TOXICOLOGICAL PROFILE FOR 

BARIUM AND BARIUM COMPOUNDS 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES 

Public Health Service 

Agency for Toxic Substances and Disease Registry
 

August 2007 
BARIUM AND BARIUM COMPOUNDS 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. 
BARIUM AND BARIUM COMPOUNDS iii 

UPDATE STATEMENT 

A Toxicological Profile for Barium and Barium Compounds, Draft for Public Comment was released in 

September 2005. This edition supersedes any previously released draft or final profile. 

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

status of previously released profiles, contact ATSDR at: 

Agency for Toxic Substances and Disease Registry
 

Division of Toxicology and Environmental Medicine/Applied Toxicology Branch 

1600 Clifton Road NE 

Mailstop F-32 

Atlanta, Georgia 30333 
BARIUM AND BARIUM COMPOUNDS iv 

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v 

FOREWORD

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

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

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

and republished as necessary. 

The ATSDR toxicological profile succinctly characterizes the toxicologic and adverse health 

effects information for the hazardous substance described therein. Each peer-reviewed profile identifies 

and reviews the key literature that describes a hazardous substance's toxicologic properties. Other 

pertinent literature is also presented, but is described in less detail than the key studies. The profile is not 

intended to be an exhaustive document; however, more comprehensive sources of specialty information 

are referenced. 

The focus of the profiles is on health and toxicologic information; therefore, each toxicological 

profile begins with a public health statement that describes, in nontechnical language, a substance's 

relevant toxicological properties. Following the public health statement is information concerning levels 

of significant human exposure and, where known, significant health effects. The adequacy of information 

to determine a substance's health effects is described in a health effects summary. Data needs that are of 

significance to protection of public health are identified by ATSDR and EPA. 

Each profile includes the following: 

(A) The examination, summary, and interpretation of available toxicologic information and 

epidemiologic evaluations on a hazardous substance to ascertain the levels of significant 

human exposure for the substance and the associated acute, subacute, and chronic health 

effects; 

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

available or in the process of development to determine levels of exposure that present a 

significant risk to human health of acute, subacute, and chronic health effects; and 

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

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

The principal audiences for the toxicological profiles are health professionals at the Federal, State, 

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

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

has been peer-reviewed. Staff of the Centers for Disease Control and Prevention and other Federal 

scientists have also reviewed the profile. In addition, this profile has been peer-reviewed by a 

nongovernmental panel and is being made available for public review. Final responsibility for the 

contents and views expressed in this toxicological profile resides with ATSDR. 
vi 

The toxicological profiles are developed in response to the Superfund Amendments and 

Reauthorization Act (SARA) of 1986 (Public Law 99-499) which amended the Comprehensive 

Environmental Response, Compensation, and Liability Act of 1980 (CERCLA or Superfund). This 

public law directed ATSDR to prepare toxicological profiles for hazardous substances most commonly 

found at facilities on the CERCLA National Priorities List and that pose the most significant potential 

threat to human health, as determined by ATSDR and the EPA. The availability of the revised priority 

list of 275 hazardous substances was announced in the Federal Register on December 7, 2005 (70 FR 

72840). For prior versions of the list of substances, see Federal Register notices dated April 17, 1987 

(52 FR 12866); October 20, 1988 (53 FR 41280); October 26, 1989 (54 FR 43619); October 17, 1990 (55 

FR 42067); October 17, 1991 (56 FR 52166); October 28, 1992 (57 FR 48801); February 28, 1994 (59 

FR 9486); April 29, 1996 (61 FR 18744); November 17, 1997 (62 FR 61332); October 21, 1999 (64 FR 

56792); October 25, 2001 (66 FR 54014); and November 7, 2003 (68 FR 63098). Section 104(i)(3) of 

CERCLA, as amended, directs the Administrator of ATSDR to prepare a toxicological profile for each 

substance on the list. 
BARIUM AND BARIUM COMPOUNDS vii 

QUICK REFERENCE FOR HEALTH CARE PROVIDERS 

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

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

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

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

answers to often-asked questions. 

Primary Chapters/Sections of Interest 

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

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

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

the general health effects observed following exposure. 

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

and assesses the significance of toxicity data to human health. 

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

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

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

reported in this section. 

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

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

following exposure. 

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

issues: 

Section 1.6 How Can (Chemical X) Affect Children? 

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

Section 3.7 Children’s Susceptibility 

Section 6.6 Exposures of Children 

Other Sections of Interest: 

Section 3.8 Biomarkers of Exposure and Effect 

Section 3.11 Methods for Reducing Toxic Effects 

ATSDR Information Center 

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

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

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

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

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

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

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

Toxicity; and numerous chemical-specific case studies. 
BARIUM AND BARIUM COMPOUNDS viii 

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

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

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

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

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

professionals treating patients exposed to hazardous materials. 

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

Other Agencies and Organizations 

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

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

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

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

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

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

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

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

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

SW, Washington, DC 20201 • Phone: 800-356-4674 or NIOSH Technical Information Branch, 

Robert A. Taft Laboratory, Mailstop C-19, 4676 Columbia Parkway, Cincinnati, OH 45226-1998 

• Phone: 800-35-NIOSH. 

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

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

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

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

Referrals 

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

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

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

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

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

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

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

Grove Village, IL 60007-1030 • Phone: 847-818-1800 • FAX: 847-818-9266. 
BARIUM AND BARIUM COMPOUNDS ix 

CONTRIBUTORS 

CHEMICAL MANAGER(S)/AUTHOR(S): 

Daphne Moffett, Ph.D. 

Cassandra Smith, M.S. 

Yee-Wan Stevens, M.S. 

ATSDR, Division of Toxicology and Environmental Medicine, Atlanta, GA 

Lisa Ingerman, Ph.D. 

Steven Swarts, Ph.D. 

Lara Chappell, 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 Applied Toxicology Branch reviews data needs sections to assure 

consistency across profiles and adherence to instructions in the Guidance. 

4. Green Border Review. Green Border review assures the consistency with ATSDR policy. 
BARIUM AND BARIUM COMPOUNDS x 

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BARIUM AND BARIUM COMPOUNDS xi 

PEER REVIEW 

A peer review panel was assembled for barium and barium. The panel consisted of the following 

members: 

1.	 Michael Dourson, Ph.D., DABT, Toxicological Excellence for Risk Assessment, Cincinnati, 

Ohio; 

2.	 Ernest Foulkes, Ph.D., University of Cincinnati, Cincinnati, Ohio; and 

3. Richard Leggett, Ph.D., Private Consultant, Knoxville, Tennessee. 

These experts collectively have knowledge of barium and barium compound's physical and chemical 

properties, toxicokinetics, key health end points, mechanisms of action, human and animal exposure, and 

quantification of risk to humans. All reviewers were selected in conformity with the conditions for peer 

review specified in Section 104(I)(13) of the Comprehensive Environmental Response, Compensation, 

and Liability Act, as amended. 

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

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

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

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

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

content. The responsibility for the content of this profile lies with the ATSDR. 
BARIUM AND BARIUM COMPOUNDS xii 

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BARIUM AND BARIUM COMPOUNDS xiii 

CONTENTS 

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

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

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

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

CONTRIBUTORS.......................................................................................................................................ix 

PEER REVIEW ...........................................................................................................................................xi 

CONTENTS...............................................................................................................................................xiii 

LIST OF FIGURES ..................................................................................................................................xvii 

LIST OF TABLES.....................................................................................................................................xix 

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

1.1 WHAT IS BARIUM?..................................................................................................................1 

1.2 WHAT HAPPENS TO BARIUM WHEN IT ENTERS THE ENVIRONMENT?.....................2 

1.3 HOW MIGHT I BE EXPOSED TO BARIUM? .........................................................................3 

1.4 HOW CAN BARIUM ENTER AND LEAVE MY BODY? ......................................................4 

1.5 HOW CAN BARIUM AFFECT MY HEALTH? .......................................................................4 

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

1.7 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO BARIUM? ......................6 

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

EXPOSED TO BARIUM? ..........................................................................................................6 

1.9 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH?.................................................................................................7 

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

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

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO BARIUM IN THE 

UNITED STATES.......................................................................................................................9 

2.2 SUMMARY OF HEALTH EFFECTS........................................................................................9 

2.3 MINIMAL RISK LEVELS (MRLs) .........................................................................................11 

3. HEALTH EFFECTS..............................................................................................................................21 

3.1 INTRODUCTION.....................................................................................................................21 

3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE ..................................21 

3.2.1 Inhalation Exposure ..............................................................................................................22 

3.2.1.1 Death ............................................................................................................................23 

3.2.1.2 Systemic Effects...........................................................................................................23 

3.2.1.3 Immunological and Lymphoreticular Effects...............................................................25 

3.2.1.4 Neurological Effects.....................................................................................................25 

3.2.1.5 Reproductive Effects....................................................................................................25 

3.2.1.6 Developmental Effects .................................................................................................26 

3.2.1.7 Cancer...........................................................................................................................26 

3.2.2 Oral Exposure........................................................................................................................26 

3.2.2.1 Death ............................................................................................................................27 

3.2.2.2 Systemic Effects...........................................................................................................28 

3.2.2.3 Immunological and Lymphoreticular Effects...............................................................53 

3.2.2.4 Neurological Effects.....................................................................................................53 

3.2.2.5 Reproductive Effects....................................................................................................54 

3.2.2.6 Developmental Effects .................................................................................................55 

3.2.2.7 Cancer...........................................................................................................................56 
BARIUM AND BARIUM COMPOUNDS xiv 

3.2.3 Dermal Exposure...................................................................................................................56 

3.2.3.1 Death ............................................................................................................................57 

3.2.3.2 Systemic Effects...........................................................................................................57 

3.2.3.3 Immunological and Lymphoreticular Effects...............................................................58 

3.2.3.4 Neurological Effects.....................................................................................................58 

3.2.3.5 Reproductive Effects....................................................................................................58 

3.2.3.6 Developmental Effects .................................................................................................58 

3.2.3.7 Cancer...........................................................................................................................58 

3.3 GENOTOXICITY .....................................................................................................................59 

3.4 TOXICOKINETICS..................................................................................................................61 

3.4.1 Absorption.............................................................................................................................61 

3.4.1.1 Inhalation Exposure......................................................................................................61 

3.4.1.2 Oral Exposure...............................................................................................................61 

3.4.1.3 Dermal Exposure ..........................................................................................................62 

3.4.2 Distribution ...........................................................................................................................62 

3.4.2.1 Inhalation Exposure......................................................................................................62 

3.4.2.2 Oral Exposure...............................................................................................................62 

3.4.2.3 Dermal Exposure ..........................................................................................................63 

3.4.2.4 Other Routes of Exposure ............................................................................................63 

3.4.3 Metabolism............................................................................................................................63 

3.4.4 Elimination and Excretion.....................................................................................................63 

3.4.4.1 Inhalation Exposure......................................................................................................63 

3.4.4.2 Oral Exposure...............................................................................................................64 

3.4.4.3 Dermal Exposure ..........................................................................................................64 

3.4.4.4 Other Routes of Exposure ............................................................................................64 

3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models .............64 

3.5 MECHANISMS OF ACTION .................................................................................................. 66 

3.5.1 Pharmacokinetic Mechanisms...............................................................................................66 

3.5.2 Mechanisms of Toxicity........................................................................................................66 

3.5.3 Animal-to-Human Extrapolations.........................................................................................68 

3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS ..........................68 

3.7 CHILDREN’S SUSCEPTIBILITY...........................................................................................69 

3.8 BIOMARKERS OF EXPOSURE AND EFFECT ....................................................................71 

3.8.1 Biomarkers Used to Identify or Quantify Exposure to Barium.............................................72 

3.8.2 Biomarkers Used to Characterize Effects Caused by Barium...............................................73 

3.9 INTERACTIONS WITH OTHER CHEMICALS ....................................................................73 

3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE............................................... 75 

3.11 METHODS FOR REDUCING TOXIC EFFECTS...................................................................75 

3.11.1 Reducing Peak Absorption Following Exposure ..............................................................76 

3.11.2 Reducing Body Burden.....................................................................................................76 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects ...........................................77 

3.12 ADEQUACY OF THE DATABASE........................................................................................77 

3.12.1 Existing Information on Health Effects of Barium and Barium Compounds...................77 

3.12.2 Identification of Data Needs .............................................................................................79 

3.12.3 Ongoing Studies................................................................................................................88 

4. CHEMICAL AND PHYSICAL INFORMATION................................................................................89 

4.1 CHEMICAL IDENTITY...........................................................................................................89 

4.2 PHYSICAL AND CHEMICAL PROPERTIES........................................................................89 
BARIUM AND BARIUM COMPOUNDS xv 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL............................................................97 

5.1 PRODUCTION .........................................................................................................................97 

5.2 IMPORT/EXPORT ...................................................................................................................98 

5.3 USE............................................................................................................................................98 

5.4 DISPOSAL..............................................................................................................................105 

6. POTENTIAL FOR HUMAN EXPOSURE .........................................................................................107 

6.1 OVERVIEW............................................................................................................................107 

6.2 RELEASES TO THE ENVIRONMENT................................................................................108 

6.2.1 Air .......................................................................................................................................109 

6.2.2 Water...................................................................................................................................115 

6.2.3 Soil ......................................................................................................................................115 

6.3 ENVIRONMENTAL FATE....................................................................................................116 

6.3.1 Transport and Partitioning...................................................................................................116 

6.3.2 Transformation and Degradation ........................................................................................118 

6.3.2.1 Air...............................................................................................................................118 

6.3.2.2 Water ..........................................................................................................................118 

6.3.2.3 Sediment and Soil.......................................................................................................119 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT...............................120 

6.4.1 Air .......................................................................................................................................120 

6.4.2 Water...................................................................................................................................121 

6.4.3 Sediment and Soil ...............................................................................................................123 

6.4.4 Other Environmental Media................................................................................................125 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE .....................................128 

6.6 EXPOSURES OF CHILDREN...............................................................................................132 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES ...........................................134 

6.8 ADEQUACY OF THE DATABASE......................................................................................135 

6.8.1 Identification of Data Needs ...............................................................................................135 

6.8.2 Ongoing Studies ..................................................................................................................138 

7. ANALYTICAL METHODS ...............................................................................................................141 

7.1 BIOLOGICAL MATERIALS.................................................................................................141 

7.2 ENVIRONMENTAL SAMPLES............................................................................................ 143 

7.3 ADEQUACY OF THE DATABASE......................................................................................146 

7.3.1 Identification of Data Needs ...............................................................................................147 

7.3.2 Ongoing Studies ..................................................................................................................148 

8. REGULATIONS AND ADVISORIES ...............................................................................................149 

9. REFERENCES ....................................................................................................................................152 

10. GLOSSARY ......................................................................................................................................179 
BARIUM AND BARIUM COMPOUNDS xvi 

APPENDICES 

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

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

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

D. INDEX ................................................................................................................................................D-1 
BARIUM AND BARIUM COMPOUNDS xvii 

LIST OF FIGURES 

3-1. Levels of Significant Exposure to Barium and Barium Compounds – Oral....................................... 43 

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

Hypothetical Chemical Substance...................................................................................................... 67 

3-3. Existing Information on Health Effects of Barium and Barium Compounds.....................................78 

6-1. Frequency of NPL Sites with Barium Contamination......................................................................108 
BARIUM AND BARIUM COMPOUNDS xviii 

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BARIUM AND BARIUM COMPOUNDS xix 

LIST OF TABLES 

3-1. Levels of Significant Exposure to Barium and Barium Compounds - Oral ....................................... 29 

3-2. Genotoxicity of Barium and Barium Compounds In Vitro.................................................................60 

4-1. Chemical Identity of Barium and Barium Compounds......................................................................90 

4-2. Physical and Chemical Properties of Barium and Barium Compounds.............................................94 

5-1. Facilities that Produce, Process, or Use Barium.................................................................................99 

5-2. Facilities that Produce, Process, or Use Barium Compounds...........................................................101 

5-3. Current U.S. Manufacturers of Barium Metal and Selected Barium Compounds............................103 

6-1. Releases to the Environment from Facilities that Produce, Process, or Use Barium .......................110 

6-2. Releases to the Environment from Facilities that Produce, Process, or Use Barium
 

Compounds.......................................................................................................................................112 

6-3. Concentrations of Barium in Surface Soils of the United States......................................................124 

6-4. Concentrations of Barium in Food Obtained from the Canadian Total Diet Study Between 

1993 and 1999 ..................................................................................................................................126 

6-5. Average Dietary Intake of Barium in Different Age/Sex Groups from the Canadian Total 

Diet Study (1993–1999) ...................................................................................................................130 

6-6. Number of Workers Potentially Exposed to Barium and Barium Compounds................................133 

6-7. Ongoing Studies on Environmental Fate and the Potential for Human Exposure to Barium
 

and Barium Compounds...................................................................................................................139 

7-1. Analytical Methods for Determining Barium in Biological Materials.............................................142 

7-2. Analytical Methods for Determining Barium in Environmental Samples........................................144 

8-1. Regulations and Guidelines Applicable to Barium and Barium Compounds...................................150 
BARIUM AND BARIUM COMPOUNDS xx 

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BARIUM AND BARIUM COMPOUNDS 1 

1. PUBLIC HEALTH STATEMENT 

This public health statement tells you about barium and barium compounds and the effects of 

exposure to these chemicals. 

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

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

long-term federal clean-up activities. Barium and barium compounds have been found in at least 

798 of the 1,684 current or former NPL sites; however, the total number of NPL sites evaluated 

for these substances is not known. This information is important because these sites may be 

sources of exposure and exposure to this substance may harm you. 

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

container, such as a drum or bottle, it enters the environment. Such a release does not always 

lead to exposure. You can be 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. 

If you are exposed to barium and barium compounds, many factors will determine whether you 

will be harmed. These factors include the dose (how much), the duration (how long), and how 

you come in contact with them. You must also consider any other chemicals you are exposed to 

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

1.1 WHAT IS BARIUM? 

Barium is a silvery-white metal that takes on a silver-yellow color when exposed to air. Barium 

occurs in nature in many different forms called compounds. These compounds are solids, 

existing as powders or crystals, and they do not burn well. Two forms of barium, barium sulfate 

and barium carbonate, are often found in nature as underground ore deposits. Barium is 

sometimes found naturally in drinking water and food. Because certain barium compounds 

(barium sulfate and barium carbonate) do not mix well with water, the amount of barium usually 

found in drinking water is small. Other barium compounds, such as barium chloride, barium 

nitrate, and barium hydroxide, are manufactured from barium sulfate. Barium compounds such 
BARIUM AND BARIUM COMPOUNDS 2 

1. PUBLIC HEALTH STATEMENT 

as barium acetate, barium chloride, barium hydroxide, barium nitrate, and barium sulfide 

dissolve more easily in water than barium sulfate and barium carbonate, but because they are not 

commonly found in nature, they do not typically end up in drinking water unless the water is 

contaminated by barium compounds that are released from waste sites. 

Barium and barium compounds are used for many important purposes. Barium sulfate ore is 

mined and used in several industries. It is used mostly by the oil and gas industries to make 

drilling muds. Drilling muds make it easier to drill through rock by keeping the drill bit 

lubricated. Barium sulfate is also used to make paints, bricks, tiles, glass, rubber, and other 

barium compounds. Some barium compounds, such as barium carbonate, barium chloride, and 

barium hydroxide, are used to make ceramics, insect and rat poisons, and additives for oils and 

fuels; in the treatment of boiler water; in the production of barium greases; as a component in 

sealants, paper manufacturing, and sugar refining; in animal and vegetable oil refining; and in the 

protection of objects made of limestone from deterioration. Barium sulfate is sometimes used by 

doctors to perform medical tests and take x-ray photographs of the stomach and intestines. 

More information on the chemical and physical properties and use of barium is found in 

Chapters 4 and 5. 

1.2 WHAT HAPPENS TO BARIUM WHEN IT ENTERS THE ENVIRONMENT? 

The length of time that barium will last in air, land, water, or sediments following release of 

barium into these media depends on the form of barium released. Barium compounds that do not 

dissolve well in water, such as barium sulfate and barium carbonate, can persist for a long time 

in the environment. Barium compounds, such as barium chloride, barium nitrate, or barium 

hydroxide, that dissolve easily in water usually do not last in these forms for a long time in the 

environment. The barium in these compounds that is dissolved in water quickly combines with 

sulfate or carbonate that are naturally found in water and become the longer lasting forms 

(barium sulfate and barium carbonate). Barium sulfate and barium carbonate are the barium 

compounds most commonly found in the soil and water. If barium sulfate and barium carbonate 
BARIUM AND BARIUM COMPOUNDS 3 

1. PUBLIC HEALTH STATEMENT 

are released onto land, they will combine with particles of soil. More information on the 

environmental fate of barium is found in Chapter 6. 

1.3 HOW MIGHT I BE EXPOSED TO BARIUM? 

Background levels of barium in the environment are very low. The air that most people breathe 

contains about 0.0015 parts of barium per billion parts of air (ppb). The air around factories that 

release barium compounds into the air has about 0.33 ppb or less of barium. Most surface water 

and public water supplies contain on average 0.030 parts of barium per million parts of water 

(ppm) or less, but can average as high as 0.30 ppm in some regions of the United States. In some 

areas that have underground water wells, drinking water may contain more barium than the 

2 ppm limit set by EPA. The highest amount measured from these water wells has been 10 ppm. 

The amount of barium found in soil ranges from about 15 to 3,500 ppm. Some foods, such as 

Brazil nuts, seaweed, fish, and certain plants, may contain high amounts of barium. The amount 

of barium found in food and water usually is not high enough to be a health concern. However, 

information is still being collected to determine if long-term exposure to low levels of barium 

causes any health problems. 

People with the greatest known risk of exposure to high levels of barium are those working in 

industries that make or use barium compounds. Most of these exposed persons breathe air that 

contains barium sulfate or barium carbonate. Sometimes they are exposed to one of the more 

harmful barium compounds (for example, barium chloride or barium hydroxide) by breathing the 

dust from these compounds or by getting them on their skin. Barium carbonate can be harmful if 

accidentally eaten because it will dissolve in the acids within the stomach unlike barium sulfate, 

which will not dissolve in the stomach. Many hazardous waste sites contain barium compounds, 

and these sites may be a source of exposure for people living and working near them. Exposure 

near hazardous waste sites may occur by breathing dust, eating soil or plants, or drinking water 

that is polluted with barium. People near these sites may also get soil or water that contains 

barium on their skin. More information on how you might be exposed to barium is found in 

Chapter 6. 
BARIUM AND BARIUM COMPOUNDS 4 

1. PUBLIC HEALTH STATEMENT 

1.4 HOW CAN BARIUM ENTER AND LEAVE MY BODY? 

Barium enters your body when you breathe air, eat food, or drink water containing barium. It 

may also enter your body to a small extent when you have direct skin contact with barium 

compounds. The amount of barium that enters the bloodstream after you breathe, eat, or drink it 

depends on the barium compound. Some barium compounds that are soluble, such as barium 

chloride, can enter bloodstream more easily than insoluble barium compounds such as barium 

sulfate. Some barium compounds (for example, barium chloride) can enter your body through 

your skin, but this is very rare and usually occurs in industrial accidents at factories where they 

make or use barium compounds. Barium at hazardous waste sites may enter your body if you 

breathe dust, eat soil or plants, or drink water polluted with barium from this area. 

Barium that enters your body by breathing, eating, or drinking is removed mainly in feces and 

urine. Most of the barium that enters your body is removed within 1–2 weeks. Most of the small 

amount of barium that stays in your body goes into the bones and teeth. More information on 

how barium enters and leaves your body is found in Chapter 3. 

1.5 HOW CAN BARIUM AFFECT MY HEALTH? 

Scientists use many tests to protect the public from harmful effects of toxic chemicals and to find 

ways for treating persons who have been harmed. 

One way to learn whether a chemical will harm people is to determine how the body absorbs, 

uses, and releases the chemical. For some chemicals, animal testing may be necessary. Animal 

testing may also help identify health effects such as cancer or birth defects. Without laboratory 

animals, scientists would lose a basic method for getting information needed to make wise 

decisions that protect public health. Scientists have the responsibility to treat research animals 

with care and compassion. Scientists must comply with strict animal care guidelines because 

laws today protect the welfare of research animals. 

The health effects associated with exposure to different barium compounds depend on how well 

the specific barium compound dissolves in water or in the stomach. For example, barium sulfate 
BARIUM AND BARIUM COMPOUNDS 5 

1. PUBLIC HEALTH STATEMENT 

does not easily dissolve in water and causes few harmful health effects. Doctors sometimes give 

barium sulfate orally or by placing it directly in the rectum of patients for purposes of making xrays of the stomach or intestines. The use of this particular barium compound in this type of 

medical test is not harmful to people. Barium compounds such as barium acetate, barium 

chloride, barium hydroxide, barium nitrate, and barium sulfide that dissolve in water can cause 

harmful health effects. Barium carbonate does not dissolve in water, but does dissolve in the 

stomach; it can also cause harmful health effects. 

Eating or drinking very large amounts of barium compounds that dissolve in water or in the 

stomach can cause changes in heart rhythm or paralysis in humans. Some people who did not 

seek medical treatment soon after eating or drinking a very large amount of barium have died. 

Some people who eat or drink somewhat smaller amounts of barium for a short period may 

experience vomiting, abdominal cramps, diarrhea, difficulties in breathing, increased or 

decreased blood pressure, numbness around the face, and muscle weakness. One study showed 

that people who drank water containing as much as 10 ppm of barium for 4 weeks did not have 

increased blood pressure or abnormal heart rhythms. The health effects of barium have been 

studied more often in experimental animals than in humans. Rats that ate or drank barium over 

short periods had swelling and irritation of the intestines, changes in organ weights, decreased 

body weight, and increased numbers of deaths. Rats and mice that drank barium over long 

periods had damage to the kidneys, decreases in body weight, and decreased survival. We have 

no information about the ability of barium to affect reproduction in humans; a study in 

experimental animals did not find reproductive effects. 

Some studies of humans and experimental animals exposed to barium in the air have reported 

damage to the lungs, but other studies have not found these effects. We have no reliable 

information about the health effects in humans or experimental animals that are exposed to 

barium by direct skin contact. 

Barium has not been shown to cause cancer in humans or in experimental animals drinking 

barium in water. The Department of Health and Human Services and the International Agency 

for Research on Cancer have not classified barium as to its carcinogenicity. The EPA has 
BARIUM AND BARIUM COMPOUNDS 6 

1. PUBLIC HEALTH STATEMENT 

determined that barium is not likely to be carcinogenic to humans following ingestion and that 

there is insufficient information to determine whether it will be carcinogenic to humans 

following inhalation exposure. 

More information on the health effects of barium can be found in Chapter 3. 

1.6 HOW CAN BARIUM AFFECT CHILDREN? 

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

conception to maturity at 18 years of age. 

We do not know whether children will be more or less sensitive than adults to barium toxicity. 

A study in rats that swallowed barium found a decrease in newborn body weight; we do not 

know if a similar effect would be seen in humans. 

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

If your doctor finds that you have been exposed to substantial amounts of barium, ask whether 

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

department to investigate. 

The greatest potential source of barium exposure is through food and drinking water. However, 

the amount of barium in foods and drinking water are typically too low to be of concern. 

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

EXPOSED TO BARIUM? 

There is no routine medical test to determine whether you have been exposed to barium. Doctors 

can measure barium in body tissues and fluids, such as bones, blood, urine, and feces, using very 

complex instruments. These tests cannot be used to predict the extent of the exposure or 

potential health effects. This is normally done only for cases of severe barium poisoning and for 

medical research. 
BARIUM AND BARIUM COMPOUNDS 7 

1. PUBLIC HEALTH STATEMENT 

More information on testing for barium exposure is found in Chapters 3 and 7. 

1.9 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH? 

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

Regulations can be enforced by law. The EPA, the Occupational Safety and Health 

Administration (OSHA), and the Food and Drug Administration (FDA) are some federal 

agencies that develop regulations for toxic substances. Recommendations provide valuable 

guidelines to protect public health, but cannot be enforced by law. The Agency for Toxic 

Substances and Disease Registry (ATSDR) and the National Institute for Occupational Safety 

and Health (NIOSH) are two federal organizations that develop recommendations for toxic 

substances. 

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

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

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

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

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

factors. 

Recommendations and regulations are also updated periodically as more information becomes 

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

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

The EPA has determined that drinking water should not contain more than 2.0 milligrams (mg) 

barium per liter (L) of water (2.0 mg/L). 

OSHA has a legally enforceable occupational exposure limit of 0.5 mg of soluble barium 

compounds per cubic meter (m3

) of air averaged over an 8-hour work day. The OSHA 8-hour 

exposure limit for barium sulfate dust in air is 15 mg/m3

 for total dust. NIOSH considers 
BARIUM AND BARIUM COMPOUNDS 8 

1. PUBLIC HEALTH STATEMENT 

exposure to barium chloride levels of 50 mg/m3 and higher as immediately dangerous to life or 

health. 

More information on government regulations can be found in Chapter 8. 

1.10 WHERE CAN I GET MORE INFORMATION? 

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

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

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

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

hazardous substances. 

