TOXICOLOGICAL PROFILE FOR 

AMERICIUM 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES 

Public Health Service 

Agency for Toxic Substances and Disease Registry
 

April 2004 
AMERICIUM 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. 
AMERICIUM iii 

UPDATE STATEMENT 

A Toxicological Profile for Americium, Draft for Public Comment, was released in May 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 


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). 
 

 

 

AMERICIUM vii 

QUICK REFERENCE FOR HEALTH CARE PROVIDERS 

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

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

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

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

answers to often-asked questions. 

Primary Chapters/Sections of Interest 

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

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

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

the general health effects observed following exposure. 

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

and assesses the significance of toxicity data to human health. 

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

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

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

reported in this section. 

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

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

observed following exposure. 

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

issues: 

Section 1.6 How Can (Chemical X) Affect Children? 

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

Section 3.7 Children’s Susceptibility 

Section 6.6 Exposures of Children 

Other Sections of Interest: 

Section 3.8 Biomarkers of Exposure and Effect 

Section 3.11 Methods for Reducing Toxic Effects 

ATSDR Information Center 

Phone: 1-888-42-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 
AMERICIUM 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: 

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/. 
AMERICIUM ix

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

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

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

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

AMERICIUM xi

CONTRIBUTORS 

CHEMICAL MANAGER(S)/AUTHOR(S): 

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

ATSDR, Division of Toxicology, Atlanta, GA 

Lisa Ingerman, Ph.D. 

Regina A. McCartney, M.S. 

Lara L. Chappell, Ph.D. 

David W. Wohlers, Ph.D. 

Gloria W. Sage, Ph.D. 

Gary L. Diamond, Ph.D. 

Michael Neal, 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. 

AMERICIUM xiii 

PEER REVIEW 

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

1. Ronald Kathren, C.H.P., D.E.E., Emeritus Professor of Pharmaceutical Science, Washington 

State University; President, The Kathren Group, Inc., Richland, WA, 

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

3. Ray D. Lloyd, Ph.D., Research Professor of Radiology, University of Utah School of Medicine, 

Salt Lake City, UT, 

4.	 Neal Stradling, Ph.D., Biokinetics Studies Group, U.K. National Radiological Protection Board, 

Chilton, Didcot, Oxon, United Kingdom, 

5.	 Raymond Guilmette, Ph.D., Los Alamos National Laboratory, Los Alamos, NM, and 

6. Melvin Sikov, Ph.D., Scientist Emeritus, Pacific Northwest National Laboratory, Richland, WA. 

These experts collectively have knowledge of amercium'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. 

 

 

 

AMERICIUM 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 AMERICIUM?...........................................................................................................2 

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

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

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

1.5 HOW CAN AMERICIUM AFFECT MY HEALTH?................................................................5 

1.6 HOW CAN AMERICIUM AFFECT CHILDREN? ...................................................................6 

1.7 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO AMERICIUM? ...............7 

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

EXPOSED TO AMERICIUM? ..................................................................................................8 

1.9 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH? ................................................................................................8 

1.10 WHERE CAN I GET MORE INFORMATION? .....................................................................10 

2. RELEVANCE TO PUBLIC HEALTH .................................................................................................11 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO AMERICIUM IN THE 

UNITED STATES....................................................................................................................11 

2.2 SUMMARY OF HEALTH EFFECTS......................................................................................12 

2.3 MINIMAL RISK LEVELS (MRLs) .........................................................................................14 

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

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

3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE ..................................17 

3.2.1 Inhalation Exposure ..............................................................................................................19 

3.2.1.1 Death ............................................................................................................................19 

3.2.1.2 Systemic Effects...........................................................................................................19 

3.2.1.3 Immunological and Lymphoreticular Effects...............................................................23 

3.2.1.4 Neurological Effects.....................................................................................................24 

3.2.1.5 Reproductive Effects....................................................................................................24 

3.2.1.6 Developmental Effects .................................................................................................24 

3.2.1.7 Cancer...........................................................................................................................24 

3.2.2 Oral Exposure........................................................................................................................24 

3.2.2.1 Death ............................................................................................................................25 

3.2.2.2 Systemic Effects...........................................................................................................25 

3.2.2.3 Immunological and Lymphoreticular Effects...............................................................25 

3.2.2.4 Neurological Effects.....................................................................................................25 

3.2.2.5 Reproductive Effects....................................................................................................25 
 

 

 

AMERICIUM xvi 

3.2.2.6 Developmental Effects .................................................................................................25 

3.2.2.7 Cancer...........................................................................................................................25 

3.2.3 Dermal Exposure...................................................................................................................25 

3.2.3.1 Death ............................................................................................................................25 

3.2.3.2 Systemic Effects...........................................................................................................25 

3.2.3.3 Immunological and Lymphoreticular Effects...............................................................26 

3.2.3.4 Neurological Effects.....................................................................................................27 

3.2.3.5 Reproductive Effects....................................................................................................27 

3.2.3.6 Developmental Effects .................................................................................................27 

3.2.3.7 Cancer...........................................................................................................................27 

3.2.4 Other Routes of Exposure .....................................................................................................27 

3.2.4.1 Death ............................................................................................................................27 

3.2.4.2 Systemic Effects...........................................................................................................27 

3.2.4.3 Immunological and Lymphoreticular Effects...............................................................28 

3.2.4.4 Neurological Effects.....................................................................................................29 

3.2.4.5 Reproductive Effects....................................................................................................29 

3.2.4.6 Developmental Effects .................................................................................................29 

3.2.4.7 Cancer...........................................................................................................................30 

3.3 GENOTOXICITY .....................................................................................................................31 

3.4 TOXICOKINETICS..................................................................................................................32 

3.4.1 Absorption.............................................................................................................................32 

3.4.1.1 Inhalation Exposure......................................................................................................32 

3.4.1.2 Oral Exposure...............................................................................................................38 

3.4.1.3 Dermal Exposure ..........................................................................................................43 

3.4.1.4 Other Routes of Exposure ............................................................................................44 

3.4.2 Distribution ...........................................................................................................................44 

3.4.2.1 Inhalation Exposure......................................................................................................44 

3.4.2.2 Oral Exposure...............................................................................................................49 

3.4.2.3 Dermal Exposure ..........................................................................................................49 

3.4.2.4 Other Routes of Exposure ............................................................................................50 

3.4.3 Metabolism............................................................................................................................51 

3.4.4 Elimination and Excretion.....................................................................................................51 

3.4.4.1 Inhalation Exposure......................................................................................................51 

3.4.4.2 Oral Exposure...............................................................................................................53 

3.4.4.3 Dermal Exposure ..........................................................................................................54 

3.4.4.4 Other Routes of Exposure ............................................................................................54 

3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models .............55 

3.5 MECHANISMS OF ACTION ..................................................................................................79 

3.5.1 Pharmacokinetic Mechanisms...............................................................................................79 

3.5.2 Mechanisms of Toxicity........................................................................................................83 

3.5.3 Animal-to-Human Extrapolations.........................................................................................83 

3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS ..........................84 

3.7 CHILDREN’S SUSCEPTIBILITY...........................................................................................85 

3.8 BIOMARKERS OF EXPOSURE AND EFFECT ....................................................................88 

3.8.1 Biomarkers Used to Identify or Quantify Exposure to Americium ......................................89 

3.8.2 Biomarkers Used to Characterize Effects Caused by Americium.........................................90 

3.9 INTERACTIONS WITH OTHER CHEMICALS ....................................................................90 

3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE...............................................91 

3.11 METHODS FOR REDUCING TOXIC EFFECTS...................................................................91 

3.11.1 Reducing Peak Absorption Following Exposure ..............................................................92 

3.11.2 Reducing Body Burden.....................................................................................................92 
 

 

AMERICIUM xvii 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects ...........................................93 

3.12 ADEQUACY OF THE DATABASE........................................................................................93 

3.12.1 Existing Information on Health Effects of Americium.....................................................93 

3.12.2 Identification of Data Needs .............................................................................................95 

3.12.3 Ongoing Studies..............................................................................................................101 

4. CHEMICAL, PHYSICAL, and RADIOLOGICAL INFORMATION ...............................................103 

4.1 CHEMICAL IDENTITY.........................................................................................................103 

4.2 PHYSICAL, CHEMICAL, AND RADIOLOGICAL PROPERTIES.....................................103 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL..........................................................113 

5.1 PRODUCTION .......................................................................................................................113 

5.2 IMPORT/EXPORT .................................................................................................................116 

5.3 USE..........................................................................................................................................116 

5.4 DISPOSAL..............................................................................................................................117 

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

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

6.2 RELEASES TO THE ENVIRONMENT................................................................................125 

6.2.1 Air .......................................................................................................................................126 

6.2.2 Water...................................................................................................................................128 

6.2.3 Soil ......................................................................................................................................129 

6.3 ENVIRONMENTAL FATE....................................................................................................130 

6.3.1 Transport and Partitioning...................................................................................................130 

6.3.2 Transformation and Degradation ........................................................................................148 

6.3.2.1 Air...............................................................................................................................148 

6.3.2.2 Water ..........................................................................................................................148 

6.3.2.3 Sediment and Soil.......................................................................................................148 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT...............................149 

6.4.1 Air .......................................................................................................................................149 

6.4.2 Water...................................................................................................................................151 

6.4.3 Sediment and Soil ...............................................................................................................154 

6.4.4 Other Environmental Media................................................................................................158 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE .....................................170 

6.6 EXPOSURES OF CHILDREN...............................................................................................176 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES ...........................................177 

6.8 ADEQUACY OF THE DATABASE......................................................................................178 

6.8.1 Identification of Data Needs ...............................................................................................178 

6.8.2 Ongoing Studies ..................................................................................................................182 

7. ANALYTICAL METHODS ...............................................................................................................183 

7.1 BIOLOGICAL MATERIALS.................................................................................................183 

7.1.1 Whole or Partial Body Measurements ................................................................................183 

7.1.2 Assay of Excreta .................................................................................................................188 

7.2 ENVIRONMENTAL SAMPLES............................................................................................190 

7.2.1 Field Measurements of Americium.....................................................................................190 

7.2.2 Laboratory Analysis of Environmental Samples.................................................................191 

7.3 ADEQUACY OF THE DATABASE......................................................................................198 

7.3.1 Identification of Data Needs ...............................................................................................198 

7.3.2 Ongoing Studies ..................................................................................................................199 
 

 

AMERICIUM xviii 

8. REGULATIONS AND ADVISORIES ...............................................................................................201 

9. REFERENCES ....................................................................................................................................209 

10. GLOSSARY ......................................................................................................................................259 

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 
 

 

AMERICIUM xix 

LIST OF FIGURES 

3-1. Conceptual Representation of a Physiologically Based Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance ......................................................................................................57 

3-2. Compartment Model to Represent Particle Deposition and Time-Dependent Particle Transport in the 

Respiratory Tract ................................................................................................................................60 

3-3. The Human Respiratory Tract Model: Absorption into Blood..........................................................66 

3-4. ICRP (1989) Model of Americium Biokinetics..................................................................................68 

3-5. Leggett (1992) Model of Americium Biokinetics ..............................................................................70 

3-6. Mewhinney and Griffith (1983) Model of Deposition and Retention of Americium in the Human 

Respiratory Tract ................................................................................................................................75 

3-7. Durbin and Schmidt (1985) Model of Distribution and Excretion of Absorbed Americium in the 

Human.................................................................................................................................................78 

3-8. Leggett (1992) Model of Deposition and Retention of Americium in the Human Respiratory
 

Tract....................................................................................................................................................80 

3-9. Existing Information on Health Effects of Americium ......................................................................94 

5-1. Production Table for 241Am ..............................................................................................................115 

6-1. Frequency of NPL Sites with Americium Contamination................................................................122 

 

 

 

AMERICIUM xxi 

LIST OF TABLES 

3-1. Retention and Absorption Estimates in Animals Exposed to Americium Compounds by 

Inhalation ............................................................................................................................................34 

3-2. Absorption Estimates in Animals Exposed to Americium Compounds by Ingestion ........................40 

3-3. Tissue Americium Levels from Human Autopsies.............................................................................46 

3-4. Reference Respiratory Values for a General Caucasian Population at Different Levels of 

Activity ...............................................................................................................................................61 

3-5. Reference Values of Parameters for the Compartment Model to Represent Time-dependent 

Particle Transport from the Human Respiratory Tract .......................................................................62 

4-1. Principal Americium Isotopes ..........................................................................................................105 

4-2. Physical and Chemical Properties of Americium and Selected Americium Compounds ................107 

4-3. Properties of Some Americium Ions.................................................................................................109 

4-4. 241Am Decay Scheme........................................................................................................................110 

4-5. 243Am Decay Scheme........................................................................................................................111 

6-1. Concentrations of 241Am in Soil and Sediment.................................................................................132 

6-2. Bioconcentration Factors for 241Am..................................................................................................145 

6-3. Concentrations of 241Am in Water....................................................................................................153 

6-4. Average Concentrations of 241Am in Food .......................................................................................159 

6-5. Concentrations of 241Am in Fauna ....................................................................................................162 

6-6. Estimated Effective 241Am Dose from Food Raised on Land Impacted by Tidal Estuaries 

along the Irish Sea.............................................................................................................................172 

7-1. Analytical Methods for Determining Americium in Biological Samples ........................................185 

7-2. Analytical Methods for Determining Americium in Environmental Samples .................................192 

8.1 Regulations and Guidelines Applicable to Americium......................................................................200 

AMERICIUM 1 

1. PUBLIC HEALTH STATEMENT 

This public health statement tells you about americium 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. Americium has been found in at least 8 of the 1,636 current 

or former NPL sites. However, the total number of NPL sites evaluated for americium is not 

known. As more sites are evaluated, the sites at which americium is found may increase. This 

information is important because exposure to americium 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 normally 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. However, 

since americium is radioactive, you can also be exposed to its radiation if you are near it. 

External or internal exposure to radiation may occur from natural or man-made sources. 

Naturally occurring sources of radiation are cosmic radiation from space or naturally occurring 

radioactive materials in our body or in soil, air, water, or building materials. Man-made sources 

of radiation 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 americium, 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 or radioactive materials you’re exposed to and 

your age, sex, diet, family traits, lifestyle, and state of health. 
AMERICIUM 2 

1. PUBLIC HEALTH STATEMENT 

1.1 WHAT IS AMERICIUM? 

Americium (pronounced, 1am-c-0ris(h)-‘-cm) is a human-made, radioactive element. There are 

no naturally occurring or stable isotopes of americium. Pure americium is a silvery metal. 

There are two important isotopes of americium, americium 241 and americium 243, also written 

as 

241Am and 243Am, and read as americium two-forty-one and americium two-forty-three. Both 

isotopes have the same chemical behavior in the environment. 

Quantities of americium, as well as other radioactive elements, can be measured in units of mass 

(grams), but are usually measured in terms of their radioactivity (curies or becquerels). Both the 

curie (Ci) and the becquerel (Bq) tell us how much a radioactive material decays every second. 

The becquerel is a new international unit and the curie is a traditional unit; both units are 

currently used in the United States. 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. 

Each radioactive isotope of an element, including americium, constantly gives off radiation, 

which changes 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. 241Am and 243Am give off alpha particles (sometimes referred to as alpha radiation) and 

change into neptunium 237 (237Np) and neptunium 239 (239Np), respectively. Neptunium is also 

radioactive, so isotopes of this element also give off radiation and change into isotopes of other 

elements. This process continues and eventually ends when stable isotopes of bismuth and lead 

are formed. 

Half-life is the term that is used to describe the rate of the decay process. Specifically, the halflife is the time it takes for half of the atoms of a radionuclide to undergo radioactive decay and 

change it into a different isotope. The half-life of 241Am is 432 years. The half-life of 243Am is 

7,370 years. 
AMERICIUM 3 

1. PUBLIC HEALTH STATEMENT 

Specific activity is a term that describes the relative rates of decay of the same mass of different 

radioactive materials. If you have 1 gram of each isotope of americium side by side, the specific 

activities would be 3.4 curies per gram for 241Am and 0.2 curies per gram for 243Am. Thus, for 

the same mass, 241Am is about 17 times more radioactive (i.e., its specific activity would be 

17 times higher) than that of 243Am. The higher the specific activity of a radioisotope, the faster 

it is decaying. 

The predominant commercial use of 241Am is in ionization-type smoke detectors. This 

application relies on the alpha particles that are produced when the isotope decays as an 

ionization source. A typical household smoke detector contains 0.9 microcuries (μCi; a μCi is 

one millionth of a curie) or 33,000 Bq of 241Am, and 1 g of americium dioxide is sufficient to 

make 5,000 smoke detectors. 241Am is also used for industrial gauging applications and in 

medical diagnostic devices. There are research applications, but no commercial applications for 

243Am. This will change if the United States and Russia turn nuclear warheads into power 

reactor fuel by making a mixed oxide fuel of uranium and plutonium. This fuel, called MOX, 

will contain both 241Am and 243Am, and the plan is to use it to make electricity. Once used, the 

spent nuclear fuel is to be sent for disposal. 

For more information about the properties and uses of americium, see Chapters 4, 5, and 6. 

1.2 WHAT HAPPENS TO AMERICIUM WHEN IT ENTERS THE ENVIRONMENT? 

241Am can be released to the environment from nuclear reactors, nuclear explosions, and 

accidents, as well as from manufacturing products containing americium (such as smoke 

detectors). Americium is a byproduct of plutonium production. 241Am is formed from the 

radioactive decay of plutonium 241 (241 Pu), which itself is produced from uranium 238 (238U) 

while it is inside an operating nuclear reactor. In the absence of clean-up procedures, radioactive 

decay is the only way for decreasing the amount of americium in the environment. Because 

241Am has a long half-life, it will be present in the environment for a long time. Since 241Pu can 

be released along with 241Am in the decay process, the amount of 241Am will slowly increase for 

decades, even in the absence of additional 241Am releases, and then slowly decrease. 
AMERICIUM 4 

1. PUBLIC HEALTH STATEMENT 

241Am released to the atmosphere will be associated with particles and will settle to earth or be 

washed from the air in precipitation (e.g., rain, snow). 241Am from atmospheric nuclear weapons 

tests may remain in the atmosphere for decades before settling to earth. For example, 241Am 

released in nuclear accidents, like the accident at Chernobyl, will stay in the lower atmosphere 

and begin to settle to earth near the site from which it was released. Larger particles will settle 

out more quickly and over a smaller area; smaller particles may remain in the atmosphere for 

several months and travel far from where they were released. Precipitation removes particles 

from the air more rapidly. 

241Am released into water from nuclear facilities will tend to stick to particles in the water or the 

sediment. 241Am deposited on soil is so strongly attached to soil particles that it does not travel 

very far into the ground. Ultimately, most americium ends up in soil or sediment. 

While plants may take up 241Am from the soil, the amount taken up is small, especially in the 

parts of the plant that are most often eaten (i.e., the fruit, grain, and seeds). While fish may take 

up 

241Am, the amount that builds up in the flesh is very small. Most of the 241Am found in 

shellfish like shrimp or mussels is contained in the shell, rather than in the edible parts of the 

animal. For more information about what happens to americium in the environment, see 

Chapter 6. 

1.3 HOW MIGHT I BE EXPOSED TO AMERICIUM? 

You may be exposed to 241Am by breathing air, drinking water, or eating food containing 241Am; 

however, the levels of 241Am in air, water, soil, and food are generally very low, and of little 

health consequence. 

People working at sites where nuclear waste is stored, in nuclear power plants, or in other 

nuclear facilities that handle 241Am may be exposed to higher levels of americium than the 

general population. People living near these sites also may be exposed to elevated levels of 

americium. People who produce or handle 241Am in smoke detectors or other devices may be 
AMERICIUM 5 

1. PUBLIC HEALTH STATEMENT 

exposed to higher levels. In the case of a nuclear accident, exposure could occur by breathing or 

eating dust containing 241Am. Even at sites that contain measurable levels of radioactive 

contamination, the amount of 241Am that is taken up into plant and animal tissue is so small that 

it is of little concern. You can find more information on how you may be exposed to americium 

in Chapter 6. 

1.4 HOW CAN AMERICIUM ENTER AND LEAVE MY BODY? 

Americium can enter your body from the air you breathe, the food you eat, or the water you 

drink, or from contact with your skin. If you breathe in air that contains americium, some forms 

of americium that dissolve easily in lung fluid stay in your lungs for hours or days. Other forms 

that do not dissolve easily in lung fluid might stay in your lungs for months or years. Some 

americium that enters your lungs may get into your blood. If you swallow americium, a very 

small amount of what enters your digestive tract may also enter your blood. Most of the 

americium entering your blood leaves your body in your urine and feces. Of the small amount 

that stays in your body, most goes to your bones, where it can remain for many decades; a 

smaller amount goes into your liver and other organs, where it may remain for a few years as the 

body clears it. 

1.5 HOW CAN AMERICIUM AFFECT MY HEALTH? 

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

who have been harmed, scientists use many tests. 

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

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

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

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

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

get information needed to make wise decisions to protect public health. Scientists have the 
AMERICIUM 6 

1. PUBLIC HEALTH STATEMENT 

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. 

In the process of radioactive decay, americium releases alpha particles and gamma rays. Alpha 

particles are relatively high energy particles, but travel only extremely short distances and do not 

penetrate the skin. However, if americium is taken into the body and enters body tissues, alpha 

particles may produce damage to nearby cells. Gamma rays can travel much greater distances 

and can penetrate the entire body. Since alpha particles do not penetrate the skin and the gamma 

rays released from americium sources are relatively low in energy, external exposure to 

americium is not usually considered to be a danger to your health. 

The radiation from americium is the primary cause of adverse health effects from absorbed 

americium. Upon entering the body by any route of exposure, americium moves relatively 

rapidly through the body and is deposited on the surfaces of the bones where it remains for a 

long time. As americium undergoes radioactive decay in the bone, alpha particles collide with 

nearby cell matter and give all of their energy to this cell matter. The gamma rays released by 

decaying americium can travel much farther before hitting cellular material, and many of these 

gamma rays leave the body without hitting or damaging any cell matter. The dose from this 

alpha and gamma radiation can cause changes in the genetic material of these cells that could 

result in health effects such as bone cancers. Exposure to extremely high levels of americium, as 

has been reported in some animal studies, has resulted in damage to organs such as the lungs, 

liver, kidneys, and thyroid. It is rare, however, that a person would be exposed to amounts of 

americium large enough to cause harmful effects in these organs. 

1.6 HOW CAN AMERICIUM AFFECT CHILDREN? 

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

to maturity at 18 years of age in humans. 

Americium accumulates in human bones and remains there for a long time. Americium emits 

radioactive alpha particles in the bone that can cause damage to the surrounding tissue. The 
AMERICIUM 7 

1. PUBLIC HEALTH STATEMENT 

body normally repairs all of the damage, but if it fails, bone cancer could result after many years. 

If americium exposure to children occurs, the exposure to the radiation from americium may be 

for a longer period of time, causing a larger radiation dose over their lifetime and increasing the 

likelihood of producing cancer. However, there are no published data showing that children are 

more susceptible than adults to radiation-induced americium toxicity. A developing baby is 

expected to have some americium in its body. It could be affected by this americium while in 

the womb if the pregnant mother has high enough levels of americium in her blood. 

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

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

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

department to investigate. 

While discharges from nuclear waste sites, nuclear reactors, or plants that manufacture ionization 

smoke detectors or gauges containing americium are regulated, it is possible that higher-thannormal levels of americium may be in soil near a nuclear waste site, nuclear reactor, or plant that 

manufactures ionization smoke detectors or gauges containing americium. If you live near any 

of these types of nuclear or manufacturing sites, discourage your children from putting their 

hands in their mouths and engaging in other hand-to-mouth activities. 

Discharge water and air emissions from facilities that make americium smoke detectors or 

gauges or produce plutonium for nuclear weapons may contain some americium. These 

operations are strictly regulated, but you can check local health advisories before consuming fish 

or other food from these waters. Nuclear reactors are not expected to discharge measurable 

amounts of americium. 

Ionization smoke detectors that contain americium are safe when installed; however, you should 

not allow your children to play with these detectors. If the detectors are damaged or are no 

longer being used, they should be promptly returned to the manufacturer for disposal. 
AMERICIUM 8 

1. PUBLIC HEALTH STATEMENT 

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

EXPOSED TO AMERICIUM? 

Physicians do not test for americium in their offices, but they can collect samples and send them 

to special laboratories or request that you be sent to such a laboratory. If you are exposed to a 

large dose of radiation from americium, your blood can be tested for signs of damage to the cell 

chromosomes. If americium were to enter your body from contaminated air, food, or water, the 

amount of americium (in Ci or Bq) can be estimated by measuring the radiation given off by the 

americium present in samples of blood, urine, teeth, or tissue. If in the lungs, the amount of 

americium can be estimated by measuring the americium gamma radiation that exits the body. 

Radiation detector systems used for these purposes are at a limited number of locations. The 

amount in your lungs and excretions fall sharply after exposure, so tests should be done as soon 

as possible. 

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 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; then they are adjusted to help protect 

people. Sometimes these not-to-exceed levels differ among federal organizations because of 
AMERICIUM 9 

1. PUBLIC HEALTH STATEMENT 

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 americium include the following: 

The USNRC established radiation dose limits to the public and to workers. To ensure that these 

limits are met, USNRC also set concentration limits for 241Am in air, water, and sewer discharge 

that can be released from licensed facilities. This ensures that the annual radiation dose will not 

exceed 0.1 rem (0.001 sievert) to the public, or 5 rem (0.05 sievert) to the worker or 50 rem 

(0.5 sievert) to their bones. The concentration limits are 0.00000000000002 microcurie per 

milliliter (2x10-14 μCi/mL) for air, 0.00000002 microcurie per milliliter (2x10-8 μCi/mL) for 

water, and 0.0000002 microcurie per milliliter (2x10-7 μCi/mL) for releases to sewers. The 

USNRC requires that intake of americium not exceed the specified annual limits on intake (ALI) 

for inhalation or oral routes of exposure. The occupational exposure limits are 6x10-3 μCi (ALI) 

for workers inhaling 241Am and 8x10-1 μCi (ALI) for ingestion of 241Am. The level of 241Am in 

workplace air, specified as the derived air concentration (DAC), is not to exceed 3x10-12 μCi/mL 

(which can be adjusted to account for work weeks shorter or longer than 40 hours). The FDA 

has set a food contamination guideline of 2 Bq/kg per kilogram (5.4x10-5 μCi/kg) for 241Am to 

protect 3-month-old children. This is the population group that would receive the highest 

radiation dose from eating food that contains americium. The EPA has established a public 

drinking water limit of 15 picocurie per liter (pCi/L). This is for the sum of all radioactive 

materials that give off alpha radiation. 241Am and 243Am are examples, but drinking water 

normally contains other alpha emitters, such as uranium, thorium, and radium. 

More information on regulations and guidelines is available in Chapter 8. 
AMERICIUM 10 

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/ 
 

 

AMERICIUM 11 

2. RELEVANCE TO PUBLIC HEALTH 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO AMERICIUM IN THE 

UNITED STATES 

Americium is a human-made, radioactive, actinide element; it has no stable isotopes. The only isotope 

used commercially is 241Am, several kilograms of which are produced annually. The only other 

americium isotope produced in macroscopic quantity (10–100 g annually) is 243Am. Both 241Am and 

243Am can be formed when either 238U (the major uranium isotope used in nuclear power reactor fuel) or 

238,239Pu (primarily used in nuclear weapons) are exposed to neutrons, as occurs in a nuclear reactor or 

nuclear explosion. Neutron activation of 238U to 239U followed by combinations of decay to 239Np and 

239Pu and neutron activation to higher masses of each produces a range of isotopes of these elements. 

Similarly, neutron activation of 238,239Pu yields higher mass isotopes. Any 241Pu or 243Pu formed by these 

processes will decay to 241Am and 243Am, respectively. The most common application of americium is in 

ionization smoke detectors; a typical home smoke detector contains about 0.9 μCi (33.3 kBq) of 

radioactivity. One gram of 241AmO2 provides enough active material for more than 5,000 smoke 

detectors. Americium is also used in a wide range of industrial gauging applications. 

Very low levels of 241Am may be found in environmental media worldwide, a legacy of atmospheric 

nuclear weapons testing that predominantly took place between 1945 and 1963. In nuclear reactors, 

241Am has been detected in primary coolant water, stack aerosols, and waste water (Rosner et al. 1978). 

Because 241Am is produced from the decay of 241Pu (half-life=14.4 years), releases of 241Pu result in 

increased environmental levels of 241Am. The maximum concentration of 241Am following an accidental 

release of 241Pu occurs 70–80 years post release (EPA 1976). Consequently, the impact of 241Am from 

atmospheric nuclear weapons testing will reach its peak in about the year 2035, when its rate of 

production from 241Pu decay equals its rate of decay. Environmental levels of 241Am will subsequently 

decline. Exposure of the general population to 241Am via air, water, soil, and food is generally very low; 

these ‘background’ levels are a result of fallout from past atmospheric nuclear weapons tests. Since 1973, 

241Am air concentrations have been <1 aCi/m3

 (1 attocurie [aCi]=1x10-18 Ci) (0.037 μBq/m3) and are 

expected to continue to decline, assuming no significant additional atmospheric nuclear testing after 1976 

(Bennett 1979). Levels around nuclear power plants are indistinguishable from fallout background levels 

(EPRI 1981). 241Am levels in surface seawater of the North Sea and North Atlantic Ocean stayed around 
AMERICIUM 12 

2. RELEVANCE TO PUBLIC HEALTH 

10 Bq/m3 (270 pCi/m3) between 1976 and 1988 (Pattenden and McKay 1994), but may be considerably 

higher near discharges from nuclear facilities. In the Food and Drug Administration (FDA) Total Diet 

Studies in 1983–1986 and 1987–1992, the concentrations of radionuclides were sufficiently low as to 

require no specific action or simple monitoring. 

2.2 SUMMARY OF HEALTH EFFECTS 

Americium exists only in the form of radioactive isotopes; there are no stable forms. Reports of adverse 

health effects in animals that were administered massive doses of americium are most certainly the result 

of the ionizing radiation, not the chemical toxicity of americium. The specific activity of 241Am is 

approximately 17 times greater than that of 243Am. Its higher specific activity and greater abundance 

make 241Am of greater health concern than 243Am. Both 241Am and 243Am release alpha particles and 

gamma rays during decay. Alpha radiation is primarily an internal hazard, and the low energy, low 

intensity gamma radiation is typically not the main health concern. The charged alpha particles generally 

travel a straight path, interacting with or colliding into other atomic particles. A collision between an 

atom and an alpha particle can result in a transfer of energy sufficient to “knock out” an electron from the 

atom, producing an ionized or excited atomic state. Alpha particles have short ranges, and those from 

americium isotopes are not able to penetrate the outer layers of skin; thus, they are not considered an 

external hazard. Once americium enters the body via ingestion, inhalation, dermal transport, or a dermal 

wound, however, the alpha particles that it emits present an internal hazard. The alpha energy induces 

rapid physical changes to localized cell matter in its path and via chemical interactions with the water in 

human cells. Radiation hydrolysis of water produces a cascade of rapid chemical reactions, forming 

ionized and excited chemical species referred to as radiolysis products. These reactive species can 

interact with biological molecules in ways that can damage cells. Cellular damage can result both directly 

from radiation interactions and indirectly from the chemical reactions involving reactive species of 

radiolysis products. The gamma rays emitted during the decay of 241Am are the only components of 

external radiation exposure, but they represent a small component of the decay scheme and are 

sufficiently low in energy and intensity so as to pose little hazard from external exposure. Internalized 

gamma rays can travel greater distances than the heavier alpha particles, but deposit a lower amount of 

energy with each interaction. Although the gamma rays emitted from the decaying americium atom are 

of low energy and intensity, their activity and energy could contribute to both localized and more distant 

cell damage. 
AMERICIUM 13 

2. RELEVANCE TO PUBLIC HEALTH 

Information regarding health effects in humans following exposure to americium is mainly limited to a 

case report of an individual accidentally exposed to high levels of americium resulting in a significant 

internal dose from americium that was absorbed via external wounds. Lymphopenia, thrombocytopenia, 

and histological signs of bone marrow peritrabecular fibrosis, bone cell depletion, and bone marrow 

atrophy were noted (Filipy et al. 1995; Priest et al. 1995). These data are supported by findings in 

laboratory animals exposed to high doses of americium. Elevated hematopoietic activity, leukopenia, 

decreased hematocrit and platelet levels, and increased cellularity in bone marrow were observed in 

animals exposed to americium via inhalation (Buldakov et al. 1972; Thomas et al. 1972) or parenteral 

injection (Dougherty 1970); these effects are likely due to the inability to support hematopoiesis and the 

reduced colony-forming capacity. Degenerative changes in bone, liver, kidneys, and thyroid have also 

been observed following inhalation (Moushatova et al. 1996; Thomas et al. 1972) or parenteral (Lloyd et 

al. 1970; Taylor et al. 1991, 1993a) exposure to 241Am. Comparisons between single exposure and 

repeated exposure studies suggest that the severity of the tissue damage increases with duration of 

exposure. Although many of the animal studies employed parenteral injection as the route of exposure, 

available inhalation data indicate similarity in targets of toxicity. The radiation dose resulting from 

inhaling large quantities of 241Am can also produce respiratory insufficiency and pneumonia (Buldakov et 

al. 1972; DOE 1978; Thomas et al. 1972). Experimental studies in animals demonstrate that internal 

exposure to the radioactive isotope, 241Am, results in the development of cancer in the tissues that 

sequester this element. Animal studies indicate increased risk of bone cancer in areas of bone containing 

relatively high levels of americium. Increases in bone cancer have occurred in dogs receiving a single 

inhalation exposure to 241AmO2 (Gillett et al. 1985) and in dogs (Jee et al. 1985; Lloyd et al. 1994a, 

1994b), rats (Carter et al. 1951), and mice (Schoeters et al. 1991; Taylor et al. 1983; Van Den Heuvel et 

al. 1995) receiving a single intraperitoneal or intravenous injection of 241Am. Studies of cancer risk 

specifically associated with exposure of humans to radioactive americium isotopes were not located. 

However, the EPA has determined that ionizing radiation is a Group A known carcinogen, and by 

extension, all radionuclides, including americium, are considered to be known carcinogens. 

Based on the outcome of accidental human exposures and experimental animal study data, as well as the 

application of physiological model simulations, the toxic effects following exposure to americium 

compounds can be predicted from the associated radiation dose. The potential for adverse health effects 

occurs when americium enters the body via ingestion, inhalation, dermal absorption, or dermal 

penetration where radiation from the americium compounds and their radioactive decay products inside 

the body can cause localized cell damage. Because americium accumulates in the bone and remains there 

for a long time, the ionizing properties of radiation from 241Am and 243Am can result in damage to the 
AMERICIUM 14 

2. RELEVANCE TO PUBLIC HEALTH 

hematopoietic system if the americium is deposited at a sufficient depth in the bone that its alpha particles 

can reach the marrow. Although human studies have not correlated americium exposure with an increase 

in cancer rate, one can calculate a theoretical risk based on dose and values from cancer risk tables. Risk 

may be significant at high doses, but such high-level exposures are not likely among the general 

population. 

2.3 MINIMAL RISK LEVELS (MRLs) 

Inhalation MRLs 

No acute-, intermediate-, or chronic-duration inhalation MRLs were derived for americium due to the lack 

of suitable human or animal data regarding health effects following inhalation exposure to americium. 

Oral MRLs 

No acute-, intermediate-, or chronic-duration oral MRLs were derived for americium due to the lack of 

suitable human or animal data regarding health effects following oral exposure to americium. 
AMERICIUM 15 

3. HEALTH EFFECTS 

3.1 INTRODUCTION 

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

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

contains descriptions and evaluations of toxicological studies and epidemiological investigations and 

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

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

The potential for adverse health effects to humans exposed to americium is dependent on the amount of 

americium isotopes (241Am and 243Am) present in the body as well as the radiation dose and dose rate that 

each produce. Both 241Am and 243Am can be formed when either 238U (the major uranium isotope used in 

nuclear power reactor fuel) or 238,239Pu (primarily used in nuclear weapons) are exposed to neutrons, as 

occurs in a nuclear reactor or nuclear explosion. Neutron activation of 238U to 239U, followed by 

combinations of decay to 239Np and 239Pu and neutron activation to higher masses of each, produces a 

range of isotopes of these elements. Similarly, neutron activation of 238,239Pu yields higher mass isotopes. 

Any 241Pu or 243Pu formed by these processes will decay to 241Am and 243Am, respectively. These can 

also be neutron activated, producing other americium isotopes (e.g., 242,244,245Am). The isotopes, 242Am 

and 243Am, are produced in lower abundance than 241Am (see Chapter 4 for decay schemes and other 

more detailed information). These americium radionuclides may be released into the atmosphere in sites 

that surround nuclear production facilities, store nuclear waste, or leak americium into the soil or 

groundwater. The radiation dose from these radionuclides can be classified as either external (if the 

source is outside the body) or internal (if the source is inside the body). 

The external dose from americium radionuclides may be attributed to the gamma radiation. Alpha 

particle decay emits alpha radiation, which cannot penetrate the outer layers of the skin, and a variety of 

low energy gamma rays, which do penetrate the skin, although rarely in sufficient quantity to exceed a 

regulatory limit. At very high doses of americium, there is increased risk for gamma radiation to cause 

dermal and subdermal effects such as erythema, ulceration, or even tissue necrosis. 
 

AMERICIUM 16 

3. HEALTH EFFECTS 

Once radioactive americium is internalized, it is distributed and excreted at a rate of transfer that is 

dependent on age. The internal radiation dose from americium is actually a measure of the amount of 

energy that the alpha and gamma emissions deposit in tissue. The short-range alpha radiation produces a 

localized dose, while the low energy gamma radiation contributes to a larger distribution of dose. 

Molecular damage results from the direct ionization of atoms that are encountered by alpha and gamma 

radiation and by interactions of resulting free radicals with nearby atoms. Tissue damage results when the 

molecular damage is extensive and not sufficiently repaired in a timely manner. 

In radiation biology, the term absorbed dose refers to the amount of energy deposited by radiation per 

unit mass of tissue, expressed in units of rad or gray (Gy) (see Appendix D for a detailed description of 

principles of ionizing radiation). The term dose equivalent (H) refers to the biologically significant dose, 

which is determined by multiplying the absorbed dose (D) by a quality factor (Q) for the type and energy 

of the radiations involved. Dose equivalent (H) is expressed as H=DxQ in units of rem or sievert (Sv). 

The quality factor (Q) for alpha radiation emitted from 241Am is rated 20 because of the high stopping 

power for charged particles. The dose equivalent (H) from internalized americium radionuclides is 

estimated using the quantity of material entering the body (via ingestion or inhalation), the biokinetic 

parameters for americium (retention, distribution, and excretion), the energies and intensities of the alpha 

and gamma radiation emitted, and the parameters describing the profile of absorbed radiation energy 

within the body. If, for example, a person ingests a given activity of 241Am (measured in curies [Ci] or 

becquerels [Bq]), the tissues of the body will absorb some of the energy of the emitted alpha and gamma 

radiation in a pattern reflecting the kinetics of distribution and elimination of the ingested 241Am, the rate 

at which the radioactive isotope decays to a stable form, and the age of the person at the time of ingestion 

(which affects both the biokinetics of the americium as well as the potential length of time over which the 

tissues can be exposed to the radiation). Each tissue, therefore, can receive a different dose equivalent. 

The total effective dose equivalent for the body will reflect the integration of the dose equivalents for the 

various tissues using a weighting scheme for the relative sensitivities of tissues and organs. 

The EPA has published a set of internal dose conversion factors for reference persons of various ages 

(newborn; 1, 5, 10, or 15 years of age; and adult) in its Federal Guidance Report No. 13 supplemental CD 

(EPA 2000). For example, the EPA has estimated that the dose equivalent following ingestion of 1 Bq of 

241Am is 2.1x10-7 Sv (assuming an integration time of 50 years for an adult following the initial 

exposure). Age-specific dose coefficients for inhalation and ingestion of any of the radioactive isotopes 

of americium by the general public can be found in ICRP publications 67 (ICRP 1993), 71 (ICRP 1995), 

and 72 (ICRP 1996). Dose coefficients for inhalation, ingestion, and submersion in a cloud of americium 
AMERICIUM 17 

3. HEALTH EFFECTS 

radionuclides can be found in U.S. EPA Federal Guidance Report No. 11 (EPA 1988). Dose coefficients 

for external exposure to radioisotopes of americium in air, surface water, or soil contaminated to various 

depths can be found in U.S. EPA Federal Guidance Report No. 12 (EPA 1993). 

3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 

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

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

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

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

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

Levels of significant exposure for each route and duration are presented in tables and illustrated in 

figures. The points in the figures showing no-observed-adverse-effect levels (NOAELs) or lowestobserved-adverse-effect levels (LOAELs) reflect the actual doses (levels of exposure) used in the studies. 

LOAELs have been classified into "less serious" or "serious" effects. "Serious" effects are those that 

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

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

or those whose significance to the organism is not entirely clear. ATSDR acknowledges that a 

considerable amount of judgment may be required in establishing whether an end point should be 

classified as a NOAEL, "less serious" LOAEL, or "serious" LOAEL, and that in some cases, there will be 

insufficient data to decide whether the effect is indicative of significant dysfunction. However, the 

Agency has established guidelines and policies that are used to classify these end points. ATSDR 

believes that there is sufficient merit in this approach to warrant an attempt at distinguishing between 

"less serious" and "serious" effects. The distinction between "less serious" effects and "serious" effects is 

considered to be important because it helps the users of the profiles to identify levels of exposure at which 

major health effects start to appear. LOAELs or NOAELs should also help in determining whether or not 

the effects vary with dose and/or duration, and place into perspective the possible significance of these 

effects to human health. 

The significance of the exposure levels shown in the Levels of Significant Exposure (LSE) tables and 

figures may differ depending on the user's perspective. Public health officials and others concerned with 

appropriate actions to take at hazardous waste sites may want information on levels of exposure 
AMERICIUM 18 

3. HEALTH EFFECTS 

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. 

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. 

Americium is a human-made element that has no stable form; all isotopes of americium are radioactive 

(see Section 4.1). Americium isotopes vary with respect to decay rates, decay chain isotopes produced, 

and specific activity (see Section 4.2). Of particular interest is 241Am, a decay product of 241Pu. 

Americium is produced in small quantities (see Section 5.1), and information regarding human exposure 

is limited. Although this Toxicological Profile is not limited to health and pharmacokinetics data for any 

particular radioisotope of americium, available studies primarily involve the isotope 241Am and, to a much 

lesser extent, 243Am. Accidental occupational or environmental exposures to 241Am in humans are usually 

associated with co-exposures to 241Pu (typically in a mixture with a range of plutonium isotopes of mass 

from 238 up to 244) and other radioactive isotopes comprising the major sources of radiation associated 

with nuclear fallout from nuclear explosions and releases from processing and fuel reprocessing plants 

(see Chapter 6). Isolated accidental exposures to household products containing 241Am (e.g., ingestion of 

241Am-containing parts of smoke detectors) have been reported, but did not result in observed adverse 

health effects. Available information on the health effects of americium is based entirely on effects 

observed in humans and animals from radioactivity attributable, at least in part, to americium exposures. 

The animal studies discussed below involve exposures to high doses of ionizing radiation from uptake of 

241Am. As with other substances, uptake and disposition of americium in the body (and, hence, the 

potential for specific health effects from internalized americium) depend upon the chemical properties of 

the particular americium compound to which one may be exposed, as well as the route of exposure (see 

Section 3.4 for more information regarding uptake and disposition of americium). Based on available 

toxicokinetic information and the emissions of americium, the major health concern is radiation damage 

from internalized americium. Health effects may be deterministic in nature or stochastic with a lengthy 

latency period, similar to those reported for other radionuclides with comparable half-lives and 

distribution schemes. Inhalation, ingestion, or dermal absorption of americium compounds (or 

compounds that generate americium via radioactive decay) in amounts large enough to pose a chemical 

health risk would be expected to result in much more significant radiation toxicity. 
 

AMERICIUM 19 

3. HEALTH EFFECTS 

3.2.1 Inhalation Exposure 

Available information from human exposures indicates that airborne americium-containing particles are 

deposited in the respiratory tract, cleared to some extent via mucociliary action, and swallowed or 

expelled (Edvardsson and Lindgren 1976; Fry 1976; Newton et al. 1983; Sanders 1974; Toohey and 

Essling 1980). Descriptions of human respiratory tract models that can be used for radiation protection 

also include relevant information regarding biokinetics of inhaled particles (ICRP 1994b, 1995; NCRP 

1997). Quantitative data for uptake fractions of americium compounds resulting in fast, medium, and 

slow systemic absorption are summarized by ICRP (1996). Supporting animal studies include inhalation 

exposure to aerosols of americium (Buldakov et al. 1972; DOE 1978; Gillett et al. 1985; Sanders and 

Mahaffey 1983; Talbot et al. 1989; Thomas et al. 1972) or intratracheal instillation of americium 

compounds (Moushatova et al. 1996). Estimates of tissue or organ body burden of americium are 

provided in some study reports to demonstrate the target areas of internal deposition of americium. 

3.2.1.1 Death 

No reports were located regarding death in humans resulting from acute-, intermediate-, or chronicduration inhalation exposure to americium. 

Death was noted within 6 months in an unspecified number of dogs following acute exposure to 241Am 

aerosols (as americium nitrate) resulting in inhaled activity of 1.5 μCi/kg (55.5 kBq/kg) (Buldakov et al. 

1972). Significant early mortality, attributed to radiation pneumonitis, was noted in rats following acute 

inhalation of 241AmO2 particles (activity median aerodynamic diameter [AMAD] 0.75–1.39 μm) resulting 

in an approximate initial lung burden of 1.3 μCi (48 kBq) and radiation dose to the lungs of 1,500 rad 

(1.5 Gy) (Sanders and Mahaffey 1983). 

3.2.1.2 Systemic Effects 

No data were located regarding gastrointestinal, dermal, or ocular effects in humans or animals following 

acute-, intermediate-, or chronic-duration inhalation exposure to americium. 
AMERICIUM 20 

3. HEALTH EFFECTS 

Respiratory Effects. No reports were located regarding respiratory effects in humans following 

acute-, intermediate-, or chronic-duration inhalation exposure to americium. External measurements of 

internally deposited 241Am in the lungs of a man exposed to americium in an occupational accident 

determined an initial lung burden of 960 kBq (26 μCi) measured 3 days after the exposure that decreased 

to 55 kBq (1.5 μCi) after 2 years (Breitenstein and Palmer 1989; Robinson et al. 1983). However, no 

pathological changes to the lung attributed to radiation exposure were identified in the autopsy of this 

man 11 years later (Filipy et al. 1995). Exposure was predominantly dermal via facial lacerations, but 

included inhalation. Toohey and Kathren (1995) estimated that the man received a total lung dose of 

1.7 Gy (170 rem) based on the Breitenstein and Palmer (1989) estimate of 1.3 Gy (130 rem) for the first 

5.7 years plus a dose of 0.4 Gy (40 rem) for the remaining 5.7 years, based on estimated lung burden at 

autopsy. See Section 3.2.3.2 for additional information regarding this case of accidental mixed exposure 

to americium. 

No reports were located regarding respiratory effects in animals following intermediate- or chronicduration inhalation exposure to americium. Respiratory insufficiency and pulmonary pneumonia were 

reported in a group of five dogs following acute exposure to 241Am aerosols (as americium nitrate) 

resulting in an inhaled activity of 1.5 μCi/kg (55.5 kBq/kg) (Buldakov et al. 1972). In another study, 

gross and microscopic lung lesions, including pleural thickening, fibrosis, mineralization, and cell 

proliferation, were noted in dogs sacrificed from 127 to 1,022 days following a 10-minute inhalation 

exposure to aerosols of 241Am dioxide (relatively insoluble) that was generated by heating 241Am oxide to 

600 oC). Exposures resulted in estimated initial 241Am body burdens between 38 and 51 μCi (1.4 and 

1.9 MBq). Increased respiratory frequency and decreased tidal volume were observed in two of the early 

sacrifices (Thomas et al. 1972). Radiation pneumonitis was observed in rats exposed once (nose-only) to 

241AmO2 aerosols resulting in a lung tissue activity level of approximately 650 nCi (24 kBq), but not at 

lung tissue activity level of 31 nCi (1.15 kBq) (DOE 1978). 

Cardiovascular Effects. No reports were located regarding cardiovascular effects in humans 

following acute-, intermediate-, or chronic-duration inhalation exposure to americium. 

No reports were located regarding cardiovascular effects in animals following intermediate- or chronicduration inhalation exposure to americium. Various effects on the cardiovascular system, including shifts 

in hemodynamics (blood pressure and flow), electrocardiographic changes, and myocardial ischemia were 

reported in a group of five dogs following acute exposure to 241Am aerosols (as americium nitrate) 

resulting in inhaled activity of 1.5 μCi/kg (55.5 kBq/kg) (Buldakov et al. 1972). 
 

 

AMERICIUM 21 

3. HEALTH EFFECTS 

Hematological Effects. Persistent clinical lymphopenia and thrombocytopenia were observed in a 

64-year-old man exposed to 241Am when an ion-exchange column containing about 100 g of 241Am 

exploded in his face (Filipy et al. 1995). The explosion resulted in contact exposure predominantly via 

lacerated skin and chemical burns on the face and neck areas as well as presumed inhalation exposure 

introducing 241Am into the surrounding tissues and blood circulatory system (Ragan et al. 1983; Robinson 

et al. 1983). The administration of chelating agents would have affected the blood concentration and 

deposition, and may have reduced the potential duration and severity of symptoms. 

No reports were located regarding hematological effects in animals following intermediate- or chronicduration inhalation exposure to americium. Leukopenia and elevated hematopoietic activity were 

reported in a group of five dogs following acute exposure to 241Am aerosols (as americium nitrate) 

resulting in inhaled activity of 1.5 μCi/kg (55.5 kBq/kg) (Buldakov et al. 1972). Hematocrit, total white 

blood cell counts, neutrophils, lymphocytes, and platelets were decreased from pre-exposure values in 

dogs following a 10-minute inhalation exposure to aerosols of 241Am (presumed to be relatively insoluble, 

having been generated by heating 241Am oxide to 600 oC), resulting in estimated initial 241Am lung 

burdens between 38 and 51 μCi (1.4 and 1.9 MBq) (Thomas et al. 1972). These values remained lower 

than pre-exposure values in the dogs individually sacrificed 127, 256, and 512 days postexposure; the 

only apparent recovery occurred in the platelet count of the dog sacrificed 1,022 days postexposure, 

reaching near pre-exposure values approximately 900 days postexposure. 

Musculoskeletal Effects. Information regarding musculoskeletal effects in humans is limited to the 

findings of bone marrow peritrabecular fibrosis and decreased cellularity in bone samples taken from the 

corpse of a 64-year-old man who had been exposed to 241Am when an ion-exchange column containing 

about 100 g of 241Am exploded in his face (Priest et al. 1995). See Section 3.2.3.2 for additional 

information regarding this accident. 

No reports were located regarding musculoskeletal effects in animals following intermediate- or chronicduration inhalation exposure to americium. Pathologic findings in the bone, including fibrosis with focal 

osteoid thickening, focal resorption, and cartilage degeneration, were observed in dogs (initial body 

weights between 8.4 and 10.6 kg) sacrificed between 127 and 1,022 days following a 10-minute 

inhalation exposure to aerosols of 241Am dioxide (presumed to be relatively insoluble, having been 

generated by heating 241Am oxide to 600 oC). Exposures resulted in estimated initial 241Am body burdens 

between 38 and 51 μCi (1.4 and 1.9 MBq) (Thomas et al. 1972). 
AMERICIUM 22 

3. HEALTH EFFECTS 

Hepatic Effects. No reports were located regarding hepatic effects in humans following acute-, 

intermediate-, or chronic-duration inhalation exposure to americium. 

No reports were located regarding hepatic effects in animals following intermediate- or chronic-duration 

inhalation exposure to americium. Changes were observed in the livers of male rats 30 days after a single 

intratracheal instillation (0.2 mL) of 241Am (as americium nitrate), resulting in an internal activity of 

0.05 μCi (1.8 kBq); the effects were predominantly hepatic parenchyma degeneration and focal necrosis 

with the effect observed in areas where blood entered the organ (Moushatova et al. 1996). Liver lesions 

(fatty changes in the centri-lobular region) were also observed in two beagle dogs 512 or 1,022 days 

following a 10-minute inhalation exposure to aerosols of 241Am dioxide (presumed to be relatively 

insoluble, having been generated by heating 241Am oxide to 600 oC). Exposures resulted in estimated 

initial 241Am body burdens between 38 and 51 μCi (1.4 and 1.9 MBq) (Thomas et al. 1972). 

Renal Effects. No reports were located regarding renal effects in humans following acute-, 

intermediate-, or chronic-duration inhalation exposure to americium. 

No reports were located regarding renal effects in animals following intermediate- or chronic-duration 

inhalation exposure to americium. Kidney lesions (generalized glomerular mesangial thickening with 

obliteration) were observed in two beagle dogs 512 or 1,022 days following a 10-minute inhalation 

exposure to aerosols of 241Am dioxide (presumed to be relatively insoluble, having been generated by 

heating 241Am oxide to 600 oC). Exposures resulted in estimated initial 241Am body burdens between 

38 and 51 μCi (1.4 and 1.9 MBq) (Thomas et al. 1972). 

Endocrine Effects. No reports were located regarding endocrine effects in humans following acute-, 

intermediate-, or chronic-duration inhalation exposure to americium. 

No reports were located regarding endocrine effects in animals following intermediate- or chronicduration inhalation exposure to americium. Thyroid gland lesions (gross atrophy, with fibrosis) were 

observed in two beagle dogs 512 or 1,022 days following a 10-minute inhalation exposure to aerosols of 

241Am dioxide (presumed to be relatively insoluble, having been generated by heating 241Am oxide to 

600 EC). Exposures resulted in estimated initial 241Am body burdens between 38 and 51 μCi (1.4 and 

1.9 MBq). Estimated radiation doses to the dogs’ thyroids increased from 30 to 900 rad (0.3–9 Gy) 
AMERICIUM 23 

3. HEALTH EFFECTS 

measured from day 127 through 1,022 days after exposure to 241Am dioxide aerosols (Thomas et al. 

1972). 

Body Weight Effects. No reports were located regarding body weight effects in humans following 

acute-, intermediate-, or chronic-duration inhalation exposure to americium. 

No reports were located regarding body weight effects in animals following intermediate- or chronicduration inhalation exposure to americium. One of four dogs lost approximately 15% of its body weight 

during the time period of 365 days to sacrifice at 512 days following a 10-minute inhalation exposure to 

aerosols of 241Am dioxide (presumed to be relatively insoluble, having been generated by heating 241Am 

oxide to 600 EC). Exposure resulted in an estimated initial body burden of 38 μCi (1.4 MBq) (Thomas et 

al. 1972). 

Metabolic Effects. No reports were located regarding metabolic effects in humans following acute-, 

intermediate-, or chronic-duration inhalation exposure to americium. 

No reports were located regarding metabolic effects in animals following intermediate- or chronicduration inhalation exposure to americium. Increased B-glucuronidase activity was reported in mice 

receiving a single 30-minute nose-only exposure to aerosols of 241Am (as americium nitrate) that resulted 

in a lung-averaged cumulative radiation dose of 2,000 rad (20 Gy) (Talbot et al. 1989). 

3.2.1.3 Immunological and Lymphoreticular Effects 

Lymphopenia was noted in a 64-year-old man exposed to 241Am when an ion-exchange column 

containing about 100 g of 241Am exploded in his face (Filipy et al. 1995), but information regarding the 

immunological consequences of this finding was not available (see Section 3.2.3.2 for additional 

information regarding this accident). 

Leukopenia was reported in a group of five dogs following acute exposure to 241Am aerosols (as 

americium nitrate) resulting in inhaled activity of 1.5 μCi/kg (55.5 kBq/kg) (Buldakov et al. 1972). Total 

white blood cell counts, neutrophils, and lymphocytes were decreased from pre-exposure values in dogs 

following a 10-minute inhalation exposure to aerosols of 241Am dioxide (presumed to be relatively 

insoluble, having been generated by heating 241Am oxide to 600 EC). Exposures resulted in estimated 
AMERICIUM 24 

3. HEALTH EFFECTS 

initial 241Am body burdens between 38 and 51 μCi (1.4 and 1.9 MBq) (Thomas et al. 1972). These values 

decreased in the dogs individually sacrificed 127, 256, and 512 days postexposure. However, no reports 

were located regarding immunological consequences of reduced leukocyte counts in animals exposed to 

americium. 

No reports were located regarding the following health effects in humans or animals following acute-, 

intermediate-, or chronic-duration inhalation exposure to americium: 

3.2.1.4 Neurological Effects 

3.2.1.5 Reproductive Effects 

3.2.1.6 Developmental Effects 

3.2.1.7 Cancer 

No reports were located regarding cancer in humans following acute-, intermediate-, or chronic-duration 

inhalation exposure to americium, and no signs of cancer were found during the autopsy of a heavily 

exposed worker who died 11 years later of unrelated causes (see Section 3.2.3.2). However, EPA 

considers all radionuclides to be known human carcinogens and has calculated cancer risk factors for 

inhaled 241Am and 243Am (see Table 8-1 in Chapter 8 for additional information). 

No reports were located regarding cancer in animals following intermediate- or chronic-duration 

inhalation exposure to americium. Osteosarcomas developed in 4 of 15 dogs surviving more than 

1,000 days following a single inhalation exposure to aerosols of 241AmO2 that resulted in initial lung 

burdens of approximately 2–6 μCi (74–222 kBq) (Gillett et al. 1985). Among the four dogs that 

developed osteosarcomas, the radiation doses to the skeleton, calculated to 1,000 days postexposure, were 

96–410 rad (0.96–4.1 Gy). 

3.2.2 Oral Exposure 

No reports were located regarding the following health effects in humans or animals following acute-, 

intermediate-, or chronic-duration oral exposure to americium: 
AMERICIUM 25 

3. HEALTH EFFECTS 

3.2.2.1 Death 

3.2.2.2 Systemic Effects 

3.2.2.3 Immunological and Lymphoreticular Effects 

3.2.2.4 Neurological Effects 

3.2.2.5 Reproductive Effects 

3.2.2.6 Developmental Effects 

3.2.2.7 Cancer 

No reports were located regarding cancer in humans following acute-, intermediate-, or chronic-duration 

oral exposure to americium, and no signs of cancer were found during the autopsy of a heavily exposed 

worker who died 11 years later of unrelated causes (see Section 3.2.3.2). EPA considers all radionuclides 

to be known human carcinogens and has calculated cancer risk factors for ingested 241Am and 243Am (see 

Table 8-1 in Chapter 8 for additional information). 

3.2.3 Dermal Exposure 

3.2.3.1 Death 

No reports were located regarding death in humans or animals following acute-, intermediate-, or chronicduration dermal exposure to americium. 

3.2.3.2 Systemic Effects 

No data were located regarding respiratory effects, cardiovascular effects, gastrointestinal effects, hepatic 

effects, renal effects, endocrine effects, dermal effects, ocular effects, body weight effects, or metabolic 

effects in humans or animals following acute-, intermediate-, or chronic-duration dermal exposure to 

americium. 
 

