TOXICOLOGICAL PROFILE FOR 

COBALT 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES 

Public Health Service 

Agency for Toxic Substances and Disease Registry
 

April 2004 
COBALT 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. 
COBALT iii 

UPDATE STATEMENT 

A Toxicological Profile for cobalt, 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). 
 

 

COBALT 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 3.8 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 
COBALT viii 

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

Toxicity; and numerous chemical-specific case studies. 

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: 
COBALT ix 

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

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

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

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

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

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

COBALT xi 

CONTRIBUTORS 

CHEMICAL MANAGER(S)/AUTHOR(S): 

Obaid M. Faroon, D.V.M., Ph.D. 

ATSDR, Division of Toxicology, Atlanta, GA 

Henry Abadin, M.S.P.H. 

ATSDR, Division of Toxicology, Atlanta, GA 

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

ATSDR, Division of Toxicology, Atlanta, GA 

Mark Osier, Ph.D., D.A.B.T. 

Syracuse Research Corporation, North Syracuse, NY 

Lara L. Chappell, Ph.D. 

Syracuse Research Corporation, North Syracuse, NY 

Gary Diamond, Ph.D. 

Syracuse Research Corporation, North Syracuse, NY 

Gloria Sage, 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. 

COBALT xiii 

PEER REVIEW 

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

1. Dr. Herman Cember, C.H.P., Ph.D., PE., Adjunct Professor, School of Health Sciences, Purdue 

University, Lafayette, Indiana; 

2.	 Dr. James Hansen, Ph.D., Environmental Contaminant Specialist, U.S. Fish and Wildlife Service, 

Spokane, WA; 

3.	 Dr. Dominique Lison, M.D., Ph.D., Vice-Chairman of the Doctoral School in Genetics and 

Immunology, Catholic University of Louvain, Brussels, Belgium, and 

4. Dr. Nancy Pedigo, Ph.D., Research Assistant Professor, Department of Pharmacology, University 

of Kentucky Medical Center, Lexington, KY. 

These experts collectively have knowledge of cobalt'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. 

COBALT 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 COBALT? ......................................................................................................................2 

1.2 WHAT HAPPENS TO COBALT WHEN IT ENTERS THE ENVIRONMENT? .........................4 

1.3 HOW MIGHT I BE EXPOSED TO COBALT? .............................................................................6 

1.4 HOW CAN COBALT ENTER AND LEAVE MY BODY?...........................................................8 

1.5 HOW CAN COBALT AFFECT MY HEALTH?............................................................................8 

1.6 HOW CAN COBALT AFFECT CHILDREN?.............................................................................12 

1.7 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO COBALT ..........................12 

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

COBALT?......................................................................................................................................13 

1.9 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH?...................................................................................................14 

1.10 WHERE CAN I GET MORE INFORMATION? .....................................................................15 

2. RELEVANCE TO PUBLIC HEALTH .................................................................................................17 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO COBALT IN THE UNITED 

STATES ..................................................................................................................................................17 

2.2 SUMMARY OF HEALTH EFFECTS ..........................................................................................18 

2.3 MINIMAL RISK LEVELS (MRLs)..............................................................................................24
 

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

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

3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE ..................................27 

3.2.1 Inhalation Exposure ..............................................................................................................29 

3.2.1.1 Death ............................................................................................................................29 

3.2.1.2 Systemic Effects...........................................................................................................30 

3.2.1.3 Immunological and Lymphoreticular Effects...............................................................50 

3.2.1.4 Neurological Effects.....................................................................................................51 

3.2.1.5 Reproductive Effects....................................................................................................51 

3.2.1.6 Developmental Effects .................................................................................................52 

3.2.1.7 Cancer...........................................................................................................................52 

3.2.2 Oral Exposure........................................................................................................................54 

3.2.2.1 Death ............................................................................................................................54 

3.2.2.2 Systemic Effects...........................................................................................................55 

3.2.2.3 Immunological and Lymphoreticular Effects...............................................................79 

3.2.2.4 Neurological Effects.....................................................................................................80 
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3.2.2.5 Reproductive Effects....................................................................................................81 

3.2.2.6 Developmental Effects .................................................................................................81 

3.2.2.7 Cancer...........................................................................................................................82 

3.2.3 Dermal Exposure...................................................................................................................83 

3.2.3.1 Death ............................................................................................................................83 

3.2.3.2 Systemic Effects...........................................................................................................83 

3.2.3.3 Immunological and Lymphoreticular Effects...............................................................84 

3.2.3.4 Neurological Effects.....................................................................................................86 

3.2.3.5 Reproductive Effects....................................................................................................86 

3.2.3.6 Developmental Effects .................................................................................................86 

3.2.3.7 Cancer...........................................................................................................................86 

3.2.4 Other Routes of Exposure .....................................................................................................86 

3.3 DISCUSSION OF HEALTH EFFECTS OF RADIOACTIVE COBALT BY ROUTE OF 

EXPOSURE ..............................................................................................................................87 

3.3.1 Inhalation Exposure ..............................................................................................................87 

3.3.1.1 Death ............................................................................................................................87 

3.3.1.2 Systemic Effects...........................................................................................................87 

3.3.1.3 Immunological and Lymphoreticular Effects...............................................................87 

3.3.1.4 Neurological Effects.....................................................................................................87 

3.3.1.5 Reproductive Effects....................................................................................................87 

3.3.1.6 Developmental Effects .................................................................................................87 

3.3.1.7 Cancer...........................................................................................................................88 

3.3.2 Oral Exposure........................................................................................................................88 

3.3.2.1 Death ............................................................................................................................88 

3.3.2.2 Systemic Effects...........................................................................................................88 

3.3.2.3 Immunological and Lymphoreticular Effects...............................................................88 

3.3.2.4 Neurological Effects.....................................................................................................88 

3.3.2.5 Reproductive Effects....................................................................................................88 

3.3.2.6 Developmental Effects .................................................................................................88 

3.3.2.7 Cancer...........................................................................................................................88 

3.3.3 External Exposure .................................................................................................................88 

3.3.3.1 Death ..........................................................................................................................106 

3.3.3.2 Systemic Effects.........................................................................................................107 

3.3.3.3 Immunological and Lymphoreticular Effects.............................................................112 

3.3.3.4 Neurological Effects...................................................................................................113 

3.3.3.5 Reproductive Effects..................................................................................................114 

3.3.3.6 Developmental Effects ...............................................................................................115 

3.3.3.7 Cancer.........................................................................................................................117 

3.3.4 Other Routes of Exposure ...................................................................................................117 

3.4 GENOTOXICITY ...................................................................................................................118 

3.5 TOXICOKINETICS................................................................................................................122 

3.5.1 Absorption...........................................................................................................................122 

3.5.1.1 Inhalation Exposure....................................................................................................122 

3.5.1.2 Oral Exposure.............................................................................................................126 

3.5.1.3 Dermal Exposure ........................................................................................................128 

3.5.1.4 Other Routes of Exposure ..........................................................................................128
 

3.5.2 Distribution .........................................................................................................................128 

3.5.2.1 Inhalation Exposure....................................................................................................129 

3.5.2.2 Oral Exposure.............................................................................................................130 
 

 

 

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3.5.2.3 Dermal Exposure ........................................................................................................130 

3.5.2.4 Other Routes of Exposure ..........................................................................................130
 

3.5.3 Metabolism..........................................................................................................................131 

3.5.4 Elimination and Excretion...................................................................................................131 

3.5.4.1 Inhalation Exposure....................................................................................................131 

3.5.4.2 Oral Exposure.............................................................................................................134 

3.5.4.3 Dermal Exposure ........................................................................................................135 

3.5.4.4 Other Routes of Exposure ..........................................................................................135
 

3.5.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models ...........137 

3.6 MECHANISMS OF ACTION ................................................................................................152 

3.6.1 Pharmacokinetic Mechanisms.............................................................................................152 

3.6.2 Mechanisms of Toxicity......................................................................................................153 

3.6.3 Animal-to-Human Extrapolations.......................................................................................157 

3.7 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS ........................157 

3.8 CHILDREN’S SUSCEPTIBILITY.........................................................................................158 

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

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

3.9.2 Biomarkers Used to Characterize Effects Caused by Cobalt ..............................................166 

3.10 INTERACTIONS WITH OTHER CHEMICALS ..................................................................166 

3.11 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE.............................................168 

3.12 METHODS FOR REDUCING TOXIC EFFECTS.................................................................169 

3.12.1 Reducing Peak Absorption Following Exposure ............................................................169 

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

3.12.3 Interfering with the Mechanism of Action for Toxic Effects .........................................170 

3.13 ADEQUACY OF THE DATABASE......................................................................................170 

3.13.1 Existing Information on Health Effects of Cobalt ..........................................................171 

3.13.2 Identification of Data Needs ...........................................................................................171 

3.13.3 Ongoing Studies..............................................................................................................182 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION............................................. 183 

4.1 CHEMICAL IDENTITY.........................................................................................................183 

4.2 PHYSICAL, CHEMICAL, AND RADIOLOGICAL PROPERTIES.....................................183 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL..........................................................195 

5.1 PRODUCTION............................................................................................................................195 

5.2 IMPORT/EXPORT......................................................................................................................201 

5.3 USE..............................................................................................................................................202 

5.4 DISPOSAL ..................................................................................................................................203 

6. POTENTIAL FOR HUMAN EXPOSURE .........................................................................................207 

6.1 OVERVIEW ................................................................................................................................207 

6.2 RELEASES TO THE ENVIRONMENT ....................................................................................212 

6.2.1 Air .......................................................................................................................................213 

6.2.2 Water...................................................................................................................................216 

6.2.3 Soil ......................................................................................................................................218 

6.3 ENVIRONMENTAL FATE........................................................................................................219 

6.3.1 Transport and Partitioning...................................................................................................219 

6.3.2 Transformation and Degradation ........................................................................................227
 

6.3.2.1 Air...............................................................................................................................227 
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6.3.2.2 Water ..........................................................................................................................227 

6.3.2.3 Sediment and Soil.......................................................................................................229 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT...............................230 

6.4.1 Air .......................................................................................................................................230 

6.4.2 Water...................................................................................................................................231 

6.4.3 Sediment and Soil ...............................................................................................................238 

6.4.4 Other Environmental Media................................................................................................241 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE .....................................246 

6.6 EXPOSURES OF CHILDREN...............................................................................................255 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES ...........................................257 

6.8 ADEQUACY OF THE DATABASE......................................................................................258 

6.8.1 Identification of Data Needs ...............................................................................................258 

6.8.2 Ongoing Studies ..................................................................................................................262 

7. ANALYTICAL METHODS ...............................................................................................................265 

7.1 BIOLOGICAL MATERIALS.................................................................................................265 

7.1.1 Internal Cobalt Measurements ............................................................................................265 

7.1.2 External Measurements.......................................................................................................270 

7.2 ENVIRONMENTAL SAMPLES............................................................................................272 

7.2.1 Field Measurements of Cobalt ............................................................................................272 

7.2.2 Laboratory Analysis of Environmental Samples.................................................................273 

7.3 ADEQUACY OF THE DATABASE......................................................................................278 

7.3.1 Identification of Data Needs ...............................................................................................278 

7.3.2 Ongoing Studies ..................................................................................................................280 

8. REGULATIONS AND ADVISORIES ...............................................................................................281 

9. REFERENCES ....................................................................................................................................301 

10. GLOSSARY ......................................................................................................................................397 

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 
COBALT xix 

LIST OF FIGURES 

3-1. Levels of Significant Exposure to Cobalt—Chemical Toxicity—Inhalation ................................ 41 

3-2. Levels of Significant Exposure to Cobalt—Chemical Toxicity—Oral ......................................... 71 

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

3-4. Transfer Parameters for Cobalt Following Inhalation of Cobalt Oxide (CO3O4) Particles, Showing 

the Fractions of the Lung Content, L(t), and Time, t, Cleared Per Day by Each Route .............. 124 

3-5. Conceptual Representation of a Physiologically Based Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance ............................................................................................... 139 

3-6. Compartment Model to Represent Particle Deposition and Time-Dependent Particle Transport in 

the Respiratory Tract.................................................................................................................... 141 

3-7. Reaction of Gases or Vapors at Various Levels of the Gas-Blood Interface............................... 144 

3-8. The Human Respiratory Tract Model: Absorption into Blood .................................................... 149 

3-9. ICRP Biokinetics Model for Cobalt............................................................................................. 151 

3-10. Relation Between Mean Cobalt Exposure and Mean Blood Concentration of Cobalt in Exposed 

Workers........................................................................................................................................ 165 

3-11. Existing Information on Health Effects of Stable Cobalt ............................................................ 172 

3-12. Existing Information on Health Effects of Radioactive Cobalt ................................................... 173 

6-1. Frequency of NPL Sites with Cobalt Contamination................................................................... 208 

6-2. Frequency of NPL Sites with 60Cobalt Contamination ................................................................ 209 

 

COBALT xxi 

LIST OF TABLES 

3-1. Levels of Significant Exposure to Cobalt—Chemical Toxicity—Inhalation ...............................31 

3-2. Levels of Significant Exposure to Cobalt—Chemical Toxicity—Oral ........................................56 

3-3. Levels of Significant Exposure to Cobalt—Chemical Toxicity—Dermal ...................................85 

3.4. Levels of Significant Exposure to Cobalt—Radiation Toxicity—External Radiation .................89 

3-5. Genotoxicity of Cobalt In Vitro ..................................................................................................119
 

3-6. Initial (Day 3) Lung Deposits of Cobalt Oxide and Summary of Lung Retention at 90 and 180 

Days ............................................................................................................................................125
 

3-7. Summary of Measurements of Retention and Excretion After Intragastric Administration of 

Cobalt Oxide (Co3O4) Particles (Mean Percentage of Recovered Activity at 7 Days After 

 Administration)...........................................................................................................................127
 

3-8. Peak Translocation and Average Mechanical Clearance Rates After Inhalation of Cobalt 

Oxide...........................................................................................................................................133
 

3-9. Summary of Measurements of Retention and Excretion of Cobalt Following Injection of Cobalt 

Nitrate Co(NO3)2 Solution (Mean Percent Recovery) ................................................................136
 

3-10. Reference Respiratory Values for a General Caucasian Population at Different Levels of 

Activity .......................................................................................................................................143
 

3-11. Reference Values of Parameters for the Compartment Model to Represent Time-dependent 

Particle Transport from the Human Respiratory Tract ...............................................................145
 

3-12. Cobalt Exposure Concentrations and Amounts in the Blood and Urine of Subjects 

Examined ....................................................................................................................................164
 

4-1. Chemical Identity of Cobalt and Selected Compounds ..............................................................184
 

4-2. Physical and Chemical Properties of Cobalt and Selected Compounds .....................................188
 

4-3. Principal Radioactive Cobalt Isotopes ........................................................................................192
 

5-1. Current U.S. Manufacturers of Cobalt Metal and Selected Cobalt Compounds.........................197
 

5-2. Facilities that Produce, Process, or Use Cobalt and Cobalt Compounds....................................199
 

6-1. Releases to the Environment from Facilities that Produce, Process, or Use Cobalt and Cobalt 

 Compounds .................................................................................................................................214
 

6-2. Concentration of Cobalt in the Atmosphere ...............................................................................232
 
COBALT xxii 

6-3. Cobalt Levels in Water ...............................................................................................................236
 

6-4. Cobalt Levels in Sediment ..........................................................................................................240
 

6-5. Cobalt Levels in Food.................................................................................................................244
 

6-6. Cobalt Content of Miscellaneous Substances .............................................................................247
 

6-7. Mean Daily Dietary Intake of Cobalt for Selected Population Groups in Canada .....................248
 

6-8. Cobalt Levels in Human Tissues and Fluids...............................................................................250
 

6-9. Ongoing Studies on Cobalt .........................................................................................................263
 

7-1. Analytical Methods for Determining Stable Cobalt in Biological Materials..............................266
 

7-2. Analytical Methods for Determining Radioactive Cobalt in Biological Samples ......................268
 

7-3. Analytical Methods for Determining Stable Cobalt in Environmental Samples ........................274
 

7-4. Analytical Methods for Determining Radioactive Cobalt in Environmental Samples ...............276
 

8-1. Regulations and Guidelines Applicable to Stable Cobalt ...........................................................282
 

8-2. Regulations and Guidelines Applicable to Radioactive Cobalt ........................................................
 
COBALT 1 

1. PUBLIC HEALTH STATEMENT 

This public health statement tells you about cobalt 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. Stable cobalt has been found in at least 426 of the 

1,636 current or former NPL sites. Radioactive cobalt, as 60Co, has been found in at least 13 of 

the 1,636 current or former NPL sites. However, the total number of NPL sites evaluated for this 

substance is not known. As more sites are evaluated, the sites at which cobalt is found may 

increase. This information is important because exposure to this substance 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 cobalt, 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. 
COBALT 2 

1. PUBLIC HEALTH STATEMENT 

1.1 WHAT IS COBALT? 

Cobalt is a naturally-occurring element that has properties similar to those of iron and nickel. It 

has an atomic number of 27. There is only one stable isotope of cobalt, which has an atomic 

mass number of 59. (An element may have several different forms, called isotopes, with 

different weights depending on the number of neutrons that it contains. The isotopes of an 

element, therefore, have different atomic mass numbers [number of protons and neutrons], 

although the atomic number [number of protons] remains the same.) However, there are many 

unstable or radioactive isotopes, two of which are commercially important, cobalt-60 and 

cobalt-57, also written as Co-60 or 60Co and Co-57 or 57Co, and read as cobalt sixty and cobalt 

fifty-seven. All isotopes of cobalt behave the same chemically and will therefore have the same 

chemical behavior in the environment and the same chemical effects on your body. However, 

isotopes have different mass numbers and the radioactive isotopes have different radioactive 

properties, such as their half-life and the nature of the radiation they give off. The half-life of a 

cobalt isotope is the time that it takes for half of that isotope to give off its radiation and change 

into a different isotope. After one half-life, one-half of the radioactivity is gone. After a second 

half-life, one-fourth of the original radioactivity is left, and so on. Radioactive isotopes are 

constantly changing into different isotopes by giving off radiation, a process referred to as 

radioactive decay. The new isotope may be a different element or the same element with a 

different mass. 

Small amounts of cobalt are naturally found in most rocks, soil, water, plants, and animals, 

typically in small amounts. Cobalt is also found in meteorites. Elemental cobalt is a hard, 

silvery grey metal. However, cobalt is usually found in the environment combined with other 

elements such as oxygen, sulfur, and arsenic. Small amounts of these chemical compounds can 

be found in rocks, soil, plants, and animals. Cobalt is even found in water in dissolved or ionic 

form, typically in small amounts. (Ions are atoms, collections of atoms, or molecules containing 

a positive or negative electric charge.) A biochemically important cobalt compound is 

vitamin B12 or cyanocobalamin. Vitamin B12 is essential for good health in animals and humans. 

Cobalt is not currently mined in the United States, but has been mined in the past. Therefore, we 
COBALT 3 

1. PUBLIC HEALTH STATEMENT 

obtain cobalt and its other chemical forms from imported materials and by recycling scrap metal 

that contains cobalt. 

Cobalt metal is usually mixed with other metals to form alloys, which are harder or more 

resistant to wear and corrosion. These alloys are used in a number of military and industrial 

applications such as aircraft engines, magnets, and grinding and cutting tools. They are also used 

in artificial hip and knee joints. Cobalt compounds are used as colorants in glass, ceramics, and 

paints, as catalysts, and as paint driers. Cobalt colorants have a characteristic blue color; 

however, not all cobalt compounds are blue. Cobalt compounds are also used as trace element 

additives in agriculture and medicine. 

Cobalt can also exist in radioactive forms. A radioactive isotope of an element constantly gives 

off radiation, which can change it into an isotope of a different element or a different isotope of 

the same element. This newly formed nuclide may be stable or radioactive. This process is 

called radioactive decay. 60Co is the most important radioisotope of cobalt. It is produced by 

bombarding natural cobalt, 59Co, with neutrons in a nuclear reactor. 60Co decays by giving off a 

beta ray (or electron), and is changed into a stable nuclide of nickel (atomic number 28). The 

half-life of 60Co is 5.27 years. The decay is accompanied by the emission of high energy 

radiation called gamma rays. 60Co is used as a source of gamma rays for sterilizing medical 

equipment and consumer products, radiation therapy for treating cancer patients, and for 

manufacturing plastics. 60Co has also been used for food irradiation; depending on the radiation 

dose, this process may be used to sterilize food, destroy pathogens, extend the shelf-life of food, 

disinfest fruits and grain, delay ripening, and retard sprouting (e.g., potatoes and onions). 57Co is 

used in medical and scientific research and has a half-life of 272 days. 57Co undergoes a decay 

process called electron capture to form a stable isotope of iron (57Fe). Another important cobalt 

isotope, 58Co, is produced when nickel is exposed to a source of neutrons. Since nickel is used in 

nuclear reactors, 58Co may be unintentionally produced and appear as a contaminant in cooling 

water released by nuclear reactors. 58Co also decays by electron capture, forming another stable 

isotope of iron (58Fe). 60Co may be similarly produced from cobalt alloys in nuclear reactors and 
COBALT 4 

1. PUBLIC HEALTH STATEMENT 

released as a contaminant in cooling water. 58Co has a half-life of 71 days and gives off beta and 

gamma radiation in the decay process. 

Quantities of radioactive cobalt are normally measured in units of radioactivity (curies or 

becquerels) rather than in units of mass (grams). The becquerel (Bq) is a new international unit, 

and the curie (Ci) is the traditional unit; both are currently used. A becquerel is the amount of 

radioactive material in which 1 atom transforms every second, and a curie is the amount of 

radioactive material in which 37 billion atoms transform every second. For an overview of basic 

radiation physics, chemistry, and biology see Appendix D of this profile. For more information 

on radiation, see the ATSDR Toxicological Profile for Ionizing Radiation. 

To learn more about the properties and uses of cobalt, see Chapters 4 and 5. 

1.2 WHAT HAPPENS TO COBALT WHEN IT ENTERS THE ENVIRONMENT? 

Cobalt may enter the environment from both natural sources and human activities. Cobalt occurs 

naturally in soil, rock, air, water, plants, and animals. It may enter air and water, and settle on 

land from windblown dust, seawater spray, volcanic eruptions, and forest fires and may 

additionally get into surface water from runoff and leaching when rainwater washes through soil 

and rock containing cobalt. Soils near ore deposits, phosphate rocks, or ore smelting facilities, 

and soils contaminated by airport traffic, highway traffic, or other industrial pollution may 

contain high concentrations of cobalt. Small amounts of cobalt may be released into the 

atmosphere from coal-fired power plants and incinerators, vehicular exhaust, industrial activities 

relating to the mining and processing of cobalt-containing ores, and the production and use of 

cobalt alloys and chemicals. 58Co and 60Co may be released to the environment as a result of 

nuclear accidents (i.e, Chernobyl), radioactive waste dumping in the sea or from radioactive 

waste landfills, and nuclear power plant operations. 

Cobalt cannot be destroyed in the environment. It can only change its form or become attached 

or separated from particles. Cobalt released from power plants and other combustion processes 
COBALT 5 

1. PUBLIC HEALTH STATEMENT 

is usually attached to very small particles. Cobalt contained in windborne soil is generally found 

in larger particles than those released from power plants. These large particles settle to the 

ground or are washed out of the air by rain. Cobalt that is attached to very small particles may 

stay in the air for many days. Cobalt released into water may stick to particles in the water 

column or to the sediment at the bottom of the body of water into which it was released, or 

remain in the water column in ionic form. The specific fate of cobalt will depend on many 

factors such as the chemistry of the water and sediment at a site as well as the cobalt 

concentration and water flow. Cobalt deposited on soil is often strongly attached to soil particles 

and therefore would not travel very far into the ground. However, the form of the cobalt and the 

nature of the soil at a particular site will affect how far cobalt will penetrate into the soil. Both in 

soil and sediment, the amount of cobalt that is mobile will increase under more acidic conditions. 

Ultimately, most cobalt ends up in the soil or sediment. 

Plants can accumulate very small amounts of cobalt from the soil, especially in the parts of the 

plant that you eat most often, such as the fruit, grain, and seeds. While animals that eat these 

plants will accumulate cobalt, cobalt is not known to biomagnify (produce increasingly higher 

concentrations) up the food chain. Therefore, vegetables, fruits, fish, and meat that you consume 

will generally not contain high amounts of cobalt. Cobalt is an essential element, required for 

good health in animals and humans, and therefore, it is important that foodstuffs contain 

adequate quantities of cobalt. 

60Co and 58Co are moderately short-lived, manufactured radioactive isotopes that are produced in 

nuclear reactors. Although these isotopes are not produced by nuclear fission, small amounts of 

these radioisotopes are also produced by the neutron interaction with the structural materials 

found in the reactor of nuclear plants, and are produced during the routine operation of nuclear 

plants. Small amounts may be released to the environment as contaminants in cooling water or 

in radioactive waste. Since these isotopes are not fission products, they are not produced in 

nuclear weapons testing and are not associated with nuclear fallout. In the environment, 

radioactive isotopes of cobalt will behave chemically like stable cobalt. However, 60Co and 58Co 
 

COBALT 6 

1. PUBLIC HEALTH STATEMENT 

will also undergo radioactive decay according to their respective half-lives, 5.27 years and 

71 days. 

For more information about what happens to cobalt in the environment, see Chapter 6. 

1.3 HOW MIGHT I BE EXPOSED TO COBALT? 

Cobalt is widely dispersed in the environment in low concentrations. You may be exposed to 

small amounts of cobalt by breathing air, drinking water, and eating food containing it. Children 

may also be exposed to cobalt by eating dirt. You may also be exposed by skin contact with soil, 

water, cobalt alloys, or other substances that contain cobalt. Analytical methods used by 

scientists to determine the levels of cobalt in the environment generally do not determine the 

specific chemical form of cobalt present. Therefore, we do not always know the chemical form 

of cobalt to which a person may be exposed. Similarly, we do not know what forms of cobalt are 

present at hazardous waste sites. Some forms of cobalt may be insoluble or so tightly attached to 

particles or embedded in minerals that they are not taken up by plants and animals. Other forms 

of cobalt that are weakly attached to particles may be taken up by plants and animals. 

The concentration of cobalt in soil varies widely, generally ranging from about 1 to 40 ppm 

(1 ppm=1 part of cobalt in a million parts of soil by weight), with an average level of 7 ppm. 

Soils containing less than about 3 ppm of cobalt are considered cobalt-deficient because plants 

growing in them do not have sufficient cobalt to meet the dietary requirements of cattle and 

sheep. Such cobalt-deficient soils are found in some areas in the southeast and northeast parts of 

the United States. On the other hand, soils near cobalt-containing mineral deposits, mining and 

smelting facilities, or industries manufacturing or using cobalt alloys or chemicals may contain 

much higher levels of cobalt. 

Usually, the air contains very small amounts of cobalt, less than 2 nanograms (1 nanogram=onebillionth part of a gram) per cubic meter (ng/m3

). The amount of cobalt that you breathe in a day 
COBALT 7 

1. PUBLIC HEALTH STATEMENT 

is much less than what you consume in food and water. You may breathe in higher levels of 

cobalt in dust in areas near cobalt-related industries or near certain hazardous waste sites. 

The concentration of cobalt in surface and groundwater in the United States is generally low— 

between 1 and 10 parts of cobalt in 1 billion parts of water (ppb) in populated areas; 

concentration may be hundreds or thousands times higher in areas that are rich in cobaltcontaining minerals or in areas near mining or smelting operations. In most drinking water, 

cobalt levels are less than 1–2 ppb. 

For most people, food is the largest source of cobalt intake. The average person consumes about 

11 micrograms of cobalt a day in their diet. Included in this food is vitamin B12, which is found 

in meat and diary products. The recommended daily intake of vitamin B12 is 6 micrograms 

(1 microgram=one-millionth part of a gram). 

You may also be exposed to higher levels of cobalt if you work in metal mining, smelting, and 

refining, in industries that make or use cutting or grinding tools, or in other industries that 

produce or use cobalt metal and cobalt compounds. If good industrial hygiene is practiced, such 

as the use of exhaust systems in the workplace, exposure can be reduced to safe levels. 

Industrial exposure results mainly from breathing cobalt-containing dust. 

When we speak of exposure to 60Co, we are interested in exposure to the radiation given off by 

this isotope, primarily the gamma rays. The general population is rarely exposed to this radiation 

unless a person is undergoing radiation therapy. However, workers at nuclear facilities, 

irradiation facilities, or nuclear waste storage sites may be exposed to 60Co or 58Co. Exposures to 

radiation at these facilities are regulated and carefully monitored and controlled. 

You can find more information on how you may be exposed to cobalt in Chapter 6. 
COBALT 8 

1. PUBLIC HEALTH STATEMENT 

1.4 HOW CAN COBALT ENTER AND LEAVE MY BODY? 

Cobalt can enter your body when you breathe in air containing cobalt dust, when you drink water 

that contains cobalt, when you eat food that contains cobalt, or when your skin touches materials 

that contain cobalt. If you breathe in air that contains cobalt dust, the amount of inhaled cobalt 

that stays in your lungs depends on the size of the dust particles. The amount that is then 

absorbed into your blood depends on how well the particles dissolve. If the particles dissolve 

easily, then it is easier for the cobalt to pass into your blood from the particles in your lungs. If 

the particles dissolve slowly, then they will remain in your lungs longer. Some of the particles 

will leave your lungs as they normally clean themselves out. Some of the particles will be 

swallowed into your stomach. The most likely way you will be exposed to excess cobalt is by 

eating contaminated food or drinking contaminated water. Levels of cobalt normally found in 

the environment, however, are not high enough to result in excess amounts of cobalt in food or 

water. The amount of cobalt that is absorbed into your body from food or water depends on 

many things including your state of health, the amount you eat or drink, and the number of days, 

weeks, or years you eat foods or drink fluids containing cobalt. If you do not have enough iron 

in your body, the body may absorb more cobalt from the foods you eat. Once cobalt enters your 

body, it is distributed into all tissues, but mainly into the liver, kidney, and bones. After cobalt is 

breathed in or eaten, some of it leaves the body quickly in the feces. The rest is absorbed into the 

blood and then into the tissues throughout the body. The absorbed cobalt leaves the body slowly, 

mainly in the urine. Studies have shown that cobalt does not readily enter the body through 

normal skin, but it can if the skin has been cut. 

Further information on how cobalt can enter or leave your body can be found in Chapter 3. 

1.5 HOW CAN COBALT 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. 
COBALT 9 

1. PUBLIC HEALTH STATEMENT 

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. 

Cobalt has both beneficial and harmful effects on human health. Cobalt is beneficial for humans 

because it is part of vitamin B12, which is essential to maintain human health. Cobalt 

(0.16–1.0 mg cobalt/kg of body weight) has also been used as a treatment for anemia (less than 

normal number of red blood cells), including in pregnant women, because it causes red blood 

cells to be produced. Cobalt also increases red blood cell production in healthy people, but only 

at very high exposure levels. Cobalt is also essential for the health of various animals, such as 

cattle and sheep. Exposure of humans and animals to levels of cobalt normally found in the 

environment is not harmful. 

When too much cobalt is taken into your body, however, harmful health effects can occur. 

Workers who breathed air containing 0.038 mg cobalt/m3 (about 100,000 times the concentration 

normally found in ambient air) for 6 hours had trouble breathing. Serious effects on the lungs, 

including asthma, pneumonia, and wheezing, have been found in people exposed to 0.005 mg 

cobalt/m3

 while working with hard metal, a cobalt-tungsten carbide alloy. People exposed to 

0.007 mg cobalt/m3

 at work have also developed allergies to cobalt that resulted in asthma and 

skin rashes. The general public, however, is not likely to be exposed to the same type or amount 

of cobalt dust that caused these effects in workers. 

In the 1960s, some breweries added cobalt salts to beer to stabilize the foam (resulting in 

exposures of 0.04–0.14 mg cobalt/kg). Some people who drank excessive amounts of beer (8– 

25 pints/day) experienced serious effects on the heart. In some cases, these effects resulted in 
COBALT 10 

1. PUBLIC HEALTH STATEMENT 

death. Nausea and vomiting were usually reported before the effects on the heart were noticed. 

Cobalt is no longer added to beer so you will not be exposed from this source. The effects on the 

heart, however, may have also been due to the fact that the beer-drinkers had protein-poor diets 

and may have already had heart damage from alcohol abuse. Effects on the heart were not seen, 

however, in people with anemia treated with up to 1 mg cobalt/kg, or in pregnant women with 

anemia treated with 0.6 mg cobalt/kg. Effects on the thyroid were found in people exposed to 

0.5 mg cobalt/kg for a few weeks. Vision problems were found in one man following treatment 

with 1.3 mg cobalt/kg for 6 weeks, but this effect has not been seen in other human or animal 

studies. 

Being exposed to radioactive cobalt may be very dangerous to your health. If you come near 

radioactive cobalt, cells in your body can become damaged from gamma rays that can penetrate 

your entire body, even if you do not touch the radioactive cobalt. Radiation from radioactive 

cobalt can also damage cells in your body if you eat, drink, breathe, or touch anything that 

contains radioactive cobalt. The amount of damage depends on the amount of radiation to which 

you are exposed, which is related to the amount of activity in the radioactive material and the 

length of time that you are exposed. Most of the information regarding health effects from 

exposure to radiation comes from exposures for only short time periods. The risk of damage 

from exposure to very low levels of radiation for long time periods is not known. If you are 

exposed to enough radiation, you might experience a reduction in white blood cell number, 

which could lower your resistance to infections. Your skin might blister or burn, and you may 

lose hair from the exposed areas. This happens to cancer patients treated with large amounts of 

radiation to kill cancer. Cells in your reproductive system could become damaged and cause 

temporary sterility. Exposure to lower levels of radiation might cause nausea, and higher levels 

can cause vomiting, diarrhea, bleeding, coma, and even death. Exposure to radiation can also 

cause changes in the genetic materials within cells and may result in the development of some 

types of cancer. 

Studies in animals suggest that exposure to high amounts of nonradioactive cobalt during 

pregnancy might affect the health of the developing fetus. Birth defects, however, have not been 
COBALT 11 

1. PUBLIC HEALTH STATEMENT 

found in children born to mothers who were treated with cobalt for anemia during pregnancy. 

The doses of cobalt used in the animal studies were much higher than the amounts of cobalt to 

which humans would normally be exposed. 

Nonradioactive cobalt has not been found to cause cancer in humans or in animals following 

exposure in the food or water. Cancer has been shown, however, in animals who breathed cobalt 

or when cobalt was placed directly into the muscle or under the skin. Based on the animal data, 

the International Agency for Research on Cancer (IARC) has determined that cobalt is possibly 

carcinogenic to humans. 

Much of our knowledge of cobalt toxicity is based on animal studies. Cobalt is essential for the 

growth and development of certain animals, such as cows and sheep. Short-term exposure of 

rats to high levels of cobalt in the air results in death and lung damage. Longer-term exposure of 

rats, guinea pigs, hamsters, and pigs to lower levels of cobalt in the air results in lung damage 

and an increase in red blood cells. Short-term exposure of rats to high levels of cobalt in the 

food or drinking water results in effects on the blood, liver, kidneys, and heart. Longer-term 

exposure of rats, mice, and guinea pigs to lower levels of cobalt in the food or drinking water 

results in effects on the same tissues (heart, liver, kidneys, and blood) as well as the testes, and 

also causes effects on behavior. Sores were seen on the skin of guinea pigs following skin 

contact with cobalt for 18 days. Generally, cobalt compounds that dissolve easily in water are 

more harmful than those that are hard to dissolve in water. 

Much of what we know about the effects of radioactive cobalt comes from studies in animals. 

The greatest danger of radiation seen in animals is the risk to the developing animal, with even 

moderate amounts of radiation causing changes in the fetus. High radiation doses in animals 

have also been shown to cause temporary or permanent sterility and changes in the lungs, which 

affected the animals’ breathing. The blood of exposed animals has lower numbers of white 

blood cells, the cells that aid in resistance to infections, and red blood cells, which carry oxygen 

in the blood. Radioactive cobalt exposures in animals have also caused genetic damage to cells, 

cancer, and even death. 
COBALT 12 

1. PUBLIC HEALTH STATEMENT 

More information on how cobalt can affect your health can be found in Chapter 3. 

1.6 HOW CAN COBALT 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 can be exposed to cobalt in the same ways as adults. In addition, cobalt may be 

transferred from the pregnant mother to the fetus or from the mother to the infant in the breast 

milk. Children may be affected by cobalt the same ways as adults. Studies in animals have 

suggested that children may absorb more cobalt from foods and liquids containing cobalt than 

adults. Babies exposed to radiation while in their mother’s womb are believed to be much more 

sensitive to the effects of radiation than adults. 

1.7 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO COBALT 

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

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

department to investigate. 

Since cobalt is naturally found in the environment, people cannot avoid being exposed to it. 

However, the relatively low concentrations present do not warrant any immediate steps to reduce 

exposure. If you are accidentally exposed to large amounts of cobalt, consult a physician 

immediately. 

Children living near waste sites containing cobalt are likely to be exposed to higher 

environmental levels of cobalt through breathing, touching soil, and eating contaminated soil. 

Some children eat a lot of dirt. You should discourage your children from eating dirt. Make sure 
COBALT 13 

1. PUBLIC HEALTH STATEMENT 

they wash their hands frequently and before eating. Discourage your children from putting their 

hands in their mouths or hand-to-mouth activity. 

You are unlikely to be exposed to high levels of radioactive cobalt unless you are exposed as part 

of a radiotherapy treatment, there is an accident involving a cobalt sterilization or radiotherapy 

unit, or there is an accidental release from a nuclear power plant. In such cases, follow the 

advice of public health officials who will publish guidelines for reducing exposure to radioactive 

material when necessary. Workers who work near or with radioactive cobalt should follow the 

workplace safety guidelines of their institution carefully to reduce the risk of accidental 

irradiation. 

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

EXPOSED TO COBALT? 

We have reliable tests that can measure cobalt in the urine and the blood for periods up to a 

few days after exposure. The amount of cobalt in your blood or urine can be used to estimate 

how much cobalt you had taken into your body. The tests are not able to accurately predict 

potential health effects following exposure to cobalt. 

It is difficult to determine whether a person has been exposed only to external radiation from 

radioactive cobalt unless the radiation dose was rather large. Health professionals examining 

people who have health problems similar to those resulting from radiation exposure would need 

to rely on additional information in order to establish if such people had been near a source of 

radioactivity. It is relatively easy to determine whether a person has been internally exposed to 

radioactive cobalt, as discussed in Chapter 7. More information on medical tests can be found in 

Chapters 3 and 7. 
COBALT 14 

1. PUBLIC HEALTH STATEMENT 

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 cobalt include the following: 

EPA requires that the federal government be notified if more than 1,000 pounds of cobalt (as the 

bromide, formate, and sulfamate compounds) are released into the environment in a 24-hour 

period. OSHA regulates levels of nonradioactive cobalt in workplace air. The limit for an 

8-hour workday, 40-hour workweek is an average of 0.1 mg/m3

. The USNRC and the 

Department of Energy (DOE) regulate occupational exposures as well as exposures of the 

general public to radioactive cobalt. 
 

 

 

 

 

 

 

 

 

 

 

COBALT 15 

1. PUBLIC HEALTH STATEMENT 

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: 

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/ 

COBALT 17 

2. RELEVANCE TO PUBLIC HEALTH 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO COBALT IN THE UNITED 

STATES 

Cobalt is a naturally-occurring element that has properties similar to those of iron and nickel. The largest 

use of metallic cobalt is in superalloys that are used in gas turbine aircraft engines. Cobalt compounds are 

used as pigments in glass, ceramics, and paints; as catalysts in the petroleum industry; as paint driers; and 

as trace element additives in agriculture and medicine. 

Cobalt may be released to the environment by human activities, as well by weathering of rocks and soil. 

The primary anthropogenic sources of cobalt in the environment are from the burning of fossil fuels, 

application of cobalt-containing sludge or phosphate fertilizers, mining and smelting of cobalt-containing 

ores, processing of cobalt-containing alloys, and industries that use or process cobalt compounds. Cobalt 

released to the atmosphere is deposited onto soil or water surfaces by wet and dry deposition. In soils, 

cobalt generally has low mobility and strong adsorption. However its mobility increases in moist, acidic 

soils. In water, cobalt largely partitions to sediment and to suspended solids in the water column; 

however, the amount that is adsorbed to suspended solids is highly variable. 

Exposure of the general population to cobalt occurs through inhalation of ambient air and ingestion of 

food and drinking water. In general, intake from food sources is much greater than from drinking water 

and air. The cobalt intake in food has been estimated to be 5.0–40.0 μg/day. Occupational exposure to 

cobalt occurs for workers in the hard metal industry (tool production, grinding, etc.) and in industries such 

as coal mining, metal mining, smelting and refining, cobalt dye painters, and the cobalt chemical 

production industry. The concentrations of cobalt in the air of hard metal manufacturing, welding, and 

grinding factories may range from 1 to 300 μg/m3

, compared to normal atmospheric levels of 0.4– 

2.0 ng/m3

. 

While there is only one stable isotope of cobalt, 59Co, there are many radioactive isotopes of cobalt. Of 

these radioactive isotopes, two are commercially important, 60Co and 57Co. 60Co is produced by 

irradiating 59Co with thermal neutrons in a nuclear reactor, and is used as a source of gamma rays for 

sterilizing medical equipment or consumer products, food irradiation, radiation therapy for treating cancer 
COBALT 18 

2. RELEVANCE TO PUBLIC HEALTH 

patients, and for manufacturing plastics. The general population is not significantly exposed to 

radioactive forms of cobalt. Cancer patients being treated with radiation therapy may be exposed to 

gamma rays from a 60Co source; however, the effects of external exposure to gamma radiation is not 

unique to 60Co, but is similar for all gamma-emitting radionuclides. Workers at nuclear facilities and 

nuclear waste storage sites may be exposed to potentially high levels of radioactive cobalt. 

2.2 SUMMARY OF HEALTH EFFECTS 

As a component of cyanocobalmin (vitamin B12), cobalt is essential in the body; the Recommended 

Dietary Allowance of vitamin B12 is 2.4 μg/day, which contains 0.1 μg of cobalt. Cobalt has been 

identified in most tissues of the body, with the highest concentrations found in the liver. 

Following inhalation exposure to cobalt-containing particles, the primary target of exposure is the 

respiratory tract. Occupational exposure of humans to cobalt metal or cobalt-containing hard metal have 

reported primarily respiratory effects, including decreased pulmonary function, asthma, interstitial lung 

disease, wheezing, and dyspnea; these effects were reported at occupational exposure levels ranging from 

0.015–0.13 mg Co/m3

. Animal studies have further identified respiratory tract hyperplasia, pulmonary 

fibrosis, and emphysema as sensitive effects of inhaled cobalt on respiratory tissues. Many of the 

respiratory tract effects are believed to be the result of the generation of oxidants and free radicals by the 

cobalt ion. In particular, hard metal (a tungsten carbide/cobalt alloy) is a potent generator of free 

electrons, resulting in the generation of active oxygen species. However, some of the respiratory effects, 

such as cobalt-induced asthma, are likely the result of immunosensitization to cobalt. 

Other sensitive targets of cobalt inhalation in humans include effects on the thyroid and allergic 

dermatitis, manifesting as eczema and erythema; it is believed that the allergic dermatitis is due, at least in 

part, to concurrent dermal exposure and the development of immunosensitization to cobalt. 

Adequate chronic studies of the oral toxicity of cobalt or cobalt compounds in humans and animals are 

not presently available. The most sensitive endpoint following oral exposure to cobalt in humans appears 

to be an increase in erythrocyte numbers (polycythemia). This effect has been observed in both normal 

subjects and in patients who were anemic as a result of being anephric. However, treatment of pregnant 

women with cobalt did not prevent the reduction in hematocrit and hemoglobin levels often found during 
COBALT 19 

2. RELEVANCE TO PUBLIC HEALTH 

pregnancy. Exposure of humans to beer containing cobalt as a foam stabilizer resulted in severe effects 

on the cardiovascular system, including cardiomyopathy and death, as well as gastrointestinal effects 

(nausea, vomiting) and hepatic necrosis. However, the subjects in these studies were alcoholics, and it is 

not known what effect excessive alcohol consumption may have played in the development of the 

observed effects. 

Following dermal exposure, the most commonly observed effect is dermatitis, as demonstrated by a large 

number of human studies. Using patch tests and intradermal injections, it has been demonstrated that the 

dermatitis is probably caused by an allergic reaction to cobalt, with the cobalt ion functioning as a hapten. 

Available studies of the carcinogenic effects of cobalt in occupationally-exposed humans have reported 

mixed results, with both positive and negative results. Lifetime inhalation of cobalt sulfate resulted in 

increased tumor incidences in both rats and mice; NTP reported that there was some evidence of 

carcinogenicity in male Fischer 344 (F344) strain rats, and clear evidence of carcinogenicity in female 

F344 strain rats and male and female B6C3F1 strain mice following inhalation exposure. Oral data on the 

carcinogenic effects of cobalt and cobalt compounds are not available. IRIS does not report a cancer 

classification for cobalt or cobalt compounds. IARC has classified cobalt and cobalt compounds as 

possibly carcinogenic to humans (Group 2B). 

A more detailed discussion of the health effects of cobalt and cobalt compounds is presented in Chapter 3. 

An enhanced discussion of sensitive end points of stable cobalt toxicity is presented below. 

Respiratory Effects. The primary effects of cobalt on respiratory tissues are seen following 

inhalation exposure, and include diminished pulmonary function, increased frequency of cough, 

respiratory inflammation, and fibrosis; reported effect levels in occupationally-exposed humans have 

ranged from 0.015–0.13 mg Co/m3

. Animal studies have further identified respiratory tract hyperplasia, 

pulmonary fibrosis, and emphysema as sensitive effects of cobalt on respiratory tissues. A number of 

these effects are believed to be the result of the generation of oxidants and free radicals by the cobalt ion. 

In vitro exposure to soluble cobalt increases indices of oxidative stress, including diminished levels of 

reduced glutathione, increased levels of oxidized glutathione, activation of the hexose monophosphate 

shunt, and free-radical-induced DNA damage. Cobalt exposure also results in sensitization of the 

immune system, which may result in asthmatic attacks following inhalation of cobalt in sensitized 

individuals. 
COBALT 20 

2. RELEVANCE TO PUBLIC HEALTH 

Hard metal is a metal alloy with a tungsten carbide and cobalt matrix. It is used to make cutting tools 

because of its hardness and resistance to high temperature. Exposure to hard metal has been shown in a 

number of studies to cause respiratory effects, including respiratory irritation, diminished pulmonary 

function, asthma, and fibrosis, at exposure levels lower than those that would produce similar effects 

following exposure to cobalt metal alone (0.007–0.14 mg Co/m3

). Studies suggest that cobalt and not 

tungsten carbide is the probable causative agent for the respiratory effects observed in hard metal workers 

(see Section 3.5). A mechanism by which hard metal may exert its effects has been proposed by a group 

of Belgian researchers. In this proposed mechanism, tungsten carbide, which is a very good conductor of 

electrons, facilitates the oxidation of cobalt metal to ionic cobalt (presumably Co2+) by transferring 

electrons from the cobalt atom to molecular oxygen adjacent to the tungsten carbide molecule. The result 

is an increased solubility of cobalt, relative to cobalt metal alone, and the generation of active oxygen 

species. In vitro evidence for this mechanism includes the ability of hard metal particles, but neither 

cobalt nor tungsten carbide alone at the same concentrations, to generate oxidant species and cause lipid 

peroxidation. Hard metal particles have also been shown to increase the levels of inducible nitric oxide 

synthase (iNOS), a gene responsive to oxidant stress. 

Hematological Effects. Exposure to cobalt and cobalt compounds has been demonstrated to increase 

levels of erythrocytes and hemoglobin in both humans and animals. Davis and Fields reported increased 

(~16–20%) erythrocyte levels in six of six healthy men exposed orally to cobalt chloride (~1 mg Co/kgday); erythrocyte counts returned to normal 9–15 days after cessation of cobalt administration. Increased 

levels of erythrocytes were also found following oral treatment of anephric patients (with resulting 

anemia) with cobalt chloride. The increase in hemoglobin resulted in a decreased need for blood 

transfusions. Treatment of pregnant women for 90 days with cobalt chloride, however, did not prevent 

the reduction in hematocrit and hemoglobin levels often found during pregnancy. 

Increased levels of hemoglobin were observed in rats and guinea pigs, but not in dogs, exposed to cobalt 

hydrocarbonyl by inhalation. Polycythemia was reported in rats, but not mice, exposed to airborne cobalt 

sulfate. Significantly increased erythrocyte (polycythemia), hematocrit, and hemoglobin levels were 

found in animals treated orally with cobalt as either a single dose or with longer-term exposure. Of 

particular note is an 8-week study in rats, which reported dose- and time-related increases in erythrocyte 

number following oral administration of cobalt chloride. 
COBALT 21 

2. RELEVANCE TO PUBLIC HEALTH 

The mechanisms regarding cobalt-induced polycythemia are not well understood. Cobalt is thought to 

inhibit heme synthesis in vivo by acting upon at least two different sites in the biosynthetic pathway. This 

inhibitory activity might result in the formation of cobalt protoporphyrin rather than heme. Cobalt 

treatment also stimulates heme oxidation in many organs, due to the induction of heme oxygenase. 

Conversely, cobalt acts, through a mechanism believed to involve a heme-containing protein, to increase 

erythropoietin, which stimulates the production of red blood cells. The regulatory mechanisms behind 

this apparent dichotomy have not been fully elucidated. 

Cardiac Effects. Cardiomyopathy has been reported in both humans and animals following exposure 

to cobalt. Occupational exposure of humans to cobalt-containing dust, either as cobalt metal or as hard 

metal, is believed to result in cardiomyopathy characterized by functional effects on the ventricles and 

enlargement of the heart, but the exposure levels associated with cardiac effects of inhaled cobalt in 

humans have not been determined. Rats exposed to 11.4 mg Co/m3

 for 13 weeks developed a mild 

cardiomyopathy; however, rats and mice exposed to 1.14 mg Co/m3

 for 2 years showed no signs of 

cardiomyopathy. 

Beer-cobalt cardiomyopathy was observed in people who heavily consumed beer that contained cobalt 

sulfate as a foam stabilizer. The beer drinkers ingested an average of 0.04 mg Co/kg/day to 0.14 mg 

Co/kg/day for a period of years. The cardiomyopathy was characterized by sinus tachycardia, left 

ventricular failure, cardiogenic shock, diminished myocardial compliance, absence of a myocardial 

response to exercise or catecholamine, enlarged heart, pericardial effusion, and extensive intracellular 

changes (changes in the myofibers, mitochondria, glycogen, and lipids). The beer-cobalt cardiomyopathy 

appeared to be similar to alcoholic cardiomyopathy and beriberi, but the onset of beer-cobalt 

cardiomyopathy was very abrupt. It should be noted, however, that the cardiomyopathy may have also 

been due to the fact that the beer-drinkers had protein-poor diets and may have had prior cardiac damage 

from alcohol abuse. Studies in animals, and limited human data, have supported this possibility, as much 

greater oral exposure levels (on the order of 8-30 mg Co/kg-day) are necessary to induce cardiac effects. 

The mechanism for cobalt-induced cardiomyopathy is not presently understood. Exposure to cobalt may 

result in accumulation in cardiac tissues, and is thought to stimulate carotid-body chemoreceptors, 

mimicking the action of hypoxia. Microscopic analysis of the hearts of those with beer-cobalt 

cardiomyopathy revealed fragmentation and degeneration of myofibers and aggregates of abnormal 

mitochondria. These mitochondrial changes are indicative of disturbances in energy production or 
COBALT 22 

2. RELEVANCE TO PUBLIC HEALTH 

utilization may possibly be related to cobalt effects on lipoic acid. Cobalt irreversibly chelates lipoic 

acids under aerobic conditions. Lipoic acid is a required cofactor for oxidative decarboxylation of 

pyruvate to acetyl CoA and of α-ketoglutarate to succinate. In the myocardium of rats treated with cobalt, 

oxidation of pyruvate or fatty acids is impaired. However, the relative contribution of these mechanisms 

to the cardiac effects of cobalt has not been determined. 

Dermal Effects. Dermatitis is a common result of dermal exposure to cobalt in humans. Using patch 

tests and intradermal injections, it has been demonstrated that the dermatitis is probably caused by an 

allergic reaction to cobalt. Exposure levels associated with the development of dermatitis have not been 

identified. It appears that cobalt metal may be a more potent allergen than some cobalt salts, as Nielsen et 

al. demonstrated that daily repeated exposure to aqueous cobalt salts did not result in hand eczema in 

patients known to have cobalt allergy. In animals, scabs and denuded areas were found after six doses of 

51.75 mg Co/kg (5 days/week) as dicobalt octacarbonyl were applied to the shaved abdomens (uncovered 

area of approximately 50 cm2

) of guinea pigs. By the 11th dose, the lesions disappeared. No adverse 

effects were observed in vehicle controls (methyl ethyl ketone). It is not known whether or not a similar 

reaction would result from metallic or inorganic forms of cobalt. 

Immunological Effects. Exposure of humans to cobalt by the inhalation and dermal routes has 

resulted in sensitization to cobalt. Exposure to inhaled cobalt chloride aerosols can precipitate an 

asthmatic attack in sensitized individuals, believed to be the result of an allergic reaction within the lungs. 

Similarly, the dermatitis seen in dermally-exposed subjects is likely the result of an allergic reaction, with 

cobalt functioning as a hapten. IgE and IgA antibodies specific to cobalt have been reported in humans. 

There is evidence that cobalt sensitivity in humans may also be regulated by T-lymphocytes; a human 

helper T-lymphocyte cell line specific for cobalt (CoCl2) has been established. Cobalt may also interact 

directly with immunologic proteins, such as antibodies or Fc receptors, to result in immunosensitization. 

In vitro, cobalt(III) has been shown to reduce the proliferation of both B and T lymphocytes, as well as 

the release of the cytokines IL-2, IL-6, and IFN-Gamma. Interrelationships exist between nickel and 

cobalt sensitization, with cross-reactivity between the two having been reported in several studies. 

Radioactive Cobalt. Exposure to radioisotopes of cobalt is also a human health concern. Energy released 

by radioactive isotopes can result in significant damage to living cells. Both 60Co and 57Co emit beta 

particles and gamma rays, which may ionize molecules within cells penetrated by these emissions and 

result in tissue damage and disruption of cellular function. The most important exposure route for 
 

COBALT 23 

2. RELEVANCE TO PUBLIC HEALTH 

radioisotopes of cobalt is external exposure to the radiation released by the radioisotopes. It should be 

noted that there is nothing unique about the effects of external exposure to 60Co and 57Co when compared 

to other gamma- and beta-emitting radionuclides. 

Generally, acute radiation doses below 15 rad (0.15 Gy) do not result in observable adverse health effects. 

At doses in the range of 15–50 rad (0.15–0.5 Gy), subclinical responses such as chromosomal breaks and 

transient changes in formed elements of the blood may be seen in sensitive individuals. Symptoms of 

acute radiation syndrome begin to be observed at radiation doses above 50 rad, characterized by transient 

hematopoietic manifestations, nausea and vomiting, and moderate leukopenia at doses near 100 rad 

(1 Gy), progressing through more serious hematopoietic symptoms, clinical signs, and gastrointestinal 

symptoms with increasing dose (100–800 rad or 1–8 Gy), and usually death in persons receiving total 

doses ≥1,000 rad (10 Gy). Other health effects from acute or continued high-level exposure to ionizing 

radiation may include reproductive, developmental, and latent cancer effects. 

Signs and symptoms of acute toxicity from external and internal exposure to high levels of radiation from 

60Co and 57Co are typical of those observed in cases of high exposure to ionizing radiation in general. 

Depending on the radiation dose, symptoms may include those typical of acute radiation syndrome 

(vomiting, nausea, and diarrhea), skin and ocular lesions, neurological signs, chromosomal abnormalities, 

compromised immune function, and death. 

Acute or repeated exposure of humans or animals to ionizing radiation (from radioisotopes of cobalt or 

other radioactive elements) may result in reduced male fertility, abnormal neurological development 

following exposure during critical stages of fetal development, and genotoxic effects such as increased 

frequencies of chromosomal aberrations, sister-chromatid exchanges, and micronucleus formation. 

Due to the ionizing properties of radionuclides such as 60Co and 57Co, increased cancer risk would be 

expected among exposed individuals. However, studies of increased cancer risk specifically associated 

with exposure of humans to radioactive cobalt isotopes were not located. Similarly, studies of the 

carcinogenic effects of radioactive cobalt isotopes in animals were not located. 
COBALT 24 

2. RELEVANCE TO PUBLIC HEALTH 

2.3 MINIMAL RISK LEVELS (MRLs) 

Inhalation MRLs 

•	 An MRL of 0.0001 mg cobalt/m3

 has been derived for chronic-duration inhalation exposure 

(>365 days) to cobalt. 

An MRL for inhalation exposure to cobalt was derived for chronic duration only. The chronic inhalation 

MRL of 0.0001 mg cobalt/m3

 was based on a no-observed-adverse-effect-level (NOAEL) of 0.0053 mg 

cobalt/m3

 and a LOAEL of 0.0151 mg cobalt/m3 (both NOAEL and LOAEL values were adjusted for 

continuous exposure prior to MRL derivation) for decreases in forced vital capacity (FVC), forced 

expiratory volume in one second (FEV1), forced expiratory flow between 25 and 75% of the FVC 

(MMEF), and mean peak expiratory flow rate (PEF) in diamond polishers (Nemery et al. 1992); a further 

discussion of the results and limitations of this study is presented in Appendix A. 

The National Toxicology Program (NTP) has conducted a chronic-duration carcinogenicity study in rats 

and mice. Exposure of rats and mice to aerosols of cobalt (as cobalt sulfate) at concentrations ranging 

from 0.11 to 1.14 mg cobalt/m3

 for 2 years resulted in a spectrum of inflammatory, fibrotic, and 

proliferative lesions in the respiratory tract of male and female rats and mice (NTP 1998). Squamous 

metaplasia of the larynx occurred in rats and mice at exposure concentrations of 0.11 mg cobalt/m3

, with 

severity of the lesion increasing with increased exposure concentration. Hyperplastic lesions of the nasal 

epithelium occurred in rats at concentrations of 0.11 mg cobalt/m3

, and in mice at concentrations of 

0.38 mg cobalt/m3

. Both sexes of rats had greatly increased incidences (>90% incidence) of alveolar 

lesions at all exposure levels, including inflammatory changes, fibrosis, and metaplasia. Similar changes 

were seen in mice at all exposure levels, though the changes in mice were less severe. The study in 

diamond polishers, being a well-conducted study in humans, was selected as the critical study for the 

derivation of a MRL because it examined a human population and identified a NOAEL, neither of which 

occurred in the NTP study. The chronic inhalation MRL was derived by adjusting the NOAEL of 

0.0053 mg Co/m3

 for intermittent exposure (adjusted to 0.0013 mg/m3 to simulate continuous exposure), 

and applying an uncertainty factor of 10 (for human variability). It should be noted that this MRL may 

not be protective for individuals already sensitive to cobalt. 

An acute inhalation MRL was not derived because the threshold was not defined for human effects and 

animal studies reported effects that were serious and occurred at levels above those reported in the few 
COBALT 25 

2. RELEVANCE TO PUBLIC HEALTH 

human studies. An acute-duration study of hard metal exposure in humans (Kusaka et al. 1986b) was not 

utilized for MRL derivation because the toxicity of hard metal is not directly due to cobalt metal, but 

rather to an interaction between cobalt metal and tungsten carbide. An intermediate-duration MRL was 

not derived because available studies did not examine the dose-response relationship at low doses; the 

chronic inhalation MRL should be protective for intermediate exposures (see Appendix A). 

Oral MRLs 

•	 An MRL of 0.01 mg Co/kg-day has been derived for intermediate-duration oral exposure 

(<365 days) to cobalt. 

An intermediate-duration MRL of 0.01 mg Co/kg/day was derived based on a LOAEL of 1 mg cobalt/kgday for polycythemia as reported in a study by Davis and Fields (1958). The authors exposed six men to 

120 or 150 mg/day of cobalt chloride (~1 mg Co/kg/day) for up to 22 days. Exposure to cobalt resulted in 

the development of polycythemia in all six patients, with increases in red blood cell numbers ranging 

from 0.5 to 1.19 million (~16–20% increase above pre-treatment levels). Polycythemic erythrocyte 

counts returned to normal 9–15 days after cessation of cobalt administration. An 8–week study in rats 

(Stanley et al. 1947) also reported increases in erythrocyte number, with a no-observed-effect-level 

(NOEL) of 0.6 mg/kg-day and a lowest-observed-effect-level (LOEL) of 1 mg/kg/day. The intermediate 

oral MRL was derived by dividing the LOAEL of 1 mg Co/kg-day by an uncertainty factor of 100 (10 for 

use of a LOAEL and 10 for human variability). 

Oral MRL values were not derived for acute or chronic exposure to cobalt. An acute MRL was not 

derived because the reported effects in animals were serious and occurred at levels above those reported 

in the few human oral studies. No chronic oral studies were available in animals; the chronic studies of 

beer-cobalt cardiomyopathy (Alexander 1969, 1972; Bonenfant et al. 1969; Morin et al. 1967, 1971; 

Sullivan et al. 1969) were not used because the effects were serious (death) and because the effects of 

concurrent alcoholism were not controlled for. Therefore, a chronic oral MRL was not derived for cobalt. 

MRLs for External Exposure to Cobalt Isotopes 

Two MRLs have been derived for ionizing radiation (Agency for Toxic Substances and Disease Registry 

1999) and are applicable to external exposure to radioisotopes of cobalt: 
C 

COBALT 26 

2. RELEVANCE TO PUBLIC HEALTH 

An MRL of 400 mrem (4.0 mSv) has been derived for acute-duration external exposure to 

ionizing radiation (14 days or less). 

The acute MRL is based on results of a study by Schull et al. (1988) in which neurological effects of 

radiation, measured by intelligence test scores, were evaluated in children 10–11 years of age who had 

been exposed at critical stages of fetal development (gestation weeks 8–15) during the atomic bombing of 

Hiroshima and Nagasaki. When IQ scores were regressed on radiation dose estimates, IQ diminished 

linearly with increasing dose, resulting in an estimated decrease in IQ score of approximately 25 points 

per 100 rad (or 100 rem in dose equivalent) or 0.25 points/rem (25 points/Sv). To derive the MRL of 

400 mrem (4.0 mSv), Agency for Toxic Substances and Disease Registry (1999) divided the dose 

associated with a predicted change of 0.25 IQ points/rem by an uncertainty factor of 3 (for human 

variability and/or the potential existence of sensitive populations). Agency for Toxic Substances and 

Disease Registry (1999) noted that a change in IQ points of 0.25 is less than the reported difference of 

0.3 IQ points between separated and unseparated identical twins (Burt 1966). 

The USNRC set a radiation exposure limit of 500 mrem (5 mSv) for pregnant working women over the 

full gestational period (USNRC 1991). For the critical gestational period of 8–15 weeks, Agency for 

Toxic Substances and Disease Registry believes that the acute MRL of 400 mrem (4 mSv) is consistent 

with the USNRC limit and could be applied to either acute (0–14-day) or intermediate (15–365-day) 

exposure periods. 

C An MRL of 100 mrem/year (1.0 mSv/year) above background has been derived for chronicduration external ionizing radiation (365 days or more). 

The MRL is based on the BEIR V (1990) report that the average annual effective dose of ionizing 

radiation to the U.S. population is 360 mrem/year (3.6 mSv/year), a dose not expected to produce adverse 

noncancerous health effects. This dose is obtained mainly by naturally-occurring radiation from external 

sources, medical uses of radiation, and radiation from consumer products. An uncertainty factor of 3 (for 

human variability) was applied to the NOAEL of 360 mrem/year to derive the MRL of 100 mrem/year. 
COBALT 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 cobalt. 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. 

Section 3.2 contains a discussion of the chemical toxicity of stable cobalt; radiation toxicity associated 

with exposure to radioactive cobalt (primarily 60Co) is discussed in Section 3.3. The chemical properties 

of stable and radioactive cobalt isotopes are identical and are described in Chapter 4. 

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

3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 

Section 3.2 discusses the chemical toxicity of stable cobalt. Radiation toxicity resulting from exposure to 

radioactive cobalt 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, 
COBALT 28 

3. HEALTH EFFECTS 

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 

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. 

Estimates of exposure levels posing minimal risk to humans (Minimal Risk Levels or MRLs) have been 

made for cobalt. 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 
 

COBALT 29 

3. HEALTH EFFECTS 

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. 

Studies have shown that soluble cobalt compounds are generally more acutely toxic than insoluble cobalt 

compounds. When expressed in terms of the cobalt ion for the sake of comparison, however, the 

differences in lethality values from the available studies are within an order of magnitude and therefore do 

not warrant presentation in separate LSE tables and figures. Therefore, data regarding both soluble and 

insoluble cobalt compounds are presented in Tables 3-1, 3-2, and 3-3. 

3.2.1 Inhalation Exposure 

3.2.1.1 Death 

Conclusive evidence for human deaths related to inhalation exposure to cobalt has not been reported; 

however, results of several studies and case reports suggest a possible relationship between exposure and 

deaths from lung cancer and cardiomyopathy, respectively. 

In general, available cohort studies in humans have not reported a significant increase in total mortality as 

a result of cobalt exposure. Several studies have noted increased mortality rates resulting from lung 

cancer following occupational exposure to cobalt, either as a mixture of cobalt compounds (Mur et al. 

1987) or as hard metal, a metal alloy with a tungsten carbide and cobalt matrix (Lasfargues et al. 1994; 

Moulin et al. 1998). Fatal cases of hard metal disease (Figueroa et al. 1992; Ruokonen et al. 1996) and 

cardiomyopathy (Barborik and Dusek 1972) believed to have resulted from occupational cobalt exposure 

have also been reported. However, in the majority of these and other reported occupational studies, coexposure to other substances was common, and was unable to be corrected for in the analysis. 

Cobalt inhalation can be lethal in animals if exposure is sufficiently high or prolonged. The acute 

LC50 for a 30-minute inhalation exposure in rats was 165 mg cobalt/m3

 as cobalt hydrocarbonyl (Palmes 

et al. 1959). Exposure to 9 mg cobalt/m3

 as cobalt hydrocarbonyl for 6 hours/day, 5 days/week for 
 

 

COBALT 30 

3. HEALTH EFFECTS 

3 months resulted in 16 deaths out of 75 rats (Palmes et al. 1959). Death was reported in rats and mice 

exposed to 19 mg cobalt/m3

 (but not 1.9 mg cobalt/m3) as cobalt sulfate over 16 days, but exposure to 

11.4 mg cobalt/m3

 over 13 weeks was lethal only to mice and not to rats (Bucher et al. 1990; NTP 1991). 

Exposure to 1.14 mg cobalt/m3

 as cobalt sulfate for 104 weeks resulted in no increase in mortality in rats 

and mice of either sex (Bucher et al. 1999; NTP 1998). Lethal levels for each species and duration 

category are recorded in Table 3-1 and plotted in Figure 3-1. 

3.2.1.2 Systemic Effects 

No data were located regarding dermal effects in humans or animals after inhalation exposure to stable 

cobalt. Inhalation of stable cobalt by humans and/or animals resulted in respiratory, cardiovascular, 

hematological, hepatic, renal, endocrine, ocular, and body weight effects. For each effect, the highest 

NOAEL values and all reliable LOAEL values for each species and duration category are reported in 

Table 3-1 and plotted in Figure 3-1. 

Respiratory Effects. Hard metal is a metal alloy with a tungsten carbide and cobalt matrix. It is used to 

make cutting tools because of its hardness and resistance to high temperature. Studies (Davison et al. 

1983; Harding 1950) suggest that cobalt (and not tungsten carbide) is the probable causative agent for the 

respiratory effects observed in hard metal workers (see Section 3.6). 

The effects of chronic occupational exposure to cobalt and cobalt compounds on the respiratory system in 

humans are well-documented. These effects include respiratory irritation, diminished pulmonary 

function, wheezing, asthma, pneumonia, and fibrosis and occurred at exposure levels ranging from 

0.007 to 0.893 mg cobalt/m3

 (exposure from 2 to 17 years) (Anttila et al. 1986; Davison et al. 1983; 

Demedts et al. 1984a, 1984b; Deng et al. 1991; Gennart and Lauwerys 1990; Gheysens et al. 1985; 

Hahtola et al. 2000; Hartung et al. 1982; Kusaka et al. 1986a, 1986b, 1996a, 1996b; Nemery et al. 1992; 

Raffn et al. 1988; Rastogi et al. 1991; Ruokonen et al. 1996; Shirakawa et al. 1988, 1989; Sprince et al. 

1988; Sundaram et al. 2001; Swennen et al. 1993; Tabatowski et al. 1988; Van Cutsem et al. 1987; 

Zanelli et al. 1994). These effects have been observed in workers employed in cobalt refineries, as well 

as hard metal workers, diamond polishers, and ceramic dish painters (painting with cobalt blue dye). 
Table 3-1 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation 

a

Key to Species 

figure (Strain) 

Exposure/ 

Duration/

Frequency 

(Specific Route) System 

NOAEL 

(mg/m3) 

LOAEL 

Less Serious 

(mg/m3) 

Serious 

(mg/m3) 

1 2 

3 4 

5 

ACUTE EXPOSURE Systemic 

Human 6 hr 

1

Rat 5 hr SD-Jcl 

2

Rat 4 d SD-Jcl 

3

Rat 30 min 

4

INTERMEDIATE EXPOSURE Death 

Rat 16 d 5 d/wk 6 hr/d 

6

Resp Resp 

Resp Resp 

2.72

7 

1.9 

2.7271.9

0.038 (bronchial irritation, reduced 

FVC) 

0.038

2.12 M (Slight damage to respiratory 

tissues, assessed by electron microscopy) 

2.12

26 (edema) 

26

83 

19 

(severe edema) 

83

(2/5 males died) 

19
Table 3-1 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation (continued) 

a

Key to Species 

figure (Strain) 

Exposure/ 

Duration/

Frequency 

(Specific Route) System 

NOAEL 

(mg/m3) 

LOAEL

Less Serious 

(mg/m3)

Serious 

(mg/m3) 

6 

7 

8 

Mouse 

7

Systemic 

Rat 

14

Rat 

15

13 wk 5 d/wk 6 hr/d

13 wk 5 d/wk 6 hr/d 

3 mo 5 d/wk 7 h/d 

Resp 

Cardio 

HematoRenal Bd Wt Resp Hemato Bd Wt 

3.8

11.4 

9 

3.811.49

0.11 (laryngial squamous metaplasia 

and polyps) 

0.11

11.4 (increase in severity of

cardiomyopathy)

11.4

b

1.14 M (polycythemia) 

1.14

11.4 (15% lower body weight in

males)

11.4

9 (lung inflamm) 

9

b

9 (10% increase in hemoglobin) 

9

11.4 

0.38 

(2 males died) 

11.4

(chronic inflammation of larynx) 

0.38
Table 3-1 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation (continued) 

a

Key to 

figure 

Species 

(Strain) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(mg/m3) 

LOAEL 

Less Serious

(mg/m3) 

Serious 

(mg/m3) 

9 Mouse 

16

16d 5 d/wk 6 hr/d 

Resp 

Cardio Gastro Musc/skel Hepatic Renal Dermal 

0.2 

76 76 76 76 76 

0.27676767676

1.9 (respiratory tract inflammation) 

1.9

19 19 

(necrosis) 

19

(necrosis) 

19
Table 3-1 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation (continued) 

a

Key to 

figure 

Species 

(Strain) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(mg/m3) 

LOAEL 

Less Serious

(mg/m3) 

Serious 

(mg/m3) 

10 

11 

Mouse 

17

Gn Pig (Hartley) 

18

13 wk 5 d/wk 6 hr/d 66 d 

Resp 

Gastro Hemato Musc/skel Hepatic Renal Dermal Bd Wt 

Resp 

11.4 11.4 11.4 11.4 11.4 11.4 

11.411.411.411.411.411.4

0.11 

11.4 

(larynx metaplasia) 

0.11

(13-20% decrease in body 

weight) 

11.4

3.8 M (acute inflam of nose) 

3.8

c

1.14 F (acute inflam of nose) 

1.14

2.4 F (Increased lung weight, 

increased retention of lavage fluid) 

2.4
Table 3-1 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation (continued) 

a

Key to Species 

figure (Strain) 

Exposure/ 

Duration/

Frequency 

(Specific Route) System 

NOAEL 

(mg/m3) 

LOAEL 

Less Serious 

(mg/m3) 

Serious 

(mg/m3) 

12 

13 14 

15 16 

Gn Pig 

19

Dog 

384

Rabbit 

24

Rabbit 

25

Rabbit 

26

3 mo 5 d/wk 7 h/d 

3 mo 3d/wk 7h/d 4 mo 5 d/wk 6 h/d 

4 mo 

4 mo 

Hemato 

Hemato Bd Wt Resp 

Resp 

Resp 

9 

0.5 M 

90.5

b

9 (5% increase in hemoglobin) 

9

9 (wt loss) 

9

0.4 (moderate lung inflammation) 

0.4

0.6 M (Histologic alterations in 

pulmonary tissue; altered BAL parameters) 

0.6

2 (severe lung inflammation) 

2
Table 3-1 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation (continued) 

a

Key to Species 

figure (Strain) 

Exposure/ 

Duration/

Frequency 

(Specific Route) System 

NOAEL 

(mg/m3) 

LOAEL

Less Serious 

(mg/m3)

Serious 

(mg/m3) 

17 

18 

19 

20 

21 

Pig 3 mo 5d/wk 6hr/d 

389

Immuno/ Lymphoret 

Rat 16 d 5 d/wk 6 hr/d 

392

Mouse 13 wk 5 d/wk 6 hr/d

393

Neurological 

Rat 16 d 5 d/wk 6 hr/d 

395

Mouse 16 d 5 d/wk 6 hr/d 

398

Resp CardioHepatic Renal Bd Wt

1 1 

11

0.1 0.1 0.1 

19 

11.4

19 

19 

(decr compliance) 

0.1

(EKG changes) 

0.1

(decr wt gain) 

0.1

(necrosis of thymus) 

19

(lymph node hyperplasia) 

11.4

(congestion of vessels in brain) 

19

(congestion of vessels in brain) 

19
Table 3-1 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation (continued) 

Exposure/ LOAEL

Duration/ a Frequency 

Key to Species NOAEL Less Serious Serious (Specific Route) figure (Strain) System (mg/m3) (mg/m3) (mg/m3) 

Reproductive 

22 Rat 16 d 5 d/wk 6 hr/d 

19 M (testes atrophy) 

19 

399

23 Mouse 13 wk 5 d/wk 6 hr/d 

1.14 M (decreased sperm motility) 11.4 (testes atrophy- increased 

1.14 length estrous cycle) 

11.4

401

CHRONIC EXPOSURE Systemic 

24 Human occup 

Resp 0.0175 (occup) 

0.0175

31

25 Human occup 

Resp 0.1355 (Decreased FEV1 and FVC (occup) ~10%; increased cough, 

sputum, dyspnea) 

0.1355

33

26 Human occup d 

Resp 0.0053 0.0151 (Decreased FEV1, FVC (occup) 

0.0053 increased cough and upper 

airway irritation) 

0.0151

37

27 Human occup 

Endocr 0.05 F (Decreased thyroid volume; (occup) 

increases in T4 and FT4I levels) 

0.05

39
Table 3-1 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation (continued) 

a

Key to Species 

figure (Strain) 

Exposure/ 

Duration/

Frequency 

(Specific Route) System 

NOAEL 

(mg/m3) 

LOAEL

Less Serious 

(mg/m3)

Serious 

(mg/m3) 

28 

29 

30 

31 32 

Human 

418

Human 

420

Human 

41

Rat (Fischer- 344) 

43

Mouse (B6C3F1)

44

occup

occup

8 yr (occup)

104 wk104 wk 

Resp 

Resp 

Resp 

Hemato Endocr Dermal Resp Resp 

0.125 

0.1250.1250.125

0.11 

(Dyspnoea and wheezing)

0.125

(Decreased red cell counts~5%; decreased totalhemoglobin ~4%)

0.125

(Slight (~7%) decrease in T3 levels) 

0.125

(Eczema and erythema) 

0.125

(Laryngial metaplasia)

0.11

0.007 

0.051 

0.11 

(asthma) 

0.007

(interst lung dis) 

0.051

(Hyper- and metaplasia of

respiratory tract tissues; pulmonary fibrosis) 

0.11
Table 3-1 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation (continued) 

a

Key to Species 

figure (Strain) 

Exposure/ 

Duration/

Frequency 

(Specific Route) System 

NOAEL 

(mg/m3) 

LOAEL

Less Serious 

(mg/m3)

Serious 

(mg/m3) 

33 

34 

35 

36 

Hamster life 5d/wk 7h/d

424

Immuno/ Lymphoret 

Human occup 

425

Human 8 yr

(occup)

46

Cancer 

Rat 104 wk (Fischer- 344) 

53

Resp 

Bd Wt 7.9 

7.9

0.007

0.125 

(sensitization) 

0.007

(Increased white cell count by19%) 

0.125

7.9 (emphysema) 

7.9

1.14 M (alveoloar/bronchiolar

neoplasms) 

1.14

1.14 F (pheochromocytoma) 

1.14

0.38 F (alveoloar/bronchiolar 

neoplasms) 

0.38
Table 3-1 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation (continued) 

a

Key to Species 

figure (Strain) 

Exposure/ 

Duration/

Frequency 

(Specific Route) System 

NOAEL 

(mg/m3) 

LOAEL

Less Serious 

(mg/m3) 

Serious 

(mg/m3) 

37 Mouse 

(B6C3F1) 

54

104 wk 

1.14 M (Combined alveolar/bronchiolar

adenoma/carcinoma) 

1.14

0.38 F (Combined alveolar/bronchiolar 

adenoma/carcinoma) 

0.38

a The number corresponds to entries in Figure 3-1.b An increase in hemoglobin or red blood cells (polycythemia) is not necessarily considered an adverse effect.c Differences in levels of health effects and cancer effect between males and females are not indicated in Figure 3-1. Where such differences exist, only the le

most sensitive gender are presented. 

d Used to derive a chronic inhalation Minimal Risk level (MRL) of 0.0001 mg Co/m3., dose adjusted for intermittent exposure, and divided by an uncertainty fa

variability). 