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

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

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

cdcinfo@cdc.gov, or by writing to: 

Agency for Toxic Substances and Disease Registry 

 Division of Toxicology and Environmental Medicine 

1600 Clifton Road NE 

 Mailstop F-32 

 Atlanta, GA 30333 

 Fax: 1-770-488-4178 

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

National Technical Information Service (NTIS) 

5285 Port Royal Road 

 Springfield, VA 22161 

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

 Web site: http://www.ntis.gov/ 
BARIUM AND BARIUM COMPOUNDS 9 

2. RELEVANCE TO PUBLIC HEALTH 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO BARIUM IN THE UNITED 

STATES 

Barium is an alkaline earth metal, principally found as barite (barium sulfate) and witherite (barium 

carbonate) ores. Barium and barium compounds have a variety of uses including as getters in electronic 

tubes (barium alloys), rodenticide (barium carbonate), colorant in paints (barium carbonate and barium 

sulfate), and x-ray contrast medium (barium sulfate). Barium naturally occurs in food and groundwater. 

Barium concentrations in drinking water in the United States typically average 30 μg/L, but can average 

as high as 302 μg/L. However, individuals residing in certain regions of Kentucky, northern Illinois, New 

Mexico, and Pennsylvania who rely on groundwater for their source of drinking water may be exposed to 

barium concentrations as high as 10 times the maximum contaminant level (MCL) in drinking water of 

2.0 mg/L. Low levels of barium are also found in ambient air; levels are typically less than 0.05 μg 

barium/m3

. 

There is little quantitative information regarding the extent of barium absorption following inhalation, 

oral, or dermal exposure. Available evidence indicates that barium is absorbed to some extent following 

inhalation, oral, and dermal exposure; however, in some cases, absorption is expected to be limited. For 

example, there is some evidence that gastrointestinal absorption of barium in humans is <5–30% of the 

administered dose. The general population can be exposed to barium via inhalation, oral, or dermal 

exposure; under most circumstances, oral exposure would be the predominant route of exposure. 

2.2 SUMMARY OF HEALTH EFFECTS 

An important factor affecting the development of adverse health effects in humans is the solubility of the 

barium compound to which the individual is exposed. Soluble barium compounds would generally be 

expected to be of greater health concern than insoluble barium compounds because of their greater 

potential for absorption. The various barium compounds have different solubilities in water and body 

fluids and therefore serve as variable sources of the Ba2+ ion. The Ba2+ ion and the soluble compounds of 

barium (notably chloride, nitrate, hydroxide) are toxic to humans. Although barium carbonate is 

relatively insoluble in water, it is toxic to humans because it is soluble in the gastrointestinal tract. The 

insoluble compounds of barium (notably sulfate) are inefficient sources of Ba2+ ion and are therefore 

generally nontoxic to humans. The insoluble, nontoxic nature of barium sulfate has made it practical to 

use this particular barium compound in medical applications as a contrast media for x-ray examination of 
BARIUM AND BARIUM COMPOUNDS 10 

2. RELEVANCE TO PUBLIC HEALTH 

the gastrointestinal tract. Barium provides an opaque contrasting medium when ingested or given by 

enema prior to x-ray examination. Under these routine medical situations, barium sulfate is generally 

safe. However, barium sulfate or other insoluble barium compounds may potentially be toxic when it is 

introduced into the gastrointestinal tract under conditions where there is colon cancer or perforations of 

the gastrointestinal tract and barium is able to enter the blood stream. 

There are a number of reports of serious health effects in individuals intentionally or accidentally exposed 

to barium carbonate or chloride. The predominant effect is hypokalemia, which can result in ventricular 

tachycardia, hypertension and/or hypotension, muscle weakness, and paralysis. Barium is a competitive 

potassium channel antagonist that blocks the passive efflux of intracellular potassium, resulting in a shift 

of potassium from extracellular to intracellular compartments. The net result of this shift is a significant 

decrease in the potassium concentration in the blood plasma. Although the case reports did not provide 

information on doses, it is likely that the doses were high. In addition to the effects associated with 

hypokalemia, gastrointestinal effects such as vomiting, abdominal cramps, and watery diarrhea are 

typically reported shortly after ingestion. Similar effects have been reported in cases of individuals 

exposed to very high concentrations of airborne barium; the effects include electrocardiogram (ECG) 

abnormalities, muscle weakness and paralysis, hypokalemia, and abdominal cramps, nausea, and 

vomiting. 

Several investigators have examined whether exposure to much lower doses of barium would adversely 

affect the cardiovascular system. A population-based study found significant increases in the risk of 

death from cardiovascular disease among residents 65 years of age and older living in communities with 

high levels of barium in the drinking water. However, these data cannot be used to establish a causal 

relationship because the study did not control for other cardiovascular risk factors or the use of water 

softeners, which would decrease barium levels and increase sodium levels. Two other studies did not find 

alterations in blood pressure and cardiac rhythm. In general, animal studies designed to assess 

cardiovascular function have not found significant alterations in blood pressure or ECG readings 

following low-dose oral exposure. One study did find significant increases in blood pressure in rats 

exposed to 0.80 mg barium/kg/day. However, the use of a low mineral diet with less than adequate levels 

of calcium may have influenced the study results. 

The available animal data provide strong evidence that the most sensitive adverse effect of barium is renal 

toxicity. There are some reports of renal effects in case reports of individuals ingesting high doses of 

barium. Nephropathy has been observed in rats and mice following long-term oral exposure to barium. 
BARIUM AND BARIUM COMPOUNDS 11 

2. RELEVANCE TO PUBLIC HEALTH 

In both species, there is a steep dose-response curve for the incidence of nephropathy. For example, 

nephropathy was not observed in mice exposed to 205 mg barium/kg/day for an intermediate duration; at 

450 mg barium/kg/day, 95% of the animals exhibited mild to moderate nephropathy. Data in mice also 

suggest that the severity and sensitivity to renal lesions is related to duration of exposure. As noted 

previously, a 205 mg barium/kg/day dose is a no effect level in mice exposed to barium chloride for 

90 days; a 2-year exposure to 200 mg barium/kg/day resulted in moderate to marked nephropathy. 

The potential for barium to induce reproductive and developmental effects has not been well investigated. 

Decreases in the number of sperm and sperm quality and a shortened estrous cycle and morphological 

alterations in the ovaries were observed in rats exposed to 2.2 mg barium/m3

 and higher in air for an 

intermediate duration. Interpretation of these data is limited by the poor reporting of the study design and 

results, in particular, whether the incidence was significantly different from controls. In general, oral 

exposure studies have not found morphological alterations in reproductive tissues of rats or mice exposed 

to 180 or 450 mg barium/kg/day, respectively, as barium chloride in drinking water for an intermediate 

duration. Additionally, no significant alterations in reproductive performance was observed in rats or 

mice exposed to 200 mg barium/kg/day as barium chloride in drinking water. Decreased pup birth weight 

and a nonsignificant decrease in litter size have been observed in the offspring of rats exposed to 

180/200 mg barium/kg/day as barium chloride in drinking water prior to mating. 

Several studies have examined the carcinogenic potential of barium following oral exposure and did not 

find significant increases in the tumor incidence. No studies have adequately assessed the carcinogenicity 

of barium following inhalation exposure. The Department of Health and Human Services (DHHS) and 

the International Agency for Research on Cancer (IARC) have not assessed the carcinogenicity of barium. 

The EPA has concluded that barium is not classifiable as to human carcinogenicity, Group D. However, 

under EPA’s revised guidelines for carcinogen risk assessment, barium is considered not likely to be 

carcinogenic to humans following oral exposure and its carcinogenic potential cannot be determined 

following inhalation exposure. 

2.3 MINIMAL RISK LEVELS (MRLs) 

Estimates of exposure levels posing minimal risk to humans (MRLs) have been made for barium. An 

MRL is defined as an estimate of daily human exposure to a substance that is likely to be without an 

appreciable risk of adverse effects (noncarcinogenic) over a specified duration of exposure. MRLs are 

derived when reliable and sufficient data exist to identify the target organ(s) of effect or the most sensitive 
BARIUM AND BARIUM COMPOUNDS 12 

2. RELEVANCE TO PUBLIC HEALTH 

health effect(s) for a specific duration within a given route of exposure. MRLs are based on 

noncancerous health effects only and do not consider carcinogenic effects. MRLs can be derived for 

acute, intermediate, and chronic duration exposures for inhalation and oral routes. Appropriate 

methodology does not exist to develop MRLs for dermal exposure. 

Although methods have been established to derive these levels (Barnes and Dourson 1988; EPA 1990), 

uncertainties are associated with these techniques. Furthermore, ATSDR acknowledges additional 

uncertainties inherent in the application of the procedures to derive less than lifetime MRLs. As an 

example, acute inhalation MRLs may not be protective for health effects that are delayed in development 

or are acquired following repeated acute insults, such as hypersensitivity reactions, asthma, or chronic 

bronchitis. As these kinds of health effects data become available and methods to assess levels of 

significant human exposure improve, these MRLs will be revised. 

Inhalation MRLs 

No acute-, intermediate-, or chronic-duration inhalation MRLs were derived for barium because studies 

evaluating the effects of barium in humans and animals following acute, intermediate, and chronic 

inhalation exposure were inadequate for establishing the exposure concentrations associated with adverse 

health effects. Five reports of occupational exposure to barium have been identified. In one study (Doig 

1976), a benign pneumoconiosis was observed in several workers exposed to barium sulfate; two other 

studies did not find barium-related alterations in the respiratory tract of workers exposed to barium sulfate 

(Seaton et al. 1986) or barium carbonate (Essing et al. 1976). Other effects reported in the occupational 

exposure studies were an increase in blood pressure (Essing et al. 1976), gastrointestinal distress, muscle 

weakness and paralysis, absence of deep tendon reflex, and decreased serum potassium levels in a worker 

exposed to barium carbonate powder (Shankle and Keane 1988). A fifth study did not find alterations in 

plasma potassium levels in welders using barium-containing electrodes (Zschiesche et al. 1992). 

Interpretation of these studies is limited by the small number of subjects, possible lack of a control group, 

and/or the lack of quantitative exposure information. 

Three animal studies evaluating the toxicity of inhaled barium have also been identified. Two of the 

studies reported adverse respiratory tract effects including lung lesions (perivascular and peribronchial 

sclerosis and focal thickening of the intraalveolar septa) in rats exposed to 3.6 mg barium/m3

 as barium 

carbonate dust 4 hours/day, 6 days/week for 4 months (Tarasenko et al. 1977) and bronchoconstriction in 

guinea pigs exposed to 0.06 mg barium/m3

/minute as barium chloride for an unspecified amount of time 
BARIUM AND BARIUM COMPOUNDS 13 

2. RELEVANCE TO PUBLIC HEALTH 

(Hicks et al. 1986). The third study (Cullen et al. 2000) did not find histological alterations in the lungs 

of rats exposed to 44.1 mg barium/m3

 as barium sulfate for 7 hours/day, 5 days/week for 119 days. 

Increases in blood pressure were observed in the Tarasenko et al. (1977) and Hicks et al. (1986) studies. 

Tarasenko et al. (1977) also reported hematological, reproductive, and developmental effects in rats 

exposed to barium carbonate dust. None of these studies provide a suitable basis for an inhalation MRL. 

The Tarasenko et al. (1977) studies are limited by poor reporting of the study design and results, lack of 

incidence data, and lack of statistical analysis for many of the end points. The Hicks et al. (1986) study 

did not report the frequency or length of exposure, the number of animals used was not clearly reported, 

and it does not appear that control animals were used. Although the Cullen et al. (2000) study was well 

reported and designed, it only examined the respiratory tract and did not identify an adverse effect level. 

Oral exposure studies identify the kidney as the most sensitive target of toxicity; this end point was not 

evaluated in the Cullen et al. (2000) study. 

Oral MRLs 

There are numerous case reports of individuals intentionally or accidentally ingesting unreported but 

presumably high doses of barium (Das and Singh 1970; Deng et al. 1991; Diengott et al. 1964; Downs et 

al. 1995; Gould et al. 1973; Jha et al. 1993; Koch et al. 2003; Lewi and Bar-Khayim 1964; McNally 1925; 

Ogen et al. 1967; Phelan et al. 1984; Silva 2003; Talwar and Sharma 1979; Wetherill et al. 1981). The 

consistently observed effects included abdominal distress (vomiting, abdominal cramping, and watery 

diarrhea), numbness around the face, muscle weakness, paralysis, and ventricular tachycardia. 

Information on the acute oral toxicity of barium is limited to two studies in rats conducted by Borzelleca 

et al. (1988). A nonsignificant increase in mortality (3/20 females compared to 0/20 in controls) was 

found in rats receiving gavage doses of 198 mg barium/kg/day as barium chloride in water for 10 days. In 

the other study conducted by this group, 15/20 animals died after a single dose of 198 mg barium/kg/day 

as barium chloride in water. In the 10-day study, significant decreases in relative kidney weight 

(kidney:brain ratio) were observed in female rats administered 66–138 mg barium/kg/day and decreases 

in blood urea nitrogen (BUN) levels were observed in female rats dosed with 66–198 mg barium/kg/day 

and male rats dosed with 198 mg barium/kg/day. The magnitude of change in BUN levels was small (less 

than 15%) and was not dose-related; the decrease in BUN was not considered to be biologically 

significant. Additionally, BUN levels are typically increased in response to kidney damage. Significant 

decreases in absolute ovary weight and relative ovary weight (ovary:brain ratio) were observed at 198 mg 

barium/kg/day in the 10-day study. The biological significance of this change in organ weight is 
BARIUM AND BARIUM COMPOUNDS 14 

2. RELEVANCE TO PUBLIC HEALTH 

questionable; no gross alterations in the ovaries were observed in this study and no histological alterations 

were observed in rats or mice exposed to barium chloride for acute, intermediate, or chronic durations to 

barium doses as high as 180 mg barium/kg/day in rats (NTP 1994) and 495 mg barium/kg/day in mice 

(NTP 1994). 

The data are considered inadequate for derivation of an acute-duration oral MRL for barium. The 

available animal studies (Borzelleca et al. 1988) have evaluated the toxicity of barium chloride in 

repeated dose studies; however, neither study identified a non-lethal biologically significant adverse 

effect level. Longer-term studies identify the kidney as the most sensitive target; however, it is not 

known if the kidney would also be the most sensitive target following acute-duration exposure. Data in 

mice suggest that the severity and sensitivity to renal lesions are related to duration of exposure. The 

intermediate-duration mouse study identified a NOAEL of 205 mg barium/kg/day; however; a 2-year 

exposure to 200 mg barium/kg/day resulted in moderate to marked nephropathy (NTP 1994). Derivation 

of an MRL using the highest identified no-observed-adverse-effect level (NOAEL) is not recommended 

at this time because critical targets of toxicity and dose-response relationships have not been established 

for this exposure category. The exposure levels are poorly characterized in the available reports of human 

poisonings, acute-duration animal studies have failed to identify the critical target of barium toxicity, and 

it is possible that the critical target (kidneys) following long-term exposure may not be a sensitive target 

following short-term exposure. 

•	 An MRL of 0.2 mg barium/kg/day has been derived for intermediate-duration oral exposure (15– 

364 days) to barium. 

Information on the oral toxicity of barium in humans following intermediate-duration oral exposure is 

limited to an experimental study in which men were exposed to 0.1 or 0.2 mg barium/kg/day as barium 

chloride in drinking water for 4 weeks (Wones et al. 1990). No significant alterations in blood pressure or 

ECG readings, relative to initial baseline measurements, were found. 

A number of animal studies have evaluated barium toxicity following intermediate-duration oral 

exposure. Several of these studies focused on the cardiovascular system or assessed cardiovascular 

function. Perry et al. (1983, 1985, 1989) reported significant increases in blood pressure in rats 

administered 8.6 or 11 mg barium/kg/day as barium chloride in drinking water for 1 or 4 months, 

respectively. NTP (1994) and McCauley et al. (1985) did not find significant alterations in blood pressure 

or ECG readings in rats exposed to 150 or 180 mg barium/kg/day in drinking water for 13 or 16 weeks, 

respectively. The reason for the differences between the results from the Perry et al. (1983, 1985, 1989) 
BARIUM AND BARIUM COMPOUNDS 15 

2. RELEVANCE TO PUBLIC HEALTH 

studies and the NTP (1994) and McCauley et al. (1985) studies is not known. It is possible that the lowmineral diet used in the Perry et al. (1983, 1985, 1989) studies influenced the results. The calcium 

content of the rye-based diet was 3.8 mg/kg, which is lower than the concentration recommended for 

maintenance, growth, and reproduction of laboratory rats (NRC 1995b). 

The results of the McCauley et al. (1985) and NTP (1994) studies suggest that the kidney is the most 

sensitive target of toxicity in rats and mice. In the McCauley et al. (1985) study, glomerular alterations 

consisting of fused podocytes and thickening of the capillary basement membrane were found in 

uninephrectomized Sprague Dawley rats, Dahl salt-sensitive rats, and Dahl salt-resistant rats exposed to 

150 mg barium/kg/day in drinking water for 16 weeks. In the NTP (1994) 13-week rat study, significant 

increases in absolute and relative kidney weights were observed in female rats exposed to 115 or 180 mg 

barium/kg/day and in males exposed to 200 mg barium/kg/day. At 200 and 180 mg barium/kg/day, 

minimal to mild dilatation of the proximal convoluted tubules of the outer medulla and renal cortex was 

observed in the males and females, respectively; an increase in mortality (30%) was also observed in the 

males exposed to 200 mg barium/kg/day. In mice, mild to moderate nephropathy (characterized as tubule 

dilatation, regeneration, and atrophy) was observed in 100% of the males exposed to 450 mg 

barium/kg/day and 90% of the females exposed to 495 mg barium/kg/day; no renal lesions were observed 

at the next lowest dose level (205 and 200 mg barium/kg/day in males and females, respectively). Other 

effects observed at the 450/495 mg barium/kg/day dose level included weight loss, spleen and thymus 

atrophy, and increased mortality (60% of the males and 70% of females died after 5 weeks of exposure). 

Other end points that have been examined in rats and mice include neurotoxicity, reproductive toxicity, 

and developmental toxicity. In male and female rats, slight decreases in undifferentiated motor activity 

were observed at 10 mg barium/kg/day and higher. However, the difference between motor activity in the 

barium-exposed rats and the controls was less than 20% and was not considered to be biologically 

significant. At 180 mg barium/kg/day, the difference was 30% in the female rats, which was considered 

to be adverse. No significant alterations were found on the remaining neurobehavioral tests (grip 

strength, tail flick latency, startle response, and hindlimb foot splay). In mice, a significant decrease in 

forelimb grip strength was observed in females exposed to 495 mg barium/kg/day; this may have been 

due to debilitation. No other alterations in neurobehavioral performance were found. No effects on 

reproductive tissues or reproductive performance were observed in rats or mice exposed to approximately 

200 mg barium/kg/day (Dietz et al. 1992; NTP 1994). Pre-mating exposure of male and female rats to 

180/200 mg barium/kg/day resulted in decreased pup birth weight and a nonsignificant decrease in litter 

size; the NOAEL for these effects was 110/115 mg barium/kg/day (Dietz et al. 1992). No developmental 
BARIUM AND BARIUM COMPOUNDS 16 

2. RELEVANCE TO PUBLIC HEALTH 

effects were observed in mice exposed to 200 mg barium/kg/day (Dietz et al. 1992). Another study 

(Tarasenko et al. 1977) also reported developmental effects (increased offspring mortality during the first 

2 months and disturbances in liver function) in an unspecified animal species; however, the lack of 

information on experimental methods, exposure conditions, and results limits the usefulness of this study 

for evaluating the potential of aluminum to induce developmental toxicity. 

Based on these data, the kidney appears to be the most sensitive target following intermediate-duration 

oral exposure to barium. Three studies identified adverse effect levels for kidney effects: (1) a lowestobserved-adverse-effect level (LOAEL) of 150 mg barium/kg/day was identified in uninephrectomized 

and salt-sensitive and salt resistant rats (McCauley et al. 1985), (2) a LOAEL of 115 mg barium/kg/day 

was identified for increased kidney weight in rats; the NOAEL was 65 mg barium/kg/day (NTP 1994), 

and (3) a LOAEL of 450 mg barium/kg/day for nephropathy in mice; the NOAEL was 205 mg 

barium/kg/day (NTP 1994). The NTP (1994) 13-week rat study, which identified the lowest LOAEL for 

a kidney effect, was selected as the basis of the intermediate-duration oral MRL; the change in kidney 

weight was considered an early indicator of potentially more serious effects in the kidney. 

In this study (NTP 1994), groups of 10 male and 10 female F344/N rats were administered 0, 125, 500, 

1,000, 2,000, or 4,000 ppm barium chloride dihydrate (0, 10, 30, 65, 110, and 200 mg barium/kg/day for 

males and 0, 10, 35, 65, 115, and 180 mg barium/kg/day for females) in drinking water for 90 days. 

Exposure-related deaths were observed during the last week of the study in 30% of the males and 10% of 

the females exposed to 200/180 mg barium/kg/day. Significant decreases in final body weights were 

observed in the 200 mg barium/kg/day males (13% lower than controls) and 180 mg barium/kg/day 

females (8% lower than controls); significant decreases in water consumption (approximately 30% lower 

than controls) were also observed at this dose level. Significant increases in absolute and relative kidney 

weights were observed in females exposed to 115 or 180 mg barium/kg/day and increases in relative 

kidney weights were also observed in males at 200 mg barium/kg/day; an increase in relative kidney 

weight was also observed in the females exposed to 65 mg barium/kg/day; The magnitude of the 

increases in relative kidney weights were 7, 14, and 19% in the females exposed to 65, 115, and 180 mg 

barium/kg/day and 12% in males exposed to 200 mg barium/kg/day. Minimal to mild, focal to multifocal 

dilatation of the proximal renal cortex was observed in three male and three female rats in the 200/180 mg 

barium/kg/day group. The small increase in relative kidney weight (7%) observed in the female rats 

exposed to 65 mg barium/kg/day was not considered biologically significant because it is not supported 

by an increase in histological alterations in the kidney at 65 or 115 mg barium/kg/day or in rats exposed 
BARIUM AND BARIUM COMPOUNDS 17 

2. RELEVANCE TO PUBLIC HEALTH 

to 75 mg barium/kg/day for 2 years (NTP 1994). Thus, this study identifies a NOAEL of 65 mg 

barium/kg/day and a LOAEL of 115 mg barium/kg/day. 

A NOAEL/LOAEL approach was used to derive the MRL because none of the available benchmark dose 

models provided an adequate fit to the absolute or relative kidney weight data. Thus, the intermediateduration oral MRL of 0.2 mg barium/kg/day was calculated by dividing the NOAEL of 65 mg 

barium/kg/day by an uncertainty factor of 100 (10 to account for animal to human extrapolation and 

10 for human variability) and a modifying factor of 3. The modifying factor of 3 was included to account 

for deficiencies in the oral toxicity database, particularly the need for an additional developmental toxicity 

study. Decreases in pup birth weight and a nonstatistically significant decrease in live litter size were 

observed in the offspring of rats exposed to 180/200 mg Ba/kg/day as barium chloride in drinking water 

prior to mating (Dietz et al. 1992). Maternal body weight gain and water consumption were not reported, 

thus it is not known if the decreases in pup body weight were secondary to maternal toxicity or direct 

effect on the fetus. No developmental effects were observed in mice at the highest dose tested (200 mg 

Ba/kg/day) (Dietz et al. 1992). One other study examined the potential for developmental toxicity in 

orally exposed animals (Tarasenko et al. 1977). However, because the study was poorly reported and no 

incidence data or statistical analysis were presented in the published paper, the reported findings of 

increased mortality and systemic toxicity in the offspring of an unspecified species orally exposed to 

barium during conception and pregnancy can not be adequately evaluated. The Dietz et al. (1992) study 

was designed to be a mating trial and did not expose the animals during gestation; thus, database is 

lacking an adequate study to evaluate the potential for barium to induce developmental effects. 

•	 An MRL of 0.2 mg barium/kg/day has been derived for chronic-duration oral exposure 

(>365 days) to barium. 

Several human and animal studies have examined the toxicity of barium following chronic-duration 

exposure. Two community-based studies have evaluated the possible association between elevated levels 

of barium in drinking water and increased risk of cardiovascular disease. No significant alterations in 

blood pressure measurements or increases in the prevalence of hypertension, heart disease, or stroke were 

found among residents of two communities with elevated (0.2 mg barium/kg/day) or low 

(0.003 mg barium/kg/day) levels of barium in drinking water (Brenniman and Levy 1985; Brenniman et 

al. 1979a, 1981). In the second study, significantly higher mortality rates, particularly among individuals 

65 years of age and older, for cardiovascular disease and heart disease (arteriosclerosis) were found in a 

community with elevated barium drinking water levels (0.06–0.3 mg barium/kg/day) as compared to a 

community with low barium levels (0.006 mg barium/kg/day) (Brenniman and Levy 1985; Brenniman et 
BARIUM AND BARIUM COMPOUNDS 18 

2. RELEVANCE TO PUBLIC HEALTH 

al. 1979a, 1981). A common limitation of both studies is the lack of information on tap water 

consumption, actual barium intakes, and duration of exposure. Additionally, the second study did not 

control for a number of potential confounding variables, particularly the use of water softeners, which 

would have resulted in a decrease in barium levels in the drinking water and an increase in sodium levels. 

Significant increases in blood pressure were observed in rats exposed to 0.8 mg barium/kg/day as barium 

chloride in drinking water for 16 months (Perry et al. 1983, 1985, 1989); the NOAEL for this effect was 

0.17 mg barium/kg/day. At higher doses (7.2 mg barium/kg/day), depressed rates of cardiac contraction, 

reduced cardiac electrical conductivity, and decreased cardiac ATP levels were observed. As noted in the 

discussion of the intermediate-duration oral MRL, interpretation of the results of this study is limited due 

to the low mineral diet, which may have supplied inadequate levels of calcium. No adverse effects were 

observed in rats exposed to 60 mg barium/kg/day as barium chloride in drinking water for 2 years (NTP 

1994), 15 mg barium/kg/day to an unspecified barium compound in drinking water for 68 weeks 

(McCauley et al. 1985), or 0.7 mg barium/kg/day as barium acetate in drinking water for a lifetime 

(Schroeder and Mitchener 1975a). In mice exposed to barium chloride in drinking water for 2 years, 

marked renal nephropathy was observed at 160 mg barium/kg/day; the increased incidence of 

nephropathy in the next lowest dose group (75 mg barium/kg/day) was not statistically significant. Other 

adverse effects observed at 160 mg barium/kg/day included weight loss and increased mortality (NTP 

1994). 

As with intermediate-duration exposure, the animal data provide suggestive evidence that the kidney is 

the most sensitive target of toxicity. A serious LOAEL of 160 mg barium/kg/day was identified for 

nephropathy in mice (NTP 1994); the NOAEL identified in this study is 75 mg/kg/day. Although no 

kidney lesions were observed in rats exposed to doses as high as 60 mg barium/kg/day (NTP 1994), the 

doses utilized in the study may not have been high enough to cause kidney damage. Biologically 

significant kidney alterations were observed at 115 mg barium/kg/day and higher in rats exposed for an 

intermediate duration (NTP 1994). The chronic-duration mouse study (NTP 1994) was selected as the 

basis of the chronic-duration MRL for barium. 

In this study (NTP 1994), groups of 60 male and 60 female B6C3F1 mice were exposed to 0, 500, 1,250, 

or 2,500 ppm barium chloride dehydrate (0, 30, 75, and 160 mg barium/kg/day for males and 0, 40, 90, 

and 200 mg barium/kg/day for females) in drinking water for 2 years. Increased mortality attributed to 

renal lesions was observed in the 160/200 mg/kg/day group. Decreased body weights (<7%) were 

observed in the barium-exposed mice. The investigators noted that a moderate to marked weight loss was 
BARIUM AND BARIUM COMPOUNDS 19 

2. RELEVANCE TO PUBLIC HEALTH 

observed in animals dying early. No significant alterations in hematology or clinical chemistry 

parameters were observed. A significant increase in the incidence of nephropathy was observed in male 

and female mice exposed to 160/200 mg/kg/day. The nephropathy was characterized by extensive 

regeneration of cortical and medullary tubule epithelium, tubule dilatation, hyaline cast formation, 

multifocal interstitial fibrosis, and glomerulosclerosis in some kidneys. The average severity of the 

nephropathy was 3.6 (moderate to marked) for both the males and females in the 160/200 mg/kg/day 

group. 

