabbit s-Hamster NOAEL - Animals NOAEL - Humans 

q-Cow a-Sheep g-Guinea Pig 
STRONTIUM 89 

3. HEALTH EFFECTS 

Gastrointestinal Effects. No studies were located regarding gastrointestinal effects in humans after 

oral exposure to radioactive strontium. Intestinal hemorrhage occurred in cows succumbing to radiation 

sickness 3 months after ingesting 44 μCi 90Sr/kg/day (1.63 MBq/kg/day) for 5 days (Cragle et al. 1969). 

It is likely that other reports of terminal hemorrhagic effects (see Hematological Effects below) following 

high doses of radiostrontium encompassed intestinal hemorrhage whether or not it was specifically 

mentioned. 

Hematological Effects. In human and animal studies, adverse hematological affects were associated 

with beta radiation of bone marrow following incorporation of radiostrontium into bone. 

The Techa River population exposed to chronic combined external gamma radiation and internal radiation 

due to 90Sr and 137Cs exhibited alterations in hematological parameters, including leukopenia, 

thrombocytopenia, and granulocytopenia (Akleyev et al. 1995). These effects were observed in a portion 

of the exposed population that received radiation doses to the bone marrow at rates in excess of 30– 

50 rem (0.3–0.5 Sv) per year. These data are omitted from Table 3-3 because exposures were to multiple 

sources of radiation. 

Among Rhesus monkeys given 1,000 μCi (37 MBq) of 90Sr over 10 days, the one with the highest dose on 

a kg body weight basis (28 μCi/kg/day; 1.0 MBq/kg/day) died from pancytopenia within 4 months of 

treatment (Casarett et al. 1962). Among young (30 days old) Long-Evans rats that were given >300 μCi 

90Sr/kg/day (11 MBq/kg/day) in drinking water for 10 days (total 460 μCi; 17 MBq), the bone marrow 

was extremely hypoplastic. Hypoplastic effects were slight among adult males given doses of 64 or 

135 μCi/kg/day or adult females given 92 or 194 μCi/kg/day (total 330 or 650 μCi; total 12.2 or 

24.1 MBq; Casarett et al. 1962). Skeletal radiation doses were about 15 times higher in the younger rats. 

In another acute study, six young female dairy cattle (three sets of twins, ages 398 and 479 days and 

weighing 145–349 kg at the start of treatment) were given 44 μCi 90Sr/kg/day (1.63 MBq/kg/day) for 

5 days (Cragle et al. 1969). All six heifers exhibited decreases in leukocyte and platelet counts by the 

first month. In surviving animals, the counts plateaued at about 60% of the normal value. In four 

animals, the youngest (398 days old) and lightest (145–212 kg) at the time of dosing, leukocyte and 

platelet counts dropped severely after 80 days, shortly before the onset of the terminal stages of radiation 

sickness. 

In an intermediate-duration study in young Long-Evans rats, moderate hypoplasia of the bone marrow 

occurred among males (87 days old) given 74 μCi/kg/day and females given 104 μCi/kg/day (2.7 and 
STRONTIUM 90 

3. HEALTH EFFECTS 

3.8 MBq/kg/day, respectively) of 90Sr in drinking water for 30 days (total 790 μCi; 29.2 MBq) (Casarett 

et al. 1962). Hypoplasia of the bone marrow leading to anemia and thrombocytopenia developed in 

Dutch rabbits that were fed approximately 6 μCi 90Sr/kg/day (218 kBq/kg/day) in pellets for 31–280 days 

(Downie et al. 1959). 

Chronic-duration studies in several species reported suppression of hematopoiesis. In albino rats fed 

≥0.5 μCi 90Sr/kg/day (18.5 kBq/kg/day) for their post-weaning lifetime, hematopoiesis was significantly 

depressed (Zapol’skaya et al. 1974). Lymphocytes were the first cells affected, then neutrophils, 

thrombocytes, and after 1 year, erythrocytes. Morphological abnormalities included binucleation. At 

0.5 μCi 90Sr/kg/day (18.5 kBq/kg/day), leukocyte numbers remained 20% depressed by the end of the 

second year. The authors calculated that the minimal dose to induce leukopenia was 150–200 rad. The 

reduction in leucocytes plateaued at about 30–35% for absorbed doses between 400 and 2,000 rad. 

Hematological effects were reported in a chronic-duration beagle study, in which animals were exposed 

to 0.002–1.2 μCi/kg/day (0.074–44.4 kBq/kg/day) of 90Sr in utero from gestational day 21, throughout 

lactation, and from weaning on day 42 to day 540 (Dungworth et al. 1969). Six years after exposure 

began, the following effects were observed at doses of 0.44 or 1.2 μCi/kg/day (14.8 or 44.4 kBq/kg/day): 

abnormal erythrocyte morphology (primarily poikilocytosis, anisocytosis, and hypochromasia, with some 

instances of macrocytosis), dose-related, radiation-induced leukopenia, an abnormal number of immature 

granulocytes, one case of unusual giant neutophils, a reduction in the number of platelets, anemia, and 

splenomegaly. Similarly, female Pitman-Moore miniature swine exposed to 3,100 μCi 90Sr/day 

(114.7 MBq/day) as strontium chloride died within 3–4 months from destruction of hematopoietic tissue 

in bone marrow, which resulted in anemia, leukopenia, thrombocytopenia, and terminal hemorrhagic 

syndrome (Clarke et al. 1972). In addition, two animals in this group developed myeloid metaplasia. 

Musculoskeletal Effects. Skeletal effects following oral exposure to radioactive strontium have 

been reported in humans and animals. Dystrophic lesions of the skeleton, primarily affecting articular 

and periarticular tissues, were observed in the Techa River populations that were chronically exposed to 

radiostrontium and other radionuclides in contaminated food and water (Akleyev et al. 1995). The 

incidence of skeletal lesions was significantly higher for mean radiation doses to the surface of bone in 

excess of 200 rem (2 Sv). 

In an acute uptake, chronic radiation study, male and female 30-day-old Long-Evans rats that were given 

300 or 390 μCi 90Sr/kg/day, respectively (11 or 14.4 MBq/kg/day) in drinking water for 5–10 days (total 

460 μCi; 17 MBq) exhibited signs of abnormal osteogenesis more than 10 months after administration 
STRONTIUM 91 

3. HEALTH EFFECTS 

(Casarett et al. 1962). As marrow failed to invade into metaphyseal cartilage, the cartilage resumed active 

proliferation. Resorption failed to occur in metaphyseal cartilage and metaphyseal spongiosa failed to 

transform to lamellar bone. Often, cartilage and fibrous marrow were incorporated into cortical bone, 

sometimes causing fracture and deformation. 

In an intermediate uptake, chronic radiation study on young (87 days old) Long-Evans rats, ingestion of 

74 (males) or 104 (females) μCi 90Sr /kg/day (2.7 or 3.8 MBq/kg/day) in drinking water for 30 days (total 

790 μCi; 28.9 MBq) adversely affected the vasculature of the bone, which interfered with the normal 

transformation of cartilage into bone (Casarett et al. 1962). At the end of the long bones, the cartilage 

discs were damaged, with detachment of primary spongiosa and failure of resorption. In another 

intermediate-duration study, numbers of osteocytes (bone cells surrounded by a mineralized matrix and 

connected by a mesh-work of processes) were reduced in Dutch rabbits that ingested approximately 6 μCi 

90Sr/kg/day (218 kBq/kg/day) in pellets for 48 days (Downie et al. 1959). 

Bone damage was a notable effect of chronic-duration oral exposure to radioactive strontium in dogs 

(Momeni et al. 1976). Groups of pregnant beagles were fed 0.002–3.6 μCi 90Sr/kg/day (0.074– 

133.2 kBq/kg/day) from gestational day 21 through lactation to PND 44, and the pups were fed the same 

doses from weaning at day 42 through day 540 (Raabe et al. 1983; White et al. 1993). Ten years from the 

start of the study, dose-related skeletal effects included mild trabecular osteopenia, endosteal and 

periosteal cortical changes (sclerosis and thickening), and mottling or focal osteolytic lesions (Momeni et 

al. 1976). These occurred in all the dogs in the 3.6 μCi/kg/day group and also in the 1.2 and 

0.4 μCi/kg/day groups (133.2, 44.4, and 14.8 kBq/kg/day, respectively). Radiation-induced 

osteodystrophy was noted in three out of four beagle dogs that received 1.2 μCi 90Sr/kg/day 

(44.4 kBq/kg/day) for life beginning at midgestion (Book et al. 1982); the average dose rate (cumulative 

dose divided by lifespan) for these dogs was 4 rad/day (0.04 Gy/day). Radiation osteonecrosis was said 

to be a common finding among female Pitman-Moore miniature swine that died with hematopoietic 

disorders or bone marrow hypoplasia after ingesting 90SrCl2 at levels between 1 and 3,100 μCi/day (0.37– 

114.7 MBq/day) until death (Clarke et al. 1972). The incidence of osteonecrosis at each dose level was 

not reported. Bone cancers that were reported in these chronic studies are discussed below in 

Section 3.3.2.7. 

Hepatic Effects. No studies were located regarding hepatic effects in humans after oral exposure to 

radioactive strontium isotopes. No studies were located regarding hepatic effects in animals after acuteor intermediate-duration oral exposure to radioactive strontium isotopes. In a chronic-duration beagle 
STRONTIUM 92 

3. HEALTH EFFECTS 

study, animals exposed to 0.4 or 1.2 μCi 90Sr/kg/day (14.8 or 44.4 kBq/kg/day) in utero from gestational 

day 21, throughout lactation, and from weaning on day 42 to day 540 exhibited only secondary hepatic 

effects (Dungworth et al. 1969). Livers were sometimes enlarged from myeloid infiltration and periacinar 

lipidosis, sometimes with terminal necrosis, in dogs with severe anemia. Since the observed myeloid 

infilitration was a secondary effect resulting from irradiation of the bone marrow, it is not categorized 

under Systemic: Hepatic Effects in Table 3-3. 

Renal Effects. No studies were located regarding renal effects in humans after oral exposure to 

radioactive strontium isotopes. Approximately 19% of adult Long-Evans rats ingesting 65 μCi 90Sr/day 

(2.41 MBq/day; 135 or 194 μCi/kg/day, 5 or 7.2 MBq/kg/day for males and females, respectively) of in 

drinking water for 10 days developed chronic interstitial nephritis, a common disease in older rats, during 

their remaining lifespan (Casarett et al. 1962). It is very unlikely that the ingestion of radiostrontium was 

related to the occurrence of nephritis. 

Ocular Effects. No studies were located regarding ocular effects in humans after oral exposure to 

radioactive strontium isotopes. 

No studies were located regarding ocular effects in animals after acute- or intermediate-duration oral 

exposure to radioactive strontium isotopes. In one chronic-duration study, 2 out of 403 beagles that had 

been exposed to 90Sr in utero from gestational day 21, during lactation, and from weaning on day 42 to 

day 540, developed a benign melanoma of the eye, but the dose-level was not reported (Raabe et al. 

1994). Statistical analysis showed that these tumors (not found in controls, but also found in dogs 

irradiated through other exposure routes, or with other radionuclides) were significantly related to 

exposure to ionizing radiation. According to a 6-year report from the same chronic-duration beagle study, 

animals exposed to 0.4 or 1.2 μCi 90Sr/kg/day (14.8 or 44.4 kBq/kg/day) in utero from gestational day 21, 

throughout lactation, and from weaning on day 42 to day 540 exhibited only indirect ocular effects 

(Dungworth et al. 1969). The eyes of dogs with a myeloproliferative disorder exhibited some slight 

degree of myeloid infiltration (see Section 3.3.2.7 Cancer). Since this was a secondary effect resulting 

from irradiation of bone marrow and not the direct response of the eye tissues to radiostrontium, it is not 

categorized under Ocular Effects in Table 3-3. 

Body Weight Effects. No studies were located regarding body weight effects in humans after oral 

exposure to radioactive strontium isotopes. No studies were located regarding body weight effects in 

animals after acute- or intermediate oral exposure to radioactive strontium. No effect on body weight was 
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3. HEALTH EFFECTS 

observed among female CF-1 mice that had been exposed to 90Sr in utero, during lactation, and up to day 

414 at doses of up to 36 μCi of 90Sr/kg/day (1.33 MBq/day) (Finkel et al. 1960). Progressive weight loss 

was observed among beagle dogs that developed anemia after having been exposed to 0.4–1.2 μCi of 

90Sr/kg/day (148–444 kBq/kg/day) from mid-gestation to age 1.5 years (Dungworth et al. 1969). 

3.3.2.3 Immunological and Lymphoreticular Effects 

Immunological changes were reported in the Techa River population that was exposed to chronic 

combined external gamma radiation and internal radiation from 90Sr and 137Cs between 1949 and 1956 

(Akleyev et al. 1995). Immunological disorders persisted for 30 years and included decreased expression 

of antigens of differentiating T-lymphocytes, decreased T-lymphoblast transformation, and reduced 

counts of large granulocytic lymphocytes. Granulocytopenia developed in a portion of the exposed 

population that received radiation to the bone marrow at rates in excess of 30–50 rem (0.3–0.5 Sv) per 

year. Akleyev et al. (1995) suggested that radiation-induced immunodeficiency may have contributed to 

the higher incidence of leukemia in the exposed population (see Section 3.3.2.7 Cancer). Clinical 

manifestations of immune insufficiency in exposed cancer patients included 3-fold increases in the 

incidences of infectious diseases (chronic pneumonia, chronic bronchitis, pulmonary tuberculosis, and 

osteomyelitis) compared to a nontumor-bearing group. These data are omitted from Table 3-3 because of 

the mixed exposures. 

No animal studies were located that described immunological effects following acute oral uptake of 

radiostrontium. Intermediate-to-chronic-duration exposures to radiostrontium resulted in impaired 

immune function in animals. In Pitman-Moore miniature pigs that were fed 625 μCi 90Sr/day 

(23.13 MBq/day) as strontium chloride for 9 months, the antibody response to inoculated Brucella 

abortus (strain 19) antigen was determined by the plate agglutination test to be less than half that of 

controls (Howard 1970). In another test, peripheral leukocyte cultures were prepared from these same 

animals at monthly intervals, in medium containing phytohemagglutinin (PHA). In pigs that were fed 

625 μCi 90Sr/day (23.13 MBq/day) for 4–5 months, peripheral lymphocytes lost the ability to respond to 

PHA stimulation; this adverse effect was sustained for at least 6 months. The author attributed these 

immunological effects to exposure to 90Sr. Myeloid metaplasia also afflicted female Pitman-Moore 

miniature swine that were fed 3,100 μCi 90Sr/day (114.7 MBq/day) until the end of life at age 3–4 months 

(Howard and Clarke 1970). The cumulative doses at the time of death ranged from 40 to 10,000 rad (0.4– 

100 Gy). 
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3. HEALTH EFFECTS 

In a 6-year status report of a chronic uptake study in which beagle dogs were exposed to 90Sr from 

midgestion to age 1.5 years, 1.3% of dogs receiving 0.4 μCi 90Sr/kg/day (14.8 kBq/kg/day) and 3.7% of 

dogs receiving 1.2 μCi 90Sr/kg/day (44.4 kBq/kg/day) developed myeloid metaplasia of the spleen 

(Dungworth et al. 1969). 

The highest reliable NOAEL values and all LOAEL values for immunological and lymphoreticular 

effects from oral exposure to radioactive strontium in each species and duration category are recorded in 

Table 3-3 and plotted in Figure 3-3. 

3.3.2.4 Neurological Effects 

Nervous system disorders (weakness, apathy, fatigue) were reported in the Techa River population that 

was chronically exposed to combined external gamma radiation and internal radiation from 90Sr and 137Cs 

(Akleyev et al. 1995). Neurological effects were observed at chronic dose rates in excess of 40–50 rad 

(0.4–0.5 Gy) per year and persisted for 14–20 years in the exposed population. However, it is not clear to 

what extent strontium-derived radiation contributed to neurological effects, compared to external gamma 

radiation. These data are omitted from Table 3-3 because of the mixed exposures. 

No studies were located that reported neurological effects in animals following oral exposure to 

radioactive strontium isotopes. 

3.3.2.5 Reproductive Effects 

No significant reproductive effects were reported in the Techa River population that was exposed to 

combined external gamma radiation and internal radiation from 90Sr and 137Cs between 1949 and 1956 

(Kossenko et al. 1994). Exposure had no effect on birth rate, fertility, or the incidence of spontaneous 

abortions in the study group that had received average doses to the gonads of up to 74 rem (0.74 Sv), 

primarily from external gamma radiation (Akleyev et al. 1995). An increase in the incidence of ectopic 

pregnancies was not dose-associated. These data are omitted from Table 3-3 because exposures were to 

multiple sources and it is probable that radiostrontium had a minor effect on the gonadal radiation dose. 

In one acute study, female rats were given a single dose of 400 μCi 90Sr/kg by gavage 1–10 days before 

impregnation (Moskalev et al. 1969). At the time of conception, the maternal skeletal dose was 800 rad 
STRONTIUM 95 

3. HEALTH EFFECTS 

(8 Gy) and soft tissue dose was 10 rad (0.1 Gy). Fetuses received skeletal doses of 20 rad (0.2 Gy). 

Under these conditions, 22% of fetuses died. In an intermediate-duration study, groups of 230– 

339 female CF-1 mice were fed 90Sr in the diet at doses between 0.03 and 31 μCi/kg/day (1.11 and 

1,147 kBq/day; Finkel et al. 1960). Dams and males bred while on the radiostrontium diet, and dams 

were maintained on diet throughout gestation and lactation. Radiostrontium feeding had no effect on 

fertility, the number of live offspring, or the number of female offspring surviving at PND 35. 

In a multigenerational study, 9-month-old female Pitman-Moore miniature swine were fed a diet 

containing between 1 and 3,100 μCi 90Sr/day (0.037 and 114.7 MBq/day) and then were bred with males 

that were only exposed to 90Sr during the period of mating (Clarke et al. 1970, 1972; McClellan et al. 

1963). Ingestion of radioactive strontium had no effect on fertility or fecundity. Pregnant sows receiving 

3,100 μCi 90Sr/day (114.7 MBq/day) did not survive to the end of the period of gestation because of bone 

marrow hypoplasia, but their fetuses were apparently normal (McClellan et al. 1963). For doses between 

1 and 625 μCi 90Sr/day (0.037 and 23.13 MBq/day), there was no significant effect on litter size, 

percentage of stillborn, or birth weight. Exposure had no effect on frequency and duration of the estrus 

cycle or in the number of repeat breedings. However, the F1 offspring of the sows ingesting 625 μCi 

90Sr/day (23.13 MBq/day) did not survive to adulthood. Survival of the F2 offspring was apparently 

similar to the F1 generation, but their reproductive capacity was not reported, since later studies focused 

on cancer effects. 

The highest reliable NOAEL values and all LOAEL values for reproductive effects from oral exposure to 

radioactive strontium in each species and duration category are recorded in Table 3-3 and plotted in 

Figure 3-3. 

3.3.2.6 Developmental Effects 

Few developmental effects were reported in the progeny of the Techa River population that was exposed 

to combined external gamma radiation and internal radiation from 90Sr and 137Cs between 1949 and 1956 

(Kossenko et al. 1994). The cohort of women in the study received radiation doses to the gonads of up to 

74 rem (0.74 Sv), primarily from external gamma radiation (Akleyev et al. 1995); the proportion of the 

dose attributable to radiostrontium was not specified, but is likely to have been relatively small. No 

increase in the incidences of spontaneous abortion, miscarriages, or stillbirths was observed. However, 

there were slight increases in child mortality from chromosomal defects and from congenital anomalies of 
STRONTIUM 96 

3. HEALTH EFFECTS 

the nervous system, circulatory system, and other unspecified anomalies in the progeny of the exposed 

group compared to controls. Considering deaths from these anomalies, from labor complications, or from 

unspecified perinatal causes, the mortality coefficient of the offspring of parents with gonadal doses of 

11 rem (0.11 Sv) was double that of the unexposed control group. Kossenko et al. (1994) calculated that 

the gonadal doses required to double the incidences of stillbirths, miscarriages, early neonatal mortality, 

or lethal developmental effects were rather high, ranging from 20 to 480 rem (0.2–4.8 Sv) for the different 

end points. These data are omitted from Table 3-3 because of the combined internal and external 

radiation exposures. 

In one animal study, CF-1 mice were exposed to 90Sr from the time of conception; breeding adults were 

fed a diet containing 0.03–31 μCi 90Sr/kg/day (1.11–1,147 kBq/kg/day), and the dams were fed the same 

diet throughout gestation and lactation (Finkel et al. 1960). The offspring were fed the same diet 

throughout their lifetimes. Gestational exposure to radiostrontium did not affect litter size or early 

survival of offspring, and no teratogenic effects were noted. However, survival of the offspring was 

shortened at doses of 3 μCi 90Sr/kg/day (111 kBq/kg/day) or higher, which was related to the higher 

incidence of bone-related cancer (see Section 3.3.2.7 Cancer). Autoradiographs demonstrated the 

uniform distribution of 90Sr in the skeleton, which probably contributed to these effects. 

In a large multigenerational study, 9-month-old female Pitman-Moore miniature swine were fed a diet 

containing between 1 and 3,100 μCi 90Sr/day (0.037 and 114.7 MBq/day) and then were bred with males 

that were only exposed to 90Sr during the period of mating (Clarke et al. 1970, 1972; McClellan et al. 

1963). Ingestion of radioactive strontium had no effect on fertility or fecundity. Fetuses were apparently 

unaffected, even those of sows that died during pregnancy from bone marrow hypoplasia after ingesting 

3,100 μCi 90Sr/day (114.7 MBq/day; McClellan et al. 1963). For doses between 1 and 625 μCi 90Sr/day 

(0.037 and 23.13 MBq/day), there was no significant effect on litter size, percentage of stillborn, or birth 

weight. In offspring of sows ingesting 625 μCi 90Sr/day (23.13 MBq/day), the weaning weight was 

reduced because radiation-induced hematopoietic effects reduced the output of milk (Clarke et al. 1970). 

After weaning, the F1 offspring were fed 90Sr in the diet at graded levels that, by 6 months, equaled the 

maternal level, 1–625 μCi 90Sr/day (0.037–23.13 MBq/day). The 625 μCi 90Sr/day (23.13 MBq/day) F1 

females did not survive to be bred at 9 months. These results indicate an age-related vulnerability to 90Sr, 

since the 625 μCi 90Sr/day (23.13 MBq/day) dosage was not lethal to the parental generation (pigs 

exposed from age 9 months). 
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3. HEALTH EFFECTS 

The highest reliable NOAEL values and all LOAEL values for developmental effects from oral exposure 

to radioactive strontium in each species and duration category are recorded in Table 3-3 and plotted in 

Figure 3-3. 

3.3.2.7 Cancer 

Epidemiological studies have found little or no association between oral exposure to radioactive strontium 

from fallout and cancer effects in humans. In an epidemiological study using the Danish cancer registry, 

no association was found between the incidence of thyroid cancer in Denmark between 1943 and 1988 

and the levels of skeletal incorporation of 90Sr from fallout (Sala and Olsen 1993). In another 

epidemiological study, data collected between 1959 and 1970 in a 90Sr monitoring program in Glasgow, 

Scotland, were used to identify three cohorts with respect to the hypothetical risk for leukemia and nonHodgkin’s lymphoma, acute myeloid leukemia, all childhood cancers combined, and bone tumors (Hole 

et al. 1993). The three cohorts were a high risk group born in 1963–1966 (exposed to high levels of 

fallout, i.e., 90Sr, at a young age), a medium risk group born in 1959–1962 (exposed to high levels at an 

older age), and a low risk group born after 1966. Cumulative incidences for all cancers, leukemia and 

non-Hodgkin’s lymphoma, and acute myeloid leukemia all showed a secular (progressive, noncyclical) 

increasing trend for children born before 1982. However, the study found no evidence for increased risks 

of total cancers, leukemia and Non-Hodgkin’s lymphoma, or acute myeloid leukemia for cohorts born 

during the period of highest fallout (radiostrontium) exposure. The few cases of bone tumors showed a 

statistically nonsignificant increase for children born during the ‘high risk’ period. 

In contrast, the Techa River population that was exposed to contaminated water and food as a result of 

releases from a nuclear weapons facility exhibited a significant increase in the incidence of leukemia 

(Kossenko 1996; Kossenko et al. 1997, 2000, 2002). An excess of leukemia cases (0.85 excess cases per 

10,000 person-year Gy (95% CI: 0.2; 1.5) was observed in groups of individuals with estimated bone 

marrow doses in excess of 10 rem (0.1 Sv), and the risk of mortality from leukemia increased with 

increasing dose (Kossenko, 1997, 2002). This finding can be related to the body burdens of 90Sr, which in 

the Techa River cohort, have been >100 times higher than fallout-related exposures during the same 

period (Shagina et al. 2000). No increase in cancer rates has been observed in the progeny of the Techa 

River cohort (Kossenko 1996). 
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3. HEALTH EFFECTS 

As shown in numerous animal studies, oral exposure to radioactive strontium may increase the incidence 

of cancers of bone and bone marrow. In a small study in which young monkeys were given 90Sr by 

gavage, one given 11.2 μCi 90Sr/kg/day (0.42 MBq/kg/day) for 5 days died of leukemia, with a final 

skeletal dose of 4,300 rad (43 Gy) 4 years after treatment (Casarett et al. 1962). Two others exposed to an 

average of 18 μCi 90Sr/kg/day (0.67 MBq/kg/day) for 10 days died from bone-associated cancers 

(chondrosarcoma, osteosarcoma) within 36 months of treatment, with estimated skeletal doses of 4,700– 

9,500 rad (47–95 Gy). 

Acute-duration experiments using Long-Evans rats demonstrated that weanlings, with their relatively 

higher rate of incorporation of strontium into the skeleton, were more vulnerable than adults to the 

carcinogenetic effects of 90Sr (Casarett et al. 1962). Weanlings (30 days old) were given 46 μCi 90Sr/day 

(1.7 MBq/day) and adults were given 33 or 65 μCi 90Sr/day (1.2 or 2.4 MBq/day) in drinking water for 

10 days; on a body weight basis, the amounts given were >300 μCi/kg/day (11 MBq/kg/day) for 

weanlings, 64 or 135 μCi/kg/day for adult males, or 92 or 194 μCi/kg/day for adult females. After 

5 months, 33 μCi (1.2 MBq) of radioisotope were detected in the skeletons of weanlings that received 

460 μCi (17 MBq), but only 1 or 2 μCi (37 or 74 kBq) were detected in the skeletons of adults that 

received 330 or 650 μCi (12.2 or 24.1 MBq), respectively. The differences in incorporation of 90Sr 

probably accounted for the age-related differences in the incidence of osteosarcoma; 17.5% of weanlings 

developed osteosarcoma compared to none of the adults. However, in the high dose adults, the overall 

incidence of malignancy (leukemia, squamous cell carcinoma of the skin, various other carcinomas) was 

more than doubled, compared to controls. At the lower dose, the overall rate of malignancies in adults 

was lower than in controls (6.25% compared to 16.2%). In an intermediate-duration experiment, in which 

male 87-day-old Long-Evans rats were given 74 μCi 90Sr/kg/day (2.7 MBq/kg/day) and females were 

given 104 μCi 90Sr/kg/day (3.8 MBq/kg/day) in drinking water for 30 days (total 790 μCi; 29.2 MBq), the 

incidence of osteosarcomas was 27.5% compared to none in the controls. Overall, the incidence of 

malignancy in the treated group was more than double that of controls; other neoplasms included 11.25% 

skin carcinoma (facial) and 6.25% leukemia. The 87-day-old rats treated for 30 days had a 5-month 

skeletal burden of about 11μCi (407 kBq), which, on a kg body weight basis, was less than one quarter 

that of weanlings treated for 10 days. This discrepancy reflects differences in rates of absorption and 

osteogenesis, which are higher in the younger rats. The older rats had a higher incidence of osteosarcoma 

than the weanlings because they survived beyond the latency period for the cancer. In another 

intermediate-duration rat study, oral exposure to 90Sr for 37 days (total dose of 790 μCi; 29.2 MBq) 

increased the incidence of osteolysis and osteogenic sarcoma by 21% (Hopkins et al. 1966). The 

radiation dose to the skeleton after 150 days was 4,000 rad (40 Gy). Young rabbits (~52 days old) that 
STRONTIUM 99 

3. HEALTH EFFECTS 

were fed an average of 6 μCi 90Sr/kg/day (218 kBq/kg/day) 90Sr in pellets for 224–280 days developed 

multiple osteogenic sarcomas in the skull and at the rapidly growing ends of the long bones within 6– 

8 months (Downie et al. 1959). 

Relatively large studies in rats, mice, dogs, and pigs demonstrated increased tumor induction following 

chronic ingestion of 90Sr. In the rat study, albino rats were fed between 0.05 and 2 μCi 90Sr/kg/day for 

their post-weaning lifetime, resulting in exposures between 0.01 and 0.4 μCi/day (Zapol’skaya et al. 

1974). In rats consuming 2 μCi 90Sr/kg/day, the number of rats with malignant tumors was 18.7%, 

compared to 1.3% for controls. At 0.5 90Sr/kg/day, the tumor incidence was 3–6 times lower (not 

specified numerically), but the outcome at 0.05 90Sr/kg/day was not reported. The most common 

malignancies were lymphosarcoma (8%), osteosarcoma (6.7%), and “leukosis” (4%). The latency periods 

were 300–540 days for lymphosarcomas and 450–660 days for “leukosis” and osteosarcoma. The 

cumulative absorbed doses averaged 1,350 rad (13.5 Gy) just before the onset of lymphosarcoma, 

2,200 rad (22 Gy) just before the onset of ‘leukosis’, and 2,400 rad (24 Gy) just before the onset of 

osteosarcoma. 

In the mouse study, mice were exposed either as adults (beginning at age 110–250 days) or from 

conception to 0.05–36 μCi 90Sr/kg/day (Finkel et al. 1960). There was a higher incidence of reticular 

tumors in blood-forming tissues, but no evidence of osteogenic sarcoma in all adult exposed groups. 

Possibly because of the experimental design-groups were not exposed simultaneously and were subjected 

to environmental differences-tumor incidence in adults did not show a clear dose-response. However, the 

tumor incidence was significantly elevated in mice exposed to 90Sr from conception. The highest dose 

level resulted in the early appearance of reticular tumors, especially lymphomas; 24% of mice at this level 

died with reticular-tissue tumors by 525 days, compared to 6% in controls. Other tumors unique to the 

high-dose level included six osteogenic sarcomas, four osteolytic tumors, and two epidermoid carcinomas 

of the oral cavity. Radiography demonstrated that radioactive strontium was ubiquitously distributed 

throughout the skeleton of mice exposed from conception. 

In the dog study, groups of pregnant beagles were fed between 0.002 and 3.6 μCi 90Sr/kg/day (0.074 and 

133.2 kBq/kg/day) from day 21 of gestation to postnatal day 42 (White et al. 1993). The pups were 

weaned and then fed a diet containing the same 90Sr/calcium ratio as the dam until day 540. Bone 

sarcoma deaths occurred in dogs ingesting between 0.13 and 3.6 μCi 90Sr/kg/day (4.8–133.2 kBq/kg/day) 

resulting in bone doses at death of 5,000–10,700 rad (50–107 Gy), but not at 0.002–0.043 μCi 90Sr/kg/day 

(0.1–1.6 kBq/kg/day) with doses to death of 100–2,300 rad (1–23 Gy). The higher the amount of 90Sr 
STRONTIUM 100 

3. HEALTH EFFECTS 

given, the earlier the age of onset of sarcomas and the more likely they were to be osteosarcomas. Of 

66 sarcomas, 75% were osteosarcomas; other types were chondrosarcoma, hemangiosarcoma, 

fibrosarcoma, and undifferentiated sarcoma. Multiple tumors occurred only at the two highest doses. 

Other cancer deaths occurred at high doses: radiation-induced myeloid leukemia (43 deaths), oral or nasal 

carcinoma (29 deaths), and periodontal carcinoma (16 deaths). The leukemic animals (average age at 

death 1,156 days) were not at risk for osteosarcoma, which had an average age of onset of 2,864 days. 

The mean cumulative skeletal doses at the time of onset in the four highest exposure groups for dogs with 

tumors were between 3,100 and 11,600 rad (31–116 Gy). The authors indicated that of the exposures that 

did not give rise to tumors, the lowest exposure (8 mrad/day; 0.08 mGy/day) was 25 times higher than 

background and the highest (146 mrad/day; 1.46 mGy/day) was 500 times higher than background. 

Therefore, lifetime chronic exposure to low linear energy transfer (LET) beta particle radiation up to 

500 times background showed no apparent carcinogenic potential in dogs. 

Stage-specific differences in carcinogenetic effects were reported in a large multigenerational study of 

female Pitman-Moore miniature swine that were fed between 1 and 3,100 μCi 90Sr/day 

(0.037–114.7 MBq/day) for life (Clarke et al. 1972; Howard 1970; Howard and Clarke 1970). In the 

parental generation, which was started on the regimen at age 9 months of age, myeloid metaplasia was 

observed at nearly all levels, and lymphoid or myeloid neoplasms were observed when between 1 and 

125 μCi 90Sr/day were ingested. The average doses to the skeleton for the parental females were between 

40 and 10,000 rad. No bone cancer occurred in the parental generation, whereas osteosarcomas occurred 

in F1 or F2 offspring exposed from conception to 125 or 625 μCi/day with average skeletal doses higher 

than 9,000 rad (90 Gy). Osteosarcoma had a longer latency period and occurred at higher exposure 

levels. Myeloid metaplasia and myeloid and lymphoid neoplasms developed sooner and more frequently 

in the F1 and F2 generations than in the parental generation. 

The cancer effect levels (CELs) resulting from oral exposure to radioactive strontium in each species and 

duration category are recorded in Table 3-3 and plotted in Figure 3-3. 

3.3.3 External Exposure 

Cardiovascular, dermal, ocular, and cancer effects have been reported following acute- or intermediateduration external exposure to beta radiation from a solid radioactive strontium source apposed to the skin 

or eye. In these studies, 90Sr was considered to be in equilibrium with 90Y; that is, following decay of 90Sr, 

some radiation emissions could be expected from decay of its transformation product, 90Y. 
STRONTIUM 101 

3. HEALTH EFFECTS 

3.3.3.1 Death 

No studies were located regarding death in humans or animals after external exposure to radioactive 

strontium. 

3.3.3.2 Systemic Effects 

No studies were located regarding respiratory, gastrointestinal, hematological, musculoskeletal, hepatic, 

renal, or endocrine effects in humans or animals after external exposure to radioactive strontium isotopes. 

Cardiovascular Effects. Exposure to excessive ionizing radiation is known to affect the integrity of 

the vasculature of the skin, increasing the permeability of the vasculature to plasma protein. A study by 

Song et al. (1968) examined the ability of several anti-inflammatory agents to suppress this radiationinduced increase in vascular permeability. Albino male guinea pigs were exposed to 3,000 rep (Roentgen 

equivalent, physical) (3,230 rad; 1 rep.0.93 rad) of particles (800 rad/min; 8.0 Gy/min) from a 90Sr/90Y 

source. Immediately after irradiation, 125I-labeled guinea pig serum albumin was injected into the heart as 

a tracer. The peak increase in vascular permeability, as measured by the ratio of accumulation of labeled 

plasma protein in the nonirradiated control and beta-irradiated skin, was determined to occur at 18 hours. 

In the group receiving no anti-inflammatory drug, the irradiated epidermis and dermis exhibited 

approximately 3- and 1.6-fold increases in the peak accumulation of plasma protein, respectively. 

The highest reliable NOAEL values and all LOAEL values for cardiovascular effects from external 

exposure to radioactive strontium in each species and duration category are recorded in Table 3-4. 

Dermal Effects. Several studies in humans and animals have reported damage to the skin following 

external exposure to radioactive strontium. Beta radiation from 90strontium has been used to treat 

hemangiomas in children and adults. One study described some delayed effects of this radiation 

treatment within patients in one medical practice in Belgrad, Yugoslavia (now Serbia; Bekerus 1970). 

The beta source was a 50 mCi 90Sr plate with a diameter of 9.9 mm. Adults were treated with an initial 

dose of 1,600 rad (16 Gy) and subsequent doses of 1,080–1,600 rad (10.8–16 Gy) in succeeding months, 
a 

Key to 

figure 

Species 

(Strain) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(rad) 

Less Serious 

(rad) 

LOAEL 

(rad) 

Serious 

ACUTE EXPOSURE Systemic 

1 Human once 

<1 min Ocular 1700 (scleral thinning in diabetic 

patient) 

Table 3-4 Levels of Significant Exposure to Strontium - Radiation Toxicity - External Radiation 

2 Mouse	 1-60 min 

once Dermal 2200 M (50% incr moist desquamation) (SAS/4) 

3 Mouse	 9 min 

Dermal	 2700 F (acute injury, scarring) once (ICR)	 

4 Mouse	 once 

Dermal 5000 M (late chronic fibrosis) (CD-1) 

5 Mouse	 once 

Dermal 5000 M (late chronic fibrosis) (CBA/ca 

agouti) 
Table 3-4 Levels of Significant Exposure to Strontium - Radiation Toxicity - External Radiation (continued) 

Exposure/ LOAEL
 

Duration/

a 

Key to Species Frequency NOAEL Less Serious Serious 

(Specific Route) figure (Strain) System (rad) (rad) (rad) 

6 Gn Pig	 1.4 to 8.3 min 

once Dermal	 1000 M (reversible 25% loss of basal (albino) cells; erythema; hair loss)	 

7 Gn Pig	 4 min 

once Cardio 3230 M (incr vascular permeability in (albino) dermis) 

8 Pig	 1-60 min 

Dermal	 2000 F (late 35% dermal atrophy) once (Large White)	 

9 Pig once 

3 to 12 min Dermal 2340 F (moist desquamation) Large White 

10 Pig	 1-60 min 

once Dermal 3000 F (50% incr moist desquamation) (Large White) 
Table 3-4 Levels of Significant Exposure to Strontium - Radiation Toxicity - External Radiation (continued) 

Exposure/ LOAEL
 

Duration/

a 

Key to Species Frequency NOAEL Less Serious Serious 

(Specific Route) figure (Strain) System (rad) (rad)	 (rad) 

11 Pig	 1-60 min 

once Dermal 3000 F (50% incr moist desquamation) (Large White) 

Cancer 

12 Mouse 1 hr 

17800 F (CEL: 1/5 fibrosarcoma once (ICR)	 of skin) 

INTERMEDIATE EXPOSURE Systemic 

13 Human	 1 yr 

~1 x/mo Dermal 220 (delayed telangiectasis, slight ~min/d atrophy) 
Table 3-4 Levels of Significant Exposure to Strontium - Radiation Toxicity - External Radiation (continued) 

Exposure/ LOAEL
 

Duration/

a 

Key to Species Frequency NOAEL Less Serious Serious 

(Specific Route) figure (Strain) System (rad) (rad) (rad) 

14 Human 3 wk 

1 x/wk Ocular 1075 (conjunctival telangiectasis, 

<1 min/d scarring; abnormal nuclei of 

conjunctival epithelium) 

Cancer 

15 Mouse 43 wks 

17800 F (CEL: 1/5 reticulocyte 1 x/wk (ICR) sarcoma) 

1 hr 

16 Mouse 177-300 d 

150 F (CEL: fibrosarcoma; 3 x/wk (ICR) squamous cell 

~min/d 

carcinoma; basal cell carcinoma) 

17 Mouse 177-300 d 

150 F (CEL: osteosarcoma) 3 x/wk (ICR) 

~min/d 

a There is no corresponding LSE figure. 1 In these studies, a solid radioactive source was placed adjacent to the eye or skin. ~ = approximately; CEL = cancer effect level; d = day(s); Gn pig = guinea pig; hr = hour(s); incr = increased; LOAEL = lowest-observed-adverse-effect level; m= no-observed-adverse-effect level 
STRONTIUM 106 

3. HEALTH EFFECTS 

not exceeding a total of 7,530 rad (75.3 Gy). Children were treated with an initial dose of 200–300 rad 

(2–3 Gy) and additional treatments over 6–16 months, for a total exposure of 2,420–6,130 rad (24.2– 

61.3 Gy) in some cases. Eight or 10 years after treatment, about a third of the patients developed delayed 

reactions to radiation: achromia, excess pigmentation, slight atrophy, and telangiectasis. The author did 

not specify the exposure levels that resulted in these effects. 

Acute dermal reactions to 90Sr have been described for depilated skin in mice, guinea pigs, and pigs. In 

mice, skin exposed to a single 2,000–5,000 rad (20–50 Gy) dose of beta radiation from a 90Sr-90Y source 

sustained an acute reaction (Hoshino and Tanooka 1975; Randall and Coggle 1995). For example, all 

mice exposed once to 5,000 rad (50 Gy) from a 1 mm diameter source developed an acute skin reaction 

with the following characteristics (Randall and Coggle 1995). After an asymptomatic period of 3 or 

4 days, the skin exhibited increasing erythema and pigmentation changes, leading to dry desquamation by 

day 10. Within a few days, exposed skin entered a period of moist desquamation, during which a serum 

scab was formed that was prevalent between days 15 and 25. Re-growth of the epithelium commenced at 

the edges of the irradiated field and from surviving hair follicles. By 1 month postirradiation, the 

epidermis was overtly normal, although histologically hyperplastic. Chronic fibrosis was a delayed skin 

reaction that was not apparent until 3–6 months postirradiation. 

Dose-related effects were noted in guinea pig skin that was treated with a 25x25 mm square 90Sr source 

(Etoh et al. 1977). At 1,000 rad, there was a transient 25% reduction in the number of basal epithelial 

cells by day 10, which approached normality by day 15. At 2,200 rad, the epithelial basal cell population 

dropped by about 60% at day 12, but was slightly above normal by day 20. At 3,000 and 5,000 rad, the 

basal epithelial cell population was reduced 75%, but hyperplasia was also detected at the margin of the 

field. Hyperplasia was maintained for the 50-day observation period following exposure to 2,200– 

5,000 rad. At 3,000 rad, erythema was noted by day 14, followed by dry desquamation and complete hair 

loss by day 21. A similar pattern, with ulceration at 1 month, was seen at 5,000 rad. 

Within certain ranges, field-size effects for acute, localized external exposures to radioactive strontium 

have been demonstrated in mice and pigs. Hopewell et al. (1986) exposed young SAS/4 male mice to 

different levels of radiation from 90Sr sources varying in diameter between 1 and 22.5 mm. The ED50 

values for moist desquamation were 2,200–2,750 rad (22–27.5 Gy) for the 22.5-mm source and 7,500– 

9,000 rad for the 5-mm source. Acute tissue breakdown was only achieved in mouse skin by very high 

doses (ED50 ≥14,000 rad) when the smallest sources were employed (≤2 mm in diameter). In a parallel 

study in pigs, moist desquamation occurred at 2,250–7,500 rad (22.5–75 Gy) and acute tissue necrosis 
STRONTIUM 107 

3. HEALTH EFFECTS 

occurred at doses of ≥14,000 rad (140 Gy) (Hopewell et al. 1985, 1986). Peel et al. (1984) compared the 

effect on pigskin of acute exposure to 90Sr sources with diameters between 1 and 40 mm. The effects of 

acute beta radiation included epithelial cell death within the first 16 weeks, and subsequently, dermal 

necrosis that was attributed to vascular damage. The rate of repair was dependent on the size of the 

exposed area, since repair was dependent upon the migration of healthy cells into the wound. Transient 

moist desquamation associated with bright red erythema was observed between 4 and 6 weeks. At ‘high’ 

doses, this intensified and the dermis became ulcerated, but healed with scarring. After doses ≥4,000 rad 

(22.5-mm source), 6,600 rad (11-mm source), or 12,500 rad (5-mm source), a dusky red or mauve 

erythema followed by dermal necrosis occurred between weeks 10 and 16. In pigs that were acutely 

exposed to the same range of 90Sr sources at the age of 3 months, dose-dependent dermal atrophy was 

detected in the irradiated field 2 years later, reaching a maximal 55% reduction in dermal thickness for all 

doses above 4,500 rad (45 Gy; Hamlet et al. 1986). Dermal atrophy was produced by doses below the 

threshold required to induce moist desquamation. The threshold dose for moist desquamation following 

irradiation by the 22.5 mm source (2,250 rad) produced a 38% thinning of the dermis. Irradiation from 

the 1-mm source produced 30% dermal thinning at the threshold (7,250 rad). Irradiation from the 5-mm 

source (2,000 rad) reduced the thickness of the dermis by 35%. For the 11–22.5-mm sources, above 

doses that caused maximal thinning (in the range of 12,000–6,250 rad, respectively), the relative dermal 

thickness increased slightly, but remained 30–40% thinner than normal. 

The highest reliable NOAEL values and all LOAEL values for dermal effects from external exposure to 

radioactive strontium in each species and duration category are recorded in Table 3-4. 

Ocular Effects. Beta radiation has been employed medically to treat pterygium, an alteration in the 

conjunctival connective tissue that results in the penetration of the superficial corneal stroma by vascular 

connective tissue (Tong et al. 1969; Wesberry and Wesberry 1993). As an adjunct to surgical removal of 

the pterygium, a solid 90Sr source is apposed to the site in order to reduce neovascularization. Several 

clinical studies reported complications resulting from this procedure. Serious effects (radiation cataracts, 

keratinization and telangiectasis of the conjunctiva) resulted from the high dose levels used when the 

technique was first employed using other beta-emitting radionuclides (Merriam 1955). Atrophy of the 

sclera occurred after a dose of 1,600 rad from 90Sr. In a later study, 78 eyes in 62 patients were treated 

with 1,080 rad (10.8 Gy) of beta radiation from a 90Sr source repeated at weekly intervals (total dose 

3,200 rad; 32 Gy; Tong et al. 1969). Because pterygia recurred within 2–18 months, six patients were retreated as before, two were given a single dose of 2,100 rad (21 Gy), and one of these two received a third 

dose of 2,100 rad (21 Gy). One eye, which had received treatments of 5,380 rad (53.8 Gy) each to two 
STRONTIUM 108 

3. HEALTH EFFECTS 

adjacent fields, developed keratitis of the cornea. Other complications noted were telangiectasis of the 

conjunctiva (27%), scarring of the conjunctiva (14%), and scarring of the cornea (3%); the authors did not 

specify the exposure levels at which these side effects occurred. A more recent study described results for 

171 eyes that had been treated with single doses of 1,700–1,800 rad (17–18 Gy) (Wesberry and Wesberry 

1993). During follow-up periods lasting between 1 and 19 years, the only complications noted were one 

case each of corneal scarring, iritis, conjunctivitis, mild irritation, and, in a diabetic patient, scleral 

thinning. A complication rate of 1.8% was reported for a study of 490 eyes (399 patients) that received 

doses between 31 and 42 Gy (3,100–4,200 rad) in four or five fractions over 29 days (Nishimura et al. 

2000). Scleral thinning, not severe enough to require treatment, was reported for four eyes in three 

patients 0.5, 2, and 9 years after treatment. Infectious scleral ulcer occurred within weeks of treatment in 

one male. Ischemic necrosis of the sclera in one male and adhesion of the eyelid and eyeball in one 

female occurred several years after repeat treatments for recurring pterygia; adhesive scarring of the 

eyelid occurred in one female 7 years after treatment. 

No studies were located regarding ocular effects in animals after external exposure to radioactive 

strontium isotopes. 

The highest reliable NOAEL values and all LOAEL values for ocular effects in humans from external 

exposure to radioactive strontium in each duration category are recorded in Table 3-4. 

No studies were located regarding the following effects in humans or animals after external exposure to 

radioactive strontium isotopes: 

3.3.3.3 Immunological and Lymphoreticular Effects 

3.3.3.4 Neurological Effects 

3.3.3.5 Reproductive Effects 

3.3.3.6 Developmental Effects 

3.3.3.7 Cancer 

Development of skin cancers in mice following localized exposure to beta radiation from a solid 90Sr-90Y 

source depended on the dose and on strain susceptibilities (Hoshino and Tanooka 1975). In experiments 
STRONTIUM 109 

3. HEALTH EFFECTS 

using a 40 mCi (1.48x109 Bq) 90Sr-90Y source that delivered doses of 290 rad/min (2.9 Gy/min) to the 

skin, ICR mice exposed to a single localized dose of 2,700 rad (27 Gy) developed an acute skin reaction 

within the first month (see Section 3.3.4.2 Dermal Effects), but did not develop skin cancer during a 

23-month observation period (Hoshino and Tanooka 1975). When the exposure was repeated 7 times for 

a total dose of 17,800 rad (178 Gy), one fibrosarcoma of the skin appeared after 10 months among five 

mice. Even extending the duration of the repeated 17,800 rad treatment for 43 weeks did not increase the 

incidence of malignant skin tumor; a single reticulocyte sarcoma developed in one out of five mice. Mice 

from a different strain, Japanese ddN, exposed to single doses of up to 17,400 rad (174 Gy) did not 

develop skin tumors during a 1-year observation period (Hoshino and Tanooka 1975). In the acute 

dermal toxicity experiments described above, Randall and Coggle (1995) selected the exposure level of 

5,000 rad (50 Gy) for their mouse studies since it is known to be a critical dose for carcinogenetic effects 

in humans exposed to ionizing radiation. 

Ootsuyama and Tanooka (1988, 1989) exposed the backs of female ICR mice to beta radiation from a 

40,000 μCi (1,500 MBq) source of 90Sr–90Y, which delivered a surface dose rate of 228 rad/minute 

(2.28 Gy/minute) and a 20–80% lower dose rate to the top of the vertebrae. Mice were irradiated 3 times 

weekly at skin entrance doses per exposure of 135–1,180 rad (1.35–11.8 Gy), and irradiation was 

continued until a palpable tumor appeared (up to 86 weeks). Tumors arising included squamous cell 

carcinomas, basal cell carcinomas, fibrosarcomas, and osteosarcomas. No skin tumors arose in mice 

receiving 135 rad/day (1.35 Gy/day). The total number of irradiations (and total dose) needed to induce 

50% incidence of skin tumors ranged from 252 sessions for a total of 37,800 rad (378 Gy) for the 

150 rad/day level and 156 sessions for a total of 192,300 rad (1,923 Gy) for the 1,180 rad/day level. 

Osteosarcomas were induced at lower doses, most frequently with skin surface doses of 250–350 rad 

(2.5–3.5 Gy) per exposure. In time, 100% of mice developed tumors in groups receiving 250–1,180 rad 

per exposure. Ootsuyama and Tanooka (1988) suggested that the 135 rad/day dose might represent a 

threshold dose, since no tumors formed. However, in their experimental design, they arbitrarily 

terminated exposures at this dose level on day 300, which conceivably could be shorter than the latency 

period for tumor development at that dose. 

The CELs resulting from external exposure to radioactive strontium in each species and duration category 

are recorded in Table 3-4. 
STRONTIUM 110 

3. HEALTH EFFECTS 

3.3.4 Other Routes of Exposure 

This section includes injection and in vitro studies that provide evidence for the biological basis of 

toxicity of stable and radioactive strontium in humans and animals. Since these studies are not directly 

relevant to general population exposure conditions, no LSE tables have been created for this section. 

Hematological Effects Hematological effects have been observed in several clinical studies in 

which 89Sr, one of the shorter-lived radioactive isotopes of strontium, has been used in cancer therapy for 

the relief of pain by irradiating and destroying tumors that have metastasized to the bone marrow 

(Baziotis et al. 1998; Ben-Josef et al. 1995b; Blake et al. 1987c; Breen et al. 1992; Kan 1995; Lee et al. 

1996; Piffanelli et al. 2001; Sciuto et al. 2001). Significant reductions in platelet and white blood cell 

counts (averaging 70 and 30%, respectively) were seen 3 months after patients were injected with a single 

therapeutic dose (40 μCi 89Sr/kg; 1.5 MBq/kg) (Lee et al. 1996). In two patients who received two doses 

of 60 μCi 89Sr/kg (2.2 MBq/kg) 6 months apart, platelet counts were significantly reduced (>30%) for at 

least 1 year. Similar effects have been observed in animals. Hypoplasia of the bone marrow has been 

observed in mice injected with 90Sr (Ito et al. 1976; Nilsson 1970) or 89Sr, the latter of which has been 

used intentionally to create mice with aplastic bone marrow (Bennett et al. 1976; Haller and Wigzell 

1977; Levy et al. 1981; Merluzzi et al. 1978; Oghiso et al. 1988; Sawyer et al. 1982). CBA/J mice 

injected with fixed doses of 89Sr that differed in the specific activity of the preparation, showed 

quantitative differences in the degree of bone marrow suppression (Shibata et al. 1985). Acute 

hematological symptoms (depression of hemopoiesis leading to anemia or hemorrhage) were observed in 

beagles beginning several weeks after injection of 64 or 98 μCi 90Sr/kg (Dougherty et al. 1972). Transient 

neutropenia occurred at the 10.8 μCi 90Sr/kg level, and prolonged (36-month) depression of all types of 

leukocytes was reported at 32.7–98 μCi 90Sr/kg. No hematological effects were noted at levels between 

0.57 and 3.46 μCi 90Sr/kg. 