Bd = body weight; Cardio = cardiovascular, d = day(s); Derm = dermal; Endocr = endocrine; F = female; Gastro = gastrointestinal; Gn Pig = guinea pig; Hemathour(s); LOAEL = lowest-observed-adverse-effect level; M = male; mo = month(s); Musc/skel = muscular/skeletal; NOAEL = no-observed-adverse-effect leveloccupational; Resp = respiratory; wk = week(s); yr = year(s). 
100 

Respiratory 

Figure 3-1. Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation 

Acute (≤14 days) 

Systemic 

mg/m3 

4r 4r 

10 

4r 2r3r

1 

0.1 

1 

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 
Death Respiratory Cardiovascular Gastrointestinal Hematological Musculoskeletal Hepatic Renal Dermal 

100 

Figure 3-1. Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation (Continu

Intermediate (15-364 days) 

Systemic 

mg/m3 

9m 9m 9m 9m 9m 

5r 9m 9m 6m 7r 10m 10m 10m 10m 10m 7r 10m 

10 8r 13d 12g 8r 

6m 

11g 

14h 5r 9m 

10m 7r 

1 17p 17p 

16h15h14h 7r 

9m 10m 7r 0.1 17p 17p 

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 
Neurological 

100 

Immuno/Lymphor Reproductive 

Figure 3-1. Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation (Continue

Intermediate (15-364 days) 

mg/m3 

18r 21m 20r 22r 19m 23m 

10 

23m 

1 

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 Endocrine Dermal Body W Immuno/L Cancer * 

10 

Respiratory eight ymphor 

Figure 3-1. Levels of Significant Exposure to Cobalt - Chemical Toxicity - Inhalation (C

Chronic (≥365 days) 

Systemic 

mg/m3 

33s 33s 

37m 36r 36r 1

37m 36r 

25 30 30 30 30 35 32m 31r 0.1 

29 27

24 26

0.01 

28 34

26

0.001 

*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. 

0.0001 

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 
COBALT 45 

3. HEALTH EFFECTS 

Kusaka et al. (1986b) described an acute exposure of 15 healthy young men to atmospheres of hard metal 

dust containing 0.038 mg cobalt/m3

 for 6 hours. Forced vital capacity (FVC) was reduced, but no doseresponse relation could be discerned. By contrast, 42 workers occupationally exposed to hard metal 

showed no decrease in ventilatory function at 0.085 mg cobalt/m3

, but significant changes in FEV1 

(forced expiratory volume in 1 second) at 0.126 mg cobalt/m3

 (Kusaka et al. 1986b). Several other 

studies of hard metal workers have shown respiratory effects, including decreased ventilatory function, 

wheezing, asthma, and fibrosis (Kusaka et al. 1996a, 1996b; Ruokonen et al. 1996; Zanelli et al. 1994), 

but have had less complete reports of exposure. 

Swennen et al. (1993) performed a cross-sectional study on 82 workers in a cobalt refinery. Workers 

were examined for cobalt in blood and urine, a number of erythropoietic variables, thyroid metabolism, 

pulmonary function, skin lesions, and several serum enzymes. The concentrations of cobalt in blood and 

in urine after the shift were significantly correlated with those in air. Workers exposed to airborne cobalt 

metal, salts, or oxides (mean concentration 0.125 mg/m3

, range 0.001–7.7 mg/m3) showed an increased 

(p<0.05) prevalence of dyspnea and wheezing and had significantly more skin lesions (eczema, erythema) 

than control workers. A dose-effect relation was found between the reduction of the FEV1 and the 

intensity of the current exposure to cobalt, as assessed by measurement of cobalt in blood, air, or urine. 

Gennart and Lauwerys (1990) examined the ventilatory functions of 48 diamond polishing workers, 

relative to 23 control workers. Exposure occurred mainly in one of two rooms, with mean airborne 

concentrations of 0.0152 and 0.1355 mg cobalt/m3

; control subjects worked in other areas of the facilities, 

where no exposure to cobalt occurred. Significant decreases in ventilatory function were found in the 

exposed workers relative to the control workers. Duration of exposure played a significant factor, with no 

significant differences in workers who had been exposed for ≤5 years; reported decreases in ventilatory 

function were noted in workers exposed for > 5 years. Inhalation exposure to cobalt salts (exposure 

levels not reported) among glass bangle workers resulted in decreases in decreased ventilatory function, 

generally restrictive in nature, relative to controls (Rastogi et al. 1991). 

Nemery et al. (1992) conducted a cross-sectional study of cobalt exposure and respiratory effects in 

diamond polishers. Exposure occurred mainly from the generation of airborne cobalt resulting from the 

use of cobalt-containing polishing discs. The study groups were composed of 194 polishers working in 

10 different workshops, and were divided into control, low-, and high-exposure groups. The lowexposure group (n=102) was exposed to an average of 0.0053 mg cobalt/m3

, based on personal sampling 
COBALT 46 

3. HEALTH EFFECTS 

measurements, while the exposure level for the high dose group (n=92) was 0.0151 mg cobalt/m3; there 

was considerable overlap in the total range of concentrations for the low- and high-exposure groups. 

Workers in the high-exposure group were more likely than those in the other groups to complain about 

respiratory symptoms; the prevalence of eye, nose, and throat irritation and cough, as well as the fraction 

of these symptoms related to work, were significantly increased in the high-exposure group. Workers in 

the high-exposure group also had significantly reduced lung function compared to controls and lowexposure group workers, as assessed by FVC, FEV1, MMEF (forced expiratory flow between 25 and 75% 

of the FVC) and mean PEF (peak expiratory flow rate). Results in the low-exposure group did not differ 

from controls. Based on the NOAEL of 0.0053 mg cobalt/m3

 for decreased ventilatory function in 

exposed workers, a chronic inhalation MRL of 1x10-4 mg cobalt/m3

 was calculated as described in 

footnote (d) in Table 3-1. It should be noted that this MRL value may not be protective for some 

hypersensitive individuals. 

As with exposures in humans, exposures of animals to cobalt-containing aerosols have resulted in 

pronounced respiratory effects. Animals exposed to aerosols of cobalt oxides and cobalt sulfate 

developed respiratory effects that varied in severity with exposure level and duration. A single 30-minute 

exposure of rats to relatively high levels (26–236 mg cobalt/m3

 as cobalt hydrocarbonyl) resulted in 

congestion, edema, and hemorrhage of the lung (Palmes et al. 1959). Prolonged exposure (3–4 months) 

of rats and rabbits to mixed cobalt oxides (0.4–9 mg cobalt/m3

) resulted in lesions in the alveolar region 

of the respiratory tract characterized histologically by nodular accumulation of Type II epithelial cells, 

accumulations of enlarged highly vacuolated macrophages, interstitial inflammation, and fibrosis 

(Johansson et al. 1984, 1987, 1991, 1992; Kyono et al. 1992; Palmes et al. 1959). In at least one instance, 

the lesions appeared to regress when exposure was terminated (Palmes et al. 1959). Guinea pigs 

sensitized to cobalt by repeated dermal application and then exposed to 2.4 mg cobalt/m3

 as cobalt 

chloride showed pulmonary inflammatory changes (altered BAL fluid recovery, increased neutrophils and 

eosinophils in the recovered BAL fluid) that were different than those in exposed animals not sensitized 

to cobalt (Camner et al. 1993). Decreased lung compliance was found in pigs exposed to 0.1 mg 

cobalt/m3

 as cobalt dust for 3 months (Kerfoot 1975). Lifetime exposure of hamsters to 7.9 mg 

cobalt/m3

 as cobalt oxide resulted in emphysema (Wehner et al. 1977). 

Necrosis and inflammation of the respiratory tract epithelium (nasal turbinates, larynx, trachea, 

bronchioles) were reported in rats exposed to 19 mg cobalt/m3

 and mice exposed to 1.9 mg cobalt/m3 or 

greater as cobalt sulfate over 16 days (Bucher et al. 1990; NTP 1991). Exposure of rats and mice to 
 

COBALT 47 

3. HEALTH EFFECTS 

cobalt as cobalt sulfate for 13 weeks resulted in adverse effects on all parts of the respiratory tract, with 

the larynx being the most sensitive part (Bucher et al. 1990; NTP 1991). At concentrations of ≥0.11 mg 

cobalt/m3

, rats and mice developed squamous metaplasia of the larynx. Histiocytic infiltrates in the lung 

were also reported at similar levels in both the rats and mice. In rats, chronic inflammation of the larynx 

was found at ≥0.38 mg cobalt/m3

, and more severe effects on the nose, larynx, and lung were reported at 

higher exposures. In mice, acute inflammation of the nose was found at ≥1.14 mg cobalt/m3

, and more 

severe effects on the nose, larynx, and lung were reported at higher exposures. Exposure of rats and mice 

to aerosols of cobalt (as cobalt sulfate) at concentrations from 0.11 to 1.14 mg cobalt/m3

 for 2 years 

resulted in a spectrum of inflammatory, fibrotic, and proliferative lesions in the respiratory tract of male 

and female rats and mice (Bucher et al. 1999; NTP 1998). Squamous metaplasia of the larynx occurred in 

rats and mice at exposure concentrations of ≥0.11 mg cobalt/m3

, with severity of the lesion increasing 

with increased cobalt concentration. Hyperplastic lesions of the nasal epithelium occurred in rats at 

concentrations of ≥0.11 mg cobalt/m3

, and in mice at concentrations of ≥0.38 mg cobalt/m3. Both sexes 

of rats had greatly increased incidences (>90% incidence) of alveolar lesions at all exposure levels, 

including inflammatory changes, fibrosis, and metaplasia. Similar changes were seen in mice at all 

exposure levels, though the changes in mice were less severe. 

Cardiovascular Effects. Occupational exposure of humans to cobalt-containing dust, either as 

cobalt metal or as hard metal, has been shown to result in cardiomyopathy, characterized by functional 

effects on the ventricles (Horowitz et al. 1988) and/or enlargement of the heart (Barborik and Dusek 

1972; Jarvis et al. 1992), but the exposure levels associated with cardiac effects of inhaled cobalt in 

humans have not been determined. Jarvis et al. (1992) reported on two patients (exposure histories not 

specified) who had been admitted to the emergency room for cardiac failures; these failures were believed 

to be associated with cobalt exposure. Barborik and Dusek (1972) reported a case of a 41-year-old man 

who was admitted to the hospital with cardiac failure following occupational exposure to cobalt; cobalt 

concentrations in heart, liver, lung, spleen, and kidney were elevated over two control patients. Horowitz 

et al. (1988) reported that in a cohort of 30 hard metal workers (exposure histories not specified), 

significant decreases in exercise right ventricular ejection fraction (EF) were seen in workers with 

abnormal chest x-rays relative to those with normal chest x-rays. It is possible that these effects were 

secondary to the respiratory effects of inhaled cobalt. It was concluded that cobalt is a weak 

cardiomyopathic agent following occupational exposure (Horowitz et al. 1988). Cardiomyopathy is a 

characteristic toxic effect of cobalt following oral exposure in both humans and animals (Section 3.2.2.2). 
COBALT 48 

3. HEALTH EFFECTS 

In rats, exposure to 11.4 mg cobalt/m3 as cobalt sulfate over 13 weeks resulted in a marginal increase in 

the severity of cardiomyopathy as compared to controls (minimal-mild in treated animals versus minimal 

in controls; 3/10 animals affected in either group) (Bucher et al. 1990; NTP 1991). Cardiomyopathy was 

not observed in mice exposed to ≤76 mg cobalt/m3

 as cobalt sulfate over 16 days (Bucher et al. 1990; 

NTP 1991), nor in mice or rats exposed to up to 1.14 mg cobalt/m3

 for 2 years (Bucher et al. 1999; NTP 

1998). Electrocardiogram abnormalities that may reflect ventricular impairment have been observed in 

miniature swine (n=5) exposed to 0.1 mg cobalt dust/m3

 for 6 hours/day, 5 days/week for 3 months 

(Kerfoot 1975). 

Gastrointestinal Effects. No studies were located regarding gastrointestinal effects in humans after 

inhalation exposure to stable cobalt. 

No histological lesions were reported in the esophagus, stomach, duodenum, ileum, jejunum, cecum, 

colon, or rectum of rats or mice of either sex exposed to 76 mg cobalt/m3

 or less as cobalt sulfate for 

16 days, up to 11.4 mg cobalt/m3

 for 13 weeks, or up to 1.14 mg cobalt/m3 for 104 weeks (Bucher et al. 

1990, 1999; NTP 1991, 1998). 

Hematological Effects. Swennen et al. (1993) reported slightly, but statistically significantly, 

decreased levels of red cells and total hemoglobin (~4–5% decreases) in a group of 82 workers 

occupationally exposed to a mean concentration of 0.125 mg cobalt/m3

 as cobalt metal dust. No other 

studies were located regarding hematological effects in humans after inhalation exposure to cobalt. 

Increased levels of hemoglobin and increased numbers of basophils and monocytes have been observed in 

rats and guinea pigs, but not in dogs, exposed to 9 mg cobalt/m3

 as cobalt hydrocarbonyl for 3 months 

(Palmes et al. 1959). Polycythemia was reported in rats, but not mice, exposed to 1.14 mg cobalt/m3

 as 

cobalt sulfate for 13 weeks (Bucher et al. 1990; NTP 1991). 

Musculoskeletal Effects. No studies were located regarding musculoskeletal effects in humans after 

inhalation exposure to cobalt. 

No histological lesions were reported in the sternebrae (segments of the sternum), including the bone 

marrow, of rats or mice exposed to ≤76 mg cobalt/m3

 as cobalt sulfate for 16 days, up to 11.4 mg 
 

COBALT 49 

3. HEALTH EFFECTS 

cobalt/m3 for 13 weeks, or up to 1.14 mg cobalt/m3 for 104 weeks (Bucher et al. 1990, 1999; NTP 1991, 

1998) (see the above section on respiratory effects for detailed descriptions of exposure conditions). 

Hepatic Effects. Congestion of the liver was observed upon autopsy of a metal worker (exposure 

history not reported) who had been occupationally exposed to an unknown level of cobalt for 4 years 

(Barborik and Dusek 1972). The cause of death was determined to be cardiomyopathy. 

Necrosis and congestion of the liver were observed in both rats and mice that died following exposure to 

19 mg cobalt/m3

 as cobalt sulfate over 16 days (Bucher et al. 1990; NTP 1991). No histological effects 

on the liver were found in pigs exposed to up to 1.0 mg cobalt/m3

 as cobalt metal dust for 3 months 

(Kerfoot 1975). 

Renal Effects. Congestion of the kidneys was observed upon autopsy of a metal worker who had 

been occupationally exposed to an unknown level of cobalt for 4 years (Barborik and Dusek 1972). The 

cause of death was determined to be cardiomyopathy. 

A significant increase in the relative weight of the kidneys was reported in male rats exposed to 0.11 mg 

cobalt/m3

 or greater as cobalt sulfate for 13 weeks (Bucher et al. 1990; NTP 1991). No effects were 

observed upon histological examination of the kidneys in rats or mice following exposure to ≤76 mg 

cobalt/m3

 as cobalt sulfate for 16 days, up to 11.4 mg cobalt/m3 for 13 weeks, or up to 1.14 mg cobalt/m3 

for 104 weeks (Bucher et al. 1990, 1999; NTP 1991, 1998). No histological effects on the kidneys were 

found in pigs exposed to up to 1.0 mg cobalt/m3

 as cobalt metal for 3 months (Kerfoot 1975). 

Dermal Effects. No studies were located regarding dermal effects in humans or animals after 

inhalation exposure to stable cobalt. 

Endocrine Effects. A group of female workers occupationally exposed to a semisoluble cobalt glaze 

(cobalt-zinc silicate, estimated concentrations of 0.05 mg Co/m3

) showed significantly elevated levels of 

serum thyroxine (T4) and free thyroxine, but no change in T3 levels (Prescott et al. 1992). In contrast to 

this, Swennen et al. (1993) reported no significant change in serum T4 levels, but a significant reduction 

in serum T3 in workers occupationally exposed to cobalt oxides, cobalt salts, and cobalt metal. 
COBALT 50 

3. HEALTH EFFECTS 

Ocular Effects. Congestion of the conjunctiva was observed in a metal worker after occupational 

exposure to an unknown level of cobalt for 4 years (Barborik and Dusek 1972); however, due to the 

nature of the exposure, this effect may also have been the result of direct dermal or ocular contact. Upon 

autopsy, the cause of death was determined to be cardiomyopathy. 

No histological lesions were reported in the eyes or on the skin of rats or mice exposed to ≤76 mg 

cobalt/m3

 as cobalt sulfate for 16 days, up to 11.4 mg cobalt/m3 for 13 weeks, or up to 1.14 mg cobalt/m3 

for 104 weeks (Bucher et al. 1990, 1999; NTP 1991, 1998). 

Body Weight Effects. Weight loss, measured individually from time of initial examination 

throughout followup, was observed in a group of five diamond polishers suffering from cobalt-induced 

interstitial lung disease (Demedts et al. 1984b), but the exposure level of cobalt was not reported. 

Decreased body weight, relative to controls at study termination, was reported in both rats and mice 

exposed to 19 mg cobalt/m3

 as cobalt sulfate over 16 days or to 11.4 mg cobalt/m3 for 13 weeks (Bucher 

et al. 1990; NTP 1991). A 13-week exposure to 11.4 mg cobalt /m3

 resulted in ruffled fur in male rats, 

with no clinical signs reported in female rats or either sex of mice (Bucher et al. 1990; NTP 1991). 

Chronic exposure of rats and mice to up to 1.14 mg cobalt/m3

 did not result in decreased body weight 

(Bucher et al. 1999; NTP 1998). 

Weight loss was found in dogs, but not rats or guinea pigs, exposed for 3 months to cobalt at a level of 

9 mg cobalt/m3

 as cobalt hydrocarbonyl (Palmes et al. 1959). Lifetime exposure of hamsters to a similar 

concentration (7.9 mg cobalt/m3

 as cobalt oxide) did not result in decreased body weight gain (Wehner et 

al. 1977). 

3.2.1.3 Immunological and Lymphoreticular Effects 

Cobalt is known to function as a hapten, resulting in the generation of antibodies against cobalt-protein 

complexes. Although the minimum exposure level associated with cobalt sensitization has not been 

determined, sensitization has been demonstrated in hard metal workers with work-related asthma who 

have experienced prolonged occupational exposure (>3 years) to levels ranging from 0.007 to 0.893 mg 

cobalt/m3

 (Shirakawa et al. 1988, 1989). The lower end of this range, 0.007 mg/m3, is reported in 
COBALT 51 

3. HEALTH EFFECTS 

Table 3-1 and plotted in Figure 3-1 as a LOAEL. The sensitization phenomenon includes the production 

of IgE and IgA antibodies to cobalt (Bencko et al. 1983; Shirakawa et al. 1988, 1989). Exposure to 

inhaled cobalt chloride aerosols can precipitate an asthmatic attack in sensitized individuals (Shirakawa et 

al. 1989), believed to be the result of an allergic reaction within the lungs. 

Necrosis of the thymus was reported in rats exposed to 19 mg cobalt/m3

 as cobalt sulfate over 16 days, 

and hyperplasia of the mediastinal lymph nodes was found in mice exposed to 11.4 mg cobalt/m3

 for 

13 weeks (Bucher et al. 1990; NTP 1991). Tests of immunological function, however, were not 

performed on the rats or mice. 

3.2.1.4 Neurological Effects 

Occupational exposure to cobalt in humans has been reported to cause several effects on the nervous 

system, including memory loss (Wechsler Memory Scale-Revised), nerve deafness, and a decreased 

visual acuity (Jordan et al. 1990; Meecham and Humphrey 1991). It should be noted, though, that both of 

these studies had small numbers of subjects (n=38 for Jordan et al. 1990, n=1 for Meecham and 

Humphrey 1991), and exposure characterization was not reported. 

Congestion in the vessels of the brain/meninges was reported in rats and mice exposed to 19 mg 

cobalt/m3

 or greater as cobalt sulfate over 16 days (Bucher et al. 1990; NTP 1991). 

3.2.1.5 Reproductive Effects 

No studies were located regarding reproductive effects in humans after inhalation exposure to cobalt. 

In animals, long-term exposure to cobalt-containing aerosols has resulted in effects on reproductive end 

points. Testicular atrophy was reported in rats, but not in mice, exposed to 19 mg cobalt/m3

 as cobalt 

sulfate over 16 days (Bucher et al. 1990; NTP 1991). Following exposure of mice to cobalt (as cobalt 

sulfate) for 13 weeks, a decrease in sperm motility was found at 1.14 mg cobalt/m3

, and testicular atrophy 

was found at 11.4 mg cobalt/m3

. A significant increase in the length of the estrous cycle was reported in 

female mice exposed to 11.4 mg cobalt/m3

 for 13 weeks (Bucher et al. 1990; NTP 1991). No effects on 
COBALT 52 

3. HEALTH EFFECTS 

the male or female reproductive systems were observed in rats similarly treated for 13 weeks (Bucher et 

al. 1990; NTP 1991), or in mice or rats exposed to up to 1.14 mg cobalt/m3

 for 104 weeks (Bucher et al. 

1999; NTP 1998). 

3.2.1.6 Developmental Effects 

No studies were located regarding developmental effects in humans or animals after inhalation exposure 

to cobalt. 

3.2.1.7 Cancer 

Several studies have evaluated the effects of inhalation of cobalt-containing compounds on possible 

carcinogenicity in humans. The mortality of a cohort of 1,143 workers in a plant that refined and 

processed cobalt and sodium was analyzed (Mur et al. 1987); the French national population mortality 

data were used as a reference population. An increase in deaths due to lung cancer was found in workers 

exposed only to cobalt (standardized mortality ratio [SMR] of 4.66; four cases in the exposed group 

versus one case in the controls). In a study within the cohort that controlled for date of birth, age at death, 

and smoking habits, 44% (four workers) in the group exposed to cobalt and 17% (three workers) in the 

group not exposed to cobalt died of lung cancer. The authors, however, indicated that the difference was 

not statistically significant and that the workers were exposed to both arsenic and nickel as well as cobalt. 

The nonneoplastic lung diseases commonly found in cobalt-exposed workers (see Section 3.2.1.2) were 

not reported in this group. These lung diseases may have been present in these workers, but if they were 

not listed as the cause of death on the death certificate, they would not have been mentioned. Inhalation 

was probably a prominent route of exposure to cobalt; however, oral and dermal exposure probably 

occurred as well. No adjustments were made for smoking habits in the larger study, and the exposure 

levels of cobalt were not reported for either study. However, a followup study of this cohort (Moulin et 

al. 1993) did not report significant increases in mortality due to respiratory or circulatory diseases. 

Similarly, no increase in the SMR for lung cancer was noted in exposed workers, relative to controls. 

While an elevated SMR for lung cancer was seen in maintenance workers (SMR=1.80, 95% confidence 

interval [CI]=0.78–3.55), it was not statistically significant, since the 95% confidence interval included an 

SMR of 1. 
COBALT 53 

3. HEALTH EFFECTS 

Lasfargues et al. (1994) reported on the mortality of a cohort of 709 male workers in a French hard metal 

plant, using the national rates for French males for comparison. The overall mortality did not differ from 

expected, but there was a significant increase in mortality due to cancer of the trachea, bronchus, and lung 

(SMR=2.13, 95% CI=1.02–3.93). Smoking alone did not account for the lung cancer excesses, although 

the influence of smoking on the observed mortality could not be entirely ruled out. 

A cohort of 5,777 males and 1,682 females who were exposed occupationally to cobalt (concentrations 

ranging from 1 to 515 μg/m3

, means of exposure levels ranging from 39.37 to 169.0 μg/m3) and tungsten 

carbide (as hard metal dust) was examined by Moulin et al. (1998). A significantly increased mortality 

rate (SMR=1.30, 95% CI=1.00–1.66) was seen for lung cancer in exposed workers, when compared to the 

national average. Within this study group, 61 cases and 180 controls were selected for a case-control 

study of cancer risk. When exposures during the last 10 years were ignored, presumably because cancer 

is a late-developing disease, a significant increase in lung cancer mortality (OR=1.93, 95% CI=1.03–3.62) 

relative to controls was seen among workers simultaneously exposed to cobalt and tungsten carbide. 

Significant trends for increasing cancer risk with increasing cumulative exposure and exposure duration 

were noted. Adjustments for smoking and for coexposures to other carcinogens did not change the 

results, though occupational risk was greatest among smokers. 

A later study by the same group (Moulin et al. 2000) examined the lung cancer mortality of 4,288 male 

and 609 female workers employed in the production of stainless and alloyed steel from 1968 to 1992. No 

significant changes in mortality rate from lung cancer were seen among exposed workers (SMR=1.19, 

95% CI=0.88–1.55), and a concurrent case control study identified no correlation between lung cancer 

excess and for exposure to cobalt (OR=0.64, 95% CI=0.33–1.25). 

Wild et al. (2000) reported on a cohort of 2,216 male hard metal workers who had been employed for at 

least 3 months; this cohort was the same as that in Moulin et al. (2000), with some modifications. The 

total mortality was not increased in workers, relative to local mortality rates. However, lung cancer 

mortality was significantly increased (SMR=1.70, 95% CI=1.24–2.26). The risks increased with 

increasing exposure scores, even after adjustment for smoking and coexposure to other known or 

suspected carcinogens. 
 

COBALT 54 

3. HEALTH EFFECTS 

Inhalation exposure to 7.9 mg cobalt/m3 as cobalt oxide intermittently for a lifetime did not increase the 

incidence of malignant or benign tumors in hamsters (Wehner et al. 1977). 

NTP (1998) exposed groups of rats and mice of both sexes to 0, 0.11, 0.38, or 1.14 mg cobalt/m3

 as cobalt 

sulfate for 2 years. Increased incidence of alveolar/bronchiolar neoplasms was noted following lifetime 

exposure of male rats to 1.14 mg cobalt/m3

 and in female rats exposed to 0.38 mg cobalt/m3 (Bucher et al. 

1999; NTP 1998). Statistical analysis revealed that tumors occurred with significantly positive trends in 

both sexes of rats. Similarly, mice of both sexes exposed to 1.14 mg cobalt/m3

 showed an increase in 

alveolar/bronchiolar neoplasms, again with lung tumors occurring with significantly positive trends. 

3.2.2 Oral Exposure 

3.2.2.1 Death 

In several studies, lethal cardiomyopathy was reported in people who consumed large quantities of beer 

containing cobalt sulfate (Alexander 1969, 1972; Bonenfant et al. 1969; Morin et al. 1967, 1971; Sullivan 

et al. 1969). The deaths occurred during the early to mid 1960s, at which time, breweries in Canada, the 

United States, and Europe were adding cobalt to beer as a foam stabilizer (Alexander 1969, 1972; 

Bonenfant et al. 1969; Morin et al. 1967, 1971; Sullivan et al. 1969); this practice has been discontinued. 

Deaths occurred following ingestion of beer containing 0.04–0.14 mg cobalt/kg/day for a period of years 

(approximately 8–30 pints of beer each day). “Acute mortality” (death within several days of admission) 

accounted for 18% of the deaths (Alexander 1972). Approximately 43% of the patients admitted to the 

hospital with cardiomyopathy died within several years of the initial hospital visit. It should be noted, 

however, that the cardiomyopathy may have also been due to the fact that the beer-drinkers had proteinpoor diets and may have had prior cardiac damage from alcohol abuse. 

Treatment of both pregnant and nonpregnant anemic patients with doses of cobalt (0.6–1 mg/kg/day) that 

were much higher than the doses in the beer did not result in mortality (Davis and Fields 1958; Holly 

1955). A 19-month-old male child who swallowed an unknown amount of a cobalt chloride solution died 

approximately 6.5 hours after ingestion, despite repeated induced vomiting, gastric lavage, and supportive 

therapy (Jacobziner and Raybin 1961). 
 

 

COBALT 55 

3. HEALTH EFFECTS 

Oral LD50 values for several cobalt compounds have been determined in Wistar rats (FDRL 1984a, 

1984b, 1984c; Singh and Junnarkar 1991; Speijers et al. 1982). The LD50 values ranged from 42.4 mg 

cobalt/kg as cobalt chloride to 317 mg cobalt/kg as cobalt carbonate. An LD50 of 3,672 mg cobalt/kg was 

also found for tricobalt tetraoxide, a highly insoluble cobalt compound (FDRL 1984c). The exact cause 

of death in rats is unknown, but effects on the heart, liver, gastrointestinal tract, and kidneys have been 

observed. In Sprague-Dawley rats, death has been reported to occur at 161 mg cobalt/kg given by gavage 

as cobalt chloride (Domingo and Llobet 1984). In male Swiss mice, the LD50 values for cobalt chloride 

and cobalt sulfate have been reported to be 89.3 and 123 mg cobalt/kg, respectively (Singh and Junnarkar 

1991). 

Following 5 weeks of exposure to 20 mg cobalt/kg/day as cobalt sulfate by gavage, 20–25% of the guinea 

pigs died (Mohiuddin et al. 1970). The animals were given cobalt sulfate alone or in combination with 

ethanol (as part of a liquid diet) to compare the effects seen in animals to those seen in humans suffering 

from beer-cobalt cardiomyopathy. Although effects on the heart were found in the treated animals, 

alcohol did not appear to intensify the toxic effect. 

The LD50 and all reliable LOAEL values for each species and duration category are reported in Table 3-2 

and plotted in Figure 3-2. 

3.2.2.2 Systemic Effects 

Oral cobalt exposure in humans and/or animals resulted in respiratory, cardiovascular, gastrointestinal, 

hematological, hepatic, renal, endocrine, dermal, ocular, hypothermic, and body weight effects. For each 

effect, the highest NOAEL values and all reliable LOAEL values for each species and duration category 

are reported in Table 3-2 and plotted in Figure 3-2. 

Respiratory Effects. In 50 patients with beer-cobalt cardiomyopathy, pulmonary rales and 

pulmonary edema were observed and were attributed to cobalt-induced cardiac failure (Morin et al. 1971). 

These patients had ingested, over a period of years, an average of 0.04 mg cobalt/kg/day in beer 

containing cobalt sulfate that was added to stabilize the foam. It should be noted that these patients 

consumed significant quantities of alcohol, and the effect that this may have had on the symptoms seen is 

not known. 
56

161.1

61

42.4

62

194

320

91

321

187

322

109

63

159

Table 3-2 Levels of Significant Exposure to Cobalt - 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 Rat 1x 

161.1 (LD50) (Sprague- (GW) 

Dawley) 

2 Rat 1x 

42.4 (LD50) (Wistar) (GW) 

3 Rat 1x 

194 (LD50) (Wistar) (GW) 

4 Rat 1 x 

91 (LD50) (Wistar) (GO) 

5 Rat 1 x 

187 (LD50) (Wistar) (GO) 

6 Rat 1 x 

109 (LD50) (Wistar) (GW) 

7 Rat 1 x 

159 (LD50) (Wistar) (GO) 
64

168

66

190

67

140

68

161

69

123

70

89.3

73

1

a

Key to 

figure 

Species 

(Strain) 

LOAEL 

NOAEL Less Serious

System 

Table 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral 

(mg/kg/day) (mg/kg/day) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) 

Serious 

(mg/kg/day) 

(continued) 

8 

(Wistar) Rat 1 x 

(GW) 168 (LD50) 

9 

(Wistar) Rat 1 x 

(GW) 190 (LD50) 

10 

(Wistar) Rat 1 x 

(GW) 140 (LD50) 

11 

(Wistar) Rat 1 x 

(GW) 161 (LD50) 

12 

(SwissWebster) Mouse 1x 

(GW) 123 (LD50) 

13 14 

(SwissWebster) Mouse 

Systemic 

Human 

1x (GW) 2 wk (C) 

Endocr 1 (decreased Iodine uptake in 

thyroid) 

89.3 (LD50) 
74

161.1

110

75

209

59

149

78

19.4

109.6

79

176.6

42.6 68.2

42.6

176.6109.6

Table 3-2 Levels of Significant Exposure to Cobalt - 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) 

15 Rat 1x 

(GW) 

Hemato 161.1 

b

(increased hematocrit 8%) 

16 Rat 1 x 

(GW) 

Other 110 209 (Clinical signs, including 

decreased activity, ataxia, diarrhea, salivation) 

17 

(SpragueDawley) Rat 1 x 

(GO) 

Other 149 (Decreased activity, diarrhea) 

18 

(Wistar) Rat 1x 

(GW) 

Renal 19.4 (Increased urinary output) 

19 

(Wistar) Rat 1 x 

(GO) 

Cardio 109.6 176.6 (proliferative interstitial tissues, 

swollen muscle fibers, focal myocardial degeneration) 

Hepatic 42.6 68.2 (hyperemia) 

Renal 42.6 (swollen proximal tubules) 176.6 (degeneration of proximal 

tubules) 

Other 109.6 (hypothermia) 
Table 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral (continued) 

Exposure/ LOAEL 

Duration/ a Frequency NOAEL Less Serious 

Key to Species Serious (Specific Route) figure (Strain) System (mg/kg/day) (mg/kg/day) (mg/kg/day) 

20 Rat 1 x 

Cardio 794.5 (hemorrhage) (Wistar) (GO) 794.5 

80

Hepatic 157.3 (hyperemia) 

157.3

Renal 157.3 (hyperemia) 

157.3

Other 157.3 (hypothermia) 

157.3

21 Mouse 48 hr 

Hemato 76.4 M (Alteration in electrophoretic (Swiss- (W) 

profile of serum proteins) Webster) 76.4

82

22 Mouse 3 mo 

Hemato 76.4 M 

(Swiss- (W) 

76.4 Webster) 

83

Neurological 

23 Rat 1x 

19.4 (Mild depression of (Wistar) (GW) 

spontaneous activity, muscle tone, and respiration) 

19.4

88
89

4.25

24.8

91

81.7

9298

0.04

99

20

101

0.07

Table 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral (continued) 

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) 

24 Rat 1x 

4.25 (Mild depression of (Wistar) (GW) 

spontaneous activity, muscle tone, and respiration) 

Developmental 

25 Rat Gd 6-15 

24.8

(GW) 

26 Mouse Gd 8-12 

(GW) 

81.7 

INTERMEDIATE EXPOSURE Death 

27 Human NR 

(W) 

0.04 (death) 

28 Gn Pig 5 wk 

(F) 

20 (death) 

Systemic 

29 Human NR 

(W) 

Cardio 0.07 (beer-cobalt cardiomyopathy) 
102

1

103

0.180.18

104

0.5

0.60.6

106

0.04

0.04

0.040.04

Table 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral (continued) 

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) 

30 Human 1x/d 25 d c 

Hemato 1 (polycythemia) (C) 

31 Human 12-32 wk 

Gastro 0.18 (nausea) (C) 

b

Hemato 0.18 (increased hemoglobin,

23-102% increase)

32 Human 90 d 

Gastro 0.5 (gastric intolerance) (C) 

Hemato 0.6 Hepatic 0.6 

33 Human NR 

Resp 0.04 (edema) (W) 

Cardio 0.04 (beer-cobalt cardiomyopathy) Gastro 0.04 (vomiting, nausea) Hepatic 0.04 (necrosis) 
107

0.54

108

0.16

109

3.79

110

4.2

a

Key to Species 

figure (Strain) 

34 Human 35 Human 36 Rat 

(SpragueDawley) 

37 Rat 

Table 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral (continued) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(mg/kg/day) 

Less Serious 

(mg/kg/day) 

LOAEL 

Serious 

(mg/kg/day) 

10-25 d 1x/d (C) 

Other 0.54 (decreased Iodine uptake) 

12-32 wk 7d/wk (C) 

Hemato 0.16 

b

(increased hemoglobin) 

4 wk (F) 

Bd Wt 3.79 M (45-65% reduction in body 

weight gain) 

8 wk 1x/d (F) 

Bd Wt 4.2 (33% decrease in body weight 

gain) 
111

30.230.2

30.2

30.2

30.230.230.2

112

26

113

8.4

a

Key to 

figure 

Species 

(Strain) 

LOAEL 

NOAEL Less Serious

System 

Table 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral 

(mg/kg/day) (mg/kg/day) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) 

Serious 

(mg/kg/day) 

(continued) 

38 Rat 3 mo 

(W) Resp 30.2 (increased lung weight 33%) 

Cardio Gastro 30.2 

30.2 (increased heart weight 9.4%) 

Hemato Musc/skel Hepatic Renal 

30.2 30.2 30.2 

30.2 (increased hematocrit 29%)c 

39 Rat 8 wk 

(F) 

Cardio 26 (degeneration) 

40 

(SpragueDawley) Rat 24 wk 

(F) 

Cardio 8.4 M (Left ventricular hypertrophy 

and impaired ventricular function) 
18

114

1818

18

18

18

0.05

115

0.5

2.5

116

12.4

12.4

a

Key to 

figure 

Species 

(Strain) 

LOAEL 

NOAEL Less Serious

System 

Table 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral 

(mg/kg/day) (mg/kg/day) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) 

Serious 

(mg/kg/day) 

(continued) 

41 Rat 4 mo 

(G) Resp 18 

Cardio 18 Gastro Hemato Hepatic Renal 

18 18 

18 

b

(erythrocytosis) 

18 (tubular necrosis) 

42 Rat 7 mo 6 d/wk 

(GW) 

Hemato 0.05 0.5 (increased RBC, hemoglobin) 

b 

Hepatic 2.5 

43 

CFY Rat 3 wk 

(G) 

Cardio 12.4 M (Incipient, multifocal 

myocytolysis, with degeneration of myofibrilles) 

Bd Wt 12.4 M (Decreased body weight 8%) 
117

1010

10

108.4

118

8.4

10.6

119

10.6

Table 3-2 Levels of Significant Exposure to Cobalt - 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) 

44 Rat 150 d 5 d/wk 

(GW) 

Hemato 10 

b

(increased hemoglobin) 

Hepatic 10 (increased weight 17%) Renal 10 (necrosis of tubular lining cells) Bd Wt 10 

45 

(SpragueDawley) Rat 8 wk 

Hemato 8.4 M 

Bd Wt 8.4 M (>20% decrease from 

appropriate control) 

46 

(SpragueDawley) Rat 12-16 d 

(W) 

Bd Wt 10.6 M 

Metab 10.6 M (Decreased serum glucose 

levels in diabetic rats, but not control rats) 
0.6

120

2.5

20

121

100

122

26

123

20

20

124

5

109

3.79

Table 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral (continued) 

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) 

47 Rat 6 wk 7 d/wk b 

Hemato 0.6 2.5 (polycythemia) (C) 

48 3 d 

(Long- Evans) (F) Rat 

Bd Wt 20 M 100 M (<20% reduction of body 

weights) 

49 

Parkes Mouse 45 d 

(W) 

Endocr 26 F (Necrosis and inflammation of 

thyroid) 

50 Gn Pig 5 wk 

(F) 

Cardio 20 (cardiomyopathy) 

Bd Wt 20 

51 Dog 4 wk 7 d/wk 

(F) 

Hemato 5 

b

(polycythemia) 

Immuno/ Lymphoret 

52 

(SpragueDawley) Rat 4 wk 

(F) 3.79 M (Atrophy of the thymus) 
0.05

125

0.5

126

20

127

20

0.05

128

0.5

2.5

129

4.96

5

130

20

a

Key to 

figure 

Species 

(Strain) 

LOAEL 

NOAEL Less Serious

System 

Table 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral 

(mg/kg/day) (mg/kg/day) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) 

Serious 

(mg/kg/day) 

(continued) 

53 Rat 7 mo 6 d/wk 

(GW) 

0.05 0.5 (decreased phagocytic ability) 

54 

Neurological 

57 d 

(Sprague- (W)Dawley) Rat 

20 M (Increased latency during 

retention testing) 

55 Rat 57 d 

(W) 

20 (increased reactivity) 

56 Rat 7 mo 6 d/wk 

(GW) 

0.05 0.5 (mildly increased latent reflex) 2.5 (pronounced increase in latent 

reflex) 

57 

(Wistar) Rat 30 d 

(W) 4.96 M (Alterations in sympathetically-induced 

contractility of vas deferens) 

58 Rat 69 d 

(F) 

5 20 (changes in schedule training, 

conditioned suppression, and mixed schedule training tests) 
131

6.44

20

132

100

551

20

550

30.2

133

13.25

5

134

20

Table 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral (continued) 

Exposure/ LOAEL 

a

Key to 

figure 

Duration/ 

Frequency 

(Specific Route) Species (Strain) System NOAEL (mg/kg/day) Less Serious (mg/kg/day) 

59 30 d 

(Wistar) (W)Rat 

6.44 M (Alterations in cholinergic 

sensitivity) 

60 3 d 

(Long- Evans) (F) Rat 

20 M 100 M (Saccharin and food aversion) 

Reproductive 

61 98 days 

(Sprague- (F)Dawley) Rat 

62 90 d 

(Sprague- (W)Dawley) Rat 

30.2 M 26% decrease in testicular 

weight 

63 98 d 7 d/wk 

(F) 

Rat 

64 69 d 

(F) 

Rat 

5 

(mg/kg/day) 

Serious 

20 M Pronounced histologic alteration

of seminiferous tubules 

13.25 (testicular degeneration) 

20 M (testicular atrophy) 
135

43.4

136

43.4

137

23

138

58.9

0.6

139

Table 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral (continued) 

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) 

65 Mouse 13 wk 

43.4 M (Irreversible testicular (CD-1) (W) degeneration) 

66 Mouse 13 wk 

43.4 M (Testicular degeneration) (CD-1) (W) 

67 Mouse 13 wk 

23 (reversible testicular (W) 

degeneration) 

68 Mouse 10 wk 

58.9 M (Reduced pregnant females and (B6C3F1) (W) pups per litter; reduced fertility) 

Developmental 

69 Human 90 d 

0.6

(C) 
141

5.4

Table 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral (continued) 

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) 

70 Rat Gd 14- Ld 21 

5.4 (stunted pup growth) (G) 

a The number corresponds to entries in Figure 3-2.b An increase in hemoglobin or red blood cells is not necessarily considered an adverse effect.c Used to derive an intermediate oral MRL; concentration was divided by an uncertainty factor of 100 (10 for use of a LOAEL and 10 for human variability), res

mg/kg/day. 

Bd Wt = body weight; (C) = capsule; Cardio = cardiovascular; d = day(s); Endocr = endocrine; (F) = feed; F = female; (G) = gavage; Gd = gestation day; (GO) gavage-water, Gastro = gastrointestinal; Hemato = hematological; hr = hour(s); Ld = lactation day; LD50 = dose producing 50% death; LOAEL = lowest-observlevel; M = male; Metab = metabolism; mo = month(s); NOAEL = no observed-adverse-effect level; NS = not specified; (W) = drinking water; wk = week(s); x = 
Death Cardiovascular Hepatic Renal Endocrine Other Neurological Developm

1000 

Hematological 

Figure 3-2. Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral 

Acute (≤14 days) 

Systemic 

mg/kg/day 

20r 

16r 3r 5r 9r 8r 19r 19r 1r 7r 11r 15r 20r 20r 17r 20r 10r 12m 6r 19r 16r 19r 100 13m 4r 21m 22m 26m 19r 

2r 19r 19r

25r 

18r 23r 

10 

24r 

1 14 

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 
Death Respiratory Cardiovascular Gastrointestinal Hematological Musculoskeletal Hepatic Renal Endocrine Bod

1000 

Figure 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral (Contin

Intermediate (15-364 days)
 

Systemic
 

mg/kg/day 

100 

38r 38r 38r 38r 38r 38r 38r 39r 49m 

28g 50g 50g 

41r 41r 41r 41r 41r 41r 

43r 

10 44r 44r 44r 

40r 45r 

51d 

36r 

47r 42r 

1 30 

32 47r 32 32 42r 

31 31 35 

0.1 

29 

42r 

27 33 33 33 33 

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 
Other Immuno/L Neurological Reproductive Developme

1000 

ntal Metabolic ymphor 

Figure 3-2 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Oral (Contin

Intermediate (15-364 days) 

mg/kg/day 

100 60r 54r 55r 58r 

68m 

46r 65m 66m 

62r 59r 

57r 58r 67m 60r 61r 64r 

52r 63r 

10 56r

70r 64r 

34 53r 56r 

1 

69 

53r 56r 

0.1 

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 
COBALT 74 

3. HEALTH EFFECTS 

A significant increase in the weight of the lungs, without morphological or histological changes, was 

found in rats that received 30.2 mg cobalt/kg/day as cobalt chloride in drinking water for 3 months, as 

compared with controls (Domingo et al. 1984). No morphological changes were seen in the lungs of rats 

treated with 18 mg cobalt/kg/day for 4 months (Holly 1955). 

Cardiovascular Effects. Beer-cobalt cardiomyopathy was observed in people who heavily 

consumed beer containing cobalt sulfate as a foam stabilizer (Alexander 1969, 1972; Bonenfant et al. 

1969; Kesteloot et al. 1968; Morin et al. 1967, 1971; Sullivan et al. 1969). The beer drinkers ingested an 

average of 0.04 mg cobalt/kg/day (Morin et al. 1971, n=50) to 0.14 mg cobalt/kg/day for a period of years 

(Alexander 1969, 1972, n=28). The cardiomyopathy was characterized by sinus tachycardia, left 

ventricular failure, cardiogenic shock, diminished myocardial compliance, absence of a myocardial 

response to exercise or catecholamine, enlarged heart, pericardial effusion, and extensive intracellular 

changes (changes in the myofibers, mitochondria, glycogen, and lipids). The beer-cobalt cardiomyopathy 

appeared to be similar to alcoholic cardiomyopathy and beriberi, but the onset of beer-cobalt 

cardiomyopathy was very abrupt. It should be noted, however, that the cardiomyopathy may have also 

been due to the fact that the beer-drinkers had protein-poor diets and may have had prior cardiac damage 

from alcohol abuse. Treatment of both pregnant and nonpregnant anemic patients for 90 days with doses 

of cobalt (0.6–1 mg/kg/day as cobalt chloride) that were much higher than the doses in the beer did not 

result in effects on the heart (Davis and Fields 1958; Holly 1955). 

Approximately 40–50% of the patients admitted to the hospital with cardiomyopathy died within several 

years of diagnosis. In a followup study of four different sites, 0–43% of the survivors, depending on the 

site, showed a residual cardiac disability and 23–41% had abnormal electrocardiograms (Alexander 

1972). 

In an experiment designed to simulate conditions leading to beer-cobalt cardiomyopathy in humans, 

guinea pigs were given 20 mg cobalt/kg/day as cobalt sulfate by gavage either alone or in combination 

with ethanol (as part of a liquid diet) for 5 weeks (Mohiuddin et al. 1970). The experiment resulted in 

cardiomyopathy, which was characterized by abnormal EKGs; increased heart weights; lesions involving 

the pericardium, myocardium, and endocardium; and disfigured mitochondria. Alcohol did not intensify 

the cardiac effects. Myocardia changes (proliferative interstitial tissue, swollen muscle fibers, and focal 

degeneration) were also found in rats following a single dose of 176.6 mg cobalt/kg administered by 
COBALT 75 

3. HEALTH EFFECTS 

gavage as cobalt fluoride or a single dose of 795 mg cobalt/kg administered as cobalt oxide (Speijers et al. 

1982). 

Three weeks of exposure to 12.4 mg cobalt/kg/day as cobalt chloride in male rats resulted in cardiac 

damage, presenting as incipient, multifocal myocytolysis, with degeneration of myofibrilles (Morvai et al. 

1993). After longer-term exposure (2–3 months) of rats to 26–30.2 mg cobalt/kg/day as cobalt sulfate in 

the diet or as cobalt chloride in the drinking water, degenerative heart lesions (Grice et al. 1969) and an 

increase in heart weight were found (Domingo et al. 1984). Exposure of rats to 8.4 mg cobalt/kg/day as 

cobalt sulfate resulted in left ventricular hypertrophy and impaired left ventricular systolic and diastolic 

functions in an isolated working rat heart model (Haga et al. 1996). Clyne et al. (2001) reported that 

exposure of rats to 8.4 mg cobalt/kg/day, as cobalt sulfate, in the diet for 24 weeks resulted in significant 

reductions in a number of enzymes in cardiac tissues, including manganese-superoxide dismutase, 

succinate-cytochrome c oxidase, NADH-cytochrome c reductase, and cytochrome c oxidase, as well as 

reducing the mitochondrial ATP production rate. 

Gastrointestinal Effects. The first signs of the beer-cobalt cardiomyopathy syndrome were 

gastrointestinal effects and included nausea, vomiting, and diarrhea (Morin et al. 1971). Signs of heart 

failure subsequently appeared. These individuals had ingested an average of 0.04 mg cobalt/kg/day for a 

period of years during which cobalt sulfate was added to beer as a foam stabilizer; however, it is likely 

that alcohol consumption was also a factor. 

In pregnant women given cobalt supplements (alone or combined with iron) to prevent the decrease in 

hematocrit and hemoglobin levels commonly found during pregnancy (n=78), a small percentage of those 

treated complained of gastric intolerance (Holly 1955). The women were treated with 0.5–0.6 mg 

cobalt/kg/day as cobalt chloride for 90 days. Nausea was reported in one anemic patient following 

treatment with 0.18 mg cobalt/kg/day as cobalt chloride (Duckham and Lee 1976b). 

No morphological changes in the gastrointestinal system were observed following exposure of 20 male 

rats for 3 months to 30.2 mg cobalt/kg/day as cobalt chloride in the drinking water (Domingo et al. 1984) 

or exposure for 4 months to 18 mg cobalt/kg/day as cobalt chloride by gavage (Holly 1955). 

Hematological Effects. Cobalt has been shown to stimulate the production of red blood cells in 

humans. Davis and Fields (1958) exposed six apparently normal men, ages 20–47, to a daily dose of 
 

 

COBALT 76 

3. HEALTH EFFECTS 

cobalt chloride, administered as a 2% solution diluted in either water or milk, for up to 22 days. Five of 

the six received 150 mg cobalt chloride per day for the entire exposure period, while the sixth was started 

on 120 mg/day and later increased to 150 mg/day. Blood samples were obtained daily from free-flowing 

punctures of fingertips at least 2 hours after eating, and at least 15 hours after the last dosage of cobalt. 

Blood was analyzed for red blood cell counts, hemoglobin percentage, leukocyte counts, reticulocyte 

percentages, and thrombocyte counts. Exposure to cobalt resulted in the development of polycythemia in 

all six subjects, with increases in red blood cell numbers ranging from 0.5 to 1.19 million (~16–20% 

increase above pretreatment levels). Polycythemic erythrocyte counts returned to normal 9–15 days after 

cessation of cobalt administration. Hemoglobin levels were also increased by cobalt treatment, though to 

a lesser extent than the erythrocyte values, with increases of 6–11% over pretreatment values. In five of 

the six subjects, reticulocyte levels were elevated, reaching at least twice the pre-experiment values. 

Thrombocyte and total leukocyte counts did not deviate significantly from pretreatment values. From the 

LOAEL of 1 mg/kg-day identified by this study, an intermediate-duration oral MRL of 1x10-2 mg/kg-day 

was derived (for derivation, see Section 2.3 and Appendix A). 

Increased levels of erythrocytes were also found following oral treatment of anephric patients (with 

resulting anemia) with 0.16–1.0 mg cobalt/kg/day daily as cobalt chloride for 3–32 weeks (Duckham and 

Lee 1976b; Taylor et al. 1977). The increase in hemoglobin resulted in a decreased need for blood 

transfusions. Treatment of pregnant women for 90 days with 0.5–0.6 mg cobalt/kg/day as cobalt chloride, 

however, did not prevent the reduction in hematocrit and hemoglobin levels often found during pregnancy 

(Holly 1955). 

Significantly increased erythrocyte (polycythemia), hematocrit, and hemoglobin levels were found in 

animals treated orally with cobalt chloride as a single dose of 161 mg cobalt/kg (Domingo and Llobet 

1984) or with longer-term exposure (3 weeks to 2 months) to ≥0.5 mg/kg/day (Brewer 1940; Davis 1937; 

Domingo et al. 1984; Holly 1955; Krasovskii and Fridlyand 1971; Murdock 1959; Stanley et al. 1947). 

Of particular note is an 8-week study in rats (Stanley et al. 1947), which reported dose- and time-related 

increases in erythrocyte number following oral administration of cobalt chloride, with an apparent 

NOAEL of 0.6 mg cobalt/kg/day and a LOAEL of 2.5 mg cobalt/kg/day. Changes in the levels of other 

blood proteins (transferrin, several haptoglobulins, and ceruloplasmin) were noted in male Swiss mice 

following 4, 24, and 48 hours of treatment with 76.4 mg cobalt/kg as cobalt chloride in the drinking water 

(Bryan and Bright 1973). Exposure for 3 weeks or 3 months to 76.4 mg cobalt/kg as cobalt chloride in 

the drinking water resulted in no alterations in serum proteins examined. 
COBALT 77 

3. HEALTH EFFECTS 

Musculoskeletal Effects. No studies were located regarding musculoskeletal effects in humans after 

oral exposure to cobalt. 

No morphological changes were found in the skeletal muscle of rats exposed to 30.2 mg cobalt/kg/day as 

cobalt chloride in the drinking water for 3 months (Domingo et al. 1984). This NOAEL in rats for 

intermediate-duration exposure is reported in Table 3-2 and plotted in Figure 3-2. 

Hepatic Effects. Liver injury was evident in patients with beer-cobalt cardiomyopathy, characterized 

by central hepatic necrosis accompanied by increased levels of serum bilirubin and serum enzymes 

(serum glutamic oxaloacetic transaminase [SGOT], serum glutamic pyruvic transaminase [SGPT], lactate 

dehydrogenase [LDH]), creatine phosphokinase, ornithine carbamyl transferase, isocitric dehydrogenase, 

aldolase) (Alexander 1972; Morin et al. 1971). The hepatic injury may have resulted from ischemia, 

secondary to the cardiac effects of cobalt, and/or from excessive alcohol consumption. The 

cardiomyopathy resulted from the ingestion of beer containing 0.04 mg cobalt/kg/day as cobalt sulfate 

that had been added as a foam stabilizer (Morin et al. 1971). Liver function tests were found to be normal 

in pregnant women receiving up to 0.6 mg cobalt/kg/day as cobalt chloride for 90 days for treatment of 

the decreases in hematocrit and hemoglobin levels commonly found during pregnancy (Holly 1955). 

Data from animals have also indicated that cobalt has hepatic effects. Hyperemia of the liver and 

cytoplasmic changes in hepatocytes (clumpy cytoplasm located along the cell membrane) were found in 

rats administered a single dose of 68.2 mg cobalt/kg as cobalt fluoride or a single dose of 157.3 mg 

cobalt/kg as cobalt oxide (Speijers et al. 1982). 

Increased liver weight (17%) was found in rats exposed to 10 mg cobalt/kg/day (as cobalt chloride) for 

5 months (Murdock 1959). No morphological or enzymatic changes were found in the livers of rats 

exposed to 2.5–30.2 mg cobalt/kg as cobalt chloride by gavage or as cobalt chloride in the drinking water 

for 3–7 months (Domingo et al. 1984; Holly 1955; Krasovskii and Fridlyand 1971). 

Renal Effects. No studies were located regarding renal effects in humans after oral exposure to 

cobalt. 
 

COBALT 78 

3. HEALTH EFFECTS 

Acute and prolonged exposure to cobalt results in renal tubular degeneration in rats. Renal injury, 

evidenced by histologic alteration of the proximal tubules, was observed in rats after a single oral 

exposure to 42 mg cobalt/kg as cobalt fluoride (Speijers et al. 1982) and after exposure to 10–18 mg 

cobalt/kg/day as cobalt chloride for 4–5 months (Holly 1955; Murdock 1959). A slightly decreased 

urinary output was observed in rats exposed to 19.4 mg cobalt/kg as cobalt sulfate, but not in rats exposed 

to 4.25 mg cobalt/kg as cobalt chloride (Singh and Junnarker 1991). 

Endocrine Effects. Roy et al. (1968) reported on 20 Québécois patients who died of beer drinkers’ 

myocardosis. Of these, 14 thyroids were available for examination. Three of those were normal, and the 

other 11 formed the basis of the study. “Abnormal” thyroids did not show gross changes, but upon 

histologic examination, they showed irregular follicle morphology and decreased follicular size. 

Kriss et al. (1955) reported on five patients who had been receiving cobalt therapy for sickle-cell anemia 

or renal amyloidosis. Three of five developed goiter, one severe, while four of five showed microscopic 

alterations of the thyroid gland. Two of the patients died from non-cobalt-related causes, while the other 

three recovered once cobalt treatment was removed. A similar study was reported by Gross et al. (1955) 

in which stable cobalt was used therapeutically in four cases of sickle-cell anemia. Treatment with cobalt 

resulted in an enlargement of the thyroid gland, which was reversible upon cessation of cobalt therapy. 

Similar effects on the thyroid, including enlargement, hyperplasia, and an increased firmness, have been 

reported in several other cases where cobalt therapy for anemia was used (Chamberlain 1961; Little and 

Sunico 1958; Soderholm et al. 1968; Washburn and Kaplan 1964). No other studies examining the 

endocrine effects of stable cobalt in humans were located. 

NTP (1998; Bucher et al. 1999) reported increased incidence of pheochromocytoma, a tumor of the 

adrenal medulla, in female rats exposed to 1.14 mg cobalt/m3

 for 2 years, but did not measure any other 

endocrine effects. Female mice exposed to 26 mg cobalt/kg-day in the drinking water for up to 45 days 

showed histopathological changes to the thyroid gland (Shrivastava et al. 1996). Cobalt significantly 

stimulated serum testosterone in mice treated orally with 23 mg cobalt/kg as cobalt chloride, though no 

dose-response relationship was present (Pedigo et al. 1988). 

Dermal Effects. Allergic dermatitis has been reported in some cobalt-sensitized people following oral 

challenge with cobalt. Several patients with eczema of the hands were challenged orally with 1 mg cobalt 

as cobalt sulfate given in tablet form once per week for 3 weeks (0.014 mg/kg/day). A flaring of the 
 

 

COBALT 79 

3. HEALTH EFFECTS 

eczema was considered to be a positive allergic response to cobalt (Veien et al. 1987). No other studies 

were located regarding dermal effects in humans or animals after oral exposure to cobalt. 

Ocular Effects. Severe visual disturbances (optic atrophy, impaired choroidal perfusion) developed in 

a man who was treated with cobalt chloride for pancytopenia and hypercellular bone marrow (Licht et al. 

1972). He received 1.3 mg cobalt/kg daily for four series of treatments with a total duration of 6 weeks. 

However, no other cases of visual disturbances due to therapeutic administration of cobalt have been 

reported, and no such effects have been observed in animals. 

Body Weight Effects. No effects on body weight in animals were found following longer-term (1– 

5 months) exposure of rats to 10–30.2 mg cobalt/kg/day as cobalt chloride (Bourg et al. 1985; Domingo et 

al. 1984; Murdock 1959) or of guinea pigs to 20 mg cobalt/kg/day as cobalt sulfate (Mohiuddin et al. 

1970). A significant decrease (33%) in body weight gain was observed following 8 weeks of exposure of 

rats to 4.2 mg cobalt/kg/day as cobalt sulfate (Clyne et al. 1988). 

Metabolic Effects. Treatment of rats with 10.6 mg Co/kg/day as CoCl2 in the drinking water for 12– 

16 days resulted in a significant decrease in serum glucose levels in diabetic rats, but not in control rats 

(Saker et al. 1998). 

Other Systemic Effects. Hypothermia occurred in rats following a single oral dose of 157 mg 

cobalt/kg given as cobalt oxide or a single oral dose of 110 mg cobalt/kg given as cobalt fluoride (Speijers 

et al. 1982). The hypothermia was time- and dose-related. Hypothermia was reported as an effect during 

LD50 studies with other cobalt compounds, but the exact dose for the onset of hypothermia with these 

compounds was not reported (Speijers et al. 1982). Other physiological signs noted in LD50 studies 

include decreased activity, ataxia, diarrhea, and salivation (FDRL 1984a, 1984b). 

3.2.2.3 Immunological and Lymphoreticular Effects 

Cobalt is known to function as a hapten, resulting in the generation of antibodies against cobalt-protein 

complexes. Allergic dermatitis has been reported in some cobalt-sensitized people following oral 

challenge with cobalt. Several patients with eczema of the hands were challenged orally with 1 mg cobalt 

as cobalt sulfate given in tablet form once per week for 3 weeks (0.014 mg/kg/day). A flaring of the 
COBALT 80 

3. HEALTH EFFECTS 

eczema was considered to be a positive allergic response to cobalt (Veien et al. 1987). Using both the 

oral challenge test and dermal patch tests, it was determined that the cobalt allergy was systemically 

induced. The exposure level associated with sensitization to cobalt was not established. After 

sensitization, allergic reactivity may be independent of dose. Cobalt has been found to be a sensitizer 

following inhalation exposure (Section 3.2.1.3). This LOAEL value was not reported in Table 3-2 

because sensitized individuals only represent a small percent of the population. 

A case report of a 6-year-old boy who had ingested approximately 1.7 mg of cobalt chloride reported 

neutropenia by 7 hours post-exposure (Mucklow et al. 1990). 

Thymic atrophy was reported in male Sprague-Dawley rats exposed to 3.79 mg cobalt/kg/day as cobalt 

chloride in the feed for 4 weeks (Chetty et al. 1979). A deterioration in immunological reactivity, 

manifested by a decline in phagocytic activity, was reported in rats following 6–7 months of treatment 

with 0.5 mg cobalt/kg or greater as cobalt chloride (Krasovskii and Fridlyand 1971). This value is 

presented in Table 3-2 and Figure 3-2. 

3.2.2.4 Neurological Effects 

No studies were located regarding neurological effects in humans after oral exposure to stable cobalt. 

Several rodent studies have identified neurological effects following cobalt exposure. In Wistar rats, a 

single gavage dose of 4.25 mg cobalt/kg as cobalt chloride resulted in a moderate reduction in 

spontaneous activity, muscle tone, touch response, and respiration, while 19.4 mg cobalt/kg as cobalt 

sulfate caused a mild reduction the same parameters (Singh and Junnarkar 1991). In rats exposed to 

4.96 mg cobalt/kg/day as cobalt chloride for 30 days in the drinking water, cobalt led to changes in 

sympathetically mediated contractile activity of isolated rat vas deferens (Mutafova-Yambolieva et al. 

1994). Rats exposed to 6.44 mg cobalt/kg/day as cobalt nitrate in the drinking water showed an increased 

sensitivity and decreased maximal response to a cholinergic agonist (Vassilev et al. 1993). In rats 

exposed to 20 mg cobalt/kg/day as cobalt chloride for 57 days in the drinking water, cobalt enhanced 

behavioral reactivity to stress (the animals were less likely to descend from a safe platform to an 

electrified grid) (Bourg et al. 1985). Rats exposed to the same dose in the diet for 69 days showed a 

slower rate of lever pressing than controls, but no change in behavioral reactivity to stress (Nation et al. 
 

COBALT 81 

3. HEALTH EFFECTS 

1983). Longer-term exposure of rats to cobalt chloride (7 months) resulted in a significant increase in the 

latent reflex period at ≥0.5 mg cobalt/kg as cobalt chloride and a pronounced neurotropic effect (disturbed 

conditioned reflexes) at 2.5 mg cobalt/kg (Krasovskii and Fridlyand 1971). 

The NOAEL value and the LOAEL value for rats for intermediate duration are reported in Table 3-2 and 

plotted in Figure 3-2. 

3.2.2.5 Reproductive Effects 

No studies were located regarding reproductive effects in humans after oral exposure to stable cobalt. 

Testicular degeneration and atrophy have been reported in rats exposed to 13.3–58.9 mg cobalt/kg/day as 

cobalt chloride for 2–3 months in the diet or drinking water (Corrier et al. 1985; Domingo et al. 1984; 

Mollenhauer et al. 1985; Nation et al. 1983; Pedigo and Vernon 1993; Pedigo et al. 1988), or in mice 

exposed to 43.4 mg cobalt/kg/day as cobalt chloride for 13 weeks in the drinking water (Anderson et al. 

1992, 1993). 

The highest NOAEL and all reliable LOAEL values for rats in the intermediate-duration category are 

reported in Table 3-2 and plotted in Figure 3-2. 

3.2.2.6 Developmental Effects 

No developmental effects on human fetuses were observed following treatment of pregnant women with 

cobalt chloride to raise hematocrit and hemoglobin levels that are often depressed during pregnancy. 

Dosages up to 0.6 mg cobalt/kg/day for 90 days were given (Holly 1955). Examination of the fetuses, 

however, was limited to the reporting of obvious birth defects, and exposure only occurred in the final 

trimester. 

Oral exposure of female rats to cobalt chloride at 5.4 or 21.8 mg cobalt/kg/day from gestation 

day 14 through lactation day 21 has been shown to result in stunted growth and decreased survival, 

respectively, of newborn pups (Domingo et al. 1985b). The effects on the offspring occurred at levels 
COBALT 82 

3. HEALTH EFFECTS 

that also caused maternal toxicity (reduced body weight and food consumption, and altered hematological 

measurements) and might therefore have been an indirect effect of maternal toxicity rather than a direct 

effect of cobalt on the fetus (Domingo et al. 1985b). Teratogenic effects were not observed. 

Szakmary et al. (2001) reported that exposure of pregnant rats to 0–38 mg Co/kg-day as cobalt sulfate did 

not result in changes in fetal death rates, maternal body weigh gain, average litter size, or average fetal or 

placental weights; however, a dose-related trend was seen for the percent of fetuses with retarded body 

weights. In contrast, no effects on fetal growth or survival were found following exposure of rats to 

24.8 mg cobalt/kg/day as cobalt chloride during gestation days 6–15 (Paternian et al. 1988). In mice, 

exposure to 81.7 mg cobalt/kg/day as cobalt chloride during gestation days 8–12 was reported to have no 

effect on fetal growth or mortality in mice (Seidenberg et al. 1986). In a later mouse study that exposed 

pregnant mice to 19 mg Co/kg-day as cobalt sulfate, no changes in litter size, postimplantation loss, or 

average fetal or placental weights were seen; the only difference seen was an increase in the percent of 

fetuses with retarded body weights (Szakmary et al. 2001). The same study reported that rabbits exposed 

to ≥ 38 mg Co/kg-day, as cobalt sulfate, showed nearly complete maternal lethality, and complete fetal 

loss. Rabbits exposed to 7.6 mg Co/kg, as cobalt sulfate, showed significant increases in mortality and 

fetal resorption, as well as an increase in fetuses with retarded body weight (Szakmary et al. 2001). The 

highest NOAEL and all reliable LOAEL values for each species and duration category are reported in 

Table 3-2 and plotted in Figure 3-2. 

3.2.2.7 Cancer 

In a survey assessing the correlation between cancer mortality and trace metals in water supplies 

(10 basins) throughout the United States, no correlation was found between cancer mortality and the level 

of cobalt in the water (Berg and Burbank 1972). Cobalt levels of 1–19 μg/L, with resulting human 

intakes ranging from 0.03 to 0.54 μg/kg/day, were reported. 

No studies were located regarding carcinogenic effects in animals after oral exposure to stable cobalt. 
COBALT 83 

3. HEALTH EFFECTS 

3.2.3 Dermal Exposure 

3.2.3.1 Death 

No studies were located regarding lethal effects in humans after dermal exposure to cobalt. 

No mortality was observed in guinea pigs dermally exposed to 51.75 mg cobalt/kg for 5 days/week as 

dicobalt octacarbonyl for a total of 18 applications (Kincaid et al. 1954). 

3.2.3.2 Systemic Effects 

No studies were located regarding respiratory, cardiovascular, gastrointestinal, hematological, 

musculoskeletal, hepatic, renal, or ocular effects in humans or animals after dermal exposure to stable 

cobalt. 

Dermal Effects. Dermatitis is a common result of dermal exposure to cobalt in humans that has been 

verified in a large number of studies (Alomar et al. 1985; Bedello et al. 1984; Dooms-Goossens et al. 

1980; Fischer and Rystedt 1983; Goossens et al. 2001; Kanerva et al. 1988, 1998; Kiec-Swierczyńska and 

Krecisz 2002; Marcussen 1963; Minamoto et al. 2002; Pryce and King 1990; Swennen et al. 1993; 

Romaguera et al. 1982; Valer et al. 1967). Using patch tests and intradermal injections, it has been 

demonstrated that the dermatitis is probably caused by an allergic reaction to cobalt. Contact allergy was 

reported in 22 of 223 (9.9%) nurses who were tested with a patch test of 1.0% cobalt chloride (KiećŚwierczyńska and Kręcisz 2000), as well as 16 of 79 (20.3%) of examined dentists (Kieć-Świerczyńska 

and Kręcisz 2002). Persons with body piercings showed an increased prevalence of allergy to cobalt, 

with the incidence of contact allergy being proportional to number of piercings (Ehrlich et al. 2001). The 

prevalence of sensitivity to cobalt following exposure to cobalt as a component of metal implants is low, 

with only 3.8% of patients developing a new sensitivity to cobalt following insertion of the implant 

(Swiontkowski et al. 2001). Exposure levels associated with the development of dermatitis have not been 

identified. It appears that the allergic properties of cobalt result mainly from exposure to the metal itself, 

rather than a salt, as Nielsen et al. (2000) demonstrated that daily repeated exposure to aqueous cobalt 

salts did not result in hand eczema in patients known to have cobalt allergy. 
COBALT 84 

3. HEALTH EFFECTS 

In animals, scabs and denuded areas were found after six doses of 51.75 mg cobalt/kg (5 days/week) as 

dicobalt octacarbonyl were applied to the shaved abdomens (uncovered area of approximately 50 cm2

) of 

guinea pigs (Kincaid et al. 1954). By the 11th dose, the lesions disappeared. No adverse effects were 

observed in vehicle controls (methyl ethyl ketone). It is not known whether or not a similar reaction 

would result from metallic or inorganic forms of cobalt. This LOAEL value is reported in Table 3-3. 

3.2.3.3 Immunological and Lymphoreticular Effects 

Cobalt-induced dermatitis is well documented in the literature, and the studies indicate that cobalt is a 

sensitizer (Alomar et al. 1985; Dooms-Goossens et al. 1980; Fischer and Rystedt 1983; Goh et al. 1986; 

Kanerva et al. 1988; Marcussen 1963; Valer et al. 1967). Patch testing and intradermal injections were 

performed, but exposure levels of cobalt were not reported. Interrelationships exist between nickel and 

cobalt sensitization (Bencko et al. 1983; Rystedt and Fisher 1983); however, the extent of any potential 

interactions between the two metals on immunologic end points is not well understood. In guinea pigs, 

nickel and cobalt sensitization appear to be interrelated and mutually enhancing (Lammintausta et al. 

1985), though cross-reactivity was not reported to occur. 

Single or multiple dermal exposures of BALB/c mice to CoCl2 in dimethylsulfoxide or in ethanol resulted 

in an increased cellular proliferation in the local lymph node assay in a concentration-dependant manner 

(Ikarashi et al. 1992a). The effect of three consecutive exposures to varying concentrations of CoCl2 in 

DMSO on lymph node proliferation was measured in rats, mice, and guinea pigs (Ikarashi et al. 1992b). 

Stimulation Indices of 3 or greater, indicated by the authors as a significant response, were reported for 

mice exposed to 1, 2.5, or 5% CoCl2, rats exposed to 2.5 or 5% CoCl2, and guinea pigs exposed to 5% 

CoCl2; these treatments resulted in dose levels of 10.8, 27, or 54.1 mg cobalt/kg/day for mice, 9.60 or 

19.2 mg cobalt/kg/day for rats, and 14.7 mg cobalt/kg/day for guinea pigs. 

No studies were located regarding the following health effects in humans or animals after dermal 

exposure to stable cobalt: 
mg/kg/day

mg/kg/day

142

mg/kg/day

143

mg/kg/day

mg/kg/day

144

mg/kg/day

mg/kg/day

145

mg/kg/day

146

LOAEL 

Table 3-3 Levels of Significant Exposure to Cobalt - Chemical Toxicity - Dermal 

Species 

(Strain) System NOAEL Less Serious 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) 

ACUTE EXPOSURE 

Immuno/ Lymphoret 

(Fischer- 344) Rat 3.84 F 

mg/kg/day 

F 

(Increased proliferation of lymphatic cells) 

9.6 

mg/kg/day 

1x/d 3d 

Serious 

IkaCh

(BALB/c) Mouse 1x or 1x/d for 3 d F10.8 

mg/kg/day (Increased proliferation of lymphatic cells) 

IkaCh

CBA/N Mouse 1x/d 3 d 5.4 F 

mg/kg/day 

F10.8 

mg/kg/day (Increased proliferation of lymphatic cells) 

IkaCh

(Hartley) Gn Pig 1x/d 3 d 7.39 F 

mg/kg/day 

F14.7 

mg/kg/day (Increased proliferation of lymphatic cells) 

IkaCh

INTERMEDIATE EXPOSURE 

Systemic 

(NS) Gn Pig 18 d 5 d/wk Dermal 51.75 

mg/kg/day (skin lesions (scabs and denuded areas) at 

application site) 

Ki

d =day(s); F = female; LOAEL = lowest-observed-adverse-effect level; NOAEL = no observed-adverse-effect level; wk = week(s); x = times. 
COBALT 86 

3. HEALTH EFFECTS 

3.2.3.4 Neurological Effects 

3.2.3.5 Reproductive Effects 

3.2.3.6 Developmental Effects 

3.2.3.7 Cancer 

No studies were located regarding carcinogenic effects in humans or animals after dermal exposure to 

cobalt. 

3.2.4 Other Routes of Exposure 

Endocrine Effects. Patients (n=12) injected with a single diagnostic dose of radioactive iodine, and 

then treated 48 hours later with 1 mg cobalt/kg/day as cobalt chloride for 2 weeks, resulted in a greatly 

reduced uptake of radioactive iodine by the thyroid in 1 week, with uptake nearing 0 by the second week 

(Roche and Layrisse 1956). When the cobalt treatment ended, the uptake values returned to normal. The 

decrease of radioactive iodine uptake found in patients administered 0.54 mg cobalt/kg/day for 10– 

25 days prior to iodine injection was found to result from cobalt blocking the organic binding of iodine 

(Paley et al. 1958). 

In various species of animals, parenteral administration of cobalt resulted in cytotoxic effects on the alpha 

cells of the pancreas (Beskid 1963; Goldner et al. 1952; Hakanson et al. 1974; Lacy and Cardeza 1958; 

Lazarus et al. 1953; Van Campenhout 1955). Because this effect has never been reported in humans or 

animals following inhalation, oral, or dermal exposure to cobalt, the relevance of the effect to humans is 

not known. 

Moger (1983) exposed primary cultures of mouse Leydig cells to 0–2.5 mM cobalt as cobalt for 3 hours, 

and measured the effects on androgen production. Cobalt exposure caused a dose-related decrease in both 

basal and LH-stimulated androgen production, with no effects on protein synthesis. The author suggested 

that these effects are the result of cobalt inhibition of calcium influx across the plasma membrane. 
 

COBALT 87 

3. HEALTH EFFECTS 

3.3 DISCUSSION OF HEALTH EFFECTS OF RADIOACTIVE COBALT BY ROUTE OF 

EXPOSURE 

Section 3.3 discusses radiation toxicity associated with exposure to radionuclides of cobalt 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. 

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 

No studies were located regarding the following health effects in humans or animals after inhalation 

exposure to radioactive cobalt: 

3.3.1.1 Death 

3.3.1.2 Systemic Effects 

3.3.1.3 Immunological and Lymphoreticular Effects 

3.3.1.4 Neurological Effects 

3.3.1.5 Reproductive Effects 

3.3.1.6 Developmental Effects 
COBALT 88 

3. HEALTH EFFECTS 

3.3.1.7 Cancer 

3.3.2 Oral Exposure 

No studies were located regarding the following health effects in humans or animals after oral exposure to 

radioactive cobalt: 

3.3.2.1 Death 

3.3.2.2 Systemic Effects 

3.3.2.3 Immunological and Lymphoreticular Effects 

3.3.2.4 Neurological Effects 

3.3.2.5 Reproductive Effects 

3.3.2.6 Developmental Effects 

3.3.2.7 Cancer 

3.3.3 External Exposure 

This section contains information regarding health effects related to external exposure to radioactive 

cobalt sources. Radionuclides of cobalt may emit beta particles and/or gamma rays, which may be a 

health hazard in living organisms because they ionize the atoms that they hit while passing through the 

tissues of the body (see Table 3-4 and Figure 3-3). Beta particles can travel appreciable distances in air, 

but travel only a few millimeters in solids. External exposure to beta particles may result in damage to 

skin and superficial body tissues at sufficiently high doses. Beta radiation is only a threat to internal 

organs if the radiation source is internalized. Gamma radiation, on the other hand, can easily pass 

completely through the human body and cause ionization of atoms in its path. For most radionuclides of 

public interest, the fraction of gamma rays that actually deposits energy and contributes to the radiation 
152

2250

155

627

156

1420

12.7

166

12.7

168

159159

a

Key to 

figure 

Species 

(Strain) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(rad) 

Less Serious 

(rad) 

LOAEL 

Serious 

(rad) 

ACUTE EXPOSURE Death 

1 Human 2250 M (Death) 

Table 3-4 Levels of Significant Exposure to Cobalt - Radiation Toxicity - External Radiation 

2 Mouse 

627 (30-day LD50 value, single (BALB/c) exposure) 

3 Mouse 1x 

1420 M (Death) CBA/Ca.Lac.C 

Systemic 

4 Human (occup) 

Gastro 12.7 Hemato 12.7 

5 Human 

Dermal 159 M (Severe alterations to skin of lef

hand) 

Ocular 159 M (Progressive occlusion of vision 

of left eye) 
171

225022502250

2250

172

1000

174

10000

176

2500

Table 3-4 Levels of Significant Exposure to Cobalt - 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 Human 

Cardio 2250 M (left ventricular hypertrophy) 

Gastro 2250 M (Pronounced atrophy in 

intestines; less severe in stomach) 

Hemato 2250 M (>35% decrease in hemogolbin 

and >90% decrease in thrombocytes) 

Renal 2250 M (Enlarged kidneys) 

7 Monkey 30 min 

Cardio 1000 M (Minor changes: increased heart (Rhesus) rate; decreased blood pressure; 

variable cardiac output and total peripheral resistance) 

8 Monkey 1 hr 

Cardio 10000 M (Pronounced decreases in (Rhesus) mean arterial blood pressure

and blood flow to the brain)

9 Rat 

Cardio 2500 M (Increased brain uptake index) (Wistar) 
178

1500

180

1000

182

13301800

186

1000

193

4355

195

800

a

Key to Species 

figure (Strain) 

10 Rat 

(SpragueDawley) 

11 Mouse 

(SwissWebster) 

12 Mouse 

CBA/Ca.Lac.C 

13 Mouse 

(SwissWebster) 

14 Dog 

(Mongrel) 

15 Dog 

(Beagle) 

Table 3-4 Levels of Significant Exposure to Cobalt - Radiation Toxicity - External Radiation (continued) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(rad) 

Less Serious 

(rad) 

LOAEL 

Serious 

(rad) 

1x 

Resp 1500 M (Severe inflammation, 

pulmonary histopathology, fibrosis) 

Gastro 1000 M (Intestinal crypt cell damage, 

including necrosis and altered mitotic figures) 

1x 

Resp 1330 M (Increased breathing rate) Dermal 1800 M (Mild epilation) 

24 hr 

Hepatic 1000 M (Transient decrease in total liver 

protein) 

198 d 

Cardio 4355 (Cardiac arrhythmia) 

10.44 min 

Gastro 800 (Repeated emesis) 
198

1730

200

900

1090

201

874

202

780 1190780 980

203

557

a

Key to Species 

figure (Strain) 

16 Rabbit 

(New Zealand) 

17 Pig 

Large White 

18 Pig 

Large White 

19 Pig 

Large White 

20 Pig 

Large White 

Table 3-4 Levels of Significant Exposure to Cobalt - Radiation Toxicity - External Radiation (continued) 

Exposure/ LOAEL 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(rad) 

Less Serious 

(rad) 

1x 

Dermal 1730 M (Alopecia) 

1x 

Resp 900 F (Reversible decrease in 

ventilation capacity) 

1x 

Renal 

1x 

Hemato 780 F (Slight decreases in 

erythrocytes, hemoglobin, and hematocrit) 

Renal 780 F (Reversible changes in effective 

renal plasma flow and glomerular filtration rate) 

1x 

Renal 

Serious 

(rad) 

1090 F (Irreversible decrease in 

ventilation capacity, histopathology, pulmonary atrophy) 

874 F (50% loss in effective renal

plasma flow)

1190 F (Severe decreases in 

erythrocytes, hemoglobin, and hematocrit) 

980 F (Persistent changes in effective 

renal plasma flow and glomerular filtration rate) 

557 F (50% loss in effective renal

plasma flow)
204

980

206

3000

49

205

77

12.7

207208

159

209

2250

Table 3-4 Levels of Significant Exposure to Cobalt - 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) 

21 Pig 1x 

Renal 980 F (Progressive inflammatory and Large White degenerative changes in the 

glomerulus) 

22 Baboon 3-4 wk, 1x/wk 

Resp 3000 (Severe pulmonary fibrosis) 

23 Ferret 2 hr 

Gastro 49 M 77 M (Emesis with wretching) 

Immuno/ Lymphoret 

24 Human (occup) 

12.7 

25 Human 

159 M (Minor reduction in white cell 

counts) 

26 Human 

2250 M (Pronounced decrease in 

lymphocytes and granulocytes) 
210

1000

150

212

450

300

214

500

217

450

218

330

220

80

a

Key to 

figure 

Species 

(Strain) 

NOAEL Less Serious

System 

Table 3-4 Levels of Significant Exposure to Cobalt - Radiation Toxicity 

(rad) (rad) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) 

LOAEL 

Serious 

- External Radiation 

(rad) 

(continued) 

27 

(SwissWebster) Mouse 24 hr 

1000 M (>50% decrease in spleen 

weight and protein; increased spleen acid phosphatase) 

28 

Neurological 

140 d 

(CD) Rat 

150 M 450 M (Reversible deficits in fixed-ratio 

behavior parameters) 

29 

(SwissWebster) Mouse 97 d 

300 M 500 M (Reversible decreases in 

aggressive behavior) 

30 31 

12 hr 

Burgundy fawn Rabbit 

Reproductive 

1x 

(SpragueDawley) Rat 

450 M (Altered firing rates and patterns 

of hippocampal neurons) 

330 M (Decreased testis weight and 

altered spermatogenesis, with some evidence of recovery) 

32 

(Wistar) Rat 1x 

80 M (Reversible decrease in 

testicular weight) 
224

100

225

50

226

260

227

260

11

228

16 560

229

210

Table 3-4 Levels of Significant Exposure to Cobalt - 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) 

Developmental 

33 Monkey 1x 

100 (Developmental retardation, Squirrel neurobehavioral deficits) 

34 Rat 1x 

50 F (Defective eye development and (Sprague- spinal curvature) Dawley)

35 Rat 1x 

260 (Testicular trophy; adrenal 

atrophy) 

36 Rat 1x 

260 M (Reduced NADPH cytochrome (Wistar) p450 reductase) 

37 Rat 4d or 6d 

11 16 (slightly decreased (2.6%) brain 560 (decreased (13.1%) brain (Wistar) weight in offspring) weight in offspring) 

38 Rat 1x 

210 M (Testicular atrophy) (Wistar)
5

230

10

50

231

25

234

100

236

200

237

20

Table 3-4 Levels of Significant Exposure to Cobalt - 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) 

39 Mouse 1x 

5 10 (Decreased brain weight 3-4%, 50 (Increased fetal mortality and (Swiss- significantly increased growth retardation) Webster) microphthalmia) 

40 Mouse 1x 

25 (Decreased body weight 5%, (Swiss- liver weight 5%, and spleen Webster) weight 12%. Decreased spleen 

cellularity.) 