 

 

AMERICIUM 26 

3. HEALTH EFFECTS 

Information regarding systemic effects in humans following dermal exposure to americium derives 

mainly from a single case in which a 64-year-old male (USTUR Case 0246) was exposed when an ionexchange column containing about 100 g of 241Am exploded in his face. Numerous studies relate various 

aspects of this accident as well as subsequent treatment and follow-up (Breitenstein and Palmer 1989; 

Filipy et al. 1995; Jech et al. 1983; McMurray 1983; Palmer et al. 1983; Robinson et al. 1983; Thompson 

1983; Toohey and Kathren 1995). The explosion resulted in contact exposure through the intact and 

lacerated skin and in presumed inhalation exposure, evident from external chest measurements of 

radioactivity. The amount of activity initially deposited on the man and his clothing was estimated to be 

1–5 Ci (37–185 GBq). Immediate treatment reduced contamination to approximately 6 mCi (222 MBq). 

By the end of the first day after the accident, the activity had been reduced to 1 mCi (37 MBq). Intense, 

long-term chelation therapy was employed to reduce body burden. Levels of 241Am in the victim’s blood 

collected the day of the exposure was estimated initially at 6.4 μCi and decreased 10-fold 6 days later to 

0.64 μCi following chelation therapy (Robinson et al. 1983). 

Hematological Effects. Significant, but transient effects on erythropoiesis were indicated by a 

decrease in erythrocyte concentration, hemoglobin concentration, and packed red cell volumes. Clinical 

lymphopenia and thrombocytopenia persisted for 5 years post-exposure. The lymphopenia had rapid 

onset and a slow recovery, although pre-exposure values were not attained by 11 years postexposure, at 

which time, the man died of unrelated causes (Filipy et al. 1995). Histopathologic examination of bone at 

autopsy revealed pathologic changes including peritrabecular fibrosis, bone cell depletion, and bone 

marrow atrophy (Priest et al. 1995), but these changes could not be directly related to estimated radiation 

dose or bone turnover rates as a result of dermal exposure. 

3.2.3.3 Immunological and Lymphoreticular Effects 

Leukopenia was observed in a 64-year-old man following 241Am exposure (Filipy et al. 1995), but 

information regarding the immunological consequences of this finding was not available. 

No reports were located regarding the following health effects in humans or animals following acute-, 

intermediate-, or chronic-duration dermal exposure to americium: 
AMERICIUM 27 

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 reports were located regarding cancer in humans following acute-, intermediate-, or chronic-duration 

dermal exposure to americium, however, no signs of cancer were found during the autopsy of a heavily 

exposed worker who died 11 years later of unrelated causes (see Section 3.2.3.2). EPA considers all 

radionuclides to be known human carcinogens and has calculated cancer risk factors for external exposure 

to 241Am and 243Am (see Table 8-1 in Chapter 8 for additional information). 

3.2.4 Other Routes of Exposure 

3.2.4.1 Death 

No reports were located regarding death in humans resulting from acute-, intermediate-, or chronicduration exposure to americium by routes other than inhalation, oral, dermal, or external exposure. 

Dose-related decreased long-term survival was observed in beagle dogs following single intravenous 

injections of 241Am at average activity levels of 1.9–2,900 nCi/kg (0.07–107 kBq/kg) (Taylor et al. 1991, 

1993a). 

3.2.4.2 Systemic Effects 

No data were located regarding systemic effects in humans following acute-, intermediate-, or chronicduration exposure to americium by routes other than inhalation, oral, dermal, or external exposure. No 

data were located regarding respiratory effects, cardiovascular effects, gastrointestinal effects, renal 

effects, dermal effects, ocular effects, or metabolic effects animals following exposure to americium by 

routes other than inhalation, oral, dermal, or external exposure. 
AMERICIUM 28 

3. HEALTH EFFECTS 

Hematological Effects. A limited study reported dose-related depressions in white blood cell counts 

in dogs that were administered single intravenous injections of 241Am at activity levels of 0.1–2.8 μCi/kg 

(3.7–103.6 kBq/kg) (Dougherty 1970). Maximum depression in granular leukocytes and monocytes was 

reached approximately 1 month post injection. Depression of lymphocytes occurred more slowly; 

minimal values were reached 1 year or more post injection, with little indication for recovery in the dogs 

receiving the two highest doses of 0.9 or 2.8 μCi/kg (33.3 or 103.6 kBq/kg). Depression of red blood 

cells was observed only in groups of dogs injected with 241Am at activity levels of ≥0.9 μCi/kg 

(33.3 kBq/kg). 

Hepatic Effects. Degenerative liver changes, severe reduction in liver weight, and early death 

(typically attributed to bone cancer) were observed in dogs following single intravenous injections of 

241Am citrate at activity levels of approximately 2.9 μCi/kg (107 kBq/kg) (Taylor et al. 1991). The 

average radiation dose to the liver in these dogs was 590 rad (5.9 Gy). Degenerative liver changes and 

early death were also reported in dogs administered single intravenous injections of 241Am at a similar 

activity level (2.8 μCi/kg or 104 kBq/kg) (Lloyd et al. 1970; Taylor et al. 1993a). 

Endocrine Effects. Thyroid weights were significantly lower in adult beagle dogs administered 

single intravenous injections of 241Am citrate at activity levels ranging from approximately 0.3 to 

2.75 μCi/kg (11–102 kBq/kg) than those of controls (Taylor et al. 1993a), resulting in thyroid doses of 8– 

2,976 rad (0.08–29.76 Gy). Histologic examination revealed follicular hyperplasia and degenerative 

cellular changes. Lower serum thyroxine levels were noted in the peripheral blood of dogs in the two 

highest exposure groups. 

3.2.4.3 Immunological and Lymphoreticular Effects 

A limited study reported dose-related depressions in white blood cell counts in dogs that were 

administered single intravenous injections of 241Am citrate at activity levels of 0.1–2.8 μCi/kg (3.7– 

103.6 kBq/kg) (Dougherty 1970). Maximum depression in granular leukocytes and monocytes was 

reached approximately 1 month post injection. Depression of lymphocytes occurred more slowly; 

minimal values were reached 1 year or more post injection. 
AMERICIUM 29 

3. HEALTH EFFECTS 

3.2.4.4 Neurological Effects 

No reports were located regarding neurological effects in humans or animals following acute-, 

intermediate-, or chronic-duration exposure to americium by routes other than inhalation, oral, dermal, or 

external exposure. 

3.2.4.5 Reproductive Effects 

No reports were located regarding reproductive effects in humans following acute-, intermediate-, or 

chronic-duration exposure to americium by routes other than inhalation, oral, dermal, or external 

exposure. 

Dose-related increased incidences of death were reported among 14- and 17-day-old fetuses of rats that 

had been administered single intravenous injections of 241Am between 1 and 10 days prior to mating 

(Moskalev et al. 1969). In this study, 241Am was administered at activity levels of 0.2–96 μCi/kg (7.4– 

3,552 kBq/kg) that produced antenatal fetal tissue doses up to 200 rad (2 Gy). During gestation, 

concentrations of 241Am were 9–15 times higher in placental tissues than in fetuses. The investigators 

indicated that death may have been the result of placental changes. 

3.2.4.6 Developmental Effects 

No reports were located regarding developmental effects in humans following acute-, intermediate-, or 

chronic-duration exposure to americium by routes other than inhalation, oral, dermal, or external 

exposure. 

Decreased fetal weight and increased fetal death were reported following single intravenous injection of 

pregnant rats with 241Am (activity level 90 μCi/kg or 3,330 kBq/kg) on gestation day 9 (Rommereim and 

Sikov 1986; Rommereim et al. 1985). The investigators indicated a tendency toward increased incidences 

of fetuses with anomalous ribs, which they attributed to americium exposure at an early critical stage of 

fetal development. 
 

AMERICIUM 30 

3. HEALTH EFFECTS 

3.2.4.7 Cancer 

No reports were located regarding carcinogenic effects in humans following acute-, intermediate-, or 

chronic-duration exposure to americium by routes other than inhalation, oral, dermal, or external 

exposure. 

Increases in bone cancers occurred in animals administered a single intraperitoneal or intravenous 

injection of 241Am and observed over their life span. Schoeters et al. (1991) reported bone tumor 

induction in mice receiving injections of 22,000 or 58,000 Bq 241Am/kg (0.59 μCi or 1.57 μCi/kg) and 

early mortality from non-neoplastic diseases in mice receiving larger activities of 190, 373, or 1,197 kBq 

241Am/kg (5.14, 10.1, or 32.4 μCi/kg). Mice administered 45,000, 90,000, or 213,000 Bq 241Am/kg (1.22, 

2.43, or 5.76 μCi) (Van Den Heuvel et al. 1995) via intravenous injection, which produced respective 

radiation doses to the femur of 2.3, 3.6, and 8.4 Gy (230, 360, and 840 rad), showed increased incidence 

for osteosarcomas at 45,000 Bq/kg (0.8 kBq/mouse). Rats administered 0.03 μCi 241Am/g via injection 

into the tail developed osteosarcomas (Carter et al. 1951). Young adult beagle dogs were administered a 

single injection of graded activities of 0.016-3.0 μCi/kg 241Am (592–111,000 Bq/kg) that resulted in bone 

sarcomas at low doses not expected to cause adverse effects. A 100% incidence of sarcomas was 

observed in the dogs receiving higher activities (Jee et al. 1985). Companion experiments using boneseeking radionuclides in beagle dogs were conducted over 35 years (1952–1987) by Lloyd et al. (1994a, 

1994b, 1995); several biological effects were observed during the lifespan of the animals. The initial 

report, a comparative toxicity study for 241Am to 226Ra, both bone-seeking internal emitters, showed 

similar ratios for relative effectiveness for bone cancer induction in dogs (Lloyd et al. 1994a) and mice 

(Taylor et al. 1983) administered 241Am via intravenous injection. Lloyd et al. (1994b) reported skeletal 

malignancies among beagles receiving graded activities of 0.07–104 kBq 241Am/kg (0.002–2.8 μCi/kg) 

via a single intravenous injection as the first of the companion experiments. In the second part of the 

experiment, Lloyd et al. (1995) conducted an analysis of all soft tissue tumors in the dogs treated by 

intravenous injection. The authors reported both positive and negative associations between exposure and 

tumor incidence, apparent in a variety of soft tissues, but the development of these tumors appeared to be 

influenced by the competing risk of death from bone cancer or other severe radiation effects (Lloyd et al. 

1995). Incidence of tumors in mice administered activities of 6, 17, or 29 kBq 241Am/kg (0.2, 0.5, or 

0.8 μCi/kg) were higher for liver (adenomas and carcinomas) than for bone sarcomas (Ellender et al. 

2000), supporting similar findings in earlier investigations. In a study of dogs administered single 

intravenous injections of 241Am that ranged from 0.07 to 107 kBq Am/kg (from 0.002 to 2.9 μCi/kg), the 

incidence of death was dose-related and was predominantly due to bone cancer (Taylor et al. 1991). 
 

AMERICIUM 31 

3. HEALTH EFFECTS 

However, the incidence of liver tumors was higher than that of bone tumors in dogs exposed to lower 

levels of 241Am. Moskalev et al. (1989) reported that injecting pregnant Wistar rats with 92.5 kBq 

241Am/kg (3.4 μCi/kg) as nitrate on gestation day 16 produced 4 osteosarcomas in 78 female and 52 male 

offspring, compared with no cancers in the controls. In a communication by Lloyd et al. (2001), the 

authors concluded that longevity of irradiated mammals exposed to low-level exposures of bone-seeking 

radionuclides was independent of dose, except for radiation-induced malignancies or other radiation 

effects. 

3.3 GENOTOXICITY 

No reports were located regarding genotoxic effects in humans following acute- or intermediate-duration 

inhalation exposure to americium. Chromosomal aberrations (symmetrical translocations and dicentrics 

and ring chromosomes) in lymphocyte preparations were elevated for an entire group of seven nuclear 

fuel production workers who were exposed for 11–22 years to external gamma radiation, with an 

additional internal exposure for six of these workers to alpha-emitting 241Am 5 years prior to the analysis 

(Bauchinger et al. 1997). The total effective dose equivalent for the workers from exposure to external 

gamma radiation and internal contamination with 241Am were: 393, 39, 207, 304, 202, 237, and 349 mSv 

(whole body) (39.3, 3.9, 20.7, 30.4, 20.2, 23.7, and 34.9 rem). In five of the six cases that included 

internal contamination, the committed effective dose equivalent from 241Am represented 5–25% of the 

total dose, the main contribution coming from external exposure to gamma radiation. In the other worker, 

internalized 241Am represented 66% of the total effective dose equivalent of 39 mSv (3.9 rem). Another 

case involved a radiation worker and his wife, college-age daughter, and 10-year-old son who were 

exposed for several years in their house to elevated levels of 241Am that resulted in body burdens of 6.5– 

89 nCi (0.24–3.3 kBq) from a source used by the father for private experiments. Chromosomal 

aberrations in isolated leukocytes were noted to be similar to those observed in other cases of accidental 

or therapeutic exposure to external radiation sources (Kelly and Dagle 1974). The cytogenetic damage 

observed was low and only grossly comparable to historical control values available to the authors. The 

limited human data do not indicate a significant genotoxic response to inhaled americium. 

No reports were located regarding genotoxic effects in animals following intermediate- or chronicduration inhalation exposure to americium. A single report regarding genotoxic effects following acute 

inhalation exposure to americium indicated decreased numbers of pulmonary alveolar macrophages 

(PAMs) (maximum decrease at day 21), increased numbers of micronuclei, and multinucleated cells in 
 

AMERICIUM 32 

3. HEALTH EFFECTS 

mice receiving a single 30-minute nose-only exposure to 241Am (as americium nitrate) producing a 

cumulative radiation dose of 2,000 rad (20 Gy) to lungs (Talbot et al. 1989). The initial alveolar 

deposition was 32.4 nCi (1.2 kBq), but rapidly declined to about 8.1 nCi (300 Bq) by 21 days and to 

approximately 2.7 nCi (100 Bq) by the end of the study (day 98). Following exposure to 241Am, 

essentially all PAMs contained 241Am; significant amounts of 241Am were still observed at each sacrifice 

time period between postexposure days 3 and 98. 

No reports were located regarding genotoxic effects in humans or animals following acute-, intermediate-, 

or chronic-duration oral or dermal exposure to americium. 

3.4 TOXICOKINETICS 

3.4.1 Absorption 

3.4.1.1 Inhalation Exposure 

Evidence for absorption of inhaled americium to blood of humans is provided by several cases of workers 

who were accidentally exposed to airborne 241Am (Edvardsson and Lindgren 1976; Fry 1976; ICRP 1996; 

Kathren et al. 2003; Newton et al. 1983; Sanders 1974; Toohey and Essling 1980). Although these cases 

do not provide a complete quantitative description of the absorption of inhaled americium in humans, they 

clearly demonstrate that inhaled americium oxides (e.g., AmO2) can be absorbed, as indicated by the 

detection of 241Am radioactivity in regions of the body such as liver and bone, and excretion in urine. 

In one case, an adult worker inhaled aerosols of plutonium and americium dioxides (239PuO2 and 

241AmO2) (Newton et al. 1983). Thoracic counts of radioactivity that were determined by an external 

radiation detector starting 7 days after the exposure showed that 241Am was removed from the chest area 

with biological half-times of 11 (80%) and 920 (20%)days. These estimates were assumed to reflect 

clearance from the lung to systemic compartments. However, fecal excretion was estimated to be 

approximately 50% of the estimated initial deposit of 241Am in the lung, suggesting that extensive 

mechanical transport to the gastrointestinal tract, typical of inhaled large particles, may have occurred. 

External counting also detected 241Am in the skull on day 913 post accident, suggesting that 241Am was 

transferred to the skeleton. 
AMERICIUM 33 

3. HEALTH EFFECTS 

In a second case, an adult worker inhaled mixed oxides of curium and americium dioxides (244CmO2 and 

241AmO2) (244Cm:241Am airborne ratio, 3:1), which resulted in the deposition of approximately 450 nCi 

(16.6 kBq) of radioactivity in the lungs, or approximately 112 nCi (4.1 kBq) of 241Am (Sanders 1974). 

Chest counts of the subject indicated that total radioactivity was retained in the lungs with a half-time 

(i.e., decay-corrected) of 28 days; however, data on the elimination of each isotope from the lung were 

not reported. Most of the elimination from the chest area was accounted for by recovery of radioactivity 

in the feces, consistent with mechanical clearance of the deposited activity to the gastrointestinal tract. 

Evidence for systemic absorption in this case was the detection of 241Am in urine; approximately 1.1 nCi 

(41 Bq, 1% of the deposited activity) of 241Am was excreted in urine in 365 days, with a half-time of 

35 days. 

In a third case, two adults accidentally inhaled 241AmO2 (particle size not specified), which resulted in the 

deposition of approximately 15 nCi (555 Bq) of activity in the lungs (Fry 1976). Chest activity measured 

over a period of 200–1,500 days after the accident indicated that the retention half-time for 241Am in the 

lungs was between 900 and 1,400 days. Activity measured over the chest, liver, and extremities (knees 

and ankles, reflecting primarily bone activity) indicated that by 324 days after the accident, approximately 

41% of the whole-body activity was in the lung, 47% was in the liver, and 12% was in bone. After 

1,392 days, lung activity had decreased to 18%, liver activity was unchanged (47%), and bone activity 

had increased to 35%. 

In a more recent case, an adult male accidentally inhaled 241Am (believed to be in oxide form), which 

resulted in an intake of approximately 6.3 kBq (170 nCi) of activity (Kathren et al. 2003). Results of 

radioactivity measurements in the chest area between days 48 and 2,135 following the accident indicated 

that 241Am was cleared from the lungs with half-times of 110 and 10,000 days. 

Additional evidence for absorption of inhaled americium, and more quantitative estimates of the extent of 

and rates of absorption, are provided by animal experiments. The lung deposition and absorption of 

inhaled aerosols of americium nitrates and oxides have been studied in experimental animals; the results 

of representative studies are provided in Table 3-1. In general, exposures were nose-only (although this 

was not always specified in the reports) to relatively well-characterized aerosols of 241Am compounds. In 

most studies, the actual exposure concentration of americium was not reported. Estimates of lung 

retention half-times reflect the rate of loss of radioactivity from the lung following any initial (3–8 days) 

loss of americium that may have been transferred to the gastrointestinal tract and excreted without 

absorption. In some studies, absorption half-times to the blood were estimated. In either case, the 
 

 

 

 

 

 

AMERICIUM 34 

3. HEALTH EFFECTS 

Table 3-1. Retention and Absorption Estimates in Animals 

Exposed to Americium Compounds by Inhalation 

Animal 

model 

Am 

species 

Stanley et al. 1982 

Exposure 

Exposure 

concentrationa 

Aerosol 

AMAD 

(μm±GSD) 

Lung deposition 

(percent of 

intake) 

Lung retention or 

absorption halflifeb 

Monkey, 

adult 

241AmO2 

(dust)c 

Aerosol No data 1.5±1.6 67 nCi 

21 ng 

47 days (89%) 

550 days (11%) 

(retention) 

Mewhinney and Muggenburg 1985 

Monkey, 

3–5 

years 

241AmO2 Aerosol, 

nose-only 

No data 1.4 75 μCi/kg 

23 μg/kg 

0.1 days (32%) 

160 days (68%) 

(retention) 

Mewhinney et al. 1982 

Dog, 

adult 

241AmO2 Aerosol, 

nose-only, 

20 minutes 

No data 0.75±1.2 41% 

60–250 nCi/kg 

18–77 ng/kg 

9 days (89%) 

283 days (11%) 

(retention) 

No data 1.5±1.07 39% 

39–240 nCi/kg 

12–74 ng/kg 

13 days (76%) 

171 days (24%) 

(retention) 

No data 3.0±1.06 30% 

30–190 nCi/kg 

12–59 ng/kg 

13 days (69%) 

167 days (31%) 

(retention) 

Stanley et al. 1982 

Dog, 

adult 

241AmO2 

(dust)c 

Aerosol No data 2.2±1.8 190 nCi 

59 ng 

39 days (67%) 

5,000 days 

(33%) 

(retention) 

Thomas et al. 1972 

Dog, 

adult 

241AmO2 Aerosol, 

nose only 

10 minutes 

2.18 Ci/m3 

673 mg/m3 

0.8– 

1.0±1.5 

50% 

2.1–3.1 μCi/kg 

0.7–1.0 μg/kg 

20–30 days 

(retention) 

Craig et al. 1975 

Dog, 

adult 

241AmO2 Aerosol, 

nose-only 

42–336 Ci/m3 

13–104 mg/m3 

1.40±1.69 No data ~60 days 

(retention) 
 

 

 

 

 

 

AMERICIUM 35 

3. HEALTH EFFECTS 

Table 3-1. Retention and Absorption Estimates in Animals 

Exposed to Americium Compounds by Inhalation 

Aerosol Lung deposition Lung retention or 

Animal Am Exposure AMAD (percent of absorption halfmodel species Exposure concentrationa (μm±GSD) intake) lifeb 

Craig et al. 1979 

Dog, 241AmO2 Aerosol, 0.66 mCi/m3 0.63±2.64 13% 20–30 days 

adult nose-only 0.20 mg/m3 1,2 nCi 120 days 

0.38 ng 400 days 

(retention) 42 mCi/m3 1.25±1.77 30% 

13 mg/m3 120 nCi 

37 ng 

340 mCi/m3 1.35±1.74 35% 

105 mg/m3 1,150 nCi 

355 ng 

Stather et al. 1979 

Hamster, 241AmO2 Aerosol No data 1.9±2.0 45 nCi/kg 11 days 

adult 14 ng/kg 200 days 

(retention) 

Stanley et al. 1982 

Rat, 241AmO2 Aerosol No data 2.3±1.7 7.8 nCi 95 days (89%) 

adult (dust)c 2.4 ng/kg	 2,800 days 

(11%) 

(retention) 

Stradling et al. 1992, 1994 

Rat, 241AmO2 Aerosol, No data 2.1±1.78 0.14 nCi/kg 2,000 days 

adult (dust)d nose-only, 0.042 ng/kg >10,000 days 

1-hour (absorption) 

Stradling and Stather 1989 

Rat, 241Am Aerosol, No data 0.3±2.5 75 nCi/kg 49 days 

adult nitrate nose-only 23 ng/kg 315 days 

1–2 hour (absorption) 

241AmO2 No data 1.4±2.0 26 nCi/kg 7,000 days 

(dust)e 8.1 ng/kg 7,000 days 

(absorption) 

241Am No data 3.8±1.6 0.51 nCi/kg 170 days 

nitrate 0.16 ng/kg 1,200 days 

(dust)f (absorption) 

241Am No data 1.8±2.4 0.11 nCi/kg 47 days 

chloride 0.035 ng/kg 1,700 days 

(dust)g (absorption) 
 

AMERICIUM 36 

3. HEALTH EFFECTS 

Table 3-1. Retention and Absorption Estimates in Animals 

Exposed to Americium Compounds by Inhalation 

Animal 

model 

Am 

species Exposure 

Exposure 

concentrationa 

Aerosol 

AMAD 

(μm±GSD) 

Lung deposition 

(percent of 

intake) 

Lung retention or 

absorption halflifeb 

Moody et al. 1991 

Rat, 

adult 

241Am 

(dust)h 

Aerosol, 

nose-only 

No data 1.26±1.29 11 nCi/kg 

3.6 ng/kg 

0.21±1.61 89 nCi/kg 

27.6 ng/kg 

1.74±1.94 47 nCi/kg 

14 ng/kg 

241Am 

(dust)i 

1.63±1.76 2.3 nCi/kg 

0.7 ng/kg 

14,000 days 

>17,000 days 

(absorption) 

5,800 days 

8,600 days 

(absorption) 

4,600 days 

>14,000 days 

(absorption) 

170 days 

290 days 

380 days 

(absorption) 

a

Where only activity was reported, mass concentration of Am was calculated assuming a specific activity of 3.24 Ci/g. b

Retention reflects total elimination from lung; absorption reflects transfer to blood 

c

Powder collected from plutonium oxide milling operation 

d

Dust from a weapons test site 

e

Dust from ambient oxidation of Pu metal 

f

Dust from corrosion of industrial process line equipment, mainly aged Pu/Am nitrate intimately mixed with corrosion 

products 

g

Dust from green salt formed in the electrorefining of Pu metal h

Dust derived from ignition of Pu (900–1,000 EC) i

Dust derived from air oxidation of molten Pu 

Note: Footnotes d-i apply to americium in a Pu-bearing matrix where Am absorption kinetics may have been determined 

by Pu dissolution. 

AMAD = activity median aerodynamic diameter; GSD = geometric standard deviation 
 

AMERICIUM 37 

3. HEALTH EFFECTS 

estimates were based on curve-fitting of the data on lung radioactivity-time profiles and other 

assumptions. Thus, some of the differences in estimates undoubtedly reflect differences in particle size 

(known to significantly affect deposition pattern within and mucociliary clearance from the respiratory 

tract), solubility in biological fluids, curve-fitting method, duration of observations, and intra-study 

variability; nevertheless, general trends are evident. Retention and systemic absorption can be described 

with two or three rate functions that represent fast and slower processes for transfer of americium from 

the lung (albeit with considerable differences in the rates reported in various studies, probably reflecting 

differences in particle size distribution, animal species, and exposure scenarios). For example, in 

monkeys exposed to aerosols of 241AmO2 (AMAD, 1.4 μm), retention half-times of 241Am were 0.1 days 

(32% of the initial deposited) and 160 days (68%) (Mewhinney and Muggenburg 1985). Stanley et al. 

(1982) also observed both fast and slower phases of lung retention in monkeys exposed to 241AmO2. 

Mewhinney et al. (1982) found that in dogs exposed to aerosols of americium dioxide (AMAD 0.8– 

3.5 μm), approximately 30–50% of the inhaled activity was deposited in the lung; for an AMAD of 

0.8 μm, the estimated retention half-times were 9 and 290 days for 89% and 11% of the lung burden, 

respectively. Within 8 days of exposure, 32% of the initial lung burden was detected in extra-respiratory 

tissues, mainly the liver (21%) and skeleton (11%). The observations of rapid and slow phases of 

retention of americium initially deposited in the respiratory tract are consistent with the results of other 

studies of dogs exposed to 241AmO2 aerosols (Craig et al. 1975; Thomas et al. 1972). Studies in rodents 

indicate that inhaled americium nitrates and chlorides are absorbed more rapidly than americium oxides 

(Stather et al. 1979b; Stradling and Stather 1989; Stradling et al. 1994). Americium oxides in dusts from 

weapon sites and industrial facilities were absorbed particularly slowly, with absorption half-times of 5– 

25 years, although this may also vary depending on the process that leads to the production of the dust. 

For example, americium oxides in dust formed during the ignition of plutonium were absorbed from the 

lung with a half-time of 0.5–1 year, whereas americium oxides produced from the air oxidation of molten 

Pu had absorption half-times exceeding 12 years (Moody et al. 1991). This may reflect differences in the 

compounds produced (e.g., Pu-Am particles that are surface but not volume oxidized) or oxide species 

formed under different conditions (e.g., temperature, etc.). 

Information on the absorption of americium from the lung also can be derived from studies in which 

americium compounds were instilled directly into the trachea. Although intratracheal instillation does not 

precisely mimic inhalation exposure, rates of absorption of the deposited americium have been shown to 

be comparable for both routes of exposure. For example, Stradling et al. (1992) estimated nearly identical 

half-times for absorption of 241Am in rats that received either intratracheal instillations of 241Am oxidecontaining dust or inhalation exposure to aerosols of the same dust (fast phase approximately 2,000 days, 
AMERICIUM 38 

3. HEALTH EFFECTS 

slower phase >10,000 days). Estimates of absorption half-times in rats that received intratracheal 

instillations of 241AmO2 in various types of dusts from weapons or fuel facilities indicate a slow and fast 

component to absorption, with the fast component ranging from 1 to 5 years, and rates of absorption 

following intratracheal instillation of americium nitrate, citrate, or hydroxide are higher than after 

instillation of americium oxides (Crawley et al. 1976; Müller et al. 1989; Stradling et al. 1989, 1992, 

1994). 

3.4.1.2 Oral Exposure 

Human studies indicate that <0.1% of the ingested activity is absorbed into blood, which is consistent 

with numerous observations that have been made in experimental animals. Infant uptake may be closer to 

0.5% (ICRP, 1996). Absorption of americium contained in shellfish (molluscs) has been studied in 

humans. Eight adult subjects (six males and two females) ingested molluscs (winkles), collected from 

marine waters near the British Nuclear Fuels facility at Sellafield, Cumbria, that contained 241Am (Hunt et 

al. 1986a, 1986b). The range in the ingested activity of 241Am was 18–76 Bq (0.49–2.1 nCi, 0.15– 

0.63 ng). Serial 24-hour urine samples were collected from each subject for up to 10 days after they 

ingested the molluscs. The fraction of the activity absorbed was estimated as the ratio of the observed 

cumulative urinary excretion of 241Am to that of the excretion predicted to occur if absorption had been 

complete. The latter was predicted using a kinetic model of excretion of absorbed americium described 

by Takada et al. (1984). The reported geometric mean absorption for the eight subjects was 

0.6x10-4 (geometric standard deviation [GSD], 0.1; range, 0.4x10-4–2.1x10-4), or 0.006% of the ingested 

activity. Seven of the initial eight subjects and one new subject participated in a subsequent study (six 

males and two females) in which the same protocol was implemented and the 241Am activity range was 

10–25 Bq (0.27–0.68 nCi, 0.083–0.21 ng) (Hunt et al. 1990). The arithmetic mean absorption fraction 

was 0.8x10-4 (range, 0.4x10-4–1.5x10-4) or 0.008% of the ingested activity. When the results of the two 

studies were combined, the arithmetic mean absorption fraction was 0.9x10-4 (range, 0.3x10-4–2.5x10-4) 

or 0.009% of the ingested activity; absorption fractions for males and females were similar. Three of the 

initial eight subjects and three new subjects participated in a third study (five males and one female) in 

which the same protocol was implemented; however, the subjects ingested cockles collected from 

Ravenglass, Cumbria for a range of ingested activity of 15–17 Bq (0.41–0.46 nCi, 0.13–0.14 ng) (Hunt 

1998). The arithmetic mean absorption fraction was 1.2x10-4 (range, 0.3x10-4–2.6x10-4) or 0.012% of the 

ingested activity. 
 

AMERICIUM 39 

3. HEALTH EFFECTS 

Information on the absorption of ingested AmO2 is provided from accidental oral exposures. In one case, 

a worker ingested a ceramic particle containing approximately 2.85 μCi (105 kBq, 0.88 μg Am) of 

241AmO2. During the first 8 days after the particle was ingested, approximately 4 pCi (0.15 Bq) or 

0.00014% of the estimated activity was excreted in the urine (Smith et al. 1983). In a second case, a 

worker swallowed two 2-mm (diameter) silver disks used in the manufacture of smoke detectors, which 

contained approximately 4.22 μCi (156 kBq, 1.3 μg) of 241Am. The subject excreted the disks in feces on 

days 16 and 24 post ingestion. Urinary 241Am excretion during this time was approximately 3 pCi 

(0.11 Bq, 0.7 ng Am) or 0.0007% of the ingested activity (Rundo et al. 1977). The time lapse between 

ingestion and fecal excretion of the disks was related to suspected delay in esophageal transit and 

infrequent bowel movements by the subject. 

Studies in nonhuman primates provide additional evidence that <0.1% of an ingested amount of 

americium is absorbed. Ham et al. (1994) estimated the gastrointestinal absorption of americium in 

marmosets by comparing the retention of 241Am in the liver and carcass after intraperitoneal injection of a 

citrate solution containing 241Am (1.6 Bq, 43 pCi, 0.012 ng Am) or after gastric intubation with 241Am 

mixed with potato powder (250 Bq, 6.7 nCi, 2.0 ng Am). The absorption fraction of 241Am mixed with 

potato powder was estimated to be approximately 6x10-4 or 0.06% of the administered activity. 

Gastrointestinal absorption of americium has also been estimated in pigs, guinea pigs, mice, and rats. The 

results of representative studies are provided in Table 3-2. Whilst these studies differ in the methodology 

used to estimate absorption, they reveal certain important trends. In general, the animal studies reveal a 

relatively low absorption of ingested americium across species (<1% in adult animals). In the pig, guinea 

pig, hamster, and rat, absorption is higher by a factor of 30–200 in neonatal animals compared with adults 

and/or progressively decreases in magnitude with age after birth (to a factor of 4 at 30 days for the guinea 

pig) (Bomford and Harrison 1986; David and Harrison 1984; Sullivan et al. 1985). Americium appears to 

be absorbed to a similar extent when it is ingested as an aqueous solution of water soluble nitrates or 

citrates or when it is incorporated into foods, such as molluscs, potato, or liver tissue (Bulman et al. 1993; 

Ham et al. 1994; Harrison et al. 1988; Hisamatsu and Takizawa 1987; Stather et al. 1979a). Absorption 

of relatively water insoluble oxides of americium is lower by a factor of 4–10 compared with the 

absorption of americium citrate, whose absorption factor is a factor of 3–6 lower than that of americium 

nitrate (Stather et al. 1979a; Sullivan 1980a, 1980b). Similarly, in rats, the absorption of americium from 

surface dust from a weapons site was lower by a factor of 10–50 compared to americium oxide or nitrate 

(Harrison et al. 1994; Sullivan 1980b). A species difference was noted; guinea pigs absorbed 5 times 

more americium than rats. Other factors that appear to increase absorption in rats include fasting 
 

 

AMERICIUM 40 

3. HEALTH EFFECTS 

Table 3-2. Absorption Estimates in Animals Exposed to Americium Compounds 

by Ingestion 

Animal model 

Marmoset, 

adult 

Dose and mediaa 

241Am in potato 

powder, single gavage 

dose, 2.0 ng 

Absorption 

(percent of dose) 

0.06 

Basis for estimate of 

absorption 

Absorption estimate based 

on comparisons with liver 

and carcass 241Am after an 

Reference 

Ham et al. 

1994 

intraperitoneal dose 

Pig, 

adult 

Pig, 

miniature 

241Am citrate aqueous 

solution, single gavage 

dose, 190 μg/kg 

241Am citrate aqueous 

solution, single gavage 

dose, 75 μg/kg 

0.16 

0.06 

Absorption estimate based 

on maximum whole-body 

241Am (8 days), without 

adjustment for excretion 

Eisele et al. 

1987 

Pig, 

neonate 

241Am nitrate aqueous 

solution, single gavage 

dose 

~3 Absorption estimate based 

on carcass 241Am (5 days), 

without adjustment for 

excretion 

Sullivan and 

Gorham 

1983 

Guinea pig, 

neonate–adult 

241Am citrate aqueous 

solution, single dose 

applied to tongue, 

0.6–0.9 μg/kg 

% 

1.1 

0.55 

0.19 

0.17 

0.06 

0.03 

0.02 

Age 

0.5 d 

1 d 

5 d 

10 d 

15 d 

20 d 

30 d 

Absorption estimate based 

on comparisons with liver 

and carcass 241Am after an 

intraperitoneal dose 

(neonates) or intravenous 

dose (adults), with 

adjustment for excretion 

Bomford and 

Harrison 

1986 

0.005 adult 

Guinea pig and 

rat, adult 

241Am in three surface 

dust samples, single 

dose applied to tongue 

(GP, 5–15 ng/kg) or 

fed (rat, 12–49 ng/kg) 

GP 

0.002 

0.005 

— 

Rat 

0.0003 

0.001 

0.001 

Absorption estimate based 

on comparisons with liver 

and carcass 241Am after an 

intraperitoneal dose, with 

adjustment for excretion 

Harrison 

et al. 1994 

Guinea pig, 

adult 

241Am nitrate, aqueous 

solution, single gavage 

dose, 2–4.4 μg 

0.017–0.031 Absorption estimate based 

on sum of liver, skeletal, 

and urine 241Am 

Sullivan 

1980a 

Hamster, 

neonate– 

weaning 

241Am nitrate, aqueous 

solution, single dose 

applied to tongue, 

1.6–2.5 ng 

% 

4.5 

1.70 

0.50 

0.006 

0.02 

Age 

1 d 

4 d 

7 d 

22 d 

30 d 

Absorption estimate based 

on comparisons with liver 

and carcass 241Am after an 

intraperitoneal dose, with 

adjustment for excretion 

David and 

Harrison 

1984 
AMERICIUM 41 

3. HEALTH EFFECTS 

Table 3-2. Absorption Estimates in Animals Exposed to Americium Compounds 

by Ingestion 

Animal model Dose and mediaa Absorption 

(percent of dose) 

Basis for estimate of 

absorption Reference 

Hamster, adult 241Am nitrate, aqueous 

solution, single gavage 

dose, 2.8 ng/kg 

241Am citrate aqueous 

solution, single gavage 

dose, 2.6 ng/kg 

0.054 

0.012 

Absorption estimate based 

on comparisons with liver 

and carcass 241Am after an 

intravenous dose, with 

adjustment for excretion 

Stather et al. 

1979 

241Am dioxide, aged 

aqueous suspension, 

single gavage dose, 

19 ng/kg 

0.0058 

241Am in liver from 0.0034 

exposed hamsters, 

single dose, 2.9 ng/kg 

Mouse, adult 241Am nitrate, aqueous 

solution, single gavage 

dose, 32 μg/kg 

241Am citrate, aqueous 

solution, single gavage 

dose, 43 μg/kg 

0.0028 

0.015 

Absorption estimate based 

on sum of 241Am in 

carcass (excluding the 

gastrointestinal tract) and 

liver 

Hisamatsu 

and 

Takizawa 

1987 

241Am in liver from 0.0024–0.0026 

exposed mice, single 

gavage dose 

Rat, adult 241Am in wild molluscs 

or 241Am nitrate 

injected into mollusc 

tissue, twice weekly for 

8 weeks 

0.026–0.12 

(wild mussels) 

0.016–0.040 

(injected mussel) 

Absorption estimate based 

on comparisons with liver 

and carcass 241Am after an 

intravenous dose, with 

adjustment for excretion, 

twice weekly for 8 weeks 

Harrison et 

al. 1988 

Rat, adult 241Am in potatoes 

exposed to 241Am, or 

injected into potatoes, 

single dose or daily for 

23 days 

0.12–0.16 Absorption estimate based 

on comparisons with liver 

and carcass 241Am after an 

intravenous or 

intraperitoneal dose, with 

adjustment for excretion 

Bulman et 

al. 1993 

Rat, adult 241Am nitrate, aqueous 

solution, single gavage 

dose, 5 μg/kg 

0.063 Absorption estimate based 

on sum of liver, skeletal, 

and urine 241Am 

Sullivan 

1980a 

Rat, adult 241Am oxide, aqueous 

suspension, single 

gavage dose, 33 μg/kg 

0.015 
AMERICIUM 42 

3. HEALTH EFFECTS 

Table 3-2. Absorption Estimates in Animals Exposed to Americium Compounds 

by Ingestion 

Animal model Dose and mediaa Absorption 

(percent of dose) 

Basis for estimate of 

absorption Reference 

Rat, adult 241Am nitrate, aqueous 

solution, single gavage 

dose, 12 μg/kg; fed or 

fasted, with or without 

Fe3+ 

0.017 (fed) 

0.124 (fast) 

1.19 (fast w/Fe3+) 

Absorption estimate based 

on sum of 241Am in 

carcass (excluding the 

gastrointestinal tract) and 

urine, Fe3+ gavage dose 

before 241Am dose 

Sullivan et 

al. 1986 

Rat, neonate 241Am nitrate, aqueous 

solution, single gavage 

dose, 0.44 μg 

4.6 Absorption estimate based 

on 241Am in carcass, 

excluding the 

gastrointestinal tract 

Sullivan 

1980b 

241Am oxide, aqueous 

solution, single gavage 

dose, 0.59 μg 

0.32 Absorption estimate based 

on 241Am in carcass, 

excluding the 

gastrointestinal tract 

Rat, 

neonate or adult 

241Am nitrate, gavage 

single dose, 285 μg/kg 

(adult), 1,380 μg/kg 

(neonate) 

% 

5.7 

0.0062 

Age 

2 d 

adult 

Absorption estimate based 

on 241Am in carcass, 

excluding the 

gastrointestinal tract 

Sullivan 

et al. 1985 

241Am citrate, aqueous 

solution, single gavage 

dose, 285 μg/kg 

(adult), 1,480 μg/kg 

(neonate) 

% 

5.9 

0.047 

Age 

2 d 

adult 

Rat, weanling 241Am nitrate, aqueous 

solution, single gavage 

dose, Fe deficient or 

replete, 7–9 μg/kg 

4.8 (Fe deficient) 

1.8 (Fe replete) 

Absorption estimate based 

on sum of 241Am in 

carcass, excluding the 

gastrointestinal tract and 

urine 

Sullivan and 

Ruemmler 

1988 

a

Where the chemical form and/or dose are not presented, these were not provided in the referenced report. Where 

only activity was reported, mass concentration of americium was calculated assuming a specific activity of 3.24 Ci/g. 

d = days; Fe = iron; GP = guinea pig 
AMERICIUM 43 

3. HEALTH EFFECTS 

compared to the fed state and iron deficiency compared with the iron-replete state (Sullivan and 

Ruemmler 1988; Sullivan et al. 1986). Concurrent oral exposure to Fe3+ and americium also appears to 

increase the absorption of ingested americium; the latter effect may result from redox reactions in the 

gastrointestinal tract catalyzed by Fe3+ (Sullivan et al. 1986). While the exact site and chemical species of 

americium that is absorbed from the gastrointestinal tract is not known, chemical speciation models 

applied to saliva and gastric fluid predict that the major species in saliva will be citrate and phosphate 

complexes, whereas in gastric fluid, the major species will be Am3+ (Webb et al. 1998). Speciation 

models for americium in the small intestine have not been reported; however, complexes with citrate, 

lactate, and phosphate would be expected based on equilibrium constants for these weak acid complexes 

and their abundance in intestinal fluid (Webb et al. 1998). 

3.4.1.3 Dermal Exposure 

Information on the dermal absorption of americium in humans or animals is extremely limited. Some 

qualitative information is available from accidental exposures that included other routes of exposure. One 

of the most well studied was an accident in which a worker received facial wounds from projectile glass 

(and other debris) and nitric acid during an explosion of a vessel containing 241Am (Filipy et al. 1995; 

McMurray 1983; Toohey and Kathren 1995). The subject also inhaled 241Am released to the air as dust 

and nitric acid aerosols, which was evident from external chest measurements of radioactivity (Palmer et 

al. 1983). Accurate estimates of dermal absorption of americium cannot be made from this case because 

of the complex exposure scenario and because of the occurrence of acid and projectile wounds to the skin 

that might have greatly affected the penetration of any americium that was deposited on the surface of the 

skin. Nevertheless, it is possible to conclude from measurements of the dermal 241Am activity soon after 

the accident and measurements of long-term excretion of 241Am that a substantial fraction of the initial 

radioactivity deposited in the area of the wounds was absorbed. Quantitative measurements of internally 

deposited 241Am in target organs were recorded from the third day following exposure to monitor rates of 

radionuclide excretion and accretion by these organs that continued up to time of death 11 years later. 

Based on measurements at day 3 postexposure, the organs that received the highest doses included the 

skin, liver, lung, and bone with estimated organ burdens of 26,000, 1,400, 960, and 480 kBq, respectively 

(Breitenstein and Palmer 1989; Robinson et al. 1983). The organ burdens of 241Am decreased under 

DTPA chelation therapy until conclusion after 5 years where monitoring data show that the activity 

decreased in the skin, entered systemic circulation, and deposited into the bone and liver. Dosimetric 

evaluation for years 6–10 following exposure showed a decrease in the skin by 93 kBq (2.5 μCi) 241Am, 
AMERICIUM 44 

3. HEALTH EFFECTS 

increased activities in the bone by about 67 kBq (1.8 μCi) and in the liver by about 7.4 kBq (0.2 μCi), and 

30 kBq (0.8 μCi) excreted via urine and feces. Over the first 60 days after the accident, dermal 241Am 

activity decreased from >5 mCi (185 MBq, 1.5 mg) to approximately 0.15 mCi, (5.5 MBq, 0.046 mg), 

largely as a result of skin decontamination procedures, although normal epidermal sloughing would be an 

expected contributor as well (Robinson et al. 1983). Cumulative urinary and fecal excretion of 241Am 

over an observation period of 5 years was estimated to be 1 mCi (37 MBq, 20% of the initial deposited 

activity), and peak body burden, excluding the skin, was estimated to have been approximately 0.08 mCi 

(3 MBq, 1.6% of the estimated initial deposited activity). Thus, the combination of transdermal injection 

and dermal absorption, under these extreme conditions of mechanical and chemical skin wounds, may 

have been as high as 20%. 

3.4.1.4 Other Routes of Exposure 

Several cases of accidental exposure to americium as a result of wound penetrations have been reported 

(Thompson 1983). These exposures have resulted in 241Am burdens in the liver and skeleton, indicating 

absorption and distribution from the wound site (McInroy et al. 1989). 

3.4.2 Distribution 

3.4.2.1 Inhalation Exposure 

The liver is the primary soft tissue site of initial accumulation of absorbed americium in humans. 

Americium deposited in bone and skeletal muscle has longer retention half-times than americium in the 

liver. Therefore, at long times after exposure (years), bone and skeletal muscle will contain a larger 

fraction of the systemic americium burden than the liver (Filipy and Kathren 1996; Kathren 1994; 

McInroy et al. 1995; Toohey and Kathren 1995). Information on the distribution of americium within the 

human liver is not available; however, studies in dogs and rats have shown that within a few days after an 

intravenous injection, hepatic 241Am is associated with lysosomes (Gruner et al. 1981; Lindenbaum and 

Rosenthal 1972; Seidel et al. 1986; Sütterlin et al. 1984). Americium in the hepatic cytosol is bound to 

ferritin and other unidentified proteins (DOE 1984; Stover et al. 1970). It is not known whether 

americium reacts with metallothionein; however, since americium forms stable complexes with 

polycarboxylate compounds such as DTPA (Lloyd et al. 1975a, 1975b), stable complexes with sulfhydryl 
 

AMERICIUM 45 

3. HEALTH EFFECTS 

groups in proteins such as metallothionein would not be expected. However, binding of 241Am to an 

unidentified low molecular weight protein fraction in a rat liver has been reported (DOE 1984). 

The United States Transuranium and Uranium Registries (USTUR) collect data on the americium content 

of human tissues obtained from autopsies. Recent data summaries reported from the USTUR show that 

after occupational inhalation exposures, 241Am activity resides primarily in the respiratory tract, skeleton, 

liver, and muscle (see Table 3-3). In three cases in which occupational exposures were believed to have 

been primarily, if not exclusively by inhalation, the following average tissue distribution was observed at 

autopsy 30 or more years after exposure: skeleton, 48%; respiratory tract, 35%; muscle, 10%; liver, 3%; 

and other issues, 4% (McInroy et al. 1989). Analyses of larger sets of USTUR cases have shown that, 

excluding the respiratory tract and other site of entry tissues (e.g., wound, gastrointestinal tract), 

approximately 80–90% of the americium in the body is associated with the skeleton, liver, and muscle, 

the skeletal:soft tissue burden ratio is approximately 3, and the highest soft-tissue concentrations are 

observed in the liver (Filipy and Kathren 1996; Filipy et al. 1994; Kathren et al. 1988). Whole-body 

counting of workers who were chronically exposed to plutonium and americium aerosols yielded a similar 

distribution of 241Am between the skeleton and soft tissue. In a separate study of 20 former workers, the 

geometric mean skeletal:liver burden ratio was 4.4 (GSD, 2.4; range, 1.2–17) (Badjin and Molokanov 

1998). Further evidence that the skeleton and liver are the primary sites of accumulation of absorbed 

americium is provided by inhalation studies conducted in monkeys (Stanley et al. 1982), dogs (Craig et al. 

1975, 1979; Mewhinney et al. 1982; Thomas et al. 1972), and rats (Stradling et al. 1992, 1994). 

Americium is also taken up by teeth. In rats, americium accumulates in the dental pulp of developing 

teeth and eventually is incorporated into the mineralized dentin (Hammerström and Nilsson 1970b). 

Information on the distribution of americium in blood after exposures to americium is available from an 

accident victim who was exposed by inhalation, dermal deposition, and wound penetration as a result of 

an explosion of a vessel containing 241Am, followed by aggressive chelation therapy (McMurray 1983). 

The internal 241Am activity was sufficiently high in this case to provide reliable estimates of blood and 

serum 241Am concentrations. Essentially all of the 241Am in blood was in the serum (Robinson et al. 

1983). Studies in animals provide further evidence that americium is confined largely to the plasma 

portion of blood. In baboons, dogs, and rats, >95% of americium in blood is associated with plasma. A 

variety of human and animal studies (in vivo and in vitro) have shown that americium in plasma binds 

extensively to proteins (80–90%), including albumin and transferrin (Boocock and Popplewell 1966; 

Bruenger et al. 1969; Cohen and Wrenn 1973; Cooper and Gowing 1981; Durbin 1973; Popplewell and 

Boocock 1967; Turner and Taylor 1968). When americium was incubated with human serum in vitro, 
AMERICIUM 46 

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Table 3-3. Tissue Americium Levels from Human Autopsies 

Mean percent of Mean percent of systemic burden 

Tissue body burden (excluding respiratory tract) 

Based on three inhalation casesa 

Respiratory tract 34.8b — 

Liver 3.3 6.3 

Skeleton 47.6 70.3 

Muscle 10.0 16.1 

Other 4.3 7.2 

Tissue Soft tissue:liver concentration ratioc

 (number of mixed exposures) 

Brain 0.08 (8)d 

Heart 0.123 (6) 

Kidneys 0.06 (38) 

Muscle 0.056 (8) 

Pancreas 0.03 (4)d 

Spleen 0.06 (38) 

Testes 0.029 (23) 

Thyroid 0.03 (21) 

a

McInroy et al. 1989 

b

Estimates of the contribution of the respiratory region to the total body burden in the three individuals from whom 

the mean value was calculated were 60.7, 23.7, and 14.7%. See McInroy et al. (1989) for additional statistical 

information. 

c

Filipy et al. 1994 

d

Calculated from Filipy and Kathren 1996 
 

 

AMERICIUM 47 

3. HEALTH EFFECTS 

<1% of the americium was ultrafilterable; however, essentially all of the americium could be rendered 

ultrafilterable by the inclusion of 50 mM citrate in the serum incubate, suggesting reversible binding of 

americium to serum proteins (Chipperfield and Taylor 1972). As noted above, bone is a primary site of 

long-term accumulation of americium in the skeleton. One human case of inhaled americium oxide 

resulted in an estimated deposition of 78 kBq (2,100 nCi) and a reported body burden of 34 kBq 

(900 nCi) after 12 years; 79% was located in the bone (Fasiska et al. 1971). In another human case, 

approximately 55% of an estimated lung deposition of 6.3 kBq (170 nCi) of 241Am was deposited in bone 

(Kathren et al. 2003). In human autopsy samples of bone, 241Am is found primarily at the cortical and 

trabecular bone surfaces (Priest et al. 1995; Schlenker et al. 1989). 

Americium that is observed in the deeper regions of human bones is thought to result from burial of 

historic surface deposits by newly accreted bone. Supporting evidence for accretion being a mode of 

redistribution of americium in bone comes from studies of monkeys, rats, and dogs that received single 

injections of 241Am (Durbin 1973; Herring et al. 1962; Lloyd et al. 1972; Nenot et al. 1972; Polig 1976; 

Priest et al. 1983). In these studies, the initial deposition of 241Am occurred at bone surfaces, including 

the periosteal and endosteal surfaces of trabecular bone and along the vascular channels of cortical bone, 

with more pronounced deposition at surfaces that were undergoing resorption, and with subsequent 

overlay of new bone (Priest et al. 1983). Because most americium in bone is associated primarily with 

the bone surface, the americium concentration in bone (per g bone ash) tends to vary with the bone ash 

content, as reflected by the variability in bone surface-to-volume ratio in a human who was 

occupationally exposed to americium (Kathren et al. 1987, 1990; Stevens et al. 1977). 

When residence times (time between exposure and autopsy) for the americium measured in autopsy cases 

are taken into consideration, the measured skeletal burdens are consistent with elimination half-times of 

approximately 50 years (McInroy et al. 1989, 1995). This value represents an average; however, in an 

individual, exchanges between bone and soft tissue stores of americium may be more rapid during periods 

of active bone metabolism such as infancy and childhood, pregnancy, and menopause (Lloyd et al. 1999). 

Studies in animals provide evidence for this concept (Durbin 1973). After an intravenous injection of 

americium citrate, skeletal tissue accumulated approximately 76% of the injected activity in neonatal dogs 

and 29% in adult dogs (Stevens et al. 1977). Higher skeletal uptakes of injected americium have also 

been observed in neonatal rats and mice, relative to adult animals (Hollins et al. 1973; Schoeters et al. 

1990) and in young rats (3 months of age) compared to old rats (13 months of age) (Sontag 1983). On the 

other hand, americium uptake into maternal bone of lactating rats was similar to that of non-lactating rats, 

while concurrent calcium uptake into bone was lower in lactating rats (Hollins and Durakovic 1972). 
AMERICIUM 48 

3. HEALTH EFFECTS 

Thus, active mobilization of bone mineral, per se, may not always promote release of americium from 

bone. 

Information on the placental transfer of inhaled americium in humans is not available. Studies in animals 

that received parenteral injections of americium show that absorbed americium is transferred to the fetus. 

To some extent, therefore, this distribution pathway would be expected after inhalation exposure (Sikov 

1987; Sikov and Kelman 1989; Stather et al. 1992). In baboons that received a single intravenous 

injection of americium citrate during the 5th month of pregnancy, approximately 0.4% of the activity was 

transferred to the fetus within 7 days post administration (Paquet et al. 1998). The fetal:maternal wholebody 241Am concentration ratio was approximately 0.1 and the tissue distribution in the fetus was similar 

to that observed in adult animals, with the skeleton and liver accounting for most of the 241Am activity in 

the body. Transfer of injected americium to the fetus has also been quantified in mice and rats that 

received intravenous injections of americium citrate during pregnancy (Sikov 1987). In both rats and 

mice, the fetal skeleton and liver were the major sites of accumulation of americium (DOE 1986; 

Hisamatsu and Takizawa 1983; Sasser et al. 1986; Schoeters et al. 1990; Van Den Heuvel et al. 1992; 

Weiss et al. 1980). In rats that received an injection of 241Am citrate on days 18 or 19 of pregnancy, fetal 

transfer was approximately 0.01% of the amount of americium administered to the dams. The 

fetal:maternal 241Am concentration ratio in rats was approximately 0.02 (Hisamatsu and Takizawa 1983). 

In mice that received an injection of 243Am citrate (0.01 μCi/mouse) on day 16 of pregnancy, fetal transfer 

was approximately 0.04% of the administered maternal amount per gram of fetus; the ratio of 243Am 

activity (μCi/g) in fetal tissue:maternal tissue exclusive of fetuses at the time of dissection was 

0.029 (Weiss et al. 1980) 

Information on the distribution of absorbed americium to mammary milk in humans is not available. 

Numerous studies in animals have shown that transfer to milk occurs and that neonates can be exposed to 

americium during lactation. These studies include experiments in which the animals were exposed by 

intravenous injection or oral administration of americium; however, the implications are relevant to any 

route of exposure, including inhalation. In rats that received an intravenous injection of americium citrate 

during lactation, approximately 0.1% of the injected activity was transferred to the nursing pups (Sasser et 

al. 1986). Oral and intravenous exposure to americium has resulted in the transfer of americium to 

mammary milk of cows, goats, and sheep (McClellan et al. 1962; Sutton et al. 1979). In a study of sheep 

that received americium chloride intravenously, the concentration of americium in mammary milk was 2– 

3 times that of maternal plasma (McClellan et al. 1962). 
AMERICIUM 49 

3. HEALTH EFFECTS 

3.4.2.2 Oral Exposure 

Although it has been demonstrated that americium can be absorbed through the gastrointestinal tract (see 

Section 3.4.1.2), the systemic distribution by the oral exposure route has been moderately characterized 

(ICRP, 1986, 1994a). However, it is reasonable to suggest that the distribution of americium absorbed 

into the systemic circulation from the gastrointestinal tract would be similar to that absorbed after 

inhalation (see Section 3.4.2.1). Studies in experimental animals support this; the major sites of 

americium accumulation after ingestion of americium are the skeleton and liver. In pigs ingesting 

americium citrate once, the distribution of the americium body burden 8 hours post ingestion, when the 

highest total body burdens were observed, was as follows: bone, 56%; liver, 29%, and muscle, 5% (Eisele 

et al. 1987). The skeleton and liver accounted for 40% (range, 8–67%) and 29% (range, 7–30%) of the 

body burden of 241Am, respectively, 7 days following a single gavage administration of americium citrate 

or nitrate to rats (Sullivan et al. 1985, 1986). Although it is possible that americium absorbed from the 

gastrointestinal tract might be taken up preferentially by the liver because of the hepatic portal blood 

flow, there is no evidence that a first pass effect substantially alters the overall tissue distribution of 

absorbed americium. For example, in marmosets that received an intravenous injection of americium 

citrate, the liver accounted for 27% of the total body burden of americium (excluding the gastrointestinal 

tract); whereas after a single gavage administration of americium in potato powder, the liver accounted 

for 31% of the body burden (oral:intravenous ratio of 1.14) (Ham et al. 1994). A similar comparison 

made in hamsters resulted in an oral:intravenous ratio for the fractional liver burden of 0.9 (Stather et al. 

1979a), and comparisons made in guinea pigs and rats resulted in ratios <1 (Bomford and Harrison 1986; 

David and Harrison 1984; Harrison et al. 1994). 

3.4.2.3 Dermal Exposure 

The tissue distribution of americium that is absorbed across the skin would be expected to be similar to 

that from other routes. Evidence for this is provided from an accident in which a worker received facial 

wounds from projectile debris and nitric acid during an explosion of a vessel containing 241Am 

(McMurray 1983; Toohey and Kathren 1995). The subject also inhaled 241Am released to the air as dust 

and nitric acid aerosols, which was evident from external chest measurements of radioactivity (Palmer et 

al. 1983). However, since the peak tissue burdens (lung, liver, and bone) of 241Am, measured 3 days after 

the accident, were collectively only 0.08 mCi, whereas the 5-year cumulative excretion of 241Am was 

approximately 1 mCi, it is almost certain that the source of most of the absorbed 241Am was the skin 
 

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3. HEALTH EFFECTS 

and/or skin wounds. The bone:liver ratio of 241Am 3 days after the exposure was approximately 3, and 

was 17–23 at autopsy 11 years after the accident. This suggests that bone and liver would be the major 

sites of accumulation of americium absorbed from the skin, as is the case for americium that is absorbed 

by other routes. The bone:liver ratio at 3 days was probably strongly affected by the aggressive DTPA 

therapy being employed at that time, since americium can be more easily removed from soft tissue 

deposition sites than from bone. Autopsy results (Toohey and Kathren 1995) were used to refine the 

estimates of organ burdens and doses and to facilitate a comparison with various models. Terminal 

burdens and tissue doses were estimated for the skeleton (490±40 kBq [13±1 μCi as average of six 

separate methods], 18 Gy [1,800 rad]), bone surface (490±40 kBq [13±1 μCi], 510 Gy [51,000 rad]), liver 

(28 kBq [0.8 μCi], 8.1 Gy [810 rad]), lung (1.9 kBq [0.05 μCi], 1.6 Gy [160 rad]), and muscle (13.5 kBq 

[0.36 μCi], 28 Gy [2,800 rad]). These USTUR measurements indicate that the long-term 241Am skeletal 

burden was 95% of the total in skeleton plus liver. This compared favorably with estimates using newer 

models (ICRP 1993; Leggett 1992), but less so when based on earlier models (ICRP 1979; ICRP 1986). 