Musculoskeletal Effects. Osteonecrosis was reported after 2 days for 2-day-old rats that were 

injected intraperitoneally with 2 mCi 90Sr/kg of body weight (Hopkins and Casarett 1972). In weanling 

rabbits, injection of 600 μCi 90Sr/kg resulted in increasing cell death of differentiating odontoblasts and 

pulp cells of immature teeth and disordered tooth structure (Rushton 1963). Mature teeth in the same 

animal, or teeth in adults injected at the age of 3 years or older, were not affected as severely. 

Immunological and Lymphoreticular Effects. Evidence from injection studies in animals 

corroborates the sensitivity of the immune system to radioactive strontium. In mice that have been 
STRONTIUM 111 

3. HEALTH EFFECTS 

injected with 89Sr or 90Sr to deplete bone marrow, NK cells are preferentially eliminated (Emmanuel et al. 

1981; Gidlund et al. 1990; Haller and Wigzell 1977; Wiltrout et al. 1989). The loss of this cell population 

results in a reduced ability to defend against lymphoid tumors (Haller and Wigzell 1977; Luevano et al. 

1981) or a transplanted methylcholanthrene-induced sarcoma (Scuderi and Rosse 1981b). In CBA/SU 

mice injected with 90Sr(NO3)2, the responsiveness of spleen cells to activation by B-cell mitogen 

lipopolysaccharide was reduced, which was attributed to the cytotoxic effect of 90Sr on bone marrow, a 

source of precursor cells for the spleen (Bierke 1990). In mice injected with 400–800 μCi 90Sr/kg to 

deplete bone marrow, the thymus went through two phases of weight loss and regeneration within 50 days 

(Järplid 1973). 

Reproductive Effects. Numerous animal studies demonstrated adverse reproductive effects of 

injected radioactive strontium. For the first 4 weeks after male CBA mice were injected intraperitoneally 

with 18 μCi of 90Sr and mated with untreated females, fetal deaths were 5–10% higher than controls 

(Lüning et al. 1963a). The increase in fetal mortality was much less (only ~2%) when the same males 

were mated 11–15 weeks postinjection (Lüning et al. 1963b). In a similar study using male C3H/He mice, 

a single injection of 1,160 μCi 90SrCl2/kg resulted in fetal death rates 7–8% higher than normal for 

matings conducted 10–40 weeks after injection (Reddi 1971). Autoradiography demonstrated that 90Sr 

selectively accumulated in testicular stem cells. 

When female CBA mice were injected with 90Sr(NO3)2 on the 19th day of pregnancy, a dose of ≥43 μCi 

90Sr(NO3)2/kg (≥1,600 kBq/kg) transiently suppressed spermatocyte maturation of the male offspring, but 

the spermatid numbers had recovered by day 56 (De Rooij and Rönnbäck 1989). After the recovery 

period, the reproductive capacity (number of litters, litter size) of male offspring at the highest dose level 

(86 μCi 90Sr(NO3)2/kg; 3,200 kBq/kg) was unaffected. No testicular effects were observed at doses of 

11 or 21 μCi 90Sr(NO3)2/kg (400 or 800 kBq/kg). Compared to the effect on male offspring, reproductive 

effects were more severe in female offspring of dams exposed to 90Sr(NO3)2 on the 19th day of pregnancy 

(Rönnbäck 1980). Dose-related decreases in the number of differentiating oocytes in the ovary were 

observed up to day 84 at all dose levels ranging from 5.5 to 43 μCi 90Sr(NO3)2/kg (200–1,600 kBq/kg). 

Injection on the 16–19th day was found to have more severe effects than injection earlier in gestation 

(Nilsson and Henricson 1969; Rönnbäck 1979). A longer-term study demonstrated that the radioactivestrontium-induced decrease in the number of oocytes in the ovary persisted for at least 10 months 

(Rönnbäck 1981b). Furthermore, the reproductive capacity (number of fertile females, number of litters, 

number of young per litter) of females treated in utero was significantly reduced at the two highest 

maternal dose levels (43 and 86 μCi 90Sr(NO3)2/kg; 1,600 and 3,200 kBq/kg). Rönnbäck (1981a) also 
STRONTIUM 112 

3. HEALTH EFFECTS 

examined the effect of exposure via lactation using CBA mice receiving 21 μCi 90Sr(NO3)2/kg 

(800 kBq/kg). Ovarian cellularity, especially the earliest stages of oogenesis, was reduced in females 

exposed in utero, whether or not they suckled milk contaminated with 90Sr. However, early stage oocyte 

numbers were somewhat improved by sucking uncontaminated milk. When unexposed newborn females 

were exposed to contaminated milk, the numbers of early stage oocytes was significantly reduced, but not 

as severely as in females exposed in utero. These studies suggest that reproductive capacity, particularly 

in females, may be adversely affected by gestational exposure to high levels of radioactive strontium. 

These levels are high compared to reported releases of 90Sr from nuclear power facilities (see Table 6-1). 

Developmental Effects. Injection of relatively high doses of radioactive strontium into pregnant 

animals resulted in severe developmental effects. A single dose of ≥764 μCi 90Sr/kg into female LongEvans rats had no effect on fetal mortality when administered on gestational day 10, but significantly 

increased fetal mortality when administered on gestational day 2 (Hopkins et al. 1967). In addition, there 

were dose-related increases in the incidence of fetuses with skeletal abnormalities (general stunting, lack 

of ossification, fusion of ribs, vertebral anomalies, missing tail). The incidence of micropthalmia was 

also significantly increased at the higher activity level (1,488 μCi 90Sr/kg). The offspring of female 

Wistar rats injected with ≥100 μCi 90Sr(NO3)2 at gestational day 18 showed no gross malformations, but 

there was a significant increase in the incidence of meningeal and pituitary tumors (Schmahl and Kollmer 

1981; Schmahl et al. 1979). This was shown to be connected with a late gestational increase in the 

transfer of transplacental strontium to the basioccipital and sphenoid bones of the skull. Tumor 

development was probably assisted by the position of the pituitary gland within the sella turcica, which 

resulted in the gland being irradiated from the ventral and lateral surfaces. The total radiation dose rate at 

that position was calculated to be between 60 and 120 rad for the lifespan of 30 months. After pregnant 

dogs were injected with 1 mCi of radiostrontium per kg (80–99% 89Sr and 1–20% 90Sr) 6 days prior to 

delivery, the puppies dying within 11 weeks exhibited abnormalities of the skeleton (underdevelopment 

of the jaws, incomplete and abnormal ossification, abnormal epiphyseal cartilage), partial atelectasis of 

the lungs, hyperplasia of lymph nodes and spleen, or deficient hematopoiesis (Finkel and Biskis 1969; 

Finkel et al. 1972). Puppies injected subcutaneously 12 days after birth showed some skull abnormalities 

and developed osteosarcomas. Effects on the reproductive system following in utero exposure to 

radioactive strontium are discussed in the preceding paragraphs. Cancer effects in animals exposed to 

radioactive strontium in utero are discussed in the next paragraph. 

Cancer. Numerous studies in several species reported the induction of malignant tumors in response to 

injection of radioactive strontium (mice: Ash and Loutit 1977; Bierke and Nilsson 1990; Ito et al. 1976; 
STRONTIUM 113 

3. HEALTH EFFECTS 

Loutit 1976; Nilsson 1971, 1972; Nilsson et al. 1980a; Reif and Triest 1982; Chinese hamsters: Benjamin 

et al. 1976b; Brooks et al. 1974; rabbits: Kshirsagar et al. 1965; Vaughan and Williamson 1969; mongrel 

dogs: Finkel and Biskis 1969; Finkel et al. 1971; beagle dogs: Lloyd et al. 1995; Taylor et al. 1966). In 

general, osteosarcomas and bone hemangiosarcomas developed at higher dose levels, and lymphomas and 

leukemias developed at lower levels. Carcinomas of soft tissues adjacent to bone also developed. The 

offspring of pregnant rats that were injected on gestational day 18 had a higher incidence of pituitary 

adenoma and meningeal sarcoma (Schmahl and Kollmer 1981; Schmahl et al. 1979). These findings 

were attributed to the higher incorporation of 90Sr to the skull at that developmental period and to the 

anatomical position of the pituitary within the sella turcica, which subjected it to radiation from all but the 

dorsal surface. The female offspring of pregnant mice that were injected intravenously with 90Sr on 

gestational day 19 developed a higher incidence of tubular adenoma of the ovaries (Rönnbäck and 

Nilsson 1982). 

3.4 GENOTOXICITY 

There is little evidence for genotoxicity of stable strontium. However, radioactive strontium isotopes 

release ionizing radiation that, within an effective radius, is known to damage DNA (see Appendix D 

Section D.4.1 Radiation Effects at the Cellular Level). Summaries of in vivo and in vitro genotoxicity 

data are presented in Tables 3-5 and 3-6, respectively. 

In Vivo Exposure 

Stable Strontium. No studies were located regarding genotoxic effects in humans following exposure to 

stable strontium. The only in vivo genotoxicity study for stable strontium in animals involved acute oral 

exposure. Oral administration of 130 mg strontium/kg body weight as strontium chloride to Swiss albino 

female mice increased the incidence of chromosomal aberrations (gaps, breaks, nondisjunction, and 

polyploidy) in bone marrow cells 5-fold after 6 hours (Ghosh et al. 1990). Genotoxicity in male mice 

administered a similar dose (140 mg/kg) was only doubled, and therefore, was less severe than in females. 

At higher doses (440–1,400 mg/kg), the incidence of chromosomal aberrations was similar in both sexes 

after 6, 12, or 24 hours. 

Radioactive Strontium. Human in vivo genotoxicity data are available from studies of the Techa River 

populations exposed to combined external gamma radiation and internal radiation from 90Sr and 137Cs 

between 1949 and 1956 and from studies on patients exposed to 89Sr as a radiopharmaceutical. The stable 
STRONTIUM 114 

3. HEALTH EFFECTS 

Table 3-5. Genotoxicity of Stable and Radioactive Strontium In Vivo 

Species (test system) End point Results Reference 

Stable Strontium 

Strontium chloride: 

Mouse (bone marrow) Chromosomal gaps, breaks, + Ghosh et al. 1990 

polyploidy, centric fusion 

Radioactive Strontium 

89Strontium chloride: 

Human (lymphocytes) Transient increase in + Watanabe et al. 1998 

micronuclei 

90Strontium: 

Human (lymphocytes) Chromosomal aberrations + Ilynskikh et al. 1999 

(rings, dicentric, tricentric) 

Mouse (skin) Unscheduled DNA synthesis + Ootsuyama and Tanooka 

1986 

Mouse (thymus, lymph Aneuploidy + Ito et al. 1976 

nodes, bone marrow) 

Chinese hamster (bone Chromosomal breaks, + Brooks and McClellan 

marrow) exchanges, rings 1969 

Miniature swine Chromosomal breaks in + Clarke et al. 1972; 

(leukocytes) leukemic cells Howard 1970 

+ = positive results; – = negative results; DNA = deoxyribonucleic acid 
STRONTIUM	 115 

3. HEALTH EFFECTS 

Table 3-6. Genotoxicity of Stable and Radioactive Strontium In Vitro 

Results 

With Without 

Species (test system) End point activation activation Reference 

Stable Strontium 

Strontium chloride: 

In vitro DNA synthesis reaction	 Lack of fidelity in DNA – – Loeb et al. 1977 

synthesis 

Prokaryotic organisms: 

Bacillus subtilis Rec- Growth inhibition – – Kanematsu et al. 

1980 

Eukaryotic cells: 

Chinese hamster ovary cells	 Reduced cloning – – Tan et al. 1984 

efficiency 

Radioactive Strontium 

90Strontium: 

Human (blood) Chromosomal rings, + de Oliveira et al. 

dicentrics, acentrics 2001 

DNA damage in + 

electrophoretic assay 

Human (lymphocytes) Micronucleus formation + Mills et al. 1996 

Human (lymphocytes) Micronucleus formation + Hall and Wells 

1988 

– = negative result; + = positive result; (+) = weakly positive result; DNA = deoxyribonucleic acid 
STRONTIUM 116 

3. HEALTH EFFECTS 

chromosomal translocation frequency in peripheral lymphocytes was evaluated in 73 radiation-exposed 

individuals from the Techa River area and 39 unexposed individuals from noncontaminated areas 

(Bauchinger et al. 1998). The mean genomic frequency of translocations per cell in the exposed group 

(12.8±1.5x10-3) was significantly elevated compared to unexposed controls (5.7±1.0x10-3). Furthermore, 

the translocation frequency per cell was significantly higher in the subgroup that had been exposed to 

radiation as teenagers (22±4.3x10-3) compared to the subgroup exposed as adults (9.7±2.3x10-3). 

Increased skeletal incorporation of radiostrontium in teenagers, leading to higher radiation doses to the 

bone marrow, probably contributed to the observed increase in translocation frequency for this subgroup. 

In a more recent study of the Techa River populations, there was a dose relationship between the 

frequency of chromosomal aberrations (dicentric, ring) in T-lymphocytes (assessed in 1994–1996) and 

whole body 90Sr activity (detected by human radiation counter in 1993) for individuals residing in the 

Muslyumovo settlement (Ilyinskikh et al. 1999). The frequency of chromosomal aberrations was 

3.8±0.8 for a non-exposed control group (whole-body 90Sr activity <100 nCi), and 8.9±0.7, 12.9±1.2, and 

18.7±1.9%, respectively, for exposed individuals with90Sr activity levels of 100–500, 500–1,000, and 

≥1,000 nCi. In a few cancer patients who were injected with 3 mCi (111 MBq) of 89SrCl2 to treat severe 

pain from multiple bone metastases, the number of micronuclei present in the lymphocytes tripled in the 

week after exposure, but declined in succeeding weeks (Watanabe et al. 1998). The authors found that 

the percentage of micronuclei, indicative of chromosomal damage, was equivalent to the damage 

observed in a separate in vitro experiment in which cells received a dose of 53 rad (0.53 Gy) by 

X-irradiation. 

In a long-term feeding study, chromosomal breaks were noted in leukocytes of miniature pigs that had 

developed leukemia as a result of exposures of 25 μCi 90Sr/day (925 kBq/day) or more for >1 year 

(Clarke et al. 1972; Howard 1970). Unexpected (“unscheduled”) DNA synthesis was detected in the skin 

of female ICR mice several hours after external exposure to 10,000–30,000 rad (100–300 Gy) from a 

90Sr-90Y disk applicator (surface dose rate 228 rad/min) (Ootsuyama and Tanooka 1986). Tritiated 

thymidine incorporation related to DNA repair was elevated to a greater degree in epithelial cells of the 

irradiated epidermis than in the dermis. This difference appeared to be intrinsic to the cell type, since 

thymidine incorporation in hair follicle epithelium situated at the same depth as fibroblastic dermal cells, 

occurred at a faster rate. The authors suggested that the somewhat slower rate of DNA repair in the 

dermis could contribute to the higher risk of cancer in the dermis, compared to the epidermis, following 

exposure to ionizing radiation. 
STRONTIUM 117 

3. HEALTH EFFECTS 

A single intraperitoneal injection of 90Sr–90Y into Chinese hamsters (200–5,000 μCi/kg) resulted in an 

increasing number of chromosomal breaks/cell over time (between 2 and 224 days), as the cumulative 

radiation dose to the skeleton increased (Brooks and McClellan 1969). The number of chromosomal 

breaks and chromatid/isochromatid deletions per bone marrow cell increased as a function of dose rate, or 

as the activity of radionuclide injected per body weight. The relative number of chromatid exchanges and 

rings and dicentrics decreased with time after exposure, whereas the number of chromosomal exchanges 

increased. Abnormal chromosomal numbers were detected in the thymus, lymph nodes, and bone 

marrow of female ICR/JCL mice as late as 90 days after interperitoneal injection with 1 mCi/kg of 90Sr 

(Ito et al. 1976). 

In Vitro Exposure 

Stable Strontium. In mutagenicity assays using the Rec-

 (recombination-repair-deficient) strain of 

Bacillus subtilis, strontium chloride had a negative effect in vitro (Kanematsu et al. 1980). Furthermore, 

in a survey of the effect of metal salts, strontium was found to have no adverse effect on the fidelity of 

DNA synthesis in vitro, which was thought to be consistent with its reported lack of mutagenicity and 

carcinogenicity (Loeb et al. 1977). 

The only stable strontium compound known to be genotoxic is strontium chromate. Strontium chromate 

induced sister chromatid exchanges in Chinese hamster ovary cells in vitro (Venier et al. 1985). In the 

Ames test using the Salmonella typhimurium strain TA100, strontium chromate induced mutations in the 

presence, but not in the absence of S9 microsomes. The genotoxicity of strontium chromate is related to 

the ability of the hexavalent chromium ion to enter cells and become metabolized, forming a reactive 

DNA-adduct. Strontium only contributes to the solubility of the salt (Elias et al. 1989, 1991). 

Radioactive Strontium. Radioactive strontium has been shown to be genotoxic to human cells in vitro. 

In lymphocytes from freshly-drawn human blood, doses of 0.2–5.0 Gy (0.002–0.05 rad) increased the 

frequency of chromosomal aberrations (de Oliveira et al. 2001). Acentric aberrations (acentrics and 

double minutes) increased at ≥0.2 Gy (0.002 rad), dicentric aberrations increased at ≥0.5 Gy (0.005 rad), 

and there was a slight indication that the frequency of centric rings increased at ≥3.0 Gy (0.03). In the 

same study, results of an electrophoretic assay (comet assay) on single exposed lymphocytes revealed that 

DNA damage (evaluated by visual inspection and tail moment) occurred at doses as low as 0.2 Gy 

(0.002 rad). The varying frequencies for the different types of chromosomal aberrations were associated 

with the number of DNA breaks required for their formation and whether one or more chromosomes were 
STRONTIUM 118 

3. HEALTH EFFECTS 

involved: acentrics requiring a single break and dicentrics requiring at least two breaks on different 

chromosomes. Dose-related increases in micronucleus formation, predominantly derived from acentric 

chromosomes, were reported in human lymphocytes irradiated at doses between 0.3 and 3.0 Gy 

(0.003 and 0.030 rad) (Hall and Wells 1988; Mill et al. 1996). 

3.5 TOXICOKINETICS 

3.5.1 Absorption 

3.5.1.1 Inhalation Exposure 

Evidence for absorption of inhaled strontium in humans is provided by several cases of accidental 

exposure of workers to airborne radiostrontium (Navarro and López 1998; Petkau and Pleskach 1972; 

Rundo and Williams 1961). Although these cases do not provide a complete quantitative description of 

the absorption of inhaled strontium in humans, they demonstrate clearly that inhaled aerosols of strontium 

compounds (e.g., SrCl2, SrTiO3) can be absorbed, as indicated by the detection of radiostrontium in urine 

and feces. 

In one case, a worker accidentally inspired an unknown quantity of 90SrCl2 (physical form unknown) and 

over the subsequent 800 days, 90Sr was excreted in the urine with half-times of 3.3 (52%), 17 (7%), and 

347 days (18%) (Petkau and Pleskach 1972). The urinary:fecal excretion ratio was 3:1. In a second case, 

a worker was exposed to 90SrCO3 (physical form unknown) with deposition within the nasal tract as well 

as the hands, face, and hair. The actual inhaled dose could not be determined; however, based on the 

excretion kinetics of 90Sr over the subsequent 300 days, the reconstructed internal dose was estimated to 

have been approximately 300–400 nCi (11.1–14.8 kBq) (Rundo and Williams 1961). Excretion in urine 

occurred with half-times of 2.2 (>90%), 15, and 175 days, and the urinary:fecal excretion ratio over the 

first 24 days was 0.71. In a third case, two workers accidentally inhaled 90SrTiO3 (physical form 

unknown), and 90Sr was detected in urine over a period of 225 days (Navarro and López 1998). 

Studies conducted in animals have shown that the rate of absorption depends on the chemical form of the 

inhaled strontium aerosol. Compounds of greater solubility are, in general, more rapidly cleared from the 

lung. For example, strontium is rapidly cleared from the lung after inhalation of SrCl2. In dogs that 

received a 2–22-minute nose-only exposure to an aerosol of 85SrCl2 (activity median aerodynamic 

diameter [AMAD] 1.4–2.7 μm, geometric standard deviation [GSD] 2.0), <1% of the initial lung burden 

remained in the lung 12 hours after the exposure; 37% of the body burden was distributed to the skeleton 
STRONTIUM 119 

3. HEALTH EFFECTS 

within 12 hours after the exposure, and 84% was in the skeleton 4 days after the exposure (Fission 

Product Inhalation Project 1967a). In contrast to the relatively rapid absorption of inhaled SrCl2, after 

exposures to strontium in particles of fused clay, absorption is much slower. In dogs that received a noseonly exposure to 90Sr in fused montmorillonite clay particles (AMAD 2.2 μm, GSD 1.7), the average halftime of elimination of strontium from the lung was 490 days (Snipes et al. 1974a, 1974b). Thus, 

strontium compounds of lower solubility are more slowly absorbed from the lung. Support for this also 

comes from studies in which the rates of absorption of various compounds of strontium were compared in 

rats. Rats were exposed to aerosols of 85Sr carbonate, phosphate, fluoride, oxide, or titanate (particle sizes 

and doses not specified) (Willard and Snyder 1966). Greater than 99% of the initial lung burden of 85Sr 

was cleared from the lung 5 days after inhalation of the carbonate, phosphate, fluoride, or oxide, whereas 

60% of the 85Sr remained in the lung after inhalation of the more insoluble strontium titanate. 

In rats exposed to airborne fly ash (sieved to have a particle diameter of distribution of 90% less than 

20 μm) for 6 hours, strontium was eliminated from the lung with a half-time of 23 days (observations 

were made for 30 days) (Srivastava et al. 1984b). One day after the exposure, the tissue:plasma strontium 

concentration ratios were 0.3–0.5 in the liver, kidney, small intestine, and heart. The report of this study 

does not indicate whether whole-body or nose-only exposures were utilized in the study; therefore, it is 

not possible to know for certain how much of the absorption may have resulted from ingestion of fly ash 

deposited on the animals. Furthermore, given the relatively large particle size of the fly ash, it is likely 

that deposition in the respiratory tract was largely in the tracheobronchial and nasopharyngeal region, 

from which the strontium may have been cleared mechanically to the esophagus and swallowed. 

Nevertheless, studies in which 89Sr-enriched fly ash was instilled into the trachea of rats indicate that 

strontium in this form was partly absorbed and appeared in plasma and other tissues within days of the 

exposure (Srivastava et al. 1984a). 

Although intratracheal instillation does not precisely replicate inhalation exposure, these studies provide 

additional evidence that strontium compounds of greater solubility are absorbed more rapidly from the 

lung. Strontium was cleared relatively rapidly from the lungs of rats that received an intratracheal dose of 

SrCl2 (half-times <1 day) and was eliminated from the body in the urine (4–6% of the initial body burden) 

and in the feces (10–18%) (Naményi et al. 1986). By contrast, in rats that received an intratracheal dose 

of 360–760 μg Sr as SrTiO3, strontium was eliminated from the lung with half-times of 0.4 days (85%) 

and 130 days (15%); the long retention phase reflects the slow absorption of the insoluble SrTiO3 

deposited in the lung, whereas the rapid phase reflects the mechanical clearance from the 

tracheobronchial region (Anderson et al. 1999b). 
STRONTIUM 120 

3. HEALTH EFFECTS 

Strontium has been shown to be absorbed from the nasopharyngeal region of the respiratory tract. In 

hamsters administered 85SrCl2 (in saline solution) directly into the nasal tract, 67% of the 85Sr was 

absorbed in 4 hours and 63% was estimated to have been absorbed directly from the nasopharynx region 

of the respiratory tract (Cuddihy and Ozog 1973). 

3.5.1.2 Oral Exposure 

The fractional absorption of ingested strontium has been estimated in healthy human subjects or hospital 

patients who received an oral dose of strontium chloride (SrCl2) or ingested strontium in the diet 

(Table 3-7). Absorption was quantified in these studies from measurements of plasma strontium 

concentration-time profiles for ingested and intravenously injected strontium (bioavailability), or from 

measurements of the difference between the amount ingested and excreted in feces (balance). 

Collectively, the results of these studies indicate that approximately 20% (range, 11–28%) of ingested 

strontium is absorbed from the gastrointestinal tract. Balance measurements can be expected to yield 

underestimates of absorption as a result of excretion of absorbed strontium in the feces (see 

Section 3.5.4); nevertheless, the two methods have yielded similar estimates of absorption. 

Vezzoli et al. (1998) compared the area under the plasma strontium concentration-time curves in adult 

males and females and found no significant difference (males, 10.6±0.6 mmol/L-minute; females, 

9.3±0.6 mmol/L-minute). The subjects included groups of healthy age-matched men and women 

(15 males, 12 females) and groups of normocalcuric patients (29 males, 18 females) who had calciumoxalate urinary tract stones. Although the fraction absorbed could not be estimated in this study because 

the area under the curve for an intravenous dose was not measured, the results suggest that there were no 

substantive differences in absorption between males and females. This conclusion may not be valid for 

physiologic states in which there is an increased demand for calcium such as pregnancy and lactation. 

Calcium absorption is higher in these states, and studies in animals suggest that strontium absorption may 

also be higher (Kostial et al. 1969b). In general, strontium absorption appears to be a good indicator of 

calcium absorption in adult humans as both elements appear to share common mechanisms of absorption 

(Bianchi et al. 1999; Blumsohn et al. 1994; Milsom et al. 1987; Reid et al. 1986; Sips et al. 1994) (see 

Section 3.6.1). 

Studies conducted in infants and children indicate that approximately 15–30% of dietary strontium is 

absorbed, similar to estimates in adults (Alexander et al. 1974; Harrison et al. 1965; Kahn et al. 1969a; 
STRONTIUM 121 

3. HEALTH EFFECTS 

Table 3-7. Summary of Estimates of Absorption of Ingested Strontium in Humans 

Dose and Absorption 

mediaa Subjects (N)b (% of dose)c Comment Reference 

Tracer 

44 mg, SrCl2 

44 mg, SrCl2 

88 mg, SrCl2 

219 mg, 

SrCl2 

Tracer 

1.45 mg/kg, 

SrCl2 

Tracer 

44 mg, SrCl2 

219 mg, 

SrCl2 

Adults (9M) 

Adults (8M) 

Adults (8M) 

Adults (8M) 

Adults 

(6M, 11F) 

Adults (3M) 

Adults 

(6M, 4F) 

Adults (12) 

Adults 

(43M, 20F) 

Adults (6M) 

Tracer in milk Adults (5) 

Tracer Adults (4F) 

28±3 

25±7 

25±6 

19±5 

20 

21 (18–24) 

22±2 

17 (8–34) 

13 

20 

11 

42 (25–59) 

Healthy adults. Absorption estimate based 

on whole body retention (R): Roral/Riv. 

Healthy, fasted subjects adults. Absorption 

estimate based on plasma AUCoral/AUCiv.

d 

Healthy fasted subjects. Absorption estimate 

based on plasma AUCoral/AUCi

. 

Healthy subjects. Dose administered with 

meal. Absorption estimate based on plasma 

AUCoral/AUCiv. 

Patients with osteoporosis or chronic renal 

failure. Dose administered with meal. 

Absorption estimate based on plasma 

AUCoral/AUCiv. 

Patients with osteoporosis. Dose 

administered with meal. Absorption estimate 

based on plasma AUCoral/AUCiv. 

Healthy fasted subjects. Absorption estimate 

based on fraction of dose in plasma at 

3 hours. 

Healthy subjects without a pre-dosing fast. 

Absorption estimate based on whole body 

counting. 

Fasted patients with growth hormone 

deficiency, osteoporosis, hypothyroidism or 

hypercalcuric urinary tract stones. Absorption 

estimate based on fraction of dose in plasma 

at 4 hours. 

Healthy fasted subjects. Absorption 

estimated from cumulative urinary excretion. 

Healthy subjects. Dose administered in milk, 

daily for 21–32 days. Absorption estimated 

from whole body retention kinetics. 

Two health subjects, two patients with 

osteoporosis. Absorption estimated from 

intake minus 20-day fecal excretion, 

corrected for fecal excretion after an 

intravenous dose. 

Likhtarev et al. 

1975 

Sips et al. 1995 

Sips et al. 1996 

Sips et al. 1996 

Blumsohn et al. 

1994 

Hart and 

Spencer 1967 

Bianchi et al. 

1999 

LeRoy et al. 

1966 

Sips et al. 1994 

Leeuwenkamp 

et al. 1990 

Rundo and 

Lilligraven 1966 

Uchiyama et al. 

1973 

0.8 mg/day Adults (11M) 18 (-17–42) Patients with various disorders, including Warren and 

diet osteoporosis. Absorption estimate based on Spencer 1976 
STRONTIUM 122 

3. HEALTH EFFECTS 

Table 3-7. Summary of Estimates of Absorption of Ingested Strontium in Humans 

Dose and Absorption 

mediaa Subjects (N)b (% of dose)c Comment Reference 

Tracer Adults (11M) 

1,500 mg/day Adults 

(5F, 1M) 

Diet Adults (9) 

5–100 mg, Children (5) 

SrCl2 4–14 years 

100 μg Infants 6–8 

breast milk days (12) 

600 μg Infants 

diet 20 days–1 

year (21) 

18 (-17–42) 

22 

(20–28) 

12 

(0–48) 

22 

15 

(-47–59) 

28 

(12–43) 

6-day balance; dietary intake minus fecal 

excretione

. 

Patients with various disorders, including 

osteoporosis. Absorption estimate based on 

estimated from 6-day balance; dietary intake 

minus fecal excretione

. 

Patients with various illnesses. Absorption 

estimated from dietary intake minus fecal 

excretion minus fecal excretion after and I.V. 

dose (endogenous fecal excretion). 

Patients with various illnesses. Absorption 

estimate based on estimated from 6-day 

balance; dietary intake minus fecal 

excretion.e 

Patients with various illnesses. Dose 

administered for 24–28 days. Absorption 

estimated from dose minus 14-day fecal 

excretion. 

Healthy breast-feeding subjects. Absorption 

estimate based on estimated from 3-day 

balance intake minus fecal excretion.e 

Healthy subjects. Absorption estimate based 

on estimated from seven sequential 28-day 

balances; dietary intake minus fecal 

excretion.e 

Warren and 

Spencer 1976 

Spencer et al. 

1960 

Spencer et al. 

1972a 

Sutton et al. 

1971b 

Harrison et al. 

1965 

Kahn et al. 

1969a 

a

Doses are in mass of strontium. 

b

Number of males (M) or females (F) is presented if reported.
 c

Values are reported means ± standard deviation; values in parentheses are reported ranges. d

AUC refers to the area under the plasma strontium concentration-time curve. e

Calculated from reported individual subject data.
 
STRONTIUM 123 

3. HEALTH EFFECTS 

Sutton et al. 1971a). Although age-related changes in strontium absorption cannot be discerned from the 

studies in humans, age-related changes in absorption of strontium have been observed in rats, suggesting 

the possibility of increased absorption of strontium during the neonatal period in humans. Adult male rats 

that received a single oral dose of 1.4 mg Sr as SrCl2 absorbed 19% (±5 standard deviation [SD]) of the 

dose (Sips et al. 1997); this value is similar to that reported for humans (Sips et al. 1995, 1996). 

However, when absorption was estimated at various ages, absorption was found to decrease from 85% of 

the dose at 15 days of age to 8% of the dose at ages older than 89 days (Forbes and Reina 1972). The 

differences between the adult estimates in these two studies may reflect the different methodologies; in 

the Sips et al. (1997) study, absorption was estimated from the area under the plasma strontium 

concentration-time curve for orally and intravenously administered strontium, whereas in the Forbes and 

Reina (1972) study, the absorption estimate was based on the measurements of 8-hour body burdens of 

strontium minus strontium in the gastrointestinal tract. 

The fractional absorption of strontium appears to increase in rats during lactation. Rats that received a 

tracer dose of 85Sr as SrCl2 in drinking water between 14 and 16 days after the start of lactation absorbed 

twice as much strontium as control rats that were not lactating and received the same oral dose of 

strontium; 11% of the dose was absorbed in lactating rats compared to 5% in controls (Kostial et al. 

1969b). Absorption was estimated in this study as the fraction of the dose in the skeleton, urine, and pups 

3 days after the start of exposure. 

The exact site of absorption of strontium in the gastrointestinal tract is not known; however, studies in 

hamsters suggest the possibility of absorption in both the stomach and small intestine. In hamsters that 

received a gavage tracer dose of 85SrCl2, 37% was absorbed, whereas 20% was absorbed when the dose 

was administered to hamsters that had their pyloric sphincter ligated (Cuddihy and Ozog 1973). Studies 

in preparations of in vitro and in situ isolated intestine of the rat provide direct evidence for strontium 

absorption in the small intestine (see Section 3.6.1). 

3.5.1.3 Dermal Exposure 

There is little evidence for systemic toxicity following dermal exposure to strontium compounds, which 

would suggest that they are not readily absorbed across the skin of humans. Ilyin et al. (1975) estimated 

absorption rates for solutions of strontium chloride across intact or abraded skin of human subjects. 

Three groups of three male volunteers received topical applications of 85Sr as strontium chloride in 
STRONTIUM 124 

3. HEALTH EFFECTS 

aqueous solution (pH 7.0) without a carrier. In the first group, intact forearm skin (average area 8 cm2) 

was exposed for 6 hours. In the second and third groups, the skin of the forearm was abraded with a 

metal grater just before the solution was applied; exposures were 6.1 cm2

 for 30 minutes and 6.9 cm2 for 

6 hours, respectively. For comparison, a fourth group received an intravenous injection of 85SrCl2. After 

exposure and decontamination of the skin, radioactivity measurements were taken over 40 days of the 85Sr 

present in the whole body, the patella, the right unexposed forearm, and, during the first 20 days, in daily 

urine samples. Absorption of strontium was estimated from whole body or partial body 85Sr burdens, or 

urinary excretion of 85Sr in comparison to the same end points after an intravenous dose of 85SrCl2. The 

absorption of radiostrontium through intact skin over 6 hours was estimated to be 0.26% (range, 0.14– 

0.37%) of the applied dose, indicating that undamaged skin is a relatively effective barrier to penetration 

by strontium. Strontium absorption was greater through scratched and abraded skin. An average of 38% 

(range, 25.5–45.8%) of the applied dose was absorbed after 30 minutes and an average of 57.4% (range of 

coefficients, 55.7–65.3%) was absorbed after 6 hours. No other studies were located regarding dermal 

absorption of strontium compounds in humans. 

An in vitro study evaluated penetration of 90Sr through abdominal skin removed from 5- or 9-day-old 

Wistar rats and arranged in vertical penetration cells (Bauerová et al. 2001). The radionuclide in a 

chloride carrier solution (0.01–1.0% strontium chloride w/v) was applied to the epidermal surface; 

radioactivity of the permeated 90Sr in the receptor chamber solution was measured by liquid scintillation 

spectrometry. Penetration was inversely related to concentration of the carrier solution. Penetration of 

the radiostrontium through the hairless skin of 5-day-old rats over 24 hours was 4 times lower than 

through the hairy skin of 9-day-old rats: at a carrier concentration of 0.1%, penetration was 0.5% for 

hairless skin of 5-day old rats compared to 2% for 9-day old rats. The authors attributed this difference to 

the barrier provided by the intact stratum corneum in 5-day skin, indicating that hair follicles in skin of 

9-day-old rats increase the permeability of skin to strontium. In experiments in which epidermal layers 

were stripped (by the 20x repeated application of adhesive tape) or entirely removed from skin of 5-dayold rats, penetration was approximately 25% over 24 hours. 
STRONTIUM 125 

3. HEALTH EFFECTS 

3.5.2 Distribution 

3.5.2.1 Inhalation Exposure 

Information on the distribution of inhaled strontium in humans is not available; however, it is reasonable 

to assume that the distribution of strontium absorbed into the systemic circulation after deposition in the 

respiratory tract would be similar to that absorbed after ingestion (see Section 3.5.2.2). 

Studies in animals have shown that strontium that is absorbed after an initial deposition in the respiratory 

tract ultimately distributes primarily to the skeleton. In dogs that received a 2–22-minute nose-only 

exposure to aerosols of 85SrCl2 (AMAD 1.4–2.7 μm, GSD 2.0), 37% of the body burden was distributed 

to the skeleton within 12 hours after the exposure and 84% was in the skeleton 4 days after the exposure 

(Fission Product Inhalation Project 1967a). Four to 6 days after a 30-minute inhalation exposure of rats 

to aerosols of 85Sr carbonate, phosphate, fluoride, or oxide (particle sizes and doses not specified), >99% 

of the body burden of 85Sr was in the skeleton (Willard and Snyder 1966). Two days after rats received a 

10-minute head-only exposure to tracer levels of 85Sr or a mixture of 85Sr and 90Sr aerosols (AMAD 

1.8–2.8), at which time radioactive strontium could no longer be detected in the lung, the concentration in 

bone was 100–2,000 times that in soft tissues (Fission Product Inhalation Project 1967b). The rank order 

of soft tissue concentrations (highest to lowest) was muscle > skin > liver > kidney. In rats exposed to 

airborne fly ash (sieved to have a particle diameter of distribution of 90% less than 20 μm) for 6 hours, 

strontium was detected in various tissues; 1 day after the exposure, the tissue:plasma strontium 

concentration ratios were 0.3–0.5 in the liver, kidney, small intestine, and heart (Srivastava et al. 1984b). 

Information on the distribution of strontium absorbed after deposition in the respiratory tract can be 

derived from studies in which strontium compounds were instilled directly into the trachea. Although 

intratracheal instillation does not precisely replicate inhalation exposure, the distribution of the absorbed 

strontium is likely to be similar to that which would be absorbed after inhalation. In rats that received an 

intratracheal dose of 89Sr-enriched fly ash (sieved to have a particle diameter of distribution of 90% less 

than 20 μm), radioactivity was eliminated from the lung and appeared in plasma and other tissues within 

days of the exposure; tissue:plasma concentration ratios were >1 (1.5–2) in the liver, kidney, stomach, 

and small intestine, and <1 (0.7–0.9) in the spleen, heart, and brain (Srivastava et al. 1984a). The 

relatively high concentrations of strontium in the gastrointestinal tract may reflect the mechanical 

clearance of strontium from the airways to the esophagus. 
STRONTIUM 126 

3. HEALTH EFFECTS 

Although placental transfer of strontium has been demonstrated in humans and animals exposed to 

strontium by other routes of exposure (see Section 3.5.2.2), only one study has examined placental 

transfer after a dose to the respiratory tract. Pregnant rats received an intratracheal dose of 89Sr-enriched 

fly ash (sieved to have a particle diameter of distribution of 90% less than 20 μm) on days 14–18 of 

gestation. The concentrations of strontium in whole fetus, liver, lung, heart, and kidney were not 

significantly different from controls that received an instillation of saline (Srivastava et al. 1990). 

3.5.2.2 Oral Exposure 

The distribution of absorbed strontium in the human body is similar to that of calcium, with 

approximately 99% of the total body burden in the skeleton (ICRP 1993). The skeletal burden of stable 

strontium has been estimated from analyses of bone samples from human autopsies (Herring and Keefer 

1971a; O’Connor et al. 1980; Papworth and Vennart 1984; Tanaka et al. 1981). Skeletal burden was 

estimated in Japanese adult males to be approximately 440 mg compared to 850 g of calcium (Tanaka et 

al. 1981). 

Papworth and Vennart (1984) analyzed published data on 90Sr and calcium concentrations in human bone 

tissues and diets of people in the United Kingdom during the period from 1955 to 1970 and concluded 

that approximately 4.75% of the dietary intake of 90Sr was taken up by the adult skeleton. Approximately 

7.5% of the cortical bone 90Sr burden was eliminated from bone each year (equivalent to elimination halftimes of approximately 9.2 years). The rate of elimination from trabecular bone was approximately 

4 times this value. The same analysis yielded estimates of skeletal uptakes of strontium that varied with 

age, being highest, approximately 10%, in infants and during adolescence, ages in which bone growth 

rates are high relative to other ages. 

Strontium distributes relatively uniformly within the bone volume where it exchanges with calcium in 

hydroxyapatite (see Section 3.6.1), although small differences in the calcium and strontium distributions 

within bone have been reported. The Sr:Ca concentration ratio in bone increases with age from 

approximately 0.3 mg strontium/g Ca at birth to a value of 0.5 in adults (Papworth and Vannart 1984; 

Tanaka et al. 1981). The Sr:Ca ratio in bone also has been shown to vary with the bone type; ratios in 

cortical bone were approximately 10–20% higher than in trabecular bone (Tanaka et al. 1981). 

Information on the distribution of strontium in soft tissue is extremely limited. In rats that were exposed 

to 3.4 mg strontium/L (as SrCl2) in drinking water for 3 months, the serum concentration of strontium was 
STRONTIUM 127 

3. HEALTH EFFECTS 

8.7 mg/L and tissue:serum strontium concentration ratios (based on the latter mean serum concentration) 

were as follows: liver, 0.7; heart, 1.2; muscle, 1.1; adrenal, 1.3; brain, 1.2; and bone, 1,300 (Skoryna 

1981b). Strontium:calcium ratios in these tissues were approximately 0.05–0.1. Tissue:plasma strontium 

concentration ratios in rats 1–5 hours after they received an intraperitoneal injection of strontium revealed 

ratios <1 in the fat, spleen, liver, ovary, testis, skeletal muscle, and heart; and values of 1.2–1.7 in the 

lung, small intestine, salivary gland, kidney, and skin (Brues et al. 1969). Tissue:plasma concentration 

ratios of seminal vesicles in mice increased to values exceeding 2 several days after an intraperitoneal 

dose of strontium (Brues et al. 1967). 

Information on the subcellular location of strontium in soft tissues is also extremely limited. In rats that 

were exposed to 1.9 mg strontium/L (as SrCl2) in drinking water for 3 months, the strontium 

concentrations (per mg protein) in the mitochondrial, lysosomal, and microsomal fractions of liver were 

approximately 5 times that of cytosol (Skoryna 1981b). A major fraction of the strontium in tissues, 

possibly as much as 50–80% appears to be bound to protein (Kshirsagar 1977). 

The partitioning of strontium in blood has not been extensively explored. The concentrations of 

strontium in the erythrocyte and plasma fractions of human blood obtained from blood banks were 

7.2 μg/L in the erythrocyte fraction and 44 μg/L in the plasma fraction, suggesting that most of the 

strontium in blood resides in the plasma (Olehy et al. 1966). The strontium concentration in serum from 

100 human subjects (health status not reported) was 53 μg/L, similar to the value reported for blood bank 

serum (Skoryna 1981b). Strontium binds to proteins in human serum; however, the specific proteins to 

which strontium binds have not been characterized. Alda and Escanero (1985) found that 45% of the 

strontium incubated with human serum at a concentration of 10 mg/L was ultrafilterable. Harrison et al. 

(1955) reported a value of 60% for the ultrafilterable fraction of plasma at a plasma concentration of 

3.5 mg/L in two subjects who received an intravenous dose of 20 or 100 mg strontium chlorides. Note 

that this concentration is 300–1,000 times that reported for serum concentrations in subjects that were not 

receiving strontium supplements (Olehy et al. 1966; Skoryna 1981b); at lower concentrations, a larger 

fraction of the serum strontium may be bound, as binding appears to be saturable (Alda and Escanero 

1985; Berg et al. 1973). Values of 40–60% bound to protein have been reported for guinea pig and rabbit 

plasma or serum, respectively (Lloyd 1968; Twardock et al. 1971). 

Strontium in the maternal skeleton can be transferred to the fetus during pregnancy. Studies of residents 

of the Techa River who were exposed to strontium as result of releases from a plutonium production plant 

provide evidence for fetal transfer of strontium (Tolstykh et al. 1998, 2001). The fetal:maternal transfer 
STRONTIUM 128 

3. HEALTH EFFECTS 

coefficient—the ratio of 90Sr concentrations in the fetal and maternal skeletons (expressed in becquerels 

per gram of calcium)—was determined for six subjects who were exposed prior to pregnancy and their 

seven stillborn infants (Tolstykh et al. 1998). The transfer coefficients varied from 0.012 to 0.24, with the 

higher values associated with maternal exposures that occurred during adulthood and lower values 

associated with maternal exposures during childhood or adolescence. The difference was not related to 

the maternal strontium burden at pregnancy and may reflect a lower availability of strontium deposited in 

cortical bone during periods of active bone growth. 

Studies in animals provide additional evidence for transfer of strontium through the placenta to the fetus. 

The fetus begins to accumulate strontium as the fetal skeleton develops. In mice, ossification of the fetal 

skeleton begins on approximately the 14th day of gestation, at which point, the fetal strontium burden 

begins to increase (Olsen and Jonsen 1979). In pregnant mice that received an injection of strontium at 

different stages of pregnancy, fetal strontium burden was 4.5% of the maternal dose administered on the 

18th day of pregnancy compared to 0.7% of the maternal dose administered on the 14th day of pregnancy 

(Rönnbäck 1986). Thus, fetal transfer was highest when the maternal dose occurred at the time of 

greatest skeletal growth. A similar observation has been made in rats; uptake of strontium by the fetus is 

highest (1–2% of an injected maternal dose) if the maternal dose is given on or after the 16th day of 

gestation when ossification of the fetal skeleton begins (Hartsook and Hershberger 1973; Wykoff 1971). 

The distribution of strontium in the fetus at the end of gestation is similar to that of the mother with most 

of the strontium burden in the skeleton. In mice, the skeletal (long bones):soft tissue concentration ratio 

was approximately 40 in both the fetuses and dams (Jacobsen et al. 1978). 

Strontium enters mammary milk in humans and can be transferred to newborns during breast feeding 

(Harrison et al. 1965). The concentration of strontium in breast milk of 12 healthy women was estimated 

to be 74 μg/L (range, 39–93) and the Sr:Ca concentration ratio was 0.24 μg strontium/mg Ca (Harrison et 

al. 1965). In a study of the transport of trace elements, the concentration of strontium in colostrum 

samples collected from 29 healthy women during the first 3 days after delivery was found to be 

comparable to that in serum from venous blood samples taken 20 minutes before delivery (Rossipal et al. 

2000). In contrast, the concentration of calcium in colostrum was significantly increased over the level in 

maternal serum, which was indicative of active transport. The authors concluded that the transfer of 

strontium was based primarily on a concentration gradient mode of action. Numerous studies in animals 

provide additional evidence for transfer of strontium from breast milk to newborns during lactation 

(Hopkins 1967; Jacobsen et al. 1978; Kostial et al. 1969b; Rönnbäck et al. 1968). In lactating rats that 

received an oral exposure to tracer concentrations 85Sr in drinking water during the 14th through 16th days 
STRONTIUM 129 

3. HEALTH EFFECTS 

of lactation, approximately 5% of the ingested dose was recovered in the nursing pups 24 hours after the 

end of the 2-day exposure (Kostial et al. 1969b). In a study in which lactating mice received an 

intraperitoneal injection of radioactive strontium, strontium levels of the nursing pups was approximately 

20% of that of the dams (Rönnbäck et al. 1968). These results are consistent with the oral exposure study 

(Kostial et al. 1969b), if one assumes that approximately 25% of the oral dose was absorbed by the dam. 

The tissue distribution of strontium in lactating mice and their offspring was found to be similar after an 

intraperitoneal dose to the dams during lactation; concentrations in bone were approximately 1,000 times 

higher than liver and kidney (Jacobsen et al. 1978). The strontium concentration in calvaria of the 

lactating pups, after 5 days of lactation, was approximately 3 times that of the dams, whereas the 

concentration in long bones of pups and dams were similar (Jacobsen et al. 1978). The difference in the 

bone concentrations in the dams and pups may reflect the relatively higher rate of bone formation in the 

pups and associated incorporation of strontium into the new bone. 

3.5.2.3 Dermal Exposure 

In volunteers who were exposed to dermally applied 85SrCl2 in the left forearm, 85Sr was detected by 

external counting of the patella and right forearm 3 and 6 hours after the exposure was initiated, 

suggesting that the absorbed strontium had been taken up by bone (Ilyin et al. 1975). Although no other 

studies were located regarding the distribution of dermally absorbed strontium, it is likely that the 

distribution would be similar to that absorbed from the oral route, with the most of the body burden in the 

skeleton (see Section 3.5.2.2). 

3.5.3 Metabolism 

The metabolism of strontium consists of binding interactions with proteins and, based on its similarity to 

calcium, probably complex formation with various inorganic anions such as carbonate and phosphate, and 

carboxylic acids such as citrate and lactate (Alda and Escanero 1985; Inoue et al. 1988; Kshirsagar 1977; 

Lloyd 1968; Twardock et al. 1971). These types of interactions would be expected for all routes of 

exposure. These types of interactions would be expected for all routes of exposure including the 

following: 
STRONTIUM 130 

3. HEALTH EFFECTS 

3.5.3.1 Inhalation Exposure 

3.5.3.2 Oral Exposure 

3.5.3.3 Dermal Exposure 

3.5.4 Elimination and Excretion 

3.5.4.1 Inhalation Exposure 

Whole body elimination times have been measured in dogs and rats that received inhalation exposures to 

SrCl2. In dogs that were exposed to aerosols of 85SrCl2 (AMAD 1.4–2.7 μm, GSD 2.0), elimination halftimes were 0.6 (59%), 9 (12%), and 300 days (29%) (Fission Product Inhalation Project 1967a). The 

rapid early phase of elimination reflects the mechanical clearance of strontium deposited in the 

tracheobronchial region of the respiratory tract and transfer to the gastrointestinal tract and feces, whereas 

the slower elimination component reflects the elimination from the skeleton. A similar pattern of 

elimination has been observed in rats. In rats that were exposed to tracer levels of 85Sr or a mixture of 

85Sr and 90Sr aerosols (AMAD 1.8–2.8), the long-term whole-body elimination half-time, measured 5– 

230 days after exposure, was 330 days (Fission Product Inhalation Project 1967b). 

Strontium that is absorbed after an initial deposition in the respiratory tract is excreted in feces and urine. 

Evidence for this comes from accidental exposures to radioactive strontium. In one case, a worker 

accidentally inspired an unknown quantity of 90SrCl2 (physical form unknown) and, over the subsequent 

800 days, the urinary:fecal excretion ratio was 3:1 (Petkau and Pleskach 1972). The urinary:fecal 

excretion ratio of 3 is consistent with observations of long-term urinary:fecal excretion ratios observed in 

people who ingested radioactive strontium or short-term ratios in people who received an intravenous 

dose of radioactive strontium (see Section 3.5.4.2). In a second case, a worker was exposed to 90SrCO3 

with deposition within the nasal tract as well as the hands, face, and hair and the urinary:fecal excretion 

ratio over the first 24 days was 0.71 (Rundo and Williams 1961). The lower ratio in this case probably 

reflects the fecal contribution of strontium that was mechanically cleared from the respiratory tract over 

the shorter observation period (24 days compared to 800 days). Similar observations have been made in 

animals. In dogs that received a 2–22-minute nose-only exposure to aerosols of 85SrCl2 (AMAD 

1.4–2.7 μm, GSD 2.0), an initially large fecal component of excretion was followed by urinary:fecal 

excretion ratios of 1.0–1.4 (Fission Product Inhalation Project 1967a). An increase over time in the 
STRONTIUM 131 

3. HEALTH EFFECTS 

urinary:fecal excretion ratios from values <1 to 2–4 has also been observed after intratracheal instillation 

of SrCl2 in rats (Fission Product Inhalation Project 1967b; Namenyi et al. 1986). 

3.5.4.2 Oral Exposure 

The long-term (decades) elimination of strontium has been studied in people who were exposed to 

strontium in the Techa River area of Russia after fission products from a plutonium production process 

were released in the area. Whole-body elimination half-times were estimated in a study population of 

361 males and 356 females to be 28 years in males and 16 years in females (Tolstykh et al. 1997). Most 

of the difference in the elimination rate estimated for males and females resulted from a pronounced 

increase in the elimination rate in females after age 50 years. The increase most likely reflects the 

increase in bone resorption that tends to occur in females after menopause. Müller et al. (1966) estimated 

a similar value, 25 years, for the long-term elimination half-time of strontium in 56 radium dial painters. 

In two dial painters, long-term elimination half-times were estimated to be 9 years (Wenger and Soucas 

1975). Estimates of the long-term elimination half-times of strontium reflect primarily the storage and 

release of strontium in bone. Over shorter time periods after exposure, faster elimination rates are 

observed that reflect soft-tissue elimination as well as elimination from a more rapidly exchangeable pool 

of strontium in bone. When whole-body elimination of a tracer dose of 85Sr was measured for periods of 

42–108 days in nine subjects, the mean elimination half-time was 91 days (±32, SD) (Likhtarev et al. 

1975). In three healthy subjects that received a single oral dose of SrCl2, the estimated average wholebody elimination half-times, estimated over 13 days, were 2 (30%) and 59 days (70%) (Uchiyama et al. 

1973). Similar short-term rates of elimination have been observed within days to a few weeks after an 

intravenous injection of SrCl2 (MacDonald et al. 1965; Newton et al. 1990). 