A benchmark analysis of the incidence data for nephropathy in mice was conducted; details of this 

analysis are presented in Appendix A. A benchmark dose (BMD) of 80.06 mg barium/kg/day, which 

corresponds to a 5% increase in the incidence of nephropathy was calculated; the 95% lower confidence 

limit on the BMD (BMDL) was 61.13 mg barium/kg/day. The BMDL05 was selected as the point of 

departure for deriving the chronic-duration oral MRL. The dose corresponding to a predicted 5% 

incidence was selected over the typically 10% incidence as a precaution due to the severity of the 

observed effects (moderate to marked severity nephropathy), which resulted in marked weight loss and 

increased mortality. Thus, the chronic-duration oral MRL of 0.2 mg barium/kg/day is based on the 

BMDL05 of 61 mg barium/kg/day in male mice and an uncertainty factor of 100 (10 to account for animal 

to human extrapolation and 10 for human variability) and a modifying factor of 3. The modifying factor 

of 3 was included to account for deficiencies in the oral toxicity database, particularly the need for an 

additional developmental toxicity study. Decreases in pup birth weight and a nonstatistically significant 

decrease in live litter size were observed in the offspring of rats exposed to 180/200 mg Ba/kg/day as 

barium chloride in drinking water prior to mating (Dietz et al. 1992). Maternal body weight gain and 

water consumption were not reported, thus it is not known if the decreases in pup body weight were 

secondary to maternal toxicity or direct effect on the fetus. No developmental effects were observed in 

mice at the highest dose tested (200 mg Ba/kg/day) (Dietz et al. 1992). One other study examined the 

potential for developmental toxicity in orally exposed animals (Tarasenko et al. 1977). However, because 

the study was poorly reported and no incidence data or statistical analysis were presented in the published 

paper, the reported findings of increased mortality and systemic toxicity in the offspring of an unspecified 

species orally exposed to barium during conception and pregnancy can not be adequately evaluated. The 

Dietz et al. (1992) study was designed to be a mating trial and did not expose the animals during 

gestation; thus, database is lacking an adequate study to evaluate the potential for barium to induce 

developmental effects. 
BARIUM AND BARIUM COMPOUNDS 20 

2. RELEVANCE TO PUBLIC HEALTH 

This page is intentionally blank. 
BARIUM AND BARIUM COMPOUNDS 21 

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 barium. 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. 

When evaluating the health effects of barium compounds, it is important to keep in mind that different 

barium compounds have different solubilities in water and body fluids and therefore serve as variable 

sources of the Ba2+ ion. The Ba2+ ion and the soluble compounds of barium (notably chloride, nitrate, and 

hydroxide) are generally highly toxic to humans and experimental animals. The insoluble barium 

compounds (notably sulfate) are inefficient sources of the Ba2+ ion and therefore are generally nontoxic. 

Although barium carbonate is insoluble in water, barium ions would be released from ingested barium 

carbonate in the acid milieu of the stomach. Throughout the following section (3.2), the health effects by 

route of exposure of both soluble and insoluble barium compounds are discussed. 

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 
BARIUM AND BARIUM COMPOUNDS 22 

3. HEALTH EFFECTS 

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

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

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

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

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

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

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

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

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

effects to human health. 

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

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

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

associated with more subtle effects in humans or animals (LOAELs) or exposure levels below which no 

adverse effects (NOAELs) have been observed. Estimates of levels posing minimal risk to humans 

(Minimal Risk Levels or MRLs) may be of interest to health professionals and citizens alike. 

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. 

3.2.1 Inhalation Exposure 

Studies evaluating the effects of barium following acute, intermediate, and chronic inhalation exposure 

are limited to several case reports of humans exposed occupationally (Doig 1976; Essing et al. 1976; 

Seaton et al. 1986; Shankle and Keane 1988), an experimental exposure to barium in welding fumes 

(Zschiesche et al. 1992), and three experimental studies with animals (Cullen et al. 2000; Hicks et al. 

1986; Tarasenko et al. 1977). These case reports and animal studies are not adequate for firmly 

establishing the health effects of barium by inhalation because of a number of significant study 

limitations. The case reports are generally inadequate because data were available for a limited number 

of exposed subjects and because exposure conditions (duration, frequency, dose) were not well 

characterized (Doig 1976; Essing et al. 1976; Seaton et al. 1986; Shankle and Keane 1988). One of the 

animal studies was limited in that apparently no control animals were used, an inhalation chamber 

providing a controlled dose and environment was not used, and there was a lack of information regarding 
BARIUM AND BARIUM COMPOUNDS 23 

3. HEALTH EFFECTS 

the vehicle used, purity of the test material, duration and frequency of exposure, and number of animals 

tested (Hicks et al. 1986). The second animal study consisted of several experiments, but was generally 

limited in that the authors provided few details regarding experimental methods, exposure conditions, and 

test results, and no information as to the number of animals tested, purity of the test material, or statistical 

methods used; furthermore, in some experiments, it was not clear whether or not control animals were 

used (Tarasenko et al. 1977). The third study examined a limited number of end points (Cullen et al. 

2000). In view of the major limitations associated with the available case reports and studies, results from 

these reports should be regarded as providing only preliminary and/or suggestive evidence that acute, 

intermediate, and chronic inhalation exposure to barium may potentially be associated with adverse health 

effects. Findings from the various case reports and animal studies are briefly described below. 

3.2.1.1 Death 

No studies were located regarding death in humans or animals after inhalation exposure to barium. 

3.2.1.2 Systemic Effects 

No studies were located regarding endocrine, dermal, or ocular effects in humans or animals after 

inhalation exposure to barium. 

Respiratory Effects. Two reports of workers exposed chronically to dust from barium sulfate 

demonstrated that this exposure had a minor effect on the lungs. In one study, a benign pneumonoconiosis was observed in several factory workers (Doig 1976). In a second study in which workers 

were exposed by mining barium sulfate, silicosis was observed but was attributed to inhalation of quartz 

(Seaton et al. 1986). In contrast, a study of workers chronically exposed to barium carbonate dust 

reported no respiratory symptoms attributable to barium exposure (Essing et al. 1976). X-ray analysis of 

the lungs also showed no abnormalities attributable to barium dust. 

Studies regarding respiratory effects in animals following inhalation exposure to barium are limited to 

three reports (Cullen et al. 2000; Hicks et al. 1986; Tarasenko et al. 1977). Pulmonary lesions 

(perivascular and peribronchial sclerosis and focal thickening of the interalveolar septa) were observed in 

rats exposed to 3.6 mg barium/m3

 as barium carbonate dust 4 hours/day, 6 days/week for 4 months 

(Tarasenko et al. 1977). Bronchoconstriction was reportedly noted in guinea pigs following inhalation for 

an unspecified period of time to 0.06 mg barium/m3

/minute as aerosolized barium chloride solution 
BARIUM AND BARIUM COMPOUNDS 24 

3. HEALTH EFFECTS 

(Hicks et al. 1986). In contrast to these finding, no adverse histological alterations were observed in the 

lungs of rats exposed to 44.1 mg barium/m3

 as barium sulfate for 119 days (Cullen et al. 2000). 

Cardiovascular Effects. Three of 12 workers chronically exposed to barium carbonate dust had 

elevated blood pressure and 2 workers had ECG abnormalities (Essing et al. 1976). However, it is 

unknown whether this represented an increased incidence because no comparison with a control 

population was performed. Increased blood pressure and cardiac irregularities were reportedly observed 

in guinea pigs exposed by inhalation for an unspecified period of time to 0.06 mg barium/m3

/minute as 

aerosolized barium chloride solution (Hicks et al. 1986). Tarasenko et al. (1977) reported a 32% increase 

in arterial pressure and alterations in ECG readings suggestive of disturbances in heart conductivity 

following proserine administration in rats exposed to 3.6 mg barium/m3

 as barium carbonate; no ECG 

alterations were observed prior to proserine administration. 

Gastrointestinal Effects. Abdominal cramps, nausea, and vomiting were experienced by a 22-yearold factory worker accidentally exposed by acute inhalation to a large but unspecified amount of barium 

carbonate powder (Shankle and Keane 1988). No animal studies were located regarding gastrointestinal 

effects in animals after inhalation exposure to barium. 

Hematological Effects. Altered hematological parameters were observed in rats following inhalation 

for an intermediate exposure period to 3.6 mg barium/m3

 as barium carbonate dust (Tarasenko et al. 

1977). Reported changes included decreased blood hemoglobin and thrombocyte count. 

Musculoskeletal Effects. After accidental exposure to a large amount of barium carbonate powder 

by acute inhalation, a 22-year-old factory worker developed progressive muscle weakness and paralysis 

of the extremities and neck (Shankle and Keane 1988); this is likely due to the low serum potassium level 

rather than a direct effect on muscle tissue. X-ray analysis of the bones and skeletal muscles of the pelvis 

and thighs of workers chronically exposed to barium carbonate dust revealed no apparent build up of 

insoluble barium in these tissues (Essing et al. 1976). No studies were located regarding musculoskeletal 

effects in animals after inhalation exposure to barium. 

Hepatic Effects. No studies were located regarding hepatic effects in humans after inhalation 

exposure to barium. Impaired detoxifying function of the liver was noted in rats exposed to 3.6 mg 

barium/m3

 as barium carbonate dust (Tarasenko et al. 1977). No other details were reported. 
BARIUM AND BARIUM COMPOUNDS 25 

3. HEALTH EFFECTS 

Renal Effects. Renal failure occurred in a 22-year-old worker accidentally exposed by acute 

inhalation to barium carbonate powder (Shankle and Keane 1988). No studies were located regarding 

renal effects in animals after inhalation exposure to barium. 

Body Weight Effects. A 21% decrease in body weight gain was observed in rats exposed to 3.6 mg 

barium/m3

 as barium carbonate dust for 4 months (Tarasenko et al. 1977). 

Metabolic Effects. Decreases in plasma potassium concentrations were observed in two groups of 

welders using barium-containing electrodes; the barium levels in the work environment were 4.4 and 

0.3 mg/m3

 (Zschiesche et al. 1992). However, this was not observed in a third group of welders exposed 

to 2.0 mg barium/m3

. A low serum potassium level was also observed in a worker accidentally exposed 

to barium carbonate powder (Shankle and Keane 1988). Additionally, the plasma potassium 

concentrations were not statistically different from levels measured prior to barium exposure. Tarasenko 

et al. (1977) reported a decrease in urinary calcium levels and increased blood phosphorus levels in rats 

exposed to 3.6 mg barium/m3

 as barium carbonate dust for an intermediate duration (Tarasenko et al. 

1977). This study also reported a decrease in blood glucose levels in barium-exposed rats. 

3.2.1.3 Immunological and Lymphoreticular Effects 

No studies were located regarding immunological effects in humans or animals after inhalation exposure 

to barium. 

3.2.1.4 Neurological Effects 

Absence of deep tendon reflexes was observed in a 22-year-old man accidentally exposed by acute 

inhalation to barium carbonate powder (Shankle and Keane 1988); as noted previously, this is probably 

due to the barium-induced low potassium levels. No studies were located regarding neurological effects 

in animals after inhalation exposure to barium. 

3.2.1.5 Reproductive Effects 

No studies were located regarding reproductive effects in humans after inhalation exposure to barium. 

Only one limited report was available regarding reproductive effects in animals following intermediate 

inhalation exposure to barium carbonate (Tarasenko et al. 1977). Disturbances in spermatogenesis, 

including decreased number of sperm, decreased percentage of motile sperm, and decreased osmotic 
BARIUM AND BARIUM COMPOUNDS 26 

3. HEALTH EFFECTS 

resistance of sperm, were reportedly observed in male rats exposed by inhalation for one cycle of 

spermatogenesis to 15.8 mg barium/m3

 as barium carbonate dust. The testicles of these treated rats 

reportedly had an increase in the number of ducts with desquamated epithelium and a reduced number of 

ducts with 12th-stage meiosis. The condition of the testicles of treated rats returned to normal 30 days 

after cessation of barium carbonate treatment (Tarasenko et al. 1977). Similar observations were noted in 

a second experiment in which male rats were exposed by inhalation for an intermediate period to 3.6 mg 

barium/m3

 as barium carbonate dust. In a third experiment by the same authors, female rats exposed by 

inhalation for an intermediate period to 2.2 or 9.4 mg barium/m3

 as barium carbonate dust reportedly 

developed a shortened estrous cycle and alterations in the morphological structure of the ovaries. 

3.2.1.6 Developmental Effects 

No studies were located regarding developmental effects in humans after inhalation exposure to barium. 

Only one limited report was available regarding developmental effects in animals after intermediate 

inhalation exposure to barium (Tarasenko et al. 1977). Reduced survival, underdevelopment, lowered 

weight gain, and various hematologic alterations (erythropenia, leukocytosis, eosinophilia, neutrophilia) 

were reported in the offspring of female rats exposed by inhalation for an intermediate period to 2.2 or 

9.4 mg barium/m3

 as barium carbonate dust (Tarasenko et al. 1977). No other significant details 

regarding this developmental study were reported. 

3.2.1.7 Cancer 

No studies were located regarding cancer in humans or animals after inhalation exposure to barium. 

3.2.2 Oral Exposure 

The majority of studies evaluating the health effects of barium are oral exposure studies. The available 

oral studies include numerous case reports of humans exposed orally to barium through accidental or 

intentional ingestion, several epidemiological and statistical investigations of humans exposed to drinking 

water containing barium, and various experimental animal studies involving acute, intermediate, or 

chronic exposure to barium either by gavage or by drinking water. Findings from the various oral studies 

are summarized below. 
BARIUM AND BARIUM COMPOUNDS 27 

3. HEALTH EFFECTS 

3.2.2.1 Death 

Death has been reported in a number of case reports of accidental or intentional ingestion of barium salts. 

The cause of death was attributed to cardiac arrest, severe gastrointestinal hemorrhage, or unknown 

causes (Das and Singh 1970; Deng et al. 1991; Diengott et al. 1964; Downs et al. 1995; Jourdan et al. 

2001; McNally 1925; Ogen et al. 1967; Talwar and Sharma 1979). Doses in these cases were not known. 

In addition to case reports of death in humans, several studies have examined mortality rates in residents 

living in communities with elevated barium levels in the drinking water (Brenniman and Levy 1985; 

Brenniman et al. 1979a, 1979b, 1981; Elwood et al. 1974; Schroeder and Kraemer 1974). Two studies 

found no statistical correlations between barium concentrations in drinking water and total mortality 

and/or cardiovascular mortality rates in exposed populations (Elwood et al. 1974; Schroeder and Kraemer 

1974). Interpretation of the study results are limited by the lack of information on exposure conditions 

(dose, duration, frequency) and the number of people exposed. Results of a third study indicated that 

relative to communities with little or no barium in drinking water, communities with elevated 

concentrations of barium in their drinking water had significantly higher mortality rates for all causes, 

heart disease, arteriosclerosis, and all cardiovascular disease (Brenniman and Levy 1985; Brenniman et al. 

1979a, 1979b, 1981). This epidemiological study had a number of confounding variables, including 

possible use in the study population of home water softeners that would remove barium from the drinking 

water, inclusion of communities that had significant changes in population, lack of a way to control for 

length of time an individual lived in a community, and widely varying concentrations of other 

contaminants (calcium, sodium, magnesium) in the drinking water. 

The LD50 values for barium chloride in rats range from 132 to 277 mg barium/kg (Borzelleca et al. 1988; 

Tardiff et al. 1980). Significant increases in mortality were observed in rats and mice exposed to 200 or 

450 mg barium/kg/day as barium chloride in drinking water for 90 days (NTP 1994). Survival was not 

affected at 110 or 205 mg barium/kg/day in the rats or mice, respectively. No changes in mortality were 

observed in rats chronically exposed to doses as high as 60 mg barium/kg/day as barium chloride in the 

drinking water (NTP 1994). An increase in mortality, attributable to nephropathy, was observed in mice 

chronically exposed to 160 mg barium/kg/day as barium chloride in drinking water (NTP 1994); the 

number of deaths was similar to controls in mice exposed to 75 mg barium/kg/day. In male mice exposed 

to 0.95 mg barium/kg/day as barium acetate in drinking water, a significant decrease in longevity (defined 

as average lifespan of the last five surviving animals) was observed; however, no significant differences 

in mean lifespan were observed (Schroeder and Mitchener 1975b). Similarly, lifespan was not 
BARIUM AND BARIUM COMPOUNDS 28 

3. HEALTH EFFECTS 

significantly altered in female mice exposed to 0.95 mg barium/kg/day (Schroeder and Mitchener 1975b) 

or male or female rats exposed to 0.7 mg barium/kg/day as barium acetate in drinking water (Schroeder 

and Mitchener 1975a). 

LD50 values and reliable LOAEL values for death in each species and duration category are recorded in 

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

3.2.2.2 Systemic Effects 

The highest NOAEL values and all reliable LOAEL values for systemic effects in each species and 

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

Respiratory Effects. Limited data are available regarding respiratory effects in animals following 

oral barium exposure. Fluid in the trachea was observed in rats receiving a single gavage dose of 198 mg 

barium/kg as barium chloride (Borzelleca et al. 1988). However, this effect was not observed when rats 

were dosed with 198 mg barium/kg/day as barium chloride for 10 days (Borzelleca et al. 1988). No 

significant alterations in lung weights, gross lesions, or histopathological alterations were observed in the 

respiratory tracts of rats and mice exposed to doses as high as 110 or 70 mg barium/kg/day, 180 or 

450 mg barium/kg/day, or 60 and 160 mg barium/kg/day for intermediate or chronic durations, 

respectively (McCauley et al. 1985; NTP 1994; Tardiff et al. 1980) or lifetime exposure to 0.7 or 0.95 mg 

barium/kg/day, respectively, as barium acetate via drinking water (Schroeder and Mitchener 1975a). 

Cardiovascular Effects. As demonstrated in numerous case reports, acute exposure to presumably 

high doses of barium carbonate, barium sulfate, or barium chloride can result in serious effects on heart 

rhythm. Barium adversely affects cardiac automaticity resulting in ventricular tachycardia and other 

disruptions of rhythm (Deng et al. 1991; Diengott et al. 1964; Downs et al. 1995; Gould et al. 1973; Jha et 

al. 1993; Koch et al. 2003; Silva 2003; Talwar and Sharma 1979; Wetherill et al. 1981). Hypotension has 

also been reported in some cases (Koch et al. 2003; Talwar and Sharma 1979). The likely cause of these 

effects was barium-induced hypokalemia. 

Several human studies have investigated a possible association between exposure to low levels of barium 

and alterations in blood pressure and cardiac rhythms. In a small-scale (11 subjects) study of individuals 

exposed to 0.1 or 0.2 mg barium/kg/day as barium chloride in drinking water for 4 weeks, no significant 

alterations in blood pressure or ECG readings were found (Wones et al. 1990). There was no significant 
55

198

59

269

34

132220

58

198198198198198198198198

Table 3-1 Levels of Significant Exposure to Barium - Oral 

Exposure/ 

Duration/ 

a 

Key to 

Figure 

Species 

(Strain) 

Frequency 

(Route) 

ACUTE EXPOSURE Death 

1 Rat 

(SpragueDawley) 

once (GW) 

System 

NOAEL 

(mg/kg/day) 

Less Serious 

(mg/kg/day) 

LOAEL 

Serious 

(mg/kg/day) 

198 (death in 15/20 rats) 

Reference Chemical Form 

Borzelleca et al. 1988 Barium chloride 

2 Rat 

(SpragueDawley) 

once (GW) 269 F (LD50 in females) Borzelleca et al. 1988 Barium chloride 

3 Rat 

(NS) 

once (GW) 132 (LD50 adult) 

220 (LD50 weanling) 

Tardiff et al. 1980 Barium chloride 

Systemic 

4 Rat 

(SpragueDawley) 

10 d 1 x/d (GW) 

Resp 198 Borzelleca et al. 1988 

Barium chloride 

Cardio 198 Gastro 198 Hemato 198 Hepatic Renal 

198 198 

Ocular 198 Bd Wt 198 
7

66 19819866

198

19866

198

66

198

66 19866 198198

119

198

57

198

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference 

Figure (Strain) (Route) System (mg/kg/day) (mg/kg/day) (mg/kg/day) Chemical Form 

5 Rat 

(SpragueDawley) 

once (GW) Resp 66 198 (fluid in trachea) Borzelleca et al. 1988 Barium chloride 

Cardio 198 Gastro 66 198 (inflammation of small 

and large intestine) 

Hemato 198 Hepatic 66 198 (decreased liver/brain 

weight ratio; darkened liver) 

Renal 66 198 (increased kidney/body 

weight ratio) 

Ocular 66 198 (ocular discharge) Bd Wt 66 198 (decreased body weight) 

Immuno/ Lymphoret 

6 Rat 

(SpragueDawley) 

Neurological 

7 Rat 

(SpragueDawley) 

10 d 1 x/d (GW) 10 d 1 x/d (GW) 

Other 198 

198 198 

Borzelleca et al. 1988 Barium chloride Borzelleca et al. 1988 Barium chloride 
53

198

60

138

198

90

200

102

450

39

0.2

15

15015

150

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference 

Figure (Strain) (Route) System (mg/kg/day) (mg/kg/day) (mg/kg/day) Chemical Form 

Reproductive 

8 Rat 

(SpragueDawley) 

once (GW) 

198 Borzelleca et al. 1988 

Barium chloride 

9 Rat 

(SpragueDawley) 

10 d 1 x/d (GW) 

138 F 198 F (decreased ovary weight 

and ovaries/brain ratio) 

Borzelleca et al. 1988 Barium chloride 

INTERMEDIATE EXPOSURE Death 

10 Rat 

(Fischer- 344) 

90 d (W) 200 M (30% mortality) NTP 1994 Barium chloride 

11 Mouse 

(B6C3F1) 

Systemic 

12 Human 

(NS) 

90 d (W) 4 wk 7 d/wk (W) 

Cardio 0.2 M 

450 M (60% mortality) NTP 1994 

Barium chloride Wones et al. 1990 Barium chloride 

13 Rat 

(Dahl) 

16 wk (W) 

Cardio 150 McCauley et al. 1985 

NR 

Renal 15 150 (fused podocytes and 

thickening of the capillary basement membrane in glomeruli) 
61

15015

150

65

37.537.537.537.537.537.537.537.5

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference 

Figure (Strain) (Route) System (mg/kg/day) (mg/kg/day) (mg/kg/day) Chemical Form 

14 Rat 

(SpragueDawley) 

16 wk (W) 

Cardio 150 McCauley et al. 1985 

NR 

Renal 15 150 (fused podocytes and 

thickening of the capillary basement membrane in glomeruli) 

15 Rat 

(SpragueDawley) 

36 wk (W) Resp 37.5 M McCauley et al. 1985 NR 

Cardio 37.5 M Gastro 37.5 M Musc/skel Hepatic Renal 

37.5 M 37.5 M 37.5 M 

Ocular 37.5 M Bd Wt 37.5 M 
72

37.537.537.537.537.537.537.537.5

88

110110110110110110110110

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/

Duration/

a Frequency Key to Species (Route) Figure (Strain) System 

16 Rat 46 wk Resp (Sprague- (W) 

Dawley) 

Cardio Gastro Musc/skel Hepatic Renal Ocular Bd Wt 

17 Rat 15 d Resp (Fischer- 344) (W) 

Cardio Gastro Hemato Hepatic Renal Bd Wt Metab 

LOAEL 

NOAEL 

(mg/kg/day) 

Less Serious 

(mg/kg/day) 

Serious 

(mg/kg/day) 

Reference Chemical Form 

37.5 F McCauley et al. 1985 

NR 

37.5 F 37.5 F 37.5 F 37.5 F 37.5 F 37.5 F 37.5 F 

110 NTP 1994 

Barium chloride 

110 

110 110 

110 110 

110 110 
89

18018018018018018065

180115

180110

200

180

77

1

8.6

78

1.2

11

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/ 

Duration/ 

a Frequency Key to Species (Route) Figure (Strain) 

18 Rat 90 d 

(Fischer- 344) (W) 

19 Rat 1 mo 

(Long- Evans) 7 d/wk 

(W) 

20 Rat 4 mo 

(Long- Evans) 7 d/wk 

(W) 

System 

Resp Cardio Gastro Hemato Musc/skel Hepatic Renal Ocular Bd Wt Metab Cardio Cardio 

NOAEL 

(mg/kg/day) 

180 F 180 F 180 F 180 F 180 F 180 F 

b

65 F 

180 F 110 M 180 F 

1 F 

1.2 F 

LOAEL 

Less Serious Serious 

(mg/kg/day) (mg/kg/day) 

180 F (dilatation of proximal 

renal cortex) 

115 F (increased kidney weight) 200 M (13% lower final body 

weight) 

8.6 F (increased blood 

pressure) 

11 F (increased blood 

pressure) 

Reference Chemical Form 

NTP 1994 Barium chloride Perry et al. 1983, 1985, Barium chloride Perry et al. 1983, 1985, Barium chloride 
87

35353535353535

100

450450450450450450205 450450205

450

450

21 22 

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/ 

Duration/ 

a Frequency Key to Species (Route) Figure (Strain) 

Rat 13 wk Charles-River 7 d/wk

(W) 

Mouse 90 d (B6C3F1) (W) 

System 

Resp Cardio Hemato Musc/skel Hepatic Renal Bd Wt Resp Cardio Gastro Hemato Musc/skel Hepatic Renal Ocular Bd Wt Metab 

LOAEL 

NOAEL Less Serious Serious Reference

(mg/kg/day) (mg/kg/day) (mg/kg/day) Chemical Form 

35 Tardiff et al. 1980 

Barium chloride 

35 35 35 35 35 

35 

450 M 450 M 

NTP 1994 Barium chloride 

450 M 450 M 450 M 450 M 205 M 450 M 

450 M (nephropathy) 

205 M 450 M (30% lower final body 

weight) 

450 M 
97

7070707070707070

120

37.5

75

37.5

123

180

122

205

450

23 

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/ 

Duration/ 

a Frequency Key to Species (Route) Figure (Strain) 

Mouse 15 d (B6C3F1) (W) 

Immuno/ Lymphoret 

24 Rat 36 wk 

(SpragueDawley) (W) 

25 Rat 46 wk 

(Sprague- (W) Dawley) 

26 Rat 90 d 

(Fischer- 344) (W) 

27 Mouse 90 d 

(B6C3F1) (W) 

System 

Resp Cardio Gastro Hemato Hepatic Renal Bd Wt Metab 

LOAEL 

NOAEL Less Serious Serious Reference

(mg/kg/day) (mg/kg/day) (mg/kg/day) Chemical Form 

70 M 

70 M 70 M 70 M 70 M 70 M 70 M 70 M 

NTP 1994 Barium chloride 

37.5 M McCauley et al. 1985 

NR 

37.5 F McCauley et al. 1985 

NR 

180 F NTP 1994 

Barium chloride 

205 M 450 M (thymic and splenic 

atrophy) 

NTP 1994 Barium chloride 
67

37.5

70

37.5

91

115

180

93

110

85

35

101

200

495

98

70

107

200180

31 32 33 

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference 

Figure (Strain) (Route) System (mg/kg/day) (mg/kg/day) (mg/kg/day) Chemical Form 

Neurological 

28 Rat 

(SpragueDawley) 

36 wk (W) 37.5 M McCauley et al. 1985 NR 

29 Rat 

(SpragueDawley) 

46 wk (W) 37.5 F McCauley et al. 1985 NR 

30 Rat 

(Fischer- 344) 

90 d (W) 115 F 180 F (decreased spontaneous motor activity) NTP 1994 Barium chloride 

Rat 15 d 110 NTP 1994 

(Fischer- 344) (W) Barium chloride 

Rat 13 wk 35 Tardiff et al. 1980 Charles-River 7 d/wk 

Barium chloride (W) 

Mouse 90 d 200 F 495 F (decreased forelimb grip NTP 1994 (B6C3F1) (W) strength) Barium chloride 

34 Mouse 

(B6C3F1) 

15 d (W) 70 M NTP 1994 Barium chloride 

Reproductive 

35 Rat 

(Fischer- 344) 

M: 60 d F: 30 d (W) 

200 M 

c

180 F 

Dietz et al. 1992 Barium chloride 
66

37.5

71

37.5

92

200180

94

110

110

205200

103

450495

38 

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference 

Figure (Strain) (Route) System (mg/kg/day) (mg/kg/day) (mg/kg/day) Chemical Form 

36 Rat 36 wk 37.5 M McCauley et al. 1985 (Sprague- (W) NR Dawley) 

37 Rat 46 wk 37.5 F McCauley et al. 1985 (Sprague- (W) NR Dawley) 

Rat 90 d 200 M NTP 1994 (Fischer- 344) (W) c Barium chloride 

180 F 

39 Rat 15 d 110 NTP 1994 

(Fischer- 344) (W) Barium chloride 

40 Mouse M: 60 d 205 M Dietz et al. 1992 F: 30 d (B6C3F1) c Barium chloride (W) 200 F 

41 Mouse 90 d c 450 M NTP 1994 

(B6C3F1) (W) Barium chloride 

495 F 
99

7085

108

115

180

109

200

105

160

73

1515151515151515

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference 

Figure (Strain) (Route) System (mg/kg/day) (mg/kg/day) (mg/kg/day) Chemical Form 

42 Mouse 15 d c 70 M NTP 1994 

(B6C3F1) (W) Barium chloride 

85 F 

Developmental 

43 Rat M: 60 d 115 F 180 F (decreased pup body Dietz et al. 1992 F: 30 d (Fischer- 344) weight and nonsignificant Barium chloride (W) decrease in litter size) 

44 Mouse 

(B6C3F1) 

M: 60 d F: 30 d (W) 

200 F Dietz et al. 1992 

Barium chloride 

CHRONIC EXPOSURE Death 

45 Mouse 

(B6C3F1) 