Another finding was that muscle was a major repository, based on the total radiation dose it received 

being larger than that of the liver, whose terminal burden was actually twice as large. 

3.4.2.4 Other Routes of Exposure 

Various cases have been reported of internal exposure to americium resulting from skin punctures with 

materials also containing plutonium. Information on the distribution of americium in these cases has been 

derived from the analysis of autopsy tissues. In most cases, the largest fraction of the 241Am activity 

measured in the body was associated with tissues near the puncture wound. In one case, 18 years after a 

puncture wound to the left hand resulting in the deposition of a splinter of plutonium metal, 80% of the 

measured 241Am activity (a product of 241Pu decay) was associated with the left arm axillary lymph nodes 

and left hand, 12% was measured in the skeleton, and 1% was measured in the liver (Popplewell and Ham 

1989). The large amount of activity associated with the left arm lymph nodes and left hand reflects the 

local accumulation of americium near the wound site. However, if such local accumulations are 

subtracted from the total body activity, then most of the systemic americium measured after puncture 

wound exposures has been associated with the skeleton (80–90%) while liver, muscle, and spleen account 

for the remainder (5–10%), with skeletal:liver ratios of approximately 9:1 (Lagerquist et al. 1972b; 

McInroy et al. 1989; Popplewell and Ham 1989). These observations are consistent with those made 

from autopsy analyses after inhalation exposures (McInroy et al. 1989). 
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3. HEALTH EFFECTS 

A large degree of variation is apparent in retention rates for americium in the liver among various animal 

species (Durbin 1973), as indicated by measured or estimated liver clearance half-times of approximately 

5–16 days in rats, 152 days in baboons, 1–10 years in dogs, and 10 years in Chinese hamsters. A liver 

clearance half-time of 2 years has been estimated for humans (Griffith et al. 1983). Refer to Section 3.5.1 

for information regarding toxicokinetic mechanisms that may play a role in interspecies differences in 

liver retention of americium. 

3.4.3 Metabolism 

The metabolism of americium involves binding interactions with proteins and probably complex 

formation with various inorganic anions, such as carbonate and phosphate, and carboxylic acids, such as 

citrate and lactate (Durbin 1973; Taylor 1973; Webb et al. 1998). These types of interactions would be 

expected for all routes of exposure. 

3.4.4 Elimination and Excretion 

3.4.4.1 Inhalation Exposure 

Americium deposited in the nasopharyngeal or tracheal-bronchial regions of the respiratory tract will 

undergo extensive mucociliary transport to the esophagus with subsequent ingestion and fecal excretion. 

Evidence for this in humans is provided by cases of accidental inhalation exposure of americium oxides in 

which a substantial fraction (>50%) of the estimated initially deposited activity was found to be excreted 

in feces during the first days to weeks after the exposure (Edvardsson and Lindgren 1976; Newton et al. 

1983; Sanders 1974). Once absorbed from the lung, americium is excreted in feces and urine. The 

relative contribution of each in humans is difficult to assess from existing data because most data are 

derived from accidental exposures, after which the victims were subjected to chelation therapy, which 

would have increased the urinary excretion of americium. Following an accidental inhalation exposure in 

which approximately 1.22 μCi (45.1 kBq) of 244Cm and 241Am (in the form of mixed oxides) were 

deposited in the respiratory tract, the cumulative 1-year excretion of radioactivity was approximately 

1,174 nCi (43.4 kBq, 96% of the deposited activity) in feces and 5.4 nCi (200 Bq, 0.4% of the deposited 

activity) in urine (Sanders 1974). The equivalent fractions of 241Am, based on measurements of the 

244Cm:241Am ratios in feces and urine, were similar, 96% in feces and 0.4% urine. The subject received 
AMERICIUM 52 

3. HEALTH EFFECTS 

14 treatments with the chelating agent, DTPA, which may have effectively increased rates of excretion of 

americium. 

Studies of excretion in animals after inhalation exposures also indicate a relatively large contribution of 

fecal excretion to the total elimination of americium that deposits in the respiratory tract. In dogs that 

inhaled an aerosol of AmO2, fecal and urinary excretion of americium during the first 10 days after 

exposure were 30 and 0.7% of the initial body burden, respectively, and were 50 and 6% of the initial 

burden, respectively, by 810 days postexposure (Craig et al. 1979). Mechanical clearance from the upper 

respiratory tract to the gastrointestinal tract would be expected to make a substantial contribution to fecal 

excretion during the first few weeks after exposure and may continue for longer periods. The observation 

that fecal excretion continued to be the main route of excretion months after the exposure suggests two 

possibilities: (1) mechanical clearance from the lower respiratory tract (e.g., lung) continues to contribute 

to fecal excretion for longer periods of time (ICRP 1994b), and (2) absorbed americium is excreted in 

feces, suggesting a role for biliary excretion (Durbin 1973). 

Lung deposition patterns and the relative contributions of the fecal and urinary pathways vary with the 

aerosol particle size. Evidence for this is provided by a study in which dogs inhaled AmO2 aerosols 

having different size distributions. As the particle size AMAD increased from 0.8 μm (±1.2 GSD) to 

3.5 μm (±1.06 GSD), the urine:fecal ratios of cumulative excretion (from days 8 to 730 after the 

exposure) decreased from 4 to 0.3 (Mewhinney et al. 1982). These observations are consistent with an 

effect of particle size on deposition patterns in the respiratory tract. Larger particles will be deposited in 

the tracheo-bronchial airways and will be subjected to mucociliary transport to the esophagus where they 

can enter the gastrointestinal tract. Therefore, the fraction of the deposited activity transferred to the 

gastrointestinal tract and excreted in the feces would be expected to increase with increasing mean 

particle size of the inhaled aerosol. The general trend of increased fecal excretion with increasing particle 

size would be expected to occur in humans, although the exact relationship between particle size and 

deposition patterns will vary across species because of species differences in airway geometry, breathing 

patterns, and air flow rates in the respiratory tract (see Section 3.4.5). 

Once absorbed into the general circulation, regardless of the route of exposure, americium is excreted in 

both feces and urine. Evidence for this derives from a human accident case study and from experiments 

in animals that received an intravenous or intramuscular injection of americium (see Section 3.4.4.4). 
 

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3.4.4.2 Oral Exposure 

Urinary excretion of ingested americium has been measured in humans who ingested shellfish (molluscs) 

that had assimilated americium from their aquatic environment. In eight adult subjects (six males and 

two females) who ingested molluscs (winkles) containing 241Am (activity range 10–25 Bq, 0.27–0.68 nCi, 

0.083–0.21 ng), the mean cumulative urinary excretion during the 7 days after ingestion was 

approximately 0.0005% and the estimated fraction of the absorbed activity excreted in the urine was 

0.07% (Hunt et al. 1990). In a similar study of six subjects (five males and one female) who ingested 

cockles collected from Ravenglass, Cumbria (activity range of 15–17 Bq, 0.41–0.46 nCi, 0.13–0.14 ng), 

the mean cumulative urinary excretion during the 7 days post ingestion was approximately 0.0009% of 

the ingested americium and the estimated portion of the absorbed activity excreted in the urine was 0.08% 

(Hunt 1998). Three of these subjects had participated in the earlier study with winkles (Hunt et al. 1990); 

urinary excretion during 3 days prior to ingestion of the cockles was used to correct for internalized 

americium from prior exposures. Measured 241Am activity in the cockles was indistinguishable from the 

cumulative activity measured in fecal samples collected from the subjects during the 7 days post 

ingestion. 

Additional information on the excretion of ingested americium derives from an accident in which a 

worker ingested a ceramic particle containing 241AmO2 (Smith et al. 1983). Five days after the accident, 

the particle, containing approximately 2.85 μCi (105 kBq) of 241Am (0.88 μg Am), was excreted in the 

feces. Previous fecal samples and one subsequent fecal sample collected the day after the particle was 

excreted had essentially no 241Am activity. During the first 8 days after the particle was ingested, 

approximately 4 pCi (0.15 Bq, 0.00007% of the estimated activity) was excreted in the urine. 

Studies in rats and guinea pigs have shown that urinary excretion is the major route of excretion of 

americium absorbed from the gastrointestinal tract during the first week after exposure in these species. 

In rats that were administered americium nitrate or citrate by gavage, 30–80% of the estimated absorbed 

activity was excreted in urine during the first 7 days post administration (Sullivan 1980a; Sullivan et al. 

1985). The wide range may reflect the uncertainty in the estimates of the relatively low fraction 

absorption of the americium. The fraction of the absorbed activity that was excreted in urine was lower in 

iron-deficient rats (35%) than in iron-replete rats (78%) (Sullivan et al. 1985). In guinea pigs, 35–50% of 

the absorbed activity was excreted in urine during the first 7 days after a single gavage dose of americium 

nitrate (Sullivan 1980a). 
 

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3. HEALTH EFFECTS 

Once absorbed into the general circulation, regardless of the route of exposure, americium is excreted in 

both feces and urine. Evidence for this derives from human accident case study and from experiments in 

animals that received an intravenous or intramuscular injection of americium (see Section 3.4.4.4). 

3.4.4.3 Dermal Exposure 

Information on the excretion of americium after dermal exposure in humans or animals is extremely 

limited. Some qualitative information is available from an accidental exposure in which a worker 

received facial wounds from projectile debris and nitric acid during an explosion of a vessel containing 

241Am (McMurray 1983). The subject also inhaled 241Am released to the air as dust and nitric acid 

aerosols, which was evident from external chest measurements of internal radioactivity; thus, excretion 

estimates reflect combined inhalation, dermal, and wound penetration exposures (Palmer et al. 1983). 

Measurements of cumulative fecal and urinary excretion of 241Am during the first years after the accident, 

and periodic measurements made from day 10 to 11 years post accident, indicated a fecal:urine excretion 

ratio of approximately 0.2–0.3, although the ratio was approximately 1 on day 3 post accident 

(Breitenstein and Palmer 1989; Robinson et al. 1983). The ratio was almost certainly affected, however, 

by initial chelation with Ca-DTPA, followed by daily intravenous therapy with the chelating agent, 

Zn-DTPA; these treatments would have increased the urinary excretion of americium (Breitenstein and 

Palmer 1989). The above not withstanding, the observations made on this subject demonstrate that fecal 

excretion was an important pathway of excretion in this subject long after mechanical clearance of 

americium from the respiratory tract would have been complete. This is consistent with observations 

made in nonhuman primates that show that americium is excreted into bile (see Section 3.4.4.4). 

However, the extent to which the biliary excretion pathway in humans might resemble that of nonhuman 

primates is not known. 

Once absorbed into the general circulation, regardless of the route of exposure, americium is excreted in 

both feces and urine. Evidence for this derives from experiments in animals that received an intravenous 

or intramuscular injection of americium (see Section 3.4.4.4). 

3.4.4.4 Other Routes of Exposure 

Measurements of fecal and urinary excretion of americium after an inhaled or ingested dose do not 

provide all of the information needed to assess the relative importance of either route in the excretion of 
 

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3. HEALTH EFFECTS 

absorbed americium. This is because inhaled americium is subject to mucociliary transport and ingestion, 

and only a small fraction of ingested americium is absorbed. Studies in which animals were parenterally 

administered americium have provided quantitative information on the routes of excretion of absorbed 

americium. The relative contribution of the fecal and urinary pathways appears to vary with species and 

time post administration; however, in general, the fecal pathway predominates. In monkeys, urinary 

excretion of radioactivity following intravenously administered americium citrate was the major route of 

excretion only during the first few weeks post administration, at which time, cumulative urinary and fecal 

excretion accounted for 10 and 3% of the administered activity, respectively (Durbin 1973). Long-term 

cumulative excretion (months to years), however, was primarily in feces, with 37% of the administered 

activity excreted in feces and 20% excreted in urine. A similar pattern of urinary and fecal excretion over 

time was evident in baboons (Cohen and Wrenn 1973; Durbin 1973; Guilmette et al. 1980). Similarly, in 

rats, dogs, and hamsters, urinary excretion of radioactivity following intramuscularly or intravenously 

injected americium citrate or chloride was the major route of excretion only during the first few days to 

weeks, with a fecal:urine excretion ratio of approximately 0.11–0.15; however, over a 1–2-year period, 

the fecal:urine ratio was approximately 5–9 (Durbin 1973; Stather et al. 1979a). 

The large contribution of the fecal route to excretion of absorbed americium appears to be the result of 

excretion of americium into the bile. In monkeys that received an intravenous injection of americium 

citrate, 241Am was detected in gall bladder bile and its concentration increased as the relative rate of fecal 

excretion increased over time post injection (Durbin 1973). Durbin (1973) estimated that at bile 

production rates similar to humans, biliary excretion could have accounted for most, if not all, of the fecal 

excretion of americium observed in the monkeys. 

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

Physiologically based pharmacokinetic (PBPK) models use mathematical descriptions of the uptake and 

disposition of chemical substances to quantitatively describe the relationships among critical biological 

processes (Krishnan et al. 1994). PBPK models are also called biologically based tissue dosimetry 

models. PBPK models are increasingly used in risk assessments, primarily to predict the concentration of 

potentially toxic moieties of a chemical that will be delivered to any given target tissue following various 

combinations of route, dose level, and test species (Clewell and Andersen 1985). Physiologically based 

pharmacodynamic (PBPD) models use mathematical descriptions of the dose-response function to 

quantitatively describe the relationship between target tissue dose and toxic end points. 
 

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PBPK/PD models refine our understanding of complex quantitative dose behaviors by helping to 

delineate and characterize the relationships between: (1) the external/exposure concentration and target 

tissue dose of the toxic moiety, and (2) the target tissue dose and observed responses (Andersen et al. 

1987; Andersen and Krishnan 1994). These models are biologically and mechanistically based and can 

be used to extrapolate the pharmacokinetic behavior of chemical substances from high to low dose, from 

route to route, between species, and between subpopulations within a species. The biological basis of 

PBPK models results in more meaningful extrapolations than those generated with the more conventional 

use of uncertainty factors. 

The PBPK model for a chemical substance is developed in four interconnected steps: (1) model 

representation, (2) model parametrization, (3) model simulation, and (4) model validation (Krishnan and 

Andersen 1994). In the early 1990s, validated PBPK models were developed for a number of 

toxicologically important chemical substances, both volatile and nonvolatile (Krishnan and Andersen 

1994; Leung 1993). PBPK models for a particular substance require estimates of the chemical substancespecific physicochemical parameters, and species-specific physiological and biological parameters. The 

numerical estimates of these model parameters are incorporated within a set of differential and algebraic 

equations that describe the pharmacokinetic processes. Solving these differential and algebraic equations 

provides the predictions of tissue dose. Computers then provide process simulations based on these 

solutions. 

The structure and mathematical expressions used in PBPK models significantly simplify the true 

complexities of biological systems. If the uptake and disposition of the chemical substance(s) is 

adequately described, however, this simplification is desirable because data are often unavailable for 

many biological processes. A simplified scheme reduces the magnitude of cumulative uncertainty. The 

adequacy of the model is, therefore, of great importance, and model validation is essential to the use of 

PBPK models in risk assessment. 

PBPK models improve the pharmacokinetic extrapolations used in risk assessments that identify the 

maximal (i.e., the safe) levels for human exposure to chemical substances (Andersen and Krishnan 1994). 

Similar models have been developed for radionuclides. These 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 3-1 shows a conceptualized representation 
 

Inhaled chemical Exhaled chemical 

Lungs 

Liver 

Fat 

Slowly 

perfused 

tissues 

Richly 

perfused 

tissues 

Kidney 

Skin 

V 

E 

N 

O 

U 

S 

B 

L 

O 

O 

D 

A 

R 

T 

E 

R 

I 

A 

L 

B 

L 

O 

O 

D 

V max K m 

Ingestion 

GI 

Tract 

Feces 

Urine

 Chemicals in air 

contacting skin 

AMERICIUM 57 

3. HEALTH EFFECTS 

Figure 3-1. Conceptual Representation of a Physiologically Based 

Pharmacokinetic (PBPK) Model for a Hypothetical 

Chemical Substance 
 

AMERICIUM 58 

3. HEALTH EFFECTS 

of a PBPK model. Figures 3-2 through 3-8 show models for radionuclides in general or specifically for 

americium. 

For radionuclides, the PBPK model is replaced with a set of sophisticated physiologically based 

biokinetic (PBBK) models for inhalation, ingestion, and submersion. These were developed to 

accomplish virtually the same end as the PBPK models above, while integrating additional parameters 

(for radioactive decay, particle and photon transport, and compound-specific factors). Goals are to 

facilitate interpreting chest monitoring and bioassay data, assessing risk, and calculating radiation doses 

to a variety of tissues throughout the body. The standard for these models has been set by the ICRP and 

their models receive international support and acceptance. ICRP periodically considers newer science in 

a type of weight of evidence approach toward improving the state of knowledge and reducing 

uncertainties associated with applying the model to any given radionuclide. ICRP publications also allow 

for the use of situation- and individual-specific data to reduce the overall uncertainty in the results. Even 

though there may be conflicting data for some parameters, such as absorption factors, one can use 

conservative values and still reach conclusions on whether the dose is below recommended limits. One of 

the strengths of the ICRP model is that it permits the use of experimentally determined material-specific 

absorption parameter values rather than requiring the use of those provided for default types. If the 

material of interest does not have absorption parameter values that correspond to those in the model (e.g., 

Type F, M, or S), the difference can have a profound effect on the assessment of intake and dose from 

bioassay measurements. This has been discussed in National Radiological Protection Board (NRPB) 

published reports on uranium (NRPB 2002). 

The ICRP (1994b, 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 americium compounds. The ICRP (1986, 1989) has a biokinetic 

model for human oral exposure that applies to americium. The National Council on Radiation Protection 

and Measurements (NCRP) has also developed a respiratory tract model for inhaled radionuclides (NCRP 

1997). At this time, the NCRP recommends the use of the ICRP model for calculating exposures for 

radiation workers and the general public. Readers interested in this topic are referred to NCRP Report 

No. 125; Deposition, Retention and Dosimetry of Inhaled Radioactive Substances (NCRP 1997). In the 

appendix to the report, NCRP provides the animal testing clearance data and equations fitting the data that 

supported the development of the human mode for americium. 
AMERICIUM 59 

3. HEALTH EFFECTS 

Human Respiratory Tract Model for Radiological Protection (ICRP 1994b) 

Deposition. The ICRP (1994b) has developed a deposition model for behavior of aerosols and vapors in 

the respiratory tract. It was developed to estimate the fractions of substances in breathing air that are 

deposited in each anatomical region of the respiratory tract. ICRP (1994b) provides inhalation dose 

coefficients that can be used to estimate radiation doses to organs and tissues throughout the body based 

on a unit intake of radioactive material. The model applies to three levels of particle solubility, a wide 

range of particle sizes (approximately 0.0005–100 μm in diameter), and parameter values that can be 

adjusted for various segments of the population (e.g., sex, age, and level of physical exertion). This 

model also allows one to evaluate the bounds of uncertainty in deposition estimates. Uncertainties arise 

from natural biological variability among individuals and the need to interpret some experimental 

evidence that remains inconclusive. It is applicable to particulate aerosols containing americium, but was 

developed for a wide variety of radionuclides and their chemical forms. 

The ICRP deposition model estimates the fraction of inhaled material initially retained in each 

compartment (see Figure 3-2). The model was developed with five compartments: (1) the anterior nasal 

passages (ET1); (2) all other extrathoracic airways (ET2) (posterior nasal passages, the naso- and 

oropharynx, and the larynx); (3) the bronchi (BB); (4) the bronchioles (bb); and (5) the alveolar 

interstitium (AI). Particles deposited in each of the regions may be removed and redistributed either 

upward into the respiratory tract or to the lymphatic system and blood by different particle removal 

mechanisms. 

For extrathoracic deposition of particles, the model uses measured airway diameters and experimental 

data, where deposition is related to particle size and airflow parameters, and scales deposition for women 

and children from adult male data. Similar to the extrathoracic region, experimental data served as the 

basis for lung (bronchi, bronchioles, and alveoli) aerosol transport and deposition. A theoretical model of 

gas transport and particle deposition was used to interpret data and to predict deposition for compartments 

and subpopulations other than adult males. Table 3-4 provides reference respiratory values for the 

general Caucasian population during various intensities of physical exertion. 

Respiratory Tract Clearance. This portion of the model identifies the principal clearance pathways 

within the respiratory tract. The model was developed to predict the retention of various radioactive 

materials. The compartmental model represents particle deposition and time-dependent particle transport 

in the respiratory tract (see Figure 3-2) with reference values presented in Table 3-5. This table provides 

clearance rates, which are expressed as a fraction per day and also as half-time (Part A), and deposition 
Sequestered in Tissue Surface 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 

AMERICIUM 60 

3. HEALTH EFFECTS 

Figure 3-2. 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 3-5. 

Source: ICRP 1994b 
 

 

 

 

 

 

 

 

 

 

 

AMERICIUM 61 

3. HEALTH EFFECTS 

Table 3-4. Reference Respiratory Values for a General Caucasian Population at 

Different Levels of Activitya
 

Breathing 

parameters: 3 months 1 year 5 years Male 

10 years 

Female Both 

15 years 

Male Female 

Adult 

Male Female 

Resting (sleeping); Maximal workload 8% 

Breathing parameters: 

VT(L) 0.04 0.07 0.17 

B(m3

h-1) 0.09 0.15 0.24 

fR(min-1) 38 34 23 

— 

— 

— 

— 

— 

— 

0.3 0.500 

0.31 0.42 

17 14 

0.417 

0.35 

14 

0.625 

0.45 

12 

0.444

0.32 

12 

Sitting awake; Maximal workload 12% 

Breathing parameters: 

VT(L) N/A 0.1 0.21 

B(m3

h-1) N/A 0.22 0.32 

fR(min-1) N/A 36 25 

— 

— 

— 

— 

— 

— 

0.33 0.533 

0.38 0.48 

19 15 

0.417 

0.40 

16 

0.750 

0.54 

12 

0.464

0.39 

14 

Light exercise; Maximal workload 32% 

Breathing parameters: 

VT(L) 0.07 0.13 0.24 

B(m3

h-1) 0.19 0.35 0.57 

fR(min-1) 48 46 39 

— 

— 

— 

— 

— 

— 

0.58 1.0 

1.12 1.38 

32 23 

0.903 

1.30 

24 

1.25 

1.5 

20 

0.992

1.25 

21 

Heavy exercise; Maximal workload 64% 

Breathing parameters: 

VT(L) N/A N/A N/A 

B(m3

h-1) N/A N/A N/A 

fR(min-1) N/A N/A N/A 

0.841 

2.22 

44 

0.667 

1.84 

46 

— 

— 

— 

1.352 

2.92 

36 

1.127 

2.57 

38 

1.923 

3.0 

26 

1.364

2.7 

33 

a

See Annex B (ICRP 1994b) for data from which these reference values were derived. 

B = ventilation rate; fR = respiration frequency; h = hour; L = liter; m = meter; min = minute; N/A = not applicable; 

VT = tidal volume 
 

AMERICIUM 62 

3. HEALTH EFFECTS 

Table 3-5. 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 1x10-4 7,000 days 

m3,10 AI3 LNTH 2x10-5 No data 

m4,7 bb1 BB1 2 8 hours 

m5,7 bb2 BB1 0.03 23 days 

m6,10 bbseq LNTH 0.01 70 days 

m7,11 BB1 ET2 10 100 minutes 

m8,11 BB2 ET2 0.03 23 days 

m9,10 BBseq LNTH 0.01 70 days 

m11,15 ET2 GI tract 100 10 minutes 

m12,13 ETseq LNET 0.001 700 days 

m14,16 ET1 Environment 1 17 hours 

See next page for Part B 
 

f s = 05. for d ae ≤ 25 . ρ χμ / m and

0 63 .( d ρ χ/ −2 5.) ae f s = 05. e for d ae > 25 . ρ χμ / m 

AMERICIUM 63 

3. HEALTH EFFECTS 

Table 3-5. Reference Values of Parameters for the Compartment Model to 

Represent Time-dependent Particle Transport from the Human Respiratory
 

Tract (continued) 

Part B
 

Partition of deposit in each region between compartmentsb 

Fraction of deposit in region 

Region or deposition site Compartment assigned to compartmentc 

ET2	 ET2 0.9995 

ETseq 0.0005 

BB	 BB1 0.993-fs 

BB2 fs 

BBseq 0.007 

Bb	 bb1 0.993-fs 

bb2 fs 

bbseq 0.007 

AI	 AI1 0.3 

AI2 0.6 

AI3 0.1 

a

The half-times are approximate since the reference values are specified for the particle transport rates and are rounded in units 

of days-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. b

See paragraph 181, Chapter 5 (ICRP 1994b) for default values used for relating fs to dae. c

It is assumed that fs is size-dependent. For modeling purposes, fs is taken to be: 

where 

fs = fraction subject to slow clearance 

dae = aerodynamic particle diameter/(μm) 

ρ = particle density (g/cm3

) 

χ = particle shape factor 

AI = alveolar-interstitial region; BB = bronchial region; bb = bronchiolar region; BBseq = compartment representing prolonged 

retention in airway walls of small fraction of particles deposited in the bronchial region; bbseq = compartment representing 

prolonged retention in airway walls of small fraction of particles deposited in the bronchiolar region; ET = extrathoracic region; 

ETseq = compartment representing prolonged retention in airway tissue of small fraction of particles deposited in the nasal 

passages; GI = gastrointestinal; LNET = lymphatics and lymph nodes that drain the extrathoracic region; LNTH = lymphatics and 

lymph nodes that drain the thoracic region 

Source: ICRP 1994b 
AMERICIUM 64 

3. HEALTH EFFECTS 

fractions (Part B) for each compartment for insoluble particles. ICRP (1994b) also developed modifying 

factors for some of the parameters, such as age, smoking, and disease status. Parameters of the clearance 

model are based on human evidence for the most part, although particle retention in airway walls is based 

on experimental data from animal experiments. 

The clearance of particles from the respiratory tract is a dynamic process. The rate of clearance generally 

changes with time from each region and by each route. Following deposition of large numbers of 

particles (acute exposure), the mass flow of material between compartments decreases 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 of material between the compartments tend 

to change. By creating a model with compartments of different clearance rates within each region (e.g., 

BB1, BB2, BBseq), the ICRP model overcomes problems associated with time-dependent functions. 

Each compartment clears to other compartments by constant rates for each pathway. 

Particle transport from all regions is toward both the lymph nodes and the pharynx, and a majority of 

deposited particles, if sufficiently large, end up being swallowed. In the front part of the nasal passages 

(ET1), nose blowing, sneezing, and wiping remove most of the deposited particles. Particles remain here 

for about a day. For particles with AMADs a few micrometers or greater, the ET1 compartment is 

probably the largest deposition site. A majority of particles deposited at the back of the nasal passages 

and in the larynx (ET2) are removed quickly by the fluids that cover the airways. In this region, particle 

clearance is completed within 15 minutes. 

Ciliary action removes deposited particles from both the bronchi and the bronchioles. Though it is 

generally thought that mucociliary action rapidly transports most particles deposited here toward the 

pharynx, a fraction of these particles is cleared more slowly. Evidence for this is found in human studies. 

For humans, retention of particles deposited in the lungs (BB and bb) is apparently biphasic. The “slow” 

action of the cilia may remove as much as half of the bronchi- and bronchiole-deposited particles. In 

human bronchi and bronchiole regions, mucus moves more slowly when it is closer to the alveoli. For the 

faster compartment, it has been estimated that it takes about 2 days for particles to travel from the 

bronchioles to the bronchi and 10 days from the bronchi to the pharynx. The second (slower) 

compartment is assumed to have approximately equal fractions deposited between BB2 and bb2, with 

both fractions having clearance half-times estimated at 20 days. Particle size is a primary determinant of 

the fraction deposited in this slow thoracic compartment. A small fraction of particles deposited in the 

BB and bb regions is retained in the airway wall for even longer periods (BBseq and bbseq). 
AMERICIUM 65 

3. HEALTH EFFECTS 

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. 

In the AI region, human lung clearance has been measured. The ICRP model uses three half-times to 

represent clearance: about 30, 60, and 10% of the particles have half times that approximate 30, 700, and 

7,000 days, respectively. Over time, AI particle transport falls, and some compounds have been found in 

lungs 10–50 years after exposure. 

Absorption into Blood. The ICRP model assumes that absorption into blood occurs at equivalent rates in 

all parts of the respiratory tract, except in the anterior nasal passages (ET1), where no absorption occurs. 

It is essentially a 2-stage process, as shown in Figure 3-3. First, there is a dissociation (dissolution) of 

particles, and then the dissolved molecules or ions diffuse across capillary walls and are taken up by the 

blood. Immediately following dissolution, rapid absorption is observed. For some elements, rapid 

absorption does not occur because of binding to respiratory-tract components. In the absence of specific 

data for specific compounds, the model uses the following default absorption rate values for those specific 

compounds that are classified as Types F (fast), M (medium), S (slow), and V (instantaneous): 

•	 For Type F, there is rapid 100% absorption within 10 minutes of the material deposited in the BB, 

bb, and AI regions and 50% absorption of material deposited in ET2. Thus, for nose breathing, 

there is rapid absorption of approximately 25% of the deposit in ET; for mouth breathing, the 

value is 50%. 

•	 For Type M, about 70% of the deposit in AI eventually reaches the blood. 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 eventually 

reaches the blood. 

•	 For Type V, complete absorption (100%) is considered to occur instantaneously (which is not 

relevant to americium compounds). 

ICRP (1995) considers the experimental data on americium nitrate, chloride, citrate, and hydroxide to 

support classification of these compounds as either Type F or M. Americium oxides are classified as 
Particulate Material 

Dissociated Material 

Bound Material 

Blood 

Source: ICRP 1994b 

Dissolution 

Uptake 

AMERICIUM 66 

3. HEALTH EFFECTS 

Figure 3-3. The Human Respiratory Tract Model: Absorption into Blood 
AMERICIUM 67 

3. HEALTH EFFECTS 

Type M. ICRP (1995) recommends assigning all americium aerosols to Type M in the absence of 

specific information supporting an alternative classification. Substance specific values should be used 

where feasible to reduce uncertainties in results. 

ICRP (1989) Americium Biokinetic Model 

Description of the model. 

ICRP (1989) developed a compartmental model of the kinetics of ingested americium in humans that is 

applicable to infants, children, adolescents, and adults. The model is a modification and expansion of a 

similar model for plutonium, described by Leggett et al. (1984, 1985). The fraction of ingested 

americium that is absorbed (uptake to blood) is assumed to vary with age and have values of 0.01 in 

infants up to 12 months of age and 0.001 from 12 months of age through adulthood (ICRP 1986). 

Absorbed americium enters the blood plasma where it distributes to the skeleton, liver, and other tissues 

(Figure 3-4). Excretion pathways included in the model are plasma to urine and liver to feces. Transfer 

rate coefficients between compartments are age-specific and, depending on the specific coefficient, values 

can change at ages 3 months, 1 year, 5 years, 10 years, 15 years, and adult (>15 years). The model 

assumes that, in adults, 50% of the americium that enters the body and is not excreted is transferred to the 

liver and 30% is transferred to the skeleton. In newborns, 70% is assumed to be transferred to the 

skeleton and 10% to the liver. Skeletal deposition is assumed to distribute into two pools: 50% goes to 

the trabecular bone surface and 50% goes to the cortical bone surface. A first-order rate coefficient for 

elimination of americium from liver to plasma is assumed to be 0.0019 day-1 (half-time, 365 days). 

Bone is divided into trabecular and cortical components, with each further divided into surface bone, bone 

volume, and bone cavity (marrow compartment). Deposition of americium is assumed to occur from 

plasma directly to bone surfaces, whereas elimination from bone occurs by transfer from the bone surface 

or volume to the marrow cavity, and then from the marrow cavity to plasma (Figure 3-4). Transfers of 

americium within the cortical or trabecular bone compartments are modeled based on assumptions about 

rates of bone formation and resorption, which are assumed to be vary with age, but are equal within a 

given age group (Leggett et al. 1982). Movement of americium to the marrow compartment is 

determined by the bone resorption rate, whereas movement from the bone surface to the bone volume is 

assumed to occur by burial of surface deposits with new bone and is determined by the bone formation 

rate. During growth, bone formation and resorption are assumed to occur at different sites within bone; 

therefore, the rate of removal of americium from the bone surface is approximated by the sum of the bone 

resorption rate (represented in the model by the movement of americium to the marrow compartment) and 
SKELETON
 

Cortical
 

Volume
 

Trabecular
 

Volume
 

Other
 

Soft
 

Tissue
 

LIVER
 

ReticuloEndothelial
 

Cells
 

H 

E Subcellular 

P Organelles A 

T 

O 

C 

Cytoplasm Y 

and T 

Membranes E 

S 

B 

L 

O 

O 

D 

Urinary
 

Tract 

Tissue
 

Feces 

Cortical
 

Surface
 

Cortical
 

Marrow
 

Trabecular
 

Surface
 

Trabecular
 

Marrow
 

Urine 

AMERICIUM 68 

3. HEALTH EFFECTS 

Figure 3-4. ICRP (1989) Model of Americium Biokinetics 
AMERICIUM 69 

3. HEALTH EFFECTS 

the rate of bone formation, which results in burial of surface deposits (represented by movement of 

americium from the bone surface to bone volume). In adults, the possibility of resorption and formation 

of bone occurring at the same site is assumed; therefore, only a portion of the bone formation rate results 

in burial of surface deposits and movement of americium from the bone surface to the bone volume. 

Validation of the model. 

The extent to which the ICRP model has been validated is not described in ICRP (1989). 

Risk assessment. 

The model has been used to establish the radiation dose (Sv) per unit of ingested 241Am activity (Bq) for 

ages 3 months to 70 years (ICRP 1989). 

Target tissues. 

The model is designed to calculate the 241Am intake that would produce the maximum allowed 

occupational radiation dose to all major organs, including the bone surfaces, bone marrow, and liver, but 

the conversion factors for other tissues and organs are published in the same tables. 

Species extrapolation.The model is based on both human and animal data. It is intended, however, for 

applications to human dosimetry. Applications to other species would require consideration of speciesspecific adjustments in model parameters. 

Interroute extrapolation. 

The model is designed to simulate oral exposures to americium. It can be applied to any other route of 

exposure for which the transfer rate to blood is available. 

Leggett (1992) Americium Biokinetic Model 

Description of the model. 

Leggett (1992) proposed a model for the retention and excretion of americium in humans. The model is a 

modification of a similar model for plutonium (Leggett et al. 1984, 1985) with the following changes 

(Figure 3-5): (1) the liver is represented as a single pool rather than having distinct pools for hepatocytes 
AMERICIUM 

SKELETON 

Cortical 

Volume 

MASSIVE 

Rapid Intermed Slow SOFT 

Turnover Turnover Turnover TISSUES 

Cortical
 

Surface
 

Cortical
 

Cavities
 Gonads 

B 

L 

O 

O 

D 

Trabecular
 

Volume
 

Trabecular
 

Surface
 

Trabecular
 

Marrow
 Liver 

KIDNEY 

Other
 

Kidney
 

Tissue
 

Urinary
 

Path
 

GI Tract
 

Contents
 

Feces 

Urinary 

Bladder 

Contents 

Urine 

70 

3. HEALTH EFFECTS 

Figure 3-5. Leggett (1992) Model of Americium Biokinetics 
 

AMERICIUM 71 

3. HEALTH EFFECTS 

and other cell types; (2) the gonads are represented by a separate compartment; (3) a kidney compartment 

is included in place of the compartment for urinary tract tissue; (4) a compartment representing the 

urinary bladder contents is included; and (5) other soft tissues are represented as having slow, 

intermediate, and fast turnover pools. 

The fraction of ingested americium that is absorbed (uptake from the small intestine to blood) is 

represented by age-specific functions that yield the following values: decreasing from 0.05 to 

0.0005 during the first 12 months, 0.0005 at 1–15 years of age, decreasing from 0.0005 to 0.0002 at 15– 

18 years of age, and 0.0002 from age 18 years through adulthood. The model assumes that, in adults, 

62% of the americium that enters the body and is not excreted is transferred to liver and 38% is 

transferred to the skeleton (skeleton:liver deposition ratio, 3:5). In newborns, 88% is assumed to be 

transferred to the skeleton and 12% to the liver (skeleton:liver deposition ratio, 7:1). The half-time for 

elimination of americium from the liver is assumed to be 365 days, although the half-time for elimination 

measured externally would be longer and would increase with increasing time after intake, due to 

recycling of americium from tissues to blood to tissues. 

Validation of the model. 

Predictions based on the model have been compared to observed urinary or fecal excretion of americium 

in humans. Model predictions agreed reasonably well with the empirical observations (Leggett 1992). 

Risk assessment. 

The Leggett (1992) model was developed to predict tissue doses and whole-body dose to people who may 

be exposed to americium and for interpretation of bioassay data for americium. The model is considered 

an updated version of the ICRP (1989) model for americium, which has been used to establish risk-based 

limits of intake of 241Am (ICRP 1989). The Leggett (1992) and ICRP (1989) models predict similar longterm average doses of americium to the liver and skeleton for an injection exposure and would be 

expected to predict similar radiation risks and risk-based intake limits (Leggett 1992). Descriptions of 

applications of the Leggett (1992) model in risk assessment have not been reported. 

Target tissues. 

The model is designed to calculate americium excretion and time courses for americium levels in the 

liver, skeleton, and gonads. This output could be used to predict radiation doses to these tissues. 
AMERICIUM 72 

3. HEALTH EFFECTS 

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, inhalation, and parenteral (e.g., injection) exposures to americium 

and cannot be applied to other routes of exposure without modification. 

ICRP (1993) Americium Biokinetic Model 

Description of the model. 

ICRP (1993) adopted the model of Leggett (1992) as its systemic biokinetic model for americium with 

the following modifications: (1) the Leggett (1992) model addresses changes throughout life in the rate 

of bone turnover, whereas the ICRP (1993) model assumes bone turnover rates to remain constant in 

adults, and (2) assumptions regarding uptake and retention by gonadal tissues of children are more 

cautious in the ICRP (1993) model compared to those used in the Leggett (1992) model. 

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 the radiation dose (Sv) per unit of ingested 241Am activity (Bq) for 

ages 3 months to 70 years (ICRP 1993). 

Target tissues. 

The model is designed to calculate the 241Am intake that would produce the maximum allowed 

occupational radiation dose to all major organs, including the bone surfaces, bone marrow, and liver, but 

the conversion factors for other tissues and organs are published in the same tables. 
 

AMERICIUM 73 

3. HEALTH EFFECTS 

Species extrapolation. 

The model is based on both human and animal data. It is intended, however, for applications to human 

dosimetry. Applications to other species would require consideration of species-specific adjustments in 

model parameters. 

Interroute extrapolation. 

The model is designed to simulate oral exposures to americium. It can be applied to any other route of 

exposure for which the transfer rate to blood is available. 

USTUR (1994) Americium Biokinetics Model 

Description of the model. 

The USTUR proposed modifications to the ICRP americium model, based on post-mortem americium 

measurements in human exposure cases (Kathren 1994). The major modifications are: (1) the initial 

deposition fraction is assumed to be skeleton 45%, liver 25%, muscle 20%, and other tissues 10%; and 

(2) the half-times for elimination of americium were assumed to be 2.5 years in liver, 10 years in muscle, 

50 years in skeleton, and 10 years in other tissues. 

Validation of the model. 

Predictions based on the model have been compared to observed post-mortem tissue americium levels in 

whole-body and tissue donations to the USTUR. Model predictions agreed reasonably well with the 

empirical observations (Kathren 1995; USTUR 1997). They, however, depend heavily on the accuracy of 

initial uptake and distribution data that, in certain cases, were difficult to reconstruct due to delays 

between times of exposure and initial analysis. 

Risk assessment. 

The USTUR (Kathren 1994) model was developed to predict tissue doses and whole-body dose to people 

who may be exposed to americium. The model has been used to verify annual limits on intake (ALIs) for 

241Am, and yielded similar, but lower limits than those estimated using the ICRP model (1989). 
 

AMERICIUM 74 

3. HEALTH EFFECTS 

Target tissues. 

The model is designed to calculate americium excretion and time courses for americium levels in the 

liver, skeleton, and gonads. This output could be used to predict radiation doses to these tissues. 

Species extrapolation. 

The model is designed for application to human dosimetry and does not apply to other species. 

Interroute extrapolation. 

The model is designed to simulate oral, inhalation, and parenteral (e.g., injection, wounds) exposures to 

americium and cannot be applied to other routes of exposure without modification. 

Mewhinney and Griffith (1983) Americium Biokinetics Model 

Description of the model. 

Mewhinney and Griffith (1983) proposed a model for the absorption and tissue distribution of inhaled 

americium dioxide in humans. The model is a modification of a model of the beagle dog (Mewhinney 

and Griffith (1982) and formed part of the basis for the Leggett (1992) model. The model is similar to 

other actinide models (ICRP 1989; Leggett 1992), but has several additional features in the respiratory 

tract portion of the model (Figure 3-6) including: (1) dissolution of particles in the respiratory tract is 

simulated with rate functions, rather than zero or first-order rate constants, that include various parameters 

of particle size and surface area that affect dissolution rate (Mercer 1967); (2) the pulmonary region 

includes three pools; a pool of deposited particulate; a pool of dissolved americium which can be rapidly 

absorbed into the blood; and a pool of locally bound americium (transformed) which can be absorbed into 

blood or mechanically cleared to the tracheobronchial region; and (3) absorption from the pulmonary 

region of the respiratory tract includes a pathway for transfer to tracheobroncheal lymph nodes. 

Excretion is assumed to be in feces, from either the intestine or from the liver to the intestine, and from 

the blood to the urine (i.e., the kidney is represented as a distribution compartment). An absorption 

fraction of 0.0005 is assumed for americium in the small intestine. 
AMERICIUM 75 

3. HEALTH EFFECTS 

Figure 3-6. Mewhinney and Griffith (1983) Model of Deposition and Retention of 

Americium in the Human Respiratory Tract 

RESPIRATORY TRACT 

Nasopharyngeal 

Tracheobronchial 

G
 

I
 

T 

R 

A 

C 

T 

Pulmonary 

B 

L 

O 

O 

D 

TracheoBronchial
 

Lymph
 

Nodes
 

Pulmonary
 

Dissolved 

Transformed
 

Pulmonary 
AMERICIUM 76 

3. HEALTH EFFECTS 

Validation of the model. 

Predictions based on the model have been compared to observed time courses for lung, liver, and skeletal 

americium burden in dogs that inhaled americium oxide (Mewhinney and Griffith 1983). Data on lung 

retention for four humans who accidentally inhaled americium were also compared to model predictions. 

The empirical observations fell within predicted retention patterns for particle sizes (AMAD) 0.5 and 

1.8 μm (Mewhinney and Griffith 1983). 

Risk assessment. 

The Mewhinney and Griffith (1983) model was developed to predict lung retention and tissue 

distributions of americium in people who may be exposed to americium. Descriptions of applications of 

the model in risk assessment have not been reported. 

Target tissues. 

The model calculates americium burdens in lung, liver, skeleton, kidney, and body. This output could be 

used to predict radiation doses to these tissues. 

Species extrapolation. 

The model is designed for applications to human dosimetry; however, it predicts reasonably well the 

retention of americium in beagle dogs as well (Mewhinney and Griffith 1982). The model cannot be 

applied to other species without modification. 

Interroute extrapolation. 

The model is designed to simulate inhalation exposures to americium; however, it could be applied to 

ingestion exposures since the model simulates the absorption of americium from the gastrointestinal tract. 

The model can be applied to other routes of exposure with modification. 

Durbin and Schmidt (1985) Americium Biokinetics Model 

Description of the model. 

Durbin and Schmidt (1985) proposed a model for tissue distribution and excretion of absorbed americium 

in humans. A unique feature of this model is that transfers from plasma to tissues are assumed to be 
AMERICIUM 77 

3. HEALTH EFFECTS 

instantaneous; therefore, a central plasma (and blood) compartment is not included in the model (see 

Figure 3-7). Tissue compartments included in the model are slow and fast turnover bone compartments, 

representing cortical and trabecular bone, respectively; liver; and slow and fast turnover for other soft 

tissue compartments. Excretion pathways include urine and feces. Urinary excretion is represented as a 

sum of the contributions from bone, liver, and other soft tissues. Fecal americium is assumed to be 

excreted from the liver. 

Validation of the model. 

Predicted skeletal americium concentrations were compared to values observed in a USTUR case and the 

predicted and observed values agreed reasonably well. However, the same USTUR case was used to 

derive values for model parameters and, therefore, agreement with the observations would be expected. 

No other validation results are described. 

Risk assessment. 

The model was developed to predict skeletal and soft tissue burdens of americium in people who may be 

exposed to americium. Comparisons of ALIs derived from the model and the ICRP (1979) model are 

presented. Descriptions of applications of the model in risk assessment have not been reported. 

Target tissues. 

The model calculates americium burdens in liver and skeleton. This output could be used to predict 

radiation doses to these tissues. 

Species extrapolation. 

The model is designed for applications to human dosimetry. The model cannot be applied to other 

species without modification. 

Interroute extrapolation. 

The model, as described in Durbin and Schmidt (1985), does not have an intake component, but it could 

be linked to an oral or inhalation intake model or a wound model to simulate the biokinetics of americium 

associated with such exposures. 
 

Urine Slow 

Bone 

Fast 

Bone 

Fast 

Other Soft 

Tissue 

Slow 

Other Soft 

Tissue 

Liver 

Feces 

Urine 

Urine Urine 

AMERICIUM 78 

3. HEALTH EFFECTS 

Figure 3-7. Durbin and Schmidt (1985) Model of Distribution and Excretion of 

Absorbed Americium in the Human
 
 

 

AMERICIUM 79 

3. HEALTH EFFECTS 

Other Models 

Leggett (1992) also proposed a respiratory tract model. Deposition of americium particles, depending on 

their size, are assumed to deposit in three compartments representing extrathoracic, fast-clearing thoracic, 

and slow-clearing thoracic regions of the respiratory tract (Figure 3-8). 

An early model to calculate doses to workers exposed to radionuclides by ingestion or inhalation was 

developed by ICRP (1979). In 1996, ICRP recommended that a task group be set up to revise the model. 

This task group developed a new model for the human alimentary tract (Métivier 2003) that has yet to be 

endorsed by the ICRP. 

A biokinetic model for radionuclide-contaminated wounds is under development by a scientific 

committee established jointly by the U.S. National Council on Radiation Protection (USNCRP) and 

ICRP, a draft of which was recently published (Guilmette and Durbin 2003). 

3.5 MECHANISMS OF ACTION 

3.5.1 Pharmacokinetic Mechanisms 

Absorption. Inhaled particulate aerosols of americium will be deposited in the respiratory tract. 

Amounts and patterns of deposition of particulates in the respiratory tract are affected by the size of the 

inhaled particles, age-related factors, breathing route (e.g., nose breathing versus mouth breathing), 

airway geometry, and airstream velocity within the respiratory tract (ICRP 1994b; James et al. 1994; Roy 

et al. 1994). In general, large particles (>2.5 μm) preferentially deposit in the nasopharyngeal region 

where high airstream velocities and airway geometry facilitate inertial impaction (Chan and Lippman 

1980; James et al. 1994). In the tracheobronchial and alveolar regions, where airstream velocities are 

lower, processes such as sedimentation and interception become important for deposition of smaller 

particles (<2.4 μm). Airflow velocity and airway geometry change with age, giving rise to age-related 

differences in particle deposition (James 1978; James et al. 1994; Phalen et al. 1985). Anatomical 

features, as well as their use (nose versus mouth breathing), also affect the intake route (nose or mouth). 

Deposition in the various regions of the respiratory tract in children may be higher or lower than in adults 

depending on particle size; for submicron particles, fractional deposition in 2-year-old children has been 

estimated to be 1.5 times greater than in adults (Xu and Yu 1986). Absorption of deposited americium is 
RESPIRATORY
 

TRACT
 

ExtraThoracic
 

S1 

S2 

S3 

G
 

I
 

T 

R 

A 

C 

T 

B 

L 

O 

O 

D 

FastThoracic
 

Slow Thoracic 

 

 

 

 

 

AMERICIUM 80 

3. HEALTH EFFECTS 

Figure 3-8. Leggett (1992) Model of Deposition and Retention of Americium in the 

Human Respiratory Tract 

AmO2 Other americium 

Pool To Half-time f Half-time f 

Extra-thoracic Blood – 0.0 0.4 days 0.05 

Gastrointestinal tract 0.4 days 1.0 0.4 days 0.95 

Fast thoracic Blood – 0.0 0.2 days 0.25 

Gastrointestinal tract 0.2 days 1.0 0.2 days 0.75 

Slow thoracic 

S1 (80%) (45%) 

Blood 

Gastrointestinal tract 

11 days 

11 days 

0.90 

0.10 

15 hours 

15 hours 

0.80 

0.20 

S2 (17%) (45%) 

Blood 

Gastrointestinal tract 

0.5 years 

0.5 years 

0.0 

1.0 

25 days 

25 days 

0.80 

0.20 

S3 (3%) (10%) 

Blood 

Gastrointestinal tract 

3 years 

3 years 

0.20 

0.80 

500 days 

500 days 

0.20 

0.80 

GI = gastrointestinal tract 
 

AMERICIUM 81 

3. HEALTH EFFECTS 

influenced by particle size and solubility as well as the pattern of regional deposition within the 

respiratory tract. Larger particles (>2.5 μm) that are primarily deposited in the ciliated airways 

(nasopharyngeal and tracheobronchial regions) can be transferred by mucociliary transport into the 

esophagus and swallowed. Particles deposited in the alveolar region can be absorbed after extracellular 

dissolution or ingestion by phagocytic cells. Americium-bearing pulmonary alveolar macrophages 

(PAMs) can either migrate to the airways where mucociliary transport to the esophagus can occur or to 

tracheobronchial lymph nodes (Taya and Mewhinney 1992; Taya et al. 1986, 1992). The relative 

contributions of these two pathways to americium absorption have not been quantified. Studies in dogs 

and monkeys have shown that americium is present in tracheobronchial lymph nodes within days after 

inhalation of americium dioxide (Mewhinney et al. 1982; Stanley et al. 1982; Thomas et al. 1972). PAMs 

isolated from dogs, monkeys, and rats demonstrated the presence of phagocytosed and dissolved 

americium dioxide particles (Taya et al. 1992). 

The site and mechanism of absorption of ingested americium are not known. Based on studies of 

plutonium, it is likely that americium absorption occurs, at least to some extent, in the small intestine. 

Studies of the absorption of plutonium in preparations of in situ isolated segments of small intestine of 

immature miniature swine indicate that absorption of actinides can occur along the entire small intestine, 

with the highest rates of absorption occurring in the duodenum (Sullivan and Gorham 1982). 

Distribution. Once americium is in systemic circulation, the route of exposure is not expected to 

affect its distribution. The mechanisms by which americium is taken up and retained in bone are only 

partially understood. The distribution of americium in bone initially is confined to bone surfaces, 

including endosteal and periosteal surfaces, and adjacent to vascular canals in cortical bone (Polig 1976; 

Priest et al. 1983, 1995; Schlenker et al. 1989). Deposition appears to be favored at sites of active bone 

resorption, and concentrations are highest in trabecular bone where there is a high surface to volume ratio 

(Kathren et al. 1987; Priest et al. 1983). Surface deposits can eventually appear in somewhat deeper 

regions of bone as a result of accretion of new bone and burial of older surface deposits (Polig 1976; 

Priest et al. 1983). The observation that americium does not distribute more uniformly in bone has been 

taken as evidence that it does not exchange readily with calcium or other minerals in the bone mineral 

matrix and that the initial interactions with bone may be with organic components of bone (Bruenger et al. 

1973; Priest et al. 1983); however, experimental evidence for this is equivocal. While americium has 

been shown to bind to the glycoprotein fraction of bovine cortical bone, even in the presence of an excess 

mass of bone mineral (Chipperfield and Taylor 1972), it also binds to bone mineral and bone calcium 

hydroxyapatite (Guilmette et al. 1998). 
 

AMERICIUM 82 

3. HEALTH EFFECTS 

The highest concentrations of americium in soft tissues occur in the liver (Filipy and Kathren 1996). The 

mechanisms of accumulation and retention of americium in liver have not been characterized. In rats and 

hamsters, americium appears to initially and extensively associate with lysosomes (Gruner et al. 1981; 

Seidel et al. 1986; Sütterlin et al. 1984). Agents that disrupt microtubules and lysosome formation and 

processing, such as colchicine and vinblastine, have been shown to decrease liver uptake of americium in 

rats (Seidel 1984, 1985). The effect is thought to involve disruption of hepatic microtubule formation, 

which is critical to the formation and intracellular processing of lysosomes, the initial site of accumulation 

of americium in the liver. The major bound form of americium in dog liver cytosol was shown to be a 

ferritin complex (Stover et al. 1970). Substantial species differences in liver retention of americium have 

been observed. Most notable is the Chinese hamster for which liver retention half-times of 3,400 days 

have been estimated, compared to 5–16 days in rat liver (Durbin 1973; McKay et al. 1972). Elimination 

of americium from liver is relatively slow in dogs (1–10 years) compared with rats and mice (Durbin 

1973; Lindenbaum and Rosenthal 1972). Mechanisms involved in the species differences in retention of 

americium in the liver have not been elucidated, although it has been proposed that animals with shorter 

retention times might be capable of excreting lysosomes in the bile (Sütterlin et al. 1984). The relatively 

slow elimination of americium from the hamster liver does not appear to be related to the initial tissue 

distribution, as the degree of association of americium with the lysosomal fraction of livers from rats and 

hamsters is similar (Sütterlin et al. 1984). 

The placental transfer of 241Am to the fetus has been studied in several animal models and in the in situ 

perfused guinea pig placenta (Sikov 1987). After injections of 241Am in mice and rats, a small fraction 

(<0.1%) of the maternal dose is transferred to the fetus (Hisamatsu and Takizawa 1983; Sikov 1987; 

Stather et al. 1992; Van Den Heuvel 1992; Weiss et al. 1980). Placental concentrations generally exceed 

those of the fetus, and concentrations in the embryo/fetal membranes are higher than in the fetus (Sikov 

1987). Mechanisms of transport across the placenta have not been elucidated. 

Metabolism. As noted in Section 3.4.3, the metabolism of americium consists of binding interactions 

with proteins and probably complex formation with various inorganic anions, such as carbonate and 

phosphate, and carboxylic acids, such as citrate and lactate (Durbin 1973; Taylor 1973; Webb et al. 1998). 

Experiments have not been conducted to determine whether americium binds to metallothionein, but such 

binding is not likely. 
 

AMERICIUM 83 

3. HEALTH EFFECTS 

Excretion. Although fecal excretion appears to be a major route of excretion of absorbed americium, 

the mechanisms by which americium is transferred to feces have not been characterized in humans. 

Injection studies in animals suggest a contribution of biliary excretion to the fecal excretion of absorbed 

americium (Durbin 1973). Similarly, the mechanisms by which americium is excreted in urine have not 

been elucidated. Renal plasma clearance has been measured in rats, dogs, and monkeys; in all three 

species, the renal clearance was <10% of the glomerular filtration rate (Durbin 1973; Lloyd et al. 1970; 

Taylor et al. 1961; Turner and Taylor 1968). However, simultaneous measurements of the renal plasma 

clearance of ultrafilterable americium and glomerular filtration rate are not available; thus, the relative 

contributions of filtration, tubular secretion, and tubular reabsorption to urinary excretion of americium 

cannot be ascertained with the available information. Studies of human urine incubated with 241Am or 

urine collected from rats that were exposed to americium indicate that the major form of americium in 

urine appears to be a low molecular weight complex (1,000–10,000 daltons) with citrate (Stradling et al. 

1976). This would be consistent with citrate complexes occurring in plasma from which they could enter 

the urine by glomerular filtration. 

3.5.2 Mechanisms of Toxicity 

Americium toxicity results primarily from the damage done by the alpha particle emitted during 

radioactive decay. This alpha particle has very limited penetration in tissue, and hence, the cellular 

damage (including damage to genomic material) occurs only in the immediate vicinity of the sequestered 

americium. Alpha particles deposit all of their energy in a short distance of travel. The large charge and 

mass of the alpha particle account for the strong interaction with surrounding cells. The transferred 

energy ionizes localized cell matter in its path directly and via hydrolysis of water (approximately 70%) 

in human cells. Radiation interaction with water produces ionized and excited water molecules referred 

to as radiolysis products. These reactive water species have sufficiently long half-times that they can 

diffuse away from the interaction site and interact with biological molecules, which can increase the 

resulting cellular damage. Thus, cellular damage can result both directly from radiation itself and 

indirectly from the chemical reactions involving reactive species of radiolysis products. 

3.5.3 Animal-to-Human Extrapolations 

Significant interspecies differences are apparent regarding liver retention rates of absorbed americium 

(Durbin 1973; Griffith et al. 1983) (see Sections 3.4.2.4 and 3.5.1 for more detailed information). 
 

AMERICIUM 84 

3. HEALTH EFFECTS 

Interspecies differences are also apparent in skeletal distribution of absorbed americium (Lynch et al. 

1989). However, no data were located to indicate significant interspecies differences in health effects 

associated with exposure to americium. 

3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS 

Recently, attention has focused on the potential hazardous effects of certain chemicals on the endocrine 

system because of the ability of these chemicals to mimic or block endogenous hormones. Chemicals 

with this type of activity are most commonly referred to as endocrine disruptors. However, appropriate 

terminology to describe such effects remains controversial. The terminology endocrine disruptors, 

initially used by 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 1997a). 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). 
AMERICIUM 85 

3. HEALTH EFFECTS 

No studies were located regarding endocrine disruptive effects in humans or animals resulting from 

exposure to americium. 

3.7 CHILDREN’S SUSCEPTIBILITY 

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

maturity at 18 years of age in humans, when all biological systems will have fully developed. Potential 

effects on offspring resulting from exposures of parental germ cells are considered, as well as any indirect 

effects on the fetus and neonate resulting from maternal exposure during gestation and lactation. 

Relevant animal and in vitro models are also discussed. 

Children are not small adults. They differ from adults in their exposures and may differ in their 

susceptibility to hazardous 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 
AMERICIUM 86 

3. HEALTH EFFECTS 

Kearns 1997; NRC 1993; Vieira et al. 1996). Whether differences in xenobiotic metabolism make the 

child more or less susceptible also depends on whether the relevant enzymes are involved in activation of 

the parent compound to its toxic form or in detoxification. There may also be differences in excretion, 

particularly in newborns who all have a low glomerular filtration rate and have not developed efficient 

tubular secretion and resorption capacities (Altman and Dittmer 1974; NRC 1993; West et al. 1948). 