Strontium that has been absorbed from the gastrointestinal tract is excreted primarily in urine and feces. 

In two dial painters, rates of urinary and fecal excretion of radium approximately 10 years after the 

exposure were approximately 0.03 and 0.01% of the body burden per 24 hours, respectively (Wenger and 

Soucas 1975). The urine:fecal excretion ratio of 3 that was observed in the radium dial workers is 

consistent with ratios of 2–6 observed several days to weeks after subjects received an intravenous 

injection of SrCl2 (Bishop et al. 1960; Blake et al. 1989a, 1989b; Likhtarev et al. 1975; Newton et al. 

1990; Samachson 1966; Snyder et al. 1964; Uchiyama et al. 1973). Thus, urine appears to be the major 

route of excretion of absorbed strontium. The observation of fecal excretion of radioactive strontium 

weeks to decades after an oral exposure or over shorter time periods after an intravenous exposure 

suggests the existence of a mechanism for transfer of absorbed strontium into gastrointestinal tract, either 
STRONTIUM 132 

3. HEALTH EFFECTS 

from the bile or directly from the plasma. Evidence for direct secretion of strontium from the plasma into 

the intestine is provided by studies in animals (see Section 3.5.1). The available information does not 

address the extent to which biliary excretion may also contribute to fecal excretion of strontium. 

As discussed in Section 3.5.2.2, absorbed strontium is eliminated in breast milk during lactation. The 

concentration of strontium in breast milk of 12 healthy women was estimated to be 74 μg/L (range, 39– 

93) and the Sr:Ca concentration ratio was 0.24 μg strontium/mg Ca (Harrison et al. 1965). 

Strontium has been detected in human saliva and seminal fluid. In healthy subjects who received a single 

intravenous injection of SrCl2, the saliva:plasma concentration ratio was 0.9 and the semen:plasma ratio 

was 0.6 (Harrison et al. 1967a). 

3.5.4.3 Dermal Exposure 

In volunteers who were exposed to dermally applied 85SrCl2 in the left forearm, 85Sr was excreted in urine 

(fecal excretion was not measured in this study) (Ilyin et al. 1975). Although no other studies were 

located regarding the excretion of dermally absorbed strontium, it is likely that the excretion would be 

similar to that absorbed from the oral route, with urinary excretion being approximately 2–3 times greater 

than fecal excretion (see Section 3.5.4.2). 

3.5.5 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. 

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 
STRONTIUM 133 

3. HEALTH EFFECTS 

tissue dose of the toxic moiety, and (2) the target tissue dose and observed responses (Andersen et al. 

1987; Andersen and Krishnan 1994). 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 parametrization, (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) is 

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). 

Similar models have been developed for radionuclides. These 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 3-4 shows a conceptualized 

representation of a PBPK model. Figures 3-5 through 3-8 show models for radionuclides in general or 

specifically for strontium. 
Lungs 

Liver 

Fat 

S low ly 

perfused 

tissues 

Richly 

perfused 

tissues 

K idney 

Skin 

V 

E 

N 

O 

U 

S 

B 

L 

O 

O 

D 

A 

R 

T 

E 

R 

I 

A 

L 

B 

L 

O 

O 

D 

V max K m 

Ingestion 

Inhaled chem ical E xhaled chem ical 

GI 

Tract 

Feces 

Urine

 C hem icals in air 

Source: adapted from Krishnan et al. 1994 contacting skin 

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. 

STRONTIUM 134 

3. HEALTH EFFECTS 

Figure 3-4. Conceptual Representation of a Physiologically Based 

Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance 
STRONTIUM 135 

3. HEALTH EFFECTS 

Human Respiratory Tract Model for Radiological Protection (ICRP 1994a). 

Deposition. The ICRP (1994a) 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 (1994a) provides inhalation dose 

coefficients that can be used to estimate the committed equivalent and effective doses to organs and 

tissues throughout the body based on a unit intake of radioactive material. The model applies to three 

levels of particle solubility and a wide range of particle sizes (approximately 0.0005–100 μm in 

diameter), and parameter values, which can be adjusted for various segments of the population (e.g., sex, 

age, 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. It is applicable to particulate 

aerosols containing strontium, but was developed for a wide variety of radionuclides and their chemical 

forms. 

The ICRP deposition model estimates the amount of inhaled material that initially enters each 

compartment (see Figure 3-5). The model was developed with the following 5 compartments: (1) the 

anterior nasal passages (ET1); (2) all other extrathoracic airways (ET2) (posterior nasal passages, the nasoand 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 from each region 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 experimental data, where deposition is related to 

particle size and airflow parameters, and scales deposition for women and children from adult male data. 

Similarly, 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 under 

several levels of activity. 

Deposition of inhaled gases and vapors is modeled as a partitioning process which depends on the 

physiological parameters noted above as well as the solubility and reactivity of compound in the 
Sequestered in Tiss Sequestered in Tiss S rface r sp rt ue S urface Tr ansp or t

AnteriorAnterior

ET1 

14 

ET1

14

1 Nasal

Extrathoracic Environment 

16 

Environment

16

Naso-oro­Naso-oropharynx 

Larynx

0.001 

ETSEQ

12 

LNET 

13 

Bronchi 

bb2 

BB2 

LNTH bbSEQ

0.03 2 

0.01 

0.01 

8 

BBSEQ 

9 

6 5

10 

Al3 

0.0001 

BB1 

bb1 

7 

4 

Al Al2 1

0.001 0.02 

3 2 1

ET GI Tract 2 

11 15 

100 

Bronchioles 

Alveolar 

Interstitium 

0.03 10 

0.00002 

0.001

ETSEQ

12

LNET

13

Bronchi

bb2

BB2

LNTH bbSEQ

0.03 2

0.01

0.01

8

BBSEQ

9

6 5

10

Al3

0.0001

BB1

bb1

7

4

Al Al2 1

0.001 0.02

3 2 1

ET GI Tract 2

11 15

100

Bronchioles

Alveolar 

Interstitium

0.03 10

0.00002

Thor acichor

*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 1994a 

STRONTIUM 136 

3. HEALTH EFFECTS 

Figure 3-5. Compartment Model to Represent Particle Deposition and 

Time-Dependent Particle Transport in the Respiratory Tract* 
STRONTIUM 137 

3. HEALTH EFFECTS 

Table 3-8. Reference Respiratory Values for a General Caucasian Population 

at Different Levels of Activity 

Activity: Resting (sleeping) Sitting awake Light exercise Heavy exercise 

Maximal workload: 8% 12% 32% 64% 

Breathing VT B fR VT B fR VT B fR VT B fR 

parameters: (L) (m3

h-1) (min-1) (L) (m3h-1) (min-1) (L) (m3h-1) (min-1) (L) (m3h-1) (min-1) 

Age Sex 

3 months 0.04 0.09 38 N/A N/A N/A 0.07 0.19 48 N/A N/A N/A 

1 year 0.07 0.15 34 0.1 0.22 36 0.13 0.35 46 N/A N/A N/A 

5 years 0.17 0.24 23 0.21 0.32 25 0.24 0.57 39 N/A N/A N/A 

10 years Male: 0.841 2.22 44 

Both: 0.667 1.84 46 

Female: 0.3 0.31 17 0.33 0.38 19 0.58 1.12 32 

15 years Male: 0.500 0.42 14 0.533 0.48 15 1.0 1.38 23 1.352 2.92 36 

Female: 0.417 0.35 14 0.417 0.40 16 0.903 1.30 24 1.127 2.57 38 

Adult Male: 0.625 0.45 12 0.750 0.54 12 1.25 1.5 20 1.923 3.0 26 

Female: 0.444 0.32 12 0.464 0.39 14 0.992 1.25 21 1.364 2.7 33 

a

See Annex B (ICRP 1994a) for data from which these reference values were derived. 

B = ventilation rate; fR = respiration frequency; h = hour; min = minute; N/A = not applicable; VT = tidal volume 
STRONTIUM	 138 

3. HEALTH EFFECTS 

respiratory tract (Figure 3-6). The ICRP (1994a) 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 of the compound that is inhaled is exhaled. Radiation doses from inhalation of SR-0 

compounds are assumed to result from the irradiation of the respiratory tract from the air spaces. 

•	 Type SR-1 compounds include soluble or reactive gases and vapors that 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 that are completely retained 

in the extrathoracic regions of the respiratory tract. SR-2 compounds include sulfur dioxide 

(SO2) and hydrogen fluoride (HF). 

Mechanical Clearance from the Respiratory Tract. 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. Figure 3-7 presents the compartmental model and is linked to the 

deposition model (Figure 3-5) and to reference values presented in Table 3-9. Table 3-9 provides 

clearance rates and deposition fractions for each compartment for insoluble particles. The table provides 

rates of insoluble particle transport for each of the compartments, expressed as a fraction per day and also 

half-time. ICRP (1994a) 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. 
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 

From ICRP 1994a 

Convection 

Diffusion 

STRONTIUM 139 

3. HEALTH EFFECTS 

Figure 3-6. Reaction of Gases or Vapors at Various Levels of the Gas-Blood 

Interface 
Figure 3-7. The Human Respiratory Tract Model: Absorption into Blood 

Particulate Material 

Bound Material 

Dissociated Material 

Particulate Material

Bound Material

Dissociated Material

Dissolution 

Uptake 

Blood

Source: ICRP 1994a 

STRONTIUM 140 

3. HEALTH EFFECTS 
STRONTIUM 141 

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-timea 

m1,4 AI1 bb1 0.02 35 days 

m2,4 AI2 bb1 0.001 700 days 

m3,4 AI3 bb1 0.0001 7,000 days 

m3,10 AI3 LNTH 0.00002 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 
STRONTIUM 142 

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-times are approximate since the reference values are specified for the particle transport rates and are 

rounded in units of d-1. A half-time 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-time of compartment Al3 is 

determined by the sum of the clearance rates from it. 

b

See paragraph 181, Chapter 5 (ICRP 1994a) for default values used for relating fs to dae. c

It is assumed that the slow-cleared fraction fs is size-dependent. For modeling purposes fs is taken to be: 

fs = 0 5. for dae ≤ 25 . ρ χμ / m and

0 63 .( d ρ χ/ − 25 .) ae fs = 0 5. e for dae > 25 . ρ χμ / m

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; d = day(s); 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 1994a 
STRONTIUM 143 

3. HEALTH EFFECTS 

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 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 mucocilliary action rapidly transports most particles deposited here toward the pharynx, a 

fraction of these particles are 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 many as half of the bronchi- and bronchiole-deposited particles. In 

human bronchi and bronchiole regions, mucus moves more slowly the closer it is 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, and both 

with clearance half-times estimated at 20 days. Particle size is a primary determinant of the 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 stay imbedded in the fluid on the 

alveolar surface or move into the lymph nodes. The one mechanism by which particles are physically 

resuspended and removed from the AI region is coughing. For modeling purposes, the AI region is 

divided into three subcompartments to represent different clearance rates, all of which are slow. 

Particle clearance from the alveolar-interstitial region has been measured in human subjects. The ICRP 

model uses two half-times to represent clearance: about 30% of the particles have a 30-day half-time, and 

the remaining 70% are given 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. 

Absorption is essentially a 2-stage process, as shown in Figure 3-7. First, there is a dissociation 
STRONTIUM	 144 

3. HEALTH EFFECTS 

(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): 

C 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 and 50% for mouth breathing. 

C		 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. 

C		 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. 

C		 For Type V, complete absorption (100%) is considered to occur instantaneously. 

ICRP (1995) considers the experimental data on strontium carbonate, and chloride, and sulfate to support 

classification of these compounds as Type F. Data on strontium particulates released from irradiated fuel 

support their classification as either Type F or M. Data on strontium in fused aluminosilicate particles 

support a classification as Type S. ICRP (1995) recommends assigning all strontium aerosols to Type M 

in the absence of specific information supporting an alternative classification. 

ICRP (1993) Strontium Biokinetics Model 

Description of the model. ICRP (1993) developed a compartmental model of the kinetics of 

alkaline earth elements, including strontium, in humans that is applicable to infants, children, adolescents, 

and adults. The model is based on a nearly identical model developed by Leggett (1992). The fraction of 

ingested strontium that is absorbed (uptake to blood) is assumed to vary with age and have values of 

0.6 in infants up to 12 months of age, 0.4 from 12 months of age through 15 years, and 0.3 from age 

15 years through adulthood. Absorbed strontium that enters the blood plasma is assumed to distribute to 

the skeleton, liver, and other tissues (Figure 3-8). Excretion pathways included in the model are plasma 

to urine, plasma to feces, and liver to feces. Transfer rate coefficients between compartments are agespecific and, depending on the specific coefficient, values can change at ages 3 months, 1 year, 5 years, 

10 years, 15 years, and adult (>15 years). The model assumes that 99% of the strontium that enters the 
Figure 3-8. ICRP (1993) Model of Strontium Biokinetics 

Feces 

Intermed 

Turnover 

Cortical 

Surface 

Trabecular 

Surface R 

B 

C 

Other 

Kidney 

Tissue 

Urinary 

Path 

KIDNEY 

Liver 1 

Liver 2 

GI Tract 

Contents 

Rapid 

Turnover 

Slow 

Turnover 

MASSIVE 

SOFT 

TISSUES 

Urinary 

Bladder 

Contents

 Cortical Volume 

Nonexch Exch 

Trabecular Volume 

Nonexch Exch 

P 

L 

A 

S 

M 

A 

P 

L 

A 

S 

M 

A 

SKELETON
 

Urine 

STRONTIUM 145 

3. HEALTH EFFECTS 
STRONTIUM 146 

3. HEALTH EFFECTS 

body and is not excreted is ultimately transferred to the skeleton and 1% is in soft tissues. Skeletal 

deposition is assumed to distribute initially to the bone surface of either cortical or trabecular bone, from 

which it can exchange relatively rapidly with calcium in plasma or more slowly with calcium in the bone 

volume. Two pools are assumed to exist within the bone volume, an exchangeable pool that 

communicates with surface bone, and a nonexchangeable pool from which strontium can be returned to 

plasma as a result of bone resorption. Approximately 55% of the transfer from plasma to bone in adults is 

to the trabecular bone surface and 45% to the cortical bone surface. 

Validation of the model. The extent to which the ICRP model has been validated is not described in 

ICRP (1993). 

Risk assessment. The model has been used to establish radiation dose equivalents (Sv/Bq) of 

ingested 89Sr and 90Sr for ages 3 months to 70 years (ICRP 1993). The model has also been applied by the 

ICRP to calculate limits on inhalation for 89Sr and 90Sr (ICRP 1995) and limits on inhalation or ingestion 

for 80Sr, 81Sr, 82Sr, 83Sr, 85Sr, 85mSr, 87mSr, 91Sr, and 92Sr (ICRP 1994b). It was used in the U.S. Federal 

Guidance Report No. 13 (EPA 2000e) to calculate inhalation risk coefficients and ingestion risk 

coefficients (separately for food and water) for the following radionuclides: 80Sr, 81Sr, 82Sr, 83Sr, 85Sr, 

85mSr, 87mSr, 89Sr, 90Sr, 91Sr, and 92Sr. 

Target tissues. The model is designed to calculate 89Sr and 90Sr intake limits, based on radiation dose 

to all major organs, including the bone surfaces, bone marrow, and liver, to which the highest doses 

would be expected. 

Species extrapolation. The model is designed for applications to human dosimetry and cannot be 

applied to other species without modification. 

Interroute extrapolation. The model is intended for application to strontium reaching blood by 

absorption from lungs, gastrointestinal tract, or wound, or by injection. 
STRONTIUM 147 

3. HEALTH EFFECTS 

3.6 MECHANISMS OF ACTION 

3.6.1 Pharmacokinetic Mechanisms 

Absorption. Airborne particulate aerosols of strontium can be deposited in the respiratory tract when 

the aerosols are inhaled. Amounts and patterns of deposition of particulates in the respiratory tract are 

affected by the size of the inhaled particles, age-related factors that determine breathing patterns (e.g., 

nose breathing vs mouth breathing), airway geometry, and airstream velocity within the respiratory tract 

(Gehr 1994; James et al. 1994; Roy et al. 1994). In general, large particles (>2.5 μm) deposit in the 

nasopharyngeal tract where high airstream velocities and airway geometry facilitate inertial impaction 

(Chan and Lippman 1980; James et al. 1994). In the tracheobronchial and alveolar regions, where 

airstream velocities are lower, processes such as sedimentation and interception become important for 

deposition of smaller particles (<2.4 μm). Breathing patterns, airflow velocity, and airway geometry 

change with age, giving rise to age-related differences in particle deposition (James 1978; James et al. 

1994; Phalen et al. 1985). Deposition in the various regions of the respiratory tract in children may be 

higher or lower than in adults depending on particle size; for submicron particles, fractional deposition in 

2-year-old children has been estimated to be 1.5 times greater than in adults (Xu and Yu 1986). 

Absorption of insoluble strontium is influenced by particle size and solubility as well as the pattern of 

regional deposition within the respiratory tract. Larger particles (>2.5 μm) that are deposited in the 

ciliated airways (nasopharyngeal and tracheobronchial regions) can be transferred by mucociliary 

transport into the esophagus and swallowed. Particles deposited in the alveolar region can be absorbed 

after extracellular dissolution or ingestion by phagocytic cells. Strontium-bearing pulmonary alveolar 

macrophages (PAMs) can migrate either to the airways where mucocilliary transport to the esophagus can 

occur or to tracheobronchial lymph nodes. The relative contributions of these two pathways to strontium 

absorption have not been quantified. 

The exact site of absorption of strontium in the gastrointestinal tract is not known; however, studies in 

hamsters suggest the possibility of absorption in both the stomach and small intestine. In hamsters that 

received a gavage tracer dose of 85SrCl2, 37% was absorbed, whereas 20% was absorbed when the dose 

was administered to hamsters that had their pyloric sphincter ligated (Cuddihy and Ozog 1973). In 

isolated, everted segments of small intestine of the rat, transfer from the mucosal (lumen) to the serosal 

(blood) side of the duodenum, jejunum, and ileum was observed. The serosal:mucosal strontium 

concentrations were approximately 0.2–0.4, whereas the ratio for calcium in preparations of duodenum 

was 1.98 (Stantic and Gruden 1974). Ratios >1 would be indicative of an active transport process; 

therefore, this study did not detect an active component of strontium transfer across the small intestine. 
STRONTIUM 148 

3. HEALTH EFFECTS 

Measurements of the rate of uptake of strontium into slices of rat small intestine when incubated with 

increasing concentrations of strontium suggested the existence of a saturable uptake mechanism in the 

intestinal epithelium (Papworth and Patrick 1970). The fractional absorption of a gavage dose of 

strontium appears to be a relatively constant ratio to that of calcium. In rats, the strontium:calcium 

absorption ratio was 0.75 over a fairly wide range of absorbed fractions of calcium (Marcus and 

Wasserman 1965). This suggests that strontium and calcium may be absorbed by similar mechanisms. 

Strontium has been shown to be a substrate for a Ca2+-ATPase on the basolateral membrane of the renal 

proximal tubule in the rat, which is thought to play an important role in the tubule reabsorption of calcium 

(Sugihira et al. 1992). 

Active vitamin D (calcitriol or 1,25(OH)2D3) has an indirect, delayed effect on the gastrointestinal 

absorption of strontium or calcium by inducing the synthesis of calcium-binding proteins in both humans 

and animals (Bianchi et al. 1999). A calcitriol-inducible Ca2+-ATPase has been shown to be important in 

the absorption of calcium in the rat intestine, and may provide a common mechanism for absorption of 

calcium and strontium (Bronner et al. 1986). Other possible common mechanisms may involve binding 

of calcium and strontium to an intracellular calcium-binding protein, calbindin-D, which is a 

1,25(OH)2D3-inducible calcium binding protein that is thought to play an important role in calcium 

absorption (Gross and Kumar 1990). In a group of 18 66-year-old women who received calcitriol at a 

daily dose of 0.5 μg of calcitriol for two years, the intestinal absorption of strontium was 13.7% compared 

to 10.4% for the untreated controls (Sairanen et al. 2000); the basal absorption percentages before 

treatment were 8.7 and 9.2%, respectively. Age-related decreases in the gastrointestinal absorption of 

strontium in men (ages 20–79) were found to be positively correlated with serum levels of insulin-like 

growth factor I (IGF-I) (Fatayerji et al. 2000). These authors proposed that IGF-I increases strontium 

absorption by maintaining the structural integrity of the intestine and the sensitivity of the intestine to 

1,25(OH)2D and increasing the synthesis of calcium-binding protein in that tissue. IGF-I also acts by 

stimulating the synthesis of 1,25(OH)2D in the kidney (Audi et al. 1999; Fatayerji et al. 2000). 

Distribution. The close similarity in the distribution of strontium and calcium derives from the ability 

of strontium to interact with ligands that normally bind calcium (Skoryna 1981b). These include 

hydroxyapatite, the main component of mineralized bone (Harrison et al. 1959; Schoenberg 1963) and a 

variety of calcium binding and transport proteins that are important in the physiological disposition of 

calcium in cells, including Ca2+-ATPases (Berman and King 1990; Mermier and Hasselbach 1976; 

Pfleger and Wolf 1975; Sugihira et al. 1992; Yu and Inesi 1995), Na+

-Ca+-antiport (McCormack and 
STRONTIUM 149 

3. HEALTH EFFECTS 

Osbaldeston 1990; Niggli 1989; Richard et al. 1989), and Ca2+ channels (Fukushi et al. 1995a, 1995b; 

Gregoire et al. 1993). 

Metabolism. As noted in Section 3.5.3, the metabolism of strontium consists of binding interactions 

with proteins and probably complex formation with various inorganic anions such as carbonate and 

phosphate, and carboxylic acids such as citrate and lactate. 

Excretion. The renal clearance of strontium has been measured in human subjects who received an 

intravenous injection of a dose of SrCl2 and is approximately 4–10 L/day and 2–3 times greater than renal 

calcium clearance (Blake et al. 1986, 1989a, 1989b; Harrison et al. 1955, 1966a; Newton et al. 1990; 

Samachson 1966). Based on these estimates, the renal clearance of strontium is substantially less than the 

product of the glomerular filtration rate in humans (approximately 180–200 L/day) and the estimated rate 

of filtration of strontium, assuming that approximately 50% of the strontium in plasma is ultrafilterable 

(Harrison et al. 1955). Thus, strontium appears to undergo net tubular reabsorption in the human kidney. 

The mechanism by which strontium is reabsorbed in the renal tubule has not been determined, although it 

is likely that it may share common transport mechanisms with calcium, possibly including the Na+

­

Ca2+-antiport, Ca2+-ATPase and membrane Ca2+ channels, all of which are thought to play a role in the 

reabsorption of calcium (Friedman and Gesek 1995). Direct evidence for this comes from in vitro studies 

of basolateral membranes isolated form the rat renal cortex (primarily proximal tubule). In this 

preparation, strontium has been shown to be a substrate for a Ca2+-ATPase, which transports calcium 

from the proximal tubular cells into the plasma (Sugihira et al. 1992). 

The observation of fecal excretion of radioactive strontium for weeks to decades after an oral exposure or 

over shorter time periods after an intravenous exposure suggests the existence of a mechanism for transfer 

of absorbed strontium into gastrointestinal tract, either from the bile or directly from the plasma. 

Evidence for direct secretion of strontium from the plasma into the intestine is provided by studies 

conducted with the in situ lumen-perfused rat intestine. When the lumen of either the small or large 

intestine was perfused (below the entrance of the bile duct) in situ, and radioactive strontium was injected 

intravenously, radioactive strontium was detected in the lumen, indicating that strontium was secreted 

from blood into the intestine (Palmer and Thompson 1961). The amount of strontium secreted into the 

small intestine was approximately 4–8 times that in the large intestine; however, the strontium:calcium 

secretion ratio was approximately 1 in the small intestine and 1.3 in the large intestine. The mechanism 

by which strontium is secreted into the intestine has not been determined. Transfer of strontium from the 

serosal (blood) side of the intestinal epithelium to the mucosal (lumen) side of the epithelium has been 
STRONTIUM 150 

3. HEALTH EFFECTS 

demonstrated in in vitro preparations of isolated rat colon mucosa. Serosal-to-mucosal transfer was 

observed to be completely dependent on the transepithelial electrochemical potential for strontium, 

completely insensitive to calcium concentration of the serosal bathing medium, and unaffected by prior 

treatment of the rats with 1,2,-dihydroxyvitamin D3, which stimulated calcium transport in the same 

preparation (Karbach and Rummel 1987). Based on these observations, transfer of strontium into the 

lumen of the colon in this preparation appeared to be explainable as a passive process. 

3.6.2 Mechanisms of Toxicity 

The fact that strontium is chemically similar to calcium allows it to exchange for calcium in bone and 

other cellular compartments that are enriched in calcium. Many enzymes that are calcium-dependent will 

function when strontium is substituted, but changes in kinetic parameters may occur. As discussed in 

Section 3.6.1, strontium can interact with secondary cell messenger systems and transporter systems that 

normally use calcium. Furthermore, as described in Section 3.2.4 (Neurological Effects), synaptic 

transmission may be variably affected by strontium. Consequently, at high concentrations, differences in 

the chemical characteristics between strontium and calcium may be the basis for neurotoxic and 

neuromuscular perturbations associated with strontium intoxication. 

Effect of Metabolism on Toxicity. Variations in the rate of absorption of soluble strontium compounds 

will affect the severity of their effects following oral exposure. One report identified polymorphisms in 

three alleles for the vitamin D receptor that imparted a 40% difference in efficiency in intestinal strontium 

absorption in humans (Gennari et al. 1997). The significance of this finding is unresolved, since other 

studies have found no link between vitamin D receptor genotypes and enteral absorption rates for calcium 

or strontium (Vezzoli et al. 2002; Wolf et al. 2000). Furthermore, no association was found between 

vitamin D receptor polymorphisms and bone mineral density when other parameters are taken into 

consideration (Poggi et al. 1999). However, daily administration of 0.5 μg of activated vitamin D to 

66-year-old women over 2 years increased both the rate of strontium absorption and the bone mineral 

density at the femoral neck and the lumbar spine (Sairanen et al. 2000). The rate of strontium 

incorporation into bone may be influenced by other factors thought to affect bone mineralization, such as 

parathyroid hormone receptor, estrogen receptor 1, and others (Audi et al. 1999; Duncan et al. 1999). 

However, the effects of these factors on strontium utilization have not been established definitively. 

Genetic variants of the parathyroid hormone receptor 1 result in either increased or decreased bone 

mineralization (Duncan et al. 1999). There is a potential physiological link between the estrogen receptor 

and vitamin D in osteoblasts, although the relationship to bone mineralization has not been established 
STRONTIUM 151 

3. HEALTH EFFECTS 

(Audi et al. 1999); vitamin D regulates the expression of P450 aromatase, an enzyme expressed in 

osteoblasts that modulates the availability of estrogen to its receptor. The cytokine interleukin-6 is 

associated with osteoclast differentiation, and therefore, could potentially be involved with the removal of 

strontium from bone (Audi et al. 1999; Duncan et al. 1999). Persons with chronic kidney failure may be 

more susceptible to effects of excess strontium because of a reduced ability to excrete strontium 

(Apostolidis et al. 1998; see Section 3.12); in this study, plasma levels of strontium were 60% higher in 

afflicted patients compared to controls. A study in rats demonstrated that protein deficiency, especially in 

combination with ethanol consumption, may increase strontium incorporation into bone while reducing 

fecal and urinary excretion of strontium (Gonzales-Reimers et al. 1999; see Section 3.12). 

Differences in bone physiology suggest that adult rats may have a higher susceptibility to stable or 

radioactive strontium effects than adult humans. Unlike most mammals (including humans), the 

epiphyseal growth plate of the long bones of rats never entirely transforms into bone after sexual 

maturity, so that bone growth continues throughout life (although reduced after the age of 12 months) 

(Leininger and Riley 1990). Thus, incorporation of strontium into the skeleton is likely to be relatively 

higher in adult rats compared to other mammals. 

Stable Strontium. The toxicity of excess stable strontium is related to its interference in biological 

processes that normally involve calcium, most notably, skeletal development. 

Calcium Absorption. In animals, excess strontium indirectly suppresses the activation of vitamin D3 in 

the kidney, which severely reduces the expression of calbindin D mRNA and the translation of 

calbindin D protein in the duodenum (Armbrecht et al. 1979, 1998; Omdahl and DeLuca 1972). As a 

result, duodenal absorption of calcium is reduced. The reported inverse correlation between the amount 

of strontium that is absorbed and the levels of parathyroid hormone (Vezzoli et al. 1998) suggest that 

changes in parathyroid hormone levels mediate this effect. While there are no data on strontium-binding 

to the calcium receptor of the parathyroid gland, it is likely that strontium binds in place of calcium, 

mimicking calcium and thereby suppressing parathyroid hormone levels. A reduction in parathyroid 

hormone levels will decrease the level of 1-hydroxylase available to activate vitamin D3. 

Bone Toxicity. In addition to its effect on calcium absorption, excess absorbed strontium adversely 

affects bone development in several ways, leading to the development of rickets in young laboratory 

animals and possibly in children under special circumstances (Özgür et al. 1996). Strontium binds 

directly to hydroxyapatite crystals, which may interfere with the normal crystalline structure of bone 
STRONTIUM 152 

3. HEALTH EFFECTS 

(Storey 1961). In addition, excess strontium may prevent the normal maturation of chondrocytes in the 

epiphyseal plates of long bones (Matsumoto 1976). Excess strontium apparently interferes with the 

mineralization of complexed acidic phospholipids that is thought to help initiate the formation of 

hydroxyapatite crystals in developing bone (Neufeld and Boskey 1994). As a result, affected bone 

contains an excess of complexed acidic phospholipid and a significantly lower ash weight. Insufficient 

mineralization reduces the strength of bones, so that the inability to resist compression from increasing 

body weight results in bone distortion (bowing). 

Anaphylactic Response After Inhalation Exposure. There was one case of anaphylaxis reported in a 

paramedic who inhaled strontium-containing smoke in an enclosed space (Federman and Sachter 1997; 

see Section 3.2.1.2). Although other irritants in the smoke may have contributed to the incident, there is 

supporting evidence that large concentrations of stable strontium can stimulate the release of histamine 

from mast cells (Alm and Bloom 1981a, 1981b; Atkinson et al. 1979; Foreman 1977; Foreman and 

Mongar 1972a, 1972b; Foreman et al. 1977). Stable strontium stimulates degranulation in several cell 

types (see Section 3.2.5 Hematological Effects) and it has been suggested that it acts by mimicking the 

receptor-linked rise in calcium that is the usual trigger for such events (Best et al. 1981). It is conceivable 

that the conditions of the paramedic’s exposure were such to result in locally high concentrations of 

strontium in the respiratory tract, thereby eliciting histamine release and contraction of smooth muscle. 

Radioactive Strontium. The adverse health effects of radioactive strontium are related to its sequestration 

in bone, the high energy of its beta emissions, and, in the case of 90Sr, its long half-life and the radiation 

from the decay product, 90Y, produced in the body after intake of 90Sr. An extensive discussion of 

ionizing radiation and its health effects is found in the Appendix D of this document and in the 

Toxicological Profile for Ionizing Radiation (Agency for Toxic Substances and Disease Registry 1999). 

There is some evidence that body size or skeletal density may affect the outcome of exposures to 

radioactive strontium. It was suggested that two cows that survived large oral doses of 90Sr owed their 

survival to their breed characteristics (Cragle et al. 1969). The massive skeletons of Holsteins have wide 

bone marrow cavities so that tissue in the center of the bone marrow is not within range of the 1 cm beta 

emissions from radiostrontium (and radioyttrium) bound to bone. Conversely, mice and rats are more 

vulnerable than large animals to radioactive strontium because all bone marrow tissues are within striking 

range. This renders rats and mice less useful than larger mammals as models for human exposure to 

radioactive strontium. In addition, adult rats are less satisfactory models than adults of other species 

because of the persistence of the epiphyseal cartilaginous plate, which will result in the incorporation of 

larger amounts of radioactive strontium into bone. 
STRONTIUM 153 

3. HEALTH EFFECTS 

Bone Toxicity. Beta emissions from radiostrontium bound to bone resulted in various bone lesions 

(trabecular osteoporosis, sclerosis, osteolytic lesions), particularly in animals that were exposed 

chronically (Book et al. 1982; Clarke et al. 1972; Momeni et al. 1976). In young rats and rabbits exposed 

orally to 90Sr, necrotic effects on the vasculature of developing bone secondarily disrupted the process of 

osteogenesis (Casarett et al. 1962; Downie et al. 1959). Disruption in the metaphyseal microvasculature 

disorganized the transformation of cartilage into bone, so that chondrocytes inappropriately resumed 

active proliferation. 

Pancytopenia. The severe reduction in hematopoetic tissue results from irradiation of the bone marrow 

by radiostrontium incorporated into bone. At high exposure levels, thrombocytopenia may lead to platelet 

loss severe enough to cause hemorrhaging and the resulting anemia will be exacerbated by destruction of 

erythropoietic tissue. Impaired immune function results from the genetic damage to lymphocytes. 

Carcinogenicity. Radioactive strontium is a genotoxic carcinogen. Following exposure in vivo, 

cytogenetic analysis has revealed aneuploidy, chromosomal breaks, gaps, rings, and exchanges (see 

Table 3-5), which are manifestations of unrepairable changes in DNA. It is generally understood that 

radiation-induced damage to genes that regulate cell growth is a major factor in the development of 

cancer in affected cells, and the observation of chromosomal breaks in leukemic cells of miniature swine 

following chronic oral exposure to 90SrCl2 is consistent with this idea (Clarke et al. 1972; Howard 1970). 

However, the specific genes involved in radiostrontium-induced malignancies have not been identified. 

Because of strontium’s chemical properties, which determine its distribution in the body, exposure to 

sufficient radiostrontium results in an increased risk of malignancy for particular tissues. In dogs, acute 

inhalation of insoluble 90Sr particles that lodged in the lungs resulted in chronic radiation exposure to the 

lungs, leading to pulmonary hemangiomas and carcinomas of pulmonary epithelia (Snipes et al. 1979). 

Other tissues were subsequently affected as the radioactive particles were cleared from the lungs. 

Following acute inhalation of soluble 90SrCl2 aerosols, some dogs developed carcinomas of nasal airway 

tissues, probably resulting from irradiation of these tissues from the 90Sr bound to the underlying bone 

(Gillett et al. 1987b). Following oral or inhalation exposures, absorbed 90Sr was distributed to bone, from 

which it irradiated the surrounding tissues and induced various kinds of osteosarcomas, as well as 

malignancies of hematopoietic tissues in bone marrow (see Section 3.3.2.7). 

Induction of Delayed Fibrosis Following External Exposure. A single high-dose external exposure to 

beta radiation can elicit acute epidermal reactions, late connective tissue damage, and carcinogenesis in 
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murine skin, as was demonstrated in experiments that used 90Sr as a convenient beta source (Randall and 

Coggle 1996; see Section 3.3.3.7). A biochemical change that is associated with both acute and late 

effects is the enhanced expression of mRNA and protein for transforming growth factor beta 1 

(TGF-beta l, Randall and Coggle 1995, 1996). Following an acute exposure to beta radiation from a 90Sr 

source that is sufficient to generate moist desquamation, CBA/ca mouse skin exhibited two separate peaks 

of TGF-beta l expression (Randall and Coggle 1996). The first, occurring within the first few weeks after 

exposure, coincided with a period of epithelial hyperplasia that occurred during and after the phase of reepithelialization. TGF-beta l expression declined to a low at 3 months postexposure, but then rose to 

another peak at about 9 months. Expression was especially high in the fibrotic dermis, which was also the 

site of skin tumors that appeared at about 9 months. TGF-beta l expression in tumors was elevated by 

1.8 to 87 times the level in unirradiated control skin from the same animal. The implication of this study 

is that sustained high expression of transforming growth factor-betal may drive the progressive fibrosis 

and, possibly, contribute to malignancy following radiation damage. Another study from this laboratory 

indicates that there may be genetic differences in the control of TGF-beta l expression, and therefore, 

susceptibility to long-term effects of radiation damage (Randall and Coggle 1995). 

3.6.3 Animal-to-Human Extrapolations 

The toxic effects of stable and radioactive strontium have been similar in all species studied. However, as 

mentioned in Section 3.6.2, adult rats are not an optimal model for bone effects in adult humans because 

of the lack of a Haversian (bone remodeling) system in the rat and because of the persistence of the 

epiphyseal cartilaginous plate into adulthood (Leininger and Riley 1990). Because the epiphyseal 

cartilage persists, the long bones of rats continue to lengthen during adulthood, and therefore, the rates of 

incorporation of strontium will be proportionally higher. This will make adult rats more susceptible to 

adverse effects of both stable and radioactive strontium. This caveat does not apply to young rats, which 

are comparable to the young of other species. In general, rodents are not optimal models for 

radiostrontium effects because their small size ensures that most of their tissues will be within the 

effective range of beta emissions from radiostrontium bound to bone. Larger laboratory animals, such as 

dogs or non-human primates, avoid the problems of both radiation scatter to adjacent tissues and closure 

of the epiphysis as they become adults. 
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3.7 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 Colborn and Clement (1992), was also used in 1996 when Congress mandated the 

Environmental Protection Agency (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), which in 1998 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 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 1997c). 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). 

No studies were located regarding endocrine disruptive effects in humans resulting from inhalation, oral, 

or dermal exposure to stable or radioactive strontium. Stable strontium, as an analog to calcium, is 

unlikely to cause endocrine disruption at normal levels of exposure. Endocrine glands, such as the 

pituitary, that are in close association with bone could potentially be damaged by irradiation from 

radioactive strontium incorporated into bone. For example, increases in tumors of the pituitary and 
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ovaries were observed in rats following gestational exposure to injected 90Sr (Rönnbäck and Nilssen 

1982; Schmahl and Kollmer 1981; Schmahl et al. 1979; Section 3.4.5.7). However, endocrine function 

was not tested in these studies. Ingested radioactive strontium had no effect on reproductive function in 

animals, suggesting that it did not affect reproductive hormones to an obvious degree (Clarke et al. 1972; 

Finkel et al. 1960). However, no study has specifically investigated the endocrine system. 

3.8 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 chemicals. 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. 

Children sometimes differ from adults in their susceptibility to hazardous chemicals, but whether there is 

a difference depends on the chemical (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). Distribution of xenobiotics may be different; for example, 

infants have a larger proportion of their bodies as extracellular water and their brains and livers are 

proportionately larger (Altman and Dittmer 1974; Fomon 1966; Fomon et al. 1982; Owen and Brozek 

1966; Widdowson and Dickerson 1964). The infant also has an immature blood-brain barrier (Adinolfi 

1985; Johanson 1980) and probably an immature blood-testis barrier (Setchell and Waites 1975). Many 

xenobiotic metabolizing enzymes have distinctive developmental patterns. At various stages of growth 
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and development, levels of particular enzymes may be higher or lower than those of adults, and 

sometimes unique enzymes may exist at particular developmental stages (Komori et al. 1990; Leeder and 

Kearns 1997; NRC 1993; Vieira et al. 1996). Whether differences in xenobiotic metabolism make the 

child more or less susceptible also depends on whether the relevant enzymes are involved in activation of 

the parent compound to its toxic form or in detoxification. 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 chemical insults. Children also 

have a longer remaining lifetime in which to express damage from chemicals; 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 chemical. 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). 

The ubiquitous nature of stable strontium in soils and water supplies, and the chemical similarity of 

strontium to calcium, ensure that strontium will unavoidably be incorporated into the human body to 

some degree. Because of the requirement for high calcium intake during the period of bone development, 

the absorption and retention of strontium is higher in children than in adults; an ICRP (1993) model 

postulates that the fractional gastrointestinal absorption of strontium by infants (up to 12 months) is 

double that of adults (see Sections 3.5.1.2 and 3.5.5). Consequently, children are more at risk than adults 

from exposures to excess stable strontium or radioactive strontium. 

Stable Strontium. A Turkish epidemiological study indicated that children with probable deficient 

vitamin D status (from insufficient exposure to sunlight) and diets low in calcium and animal protein were 

more likely to develop rickets as a result of exposure to excess dietary strontium (Özgür et al. 1996). The 

rachitic signs of craniotabes, rachitic rosary, bulging at the wrist, genu valgus, genu varus, and delayed 

closure of the fontanelles represented biomarkers of effect in children exposed to excess strontium. This 

study is consistent with numerous animal studies that demonstrated abnormal skeletal development (i.e., 

rickets) in young animals exposed to sufficiently high levels of dietary strontium (Kshirsagar 1976; 

Matsumoto 1976; Morohashi et al. 1994; Reinholt et al. 1985; Storey 1961, 1962; Svensson et al. 1985, 
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1987). Young rats may be sensitive to levels of ingested strontium that have no effect on adults (Storey 

1961). 

Children or young animals are likely to be more sensitive than adults to excess strontium, in part, because 

the rates of intestinal strontium absorption may be higher, although this has not been consistently 

demonstrated in humans (see Section 3.5.1.2 and Table 3-7). The ICRP (1993) biokinetic model for 

strontium assumes that the fraction of ingested strontium that is absorbed decreases from 0.6 in infancy to 

0.3 in adulthood (see Section 3.5.5); some models assume the absorbed dose may be 8 times higher in 

infants compared to adults (NCRP 1991). These estimates are consistent with rat studies in which rates of 

strontium absorption were much higher (4–8 times) in weanlings compared to adults (Forbes and Reina 

1972; Harrison et al. 1966b). This age-dependent difference in absorption may be partly explained by the 

duodenal level of vitamin-D-dependent calbindin D protein (a calcium-binding protein involved in 

absorption), which is much lower in old rats than in young rats (Armbrecht et al. 1979). Armbrecht et al. 

(1998) have demonstrated that the translation of calbindin D-9k mRNA into protein declines in the rat 

duodenum with age and this would be expected to reduce the rates of intestinal absorption of calcium and 

strontium in older animals. 

Children are particularly vulnerable to excess strontium because the immature skeleton has a high rate of 

bone remodeling, and strontium adversely affects bone development in several ways, as demonstrated in 

animal studies. In chickens and rats, excess strontium suppresses the activation of vitamin D3 in the 

kidney, which severely reduces the expression of calbindin D mRNA and the translation of calbindin D 

protein in the duodenum (Armbrecht et al. 1979, 1998; Omdahl and DeLuca 1972). As a result, duodenal 

absorption of calcium is reduced. Strontium also binds directly to hydroxyapatite crystals, which may 

interfere with the normal crystalline structure of bone in rats (Storey 1961). In addition, excess strontium 

may prevent the normal maturation of chondrocytes in the epiphyseal plates of long bones of rats 

(Matsumoto 1976). Excess strontium apparently interferes with the mineralization of complexed acidic 

phospholipids that is thought to help initiate the formation of hydroxyapatite crystals in developing bone 

(Neufeld and Boskey 1994). As a result, affected bone contains an excess of complexed acidic 

phospholipid and a significantly lower ash weight. This finding is consistent with the reduced rate of 

matrix vesicle degradation observed by Reinholt et al. (1984) in rachitic cartilage in strontium-treated 

rats. 

The placenta does not accumulate strontium nor does it prevent transfer of strontium to the fetus 

following maternal exposure (see Section 3.5.2.2). However, no studies were located that addressed 
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developmental effects following maternal exposure to stable strontium in humans or animals. Stable 

strontium is also transferred to nursing infants through breast milk of exposed mothers at a ratio of 

approximately 0.24 μg strontium/mg Ca (Harrison et al. 1965). These levels are unlikely to be 

sufficiently high to perturb bone development in the fetus. Strontium stored in maternal bone because of 

prior exposure can be mobilized during pregnancy or lactation, resulting in fetal or infant exposure 

(Tolstykh et al. 1998). 

Alginates, carbohydrates rich in guluronic acid, have been found to reduce peak exposure to strontium 

(see Section 3.12.1). Sutton et al. (1971a) showed that gastrointestinal absorption of stable 84Sr was 

reduced 4-fold in children who were simultaneously given 10% sodium alginate-97% guluronic acid. 

Exposure to sunlight to enhance vitamin D status and diets with adequate calcium, phosphorus and 

protein may be considered to some degree protective against the effects of stable strontium (see 

Section 3.12). 

Radioactive Strontium. During the period of above-ground nuclear weapons testing, the possible effects 

in children resulting from exposure to 90Sr in radioactive fallout was a matter of concern. However, no 

studies have been able to identify unequivocally any increase in infant mortality, childhood cancers, or 

genetic damage in humans that could be attributed to oral or inhalation exposure to 90Sr in fallout (NCRP 

1991; Shaw and Smith 1970). In the Techa River populations that received higher oral doses of radiation, 

including radiostrontium, individuals who were exposed as teenagers exhibited a significantly higher 

frequency of stable chromosomal translocations compared to individuals who were exposed as adults 

(Bauchinger et al. 1998). Adverse pregnancy outcomes (mortality from developmental anomalies, 

chromosomal anomalies, labor complications, and other unspecified perinatal conditions) were elevated 

in the progeny of exposed individuals from the Techa River cohort, 60% of whom were exposed to 

radiation as teenagers (Kossenko et al. 1994). However, Kossenko et al. (1994) calculated that relatively 

high radiation doses (20–480 rem or 0.2–4.8 Sv) to the parental gonad would be required to double the 

incidences of stillbirths, miscarriages, early neonatal mortality, or lethal developmental effects. (Note 

that the gonadal radiation doses may have primarily been caused by exposure to external gamma radiation 

[Akleyev et al. 1995]). No increase in cancer incidence was observed among the progeny of the exposed 

Techa River population (Kossenko 1996). Dermal effects (slight dermal atrophy, telangectiasis, and 

pigmentation changes) were reported as delayed reactions to superficial 90Sr treatments for facial 

hemangiomas in adults and children (Bekerus 1970). However, this study did not compare the relative 

sensitivity of children and adults. 
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It would not be expected that the immediate consequences of radioactive strontium exposure would differ 

in children and adults at the cellular level; that is, the initial damage to proteins and nucleic acids caused 

by ionizing radiation would be the same. Thus, children and adults might be expected to have similar 

effects following exposure to solid radiostrontium sources apposed to the skin or to insoluble particles of 

radiostrontium lodged in the lungs. However, as discussed in Appendix Section D.4.1, ionizing radiation 

is more damaging to actively mitotic cells than to differentiated postmitotic cells, largely because genetic 

lesions become permanent when cell division occurs before repair can occur. Since children have 

proportionally more mitotic cells than adults, the biological effect of radiation exposure in children would 

be expected to be proportionally more severe. Other developmental aspects contribute to the higher 

potential vulnerability of children to radiation effects. One is the higher rate of gastrointestinal absorption 

in children, as discussed for Stable Strontium, above. In addition, animal studies indicate that the young 

are more vulnerable than adults to inhalation or oral exposures to radioactive strontium in soluble form, 

because of higher rates of retention in the developing skeleton (see Stable Strontium section above). 

Thus, a given absorbed dose of soluble radiostrontium will have a longer biological half-life in young 

animals compared to adults, leading to higher cumulative radiation doses to bone and surrounding soft 

tissues and more severe adverse effects (see Section 3.3). Examples of this age-related difference in 

severity are discussed under Section 3.2.2.2 Musculoskeletal Effects (especially Storey 1961, the basis for 

the intermediate oral MRL) and Section 3.3.2.2 Hematological Effects (Cragle et al. 1969), and 

Section 3.3.2.6 Reproductive Effects (Clarke et al. 1970). Young animals exhibit the same types of 

effects as adults (e.g., malignancies), in addition to other effects specific to their developmental stage. 

For example, radioactive strontium disturbed osteogenesis of long bones in young rats by damaging the 

epiphyseal cartilaginous discs, and the vasculature that supports resorption (Casarett et al. 1962). In 

weanling rats, irradiation of the marrow prevented its invasion of metaphyseal cartilage, thereby causing 

cartilage to resume active proliferation, rather than undergo transformation into bone. Because of 

disruption of these processes, cartilage and fibrous marrow were sometimes incorporated into cortical 

bone, resulting in weakness or fracture. For all species studied, a long-term effect of 90Sr incorporation in 

young animals or in utero was a higher incidence of bone-associated cancers compared to animals 

exposed as adults (Clarke et al. 1972; Finkel et al. 1960; White et al. 1993). Size differences may 

contribute to the possible higher vulnerability of children to bone marrow effects from retained 

radiostrontium. Since bone marrow cavities in children have smaller diameters, a larger proportion of the 

hemopoietic bone marrow is within the approximate centimeter range of beta radiation emitted from 

radiostrontium bound to the endochondral surface. 
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There are two theoretical ways in which the fetus might be exposed to radiation from the decay of 

radioactive strontium: from transfer of strontium across the placenta or from proximity to radiation 

emitted from the maternal body. Placental transfer of radioactive strontium to the fetus has been 

demonstrated in humans (Sikov et al. 1991, Stather et al. 1992) and animals (rodent: Onyskowova and 

Josifko 1985, Taylor and Bligh 1992; pig: Palmer et al. 1969). Studies of residents of the Techa River 

who were exposed to strontium as a result of an accident at a plutonium production plant provide 

evidence that fetal exposures can result from previous maternal exposures. The fetal:maternal strontium 

concentration ratio in four subjects who were exposed prior to pregnancy varied from 0.012 to 0.24, with 

the higher values associated with maternal exposures that occurred during adulthood and lower values 

associated with maternal exposures during childhood or adolescence (Tolstykh et al. 1998). A dosimetry 

study in minipigs determined that exposure of the fetal thymus (ages 55–110 days of gestation) to 

radiostrontium (90Sr–90Y) is related to the amount that is incorporated by the fetus after placental transfer; 

no appreciable radiation reached the thymus from radiostrontium in the maternal uterine wall (Palmer et 

al. 1969). Palmer et al. (1969) indicated that results might vary for other organs, for younger fetuses 

(which may be relatively closer to the maternal uterine wall or pelvic bone), or for single fetuses 

compared to multiple fetuses (as in the pig). As discussed in Section 4.2, strontium isotopes and their 

transformation product isotopes differ with respect to their emission energies; this factor is another 

variable that will determine whether the fetus is subject to radiation from the maternal body. 

Animal studies demonstrate that the developmental consequences of injecting pregnant females with 

radioactive strontium are qualitatively different depending on the gestational day of administration 

(Finkel and Biskis 1969; Finkel et al. 1972; Hopkins et al. 1967). This is partly related to temporal 

differences in the onset of osteogenic activity and calcification in different parts of the skeleton. For 

example, the increase in calcification of the basioccipital and sphenoid bones of the skull occurring by 

gestational day 18 of the rat probably contributed to the development of pituitary gland tumors after an 

injection of 90Sr was administered that day (Schmahl and Kollmer 1981; Schmahl et al. 1979). A single 

injection administered to pregnant mice late in gestation transiently affected fertility of male offspring by 

suppressing spermatocyte maturation, but severely depressed oocyte maturation of the female offspring 

(De Rooij and Rönnbäck 1989; Nilsson and Henricson 1969; Rönnbäck 1979, 1980, 1981a, 1981b). 

Radioactive strontium, like stable strontium, can be transferred to infants through breast milk of exposed 

mothers (Harrison et al. 1965). Rönnbäck (1981a) demonstrated that the numbers of oocytes (all stages) 

in the ovary was reduced in neonatal mice that were exposed to radioactive strontium in the milk of 

surrogate females that had been given high doses by injection. 
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Various methods for reducing the body burden and toxic effect of radioactive strontium have been 

investigated (see Section 3.12). Only the administration of alginates high in guluronic acid, described in 

the previous section, has been validated in children (Sutton et al. 1971a). A single oral dose of aluminum 

phosphate antacid gel taken soon after exposure is a recommended treatment for reducing absorption of 

ingested strontium (Ellenhorn et al. 1997; Haddad et al. 1998). This would be a suitable treatment for 

children as long as the dosage recommendations were followed, since excess ingestion of aluminum 

phosphate can cause rickets (Chines and Pacifici 1990; Pivnick et al. 1995). A diet high in calcium would 

tend to reduce the incorporation of radioactive strontium into bone (Steinbach 1968). 

3.9 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). 

Due to a nascent understanding of the use and interpretation of biomarkers, implementation of biomarkers 

as tools of exposure in the general population is very limited. A biomarker of exposure is 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). The 

preferred biomarkers of exposure are generally the substance itself or substance-specific metabolites 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. The substance being measured may be a metabolite of another xenobiotic 

substance (e.g., high urinary levels of phenol can result from exposure to several different aromatic 

compounds). Depending on the properties of the substance (e.g., biologic half-life) and environmental 

conditions (e.g., duration and route of exposure), the substance and all of its metabolites 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 strontium 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 
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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 strontium 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 xenobiotic 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”. 

3.9.1 Biomarkers Used to Identify or Quantify Exposure to Strontium 

The biomarkers to quantify exposure to stable or radioactive strontium are similar in children and adults. 