2 yr (W) 160 M (increased mortality) NTP 1994 Barium chloride 

Systemic 

46 Rat 

(SpragueDawley) 

68 wk (W) Resp 15 M McCauley et al. 1985 NR 

Cardio 15 M Gastro 15 M Musc/skel 15 M Hepatic 15 M Renal 15 M Ocular 15 M Bd Wt 15 M 
95

60606060606060606060

46

0.17

0.87.2

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference 

Figure (Strain) (Route) System (mg/kg/day) (mg/kg/day) (mg/kg/day) Chemical Form 

47 Rat 

(Fischer- 344) 

2 yr (W) Resp 60 M NTP 1994 Barium chloride 

Cardio 60 M Gastro 60 M Hemato 60 M Musc/skel 60 M Hepatic 60 M Renal 60 M Ocular 60 M Bd Wt 60 M Metab 60 M 

48 Rat 

(Long- Evans) 

16 mo 7 d/wk (W) 

Cardio 0.17 F 0.8 F (increased blood 

pressure) 

Perry et al. 1983, 1985, Barium chloride 

7.2 F (depressed rates of 

cardiac contraction and electrical conductivity) 
104

16016016016016016075 16016075 160

63

15

124

60

125

75

160

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/ 

Duration/ 

a Frequency Key to Species (Route) Figure (Strain) 

49 Mouse 2 yr 

(B6C3F1) (W) 

Immuno/ Lymphoret 

50 Rat 68 wk 

(Sprague- (W) Dawley) 

51 Rat 2 yr 

(Fischer- 344) (W) 

52 Mouse 2 yr 

(B6C3F1) (W) 

System 

Resp Cardio Gastro Hemato Musc/skel Hepatic Renal Ocular Bd Wt 

NOAEL 

(mg/kg/day) 

160 M 160 M 160 M 160 M 160 M 160 M 

d

75 M 

160 M 

75 M 

15 M 60 M 75 M 

Less Serious 

(mg/kg/day) 

160 M (lymphoid depletion in 

the spleen and decreased relative and absolute spleen weight) 

LOAEL 

Serious 

(mg/kg/day) 

160 M (marked nephropathy) 160 M (weight loss) 

Reference Chemical Form 

NTP 1994 Barium chloride McCauley et al. 1985 NR NTP 1994 Barium chloride NTP 1994 Barium chloride 
74

15

126

60

127

160

62

15

96

6075

106

160200

Table 3-1 Levels of Significant Exposure to Barium - Oral (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference 

Figure (Strain) (Route) System (mg/kg/day) (mg/kg/day) (mg/kg/day) Chemical Form 

Neurological 

53 Rat 

(SpragueDawley) 

68 wk (W) 

15 M McCauley et al. 1985 

NR 

54 Rat 

(Fischer- 344) 

2 yr (W) 

60 M NTP 1994 

Barium chloride 

55 Mouse 

(B6C3F1) 

Reproductive 

56 Rat 

(SpragueDawley) 

2 yr (W) 68 wk (W) 

160 M 

15 M 

NTP 1994 Barium chloride McCauley et al. 1985 NR 

57 Rat 2 yr c 60 M NTP 1994 

(Fischer- 344) (W) Barium chloride 

75 F 

58 Mouse 2 yr c 160 M NTP 1994 

(B6C3F1) (W) Barium chloride 

200 F 

a The number corresponds to entries in Figure 3-1. b Used to derive an intermediate duration oral minimal risk level (MRL) of 0.2 mg barium/kg/day; dose divided by an uncertainty factor of 100 (10 for extrapolation fhumans and 10 for human variability) and modifying factor of 3 to account for database deficiencies. c Differences in levels of health effects and cancer effects between male and females are not indicated in Figure 3-1. Where such differences exist, only the levels most sensitive gender are presented. d The chronic-duration oral MRL of 0.2 mg barium/kg/day was calculated using benchmark dose analysis. The BMDL5 of 61 mg barium/kg/day was divided by an uof 100 (10 to account for extrapolation from animals to humans and 10 for human variability) and modifying factor of 3 to account for database deficiencies. Cardio = cardiovascular; d = day; F = female; Gastro = gastrointestinal; (GW) = gavage in water; Hemato = hematological; LD50 = lethal dose, 50% kill; M = male; mMusc/skel = musculoskeletal; NS = not specified; NR = not reported; Resp = respiratory; (W) = drinking water; wk = week; x = time(s); yr = year 
Death 

Respiratory Cardiovascular Gastrointestinal Hematological Hepatic Renal Ocular Body Weight Other Immuno/Lymphor Neurological 

1000 

Figure 3-1 Levels of Significant Exposure to Barium - Oral
	

Acute (≤14 days)
	

Systemic 

mg/kg/day 

2r 

3r
	

1r
	 4r 5r 4r 5r 4r 5r 4r 5r 4r 5r 4r 5r 4r 5r 4r 5r 5r 6r 7r 

3r 

100 

5r 5r 5r 5r 5r 5r 

10 

c-Cat 

d-Dog

r-Rat 

p-Pig

q-Cow

 -Humans 

k-Monkey

m-Mouse 

h-Rabbit 

a-Sheep 

f-Ferret 

j-Pigeon

e-Gerbil 

s-Hamster 

g-Guinea Pig 

n-Mink 

o-Other

 Cancer Effect Level-Animals

 LOAEL, More Serious-Animals

LOAEL, Less Serious-Animals

NOAEL - Animals

 Cancer Effect Level-Humans

 LOAEL, More Serious-Humans

LOAEL, Less Serious-Humans

NOAEL - Humans

 LD50/LC50

 for effects

 other than

 Cancer 

Minimal Risk Level 
Reproductive 

Figure 3-1 Levels of Significant Exposure to Barium - Oral (Continued)
 

Acute (≤14 days)
	

mg/kg/day 

1000 

8r 9r 

9r 

100 

10 

c-Cat 

d-Dog

r-Rat 

p-Pig

q-Cow

 -Humans 

k-Monkey

m-Mouse 

h-Rabbit 

a-Sheep 

f-Ferret 

j-Pigeon

e-Gerbil 

s-Hamster 

g-Guinea Pig 

n-Mink 

o-Other

 Cancer Effect Level-Animals

 LOAEL, More Serious-Animals

LOAEL, Less Serious-Animals

NOAEL - Animals

 Cancer Effect Level-Humans

 LOAEL, More Serious-Humans

LOAEL, Less Serious-Humans

NOAEL - Humans

 LD50/LC50

Minimal Risk Level

 for effects

 other than

 Cancer 
Death 

Respiratory Cardiovascular Gastrointestinal Hematological Musculoskeletal Hepatic Renal 

Figure 3-1 Levels of Significant Exposure to Barium - Oral (Continued)
 

Intermediate (15-364 days)
	

Systemic 

mg/kg/day 

1000 

11m 22m 22m 

10r 18r 

13r 14r 

17r 100 

23m 23m 

15r 16r 15r 21r 

10 

1 

12 

0.1 

22m 

15r 

22m 22m 

22m 18r 18r 

13r 

17r 

23m 23m 

16r 15r 16r 21r 21r 

13r 

18r 

14r 

17r 

18r 

15r 16r 

14r 

18r 

17r 

16r 

20r 

19r 

20r 

19r 

c-Cat 

d-Dog

r-Rat 

p-Pig

q-Cow

 -Humans 

k-Monkey

m-Mouse 

h-Rabbit 

a-Sheep 

f-Ferret 

j-Pigeon

e-Gerbil 

s-Hamster 

g-Guinea Pig 

n-Mink 

o-Other

 Cancer Effect Level-Animals

 LOAEL, More Serious-Animals

LOAEL, Less Serious-Animals

NOAEL - Animals

 Cancer Effect Level-Humans

 LOAEL, More Serious-Humans

LOAEL, Less Serious-Humans

NOAEL - Humans

 LD50/LC50

 for effects

 other than

 Cancer 

Minimal Risk Level 

22m 22m 

18r 18r 

17r 17r 

23m 23m 

15r 16r 21r 21r 
Renal 

Ocular Body Weight Metabolic Immuno/Lymphor Neurological Reproductive Developmental 

Figure 3-1 Levels of Significant Exposure to Barium - Oral (Continued)
 

Intermediate (15-364 days)
	

Systemic 

mg/kg/day 

1000 

18r 100 

21r 

10 

1 

0.1 

33m 22m 22m 22m 27m 41m 

22m 18r 27m 33m 40m 44m 18r 18r 26r 30r 35r 38r 43r 

17r 18r 17r 30r 31r 39r 43r

23m 23m 34m 42m 

15r 16r 15r 16r 24r 25r 28r 29r 36r 37r 21r 32r 

c-Cat 

d-Dog

r-Rat 

p-Pig

q-Cow

 -Humans 

k-Monkey

m-Mouse 

h-Rabbit 

a-Sheep 

f-Ferret 

j-Pigeon

e-Gerbil 

s-Hamster 

g-Guinea Pig 

n-Mink 

o-Other

 Cancer Effect Level-Animals

 LOAEL, More Serious-Animals

LOAEL, Less Serious-Animals

NOAEL - Animals

 Cancer Effect Level-Humans

 LOAEL, More Serious-Humans

LOAEL, Less Serious-Humans

NOAEL - Humans

 LD50/LC50

Minimal Risk Level

 for effects

 other than

 Cancer 
Death 

Respiratory Cardiovascular Gastrointestinal Hematological Musculoskeletal Hepatic Renal Ocular Body Weight Metabolic Immuno/Lymphor Neurological Reproductive 

Figure 3-1 Levels of Significant Exposure to Barium - Oral (Continued)

Chronic (≥365 days) 

Systemic 

mg/kg/day 

1000 

45m 49m 49m 49m 49m 49m 49m 49m 49m 49m 52m 55m 58m 

100 

49m 49m 52m 

47r 47r 47r 47r 47r 47r 47r 47r 47r 47r 51r 54r 57r 

46r 46r 46r 46r 46r 46r 46r 46r 50r 53r 56r 

10 

48r 

1 

48r 

48r 

0.1 

c-Cat 

d-Dog

r-Rat 

p-Pig

q-Cow

 -Humans 

k-Monkey

m-Mouse 

h-Rabbit 

a-Sheep 

f-Ferret 

j-Pigeon

e-Gerbil 

s-Hamster 

g-Guinea Pig 

n-Mink 

o-Other

 Cancer Effect Level-Animals

 LOAEL, More Serious-Animals

LOAEL, Less Serious-Animals

NOAEL - Animals

 Cancer Effect Level-Humans

 LOAEL, More Serious-Humans

LOAEL, Less Serious-Humans

NOAEL - Humans

 LD50/LC50

 for effects

 other than

 Cancer 

Minimal Risk Level 
BARIUM AND BARIUM COMPOUNDS 48 

3. HEALTH EFFECTS 

alteration in blood pressure measurements or alterations in hypertension, heart disease, or stroke among 

residents of two communities with elevated (0.2 mg barium/kg/day) or low (0.003 mg barium/kg/day) 

levels of barium in drinking water (Brenniman and Levy 1985; Brenniman et al. 1979a, 1981). 

Interpretation of this study is limited by the lack of information on tap water consumption, and the fact 

that blood pressure was measured 3 times in a single 20-minute period and not repeatedly over a longer 

period, and the incidence of hypertension, stroke, and heart disease was taken from subject-completed 

questionnaires and not confirmed by testing or examination of medical records. Brenniman and 

associates (Brenniman and Levy 1985; Brenniman et al. 1979a, 1981) also conducted a mortality study of 

residents living in communities with elevated or low barium levels in drinking water. Significantly 

higher mortality rates for cardiovascular disease and heart disease (arteriosclerosis) were found in the 

elevated barium communities (0.06–0.3 mg barium/kg/day) than in the low barium communities 

(0.006 mg barium/kg/day). The largest difference between the groups was in individuals 65 years of age 

and older. These results should be interpreted cautiously because the study did not control for a number 

of potential confounding variables such as the use of water softeners, which would reduce the amount of 

barium and increase sodium levels, duration of exposure, or actual barium intakes. 

Several animal studies have examined potential cardiovascular end points following acute-, intermediate-, 

or chronic-duration exposures. No histological alterations have been observed in the hearts of rats and 

mice exposed to barium chloride, barium acetate, or an unspecified barium compound for intermediate or 

chronic durations (Borzelleca et al. 1988; McCauley et al. 1985; NTP 1994; Perry et al. 1983, 1985, 1989; 

Schroeder and Mitchener 1975a; Tardiff et al. 1980). Significant increases in systolic blood pressure 

were observed in rats exposed to 8.6 or 11 mg barium/kg/day for 1 or 4 months, respectively; no effect 

levels were 1.0 and 1.2 mg barium/kg/day (Perry et al. 1983, 1985, 1989). When the duration of exposure 

was longer (8–16 months), the LOAEL for increased blood pressure was 0.80 mg barium/kg/day and the 

NOAEL was 0.17 mg barium/kg/day (Perry et al. 1983, 1985, 1989). Depressed rates of cardiac 

contraction and cardiac conductivity and decreased cardiac ATP levels were observed in another group of 

rats exposed to 7.2 mg barium/kg/day. In contrast to the findings in the Perry study (1983, 1985, 1989), 

no significant alterations in blood pressure were observed in rats exposed to up to 150 mg barium/kg/day 

in drinking water for 16 weeks (McCauley et al. 1985); it should be noted that the McCauley et al. (1985) 

studies were conducted in uninephrectomized rats or Dahl salt-sensitive and salt-resistant rats. NTP 

(1994) also found no significant alterations in blood pressure, heart rate, or ECG readings in rats exposed 

to 180 mg barium/kg/day for 45 or 90 days. The low metal diet used in the Perry et al. (1983, 1985, 

1989) study may have influenced the study outcome. 
BARIUM AND BARIUM COMPOUNDS 49 

3. HEALTH EFFECTS 

Gastrointestinal Effects. All cases of acute oral barium poisoning in adults exhibit gastrointestinal 

disturbances as the initial symptoms. These include gastric pain, vomiting, and diarrhea (Das and Singh 

1970; Diengott et al. 1964; Downs et al. 1995; Gould et al. 1973; Jha et al. 1993; Lewi and Bar-Khayim 

1964; McNally 1925; Morton 1945; Ogen et al. 1967; Phelan et al. 1984; Silva 2003; Talwar and Sharma 

1979; Wetherill et al. 1981). In one case, severe gastrointestinal hemorrhage occurred in an adult male 

victim (Diengott et al. 1964). 

Although gastrointestinal effects have been observed in some animal studies, most studies have not found 

effects. Inflammation of the intestines was noted in rats receiving a single gavage dose of 198 mg 

barium/kg as barium chloride (Borzelleca et al. 1988); but not in rats administered 10 doses of 198 mg 

barium/kg/day (Borzelleca et al. 1988). Stomach rupture, bowel obstruction, and gastrointestinal 

hemorrhage have been observed in rats dosed with barium sulfate; however, those adverse effects were 

most likely due to the massive doses of barium sulfate used in the study (25–40% of body weight) and not 

necessarily to barium toxicity (Boyd and Abel 1966). A 15-day exposure of male and female rats and 

mice to 110 or 70 mg barium/kg/day as barium chloride in drinking water, respectively, did not result in 

histological alterations in the gastrointestinal tract (NTP 1994). No gross or microscopic lesions of the 

esophagus, stomach, pancreas, small intestines, or colon were noted in several intermediate and chronic 

experiments in which male and female rats were exposed to doses as high as 180 mg barium/kg/day as an 

unspecified barium compound or barium chloride in drinking water (McCauley et al. 1985; NTP 1994) or 

male and female mice exposed to doses as high as 450 mg barium/kg/day as barium chloride (NTP 1994). 

Hematological Effects. Results of animal studies indicate that acute, intermediate, and chronic oral 

exposure to barium is not associated with any adverse hematological effects. No alterations were found 

in rats administered 198 mg barium/kg/day as barium chloride for 10 days (Borzelleca et al. 1988) or in 

rats or mice exposed to 110 or 70 mg/kg/day, respectively, as barium chloride in drinking water for 

15 days (NTP 1994). Intermediate and chronic oral exposure of rats to barium acetate and barium 

chloride in drinking water has not been associated with any significant or treatment-related changes in a 

variety of hematological parameters (NTP 1994; Tardiff et al. 1980). Elemental barium doses in these 

intermediate and chronic drinking water studies ranged from 15 to 450 mg/kg/day. 

Musculoskeletal Effects. The predominant musculoskeletal effect observed in cases of barium 

toxicity in humans is progressive muscle weakness, often leading to partial or total paralysis (Das and 

Singh 1970; Diengott et al. 1964; Gould et al. 1973; Lewi and Bar-Khayim 1964; McNally 1925; Morton 

1945; Ogen et al. 1967; Phelan et al. 1984; Wetherill et al. 1981). In severe cases, the paralysis affects 
BARIUM AND BARIUM COMPOUNDS 50 

3. HEALTH EFFECTS 

the respiratory system (Das and Singh 1970; Gould et al. 1973; Lewi and Bar-Khayim 1964; Morton 

1945; Ogen et al. 1967; Phelan et al. 1984; Wetherill et al. 1981). The likely cause of the muscle 

weakness was the barium-induced hypokalemia rather than a direct effect on muscles. 

Very limited animal data are available regarding the musculoskeletal effects of barium following oral 

exposure. No gross and microscopic lesions were observed in skeletal system of several intermediate and 

chronic experiments in which rats were exposed to an unspecified barium compound or barium chloride 

in drinking water at doses as high as 180 mg barium/kg/day for intermediate duration and as high as 

60 mg barium/kg/day for chronic duration (McCauley et al. 1985; NTP 1994; Tardiff et al. 1980); 

similarly, no effects were observed in mice exposed to 450 or 160 mg barium/kg/day as barium chloride 

in drinking water for intermediate or chronic durations, respectively (NTP 1994). 

Hepatic Effects. In one case study involving accidental acute ingestion of barium carbonate in an 

adult female, some degeneration of the liver was noted post-mortem (McNally 1925). Adverse hepatic 

effects in animals following oral barium exposure have been minor or have not been observed. Decreased 

liver/brain weight ratio and darkened liver were observed in rats administered a single gavage dose of 

198 mg barium/kg as barium chloride; however, these changes were not associated with any microscopic 

hepatic lesions or alterations in serum enzymes (e.g., serum glutamic-oxaloacetic transaminase [SGOT], 

serum glutamic pyruvic transaminase [SGPT], alkaline phosphatase). No histological or liver weight 

alterations were observed in rats dosed with 198 mg barium/kg/day as barium chloride for 1 or 10 days 

(Borzelleca et al. 1988) or in rats and mice exposed to 110 or 70 mg barium/kg/day, respectively, as 

barium chloride in drinking water for 15 days (NTP 1994). Intermediate and chronic studies involving 

oral exposure of rats or mice to barium in drinking water did not find significant alterations in liver 

weight or liver histopathology following exposure to doses as high as 180 mg barium/kg/day for rats and 

450 mg barium/kg/day for mice (McCauley et al. 1985; NTP 1994; Schroeder and Mitchener 1975a, 

1975b; Tardiff et al. 1980). 

Renal Effects. Toxic effects on the kidneys have been observed in several adult cases of acute barium 

poisoning. Effects include hemoglobin in the urine (Gould et al. 1973) (which may be indicative of 

kidney damage), renal insufficiency (Lewi and Bar-Khayim 1964; Phelan et al. 1984), degeneration of the 

kidneys (McNally 1925), and acute renal failure (Wetherill et al. 1981). 

Studies in animals suggest that the kidney is a critical target of barium toxicity. An increase in relative 

kidney weight (kidney/brain weight ratio) was observed in male and female rats receiving a single gavage 
BARIUM AND BARIUM COMPOUNDS 51 

3. HEALTH EFFECTS 

dose of 198 mg barium/kg/day as barium chloride in water (Borzelleca et al. 1988). Increases in relative 

kidney weight (kidney to brain weight ratio) were also observed in female rats receiving gavage doses of 

66, 96, or 138 mg barium/kg/day as barium chloride in water for 10 days, but not at 198 mg 

barium/kg/day (Borzelleca et al. 1988). Significant reductions in blood urea nitrogen (BUN) were also 

observed in females exposed to 66–198 mg barium/kg/day and in males exposed to 198 mg 

barium/kg/day. The changes in BUN levels were not considered to be biologically significant because 

BUN levels are typically increased in response to kidney damage, the magnitude of change was slight 

(less than 15%), and there were no differences between the barium-exposed groups. The changes in 

relative kidney weights or BUN levels were not associated with gross or microscopic renal lesions. 

Studies of rats and mice did not find significant alterations in kidney weights or the incidence of renal 

lesions following a 15-day exposure to 110 or 70 mg barium/kg/day, respectively, as barium chloride in 

drinking water (NTP 1994). 

Exposure of rats to doses as high as 65 mg barium/kg/day for an intermediate duration did not result in 

any alterations in kidney weight or the occurrence of histopathological lesions (McCauley et al. 1985; 

NTP 1994; Tardiff et al. 1980). At 115 mg barium/kg/day, significant increases in absolute and relative 

kidney weights were observed in female rats (NTP 1994). Electron microscopy detected glomerular 

lesions consisting of fused podocyte processes and thickening of the capillary basement membrane in rats 

exposed to 150 mg barium/kg/day (McCauley et al. 1985). At slightly higher doses (180 mg 

barium/kg/day), minimal to mild dilatation of the proximal convoluted tubules of the outer medulla and 

renal cortex was observed in male and female rats (NTP 1994). In mice, nephropathy characterized by 

mild to moderate tubule dilatation, regeneration, and atrophy was observed in males and females exposed 

to 450 mg barium/kg/day as barium chloride, but not to 205 mg barium/kg/day (NTP 1994). 

Three chronic-duration studies assessed the renal toxicity of barium. No adverse effects were observed in 

rats exposed via drinking water to 15 mg barium/kg/day of an unspecified barium compound for 68 weeks 

(McCauley et al. 1985), 60 mg barium/kg/day as barium chloride for 2 years (NTP 1994), or lifetime 

exposure to 0.7 mg barium/kg/day as barium acetate (Schroeder and Mitchener 1975a). In mice, exposure 

to 160–200 mg barium/kg/day resulted in moderate to marked nephropathy, characterized by extensive 

regeneration of cortical and medullary tubule epithelium, tubule dilatation, hyaline cast formation, 

interstitial fibrosis, and glomerulosclerosis (NTP 1994); at the next lowest dose tested (75 mg 

barium/kg/day), the incidence of nephropathy did not differ from controls. No kidney lesions were 

observed in mice following lifetime exposure to 0.95 mg barium/kg/day as barium acetate (Schroeder and 

Mitchener 1975b). 
BARIUM AND BARIUM COMPOUNDS 52 

3. HEALTH EFFECTS 

Dermal Effects. No studies were located regarding dermal effects in humans or animals after oral 

exposure to barium. 

Ocular Effects. No studies were located regarding ocular effects in humans after oral exposure to 

barium. In studies with Sprague-Dawley rats, ocular discharge following administration of a single 

gavage dose of 198 mg barium/kg/day as barium chloride (Borzelleca et al. 1988); this was not reported 

in rats dosed for 10 days (Borzelleca et al. 1988). A nonsignificant increase in retinal dystrophy was 

observed in rats following intermediate and chronic oral exposure to 12–37.5 mg barium/kg/day as an 

unspecified barium compound (McCauley et al. 1985). Although the retinal dystrophy was statistically 

insignificant, a dose-related trend was observed if different duration exposure groups were combined 

(McCauley et al. 1985). Both ocular discharge and retinal dystrophy are commonly observed in SpragueDawley rats; consequently, the ocular lesions noted in these animal studies cannot necessarily be 

attributed to oral barium exposure. Ocular lesions were not observed in F344 rats or B6C3F1 mice 

exposed to barium chloride in drinking water for 90 days or 2 years to doses as high as 180 mg 

barium/kg/day in rats and 450 mg barium/kg/day in mice (NTP 1994). 

Body Weight Effects. Body weight has been monitored in a number of acute, intermediate, and 

chronic studies in which rats and mice were exposed orally to barium compounds (Borzelleca et al. 1988; 

McCauley et al. 1985; NTP 1994; Perry et al. 1983, 1985, 1989; Schroeder and Mitchener 1975a, 1975b; 

Tardiff et al. 1980). In general, body weight effects have only been observed at lethal doses. A decrease 

in body weight was observed in rats receiving a single gavage dose of 198 mg barium/kg/day as barium 

chloride (Borzelleca et al. 1988), in rats exposed to 200 mg barium/kg/day as barium chloride in drinking 

water for an intermediate duration (NTP 1994), and in mice exposed to 450 or 160 mg barium/kg/day as 

barium chloride in drinking water for intermediate and chronic durations, respectively (NTP 1994). 

Metabolic Effects. Hypokalemia is a common finding in cases of severe barium poisoning (Deng et 

al. 1991; Diengott et al. 1964; Downs et al. 1995; Gould et al. 1973; Jha et al. 1993; Koch et al. 2003; 

Lewi and Bar-Khayim 1964; Phelan et al. 1984; Talwar and Sharma 1979; Wetherill et al. 1981). In a 

group of cases examined by Deng et al. (1991), serum potassium levels ranged from 0.8 to 2.7 mEq/L; 

normal values range from 3.5 to 5 mEq/L. Alterations in serum potassium levels have not been reported 

in rats exposed to 110 or 180 mg barium/kg/day as barium chloride in drinking water for 15 or 90 days,, 

respectively (NTP 1994). 
BARIUM AND BARIUM COMPOUNDS 53 

3. HEALTH EFFECTS 

3.2.2.3 Immunological and Lymphoreticular Effects 

No studies were located regarding immunological effects in humans after oral exposure to barium. 

Several animal studies have examined potential lymphoreticular effects, particularly damage to the 

thymus, spleen, and lymph nodes. Acute gavage exposure of rats to doses as high as 198 mg 

barium/kg/day as barium chloride for 1 or 10 days was not associated with any changes in thymus weight 

or any gross lesions of the thymus (Borzelleca et al. 1988). Intermediate and chronic oral exposure of rats 

to nominal concentrations of barium in drinking water of 37.5 and 15 mg/kg/day, respectively, of an 

unspecified barium compound was not associated with lesions of the lymph nodes or thymus upon gross 

and histopathologic examination (McCauley et al. 1985). No histopathological alterations were observed 

in the spleen or thymus of rats exposed to 180 or 60 mg barium/kg/day for an intermediate or chronic 

duration, respectively (NTP 1994). In mice, thymic and splenic atrophy were observed at 450 mg 

barium/kg/day after intermediate exposure and lymphoid depletion in the spleen and decreased spleen 

weight were observed at 160 mg barium/kg/day after chronic exposure (NTP 1994). These effects were 

probably secondary to the severe nephropathy and weight loss observed at these doses. 

No studies have assessed the potential of barium to impair immune function. 

The highest NOAEL values for lymphoreticular effects in each species and duration category are recorded 

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

3.2.2.4 Neurological Effects 

Numbness and tingling around the mouth and neck were sometimes among the first symptoms of barium 

toxicity in humans (Lewi and Bar-Khayim 1964; Morton 1945). Occasionally, these neurological 

symptoms extended to the extremities (Das and Singh 1970; Lewi and Bar-Khayim 1964). Partial and 

complete paralysis occurred in severe cases, often accompanied by an absence of deep tendon reflexes 

(Das and Singh 1970; Diengott et al. 1964; Gould et al. 1973; Lewi and Bar-Khayim 1964; Morton 1945; 

Ogen et al. 1967; Phelan et al. 1984; Wetherill et al. 1981). Post-mortem examination in one case of 

poisoning by ingestion of barium sulfide revealed brain congestion and edema (McNally 1925). 

Animal studies have not found significant alterations in brain weight or histopathology following acute 

gavage exposure of rats for 1 or 10 days to doses as high as 198 mg barium/kg/day as barium chloride 

(Borzelleca et al. 1988), intermediate oral exposure of rats to doses as high as 115 mg barium/kg/day in 

drinking water (McCauley et al. 1985; NTP 1994; Tardiff et al. 1980), intermediate-duration exposure of 
BARIUM AND BARIUM COMPOUNDS 54 

3. HEALTH EFFECTS 

mice to doses less than 450 mg barium/kg/day as barium chloride in drinking water (NTP 1994), or 

chronic exposure of rats and mice to doses greater than 60 or 160 mg barium/kg/day as barium chloride in 

drinking water, respectively (NTP 1994). Neurobehavioral performance (spontaneous motor activity, grip 

strength, tail flick latency, startle response, hindlimb foot splay) was evaluated in rats and mice exposed 

to barium chloride for 15 or 90 days (NTP 1994). No alterations were observed in rats or mice following 

a 15-day exposure to 110 or 70 mg barium/kg/day. Slight decreases in motor activity were observed in 

rats exposed to 10–115 mg barium/kg/day for 90 days; these changes were not considered to be 

biologically significant. However, in female rats exposed to 180 mg barium/kg/day, spontaneous motor 

activity was 30% lower than controls; this difference was considered to be biologically significant. In 

mice, the only alteration noted was a decrease in forelimb grip strength in females exposed to 495 mg 

barium/kg/day for 90 days; the investigators noted that this may have been due to debilitation. The 

highest NOAEL values and reliable LOAEL values for neurological effects in each species and duration 

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

3.2.2.5 Reproductive Effects 

No studies were located regarding reproductive effects in humans after oral exposure to barium. 