41 Mouse 1x 

100 M (Increased number of (B6C3F1) tumor-bearing animals after in

utero exposure)

42 Mouse 1x 

200 (Atrophy or lack of development (Swiss- of corpus callosum) Webster)

43 Mouse 6d 

20 F (Altered neurobehavioral 

parameters, growth retardation) 
238

50

239

200

240

83

242

15.6

16

245

83

247

96

Table 3-4 Levels of Significant Exposure to Cobalt - Radiation Toxicity - External Radiation (continued) 

Exposure/ LOAEL 

a

Key to 

figure 

Species 

(Strain) 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(rad) 

Less Serious 

(rad) 

44 

LACA Mouse 1x 

45 

(Golden Syrian) Hamster 1x 

46 

(Beagle) Dog 1x 

47 

(Beagle) Dog 1x 

48 

(Beagle) Dog 1x 16 83 (Hypodontia) 

49 

(Beagle) Dog 1x 

Serious 

(rad) 

50 (Delayed development, altered

hindlimb splay)

200 F (Severe developmental 

abnormalities of multiple organ systems, embryo death) 

83 (Increased risk of thyroid

neoplasia)

15.6 (Increased cancer-related 

mortality - multiple tumor types) 

96 (Optic atrophy/degeneration) 
260

15.6

263

7500

272

4800

277

4623

278

3600

279

4056

Table 3-4 Levels of Significant Exposure to Cobalt - Radiation Toxicity - External Radiation (continued) 

a 

System 

Key to 

figure 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) Species (Strain) NOAEL (rad) 

LOAEL 

Less Serious Serious 

(rad) (rad) 

Cancer 

50 1x 

(Beagle) Dog 15.6 (Increased cancer-related 

mortality) 

INTERMEDIATE EXPOSURE Death 

51 Human 7500 F (Death) 

Systemic 

52 Ocular Human 4800 F (Progressive visual impairment 

and blindness) 

53 Cardio 22 - 35 d 

teletherapy 

Human 4623 (Persistent pericarditis) 

54 Gastro Human 18 d 3600 (Loose bowel movements, 

impaired absorption of vitamin B12) 

55 

Dermal 

Human 17 d

4056 F (Comedones, which were 

resolved with treatment) 
282

7500

2400

283284

4700

2400

289

4800 7200

292

1125

293

1125

Table 3-4 Levels of Significant Exposure to Cobalt - Radiation Toxicity - External Radiation (continued) 

a

Key to 

figure 

Species 

(Strain) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(rad) 

Less Serious 

(rad) 

LOAEL 

Serious 

(rad) 

56 Human Gastro 7500 F (Severe gastrointestinal 

necrosis and fibrosis) 

57 Human 3 yr Other 2400 

58 Human 7 wk 

Dermal 4700 (Reversible changes in skin 

pigmentation) 

59 

(albino) Rat 10 wk 

Other 2400 M 4800 M (Transient alterations in incisor 

histopathology) 

7200 M (Lasting alterations in incisor 

histopathology) 

60 61 

150-300 d 

(Beagle) Dog 

Immuno/ Lymphoret 

150-300 d 

(Beagle) Dog 

Hemato 1125 M (Aplastic anemia) 

1125 M (Dose- and time-related 

reduction in granulocytes, monocytes, and lymphocytes) 
294

4800

295

13150

296

55005000

298

6600

299

1282

304

1800

305

25150

Table 3-4 Levels of Significant Exposure to Cobalt - Radiation Toxicity - External Radiation (continued) 

a

Key to 

figure 

Species 

(Strain) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(rad) 

Less Serious 

(rad) 

LOAEL 

Serious 

(rad) 

Neurological 

62 Human 

4800 F (Optic nerve damage, resulting 

in visual impairment and blindness) 

63 Human 9 mo 

13150 F (Neural necrosis and gliosis) 

64 Human 

5500 M (Partial paralysis secondary to 

radiation myelopathy) 

b

5000 F (Partial paralysis secondary to 

radiation myelopathy) 

Reproductive 

65 Human 47 d 

6600 M (Calcification of the prostate) 

66 Mouse 32 wk 

1282 F (Decreased offspring per litter 

and sterility) 

Cancer 

67 Human NS 

1800 F (Basal cell carcinoma) 

68 Human 8 mo 

25150 M (Multiple basal cell carcinomas) 
307

13150

Table 3-4 Levels of Significant Exposure to Cobalt - Radiation Toxicity - External Radiation (continued) 

a

Key to 

figure 

Species 

(Strain) 

Exposure/ 

Duration/ 

Frequency 

(Specific Route) System 

NOAEL 

(rad) 

Less Serious 

(rad) 

LOAEL 

Serious 

(rad) 

CHRONIC EXPOSURE 

69 

Systemic 

Human 3 yr Cardio 13150 F (Endothelial hyperplasia, 

dysplasia, and fibrosis) 

a The number corresponds to entries in Figure 3-3. b Differences in levels of health and cancer effects between males and females are not indicated in Figure 3-3. Where such differences exits, only the levels o

sensitive gender are represented. 

Bd Wt = body weight; Cardio = cardiovascular; d = day(s); Endocr = endocrine; F = female; Gastro = gastrointestinal; Hemato = hematological; hr = hour(s); LOlowest-observed-adverse-effect level; M = male; Metab = metabolism; min = minute(s); mo = month(s); NOAEL = no observed-adverse-effect level; NS = not occupational; Resp = respiratory; wk = week(s); yr = year(s). 
Death Respiratory Cardiovascular Gastrointestinal Hematological Renal Dermal Ocular Immuno/L Neu

100000 

Hepatic ymphor 

Figure 3-3. Levels of Significant Exposure to Cobalt - Radiation Toxicity - External Radiation 

Acute (≤14 days)
 

Systemic
 

rad 

10000 8k
 

14d
 

22k 9r 1 6 6 6 6 26 

12m 16h

3m 10r 12m 19p 17p 1000 17p 7k 11m 13m 19p 21p 27m 18p 15d 19p 19p 2m 20p 29m 

2

5 5 25 2

100 

23f 23f 4 4 24 

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 
Developmental Cancer * 

Figure 3-3. Levels of Significant Exposure to Cobalt - Radiation Toxicity - External Radiation (

Acute (≤14 days) 

rad 

100000 

10000 

1000 

37r 

35r 36r 

45s 42m 38r

100 49d 33k 41m 46d 48d 

39m 44m 34r
 

40m
 

43m 

47d 48d 37r 50d 

37r 10 39m
 

39m
 

*Doses represent the lowest dose tested per study that produced a tumorigenic 

1 response and do not imply the existence of a threshold for the cancer endpoint.

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 
Death Cardiovascular Gastrointestinal Hematological Ocular Immuno/L Neurological Reproductive Cancer * 

100000 

Dermal Other ymphor 

Figure 3-3. Levels of Significant Exposure to Cobalt - Radiation Toxicity - External Radiation (

Intermediate (15-364 days) 

Systemic 

rad 

68
 

63
 

10000
 

51
 56
 59r 

65
 

64
 58
 52
 59r 62


55
 

53
 

54
 

57
 59r 

67
 

66m 

60d 61d *Doses represent the lowest dose tested per study that pro

1000
 response and do not imply the existence of a threshold for t

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 
100000 

Cardiovascular 

Figure 3-3. Levels of Significant Exposure to Cobalt - Radiation Toxicity - External Radiation (C

Chronic (≥365 days) 

Systemic 

rad 

69 

10000 

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 
 

 

 

COBALT 106 

3. HEALTH EFFECTS 

dose increases with tissue density (resulting in a higher dose to bone than soft tissue) and decreases with 

energy. Several feet of concrete or a few inches of lead are typical shield thicknesses for protection from 

gamma rays. Because it is so highly penetrating, gamma radiation released by radionuclides such as 

cobalt may be a radiation hazard to internal organs (Agency for Toxic Substances and Disease Registry 

1999; EPA 1997b). 60Co gamma rays are commonly used for human radiotherapy. The purpose of this 

section is to provide information regarding health effects associated with external exposure to a 

radioactive cobalt source. These health effects are not specific to cobalt, but apply to any radionuclide 

delivering the same beta and gamma radiation dose at a comparable dose rate. Refer to Agency for Toxic 

Substances and Disease Registry (1999) for a detailed description of health effects from external exposure 

to ionizing radiation in general. 

3.3.3.1 Death 

Exposure to high levels of external radiation, including radiation from cobalt radionuclides, may result in 

mortality when the whole body dose exceeds 300 rads. Stavem et al. (1985) reported a case in which a 

worker was exposed to 2,250 rad (22.5 Gy) within a few minutes time, resulting in death due to acute 

radiation sickness (depressed leukocyte counts, vomiting, diarrhea, etc.). Complications resulting from 

cobalt radiotherapy resulted in the death of a patient from severe gastrointestinal complications (Roschler 

and Woodard 1969). 

Norris and Poole (1969) reported on the mortality of dogs exposed to 60Co gamma rays at a rate of 35 rad 

(0.35 Gy) per day for 40 days, resulting in a cumulative exposure of 1,400 rad (14 Gy). Twelve of 

40 animals died prior to termination of the 40-day exposure period, 13 of 40 died within the 23-day postexposure observation period, and 15 survived to the end of the study period, indicating an LD50 of 

<1,400 rad at 35 rad/day. Darwezah et al. (1988) reported single, whole-body exposure LD50 values in 

mice of 913 rad (9.13 Gy) and 627 rad (6.27 Gy) at 6 and 30 days post-irradiation, respectfully. Down et 

al. (1986) reported a slightly higher LD50 of 1,400–1,450 rad (14–14.5 Gy) for 60Co thoracic irradiation in 

mice at 26 days postirradiation. Several studies have demonstrated that decreasing the dose rate or the 

portion of the body exposed will increase the LD50 for 60Co gamma rays (Darwezah et al. 1988; Down et 

al. 1986; Hanks et al. 1966; Page et al. 1968). 
COBALT 107 

3. HEALTH EFFECTS 

3.3.3.2 Systemic Effects 

Respiratory Effects. Ionizing radiation is known to exert dramatic effects on the tissue of the lung 

(Agency for Toxic Substances and Disease Registry 1999; Davis et al. 1992; Libshitz 1993; Roswit and 

White 1977), particularly at the high doses used in radiotherapy. The first phase of damage usually 

consists of radiation pneumonitis, which occurs between 3 and 13 weeks after irradiation and is 

characterized by low-grade fever, mild exertional dyspnea, congestion, and unproductive cough. The 

second phase is characterized by radiation-induced lung fibrosis, emphysema, and pleural thickening. 

Patients receiving radiotherapy treatment regimens of ≥4,000 rad (40 Gy) to the chest region almost 

always develop radiographic changes in the lung (Davis et al. 1992), whereas lower therapeutic doses 

(2,500–3,000 rad, 25–30 Gy) generally result in a lower risk of adverse pulmonary symptoms (Davis et 

al. 1992; Roswit and White 1977). Prophylactic protective measures may be taken, and these symptoms 

may be treated later if detected early enough in their progression (Roswit and White 1977). 

At similar doses, studies in animals, including rats, mice, baboons, and pigs, using 60Co radiation have 

also shown radiation pneumonitis and fibrosis, similar to effects seen in humans (Collins et al. 1978; 

Down et al. 1986; Lafuma et al. 1987; Rezvani et al. 1989). Other respiratory changes seen in animal 

experiments included an increased breathing rate, effects on the surfactant system, edema, increased 

pleural fluid content, pulmonary atrophy, and histologic alterations of the lung parenchyma (BelletBarthas et al. 1980; Collins et al. 1978; Down et al. 1986; Lafuma et al. 1987). 

Cardiovascular Effects. Martin et al. (1975) reported that 24 of 81 patients who underwent 60Co 

teletherapy for Hodgkin’s disease, using an upper mantle treatment regimen of 4,000 rad (40 Gy) over 

22–35 days, developed radiation-related pericarditis. In 14 of these patients, the condition was transient, 

while it persisted in the other 10 patients. Llena et al. (1976) presented a case wherein a 51-year-old 

woman who had received a localized dose of 13,150 rad (131.5 Gy) of 60Co radiation between the 

nasopharynx and cervical lymph nodes as part of radiotherapy developed severe alterations in the 

endothelial cells of the brain, including proliferation, increased cytoplasmic organelles, and infoldings of 

the plasma membrane. 

Whole-body exposure of Rhesus monkeys to 10,000 rad (100 Gy) over a 90-second period resulted in 

dramatic decreases in mean systemic arterial blood pressure, as well as in mean blood flow in the pons 

and pre-central gyrus, beginning at 10 minutes post-irradiation and persisting throughout the 60-minute 
COBALT 108 

3. HEALTH EFFECTS 

observation period (Cockerham et al. 1986). Bruner (1977) examined cardiovascular parameters in 

Rhesus monkeys exposed to 1,000 rad (10 Gy) at rates of 129–164 rad/minute (1.29–1.64 Gy/minute). 

Heart rate was elevated post-exposure, blood pressure was reduced near the end of exposure and 

thereafter, cardiac output increased at the end of exposure, but thereafter fell to below control levels, and 

total peripheral resistance to blood flow decreased at early times post-exposure, but thereafter rose to 

above control levels. Ten of 12 dogs irradiated with 4,355–5,655 rad (43.6–56.6 Gy), focused on the 

interatrial septum of the heart, developed cardiac arrhythmias (Dick et al. 1979). The permeability of the 

blood-brain barrier was significantly increased, particularly for hydrophillic compounds, in rats exposed 

to 2,500 rad (25 Gy) from a 60Co source (Bezek et al. 1990). 

Gastrointestinal Effects. A worker accidentally exposed to an acute whole-body dose of 2,250 rad 

(22.5 Gy) showed slight atrophy of the stomach glands, marked atrophy in the small intestine, and total 

atrophy of the glands in the large intestine (Stavem et al. 1985). Two years after a woman received 60Co 

radiation therapy amounting to 4,000 rad (40 Gy) anteriorly and 3,500 rad (35 Gy) posteriorly over a 

6-week period, she reported severe gastrointestinal difficulties, including epigastric pain, vomiting, 

bloody stools, and weight loss (Roschler and Woodard 1969), eventually resulting in death. Autopsy 

revealed dense fibrous layers around the sacrum, with severe fibrosis confirmed by microscopic 

examination. Cobalt radiotherapy for carcinoma of the bladder (~3,100–3,600 rad, 31–36 Gy, over 

18 days) resulted in loose bowel movements and a decreased absorption of vitamin B12 following oral 

exposure in 8 of 14 patients (McBrien 1973). No gastrointestinal symptoms were reported in three 

workers who were accidentally exposed to much lower exposure levels, ranging from 2.24 to 12.7 rad 

(0.022–0.127 Gy) (House et al. 1992). 

Exposure of male Sprague-Dawley rats to 850 rad (8.5 Gy) of 60Co gamma radiation resulted in marked 

alterations in drug absorption, primarily due to a decrease in gastric emptying rate (Brady and Hayton 

1977b). Exposure of young adult beagle dogs to 800 rad (8 Gy) of 60Co radiation at a rate of 

177.5 rad/minute (1.775 Gy/minute) resulted in a 100% emesis rate within 10 hours post-irradiation, with 

an average of 2.4 episodes per animal and an average time to emesis of 82 minutes (Gomez-d-Segura et 

al. 1998). King (1988a) reported a NOAEL of 49 rad (0.49 Gy) and an EC50 of 77 rad (0.77 Gy) for 

emesis and wretching following exposure of male ferrets to 60Co gamma radiation. Exposure of male 

Swiss mice to 1,000 rad (10 Gy) of 60Co radiation resulted in necrosis of the intestinal crypt cells (Devi et 

al. 1979). 
COBALT 109 

3. HEALTH EFFECTS 

Hematological Effects. No changes in hematologic parameters were reported in three workers who 

were accidentally exposed to levels ranging from 2.24 to 12.7 rad (0.022–0.127 Gy) (House et al. 1992). 

Hashimoto and Mitsuyasu (1967) reported that in 50 of 58 patients receiving local radiotherapy, irradiated 

bone marrow was more hypoplastic in the hematopoietic elements than in non-irradiated marrow in the 

same individual. A male worker exposed to 159 rad (1.59 Gy) showed minor reductions in leukocytes, 

neutrophils, and lymphocytes (Klener et al. 1986). Stavem et al. (1985) reported that a male worker 

exposed to 2,250 rad (22.5 Gy) showed a progressive decrease in hemoglobin and circulating 

thrombocytes prior to death. Autopsy showed a pronounced hypocellularity of the bone marrow. 

Seed et al. (1989) exposed male Beagle dogs to 7.5 rad/day (0.075 Gy/day) gamma radiation for 

150–700 days from a 60Co source. The irradiated dogs initially showed a significant suppression, 

compared with levels from the control animals, of the five circulating types of cells studied (granulocytes, 

monocytes, platelets, erythrocytes, and lymphocytes), which lasted ~250 days; this was followed by a 

recovery phase for the remainder of the study period. Hashimoto and Mitsuyasu (1967) exposed guinea 

pigs to whole-body 60Co radiation, and reported an initial hypoplasia of the bone marrow followed by 

recovery of hematopoietic activity by 3 weeks post-irradiation. Robbins et al. (1989b) reported 

significant reductions in erythrocyte count, hematocrit, and hemoglobin levels within 6–8 weeks of 

irradiation of the kidneys of female pigs with 980–1,400 rad (9.8–14 Gy) of 60Co gamma rays. 

Musculoskeletal Effects. No studies were located regarding musculoskeletal effects in humans or 

animals following external exposure to 60Co radiation. These tissues are among the most radioresistant in 

both humans and animals. 

Hepatic Effects. No studies were located regarding hepatic effects in humans following external 

exposure to 60Co radiation. 

No changes in liver weight were seen in male Swiss mice exposed to 1,000 rad (10 Gy) of 60Co radiation 

and examined every 4 hours for 24 hours post-irradiation (Mazur et al. 1991). Andrzejewski et al. (1980) 

reported increased respiration rates in rat liver mitochondria after whole-body exposure to 1,000 or 

3,000 rad (10 or 30 Gy) of 60Co radiation; the increase was greater and more persistent at the higher dose 

level. 
COBALT 110 

3. HEALTH EFFECTS 

Renal Effects. Stavem et al. (1985) reported that a 64-year-old man who accidentally received a fatal 

dose (2,250 rad) of cobalt radiation developed enlarged kidneys. No other studies were located regarding 

renal effects in humans after external exposure to cobalt radiation. 

Robbins et al. (1989a, 1989b, 1989c, 1991a, 1991b) performed a series of studies in female White pigs 

wherein the kidneys of the animals were exposed to single doses of 780–1,400 rad (7.8–14 Gy) of 60Co 

radiation and examined for periods up to 24 weeks postirradiation. Irradiation resulted in an initial 

increase in glomerular filtration rate (GFR), followed by a dose-related decrease in the GFR, beginning at 

4 weeks postexposure. Effective renal plasma flow (ERPF) was also decreased in a dose-related manner 

beginning at 4 weeks postexposure, but did not show the initial increase seen in GFR. Some recovery of 

GFR and ERPF occurred by 24 weeks postirradiation, though values were still significantly reduced 

below controls in all groups but the 780 rad (7.8 Gy) group. Histology was performed on animals 

exposed to 980 rad (9.8 Gy) and killed between 2 and 24 weeks after exposure. Beginning at 2 weeks 

postirradiation, increased numbers of inflammatory cells were present within the glomerulus, and there 

was an increase in mesangial matrix and number of mesangial cells. The glomerular changes continued 

to progress in severity throughout the observation period, with generalized thickening of the capillary 

walls, extensive duplication of the basement membrane, and progressive inflammation. Tubular changes 

appeared to be maximal at 6 weeks, including focal degeneration and necrosis, with partial recovery at 

later timepoints. 

Endocrine Effects. Prager et al. (1972) reported that 5 of 23 patients receiving cobalt radiotherapy 

(3,900–4,600 rad, 39–46 Gy) for Hodgkin’s disease developed hypothyroidism, with substantial decreases 

in levels of T4 relative to patients with normal thyroids. Chang et al. (2001) examined the residents of 

60Co-contaminated buildings for effects on the thyroid. There was an increased prevalence of goiter in 

males of all ages and females <15 years of age, as well as a dose-related increase in the prevalence of 

thyroid cysts in females of all ages, and elevated tri-iodothyronine levels in males <15 years of age. No 

other studies examining the endocrine effects of radioactive cobalt exposure, either internal or external, in 

humans were located. 

Whole-body acute exposure of rats to 330 rad (3.3 Gy) did not affect FSH, LH, or testosterone levels 

(Cunningham and Huckins 1978). Similarly, male Wistar rats exposed to a single dose of 80 rad (0.8 Gy) 

of testicular radiation showed no changes in FSH, LH, prolactin, or testosterone (Laporte et al. 1985). No 
 

 

 

COBALT 111 

3. HEALTH EFFECTS 

other studies examining the endocrine effects of radioactive cobalt exposure, either internal or external, in 

animals were located. 

Dermal Effects. Several studies in humans have demonstrated that high-dose exposure to cobalt 

radiation can result in damage to the skin. Klener et al. (1986) described the accidental irradiation of a 

worker who was attempting to bring under control a sealed 60Co source. The patient’s left palm (the 

patient was left-handed) developed an irregular oval defect 3x4 cm with whitish edges and bleeding, as 

well as superficial lesions on the third and fourth finger. Considerable spontaneous pain required the 

administration of analgesics. The lesions showed no tendency to heal, instead spreading to the adjacent 

digits. After several failed skin graft attempts, the condition worsened, necessitating the amputation of 

fingers five through two. Walter (1980) reported that a patient who had undergone 60Co radiotherapy 

(dose not reported) of the forehead and scalp developed a pronounced acneform reaction, characterized 

primarily by alopecia with multiple open comedones on the scalp and forehead, and hair loss. With 

treatment, the comedones were 80% cleared at 9 months post-diagnosis (13 months post-treatment), but 

no hair regrowth was noted. Myskowski and Safai (1981) have likewise reported localized comedones in 

a patient following 4,056 rad (40.6 Gy) of 60Co radiotherapy. Van Oort et al. (1984) reported that patients 

receiving 4,700–6,000 rad (47–60 Gy) of 60Co radiotherapy over a 7-week period showed significant 

differences in baseline color of the skin, primarily erythema, and pigmentation, beginning the third week 

of exposure and persisting throughout the fifth week postirradiation (study week 12). Johansson et al. 

(2000) reported that 86% of women who had been treated with 5,400–5,700 rad (54–57 Gy) after a 

radical mastectomy developed fibrosis of the skin of the treated area. 

Cox et al. (1981) reported a dose-related loss of hair in rabbits exposed to 1,730–3,210 rad 

(17.3–32.1 Gy) 60Co gamma rays, targeted at the skin near the eyes or of the ears, with recovery initially 

noted in animals exposed to 2,140 rad (<21.4 Gy) by day 200 postirradiation. Beginning at day 

500 postirradiation, a substantial loss of hair again was seen, persisting throughout the end of the study. 

Mice exposed to 1,800 rad (18 Gy) of 60Co radiation showed a slight increase in epilation score (Down et 

al. 1986). 

Ocular Effects. Exposure to high-dose radiation from cobalt sources has been shown to result in 

effects on the eye, in particular the development of cataracts. Augsburger and Shields (1985) described 

13 patients who developed cataracts following 60Co plaque radiotherapy; estimated doses to the eyes 

ranged from 2,000 to 10,000 rad (20–100 Gy). Fishman et al. (1976) reported on two patients who 
 

 

 

COBALT 112 

3. HEALTH EFFECTS 

received head-only 60Co radiotherapy, in combination with chemotherapy, for the treatment of acute 

lymphocytic leukemia. Both patients, who received 2,400 rad (24 Gy) over an initial 16-day course of 

treatment followed later by either 2,400 or 2,500 rad (24 or 25 Gy) in followup therapy, developed 

progressively severe vision disorders, resulting in partial or total blindness. Exposure of a male worker to 

a whole-body dose of 159 rad (1.59 Gy) of 60Co radiation resulted in a progressive deterioration of visual 

acuity, due to cataract development, in the left eye (which was more exposed than the right) over time 

(Klener et al. 1986). Chen et al. (2001) evaluated subjects that had been exposed to 120–194 mSv (range: 

1.11–1493.4 mSv) for an undisclosed period of time for lenticular opacities. Subjects <20 years old 

showed a dose-dependent increase in the numbers of focal lens defects, while for those aged 20–40 and 

>40, no such statistical correlation was seen. 

Other Systemic Effects. Thibadoux et al. (1980) reported that of 61 children receiving a course of 

2,400 rad (24 Gy) of cranial radiotherapy, none developed significant reductions in hearing levels by the 

end of the third year after irradiation. 

Taiwanese children (48 boys, 37 girls) who were raised in apartments contaminated with 60Co were 

compared to 21,898 age- and sex-matched nonexposed children from a nationwide surveillance program 

(Wang et al. 2001). After adjusting for effects from parental heights and body mass index, clear doserelated decreases in height percentile (HP) and age-specific relative height differences (RHD) were seen 

in exposed boys, but not in exposed girls. Average cumulative doses were 120.8 and 129.9 mSv for the 

boys and girls, respectively. 

Sweeney et al. (1977) examined the effects of 60Co radiation on the teeth of rats exposed to 0, 2,400, 

4,800, or 7,200 rad (0, 24, 48, or 72 Gy). Animals exposed to 4,800 rad (48 Gy) showed transient effects 

on the incisors only, while at 7,200 rad (72 Gy), the effects lasted throughout the 10-week study period. 

3.3.3.3 Immunological and Lymphoreticular Effects 

A worker accidentally exposed to an acute dose of 2,250 rad (22.5 Gy) showed a rapid fall in circulating 

lymphocytes and granulocytes prior to death (Stavem et al. 1985). Chronic exposure to low amounts of 

60Co radiation in people living in a contaminated building significantly reduced the numbers of circulating 

CD4+ lymphocytes in the blood (Chang et al. 1997, 1999b); mean total radiation dose was estimated to be 
 

 

COBALT 113 

3. HEALTH EFFECTS 

0.169 Gy (16.9 rad) over a 2–13-year period. Similarly, children chronically-exposed to low levels 

(estimated dose of 0.002–0.085 Gy [0.2–8.5 rad]) of 60Co radiation in a contaminated kindergarten 

building showed significant decreases in total leucocytes and neutrophils, but an increase in eosinophils, 

5–7 years after exposure had ceased (Chang et al. 1999a). 

In male Swiss mice exposed to 1,000 rad (10 Gy) of 60Co radiation, significant decreases in weight of the 

spleen were seen as early as 1 hour post-exposure and persisted throughout the following 24 hours (Mazur 

et al. 1991). Spleen acid phosphatase activity, expressed as activity per gram of protein, was significantly 

increased in irradiated animals beginning at 13 hours post-exposure. 

3.3.3.4 Neurological Effects 

Exposure of both humans and animals to high doses of cobalt radiation has been shown to result in 

damage to nervous tissue, particularly peripheral nerves. Llena et al. (1976) presented a case wherein a 

51-year-old woman who had received 13,150 rad (131.5 Gy) of 60Co radiation between the nasopharynx 

and cervical lymph nodes as part of radiotherapy developed focal necrosis of the brain in the frontal lobe, 

as confirmed by gross and microscopic examination. Fishman et al. (1976) reported on two patients who 

received head-only 60Co radiotherapy, in combination with chemotherapy, for the treatment of acute 

lymphocytic leukemia. Both patients, who received 2,400 rad (24 Gy) over an initial 16-day course of 

treatment followed later by either 2,400 or 2,500 rad (24 or 25 Gy) in followup therapy, developed 

progressively severe vision disorders, resulting in partial or total blindness. Histopathology from one 

patient demonstrated severe alterations in the optic nerve, including severe atrophy, terminal beading, 

lack of myelin, and calcification. Sanyal et al. (1979) reported on five patients who received doses of 

4,500–6,000 rad (45–60 Gy) 60Co radiation as radiotherapy, who developed varying degrees of 

myelopathy, resulting in minimal to mild paralysis. In patients that had been treated with 60Co radiation 

(total dose of 54–57 Gy, or 5,400–5,700 rad) following mastectomy, 63% developed brachial plexus 

neuropathy and 5% developed vocal chord paresis over the 30-year period reported by the study 

(Johansson et al. 2000). 

Mele et al. (1988) exposed male rats to 50, 150, or 450 rad (0.5, 1.5, or 4.5 Gy) 3 times, at 43-day 

intervals, and examined them for changes in behavior daily for 30 days following each exposure. Rats 

exposed to 450 rad (4.5 Gy), but not those exposed to 150 rad (1.5 Gy) or 50 rad (0.5 Gy), showed 
 

 

COBALT 114 

3. HEALTH EFFECTS 

significant deficits in fixed-ratio response rates and running rates after each exposure, beginning the day 

after exposure and persisting for 4–5 days, after which both rates returned to normal. After the third 

exposure, all rats were exposed to 650 rad (6.5 Gy), which resulted in similar performance decrements as 

were seen in the 450 rad (4.5 Gy) animals, again beginning 24 hours after exposure, with previous 

exposure resulting in no differences in behavioral parameters. Maier and Landauer (1989) reported 

significant decreases in offensive behavior in mice acutely exposed to whole-body doses of 500 or 

700 rad (5 or 7 Gy), but not those exposed to 300 rad (3 Gy), with changes occurring in the second week 

postirradiation and responses returning to normal by day 19 postirradiation. Rabin et al. (1998) reported 

that exposure of rats to 60Co radiation (up to 30 Gy or 3,000 rad) showed a dose-related decrease in the 

acquisition of controlled taste aversion behavior. Bassant and Court (1978) reported that rabbits exposed 

to 450 rad (4.5 Gy) of 60Co radiation whole-body showed an altered activity of hippocampal cells, with a 

slowed mean discharge rate and increased interspike variability persisting for at least 12 hours 

postirradiation. 

3.3.3.5 Reproductive Effects 

Ionizing radiation in general, and gamma-emitting isotopes in particular, is known to have profound 

effects on reproductive tissues, with effects seen primarily in rapidly-dividing germ cells resulting in 

temporary or permanent sterility in both sexes, as well as other effects (Agency for Toxic Substances and 

Disease Registry 1999). These effects are usually observed only at high radiation doses. Keys and Reed 

(1980) reported a case of a man who, as treatment for a prostate tumor, received an estimated dose of 

6,600 rad (66 Gy) to the prostate over a 47-day period, and who later developed a severe prostatic 

calcification necessitating surgical correction. 

60Co radiation at high doses has been shown to elicit profound decrements in reproductive ability in 

animal species. Whole-body acute exposure of rats to 330 rad (3.3 Gy) decreased testicular weights 

beginning at 22 days postirradiation, with recovery of testicular weight beginning about day 

65 (Cunningham and Huckins 1978). Histologic examination of the testes revealed destruction of the 

spermatogonial population, with a slow recovery as the spermatogonial population was rebuilt from the 

surviving stem cells. Searl et al. (1976) reported that exposure of male mice to 1,128 rad (11.3 Gy) over a 

28-week period resulted in significant reductions of testis mass and epididymal sperm count. Male Wistar 

rats exposed to a single dose of 80 rad (0.8 Gy) to the testes showed increased tubular fluid production 
COBALT 115 

3. HEALTH EFFECTS 

and decreased testicular weight at 30 and 45 days postirradiation, but not at later time points (Laporte et 

al. 1985). Single doses of >100 rad (1 Gy) of 60Co radiation caused decreased fertility in exposed female 

mice (Philippe 1975). Continuous exposure of female mice to an average daily dose of 8 or 16 rad/day 

(0.08 or 0.16 Gy/day) caused a decreased number of offspring per litter and decreased reproductive 

performance, with 100% sterility occurring at 32 weeks of exposure at 8 rad/day (0.08 Gy/day) or 

20 weeks of exposure at 16 rad/day (0.16 Gy/day) (Searl et al. 1980). Female rabbits exposed to 400 rad 

(4 Gy) prior to implantation showed dramatic decreases in implantation (Chang et al. 1963). 

3.3.3.6 Developmental Effects 

No studies were located regarding developmental effects in humans after external exposure to cobalt 

radiation. 

In utero exposure to cobalt radiation has been extensively studied in animal species, and may elicit 

substantial effects across many organ systems of the developing organism. Effects have been noted 

following single-dose exposures as low as 10 rad (0.10 Gy) in mice (Devi et al. 1994; Wang et al. 1993), 

50 rad (0.5 Gy) in rats (Bruni et al. 1994), 200 rad (2 Gy) in hamsters (Harvey and Chang 1962), 250 rad 

in rabbits (Chang et al. 1963), 15.6 rad (0.16 Gy) in dogs (Benjamin et al. 1998a, 1998b), and 100 rad 

(1 Gy) in monkeys (Brizzee et al. 1978). Organs known to be affected include the brain (Brizzee et al. 

1978; Bruni et al. 1994; Devi et al. 1994; Hamilton et al. 1989; Reyners et al. 1992; Schmidt and Lent 

1987), eyes (Brizzee et al. 1978; Bruni et al. 1994; Schweitzer et al. 1987), hair (Hirobe 1994; Hirobe and 

Zhou 1990), kidney (Benjamin et al. 1998a; Brizzee et al. 1978), liver (Devi et al. 1998), ovaries (Inano et 

al. 1989), pituitary (Brizzee et al. 1978), skeleton (including cleft palate, shortened digits, fused digits, 

and other gross abnormalities) (Bruni et al. 1994; Chang et al. 1963; Harvey and Chang 1962), spleen 

(Devi et al. 1998), teeth (Lee et al. 1989), testes (Inano et al. 1989; Suzuki et al. 1990), and thyroid 

(Benjamin et al. 1997). 60Co radiation in utero has also shown to cause functional alterations, including 

postnatal growth retardation (Wang et al. 1993; Zhong et al. 1996), neurobehavioral changes (Brizzee et 

al. 1978; Wang et al. 1993), hormonal production (Brizzee et al. 1978; Inano et al. 1989; Suzuki et al. 

1990), alterations in hepatic enzymes (Inano et al. 1990), and diabetes mellitus (Benjamin et al. 1998a). 

In utero irradiation with cobalt also leads to increased tumor incidence later in life (Benjamin et al. 1991, 

1997, 1998b; Nitta et al. 1992). 
 

 

 

 

COBALT 116 

3. HEALTH EFFECTS 

Devi et al. (1994) exposed pregnant mice to a single dose of 0–50 rad (0–0.50 Gy) of 60Co radiation on 

day 11.5 of gestation. A significant decrease in pup brain weight and an increase in the incidence of 

microphthalmia was seen at 10 rad (0.10 Gy), with decreases in head width, head length, body length, and 

body weight occurring at higher doses. A later study (Devi et al. 1998) found decreases in body weight, 

liver weight, and spleen weight in pups 72 hours after irradiation with 25 rad (0.25 Gy) of 60Co radiation 

on day 17 of gestation. Male offspring, but not female offspring, of mice exposed to 50 rad (0.5 Gy) on 

gestation day 9 showed decreased body weights on postnatal days 0, 3, and 7, while offspring of both 

sexes showed delays in pinna detachment, incisor eruption, eye opening, and testes descent (Zhong et al. 

1996). Wang et al. (1993) reported that mice exposed to a cumulative in utero dose of 10 rad (0.10 Gy) 

showed alterations in visual placing reflex tests, while those exposed to 20 or 40 rad (0.20 or 0.40 Gy) 

showed decreased mean body weight, delayed eye opening, and alterations in the air righting reflex. 

Rats exposed to 50 rad (0.50 Gy) of 60Co radiation on gestational day 9.5 showed histologic damage to 

the neuro-epithelium 4 hours post-exposure, with abnormal flexion of the embryo and abnormal flexion 

of the head at 48 hours post-exposure (Bruni et al. 1994). At birth, rats showed increased incidence of 

defective eye development, spinal curvature, and visceral anomalies. Reyners et al. (1992) reported 

decreased brain weight in 3-month-old rats that had been exposed to cumulative doses of 160 rad (1.6 Gy) 

over gestation days 12–16 or 170 rad (1.7 Gy) over gestation days 14–20. Male rats exposed to 210 rad 

(2.1 Gy) on day 20 of gestation showed atrophy of the testes, prostates, and seminal vesicles, as well as a 

complete disappearance of germinal cells within the testes, on postnatal day 70 (Suzuki et al. 1990). 

Inano et al. (1989) exposed rats on gestation day 20 to 260 rad (2.6 Gy) of 60Co radiation. Seminiferous 

tubules of male offspring and ovaries of female offspring showed pronounced atrophy, and steroid 

hormone production was significantly altered. 

Benjamin et al. (1997, 1998a, 1998b) exposed groups of pregnant Beagle dogs to 15.6–17.5 or 

80.8–88.3 rad (0.15–0.175 or 0.8–0.88 Gy) of 60Co radiation on day 8, 28, or 55 post-breeding. Animals 

were allowed to live their full life span and were observed for radiation-related illnesses and cause of 

death. No change in the mean age at death was seen as a result of exposure. Males exposed to either 

exposure level at day 55 post-breeding, but not females at any time or males exposed at days 8 or 28, 

showed an increase in deaths due to renal disease. High-dose females exposed on days 28 or 55 showed 

an increase in the frequency of diabetes mellitus. Both sexes showed an increase in malignant neoplasias 

in general when exposed to radiation at 8 or 55 days postcoitus, but not at 28 days, while females exposed 

on day 55 also showed an increase in lymphoid neoplasia. A similar exposure on day 28 or 55 postcoitus 
COBALT 117 

3. HEALTH EFFECTS 

also resulted in a dose-dependent decrease in brain weight (Hamilton et al. 1989). In utero radiation of 

dogs to higher doses (100–380 rad [1–3.8 Gy]) resulted in retinal dysplasia and atrophy (Schweitzer et al. 

1987). 

3.3.3.7 Cancer 

The carcinogenic effects of high doses of ionizing radiation have been well documented (Agency for 

Toxic Substances and Disease Registry 1999), though the effects of lower doses are less clearly defined. 

Duncan et al. (1977) reported on a cohort of patients who had received radiotherapy for carcinoma of the 

cervix. Eight of 2,674 patients developed bladder tumors within 6 months to 20 years following 

irradiation; the incidence rate was over 57 times greater than the general female population. All eight 

patients had received high (therapeutic) doses of 60Co irradiation, though five of the eight also received 

radium therapy in conjunction with 60Co irradiation. Wollenberg et al. (1995) presented a case of a 

55-year-old farmer who received a total of 25,150 rad (251.5 Gy) distributed over six areas of the body 

over an 8-month period as a 60Co teletherapy treatment regimen. Twenty years after irradiation, the 

patient developed a total of 43 basal cell carcinomas of the skin over the treated areas, all of which were 

successfully removed with cryosurgery. A 2-year-old girl exposed to 1,800 rad (18 Gy) of 60Co radiation 

as part of a treatment regimen for acute lymphoblastic leukemia L1 developed, at age 12, a basal cell 

carcinoma of the scalp (Garcia-Silva et al. 1996). Three patients receiving cobalt irradiation as part of a 

chemotherapy/radiation treatment developed basal cell carcinoma of the scalp 8–15 years after treatment 

in the area of radiation treatment (Dinehart et al. 1991). 

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 cobalt 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. 
COBALT 118 

3. HEALTH EFFECTS 

3.4 GENOTOXICITY 

Stable Cobalt. No studies were located regarding genotoxic effects in humans following oral or dermal 

exposure to cobalt. No studies were located regarding genotoxic effects in animals following inhalation 

exposure to cobalt. 

Gennart et al. (1993) examined a cohort of 26 male workers who had been occupationally-exposed to 

cobalt, chromium, nickel, and iron. Analysis of variance on sister-chromatid exchange rank values 

revealed that exposure status (exposed vs. controls) and smoking habits had statistically significant 

effects. De Boeck et al. (2000) reported no significant change in the comet assay on lymphocytes from 

nonsmoking workers who had been occupationally exposed to cobalt or hard metal dusts; a positive 

association was found between hard metal exposure and increased micronucleus formation in smokers 

only. 

Single oral exposure of male Swiss mice to 0, 4.96, 9.92, or 19.8 mg cobalt/kg as cobalt chloride resulted 

in significantly increased percentages of both chromosomal breaks and chromosomal aberrations in bone 

marrow cells, with significant linear trends toward increasing aberrations with increased exposure (Palit et 

al. 1991a, 1991b, 1991c, 1991d). 

Results of genetic testing of cobalt are presented in Table 3-5. Several different forms of cobalt, 

including cobalt chloride and cobalt sulfide, were tested. No profound differences were found among the 

various forms. 

Cobalt was found to be generally nonmutagenic in bacteria (Salmonella typhimurium, Escherichia coli) 

and yeast when compounds with a valence state of II were tested (Arlauskas et al. 1985; Fukunaga et al. 

1982; Kanematsu et al. 1980; Kharab and Singh 1985; Ogawa et al. 1986; Singh 1983; Tso and Fung 

1981). A very weak mutagenic response was found with Bacillus subtilis (Kanematsu et al. 1980). A 

mutagenic response to cobalt was found, however, when compounds with a valence state of III were 

tested in S. typhimurium and E. coli (Schultz et al. 1982). The authors suggested that this may be due to 

the formation of cobalt(III) complexes that are inert to ligand substitution, allowing optimal interaction of 

cobalt with genetic material (Schultz et al. 1982). Other studies have shown cobalt to be a comutagen in 

combination with 4-substituted pyridines in S. typhimurium (Ogawa et al. 1988). It has been reported that 

cobalt acts as an antimutagen in bacterial (S. typhimurium, B. subtilis, E. coli) and yeast test systems 
 

 

 

 

 

 

 

COBALT 119 

3. HEALTH EFFECTS 

Table 3-5. Genotoxicity of Cobalt In Vitro 

Results 

With Without Valence 

Species (test system) End point activation activation Reference state 

Stable Cobalt 

Prokaryotic organisms: 

Salmonella typhimurium 

(plate incorporation) 

Gene mutations No data – Tso and Fung 

1981 

II 

S. typhimurium (plate 

incorporation) 

Gene mutations No data – Arlauskas et al. 

1985 

II 

S. typhimurium (plate 

incorporation) 

Gene mutations No data – Ogawa et al. 1986 II 

S. typhimurium (plate 

incorporation) 

Gene mutations No data + Schultz et al. 1982 III 

Bacillus subtilis (rec assay) Gene mutations No data (+) Kanematsu et al. 

1980 

II 

Escherichia coli (reversion 

assay) 

Gene mutations No data – Kanematsu et al. 

1980 

II 

E. coli (repair assay) DNA damage No data + Schultz et al. 1982 III 

Eukaryotic organisms: 

Fungi: 

Saccharomyces cerevisiae 

(plate assay) 

Reversion No data – Kharab and Singh 

1985 

II 

S. cerevisiae (plate assay) Reversion No data – Fukunaga et al. 

1982 

II 

S. cerevisiae (plate assay) Reversion No data – Singh 1983 II 

S. cerevisiae (plate assay) Conversion No data + Kharab and Singh 

1985 

II 

S. cerevisiae (plate assay) Conversion No data + Fukunaga et al. 

1982 

II 

S. cerevisiae (plate assay) Conversion No data + Singh 1983 II 

Mammalian cells: 

Hamster ovary cells Clastogenic 

effects 

No data + Hamilton-Koch et 

al. 1986 

II 

Hamster embryo cells Transformation No data + Costa et al. 1982 II 

Human lymphocytes Sister chromatid 

exchange 

No data + Andersen 1983 II 

Human HeLa cells Inhibition of DNA No data + Painter and II 

synthesis Howard 1982 

Human diploid fibroblasts DNA damage No data + Hamilton-Koch et 

al. 1986 

II 
 

 

 

 

 

 

 

COBALT 120 

3. HEALTH EFFECTS 

Table 3-5. Genotoxicity of Cobalt In Vitro 

Results 

With Without Valence 

Species (test system) End point activation activation Reference state 

Radioactive Cobalt 

Mammalian cells: 

Chinese hamster ovary DNA amplification No data + Luecke-Huhle et N/A 

cells al. 1986 

Hamster embryo cells DNA amplification No data + Luecke-Huhle et N/A 

al. 1990 

 Mouse lymphosarcoma Chromosomal No data + Juraskova and N/A 

cells aberrations Drasil 1987 

 Mouse lymphosarcoma Sister-chromatid No data + Juraskova and N/A 

cells exchanges Drasil 1987 

 Human lymphocytes Chromosomal No data + Koksal et al. 1995 N/A 

aberrations 

 Human lymphocytes Micronucleus No data + Koksal et al. 1996 N/A 

formation 

Human leukocytes DNA strand No data + Rueff et al. 1993 N/A 

breaks 

 Human leukocytes Chromosomal No data + Rueff et al. 1993 N/A 

aberrations 

 Human leukocytes Chromosome No data + Lindahl-Kiessling N/A 

breaks et al. 1970 

Human fibroblasts Transformation No data + Namba et al. 1981 N/A 

Human fibroblasts Transformation No data + Namba et al. 1985 N/A 

Human fibroblasts DNA strand No data + Coquerelle et al. N/A 

breaks 1987 

Human fibroblasts Transformation No data + Namba et al. 1988 N/A 

 Human fibroblasts Retinoblastoma No data + Endo et al. 1993 N/A 

gene alterations 

Human fibroblasts DNA strand No data + Dolling et al. 1998 N/A 

breaks 

Human kidney cells DNA strand No data + Feinendegen et al. N/A 

breaks 1977 

Human kidney cells DNA strand No data + Feinendegen et al. N/A 

breaks 1978 

DNA = deoxyribonucleic acid; + = positive results; – = negative results; (+) = weakly positive results 
COBALT 121 

3. HEALTH EFFECTS 

(Saccharomyces cerevisiae) (Inoue et al. 1981; Kada et al. 1986; Kuroda and Inoue 1988). A possible 

explanation was that cobalt acts by correcting the error-proneness of deoxyribonucleic acid (DNA) 

replicating enzymes by improving their performance in DNA synthesis (Inoue et al. 1981; Kada et al. 

1986; Kuroda and Inoue 1988). However, cobalt has also been shown to increase the frequency of 

genetic conversions in S. cerevisiae (Kharab and Singh 1985; Singh 1983). The reasons for this apparent 

dichotomy in yeast cells is not known. 

In contrast to the results seen in bacteria, stable cobalt compounds were generally found to be genotoxic 

or mutagenic in mammalian assay systems. Exposure to cobalt compounds (metal, salts, or hard metal) 

has been shown to produce clastogenic effects in mammalian cells, including human lymphocytes (Anard 

et al. 1997; Hamilton-Koch et al. 1986; Painter and Howard 1982); transformation in hamster cells (Costa 

et al. 1982); sister chromatid exchanges in human lymphocytes (Andersen 1983); and micronucleus 

formation in mouse bone marrow cells (Suzuki et al. 1993) and human lymphocytes (Capomazza and 

Botta 1991; Olivero et al. 1995; Van Goethem et al. 1997). Hard metal is generally more genotoxic in in 

vitro tests than other cobalt compounds. Cobalt ions are also thought to inhibit DNA repair in 

mammalian cells by interaction with zinc-finger proteins involved in DNA excision repair (Asmuß et al. 

2000; De Boeck et al. 1998; Hartwig et al. 1991; Kasten et al. 1997; Sarkar 1995). 

Thirty hours following single intraperitoneal injection of cobalt(II) chloride in BALB/c mice, an increase 

in micronucleus formation was seen at 12.4 or 22.3 mg cobalt/kg (as cobalt chloride), but not at 

6.19 mg/kg (Suzuki et al. 1993). Single injection of mg cobalt/kg (as cobalt chloride) resulted in 

significantly increased micronucleus formation at 24 hours post-injection, but not at 12, 48, 72, or 

96 hours. Two or 10 days following intraperitoneal injection of male and female F344 rats with 3 or 6 mg 

cobalt/kg, increased levels of oxidatively-damaged DNA bases were noted in the liver, kidney, and to a 

lesser extent, the lung (Kasprzak et al. 1994). 

Radioactive Cobalt. The ability of ionizing radiation to induce genotoxic damage is well-documented 

(Agency for Toxic Substances and Disease Registry 1999). Chang et al. (1999c) reported increased 

micronucleus frequency, both of single and multiple nucleates, in 48 people who had been exposed to 

12–1,600 rad (0.12–16 Gy) over a 2–10-year period as a result of a building contaminated with 60Cocontaining steel. Subjects who had left the building showed a decrease in micronucleus formation that 

correlated with time since cessation of exposure. Three workers accidentally exposed to 2.2–12.7 rad 

(0.022–0.127 Gy) showed no elevation in frequency of chromosome alterations (House et al. 1992). Ten 
COBALT 122 

3. HEALTH EFFECTS 

children who received chemotherapy and 1,725–2,405 rad (17.25–24.05 Gy) as cobalt radiotherapy for 

acute lymphatic leukemia showed no clastogenic changes after chemotherapy but before irradiation. 

After radiotherapy, significant dose-related increases in chromosomal aberrations were seen (Rauscher 

and Bauchinger 1983). 

Radiation from cobalt isotopes has been shown to induce numerous genetic changes, including 

translocations (Gilot-Delhalle et al. 1988; Grahn and Carnes 1988; Grahn et al. 1983; Searl et al. 1976), 

decreased DNA synthesis (Lohmann et al. 1966), dominant lethal mutations (Grahn et al. 1988; Searl et 

al. 1976; Zhou et al. 1986), chromosome deletions (Brooks et al. 1971b, 1974), polycentrics (Brooks et al. 

1971a, 1974), and aberrations (Brooks et al. 1971a, 1971b) in exposed animals. 

Radiation from cobalt isotopes was genotoxic in several assay systems in mammalian cells: DNA 

amplification in hamster cells (Lucke-Huhle et al. 1986, 1990); chromosomal aberrations and sisterchromatid exchanges in mouse lymphosarcoma cells (Juraskova and Drasil 1987); chromosomal 

aberrations and micronucleus formation in human lymphocytes (Koksal et al. 1995, 1996; Schmid et al. 

2002); DNA breakage in human leukocytes (Lindahl-Kiessling et al. 1970; Reuff et al. 1993), kidney cells 

(Feinendegen et al. 1977), and fibroblasts (Coquerelle et al. 1987; Dolling et al. 1998); chromosomal 

aberrations in human leukocytes (Reuff et al. 1993); transformation of human fibroblasts (Namba et al. 

1981, 1985, 1988); and retinoblastoma gene alterations in human fibroblasts (Endo et al. 1993). 

3.5 TOXICOKINETICS 

3.5.1 Absorption 

3.5.1.1 Inhalation Exposure 

Inhaled cobalt particles are deposited in the upper and lower respiratory tract and cobalt is subsequently 

absorbed by several mechanisms (Casarett and Doull 1986); however, two of these mechanisms in 

particular appear to be most relevant. The deposition pattern in the respiratory tract is related to particle 

size, which determines the degree to which particles are affected by inertial impaction, sedimentation, 

diffusion, and electrostatic precipitation. Large particles (diameter >2 μm) tend to deposit in the upper 

respiratory tract where high airstream velocities and airway geometry promote inertial impaction of larger 

particles. Smaller particles escape inertial impaction and enter the lower respiratory tract where lower 
COBALT 123 

3. HEALTH EFFECTS 

airstream velocities and airway geometry favor the process of sedimentation, diffusion, and electrostatic 

precipitation of small particles. Fractional deposition can be expected to vary considerably with age, 

particle size, and breathing patterns (see Table 3-10). Fractional deposition of inhaled cobalt oxide 

particles in humans varied from approximately 50% of the inhaled dose for particles with a geometric 

mean diameter of 0.8 μm to approximately 75% of the inhaled dose for particles with a geometric mean 

diameter of 1.7 μm (Foster et al. 1989). 

The transfer pathways of cobalt oxide (57Co used as a tracer) from the lungs in humans and animals are 

shown in Figure 3-4. Particles of cobalt deposited in the respiratory tract can be absorbed into the blood 

after dissolution (S(t)) or mechanically transferred to the gastrointestinal tract by mucociliary action of the 

respiratory tract and swallowing action (M(t)). Only a portion (probably <50%) of the cobalt that enters 

the gastrointestinal tract will be absorbed into the body. The relative magnitude of the translocation and 

mechanical clearance pathways depends on the size and solubility of the cobalt particles that are inhaled. 

Large particles (>2 μm) will tend to deposit in the middle and upper airways where mechanical clearance 

mechanisms predominate over translocation. Smaller particles that enter the lower respiratory tract will 

tend to remain until dissolved or phagocytized by macrophages and translocation occurs. The sum of the 

activities of translocation and mechanical clearance determine the kinetics of absorption of inhaled cobalt. 

In humans, the ratio of translocation (S(t)) to mechanical clearance (M(t)) is approximately 5–1 for 

particle sizes ranging from 0.8 to 1.7 μm (mean geometric diameter) (Foster et al. 1989). 

Data on retention of cobalt oxide (57Co used as a tracer) in the respiratory tracts of humans and several 

animal species are summarized in Table 3-6. Considerable variability exists among species. In humans, 

almost one-half of the original lung burden persisted 6 months after exposure; in rats, clearance of cobalt 

from the lungs was nearly complete after 6 months. The elimination half-time for cobalt in the human 

lung increased with increasing time after exposure (Foster et al. 1989; Sedlet et al. 1958). This may 

reflect slower clearance of cobalt that is bound to cellular components in the lung (Kreyling et al. 1985, 

1986). 
 

Lungs 

Blood GI Tract

Urine Feces

S(t) M(t)

buS(t) bfS(t) guM(t) gfM(t) 

U(t) F(t) 

COBALT 124 

3. HEALTH EFFECTS 

Figure 3-4. Transfer Parameters for Cobalt Following Inhalation of Cobalt Oxide* 

(CO3O4) Particles, Showing the Fractions of the Lung Content, L(t), and Time, t, 

Cleared Per Day by Each Route** 

GI tract = gastrointestinal tract; 

bfS(t) = fraction of cobalt excreted in the feces after translocation; 

buS(t) = fraction of cobalt excreted in the urine after translocation; 

F(t) = fecal excretion rate; 

gfM(t) = fraction of cobalt excreted in the feces after mechanic clearance to the gastrointestinal tract; 

guM(t) = fraction of cobalt excreted in the urine after mechanic clearance to the gastrointestinal tract; 

M(t) = rate of mechanical transport of cobalt particles from the lungs to the gastrointestinal tract; 

S(t) = rate of translocation of cobalt from the lungs to the blood; 

U(t) = urinary excretion rate 

*Cobalt-57 tracer used 

**Derived from Bailey et al. 1989 
 

 

COBALT 125 

3. HEALTH EFFECTS 

Table 3-6. Initial (Day 3) Lung Deposits of Cobalt Oxide and Summary of Lung 

Retention at 90 and 180 Daysa,b
 

Mean initial 57Co activity in Lung retention Lung retention 

lung L(3) (kBq) L(90)/L(3) (%) L(180)/L(3) (%) 

Species (strain) 0.8 μm 1.7 μm 0.8 μm 1.7 μm 0.8 μm 1.7 μm 

Human 53 42 64 75 45 56 

Baboon 2,100 1,700 55 55 26 37 

Beagle dog 1,150 1,450 27 45 5.5 12 

Guinea pig (Harwell) 8.4 1.4 49 46 8.3 15 

Rat (HMT, 1985) 10.8 4.7 5.2 20 1.3 8.0 

Rat (HMT, 1986) 3.2 0.7 5.3 18 1.2 9.2 

Rat (F344, SPF) 8.8 4.4 14 25 4.7 9.2 

Rat (Sprague-Dawley) 0.9 0.10 8 39 1 15 

Syrian hamster 4.0 1.2 21 35 3.4 12 

Mouse (CBA/H) 1.8 No data 15 No data 2.8 No data 

a

Derived from Bailey et al. 1989 

b

Cobalt-57 used as tracer 
 

 

COBALT 126 

3. HEALTH EFFECTS 

3.5.1.2 Oral Exposure 

Gastrointestinal absorption of cobalt in humans varies considerably (18–97% of the given dose) based on 

the type and dose of cobalt compound given and the nutritional status of the subjects (Harp and Scoular 

1952; Smith et al. 1972; Sorbie et al. 1971; Valberg et al. 1969). More cobalt was absorbed through the 

gastrointestinal tract of humans when the body was deficient in iron (31–71% in iron deficiency; 18–44% 

in controls) (Sorbie et al. 1971; Valberg et al. 1969). One study in humans has shown that oral exposure 

to cobalt chloride resulted in significantly higher urinary excretion in females relative to males 

(Christensen et al. 1993). 

In animal studies, many factors have been shown to influence the absorption of cobalt compounds 

following oral exposure. In several studies in rats (Ayala-Fierro et al. 1999; Barnaby et al. 1968; Hollins 

and McCullough 1971; Kirchgessner et al. 1994; Schade et al. 1970; Taylor 1962), soluble cobalt chloride 

was absorbed in the range of 13–34%, whereas physiologically insoluble cobalt oxide particles have been 

shown to be poorly absorbed, in the range of 1–3% (Bailey et al. 1989; Collier et al. 1989; Patrick et al. 

1989). The particle size of the given dose of cobalt oxide had no significant effect on gastrointestinal 

absorption (Table 3-7). Administration of cobalt chloride labeled with radioactive 58Co and complexed 

with histidine, lysine, glycylglycine, ethylenediaminetetraacetic acid (EDTA), casein, or glycine resulted 

in decreased gastrointestinal absorption of cobalt; administration of cobalt chloride (with 58Co tracer) in 

cows' milk permitted a significantly greater (about 40%) absorption through the gastrointestinal tract 

(Taylor 1962). The same study found that while there was no difference in the chlorides of cobalt(II) and 

cobalt(III), a cobalt(II) glycine complex was absorbed in greater quantities than a cobalt(III) glycine 

complex. Other studies have also demonstrated that the chemical form of the cobalt compound can affect 

the absorption of cobalt following oral exposure (Deka et al. 1981; Firriolo et al. 1999; Inaba et al. 1980; 

Kinoshita and Fujita 1972), with more water-soluble compounds generally showing greater absorption. 

Iron deficiency led to increased absorption of cobalt from the gastrointestinal tract, and simultaneous 

administration of cobalt and iron reduced the amount of cobalt absorbed (Reuber et al. 1994; Schade et al. 

1970). Increasing oral doses of cobalt resulted in decreased fractional absorption (Houk et al. 1946; 

Kirchgessner et al. 1994; Taylor 1962), and more soluble forms of cobalt were better absorbed than less 

soluble compounds (Kreyling et al. 1986). Absorption is 3- to 15-fold greater in younger animals (rats 

and guinea pigs examined from days 1–60 of life) than in adult (200 days of age) animals (Naylor and 
 

 

COBALT 127 

3. HEALTH EFFECTS 

Table 3-7. Summary of Measurements of Retention and Excretion After 

Intragastric Administration of Cobalt Oxide (Co3O4) Particles (Mean 

Percentage of Recovered Activity at 7 Days After Administration)a,b
 

Cumulative fecal Whole body Cumulative urinary 

Species excretion retention excretion Absorption 

(strain) 0.8 μm 1.7 μm 0.8 μm 1.7 μm 0.8 μm 1.7 μm 0.8 μm 1.7 μm 

Baboon 97.8 98.4 0.12 0.20 2.0 1.4 2.6 1.9 

Guinea pig 98.7 97.6 0.16 0.66 1.1 1.9 1.3 2.3 

Rat (HMT) 96.3 99.4 0.09 0.02 2.8 0.6 3.9 1.0 

Rat 99.6 99.7 0.04 0.03 0.4 0.3 0.4 0.3 

(F-344) 

Hamster 96.0 96.3 0.50 0.18 3.5 3.5 5.1 5.1 

Mouse 99.1 No data 0.3 No data 0.6 No data 0.8 No data 

(CBA/H) 

a

Derived from Bailey et al. 1989 

b

Cobalt-57 used as tracer 
COBALT 128 

3. HEALTH EFFECTS 

Harrison 1995). Species differences in absorption of cobalt oxide do not appear to exist (Bailey et al. 

1989), but absorption of soluble cobalt compounds is greater in rats (13–34%) than in dairy cows (1–2%) 

and guinea pigs (4–5%) following oral exposure (Ayala-Fierro et al. 1999; Barnaby et al. 1968; Hollins 

and McCullough 1971; Kirchgessner et al. 1994; Naylor and Harrison 1995; Schade et al. 1970; Taylor 

1962; van Bruwaene et al. 1984). 

3.5.1.3 Dermal Exposure 

Four humans who placed their right hands into a box filled with hard metal dust (~5–15% cobalt metal, 

95–85% tungsten carbide) for 90 minutes showed an increase in urinary cobalt levels by an order of 

magnitude in the post-exposure samples, remaining elevated for as long as 48–60 hours (Scansetti et al. 

1994). Similarly, cobalt was detected in the fingernails of three volunteers who placed their fingers in 

cobalt solution 10 minutes/day for 7 days (Nielsen et al. 2000), even after the cessation of exposure. 

These findings demonstrate that cobalt from these metal dusts can be absorbed through the skin. The 

absorption of 2.2x10-5 mg 60Co/kg as cobalt chloride in 1.4N HCl through 1 cm2

 of intact or abraded skin 

of guinea pigs was examined by Inaba and Suzuki-Yasumoto (1979). Absorption through intact skin was 

very small (<1%), while absorption through abraded skin was almost 80% 3 hours after exposure. A 

study in hamsters (Lacy et al. 1996) also reported a low amount of absorption of cobalt through 

unabraded skin. 

3.5.1.4 Other Routes of Exposure 

No studies were located regarding absorption of cobalt in humans or animals after other routes of 

exposure. 

3.5.2 Distribution 

As a component of vitamin B12, cobalt is an essential element and, therefore, is found in most body 

tissues. It has been identified in liver, muscle, lung, lymph nodes, heart, skin, bone, hair, stomach, brain, 

pancreatic juice, kidneys, plasma, and urinary bladder of nonexposed subjects, with the highest cobalt 

concentration found in the liver (Collecchi et al. 1986; Forbes et al. 1954; Hewitt 1988; Ishihara et al. 
COBALT 129 

3. HEALTH EFFECTS 

1987; Muramatsu and Parr 1988; Teraoka 1981; Yamagata et al. 1962; Yukawa et al. 1980) (see 

Chapter 6 for more information). Tissue levels reflected exposure from all routes. The total body content 

of cobalt has been estimated at 1.1–1.5 mg (ICRP 1979; Yamagata et al. 1962); about 0.11 mg was found 

in the liver (ICRP 1979). 

In patients with laryngeal carcinoma, levels of cobalt in the tumor were significantly higher (p<0.001) 

than levels in the nonmalignant tissues around the tumor (68.7 ng/g tissue versus 39.6 ng/g) (Collecchi et 

al. 1986). The mean cobalt concentrations in plasma (18.3 ng/mL) were also significantly higher in these 

patients than in the comparison population (0.73 ng/mL). The clinical significance of these findings is 

not known. 

3.5.2.1 Inhalation Exposure 

In workers occupationally exposed to airborne cobalt, increased cobalt levels were found in tissues at 

death. Significant increases in cobalt in the lung have been found in copper smelter and metal workers 

and coal miners occupationally exposed to cobalt (Gerhardsson et al. 1984; Hewitt 1988; Hillerdal and 

Hartung 1983; Teraoka 1981). No increase in liver or kidney cobalt levels were found in the copper 

smelter workers as compared to controls (Gerhardsson et al. 1984). In metal workers, increased cobalt 

levels were also found in the lymph nodes, liver, spleen, and kidneys (Hillerdal and Hartung 1983; 

Teraoka 1981). 

The tissue distribution of cobalt in animals is similar to that in humans, with marked increases in the 

concentration of cobalt in the lungs following inhalation exposure (Barnes et al. 1976; Brune et al. 1980; 

Collier et al. 1991; Kreyling et al. 1986; Kyono et al. 1992; Patrick et al. 1989; Talbot and Morgan 1989). 

Histologically, the particles of cobalt in the lung are found in macrophages within the bronchial wall or in 

the interstitium close to the terminal bronchioli (Brune et al. 1980). Significant concentrations of cobalt 

have been found in the liver, kidney, trachea, spleen, bones, and heart (Barnes et al. 1976; Brune et al. 

1980; Kerfoot 1975; Kreyling et al. 1986; Wehner and Craig 1972), with the greatest concentrations in the 

liver and the kidney (Kerfoot 1975; Wehner and Craig 1972). 
COBALT 130 

3. HEALTH EFFECTS 

3.5.2.2 Oral Exposure 

No studies were located regarding distribution in humans after oral exposure to cobalt. 

In animals, the cobalt absorbed through the gastrointestinal tract was primarily retained in the liver 

(Ayala-Fierro et al. 1999; Greenberg et al. 1943; Simesen 1939). Appreciable levels were also found in 

the kidneys, heart, stomach, and intestines (Ayala-Fierro et al. 1999; Persson et al. 1992; Simesen 1939). 

Following a single oral dose of cobalt napthenate, appreciable levels of cobalt were found in the heart, 

liver, and kidney, but not in the spleen or testes (Firriolo et al. 1999). Following oral exposure to 

pregnant rats, a dose-dependent increase in cobalt levels in fetal blood and amniotic fluid was seen 

(Szakmary et al. 2001). 

Following longer-term exposure (8 weeks) to cobalt sulfate in the diet, exposed rats showed a 30-fold 

increase in the cobalt concentration in the myocardium, a 26-fold increase in the concentration in the 

soleus muscle, and a 100-fold increase in the concentration in serum compared with nonexposed controls 

(Clyne et al. 1988; Pehrsson et al. 1991). Long-term oral exposure of rats to cobalt chloride resulted in 

significantly increased levels of cobalt in the liver, kidney, muscle, brain, and testes of treated rats 

(Barnaby et al. 1968; Bourg et al. 1985; Thomas et al. 1976). 

3.5.2.3 Dermal Exposure 

No studies were located regarding distribution in humans or animals after dermal exposure to cobalt. 

3.5.2.4 Other Routes of Exposure 

Following intravenous injection of cobalt chloride (as a combination of radioactive 55CoCl2 and 56CoCl2) 

in two humans, the liver and bladder contained the highest portions of cobalt (Jansen et al. 1996). 

Distribution in animals after an intravenous dose appears to be similar to what we know of cobalt 

distribution in humans following injection of cobalt compounds. Two hours after intravenous injection of 

cobalt chloride (with a radioactive 57Co tracer) in rats, accumulation was found in the liver (22.8% of the 

dose), kidneys (10.2%), and intestines (3.16%) (Gregus and Klaassen 1986). Similar results (29% liver, 
COBALT 131 

3. HEALTH EFFECTS 

10% kidneys, 4.6% intestines) were found following intracardiac injection of cobalt nitrate in rats (Patrick 

et al. 1989) or intravenous injection of a combination of radioactive 55CoCl2 and 56CoCl2 in rats (exact 

percentages were not provided) (Jansen et al. 1996). One hundred days after intravenous injection of 

60CoCl2 in rats, the greatest concentrations were found in spleen>heart>bone, while liver and kidney, 

initially the highest in cobalt, contained comparatively low amounts of cobalt (Thomas et al. 1976). 

Similar results were seen 132 days following an intraperitoneal injection of 60CoCl2 in rats (Barnaby et al. 

1968). Intramuscular injection of cobalt mesoporphyrin in rats yielded the greatest levels of cobalt in 

liver and blood, followed by kidney, lung, spleen, adrenal glands, and heart at 7 days post-injection and 

later (Feng et al. 1998). Four weeks after subcutaneous administration of cobalt protoporphyrin, the 

greatest tissue levels of cobalt occurred in the kidney, followed by spleen, liver, lung, thymus, and gonads 

(Rosenberg 1993). When cobalt (with a 57Co tracer) encapsulated in liposomes was intravenously 

injected into rats, decreased distribution to the heart (40% less than animals receiving cobalt chloride), 

kidneys, and carcass, and increased distribution to the spleen and bones were found (Szebeni et al. 1989). 

3.5.3 Metabolism 

Cobalt is essential in the body because it is a component of cyanocobalamin (vitamin B12) (Vouk 1986). 

Vitamin B12 acts as coenzyme in many enzymatic reactions, most notably a methyl transfer reaction that 

converts homocysteine to methionine and for a separate reaction that converts L-methylmalonylcoenzyme 

A (CoA) to succinyl-CoA (Institute of Medicine 2000). Vitamin B12 is also a part of some enzymes 

involved in hematopoiesis; deficiency can lead to pernicious anemia (Domingo 1989). No other essential 

function of cobalt has been reported. The Recommended Dietary Allowance (RDA) for vitamin B12 for 

adults is 2.4 μg/day, which contains 0.1 μg of cobalt (Institute of Medicine 2000). 

3.5.4 Elimination and Excretion 

3.5.4.1 Inhalation Exposure 

No data are available on the clearance of soluble cobalt particles in humans. Following exposure of 

humans to physiologically insoluble cobalt compounds (cobalt metal, cobalt oxides), clearance from the 

body, assessed by both urinary/fecal clearance and a reduction in whole-body retention, appears to follow 
 

 

COBALT 132 

3. HEALTH EFFECTS 

three-phase kinetics. The first phase, likely representing mucociliary clearance of particles deposited in 

the tracheobronchial region, has a half-time on the order of 2–44 hours (Apostoli et al. 1994; Mosconi et 

al. 1994b). The second phase, with a half-time on the order of 10–78 days, may represent macrophagemediated clearance of cobalt particles from the lung (Beleznay and Osvay 1994; Mosconi et al. 1994b). 

The third clearance phase, representing long-term clearance from the lungs, has a half-time on the order 

of years (Bailey et al. 1989; Beleznay and Osvay 1994; Mosconi et al. 1994b; Newton and Rundo 1971). 

Following a controlled aerosol exposure in humans, about 40% of the initial lung burden of inhaled cobalt 

oxide (with a 57Co tracer) was retained for a period of 6 months after exposure (Foster et al. 1989). 

Within the first week, about 17% of the initial lung burden was eliminated, with the majority (about 90%) 

mechanically cleared to the gastrointestinal tract and excreted in the feces (Foster et al. 1989). Six 

months after exposure, a cumulative elimination of 33% of the initial lung burden was found in the urine 

and 28% was found in the feces (Foster et al. 1989). The ratio of peak absorption rate to average 

mechanical clearance rate (Figure 3-4 and Table 3-8) was about 5 to 1. The elimination of cobalt 

following inhalation exposure was affected by the time after exposure (urinary excretion increases as time 

increases) and particle size (more cobalt is initially mechanically cleared to the gastrointestinal tract when 

the aerosol consists of bigger particles) (Bailey et al. 1989; Foster et al. 1989). 

In animals, the solubility of the cobalt compound appears to greatly affect its long-term clearance. 

Studies with cobalt oxides have shown that the more soluble CoO is cleared from the lungs at a greater 

rate than the less soluble Co3O4 (Barnes et al. 1976; Kreyling 1984a). More soluble cobalt compounds 

are absorbed into the blood at a greater rate, and excreted in the urine and, to a lesser extent, the feces 

(Barnes et al. 1976). The rate of urinary excretion appears to correlate with the rate of translocation of 

cobalt from the lungs to the blood, and the rate of fecal clearance with the rate of mechanical clearance of 

cobalt from the lungs to the gastrointestinal tract (Andre et al. 1989; Bailey et al. 1989; Collier et al. 1989; 

Kreyling et al. 1986, 1989; Patrick et al. 1989; Talbot and Morgan 1989). Following an initial high rate 

of fecal clearance, urinary excretion was the primary route of cobalt elimination after a single inhalation 

exposure (2 weeks of observation) (Palmes et al. 1959) or 3 months of exposure (Kerfoot 1975; Palmes et 

al. 1959). In several species of animals, most of the inhaled Co3O4 (with a 57Co tracer) following a single 

exposure was cleared from the lungs by 6 months after exposure (Table 3-6) (Andre et al. 1989; Bailey et 

al. 1989; Collier et al. 1989; Kreyling et al. 1989; Patrick et al. 1989; Talbot and Morgan 1989). The 

peak translocation and average mechanical clearance of cobalt from the lungs for different species are 

reported in Table 3-8, with the rate (high to low) following as mouse > rat > hamster > guinea pig > 

baboon, human > beagle dog. 
 

 

COBALT 133 

3. HEALTH EFFECTS 

Table 3-8. Peak Translocation and Average Mechanical Clearance Rates After 

Inhalation of Cobalt Oxidea,b
 

Percent of lung content cleared per day 

Species (strain) 0.8 μm 

Translocation at peak 

Peak day 1.7 μm Peak day 

Average mechanical 

clearancec 

Human 0.45 180 0.5 180 0.1 

Baboon 0.6 180 0.2 d 0.1 

Beagle dog 2.1 85 1.7 180 0.03 

Guinea pig 2.1 180 1.0 75 0.3 

Rat HMT 2.4 40 0.6 d 0.9 

Rat (F-344) 1.1 10 0.4 d 1.0 

Hamster 1.8 180 0.7 180 0.8 

Mouse 1.7 180 No data No data 1.05 

a

Derived from Bailey et al. 1989 

b

Cobalt-57 used as tracer 

c

Clearance rates were virtually identical in both particle size groups 

d

Constant value over 180 days 
COBALT 134 

3. HEALTH EFFECTS 

3.5.4.2 Oral Exposure 

In humans orally exposed to cobalt, fecal elimination, which is the primary route of elimination, varies 

considerably (3–99% of the dose) and depends on the amount and type of cobalt given and on the 

nutritional status of the subjects (Section 3.5.1.2) (Harp and Scoular 1952; Paley et al. 1958; Smith et al. 

1972; Sorbie et al. 1971; Valberg et al. 1969). Within days after oral exposure, 10 times more cobalt was 

excreted in feces than in the urine (Paley et al. 1958). Less cobalt was eliminated in the feces (more was 

absorbed) in subjects with an iron deficiency (Sorbie et al. 1971; Valberg et al. 1969). 

Fecal elimination of cobalt is the primary route of elimination in animals following oral exposure and 

depends mainly upon the particle solubility (decreasing fecal clearance with increasing solubility) of the 

cobalt compound. The cumulative urinary and fecal elimination in several species following oral 

administration of Co3O4 (with a 57Co tracer) is reported in Table 3-7 (Bailey et al. 1989). Following oral 

administration in several species, very little Co3O4 was absorbed through the gastrointestinal tract and 

most (>96%) was quickly eliminated in the feces. No significant differences in elimination of 

Co3O4 were found among species of animals (Andre et al. 1989; Bailey et al. 1989; Collier et al. 1989; 

Patrick et al. 1989; Talbot and Morgan 1989). For the more soluble cobalt(II) chloride, reported fecal 

elimination levels have ranged from 70 to 83% of the administered dose for rats, with urinary excretion 

accounting for the majority of the remainder of the dose (Ayala-Fierro et al. 1999; Barnaby et al. 1968; 

Hollins and McCullough 1971). In lactating dairy cows, about 97% of an oral dose of cobalt chloride was 

recovered in the feces by day 70 post-exposure, while the urine and milk contained 0.26 and 0.012% of 

the dose, respectively (van Bruwaene et al. 1984). Following a single exposure in beagle dogs, more 

Co3O4 (physiologically insoluble) was eliminated in the feces (90% in the feces and 5% in the urine) than 

following an exposure to cobalt nitrate (soluble) (70% in the feces and 25% in the urine) (Kreyling et al. 

1986). 

As is the case for absorption of cobalt compounds, the iron status of the animal also appears to affect the 

elimination of cobalt compounds. Following oral exposure, iron-deficient rats eliminated less of a given 

dose in the feces than normal rats, while co-administration of iron compounds resulted in an increased 

fecal excretion of cobalt compounds (Reuber et al. 1994; Schade et al. 1970). 
COBALT 135 

3. HEALTH EFFECTS 

3.5.4.3 Dermal Exposure 

No studies were located regarding excretion in humans after dermal exposure to cobalt. 