Stable strontium is ubiquitous in the diet and can be measured in urine, blood and feces by a number of 

methods outlined in Section 7.1. After exposure, approximately 99% of the absorbed strontium that is 

retained is found in bone and connective tissues (Schroeder et al. 1972). Normal background levels of 

strontium were measured by emission spectrography in cadaver tissue from 168 American subjects 

(Tipton 1981; Tipton and Cook 1963). Average strontium levels in human tissues expressed as ppm ash 

were as follows: rib bone 110 ppm, vertebra 100 ppm, aorta 33 ppm, ileum 25 ppm, duodenum 11 ppm, 

lung 8.2 ppm, kidney 5.2, heart 2.6 ppm, and liver 1.6 ppm. In a small group of adult males, the mean 

strontium concentration in plasma was 29 μg/L (Sutton et al. 1971b). 

Soluble radioactive strontium can be detected in urine, blood, or feces by liquid scintillation counting. 

Whole body counters (or chest counters for inhalation exposures) can measure internal radioactive 

strontium deposited in bone following high level exposures (see Section 7.1.1). Children tend to 

incorporate strontium more homogenously throughout bone than is the case for adults. 
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3.9.2 Biomarkers Used to Characterize Effects Caused by Strontium 

Deformities of bone in response to excess strontium can be detected by radiography. Exposure to excess 

stable strontium may cause specific abnormalities in bone calcification that can lead to obvious bone 

deformities, particularly in the young. Such ‘rachitic’ signs in children include craniotabes, rachitic 

rosary, conspicuous bulging at the wrist, genu valgus, genu varus, and delayed closure of the fontanelles 

(Özgür et al. 1996). However, excess exposure to other metals, such as aluminum (Bhattacharyya et al. 

1995; Carmichael et al. 1984; Chines and Pacifici 1990; Pivnick et al. 1995; Woodson 1998) or 

deficiencies in calcium, vitamin D, and/or phosphate can generate the same effects. Thus, this is not a 

specific biomarker for strontium, but can be confirmatory. Although bone biopsies can measure 

strontium chemically, these tests are not warranted because of the relatively high risk/benefit ratio. 

Exposure to radioactive strontium may result in lowered blood cell counts, which can be detected using 

standard clinical laboratory methods. However, exposure to other sources of ionizing radiation has 

similar effects. Sufficiently high exposures to radioactive strontium can result in genetic damage to 

tissues adjacent to bone. Recently, Sutherland et al. (2000a, 2000b) developed a molecular biological 

strategy to identify clustered lesions in DNA resulting from in vitro cellular exposure to gamma radiation. 

It is possible that this technique might be adapted to evaluate genetic damage in blood cells following 

exposure to radioactive strontium, although, again, it would not be specific for radiostrontium, but rather 

for ionizing radiation. It is uncertain whether the technique would be applicable for the chronic exposures 

characteristic of absorbed radiostrontium compared to the acute high-dose exposures for which it was 

designed. 

3.10 INTERACTIONS WITH OTHER CHEMICALS 

Several agents reduce the absorption or retention of strontium, reducing its toxic effects (see 

Section 3.12). 

Calcium. Strontium has chemical properties similar to calcium, but is less efficient than calcium in most 

biological processes. Calcium and strontium appear to compete for the same transporter elements in the 

intestine (Bianchi et al. 1999; Blumsohn et al. 1994; Milsom et al. 1987; Reid et al. 1986; Sips et al. 

1994), but calcium is preferentially absorbed. Co-administration strontium and calcium reduces the 
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uptake of strontium and also reduces skeletal retention of strontium (Palmer et al. 1958; Roushdy et al. 

1980, 1981; Steinbach 1968). 

Anions. Oral administration of phosphate, as aluminum phosphate antacid gel, reduces the 

gastrointestinal absorption of strontium by increasing its excretion in feces (Carr and Nolan 1968; Keslev 

et al. 1972; Spencer et al. 1969a, 1969b). Oral administration of sulfates at the same time as strontium 

reduces its retention in the skeleton (Volf 1964). These agents are discussed in Section 3.12.1. 

3.11 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE 

A susceptible population will exhibit a different or enhanced response to strontium than will most persons 

exposed to the same level of strontium in the environment. Reasons may include genetic makeup, age, 

health and nutritional status, and exposure to other toxic substances (e.g., cigarette smoke). These 

parameters result in reduced detoxification or excretion of strontium, or compromised function of organs 

affected by strontium. Populations who are at greater risk due to their unusually high exposure to 

strontium are discussed in Section 6.7, Populations With Potentially High Exposures. 

In general, children, who are in the stage of active bone synthesis and growth, are more vulnerable to 

adverse effects of strontium. A more detailed discussion of children’s susceptibility can be found in 

Section 3.8. The following discussion is limited to other individual variations or health conditions that 

may modify the usual effects of strontium. 

Protein Deficiency and Ethanol Consumption. Protein-deficient diets may increase the adverse effects 

of exposure to excess stable strontium or to radioactive strontium, by reducing clearance and increasing 

incorporation into bone. A metabolic experiment in adult male Wistar rats showed that consumption of a 

protein-deficient diet increased the intestinal absorption of dietary strontium and its incorporation into 

bone, while reducing fecal and urinary excretion of strontium (Gonzales-Reimers et al. 1999). When rats 

were given ethanol in addition to the protein-deficient diet, incorporation of strontium into bone was 

significantly enhanced, although ethanol given with a protein-normal diet tended to reduce strontium 

incorporation through its diuretic effects. 

Renal Disorders. Patients with chronic kidney failure may be more susceptible to excess strontium than 

the general population, because of a reduced ability to excrete strontium and retain calcium (Apostolidis 

et al. 1998). In such patients, plasma levels of strontium were found to be 60% higher compared to 
STRONTIUM 166 

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controls. In a variety of studies, uremic patients on dialysis were found to have significantly higher levels 

of strontium in serum, muscle, and brain tissue compared to normal undialized controls (Alfrey et al. 

1975; Couttenye et al. 1999; D’Haese and De Broe 1996; D’Haese et al. 1999, 2000; Krachler et al. 2000; 

Schrooten et al. 1999). Although the high level of strontium in serum in uremic patients was correlated 

with the high level of strontium in the local tap water, it is also possible that uremic patients may have 

reduced rates of strontium excretion. 

Paget’s Disease (osteitis deformans). Patients with Paget’s disease (osteitis deformans) had a higher than 

normal retention rate following administration of 85Sr (Tothill et al. 1983). Part-body retention 

measurements demonstrated that diseased bone had relatively higher uptakes of strontium compared to 

undiseased bone. Pagetic bone contains a higher proportion of small mineral crystals with greater surface 

area, which accounts for its increased ability to accumulate strontium. Reflecting the high degree of 

osteoclast activity in Paget’s disease, diseased bone had an increased turnover of 85Sr, compared to 

undiseased bone in the same patient. Since bone metabolism is locally accelerated in persons with this 

disease, they are likely to develop higher body burdens of radioactive strontium than healthy adults. 

Rheumatoid Arthritis or Seronegative Spondarthritis. Patients with active rheumatoid arthritis or 

seronegative spondarthritis were found to have significantly higher levels of strontium and calcium in 

their granulocytes (Hällgren et al. 1984). The strontium overload was thought to be linked to the degree 

of inflammation and was positively related to serum levels of the acute-phase protein haptoglobin; 

corticosteroid therapy differentially reduced the strontium content of granulocytes compared to calcium. 

It is not known whether granulocytes in persons with active disease would take up relatively more 

radiostrontium from plasma, and therefore incur more damage, than would be the case for otherwise 

healthy individuals under an identical exposure scenario. 

Diabetes. Persons with diabetes may be more vulnerable to adverse effects from dermally-applied 

radioactive strontium. Thinning of the sclera developed in a diabetic patient who had been treated for 

pterygium with a single dose (1,700–1,800 rad; 17–18 Gy) of 90Sr (Wesberry and Wesberry 1993; see 

Section 3.3.3.2). This reaction was not observed in 170 other eyes treated at that dose level; however, the 

authors did not state whether other diabetics were in the group that was unaffected. Conversely, in rats 

made diabetic by injection of streptozotocin, the absorption of strontium in the duodenum was 

significantly reduced, which would appear to be protective (Miller and Schedl 1976). 
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Genetic Polymorphisms. Polymorphisms in genes that may affect rates of strontium (calcium) absorption 

and bone mineralization are currently under investigation. In a study of postmenopausal women with 

osteoporosis, polymorphisms of vitamin D receptor genes apparently caused a 40% variation in the rate of 

strontium absorption (Gennari et al. 1997); however, another study found no association between vitamin 

D receptor polymorphisms and bone mineral density in osteoporotic women (Poggi et al. 1999). 

Similarly, 3’-end region polymorphisms of the vitamin D receptor were found to have no effect on enteral 

strontium absorption or bone mineral density in patients with calcium kidney stone disease (Vezzoli et al. 

2002). Insulin-like growth factor (IGF-I) is correlated with age-related changes in strontium absorption in 

men (Fatayerji et al. 2000), but polymorphisms have not been evaluated. Other candidate genes that may 

affect bone mineralization include the parathyroid hormone receptor 1, the estradiol receptor, collagen 

type I alpha 1, transforming growth factor-beta 1, interleukin-6, calcitonin receptor, alpha2-HSglycoprotein, osteocalcin, calcium-sensing receptor, interleukin-1 receptor antagonist, beta-3-adrenergic 

receptor, apolipoprotein E, glucocorticoid receptor, and epidermal growth factor (Audi et al. 1999; 

Duncan et al. 1999). The relative contribution of these factors on bone mineralization has yet to be 

clarified and whether any polymorphisms increase susceptibility to adverse effects of strontium remains 

to be determined. 

3.12 METHODS FOR REDUCING TOXIC EFFECTS 

This section will describe clinical practice and research concerning methods for reducing toxic effects of 

exposure to strontium. However, because some of the treatments discussed may be experimental and 

unproven, this section should not be used as a guide for treatment of exposures to strontium. When 

specific exposures have occurred, poison control centers and medical toxicologists should be consulted 

for medical advice. The following texts provide specific information about treatment following exposures 

to strontium: 

Ellenhorn MJ, Schonwald S, Ordog G, et al., eds. 1997. Medical toxicology: Diagnosis and treatment of 

human poisoning. 2nd ed. Baltimore, MD: Williams & Wilkins, 1682–1723. 

Haddad LM, Shannon MW, Winchester JF, eds. 1998. Clinical management of poisoning and drug 

overdose. 3rd ed. Philadelphia, PA: W.B. Saunders, 413–425. 

Viccellio P, ed. 1998. Emergency toxicology. 2nd ed. Philadelphia, PA: Lippincott-Raven, 991–996. 
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3.12.1 Reducing Peak Absorption Following Exposure 

Human exposure to strontium and its compounds occurs primarily by inhalation and ingestion, since 

absorption is poor following dermal contact. Current suggestions for reducing absorption of 

radiostrontium include ingestion of antacids containing aluminum phosphate (Ellenhorn et al. 1997; 

Haddad et al. 1998). Treatment is most effective when it is initiated within 2 hours of exposure. 

The threat of nuclear fallout from atomic weapons testing was the impetus for a large number of studies 

that investigated methods to prevent absorption of radiostrontium, while not adversely affecting the 

absorption of calcium. Reasonably effective strategies have included alginates, aluminum phosphate, and 

sulfates. Less effective or less practical strategies have included cold, diet, dietary fiber, flavones, and 

stable strontium. 

Alginates. Alginates are carbohydrates derived from seaweed that have been found to reduce the 

absorption of strontium in humans and animals, without significantly affecting the absorption of calcium. 

When 10% sodium alginate-97% guluronic acid was given orally along with the stable marker 84SrCl2 to 

children (ages 2.5–10 years), plasma 84Sr was reduced by 75% and urinary excretion of the tracer was 

reduced 72% (Sutton et al. 1971a). The authors concluded that absorption was reduced 4-fold. In adults, 

sodium alginate extracts administered as a liquid or in bread, reduced strontium absorption by 50% in 

humans and 3-fold in rats (Gong et al. 1991). Alginates with a high guluronic acid/mannuronic acid ratio 

were found to be more effective in humans and rats (Carr and Nolan 1968; Gong et al. 1991). Sodium 

alginate administered orally to rats effectively reduced the whole body retention of 85strontium that had 

been administered intratracheally (Naményi et al. 1986). Calcium alginate added to the diet of female 

goats reduced the transfer of 85strontium to milk, which was attributed to a reduction in strontium 

absorption (Beresford et al. 1999). In rats given 89Sr and 45Ca by gavage, alginate treatment, particularly 

in combination with stable calcium, differentially increased the fecal excretion of 89Sr and reduced the 

skeletal retention of 89Sr (Light et al. 1970a). 

Aluminum Phosphate Antacid Gel. Aluminum phosphate antacid gels, administered just prior to or 

shortly after oral strontium exposure, have been shown to reduce absorption of strontium by increasing its 

excretion in feces in humans (Spencer et al. 1969a, 1969b), rats (Carr and Nolan 1968), and mice (Keslev 

et al. 1972). A practical advantage of this treatment is that the gels are readily available as over-thecounter pharmaceuticals. In elderly men who had been maintained on a low calcium diet for several 

weeks, oral administration of an antacid gel just prior to oral 85Sr/45Ca exposure reduced plasma 
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radiostrontium levels by 88%, but reduced radiocalcium levels by only 38% (Spencer et al. 1969a). In the 

same study group, antacid treatment reduced strontium absorption by 57% when given 0.5 hours after 

exposure, but by only 43%, 1 hour after exposure (Spencer et al. 1969b). In similar studies on rats fed 

antacid for several days prior to exposure, the absorption of strontium was reduced by 83%, whereas there 

was no effect on the absorption of calcium (Carr and Nolan 1968). In mice, an aluminum phosphate gel 

reduced the absorption of strontium by about 13-fold and of calcium by about 3-fold (Keslev et al. 1972). 

Sulfates. In rats orally exposed to radiostrontium and monitored on day 2, oral administration of barium 

sulfate in combination with sodium sulfate or magnesium sulfate reduced radiostrontium retention in the 

femur by nearly 80% (Volf 1964). Treatment was effective if given within 10 minutes of exposure, but 

not if delayed more than 80 minutes. Strontium sulfate was less effective, reducing radiostrontium 

retention by only 30%. Volf (1964) did not determine whether the effectiveness of the barium sulfate 

combination therapy was a result of increased diuresis or decreased bioavailability by means of 

adsorption to radiostrontium in the intestine. 

The following treatments have been shown to be less effective or less practical. 

Diet or Dietary Fiber. A pulverized solid diet administered to rat sucklings over 8 hours resulted in 10– 

20% less whole body retention of 85Sr (reduced absorption) than cow milk (Kostial et al. 1981b, 1984). 

Supplementing cow milk with trace elements did not improve its effectiveness, ruling out the possibility 

that trace elements in the food competitively inhibited intracellular transport of ingested strontium. 

Rather, the authors suggested that the solid diet contained ligands for strontium that reduced the amount 

of strontium available for transport. Another study demonstrated that the inclusion of cellulose fiber into 

the diet of suckling rats decreased the retention of simultaneously administered 85Sr/45Ca by 20% 

(Momčilovič and Gruden 1981). However, cellulose fiber was less satisfactory than alginates, both in 

effectiveness and in the lack of discrimination between strontium and calcium. 

Flavones. In rats given doses of flavone (Ipriflavone, 7-isopropyl-isoflavone, or Morin, 

2',2,4',5,7-pentahydroxy-flavone) for 3 weeks prior to acute oral exposure to radiostrontium, the whole 

body retention of radiostrontium was reduced by 50 and 30%, respectively, after 1 month (Gachályi et al. 

1988). Similar experiments on pregnant rats demonstrated that both flavones reduced fetal uptake of 

radiostrontium administered to dams on gestational days 17/18 and 19/20. No studies were located that 

demonstrated the usefulness of flavones for emergency situations, rather than as pretreatments. 
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Stable Strontium. In weanling rats previously given varying amounts of strontium lactate in the diet, 4 or 

6% strontium lowered the retention of injected radiostrontium to a greater extent than the retention of 

injected radiocalcium (Teree et al. 1965). The disadvantage of this treatment is the adverse effect on bone 

development caused by excess stable strontium. 

3.12.2 Reducing Body Burden 

Absorption of strontium can vary with the chemical form of the compound and its solubility. Those 

strontium compounds that are readily absorbed following inhalation or oral exposure are rapidly 

distributed throughout the body (see Section 3.5). Because of its similarity to calcium, strontium entering 

the circulation preferentially accumulates in bone. Methods for reducing the body burden of 

radiostrontium that have been tested in animals include calcium, chelators (with variable results), 

hemodialysis, and magnesium sulfate. Exposure to cold temperatures, use of the few pharmacological 

agents that have been tested, and use of stable strontium are less satisfactory treatments. 

Calcium. In human patients with osteoporosis who were injected with tracer doses of 85SrCl2, 

intravenous infusions of calcium gluconate significantly increased urinary excretion of strontium, but had 

no effect on fecal excretion (Spencer et al. 1967d). This effect was attributed to the decreased renal 

tubular reabsorption of calcium under these conditions. Calcium gluconate was more effective than 

magnesium chloride tested in the same study. A 10-day series of injections with a combination of 

calcium and calciferol reduced the retention of 90Sr in rabbits by 70%, if the treatments started as soon as 

24 hours after exposure (George et al. 1979). If treatments were delayed 96 hours, the removal of 

strontium was reduced by 50%. Slightly less effective treatments included calcium alone, sodium citrate, 

or a combination of calcium and magnesium, which reduced strontium retention by 40, 30, and 20%, 

respectively. A 3-week diet high in calcium and low in phosphorus, initiated 24 hours after injection of 

90Sr into rats, significantly reduced the incorporation of the isotope into bone (Steinbach 1968). In rats, 

pretreatment with diets rich or adequate in calcium tend to result in lower accumulations of 

radiostrontium in bone following exposure than diets poor in calcium (Palmer et al. 1958; Roushdy et al. 

1980, 1981). However, administration of a high-calcium diet to rats following a month-long parenteral 

exposure to radiostrontium, only slightly reduced the strontium content of the femur after 65 days (Ray et 

al. 1956). 

Chelators. Chelators are not effective once strontium has become incorporated into hydroxyapatite. A 

variety of chelators have been tested in rodents, with variable results. In general, chelators did not 
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successfully increase the excretion of radiostrontium, if administered 6 or 24 hours after exposure (e.g., 

Llobet et al. 1991a, 1991b, 1992a). In tests on rats, the cryptator hexaoxa-diamine macrobicycle was 

effective when given simultaneously with radiostrontium (Müller 1970). The aza crown ether 2NaCa 

Kryptofix 22 was effective in tests on mice and rats when administered intravenously or intratracheally 

within 1 hour of exposure to radiostrontium (Varga et al. 1994). Other aza crown ethers and other 

chelators have been tested on mice following parenteral exposure to strontium, but their effectiveness has 

been so variable and no consistent conclusions can be drawn (Colomina et al. 1991; Llobet et al. 1992b; 

Ortega et al. 1989). For example, Na2Ca EGTA (Na2Ca ethylenglycol-bis-(β-amino-ethyl-ether)-N,N’­

tetraacetic acid) increased fecal excretion of subcutaneously administered strontium (nitrate), but 

decreased urinary excretion to the same degree, and thus, there was no net change (Colomina et al. 1991). 

Chelators that were not at all effective in rodent studies include monosodium glutamate, Tiron 

(4,5-dihydroxy-1,3-benzene-disulfonic acid), DMSA (2,3-dimercaptosuccinic acid), succinic acid, malic 

acid, CaNa2CTDA (cyclohexanediaminetetraacetic acid), and THPC, a cyclic derivative of EDTA 

(Kostial et al. 1979; Llobet et al. 1992b; Ortega et al. 1989). 

The chelating agent, zirconium citrate, administered intraperitoneally in several injections soon after 

parenteral exposure to 90Sr, significantly reduced the number of mice with bone tumors, reduced the 

multiplicity of tumors, and delayed the onset of tumors (Zander-Principati and Kuzma 1964). 

Measurements of external brehmsstrahlung emissions 10–12 months later demonstrated that mice treated 

with zirconium citrate had a reduced body burden of radiostrontium, which is the likely cause of the 

reduced tumor rate. One source of uncertainty regarding this study, despite the claims of low toxicity for 

zirconium citrate, is the unexplained reduction in lifespan in all the groups treated with the chelator. 

Cold. In mice exposed to low temperature (9 EC), the rate of urinary excretion of a radiostrontium tracer 

was increased (Wedin 1972; Wedin et al. 1972). This was attributed to a specific effect of cold on the 

rate of diuresis. However, since the rate of calcium excretion was not measured in this study, but is also 

known to be increased by cold, the usefulness of this finding is not clear. Urinary excretion rates of 

radioactive strontium in mice intraperitoneally injected with 85Sr were increased about 10% by transfer to 

4 EC (Nilsson and Rönnbäck 1988). 

Hemodialysis. Hemodialysis is only effective if administered soon after exposure to strontium. In 

100-day-old calves injected with 85Sr, a 12-hour hemodialysis session administered 4, 14, or 24 hours 
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later resulted in removal of only 14, 4, and 2.5% of the administered dose, respectively (Downey et al. 

1964). 

Magnesium. In human patients with osteoporosis who were injected with tracer doses of 85SrCl2, 

intravenous infusions of magnesium chloride significantly increased urinary excretion of strontium, but 

had no effect on fecal excretion (Spencer et al. 1967a). Magnesium chloride was not as effective as 

calcium gluconate tested in the same study. Magnesium sulfate injected 10 minutes after 85SrCl2 

significantly reduced the body burden of strontium in rats, irrespective of the dietary calcium or 

vitamin D status (Roushdy et al. 1980, 1981). 

Pharmacological Agents. Tests of the effectiveness of hormones or drugs in reducing the body burden of 

strontium have been disappointing. In rats, progesterone had no significant effect on radiostrontium 

retention, whereas estrogen actually increased the amount of 90Sr in the femur (Steinbach 1968). In 

rabbits, the steroid prednislone, thyroxine, and the diuretic furosemide removed only about 30, 15, and 

10%, respectively, of the administered dose of 90Sr (George et al. 1979). 

Phosphorus-reduced Diet. A diet low in phosphorus (0.017%, Ca/P ratio of 21.5) was most effective in 

mobilizing radiostrontium from the rat skeleton (Ray et al. 1956). Nearly 85% of the strontium 

incorporated into the femur was removed by the 50th day; only 0.24% of the injected dose remained in the 

femur. However, this diet caused serious adverse effects: minimal increase in body weight, delayed 

growth and narrowing of epiphyseal discs in the tibia, reduced ash weight of the femur, and poor health 

necessitating termination of the experiment. Consumption for 64 days of a diet ‘subminimal’ in 

phosphorus (0.21%, Ca/P ratio of 2.19) removed nearly 64% of the radiostrontium incorporated into the 

femur. Rats exhibited normal body weight gain and ash weight of the femur, but there were 

histopathological changes in the epiphyseal discs and trabeculae of the tibia. Although the low and 

‘subminimal’ phosphorus diets were relatively effective in reducing the body burden of radiostrontium, 

the potential for adverse health effects from inadequate phosphorus intake reduces the value of this 

strategy. 

Strontium-free Diet. In young rats maintained on a diet high in strontium for 28 days, returning to a 

normal diet low in strontium noticeably reversed the adverse effect on bone mineralization (Johnson et al. 

1968). The reduced percentage of ash in bone began to show improvement after 2 weeks and was nearly 

normal after 5 weeks. In addition, the abnormal deposition of osteoid in vertebrae was repaired. 
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3. HEALTH EFFECTS 

3.12.3 Interfering with the Mechanism of Action for Toxic Effects 

Hyperbaric oxygen therapy was successfully used to treat a case of scleral necrosis resulting from 90Sr 

therapy following pterygiectomy (Green and Brannen 1995). Repeated hyperoxygenation enhanced 

neovascularization and regrowth of the scleral tissue that had become avascular and abnormally thin as a 

result of exposure to beta radiation. 

In tests on irradiated skin of guinea pigs, anti-inflammatory compounds reduced the permeability of the 

dermal vasculature to plasma proteins by up to 30% (Song et al. 1968). However, since drug treatment 

was administered both before and after irradiation, this study is not definitive proof of the efficacy of 

these compounds. 

3.13 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 strontium 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 strontium. 

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. 

3.13.1 Existing Information on Health Effects of Strontium 

The existing data on health effects of inhalation, oral, and dermal exposure of humans and animals are 

summarized in Figure 3-9 for stable strontium and in Figure 3-10 for radioactive strontium. The purpose 

of these figures is to illustrate the existing information concerning the health effects of strontium. Each 

dot in the figure indicates that one or more studies provide information associated with that particular 
STRONTIUM 174 

3. HEALTH EFFECTS 

Figure 3-9. Existing Information on Health Effects of Stable Strontium 

Death

Acute 

Intermediate 

Chronic 

Immunologic/Lymphoretic 

Neurologic 

Reproductive 

Developmental 

Genotoxic 

Cancer 

Systemic 

Human 

Inhalation 

Oral 

Dermal 

Death

Acute 

Intermediate 

Chronic 

Immunologic/Lymphoretic 

Neurologic 

Reproductive 

Developmental 

Genotoxic 

Cancer 

Systemic 

Animal 

Inhalation 

Oral 

Dermal 

Existing Studies 
STRONTIUM 175 

3. HEALTH EFFECTS 

Figure 3-10. Existing Information on Health Effects of 

Radioactive Strontium 

Existing Studies 

Human 

Animal 

Inhalation 

Oral 

Dermal 

Death

Acute 

Intermediate 

Chronic 

Immunologic/Lymphoretic 

Neurologic 

Reproductive 

Developmental 

Genotoxic 

Cancer 

Systemic 

External 

Inhalation 

Oral 

Dermal 

Death

Acute 

Intermediate 

Chronic 

Immunologic/Lymphoretic 

Neurologic 

Reproductive 

Developmental 

Genotoxic 

Cancer 

Systemic 

External 
STRONTIUM 176 

3. HEALTH EFFECTS 

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. Generally, ATSDR defines a data gap more broadly as any 

substance-specific information missing from the scientific literature. 

3.13.2 Identification of Data Needs 

In the following discussion, the toxicity (carcinogenicity) of inhaled strontium chromate is omitted, since 

its adverse effects are attributed to hexavalent chromium (see Section 3.2.1.7). Unless otherwise stated, 

the proposed investigations refer to studies of health effects in animals. 

Acute-Duration Exposure. 

Stable Strontium. Information from injection and kinetic studies in humans and oral, inhalation, and 

injection studies in animals indicates that bone is the primary target tissue of absorbed stable strontium. 

The acute database is inadequate for deriving MRLs. A data need for an acute inhalation study is 

discussed under Data Needs for Immunotoxicity. Animal studies have shown that stable strontium is not 

toxic at low doses (Kroes et al. 1977). On the other hand, high oral doses of stable strontium can severely 

depress the serum levels of 1,25-dihydroxyvitamin D in rats within a week, which has an adverse effect 

on calcium absorption (Armbrecht et al. 1979, 1998). Of the two available acute oral toxicity studies, one 

employed ineffective doses, and the other used a single high dose (Kroes et al. 1977; Kshirsagar 1976). 

Thus, there is a need for an acute-duration oral study that would enable an analysis of dose-response 

relationships with regard to strontium ingestion and skeletal effects. Consideration should be given to 

comparing the relative effects of different forms of strontium (e.g., strontium chloride, strontium 

carbonate, strontium phosphate), and different modes of delivery (in food, in water), since these factors 

probably affect the bioavailability of ingested strontium. In addition, such a study could provide a basis 

for investigating possible biomarkers of effect (by monitoring changes in the serum levels of vitamin D, 

1,25-dihydroxyvitamin D, calcium, phosphorus, phosphatases, and other biomarkers) that could be used 

to characterize the early systemic response to strontium. 
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Radioactive Strontium. Acute-duration inhalation or oral administration of radioactive strontium caused 

adverse effects. No dermal studies were conducted. Rather, external studies used solid strontium 

apposed to the skin, which did not provide an opportunity for dermal absorption (Hoshino and Tanooka 

1975; Randall and Coggle 1995; Song et al. 1968). In dogs, inhalation of relatively insoluble particles of 

radiostrontium resulted in prominent damage to pulmonary tissues (Benjamin et al. 1975, 1976c; Snipes 

et al. 1979). Inhalation or ingestion of soluble radiostrontium resulted in radiostrontium incorporation 

into bone and subsequent chronic radiation exposure of the surrounding tissues (inhalation: Gillett et al. 

1987a, 1987b; oral: Casarett et al. 1962; Cragle et al. 1969). No inhalation or oral MRLs could be 

derived because the effects of exposure, even at the lowest levels, were serious. There is a need for an 

inhalation study using soluble strontium aerosols that would test a lower range of exposure levels than 

had previously been employed, primarily to assess the effects on the lymphocyte population; existing 

studies found chronic depression of lymphocyte numbers even at the lowest concentrations. Existing 

acute-duration oral studies are inadequate because either the study size was small and/or a single dose was 

used. There is a need for an acute oral multi-dose study, in particular, one comparing effects in young 

and adult animals, primarily for the purpose of relating genotoxicity to dosage. Dermal studies using 

strontium applied to the skin should be conducted to evaluate systemic effects that might occur following 

the kind of exposure that might occur in the vicinity of a hazardous waste site. 

Intermediate-Duration Exposure. 

Stable Strontium. An intermediate oral MRL was derived on the basis of a study that showed young rats 

were more susceptible to adverse skeletal effects (rickets) than adults (Storey 1961). A considerable 

number of studies support this finding (see Section 3.2.2.2 Musculoskeletal Effects). No intermediate 

inhalation study was located. The necessity for an intermediate inhalation study should be evaluated once 

the data from the proposed acute inhalation study are assessed. No intermediate dermal study was 

located, but given the low cytotoxicity of stable strontium, such a study does not seem necessary. 

Radioactive Strontium. No intermediate-duration inhalation, oral, or dermal studies were located. There 

is a need for intermediate-duration inhalation and oral studies, using low levels of exposure, to help define 

the risk associated with longer-term exposures, such as may occur from radiostrontium releases at nuclear 

fuel reprocessing facilities or nuclear power plants into air, into drinking water, or settling onto croplands. 

The primary focus of these studies should be hematological and immunological effects. Some 

information is available in intermediate external studies, but in these, radiostrontium was not applied to 

the skin in a form that could be absorbed. Dermal studies need to be conducted to assess the systemic 

risks that children might incur by playing in the open after radiostrontium has settled on the ground. 
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Chronic-Duration Exposure and Cancer. 

Stable Strontium. There were no adequate chronic-duration studies of stable strontium effects in humans 

or animals. In a review paper, Skoryna (1981a) briefly mentioned that oral administration of low doses of 

strontium had no adverse effect in rats over a 3-year period or over several generations, but provided no 

experimental details. A chronic-duration oral study would be useful for evaluating the long-term health 

effects of strontium ingestion. Some consideration should be given to comparing the effects of 

compounds having different chemical properties (e.g., strontium chloride, strontium carbonate, and 

strontium phosphate). 

Although there are no chronic studies of stable strontium exposure, the rest of the database provides no 

evidence to suspect that stable strontium might be carcinogenic. It does not appear that a long-term 

carcinogenesis study would prove useful. 

Radioactive Strontium. There is no chronic inhalation study for radioactive strontium. Such a study 

should be considered after an intermediate inhalation study is conducted, as a means of evaluating longterm exposure to low levels of radioactivity on the immune system. The Techa River cohort represents 

the major source of information regarding the health effects of chronic exposure to radiostrontium: 

suppression of hematopoiesis and immune function (Akleyev et al. 1995). Chronic oral administration of 

radioactive strontium has been shown to suppress hematopoiesis and lymphocyte function in animals 

(Dungworth et al. 1969; Howard 1970). Since these effects were observed at the lowest exposure levels, 

chronic oral studies using even lower exposure levels are needed to evaluate potential adverse effects on 

the immune system. A single clinical study reported late-developing changes in the skin following 

chronic application of solid strontium (external exposure) to treat hemangioma (Bekerus 1970). It is not 

clear that the database needs a chronic dermal study of radiostrontium applied to the skin in a form that 

might be absorbed, since significant dermal absorption of strontium only occurs through abraded skin (see 

Section 3.5.1.3). 

An increase in the incidence of leukemia has been reported in the Techa River cohort, which received 

doses of 10 rem (0.1 Sv) or more from radioactive strontium (Kossenko 1996; Kossenko et al. 2000). 

Chronic oral administration of radioactive strontium was shown to increase the incidence of boneassociated cancer in animals (Book et al. 1982; Clarke et al. 1972; Finkel et al. 1960; White et al. 1993; 

Zapol’skaya et al. 1974). No chronic inhalation or dermal studies were located. Since the dynamics of 

strontium uptake into bone are known, estimations of the risk of cancer in humans following inhalation 
STRONTIUM 179 

3. HEALTH EFFECTS 

exposure can be derived using dose-response data from the Techa River cohort and the beagle inhalation 

studies. There is no realistic scenario for chronic dermal exposure at damaging levels. 

Genotoxicity. 

Stable Strontium. In vitro studies listed in Table 3-6 demonstrate a lack of adverse effects from treatment 

with stable strontium. A single gavage study in mice is the only evidence for genotoxicity of stable 

strontium (at doses of 140–1,400 mg/kg), but it seems likely that the bolus delivery may have influenced 

the outcome (Ghosh et al. 1990). None of the intermediate-duration studies (no chronic study is 

available) presented any evidence of effects that could be attributed to genotoxicity. Additional 

genotoxicity studies on stable strontium appear to be unnecessary. 

Radioactive Strontium. The genotoxicity of radioactive strontium is well-documented. In the Techa 

River cohort, an elevated frequency of stable chromosomal translocations was observed (Bauchinger et al. 

1998). Other evidence includes in vitro cytogenetic studies (see Table 3–6), and, by implication, the 

increased cancer rates that were observed in most investigations (see Data Needs for Cancer). However, 

the mechanism of radiostrontium genotoxicity (i.e., the specific DNA alterations that occur following 

exposure) has yet to be characterized. Recently, Sutherland et al. (2000a, 2000b) developed molecular 

biological assays for characterizing clustered DNA lesions caused by exposure to gamma radiation. If 

such a technique were to be developed for radiostrontium-exposed cells, it might provide a means of 

recording molecular damage. 

Reproductive Toxicity. 

Stable Strontium. There is no evidence regarding the effect of stable strontium on reproduction, but 

levels of exposure possible by inhalation or dermal routes are not likely to be harmful. Stable strontium 

was found to have beneficial effects when it was used in solutions designed for testing the functional 

capacity of human spermatozoa in vitro (Mortimer 1986; Mortimer et al. 1986). The possible 

consequences of excess strontium ingestion on reproduction need to be explored. Such experiments 

should compare the relative toxicity of stable strontium compounds that have different properties and may 

have different rates of absorption (e.g., strontium chloride, strontium carbonate and strontium phosphate). 

Radioactive Strontium. In the Techa River cohort, average radiation doses to the gonads of up to 74 rem 

(0.74 Sv) had no effect on birth rate, fertility, or the incidence of spontaneous abortions (Kossenko et al. 

1994). However, the contribution of radiostrontium to the gonadal radiation dose is likely to have been 
STRONTIUM 180 

3. HEALTH EFFECTS 

negligible compared to that of external gamma radiation. Multigenerational oral studies in animals 

demonstrated a dose-dependent effect of radioactive strontium on reproduction. In pigs, only the highest 

doses affected fetal survival, and in those treated as adults, there was no effect on litter size, percentage of 

stillborn, or birth weight (Clarke et al. 1970, 1972; McClellan et al. 1963). Injection studies have reported 

a higher incidence of adverse reproductive effects, perhaps because of the higher dose levels. Injection of 

male mice prior to mating increase the rate of fetal death, and there is some evidence that radioactive 

strontium selectively accumulates in the testis (Reddi 1971). Injection of pregnant female mice reduced 

the reproductive capacity of female offspring, reducing the numbers of oocytes of all stages in the ovary 

(Rönnbäck 1981a, 1981b). Thus, the fetal reproductive system appears to be vulnerable to radioactive 

strontium. Further studies to evaluate the dose-response of gonadal effects, including cytogenetic aspects, 

would appear to be warranted. 

Developmental Toxicity. 

Stable Strontium. The main developmental effect of stable strontium is impaired bone development 

(rickets) following oral exposure at high doses (Johnson et al. 1968; Kshirsagar 1976; Marie and Hott 

1986; Neufeld and Boskey 1994; Ögzur et al. 1996; Reinholt et al. 1984; Storey et al. 1961, 1962). 

Inhalation and dermal exposures are unlikely to be high enough to have an adverse effect. The oral 

developmental toxicity studies have concentrated on the initiation of rickets in young children or young 

animals during the postnatal or juvenile periods, but none have addressed the effect of maternal exposures 

on the fetus during gestation or on the neonate during lactation. The relative effectiveness of strontium 

compounds that have different properties (e.g., strontium chloride, strontium carbonate, and strontium 

phosphate) needs to be evaluated with regard to maternal absorption, placental transfer, fetal toxicity, and 

postnatal toxicity during lactation. In addition, behavioral testing should be conducted on the young 

animals to determine whether there are any neurological consequences of fetal exposure to excess stable 

strontium. 

Radioactive Strontium. In the Techa River cohort, individuals who were exposed to high levels of 

radiostrontium as teenagers had a higher frequency of stable transformations than those who were adults 

at the time (Bauchinger et al. 1998); the differences were attributed to increased skeletal incorporation of 

radiostrontium in the young. The progeny of the exposed cohort showed an elevated incidence of adverse 

pregnancy outcomes (mortality from developmental anomalies, chromosomal anomalies, labor 

complications, and other unspecified perinatal conditions), but no increase in the incidence of cancer 

(Kossenko et al. 1994). Multigenerational oral studies in animals showed no teratogenic effect of 

radioactive strontium administered from the time of conception, but showed reduced survival of the F1 
STRONTIUM 181 

3. HEALTH EFFECTS 

generation because of an increased incidence of bone-associated cancer (Clarke et al. 1970; Finkel et al. 

1960; McClellan et al. 1963). Injection of high doses of radioactive strontium during gestation had 

teratogenic effects on the fetus, primarily skeletal abnormalities (Hopkins et al. 1967; Finkel and Biskis 

1969). Injections had qualitatively different effects depending on the day of gestation, because of 

regional differences in rates of bone mineralization during gestation. More information is needed 

regarding the effect of the timing of maternal exposure relative to developmental stages. In addition, 

developmental studies that evaluate neurological effects in the offspring are needed. 

Immunotoxicity. 

Stable Strontium. There is no evidence that oral or dermal exposures to stable strontium affect the 

immune system. However, one case report described an anaphylactic reaction to inhalation of smoke that 

contained ~30% strontium among other irritants (Federman and Sachter 1997). Strontium’s possible 

involvement is supported by reports that excess strontium elicits degranulation of mast cells in vitro, 

causing histamine release (Alm and Bloom 1981a, 1981b; Atkinson et al. 1979; Foreman 1977; Foreman 

and Mongar 1972a, 1972b; Foreman et al. 1977). For this reason, a short-term inhalation study would 

help to determine whether strontium by itself can elicit anaphylaxis and, if so, identify the effective 

concentration levels. 

Radioactive Strontium. There is evidence that immunosuppression, resulting from irradiation of bone 

marrow, may occur in humans and animals following absorption of radioactive strontium. 

Immunological effects were noted in the Techa River cohort, which received relatively high radiation 

doses to bone marrow following ingestion of food and water contaminated with radiostrontium (Akleyev 

et al. 1995). In animal studies, the lowest applied inhalation or oral doses were reported to result in 

lymphopenia lasting as long as 2 years (Benjamin et al. 1976c; Howard 1970; Jones et al. 1976). There 

appears to be a need for studies that examine the effect of a lower range of exposures on immune 

function. Another reason for such studies comes from the reports demonstrating that NK cells may be 

preferentially eliminated following injection of 89Sr or 90Sr (Emmanuel et al. 1981; Gidlund et al. 1990; 

Haller and Wigzell 1977; Wiltrout et al. 1989), with the result that the organism’s ability to defend 

against lymphoid tumors is impaired (Haller and Wigzell 1977; Luevano et al. 1981). The implication is 

that reduced cellular defenses may compound the effect of genotoxicity, increasing the risk of cancer. 

However, it is not known whether NK cells are equally vulnerable at lower exposure levels. 
STRONTIUM 182 

3. HEALTH EFFECTS 

Neurotoxicity. 

Stable Strontium. The only evidence for neurotoxicity of stable strontium is a report of hindlimb 

paralysis following intermediate-duration ingestion of excess strontium (Johnson et al. 1968). Given the 

absence of any other evidence for neurotoxicity, it is possible that, in this case, the paralysis may have 

resulted from compression of the hypertrophic epiphyseal cartilage, which was insufficiently mineralized 

to support the weight of the body. Additional neurotoxicity studies in adult animals for stable strontium 

do not appear to be necessary. 

Radioactive Strontium. Neurological effects were reported in the Techa River population that was 

exposed to radiostrontium from water and food contaminated from releases at a plutonium processing 

plant between 1949 and 1956 (Akleyev et al. 1995). However, external gamma radiation, also released at 

this time, undoubtedly contributed to these effects. A single instance of epilepsy in a dog exposed by 

inhalation to a high concentration represents the only evidence for neurotoxicity of radioactive strontium 

in animals (Gillett et al. 1987b). The authors concluded that epilepsy was not related to treatment. 

However, no studies have specifically measured behavioral or neurological deficits in exposed animals. 

The database needs studies that measure neurological effects in offspring following exposure in utero 

and/or during lactation. 

Epidemiological and Human Dosimetry Studies. 

Stable Strontium. Strontium is ubiquitous in the environment, so everyone is exposed to it to some 

degree. Children who exhibit pica behavior or persons living in areas with high levels of strontium in the 

drinking water may have higher exposures than the general population. A Turkish epidemiological study 

demonstrated a higher incidence of rickets among children living in rural communities whose diet was 

based on grain crops grown in local soil containing high levels of strontium (Özgür et al. 1996). This 

study did not attempt to measure strontium levels in the affected children. In addition, this study may not 

be directly applicable to conditions in the United States, given the different diet and the availability of 

foods from a wider geographic range. One epidemiological study found that relatively high levels of 

strontium in the drinking water had no adverse effect on cardiovascular health, and, in fact appeared to 

have a beneficial effect on the rate of mortality from hypertension with heart disease (Dawson et al. 

1978). Information regarding the higher levels in drinking water could be used to design animal 

experiments for evaluating chronic exposure effects, which are currently lacking in the database. In one 

case-control study that tried to account for the higher incidence of liver cancer in 1984 on Chongming 
STRONTIUM 183 

3. HEALTH EFFECTS 

Island in China, no association was found with the levels of stable strontium detected in hair (Wang et al. 

1990). 

Radioactive Strontium. Dosimetry data are available for approximately 16,000 members of the Techa 

River population that was exposed to radiostrontium because of releases from a plutonium processing 

plant between 1949 and 1956 (Kossenko et al. 1997). Since exposure levels in this population were 30– 

100 times higher than the maximum exposure from global fallout, this cohort represents the largest group 

of subjects available for examining health effects of chronic radiation exposure. Subpopulations living in 

certain regions within the Techa River area received different levels of exposure, so that dose 

relationships are being established for health effects. In addition, investigators have been able to examine 

the effect of developmental age at the time of exposure on health outcomes. Although individuals were 

exposed to multiple sources of radiation during the first years (including 137Cs bound in soft tissues), in 

recent decades, their radiation exposure was primarily from 90Sr incorporated into bone. The health 

effects have been similar to those observed for animals exposed chronically to radiostrontium, and have 

included suppression of hematopoeisis and leukemia (Akleyev et al. 1995; Kossenko 1996; Kossenko et 

al. 1997, 2000). 

A Danish epidemiological study found no association between the incidence of thyroid cancer in 

Denmark between 1943 and 1988 and the levels of skeletal incorporation of 90Sr from fallout (Sala and 

Olsen 1993). However, the reason for this study is uncertain since strontium is not taken up preferentially 

in the thyroid, unlike iodine, which is incorporated into thyroid hormones (T3 and T4). A Scottish 

epidemiological study found no evidence for increased risks of total cancers, leukemia and nonHodgkin’s lymphoma, or acute myeloid leukemia for cohorts of children born during the period of highest 

fallout (radiostrontium) exposure (Hole et al. 1993). The few cases of bone tumors showed a 

nonsignificant increase for children born during the ‘high risk’ period. The reduction in fallout from 

above-ground nuclear weapons testing has reduced the exposure of the general population to radioactive 

strontium. Currently, populations working at or living in the vicinity of nuclear power plants or 

reprocessing facilities might have higher than background exposures. Workers at the facilities may have 

less exposure because protective equipment and safety procedures are in use. Environmental levels of 

radiostrontium that are measured near these facilities could be used to guide exposure levels in the 

toxicity experiments proposed above. 
STRONTIUM 184 

3. HEALTH EFFECTS 

Biomarkers of Exposure and Effect. 

Exposure. 

Stable Strontium. Levels of stable strontium can be measured in blood or urine to determine exposures 

of any duration. Within a few days, most of the retained strontium is found in bone, but because of bone 

remodeling, strontium will be released over time and be detectable in blood and urine. Inductively 

coupled plasma mass spectroscopy (ICP-MS) was able to detect strontium in amniotic fluid and maternal 

plasma at levels of 0.03 and 0.06 ppb, respectively, in untreated humans (Silberstein et al. 2001). The 

sensitivity of this method is adequate to detect unusual accumulations of strontium. No additional 

biomarkers of exposure to stable strontium appear to be needed. 

Radioactive Strontium. Exposures to radioactive strontium can be determined readily by measuring 

levels of radioactivity in blood or urine by liquid scintillation counting techniques. In addition, whole 

body counters can determine the level of radiostrontium retained in the skeleton. There appears to be no 

need for additional biomarkers of exposure to radioactive strontium. 

Effect. 

Stable Strontium. The typical signs of rickets (craniotabes, rachitic rosary, bulging at the wrist, genu 

valgus, genu varus, and delayed closure of the fontanelles) represent biomarkers of exposure to excess 

stable strontium in children (Özgür et al. 1996). Excess strontium ingestion has been shown to depress 

serum levels of 1,25-dihydroxyvitamin D in rats (Armbrecht et al. 1998). Since vitamin D insufficiency 

by itself can also cause rickets, measurement of both vitamin D levels and strontium levels in serum 

would be required to determine the role of strontium in a particular case. As mentioned above (Data 

Needs for Acute-Duration Studies), the proposed toxicity studies could be used to develop biomarkers for 

early effects following exposure to excess strontium. An array of biomarkers could possibly be 

developed to monitor the course of pathology before the signs of rickets fully appear. 

Radioactive Strontium. A reduction in blood cell counts is a biomarker of effect for radioactive 

strontium. However, many other conditions can have the same result. Cytogenetic analysis of blood cells 

can reveal whether exposure to radioactive strontium has been sufficient to cause genotoxicity (see 

Table 3-5). A new method for evaluating DNA damage in cells exposed to gamma radiation has been 

developed using molecular biological techniques (Sutherland et al. 2000a, 2000b). It may be possible to 
STRONTIUM 185 

3. HEALTH EFFECTS 

develop such an assay for evaluating exposure to radioactive strontium, which would also specifically 

identify the kind of DNA lesions produced. 

Absorption, Distribution, Metabolism, and Excretion. More information is needed comparing 

the relative rates of absorption for different chemical forms of strontium that may vary in solubility. 

Solubility differences would affect the duration of residence of particles in the lung, which might have 

significant effects in the case of radiostrontium exposure. A comparison of gastrointestinal absorption 

rates for different chemical forms and for different vehicles of administration (food or water) has not been 

conducted. Results of such studies would help predict outcomes following different kinds of exposure. 

Nothing is known regarding dermal absorption of strontium taken up in soil, which is a type of exposure 

that children would be likely to encounter. However, studies of dermal absorption from soil would be of 

low priority given that significant dermal absorption of soluble strontium only occurred through abraded 

skin (See Section 3.5.1.3) and the amounts available from dry soil would be biologically insignificant 

under any realistic exposure scenario. Absorbed strontium is understood to distribute primarily to the 

bone and to be retained longer in the young than in adults. The combination of the ICRP PBPK model for 

strontium and animal-based studies on Observed Ratios of strontium and calcium (Comar and Wasserman 

1964) is sufficient to estimate strontium turnover during pregnancy and lactation and in the elderly. 

Comparative Toxicokinetics. The target organ for stable and radioactive strontium is the same in 

humans and animals, namely, bone. Young rats can serve as a model for children’s exposures, but adult 

rats are less suitable, since the epiphyseal plate remains cartilaginous into adulthood (Leininger and Riley 

1990). For this reason, adult rats could be expected to incorporate proportionally higher levels of 

strontium than adult humans. Furthermore, remodeling of bone in rats is not analogous to that in humans. 

The rat would probably not be a good model for evaluating placental transfer of strontium to the fetus 

because of differences in placental tissue organization. 

Methods for Reducing Toxic Effects. Both stable and radioactive strontium are readily absorbed by 

the intestine, apparently through calcium transporter elements (Bianchi et al. 1999; Blumsohn et al. 1994; 

Milsom et al. 1987; Reid et al. 1986; Sips et al. 1994). Numerous methods have been tested for 

alleviating the effects of exposure to strontium (see Section 3.12). Oral administration of alginates with a 

high guluronic acid content or a single dose of aluminum phosphate antacid gel are currently 

recommended for reducing peak absorption of strontium shortly after exposure. The toxicities of excess 

stable and radioactive strontium are related to their rapid sequestration into bone. Most strategies for 

treatment involve high calcium in combination with other agents to enhance the replacement of strontium 
STRONTIUM 186 

3. HEALTH EFFECTS 

in bone by calcium. There does not appear to be a need for new studies at this time. However, as 

mentioned in Section 3.6.2, polymorphisms in genetic factors that may affect rates of strontium 

absorption and bone mineralization are currently under investigation and potentially could regulate the 

effectiveness of treatment. If relevant polymorphisms are identified, then the existing methods for 

reducing toxic effects should be tested using stable strontium tracers to determine whether genetic factors 

affect the outcome of treatment. 

Children’s Susceptibility. 

Stable Strontium. The effect of excess stable strontium ingestion on bone development is well 

documented: strontium-induced rickets has been reported in children and young animals. The particular 

vulnerability of children, because of the immaturity of the skeleton, is well understood. The intestinal 

rate of strontium absorption and the retention of strontium in the developing bone is known to be higher 

in infants and children than in adults. It is known that the fetus can be exposed to strontium following 

previous maternal exposure, but adequate information regarding changes in the rates of strontium 

mobilization from the maternal skeleton or changes in rates of intestinal absorption of strontium during 

the course of pregnancy is lacking. There is a need for studies to develop this information to fill in gaps 

in existing PBPK models for strontium; this effort would have the additional benefit of being applicable 

to other bone-seeking radioisotopes. Another issue to be considered is the relative bioavailability of 

strontium in the different chemical compounds (e.g., strontium chloride, strontium carbonate, strontium 

phosphate). Since children may be exposed to strontium by pica behavior, there is a need for animal 

studies that would investigate variations in absorption (bioavailability) when strontium is ingested in the 

form of soil. 

Biomarkers of exposure and effect are established for children. Since the primary biomarker of effect, 

rickets, is a late-stage phenomenon, it would be useful to precisely establish a constellation of biomarkers 

that would identify a precursor condition. Such markers might include relative serum levels of vitamin D, 

calcium, phosphorus, and alkaline phosphatases, as well as strontium itself. The alginate method for 

reducing peak absorption of strontium has been validated in children (Sutton et al. 1971a). 

Radioactive Strontium. Numerous oral exposures have demonstrated the enhanced risk of reproductive 

effects and cancer in animals exposed to radiostrontium in utero or during lactation. At the higher levels 

used in injection studies, teratogenic effects were observed on bone development. The possibility of 

neurological deficits from gestational exposure to radioactive strontium, resulting from radiostrontium 

incorporation into the cranium and subsequent irradiation of adjacent brain tissue, should be explored. 
STRONTIUM 187 

3. HEALTH EFFECTS 

The toxicokinetic and bioavailability issues mentioned in the previous section on stable strontium apply 

to radioactive strontium. Low-level exposure studies should be conducted to evaluate possible 

impairment of immune function, which results from irradiation of bone marrow by radiostrontium 

incorporated into bone and which has been observed in animal studies at higher levels. 

Radioactive strontium is its own biomarker of exposure in children and adults. The primary biomarkers 

of effect, also applicable to children and adults, are a reduction in lymphocyte and other blood cell counts, 

which closely match the intensity of exposure. The alginate method for reducing peak absorption, 

described above, has been validated for children (Sutton et al. 1971a). It is not clear whether another 

recommended treatment, a single dose of aluminum phosphate antacid gel, would be safe for children, 

since it can have toxic effects in children at high doses. Either method would only be effective if 

administered very soon after exposure (within an hour). 

Data needs relating to both prenatal and childhood exposures and developmental effects expressed either 

prenatally or during childhood, are discussed in detail in the Developmental Toxicity subsection above. 

Child health data needs relating to exposure are discussed in 6.8.1 Identification of Data Needs: 

Exposures of Children. 