Children and adults may differ in their capacity to repair damage from chemical insults. Children also 

have a longer remaining lifetime in which to express damage from chemicals; this potential is particularly 

relevant to cancer. 

Certain characteristics of the developing human may increase exposure or susceptibility, whereas others 

may decrease susceptibility to the same chemical. For example, although infants breathe more air per 

kilogram of body weight than adults breathe, this difference might be somewhat counterbalanced by their 

alveoli being less developed, which results in a disproportionately smaller surface area for alveolar 

absorption (NRC 1993). 

No studies were located in which comparisons were made between the sensitivity of children and adults 

to the toxicity of americium. Some studies indicate that radiation effects may be greater per unit dose in 

children than in adults. However, study of bone cancer induction from injected 239Pu or 226Ra in dogs 

suggests that, on a per Gy basis, dogs exposed at 3 months of age were less sensitive than dogs exposed at 

1.5 years of age (Lloyd et al. 1999). Both plutonium and radium are alpha-emitters that accumulate in 

bone, as does americium. No direct evidence was located to indicate that the pharmacokinetics of 

americium in children may be different from that in adults. Based on dosimetric considerations related to 

differences in the parameters of available models, as well as studies in animals, it seems likely that 

children may be more susceptible to americium toxicity than adults by virtue of age-related differences in 

pharmacokinetics or radiosensitivity. Therefore, a potential for increased risk of effects to the bones of 

children is attributed to the uptake and long-term biological storage of 241Am in the bone during critical 

periods of growth, which may result in genetic damage and an increased risk for cancer. Differences in 

airway geometry and airflow rates between children and adults would be expected to result in higher 

fractional deposition of inhaled submicron particles in children than in adults (Xu and Yu 1986) (see 

Section 3.5.1). Thus, children who are exposed to americium aerosols may receive a higher dose to the 

lung and greater absorption than would similarly exposed adults (ICRP 1995). 

Studies of experimental animals indicate that absorption of ingested americium may be as much as 

200 times greater in neonates than in adults (Bomford and Harrison 1986; David and Harrison 1984; 
AMERICIUM 87 

3. HEALTH EFFECTS 

Sullivan et al. 1985) (see Section 3.4.1.2 and Table 3-2). Thus, infants exposed to levels of americium in 

food or water similar as adults, or who ingest similar amounts of americium subsequent to an inhalation 

exposure, may absorb more americium and acquire a higher internal burden of americium. The ICRP 

(1989, 1994b, 1995) assumes age-related differences in intestinal absorption of americium swallowed 

following clearance from the lungs. The fractional absorption value employed for a 3-month-old infant is 

a factor of 10 higher than for an adult. 

Absorption of americium is greater in iron-deficient animals than in iron-replete adult animals (Sullivan 

and Ruemmler 1988; Sullivan et al. 1986) (see Section 3.4.1.2). Concurrent oral exposure to Fe3+ and 

americium also appears to increase the absorption of ingested americium; the latter effect may result from 

redox reactions in the gastrointestinal tract catalyzed by Fe3+ (Sullivan et al. 1986). These differences are 

accounted for in the discussions and dosimetric/metabolic models of the ICRP (1989, 1993) and the NEA 

(1988). 

As inherent in these ICRP (1989, 1993) models, deposition of americium in bone occurs predominantly at 

bone surfaces that are actively undergoing resorption; therefore, exchanges between bone and soft tissue 

stores of americium would be expected to be more rapid during periods of active bone metabolism such 

as infancy and childhood, pregnancy, and menopause. Higher skeletal accumulation of americium has 

been observed in neonatal animals that received americium intravenously than in similarly exposed adult 

animals (Hollins et al. 1973; Schoeters et al. 1990; Stevens et al. 1977) and in young rats (3 months of 

age) compared to old rats (13 months of age) (Sontag 1983). This suggests the possibility that infants and 

children may accumulate higher concentrations of americium in bone than similarly exposed adults. On 

the other hand, americium uptake into maternal bone of lactating rats was similar to that of nonlactating 

rats, while concurrent calcium uptake into bone was lower in lactating rats (Hollins and Durakovic 1972). 

Thus, active mobilization of bone mineral, per se, may not always promote release of americium from 

bone (see Section 3.4.2.1). Studies of other bone-seeking radionuclides indicate that vulnerability may be 

higher in adolescence and early adulthood than during earlier development or later adulthood (Carnes et 

al. 1997; Lloyd et al. 1999). 

Information on the transplacental transfer of americium in humans is not available directly, but the 

information from experiments with americium and other actinides has been used to derive biokinetic 

models and perform dosimetric models for the human (NCRP 1998; Sikov and Kelman 1989; USNRC 

1996). Studies in animals that received parenteral injections of americium have shown that absorbed 

americium is partially transferred to the fetus (Hisamatsu and Takizawa 1983; Paquet et al. 1998; Sasser 
AMERICIUM 88 

3. HEALTH EFFECTS 

et al. 1986; Schoeters et al. 1990; Weiss et al. 1980) (see Section 3.4.2.1). Limited reports indicate that 

relatively large doses of 241Am may induce fetal death and teratogenic effects in rodents (Moskalev et al. 

1969; Rommerein and Sikov 1986). 

Information on the distribution of absorbed americium to mammary milk in humans is not available; 

however, maternal (oral or intravenous) exposures of animals, including cows and goats, have shown that 

transfer to milk occurs and that neonates can be exposed to americium during lactation (McClellan et al. 

1962; Sasser et al. 1986; Sutton et al. 1979) (see Section 3.4.2.1). Thus, it is possible that children who 

breast feed from mothers who have been exposed to americium, or who ingest milk from cows or other 

livestock that have been exposed to americium, may also be exposed to americium. 

Bone serves as a long-term reservoir of americium in the body. The kinetics of bone formation and 

remodeling appear to be important factors in the overall biokinetics of americium in experimental animals 

(ICRP 1989, 1993). Quantitative evidence for their effects in humans has not been characterized, but 

exchanges between bone and soft tissue stores of americium would be expected to be more rapid during 

periods of active bone metabolism such as infancy and childhood, pregnancy, and menopause (see 

Section 3.4.2.1). Thus, it is possible that, in humans, some of the maternal bone americium stores may be 

transferred to the fetus during gestation and may be incorporated into fetal bone during the development 

of the fetal skeleton. However, the finding of similar americium uptake in maternal bone of lactating and 

nonlactating rats (Hollins and Durakovic 1972) may be an indication that active bone metabolism is not 

necessarily a major source of americium release from bone at this maternal stage. 

3.8 BIOMARKERS OF EXPOSURE AND EFFECT 

Biomarkers are broadly defined as indicators signaling events in biologic systems or samples. They have 

been classified as markers of exposure, markers of effect, and markers of susceptibility (NAS/NRC 

1989). 

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 
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3. HEALTH EFFECTS 

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., biological half-life) and environmental 

conditions (e.g., duration and route of exposure), the substance and all of its metabolites may have left the 

body by the time samples can be taken. It may be difficult to identify individuals exposed to hazardous 

substances that are commonly found in body tissues and fluids (e.g., essential mineral nutrients such as 

copper, zinc, and selenium). Biomarkers of exposure to americium are discussed in Section 3.8.1. 

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 americium are discussed in Section 3.8.2. 

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 3.10 “Populations That Are Unusually Susceptible”. 

3.8.1 Biomarkers Used to Identify or Quantify Exposure to Americium 

Biomarkers or tests to identify or quantify exposure to americium are available only at a limited number 

of government or nuclear facilities, or through contractors engaged in this type work. Americium is a 

radioactive element. Internalized americium can be quantified through the use of in vivo radiation 

counters that measure the gamma emissions specific to each isotope of americium (Graham and Kirkman 

1983; Palmer and Rhoads 1989; Palmer et al. 1983). Americium within the body can be inferred from 

radioassays of urine, feces, or tissue samples by gross alpha analysis, alpha spectroscopy, gamma-ray 
AMERICIUM 90 

3. HEALTH EFFECTS 

spectroscopy, mass spectrometry, and liquid scintillation techniques (Alvarez and Navarro 1996; Dacheux 

and Aupiais 1997; DOE 1997b; Guilmette 1986; McInroy et al. 1985). Americium radioactivity can be 

measured in the teeth of rats, where it accumulates in the dental pulp of developing teeth and eventually is 

incorporated into the mineralized dentin (Hammerström and Nilsson 1970b), so it may be feasible to 

analyze human teeth for americium. 

3.8.2 Biomarkers Used to Characterize Effects Caused by Americium 

Although a sufficiently high dose of americium may produce chromosomal aberrations in lymphocytes 

(Bauchinger et al. 1997; Kelly and Dagle 1974), these effects are not specific to americium or to ionizing 

radiation in general. 

3.9 INTERACTIONS WITH OTHER CHEMICALS 

Ethanol may enhance the fecal excretion of absorbed americium. In baboons that received repeated oral 

doses of ethanol (1 mL ethanol/kg body weight), 3–6 months after receiving americium citrate 

intravenously, fecal excretion was approximately 2.5 times that of baboons that received water in place of 

the ethanol dose (Cohen et al. 1978). Long-term ethanol consumption accelerated the elimination of 

americium from the livers of beagle dogs that had been administered single intravenous injections of 

241Am (Taylor et al. 1992). The risk of americium-induced liver tumors, however, was 2–3 times higher 

in the ethanol-treated dogs than in similarly 241Am-injected dogs not consuming ethanol. 

Colchicine (a drug used in treatment of gout) and vinblastine (a cancer chemotherapy agent) may 

decrease liver uptake of americium. In rats that received an intraperitoneal injection of either colchicine 

and vinblastine prior to an intravenous or intramuscular injection of americium citrate, liver uptake of 

americium was lower, relative to controls, and kidney and skeletal americium uptakes were higher (Seidel 

1984, 1985). The effect is thought to involve disruption of hepatic microtubule formation, which is 

critical to the formation and intracellular processing of lysosomes, the initial site of accumulation of 

americium in the liver. 
 

 

 

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3. HEALTH EFFECTS 

3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE 

A susceptible population will exhibit a different or enhanced response to americium than will most 

persons exposed to the same level of americium 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 241Am, or compromised function of 

organs affected by 241Am. Populations who are at greater risk due to their unusually high exposure to 

241Am are discussed in Section 6.7, Populations With Potentially High Exposures. 

As discussed in Section 3.7, theoretical pharmacokinetics consideration suggests that children may be at 

greater risk from the effects of exposure to americium. Furthermore, some studies indicate that children 

may be more susceptible than adults to radiation-induced adverse effects. A study of bone cancer 

induction from injected 239Pu or 226Ra in dogs suggests that, on a per Gy basis, dogs exposed as young 

adults (1.5 years of age) were more susceptible than either juveniles exposed at 3 months of age or older 

adults (5 years of age) (Lloyd et al. 1999). Both plutonium and radium are alpha-emitters that accumulate 

in bone, as does alpha-emitting americium. 

3.11 METHODS FOR REDUCING TOXIC EFFECTS 

This section will describe clinical practice and research concerning methods for reducing toxic effects of 

exposure to americium. 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 americium. When 

specific exposures have occurred, the Radiological Emergency Assessment Center/Training Site, poison 

control centers and medical toxicologists should be consulted for medical advice. The following texts 

provide specific information about treatment following exposures to americium: 

Ellenhorn MJ, Schonwald S, Ordog G, et al., eds. 1997. Medical toxicology: Diagnosis and Treatment of 

Human Poisoning. 2nd Baltimore (Williams & Wilkins), 1682-1723. 

Haddad LM, Shannon MW, Winchester JF, eds. 1998. Clinical Management of Poisoning and Drug 

Overdose. 3rd edition. Philadelphia (W.B. Saunders), 413-425. 

Viccellio P, ed. 1998. Emergency Toxicology. 2nd edition. Philadelphia (Lippincott-Raven), 991-996. 
 

 

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3.11.1 Reducing Peak Absorption Following Exposure 

Topical applications of saline containing DTPA, tartaric acid, or citric acid (e.g., Schubert’s solution) 

have been used to remove americium from the skin and wounds after accidental dermal exposures 

(Breitenstein 1983). These agents form stable, water-soluble complexes with americium. Based on 

experiments with laboratory animals, it appears that aerosols of DTPA may reduce the absorption of 

soluble forms of inhaled americium compounds (Stradling et al. 2000). Postexposure treatments that are 

effective in reducing toxic effects of radionuclides such as americium typically concentrate on 

decorporation (removal of americium from the body following absorption) and are discussed in 

Section 3.11.2. 

3.11.2 Reducing Body Burden 

Calcium or zinc complexes of polycarboxylate compounds such as DTPA or ethylenediaminetetratacetic 

acid (EDTA) have been used as chelating agents to accelerate the urinary excretion of americium in 

humans who were accidentally exposed to americium (Breitenstein 1983; Doerfel and Oliveira 1989; 

Durbin 1973; Fasiska et al. 1971). Extended chelation therapy was considered to have been a primary 

factor in the long-term survival of a man who had been accidentally exposed to a massive amount of 

241Am (Breitenstein and Palmer 1989; Filipy et al. 1995; Toohey and Kathren 1995). Immediate and 

continued DTPA treatment of rats that had been exposed to 241AmO2 by inhalation resulted in the neartotal blockage of 241Am translocation to liver and bone (Guilmette et al. 1988). Continuous subcutaneous 

infusion of DTPA was more effective in blocking the uptake than were periodic intravenous injections. 

Dogs receiving DTPA treatments following single intravenous injections of 241Am at activity levels of 

approximately 11 kBq/kg (297 nCi/kg) exhibited greater longevity and lower rates of bone cancer than 

241Am-treated dogs not given subsequent DTPA treatment (Lloyd et al. 1998). DTPA and EDTA form 

relatively stable complexes with americium in the extracellular fluid that can be excreted in the urine 

(Durbin 1973; Taylor 1973). The calcium and zinc complexes are used to decrease the risk of calcium 

and zinc depletion. Both DTPA and EDTA appear to affect primarily the americium in soft tissues, 

which exchanges more rapidly with americium in plasma than does americium in bone. As a result, 

treatments with DTPA or EDTA may have only a marginal effect on bone americium levels (Durbin 

1973). In a study in rats, DTPA treatment, administered beginning 1.5 hours following intravenously 

administered 241Am citrate, decreased bone 241Am levels in trabecular bone at locations where bone 

resorption and remodeling occurred, but had little effect on americium levels in cortical bone (Polig 
 

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3. HEALTH EFFECTS 

1976). This effect may have resulted from accelerated excretion and, therefore, diminished redeposition 

of americium released during bone resorption. 

Hydroxypyridonate ligands such as octadentate 3,4,3-LI(1,2-HOPO) and hexadentate TREN-Me3,2-HOPO) have been shown to be highly effective chelating agents in laboratory animals (Durbin et al. 

1994; Stradling et al. 2000). Recent in vitro studies have indicated that octadentate 3,4,3-LI(1,2-HOPO) 

may be effective in decorporation of americium from bone tissues (Guilmette et al. 2003). 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects 

No data were located regarding reduction of the toxic effects of radioactive americium through interfering 

with mechanisms of action. 

3.12 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of americium 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 americium. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 

3.12.1 Existing Information on Health Effects of Americium 

The existing data on health effects of inhalation, oral, and dermal exposure of humans and animals to 

americium are summarized in Figure 3-9. The purpose of this figure is to illustrate the existing 
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3. HEALTH EFFECTS 

Figure 3-9. Existing Information on Health Effects of Americium 

Inhalation 

Oral 

Dermal 

Death

Acute

Intermediate 

Chronic 

Immunologic/Lymphoretic 

Neurologic 

Reproductive 

Developmental 

Genotoxic 

Cancer 

Systemic 

External 

Human 

Inhalation 

Oral 

Dermal 

External 

De

h

Acu e 

Inte

ediate 

C r

c 

Im

o g

/Lymphoreti

e

e

e

at

t

rm

o h

ni

mun lo

ic

c 

N urologic 

R productive 

Developmental 

G notoxic 

Cancer 

Systemic 

Animal 

Existing Studies 
 

AMERICIUM 95 

3. HEALTH EFFECTS 

information concerning the health effects of americium. 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. 

Information regarding health effects following exposure to americium is mainly limited to reports of acute 

exposure. Accidental occupational overexposure of a 64-year-old man resulted in signs of hematological 

and bone marrow damage. Animal studies indicate that overexposure to americium can result in 

compromised hematological and immunological systems, as well as degenerative changes in the bone, 

liver, kidneys, and thyroid, and bone and liver cancer in long-term surviving animals. Although most 

studies employed parenteral injection as the route of exposure, available inhalation data indicate similarity 

in targets of toxicity. Data regarding health effects related to oral or dermal exposure are lacking for both 

humans and animals. Levels of radioactivity from americium employed in animal studies are much 

higher than those likely to be environmentally experienced by humans. Therefore, americium does not 

likely pose an immediate health concern to humans. 

3.12.2 Identification of Data Needs 

Acute-Duration Exposure. Human data regarding acute adverse health effects resulting from 

exposure to americium are limited to the accidental occupational overexposure (inhalation, dermal, 

subcutaneous) of a 64-year-old man in whom possible hematological and bone marrow changes may have 

been elicited (Filipy et al. 1995; Priest et al. 1995). Overexposure of animals to americium by the 

inhalation exposure route resulted in compromised respiratory function and radiation pneumonitis 

(Buldakov et al. 1972; DOE 1978; Thomas et al. 1972), persistent depressed blood values (Buldakov et 

al. 1972; Thomas et al. 1972), degenerative changes in bone, liver and kidney lesions, and gross atrophy 

and fibrosis of the thyroid gland (Thomas et al. 1972). Following acute inhalation exposure to 

americium, 4 of 15 dogs surviving more than 1,000 days developed osteosarcomas (Gillett et al. 1985). 

With the exception of the respiratory effects following inhalation exposure, the other targets of toxicity 

were likewise identified in animals administered single parenteral injections of americium at relatively 
 

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high levels of radioactivity (Carter et al. 1951; Dougherty 1970; Jee et al. 1985; Lloyd et al. 1970, 1994a, 

1994b; Schoeters et al. 1991; Taylor et al. 1983, 1991, 1993a; Van Den Heuvel et al. 1995). Acuteduration inhalation and oral MRLs were not derived for radioactive americium due to a lack of human or 

animal data. To generate appropriate data for deriving acute-duration inhalation and oral MRLs for 

radioactive americium, at least one comprehensive acute inhalation study and one acute oral toxicity 

study of at least one animal species exposed to several dose levels would be needed. Such studies could 

be designed to also generate data regarding potential age-related differences in toxicity. However, since 

americium is not found naturally, and is produced and used in small quantities, the risk of overexposure to 

americium in humans should be low. Thus, additional studies may not be presently needed. 

Intermediate-Duration Exposure. A single report indicated the potential for cytogenetic damage in 

a radiation worker and his family members following exposure to an americium source used by the father 

for private experiments at home for several years. No additional human or animal data were located. 

Intermediate-duration inhalation and oral MRLs were not derived for americium due to the lack of human 

or animal data. To generate appropriate data for deriving intermediate-duration inhalation and oral MRLs 

for americium, at least one comprehensive intermediate-duration inhalation and one intermediate-duration 

oral toxicity study of at least one animal species exposed to several dose levels would be needed. Such 

studies could be designed to also generate data regarding potential age-related differences in toxicity. 

However, since americium is not found naturally, and is produced and used in small quantities, the risk of 

overexposure to americium in humans should be low. Thus, additional studies may not be presently 

needed. 

Chronic-Duration Exposure and Cancer. No data were located regarding chronic-duration 

exposure of humans or animals to americium. Chronic-duration inhalation and oral MRLs were not 

derived for americium due to the lack of human or animal data. To generate appropriate data for deriving 

chronic-duration inhalation and oral MRLs for americium, at least one comprehensive chronic-duration 

inhalation and one chronic-duration oral toxicity study of at least one animal species exposed to several 

dose levels would be needed. Such studies could be designed to also generate data regarding potential 

age-related differences in toxicity. However, since americium is not found naturally, and is produced and 

used in small quantities, the risk of overexposure to americium in humans should be low. Thus, 

additional studies may not be presently needed. 

Genotoxicity. Chromosomal aberrations have been reported in lymphocytes following exposure to 

241Am (Bauchinger et al. 1997; Kelly and Dagle 1974). A single animal study reported increased 
 

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numbers of micronucleated and multinucleated pulmonary alveolar macrophages in lung lavage of mice 

that had been exposed to 241Am by inhalation (Talbot et al. 1989). External and internal exposure to 

radioactivity is a genotoxicity concern. External exposure to gamma-emitting americium would be 

expected to result in genotoxic effects similar to those observed following external exposure to any other 

gamma-emitting radionuclide (see ATSDR 1999 for more information on ionizing radiation). 

Internalized americium could cause damage to nearby cellular components that might be encountered by 

high energy alpha particles emitted from americium. Additional genotoxicity studies could be designed 

to assess the potential for genotoxicity from internalized americium, with special emphasis on bloodforming cells. 

Reproductive Toxicity. No reports were located regarding reproductive effects in humans or 

animals following inhalation, oral, or dermal exposure to americium. In a limited study, increased 

incidences of fetal death were observed following single intravenous injections of 241Am, administered to 

female rats prior to mating (Moskalev et al. 1969). Concentrations of 241Am were much higher in 

placental tissues than in fetuses, and the investigators indicated that death may have been the result of 

placental changes. Animal studies could be designed to assess the potential for the reproductive toxicity 

of americium. 

Developmental Toxicity. Data concerning developmental effects related to exposure to americium 

are restricted to a single report of decreased fetal weight, increased fetal death, and a tendency toward 

increased incidences of fetuses with anomalous ribs following exposure of pregnant rats with single 

intravenous injections of 241Am (Rommerein and Sikov 1986). Animal studies could be designed to 

further assess the potential for the developmental toxicity of americium. 

Immunotoxicity. Information regarding the immunotoxicity of americium is limited to a report of 

lymphopenia in a man following accidental overexposure when a glass column containing 241Am blew up 

in his face (Filipy et al. 1995) and reports of depressed white blood cell counts in dogs exposed to 241Am 

by inhalation (Buldakov et al. 1972; Thomas et al. 1972) or intravenous injection (Dougherty 1970). 

Additional animal studies could be designed to assess dose-response relationships. 

Neurotoxicity. No data were located regarding neurotoxicity in humans or animals following 

exposure to americium. Neurotoxic effects, noted in humans suffering from acute radiation syndrome due 

to ionizing radiation exposure, are well-characterized (see ATSDR 1999 for detailed information on the 

effects of ionizing radiation). External overexposure to any gamma-emitting source could result in 
AMERICIUM 98 

3. HEALTH EFFECTS 

neurotoxic effects. However, it is extremely unlikely that an americium source capable of producing such 

an overexposure would be encountered. Studies concerning the potential of americium to induce 

neurotoxicity do not appear to be needed at present. 

Epidemiological and Human Dosimetry Studies. Epidemiological studies of radiation dose 

typically involve estimates of exposure that are based on whole-body measurements of internallydeposited americium. A need remains for epidemiological data that can provide quantitative human doseresponse information while supplying additional information on the health effects of exposure to ionizing 

radiation and americium; in particular, for cases of known internal exposure. 

Biomarkers of Exposure and Effect. 

Exposure. Americium may be detected during in vivo counting as well as in samples of urine, blood, 

feces, or body tissues. Due to the relatively long biological half-time of americium in skeleton, shortterm exposures cannot be readily distinguished from longer-term ones. An increased understanding of the 

biokinetics and health effects of internalized americium can be achieved through continued monitoring of 

individuals following known overexposure to americium. 

Effect. Chromosomal aberrations have been reported in lymphocytes following exposure to 241Am 

(Bauchinger et al. 1997; Kelly and Dagle 1974). Additionally, high radiation doses from internally 

deposited americium can cause bone marrow changes and altered blood values (Filipy et al. 1995; Priest 

et al. 1995). However, none of these effects are specific to americium. 

Absorption, Distribution, Metabolism, and Excretion. Inhaled americium can be absorbed and 

transferred to the blood (Edvardsson and Lindgren 1976; Fry 1976; Newton et al. 1983; Sanders 1974; 

Toohey and Essling 1980). Limited information indicates that americium is rather poorly absorbed via 

the gastrointestinal tract (Hunt 1998; Hunt et al. 1986a, 1986b). Once americium reaches the blood, it is 

distributed throughout the body, accumulating mainly in the skeleton, liver, and muscle (Filipy and 

Kathren 1996; Filipy et al. 1994; Kathren et al. 1988; McInroy et al. 1989). Animal studies indicate that 

americium can pass through the placental barrier of a pregnant mother to a developing fetus (DOE 1986; 

Hisamatsu and Takizawa 1983; Paquet et al. 1998; Sasser et al. 1986; Schoeters et al. 1990; Sikov 1987; 

Van Den Heuvel et al. 1992; Weiss et al. 1980), and also can be distributed to the breast milk of lactating 

mothers (McClellan et al. 1962; Sasser et al. 1986; Sutton et al. 1979). The metabolism of americium 

consists of binding interactions with proteins and probably complex formation with various inorganic 

anions, such as carbonate and phosphate, and carboxylic acids, such as citrate and lactate (Durbin 1973; 
AMERICIUM 99 

3. HEALTH EFFECTS 

Taylor 1973; Webb et al. 1998). Americium is slowly eliminated from soft tissues and bone, but may 

remain in the skeleton for much longer periods. Once absorbed into the general circulation, americium is 

excreted in both feces and urine (Cohen and Wrenn 1973; Durbin 1973; Guilmette et al. 1980; Stather et 

al. 1979a). Additional quantitative toxicokinetic studies could be designed to further assess absorption 

following inhalation, oral, and dermal exposure, as well as age-related differences in the toxicokinetics of 

americium. However, the predominant data need for americium, and other sources of internal radiation 

exposure, is the validation (through biokinetic studies) and refinement of the models that describe internal 

distribution from which the radiation dose derives. 

Comparative Toxicokinetics. Toxicokinetic properties of americium are generally similar in 

humans and animals. Inhaled americium, in relatively soluble forms, is readily absorbed in the 

respiratory system of humans and animals. Ingested americium is not absorbed to any great extent in 

humans or animals. Distribution patterns are generally similar; americium is found in highest 

concentrations in the skeleton, liver, and muscle of humans and animals. Although studies were not 

located regarding transfer of americium from mother to developing fetus, studies in animals suggest that 

americium could be incorporated by a fetus following inhalation exposure of the pregnant mother. 

Methods for Reducing Toxic Effects. Topical applications of saline containing DTPA, tartaric 

acid, or citric acid (e.g., Schubert’s solution) have been used to remove americium from the skin and 

wounds after accidental dermal exposures. These agents form stable, water soluble complexes with 

americium. Calcium or zinc complexes of DTPA have been used as chelating agents to accelerate the 

urinary excretion of americium. Hydroxypyridonate ligands such as octadentate 3,4,3-LI(1,2-HOPO) and 

hexadentate TREN-Me-3,2-HOPO) have been shown to be highly effective chelating agents in laboratory 

animals (Durbin et al. 1994; Stradling et al. 2000). Recent in vitro studies have indicated that octadentate 

3,4,3-LI(1,2-HOPO) may be effective in decorporation of americium from bone tissues (Guilmette et al. 

2000). 

Children’s Susceptibility. Some studies suggest that children, especially neonates, may be more 

susceptible than adults to radiation-induced adverse effects.. However, animal studies indicate that 

juvenile dogs are less susceptible than adults to americium-induced bone cancer (Lloyd et al. 1999). No 

direct evidence was located to indicate that the pharmacokinetics of americium in children may be 

different from that in adults. Based on dosimetric considerations related to differences in the parameters 

of available models, as well as studies in animals, it seems likely that children may be more susceptible to 

the radiological effects of americium than are adults by virtue of age-related differences in 
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3. HEALTH EFFECTS 

pharmacokinetics. Absorption of ingested americium may be as much as 200 times greater in neonatal 

animals than in adults (Bomford and Harrison 1986; David and Harrison 1984; Sullivan et al. 1985). 

As inherent in ICRP (1989, 1993) models, deposition of americium in bone occurs predominantly at bone 

surfaces that are actively undergoing resorption; therefore, exchanges between bone and soft tissue stores 

of americium would be expected to be more rapid during periods of active bone metabolism such as 

infancy and childhood, pregnancy, and menopause. Higher skeletal accumulation of americium has been 

observed in neonatal animals that received americium intravenously than in similarly exposed adult 

animals (Hollins et al. 1973; Schoeters et al. 1990; Stevens et al. 1977) and in young rats (3 months of 

age) compared to old rats (13 months of age) (Sontag 1983). This suggests the possibility that infants and 

children may accumulate higher concentrations of americium in bone than similarly exposed adults. 

Studies of other bone-seeking radionuclides provide further support for increased vulnerability during 

periods of rapid bone growth such as adolescence (Carnes et al. 1997; Lloyd et al. 1999). 

Information on the transplacental transfer of americium in humans is not available. Studies in animals 

that received parenteral injections of americium have shown that absorbed americium is transferred to the 

fetus (Hisamatsu and Takizawa 1983; Paquet et al. 1998; Sasser et al. 1986; Schoeters et al. 1990; Weiss 

et al. 1980). 

Information on the distribution of absorbed americium to mammary milk in humans is not available; 

however, maternal (oral or intravenous) exposures of animals, including cows and goats, have shown that 

transfer to milk occurs and that neonates can be exposed to americium during lactation (McClellan et al. 

1962; Sasser et al. 1986; Sutton et al. 1979). 

Exchanges between bone and soft tissue stores of americium would be expected to be more rapid during 

periods of active bone metabolism such as infancy and childhood, pregnancy, and menopause. Thus, it is 

possible that, in humans, some of the maternal bone americium stores may be transferred to the fetus 

during gestation and may be incorporated into fetal bone during the development of the fetal skeleton. 

Child health data needs relating to exposure are discussed in 6.8.1 Identification of Data Needs: 

Exposures of Children. 
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3.12.3 Ongoing Studies 

No ongoing studies examining adverse health effects in mammalian species exposed to americium were 

identified in the Federal Research in Progress database (FEDRIP 2004) or are currently listed by the 

Argonne National Laboratory (ANL) for the Department of Energy (DOE). 

 

 

AMERICIUM 103 

4. CHEMICAL, PHYSICAL, and RADIOLOGICAL INFORMATION 

4.1 CHEMICAL IDENTITY 

Americium is a human-made actinide element (atomic number 95) and has no stable isotopes. It was 

discovered by Glen Seaborg, Leon Morgan, Ralph James, and Albert Ghiorso in 1944 and isolated by 

B.B. Cunningham as the isotope 241Am in Am(OH)3 in the fall of 1945. It was named after the Americas 

(Seaborg 1991; Seaborg and Loveland 1990). Actinides are the 15 elements starting with actinium, 

atomic number 89, and extending to lawrencium, atomic number 103. All of the isotopes of these 

elements are radioactive. Of the 15 americium isotopes and isomers currently identified, the longest-lived 

is 243Am. 

4.2 PHYSICAL, CHEMICAL, AND RADIOLOGICAL PROPERTIES 

Americium is a silvery, ductile, very maleable, non-magnetic metal. Americium melts at 1,176 oC, boils 

at 2,011 oC, and has an electron configuration of 5f7

7s2. The Chemical Abstract Service (CAS) registry 

numbers, decay modes, half-lives, and specific activities of the four principal americium isotopes and 

isomers, 241Am,242mAm, 242Am, and 243Am, are presented in Table 4-1. 241Am and 243Am decay by alpha 

emission forming neptunium (atomic number 93), 237Np (t1⁄2=2.14x106

 years) and 239Np (t1⁄2=2.355 days) as 

the respective products. 239Np subsequently decays to 239Pu (t1⁄2=2.411x104 years), and then to 235U, which 

is also a naturally-occurring isotope of uranium. The decay of 241Am to 237Np is accompanied by a 

predominant gamma ray photon of 59.54 keV. 242mAm is an isomer (long-lived excited state of the 

nucleus) of 242Am and has a half-life of 141 years; 95.5% of 242mAm undergoes an isomeric transition to 

242Am (t1⁄2=16.02 hours) with the emission of a 48.6 keV gamma ray, and 0.5% decays by alpha emission 

to 238Np. 242Am primarily (87%) undergoes beta decay to curium 242 (atomic number 96) 

(t1⁄2=162.8 days), which decays to 238Pu (t1⁄2=87.74 years) and then to 234U (t1⁄2=2.45x105

 years) (another 

naturally-occurring uranium isotope); 17% undergoes electron capture to 242Pu (t1⁄2=3.76x105 years). 

241Am has a high specific activity of 3.428 Ci/g (0.1268 TBq/g), emitting ~7x109

 alpha particles/mg/ 

minute. 243Am has a specific alpha activity about 17 times lower than 241Am and is therefore more 

attractive for chemical investigations of the element (ICRP 1983; Lide 1998; O’Neil 2001; Seaborg 

1991). 
 

 

 

AMERICIUM 104 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-1. Principal Americium Isotopes 

Particle energy 

Isotopea 

CAS 

Registry 

No. 

Decay mode/ 

percent 

(product) 

Decay mode 

energy(MeV) 

Energy 

(MeV) 

Intensity 

(percent) 

Half-life 

(years) 

Specific 

activityb 

(Ci/g) 

Gamma 

energy 

(keV) 

241Am 14596-10-2 

86954-36-1c 

" (23 

9 

7 

3Np) 5.637 5.4431 

5.4857 

5.3884 

Others 

12.8 

85.2 

1.4 

<1 

432.2 3.43 26.34 

33.192 

59.536 

242mAm 13981-54-9 I.T./95.5 

(

242Am) 

0.048 141 10.5 48.63 

" /0.5(23 

9 

8 

3Np) 5.62 5.141 

5.2070 

0.026 

0.4 

86.48 

109.44 

163.04 

242Am 13981-54-9 $-

/83 (24 

9 

2 

6Cm) 0.665 0.63 46 16.02 

hours 

808,000 42.2 

EC/17 (24 

9 

2 

4Pu) 0.750 0.67 37 44.53 

243Am 14993-75-0 " (23 

9 

9 

3Np) 5.438 5.1798 

5.2343 

5.2766 

Others 

1.1 

11 

88 

<1 

7,370 0.199 43.54 

74.67 

86.57 

117.70 

141.97 

a

An m after the atomic mass indicates one of multiple isomers of a given atomic mass. b

LANL 1999 (1 Ci=0.037 TBq) 

c

CAS Registry Number for 241Am3+ ion 

Source: Baum 2002; DOE 1997b; ICRP 1983; LBL 2000; Lide 1998 
AMERICIUM 105 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

The known oxidation states of americium are +2, +3, +4, +5, and +6. However, the stable oxidation 

states are +3 and +4; the common oxidation state is +3, in which state, the behavior of americium and 

other actinides is similar to the lanthanides. The trivalent state is the only state of importance in 

biological systems. The +2 oxidation state is very unstable and has only been produced in solid 

compounds. The stability of the americium oxidation states higher than +3 is less than that of uranium, 

neptunium, and plutonium (Cotton and Wilkinson 1980; Nenot and Stather 1979; Seaborg 1991). Am+3 

hydrolyzes and forms weak complexes with serum proteins and other ligands. The physical and chemical 

properties of americium and selected americium compounds are shown in Table 4-2. Properties of some 

americium ions are shown in Table 4-3. The decay schemes for 241Am and 243Am are shown in 

Tables 4-4 and 4-5. 
 

 

 

 

AMERICIUM 106 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Americium and 

Selected Americium Compounds 

Value 

Property Americium 

Atomic/molecular weighta 243 

Americium(II) oxide 

275 

Americium(III) 

oxide 

534 

Americium(III) 

chloride 

349 

Chemical formula Am AmO2 Am2O3 AmCl3 

Synonyms 

Chemical Abstracts 

Service Registry No. 

No data 

7440-35-9b 

No data 

12005-67-3 

No data 

12254-64-7 

No data 

13464-46-5 

Color Silvery Black Tan Pink 

Physical form Solid metal Cubic crystals Hexagonal 

crystals 

Hexagonal 

crystals 

Odor No data No data No data No data 

Melting point, EC 1,176 >1,000 (decomposes) No data 500 

Boiling point, EC 2,011 Not relevant No data No data 

Autoignition temperature No data Not relevant Not relevant Not relevant 

Solubility: 

 Water 

 Other solvents 

Insoluble 

Soluble in acid 

No data 

Soluble in acid 

No data 

Soluble in acid 

Soluble 

No data 

Density, g/cm3 12 11.68 11.77 5.87 

Partition coefficients No data No data No data No data 

Vapor pressure No data No data No data No data 

Refractive index No data No data No data No data 
 

AMERICIUM 107 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Americium and 

Selected Americium Compounds 

Value 

Property Americium(III) fluoride Americium nitrate Americium citrate 

Atomic/molecular weighta 300 429 432 

Chemical formula AmF3 Am(NO3)3 AmC6H5O7 

Synonyms No data Americium trinitrate No data 

Chemical Abstracts Service 13708-80-0 25933-53-3 11078-88-9 

Registry No. 

Color Pink No data No data 

Physical form Hexagonal crystals No data No data 

Odor No data No data No data 

Melting point, EC 1,393 No data No data 

Boiling point, EC No data No data No data 

Autoignition temperature Not relevant Not relevant Not relevant 

Solubility: 

 Water No data No data No data 

 Other solvents No data No data No data 

Density, g/cm3 9.53 No data No data 

Partition coefficients No data No data No data 

Vapor pressure No data No data No data 

Refractive index No data No data No data 

a

Calculated for 243Am b

This is also a generic CAS Registry Number for americium (unspecified form). 

Source: Chemical Abstract Service 2000; Lide 1994, 1998, 2000 
AMERICIUM 108 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-3. Properties of Some Americium Ions 

Ion Color Stability 

Am3+ Pink or yellow Stable; difficult to oxidize 

Am4+ Color unknown Occurs in solution only as complex 

fluoride and carbonate ions 

AmO2 

+

 Yellow Disproportionates in strong acid; 

reduces fairly rapidly under action of 

own alpha emissions (241Am) at low 

acidification 

AmO2 

2+ Rum colored Easily reduced; reduces fairly rapidly 

under the action of its own alpha 

radiation (241Am) 

Source: Seaborg 1991 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

AMERICIUM 109 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-4. 241Am Decay Schemea 

Nuclide Half-life 

Energies and intensities of emitted radiation 

Alpha (α) Beta (β) max Gamma (γ) 

keV % MeV % keV % 

241Am 

↓

432.2 years 5,485 

5,443 

84.5 

13.0 

13.9 

59.5 

26.3 

42 

35.9 

2.4 

237Np 

↓

2.144x106 

years 

4,788 

4,771 

4,766 

4,639 

4,664 

47 

25 

8 

6.2 

3.3 

13.3 

29.4 

86.5 

8.2 

95.9 

58 

15 

12.4 

9 

2.7 

233Pa 

↓

26.97 days 232 

156 

260 

174 

572 

40 

27.7 

17 

16.4 

4 

13.6 

312.2 

98.4 

94.7 

111.0 

56 

38.6 

17.7 

10.9 

8.2 

233U 

↓

1.592x105 

years 

4,824 

4,784 

84.4 

13.2 

13.0 6.0 

229Th 

↓

7,340 years 4,845 

4,901 

4,815 

5,053 

4,968 

56.2 

10.2 

9.3 

6.6 

6.0 

12.3 

88.5 

85.4 

100.0 

11.1 

79 

24.7 

15.0 

11.3 

8 

225Ra 

↓

14.9 days 331 

371 

69.5 

30.5 

40.0 

12.7 

30.0 

15.2 

225Ac 

↓

10.0 days 5,830 

5,792 

5,791 

5,732 

5,637 

50.7 

18.1 

8.6 

8.0 

4.4 

12.0 

10.6 

20.9 

9.3 

221Fr 

↓

4.9 minutes 6,341 

6,126 

83.4 

15.1 

218.2 

11.4 

11.6 

2.2 

217At ↓ 0.323 seconds 7,066 99.9 258.5 0.056 

213Bi 

97.84% ↓ 2.16% 

45.59 minutes 5,869 1.94 1422 

982 

65.9 

31.0 

440.5 

79.3 

26.1 

2.0 

213Po 

↓

209Tl 

↓

 3.65 microseconds 

2.2 minutes 

8,376 100.0 

660 98.8 

778.8 

1567.1 

465.1 

117.2 

75.0 

10.6 

0.005 

99.8 

96.9 

84.3 

10.7 

9.4 

209Pb ↓ 3.253 hours 0.644 100 

209Bi stable 

a

Minimum intensity 2%, up to five energies, with at least one entry per radiation type (DOE 2003) 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

AMERICIUM 110 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-5. 243Am Decay Schemea 

Nuclide Half-life 

Energies and intensities of emitted radiation 

Alpha (α) Beta (β) max Gamma (γ) 

keV % MeV % keV % 

243Am 

↓

7,370 years 5,275 

5,233 

5,181 

87.4 

11.0 

1.1 

74.7 

13.9 

43.5 

68.2 

21.4 

5.9 

239Np 

↓

2.3565 days 436.5 

330.4 

391.9 

714.1 

45 

40.5 

11 

2.0 

14.3 

106.1 

103.8 

277.6 

99.6 

63 

27.2 

22.5 

14.4 

14.0 

239Pu 

↓

24,110 years 5,157 

5,144 

5,106 

73.3 

15.1 

11.5 

13.6 4.9 

235U 

↓

703,800,000 

years 

4,398 

4,366 

4,215 

4,596 

4,325 

55 

17.0 

5.7 

5.0 

4.4 

185.7 

13.0 

143.8 

93.4 

163.3 

57.2 

36 

11.0 

5.8 

5.1 

231Th 

↓

25.52 hours 288.1 

305.3 

206.0 

287.2 

142.2 

40 

33 

12.8 

12 

2.8 

13.3 

25.6 

84.2 

72 

14.1 

6.6 

231Pa 

↓

32,760 years 5,014 

4,951 

5,028 

5,059 

4,736 

25.4 

22.8 

20.0 

11.0 

8.4 

12.7 

27.4 

300.0 

302.6 

36 

10.3 

2.5 

2.2 

227Ac 

↓

98+% 1.4% 

21.772 years 4,953 0.658 44.8 

35.5 

20.3 

53 

35 

10 

12.0 0.088 

227Th 

↓

223Fr 

↓

18.68 days 6,038 

5,978 

5,757 

5,709 

5,713 

24.2 

23.5 

20.4 

8.3 

4.9 

12.3 

236.0 

50.1 

256.2 

329.8 

40 

12.9 

8.4 

7.0 

2.9 

22.00 minutes 1,099.,0 

1,069.4 

914.3 

70 

15.0 

10.1 

50.1 

12.3 

79.7 

234.8 

49.8 

34 

30 

8.7 

3.0 

2.8 

223Ra 

↓

11.43 days 5,716 

5,607 

5,747 

5,540 

5,434 

51.6 

25.2 

9.0 

9.0 

2.2 

83.8 

11.7 

81.1 

269.5 

94.9 

25.4 

25 

15.3 

13.9 

11.5 
 

 

 

 

 

 

 

 

 

 

 

AMERICIUM 111 

4. CHEMICAL, PHYSICAL, AND RADIOLOGICAL INFORMATION 

Table 4-5. 243Am Decay Schemea 

Nuclide Half-life 

Energies and intensities of emitted radiation 

Alpha (α) Beta (β) max Gamma (γ) 

keV % MeV % keV % 

219Rn 

↓

3.96 seconds 6,819 

6,553 

6,425 

79.4 

12.9 

7.5 

271.2 

401.8 

10.8 

6.6 

215Po ↓ 1.781 milli- 7,386 100.0 

seconds 

211Pb 36.1 minutes 1379 91.3 404.9 3.8 

↓ 547 6.3 832.0 3.5 

211Bi 

↓

2.14 minutes 6,623 

6,278 

83.5 

16.2 

351.1 12.9 

207Tl ↓ 4.77 minutes 1427 99.7 897.8 0.26 

207Pb stable 

a Minimum intensity 2%, up to five energies, with at least one entry per radiation type (DOE 2003) 

AMERICIUM 113 

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

5.1 PRODUCTION 

Americium does not occur in nature. Although the amount of 241Am produced is believed to be several 

kilograms a year, the only isotope produced for commercial use is 241Am. No production figures were 

available in the published literature. The amount of 243Am available ranges from 10 to 100 g (Seaborg 

and Loveland 1990). 

241Am and 243Am can be made from 239U or 239Pu by neutron activation involving an operating nuclear 

reactor or nuclear bomb detonation. In this process, neutron activation of 238U can produce uranium 

isotopes up to at least 241U, and each of these beta decays to a neptunium isotope of the same mass. 

Neutron activation of neptunium can produce isotopes starting with 239Np up through at least 244Np, and 

each of these isotopes beta decays to a plutonium isotope of the same mass. Neutron activation of 

plutonium isotopes starting with 239Pu can produce isotopes through at least 246Pu, and of these, 241Pu, 

243Pu, 245Pu, and 246Pu beta decay to americium isotopes of the same mass. 241Am can be produced more 

directly through alpha bombardment of 238U to 241Pu (238U [α,n] 241Pu), and its subsequent beta decay. 

Each of these americium isotopes can also be neutron activated to isotopes up through at least 246Am. The 

amount of any product is a function of the starting mass of either 238U or 239Pu and the neutron fluence 

over the activation period balanced by the natural radioactive decay of the isotopes being formed. For 

example, an atom of 239Pu will naturally decay to 235U, unless it is first neutron activated to 240Pu. 240Pu 

will alpha decay to 236U, unless first activated to 241Pu. 241Pu will beta decay to 241Am, unless first neutron 

activated to 242Pu. These processes can be managed through focused radiochemical separation or by the 

addition of special processing (proton bombardment) to help direct the effort toward a particular isotopic 

product (Parrington et al. 1996). In general, lower mass isotopes are preferentially produced in the 

relatively low fluxes available inside nuclear reactors, while higher masses are more feasibly produced in 

extreme flux conditions present inside a nuclear detonation. These processes are summarized in 

Figure 5-1. 

The relative activities of americium isotopes for a typical pressurized-water reactor (PWR) fuel assembly 

are 1,500, 7.2, and 20 Ci (56, 0.27, and 0.74 TBq) for 241Am, 242Am, and 243Am, respectively (DOE 
AMERICIUM 114 

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

Figure 5-1. Production Table for 241Am 

Americium 

Plutonium 

Neptunium 

Uranium 

241Am 242Am 243Am 244Am 245Am 246Am 

239Pu 240Pu 241Pu 242Pu 243Pu 244Pu 245Pu 246Pu 

237Np 238Np 239Np 240Np 241Np 242Np 243Np 244Np 

235U 236U 237U 238U 239U 240U 242U 

238Pu 237Pu 

Legend: Neutron activation (n,ƒÁ) reaction more significant to Am-241,243 formation 

Neutron activation (n,ƒÁ) reaction less significant to Am-241,243 formation 

Neutron activation (n, 2n reaction)
 

Beta decay (significant to Am-241,243 formation)
 

Alpha decay
 

*developed from Parrington et al. (1996) 
 

 

 

 

AMERICIUM 115 

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

2002a). The respective activity ratios for a typical boiling water reactor (BWR) are 370, 2.1, and 4.8 Ci 

(14, 0.078, and 0.18 TBq). There are 78 PWRs and 40 BWRs in the United States, several of which have 

ceased operation. Total projected inventories of these three radionuclides for all reactors are 2.2x108

, 

1.6x106

, and 1.9x106 Ci (8.1x106, 5.9x104, and 7.0x104 TBq), respectively. The post-irradiation 

americium content of typical PWR and BWR fuel assemblies are 600 g (0.09%) and 220 g (0.07%), 

respectively. 

The ratio of plutonium isotopes to 241Am is often reported in monitoring studies as it is an important tool 

in dose assessment by enabling a determination of plutonium concentrations. 243Am is produced directly 

by the capture of two neutrons by 241Am. The parent of 241Am is 241Pu, which constitutes about 12% of 

the 1% content of a typical spent fuel rod from a nuclear reactor, and has a half-life of 14.4 years. 

Separation of 241Am from its parent, 241Pu, and the other isotopes present can be effected by precipitation, 

ion exchange, or solvent extraction. 

Americium metal has been obtained by heating americium oxide, Am2O3, with lanthanum at 1,200 EC; 

americium, which is more volatile than other actinides, volatilizes and can readily be separated from other 

actinides. AmO2 can be obtained by igniting most trivalent americium compounds (Budavari 1996; 

Cotton and Wilkinson 1980; UIC 1997). 

5.2 IMPORT/EXPORT 

No U.S. import or export information is available for americium. 

5.3 USE 

241Am has a long half-life and a predominant gamma ray energy of 59.5 keV, which makes it useful for a 

wide range of industrial gauging applications and for diagnosing certain thyroid disorders (Seaborg 1991). 

The most common application of americium is in ionization smoke detectors, and most of the several 

kilograms of americium produced each year are used for this purpose. Smoke detectors today typically 

contain approximately 1 μCi (37 kBq) of 241Am (EPA 2004b). One gram of americium dioxide, AmO2, 

provides enough active material for more than 5,000 smoke detectors. In the 1980s, annual sales of 

smoke detectors approached 12 million units. A mixture of 241Am and beryllium known as 241Am-Be is 

used as a neutron source in non-destructive testing of machinery and equipment, and as a thickness gauge 
 

AMERICIUM 116 

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

in the glass industry (UIC 1997). 241Am is used worldwide to measure the rate of production by oil wells 

(Seaborg 1991). No commercial uses for other americium isotopes were found. However, 243Am can be 

used as a target material for the production of transcurium elements in high neutron flux reactors 

(Budavari 1996). 243Am is also the preferred isotope for investigating the chemical properties of 

americium, because its lower specific activity and gamma emissions relative to 241Am, which produce a 

lower radiation field for researchers and a lower radiation dose to experimental animals. 

5.4 DISPOSAL 

Radioactive wastes are categorized according to their origin, the type of waste present, and their level of 

activity. The first distinction is between defense waste and commercial waste. The former was generated 

during and after World War II, principally at DOE’s facilities at Hanford, Washington; Savannah River, 

South Carolina; and Idaho Falls, Idaho where plutonium and other isotopes were separated from 

production reactor or nuclear-powered naval vessel spent fuel. Commercial waste is produced by nuclear 

power plants, except for the long defunct commercial reprocessing facility at West Valley, New York. 

Nuclear waste is classified as transuranic waste (TRU), high-level waste (HLW), spent nuclear fuel 

(SNF), uranium and thorium mill tailings (UMT), and low-level waste (LLW). LLW is further 

differentiated into four classes, A, B, C, and greater than class C, according to increasing level of activity 

(listed in Tables 1 and 2 of 10 CFR 61.55 for long and short half-life radionuclides, respectively), with 

specific disposal requirements (USNRC 2004a). SNF, HLW, TRU, and greater than class C (GTCC) 

waste are not generally suitable for near-surface disposal (EPA 2004d). Class C waste would include 

much of the operating and decommissioning waste from nuclear power plants, typical radioactive material 

licensee facilities, and sealed radioisotope sources. LLW (less GTCC) is currently accepted at three sites 

(Barnwell, South Carolina; Envirocare, Utah; and Richland, Washington). Defense TRU is currently 

being buried at the Waste Isolation Pilot Plant (WIPP) 2,150 feet below ground in a geologically inactive 

salt deposit near Carlsbad, New Mexico (EPA 2004e). GTCC, HLW, and SNF are destined for disposal 

at a HLW site, which is likely to be at Yucca Mountain, Nevada (USNRC 2004b). Yucca’s 25-foot 

diameter main access tunnel and test disposal drifts have been bored, and research is underway to test and 

reduce uncertainties associated with various modeling parameters used to provide assurance that isolation 

of the waste from the biosphere for 10,000 years will be feasible (DOE 2004). If LLW also contains 

hazardous material (i.e., toxic, corrosive, inflammable, or oxidizing), it is termed low level mixed waste 

(LLMW). EPA is considering the feasibility of disposing of some LLMW in RCRA-C landfills, and the 

EPA public comment period ended in April, 2004. Large volumes of mixed chemical and radioactive 
AMERICIUM 117 

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

liquid waste at the Hanford Reservation are slated for disposal at the future HLW repository; however, 

Hanford is considering managing the waste in a way that destroys the volatile organics and PCBs, 

separating the resulting waste into low and high level component streams, vitrifying each, disposing of 

the low activity waste on site in a virtual LLW facility, and holding the vitrified HLW until Yucca or the 

selected facility opens. UMT waste does not concern americium (DOE 1999a; Murray 1994). 

TRU contains radionuclides, like 241Am and 243Am, which follow uranium in the periodic table and have 

half-lives >20 years. If its level of activity is less than 100 nanocuries (nCi) (3.7 kBq) of alpha-emitters 

per gram of waste material (up from 10 nCi/g in 1982), the waste can be disposed of by shallow burial. 

Wastes with TRU concentrations >100 nCi/g go to WIPP. TRU generally has low levels of radioactivity, 

generates very little heat, contains volatile organics, and is grouped as contact handled (CH) with surface 

radiation levels not exceeding 200 mrem per hour, or remote handled (RH) waste with surface levels 

above 200 but not exceeding 1,000 mrem per hour (EPA 2004d). 

HLW includes spent fuel that is contained in fuel rods that have been used in a nuclear reactor and fuel 

reprocessing liquids, concentrates, and solids. These fuel rods will contain some level of transuranic 

elements. After removal, these rods are placed in 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 radioactivity and 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 USNRC has issued standards 

for the disposal of HLW (10 CFR 61), and the DOE is pursuing the establishment of an HLW facility. 

Efforts to establish an HLW facility, which began over 2 decades ago, have experienced many delays. 

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 underground tunnel system and several of its 

operational facilities have been completed through 2004. The facility is projected to begin operation 

(accept HLW) in 2010, and efforts are underway to consider establishing a nearby interim storage facility 

should that date need to be extended beyond the capacity of utilities to provide onsite storage of their SNF 

(DOE 2002b, 2004). 

LLW is officially defined as radioactive waste other than those previously defined. These wastes come 

from reactors and institutions such as hospitals, universities, and research centers. Most LLW contains 

very little or low concentrations of primarily short-lived radioactivity and essentially no transuranic 

elements. It requires little or no shielding or special handling, and may be disposed of by shallow burial. 
AMERICIUM 118 

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

However, some LLW contains sufficient quantities of radioactivity as to require special treatment. 

USNRC regulations for LLW disposal (10 CFR 61) permit shallow land burial, and the three states with 

licensed LLW disposal facilities (South Carolin, Utah, and Washington), as USNRC agreement states, 

have enacted more stringent regulations (Eisenbud 1987; Murray 1994; USNRC 2004c). The EPA is 

developing cleanup regulations as well as general environmental standards for LLW disposal that would 

apply to DOE facilities (EPA 2001d). The standards will facilitate planning and reduce costs for cleanup 

and disposal. There are currently 23 DOE and commercial LLW disposal sites in the United States (EPA 

2001d). While some LLW facilities are closed, they are continuously monitored to detect releases of 

radioactivity into the environment. The Manifest Information Management System (MIMS), maintained 

by the Idaho National Environmental and Engineering Laboratory (INEEL), contains information on lowlevel radioactive waste shipments received at commercial low-level radioactive waste disposal facilities at 

Barnwell, South Carolina (January 1, 1986–present); Beaty, Nevada (April 1, 1986–December 31, 1992); 

Richland, Washington (January 1, 1986–present); and Envirocare, Utah (January 1, 1998–December 31, 

1999). In 1999, 3.67 Ci (136 GBq) of 241Am and <0.01 Ci (<0.4 GBq) of 243Am LLW was received at 

these facilities from academic, industrial, government, and utility generators throughout the United States 

(INEEL 2000). 

The USNRC and EPA each have responsibilities for regulating the cleanup of radioactivity and 

decommissioning of USNRC licensed sites. USNRC and EPA reached an agreement in 2002, in response 

to Congressional mandate, to preclude double regulation of these efforts. The agreement provides that 

EPA will defer exercise of authority under Comprehensive Environmental Response, Compensation, and 

Liability Act (CERCLA) for the majority of facilities decommissioned under USNRC authority. It also 

contains provisions for joint consultation when certain EPA parameters are exceeded, including 

groundwater exceeding EPA-permitted levels, USNRC contemplation of restricted release or alternate 

release criteria, and residual soil radioactivity concentrations exceeding those in the agreement (USNRC 

2002). 

At present, DOE stores most of its spent fuel and HLW at three primary locations: the Hanford site in 

Washington, the INEEL in Idaho, and the Savannah River Site in South Carolina, representing 86% of the 

volume and 98% of the metal mass. Some HLW/SNF is also stored at Oak Ridge National Laboratory in 

Tennessee, the West Valley site in New York, and the dry storage facility at Fort St. Vrain in Colorado 

(DOE 2002c). 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 1999a). The DOE National 

Spent Fuel Program maintains a spent nuclear fuel database that lists the total volume, mass, and metric 
AMERICIUM 119 

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

tons of heavy metal (MTHM) of 16 DOE categories of spent nuclear fuel stored in each of the three 

locations. The categories having the highest 241Am activities per spent nuclear fuel canister (decayed to 

2030) are ‘uranium metal’, ‘mixed oxides’, and ‘plutonium/uranium carbide, nongraphite’. The 241Am 

solid waste stored on the Hanford site in 1998 included 2.3 Ci (85 GBq) as LLW and 11 Ci (410 GBq) as 

TRU (Hanford 1999). Between 1945 and 1970, the Farallon Islands Nuclear Waste Dump Site 

(FINWDS), approximately 30 miles west of San Francisco, received at least 500 TBq (14,000 Ci) of 

reportedly low-level nuclear waste, concrete-encapsulated in at least 47,500 55-gallon, 16-gauge steel 

drums (life-expectancy ~30 years in sea water) (Suchanek et al. 1996). These were deposited at three 

sites 100, 900, and 1,800 m deep. 

According to EPA (2004a), smoke detectors (with the batteries removed) can be disposed of in the trash. 

However, EPA also notes that state and local practices for the safe disposal of smoke detectors vary. 

Some state radiation control programs conduct annual collection programs for smoke detectors, while 

other state and local governments recommend that the smoke detector be returned to the supplier (EPA 

2004b). 

 

 

AMERICIUM 121 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.1 OVERVIEW 

Americium has been identified in at least 8 of the 1,636 hazardous waste sites that have been proposed for 

inclusion on the EPA National Priorities List (NPL) (HazDat 2004). However, the number of sites 

evaluated for americium is not known. The frequency of these sites can be seen in Figure 6-1. Of these 

sites, all are located within the United States. 