Lacy et al. (1996) reported that the majority of the absorbed dose of CoCl2 was excreted in the urine 

48 hours after a single dermal exposure in Syrian hamsters. No other studies were located regarding 

excretion in animals after dermal exposure to cobalt. 

3.5.4.4 Other Routes of Exposure 

Following intravenous injection of cobalt chloride in humans, about 30% of the dose was excreted in the 

urine within 24 hours (Smith et al. 1972), 56–73% was excreted within 48 hours (Paley et al. 1958), and 

57% was excreted within 2 weeks (Kent and McCance 1941). 

Following intravenous injection of cobalt nitrate (with a 57Co tracer) in various species of animals, most 

of the injected dose was excreted in the urine; about 80% of the given dose was excreted in the urine 

within 21 days (Table 3-9) (Andre et al. 1989; Bailey et al. 1989; Collier et al. 1989; Patrick et al. 1989; 

Talbot and Morgan 1989). Other investigators have also found that the urine is the primary route of 

cobalt excretion following intravenous administration (Ayala-Fierro et al. 1999; Barnaby et al. 1968; 

Gregus and Klaassen 1986; Kreyling et al. 1986; Onkelinx 1976; Thomas et al. 1976). Most of the 

remaining cobalt (5–30% of the total dose) after intravenous exposure was excreted in the feces, with the 

majority of studies reporting very little long-term retention. Excretion of cobalt (about 2–7% of the 

injected dose) in the bile was also reported (Cikrt and Tich 1981; Gregus and Klaasen 1986; Sheline et al. 

1945). Elimination following intraperitoneal injection is similar to that seen following intravenous 

exposure, with urinary excretion being the major route of elimination, and fecal excretion accounting for 

the majority of the remainder of the dose (Barnaby et al. 1968; Hollins and McCullough 1971; Talbot and 

Morgan 1989), though long-term clearance may be more balanced between the two (Hollins and 

McCullough 1971). Following subcutaneous injection, both CoCl2 and Co(NO3)2 were cleared rapidly 

from the body (Rosenberg 1993; Talbot and Morgan 1989), with the urine being the major route of 

clearance (Talbot and Morgan 1989). 
 

 

COBALT 136 

3. HEALTH EFFECTS 

Table 3-9. Summary of Measurements of Retention and Excretion of Cobalt 

Following Injection of Cobalt Nitrate Co(NO3)2 Solution (Mean Percent 

Recovery)a,b 

Whole body retention on Cumulative urinary Cumulative fecal 

Species day excretion on day excretion on day 

(strain) 1 7 21 1 7 21 1 7 21 

Baboon No data No data No data 57 74 80 5 17 20 

Beagle dog No data No data No data 71 86 87 3.4 4.4 4.9 

Guinea pig 34 8 3.5 64 82 85 2.2 10 12 

Rat (HMT) 18 4.2 1.9 64 72 74 18 24 24 

Rat (F-344) No data No data 2.9 No data No data 80 No data No data 18 

Hamster 27 4.3 1.9 55 68 69 17 28 29 

Mouse 23 2.9 1.1 59 71 72 18 26 27 

a

Derived from Bailey et al. 1989 

b

Cobalt-57 used as tracer 
COBALT 137 

3. HEALTH EFFECTS 

Following injection, studies have shown that the chemical form of the cobalt compound can affect its 

elimination. Subcutaneous injection of cobalt protoporphyrin in rats, in which the cobalt atom is chelated 

within the porphyrin ring, resulted in a slower elimination from the body than cobalt chloride, with 

significant cobalt levels (~20% of initial injection) still present in the body 14 days after exposure 

(Rosenberg 1993). Likewise, intramuscular injection of cobalt mesoporphyrin resulted in primarily in 

fecal excretion, with a high systemic retention (Feng et al. 1998). It therefore appears that a greater 

solubility leads to fast elimination, mainly in the urine, while a less soluble compound will be retained for 

longer periods and eliminated to a greater extent in the feces. 

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 

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 
COBALT 138 

3. HEALTH EFFECTS 

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 3-5 shows a conceptualized 

representation of a PBPK model. Figures 3-6 through 3-9 show models for radionuclides in general or 

specifically for cobalt. 

The ICRP (1995) developed a Human Respiratory Tract Model for Radiological Protection, which 

contains respiratory tract deposition and clearance compartmental models for inhalation exposure that 

may be applied to particulate aerosols of cobalt compounds. The ICRP (1993) also developed a 

3-compartment biokinetic model for human oral exposure that applies to cobalt. EPA (1998) has adopted 

the ICRP (1993, 1995) models for assessment of radiologic cancer risks from cobalt exposures. The 

National Council on Radiation Protection and Measurement (NCRP) has also developed a respiratory 

tract model for inhaled radionuclides (NCRP 1997). At this time, the NCRP recommends the use of the 
 

 

Skin 

Kidney 

Richly

perfused

tissues 

Slowly

perfused

tissues 

Fat 

Liver 

Lungs 

A 

R 

T 

E 

R 

I 

A 

L 

B 

L 

O 

O 

D 

V 

E 

N 

O 

U 

S 

B 

L 

O 

O 

D 

GI 

Tract 

Vmax Km 

Urine 

Inhaled chemical Exhaled chemical 

Ingestion 

Feces 

Chemicals in air 

contacting skin 

COBALT 139 

3. HEALTH EFFECTS 

Figure 3-5. Conceptual Representation of a Physiologically Based 

Pharmacokinetic (PBPK) Model for a Hypothetical 

Chemical Substance 

Source: adapted from Krishnan et al. 1994 

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. 
COBALT 140 

3. HEALTH EFFECTS 

ICRP model for calculating doses for radiation workers and the general public. Readers interested in this 

topic are referred to NCRP Report No. 125; Deposition, Retention and Dosimetry of Inhaled Radioactive 

Substances (NCRP 1997). In the appendix to the report, NCRP provides the animal testing clearance data 

and equations fitting the data which supported the development of the human model for cobalt 

Human Respiratory Tract Model for Radiological Protection (ICRP 1994). 

Respiratory Tract Deposition. The ICRP (1994) has developed a physiologically-based 

pharmacokinetic model for behavior of aerosols and vapors in the respiratory tract. ICRP (1994) provides 

inhalation dose coefficients that can be used to estimate the committed equivalent and the effective doses 

to organs and tissues throughout the body based on a unit intake of radioactive material and the 

anticipated distribution and retention of the material, its radioactive decay, and the energy of the 

radiationemitted from the material and absorbed by tissues. The model applies to three levels of particle 

solubility, a wide range of particle sizes (approximately 0.0005–100 μm in diameter), and parameter 

values that can be adjusted for various segments of the population (e.g., sex, age, 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 

cobalt, and was developed for a wide variety of radionuclides and their chemical forms. 

The ICRP deposition model estimates the fraction of inhaled particle mass that initially deposits in each 

compartment (Figure 3-6). The model was developed with 5 compartments: (1) the anterior nasal 

passages (ET1); (2) all other extrathoracic airways (ET2) (posterior nasal passages, the naso- and 

oropharynx, and the larynx); (3) the bronchi (BB); (4) the bronchioles (bb); and (5) the alveolar 

interstitium (AI). Particles deposited in each of the regions may be removed 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 
 

Sequestered in Tissue Surface Turface Transport 

Anterior
 

Nasal
 

Naso-oro-­

pharynx 

Larynx 

0.001

Extrathoracic

ETSEQ

12

LNET

13

Bronchi

bb2

BB2

LNTH

bbSEQ

0.03 2

0.01

0.01

8

BBSEQ

9

Thoracic

6 5

10

Al3

0.0001

BB1

bb1

7

4

Al Al2 1

0.001 0.02

3 2 1

GI Tract

Environment

16

ET2

ET1

14

11 15

100

1

Bronchioles

Alveolar 

Interstitium

0.03 10

0.00002

0.001 

Extrathoracic 

ETSEQ 

12 

LNET 

13 

Bronchi 

bb2 

BB2 

LNTH 

bbSEQ

0.03 2 

0.01 

0.01 

8 

BBSEQ

9

SEQ 

9 

Thoracic 

6 5

10 

Al3 

0.0001 

BB1 

bb1 

7 

4 

Al Al2 1

0.001 0.02 

3 2 1

GI Tract 

Environment 

16 

ET2

ET1

14

11

ET2 

ET1 

14 

11 15 

100 

1 

Bronchioles 

Alveolar 

Interstitium 

0.03 10 

0.00002 

COBALT 141 

3. HEALTH EFFECTS 

Figure 3-6. Compartment Model to Represent Particle Deposition and 

Time-Dependent Particle Transport in the Respiratory Tract* 

*Compartment numbers shown in lower right corners are used to define clearance pathways. The clearance rates, 

half-lives, and fractions by compartment, as well as the compartment abbreviations are presented in Table 3-11. 

Source: ICRP 1994b 
 

 

COBALT	 142 

3. HEALTH EFFECTS 

was used to interpret data and to predict deposition for compartments and subpopulations other than adult 

males. Table 3-10 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 

respiratory tract (Figure 3-7). The ICRP (1994) model defines three categories of solubility and 

reactivity: SR-0, SR-1, and SR-2: 

•	 Type SR-0 compounds include insoluble and nonreactive gases (e.g., inert gases such as H2, He). 

These compounds do not significantly interact with the respiratory tract tissues and essentially all 

compound inhaled is exhaled. Radiation doses from inhalation 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 type compounds include sulfur dioxide 

(SO2) and hydrogen fluoride (HF). 

Respiratory Tract Mechanical (Particle) Clearance. This portion of the model identifies the 

principal clearance pathways within the respiratory tract. The model was developed to predict the 

retention of various chemical materials. The compartmental model is linked to the deposition model (see 

Figure 3-6) and to reference values presented in Table 3-11. This table provides deposition fractions and 

clearance rates for each compartment for insoluble particles. The table provides rates of insoluble particle 

transport for each of the compartments, expressed as a fraction of the deposit per day and also as 

clearance half-time. ICRP (1994) 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 deposited 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 
 

 

 

 

 

 

 

COBALT 143 

3. HEALTH EFFECTS 

Table 3-10. Reference Respiratory Values for a General Caucasian Population at 

Different Levels of Activitya
 

Activity: Resting (sleeping) Sitting awake Light exercise Heavy exercise 

Maximal 

workload: 8% 12% 32% 64% 

Breathing 

parametersb VT 

(L) 

B 

(m3

h-1) 

fR 

(min-1) 

VT 

(L) 

B 

(m3h-1) 

fR 

(min-1) 

VT 

(L) 

B 

(m3h-1) 

fR 

(min-1) 

VT 

(L) 

B fR 

(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 

 Female: 0.667 1.84 46 

Both: 0.3 0.31 17 0.33 0.38 19 0.58 1.12 32 

15 years Male: 0.50 0.42 14 0.533 0.48 15 1.0 1.38 23 1.352 2.92 36 

 Female: 0.42 0.35 14 0.417 0.40 16 0.903 1.30 24 1.127 2.57 38 

Adult Male: 0.63 0.45 12 0.750 0.54 12 1.25 1.5 20 1.923 3.0 26 

 Female: 0.44 0.32 12 0.464 0.39 14 0.992 1.25 21 1.364 2.7 33 

a

See Annex B (ICRP 1994) for data from which these reference values were derived. b

VT = Tidal volume, B = ventilation rate, fR = respiration frequency 

h = hour; L = liter(s); min = minute(s); N/A = not applicable 
 

Airway Uptake Gas or Vapor 

Lumen 

Airway 

Fluid 

Tissue 

Blood Blood 

Sb 

Reaction 

Product 

Reaction 

Product 

Bound 

Material 

Gas/Vapor 

Gas/Vapor 

Reaction 

Product Gas/Vapor 

Source: ICRP 1994b 

Convection 

Diffusion 

COBALT 144 

3. HEALTH EFFECTS 

Figure 3-7. Reaction of Gases or Vapors at Various Levels of the Gas-Blood 

Interface 
 

 

COBALT 145 

3. HEALTH EFFECTS 

Table 3-11. 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 — 

m4,7 bb1 BB1 2 8 hours 

m5,7 bb2 BB1 0.03 23 days 

m6,10 bbseq LNTH 0.01 70 days 

m7,11 BB1 ET2 10 100 minutes 

m8,11 BB2 ET2 0.03 23 days 

m9,10 BBseq LNTH 0.01 70 days 

m11,15 ET2 GI tract 100 10 minutes 

m12,13 ETseq LNET 0.001 700 days 

m14,16 ET1 Environment 1 17 hours 

See next page for Part B 
 

 

 

 

 

COBALT	 146 

3. HEALTH EFFECTS 

Table 3-11. 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 assigned to 

Region or deposition site Compartment 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 day-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 1994) for default values used for relating fs to dae. c

It is assumed that fs is size-dependent. For modeling purposes, fs is taken to be: 

fs = 05. for dae ≤ 25 . ρ χμ / m and

0 63 .( d ρ χ/ −2 5.) ae fs = 05. e for dae > 25 . ρ χμ / m

where: 

fs = fraction subject to slow clearance 

dae = aerodynamic particle diameter/(μm) 

ρ = particle density (g/cm3

) 

χ = particle shape factor 

AI = alveolar-interstitial region; BB = bronchial region; bb = bronchiolar region; BBseq = compartment representing 

prolonged retention in airway walls of small fraction of particles deposited in the bronchial region; 

bbseq = compartment representing prolonged retention in airway walls of small fraction of particles deposited in the 

bronchiolar region; ET = extrathoracic region; Etseq = compartment representing prolonged retention in airway tissue 

of small fraction of particles deposited in the nasal passages; LNET = lymphatics and lymph nodes that drain the 

extrathoracic region; LNTH = lymphatics and lymph nodes that drain the thoracic region 

Source: ICRP 1994 
COBALT 147 

3. HEALTH EFFECTS 

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 sub-compartments of 

different clearance rates within each region (e.g., BB1, BB2, BBseq), the ICRP model overcomes 

problems associated with time-dependent functions. Each compartment clears to other compartments by 

constant rates for each pathway. 

Particle transport from all regions is toward both the lymph nodes and the pharynx, and a majority of 

deposited particles end up being swallowed. In the front part of the nasal passages (ET1), nose blowing, 

sneezing, and wiping remove most of the deposited particles. Particles remain here for about a day. For 

particles with AMADs a few micrometers or greater, the ET1 compartment is probably the largest 

deposition site. The 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 to the alveoli it is. 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 (BB2 and bb2) is assumed to have fractions of the inhaled particles, 

depending on the particle size, deposited in BB2 and bb2; both have clearance half-times estimated at 

20 days. 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 2 half-times to represent clearance: about 30% of the particles have a 30-day half-time, and 
COBALT	 148 

3. HEALTH EFFECTS 

the remaining 70% are given a half-time of several hundred days. Over time, the AI particle transport rate 

falls and some compounds have been found in lungs 10–50 years after exposure. 

Absorption into Blood. The ICRP model assumes that absorption into blood occurs at equivalent rates in 

all parts of the respiratory tract, except in the anterior nasal passages (ET1), where no absorption occurs. 

It is essentially a 2-stage process, as shown in Figure 3-8. First, there is a dissociation (dissolution) of 

particles; then, the dissolved molecules or ions diffuse across capillary walls and are taken up by the 

blood. Immediately following dissolution, rapid absorption is observed. For some elements, rapid 

absorption does not occur because of binding to respiratory-tract components. In the absence of data for 

specific compounds, the model uses the following default absorption rate values for those compounds that 

are classified as Types F (fast), M (medium), S (slow), and V (instantaneous): 

•	 For Type F, there is rapid 100% absorption within 10 minutes of the material deposited in the BB, 

bb, and AI regions, and 50% of material deposited in ET2. Thus, for nose breathing, there is rapid 

absorption of approximately 25% of the deposit in ET and 50% for mouth breathing. 

•	 For Type M, about 70% of the deposit in AI reaches the blood eventually. There is rapid 

absorption of about 10% of the deposit in BB and bb, and 5% of material deposited in ET2. Thus, 

there is rapid absorption of approximately 2.5% of the deposit in ET for nose breathing, and 5% 

for mouth breathing. 

•	 For Type S, 0.1% is absorbed within 10 minutes and 99.9% is absorbed within 7,000 days, so 

there is little absorption from ET, BB, or bb, and about 10% of the deposit in AI reaches the 

blood eventually. 

•	 For Type V, complete absorption (100%) is considered to occur instantaneously. 

ICRP (1995) considers the experimental and human data to support the following classifications: cobalt 

chloride and nitrate, Type F; cobalt oxides, Type M or S; cobalt in fused aluminosilicate or polystyrene, 

Type S; cobalt in mineral dusts such as fly ash and volcanic ash, Type M; cobalt metal and metal alloys, 

M or S. ICRP (1995) recommends assigning all cobalt aerosols to Type M in the absence of specific 

information supporting an alternative classification. 
 

Particulate Material 

Dissolution 

Dissociated Material 

Bound Material 

B loo d 

Uptake 

Source: ICRP 1994 

COBALT 149 

3. HEALTH EFFECTS 

Figure 3-8. The Human Respiratory Tract Model: Absorption into Blood 
COBALT 150 

3. HEALTH EFFECTS 

ICRP (1993) Cobalt Biokinetics Model. 

Description of the model. 

ICRP (1979, 1993) developed a 3-compartment model of the kinetics of ingested cobalt in humans that is 

applicable to infants, children, adolescents, and adults. Absorption of ingested cobalt is assumed to be 

60% in infants up to 3 months of age, 30% from 3 months to 15 years of age, and 10% after age 15 years. 

Absorbed cobalt is assumed to distribute as follows: 50% is excreted (urine and feces combined in a 

6:1 ratio), 5% is transferred to the liver, and 45% is transferred to other tissues (Figure 3-9). Elimination 

from tissue compartments is described by three first order rate constants representing slow, medium, and 

fast elimination pools with half-times of 6, 60, and 800 days, respectively. The elimination half-times are 

assumed to be independent of age. 

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 57Co, 58Co, and 60Co 

for ages 3 months to 70 years (ICRP 1993). 

Target tissues. 

The model can be used to estimate the radiation dose from cobalt radionuclides to all major organs and 

can be applied to environmental and occupational exposures. 

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 designed to simulate oral exposures to cobalt and cannot be applied to other routes of 

exposure without modification. 
 

Figure 3-9. ICRP Biokinetics Model for Cobalt 

Gastrointestinal or
 

Respiratory Tract
 

Transfer Compartment 

Other Tissues Liver 

50% 

45% 5% 

(0.5 d) 

(6, 60, 800 d) (6, 60, 800 d) 

Urine and Feces (6:1 ratio) 

COBALT 151 

3. HEALTH EFFECTS 

Absorbed cobalt enters a virtual transfer compartment from which unidirectional transfer to tissues is assumed to 

occur. Percentages shown are of the initial amounts absorbed. Numbers in parentheses are elimination half-times to 

urine and feces combined (d=days. Liver other tissues are assumed to have fast, medium, and slow elimination 

pools. 
COBALT 152 

3. HEALTH EFFECTS 

3.6 MECHANISMS OF ACTION 

3.6.1 Pharmacokinetic Mechanisms 

Absorption. Following inhalation exposure, the absorption of deposited cobalt compounds seems to 

be related to their biological solubility. Cobalt compounds deposit in the lungs based on their aerosol 

characteristics. Physiologically insoluble cobalt particles are generally cleared by phagocytosis and/or 

mucociliary transport, and thus, have a low systemic absorption. To some extent, cobalt particles may be 

dissolved within alveolar macrophages (Kreyling et al. 1990). More soluble forms of cobalt may enter 

the bloodstream through the alveolar or bronchial walls. 

Following oral exposure, the absorption of cobalt varies with the amount given, with a greater dose 

leading to 4- to 20-fold greater fractional absorption (Smith et al. 1972). Nutritional status also seems to 

be an important factor in cobalt absorption, with both overnight fasting and iron deficiency resulting in 

increased cobalt absorption (Smith et al. 1972; Sorbie et al. 1971; Valberg et al. 1969). It has been 

suggested that cobalt and iron share a common absorptive pathway in the intestines, though the cobalt 

absorption takes place without ferritin (Reuber et al. 1994; Schade et al. 1970; Thomson et al. 1971). 

Solubility of the cobalt compound is also an important factor regarding the absorption following oral 

exposure, with increasing solubility resulting in increasing absorption (Christensen et al. 1993). One 

study in humans showed that oral exposure to cobalt resulted in significantly higher urinary excretion in 

females relative to males (Christensen et al. 1993), but these results have not been verified by other 

studies. A complex, specific pathway exists for the absorption of vitamin B12, whereby the molecule 

interacts with several factors in the stomach and intestine to facilitate absorption (for review, see RusselJones and Alpers 1999). 

Dermal absorption of cobalt compounds depends greatly on whether the skin is intact or damaged. 

Absorption through intact skin is comparatively low, while absorption through damaged skin is much 

higher (Inaba and Suzuki-Yasumoto 1979; Lacy et al. 1996). 

Distribution. As a component of vitamin B12, cobalt is found in most body tissues. Absorbed cobalt is 

transported throughout the body in the blood, with greatest levels found in the liver, followed by the 

kidney (Ayala-Fierro et al. 1999; Greenberg et al. 1943; Gregus and Klaassen 1986; Patrick et al. 1989). 
 

 

COBALT 153 

3. HEALTH EFFECTS 

Following inhalation exposure, significant levels of cobalt are found in the lungs of exposed humans and 

animals (Barnes et al. 1976; Brune et al. 1980; Collier et al. 1991; Gerhardsson et al. 1984; Hewitt 1988; 

Hillerdal and Hartung 1983; Kreyling et al. 1986; Kyono et al. 1992; Patrick et al. 1989; Talbot and 

Morgan 1989; Teraoka 1981). Within the lung, physiologically insoluble cobalt particles tend to be 

located within macrophages within the bronchial wall or in the interstitium close to the terminal 

bronchioli (Brune et al. 1980). 

Excretion. Following inhalation exposure, the rate of urinary excretion appears to correlate with the 

rate of translocation of cobalt from the lungs to the blood, and the rate of fecal clearance with the rate of 

mechanical clearance of cobalt from the lungs to the gastrointestinal tract (Andre et al. 1989; Bailey et al. 

1989; Collier et al. 1989; Kerfoot 1975; Kreyling et al. 1986, 1989; Palmes et al. 1959; Patrick et al. 

1989; Talbot and Morgan 1989). Likewise, the majority of absorbed cobalt following oral exposure is 

rapidly removed from the body by excretion in the urine, and to a lesser extent in the bile and feces, with 

fecal elimination being the primary method of excretion for physiologically insoluble cobalt compounds 

in both humans and animals (Andre et al. 1989; Bailey et al. 1989; Collier et al. 1989; Harp and Scoular 

1952; Paley et al. 1958; Patrick et al. 1989; Smith et al. 1972; Sorbie et al. 1971; Talbot and Morgan 

1989; Valberg et al. 1969). The primary route for excretion following dermal exposure is the urine (Lacy 

et al. 1996; Scansetti et al. 1994). 

3.6.2 Mechanisms of Toxicity 

Stable Cobalt. The exact mechanisms by which cobalt exerts its effects on cells are not completely 

understood. However, a number of potential mechanisms have been identified. Several studies have 

demonstrated that hard metal, a metal alloy with a tungsten carbide and cobalt matrix, is considerably 

more toxic than either cobalt or tungsten carbide alone. A mechanism by which hard metal may exert its 

effects has been proposed by a group of Belgian researchers (Lasfargues et al. 1995; Lison et al. 1995, 

1996). In this proposed mechanism, tungsten carbide, which is a very good conductor of electrons, 

facilitates the oxidation of cobalt metal to ionic cobalt (presumably Co2+) by transferring electrons from 

the cobalt atom to molecular oxygen adjacent to the tungsten carbide molecule. The result is an increased 

solubility of cobalt, relative to cobalt metal alone, and the generation of active oxygen species. The 

cobalt ions formed may be absorbed into the blood and transported throughout the body, where they may 

elicit effects by the above mechanisms. In vitro evidence for this mechanism includes the ability of hard 
 

 

 

 

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3. HEALTH EFFECTS 

metal particles, but neither cobalt nor tungsten carbide alone, to generate substantial levels of oxidant 

species and cause significant lipid peroxidation (Lison et al. 1995; Zanetti and Fubini 1997). Hard metal 

particles have also been shown to increase the levels of inducible nitric oxide synthase (iNOS), a gene 

responsive to oxidant stress (Rengasamy et al. 1999). 

Another potential mechanism for cobalt toxicity is through oxidant-based and free radical-based 

processes. Exposure to soluble cobalt increases indices of oxidative stress, including diminished levels of 

reduced glutathione, increased levels of oxidized glutathione, activation of the hexose monophosphate 

shunt, and free-radical-induced DNA damage (Hoet et al. 2002; Kasprzak et al. 1994; Lewis et al. 1991; 

Zhang et al. 1998a); hydrogen peroxide appears to be a necessary cofactor for cobalt-induced oxidative 

DNA damage (Ivancsits et al. 2002). Cobalt has been shown to generate oxygen radicals, including 

superoxide, both in vitro and in vivo (Kadiiska et al. 1989; Kawanishi et al. 1994; Moorhouse et al. 1985), 

through what may be a Fenton-type mechanism (Lloyd et al. 1997). In vivo exposure to cobalt in rats and 

guinea pigs resulted in increased lipid peroxidation in the liver (Christova et al. 2001, 2002; Sunderman 

and Zaharia 1988), as well as changes in reduced glutathione and hepatic levels of superoxide dismutase, 

catalase, heme oxygenase, and glutathione peroxidase (Christova et al. 2001, 2002). Exposure to cobalt 

results in accumulation in cardiac tissues, and is thought to stimulate carotid-body chemoreceptors, 

mimicking the action of hypoxia (Di Giulio et al. 1990, 1991; Hatori et al. 1993; Morelli et al. 1994). 

Cobalt administration to a neuroblastoma/glioma cell line resulted in an upregulation of opioid delta 

receptors, through a mechanism similar to that of hypoxia (Mayfield et al. 1994). Exposure to cobalt also 

elicits effects on a number of genes known to be sensitive to oxidant status, including hypoxia-inducible 

factor 1, erythropoietin, vascular endothelial growth factor, catalase, and monooxygenase enzymes (Bunn 

et al. 1998; Daghman et al. 1999; Dalvi and Robbins 1978; Di Giulio et al. 1991; Goldberg et al. 1988, 

1994; Ho and Bunn 1996; Hoet et al. 2002; Ladoux and Frelin 1994; Legrum et al. 1979; Semenza et al. 

1994; Yasukochi et al. 1974), and may also lead, through these genes or other pathways, to the induction 

of apoptosis (Zou et al. 2001). 

Soluble cobalt has also been shown to alter calcium influx into cells, functioning as a blocker of inorganic 

calcium channels (Henquin et al. 1983; Moger 1983; Yamatani et al. 1998). This mechanism has been 

linked to a reduction of steroidogenesis in isolated mouse Leydig cells (Moger 1983). Additionally, 

soluble cobalt has been shown to alter the inorganic calcium influx in liver cells after exposure to 

glucagon (Yamatani et al. 1998), and calcium influx into pancreatic β cells (Henquin et al. 1983) and 
COBALT 155 

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isolated rat islets (Henquin and Lambert 1975). Cobalt may also affect neuromuscular transmission 

though antagonism with calcium (Weakly 1973). 

Another potential mechanism of cobalt toxicity is relevant to cobalt cardiomyopathy. As mentioned 

previously, cobalt accumulated in the heart of beer drinkers. Microscopic analysis revealed fragmentation 

and degeneration of myofibers and aggregates of abnormal mitochondria (Ferrans et al. 1964). These 

mitochondrial changes are indicative of disturbances in energy production or utilization possibly related 

to cobalt effects on lipoic acid. Cobalt irreversibly chelates lipoic acids under aerobic conditions (Webb 

1982). Lipoic acid is a required cofactor for oxidative decarboxylation of pyruvate to acetyl CoA and of 

α-ketoglutarate to succinate (Lehninger 1982). In the myocadrium of rats treated with cobalt, oxidation of 

pyruvate or fatty acids is impaired (Wiberg 1968). 

A number of investigators have reported that cobalt ions can result in increased damage to DNA when coexposed with oxidants in vitro, such as UV radiation or H2O2 (De Boeck et al. 1998; Hartwig et al. 1991; 

Nackerdien et al. 1991). It is believed that cobalt acts by inhibition of DNA repair, particularly the 

incision and polymerization steps (Asmuß et al. 2000; Kasten et al. 1997), accomplishing this through 

interaction with zinc finger DNA repair proteins (Asmuß et al. 2000; Sarkar 1995). 

Another potentially important mechanism by which cobalt may exert effects is through its effects on 

heme and heme-containing enzymes. Cobalt is thought to inhibit heme synthesis in vivo by acting upon 

at least two different sites in the biosynthetic pathway: synthesis of 5-aminolevulinate and conversion of 

5-aminolevulinate into heme (de Matteis and Gibbs 1977). This inhibitory activity might result in the 

formation of cobalt protoporphyrin rather than heme (Sinclair et al. 1979). Cobalt treatment also 

stimulates heme oxidation in many organs, due to the induction of heme oxygenase (for review, see 

Sunderman 1987). Effects on heme synthesis may potentially affect a wide variety of heme-containing 

proteins, including monooxygenase enzymes (i.e., cytochromes P450) and catalase (Legrum et al. 1979; 

Yasukochi et al. 1974). Conversely, cobalt acts, through a mechanism believed to involve a hemecontaining protein, to increase erythropoietin, which stimulates the production of red blood cells 

(Di Giulio et al. 1991; Goldberg et al. 1988; Smith and Fisher 1973). The regulatory mechanisms behind 

this apparent dichotomy have not been fully elucidated. 

Another potential mechanism by which cobalt may exert its effects is through interactions with the 

immune system. Exposure of humans to cobalt by the inhalation and dermal routes have resulted in 
 

 

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sensitization to cobalt (Alomar et al. 1985; Bencko et al. 1983; Dooms-Goossens et al. 1980; Fischer and 

Rystedt 1983; Goh et al. 1986; Kanerva et al. 1988; Marcussen 1963; Shirakawa et al. 1988, 1989; Valer 

et al. 1967). Exposure to inhaled cobalt chloride aerosols can precipitate an asthmatic attack in sensitized 

individuals (Shirakawa et al. 1989), suggesting cobalt sensitization as one mechanism by which cobaltinduced asthma may be produced. IgE and IgA antibodies specific to cobalt have been reported in 

humans (Bencko et al. 1983; Shirakawa et al. 1988, 1989). There is evidence that cobalt sensitivity in 

humans may to be regulated by T-lymphocytes (Katsarou et al. 1997). A human helper T-lymphocyte 

cell line specific for cobalt (CoCl2) has been established (Löfström and Wigzell 1986). Cobalt may also 

interact directly with immunologic proteins, such as antibodies or Fc receptors, to result in 

immunosensitization (Cirla 1994). In vitro, cobalt(II) has been shown to reduce the proliferation of both 

B and T lymphocytes, as well as the release of the cytokines IL-2, IL-6, and IFN-Gamma (Wang et al. 

1996). Interrelationships exist between nickel and cobalt sensitization (Bencko et al. 1983; Rystedt and 

Fisher 1983); however, the extent of any potential interactions between the two metals on immunologic 

end points is not well understood. In guinea pigs, nickel and cobalt sensitization appear to be interrelated 

and mutually enhancing (Lammintausta et al. 1985), though cross-reactivity was not reported to occur. 

Cobalt has been shown to have a number of effects on glucose metabolism. Treatment of animals with 

cobalt results in a depression of serum (Eaton and Pommer 1973; Ybarra et al. 1997) or tissue (Wiberg 

1968) glucose levels. In rats made diabetic by pretreatment with streptozotocin, this depression was 

persistent, whereas it was transient in normal rats (Ybarra et al. 1997). Many of the effects of cobalt on 

glucose metabolism are thought to result from alterations in the expression of the glut family of glucose 

transport proteins, a family of facilitative Na+-independent transport proteins thought to mediate noninsulin-dependent transport of glucose. Exposure to soluble cobalt results in increased expression of 

these genes, particularly GLUT1, in cells of the liver, kidney cortex, myocardium, skeletal muscle, and 

cerebrum (Behrooz and Ismail-Beigi 1997; Ybarra et al. 1997). Cobalt also reduces the amount of 

glucose produced in liver cells following stimulation with glucagon (Eaton and Pommer 1973; Yamatani 

et al. 1998), as well as reducing insulin release in isolated rat islets (Henquin and Lambert 1975). 

Radioactive Cobalt. Due to the nature of its ionizing radiation, radioactive cobalt can present a health 

hazard. Highly-penetrating gamma emissions are the major source of damage to tissues and internal 

organs following external exposure to radioactive cobalt isotopes. If radioactive cobalt is internalized, 

nearby tissues are at highest risk for damage due to the release of beta particles. In either case, exposure 

to ionizing radiation results in an increased risk of cellular damage. Both beta and gamma radiations are 
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capable of producing ionization events when they hit cellular molecules, including DNA, RNA, or lipids. 

Ionized molecules within irradiated cells may be repaired quickly to prevent further damage. On the 

other hand, irreparable damage may be imposed on cellular materials, such as DNA, which might 

ultimately result in either cell death or the formation of cancerous tumors. Very large acute radiation 

doses can damage or kill enough cells to cause the disruption of organ systems, resulting in acute 

radiation syndrome or even death. Human and animal data indicate that sufficiently high exposures to 

cobalt radiation can result in adverse effects such as reduced fertility, abnormal development, 

genotoxicity, pulmonary fibrosis, gastrointestinal atrophy and fibrosis, hematological and lymphoreticular 

disorders, cancer, and death (Chang et al. 1999b; Davis et al. 1992; Dinehart et al. 1991; Hashimoto and 

Mitsuyasu 1967; Klener et al. 1986; Libshitz 1993; Myskowski and Safai 1981; Rauscher and Bauchinger 

1983; Roschler and Woodard 1969; Roswit and White 1977; Stavem et al. 1985; Van Oort et al. 1984). 

For a more complete discussion of the mechanisms associated with the toxic effects of ionizing radiation, 

refer to Chapter 5 of the Toxicological Profile for Ionizing Radiation (Agency for Toxic Substances and 

Disease Registry 1999). 

3.6.3 Animal-to-Human Extrapolations 

Bailey et al. (1989) reported a wide variation across species, including man, in the retention and clearance 

of inhaled physiologically insoluble 57Co particles (see Table 3-8), noting that this variation illustrates 

the potential difficulty of extrapolating the results of animal lung retention experiments to human even 

qualitatively. Species differences in absorption of physiologically insoluble cobalt oxide following oral 

exposure do not appear to exist (Bailey et al. 1989), although humans were not examined. Absorption of 

soluble cobalt compounds is greater in rats (13–34%) than in dairy cows (1–2%) and guinea pigs (4–5%) 

following oral exposure (Ayala-Fierro et al. 1999; Barnaby et al. 1968; Hollins and McCullough 1971; 

Kirchgessner et al. 1994; Naylor and Harrison 1995; Schade et al. 1970; Taylor 1962; van Bruwaene et al. 

1984). 

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 
 

 

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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). 

The available human and animal data suggest that the endocrine system, particularly the thyroid gland, 

may be a target of stable and radioactive cobalt toxicity. These effects are discussed in Sections 3.2 and 

3.3 under Systemic Effects. 

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 
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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 

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 
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3. HEALTH EFFECTS 

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). 

Though human data are lacking, animal studies have suggested several differences in pharmacokinetic 

behavior of cobalt compounds between children and adults. Following inhalation exposure to Co3O4, 

deposition tended to increase with age, though no significant differences were reported (Collier et al. 

1991). The youngest animals exposed (3 weeks postnatal) had the lowest fractional retention 182 days 

postexposure, though no differences were seen at day 7 or 83. The authors attributed this to a faster rate 

of translocation of cobalt from the lung to the blood, which could enhance subsequent excretion. Naylor 

and Harrison (1995) reported that in rats and guinea pigs, fractional absorption of cobalt following oral 

exposure was highest at 1 day after birth, and diminished rapidly with time thereafter. Collier et al. 

(1991) reported no difference in absorption of cobalt nitrate following oral exposure to animals aged 3– 

46 weeks, which is in agreement with the results of the later portion of the Naylor and Harrison (1995) 

study. No PBPK models specific for cobalt exposures to children were located. However, the ICRP 

Human Respiratory Tract Model is applicable to children, and may be used for children if the appropriate 

values for the parameters are used. 

Once in the bloodstream, soluble cobalt compounds have been shown, in animal studies, to cross the 

placenta and enter the fetus. Twenty-four hours after intravenous injection of cobalt chloride in rats, 

0.14% of the dose was found in the fetus, 0.19% in the chorioallantoic placenta, and 0.22% in the yolk sac 

(Zylicz et al. 1975). Several other rat studies (Nishimura et al. 1978; Zylicz et al. 1975, 1976) have 

demonstrated that the amount of cobalt crossing the placenta following intravenous injection is greater in 

later gestation stages, though the percent of the maternal dose reaching the fetus is still relatively low (in 

<1% of the maternal dose). The fetal uptake of cobalt following intravenous administration to the mother 

was increased when the cobalt was given as cyanocobalmin, relative to cobalt chloride (~5% of the 

maternal dose for cyanocobalmin, compared to <1% for cobalt chloride) (Nishimura et al. 1978), 

indicating that the form of the cobalt compound may affect its availability to the fetus. 
COBALT 161 

3. HEALTH EFFECTS 

Cobalt has been detected in human breast milk (Byczkowski et al. 1994; Kratchler et al. 1998). In 

general, physiological concentrations of cobalt in breast milk are very low, on the order of parts per 

billion (Byczkowski et al. 1994). Animal studies are in agreement with this observation. By day 70 postexposure in lactating dairy cows orally exposed to cobalt chloride, the milk contained 0.012% of the dose 

(van Bruwaene et al. 1984). One to two percent of cobalt given intravenously to mother rats as 

cyanocobalmin was transferred to offspring via the breast milk (Nishimura et al. 1978). 

Health Effects from Exposure to Stable Cobalt. Available data have not clearly defined whether 

children are at greater risk from exposure to stable cobalt than adults. Studies in adult humans have 

identified several health effects of cobalt compounds following inhalation, oral, or dermal exposure. Data 

on effects of cobalt in children following inhalation exposures are lacking. Jacobziner and Raybin (1961) 

reported on two cases of children who had accidentally ingested unknown amounts of cobalt chloride; a 

19-month-old male died approximately 6.5 hours after ingestion, whereas a 3-year-old male was given 

medical treatment and showed no symptoms after ingestion. Several studies (Chamberlain 1961; Little 

and Sunico 1958; Sederholm et al. 1968; Washburn and Kaplan 1964) have reported enlarged thyroid 

glands in children given cobalt chloride for treatment of anemia; removal of cobalt therapy resulted in a 

return to normal thyroid size. Patch testing of children aged 4–14 years revealed a 13.3% dermal 

sensitization rate to cobalt chloride (Romaguera and Vilaplana 1998). More girls reacted positively than 

boys, which the authors attributed to the wearing of costume jewelry, which often contains cobalt, and the 

resulting exposure. 

Offspring of mice intravenously injected with approximately 1.2 mg cobalt/kg at day 8 of gestation, but 

not at day 3, showed a significant increase in the number of skeletons with delayed ossification (Wilde 

1984). Other studies, however, have not shown developmental effects of stable cobalt compounds, or 

have shown effects only at maternally toxic doses (Domingo et al. 1985b; Paternian et al. 1988; 

Seidenberg 1986). 

Health Effects from Exposure to Radioactive Cobalt. Taiwanese children (48 boys, 37 girls) who were 

raised in apartments contaminated with 60Co were compared to 21,898 age- and sex-matched non-exposed 

children from a nationwide surveillance program (Wang et al. 2001). After adjusting for effects from 

parental heights and body mass index, clear dose-related decreases in height percentile (HP) and agespecific relative height differences (RHD) were seen in exposed boys, but not in exposed girls. Average 
COBALT 162 

3. HEALTH EFFECTS 

cumulative exposures were 120.8 and 129.9 mSv (equivalent to ~12.1 or 13 rad) for the boys and girls, 

respectively. 

No other studies of human children exposed to radioactive cobalt or cobalt radiation were located. As 

rapidly-dividing cells are more sensitive to radiation, the developing fetus and growing children are 

expected to be more sensitive to cobalt radiation than adults. 

Animal studies have shown that exposures to external radiation from cobalt isotopes (as low as 10 rad 

[0.1 Gy] in mice) may have a dramatic effect on the developing fetus (see Section 3.2.4.6 and Agency for 

Toxic Substances and Disease Registry 1999). Exposure duration, gestational day, and dose all influence 

the effect of cobalt radiation on the developing organism. Radiation exposure to very young dogs (80 rad 

[0.8 Gy] on day 2 or 70 postpartum) has resulted in an increased incidence of diabetes mellitus, renal 

disease, and cancer (Benjamin et al. 1998a, 1998b). 

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 
 

 

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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 cobalt are discussed in Section 3.9.1. 

Biomarkers of effect are defined as any measurable biochemical, physiologic, or other alteration within an 

organism that, depending on magnitude, can be recognized as an established or potential health 

impairment or disease (NAS/NRC 1989). This definition encompasses biochemical or cellular signals of 

tissue dysfunction (e.g., increased liver enzyme activity or pathologic changes in female genital epithelial 

cells), as well as physiologic signs of dysfunction such as increased blood pressure or decreased lung 

capacity. Note that these markers are not often substance specific. They also may not be directly 

adverse, but can indicate potential health impairment (e.g., DNA adducts). Biomarkers of effects caused 

by cobalt 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 Cobalt 

Biomonitoring data exist that demonstrate a positive correlation between occupational exposure levels of 

cobalt and the levels of cobalt in both the urine and blood (Table 3-12) (Alexandersson 1988; Ichikawa et 

al. 1985; Lison et al. 1994; Nemery et al. 1992; Scansetti et al. 1985). Available studies of unexposed 

humans have reported cobalt blood levels of 0.05–0.19 μg/dL and urinary cobalt levels of 0.04–2 μg/dL 

(Alexandersson 1988; Ichikawa et al. 1985). Figure 3-10 graphically presents the cobalt exposure data 

and cobalt in blood data presented in Table 3-12 (Ichikawa et al. 1985). The highest excretion rate of 

cobalt in urine occurs during the first 24 hours after short-term exposure; therefore, subjects should be 

tested quickly to assess whether cobalt exposure has occurred (Alexandersson 1988). Occupational 

exposure to 0.1 mg/m3

 cobalt resulted in blood levels of cobalt ranging (95% CI) from 0.57 to 0.79 μg/dL, 

compared to 0.19 μg/dL in unexposed workers, and urinary levels from 59 to 78 μg/L, compared to 

2 μg/L in unexposed workers (Ichikawa et al. 1985). Correlations between recent exposure and cobalt 

levels in the blood or urine are more consistent for soluble cobalt compounds (metal, salts, and hard 
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3. HEALTH EFFECTS 

Table 3-12. Cobalt Exposure Concentrations and Amounts in the Blood and 

Urine of Subjects Examineda
 

Cobalt in airb Cobalt in bloodb Cobalt in urineb 

Subjects Number mean±SD μg/m3 mean±SD μg/dL mean±SD μg/L 

Powder handlers 2 186±108 (110–262) 1.08±0.28 (0.88–1.28) 148±13 (138–158) 

Rubber press 6 367±324 (92–859) 1.87±1.96 (0.40–5.30) 235±182 (41–392) 

operators 

Automatic press 11 56±60 (9–210) 0.57±0.53 (0.10–0.95) 34±43 (4–73) 

operators 

Shapers (lathing) 7 33±15 (15–62) 0.67±0.44 (0.14–1.34) 33±30 (11–95) 

Shapers (sawing) 21 50±35 (8–144) 0.52±0.31 (0.15–1.15) 41±60 (6–266) 

Sintering workers 21 28±30 (4–145) 0.26±0.10 (0.09–0.45) 10±10 (2–46) 

Wet grinders 

A 27 44±48 (4–227) 0.42±0.31 (0.10–1.30) 35±34 (2–180) 

B 18 45±50 (3–161) 0.33±0.10 (0.16–0.52) 19±15 (2–67) 

C 12 92±92 (15–291) 0.43±0.39 (0.12–1.90) 68±87 (3–265) 

D 25 44±54 (3–205) 0.35±0.20 (0.10–1.00) 17±16 (1–69) 

Workers using 25 317±307 (7–1,203) 0.65±0.86 (0.20–3.90) 26±30 (1–119) 

respirators 

Office workers 20 No data 0.19±0.11 (0.08–0.40) 2±1 (1–4) 

a

Adapted from Ichikawa et al. 1985 

b

The range of each value is given in parentheses. 

SD = standard deviation 
 

:g/dl 

2.5 

2 

1.5 

1 

0.5 

0 

y = 0.0044 x +0.23

r = 0.96 

P<0.001 

0 100 200 300 400 :g/m3 

COBALT IN AIR 

*Adapted from Ichikawa et al. 1985 

COBALT 165 

3. HEALTH EFFECTS 

Figure 3-10. Relation Between Mean Cobalt Exposure and Mean Blood 

Concentration of Cobalt in Exposed Workers* 
 

 

COBALT 166 

3. HEALTH EFFECTS 

metals), while blood and/or urinary cobalt levels are less reflective of recent exposure for less soluble 

compounds (cobalt oxides) (Lison et al. 1994). 

Sensitive serum protein responses were found in animals exposed to cobalt at levels below those 

necessary to produce hematopoietic effects (Stokinger and Wagner 1958). These serum protein responses 

included an increase in alpha globulin fractions of serum proteins and associated serum neuraminic acid. 

The responses were observed in rabbits and dogs following both inhalation and injection of cobalt. The 

authors indicated that this increase was a unique response to cobalt exposure. The characteristics of the 

response were similar to those of the erythropoietic response found following exposure to higher levels of 

cobalt; the response is delayed, does not occur in all animals within a given exposure group, is not of 

great magnitude, and is not persistent (Stokinger and Wagner 1958). 

Biomarkers specific for exposure to cobalt radioisotopes have not been reported. 

3.9.2 Biomarkers Used to Characterize Effects Caused by Cobalt 

Sensitization to cobalt results in cobalt-specific changes in serum antibodies (IgE and IgA) that may be 

monitored to determine if sensitization, or additional exposure, to cobalt has occurred (Bencko et al. 

1983; Shirakawa et al. 1988, 1989). 

No biomarkers specific for effects of radioactive cobalt isotopes have been reported. Biomarkers for 

response to ionizing radiation are discussed in Agency for Toxic Substances and Disease Registry (1999). 

3.10 INTERACTIONS WITH OTHER CHEMICALS 

A major medical use of cobalt is in combination with bleomycin, an antineoplastic antibiotic, as a tumorlocalizing and therapeutic agent (Goodwin and Meares 1976; Hansen et al. 1976; Kapstad 1978, 1979). 

The anti-tumor effects of the two agents are amplified when given in combination with each other. The 

complex, wherein cobalt is coordinately bound to the bleomycin molecule, is intravenously injected and 

acts by binding to and cleaving the DNA in the tumor cells (Kakinuma and Orii 1982). 
 

 

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The interaction of cobalt with various chelators has been investigated in animals for mitigation of the 

toxicity of cobalt (Baker et al. 1987; Domingo et al. 1983; Llobet et al. 1988). Glutathione, N-acetylL-cysteine (NAC) and diethylenetriaminepentaacetic acid (DTPA), administered to rats previously 

exposed to cobalt, significantly increased urinary excretion of cobalt, while EDTA, NAC, and 2,3-dimercaptosuccinic acid (DMSA) increased fecal excretion. NAC was the most effective chelator because 

it increased both urinary and fecal excretion of cobalt while decreasing its levels in liver and spleen 

(Llobet et al. 1988). Cysteine, also acting as a chelator, mitigated the toxicity of cobalt when both 

chemicals were given to chicks in the feed (Baker et al. 1987). 

A number of studies have suggested an association between cobalt ions and calcium ions. Soluble cobalt 

has also been shown to alter calcium influx into cells, functioning as a blocker of inorganic calcium 

channels (Henquin et al. 1983; Moger 1983; Yamatani et al. 1998). This mechanism has been linked to a 

reduction of steroidogenesis in isolated mouse Leydig cells (Moger 1983). Additionally, soluble cobalt 

has been shown to alter the inorganic calcium influx in liver cells after exposure to glucagon (Yamatani et 

al. 1998), and calcium influx into pancreatic β cells (Henquin et al. 1983) and isolated rat islets (Henquin 

and Lambert 1975). Cobalt may also affect neuromuscular transmission through antagonism with 

calcium (Weakly 1973). 

Hard metal, consisting of 5–10% cobalt with the balance being tungsten carbide, has been shown to be 

considerably more toxic than cobalt alone, resulting from interactions between particles of cobalt metal 

and tungsten carbide particles. The mechanisms responsible for this interaction are discussed in 

Section 3.6.2. 

An interrelationship between cobalt and nickel sensitization has been reported in individuals exposed to 

the two metals (Rystedt and Fisher 1983; Veien et al. 1987), as well as in animal studies (Wahlberg and 

Lidén 2000). It was concluded that the combination of nickel sensitivity and irritant eczema resulted in a 

high risk for developing an allergy to cobalt. Studies of cultured alveolar type II cells showed a 

synergistic (greater than additive) response to co-exposure to cobalt and nickel chlorides (Cross et al. 

2001). 
 

 

COBALT 168 

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3.11 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE 

A susceptible population will exhibit a different or enhanced response to cobalt than will most persons 

exposed to the same level of cobalt 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 cobalt, or compromised function of organs affected by 

cobalt. Populations who are at greater risk due to their unusually high exposure to cobalt are discussed in 

Section 6.7, Populations With Potentially High Exposures. 

Individuals who are already sensitized to cobalt may be unusually susceptible because cobalt exposure 

may trigger asthmatic attacks (Shirakawa et al. 1988, 1989). Sensitization to cobalt results in cobaltspecific changes in serum antibodies (IgE and IgA) (Bencko et al. 1983; Shirakawa et al. 1988, 1989). 

Potolicchio et al. (1997, 1999) have suggested that individuals with a polymorphism in the HLA-DP gene 

(presence of glutamate 69 in the β chain) may be more susceptible to hard metal lung disease. Individuals 

with ongoing respiratory illness may also be more susceptible to the effects of inhaled cobalt. Following 

oral exposure, individuals with iron deficiency may at greater risk, as animal studies have shown an 

increased absorption of cobalt compounds in iron-deficient animals (Reuber et al. 1994; Schade et al. 

1970). Studies of beer-cobalt cardiomyopathy have suggested that individuals with high alcohol 

consumption may be more susceptible to health effects of cobalt (Alexander 1969, 1972; Morin et al. 

1971). 

Ionizing radiation has greater effects on rapidly-dividing cells than on those that divide at a slower rate. 

The most sensitive population to exposure to cobalt radiation is likely to be the developing fetus, as even 

moderate exposures to cobalt radiation have been shown to cause dramatic effects on the developing fetus 

in animal studies (see Section 3.2.4.6), Likewise, growing children are likely to be more susceptible to 

cobalt radiation than adults, and people who are immunocompromised, have existing lung diseases, or 

who have defects in genetic repair enzymes would be expected to show an increased susceptibility to 

cobalt radiation. A detailed discussion on the effects of ionizing radiation in children can be found in 

Agency for Toxic Substances and Disease Registry (1999). 
COBALT 169 

3. HEALTH EFFECTS 

3.12 METHODS FOR REDUCING TOXIC EFFECTS 

This section will describe clinical practice and research concerning methods for reducing toxic effects of 

exposure to cobalt. 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 cobalt. 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 

cobalt: 

Ellenhorn MJ, Schonwald S, Ordog G, et al., eds. 1997. Medical toxicology: Diagnosis and treatment of 

human poisoning. 2nd edition. Baltimore, MD: Williams & Wilkins, 1682–1723. 

Goldfrank, LR, Flomenbaum, NE, Lewin, NA, et al., eds. 1998. Toxicological emergencies. 6th edition. 

Connecticut: Appleton & Lange, 481t, 489, 490t, 1338–1339. 

REAC/TS. Radiation Emergency Assistance Center/Training Site. www.orau.gov/reacts/. 

3.12.1 Reducing Peak Absorption Following Exposure 

Methods for reducing peak absorption are similar for both the stable and radioactive forms of cobalt. 

General management and treatment of patients following acute exposure to cobalt includes removal of the 

victim from the contaminated area, and removal and isolation of contaminated clothing, jewelry, and 

shoes (Bronstein and Currance 1988; Stutz and Janusz 1988). The excess solid contaminant is gently 

brushed away, and excess liquids are blotted with absorbent material. If the victim is in respiratory 

distress, ventilation assistance is provided and oxygen is administered. Measures that are appropriate to 

the route of exposure are then taken to remove cobalt from the body. Following ocular exposure, the eyes 

are immediately flushed thoroughly with water. Skin is washed immediately with soap or mild detergent 

and water. Some evidence has been presented that the use of cheating creams on the skin can reduce the 

occurrence of symptoms in allergic persons (Wöhrl et al. 2001). Following ingestion of cobalt, two 

conflicting forms of treatment have been recommended. Stutz and Janusz (1988) recommend that victims 

over 1 year old be given ipecac, followed by activated charcoal (after vomiting). A cathartic, such as 

magnesium sulfate in water, is then administered to adults and children. Bronstein and Currance (1988) 

recommend that the victim be given water for dilution of the cobalt; however, they recommend that 

emetics not be administered. Following all routes of exposure, victims are monitored for pulmonary 

edema, circulatory collapse, and shock, and treated as necessary. 
 

 

COBALT 170 

3. HEALTH EFFECTS 

3.12.2 Reducing Body Burden 

Chelation therapy with EDTA or dimercaprol can be effectively used if necessary (Goldfrank et al. 1990; 

Haddad and Winchester 1990; Stutz and Janusz 1988). Animal studies have investigated the 

effectiveness of various chelating agents for mitigating the toxicity of cobalt (Baker et al. 1987; Domingo 

et al. 1983; Llobet et al. 1988). NAC was found to be the most effective chelator because it increased 

both urinary and fecal excretion of cobalt as well as decreased the levels of cobalt in the liver and spleen 

(Llobet et al. 1988). These chelators react chemically with cobalt, so they are effective for both stable 

and radioactive cobalt isotopes. For more complete information on treatment of specific symptoms, refer 

to Bronstein and Currance (1988) and Stutz and Janusz (1988). 

3.12.3 Interfering with the Mechanism of Action for Toxic Effects 

No studies were located in humans or animals regarding interfering with the mechanism of action of 

stable or radioactive cobalt 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 cobalt 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 cobalt. 

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. 
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3. HEALTH EFFECTS 

3.13.1 Existing Information on Health Effects of Cobalt 

The existing data on health effects of inhalation, oral, and dermal exposure of humans and animals are 

summarized in Figure 3-11 for stable cobalt and in Figure 3-12 for radioactive cobalt. The purpose of 

these figures is to illustrate the existing information concerning the health effects of cobalt. Each dot in 

the figure indicates that one or more studies provide information associated with that particular effect. 

The dot does not necessarily imply anything about the quality of the study or studies, nor should missing 

information in this figure be interpreted as a “data need”. A data need, as defined in ATSDR’s Decision 

Guide for Identifying Substance-Specific Data Needs Related to Toxicological Profiles (Agency for Toxic 

Substances and Disease Registry 1989), is substance-specific information necessary to conduct 

comprehensive public health assessments. Generally, ATSDR defines a data gap more broadly as any 

substance-specific information missing from the scientific literature. 

Figures 3-11 and 3-12 represent studies conducted with all forms of cobalt. The effects of cobalt have 

been studied in humans following both inhalation and oral exposure. Human dermal studies designed to 

investigate nondermal systemic effects of cobalt have been reported. Similarly, the effects of cobalt in 

animals have been studied following inhalation and oral exposure. Few dermal studies are available. 

3.13.2 Identification of Data Needs 

Stable Cobalt. Effects in humans following acute inhalation, oral, and dermal exposures to cobalt have 

been reported. In humans, the primary targets following acute exposure to cobalt include the respiratory 

system following inhalation exposure (Kusaka et al. 1986a), the thymus following oral exposure (Roche 

and Layrisse 1956), and the immunological system following dermal exposure (Alomar et al. 1985; 

Fischer and Rystedt 1983; Kanerva et al. 1988). Acute oral studies in animals have also identified the 

cardiovascular and hematopoietic systems as targets of cobalt toxicity (Domingo and Llobet 1984; 

Speijers et al. 1982). Although acute exposure levels associated with some of these effects in humans 

have been reported, the minimal acute exposure levels required to produce these effects are not known 

because few acute human studies exist. The results of animal studies of the acute toxicity of cobalt have 

been used to determine dose levels that produce death and respiratory effects following inhalation 

exposure, death and various systemic effects following oral exposure, and dermal and immunological 

effects following dermal exposure. 
 

Figure 3-11. Existing Information on Health Effects of Stable Cobalt 

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 

COBALT 172 

3. HEALTH EFFECTS 
 

Death

Acute 

Intermediate 

Chronic 

Immunologic/Lymphoretic 

Neurologic 

Reproductive 

Developmental 

Genotoxic 

Cancer 

Systemic 

Inhalation 

Oral 

Dermal 

External 

Human 

Death

Acute 

Intermediate 

Chronic 

Immunologic/Lymphoretic 

Neurologic 

Reproductive 

Developmental 

Genotoxic 

Cancer 

Systemic 

Inhalation 

Oral 

Dermal 

External 

Animal 

Existing Studies 

COBALT 173 

3. HEALTH EFFECTS 

Figure 3-12. Existing Information on Health Effects of Radioactive Cobalt 
COBALT 174 

3. HEALTH EFFECTS 

There were insufficient data for derivation of inhalation or oral acute MRLs because reported effects were 

severe and occurred at levels above those reported in the few human studies. Animal studies that identify 

minimally effective inhalation and oral exposure levels for the various cobalt compounds would be useful 

in estimating acute MRLs for each cobalt compound. Acute dermal studies would enable the 

determination of hazardous levels for this route of exposure. Because a small portion of the cobalt taken 

into the body is retained for a relatively long time, studies on the long-term consequences of acute 

exposure on the heart, respiratory tract, hematological system, and immune response could provide 

information about the potential for chronic effects of acute exposures in humans. Knowledge about the 

acute toxicity of cobalt is important because people living near hazardous waste sites might be exposed 

for brief periods. 

Radioactive Cobalt. Data on health effects following acute exposure to radioactive cobalt by the 

inhalation, oral, or dermal routes are lacking. Because all cobalt radioisotopes are man-made (see 

Chapter 5), only low-level exposure to radioactive cobalt in the environment by these routes is likely to 

occur. A number of health effects have been seen following cases of accidental acute exposure to high 

levels of external cobalt radiation in humans, including death, gastrointestinal disorders, hematological 

alterations, and dermal lesions (Klener et al. 1986; Stavem et al. 1985). Acute-exposure animal studies 

have shown pronounced effects, including death, cardiovascular changes, gastrointestinal effects, kidney 

effects, and neurobehavioral changes (Brady and Hayton 1977b; Bruner 1977; Cockerham et al. 1986; 

Darwezah et al. 1988; Down et al. 1986; Gomez-d-Segura et al. 1998; Hanks et al. 1966; King 1988a; 

Mele et al. 1988; Page et al. 1968; Robbins 1989a, 1989b, 1989c, 1991a). The most pronounced effects 

in animals following acute exposure to cobalt radiation have been reproductive and developmental effects 

(see Sections 3.2.4.5 and 3.2.4.6). Agency for Toxic Substances and Disease Registry (1999) has derived 

an acute MRL for external exposure to ionizing radiation, which is applicable to external exposures to 

cobalt radiation, so additional data for the derivation of an MRL are not needed. 

Intermediate-Duration Exposure. 

Stable Cobalt. Information on oral exposure of humans to cobalt, in the form of cobalt chloride added to 

beer as a foam stabilizer, provides the only human data available for exposure of intermediate duration 

(Alexander 1969, 1972; Morin et al. 1971). Inhalation and dermal data in humans were not located for 

this duration of exposure. The cardiac and hematopoietic systems are the primary targets in humans 

following oral exposure to cobalt. Some exposure levels associated with cardiomyopathy have been 
 

 

 

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3. HEALTH EFFECTS 

reported following oral exposure, but the minimal exposure level required to produce this effect in 

humans is not known (Alexander 1969, 1972; Morin et al. 1971). Oral studies in animals reported dose 

levels associated with death, various systemic and neurological effects, and effects on reproduction and 

development (Domingo et al. 1984, 1985b; Krasovskii and Fridlyand 1971; Mohiuddin 1970; 

Mollenhauer et al. 1985; Pedigo et al. 1988). Intermediate-duration inhalation studies in animals reported 

that the respiratory tract is the target of the toxicity of inhaled cobalt (Bucher et al. 1990; Johansson et al. 

1987; Kerfoot 1975; NTP 1991; Palmes et al. 1959). Animal studies were insufficient for derivation of an 

intermediate-duration MRL for oral exposure, since the reported effects were severe and the effects 

occurred at levels above those reported in the few human studies. Dermal data in animals were not 

located. Animal studies that investigate the possible toxic interaction between cobalt and alcohol may be 

helpful in understanding the role of cobalt in the cardiomyopathy reported in the heavy beer drinkers 

(Alexander 1969, 1972; Morin et al. 1971). One such study in guinea pigs already exists (Mohiuddin et 

al. 1970), but this study used a single, high dose of cobalt. Studies using a series of lower doses, both 

with and without alcohol preexposure, would be helpful in determining the threshold for the cardiac 

effects. Intermediate-duration dermal studies would enable determination of hazardous levels for this 

route of exposure. Intermediate-duration toxicity information is important because people living near 

hazardous waste sites might be exposed for corresponding time periods. 

Radioactive Cobalt. Data on health effects following acute exposure to radioactive cobalt by the 

inhalation, oral, or dermal routes are lacking. Because cobalt radioisotopes are man-made (see 

Chapter 5), only low-level exposure to radioactive cobalt in the environment by these routes is likely to 

occur. Substantial human data exist concerning intermediate-duration exposure to external radiation, as 

radiotherapy treatment regimens fall into this duration category. Animal data from intermediate-duration 

external exposure also exist, but are less numerous. Additional intermediate-duration studies are not 

likely to provide substantial additions to our knowledge of radiation-induced toxic effects. 

Chronic-Duration Exposure and Cancer. 

Stable Cobalt. Chronic inhalation exposure levels in humans associated with respiratory effects have 

been reported (Gennart and Lauwerys 1990; Nemery et al. 1992; Shirakawa et al. 1988; Sprince et al. 

1988). In humans, the respiratory system is the primary target following chronic inhalation exposure. A 

chronic-duration inhalation MRL was derived from a NOAEL for decreased ventilatory function in 

exposed workers (Nemery et al. 1992). Wehner et al. (1977) reported no adverse effects in hamsters 
 

 

COBALT 176 

3. HEALTH EFFECTS 

exposed chronically to cobalt oxide. NTP (1998; Bucher et al. 1999) exposed rats and mice to cobalt 

sulfate for 2 years, reporting pronounced effects on the respiratory tract, including hyperplasia, 

inflammation, fibrosis, and metaplasia; an increased incidence of cancer was also reported. Chronic oral 

or dermal studies have not been reported in either humans or animals. Animal studies that identify 

minimally effective chronic oral exposure levels would be useful for estimating a chronic MRL. Chronic 

dermal studies would enable determination of hazardous levels for this route of exposure. Chronic 

toxicity information is important because people living near hazardous waste sites might be exposed to 

cobalt for many years. 

Several studies of hard metal exposure in humans have reported increases in lung cancer mortality from 

occupational inhalation exposure to hard metal (Lasfargues et al. 1994; Moulin et al. 1998; Wild et al. 

2000). In humans, cancer has not been reported following exposure to cobalt by the oral or dermal routes. 

An increased incidence of alveolar/bronchiolar neoplasms was noted following lifetime exposure of male 

rats to 1.14 mg cobalt/m3

 and in female rats to 0.38 mg cobalt/m3 as cobalt sulfate, with tumors occurring 

in both sexes with significantly positive trends (Bucher et al. 1999; NTP 1998). Similarly, mice of both 

sexes exposed to 1.14 mg cobalt/m3

 showed an increase in alveolar/bronchiolar neoplasms, again with 

lung tumors occurring with significantly positive trends. Parenteral exposure to cobalt has been found to 

induce tumors (Gilman 1962; Gilman and Ruckerbauer 1962; Heath 1956, 1969; Heath and Daniel 1962; 

Shabaan et al. 1977). Further chronic exposure studies by the oral and dermal routes may determine the 

actual carcinogenic potential of cobalt. Also, studies examining the effect of cobalt speciation (i.e., cobalt 

metal vs. cobalt sulfate) would add to our understanding of the carcinogenic potential of cobalt. 

Radioactive Cobalt. Data on health effects following chronic exposure to radioactive cobalt by the 

inhalation, oral, or dermal routes are lacking. Because cobalt radioisotopes are man-made (see 

Chapter 5), only low-level exposure to radioactive cobalt in the environment by these routes is likely to 

occur. Limited data exist on chronic exposure to cobalt radiation in humans, with genotoxicity, 

immunologic effects, and cancer being the primary end points examined. Animal data are similarly 

limited. Additional human or animal data following chronic exposure to external cobalt radiation would 

be useful in further identifying possible long-term health effects or susceptible populations. Agency for 

Toxic Substances and Disease Registry (1999) has derived a chronic-duration MRL for external radiation 

exposure, which is applicable to external exposures to cobalt radiation, so additional data for the 

derivation of an MRL are not needed. 
 

 

 

COBALT 177 

3. HEALTH EFFECTS 

Genotoxicity. 

Stable Cobalt. Gennart et al. (1993) reported an increase in sister-chromatid exchanges in workers 

exposed to a mixture of cobalt, chromium, nickel, and iron. De Boeck et al. (2000) reported no 

significant change in the comet assay on lymphocytes from nonsmoking workers who were 

occupationally exposed to cobalt or hard metal dusts; a positive association was found between hard 

metal exposure and increased micronucleus formation in smokers only. 

Data regarding the mutagenic action of cobalt in bacterial cell lines and mammalian cell lines have been 

reported in the literature (Hamilton-Koch et al. 1986; Kharab and Singh 1985; Ogawa et al. 1986). In 

vivo mutagenicity studies in animals following inhalation, oral, or dermal exposure to cobalt would be 

helpful in ascertaining its true mutagenic potential. Further studies examining the differences in 

genotoxicity between different valence states of cobalt would also be useful. 

Radioactive Cobalt. Data on genotoxic effects following exposure to radioactive cobalt by the inhalation, 

oral, or dermal routes are lacking. Because cobalt radioisotopes are man-made (see Chapter 5), only lowlevel exposure to radioactive cobalt in the environment by these routes is likely to occur. Several studies 

have demonstrated genotoxic effects in humans exposed to external cobalt radiation (Chang et al.1999c; 

House et al. 1992; Rauscher and Bauchinger 1983). Numerous data from animal studies exist 

demonstrating the genotoxic effects of ionizing radiation, including cobalt radiation. 

Reproductive Toxicity. 

Stable Cobalt. No studies were located regarding the reproductive effects of cobalt in humans following 

exposure by any route. Inhalation and oral studies in male animals have demonstrated adverse effects on 

reproductive organs (Anderson et al. 1992, 1993; Bucher et al. 1990; Corrier et al. 1985; Domingo et al. 

1985b; Mollenhauer et al. 1985; NTP 1991; Pedigo et al. 1988). One study also reported effects on the 

estrous cycle in mice following inhalation exposure (Bucher et al. 1990; NTP 1991). Multigenerational 

studies would be helpful in assessing the significance of these effects on reproductive performance. 

Radioactive Cobalt. Data on reproductive effects following exposure to radioactive cobalt by the 

inhalation, oral, or dermal routes are lacking. Because cobalt radioisotopes are man-made (see 

Chapter 5), only low-level exposure to radioactive cobalt in the environment by these routes is likely to 

occur. Human data on reproductive effects following external exposure to cobalt radiation are lacking, 
COBALT 178 

3. HEALTH EFFECTS 

but are sufficiently understood for gamma radiation. Available animal studies are limited, but have 

demonstrated radiation-induced deficits on reproductive ability in both genders (Cunningham and 

Huckins 1978; Laporte et al. 1985; Searl et al. 1976, 1980). Additional data in humans and animals 

would be helpful in refining minimal effective doses for radiation effects on reproduction. 

Developmental Toxicity. 

Stable Cobalt. No developmental effects were observed in the children of 78 women given cobalt 

chloride orally during pregnancy for treatment of anemia (Holly 1955); however, only a limited 

examination of offspring was reported, and details of examined end points were not reported. No studies 

of developmental effects by other routes of exposure in humans were located. Developmental effects in 

animals following oral exposure during gestation, however, have been observed (Domingo et al. 1985b). 

Further developmental studies in animals by all relevant routes of exposure (inhalation, oral, dermal) may 

clarify the potential developmental effects of cobalt in humans. 

Radioactive Cobalt. Data on developmental effects following exposure to radioactive cobalt by the 

inhalation, oral, or dermal routes are lacking. Because cobalt radioisotopes are man-made (see 

Chapter 5), only low-level exposure to radioactive cobalt in the environment by these routes is likely to 

occur. No human studies describing developmental effects of exposure to external cobalt radiation were 

located. Extensive data from animal studies have shown that even acute exposures to small amounts of 

cobalt radiation may elicit profound effects on the developing organism (see Section 3.2.4.6). The effects 

of ionizing radiation on the developing organism are also described in the Agency for Toxic Substances 

and Disease Registry Toxicological Profile for Ionizing Radiation (1999). 

Immunotoxicity. 

Stable Cobalt. Humans have been shown to develop sensitivity to cobalt following occupational 

exposure (Bencko et al. 1983; Shirakawa et al. 1988, 1989). No immunological effects were observed 

following oral exposure of humans to cobalt. Similar evidence of sensitization has been reported in 

animals (Lammintausta et al. 1985). Studies examining the mechanism of sensitization might be helpful 

in fully understanding and treating this effect in humans. A battery of immune function tests would 

further assess the immunotoxicity of cobalt in humans and animals. 
COBALT 179 

3. HEALTH EFFECTS 

Radioactive Cobalt. Data on immunotoxic effects following exposure to radioactive cobalt by the 

inhalation, oral, or dermal routes are lacking. Because cobalt radioisotopes are man-made (see 

Chapter 5), only low-level exposure to radioactive cobalt in the environment by these routes is likely to 

occur. Following external exposure to cobalt radiation, above levels normally encountered except for 

medical procedures, decreases in white blood cell counts have been seen in both humans and animals. 

Further studies on the immunotoxic effects of external cobalt radiation would be useful in refining the 

minimum effective dose. 

Neurotoxicity. 

Stable Cobalt. No studies were located regarding neurotoxic effects of cobalt in humans following oral 

or dermal exposure. Two occupational inhalation exposure studies have reported memory deficits, optic 

atrophy, or nerve deafness in humans exposed to cobalt (Jordan et al. 1990; Meecham and Humphrey 

1991). In animals, alterations in several neurologic parameters were found following oral exposure 

(Bourg et al. 1985; Krasovskii and Fridlyand 1971; Mutafova-Yambolieva et al. 1994; Nation et al. 1983; 

Singh and Junnarkar 1991; Vassilev et al. 1993; Wellman et al. 1984). Additional studies in animals 

would assist in determining whether these neurological effects have any relevance to potential effects in 

humans. 

Radioactive Cobalt. Data on neurotoxic effects following exposure to radioactive cobalt by the 

inhalation, oral, or dermal routes are lacking. Because cobalt radioisotopes are man-made (see 

Chapter 5), only low-level exposure to radioactive cobalt in the environment by these routes is likely to 

occur. Human data following cobalt radiotherapy have demonstrated effects believed to result from 

neurological damage, but data are limited, doses were extreme, and effects have not been wellcharacterized. Several animal studies have shown neurobehavioral or neurophysiological changes 

following exposure to cobalt radiation (Bassant and Court 1978; Maier and Landauer 1989; Mele et al. 

1988). 

Epidemiological and Human Dosimetry Studies. 

Stable Cobalt. Epidemiological studies relating to cobalt exposure are available in the literature. Studies 

of persons exposed to cobalt occupationally are available (Kusaka et al. 1986a, 1986b; Shirakawa et al. 

1988, 1989; Sprince et al. 1988), dietetically (beer drinkers) (Alexander 1969, 1972; Morin et al. 1971), 

and medically (cobalt given to alleviate anemia) (Davis and Fields 1958; Holly 1955; Taylor et al. 1977). 
COBALT 180 

3. HEALTH EFFECTS 

Further studies assessing the cause/effect relationship between cobalt exposure and human health effects 

would be helpful in monitoring individuals living near a hazardous waste site to verify that documented 

exposure levels are not associated with adverse health effects. 

Radioactive Cobalt. Epidemiological data on exposure to radioactive cobalt by the inhalation, oral, or 

dermal routes are lacking. Because cobalt radioisotopes are man-made (see Chapter 5), only low-level 

exposure to radioactive cobalt in the environment by these routes is likely to occur. Human external 

exposures to cobalt radiation have been documented in the literature. Radiotherapy exposures, though to 

extremely high radiation doses, are generally well-controlled and documented, whereas environmental 

and accidental workplace exposures are less frequent and less well-documented. 

Biomarkers of Exposure and Effect. 

Exposure. 

Stable Cobalt. Information is available on the monitoring of cobalt exposure by the quantification of 

cobalt in urine and blood (Alexandersson 1988; Ichikawa et al. 1985; Scansetti et al. 1985). A portion of 

inhaled cobalt is rapidly excreted in the feces, and the amount retained in the body tends to be steadily 

excreted over time. Levels in body fluids, therefore, can be monitored up to several days after exposure. 

Many different methods for the detection of cobalt in body fluids have been reported (Section 7.1). 

Radioactive Cobalt. No information is available regarding biomarkers specific for exposure to cobalt 

radionuclides by the inhalation, oral, dermal, or external exposure routes. Biomarkers for exposure to 

ionizing radiation are discussed in Agency for Toxic Substances and Disease Registry (1999). Personal 

dosimeters (film or luminescent) are an artificial surrogate to measure the amount of exposure to external 

beta or gamma radiation, though these are not specific for radiation from cobalt radionuclides. 

Effect. 

Stable Cobalt. Alterations in serum proteins and changes in serum antibodies have been found that are 

specific for cobalt exposure (Stokinger and Wagner 1958). These changes may be the earliest indication 

of the effects of cobalt exposure. Further studies may reveal other cobalt-specific biomarkers that, in 
COBALT 181 

3. HEALTH EFFECTS 

combination with these changes, may alert health professionals to cobalt exposure before serious 

toxicological effects occur. 

Radioactive Cobalt. While in many cases radioactive cobalt itself can be measured following exposure, 

no information is available regarding biomarkers specific for effects of cobalt radionuclides following 

exposure by the inhalation, oral, dermal, or external exposure routes. Biomarkers for effects of ionizing 

radiation are discussed in Agency for Toxic Substances and Disease Registry (1999), and include changes 

in levels of formed elements of the blood as some of the most sensitive indicators. These biomarkers are 

believed to be suitable for monitoring exposure to cobalt radiation. 

Absorption, Distribution, Metabolism, and Excretion. Pharmacokinetic data in humans indicate 

that cobalt is absorbed through the lungs (Foster et al. 1989) and the gastrointestinal tract (Harp and 

Scoular 1952; Sorbie et al. 1971; Valberg et al. 1969), that cobalt is well distributed in the body with the 

highest concentration being found in the lungs following inhalation (Gerhardsson et al. 1984; Hewitt 

1988; Hillerdal and Hartung 1983; Teraoka 1981), and that some of the inhaled or ingested cobalt is 

rapidly excreted in the feces, with the amount retained in the body being excreted slowly, primarily in the 

urine (Foster et al. 1989; Paley et al. 1958; Smith et al. 1972). Pharmacokinetic studies in animals 

following inhalation and oral exposure have demonstrated similar responses (Andre et al. 1989; Bailey et 

al. 1989; Collier et al. 1989; Foster et al. 1989; Patrick et al. 1989; Talbot and Morgan 1989). Few data 

exist regarding the pharmacokinetics of cobalt following dermal exposure, though what data are available 

demonstrate that cobalt can be absorbed in small quantities through human (Scansetti et al. 1994) and 

animal (Inaba and Suzuki-Yasumoto 1979; Lacy et al. 1996) skin, with greater absorption occurring 

through damaged than intact skin. 

Comparative Toxicokinetics. Several inhalation and oral studies have compared the toxicokinetics 

of cobalt in several different species of animals, including humans (Andre et al. 1989; Bailey et al. 1989; 

Collier et al. 1989; Foster et al. 1989; Patrick et al. 1989; Talbot and Morgan 1989). No comparative 

pharmacokinetic studies following dermal exposure were located. These studies would be useful because 

humans are exposed via the skin in the workplace and may potentially be exposed via this route at waste 

sites. 
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3. HEALTH EFFECTS 

Methods for Reducing Toxic Effects. 

Stable and Radioactive Cobalt. Chelation therapy is expected to apply equally well to stable and 

radioactive cobalt isotopes. EDTA or British anti-lewisite (BAL) has been shown to effectively mitigate 

the toxicity of cobalt in humans (Goldfrank et al. 1990; Haddad and Winchester 1990; Stutz and Janusz 

1988). In animal studies examining the effectiveness of various chelators, n-acetyl cysteine (NAC) was 

shown to be the most effective (Llobet et al. 1988). It would be useful to determine the effective dose of 

NAC in humans. Studies examining the effectiveness of other chelating agents may be helpful in 

determining the most effective chelation therapy for humans. 

Children’s Susceptibility. 

Stable Cobalt. Data comparing the susceptibility of children to cobalt compounds are limited. Animal 

studies have suggested that absorption following inhalation or oral exposure may be greater in very young 

animals, resulting in increased systemic dose. Data are not available on the differences between children 

and adults following dermal exposure. Further studies on the susceptibility of young animals relative to 

adult animals may be useful in determining whether children are at greater risk from exposure to cobalt in 

the environment than adults. 

Radioactive Cobalt. No data are available on whether children are more susceptible to the effects of 

radioactive cobalt compounds than adults. Animal studies have shown that exposure in utero to even 

moderate amounts of cobalt radiation can cause dramatic effects in the developing organism. It would be 

expected that children would be more susceptible to the effects of external cobalt radiation, due to the 

greater percentage of rapidly-dividing cells during growth. 

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 

Relevant ongoing studies were not located for cobalt. 
COBALT 183 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

4.1 CHEMICAL IDENTITY 

Cobalt is a naturally-occurring element that appears in the first transition series of Group 9 (VIII) of the 

periodic table along with iron and nickel. There is only one stable isotope of cobalt, 59Co. There are 

about 26 known radioactive isotopes of cobalt, of which only two are of commercial importance, 60Co and 

57Co. 60Co, a commonly-used source of gamma radiation, is the most important radionuclide. It may be a 

low-level contaminant of cooling water released by nuclear reactors. Table 4-1 summarizes information 

on the chemical identity of elemental cobalt and some common cobalt compounds. 