However, limited data are available from acute, intermediate, and chronic animal studies in which certain 

reproductive organs were weighed and examined grossly and microscopically following oral barium 

exposure. Gavage exposure of rats to doses of 198 mg barium/kg/day as barium chloride for 10 days 

resulted in decreased ovary weight and decreased ovary/brain weight ratio (Borzelleca et al. 1988); no 

alterations were observed after a single gavage dose with 198 mg barium/kg/day (Borzelleca et al. 1988). 

Neither study found changes in testicular weight, and no gross lesions of the ovaries or testes were 

observed at this dose. No histological alterations were observed in the reproductive tissues of male and 

female rats and mice exposed to 110 mg barium/kg/day (rats) or 70/85 mg barium/kg/day (mice) as 

barium chloride in drinking water (NTP 1994). Intermediate and chronic oral exposure of rats to barium 

in drinking water at doses of 200 mg barium/kg/day and lower was not associated with any gross or 

histopathologic lesions of the uterus, ovaries, or testes (Dietz et al. 1992; McCauley et al. 1985; NTP 

1994). Similarly, no histopathological alterations were observed in reproductive tissues of mice exposed 

to 495 mg barium/kg/day and lower for an intermediate duration (NTP 1994) or 160 mg barium/kg/day or 

lower for a chronic duration (NTP 1994). Additionally, no alterations in epididymal sperm counts, sperm 

motility, or sperm morphology were observed in rats or mice exposed to 200 or 205 mg barium/kg/day, 

respectively, as barium chloride in drinking water for 60 days (Dietz et al. 1992). 
BARIUM AND BARIUM COMPOUNDS 55 

3. HEALTH EFFECTS 

There are limited data on the potential of barium to impair reproductive function. No significant 

alterations in pregnancy rate or gestation length were observed in rats or mice exposed to approximately 

200 mg barium/kg/day as barium chloride in drinking water (Dietz et al. 1992); the males were exposed 

for 60 days prior to mating and the females were exposed for 30 days. 

The highest NOAEL values and all reliable LOAEL values for reproductive effects in each species and 

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

3.2.2.6 Developmental Effects 

Studies regarding developmental effects of barium following oral exposure are limited to one human 

study (Morton et al. 1976) and three animal studies (Dietz et al. 1992; Tarasenko et al. 1977). A 

statistically significant negative correlation was found between barium concentrations in drinking water 

and human congenital malformation rates of the central nervous system in South Wales (Morton et al. 

1976). A negative correlation implies that as the barium concentration in drinking water increased, the 

rate of central nervous system malformations decreased. This statistical study is of limited value in 

identifying a NOAEL for developmental effects because exposure conditions (duration and frequency of 

exposure, dose, number of subjects exposed) were not characterized. 

Developmental effects were reported in a study in which an unspecified animal species was orally 

administered a dose of barium carbonate that was equal to 1/16 of the LD50 for 24 days prior to 

conception and pregnancy (Tarasenko et al. 1977). Reported effects in offspring included increased 

mortality during the first 2 months, increased leukocyte count, disturbances in liver function, and 

increased urinary excretion of hippuric acid. This study is inadequate for evaluating developmental 

effects of oral barium exposure because of major study limitations. These limitations include a general 

lack of information provided by the authors regarding experimental methods, exposure conditions, and 

test results, and no information as to the species and number of animals tested, the purity of the test 

material, the statistical methods used, and whether or not controls were used. 

In studies by Dietz et al. (1992), male rats and mice were exposed to barium chloride in drinking water 

for 60 days and mated to females exposed to barium chloride for 30 days. In the rats, exposure to 

180/200 mg barium/kg/day resulted in significant decreases in pup birth weights. Decreases in the live 

litter size at postnatal days 0 and 5 were also observed in the 180/200 mg barium/kg/day group, but the 

difference was not statistically significant; litter sizes were 9.0 and 9.3 pups in controls on days 0 and 5, 
BARIUM AND BARIUM COMPOUNDS 56 

3. HEALTH EFFECTS 

and 7.2 and 7.1 pups on days 0 and 5 in the 200 mg barium/kg/day group. No adverse developmental 

effects were observed in the mice (highest dose tested was 200 mg barium/kg/day). 

The highest NOAEL values and all reliable LOAEL values for developmental effects in each species and 

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

3.2.2.7 Cancer 

No studies were located regarding cancer in humans after oral exposure to barium. Several animal studies 

evaluated the induction of tumors following chronic oral exposure to barium (NTP 1994; Schroeder and 

Mitchener 1975a, 1975b). In studies by Schroeder and Mitchener (1975a, 1975b), rats and mice were 

exposed to 0.7 and 0.95 mg barium/kg/day, respectively, as barium acetate in drinking water for lifetime. 

No differences in the incidence of tumors were noted between treated animals and vehicle controls in 

either study. These studies are inadequate for evaluating the carcinogenic potential of barium because 

insufficient numbers of animals were used for a carcinogenicity study, it was not determined whether or 

not a maximum tolerated dose was achieved, a complete histological examination was not performed, the 

purity of the test material was not specified, and only one exposure dose was used in each study. Studies 

conducted by the NTP (1994) are considered adequate for carcinogenicity assessment. In rats exposed to 

doses as high as 60–75 mg barium/kg/day as barium chloride in drinking water, significant negative 

trends for mononuclear cell leukemia, adrenal medulla pheochromocytoma, and mammary gland 

neoplasms were found. No significant increases in malignant tumors were observed. Similarly, no 

increases in malignant tumor incidences were observed in mice chronically exposed to doses up to 160– 

200 mg barium/kg/day as barium chloride in drinking water. 

3.2.3 Dermal Exposure 

Limited information is available regarding the health effects of barium following dermal exposure. 

Barium salts would be expected to have a local effect on skin surfaces and would not likely be absorbed 

systematically to any great extent. Available studies include a case report of an individual exposed 

dermally to molten barium chloride (Stewart and Hummel 1984), a skin irritation study evaluating barium 

carbonate in experimental animals (Tarasenko et al. 1977), and a skin-painting study in which mice were 

exposed dermally to a barium hydroxide extract of tobacco leaf (Van Duuren et al. 1968). No reliable 

information was available from any of these dermal studies to identify study NOAELs or LOAELs for 

barium. In the case report (Stewart and Hummel 1984), the dermal burns that developed in the individual 
BARIUM AND BARIUM COMPOUNDS 57 

3. HEALTH EFFECTS 

exposed to molten barium chloride may potentially have contributed to some of the reported health 

effects, which are described briefly in Section 3.2.3.2 (Systemic Effects). 

3.2.3.1 Death 

No studies were located regarding death in humans or animals after dermal exposure to barium. 

3.2.3.2 Systemic Effects 

No studies were located regarding respiratory, hematological, musculoskeletal, hepatic, renal, endocrine, 

or body weight effects in humans or animals after dermal exposure to barium. 

Cardiovascular Effects. An abnormal electrocardiogram was observed in a 62-year-old man burned 

by molten barium chloride (Stewart and Hummel 1984). No studies were located regarding 

cardiovascular effects in animals after dermal exposure to barium. 

Gastrointestinal Effects. A 62-year-old man experienced vomiting after he was accidentally burned 

by molten barium chloride (Stewart and Hummel 1984). No studies were located regarding 

gastrointestinal effects in animals after dermal exposure to barium. 

Dermal Effects. Molten barium chloride induced burns on the skin of a 62-year-old man who was 

accidentally exposed through an explosion. The dermal burns, however, were very probably due to the 

molten nature of the material and not necessarily to barium chloride (Stewart and Hummel 1984). 

The dermal effects of barium carbonate were examined in a study with rats and rabbits (Tarasenko et al. 

1977). When barium carbonate in lanolin was applied to the skin, ulcers developed. These dermal 

lesions reportedly disappeared within a month when dermal treatment was discontinued. Although these 

findings suggest that barium carbonate may be a dermal irritant, these particular investigations are 

inadequate for establishing the dermal effects of barium because of a number of significant study 

limitations. The authors provided few details regarding experimental methods and results, and no 

information as to the concentration of barium carbonate used, the number of animals used, and whether or 

not controls were used. 

Ocular Effects. Information on the ocular toxicity of barium is limited to a study conducted by 

Tarasenko et al. (1977) in rats and rabbits. When barium carbonate powder was introduced into the 
BARIUM AND BARIUM COMPOUNDS 58 

3. HEALTH EFFECTS 

conjunctival sac, purulent discharge, conjunctivitis, and slight opacity of the cornea developed. As noted 

in the Dermal Effects section, interpretation of these results is limited by the poor reporting of study 

methods and results, lack of information on barium carbonate concentration, and whether controls were 

used. 

Metabolic Effects. A 62-year-old victim accidentally exposed to molten barium chloride had a 

depressed plasma potassium level when admitted to the hospital (Stewart and Hummel 1984). 

No studies were located regarding the following health effects in humans or animals after dermal 

exposure to barium: 

3.2.3.3 Immunological and Lymphoreticular Effects 

3.2.3.4 Neurological Effects 

3.2.3.5 Reproductive Effects 

3.2.3.6 Developmental Effects 

3.2.3.7 Cancer 

No studies were located regarding cancer in humans after dermal exposure to barium. Dysplasia of the 

cervical epithelium was reportedly induced in a woman who had a barium chloride solution applied to her 

cervix (Ayre 1966). The use of dimethyl sulfoxide in combination with the barium chloride solution 

reportedly enhanced the ability of barium chloride to induce dysplasia. Dysplasia can be regarded as a 

potential precancerous lesion. The significance of the observations reported in this study are difficult to 

assess, since only one subject was exposed and because there have been no reports of similar findings in 

other human or animal studies. Also, the vehicle used was not specified in this study. 

No studies were located regarding cancer in animals after dermal exposure to barium. However, results 

of one skin-painting study with mice suggest that barium hydroxide extract derived from tobacco leaf 

may act as a tumor-promoting agent (Van Duuren et al. 1968); the purity of the barium hydroxide extract 

was not reported. In this study, mice were treated dermally for an unspecified period of time with either 

barium hydroxide extract alone, 7,12-dimethylbenz(a)anthracene (DMBA) alone (an initiating agent), or a 

combination of DMBA and barium hydroxide extract. After 1 year, none of the mice treated with barium 

hydroxide extract developed skin tumors. However, 3 out of 20 mice treated with DMBA alone and 7 out 

of 20 mice treated with a combination of both barium hydroxide extract and DMBA developed skin 
BARIUM AND BARIUM COMPOUNDS 59 

3. HEALTH EFFECTS 

papillomas and carcinomas. These results provide limited, but suggestive evidence that barium hydroxide 

extract of tobacco leaf acted as a tumor-promoting agent. However, it can not be determined whether or 

not this apparent positive tumorigenic response was due to barium hydroxide or some other component of 

the barium hydroxide tobacco leaf extract. 

3.3 GENOTOXICITY 

In vivo studies of barium genotoxicity are limited to a study in Drosophila melanogaster. In this study, 

positive results were found in the somatic mutation and recombination test when high levels of barium 

nitrate were used; the results were inconclusive at low barium nitrate levels (Yesilada 2001). In vitro 

studies were limited and summarized in Table 3-2. No significant alterations in gene mutation frequency 

were observed in Salmonella typhimurium (Monaco et al. 1990, 1991; NTP 1994) or Escherichia coli 

(Rossman et al. 1991). Similarly, barium chloride or barium nitrate did not result in deoxyribonucleic 

acid (DNA) damage in Bacillus subtilis (Kanematsu et al. 1980; Nishioka 1975). Tests of the fidelity of 

DNA synthesis using an avian myeloblastosis virus (AMV) DNA polymerase system showed that neither 

barium acetate nor barium chloride affect the accuracy of DNA replication (Sirover and Loeb 1976a, 

1976b). However, studies with a DNA polymerase I system from Micrococcus luteus, demonstrated that 

concentrations of barium ion ≤0.1 mM stimulated DNA polymerase activity while concentrations greater 

than this inhibited polymerase activity (Korman et al. 1978). The significance of the inhibitory and 

stimulatory effects has not been determined. Results from an experiment designed to test the effect of 

barium chloride on sporulation frequency, recombination frequency, and meiotic failures in 

Saccharomyces cerevisiae demonstrated a definite inhibition of sporulation. Effects on recombination 

frequency and meiotic failures were ambiguous. Barium chloride may have caused a marginal increase in 

recombination frequency and information of diploid clones (Sora et al. 1986), but the data are 

inconclusive. In mammalian test systems, barium chloride did not increase the frequency of sister 

chromatid exchange or chromosome aberrations in Chinese hamster cells (NTP 1994). However, an 

increase in gene mutations was observed at the TK locus of L5178Y mouse lymphoma cells in the 

presence of metabolic activation, but not without metabolic activation (NTP 1994). 
BARIUM AND BARIUM COMPOUNDS 60 

3. HEALTH EFFECTS 

Table 3-2. Genotoxicity of Barium and Barium Compounds In Vitro 

Species (test system) End point Results Reference Compound 

Prokaryotic organisms: 

Salmonella typhimurium	 Gene mutation – Monaco et al. 1990, Barium chloride 

frequency 1991; NTP 1994 

(with or without S9 

activation) 

Escherichia coli Gene mutation – Rossman et al. 1991 Barium chloride 

WP2s(λ) frequency 

Bacillus subtilis DNA damage – Kanematsu et al. 1980; Barium chloride, 

(rec assay) Nishioka 1975 barium nitrate 

Eukaryotic organisms: 

Fungi 

Saccharomyces Meiosis – Sora et al. 1986 Barium chloride 

cerevesiae 

Avian myeloblastosis DNA synthesis – Sirover and Loeb 1976a, Barium chloride, 

virus DNA polymerase 1976b barium acetate 

 Mammalian cells: 

CHO cells Sister chromatid – NTP 1994 Barium chloride 

exchange 

(with or without S9 

activation) 

CHO cells Chromosome – NTP 1994 Barium chloride 

aberration 

(with or without S9 

activation) 

Mouse lymphoma cells Gene mutation at TK NTP 1994 Barium chloride 

locus 

With S9 activation + 

Without S9 activation – 

– = negative result; + = positive result; CHO = Chinese hamster ovary 
BARIUM AND BARIUM COMPOUNDS 61 

3. HEALTH EFFECTS 

3.4 TOXICOKINETICS 

3.4.1 Absorption 

3.4.1.1 Inhalation Exposure 

No studies were located regarding absorption of barium in humans following inhalation exposure. 

Several animal studies have investigated the absorption of barium chloride or barium sulfate following 

inhalation, intratracheal injection, or nasal deposition. The results of these studies suggest that the rate 

and extent of absorption of barium from the respiratory tract depend on the exposure level, how much 

barium reaches the alveolar spaces, the clearance rate from the upper respiratory tract, and the solubility 

of the particular form of barium that was administered. Approximately 50–75% of inhaled barium 

chloride or barium sulfate is absorbed from the respiratory tract (Cuddihy and Griffith 1972; Morrow et 

al. 1968); approximately 65% of the barium chloride deposited in the nose is absorbed (Cuddihy and 

Ozog 1973b). Most of the barium absorption occurs within the first 24 hours (Cuddihy and Griffith 1972; 

Cuddihy et al. 1974). Barium chloride appears to be more rapidly absorbed than barium sulfate (Cuddihy 

et al. 1974), although the differences in particle size (AMADs of 2.3 and 1.0 μm for barium chloride and 

barium sulfate, respectively) may have influenced the absorption rate. In contrast to the rapid absorption 

of barium following inhalation or nasal deposition, most of the barium sulfate that is injected directly into 

the trachea of rats can be taken up into the epithelium membranes and remains in these membranes for at 

least a few weeks (Gore and Patrick 1982; Takahashi and Patrick 1987), suggesting that clearance in the 

upper respiratory tract is more efficient than in the trachea. Following intratracheal injection, the 

clearance of barium sulfate from the lungs was independent of lung burden over the range of 23.3– 

2,330 μg (Cember et al. 1961); this is consistent with the lack of evidence of lung overload following 

intermediate-duration inhalation exposure to 37.5 or 75 mg/m3

 barium sulfate (MMAD 4.3 μm, σg 1.7) 

(Cullen et al. 2000). Species differences in the retention of intratracheally administered radiolabelled 

(

133Ba) barium sulfate have been found. The percentages of 133Ba retained in the trachea 1 week after 

administration were 0.41, 0.145, 0.044, and 0.043% in rats, rabbits, dogs, and monkeys, respectively 

(Takahashi and Patrick 1987; Takahashi et al. 1993). 

3.4.1.2 Oral Exposure 

The absorption of barium from the gastrointestinal tract is compound dependent. Barium sulfate is 

extremely insoluble and very little, if any, ingested barium sulfate is absorbed. Acid-soluble barium 

compounds, such as barium chloride and barium carbonate, are absorbed through the gastrointestinal 
BARIUM AND BARIUM COMPOUNDS 62 

3. HEALTH EFFECTS 

tract, although the amount of barium absorbed is highly variable. Older human studies estimated that 

barium was poorly absorbed; approximately 1–15% of the ingested dose was estimated to be absorbed 

(Harrision et al. 1956; LeRoy et al. 1966; Schroeder et al. 1972; Tipton et al. 1969). A re-examination of 

the methods used in these studies found a number of flaws; Leggett (1992) estimated that barium 

absorption in these studies was approximately 3–60%. Studies in adult rats and dogs estimated fractional 

absorption at 7% (Cuddihy and Griffith 1972; Taylor et al. 1962). Several unpublished animal studies 

discussed by Leggett (1992) found absorption rates of 1–50%. Experiments in rats have shown that 

younger animals (22 days old or less) absorb about 10 times more barium chloride from the 

gastrointestinal tract (63–84%) than do older animals (about 7%) (Taylor et al. 1962). Absorption was 

higher in fasted adult rats (20%) as compared to fed rats (7%). The International Commission for 

Radiation Protection (ICRP) estimates that the gastrointestinal absorption of barium is 20% in adults, 

30% for children aged 1–15 years, and 60% in infants (ICRP 1993). 

3.4.1.3 Dermal Exposure 

No studies were located regarding absorption of barium in humans after dermal exposure. One animal 

study showed that barium applied to the skin of piglets was found in the various layers of the skin 

(Shvydko et al. 1971). Barium is not expected to cross the intact skin because of the high polarity of the 

forms in which it is most commonly encountered. 

3.4.2 Distribution 

3.4.2.1 Inhalation Exposure 

Shortly after dogs were exposed to radiolabelled (140Ba) barium chloride, elevated activity was found in 

the upper respiratory tract, stomach, and small intestine (30% of initial burden), lungs and 

tracheobronchial tissue (6%), and various internal organs (64%) (Cuddihy and Griffith 1972). One day 

post-exposure, 44% of the label was detected in the skeleton, 1% in blood, and 4% in muscle; 26% of the 

dose was excreted. 

3.4.2.2 Oral Exposure 

In humans, barium is predominantly found in bone; approximately 90% of the barium in the body was 

detected in the bone (Schroeder et al. 1972). Approximately 1–2% of the total body burden was found in 

muscle, adipose, skin, and connective tissue. This information is supported by a number of studies 
BARIUM AND BARIUM COMPOUNDS 63 

3. HEALTH EFFECTS 

(Bauer et al. 1957; Losee et al. 1974; Miller et al. 1985; Sowden 1958; Sowden and Stitch 1957; Sowden 

and Pirie 1958). Significant increases in the levels of barium in bone were found in rats administered 

barium chloride in the diet or barium as a component of Brazil nuts for 29 days (Stoewsand et al. 1988); 

this study did not examine other tissues. A study by McCauley and Washington (1983) in which rats 

were exposed to barium chloride and barium carbonate in drinking water found the following non-skeletal 

distribution (skeletal tissue was not examined in the study) 24 hours after ingestion: heart > eye > 

skeletal muscle > kidney > blood > liver. 

3.4.2.3 Dermal Exposure 

No studies were located regarding distribution of barium in humans or animals after dermal exposure. 

3.4.2.4 Other Routes of Exposure 

Human injection studies support the findings of the inhalation and oral exposure studies. Barium is 

rapidly cleared from the blood and distributed to bone (Bauer et al. 1957; Harrison et al. 1966, 1967; 

Newton et al. 1991). A long-term study of barium retention in humans injected with 133Ba found that 

after the first couple of years, bone turnover was the most significant contributor to barium losses from 

the skeleton (Newton et al. 2001). 

3.4.3 Metabolism 

Barium is not metabolized in the body, but it may be transported or incorporated into complexes or 

tissues. 

3.4.4 Elimination and Excretion 

3.4.4.1 Inhalation Exposure 

No studies have been located regarding excretion of barium following inhalation exposure in humans. 

Studies in animals demonstrate that the fecal excretion of barium exceeds urinary excretion (Cember et al. 

1961; Cuddihy and Griffith 1972; Cuddihy et al. 1974). In dogs, 30% of the total barium excretion was 

accounted for by urine (Morrow et al. 1964). 
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3. HEALTH EFFECTS 

3.4.4.2 Oral Exposure 

A study of two humans ingesting a normal diet found that fecal excretion of barium was 2–3 times higher 

than urinary excretion over a 30-day period (Tipton et al. 1966). A 29-day rat study also demonstrated 

that the feces was the primary route of excretion following exposure to barium chloride in the diet or 

barium from brazil nuts (Stoewsand et al. 1988). 

3.4.4.3 Dermal Exposure 

No studies were located regarding excretion of barium in humans or animals after dermal exposure. 

3.4.4.4 Other Routes of Exposure 

Several human studies have examined the excretion of barium following parenteral administration. These 

studies confirm the findings of the inhalation or oral exposure studies that barium is primarily excreted in 

the feces. In a study, one subject receiving an intravenous injection of 133Ba, 84% of the radiolabelled 

barium was excreted within the first 6 days, primarily in the feces (75% of total dose) (Harrison et al. 

1967; Newton et al. 1977). The ratio of fecal to urinary barium excretion in six subjects injected with 

133Ba ranged from 6 to 15 for the first 2 weeks (Newton et al. 1991). 

A study in rats (Edel et al. 1991) found that biliary excretion did not significantly contribute to the total 

amount of barium excreted in the feces, suggesting that other physiological routes were responsible for 

fecal barium. A study of rabbits administered an intravenous injection of radiolabelled barium also found 

that barium was primarily excreted in the feces. After the first day, fecal excretion was approximately 

twice as high as urinary excretion. The barium was primarily excreted in the first 5 days after exposure; 

after 9 days, approximately 50% of the dose was excreted (Liniecki 1971). 

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 
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pharmacodynamic (PBPD) models use mathematical descriptions of the dose-response function to 

quantitatively describe the relationship between target tissue dose and toxic end points. 

PBPK/PD models refine our understanding of complex quantitative dose behaviors by helping to 

delineate and characterize the relationships between: (1) the external/exposure concentration and target 

tissue dose of the toxic moiety, and (2) the target tissue dose and observed responses (Andersen and 

Krishnan 1994; Andersen et al. 1987). These models are biologically and mechanistically based and can 

be used to extrapolate the pharmacokinetic behavior of chemical substances from high to low dose, from 

route to route, between species, and between subpopulations within a species. The biological basis of 

PBPK models results in more meaningful extrapolations than those generated with the more conventional 

use of uncertainty factors. 

The PBPK model for a chemical substance is developed in four interconnected steps: (1) model 

representation, (2) model parameterization, (3) model simulation, and (4) model validation (Krishnan and 

Andersen 1994). In the early 1990s, validated PBPK models were developed for a number of 

toxicologically important chemical substances, both volatile and nonvolatile (Krishnan and Andersen 

1994; Leung 1993). PBPK models for a particular substance require estimates of the chemical substancespecific physicochemical parameters, and species-specific physiological and biological parameters. The 

numerical estimates of these model parameters are incorporated within a set of differential and algebraic 

equations that describe the pharmacokinetic processes. Solving these differential and algebraic equations 

provides the predictions of tissue dose. Computers then provide process simulations based on these 

solutions. 

The structure and mathematical expressions used in PBPK models significantly simplify the true 

complexities of biological systems. If the uptake and disposition of the chemical substance(s) are 

adequately described, however, this simplification is desirable because data are often unavailable for 

many biological processes. A simplified scheme reduces the magnitude of cumulative uncertainty. The 

adequacy of the model is, therefore, of great importance, and model validation is essential to the use of 

PBPK models in risk assessment. 

PBPK models improve the pharmacokinetic extrapolations used in risk assessments that identify the 

maximal (i.e., the safe) levels for human exposure to chemical substances (Andersen and Krishnan 1994). 

PBPK models provide a scientifically sound means to predict the target tissue dose of chemicals in 

humans who are exposed to environmental levels (for example, levels that might occur at hazardous waste 
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3. HEALTH EFFECTS 

sites) based on the results of studies where doses were higher or were administered in different species. 

Figure 3-2 shows a conceptualized representation of a PBPK model. 

If PBPK models for barium exist, the overall results and individual models are discussed in this section in 

terms of their use in risk assessment, tissue dosimetry, and dose, route, and species extrapolations. 

No information on available PBPK models for barium has been identified. 

3.5 MECHANISMS OF ACTION 

3.5.1 Pharmacokinetic Mechanisms 

No studies were located for animals or humans that describe observed mechanisms for barium absorption 

across the skin, lung, or gut or barium distribution, metabolism, or excretion. 

3.5.2 Mechanisms of Toxicity 

The mechanism of barium toxicity has not been fully elucidated. Presumably, high-dose exposure to 

barium consistently results in a number of effects including ventricular tachycardia, hypertension and/or 

hypotension, and muscle weakness and paralysis (Deng et al. 1991; Diengott et al. 1964; Downs et al. 

1995; Gould et al. 1973; Jha et al. 1993; Koch et al. 2003; Talwar and Sharma 1979; Wetherill et al. 

1981). There is strong evidence that many of these effects result from increases in intracellular potassium 

levels. Barium is a competitive potassium channel antagonist that blocks the passive efflux of 

intracellular potassium, resulting in a shift of potassium from extracellular to intracellular compartments 

(Roza and Berman 1971). The intracellular translocation of potassium results in a decreased resting 

membrane potential, making the muscle fibers electrically unexcitable and causing paralysis (Koch et al. 

2003). Hypokalemia (serum potassium levels below 3.5 mEq/L) has been reported in a number of 

individuals exposed to high doses of barium (Deng et al. 1991; Diengott et al. 1964; Downs et al. 1995; 

Gould et al. 1973; Jha et al. 1993; Koch et al. 2003; Lewi and Bar-Khayim 1964; Phelan et al. 1984; 

Talwar and Sharma 1979; Wetherill et al. 1981). Intravenous infusion of potassium often relieves many 

of the symptoms of barium toxicity (Dreisbach and Robertson 1987; Haddad and Winchester 1990; 

Proctor et al. 1988). However, there is also evidence that some of these effects may be due to bariuminduced neuromuscular blockade and membrane depolarization (Phelan et al. 1984; Thomas et al. 1998). 

Two investigators (Phelan et al. 1984; Thomas et al. 1998) have shown an apparent direct relationship 
3. HEALTH EFFECTS 

Figure 3-2. Conceptual Representation of a Physiologically Based 

Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance 

Inhaled chem ic al E x haled chem ic al 

Lungs 

Liver 

F a t 

S lo w ly 

perfu sed 

tissues 

R ic h ly 

perfu sed 

tissues 

K idney 

S k in 

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 m a x 

K m 

Ingestion 

GI 

T ra c t 

F e c e s 

U rin e

 C hem ic als 

contacting skin 

BARIUM AND BARIUM COMPOUNDS 67 

Note: This is a conceptual representation of a physiologically based pharmacokinetic (PBPK) model for a 

hypothetical chemical substance. The chemical substance is shown to be absorbed via the skin, by inhalation, or by 

ingestion, metabolized in the liver, and excreted in the urine or by exhalation. 

Source: adapted from Krishnan and Andersen 1994 
BARIUM AND BARIUM COMPOUNDS 68 

3. HEALTH EFFECTS 

between serum barium levels and the degree of paralysis or muscle weakness in two individuals orally 

exposed to barium. 

3.5.3 Animal-to-Human Extrapolations 

Most of the available data in humans comes from case reports involving acute oral exposure to 

presumably high doses of barium; the primary effects noted were gastrointestinal distress and effects 

associated with hypokalemia (e.g., ventricular tachycardia, hypo or hypertension, paralysis). Only one 

human exposure study (Wones et al. 1990) provided reliable information on exposure level; this study did 

not find any significant alterations in blood pressure in subjects exposed to relatively low doses of 

barium. The available data in laboratory animals suggest that toxicity of ingested barium is similar across 

species. Studies conducted by the NTP (1994) in rats and mice found similar targets of toxicity; although 

some differences in sensitivity were found between the species. Following intermediate-duration 

exposure, renal effects were observed at lower doses in rats (115 mg barium/kg/day) than in mice 

(450 mg barium/kg/day). However, NTP (1994) concluded that rats and mice were equally sensitive to 

the barium-induced renal effects because adverse effect levels when estimated on a per unit surface area 

basis were similar for the two species. In the absence of contrary data, it is assumed that humans and 

animals would have similar targets of toxicity and equal sensitivity. 