Americium is a human-made element. In the environment, 241Am is present as a result of basically three 

sources: fallout from nuclear explosions, releases from nuclear reactors and reprocessing plants, and 

production and disposal of smoke detectors by producers and consumers. The majority of the americium 

present in the environment was the result of atmospheric nuclear weapons testing during the 1950s and 

1960s (EPA 2004c). Additionally, there are accidental releases such as the Chernobyl accident, the burnup of a satellite powered by the aerospace reactor SNAP 9A, and the crash of a B-52 aircraft carrying 

nuclear weapons in Thule, Greenland. Today, 241Am along with 90Sr, 137Cs, 238Pu, 239Pu, and 240Pu, are the 

isotopes that produce the majority of radiation associated with nuclear fallout (DOE 1997a). Low levels 

of 241Am may be found in environmental media worldwide from atmospheric nuclear weapons tests; these 

levels are referred to as fallout background levels. In nuclear reactors, 241Am has been detected in 

primary coolant water, stack aerosols, and waste water (Rosner et al. 1978). Because 241Am is produced 

from the decay of 241Pu (half-life=14.4 years), releases of 241Pu will result in an ingrowth of 241Am; 

clearly, releases of 241Pu and 241Am must be considered collectively. The maximum quantity of 241Am 

following an accidental release of 241Pu occurs in 70–80 years following the production of the 241Pu (EPA 

1976). Consequently, the impact of 241Am from atmospheric nuclear weapons testing will reach its peak 

in about the year 2035 and then, based on this model, levels will decline according to its combined rate of 

formation and decay. It should be noted that when the 241Am level reaches its peak, there will still be 

241Pu remaining. 241Am is used commercially as an ionization source in smoke detectors and it may be 

released into the environment from its production, use, and disposal. 241Am is the only americium isotope 

that is used commercially. 

Americium released to the atmosphere will be associated with particulate matter and will be deposited on 

land or surface water by dry or wet deposition (Essien et al. 1985). Dry deposition results from 
AMERICIUM 122 

6. POTENTIAL FOR HUMAN EXPOSURE 

Figure 6-1. Frequency of NPL Sites with Americium Contamination 

Frequency of 

NPL Sites 

<= 1 

1 - 2 

Derived from HazDat 2004 
AMERICIUM 123 

6. POTENTIAL FOR HUMAN EXPOSURE 

gravitational settling and impaction on surfaces. Wet deposition returns americium to earth in 

precipitation. Radionuclides resulting from atmospheric weapons tests are often injected into the lower 

stratosphere, while other atmospheric releases are into the troposphere. The residence time of particles in 

the atmosphere will depend on their aerodynamic size, as well as the altitude, latitude, season, and 

hemisphere because of atmospheric circulatory patterns. For example, residence half-times of particles in 

the lower stratosphere range from 3 to 12 months in polar regions and from 8 to 24 months in equatorial 

regions, with removal being highest in the spring and lowest in the fall. Half-times for particles in the 

troposphere are about 1 month. Larger particles will remain in the atmosphere for shorter periods of time 

and are deposited closer to their emission source, while smaller particles remain in the air for longer 

periods of time and are deposited farther from their source. In the absence of actual measurements, the 

deposition of 241Am in a region can be estimated by using the relationship between air concentration and 

deposition quantities for other isotopes that are attached to particulate matter in air. Using this 

methodology, the annual deposition of 241Am in New York was estimated to have reached a maximum of 

0.010 mCi/km2

 (0.37 MBq/km2) in 1964 (Bennett 1979). The cumulative 241Am deposition in the 

year 2000 is estimated to be 0.058 mCi/km2 (2.1 MBq/km2

). If the ingrowth from 241Pu decay is included, 

the cumulative 241Am deposited by the year 2000 would be 0.80 mCi/km2

 (30 MBq/km2). Americium 

may also be injected into the atmosphere from water surfaces by the action of bubbles scavenging the 

water column and wave action (McKay et al. 1994; Walker et al. 1986). Similarly, 241Am-contaminated 

soil may be released into air by wind action. 

Americium released to water in effluent, runoff, or atmospheric deposition adsorbs to particulate matter 

and is rapidly depleted from the water column and deposited in surface sediment (Murray and Avogadro 

1979). Adsorption is very high with distribution coefficients between the particulate-associated phase and 

the dissolved phase in sediment and water of the order of 105

–106 (Davis et al. 1997; NRC 1981; 

Pattenden and McKay 1994). Aquatic organisms can bioaccumulate americium via intake from the water 

or ingestion of sediment or organisms lower on the food scale. In crustacean zooplankton, crustaceans, 

and molluscs, americium is accumulated from water by passive absorption onto exoskeletons (Fisher et al. 

1983). Ingested in suspended diatoms or other food, americium largely passes through the gut and is 

eliminated. Biogenic debris from these animals, such as fecal pellets and discarded molts, facilitates 

vertical transport of 241Am into the depths and sediment. 

If land deposition occurs, americium will sorb to the soil, leach into the subsurface soil, and redistribute 

by the action of wind, water, or biotic transport. Small mammals inhabiting areas containing radioactive 

contamination or radioactive waste sites may become contaminated with americium by consuming 
 

AMERICIUM 124 

6. POTENTIAL FOR HUMAN EXPOSURE 

contaminated soil or plants and disturb 241Am-contaminated soil through their burrowing and excavating 

activities. In addition, small mammals may be consumed by animals higher in the food chain such as 

hawks and coyotes, which would add to the dispersal of americium from disposal areas. Since fallout 

241Am is accompanied by its precursor, 241Pu, which also leaches into the ground, the amount of 241Am at 

a depth is a function of the leaching of both the americium and plutonium as well as the decay of these 

isotopes. Fallout 241Am is predominantly retained to the upper few centimeters of soil where it is 

associated with organic matter and bound to manganese and iron oxides (Bennett 1976; Bunzl et al. 1995; 

Vyas and Mistry 1980). However, transuranic radionuclides, including americium, have been found to 

migrate in groundwater, and have traveled underground from 80 to over 3,000 meters at several national 

laboratories. Colloidal materials can be mobile in groundwater systems for great distances and are 

capable of binding and transporting radionuclide contaminants, including americium, in subsurface 

systems (McCarthy et al. 1998a, 1998b; Penrose et al. 1990). 

Americium may be taken up from the soil by plants and translocated to other parts of the plants. 241Amcontaminated dust may also be deposited on the above-ground parts of the plant. Uptake of 241Am from 

soil is low (Bennett 1979; EPA 1979; Nisbet and Shaw 1994; Romney et al. 1981; Schultz et al. 1976; 

Zach 1985). Uptake from soil is a function of the chemical species, soil chemistry, plant species, and 

environmental conditions. Concentration ratios of 241Am in plants to that in soil range over about 2 orders 

of magnitude depending on crop and soil type. Uptake is higher under acidic conditions and lower in soil 

with high fractions of organic matter that play an important role in complexing americium, making it less 

available for uptake. Translocation of transuranic elements taken up through the roots into seeds and fruit 

is generally very low (Bennett 1979; Schreckhise and Cline 1980). Concentration ratios in seed, grain, 

and fruit range from 10-6 to 10-4, about a factor of 10 lower than in foliage. Animals can accumulate 

americium by eating contaminated plants as well as by ingesting soil or other animals and by breathing 

air. Biological uptake in aquatic organisms may depend on factors such as temperature, time after intake, 

season of the year, and water quality. The bioconcentration of 241Am in fish is low, especially to the 

edible parts of the fish (DOE 1996). In a study performed in a nuclear waste pond where the levels of 

241Am were about 3 orders of magnitude above background levels, concentrations in fish filet were rarely 

>10 times that of controls (Emery et al. 1981). In marine organisms consumed by humans, uptake is 

generally highest in mussels where the target organs are mainly the digestive gland, gill, and exoskeleton 

(Chassard-Bouchaud 1996; Fisher et al. 1996; Hamilton and Clifton 1980). Transfer coefficients have 

been reported for many of these processes. Available evidence suggests that americium is not 

biomagnified up the food chain to humans (Bulman 1978; Jaakkola et al. 1977). More recent reports on 

the biomagnification of americium have not been located. 
 

 

AMERICIUM 125 

6. POTENTIAL FOR HUMAN EXPOSURE 

Exposures of the general population to 241Am via air, water, soil, and food are generally very low; these 

‘background’ levels are a result of fallout from past atmospheric nuclear weapons tests. Since 1973, 

241Am air concentrations have been <10-18 Ci/m3

 (0.037 μBq/m3) and are continuing to decline (Bennett 

1979). The United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) (2000) 

reported that deposition and air concentrations of radionuclides from fallout dropped rapidly once 

atmospheric testing ceased in 1980. Inhalation exposures for even long-lived transuranic radionuclides 

became insignificant after 1985. Levels around nuclear power plants are indistinguishable from fallout 

background (EPRI 1981). 241Am levels in surface seawater of the North Sea and North Atlantic Ocean 

stayed around 10 Bq/m3

 (270 pCi/m3) between 1976 and 1988 (Pattenden and McKay 1994), but may be 

considerably higher near discharges from nuclear facilities. 241Am in soil resulting from cumulative 

deposition and ingrowth in the New York region should reach a maximum of 0.88 mCi/km2 

(33 MBq/km2

) in the year 2035. In the FDA Total Diet Studies in 1983–1986 and 1987–1992, the 

concentrations of radionuclides were sufficiently low as to require no specific action or simple 

monitoring. 

The general population may be exposed to elevated levels of 241Am from nuclear accidents or from 

residing in areas in the proximity of hazardous waste sites where this radionuclide is present. Exposure is 

generally through the inhalation and ingestion of dust from these sites. Workers involved in producing 

ionization smoke detectors or other devices containing 241Am, workers at nuclear reactors or Department 

of Energy (DOE) facilities, and workers who use americium-containing devices (neutron backscatter 

sources for checking roof leaks and road undermining, and well logging equipment) may also be exposed 

to higher levels of 241Am. In the environment and most occupational situations, americium is usually 

encountered in combination with plutonium and curium; exposure to americium alone is unlikely. 

Elevated levels of 241Am have been identified in at least 8 of the 1,636 current or former EPA NPL 

hazardous waste sites (HazDat 2004). However, the number of sites evaluated for americium is not 

known. The distribution of these sites within the United States is shown in Figure 6-1. 

6.2 RELEASES TO THE ENVIRONMENT 

Throughout this chapter, the units used to express concentration or intake of 241Am are the same units 

reported by the authors, which may be followed by converted units in parenthesis. Concentrations of 

241Am are generally expressed in terms of activity, either in the conventional unit, the curie (Ci) or the SI 
AMERICIUM 126 

6. POTENTIAL FOR HUMAN EXPOSURE 

unit, the becquerel (Bq), where 1 Ci=3.7x1010 Bq=0.037 TBq or 1 Bq=2.7x10-11 Ci=27 pCi. Activities 

may be converted into mass units using the specific activity, 3.43 Ci/g. It should be remembered that 

since 241Pu (half-life=14.4 years) decays into 241Am, over time, inventories of 241Am will be augmented by 

releases of 241Pu. The ratio of americium to plutonium isotopes is often used to characterize the nature of 

a radionuclide source. 

6.2.1 Air 

241Am has been detected in air at 3 of the 1,636 current or former NPL hazardous waste sites where it was 

detected in some environmental media (HazDat 2004). 

241Am is released into the atmosphere primarily by nuclear reactor operations, nuclear accidents, and 

nuclear weapons testing, but previous releases from plutonium production reactors have ended since they 

are no longer operational. The 241Am released is augmented by the decay of 241Pu released during these 

events. The amount of 241Am released is often estimated by the amount deposited on earth. In 1982, 

UNSCEAR estimated that the integrated deposition density of 241Am in the north temperate zone of the 

earth was 25 Bq/m2 (0.68 nCi/m2

) (Suchanek et al. 1996). Since then, the effective deposition of 241Am 

has grown by 1 Bq/m2

 (0.03 nCi/m2) per year because of the radioactive decay of 730 Bq/m2 (20 nCi/m2) 

of deposited 241Pu (to approximately 45 Bq/m2 [1.2 nCi/m2

]). 

In atmospheric nuclear weapons tests, radionuclides are often injected into the stratosphere. The amount 

of 241Am present in the atmosphere from nuclear weapons testing depends on the amount of unfissioned 

241Am and 241Pu, as well as lower isotopes of plutonium neutron activated to 241Pu during detonation and 

injected into the atmosphere, and the transport and residence time of both 241Am and its precursor in the 

various atmospheric compartments (e.g., stratosphere and troposphere). For a particular weapon’s test, 

this will depend on such factors as the amount of plutonium and americium in the weapon, detonation 

yield, altitude and latitude of the detonation, and season. High-yield U.S. tests were characterized by very 

high ratios of 241Pu/239,240Pu, and these would produce relatively large quantities of 241Am (Roos et al. 

1994). At this time, the legacy of past atmosphere nuclear weapons tests is a fairly uniform low level 

radiation background. The peak global activity of 241Am resulting from nuclear weapons testing between 

1951 and 1978 and receiving global distribution is estimated to be 130 kCi (4,800 TBq), taking into 

account the simultaneous production of 241Am from 241Pu and its decay (Bennett 1979). At the same 

time, it should be realized that the detonation of uranium bombs can produce some americium. 
 

AMERICIUM 127 

6. POTENTIAL FOR HUMAN EXPOSURE 

The reactor accident at Chernobyl in April 1986 released radionuclides into the atmosphere, mostly 

between April 26 and May 6. Estimates of quantities released are based on observations of deposition 

within 30 km of the reactor. Releases in this area were predominantly highly irradiated fuel particles. It 

is estimated that the discharge of 241Pu through May 6, 1986 was 5,200 TBq (140 kCi), which amounted 

to 3% of the reactor content of this radionuclide (Askbrant et al. 1996; Pattenden and McKay 1994). The 

material was released mainly in the lower troposphere. 

Subsequent to the primary events releasing radionuclides into the atmosphere, radionuclides can enter the 

atmosphere from resuspension of soil particles and forest fires (Lujaniene et al. 1999). Resuspension 

studies performed with 241Am indicate that the activity to mass ratio is greatest for particles <45 μm in 

diameter (Cooper et al. 1994). Therefore, the fine, resuspended soil released into the air would have a 

higher concentration of 241Am than the remaining surface soil. This enhancement factor for resuspended 

soil in the inhalable fraction (<7 μm) ranged from 5.4 to 32.5 at six sites at Taranaki, a weapons testing 

range at Maralinga, South Australia (Cooper et al. 1994). Another potential source of release is from 

windblown soil from LLW disposal sites. While low-level radioactive waste is required to be buried in a 

manner protective of near-term release, biotic transport by plants and small mammals may transport 

americium to the soil surface where it is accessible to wind. In order to predict the impact of biotic 

transport, a model was applied to six composite waste streams containing isotopic concentrations for the 

western United States prepared by the USNRC to which current and past LLW disposal conditions 

applied. The containers and wastes were assumed to decompose with a 35-year half-life and active biotic 

transport was assumed to occur for 100 years following site closure and before institutional control of the 

site was lost. After 100 years, the activity at the soil surface (assumed to be uniformly mixed in the upper 

0.5 m of the entire burial ground) was estimated to be 8.7x103

 and 2.8x105 pCi/m2 (0.32 and 10 kBq/m2) 

for 243Am and 241Am, respectively (Kennedy et al. 1985). 

241Am is released to the atmosphere at DOE facilities. Air sampling data were used to estimate effluent 

release from the Savannah River Site (SRS) from the plant’s start-up in 1954 through 1989 (DOE 1991a). 

From this monitoring, it was estimated that 5.49 mCi (200 MBq) of 241Am was released to the atmosphere 

between 1977 and 1989. The SRS was a major U.S. nuclear production facility and included five nuclear 

reactors, a fuel and target fabrication plant, a naval fuel materials facility, two chemical separation plants, 

a heavy water production plant, and a laboratory. Between 1977 and 1996, the total reported release from 

the SRS of 241Am to the atmosphere was 0.0061 Ci (230 MBq). Prior to 1977, no specific anaylsis for 

241Am was done (DOE 1998). In 1999, the total reported releases to atmosphere from the SRS were 
 

 

AMERICIUM 128 

6. POTENTIAL FOR HUMAN EXPOSURE 

3.86x10-5 and 4.28x10-6 Ci (1.43 and 0.158 MBq) for 241Am and 243Am, respectively (DOE 1999b). 

241Am has been identified in air at the Hanford Site, Washington; Idaho National Engineering and 

Environmental Laboratory (INEEL), Idaho; and Los Alamos National Laboratory, New Mexico. A 

maximum concentration of 13 MBq/L (350 μCi/L) was measured in 1991 in air at a point source (stack) 

at Hanford (HazDat 2004). In 1994, atmospheric discharges of 241Am from four areas at the Hanford Site 

ranged from 0.067 to 66 μCi (2.5–2,400 kBq) (PNL 2000). 

6.2.2 Water 

241Am has been detected in surface water samples at 2 and in groundwater at 1 of 1,636 NPL hazardous 

waste sites where americium has been identified in some environmental component (HazDat 2004). 

Americium is released into surface water primarily from plutonium production reactors, nuclear fuel 

reprocessing facilities, or nuclear accidents. It may also be released from radioactive waste storage 

facilities. Since 241Pu decays into 241Am, 241Am is also released as a result of 241Pu releases. Water 

sampling data were used to estimate effluent releases from the SRS from the plant’s startup in 

1954 through 1989 (DOE 1991a). From this monitoring, it was estimated that 290 mCi (11 GBq) of 

241Am was released into seepage basins between 1977 and 1989; however, no 241Am was released directly 

into streams. In 1999, 1.34x10-5Ci (0.496 MBq) of 241Am was released from the SRS into surface waters 

(DOE 1999b). 

Radionuclides have been released since 1952 at Sellafield, United Kingdom on the Irish Sea by the 

British Nuclear Fuels Limited (BNFL) reprocessing plant and, before that, by two plutonium-producing 

nuclear reactors. In 1988, the estimated environmental inventory of 241Am from all previous operations 

totaled 859 TBq (23.2 kCi), consisting of 537 TBq (14.5 kCi) actually released plus 322 TBq (8.7 kCi) 

produced from the decay of 241Pu that was also released. Annual discharges of 241Am from Sellafield 

ranged from 4.5 to 120 TBq/year (120–3,200 Ci/year) between 1964 and 1989, while those for 241Pu 

ranged from 1 to 2,800 TBq/year (27–76,000 Ci/year) between 1952 and 1989; maximum annual 

discharges occurred in 1973 for 241Pu and 1974 for 241Am (Pattenden and McKay 1994). The annual 

liquid effluent discharges from a typical U.K. Magnox Station contained 34.3–121 Bq/L (0.926– 

3.27 nCi/L) of 241Am for the years 1991–1995 (Ware et al. 1998). These discharges are from the final 

monitoring and delay tank. (Magnox, an alloy of magnesium oxide and aluminum, has been used as a 

protective covering or cladding material for fuel elements in British nuclear reactors. The name 
AMERICIUM 129 

6. POTENTIAL FOR HUMAN EXPOSURE 

"Magnox" is widely used to refer to the early gas cooled because it provides a simple way to uniquely 

identify the group.) 

241Am was identified in surface water at Oak Ridge, Tennessee and Paducah Gaseous Diffusion Plant, 

Kentucky, as well as in groundwater as an unspecified form at the Hanford, Washington and Rocky Flats, 

Colorado NPL sites (HazDat 2004). The distribution of NPL sites is shown in Figure 6-1. 

6.2.3 Soil 

241Am was detected in soil and sediment at 5 and 2 of the 1,636 NPL hazardous waste sites, respectively, 

where it was detected in some environmental media (HazDat 2004). 

As a manufactured element, americium is not naturally present in the environment. Contamination of the 

soil can occur either from deposition of americium or precursor plutonium originally discharged into the 

atmosphere, or from waste products discharged directly into or on the ground. Except for the reentry into 

the atmosphere of the SNAP 9A satellite and the French atmospheric tests in the Mururoa Atoll between 

1966 and 1974 that occurred in the southern hemisphere, the main events resulting in the deposition of 

artificial radionuclides occurred in the northern hemisphere. As a consequence, there is a progressive 

decline in the levels of artificial radioactivity from northern to southern latitudes. Recent studies of the 

multi-isotopic radioactive content in ice layers in Antarctica have determined that 0.21 Bq/m2 

(5.7 pCi/m2

) of 241Am was deposited in fallout between 1969 and 1993 (Baeza et al. 1999). Therefore, the 

mean annual fallout in Antarctica is about 8.3 mBq/m2

 (0.22 pCi/m2). 

The USNRC has projected the activities and volumes of low level radioactive waste from all sources 

buried at commercial nuclear waste burial sites to the year 2000 using information from the INEEL waste 

retrieval project and assuming that the waste disposal practices then used would continue into the future. 

The estimated 20-year decayed 241Am and 243Am concentrations were 380 and 230 pCi/m3

 (14 and 

8.5 Bq/m3

), respectively (Kennedy et al. 1985). 

The largest releases of 241Am to soil in the United States occur at DOE facilities. The 241Am inventory in 

surface soil at the Nevada Test Site (NTS) estimated as part of the DOE’s Radionuclide Inventory and 

Distribution Program between 1981 and 1986 was 150 Ci (5,600 GBq) (DOE 1991b). The highest 

concentration of 241Am was found in the Yucca Flats area. The United States began testing nuclear 
 

AMERICIUM 130 

6. POTENTIAL FOR HUMAN EXPOSURE 

weapons at the NTS in January 1951. Since then, the NTS has become the primary site for testing nuclear 

weapons and studying the effect of these weapons on structures and military equipment; >600 nuclear 

explosions have taken place at this site. At Rocky Flats, 241Am contamination in soil was largely formed 

from 241Pu in the storage tanks or in the ground (Litaor et al. 1996). Waste oil stored in the tanks was 

from processing weapons-grade plutonium, which contained 0.58% 241Pu and <10-4% 241Am. Between 

1978 and 1981, 48 and 179 kCi (1,800 and 6,600 TBq) of 241Am and 241Pu, respectively, were disposed in 

the Subsurface Disposal Area of INEEL (Arthur and Janke 1986). No estimates are available of the 

quantities of these isotopes disposed of between 1952 and 1971 at the Radioactive Waste Disposal 

Complex of INEEL. 241Am is present at plutonium facilities and at plutonium reclamation facilities 

where 241Am is routinely separated from plutonium. The Hanford plant was the site of a 1976 column 

explosion, which resulted in extensive contamination and worker exposure (PNL 2000). 

6.3 ENVIRONMENTAL FATE 

6.3.1 Transport and Partitioning 

Atmospheric Transport. In the atmosphere, americium is associated with particulate matter and the 

transport of americium in air will therefore be governed by that of its host particles (Bennett 1979). 

Radionuclides resulting from atmospheric weapons tests are often injected into the lower stratosphere, 

while other atmospheric releases are into the troposphere. The residence time of particles in the 

atmosphere will depend on the aerodynamic particle size, altitude, latitude, season, and hemisphere 

because of atmospheric circulatory patterns. For example, residence half-lives of particles in the lower 

stratosphere range from 3 to 12 months in polar regions and from 8 to 24 months in equatorial regions, 

with removal being highest in the spring and lowest in the fall. Half-lives for particles in the troposphere 

are about 1 month. Larger particles will remain in the atmosphere for short periods of time and are 

deposited closer to their emission source, while small particles remain in the air for longer periods of time 

and are deposited further from their source. There are three deposition mechanisms: rain-out caused by 

droplet formation on aerosols within clouds, wash-out by falling precipitation, and dry deposition of 

particles onto the ground. Rain-out is the most important deposition process for americium, wash-out 

occurs relatively slowly and is dependent on the solubility of the pollutant in rainwater, and dry 

deposition makes an important contribution in areas of low rainfall. Therefore, deposition of 241Amcontaining particulate matter will depend on location, season, and meteorological conditions. In the 

absence of actual measurements, the deposition of 241Am in a region can be estimated by using the 

relationship between air concentration and deposition quantities for other isotopes that are attached to 
AMERICIUM 131 

6. POTENTIAL FOR HUMAN EXPOSURE 

particulate matter in air. In this way, using the average annual air concentration to annual deposition rate 

for strontium 90 (90Sr), the deposition rate of 241Am in the New York area was estimated to reach a 

maximum of 10 μCi/km2

 (37 kBq/km2) in 1964 and decline thereafter to 0.06 μCi/km2 (2.2 kBq/km2) by 

1981 (Bennett 1979). This would be expected to result in cumulative 241Am deposit of 58 μCi/km2 

(2.1 MBq/km2

) in the New York region in 2000, assuming no additional atmospheric nuclear testing after 

1976. If the ingrowth from 241Pu decay is included, the cumulative 241Am deposit in the year 2000 would 

be 800 μCi/km2

 (30 MBq/km2). 

Sea-air Transport. Sea-air transport may occur as a result of bubble scavenging in the water column 

coupled with ejection into the air when bubbles burst on the water surface. Laboratory and field studies 

of this process showed respective 241Am enrichments in aerosols of 92–580 and 20–40 over that in the 

bulk seawater (Belot et al. 1982; McKay et al. 1994; Walker et al. 1986). In extensive field studies, 

Mackay et al. (1994) found clear evidence of localized temporal and spatial variability in the enrichment 

of americium in sea spray over that in adjacent surf-zone seawater. While the enrichment is typically 

between 50 and 80, it ranges from 4 to 400. The aerosols produced by the sea spray are deposited nearby. 

Coastal strips in Cumbria, England have elevated levels of 241Am from sea spray (Pattenden and McKay 

1994; Walker et al. 1986). The water in this region of the Irish Sea receives effluent from the BNFL 

Sellafeld reprocessing plant. Studies of coastal soils in Northern Scotland are also believed to obtain their 

241Am contamination from the sea, albeit by a different mechanism. The activity level decreases with 

distance from the sea and is indistinguishable from background levels more than a few hundred meters 

inland. The actinide levels in these soils are in excess of those due to past nuclear explosions. The 

influence of sea spray was ruled out because of the much lower actinide concentrations in the Scottish 

water compared with that in the Irish Sea. In Northern Scotland, a stable foam or spume is formed along 

the coast that collects in rocky inlets. It is thought that this spume, which is rich in particulate matter and 

actinides, builds up in inlets, both overflowing onto the surrounding land and blowing inland on onshore 

wind (Pattenden and McKay 1994). 

Leaching in Soil. After being deposited on soil, 241Am may then leach into the soil. Since fallout of 

241Am is accompanied by its precursor, 241Pu, which also leaches into the ground, in addition to being 

mobilized by colloidal action, the amount of 241Am at a depth is a function of the leaching of both 

americium and plutonium, the colloidal movement of plutonium, and the decay of these isotopes. A 

depth profile of fallout americium was performed on samples at a representative site in North Eastham, 

Massachusetts in 1972 (see Table 6-1). Sixty-two percent of the activity resided in the upper 2 cm of soil 

and an additional 21% in the 2–4 cm depth (Bennett 1976). A comparison of modeling and experimental 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

AMERICIUM	 132 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-1. Concentrations of 241Am in Soil and Sediment 

Site/sample type Depth, Number of 

(year) cm samples Concentration Unitsa Type Reference 

Bikini Atoll (not specified)b

, U.S. Nuclear Test Site from 1946 to 1958, including BRAVO 

explosion on 3/1/54 

Robison 

et al. 1997b 

Interior of 

island 

0–5 157 0.26 (0.30) Bq/g d.w. Median 

(mean) 

5–10 151 0.19 (0.27) Bq/g d.w. Median 

(mean) 

10–15 127 0.081 (0.18) Bq/g d.w. Median 

(mean) 

15–25 80 0.026 (0.11) Bq/g d.w. Median 

(mean) 

25–40 59 0.012 (0.051) Bq/g d.w. Median 

(mean) 

40–60 23 0.017 (0.035) Bq/g d.w. Median 

(mean) 

0–40 53 0.11 (0.14) Bq/g d.w. Median 

(mean) 

Village area 0–5 63 0.11 (0.22) Bq/g d.w. Median 

(mean) 

5–10 62 0.13 (0.20) Bq/g d.w. Median 

(mean) 

10–15 63 0.12 (0.19) Bq/g d.w. Median 

(mean) 

15–25 59 0.064 (0.15) Bq/g d.w. Median 

(mean) 

25–40 52 0.059 (0.13) Bq/g d.w. Median 

(mean) 

40–60 20 0.012 (0.11) Bq/g d.w. Median 

(mean) 

0–40 51 0.13 (0.17) Bq/g d.w. Median 

(mean) 

Northern Marshall Islands Radiological Survey (NMIRS)c

, site of U.S. atmospheric Robison 

weapons testing from 1946 to 1958, including BRAVO explosion on 3/1/54 et al. 1997a 

16 Atolls/islands 0–5 182 0.49–569 Bq/g d.w. Range of 

means 

5–10 182 0.26–435 Bq/g d.w.	 Range of 

means 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

AMERICIUM	 133 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-1. Concentrations of 241Am in Soil and Sediment 

Site/sample type Depth, Number of 

(year) cm samples Concentration Unitsa Type Reference 

10–15 182 0.47–207 Bq/g d.w.	 Range of 

means 

15–25 182 0.15–48 Bq/g d.w.	 Range of 

means 

25–40 182 0.038–21 Bq/g d.w.	 Range of 

means 

Nuclear Weapons Testing Range, Maralinga, South Australia, site of 12 hydronuclear 

experiments at Taranaki in 1960, 1961, and 1963 (Vixen B Trials) in which 22.2 kg of 

plutonium was dispersed, having been ejected 2,500 feet vertically into the atmosphere. 

Cooper et 

al. 1994 

Taranaki, 

5 sites 

0–1 1 0.227–4.40 Bq/g d.w. Range 

1–2 1 0.026–0.799 Bq/g d.w. Range 

2–3 1 0.005–0.099 Bq/g d.w. Range 

3–4 1 0.009–0.022 Bq/g d.w. Range 

4–5 1 0.004–0.019 Bq/g d.w. Range 

Lake Michigan, site 7 km from Grandhaven, Michigan, water depth 67 m (cores and 

sediment trap at 60 m) 

Alberts et 

al. 1989 

Core 0–1 NS 651±118 μBq/g 

d.w. 

Mean±SD 

1–2 NS 1,147±111 μBq/g 

d.w. 

Mean±SD 

2–3 NS 1,427±181 μBq/g 

d.w. 

Mean±SD 

3–4 NS 1,110±148 μBq/g 

d.w. 

Mean±SD 

4–5 NS 363±67 μBq/g 

d.w. 

Mean±SD 

Suspended 

sediment, 60 m 

NS 555±107 μBq/g 

d.w. 

Mean±SD 

Cruise of RV Scotia, Orkney Islands, and northeast Scottish coast Pattenden 

and McKay 

1994 

Bottom 

sediment 

Surface NS 0.44–21 mBq/g 

d.w. 

Range 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

AMERICIUM 134 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-1. Concentrations of 241Am in Soil and Sediment 

Site/sample type 

(year) 

Depth, 

cm 

Number of 

samples Concentration Unitsa Type Reference 

Savannah River Estuary sedimentd DOE 1980 

Tidal 

freshwater 

0–5 NS 426±150 μBq/g 

d.w. 

Mean±SD 

5–15 NS 140±70 μBq/g 

d.w. 

Mean±SD 

15–30 NS 200±70 μBq/g 

d.w. 

Mean±SD 

30–50 NS 74±30 μBq/g 

d.w. 

Mean±SD 

50–70 NS 8.5±8.5 μBq/g 

d.w. 

Mean±SD 

Mouth of 

estuary 

0–5 NS 411±63 μBq/g 

d.w. 

Mean±SD 

5–15 NS 110±85 μBq/g 

d.w. 

Mean±SD 

15–25 NS 67±20 μBq/g 

d.w. 

Mean±SD 

Soil in northeastern United States from 1970 to 1974, undisturbed soil unless otherwise Bennett 

indicatede 1979 

Brookhaven, 0–5 1 16f mBq/km2
 

New York
 

North 0–30 1 17f mBq/km2
 

Eastham, 

Massachusetts
 

0–30 2 18f mBq/km2 Mean 

North Eastham, 0–25 5 19f mBq/km2 Mean
 

Massachusettscultivated soil
 

North Eastham, Massachusetts, background falloute Bennett 

1979 

0–2 NS 8.1±2 mBq/km2 Mean±SD 

2–4 NS 2.7±0.3 mBq/km2 Mean±SD 

4–6 NS 1.1±0.2 mBq/km2 Mean±SD 

6–8 NS 0.59±0.1 mBq/km2 Mean±SD 

8–10 NS 0.1±0.07 mBq/km2 Mean±SD 

10–12 NS 0.1±0.07 mBq/km2 Mean±SD 
 

 

AMERICIUM 

6. POTENTIAL FOR HUMAN EXPOSURE 

135 

Table 6-1. Concentrations of 241Am in Soil and Sediment 

Site/sample type 

(year) 

Depth, 

cm 

12–14 

0–30 

Number of 

samples 

NS 

NS 

Concentration 

0.1±0.04 

19±2 

Unitsa 

mBq/km2 

mBq/km2 

Type 

Mean±SD 

Mean±SD 

Reference 

a

conversion: 1 Bq=2.7x10-11 Ci=27 pCi b

Continuous monitoring program 1975–1993; decay corrected to 1999 

c

Decay corrected to 1996 

d

Concentration units converted from fCi/g 

e

Concentration units converted from mCi/km2 

f

Decay corrected to sampling date 

d.w. = dry weight; NMIRS = Northern Marshall Islands Radiological Survey; NS = not specified; SD = standard 

deviation 
AMERICIUM 136 

6. POTENTIAL FOR HUMAN EXPOSURE 

results indicates that americium is slightly less mobile than plutonium in this soil. Leaching studies of 

surface-deposited 241Am in three Indian soils of widely differing characteristics, namely laterite, medium 

black, and alluvial, were conducted in soil columns using simulated rain corresponding to the mean 

annual precipitation (Vyas and Mistry 1980). It was found that 98% of the americium was retained in 

upper 2 cm of soil; amending the soil with organic matter only slightly reduced its mobility. The greatest 

retention was obtained with the medium black and laterite soils, where >99% of the 241Am was found in 

the upper 1 cm. In 1990, Bunzl et al. (1994) investigated the residence time, and consequently the 

migration rates, of fallout 241Am in a typical undisturbed grassland soil (Alfisol) in Germany. Since 

241Am is present from its own deposition and also due to ingrowth from 241Pu, the residence time of 

plutonium also had to be determined and a compartment model had to be employed. The residence halftime in a particular zone and mean migration rates of americium at various soil depths were (depth, 

residence half-time, mean migration rate): 0–2 cm, 8 years, 0.3 cm/year; 2–5 cm, 8 years, 0.4 cm/year; 5– 

10 cm, 10 years, 0.50 cm/year; 10–15 cm, 10 years, 0.5 cm/year; 15–20 cm, 4 years, 1 cm/year; and 20– 

30 cm, 9 years, 1 cm/year. The migration rates were similar to, but somewhat greater than, those of 

plutonium. After a period of 30 years, the 241Am concentration on the surface layer was significantly 

diminished as a result of the migration. Stability constants for Am(III) indicate strong complexation with 

soil organic matter, and this could explain its increased mobility with depth. In another study, Bunzl et al. 

(1995) investigated the association of 241Am from global fallout with various soil components in six 

successive layers of undisturbed grassland in Germany from 0 to 30 cm using a sequential extraction 

procedure. In this way, the fractions that were readily exchangeable, bound to iron and manganese 

oxides, bound to organic matter, and bound to mineral (residual fraction) were identified. The association 

of a chemical with soil components controls their availability for plant uptake and transport. The 

americium was mainly deposited on the soil surface 30–40 years ago as a result of atmospheric nuclear 

weapon tests. The total deposition (i.e., sum over all layers) of 241Am was 18±2 Bq/m2

 (490±50 pCi/m2). 

On a Bq/kg basis, the data show that the highest activity was contained in the 2–5 cm layer, slightly less 

was present in the 5–10 cm layer, and activity declined markedly below 10 cm. On a Bq/m2

-cm thickness 

basis, the maximum activity was in the 5–10 cm layer. The attachment of americium to soil component 

varied considerably with soil layer. The largest amount of 241Am was attached to organic matter, 18– 

74%, depending on the soil layer. A substantial fraction, 12–64%, was bound to oxides. In the 5–10 cm 

layer, the 241Am in the readily exchangeable fraction was a minimum, 1.5%, while that attached to soil 

minerals was a maximum, 68%. In contrast, very little 241Am (<0.5%) was bound to mineral in the 

surface (0–2 cm) layer and the deepest soil layers (15–20 and 20–30 cm). Compared with plutonium, 

much more americium is contained in the exchangeable fraction, a result that has been ascribed to 

americium’s greater hydrolyzability. Americium has also been shown to be largely associated with the 
 

AMERICIUM 137 

6. POTENTIAL FOR HUMAN EXPOSURE 

high molecular weight organic factions of dissolved organic matter in the soil solution of two grassland 

soils, a soddy podzolic soil and a peat soil, in the vicinity of the nuclear reactor at Chernobyl. The 

distribution coefficients for 241Am in these soils were (soil type [depth], Kd in mL/g): soddy podzolic— 

sod layer (0–2 cm), 1,220; soddy podzolic—mineral layer (2–5 cm), 810; peat (0–2 cm), 2,760; and peat 

(2–5 cm), 4,550 (Bunzl et al. 1998). While it was similarly shown that the concentration of 241Am was 2– 

3 times higher in organic matter than in whole sediment from Lake Michigan, organic matter was a very 

minor constituent of the sediment (<0.5%), so organic matter was associated with a smaller percentage of 

americium despite its higher concentration (Alberts et al. 1989). The bulk of the 241Am in Lake Michigan 

was found in the hydrous oxides fraction of both the sediment core samples and the suspended particulate 

matter. 

While laboratory studies predicted very little movement of actinides in subsurface environments, these 

radionuclides have been found to migrate in groundwater, and have traveled underground from 80 to over 

3,000 meters at Los Alamos National Laboratory (LANL), New Mexico and Oak Ridge National 

Laboratories (ORNL), Tennessee. Colloidal materials, which can be mobile in underground systems over 

large distances, can bind and transport radionuclide contaminants in subsurface systems (McCarthy et al. 

1998a, 1998b; Penrose et al. 1990). 

Sorption to Sediment and Particles in Water. When discharged into water, americium rapidly sorbs onto 

particulate matter in the water column, settles, and adsorbs to bottom sediment (Murray and Avogadro 

1979). The distribution coefficient, Kd, of americium between the particulate-associated phase and the 

dissolved phase is 2.0x106 (Pattenden and McKay 1994). The sediment-water distribution coefficient, Kd, 

was also 2.0x106

 for intertidal sediment from the Ravenglass estuary near Sellafield, United Kingdom, in 

agreement with other investigators (Davis et al. 1997). Equilibrium was established in 30 minutes. 

Adsorption is greatest for fine-grained particles. A large fraction of the heavier sediment particles will 

settle out quickly and remain close to the source. Finer particles (and soluble species) will remain 

suspended for longer periods and be dispersed by currents and tides. The distribution in sediment will be 

site specific, being largely determined by hydrology and the nature of the underlying sediment. Being a 

particle-reactive nuclide, like plutonium, americium’s distribution in sediment after release will mirror 

that of plutonium, although its loss from the water column appears to be more rapid. The distribution of 

americium released from the BNFL reprocessing plant at Sellafield, United Kingdom near the Irish Sea 

changed very little between 1978 and 1988 (McCartney et al. 1994). Americium in the effluent was 

entirely as Am(III). In their study of actinide activity in waters entering the northern North Sea, Murray 

et al. (1978) noted that the activity level of 241Am relative to 238,239,240Pu near the northwest coast of 
 

AMERICIUM 138 

6. POTENTIAL FOR HUMAN EXPOSURE 

Scotland was very low, 0.06. Assuming that the contamination was derived from discharges into the Irish 

Sea 2–2.5 years earlier and 300–500 km to the south where Am-to-Pu alpha activity ratios varied from 

0.9 to 2.56, there was a decrease of about 1.7 in the ratio from the point of discharge in spite of the 

increase in 241Am due to the decay of 241Pu. Similar results have been observed during the transport of 

actinides discharged from the nuclear fuel reprocessing plant at La Hague, France and in the case of 

fallout into Mediterranean waters (Murray et al. 1979). These observations have been ascribed to 

americium’s greater adsorption to suspended particulate matter, which then settle out; americium 

consequently disappears more rapidly from surface water than plutonium. Support for this conclusion 

was found in another study where the percentage activities associated with suspended materials were 

36±8 and 80±7 for plutonium and americium, respectively, <10 km from the point of discharge. 

Therefore, twice as much americium was associated with suspended matter than plutonium. At a distance 

of 100 km from the point of discharge, this fraction was still >50%. Core profiles of sediment in the 

northeast Irish field reveal major subsurface peaks of Sellafield-derived 241Am in both the solid phase and 

interstitial water (Malcolm et al. 1990b). These peaks were not related to the distribution of organic 

carbon or iron or magnesium oxides in the sediment or composition of the interstitial water, but rather 

resembled the discharge of 241Am and plutonium. Studies of radionuclide concentrations in sediment 

cores from the Ravenglass salt marsh in West Cumbria, United Kingdom, suggest that the concentration 

profile of 241Am in sediment bear a qualitative resemblance to the Sellafield discharge patterns and to 

other cores from the eastern Irish Sea coastline. A maximum concentration of 29,300 Bq/kg 

(0.792 μCi/kg) dry weight was found in the sediment core at 8.9 cm. This maximum concentration for 

241Am is in the correct section of the sediment core to correlate with discharges in 1974 based on a 

sedimentation rate of 4 mm/year (Morris et al. 2000). 

Davis et al. (1997) investigated how various environmental factors influenced Kd. The presence of CO2 

gas had a marked effect, increasing the amount of americium leached from sediment by a factor of 40. 

The increase is attributable to the presence of stable americium-carbonate complexes in seawater and, to a 

lesser extent, the accompanying decrease in pH to 5.5 as a result of purging with CO2. Experiments on 

the effect of pH on Kd suggested that desorption of americium from sediment at low salinity is due to low 

pH rather than to a drop in ionic strength. Therefore, the effect of low salinity and low pH in an estuary at 

low tide and when fresh water is backed up by the incoming tide is the remobilization of 241Am. 

Resorption to sediment entering the estuary from rivers will result in the redistribution of activity. 

The disposal of large quantities of radionuclides in Arctic seas has raised concern about the behavior of 

these chemicals in these waters. Fisher et al. (1999) found that the mean (range) Kd of americium in Kara 
 

AMERICIUM 139 

6. POTENTIAL FOR HUMAN EXPOSURE 

Sea sediment was 1x106 (1x105–3x106) mL/g, which is in accord with that for temperate coastal sediment, 

2x106

 (1x105–2x107) mL/g. The mean Kd values for americium in two areas in the Kara Sea, an Arctic 

bay where radionuclides have been dumped, were 4.3x104

 and 35x104 for ambient water column samples 

and 57x104

 and 16x104 for bottom sediment samples (Carroll and Harms 1999; Carroll et al. 1999). The 

mean sediment water distribution function recommended by the International Atomic Energy Agency 

(IAEA) is 2x106

 (range 2x105–2x107). Therefore, use of the IAEA value in risk assessment modeling 

would underestimate the americium concentration in seawater. Carroll et al. (1999) stressed that for 

particle-reactive elements like americium, it is important to use site-specific information for Kd. 

Extensive adsorption determinations of 241Am were obtained in freshwater, estuarine, and marine 

sediment-water systems (NRC 1981). The Kd values for sorption range from 104

 to 106 mL/g, accounting 

for upward of 95% removal of americium to the solid phase. There were no apparent trends in Kd with 

salinity. There was an increase in Kd with increasing pH that is typical of hydrolyzable metal ions. The 

Kd declined with increasing sediment concentration. The mean sediment-water distribution coefficients 

obtained were (sample type, Kd with standard deviation [SD]x10-4): Lake Michigan—three sites, 

54.8 (37.3); Clinch River, Tennessee, 73.3 (36.4); Hudson River estuary—three sites, 6.76 (2.43)– 

29.6 (8.8); Lake Washington, Washington, 18.0 (4.3); Lake Nitinat, Washington—anoxic marine, 

25.4 (3.1); Washington Continental Shelf, 10.3 (1.8); Sinclair Inlet, Puget Sound, Washington, 

45.4 (12.0); Saanich Inlet, British Columbia—anoxic fjord, 37.1 (8.4); and Skagit Bay, Puget Sound, 

Washington—estuary—two sites, 26.8 (7.4) and 38.0 (10.6). Sediment-water distribution coefficients for 

241Am in various environments obtained from the literature include (site, Kd in mL/g): Lake Michigan, 

>50x104

; Hanford, U-Pond, 1.9x104 and 8.7x104; and Rocky Flats, Pond A, 0.65x104 (NRC 1981). 

Laboratory measurements yielded Kd values of 5,000 and 400 in Dutch subsoil and river sand, 

respectively (NRC 1981). 

Despite its high absorptivity, americium has migrated into groundwater and traveled underground at 

several national laboratories; the mobile forms were colloids and anionic complexes (McCarthy et al. 

1998a, 1998b; Penrose et al. 1990; Toran 1994). Artinger et al. (1998) found that increasing 

concentrations of humic substances reduced americium adsorption on sandy aquifer material, confirming 

the involvement of colloid-sorbed americium in its subsurface transport. The leachability of 

radionuclides in waste was assessed in soil column experiments in Carjo loam soil (B horizon) collected 

in the vicinity of the low level radioactive burial site at Los Alamos. In the case of 241Am, 90% was 

retained in the silica sand layer placed on top of the soil column, 5% was in the upper 5 cm of the column, 

and the remainder was distributed at greater depths. In batch experiments, 40 and 49% of soluble 241Am 
AMERICIUM 140 

6. POTENTIAL FOR HUMAN EXPOSURE 

in waste, 0.3% of the total 241Am present, sorbed to Puyo sandy loam and Carjo loam, respectively 

(Fowler et al. 1981). While americium should strongly adsorb to silicates and mineral oxides of the 

highly weathered shale saprolite in the unlined disposal trenches used for transuranic waste (TRU) at Oak 

Ridge National Laboratory, rapid migration in groundwater with little retardation over distances of 

80 meters has been observed (McCarthy et al. 1998a, 1998b). This occurred when seasonal fluctuations 

in the water table permitted groundwater to contact TRU in the trenches. As a result of laboratory studies, 

the mobilization and transport of americium has been demonstrated to result from complexation of the 

actinide by natural organic matter. Storm events aid the mobilization by providing the physical 

connection between the TRU and groundwater and increasing the amount of organic matter in the soil 

solution and groundwater. 

In the absence of natural organic matter, the adsorption coefficient on the site-specific saprolite was 

8,900. A similar situation was documented in Los Alamos where nuclear wastes infiltrated a small 

aquifer. While the movement of 241Am was predicted to be limited to a few meters, the actinide was 

detectable in monitoring wells as far as 3,390 m downgradient from the discharge (Penrose et al. 1990). 

Further investigation indicated that the mobile americium was tightly bound to colloidal material between 

25 and 450 nm in dimension. The distributions of 241Am activity with colloid particle size (<450 nm) in 

the well water were (particle size, percent): 25–450 nm, 28%; 5–25 nm, 0.75%; 2–5 nm, 26%; and <2 nm 

(filtrate), 43%. The unbound americium fraction appeared to be a stable anionic complex of unknown 

composition. At other sites at Los Alamos, contaminated plumes traveled 30 m in <30 years and 40 m in 

<20 years (Nyhan et al. 1985; Toran 1994). Migration appeared to be related to the water content of the 

tuff (a rock composed of the finer kinds of volcanic detritus usually fused together by heat) bed 

underlying the disposal site, and not simply to fractures in the rock (Nyhan et al. 1985). Investigation of 

the possible mobility of 241Am in soils around Rocky Flats contaminated by leaking drums under 

simulated conditions of extreme rain events found that 90% of 241Am activity resided in the upper 12 cm 

of soil, below which it rapidly decreased; 241Am activity in interstitial water never exceeded 0.4 Bq/L 

(11 pCi/L) at the deepest sampling layers even in a 100-year rain event (Litaor et al. 1996). However, 

evidence was found, in line with other investigators, that actinides may move to greater depths in 

macropores possibly formed by decaying root channels or other biological processes. 

The behavior of colloidal americium was studied in an oligotrophic soft water lake used as the source of 

cooling water for a nuclear power plant in Wales (Orlandini et al. 1990). 241Am concentrations in the 

dissolved fraction (≤450 nm) were 5.8–18.2 fCi/L (210–673 μBq/L). Most of the americium was 

distributed in two size ranges, filterable particles (≥450 nm) that contained ~37% of the activity and 
AMERICIUM 141 

6. POTENTIAL FOR HUMAN EXPOSURE 

medium-sized colloids (5–100 nm) that contained ~54% of the activity; only a small fraction (~7%) of 

americium was ‘dissolved’ or in true solution, size <1.5 nm (3,000 molecular weight [MW]), where the 

americium would occur as free ions. The Kd of americium to filterable particles (≥450 nm), the minimum 

particle size that would settle by gravity, was found to be 470,000; the Kd of americium to colloidal 

particles was estimated to be about a factor of 20 higher. Lower Kd values obtained for 241Am in dialysis 

experiments, which restrict the size of particles, compared to those obtained in shaking sorption 

experiments is a further indication that chemical species affects sorption (NRC 1981). 

Distribution of 241Am in a dialysis system containing sediment, phytoplankton, and detrital matter 

established that a substantial amount of americium accumulated in all three phases both in fresh and 

marine waters (NRC 1981). The adsorption process was not reversible, and the longer the americium was 

adsorbed, the more difficult the chemical was to desorb. Appreciable amounts of americium have been 

shown to adsorb to bacterial cells such as those found in the Waste Isolation Pilot Plant in New Mexico 

(Francis et al. 1998). There is a potential that americium attached to biocolloids may facilitate its 

transport from the waste site. 

Biotic Transport. Biotic transport can be defined as the actions of plants and animals that result in the 

transport of a radioactive material or other substance from a waste site to locations where it can enter 

pathways that may result in exposure to humans. Small mammals inhabiting areas containing radioactive 

contamination or radioactive waste sites may become contaminated with americium by consuming 

contaminated soil or plants and may disturb americium-contaminated soil through their burrowing and 

excavating activities. These animals may therefore affect the distribution of americium within the waste 

site or transport americium to previously uncontaminated areas. In addition, small mammals may be 

consumed by animals higher in the food chain, such as hawks and coyotes, which would add to the 

dispersal of americium from disposal areas. However, results of studies of numerous species of wildlife 

that inhabit the waste disposal area at INEEL indicate that wildlife do not contribute significantly to the 

spread of radionuclides to the surrounding environment (Arthur and Janke 1986). What may be more 

significant is the contribution of biotic intrusion on the soil covering the waste areas and the effect on 

moisture infiltration rates. A study was conducted of the dispersal of radioactive isotopes by deer mice at 

the Subsurface Disposal Area (SDA) at INEEL in southwest Idaho (Arthur et al. 1987). These animals, 

which make up 69% of the small mammal biomass at the SDA, contained significantly higher levels of 

241Am than in control areas; the isotope accumulated primarily in the pelt and lung tissue, but also the 

gastrointestinal tract. Of the 22.8 μCi (0.844 MBq) radionuclide inventory estimated to be contained in 

deer mice inhabiting the SDA during a 1-year period, about 8.4 μCi (0.31 MBq) was estimated to have 
 

AMERICIUM 142 

6. POTENTIAL FOR HUMAN EXPOSURE 

been transported off site, of which about 1% was the transuranic radionuclides 238Pu, 239+240Pu, and 241Am. 

These transuranic radionuclides also make up about 1% of the 28.8 μCi (1.07 MBq) inventory present in 

deer mice feces. It was estimated that during 1978–1979, deer mice excavated 12,450 kg of contaminated 

soil to the surface, which could be further dispersed by wind. Evidence of burrowing activity by 

earthworms and ants were also found at Rocky Flats, Colorado and other sites (Litaor et al. 1994). 

Models have been developed to estimate the amount of radioactivity transported to the surface as a result 

of burrowing activity by animals and plant uptake at a generic LLW disposal site in an arid region 

(Kennedy et al. 1985). It was found that for 243Am, plants were about 200 times more effective at 

transporting waste to the surface than burrowing animals. These results indicate that long-term biotic 

transport may affect the integrity of land burial, redistributing radionuclides such that they become a 

source of human exposure. Biotic transport will be affected by the oxygenation of soil, as waterlogged 

and anaerobic soils are less likely to be disturbed by earthworms and other burrowing animals (Livens 

and Hursthouse 1993). 

Uptake by Plants. The uptake of chemicals by plants and their ingestion and bioaccumulation by animals 

is one mechanism by which a chemical present in soil, air, and water enters into the food chain of 

humans. Plants may become contaminated with americium as a result of uptake via the root and 

deposition on the upper part of the plant. Direct deposition occurs during the deposition period, but 

surface contamination may also occur from resuspension of or direct contact with contaminated soil. 

Surface deposits may be reduced by weathering or by washing or processing, thereby reducing the 

amount of americium consumed by humans. Some studies indicate that foliar uptake and subsequent 

translocation, which is affected by rainfall and size of the deposited particles, may rival the soil-root 

pathway in magnitude (Cataldo et al. 1980). Translocation of transuranic elements taken up through the 

roots into seeds and fruit is generally very low (Bennett 1979). Uptake in seeds is significantly lower 

than for other above ground plant parts, and legumes accumulate about 10 times more than grasses 

(Schreckhise and Cline 1980). 

Plant uptake from soil depends on factors such as the form and availability of the chemical, soil 

chemistry, plant species, and environmental conditions. Various studies indicate that 241Am uptake by 

plants is on the order of 10-2 to 10-6, about an order of magnitude greater than 239Pu under the same 

conditions (Bennett 1979; EPA 1979; Romney et al. 1981; Schultz et al. 1976; Zach 1985). Uptake is 

somewhat greater under acidic conditions and greater to the leaves than to the grain or fruit. Plant uptake 

experiments with potatoes, peas, and corn were performed using ‘fallout background’ soil in North 

Eastham, Massachusetts. The 241Am in the plant was compared with the average activity in the upper 
 

AMERICIUM 143 

6. POTENTIAL FOR HUMAN EXPOSURE 

30 cm of dried soil, 0.0033 Bq/g (89 fCi/g). The concentration ratios (CRs) (activity per unit wet weight 

of plant/activity per unit dry weight of soil), also referred to as the transfer coefficient, were 1.7x10-3 for 

husked corn plus cob, 1.0x10-3 for peeled potatoes, and <1.6x10-3 for shelled peas (Bennett 1979). Flours 

that were milled from crops of wheat, rye, barley, and oats grown on German soil where radionuclides 

resulted exclusively from global fallout contained #5.2, 11, 31, and 70 μBq/kg (1.9 fCi/kg) of 241Am, 

respectively (Bunzl and Kracke 1987). The respective soil to plant transfer factors were #0.86x10-4, 

1.5x104

, 4.7x10-4, and 37x10-4. The concentration of 241Am in the bran was a factor of 10–38 higher than 

in the flour for wheat, rye, and oats. Romney et al. (1981) studied 241Am uptake in crops of peas, 

soybeans, tomatoes, and wheat grown in seven soils representative of major food production areas of the 

United States. The CRs in the foliage ranged from 10-5 to 10-2 and the CRs in the seed, grain, and fruit 

parts ranged from 10-6 to 10-4, about a factor of 10 lower than in the foliage. Uptake varied among the 

difference soils by a factor of about 100. However, Schulz et al. (1976) obtained less of a variation in 

uptake of 241Am by wheat in three California soils. The CRs were 6.3x10-6, 16.4x10-6, and 6.1x10-6 in 

Aiken (a slightly acidic forest soil), Yolo (an agricultural soil), and Panoche (a calcareous soil) soil, 

respectively. The CRs for 239, 240Pu were approximately the same. Nisbet and Shaw (1994) obtained CRs 

ranging from 0.04x10-4 to 4x10-4 for 241Am for carrots, cabbage, and barley grown in artificiallycontaminated peat, loam, and sand soils; the CRs were in the order carrot > cabbage > barley. The CRs 

therefore ranged over 2 orders of magnitude with crop and soil type. Uptake was lowest in peat soil 

where the organic matter plays an important role in complexing the ions, making them less available for 

uptake. The CR remained unchanged for plants grown ≥3 years after contamination of the soil. The soilplant transfer appears to be related to the concentration of 241Am in the soil solution, rather than the bulk 

soil. While Livens et al. (1994) obtained plant-soil CRs for 241Am in the range of 10-5–10-6, the plant-soil 

solution CR obtained was much higher, 210–640 L/kg (Bennett 1979). The concentration ratio for 241Am 

in composite vegatation samples (grasses and herbaceous species) collected in Lady Wood, a coniferous 

wood located 500 meters northeast of BNFL Sellafield, Cumbria, United Kingdom, ranged from 0.02 to 

0.32 (Copplestone et al. 1999). Amendment of soil with lime and organic matter decreases uptake 

(Adriano 1979; Hoyt and Adriano 1979). This is thought to reduce the solubility or increase americium 

binding, thereby reducing its availability. 

The uptake of radionuclides into plants from soil at contaminated sites at DOE facilities and elsewhere 

has been the impetus for several studies. Such concerns led to experiments conducted in May 1996 at the 

Los Alamos National Laboratory (LANL), New Mexico using stream channel sediment from Los Alamos 

Canyon (LAC). This stream received various amounts of untreated radioactive waste in the 1940s 

(Fresquez et al. 1998b). Pinto beans, sweet corn, and zucchini were grown in this contaminated soil as 
AMERICIUM 144 

6. POTENTIAL FOR HUMAN EXPOSURE 

well as in soil from seven regional background locations (RBG) between 32 and 96 km around the LANL. 

The radionuclide content of this latter soil is reflective of global fallout. The 241Am levels in LAC and 

RBG soils were 0.708 and 0.005 pCi/g dry weight (0.0262 and 0.0002 Bq/g), respectively. The mean 

241Am concentrations (dry weight basis) in edible tissue of crops grown on LAC soil and RBG soil were 

(crop, LAC level [pCi/g (μBq/g)], RBG level [pCi/g (μBq/g)]): beans, 21.5x10-5 (7.96), 7.0x10-5 (2.6); 

corn, 27.8x10-5 (10.3), 4.1x10-5 (1.5); and zucchini, 182.5x10-5 (67.5), 27.1x10-5 (10.0). The CRs (activity 

of 241Am in dry plant tissue to that in dry soil) in the edible LAC crop tissues were (crop, concentration 

ratio): LAC beans, 3.04x10-4; LAC corn, 3.93x10-4; and LAC zucchini, 25.78x10-4. These ratios are much 

lower than those in composite nonedible crop tissue, which ranged from 48x10-4 to 740x10-4. The mean 

concentration (dry weight) of 241Am found for pinon pine nuts collected around LANL was 9.8x10-5 pCi/g 

(3.6 μBq/g) with a mean concentration ratio to soil of 0.0193 (dry basis) (Fresquez et al. 2000). A garden 

plot was established on a portion of a drained contaminated pond at the Savannah River Site (SRS) 

having a mean 241Am concentration of 1.60±0.59 Bq/kg (43.2±15.9 pCi/kg) in soil (0–15 cm). Geometric 

mean concentration ratios of 241Am (Bq/kg dry plant/Bq/kg dry soil) in the various crops were: corn 

kernel, 0.0011; corn husk, 0.0016; bush beans, 0.0072; turnip green, 0.0528; and turnip tuber, 0.0053 

(Whicker et al. 1999). Uptake for americium was similar to that of curium, but was much higher than for 

plutonium, thorium, and uranium. Based on the conditions of the study, it was thought that root uptake 

was the primary mechanism of plant contamination. The concentration ratios for americium are about an 

order of magnitude higher than a similar study in Tennessee. Since it has been demonstrated that liming 

decreased uptake, the high uptakes in the SRS study have been ascribed to the acidity of the soil (pH 

3.8-4.5 vs. 7–7.5). SRS served as a primary source of reactor-produced nuclear materials, primarily 

plutonium and tritium, for nearly 4 decades. The CR for 241Am in barley grown on contaminated soil at 

the Nevada Test Site was of the order of 10-4 for vegetative growth and 25–100 times lower for the grain 

(Schulz et al. 1976). Similar CRs (3x10-4–7x10-4) were obtained for green and root vegetables on land 

reclaimed from the sea that was contaminated with Sellafield discharges (Green and Wilkins 1995); an 

earlier study with potatoes, obtained CRs about an order of magnitude less (Popplewell et al. 1984). 