4.2 PHYSICAL, CHEMICAL, AND RADIOLOGICAL PROPERTIES 

Cobalt commonly occurs in the 0, +2, and +3 valence states. Compounds containing cobalt in the -1, +1, 

+4, and +5 oxidation state are few and uncommon (Cotton and Wilkinson 1980). Cobalt (II) is much 

more stable than Co(III), and Co3+ is a sufficiently powerful oxidizing agent to oxidize water, liberating 

oxygen. Table 4-2 summarizes important physical and chemical properties of elemental cobalt and some 

common cobalt compounds. These properties are similar to those of its neighbors in Group 9 of the 

periodic table, iron and nickel. Metallic cobalt, Co(0), occurs as two allotropic forms, hexagonal and 

cubic; the hexagonal form is stable at room temperature. A biochemically important cobalt compound is 

vitamin B12, or cyanocobalamin, in which cobalt is complexed with four pyrrole nuclei joined in a ring 

called the corrinoid ligand system (similar to porphyrin). 

The Chemical Abstract Service (CAS) registry numbers, decay modes, half-lives, and specific activity of 

the three principal radioactive cobalt isotopes, 57Co, 58Co, and 60Co, are presented in Table 4-3. 60Co 

(half-life of 5.27 years) decays by beta decay to nickel-60, a stable isotope (ICRP 1983; Lide 1998). 

60 60 0 

27Co→28Ni+−1e + γ
 

Table 4-1. Chemical Identity of Cobalt and Selected Compounds 

Characteristic Cobalt Cobalt(II) acetate Cobalt(III) acetate Cobalt(II) carbonate 

Synonym(s) Cobalt-59, Cobaltous acetate, Cobaltic acetate, 

cobalt metal cobalt diacetate cobalt triacetate 

Registered trade No data No data No data 

name(s) 

Chemical formula Co Co(C2H4O2)2 Co(C2H4O2)3

Chemical structure Co O O 

C C O O Co O Co O C C O 

O O C O 

Identification numbers: 

 CAS registry 7440-48-4 71-48-7 917-69-1 

 NIOSH RTECS GF8750000 AG3150000 No data 

 EPA hazardous No data No data No data 

waste 

OHM/TADS No data No data No data 

 DOT/UN/NA/IMCO UN1318 No data No data 
 shippinga

HSDB 519 997 No data 

NCI C60311 No data No data 

Cobaltous carbonate; 

carbonic acid; cobalt (+2) 

salt 

No data 

 CoCO3 

O 

O Co

O 

513-79-10 

FF9450050 

No data 

No data 

No data 

No data 

No data 

COBALT 184 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 
 

Table 4-1. Chemical Identity of Cobalt and Selected Compounds 

Characteristic Cobalt carbonyl Cobalt(II) chloride 

Cobalt(II) 

hydroxide 

Cobalt(II) mesoporphyrin 

Synonym(s) Dicobalt octacarbonyl; cobalt 

tetracarbonyl 

Registered trade No data 

name(s) 

Chemical formula Co2(CO)8

Chemical structure O	 O 

C O C C 

O C Co Co C O 

C C
 C

O
 O

O 

Identification numbers: 

 CAS registry 10210-68-1 

NIOSH RTECS GG0300000 

 EPA hazardous No data 

waste 

OHM/TADS No data 

 DOT/UN/NA/IMCO No data 

shipping 

HSDB 6345 

NCI No data 

Cobalt dichloride; 

cobaltous chloride 

No data 

 CoCl2

Cl 

Co 

C l

7646-79-9 

GF9800000 

No data 

7217328 

No data 

1000 

No data 

Cobaltous hydroxide; cobalt 

dihydroxide 

No data 

 Co(OH)2

HO Co OH 

21041-93-0 

No data 

No data 

No data 

No data 

No data 

No data 

Cobalt mesoporphyrin IX Cobaltiprotoporphyrin 

No data 

 C34H34CoN4O4 

No data

21158-51-0 

No data 

No data 

No data 

No data 

No data 

No data 

COBALT	 185 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 
 

Table 4-1. Chemical Identity of Cobalt and Selected Compounds 

Cobalt(II) Cobalt(II) 

Characteristic naphthenate nitrate Cobalt(II) oxide Cobalt(III) oxide 

Synonym(s) Naftolite; Cobaltous Black 13; C.I. 77322; Cobalt black; cobaltic 

naphthenic acid, nitrate cobalt monoxide; oxide; cobalt sesquioxide; 

cobalt salt cobaltous oxide cobalt trioxide; C.I. 77323 

Registered trade No data No data C.I. Pigment No data 

name(s) Black 13; Zaffre 

Chemical formula Co(C11H10O2)2 Co(No3)2•6H20 CoO Co2O3 

Chemical structure Co O O Co O Co O

O O 

C Co O N O Co 

O O

2 C 

O 

Identification numbers: 

 CAS registry 10210-68-1 7646-79-9 21041-93-0 21158-51-0 

NIOSH RTECS GG0300000 GF9800000 No data No data 

 EPA hazardous No data No data No data No data 

waste 

OHM/TADS No data 7217328 No data No data 

 DOT/UN/NA/IMCO No data No data No data No data 

shipping 

HSDB 6345 1000 No data No data 

NCI No data No data No data No data 

COBALT	 186 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 
 

Table 4-1. Chemical Identity of Cobalt and Selected Compounds 

Characteristic Cobalt(II, III) oxide Cobalt(II) sulfate 

Synonym(s) 

Registered trade name(s) 

Chemical formula 

Chemical structure 

Identification numbers: 

 CAS registry 

 NIOSH RTECS 

EPA hazardous waste 

 OHM/TADS 

 DOT/UN/NA/IMCO 

shipping 

HSDB 

NCI 

Cobaltic-cobaltous oxide; cobalt tetraoxide, tricobalt tetraoxide, cobaltosic 

oxide; cobalt black; C.I. Pigment Black 13 

No data 

Co3O4

Co=OO=Co–O–Co=O 

1308-06-1 

No data 

No data 

No data 

No data 

No data 

No data 

Cobalt sulfate; cobaltous 

sulfate 

No data 

 CoSO4 

O O 

Co S 

O O 

10124-43-3 

GG3100000 

No data 

7217330 

No data 

240 

No data 

a

The identification number for radioactive materials is UN2910 

CAS = Chemical Abstract Service; 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 

Source: Budavari 1996; HSDB 2001; RTECS 1987 

COBALT 187 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 
COBALT 188 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Cobalt and Selected Compounds 

Property Cobalt Cobalt(II) acetate Cobalt(III) acetate Cobalt(II) carbonate 

Molecular weight 58.93 177.03 236.07 118.94 

Color Silvery gray Light pink Dark green Red 

Physical state Solid Solid Solid Solid 

Melting point, °C 1,495 No data Decomposes at 

100 °C 

Decomposes 

Boiling point, °C 

Density, g/cm3 

2,870 

8.9 (20 °C) 

No data 

No data 

Not relevant 

No data 

Not relevant 

4.13 

Odor No data No data No data No data 

Odor threshold: 

 Water No data No data No data No data 

Air No data No data No data No data 

Solubility: 

 Water Insoluble Soluble Soluble 0.18 g/100 g H2O at 

15 °C 

 Organic 

solvent(s) 

Insoluble 2.1 g/100 g 

methanol at 15 °C 

soluble in alcohol, 

acetic acid 

Insoluble in ethanol 

Partition coefficients: 

 Log Kow

 Log Koc 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

No data 

Vapor pressure 1 mmHg at 

1,910 °C 

No data No data No data 

Henry’s law constant No data No data No data No data 

Autoignition 

temperature 

760 °C for dust 

cloud 

No data No data No data 

Flashpoint No data No data No data No data 

Flammability limits 

Conversion factors 

No data 

Not relevanta

No data 

 Not relevanta

No data 

 Not relevanta

No data 

 Not relevanta 

Explosive limits No data No data No data No data 
 

 

COBALT 189 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Cobalt and Selected Compounds 

Cobalt(II) 

Property Cobalt carbonyl Cobalt(II) chloride Cobalt(II) hydroxide mesoporphyrin 

Molecular weight 341.9 129.84 92.95 621.2b 

Color Orange (white Blue Rose red or blue No data 

when pure) green 

Physical state Solid Solid Solid No data 

Melting point, °C 51 724 No data No data 

Boiling point, °C Decomposes 1,049 No data No data 

Density, g/cm3 1.73 at 18 °C 3.356 (36 °C) 3.597 at 15 °C No data 

Odor No data No data No data No data 

Odor threshold: 

 Water No data No data No data No data 

Air No data No data No data No data 

Solubility: 

 Water Insoluble 450 g/L at 7 °C 0.0032 g/L No data 

 Organic Soluble in ether; 544 g/L in ethanol; No data No data 

solvent(s) insoluble in 86 g/L in acetone 

naphtha 

Partition coefficients: 

 Log Kow No data No data No data No data 

 Log Koc No data No data No data No data 

Vapor pressure 199.5 at 25 °C No data No data No data 

Henry’s law constant No data No data No data No data 

Autoignition No data No data No data No data 

temperature, °C 

Flashpoint, °C No data No data No data No data 

Flammability limits No data No data No data No data 

Conversion factors Not relevanta

 Not relevanta Not relevanta Not relevanta 

Explosive limits No data No data No data No data 
COBALT 190 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Cobalt and Selected Compounds 

Cobalt(II) 

Property naphthenate Cobalt(II) nitrate Cobalt(II) oxide Cobalt(III) oxide 

Molecular weight 407 182.94 74.93 165.86 

Color No data Red Pink Black-gray 

Physical state Solid Solid Solid Solid 

Melting point, °C 140 Decomposes at 100– 

105b 

1,795 895 

(decomposes) 

Boiling point, °C No data Not relevant No data Not relevant 

Density g/cm3

 0.9 2.49b 6.45 5.18 

Odor No data No data No data No data 

Odor threshold: 

 Water No data No data No data No data 

Air No data No data No data No data 

Solubility: 

 Water Insoluble 133.8 at 0 °Cc Insoluble Insoluble 

 Organic No data Soluble in ethanol, Insoluble in Insoluble in 

solvent(s) acetone alcohol ethanol 

Partition coefficients: 

 Log Kow No data No data No data No data 

Log Kow No data No data No data No data 

Vapor pressure No data No data No data No data 

Henry’s law constant No data No data No data No data 

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 

Conversion factors Not relevanta

 Not relevanta Not relevanta Not relevanta 

Explosive limits No data No data No data No data 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

COBALT 191 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Cobalt and Selected Compounds 

Property Cobalt(II, III) oxide Cobalt(II) sulfate 

Molecular weight 250.80 154.99 

Color Black Dark blue 

Physical state Solid Solid 

Melting point, °C -O2 at 900–950 Decomposes at 735 °C 

Boiling point, °C 

Density g/cm3

Not relevant 

6.07 

Not relevant 

3.71 

Odor No data No data 

Odor threshold: 

 Water No data No data 

Air No data No data 

Solubility: 

 Water 

 Organic solvent(s) 

Insoluble 

No data 

3.83 g/100 mL H2O at 25 °C 

1.04 g/100 mL methanol at 18 °C 

Partition coefficients: 

 Log Kow 

Log Kow 

No data 

No data 

No data 

No data 

Vapor pressure No data No data 

Henry’s law constant No data No data 

Autoignition temperature No data No data 

Flashpoint No data No data 

Flammability limits 

Conversion factors 

No data 

Not relevanta

No data 

 Not relevanta 

Explosive limits No data No data 

a

Substances exist in the atmosphere in the particulate state, and the concentration is expressed in weight per cubic 

meter 

b

CAS Online 

c

Hexahydrate 

Source: Budavari 1996; HSDB 2001, 2004; Lide 1994; Stockinger 1981; Weast 1985 
 

 

 

 

 

COBALT 192 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-3. Principal Radioactive Cobalt Isotopes 

 Beta radiation Gamma radiation 

Isotope 

CAS 

registry no. 

Decay mode 

(product) 

Decay mode 

energy (MeV) 

55Co 13982-25-7 E.C. β+ 

(

55Fe) 

3.452 

Energy 

(MeV) 

1.498 

1.021 

Intensity 

(percent) 

46 

25.6 

Energy 

(MeV) 

0.9312 

0.4772 

Intensity 

(percent) Half-life 

75 

20 

17.53 

hours 

2.043 10.7 1.408 16.88 

57Co 13981-50-5 E.C. (57Fe) 0.836 0.700 99.8 0.1221 

0.1365 

85.6 

10.7 

271.8 

days 

0.014 9.2 

58Co 13981-38-9 E.C. β+ 

(

58Fe) 

2.30 1.4966 

0.4746 

83.9 

14.9 

0.811 99 70.86 

days 

60Co 10198-40-0 β-

(

60Ni) 2.824 0.3181 99.9 1.173 

1.332 

100 

100 

5.271 

years 

Β–

 = negative beta emission; β+ = positron emission; E.C. = orbital electron capture 

Source: ICRP 1983; LBNL 2000; Lide 1998 
 

 

COBALT 193 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

The decay is accompanied by the emission of 1.173 and 1.332 MeV gamma rays. 57Co (half-life of 

271.8 days) and 58Co (half-life of 70.9 days) decay by electron capture and electron capture/position (β+) 

emission to 57Fe and 58Fe, respectively. These decay processes are also accompanied by gamma 

emissions (Table 4-3). 

COBALT 195 

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

5.1 PRODUCTION 

Cobalt is the 33rd most abundant element, comprising approximately 0.0025% of the weight of the earth’s 

crust. It is often found in association with nickel, silver, lead, copper, and iron ores and occurs in mineral 

form as arsenides, sulfides, and oxides. The most import cobalt minerals are: linnaeite, Co3S4; carrolite, 

CuCo2S4; safflorite, CoAs2; skutterudite, CoAs3; erythrite, Co3(AsO4)2•8H2O; and glaucodot, CoAsS 

(Hodge 1993; IARC 1991; Merian 1985; Smith and Carson 1981). The largest cobalt reserves are in the 

Congo (Kinshasa), Cuba, Australia, New Caledonia, United States, and Zambia. Most of the U.S. cobalt 

deposits are in Minnesota, but other important deposits are in Alaska, California, Idaho, Missouri, 

Montana, and Oregon. Cobalt production from these deposits, with the exception of Idaho and Missouri, 

would be as a byproduct of another metal (USGS 2004). Cobalt is also found in meteorites and deep sea 

nodules. 

The production of pure metal from these ores depends on the nature of the ore. Sulfide ores are first 

finely ground (i.e., milled) and the sulfides are separated by a floatation process with the aid of frothers 

(i.e., C5–C8 alcohols, glycols, or polyethylene or polypropylene glycol ethers). The concentrated product 

is subjected to heating in air (roasting) to form oxides or sulfates from the sulfide, which are more easily 

reduced. The resulting matte is leached with water and the cobalt sulfate leachate is precipitated as its 

hydroxide by the addition of lime. The hydroxide is dissolved in sulfuric acid, and the resulting cobalt 

sulfate is electrolyzed to yield metallic cobalt. For the cobalt-rich mineral cobaltite, a leaching process 

with either ammonia or acid under pressure and elevated temperatures has been used to extract cobalt. 

The solution is purified to remove iron and is subsequently reduced by hydrogen in the presence of a 

catalyst under elevated temperature and pressure to obtain fine cobalt powder (Duby 1995; Nagaraj 1995; 

Planinsek and Newkirk 1979). 

Except for a negligible amount of byproduct cobalt produced from some mining operations, no cobalt is 

presently mined or refined in the United States. In addition to byproduct production, U.S. production is 

derived from scrap (secondary production). In 2003, an estimated 2,200 metric tons of cobalt were 

recycled from scrap (USGS 2004). Since 1993, production has been supplemented by sales of excess 

cobalt from the National Defense Stockpile (NDS), which the government maintains for military, 
 

 

COBALT 196 

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

industrial, and essential civilian use during national emergencies. In fiscal year 2002, 2,720 metric tons 

of cobalt were released from the NDS. In 2001, the United States did not mine or refine cobalt, with the 

exception of small amounts of byproduct cobalt produced from mining operations in Missouri and 

Montana. The 2002 U.S. consumption of cobalt metal, organic and inorganic cobalt compounds, and 

purchased scrap (in terms of cobalt content) was 3,870, 1,270, and 2,800 metric tons, respectively (USGS 

2002). 

Current U.S. manufacturers of selected cobalt compounds are given in Table 5-1. Table 5-2 lists facilities 

in each state that manufacture, process, or use cobalt or cobalt compounds, the intended use, and the 

range of maximum amounts of these substances that are stored on site. In 2000, there were 618 reporting 

facilities that produced, processed, or used cobalt or cobalt compounds in the United States. The data 

listed in Table 5-2 are derived from the Toxics Chemicals Release Inventory (TRI) (TRI01 2004). Only 

certain types of facilities were required to report. Therefore, this is not an exhaustive list. 

60Co is produced by irradiating stable cobalt, 59Co, with thermal neutrons in a nuclear reactor: 

59Co(n,γ)60Co. The neutron flux employed is 1012–1015 

n/cm2-sec and the conversion is 99%. The 

maximum specific activity obtained is 3.7x1013 Bq/g (1,000 Ci/g). Commercial 60Co sources used for 

bacterial sterilization are made into rods with double metal shielding. The individual sources have an 

activity of about 2x1014–6x1014 Bq (6–15 kCi). The annual output of 60Co was about 2x1018–3x1018 Bq 

(50–80 MCi) in the early 1990s. In 1991, there were 170 gamma irradiation systems operating in 

45 countries having a total activity of about 6x1018 Bq (160 MCi) (Zyball 1993). Producers of 60Co 

include MDS Nordion in Canada, AEA Technology (formerly Amersham QSA) in the United Kingdom, 

and Neutron Products in Dickerson, Maryland. 

58Co is not produced commercially. It can be produced by irradiating 58Ni, a stable isotope, with 

neutrons, followed by positron decay: 58Ni(n,γ)

58Co. It can be produced in a nuclear reactor or a 

cyclotron. Both 60Co and 58Co may be produced unintentionally in reactors. These are the dominant 

sources of residual radiation in the primary circuit outside the reactor core of nuclear plants and are 

formed by neutron absorption of 59Co and 58Ni, both stable isotopes commonly used in plant construction 

materials (Taylor 1996). 60Co is commonly found as one of the radionuclides present in the low-level 

radioactive waste discharges from many nuclear power plants; however, amounts rarely make a 

significant contribution to the radiation exposure of the public (Leonard et al. 1993a). The geometric 
COBALT 197 

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

Table 5-1. Current U.S. Manufacturers of Cobalt Metal and Selected Cobalt 

Compoundsa 

Company Location 

Cobalt metalb: 

 Kennametal, Inc. Latrobe, Pennsylvania 

OM Group, Inc. Cleveland, Ohio 

Cobalt (II) acetate: 

The IMC Group Shelby, North Carolina 

McGean-Rohco, Inc., McGean Specialty Chemicals Division Cleveland, Ohio 

OM Group, Inc. Franklin, Pennsylvania 

The Shepard Chemical Company Cincinnati, Ohio 

Cobalt (II) carbonate: 

The IMC Group Shelby, North Carolina 

McGean-Rohco, Inc., McGean Specialty Chemicals Division Cleveland, Ohio 

 OMG Apex St. George, Utah 

OM Group, Inc. Franklin, Pennsylvania 

The Shepherd Chemical Co. Cincinnati, Ohio 

Cobalt (II) chloride: 

The IMC Group Shelby, North Carolina 

Johson Matthey, Inc., Alfa Aesar Ward Hill, Massachusetts 

McGean-Rohco, Inc., McGean Specialty Chemicals Division Cleveland, Ohio 

OM Group. Inc. Franklin, Pennsylvania 

The Shepard Chemical Company Cincinnati, Ohio 

Cobalt (II) hydroxide: 

McGean-Rohco, Inc., McGean Specialty Chemicals Division Cleveland, Ohio 

OM Group, Inc. Franklin, Pennsylvania 

The Shepard Chemical Company Cincinnati, Ohio 

Cobalt (II) nitrate: 

The IMC Group Shelby, North Carolina 

Johnson Matthey, Inc., Alfa Aesar Ward Hill, Massachusetts 

McGean-Rohco, Inc., McGean Specialty Chemicals Division Cleveland, Ohio 

 OMG Apex St. George, Utah 

OM Group, Inc. Franklin, Pennsylvania 

The Shepard Chemical Company Cincinnati, Ohio 

Umicore USA, Inc., Cobalt Products Laurinburg, North Carolina 

Cobalt (II) oxide: 

 OMG Apex St. George, Utah 

The Shepard Chemical Company Cincinnati, Ohio 
COBALT 198 

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

Table 5-1. Current U.S. Manufacturers of Cobalt Metal and Selected Cobalt 

Compoundsa 

Cobalt (III) oxide: 

Johnson Matthey, Inc., Alfa Aesar Ward Hill, Massachusetts 

 Mallinckrodt Baker, Inc. Phillipsburg, New Jersey 

McGean-Rohco, Inc., McGean Specialty Chemicals Division Cleveland, Ohio 

OM Group, Inc. Franklin, Pennsylvania 

Osram Sylvania Inc. Towanda, Pennsylvania 

Cobalt (II) sulfate: 

The IMC Group Shelby, North Carolina 

McGean-Rohco, Inc., McGean Specialty Chemicals Division Cleveland, Ohio 

 OMG Apex St. George, Utah 

OM Group, Inc. Franklin, Pennsylvania 

The Shepard Chemical Company Cincinnati, Ohio 

a

Derived from Stanford Research Institute (SRI) 2003, except where otherwise noted. SRI reports production of 

chemicals produced in commercial quantities (defined as exceeding 5,000 pounds or $10,000 in value annually) by 

the companies listed 

b

U.S. members of The Cobalt Development Institute that are listed as producers of cobalt powder or hard metal 

products 
COBALT 199 

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

Table 5-2. Facilities that Produce, Process, or Use Cobalt and Cobalt 

Compounds 

Number of Minimum amount Maximum amount 

Statea facilities on site in poundsb on site in poundsb Activities and usesc 

AK 2 10,000 999,999 1, 5, 7, 12 

AL 22 100 999,999 1, 2, 3, 4, 5, 6, 7, 8,9, 10, 12, 13 

AR 9 100 99,999 1, 5, 7, 8,9 

AZ 12 1,000 49,999,999 1, 2, 3, 5, 7, 8,9, 10, 12, 13, 14 

CA 28 0 9,999,999 1, 2, 3, 5, 6, 7, 8,9, 10, 11, 12 

CO 1 10,000 99,999 12 

CT 9 0 999,999 2, 3, 7, 8 

DE 2 1,000 9,999 1, 5,9, 13 

FL 11 0 99,999 1, 2, 3, 4, 5, 6, 7, 8,9, 12, 13, 14 

GA 17 100 999,999 1, 2, 3, 4, 5, 6, 7, 8,9, 11, 12, 13 

IA 6 100 99,999 3, 4, 7, 8, 12 

ID 2 100,000 999,999 1, 3, 5, 12 

IL 24 100 9,999,999 1, 2, 3, 4, 5, 6, 7, 8,9, 10, 11, 12, 13, 14 

IN 42 100 999,999 1, 2, 3, 4, 5, 6, 7, 8,9, 10, 11, 12, 13, 14 

KS 5 10,000 99,999 1, 3, 5, 6, 7, 8,9, 10, 11, 12, 13 

KY 22 100 999,999 1, 2, 3, 4, 5, 6, 7, 8,9, 12, 13, 14 

LA 15 1,000 999,999 1, 2, 3, 4, 5, 6, 8, 10, 12, 13, 14 

MA 11 100 99,999 1, 5, 8,9, 12 

MD 6 1,000 99,999 1, 2, 3, 4, 5, 6, 7,9, 13 

ME 2 100 99,999 1, 5, 8 

MI 24 0 999,999 1, 2, 3, 4, 5, 7, 8,9, 11, 12, 13, 14 

MN 6 100 99,999 1, 2, 5, 7, 8,9, 10, 12, 13, 14 

MO 5 1,000 999,999 1, 2, 3, 4, 5, 6, 8,9, 12, 13, 14 

MS 7 100 99,999 1, 5, 6, 7, 8, 10 

MT 1 10,000 99,999 1, 5, 12, 14 

NC 24 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8,9, 10, 12, 13, 14 

ND 4 1,000 99,999 1, 5, 7, 12, 13, 14 

NE 1 1,000 9,999 8, 11 

NH 1 100 999 8 

NJ 14 1,000 9,999,999 1, 3, 4, 5, 6, 7, 8, 10, 12, 14 

NM 6 1,000 9,999,999 1, 3, 4, 5, 7, 8,9, 11, 12, 13 

NV 8 1,000 10,000,000,000 1, 5, 6, 8, 12, 13, 14 

NY 12 1,000 99,999 1, 2, 3, 4, 5, 7, 8,9, 11, 12 

OH 44 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8,9, 11, 12, 13, 14 

OK 14 100 999,999 1, 2, 3, 5, 6, 7, 8,9, 10, 11, 12 

OR 6 1,000 99,999 1, 5, 7, 8, 12 

PA 44 100 9,999,999 1, 2, 3, 4, 5, 6, 7, 8,9, 10, 11, 12, 13, 14 
COBALT 200 

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

Table 5-2. Facilities that Produce, Process, or Use Cobalt and Cobalt 

Compounds 

Number of Minimum amount Maximum amount 

Statea facilities on site in poundsb on site in poundsb Activities and usesc 

PR 2 1,000 99,999 8,9 

RI 1 100,000 999,999 8 

SC 26 100 9,999,999 1, 2, 3, 4, 5, 6, 7, 8,9, 10, 11, 12, 13 

SD 1 10,000 99,999 7 

TN 18 0 999,999 1, 2, 3, 4, 5, 6, 7, 8,9, 10, 12, 13 

TX 45 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8,9, 10, 11, 12, 13, 14 

UT 6 1,000 9,999,999 1, 3, 4, 5, 7, 8,9, 12, 13 

VA 9 10,000 999,999 1, 2, 3, 4, 5, 6, 7, 8 

VI 1 10,000 99,999 10 

WA 2 10,000 99,999 1, 3, 4, 5,9, 10, 11, 12, 13 

WI 20 100 999,999 1, 3, 4, 5, 7, 8,9, 11, 12, 13, 14 

WV 13 100 999,999 1, 2, 3, 4, 5, 7, 8,9, 11, 12, 13, 14 

WY 2 0 99,999 1, 5,9, 12, 13 

Source: TRI01 2004 

a

Post office state abbreviations used 

b

Amounts on site reported by facilities in each state 

c

Activities/Uses: 

1. Produce 6. Impurity 11. Chemical Processing Aid 

2. Import 7. Reactant 12. Manufacturing Aid 

3. Onsite use/processing 8. Formulation Component 13. Ancillary/Other Uses 

4. Sale/Distribution 9. Article Component 14. Process Impurity 

5. Byproduct 10. Repackaging 
 

 

 

COBALT 201 

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

mean release of 60Co in liquid effluents of light-water nuclear power stations was reported as in the early 

1970s as 0.0805 Ci/year (3.0 GBq) (Morgan 1976). 

The 60Co activities for a representative pressurized-water reactor (PWR) and boiling water reactor (BWR) 

fuel assemblies are 1,100 and 170 Ci (41 and 6.3 TBq), respectively. There are 78 PWR and 40 BWR 

reactors in the United States, several of which have ceased operation. The postirradiation cobalt content 

of typical PWR and BWR reactor fuel assemblies are 38 g (0.01%) and 26 g (0.01%), respectively (DOE 

2002). 

55Co may be produced by applying 12 MeV indirect deuteron energy to 54Fe (54Fe(d,n)55Co), 40 MeV 

protons to natural iron (56Fe(p,2n)55Co), or 20 MeV protons to natural nickel foil (58Ni(p,α)

55Co) followed 

by separation of the 55Co on an ion exchange column (Wolf 1955). Due to the short half-life (17.5 hours), 

however, 55Co would not be persistent in the environment or in waste sites. 57Co (half-life of 270 days) is 

produced by AEA Technology (formerly Amersham QSA) in the United Kingdom (Web Research Co. 

1999). 

5.2 IMPORT/EXPORT 

In 2002, 8,450 metric tons of cobalt were imported into the United States compared with 7,670, 8,150, 

8,770, and 9,410 metric tons in 1998, 1999, 2000, and 2001 (USGS 2002). Between 1999 and 2002, 

Finland, Norway, Russia, and Canada supplied 24, 18, 13, and 10% of cobalt, respectively (USGS 2004). 

Imports for 2002 by form included (form, metric tons cobalt content): metal, 6,800; oxides and 

hydroxides, 936; acetates, 84; carbonates, 60; chlorides, 22; and sulfates 545. Cobalt exports for 1999, 

2000, 2001, and 2002 were 1,550, 2,630, 3,210, and 2,080 metric tons, respectively; exports estimated in 

2002 are 2,500 metric tons (USGS 2002; 2004). 

60Co and 57Co are produced in Canada and in the United Kingdom and are imported from these countries. 

No import and export quantities for cobalt radioisotopes were available. 
 

 

 

COBALT 202 

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

5.3 USE 

The United States is the world’s largest consumer of cobalt. Cobalt is used in a number of essential 

military and industrial applications. The largest use of metallic cobalt is in superalloys that are used in 

gas turbines aircraft engines. Superalloys are alloys developed for applications where elevated 

temperatures and high mechanical stress are encountered. It is also used in magnetic alloys and alloys 

that are required for purposes requiring hardness, wear resistance, and corrosion resistance. Cobalt is 

used as a binder for tungsten carbide (cemented carbides) cutting tools to increase impact strength. 

Cobalt compounds are used as pigments in glass, ceramics, and paints; as catalysts in the petroleum 

industry; as paint driers; and as trace element additives in agriculture and medicine. 

Over 40% of nonmetallic cobalt is used in catalysis, and most cobalt catalysts are used in 

hydrotreating/desulfurization in the oil and gas industry, the production of terephthalic acid and 

dimethylterephthalate, and the production of aldehydes using the high pressure oxo process 

(hydroformylation). Cobalt chemicals primarily used as catalysts include cobalt(III) acetate, cobalt(II) 

bromide, carbonate, manganate, oxalate, and sulfide, cobalt carbonyl, and cobalt naphthenate. Cobalt 

carbonate and chromate are mainly used as pigments and cobalt(II) acetate, 2-ethylhexanoate, linoleate, 

naphthenate, nitrate, oleate, and stearate are mainly used as driers. Cobalt has been used for hundreds of 

years as a blue colorant in glass, ceramics, and paints (Richardson 1993). 

A growing use for cobalt is as an addition to the Ni/Cd, Ni-metal hydride battery or as the main 

component of the lithium ion cell (LiCoO2). In 2002, the reported U.S. cobalt consumption was 

7,930 metric tons with a use pattern of (end use, metric tons cobalt content, percent): superalloys, 3,700, 

46.7%; steel alloys, 555, 7.0%; other alloys, including magnetic alloys, 1,050, 13.2%; cemented carbides, 

617, 7.8%; chemical and ceramic use, 1,950, 24.6%; and miscellany, 63, 0.8%. Cobalt is also used a 

target material in electrical x-ray generators (Cobalt Development Institute 2004; Donaldson 1986; Hodge 

1993; IARC 1991; Richardson 1993; USGS 2002). 

Gamma rays from 60Co are used medically to treat cancer and industrially to sterilize medical and 

consumer products, to crosslink, graft and degrade plastics, and as an external source in radiography and 

radiotherapy. 60Co, along with iridium 192 (192Ir), are the most commonly used isotopes in industrial 

radiography. In this application, 60Co is used for nondestructive testing of high-stress alloy parts, such as 

pipeline weld joints, steel structures, boilers, and aircraft and ship parts. Radiography may be conducted 
 

 

COBALT 203 

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

at permanent, specially shielded facilities or temporary sites in the field (USNRC 1999). 60Co is used in 

chemical and metallurgical analysis and as a tracer in biological studies. In 1990, about 95% of installed 

60Co activity was used for the sterilization of medical devices; about 45% of medical devices were 

sterilized using radiation. 60Co is also a source of gamma rays used for food irradiation; depending on the 

dose levels, irradiation may be used to sterilize food, destroy pathogens, extend the shelf-life of food, 

disinfest fruits and grain, delay ripening, and retard sprouting (e.g., potatoes and onions). Sludge, waste 

water, and wood may also be treated with gamma rays to kill harmful organisms. 

57Co decays to an excited state of 57Fe, the most widely used x-ray source in Mössbauer spectroscopy 

(Hodge 1993; Richardson 1993). It is also made into standards and sources for dose calibrators, gamma 

cameras, and gauges, and is used as markers and rulers to help estimate organ size/location. It is also 

used in in vitro diagnostic kits for the study of anemia related to vitamin B12 deficiency/malabsorption 

(MDS Nordion 2000). 55Co-bleomycin has been used for scanning malignant tumors (e.g., lung and brain 

cancer) and is a practical isotope for positron emission tomography (PET) studies because it mainly 

(81%) decays by positron emission. 

5.4 DISPOSAL 

There is a paucity of data on the methods of disposal of cobalt and its compounds. Due to the lack of 

natural sources of economically extractable ores in the United States, cobalt is entirely imported in the 

United States, and it is considered a strategic mineral. It is economical to recycle certain cobalt wastes 

rather than to dispose of them. Recycling of superalloy scrap is an important method for the recovery of 

cobalt. About 2,200 metric tons of cobalt were recycled from purchased scrap in 2003. This was about 

28% of reported consumption for the year (USGS 2004). According to TRI (TRI01 2004), 7.14 and 

1.42 million pounds of cobalt and cobalt compounds combined were recycled onsite and offsite, 

respectively, in 2001. Waste containing cobalt dust and, presumably, waste containing cobalt in the solid 

state may be placed in sealed containers and disposed of in a secured sanitary landfill (HSDB 1989). 

Waste water containing cobalt can be treated before disposal, for instance, by precipitation of carbonate 

or hydroxide of cobalt or by passage through an ion-exchange resin (Clifford et al. 1986). According to 

TRI (TRI01 2004), 1,619,874 pounds of cobalt and cobalt compounds, were transferred offsite for 

disposal, in processes such as solidification/stabilization and waste water treatment, including publicly 

operated treatment plants (POTWs). The amount of cobalt so transferred by state is shown in Table 6-1. 
 

 

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

In August 1998, EPA issued a final rule listing spent hydrotreated and hydrorefined catalysts as hazardous 

waste under the Resource Conservation and Recovery Act (USGS 1998). Listing under this act requires 

that releases of these substances will be subject to certain management and treatment standards and 

emergency notification requirements. Information regarding effluent guidelines and standards for cobalt 

may be found in Title 40 of the Code of Federal Regulations, Parts 421.230, 421.310, and 471.30. 

60Co sources used for irradiation purposes are valuable and are not to be discarded. However, some 

radioactive cobalt isotopes may occur in waste material from nuclear reactors. Radioactive waste is 

categorized according to origin, type of waste present, and level of activity. Radioactive cobalt isotopes 

may be commingled with other radioactive isotopes. The first distinction in radioactive waste is between 

defense waste and commercial waste, the former being generated during and after World War II 

principally at the Department of Energy (DOE) facilities at Hanford, Washington; Savannah River, South 

Carolina; and Idaho Falls, Idaho, where plutonium and other isotopes were separated from production 

reactor spent fuel or nuclear-powered naval vessels. Commercial wastes are produced predominantly by 

nuclear power plants as well as the long defunct commercial reprocessing facility at West Valley, New 

York and manufacturers of radioisotopes used in nuclear medicine for the treatment and diagnosis of 

disease. Nuclear waste is also classified as high-level waste (HLW), transuranic waste (TRU), and lowlevel waste (LLW). LLW is further differentiated into three classes, A, B, and C, according to increasing 

of the level of activity. A fourth category, commercial greater-than-class-C LLW (listed in 10 CFR 

61.55 Tables 1 and 2 for long and short half-life radionuclides, respectively) is not generally suitable for 

near-surface disposal. This could include operating and decommissioning waste from nuclear power 

plant and sealed radioisotope sources. The final disposition for this waste has not been determined. If 

LLW also contains nonradioactive hazardous material (i.e., that which is toxic, corrosive, inflammable, or 

explosive), it is termed mixed waste. Mine tailings from uranium mining is yet another category of 

radioactive waste (DOE 1999; Murray 1994). While radioactive cobalt would not ordinarily be found in 

HLW or TRU, the definitions of these are included below for completion. 

TRUs are those containing isotopes, like plutonium, that are above uranium in the periodic table and 

whose half-lives are >20 years. If their level of activity is <100 nanocuries (nCi) (<3,700 becquerels[Bq]) 

of alpha-emitters per gram of waste material (up from 10 nCi/g in 1982), the waste could be disposed of 

by shallow burial. Otherwise, the waste must be placed in retrievable storage for eventual transfer to a 
COBALT 205 

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

permanent repository. The level of radioactivity in TRUs is generally low; they generate very little heat 

and can be handled by ordinary means without remote control (Eisenbud 1987, Murray 1994). 

HLW includes spent fuels that are contained in fuel rods that have been used in a nuclear reactor. These 

may contain small amounts of transuranic elements. After removal from the reactor, these rods are placed 

into pools adjacent to the commercial nuclear power plants and DOE facilities where they were produced. 

It was originally intended that the fuel rods remain in these pools for only about 6 months to allow for a 

reduction in short-lived radioactivity and rate of heat production temperature and then be transferred to a 

reprocessing or storage facility. There is no commercial reprocessing facility or permanent disposal 

facility for HLW operating in the United States. The U.S. Nuclear Regulatory Commission (USNRC) has 

issued standards for the disposal of HLW (10 CFR 60), and the DOE is pursuing the establishment of an 

HLW facility in Yucca Mountain, Nevada. Efforts to establish an HLW facility, which began over 

2 decades ago, have experienced many delays (Eisenbud 1987; Murray 1994). However, in July, 2002, 

the U.S. Congress and the President selected Yucca Mountain, Nevada as the nation’s first long-term 

repository for HLW. The facility is projected to begin operation in 2010, and efforts are underway to 

consider establishing a nearby interim facility (DOE 2002b). 

LLWs are officially defined as wastes other than those previously defined. These wastes come from 

certain reactor operations and from manufacturers of radioisotopes used in nuclear medicine and 

institutions such as hospitals, universities, and research centers. Most LLW contain very little 

radioactivity and contain practically no transuranic elements. It requires little or no shielding or special 

handling and may be disposed of by shallow burial. However, some LLW contains sufficient 

radioactivity as to require special treatment. Although USNRC regulations for LLW disposal (10 CFR 

61) permit shallow land burial, many states have enacted more stringent regulations that require artificial 

containment of the waste in addition to natural containment (Eisenbud 1987; Murray 1994). The EPA has 

the authority to set generally acceptable environmental standards for LLW that would be implemented by 

the US NRC and DOE (EPA 2004). The Manifest Information Management System (MIMS), maintained 

by the Idaho National Engineering and Environmental Laboratory (INEEL), contains information on lowlevel radioactive waste shipments received at commercial low-level radioactive waste disposal facilities at 

Barnwell, South Carolina (1/1/86–present), Beaty, Nevada (4/1/86–12/31/92), Richland, 

Washington(1/1/86–present), and Envirocare, Utah (1/1/98–12/31/99). In 1999, 17 Ci (0.63 TBq) of 

57Co, 1,300 Ci (48 TBq) of 58Co, and 1.08x106

 Ci (4.00x104 TBq) of 60Co contained in LLW was received 

at these facilities from academic, industrial, government, and utility generators throughout the United 
COBALT 206 

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

States (INEL 2000). In addition, 4.26 Ci (0.158 TBq) of 57Co of NARM (“naturally occurring and 

accelerator-related waste”) was received. 

At present, DOE stores most of its spent fuel at three primary locations: the Hanford site, Washington, 

the Idaho National Engineering and Environmental Laboratory (INEEL), Idaho, and the Savannah River 

site, South Carolina. Some spent fuel is also stored at the dry storage facility at Fort St. Vrain in 

Colorado. Much smaller amounts of spent nuclear fuel stored at other sites were to be shipped to the 

three prime sites for storage and preparation for ultimate disposal (DOE 1999). The DOE National Spent 

Fuel Program maintains a spent nuclear fuel database that lists the total volume, mass, and metric tons 

heavy metal (MTHM) of 16 DOE categories of spent nuclear fuel stored in each of the three locations. 

The categories having the highest 60Co activities per spent nuclear fuel canister (decayed to 2030) are 

‘naval surface ship fuel’ and ‘naval submarine fuel’. The 58Co and 60Co solid wastes stored on the 

Hanford site in 1998 as LLW were 2,600 and 6,900 Ci (96 and 260 TBq), respectively (Hanford 1999). 

In addition, 40 Ci (1.5 TBq) of 60Co was included in TRU. 

In commercial irradiators, additional quantities of 60Co are added, usually once a year to maintain 

preferred radiation levels of the source (MDS Nordion 2000). 60Co sources are removed from the facility 

at the end of their useful life, which is typically 20 years. In general, manufacturers of 60Co sources 

guarantee to accept the sources they originally supplied. These old sources may be reencapsulated, 

reprocessed, or recycled when technically, environmentally, and economically feasible. 
 

 

COBALT 207 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.1 OVERVIEW 

Stable cobalt has been identified in at least 426 of the 1,636 hazardous waste sites that have been 

proposed for inclusion on the EPA National Priorities List (NPL) (HazDat 2004). Radioactive cobalt as 

60Co has been identified in at least 13 of the 1,636 hazardous waste sites that have been proposed for 

inclusion on the EPA NPL (HazDat 2004). However, the number of sites evaluated for stable cobalt and 

60Co is not known. The frequency of these sites can be seen in Figures 6-1 and 6-2, respectively. Of the 

cobalt sites, 421 are located within the United States, 1 is located in Guam (not shown), 3 are located in 

the Commonwealth of Puerto Rico (not shown), and 1 is located in the Virgin Islands (not shown). All of 

the sites at which 60Co has been identified are located within the United States. 

Cobalt occurs naturally in the earth's crust, and therefore, in soil. Low levels of cobalt also occur 

naturally in seawater and in some surface water and groundwater (Smith and Carson 1981). However, 

elevated levels of cobalt in soil and water may result from anthropogenic activities such as the mining and 

processing of cobalt-bearing ores, the application of cobalt-containing sludge or phosphate fertilizers to 

soil, the disposal of cobalt-containing wastes, and atmospheric deposition from activities such as the 

burning of fossil fuels and smelting and refining of metals (Smith and Carson 1981). Cobalt is released 

into the atmosphere from both anthropogenic and natural sources. However, emissions from natural 

sources are estimated to slightly exceed those from manufactured sources. Natural sources include 

windblown soil, seawater spray, volcanic eruptions, and forest fires. Primary anthropogenic sources 

include fossil fuel and waste combustion, vehicular and aircraft exhausts, processing of cobalt and cobaltcontaining alloys, copper and nickel smelting and refining, and the manufacture and use of cobalt 

chemicals and fertilizers derived from phosphate rocks (Barceloux 1999; Lantzy and Mackenzie 1979; 

Nriagu 1989; Smith and Carson 1981). 60Co and 58Co, both radioactive forms of cobalt, may be released 

to the environment as a result of nuclear research and development, nuclear accidents, operation of 

nuclear power plants, and radioactive waste dumping in the sea or in radioactive waste landfills. 

Cobalt compounds are nonvolatile and cobalt will be emitted to the atmosphere only in particulate form. 

Their transport in air depends on their form, particle size and density, and meteorological conditions. 

Cobalt so released will return to land or surface water as wet or dry deposition. Coarse particles, those 
COBALT 208 

6. POTENTIAL FOR HUMAN EXPOSURE 

Figure 6-1. Frequency of NPL Sites with Cobalt Contamination 

Frequency of 

NPL Sites 

Derived from HazDat 2004 

<= 4 

4 - 7 

7 - 10 

10 - 16 

16 - 23 

23 - 36 
COBALT 209 

6. POTENTIAL FOR HUMAN EXPOSURE 

Figure 6-2. Frequency of NPL Sites with 60Cobalt Contamination 

Frequency of 

NPL Sites 

1 

3 

Derived from HazDat 2004 
 

 

COBALT 210 

6. POTENTIAL FOR HUMAN EXPOSURE 

with aerodynamic diameters >2 μm (such as those obtained during ore processing), may deposit within 

10 km from the point of emission; finer particles (such as is obtained from thermal processes) may travel 

longer distances. It is generally assumed that anthropogenic cobalt originating from combustion sources 

exists primarily as the oxide; arsenides or sulfides may be released during mining and ore processing 

(Schroeder et al. 1987). Frequently, sediment and soil are the ultimate sinks for cobalt; however, this 

process is dynamic, and cobalt can be released into the water depending upon conditions. Soluble cobalt 

released into waterways will sorb to particles and may settle into the sediment or be sorbed directly by 

sediment. It may precipitate out as carbonates and hydroxides or with mineral oxides. It may also sorb to 

or complex with humic acid substances in the water. These processes are sensitive to environmental 

factors such as pH and the proportion of dissolved cobalt will be higher at low pH. In the case of 60Co 

released into an experimental lake in northwestern Ontario, cobalt’s half-life in the water column was 

11 days; 5% of added 60Co remained in the water after 100 days (Bird et al. 1998a). Cobalt can also be 

transported in dissolved form or as suspended sediment by rivers to lakes and the sea or by ocean 

currents. The proportion of cobalt transported in each form is highly variable (Smith and Carson 1981). 

In deep sediment where water is anoxic and hydrogen sulfide is present, some mobilization of cobalt from 

sediment may occur, probably due to the formation of bisulfides and polysulfides (Bargagli 2000; 

Brügmann 1988; Finney and Huh 1989; Glooschenko et al. 1981; Knauer et al. 1982; Nriagu and Coker 

1980; Shine et al. 1995; Smith and Carson 1981; Szefer et al. 1996; Windom et al. 1989). Cobalt adsorbs 

rapidly and strongly to soil and sediment in which it is retained by metal oxides, crystalline minerals, and 

natural organic matter. The mobility of cobalt sediment depends on the nature of the soil or sediment; it 

increases with decreasing pH and redox potential (Eh) and in the presence of chelating/complexing agents 

(Brooks et al. 1998; Buchter et al. 1989; King 1988b; McLaren et al. 1986; Schnitzer 1969; Smith and 

Carson 1981; Swanson 1984; Yashuda et al. 1995). 

While cobalt may be taken up from soil by plants, the translocation of cobalt from roots to above-ground 

parts of plants is not significant in most soils; the transfer coefficient (concentration in plant/concentration 

in soil) for cobalt is generally 0.01–0.3 (Mascanzoni 1989; Mermut et al. 1996, Smith and Carson 1981). 

However, in highly acidic soils (pH as low as 3.3) and in some higher plants (plants excluding algae), 

significantly higher transfer has been observed (Boikat et al. 1985; Francis et al. 1985; Jenkins 1980; 

Kloke et al. 1984; Mejstrik and Svacha 1988; Palko and Yli-Hala 1988; Tolle et al.1983; Watabe et al. 

1984). The bioaccumulation factors (dry weight basis) for cobalt in marine fish and freshwater fish are 

~100–4,000 and <10–1,000, respectively; accumulation is largely in the viscera and on the skin, as 
 

 

COBALT 211 

6. POTENTIAL FOR HUMAN EXPOSURE 

opposed to the edible parts of the fish. Cobalt does not biomagnify up the food chain (Barceloux 1999; 

Evans et al. 1988; Freitas et al. 1988; Smith and Carson 1981). 

Atmospheric cobalt is associated with particulate matter. Mean cobalt levels in air at unpolluted sites are 

generally <1–2 ng/m3

. In several open-ocean environments, geometric mean concentrations ranged from 

0.0004 to 0.08 ng/m3

 (Chester et al. 1991). However, in source areas, cobalt levels may exceed 10 ng/m3; 

the highest average cobalt concentration recorded was 48 ng/m3

 at the site of a nickel refinery in Wales 

(Hamilton 1994; Smith and Carson 1981). By comparison, the Occupational Safety and Health 

Administration (OSHA) limit for airborne stable cobalt is 100,000 ng/m3

. While 60Co has been detected 

in some air samples at the Hanford, Washington site and Oak Ridge National Laboratories, Tennessee, 

levels were not reported (HazDat 2004; PNNL 1996). 

The concentrations of stable cobalt in surface and groundwater in the United States are generally low; 

<1 μg/L in pristine areas and 1–10 μg/L in populated areas (Hamilton 1994; Smith and Carson 1981). 

However, cobalt levels may be considerably higher in mining or agricultural areas. Cobalt concentrations 

in surface water and groundwater samples collected in 1992 from area creeks near the Blackbird Mine in 

Idaho, one of the large deposits of cobalt in North America where mining occurred from the late 1800s to 

1982, were reported to range from <1 to 625,000 μg/L, and from not detected to 315,000 μg/L, 

respectively (ATSDR 1995). Cobalt levels in most drinking water is <1–2 μg/L although levels as high as 

107 μg/L have been recorded (Greathouse and Craun 1978; Meranger et al. 1981; NAS 1977; Smith and 

Carson 1981). 

Little data are available on the levels of 60Co in water. In 1989, subsequent to the largest effluent 

discharge from the Steam Generating Heavy Water Reactor at Winfrith on the south coast of England, 

60Co levels in offshore seawater from 18 sites contained 0.06–2.22 mBq/L (1.6–69 fCi) of particulate 

60Co, 0.30–10.3 mBq/L (8–280 fCi) of soluble 60Co(II), and 0.12–1.55 mBq/L (3.2–42 fCi) of soluble 

60Co(III) (Leonard et al. 1993a). The U.S. NRC discharge limit is 111,000 mBq/L (3x106

 fCi/L) (USNRC 

1991). 

The average concentrations of cobalt in the earth's crust are 20–25 mg/kg (Abbasi et al. 1989; Merian 

1985; Smith and Carson 1981). Most soils contain 1–40 mg cobalt/kg; the average cobalt concentration 

in U.S. soils is 7.2 mg/kg (Smith and Carson 1981). Soils containing <0.5–3 mg cobalt/kg are considered 

cobalt-deficient because plants growing on them have insufficient cobalt (<0.08–0.1 mg/kg) to meet the 
COBALT 212 

6. POTENTIAL FOR HUMAN EXPOSURE 

dietary requirements of cattle and sheep. Cobalt-deficient soils are found in some areas of the 

southeastern and northeastern United States. Soils near ore deposits, phosphate rocks, or ore smelting 

facilities, and soils contaminated by airport traffic, highway traffic, or other industrial pollution may 

contain high concentrations of cobalt; concentrations up to 800 mg/kg have been detected in such areas 

(Kloke et al. 1984; Smith and Carson 1981). Cobalt concentrations in 28 samples collected from surface 

deposits in the Big Deer and Blackbird Creek drainage basins near a site of former cobalt mining in Idaho 

ranged from 26.5 to 7,410 mg/kg (ATSDR 1995). 

The level of cobalt in most foods is low. However, food is the largest source of exposure to cobalt in the 

general population. The estimated average daily dietary intake of cobalt in Canada was 11 μg/day. Food 

groups contributing most heavily to this intake were bakery goods and cereals (29.8%) and vegetables 

(21.9%) (Dabeka and McKenzie 1995). No estimates of the average dietary input of cobalt in the United 

States were located. People living near mining and smelting facilities or metal shops where cobalt is used 

in grinding tools may be exposed to higher levels of cobalt in air or soil. Similarly, people living near 

hazardous waste sites may be exposed to higher levels of cobalt in these media. Contaminated soils pose 

a hazardous exposure pathway to children because of both hand-to-mouth behavior and intentional 

ingestion of soil (pica) that contain metals and other contaminants (Hamel et al. 1998). However, much 

of the cobalt in soil may not be in a form that is available for uptake by the body. People who work in the 

hard metal industry, metal mining, smelting, and refining or other industries that produce or use cobalt 

and cobalt compounds may be exposed to substantially higher levels of cobalt, mainly from dusts or 

aerosols in air. Workers at nuclear facilities, irradiation facilities, or nuclear waste storage sites may be 

exposed to radioisotopes of cobalt. Exposure would generally be to radiation produced by these isotopes 

(e.g., gamma radiation from 60Co). 

6.2 RELEASES TO THE ENVIRONMENT 

Stable cobalt has been identified in a variety of environmental media (air, surface water, leachate, 

groundwater, soil, and sediment) collected at 426 of 1,636 current or former NPL hazardous waste sites 

(HazDat 2004). 60Co has been identified in a variety of environmental media (air, surface water, leachate, 

groundwater, soil, and sediment) collected at 13 of 1,636 current or former NPL hazardous waste sites 

(HazDat 2004). 
 

 

COBALT 213 

6. POTENTIAL FOR HUMAN EXPOSURE 

According to the Toxic Chemical Release Inventory (TRI), in 2001, total releases of cobalt and cobalt 

compounds to the environment (including air, water, soil, and underground injection) from 605 reporting 

facilities that produced, processed, or used cobalt or cobalt compounds were 16,443,429 pounds (TRI01 

2004). Table 6-1 lists amounts released from these facilities grouped by state. In addition, 

1,619,874 pounds of cobalt and cobalt compounds were transferred offsite by these facilities (TRI01 

2004). Starting in 1998, metal mining, coal mining, electric utilities, and Resource Conservation and 

Recovery Act (RCRA)/solvent recovery industries are required to report, to the TRI, industries with 

potentially large releases of cobalt and cobalt compounds. Industrial sectors producing, processing, or 

using cobalt that contributed the greatest environmental releases in 2001 were primary metals and 

RCRA/solvent recovery with 141,554 and 531,427 pounds, respectively. Industrial sectors producing, 

processing, or using cobalt compounds that contributed the greatest environmental releases in 2001 were 

metal mining and electrical utilities with 10,228,193 and 3,652,398, pounds, respectively. 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 

The sources of cobalt in the atmosphere are both natural and anthropogenic (Barceloux 1999). Natural 

sources include wind-blown continental dust, seawater spray, volcanoes, forest fires, and continental and 

marine biogenic emissions. The worldwide emission of cobalt from natural sources has been estimated to 

range from 13 to 15 million pounds/year (Lantzy and Mackenzie 1979; Nriagu 1989). The global 

atmospheric emission of cobalt from anthropogenic sources is an estimated 9.7 million pounds/year. 

Therefore, natural sources contribute slightly more to cobalt emissions in the atmosphere than 

anthropogenic sources (Lantzy and Mackenzie 1979). The primary anthropogenic sources of cobalt in the 

atmosphere are the burning of fossil fuels and sewage sludge, phosphate fertilizers, mining and smelting 

of cobalt-containing ores, processing of cobalt-containing alloys, and industries that use or process cobalt 

compounds. Small amounts of cobalt are found in coal, crude oils, and oil shales. Therefore, burning of 

these fossil fuels for power generation will emit cobalt into the atmosphere. The cobalt contents of the fly 

ash and flue gases of a coal-burning power plant are approximately 25 mg/kg and 100–700 μg/L, 

respectively. Gasoline contains <0.1 mg cobalt/kg, but catalytic converters may contain cobalt; therefore, 

emissions from vehicular exhaust are also a source of atmospheric cobalt (Abbasi et al. 1989; Holcombe 
COBALT 214 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-1. Releases to the Environment from Facilities that Produce, Process, or 

Use Cobalt and Cobalt Compoundsa
 

Reported amounts released in pounds per yearb 

Number Under- Total on and 

of ground Total on-site Total off- off-site 

Statec facilities Aird

 Water injection Land releasee site releasef release 

AK 2 23 0 16,000 546,463 562,486 0 562,486 

AL 21 5,893 8,612 0 315,853 330,358 30,040 360,398 

AR 9 921 142 0 8,301 9,364 2,015 11,379 

AZ 12 1,029 0 0 1,061,035 1,062,064 2,266 1,064,330 

CA 26 646 20 0 307,654 308,320 7,463 315,783 

CO 1 3 1 0 12,026 12,030 0 12,030 

CT 9 632 65 0 0 697 4,133 4,830 

DE 2 1,265 52 0 52 1,369 27,444 28,813 

FL 11 2,397 345 0 93,049 95,791 15,464 111,255 

GA 17 3,508 268 0 282,610 286,386 12,461 298,847 

IA 6 566 0 0 0 566 2,123 2,689 

ID 2 74 5 0 395,424 395,503 0 395,503 

IL 23 1,630 1,278 0 16,999 19,907 102,088 121,995 

IN 42 7,005 351 0 279,122 286,478 64,293 350,771 

KS 5 4,269 0 0 10,200 14,469 3,859 18,328 

KY 22 3,184 542 0 478,855 482,581 13,269 495,850 

LA 15 385 8,477 2,700 66,858 78,420 91,274 169,694 

MA 11 794 780 0 5 1,579 17,403 18,982 

MD 6 2,472 15 0 6,629 9,116 45,382 54,498 

ME 2 66 0 0 0 66 700 766 

MI 24 4,699 559 0 125,405 130,663 33,737 164,400 

MN 5 255 No data 0 0 255 7,666 7,921 

MO 5 1,457 8 0 559,401 560,866 0 560,866 

MS 7 386 120 12,000 44 12,550 3,044 15,594 

MT 1 250 No data 0 31,000 31,250 505 31,755 

NC 24 6,593 8,257 0 194,974 209,824 216,849 426,673 

ND 4 1,165 21 0 108,300 109,486 39,842 149,328 

NE 1 0 27 0 0 27 3,982 4,009 

NH 1 0 No data 0 0 0 No data 0 

NJ 12 1,191 26 0 413 1,630 26,894 28,524 

NM 6 498 1 0 4,257,140 4,257,639 69 4,257,708 

NV 8 678 0 0 4,099,136 4,099,814 9,950 4,109,764 

NY 12 755 44 0 11,843 12,642 14,322 26,964 

OH 44 4,977 771 1,100 310,653 317,501 96,116 413,617 

OK 13 1,357 158 0 5,677 7,192 20,760 27,952 
COBALT 215 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-1. Releases to the Environment from Facilities that Produce, Process, or 

Use Cobalt and Cobalt Compoundsa
 

Reported amounts released in pounds per yearb 

Number Under- Total on and 

of ground Total on-site Total off- off-site 

Statec facilities Aird

 Water injection Land releasee site releasef release 

OR 6 1,262 20 0 16,487 17,769 2,862 20,631 

PA 44 6,169 3,176 0 51,350 60,695 221,662 282,357 

PR 2 2 No data 0 0 2 2,871 2,873 

RI 1 1 1 0 0 2 50 52 

SC 25 1,579 10,970 0 43,488 56,037 70,316 126,353 

SD 1 0 No data 0 0 0 0 0 

TN 18 5,560 4,013 0 330,615 340,188 36,520 376,708 

TX 44 8,126 784 3,730 150,470 163,110 95,840 258,950 

UT 6 278 No data 0 23,350 23,628 126,502 150,130 

VA 9 1,451 518 0 89,388 91,357 9,683 101,040 

VI 1 0 0 0 0 0 0 0 

WA 2 72 91 0 106,618 106,781 5,112 111,893 

WI 20 1,098 5 0 8 1,111 95,996 97,107 

WV 13 1,341 566 0 212,254 214,161 37,047 251,208 

WY 2 898 No data 0 38,927 39,825 0 39,825 

Total 605 88,860 51,089 35,530 14,648,076 14,823,555 1,619,874 16,443,429 

Source: TRI01 2004 

a

The TRI data should be used with caution since only certain types of facilities are required to report. This is not an 

exhaustive list. Data are rounded to nearest whole number.
 b

Data in TRI are maximum amounts released by each facility.
 c

Post office state abbreviations are used. 

d

The sum of fugitive and stack releases are included in releases to air by a given facility.
 e

The sum of all releases of the chemical to air, land, water, and underground injection wells. 

f

Total amount of chemical transferred off-site, including to publicly owned treatment works (POTW). 
 

 

COBALT 216 

6. POTENTIAL FOR HUMAN EXPOSURE 

et al. 1985; Ondov et al. 1982; Smith and Carson 1981). Cobalt has been detected in cigarette tobacco 

and therefore, smoking is a potential source of atmospheric cobalt that could impact on indoor air quality 

(Munita and Mazzilli 1986). 

Stable cobalt has been identified in air samples collected at 5 of the 426 current or former NPL hazardous 

waste sites where it was detected in some environmental media (i.e., air, soil, sediment, or water) (HazDat 

2004). 60Co has been identified in air samples collected at 2 of the 13 current or former NPL hazardous 

waste sites where it was detected in some environmental media (HazDat 2004). 

Air sampling data were used to estimate 60Co release from the Savannah River Site (SRS) from the plant’s 

start up in 1954 to 1989 (DOE 1991). From this monitoring, it was estimated that 0.092 Ci (3.4 GBq) of 

60Co was released to the atmosphere between 1968 and 1986. Total releases of 60Co to the atmosphere 

from the SRS between 1968 and 1996 were 0.092 Ci (3.4 GBq) (DOE 1998). Data were not reported for 

all years in this interval. In 1999, atmospheric releases of 57Co, 58Co, and 60Co as particulates were 

4.71x10-8, 1.27x10-4, and 1.30x10-4 Ci (0.00174, 4.70, and 4.81 MBq), respectively (DOE 1999). The 

SRS was a major production facility to the U.S. defense program and included five nuclear reactors, a fuel 

fabrication plant, a naval fuel materials facility, two chemical separation plants, a heavy water production 

plant, and a laboratory. 60Co has also been detected in air samples at the Hanford site and Oak Ridge 

National Laboratories (HazDat 2004; PNNL 1996). 

According to the TRI, in 2001, releases of 88,860 pounds of cobalt and cobalt compounds to air from 

605 reporting facilities accounted for 0.5% of the total onsite environmental releases of these substances 

(TRI01 2004). The industrial sectors contributing the largest release of cobalt and cobalt compounds to 

air were electrical utilities, chemicals, and primary metals. Table 6-1 lists the amounts of cobalt and 

cobalt compounds released to air from these facilities grouped by state. The TRI data should be used with 

caution, however, since only certain types of facilities are required to report. This is not an exhaustive 

list. 

6.2.2 Water 

Compounds of cobalt occur naturally in seawater and in some surface, spring, and groundwater (Smith 

and Carson 1981). Cobalt is also released into water from anthropogenic sources. While there has been 
 

 

COBALT 217 

6. POTENTIAL FOR HUMAN EXPOSURE 

no mine production of cobalt in the United States in recent years, cobalt is a byproduct or coproduct of the 

refining of other mined metals such as copper and nickel. Historic mining operations that processed 

cobalt containing ores may continue to release cobalt into surface water and groundwater. Waste water 

from the recovery of cobalt from imported matte or scrap metal, refining of copper and nickel, or during 

the manufacture of cobalt chemicals are sources of cobalt in water (Smith and Carson 1981). Process 

water and effluent from coal gasification and residue from solvent-refined coal contain cobalt. The 

accidental discharge of activated sludge and sewage may be important sources of cobalamins in 

waterways, together with bioconcentration by benthic organisms (Smith and Carson 1981). The 

discharge of waste water by user industries, such as paint and pigment manufacture, also contributes to 

the release of cobalt into water. In one case, manufacturers of nickel-cadmium batteries operating 

between 1953 and 1979 discharged cobalt from a battery factory to the Hudson River in Foundry Cove, 

New York, of which 1.2 metric tons are estimated to be present in the eastern cove (Knutson et al. 1987). 

Atmospheric deposition is an additional source of cobalt in water. Lake Huron receives an estimated 76% 

of its cobalt input from natural sources and 24% from anthropogenic sources. The corresponding 

estimated values for Lake Superior are 85.4 and 14.6% (Smith and Carson 1981). In these Great Lakes, it 

therefore appears that natural inputs of cobalt far exceed anthropogenic ones. 

Cobalt has been identified in groundwater and surface water at 255 and 106 sites, respectively, of the 

426 NPL hazardous waste sites, where it was detected in some environmental media (i.e., air, soil, 

sediment, or water) (HazDat 2004). 60Co has been identified in groundwater and surface water at 4 and 

2 sites, respectively, of the 13 NPL hazardous waste sites, where it was detected in some environmental 

media (HazDat 2004). 

According to the TRI, in 2001, the reported releases of 51,089 pounds of cobalt and cobalt compounds to 

water from 605 reporting facilities accounted for 0.3% of the total onsite environmental releases of these 

substances (TRI01 2004). Table 6-1 lists the amounts of cobalt and cobalt compounds released to water 

from these facilities grouped by state. As of 1998, TRI no longer separately collects data on substances 

released indirectly to Publicly-Owned Treatment Works (POTWs), part of which may ultimately be 

released to surface waters. The TRI data should be used with caution, however, since only certain types 

of facilities are required to report. This is not an exhaustive list. 

60Co is present in the low-level aqueous radioactive waste discharges from many nuclear power plants. 

Alloys that contain stable cobalt (59Co), such as stellite, used in piping of nuclear reactors corrode and 
COBALT 218 

6. POTENTIAL FOR HUMAN EXPOSURE 

may be activated, producing 60Co, which accumulates in the reactor and must be periodically 

decontaminated. A common decontaminating agent includes a reducing metal ion (e.g., vanadium(II)) 

and a chelating agent (e.g., picolinate) resulting in low-level discharges of uncomplexed 60Co(II) and 

complexed 60Co(III). While soluble ionic and particulate forms predominate, at some sites stable, 

nonionic trivalent complexes of cobalt are present (Leonard et al. 1993a, 1993b; USNRC 2000d). For 

example, in 1987–1989 samples of treated effluent from the Steam Generating Heavy Water Reactor at 

Winfrith on the south coast of England, the percent of 60Co as Co(III) picolinate ranged from 6.2 to 

75.4%. Between 1978 and 1988, 12 TBq (320 Ci) of 60Co was released into the Irish Sea by the British 

Nuclear Fuels reprocessing plant at Sellafield, United Kingdom (McCartney et al. 1994). These 

discharges are believed to be Co(II) (Leonard et al. 1993a). Both 58Co and 60Co are discharged into the 

Rhone River by the nuclear power plant at Bugey, France. This facility, which consists of a natural 

Uranium-Graphite-Gas unit and four pressurized water reactor (PWR) units, two of which are cooled by 

Rhone River water, discharged about 406 and 280 GBq (11.0 and 7.56 Ci) of 58Co and 60Co, respectively, 

in liquid waste during 1986–1990 (Beaugelin-Seiler et al. 1994). 

Water sampling data were used to estimate effluent release from the SRS from the plant’s start up in 

1954 to 1989 (DOE 1991). From this monitoring, it was estimated that 17.8 Ci (659 GBq) of 60Co were 

released into seepage basins and 66.4 Ci (2,460 GBq) were released into streams between 1955 and 1988. 

In addition, 2.7 Ci (100 GBq) of 58Co were released into seepage basins between 1971 and 1988; no 58Co 

was released into streams. Total releases of 60Co to streams from the SRS for 1954–1995 were 66 Ci 

(2,400 GBq) (DOE 1998). No data were reported from 1985 to 1994. In 1999, 4.94x10-4 Ci 

(0.0183 GBq) of 60Co was released to surface waters at the SRS (DOE 1999). 60Co has also been reported 

in surface water at, Hanford, Washington, and Oak Ridge National Laboratories, and groundwater at 

Brook Industrial Park, New Jersey, the Hanford site and Oak Ridge National Laboratories, Tennessee 

(HazDat 2004). The Columbia River receives discharges from the unconfined aquifer underlying the 

Hanford Site via subsurface and surface (riverbank springs) discharges. This aquifer is contaminated by 

leachate from past waste-disposal practices at the site. 

6.2.3 Soil 

Cobalt occurs naturally in the earth's crust, and therefore, in soil. However, elevated levels of cobalt in 

soil may result from anthropogenic activities such as the mining and processing of cobalt-bearing ores, 
 

 

COBALT 219 

6. POTENTIAL FOR HUMAN EXPOSURE 

the application of cobalt-containing sludge or phosphate fertilizers to soil, the disposal of cobaltcontaining wastes, and atmospheric deposition from activities such as burning of fossil fuels, smelting, 

and metal refining (Smith and Carson 1981). 

Cobalt has been identified in soil at 219 sites and sediment at 143 sites collected from 426 NPL hazardous 

waste sites, where it was detected in some environmental media (i.e., air, soil, sediment, or water) 

(HazDat 2004). 60Co has been identified in soil at 8 sites and sediment at 2 sites collected from 13 NPL 

hazardous waste sites, where it was detected in some environmental media (HazDat 2004). 60Co has been 

detected onsite in soils at the Hanford Site, Washington; INEEL, Idaho; Lawrence Livermore National 

Laboratory, Main Site, California; and Robins Air Force Base, Georgia at maximum concentrations of 

87.7, 570, 0.21, and 0.07 pCi/g (3.24, 21, 0.0078, and 0.003 Bq/g) (HazDat 2004). 

According to the TRI, in 2001, reported releases of 14,646,076 pounds of cobalt and cobalt compounds to 

land from 605 reporting facilities accounted for 98.8% of the total onsite environmental releases of these 

substances (TRI01 2004). An additional 35,530 pounds, accounting for 0.2% of the total onsite 

environmental releases were injected underground (TRI01 2004). Industrial sectors contributing the 

largest releases of cobalt and cobalt compounds to land were metal mining and electrical utilities with 

10,210,508 and 3,197,209 pounds, respectively. Table 6-1 lists the amounts of cobalt and cobalt 

compounds released on land from these facilities grouped by state. The TRI data should be used with 

caution, however, since only certain types of facilities are required to report. This is not an exhaustive 

list. 

6.3 ENVIRONMENTAL FATE 

6.3.1 Transport and Partitioning 

Cobalt compounds are nonvolatile, and thus, cobalt is emitted to the atmosphere in particulate form. The 

transport of cobalt in air depends on its particle size and density, and meteorological conditions; it can be 

returned to land or surface water by rain or it may settle to the ground by dry deposition. In nonarid 

areas, wet deposition may exceed dry deposition (Arimoto et al. 1985; Erlandsson et al. 1983). Coarse 

particles, with aerodynamic diameters >2 μm (such as those obtained during ore processing), may deposit 

within 10 km from the point of emission; finer particles may travel longer distances. It is the larger 
 

 

COBALT 220 

6. POTENTIAL FOR HUMAN EXPOSURE 

particles that may be responsible for elevated local concentrations around emission sources. The mass 

median diameter for cobalt particles emitted from a power generator with a stack emission controlled by 

an electrostatic precipitator or scrubber ranged from <2 to 12 μm. The mass median diameter of cobalt in 

the ambient atmosphere is about 2.6 μm (Milford and Davidson 1985). Golomb et al. (1997) report 

average total (wet+dry) deposition rates of cobalt to Massachusetts Bay during the period September 15, 

1992 to September 16, 1993. The total deposition rate was 58 μg/m2

-year, of which 47 μg/m2-year was 

dry deposition and 12 μg/m2

-year was wet deposition. Total cobalt deposition flux at a site in the Rhone 

delta in southern France in 1988–1989 was 0.42±0.23 kg/km2

-year with 0.15 kg/km2-year in the form of 

wet deposition (Guieu et al. 1991). 

As with most metals, sediment and soil are frequently the final repository for cobalt released into the 

environment, although the process is dynamic, and cobalt can be released into the water depending upon 

conditions. Cobalt released into waterways may sorb to particles and settle into the sediment or be sorbed 

directly into the sediment. However, complexation cobalt to dissolved organic substances can 

significantly reduce sorption to sediment particles (Albrecht 2003). Studies by Jackman et al. (2001) 

suggest that interparticle migration of cobalt can influence the transport of metal ions, including cobalt, in 

sediments. For example, migration of a metal ion from a highly mobile sediment particle, such as clay, to 

less mobile gravels will slow the transport of that metal. Cobalt can also be transported in dissolved form 

or as suspended sediment by rivers to lakes and the sea or by ocean currents. Sediment in areas of active 

sedimentation would receive a large portion of the suspended sediment. In the case of the Peach Bottom 

Atomic Power Plant where 60Co is released into the Conowingo Reservoir, an impoundment of the lower 

Susquehanna River, <20% of the radionuclide is trapped in the reservoir sediment, the rest being 

transported downstream and into the Chesapeake Bay (McLean and Summers 1990). It is often assumed 

that the primary mode of transport of heavy metals in aquatic systems is as suspended solids (Beijer and 

Jernelov 1986). However, in the case of cobalt, the percent that is transported by suspended solids is 

highly variable. Examples of the percentage of cobalt transported in suspended solids include (water 

body, percent): Main River (Germany), 33.4–42.2%; Susquehanna River (near its source in New York), 

9%; New Hope River (North Carolina), 92%; Yukon River, >98%; Danube Rive (1961–1970), 27.4– 

85.9%; Columbia River (60Co, downstream of the Hanford site), 95–98%; Strait of Juan de Fuca (Puget 

Sound, Washington), 11–15%; North Sea, 34%; and Lake Washington (Washington), 0% (Smith and 

Carson 1981). 
COBALT 221 

6. POTENTIAL FOR HUMAN EXPOSURE 

In the oxic zones of many surface waters, dissolved cobalt levels decrease with increasing depth. This 

may be due to cobalt’s continuous input into surface water from discharges or to increased adsorption and 

precipitation of the soluble forms with increasing depth. The fact that cobalt concentration profiles in 

deep water follow manganese and aluminum profiles strongly suggests that dissolved cobalt is 

precipitated in the adsorbed state with oxides of iron and manganese and with crystalline sediments such 

as aluminosilicate and goethite. A part of the cobalt may also precipitate out as carbonate and hydroxide 

in water. The higher concentration of organic pollutants in polluted water probably results in the 

formation of higher concentrations of soluble organic complexes. In a deep sediment where the water 

was anoxic and contained hydrogen sulfide, some mobilization of cobalt was observed, probably due to 

the formation of bisulfide and polysulfide complexes (Bargagli 2000; Brügmann 1988; Finney and Huh 

1989; Glooschenko et al. 1981; Knauer et al. 1982; Nriagu and Coker 1980; Shine et al. 1995; Smith and 

Carson 1981; Szefer et al. 1996; Windom et al. 1989). 

Cobalt strongly binds to humic substances naturally present in aquatic environments. Humic acids can be 

modified by UV light and bacterial decomposition, which may change their binding characteristics over 

time. The lability of the complexes is strongly influenced by pH, the nature of the humic material, and 

the metal-to-humic substance ratio. The lability of cobalt-humate complexes decreases in time (“aging 

effect”) (Burba et al. 1994). The “aging effect” indicates that after a period of time (~12 hours), 

complexes that were initially formed are transformed into stronger ones from which the metal ion is less 

readily dislodged. In the Scheldt Estuary and the Irish Sea, between 45 and 100% of dissolved cobalt was 

found to occur in these very strong complexes (Zhang et al. 1990). Aquifer material from the 

contaminated aquifer at a low-level infiltration pit at the Chalk River Nuclear Laboratories in Canada was 

analyzed to assess the nature of the adsorbed 60Co using sequential leaching techniques (Killey et al. 

1984). Of the sediment-bound 60Co, <10% was exchangeable, 5–35% was retained by iron oxide, and 

55–>90% was fixed. Over 80% of the dissolved 60Co was present as weakly anionic hydrophilic organic 

complexes. The average Kd for 60Co between particulate matter and Po River (Italy) water was 451 m3

/kg 

over a 2-year monitoring period (Pettine et al. (1994). The mean Kd for 60Co in Arctic surface sediment 

(Kara Sea) where large quantities of radioactive waste by the former Soviet Union was disposed was 

1x105

 L/kg (range 1x103–7x105), which is comparable to that in temperate coastal regions, 2x105 L/kg 

(range, 2x104

–1x106) (Fisher et al. 1999). 

The distribution coefficient of cobalt may vary considerably in the same sediment in response to 

conditions affecting the pH, redox conditions, ionic strength, and amount of dissolved organic matter 
COBALT 222 

6. POTENTIAL FOR HUMAN EXPOSURE 

(Mahara and Kudo 1981b). Uptake of 60Co from the water by sediment increased rapidly as the pH was 

increased from 5 to 7–7.5 and then slightly decrease (Benes et al. 1989a, 1989b). Therefore, pH would be 

an important factor affecting the migration of cobalt in surface water. Uptake was little affected by 

changes in liquid-to-solids ratio and ionic strength. 60Co is more mobile in anaerobic marine aquatic 

environments than in freshwater aerobic ones (Mahara and Kudo 1981b). Therefore, 60Co waste is most 

suitably stored underground in aerated zones away from possible seawater intrusions. In seawatersediment systems under anaerobic conditions 60Co was 250 times more mobile than 60Co in freshwatersediment systems under aerobic conditions. Under anaerobic conditions, 30% of the 60Co added to a 

sediment-freshwater system was ‘exchangeable’ and therefore potentially mobile, while under aerobic 

conditions, 98% of the 60Co was permanently fixed. Most of the mobile 60Co produced under anaerobic 

conditions in seawater consisted of nonionic cobalt associated with low molecular weight organic 

substances that were stable to changes in pH; the exchangeable 60Co appeared to be mostly ionic. 

Bird et al. (1998b) added 60Co to the anoxic hypolimnion of a Canadian Shield lake to simulate a nuclear 

waste scenario where radionuclides entered the bottom waters of a lake, and evaluated its behavior over 

5 years. This situation was considered to be a likely pathway by which nuclear fuel waste stored deep 

underground in the plutonic (igneous) rock of this region would reach the surface environment via deep 

groundwater flow into the bottom waters of a lake. It was felt that adding a redox sensitive element such 

as cobalt to the anoxic hypolimnion might be different from adding it to the epilimnion. Monitoring 

vertical profiles in the lake established that the cobalt remained confined to the anoxic hypolimnion prior 

to the fall turnover (first 72 days) when mixing occurred throughout the water column. After 358 days, 

only about 4% of the 60Co remained in the water. After the second year, approximately 2% of the 60Co 

remained and after 5 years, only 0.4%. These results mirror previous experiments in which the 60Co was 

added to the epilimnion, therefore establishing that there is little difference in the overall behavior of 

cobalt when added to the epilimnion or hypolimnion. The loss rate coefficient of 60Co was 0.036/day 

(half-life=19 days) between days 90 and 131 (lake mixing) during which time, the cobalt sorbed to the 

suspended sediment and bottom sediment under anoxic conditions. Loss was to the sediment as there was 

no hydrological loss from the lake. In the previous experiment in which 60Co was added to the 

epilimnion, the initial loss rate coefficient was somewhat higher, 0.056/day (half-life=12 days). 

Following the initial loss, 60Co continued to be slowly removed from the water (loss rate coefficient 

0.002/day; half-life=347 days); after 328 days, 60Co was no longer detectable in the epilimnion. The halflife of 60Co in the water column of an experimental lake in northwestern Ontario was 11 days; 5% of 

added 60Co remained in the water after 100 days (Bird et al. 1998b). The redox potential also affects the 
COBALT 223 

6. POTENTIAL FOR HUMAN EXPOSURE 

behavior of cobalt in sediment. Under moderately reducing conditions, cobalt is released from sediment 

as Co2+ and forms CoS in the presence of sulfide. The concentration of cobalt in the bottom water 

increases as the water becomes more anoxic (Brügmann 1988; Smith and Carson 1981). 

The mobility of cobalt in soil is inversely related to how strongly it is adsorbed by soil constituents. 

Cobalt may be retained by mineral oxides such as iron and manganese oxide, crystalline materials such as 

aluminosilicate and goethite, and natural organic substances in soil. Sorption of cobalt to soil occurs 

rapidly (within 1–2 hours). Soil-derived oxide materials were found to adsorb greater amounts of cobalt 

than other materials examined, although substantial amounts were also adsorbed by organic materials. 