3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS 

Recently, attention has focused on the potential hazardous effects of certain chemicals on the endocrine 

system because of the ability of these chemicals to mimic or block endogenous hormones. Chemicals 

with this type of activity are most commonly referred to as endocrine disruptors. However, appropriate 

terminology to describe such effects remains controversial. The terminology endocrine disruptors, 

initially used by Thomas and Colborn (1992), was also used in 1996 when Congress mandated the EPA to 

develop a screening program for “...certain substances [which] may have an effect produced by a 

naturally occurring estrogen, or other such endocrine effect[s]...”. To meet this mandate, EPA convened a 

panel called the Endocrine Disruptors Screening and Testing Advisory Committee (EDSTAC), and in 

1998, the EDSTAC completed its deliberations and made recommendations to EPA concerning endocrine 

disruptors. In 1999, the National Academy of Sciences released a report that referred to these same types 

of chemicals as hormonally active agents. The terminology endocrine modulators has also been used to 

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 
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chemicals do not pose a significant health risk, particularly in view of the fact that hormone mimics exist 

in the natural environment. Examples of natural hormone mimics are the isoflavinoid phytoestrogens 

(Adlercreutz 1995; Livingston 1978; Mayr et al. 1992). These chemicals are derived from plants and are 

similar in structure and action to endogenous estrogen. Although the public health significance and 

descriptive terminology of substances capable of affecting the endocrine system remains controversial, 

scientists agree that these chemicals may affect the synthesis, secretion, transport, binding, action, or 

elimination of natural hormones in the body responsible for maintaining homeostasis, reproduction, 

development, and/or behavior (EPA 1997). Stated differently, such compounds may cause toxicities that 

are mediated through the neuroendocrine axis. As a result, these chemicals may play a role in altering, 

for example, metabolic, sexual, immune, and neurobehavioral function. Such chemicals are also thought 

to be involved in inducing breast, testicular, and prostate cancers, as well as endometriosis (Berger 1994; 

Giwercman et al. 1993; Hoel et al. 1992). 

No studies were located regarding endocrine disruption in human and/or animals after exposure to 

barium; additionally, in vitro studies were not located. 

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 
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3. HEALTH EFFECTS 

may not be evident until a later stage of development. There are often differences in pharmacokinetics 

and metabolism between children and adults. For example, absorption may be different in neonates 

because of the immaturity of their gastrointestinal tract and their larger skin surface area in proportion to 

body weight (Morselli et al. 1980; NRC 1993); the gastrointestinal absorption of lead is greatest in infants 

and young children (Ziegler et al. 1978). Distribution of xenobiotics may be different; for example, 

infants have a larger proportion of their bodies as extracellular water, and their brains and livers are 

proportionately larger (Altman and Dittmer 1974; Fomon 1966; Fomon et al. 1982; Owen and Brozek 

1966; Widdowson and Dickerson 1964). The infant also has an immature blood-brain barrier (Adinolfi 

1985; Johanson 1980) and probably an immature blood-testis barrier (Setchell and Waites 1975). Many 

xenobiotic metabolizing enzymes have distinctive developmental patterns. At various stages of growth 

and development, levels of particular enzymes may be higher or lower than those of adults, and 

sometimes unique enzymes may exist at particular developmental stages (Komori et al. 1990; Leeder and 

Kearns 1997; NRC 1993; Vieira et al. 1996). Whether differences in xenobiotic metabolism make the 

child more or less susceptible also depends on whether the relevant enzymes are involved in activation of 

the parent compound to its toxic form or in detoxification. There may also be differences in excretion, 

particularly in newborns who all have a low glomerular filtration rate and have not developed efficient 

tubular secretion and resorption capacities (Altman and Dittmer 1974; NRC 1993; West et al. 1948). 

Children and adults may differ in their capacity to repair damage from chemical insults. Children also 

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). 

There is limited information on age-related differences in the toxicity of barium in humans or animals. 

Deng et al. (1991) and Lewi and Bar-Khayim (1964) reported cases from two food poisoning incidents 

that involved exposure of adults and children. Both reports noted that children did not seem to be 

affected by the barium carbonate exposure; however, these data should be interpreted cautiously because 

neither involved examination of exposed children and no information is available on barium carbonate 

intake. There are limited data on the developmental toxicity of barium in laboratory animals. The body 

weights of the offspring of rats exposed to barium chloride prior to mating were significantly lower than 
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3. HEALTH EFFECTS 

control pup body weights. A decrease in litter size was also observed, although the difference was not 

statistically significant (Dietz et al. 1992). No developmental effects were observed in the offspring of 

mice exposed to barium chloride prior to mating (Dietz et al. 1992). Reduced survival and decreased 

body weight were observed in the offspring of rats exposed to barium carbonate dust (Tarasenko et al. 

1977); however, poor reporting of the study methods and results limits the interpretation of the Tarasenko 

et al. (1977) study. 

There are some data suggesting possible age-related differences in toxicokinetic properties of barium. A 

higher rate (about 10 times higher) of absorption was found in younger rats compared to older rats 

(Taylor et al. 1962). A study of cadmium and mercury also found higher permeability in the jejunum of 

immature rats as compared to mature animals (Foulkes and Bergman 1993). An unpublished study by 

Della Rosa summarized by ICRP (1993) found higher barium retention in dogs aged 43 (2.3% retained) 

or 150 (2.0%) days, compared to dogs aged 250 days (0.8%) or adult dogs (0.4–0.6%). Information on 

biomarkers, interactions, and methods for reducing toxic effects of barium (discussed in Sections 3.8, 

3.10, and 3.11) comes from studies in adults and mature animals; no child-specific information was 

identified. In the absence of data to the contrary, it is assumed that this information will also be 

applicable to children. 

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, substance-specific metabolites in 

readily obtainable body fluid(s), or excreta. However, several factors can confound the use and 

interpretation of biomarkers of exposure. The body burden of a substance may be the result of exposures 

from more than one source. The substance being measured may be a metabolite of another xenobiotic 

substance (e.g., high urinary levels of phenol can result from exposure to several different aromatic 

compounds). Depending on the properties of the substance (e.g., biologic half-life) and environmental 
BARIUM AND BARIUM COMPOUNDS 72 

3. HEALTH EFFECTS 

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 barium 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 barium 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. 

At present, there are no well-established biomarkers of exposure and effect for barium. Data suggesting 

possible biomarkers are presented below. 

3.8.1 Biomarkers Used to Identify or Quantify Exposure to Barium 

Barium can be measured in bone, blood, urine, and feces. It has been shown to be sequestered in bone 

and teeth and excreted in feces and urine. Background levels of barium in bone are approximately 2 μg/g 

wet weight (ICRP 1974; Schroeder et al. 1972). Background levels of barium in blood, urine, and feces 

will vary with daily intake of barium. However, the following levels have been reported: bone, 2 ppm 

(ICRP 1974; Schroeder et al. 1972); feces, 690–1,215 μg/day (ICRP 1974; Schroeder et al. 1972; Tipton 

et al. 1969); and urine, 17–50 μg/day (ICRP 1974; Schroeder et al. 1972; Tipton et al. 1969). In the 

United States, the geometric mean concentration of barium in the urine is approximately 1.5 μg/L (CDC 

2005). There are no data correlating bone, blood, urine, or feces levels of barium with specific exposure 

levels. For more detailed information on the toxicokinetics of barium, see Section 3.4. 
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3. HEALTH EFFECTS 

3.8.2 Biomarkers Used to Characterize Effects Caused by Barium 

Reports of individuals exposed to high levels of barium suggest that cardiovascular, nervous, and 

gastrointestinal systems are targets of barium toxicity (Das and Singh 1970; Deng et al. 1991; Diengott et 

al. 1964; Downs et al. 1995; Gould et al. 1973; Jha et al. 1993; Koch et al. 2003; Lewi and Bar-Khayim 

1964; McNally 1925; Ogen et al. 1967; Phelan et al. 1984; Talwar and Sharma 1979; Wetherill et al. 

1981). The likely cause of most of these effects is barium induced hypokalemia. Gastrointestinal 

disturbances are usually the first symptoms of acute barium exposure. Hypokalemia, hypertension, and 

abnormalities in heart rhythm frequently occur shortly afterwards. General muscle weakness is a frequent 

symptom, sometimes followed by paralysis. Nerve conduction is often affected, resulting in numbness 

and tingling of the mouth, neck and extremities. Loss of deep tendon reflexes may also occur. Not all 

symptoms appear in every case of acute barium poisoning. Although the observation of hypokalemia and 

gastrointestinal upset may be indicative of exposure to high doses of barium, other toxicants and disease 

states can produce these effects. 

Animal studies also suggest that the kidney is a target of barium toxicity; the observed nephropathy is not 

specific to barium and would not be a sensitive biomarker of effect. 

3.9 INTERACTIONS WITH OTHER CHEMICALS 

There are no data regarding the interaction between barium and various chemicals potentially found at 

hazardous waste sites. However, there are data that suggest that barium may interact with other cations 

and certain prescription drugs. Drug interactions are of relevance because individuals exposed to barium 

by living or working near hazardous waste sites contaminated with this substance may also be taking 

prescription drugs. 

The cations potassium, calcium, and magnesium also interact with barium. Barium exposure, for 

example, may cause a buildup of potassium inside the cell resulting in extracellular hypokalemia, which 

is believed to mediate barium-induced paralysis. In fact, potassium is a powerful antagonist of the 

cardiotoxic and paralyzing effects of barium in animals (Foster et al. 1977; Jaklinski et al. 1967; Roza and 

Berman 1971; Schott and McArdle 1974) and is used as an antidote in cases of acute barium poisoning. 

Calcium and magnesium suppress uptake of barium by pancreatic islets in vitro. Conversely, barium, in 

low concentrations, stimulates calcium uptake in these cells. Although the data are insufficient to 
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3. HEALTH EFFECTS 

determine the significance of these findings to human health effects, displacement of calcium may be the 

mechanism by which barium stimulates insulin release (Berggren et al. 1983). 

Among the drugs that are known to interact with barium, the barbiturates sodium pentobarbital and 

phenobarbital, were found to have an increased depressive effect on the hearts of rats exposed to barium 

(Kopp et al. 1985; Perry et al. 1983, 1989). This hypersensitivity of the cardiovascular system to 

anesthesia was not observed in similarly treated animals that were anesthetized with xylazine plus 

ketamine. Results of the study indicated that the hypersensitivity was specific to the barbiturates and not 

a generalized effect of anesthesia (Kopp et al. 1985). 

Other medically prescribed drugs interact with barium. Experiments with mice indicated that atropine 

significantly antagonized antinociception and death induced by intracerebroventricular injection of 

barium chloride (Segreti et al. 1979; Welch et al. 1983). These same studies also found that naloxone, a 

narcotic antagonist, inhibited the lethal toxicity of barium (Segreti et al. 1979; Welch et al. 1983). 

Propranolol had no effect on barium-induced paralysis in rats (Schott and McArdle 1974). Verapamil 

rapidly abolished cardiac dysrhythmias in rabbits injected with barium chloride (Mattila et al. 1986). In 

the same study, pretreatment with the tricyclic antidepressant, doxepin, was found to offer some 

protection against barium-induced dysrhythmias (Mattila et al. 1986). Ouabain, which is an inhibitor of 

Na+

-K+ ATPase, while not widely prescribed, has been shown to rapidly reverse the paralyzing effects of 

barium. It has been hypothesized that ouabain works by reducing barium-induced hypokalemia by 

allowing some intracellular potassium to escape. However, this hypothesis has not yet been proved or 

disproved because of the complexity of the mechanism involved (Schott and McArdle 1974). 

Other substances can affect barium pharmacokinetics. One study showed that sodium alginate could 

reduce retention of orally administered barium, possibly by inhibiting absorption in the gut (Sutton et al. 

1972). This could be useful in treating cases of acute barium ingestion. Lysine and lactose increase 

absorption of barium and could increase the toxic effects of oral exposure (Lengemann 1959). 

A human study involving one adult female was performed by applying barium chloride, alone and in 

combination, with dimethyl sulfoxide to the cervical epithelium. Dimethyl sulfoxide significantly 

enhanced the ability of barium chloride to induce dysplasia with unusual cell formation in the cervical 

epithelium (Ayre 1966). The significance of this is difficult to determine since there was only one 

subject, there were no controls, and few details of the experiment were provided. 
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3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE 

A susceptible population will exhibit a different or enhanced response to barium than will most persons 

exposed to the same level of barium 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 barium, or compromised function of organs 

affected by barium. Populations who are at greater risk due to their unusually high exposure to barium 

are discussed in Section 6.7, Populations with Potentially High Exposures. 

The limited data available suggest that certain subgroups of the population may be more susceptible to 

barium exposure than the general population. These include people with cardiovascular problems or lung 

disease, those taking certain prescription drugs, children, pregnant women, and smokers. 

Animal studies suggest that the kidney may be a sensitive target of barium toxicity; thus, individuals with 

impaired renal function may have a higher risk of developing barium-induced kidney damage. There is 

suggestive evidence that barium may affect blood pressure. Therefore, humans with hypertension could 

be at increased risk from either chronic, intermediate, or acute barium exposure. Barbiturates have been 

shown to have an enhanced depressant effect on the heart in barium-exposed animals (Kopp et al. 1985; 

Perry et al. 1983, 1989). Individuals on this type of medication may experience an increased risk of heart 

problems on exposure to barium. 

Since exposure to high doses of barium has been repeatedly demonstrated to significantly decrease serum 

potassium in both humans and animals (Foster et al. 1977; Gould et al. 1973; Phelan et al. 1984; Roza and 

Berman 1971), individuals taking diuretics may have a more severe hypokalemic reaction to barium 

toxicity. 

3.11 METHODS FOR REDUCING TOXIC EFFECTS 

This section will describe clinical practice and research concerning methods for reducing toxic effects of 

exposure to barium. 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 barium. When specific 

exposures have occurred, poison control centers and medical toxicologists should be consulted for 
 

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medical advice. The following texts provide specific information about treatment following exposures to 

barium: 

Dreisbach RH, Robertson WO, eds. 1987. Handbook of poisoning: Prevention, diagnosis and treatment. 

12th ed. Norwalk, CT: Appleton & Lange, 119-120. 

Haddad LM, Winchester JF, eds. 1990. Clinical management of poisoning and drug overdose. 2nd ed. 

Philadelphia, PA: WB Saunders Company, 1129. 

3.11.1 Reducing Peak Absorption Following Exposure 

The general population is typically exposed to barium through consumption of food and drinking water; 

workers may also be exposed to barium via inhalation or dermal contact. General recommendations for 

reducing absorption of barium following exposure have included removing the exposed individual from 

the contaminated area and removing contaminated clothing, followed by washing with mild soap and 

water. If the eyes and skin were exposed, they are flushed with water. Lavage or emesis has also been 

suggested; however, high concentrations of barium cause nausea and emesis should not be induced in 

cases where substantial vomiting has already occurred (Haddad and Winchester 1990). Furthermore, 

there is a risk of aspiration of vomitus during emesis. Administration of soluble sulfates orally will also 

limit absorption of barium by causing precipitation of an insoluble form of barium (barium sulfate) 

(Dreisbach and Robertson 1987; Haddad and Winchester 1990). However, intravenous administration of 

sulfate salts should be avoided because barium precipitate in the kidneys will cause renal failure 

(Dreisbach and Robertson 1987; Koch et al. 2003). 

3.11.2 Reducing Body Burden 

Barium is primarily distributed to the bone and teeth; it is not known if the barium distributed to these 

tissues would result in toxicity. A method for reducing the levels of barium in bone and teeth has not 

been identified. Removal of barium from the bloodstream may be facilitated by infusing with saline and 

inducing saline diuresis (Dreisbach and Robertson 1987). As described in several case reports of barium 

poisoning (Bahlmann et al. 2005; Koch et al. 2003; Thomas et al. 1998; Wells and Wood 2001), 

hemodialysis resulted in significant decreases in the levels of barium in the blood and improved clinical 

signs. 
BARIUM AND BARIUM COMPOUNDS 77 

3. HEALTH EFFECTS 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects 

Hypokalemia is commonly seen in cases of acute barium toxicity and may be responsible for some of the 

symptoms of barium poisoning (Proctor et al. 1988). Plasma potassium should be monitored and 

hypokalemia may be relieved by intravenous infusion of potassium (Dreisbach and Robertson 1987; 

Haddad and Winchester 1990; Proctor et al. 1988). 

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 barium and compounds 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 barium and compounds. 

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 Barium and Barium Compounds 

The existing data on health effects of inhalation, oral, and dermal exposure of humans and animals to 

barium and barium compounds are summarized in Figure 3-3. The purpose of this figure is to illustrate 

the existing information concerning the health effects of barium. 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. 
3. HEALTH EFFECTS 

Figure 3-3. Existing Information on Health Effects of Barium and Barium 

Compounds 

D t

I

ea h

Acute 

Intermediate 

C ronic 

i 

h 

t c 

Neurologic 

Reproductive 

Developmental 

Genotoxic 

Systemic 

h 

mmunolog c/Lymp ore i 

Cancer 

Inhalation 

Oral 

Dermal 

Human 

eath

Acute 

Intermediate 

Chronic 

I 

l i 

h 

t c 

Neurologic 

Reproductive 

Developmental 

Genotoxic 

Cancer 

Systemic 

D 

mmuno og c/Lymp ore i 

Inhalation 

Oral 

Dermal 

Animal 

Existing Studies 

BARIUM AND BARIUM COMPOUNDS 78 
BARIUM AND BARIUM COMPOUNDS 79 

3. HEALTH EFFECTS 

There is little information regarding health effects in humans following inhalation, oral, or dermal 

exposure to barium and barium compounds (Figure 3-3). Inhalation studies are limited to several case 

reports of individuals exposed acutely or chronically through occupational exposure (Doig 1976; Essing 

et al. 1976; Seaton et al. 1986; Shankle and Keane 1988). A number of case reports of acute oral 

exposure to high doses of barium have been identified (Das and Singh 1970; Deng et al. 1991; Diengott et 

al. 1964; Downs et al. 1995; Gould et al. 1973; Jha et al. 1993; Koch et al. 2003; Lewi and Bar-Khayim 

1964; McNally 1925; Ogen et al. 1967; Phelan et al. 1984; Talwar and Sharma 1979; Wetherill et al. 

1981). Additionally, there is information from a single intermediate-duration experimental study (Wones 

et al. 1990) and several human epidemiological studies or statistical studies examining mortality and 

morbidity rates in communities having exposure to barium through drinking water supplies (Brenniman 

and Levy 1985; Brenniman et al. 1979a, 1979b, 1981; Elwood et al. 1974; Schroeder and Kraemer 1974). 

Dermal studies are limited to one case report of an exposed individual (Stewart and Hummel 1984). 

The majority of studies conducted on animals have been oral exposure studies (Figure 3-3). Available 

inhalation studies with experimental animals (Hicks et al. 1986; Tarasenko et al. 1977) can only suggest 

information on the health effects of barium because these studies have a number of limitations and 

deficiencies; a third inhalation study (Cullen et al. 2000) is limited to the examination of the respiratory 

tract. The available oral studies have examined a number of end points, although most studies focused on 

various systemic effects for acute (Borzelleca et al. 1988; Boyd and Abel 1966; Tardiff et al. 1980), 

intermediate (Dietz et al. 1992; McCauley et al. 1985; NTP 1994; Perry et al. 1983, 1985, 1989; 

Tarasenko et al. 1977; Tardiff et al. 1980), and chronic exposure (Kopp et al. 1985; McCauley et al. 1985; 

NTP 1994; Perry et al. 1983, 1985, 1989; Schroeder and Mitchener 1975a, 1975b). Dermal studies with 

experimental animals are limited to one skin irritation study (Tarasenko et al. 1977) and one study 

evaluating the tumor-promoting activity of barium (Van Duuren et al. 1968). 

3.12.2 Identification of Data Needs 

Acute-Duration Exposure. There are limited data on the acute toxicity of barium following 

inhalation, oral, or dermal exposure. Data on the toxicity of inhaled barium are limited to a human 

experimental study in which welders were exposed to fumes from barium-containing electrodes 

(Zschiesche et al. 1992), a case of a worker exposed to a large amount barium carbonate dust (Shankle 

and Keane 1988), and a study in which guinea pigs were exposed to a single concentration of barium 

chloride for unspecific amount of time (Hicks et al. 1986). Although none of these studies are suitable for 

derivation of an MRL, the Hicks et al. (1986) study does identify two potential end points (increased 
BARIUM AND BARIUM COMPOUNDS 80 

3. HEALTH EFFECTS 

blood pressure and bronchoconstriction). Additional inhalation studies are needed to fully evaluate the 

toxicity of barium and establish concentration-response relationships. 

Most of the available information on the acute toxicity of barium comes from human case reports 

involving oral exposure to soluble barium compounds and oral toxicity studies in animals. There are a 

number of case reports of individuals accidentally or intentionally ingesting large doses of barium (Das 

and Singh 1970; Deng et al. 1991; Diengott et al. 1964; Downs et al. 1995; Gould et al. 1973; Jha et al. 

1993; Koch et al. 2003; Lewi and Bar-Khayim 1964; McNally 1925; Ogen et al. 1967; Phelan et al. 1984; 

Talwar and Sharma 1979; Wetherill et al. 1981). In general, dose levels were not reported; based on the 

severity of the observed effects, it is likely that the doses were very high. The observed effects included 

effects associated with hypokalemia (cardiac arrest, ventricular tachycardia, muscle weakness, and 

paralysis), gastrointestinal distress (vomiting, gastric pain, and diarrhea), and kidney damage (hemoglobin 

in the urine, renal insufficiency, degeneration, and acute renal failure). Several studies in experimental 

animals have examined the acute oral toxicity of barium chloride (Borzelleca et al. 1988; Tardiff et al. 

1980). These studies have determined LD50 values and evaluated potential systemic, neurological, and 

reproductive end points. These studies have not consistently identified targets of toxicity or adverse 

effect levels. The available data were considered inadequate for derivation of an acute oral MRL. 

Human data consistently identify the gastrointestinal tract as a target of barium toxicity; most case reports 

of individuals ingesting soluble barium compounds report vomiting, diarrhea, and/or abdominal pain as 

one of the early signs of toxicity. However, none of the animal studies have adequately investigated this 

end point; rodents are not a good model for examining gastrointestinal irritation. Animal studies are 

needed to identify the critical targets of barium toxicity and establish dose-response relationships; these 

studies should include a more appropriate animal model for investigating potential gastrointestinal effects. 

Two studies have examined the dermal toxicity of barium. One is a case report on an individual burned 

with molten barium chloride (Stewart and Hummel 1984); extrapolation of the results of this study to 

environmental exposure scenarios is complicated by the thermal burns. Tarasenko et al. (1977) examined 

the dermal and ocular toxicity of barium carbonate in several animal species. Poor reporting of the 

experimental design and results limits the interpretation of the study. Additional dermal toxicity studies 

are needed for several barium compounds to confirm the Tarasenko et al. (1977) study findings that 

barium is a local irritant and to establish the existence of remote toxicity. 

Intermediate-Duration Exposure. No human studies have examined the toxicity of barium in 

humans following intermediate-duration inhalation exposure. Two animal studies have been identified 
BARIUM AND BARIUM COMPOUNDS 81 

3. HEALTH EFFECTS 

(Cullen et al. 2000; Tarasenko et al. 1977). The Tarasenko et al. (1977) study examined systemic, 

reproductive, and developmental end points. However, interpretation of the results is limited by poor 

reporting of the study design and results. The Cullen et al. (2000) study only examined the respiratory 

tract. As these studies were considered inadequate for development of an inhalation MRL, additional 

studies examining a variety of end points are needed to identify the critical targets of barium toxicity and 

to establish concentration-response relationships. 

One human experimental study examined the cardiovascular toxicity of barium (Wones et al. 1990) 

following oral exposure; no adverse effects were found. Several animal studies also examined the oral 

systemic toxicity (McCauley et al. 1985; NTP 1994; Perry et al. 1983, 1985, 1989; Tardiff et al. 1980), 

neurotoxicity (NTP 1994), reproductive toxicity (Dietz et al. 1992), and developmental toxicity (Dietz et 

al. 1992; Tarasenko et al. 1977) of barium. The results of these studies suggest that the kidney is the most 

sensitive target of toxicity following intermediate-duration oral exposure. An intermediate-duration oral 

MRL based on kidney effects in rats exposed to barium chloride for 13 weeks (NTP 1994) has been 

derived. 

Information on the oral toxicity of barium following intermediate-duration exposure comes from a human 

experimental study examining cardiovascular toxicity (Wones et al. 1990) and several animal studies 

examining systemic toxicity (McCauley et al. 1985; NTP 1994; Perry et al. 1983, 1985, 1989; Tardiff et 

al. 1980), neurotoxicity (NTP 1994), reproductive toxicity (Dietz et al. 1992; NTP 1994), and 

developmental toxicity (Dietz et al. 1992). The human study did not find significant alterations in blood 

pressure or ECG readings in adults exposed to fairly low doses (Wones et al. 1990). Effects observed in 

the animal studies include increased blood pressure (Perry et al. 1983, 1985, 1989), kidney damage 

(glomerular alterations consisting of fused podocytes and thickening of the capillary basement membrane 

and mild to moderate nephropathy) (McCauley et al. 1985; NTP 1994), and developmental toxicity 

(decreased pup birth weight) (Dietz et al. 1992). The increase in blood pressure was observed at the 

lowest adverse effect level; however, two other studies (McCauley et al. 1985; NTP 1994) did not find 

significant alterations in blood pressure or ECG readings in rats exposed to higher doses of barium. The 

low-mineral diet used in the Perry et al. (1983, 1985, 1989) studies may have influenced the results. The 

calcium content of the rye-based diet was 3.8 mg/kg, which is lower than the concentration recommended 

for maintenance, growth, and reproduction of laboratory rats (NRC 1995). Additional studies are needed 

to support this hypothesis. The results of the McCauley et al. (1985) and NTP (1994) studies suggest that 

the kidney is the most sensitive target of toxicity in rats and mice following intermediate-duration oral 
BARIUM AND BARIUM COMPOUNDS 82 

3. HEALTH EFFECTS 

exposure; an intermediate-duration oral MRL was derived based on kidney effects observed in rats 

exposed to barium chloride for 13 weeks (NTP 1994). 

No studies have examined the toxicity in humans or animals following intermediate-duration dermal 

exposure. Studies are needed to assess the potential toxicity of various barium compounds and to 

establish whether dermal exposure would result in remote toxicity. 

Chronic-Duration Exposure and Cancer. The toxicity of barium following chronic-duration 

inhalation exposure is limited to three occupational exposure studies (Doig 1976; Essing et al. 1976; 

Seaton et al. 1986). These studies focused on potential respiratory tract effects and are limited by coexposure to other compounds, small number of tested workers, and/or lack of a comparison group. Welldesigned studies examining a number of potential end points are needed to identify the critical targets of 

barium toxicity and establish concentration-response relationships. These studies would be useful for 

deriving a chronic-duration inhalation MRL for barium. 

Three groups of investigators have examined the effect of living in a community with elevated barium 

levels in the drinking water and the risk of mortality and cardiovascular effects (Brenniman and Levy 

1985; Brenniman et al. 1979a, 1979b, 1981; Elwood et al. 1974; Schroeder and Kraemer 1974). These 

studies are limited by a number of factors including the lack of information on barium ingestion levels 

and the possible use of water softeners, which may have removed barium from the drinking water and 

increased the sodium content of the water. Several studies in rats and mice have examined the chronic 

toxicity of barium (NTP 1994; Perry et al. 1989; Schroeder and Mitchener 1975a, 1975b). The Perry et 

al. (1989) study found significant increases in systolic blood pressure in rats fed a relatively low 

concentration of barium in the diet; however, the contribution of the low mineral basal diet to the 

observed effect is not known. Several rat studies did not find adverse effects at the highest doses tested 

(McCauley et al. 1985; NTP 1994; Schroeder and Mitchener 1975a). Marked renal nephropathy was 

observed in mice (NTP 1994); this study and effect were the basis of the chronic-duration MRL for 

barium. The available toxicokinetic data suggest that barium accumulates in bone; it is not known if this 

accumulation would result in adverse effects. Studies designed to test the possible association between 

high levels of barium in bone and adverse bone effects would be useful. 

Data on the dermal toxicity of barium are limited to a skin tumor promotion study using barium 

hydroxide extract from tobacco plants (Van Duuren et al. 1968); the study did not examine noncancerous 
BARIUM AND BARIUM COMPOUNDS 83 

3. HEALTH EFFECTS 

end points. Additional dermal exposure studies are needed to evaluate whether various barium 

compounds are irritants and can cause remote-site toxicity. 

No studies assessing the carcinogenicity of barium following chronic inhalation exposure were identified. 