Bioconcentration in Aquatic Organisms. Transuranic elements are generally associated with the gut or 

external surfaces of aquatic organisms. Bioconcentration factors (BCFs) for 241Am measured at a pond at 

Savannah River, Georgia for fish and other plants and animals are presented in Table 6-2. In a study 

performed at a nuclear waste pond at Hanford, the maximum concentration of actinides, including 241Am, 

that would accumulate in the whole fish and fish fillet were measured. In this waste pond, the sediment 

concentration of 241Am was about 150 pCi/g (5.5 Bq/g), approximately 3 orders of magnitude above 

background levels (Emery et al. 1981). Both the bluegill and largemouth bass were studied. The 
 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-2. Bioconcentration Factors for 241Am 

Bioconcentration factora 

Species Value Mean Number of samples Site 

Large-mouth bass, muscle 

Fish muscle 

2,500 

50 

1 SRS 

Literature valueb 

Fish muscle 25 USNRCc 

Bullhead catfish, bone 4,200 1 SRS 

Macroinvertebrates, larvae 78,000–240,000 2 SRS 

Macrophyte, rooted vascular 

Macrophyte, floating vascular 

Turtle, muscle 

1,400–21,000 

75,000 

5,600 

3 

1 

1 

SRS 

SRS 

SRS 

American coot, muscle 650 1 SRS 

Bahia grass 0.03–0.12 

2.3x10-7–0.005 

0.067 6 SRS 

Literature valueb 

2.5x10-4 USNRCc 

Pine tree leaves 0.0052–0.021 0.013 2 SRS 

0.0001–0.1 Literature valueb 

a

The bioconcentration factor is the concentration in organism dry weight/concentration in medium (i.e., water, soil as 

appropriate). 

b

Values obtained from various literature sources cited in DOE 1996 

c

USNRC values cited in DOE 1996 

USNRC = U.S. Nuclear Regulatory Commission; SRS = Savannah River Site 

Source: DOE 1996 
 

AMERICIUM 146 

6. POTENTIAL FOR HUMAN EXPOSURE 

concentration of 241Am in the water was about 0.2 fCi/mL (7 μBq/mL). The results from the Hanford 

study indicate that both short- and long-term uptake of americium were low; that uptake was similar for 

short-term (5 days) and long-term (430 days), experiments; and that direct sediment-to-fish transfer was 

the primary route for americium uptake. In both species of fish, there were only a few cases where fillet 

concentrations were >10 times those in controls. The maximum concentration of 241Am obtained in bass 

and bluegill were 0.030 and 0.028 pCi/g (1.1 and 1.0 mBq/mL) dry weight in fillet and 0.067 and 

2.0 pCi/g dry weight (2.5 and 74 mBq/mL) in whole fish (Emery et al. 1981). 

In marine organisms, the target organs and tissues of americium bioaccumulation are mainly the digestive 

gland, gill, and exoskeleton (Chassard-Bouchaud 1996). Uptake in mussels appears to be primarily from 

seawater rather than ingested sediment (Hamilton and Clifton 1980). Americium taken up by mussels 

from water was primarily associated with the shell, while that obtained from food was bound to soft tissue 

(Fisher et al. 1996). Absorption efficiencies from ingested food in mussels were also critical in 

determining bioaccumulation. Clifton et al. (1983) studied the depuration profiles in mussel populations 

chronically exposed to radioactive waste discharges from the BNFL reprocessing plant at Sellafield, 

Cumbria, into the northeast Irish Sea. Apart from clearance from the digestive tract (half-life of 

0.9 hours), the half-time of 241Am is 303 days. Essentially all of the 241Am taken up by a euphausiid, a 

shrimp-like zooplankton, was by passive adsorption onto exoskeletons, so that negligible americium was 

retained by the animal after molting (Fisher et al. 1983). Wet weight concentration factors were of the 

order of 100 after a week of exposure, with the BCFs varying linearly with the surface area-to-weight 

ratio of the organism. Americium was also taken up by feeding on suspensions of diatoms, but there was 

negligible assimilation and most americium passed through the gut and was defecated. 

Uptake and retention of americium by benthic organisms is quite variable (Fowler and Carvalho 1985). 

In general, filter feeders such as tunicates can clear particles containing 241Am from seawater by filtration 

through the granchial basket and accumulate small amounts in internal tissue. Mucous feeding guilds of 

suspension-feeders like crinoids do not efficiently trap americium; uptake appears to occur by 

complexation or adsorption of dissolved americium to the body wall. Echinoderms and some large 

crustaceans assimilated americium with their ingested prey, although large differences in half-times and 

assimilation efficiencies in different groups suggest different feeding-digestion physiologies. Uptake in 

benthic marine isopods, is to a great extent, by surface adsorption to the exoskeleton and to a lesser extent 

through the gut, digestive gland, muscle, and haemolymph (Carvalho and Fowler 1985). The half-time in 

the long-lived compartment was 261 days. Elimination from the internal tissue was more rapid than from 

the exoskeleton. The fraction assimilated into tissue from food was <5%. The transfer of 241Am from 
AMERICIUM 147 

6. POTENTIAL FOR HUMAN EXPOSURE 

marine sediments contaminated by nuclear tests to benthic polychaetes was <1% (dry weight) (Hamilton 

et al. 1991). 

The biological uptake in aquatic organisms may depend on factors such as temperature, time after intake, 

season of the year, and water quality. In the brittle star (Ophiothrix fragilis), a species that dominates 

Arctic benthic communities, the initial uptake was 3 times greater at 12 EC than at 2 EC, but depuration 

was not temperature dependent (Hutchins et al. 1996a). After 14 days, the BCF was 48 at 2 EC and 53 at 

12 EC. In the sea star (Asteruas forbesi), another Arctic organism, temperature greatly enhanced the 

retention of americium ingested in food (Hutchins et al. 1996b). The biological half-time of americium 

ingested in food was 31 days at 12 EC and essentially infinite at 2 EC. Experiments performed on the 

freshwater snail (Lymnaea stagnalis) found higher 241Am uptakes from mesotrophic pond water at acid 

pH 5.0 than at pH 8.0 (Thiels et al. 1984). In summer, the BCF in the freshwater snail was more than 

twice as high in acidic media as in alkaline media. In addition, uptake was a function of season, being 

greater in August than in December. This has been ascribed to changes in metabolic rate with changing 

photoperiods. Uptake of 241Am by two freshwater benthic invertebrates, Hyallella and Tubifex, from 

water was two orders of magnitude higher than from detritus or sand, suggesting that soluble 241Am is the 

principal route of uptake and that desorption from particulate matter must occur before the substance is 

available for uptake (Sibley and Stohr 1990). No uptake was observed from labeled National Bureau of 

Standards (NBS) standard sediment. 

Mahon (1982) measured BCFs of 1,576 and 459 in algae and plankton, respectively. Horikoshi et al. 

(1981) determined BCFs in several species of bacteria that ranged from 2,794 to 354,000; however, 

bioconcentration by the bacteria represented adsorption onto the cell surfaces of the bacteria rather than 

true biological uptake. 

Biomagnification in the Food Chain. The available evidence suggests that the transport of americium 

up the food chain to man is slight (Bulman 1978). Americium in the food chain, lichen-reindeer-man, 

was studied by determining the concentrations 241Am in lichen and reindeer liver in Finnish Lapland 

(Jaakkola et al. 1977). During 1963–1974, 241Am in lichen ranged from 1 to 40 pCi/kg 

(0.037-1.48 Bq/kg) dry weight. Levels in six reindeer livers in 1974–1976 contained 0.3–5.4 pCi/kg 

(0.01-0.20 Bq/kg) fresh weight. 
AMERICIUM 148 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.3.2 Transformation and Degradation 

Americium isotopes are transformed by radioactive decay. However, the half-lives of the principal 

americium isotopes, 241Am and 243Am, are very long, 432.2 and 7,370 years, respectively (Baum et al. 

2002), and there is only a small amount of transformation over a human lifetime. 241Am is formed by the 

decay of 241Pu (half-life of 14.4 years) (Baum et al. 2002) and this can lead to a significant transformation 

of that isotope to 241Am in humans, especially for 241Pu that is fixed in the bone. 

6.3.2.1 Air 

There is limited information available regarding the abiotic transformation of americium in the 

atmosphere. Oxidation is the most common reaction that occurs in the atmosphere. This would not be 

expected for americium compounds, which are generally present in the +3 oxidation state under 

environmental conditions. 

6.3.2.2 Water 

The principal abiotic processes affecting americium in water are precipitation and complex formation. In 

natural waters, americium solubility is limited by the formation of hydroxyl-carbonate (AmOHCO3) 

precipitates. Solubility is unaffected by redox condition. Increased solubility at higher temperatures may 

be relevant in the environment of radionuclide repositories. In environmental waters, americium occurs 

in the +3 oxidation state; oxidation-reduction reactions are not significant (Toran 1994). 

6.3.2.3 Sediment and Soil 

Americium will occur in soil in the trivalent state. The transformations that may occur would involve 

complexation with inorganic and organic ligands (see Section 6.3.1) and precipitation reactions with 

anions and other substances present in the soil solution. The 241Am occurring as an ingrowth progeny of 

241Pu and trapped in a plutonium matrix will exhibit solubility and biokinetic characteristics of plutonium, 

rather than americium. 
AMERICIUM 149 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 

In 1973, the EPA established The Environmental Radiation Monitoring System (ERAMS), a nationwide 

network for obtaining data in environmental samples. ERAMS consists of a network of sampling stations 

that provide air, surface and drinking water, and milk samples that the EPA uses to obtain environmental 

concentrations of radioactive material. The objective of this system is to identify trends in the 

accumulation of long-lived radionuclides in the environment (EPA 2000b). Sampling locations for 

ERAMS are located near primary population centers to provide optimal population coverage. ERAMS 

does not analyze samples for americium, but does measure concentrations of 238,239/240Pu in air, from 

which it may be possible to infer levels of 241 Pu and 241 Am. The most recent ERAMS report containing 

plutonium data is that covering January–December 1998 composites (EPA 2000b). 

6.4.1 Air 

The annual average 241Am concentration in surface air in the mid-latitudes resulting from nuclear testing 

between 1951 and 1978 was estimated using the atmospheric transport model and the amount of 241Am 

that would have been produced as a result of the testing. The results show a rapid increase in 241Am 

surface air concentrations, which reached a maximum of 23 aCi/m3

 (1 aCi=10-18 Ci) (0.85 μBq/m3) in 

1963–1964. Since 1973, levels have been <1 aCi/m3

 (0.037 μBq/m3) and are continuing to decline, 

assuming no additional atmospheric nuclear testing (Bennett 1979). Measurement of these low 1973 

levels would have required large sample volumes and exceedingly long sampling periods at common 

sampling rates. Integral concentration over the entire fallout period is estimated to be 0.12 fCi-year/m3 

(4.4 μBq-year/m3

). Confirmation for these concentration estimates comes from two sources: comparison 

with plutonium fallout and cumulative deposits of 241Am activity in soil, which is a reflection of integral 

air concentrations. UNSCEAR (2000) reported that deposition and air concentrations of radionuclides 

from fallout dropped rapidly once atmospheric testing ceased in 1980. Inhalation exposures for even 

long-lived transuranic radionuclides became insignificant after 1985. 

The Electric Power Research Institute (EPRI 1981) conducted a survey of transuranic radionuclides in the 

terrestrial environs of nuclear power plants in the United States in 1978–1979. The plants included two 

pressurized water reactors (PWRs) and two boiling water reactors (BWRs) that were of modern design 

and had been in operation at least 3 years. The 241Am air concentrations around all of the power plants 

were extremely low and indistinguishable from fallout background. 
 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

Selected radionuclide levels in air were measured at Bragin, 55 km north of Chernobyl for 18 days from 

April 28, 1986, 2 days after the start of releases from the Chernobyl accident, until May 15. The mean 

activity concentration of 241Am during this period was 40 μBq/m3

 (1.1 fCi/m3) and the mean total 

radionuclide activity was 20 Bq/m3

 (0.54 nCi/m3) (Knatko et al. 1993). Debris from the Chernobyl 

accident arrived in Denmark 1.5 days after the explosion. Air samples collected at Roskilde, Denmark on 

April 27–28, contained a mean air concentration of 241Am of 5.2 μBq/m3

 (0.14 fCi/m3). In May 1986, the 

mean concentration was 11 μBq/m3

 (0.30 fCi/m3) (Aarkrog 1988). Whereas debris from nuclear weapons 

testing is injected into the stratosphere, debris from Chernobyl was injected into the troposphere. As the 

mean residence time in the troposphere is 20–40 days, it would appear that the fallout would have 

decreased to very low levels by the end of 1986. However, from the levels of other radioactive elements, 

this was not the case. Sequential extraction studies were performed on aerosols collected in Lithuania 

after dust storms in September 1992 carried radioactive aerosols to the region from contaminated areas of 

the Ukraine and Belarus. The fraction distribution of 241Am in the aerosol samples was approximately 

(fraction, percent): organically-bound, 18%; oxide-bound, 10%; acid-soluble, 36%; and residual, 32% 

(Lujaniene et al. 1999). Little americium was found in the more readily extractable ‘exchangeable and 

water soluble’ and ‘specifically adsorbed’ fractions. 

The accident at the Three Mile Island nuclear reactor in March 1979 resulted in contamination of the 

containment and auxiliary buildings. An aerosol sample from the auxiliary building obtained by filtering 

about 1.4x109

 cm3 of air through a fiberglass filter for 8 days contained an estimated total transuranic 

actinide radioactivity of 13 Bq (350 pCi), for an average concentration of 0.0093 Bq/m3

 (0.25 pCi/m3) 

(assuming no oversampling in the confined space) of which 241Am was the major contributor (Kanapilly 

et al. 1983). 

Air monitoring of 241Am was started at Hanford in 1993 to estimate regional background concentrations 

of the radionuclide before large-scale remediation work commenced (PNL 2000). Maximum and mean 

onsite levels of 241Am were 0.50 and 0.46 aCi/m3

 (0.019 and 0.017 μBq/m3) in 1994 compared with 

0.90 and 0.41 aCi/m3

 (0.033 and 0.015 μBq/m3) in 1993. Concentrations were not measurable at 

perimeter sites or at distant community-operated surveillance stations in 1994 (PNL 1995). 

Annual average 241Am air concentrations of 2.9x10-5, 1.4x10-5, and 0.55x10-5 pCi/m3

 (1.1, 0.52, and 

0.20 μBq/m3

) at the 100-K Area, and 2.5x10-5, 1.6x10-5, and 0.32x10-5 pCi/m3 (0.93, 0.59, and 

0.12 μBq/m3

) at the 200-East Area of the Hanford site were measured in 1999, 2000, and 2001, 
 

 

AMERICIUM 151 

6. POTENTIAL FOR HUMAN EXPOSURE 

respectively. No data were reported for 241Am levels measured at distant community sites. Average gross 

alpha concentrations in air on the Hanford Site in 1999, 2000, and 2001 were comparable to levels 

measured at distance stations. These data indicate that the onsite levels were likely to be due to natural 

sources and worldwide radioactive fallout (PNNL 2000, 2001, 2002). 241Am was detected in 15 quarterly 

air samples measured at distant sites, boundary sites, and the INEEL site in 2002. Concentrations ranged 

from 1.6x10-12 to 8.4x10-12 pCi/mL of air (5.9x10-8–31x10-8 μBq/mL). 241Am was not detected in the 

other 16 samples. Concentrations were within historical measurements and were below regulatory 

standards (DOE 2003b). 

In an attempt to obtain background 241Am concentrations around the Waste Isolation Pilot Plant (WIPP) 

in southeastern New Mexico, a plant developed for demonstrating the safe disposal of transuranic waste, 

high volume samples were obtained continuously over a 14-day period between February 23 and 

May 6, 1996 1 km from the facility. Samplers concurrently obtained total suspended solids (TSP) and 

particles >10 μm (PM10) at a 5-m level elevation and PM10 at a 2-m level. The activities of 241Am were 

8±2, 6±2, and 11±1 nBq/m3

 (0.2±0.05, 0.16±0.054, and 0.31±0.03 aCi/m3) in the PM10-2 m, PM10-5 m, 

and TSP-5 m samples, respectively (Lee et al. 1998). Approximately 50% of the 241Am activity 

concentration was in the PM10 fraction. Using values for the 239,240Pu concentrations measured at the site 

and those obtained in the early 1980s and estimated mean residence times for Pu in the troposphere and 

stratosphere, it is likely that the observed 241Am levels reflect resuspension of dust contamination at the 

WIPP site and not background 241Am levels. Present background levels result from past atmospheric 

nuclear testing and would be fairly uniform throughout the northern hemisphere. 

6.4.2 Water 

241Am may enter surface water from nuclear power plants sited on the shores. A region of possible 

concentration is the Great Lakes where 35 nuclear facilities are located in the lakes basin. A sample of 

water from Lake Ontario collected in 1985 and filtered through a 0.45-μm Millipore filter contained 

0.3 mBq 241Am/L (8 fCi/L) (Platford and Joshi 1986). A few water samples from the Savannah River, 

which received runoff and discharges from the DOE Savannah River Plant, contained 0.05 fCi 241Am/L 

(2 μBq/L), about the same levels as other American rivers (DOE 1980). 

In some surface waters that have been contaminated by waste discharge, the concentrations of americium 

may be higher than background levels. For example, at times, measurable levels of 241Am have been 
 

AMERICIUM 152 

6. POTENTIAL FOR HUMAN EXPOSURE 

detected in the creek where waste water is discharged from Argonne National Laboratory’s treatment 

plant. However, this creek is not used for drinking water and no 241Am has been detected in the Des 

Plains River into which it empties (ANL 1999). While 241Am is associated with waste from the Hanford 

site operations, concentrations in groundwater were considered low (no value was given) and were not 

discussed in the PNNL (2002) report. The 1995–1996 levels of 241Am in rivers and lakes in the exclusion 

zone of the Chernobyl Nuclear Power Plant ranged from 20 to 200 μBq/L (0.5–5 fCi/L) with 70% of the 

radioactivity being contained in the particulate phase (Matsunaga et al. 1998). The particles appear to 

have originated from the erosion of surface soil in the area. 

The concentration of 241Am in filtered seawater is very variable. Some 241Am levels (filtered through a 

0.22 μm filter) are (site, date, and concentration): Arctic Ocean, 7/81, 1.77 μBq/L (0.048 fCi/L); English 

Chanel, 4/85, 4.96 μBq/L (0.13 fCi/L); and Eastern Irish Sea, 4/84, 4,840 μBq/L (131 fCi/L) (Lovett et al. 

1990). 241Am concentrations in filtered seawater in the North Channel of the Irish Sea were about 

200 and 120 mBq/m3

 (5.4 and 3.2 pCi/m3) in 1979 and 1986, respectively (Pattenden and McKay 1994). 

Because of the higher sediment load, near shore water generally has a larger fraction of americium bound 

to particles, and therefore, seawater from the northern coast of Scotland (which is impacted by the United 

Kingdom Atomic Energy Agency [UKAEA] Technology Dounreay Establishment, a nuclear research and 

development facility at Dounreay, Scotland) shows a large variation in near-shore concentrations (see 

Table 6-3). Levels were much higher in the immediate vicinity of Dounreay than elsewhere along the 

coast. The 1984 level was unusually high because the monthly discharge from the plant before the 

sampling was 40 times the mean monthly level. Time series measurements on seaweeds and winkles 

show that the americium levels peaked in the early 1980s and then declined by 1989, when levels were 

the lowest they had been in 12 years. In comparison, offshore 241Am levels in surface seawater of the 

North Sea and North Atlantic Ocean has remained relatively constant, at around 10 Bq/m3

 (270 pCi/m3), 

between 1976 and 1988 (Pattenden and McKay 1994). Nearshore levels of 241Am were much greater than 

offshore concentrations, and the activity in the dissolved and particle-associated fractions were broadly 

similar. 

Mururoa and Fangataufa Atolls were used from 1975 to 1996 for underground testing of nuclear weapons. 

Of the nine sites at Mururoa sampled for underground water, two, Aristee and Ceto, had measurable 

241Am concentrations, 0.064 and 0.104 mBq/L (1.7 and 2.8 fCi/L), respectively. The remaining seven 

sites at Mururoa and the two sites at Fangautaufa had 241Am had concentrations below the detection limit 

(<0.002–<0.008 mBq/L [<0.05–<0.2 fCi/L]). At Aristee and Ceto, the 241Am concentrations in the 

particle fraction of groundwater samples were 0.037 and 0.114 mBq/L (1.0 and 3.08 fCi/L) of filtered 
 

 

 

 

 

 

 

 

 

 

AMERICIUM 153 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-3. Concentrations of 241Am in Water 

Concentration 

Number of 

Site/sample type Year samples (mBq/m3

) (pCi/m3) Type 

Dounreay, Scotland (north coast) near U.K. AEA Technology Dounreay Establishment R&D (nuclear 

reactor, reprocessing) 

Filtered seawater 1984 13 6,058±9,912 164±268 Mean±SD 

(0.45 μm) 

1985 16 36±18 0.97±0.49 Mean±SD 

1986 14 47±62 1.3±1.7 Mean±SD 

1987 30 15±17 0.41±0.46 Mean±SD 

Unfiltered 1986 14 110±147 3.0±4.0 Mean±SD 

seawater 

1987 30 35±65 0.95±1.8 Mean±SD 

Scotland mainland and some island coasts (near shore) 

Filtered seawater 

(13 sites) 

1982 NR 1.9–140 0.051–3.78 Range 

Cruise of RV Scotia, Orkney Islands, and northeast Scottish coast 

Near surface 

unfiltered 

seawater 

1982 NR 6–270 0.2–7.3 Range 

30–40 m 

unfiltered 

seawater 

NR 220–650 5.9–17.6 Range 

NR = not reported; R&D = Research and Development; SD = standard deviation; U.K. AEA = United Kingdom 

Atomic Energy Agency 

Source: Pattenden and McKay 1994 
 

AMERICIUM 154 

6. POTENTIAL FOR HUMAN EXPOSURE 

water, respectively, and at the remaining seven sites at Mururoa, the 241Am concentrations were below the 

detection limit (<0.003–<0.001 mBq/L [0.08–0.03 fCi/L]. At the two Fangatufa Atoll sites, 241Am 

concentrations were 0.016 and 0.006 mBq/L (0.43 and 0.16 fCi/L) of filtered water (Mulsow et al. 1999). 

The concentration of 241Am in New York City tap water in 1974 was estimated to be 0.03 fCi/L (1 μBq/L) 

based on the average 241Am/239,240Pu ratio of 0.10 obtained in 1975–1976 and the 1974 239,240Pu 

concentration (Bennett 1979). 

6.4.3 Sediment and Soil 

Soil may become contaminated with 241Am from the deposition of the element released to the atmosphere 

from nuclear weapons’ testing and nuclear reactors, or secondarily, from the resuspension of 

contaminated soil. 241Am levels may then increase due to ingrowth from the decay of 241Pu (half-life 

14.4 years). Soil surveillance provides baseline information with which unplanned releases can be 

compared, and long-term contamination trends can be determined. It also provides information about 

direct exposure to humans (inhalation of dust, ingestion of dirt) as well as potential sources of exposure 

(contamination of groundwater, uptake into plants and animals). The concentrations of 241Am in soil 

samples from the northeastern United States from 1970 to 1974 are shown in Table 6-1. The areal 

activity at the sampling date ranged from 0.37 to 0.49 mCi/km2

 (14–18 MBq/km2), which compares well 

with that calculated from estimated values obtained from releases from nuclear weapons testing combined 

with an atmospheric transport model (Bennett 1979). 241Am in soil resulting from cumulative deposition 

in the New York region was estimated as being fairly constant since about 1969 at about 0.060 mCi/km2 

(2 MBq/km2

), whereas 241Pu peaked at about 20.1 mCi/km2 (744 MBq/km2) in 1965. The decay of 241Pu 

adds to the cumulative deposits of 241Am in soil, bringing the total 241Am to about 0.8 mCi/km2 

(30 MBq/km2

). The 241Am inventory should reach a maximum of 0.88 mCi/km2 (33 MBq/km2) in 2035. 

The radioactive decay of 241Am will then exceed its ingrowth, and the cumulative deposits of 241Am will 

then slowly be depleted. 

Nuclear Power Plants. EPRI (1981) conducted a survey of transuranic radionuclides in the terrestrial 

environs of nuclear power plants in 1978–1979. The plants included two PWRs and two BWRs that were 

of modern design and had been in operation at least 3 years. The 241Am levels in soil samples collected 

around all of the power plants were indistinguishable from fallout background. 
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6. POTENTIAL FOR HUMAN EXPOSURE 

A survey of Big Trees Park was conducted in 1998 after soil samples taken in the park in 1993 and 1995 

revealed higher-than-expected concentrations of plutonium (LLNL 1999). Big Trees Park is a public park 

in the city of Livermore, California located about one-half mile from Lawrence Livermore National 

Laboratory (LLNL). The pattern of 241Am distribution was the same as that for plutonium with levels 

significantly higher inside ornamental tree wells than outside the wells or at depths. Activity levels were 

well below EPA’s residential preliminary remediation goal of 2.5 pCi/g (93 mBq/g), which may have 

necessitated cleanup. The source of the contamination was most likely sewage sludge from LLNL that 

was applied to the ornamental trees in the park. 

Great Britain. In 1993, the Ministry of Agriculture, Fisheries, and Food (MAFF) in the United Kingdom 

systematically surveyed the concentrations of 241Am in soil and grass samples near 18 nuclear sites in 

England and Wales (Sanchez et al. 1996). 241Am was detected in most soil samples; the range was 0.03– 

0.40 Bq/kg (0.8–11 pCi/kg) soil; three samples were below the detection limit. Sanchez et al. (1998) 

measured the 241Am activity in root mat samples from tide washed pastures in 17 estuaries spanning the 

eastern seaboard of the Irish Sea from Solway in northwest England to David’s Head in southern Wales. 

Fourteen of the pastures had detectable levels of 241Am with median levels of 64–5,570 Bq/kg (1.7– 

150 nCi/kg) dry weight and individual samples of 14–10,230 Bq/kg (0.38–276 nCi/kg) dry weight. 241Am 

accumulations in soils (to 10–15 cm depth) near Greeny Geo, Scotland ranged from 2,000 to 

11,400 Bq/m2 (54–308 nCi/m2

) (Pattenden and McKay 1994). This coastal area is contaminated by foam 

or spume that forms in seawater in rocky inlets and blows over the land. The seawater in the area 

receives discharges from the BNFL Sellafield facility. Sediment from two Harbors on the Isle of Mann, 

which is impacted by the reprocessing plant at Sellafield in the United Kingdom, contained 241Am ranging 

from <2.0 to 8.1 Bq/kg (<50–220 pCi/kg) dry weight during 1990–1993 (McKenna and Longworth 

1995). Nearshore sediment core samples taken at several sites off the northern coast of Scotland (see 

Table 6-1) had fairly constant 241Am levels with depth showing that mixing had occurred to a depth of 

74 cm (Pattenden and McKay 1994). 241Am concentrations found in a sand dune ecosystem near the 

British Nuclear Fuels reprocessing plant at Sellafield, Cumbria United Kingdom, were 183–250 Bq/kg 

(4.95–6.76 nCi/kg) (Copplestone et al. 2001). 

Los Alamos National Laboratory. Soil surveillance is conducted at national laboratories to monitor the 

levels of radionuclides and ascertain their possible migration. Data from such a program at the LANL in 

1974–1996 was evaluated to ascertain whether there were changes in radionuclide concentrations during 

that period and whether changes could be ascribed to air emissions and fugitive dust (Fresquez et al. 

1998a). Surface samples (0–5 cm) were obtained on-site and from perimeter and background sites. 
AMERICIUM 156 

6. POTENTIAL FOR HUMAN EXPOSURE 

Americium levels at LANL sites were significantly higher than at background sites. The mean 1974– 

1996 concentrations of 241Am in soil at LANL and background sites were 0.011±0.006 and 

0.006±0.002 pCi/g (0.41±0.22 and 0.22±0.07 mBq/g) dry weight, respectively. Sediment 2.1 km 

downstream of a National Pollutant Discharge Elimination System (NPDES) outfall in Mortandad 

Canyon, Los Alamos County, New Mexico in 1994 contained high levels, 8.93 pCi/g (330 Bq/g) dry 

weight, of 241Am. However, the 241Am concentrations in sediment upstream of the outfall and 4.0 km 

downstream below a sediment trap were below upper limits of regional background levels, 0.023 pCi/g 

(0.85 Bq/g) dry weight. (Bennett et al. 1996). 

Brookhaven National Laboratory. Sediment samples were analyzed from the Peconic River system on 

Long Island, NY, downstream of Brookhaven National Laboratory (BNL). Near the sewage treatment 

plant closest to BNL, respective mean concentrations (dry weight) of 241Am from three locations at four 

depth intervals (0.00-0.06, 0.06-0.15, 0.15-0.24, and 0.24-0.37 m) were 31, 24, 5.6, and 1.7 Bq/kg (0.83, 

0.64, 0.15, and 0.045 nCi/kg). At one location at the BNL property boundary mean concentrations of 

241Am were 18, 2.8, 0.29, and 0.28 Bq/kg (0.49, 0.076, 0.0078, and 0.0076 pCi/kg), respectively, for the 

same depth intervals. Sediment samples from a control river, Connetquot River, were 1.4 and 0.74 Bq/kg 

(0.038 and 0.020 nCi/kg) (0.00-0.06 m) and 0.30 and 0.081 Bq/kg (0.0081 and 0.00022 nCi/kg) 

(0.06-0.15 m) in two locations (Rapiejko et al. 2001). 

Rocky Flats. Rocky Flats (RF), near Golden, Colorado, was contaminated with 241Am as a result of past 

waste storage practices, which resulted in drums leaking contaminated oil (Litaor et al. 1994). Sampling 

was performed in four regions of expected actinide activity (26 pits) east of RF. Activity decreased with 

increasing distance east of the former storage site and was predominantly confined to the upper 12 inches 

of soil. The mean 241Am activities in the upper 3 inches of soil in the four regions were 1,653, 47.4, 2.9, 

and 3.7 Bq/kg (44.6, 1.28, 0.078, and 0.100 nCi/kg). In the region with the highest activity, the mean 

concentrations were 1,653, 1,063, 758, 595, 122, and 2.6 Bq/kg (44.6, 28.7, 20.5, 16.1, 3.3, and 

0.070 nCi/kg) at depths of 0–3, 3–6, 6–9, 9–12, 12–18, and 36–48 inches, respectively, indicating 

significant retention near the surface (Litaor et al. 1994). Soil sampled at 118 plots around RF contained 

241Am ranging from 0.18 to 9,990 Bq/kg (0.0049–270 nCi/kg) with a mean and SD of 321 and 

1,143 Bq/kg (8.67 and 30.9 nCi/kg), respectively (Litaor 1995). The distribution pattern reflects wind 

dispersion consistent with the prevailing winds at RF. 

Idaho National Engineering and Environmental Laboratory. 241Am contamination occurred outside the 

Subsurface Disposal Area (SDA) to a distance of 2,500 meters at the INEEL. Maximum concentrations 
 

AMERICIUM 157 

6. POTENTIAL FOR HUMAN EXPOSURE 

of 241Am, 2,048 nCi/m2 (75.8 kBq/m2) in the 0–4 cm surface layer, near the perimeter of the SDA, were 

thought to be due to flooding and to localized drainage of water, while low concentrations away from the 

SDA perimeter area resulted from wind transport (Markham et al. 1978). With the exception of samples 

collected from the Waste Experimental Reduction Facility, soil samples collected in 2002 from within the 

INEEL ranged from not detected to 0.889 pCi/ g (dry weight) and were within the background range for 

the INEEL and surrounding areas. These levels were attributable to past fallout. Soil samples collected 

from the perimeter and off-site around INEEL ranged from approximately 0.001 to 0.015 pCi/g (dry 

weight). There were no significant differences in 241Am concentrations between boundary and distant 

samples, indicating that INEEL inputs did not contribute significantly to these concentrations (DOE 

2003b). 

Superfund National Priorities List (NPL) Sites. 241Am has been detected in soil at 5 of the 1,636 NPL 

hazardous waste sites where americium has been identified in some environmental compartment (HazDat 

2004); it was found in sediment at two of these sites. The distribution of Superfund NPL sites is shown in 

Figure 6-1. 

Chernobyl. 241Am, in five samples of surface soil collected 1.5–15 km from the Chernobyl accident in 

July 1987, was predominantly in the 0.005–0.25 mm size fraction of soil, which comprised 65% of the 

mass (Berezhnoi et al. 1991). 

Bikini Atoll. Bikini Atoll was the site of 23 nuclear detonations between 1946 and 1958. Surface soil 

collected at 20 sites on Bikini Atoll in 1972 contained 1.2–45 pCi/g (0.044–1.7 Bq/g) of 241Am (Nevissi et 

al. 1976). This level will increase for several decades as a result of ingrowth from 241Pu before it begins 

to decrease, unless weathering causes the americium and plutonium to spread away from the surface and 

cause the concentration to decrease. 

More recent mean surface soil (0–5 cm) 241Am concentrations were 0.30 and 0.22 Bq/g (8 and 5.9 pCi/g) 

for the interior of the island and the village area, respectively (Robison et al. 1997b). This indicates either 

that soil samples were collected at too great a depth (adding uncontaminated soil from deeper layers) or 

that weathering of surface media carried contamination into deeper layers (results in decreased 

concentrations for the samples). Concentrations of 241Am in sediment from the surface of the lagoon floor 

ranged from 0.010 to >12 Bq/g from (0.27 to >320 pCi/g) with 1.1 and 0.60 Bg/g (30 and 16 pCi/g) being 

the average concentrations associated with fine and coarse sediments, respectively. The highest 241Am 

concentrations were found in surface sediments (0–2 cm) in the northwestern area of the lagoon, which 
 

 

 

AMERICIUM 158 

6. POTENTIAL FOR HUMAN EXPOSURE 

was adjacent to the locations of the largest explosions. The 241Am concentrations were reported to 

decrease from north to south and from east to west (Robison and Noshkin 1999). 

Alaska. The National Oceanic and Atmospheric Administration (NOAA) conducted a study in the 

Beaufort Sea in northwestern Alaska during the summer of 1993 to ascertain the levels of radionuclide 

activity in the U.S. Arctic (DOE 1997). 241Am was present in sediment at detectable levels at 8 of the 

13 sites sampled, ranging from 0.06 to 0.12 Bq/kg (1.6–3.2 pCi/kg). From the average ratio of 

241Am:239+240Pu, it was concluded that the americium originated from global fallout. 

The Great Lakes. In 1976, sediment at several sites was sampled in Lakes Erie and Ontario. 241Am was 

detected at only one site in Lake Erie, a site influenced by the Nuclear Fuels Reprocessing plant at West 

Valley, New York (U.S. Energy Research and Development Administration 1977). Levels of 241Am 

increased with depth at concentrations of 3.4, 7.9, 11.1, and 11.8 Bq/kg (92, 210, 300, and 319 pCi/kg) 

dry weight at 0–2, 2–4, 4-6, and 6–8 cm, respectively. 

Arctic. 241Am concentrations were measured in the surface marine sediments collected in the 

Spitsbergen-Bear Island region, located between the Arctic Ocean, Barents, Greenland, and Norwegian 

Seas, an area important to Norwegian fisheries. Highest concentrations (dry weight) were found in the 

Spitsbergen area, ranging from 0.37 to 0.85 Bq/kg (10–23 pCi/kg). Lower levels were found in the 

deeper parts of the Norwegian Sea, ranging from 0.30 to 0.007 Bq/kg (8.1–0.2 pCi/kg) (Heldal et al. 

2002). 

6.4.4 Other Environmental Media 

Concentrations of 241Am have been determined in various foods (Table 6-4) and biota (Table 6-5), some 

of which may be eaten by humans. Levels in food items and animals include those from diet studies as 

well as from areas contaminated by nuclear weapons testing and fuel reprocessing. The highest levels 

were in clams, crabs, and lobsters (up to 0.46 Bq/kg [12 pCi/kg]). In studies at DOE facilities and in the 

vicinity of the BNFL reprocessing plant at Sellafield and the Ravenglass Estuary, where pastures are 

subject to tidal inundations with seawater receiving discharges from the plant, results clearly show the 

effect on animals from feeding on contaminated pasture land (Arthur and Janke 1986; Bradford and 

Curtis 1984; DOE 1979c; Janke and Arthur 1985). 
 

AMERICIUM 159 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-4. Average Concentrations of 241Am in Food 

Concentrationa 

Local Food mBq/kg fCi/kg Reference 

Bikini Atollb

, U.S. Nuclear Test Site from 1946 to 1958, including BRAVO 

explosion on 3/1/54 

Reef fish
 

Tuna
 

Mahi mahi
 

Marine crabs
 

Lobster
 

Clams
 

Coconut crabs
 

Land crabs
 

Octopus
 

Turtle
 

Chicken, muscle
 

Pork, muscle
 

Eggs, chicken
 

Pandanus fruit (n=69)
 

Breadfruit (n=41)
 

Coconut juice, drinking 

(n=747)
 

Coconut meat, drinking 

(n=812)
 

Copra meat (n=188)
 

Papaya (n=93)
 

Squash (n=53)
 

Pumpkin 

Banana (n=39)
 

Citrus
 

Rain water
 

Well water
 

6.5 180
 

1.3 35
 

1.3 35
 

26 700
 

26 700
 

460 12,000
 

28 760
 

28 760
 

6.5 180
 

6.5 180
 

6.0 160
 

6.0 160
 

6.0 160
 

3.8 100
 

1.2 32
 

8.5 230
 

3.6 97
 

1.1 30
 

0.36 9.7 

3.0 81
 

3.0 81
 

0.36 9.7 

0.36 9.7 

0.0037 0.10 

0.044 1.2 

Robison et al. 

1997b 
AMERICIUM 160 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-4. Average Concentrations of 241Am in Food 

Concentrationa 

Local Food mBq/kg fCi/kg Reference 

Northern Marshall Islands Radiological Survey (NMIRS)c

, fallout from U.S. Robison et al. 

atmospheric weapons testing from 1946 to 1958, including BRAVO explosion on 1997a 

3/1/54 

Reef fish, muscle; <0.23–1.4 <6.2–38 

11 atolls/islands
 

Pelagic fish, muscle; <0.14–0.27 <3.8–7.3
 

9 atolls/islands
 

Clams, soft parts; <1.4–46 <38–1,200
 

10 atolls/islands
 

Pork; 6 atolls/islands <0.11–2.8 <3.0–76
 

Chicken; 4 atolls/islands 1.2–4.1 32–110
 

Coconut crab; 4.3–28 120–760
 

2 atolls/islands
 

Drinking coconut meat; <1.3 <35 

5 atolls/islands
 

Copra meat; <0.42–7.4 <11–200
 

10 atolls/islands
 

Pandanus; <0.23–8.5 <6.2–230
 

12 atolls/islands
 

Breadfruit; 7 atolls/islands 0.26–8.2 7.0–220
 

Total Diet Study—New York, 1974d Bennett 1979 

Shellfish 0.48±0.15 13±4 

Whole grain products 0.074±0.044 2.0±1.2 

Bakery products 0.063±0.02 1.7±0.6 

Fresh vegetables 0.048±0.015 1.3±0.4 

Fresh fruit 0.041±0.015 1.1±0.4 

Root vegetables 0.030±0.007 0.80±0.19 

Dry beans 0.022±0.012 0.60±0.34 

Poultry 0.019±0.011 0.52±0.31 

Potatoes (peeled) 0.013±0.002 0.36±0.06 

Flour 0.013±0.007 0.36±0.18 

Fruit juice 0.011±0.006 0.29±0.16 
AMERICIUM 161 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-4. Average Concentrations of 241Am in Food 

Concentrationa 

Local Food mBq/kg fCi/kg Reference 

Meat 0.010±0.006 0.28±0.17 

Rice 0.010±0.012 0.27±0.34 

Milk 0.0093±0.0004 0.25±0.01 

Fresh fish 0.0089±0.0030 0.24±0.08 

Eggs 0.0059±0.002 0.16±0.06 

Macaroni 0.0059±0.009 0.16±0.25 

Canned fruit 0.0026±0.0033 0.07±0.09 

Near Sellafield, England, 1994 Fulker et al. 1998 

Honey 0.0007 0.02 

Blackberry 0.043 1.2 

Pheasant 0.029 0.78 

Mushrooms 0.0065 0.18 

a

Concentrations on a wet or fresh weight basis. Concentrations originally expressed in mBq/kg unless otherwise
 

indicated. 

b

Terrestrial food is from a continuous monitoring program in 1975–1993; marine food is from a 1988 report. 

c

Decay correction to 1996. 

d

Concentrations originally expressed as pCi/kg.
 
 

 

AMERICIUM	 162 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-5. Concentrations of 241Am in Fauna 

Species Sample Location Concentration Unitsa Type Reference 

Fish 

Farallon Islands Nuclear Waste Disposal Site (FINWDS) and Point Arena (reference site), Suchanek 

1986–1987 et al. 1996 

Dover sole Flesh FINWDS 1,630±2,360 mBq/kg Mean±SD 

(n=3) w.w. 

Point Arena 126±88 

(n=6) 

Sablefish Flesh FINWDS 2,850 mBq/kg Mean±SD 

(n=1) w.w. 

Point Arena 

(n=5) 1,000±1,400 

Thornyheads Flesh FINWDS 186±35 mBq/kg Mean±SD 

(n=2) w.w. 

Point Arena 299±157 

(n=3) 

Vicinity of Los Alamos National Laboratory, 1997, Bottom-feeding fish (n=10/site) Fresquez 

et al. 1999 

Fish (2 sites) Muscle+bone Reservoirs 1.7 (19.8) 10-5 pCi/g Mean (SD) 

d.w. 

Fish (4 sites) Muscle+bone Rio Grande 84.1 (54.6) 10-5 pCi/g Mean (SD) 

d.w. 

Fish (5 sites) Viscera Rio Grande 31.2–198.0 10-5 pCi/g Range of 

d.w. means 

Fish from Irish ports possibly impacted by Sellafield, 1988–1997	 Ryan et al. 

1999 

Plaice Edible 0.4–144 mBq/kg Range of 

portion w.w. means 

Whiting Edible 0.42–2.8 mBq/kg Range of 

portion w.w. means 

Cod Edible 0.62–26 mBq/kg Range of 

portion w.w. means 

Crustacea 

Fish ports possibly impacted by Sellafield, 1988–1997 Ryan et al. 

1999 

Prawns Edible 12–138 mBq/kg Range of 

portion w.w. means 

North Eastern Irish Sea, Sellafield coastal area, U.K., commercially caught crabs and Swift and 

European lobsters, 1997 Nicholson 

2001 

crab (n=34) Edible 1.7(0.8) Bq/kg Mean(SD) 

portion w.w. 

lobster Edible 8.3(11.3) Bq/kg Mean(SD) 

(n=35) portion w.w. 
 

 

AMERICIUM 163 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-5. Concentrations of 241Am in Fauna 

Species Sample Location Concentration Unitsa Type 

Bivalves 

Farallon Islands Nuclear Waste Dump Site (FINWDS) and Point Arena (reference site), 

1986–1987 

Reference 

Suchanek 

et al. 1996 

Mussels Flesh FINWDS 

(n=1) 

6 mBq/kg 

w.w. 

Mean 

Mussels Flesh Point Arena 126±88 Bq/kg d.w. Mean±SD 

(n=2) 

U.S. Mussels Watch, 1976–1978 (East Coast: Maine-Virginia; East/Gulf Coast: VirginiaTexas; West Coast: Washington-California) 

EPA 1984 

Mussels and 

oysters 

Flesh East coast 0.43–0.65 

(0.03–1.7) 

Bq/kg d.w. Range of 

means 

(range) 

Mussels and 

oysters 

Flesh East/Gulf 

coasts 

0.32–0.60 

(0.03–1.95) 

Bq/kg d.w. Range of 

means 

(range) 

Mussels and Flesh West coast 0.49 Bq/kg d.w. Range of 

oysters (0.14–18.5) means 

(range) 

Carlinford, Ireland (port city), impact from Sellafield Reprocessing Plant, 1991–1997 Ryan et al. 

1999 

Mussels Edible 

portion 

 <11–109 (69) mBq/kg 

w.w. 

Range of 

means 

(median) 

Oysters Edible 14–27 mBq/kg Range of 

portion w.w. means 

Irish Sea, site impacted by Windscale Reprocessing Plant and reference sites, 1977 EPA 1984 

Mussels Flesh Isle of Man 550 (55) Bq/kg d.w. Mean (SD) 

Mussels Flesh Ravenglass 

estuary 

63.9x103 

(6,390) 

Bq/kg d.w. Mean (SD) 

Mussels Flesh Ebro 0.52–0.88 Bq/kg d.w. Range of 

(2 sites) estuary, means 

Spain 

Sea 

mammals 

North Rona and Isle of May, Scotland, Possible impact from Sellafield and Chernobyl, 

1987 

Anderson et 

al. 1990 

Grey seals 

(n=8) 

Milk <0.2–<0.3 Bq/L Range 

Grey seals 

(n=2) 

Liver <0.3 Bq/kg f.w. Range 

Grey seals 

(n=3) 

Muscle <0.3 Bq/kg f.w. Range 
 

AMERICIUM 164 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-5. Concentrations of 241Am in Fauna 

Species Sample Location Concentration Unitsa

Mammals 

Halla, Finland, reindeer graze on lichen impacted by Chernobyl fallout 

Type Reference 

Paatero 

and 

Jaakkola 

1998 

Reindeer Meat 0.014 (0.003) Bq/kg d.w. Mean (SD) 

Reindeer Liver 0.013 (0.004) Bq/kg d.w. Mean (SD) 

Reindeer Kidney 0.0043 

(0.0010) 

Bq/kg d.w. Mean (SD) 

Material Disposal Area G, Los Alamos National Laboratory, New Mexico, mule deer and 

Rocky Mountain elk, 1991–1998 

Ferenbaugh 

et al 2002 

Deer (n=11) Muscle 0.28 (0.22) mBq/kg 

w.w. 

Mean (SD) 

Elk (n=21) Muscle 0.47 (0.34) mBq/kg 

w.w. 

Mean (SD) 

Nevada Test Site: Area 13 (outer compound) and near Area 13, but outside the area, 

1973–1976 

DOE 1979 

Cattle 

(11 animals) 

Muscle Area 13 0.020–0.17 pCi/kg 

w.w. 

Range 

Cattle 

(4 animals) 

Muscle Near Areas 

13 

<0.05–<0.11 pCi/kg 

w.w. 

Range 

Fox (adult) Muscle Area 13 25.0 pCi/kg 

w.w. 

Fox (adult) Muscle Area 13 17.0 pCi/kg 

w.w. 

Coyote Muscle Area 13 4.7 pCi/kg 

w.w. 

Vicinity of Sellafield and the Ravenglass Estuary, England, 1977–1982 Bradford 

and Curtis 

1984 

Cattle Liver Sellafield 

(n=1) 

Ravenglass 

(n=3) 

Control 

(n=2) 

0.23 

0.037–0.48 

0.003, 0.005 

Bq/kg f.w. 

Range 

Cattle Meat Ravenglass 0.002, 0.012 Bq/kg f.w. 

(n=2) 

Control 0.008 

(n=1) 
AMERICIUM 

6. POTENTIAL FOR HUMAN EXPOSURE 

165 

Table 6-5. Concentrations of 241Am in Fauna 

Species Sample Location Concentration Unitsa Type Reference 

Cattle Lung Ravenglass 0.05–0.085 Bq/kg f.w. Range 

(n=3) 

Control 0.003, 0.002 (n=2) 

Cattle Bone Ravenglass 0.25–0.29 Bq/kg f.w. Range 

(n=3) 

Control 0.013, 0.018 (n=2) 

Sheep Meat Ravenglass 0.040–0.064 Bq/kg f.w. Range 

(n=3) 

Control 0.0038 

(n=1) 

Sheep Liver Ravenglass 2.6–6.6 Bq/kg f.w. Range 

(n=3) 

Control 0.006–0.0012 

(n=2) 

Sheep Lung Ravenglass 0.018–0.24 Bq/kg f.w. Range 

(n=3) 

Control 0.017 

(n=1) 

Sheep Bone Ravenglass 0.79–1.7 Bq/kg f.w. Range 

(n=3) 

Control 0.006 

(n=1) 

Idaho National Engineering Laboratory–Subsurface Disposal Area (SDA) and control 

area, 1978–1979 

Coyote Feces SDA (n=24) 0.4±0.9 pCi/kg Mean±SD 

Control 0.003±0.002 w.w. 

(n=12) 

Cottontail Carcass SDA (n=10) 0.010±0.009 pCi/kg Mean±SD 

rabbit Control 0.001±0.001 w.w. 

(n=5) 

Cottontail Hide SDA (n=10) 0.029±0.046 pCi/kg Mean±SD 

rabbit Control 0.002±0.001 w.w. 

(n=5) 

Deer mice Carcass	 SDA (n=21) 0.010±0.02 pCi/kg Mean±SD 

Control 0.003±0.002 w.w. 

(n=5) 

Arthur and 

Janke 

1986; 

Janke and 

Arthur 1985 
 

 

AMERICIUM	 166 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-5. Concentrations of 241Am in Fauna 

Species Sample Location Concentration Unitsa Type Reference 

Deer mice Hide SDA (n=21) 0.27±0.83 pCi/kg Mean±SD 

Control 0.039±0.050 w.w. 

(n=5) 

Invertebrates 

Idaho National Engineering Laboratory, Subsurface Disposal Area (SDA) and control Arthur and 

area, 1978–1979 Janke 1986 

Invertebrates Composite SDA (n=3) 0.022±0.020 pCi/kg Mean±SD 

Control <0.004 w.w. 

(n=1) 

a

conversion: 1 Ci=3.7x1010 Bq=0.037 TBq or 1 Bq=2.7x10-11 Ci=27 pCi 

d.w. = dry weight; FINWDS = Farallon Islands Nuclear Waste Dump Site; f.w. = fat weight basis; n = number of 

samples; SD = standard deviation; SDA = subsurface disposal area; w.w. = wet weight 
AMERICIUM 167 

6. POTENTIAL FOR HUMAN EXPOSURE 

As part of the U.S. Mussel Watch program, monthly samples of mussels were collected from Bodega 

Head, California and Narragansett Bay, Rhode Island in 1977 and 1978 (Goldberg 1986). The mean 

concentration of 241Am in samples ranged from 4.2 to 11.6 Bq/kg (0.11–0.31 nCi/kg) dry weight at 

Bodega Head and from 0.2 to 0.7 Bq/kg (0.005–0.02 nCi/kg) dry weight at Narragansett Bay. No 

seasonal pattern was evident. The ratio of 241Am to 239+240Pu ranged from 1.3 to 5.3 on the west coast site 

and from 0.2 to 1.0 on the east coast. A surveillance program of U.S. coastal waters involving somewhat 

over 100 sites was another component of the Mussel Watch program. The flesh of both oysters and 

mussels, collected from the three major coastlines of the United States in 1976, 1977, and 1978, was 

analyzed (EPA 1984). The results are included in Table 6-5. The levels of 241Am were higher on the 

west coast, which was ascribed to seasonal upwelling of the 241Pu- and 241Am-rich mid-depth north 

Pacific Ocean waters (affected by nuclear weapons test fallout), rather than from releases from the lowlevel nuclear waste site off the Farallon Islands. Another factor is the association of 241Am with fine 

particles and the greater exposure of west coast bivalves to open ocean fine particles than east coast 

bivalves. Paradoxically, americium does not show the same seasonal fluctuations associated with 

upwelling as plutonium; this may be due to americium’s greater adsorptivity and associated removal from 

the water column, or its slower uptake in bivalves. The NOAA conducted a study in the Beaufort Sea in 

northwestern Alaska during the summer of 1993 to ascertain the levels of radionuclide activity in the U.S. 

Arctic (DOE 1997a). As part of this study, 241Am was determined in ashed samples of a variety of biota, 

including fish, invertebrates, crustaceans, whales, seal, and ducks, collected mostly in the coastal waters 

off Barrows, Alaska and analyzed by high-resolution gamma spectroscopy. 241Am was not detectable in 

any of the samples (detection limits ≤0.6–≤80 mBq/kg [<20–<2,000 fCi/kg]). 

Fish and mussels were sampled near the Farallon Islands Nuclear Waste Dump Site (FINWDS), 

approximately 30 miles west of San Francisco and a reference site (see Table 6-5) (Suchanek et al. 1996). 

While many of the drums have been breached or are nearing their expected lifetime, no statistical 

difference was found between the levels of 241Am in the FINWDS fish and those from the reference site. 

A simple explanation is the fact that the fish species tested are quite mobile. However, 241Am levels 

found in fish samples, 1.0 and 1.5 Bq/kg (27 and 41 pCi/kg), were higher than comparable fish muscle 

reported from relatively contaminated sites such as the Pacific Testing Grounds in Micronesia and in the 

Irish Sea near the Windscale Nuclear Plant at Sellafield, none of which exceeded 0.74 Bq/kg (20 pCi/kg). 

241Am concentrations were determined in fish and shellfish collected in 1990 from fish markets in the 

vicinity of the Vandellós I nuclear power plant (NPP) on the Spanish Mediterranean coast. The 

Vandellós I NPP was decommissioned after 1989. Mean 241Am concentrations (dry weight) for large 

prawn, mollusc, red mullet, and hake collected near the Vandellós I NPP for were 62, 25, 54, and 
 

AMERICIUM 168 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.0 mBq/kg (1.7, 0.68, 1.5, and 0.16 pCi/kg), respectively. At other locations along the Catalan coast, 

mean 241Am concentrations were 5.2, 10, 3.0, and 5.2 mBq/kg (0.14, 0.27, 0.081, and 0.14 pCi/kg), 

respectively, for the same species (Sanchez-Cabeza and Molero 2000). As part of the Environmental 

Surveillance Program (at LANL), bottom-feeding fish were collected from reservoirs upstream and 

downstream from LANL in September 1997, as well as from five sites on the Rio Grande River starting at 

one site about 1 mile upstream of any stream crossing LANL land and analyzed for 241Am and other 

radionuclides (Fresquez et al. 1999). The concentration of 241Am in muscle + bone in fish collected in the 

reservoirs was significantly lower than that collected in the river (see Table 6-5). Mussel samples 

collected from two sites in the Irish Sea where the Windscale nuclear reprocessing plant is located show 

the influence of low levels of radionuclides from the nuclear fuel cycle (Table 6-5). The 241Am found in 

the mussels were orders of magnitude higher than those on the U.S. coast. The Isle of Mann site is in the 

middle of the Irish Sea about 50 km from Windscale and the Ravenglass estuary site is 16 km to the south 

of the plant. The 241Am input into the Irish Sea from fallout is dwarfed by the contribution by the 

Sellafield reprocessing facility in England. Observations from surveys of 241Am in edible parts of fish 

and shellfish sampled from commercial landings at major Irish shipping ports between 1988 and 1997 

(Table 6-5) indicate that activity levels in fish landed at northeast Irish ports have remained low, generally 

a fraction of a mBq/kg wet weight, while those in mussel, prawns, and oysters are much higher and have 

fluctuated in activity (up to 180 mBq/kg [4.9 pCi/kg] wet weight in prawns) over time (Ryan et al. 1999). 

Concentrations of 241Am in the edible portions of molluscs (Adamussium colbecki) and fish (Trematomus 

bernacchii) collected during the years 1987–1996 from Terra Nova Bay (Ross Sea) in Antarctic were 

reported to be 0.0087 and 0.0006 Bq/kg (0.24 and 0.02 pCi/kg), dry weight, respectively (Marzano et al. 

2000). 

Enewetak and Bikini Atolls were used for nuclear weapons testing by the United States between 1946 and 

1958. Log mean normal concentrations (wet weight) of 241Am found in fish muscle and invertebrate flesh 

collected since 1976 and decay corrected from collection date to October 1998 were determined. At 

Enewetak Atoll, concentrations of 241Am in reef fish, pelagic fish, mollusks, and crustaceans were 0.0050, 

0.0024, 0.0010, and <0.1 Bq/kg (0.14, 0.064, 0.027, and <2.7 pCi/kg), respectively. At Bikini Atoll, 

241Am concentrations in reef fish, pelagic fish, mollusks, and crustaceans were 0.0072, 0.0018, 0.32, and 

<0.1 Bq/kg (0.19, 0.049, 8.6, and <2.7 pCi/kg), respectively. 241Am concentrations were higher in the 

surface sediments at Bikini Atoll, ranging from 10 to >12,000 Bq/kg (0.27–>320 nCi/kg) as compared to 

Enewetak Atoll, ranging from <1 to 1,300 Bq/kg (0.027–35 nCi/kg). The authors noted that it is difficult 

to conclude that there is a difference in the mean concentrations of radionuclides in the muscles of fish 

from Bikini Atoll as compared to Enewetak Atoll, and that this supports earlier studies that found that at 
 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

Bikini and Enewetak Atolls, the transuranics in some fish may be unrelated to the environmental 

concentrations (Robison and Noshkin 1999). 

Fish samples were analyzed from the Peconic River system on Long Island, New York, downstream of 

BNL. Near the sewage treatment plant closest to BNL, mean concentrations of 241Am were 0.070 and 

0.019 Bq/kg (1.9 and 0.51 pCi/kg) in bullhead catfish and chain pickerel (whole fish), respectively. A 

mean 241Am concentration in bullhead catfish from a control river, Connetquot River, was <0.02 Bq/kg 

(<0.54 pCi/kg). In ponds farther downstream of BNL and the sewage treatment plant 241Am 

concentrations were <0.03 Bq/kg (<0.8 pCi/kg) for all fish and <0.07 Bq/kg (<2 pCi/kg) for mussel flesh 

(Rapiejko et al. 2001). 

Fifteen cattle grazing for 1,064 days on a site at the Nellis Bombing and Gunnery Range, Nevada, where 

a nuclear device was explosively destroyed 16 years previously, had 241Am levels ranging from 0.74 to 

590 mBq/kg (0.02–16 pCi/kg) wet weight, 4.4 mBq/kg (0.10 pCi/kg) geometric mean in muscle (Gilbert 

et al. 1989). Levels in liver and kidney were much higher, 72 and 11 mBq/kg (1.9 and 0.30 pCi/kg), 

geometric mean, respectively. 