Clay minerals sorbed relatively smaller amounts of cobalt (McLaren et al. 1986). In addition, little cobalt 

was desorbed from soil oxides while substantial amounts desorbed from humic acids and montorillonite. 

In clay soil, adsorption may be due to ion exchange at the cationic sites on clay with either simple ionic 

cobalt or hydrolyzed ionic species such as CoOH+

. Adsorption of cobalt onto iron and manganese 

increases with pH (Brooks et al. 1998). In addition, as pH increases, insoluble hydroxides or carbonates 

may form, which would also reduce cobalt mobility. Conversely, sorption onto mobile colloids would 

enhance its mobility. In most soils, cobalt is more mobile than lead, chromium (II), zinc, and nickel, but 

less mobile than cadmium (Baes and Sharp 1983; King 1988b; Mahara and Kudo 1981b; Smith and 

Carson 1981). In several studies, the Kd of cobalt in a variety of soils ranged from 0.2 to 3,800. The 

geometric mean, minimum, median, and maximum Kds of 60Co in 36 Japanese agricultural soils were 

1,840, 130, 1,735, and 104,000 L/kg, respectively (Yasuda et al. 1995). The soil properties showing the 

highest correlation with Kd were exchangeable calcium, pH, water content, and cation exchange capacity 

(CEC). In 11 U.S. soils, the mean Freundlich KF and n values were 37 L/kg and 0.754, respectively; KF 

values ranged from 2.6 to 363 L/kg and correlated with soil pH and CEC (Buchter et al. 1989). In 

13 soils from the southeastern United States whose soil pH ranged from 3.9 to 6.5, cobalt sorption ranged 

from 15 to 93%; soil pH accounted for 84–95% of the variation in sorption (King 1988b). 

Organic complexing agents such as ethylenediaminetetraacetic acid (EDTA), which are used for 

decontamination operations at nuclear facilities, greatly enhance the mobility of cobalt in soil. Other 

organic complexing agents, such as those obtained from plant decay, may also increase cobalt mobility in 

soil. However, both types of complexes decrease cobalt uptake by plants (Killey et al. 1984; McLaren et 

al. 1986; Toste et al. 1984). Addition of sewage sludge to soil also increases the mobility of cobalt, 

perhaps due to organic complexation of cobalt (Gerritse et al. 1982; Williams et al. 1985). 
 

 

COBALT 224 

6. POTENTIAL FOR HUMAN EXPOSURE 

Leaching of cobalt has been observed from municipal and low-level radioactive waste sites (Cyr et al. 

1987; Czyscinski et al. 1982; Friedman and Kelmers 1988). The mobility of cobalt was assessed in two 

soils from the Cabriolet and Little Feller event sites at the Nevada Test site as a function of various 

parameters such as pH, ionic strength, cobalt concentrations, soil solids concentrations, and particle size 

distribution (DOE 1996). Cobalt was quantitatively sorbed on these soils (at least 90% sorbed) when the 

pH was above 7 and the solid concentration was at least 20 g/L. The experiments suggest that binding is 

principally on amphoteric surface-hydroxyl surfaces. Since the pH of these soils is around 8, cobalt 

would bind strongly under normal environmental conditions. Migration would be severely retarded under 

all but the most extreme conditions, e.g., pH of 4 or below and high ionic strength soil solutions 

(approximately 0.1 M). In addition, unrealistically large quantities of water would be needed to displace 

cobalt from the upper layers of the soil profile. 

Cobalt may be taken up from soil by plants. Surface deposition of cobalt on leaves of plants from 

airborne particles may also occur. Elevated levels of cobalt have been found in the roots of sugar beets 

and potato tubers in soils with high cobalt concentrations (e.g., fly ash-amended soil) due to absorption of 

cobalt from soil. However, the translocation of cobalt from roots to above-ground parts of plants is not 

significant in most soils, as indicated by the lack of cobalt in seeds of barley, oats, and wheat grown in 

high-cobalt soil (Mermut et al. 1996; Smith and Carson 1981). Mermut et al. (1996) found 0.01– 

0.02 mg/kg in 10 samples of durum wheat grain from different areas of Saskatchewan where surface soil 

cobalt levels ranged from 3.7 to 16.4 mg/kg. The enrichment ratio, defined as the concentration in a plant 

grown in amended soil (fly ash) over the concentration in unamended soil, was about 1. Other authors 

have determined the transfer coefficient (concentration in plant/concentration in soil) for cobalt to be 

0.01–0.3. The mean 57Co soil-plant transfer factors obtained for clover from eight soils over a 4-year 

period ranged from 0.02 to 0.35, in good agreement with results of other investigators (Mascanzoni 

1989). However, in highly acidic soil (pH as low as 3.3), significantly higher than normal concentrations 

of cobalt were found in rye grass foliage, oats, and barley. For example, cobalt concentrations in rye 

grass grown in unlimed soil (pH<5.0) was 19.7 mg/kg compared with 1.1 mg/kg in rye grass grown in 

limed soil (pH>5.0) (Boikat et al. 1985; Francis et al. 1985; Kloke et al. 1984; Mejstrik and Svacha 1988; 

Palko and Yli-Hala 1988; Tolle et al. 1983; Watabe et al. 1984). Soil and plant samples taken in the 

30-km zone around Chernobyl indicated that 60Co was not accumulated by plants and mushrooms (Lux et 

al. 1995). Transfer factors obtained in 1992 ranged from 0.005 to 0.16 and those obtained in 1993 ranged 

from <0.001 to 0.008. Studies investigating the uptake of 60Co by tomato plants watered with 60Cocontaminated water showed that tomato plants absorbed <2% of the activity available from the soil. The 
COBALT 225 

6. POTENTIAL FOR HUMAN EXPOSURE 

absorption was 6 times higher if the plants were watered aerially rather than ground watering. Using 

either watering method, >90% of the activity was absorbed by the stems and leaves (Sabbarese et al. 

2002). Soil to plant transfer factors for 60Co were determined for plants grown in containers with soil 

contaminated with 65Zn and 60Co over a 3-year period under outdoor tropical conditions. Average transfer 

factors for 60Co over the 3-year period ranged from a high for spinach (1.030) to a low for rice (0.087) 

(Mollah and Begum 2001). 

60Co is taken up by phytoplankton and unicellular algae (Senenastrum capricornutum) with concentration 

factors (dry weight) ranging from 15,000 to 40,000 and 2,300 to 18,000, respectively (Corisco and 

Carreiro 1999). Elimination experiments with the algae indicate a two component biological half-life, 

1 hour and 11 days, respectively, and suggest that the cobalt might be absorbed not only on the surface, 

but also intracellularly. Since these organisms are at the bottom of the food chain, they could play an 

important role in the trophic transfer of 60Co released into waterways by nuclear facilities. However, 

cobalt levels generally diminish with increasing trophic levels in a food chain (Smith and Carson 1981). 

The low levels of cobalt in fish may also reflect cobalt’s strong binding to particles and sediment. The 

bioaccumulation factors (dry weight basis) for cobalt in marine and freshwater fish are ~100–4,000 and 

<10–1,000, respectively; accumulation in the muscle of marine fish is 5–500 (Smith and Carson 1981). 

Cobalt largely accumulates in the viscera and on the skin, as opposed to the edible parts of the fish. In 

carp, accumulation from water accounted for 75% of 60Co accumulated from both water and food; 

accumulation from water and food was additive (Baudin and Fritsch 1989). Depuration half-lives were 

53 and 87 days for fish contaminated from food and water, respectively. In the case of an accidental 

release of 60Co into waterways, the implication is that effects would manifest themselves rapidly since the 

primary route of exposure is from water rather than food. Uptake of 60Co by biota in lakes in 

northwestern Ontario was not affected by the tropic status of the lakes (Bird et al. 1998a). Uptake of 60Co 

was very low in whitefish, with concentrations being highest in kidney and undetectable in muscle. 

Similarly, while accumulation of 60Co by carp from food was dependent on food type, the transfer factor 

was very low, approximately 0.01, and no long-term bioaccumulation of the radionuclide occurred 

(Baudin and Fritsch 1987; Baudin et al. 1990). Accumulation of 60Co from food for rainbow trout 

showed that after the 42-day exposure period, the highest concentrations of 60Co were found in the 

kidneys, secondary gut, and viscera, and the trophic transfer factor was 0.0186. After 73 days of 

depuration, residual 60Co concentrations were the highest in the kidneys, viscera, and fins (Baudin et al. 

2000). In the experiment described above in which Bird et al. (1998a) added 60Co to the anoxic 
 

 

COBALT 226 

6. POTENTIAL FOR HUMAN EXPOSURE 

hypolimnion of a Canadian Shield lake to simulate a nuclear waste scenario where radionuclides entered 

the bottom waters of a lake, 60Co levels in biota were low because of the rapid loss of cobalt to the 

sediment. Levels in forage fish, minnows, and sculpins were low, <0.3 Bq/g (8 pCi/g) dry weight; an 

occasional high level, ~4 Bq/g (110 pCi/g) dry weight, in slimy sculpin was thought to reflect the 

presence of detritus in the gut of the fish. Epilimnion additions of 60Co in an earlier study resulted in 

lower maximum concentrations in fish, 0.07, 0.11, and 0.01 Bq/g (2, 3.0, and 0.3 pCi/g) dry weight in 

pearl dace, fathead minnows, and slimy sculpins, respectively, when similar quantities of radioactive 

cobalt were added to the lake. 

Concentration factors have also been reported for various other aquatic organisms. Freshwater mollusks 

have concentration factors of 100–14,000 (~1–300 in soft tissue). Much of the cobalt taken up by 

mollusks and crustacae from water or sediment is adsorbed to the shell or exoskeleton; very little cobalt is 

generally accumulated in the edible parts (Amiard and Amiard-Triquet 1979; Smith and Carson 1981). A 

concentration factor for 60Co of 265 mL/g (wet weight) was determined for Daphnia magna in laboratory 

studies. The rapid decrease in radioactivity during the depuration phase indicated that adsorption to the 

surface was the major contamination process (Adam et al. 2001). However, the digestive glands of 

crustaceans, which are sometimes eaten by humans, may accumulate high levels of 60Co. Five different 

species of marine mollusks had whole-body 60Co concentration factors between 6.3 and 84 after 1-month 

exposure to 60Co in seawater (Carvalho 1987). The shell accounted for more than half of the bodyburden. Among the soft tissue, the gills and viscera had the highest concentrations factors and the muscle 

had the lowest. Fisher et al. (1996) studied the release of 60Co accumulated in mussels from water and 

ingested phytoplankton. In each case, there was a slow and fast component to the release; the rapid 

release was in the form of fecal pellets if uptake was from food and from desorption from the shell if 

uptake was from the dissolved phase. Biological half-lives obtained in laboratory studies were about 12– 

21 days from both the shell and soft parts. Higher absorption efficiencies and lower efflux rates were 

obtained for cobalamins than for inorganic cobalt, suggesting that it is a more bioavailable form of cobalt 

for mussels. Cobalt from fecal pellets is rapidly released into the overlying water and may play a role in 

its geochemical cycling (Fisher et al. 1996). The concentration of cobalt in clams in the Indian River 

Lagoon, Florida did not correlate with levels found in either water or sediment (Trocine and Trefry 1996). 

Kinetics of bioaccumulation of 57Co from water and depuration by starfish (Asterias rubens) were carried 

out in laboratory studies. After 32 days of exposure to seawater containing 57Co, whole body uptake from 

seawater reached a concentration factor of 23 (wet weight). 57Co was released with a half-life of 27 days 

after removal to uncontaminated water. Comparison of the kinetics of loss of 57Co following exposure to 
COBALT 227 

6. POTENTIAL FOR HUMAN EXPOSURE 

57Co-contaminated food versus exposure from 57Co-contaminated water indicate that A. rubens 

accumulates 57Co predominately from seawater rather than from food (Warnau et al. 1999). 

6.3.2 Transformation and Degradation 

6.3.2.1 Air 

There is a paucity of data in the literature regarding the chemical forms of cobalt in air and their 

transformations in the atmosphere. It is generally assumed that anthropogenic cobalt originating from 

combustion sources exists primarily as the oxide (Schroeder et al. 1987). In addition, cobalt may be 

released into the atmosphere as its arsenide or sulfide during ore extraction processes. It is not clear if 

these species are transformed in the atmosphere. Should a relatively insoluble species such as the oxide 

be transformed into a more soluble form such as the sulfate, one would expect greater quantities to be 

washed out of the atmosphere in rain. 

6.3.2.2 Water 

Many factors control the speciation and fate of cobalt in natural waters and sediments. These include the 

presence of organic ligands (e.g., humic acids, EDTA), the presence and concentration of anions (Cl-

, 

OH-

, CO3

-2, HCO3-

, SO4

-2), pH, and redox potential (Eh). Modeling the chemical speciation of a metal in 

water depends upon the environmental factors assumed and the stability constants of the various 

complexes. Mantoura et al. (1978) predicted the equilibrium levels of Co2+ species in fresh water to 

follow the order: free Co+2≥ CoCO3>CoHCO3

+

>>CoSO4≥Co•humic acid. However, the mole percent of 

various cobalt species in a Welsh lake was found to be: free Co+2, 76%; CoCO3, 9.8%; CoHCO3

+

, 9.6%; 

humate complexes, 4.0%; and CoSO4, 0.4%. The rank order of species concentration in seawater was 

estimated to be: CoCO3>free Co+2>CoSO4≥CoHCO3

+

. In another model, the speciation of cobalt was 

completely different with CoCl+

>free Co+2>CoCO3>CoSO4 (Smith and Carson 1981). More recently, 

Tipping et al. (1998) estimated the equilibrium speciation of cobalt in riverine, estuarine, and marine 

surface water of the Humber system (England). In all but seawater, cobalt complexes with carbonate 

- (HCO3 and CO3

2-) constituted about 70% of dissolved cobalt while the free Co2+ ion, was a major 
COBALT 228 

6. POTENTIAL FOR HUMAN EXPOSURE 

species, ~25%, which is much lower than the 61% predicted by Mantoura et al. (1978). As the alkalinity 

of the water increases, the proportion of cobalt complexed with carbonate increases at the expense of free 

Co2+. The proportion, but not the concentration, of cobalt that exists as the free ion and the carbonate 

complexes in river water is independent of the level of fulvic acid in the water. In seawater, the carbonate 

species and the free aqua species assume roughly equal importance. The proportion of dissolved cobalt 

complexed with fulvic acid decreased with increasing salinity. About 20% of cobalt in seawater was 

estimated to be present as complexes with sulfate. In a bioconcentration study in which CoCl2 was 

initially added to the seawater, at month’s end, the cationic form of cobalt was progressively converted 

into anionic and neutral forms, possibly as a result of complexation with organic ligands (Carvalho 1987). 

Addition of humic acid to natural waters may merely increase the concentration of colloidal dispersed 

metal rather than form truly soluble humic complexes. In water that contains high organic wastes such as 

was the case in the Rhone River in France, cobalt was almost completely complexed. A recent study 

determined that the distribution of 60Co in the Rhone River sampled at Arles, France was 45% in the 

particulate phase, 30% in the dissolved phase, and 25% in the colloidal phase (Eyrolle and Charmasson 

2001). Cobalt forms complexes with EDTA that are very stable environmentally. EDTA is often used in 

agriculture, food and drug processing, photography, and textile and paper manufacturing, and therefore, it 

is a likely constituent of industrial discharges. 

Acidity and redox potential have an effect on the behavior of cobalt in water. The adsorption of cobalt by 

particulate matter decreases with decreasing pH, since the increasing H+

 concentration competes with 

metal binding sites. This may lead to increased concentrations of dissolved cobalt at low pH. The effect 

of Eh (redox potential) on the speciation of cobalt has been shown by the increase in the concentration of 

dissolved cobalt by orders of magnitude with increasing depth in certain parts of Baltic waters. The 

increase in the concentration of dissolved cobalt may be due to the formation of soluble bisulfide and 

polysulfide complexes in the anoxic zones. The residence time of soluble cobalt in seawater has been 

estimated to range from <1 to 52 years (Brugmann 1988; Knauer et al. 1982; Smith and Carson 1981). 

Vitamin B12, which contains cobalt, is synthesized by 58 species of seven genuses of bacteria as well as 

blue-green algae and actinomycetes (mold-like bacteria). Consequently, vitamin B12 levels in marine 

water range from very low levels in some open ocean water to much higher levels in some coastal waters. 

Freshwater environments have comparable levels of vitamin B12. The high level of cobalamins in coastal 
COBALT 229 

6. POTENTIAL FOR HUMAN EXPOSURE 

water appears to be related to the occurrence of macrophytes in these areas with their high concentrations 

of vitamin B12. Cobalamins are released into the water when the organisms die (Smith and Carson 1981). 

Alkaline thermal groundwater in granitic areas have been studied as possible waste disposal sites for 

radioactive waste (Alaux-Negrel et al. 1993). Water in these areas is characterized by high pH, low CO2 

partial pressure, and generally low redox potential; sulfide concentrations are in the range of 10-4 to 

10-3 mol/L. The solubility of cobalt is controlled by the solubility of CoS (log K1 and log K2 being 

5.7 and 8.7 at 25°C) and therefore, levels of cobalt are very low, 10-8–10-10 mol/L. 

The 60Co (III) picolinate complex that is released into water by some nuclear reactors does not break 

down immediately on release into seawater, but rather can coexist with the 60Co (II) forms for lengthy 

periods in the environment (Leonard et al. 1993a, 1993b). Studies indicate that several processes occur to 

the Co(III) organic complexes, including reduction to the inorganic form, sorption of both species to 

particulate matter, and transformations of the uncomplexed species. It is possible that this more soluble 

and uncharged form of radioactive cobalt will increase the dispersion of 60Co from its point of discharge. 

6.3.2.3 Sediment and Soil 

The speciation of cobalt in soil or sediment depends on the nature of the soil or sediment, concentration of 

chelating/complexing agents, pH, and redox potential (Eh) of the soil. Dissolved cobalt may be absorbed 

by ion exchange and other mechanisms, or may form complexes with fulvic acids, humic acid, or other 

organic ligands in soil. The humic and fulvic complexes of cobalt are not very stable compared with 

those of copper, lead, iron, and nickel. The speciation of cobalt in sediment from nine sites in the Red 

Sea, a sea that is unique in that it has no permanent streams flowing into it, was assessed using a 

sequential extraction technique (Hanna 1992). The mean percentages contained in the various fractions 

were: exchangeable, 5.5%; carbonate, 5%; Fe/Mn oxides, 24%; organic, 30.4%; sulfides, 13%; and 

lithogenous, 22%. While the mean concentration of cobalt in the sediment increased from 0.003 to 

0.006 ppb between 1934 and 1984, its distribution among the different phases did not change appreciably. 

The reduction of soil Eh, which may occur when soil is flooded or in deeper layers of soil that are 

oxygen-depleted, may change the speciation of cobalt. This may result in the reduction of soil iron and 

manganese and the subsequent release of adsorbed cobalt from the mineral oxides. Similarly, a decrease 
COBALT 230 

6. POTENTIAL FOR HUMAN EXPOSURE 

in soil pH may result in the solubilization of precipitated cobalt and desorption of sorbed cobalt, resulting 

in increased cobalt mobility (Smith and Carson 1981). Co2+ may also be oxidized to Co3+ by manganese 

oxides, a common component of soils and aquifer material, with subsequent surface precipitation 

(Brusseau and Zachara 1993). This process may affect transport of cobalt in the subsurface environment. 

EDTA complexes of cobalt are very stable and are likely to form in soils containing EDTA. EDTA is 

widely used as a decontaminating agent at nuclear facilities. Although cobalt-EDTA complexes are 

adsorbed by some soils, the mobility of cobalt in soil may increase as a result of complex formation 

(Schnitzer 1969; Smith and Carson 1981; Swanson 1984). 60Co that is disposed of in shallow land 

trenches have sometimes been found to migrate more rapidly than expected from the disposal sites. 

Organic chelating agents are frequently present at these sites and would possibly increase the solubility 

and transport of the radionuclide. 

Bacterial action can affect the mobility of a substance by mediating reactions or by participating in 

reactions that lower the pH. Another way of influencing radionuclide mobility is by degrading 

complexing agents used in cleaning reactors (e.g., citric acid), thereby releasing the radionuclide. 

However, experiments on the fate and transport of cobalt released upon the biodegradation of the 

complexing ligand indicate that results are not always predictable; the means of ligand removal and the 

geochemical environment are important factors that must be considered (Brooks et al. 1998). 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 

Cobalt concentrations in environmental media, including food and human tissue, have been exhaustively 

tabulated by Smith and Carson (1981) and Young (1979). The International Agency for Research on 

Cancer (IARC 1991) contains reviews of more recent studies, but is primarily focused on occupational 

exposures and body burdens of cobalt. 

6.4.1 Air 

Atmospheric cobalt is associated with particulate matter. Mean cobalt levels in air at unpolluted sites are 

generally <1–2 ng/m3

 (Hamilton 1994; Smith and Carson 1981). At the South Pole, cobalt levels of 

0.00049±0.00015 ng/m3

 were recorded in 1974–1975 (Maenhaut et al. 1979). Geometric mean cobalt 
 

 

 

COBALT 231 

6. POTENTIAL FOR HUMAN EXPOSURE 

levels in several open-ocean environments ranged from 0.0004 to 0.08 ng/m3 (Chester et al. 1991). The 

average annual PM-10 (particles with diameters ≤10 μm) cobalt concentration at Nahant, Massachusetts 

(near Boston) in 1992–1993 was 1.7 ng/m3

 (Golomb et al. 1997). Half of the cobalt was contained in fine 

particles (<2.5 μm) and half in coarse particles (2.5–10 μm). The mean cobalt level in southern Norway 

in 1985–1986 (n=346) was 0.10 ng/m3

 with 35% of the samples falling below the detection limit of 

0.04 ng/m3

 (Amundsen et al. 1992). Atmospheric cobalt levels in industrial settings may exceed 

10 ng/m3

. The highest recorded average cobalt concentration in air was 48 ng/m3 in Clydach, Wales at 

the site, where nickel and cobalt were refined (Smith and Carson 1981). Some ambient atmospheric 

levels of cobalt are given in Table 6-2. These data show the contribution of anthropogenic sources in 

increasing the level of cobalt in the ambient air. Typical occupational cobalt levels are 1.0x104

– 

1.7x106

 ng/m3 (Barceloux 1999; IARC 1991). While 60Co has been detected in air samples at the Hanford 

site and Oak Ridge National Laboratories, levels were not reported (HazDat 2004; PNNL 1996). In 1995, 

the concentration of 60Co in air at the Hanford site was below the detection limit in over 88% of the air 

samples. 

6.4.2 Water 

The concentrations of cobalt in surface water and groundwater in the United States are generally low, 

<1 μg/L in pristine areas and 1–10 μg/L in populated areas (Hamilton 1994; Smith and Carson 1981). 

However, cobalt levels may be considerably higher in mining or agricultural areas. Levels as high as 

4,500 μg/L were reported in Mineral Creek, Arizona, near a copper mine and smelter; levels of 

6,500 μg/L were reported in the Little St. Francis River, which receives effluent from cobalt mining and 

milling operations (Smith and Carson 1981). Mining at Blackbird Mine in Idaho, one of the large 

deposits of cobalt in North America, occurred from the late 1800s to 1982. Cobalt concentration in 

surface water and groundwater samples collected in 1992 from area creeks near this mine were reported 

to range from <1 to 625,000 μg/L, and from not detected to 315,000 μg/L respectively (ATSDR 1995), 

Eckel and Jacob (1988) analyzed U.S. Geological Survey (USGS) data for 6,805 ambient surface water 

stations and estimated the geometric mean and median dissolved cobalt concentration as 2.9 and 2.0 μg/L, 

respectively. Mean cobalt levels reported in seawater range from 0.078 μg/L in the Caribbean Sea to 

0.39 μg/L in the Indian Ocean (Hamilton 1994). Vitamin B12 is synthesized by bacteria, macrophytes, 
 

 

 

 

 

 

 

 

 

 

COBALT 232 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-2. Concentration of Cobalt in the Atmosphere 

Possible 

Location source/activity Concentrationa Units Type Reference 

Ambient levels—remote 

South Pole, 1974–1975 Crustal material 0.00049±0.00015 ng/m3

 Mean±SD Maenhaut et 

al. 1979 

Open-ocean 0.0004–0.08 ng/m3

 Geomean Chester et al. 

range 1991 

North Atlantic 0.006–0.09 ng/m3

 Range Smith and 

Carson 1981 

Baltic Sea, 1983 0.09, 0.01–0.43 ng/m3 Mean, range Hasanen etal. 

1990 

Remote sites 0.001–0.9 ng/m3

 Range Schroeder et 

al. 1987 

Ambient levels—rural/suburban/urban 

Rural sites 0.08–10.1 ng/m3

 Range Schroeder et 

al. 1987 

Massachusetts, Nahant, 1.7 ng/m3

 Annual Golomb et al. 

1992–1993 mean 1997 

Urban sites Schroeder et 

al. 1987 

 United States 0.2–83 ng/m3

 Range 

 Canada 1–7.9 

 Europe 0.4–18.3 

Texas state average 2.0 ng/m3

 Mean Wiersema et 

(1978–1982) al. 1984 

Illinois, urban air Sweet et al. 

(<2.5 μm; 2.5–10 μm) 1993 

Bondville, Ill (rural) Background 0.2; 0.1 ng/m3

 Mean (fine; 

coarse) 

 Southeast Chicago Steel mills 0.4; 0.4 

East St. Louis Smelters 0.5; 0.4 

Washington, DC (1974) Urban area 1.1 ng/m3

 Mean Smith and 

Carson 1981 

Ambient levels—industrial 

Maryland, Baltimore Ondov et al. 

Harbor Tunnel 1982 

(1973–1974) 

Air outside Vehicular exhaust 0.8–1.9 ng/m3

 Range 

Air inside Vehicular exhaust 2.2–5.3 

Ohio, Cleveland Be-Cu alloy and other 610 ng/m3

 Maximum Smith and 

industrial activities Carson 1981 

Texas, El Paso Industrial 127 ng/m3

 Maximum Wiersema et 

(1978–1982) al. 1984 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

COBALT 233 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-2. Concentration of Cobalt in the Atmosphere 

Possible 

Location source/activity Concentrationa Units Type Reference 

Texas, Houston (1978– Urban area 81 ng/m3 Maximum Wiersema et 

1982) al. 1984 

Arizona, Tucson Smith and 

Carson 1981 

 Urban Copper smelting 1.9 ng/m3

 Mean 

Rural 0.7 

Maryland, Chalk Point Coal-burning power 3.86 ng/m3

 Mean Smith and 

Generator plant Carson 1981 

Wales, Clydach Nickel refining 48, 3–300 ng/m3 Mean, range Smith and 

Carson 1981 

Wales, Llausamlet and Towns near Clydach 3.8 Mean Smith and 

Trebanos Carson 1981 

Occupational air levels 

Northern Italy, exposure Diamond abrasive Mosconi et al. 

survey, 1991, area mfg. 1994a 

monitoring (n=259) 

Mould-filling 220, 47–960 ng/m3

 Median, 

range 

Sintering 101.5, 32–240 

Grinding 22, 15–45 

Mechanical­ 20, 12–44 

working 

 Grinding 5, 2.5–94 

Tool production 6, 5–47 

Hard metal alloy filing 2, 0.8–3 

Other 2.7, 2.3–15 

Northern Italy, exposure Diamond abrasive Mosconi et al. 

survey, 1991, personal mfg. 1994a 

sampling (n=259) 

Mould-filling 382, 76–2,600 ng/m3

 Median, 

range 

Sintering 309, 238–413 

Grinding 230, 82–690 

Mechanical­ 40, 7.1–65 

working 

 Grinding 9.3, 1.5–178 

Tool production 17, 4–28 

Hard metal alloy 5, 1–107 

filling 

Other 50, 10–290 
 

 

 

 

 

 

 

 

 

 

 

COBALT 234 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-2. Concentration of Cobalt in the Atmosphere 

Possible 

Location source/activity Concentrationa Units Type Reference 

Japan, personal sampling, Powder preparation Kumagai et al. 

hard metal tool 1996 

manufacture, 8-hour 

TWA, 356 workers 

(n=935) 

Rotation 459, 7–6,390 μg/m3

 Mean, range 

Full-time 147, 26–378 

Press 

Rubber 339, 48–2,910 

Steel 47, 6–248 

Shaping 97, 4–1,160 

Sintering 24, 1–145 

Blasting 2, 1–4 

Electron 3, 1–23 

discharging 

Grinding 45, 1–482 

geomean = geometric mean; SD = standard deviation; TWA = time weighted average 
 

 

 

COBALT 235 

6. POTENTIAL FOR HUMAN EXPOSURE 

blue-green algae, and actinomycetes, and cobalt levels in oceans often correlate with biological 

productivity. In the Baltic Sea, dissolved cobalt levels that are 1.0 ng/L near the surface, increase to 

71.0 ng/L at a depth of 200 m (Brügmann 1988). The rise in dissolved cobalt is coincident with the onset 

of anoxic conditions and the presence of hydrogen sulfide, indicating that soluble bisulfide and 

polysulfide complexes may be present. Some cobalt levels reported in water are given in Table 6-3. 

In a 1962–1967 survey, cobalt was detected in 2.8% of 1,577 U.S. raw surface waters from which 

drinking water is derived; the detection limit was 1 μg/L and the maximum concentration was 48 μg/L 

(NAS 1977). Of 380 U.S. finished drinking waters, only 0.5% contained cobalt levels exceeding 1 μg/L; 

the maximum concentration found was 29 μg/L (NAS 1977). These values are higher than the respective 

median and maximum levels of <2.0 and 6.0 μg/L found in Canadian finished drinking water (Meranger 

et al. 1981). Meranger et al. (1981) tested source water and drinking water in 71 municipalities across 

Canada and concluded that, in general, both surface water and groundwater used for drinking water 

supplies contain negligible amounts of cobalt. Greathouse and Craun (1978) analyzed 3,834 grab samples 

of household tap water from 35 geographical areas in the United States for 28 trace elements. Cobalt was 

found in 9.8% of the samples at concentrations ranging from 2.6 to 107 μg/L. It is not clear whether these 

higher levels could indicate that cobalt was picked up in the distribution system. In the earlier National 

Community Water Supply Study (2,500 samples), 62% of the samples contained <1 μg Co/L; the average 

and maximum cobalt concentrations were 2.2 and 19 μg/L, respectively (Smith and Carson 1981). Cobalt 

was not detected (detection limit 8 μg/L) in a 1982–1983 survey of drinking water in Norway that 

covered 384 waterworks serving 70.9% of the Norwegian population (Flaten 1991). 

The mean concentrations of cobalt in rain is around 0.03–1.7 μg/L, with levels generally ranging from 

0.002 μg/L at Enewetak Atoll to about 2.9 μg/L in the Swansea Valley, Wales (Arimoto et al. 1985; 

Dasch and Wolff 1989; Hansson et al. 1988; Heaton et al. 1990; Helmers and Schrems 1995; Nimmo and 

Chester 1993; Nimmo and Fones 1997; Smith and Carson 1981). The highest recorded level of cobalt in 

precipitation was 68.9 μg/L in the vicinity of a nickel smelter in Monchegorsk in the Russian Arctic 

(Reimann et al. 1997). An analysis of rain in the Mediterranean and urban and coastal sites in northwest 

England showed that about 33–44% of the cobalt occurred as very stable dissolved organic complexes 

(Nimmo and Chester 1993; Nimmo and Fones 1997). 

As it was pointed out in Section 6.3.2.2, 60Co discharged from the Steam Generating Heavy Water 

Reactor at Winfrith on the south coast of England was shown to be largely in the form of the nonionic 
 

 

 

 

 

 

 

 

 

 

COBALT 236 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-3. Cobalt Levels in Water 

Nature/location of water Level Units Type Reference 

Sea water 

Florida (Indian River 

Lagoon) (43 sites) 

0.031, 50 μg/L Mean, range Trocine and Trefry 

1996 

California (Baja) 2–45 km 

offshore (n=11) 

0.022–0.17 nM Range Sañudo-Wilhelmy and 

Flegal 1996 

<100 m off shore (n=11) 0.11–0.59 

Agean Sea, 1994; 8 sites 

(dissolved) 

0.168–0.632, 1.917 nM Range of 

means, 

maximum 

Voutsinou-Taliadouri 

1997 

Baltic Sea (Gotland Deep 

site) 

Brügmann 1988 

10 m 1.0 ng/L Mean 

(dissolved Co) 

50 m 1.0 

100 m 3.5 

150 m 4.2 

200 m (anoxic) 71.0 

235 m (anoxic) 49.2 

Seawater background 0.04 μg/L Bargagli 2000 

Seawater 0.27 μg/L Mean Abbasi et al. 1989 

Fresh surface water 

Freshwater background 0.05 μg/L Bargagli 2000 

U.S. ambient surface water 

(6,805 stations) 

<2.9, 2.0 μg/L Mean, median Eckel and Jacob 1988 

Five Great Lakes waters ND–0.09 μg/L Range Rossmann and Barres 

1988 

Japan, unpolluted lake <0.004 μg/L Nojiri et al. 1985 

Norway, 11 rivers 0.94 μg/L Maximum Flaten 1991 

Streams near populated 

areas 

1–10 μg/L Range Smith and Carson 

1981 

Streams in agricultural and 

mining areas 

11–50 μg/L Range Smith and Carson 

1981 

Suspended solids in rivers 7–94 mg/kg Range Smith and Carson 

1981 

Groundwater 

Canada (Chalk River nuclear 

waste site) 

0.0001–0.002 μg/L Cassidy et al. 1982 

 Colorado (Denver)–shallow 

groundwater, (n=30) 

<1 (<1–9) μg/L Median, range Bruce and McMahon 

1996 
 

 

 

 

 

 

 

 

 

 

 

COBALT 237 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-3. Cobalt Levels in Water 

Nature/location of water Level Units Type Reference 

Drinking water 

Canadian drinking water Meranger et al. 1981 

(71 municipalities) 

Raw: <2.0 μg/L Median 

Treated: <2.0 

Distributed: ≤2.0 

Precipitation

 Massachusetts, 1984 0.045 (0.008), 0.02– μg/L Mean (SD), Dasch and Wolff 1989 

(12 events) 0.12 range 

Rhode Island (rain/snow), 0.038 (0.067) ppb Median (mean) Heaton et al. 1990 

1985 (n=269) 

0.001–0.80 Range 

 Western Mediterranean, Nimmo and Chester 

1988–1989 1993 

Total cobalt 0.029–0.134, 0.043 μg/L Range, mean 

Labile cobalt 0.009–0.104, 0.025 

Organic cobalt ND–0.613, 0.019 

Arctic (7 sites in Finland, <0.02–1.07, 3.32 μg/L Median range, Reimann et al. 1997 

Norway, Russia) maximum 

 Russia (Monchegorsk), 11.8, 68.9 Median, 

nickel smelter maximum 

ND = not detected; SD = standard deviation 
 

 

COBALT 238 

6. POTENTIAL FOR HUMAN EXPOSURE 

trivalent complex, 60Co(III) picolinate. The 60Co(III) species is not immediately reduced to the more 

particle-reactive divalent form, and both oxidation states may coexist for long periods of time in the 

environment. The proportion of the more soluble and mobile 60Co(III) would be expected to increase 

with time and distance from the point of discharge. Shoreline water samples (n=22) taken in 1987–1988 

at two locations in the vicinity of the discharge from the Steam Generating Heavy Water Reactor at 

Winfrith contained 0.3–16.2 mBq/L (8–437 fCi/L) of particulate 60Co, 2.8–44.4 mBq/L (76–1,200 fCi/L) 

of soluble 60Co(II), and 0.2–4.8 mBq/L (5–130 fCi/L) of soluble 60Co(III) (Leonard et al. 1993). The 

percent of the soluble 60Co present as Co(III) ranged from 4.3 to 18.6%. In 1989, in conjunction with the 

largest discharge of effluent from the plant, offshore seawater samples from 18 sites contained 

0.06–2.22 mBq/L (2–60 fCi/L) of particulate 60Co, 0.30–10.3 mBq/L (8.1–278 fCi/L) of soluble 60Co(II), 

and 0.12–1.55 mBq/L (3.2–41.9 fCi/L) of soluble 60Co(III). The percent of the soluble 60Co present as 

Co(III) ranged from 6.0 to 28.6%. 

6.4.3 Sediment and Soil 

Cobalt is the 33rd most abundant element in the earth’s crust. Its average concentrations in the earth's 

crust and in igneous rocks are 20–25 and 18 mg/kg, respectively (Abbasi et al. 1989; Merian 1985; Smith 

and Carson 1981). Trace metals in soils may originate from parent rock or from anthropogenic sources, 

primarily fertilizers, pesticides, and herbicides. Most soils contain 1–40 mg cobalt/kg. The average 

cobalt concentration in U.S. soils is 7.2 mg/kg (Smith and Carson 1981). Soils containing <0.5–3 mg 

cobalt/kg are considered cobalt-deficient because plants growing on them have insufficient cobalt 

(<0.08–0.1 mg/kg) to meet the dietary requirements of cattle and sheep. Cobalt-deficient soils include the 

humus podzols of the southeastern United States, and the podzols, brown podzolic soils, and humus 

groundwater podzols in the northeastern parts of the United States. (Podzols are generally coarsetextured soils.) The cobalt content of surface soils from 13 sites in the brown and dark brown soil zones 

of southwestern Saskatchewan ranged from 3.7 to 16.0 mg/kg and only in one case was the soil 

appreciably elevated above the corresponding parent material (Mermut et al. 1996). Fertilizers used in 

this agricultural area contained 0.12–102 mg Co/kg, with a median of 5.7 mg/kg. 

Mean cobalt concentrations in surface soil from nine sites on two active volcanic islands off of Sicily 

ranged from 5.1 to 59.0 mg/kg (Bargagli et al. 1991). Soils near ore deposits, phosphate rocks, or ore 
 

 

COBALT 239 

6. POTENTIAL FOR HUMAN EXPOSURE 

smelting facilities, and soils contaminated by airport traffic, highway traffic, or other industrial pollution 

may contain much higher concentrations of cobalt; concentrations up to 800 mg/kg have been detected in 

such areas (Kloke et al. 1984; Smith and Carson 1981). Cobalt concentrations from 28 samples collected 

from surface deposits in the Big Deer and Blackbird Creek drainage basins in Idaho near the Blackbird 

Mine ranged from 26.5 to 7,410 mg/kg (Agency for Toxic Substances and Disease Registry 1995). Soils 

around the large copper-nickel smelters in Sudbury, Ontario have been shown to contain high levels of 

cobalt. Fifty kilometers from the smelters, cobalt levels in surface soil were 19 mg/kg. These levels 

increased to 48 mg/kg at 19 km, 33 mg/kg at 10 km, and 42–154 mg/kg between 0.8 and 1.3 km from the 

smelter (Smith and Carson 1981). Soils around a cemented tungsten carbide tool grinding factory 

contained cobalt levels as high as 12,700 mg/kg, almost 2,000 times the average in U.S. soils (Abraham 

and Hunt 1995). However, neighborhood soils between 30 and 160 meters from the factory only 

contained 12–18 mg Co/kg. 

Unpolluted freshwater sediment contains about the same levels of cobalt as does cobalt-sufficient soil, 

generally <20 mg/kg (Smith and Carson 1981). In the Hudson River Estuary, cobalt levels in suspended 

sediment were an order of magnitude higher than in bottom sediment (Gibbs 1994). This can be 

attributed to the finer grain size of suspended sediment or local sources. Cobalt levels in core samples 

(surface to 42 cm deep) from the Upper St. Lawrence Estuary were independent of depth, indicating the 

lack of any recent significant anthropogenic releases (Coakley et al. 1993). Cobalt levels in sediment are 

shown in Table 6-4. 

No broad-based monitoring studies of 60Co or other radioactive cobalt isotopes in soil or sediment were 

found in the literature. Soil samples from the O-horizon taken from three sites in the 30-km zone around 

Chernobyl in 1992 and again in 1993 contained 14–290 and 4.5–245 Bq/kg (380–7,800 and 120– 

6,620 pCi/kg) dry weight of 60Co, respectively (Lux et al. 1995). The Columbia River receives 

radiological contaminants along the Hanford Reach primarily through seepage of contaminated 

groundwater. The regional median concentration of 60Co in sediment was highest along the Hanford 

reach, approximately 0.09 pCi/g (0.003 Bq/g) (PNNL 1996). 60Co activity in a sediment cores in water 

off of Southampton in southern England contained up to 28 Bq/kg (760 pCi/kg) in the upper 3 cm; no 

activity was found below 12.5 cm (Croudace and Cundy 1995). Discharges of treated effluent occurred 

on closing a steam generating heavy water reactor west of where the sampling was done. The maximum 

discharge occurred in 1980–1981; however, no value was reported (Croudace and Cundy 1995). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

COBALT 240 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-4. Cobalt Levels in Sediment 

Nature/location of sediment Level Units Type Reference 

Freshwater 

Polluted lakes and rivers 0.16–133 mg/kg Range Smith and Carson 

1981 

Lake Ontario near Miesissaqua, Canada 4.1–19.8 mg/kg Range Glooschenko et al. 

1981 

Hudson River, Foundry Cove, 1983, Ni-Cd 

battery plant, 1953–1979, surficial (0–5 

cm) sediment, 16 sites 

18–700 mg/kg Range Knutson et al. 1987 

Estuaries and Marine 

Hudson River Estuary (0–80 km from 

ocean), 1991 

Gibbs 1994 

Bottom sediment 1–13 mg/kg Range 

Suspended sediment (near surface) 30–140 

Upper St. Lawrence Estuary, 1989–1990 Coakley et al. 1993 

Core C168 3.1 (0.6) mg/kg Mean (SD) 

Cores LE and LO 2.7 (0.5) 

Massachusetts, New Bedford Harbor- core 

(0–25 cm) 

Shine et al. 1995 

Outer Harbor 7.03, 3.64–9.79, 

range 

Inner Harbor 6.38, 2.62–10.52 

Buzzards Bay (control site) 4.76, 1.64–8.19 

Indian River Lagoon, Florida (43 sites) 2.3, 0.4–6.3 mg/kg Mean, 

range 

Trocine and Trefry 

1996 

Gulf of Mexico Villanueva and 

Botello 1998 

Coastal areas (11 sites) 12.30–36.26 mg/kg Range of 

means 

Continental shelf (3 sites) 6.39–21.00 

Antarctica (Ross Sea) continental shelf 

(n=12) 

19, 0.10–13 mg/kg Mean, 

range 

Bargagli 2000 

Northern Arctic Alaska, continental shelf 

(n=136) 

9, 3.3–18 mg/kg Mean, 

range 

Bargagli 2000 

Chukchi Sea, northeast Alaska 

(31 stations, surficial sediment) 

32.7, 19–74 mg/kg Mean, 

range 

Naidu et al. 1997 

Baltic Sea, southern, off Poland (surficial 

sediment) 

0.69–18.10 mg/kg Range Szefer et al. 1996 

Baltic Sea (Gotland Deep site) 19, 11–33 mg/kg Mean, Brügmann 1988 

range 

SD = standard deviation 
 

 

 

COBALT 241 

6. POTENTIAL FOR HUMAN EXPOSURE 

Sediment samples were analyzed from the Peconic River system on Long Island, New York, downstream 

of Brookhaven National Laboratory (BNL). Near the sewage treatment plant, closest to the BNL, mean 

concentrations of 60Co from three locations at the depth intervals 0.00–0.06, 0.06–0.15, 0.15–0.24, and 

0.24–0.37 meters were 9.6, 6.7, 9.6, and 10.5 Bq/kg (0.25, 0.18, 0.25, and 0.28 nCi/kg) dry weight, 

respectively. At one location at the BNL property boundary, mean concentrations of 60Co, using the same 

depth intervals, were 5.8 Bq/kg (0.16 nCi/kg) dry weight for the 0.00–0.06 m depth and <4 Bq/kg 

(<0.11 nCi/kg) dry weight for the remaining depth intervals. Sediment samples from a control river, 

Connetquot River, were <4 Bq/kg (<0.11 nCi/kg) in two locations at two depths (0.00–0.06 and 0.06– 

0.15 m) (Rapiejko et al. 2001). 

Mururoa and Fangataufa Atolls were used for underground testing of nuclear weapons from 1975 to 1996. 

60Co was detected in the particle fraction of water in measurable levels at two of the nine Mururoa Atoll 

sites, Aristee and Ceto, at 0.58 and 1.06 mBq/L (0.016 and 0.029 pCi/L), respectively. 60Co levels were 

found at levels below the detection limit, <0.1 mBq/L (<0.003 pCi/L), at the two Fangataufa Atoll sites 

and at the seven other Muruoa Atoll sites (Mulsow et al. 1999). Concentrations of 60Co of soil samples 

used for growing onion, potatoes, tomatoes, cabbage, and maize in the Bulgarian village, Ostrov, in the 

vicinity (approximately 25–30 km) of the “Kozloduy” nuclear power plant were <8, 3, 320, 330, and 

180 mBq/kg (2, 8.1, 8.6, 8.9, and 4.9 pCi/kg), respectively (Djingova and Kuleff 2002). 

6.4.4 Other Environmental Media 

The cobalt content of plants depends on the plant, the cobalt content of the soil, and numerous 

environmental factors. The mean cobalt concentration reported for terrestrial plants was 0.48 μg/g, while 

the mean and median levels for freshwater vascular plants were 0.48 and 0.32 μg/g, respectively 

(Outridge and Noller 1991). The median cobalt level in freshwater vascular plants from polluted waters 

was about the same as in unpolluted waters, 0.37 μg/g, although extremely high levels of cobalt, up to 

860 μg/g, was reported in one species, Myriophyllum verticillatum, from central Ontario lakes. Grasses 

normally contain 0.2–0.35 μg/g of cobalt, but grasses from cobalt-deficient regions contain only 

0.02–0.06 μg/g of cobalt (Hamilton 1994). Durum wheat grown in southeastern Saskatchewan contained 

0.01–0.02 mg/kg dry weight (Mermut et al. 1996). In view of the cobalt content of the soil and the fact 

that almost half of the cobalt in fertilizers used in the area was in a readily available form, the uptake of 

cobalt by wheat was negligible. 
COBALT 242 

6. POTENTIAL FOR HUMAN EXPOSURE 

60Co levels in plants and mushrooms in the 30-km zone around Chernobyl were mostly below the 

detection limit in samples obtained in 1992 and 1993; the highest activity recorded was 3.9 Bq/kg 

(110 pCi/kg) dry weight in Athyrium filix femina (Lux et al. 1995). 

Cobalt concentrations have been reported in various aquatic animals and seabirds. Eel and a freshwater 

fish from three Dutch polder lakes contained 2.5–25.0 and 2.50–5.63 mg cobalt/kg wet weight, 

respectively, (Badsha and Goldspink 1988). Muscle tissue of ocean fish and rock crabs caught near dump 

sites off New York City, New Haven, Connecticut, and Delaware Bay contained 10–40 and 16.0 μg/kg, 

respectively (Greig and Jones 1976). In a study of the levels and distribution of 14 elements in oceanic 

seabirds, the concentration of cobalt, an essential element, appeared to be highly regulated, with over 80% 

of the body burden residing in the skeleton. The mean cobalt concentration in the livers of 11 seabird 

species ranged from 0.048 to 0.078 μg/g dry weight, and cobalt had the lowest coefficient of variation in 

the different species of the elements studied (Kim et al. 1998a). In another study in Antarctica, mean 

cobalt levels in fish and amphipods were 0.11–0.14 and 1.01 μg/g dry weight, respectively, while those in 

the tissue of penguin and other sea birds ranged from 0.09 to 0.11 μg/g (Szefer et al. 1993). The 

concentration of cobalt in the tissue of 14 bluefin tuna caught by various commercial fishing vessels off 

Newfoundland was essentially the same, 0.01±0.004 μg/g (Hellou et al. 1992a). Similarly, in a broad 

survey of contaminant levels in nine species of fish and fiddler crabs from 11 sites in the lower Savannah 

River, Georgia and the Savannah National Wildlife Refuge, mean cobalt levels among different species 

and sites were statistically indistinguishable (Winger et al. 1990). These and other studies indicate that 

cobalt does not biomagnify up the food chain (Smith and Carson 1981). While high levels of cobalt were 

found in sediment from the Tigris River in Turkey and low levels in the water, cobalt was not detected in 

two species of fish, Cyprinion macrostomus and Garra rufa (Gümgüm et al. 1994). Cobalt was detected 

in two other species of fish collect between 1995 and 1996 in the upper Sakarya river basin, Turkey. 

Cobalt concentrations ranged from 0.038 to 0.154 μg/g dry weight for Cyprinus caprio and from 0.045 to 

0.062 μg/g dry weight for Barbus plebejus (Barlas 1999). 

60Co was not detected in fish and mussel samples analyzed from the Peconic River system on Long 

Island, New York, downstream of the BNL. The lower detection limit for 60Co was 0.4 Bq/kg 

(10 pCi/kg). 60Co had been detected in sediment samples from this area (Section 6.4.3) (Rapiejko et al. 

2001). 
COBALT 243 

6. POTENTIAL FOR HUMAN EXPOSURE 

Some female birds sequester metals into their eggs under certain conditions, a phenomenon that may 

jeopardize the developing embryos. The geometric mean concentrations of cobalt in tern eggs collected 

from coastal New Jersey in 1971 and 1982 were 0.48 and 0.50 mg/kg, respectively. Unlike the levels of 

seven other common metals (e.g., mercury, cadmium, copper, lead, manganese, nickel, and zinc), the 

level of cobalt in tern eggs (and in the environment) showed no decline over the 11-year period (Burger 

and Gochfeld 1988). 

Table 6-5 shows the levels of cobalt in food items and food categories from different countries. The level 

of cobalt in most Canadian foods was low; items with the highest concentrations in this study were 

waffles (0.076 μg/g), corn cereal (0.074 μg/g), and potato chips (0.070 μg/g) (Dabeka and McKenzie 

1995). Green leafy vegetables and fresh cereals are the richest sources of cobalt (0.2–0.6 μg/g dry 

weight), while dairy products, refined cereals, and sugar contain the least cobalt (0.1–0.3 μg/g dry weight) 

(Barceloux 1999). The levels of cobalt were determined in 50 different food items, mainly meat, fish, 

fruit, vegetables, pulses, and cereals on the Swedish market during the years 1983–1990 (Jorhem and 

Sundström 1993). Beef liver and seeds were fairly high in cobalt and fish, fruit, and root and leafy 

vegetables were under 0.01 μg cobalt/g fresh weight. The cobalt levels in μg/g fresh weight were highest 

in alfalfa seeds, 0.86; linseed, 0.56; milk chocolate, 0.34; dark chocolate, 0.24; white poppy seeds, 0.30; 

blue poppy seeds, 0.15; soya beans, 0.084; green lentils, 0.054; and beef liver, 0.043. The cobalt content 

of 20 brands of alcoholic and nonalcoholic beer widely consumed in Spain ranged from 0.16 to 0.56 μg/L 

with a median of 0.39 μg/L (Cameán et al. 1998). Cobalt, which was at one time added to beer to 

increase the foam head, has been associated with cardiomyopathies (heart disease) in heavy beer drinkers. 

A study of radionuclide levels in various foods and drinks in Hong Kong found that the 60Co content in 

nearly all foods and drinks used in the study were below the minimal detection limit (Yu and Mao 1999). 

Analysis of wild plants in Bulgaria in villages near the “Kozloduy” nuclear power plant showed that the 

concentrations of 60Co were below the detection limit. Mean activity concentrations of 60Co in edible 

plants in this region were mostly <0.04 Bg/kg (<1 pCi/kg) (Djingova and Kuleff 2002). 

Stable cobalt is present in various consumer products including cleaners, detergents, and soaps, which 

have resulted in dermatitis in sensitive individuals (Kokelj et al. 1994; Vilaplana et al. 1987). Tobacco 

contains about <0.3–2.3 μg Co/g dry weight and approximately 0.5% of the cobalt appears in mainstream 

smoke (Barceloux 1999; Munita and Mazzilli 1986; Ostapczuk et al. 1987; Stebbens et al. 1992). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

COBALT 244 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-5. Cobalt Levels in Food 

Food item Level Unitsa Type Reference 

Infant formulas/milk 

Evaporated milk (n=21) 0.74, 0.52–2.6 μg/kgb Median, range Dabeka 1989 

Ready-to-use formula (n=49) 0.53, 0.21–5.2 μg/kgb Median, range Dabeka 1989 

Milk-based (n=33) 0.40, 0.21–0.99 

No added iron (n=6) 0.36, 0.21–0.61 

Added iron (n=27) 0.87, 0.41–0.99 

Soy-based (n=16) 2.27, 1.71–5.2 

Concentrated liquid formula (n=50) 2.27,0.25–11.8 μg/kgb Median, range Dabeka 1989 

Milk-based (n=34) 1.57, 0.25–3.11 

No added iron (n=20) 1.06, 0.25–1.77 

Added iron (n=14) 2.59, 2.03–3.11 

Soy-based (n=16) 4.33, 2.7–11.8 

Powdered formula (n=64) 9.54, 2.6–53 μg/kgb Median, range Dabeka 1989 

Milk-based (n=36) 4.96, 2.6–10.6 

No added iron (n=23) 4.24, 2.6–9.6 

Added iron (n=13) 8.26, 5.1–10.6 

Soy-based (n=28) 20.0, 10.6–53 

Agricultural crops 

Cabbage, United States 0.2 mg/kgc Typical level NAS 1977 

Corn seed, United States 0.01 mg/kgc Typical level NAS 1977 

Fruits, 12 types, Poland 0.01–0.02 mg/kg Range Bulinski et al. 1986 

Lettuce, Sweden 1983–1990 (n=7) 0.002, 0.006 mg/kg Mean, Jorhem and 

maximum Sundström 1993 

Lettuce, United States 0.2 mg/kgc Typical level NAS 1977 

Onions, 11 Danish sites (n=110) 1.51, 0.119–5.1 μg/kg Median, range Bibak et al. 1998a 

Peas, 10 Danish sites (n=93) 4.6, 0.57–17 μg/kg Median, range Bibak et al. 1998b 

Potatoes, Sweden (n=8) 0.008, 0.017 mg/kg Mean, Jorhem and 

maximum Sundström 1993 

Spinach, United States 0.4–0.6 mg/kgc Typical range NAS 1977 

 Strawberries, Sweden (n=10) 0.004, 0.010 mg/kg Mean, Jorhem and 

maximum Sundström 1993 

Vegetables, 30 types, Poland 0.008–0.032 mg/kg Range Bulinski et al. 1986 

White flour, United States 0.003 mg/kgc Typical level NAS 1977 

Meat, fish, beverages 

Beef, Sweden (n=3) 0.001, 0.001 mg/kg Range, Jorhem and 

maximum Sundström 1993 

Beef liver, Sweden (n=3) 0.043, 0.074 mg/kg Range, Jorhem and 

maximum Sundström 1993 

Beef kidney, Sweden (n=3) 0.008, 0.010 mg/kg Range, Jorhem and 

maximum Sundström 1993 
 

 

 

 

 

COBALT 245 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-5. Cobalt Levels in Food 

Food item Level Unitsa Type Reference 

Beer, Spain, 20 brands 0.39, 0.16–0.56 μg/L Median, range Cameán et al. 1998 

 Cocoa, Germany 1.31 mg/kgc Ostapczuk et al. 

1987 

Coffee (whole), South Africa 0.93 mg/kgc Horwitz and Van der 

Linden 1974 

Coffee (whole), Germany (61% 0.11–0.31 mg/kgc Range Ostapczuk et al. 

water extractable) 1987 

Fish, Sweden, 10 varieties (n=40) <0.001–.008, mg/kg Range of mean, Jorhem and 

0.020 maximum Sundström 1993 

Pork, Sweden (n=36) 0.001, 0.012 mg/kg Range, Jorhem and 

maximum Sundström 1993 

Pork liver, Sweden (n=36) 0.010, 0.023 mg/kg Range, Jorhem and 

maximum Sundström 1993 

Pork kidney, Sweden (n=36) 0.004, 0.011 mg/kg Range, Jorhem and 

maximum Sundström 1993 

Tea (whole), South Africa 0.2 mg/kgc Horwitz and Van der 

Linden 1974 

Tea (whole), Germany (40% water 0.18–6.7 mg/kgc Range Ostapczuk et al. 

extractable) 1987 

Food categories 

Bakery good/ cereals, Canada 10.9, 75.7 μg/kg Median, Dakeba and 

(n=24) maximum McKenzie 1995 

Beverages, Canada (n=7) 5.9, 9.1 μg/kg Median, Dakeba and 

maximum McKenzie 1995 

Fats and oils, Canada (n=3) <2.6, 37.6 μg/kg Median, Dakeba and 

maximum McKenzie 1995 

Fish, Canada (n=6) 18.6, 14.3–29.4 μg/kg Median, range Dakeba and 

McKenzie 1995 

Fruits and fruit juices, Canada <6.6, 35.7 μg/kg Median, Dakeba and 

(n=25) maximum McKenzie 1995 

Meat and poultry, Canada (n=18) <5.5, 38.2 μg/kg Median, Dakeba and 

maximum McKenzie 1995 

Milk and milk products, Canada <1.4, 18.9 μg/kg Median, Dakeba and 

(n=13) maximum McKenzie 1995 

Soups, Canada (n=4) 5.6, 8.5 μg/kg Median, Dakeba and 

maximum McKenzie 1995 

Sugar and candy, Canada (n=7) <0.4, 3.5 μg/kg Median, Dakeba and 

maximum McKenzie 1995 

Vegetables, Canada (n=38) 2.4, 18.1 μg/kg Median, Dakeba and 

maximum McKenzie 1995 

a

Produce on a fresh weight basis, unless otherwise specified b

As sold 

c

Dry weight basis 
 

 

COBALT 246 

6. POTENTIAL FOR HUMAN EXPOSURE 

The cobalt content of sewage sludge, incinerator ash, fertilizers, soil amendments, and other substances 

appears in Table 6-6. The concentration of cobalt in U.S. coal averages about 5 mg/kg, levels in crude oil 

and fuel oil are 0.001–10 and 0.03–0.3 mg/kg, respectively, and those in gasoline are <0.1 mg/kg (Smith 

and Carson 1981). Cobalt levels were below the detection limit of 0.05 ppm dry weight in all but 1 of 

26 samples of composted yard waste, sewage sludge, and municipal solid waste samples nationwide in 

1991. The one positive sample of composted yard waste contained 1.53 ppm of cobalt (Lisk et al. 1992). 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE 

Exposure of the general population to cobalt occurs through inhalation of ambient air and ingestion of 

food and drinking water. In general, intake from food is much greater than from drinking water, which in 

turn, is much greater than from air. From the limited monitoring data available, the average concentration 

of cobalt in ambient air in the United States is approximately 0.4 ng/m3

. However, levels may be orders 

of magnitude higher in source areas. Therefore, intake to cobalt in air will vary substantially from 

nonsource areas to areas with cobalt-related industries. Similarly, the median cobalt concentration in U.S. 

drinking water is <2.0 μg/L; however, values as high as 107 μg/L have been reported in surveys of water 

supplies (Smith and Carson 1981). Therefore, exposure from drinking water may vary considerably from 

one location to another. In Canada, the daily cobalt intake of the average adult from drinking water is 

≤2.6 μg; this could increase to 10 μg for those living in areas with the highest cobalt levels (Meranger et 

al. 1981). 

General population exposure to cobalt from food is highly variable and normally higher than intake from 

drinking water. Most of the cobalt ingested is inorganic; vitamin B12, which occurs almost entirely in 

food of animal origin, constitutes only a very small fraction of cobalt intake. The cobalt intake in food 

has been estimated to be 5.0–40.0 μg/day (Jenkins 1980). The daily cobalt intake, including food, water, 

and beverages of two men that were followed for 50 weeks was much higher, 310 and 470 μg (Smith and 

Carson 1981). The estimated average daily cobalt intake from diet in Canada was 11 μg/day; the intake 

varied from 4 to 15 μg/day between the various age/sex groups (Table 6-7) (Barceloux 1999; Dabeka and 

McKenzie 1995). The contributions of various food groups to cobalt intake in this study were (category, 

contribution of dietary intake): bakery goods and cereals, 29.8%; vegetables, 21.9%; beverages, 9.8%; 

milk and milk products, 9.4%; meat and poultry, 9.1%; soups, 6.4%; fruit and fruit juices, 5.0%; sugar 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

COBALT 247 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-6. Cobalt Content of Miscellaneous Substances 

Substance/source Level Units Type Reference 

Bituminous coal used for power 6.4 mg/kg Median Rubin 1999 

generation 

Coal, United States ~5 mg/kg Mean Smith and Carson 1981 

Fly ash ~25 mg/kg Mean Smith and Carson 1981 

MSW Incinerator ash, Mississippi Buchholz and Landsberger 

1995 

Fly ash (n=30) 11.3–13.5 μg/g Range 

Bottom ash (n=30) 65.2–90.3 

Combined ash (n=30) 24.8–30.5 

MSW Incinerator ash, United States, 1987 Mumma et al. 1990 

Fly ash (n=5) 18.2–54.0 μg/g Range 

Bottom ash (n=7) 13.5–35.1 

Combined ash (n=8) 11.2–43.4 

Compost, Toronto Evans and Tan 1998 

Residential compost 8.1, 3.2–12 mg/kg Median, range 

Greenhouse finished compost 6.1±1.03 Mean ± SD 

Sewage sludge 

16 large U.S. cities 11.3, 6.08– mg/kg Median, range Gutenmann et al 1994 

29.1 

32 U.S. cities 7.2, 2.4– mg/kg Median, range Mumma et al. 1984 

30.1 

Cow manure (comparison) 

Miscellaneous soil amendmentsa 

6.1 mg/kg Mumma et al. 1984 

Raven and Loeppert 1997

 Compost 3.55, 3.57 mg/kg Individual 

means 

Diammonium phosphate 3.24, 0.68 

Dolomite 0.33 

 Manure 2.23 

Monoammonium phosphate 0.78, 3.38 

Rock phosphate, Tilemsi 19.6 

Rock phosphate, North Carolina <0.08 

Sewage sludge, Austinite 4.10 

Sewage sludge, Milorganite 4.07 

 Triple superphosphate 6.61, 2.24 

Street dust, New York City 8.7–12.9 μg/g Range Fergusson and Ryan 1984 

a

The rest of the 24 fertilizers and soil amendments tested were below the detection limit (typically <0.07 ppm) 

MSW = municipal solid waste; SD = standard deviation 
COBALT 248 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-7. Mean Daily Dietary Intake of Cobalt for Selected Population Groups in 

Canada 

Group Mean daily intake (μg/day) 

1–4 years 7 

5–11 years 10 

12–19 years; male 14 

12–19 years; female 10 

20–39 years; male 15 

20–39 years; female 9 

40–65 years; male 12 

40–65 years; female 9 

65+; male 10 

65+; male 8 

Source: Dabeka and McKenzie 1995 
 

 

 

COBALT 249 

6. POTENTIAL FOR HUMAN EXPOSURE 

and candies, 2.8%; fish, 2.7%; fats and oils, 2.2%; and miscellaneous, 1.1%. The average daily intake of 

cobalt in France was estimated to be 29 μg/day (Biego et al. 1998). In this study, foods were divided into 

nine categories. The foods accounting for the greatest contributions of cobalt intake were milk and dairy 

products, fish-crustaceans, and condiments-sugar oil, respectively contributing 32, 20, and 16% to the 

daily intake. The U.S. Department of Agriculture (USDA) conducted a special exploratory study in 

1985–1986 to determine the concentration of trace metals in tissue of health livestock and poultry 

randomly selected from those slaughtered. Between 0.6 and 5.9% of samples in the 11 production classes 

had levels of cobalt that exceeded the lowest reliable quantitation level of 0.15 ppm (0.15 mg/kg) and the 

mean of positive samples ranged from 0.20 to 0.23 ppm in all classes but heifer/steer, which had a level of 

1.92 ppm (Coleman et al. 1992). Cobalt, which has been added to beer to increase the foam head, has 

been associated with cardiomyopathies (heart disease) in heavy beer drinkers. However, according to a 

recent Spanish study, the low levels of cobalt presently found in beer do not make a significant 

contribution to the total cobalt intake in heavy beer drinkers (Cameán et al. 1998). Smokers may be 

exposed to cobalt in mainstream smoke, but the level of exposure has not been assessed (Barceloux 

1999). 

Since cobalt and other heavy metals have been used on hand-painted china, a study was conducted to see 

whether these metals are released into food under acidic conditions. Forty-six samples of porcelain 

dinnerware from Europe or Asia that were manufactured before the mid-1970s and had hand-painted 

designs over the glaze were filled with 4% acetic acid to within 7 mm of the rim and analyzed after 

24 hours (Sheets 1998). Of these, 36 samples released <0.02 μg/mL of cobalt and 10 released 0.020– 

2.9 μg/mL. The Food and Drug Administration (FDA) has not established dinnerware extraction limits 

for cobalt. 

Data are lacking on the levels of cobalt in tissues and fluids of the general populations in the United 

States; values from various countries are given in Table 6-8. This table shows that cobalt concentrations 

are greatest in nail, hair, and bone. The differences in cobalt levels in similar human tissues (e.g., hair, 

nail) in different countries may be due to differences in dietary and living habits and levels of cobalt in 

food (Takagi et al. 1988). The total amount of cobalt in the body of an adult as vitamin B12 is about 

0.25 mg, of which 50–90% in contained in the liver (IARC 1991). 

A recent study in the United States determined the concentrations of trace metals in seminal plasma in 

industrial workers in a petroleum refinery, smelter, and chemical plant as compared with those of hospital 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-8. Cobalt Levels in Human Tissues and Fluids 

Tissue or fluid Level Unitsa Type Reference 

Urine, U.S., NHANES, representative 

population (n=1007) 

0.36, 0.11–0.89 μg/L Geomean, 10th– 

90th percentile 

CDC 2001 

Urine, U.S., NHANES 1999–2000, 

Total, age 6 and older (n=2,465) 

0.372, 0.130–1.32 μg/L Geomean, 10th– 

95th percentile 

CDC 2003 

6–11 years (n=340) 0.498, 0.130–1.32 

12–19 years (n=719) 0.517, 0.200–1.52 

20 years and older (n=1,406) 0.339, 0.120–1.28 

 Males (n=1,227) 0.369, 0.150–1.01 

Females (n=1,238) 0.375, 0.120–1.49 

Mexican Americans (n=884) 0.415, 0.130–1.47 

Non-Hispanic blacks (n=568) 0.433, 0.160–1.45 

Non-Hispanic whites (n=822) 0.365, 0.120–1.29 

Urine, The Netherlands <0.2–1.2 μg/L Range Bouman et al. 

1986 

Urine, Sweden 0.5, 0.1–2.2 μg/L Mean, range Alexandersson 

1988 

Urine, Denmark (3 reference groups) Poulsen et al. 1994 

Unexposed control females (n=46) 1.5, LOD–20.5 nmolb

 Mean, range 

Unexposed males (n=12) 0.9, LOD–2.31 

Unexposed females (n=11) 5.9, LOD–25.02 

Urine, hip arthroplasty patients, 0.9–1.05 μg/L Range IARC 1991 

observed 7–15 years (n=17) 

Urine, hip arthroplasty patients, 3.8 μg/L Mean IARC 1991 

observed 5–15.5 years (n=10) 

Urine, 48 metal sharpening workers in 0–40.3, 86 μg/L Range of means, Imbrogno et al. 

12 Italian factories maximum 1994 

Urine, 12 female cobalt powder Ferdenzi et al. 

sintering workers, Italy 1994 

Monday, before shift 25, 1–51 μg/L Mean, range 

Friday, before shift 29, 3–159 

Friday, end-of shift 85, 6–505 

After 3-week holiday 11, 4–34 

Urine, Italian workers wet grinding of Sesana et al. 1994 

hard metal tools (end of shift) 

Factory A no local exhausts (n=3) 138.3 (108), 123.7 μg/L Mean (SD) 

(74) Monday, Friday 

Factory B local exhausts (n=5) 15.3 (7.7), 24.4 

(14.1) 

Factory C local exhausts (n=3) 48.2 (7.3), 74.7 

(13) 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

COBALT 251 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-8. Cobalt Levels in Human Tissues and Fluids 

Tissue or fluid Level Unitsa Type Reference 

Urine, Northern Italy, 1991, Mosconi et al. 

occupational exposure survey, 1994 

314 exposed people 

Diamond abrasive production 

 Mould-filling 320, 587, 39– μg/L Median, mean, 

2,100 range 

Sintering 168, 193, 02–390 

 Grinding 61, 151, 34–520 

 Mechanical-working 50, 67, 143–165 

Grinding 15, 32, 0.8–730 

Tool production 12, 19, 0.8–100 

Hard metal alloy filling 5, 5, 0.8–18 

Other 1, 2.9, 0.8–72
 

Blood, Denmark, porcelain factory Raffn et al. 1988 

Plate painters, off work for 6 weeks 8.05, 1.70–22.1 nmol/L Mean, range
 

(n=46)
 

Plate painters, working 4 weeks 36.7, 3.40–407
 

(n=46) 

Top glaze painters (unexposed) 4.04, <1.70–10.2 

(n=51) 

Urine, Denmark, porcelain factory Raffn et al. 1988 

Plate painters, off work for 6 weeks 81.8, <1.70–445 nmol/L Mean, range
 

(n=46)
 

Plate painters, working 4 weeks 1,308, 37.4–
 

(n=46) 14,397 

Top glaze painters (unexposed) 16.0, <1.70–234 

(n=51) 

Plasma, Sweden 0.1–1.2 μg/L Range Alexandersson 

1988 

Whole Blood, Denmark (3 Reference Poulsen et al. 1994 

groups) 

Unexposed control females (n=46) 4.1, <1.7–10.2 nmol/L Mean, range 

Unexposed males (n=12) 3.1, <1.7–6.8 

Unexposed females (n=11) 7.6, <1.7–30.5 

Lung, Sweden Gerhardsson et al. 

1988 

Rural 0.007 mg/kg Mean 

 Urban 0.011 

Liver Tissue, United Kingdom, 17.4±11.3 (15.9) ng/g mean±SD Patriarca et al. 

newborns and infants that died from wet (median) 1999 

SIDS (n=157) mass 

Liver, New Zealand (n=96) 0.120 mg/kg Mean IARC 1991 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-8. Cobalt Levels in Human Tissues and Fluids 

Tissue or fluid Level Unitsa Type Reference 

Tissue, Japan Yamagata et al. 

1962 

 Pectoral muscle 0.016 mg/kg Mean 

 Rib bone 0.036 

Stomach 0.021 

Liver 0.017 

Brain 0.0055 

 Urinary bladder 0.0055 

Kidney 0.012 

Aorta 0.021 

Nails Takagi et al. 1988 

 Canada (n=40) 0.09 mg/kg Mean 

 India (n=100) 0.06 

 Japan (n=252) 0.17 

 Poland (n=49) 0.04 

U.S. (n=71) 0.06 

Adipose tissue 0.035–0.078 mg/kg Range EPA 1986 

Hair Takagi et al. 1986 

 Canada (n=92) 0.043 mg/kg Mean 

 India (n=255) 0.051 

 Japan (n=457) 0.18 

Poland (n=46) 0.022 

United States (n=55) 0.047 

Hair, Italy Vienna et al. 1995 

Male biology students (n=20) 0.007, 0.001–0.07 mg/kg Geomean, range 

Female biology students (n=20) 0.017, 0.001–0.28 

Hair, Pakistan	 Ashraf et al. 1995 

Rural (n=28) 2.05, 0.10–4.80 mg/kg Mean, range 

Urban (n=39) 3.86, 1.10–5.90 

a

fresh weight, unless otherwise specified 

b

creatinine basis 

geomean = geometric mean; LOD = limit of detection; NHANES = Nation Health and Nutrition Examination Survey; 

SD = standard deviation; SIDS = sudden infant death syndrome 
 

 

COBALT 253 

6. POTENTIAL FOR HUMAN EXPOSURE 

workers (control group). There were four groups each with 50 adult men. The mean cobalt 

concentrations (μg/dL), including standard errors, were determined to be 31±2 (hospital workers), 

25±0.8 (metal ore smelter workers), 19±0.6 (petroleum refinery workers), and 22±1 (chemical workers) 

(Dawson et al. 2000). 

Surgical implants for knee and hip replacements often use cobalt-containing alloys, which may lead to 

elevated cobalt levels in body fluids. Indeed, cobalt levels in serum and urine have been used as an index 

of prosthesis wear. In some cases, significant increases in cobalt levels have been observed, while in 

other cases, elevations were much lower or only sporadic (IARC 1991). These differences have been 

ascribed to greater release rates from metal to metal than metal to polyethylene articular surfaces as well 

to differences in the cobalt-containing alloys. 

There are several reports of cobalt exposure among occupational groups. The concentrations of cobalt in 

the air of hard metal manufacturing, welding, and grinding factories may range from 1 to 300 μg/m3

, 

compared to normal atmospheric levels of 0.4–2.0 ng/m3

 (Burr and Sinks 1989; Haddad and Zikovsky 

1985; Koponen et al. 1982; Lichtenstein et al. 1975). The maximum OSHA permissible level is 

100 μg/m3

. The concentration of cobalt in the dust of an electric welding factory was 4.2 μg/g compared 

to its normal dust level of 0.1–1.0 μg/g (Baumgardt et al. 1986). The higher rate of exposure to cobalt for 

occupational groups is also reflected in the higher cobalt content in tissues and body fluids of living and 

deceased workers in this group. The levels of cobalt in the urine of workers in the hard metal industry 

varied with the levels of cobalt concentration in the working atmosphere. At a concentration of 

0.09 mg/m3

, the urinary excretion of cobalt exceeded normal values by orders of magnitude. When the 

cobalt concentration in the working atmosphere was 0.01 mg/m3

 or lower, urinary cobalt excretion was 

4–10 times higher than normal level (Alexandersson 1988; Scansetti et al. 1985). At high exposure 

levels, the cobalt concentration in blood was 20 times higher than normal; in the low exposure group, it 

was only slightly higher than in the control group (Alexandersson 1988). 

An extensive survey of workers potentially exposed to cobalt in the Bergamo Province in northern Italy in 

1991 identified 403 exposed workers in different production areas (Mosconi et al. 1994a). Significant 

cobalt exposure occurred especially for operators working in diamond abrasive production, and in 

particular, in mold filling and sintering units where environmental limits are regularly exceeded. 

Exposure in tool production, tool sharpening, and hard metal alloy filling is much more restrained. 
 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

Occupational cobalt air levels and urinary excretion levels recorded in the survey appear in Tables 6-2 

and 6-8. 

Several studies of cobalt concentrations in air in the hard metal industry have been reported. In the hard 

metal industry in Japan, Kumagai et al. (1996) found that mean 8-hour time weighted averages (TWAs) 

of airborne cobalt were >50 μg/m3

 for workers involved in powder preparation (rotation), powder 

preparation (full-time), rubber press, and shaping operations; mean atmospheric concentrations were 459, 

147, 339, and 97 μg/m3

, respectively. Workers involved in the manufacture and maintenance of hard 

metal and stellite blades in Finland were exposed to breathing zone cobalt concentrations ranging from 

2 to 240 μg/m3

, with a geometric mean of 17 μg/m3 (Linnainmaa et al. 1996). The average proportion of 

water soluble cobalt in airborne cobalt was 68% (range 14–100%). Wet grinding was not sufficient to 

adequately control cobalt levels and coolant cobalt levels were high. In a group of 12 factories in Italy in 

which 48 workers were tested who had been exposed to cobalt in operations such as sharpening with 

diamond grinding stones, the mean concentration of cobalt in air was 21.2 and 137.7 μg/m3

 (Permissible 

exposure limit [PEL]-TWA 100 μg/m3

) in work places with and without dust ventilation, respectively 

(Imbrogno et al. 1994). 

Urine concentrations have been used to monitor workers' exposure to airborne cobalt. Ferdenzi et al. 

(1994) obtained a correlation between Friday TWA air cobalt levels and Friday end-of-shift urine levels 

among women in the powder sintering industry. Median urinary cobalt concentrations were 25 (range: 1– 

51) and 29 (3–159) μg/L, on Monday and Friday before the shift, respectively, and 85 (6–505) μg/L on 

Friday after the shift. Imbrogno and Alborghetti (1994) evaluated the levels of occupational exposure to 

cobalt during dry and/or wet hard metal sharpening. The mean urine cobalt level in the workers in 

12 factories was found to range from 0 to 40.3 μg/L and the maximum was 86 μg/L. The average urinary 

cobalt level among workers using wet/mixed sharpening methods was 4 times higher than those using dry 

sharpening methods; 21.38 μg/L as compared to 5 μg/L, respectively. Gallorini et al. (1994) found that 

the ratio of inorganic to organic cobalt in the urine of hard metal workers was 2.3 compared to 1.01 in 

controls; the ratio was constant over the range of urinary cobalt levels analyzed (180–1,254 μg/L). 

Exposure to cobalt during the wet grinding of hard metal tools (Widia tools) used in the wood industry 

produced exposure to cobalt above the PEL-TWA of 100 μg/m3

 (Sesana et al. 1994). However, exhausts 

near the grinding wheels were shown to substantially reduce exposure levels (see Table 6-8). In the 

processing department of a small company producing carbide tip saw blades for the woodworking 

industry, area air sampling showed that exposure levels were low in all departments except tip grinding 
COBALT 255 

6. POTENTIAL FOR HUMAN EXPOSURE 

where wet and dry tip grinding areas contained 55 and 21 μg/m3 of cobalt, respectively, for the total 

collection method (Stebbins et al. 1992). For the method collecting respirable particles, cobalt levels 

ranged from 2 to 28 μg/m3

. Wet grinding is a traditional method for controlling dust during grinding. 

However, some coolants may contain significant concentrations of cobalt (in this case, 61–538 mg/mL) 

that can contribute to exposure during grinding (Stebbins et al. 1992). Among cobalt blue dye plate 

painters in a porcelain factory in Denmark, the blood and urine cobalt levels were, respectively, 2–4 and 

5–15 times higher than in control groups (Raffn et al. 1988). Similarly, lungs taken from deceased, 

occupationally exposed workers also had higher levels of cobalt than lungs from control groups. Lungs 

of deceased hard metal industry workers in Sweden contained 2.5–4 times higher levels of cobalt than 

control lungs (Gerhardsson et al. 1988). Similarly, the lungs of coal miners from England contained 

6 times higher cobalt levels than control lungs (Hewitt 1988). 

Exposure to radioactive cobalt can occur through various means. Workers at nuclear facilities, irradiation 

facilities, or nuclear waste storage sites may be accidentally exposed to radioisotopes of cobalt. Also, 

workers using cobalt isotopes in tracer studies, in calibration or other devices, or 57Co in Mössbauer 

spectroscopy, may be exposed to radioactive cobalt. Exposure would generally be to radiation produced 

by these isotopes (e.g., gamma radiation from 60Co). Patients receiving 60Co radiotherapy will obviously 

be exposed to its radiation. According to the USNRC (1999), the collective intake of 60Co by ingestion 

and inhalation at power reactors in 1998 was 352 μCi (13 MBq) for 25 intake records and 27,000 μCi 

(1,000 MBq) for 281 intake records (USNRC 1999). The collective intake at fuel fabrication facilities 

was 0.486 μCi (0.180 MBq) for 502 intake records. The USNRC occupational inhalation annual limits of 

intake (ALIs) for 60Co are 200 μCi (7.4 MBq) for all compounds, except oxides, hydroxides, halides, and 

nitrates, and 30 μCi (1.1 MBq) for compounds of oxides, hydroxides, halides, and nitrates (USNRC 

2001k). 