3.13.3 Ongoing Studies 

Stable Strontium. Two currently funded research programs that specifically mention stable strontium are 

probably using it as a surrogate for calcium in physiological experiments. In a study sponsored by the 

National Institute of Mental Health, Dr. J.A. Dzubay (1997) of the Oregon Health Sciences University is 

conducting in vitro experiments on the activity of NMDA (N-methyl D-aspartate) channels in the 

hippocampus; these are membrane channels controlled by NMDA receptors that regulate the influx of 

calcium into neurons. In work funded by the National Institute of Neurological Disorders and Stroke, Dr. 

David Lovinger (1999) of Vanderbilt University Medical Center is studying glutamatergic and 

dopaminergic synaptic transmission in the neostriatum. In a third study, sponsored by the National 

Institute of General Medical Sciences, Dr. J. Bell (1998) of Fayetteville State University in North 

Carolina is examining the effect of metal salts on the fidelity of DNA synthesis. It appears that this 

research may provide additional genotoxicity information regarding stable strontium. 
STRONTIUM 188 

3. HEALTH EFFECTS 

Radioactive Strontium. The single largest population available for studying the long-term health effects 

of radiostrontium is the Techa River cohort that was exposed from contaminated drinking water and food 

following releases from a plutonium processing plant between 1949 and 1956 (Akleyev et al. 1995; 

Bauchinger et al. 1998; Kossenko 1996; Kossenko et al. 1994, 1997, 2000; Shagina et al. 2000; Tolstykh 

et al. 1998). In addition to the studies reviewed in this toxicological profile, further analysis of this 

population is expected to continue under the auspices of the Urals Research Center for Radiation 

Medicine. 

Additional information regarding the toxicity of radioactive strontium is likely to emerge from studies 

related to the therapeutic use of strontium isotopes. In programs funded by the National Heart Lung and 

Blood Institute, Dr. Sou-Tung Chiu-Tsao (1999) of the Beth-Israel Medical Center, New York, and Dr. 

Ravinder Nath (1999) of Yale University Medical Center, are investigating 90Sr along with other isotopes 

for intravascular brachytherapy delivered at the time of angioplasty. Dr. Carl J. Pepine (1998) of the 

Department of Veterans Affairs Medical Center, Gainesville, Florida, is conducting a clinical trial to 

evaluate a commercial product for intravascular brachytherapy. Dr. Timothy Kuzel (1999) of the 

Department of Veterans Affairs Medical Center, Chicago, Illinois, is conducting a Phase I/II trial of 89Sr 

in conjunction with mitoxantrone and hydrocortisone in the treatment of bone metastases in patients with 

hormone-refractory prostate cancer. In work funded by the National Center of Research Resources, Dr. 

Franco Muggia (1999) of the New York University Medical Center is conducting an open label Phase II 

study to evaluate the effect and toxicity of Doxil, a liposomal encapsulated doxirubicin, and 89Sr in 

combination for treating hormone-refractory metastatic prostate cancer. In a study sponsored by the 

National Institute on Deafness and Other Communication Disorders, Dr. Gina M. Nelson (1999) of the 

University of Alabama at Birmingham is conducting laboratory tests in rodents in order to develop a 

radiation treatment for cancer of the mouth that will be less likely to destroy the sense of taste than 

current procedures. Radiostrontium will be held in a device to expose the tongue to beta radiation. 
STRONTIUM 189 

4. CHEMICAL, PHYSICAL, and RADIOLOGICAL INFORMATION 

4.1 CHEMICAL IDENTITY 

Strontium is an alkaline earth element in Group IIA of the periodic table. Because of its high reactivity, 

elemental (or metallic) strontium is not found in nature; it exists only as molecular compounds with other 

elements. The chemical information for elemental strontium and some of its compounds is listed in 

Table 4-1. Radioactive isotopes of strontium (e.g., 89Sr and 90Sr, see Section 4.2) are the primary cause of 

concern with regard to human health (see Chapter 3). 

4.2 PHYSICAL, CHEMICAL, AND RADIOLOGICAL PROPERTIES 

The physical properties of strontium metal and selected strontium compounds are listed in Table 4-2. The 

percent occurrence of strontium isotopes and the radiologic properties of strontium isotopes are listed in 

Table 4-3. 

Strontium can exist in two oxidation states: 0 and +2. Under normal environmental conditions, only the 

+2 oxidation state is stable enough to be of practical importance since it readily reacts with both water 

and oxygen (Cotton and Wilkenson 1980; Hibbins 1997). There are 26 isotopes of strontium, 4 of which 

occur naturally. The four stable isotopes, 84Sr, 86Sr, 87Sr, and 88Sr, are sometimes referred to as stable 

strontium. The most important radioactive isotopes, 89Sr and 90Sr, are formed during nuclear reactor 

operations and during nuclear explosions by the nuclear fission of 235U, 238U, or 239Pu. For example, 235U 

is split into smaller atomic mass fragments such as 90Sr by a nuclear chain reaction initiated by high 

energy neutrons of approximately 1 million electron volts (or 1 MeV). These smaller atomic mass 

fragments are referred to as fission by-products. This process is illustrated below: 

235U + 1

n 6 90Sr + 89Sr + other fission by-products 

90Sr is the more dangerous of the two isotopes due to its long half-life (29 years). 90Sr decays by emission 

of a beta-particle with a maximum energy of 0.546 MeV and the creation of an 90Y isotope, or progeny 

product. Unlike other radioactive isotopes that decay by beta-emission, 90Sr does not directly release high 

energy photons or gamma-ray radiation (γ). However, the progeny product of 90Sr, 90Y, is both a betaparticle (2.28 MeV maximum energy) emitter and to a minor degree for 0.02% of all disintegrations, a 
STRONTIUM 190 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-1. Chemical Identity of Strontium and Strontium Compounds 

Strontium Strontium Strontium Strontium 

Property Strontium (0) acetate carbonate chloride chromate 

Chemical formula Sr C4H6O4Sr CO3Sr Cl2Sr CrH2O4Sr 

Chemical structure Sr Sr(O2CCH3)2 SrCO3 SrCl2 SrCrO4 

O O O -

O
 

Sr+2
 Sr+2 O Cr OSr O- O Cl- Cl-

-

O OO- Sr+2 

Sr+2 

Synonyms None Strontium Carbonic acid, Strontium Chromic acid, 

diacetate strontium salt dichloride strontium salt 

(1:1); 

strontianite 

Trade names No data No data No data No data No data 

Identification numbers 

 CAS registry 7440-24-6 543-94-2 1633-05-2 10476-85-4 7789-06-2 

 NIOSH RTECS WK7849000 AJ4725000 No data WK8400000 GB3240000 

 EPA hazardous No data No data No data No data D007 

 waste 

OHM/TADS No data No data No data No data No data 

 DOT/UN/NA/IMO UN 1383/IMO No data No data No data 9149/NA 9149 

 shipping 4.2 

HSDB 2545 No data 5845 No data 2545 

NCI No data 75799 112224 No data No data 

STCC No data No data No data No data 49 633 77 
STRONTIUM 191 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-1. Chemical Identity of Strontium and Strontium Compounds 

Strontium Strontium Strontium Strontium Strontium 

Property fluoride hydroxide nitrate phosphate oxide 

Chemical formula F2Sr H2O2Sr N2O6Sr O8P2Sr3 OSr 

Chemical structure SrF2 Sr(OH)2 Sr(NO3)2 Sr3(PO4)2 SrO 

O 

O 

N+ P O -

O O -

O O

Sr+2 Sr+2 Sr+2
 

Sr+2 Sr+2 Sr+ Sr O F- F- OH- OH- -

O O

O N+ -

O 

O P 

O O 

Synonyms Strontium Strontium Nitrate de No data Strontia, 

difluoride hydrate strontium strontium 

(French); monoxide 

Nitric acid, 

strontium 

salt; 

strontium 

dinitrate; 

strontium(II) 

nitrate (1:2) 

Trade names No data No data No data No data No data 

Identification 

numbers

 CAS registry 7783-48-4 18480-07-4 10042-76-9 7446-28-8 1314-11-0

NIOSH WK8925000 WK9100000 WK9800000 No data No data

RTECS 

 EPA hazardous No data No data No data No data No data

 waste 

 OHM/TADS No data No data No data No data No data

 DOT/UN/NA/IMO No data No data UN 1507 No data No data

 shipping Oxidizer 

IMO 5.1 

HSDB
 No data No data No data No data No data

NCI
 No data No data No data No data No data

STCC
 No data No data 49 187 54 No data No data 

­

­

­

­

­

­
STRONTIUM 192 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-1. Chemical Identity of Strontium and Strontium Compounds 

Strontium Strontium Strontium Strontium 

Property peroxide sulfate sulfide titanate 

Chemical formula O2Sr O4SSr SSr O3SrTi 

Chemical structure SrO2 SrSO4 SrS SrTiO3 

O O 

Sr+2 

O S O- Ti 

Sr S -

O O- -

O OO- Sr+2 

Sr+2 

Synonyms Strontium Celestine, Strontium No data 

dioxide celestite monosulfide 

Trade names No data No data No data No data 

Identification numbers

 CAS registry
 1314-18-7 7759-02-6 1314-96-1 12060-59-2

 NIOSH RTECS
 WL0100000 No data WL0400000 No data

 EPA hazardous No data No data P107/D003 No data

 waste 

 OHM/TADS No data No data No data No data

 DOT/UN/NA/IMO UN 1509 No data No data No data

 shipping Oxidizer 

IMO 5.1 

HSDB
 788 No data 12 No data

NCI
 No data No data No data No data

STCC
 49 187 55 No data No data No data 

CAS = Chemical Abstracts Services; DOT/UN/NA/IMCO = Department of Transportation/United Nations/North 

America/International Maritime Dangerous Goods Code; EPA = Environmental Protection Agency; 

HSDB = Hazardous Substances 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; STCC = Standard Transportation Commercial Code 

Source: ChemFinder 2002; HSDB 2002; Lide 2000 
STRONTIUM 193 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Strontium and 

Strontium Compoundsa 

Property Strontium (0) 

Strontium 

acetateb,c 

Strontium 

carbonateb,c 

Strontium 

chloridec 

Strontium 

chromate 

Molecular weight, 87.62 205.71 147.63 158.53 203.62 

g/mole 

Color Pale yellow White White White Yellow 

Physical state 

Melting point 

Solid 

777 °C 

Solid 

Decomposes 

Solid 

1,497 °Cd 

Solid 

875 °C 

Solid 

No data 

Boiling point 1,382 °C Not applicable Decomposes at 1,250 °C No data 

Density, g/cm3 2.64 2.099 

1,100 °C 

3.5 3.05 3.90 

Odor No data No data Odorless No data No data 

Odor threshold:

 Water No data No data No data No data No data

 Air No data No data No data No data No data 

Solubility:

 Water Decomposes 369 g/L (cold) 0.11 g/L at 538 g/L 30 g/L at 

18 °C at 20 °C 100 °C

 Organic Alcohol Alcohol, No data Alcohol, Acetic acid 

 solvents(s) slightly acetone 

Partition 

coefficients:

 Log Kow No data No data No data No data No data

 Log Koc No data No data No data No data No data 

Vapor pressure 5 mmHg No data No data No data No data 

at 847 °C 

Henry’s Law No data No data No data No data No data 

constant 

Autoignition No data No data No data No data No data 

temperature 

Flashpoint No data No data No data No data No data 

Flammability limits No data No data No data No data No data 

Explosive limits No data No data No data No data No data 
STRONTIUM 194 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Strontium and 

Strontium Compoundsa 

Property 

Strontium 

fluoridee,c 

Strontium 

hydroxidec 

Strontium 

nitratec 

Strontium 

phosphatef 

Strontium 

oxidec 

Molecular weight, 

g/mole 

Color 

Physical state 

Melting point 

Boiling point 

Density, g/cm3 

Odor 

Odor threshold:

125.62 

White 

Solid 

Decomposes 

>100 °C 

2,489 °C 

4.24 

No data 

121.64 

Colorless 

Solid 

375 °C 

No data 

3.63 

No data 

211.63 

Colorless 

Solid 

570 °C 

645 °C 

2.98 

Odorless 

452.80 

White 

Solid 

No data 

No data 

No data 

No data 

103.62 

Yellow 

Solid 

2,430 °C 

3,000 °C 

4.56 

No data 

 Water 

Air 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data

No data 

Solubility:

 Water 

 Organic 

 solvents(s) 

0.12 g/L 

at 18 °C 

Alcohol, acetone 

470 g/L 

at 100 °C 

Alcohol 

790 g/L 

at 18 °C 

Slightly in 

alcohol and 

acetone 

Insoluble 

No data 

229 g/L 

at 100 °C 

Slightly in 

alcohol 

Partition 

coefficients:

 Log Kow 

 Log Koc 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data

No data 

Vapor pressure 

Henry’s Law 

constant 

1 mmHg 

at 921 °C 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

Autoignition 

temperature 

No data No data No data No data No data 

Flashpoint 

Flammability limits 

Explosive limits 

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 

No data 

No data 
STRONTIUM 195 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Strontium and 

Strontium Compoundsa
 

Strontium Strontium Strontium Strontium 

Property peroxide sulfate sulfide titanate 

Molecular weight, 119.63 183.68 119.70 183.52 

g/mole 

Color White Colorless Gray White 

Physical state Solid Solid Solid Solid 

Melting point Decomposes at 1,605 °C >2,000 °C No data 

215 °C 

Boiling point No applicable No data No data No data 

Density, g/cm3 4.56 3.96 3.70 4.810 

Odor Odorless No data Hydrogen No data 

sulfide in moist 

air 

Odor threshold:

 Water Not applicable No data No data No data

 Air Not applicable No data No data No data 

Solubility:

 Water Decomposes 0.14g/L at Decomposes Insoluble

30 °C 

 Organic Alcohol Slightly in No data No data 

 solvents(s) alcohol 

Partition 

coefficients:

 Log Kow No data No data No data No data

 Log Koc No data No data No data No data 

Vapor pressure No data No data No data No data 

Henry’s Law No data No data No data No data 

constant 

Autoignition No data No data No data No data 

temperature 

Flashpoint No data No data No data No data 

Flammability limits No data No data No data No data 

Explosive limits No data No data No data No data 

a

Source: HSDB 2002, unless otherwise stated 

b

Merck 1989 

c

Lide 1995 

d

At 69 atmospheres pressure 

e

Sigma-Aldrich 2000 

f

Lide 2000 
STRONTIUM 196 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-3. Percent Natural Occurrence and Radioactive Properties 

of Isotopes of Strontium 

Natural 

CAS registry abundance Beta energies, 

Isotope number (by weight %) MeV Half-life Activity, Ci/gram 

84Sr 15758-49-3 0.56 No data Stable No data 

85Sr 13967-73-2 No data 1.065a 65 days 35,400 

86Sr 13982-14-4 9.86 No data Stable No data 

87Sr 13982-64-4 7.00 No data Stable No data 

88Sr 14119-10-9 82.58 No data Stable No data 

89Sr 14158-27-1 No data 1.495 51 days 27,800 

90Sr 10098-97-2 No data 0.546 29 years 143 

91Sr 14331-91-0 No data 2.707 10 hours 3.4x106 

92Sr 14928-29-1 No data 1.911 3 hours 1.1x107 

a

Decay mechanism by electron capture with gamma emission 

Source: Lide 1995 
6

STRONTIUM	 197 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

beta-particle and gamma-ray (2.19 keV) emitter. The decay product of 90Y is 90Zr, a stable isotope. The 

reaction is: 

90Sr (t1⁄2=29 yrs) 6 90Y (t1⁄2=64 hrs) + β-

(0.546MeV) 6	 90Zr (stable) + β-

(2.28 MeV) (99.98 %)
 

90Zr (stable) + β-

(0.523 MeV) + γ(1.75 MeV) 

89Sr, like 90Sr, is a fission product of 235U, 238U, or 239Pu. It decays to 89Y by emission of a beta-particle of 

1.495 MeV 89Y. 89Sr has half-life of 51 days (Lide 1995). 

STRONTIUM 199 

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

5.1 PRODUCTION 

Strontium is a naturally occurring element that makes up approximately 0.02–0.03% of the earth’s crust. 

In nature, strontium is present in igneous rocks in amounts averaging 375 ppm. The principal strontium 

minerals of commercial interest are celestite (SrSO4) and strontianite (SrCO3). Strontium is also a minor 

component of other mineral deposits and may occur in or near sedimentary rocks associated with beds or 

lenses of gypsum, anhydrite, and rock salt; in veins associated with limestone and dolomite; or dispersed 

in shales, marls, and sandstones. In the United States, there are deposits of celestite in Texas, 

Washington, Arizona, Ohio, and California. The U.S. Geological Survey (USGS) estimated U.S. 

resources of celestite and strontianite at 2,500,000 tons, containing 1,130,000 tons of strontium (Adams 

1975). However, domestic deposits of these minerals are not economically exploitable, and strontium has 

not been mined in the United States since 1959. 

Celestite is converted to SrCO3, the common commercial form of strontium. The black ash method 

(alternatively known as the calcining method) and the soda method (also known as direct conversion) are 

the two most common recovery techniques for strontium. The black ash method produces chemical grade 

strontium carbonates, which are 98% strontium carbonate and 2% byproducts and impurities. The soda 

ash method produces technical grade strontium carbonates, containing at least 97% strontium carbonate. 

The black ash method is the preferred means of strontium carbonate production because it yields a highergrade product (USGS 1998). 

During World War II, the U.S. government began stockpiling celestite for defense applications. In 1963, 

Congress determined that the stockpile was unnecessary, and by 1973, all of the stockpiled high-grade 

celestite was sold. The remaining low-grade celestite material, approximately 12,000 metric tons, has 

been listed by the Defense National Stockpile Center of the Defense Logistics Agency as valueless. In 

1998, Congress authorized the remaining stockpile for disposal. The only U.S. strontium carbonate 

producer using celestite is the Chemical Products Corporation of Cartersville, Georgia. A number of U.S. 

companies manufacture strontium compounds from strontium carbonate. Mallinkrodt Inc. of St. Louis, 

Missouri, produces strontium chloride, and Rockwood Pigments Corporation of Beltsville, Maryland, 

produces strontium chromate. Production of other strontium compounds is on a limited scale (USGS 

1998, 1999). 
STRONTIUM 200 

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

Radioactive strontium, or 89Sr and 90Sr, does not occur in nature. It is the direct result of anthropogenic 

activity. As discussed in Chapter 4, 89Sr and 90Sr are produced by nuclear fission. Nearly all of the 90Sr 

generated in the United States is present in spent nuclear reactor fuel rods. These fuel rods are currently 

located at the commercial reactor facilities or at Department of Energy (DOE) facilities across the United 

States. After 1 year of decay of nuclear fuel rods, 90Sr represents 3.7% by mass of the total fission 

product inventory. A limited amount of 89Sr and 90Sr is produced for industrial, scientific, and medicinal 

applications through the process of fission product recovery. During the period of 1974–1984, 90Sr was 

recovered and converted into solid forms. Typically, 90Sr is combined with fluorine to produce strontium 

fluoride (90SrF2) or with chlorine (Cl2) to produce strontium chloride (90SrCl2). These solids were placed 

in double walled capsules to be used for commercial and medical applications. 90Sr is available from 

Pacific Northwest National Laboratory located at the DOE facility in Hanford, Washington. The Hanford 

inventory of 90Sr embodies one of the largest sources of this nuclide in the world (DOE 1996b, 1996c). 

5.2 IMPORT/EXPORT 

In 2001, 100% of celestite used in the United States was imported from Mexico. Of the 38,500 metric 

tons of strontium minerals and compounds imported in 2001, approximately 94% were imported from 

Mexico, 6% from Germany, and 2% from other countries. From the period of 1954–1974, demand for 

strontium imports (both mineral and compound) has steadily increased from approximately 3,200 to 

16,000 metric tons. From 1994 to 2001, the importation of strontium minerals and compounds for 

consumption has remained relatively steady at approximately 31,000–38,500 metric tons. The apparent 

consumption of all strontium imports in the United States is 97%. The total export volume of strontium 

compounds during 1993–2001 was more than 20 times lower than the quantities of strontium minerals 

and compounds imported during the same period. Exports of strontium compounds has varied from 

1,120 metric tons in 1994 to 1,040 metric tons in 2001 (USGS 1998, 1999, 2002). 

5.3 USE 

In 2001, more than 85% of all strontium consumed in the United States was used in the manufacture of 

ceramics and glass products, primarily in television faceplate glass and secondarily in ceramic ferrite 

magnets (strontium ferrite) and other ceramic and glass applications. All color televisions and other 

devices containing cathode-ray tubes (CRT) sold in the United States are required by law to contain 
STRONTIUM 201 

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

strontium in the faceplate glass of the picture tube to block x-ray emissions. Major manufacturers of 

television picture tube glass incorporate about 8% by weight of strontium oxide (SrO) into the glass 

faceplate material. Strontium is added to the glass melt in the form of strontium carbonate. Upon heating 

and solidification, it is transformed to SrO. Other uses for strontium compounds include pyrotechnics 

(strontium nitrate), paint pigments (strontium chromate), fluorescent lights (strontium phosphate), getters 

in zinc production (strontium carbonate), alloy (strontium metal), and medicines (strontium chloride, 

strontium peroxide). Strontium metal has limited commercial use. One minor use of strontium is as an 

alloy material for the production of aluminum castings. Most commercial uses of strontium compounds 

and products use strontium carbonate as the feed material (Hibbins 1997; USGS 1999, 2002). 

The radioactive isotope 89Sr (also known by the pharmaceutical brand name MetastronTM) is used as a 

cancer therapeutic to alleviate bone pain. 85Sr has been used in medical applications, such as radiologic 

imagining of bones, in minor commercial applications, such in radioisotope thermoelectric generators 

(RTG), as a beta-particle standard source, and in instruments that measure thickness and density of 

materials (Murray 1994). 90Sr has been used in RTGs at remote locations (e.g., lighthouses) throughout 

the former Soviet Union (Alimov 2003). Many of these 90Sr RTGs in the former Soviet Union are 

completely unguarded against potential thieves or intruders, lacking such minimal security measures as 

fences or even signs warning of radioactive dangers. The biggest danger coming from these unprotected 

RTGs is their availability to terrorists who can use the radioactive materials (e.g., 90Sr) contained in them 

to make so-called “dirty bombs”, which are bombs that are triggered by standard explosives, but disperse 

radioactivity. 

5.4 DISPOSAL 

Most nonradioactive strontium minerals, strontium compounds, and strontium-containing materials do not 

require special disposal and handling requirements. However, some chemical forms may be classified as 

hazardous materials if the compound is chemically reactive, flammable, or toxic. Care should be taken to 

read and understand all of the hazards, precautions, and safety procedures for each specific chemical 

form. In addition, all federal, state, and local laws and regulations should be investigated and 

subsequently followed with regard to disposal and handling of the specific chemical form of the strontium 

compound or material. 

Radioactive strontium does require special disposal and handling requirements and is regulated by the 

Nuclear Regulatory Commission (USNRC). Radioactive waste-containing radioactive strontium can be 
STRONTIUM 202 

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

grouped into three categories: low-level waste (LLW); high-level waste (HLW) and spent nuclear fuel; 

and mixed waste. As defined by the Nuclear Waste Policy Act, high-level radioactive waste is “the 

highly radioactive material resulting from the reprocessing of spent nuclear fuel, including liquid waste 

produced directly in reprocessing and any solid material derived from such liquid waste that contains 

fission products in sufficient concentration.” However, most classifications of HLW also include spent 

nuclear fuel. Most HLW was generated from the production of plutonium. A small fraction is related to 

the recovery of enriched uranium from naval reactor fuel. This waste typically contains highly 

radioactive, short-lived high activity fission by-products as well as other long-lived isotopes, hazardous 

chemicals, and toxic heavy metals. 90Sr contamination is only a small fraction of the activity of HLW. 

Liquid HLW is typically stored in large underground tanks of either stainless steel or carbon steel, 

depending on whether they are acid or alkaline solutions. There are about 100 million gallons of highlevel liquid waste stored in underground tanks in Washington, South Carolina, Idaho, and New York. 

These tanks contain a variety of radioactive liquids, solids, and sludges. Some of the liquid wastes have 

been solidified into glass, ceramic slag, salt cakes, and sludges (DOE 1996a; Murray 1994). 

Spent nuclear fuels, such as fuel elements and irradiated targets used in nuclear reactors, are currently 

disposed of at the commercial nuclear power plants and DOE facilities where they were produced. Spent 

fuel is highly radioactive due to the large concentration of fission products and must be stored in special 

water-cooled pools that shield and cool the material. Most of the 90Sr remains trapped in the spent fuel 

rod matrix and is never released. Roughly all DOE spent fuel, about 3,000 metric tons, is stored at four 

sites: Hanford, Savannah River, Idaho National Engineering Laboratory, and West Valley, New York. 

Commercial reactors have generated more than 30,000 metric tons of spent fuel. The spent fuel from 

these facilities is stored at the more than 100 commercial nuclear reactor sites around the United States. 

The establishment of an HLW and spent fuel repository for both DOE and commercial waste is currently 

under evaluation at Yucca Flats, Nevada. It is not projected to be in operation until after the year 2010 

(DOE 1996b; Eisenbud 1987; Murray 1994). 

Mixed waste contains both radioactive and chemically hazardous materials such as toxic, corrosive, 

flammable, or explosive materials. The radioactive component may be either HLW or LLW. All liquid 

HLW is mixed waste, usually in the presence of organic solvents or heavy metals in addition to 

radioactive components. Disposal of mixed wastes is regulated by EPA under the Resource Conservation 

and Recovery Act (RCRA) and by the USNRC under the Atomic Energy Act. EPA and USNRC have 

developed special procedures on how to handle and dispose of this special category. DOE operates an 

incinerator in Oak Ridge, Tennessee that burns mixed hazardous radioactive wastes (DOE 1996a). 
STRONTIUM 203 

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

Low-level waste is all radioactive waste that cannot be classified as HLW, spent fuel, or mixed waste. 

Low-level does not necessarily mean low radioactivity or low environmental hazards. However, the bulk 

of LLW has relatively little radioactivity and practically no transuranic elements. Thus, LLW usually 

does not require shielding from radioactivity or heat removal equipment. Most LLW is acceptable for 

near-surface land disposal. LLW types that may be contaminated with 90Sr include both wet and dry 

wastes. Examples of the physical form of LLW are spent ion exchange resins, filter sludges, filter 

cartridges, evaporator bottoms, compactable trash, non-compactable trash, irradiated components, ashes 

produced from the incineration of combustible material, contaminated detergents or solvents, organic 

liquids, and discarded contaminated equipment or tools. Of the LLW generated today, approximately 

64% of the volume and 70% of the radioactivity are generated as a result of nuclear power plant activities 

or supporting fuel cycle operations. Other sources of LLW are industrial, academic, government, and 

medical. Radiostrontium contamination accounts for only a small fraction of the activity of LLW. LLW 

is typically packaged in drums or boxes and buried in shallow pits or trenches. Approximately 3 million 

cubic meters of LLW generated in the United States have been disposed of this way. LLW from DOE 

sources is currently disposed of at several DOE facilities across the United States. Only two sites accept 

non-DOE LLW, Barnwell, South Carolina and Richland, Washington. Over half of the LLW in the 

eastern United States is disposed of at the Barnwell site. As required by the Federal LLRW (Low Level 

Radioactive Waste) Policy Act in 1980 and in the 1985 amendments, states or interstate compacts are 

required to build facilities to contain LLW generated from sources within their boundaries. However, 

other than Barnwell, South Carolina and Richland, Washington sites, no other facility in the United States 

is currently accepting LLW from non-DOE sources. Currently, many generators store LLW on-site until 

additional facilities can be constructed in the future (DOE 1996a; Eisenbud 1987; Murray 1994). 

STRONTIUM 205 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.1 OVERVIEW 

Strontium and 90Sr have been identified in at least 102 and 12, respectively, of the 1,636 hazardous waste 

sites that have been proposed for inclusion on the EPA National Priorities List (NPL) (HazDat 2003). 

However, the number of sites evaluated for strontium and strontium-90 are not known. The frequency of 

these sites can be seen in Figures 6-1 and 6-2, respectively. Of these sites, all are located within the 

United States and none are located in the Commonwealth of Puerto Rico. 

Strontium is widely distributed in the earth’s crust and oceans. Strontium is released into the atmosphere 

primarily as a result of natural sources, such as entrainment of dust particles and resuspension of soil. 

Radioactive strontium is released into the environment as a direct result of anthropogenic activities. 

Stable strontium can neither be created nor destroyed. However, strontium compounds may transform 

into other chemical compounds. Radioactive strontium is formed by nuclear reactions. Radioactive 

decay is the only mechanism for decreasing the concentration of radiostrontium. The half-life of 90Sr is 

29 years. Eventually, all of the radioactive strontium will be converted to stable zirconium (see 

Section 4.2). 

Strontium present in the atmosphere is in the form of wet or dry aerosols. The principal chemical species 

in the air is strontium oxide (SrO). Strontium oxide will react rapidly in the presence of moisture to form 

Sr+2 and SrOH+

 ions. Strontium is dispersed by atmospheric cycling and is subsequently deposited by wet 

deposition on the earth’s surface. In surface water and groundwater, strontium exists primarily as a 

hydrated ion. Strontium can form ionic complexes with other inorganic or organic substances. Strontium 

is relatively mobile in water. However, the formation of insoluble complexes or sorption of strontium to 

soils can reduce its mobility in water. Strontium sorbs to soils by ion exchange, and tends to be more 

mobile in soils with a high concentration of exchangeable ions or in soils with low cation exchange 

capacities. Strontium is taken up and retained by aquatic and terrestrial plants and is concentrated in the 

boney tissues of animals that eat contaminated vegetation. The average concentration of strontium in 

urban air is 20 ng/m3

 (Dzubay and Stevens 1975). The concentration of 90Sr in the atmosphere has 

steadily decreased since its maximum concentration in 1963. The mean concentration of strontium in 

U.S. surface water is <1 mg/L. Dissolved strontium has been detected in groundwater and surface water 

used for drinking water supplies with average concentrations of 0.81 and 1.1 mg/L, respectively (EPA 
STRONTIUM 206 

6. POTENTIAL FOR HUMAN EXPOSURE 

Figure 6-1. Frequency of NPL Sites with Strontium Contamination 

Frequency of 

NPL Sites

Derived from HazDat 2003 

2 

3 

5 

6 

8 

10 
STRONTIUM 207 

6. POTENTIAL FOR HUMAN EXPOSURE 

Figure 6-2. Frequency of NPL Sites with Strontium-90 Contamination 

Frequency of 

NPL Sites

1
 

2
 

3
 

Derived from HazDat 2003
 
STRONTIUM 208 

6. POTENTIAL FOR HUMAN EXPOSURE 

2002b). The median concentration of 90Sr in drinking water for 1995 was 0.1 pCi/L (3.7 mBq/L). Human 

exposure to strontium and radiostrontium can result from consumption of food, drinking water, or 

incidental ingestion of soil or dust contaminated with strontium. Food and drinking water are the largest 

sources of exposure to strontium and radiostrontium. Grain, leafy vegetables, and dairy products 

contribute the greatest percentage of dietary strontium and radiostrontium to humans. 

6.2 RELEASES TO THE ENVIRONMENT 

The TRI data should be used with caution because only certain types of facilities are required to report. 

This is not an exhaustive list. 

6.2.1 Air 

Strontium naturally occurs in the earth’s crust and is released into the atmosphere as a result of natural 

processes such as entrainment of dust particles, resuspension of soil by wind, and sea spray. Entrainment 

of soil and dust particles with significant concentrations of strontium would be most significant in areas 

with higher soil strontium concentrations. Coastal regions have higher concentrations of strontium due to 

sea spray (Capo et al. 1998). Human activities, including milling and processing of strontium 

compounds, burning of coal, land application of phosphate fertilizers, and using pyrotechnic devices, 

release strontium into the atmosphere (Lee and von Lehmden 1973; Ondov et al. 1989; Perry 1999; Que 

Hee et al. 1982; Raven and Loeppert 1997). The effect of these activities is illustrated by the deposition 

rates of strontium measured in peat cores of northern Indiana. Deposition has increased by a factor of 

7 from 8.1 mg strontium/m2

/year in presettlement times (1339–1656) to 57.0 mg strontium/m2/year 

between 1970 and 1973 (Cole et al. 1990). 

Strontium discharged into the atmosphere from the operation of coal fired power plants depends on the 

strontium concentration in coal, the amount of coal burned, and the efficiency of fly ash recovery. 

Approximately 90% of coal mass is consumed during the combustion process, leaving 10% as a residual 

nonvolatile material (fly ash) containing 100–4,000 ppm (or mg/kg) of strontium (Furr et al. 1977). 

Atmospheric concentrations of strontium emitted from coal fired power plants have been found to range 

from 17 to 2,718 μg/m3

 in the western United States and are approximately 9,786 μg/m3 in the eastern 

United States (Ondov et al. 1989; Que Hee et al. 1982). Phosphate fertilizers are known to contain 

between 20 and 4,000 μg strontium/g solid by weight (Lee and von Lehmden 1973; Raven and Loeppert 
STRONTIUM 209 

6. POTENTIAL FOR HUMAN EXPOSURE 

1997). Strontium can be released into the atmosphere in windblown soil to which phosphate fertilizers 

have been applied. Pyrotechnic displays release low levels of strontium on the order of 9 ng/m3

 in the 

immediate environment of the display (Perry 1999). 

Strontium has been identified in air at 9 sites collected from the 102 NPL hazardous waste sites where it 

was detected in some environmental media (HazDat 2003). 

Radioactive strontium (e.g., 90Sr) was released into the atmosphere from aboveground testing of nuclear 

weapons during the period of 1945–1980. Nuclear weapon testing injects radioactive material into the 

stratosphere, which results in wide dispersal of radionuclides. However, atmospheric deposition of 90Sr 

has steadily decreased from a high in 1963 of approximately 1.10x108

 GBq (3.0 MCi) to <3,000 Ci in 

1990, which suggests that global concentrations of 90Sr in the atmosphere have declined (DOE 1996c). 

Other sources of regional contamination from radiostrontium include large-scale nuclear power plant 

accidents such as the Chernobyl disaster in the Ukraine (April 1986), which resulted in releases of about 

2.2 MCi (8.1x107

 GBq) of 89Sr and 0.22 MCi (8.1x106 GBq) of 90Sr into the atmosphere (Eisenbud 1987). 

However, although some 90Sr reached the upper atmosphere and was subsequently transported around the 

world, most of the radiostrontium was deposited as regional fallout in eastern Europe (Eisenbud 1987). 

Routine releases of radiostrontium in 1993 from the operation of nuclear power plants around the United 

States are summarized in Table 6-1 (USNRC 1993a). In 1993, releases of radiostrontium (i.e., 89Sr, 90Sr, 

and 91Sr) for boiling water reactors (BWR) and pressurized water reactors (PWR) (the two common 

designs of nuclear reactors in the United States) were 72.1 and 3.3 mCi (2.67 and 0.12 GBq), 

respectively. The total annual releases of radiostrontium from nuclear power plants in the United States 

(75.4 mCi or 2.79 GBq) are insignificant compared to releases of 90Sr from the testing of nuclear 

weapons. In the former Soviet Union between the years 1949 and 1956, large-scale environmental 

contamination occurred in the region surrounding the Mayak plutonium production complex in the Ural 

region of Russia (Eisenbud and Gesell 1997). Releases of radioactive liquid wastes into the Techa River, 

both planned and accidental, of about 1017 Bq (2.7 MCi) resulted. 90Sr contributed about 12% (or 

0.23 MCi) to the total activity released (Tokareva et al. 2000). Other minor releases of 90Sr have involved 

accidents with rockets or satellites that have disintegrated in the atmosphere. The Soviet satellite 

Cosmos 954 powered by a plutonium fueled nuclear reactor released 3.1x103

 GBq (83 Ci) of 90Sr to the 

regional atmosphere in northern Canada in 1978 (Eisenbud 1987). The Department of Energy (DOE) and 

its predecessor agencies have been involved in operations that have released radiostrontium into the 

atmosphere. Over the 43-year operating period at the DOE Savannah River Site in South Carolina, about 

1.1x102

 GBq (3 Ci) of 90Sr were released into the atmosphere, primarily from the chemical separation and 
STRONTIUM 210 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-1. Radiostrontium Releases from Nuclear Power Plants for 1993 

Annual total site environmental releases for 1993 

Water Air 

Installation Locationa 89Sr, 90Sr, 91Sr, 92Sr, mCi 89Sr, mCi 90Sr, 91Sr, 

mCi mCi mCi mCi mCi 

Boiling Water Reactors

 Browns Ferryb Decatur, AL 41.1 2.05 No data 0.40 0.19 No data No data

 Brunswickb

 Wilmington, No data No data No data 0.0062 0.099 0.0027 No data 

NC 

Clinton Clinton, IL No data No data No data No data 0.06 No data No data

 Cooper Omaha, NE 4.69 15.8 No data 0.082 No data No data No data

 Dresdenb Joliet, IL 0.056 0.085 No data No data 0.67 0.004 No data 

Duane Arnold Cedar Rapids, No data No data No data No data 0.018 0.0009 No data 

IA 

Edwin I. Hatch Baxley, GA 6.29 0.43 5.20 0.65 12.0 0.24 No data

 Fermi Laguna 0.19 No data No data No data 0.14 0.0003 4.0 

Beach, MI 

Grand Gulf Vicksburg, MS 0.32 0.29 No data No data 0.003 0.002 No data

 Hope Creek Wilmington, No data No data No data No data No data No data No data

DE 

 Humbolt Bayb Eureka, CA No data 36.5 No data No data No data 0.002 No data

 James A. Syracuse, NY 0.44 No data No data No data 0.045 7.3x10-7 No data

Fitzpatrick 

 LaCrosseb

 LaCross, WI No data 0.28 No data No data No data 0.0003 No data 

LaSalle Ottawa, IL No data No data No data No data No data No data No data

 Limerick Phildelphia, 20.0 0.44 No data No data 16.4 0.31 No data

PA 

Millstone New London, 3.30 0.15 No data 0.55 0.22 0.0006 No data 

CT 

Monticello St.Cloud, MN No data No data No data No data 0.59 0.003 No data 

Nine Mile Point Oswego, NY <0.0001 No data No data No data 5.90 0.004 No data 

Oyster Creek Toms River, No data No data No data No data 1.17 0.014 No data 

NJ 

Peach Bottom Lancaster. PA 0.19 0.056 No data No data 4.9 0.021 3.76

 Perry Painesville, 0.22 0.008 No data No data 1.8 0.009 4.87

OH 

Pilgram Boston, MA 1.63 0.086 No data No data 5.8 0.024 No data 

Quad-Cites Moline, IL 0.050 0.018 No data 0.12 0.61 0.0014 No data 

River Bend Baton Rouge, 5.3 0.31 No data No data 0.30 0.0095 No data

LA 

 Shoreham Brookhaven, 0.025 No data No data No data No data No data No data 

NY 

Susquehanna Berwick, PA 0.0088 No data No data 0.0011 0.0003 No data No data

 Vermont Yankee Brattleboro, No data No data No data No data 2.83 0.054 No data 

VT 

WNP-2 Richland, WA 0.55 0.057 No data No data 3.5 0.012 1.61 
STRONTIUM 211 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-1. Radiostrontium Releases from Nuclear Power Plants for 1993 

Annual total site environmental releases for 1993 

Water Air 

Installation Locationa 89Sr, 90Sr, 91Sr, 92Sr, mCi 89Sr, mCi 90Sr, 91Sr, 

mCi mCi mCi mCi mCi 

Total 84.4 56.6 5.20 1.81 57.2 0.72 14.2 

Pressurized Water Reactors 

 Arkansas One Russellville, 2.81 1.17 No data 0.59 0.000955 No data No data

AR 

 Beaver Valley Shippingport, No data No data No data 0.08 No data No data No data 

PA 

Big Rock Point Charlevoix, MI 0.02 0.17 No data No data 0.21 0.006 2.73 

Braidwood Joliet, IL 3.68 158.4 No data 0.017 No data No data No data

 Byron Byron, IL 152.4 0.56 No data No data No data No data No data 

Callaway Fulton, MO 17.6 1.12 No data No data 0.004 No data No data

 Calvert Cliffs Washington, 0.83 0.37 No data No data No data No data No data 

DC 

Catawaba Rock Hill, SC No data No data No data 0.41 No data No data No data 

Comache Peak Glen Rose, TX No data No data No data 0.029 No data No data No data 

Crystal River Tampa, FL 3.03 10.2 No data 3.57 0.001 0.001 No data 

Davis-Besse Toledo, OH No data No data No data No data No data No data No data 

Diablo Canyon San Luis 0.16 0.057 No data 0.003 No data No data No data 

Obispo, CA 

Donald C. Cook St. Joseph, MI No data 0.029 No data No data 0.080 0.0005 No data

 Fort Calhoun Omaha, NE 0.61 0.77 No data No data No data 0.0007 No data 

H.B. Robinson Hartsville, SC No data No data No data No data No data No data No data

 Haddam Neck Middletown, 0.076 1.52 No data No data 0.0002 0.0002 No data

CT 

 Harrisb Raleigh, NC No data No data No data No data No data No data No data

 Indian Pointb Peekskill, NY 0.077 0.007 No data No data No data No data No data

 Joseph M. Dothan, AL No data 0.028 No data 0.10 No data No data No data 

Farley 

Kewaunee Green Bay, WI 0.92 0.051 No data No data No data No data No data 

Maine Yankee Wicassett, ME 0.15 No data No data No data No data No data No data 

McGuire Charlotte, NC 0.20 No data No data No data No data No data No data

 North Annac

 NW No data No data No data No data No data No data No data 

Richmond, VA 

Oconee Greenville, SC No data No data No data No data No data No data No data

 Palisades South Haven, 0.003 0.012 No data No data 0.011 0.0042 No data 

MI 

Palo Verde Phoenix, AZ No data No data No data No data 0.19 0.0009 No data

 Point Beach Manitowoc, WI 0.012 0.11 0.0052 No data No data 0.0001 No data

 Prairie Island Minneapolis, No data No data No data 0.029 0.0006 0.0003 No data 

MN 

R.E. Ginna Rochester, NY 0.30 0.090 No data No data No data No data No data 
STRONTIUM 212 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-1. Radiostrontium Releases from Nuclear Power Plants for 1993 

Annual total site environmental releases for 1993 

Water Air 

Installation Locationa 89Sr, 90Sr, 91Sr, 92Sr, mCi 89Sr, mCi 90Sr, 91Sr, 

mCi mCi mCi mCi mCi 

 Rancho Secob Sacramento, No data 0.0013 No data No data No data No data No data

CA 

 San Onofreb

 San Clemente, 4.26 0.36 No data 0.48 No data No data No data

CA 

 Seabrook Portsmouth, No data No data No data No data No data No data No data

NH 

Sequoyah Daisy, TN 0.35 0.29 0.023 0.54 No data No data No data 

South Texas Bay City, TX No data No data No data No data No data No data No data 

St. Lucie Ft. Pierce, FL 1.21 1.83 No data No data No data 0.0012 No data 

Summer Columbia, SC 0.0007 0.021 No data No data No data No data No data

 Surry Newport No data No data No data No data No data No data No data

News, VA 

 Three Mile Harrisburg, PA 0.034 0.83 No data No data No data 0.0003 No data

Islandb 

 Trojanb Portland, OR 0.24 0.029 No data No data No data No data No data

 Turkey Pointb

 Florida City, 12.7 3.55 No data No data No data No data No data

FL 

Vogtle Augusta, GA 1.64 0.19 No data No data 0.0025 0.0003 No data

 Waterford New Orleans, No data No data No data 0.23 No data No data No data 

LA 

Wolf Creek Burlington, KS No data 0.092 0.0087 No data No data No data No data

 Yankee Roweb Greenfield, MA No data No data No data No data No data No data No data 

Zion Waukegan, IL No data No data No data 5.93 No data No data No data 

Total 207.1 182.8 0.04 11.5 0.50 0.02 2.73 

a

Post office state abbreviations used 

b

Facilities that are permanently or indefinitely shut down c

Air 85Sr 8.17x106 

Source: NRC 1993b 
STRONTIUM 213 

6. POTENTIAL FOR HUMAN EXPOSURE 

reprocessing of nuclear fuel (Carlton et al. 1998, 1999). Between 1944 and 1972, about 64 Ci 

(2.4x103

 GBq) of 90Sr and 700 Ci (2.6x104 GBq) of 89Sr was released into the atmosphere at the DOE 

Hanford site in Washington state from the routine operation of chemical plants used to separate plutonium 

from spent reactor fuel (CDC 1994). 

90Sr has been identified in air at 3 sites collected from the 12 NPL hazardous waste sites where it was 

detected in some environmental media (HazDat 2003). 

6.2.2 Water 

Releases of strontium to surface water and groundwater results from the natural weathering of rocks and 

soils and from the discharge of waste water directly into streams and aquifers. Intentional and 

unintentional releases of radioactive strontium directly into streams have occurred at DOE sites across the 

country. Over the period of 1954–1989, about 104 Ci (3.8x103

 GBq) of 90Sr and 216 Ci (8.0x103 GBq) of 

89Sr were released to streams in the vicinity of the Savannah River Site (Carlton et al. 1998; Cummins et 

al. 1991). During the period from 1952 to 1991, >129 Ci of 90Sr in waste water was discharged into pits, 

wells, and infiltration ponds at the Idaho Chemical Processing Plant in Idaho, some of which may have 

found its way into surface or groundwater (Bartholomay et al. 1995). Minor releases of radioactive 

strontium to water occur annually from nuclear power plants. Table 6-1 summarizes the releases of 

radioactive strontium from nuclear power plants into surface waters in 1993 (USNRC 1993a). Releases 

of radiostrontium (i.e., 89Sr, 90Sr, 91Sr, and 92Sr) into surface waters in 1993 from BWR and PWR were 

146.2 mCi (5.41 GBq) and 401.4 mCi (14.9 GBq), respectively. 

Strontium has been identified in surface water and groundwater at 25 and 55 sites, respectively, collected 

from the 102 NPL hazardous waste sites where it was detected in some environmental media. 90Sr has 

been identified in surface water and groundwater at 3 and 7 sites, respectively, collected from the 12 NPL 

hazardous waste sites where it was detected in some environmental media (HazDat 2003). 

6.2.3 Soil 

Strontium is ubiquitous in the environment and is present in nearly all rocks and soils. It is released to 

land in solid waste and from the use of phosphate fertilizers. 90Sr is found in nearly all soils in the United 

States. 90Sr that is deposited at a specific site varies widely, depending primarily on rainfall. Intentional 
STRONTIUM 214 

6. POTENTIAL FOR HUMAN EXPOSURE 

and unintentional releases of radioactive strontium have occurred at DOE sites across the country. 

Between 1954 and 1989 at the Savannah River Site, 105 Ci (3.9x103

 GBq) of 89Sr and 299 Ci 

(1.1x104

 GBq) of 90Sr were released into onsite seepage basins (DOE 1991). About 100 million gallons 

of liquid HLW are stored in underground tanks in Hanford, Washington, Savannah River, South Carolina, 

Idaho National Engineering Laboratory, Idaho, and West Valley, New York; these tanks contain a variety 

of radioactive liquids, solids, and sludges with unknown characteristics. Sixty-seven tanks at the Hanford 

site have suspected leaks of HLW into the surrounding soil. The largest three confirmed leaks at the 

Hanford site have released 115,000, 70,000, and 55,000 gallons of HLW, respectively, which may contain 

90Sr as well as other radionuclides (DOE 1996a). 

Strontium has been identified in soil and sediment at 32 and 16 sites, respectively, collected from the 

102 NPL hazardous waste sites where it was detected in some environmental media. 90Sr has been 

identified in soil and sediment at 3 and 1 sites, respectively, collected from the 12 NPL hazardous waste 

sites where it was detected in some environmental media (HazDat 2003). 

6.3 ENVIRONMENTAL FATE 

6.3.1 Transport and Partitioning 

Strontium, present in crustal materials, is released by the weathering force of wind and water. Strontium 

leaves the oceans, the largest reservoir of dissolved strontium, by deposition in marine carbonate 

sediment. Some strontium is transported from oceans to the atmosphere in sea spray, returning to the 

terrestrial environment in the form of precipitation (Capo et al. 1998). 

Strontium released into the atmosphere from natural and anthropogenetic activities is transported and 

redeposited on the earth by dry or wet deposition. Dry deposition results from gravitational settling, 

impact, and sorption on surfaces (NCRP 1984). Experimental data on dry deposition of strontium, 

present in the ambient atmosphere, is limited. Rain, sleet, snow, or other forms of moisture can wash 

airborne particles containing strontium from the atmosphere by the process of wet deposition. Wet 

deposition depends on conditions such as particle solubility, air concentration, rain drop size distribution, 

and rain fall rate (NCRP 1984). Hirose et al. (1993) examined the mechanism of aerial deposition of 90Sr 

derived from the Chernobyl accident, and found that 96% of atmospheric 90Sr returned to earth as wet 

deposition. 
STRONTIUM 215 

6. POTENTIAL FOR HUMAN EXPOSURE 

Like calcium, strontium has moderate mobility in soils and sediments, and sorbs moderately to metal 

oxides and clays (Hayes and Traina 1998). The Sr2+ ion is strongly hydrated and is firmly coordinated 

with six or more water molecules in aqueous solution. When Sr2+ ions sorb on negatively charged 

mineral surface sites, the hydration sphere is retained (O’Day et al. 2000). Strontium sorbs as hydrated 

ions on the surface of clay minerals (kaolinite), weathered minerals (amorphous silica), and iron oxides 

(Sahai et al. 2000). Sorbed carbonate on iron oxides enhances the sorption of Sr2+ and permits the 

nucleation of Sr2+ as strontium carbonate (Sahai et al. 2000). On calcite (calcium carbonate), Sr2+ 

sorption occurs by electrostatic attraction as hydrated ions. However, at higher concentrations, 

precipitation of strontianite (strontium carbonate) occurs, and strontium is likely to be less mobile 

(Parkman et al. 1998). 

A wide variation of Kd values have been published in the literature for Sr2+ sorption (NCRP 1984) that 

reflect differences in soil and sediment conditions as well as the analytical techniques used (Bunde et al. 

1997). The in situ Kd values of stable strontium and 90Sr determined in soil cores taken from the fallout 

area of the 1945 blast in Nagasaki, Japan were 496 and 300 L/kg, respectively (Mahara 1993). Migration 

rates for 90Sr in soils from this area were estimated to be 4.2 mm/year when the percolation rate of soil 

water was 2,500 mm/year. Most 90Sr remained close to the soil surface in these soils. In 1996, at most 

sites in the contaminated zone near Chernobyl, the main content of 90Sr (more than 95% of activity) was 

located in the upper 30-cm layer. Only at a few sites (<1% of all sites) had a significant part of the 90Sr 

(>20%) migrate deeper than 30 cm (Kashparov et al. 2001). A high migration ability of 90Sr is observed 

only in low-humus sands. In soils from Belarus near the Chernobyl accident site, Kd values were 43, 59, 

and 150 L/kg for soddy-podzolic, soddy-loamy sandy, and peaty-gley soils, respectively (Sokolik et al. 

2001). Organic matter in soils has a substantial effect on the transport of strontium through soils into 

groundwater. Kd values decreased down the soil profile in Podzol forest soil with an organic rich top soil 

and lower clay layers, from 140 to 44 L/kg (Bunzl and Schimmack 1989). Sr2+ chemically complexes 

with organic matter by partially neutralizing exchangeable sites on organic matter resulting in the 

precipitation of organic matter-Sr2+ complexes (Helal et al. 1998a). High concentrations of ion 

exchangeable Ca2+ in soil enhances the complexation of Sr2+ with organic matter and increases the 

removal of Sr2+ from solution, which results in reduced Sr2+ mobility (Helal et al. 1998a). However, 

nitrate fertilizers inhibit the formation of Sr2+-organic matter complexes and increase Sr2+ mobility (Helal 

et al. 1998b). Kd values of 15–40 L/kg were measured for 90Sr2+ in aquifer sediments near Liquid Waste 

Disposal Facilities at the Hanford site in Washington, where rapid ion exchange dominates (DOE 1996d). 

Kd was measured for 90Sr2+ in aquifer sediments beneath waste water ponds that contained high salt 

concentrations at the Idaho National Environmental and Engineering Laboratory (INEEL) (Bunde et al. 
STRONTIUM 216 

6. POTENTIAL FOR HUMAN EXPOSURE 

1998); and values ranged from 56 to 62 L/kg at initial concentrations of sodium and potassium of 300 and 

150 mg/L, respectively. For initial aqueous concentrations of sodium between 1,000 and 5,000 mg/L, Kd 

values were 4.7 and 19 L/kg, respectively. At the Chalk River Nuclear Laboratory in Ontario, Canada, a 

90Sr waste plume in groundwater initially advanced rapidly as 90Sr was out competed by high 

concentrations of Ca2+ and Mg2+ for sorption sites in sediments, and as concentrations of Ca2+ and Mg2+ 

declined, the migration of the 90Sr plume slowed (Toran 1994). High salt concentrations (marine, brines, 

or high salinity water) can increase the mobility of 90Sr2+ by decreasing strontium sorption to sediments 

(Bunde et al. 1997, 1998) and increase the transport of strontium with the environmental cycling of water. 