The carcinogenicity of ingested barium has been assessed in several long-term oral exposure studies in 

rats and mice (McCauley et al. 1985; NTP 1994; Schroeder and Mitchener 1975a, 1975b). These studies 

did not find significant increases in the incidence of neoplastic lesions in either species. Although a study 

by Van Duuren et al. (1968) provided evidence suggesting that barium hydroxide extract derived from 

tobacco leaf may act as a tumor-promoting agent when applied with a tumor initiating agent, there are no 

studies to assess barium’s potential to be a complete carcinogen following dermal exposure. Based on the 

results of the oral study, it can be predicted that inhalation or dermal exposure to barium would not result 

in remote site carcinogenicity; however, it is not known if long-term exposure would result in respiratory 

tract cancer following inhalation exposure or skin cancer following dermal exposure. Inhalation and 

dermal exposure cancer studies are needed to address these questions. 

Genotoxicity. The genotoxicity of barium has not been well characterized. One study used an in vivo 

assay to assess genotoxic potential (Yesilada 2001); increases in somatic mutations were observed in 

D. melanogaster following exposure to high levels of barium nitrate. The available data utilizing in vitro 

assays have not found significant alterations in gene mutation frequency or DNA damage in nonmammalian systems (Kanematsu et al. 1980; Monaco et al. 1990, 1991; Nishioka 1975; NTP 1994; 

Rossman et al. 1991; Sirover and Loeb 1976a, 1976b). In mammalian test systems, barium did not have 

clastogenic effects (NTP 1994), but did increase the frequency of gene mutation (NTP 1994). The 

available data are inadequate to thoroughly assess the genotoxic potential of barium; additionally studies, 

particularly in vivo assays, are needed. 

Reproductive Toxicity. The reproductive effects of barium have not been thoroughly studied. There 

are no studies regarding reproductive effects in humans following barium exposure. Several animal 

studies have examined potential end points of reproductive toxicity. In the only inhalation exposure study 

(Tarasenko et al. 1977), a number of adverse effects were reported, including disturbances in 

spermatogenesis, shortened estrus cycle, and histological damage to the testes and ovaries. However, 

limited reporting of the study design and results and the lack of incidence data and statistical analysis 

limit the interpretation of the study results. Although a 10-day gavage study found significant decreases 

in relative and absolute ovary weights (Borzelleca et al. 1988), other oral exposure studies have not found 

alterations in organ weights or histological alterations in reproductive tissues following acute-, 
BARIUM AND BARIUM COMPOUNDS 84 

3. HEALTH EFFECTS 

intermediate-, or chronic-duration exposure (McCauley et al. 1985; NTP 1994). Additionally, no 

alterations in sperm morphology, motility, or counts were observed in rats or mice exposed to barium in 

drinking water for 60 days (Dietz et al. 1992). Only one oral study evaluated reproductive function (Dietz 

et al. 1992) and found no alterations in pregnancy rate or gestation length in rats or mice. A twogeneration study would be useful for further evaluating the potential reproductive toxicity of barium. No 

dermal exposure studies examining reproductive end points were identified; based on available 

toxicokinetic data. Additional studies are needed to further assess if reproductive toxicity is an end point 

of concern for barium. 

Developmental Toxicity. The developmental effects of barium have not been studied extensively in 

either humans or animals. One limited statistical study evaluated the degree of correlation between 

barium concentrations in drinking water and human congenital malformation rates of the central nervous 

system (Morton et al. 1976). Results of the study indicated there was a negative statistical correlation 

between these parameters, implying that a lower risk of congenital abnormalities was found in 

populations with higher barium levels. Two animal studies evaluated the potential developmental toxicity 

of barium. Reduced survival, underdevelopment, lowered body weight, decreased lability of the 

peripheral nervous system, and various blood disorders were reportedly noted in the offspring of rats 

following inhalation to barium for an intermediate exposure period (Tarasenko et al. 1977). The 

investigators also noted increased mortality and systemic toxicity in the offspring of rats orally exposed to 

barium during conception and pregnancy. As noted previously, interpretation of the results from the 

Tarasenko et al. (1977) studies are limited because the studies were poorly reported and no incidence data 

or statistical analysis were reported. In a mating study involving oral exposure to barium chloride prior to 

mating (Dietz et al. 1992), decreases in pup birth weight and a nonstatistically significant decrease in live 

litter size were observed in rats; no adverse effects were observed in mice. It is not known if the decrease 

in body weight observed in the rat offspring was secondary to maternal toxicity or was a direct effect on 

the fetus. Additional developmental toxicity studies, particularly studies involving oral exposure during 

gestation and lactation, would be useful to confirm the results of the Tarasenko et al. (1977) and Dietz et 

al. (1992) studies. Developmental toxicity studies via dermal exposure are also needed because this end 

point has not been evaluated for this route of exposure. 

Immunotoxicity. The effect of barium on the immune system has not been well studied. No studies 

were available regarding immunological effects in humans or animals following inhalation, oral, or 

dermal exposure to barium. Several oral exposure studies in animals examining lymphoreticular end 

points such as thymus and lymph node histopathology have not reported adverse effects at nonlethal 
 

 

BARIUM AND BARIUM COMPOUNDS 85 

3. HEALTH EFFECTS 

doses (Borzelleca et al. 1988; McCauley et al. 1985; NTP 1994). Screening studies are needed to 

evaluate the potential immunotoxicity of barium following inhalation, oral, or dermal exposure. 

Neurotoxicity. Exposure to high oral doses of barium is associated with numbness and tingling 

around the mouth and neck (Lewi and Bar-Khayim 1964; Morton 1945); higher doses can result in partial 

or complete paralysis (Das and Singh 1970; Diengott et al. 1964; Gould et al. 1973; Lewi and BarKhayim 1964; Morton 1945; Ogen et al. 1967; Phelan et al. 1984; Wetherill et al. 1981). Absence of a 

deep tendon reflex has been reported in an individual exposed to airborne barium carbonate powder 

(Shankle and Keane 1988). Oral exposure of rats and mice to barium has not been associated with 

changes in brain weight or gross or microscopic lesions of the brain (Borzelleca et al. 1988; McCauley et 

al. 1985; NTP 1994; Tardiff et al. 1980). NTP (1994) evaluated neurobehavioral performance in rats and 

mice exposed to barium chloride in drinking water for acute or intermediate durations. Decreases in 

spontaneous motor activity were observed in rats exposed for an intermediate duration. Decreased grip 

strength was also observed in mice; however, this was likely due to debilitation rather than neurotoxicity. 

The human data demonstrate that at presumably high doses, barium affects action potentials of muscles 

and nerve cells by increasing cellular potassium levels. However, oral studies are needed to establish a 

dose-response relationship for these neurological effects. No data were available regarding neurological 

effects in animals following inhalation exposure or humans and/or animals following dermal exposure. 

Additional studies would be useful to further evaluate the neurotoxic potential of barium. 

Epidemiological and Human Dosimetry Studies. A limited number of epidemiological and 

human dosimetry studies evaluating the health effects of barium are available (Brenniman and Levy 1985; 

Brenniman et al. 1979a, 1979b, 1981; Elwood et al. 1974; Schroeder and Kraemer 1974; Wones et al. 

1990). These studies have primarily focused on the potential of barium to adversely affect cardiovascular 

function by altering blood pressure or increasing the risk of death due to cardiovascular disease; 

consistent results have not been found. However, all of the available human studies on barium have 

limitations and/or confounding variables that make it difficult to draw firm conclusions regarding the 

health effects of barium (see Sections 3.2.2.1 and 3.2.2.2 for discussions on the specific limitations 

associated with available epidemiological and human dosimetry studies). Several human studies have 

also examined the potential toxicity of inhaled barium to the respiratory tract or cardiovascular system 

(Doig 1976; Essing et al. 1976; Seaton et al. 1986). As with the oral studies, limitations in the study 

reporting or confounding variables preclude using the studies to establish causal relationships. In addition 

to these epidemiological or experimental studies, there are numerous case reports of individuals ingesting 

large doses of barium (Das and Singh 1970; Deng et al. 1991; Diengott et al. 1964; Downs et al. 1995; 
 

BARIUM AND BARIUM COMPOUNDS 86 

3. HEALTH EFFECTS 

Gould et al. 1973; Koch et al. 2003; Lewi and Bar-Khayim 1964; McNally 1925; Ogen et al. 1967; 

Phelan et al. 1984; Talwar and Sharma 1979; Wetherill et al. 1981) or exposed to airborne barium 

carbonate (Shankle and Keane 1988). In general, these studies reported serious health effects such as 

death, ventricular tachycardia, and paralysis. Animal studies provide evidence that the kidney is a 

sensitive target of toxicity; there is also some evidence that the cardiovascular and neurological systems 

and the developing organisms are targets of barium toxicity (Dietz et al. 1992; McCauley et al. 1985; 

NTP 1994; Perry et al. 1983, 1985, 1989). Additional epidemiological and/or human dosimetry studies 

would be useful to determine the effects of low doses of barium on these end points. Studies of workers 

exposed to airborne barium would also be useful for establishing the toxicity of barium to the respiratory 

tract. 

Biomarkers of Exposure and Effect. 

Exposure. There are no established biomarkers of exposure for barium. Analytical methods exist for 

measuring barium in blood, urine, feces, and biological tissues (Mauras and Allain 1979; Schramel 1988; 

Shiraishi et al. 1987); however, there are no data correlating levels of barium in these tissues and fluids 

with exposure. Studies associating barium levels in biological media (such as blood or urine) with 

exposure concentrations or doses would be useful for establishing biomarkers of exposure. 

Effect. Symptoms of barium toxicity, such as hypokalemia, gastrointestinal upset, hyper- or hypotension, ventricular tachycardia, and numbness and tingling around the mouth and neck (Das and Singh 

1970; Deng et al. 1991; Diengott et al. 1964; Downs et al. 1995; Gould et al. 1973; Koch et al. 2003; 

Lewi and Bar-Khayim 1964; McNally 1925; Ogen et al. 1967; Phelan et al. 1984; Talwar and Sharma 

1979; Wetherill et al. 1981) are well documented. However, there are no quantitative studies correlating 

these effects with dose and these effects are not specific to barium toxicity. For purposes of facilitating 

medical surveillance, studies to determine useful biomarkers of effect for barium, particularly effects 

associated with low doses of barium, would be useful. 

Absorption, Distribution, Metabolism, and Excretion. The database on absorption, distribution, 

metabolism, and excretion of barium is limited. Existing studies indicate that barium is absorbed from 

the respiratory tract (Cuddihy and Griffith 1972; Cuddihy and Ozog 1973b; Morrow et al. 1968) and 

gastrointestinal tract (Cuddihy and Griffith 1972; Harrison et al. 1956; Leggett 1992; LeRoy et al. 1966; 

Schroeder et al. 1972; Taylor et al. 1962;Tipton et al. 1969), primarily deposited in the bones and teeth 

(Bauer et al. 1957; Cuddihy and Griffith 1972; Losee et al. 1974; Miller et al. 1985; Sowden 1958; 
BARIUM AND BARIUM COMPOUNDS 87 

3. HEALTH EFFECTS 

Sowden and Pirie 1958; Sowden and Stitch 1957), and excreted mostly in feces and urine (Cuddihy and 

Griffith 1972; Tipton et al. 1966). Deposition in bones and teeth and excretion in feces and urine appear 

to be independent of the route of exposure. Essentially no data exist on absorption, distribution, or 

excretion following dermal exposure; however, this route is not considered to be a significant source of 

exposure to barium. No significant data exist on the metabolism of barium compounds in the body. 

Additional studies evaluating the binding and/or complexing of barium and barium compounds with 

biological macromolecules or organic molecules in the body would be useful. Studies quantifying the 

extent of absorption following inhalation, oral, and dermal exposure also would be useful because of 

limited absorption data. A wide variety of individual differences in absorption efficiencies have been 

detected in the available human studies; studies examining factors influencing barium absorption would 

be useful. 

Comparative Toxicokinetics. Based on available data, there do not appear to be significant 

differences in the toxicokinetics of barium between species (Chou and Chin 1943; Cuddihy and Griffith 

1972; McCauley and Washington 1983), although there is some indication that a larger percentage of 

absorbed barium is excreted in the feces of humans compared to that of experimental animals. However, 

there are not enough similar studies on different species to determine this with certainty. Studies on 

different species would increase confidence in the reliability of the existing database. 

Methods for Reducing Toxic Effects. Methods have been reported for limiting oral and dermal 

absorption of barium compounds (Bronstein and Currance 1988; Dreisbach and Robertson 1987; Haddad 

and Winchester 1990) and for counteracting the hypokalemia that is produced by barium in acute highlevel exposure situations (Dreisbach and Robertson 1987; Haddad and Winchester 1990; Proctor et al. 

1988). Contradictions exist in the literature regarding the efficacy or desirability of administering emetics 

(Bronstein and Currance 1988; Ellenhorn and Barceloux 1988; Haddad and Winchester 1990). 

Additional studies clarifying this issue would be helpful. Also, studies directed at finding a more efficient 

way to remove barium from the body would be useful. It is unclear whether mechanisms other than 

hypokalemia contribute to the toxic effects produced in acute high-level exposure situations. Additional 

information on the mechanisms responsible for the toxic effects of barium could aid in the development 

of effective treatments. Magnesium has been reported to antagonize the neuromuscular effects 

(Dreisbach and Robertson 1987). Additional studies examining the efficacy of administering soluble 

magnesium salts to antagonize the effects of barium would also be helpful. No information was located 

on treatment strategies for long-term low-level exposures. Research on procedures for mitigating such 

chronic exposure situations would be helpful. 
BARIUM AND BARIUM COMPOUNDS 88 

3. HEALTH EFFECTS 

Children’s Susceptibility. Data needs relating to both prenatal and childhood exposures, and 

developmental effects expressed either prenatally or during childhood, are discussed in detail in the 

Developmental Toxicity subsection above. 

There is very little information on the toxicity of barium in children. Two reports of food poisonings with 

barium carbonate (Deng et al. 1991; Lewi and Bar-Khayim 1964) provide some suggestive information 

that children may not be as sensitive as adults to barium carbonate toxicity; however, the lack of detailed 

examination of the exposed children and lack of exposure information limits the interpretation of these 

data. No human or animal toxicity studies have been designed to assess possible differences in the 

toxicity of barium. There is some information suggesting that infants and young children may have a 

higher barium absorption rate than adults (ICRP 1993; Taylor et al. 1962). Other potential toxicokinetic 

differences have not been thoroughly investigated. Additional studies are needed to evaluate potential 

age-specific differences in toxicity and toxicokinetics. 

Child health data needs relating to exposure are discussed in Section 6.8.1, Identification of Data Needs: 

Exposures of Children. 

3.12.3 Ongoing Studies 

No ongoing studies were reported in the FEDRIP (2006) database. 
BARIUM AND BARIUM COMPOUNDS 89 

4. CHEMICAL AND PHYSICAL INFORMATION 

4.1 CHEMICAL IDENTITY 

Barium is an alkaline earth metal with an atomic number of 56 and is classified in Group IIA of the 

periodic table of elements. Its outer shell of electrons has a 6s2

 configuration. Because barium is highly 

reactive, it exists in the environment in the +2 oxidation state, which is its only oxidation state. 

Barium forms useful alloys with aluminum and magnesium, which are used as getters in electronic tubes 

to remove residual gases (Genter 2001). Barium is also used as a deoxidizer for steel and other metals 

(Boffito 2002). 

Barium reacts with several other elements to form commercially-important compounds. Of these, eight 

barium compounds are covered in this chapter: barium acetate, barium carbonate, barium chloride, 

barium cyanide, barium, hydroxide, barium oxide, barium sulfate, and barium sulfide. Their chemical 

formulas, structures, synonyms, and identification numbers, in addition to those for barium metal, are 

listed in Table 4-1. 

4.2 PHYSICAL AND CHEMICAL PROPERTIES 

Metallic barium is a silvery-white soft metal, but takes on a silver-yellow color when exposed to air 

(Boffito 2002; Genter 2001). Like other alkaline earth metals, barium decomposes in water, evolving 

hydrogen gas. Barium oxidizes readily in moist air. In powdered form, barium reacts violently with air. 

Because of its high reactivity, barium does not exist as the metal in the environment; it exists in a 

combined state with other elements. 

The barium compounds, barium acetate, barium chloride, barium cyanide, barium hydroxide, and barium 

oxide, are quite soluble in water. Barium carbonate and sulfate are poorly soluble in water. Barium oxide 

reacts rapidly with carbon dioxide in water to form barium hydroxide and barium carbonate (Dibello et al. 

2003). Barium sulfide slowly decomposes in water, forming barium hydroxide and barium hydrosulfide. 

Barium sulfide is also known to undergo slow oxidation in solution to form elemental sulfur and various 

oxidized sulfur species including the sulfite, thiosulfate, polythionates, and sulfate. The water solubility 

of barium compounds increases with decreasing pH (IPCS 1991). 
BARIUM AND BARIUM COMPOUNDS 90 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-1. Chemical Identity of Barium and Barium Compoundsa 

Characteristic Barium Barium acetate Barium carbonate 

Synonyms No data Acetic acid, barium salt; Carbonic acid, barium salt; 

barium diacetate barium monocarbonate; 

Pigment White 10; BW-C3; 

BW-P 

Trade names No data No data No data 

Chemical formula Ba Ba(C2H3O2)2 BaCO3 

Chemical structure Ba [Ba2+] [CO3

2-] 

O 2+

Ba 

H3C O 2 

Identification numbers: 

 CAS registry 7440-39-3 543-80-6 513-77-9 

 NIOSH RTECS CQ8370000b

 AF4550000b CQ8600000b

 EPA hazardous D005 No data D005 

waste 

 DOT/UN/NA/IMCO UN1440/IMO 4.3 No data UN 1564/IMO 6.1 

shipping 

HSDB 4481 No data 950 

EINECS 231-149-1 208-849-0 208-167-3 

NCI No data No data No data 
BARIUM AND BARIUM COMPOUNDS 91 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-1. Chemical Identity of Barium and Barium Compoundsa 

Characteristic Barium chloride Barium cyanide Barium hydroxide 

Synonyms Barium dichloride; Barium dicyanide Barium dihydroxide; barium 

NCI-C61074; SBa 0108E hydroxide lime; caustic 

baryta 

Trade names No data No data No data 

Chemical formula BaCl2 Ba(CN)2 Ba(OH)2 

Chemical structure [Ba2+] [Cl–

]2 [Ba2+] [CN–]2 [Ba2+] [OH–]2 

Identification numbers: 

 CAS registry 10361-37-2 542-62-1 17194-00-2 

 NIOSH RTECS CQ8750000b CQ8785000b CQ9200000b 

 EPA hazardous D005 PO13/D003/D005 D005 

waste 

 DOT/UN/NA/IMCO UN 1564/IMO 6.1 UN 1565/IMO 6.1 UN 1564/IMO 6.1 

shipping 

HSDB 2633 403 1605 

EINECS 233-788-1 208-822-3 241-234-5 

NCI No data No data No data 
 

BARIUM AND BARIUM COMPOUNDS 92 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-1. Chemical Identity of Barium and Barium Compoundsa 

Characteristic Barium oxide Barium sulfate Barium sulfide 

Synonyms Barium monoxide; barium Artificial heavy spar; Barium suphide 

protoxide; baryta; calcined artificial barite; baridol; 

baryta barytes; blanc fixe; C.I. 

Pigment White 21; 

Citobaryum; Enamel 

White; E-Z-Paque; 

Solbar; precipitated 

barium sulphate; sulfuric 

acid, barium saltf 

Trade names No data No data No data 

Chemical formula BaO BaSO4 BaS 

Chemical structure [Ba2+] [O2-] [Ba2+] [SO4

2-] [Ba2+] [S2-] 

Identification numbers: 

 CAS registry 1304-28-5 7727-43-7 21109-95-5 

 NIOSH RTECS CQ9800000b

 CR0600000b CR0660000b

 EPA hazardous No data D005 No data 

waste 

 DOT/UN/NA/IMCO UN1884 UN1564/IMO6.1 UN1564/IMDG6.1c 

shipping 

EINECS 215-127-9 231-784-4 244-214-4 

HSDB No data 5041 No data 

NCI No data No data No data 

a

All information obtained from HSDB 2007 and ChemIDplus 2007 except where noted b

RTECS 2007 

c

Kresse et al. 2007 

CAS = Chemical Abstracts Service; DOT/UN/NA/IMCO = Department of Transportation/United Nations/North 

America/Intergovernmental Maritime Dangerous Goods Code; EINECS = European Inventory of Existing 

Commercial chemical Substances; EPA = Environmental Protection Agency; HSDB = Hazardous Substances Data 

Bank; NCI = National Cancer Institute; NIOSH = National Institute for Occupational Safety and Health; 

RTECS = Registry of Toxic Effects of Chemical Substances 
BARIUM AND BARIUM COMPOUNDS 93 

4. CHEMICAL AND PHYSICAL INFORMATION 

Information regarding the physical and chemical properties of barium and barium compounds is located 

in Table 4-2. 
BARIUM AND BARIUM COMPOUNDS 94 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Barium and Barium Compoundsa 

Property Barium Barium acetate Barium carbonate 

Molecular weight 137.327 255.416 (anhydrous) 197.336 

273.431 (monohydrate) 

Physical description Silvery-yellow metal; White powder White orthorhombic crystals 

cubic (anhydrous); white 

crystals (monohydrate) 

Melting point 727 °C Decomposes at 110 °C 1,555 °C 

(monohydrate) 

Boling point 1,897 °C No data No data 

Density 3.62 g/cm3 2.47 g/cm3 4.2865 g/cm3 

(anhydrous); 

2.19 g/cm3 

(monohydrate) 

Specific gravity No data 2.02 (below 24.7 °C)b

 No data 

Odor No data No data Odorlessc 

Odor threshold No data No data No data 

Solubility: 

Water Reacts with water 79.2 g/100 g water at 0.0014 g/100 g water at 

25 °C 20 °C; soluble in dilute HCl, 

HNO3, and acetic acidd

; 

soluble in NH4Cl and NH4NO3 

solutionsd 

Organic solvents Slightly soluble in Slightly soluble in Insoluble in alcohole 

ethanol ethanol (monohydrate) 

Partition coefficients No data No data No data 

Vapor pressure 6.65x10-4 mmHg (at 

630 °C)f

; 0.998 mmHg 

(at 1,050 °C)f 

No data Essentially zerog 

Henry’s law coefficients No data No data No data 

Autoignition temperature No data No data Nonflammablec 

Flashpoint No data No data Nonflammablec 

Flammability limits Explosion hazard if No data Nonflammablec 

exposed to moist aird 

Conversion factors No data No data No data 

Explosive limits No data No data No data 
BARIUM AND BARIUM COMPOUNDS 95 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Barium and Barium Compoundsa 

Property Barium chloride Barium cyanide Barium hydroxide 

Molecular weight 208.232 (anhydrous); 189.361 171.342 (anhydrous); 189.357 

244.263 (dihydrate)e (monohydrate); 315.464 

(octahydrate) 

Physical description White hygroscopic White crystalline White powder (anhydrous, 

orthorhombic crystals powder monohydrate); white 

(anhydrous); white monoclinic crystals 

monoclinic crystals (octahydrate) 

(dihydrate) 

Melting point	 962 °C (anhydrous); No data 408 °C (anhydrous); 

decomposes at decomposes at 78 °C 

approximately 120 °C (octahydrate) 

(dihydrate) 

Boling point 1,560 °C (anhydrous) No data No data 

Density 3.9 g/cm3

 (anhydrous); No data 3.743 g/cm3 (monohydrate); 

3.097 g/cm3 2.18 g/cm3

 (octahydrate) 

(dihydrate) 

Specific gravity No data No data 4.495 (anhydrous)h 

Odor Odorlessg No data No data 

Odor threshold No data No data No data 

Solubility: 

Water 37.0 g/100 g water at 800 g/L (at 14 °C)e 4.91 g/100 g water at 25 °C 

25 °C 

Organic solvents Insoluble in ethanol 180 g/L (in 70% alcohol Soluble in methanold 

(dehydrate) at 14 °C)e 

Partition coefficients No data No data No data 

Vapor pressure Essentially zerog No data 0 mm Hg at 15 °C 

(monohydrate)i

; 11.4 mm Hg 

at 15 °C (water vapor 

pressure of octahydrate)i 

Henry’s law coefficients No data No data No data 

Autoignition temperature No data Nonflammablec No data 

Flashpoint No data Nonflammablec No data 

Flammability limits No data Nonflammablec No data 

Conversion factors No data No data No data 

Explosive limits No data No data Explosive >216 °Cj 
BARIUM AND BARIUM COMPOUNDS 96 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of Barium and Barium Compoundsa 

Property Barium oxide Barium sulfate Barium sulfide 

Molecular weight 

Physical description 

Melting point 

Boling point 

Density 

Specific gravity 

Odor 

Odor threshold 

Solubility: 

Water 

Organic solvents 

Partition coefficients 

Vapor pressure 

Henry’s law coefficients 

Autoignition temperature 

Flashpoint 

Flammability limits 

Conversion factors 

Explosive limits 

153.326 

White-yellow powder; 

cubic and hexagonal 

crystals 

1,972 °C 

No data 

5.72 g/cm3

 (cubic) 

5.32 (hexagonal)b 

Odorlessg 

No data 

1.5 g/100 g water at 

20 °C 

Soluble in ethanol; 

insoluble in acetone 

No data 

Essentially zerog 

No data 

No data 

No data 

Produces heat on 

contact with water or 

steamk 

No data 

Contact with CO2 may 

cause explosionk 

233.391 

White orthorhombic 

crystals 

1,580 °C 

No data 

4.49 g/cm3 

4.50b 

 Odorlessd 

No data 

00.00031 g/100 g water 

at 20 °C 

Insoluble in ethanol 

No data 

No data 

No data 

No data 

No data 

Noncombustiblek 

No data 

Heating with aluminum 

may cause violent 

explosionsk 

169.393 

Colorless cubic crystals or 

gray powder 

2,229 °C 

No data 

4.3 g/cm3 

No data 

 Sulfurous 

No data 

8.94 g/100 g water at 25 °C 

No data 

No data 

No data 

No data 

No data 

No data 

Flammable by spontaneous 

chemical reactionsk 

No data 

Air, moisture, or acid fumes 

may cause it to ignitek 

a

All information obtained from Lide 2005 except where noted

b

Dibello et al. 2003 

c

DOT 2005 

d

Budavari et al. 2001 

e

Weast 1989 

f

Boffito 2002 

g

NIOSH/OSHA 1978

h

Perry and Chilton 1973 

i

Preisman and Davis 1948 

j

HSDB 2007 

k

Lewis 2000 
BARIUM AND BARIUM COMPOUNDS 97 

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

5.1 PRODUCTION 

Barium is a dense alkaline earth metal that occurs naturally in ore deposits and makes up 0.05% of the 

Earth's crust (Genter 2001). Barium and its compounds may be found in nature or produced industrially 

for various uses. The largest natural source of barium is barite ore, which is composed largely of barium 

sulfate and is found in beds or masses in limestone, dolomite, shales, and other sedimentary formations 

(Miner 1969b). The major impurities in crude barite ore are iron(III) oxide, aluminum oxide, silica, and 

strontium sulfate (WHO 2001). Crude barite is turned into crushed barite which not only has its own 

industrial uses but also serves, in turn, as the source for the production of other barium compounds. 

Crushed barite is first converted to barium sulfide by high-temperature, solid-phase reduction with a 

carbonaceous reducing agent. Barium sulfide is the starting point for the chemical manufacture of most 

other barium compounds (Dibello et al. 2003). One such useful compound is lithophone consisting of 

28% zinc sulfide (ZnS) and 72% barium sulfate (BaSO4), which is used as a white pigment in paints. 

Barium sulfate is produced from high-grade (75–98%) ore in association with granite and shale, crushed, 

and then beneficiated by washing, jigging, heavy-media separation, tabling, floatation, or magnetic 

separation (Stokinger 1981; USGS 2004). Barium carbonate (BaCO3) occurs in nature as witherite; 

however, it has little economic significance due to its rareness, impurities, and almost fully depleted 

deposits (Kresse et al. 2007). 

In 2005, the major producer of barite in the United States was from mines in Nevada. Significantly 

smaller amounts were produced from a single mine in Georgia. Total U.S. production for 2004 was 

532,000 metric tons, a figure that represented 7.3% of world production. This production figure is 14% 

higher than for 2003. In 2004, 24 grinding plants within the United States produced 2,440,000 metric 

tons of ground or crushed (processed) barite ore. Fourteen facilities, 6 in Louisiana and 8 in Texas, 

produced American Petroleum Institute (API)-grade barite in 2004. These stand-alone grinding plants 

received barite from China and India for grinding to API specifications for the oil and gas drilling 

markets. Of the total production of ground and crushed barite ore in 2004, 94% (2,300,000 metric tons) 

was used in well drilling operations. Louisiana and Texas were the major U.S. consumers of processed 

barite ore (1,803,000 metric tons); much of this consumption was driven by exploration for natural gas. 