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 3.8 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 
COBALT 256 

6. POTENTIAL FOR HUMAN EXPOSURE 

larger skin surface in proportion to their body volume. A child’s diet often differs from that of adults. 

The developing human’s source of nutrition changes with age: from placental nourishment to breast milk 

or formula to the diet of older children who eat more of certain types of foods than adults. A child’s 

behavior and lifestyle also influence exposure. Children crawl on the floor, put things in their mouths, 

sometimes eat inappropriate things (such as dirt or paint chips), and spend more time outdoors. Children 

also are closer to the ground, and they do not use the judgment of adults to avoid hazards (NRC 1993). 

As with adults, most children are exposed to cobalt largely through their diet. Dabeka and McKenzie 

(1995) estimated that the dietary cobalt intake by Canadian children ages 1–19 ranged from 7 to 

14 mg/day (see Table 6-7). Milk constitutes a larger part of children’s diets than that of adults, and 

infants may consume infant formula. Cobalt concentrations ranging from 0.3 to 0.8 ng/g in cow’s milk 

were reported by Iyengar (1982). The levels of cobalt in human milk from Nigeria, Zaire, Guatemala, 

Hungary, Philippines, and Sweden ranged from 150 (Hungary) to 1,400 ng/g (Philippines), median 

320 ng/g (Nriagru 1992). Garg et al. (1993) reported much lower cobalt levels in three samples of human 

milk in India, 2.42 ng/g, and reported a cobalt concentration of 5.07 ng/g in cow’s milk in India. Dakeba 

(1989) determined cobalt levels in various infant formulas (see Table 6-5). Milk-based infant formulas 

and evaporated milk contained <1 ng/g of cobalt on a “ready-to-use” basis. Milk-based formulas with 

added iron contained about twice the cobalt as those with no added iron and soy-based formulas contained 

about 5 times more cobalt. The influence of added iron suggests that the cobalt in formula is not 

primarily from vitamin B12. Using literature values of cobalt in food, Dakeba also estimated that infants 

0–12 months old ingest an average of 0.52 μg Co/kg-day (3.93 μg/day) from food and water and that for 

an infant, 0–12 months old, the total dietary cobalt intake would range from 0.42 μg/kg-day (3.39 μg/day) 

for a breast or milk-based formula fed infant to 1.0 μg/kg-day (7.33 μg/day) for an infant fed soy-based 

formula powder. The recommended dietary allowance for Canadian infants is 0.012 μg/day cobalt as 

vitamin B12. In a 1967 study of the total dietary intake of some trace elements, excluding drinking water, 

of institutionalized children aged 9–12 in 28 U.S. cities, cobalt intake ranged from 0.297 to 1.767 mg/day 

with a mean value of 1.024 mg/day (Murthy et al. 1971). 

Exposure to stable cobalt in communities near mining and smelting facilities or metal shops where cobalt 

is used in grinding tools is a public health concern, especially for infants and children. Since cobalt 

remains in the surface soil indefinitely and long past land uses may be forgotten, people may not realize 

that they are living in areas where high levels of cobalt may occur in soil. Contaminated soils pose a 

particular hazard to children because of both hand-to-mouth behavior and intentional ingestion of soil that 
COBALT 257 

6. POTENTIAL FOR HUMAN EXPOSURE 

contain metals and other contaminants (Hamel et al. 1998). In these communities, cobalt may have been 

tracked in from outdoors and contaminate carpeting. Cobalt-containing dust may be brought home in the 

clothing of parents working in industries where they are exposed to cobalt. Children may be exposed to 

this cobalt while crawling around or playing on contaminated carpeting. Exposure may also result from 

dermal contact with soil, or by inhaling dust and then swallowing it after mucociliary transport up out of 

the lungs. Because there is little absorption of cobalt through the skin following dermal exposure, and 

because much of the cobalt in soil is embedded in or adsorbed to soil particles or insoluble, it may not be 

in a form accessible for uptake by the body, and therefore may not pose a serious health hazard. 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 

In addition to workers in the hard metal industry (tool production, grinding, etc.) and industries such as 

coal mining, metal mining, smelting and refining, cobalt dye painters, and the cobalt chemical production, 

the general population living near these industrial sites may be exposed to high levels of cobalt in air and 

in soil. Exposure to cobalt during the wet grinding of hard metal tools is especially high when local 

exhausts are not in use (Sesana et al. 1994). People living near hazardous waste sites may be exposed to 

cobalt by inhaling dust from contaminated sites or through dermal contact with cobalt-contaminated soil. 

In the case of children playing in and around unrestricted landfill sites, exposure via dermal and ingestion 

routes is possible. The general populations in agricultural areas that use sewage sludge or cobaltcontaining fertilizers or other soil amendments may be exposed to higher levels of cobalt via inhalation of 

dust or dermal contact with the soil. However, no experimental evidence of higher than normal exposures 

for these population groups was found in the literature. People who live in areas that naturally contain 

higher levels of cobalt minerals may also be exposed to higher levels of cobalt from both the inhalation 

and dermal contact routes. 

The higher exposure of cobalt in patients with cobalt-chromium knee implants has been demonstrated by 

the slightly higher levels of cobalt in whole blood, serum, and urine, and by very high levels of cobalt in 

bone of these patients (IARC 1991; Ostapczuk et al. 1985; Sunderman et al. 1989). Prosthetic devices 

that contain polyethylene components to avoid metal-to-metal contact do not appear to cause elevated 

levels of cobalt in tissues and body fluids (IARC 1991; Ostapczuk et al. 1985; Sunderman et al. 1989). 

People who use cobalt supplements as a treatment for anemia and those who take large amounts of 

vitamin B-12 as a dietary supplement would have higher intakes of cobalt than the general population. 
 

 

 

COBALT 258 

6. POTENTIAL FOR HUMAN EXPOSURE 

Workers at nuclear facilities and nuclear waste storage sites may be exposed to potentially high levels of 

radiation exposure from 60Co and 58Co. Workers at irradiation facilities using 60Co may be exposed to 

potentially high levels of gamma radiation exposure from this isotope. Patients receiving 60Co 

radiotherapy will intentionally be exposed to high levels of gamma radiation. 

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 cobalt 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 cobalt. 

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, Chemical and Radiological Properties. As can be seen from Table 4-2 and 

Section 4.2, the relevant physical and chemical properties of cobalt and its compounds are sufficiently 

known to enable prediction of environmental fate and transport of cobalt compounds (Budavari 1996; 

Lide 1994; Stokinger 1981; Weast 1985). Information on the radiological properties of important cobalt 

isotopes are also well known (see Table 4-3) (ICRP 1983; Lide 1994). No data needs were identified. 

Production, Import/Export, Use, Release, and Disposal. Information on the production, 

import/export, use, release, and disposal of a chemical is important because it is an indicator of possible 

environmental contamination and human exposure. Large releases and consumer use would indicate 
 

 

COBALT 259 

6. POTENTIAL FOR HUMAN EXPOSURE 

higher general population exposure from environmental sources (e.g., air, drinking water, and food) and 

use of consumer products. Occupational exposure may also increase with increased production and use. 

U.S. production of cobalt is derived primarily from scrap (secondary production). Information is 

available on cobalt consumption derived from secondary production, import/export, and release of cobalt 

from the National Defense Stockpile (USGS 1998, 1999, 2002). However, production volumes of 

individual cobalt compounds are not available and information on the production of individual 

compounds would be useful in assessing exposure to specific cobalt compounds. Radioactive cobalt 

isotopes, primarily 60Co and 57Co, are not commercially produced in the United States, but rather are 

imported from Canada and the United Kingdom; consumption amounts are not available. Information on 

the uses of cobalt is available (Cobalt Development Institute 2004; Donaldson 1986; Hodge 1993; IARC 

1991; Richardson 1993; USGS 1998, 2002). Cobalt-containing products are mostly used in the 

workplace, although some consumer products contain cobalt. 

According to the Emergency Planning and Community Right-to-Know Act of 1986, 42 U.S.C. 

Section 11023, industries are required to submit chemical release and offsite transfer information to the 

EPA. The TRI for 2001 is currently available (TRI01 2004). Starting in 1998, metal mining, coal 

mining, electric utilities, and RCRA/solvent recovery industries were required to report to the TRI. These 

sectors include those contributing greatest environmental releases of cobalt and cobalt compounds, giving 

us a much more complete picture of cobalt releases to the environment. The TRI also contains 

information on the onsite and offsite disposal and management of wastes (e.g., recycling, treatment, 

transfer to publicly owned treatment works [POTWs]). EPA guidelines address the disposal of hazardous 

cobalt wastes. The TRI database will be updated yearly and provides a list of industrial production 

facilities and emissions. The TRI data should be used with caution since the 1987 data represent firsttime reporting by these facilities. Only certain types of facilities were required to report. This is not an 

exhaustive list. 

Environmental Fate. There are data that permit assessment of the environmental fate and transport of 

cobalt in water and soil (Section 6.3). Frequently, sediment and soil are the ultimate sinks for cobalt; 

however, this process is dynamic, and cobalt can be released into the water depending upon conditions. 

There is a paucity of data in the literature regarding the chemical forms of cobalt released to the 

atmosphere and their transformations in air and this information would facilitate the determination of the 

transport and persistence of cobalt in the atmosphere. Additional data elucidating the mode of speciation 
COBALT 260 

6. POTENTIAL FOR HUMAN EXPOSURE 

of cobalt in water and soil would also be desirable. For example, under what circumstances Co(III) 

compounds might be formed in the environment and how long. 

Bioavailability from Environmental Media. Absorption by the inhalation and oral routes in 

humans has been studied, but the results vary considerably (see Section 3.5.1) (Foster et al. 1989; Harp 

and Scoular 1952; Sedlet et al. 1958; Sorbie et al. 1971; Valberg et al. 1969). These variations were 

attributed to differences in the types and doses of cobalt compounds given, to the nutritional status of the 

subjects following oral exposure, and to particle size differences following inhalation exposure. 

Additional data assessing the absorption of cobalt following soil ingestion by children may be helpful. 

Data in animals are plentiful for both inhalation and oral routes and correlate well with the human data 

(Andre et al. 1989; Bailey et al. 1989; Collier et al. 1989; Kreyling et al. 1986; Patrick et al. 1989; Talbot 

and Morgan 1989). Data in animals following dermal exposure suggested that cobalt is not absorbed well 

through intact skin, but is rapidly taken up through damaged skin. Data regarding the bioavailability of 

cobalt following dermal exposure are important because dermal exposure to cobalt in the workplace is 

probable. 

Food Chain Bioaccumulation. Bioaccumulation in the food chain is important in assessing the 

human exposure to cobalt from the consumption of food. Data are available that indicate that cobalt is 

not taken up appreciably by plants and does not biomagnify up the food chain (Baudin and Fritsch 1987; 

Baudin et al. 1990; Boikat et al. 1985; Francis et al. 1985; Kloke et al. 1984; Lux et al. 1995; Mascanzoni 

1989; Mejstrik and Svacha 1988; Mermut et al. 1996; Palko and Yli-Hala 1988; Smith and Carson 1981; 

Tolle et al. 1983; Watabe et al. 1984). 

Exposure Levels in Environmental Media. Monitoring data on levels of cobalt in air, water, and 

food permits the estimation of exposure from these sources. Data are available on the cobalt levels in 

ambient air (Golomb et al. 1997; Hasanen et al. 1990; Schroeder et al. 1987; Smith and Carson 1981; 

Sweet et al. 1993; Wiersema et al. 1984). However, the data are not sufficiently recent or broad-based for 

estimating the current levels of exposure to cobalt in the general U.S. population and particularly those 

living near cobalt-containing hazardous waste sites. In addition, in only isolated studies was there an 

assessment of the concentration of cobalt associated with coarse and fine particles (Sweet et al. 1993) or 

an average annual level obtained at a site (Golomb et al. 1997). Similarly, levels of cobalt in ambient 

water, while generally low, are also not sufficiently broad-based or recent to be satisfactory (Bargagli 

2000; Bruce and McMahon 1996; Cassidy et al. 1982; Eckel and Jacob 1988; Flaten 1991; Nojiri et al. 
 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

1985; Rossmann and Barres 1988; Smith and Carson 1981). This deficiency may be satisfied when the 

EPA’s improved and updated STORET database becomes available. Cobalt levels in Canadian drinking 

water are ≤2.0 mg/L (Meranger et al. 1981). However, U.S. drinking water levels have not been reported 

and would be useful. The levels of cobalt in sediment are available (Bargagli 2000; Coakley et al. 1993; 

Gibbs 1994; Glooschenko et al. 1981; Knutson et al. 1987; Naidu et al. 1997; Shine et al. 1995; Smith and 

Carson 1981; Trocine and Trefry 1996; Villanueva and Botello 1998), but more data on levels in soil and 

in the vicinity of industrial and hazardous waste sites would be useful. Few data on the levels of cobalt in 

U.S. foods are available, although studies from Canada and Sweden are available that indicate that cobalt 

levels in food items are generally low (Barceloux 1999; Dabeka and McKenzie 1995; Jorhem and 

Sundström 1993). In particular, total diet studies of cobalt in U.S. food is lacking. A Canadian total diet 

study estimated average daily cobalt intake to range from 7 to 15 μg/day for different age-sex groups 

(Dabeka and McKenzie 1995). 

Few data are available on levels of 60Co and other cobalt isotopes in environmental media. 

Exposure Levels in Humans. The levels of cobalt in hair, nail, and adipose tissues of the general 

U.S. population are known (EPA 1986; Takagi et al. 1986, 1988). No reliable data on the levels of this 

substance in blood (or plasma) and urine of the general U.S. population were found, although such data 

are available for certain European populations including occupationally-exposed groups (Table 6-8). 

These data may be important for establishing the background exposure level of cobalt. No data on the 

levels of cobalt in any body tissue or fluid for populations living near hazardous waste sites are available. 

Such data would be important in assessing the exposure levels of this group of people. 

Exposures of Children. Dabeka (1989) reported the levels of cobalt in various formulas and milk 

products consumed by children in Canada, and Dabeka and McKenzie (1995) determined the mean 

dietary intake of Canadian children as young as 1–4 years of age. Nriagru (1992) reported levels of 

cobalt in human milk from several countries. No analogous U.S. studies were found. Cobalt levels is the 

tissue and body fluids of children have not been found. 

Child health data needs relating to susceptibility are discussed in 3.13.2 Identification of Data Needs: 

Children’s Susceptibility. 
 

 

 

COBALT 262 

6. POTENTIAL FOR HUMAN EXPOSURE 

Exposure Registries. No exposure registries for cobalt were located. This compound is not 

currently one of the compounds for which a subregistry has been established in the National Exposure 

Registry. The compound 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 

the exposure to cobalt and its compounds. 

6.8.2 Ongoing Studies 

The Federal Research in Progress (FEDRIP 2002, 2004) 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 6-9. 

Remedial investigations and feasibility studies conducted at the NPL sites known to be contaminated with 

cobalt, such as the Blackbird Mine in Idaho, will add to the available database on exposure levels in 

environmental media, exposure levels in humans, and exposure registries, and will increase the current 

knowledge regarding the transport and transformation of cobalt in the environment. 

The Cobalt Development Institute (CDI) is implementing a research program to assess environmental 

risks posed by the manufacture and use of cobalt and cobalt compounds. Studies that are underway 

include the assessment of seasonal and background variability of cobalt compounds in aquatic 

environment and a literature survey for existing data on the effects of cobalt and cobalt compounds in 

soils and sediment. Environmental studies proposed for 2002 included the assessment of seasonal and 

background variability of cobalt compounds in soils and sediments and a literature survey for existing 

data on the effects of cobalt and cobalt compounds on marine environments. 
COBALT 263 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-9. Ongoing Studies on Cobalt 

Investigator Affiliation Research description Sponsor 

Hamilton, JW Dartmouth College, 

Hanover, New 

Hampshire 

The overall goal of the Dartmouth Superfund Basic 

Research Program (SBRP) Project, Toxic Metals in 

the Northeast: From Biological to Environmental 

Implications is to determine the impact of toxic metals 

found at waste sites, including Superfund sites on 

human health and the environment. The programwide focus of this research program is on toxic 

metals, particularly on arsenic, and also chromium, 

nickel, cadmium, mercury, cobalt, and lead. 

NIH 

Jones, BT Wake Forest 

University, WinstonSalem, North 

The investigators developing a novel, low-cost, 

portable instrument for the simultaneous 

determination of trace radioactive elements in nuclear 

NSF 

Carolina forensic samples. At issue is the routine, inexpensive 

sampling for radioactivity that could be released on 

transport or storage of potential "dirty bomb" material. 

The instrument to be developed is expected to 

provide analytical figures comparable to inductively 

coupled plasma mass spectrometry, but the 

instrument is much lower cost and more portable. 

The specific objectives of the project include 

determination of the analytical figures of merit for 

elements including cobalt, cesium, and strontium, and 

analysis of real samples such as soil, urban dust, 

water and agricultural materials. 

KpomblekouAdemawou, K 

Ankumah, RO 

Tuskegee University, 

Tuskegee, Alabama 

This project will investigate if excessive accumulation 

of some trace elements, added to poultry diet and 

excreted through feces, affects nitrogen 

transformation in broiler (chicken) litter amended soils 

and if this compromises safe food and feed 

production. The goals of this work are (1) to study 

the effects of concentrations of key trace elements 

(e.g., As, Cd, Co, Cr, Cu, Mn, Ni, Pb, Se, and Zn) 

found in broiler litter on nitrogen transformation in 

litter amended soils, (2) to assess the effects of 

temperature on the nitrogen transformation in the 

presence of trace elements and (3) to assess the fate 

of trace elements in sudax (Sorghum bicolor) grown 

in trace element-enriched broiler litter amended soils. 

USDA 

Longnecker, M NIEHS, NIH Evaluate the use of toenail levels as a measure of 

exposure by analyzing toenail and whole-diet 

homogenates by neutron activation analysis. 

Toenails reflect exposure over a longer period of time 

than do blood or urine measures, and are less likely 

to be influenced by contamination than hair. 

NIEHS 
 

 

COBALT 264 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-9. Ongoing Studies on Cobalt 

Investigator Affiliation Research description Sponsor 

Saito, MA Woods Hole This research will examine the influence of cobalt and NSF 

Oceanographic 

Institution, Woods 

Hole, MA 

cadmium speciation on Synechococcus and 

Crocosphaera at two sites in the Pacific Ocean. In 

addition, the distribution of cobalt across transects in 

the Eastern Equatorial Pacific will be determined to 

improve understanding of the global biogeochemical 

cycle of cobalt. 

Tavlarides, LL Syracuse University, 

Syracuse, New York 

This work will be towards the development of sol-gel 

synthesis methods for organo-ceramic adsorbants for 

the extraction of toxic and valuable metal ions, such 

NSF 

as cobalt, chromium, and arsenic ions from aqueous 

streams. 

NIEHS = National Institute of Environmental Health Sciences; NIH = National Institute of Health; NSF = National 

Science Foundation USDA = U.S. Department of Agriculture; USDOE = U.S. Department of Energy 
COBALT 265 

7. ANALYTICAL METHODS 

The purpose of this chapter is to describe the analytical methods that are available for detecting, 

measuring, and/or monitoring cobalt, its metabolites, and other biomarkers of exposure and effect to 

cobalt. 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. 

7.1 BIOLOGICAL MATERIALS 

Entry of cobalt and its radioisotopes into the human body can be gained through ingestion, inhalation, or 

penetration through skin. The quantities of cobalt within the body can be assessed through the use of 

bioassays that are comprised of either in vivo and/or in vitro measurements. In vivo measurements can be 

obtained through techniques that directly quantitate internally deposited cobalt using, for example, whole 

body counters. These in vivo measurement techniques are commonly used to measure body burdens of 

cobalt radioisotopes (i.e., 60Co), but cannot be used to assess the stable isotope of cobalt (59Co). Instead, 

in vitro measurements provide an estimate of internally deposited cobalt (both the stable and radioactive 

isotopes), utilizing techniques that measure cobalt in body fluids, feces, or other human samples. 

Examples of these analytical techniques are given in NRCP Report No. 87 (1987) and are also listed in 

Tables 7-1 and 7-2. 

7.1.1 Internal Cobalt Measurements 

In vivo measurement techniques are the most direct and widely used approach for assessing the burden of 

cobalt radioisotopes within the body. The in vivo measurement of these radioisotopes within the body is 
COBALT	 266 

7. ANALYTICAL METHODS 

Table 7-1. Analytical Methods for Determining Stable Cobalt in Biological 

Materials 

Sample Analytical Sample Percent 

matrix Preparation method method detection limit recovery Reference 

Urine Direct injection 

Addition of magnesium 

nitrate and nitric acid matrix 

modifiers and equal volume 

dilution of sample with 

water 

Sample chelated with 

dithiocarbamic acid 

derivative, solvent 

extracted 

Sample wet digested with 

acid and chelated with 2,3­

butanedion dioxide and 

complex preconcentrated 

at hanging mercury drop 

electrode 

Direct injection 

Whole Sample diluted with a 

blood homogenizer 

Sample wet digested with 

acid and chelated with 

2,3-butanedion dioxine and 

complex preconcentrated 

at hanging mercury drop 

electrode 

 Sample acid digested, 

complexed with thiocyanate 

and N-phenylcinnamohydroxamic acid and extracted into ethyl acetate 

Serum Direct injection 

GF-AAS with 

Zeeman background correction 

GF-AAS with 

Zeeman background correction 

GF-AAS with 

Zeeman background correction 

DPCSV 

GF-AAS with 

Zeeman background correction 

GF-AAS with D2 

background 

correction 

DPCSV 

Colorimetric 

GF-AA with 

Zeeman background correction 

0.3 μg/L 

2.4 μg/L 

0.1 μg/L 

0.2 μg/L 

0.1 μg/L 

2 μg/L 

0.8 μg/L 

0.15 mg/L 

0.02 μg/L 

101% at Bouman et al. 

40μg/L 1986 

107.6% at Kimberly et al. 

50 μg/L 1987 

No data Alexandersson 

1988; Ichikawa 

et al. 1985 

No data Heinrick and 

Angerer 1984 

No data Sunderman et 

al. 1989 

No data Heinrick and 

Angerer 1984 

No data Heinrich and 

Angerer 1984

No data Afeworki and 

Chandravanshi 

1987 

No data Sunderman et 

al. 1989 
COBALT 267 

7. ANALYTICAL METHODS 

Table 7-1. Analytical Methods for Determining Stable Cobalt in Biological 

Materials 

Sample Analytical Sample Percent 

matrix Preparation method method detection limit recovery Reference 

Blood or Acid digestion ICP-AES (NIOSH 10 μg/g 81% at NIOSH 1984 

tissue method 8005) (blood); 110 μg/L 

0.2 μg/g (blood) 

(tissue) 

D2 = deuterium; DPCSV = differential pulse cathodic stripping voltammetry; GF-AAS = graphite furnace atomic 

absorption spectrometry; ICP-AES = inductively coupled plasma-atomic emission spectrometry; NIOSH = National 

Institute for Occupational Safety and Health 
 

 

COBALT 268 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining Radioactive Cobalt in Biological 

Samples 

Sample 

matrix Preparation method 

Analytical 

method 

Sample 

detection limita 

Percent 

recovery Reference 

Urine Direct count of sample γ-spectrometry 

with NaI detector 

No data (<MDL) No data Miltenberger 

et al. 1981 

Soft 

tissue 

Sample wet-ashed γ-spectrometry 

(NaI) 

No data No data Baratta et al. 

1969 

Sample directly counted in 

detector 

γ-spectrometry 5 pCi/g No data Rabon and 

Johnson 1973 

Sample digested in acid, 

oxidized with HClO4, concentrated by precipitation 

with AMP, purified by resin 

column, precipitated with 

hexachloroplatinic acid 

-counter 0.1 pCi/g 40–85% Nevissi 1992 

Feces Direct count of sample γ-spectrometry No data No data Smith et al. 

1972 

Blood Red cells separated from 

plasma and washed 

γ-spectrometry 

with NaI detector 

No data No data Smith et al. 

1972 

a

1 Bq=2.7x10-11 Ci=27 pCi 

AMP = ammonium molybdophosphate; MDL = minimum detectable level; NaI = sodium iodide 
 

 

COBALT 269 

7. ANALYTICAL METHODS 

performed with various radiation detectors and associated electronic devices that are collectively known 

as whole body counters. These radiation detectors commonly utilize sodium iodide (NaI), hyperpure 

germanium, and organic liquid scintillation detectors to measure the 1,172 and 1,332 keV gamma rays 

from the decay of 60Co. Because of the relatively low attenuation of the high energy gamma rays emitted 

from 60Co by most tissues, cobalt radioisotopes can easily be detected and quantified using whole body 

counting techniques (Lessard et al. 1984; NCRP 1987; Raghavendran et al. 1978; Smith et al. 1972; Sun 

et al. 1997). Many configurations of the whole body counter and scanning methods have been utilized, 

ranging from unshielded single-crystal field detectors to shielded, multi-detector scanning detectors 

(IAEA 1962, 1970, 1972, 1976, 1985; NCRP 1987). Where appropriate, shielding of the room that 

houses the whole body counter and/or the detector is often used to increase the detection sensitivity of the 

equipment by minimizing background radiation. Additionally, care must be exercised to insure that 

external contamination with radioactive cobalt or other gamma-emitting radioisotopes on the clothing or 

skin of the individual to be scanned has been removed. Also, in vitro measurements of cobalt (see 

Section 7.1.2) are often used in conjunction with whole body counting when monitoring individuals 

working with cobalt, especially in conjunction with the assessment of individuals who have experienced 

accidental exposures to cobalt (Bhat et al. 1973). 

Calibration of whole body counters is achieved through the use of tissue-equivalent phantoms. These 

phantoms are constructed to mimic the shape and density of the anatomical structure using tissue 

equivalent materials such as water-filled canisters or masonite (Barnaby and Smith 1971; Bhat et al. 1973; 

Sun et al. 1997). For example, the bottle mannequin absorber (BOMAB) consists of a series of waterfilled polyethylene canisters constructed into seated or reclined human forms (Sun et al. 1997). 60Co 

standards are measured either as point sources along the phantom or dissolved within the water-filled 

canisters. Comparisons of the actual counts obtained from the phantom to the known activity of the 

cobalt standards are used to determine the efficiency of the counting technique and, thus, provide the 

basis for calibrating the technique. Even so, differences in whole body measurement techniques, 

calibration methods, and background radiation count calculations between different laboratories can 

complicate the direct comparisons of body burden measurements and clearance rates for cobalt 

radioisotopes and should be taken into consideration when comparing data obtained from independent 

laboratories. 
COBALT 270 

7. ANALYTICAL METHODS 

7.1.2 External Measurements 

In vitro analyses of cobalt are routinely performed in situations where in vivo analyses can not be 

obtained or in support of an in vivo monitoring program. Urine and feces are the preferred samples for in 

vitro analyses of cobalt, although other sample types, such as tissue, bone, or blood, can also be used on a 

more limited basis. Urine provides for an analysis of soluble (inorganic) cobalt, fecal analysis can be 

used to assess the cobalt (organic) that is eliminated into the gut or the fraction of ingested cobalt not 

absorbed by the gut, and tissue/blood/bone are used to assess whole or regional body burdens of cobalt 

(NCRP 1987; Smith et al. 1972). 

The analytical methods for determining the stable cobalt isotope, 59Co, in biological matrices are given in 

Table 7-1. For accurate determination of cobalt, contamination of samples during sample collection, 

storage, and treatment must be avoided, particularly for biological samples containing low levels of 

cobalt. Cobalt contamination in blood samples has been reported from disposable syringes and technicalgrade anticoagulants. Menghini needles, often used for liver biopsy, and mortar, pestles, and grinding 

devices used for homogeneous mixing may contaminate samples. Other sources of contamination may be 

collection and storage containers and chemical reagents used for preparing samples. In fact, sample 

contamination was responsible for erroneous reports in the earlier literature of grossly high levels of 

cobalt in biological specimens of unexposed persons. Therefore, blanks should always be run with the 

samples. 

The commonly used classical methods for determining stable cobalt in biological samples are 

polarographic and colorimetric methods. Details about these methods are given by Saltzman and Keenan 

(1957). Since these older methods have interference problems and are unsuitable for determining low 

levels of cobalt in many biological samples, the samples are pretreated before quantification. 

Precipitation, chelation, chromatography, and ion-exchange are some of the methods used for this 

purpose. In recent years, the two single-element instrumental techniques most frequently used methods 

for determining cobalt are graphite furnace-atomic absorption spectrometry (GF-AAS) (also called 

electrothermal atomic absorption spectrometry) and differential pulse anodic stripping voltammetry 

(DPAVS). Multi-element techniques commonly used for cobalt determination are neutron activation 

analysis and inductively coupled plasma-atomic emission spectrometry (ICP-AES). Several other 

methods are available for determining stable cobalt in biological samples; these include x-ray 

fluorescence and Spark source mass spectrometry (Adeloju et al. 1985; Smith and Carson 1981). 
 

 

 

COBALT 271 

7. ANALYTICAL METHODS 

For the in vitro analysis of cobalt radioisotopes in human samples, the majority of the analytical methods 

measure the cobalt radioisotopes directly in the samples, without the requirement for an extensive sample 

preparation procedure, using gamma spectrometry techniques. Of the cobalt radioisotopes that have been 

detected in the environment (e.g., 57Co, 58Co, and 60Co), 60Co is the most common. Consequently, most of 

the analytical methods that will be described in this chapter are those developed for the detection and 

quantitation of 60Co in biological (see Table 7-2) and environmental samples (see Table 7-4). 

The radiochemical analysis of 60Co in urine has been used in conjunction with whole body scanning 

methods to assess acute and long-term body burdens of this isotope. The analysis of 60Co in urine is the 

same as that described for a standardized method of analysis of cesium radioisotopes in urine (Gautier 

1983). A urine sample of approximately 2 L is collected (either over 24 hours or before and after 

bedtime) and a 1-L aliquot is transferred to a Marinelli beaker for counting in a gamma-ray spectrometer 

(Gautier 1983). This simple procedure offers high recoveries of cobalt (98%) and the minimum detection 

sensitivity (100 pCi/L [3.7 Bq/L]) that is required to evaluate individuals for exposures to radioactive 

cobalt (Gautier 1983). Direct counting methods are also used for the analysis of cobalt radioisotopes in 

tissues, feces, and blood (Smith et al. 1972, Table 7-2). However, some of these methods may require 

sample preparation to reduce volume or increase concentration. 

Accuracy of in vivo and in vitro measurements of cobalt is determined through the use of standard, 

certified solutions or radioactive sources with known concentrations or activities of cobalt. Certified 

standards for stable cobalt can be obtained through a number of commercial sources. The primary source 

of certified cobalt radioisotope standards is the National Institute of Standards and Technology (NIST). 

Gamma ray point sources for 60Co (SRM 4200, 60,000 Bq [1.6 μCi] and SRM 4207, 300,000 Bq 

[56 μCi]) and standard solutions of 60Co (SRM 4233, 600,000 Bq/g [16 μCi/g]) are available from NIST. 

Also, the determination of accuracy of a method often requires standard reference materials (SRMs). 

Unfortunately, very few biological SRMs are available. An SRM for cobalt in animal muscle is available 

from the International Atomic Energy Agency (IAEA), Vienna; an SRM for bovine liver (SRM-1577) is 

available from NIST (formerly the National Bureau of Standards) (Adeloju et al. 1985; Smith and Carson 

1981). 
 

 

COBALT 272 

7. ANALYTICAL METHODS 

7.2 ENVIRONMENTAL SAMPLES 

There are two common approaches for measuring cobalt in the environment. Cobalt radioisotopes can 

either be measured directly in the field (in situ) using portable survey instruments or samples can be 

procured from the field and returned to the laboratory for quantitation. However, quantitation of the 

stable cobalt isotope 59Co in environmental samples is generally conducted in the laboratory. 

7.2.1 Field Measurements of Cobalt 

In situ measurement techniques are extremely useful for the rapid characterization of radionuclide 

contamination in the environment, such as soils, sediments, and vegetation, or when monitoring personnel 

for exposure to radionuclides. The measurement of gamma-ray-emitting radionuclides, like cobalt, in the 

environment is conducted with portable survey instruments such as Gieger-Mueller detectors, sodium 

iodide scintillation detectors, and gamma-ray spectrometers. However, the use of gamma-ray 

spectrometers in field survey equipment is preferred for measuring cobalt in the field because of its 

selectivity and sensitivity. The relatively high energy and penetrability of the gamma ray that is emitted 

during the decay of 60Co provides an advantage for assessing the level of cobalt both on and below the 

surface using portable field survey instruments such as the gamma-ray spectrometer. These gamma-ray 

spectrometers are equipped with a high purity germanium detector that is able to selectively and 

sensitively differentiate the 1,173 and 1,332 keV gamma rays emitted from 60Co from the gamma-rays 

emitted from other radionuclides, for example 40K or 137Cs (USNRC 1997). Minimum detectable 

activities (MDAs) of 0.005 Bq/g (0.05 pCi/g) for 60Co are routinely achieved using p-type germanium 

gamma-ray spectrometers with 10-minute counting times (USNRC 1997). However, counting errors can 

occur where the simultaneous detection of the 1,173 and 1,332 keV gamma rays produces a sum peak at 

2,505 keV or a count in the continuum between the individual peaks and the sum peak (APHA 1998; 

USNRC 1997). These errors can be minimized by changing the geometry of the detector or the distance 

of the detector from the source of radioactivity. Computational methods have been derived to aid in 

determining the concentrations and distributions of 60Co in different soil types and depths (USNRC 

1997). The concentrations and distributions of 60Co that have been derived from the computational 

analysis of the survey data are often verified by laboratory-based analyses of soil samples procured from 

the survey area. 
COBALT 273 

7. ANALYTICAL METHODS 

7.2.2 Laboratory Analysis of Environmental Samples 

Analytical methods for quantifying stable cobalt and cobalt radioisotopes in environmental samples (e.g. 

air, water, soil, and biota) are summarized in Tables 7-3 (59Co) and 7-4 (60Co). The methods that are 

commonly used in the analysis of stable cobalt are based on instrumental analytical techniques, such as 

atomic absorption spectrometry (AAS), instrumental neutron activation analysis (INAA), and mass 

spectrometry (MS). The analysis of 60Co can be determined either as total mass or total activity, 

depending on the analytical technique that is used. Typically, radiochemical methods of analysis 

employing gamma-ray spectrometry techniques are used to quantitate 60Co in environmental samples. 

Analytical methods for determining stable cobalt in environmental samples are given in Table 7-3. Since 

cobalt exists in the particulate form in the atmosphere, it is sampled by drawing air through a metal-free 

filter (usually cellulose ester membrane), and the metal is quantified in the collected particles. Sample 

treatment prior to quantification is important for environmental samples. For example, the use of sodium 

carbonate for dry ashing plant materials results in poor cobalt recovery. Low-temperature ashing may be 

inadequate for some samples, and losses may occur during rigorous dry ashing. Wet ashing is the 

preferred method when sample treatment is necessary. Wet extraction with dilute nitric acid is most 

suitable for analyzing cobalt in dust samples. In some samples, the determination of soluble and 

insoluble cobalt is important, and analytical methods used to determine cobalt in filtered and unfiltered 

samples are available for this purpose. 

As in the case of biological samples, contamination of environmental samples during sample collection, 

storage, and treatment should be avoided. Loss of cobalt from aqueous samples due to adsorption on 

storage containers should be avoided by using polyethylene or similar containers and acidifying the 

solution to the proper pH (Smith and Carson 1981). Because of its rapidity, accuracy, and low detection 

limit, GF-AAS with Zeeman background correction is the most commonly used method for quantifying 

cobalt in environmental samples. To meet the detection limits of the available analytical methods, 

preconcentration prior to quantification may be necessary for some samples (e.g., seawater). A few 

commonly used methods for determining cobalt in environmental samples are given in Table 7-3. Other 

less frequently used methods are inductively coupled plasma-mass spectrometry (ICP-MS) (Henshaw 

et al. 1989; McLaren et al. 1985), gas, liquid, and ion chromatography with colorimetric, electron capture, 

and electrochemical detection (Bond and Wallace 1984; Carvajal and Zienius 1986; Cheam and Li 1988; 

King and Fritz 1987; Schaller and Neeb 1987), photoacoustic spectroscopy with colorimetry (Kitamori 
 

 

COBALT 274 

7. ANALYTICAL METHODS 

Table 7-3. Analytical Methods for Determining Stable Cobalt in Environmental 

Samples 

Sample 

Sample Analytical detection Percent 

matrix Preparation method method limit recovery Reference 

Air Weighed filter irradiated INAA 0.17 μg/m3 No data Haddad and 

(workplace) in a reactor Zikovsky 

1985 

Sample filter digested Flame-AAS with 0.4 μg/m3 98% with 12– NIOSH 1984 

by wet acid ashing background 96 μg spiked 

correction (NIOSH filter 

method 7027) 

Sample filter digested ICP-AES (NIOSH 0.5 μg/m3

 95–100% with NIOSH 1984 

by wet acid ashing method 7300) 2.5– 

1,000 spiked 

filter 

Water (low Direct injection GF-AAS with <0.5 μg/L 93–115% at Fishman 

ionic strength) Zeeman or 8.5–30 μg/L et al. 1986 

deuterium background correction 

Lake water Sample complexed with ICP-AES <0.004 μg/L No data Nojiri et al. 

8-hydroxyquinoline 1985 

absorbed on a column, 

desorbed and digested 

with acid 

Rainwater Sample preconcentrated PIXE 0.08 μg/L No data Hansson 

onto polystyrene films et al. 1988 

by spray-drying 

Seawater Sample complexed with GF-AAS with 0.0002 μg/L 90% Nakashima 

8-hydroxyquinoline Zeeman back­ et al. 1988 

absorbed on a column, ground correction 

desorbed and digested 

with acid 

Water and Direct aspiration of Flame-AAS (EPA 0.05 mg/L 97–98% at 0.2– EPA 1983 

waste water sample method 219.1) 5.0 mg/L 

Direct injection GF-AAS with 1 μg/L No data EPA 1983 

background 

correction (EPA 

method 219.2) 

Groundwater Direct aspiration Flame-AAS with 0.05 mg/L 97–98% at 0.2– EPA 1986b 

or leachate background 5.0 mg/L 

correction (EPA 

method 7200) 

Groundwater Direct injection GF-AAS with 1 μg/L No data EPA 1986b 

or leachate background 

correction (EPA 

method 7201) 
 

 

COBALT 275 

7. ANALYTICAL METHODS 

Table 7-3. Analytical Methods for Determining Stable Cobalt in Environmental 

Samples 

Sample 

Sample Analytical detection Percent 

matrix Preparation method method limit recovery Reference 

Food Sample digested with GF-AAS with 1.88 μg/L in 100–107% at Barbera and 

acid background dissolved 0.2–0.6 mg/kg Farre 1988 

correction extract (leaves, liver) 

Milled Wheat Wet ashing (HNO3), ET-AAS 20 ng/L approximately González et 

preconcentration and 100% al. 2000 

chelation 

AAS = atomic absorption spectrometry; EPA = Environmental Protection Agency; ET-AAS = electrothermal atomic 

absorption spectrometry; GF-AAS= graphite furnace atomic absorption spectrometry; ICP-AES = inductively coupled 

plasma-atomic emission spectrometry; INAA = instrumental neutron activation analysis; NIOSH = National Institute 

for Occupational Safety and Health; PIXE = photon induced x-ray emission 
COBALT 276 

7. ANALYTICAL METHODS 

Table 7-4. Analytical Methods for Determining Radioactive Cobalt 

in Environmental Samples 

Sample 

Sample detection Percent 

matrix Preparation method Analytical method limita recovery Reference 

Air Direct count of sample γ-spectrometry with 0.001 pCi/m3 No data USAEC 1974a 

collected on paper filter Ge/Li detector 

Air Sample filter ashed Scintillation counter No data No data De Franceschi 

with NaI detector et al. 1974 

Drinking Direct count of sample γ-spectrometry with <2 pCi/L 99% APHA 1998 

water Ge detector 

Drinking Direct count of sample γ-spectrometry 2 pCi/L No data USAEC 1974b 

water 

Water Direct count of sample γ-spectrometry with 2 pCi/L No data ASTM 1999 

Ge/Li detector 

Water Direct count of sample γ-spectrometry 10 pCi/L No data Cahill et al. 

1972 

Seawater Sample concentrated Scintillation 50 fCi/L 92–95% Hiraide et al. 

using continuous-flow detector 1984 

coprecipitation-flotation 

separation technique 

Sediments Sample dried and ground γ-spectrometry 0.04 pCi/g No data Cahill et al. 

1972 

Fish Samples dried and ashed γ-spectrometry 0.001 pCi/g No data Cushing et al. 

(DW) 1981 

Mollusc Samples dried and ashed γ-spectrometry <0.01 pCi/g No data De Franceschi 

et al. 1976 

a

1 Bq=2.7x10-11 Ci=27 pCi 

DW = dry weight; Ge/Li = lithium drifted geranium; NaI = sodium iodide 
COBALT 277 

7. ANALYTICAL METHODS 

et al. 1986), electrothermal vaporization with ICP-AES (Malinski et al. 1988) and chemiluminescence 

with spectrofluorimetry (Jones et al. 1989). 

Analytical methods for determining cobalt radioisotopes in the environment are shown in Table 7-4. The 

analysis of cobalt in air is based on quantifying cobalt within aerosols or particles that become trapped on 

cellulose (paper) or glass fiber filters after a calibrated amount of air is passed through the filters. Since 

the cobalt radioisotopes do not occur naturally, but may be released as a result of nuclear weapons testing 

(which has been discontinued for several years), neutron-activation of specific materials (e.g., cobalt 

containing alloys used in piping of nuclear reactors), or a severe core damage accident in a nuclear plant, 

the amounts of these isotopes within the ambient environment are near or below the minimum detectable 

levels for these isotopes (DOE 1995). However, trace amounts of 60Co can be detected in air, water, and 

sediments within or near nuclear weapons or fuel production facilities, nuclear reactors, and nuclear waste 

storage sites (DOE 1995; Boccolini et al. 1976; USAEC 1973). Analysis of cobalt radioisotopes in air 

filters, water, sediments, vegetation, and biota can be performed directly using gamma-ray spectrometry, 

or following some sample preparation (e.g., drying, ashing, or extraction) (Boccolini et al. 1976; Cahill et 

al. 1972; Cushing 1981; Hiraid et al. 1984; Windham and Phillips 1973). 

The detection limits, accuracy, and precision of any analytical methodology are important parameters in 

determining the appropriateness of a method for quantifying a specific analyte at the desired level of 

sensitivity within a particular matrix. The Lower Limit of Detection (LLD) has been adopted to refer to 

the intrinsic detection capability of a measurement procedure (sampling through data reduction and 

reporting) to aid in determining which method is best suited for the required sample quantitation (USNRC 

1984). Several factors influence the LLD, including background, size or concentration of sample, 

detector sensitivity and recovery of desired analyte during sample isolation and purification, level of 

interfering contaminants, and, particularly, counting time. Because of these variables, the LLDs between 

laboratories, utilizing the same or similar measurement procedures, will vary. 

The accuracy of a measurement technique in determining the quantity of a particular analyte in 

environmental samples is greatly dependent on the availability of standard reference materials. Several 

SRMs for cobalt in environmental samples are also available. Some of these are coal, fly ash, diet, and 

orchard leaf SRMs available from NIST. The Community Bureau of Reference, European Communities 

offers SRMs for cobalt in sludges, and an SRM for cobalt in thin polymer films is available from NIST 

for x-ray fluorescence analysis in aerosol particle samples (Dzubay et al. 1988; Miller-Ihli and Wolf 
 

 

 

 

COBALT 278 

7. ANALYTICAL METHODS 

1986; Schramel 1989; Smith and Carson 1981; Tinsley et al. 1983). Gamma ray point sources for 60Co 

(SRM 4200, 60,000 Bq [1.6 μCi] and SRM 4207, 300,000 Bq [56 μCi]) and standard solutions of 60Co 

(SRM 4233, 600,000 Bq/g [16 μCi/g]) are available from NIST. 

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 cobalt 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 cobalt. 

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. 

7.3.1 Identification of Data Needs 

Methods for Determining Biomarkers of Exposure and Effect. Cobalt concentrations in blood 

or urine can serve as exposure indicator (Alexandersson 1988; Ichikawa et al. 1985; Scansetti et al. 1985). 

The available analytical methods are capable of determining the levels of cobalt in both the blood and 

urine of normal and occupationally exposed persons (Table 7-1). For the quantitation of cobalt 

radioisotopes, whole body counters can be used to assess radioactive cobalt body burdens that have 

occurred both from acute and chronic exposures to cobalt radioisotopes (Bhat et al. 1973; NCRP 1987). 

In vitro analytical methods are available for analyzing cobalt radioisotopes in urine, feces, and tissues 

obtained from normal and occupationally exposed persons (Table 7-2). 
COBALT 279 

7. ANALYTICAL METHODS 

Sensitive serum protein responses were found in animals exposed to cobalt at levels below those that 

produce hematopoietic effects. This unique serum protein response to cobalt exposure includes an 

increase in alpha globulin fractions of serum proteins and associated serum neuraminic acid. Details of 

this effect are given in Chapters 2 and 3. If similar changes occur in humans, this measurement may
 

provide the earliest indications of effects of cobalt exposure. The available analytical methods are 

capable of determining these effects of cobalt exposure. 

Methods for Determining Parent Compounds and Degradation Products in Environmental 

Media. Analytical methods with good sensitivity and specificity are available for determining cobalt in 

air, water, soil, and other environmental media (Table 7-3). Analytical methods for cobalt, like those for 

most metals, measure total metal content rather than the particular compound. Therefore, analytical 

methods do not generally differentiate between the parent compound and a transformation product as 

would be the case, for example, were cobalt oxide to be converted to cobalt sulfate. (An exception to this 

would be the case of radioactive decay in which the parent could be readily distinguished from the decay
 

product.) Analytical methods with the capability of distinguishing between different cobalt species would 

be important an important tool for assessing the fate of cobalt compounds in the environment. However, 

methods for quantifying specific cobalt compounds were not found in the literature. 

The levels of the parent compound or its reaction products in different environmental media can be used 

to assess the exposure to cobalt by humans through the inhalation of air and ingestion of food and 

drinking water. In the case of cobalt, a correlation between its levels in environmental media (e.g., 

occupational air) and in biological tissues and body fluids has been found (Alexandersson 1988; Ichikawa 

et al. 1985; Scansetti et al. 1985). Therefore, it is possible to estimate the total body burden of cobalt in 

workers exposed to airborne cobalt vapor and fumes from its concentration in workplace air. 

For cobalt radioisotopes, analytical methods also exist that have good sensitivity and specificity for 

determining radioactive cobalt in air, water, soil, and other environmental media are available (Table 7-4). 

Because 60Co decays to the stable element 60Ni, there is no need to develop methods to detect and 

quantify the decay products. 
COBALT 280 

7. ANALYTICAL METHODS 

7.3.2 Ongoing Studies 

Two studies involving analytical techniques for cobalt was listed in the Federal Research in Progress 

database (FEDRIP 2002, 2004). N.J. Miller-Ihli and co-workers of the Agricultural Research Service in 

Beltsville, Maryland are developing single and multielement methods for the determination of trace 

elements of nutritional and health concern. This work will develop new/improved methods permitting 

direct analysis of solids by GF-AAS and ICP-MS, as well as methods for the determination of different 

chemical forms of these elements by coupling capillary zone electrophoresis with inductively coupled 

plasma mass spectrometry (ICP-MS). This research is supported by the U.S. Department of Agriculture 

(USDA) Agricultural Research Service. B.T. Jones of Wake Forest University in Winston-Salem, North 

Carolina along with C. Calloway of Winthrop College, South Carolina, are working to develop a novel, 

low-cost, portable instrument for the simultaneous determination of trace radioactive elements in nuclear 

forensic samples. The instrument to be developed is expected to provide analytical figures comparable to 

ICP-MS, but the instrument is much lower cost and more portable. The specific objectives of the project 

include determination of the analytical figures of merit for elements including cobalt, cesium, and 

strontium, and analysis of real samples such as soil, urban dust, water, and agricultural materials. 
 

 

COBALT 281 

8. REGULATIONS AND ADVISORIES 

International and national guidelines and state regulations regarding exposure to stable cobalt and its 

compounds are summarized in Table 8-1. The regulations regarding radioactive cobalt are summarized in 

Table 8-2. 

Stable Cobalt. An MRL of 1x10-4 mg cobalt/m3

 has been derived for chronic-duration inhalation 

exposure. The MRL is based on a NOAEL of 0.0053 mg cobalt/m3

 for decreased respiratory function in 

exposed workers (Nemery et al. 1992). An MRL of 1x10-2 mg/kg-day has been derived for intermediateduration oral exposure, based on a LOAEL of 1 mg/kg-day for polycythemia in human volunteers (Davis 

and Fields 1958). No other inhalation or oral MRLs were derived. 

The EPA has not derived an RfC or RfD for cobalt and compounds. Similarly, no cancer classification 

has been performed by the EPA (IRIS 2000). The American Conference of Governmental Industrial 

Hygienists (ACGIH) has given cobalt a classification of A3, confirmed animal carcinogen with unknown 

relevance to humans, and established an 8-hour time-weighted average (TWA) of 0.02 mg/m3

 for 

occupational exposure (ACGIH 2000). The Occupational Safety and Health Administration (OSHA) has 

promulgated an 8-hour permissible exposure limit (PEL) of 0.1 mg/m3

 (OSHA 2001e), and the National 

Institute for Occupational Safety and Health (NIOSH) recommends an 8-hour TWA of 0.05 mg/m3 

(NIOSH 2001). IARC (2001b) reports that cobalt and cobalt compounds are possibly carcinogenic to 

humans (Group 2B), based on sufficient evidence for cobalt metal and cobalt oxides and limited evidence 

for cobalt chloride and cobalt sulfate. 

Cobalt and its compounds are regulated by the Clean Water Effluent Guidelines for the following 

industrial point sources: nonferrous metal manufacturing, asbestos, timber products processing, paving 

and roofing, paint formulating, ink formulating, gum and wood, carbon black, and battery manufacturing 

(EPA 1988). 

Radioactive Cobalt. No MRLs were derived for inhalation or oral exposure to radioactive cobalt. MRLs 

for acute and chronic exposure to ionizing radiation exist (Agency for Toxic Substances and Disease 

Registry 1999) and are applicable to cobalt. The EPA has not derived an RfC or RfD for radioactive 
 

 

 

COBALT	 282 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Stable Cobalt 

Agency Description Information Reference 

INTERNATIONAL 

Guidelines: 

IARC Carcinogenicity classification 

Cobalt and cobalt compoundsa 

NATIONAL 

Regulations and 

Guidelines: 

a. Air 

ACGIH TLV-TWA 

Cobalt, elemental, and inorganic 

compounds (as Co) 

NIOSH REL (TWA) 

Cobalt metal, dust, and fumes

 (as Co) 

IDLH 

Cobalt metal, dust, and fumes

 (as Co) 

OSHA PEL (8-hour TWA) for general industry 

Cobalt metal, dust, and fumes

 (as Co) 

PEL (8-hour TWA) for construction 

industry 

Cobalt metal, dust, and fumes

 (as Co) 

PEL (8-hour TWA) for shipyard 

industry 

Cobalt metal, dust, and fumes

 (as Co) 

USC HAP (cobalt compounds) 

b. Water 

EPA NPDES permit application testing 

requirements; conventional and 

nonconventional pollutants required to 

be tested by existing dischargers if 

expected to be present 

BPT effluent limitations 

Maximum for 1 day 

Average of daily values for 

30 consecutive days 

 Groundwater monitoring 

 Suggested method 

 6010 

 7200 

 7201 

Group 2Bb 

0.02 mg/m3 

0.05 mg/m3 

20 mg/m3 

0.1 mg/m3 

0.1 mg/m3 

0.1 mg/m3 

3x10-4 kg/kkg 

1.2x10-4 kg/kkg 

PQL 

70 μg/L 

500 μg/L 

10 μg/L 

IARC 2001b 

ACGIH 2000 

NIOSH 2001 

OSHA 2001e 

29CFR1910.1000 

Table Z 

OSHA 2001d 

29CFR1926.55 

OSHA 2001c 

29CFR1915.1000 

USC 2001a 

42USC7412 

 EPA 2001g 

40CFR122 

Appendix D 

Table IV 

EPA 2001b 

40CFR415.652

EPA 2001d 

40CFR264 

Appendix IX 
COBALT 

8. REGULATIONS AND ADVISORIES 

283 

Table 8-1. Regulations and Guidelines Applicable to Stable Cobalt 

Agency Description Information Reference 

NATIONAL (cont.) 

c. Food 

FDA 

d. Other 

ACGIH 

EPA 

EPA 

Drug products withdrawn or removed 

from the market for reasons of safety 

or effectiveness 

New drug status accorded through 

rulemaking procedures 

Over-the-counter drugs; recommended 

warning and caution statement for 

cobalt as a cobalt salt 

Substances generally recognized as 

safe; trace minerals added to animal 

feeds 

Substances prohibited from use in 

human food 

Carcinogenicity classification 

Cobalt, elemental, and inorganic 

compounds (as Co) 

BEI 

Cobalt in urine—end of shift at

 end of workweek 

Cobalt in blood—end of shift at

 end of workweek 

Carcinogenicity classification 

RfC 

RfD 

Toxic chemical release reporting; 

Community Right-to-Know; effective 

date 

 Hazardous waste; identification and 

listing 

TSCA; health and safety data reporting 

Municipal solid waste landfills; 

hazardous constituent for detection 

monitoring 

 Suggested method 

 6010 

 7200 

 7201 

Reportable quantity (cobalt 

compounds) 

All drug products containing 

cobalt salts (except 

radioactive forms of cobalt 

and its salts and cobalamin 

and its derivatives) 

Cobalt preparations intended 

for use by man 

Required on articles 

containing ≥0.5 μg per dose 

and ≥2 μg per 24-hour period 

Cobalt acetate 

Cobalt carbonate 

Cobalt chloride 

Cobalt oxide 

Cobalt sulfate 

Cobaltous salts and its 

derivatives 

A3c 

15 μg/L 

1 μg/L 

No data 

01/01/87

Contain ≤1 ppmv in synthesis 

gas fuel generated from 

hazardous waste 

PQL 

70 μg/L 

500 μg/L 

10 μg/L 

1 pound 

FDA 2000a 

21CFR216.24 

FDA 2000b 

21CFR310.502 

(a)(7) 

FDA 2000e 

21CFR369.20 

FDA 2000f 

21CFR582.20 

FDA 2000g 

21CFR189.120 

ACGIH 2000 

IRIS 2000 

 EPA 2001c 

40CFR372.65(a) 

EPA 2001e 

40CFR261.38 

(b)(5) 

EPA 2001j 

40CFR716.120 

EPA 2001f 

40CFR258 

Appendix I and II 

EPA 2001h 

40CFR302.4 
 

 

 

 

 

 

 

 

 

 

COBALT	 284 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Stable Cobalt 

Agency Description Information Reference 

NATIONAL (cont.) 

USC Superfund imposition of tax on cobalt $4.45 per ton USC 2001c 

26USC4661 

Exemption of tax imposed on recycled USC 2001b 

cobalt 26USC4662 

STATE 

Regulations and 

Guidelines 

a. Air 

Alabama HAP (cobalt compounds) BNA 2001 

Alaska Air contaminant standard (TWA) BNA 2001 

Cobalt metal, dust, and fumes 0.05 mg/m3 

California Airborne contaminant (cobalt metal, BNA 2001 

dust, and fumes) 

HAP (cobalt compounds) BNA 2001 

Toxic air contaminant (cobalt CA Air Resources 

compounds) Board 2000 

Colorado HAP (cobalt metal, dust, and fumes) BNA 2001 

“High-concern” pollutant (cobalt and BNA 2001 

compounds) 

Reportable pollutants (cobalt metal, CO Dept. of Public 

dust, and fumes) Health and 

Environment 2000 

Connecticut HAP—hazard limiting value (cobalt BNA 2001 

metal, dust, and fumes) 

 8 hours 

 30 minutes 

2 μg/m3 

10 μg/m3 

 Delaware Reportable quantities DE Air Quality 

 Cobalt carbonyl 1 pound Management 2000 

 Cobaltous sulfamate 1,000 pounds 

 Cobalt, ((2,2'-(ethane­ 1 pound 

 diylbis(nitrilomethylidyne) 

Hawaii Air contaminant limit (PEL-TWA) 

Cobalt metal, dust, and fumes 0.05 mg/m3 BNA 2001 

HAP (cobalt compounds) BNA 2001 

Idaho TAP non-carcinogenic increments ID Dept. of 

Cobalt carbonyl and cobalt Environmental Quality 

 hydrocarbonyl (as Co) 

OEL 

EL 

AAC (24-hour average) 

1x10-1 mg/m3 

7x10-3 pounds/hour 

5x10-3 mg/m3 

2000 

Cobalt metal, dust, and fumes 

OEL 

EL 

AAC (24-hour average) 

5x10-2 mg/m3 

3.3x10-3 pounds/hour 

2.5x10-3 mg/m3 

Illinois Toxic air contaminant (cobalt) IL EPA 2000a 

Kansas HAP (cobalt compounds) KS Dept. of Health 

and Environment 

2000 
 

 

 

 

 

 

 

 

COBALT 

8. REGULATIONS AND ADVISORIES 

285 

Table 8-1. Regulations and Guidelines Applicable to Stable Cobalt 

Agency Description Information Reference 

STATE (cont.) 

Kentucky 

Louisiana 

Maine 

Maryland 

Michigan 

Minnesota 

Missouri 

 Montana 

Nebraska 

New Mexico 

New York 

North Carolina 

Ohio 

Oregon 

Rhode Island 

South Carolina 

Texas 

Vermont 

Washington 

HAP (cobalt compounds) 

Toxic air pollutant (cobalt compounds 

Emissions standards 

Toxic air pollutant (cobalt compounds) 

High concern toxic air pollutants 

(cobalt compounds) 

HAP threshold (cobalt metal and 

cobalt carbonyl) 

HAP (cobalt compounds) 

Occupational air contaminant (cobalt 

metal, dust, and fumes) 

HAP (cobalt compounds and cobalt) 

Toxic air pollutant (cobalt metal, dust, 

and fumes [as Co]) 

OEL 

Emissions 

Annual guideline concentrations 

Dangerous air contaminants (TLV) for 

cobalt metal, dust, and fumes 

HAP (cobalt compounds) 

Transition limits (PEL) 

Cobalt metal, dust, and fumes 

Final rule limits (TWA) 

Cobalt metal, dust, and fumes 

PEL-TWA (cobalt metal, dust, and 

fumes) 

TRI 

Air contaminant (cobalt metal, dust, 

and fumes) 

HAP (cobalt compounds) 

Toxic air emissions (MAC) for cobalt 

compounds 

HAP (cobalt metal, dust, and fumes) 

HAP (cobalt compounds) 

Hazardous ambient air standards 

 Cobalt compounds 

Annual average 

Averaging time
 

Action level 

Class B TAP and ASIL 

(24-hour average) 

Cobalt metal, dust and fumes 

Cobalt carbonyl and cobalt 

 hydrocarbonyl 

2,000 pounds 

0.1 tons/year 

0.1 mg/m3

1x10-1 mg/m3 

6.67x10-3 pounds/hour 

5x10-3 μg/m3 

0.1 mg/m3

0.1 mg/m3 

0.05 mg/m3 

0.05 mg/m3

0.1 mg/m3

0.25 μg/m3

0.1 mg/m3

0.12 μg/m3 

24 hours 

6.2x10-3 pounds/8 hours 

0.17 μg/m3 

0.33 μg/m3 

BNA 2001 

BNA 2001 

BNA 2001 

BNA 2001 

 BNA 2001 

BNA 2001 

BNA 2001 

 BNA 2001 

BNA 2001 

BNA 2001 

NYS Dept. of 

Environmental 

Conservation 2000 

 BNA 2001 

BNA 2001 

BNA 2001 

 BNA 2001 

Ohio EPA 2000 

 BNA 2001 

BNA 2001 

 BNA 2001 

 BNA 2001 

BNA 2001 

BNA 2001 

WA Dept. of Ecology 

2000 
 

 

 

 

COBALT 

8. REGULATIONS AND ADVISORIES 

286 

Table 8-1. Regulations and Guidelines Applicable to Stable Cobalt 

Agency Description Information Reference 

STATE (cont.) 

 Wisconsin 

b. Water 

 Alabama 

 Arizona 

Arkansas 

California 

Colorado 

 Delaware 

Illinois 

Kentucky 

 Louisiana 

 Massachusetts 

 Minnesota 

Thresholds for HAPs 

 Cobalt carbonyl 

Cobalt metal, dust, and fumes 

HAP—existing sources 

AAC <25 feet 

AAC ≥25 feet 

Groundwater monitoring (cobalt) 

 Suggested methods 

 6010 

 7200 

 7201 

Drinking water guideline 

Groundwater monitoring (cobalt) 

 Suggested methods 

 6010 

 7200 

 7201 

Chemicals known to cause cancer or 

reproductive toxicity; date of initial 

appearance on the list 

Cobalt metal powder 

 Cobalt[II] oxide 

 Cobalt sulfate heptahydrate 

Groundwater standard (cobalt) 

Groundwater monitoring (cobalt) 

 Suggested methods 

 6010 

 7200 

 7201 

Groundwater quality standards for 

Class II 

Hazardous waste constituent for 

groundwater monitoring (cobalt) 

Groundwater monitoring (cobalt) 

 Suggested methods 

 6010 

 7200 

 7201 

Groundwater monitoring (cobalt) 

 Suggested methods 

 6010 

 7200 

 7201 

Drinking water guideline 

Groundwater protection hazardous 

constituent for cobalt (total) 

0.1 tons/year 

0.1 tons/year 

4.08x10-3 pounds/hour 

1.704x10-2 pounds/hour 

PQL 

70 μg/L 

500 μg/L 

10 μg/L 

0.70 μg/L 

PQL 

70 μg/L 

500 μg/L 

10 μg/L 

07/01/92 

07/01/92 

06/02/00 

0.05 mg/L 

PQL 

70 μg/L 

500 μg/L 

10 μg/L 

1 mg/L 

PQL 

70 μg/L 

500 μg/L 

10 μg/L 

PQL 

70 μg/L 

500 μg/L 

10 μg/L 

2 μg/L 

BNA 2001 

WI Dept. of Natural 

Resources 1999 

BNA 2001 

FSTRAC 1999

BNA 2001 

Cal/EPA 2000 

BNA 2001 

BNA 2001 

IL EPA 2000b 

 BNA 2001 

BNA 2001 

BNA 2001 

FSTRAC 1995 

 BNA 2001 
 

 

 

COBALT 287 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Stable Cobalt 

Agency Description Information Reference 

STATE (cont.) 

Missouri Water quality standards 

 Livestock, wildlife watering 

 Groundwater 

1x103 μg/L 

1x103 μg/L 

BNA 2001 

New Mexico Standards for groundwater of 0.05 mg/L BNA 2001 

10,000 mg/L TDS concentration or 

less (cobalt) 

New York Groundwater monitoring (cobalt) BNA 2001 

 Suggested methods PQL 

 6010 70 μg/L 

 7200 500 μg/L 

 7201 10 μg/L 

Tennessee Effluent limitations—daily maximum 10 mg/L BNA 2001 

concentration (cobalt) 

 Wisconsin Drinking water guideline 40 μg/L FSTRAC 1999 

Groundwater standards (cobalt) BNA 2001 

 Enforcement standard 40 μg/L 

Preventive action limit 8 μg/L 

c. Food No data 

d. Other 

Alabama Detection limit values for comparable 4.6 mg/kg at BNA 2001 

fuel specification for cobalt; 10,000 BTU/pound 

concentration limit 

Arizona Soil remediation levels (cobalt) 

 Residential 

 Non-residential 

4.6x103

 mg/kg 

9.7x104

 mg/kg 

BNA 2001 

Arkansas Detection limit values for comparable 4.6 mg/kg at BNA 2001 

fuel specification for cobalt; 10,000 BTU/pound 

concentration limit 

Solid waste management (cobalt) BNA 2001 

 Suggested methods PQL 

 6010 70 μg/L 

 7200 500 μg/L 

 7201 10 μg/L 

California Characteristics of toxicity for cobalt BNA 2001 

and cobalt compounds 

 STLC 80 mg/L 

 TTLC 8,000 mg/kg (wet-weight) 

Chemicals known to cause cancer or 07/01/92 BNA 2001 

reproductive toxicity (cobalt metal 

powder); initial appearance on the list 

Hazardous substance (cobalt, cobalt BNA 2001 

carbonyl, and cobalt hydrocarbonyl) 

Delaware Detection limit values for comparable 4.6 mg/kg at BNA 2001 

fuel specification for cobalt; 10,000 BTU/pound 

concentration limit 

Florida Toxic substance in the workplace BNA 2001 

(cobalt metal, dust, and fumes) 

Georgia Soil concentration (cobalt) 20 mg/kg BNA 2001 
 

 

COBALT 

8. REGULATIONS AND ADVISORIES 

288 

Table 8-1. Regulations and Guidelines Applicable to Stable Cobalt 

Agency Description Information Reference 

STATE (cont.) 

Illinois Analytical parameters and required 

quantitation limits for cobalt 

 Water 

BNA 2001 

Soil 

Method 

50 μg/L 

10 mg/kg 

6010A 

Indiana Constituent subject to assessment 

monitoring (cobalt [total and 

dissolved]) 

 BNA 2001 

Maine Screening standards for beneficial use 

(cobalt) 

5,875 mg/kg (dry weight) BNA 2001 

 Michigan Identification and listing of hazardous 

waste (cobalt) 

When in the form of 

100 microns or less 

BNA 2001 

 Minnesota Hazardous substance BNA 2001 

Cobalt metal, dust, and fumes

 (as Co) 

Cobalt carbonyl (as Co) 

Cobalt, elemental and inorganic 

compounds (as Co) 

Cobalt hydrocarbonyl (as Co)

Missouri Hazardous constituent (cobalt [total]) BNA 2001 

New Jersey Hazardous substance 

 Cobalt 

 BNA 2001 

 Cobalt carbonyl 

 Cobalt compounds 

New York Occupational lung disease; hard metal 

disease 

Cobalt BNA 2001 

Ohio Toxic release inventory BNA 2001 

Oklahoma Fertilizer labels and labeling; minimum 

percentage accepted for registration 

(cobalt) 

5x10-4 percent BNA 2001 
COBALT 289 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Stable Cobalt 

Agency Description Information Reference 

Oregon Toxic substance (cobalt) BNA 2001 

Pennsylvania Hazardous substance (cobalt and BNA 2001 

cobalt fumes) 

a

Cobalt compounds: includes cobalt(II) carbonate, cobalt(II) chloride, cobalt(II) nitrate, cobalt(II) oxide, cobalt(II,III)
 

oxide, cobalt(III) oxide, and cobalt(II) sulfate b

Group 2B: possibly carcinogenic to humans 

c

A3: confirmed animal carcinogen with unknown relevance to humans 

AAC = acceptable ambient concentrations; ACGIH = American Conference of Governmental Industrial Hygienists; 

ASIL = acceptable source impact level; BEI = biological exposure indices; BNA = Bureau of National Affairs; 

BPT = best practicable control technology; BTU = British thermal unit; CFR = Code of Federal Regulations; 

EL = emissions levels; EPA = Environmental Protection Agency; FDA = Food and Drug Administration; 

FSTRAC = Federal-State Toxicology and Risk Analysis Committee; HAP = hazardous air pollutant; 

IARC = International Agency for Research on Cancer; IDLH = immediately dangerous to life and health; 

IRIS = Integrated Risk Information System; MAC = maximum allowable concentration; NIOSH = National Institute for 

Occupational Safety and Health; NPDES = National Pollutant Discharge Elimination System; OEL = occupational 

exposure limit; OSHA = Occupational Safety and Health Administration; PEL = permissible exposure limit; 

PQL = practical quantitation limit; REL = recommended exposure limit; RfC = reference concentration; 

RfD = reference dose; STLC = soluble threshold limit concentrations; TAP = toxic air pollutant; TDS = total dissolved 

solids; TLV = threshold limit value; TRI = Toxic Release Inventory; TSCA = Toxic Substances Control Act; 

TTLC = total threshold limit concentrations; TWA = time-weighted averages; USC = United States Code
 
 

 

 

 

 

 

 

 

COBALT 290 

Table 8-2. 

8. REGULATIONS

Regulations and Guidelin

 AND ADVISORIES 

es Applicable to Radioactive Cobalt 

Agency Description Information Reference 

INTERNATIONAL 

Guidelines: 

IARC Carcinogenicity classification Group 1 (carcinogenic to 

humans) 

IARC 2001b 

ICRP Occupational dose limits; 

effective dose 

20 mSv per year, averaged 

over defined periods of 5 years 

ICRP 1991 

Annual equivalent dose 

Lens of the eye 

Skin 

150 mSv 

500 mSv 

Hands and feet 500 mSv 

General population dose limits; 

effective dose 

1 mSv in a year ICRP 1991 

Annual equivalent dose 

Lens of eye 

Skin 

15 mSv 

50 mSv 

WHO Drinking water quality No data 

NATIONAL 

Regulations and 

Guidelines: 

a. Air 

ACGIH All radiation exposures must 

be kept as low as reasonably 

achievable 

 ACGIH 2000

 Effective dose ACGIH 2000 

Any single year 

Averaged over 5 years 

50 mSv 

20 mSv per year 

Annual equivalent dose 

Lens of the eye 

 Skin 

150 mSv 

500 mSv 

Hands and feet 500 mSv 

Embryo-fetus exposures once 

the pregnancy is known 

Monthly equivalent dose 

Dose to the surface of 

0.5 mSv 

2 mSv for the remainder of the 

women’s abdomen (lower 

trunk) 

Intake of radionuclide 

pregnancy 

1/20 of the ALI 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

COBALT 291 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Cobalt 

Agency Description Information Reference 

NATIONAL (cont.)

 DOE Radiation standards DOE 2000 

 Inhalation DAC (μCi/mL) 55Co 

56Co 

57Co 

58mCo 

58Co 

60mCo 

60Co 

61Co 

62mCo 

Class Wa 

1x10-6 

1x10-7 

1x10-6 

4x10-5 

5x10-7 

2x10-3 

7x10-8 

3x10-5 

7x10-5 

Class Yb 

1x10-6 

8x10-8 

3x10-7 

3x10-5 

3x10-7 

1x10-3 

1x10-8 

2x10-5 

7x10-5 

10CFR835 

Appendix A 

Radiation standards for air 1x10-3 DOE 2000 

immersion DACc (μCi/mL) for 

60mCo 

10CFR835 

Appendix C 

NIOSH REL No data 

USNRC Effluent concentrations—air 

55Co 

Class Wd 

Class Ye 

56Co 

Class Wd 

Class Ye 

57Co 

Class Wd 

Class Ye 

58Co 

Class Wd 

Class Ye 

58mCo 

Class Wd 

Class Ye 

60Co 

Class Wd 

Class Ye 

60mCo 

Class Wd 

Class Ye 

61Co 

Class Wd 

Class Ye 

62mCo 

Class Wd 

Class Ye 

ALI (μCi/mL) 

4x10-9 

4x10-9 

4x10-10 

3x10-10 

4x10-9 

9x10-10 

2x10-9 

1x10-9 

1x10-7 

9x10-8 

2x10-10 

5x10-11 

6x10-6 

4x10-6 

9x10-8 

8x10-8 

2x10-7 

2x10-7 

USNRC 2001k 

10CFR20 

Appendix B 

Table 2 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

COBALT	 292 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Cobalt 

Agency Description Information	 Reference 

NATIONAL (cont.)

 USNRC Occupational values 

Inhalation 

55Co 

Class Wd 

Class Ye 

56Co 

Class Wd 

Class Ye 

57Co 

Class Wd 

Class Ye 

58Co 

Class Wd 

Class Ye 

58mCo 

Class Wd 

Class Ye 

60Co 

Class Wd 

Class Ye 

60mCo 

Class Wd 

Class Ye 

6

1Co 

Class Wd 

Class Ye 

62mCo 

Class Wd 

Class Ye 

OSHA Safety and health regulations 

for construction—ionizing 

radiation 

Toxic and hazardous 

substances—ionizing radiation

b. Water 

EPA Drinking water standards 

Beta particle and photon 

activity (formerly man-made 

radionuclides)

 MCL 

Caner risk at 10-4 

Gross alpha particle activity 

MCL 

Caner risk at 10-4 

ALI (μCi) 

3x103 

3x103 

3x102 

2x102 

3x103 

7x102 

1x103 

7x102 

9x104 

6x104 

2x102 

3x101 

4x106 

3x106 

6x104 

6x104 

2x105 

2x105 

4 mrem 

4 mrem/year 

15 pCi/L 

15 pCi/L 

USNRC 2001k 

10CFR20 

DAC (μCi/mL) Appendix B 

1x10-6 Table 1 

1x10-6 

1x10-7 

8x10-8 

1x10-6 

3x10-7 

5x10-7 

3x10-7 

4x10-5 

3x10-5 

7x10-8 

1x10-8 

2x10-3 

1x10-3 

3x10-5 

2x10-5 

7x10-5 

6x10-5 

 OSHA 2001e 

29CFR1926.53 

 OSHA 2001d 

29CFR1910.1096 

EPA 2000 

Carcinogenic classification Group A (human carcinogen) 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

COBALT	 293 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Cobalt 

Agency Description Information	 Reference 

NATIONAL (cont.)

 USNRC Effluent concentrations 

 Water 

55Co 

Class Wd 

56Co 

Class Wd 

57Co 

Class Wd 

58Co 

Class Wd 

58mCo 

Class Wd 

60Co 

Class Wd 

60mCo 

Class Wd 

61Co 

Class Wd 

62mCo 

Class Wd 

Releases to sewers—monthly 

average concentration 55Co 

Class Wd 

56Co 

Class Wd 

57Co 

Class Wd 

58Co 

Class Wd 

58mCo 

Class Wd 

60Co 

Class Wd 

60mCo 

Class Wd 

61Co 

Class Wd 

62mCo 

Class Wd 

c. Food and Drug 

FDA Ionizing radiation for the 

treatment of poultry feed and 

poultry feed ingredients 

(energy sources ) 

 Requirements regarding 

certain radioactive drugs for 

58Co or 60Co 

ALI (μCi/mL) 

2x10-5 

6x10-6 

6x10-5 

2x10-5 

8x10-4 

3x10-6 

2x10-2 

3x10-4 

7x10-4 

ALI (μCi/mL) 

2x10-4 

6x10-5 

6x10-4 

2x10-4 

8x10-3 

3x10-5 

2x10-1 

3x10-3 

7x10-3 

Ioninzing radiation is limited to 

gamma rays from sealed units 

of 60CO 

Labeled cyanocobalamin for 

use in intestinal absorption 

studies 

USNRC 2001k 

10CFR20 

Appendix B 

Table 2 

USNRC 2001k 

10CFR20 

Appendix B 

Table 3 

FDA 1999 

21CFR579.40 

FDA 2000d 

21CFR310.503(c) 
 

 

COBALT 294 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Cobalt 

Agency Description Information Reference 

NATIONAL (cont.)

FDA Sources of radiation used for FDA 2000c 

inspection of food, packaged 

food, and controlling food 

processing 

21CFR179.21 

(a)(2) 

d. Other 

DOE Values for establishing sealed 

radioactive source 

DOE 2000 

10CFR835 

accountability and radioactive 

material posting and labeling 

requirements 56Co 

Activity (μCi) 

4.0x101 

Appendix E 

57Co 2.3x102 

58Co 1.4x102 

60Co 1.8x101 

DOT Activity values (Ci) 55Co 

A1 

13.5 

A2 

13.5 

DOT 2001a 

49CFR173.435 

56Co 8.11 8.11 Table 

57Co 216 216 

58mCo 1080 1080 

58Co 

60Co 

27.0 

10.8 

27.0 

10.8 

Superfund, reportable quantity 

(Ci) (pounds) 55Co 10 

DOT 2001b 

49CFR172.101 

Appendix A 56Co 10 Table 2 

57Co 

58Co 

100 

10 

58mCo 

60Co 

1,000 

10 

60mCo 

61Co 

62mCo 

1,000 

1,000 

1,000 

EPA Carcinogenicity classification 

RfC 

No data IRIS 2000 

RfD 

Annual possession quantities 

for environmental compliance 

(Ci/year) 56Co 

Solid 

2.3 

Gas 

2.3x10-6 

Liquid/ 

Powder 

2.3x10-3 

EPA 2001a 

40CFR61 

Appendix E 

Table 1 

57Co 1.8x104 1.8x10-2 1.8x101 

58Co 2.5x10 2.5 -6 2.5x10-3 

58mCo 2.3x10 2.3 -6 2.3x10-3 

60Co 4.6x104 4.6x10-2 4.6x101 

60mCo 7.0x106 7.0 7.0x103 

61Co 9.8x105 9.8x10-1 9.8x102 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

COBALT 295 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Cobalt 

Agency Description Information Reference 

NATIONAL (cont.)

EPA Concentration levels for EPA 2001a 

environmental compliance 

(Ci/m3

) 56Co 1.8x10-13 

40CFR61 

Appendix E 

Table 2 

57Co 1.3x10-12 

58Co 6.7x10-13 

58mCo 1.2x10-10 

60Co 1.7x10-14 

60mCo 4.3x10-9 

61Co 4.5x10-9 

 Carcinogenicity—slope factors EPA 2002 

Lifetime risk per pCi—

 ingestion 

Water 

EPA 2002 

57Co 1.04x10-12 

58mCo 2.95x10-12 

58Co 1.26x10-13 

60Co 1.57x10-11 

Lifetime risk per pCi—

 ingestion 

Food 

EPA 2002 

57Co 1.49x10-12 

58mCo 4.18x10-12 

58Co 1.83x10-13 

60Co 2.23x10-11 

Lifetime risk per pCi—

 ingestion 

Soil 

EPA 2002 

57Co 2.78x10-12 

58mCo 7.44x10-12 

58Co 3.47x10-13 

60Co 4.03x10-11 

Lifetime risk per pCi—

 inhalation 

EPA 2002 

57Co 2.09x10-12 

58mCo 5.99x10-12 

58Co 6.88x10-14 

60Co 3.58x10-11 

External exposure— 

risk/year per pCi/g soil 57Co 3.55x10-7 

EPA 2002 

58mCo 4.48x10-6 

58Co 1.00x10-12 

60Co 1.24x10-5 
 

 

 

 

 

 

 

 

 

 

 

 

 

COBALT 296 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Cobalt 

Agency Description Information Reference 

NATIONAL (cont.)