Strontium is not necessary for growth or reproduction for most plants, but is typically absorbed to satisfy 

the plant’s metabolic requirements for calcium (NCRP 1984). Soil to plant concentration ratios for 

strontium (the ratio of the concentration of strontium in wet vegetation to the concentration of strontium 

in dry soil) are 0.017–1.0 (NCRP 1984), and indicate that strontium can be easily absorbed into plants 

from soil. The uptake of strontium by plants is greatest in sandy soils having low clay and organic matter 

content (Baes et al. 1986). The concentration of nutritive mineral elements in soil such as calcium lower 

the intake of strontium to the aboveground phytomass. The average reduction of the soil-to-plant 

concentration ratios for 90Sr caused by amendment with Ca or K is around 50–60% (Lembrechts 1993). 

Strontium may be deposited on plant surfaces from the atmosphere, remain on the plant, be washed off, or 

be absorbed directly into the plant through leaves. Contamination by direct deposition on foliage surfaces 

is predominantly a short-term mechanism with a weathering half-life of approximately 14 days (Lassey 

1979). Carini et al. (1999) examined the mechanism of translocation in three species of fruit-bearing 

plants exposed to aerial deposition of 85Sr and found that translocation of 85Sr is localized to the area of 

contamination on the plant. However, uptake of strontium through the leaves is minor compared to root 

uptake. Once absorbed in the plant, strontium translocates to other parts of the plant, such as the leaves or 

fruit. Translocation of strontium in plants is affected by the particular species and stage of organism 

growth, and the most metabolically active parts (growing) will accumulate higher concentrations of 

strontium (Kodaira et al. 1973). 

Strontium, taken up by plants and translocated to the aboveground plant compartments, has been observed 

for deep-rooted plants such as chasima (Chrysothamnus nauseosus), mulberry vegetation (Morus alba), 

quaking aspen (Populus tremuloides), and red maple (Acer rubrum) growing on top of low level waste 

burial sites or contaminated soils (Cooper and Rahman 1994; DOE 1995; Fresquez et al. 1996a). The top 

growth of the plant material releases strontium to the soil surface through leaf fall. Downward migration 
STRONTIUM 217 

6. POTENTIAL FOR HUMAN EXPOSURE 

of 90Sr is slowed by recycling of the contaminated litter by vegetation (Cooper and Rahman 1994). 

Subsurface 90Sr can be transported from soil to top soil by burrowing animals, and is spread to the 

surrounding environment via animal tissues and fecal deposits. At the Subsurface Disposal Area at the 

INEL, deer mice had the highest contamination of all animals from ingestion of 90Sr-contaminated low 

level nuclear waste. In addition, the biotic intrusion of soils covering the waste site brings water 

infiltration into buried LLW (Arthur and Janke 1986). 

The uptake or bioaccumulation of strontium by plants and organisms is the mechanism by which 

strontium in air, water, and soil enters into the food chain of humans. Bioconcentration factors (BCFs) 

have been measured by several investigators in both aquatic and terrestrial organisms for 90Sr (NCRP 

1984). BCF values for 90Sr in aquatic, terrestrial, and wetland ecosystems at the Savannah River Site 

were reported by Friday (1996) and are summarized in Table 6-2. The study illustrates that the organisms 

with the highest uptake are aquatic organisms such as fish (large-mouthed bass), macroinvertebrates 

(insects), macrophytes (white-water lilies and bladderwort), and zooplankton. Because of the similarity 

of strontium to calcium, boney fish had a very high BCF, with a value >50,000 measured in the boney 

tissue (Friday 1996). In the muscle tissue of boney fish, BCF values for 90Sr ranged from high (benthic 

invertebrate and fish feeders; 610) to very high (piscivores; 3,400). Because strontium and calcium are 

chemically similar, the concentration of calcium in water can influence the bioaccumulation of strontium 

in biota. Organisms such as fish bioaccumulate strontium with an inverse correlation to levels of calcium 

in water. However, this correlation is not universal and does not apply to other organisms such as algae 

and plants (NCRP 1984). 

6.3.2 Transformation and Degradation 

Because strontium is an element, its atoms do not degrade by environmental processes such as hydrolysis 

or biodegradation. However, radioactive strontium will be subject to radioactive decay and 

transformation to other elements. Eventually, all of the radioactive strontium will be transformed into 

stable zirconium by the process of radioactive decay (see Section 4.2): 

90Sr (t1⁄2 = 29 years) – 90Y (t1⁄2 = 64 hours) + β- – 90Zr (stable) + βBoth radioactive and nonradioactive strontium compounds are subject to both biotic and abiotic 

transformation mechanisms. 
STRONTIUM 218 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-2. Selected Bioconcentration Factors for 90Sr in Aquatic, Wetland, and 

Terrestrial Ecosystems at the Savannah River Site 

Bioconcentration factors for 90Sr 

Organism Minimum Maximum Mean 

Algae 600 

Clam, shell 1,300 

Fish muscle 

Insect and bottom invertebrate feeders 

 Piscivores 

Benthic invertebrate and fish feeders 

<48 

3,400 

610 

Fish bone 

Insect and bottom invertebrate feeders 

 Piscivores 

Benthic invertebrate and fish feeders 

Detritus and plankton feeders 

2,400 

63,000 

57,000 

51,000 

Macroinvertebrates, larvae 520 54,000 27,300 

Macrohytes (rooted vascular) 2,100 8,500 5,500 

Macrophytes (floating vascular) 9,400 

Zooplankton 3,900 

Corn

 Grain 

 Leaves 

0.15 

13.1 

Pine tree, leaves 0.88 1.69 1.29 

Soybeans 2.51 

Tree (maple, sweetgum, and poplar) 

 Wood

 Bark

 Leaf 

0.81 

11 

3.8 

Source: Friday 1996 
STRONTIUM 219 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.3.2.1 Air 

The presence of strontium and radioactive strontium compounds in the atmosphere results from both 

natural and anthropogenetic activities (see Section 6.2.1). Strontium is emitted into the atmosphere as 

strontium oxide (SrO) during thermal processes. SrO is unstable and reacts with moisture or carbon 

dioxide in the air to form strontium hydroxide (Sr[OH]2) or strontium carbonate (SrCO3), respectively. 

Sr[OH]2 in contact with water in clouds or during washout by rain will ionize to form Sr2+ and SrOH+ ions. 

There is no evidence in the literature for interaction of SrO with other compounds in the atmosphere. 

6.3.2.2 Water 

Strontium exists almost exclusively in the environment as a +2 cation, and will form different species, 

some of which are more soluble than others. Because the different species have different solubilities, they 

will have different mobilities in the environment and different exposure potentials. Strontium exists as a 

hydrated cation, an ionic solution complex, or an ionic salt. In the environment, typical solution species 

for strontium are Sr2+ and SrOH+

, and some strontium compounds (SrCO3 and SrSO4) are practically 

insoluble in neutral water (Cotton and Wilkenson 1980; see Table 4-2). 

6.3.2.3 Sediment and Soil 

The principal abiotic processes that transform strontium in soils and sediments are mediated by sorption 

and desorption reactions between the soil solution and matrix (precipitation, complexation, and ion 

exchange), and controlled by pH, ionic strength, solution speciation, mineral composition, organic matter, 

biological organisms, and temperature (see Section 6.3.1). For many soil systems, in the short term, 

strontium sorption is dominated by simple ion exchange, and strontium ions are readily exchangeable. At 

longer timescales, however, strontium ions may relocated into sterically hindered sites that are not readily 

exchangeable (Bunker et al. 2000). 

In the vicinity of the Chernobyl accident site, 90Sr has leached from “hot” fuel particles (which have 

dissolved) and now may interact with natural soil components (Sokolik et al. 2001). In situations where 

soil is incorporated into a nuclear fireball (e.g., Semipalatinsk Nuclear Test Site, Kazakhstan), the 

resulting fused silicates that form are usually comparatively insoluble. Typically, 90Sr in these particles 
STRONTIUM 220 

6. POTENTIAL FOR HUMAN EXPOSURE 

are tightly bound with the majority of 90Sr undergoing radioactive decay before being released by 

weathering (Gastberger et al. 2000). 

6.3.2.4 Other Media 

No data were located in the literature on the transport or degradation of stable or radioactive strontium in 

other media. 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 

Strontium is widely distributed throughout the earth and has continuously cycled between the atmosphere, 

biosphere, hydrosphere, and lithosphere for many millions of years. Table 6-3 illustrates the average or 

range of concentrations of strontium in earth materials (Capo et al. 1998). Anthropogenic activities have 

increased local concentrations of strontium as a consequence of the development of an industrialized 

human society. Before the 1940s, radioactive strontium was not present in the environment at any 

measurable levels. 

In the United States, commercial nuclear power plant operators are required to monitor and report any 

detectable quantities of radioactive materials released to the environment (USNRC 1996). Table 6-1 

summarizes releases of radiostrontium isotopes with half-lives >8 hours to the atmosphere and water for 

1993 from PWR and BWR nuclear power plants. Nearly all of the radioactive material reported as 

released in effluents are from planned releases from normal plant operation or anticipated operational 

occurrences. The latter includes unplanned releases of radioactive materials from miscellaneous actions 

such as equipment failure, operator error, or procedure error, and are not of such consequence as to be 

considered an accident (USNRC 1993a). 

6.4.1 Air 

According to two surveys, the strontium content in urban air ranges from 4 to 100 ng/m3

 and averages 

20 ng/m3

 (Dzubay and Stevens 1975). The arithmetic mean concentration of strontium in urban air was 

measured as 29.1 ng/m3

 in the Los Angeles basin during 1985 (Witz et al. 1986). Urban air in Illinois 

between 1985 and 1988 averaged 0.9–4.8 ng/m3

 (Sweet et al. 1993). Areas where higher strontium 
STRONTIUM 221 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-3. Average or Ranges of Concentration of Strontium in Earth Materials 

Material Concentration of strontium 

Geologic (ppm) 

 Average crust 

Exposed upper crust 

Soil: 

Soil minerals 

Soil (labile) 

Individual rock types: 

Basalt 

Carbonate 

High-Ca granite 

Low-Ca granite 

Sandstone 

Shale 

370 

337

240 

0.2–20 

465 

610 

440 

100 

20 

300 

Biologic (ppm)

 Wood 

 Roots (spruce) 

 Conifer needles 

8–2,500

19

2–20 

Hydrologic (μg/L)

 Seawater 

 Rivers 

Rain 

Snow 

7,620

6–800

0.7–383

0.01–0.76 

Source: Capo et al. 1998 
STRONTIUM 222 

6. POTENTIAL FOR HUMAN EXPOSURE 

concentrations are prevalent are near coal burning plants where strontium can be released with stack 

emissions (as discussed in Section 6.2.1). 

Before the 1940s, radiostrontium was not present in the air at any significant concentrations. 

Concentrations of 90Sr in the atmosphere peaked at about 10 MCi (0.37 GBq) in 1963 coincident with the 

period of extensive atmospheric nuclear weapons testing. Since the signing of the Nuclear Test Ban 

Treaty of 1963, the concentration of 90Sr has steadily dropped through the latter 35 years by deposition 

and radioactive decay (DOE 1996c; Eisenbud 1987). Recent levels of 90Sr in air were not located. 

6.4.2 Water 

Surveys of strontium in surface waters and municipal water supplies across the United States show that 

strontium is present in nearly all fresh waters in amounts <1 mg/L (USGS 1963). The National Drinking 

Water Contaminant Occurrence Database (NDOD), which contains data from public water supplies 

(PWS), where testing is performed at many points in the system, including the intake and at various 

points in the treatment and distribution systems, as well as at the point where the drinking water can be 

labeled "finished", lists the number of detections and concentrations of strontium. The average 

concentrations of strontium in PWS waters from the United States derived from surface water and 

groundwater were 1.10 (range, 0.2–3.68 mg/L) and 0.81 mg/L (range, 0.010–3.5 mg/L), respectively 

(EPA 2002b). The average concentrations of strontium in streams of the United States are between 0.5 

and 1.5 mg/L. Strontium concentrations >1 mg/L are found in streams of the southwest, where the total 

dissolved solids content is the highest of any area of the continental United States. Streams of most of the 

Atlantic slope basins, southern United States, upper Great Lakes region, and Pacific northwest contain 

concentrations of strontium that are generally <0.5 mg/L strontium (USGS 1963). Some exceptions are 

areas where there are celestite-rich limestone deposits, such as regions of northwestern Ohio and eastern 

Florida (USGS 1963). The average concentration of strontium in sea water is approximately 8 mg/L 

(Demayo 1986). In groundwater, the average concentration of strontium is <0.5 mg/L. High 

concentrations of strontium, >1 mg/L, have been in observed in the southwestern United States. 

Unusually high concentrations of strontium, >20 mg/L, have been observed for some wells in central 

Wisconsin (USGS 1963). The NDOD lists the number of detections and concentrations of strontium in 

groundwater and surface water at several locations around the United States from ambient water samples 

(EPA 2002b). Dissolved strontium was detected in groundwater at 4,353 of 4,383 sites (99.3% of sites), 

with an average concentration of 1.6 mg/L (range, 0.0009–200 mg/L). The average dissolved strontium 

concentration in lake/reservoirs and springs were 1.09 mg/L (97.6% of sites; range, 0.002–170 mg/L) and 
STRONTIUM 223 

6. POTENTIAL FOR HUMAN EXPOSURE 

0.64 mg/L (100% of sites; range, 0.028–3.2 mg/L), respectively. In other surface waters, dissolved 

strontium was detected at 1,572 of 1,595 sites (98.6% of sites), with an average concentration of 362 μg/L 

(range, 0.0005–30 mg/L). The concentration of dissolved strontium in publicly owned treatment works 

(POTW) influents was between 0.025 and 0.45 mg/L (EPA 1981). The average concentrations of 

strontium in rain and snow were 0.7–383 and 0.01–0.76 μg/L, respectively (Capo et al. 1998). 

90Sr concentration in surface waters of the north Pacific Ocean has decreased steadily since the early 

1960s to present day levels of approximately 23–81 pCi/m3

 (1–3 Bq 90Sr/m3) sea water. This value is 

estimated by dividing the concentration levels for 137Cs by the global fallout activity ratio measured for 

137Cs/90Sr of 1.5 (Hamilton et al. 1996). The EPA ERAMS program monitors ambient concentrations of 

90Sr in drinking water at 78 sites. ERAMS data serve to assess trends and anomalies in concentrations, 

and to compare with standards set forth in the EPA National Interim Primary Drinking Water 

Regulations. Table 6-4 summarizes drinking water composite samples for the period of January– 

December in 1995 taken at the 78 sites in major population centers or near selected nuclear facilities 

(EPA 2000a). The median concentration of 90Sr in drinking water for this period was 0.1 pCi/L (4 mBq). 

Sites with above average levels of 90Sr, Detroit and Niagara Falls, recorded levels of 0.4 and 0.5 pCi/L 

(~15 mBq/L), respectively. In a 1974 study, a concentration of 0.09 pCi/L 90Sr (3 mBq/L) in drinking 

water was measured in Los Angeles, California (Kraybill 1983). In a survey that examined 169 wells 

used for public drinking water in California (Storm 1994), 16 wells measured recordable concentrations 

of 90Sr, with an average concentration of 105 pCi/L (4 Bq/L). The NDOD lists the number of detections 

of 90Sr in ambient groundwater at several locations around the United States. Dissolved 90Sr was detected 

in groundwater at 18 out of 104 sites (17%), with an average concentration of 1.46 nCi/L (53.9 Bq) (EPA 

2002b). The concentrations of 90Sr in groundwater at the 91 waste sites located at 18 DOE facilities were 

between 0.05 and 231,000 pCi/L (2 mBq and 9 kBq) (DOE 1992). River water taken from the Ebro River 

basin (Northeast Spain) during 1994 had a mean 90Sr level of 6.6 mBq (0.18 pCi) and ranged from 5.9 to 

7.6 mBq/L (0.16 to 0.21 pCi/L) (Pujol and Sanchez-Cabeza 2000). 90Sr in the Ebro River waters could be 

attributed solely to global fallout. The DOE Environmental Measurements Laboratory program measures 

the 90Sr content of wet deposition in selected sites across the world to determine global trends in 90Sr 

deposition. The data for the year 1990 are presented in Table 6-5 for cities in the United States. The 

average total annual wet deposition of 90Sr in the United States was 5 pCi/m2

 (0.2 Bq/m2) during this 

period. The precipitation samples with the highest total 90Sr concentrations were obtained from New 

York City and Nome, Alaska with annual totals of 10 and 8 pCi/m2

 (0.4 and 0.3 Bq/m2), respectively. In 

all cases, the 90Sr concentrations in rain were low, which suggests that the atmospheric content of 90Sr in 

1990 was small and decreasing (DOE 1996c). 
STRONTIUM 224 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-4. 90Sr in Drinking Water (Composites) for January–December 1995 

90Sr 

Statea City Total solids (mg/L) pCi/L ±2F

AK Fairbanks 162.0 0.0 0.2 

AL Dothan 160.0 0.1 0.1 

AL Montgomery 55.2 0.1 0.2 

AL Muscle Shoals 82.0 0.2 0.2 

AL Scottsboro 87.0 0.2 0.2 

AR Little Rock 28.8 0.0 0.2 

CA Berkeley 8.0 0.1 0.2 

CA Los Angeles 318.0 0.0 0.1 

CO Denver 140.0 0.0 0.2 

CO Platteville 138.0 0.0 0.2 

CT Hartford 36.6 0.3 0.2 

DE Dover 191.0 ND — 

FL Miami 150.0 0.2 0.2 

FL Tampa 252.0 0.3 0.2 

GA Baxley 165.0 0.0 0.2 

GA Savannah 147.0 ND — 

HI Honolulu 208.0 0.1 0.1 

IA Cedar Rapids 121.0 0.1 0.2 

ID Boise 95.5 ND — 

ID Idaho Falls 219.0 ND — 

IL Morris 474.0 ND — 

IL West Chicago 337.0 0.1 0.1 

KS Topeka 364.0 0.2 0.2 

LA New Orleans 226.0 0.2 0.2 

MA Lawrence 93.8 0.2 0.2 

MD Baltimore 89.8 0.1 0.2 

MD Conowingo 155.0 0.1 0.2 

ME Augusta 85.2 0.3 0.2 
STRONTIUM 225 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-4. 90Sr in Drinking Water (Composites) for January–December 1995 

90Sr 

Statea City Total solids (mg/L) pCi/L ±2F

MI Detroit 79.8 0.4 0.2 

MI Grand Rapids 125.0 0.3 0.2 

MN Minneapolis 93.8 0.3 0.2 

MN Red Wing 238.0 0.0 0.2 

MO Jefferson City 283.0 0.0 0.2 

MS Jackson 86.8 0.2 0.2 

MS Port Gibson 313.0 0.0 0.1 

MT Helena 61.8 0.1 0.2 

NC Charlotte 46.8 0.1 0.2 

NC Wilmington 110.0 0.2 0.2 

ND Bismarck 329.0 0.0 0.2 

NE Lincoln 305.0 0.1 0.2 

NH Concord 81.2 0.1 0.2 

NJ Trenton 92.7 0.1 0.2 

NJ Waretown 52.0 0.0 0.2 

NM Santa Fe 279.0 ND — 

NV Las Vegas 248.0 0.1 0.2 

NY Albany 68.8 0.3 0.2 

NY New York City 44.5 0.0 0.2 

NY Niagara Falls 99.2 0.5 0.2 

NY Syracuse 94.8 0.3 0.2 

OH Cincinnati 198.0 0.2 0.2 

OH Columbus 362.0 0.0 0.3 

OH East Liverpool 215.0 0.3 0.2 

OH Painesville 126.0 0.2 0.3 

OH Toledo 148.0 0.3 0.3 

OK Oklahoma City 62.6 0.3 0.2 

OR Portland 19.2 0.1 0.2 
STRONTIUM 226 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-4. 90Sr in Drinking Water (Composites) for January–December 1995 

90Sr 

Statea City Total solids (mg/L) pCi/L ±2F

PA Columbia 121.0 0.1 0.2 

PA Harrisburg 51.2 0.1 0.2 

PA Philadelphia 165.0 0.0 0.2 

PA Philadelphia- 207.0 0.1 0.2 

Queen 

PA Philadelphia-Baxter 101.0 0.2 0.2 

PA Pittsburgh 178.0 0.2 0.2 

PC Corozal 71.6 0.1 0.2 

RI Providence 52.8 0.3 0.2 

SC Barnwell 73.6 0.0 0.2 

SC Columbia 28.2 0.0 0.2 

SC Jenkinsville 165.0 ND — 

SC Seneca 35.2 0.1 0.2 

TN Chattanooga 82.2 0.2 0.2 

TN Knoxville 93.8 0.0 0.2 

TX Austin 180.0 0.0 0.2 

VA Doswell 193.0 0.0 0.2 

VA Lynchburg 45.2 0.1 0.2 

VA Virginia Beach 91.2 0.3 0.2 

WA Richland 77.2 0.1 0.2 

WA Seattle 29.8 0.0 0.2 

WI Genoa City 194.0 ND — 

WI Madison 234.0 ND — 

a

Post office state abbreviations used 

ND = not detected; 

2F = counting error term reported at the 2F (95%) confidence level 

Source: EPA 1995 
STRONTIUM 227 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-5. Quarterly and Annual Deposition of 90Sr in Selected U.S. Cites for the 

Year 1990 

Quarter Annual total 

Location 

First Second 

90Sr 

Depositiona 

Precipitationb 

90Sr 

Depositiona 

Precipitationb 

Third 

90Sr 

Depositiona 

Precipitationb 

Fourth 

90Sr 

Depositiona 

Precipitationb 

90Sr 

Depositiona 

Precipitationb 

Anchorage, 

Alaska 

0.0 8.5 0.0 6.5 — 15.9 — 29.7 0.0 60.5 

Argonne, 

Illinois 

0.1 18.6 0.1 33.4 0.1 26.9 0.0 29.5 0.2 108.4 

Birmingham, 

Alabama 

0.1 50.6 0.0 22.2 0.0 14.7 0.0 31.7 0.1 119.3 

Chester, New 

Jersey 

Cold Bay, 

Alaska 

0.0 

0.0 

23.2 

20.3 

0.1 

0.0 

44.7 

14.7 

0.1 

0.1 

39.2 

29.5 

0.1 

0.0 

39.3 

31.1 

0.2 

0.1 

146.4 

95.5 

Fairbanks, 

Alaska 

0.0 3.4 0.0 5.6 0.1 25.9 0.1 12.1 0.2 47.1 

Houston, 

Texas 

0.0 31.4 0.0 26.0 0.0 22.0 0.0 21.8 0.0 101.2 

Lihue, Hawaii 0.0 36.7 0.0 14.5 0.0 12.2 0.1 36.6 0.1 100.0 

Mauna Loa, 

Hawaii 

0.0 54.5 0.0 0.3 0.1 7.5 0.0 44.9 0.1 107.2 

Miami, 

Florida 

0.0 9.4 0.0 54.8 0.0 48.0 0.1 19.1 0.2 131.1 

New York, 

New York 

— 28.7 0.1 42.5 0.1 46.0 0.1 37.5 0.4 154.7 

Nome, Alaska 0.1 5.4 0.0 10.8 0.2 27.0 0.1 13.2 0.3 56.3 

Vermillion, 

South Dakota 

0.0 5.5 0.0 28.7 0.0 20.6 0.0 6.0 0.1 60.7 

West Los 

Angeles, 

California 

0.1 16.7 0.1 5.3 0.1 0.1 0.0 4.1 0.2 26.2 

Wooster, 

Ohio 

0.0 16.5 0.1 28.0 0.0 43.5 0.0 36.9 0.1 124.8 

Average 0.03 22.0 0.03 22.5 0.06 25.3 0.04 26.2 0.2 96.0 

a

In Bq/m3 

b

In cm 

Source: DOE 1996d 
STRONTIUM 228 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.4.3 Sediment and Soil 

Table 6-3 summarizes the average or range of concentrations of strontium in soils and bedrock minerals. 

The average concentrations of strontium in the earth’s crust and the exposed upper crust are 370 and 

337 mg/kg, respectively. Soils, on average, have approximately 240 mg/kg Sr (Capo et al. 1998; EPA 

1995a). Some materials, such as soil amendments, are routinely applied to agricultural lands. Typical 

concentrations of strontium in soil amendments are: POTW sewage sludges, 250±192 ppm (mg/kg dry 

weight); phosphate fertilizers, 610 mg/kg; limestone, 610 mg/kg; and manure, 80 mg/kg dry weight (EPA 

1995a; Mumma et al. 1984). 

The background level of 90Sr in soils of the United States from global fallout will depend upon the 

historical transport and deposition inventory at that particular location. The mean regional background 

concentration of 90Sr in soils in proximity to the Los Alamos National Laboratory from 1974 to 1994 was 

320±250 pCi/kg dry weight soil (Fresquez et al. 1996b). This value has decreased with time due to 

radioactive decay of 90Sr. The range of concentrations for 90Sr in soils and sediments at 91 waste sites 

located at the 18 DOE facilities around the United States was 0.02–540,000 pCi/kg (DOE 1992). The 

total content of 90Sr on surface soil in the 30 km contaminated zone around Chernobyl accident site in the 

Ukraine (not including the reactor site and waste storage) was about 8.1x1014 Bq (2.2x107

 Ci) in 1997, 

which corresponds to about 0.4–0.5% of the Chernobyl reactor inventory at the time of the accident 

(Kashparov et al. 2001). Ten years after the accident, about 95% of the 90Sr activity is associated with the 

upper 10–20 cm layer of soil for most of the soils in this area. Mean 90Sr activity in soil at a Chernobylcontaminated field site in the Ukraine was 36 Bq dry weight (0.97 nCi dry weight) (Malek et al. 2002). 

Levels of 90Sr in soils from Belarus situated at a distance of ~40 km from the Chernobyl accident site 

ranged from 50 to 640 kBq/m2

 (1.4–17 μCi/m2), while levels at a distance of 200–250 km ranged from 

10–80 kBq/m2

 (270–2,200 nCi/m2) (Sokolik et al. 2001). 

The mean activity of 90Sr in lacustrine and marine sediments from Antarctica in 1989–1996 ranged from 

0.17 to 0.76 Bq/kg dry weight (4.59–20.5 pCi/kg dry weight) and from <0.10 to 0.21 Bq/kg dry weight 

(<2.7–5.78 pCi/kg dry weight), respectively (Jia et al. 1999). The 90Sr activities in marine sediments 

ranged from 117 to 1,277 mBq/kg (3.16 and 34.5 pCi/kg) and from 304 to 1,799 mBq/kg 

(8.21–48.6 pCi/kg) at two sites off atomic power stations in South Korea (Yang et al. 2002). 90Sr2+ ions in 

sediments are characterized by reversible ion exchange processes that lead to low 90Sr activity in 

sediments (Jia et al. 1999). 
STRONTIUM 229 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.4.4 Other Environmental Media 

The range of concentrations of strontium in fruits and vegetables is summarized in Table 6-6 (Barnes 

1997). The highest concentrations are observed in leafy vegetables, such as cabbage (64.2 mg Sr/kg dry 

weight) (USGS 1980). 

The range of concentrations of 90Sr in food stuffs is summarized in Table 6-7. The highest concentrations 

were observed in fresh vegetables (8.8 pCi/kg dry weight=0.33 Bq/kg dry weight) and dry beans 

(15.9 pCi/kg dry weight=0.59 Bq/kg dry weight) (Eisenbud 1987). The U.S. Food and Drug 

Administration Radionuclides in Foods program monitors radionuclides (e.g., 90Sr) in the food supply as 

part of the Total Diet Study (TDS). For the years 1994 and 1995, about 60 foods with historically high 

90Sr levels were analyzed (Capar and Cunningham 2000). 90Sr was detected in about 65% of these foods. 

The greatest concentration was in mixed nuts at 2 Bq/kg (50 pCi). Approximately 200 reactor-survey 

food test portions, including raw vegetables, food crops (primarily fruits), fish, and milk, were collected 

in the vicinities of 33 nuclear reactors (Cunningham et al. 1994). Ninety-four percent of the reactorsurvey food test portions had 90Sr activities between 0 and 0.74 Bq/kg (0 and 20 pCi), and 6% had activity 

concentration between 0.74 and 7.4 Bq/kg (20 and 200 pCi/kg). The EPA ERAMS program monitors 

ambient concentrations of 90Sr in pasteurized milk at 42 sites in major population centers, and is used to 

assess trends and anomalies in concentrations. Table 6-8 summaries pasteurized milk samples for the 

period of July 1997 (EPA 2002b). The average concentration of 90Sr in pasteurized milk during this 

period for the 42 sites was 0.9 pCi/L (33 mBq/L). Sites with above average levels of 90Sr in pasteurized 

milk were observed at (listed in order of decreasing activity of 90Sr): Minot, North Dakota; Grand Rapids, 

Michigan; Spokane, Washington; Cleveland, Ohio; Cincinnati, Ohio; Memphis, Tennessee; St. Paul, 

Minnesota; Chicago, Illinois; Detroit, Michigan; San Francisco, California; Baltimore, Maryland; and 

Wilmington, Delaware. Dietary intake of 90Sr peaked in 1965 at 1.1 Bq/day (30 pCi/day), during a period 

of atmospheric testing of nuclear weapons, and has continued to decline to <0.05 Bq/day (<1.2 pCi/day) 

after 1987 (Cunningham et al. 1989). Dietary intake of 90Sr in the United States from 1961 to 1991 is 

illustrated in Figure 6-3. 

Sato et al. (1977) determined the concentration of strontium in tobacco leaves as 141 μg/g. The average 

concentration of strontium in the ash of 12 brands of cigarettes was measured as 373 μg/g (Iskander 

1986). No significant difference was observed in the concentration of strontium in the cigarette filter 

before and after smoking (Sato et al. 1977). The ranges of concentrations of strontium in waste materials 

are: municipal solid waste (MSW) 11–35 μg/g; incineration fly ash 110–220 μg/g (Lisk 1988); coal fly 
STRONTIUM 230 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-6. Concentration of Strontium in Fruit Juices and Produce 

Fruit juice and produce Average liquid concentration Average solid concentration 

(μg/L)a (ppm)b 

Apple 13.58 

Apple juice 0.1271 

Banana 0.1297 

Bean: 

Dry 6.63 

Snap 21.7 

Blackberry 0.2619 

Boysenberry 0.9523 

Cabbage 64.17 

Corn: 

Sweet 0.416 

Cucumber 24 

Currant: 

Red 1.251 

Grape: 

American 25.6 

 Concord 0.3661 

 European 38.4 

Red 0.1086 

White 0.6318 

Kiwi 1.744 

Lemon products: 

Lemon 0.0986 

Bottled 0.5334 

 Lemonade 0.1653 

Lettuce 22.26 

Lime 0.3464 

Mango 0.5121 

Orange 25.56 

Orange juice

 Brazilian 0.0417 

California 0.5368 

 Florida 0.0933 

 Navel 0.5209 

 Pineapple 0.1612 

Papaya 1.690 

Peach 3.082 

Pear 0.5912 

Pineapple 0.0604 
STRONTIUM	 231 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-6. Concentration of Strontium in Fruit Juices and Produce 

Fruit juice and produce	 Average liquid concentration Average solid concentration 

(μg/L)a (ppm)b 

Potato	 2.562 

Raspberry	 2.232 

Strawberry	 0.3001 

Tangerine	 0.0828 

Tomato	 9.96 

Tomato sauce	 0.8894 

a

Barnes 1997 

b

USGS 1980; values are parts per million, dry weight 
Table 6-7. 90Sr in the Human Diets During 1982 

New York City San Francisco 

Diet category 

Intake 

kg/year g Ca/year 

Percent Percent Percent 

yearly pCi pCi yearly pCi pCi yearly 

intake Ca 90Sr/kg 90Sr/year intake 90Sr 90Sr/kg 90Sr/year intake 90Sr 

Dairy products 

Fresh vegetables 

Canned 

vegetables 

Root vegetables 

Potatoes 

Dry beans 

Total (vegetables) 

Fresh fruit 

Canned fruit 

Fruit juice 

Total (fruits) 

Bakery products 

Flour 

Whole grain 

products 

Macaroni 

Rice 

Total (grains) 

Meat 

Poultry 

Eggs 

Fresh fish 

Shell fish 

Total (meat, eggs, 

and fish) 

Yearly intake 

Ca (total) 

90Sr (total) 

Ratio of 

90Sr/Ca 

Daily intake 

200 

48 

22 

10 

38 

3 

59 

11 

28 

44 

34 

11 

3 

3 

79 

20 

15 

8 

1 

-

216.0 

18.7 

4.4 

3.8 

3.8 

2.1 

9.4 

0.6 

2.5 

53.7 

6.5 

10.3 

0.6 

1.1 

12.6 

6.0 

8.7 

7.6 

1.6 

-

370 g 

58 

9 

3 

20 

10 

3.2 

8.8 

5.4 

3.4 

2.3 

15.9 

2.6 

1.1 

1.7 

3.0 

4.5 

6.2 

2.4 

0.6 

0.4 

0.3 

0.6 

0.2 

0.2 

-

641 

422 

119 

34 

88 

48 

152 

12 

48 

131 

153 

69 

7 

2 

35 

6 

10 

1 

<1 

-

1978 pCi 

5.3 pCi

90Sr/g Ca 

54 

pCi/day 

32 

36 

11 

18 

3 

1.0 

2.4 

2.9 

3.8 

2.1 

7.9 

1.3 

0.8 

1.4 

1.9 

3.5 

2.9 

2.3 

0.8 

0.4 

0.3 

0.6 

0.1 

0.7 

-

200 

116 

64 

38 

79 

54 

77 

9 

40 

84 

119 

32 

7 

2 

31 

5 

8 

1 

1 

-

967 pCi 

2.6 pCi

90Sr/g Ca 

2.6 

pCi/day 

21 

36 

13 

25 

5 

1 pCi=37 mBq (conversion factor) 

Source: DOE 1984 

STRONTIUM 232 

6. POTENTIAL FOR HUMAN EXPOSURE 
STRONTIUM 

6. POTENTIAL FOR HUMAN EXPOSURE 

233 

Statea 

AL 

CA 

CA 

CA 

CO 

CT 

DE 

FL 

GA 

HI 

IA 

IL 

IN 

KY 

MA 

MD 

MI 

MN 

MN 

MO 

MS 

NC 

ND 

NJ 

NM 

NV 

NY 

NY 

OH 

Table 6-8. 90Sr in Pasteurized Milk in July 1997 

City 90Sr (pCi/L) 

Montgomery 0.98 

Los Angeles 0.66 

Sacramento 0.26 

San Francisco 1.24 

Denver 0.41 

Hartford 1.31 

Wilmington 1.00 

Tampa 0.59 

Atlanta 0.56 

Honolulu 0.38 

Des Moines 0.40 

Chicago 1.38 

Indianapolis 0.96 

Louisville 0.20 

Boston 0.77 

Baltimore 1.06 

Detroit 1.34 

Grand Rapids 1.78 

St. Paul 1.44 

Kansas City 1.14 

Jackson — 

Charlotte 1.25 

Minot 2.12 

Trenton 0.75 

Albuquerque 0.53 

Las Vegas 0.20 

Buffalo 0.75 

Syracuse 0.94 

Cincinnati 1.60 
STRONTIUM 

6. POTENTIAL FOR HUMAN EXPOSURE 

234 

Statea 

OH 

OR 

PA 

PA 

PC 

PR 

SC 

TN 

TX 

TX 

VA 

VT 

WA 

WA 

Table 6-8. 90Sr in Pasteurized Milk in July 1997 

City 90Sr (pCi/L) 

Cleveland 1.60 

Portland 0.79 

Philadelphia 0.84 

Pittsburgh 0.23 

Cristobal 0.27 

San Juan 0.51 

Charleston 0.73 

Memphis 1.54 

Austin 0.29 

Ft. Worth 0.50 

Norfolk 0.89 

Burlington 1.10 

Seattle 0.49 

Spokane 1.71 

a

Post office state abbreviations used 

Source: EPA 2000b 
STRONTIUM 235 

6. POTENTIAL FOR HUMAN EXPOSURE 

Figure 6-3. U.S. Daily Dietary Intake of 90Sr, 1961–1992 

90 Sr (Bq/day) 

0.0 

0.2 

0.4 

0.6 

0.8 

1.0 

1.2 

1.4 

1.6 

1960 1965 1970 1975 1980 1985 1990 1995
 

Year
 

Source: Cunningham et al. 1994 
STRONTIUM 236 

6. POTENTIAL FOR HUMAN EXPOSURE 

ash 30–7,600 μg/g; coal bottom ash 170–6,400 μg/g; flue-gas desulfurization by-products 70–3,000 μg/g; 

oil ash 50–920 μg/g; (Eary et al. 1990); and compost 260–420 μg/g (Evans and Tan 1998). 

Levels of 90Sr were measured in tissue samples of animals killed by motorists near the low-level 

radioactive disposal site at Los Alamos National Laboratory and from background locations. The mean 

concentration of 90Sr in tissues from deer and elk killed near the low-level radioactive disposal site were 

460 and 230 mBq/kg (12 and 7.0 pCi), respectively, while concentrations at background locations were 

130 and 6.3 mBq/kg (3.5 and 1.7 pCi), respectively (Ferenbaugh et al. 2002). Between 1994 and 1996, 

levels of skeletal 90Sr in small mammals in the Exclusion Zone at Chernobyl, Ukraine averaged 297 Bq/g 

(8.0 nCi/g) (Chesser et al. 2000). 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE 

The primary routes of human exposure to strontium are from inhalation of aerosols and ingestion of food 

and drinking water containing strontium. The intake of strontium, therefore, depends upon the 

concentration of strontium in air, drinking water, and in the food items that comprise a person’s diet, 

which may be highly variable. The average concentration of strontium in urban air is about 20 ng 

strontium/m3

 (see Section 6.4.1). Assuming that an adult breathes approximately 20 m3 of air per day, the 

inhalation exposure would be 400 ng strontium/day. This value may be somewhat higher for persons 

living near sources of strontium emission. Workers employed at industrial facilities that produce, 

process, and use strontium and strontium compounds will have higher exposures. Similarly, strontium is 

taken into the body by ingestion of drinking water. Using the concentration of strontium in U.S. drinking 

water to be 1 mg/L (see Section 6.4.2), and the consumption rate as 2 L/day, the strontium intake from 

drinking water would be 2 mg/day. In a 1994 total diet study in the United Kingdom, the total dietary 

exposure to stable strontium was estimated at 1.3 mg/day (Ysart et al. 1999). As part of an Australian 

Market Basket Survey in 1994, the estimated daily intakes of strontium for female adults ranged from 

0.89 to 1.2 mg/day (Gulson et al. 2001). Combining air, water, and diet exposures estimates, the total 

daily exposure to strontium is ~3.3 mg/day. 

External exposure to 90Sr is not a concern because of minor emission of penetrating radiation from 90Sr. 

No estimate of the concentration of 90Sr in air is available (see Section 6.4.1). However, it is assumed that 

ambient concentrations of 90Sr in the atmosphere are small relative to exposures from water and diet. If 

the concentration of 90Sr in average U.S. drinking water is estimated as 0.1 pCi/L (4 mBq/L) or one 

radiochemical event per 5–10 minutes (see Section 6.4.2), and the consumption rate of drinking water by 
STRONTIUM 237 

6. POTENTIAL FOR HUMAN EXPOSURE 

a normal adult is assumed to be 2 L/day, then the exposure from drinking water would be 0.2 pCi 

(7 mBq) per day. Since the inception of the TDS Radionuclides in Foods program in 1961, intake levels 

of 90Sr in food have steadily declined from a peak level in 1965 of 1.1 Bq/day (30 pCi/day), to below 

0.2 Bq/day (5 pCi/day) (Cunningham et al. 1989). A DOE Environmental Measurements Laboratory 

study estimated the average dietary intake of 90Sr from 19 diet categories for individuals living in the 

urban areas of New York City and San Francisco. Table 6-6 summarizes the data from this study (DOE 

1984). For both locations, vegetables accounted for more than a third of the yearly dietary intake of 90Sr 

at 36%. In the vegetable group, fresh vegetables were the largest contributors of 90Sr dietary intakes. The 

next largest contributor of 90Sr was grains and dairy products. Using a conservative estimate of total 

dietary exposure for 90Sr of 5 pCi/day (0.19 Bq/day) and drinking water exposure of 0.2 pCi/day 

(7 mBq/day), the total estimated daily exposure to strontium is approximately 5.2 pCi/day (0.19 Bq/day). 

Current population exposure levels to 90Sr will be lower than this value as a result of decreasing 

concentrations of 90Sr in the environment. However, this value may be somewhat higher for persons 

living near sources of 90Sr, such as DOE facilities, and for workers employed at government facilities that 

produce, process, and use 90Sr and 90Sr waste compounds. 

Table 6-9 summarizes measurements of concentrations of strontium in human tissues and body fluids 

resulting from consumption of food and water and from natural background sources (Tsalev 1984); these 

are nonoccupationally exposed populations. The highest concentrations of strontium are in the bones and 

teeth (Iyengar et al. 1978; Tsalev 1984). 

The distributions of 90Sr in the body are significantly different for males and females. As expected, the 

highest concentrations of 90Sr are measured in the boney tissue. Males and females averaged 10.4 and 

65 pCi/kg (0.38 and 2.4 Bq/kg) wet weight, respectively. Males had a much higher concentration of 90Sr 

in the muscular tissue compared to females. The heart and psoas muscles had respective concentrations 

of 90Sr for men averaging 13.9 and 18.7 pCi/kg (0.51 and 0.69 Bq) wet weight versus respective 

concentrations of 7.4 and 1.9 pCi/kg (0.27 Bq/kg and 70 mBq/kg) wet weight for females (Baratta and 

Ferri 1966). Approximately 1,000 human teeth, collected in southern Ukraine in 1990–1991, had 90Sr 

activities ranging from 1.0 to 16.3 mBq/g ash (0.027–0.44 pCi/q ash) (Kulev et al. 1994). 

Strontium can be released into the atmosphere as a result of glass manufacturing. In one study, the 

median ambient air concentration of strontium that both art glass makers and formers were chronically 

exposed was 0.1 μg strontium/m3

 (Apostoli et al. 1998). A National Occupational Exposure Survey 

conducted by NIOSH during 1981–1983 estimated the number of workers potentially exposed to 
STRONTIUM 238 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-9. Strontium Concentrations in Human Body Fluids and Tissues 

Sample Unitsa Mean Range 

Blood μg/L 27 No data 

Bone μg/g 138 63–281 

Brain μg/g 0.08 No data 

Dental plaque μg/g 48 <0.5–1,880 

Erythrocytes μg/L 7.2 No data 

Feces μg/day 1.5 No data 

Hair μg/g 4.2 0.75–10.8 

Kidney μg/g 0.1 No data 

Liver μg/g 0.15 No data 

Lung μg/g 0.38 No data 

Milk μg/L 20 17–295 

Muscle μg/g 0.05 No data 

Nails (finger) μg/g(dry weight) No data 0.43–0.86 

Plasma or serum μg/L 40 10–70 

Saliva μg/L 11 8–63 

Sweat mg/7 hour 0.96 No data 

Tooth (dentin) μg/g 115 14–286 

Tooth (enamel) μg/g 128 14–286 

Urine μg/L No data <0.01–0.03 

a

Values are per wet weight unless otherwise noted. 

Source: Tsalev 1984 
STRONTIUM 239 

6. POTENTIAL FOR HUMAN EXPOSURE 

strontium compounds in the workplace: strontium chloride (8,289), strontium fluoride (5,607), strontium 

hydroxide (385), and strontium nitrate (1,895) (NOES 1983). 

Workers engaged in nuclear fuel cycle operations, such as the handling of radioactive strontium wastes, 

decontamination and decommissioning workers, contaminated soils, and waters may be potentially 

exposed to radioactive strontium. A case of accidental inhalation and dermal exposure to strontium 

titanate contaminated with 90Sr used for lightning rods was recorded, which resulted in an exposure of 

approximately 105

 Bq (2.7 mCi) to the workers (Navarro and Lopez 1998). 

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 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 (USNRC 

1993a). 

As part of an Australian Market Basket Survey in 1994, the estimated daily intakes of strontium for 

6-month-old infants fed exclusively breast milk or infant formula were 47 and 254 μg/day, respectively 

(Gulson et al. 2001). The mean concentration of strontium in amniotic fluid and placenta ranged from 

0.03 to 0.05 mg/L and from 1.6 to 3.2 μg/L, respectively, for mothers from Portugal (Carvalho et al. 

2001). Harrison (1965) notes that strontium in human breast milk is transferred to newborns during 

breast feeding. 

Specific information on the exposure of children to radiostrontium is limited. As for adults in the general 

population, small exposures to children occur from normal ingestion of food and drinking water and 

inhaling air. These exposures may be higher in areas near nuclear fuel processing sites and hazardous 
STRONTIUM 240 

6. POTENTIAL FOR HUMAN EXPOSURE 

waste sites containing radiostrontium. Future accidental exposures could potentially occur from nuclear 

weapons detonation and consequent contamination of air, water, and food. 

Children typically ingest a higher percentage of diary products compared to adults. Levels of 90Sr in body 

tissues tend to increase with age (Glowiak and Pacyna 1978). In a study in the Soviet Union between 

1959 and 1971, children were reported to have elevated levels of 90Sr in bone tissue between the ages of 

1 and 4 years (Marei et al. 1976). The elevated levels of 90Sr for children of this age were determined to 

be a direct result of diet, primarily from 90Sr contaminated cow’s milk. In a 1978 study in Poland, 

females between 0 and 20 years of age had the highest level of 90Sr accumulation in the gonad tissues for 

all age levels (Glowiak and Pacyna 1978). No explanation as to a cause for this accumulation was 

provided. For 1979–1994 births, the average concentration of 90Sr in deciduous teeth from children of 

Western Suffolk County (New York), Eastern Suffolk County (New York), Dade County (Miami, 

Florida), and Ocean County (New Jersey) were 1.56, 1.02, 2.80, and 1.54 pCi/g calcium, respectively 

(Gould et al. 2000). No additional information is available on whether children differ from adults in their 

weight-adjusted intake of strontium. There is no information on 90Sr levels in amniotic fluid, meconium, 

cord blood, neonatal blood, or breast milk. 

At hazardous waste sites, radiostrontium that is found in excess of natural background levels is most 

likely to be in soil and presents a special hazard for young children. Hand-to-mouth activity resulting in 

inadvertent soil consumption or intentional consumption of soil (pica behavior) will result in oral 

exposure to radiostrontium. Young children often play close to the ground and frequently play in dirt, 

which increases their dermal exposure to radiostrontium in dust and soil. The degree of hazard in each 

case depends on the form of strontium present at the waste site. 

Compared to adults, the potential for radiostrontium exposure is greater for children who consume foods 

(e.g., milk, grains) produced in areas with elevated concentrations of radiostrontium in the soil and for 

children with elevated concentrations of radiostrontium in their drinking water. Children are more likely 

to be exposed to 90Sr in cow’s milk produced in contaminated areas. Table 6-8 summaries pasteurized 

milk samples in the United States for July 1997 (EPA 2002b). The average concentration of 90Sr in 

pasteurized milk during this period was 0.9 pCi/L (33 mBq/L). 

Other home exposures are unlikely since no household products or products used in crafts, hobbies, or 

cottage industries contain significant amounts of radiostrontium. Radiostrontium exposure to children 

from parents’ work clothes, skin, hair, tools, or other objects from the workplace is possible if the parent 
STRONTIUM 241 

6. POTENTIAL FOR HUMAN EXPOSURE 

is exposed to radiostrontium at work. However, no specific cases of home contamination with 

radiostrontium were located in the literature. 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 

Cigarettes and tobacco leaves are known to contain strontium, and individuals who smoke may be 

exposed to higher levels of strontium. Strontium has been found in the tobacco leaves and ash of 

cigarettes at average levels of 141 and 373 mg/kg, respectively (Iskander 1986). 

The potential for 90Sr exposure is greater for individuals who consume foods grown in areas with elevated 

concentrations of 90Sr in soil, and for individuals with elevated concentrations of 90Sr in drinking water. 

Industries where higher exposures to 90Sr are known to occur include nuclear weapons test sites, nuclear 

weapons production, and nuclear reactors facilities. Populations with potentially high exposure include 

DOE employees involved in heavy construction, decontamination activities, chemical processing, and 

fabrication. 

Populations with a relatively short food chains (e.g., Arctic peoples) and a higher per capita consumption 

of country foods that have elevated levels of contamination from radionuclides, will have a higher 

exposure to 90Sr (Barrie et al. 1992). Caribou or reindeer feeding on arctic vegetation are more likely to 

accumulate higher body burdens of 90Sr in edible tissues than other herbivorous animals with less 

restrictive diets (Witkamp 1966). Concentrations of 90Sr in caribou meat per gram of calcium were high 

(150 pCi/g Ca) compared with those of Alaskan-grown cabbage (6 pCi/g Ca) and potatoes (8 pCi/g Ca), 

marine fish (5 pCi/g Ca), and whale meat (1 pCi/g Ca). Arctic peoples, who depend on caribou and 

reindeer for sustenance, may have an elevated body burden of 90Sr compared to other people who 

consume a more varied diet (Witkamp 1966). However, the 1966 peak levels reported in this study are 

expected to have fallen to minuscule levels since the Test Ban Treaty of 1962. 

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 strontium is available. Where adequate information is not 

available, ATSDR, in conjunction with the National Toxicology Program (NTP), is required to assure the 
STRONTIUM 242 

6. POTENTIAL FOR HUMAN EXPOSURE 

initiation of a program of research designed to determine the health effects (and techniques for developing 

methods to determine such health effects) of strontium. 

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. Relevant data on the physical and chemical properties of 

strontium and strontium compounds are available in the literature and are sufficient to permit estimation 

of its environmental fate (ChemFinder 2002; Cotton and Wilkenson 1980; Hibbins 1997; HSDB 2002; 

Lide 1995, 2000; Merck 1989; Sigma-Aldrich 2000). The physical and chemical properties of 

radiostrontium and radiostronium compounds are expected to be equivalent to those for stable strontium. 

Data on the radioactive properties of isotopes of strontium are available (Lide 1995). 

Production, Import/Export, Use, Release, and Disposal. Data regarding the past and present 

production and import/export volumes for strontium are available (Adams 1975; USGS 1998, 1999, 

2002). The uses of strontium and strontium compounds are well known with more than 85% of all 

strontium consumed in the United States used in the manufacture of ceramics and glass products (Hibbins 

1997; USGS 1999, 2002). Strontium is found in food products such as fruits and vegetables (Barnes 

1997; USGS 1980). Since strontium is not covered under Superfund Amendments and Reauthorization 

Act (SARA), Title III, manufacturers and users are not required to report releases to the EPA’s Toxics 

Release Inventory (TRI). Most nonradioactive strontium minerals, strontium compounds, and strontiumcontaining materials do not require special disposal and handling requirements. 

Data regarding the past and present production and import/export volumes for radiostrontium are limited 

(DOE 1996b, 1996c). The uses of radiostrontium and radiostrontium compounds are restricted primarily 

to medicinal, analytical, and power generation applications (Alimov 2003; Murray 1994). Radioactive 

strontium (e.g., 90Sr) was released into the atmosphere from aboveground testing of nuclear weapons 

during the period of 1945–1980. Nuclear weapon testing injects radioactive material into the 

stratosphere, which results in wide dispersal of radionuclides. However, atmospheric deposition of 90Sr 
STRONTIUM 243 

6. POTENTIAL FOR HUMAN EXPOSURE 

has steadily decreased from a high in 1963 of approximately 1.10x108 GBq (3.0 MCi) to <3,000 Ci in 

1990, which suggests that global concentrations of 90Sr in the atmosphere have declined (DOE 1996c). 

The disposal of radiostrontium and radiostrontium contaminated wastes is governed by the U.S. Nuclear 

Regulatory Commission (USNRC) regulations, and releases of radiostrontium and radiostrontium 

contaminated wastes are governed by USNRC and EPA regulations. 

Environmental Fate. Information about the partitioning and mobility of strontium and strontium 

compounds in the environment is available (Bunde et al. 1997; Bunzl and Schimmack 1989; Hayes and 

Traina 1998; Helal et al. 1998a, 1998b; O’Day et al. 2000; Parkman et al. 1998; Sahai et al. 2000). 

Strontium released into the atmosphere from natural and anthropogenetic activities is transported and 

redeposited on the earth by dry or wet deposition (NCRP 1984). Because strontium is an element, its 

atoms do not degrade by environmental processes such as hydrolysis or biodegradation. 

Information about the partitioning and mobility of 90Sr in environment is available (Bunde et al. 1997, 

1998; DOE 1996d; Kashparov et al. 2001; Mahara 1993; Sokolik et al. 2001; Toran 1994). 