In 1993, the MAFF, United Kingdom systematically surveyed the concentrations of 241Am in grass 

samples near 18 nuclear sites in England and Wales (Sanchez et al. 1996). 241Am levels in vegetation 

samples were <0.10 Bq/kg (<2.7 pCi/kg). Sanchez et al. (1998) measured the 241Am activity in vegetation 

from tide-washed pastures in 17 estuaries spanning the eastern seaboard of the Irish Sea from Solway in 

northwest England to David’s Head in southern Wales. In 11 of the pastures, the median level of 241Am 

in vegetation ranged from 14 to 575 Bq/kg (0.38–15.5 nCi/kg) dry weight; the others were <1 Bq/kg 

(<30 pCi/kg) dry weight. 241Am levels in individual samples in the 11 pastures were 13–1,260 Bq/kg 

(0.35–34 nCi/kg) dry weight. 

Brauning et al. (1986) reported radioactivity levels in municipal sludge. Sludge from Stickney, Illinois 

that was used as an organic fertilizer contained 3.3 and 1.5 fCi/g (14 and 575 Bq/kg) dry weight of 241Am 

in 1974 and 1975, respectively. Potential sources in this case were thought to be from background 

concentrations and fallout from nuclear weapons testing. In Texas, 241Am was present in sludge samples 

in 1983 and 1986 from a facility that received sanitary waste from the Gulf Nuclear, Inc. facility. 

Potential sources of radionuclides in the sludge were industrial wastes. Two incidents of contaminated 

sludge from companies producing foils for smoke detectors occurred in New York State. One of the 

receiving facilities that incinerated its sludge had 180–750 pCi/g (6.7–28 Bq/g) of 241Am in dried 
AMERICIUM 170 

6. POTENTIAL FOR HUMAN EXPOSURE 

incinerator ash between April 17, and May 7, 1984, after which it dropped to 13 pCi/g (0.48 Bq/g), 

corresponding to a sludge concentration of 5.2 pCi/g (0.19 Bq/g). During the latter half of 1984 and 

1985, the 241Am concentrations in sludge were 3.5 and 2.5 pCi/g (130 and 93 mBq/g), respectively. In the 

second incident, 241Am in sludge was as high as 120 pCi/g (4,400 mBq/g) in 1984, but dropped to an 

average of 24.8 pCi/g (920 mBq/g) in the latter half of 1985. This facility placed its sludge in landfills 

(Brauning et al. 1986). 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE 

Americium in the environment may be transferred to humans by inhalation and ingestion of food and, in 

the case of children, ingestion of soil; in general, intake of americium should be small. Much of the 

241Am so taken is found in the lungs, skeleton, and liver. In addition to the 241Am taken up, additional 

241Am is produced by the decay of 241Pu that has been inhaled or ingested and absorbed. No data on the 

body burden of 241Am in the general population were found. However, the body burden from fallout was 

estimated from the concentration of 241Am in air and estimates of intake by ingestion. The modeling 

study indicated that most of the 241Am body burden, 89% in 1978, was due to ingrowth from 241Pu. The 

model also estimated that the contribution of ingestion to the 241Am body burden was <1% of that due to 

inhalation. The total skeletal burden for 1970–1974 in New York was estimated from ashed skeletal 

samples to be 0.27 pCi (10 mBq) (Bennett 1979). UNSCEAR (2000) reported that inhalation exposures 

for even long-lived transuranic radionuclides became insignificant after 1985. 

Ash from a 1974 90Sr total diet study in New York consisting of representational foods from 19 separate 

categories was analyzed for 241Am to ascertain the dietary intake of the radionuclide from fallout (Bennett 

1979). It was estimated that over 95% of the 241Am transfer to food was from cumulative deposits in soil, 

rather than from direct deposition. The highest concentrations of 241Am in food occurred in shellfish, 

followed by grain products and fresh fruits and vegetables. The lowest concentrations were in meat, milk, 

eggs, fish, and processed foods. The same patterns of concentrations were obtained for 239,240Pu. The 

activity levels of 241Am in foods from New York from a total diet study, and in areas near nuclear 

weapons test sites and a fuel reprocessing facility are shown in Table 6-4. Using dietary consumption 

estimates and the activity levels in the food items and tap water, the 241Am ingestion intake for a New 

Yorker was 0.40±0.05 pCi/year (15±2 mBq/year) in 1974. The concentration of 241Am in tap water was 

estimated at 30±3 aCi/kg (1±0.1 μBq/kg) with 1,200 kg of water being consumed in a year. The food 

samples obtained in 1974 occurred at a time when direct deposition from fallout was very low and the 
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6. POTENTIAL FOR HUMAN EXPOSURE 

concentration of 241Am in food was largely a result of uptake from soil derived from cumulative deposits. 

Direct deposition from fallout was greatest in 1963–1964. Additionally, direct deposition is a much less 

significant means of plants acquiring activity than root uptake. The 241Am intake in diet from fallout will 

continue to increase due to ingrowth from 241Pu until the cumulative deposit reaches its projected 

maximum of 0.88 mCi/km2

 (33 MBq/km2) in the year 2035, at which time, the dietary intake of 241Am 

will have reached a maximum of 0.7 pCi/year (26 mBq/year) (Bennett 1979). 

As part of its Radionuclides in Food Program, the FDA determined concentrations of radionuclides in 

their Total Diet Study of food originating from the vicinity of nuclear reactors including raw vegetables, 

food crops (primarily fruits), fish, and milk. While not specifically analyzed for, 241Am concentrations of 

radionuclides in both of these surveys in 1983–1986 and 1987–1992 were sufficiently low as to require 

no specific action or simple monitoring. Imported foods were extensively monitored starting in May 

1986 for contamination resulting from the Chernobyl accident. While 241Am was identified in samples of 

imported food that probably originated from Chernobyl, the vast majority of samples were below FDA’s 

level of concern with only one oregano and three cheese shipments being detained (Cunningham et al. 

1989, 1994). FDA has since published guidelines for radionuclide concentrations, including isotopes of 

americium and plutonium, in food (FDA 1998). 

A study in the Ravenglass estuary, where tidal action inundates pasture land with water that receives 

discharges from the BNF reprocessing plan in Sellafield, concluded that consumption of a diet consisting 

of locally produced food would result in dose levels far below recommended limits (Bradford and Curtis 

1984). Sanchez et al. (1998) measured the 241Am activity in vegetation from tide washed pastures in 

17 estuaries spanning the eastern seaboard of the Irish Sea from Solway in northwest England to David’s 

Head in southern Wales. From the mean and median 241Am activity in grass and appropriately reduced 

transfer factors, they predicted the activity in animal products, namely milk, beef, beef liver, lamb, and 

lamb liver. From this, they estimated the committed effective dose for a 1-year-old child, a 10-year-old 

child, and an adult from eating these foods. Assuming that the land above the high water mark was to be 

reclaimed for growing vegetables, the authors calculated estimates of dose derived from consumption of 

potatoes, which were determined to be the critical vegetable group in terms of radionuclide 

contamination. The results are shown in Table 6-6, in which the relative doses for the various foods are 

beef liver>potatoes>lamb liver>beef>milk>lamb. 

Using transfer factors derived for uptake into plants and animals, Friberg and Vesanen (1999) have listed 

critical activity levels for combined α-emitting isotopes of Pu, Am, and Cm and other nuclides deposited 
 

 

 

 

 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-6. Estimated Effective 241Am Dose from Food Raised on Land Impacted 

by Tidal Estuaries along the Irish Sea 

241Am Committed effective dose (μSv) from 

241Amb Food item Transfer factors concentrationa 

Mean Median Mean Median Adult 10-year old 1-year old 

Milk 1.0x10-7 1.0x10-7 6.3x10-4 2.5x10-4 0.01 0.02 0.03
 

Beef 1.0x10-5 1.0x10-5 0.06 0.02 0.2 0.2 0.07
 

Beef liver 2.0x10-3 2.0x10-3 12.61 4.94 14.6 8.3 4.9
 

Lamb 4.0x10-5 4.0x10-5 0.03 0.01 0.05 0.03 0.01
 

Lamb liver 3.0x10-3 3.0x10-3 2.18 0.86 2.5 1.4 0.8
 

Potatoes 3.3 3.1 1.2
 

a

Food concentrations were estimated from measured 241Am levels in grass (485 Bq/kg dry weight mean, 

190 Bq/kg dry weight median), by applying grass-to-food transfer factors. Units are Bq/L for milk and Bq/kg fresh 

weight for other food items. 

b

The average consumption rates for the animal products were obtained from Byrom et al. (1995) and the dose 

coefficients were taken from SEPA (2000) (conversion: 1 Sv=100 rem). 

Source: Sanchez et al. 1998 
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6. POTENTIAL FOR HUMAN EXPOSURE 

on soil and pasture vegetation from a nuclear accident required to exceed the action level for foodstuffs 

recommended by the IAEA. Critical activity levels for the α-emitting isotopes of Pu, Am, and Cm were 

determined to be 8 kBq/kg (0.2 μCi/kg) for soil top-layer and 3.5 kBq/kg (0.095 μCi/kg) for pasture 

vegetation. The lowest detection limit required for the α-emitting isotopes of Pu, Am, and Cm was 

determined to be 2 kBq/kg (0.05 μCi/kg). Detection limits for the α-emitting isotopes of Pu, Am, and Cm 

achieved with thorough radioanalytical procedures have been reported as low as 0.07 Bg/kg (2 pCi/kg) in 

soil (Friberg and Vesanen 1999). 

The consumption of fish exposed to actinide contamination is a potential source of 241Am exposure. This 

potential source of exposure has been evaluated by measuring the concentration of 241Am in bass and 

bluegill living in a nuclear waste pond on the Hanford site where the levels of 241Am in sediments are 

approximately 3 orders of magnitude above background levels. Assuming that actinide behavior in the 

body is similar to that defined by the International Commission on Radiation Protection (ICRP) for 

Standard Man, the maximum levels occurring in fish fillets after 1 year in the waste pond (see Table 6-5) 

would not be sufficient to produce a significant radiation dose to a human eating 1 pound of fish fillets 

every day for 70 years (Emery et al. 1981). Similarly, the consumption of fish from the Farallon Islands 

Nuclear Waste Dump Site off of San Francisco is expected to add ~1.5% to the typical annual dose to the 

whole body effective dose equivalent value to pooled radionuclide concentrations committed to age 70 

(Suchanek et al. 1996). This increase is derived largely from the ingestion of 241Am. 

Lichens are very efficient collectors of deposited radionuclides. Since caribou and reindeer depend on 

lichens for food during the winter season, the lichen-reindeer/caribou-human pathway can lead to elevated 

exposures to indigenous Inuit and Sami populations who eat large quantities of meat and organs from 

caribou and reindeer. Reindeer tissue samples were analyzed for transuranium elements in Finland 

following the Chernobyl accident in 1986. Paatero and Jaakkola (1998) established that americium was 

transferred from lichen to reindeer via the gastrointestinal tract and not inhalation, and obtained a 

gastrointestinal-tract absorption coefficient of 0.00075 for 241Am. This gastrointestinal-tract absorption 

coefficient is similar to that estimated for humans (0.0006–0.0008, see Section 3.3.1.2). Concentrations 

of 241Am in reindeer resulting from Chernobyl fallout appear in Table 6-5. Global fallout of plutonium, 

which correlates with that of americium, was considerably higher than Chernobyl fallout, ca. 70 Bq/m2 

(2 pCi/m2

) compared to 1.5 Bq/m2 (0.04 pCi/m2) (Paatero and Jaakkola 1998). Based on 241Am 

concentrations in reindeer in Finnish Lapland, estimated 241Am intake is 2 pCi/year (74 mBq/year) for 

men and 1 pCi/year (37 mBq/year) for women (Jaakkola et al. 1977). 
 

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6. POTENTIAL FOR HUMAN EXPOSURE 

A modeling study for estimating exposure to man from dumping of radioactive waste in the Arctic Seas 

concluded that ingestion of molluscs was the dominant pathway for 241Am, and that 241Am along with 

239Pu would dominate the collective dose at longer time scales (Nielsen et al. 1997). Another modeling 

study dealing with the effect of long-term release of 241Am into an estuarine coastal sea ecosystem found 

that the greatest intake by man is from eating marine food items such as seaweed, molluscs, crustaceans, 

and fish (Murray and Avogadro 1979). Another important route of exposure is the inhalation of 

contaminated airborne coastal sediment. Ingestion of sediment by children and the contamination of 

crops by airborne sediment were estimated to be of minor importance. Radiation from contaminated mud 

flats and direct exposure from water were considered to be of little consequence. A survey of 241Am and 

plutonium in fish and shellfish in Ireland between 1988 and 1997 estimated that the mean doses from 

241Am for the typical and heavy Irish consumer were 0.024 and 0.104 μSv/year (2.4 and 10.4 μrem/year), 

respectively (Ryan et al. 1999). Americium contributes somewhat over a quarter of the combined 

plutonium-americium dose. In 1988, this combined dose was roughly 10% of that which the typical Irish 

seafood consumer obtained from 137Cs; in 1997, this percentage had increased to 48%. 

Both the general population and workers may be exposed to 241Am from the production, distribution, and 

use of ionization chamber smoke detectors. The USNRC investigated exposure relating to this device. 

Their 1979 report concluded that the sum of doses to the population resulting from production, 

distribution, use, and disposal of 14 million smoke detectors containing 3 μCi (100 kBq) of 241Am each 

(over 3 times that presently used) that were distributed in 1978 would result in a collective total body dose 

of 1,100 person-rem (11 person-Sv)—much lower than that which could potentially result in one cancer 

death (USNRC 1979). The risks reported in the 1979 report may be overestimates for current times, since 

radiation risk coefficients have changed and the amount of americium used per unit has been reduced. 

More recent information also indicates that exposure to 241Am in a home smoke detector is negligible 

(<0.01 mrem/year [<1x10-7 Sv/year]). Smoke detectors today typically contain approximately 1 μCi 

(37 kBq) of 241Am (EPA 2004b). Exposure to 241Am could result from improper disposal of smoke 

detectors; for example, if a detector was broken and then disposed of in a municipal landfill or 

incinerated. The 241Am from the broken detector could be consumed by a child, but uptake would be 

negligible based on human study results (Rundo et al. 1977). 

Occupational exposure to 241Am may occur to workers manufacturing the 241Am-containing foil used in 

ionization-type smoke detectors or assembling the device. Two manufacturers of the 241Am foils were 

surveyed in 1977 (USNRC 1979). One reported an external population dose of 0.8 person-rem per curie 

(0.2 person-pSv/Bq) of 241Am processed for the 150 workers involved and the 16.6 Ci (0.614 TBq) of 
 

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6. POTENTIAL FOR HUMAN EXPOSURE 

241Am they processed. The maximum dose for an individual was approximately 0.8 rem (8 mSv). The 

second manufacturer reported 0.2 person-rem per curie (0.05 person-pSv/Bq) of 241Am processed. It 

should be noted that manufacturers of ionization chamber smoke detectors must be licensed by the 

USNRC or an agreement state, and that certain work practices are required to minimize exposure. 

Workers wear shoe covers, lab coats, and gloves, and wipe tests are performed weekly. During the 

manufacture of the smoke detector units, one manufacturer reported the yearly external doses among 

badged workers in 1978: 40% had no measurable dose, 40% had <100 mrem (<1 mSv), 15% had doses 

between 250 and 500 mrem (2.5 and 5.0 mSv), 4% had doses between 500 and 750 mrem (5.0 and 

7.5 mSv), and one individual had a dose between 750 and 1,000 mrem (7.5 and 10 mSv). The total 

occupational dose in the ionization chamber smoke detector industry in 1978 was estimated to range from 

15 to 48 person-rem. The external doses to people involved in the distribution and retail sale of smoke 

detectors would be much less. The hand dose to installers is estimated to be 0.6 μrem (6 nSv) per unit 

installed. An individual having one detector in the hallway and one in the bedroom would have an annual 

dose of 9.3 μrem (93 nSv). 

Workers at plutonium reprocessing facilities, nuclear reactors, or transuranium and low level waste 

storage facilities, or those engaged in the production or processing of 243Am or 241Am may be 

occupationally exposed to americium. In addition, workers at sites where nuclear testing was conducted 

may also be exposed to americium. Workers in nuclear power stations may be exposed to airborne 

radionuclides. The USNRC publishes annual reports on occupational radiation exposure at USNRClicensed facilities. Monthly cumulative 24-hour air filter samples were obtained from five different 

working areas of a BWR in India during normal operation and during refueling in order to measure the 

concentrations of transuranic radionuclides, including americium, in air. The average air 241Am 

concentrations during normal operation were (work area, concentration in mBq/m3

 [fCi/m3]): reactor 

building—103 feet elevation, 0.95 (26); reactor building—143 feet elevation, 0.22 (5.9); reactor 

building—200 feet elevation, 0.25 (6.8); turbine building—133 feet elevation, 0.07 (1.9); and radwaste 

building—2.50 (68) (Hedge and Bhat 1983). During refueling, the respective concentrations were: 1.64, 

1.33, 0.78, 0.19, and 6.34 mBq/m3

 (44.3, 35.9, 21, 5.1, and 171 fCi/m3). The derived air concentration 

recommended by the ICRP for occupational exposure is 80.0 mBq/m3

 (2,200 fCi/m3) (Hedge and Bhat 

1983). In 1997, the French radiation protection office conducted monitoring (24-hour urine 

analysis/whole body activity measurements) of workers in the non-nuclear energy field (i.e., nuclear 

medicine, research laboratories, and non-nuclear industries) to ascertain the occupational intake of 

radionuclides (De Vathaire et al. 1998). 241Am was not detected in samples from any of the 37 workers 

who worked with the radionuclide. 
 

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6. POTENTIAL FOR HUMAN EXPOSURE 

The U.S. Transuranium and Uranium Registries (USTUR) include The National Human Radiobiology 

Tissue Repository, which contains postmortem tissue from persons (primarily workers) with documented 

intakes of uranium or transuranic elements, such as americium. The USTUR publishes annual reports 

detailing cases of accidental exposure and tissue levels of the different radioactive isotopes. These reports 

and other information are available over the internet at http://www.tricity.wsu.edu/ustur/. Exposure is 

generally by inhalation, but entry into the body may also occur through wounds. Americium is largely 

retained in the lung, skeleton, and liver, but after long term exposure, significant amounts of 241Am are 

found in the muscle, respiratory tract, and other soft tissue (Filipy et al. 1994; McInroy et al. 1989). In 

25 USTUR cases involving the registry of individuals who typically had ≥20 years of employment in 

facilities where 241Am was processed and who were likely to have had chronic, low-level inhalation 

exposure to the actinide, the 241Am organ content of the liver and skeleton ranged from 0.01 to 554 Bq 

(0.26 Bq, median) (0.3–15,000 pCi, 7.0 pCi, median) and from 0.04 to 6,623 Bq (0.99 Bq, median) (1– 

179,000 pCi, 27 pCi, median), respectively (Kathren et al. 1988). Seventy-five percent of the combined 

activity in the liver and skeleton resided in the skeleton (see Section 3.4). Measurements of 241Am were 

performed on the skulls of 66 residents of the Caithness area of Scotland near the Dounreay Nuclear 

Establishment between October 1990 and December 1991. No 241Am was detected in any of these 

subjects (Ham et al. 2003). 

6.6 EXPOSURES OF CHILDREN 

This section focuses on exposures from conception to maturity at 18 years in humans. Differences from 

adults in susceptibility to hazardous substances are discussed in 3.7 Children’s Susceptibility. 

Children are not small adults. A child’s exposure may differ from an adult’s exposure in many ways. 

Children drink more fluids, eat more food, breathe more air per kilogram of body weight, and have a 

larger skin surface in proportion to their body volume. A child’s diet often differs from that of adults. 

The developing human’s source of nutrition changes with age: from placental nourishment to breast milk 

or formula to the diet of older children who eat more of certain types of foods than adults. A child’s 

behavior and lifestyle also influence exposure. Children crawl on the floor, put things in their mouths, 

sometimes eat inappropriate things (such as dirt or paint chips), and spend more time outdoors. Children 

also are closer to the ground, and they do not use the judgment of adults to avoid hazards (NRC 1993). 
 

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6. POTENTIAL FOR HUMAN EXPOSURE 

Specific information on the exposure of children to americium is not available. As for adults in the 

general population, small exposures to 241Am occur from normal ingestion of food and drinking water and 

inhaling air. While the potential for americium exposure is greater for children who consume foods 

grown in areas with elevated levels of americium in the soil, the uptake of americium into plants and 

animals is very low. Children may be exposed to a substance brought into the home on parents’ work 

clothes, skin, hair, tools, or other objects from the workplace; however, with one exception, no instances 

of americium exposure in children by this route were found in the literature. In this case, a man who did 

some experiments using an americium source brought home a secondary source and stored it in a dresser 

drawer (Kelly and Dagle 1974). No information was located on americium levels in amniotic fluid, 

meconium, cord blood, neonatal blood, or breast milk, or other potential measurements relating to fetal or 

childhood body burdens. 

241Am may also find its way into municipal landfills because of improper disposal of smoke detectors or 

rubble of buildings containing smoke detectors. Smoke detectors may be broken, exposing the 241Am 

ionization source. Young children might get access to the 241Am and ingest it, although a human study 

indicates that uptake from ingesting the americium source from a smoke detector is insignificant (Rundo 

et al. 1977). At hazardous waste sites, americium that is found in excess of fallout background levels is 

most likely to be in soil and presents a special hazard for young children. Hand-to-mouth activity and 

inadvertent or intentional (pica) eating of contaminated dirt will result in oral exposure to americium. 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 

Occupational exposures and general population exposures to potentially high levels of 241Am and other 

radionuclides might occur to people occupying land like the southern Solway and Dee marshes, areas 

tidally inundated by water contaminated by the BNFL nuclear fuel reprocessing plant at Sellafield, United 

Kingdom plant in England (Rose et al. 1996). Modeling studies of human populations exposed to 241Am 

in such coastal environments show that the highest levels of 241Am would occur in sediment and marine 

organisms, especially molluscs and seaweed (Murray and Avogadro 1979). These human populations 

include farm workers and turf cutters and recreational users such as birdwatchers, hikers, fishermen, and 

bird shooters, as well as those who consume contaminated marsh produce, molluscs, and seaweed. 

Exposure routes would be ingestion and inhalation of dust. Even so, the dose rates that would be received 

by these pathways are very low (Murray and Avogadro 1979). 
 

 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

Populations with potentially high exposure to 241Am from commercial devices such as ionization chamber 

smoke detectors might include production workers and firemen attending to fires in production facilities, 

or warehouses where a large number of sources or devices are housed. 

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 americium 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 americium. 

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. Data on the physical and chemical properties 

of americium and americium compounds are available in the literature (Cotton and Wilkinson 1980; Lide 

1994, 1998; Nenot and Stather 1980; Seaborg 1991). Data are also available on the radiological 

properties of americium isotopes (Baum et al. 2002; DOE 2003a; ICRP 1983; Lide 1998). 

Production, Import/Export, Use, Release, and Disposal. Data regarding the past and present 

production and import/export volumes for 241Am and 243Am are not available. The limited commercial 

use of 241Am provides a good estimate of probable production volumes. The uses of americium are 

known (Budavari 1996; Seaborg 1991; UIC 1997; USNRC 1979). However, information on the 

production, import/export volumes, and the amounts of 241Am used in various devices would be useful for 

estimating exposure. Estimates of the amounts of 241Am released as a result of nuclear tests and accidents 

are available (Bennett 1979; Suchanek et al. 1996). The disposal of americium is governed by the 
 

AMERICIUM 179 

6. POTENTIAL FOR HUMAN EXPOSURE 

USNRC regulations (10 CFR 61). The Manifest Information Management System (MIMS), maintained 

by the INEEL, contains information on low-level radioactive waste shipments received at commercial 

low-level radioactive waste disposal facilities and the WIPP transuranic waste facility (INEEL 2000). 

The DOE stores most of its spent fuel at three primary locations: the Hanford site, Washington, the 

INEEL, Idaho, and the Savannah River Site, South Carolina. The DOE National Spent Fuel Program 

maintains a database of spent nuclear fuel stored in each of the three locations (DOE 1999a). Information 

concerning the americium content of civilian nuclear power plants and naval nuclear propulsion plant 

spent fuel now in storage and awaiting disposition would be useful for estimating the amount of 

americium stored in the country. 

Environmental Fate. The environmental fate of americium has been extensively studied in relation 

to its introduction into the Irish Sea from the BNFL nuclear fuel reprocessing plant at Sellafield, United 

Kingdom (Belot et al. 1982; Bennett 1976; Bunzl et al. 1994, 1995; Malcolm et al. 1990b; McCartney 

et al. 1994; McKay et al. 1994; Murray et al. 1978, 1979; Pattenden and McKay 1994; Walker et al. 

1986). 

Other studies have investigated transport in soil and at DOE waste disposal sites (Fowler et al. 1981; 

McCarthy et al. 1998a, 1998b; Penrose et al. 1990). As a result of these studies, the environmental fate of 

americium is reasonably well understood. However, DOE has begun using the RESRAD Biota computer 

program, and it would be useful to validate uncertainties in associated input parameter values used in the 

model. 

Bioavailability from Environmental Media. The absorption and distribution of americium as a 

result of inhalation and ingestion exposures have been discussed in Sections 3.3.1 and 3.3.2. EPA lists 

identical uptake factors for inhaled and ingested americium (as well as all of the other transuranics other 

than plutonium) regardless of compound solubility, indicating that the knowledge base for americium is 

not sufficiently developed to quantify the differences that are recognized for most other elements, and 

additional studies would be helpful. 

Food Chain Bioaccumulation. Information about the levels of americium in aquatic and terrestrial 

organisms and its bioaccumulation in these organisms is available (DOE 1996; Fresquez et al. 1999; 

Suchanek et al. 1996). Data are also available on the uptake of americium in plants (Bennett 1979; 

Cataldo et al. 1980; EPA 1979; Romney et al. 1981; Schreckhise and Cline 1980; Schulz et al. 1976; Zach 
 

 

 

 

AMERICIUM 180 

6. POTENTIAL FOR HUMAN EXPOSURE 

1985) and levels in food (Bennett 1979; Cunningham et al. 1989, 1994; Robison et al. 1997a, 1997b). 

These data indicate that americium does not biomagnify in the food chain (Bennett 1979; Bulman 1978). 

Exposure Levels in Environmental Media. Monitoring data for the levels of americium in 

contaminated media at hazardous waste sites would be useful. These data can then be used to estimate 

the intake and body burden of americium and assess the potential risk of adverse health effects in 

populations living in the vicinity of these sites. 

Information is available on the levels of 241Am in soil and sediment in areas affected only by global 

fallout, at DOE installations and other nuclear facilities, and at sites of nuclear explosions and accidents 

(Alberts et al. 1989; Bennett 1979; Cooper et al. 1994; DOE 1980; Pattenden and McKay 1994; Robison 

et al. 1997a, 1997b; Sanchez et al. 1996). 241Am levels in soil around nuclear power plants in the United 

States were indistinguishable from fallout background (EPRI 1981). 

For the Radionuclides in Food Program, the FDA determined concentrations of radionuclide activity in 

their Total Diet Study. Levels of 241Am in both the 1983–1986 and 1987–1992 studies were sufficiently 

low as to require no specific action or simple monitoring (Cunningham et al. 1989, 1994). 

The FDA (1998) has published derived intervention levels for 241Am in food at which action should be 

considered. Dietary values are 2.0 Bq/kg for 3-month-old children, increasing to 17 Bq/kg for 1-year-old 

children, and then decreasing to 8.8 Bq/kg for adults. Since 1973, background fallout levels of 241Am in 

air have been <1 aCi/m3

 (1 aCi=10-18 Ci) (0.037 μBq/m3) and are continuing to decline (Bennett 1979). 

Levels in tap water are sufficiently low that levels must be estimated (Bennett 1979). 

UNSCEAR (2000) reported that deposition and air concentrations of radionuclides from fallout dropped 

rapidly once atmospheric testing ceased in 1980. Inhalation exposures for even long-lived transuranic 

radionuclides became insignificant after 1985. 

Exposure Levels in Humans. Although some data on the levels of americium in human tissues 

exposed to natural background levels (food, water, and air) are available, few measurements have been 

made on the americium content in human tissues. The principal source of information about 

occupationally exposed individuals is the USTUR database, established to document levels and 

distribution of uranium and transuranium isotopes in human tissues for occupationally exposed workers 

(USTUR 1999). Several major database files are available. The Radiochemical file contains information 

about radiochemical analysis of tissue donations from occupationally exposed individuals. The Health 
AMERICIUM 181 

6. POTENTIAL FOR HUMAN EXPOSURE 

Physics file contains bioassay and other health physics data. These two databases are regularly updated. 

The Medical file contains abstracted personal, medical, and clinical data; the Pathology file contains 

autopsy and pathology information; and the Skeletal Estimate file contains estimated actinide 

concentrations for unanalyzed half skeletons from donors (USTUR 1999). The DOE has developed the 

Comprehensive Epidemiologic Data Resource (CEDR) Program to provide public access to health and 

exposure data concerning DOE installations. In addition, studies relating to populations residing near 

DOE installations, and other studies of radiation exposures and health effects, such as atomic bomb 

survivors, are included in CEDR (CEDR 2000). Additional research is needed to reassess the magnitude 

of any health risks associated with exposure to americium from smoke detector damage under realistic 

scenarios. 

Exposures of Children. Children will be exposed to americium in the same manner as adults in the 

general population (i.e., ingestion of food and water and inhalation of air). Americium is potentially 

found at hazardous waste sites at elevated levels. Since children may have oral exposure to soil through 

hand-to-mouth activity, bioavailability studies of americium in soil via the oral route may be useful to 

assess the risk of this type of exposure. 

Child health data needs relating to susceptibility are discussed in 3.13.2 Identification of Data Needs: 

Children’s Susceptibility. 

Exposure Registries. Americium is not currently one of the chemicals for which a subregistry has 

been established in the National Exposure Registry. Americium 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 americium. 

Other exposure registries are available for americium. The USTUR established a database to document 

levels and distribution of uranium and transuranium isotopes in human tissues for occupationally exposed 

workers who donate their bodies to science (USTUR 1999). The DOE has developed the CEDR Program 

to provide public access to health and exposure data concerning DOE installations. In addition, studies 

relating to populations residing near DOE installations, as well as other studies of radiation exposures and 

health effects, such as atomic bomb survivors, are included in CEDR (CEDR 2000). 
AMERICIUM 182 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.8.2 Ongoing Studies 

The Federal Research in Progress database lists ongoing studies about environmental effects of 

americium (FEDRIP 2004). The one current study listed in the FEDRIP database was R.D. Lloyd of the 

University of Utah at Salt Lake City, studying the consequences of exposure to a bone-seeking 

radionuclide, 239Pu. These studies will provide new knowledge on the biological behavior of plutonium 

and other bone-seeking radionuclides, including americium, and improve the capability to predict the 

risks of exposure. This research is supported by the National Cancer Institute. The International Science 

and Technology Center (ISTC), headquartered in Moscow, which began operations on March 3, 1994, 

also is active in research concerning transuranic elements. 
 

AMERICIUM 183 

7. ANALYTICAL METHODS 

The purpose of this chapter is to describe the analytical methods that are available for detecting, 

measuring, and/or monitoring americium, its metabolites, and other biomarkers of exposure and effect to 

americium. 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 americium into the human body can occur through ingestion, inhalation, or penetration through 

skin or via wounds. The quantities of americium within the body can be assessed from the use of 

bioassays, which include in vivo measurements and/or in vitro measurements. In vivo measurements can 

be obtained through techniques that directly quantify internally deposited americium (using, for example, 

a whole body counter). Conversely, in vitro measurements provide an estimate of internally deposited 

americium, utilizing techniques that measure americium in body fluids, feces, urine, or tissue obtain 

through an autopsy. Examples of these analytical techniques are given in NCRP Report No. 87 (1987) 

and are also listed in Table 7-1. The ultimate aim of making such measurements is to estimate intake and 

radiation dose. In-vitro measurements provide an assessment of intake and dose only when the data are 

interpolated using appropriate biokinetic models, taking account of pattern of exposure, chemical form, 

and other parameters. 

7.1.1 Whole or Partial Body Measurements 

In vivo measurement techniques are the most direct and widely used approach for assessing the content of 

many radioisotopes, including americium, within the body. The in vivo measurement of americium 

within the body is performed with various radiation detectors and associated electronic devices, which are 
AMERICIUM 184 

7. ANALYTICAL METHODS 

Table 7-1. Analytical Methods for Determining Americium 

in Biological Samples 

Sample 

matrix Sample preparation 

Analytical 

method Detection limita Accuracy Reference 

Urine None Gamma-ray 

spectroscopy 

0.08 nCi/ 

200 cm3 

No data Ide et al. 

1985 

(phoswich 

detector) 

Urine Co-precipitation with 

oxalate 

α-spectroscopy 0.08 pCi/ 

80 cm3 

No data Ide et al. 

1985 

Urine None Gamma-ray 

spectroscopy 

0.04 pCi/cm3

 95% at 

0.04 pCi/cm3 

Guilmette 

1986 

Urine Sample wet ashed, 

treated with HNO3 

α-liquid 

scintillation 

0.7 pCi/ 

125 cm3 

95% at 

0.01– 

Guilmette 

and Bay 

Urine 

and H2O2 

Sample wet ashed, Liquid 14 pCi/100 cm3

1,000 nCi 

 96% at 

1981 

Ham et al. 

purified by solvent scintillation 20,000 dpm 1977 

Urine 

extraction 

Sample with 241Am α-liquid 0.02 pCi/L 

spike 

96% at Hafez and 

spike co-precipitated scintillation 20 dpm spike Hafez 1992 

with CaHPO4 then 

with oxalate, 

purification by 

diglycol succinate 

column 

Urine Sample cleaned-up Biphasic liquid 1 pCi/200 cm3

 84% Bomben et 

by co-precipitation, scintillation al. 1994 

treated with HNO3 

and H2O2, wet ashed 

Urine Spiked sample 

clean-up by coα-spectroscopy 0.016 pCi/ 800 cm3 

95% at 

0.1–100 pCi/ 

Goldstein et 

al. 1997 

precipitation, purified sample 

by TRU-spec column 

and electrodeposition 

Soft 

tissue 

Sample wet ashed, 

spiked with 243Am, 

α-spectroscopy No data 98% McInroy et al. 

1985 

purified by anion 

exchange, solvent 

extraction, and 

electrodeposition 

Soft Spiked sample wet α-spectroscopy No data 53% Qu et al. 

tissue ashed, treated with 1998 

HNO3/H2O2, purified 

by A-CU column, 

anion exchange, 

TRU-spec column, 

and electrodeposition 

Soft 

tissue 

Sample wet ashed, 

purified by solvent 

Liquid 

scintillation 

1.3 pCi/ 

100 cm3 

96% at 

20,000 dpm 

Ham et al. 

1977 

extraction spike 
AMERICIUM 185 

7. ANALYTICAL METHODS 

Table 7-1. Analytical Methods for Determining Americium 

in Biological Samples 

Sample 

matrix Sample preparation 

Analytical 

method Detection limita Accuracy Reference 

Soft 

tissue 

Bone 

Bone 

Sample wet ashed, 

purified by solvent 

extraction 

Sample wet ashed, 

purified by solvent 

extraction 

Sample wet ashed, 

spiked with 243Am, 

and purified by anion 

exchange resin 

column, solvent 

α-liquid 

scintillation 

α-liquid 

scintillation 

α-spectroscopy 

0.7 pCi/g 

0.7 pCi/g 

No data 

99% at 

3,000 dpm 

spike 

99% at 

3,000 dpm 

spike 

98% 

Guilmette 

and Bay 

1981 

Guilmette 

and Bay 

1981 

McInroy et al. 

1985 

extraction, and 

Feces 

Feces 

Feces 

Teeth 

electrodeposition 

Sample wet ashed, 

purified by solvent 

extraction 

Sample wet ashed, 

purified by solvent 

extraction 

None 

Sample dissolved in 

HNO3, purified by 

TRU-spec column 

and electrode 

Liquid 

scintillation 

α-liquid 

scintillation 

Phoswich 

detector 

α-spectroscopy 

13 pCi/g 

1.3 pCi/sample 

0.02–0.09 nCi/ 

200g 

2.7 fCi/sample 

91% at 

20,000 dpm 

spike 

96% at 

3,000 dpm 

spike 

No data 

98% 

Ham et al. 

1977 

Guilmette 

and Bay 

1981 

Kramer et al. 

1989 

Culot et al. 

1997 

Whole 

organs 

and 

position 

Animal placed, 

backbone down, in 

lucite box, and 

Gamma-ray 

spectroscopy 

No data No data Lloyd et al. 

1970 

tissues positioned 33 cm 

from NaI(Tl) crystal; 

livers and other 

tissues were 

counted between 

two NaI(Tl) crystals 

a

1 Ci=3.7x1010 Bq=0.037 TBq or 1 Bq=2.7x10-11 Ci=27 pCi; 1 Ci=2.2x1012 dpm 

TRU = transuranic 
 

AMERICIUM 186 

7. ANALYTICAL METHODS 

collectively known as whole body counters. These radiation detectors commonly utilize hyperpure 

germanium to detect the 59.5 keV gamma-ray that 241Am promptly emits in 35.9% of its alpha decays to 

237Np (DOE 1979b, 2003a; Palmer et al. 1983). 

Because the attenuation half thicknesses for the 59.5 keV gamma-ray are 3.5 cm for soft tissues and 

1.3 cm for bone, 241Am that has been deposited into specific organs or tissues, such as the lungs, liver, 

bones (e.g., skull or knee cap), or lymph nodes, can be detected and quantified using whole body or 

partial body counting techniques that appropriately account for attenuation by internal organs (Graham 

and Kirkman 1983; Palmer and Rhoads 1989; Palmer et al. 1983). Many configurations of the whole 

body counter have been utilized, ranging from the more common single-detector chest detectors to 

multiple-detector arrays (e.g., four HPGE detectors, two each of front and back over the lungs or 

abdomen) or linear whole body scanners that can be utilized to assess the regional distributions of 241Am 

over the entire length of the body (Palmer et al. 1983; Toohey and Essling 1980). 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. Also, in vitro measurements 

of americium (see Section 7.1.2) are often used in conjunction with whole body counting when 

monitoring individuals working with americium. 

Calibration of whole body counters is performed so that the operator can obtain a more accurate and 

unbiased estimate of internalized americium activity. The equipment calibration is achieved through the 

use of tissue-equivalent phantoms that are constructed to mimic the shape and density of the anatomical 

structure (e.g., the human torso), using tissue equivalent materials such as polystyrene or epoxides. In 

some phantoms, a human rib cage is added to account for the attenuation of gamma-rays by bone in the 

whole body counts (DOE 1979b). Americium standards are inserted or molded into the phantom at 

locations where this radionuclide is expected to accumulate, such as in the lung, liver, or bone. 

Comparisons of the activity obtained from the phantom to the known activity of the americium standards 

are used to determine the efficiency of the counting technique and, thus, provide the basis for calibrating 

the technique. Calibration of whole body counters can be further refined by obtaining actual anatomical 

measurements of the individual to be measured. For example, chest wall thickness measurements using 

ultrasound techniques are used to account for the variability in attenuation that result from individual 

differences in the chest wall thickness and improving the calibration of chest counts of americium (DOE 

1979b). Another approach to refining the calibration of whole body counters is the comparison of 

external measurements to the actual americium content in organs and bone of cadavers (Palmer et al. 

1985). These refinements in calibration phantoms can lead to more accurate and less biased assessments 
 

AMERICIUM 187 

7. ANALYTICAL METHODS 

of the total body or organ burden of americium. The calibration may include an assessment of the 

detection limit for the system or for the specific analytical protocol being used. 

In assessing initial exposure, whole body counting techniques measure the amounts of americium that 

have been retained within organs or tissues. In cases of accidental ingestion, some of the americium may 

have been excreted in the urine or feces before exposure is assessed. In particular, soluble forms of 

americium are thought to be readily excreted through the urine. Long-term assessment of americium 

burden within an individual can be complicated by the mobilization of americium from the original site of 

deposition (e.g., the lung) to other sites within the body, such as the liver or bone (Fry 1976). This can 

lead to either overestimates or underestimates of the overall total body burden of americium, depending 

on the regions in which the americium counts are obtained relative to the shift in radionuclide 

distribution, and if local concentrations have been augmented by mobilization of americium from other 

tissues. Overestimates can also occur in cases where external contamination in the vicinity of a detector 

contributes to the collected spectrum. Showering immediately before monitoring to remove potential 

contamination should help reduce variability in temporal results and minimize the potential for obtaining 

false positive results. Additionally, the retention (biological half-life) of americium within the body can 

vary greatly between individuals (Fry 1976). Direct comparisons of americium body burdens and 

clearance rates between laboratories can be complicated by the differing whole body measurement 

techniques, calibration methods, and methods used to account for normal background radiation counts 

that are utilized within the different laboratories (DOE 1979b). These variations are largely resolved by 

performing periodic internal monitoring and adjusting the model parameters to account for the 

individual’s actual distributed retention. 

7.1.2 Assay of Excreta 

In vitro analyses of americium are routinely performed in situations where in vivo analyses cannot be 

obtained, where in vivo measurements will not provide the information needed, or in support of an in vivo 

monitoring program. Urine is the preferred sample for in vitro analyses of americium, although other 

sample types, such as feces, tissue, bone, or blood, can also be used on a more limited basis. Urine 

provides for an analysis of soluble or transportable americium, fecal analysis can be used to measure 

gastrointestinal clearance of ingested material plus bile-related systemic clearance, and tissue is used to 

assess whole or regional body burdens of americium (Guilmette and Bay 1981; Ide 1986; Ide et al. 1985; 

McInroy et al. 1985). 
AMERICIUM 188 

7. ANALYTICAL METHODS 

There are a number of methods that have the selectivity, and/or sensitivity, to measure americium in 

biological matrices including spectrophotometry, fluorimetry, mass spectrometry (MS), and radioassays 

(Dacheux and Aupias 1998; Hafez and Hafez 1992; Poupard and Jouniaux 1990; Thouvenot et al. 1993). 

Of these methods, radioassays (e.g., gross alpha analysis, alpha spectroscopy, gamma-ray spectroscopy, 

liquid scintillation techniques) are preferred because of their ease of use, detection sensitivity, and 

rapidity of analysis (Alvarez and Navarro 1996; Dacheux and Aupiais 1997; Guilmette 1986). These 

methods typically involve a preliminary concentration step and wet/dry ashing of the sample that is often 

followed by an oxidation of the radionuclides in the sample residue. To remove the possible interferences 

of other elements and alpha-emitters, ion exchange, co-precipitation, and adsorption techniques are 

applied to the purified sample before alpha or liquid scintillation techniques are applied (see Table 7-1). 

Radioassays can also be applied to the measurement of americium in fecal samples, as well as tissue and 

bone samples obtained from autopsy, using methods that are similar to those described for urinalysis, 

except for some additional purification and extraction steps that are required to remove interfering 

materials such as iron (Guilmette and Bay 1981; Hafez and Hafez 1992; Ham et al. 1977; Qu et al. 1998). 

Of the radioassays that are commonly used to quantify americium, α-spectroscopy is used when isotopic 

analyses of americium must be conducted (e.g., to obtain distinct results for 241Am and 243Am). 243Am is 

often added as a tracer to estimate the recovery (efficiency of the radiochemical sample preparation 

method for removing americium from a biological matrix). The α-spectroscopy technique differentiates 

between the two americium isotopes based on the difference in the energies of the alpha particles that are 

emitted from 241Am and 243Am, and then quantifies the amounts present in the sample by considering the 

system’s response to each, its detection efficiency, and the frequency with which the individual alpha 

particles are emitted. If 243Am is to be analyzed in a sample, 241Am can be used as a tracer. If a sample 

needs to be monitored for both 241Am and 243Am, the sample is split prior to adding the tracer and two 

analyses are performed (PNNL 2003). Mass spectrometric techniques, especially those using double 

focusing magnet spectrometers, are also capable of isotopic quantification of americium (Dacheux and 

Aupiais 1998; Poupard and Jouniaux 1990). These techniques are more rapid than the α-spectroscopy 

detection method, but the costs have been much higher. The cost of mass spectrometers, however, has 

decreased in recent years, making the cost of analyzing samples by mass spectrometry and α-spectroscopy 

more comparable. The breakeven point will depend on the sample throughput rate. Higher sensitivity 

can also be achieved with α-spectroscopy by resorting to long sampling times, sometimes referred to as 

time-averaging. 
 

AMERICIUM 189 

7. ANALYTICAL METHODS 

Accuracy and bias of in vivo and in vitro measurements of americium are determined through the use of 

standard, certified radioactive sources with known concentrations of americium. The primary source of 

certified americium standards is the National Institute of Standards and Technology (NIST). Secondary 

and tertiary level laboratories can also prepare, certify, and sell such sources, and the Health Physics 

Society is developing an accreditation program for providers who wish their products to be recognized as 

NIST-traceable (HPS 2004). Standard solutions are available for 241Am (SRM 4322, 40 Bq/g [1.1 nCi/g]) 

and 243Am (SRM 4332, 40 Bq/g [1.1 nCi/g]). Standard Reference Materials for human lung (SRM 4351) 

and human liver (SRM 4352) are also available from NIST. 

7.2 ENVIRONMENTAL SAMPLES 

There are two common approaches for measuring americium in the environment. Americium can either 

be measured directly in the field (in situ) using portable survey instruments or be quantified from samples 

that were procured from the field and returned to the laboratory. 

7.2.1 Field Measurements of Americium 

In situ measurement techniques are extremely useful for the rapid characterization of radionuclide 

contamination in the environment, such as surface soils, sediments, and vegetation, or when monitoring 

personnel for internal exposure from or external contamination with americium. Information regarding 

field measurement methods, minimum detectable concentrations, and soil-to-plant concentration factors is 

available for various radionuclides, including americium (MARSSIM 2000; NRC 1992, 1998b). The 

measurement of radionuclides in the environment is conducted with portable survey instruments that are 

equipped with α-scintillators or gamma-ray spectrometers. The use of gamma-ray spectrometers is 

preferred for measuring americium in the field, especially in the presence of plutonium isotopes. The 

reason is that the low-energy 241Am gamma-ray photons are more penetrating than lower energy x-rays 

from 238,239Pu for which it is a surrogate radionucide. This makes measurements less affected by surface 

type and texture and by the presence of vegetation and surrounding soil (Byrne and Komosa 1993). This 

provides the advantage for assessing the level of americium both on and below the surface (e.g., up to 

3-cm depth in some soils). These gamma-ray spectrometers are equipped with either a thin phoswich 

type detector or a high purity germanium detector that is able to distinguish the 59.5 keV gamma-ray 

emitted from 241Am from most environmental gamma-rays emitted from other radionuclides (Fong and 

Alvarez 1997). Another advantage of these spectrometers is the ability to discriminate the 59.5 keV 
AMERICIUM 190 

7. ANALYTICAL METHODS 

photons of 241Am from the much lower energy photons emitted from 239Pu and 240Pu, which are usually 

associated with americium. Minimum detectable activities (MDAs) of 0.4 Bq/g (10 pCi/g) for 241Am are 

routinely achieved, with MDAs as low as 0.04 Bq/g (1 pCi/g) obtained with longer counting times 

(-30 days). 

One of the limitations of the portable field survey instruments in the measurement of americium is that 

their quantitative accuracy depends on how well the lateral and vertical distribution of americium in the 

soil compares with the calibration parameters used. These methods can provide a rapid assessment of 

americium levels on or below surfaces in a particular environment; however, laboratory-based analyses of 

samples procured from these environmental surfaces must be performed in order to ensure accurate 

quantification of americium (and other radionuclides). This is due, in part, to the strong self absorption of 

the 59.5 keV gamma-ray by environmental media, such as soil. Consequently, uncertainty in the depth 

distribution of americium and density of the environmental media may contribute to a >30% error in the 

field survey measurements. Refinements in calibration strategies are currently being developed to 

improve both the precision and the accuracy (10%) of gamma-ray spectroscopy measurements of 

americium within contaminated soils (Fong and Alvarez 1997). 

7.2.2 Laboratory Analysis of Environmental Samples 

Analytical methods for quantifying americium in environmental samples are summarized in Table 7-2. 

The methods that are commonly used in the analysis of americium based on activity are gross α analysis, 

α-spectroscopy, and gamma-ray spectroscopy. MS detection techniques are used to measure the mass of 

americium in environmental samples. The mass-activity conversion factor for 241Am is 0.29 μCi/μg 

(11 kBq/μg) or 3.43 μg/μCi (0.091 μg/kBq) (Harvey et al. 1993). 

The analysis of americium in air is based on the quantification of americium within particulates that 

become trapped on cellulose or glass fiber filters after a calibrated amount of air is pulled through the 

filters. The analysis for americium on a glass fiber filter is straight forward using gamma spectroscopy, 

but can be a rather complex procedure involving many solvent extraction and column purification steps, 

followed by electrodeposition and α-spectroscopy. The extensive purification is required to prevent 

impurities within the sample from absorbing or reducing the energy of emitted alpha particles, termed 

self-absorption. Alpha-emitting contaminants must also be removed (e.g., 238Pu) from the samples to 
AMERICIUM	 191 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining Americium in 

Environmental Samples 

Sample Analytical 

matrix Sample preparation method Detection limita

 Accuracy Reference 

Air Sample collection on 

cellulose filter, dry ashed, 

solvent extracted 

Air Filter wet ashed in 

HNO3/HF, purified with 

cation and anion 

exchange columns and 

electrodeposition 

Air Cellulose filter dry ashed, 

dissolved in HNO3/HF, 

H2O2/HClO4, purified with 

anion exchange, TRUspec columns followed by 

electrodeposition. 

Water Sample fusion with 

pyrosulfate, precipitated 

with barium sulfate 

Water Wet ashed, purified by 

solvent extraction 

Water Treated with HNO3/H2O2, 

HF/HCl, anion exchange, 

TRU-spec column, 

electrodeposition 

Water Solvent extracted 

Sea water Co-precipitation with iron 

hydroxide, purified by 

anion exchange, coprecipitation with BiPO4, 

cation exchange, electrodeposition 

Sediments	 Sample fusion with KF 

and pyrosulfate, coprecipitate with BaSO4 

Sediments Sample leached with 

HNO3/HF, filtered, purified 

by KL-HDEHP resin 

columns, solvent 

extracted, and electrodeposition 

Sediments None 

Soil Sample fusion with KF 

and pyrosulfate, coprecipitate with BaSO4 

Biphasic liquid 1 pCi 

scintillation 

α-spectroscopy No data 

α-spectroscopy 0.023 pCi/sample 

Scintillation No data 

counter 

Biphasic liquid 1 pCi/sample 

scintillation 

α-spectroscopy 0.026 pCi/L 

PERALS 0.007 pCi/L 

α-spectroscopy No data 

Scintillation No data 

counter 

α-spectroscopy No data 

Gamma-ray 0.02–0.06 pCi/g 

spectroscopy 

Scintillation No data 

counter 

95% Bomben 

et al. 1994 

No data Knab 1979 

102% Goldstein 

et al. 1997 

99.5% Sill and 

Williams 

1969 

95% Bomben 

et al. 1994 

101% Goldstein 

et al. 1997 

104% Dacheux 

and Aupiais 

1998 

64–79% Lovette 

et al. 1990 

No data Sill and 

Williams 

1969 

95–99% Guogang 

et al. 1998 

108–118% Joshi 1989 

No data Sill and 

Williams 

1969 
 

 

AMERICIUM	 192 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining Americium in 

Environmental Samples 

Sample Analytical 

matrix Sample preparation method Detection limita

 Accuracy Reference 

Soil Wet ash in HNO3/HF, 

purified with cation and 

anion exchange columns, 

electrodeposition 

Soil Dry ash, digest in 

HNO3/HCl, anion 

exchange, Ca-oxalate and 

Fe (OH)2 coprecipitation, 

anion exchange, electrodeposition 

Soil Sample leached with 

HNO3/HF, filtered, purified 

by KL-HDEHP resin 

columns, solvent 

extracted, and electrodeposition 

Soil None 

Vegetation Ashed, HNO3/HF, 

(grasses) precipitation with oxalate 

and La, anion exchange, 

solvent extraction 

Vegetation Ashed, digested with 

HNO3-H2O2, oxalate and 

Fe precipitations, anion 

exchange, solvent 

extraction, electrodeposition 

Vegetation Ashed, digested with 

HNO3-HCl, anion 

exchange, Ca-oxalate and 

Fe precipitations, anion 

exchange, electrodeposition 

Lichen, Ashed, leached with HCl, 

moss Microthene-TNOA and 

KL-HDEHP column 

extractions, solvent 

extraction, electrodeposition 

α-spectroscopy No data 

α-spectroscopy 27 pCi/g 

α-spectroscopy No data 

Gamma-ray 0.02–0.06 pCi/g 

spectroscopy 

α-spectroscopy 0.011 pCi/g 

α-spectroscopy 0.3 fCi/g 

α-spectroscopy 27 pCi/g 

α-spectroscopy 0.9 fCi/g 

No data Knab 1979 

75–92% Sanchez 

and 

Singleton 

1996 

95–99% Guogang 

et al. 1998 

108–118% Joshi 1989 

No data Bunzl and 

Kracke 

1990 

73–109% Cooper 

et al. 1993 

75–92% Sanchez 

and 

Singleton 

1996 

No data Jia et al. 

1997 
AMERICIUM 

7. ANALYTICAL METHODS 

193 

Table 7-2. Analytical Methods for Determining Americium in 

Environmental Samples 

Sample 

matrix 

Biota 

Sample preparation 

Ashed, digested with 

HNO3-H2O2, oxalate, and 

Fe precipitations, anion 

exchange, solvent 

extraction, electrodeposition 

Analytical 

method 

α-spectroscopy 

Detection limita

0.3 fCi/g 

 Accuracy 

98–100% 

480% 

(shrimp) 

Reference 

Cooper 

et al. 1993 

a

1 Bq=2.7x10-11 Ci=27 pCi; 27 fCi=1 mBq 

KL-HDEHP = 50% di(2-ethylhexyl) phosphoric acid, 60–100 mesh resin; PERALS = Photon/electron rejecting alpha 

liquid scintillation; TNOA = tri-n-octylamine; TRU = transuranic 
AMERICIUM 194 

7. ANALYTICAL METHODS 

prevent these materials from interfering with the α-spectroscopy measurements of 241Am and 243Am 

(ASTM 1997; Lovette et al. 1990). Initially, the filter media is dissolved with HNO3 and H2O2, the 

residue is wet ashed with HNO3 and then purified using anion exchange chromatography, the solvent is 

extracted with 50% bis-(2-ethylhexyl) phosphoric acid (HDEHP) in toluene, the sample is again passed 

through an anion exchange column, and then the sample is oxidized with HNO3 and H2O2. 243Am is 

commonly used as a surrogate for quantifying the chemical recovery of 241Am during sample preparation, 

so quantification of 241Am in a sample involves α-spectrometric analysis of both isotopes. Preparation of 

the purified filter sample for α-spectroscopy requires electrodeposition of the americium from a sulfate 

solution onto a stainless steel or platinum disc from which alpha counts are obtained during the αspectroscopy analysis (DOE 1997b). The accuracy of this method of analysis for americium can vary 

between 85 and 102% and the MDA often ranges between 0.032 and 0.023 pCi/sample (1.2 and 

0.85 mBq/sample) (Goldstein et al. 1997). 

For the analysis of americium in water, there is a broad array of available sample preparation and 

detection methodologies (see Table 7-2). Many of the common and standardized analytical 

methodologies typically include the minimization of sample volume, purification through coprecipitation, anion exchange column chromatography, and solvent extraction techniques followed by 

radiochemical detection of americium in the purified sample. Gross alpha analysis or liquid scintillation 

are common detection techniques that are utilized to quantify americium in these methods. However, if 

lower detection sensitivity or isotopic determination is required, then α-spectroscopy is the preferred 

method to quantify 241Am (Dacheux and Aupiais 1997; DOE 1997b; Goldstein et al. 1997; Harvey et al. 

1993; Sill and Williams 1969). These detection methods can provide measurements of total americium 

activity within a sample, especially when appropriate steps have been taken to purify the sample of 

interfering materials or minimize the influence of other radionuclides on radiochemical activity (Dazhu et 

al. 1991). The presence of alpha emitting radionuclides in the sample can contribute to the alpha counts 

measured in radiochemical detection methods and, thus, affect the accuracy of the assay for determining 

the quantity of americium within a sample. 

There are methods available to quantify the total mass of americium in environmental samples. Mass 

spectrometric methods provide total mass measurements of americium isotopes (Dacheux and Aupiais 

1997, 1998; Halverson 1984; Harvey et al. 1993); however, these detection methods have not gained the 

same popularity as is found for the radiochemical detection methods. This may relate to the higher 

purchase price of an MS system, the increased knowledge required to operate the equipment, and the 

selection by EPA of α-spectroscopy for use in its standard analytical methods. Fluorimetric methods, 
AMERICIUM 195 

7. ANALYTICAL METHODS 

which are commonly used to determine the total mass of uranium and curium in environmental samples, 

have limited utility to quantify americium, due to the low quantum yield of fluorescence for americium 

(Thouvenot et al. 1993). 

Several rapid analysis techniques involving gamma spectroscopy or spectrometry have been developed 

that require either no or minimal sample preparation that can, under optimized conditions, provide the 

required selectivity and sensitivity to quantify americium in environmental samples, such as soils and 

sediments (Byrne and Komosa 1993; Cutshall et al. 1983; Guilmette 1986; Joshi 1989). These techniques 

utilize either an intrinsic germanium detector or a phoswich-based cesium-sodium iodide low energy 

photon detector that detects the gamma-rays emitted from 241Am in a neat (undiluted) or ashed 

environmental or biological sample. On average, these methods have a minimum significant measurable 

activity (MSMA) of approximately 1 pCi/sample (0.037 Bq/sample). To achieve this low MSMA, the 

counting efficiency of the detector must be standardized against the sample size and composition in order 

to assure the desired accuracy of the assay (Cutshall et al. 1983; Joshi 1989). Using a germanium detector 

with its vastly superior energy resolution facilitates the identification of multiple isotopes in the same 

sample without photopeak interference. It is the detector of choice for analyzing samples (and performing 

internal monitoring on individuals) by gamma spectroscopy. The disadvantages of using germanium are 

its greater purchase price and requirement to be cooled with liquid nitrogen or by electrocryogenic means 

whenever it is in use. One limitation of the phoswich assays is the need to know the isotopic composition 

of the sample since the x-rays that accompany the decay of other radionuclides may also be counted by 

the phoswich detector, which is typically calibrated with a wide energy window that focuses on the 59.5 

keV photon, but also detects higher energy x-rays and Compton scattered photons. 

Several methods have been described in the Multi-Agency Radiation Survey and Site Investigation 

Manual (MARSSIM 2000) for the survey and investigation of sites contaminated with radioactive 

materials. At the high end of the survey instruments, costing over $1,000,000 in 1995, is an inductively 

coupled plasma-mass spectrometer (ICP-MS) with a laser added to the front end to vaporize small 

portions of a surface or a volumetric material to be analyzed (laser ablation), thereby avoiding physical 

sample collection. Prices in 2002 were a factor of two or three lower for an inductively coupled plasma 

double focusing magnet mass spectrometer capable of very accurate americium isotopic measurements. 