 EPA Superfund, reportable 

quantities (Ci) (pounds) 55Co 

56Co 

10 

10 

EPA 2001i 

40CFR302.4 

Appendix B 

57Co 

58mCo 

58Co 

100 

1,000 

10 

60mCo 

60Co 

1,000 

10 

61Co 

62mCo 

1,000 

1,000 

NCRP Occupational exposures NCRP1993 

Effective dose limits 

Annual 50 mSv 

Cummulative 10 mSv x age 

Equivalent dose annual 

limits 150 mSv 

Lens of eye 

Skin, hands, and feet 

500 mSv 

Public exposures (annual) 

Effective dose limits, 1 mSv 

continuous or frequent 

exposure 

Effective dose limits, 5 mSv 

 infrequent exposures 

Equivalent dose limits 

Lens of eye 

Skin, hands, and feet 

15 mSv 

50 mSv 

Embryo and fetus 

 exposures (monthly) 

Effective dose limit 0.5 mSv 

USNRC Activity values for 

radionuclides (Ci) 55Co 

A1 

13.5 

A2 

13.5 

USNRC 2001a 

10CFR71 

56Co 8.11 8.11 

57Co 216 216 

58mCo 

58Co 

1080 

27.0 

1080 

27.0 

60Co 10.8 10.8 

Byproduct material listing; 

exempt concentrations 

Liquid and solid 

 concentration (μCi/mL2

) 57C 5x10-3 

USNRC 2001e 

10CFR30.70 

Schedule A 

58C 1x10-3 

60C 5x10-4 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

COBALT 297 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Cobalt 

Agency Description Information Reference 

NATIONAL (cont.)

USNRC Byproduct material listing (μCi) 58mCo 

58Co 

60Co 

Byproduct material listing (Ci) 58mCo 

58Co 

60Co 

Items containing byproduct 

material listing—60Co (μCi)

 Electron tubes 

Spark gap irradiators 

 Medical use—60Co as a 

source for brachytherapy 

 Occupational values—oral 

ingestion 55Co 

Class Wd 

56Co 

Class Wd 

Class Ye
 57Co 

Class Wd 

Class Ye
 58Co 

Class Wd 

Class Ye
 58mCo 

Class Wd 

60Co 

Class Wd 

Class Ye
 60mCo 

Class Wd 

St. wall 

61Co 

Class Wd 

Class Ye
 62mCo 

Class Wd 

St. wall 

10 

10 

1 

Column If Column IIg 

100 1.0 

1.0 0.01 

0.1 1x10-4 

1.0 

1.0 

As a sealed source in needles 

and applicator cells for topical, 

interstitial, and intracavitary 

treatment of cancer 

ALI (μCi) 

1x103 

5x102 

4x102 

8x103 

4x103 

2x103 

1x103 

6x104 

5x102 

2x102 

1x106 

1x106 

2x104 

2x104 

5x104 

4x104 

USNRC 2001b 

10CFR30.71 

Schedule B 

USNRC 2001c 

10CFR33.100 

Schedule A 

USNRC 2001d 

10CFR30.15(a)(8) 

USNRC 2001h 

10CFR35.400

USNRC 2001k 

10CFR20 

Appendix B 

Table 1 
 

 

 

 

COBALT	 298 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Cobalt 

Agency Description Information	 Reference 

NATIONAL (cont.)

USNRC Quantities of radioactive USNRC 2001g 

material requiring labeling 10CFR30 

(μCi) Appendix B 58mCo 10 

58Co 10 

60Co 1 

Quantities of licensed material USNRC 2001i 

requiring labeling (μCi) 10CFR20 

55Co Appendix C 56Co 100 

57Co 10 

58mCo 100 

58Co 1,000

60mCo 100 

60Co 1,000

61Co 1 

62mCo 1,000 

1,000 

Quantities of radioactive USNRC 2001j 

materials requiring need for an 10CFR30.72 

emergency plan Schedule C 

 Release fraction 0.001% 

 Quantity (Ci) 5,000 

 Radioactive waste USNRC 2001l 

classification 10CFR61.55 

Class A (Ci/m3) 

60Co ≤700 

Reports of individual USNRC 2001f 

monitoring—processing or 10CFR20.2206 

manufacturing for distribution, (a)(7) 

byproduct material in 

quantities exceeding 60Co (Ci) 1.0 

STATE 

Regulations and 

Guidelines: 

a. Air 

Alabama HAP—radionuclides BNA 2001 

California HAP—radionuclides BNA 2001 

 Hawaii HAP—radionuclides BNA 2001 

Illinois Toxic air contaminant— BNA 2001 

radionuclides 

 Kansas HAP—radionuclides BNA 2001 

Kentucky HAP—radionuclides BNA 2001 

 Minnesota HAP—radionuclides BNA 2001 

 Missouri HAP—radionuclides BNA 2001 
 

 

COBALT 299 

8. REGULATIONS AND ADVISORIES 

Table 8-2. Regulations and Guidelines Applicable to Radioactive Cobalt 

Agency Description Information Reference 

STATE (cont.)

 Nebraska HAP—radionuclides BNA 2001 

New York HAP—radionuclides BNA 2001 

Rhode Island HAP—radionuclides BNA 2001 

Wyoming HAP—radionuclides BNA 2001 

a

Class W: refers to the approximate length of retention in the pulmonary region which is 10–100 days for this class b

Class Y: refers to the approximate length of retention in the pulmonary region which is greater than 100 days for this 

class 

c

Air immersion DAC values: based on a stochastic dose limit of 5 rems (0.05 Sv) per year or a nonstochastic (organ) 

dose limit of 50 rems (0.5 Sv) per year 

d

Class W: all compounds except those given for Y 

e

Class Y: oxides, hydroxides, halides, and nitrates 

f

Column I: gas concentration 

g

Column II: liquid and solid concentration 

ACGIH = American Conference of Governmental Industrial Hygienists; ALI = annual limits on intake; BNA = Bureau 

of National Affairs; CFR = Code of Federal Regulations; DAC = derived air concentrations; DOE = Department of 

Energy; DOT = Department of Transportation; EPA = Environmental Protection Agency; FDA = Food and Drug 

Administration; IARC = International Agency for Research on Cancer; ICRP = International Commission on 

Radiological Protection; IRIS = Integrated Risk Information System; mSv = millisievert; NCRP = National Council on 

Radiation Protection; NIOSH = National Institute for Occupational Safety and Health; OSHA = Occupational Safety 

and Health Administration; PEL = permissible exposure limit; REL = recommended exposure limit; RfC = reference 

concentration; RfD = reference dose; TLV = threshold limit value; TWA = time-weighted averages; USNRC = U.S. 

Nuclear Regulatory Commission; WHO = World Health Organization 
COBALT 300 

8. REGULATIONS AND ADVISORIES 

cobalt (IRIS 2000). Slope factors have been derived for exposure to cobalt radioisotopes (EPA 2002). 

The slope factors for 60Co are 1.57x10-11, 2.23x10-11, and 4.03x10-11/pCi for ingestion of water, food, and 

soil, respectively. The slope factor for inhalation exposure is 3.58x10-11/pCi, and 1.24x10-5/year/pCi/g 

soil for external exposure. The slope factors for 58Co are 1.26x10-13,, 1.83x10-13,, and 3.47x10-13/pCi for 

ingestion of water, food, and soil, respectively. The slope factor for inhalation exposure is 6.88x10-14/pCi 

for inhalation exposure, and 1.00x10-12/year/pCi/g soil for external exposure. The slope factors for 58mCo 

are 2.95x10-12,, 4.18x10-12,, and 7.44x10-12/pCi for ingestion of water, food, and soil, respectively. The 

slope factor for inhalation exposure is 5.99x10-14/pCi for inhalation exposure, and 4.48x10-6/year/pCi/g 

soil for external exposure. The slope factors for 57Co are 1.04x10-12, 1.49x10-12, and 2.78x10-12/pCi for 

ingestion of water, food, and soil, respectively. The slope factor for inhalation exposure is 2.09x10-12/pCi 

for ingestion, and 3.55x10-7/year/pCi/g soil for external exposure. 
 

 

 

 

 

 

 

 

 

 

 

_______________________ 

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*Zhang C, Cai W, Li Y, et al. 1998a. Quantitative analysis of calcitonin gene-related peptide- and 

neuropeptide Y-immunoreactive nerve fibers in mesenteric blood vessels of rats irradiated with cobalt-60 

gamma rays. Radiat Res 149:19-26. 

*Zhang H, Van Den Berg CMG, Wollast R. 1990. The determination of interactions of cobalt (II) with 

organic compounds in seawater using cathodic stripping voltammetry. Mar Chem 28:285-300. 

Zhang Q, Kusaka Y, Sato K, et al. 1998b. Differences in the extent of inflammation caused by 

intratracheal exposure to three ultrafine metals: Role of free radicals. J Toxicol Environ Health, Part A 

53:423-438. 

Zhang Q, Kusaka Y, Sato K, et al. 1999. Tumor necrosis factor-alpha release from rat pulmonary 

leukocytes exposed to ultrafine cobalt: in vivo and in vitro studies. Environ Health Prev Med 4:87-91. 

*Zhao D, Feng G, Wu X, et al. 1985. Seizures induced by intraventricular microinjection of ionized 

cobalt in the rat - a new experimental model of epilepsy. Brain Res 342:323-329. 

*Zhong DZ, Pei C, Xiu-Qin L. 1996. Neurobehavioral study of prenatal exposure to hyperthermia 

combined with irradiation in mice. Neurotoxicol Teratol 18:(6)703-709. 

*Zhou X-Y, Dong J-C, Geng X-S, et al. 1986. Tritium beta-ray and 60Co gamma-ray caused dominant 

lethal mutation in mice. Chin Med J 99(5):420-423. 

*Ziegler EE, Edwards BB, Jensen RL, et al. 1978. Absorption and retention of lead by infants. Pediatr 

Res 12:29-34. 

*Zou W, Yan M, Xu W, et al. 2001. Cobalt chloride induces PC12 celss apoptosis through reactive 

oxygen species and accompanied by AP-1 activation. J. Neurosci Res 64 (6):646-53. 

*Zyball A. 1993. Radionuclides. In: Elvers B, Hawkins S, Russey W, et al., eds. Ullman's 

encyclopedia of industrial chemistry. New York, NY: VCH, Vol. A22, 553-560. 

*Zylicz E, Zablotna R, Geisler J, et al. 1975. Effects of DTPA on the deposition of 65Zn, 60Co and 144Ce 

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*Zylicz E, Zablotna R, Szot Z. 1976. Placental transfer of 60Co as a function of gestation age. 

Nukleonika 12:1204-1210. 
COBALT 397 

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. 
COBALT 398 

10. GLOSSARY 

Acute Exposure, Chemical—Exposure to a chemical for a duration of 14 days or less, as specified in the 

Toxicological Profiles. 

Acute Exposure, Radiation—The absorption of a relatively large amount of radiation (or intake of a 

radioactive material) over a short period of time. 

Acute Radiation Syndrome—The symptoms which taken together characterize a person suffering from 

the effects of intense radiation. The effects occur within hours or days. 

Ad libitum—Available in excess and freely accessible. 

Adsorption Coefficient (Koc)—The ratio of the amount of a chemical adsorbed per unit surface area or 

per unit weight of organic carbon of a specific particle size in the soil or sediment to the concentration of 

the chemical in solution at equilibrium. 

Adsorption Ratio (Kd)—See Distribution Coefficient. 

Alpha Particle—A positively charged particle ejected spontaneously from the nuclei of some radioactive 

elements. It is identical to a helium nucleus, i.e., 2 neutrons and two protons, with a mass number of 4 

and an electrostatic charge of +2. 

Alpha Track—The track of ionized atoms (pattern of ionization) left in a medium by an alpha particle 

that has traveled through the medium. 

Annihilation (Positron-Electron)—An interaction between a positive and a negative electron in which 

they both disappear; their rest mass, being converted into electromagnetic radiation (called annihilation 

radiation) with two 0.51 MeV gamma photons emitted at an angle of 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. 
 

 

 

COBALT 399 

10. GLOSSARY 

Attenuation—A process by which a beam from a source of radiation is reduced in intensity by 

absorption and scattering when passing through some material. 

Attenuation Coefficient—The fractional reduction in the intensity of a beam of radiation as it passes 

through an absorbing medium. It may be expressed as reduction per unit distance, per unit mass 

thickness, or per atom, and is called the linear, mass, or atomic attenuation coefficient, respectively. 

Auger Effect—The emission of an electron from the extranuclear portion of an excited atom when the 

atom undergoes a transition to a less excited state. 

Background Radiation—The amount of radiation to which a member of the general population is 

exposed from natural sources, such as terrestrial radiation from naturally occurring radionuclides in the 

soil, cosmic radiation originating from outer space, and naturally occurring radionuclides deposited in the 

human body. 

Becquerel (Bq)—International System of Units unit of activity and equals that quantity of radioactive 

material in which one transformation (disintegration) occurs per second (see Units). 

 Terabecquerel (TBq)—One trillion becquerel. 

 Gigabecquerel (GBq)—One billion becquerel. 

 Megabecquerel (MBq)—One million becquerel. 

 Kilobecquerel (kBq))—One thousand becquerel.

 Millibecquerel (mBq)—One-thousandth of a becquerel. 

 Microbecquerel (μBq)—One-millionth of a becquerel. 

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. 
 

 

COBALT 400 

10. GLOSSARY 

Body Burden, Radioactivity—The amount of radioactive material found in an animal or human body. 

Bone Seeker—Any compound or ion which migrates in the body and preferentially deposits into bone. 

Branching—The occurrence of two or more modes by which a radionuclide can undergo radioactive 

decay. For example, 214Bi can undergo alpha or beta minus decay, 64Cu can undergo beta minus, beta 

plus, or electron capture decay. An individual atom of a nuclide exhibiting branching disintegrates by one 

mode only. The fraction disintegrating by a particular mode is the "branching fraction" for that mode. 

The "branching ratio" is the ratio of two specified branching fractions (also called multiple 

disintegration). 

Bremsstrahlung—X rays that are produced when a charged particle accelerates (speeds up, slows down, 

or changes direction) in the strong field of a nucleus. 

Buildup Factor—The ratio of the radiation intensity, including both primary and scattered radiation, to 

the intensity of the primary (unscattered) radiation. 

Cancer Effect Level (CEL)—The lowest dose of chemical or radiation in a study, or group of studies, 

that produces significant increases in the incidence of cancer (or tumors) between the exposed population 

and its appropriate control. 

Capture, Electron—A mode of radioactive decay involving the capture of an orbital electron by its 

nucleus. Capture from a particular electron shell, e.g., K or L shells, is designated as "K-electron capture" 

or "L-electron capture." 

Capture, K-Electron—Electron capture from the K shell by the nucleus of the atom. Also loosely used 

to designate any orbital electron capture process. 

Carcinogen—A chemical or radiation that is capable of inducing cancer. 

Carcinoma—Malignant neoplasm composed of epithelial cells, regardless of their derivation. 

Case-Control Study—A type of epidemiological study which examines the relationship between a 

particular outcome (disease or condition) and a variety of potential causative agents (such as toxic 

chemicals). In a case-controlled study, a group of people with a specified and well-defined outcome is 

identified and compared to a similar group of people without outcome. 

Case Report—Describes a single individual with a particular disease or exposure. These may suggest 

some potential topics for scientific research but are not actual research studies. 

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. 
COBALT 401 

10. GLOSSARY 

Cohort Study—A type of epidemiological study of a specific group or groups of people who have had a 

common insult (e.g., exposure to an agent suspected of causing disease or a common disease) and are 

followed forward from exposure to outcome. At least one exposed group is compared to one unexposed 

group. 

Collective Dose—The sum of the individual doses received in a given period of time by a specified 

population from exposure to a specified source of radiation. Collective dose is expressed in units such as 

man-rem and person-sievert. 

Compton Effect—An attenuation process observed for x- or gamma radiation in which an incident 

photon interacts with an orbital electron of an atom to produce a recoil electron and a scattered photon 

whose energy is less than the incident photon. 

Containment—The confinement of a chemical or radioactive substance in such a way that it is prevented 

from being dispersed from its container or into the environment, or is released only at a specified rate. 

Contamination—Deposition of a stable or radioactive substance in any place where it is not desired. 

Cosmic Rays—High-energy particulate and electromagnetic radiations that originate outside the earth's 

atmosphere and interact with the atmosphere to produce a shower of secondary cosmic rays. 

Count (Radiation Measurements)—The external indication of a radiation-measuring device designed to 

enumerate ionizing events. It refers to a single detected event. The term “count rate” refers to the total 

number registered in a given period of time. The term is sometimes erroneously used to designate a 

disintegration, ionizing event, or voltage pulse. 

Counter, Gas-flow Proportional (GPC)—An instrument for detecting beta particle radiation. Beta 

particles are detected by ionization of the counter gas which results in an electrical impulse at an anode 

wire. 

Counter, Geiger-Mueller (GM counter)—Highly sensitive, gas-filled radiation-measuring device that 

detects (counts) individual photons or particulate radiation. 

Counter, Scintillation—The combination of a crystal or phosphor, photomultiplier tube, and associated 

circuits for counting light emissions produced in the phosphors by ionizing radiation. Scintillation 

counters generally are more sensitive than GM counters for gamma radiation. 

Counting, Cerenkov—Relatively energetic β-particles pass through a transparent medium of high 

refractive index and a highly-directional, bluish-white light ("Cerenkov" light) is emitted. This light is 

detected using liquid scintillation counting equipment. 

Cross-sectional Study—A type of epidemiological study of a group or groups which examines the 

relationship between exposure and outcome to a chemical or to chemicals at one point in time. 

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). 
COBALT 402 

10. GLOSSARY 

 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 

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: 
COBALT 403 

10. GLOSSARY 

[C] K = s 

d [C]w , Units = (L solution)/(kg solid), 

where [C]s is the concentration of the chemical associated with the solid phase in units of (mg)/(kg solid), 

and [C]w is the concentration of the chemical in the aqueous phase in units of (mg)/(L solution). As the 

magnitude of Kd decreases, the potential mobility of the chemical to groundwater systems increases and 

vice versa. 

Dose—A general term denoting the quantity of a substance, radiation, or energy absorbed. For special 

purposes it must be appropriately qualified. If unqualified, it refers to radiation absorbed dose. 

Absorbed Dose—The energy imparted to matter by ionizing radiation per unit mass of irradiated 

material at the place of interest. The unit of absorbed dose is the rad. One rad equals 100 ergs 

per gram. In SI units, the absorbed dose is the gray which is 1 J/kg (see Rad). 

Cumulative Dose (Radiation)—The total dose resulting from repeated or continuous exposures 

to radiation. 

Dose Assessment—An estimate of the radiation dose to an individual or a population group usually by 

means of predictive modeling techniques, sometimes supplemented by the results of measurement. 

Dose Equivalent (DE)—A quantity used in radiation safety practice to account for the relative biological 

effectiveness of the several types of radiation. It expresses all radiations on a common scale for 

calculating the effective absorbed dose. The NRC defines it as the product of the absorbed dose, the 

quality factor, and all other modifying factors at the location of interest. ICRP has changed its definition 

to be the product of the absorbed dose and the radiation weighting factor. (The unit of dose equivalent is 

the rem. In SI units, the dose equivalent is the sievert, which equals 100 rem.) 

Dose, Fractionation—A method of administering therapeutic radiation in which relatively small doses 

are given daily or at longer intervals. 

Dose, Protraction—A method of administering therapeutic radiation by delivering it continuously over a 

relatively long period at a low dose rate. 

Dose, Radiation—The amount of energy imparted to matter by ionizing radiation per unit mass of the 

matter, usually expressed as the unit rad, or in SI units, the gray. 100 rad'1 gray (Gy) (see Absorbed 

Dose). 

Committed Dose Equivalent (HT,50)—The dose equivalent to organs or tissues of reference (T) 

that will be received from an intake of radioactive material by an individual during the 50 years 

following the intake. 

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 
COBALT 404 

10. GLOSSARY 

that of a uniform whole body exposure. Effective dose is calculated as the sum of products of the 

equivalent dose and the tissue weighting factor (wT) for each tissue exposed. (E = ∑DT,R wR wT)). 

Effective Dose Equivalent (HE)—This dose type is limited to internal exposures and is the sum 

of the products of the dose equivalent to the organ or tissue (HT) and the weighting factors (wT) 

applicable to each of the body organs or tissues that are irradiated. (HE = ∑wT HT). 

Equivalent Dose—A dose quantity that places the biological effect of all radiation types on a 

common scale for calculating tissue damage. Alpha particles, for example, are considered to 

cause 20 times more damage than gamma rays. Equivalent dose is calculated as the sum of 

products of the average absorbed dose (in gray) in an organ or tissue (DT,R) from each type of 

radiation and the radiation weighting factor (wR) for that radiation (∑DT,R wR). 

External Dose—That portion of the dose equivalent received from radiation sources outside the 

body. 

Internal Dose—That portion of the dose equivalent received from radioactive material taken into 

the body. 

Limit—A permissible upper bound on the radiation dose. 

Maximum Permissible Dose (MPD)—The greatest dose equivalent that a person or specified 

part thereof shall be allowed to receive in a given period of time. 

Median Lethal Dose (MLD)—Dose of radiation required to kill, within a specified period 

(usually 30 days), 50% of the individuals in a large group of animals or organisms. Also called 

the LD50, or LD50/30 if for 30 days. 

Threshold Dose—The minimum absorbed dose that will produce a detectable degree of any 

given effect. 

Tissue Dose—Absorbed dose received by tissue in the region of interest, expressed in rad (see 

Dose, Gray, and Rad). 

Dose Rate—The amount of radiation dose delivered per unit time. Generically, the rate at which 

radiation dose is delivered to any material or tissue. 

Dose-Response Relationship—The quantitative relationship between the amount of exposure to a 

toxicant and the incidence of the adverse effects. 

Dosimetry—Quantification of radiation doses to cells, tissues, organs, individuals or populations 

resulting from radiation exposures. 

Early Effects (of radiation exposure)—Effects that appear within 60 days of an acute exposure. 

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). 
COBALT 405 

10. GLOSSARY 

Electron Volt—A unit of energy equivalent to the energy gained by an electron in passing through a 

potential difference of one volt. Larger multiple units of the electron volt are frequently used: keV for 

thousand or kilo electron volts; MeV for million or mega electron volts (eV). 1 eV=1.6x10-12 erg. 

Embryotoxicity and Fetotoxicity—Any toxic effect on the conceptus as a result of prenatal exposure to 

a chemical; the distinguishing feature between the two terms is the stage of development during which the 

insult occurred. The terms, as used here, include malformations and variations, altered growth, and in 

utero death. 

Energy—Capacity for doing work. Gravitationally, "potential energy" is the energy inherent in a mass 

because of its spatial relation to other masses. Chemically or radiologically, “potential energy” is the 

energy released when a chemical reaction or radiological transformation goes to completion. "Kinetic 

energy" is the energy possessed by a mass because of its motion (SI unit: joules): 

Binding Energy (Electron)—The amount of energy that must be expended to remove an 

electron from an atom. 

Binding Energy (Nuclear)—The energy represented by the difference in mass between the sum 

of the component parts and the actual mass of the nucleus. It represents the amount of energy 

that must be expended to break a nucleus into its component neutrons and protons. 

Excitation Energy—The energy required to change a system from its ground state to an excited 

state. Each different excited state has a different excitation energy. 

Ionizing Energy—The energy required to knock an electron out of an atom. The average energy 

lost by electrons or beta particles in producing an ion pair in air or in soft tissue is about 34 eV. 

Radiant Energy—The energy of electromagnetic radiation, such as radio waves, visible light, x 

and gamma rays. 

Enrichment, Isotopic—An isotopic separation process by which the relative abundances of the isotopes 

of a given element are altered, thus producing a form of the element that has been enriched in one or more 

isotopes and depleted in others. In uranium enrichment, the percentage of uranium-235 in natural 

uranium can be increased from 0.7% to >90% in a gaseous diffusion process based on the different 

thermal velocities of the constituents of natural uranium (234U, 235U, 238U) in the molecular form UF6. 

EPA Health Advisory—An estimate of acceptable drinking water levels for a chemical substance based 

on health effects information. A health advisory is not a legally enforceable federal standard, but serves 

as technical guidance to assist federal, state, and local officials. 

Epidemiology—Refers to the investigation of factors that determine the frequency and distribution of 

disease or other health-related conditions within a defined human population during a specified period. 

Equilibrium, Radioactive—In a radioactive series, the state which prevails when the ratios between the 

activities of two or more successive members of the series remains constant. 

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 
COBALT 406 

10. GLOSSARY 

the series disintegrate in unit time. This condition is never exactly attained, but is essentially 

established in such a case as 226Ra and its transformation series to stable 206Pb. The half-life of 

226Ra is about 1,600 years; of 222Rn, approximately 3.82 days, and of each of the subsequent 

members, a few minutes. After about a month, essentially the equilibrium amount of radon is 

present; then (and for a long time) all members of the series disintegrate the same number of 

atoms per unit time. At this time, the activity of the daughter is equal to the activity of the parent. 

Transient Equilibrium—If the half-life of the parent is short enough so the quantity present 

decreases appreciably during the period under consideration, but is still longer than that of 

successive members of the series, a stage of equilibrium will be reached after which all members 

of the series decrease in activity exponentially with the period of the parent. At this time, the 

ratio of the parent activity to the daughter activity is constant. 

Equilibrium, Electron—The condition in a radiation field where the energy of the electrons entering a 

volume equals the energy of the electrons leaving that volume. 

Excitation—The addition of energy to a system, thereby transferring it from its ground state to an excited 

state. Excitation of a nucleus, an atom, or a molecule can result from absorption of photons or from 

inelastic collisions with other particles. The excited state of an atom is an unstable or metastable state and 

will return to ground state by radiation of the excess energy. 

Exposure (Chemical)—Contact of an organism with a chemical or physical agent. Exposure is 

quantified as the amount of the agent available at the exchange boundaries of the organism (e.g., skin, 

lungs, gut) and available for absorption. 

Exposure (Radiation)—Subjection to ionizing radiation or to a radioactive material. For example, 

exposure in air is a measure of the ionization produced in air by x or gamma radiation; the sum of the 

electric charges on all ions of one sign produced in air when all electrons liberated by photons in a 

volume of air are completely stopped in air (dQ), divided by the mass of the air in the volume (dm). The 

unit of exposure in air is the roentgen, or coulomb per kilogram (SI units). One roentgen is equal to 

2.58x10-4 coulomb per kilogram (C/kg). 

Fission, Nuclear—A nuclear transformation characterized by the splitting of a nucleus into at least two 

other nuclei with emission of several neutrons, accompanied by the release of a relatively large amount of 

energy. 

Gamma Ray, Penetrating—Short wavelength electromagnetic radiation of nuclear origin. 

Genetic Effect of Radiation—Inheritable change, chiefly mutations, produced by the absorption of 

ionizing radiation by germ cells. Genetic effects have not been observed in any human population 

exposed at any dose level. 

Genotoxicity—A specific adverse effect on the genome of living cells that, upon the duplication of 

affected cells, can be expressed as a mutagenic, clastogenic or carcinogenic event because of specific 

alteration of the molecular structure of the genome. 

Gray (Gy)—SI unit of absorbed dose, 1 J/kg. One gray equals 100 rad (see Units). 

Half-life, Effective—See Half-Time, Effective. 
 

 

COBALT 407 

10. GLOSSARY 

Half-life, Radioactive—Time required for a radioactive substance to lose 50% of its activity by decay. 

Each radio-nuclide has a unique physical half-life. Known also as physical half-time and symbolized as 

Tr or Trad. 

Half-time, Biological—Time required for an organ, tissue, or the whole body to eliminate one-half of any 

absorbed substance by regular processes of elimination. This is the same for both stable and radioactive 

isotopes of a particular element, and is sometimes referred to as half-time, symbolized as tbiol or Tb. 

Half-time, Effective—Time required for a radioactive element in an organ, tissue, or the whole body to 

be diminished 50% as a result of the combined action of radioactive decay and biological elimination, 

symbolized as Te or Teff. 

Biological half-time × Radioactive half-life Effective half-time = Biological half-time + Radioactive half-life 

Immediately Dangerous to Life or Health (IDLH)—The maximum environmental concentration of a 

contaminant from which one could escape within 30 minutes without any escape-impairing symptoms or 

irreversible health effects. 

Immunologic Toxicity—The occurrence of adverse effects on the immune system that may result from 

exposure to environmental agents such as chemicals. 

Immunological Effects—Functional changes in the immune response. 

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 
 

 

COBALT 408 

10. GLOSSARY 

rays. (2) In counter tubes: the total ionization produced by incident radiation without gas 

amplification. 

Specific Ionization—Number of ion pairs per unit length of path of ionizing radiation in a 

medium; e.g., per centimeter of air or per micrometer of tissue. 

Total Ionization—The total electric charge of one sign on the ions produced by radiation in the 

process of losing its kinetic energy. For a given gas, the total ionization is closely proportional to 

the initial ionization and is nearly independent of the nature of the ionizing radiation. It is 

frequently used as a measure of absorption of radiation energy. 

Ionization Density—Number of ion pairs per unit volume. 

Ionization Path (Track)—The trail of ion pairs produced by an ionizing particle in its passage through 

matter. 

Ionizing Radiation—Any radiation capable of knocking electrons out of atoms and producing ions. 

Examples: alpha, beta, gamma and x rays, and neutrons. 

Isobars—Nuclides having the same mass number but different atomic numbers. 

Isomers—Nuclides having the same number of neutrons and protons but capable of existing, for a 

measurable time, in different quantum states with different energies and radioactive properties. 

Commonly the isomer of higher energy decays to one with lower energy by the process of isomeric 

transition. 

Isotopes—Nuclides having the same number of protons in their nuclei, and hence the same atomic 

number, but differing in the number of neutrons, and therefore in the mass number. Identical chemical 

properties exist in isotopes of a particular element. The term should not be used as a synonym for nuclide 

because isotopes refer specifically to different nuclei of the same element. 

 Stable Isotope—A nonradioactive isotope of an element. 

Joule—The S.I. unit for work and energy. It is equal to the work done by raising a mass of one newton 

through a distance of one meter (J = Nm), which corresponds to about 0.7 ft-pound. 

Kerma (k)—A measure of the kinetic energy transferred from gamma rays or neutrons to a unit mass of 

absorbing medium in the initial collision between the radiation and the absorber atoms. The SI unit is 

J/kg. The special name of this unit is the rad (traditional system of units) or Gray (SI). 

Labeled Compound—A compound containing one or more radioactive atoms intentionally added to its 

structure. By observations of radioactivity or isotopic composition, this compound or its fragments may 

be followed through physical, chemical, or biological processes. 

Late Effects (of radiation exposure)—Effects which appear 60 days or more following an acute 

exposure. 

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. 
COBALT 409 

10. GLOSSARY 

Lethal Concentration(Lo) (LCLo)—The lowest concentration of a chemical in air that has been reported 

to have caused death in humans or animals. 

Lethal Concentration(50) (LC50)—A calculated concentration of a chemical in air to which exposure for 

a specific length of time is expected to cause death in 50% of a defined experimental animal population 

within a specified time, usually 30 days. 

Lethal Dose(Lo) (LDLo)—The lowest dose of a chemical introduced by a route other than inhalation that is 

expected to have caused death in humans or animals within a specified time, usually 30 days. 

Lethal Dose(50) (LD50)—The dose of a chemical which has been calculated to cause death in 50% of a 

defined experimental animal population. 

Lethal Time(50) (LT50)—A calculated period of time within which a specific concentration of a chemical 

is expected to cause death in 50% of a defined experimental animal population. 

Linear Energy Transfer (LET)—A measure of the energy that a charged particle transfers to a material 

per unit path length. 

Average LET—The energy of a charged particle divided by the length of the path over which it 

deposits all its energy in a material. This is averaged over a number of particles. 

High-LET—Energy transfer characteristic of heavy charged particles such as protons and alpha 

particles where the distance between ionizing events is small on the scale of a cellular nucleus. 

Low-LET—Energy transfer characteristic of light charged particles such as electrons produced 

by x and gamma rays where the distance between ionizing events is large on the scale of a 

cellular nucleus. 

Lowest-Observed-Adverse-Effect Level (LOAEL)—The lowest dose of chemical in a study, or group 

of studies, that produces statistically or biologically significant increases in frequency or severity of 

adverse effects between the exposed population and its appropriate control. 

Lung Clearance Class (fast, F; medium, M; slow, S)—A classification scheme for inhaled material 

according to its rate of clearance from the pulmonary region of the lungs to the blood and the 

gastrointestinal tract. 

Lymphoreticular Effects—Represent morphological effects involving lymphatic tissues such as the 

lymph nodes, spleen, and thymus. 

Malformations—Permanent structural changes that may adversely affect survival, development, or 

function. 

Mass Numbers (A)—The number of nucleons (protons and neutrons) in the nucleus of an atom. 

Minimal Risk Level—An estimate of daily human exposure to a substance that is likely to be without an 

appreciable risk of adverse noncancerous effects over a specified duration of exposure. 
COBALT 410 

10. GLOSSARY 

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. 

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. 
COBALT 411 

10. GLOSSARY 

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. 

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). 
 

 

 

COBALT 412 

10. GLOSSARY 

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." 

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). 
COBALT 413 

10. GLOSSARY 

Radiation, Monoenergetic—Radiation of a given type in which all particles or photons originate 

with and have the same energy. 

Radiation, Scattered—Radiation which during its passage through a substance, has been 

deviated in direction. It may also have been modified by a decrease in energy. 

Radiation, Secondary—A particle or ray that is produced when the primary radiation interacts 

with a material, and which has sufficient energy to produce its own ionization, such as 

bremsstrahlung or electrons knocked from atomic orbitals with enough energy to then produce 

ionization (see Delta Rays). 

Radiation Weighting Factor (also called Quality Factor)—In radiation protection, a factor (1 for xrays, gamma rays, beta particles; 20 for alpha particles) weighting the absorbed dose of radiation of a 

specific type and energy for its effect on tissue. 

Radioactive Material—Material containing radioactive atoms. 

Radioactivity—Spontaneous nuclear transformations that result in the formation of new elements. These 

transformations are accomplished by emission of alpha or beta particles from the nucleus or by the 

capture of an orbital electron. Each of these reactions may or may not be accompanied by a gamma 

photon. 

Radioactivity, Artificial—Man-made radioactivity produced by particle bombardment or 

nuclear fission, as opposed to naturally occurring radioactivity. 

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. 
COBALT 414 

10. GLOSSARY 

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). 

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. 
COBALT 415 

10. GLOSSARY 

Sievert (Sv)—The SI unit of any of the quantities expressed as dose equivalent. The dose equivalent in 

sieverts is equal to the absorbed dose, in gray, multiplied by the quality factor (1 sievert equals 100 rem). 

The sievert is also the SI unit for effective dose equivalent, which is the sum of the products of the dose 

equivalent to each organ or tissue and its corresponding tissue weighting factor. 

Specific-Activity—Radioactivity per unit mass of a radionuclide, expressed, for example, as Ci/gram or 

Bq/kilogram. 

Specific Energy—The actual energy per unit mass deposited per unit volume in a small target, such as 

the cell or cell nucleus, as the result of one or more energy-depositing events. This is a stochastic 

quantity as opposed to the average value over a large number of instance (i.e., the absorbed dose). 

Standardized Mortality Ratio (SMR)—A ratio of the observed number of deaths and the expected 

number of deaths in a specific standard population. 

Stochastic Effect—A health effect that occurs randomly and for which the probability of the effect 

occurring, rather than its severity, is assumed to be a linear function of dose without a threshold (also 

called a nondeterministic effect). 

Stopping Power—The average rate of energy loss of a charged particle per unit thickness of a material or 

per unit mass of material traversed. 

Surface-seeking Radionuclide—A bone-seeking internal emitter that deposits and remains on the bone 

surface for a long period of time, although it may eventually diffuse into the bone mineral. This contrasts 

with a volume seeker, which deposits more uniformly throughout the bone volume. 

Target Organ Toxicity—This term covers a broad range of adverse effects on target organs or 

physiological systems (e.g., renal, cardiovascular) extending from those arising through a single limited 

exposure to those assumed over a lifetime of exposure to a chemical. 

Target Theory (Hit Theory)—A theory explaining some biological effects of radiation on the basis that 

ionization, occurring in a discrete volume (the target) within the cell, directly causes a lesion which 

subsequently results in a physiological response to the damage at that location. One, two, or more "hits" 

(ionizing events within the target) may be necessary to elicit the response. 

Teratogen—A chemical that causes birth defects. 

Threshold Limit Value (TLV®)—The maximum concentration of a substance to which most workers 

can be exposed without adverse effect. TLV is a term used exclusively by the ACGIH. Other terms used 

to express similar concepts are the MAC (Maximum Allowable Concentration) and PEL (Permissible 

Exposure Limits). 

Time-Weighted Average (TWA)—An allowable exposure concentration averaged over a normal 8-hour 

workday or 40-hour workweek. 
COBALT 416 

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. 
 

 

 

COBALT 417 

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. 

COBALT 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 
COBALT 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. 
 

 

 

COBALT A-3 

APPENDIX A 

MINIMAL RISK LEVEL (MRL) WORKSHEET 

Chemical Name: Cobalt 

CAS Number: 10026-24-1 

Date: March 2004 

Profile Status: Final 

Route: [x] Inhalation [ ] Oral 

Duration: [ ] Acute [ ] Intermediate [x] Chronic 

Key to figure: 26 

Species: human 

Minimal Risk Level: 1x10-4 [ ] mg/kg/day [ ] ppm [x] mg/m3 

Reference: 

Nemery B, Casier P, Roosels D, et al. 1992. Survey of cobalt exposure and respiratory health in 

diamond polishers. Am Rev Respir Dis 145:610-616. 

Experimental design: 

Nemery et al. (1992) conducted a cross-sectional study of cobalt exposure and respiratory effects in 

diamond polishers. The study group was composed of 194 polishers working in 10 different workshops. 

In two of these workshops (#1, 2), the workers used cast iron polishing disks almost exclusively, and in 

the others, they used cobalt-containing disks primarily. The number of subjects from each workshop 

varied from 6 to 28 and the participation rate varied from 56 to 100%. The low participation in some 

workshops reflects the fact that only workers who used cobalt disks were initially asked to be in the study, 

rather than a high refusal rate (only eight refusals were documented). More than a year after the polishing 

workshops were studied, an additional three workshops with workers engaged in sawing diamonds, 

cleaving diamonds, or drawing jewelry were studied as an unexposed control group (n=59 workers). 

Subjects were asked to fill out a questionnaire regarding employment history, working conditions, 

medical history, respiratory symptoms, and smoking habits, to give a urine sample for cobalt 

determination, and to undergo a clinical examination and lung function tests. Both area air samples and 

personal air samples were collected (always on a Thursday). Sampling for area air determinations started 

2 hours after work began and continued until 1 hour before the end of the work day. Personal air samples 

were collected from the breathing zone of a few workers per workshop for four successive 1-hour periods. 

Air samples were analyzed for cobalt and iron. In addition, personal air samplers were used to sample the 

air 1 cm above the polishing disks. These samples were analyzed for the entire spectrum of mineral and 

metallic compounds. Air samples were not obtained at one of the polishing workshops (#4), but this 

workshop was reported to be almost identical to an adjoining workshop (#3) for which samples were 

obtained. Urinary cobalt levels were similar between workers in these two workshops, so exposure was 

considered to be similar as well. It is important to note that the study authors suggested that the available 

methods used for air sampling may have underestimated the exposure levels. 

There was a good correlation (R=0.92) between the results of area and personal air sampling, with area air 

sampling reporting lower concentrations than personal air samples in all workshops except one (#9) 

(Nemery et al. 1992). In this workshop, personal air samples appeared to be artificially low in 

comparison to area air samples and urinary cobalt levels of the workers. When this workshop was 

excluded, there was a good correlation (R=0.85–0.88) between urinary cobalt and cobalt in the air. Based 

on urinary cobalt levels, the concentration of cobalt expected in personal air samples from workshop #9 

was about 45 μg/m3

 (the mean value actually reported was 6 μg/m3). The polishing workshops were 

divided into two groups: those with low exposure to cobalt (#1–5, n=102) and those with high exposure to 
 

 

COBALT A-4 

APPENDIX A 

cobalt (#6–10, n=91). Mean cobalt exposure concentrations were 0.4, 1.6, and 10.2 μg/m3 by area air 

sampling and 0.4, 5.3, and 15.1 μg/m3

 by personal air sampling in the control, low-exposure, and highexposure groups, respectively. The inclusion of the apparently biased personal air samples from 

workshop #9 means that the reported mean cobalt exposure in the high-exposure group obtained by 

personal air sampling (15.1 μg/m3

) may be lower than the true value. Air concentrations of iron were 

highest in the two polishing workshops that used iron disks and the sawing workshop (highest value 

=62 μg/m3

), and were not correlated with cobalt levels. Analysis of samples taken near the disks showed 

the presence of cobalt, with occasional traces of copper, zinc, titanium, manganese, chromium, silicates, 

and silicon dioxide. No tungsten was detected. There is a possibility that some workers had previously 

been exposed to asbestos, since pastes containing asbestos had been used in the past to glue the diamonds 

onto holders. However, the degree of asbestos exposure had apparently been insufficient to produce 

functional impairment. The researchers considered cobalt to be the only relevant exposure. Smoking 

habits were similar in workers from the high-exposure, low-exposure, and control groups. Duration of 

exposure was not discussed. 

Effects noted in study and corresponding doses: 

Workers in the high-exposure group were more likely than those in the other groups to complain about 

respiratory symptoms; the prevalences of eye, nose, and throat irritation and cough, and the fraction of 

these symptoms related to work, were significantly increased in the high-exposure group (Nemery et al. 

1992). Workers in the high-exposure group also had significantly reduced lung function compared to 

controls and low-exposure group workers, as assessed by FVC (forced vital capacity), FEV1 (forced 

expiratory volume in 1 second), MMEF (forced expiratory flow between 25 and 75% of the FVC), and 

mean PEF (peak expiratory flow rate), although the prevalence of abnormal values did not differ 

significantly between exposure categories. Results in the low-exposure group did not differ from 

controls. Two-way analysis of variance was used to show that the effect on spirometric parameters in the 

high exposure group was present in both men and women. Women seemed to be affected more than men, 

but the interaction between exposure and sex was not significant. Smoking was found to exert a strong 

effect on lung function, but lung function level remained negatively correlated with exposure to cobalt, 

independently of smoking. 

Dose and end point used for MRL derivation: 

[x] NOAEL [ ] LOAEL 

Nemery et al. (1992) established a NOAEL of 0.0053 mg cobalt/m3

 for effects on pulmonary function 

(decreased values upon spirometric examination). 

Uncertainty Factors used in MRL derivation: 

[x] 1 [ ] 3 [ ] 10 (for use of a NOAEL) 

[x] 1 [ ] 3 [ ] 10 (for extrapolation from animals to humans) 

[ ] 1 [ ] 3 [x] 10 (for human variability) 

The chronic inhalation MRL for cobalt is derived as follows: 

MRL = NOAEL[ADJ] ÷ UF 

MRL = 0.0013 mg cobalt/m3

 ÷ 10 

MRL = 1x10-4 mg cobalt/m3 

Was a conversion used from ppm in food or water to a mg/body weight dose? No. 

Was a conversion used from intermittent to continuous exposure? If so, explain: 
COBALT A-5 

APPENDIX A 

0.0053 mg cobalt/m3 * (8 hours/24 hours) * (5 days/7 days) = 0.0013 mg cobalt/m3 continuous exposure. 

If an inhalation study in animals, list the conversion factors used in determining human equivalent dose: 

NA. 

Other additional studies or pertinent information which lend support to this MRL: 

Necrosis and inflammation of the respiratory tract epithelium (larynx, trachea, bronchioles, nasal 

turbinates) were reported in rats exposed to 19 mg cobalt/m3

 and mice exposed to 1.9 mg cobalt/m3 (and 

above) as cobalt sulfate over 16 days (NTP 1991). Exposure of rats and mice to cobalt as cobalt sulfate 

for 13 weeks resulted in adverse effects on all parts of the respiratory tract, with the larynx being the most 

sensitive part (NTP 1991). At concentrations of ≥0.11 mg cobalt/m3

, rats and mice had squamous 

metaplasia of the larynx. Histiocytic infiltrates in the lung were also reported at similar levels in both the 

rats and mice. In rats, chronic inflammation of the larynx was found at ≥0.38 mg cobalt/m3

, and more 

severe effects on the larynx, nose, and lung were reported at higher exposures. In mice, acute 

inflammation of the nose was found at ≥1.14 mg cobalt/m3

, and more severe effects on the larynx, nose, 

and lung were reported at higher exposures. 

Exposure of rats and mice to aerosols of cobalt (as cobalt sulfate) at concentrations from 0.11 to 1.14 mg 

cobalt/m3

 for 2 years resulted in a spectrum of inflammatory, fibrotic, and proliferative lesions in the 

respiratory tract of male and female rats and mice (NTP 1998). Squamous metaplasia of the larynx 

occurred in rats and mice at exposure concentrations of ≥0.11 mg cobalt/m3

, with severity of the lesion 

increasing with increased exposure concentration. Hyperplastic lesions of the nasal epithelium occurred 

in rats at concentrations of ≥0.11 mg cobalt/m3

, and in mice at concentrations of ≥0.38 mg cobalt/m3. 

Both sexes of rats had greatly increased incidences (>90% incidence) of alveolar lesions at all exposure 

levels, including inflammatory changes, fibrosis, and metaplasia. Similar changes were seen in mice at 

all exposure levels, though the changes in mice were less severe. 

Both studies by NTP (1991, 1998) failed to define a NOAEL, with the lowest concentration examined 

(0.11 mg/m3

) a LOAEL for a variety of respiratory effects. If an MRL were to be calculated based upon 

these studies, it would be as follows: 

Duration adjustment: 0.11 mg cobalt/m3

 * (6 h/24 h) * (5 d/7 d) = 0.020 mg cobalt/m3 continuous 

exposure. 

Calculation of human equivalent concentration: 

If fractional depositions in humans and animals are assumed to be equal, then: 

RDDR = VE(animal)/SET(animal) ÷ VE(human)/SET(human) = 0.24 m3

/day / 15 cm2 ÷ 20 m3/day / 200 cm2 

RDDR = 0.16 

LOAEL[HEC] = LOAEL[ADJ] * RDDR 

= 0.020 mg cobalt/m3

 * 0.16 = 0.0032 mg cobalt/m3 

To the LOAEL[HEC], an uncertainty factor of 300 (10 for use of a LOAEL, 3 for animal to human 

extrapolation, and 10 for human variability) to derive an MRL of 1x10-5 mg/m3

. This number is an order 

of magnitude lower than the number derived from the Nemery et al. (1992) data, reflecting the fact that it 

is derived from animal data, not from a human study, and is based on a LOAEL, not a NOAEL. As the 

Nemery et al. (1992) study was a well-performed study in humans that defined a NOAEL and LOAEL, it 

was selected as the basis for derivation of the MRL. 

Agency Contact (Chemical Manager): Obaid Faroon D.V.M., Ph.D. 
 

 

 

 

COBALT A-6 

APPENDIX A 

MINIMAL RISK LEVEL (MRL) WORKSHEET 

Chemical Name: Cobalt 

CAS Number: 10026-24-1 

Date: March 2004 

Profile Status: Final 

Route: [ ] Inhalation [x] Oral 

Duration: [ ] Acute [x] Intermediate [ ] Chronic 

Key to figure: 30 

Species: human 

Minimal Risk Level: 1x10-4 [x] mg/kg/day [ ] ppm [ ] mg/m3 

Reference: 

Davis, J.E. and Fields, J.P. 1958. Experimental production of polycythemia in humans by administration 

of cobalt chloride. Proc Soc Exp Biol Med 99:493-495. 

Experimental design: 

Six apparently normal men, ages 20–47, were administered a daily dose of cobalt chloride, administered 

as a 2% solution diluted in either water or milk, for up to 22 days. Five of the six received 150 mg cobalt 

chloride per day for the entire exposure period, while the sixth was started on 120 mg/day and later 

increased to 150 mg/day. Blood samples were obtained daily from free-flowing punctures of fingertips at 

least 2 hours after eating, and at least 15 hours after the last dosage of cobalt. Blood was analyzed for red 

blood cell counts, hemoglobin percentage, leukocyte counts, reticulocyte percentages, and thrombocyte 

counts. 

Effects noted in study and corresponding doses: 

Exposure to cobalt resulted in the development of polycythemia in all six subjects, with increases in red 

blood cell numbers ranging from 0.5 to 1.19 million (~16–20% increase above pre-treatment levels). 

Polycythemic erythrocyte counts returned to normal 9–15 days after cessation of cobalt administration. 

Hemoglobin levels were also increased by cobalt treatment, though to a lesser extent than the erythrocyte 

values, with increases of 6–11% over pretreatment values. In five of the six subjects, reticulocyte levels 

were elevated, reaching at least twice the pre-experiment values. Thrombocyte and total leukocyte counts 

did not deviate significantly from pretreatment values. 

Dose end point used for MRL derivation: 

[ ] NOAEL [x] LOAEL 

Davis and Fields (1958) identified a LOAEL of 150 mg cobalt chloride per day for increased levels of 

erythrocytes in volunteers. 150 mg cobalt chloride/day corresponds to ~1 mg Co/kg/day, assuming a 

reference body weight of 70 kg. Available animal studies, presented below, lend support to this LOAEL, 

having demonstrated LOAEL values within half an order of magnitude of that identified by Davis and 

Fields (1958). 

Uncertainty factors used in MRL derivation: 

[ ] 1 [ ] 3 [x] 10 (for use of a LOAEL) 
 

 

COBALT A-7 

APPENDIX A 

[x] 1 [ ] 3 [ ] 10 (for extrapolation from animals to humans) 

[ ] 1 [ ] 3 [x] 10 (for human variability) 

The intermediate oral MRL for cobalt is derived as follows: 

MRL = LOAEL ÷ UF 

MRL = 1 mg cobalt/kg-day ÷ 100 

MRL = 1x10-2 mg cobalt/kg-day 

Was a conversion factor used from ppm in food or water to a mg/body weight dose? No. 

Was a conversion used from intermittent to continuous exposure? If so, explain: No. 

If an inhalation study in animals, list conversion factors used in determining human equivalent dose: Not 

applicable. 

Other additional studies or pertinent information that lend support to this MRL: 

No other studies of the effect of intermediate oral cobalt exposure on erythrocyte levels in healthy human 

subjects were identified in a search of the literature. Treatment of pregnant women for 90 days with 0.5– 

0.6 mg cobalt/kg/day as cobalt chloride did not prevent the reduction in hematocrit and hemoglobin levels 

often found during pregnancy (Holly 1955). However, treatment of anephric patients (with resulting 

anemia) with 0.16–1.0 mg cobalt/kg/day daily as cobalt chloride for 3–32 weeks resulted in increased 

levels of circulating erythrocytes and a decreased need for transfusions (Duckham and Lee 1976b; Taylor 

et al. 1977). While these studies provide additional evidence that exposure to cobalt can increase 

erythrocyte levels in humans, the fact that the patients were anephric makes definitive interpretation of the 

results more difficult. 

Roche and Layrisse (1956) exposed volunteers to similar levels (150 mg CoCl2/day) of cobalt, and 

reported a reversible decrease in uptake of 131I by the thyroid. The decreased uptake is believed to result 

from cobalt blocking the organic binding of iodine (Paley et al. 1958). This observation adds support to 

the choice of effect level, as a similar exposure resulted in measurable effects in volunteers, though 

whether the changes in iodine uptake operate through the same mechanisms as the changes in erythrocyte 

numbers has not been determined. 

Stanley et al. (1947) exposed groups (n=4, 6 for controls) of 6 Sprague-Dawley rats to 0, 0.62, 2.5, or 

10 mg cobalt/kg/day (0, 2.5, 10, or 40 mg/kg-day of CoCl2@6H2O) in gelatin capsules for 8 weeks. Blood 

counts and hemoglobin levels were examined at the beginning of the experiment and at 2-week intervals. 

Rats exposed to 0.62 mg cobalt/kg-day showed no change in erythrocyte number. At 2.5 mg cobalt/kgday, a progressive increase in erythrocyte number was seen, increasing up to a maximum of 17% above 

pretreatment values on week 6. At the highest exposure level, a progressive increase in erythrocyte 

numbers was seen, reaching 29% above pretreatment values at 8 weeks of exposure. Statistical analyses 

of the group means were not provided, and the study provided only mean values of the measurements, 

precluding statistical analysis. However, if a 10% change is assumed to be an effect level, exposure to 

2.5 mg cobalt/kg-day was the LOAEL for this study, with a NOAEL of 0.62 mg cobalt/kg-day. 

Krasovskii and Fridyland (1971) exposed groups of rats to 0, 0.05, 0.5, or 2.5 mg Co/kg/day for up to 

7 months. In the 2.5 mg/kg-day group, a persistent increase in erythrocyte levels was seen. The increase 

was transient in the 0.5 mg/kg/day rats, and was not present in rats exposed to 0.05 mg/kg/day. However, 

numerical data were not presented and statistical significance was not reported. 
COBALT A-8 

APPENDIX A 

A number of other studies in animals have reported increases in erythrocyte levels following intermediate 

oral administration of cobalt compounds (see the LSE table for further details of these studies). However, 

the majority of them have considerable methodological limitations, including examination of either very 

high exposure levels or only one exposure level, limited reporting of results, or limited or no statistical 

analysis. 

Whether or not polycythemia, a condition wherein an excess of erythrocytes is produced, constitutes an 

adverse effect is open to interpretation. At the levels seen in the available studies, and in particular in the 

Davis and Fields (1958) study, the subjects would be expected to be asymptomatic. However, data on the 

long-term effects of elevated erythrocyte levels are not available. As such, this end point was considered 

an adverse effect as a health-protective assumption, and was utilized as a critical end point for MRL 

derivation. 

Agency Contact (Chemical Manager): Obaid Faroon D.V.M., Ph.D. 
 

COBALT A-9 

APPENDIX A 

MINIMAL RISK LEVEL (MRL) WORKSHEET 

Chemical name: Radioactive Cobalt 

CAS number: Multiple 

Date:March 2004 

Profile status: Final 

Route: [ ] Inhalation [ ] Oral [x] External 

Duration: [x] Acute [ ] Intermediate [ ] Chronic 

Species: Human 

Minimal Risk Level: 4 [ ] mg/kg/day [ ] ppm [ ] mg/m3

 [x] mSv (400 mrem) 

References: 

Schull WJ, Otake M, Yoshimaru H. 1988. Effect on intelligence test score of prenatal exposure to 

ionizing radiation in Hiroshima and Nagasaki: A comparison of the T65DR and DS86 dosimetry 

systems. Radiation Effects Research Foundation (RERF) Technical Report No. 3-88. Hirroshima, Japan. 

NTIS Report Number: DE89-906462. 

Burt C. 1966. The genetic determination of differences in intelligence: A study of monozygotic twins 

reared together and apart. Brit J Psychol 57(1&2):137-153. 

Experimental design: 

Schull et al. (1988) study: Schull et al. (1988) evaluated the quantitative effect of exposure to ionizing 

radiation on the developing fetal and embryonic human brain. The end point measured was changes in 

intelligence test scores. The effects on individuals exposed in utero to the atomic bombing of Hiroshima 

and Nagasaki were based on the original PE86 samples (n=1,759; data on available intelligence testing) 

and a clinical sample (n=1,598). The original PE86 sample included virtually all prenatally exposed 

individuals who received tissue-absorbed doses of 0.50 Gy or more. There were many more individuals 

in the dose range 0–0.49 Gy in the PE86 sample than in the clinical sample. The clinical sample does not 

include children prenatally exposed at distances between 2,000 and 2,999 m in Hiroshima and Nagasaki. 

Children exposed at greater distances or not present in the city were selected as controls. In 1955–1956, 

Tanaka-B (emphasis on word-sense, arithmetic abilities, and the like, which were associated with the 

more subtle processing of visual clues than their simple recognition and depended more on 

connectedness) and the Koga (emphasis on perception of spatial relationships) intelligence tests were 

conducted in Nagasaki and the Koga test in Hiroshima. 

Burt (1966) study: This study determined differences in intelligence in monozygotic twins reared 

together (n=95) and apart (n=53). All tests conducted in school consisted of (1) a group test of 

intelligence containing both non-verbal and verbal items, (2) an individual test (the London Revision of 

the Terman-Binet Scale) used primarily for standardization and for doubtful cases, and (3) a set of 

performance tests, based on the Pitner-Paterson tests and standardization. The methods and standard 

remained much the same throughout the study. Some of the reasons for separation of the twins were 

given as follows: death of the mother (n=9), unable to bring them up properly, mother's poor health 

(n=12), unmarried (n=6), and economic difficulties. The children were brought up by parents or foster 

parents (occupation ranged from unskilled to professional). IQ scores in the study group ranged from 

66 to 137. The standard deviation of the group of separated monozygotic twins was reported at 15.3 as 

compared to 15.0 of ordinary siblings. Twins brought up in different environments were compared with 

those brought up in similar circumstances. 
 

 

 

COBALT A-10 

APPENDIX A 

Effects noted in study and corresponding doses: 

Schull et al. (1986) study: No evidence of radiation-related effect on intelligence was observed among 

individuals exposed within 0–7 weeks after fertilization or in the 26th or subsequent weeks. The highest 

risk of radiation damage to the embryonic and fetal brain occurs 8–15-weeks after fertilization under both 

dosimetric systems. The regression of intelligence score on estimated DS86 uterine absorbed dose is 

linear with dose, and the diminution in intelligence score is 21–29 points per Gy for the 8–15-week group 

and 10–26 points per Gy for the 16–25-week group. The results for 8–15 weeks applies regardless 

whether or not the mentally retarded individuals were included. The cumulative distribution of test scores 

suggested a progressive shift downwards in individual scores with increasing exposure. The mean IQ 

scores decrease significantly and systematically with uterine or fetal tissue dose within the 8–15- and 

16–25-week groups. 

In summary, analysis of intelligence test scores at 10–11 years of age of individuals exposed prenatally 

showed that: 

•	 There is no evidence of a radiation-related effect on intelligence scores among those individuals 

exposed within 0–7 weeks of fertilization or in the 26th week of gestation and beyond; 

•	 The cumulative distribution of test scores suggests a progressive shift downwards in intelligence 

scores with increasing exposure to ionizing radiation (dose-response relationship). 

•	 The most sensitive group was the 8–15 weeks exposure group. The regression in intelligence 

scores was found to be linear, with 1 Gy dose resulting in a 21–29 point decline in intelligence 

scores. 

•	 There was no indication of groups of individuals with differing sensitivities to radiation. 

Burt (1966) study: The average intelligence of the twins measured on a conventional IQ scale (SD=15) 

was 97.8 for the separated monozygotes, 98.1 for monozygotes brought up together, 99.3 for the 

dizygotes as compared with 100.2 for the siblings, and 100.0 for the population as a whole. The 

difference of 0.3 IQ point between the separated and unseparated identical twins is considered a NOAEL 

for this study. 

Dose endpoint used for MRL derivation: 

[x] NOAEL [ ] LOAEL 0.3 IQ point reduction in twins, between those raised together and those raised 

apart. 

Uncertainty factors (UF) used in MRL derivation: 

[x] 1 [ ] 3 [ ] 10 (for use of a NOAEL) 

[x] 1 [ ] 3 [ ] 10 (for extrapolation from animals to humans) 

[ ] 1 [x] 3 [ ] 10 (for human variability/sensitive population) 

Was a conversion factor used from ppm in food or water to a mg/body weight dose? If so, explain: No. 

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? No. 
COBALT A-11 

APPENDIX A 

Other additional studies or pertinent information that lend support to this MRL: 

Husen (1959) reported a study involving 269 pairs of Swedish monozygotic (identical) twins where the 

intrapair IQ difference was 4 IQ points for a combination of twins raised together and apart. This is 

somewhat lower than the value of 7 IQ points for identical twins raised apart, and just larger than the 

range of IQ scores for Washington, DC children repetitively tested (Jacobi and Glauberman 1995). 

Supporting evidence for the acute MRL is provided by Jacobi and Glauberman (1995). Children in the 

1st, 3rd, and 5th grades born in Washington, DC were tested, and average IQ levels of 94.2, 97.6, and 94.6, 

respectively, were reported. The range of 3.4 IQ points is considered to be a LOAEL for this study, 

which, if used for MRL derivation, would yield an MRL of 0.004 Sv (3.4 IQ points x 1 Sv/25 IQ points 

÷ 30 [10 for use of a LOAEL and 3 for a sensitive population]). 

Additional supporting evidence for the acute MRL is provided by Berger et al. 1997, in a case study of 

accidental radiation injury to the hand. A Mexican engineer suffered an accidental injury to the hand 

while repairing an x-ray spectrometer. The day after the accident, his symptoms included a tingling 

sensation and itching in the index and middle fingers. On days 4 and 7, a "pinching" sensation, swelling, 

and slight erythema were observed. By day 7, the tip of his index fingers was erythematous and a large 

blister developed with swelling on other fingers. On day 10, examination by a physician showed that the 

lesions had worsened and the fingers and palms were discolored. On day 10, he was admitted to the 

hospital where hyperbaric oxygen therapy was administered without success. One month after the 

accident, the patient entered the hospital again with pain, discoloration, and desquamation of his hand. 

Clinical examination showed decreased circulation in the entire hand, most notably in the index and 

middle finger. Total white blood count decreased to 3,000/μL (normal range 4,300–10,800/μL). 

Cytogenic studies of peripheral blood lymphocytes revealed four dicentrics, two rings, and eight 

chromosomal fragments in the 300 metaphases studied. The estimated whole body dose was reported to 

be 0.382 Gy (38.2 rad). This dose is a potential LOAEL for acute ionizing radiation and would yield an 

MRL of 0.004 Sv (0.38 Sv ÷100 [10 for use of LOAEL and 10 for sensitive human population]). 

The USNRC set a radiation exposure limit of 0.5 rem (50 mSv) for pregnant working women over the full 

gestational period (USNRC 1991). For the critical gestational period of 8–15 weeks, ATSDR believes 

that the conservative acute MRL of 4 mSv is consistent with the USNRC limit and could be applied to 

either acute (0–14-day) or intermediate (15–365-day) exposure periods. 

Calculations 

Given: 0.3 IQ point is a NOAEL. A 1 Sv dose results in a 25 IQ point reduction (range=21–29 points; 

mean=25) and provides a conversion factor from IQ prediction to radiation dose. Assume that the 

radiation dose and the subsequent reduction in IQ is a linear relationship. 

MRL = NOAEL x CF ÷ UF 

MRL = 0.3 x 1/25 ÷ 3 

MRL = 0.004 Sv = 4 mSv (400 mrem) 

Agency Contact (Chemical Manager): Obaid Faroon D.V.M., Ph.D. 
 

 

 

 

 

 

COBALT A-12 

APPENDIX A 

MINIMAL RISK LEVEL (MRL) WORKSHEET 

Chemical Name: Radioactive Cobalt 

CAS Number: Multiple 

Date: March 2004 

Profile Status: Final 

Route: [ ] Inhalation [ ] Oral [X] External 

Duration: [ ] Acute [ ] Intermediate [X] Chronic 

Species: Human 

Minimal Risk Level: 1 [ ] mg/kg/day [ ] ppm [ ] mg/m3

 [X] mSv/year (100 mrem/year) 

Reference: BEIR V. 1990. Health effects of exposure to low levels of ionizing radiation. Committee on 

the Biological Effects of Ionizing Radiations, National Research Council. National Academy Press. 

Washington, DC. 

Experimental design: Not applicable 

Effects noted in study and corresponding doses: No individual studies were identified that could be used 

to base a chronic-duration external exposure MRL that did not result in a cancer-producing end point. 

However, two sources of information were identified that did provide doses of ionizing radiation that 

have not been reported to be associated with detrimental effects (NOAELs). These sources provide 

estimates of background levels of primarily natural sources of ionizing radiation that have not been 

implicated in producing cancerous or noncancerous toxicological endpoints. BEIR V states that the 

average annual effective dose to the U.S. population is 3.6 mSv/year. A total annual effective dose 

equivalent of 3.6 mSv (360 mrem)/year to members of the U.S. population is obtained mainly by 

naturally occurring radiation from external sources, medical uses of radiation, and radiation from 

consumer products. The largest contribution (82%) is from natural sources, two-thirds of which is from 

naturally occurring radon and its decay products. Specific sources of this radiation are demonstrated in 

Table A-1. 

The annual dose of 3.6 mSv per year has not been associated with adverse health effects or increases in 

the incidences of any type of cancers in humans or other animals. 

Dose and end point used for MRL derivation: 3.6 mSv/year 

[X] NOAEL [ ] LOAEL 3.6 mSv/year 

Uncertainty Factors used in MRL derivation: 

[X] 1 [ ] 3 [ ] 10 (for use of a NOAEL) 

[X] 1 [ ] 3 [ ] 10 (for extrapolation from animals to humans) 

[ ] 1 [X] 3 [ ] 10 (for human variability) 

Was a conversion used from ppm in food or water to a mg/body weight dose? No. 
 

 

 

 

 

 

 

 

 

Nuclear Medicine 

4% 

X Rays 

11% 

Consumer 

Other 

<1% 

Terrestrial 

8% 

Cosmic 

8% 

Natural Internal 

11% 

Radon 

55% 

Products 3% 

COBALT A-13 

APPENDIX A 

Table A-1. Average Annual Effective Dose Equivalent from Ionizing Radiation to a 

Member of the U.S. Populationa
 

Effective dose equivalent 

Percent of total 

Source mSv dose 

Natural 

Radonb

 2.0 55 

Cosmic 0.27 8.0 

Terrestrial 0.28 8.0 

Internal 0.39 11 

Total natural 3.0 82 

Artificial 

Medical 

X-ray 0.39 11 

Nuclear 0.14 4.0 

Consumer 0.10 3.0 

products 

Other 

Occupational <0.01 <0.3 

Nuclear fuel <0.01 <0.03 

cycle 

Fallout <0.01 <0.03 

Miscellaneousc

 <0.01 <0.03 

Total artificial 0.63 18 

Total natural 3.6 100 

and artificial 

a

Adapted from BEIR V, Table 1-3 , page 18. b

Dose equivalent to bronchi from radon daughter products 

c

DOE facilities, smelter, transportation, etc. 
COBALT A-14 

APPENDIX A 

If an inhalation study in animals, list the conversion factors used in determining human equivalent dose: 

Not applicable. 

Was a conversion used from intermittent to continuous exposure? No. 

Other additional studies or pertinent information which lend support to this MRL: ICRP has developed 

recommended dose limits for occupational and public exposure to ionizing radiation sources. The ICRP 

recommends limiting public exposure to 1 mSv/year (100 mrem/year), but does note that values at high 

altitudes above sea level and in some geological areas can sometimes be twice that value (≥2 mSv). In 

Annex C of ICRP 60, the commission provides data that suggests increasing the dose from 1 mSv to 

5 mSv results in a very small, but detectable, increase in age-specific human mortality rate. ICRP states 

that the value of 1 mSv/year was chosen over the 5 mSv value because 5 mSv/year (500 mrem/year) 

causes this increase in age specific mortality rate, and 1 mSv/year (100 mrem/year) is typical of the 

annual effective dose from background, less radon (ICRP 1991). The 1 mSv estimate may underestimate 

the annual exposure to external sources of ionizing radiation to the U.S. population, as it does not include 

radiation from radon. Conversely, the 5 mSv estimate may be high, in that increases in mortality rate 

been reported. The most useful estimate appears to be the BEIR V estimate of 3.6 mSv, in that it 

accounts for an annual exposure to radon, is specific to the U.S. population, has not been associated with 

increases mortality, and it falls short of the 5 mSv value associated with small increases in human 

mortality. 

Calculations: 

MRL = NOAEL(ADJ) ÷ UF 

MRL = 3.6 mSv/year ÷ 3 

MRL = 1.20 mSv/year 

MRL = 1.0 mSv/year =100 mrem/year above background 

Agency Contact (Chemical Manager): Obaid Faroon D.V.M., Ph.D. 

COBALT 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. 
 

 

COBALT 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. 

LEGEND 
COBALT B-3 

APPENDIX B 

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 3.5, "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"). 
COBALT 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. 

(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*). 
COBALT B-5 

APPENDIX B 

(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 


COBALT 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 
 

 

COBALT 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 
 

 

COBALT 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 
COBALT 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 
COBALT 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 

COBALT 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. 
COBALT 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. 
 

 

 

 

 

 

 

 

 

COBALT 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. 
 

 

 

COBALT 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 

particles, lose energy rapidly with distance and, therefore, do not penetrate deeply. The result of these 
 

 

COBALT D-5 

APPENDIX D 

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 

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; 

1

 Neutrinos also accompany negative beta particles and positron emissions 
 

 

COBALT D-6 

APPENDIX D 

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 

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). 
COBALT D-7 

APPENDIX D 

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 

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. 
 

 

COBALT D-8 

APPENDIX D 

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 

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. 
COBALT D-9 

APPENDIX D 

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. 
COBALT 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 
 

 

COBALT 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 
 

 

 

COBALT 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. 
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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. 
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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. 
 

 

 

 

 

 

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APPENDIX E. INDEX 

adipose tissue.............................................................................................................................................................261 

adrenal gland .............................................................................................................................................................131 

adrenal glands............................................................................................................................................................131 

adsorption ....................................................................................................................................17, 220, 223, 226, 228 

aerobic .........................................................................................................................................................22, 155, 222 

air.........................................4, 6, 7, 9, 11, 14, 17, 45, 88, 116, 142, 159, 195, 207, 211, 212, 213, 215, 216, 217, 219, 

227, 230, 232, 233, 246, 253, 254, 255, 257, 258, 259, 260
 

ambient air.......................................................................................................................................9, 17, 231, 246, 260 

anaerobic....................................................................................................................................................................222 

Arctic.................................................................................................................................................221, 235, 237, 240 

average daily dose .....................................................................................................................................................114 

average daily intake...................................................................................................................................................249 

bioaccumulation ........................................................................................................................................210, 225, 226 

bioavailability ............................................................................................................................................................260 

bioconcentration ................................................................................................................................................217, 228 

biodegradation ...........................................................................................................................................................230 

biomagnify.............................................................................................................................................5, 211, 242, 260 

biomarker...........................................................................................................................................................162, 163 

birds...................................................................................................................................................................242, 243 

blood......................................................7, 9, 10, 11, 13, 20, 21, 23, 25, 45, 75, 76, 107, 112, 123, 124, 130, 131, 132, 

140, 148, 152, 153, 155, 159, 160, 163, 166, 179, 180, 181, 253, 255, 257, 261, 263
 

body weight effects................................................................................................................................................30, 55 

breast milk ...................................................................................................................................................11, 160, 256 

cancer............................................................3, 8, 10, 11, 17, 19, 23, 29, 52, 53, 82, 138, 157, 159, 162, 176, 202, 203
 

carcinogenic....................................................................................................... 10, 19, 24, 27, 28, 82, 86, 87, 117, 176
 

carcinogenicity ................................................................................................................................................19, 24, 52 

carcinoma ..................................................................................................................................................108, 117, 129 

chromosomal abnormalities.........................................................................................................................................23 

chronic inhalation exposure.......................................................................................................................................175 

crustaceans.........................................................................................................................................................226, 249 

deoxyribonucleic acid........................................................................................................................................120, 121 

dermal effects ..................................................................................................................................................30, 49, 79 

DNA .................................................................................................... 19, 119, 120, 121, 122, 154, 155, 156, 163, 166
 

dog.....................................................................................................................................................125, 132, 133, 136 

dye .........................................................................................................................................................17, 30, 255, 257 

endocrine effects..........................................................................................................................................78, 110, 111 

FDA.....................................................................................................................................................................13, 249 

FEDRIP .....................................................................................................................................................................262 

fetus .................................................................................................................................10, 11, 82, 158, 160, 162, 168 

fish.................................................................................................................................5, 210, 225, 242, 243, 244, 249 

Food and Drug Administration............................................................................................................................13, 249 

fruits...................................................................................................................................................................3, 5, 203 

FSH............................................................................................................................................................................110 

gastrointestinal effects .............................................................................................................................18, 48, 75, 174 

general population ........................................................................................... 7, 17, 117, 162, 212, 246, 249, 257, 258
 

glutathione peroxidase...............................................................................................................................................154 

goiter....................................................................................................................................................................78, 110 

grass...........................................................................................................................................................................224 

groundwater........................................................... 6, 207, 211, 212, 216, 217, 218, 222, 228, 231, 235, 236, 238, 239
 

half-life ...................................................................................... 2, 3, 146, 162, 183, 193, 201, 204, 210, 222, 225, 226
 

hematological effects...................................................................................................................................................48 

hepatic effects......................................................................................................................................................77, 109 

IgA.................................................................................................................................................22, 51, 156, 166, 168 
 

 

 

 

 

 

 

COBALT E-2 

APPENDIX E 

immune system....................................................................................................................................................19, 155 

immunological effects .......................................................................................................................................171, 178 

kidney .............................................................. 8, 47, 115, 120, 121, 122, 129, 130, 131, 152, 156, 174, 225, 244, 245
 

kidney effects.............................................................................................................................................................174 

Kow .....................................................................................................................................................188, 189, 190, 191 

lake ............................................................................................................................................210, 222, 225, 227, 236 

LD50 .........................................................................................................................................................54, 55, 79, 106 

leukemia ............................................................................................................................................112, 113, 117, 122 

LH........................................................................................................................................................................86, 110 

liver....................................................8, 11, 18, 47, 49, 55, 77, 109, 115, 116, 121, 128, 129, 130, 139, 150, 152, 154,
 

156, 163, 167, 170, 243, 244, 245, 249
 

LOAEL................................................................................................ 24, 25, 27, 28, 30, 50, 55, 76, 80, 81, 82, 84, 87 

LOAELs ..........................................................................................................................................................27, 28, 87 

lowest-observed-adverse-effect level ..........................................................................................................................27 

lowest-observed-adverse-effect levels.........................................................................................................................27 

lung11, 18, 29, 46, 47, 50, 52, 53, 54, 107, 121, 123, 125, 128, 129, 131, 133, 140, 153, 157, 160, 163, 168, 176, 203
 

lymph..................................................................................................................... 51, 84, 107, 113, 128, 129, 146, 147
 

lymphatic ...........................................................................................................................................................122, 140 

marine................................................................................................................ 210, 213, 222, 225, 226, 227, 228, 262
 

milk.............................................................................................. 76, 126, 134, 160, 243, 244, 245, 246, 249, 256, 261
 

Minimal Risk Level.....................................................................................................................................................28 

MRL ................................................................................................................ 20, 24, 25, 28, 29, 46, 76, 174, 175, 176 

musculoskeletal effects..................................................................................................................................48, 77, 109 

National Priorities List...........................................................................................................................................1, 207 

neurobehavioral .................................................................................................................................115, 158, 174, 179 

neurophysiological.....................................................................................................................................................179 

NIOSH.........................................................................................................................................13, 184, 185, 186, 187 

NOAEL ........................................................................................... 24, 27, 28, 30, 46, 55, 76, 77, 81, 82, 87, 108, 175
 

no-observed-adverse-effect level.................................................................................................................................27 

NPL ............................................................................................................... 1, 207, 208, 209, 212, 216, 217, 219, 262
 

ocean.................................................................................................................. 210, 211, 220, 228, 230, 232, 240, 242
 

ocular effects ...............................................................................................................................................................83 

OR .......................................................................................................................................................53, 199, 215, 230 

particulate .......................................................................... 138, 140, 191, 207, 211, 218, 219, 221, 228, 229, 230, 238 

particulates.................................................................................................................................................................216 

PBPD.........................................................................................................................................................................137 

PBPK.................................................................................................................................................137, 138, 139, 160 

PEL............................................................................................................................................................................254 

pharmacodynamic......................................................................................................................................................137 

pharmacokinetic.........................................................................................................................137, 138, 140, 160, 181 

physiologically based pharmacokinetic .....................................................................................................................139 

precipitation...............................................................................................................................122, 203, 220, 229, 235 

public health .................................................................................................................... 1, 8, 12, 13, 27, 158, 171, 256 

pulmonary fibrosis.........................................................................................................................................18, 19, 157 

RCRA ................................................................................................................................................................213, 259 

RDA...........................................................................................................................................................................131 

recommended dietary allowance ...............................................................................................................................256 

reflexes ........................................................................................................................................................................81 

regulations .....................................................................................................................................................13, 14, 205 

renal effects .........................................................................................................................................................77, 110 

reproductive effect.........................................................................................................................................51, 81, 177 

reproductive system...............................................................................................................................................10, 51 

Resource Conservation and Recovery Act ........................................................................................................203, 213 

respiratory effect...................................................................................................... 18, 20, 30, 45, 46, 47, 49, 171, 175
 

salivation......................................................................................................................................................................79 

sculpin .......................................................................................................................................................................226 

sea..................................................................................................................................4, 195, 207, 210, 220, 229, 242 
 

 

 

 

 

 

 

COBALT E-3 

APPENDIX E 

sediment............................4, 17, 210, 212, 216, 217, 219, 220, 221, 222, 225, 226, 229, 239, 240, 242, 259, 261, 262 

sedimentation.....................................................................................................................................................122, 220 

selenium.....................................................................................................................................................................162 

serum ..................................................................................... 45, 49, 76, 77, 78, 79, 130, 156, 166, 168, 180, 253, 257 

SMR.......................................................................................................................................................................52, 53 

soil .......................................................1, 2, 4, 5, 6, 12, 14, 17, 207, 210, 212, 213, 216, 217, 218, 219, 220, 223, 224, 

229, 230, 238, 239, 241, 246, 247, 256, 257, 259, 260, 261, 263
 

solubility...................................................................................... 20, 123, 132, 134, 137, 140, 142, 152, 153, 229, 230
 

standardized mortality ratio .........................................................................................................................................52 

sulfides.......................................................................................................................................................195, 210, 229 

Superfund ..................................................................................................................................................................263 

surface water.................................................................. 4, 207, 211, 212, 217, 218, 219, 220, 221, 227, 231, 235, 236
 

T3.................................................................................................................................................................................49 

T4.........................................................................................................................................................................49, 110 

thyroid ................................................................................................................... 9, 18, 45, 78, 86, 110, 115, 158, 161
 

thyroxine......................................................................................................................................................................49 

tomato................................................................................................................................................................224, 241 

total diet studies.........................................................................................................................................................261 

toxicokinetic ................................................................................................................................................................27 

transport......................124, 140, 142, 146, 147, 148, 152, 156, 158, 207, 219, 220, 229, 230, 257, 258, 259, 262, 263 

TRI..................................................................................................................... 196, 203, 213, 215, 216, 217, 219, 259
 

trophic transfer...........................................................................................................................................................225 

tumors....................................................................................................................................53, 54, 117, 157, 176, 203 

tuna ............................................................................................................................................................................242 

TWA..................................................................................................................................................................234, 254 

Type I ..........................................................................................................................................................................46 

Type II .........................................................................................................................................................................46 

U.S. Department of Agriculture.........................................................................................................................249, 264 

USDA ........................................................................................................................................................249, 263, 264 

water ........................................................................... 2, 3, 4, 5, 6, 7, 10, 11, 14, 17, 74, 75, 76, 77, 78, 79, 80, 81, 82, 

...........................................................126, 159, 169, 183, 195, 201, 203, 207, 210, 211, 212, 213, 215, 216, 217, 218,
 

219, 220, 221, 222, 223, 224, 225, 226, 227, 228, 229, 231, 235, 236, 238, 239, 241, 242, 245, 246, 254, 

256, 258, 259, 260, 263