Radiostrontium released into the atmosphere from anthropogenetic activities is transported and 

redeposited on the earth by dry or wet deposition (NCRP 1984). Radiostrontium does not degrade by 

environmental processes such as hydrolysis or biodegradation. However, radioactive strontium will be 

subject to radioactive decay and transformation to other elements. Eventually, all of the radioactive 

strontium will be transformed into stable zirconium by the process of radioactive decay. Additional 

information on the environmental fate of 90Sr in different forms of mixed waste may be beneficial. 

Studies investigating mixed waste matrixes may be useful information for accessing the current and 

potential risk of the storage of liquid HLW in buried underground tanks. Mixed waste forms that pose the 

highest potential risk include mixtures such as metals-radiostrontium, metals-radiostrontium-organic 

acids, metals-radiostrontium-complexing agents, and metals-radiostrontium-ketones (DOE 1992). 

Bioavailability from Environmental Media. The absorption and distribution of strontium and 

radiostrontium as a result of inhalation, dermal, or oral exposures have been discussed in Sections 3.5.1 

and 3.5.2. Limited information on the bioavailability of strontium and radiostrontium from 

environmental media (e.g., plants and animals) is available. Additional studies on the bioavailability of 

strontium and radiostrontium from environmental media would be useful. 

Food Chain Bioaccumulation. The uptake or bioaccumulation of strontium and radiostrontium by 

plants and organisms is the mechanism by which strontium and radiostrontium in air, water, and soil enter 
STRONTIUM 244 

6. POTENTIAL FOR HUMAN EXPOSURE 

into the food chain of humans. Information on tissue levels of strontium and radiostrontium indicating 

storage in the organism as a result of exposure to contaminated media would be useful. Information on 

whether strontium and radiostrontium are biomagnified (increased levels in predators resulting from the 

consumption of contaminated prey organisms) would also be helpful. 

Exposure Levels in Environmental Media. Strontium has been detected in air (Dzubay and 

Stevens 1975; Sweet et al. 1993; Witz et al. 1986), water (Capo et al. 1998; EPA 1981, 2002b; USGS 

1963), soil (Capo et al. 1998; EPA 1995a), plants (Sato et al. 1977), and foodstuff (Barnes 1997; USGS 

1980). Reliable monitoring data for the levels of strontium in contaminated media at hazardous waste 

sites are needed so that the information obtained on levels of strontium in the environment can be used in 

combination with the known body burden of strontium to assess the potential risk of adverse health 

effects in populations living in the vicinity of hazardous waste sites. In a 1994 total diet study in the 

United Kingdom, the total dietary exposure to stable strontium was estimated at 1.3 mg/day (Ysart et al. 

1999). As part of an Australian Market Basket Survey in 1994, the estimated daily intakes of strontium 

for female adults ranged from 0.89 to 1.2 mg/day (Gulson et al. 2001). Combining air, water, and diet 

exposures estimates, the total daily exposure to strontium is ~3.3 mg/day. 

Radiostrontium has been detected in air (DOE 1996c; Eisenbud 1987), water (DOE 1992, 1996c; EPA 

2000a, 2002b; Hamilton et al. 1996; Kraybill 1983; Pujol and Sanchez-Cabeza 2000), soil (DOE 1992; 

Fresquez et al. 1996b; Kashparov et al. 2001; Malek et al. 2002; Sokolik et al. 2001), and foodstuffs 

(Capar and Cunningham 2000; Cunningham et al. 1989, 1994; Eisenbud 1987; EPA 2002b). Information 

on levels of radiostrontium is needed. Exposure levels of 90Sr in environmental media have decreased as 

a result of radioactive decay from a high in the 1960s. However, updated information on the 

concentration levels in air, water, soil, and food (e.g., milk products) may be useful. Specific monitoring 

of radiostrontium in airborne particulates may also be beneficial. Reliable monitoring data for the levels 

of radiostrontium in contaminated media at hazardous waste sites may be useful so that the information 

obtained on levels of radiostrontium in the environment can be used in combination with the known body 

burden of radiostrontium to assess the potential risk of adverse health effects in populations living in the 

vicinity of hazardous waste sites. Using a conservative estimate of total dietary exposure for 90Sr of 

5 pCi/day (0.19 Bq/day) (Cunningham et al. 1989) and drinking water exposure of 0.2 pCi/day 

(7 mBq/day) (EPA 2000a), the total estimated daily exposure to strontium is approximately 5.2 pCi/day 

(0.19 Bq/day). 
STRONTIUM 245 

6. POTENTIAL FOR HUMAN EXPOSURE 

Exposure Levels in Humans. Strontium has been detected in human tissues, as illustrated in 

Table 6-9 (Tsalev 1984). The highest concentrations of strontium are in the bones and teeth (Iyengar et 

al. 1978; Tsalev 1984). However, these data are not current (within 3 years). Additional human tissue 

monitoring data for strontium is needed for populations surrounding hazardous waste sites. This 

information is necessary for assessing the need to conduct health studies on these populations. 

90Sr has been detected in human tissues with the highest concentrations measured in boney tissues 

(Baratta and Ferri 1966; Kulev et al. 1994). However, these data are not current (within 3 years). 

Exposure levels of humans to 90Sr have decreased as a result of radioactive decay from a high in the 

1960s. Additional human tissue monitoring data for radiostrontium is needed for populations surrounding 

hazardous waste sites. This information is necessary for assessing the need to conduct health studies on 

these populations. 

Exposures of Children. Children are exposed to strontium in the same manner as adults, primarily 

by food and water intake. No information was available on unique exposure pathways for children (e.g., 

pica children, dermal). However, children typically ingest a higher percentage of diary products 

compared to adults. Data exist on the levels of strontium in human breast milk (Gulson et al. 2001). 

Additional body burden studies on children are needed for strontium. Additional studies are needed to 

determine whether children are different in their weight-adjusted intake of strontium. Better and more 

recent information on exposure levels of strontium to children may be beneficial. 

Children are exposed to radiostrontium in the same manner as adults, primarily by food and water intake. 

No information was available on unique exposure pathways for children (e.g., pica children, dermal). 

However, children typically ingest a higher percentage of diary products compared to adults. Exposure 

levels of children to 90Sr have decreased as a result of radioactive decay from a high in the 1960s. Data 

exist on the levels of 90Sr in deciduous teeth (Gould et al. 2000). Additional body burden studies on 

children are needed for radiostrontium. Additional studies are needed to determine whether children are 

different in their weight-adjusted intake of radiostrontium. Better and more recent information on 

exposure levels of radiostrontium to children may be beneficial. 

Child health data needs relating to susceptibility are discussed in Section 3.13.2 Identification of Data 

Needs: Children’s Susceptibility. 
STRONTIUM 246 

6. POTENTIAL FOR HUMAN EXPOSURE 

Exposure Registries. No exposure registries for strontium or radiostrontium were located. These 

substances are not currently compounds for which a subregistry has been established in the National 

Exposure Registry. These substances will be considered in the future when chemical selection is made 

for subregistries 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. 

6.8.2 Ongoing Studies 

The Federal Research in Progress (FEDRIP 2002) database provides additional information obtainable 

from a few ongoing studies that may fill in some of the data needs identified in Section 6.8.1. These 

studies are summarized in Table 6-10. 
STRONTIUM	 247 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-10. Ongoing Studies on the Environmental Effects of Strontiuma 

Investigator Affiliation Study Sponsor 

Ron, Elaine NIH Studies of populations exposed to occupational NIH 

sources of radiation 

Helt, JE ANL Waste volume reduction using surface DOE-OEM 

characterization and decontamination by laser 

ablation 

Todd, Terry A INEEL Laboratory radioactive waste solvent extraction DOE-OEM 

and ion exchange 

Smith, Robert W INEEL Calcite precipitation and trace metal partitioning DOE-OEM 

in groundwater and the vadose zone: 

Remediation of 90Sr and other divalent metals 

and radionuclides in arid western environments 

Louie, Gary D PNNL Chemical separations for nuclear waste disposal DOE-OEM 

Louie, Gary D PNNL Chemical speciation of strontium, americium, and DOE-OEM 

curium in waste 

ANL = Argonne National Laboratory; DOE-OEM = Department of Energy-Office of Environmental Management; 

INEEL = Idaho National Engineering and Environmental Laboratory; NIH = National Institute of Health; PNNL = 

Pacific Northwest National Laboratory 

a

Source: FEDRIP 2002 

STRONTIUM 249 

7. ANALYTICAL METHODS 

The purpose of this chapter is to describe the analytical methods that are available for detecting, 

measuring, and/or monitoring strontium, its metabolites, and other biomarkers of exposure and effect to 

strontium. 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) and the American Public Health Association (APHA). 

Additionally, analytical methods are included that modify previously used methods to obtain lower 

detection limits and/or to improve accuracy and precision. 

Its companion manual, the Draft Multi-Agency Radiological Laboratory Analytical Protocols (MARLAP) 

manual, robustly describes relevant analytical equipment and methods, and became available for public 

comment in July 2001 (MARLAP 2001). 

7.1 BIOLOGICAL MATERIALS 

Strontium can enter the human body through inhalation, ingestion, or penetration through the skin. 

Measurement of the quantities of radiostrontium in the body can be performed by two primary methods, 

in vivo measurements and in vitro measurements. These types of measurements are called bioassays. 

In vivo techniques measure the quantities of internally deposited radiostrontium directly using a whole 

body counter, while in vitro techniques permit estimation of internally deposited strontium by analysis of 

body fluids, excreta, or (in rare instances) tissues obtained through biopsy or postmortem tissue 

sectioning. Some of these analytical methods are summarized in Table 7-1. 

7.1.1 Internal Strontium Measurements 

In vivo (or direct) measurements of radioactive strontium in the body are made with radiation detector 

systems and associated electronics called whole body counters that measure radiation as it leaves the body 

from internally deposited radioactive strontium. This system measures the emission of gamma rays or 

x-rays from internally deposited radionuclides. These counters are insensitive to beta particles emitted 
STRONTIUM 250 

7. ANALYTICAL METHODS 

Table 7-1. Analytical Methods for Determining Strontium in Biological Samples 

Sample Analytical Detection Percent 

matrix Sample preparation method limit recovery Reference 

Blood Acidification with nitric GFAAS 0.13 mg/L 94.5–102.5 Burguera et al. 

acid; dilution; addition of 1999 

La matrix modifier 

Blood Acid digestion; iron TRXF 0.04 μg/mL No data Prange et al. 1989 

extraction; clean-up by ion 

exchange; thin film 

deposition 

Blood Acid digestion; dilution ICP-AES 0.3 μg/L 113 NIOSH 1994; 

Piette et al. 1994 

Blood serum Dry ashing; neutron TNA 0.02 μg/mL 75–90 Teree and Cohn 

activation; chemical 1966 

separation 

Blood serum Acidification and dilution ICP-MS No data 99 Muñiz et al. 1999 

Bone Acidification with nitric GFAAS 0.13 mg/L 96.5–102.9 Burguera et al. 

acid; dilution; addition of 1999 

La matrix modifier. 

Bone Acid digestion ICP-MS 6 μg/g dry No data Outridge et al. 1996 

weight 

Bone ash Acid dissolution; clean-up β-GPC No data No data Mutschke and 

by coprecipitation and Pribilla 1967 

scavenging 

Hair Ashed PIXE 1 μg/g No data Clayton and 

Wooller 1985 

Tissues Acid digestion; dilution ICP-AES No data 113 NIOSH 1994 

Tissues Complexometric digestion GFAAS 2.2 ng/g 99±4.2 D’Haese et al. 1996 

in TMAH/EDTA matrix 

with heat 

Urine Acidification with nitric GFAAS 0.13 mg/L 98.8–101.5 Burguera et al. 

acid; dilution; addition of 1999 

La matrix modifier 

Urine Coprecipitation with LSC 7 dpm/L 95±5 Dietz et al. 1991 

calcium phosphate; (0.82 Bq/L 

sample wet ashed with or 

nitric acid; extraction and 22 pCi/L) 

separation on Crown 

ether loaded 

chromatographic column 

Urine Wet ashed; precipitation LSC 0.6 pCi 100 Kramer and Davies 

with oxalate; acid (22 mBq) 1982 

dissolution; chemical 

extraction 

β-GPC (total radioactive strontium) = beta gas proportional counter; Bq = Becquerel; dpm = disintegrations per 

minute; EDTA = ethylenediamine tetraacetic acid; GFAAS (total strontium) = graphite furnace atomic absorption 

spectroscopy; ICP-AES (total strontium) = inductively coupled plasma atomic emission spectroscopy; ICP-MS 

(isotopic strontium composition) = inductively coupled plasma-mass spectrometry; La = Lanthanum; LSC (isotopic 

quanitification of 89Sr and 90Sr) = liquid scintillation counting; pCi = pico curies (10-12 curies); PIXE (total 

strontium) = proton induced x-ray emission; TMAH = tetramethylammonium hydroxide; TNA (total 

strontium) = thermal neutron activation and radiometric measurement; TRXF (total strontium) = total-reflection x-ray 

fluorescence 
STRONTIUM 251 

7. ANALYTICAL METHODS 

from radiostrontium; thus, the utility for radiostrontium is limited to high exposure measurements. In 

vivo assays are the most direct method of quantifying internally deposited radioactive materials. The 

determinations of 90Sr levels are achieved by measuring, with a phoswich detector, the bremsstrahlung of 

the 90Y beta rays (photons with energies ranging from 30 to 160 keV). The most commonly used 

detectors for measurement of 90Y bremsstrahlung (i.e., electromagnetic radiation) by in vivo counting are 

sodium iodide or phoswich (NaI and CsI sandwich) (Tokareva et al. 2000). For whole-body counting, a 

scanning-bed geometry in a special shielding room is typically used. Although whole body counters may 

be used in many configurations, a chest counter is usually used for inhaled radioactive materials. In vivo 

analysis is widely used throughout the nuclear industry, both commercial and government, for quantifying 

levels of insoluble radioactive materials in the body (Kozheurov 1994). 

In vivo counting systems are calibrated using tissue-equivalent phantoms. These phantoms have shapes 

similar to the human torso and are made of polystyrene or other tissue equivalent material. Standard 

radioactive strontium sources of known activity are inserted at locations where strontium would be 

expected to accumulate in a human body. Relationships are determined between the radioactive 

strontium activity measured by the detection system and the known activity in the phantom (Kozheurov 

1994). 

7.1.2 In Vivo and In Vitro Radiostrontium Measurements 

In vitro radioactive strontium analyses are routinely performed in support of a personnel monitoring 

program or in cases where the size of an operation does not justify the cost of whole body counter 

facilities. These analyses are usually done on urine samples, but other types of body materials (e.g., feces 

or blood) may also be used. Urinalysis is effective for analysis of transportable or soluble strontium. 

Strontium may also be measured in fecal material using the same methods identified above for urinalyses, 

except that this matrix requires extensive preparation. 

7.2 ENVIRONMENTAL SAMPLES 

Two types of methods are commonly used for measurement of strontium and radiostrontium in 

environmental samples. The first is field surveys using portable survey instruments, and the second is 

analysis of samples procured in the field that are returned to the laboratory for quantification. 
STRONTIUM 252 

7. ANALYTICAL METHODS 

7.2.1 Field Measurements of Radiostrontium 

Radiostrontium measurements in the field are typically qualitative in nature in that the instruments simply 

respond to beta emissions, regardless of their origin. However, the levels can be measured quantitatively 

if key parameters are known, such as the relative abundances of all beta-emitting isotopes present, the 

thickness of the layer being assessed, and the detection efficiency of the instrument for the type of surface 

being assessed. Measurements in the past have typically been made using portable, hand-held GeigerMueller or beta scintillation detectors equipped with a count rate meter, which detect beta radiation while 

discriminating against other forms of ionizing radiation in the same area. Survey instruments can provide 

a quick estimate or a measure of the level of activity that might be present. However, more accurate 

measurements of radioactive strontium may require that samples be taken for laboratory analyses. 

7.2.2 Laboratory Analysis of Environmental Samples 

Analytical methods for measuring strontium in environmental samples are summarized in Table 7-2. The 

available methods can be divided into two groups: chemical methods to determine the total mass of 

strontium in a sample and radiological methods to determine amounts of radioactive isotopes. 

Environmental media that have been tested for strontium include air filters, swipes, biota, water, soil, and 

others. A full range of laboratory analysis methods has been used to quantify the total strontium or its 

radioactive isotopes. 

The chemical methods for detecting total strontium include spectrophotometry, fluorometry, kinetic 

phosphorescence, atomic absorption spectroscopy (e.g., flame and graphite furnaces), energy dispersive 

x-ray analysis (i.e., EDAX), x-ray fluorescence spectrometry, and inductively coupled plasma 

spectroscopy-atomic emission and mass spectrometry applications (i.e., ICP-AES and ICP-MS). 

The quantity of radioactive strontium is typically determined by gas-flow proportional, liquid 

scintillation, and Cherenkov counting techniques (Scarpitta et al. 1999). The standard EPA analytical 

procedure to determine radiostrontium in water is Method 905.0, and several methods are permutations of 

this procedure. A stable strontium carrier is added to the water sample so that 89Sr and 90Sr are 

precipitated as insoluble carbonates. The sample then undergoes a preliminary counting that represents 

the total strontium activity (89, 90Sr) plus a small fraction of 90Y that has grown in by radioactive decay. 
STRONTIUM	 253 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining Strontium in 

Environmental Samples 

Sample Percent 

Sample matrix Sample preparation Analytical method detection limit recovery References 

Air	 Particulate collection 

on cellulose filter; 

acid digestion 

Water	 Acid digestion 

Water	 Filtration; acid 

digestion; add matrix 

modifier 

Water	 Wet acid digestion 

Drinking, raw, Wet acid digestion; 

and waste addition of Sr carrier 

water	 and precipitation as 

SrCO3; extraction of 

Yttrium; precipitation 

of Yttrium oxalate. 

Water	 Complex EDTA; ion 

chromatography; 

precipitate Sr effluent 

fraction as SrCO3 

Water (high Sr Ion chromatography; 

concentration)	 dilution 

Saline water	 Dilution 

Soils and Digest organic 

sediments	 matter; pyrosulfate 

fusion; dissolve 

condensed 

phosphates 

Soils and Fuse with NaOHsediments	 Na2CO3; dissolve in 

acid; ion exchange 

Vegetation and Dry ash; 

food	 complexation with 

EDTA; ion exchange 

chromatography; 

precipitate Sr effluent 

fraction as SrCO3 

Milk	 Complexation of Y in 

growth; extraction; 

precipitation as 

oxalate 

FAAS (Method D4185) 

Spectrophotometric 

measurement (total 

strontium) (Method 911.03) 

FAAS (Method D3920; 

7780) 

ICP-AES (Method 200.15) 

β-GPC (Method 973.66; 

7500-Sr) 

β-GPC (Method 008) 

β-GPC 

FAAS (Method D3352) 

β-GPC 

β-GPC (Method 008-S) 

β-GPC (Method 008-V) 

β-GPC (Method 974.37) 

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	 ATSM 1999 

No data	 AOAC 1990 

No data	 ASTM 1999; 

OSW 1992 

No data	 EMMI 2000a 

93–99	 AOAC 1990; 

APHA 1992 

No data	 EMMI 2000b 

No data	 EMMI 2000c, 

2000d 

100–106 ASTM 1999 

No data	 EMMI 2000c, 

2000d 

No data	 EMMI 2000b 

No data EMMI 2000b 

No data	 AOAC 1990 

89Sr and 90Sr measured separately by measuring 90Y in-growth 

ß-GPC (total radioactive strontium) = beta gas proportional counter; EDTA = ethylenediamine tetraacetic acid; FAAS 

(total strontium) = flame atomic absorption spectroscopy; ICP-AES (total strontium) = inductively coupled plasma 

atomic emission spectroscopy 
STRONTIUM 254 

The 90Y is allowed to reach equilibrium (e.g., approximately a 2-week period) and then is separated with 

stable yttrium-carrier as yttrium hydroxide (i.e., Y(OH)3 ). The Y(OH)3 precipitates are converted to the 

oxalate and the solid oxalate is beta counted in a low background gas-flow proportional counter. The 90Sr 

concentration is determined from the 90Y activity and the 89Sr concentration by difference. Variations of 

the above method involve different techniques of selectively separating strontium from environmental 

samples. Using the various separation methods already described, Cherenkov counting, in conjunction 

with liquid scintillation, has also been use to detect 90Sr by measuring the concentration of its progeny, 

90Y, in solution (Scarpitta et al. 1999). 

Horwitz et al. (1991) developed an extraction chromatography technique in which strontium can be 

selectively separated from other interfering radionuclides such as alkaline and alkaline earth element ions. 

The technique uses an extraction column (e.g., Sr-resin) with a crown ether (4,4’(5’)-bis(tertbutylcyclohexano)-18-crown-6) sorbed on an inert polymeric porous support. A sample with 90Sr 

digested in concentrated nitric acid is diluted and loaded on the Sr-resin column in ~3 M nitric acid. 

Interfering elements are removed from the column with ~1 M nitric acid and strontium ions are 

subsequently eluted with a dilute acid solution. 90Sr ions are then beta counted using a low background 

gas flow proportional counter or Cherenkov counting of 90Y as previously discussed (Grahek et al. 1999; 

Torres et al. 2000, 2002). One disadvantage with this technique is some ions interfere with the strontium 

separation. For example, potassium diminishes the capacity of the Sr-resin column to retain strontium; 

lead also shows a very strong retention on the Sr-resin and irreversibly blocks Sr adsorption sites (Miró et 

al. 2002). Recently, improvements have been made to the extraction process using a wetting film 

technique, which has been shown to reduce ionic interferences (Miró et al. 2002). 

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 strontium 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 strontium. 

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 
STRONTIUM 255 

8. REGULATIONS AND ADVISORIES 

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. 

7.3.1 Identification of Data Needs 

Methods for Determining Biomarkers of Exposure and Effect. Analytical methods with 

satisfactory sensitivity and precision are available to determine the levels of strontium in human tissues 

and body fluids. Strontium and radiostrontium are found in essentially all food, water, and air, so 

everyone is exposed to some levels. Recently, Sutherland et al. (2000a, 2000b) developed a molecular 

biological strategy to identify clustered lesions in DNA resulting from in vitro cellular exposure to 

gamma radiation. It is possible that this technique might be adapted to evaluate genetic damage in blood 

cells following exposure to radioactive strontium. This method, however, will not be specific for 90Sr 

effects. 

Methods for Determining Parent Compounds and Degradation Products in Environmental 

Media. Analytical methods with the required sensitivity and accuracy are available for quantification 

of strontium, both total and isotopic, in environmental matrices (Table 7-2). Knowledge of the levels of 

strontium in various environmental media, along with the appropriate modeling (see Chapters 3 and 5), 

can be used to evaluate potential human exposures through inhalation and ingestion pathways. 

7.3.2 Ongoing Studies 

No ongoing studies investigating new methods for detection and speciation of strontium or radiostrontium 

were identified in the Federal Research in Progress database (FEDRIP 2002). 

STRONTIUM 257 

8. REGULATIONS AND ADVISORIES 

The international, national, and state regulations and guidelines regarding stable strontium in air, water, 

and other media are summarized in Table 8-1. The regulations and guidelines regarding radioactive 

strontium are summarized in Tables 8-2 and 8-3. 

Stable Strontium. An MRL of 2.0 mg strontium/kg/day for intermediate-duration oral exposure to 

strontium was calculated by dividing a NOAEL of 140 mg strontium/kg/day for skeletal toxicity in young 

rats (Storey 1961) by an uncertainty factor of 30 and a modifying factor of 3 (see Appendix A). 

The EPA derived a chronic reference dose (RfD) of 0.6 mg/kg/day for strontium (IRIS 2002). The RfD is 

based on a NOAEL of 190 mg strontium/kg/day for skeletal toxicity in young rats (Storey 1961). 

The EPA has not classified stable strontium for human carcinogenicity (IRIS 2002). A number of 

agencies have classified strontium chromate as a human carcinogen by the inhalation route, on the basis 

of occupational and animal studies. The carcinogenicity of strontium chromate is attributed to the 

hexavalent chromium ion and not to strontium. The American Conference of Governmental Industrial 

Hygienists (ACGIH) has given strontium chromate the classification A2, suspected human carcinogen, 

and has established an 8-hour time-weighted-average (TWA) of 0.0005 mg/m3

 for occupational exposure 

(ACGIH 2002). The International Agency for Research on Cancer (IARC) has assigned strontium 

chromate, along with other chromates, to Group 1, as a human carcinogen (IARC 1990, 2002a). No other 

stable strontium compound is listed by IARC. 

Radioactive Strontium. No MRLs were derived for inhalation or oral exposures to radioactive strontium. 

The EPA has not derived reference concentrations (RfCs) or RfDs for radioactive strontium (IRIS 2002), 

nor does the Integrated Risk Information System (IRIS) database provide cancer assessments for 

radioisotopes of strontium. This function is the responsibility of the EPA Office of Radiation and Indoor 

Air (ORIA). All radionuclides, including radioisotopes of strontium, are classified as known human 

(Group A) carcinogens. This classification is based on results of epidemiological studies of Japanese 

atomic bomb survivors, underground uranium miners, radium dial painters, and patients subjected to a 

variety of radiation treatments, as well as results of laboratory animal research and mammalian tissue 

culture studies. ORIA has published cancer slope factors (mortality and morbidity cancer risk estimates) 

for all known radionuclides, by various exposure routes (inhalation, drinking water ingestion, food 

ingestion, soil ingestion, immersion in a cloud, and external exposure from contaminated soil) for five age 
STRONTIUM	 258 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Stable Strontium 

Agency Description Information Reference 

INTERNATIONAL 

Guidelines: 

 IARC Carcinogenicity classification IARC 1990, 

 Strontium chromate Group 1a 2001a 

NATIONAL 

Regulations and 

Guidelines: 

a. Air 

ACGIH TLV (8-hour TWA) ACGIH 2002

 Strontium chromate 10x5-4 mg/m3 

EPA HAP HSDB 2001 

 Strontium chromate 

NIOSH REL No data 

OSHA PEL No data 

b. Water 

EPA Drinking water guideline 4 mg/L HSDB 2001 

 Health Advisories EPA 2000d 

 10-kg child 

1 Day 25 mg/L 

10 Day 25 mg/L 

Lifetime 4 mg/L 

DWEL 20 mg/L 

USNRC Maximum ambient environmental level 10 mg/L HSDB 2001 

in potable water 

c. Food No data 

d. Other 

ACGIH Carcinogenicity classification ACGIH 2002

 Strontium chromate A2b 

EPA Carcinogenicity classification Group Dc

 EPA 2000d 

RfD 6x10-1 mg/kg/day IRIS 2001 

 Reportable quantity EPA 2001a 

 Strontium chromate 1,000 pounds 40CFR302.4 

Toxic pollutants and hazardous EPA 2001b 

substances required to be identified 40CFR122, 

Appendix D 

STATE 

a. Air No data 

b. Water 

Florida Drinking water guideline 4.2 mg/L HSDB 2001 

Maine Drinking water guideline 2.4 mg/L HSDB 2001 

c. Food No data 

d. Other 

Arizona Soil remediation levels BNA 2001 

 Residential 4.6x104 mg/kg
 

 Non residential 1x106 mg/kg 
STRONTIUM 259 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Stable Strontium 

Agency Description Information Reference 

STATE (cont.) 

Florida Toxic substances in the workplace; Strontium chromate BNA 2001 

Florida substance list 

a

Group 1: carcinogenic to humans (refers to hexavalent chromium) 

b

A2: suspected human carcinogen (refers to hexavalent chromium) 

c

Group D: not classifiable as to human carcinogenicity 

ACGIH = American Conference of Governmental Industrial Hygienists; BNA = Bureau of National Affairs; 

CFR = Code of Federal Regulations; DWEL = drinking water equivalent level; EPA = Environmental Protection 

Agency; HAP = hazardous air pollutant; HSDB = Hazardous Substances Data Bank; IARC = International Agency for 

Research on Cancer; IRIS = Integrated Risk Information System; NIOSH = National Institute for Occupational Safety 

and Health; OSHA = Occupational Safety and Health Administration; PEL = permissible exposure limit; 

REL = recommended exposure limit; RfD = reference dose; TLV = threshold limit values; TWA = time-weighted 

averages; USNRC = National Research Council 
STRONTIUM	 260 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

INTERNATIONAL 

Guidelines: 

a. Occupational 

ICRP 

b. General Population 

IARC 

ICRP 

NATIONAL 

Regulations: 

a. Air 

EPA 

OSHA 

USNRC 

Recommended dose limitsa; 

effective dose 

Annual equivalent dose 

Lens of the eye 

Skinc
 

Hands and feet 

Carcinogenicity classification 

Recommended dose limitsa

 Effective dose 

Annual equivalent dose in 

Lens of the eye 

Skinc 

Hands and feet 

Concentration levels for 

environmental compliance for 

90Sr 

Methods for estimating 

radionuclide emissions 

Test method for measuring 

radionuclide emissions from 

stationary sources 

Safety and health regulations 

for construction for ionizing 

radiation 

Toxic and hazardous 

substances for ionizing 

radiation 

Effluent concentrations in air 

90Sr 

Class Df 

Class Yg 

 Occupational values via 

inhalation 

90Sr 

Class Df 

Class Yg 

20 mSv per year, 

averaged over defined 

period of 5 yearsb 

ICRP 1994b 

150 mSv 

500 mSv 

500 mSv 

Group 1d

 IARC 2001b, 

2001c 

1 mSv per yeare 

ICRP 1994b 

15 mSv 

50 mSv 

No data 

1.9x10-14 Ci/m3

Method 114 

10CFR20 regulations 

apply 

 EPA 2001d 

40CFR61, 

Appendix E 

 EPA 2001m 

40CFR61, 

Appendix D 

EPA 2001e 

40CFR61, 

Appendix B 

OSHA 2001 

29CFR1926.53 

 OSHA 2000 

29CFR1910.1096 

3x10-11 μCi/mL 

6x10-12 μCi/mL 

ALI 

(μCi) 

2x101 

4x100 

DAC(μCi/mL) 

8x10-9 

2x10-9 

USNRC 2001g 

10CFR20, 

Appendix B 

USNRC 2001g 

10CFR20, 

Appendix B 
STRONTIUM	 261 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

NATIONAL (cont.) 

b. Water 

EPA 

USNRC 

c. Food 

FDA 

d. Other: Occupational 

DOE 

Analytical methods for 

radioactivity of 90Sr 

Detection limits for man-made 

beta particle and photon 

emitters for 90Sr 

Maximum contaminant levels 

in community water systems; 

average annual concentrations 

assumed to produce a total 

body or organ dose of 

4 millirem/year 90Sr 

 Critical organ 

Monitoring frequency for 

radioactivity in community 

water systems; annual 

monitoring 

Effluent concentrations in 

water 

90Sr 

Class Df 

Releases to sewers; monthly 

average concentration 90Sr 

Class Df 

Sources of radiation used for 

inspection of food; sealed 

units producing radiation 

Individual monitoring 

Limits for members of the 

public entering a controlled 

area (total effective dose 

equivalent in a year) 

Limits for the embryo/fetus 

from conception to birth 

Occupational dose limits for 

general employees; total 

effective dose equivalent 

Radio chemical EPA 2001g 

40CFR141.25 

(a) 

2 pCi/L EPA 2001g 

40CFR141.25 

(c)(2), 

Table B 

EPA 2001f 

40CFR141.16 

8 pCi/L 

Bone marrow 

Analysis of four EPA 2001h 

quarterly samples 40CFR141.26 

(b)(4) 

USNRC 2001g 

10CFR20, 

5x10-7 μCi/mL 

Appendix B 

USNRC 2001g 

10CFR20, 

5x10-6 μCi/mL 

Appendix B 

≤2.2 million electron FDA 2000 

volts 21CFR179.21 

DOE 2001a 

10CFR835.402 

0.01 rem (0.001 Sv) DOE 2001b 

10CFR835.208 

0.5 rem (0.005 Sv) DOE 2001c 

10CFR835.206 

5 rems (0.05 Sv) DOE 2001d 

10CFR835.202 
STRONTIUM	 262 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

NATIONAL (cont.) 

DOE Occupational dose limits for 

general employees; sum of the 

deep dose equivalent for 

external exposures and the 

committed dose equivalent to 

any organ or tissue other than 

the lens of the eye 

Occupational dose limits for 

general employees 

Lens of the eye dose 

equivalent 

Shallow dose equivalent to 

the skin or to any extremity 

Planned special exposures 

Occupational dose limits for 

minors (total effective dose 

equivalent in a year) 

Radiation standards; inhaled 

air DAC for lung retention 90Sr 

Class Dh 

Class Wi 

Class Yj 

DOT Activity values for radionuclides 

90Sr 

A1 

A2 

Carriage by public highway; 

requirements for Class 7 

(radioactive material); total 

transport index number 

General requirements for 

shipments and packages; 

Class 7 (radioactive) materials 

Scope and definitions 

General design requirements 

Table of activity limitsexcepted quantities and 

articles

General requirements for 

shipments and packages; 

Class 7 (radioactive) materials 

50 rems (0.5 Sv) DOE 2001d 

10CFR835.202 

DOE 2001d 

10CFR835.202 

15 rems (0.15 Sv) 

50 rems (0.5 Sv) 

0.1 rem (0.001 Sv) DOE 2001e 

10CFR835.207 

DOE 2000b 

10CFR835, 

Appendix A 

8x10-9 μCi/mL 

No data 

2x10-9 μCi/mL 

DOT 2001b 

49CFR173.435 

5.41 Ci 

2.70 Ci 

50 DOT 2001c 

49CFR177.842 

 DOT 2001d 

49CFR173 

Subpart I 

49CFR173.401 

thru 403 

49CFR173.410 

 49CFR173.425 

 DOT 2001d 

49CFR173 

Subpart I 
STRONTIUM	 263 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

NATIONAL (cont.) 

DOT Requirements for determining 

A1 and A2 values for radionuclides and for the listing of 

radionuclides on shipping 

papers and labels 

Radiation level limitations; any 

normally occupied space 

except carriers operating 

under the provisions of a state 

or federally regulated radiation 

protection program and 

wearing radiation dosimetry 

devices 

Radiation level limitations; any 

point 2 meters (6.6 feet) from 

the outer lateral surfaces, 

excluding top and underside 

Radiation level limitations; 

external surface radiation level 

not to be exceeded under 

conditions normally incident to 

transportation packages 

exceeding the radiation limit 

Transport by exclusive use 

shipment 

 Conditional maximum 

radiation level 

Outer surface of vehicles 

including top and underside 

Superfund; reportable quantity 

for 90Sr 

e. Other: General Population 

EPA Annual possession quantities 

for environmental compliance 

of 90Sr 

 Gaseous form 

 Liquid/powder forms 

 Solid form 

0.02 mSv/hour 

(2 mrem/hour) 

0.1 mSv/hour 

(10 mrem/hour) 

2 mSv/hour 

(200 mrem/hour) and 

the transport index (TI) 

is less than 10 

10 mSv/hour 

(1,000 mrem/hour) 

2 mSv/hour 

(200 mrem/hour) 

0.1 pounds 

5.2x10-4 Ci/year 

5.2x10-1 Ci/year 

5.2x102

 Ci/year 

 DOT 2001d 

49CFR173.433 

DOT 2001e 

49CFR173.441 

DOT 2001e 

49CFR173.441 

DOT 2001e 

49CFR173.441 

DOT 2001a 

49CFR172.101, 

Appendix A, 

Table 2 

EPA 2001d 

40CFR61, 

Appendix E 
STRONTIUM 264 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

NATIONAL (cont.) 

EPA Environmental standards for EPA 2001i 

management and storage of 40CFR191, 

spent nuclear fuel, high-level Subpart A 

and transuranic radioactive 

wastes; applicability and 

definitions 

 Whole body 25 mrem 

Thyroid 75 mrem 

 Other critical organs 25 mrem 

Environmental standards for EPA 2001i 

disposal of spent nuclear fuel, 40CFR191, 

high-level and transuranic Subpart B 

radioactive wastes; 

applicability, definitions, 

containment and individual 

protection requirements 

Environmental standards for 1,000/1,000 MTHM EPA 2001i 

groundwater protection of 40CFR191, 

spent nuclear fuel, high-level Subpart C 

and transuranic radioactive 

wastes; applicability and 

definitions; release limits for 

containment requirements of 

90Sr 

Hazardous waste injection D004–D011 wastes EPA 2001j 

restrictions; waste specific 40CFR148.18 

prohibitions; newly listed and 

identified wastes 

Land disposal restrictions; EPA 2001l 

effective dates of injected 40CFR268, 

prohibited hazardous wastes Appendix VIII 

Radioactive waste; release 1,000 Ci EPA 2001c 

limits for containment 

requirementsk for 90Sr 

40CFR191, 

Appendix A 

Reportable quantity of 90Sr 1x10-1 Ci EPA 2001e 

40CFR302.4, 

Appendix B 

Standards for the control of EPA 2001k 

residual radioactive materials 40CFR192, 

from inactive uranium Subpart A 

processing sites; definitions; 

control of residual radioactive 

materials and their listed 

constituents 
STRONTIUM	 265 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

NATIONAL (cont.) 

EPA Standards for cleanup of land 

and buildings contaminated 

with residual radioactive 

materials from inactive 

uranium processing sites 

Guidance for implementation 

Standards for management of 

uranium byproduct materials 

pursuant to Section 84 of the 

Atomic Energy Act of 1954, as 

amended 

Standards for management of 

thorium byproduct materials 

pursuant to Section 84 of the 

Atomic Energy Act of 1954, as 

amended 

 Underground injection control 

regulations for Class V 

injection wells 

USNRC Activity values for radionuclides (90Sr) 

A1

 A2

 Specific gravity 

Byproduct material listing 

(

90Sr) 

 Column 1 

 Column 2 

Byproduct material listing 

Dose to an embryo/fetus 

(dose equivalent during the 

entire pregnancy) 

 Licensing ice detection 

devices (90Sr) 

Occupational dose limits for 

adults (total effective dose 

equivalent) in a year 

Sum of the deep-dose 

equivalent and the committed 

dose equivalent to any 

individual organ or tissue 

other than the lens of the eye 

 EPA 2001k 

40CFR192, 

Subpart B 

EPA 2001k 

40CFR192, 

Subpart C 

 EPA 2001k 

40CFR192, 

Subpart D 

 EPA 2001k 

40CFR192, 

Subpart E 

 EPA 2001n 

63FR40586 

USNRC 2001i 

10CFR71, 

5.41 Ci Table A-1 

2.70 Ci 

1.4x102

 Ci 

USNRC 2001b 

10CFR33.100, 

1x10-2 Ci Schedule A 

1x19-4 Ci 

0.1 μCi USNRC 2001a 

10CFR30.71, 

Schedule B 

0.5 rem (5 mSv) USNRC 2001m 

10CFR20.1208 

≤50 μCi USNRC 2001c 

10CFR31.10 

5 rems (0.05 Sv) USNRC 2001n 

10CFR20.1201 

50 rems (0.5 Sv) USNRC 2001n 

10CFR20.1201 
STRONTIUM	 266 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

NATIONAL (cont.) 

USNRC Annual limits to the lens of the 

eye, to the skin, and to the 

extremities 

Lens dose equivalent 

Shallow-dose equivalent to 

the skin or to any extremity 

Occupational dose limits for 

minors 

Occupational values for oral 

ingestion (ALI) of 90Sr 

 Class Df 

 Medical use—90Sr as a use of 

unsealed byproduct material 

for uptake, dilution, and 

excretion studies 

 Medical use—90Sr as a sealed 

source in an applicator for 

treatment of superficial eye 

conditions 

Physical protection for spent 

nuclear fuel and high-level 

radioactive waste 

 Radioactive waste; 

classification of 90Sr 

 Column 1l

 Column 2 

 Column 3 

Standards for protection 

against radiation—dose limits 

for individual members of the 

public; total effective dose 

equivalent to individual 

Standards for protection 

against radiation; dose limits 

for individual members of the 

public; dose from external 

source 

 Quality assurance—90Sr 

Quantity of licensed material 

requiring labeling containing 

90Sr 

USNRC 2001n 

10CFR20.1201 

15 rems (0.15 Sv) 

50 rems (0.50 Sv) 

10% of the annual dose USNRC 2001o 

limits specified for adult 10CFR20.1207 

workers in 10 CFR 

20.1201 

USNRC 2001g 

10CFR20, 

3x101

 μCi (bone surf) Appendix B 

4x101 

 USNRC 2001k 

10CFR35.100

 USNRC 2001j 

10CFR35.4000 

 USNRC 2001p 

63FR26955 

USNRC 2001l 

10CFR61.55 

0.04 Ci/m3 

150 Ci/m3 

7,000 Ci/m3 

0.1 rem/year USNRC 2001q 

10CFR20.1301 

0.002 rem/hour USNRC 2001q 

10CFR20.1301 

USNRC 2001h 

10CFR32.62 

1.2x10-1 μCi USNRC 2001d 

10CFR30, 

Appendix B 
STRONTIUM	 267 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

NATIONAL (cont.) 

USNRC Quantity of radioactive 

material requiring need for an 

emergency plan for 

responding to a release (90Sr) 

 Release fraction 

Quantity 

Standards for protection 

against radiation; quantity of 

licensed material requiring 

labeling (90Sr) 

NATIONAL 

Guidelines: 

a. Air 

ACGIH TLV-TWA (90Sr) 

 Effective dose 

Any single year 

Averaged over 5 years 

Annual equivalent dose to 

Lens of the eye 

 Skin 

Hands and feet 

Embryo-fetus exposures once 

the pregnancy is known 

Monthly equivalent dose 

Dose to the surface of 

women’s abdomen (lower 

trunk) 

Intake of radionuclide 

NIOSH REL (TWA) 

b. Water 

EPA MCLG for beta particles 

MCL for beta particles 

Health advisory for beta 

particle activity in drinking 

water 

Cancer group 

c. Food 

FDA Derived intervention leveln 

(DIL; Bq/kg food) for in 

accidentally-contaminated 

human food 

89Sr 

90Sr 

USNRC 2001f 

10CFR30.72, 

Schedule C 

0.01% 

90 Ci 

1x10-1 μCi USNRC 2001e 

10CFR20, 

Appendix C 

Rdiation exposures 

must be kept as low as 

reasonable achievable 

50 mSv 

20 mSv 

150 mSv 

500 mSv 

500 mSv 

ACGIH 2002

ACGIH 2002 

ACGIH 2002 

ACGIH 2002 

0.5 mSv 

2 mSv for the remainder 

of the pregnancy 

1/20 ALI 

No data 

No final MCLG, but zero 

proposed in 1991 

4 mrem 

4 mrem/year at 10-4 

cancer risk 

EPA 2000d 

EPA 2000d 

EPA 2000d 

Group Am EPA 2000d 

FDA 1998 

400o 

160p 
STRONTIUM	 268 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

NATIONAL (cont.) 

d. Other 

EPA Effective dose equivalent 

Adult 

Lens of the eye 

All other organs 

Juvenile workers (<18 years 

old) 

 Pregnant workers 

Carcinogenicity slope factorsq 

Ingestion—lifetime excess 

total cancer risk/pCi 

Water 

82Sr 

85Sr 

85mSr 

89Sr 

90Sr 

90+disentegrationSr 

91Sr 

92Sr 

Carcinogenicity slope factorsq 

Ingestion—lifetime excess 

total cancer risk/pCi 

Food 

82Sr 

85Sr 

85mSr 

89Sr 

90Sr 

90+disentegrationSr 

91Sr 

92Sr 

Carcinogenicity slope factorsq 

Ingestion—lifetime excess 

total cancer risk/pCi 

Soil 

82Sr 

85Sr 

85mSr 

89Sr 

90Sr 

90+disentegrationSr 

91Sr 

92Sr 

5 rem/year 

15 rem/year 

50 rem/year 

0.5 rem/year 

0.5 rem/gestation period 

3.13x10-11 

2.26x10-12 

1.67x10-14 

1.28x10-11 

5.59x10-11 

7.40x10-11 

3.22x10-12 

2.25x10-12 

4.48x10-11 

3.11x10-12 

2.31x10-14 

1.84x10-11 

6.88x10-11 

9.53x10-11 

4.66x10-12 

3.26x10-12 

8.47x10-11 

5.03x10-12 

3.74x10-14 

3.47x10-11 

9.18x10-11 

1.44x10-10 

8.81x10-12 

6.18x10-12 

EPA 1987 

Federal Register 

Part II 

EPA 2002 

EPA 2002 

EPA 2002 
STRONTIUM 269 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

NATIONAL (cont.) 

EPA Carcinogenicity slope factorsr 

Inhalation—lifetime excess 

EPA 2002 

total cancer risk/pCi 82Sr 3.69x10-11 

85Sr 2.56x10-12 

85mSr 8.32x10-15 

89Sr 2.34x10-11 

90Sr 1.05x10-10 

90+disentegrationSr 1.13x10-10 

91Sr 1.70x10-12 

92Sr 1.03x10-12 

Carcinogenicity slope factorss 

External exposure—risk/year 

per pCi/g in soil 82Sr 5.00x10-11 

EPA 2002 

85Sr 2.20x10-6 

85mSr 8.21x10-7 

89Sr 7.19x10-9 

90Sr 4.82x10-10 

90+disentegrationSr 1.96x10-8 

91Sr 3.30x10-6 

92Sr 6.69x10-6 

NCRP Occupational exposurest 

Effective dose limits 

NCRP 1993 

Annual 50 mSv 

Cumulative 10 mSv x age 

 Occupational exposurest 

Equivalent dose annual limits 

for tissues and organs 

Lens of eye 

Skin, hands, and feet 

150 mSv 

500 mSv 

NCRP 1993 

Public exposures (annual) 

Effective dose limit, 1 mSv 

NCRP 1993 

continuous or frequent 

exposures 

Public exposures (annual) 

Effective dose limit, infrequent 

exposuret 

5 mSv 

NCRP 1993 

Public exposures (annual) 

Equivalent dose limits for 

tissues and organst 

Lens of eye 

Skin, hands, and feet 

15 mSv 

50 mSv 

NCRP 1993 
STRONTIUM 270 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

STATE 

a. Air 

Arkansas 

Illinois 

Concentrations in air above 

natural background (90Sr) 

 Occupational 

Non occupational 

Concentrations in air above 

natural background 

S 1x10-9 μCi/mL 

I 5x10-9 μCi/mL 

S 3x10-11 μCi/mL 

I 2x10-10 μCi/mL 

S 3x10-11 μCi/mL 

I 2x10-10 μCi/mL 

BNA 2001 

BNA 2001 

New Jersey Maximum permissible average 

concentrations of radioactive 

materials in air (85mSr) 

 Occupational

 Non occupational 

S 4x10-5 μCi/mL 

I 3x10-5 μCi/mL 

S 1x10-6 μCi/mL 

I 1x10-6 μCi/mL 

BNA 2001 

b. Water 

Alabama 

Alaska 

Drinking water guidelines 

MCL for drinking water (90Sr ) 

8 pCi/L 

8 pCi/L 

HSDB 2001 

ADEC 2000 

Arkansas Concentrations in water above 

natural background (90Sr) 

 Occupational

 Non occupational 

S 1x10-5 μCi/mL 

I 1x10-3 μCi/mL 

S 3x10-7 μCi/mL 

I 4x10-5 μCi/mL 

BNA 2001 

California Drinking water guidelines 

Primary MCL (90Sr ) 

8 pCi/L 

8 pCi/L 

HSDB 2001 

CA Department 

of Health 

Services 2000 

Colorado Standards applicable to 

surface waters 

8 pCi/L BNA 2001 

 Groundwater quality 

standards 

8 pCi/L BNA 2001 

Connecticut Drinking water guidelines 8 pCi/L HSDB 2001 

Florida Drinking water guidelines 

MCL for groundwater (90Sr) 

4,200 μg/L 

8 pCi/L 

HSDB 2001 

FL DEP 2000 

Idaho Primary constituent standards 

for groundwater (90Sr) 

8 pCi/L ID Department of 

Health & Welfare 

1999 

Illinois Drinking water guidelines 

Water quality standard (90Sr) 

8 pCi/L 

1 and 2 pCi/L 

HSDB 2001 

IL Environmental 

Protection 

Agency 1999 
STRONTIUM	 271 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

STATE (cont.) 

New Jersey Maximum permissible average 

concentrations of radioactive 

materials in water (85mSr) 

 Occupational

 Non occupational 

Indiana Maximum contaminant levels 

in community water systems; 

average annual concentrations assumed to produce a 

total body or organ dose of 

4 millirem/year 90Sr 

 Critical organ 

Maine Drinking water guidelines 

Michigan Maximum contaminant levels 

in community water systems; 

average annual 

concentrations assumed to 

produce a total body or organ 

dose of 4 millirem/year 90Sr 

 Critical organ 

New Hampshire Drinking water guidelines 

Wisconsin Drinking water guidelines 

c. Food 

d. Other 

Arkansas Determination of A1 and A2 

quantities (90Sr) 

A1

 A2

 Specific gravity 

Standard for protection 

against radiation 

Colorado Determination of A1 and A2 

(

90Sr) 

A1

 A2 

Delaware Average annual concentration 

assumed to produce a total 

body or organ dose of 

4 rem/year (90Sr) 

Critical organ (bone marrow) 

Nevada Quantities of radioactive 

material for signs, labels, and 

signals 

BNA 2001 

S 0.2 μCi/mL 

I 0.2 μCi/mL 

S 0.007 μCi/mL 

I 0.007 μCi/mL 

IN General 

Assembly 2000 

8 pCi/L 

Bone marrow 

2,400 μg/L HSDB 2001 

MDEQ 2000 

8 pCi/L 

Bone marrow 

8 pCi/L HSDB 2001 

8 pCi/L HSDB 2001 

No data 

BNA 2001 

10 Ci 

0.4 Ci 

1.5x102

 Ci/g 

0.1 μCi BNA 2001 

BNA 2001 

5.41 Ci 

2.70 Ci 

BNA 2001 

8 pCi/L 

0.1 μCi BNA 2001 
STRONTIUM 272 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Strontium 

Agency Description Information Reference 

a

The limits apply to the sum of the relevant doses from external exposure in the specified period and the 50-year 

committed dose (to age 70 years for children) from intakes in the same period.

b

With the further provision that the effective dose should not exceed 50 mSv in any single year. Additional 

restrictions apply to the occupational exposure of pregnant women. c

The limitation on the effective dose provides sufficient protection for the skin against stochastic effects. An additional 

limit is needed for localized exposures in order to prevent deterministic effects. d

Group 1: human carcinogen 

e

In special circumstances, a higher value of effective dose could be allowed in a single year, provided that the 

average over 5 years does not exceed 1 mSv per year.

f

Class D: all soluble compounds except SrTiO 

g

Class Y: all insoluble compounds and SrTiO 

h

Class D: refers to materials with retention times in the pulmonary region of <10 days 

i

Class W: refers to materials with retention times in the pulmonary region of 10–100 days 

j

Class Y: refers to materials with retention times in the pulmonary region of >100 days

k

Release limit per 1,000 metric tons of heavy metal (MTHM) or other unit of waste l

Column 1: The sum of the fractions rule for mixtures of radionuclides. For determining classification for waste that 

contains a mixture of radionuclides, it is necessary to determine the sum of fractions by dividing each nuclide’s 

concentration by the appropriate limit and adding the resulting values. The appropriate limits must all be taken from 

the same column of the same table. The sum of the fractions for the column must be less than 1.0 if the waste class 

is to be determined by the column. Example: A waste contains 90Sr in a concentration of 50 Ci/m3 and 137Cs of 22 

Ci/m3

. Since the concentrations both exceed the values in Column 1, Table 2, they must be compared to Column 2 

values. For 90Sr fraction 50/150=0.33; for 137Cs fraction, 22/44=0.5; the sum of the fractions=0.83. Since the sum is 

less than 1.0, the waste is Class B. 

mGroup A: human carcinogen 

n

Derived intervention levels (DIL) are concentrations of radioactivity in food whose consumption would deliver a 

committed effective dose equivalent equal to the most limiting of the protection action guides (PAGs) developed by 

FDA (1998). 

o

The FDA-recommended Derived Intervention Level (DIL) for radionuclides of 89Sr, is defined as the DIL for the most 

sensitive age group (3 months) that was calculated from the most limiting Protective Action Goal (PAG; 50 mSv 

committed dose equivalent to the bone). 

p

The FDA-recommended Derived Intervention Level (DIL) for radionuclides of 90Sr, is defined as the DIL for the most 

sensitive age group (15 years) that was calculated from the most limiting Protective Action Goal (PAG; 50 mSv 

committed dose equivalent to the bone). 

q

Radioactive slope factors calculated by EPA’s Office of Radiation and Indoor Air (ORIA). Slope factors are central 

estimates in a linear model of the age-averaged, lifetime attributable radiation cancer incidence (fatal and nonfatal 

cancer) risk per unit of activity ingested, expressed as risk per picocurie (pCi). 

r

Inhalation slope factors are central estimates in a linear model of the age-average, lifetime attributable radiation 

cancer incidence (fatal and nonfatal cancer) risk per unit of activity inhaled, expressed as risk per picocurie (pCi). s

External slope factors are central estimates of the lifetime attributable radiation cancer incidence risk for each year of 

exposure to external radiation from photon-emitting radionuclides distributed uniformly in a thick layer of soil, 

expressed as risk/year per pCu per gram of soil. 

t

Sum of external and internal exposures but excluding doses from natural sources. 