The quantity of americium in soil, sediments, vegetation, and biota is determined using methods similar 

to those described above. For example, in a standardized method developed by DOE (1997b), soil 

samples are dissolved with a series of acid treatments (e.g., HNO3, HF) and initially purified through co­
AMERICIUM 196 

7. ANALYTICAL METHODS 

precipitation using calcium oxalate followed by co-precipitation with an Fe carrier. A final purification of 

the sample is achieved by passing the sample through a series of anion exchange columns (e.g., HNO3, 

HCl, and NH4SCN), followed by electrodeposition of the americium (chloride form) onto a platinum disc 

in preparation for α-spectroscopy analysis. 

In another standardized method developed for the analysis of americium in soil (ASTM 1997), a different 

approach is taken towards purifying the dissolved soil sample that relies on a series of co-precipitations 

and solvent extractions to prepare the soil sample for α-spectroscopy analysis. After the soil has been 

dissolved, the sample is initially purified by co-precipitation with barium sulfate, followed by solvent 

extraction of the redissolved precipitate with 15% HDEHP in n-hexane. The extracted trivalent actinides 

and lanthanides are stripped from the organic phase using nitric acid containing sodium bromate. The 

subsequent solution containing the trivalent actinides and lanthanides is extracted again with 15% 

HDEHP in n-hexane to remove plutonium, thorium, and tetravalent curium. The aqueous phase is further 

purified through co-precipitation with a lanthanum carrier to isolate the rare earth fluorides followed by a 

treatment using silver nitrate and ammonium persulfate/ammonium fluoride to precipitate all remaining 

rare earth fluorides, except for hexavalent americium fluoride. The hexavalent americium is reduced back 

to the trivalent state using hydrogen peroxide and then reprecipitated with a neodymium carrier in 

preparation for α-spectroscopy analysis. Both the DOE and the American Society for Testing and 

Materials (ASTM) methods of analysis provide good precision (<6% standard derivation) with no 

statistically significant bias (at the 5% level) observed. Analysis of americium in sediments, vegetation, 

and biota can also be performed using variations of the abovementioned methods or other methods, as 

exemplified in Table 7-2. 

The detection limits, accuracy, and precision of any analytical methodology, as well as the composition of 

the sample medium, are important parameters in determining the appropriateness of a method to quantify 

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 quantification (NRC 1984). Several factors influence the LLD, including 

background counting rates, size or concentration of sample, detector sensitivity, 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 and for samples in the same 

laboratory, utilizing the same or similar measurement procedures, will vary. 
 

 

AMERICIUM 197 

7. ANALYTICAL METHODS 

The accuracy of a measurement technique in determining the quantity of a particular analyte in 

environmental samples is greatly dependent on the reliability of the calibrating technique. Thus, the 

availability of standard, certified radiation sources with known concentrations of americium are required 

in order to ensure the reliability of the calibration methods and the accuracy of americium measurements 

in environmental samples. The primary source of certified americium standards is the NIST. Standard 

solutions of 241Am (SRM 4322, 40 Bq/g [1.1 nCi/g]) and 243Am (SRM 4332, 40 Bq/g [1.1 nCi/g]) are 

available. Standard reference materials are also available from NIST and the International Atomic 

Energy Agency (IAEA) for a number of environmental matrices; for example, soils and sediments (Rocky 

Flats Soil [SRM 4353], river sediment [SRM 4350B], and Peruvian soil [SRM 4355] and sediments 

[IAEA 367, IAEA 135]). 

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 americium 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 americium. 

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. Analytical methods with 

satisfactory sensitivity and precision are available to determine the levels of americium in human tissues 

and body fluids. 
 

 

AMERICIUM 198 

7. ANALYTICAL METHODS 

Methods for Determining Parent Compounds and Degradation Products in Environmental 

Media. Analytical methods with the required sensitivity and accuracy are available for quantification 

of americium, both total and isotopic, in environmental matrices (see Table 7-2). 

Whether in the environment or in the human body, americium will undergo radioactive decay to form a 

series of radioactive nuclides that end in a stable isotope of lead (for 243Am) or bismuth (for 241Am) (see 

Chapter 4). The decay series proceeds slowly due to the long half-lives of some of the intermediate decay 

series isotopes. Therefore, more sensitive analytical methods for accurately measuring very low levels of 

these radionuclides would be useful. Practically speaking, since 239Pu (for 243Am) and 237Np (for 241Am) 

have such extremely long half-lives, 2.41x104

 and 2.14x106 years, respectively, few decay products need 

to be considered since they would only begin to achieve measurable levels in the distant future. 

7.3.2 Ongoing Studies 

The Federal Research in Progress (FEDRIP 2004) database did not list any current studies involving 

developments in analytical techniques related to americium. 
AMERICIUM 199 

8. REGULATIONS AND ADVISORIES 

The international, national, and state regulations and guidelines regarding americium in air, water, and 

other media are summarized in Table 8-1. 

The USNRC maintains a database of information regarding licensees authorized to possess americium 

isotopes (241Am through 244Am) within the 18 non-Agreement States (states not committed to selfregulation). This database includes more than 2,000 records of licensees and site possession limits in the 

microcurie to curie range. The isotope, 241Am, accounts for most of the licenses. Such records for 

USNRC Agreement States are maintained by the individual state radioactive material regulatory 

organizations. The USNRC and EPA each have responsibilities for regulating the cleanup of 

radioactivity and decommissioning of USNRC licensed sites. USNRC and EPA reached an agreement in 

2002, in response to Congressional mandate, to preclude double regulation of these efforts. The 

agreement provides that EPA will defer exercise of authority under CERCLA for the majority of facilities 

decommissioned under USNRC authority. It also contains provisions for joint consultation when certain 

EPA parameters are exceeded, including groundwater exceeding EPA-permitted levels, USNRC 

contemplation of restricted release or alternate release criteria, and residual soil radioactivity 

concentrations exceeding those in the agreement (USNRC 2002). 

No inhalation or oral MRLs were derived for americium or americium compounds. 

The EPA IRIS database has withdrawn its cancer classification for radionuclides, but the EPA Office of 

Air and Radiation believes that all radionuclides, including the americium isotopes, should be considered 

to be known carcinogens, and has assigned them to Group A. Carcinogenic toxicity values for 241Am are 

listed in EPA’s Federal Radiation Guidance Report No. 13 (EPA 2000a). Lifetime excess total cancer 

risk per unit intake are included for inhalation (Table 2.1), drinking water ingestion (Table 2.2), and 

submersion, ground plane exposure, and soil intake (Table 2.3). Media-specific usage rates (Table 3.1) 

provide a means of adjusting the values to be compatible with specific population groups (e.g., tap water 

intakes range from a low of 0.188 L/day for a newborn female to a high of 1.643 L/day for a 50-year-old 

male, with a societal average of 1.11 L/day). The EPA has not derived reference concentrations (RfCs) or 

reference doses (RfDs) for americium (IRIS 2002), but has derived a maximum contaminant level (MCL) 

of 15 pCi/L for total alpha-emitters (including americium), less uranium and radon (EPA 2000c). 
 

 

 

 

 

 

 

AMERICIUM	 200 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Americium 

Agency Description Information Reference 

INTERNATIONAL 

Guidelines: 

IARC 

NATIONAL 

Guidelines: 

a. Air 

ACGIH Effective dose 

 Any single year 

Averaged over 5 years 

Annual equivalent dose to 

Lens of the eye 

Skin 

Hands and feet 

Embryo-fetus exposures once the 

pregnancy is known 

Monthly equivalent dose 

Dose to the surface of women’s 

abdomen (lower trunk) 

Intake of radionuclide 

NIOSH REL (10-hour TWA) 

NATIONAL 

Regulations: 

EPA Concentration levels for 

environmental compliance 241Am 242Am 243Am 

OSHA PEL (8-hour TWA) 

USNRC Occupational values—inhalation 241Am 242Am 243Am 

 Effluent concentrations—air 241Am 242Am 243Am 

b. Water 

USNRC Effluent concentrations—water 241Am 242Am 243Am 

EPA Drinking water

 Gross alpha activity, less U, Rn 

c. Food 

FDA Derived intervention levela

 (DIL; 

Bq/kg food) for 241Am in accidentallycontaminated human food 

No data 

50 mSv 

20 mSv 

150 mSv 

500 mSv 

500 mSv 

0.5 mSv 

2 mSv for the remainder of 

the pregnancy 

1/20 ALI 

No data 

1.9x10-15 Ci/m3 

1.5x10-11 Ci/m3 

1.8x10-15 Ci/m3 

No data 

ALI(μCi) DAC(μCi/mL) 

6x10-3 3x10-12 

8x101 4x10-8 

6x10-3 3x10-12 

2x10-14 μCi/mL 

1x10-10 μCi/mL 

2x10-14 μCi/mL 

2x10-8 μCi/mL 

5x10-5 μCi/mL 

2x10-8 μCi/mL 

15 pCi/L 

2.0 

ACGIH 2002 

EPA 2001a 

40CFR61, 

Appendix E 

USNRC 2001a 

10CFR20, 

Appendix B 

USNRC 2001a 

10CFR20, 

Appendix B 

USNRC 2001a 

10CFR20, 

Appendix B 

EPA 2000c 

FDA 1998 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

AMERICIUM 

8. REGULATIONS AND ADVISORIES 

201 

Agency 

Table 8-1. Regulations and Guidelines Applicable to Americium 

Description Information Reference 

NATIONAL (cont.) 

c. Food 

Sources of radiation used for 

inspection of food; sealed units 

producing radiation—241Am 

DOT Activity values for radionuclides in 

transport 241Am, 242Am, and 243Am 

A1 

A2 

EPA Annual possession quantities for 

environmental compliance 241Am 

Gaseous form 

Liquid/powder forms 

Solid form 242Am 

Gaseous form 

Liquid/powder forms 

Solid form 243Am 

Gaseous form 

Liquid/powder forms 

Solid form 

Radioactive waste—release limits for 

containment requirementsb 

241Am or 243Am 

 Reportable quantity 241Am 242Am 243Am 

 Carcinogenicity—slope factorsc 

Ingestion—lifetime excess total 

 cancer risk/pCi 

Water 241Am 243Am 

Food 241Am 243Am 

Soil 241Am 243Am 

Carcinogenicity—slope factorsc 

Inhalation—lifetime excess total 

 cancer risk/pCi 241Am 243Am 

External exposure—risk/year per 

pCi/g in soil 241Am 243Am 

10 Gy maximum allowed dose FDA 2000 

to food 21CFR179.21 

DOT 2001 

40CFR173.435 

5.41x101

 Ci 

5.41x10-3 Ci 

EPA 2001a 

40CFR61, 

2.3x10-6 Ci/year 

2.3x10-3 Ci/year 

2.3x100

 Ci/year 

Appendix E 

1.8x10-2 Ci/year 

1.8x101

 Ci/year 

1.8x104

 Ci/year 

2.3x10-6 Ci/year 

2.3x10-3 Ci/year 

2.3x100

 Ci/year 

EPA 2001b 

1x102

 Ci 

40CFR191, Appendix 

A 

EPA 2001c 

1x10-2 Ci 

1x102

 Ci 

1x10-2 Ci 

40CFR302.4, 

Appendix B 

 EPA 2002 

1.04x10-10 

1.03x10-10 

1.34x10-10 

1.34x10-10 

2.17x10-10 

2.17x10-10 

 EPA 2002 

2.81x10-8 

2.70x10-8 

2.76x10-8 

9.47x10-8 
 

 

 

 

 

 

 

 

 

 

AMERICIUM	 202 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Americium 

Agency Description Information Reference 

NATIONAL (cont.) 

USNRC Activity values for radionuclides in 

transport 241Am, 242Am, and 243Am 

A1 

A2 

Specific activity 241Am 242Am 243Am 

Byproduct material for in vitro clinical 

or laboratory testing—241Am 

Calibration or reference sources; 

shall not possess at any one time, at 

any one location of storage or use of 

241Am 

Exemption for low-level materials; 

contains only Americium in special 

form 

Export of byproduct material 

General applicability to domestic 

licensing of byproduct material; 

quantity of licensed material requiring 

labeling 241Am 

Ionizing radiation measuring 

instruments containing, for purposes 

of internal calibration or 

standardization, one or more sources 

of byproduct material; exempt 

quantities of 241Am 

Occupational values—oral ingestion 

(ALI) 241Am 242Am 243Am 

USNRC Quantity of radioactive material 

requiring need for an emergency plan 

for responding to a release—241Am, 242Am, and 243Am 

 Release fraction

 Quantity 

Standards for protection against 

radiation—quantity of licensed 

material requiring labeling 241Am 242Am 243Am 

5.41x101

 Ci 

5.41x10-3 Ci 

3.4 Ci/g 

1.0x101

 Ci/g 

2.0x10-1 Ci/g 

≤0.005 μCi 

≤5 μCi 

Aggregate radioactivity 

≤20 Ci 

≤1 Ci/shipment or 

≤100 Ci/year 

1x10-2 μCi 

0.05 μCi 

8x10-1 μCi 

4x103

 μCi 

8x10-1 μCi 

0.001% 

2 Ci 

1x10-3 μCi 

1x101

 μCi 

1x10-3 μCi 

USNRC 2001b 

10CFR71, 

Table A-1 

USNRC 2001c 

10CFR31.11 

USNRC 2001d 

10CFR31.8 

USNRC 2001e 

10CFR71.10 

USNRC 2001f 

10CFR110.23 

USNRC 2001g 

10CFR30, 

Appendix B 

USNRC 2001g 

10CFR30.15(a)(9) 

USNRC 2001a 

10CFR20, 

Appendix B 

USNRC 2001h 

10CFR30.72, 

Schedule C 

USNRC 2001i 

10CFR20, 

Appendix C 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

AMERICIUM 

8. REGULATIONS AND ADVISORIES 

203 

Agency 

Table 8-1. Regulations and Guidelines Applicable to Americium 

Description Information Reference 

STATEd 

a. Air 

Illinois Concentrations in air above natural 

background 241Am S 

 242mAm 

I 

S 

242Am 

I 

S 

243Am 

I 

S 

244Am 

I 

S 

I 

New Jersey Maximum permissible average 

concentrations in air 

 Occupational (40-hour week) 241Am S 

242mAm 

I 

S 

242Am 

I 

S 

243Am 

I 

S 

244Am 

I 

S 

I 

New Jersey Maximum permissible average 

concentrations in air 

 Non-occupational 241Am S 

242mAm 

I 

S 

242Am 

I 

S 

243Am 

I 

S 

244Am 

I 

S 

I 

b. Water 

Colorado Standards applicable to surface 

waters—241Am 

15 pCi/L 

Groundwater levels of radioactive 

materials shall not exceed this 

15 pCi/L 

amount—Am 

BNA 2001 

2x10-13 μCi/mL 

4x10-12 μCi/mL 

2x10-13 μCi/mL 

9x10-12 μCi/mL 

1x10-9 μCi/mL 

2x10-9 μCi/mL 

2x10-13 μCi/mL 

4x10-12 μCi/mL 

1x10-7 μCi/mL 

8x10-7 μCi/mL 

BNA 2001 

6x10-12 μCi/mL 

1x10-10 μCi/mL 

6x10-12 μCi/mL 

3x10-10 μCi/mL 

4x10-8 μCi/mL 

5x10-8 μCi/mL 

6x10-12 μCi/mL 

1x10-10 μCi/mL 

4x10-6 μCi/mL 

2x10-5 μCi/mL 

BNA 2001 

2x10-13 μCi/mL 

4x10-12 μCi/mL 

2x10-13 μCi/mL 

9x10-12 μCi/mL 

1x10-9 μCi/mL 

2x10-9 μCi/mL 

2x10-13 μCi/mL 

4x10-12 μCi/mL 

1x10-7 μCi/mL 

8x10-7 μCi/mL 

BNA 2001 

CO Dept of Public 

Health and Environ 

1999 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

AMERICIUM	 204 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Americium 

Agency Description Information Reference 

STATE (cont.) 

New Jersey Maximum permissible average 

concentrations in water 

 Occupational (40-hour week) 241Am 

242mAm 

242Am 

243Am 

244Am 

Maximum permissible average 

concentrations in water 

 Non-occupational 241Am 

242mAm 

242Am 

243Am 

244Am 

c. Food 

d. Other 

Arkansas Determination of A1and A2 quantities 

for transportation 241Am 

A1 

A2 

Specific activity 243Am 

A1 

A2 

Specific activity 

Standards for protection against 

radiation—241Am 

California Ionizing radiation measuring 

instruments containing, for purposes 

of internal calibration or 

standardization, one or more source 

of radioactive material; 241Am is 

considered an exempt quantity 

Colorado	 Determination of A1and A2 for 

transportation 241Am, 242mAm, and 243Am 

A1 

A2 

S 1x10-4 μCi/mL 

I 8x10-4 μCi/mL 

S 1x10-4 μCi/mL 

I 3x10-3 μCi/mL 

S 4x10-3 μCi/mL 

I 4x10-3 μCi/mL 

S 1x10-4 μCi/mL 

I 8x10-4 μCi/mL 

S 1x10-1 μCi/mL 

I 1x10-1 μCi/mL 

S 4x10-6 μCi/mL 

I 2x10-5 μCi/mL 

S 4x10-6 μCi/mL 

I 9x10-5 μCi/mL 

S 1x10-4 μCi/mL 

I 1x10-4 μCi/mL 

S 4x10-6 μCi/mL 

I 3x10-5 μCi/mL 

S 5x10-3 μCi/mL 

I 5x10-3 μCi/mL 

No data 

8 Ci 

0.008 Ci 

3.2 Ci/g 

8 Ci 

0.008 Ci 

1.9x10-1 Ci/g 

0.01 μCi 

<0.05 μCi 

54.1 Ci 

5.41x10-3 Ci 

BNA 2001 

BNA 2001 

BNA 2001 

BNA 2001 

BNA 2001 

BNA 2001 
 

 

 

AMERICIUM 205 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Americium 

Agency Description Information Reference 

STATE (cont.) 

Florida Quantity of radioactive material BNA 2001 

requiring need for an emergency plan 

for responding to a release 241Am, 242Am, and 243Am 

Release fraction 0.001% 

Quantity 2 Ci 

Georgia Packages transported between Not to exceed 20 Ci BNA 2001 

locations within the U.S. which 

contain only Am or Pu in special form 

with an aggregate radioactivity 

Mississippi Packages transported between Not to exceed 20 Ci BNA 2001 

locations within the U.S. which 

contain only Am or Pu in special form 

with an aggregate radioactivity 

a

The FDA-recommended Derived Intervention Level (DIL) for radionuclides of 241Am, is defined as the DIL for the most 

sensitive age group (3 months) that was calculated from the most limiting Protective Action Goal (PAG; 50 mSv 

committed dose equivalent to the bone). 

b

Release limit per 1,000 metric tons of heavy metal (MTHM) or other unit of waste. c

Radionuclide slope factors are calculated by EPA’s Office of Radiation and Indoor Air (ORIA) to assist HEAST users with 

risk-related evaluations and decision-making at various stages of the remediation process. Ingestion and inhalation slope 

factors are central estimates in a linear model of the age-averaged, lifetime attributable radiation cancer incidence (fatal 

and nonfatal cancer) risk per unit of activity inhaled or ingested, expressed as risk/picocurie (pCi). External exposure 

slope factors are central estimates of the lifetime attributable radiation cancer incidence risk for each year of exposure to 

external radiation from photon-emitting radionuclides distributed uniformly in a thick layer of soil, and are expressed as 

risk/year per pCi/gram of soil. 

d

The states included in this section are only those that were available from the BNA database. 

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 concentration; DIL = Derived Intervention Level; 

DOE = Department of Energy; DOT = Department of Transportation; EPA = Environmental Protection Agency; 

FDA = Food and Drug Administration; I = insoluble; IARC = International Agency for Research on Cancer; 

mSv = millisievert; NIOSH = National Institute for Occupational Safety and Health; OSHA = Occupational Safety and 

Health Administration; PAG = protective action goal; PEL = permissible exposure limit; S = soluble; REL = recommended 

exposure limit; TLV = threshold limit value; TWA = time-weighted average; USNRC = U.S. Nuclear Regulatory 

Commission 

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*Weiss JF, Walburg HE, McDowell WJ. 1980. Placental transfer of americium and plutonium in mice. 

Health Phys 39:903-911. 

*West JR, Smith HW, Chasis H. 1948. Glomerular filtration rate, effective renal blood flow, and 

maximal tubular excretory capacity in infancy. J Pediatr 32:10-18. 

*Whicker FW, Hinton TG, Orlandini KA, et al. 1999. Uptake of natural and anthropogenic actinides in 

vegetable crops grown on a contaminated lake bed. J Environ Radioact 45:1-12. 

*Widdowson EM, Dickerson JWT. 1964. Chemical composition of the body. In: Comar CL, Bronner 

F, eds. Mineral metabolism: An advanced treatise. Volume II: The Elements Part A. New York: 

Academic Press. 

Withers EH, Page DL, Hollifield J, et al. 1975. Carcinoma of the thyroid with description of a new 

scanning technic. Am J Surg 130(4):395-398. 

Wuu J-L, Yuan M-C, Su S-H, et al. 2002. The alpha and beta emitter measurement system in INER. 

Appl Radiat Isot 56:261-264. 
AMERICIUM 255 

9. REFERENCES 

*Xu GB, Yu CP. 1986. Effects of age on deposition of inhaled particles in the human lung. Aerosol Sci 

Technol 5:349-357. 

Yamamoto M, Komura K, Sakanoue M, et al. 1985. Pu isotopes, 241Am and 137Cs in soils from the 

atomic bombed areas in Nagasaki and Hiroshima. J Radiat Res 26:211-223. 

*Zach R. 1985. Contribution of inhalation by food animals to man's ingestion dose. Health Phys 

49(5):737-745. 

*Ziegler EE, Edwards BB, Jensen RL, et al. 1978. Absorption and retention of lead by infants. Pediatr 

Res 12:29-34. 

AMERICIUM 257 

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. 
AMERICIUM 258 

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. 
 

 

 

AMERICIUM 259 

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. 

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. 
 

 

AMERICIUM 260 

10. GLOSSARY 

Branching—The occurrence of two or more modes by which a radionuclide can undergo radioactive 

decay. For example, 214Bi can undergo alpha or beta minus decay, 64Cu can undergo beta minus, beta 

plus, or electron capture decay. An individual atom of a nuclide exhibiting branching disintegrates by one 

mode only. The fraction disintegrating by a particular mode is the "branching fraction" for that mode. 

The "branching ratio" is the ratio of two specified branching fractions (also called multiple 

disintegration). 

Bremsstrahlung—X rays that are produced when a charged particle accelerates (speeds up, slows down, 

or changes direction) in the strong field of a nucleus. 

Buildup Factor—The ratio of the radiation intensity, including both primary and scattered radiation, to 

the intensity of the primary (unscattered) radiation. 

Cancer Effect Level (CEL)—The lowest dose of chemical or radiation in a study, or group of studies, 

that produces significant increases in the incidence of cancer (or tumors) between the exposed population 

and its appropriate control. 

Capture, Electron—A mode of radioactive decay involving the capture of an orbital electron by its 

nucleus. Capture from a particular electron shell, e.g., K or L shells, is designated as "K-electron capture" 

or "L-electron capture." 

Capture, K-Electron—Electron capture from the K shell by the nucleus of the atom. Also loosely used 

to designate any orbital electron capture process. 

Carcinogen—A chemical or radiation that is capable of inducing cancer. 

Carcinoma—Malignant neoplasm composed of epithelial cells, regardless of their derivation. 

Case-Control Study—A type of epidemiological study which examines the relationship between a 

particular outcome (disease or condition) and a variety of potential causative agents (such as toxic 

chemicals). In a case-controlled study, a group of people with a specified and well-defined outcome is 

identified and compared to a similar group of people without outcome. 

Case Report—Describes a single individual with a particular disease or exposure. These may suggest 

some potential topics for scientific research but are not actual research studies. 

Cataract—A clouding of the crystalline lens of the eye which obstructs the passage of light. 

Ceiling Value—A concentration of a substance that should not be exceeded, even temporarily. 

Charged Particle—A nuclear particle, atom, or molecule carrying a positive or negative charge. 

Chronic Exposure—A long-term, continuous exposure to a chemical or radioactive material. For 

example, exposure to a chemical for 365 days or more, as specified in the Toxicological Profiles. 

Cohort Study—A type of epidemiological study of a specific group or groups of people who have had a 

common insult (e.g., exposure to an agent suspected of causing disease or a common disease) and are 

followed forward from exposure to outcome. At least one exposed group is compared to one unexposed 

group. 
AMERICIUM 261 

10. GLOSSARY 

Collective Dose—The sum of the individual doses received in a given period of time by a specified 

population from exposure to a specified source of radiation. Collective dose is expressed in units such as 

man-rem and person-sievert. 

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. 

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. 
AMERICIUM 262 

10. GLOSSARY 

Curie (Ci)—A unit of radioactivity. One curie equals that quantity of radioactive material in which there 

are 3.7x1010 nuclear transformations per second. The activity of 1 gram of radium is approximately 1 Ci. 

Attocurie (aCi)—One-thousandth of a femtocurie (3.7x10-8 disintegrations per second). 

 Femtocurie (fCi)—One-billionth of a microcurie (3.7x10-5 disintegrations per second).

 Megacurie (MCi)—One million curies (3.7x1016 disintegrations per second). 

 Microcurie (μCi)—One-millionth of a curie (3.7x104

 disintegrations per second). 

 Millicurie (mCi)—One-thousandth of a curie (3.7x107 disintegrations per second). 

 Nanocurie (nCi)—One-billionth of a curie (3.7x101 disintegrations per second). 

 Picocurie (pCi)—One-millionth of a microcurie (3.7x10-2 disintegrations per second). 

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.) 
AMERICIUM 263 

10. GLOSSARY 

Disintegration, Nuclear—A spontaneous nuclear transformation (radioactivity) characterized by the 

emission of energy and mass from the nucleus. When large numbers of nuclei are involved, the process is 

characterized by a definite half-life (see Transformation, Nuclear). 

Distribution Coefficient (Kd)—Describes the distribution of a chemical between the solid and aqueous 

phase at thermodynamic equilibrium, is given as follows: 

[C]s Kd = [C]w , Units = (L solution)/(kg solid), 

where [C]s is the concentration of the chemical associated with the solid phase in units of (mg)/(kg solid), 

and [C]w is the concentration of the chemical in the aqueous phase in units of (mg)/(L solution). As the 

magnitude of Kd decreases, the potential mobility of the chemical to groundwater systems increases and 

vice versa. 

Dose—A general term denoting the quantity of a substance, radiation, or energy absorbed. For special 

purposes it must be appropriately qualified. If unqualified, it refers to radiation absorbed dose. 

Absorbed Dose—The energy imparted to matter by ionizing radiation per unit mass of irradiated 

material at the place of interest. The unit of absorbed dose is the rad. One rad equals 100 ergs 

per gram. In SI units, the absorbed dose is the gray which is 1 J/kg (see Rad). 

Cumulative Dose (Radiation)—The total dose resulting from repeated or continuous exposures 

to radiation. 

Dose Assessment—An estimate of the radiation dose to an individual or a population group usually by 

means of predictive modeling techniques, sometimes supplemented by the results of measurement. 

Dose Equivalent (DE)—A quantity used in radiation safety practice to account for the relative biological 

effectiveness of the several types of radiation. It expresses all radiations on a common scale for 

calculating the effective absorbed dose. The NRC defines it as the product of the absorbed dose, the 

quality factor, and all other modifying factors at the location of interest. ICRP has changed its definition 

to be the product of the absorbed dose and the radiation weighting factor. (The unit of dose equivalent is 

the rem. In SI units, the dose equivalent is the sievert, which equals 100 rem.) 

Dose, Fractionation—A method of administering therapeutic radiation in which relatively small doses 

are given daily or at longer intervals. 

Dose, Protraction—A method of administering therapeutic radiation by delivering it continuously over a 

relatively long period at a low dose rate. 

Dose, Radiation—The amount of energy imparted to matter by ionizing radiation per unit mass of the 

matter, usually expressed as the unit rad, or in SI units, the gray. 100 rad'1 gray (Gy) (see Absorbed 

Dose). 

Committed Dose Equivalent (HT,50)—The dose equivalent to organs or tissues of reference (T) 

that will be received from an intake of radioactive material by an individual during the 50 years 

following the intake. 
AMERICIUM 264 

10. GLOSSARY 

Committed Effective Dose Equivalent (HE,50)—The sum of the products of the weighting 

factors applicable to each of the body organs or tissues that are irradiated and the committed dose 

equivalent to those organs or tissues. 

Effective Dose —A dose value that attempts to normalize the detriment to the body (for cancer 

mortality and morbidity, hereditary effects, and years of life lost) from a non-uniform exposure to 

that of a uniform whole body exposure. Effective dose is calculated as the sum of products of the 

equivalent dose and the tissue weighting factor (wT) for each tissue exposed. (E = ∑DT,R wR wT)). 

Effective Dose Equivalent (HE)—This dose type is limited to internal exposures and is the sum 

of the products of the dose equivalent to the organ or tissue (HT) and the weighting factors (wT) 

applicable to each of the body organs or tissues that are irradiated. (HE = ∑wT HT). 

Equivalent Dose—A dose quantity that places the biological effect of all radiation types on a 

common scale for calculating tissue damage. Alpha particles, for example, are considered to 

cause 20 times more damage than gamma rays. Equivalent dose is calculated as the sum of 

products of the average absorbed dose (in gray) in an organ or tissue (DT,R) from each type of 

radiation and the radiation weighting factor (wR) for that radiation (∑DT,R wR). 

External Dose—That portion of the dose equivalent received from radiation sources outside the 

body. 

Internal Dose—That portion of the dose equivalent received from radioactive material taken into 

the body. 

Limit—A permissible upper bound on the radiation dose. 

Maximum Permissible Dose (MPD)—The greatest dose equivalent that a person or specified 

part thereof shall be allowed to receive in a given period of time. 

Median Lethal Dose (MLD)—Dose of radiation required to kill, within a specified period 

(usually 30 days), 50% of the individuals in a large group of animals or organisms. Also called 

the LD50, or LD50/30 if for 30 days. 

Threshold Dose—The minimum absorbed dose that will produce a detectable degree of any 

given effect. 

Tissue Dose—Absorbed dose received by tissue in the region of interest, expressed in rad (see 

Dose, Gray, and Rad). 

Dose Rate—The amount of radiation dose delivered per unit time. Generically, the rate at which 

radiation dose is delivered to any material or tissue. 

Dose-Response Relationship—The quantitative relationship between the amount of exposure to a 

toxicant and the incidence of the adverse effects. 

Dosimetry—Quantification of radiation doses to cells, tissues, organs, individuals or populations 

resulting from radiation exposures. 

Early Effects (of radiation exposure)—Effects that appear within 60 days of an acute exposure. 
AMERICIUM 265 

10. GLOSSARY 

Electron—A stable elementary particle having an electric charge equal to ±1.60210x10-19 C (Coulombs) 

and a rest mass equal to 9.1091x10-31 kg. A positron is a positively charged "electron" (see Positron). 

Electron Volt—A unit of energy equivalent to the energy gained by an electron in passing through a 

potential difference of one volt. Larger multiple units of the electron volt are frequently used: keV for 

thousand or kilo electron volts; MeV for million or mega electron volts (eV). 1 eV=1.6x10-12 erg. 

Embryotoxicity and Fetotoxicity—Any toxic effect on the conceptus as a result of prenatal exposure to 

a chemical; the distinguishing feature between the two terms is the stage of development during which the 

insult occurred. The terms, as used here, include malformations and variations, altered growth, and in 

utero death. 

Energy—Capacity for doing work. Gravitationally, "potential energy" is the energy inherent in a mass 

because of its spatial relation to other masses. Chemically or radiologically, “potential energy” is the 

energy released when a chemical reaction or radiological transformation goes to completion. "Kinetic 

energy" is the energy possessed by a mass because of its motion (SI unit: joules): 

Binding Energy (Electron)—The amount of energy that must be expended to remove an 

electron from an atom. 

Binding Energy (Nuclear)—The energy represented by the difference in mass between the sum 

of the component parts and the actual mass of the nucleus. It represents the amount of energy 

that must be expended to break a nucleus into its component neutrons and protons. 

Excitation Energy—The energy required to change a system from its ground state to an excited 

state. Each different excited state has a different excitation energy. 

Ionizing Energy—The energy required to knock an electron out of an atom. The average energy 

lost by electrons or beta particles in producing an ion pair in air or in soft tissue is about 34 eV. 

Radiant Energy—The energy of electromagnetic radiation, such as radio waves, visible light, x 

and gamma rays. 

Enrichment, Isotopic—An isotopic separation process by which the relative abundances of the isotopes 

of a given element are altered, thus producing a form of the element that has been enriched in one or more 

isotopes and depleted in others. In uranium enrichment, the percentage of uranium-235 in natural 

uranium can be increased from 0.7% to >90% in a gaseous diffusion process based on the different 

thermal velocities of the constituents of natural uranium (234U, 235U, 238U) in the molecular form UF6. 

EPA Health Advisory—An estimate of acceptable drinking water levels for a chemical substance based 

on health effects information. A health advisory is not a legally enforceable federal standard, but serves 

as technical guidance to assist federal, state, and local officials. 

Epidemiology—Refers to the investigation of factors that determine the frequency and distribution of 

disease or other health-related conditions within a defined human population during a specified period. 

Equilibrium, Radioactive—In a radioactive series, the state which prevails when the ratios between the 

activities of two or more successive members of the series remains constant. 

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 
AMERICIUM 266 

10. GLOSSARY 

attain equilibrium) then, after equilibrium is reached, equal numbers of atoms of all members of 

the series disintegrate in unit time. This condition is never exactly attained, but is essentially 

established in such a case as 226Ra and its transformation series to stable 206Pb. The half-life of 

226Ra is about 1,600 years; of 222Rn, approximately 3.82 days, and of each of the subsequent 

members, a few minutes. After about a month, essentially the equilibrium amount of radon is 

present; then (and for a long time) all members of the series disintegrate the same number of 

atoms per unit time. At this time, the activity of the daughter is equal to the activity of the parent. 

Transient Equilibrium—If the half-life of the parent is short enough so the quantity present 

decreases appreciably during the period under consideration, but is still longer than that of 

successive members of the series, a stage of equilibrium will be reached after which all members 

of the series decrease in activity exponentially with the period of the parent. At this time, the 

ratio of the parent activity to the daughter activity is constant. 

Equilibrium, Electron—The condition in a radiation field where the energy of the electrons entering a 

volume equals the energy of the electrons leaving that volume. 

Excitation—The addition of energy to a system, thereby transferring it from its ground state to an excited 

state. Excitation of a nucleus, an atom, or a molecule can result from absorption of photons or from 

inelastic collisions with other particles. The excited state of an atom is an unstable or metastable state and 

will return to ground state by radiation of the excess energy. 

Exposure (Chemical)—Contact of an organism with a chemical or physical agent. Exposure is 

quantified as the amount of the agent available at the exchange boundaries of the organism (e.g., skin, 

lungs, gut) and available for absorption. 

Exposure (Radiation)—Subjection to ionizing radiation or to a radioactive material. For example, 

exposure in air is a measure of the ionization produced in air by x or gamma radiation; the sum of the 

electric charges on all ions of one sign produced in air when all electrons liberated by photons in a 

volume of air are completely stopped in air (dQ), divided by the mass of the air in the volume (dm). The 

unit of exposure in air is the roentgen, or coulomb per kilogram (SI units). One roentgen is equal to 

2.58x10-4 coulomb per kilogram (C/kg). 

Fission, Nuclear—A nuclear transformation characterized by the splitting of a nucleus into at least two 

other nuclei with emission of several neutrons, accompanied by the release of a relatively large amount of 

energy. 

Gamma Ray, Penetrating—Short wavelength electromagnetic radiation of nuclear origin. 

Genetic Effect of Radiation—Inheritable change, chiefly mutations, produced by the absorption of 

ionizing radiation by germ cells. Genetic effects have not been observed in any human population 

exposed at any dose level. 

Genotoxicity—A specific adverse effect on the genome of living cells that, upon the duplication of 

affected cells, can be expressed as a mutagenic, clastogenic or carcinogenic event because of specific 

alteration of the molecular structure of the genome. 

Gray (Gy)—SI unit of absorbed dose, 1 J/kg. One gray equals 100 rad (see Units). 

Half-life, Effective—See Half-time, Effective. 
 

 

AMERICIUM 267 

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 

rays. (2) In counter tubes: the total ionization produced by incident radiation without gas 

amplification. 
 

 

AMERICIUM 268 

10. GLOSSARY 

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. 

Lethal Concentration(Lo) (LCLo)—The lowest concentration of a chemical in air that has been reported 

to have caused death in humans or animals. 
AMERICIUM 269 

10. GLOSSARY 

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. 

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. 
AMERICIUM 270 

10. GLOSSARY 

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. 

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 
AMERICIUM 271 

10. GLOSSARY 

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). 
 

 

 

 

AMERICIUM 272 

10. GLOSSARY 

Prefix—A modifier that allows units of measure to be expressed as submultiples or multiples of the 

primary unit (e.g., 10-3 curie is 1 mCi and 103

 becquerels 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 

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. 
AMERICIUM 273 

10. GLOSSARY 

Radiation, Characteristic (Discrete)—Radiation originating from an excited atom after removal 

of an electron from an atom. The wavelength of the emitted radiation is specific, depending only 

on the element and particular energy levels involved. 

Radiation, External—Radiation from a source outside the body. 

Radiation, Internal—Radiation from a source within the body (as a result of deposition of 

radionuclides in body tissues). 

Radiation, Ionizing—Any electromagnetic or particulate radiation capable of producing ions, 

directly or indirectly, in its passage through matter (see Radiation). 

Radiation, Monoenergetic—Radiation of a given type in which all particles or photons originate 

with and have the same energy. 

Radiation, Scattered—Radiation which during its passage through a substance, has been 

deviated in direction. It may also have been modified by a decrease in energy. 

Radiation, Secondary—A particle or ray that is produced when the primary radiation interacts 

with a material, and which has sufficient energy to produce its own ionization, such as 

bremsstrahlung or electrons knocked from atomic orbitals with enough energy to then produce 

ionization (see Delta Rays). 

Radiation Weighting Factor (also called Quality Factor)—In radiation protection, a factor (1 for xrays, gamma rays, beta particles; 20 for alpha particles) weighting the absorbed dose of radiation of a 

specific type and energy for its effect on tissue. 

Radioactive Material—Material containing radioactive atoms. 

Radioactivity—Spontaneous nuclear transformations that result in the formation of new elements. These 

transformations are accomplished by emission of alpha or beta particles from the nucleus or by the 

capture of an orbital electron. Each of these reactions may or may not be accompanied by a gamma 

photon. 

Radioactivity, Artificial—Man-made radioactivity produced by particle bombardment or 

nuclear fission, as opposed to naturally occurring radioactivity. 

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. 
AMERICIUM 274 

10. GLOSSARY 

Radiosensitivity—Relative susceptibility of cells, tissues, organs, organisms, or any living substance to 

the injurious action of radiation. Radiosensitivity and its antonym, radioresistance, are used 

comparatively, rather than absolutely. 

Reference Dose (RfD)—An estimate of the daily exposure of the human population to a potential hazard 

that is likely to be without risk of deleterious effects during a lifetime. The RfD is operationally derived 

from the NOAEL (from animal and human studies) by a consistent application of uncertainty factors that 

reflect various types of data used to estimate RfDs and an additional modifying factor, which is based on 

a professional judgment of the entire database on the chemical. The RfDs are not applicable to nonthreshold effects such as cancer. 

Relative Biological Effectiveness (RBE)—The RBE is a factor used to compare the biological 

effectiveness of absorbed radiation doses (i.e., rad) due to different types of ionizing radiation. More 

specifically, it is the experimentally determined ratio of an absorbed dose of a radiation in question to the 

absorbed dose of a reference radiation (typically 60Co gamma rays or 200 kVp x rays) required to produce 

an identical biological effect in a particular experimental organism or tissue (see Quality Factor). 

Rem—The traditional unit of dose equivalent that is used in the regulatory, administrative, and 

engineering design aspects of radiation safety practice. The dose equivalent in rem is numerically equal 

to the absorbed dose in rad multiplied by the quality factor (1 rem is equal to 0.01 sievert). 

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. 
AMERICIUM 275 

10. GLOSSARY 

SI Units—The International System of Units as defined by the General Conference of Weights and 

Measures in 1960. These units are generally based on the meter/kilogram/second units, with special 

quantities for radiation including the becquerel, gray, and sievert. 

Sickness, Acute Radiation (Syndrome)—The complex symptoms and signs characterizing the condition 

resulting from excessive exposure of the whole body (or large part) to ionizing radiation. The earliest of 

these symptoms are nausea, fatigue, vomiting, and diarrhea, and may be followed by loss of hair 

(epilation), hemorrhage, inflammation of the mouth and throat, and general loss of energy. In severe 

cases, where the radiation dose is relatively high (over several hundred rad or several gray), death may 

occur within two to four weeks. Those who survive six weeks after exposure of a single high dose of 

radiation may generally be expected to recover. 

Sievert (Sv)—The SI unit of any of the quantities expressed as dose equivalent. The dose equivalent in 

sieverts is equal to the absorbed dose, in gray, multiplied by the quality factor (1 sievert equals 100 rem). 

The sievert is also the SI unit for effective dose equivalent, which is the sum of the products of the dose 

equivalent to each organ or tissue and its corresponding tissue weighting factor. 

Specific-Activity—Radioactivity per unit mass of a radionuclide, expressed, for example, as Ci/gram or 

Bq/kilogram. 

Specific Energy—The actual energy per unit mass deposited per unit volume in a small target, such as 

the cell or cell nucleus, as the result of one or more energy-depositing events. This is a stochastic 

quantity as opposed to the average value over a large number of instance (i.e., the absorbed dose). 

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. 
AMERICIUM 276 

10. GLOSSARY 

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. 

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 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 

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. 
 

 

 

AMERICIUM 277 

10. GLOSSARY 

Tritium—The hydrogen isotope with one proton and two neutrons in the nucleus (Symbol: 3H). 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. 

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 
AMERICIUM 278 

10. GLOSSARY 

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. 
AMERICIUM 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. 
AMERICIUM A-2 

APPENDIX A 

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 

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. 
AMERICIUM 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 
 

 

 

AMERICIUM B-2 

APPENDIX B 

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. 

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. 
AMERICIUM	 B-3 

APPENDIX B 

LEGEND 

See Sample LSE Table 3-1 (page B-6) 

(1) Route of Exposure. One of the first considerations when reviewing the toxicity of a substance 

using these tables and figures should be the relevant and appropriate route of exposure. Typically 

when sufficient data exists, three LSE tables and two LSE figures are presented in the document. 

The three LSE tables present data on the three principal routes of exposure, i.e., inhalation, oral, 

and dermal (LSE Table 3-1, 3-2, and 3-3, respectively). LSE figures are limited to the inhalation 

(LSE Figure 3-1) and oral (LSE Figure 3-2) routes. Not all substances will have data on each 

route of exposure and will not, therefore, have all five of the tables and figures. 

(2) Exposure Period. Three exposure periods—acute (less than 15 days), intermediate (15– 

364 days), and chronic (365 days or more)—are presented within each relevant route of exposure. 

In this example, an inhalation study of intermediate exposure duration is reported. For quick 

reference to health effects occurring from a known length of exposure, locate the applicable 

exposure period within the LSE table and figure. 

(3) Health Effect. The major categories of health effects included in LSE tables and figures are 

death, systemic, immunological, neurological, developmental, reproductive, and cancer. 

NOAELs and LOAELs can be reported in the tables and figures for all effects but cancer. 

Systemic effects are further defined in the "System" column of the LSE table (see key number 

18). 

(4) Key to Figure. Each key number in the LSE table links study information to one or more data 

points using the same key number in the corresponding LSE figure. In this example, the study 

represented by key number 18 has been used to derive a NOAEL and a Less Serious LOAEL 

(also see the two "18r" data points in sample Figure 3-1). 

(5) Species. The test species, whether animal or human, are identified in this column. Chapter 2, 

"Relevance to Public Health," covers the relevance of animal data to human toxicity and 

Section 3.5, "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, 
AMERICIUM	 B-4 

APPENDIX B 

which was used to derive an intermediate exposure, inhalation MRL of 0.005 ppm (see 

footnote "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. 
AMERICIUM	 B-5 

APPENDIX B 

(18)	 Estimated Upper-Bound Human Cancer Risk Levels. This is the range associated with the upperbound for lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. These risk levels are derived 

from the EPA's Human Health Assessment Group's upper-bound estimates of the slope of the 

cancer dose response curve at low dose levels (q1*). 

(19) Key to LSE Figure. The Key explains the abbreviations and symbols used in the figure. 
1 2 

SAMPLE 

→ TABLE 3-1. Levels of Significant Exposure to [Chemical x] – Inhalation 

LOAEL (effect) 

Exposure Less serious (ppm) Serious (ppm) frequency/ NOAEL 

Key to figurea Species duration System (ppm) Re

3 

→→

6 ↓

5 

↓

INTERMEDIATE EXPOSURE Systemic 

7 

↓

8 

↓

9 

↓

10 

4 →

Rat Rat Rat Mouse 

18 CHRONIC EXPOSURE Cancer 38 39 40 

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 

Resp 3b 

11 ↓20 10 10 

10 (hyperplasia) 

NiWNTNT

(CEL, multiple organs) (CEL, lung tumors, nasal tumors) (CEL, lung tumors, hemangiosarcomas) 

12 → a The number corresponds to entries in Figure 3-1. 

b Used to derive an intermediate inhalation Minimal Risk Level (MRL) of 5x10-3 ppm; dose adjusted for intermittent eby an uncertainty factor of 100 (10 for extrapolation from animal to humans, 10 for human variability). 


AMERICIUM 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 
 

 

AMERICIUM C-2 

APPENDIX C 

DNA deoxyribonucleic acid 

DOD Department of Defense 

DOE Department of Energy 

DOL Department of Labor 

DOT Department of Transportation 

DOT/UN/ Department of Transportation/United Nations/ 

NA/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 
 

 

AMERICIUM C-3 

APPENDIX C 

m meter 

MA trans,trans-muconic acid 

MAL maximum allowable level 

mCi millicurie 

MCL maximum contaminant level 

MCLG maximum contaminant level goal 

MF modifying factor 

MFO mixed function oxidase 

mg milligram 

mL milliliter 

mm millimeter 

mmHg millimeters of mercury 

mmol millimole 

mppcf millions of particles per cubic foot 

MRL Minimal Risk Level 

MS mass spectrometry 

NAAQS National Ambient Air Quality Standard 

NAS National Academy of Science 

NATICH National Air Toxics Information Clearinghouse 

NATO North Atlantic Treaty Organization 

NCE normochromatic erythrocytes 

NCEH National Center for Environmental Health 

NCI National Cancer Institute 

ND not detected 

NFPA National Fire Protection Association 

ng nanogram 

NHANES National Health and Nutrition Examination Survey 

NIEHS National Institute of Environmental Health Sciences 

NIOSH National Institute for Occupational Safety and Health 

NIOSHTIC NIOSH's Computerized Information Retrieval System 

NLM National Library of Medicine 

nm nanometer 

nmol nanomole 

NOAEL no-observed-adverse-effect level 

NOES National Occupational Exposure Survey 

NOHS National Occupational Hazard Survey 

NPD nitrogen phosphorus detection 

NPDES National Pollutant Discharge Elimination System 

NPL National Priorities List 

NR not reported 

NRC National Research Council 

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 
AMERICIUM C-4 

APPENDIX C 

OR odds ratio 

OSHA Occupational Safety and Health Administration 

OSW Office of Solid Waste, EPA 

OTS Office of Toxic Substances 

OW Office of Water 

OWRS Office of Water Regulations and Standards, EPA 

PAH polycyclic aromatic hydrocarbon 

PBPD physiologically based pharmacodynamic 

PBPK physiologically based pharmacokinetic 

PCE polychromatic erythrocytes 

PEL permissible exposure limit 

pg picogram 

PHS Public Health Service 

PID photo ionization detector 

pmol picomole 

PMR proportionate mortality ratio 

ppb parts per billion 

ppm parts per million 

ppt parts per trillion 

PSNS pretreatment standards for new sources 

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 
AMERICIUM C-5 

VOC 

WBC 

WHO 

> ≥

= 

< ≤

% αβγδ

μm

μg q1

* 

– 

+ 

(+) 

(–) 

APPENDIX C 

volatile organic compound 

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 

AMERICIUM 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 
AMERICIUM D-2 

APPENDIX D 

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. 

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 
 

 

 

 

 

 

 

 

AMERICIUM D-3 

APPENDIX D 

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. 

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 
 

 

 

 

AMERICIUM D-4 

APPENDIX D 

(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. 

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. 
 

 

AMERICIUM D-5 

APPENDIX D 

Mass, charge, and velocity of a particle, as well as the electron density of the material with which it 

interacts, all affect the rate at which ionization occurs. The higher the charge of the particle and the lower 

the velocity, the greater the propensity to cause ionization. Heavy, highly charged particles, such as alpha 

particles, lose energy rapidly with distance and, therefore, do not penetrate deeply. The result of these 

interaction processes is a gradual slowing down of any incident particle until it is brought to rest or 

"stopped" at the end of its range. 

D.2.4 Characteristics of Emitted Radiation 

D.2.4.1 Alpha Emission. In alpha emission, an alpha particle consisting of two protons and two 

neutrons is emitted with a resulting decrease in the atomic mass number by four and reduction of the 

atomic number of two, thereby changing the parent to a different element. The alpha particle is identical 

to a helium nucleus consisting of two neutrons and two protons. It results from the radioactive decay of 

some heavy elements such as uranium, plutonium, radium, thorium, and radon. 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. 

1

 Neutrinos also accompany negative beta particles and positron emissions 
 

 

AMERICIUM D-6 

APPENDIX D 

D.2.4.2.3 Gamma Emission. Radioactive decay by alpha, beta, or positron emission, or electron 

capture often leaves some of the energy resulting from these changes in the nucleus. As a result, the 

nucleus is raised to an excited level. None of these excited nuclei can remain in this high-energy state. 

Nuclei release this energy returning to ground state or to the lowest possible stable energy level. The 

energy released is in the form of gamma radiation (high energy photons) and has an energy equal to the 

change in the energy state of the nucleus. Gamma and x rays behave similarly but differ in their origin; 

gamma emissions originate in the nucleus while x rays originate in the orbital electron structure or from 

rapidly changing the velocity of an electron (e.g., as occurs when shielding high energy beta particles or 

stopping the electron beam in an x ray tube). 

D.3 ESTIMATION OF ENERGY DEPOSITION IN HUMAN TISSUES 

Two forms of potential radiation exposures can result: internal and external. The term exposure denotes 

physical interaction of the radiation emitted from the radioactive material with cells and tissues of the 

human body. An exposure can be "acute" or "chronic" depending on how long an individual or organ is 

exposed to the radiation. Internal exposures occur when radionuclides, which have entered the body (e.g., 

through the inhalation, ingestion, or dermal pathways), undergo radioactive decay resulting in the 

deposition of energy to internal organs. External exposures occur when radiation enters the body directly 

from sources located outside the body, such as radiation emitters from radionuclides on ground surfaces, 

dissolved in water, or dispersed in the air. In general, external exposures are from material emitting 

gamma radiation, which readily penetrate the skin and internal organs. Beta and alpha radiation from 

external sources are far less penetrating and deposit their energy primarily on the skin's outer layer. 

Consequently, their contribution to the absorbed dose of the total body dose, compared to that deposited 

by gamma rays, may be negligible. 

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 
AMERICIUM D-7 

APPENDIX D 

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). 

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 
 

 

AMERICIUM D-8 

APPENDIX D 

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. 

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 
AMERICIUM D-9 

APPENDIX D 

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. 

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 using the formula H = D x Q. The NCRP similarly 

defines equivalent dose, H, as the product of the absorbed dose, D, and the radiation weighting factor, wr 

in the equation H = Dwr. 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. 
 

 

 

 

 

AMERICIUM D-10 

APPENDIX D 

Table D-3. Quality Factors (Q) and Radiation Weighting Factors 

Type of radiation Quality factor (Q) Radiation Weighting Factor (wr) 

X, gamma, or beta radiation 1 1 

Alpha particles, multiple-charged 20 20 

particles, fission fragments and 

heavy particles of unknown charge 

Neutrons (100 keV to 2 MeV), 7.5–11 20 

protons, alpha particles, charged 

particles of unknown energy depending on energy 

Neutrons of unknown energy 10 

Thermal neutrons 2 5 

High-energy protons 10 5 

Source: USNRC. 2004. Standards for the protection against radiation, tables 1004(b).1 and 1004(b).2. 10 CFR 20.1004. 

U.S. Nuclear Regulatory Commission, Washington, D.C. 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) is 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 = ∑ Wt Ht 

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. 
 

 

AMERICIUM D-11 

APPENDIX D 

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 

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. 
 

 

AMERICIUM 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 trans- becquerel (Bq) s-1 

formations s-1 

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. 

Brodsky A. 1996. Review of radiation risks and uranium toxicity with application to decisions 

associated with decommissioning clean-up criteria. Hebron,Connecticut: RSA Publications. 
AMERICIUM D-13 

APPENDIX D 

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. 

NCRP. 1985. A handbook of radioactivity measurements procedures. 2nd ed. National Council on 

Radiation Protection and Measurements. Report No. 58. Bethesda, MD: 
AMERICIUM D-14 

APPENDIX D 

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. 
AMERICIUM E-1 

APPENDIX E. INDEX 

absorbed dose........................................................................................................................................ 16, 93 

adsorbed ............................................................................................................................................ 145, 154 

adsorption.................................................................................................. 142, 143, 144, 145, 150, 151, 194 

anaerobic................................................................................................................................................... 146 

bioaccumulation........................................................................................................................ 146, 150, 185 

bioavailability ........................................................................................................................................... 187 

bioconcentration factor ............................................................................................................................. 149 

biokinetic .............................................................................................. 16, 60, 62, 76, 84, 91, 103, 152, 189 

biokinetics......................................................................................................................... 16, 19, 82, 92, 103 

biological half-time..................................................................................................................... 32, 103, 151 

biological half-times ................................................................................................................................... 32 

biomarker .............................................................................................................................................. 92, 93 

biomarkers .................................................................................................................................... 92, 93, 189 

blood cell count....................................................................................................................... 21, 23, 28, 102 

blood cell counts ..................................................................................................................... 21, 23, 28, 102 

body weight effects ............................................................................................................................... 23, 25 

breast milk................................................................................................................................. 103, 182, 183 

cancer ...............................5, 7, 13, 14, 24, 25, 27, 28, 30, 89, 90, 95, 97, 100, 104, 180, 205, 207, 208, 212 

carcinogen................................................................................................................................................... 13 

carcinogenic .......................................................................................................................................... 17, 30 

carcinomas .................................................................................................................................................. 30 

cardiovascular ................................................................................................................................. 20, 25, 27 

cardiovascular effects...................................................................................................................... 20, 25, 27 

caribou ...................................................................................................................................................... 179 

Chernobyl...................................................................... 4, 125, 131, 141, 154, 156, 162, 168, 169, 176, 179 

chromosomal aberrations ............................................................................................................................ 94 

clearance ..............................................................32, 33, 38, 53, 55, 57, 62, 63, 64, 67, 68, 86, 90, 150, 193 

crustaceans ................................................................................................................ 127, 150, 172, 173, 180 

death............................................................................................ 17, 19, 25, 27, 28, 29, 30, 45, 91, 102, 180
 

dermal effects........................................................................................................................................ 25, 27 

DNA............................................................................................................................................................ 93 

dose coefficients............................................................................................................................ 16, 62, 178 

dose equivalent...................................................................................................................... 16, 31, 179, 212 

elimination half-time................................................................................................................................... 50 

elimination half-times ................................................................................................................................. 50 

endocrine................................................................................................................................... 22, 25, 87, 88 

endocrine effects ............................................................................................................................. 22, 25, 28 

erythema...................................................................................................................................................... 15 

external radiation .................................................................................................................... 12, 31, 32, 212 

fetal tissue ............................................................................................................................................. 29, 51 

fetus..................................................................................................... 50, 86, 89, 91, 92, 103, 104, 105, 206 

fractional absorption ................................................................................................................................... 90 

gastrointestinal effects .......................................................................................................................... 25, 27 

general population....................................................................... 4, 11, 14, 92, 129, 175, 180, 182, 183, 187
 

genotoxic................................................................................................................................. 17, 31, 32, 101 

genotoxicity............................................................................................................................................... 101 
 

 

AMERICIUM E-2 

APPENDIX E 

groundwater ................................................................ 15, 122, 128, 132, 133, 141, 143, 156, 157, 159, 205
 

half-life...............................................2, 3, 11, 35, 67, 92, 107, 119, 120, 125, 130, 131, 150, 152, 159, 193 

Hematological Effects..................................................................................................................... 21, 26, 28 

hematopoietic.................................................................................................................................. 13, 14, 21 

hepatic effects ................................................................................................................................. 22, 25, 28 

hydrolysis.............................................................................................................................................. 12, 87 

immunological .................................................................................................................. 17, 23, 24, 26, 100 

leukopenia................................................................................................................................................... 13 

lichen......................................................................................................................................... 151, 169, 179 

lichens ....................................................................................................................................................... 179 

lymphatic .................................................................................................................................................... 63 

metabolic effects ................................................................................................................................... 23, 27 

micronuclei ................................................................................................................................................. 31 

milk ....................................................................................... 51, 91, 103, 105, 153, 175, 176, 178, 182, 183 

mucociliary ............................................................................................................. 19, 38, 54, 55, 57, 68, 84 

musculoskeletal effects ............................................................................................................................... 21 

neonatal........................................................................................................................... 40, 50, 91, 104, 183 

neoplastic .................................................................................................................................................... 30 

neurobehavioral........................................................................................................................................... 88 

nuclear.................................1, 3, 4, 7, 11, 15, 18, 31, 93, 117, 119, 120, 121, 122, 125, 128, 129, 130, 131, 

132, 133, 135, 140, 142, 144, 148, 151, 153, 154, 155, 156, 158, 159, 160, 162, 

 163, 172, 173, 174, 175, 176, 179, 181, 183, 184, 185, 186 

ocular effects................................................................................................................................... 19, 25, 27 

pharmacodynamic....................................................................................................................................... 58 

pharmacokinetic.............................................................................................................................. 58, 59, 61 

pharmacokinetics .............................................................................................................. 18, 89, 90, 95, 104 

placenta ....................................................................................................................................................... 86 

placental barrier ........................................................................................................................................ 103 

radiation syndrome.................................................................................................................................... 102 

rate constant ................................................................................................................................................ 78 

rate constants............................................................................................................................................... 78 

reindeer ..................................................................................................................................... 151, 169, 179 

renal effects..................................................................................................................................... 22, 25, 27 

retention ...............16, 33, 35, 36, 38, 40, 46, 53, 63, 67, 68, 73, 76, 78, 80, 85, 87, 140, 150, 151, 161, 193 

sequestered.................................................................................................................................................. 87 

solubility ......................................................................................................... 38, 62, 84, 134, 147, 152, 185 

thrombocytopenia ........................................................................................................................... 13, 21, 26 

thyroid............................................................................................................................... 6, 13, 28, 100, 119 

thyroxine ..................................................................................................................................................... 28 

toxicokinetic............................................................................................................................ 15, 18, 54, 103 

toxicokinetics ............................................................................................................................................ 103 

tumors ................................................................................................................................................... 30, 95 

weanling...................................................................................................................................................... 44