ACGIH = American Conference of Governmental Industrial Hygienists; ADEC = Alaska Department of Environmental 

Conservation; ALI = annual limits on intake; BNA = Bureau of National Affairs; CFR = Code of Federal Regulations; 

DAC = derived air concentration; DEP = Department of Environmental Protection; DOE = Department of Energy; 

DOT = Department of Transportation; EPA = Environmental Protection Agency; FDA = Food and Drug 

Administration; HSDB = Hazardous Substances Data Bank; I = insoluble; IARC = International Agency for Research 

on Cancer; ICRP = International Commission on Radiological Protection; MCL = maximum contaminant level; 

MCLG = maximum contaminant level goal; MDEQ = Michigan Department of Environmental Quality; 

mSv = millisievert; MTHM = metric tons of heavy metal; NCRP = National Council on Radiation Protection; 

NIOSH = National Institute for Occupational Safety and Health; USNRC = Nuclear Regulatory Commission; 

OSHA = Occupational Safety and Health Administration; PAG = protective action guide; REL = recommended 

exposure limit; S = soluble; TWA = time-weighted average 
STRONTIUM	 273 

8. REGULATIONS AND ADVISORIES 

Table 8-3. Effective Dose Coefficientsa (e(50)) and Annual Limits on Intakeb (ALI) 

for Occupational Exposures to Radioactive Strontium Isotopes 

Radionuclide Inhalation, 1μm AMADc Inhalation, 5μm AMAD Ingestion 

Absorp- einh (50) ALI ALI einh (50) ALI ALI eing (50) ALI ALI 

Half-life tion type f1d (Bq) (mCi) (Bq) (mCi) (Bq) (mCi) 80Sr 

1.67 hr fast 0.3 7.6x10-11 2.6x108 7.11 1.3x10-10 1.5x108 4.158 3.4x10-10 5.9x107 1.590

 slow 0.01 1.4x10-10 1.4x108 3.86 2.1x10-10 9.5x107 2.574 3.5x10-10 5.7x107 1.544 81Sr 

0.425 hr fast 0.3 2.2x10-11 9.1x108 24.57 3.9x10-11 5.1x108 13.860 7.7x10-11 2.6x108 7.020 

 slow 0.01 3.8x10-11 5.3x108 14.22 6.1x10-11 3.3x108 8.861 7.8x10-11 2.6x108 6.93 82Sr 

25.0 d fast 0.3 2.2x10-9 9.1x106 0.245 3.3x10-9 6.1x106 0.164 6.1x10-9 3.3x106 0.089

 slow 0.01 1.0x10-8 2.0x106 0.054 7.7x10-9 2.6x106 0.070 6.0x10-9 3.3x106 0.090 83Sr 

1.35 d fast 0.3 1.7x10-10 1.2x108 3.179 3.0x10-10 6.7x107 1.801 4.9x10-10 4.1x107 1.103

 slow 0.01 3.4x10-10 5.9x107 1.589 4.9x10-10 4.1x107 1.103 5.8x10-10 3.5x107 0.932 85Sr 

64.8 d fast 0.3 3.9x10-10 5.1x107 1.386 5.6x10-10 3.6x107 0.965 5.6x10-10 3.6x107 0.965

 slow 0.01 7.7x10-10 2.6x107 0.702 6.4x10-10 3.1x107 0.845 3.3x10-10 6.1x107 1.638 85mSr 

1.16 hr fast 0.3 3.1x10-12 6.5x109 174.00 5.6x10-12 3.6x109 96.53 6.1x10-12 3.3x109 88.61 

 slow 0.01 4.5x10-12 4.4x109 120.00 7.4x10-12 2.7x109 73.05 6.1x10-12 3.3x109 88.61 87mSr 

2.8 hr fast 0.3 1.2x10-11 1.7x109 45.05 2.2x10-11 9.1x108 24.57 3.0x10-11 6.7x108 18.02 

 slow 0.01 2.2x10-11 9.1x108 24.57 3.5x10-11 5.7x108 15.44 3.3x10-11 6.1x108 16.38 89Sr 

50.5 d fast 0.3 1.0x10-9 2.0x107 0.540 1.4x10-9 1.4x107 0.386 2.6x10-9 7.7x106 0.208

 slow 0.01 7.5x10-9 2.7x106 0.072 5.6x10-9 3.6x106 0.097 2.3x10-9 8.7x106 0.235 90Sr 

29.1 yr fast 0.3 2.4x10-8 8.3x105 0.023 3.0x10-8 6.7x105 0.018 2.8x10-8 7.1x105 0.019

 slow 0.01 1.5x10-7 1.3x105 0.004 7.7x10-8 2.6x105 0.007 2.7x10-9 7.4x106 0.200 91Sr 

9.5 hr fast 0.3 1.7x10-10 1.2x108 3.180 2.9x10-10 6.9x107 1.864 6.5x10-10 3.1x107 0.832

 slow 0.01 4.1x10-10 4.9x107 1.318 5.7x10-10 3.5x107 0.948 7.6x10-10 2.6x107 0.711 92Sr 

2.7 hr fast 0.3 1.1x10-10 1.8x108 4.914 1.8x10-10 1.1x108 3.003 4.3x10-10 4.7x107 1.257

 slow 0.01 2.3x10-10 8.7x107 2.350 3.4x10-10 5.9x107 1.590 4.9x10-10 4.1x107 1.103 

a

ICRP (1994)

b

For internal exposures, ICRP (1994) recommends an effective dose limit of 100 mSv over 5 years (averaging 20 mSv 

per year). The Annual Limits on Intake (ALI in Bequerels) were calculated by dividing the annual effective dose limit 

(0.02 Sv) by the dose coefficient (e(50)) in Sieverts/Bequerel. c

ICRP (1994) calculated inhalation dose coefficients for particles with AMAD of 1 or 5 μm. 

d

Fractional absorption factor used by ICRP (1994: Annexes E and F) to calculate effective dose coefficients. A value 

of 0.3 was used for unspecified strontium compounds and 0.01 was used for strontium titanate. 

ALI = Annual Limits on Intake; AMAD = Activity Median Average Diameters; Bq = Bequerels; Ci = Curies; d = day; 

hr = hour; yr = year 
STRONTIUM 274 

8. REGULATIONS AND ADVISORIES 

groups and 14 radiogenic cancer cites (EPA 2000e). These factors are used to calculate the lifetime 

excess total cancer risk per unit intake or exposure to radiation (under the different exposure scenarios). 

Slope factors for radioactive strontium isotopes are listed in Table 8-2. IARC has determined that all 

internally deposited beta emitters, including radioactive strontium, are carcinogenic to humans and has 

assigned them to Group 1 (IARC 2001, 2002b). 

Because of the potential for ionizing radiation to cause deterministic (acute radiation syndrome) and 

nondeterministic (cancer) health effects in exposed individuals, safe dose guidelines and regulations have 

been established for radionuclides in air and water by a number of international and national agencies 

(Tables 8-2 and 8-3). Regulations and guidelines that protect against deterministic effects are based on 

identified acute thresholds doses for those effects, with a reduction to protect sensitive populations and 

provide safety margins to account for uncertainties. Those that protect against nondeterministic effects 

use the observed frequencies with which those effects occur at high doses, account for uncertainties that 

may exist, and assume a linear dose-effect relationship to calculate the doses at which the effects would 

be presumed to occur at some acceptable frequency, such as the range of 10-4–10-

6, which EPA often 

considers. This proportionality assumes a linear no threshold (LNT) dose effect curve. During the last 

decade, there have been reductions in LNT-based public radiation dose limits and site cleanup levels that 

have increased the scope and cost of medical, occupational, and environmental radiation protection 

efforts. Some recent studies found a reduction in health effects when the dose was delivered at lower 

dose rates, indicating a potential application to future protection guidelines and regulations. 

The International Commission on Radiological Protection (ICRP) provides guidance on the fundamental 

principles regarding the biological effects of exposure to ionizing radiation and recommends exposure 

limits based on these analyses. In the United States, the National Council on Radiation Protection and 

Measurements (NCRP) was chartered in 1964 by the U.S. Congress to: (1) disseminate information of 

public interest and recommend radiation levels to protect the public, (2) support cooperation among 

organizations concerned with radiation protection, (3) develop basic concepts about radiation protection, 

and (4) cooperate with the ICRP and the International Commission on Radiation Units and 

Measurements. Even though the NCRP is a nongovernmental organization, it provides recommendations 

that guide the establishment of federal radiation policies, agency requirements, and statutory laws. 

Through the governmental agencies that rely on NCRP recommendations, the work of this organization 

has a significant impact on the many activities in the United States involving the use of radiation and 

radioactive materials. 
STRONTIUM 275 

8. REGULATIONS AND ADVISORIES 

The EPA sets radiation safety policy and basic safety standards. The execution of this policy is assigned 

to the various regulatory agencies, including the EPA itself, for application to the specific activities that 

they regulate. The U.S. Nuclear Regulatory Commission (USNRC), an independent government agency, 

regulates commercial nuclear power reactors; research/test/training reactors; fuel cycle facilities; and the 

transport, storage, and disposal of nuclear materials and waste (USNRC 1997). The EPA is responsible 

for protecting the public and the environment and for cleanup of radioactively contaminated sites (EPA 

1997a). 

The Food and Drug Administration (FDA) develops standards for radioactive material concentrations in 

food (FDA 1998) and in medical devices used in radiation therapy (FDA 1997). The FDA recently 

updated its guidance document that presents recommended action levels for accidental radioactive 

contamination of foods, both domestic and imported (FDA 1998). These derived intervention levels 

(DILs) are estimated levels in food that could lead to individuals receiving a radiation equivalent dose 

equal to the FDA protection action guide (PAG) that is set as the more limiting of either 0.5 rem (5 mSv) 

for committed effective dose or 5 rem (50 mSv) committed dose equivalent to any individual tissue or 

organ. Derived intervention levels, which are based on food intake rates, are calculated for different age 

groups and the DIL for the most vulnerable group is then adopted to provide a conservative margin of 

safety for the entire population. For 90Sr, with a half-life of 29 years, the DIL is based on the dose to the 

bone surface in 15-year-old individuals, who have the highest rate of bone growth. For 89Sr, with a halflife of 50.5 days, 3-month-old infants represent the most sensitive group because of the higher doses to 

the lower intestine from milk consumption. Table 8-2 presents the DILs adopted for the two strontium 

isotopes. 

Transport of radioactive materials is regulated by the Department of Transportation (DOT) in conjunction 

with the USNRC. Coordinating government emergency response to accidents involving radioactive 

materials is the responsibility of the Federal Emergency Management Administration (FEMA). 

National regulations governing the occupational exposure to ionizing radiation include USNRC 

regulations (10 CFR 20), the Occupational Safety and Health Administration (OSHA) standards for 

ionizing radiation (29 CFR 1910.1096), and the Department of Energy (DOE) standards for occupational 

radiation protection (10 CFR 835). National regulations concerning general population exposure to 

radiation have been developed as proposed by the EPA and as finalized by the USNRC based on the dose 

limit recommendations of the ICRP (ICRP 1996) and the NCRP (NCRP 1993). The EPA and USNRC 
STRONTIUM 276 

8. REGULATIONS AND ADVISORIES 

also use the BEIR reports of the National Academy of Sciences and the UNSCEAR reports on biological 

effects to help develop the U.S. standards in line with the NCRP and the ICRP consensus standards. 

Currently, there are 29 "NRC Agreement States." An agreement state is any state that has entered into an 

agreement with the USNRC under Section 274 of the Atomic Energy Act of 1954, as amended. The 

USNRC relinquishes to these states the majority of its regulatory authority over source, by-product, and 

special nuclear material in quantities not sufficient to form a critical mass. However, the regulation of 

nuclear reactors is under USNRC jurisdiction. In the remaining states, USNRC still handles all of the 

inspection, enforcement, and licensing responsibilities. 

The basic philosophy of radiation safety is to minimize unnecessary radiation exposure. The specific 

objectives of radiation safety guidance as stated by NCRP are (1) to prevent the occurrence of severe 

radiation-induced deterministic (nonstochastic) disease, and (2) to limit the risk of the nondeterministic 

(stochastic) effects (fatal cancer and genetic effects) to a reasonable level compared with nonradiation 

risks and in relation to societal needs, benefits gained, and economic factors. In addition to regulations 

that set upper limits on radiation dose, the concept of ALARA (As Low As Reasonably Achievable) was 

introduced to ensure that workplace endeavors resulting in exposures to radiation provide sufficient 

benefits that offset any potential detriment they cause (ACGIH 2002). The goal is not to eliminate all 

radiation exposure, which would not be possible, but instead to strive for an appropriate balance between 

protection of public health and reasonable costs (economic, social, etc.) while maintaining desirable dose 

limits. The ACGIH has adopted the occupational exposure guidance of the ICRP (ACGIH 2002). 
_______________________ 

STRONTIUM 277 

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Wigström H, Swann JW. 1980. Strontium supports synaptic transmission and long lasting potentiation in 

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*Williams MW, Hoeschele JD, Turner JE, et al. 1982. Chemical softness and acute metal toxicity in 

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Wing KR. 1975. Turnover of 65Zn and 85Sr in growing rats: A comparative investigation. Acta Radiol 

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*Witkamp M. 1966. Biological concentrations of 137Cs and 90Sr in arctic food chains. Nuclear Safety 

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STRONTIUM 367 

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. 

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. 

Acute Exposure, Chemical—Exposure to a chemical for a duration of 14 days or less, as specified in the 

Toxicological Profiles. 
STRONTIUM 368 

10. GLOSSARY 

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 180E 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. 

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. 
STRONTIUM 369 

10. GLOSSARY 

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. 

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. 

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. 
STRONTIUM 370 

10. GLOSSARY 

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. 

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. 

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. 
STRONTIUM 371 

10. GLOSSARY 

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. 

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). 

Daughter Products—See Progeny and Decay Product 
STRONTIUM 372 

10. GLOSSARY 

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). 

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. 

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. 
STRONTIUM 373 

10. GLOSSARY 

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. 

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). 
STRONTIUM 374 

10. GLOSSARY 

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. 

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. 
STRONTIUM 375 

10. GLOSSARY 

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. 

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. 
STRONTIUM 376 

10. GLOSSARY 

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). 

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. 
STRONTIUM 377 

10. GLOSSARY 

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. 

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.” 

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." 

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. 

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. 
STRONTIUM 378 

10. GLOSSARY 

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. 

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. 
STRONTIUM 379 

10. GLOSSARY 

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. 

Morbidity—State of being diseased; morbidity rate is the incidence or prevalence of disease in a specific 

population. 

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. 
STRONTIUM 380 

10. GLOSSARY 

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. 

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. 

Odds Ratio (OR)—A means of measuring the association between an exposure (such as toxic substances 

and a disease or condition) which represents the best estimate of relative risk (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). An odds ratio of greater than 1 is considered to indicate greater risk 

of disease in the exposed group compared to the unexposed. 

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. 

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. 
STRONTIUM 381 

10. GLOSSARY 

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. 

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). 

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. 

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. 

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." 
STRONTIUM 382 

10. GLOSSARY 

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). 

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). 
STRONTIUM 383 

10. GLOSSARY 

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. 

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. 

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). 

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). 
STRONTIUM 384 

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. 

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. 

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). 
STRONTIUM 385 

10. GLOSSARY 

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. 
STRONTIUM 386 

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. 
STRONTIUM 387 

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. 

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. 

STRONTIUM 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 
STRONTIUM 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, expert panel peer reviews, and agency-wide 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, Agency for Toxic Substances and Disease 

Registry, 1600 Clifton Road NE, Mailstop F-32, Atlanta, Georgia 30333. 
STRONTIUM A-3 

APPENDIX A 

MINIMAL RISK LEVEL (MRL) WORKSHEET 

Chemical name(s): Strontium 

CAS number(s): 7440-24-6 

Date: March 2004 

Profile status: Third draft, post-public 

Route: [ ] Inhalation [X] Oral 

Duration: [ ] Acute [X] Intermediate [ ] Chronic 

Key to figure: 16 

Species: Rat 

MRL: 2.0 [X] mg/kg/day [ ] ppm [ ] mg/m3 

Reference: Storey E. 1961. Strontium ‘rickets’: Bone calcium and strontium changes. Austral Ann 

Med 10:213-222. 

Experimental design: Groups of five young (40–60 g) and three adult (200–250 g) female rats were fed a 

diet containing 1.6% calcium, 0.9% phosphorus, and 0, 0.19, 0.38, 0.75, 1.0 (young only), 1.5, or 3% 

strontium as strontium carbonate for 20 days. Initial and final body weights were recorded. Terminal 

levels of calcium and strontium were measured in serum and in five selected ashed bones for each dose 

level. Both tibia from each animal were processed histologically, and the proximal epiphyseal cartilages 

were measured. 

Effects noted in study and corresponding doses: The strontium intakes were calculated to be 0, 140, 550, 

1,080, 1,460, 2,220, or 4,975 mg strontium/kg/day in young rats, and 0, 170, 350, 690, 1,370, or 2,750 mg 

strontium/kg/day in adult rats. The serum calcium levels were not significantly changed in either young 

or adult animals, but at the high doses, the serum calcium/strontium ratio was about 1 in young rats and 

1.4 in adults. In young rats, increased strontium ingestion resulted in abnormal thickening of the 

epiphyseal cartilage plate, approximately doubled at the highest dose. No histological effect was noted at 

the lowest dose (140 mg strontium/kg/day), but alterations in the appearance of the cartilage plate 

(irregular, thicker, with areas of uncalcified bone matrix in the distal ends of the metaphyseal trabeculae 

and proximal end of the diaphysis) were observed at 550 mg strontium/kg/day. Irregularities in the 

organization of the cells of hypertrophic zone, in the pattern of calcification, and in the deposition of 

osteoid were more conspicuous with increasing dose. In tibias, the dry weight, ash weight, ash 

percentage, and calcium in ash were significantly reduced with increased strontium intake. Adult rats 

were less affected by strontium ingestion than young animals. In adult rats, the no-effect level was 

690 mg strontium/kg/day. In adults, changes in tibia histology (thicker epiphyseal cartilage, increased 

width of metaphyseal osteoid seams) were noted at or above 1,370 mg strontium/kg/day. At 2,750 mg 

strontium/kg/day, osteoid tissue was deposited near vascular canals and the areas of bone resorption were 

reduced. In adult rat tibias, the dry weight, ash weight, ash percentage, and calcium in ash were only 

significantly affected at the highest dose. This study demonstrates the difference in sensitivity to 

strontium between young and old animals. The LOAEL for the young rats (550 mg/strontium/kg/day) is 

a NOAEL for the adults (<690 mg strontium/kg/day). 

Dose and end point used for MRL derivation: 

This study identifies a NOAEL of 140 mg/kg/day for skeletal toxicity in young rats. 

[X] NOAEL [] LOAEL: 
 

 

STRONTIUM A-4 

APPENDIX A 

Uncertainty factors used in MRL derivation: 

[ ] 1 [ ] 3 [] 10 (for use of a LOAEL) 

[ ] 1 [] 3 [X] 10 (for extrapolation from animals to humans) 

[ ] 1 [X ] 3 [] 10 (for human variability)
 

Modifying factor used in MRL derivation: 3 

MRL = NOAEL / (UF)(MF) = 140 mg/kg/day / (30)(3) = 2 mg/kg/day
 

Was a conversion factor used from ppm in food or water to a mg/body weight dose?
 

Food intake was based upon an allometric equation using the average body weight in kg (EPA 1988): 

F = 0.056 x bw0.6611 . 

If an inhalation study in animals, list conversion factors used in determining human equivalent dose: NA 

Was a conversion used from intermittent to continuous exposure? If so, explain: NA 

Other additional studies or pertinent information that lend support to this MRL: If an MRL were to be 

derived from the adult rat NOAEL of 690 mg/kg/day, then an uncertainty factor of 100 would be applied 

(10 for interspecies extrapolation and 10 for human variability), giving a value of 

690/100=6.9 mg/kg/day. Because the young rats represent a sensitive population, just as juveniles would 

be the most sensitive human group, the selection of the NOAEL implicitly factors in human variability to 

some degree. Therefore, a smaller uncertainty factor is chosen for intraspecies extrapolation (3 for human 

variability). However, since the study duration was only 20 days, there is uncertainty whether the 

NOAEL would be valid for intermediate exposures extending up to 1 year. In addition, the focus of the 

study was skeletal effects, and no other organ system was examined. To adjust for these potential sources 

of uncertainty, a modifying factor of 3 is applied to the NOAEL. The MRL is derived using the young rat 

NOAEL of 140 mg/kg/day and a total uncertainty factor of 30 (10 for interspecies extrapolation and 3 for 

human variability), and a modifying factor of 3 (for short study duration and limited end point 

evaluation), giving a value of 140/(30x )=1.6 mg/kg/day; rounding off to whole numbers, the intermediate 

oral MRL is 2.0 mg/kg/day. 

Abnormal bone mineralization (rickets) resulting from ingestion of excess strontium has been observed in 

many rodent studies. Several studies identified a similar NOAEL (110–168 mg strontium/kg/day) in 

weanling rats (Grynpas et al. 1996; Kroes et al. 1977; Morohashi et al. 1994). Similar LOAELs 

(500–565 mg strontium/kg/day) for abnormal bone mineralization in weanling rats have been reported 

(Johnson et al. 1968; Morohashi et al. 1994; Neufeld and Boskey 1994). Slight skeletal effects were 

noted in mice at 350 mg/kg/day (Marie and Hott 1986). The relevance of the rodent studies to humans is 

suggested by a Turkish epidemiological study indicating that excess oral exposure to strontium may

contribute to the development of rickets in children (Ögzür et al. 1996). 

The skeletal effects of excess strontium are known to be related to its chemical similarity to calcium. 

Excess strontium adversely affects bone development in several ways. In chickens and rats, excess 

strontium suppresses the activation of vitamin D3 in the kidney, which severely reduces the expression of 

calbindin D mRNA and the translation of calbindin D protein in the duodenum (Armbrecht et al. 1979, 

1998; Omdahl and DeLuca 1972). As a result, duodenal absorption of calcium is reduced. Strontium 

also binds directly to hydroxyapatite crystals, which may interfere with the normal crystalline structure of 

bone in rats (Storey 1961). In addition, excess strontium may prevent the normal maturation of 

chondrocytes in the epiphyseal plates of long bones of rats (Matsumoto 1976). Excess strontium 

apparently interferes with the mineralization of complexed acidic phospholipids that is thought to help 
STRONTIUM A-5 

APPENDIX A 

initiate the formation of hydroxyapatite crystals in developing bone (Neufeld and Boskey 1994). As a 

result, affected bone contains an excess of complexed acidic phospholipid and a significantly lower ash 

weight, reducing its strength. 

STRONTIUM 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. 
STRONTIUM 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 3.10, "Interactions with Other Substances,” and Section 3.11, "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. 
STRONTIUM	 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 exists, 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 Table 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 

regimen 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"). 
STRONTIUM	 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 38r 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. 
STRONTIUM	 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. 
Serious (ppm) (CEL, multiple organs) (CEL, lung tumors, nasal tumors) (CEL, lung tumors, hemangiosarcomas) 

11 ↓20 10 10 

LOAEL (effect) Less serious (ppm) 

9 

↓

10 (hyperplasia) 

SAMPLE 

NOAEL (ppm) 8 ↓3b 

System 7 ↓Resp 

Exposure frequency/ duration 6 ↓13 wk 5 d/wk 6 hr/d 18 mo 5 d/wk 7 hr/d 89-104 wk 5 d/wk 6 hr/d 79-103 wk 5 d/wk 6 hr/d 

Species 5 

↓

Rat Rat Rat Mouse 

TABLE 3-1. Levels of Significant Exposure to [Chemical x] – Inhalation 

Key to figurea 

INTERMEDIATE EXPOSURE Systemic 18 CHRONIC EXPOSURE Cancer 38 39 40 

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 intermittenby an uncertainty factor of 100 (10 for extrapolation from animal to humans, 10 for human variability). 

→→→→→

1 2 3 4 12 


STRONTIUM C-1 

APPENDIX C. ACRONYMS, ABBREVIATIONS, AND SYMBOLS 

Some terms are generic and may not be used in this profile. 

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 

ALI annual limit on intake 

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 

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 

BMR benchmark response 

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 

CWA Clean Water Act 

DAC derived air concentration 

DHEW Department of Health, Education, and Welfare 

DHHS Department of Health and Human Services 

DNA deoxyribonucleic acid 

DOD Department of Defense 
STRONTIUM C-2 

APPENDIX C 

DOE Department of Energy 

DOL Department of Labor 

DOT Department of Transportation 

DOT/UN/ Department of Transportation/United Nations/ 

NA/IMCO North America/International 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 

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 

LT50 lethal time, 50% kill 

m meter 

MA trans,trans-muconic acid 
STRONTIUM C-3 

APPENDIX C 

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 

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 

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 
STRONTIUM C-4 

APPENDIX C 

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 

RBC red blood cell 

REL recommended exposure level/limit 

RfC reference concentration 

RfD reference dose 

RNA ribonucleic acid 

RQ reportable quantity 

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 

UF uncertainty factor 

U.S. United States 

USDA United States Department of Agriculture 

USGS United States Geological Survey 

USNRC United States Nuclear Regulatory Commission 

VOC volatile organic compound 
STRONTIUM C-5 

WBC 

WHO 

> ≥

= 

< ≤

% αβγδ

μm

μg q1

* 

– 

+ 

(+) 

(–) 

APPENDIX C 

white blood cell 

World Health Organization 

greater than 

greater than or equal to 

equal to 

less than 

less than or equal to 

percent 

alpha 

beta 

 gamma 

delta 

 micrometer 

microgram 

cancer slope factor 

negative 

positive 

weakly positive result 

weakly negative result 
STRONTIUM 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), 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 (manmade). Naturally-occurring radioactive materials (NORMs) exist 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 (hydrogen3) 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 stable atoms with particles, such as neutrons or protons, directed at 

the stable atoms with high velocity. These artificially produced radioactive elements usually decay by 

emission of particles, such as positive or negative beta particles and one or more high energy photons 

(gamma rays). Unstable (radioactive) atoms of any element can be produced. 
STRONTIUM D-2 

APPENDIX D 

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. 

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 (radionuclide) will release energy (decay) in various ways and transform to 

stable atoms or to other radioactive species called 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 daughter 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 effect 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 that quantity of radioactive material in which there are: 

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, TR, i.e., the time 

it takes for a specified source material to decay to half its initial activity. The specific activity is the 

activity of a radionuclide per mass of that radionuclide. If properly qualified, it can refer to activity per 

unit mass of related materials, such as the element itself or a chemical compound labeled with the 

radionuclide. The higher the specific activity of a radioisotope, the faster it is decaying. 
STRONTIUM D-3 

APPENDIX D 

The activity of a radionuclide at time t may be calculated by: 

-0.693t/Trad A = Aoe

where A is the activity in dps or curies or becquerels, Ao is the activity at time zero, t is the time at which 

measured, and Trad is the radiological half-life of the radionuclide (Trad 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 half-life and is expressed in any suitable unit of time. 

Table D-1. Characteristics of Nuclear Radiations 

Typical Path lengthb 

Radiation Rest massa Charge energy range Air Solid Comments 

Alpha (α) 4.00 amu +2 4–10 MeV 5–10 cm 25–80 μm Identical to ionized 

He nucleus 

Negatron (β–

) 5.48x10-4 amu; –1 0–4 MeV 0–10 m 0–1 cm Identical to electron 

0.51 MeV 

Positron (β+

) 5.48x10-4 amu; +1 0-4 MeV 0–10 m 0–1 cm Identical to electron 

0.51 MeV except for sign of 

charge 

Neutron 1.0086 amu; 0 0–15 MeV b b Free half-life: 16 

939.55 MeV min 

X ray (e.m. – 0 5 keV–100 keV b b Photon from 

photon) transition of an 

electron between 

atomic orbits 

Gamma (p) – 0 10 keV–3 MeV b b Photon from 

nuclear (e.m. photon) 

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 of a radionuclide per mass of 

that radionuclide. This activity is usually expressed in curies per gram and may be calculated by 

curies/gram = 1.3x108

 / (Trad) (atomic weight) or 

[3.577 x 105 x mass(g)] / [Trad x atomic weight] 

where Trad is 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 

(Tbiol) 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. 
STRONTIUM D-4 

APPENDIX D 

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 = (Tbiol x Trad) / (Tbiol + Trad). 

Table D-2 presents representative effective half-lives of particular interest. 

Table D-2. Half-Lives of Some Radionuclides in Adult Body Organs 

Half-lifea 

Radionuclide Critical organ Physical Biological Effective 

Uranium 238 

Hydrogen 3b 

Kidney 

Whole body 

4,460,000,000 y 

12.3 y 

4 d 

10 d 

4 d 

10 d 

(Tritium) 

Iodine 131 Thyroid 8 d 80 d 7.3 d 

Strontium 90 Bone 28 y 50 y 18 y 

Plutonium 239 Bone surface 24,400 y 50 y 50 y 

Lung 24,400 y 500 d 474 d 

Cobalt 60 Whole body 5.3 y 99.5 d 95 d 

Iron 55 Spleen 2.7 y 600 d 388 d 

Iron 59 Spleen 45.1 d 600 d 42 d 

Manganese 54 Liver 303 d 25 d 23 d 

Cesium 137 Whole body 30 y 70 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 ultraviolet 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) 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 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 
STRONTIUM D-5 

APPENDIX D 

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. The alpha particles 

emitted by a given radionuclide have the same energy and intensity combination. 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 (&) is a high-velocity electron ejected from a disintegrating 

nucleus. The particle may be either a negatively charged electron, termed a negatron (&-) or a positively 

charged electron, termed a positron (&+). Although the precise definition of "beta emission" refers to 

both &- and &+, common usage of the term generally applies only to the negative particle, as distinguished 

from the positron emission, which refers to the &+ particle. 

D.2.4.2.1 Beta Negative Emission. Beta particle (&-) 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 of betas is much less in tissue than in air. 

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 (&+) 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 & 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 

1

 Neutrinos also accompany negative beta particles and positron emissions 
STRONTIUM D-6 

APPENDIX D 

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. 

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. 

D.3.1 Dose/Exposure Units 

D.3.1.1 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 a dose of 1 R is about 0.0096 joules (J) /kg of tissue. 

D.3.1.2 Absorbed Dose and Absorbed Dose Rate. The absorbed dose is defined as the energy 

imparted by radiation to a unit mass of the tissue or organ. The unit of absorbed dose is the rad; 1 rad = 

100 erg/gram = 0.01 J/kg in any medium. An exposure of 1 R results in a dose to soft tissue of 

approximately 0.01 J/kg. The SI unit is the gray which is equivalent to 100 rad or 1 J/kg. Internal and 

external exposures from 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 in units of rad/unit time. 

D.3.1.3 Working Levels and Working Level Months. 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 daughters (through polonium-214), per liter of air, that will result in the emission of 

1.3x105

 MeV of alpha energy. An activity concentration of 100 pCi radon-222/L of air, in equilibrium 

with its daughters, corresponds approximately to a potential alpha-energy concentration of 1 WL. The 

WL unit can also be used for thoron daughters. In this case, 1.3x105

 MeV of alpha energy (1 WL) is 

released by the thoron daughters in equilibrium with 7.5 pCi thoron/L. The potential alpha energy 

exposure of miners is commonly expressed in the unit Working Level Month (WLM). One WLM 
STRONTIUM D-7 

APPENDIX D 

corresponds to exposure to a 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.3.2 Dosimetry Models 

Dosimetry models are used to estimate the dose from internally deposited to 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 and inhalation of low levels of naturally occurring 

radionuclides as well as radionuclides from nuclear weapons testing. 

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.3.2.1 Ingestion. Ingestion of radioactive materials is most likely to occur from contaminated 

foodstuffs or water or eventual ingestion of inhaled compounds initially deposited in the lung. Ingestion 

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.3.2.2 Inhalation. The inhalation route of exposure has 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 of the particles being inhaled. After the particle is deposited, the 

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 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.3.3 Internal Emitters 

An internal emitter is a radionuclide that is inside the body. The absorbed dose from internally deposited 

radionuclide depends on the energy absorbed per unit mass by the irradiated tissue. For a radionuclide 

distributed uniformly throughout an infinitely large medium, the concentration of absorbed energy must 

be equal to the concentration of energy emitted by the radionuclide. 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 radionuclide 

emissions are penetrating radiation, and a substantial fraction of gamma energy may be absorbed in 
STRONTIUM D-8 

APPENDIX D 

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.4 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. 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; Hobbs and McClellan 1986; ICRP 1984; Mettler and Moseley 1985; Rubin and Casarett 

1968). 

D.4.1 Radiation Effects at the Cellular Level 

According to Mettler and Moseley (1985), at acute doses up to 10 rad (100 mGy), single strand breaks in 

DNA may be produced. These single strand breaks may be repaired rapidly. With doses in the range of 

50–500 rad (0.5–5 Gy), 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 500 rad (5 Gy), direct cell death before division (interphase death) may occur from 

the direct interaction of free-radicals with essential cellular macromolecules. Morphological changes at 

the cellular level, the severity of which are dose-dependent, 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 or cellular mutations, which may result in 

abnormal tissue. 

D.4.2 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, which may progress to 
STRONTIUM D-9 

APPENDIX D 

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 fibrosis and occlusion 

of the microcirculation. 

D.4.3 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. The 

development of cancer is not an immediate effect. Radiation-induced leukemia has the shortest latent 

period at about 2 years, while other radiation induced cancers, such as osteosarcoma, have latent periods 

greater than 20 years. 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 at any site within the body; however, 

some sites appear to be more common than others, such as the breast, lung, stomach, and thyroid. 

DNA is the 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. However, for effects other than cancer, 

there is little evidence of human effects at low levels of exposure. 

D.5 UNITS IN RADIATION PROTECTION AND REGULATION 

D.5.1 Dose Equivalent (or Equivalent Dose) 

Dose equivalent (as measured in rem or sievert) is a special radiation protection quantity that is used for 

administrative and radiation safety purposes to express the absorbed dose in a manner which considers the 

difference in biological effectiveness of various kinds of ionizing radiation. ICRP (1990) changed this 

term to equivalent dose, but it has not yet been adopted by the USNRC or DOE. 

The USNRC defines the dose equivalent, H, as the product of the absorbed dose, D, and the quality 

factor, Q, at the point of interest in biological tissue. This relationship is expressed as H = D x Q. The 

dose equivalent concept is applicable only to doses that are not great enough to produce biomedical 

effects. 

The quality factor or radiation weighting factor 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 Q 

to define the quantity, rem, which was of use in risk assessment. The generally accepted values for 

quality factors and radiation weighting factors for various radiation types are provided in Table D-3. The 

dose equivalent rate is the time rate of change of the dose equivalent to organs and tissues and is 

expressed as rem/unit time or sievert/unit time. 
STRONTIUM D-10 

APPENDIX D 

Table D-3. Quality Factors (Q) and Absorbed Dose Equivalencies 

Type of radiation Quality factor (Q) Radiation weighting factor (wr)* 

X, gamma, or beta radiation 1 1 

Alpha particles, multiple- 20 0.05 

charged particles, fission 

fragments and heavy particles of 

unknown charge 

Neutrons (other than thermal >> 10 20 

100 keV to 2 MeV), protons, 

alpha particles, charged 

particles of unknown energy 

Neutrons of unknown energy 10 

High-energy protons 10 0.1 

Thermal neutrons 5 

*Absorbed dose in rad equal to 1 rem or the absorbed dose in gray equal to 1 sievert. 

Source: USNRC. 2004. Standards for the protection against radiation, table 1004(b).1. 10 CFR 20.1004. U.S. Nuclear
 

Regulatory Commission, Washington, D.C. NCRP 1993. 

D.5.2 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 biologic effect under the 

same conditions. Gamma rays from cobalt-60 and 200–250 kVp x-rays have been used as reference 

standards. The term RBE has been widely used in experimental radiobiology, and the term quality factor 

(or radiation weighting factor) used in calculations of dose equivalents for radiation safety purposes 

(ICRP 1977; NCRP 1971; UNSCEAR 1982). Any RBE value applies only to a specific biological end 

point, in a specific exposure, under specific conditions to a specific species. There are no generally 

applicable values of RBE since RBEs are specific to a given exposure scenario. 

D.5.3 Effective Dose Equivalent (or Effective Dose) 

The absorbed dose is usually defined as the mean energy imparted per unit mass to 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. In an attempt to compare detriment from absorbed 

dose of a limited portion of the body with the detriment from total body dose, the ICRP (1977) has 

derived a concept of effective dose equivalent. ICRP (1990) changed this term to effective dose, but it 

has not yet been adopted by the USNRC or DOE. 

The effective dose equivalent, HE, is 

HE = (the sum of) Wt Ht 
STRONTIUM D-11 

APPENDIX D 

where Ht is the dose equivalent (or equivalent dose) in the tissue t, Wt is the tissue weighting factor in that 

tissue, 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). Tissue weighting factors for selected tissues are listed in Table D-4. 

D.5.4 SI Units 

The ICRU (1980), ICRP (1984), and NCRP (1985) now recommend that the 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 customary units and the international system of units (SI) for 

radiological quantities is shown in Table D-5. 

Table D-4. Tissue Weighting Factors for Calculating Effective Dose 

Equivalent and Effective Dose for Selected Tissues
 

Tissue weighting factor 

Tissue NCRP115/ ICRP60 USNRC/ICRP26 

Bladder 0.05 – 

Bone marrow 0.12 0.12 

Bone surface 0.01 0.03 

Breast 0.05 0.15 

Colon 0.12 – 

Esophagus 0.05 – 

Gonads 0.20 0.25 

Liver 0.05 – 

Lung 0.12 0.12 

Skin 0.01 – 

Stomach 0.12 – 

Thyroid 0.05 0.03 

Remainder 0.05 0.30 

Total 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 

USNRC = Nuclear Regulatory Commission, Title 10, Code of Federal Regulations, Part 20 
STRONTIUM D-12 

APPENDIX D 

Table D-5. Comparison of Common and SI Units for Radiation Quantities 

Customary 

Quantity units Definition SI units Definition 

Activity (A) curie (Ci) 3.7x1010 becquerel (Bq) s-1 

transformations s1 

Absorbed dose (D) rad 10-2 Jkg-1 gray (Gy) Jkg-1 

-1 -1 Absorbed dose rate rad per second 10-2 Jkg-1s gray per second Jkg-1 s

(Ď) (rad s-1) (Gy s-1) 

Dose equivalent (H) rem 10-2 Jkg-1 sievert (Sv) Jkg-1 

-1 -1 Dose equivalent rate rem per second 10-2 Jkg-1s sievert per second Jkg-1 s

( ) (rem s-1) (Sv s-1) 

Effective dose rem 10-2 Jkg-1 Sievert (Sv) Jkg-1 

Equivalent dose (H) rem 10-2 Jkg-1 Sievert (Sv) Jkg-1 

Linear energy kiloelectron 1.602x10-10 Jm-1 kiloelectron volts 1.602x10-10 Jm-1 

transfer (LET) volts per per micrometer 

micrometer (keV μm-1) 

(keV μm-1) 

Jkg-1 = Joules per kilogram; Jkg-1s

-1 = Joules per kilogram per second; Jm-1 = Joules per meter; s-1 = per second 

REFERENCES FOR APPENDIX D 

ATSDR. 1990a. Toxicological profile for thorium. U.S. Department of Health and Human Services. 

Public Health Service. Agency for Toxic Substances and Disease Registry. Atlanta, GA. 

ATSDR. 1990b. Toxicological profile for radium. U.S. Department of Health and Human Services. 

Public Health Service. Agency for Toxic Substances and Disease Registry. Atlanta, GA. 

ATSDR. 1990c. Toxicological profile for radon. U.S. Department of Health and Human Services. 

Public Health Service. Agency for Toxic Substances and Disease Registry. Atlanta, GA. 

ATSDR. 1999. Toxicological profile for uranium. U.S. Department of Health and Human Services. 

Public Health Service. Agency for Toxic Substances and Disease Registry. Atlanta, GA. 

BEIR III. 1980. The effects on populations of exposure to low levels of ionizing radiation. Committee 

on the Biological Effects of Ionizing Radiations, National Research Council. Washington, DC: National 

Academy Press. 

BEIR IV. 1988. Health risks of radon and other internally deposited alpha emitters. Committee on the 

Biological Effects of Ionizing Radiations, National Research Council. Washington, DC: National 

Academy Press. 

BEIR V. 1988. Health effects of exposure to low levels of ionizing radiation. Committee on the 

Biological Effects of Ionizing Radiations, National Research Council. Washington, DC: National 

Academy Press. 
STRONTIUM D-13 

APPENDIX D 

Brodsky A. 1996. Review of radiation risks and uranium toxicity with application to decisions 

associated with decommissioning clean-up criteria. Hebron,Connecticut: RSA Publications. 

Cember H. 1996. Introduction to health physics. New York., NY: McGraw Hill. 

Early P, Razzak M, Sodee D. 1979. Nuclear medicine technology. 2nd ed. St. Louis: C.V. Mosby
 

Company.
 

Eichholz G. 1982. Environmental aspects of nuclear power. Ann Arbor, MI: Ann Arbor Science. 

Hendee W. 1973. Radioactive isotopes in biological research. New York, NY: John Wiley and Sons. 

Hobbs C, McClellan R. 1986. Radiation and radioactive materials. In: Doull J, et al., eds. Casarett and 

Doull's Toxicology. 3rd ed. New York, NY: Macmillan Publishing Co., Inc., 497-530. 

ICRP. 1977. International Commission on Radiological Protection. Recommendations of the 

International Commission on Radiological Protection. ICRP Publication 26. Vol 1. No. 3. Oxford: 

Pergamon Press. 

ICRP. 1979. International Commission on Radiological Protection. Limits for intakes of radionuclides 

by workers. ICRP Publication 20. Vol. 3. No. 1-4. Oxford: Pergamon Press. 

ICRP. 1979. Limits for Intakes of Radionuclides by Workers. Publication 30. International 

Commission on Radiological Protection. Pergamon Press. 

ICRP. 1984. International Commission on Radiological Protection. A compilation of the major concepts 

and quantities in use by ICRP. ICRP Publication 42. Oxford: Pergamon Press. 

ICRP. 1990. International Commission on Radiological Protection 1990 Recommendations of the ICRP 

ICRU. 1980. International Commission on Radiation Units and Measurements. ICRU Report No. 33. 

Washington, DC. 

James A. 1987. A reconsideration of cells at risk and other key factors in radon daughter dosimetry. In: 

Hopke P, ed. Radon and its decay products: Occurrence, properties and health effects. ACS Symposium 

Series 331. Washington, DC: American Chemical Society, 400-418. 

James A, Roy M. 1987. Dosimetric lung models. In: Gerber G, et al., ed. Age-related factors in 

radionuclide metabolism and dosimetry. Boston: Martinus Nijhoff Publishers, 95-108. 

Kondo S. 1993. Health effects of low-level radiation. Kinki University Press, Osaka, Japan (available 

from Medical Physics Publishing, Madison, Wisconsin). 

Kato H, Schull W. 1982. Studies of the mortality of A-bomb survivors. Report 7 Part 8, Cancer 

mortality among atomic bomb survivors, 1950-78. Radiat Res 90;395-432. 

Mettler F, Moseley R. 1985. Medical effects of ionizing radiation. New York: Grune and Stratton. 

NCRP. 1971. Basic radiation protection criteria. National Council on Radiation Protection and 

Measurements. Report No. 39. Washington, DC. 
STRONTIUM D-14 

APPENDIX D 

NCRP. 1985. A handbook of radioactivity measurements procedures. 2nd ed. National Council on 

Radiation Protection and Measurements. Report No. 58. Bethesda, MD: 

NCRP. 1993. Risk estimates for radiation protection. National Council on Radiation Protection and 

Measurements. Report 115. Bethesda, Maryland 

Otake M, Schull W. 1984. Mental retardation in children exposed in utero to the atomic bombs: A 

reassessment. Technical Report RERF TR 1-83, Radiation Effects Research Foundation, Japan. 

Rubin P, Casarett G. 1968. Clinical radiation pathology. Philadelphia: W.B. Sanders Company, 33. 

UNSCEAR. 1977. United Nations Scientific Committee on the Effects of Atomic Radiation. Sources 

and effects of ionizing radiation. New York: United Nations. 

UNSCEAR. 1982. United Nations Scientific Committee on the Effects of Atomic Radiation. Ionizing 

radiation: 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. 1999. Standards for the protection against radiation, table 1004(b).1. 10 CFR 20.1004. U.S. 

Nuclear Regulatory Commission, Washington, D.C. 
STRONTIUM E-1 

APPENDIX E. INDEX 

acetylcholine................................................................................................................................................................61 

acute inhalation exposure ............................................................................................................................................73 

adenocarcinoma...........................................................................................................................................................75 

adsorption ..........................................................................................................................................................169, 254 

air...................................2, 3, 4, 11, 12, 15, 30, 135, 138, 157, 177, 195, 205, 209, 213, 214, 217, 219, 220, 222, 236, 

239, 243, 244, 252, 255, 257, 259, 260, 262, 270, 272, 274
 

ambient air.................................................................................................................................................................237 

Arctic .........................................................................................................................................................................241 

bass ............................................................................................................................................................................217 

BCF (see bioconcentration factor).............................................................................................................................217 

bioaccumulation ................................................................................................................................................217, 243 

bioavailability ....................................................................................................................120, 169, 176, 186, 187, 243 

bioconcentration factor (see BCF).....................................................................................................................217, 218 

biodegradation ...................................................................................................................................................217, 243 

biomarker...........................................................................................................................162, 163, 164, 184, 186, 187 

birds.............................................................................................................................................................................55 

birth weight....................................................................................................................................................95, 96, 180 

blood............................................7, 10, 22, 60, 61, 72, 73, 99, 110, 115, 117, 127, 128, 135, 143, 144, 146, 147, 149,
 

156, 163, 164, 184, 187, 240, 251, 255 

body weight effects....................................................................................................................................25, 55, 73, 92 

breast milk ..................................................................................................... 9, 122, 128, 132, 159, 161, 239, 240, 245 

cancer...........................................3, 6, 7, 8, 9, 15, 20, 21, 27, 28, 32, 33, 35, 59, 62, 74, 75, 76, 77, 93, 95, 96, 97, 98, 

100, 109, 110, 116, 153, 157, 159, 178, 179, 180, 181, 182, 183, 186, 188, 201, 257, 267, 

268, 269, 272, 274, 276
 

carcinogen......................................................................................................................7, 8, 16, 21, 153, 257, 259, 272
 

carcinogenic............................................................................................... 8, 16, 22, 27, 31, 32, 62, 100, 178, 259, 274
 

carcinogenicity ............................................................................................................................35, 117, 176, 257, 259 

carcinoma ....................................................................................................................................22, 35, 65, 75, 98, 100 

cardiovascular effects ........................................................................................................................33, 48, 70, 80, 101 

deoxyribonucleic acid (see DNA)......................................................................................................................114, 115 

Department of Health and Human Services...................................................................................................................7 

dermal effects ............................................................................................................................................................107 

DNA (see deoxyribonucleic acid).................................. 8, 113, 114, 115, 116, 117, 153, 163, 164, 179, 184, 187, 255 

dog...............................................................................................................................................71, 73, 74, 76, 99, 182 

endocrine effects..................................................................................................................................................55, 101 

estrogen receptor........................................................................................................................................................150 

FDA (see Food and Drug Administration) ..................................................................................11, 261, 267, 272, 275
 

Federal Research in Progress (see FEDRIP) .....................................................................................................246, 255 

FEDRIP (see Federal Research in Progress) .............................................................................................246, 247, 255 

fetus ................................................................. 9, 76, 126, 127, 128, 156, 158, 161, 180, 181, 185, 186, 261, 265, 267
 

fish.....................................................................................................................................4, 5, 217, 218, 229, 232, 241 

Food and Drug Administration (see FDA) ..........................................................................................11, 229, 272, 275 

fruits...............................................................................................................................................15, 27, 229, 232, 242 

gastrointestinal effects ...........................................................................................................................................48, 89 

general population ......................................................................... 8, 15, 16, 18, 60, 110, 162, 165, 182, 183, 239, 275 

groundwater................................................................................................... 4, 205, 213, 215, 222, 223, 247, 264, 270
 

half-life ................................................................................ 2, 15, 18, 28, 142, 152, 160, 162, 189, 197, 205, 216, 275
 

hematological effects...............................................................................................................................26, 50, 71, 110 

hepatic effects..................................................................................................................................................54, 72, 91 

hydrolysis ..........................................................................................................................................................217, 243 

immune system........................................................................................................................21, 29, 73, 110, 178, 181 

immunological effects .......................................................................................................................23, 34, 73, 93, 177 

insects ........................................................................................................................................................................217 
STRONTIUM E-2 

APPENDIX E 

Integrated Risk Information System..................................................................................................................257, 259 

intermediate oral exposure...........................................................................................................................................92 

kidney .......................................................................... 55, 119, 125, 126, 127, 129, 148, 149, 151, 158, 163, 165, 167 

Kow .............................................................................................................................................................193, 194, 195 

lake ............................................................................................................................................................................222 

LD50 .......................................................................................................................................................................25, 36 

leukemia ........................................................................ 8, 9, 21, 26, 28, 65, 75, 76, 77, 93, 97, 98, 100, 116, 178, 183
 

liver...................................................................... 20, 59, 63, 72, 76, 119, 125, 126, 127, 129, 134, 144, 146, 163, 182
 

LOAEL (see lowest-observed-adverse-effect level).......... 24, 31, 36, 58, 62, 65, 74, 76, 80, 94, 95, 97, 101, 107, 108 

lowest-observed-adverse-effect level (see LOAEL)..............................................................................................24, 31 

lung........................................5, 8, 12, 18, 20, 21, 22, 23, 33, 35, 63, 64, 65, 70, 71, 72, 73, 75, 76, 80, 118, 119, 125,
 

126, 127, 135, 163, 185, 262
 

lymph......................................................................................................... 19, 63, 73, 76, 112, 114, 117, 142, 143, 147
 

lymphatic ...................................................................................................................................................................135 

lymphoreticular effects ..........................................................................................................................................58, 94 

marine................................................................................................................................................214, 216, 228, 241 

mass spectroscopy .....................................................................................................................................................184 

mast cell.......................................................................................................................................................61, 152, 181 

melanoma ....................................................................................................................................................................92 

milk................................................................ 8, 9, 19, 96, 112, 121, 128, 132, 161, 168, 169, 229, 239, 240, 244, 275
 

Minimal Risk Level (see MRL)...................................................................................................................................32 

miscarriages.........................................................................................................................................................95, 159 

MRL (see Minimal Risk Level)........................................................................... 23, 24, 25, 26, 32, 160, 176, 177, 257
 

musculoskeletal effects..........................................................................................................................................50, 51 

National Priorities List (see NPL) .........................................................................................................................1, 205 

neurobehavioral .........................................................................................................................................................155 

neurophysiological.......................................................................................................................................................17 

neurotransmitter...........................................................................................................................................................61 

NIOSH......................................................................................... 11, 190, 191, 192, 237, 249, 250, 258, 259, 267, 272 

NOAEL (see no-observed-adverse-effect level)........................... 24, 25, 31, 32, 36, 58, 62, 65, 74, 76, 80, 94, 95, 97, 

101, 107, 108, 257 

NOES.........................................................................................................................................................................239 

non-Hodgkin’s lymphoma...................................................................................................................................97, 183 

no-observed-adverse-effect level (see NOAEL)....................................................................................................24, 31 

NPL (see National Priorities List) .................................................................................1, 205, 206, 207, 209, 213, 214
 

ocular effects .....................................................................................................................................33, 36, 65, 92, 108 

odds ratio (see OR)......................................................................................................................................................50 

OR (see odds ratio)............................................................................................................................212, 220, 225, 234 

particulate ....................................................................................................................................................63, 135, 147 

particulates...........................................................................................................................................34, 144, 147, 244 

PBPD (see physiologically based pharmacodynamic)...............................................................................................132 

PBPK (see physiologically based pharmacokinetic) .................................................................132, 133, 134, 185, 186 

PEL (see permissible exposure limit) ................................................................................................................258, 259 

permissible exposure limit (see PEL) ........................................................................................................................259 

pharmacodynamic......................................................................................................................................................132 

pharmacokinetic.................................................................................................................................................132, 133 

physiologically based pharmacodynamic (see PBPD)...............................................................................................132 

physiologically based pharmacokinetic (see PBPK) .................................................................................................134 

plankton .....................................................................................................................................................................218 

precipitation............................................................................................................... 214, 215, 219, 223, 247, 250, 253
 

public health .................................................................................................................... 1, 6, 11, 27, 31, 155, 176, 276 

pulmonary fibrosis...........................................................................................................................................18, 65, 70 

RCRA (see Resource Conservation and Recovery Act)............................................................................................202 

reference dose (see RfD) ...................................................................................................................................257, 259 

regulations ............................................................................................. 11, 12, 201, 243, 257, 260, 265, 274, 275, 276
 

renal effects .....................................................................................................................................................55, 72, 92