The demand for barite in the United States is expected to increase, while the level of drilling activity in 

North America remains high due to a strong demand in the United States for natural gas. The remaining 

6% (142,000 metric tons) was used as filler and extenders and in the manufacture of glass and barium 

chemicals, such as barium sulfide (USGS 2004, 2006). A list of production and processing facilities for 
BARIUM AND BARIUM COMPOUNDS 98 

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

barium and barium compounds in the United States along with the production or processing volume for 

each are provided in Tables 5-1 and 5-2 (TRI04 2006). A listing of specific manufactures of barite and 

barium compounds is given in Table 5-3. 

5.2 IMPORT/EXPORT 

For the year 2004, U.S. imports of crude barite ore totaled 1,960,000 metric tons, which was a 17% 

increase from levels reported in 2003. Estimates for 2005 predict a 17% increase in imports to 

2,350,000 metric tons. Export volumes were at 70,000 metric tons, a 37% increase from 2003 levels. 

Estimates indicate a 22% increase in exports to 90,000 metric tons in 2005. Import of barium chloride, 

barium nitrate, and barium carbonate amounted to 130, 4,300, and 10,200 metric tons in 2004, 

respectively. Imports of barium oxide, hydroxide, and peroxides were reported to be 3,540 metric tons 

(USGS 2004, 2006). 

5.3 USE 

Barium and its compounds are used in oil and gas drilling muds, automotive paints, stabilizers for 

plastics, case hardening steels, bricks, tiles, lubricating oils, and jet fuel as well as in various types of 

pesticides (Bodek et al. 1988; Venugopal and Luckey 1978; WHO 2001). The largest use of mined 

barite, which accounts for 94% of the total output, is oil and gas well drilling (USGS 2006). The rest of 

barite ore (or crude barium sulfate) is utilized frequently as a colorant in paint, as a flux to reduce melting 

temperature in the manufacture of glass, and as a filler in plastics, rubber, and brake linings as well as in 

the production of other barium compounds (Dibello et al. 2003). Such barium compounds as the 

carbonate, chloride, and hydroxide are important in the brick, ceramic, photographic, and chemical 

manufacturing industries (Bodek et al. 1988). 

Industrial uses of barium and its compounds are wide and varied. Barium metal and its alloys, for 

example, are often used as "getters" to remove gases from vacuum tubes due to their ability to absorb 

gases (Stokinger 1981). One of barium carbonate's major uses is as a rodenticide (Meister 2004; 

Worthing 1987); however, it also plays an important role in the brick, tile, ceramics, oil drilling, and 

chemical manufacturing industries (Dibello et al. 2003; ILO 1983). Barium sulfate, in the chemically 

treated, blanc fixe form, is used in high-quality paints as well as in glass- and papermaking (ILO 1983; 

Kresse et al. 2007). Barium sulfate is also added to concrete to increase the radiation shielding of this 

material. The chloride is used for chlorine and sodium hydroxide manufacture, as a flux for aluminum 

alloys, in pigment and textile dye manufacture, and in the treatment of boiler water (Dibello et al. 2003). 
BARIUM AND BARIUM COMPOUNDS 99 

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

Table 5-1. Facilities that Produce, Process, or Use Barium 

Minimum Maximum 

Number of amount on site amount on site 

Statea facilities in poundsb in poundsb Activities and usesc 

AK 8 0 999,999 1, 5, 12, 13, 14 

AL 23 0 999,999 1, 2, 3, 5, 6, 7, 8, 10, 11, 12, 13, 14 

AR 10 0 49,999,999 1, 3, 5, 7, 8, 11, 12 

AZ 8 0 9,999,999 1, 5, 7, 10, 13 

CA 34 0 9,999,999 1, 2, 3, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

CO 8 100 99,999 2, 6, 7, 8, 12, 14 

CT 3 100 999,999 1, 2, 4, 6, 7, 8, 9, 12 

DE 4 100,000 999,999 2, 3, 9, 13, 14 

FL 2 0 999,999 1, 5, 8 

GA 13 0 49,999,999 1, 2, 3, 4, 6, 7, 8, 14 

IA 12 0 999,999 1, 2, 5, 7, 10, 11, 12 

ID 7 10,000 999,999 1, 3, 5, 12, 13 

IL 22 100 49,999,999 1, 2, 3, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

IN 19 0 9,999,999 1, 2, 3, 5, 6, 7, 8, 9, 10, 11, 12 

KS 13 0 999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 12, 13 

KY 14 0 999,999 1, 2, 3, 4, 5, 6, 7, 8, 9 

LA 6 0 99,999 1, 5, 6, 8, 12 

MA 6 1,000 99,999 1, 3, 7, 8, 11 

MD 7 100 999,999 1, 2, 3, 4, 5, 6, 7, 8, 11, 12 

ME 4 100 99,999 1, 5, 8, 13 

MI 36 0 999,999 1, 3, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

MN 21 100 999,999 1, 3, 4, 5, 7, 8, 9, 10, 11, 12, 13, 14 

MO 11 0 999,999 1, 3, 4, 5, 6, 7, 8, 9, 13, 14 

MS 10 100 999,999 2, 3, 7, 8, 11 

MT 3 10,000 99,999 1, 5, 8, 9, 12 

NC 18 0 999,999 1, 2, 3, 5, 6, 7, 8, 10, 11, 12, 13 

ND 1 100,000 999,999 1, 5, 9, 12 

NE 14 100 9,999,999 1, 2, 3, 4, 5, 7, 8, 9, 11, 12, 13, 14 

NJ 17 0 999,999 2, 3, 6, 7, 8, 10, 11 

NM 6 0 49,999,999 6, 7, 8, 9, 11, 12, 14 

NV 6 100 9,999,999 1, 5, 6, 7, 10, 13 

NY 20 0 999,999 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 13 

OH 54 0 999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

OK 19 0 999,999 1, 2, 3, 5, 7, 8, 11, 12, 13 

OR 9 0 999,999 1, 2, 3, 5, 6, 7, 12, 13 

PA 27 0 999,999 1, 2, 3, 5, 6, 7, 8, 10, 11, 12, 13 

PR 2 10,000 999,999 12 

RI 3 10,000 99,999 2, 3, 4, 6, 7 

SC 21 0 999,999 1, 2, 3, 4, 5, 6, 7, 8, 11, 12 

SD 2 100,000 999,999 1, 5, 12, 14 
BARIUM AND BARIUM COMPOUNDS 100 

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

Table 5-1. Facilities that Produce, Process, or Use Barium 

Minimum Maximum 

Number of amount on site amount on site 

Statea facilities in poundsb in poundsb Activities and usesc 

TN 19 100 999,999 1, 2, 3, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

TX 46 0 9,999,999 1, 2, 3, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

UT 9 1,000 999,999 1, 2, 3, 5, 7, 8, 11, 12 

VA 15 0 999,999 1, 2, 5, 6, 7, 8, 10, 12 

VT 1 1,000 9,999 11 

WA 3 0 999,999 2, 5, 7, 8, 12, 13, 14 

WI 13 0 999,999 1, 3, 5, 6, 7, 8, 10, 11, 12, 14 

WV 10 0 999,999 2, 3, 7, 8, 10, 12 

WY 2 0 999 1, 2, 13 

a

Post office state abbreviations used 

b

Amounts on site reported by facilities in each state 

c

Activities/Uses: 

1. Produce 

2. Import 

3. Onsite use/processing 

4. Sale/Distribution 

5. Byproduct 

6. Impurity 

7. Reactant 

8. Formulation Component 

9. Article Component 

10. Repackaging 

11. Chemical Processing Aid 

12. Manufacturing Aid 

13. Ancillary/Other Uses 

14. Process Impurity 

Source: TRI04 2006 (Data are from 2004) 
BARIUM AND BARIUM COMPOUNDS 101 

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

Table 5-2. Facilities that Produce, Process, or Use Barium Compounds 

Minimum Maximum 

Number of amount on site amount on site 

Statea facilities in poundsb in poundsb Activities and usesc 

AK 4 0 9,999,999 1, 5, 12, 14 

AL 58 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

AR 47 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

AZ 41 100 99,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

CA 89 0 99,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

CO 41 0 9,999,999 1, 3, 4, 5, 6, 7, 8, 9, 12, 13, 14 

CT 25 100 999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 12, 13 

DE 17 0 999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 11, 12, 13 

FL 51 0 999,999 1, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

GA 79 0 49,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

HI 2 1,000 99,999 1, 5, 10 

IA 42 100 999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

ID 14 0 9,999,999 1, 2, 3, 5, 7, 8, 10, 11, 12, 13, 14 

IL 136 0 999,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

IN 109 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

KS 48 0 499,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 11, 12, 13, 14 

KY 80 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

LA 56 0 499,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 12, 13, 14 

MA 42 0 49,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13 

MD 52 100 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13 

ME 25 0 99,999 1, 2, 3, 5, 7, 8, 10, 11, 12, 13 

MI 125 0 499,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

MN 46 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

MO 68 0 499,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 12, 13, 14 

MS 39 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

MT 14 100 9,999,999 1, 3, 4, 5, 6, 7, 9, 12, 13, 14 

NC 77 0 49,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

ND 18 0 9,999,999 1, 5, 8, 9, 12, 13, 14 

NE 32 0 9,999,999 1, 3, 4, 5, 6, 7, 8, 9, 11, 12, 13 

NH 10 0 99,999 1, 2, 3, 4, 5, 7, 8, 9, 10, 12 

NJ 103 0 49,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

NM 21 0 9,999,999 1, 3, 4, 5, 6, 7, 8, 9, 11, 12, 13, 14 

NV 19 0 499,999,999 1, 2, 3, 4, 5, 7, 8, 9, 12, 13 

NY 121 0 499,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

OH 169 0 499,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

OK 43 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

OR 27 0 999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 12, 13 

PA 153 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 
BARIUM AND BARIUM COMPOUNDS 102 

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

Table 5-2. Facilities that Produce, Process, or Use Barium Compounds 

Minimum Maximum 

Number of amount on site amount on site 

Statea facilities in poundsb in poundsb Activities and usesc 

PR 3 10,000 999,999 1, 2, 4, 5, 6 

RI 12 100 99,999 2, 3, 4, 6, 7, 8, 11 

SC 50 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

SD 7 1,000 999,999 1, 5, 7, 8, 9, 12, 13 

TN 71 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

TX 114 0 499,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

UT 41 0 99,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

VA 44 0 999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 11, 12, 13, 14 

VT 6 1,000 99,999 1, 5, 7, 8, 11 

WA 26 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13 

WI 54 0 9,999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

WV 34 0 999,999 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14 

WY 23 0 9,999,999 1, 3, 4, 5, 9, 12, 13, 14 

a

Post office state abbreviations used 

b

Amounts on site reported by facilities in each state 

c

Activities/Uses: 

1. Produce 6. Impurity 11. Chemical Processing Aid 

2. Import 7. Reactant 12. Manufacturing Aid 

3. Onsite use/processing 8. Formulation Component 13. Ancillary/Other Uses 

4. Sale/Distribution 9. Article Component 14. Process Impurity 

5. Byproduct 10. Repackaging 

Source: TRI04 2006 (Data are from 2004) 
BARIUM AND BARIUM COMPOUNDS 103 

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

Table 5-3. Current U.S. Manufacturers of Barium Metal and Selected Barium 

Compoundsa 

Company Location 

Barite (barium sulfate, natural): 

CIMBAR Performance Minerals	 Cadet, Missouri 

Cartersville, Georgia 

Chatsworth, Georgia 

Elementis Pigments, Inc. East St. Louis, Illinois 

Huber Engineered Materials Division Quincy, Illinois 

M-I, SWACO Amelia, Louisiana 

Battle Mountain, Nevada 

Galveston, Texas 

Westlake, Louisiana 

New Riverdale Ochre Company, Inc. Cartersville, Georgia 

Unimin Corporation Plant location not specified 

Barium sulfate (synthetic): 

Barium and Chemicals, Inc. Steubenville, Ohio 

CIMBAR Performance Minerals Cartersville, Georgia 

GFS Chemicals, Inc. Columbus, Ohio 

Johnson Matthey, Inc. Alfa Aesar Ward Hill, Massachusetts 

Mineral and Pigment Solutions, Inc. South Plainfield, New Jersey 

Barium acetate: 

Barium and Chemicals, Inc. Steubenville, Ohio 

Barium carbonate: 

Barium and Chemicals, Inc. Steubenville, Ohio 

CERAC, Inc. Milwaukee, Wisconsin 

Chemical Products Corporation Cartersville, Georgia 

Johnson Matthey, Inc. Alfa Aesar Ward Hill, Massachusetts 

Mallinckrodt Inc. Pharmaceuticals Group St. Louis, Missouri 

Osram Sylvania Inc. Towanda, Pennsylvania 

Barium chloride: 

Barium and Chemicals, Inc. Steubenville, Ohio 

Chemical Products Corporation Cartersville, Georgia 

GFS Chemical, Inc. Columbus, Ohio 

Johnson Matthey, Inc. Alfa Aesar Ward Hill, Massachusetts 

Mallinckrodt Inc. Pharmaceuticals Group St. Louis, Missouri 

Osram Sylvania Inc. Towanda, Pennsylvania 

Barium hydroxide: 

Barium and Chemicals, Inc.b,c,d Steubenville, Ohio 

Johnson Matthey, Inc. Alfa Aesarb,c Ward Hill, Massachusetts 

Mallinckrodt, Inc. Pharmaceuticals Groupe St. Louis, Missouri 

Barium oxide: 

Barium and Chemicals, Inc. Steubenville, Ohio 
BARIUM AND BARIUM COMPOUNDS 104 

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

Table 5-3. Current U.S. Manufacturers of Barium Metal and Selected Barium 

Compoundsa 

Company Location 

Barium sulfide: 

Barium and Chemicals, Inc. Steubenville, Ohio 

Chemical Products Corporation Cartersville, Georgia 

Johnson Matthey, Inc. Alfa Aesar Ward Hill, Massachusetts 

a

Derived from SRI 2006 unless otherwise noted. SRI reports production of chemicals produced in commercial 

quantities (defined as exceeding 5,000 pounds or $10,000 in value annually) by the companies listed. b

Barium hydroxide, anhydrous [Ba(OH)2] c

Barium hydroxide octahydrate [Ba(OH)2 • 8H2O] d

Barium hydroxide monohydrate [Ba(OH)2• H2O] e

Barium hydroxide, hydration not specified 
BARIUM AND BARIUM COMPOUNDS 105 

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

Barium oxide is used to dry gases and solvents, strengthen ceramics, and as a component in some 

specialty cements. Barium hydroxide plays a role in glass manufacturing, synthetic rubber vulcanization, 

in the production of barium greases and plasticizers, as a component in sealants, pigment dispersion, 

paper manufacturing, sugar refining, in animal and vegetable oil refining, and in the protection of objects 

made of limestone from deterioration. Barium acetate is used in printing fabrics, in lubricating grease, 

and as a catalyst for organic reactions. Finally, the main function of barium sulfide is to act as a starting 

point for the production of a number of other barium compounds (Dibello et al. 2003; ILO 1983). This 

compound is also used in the production of thin-film electroluminescent phosphors and the vulcanization 

of carbon black-filled neoprene rubbers. 

Barium and its compounds have several important medical uses as well. Barium chloride was formerly 

used in treating complete heart block, because periods of marked bradycardia and asystole were prevented 

through its use. This use was abandoned, however, mainly due to barium chloride's toxicity (Hayes 

1982). Characterized by extreme insolubility, chemically pure barium sulfate is non toxic to humans. It 

is frequently utilized as a benign, radiopaque aid to x-ray diagnosis in colorectal and some upper 

gastrointestinal examinations, because it is normally not absorbed by the body after oral intake (de Zwart 

et al. 2001; Doull et al. 1980; ILO 1983; Lin 1996; Newman 1998; Pijl et al. 2002; Rae 1977). 

5.4 DISPOSAL 

In case of a spill, it is suggested that persons not wearing protective equipment be restricted from the area. 

Furthermore, ventilation should be provided in the room and the spilled material collected in as safe a 

manner as possible. Persons in charge of vessels or facilities are required to notify the National Response 

Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount 

equal to or greater than its reportable quantity of 1,000 pounds or 454 kg (HSDB 2007). Barium 

compounds (particularly soluble ones) should be placed in sealed containers and reclaimed or disposed of 

in a secured sanitary landfill (IPCS 1991; NIOSH/OSHA 1978). It is also suggested that all federal, state, 

and local regulations concerning barium disposal should be followed (HSDB 2007). No other guidelines 

or regulations concerning disposal of barium and its compounds were found. 
BARIUM AND BARIUM COMPOUNDS 106 

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

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BARIUM AND BARIUM COMPOUNDS 107 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.1 OVERVIEW 

Barium has been identified in at least 798 of the 1,684 hazardous waste sites that have been proposed for 

inclusion on the EPA National Priorities List (NPL) (HazDat 2006). However, the number of sites 

evaluated for barium is not known. The frequency of these sites can be seen in Figure 6-1. Of these sites, 

794 are located within the United States, 1 is in the Territory of Guam, and 3 are located in the 

Commonwealth of Puerto Rico (the Territory of Guam and the Commonwealth of Puerto Rico are not 

shown). 

Barium is a naturally occurring component of minerals that are found in small but widely distributed 

amounts in the earth's crust, especially in igneous rocks, sandstone, shale, and coal (Kunesh 1978; Miner 

1969a). Barium enters the environment naturally through the weathering of rocks and minerals. 

Anthropogenic releases are primarily associated with industrial processes. Barium is present in the 

atmosphere, urban and rural surface water, soils, and many foods. 

Under natural conditions, barium is stable in the +2 valence state and is found primarily in the form of 

inorganic complexes. Conditions such as pH, Eh (oxidation-reduction potential), cation exchange 

capacity, and the presence of sulfate, carbonate, and metal oxides (e.g., oxides of aluminum, manganese, 

silicon, and titanium) will affect the partitioning of barium and its compounds in the environment. The 

major features of the biogeochemical cycle of barium include wet and dry deposition to land and surface 

water, leaching from geological formations to groundwater, adsorption to soil and sediment particulates, 

and biomagnification in terrestrial and aquatic food chains. 

The general population is exposed to barium through consumption of drinking water and foods, usually at 

low levels. Workers in barium mining or processing industries and individuals who reside near such 

industries might be exposed to relatively high levels, primarily through the inhalation of fugitive dust 

containing barium compounds. The most recent occupational exposure estimates indicate that about 

10,000 people were potentially exposed to barium and about 474,000 to barium compounds in workplace 

environments in the United States in 1980 (NIOSH 1989a). 

BARIUM AND BARIUM COMPOUNDS 109 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.2 RELEASES TO THE ENVIRONMENT 

The Toxics Release Inventory (TRI) data should be used with caution because only certain types of 

facilities are required to report (EPA 2005d). This is not an exhaustive list. Manufacturing and 

processing facilities are required to report information to the TRI only if they employ 10 or more full-time 

employees; if their facility is included in Standard Industrial Classification (SIC) Codes 10 (except 1011, 

1081, and 1094), 12 (except 1241), 20–39, 4911 (limited to facilities that combust coal and/or oil for the 

purpose of generating electricity for distribution in commerce), 4931 (limited to facilities that combust 

coal and/or oil for the purpose of generating electricity for distribution in commerce), 4939 (limited to 

facilities that combust coal and/or oil for the purpose of generating electricity for distribution in 

commerce), 4953 (limited to facilities regulated under RCRA Subtitle C, 42 U.S.C. section 6921 et seq.), 

5169, 5171, and 7389 (limited S.C. section 6921 et seq.), 5169, 5171, and 7389 (limited to facilities 

primarily engaged in solvents recovery services on a contract or fee basis); and if their facility produces, 

imports, or processes ≥25,000 pounds of any TRI chemical or otherwise uses >10,000 pounds of a TRI 

chemical in a calendar year (EPA 2005d). 

Barium is a highly reactive metal that occurs naturally only in a combined state. The element is released 

to environmental media by both natural processes and anthropogenic sources. 

According to the SARA Section 313 Toxics Release Inventory (TRI), an estimated total of 230 million 

pounds (105,000 metric tons) of barium and barium compounds were released to the environment from 

manufacturing and processing facilities in the United States in 2004 (TRI04 2006) (see Tables 6-1 and 

6-2). Most of these barium releases were to land. The TRI data must be viewed with caution since only 

certain types of facilities were required to report. This is not an exhaustive list. 

6.2.1 Air 

Estimated combined releases of 2.51 million pounds (1,140 metric tons) of barium (0.35 million pounds) 

and barium compounds (2.16 million pounds) to the atmosphere from 1,107 domestic manufacturing and 

processing facilities in 2004, accounted for about 1.09% of the estimated total environmental releases 

from facilities required to report to the TRI (TRI04 2006). These releases are summarized in Tables 6-1 

and 6-2. 

Barium is released primarily to the atmosphere as a result of industrial emissions during the mining, 

refining, and production of barium and barium chemicals, fossil fuel combustion (Miner 1969a), and 
BARIUM AND BARIUM COMPOUNDS 110 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-1. Releases to the Environment from Facilities that Produce, Process, or 

Use Bariuma
 

Reported amounts released in pounds per yearb 

Total release 

Statec

 RFd Aire Waterf UIg Landh Otheri On-sitej

 Off-sitek 

On- and 

off-site 

AK 3 24,620 0 0 306,812 0 146,620 184,812 331,432 

AL 5 6,963 504 0 39,889 4,748 7,459 44,645 52,104 

AZ 2 1,062 0 0 1,950,946 0 1,823,807 128,201 1,952,008 

CA 2 1,911 0 0 797,507 78 799,418 78 799,496 

CO 1 0 0 No data 0 0 No data 0 0 

CT 1 4 4 0 0 3,515 4 3,519 3,523 

DE 1 20 64 0 0 0 84 0 84 

GA 4 81 0 0 3,757 0 81 3,757 3,837 

IA 4 36,228 0 0 163 0 36,228 163 36,391 

ID 1 14 0 0 130,611 0 130,625 0 130,625 

IL 3 9,428 61 0 45,553 0 9,489 45,553 55,042 

IN 2 10 255 0 18,074 16,900 10 35,229 35,239 

KS 2 7,501 0 0 161,964 526,878 169,465 526,878 696,343 

KY 2 75,258 0 0 0 0 75,258 0 75,258 

MI 5 230 666 0 44,245 271,175 896 315,420 316,316 

MN 2 114,719 0 0 694 0 114,719 694 115,413 

MO 1 0 0 0 0 81 0 81 81 

NC 3 11 0 0 1,559 0 11 1,559 1,570 

NE 6 23,979 3,320 0 37,786 362,667 65,080 362,672 427,752 

NJ 2 89 0 0 30 272 89 302 391 

NM 1 0 0 0 0 0 0 0 0 

NV 2 1,243 0 0 817,749 0 818,992 0 818,992 

NY 5 35,001 137 0 3,073 15,991 35,140 19,062 54,202 

OH 14 866 372 16,649 287,615 6,472 220,822 91,152 311,974 

OK 1 1,906 5 0 250 0 1,906 255 2,161 

OR 1 0 0 0 230,293 1 230,293 1 230,294 

PA 4 756 0 0 344,131 51,746 322,501 74,132 396,633 

SC 2 253 0 0 0 72 253 72 325 

SD 1 500 0 0 39,480 0 39,980 0 39,980 

TN 1 0 0 No data 0 0 No data 0 0 

TX 9 7,392 4,029 0 71,083 7 81,473 1,038 82,511 

UT 2 10 0 0 31,035 0 31,010 35 31,045 

VA 2 0 1,900 0 111,900 0 95,900 17,900 113,800 

WI 1 0 0 0 257,400 0 0 257,400 257,400 
BARIUM AND BARIUM COMPOUNDS 111 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-1. Releases to the Environment from Facilities that Produce, Process, or 

Use Bariuma
 

Reported amounts released in pounds per yearb 

Total release 

Statec

 RFd Aire Waterf UIg Landh Otheri On-sitej

 Off-sitek 

On- and 

off-site 

WV 2 4,214 10 0 77,821 201 82,045 202 82,246 

Total 100 354,269 11,327 16,649 5,811,421 1,260,803 5,339,658 2,114,811 7,454,470 

a

The TRI data should be used with caution since only certain types of facilities are required to report. This is not an 

exhaustive list. Data are rounded to nearest whole number.
 b

Data in TRI are maximum amounts released by each facility.
 c

Post office state abbreviations are used. 

d

Number of reporting facilities.
 e

The sum of fugitive and point source releases are included in releases to air by a given facility. f

Surface water discharges, waste water treatment-(metals only), and publicly owned treatment works (POTWs) (metal 

and metal compounds). 

g

Class I wells, Class II-V wells, and underground injection. 

h

Resource Conservation and Recovery Act (RCRA) subtitle C landfills; other on-site landfills, land treatment, surface 

impoundments, other land disposal, other landfills. i

Storage only, solidification/stabilization (metals only), other off-site management, transfers to waste broker for 

disposal, unknown 

j

The sum of all releases of the chemical to air, land, water, and underground injection wells. k

Total amount of chemical transferred off-site, including to POTWs. 

RF = reporting facilities; UI = underground injection 

Source: TRI04 2006 (Data are from 2004) 
BARIUM AND BARIUM COMPOUNDS 112 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-2. Releases to the Environment from Facilities that Produce, Process, or 

Use Barium Compoundsa
 

Reported amounts released in pounds per yearb 

Total release 

On- and 

Statec

 RFd Aire Waterf UIg Landh Otheri On-sitej

 Off-sitek off-site 

AK 1 16,122 0 0 16,122 0 32,244 0 32,244 

AL 34 69,621 94,049 3,900 11,966,847 67,278 12,062,542 139,153 12,201,695 

AR 16 28,134 107,680 0 2,906,741 44,565 3,038,693 48,427 3,087,120 

AZ 10 11,779 0 0 3,951,882 61 3,962,437 1,285 3,963,722 

CA 14 8,998 514 0 56,003 3,624 20,826 48,313 69,139 

CO 18 14,440 2,232 0 8,687,234 7,500 5,019,424 3,691,982 8,711,406 

CT 4 505 5 0 66,963 22,315 540 89,248 89,788 

DE 3 17,256 9,034 0 480,594 121,025 486,290 141,619 627,909 

FL 22 49,588 9,750 0 2,232,733 216,852 2,134,494 374,429 2,508,924 

GA 29 61,732 112,867 0 8,660,091 19,737 8,798,097 56,330 8,854,427 

HI 1 45 0 0 29,331 0 45 29,331 29,376 

IA 24 142,028 3,709 0 4,358,835 229,865 3,293,915 1,440,522 4,734,437 

ID 6 8,334 11,400 0 137,167 83 98,901 58,083 156,984 

IL 56 218,005 114,459 0 13,593,791 370,276 6,061,909 8,234,621 14,296,530 

IN 45 72,823 31,471 0 8,274,849 82,196 7,095,068 1,366,271 8,461,340 

KS 12 78,277 938 0 4,774,271 250 4,853,486 250 4,853,736 

KY 38 49,663 76,268 0 7,134,938 211,117 5,405,100 2,066,886 7,471,986 

LA 17 70,200 40,931 1,367 4,315,727 8,307 4,411,344 25,188 4,436,532 

MA 14 2,275 1,283 0 257,892 21,982 20,043 263,389 283,432 

MD 18 9,340 1,880 59 468,562 697,038 90,155 1,086,724 1,176,879 

ME 6 1,301 4,100 0 81,692 0 71,193 15,900 87,093 

MI 32 55,968 125,134 56 10,513,385 24,961 7,965,087 2,754,417 10,719,504 

MN 22 48,772 22,540 0 8,233,091 71,522 7,430,251 945,673 8,375,924 

MO 30 231,257 11,722 0 10,226,716 731 10,356,850 113,576 10,470,426 

MS 16 5,973 14,703 0 1,626,877 528 1,627,878 20,203 1,648,081 

MT 6 111,530 781 0 8,892,216 175,814 8,951,015 229,325 9,180,340 

NC 31 30,632 68,807 0 3,082,682 171,007 2,921,804 431,324 3,353,127 

ND 9 39,926 24,052 0 13,826,846 6,786 7,126,843 6,770,767 13,897,610 

NE 11 37,560 52 0 3,982,921 6,350 3,739,570 287,313 4,026,883 

NH 5 1,532 0 0 26,500 1,583 9,632 19,983 29,615 

NJ 20 7,826 9,949 0 96,325 297,053 7,832 403,321 411,153 

NM 6 13,400 250 0 5,210,450 750 5,204,409 20,441 5,224,850 

NV 4 25,974 0 0 1,432,649 37 1,458,623 37 1,458,660 

NY 24 18,085 136,769 0 1,454,199 311,766 790,432 1,130,387 1,920,819 

OH 94 43,103 82,835 319 8,642,836 424,109 5,383,148 3,810,054 9,193,202 

OK 12 25,481 11,600 0 2,005,538 19 1,737,944 304,694 2,042,638 

OR 5 12,393 2,120 0 115,146 0 100,513 29,146 129,659 
BARIUM AND BARIUM COMPOUNDS 113 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-2. Releases to the Environment from Facilities that Produce, Process, or 

Use Barium Compoundsa
 

Reported amounts released in pounds per yearb 

Total release 

On- and 

Statec

 RFd Aire Waterf UIg Landh Otheri On-sitej

 Off-sitek off-site 

PA 72 50,576 40,857 250 3,948,212 422,230 1,469,982 2,992,143 4,462,125 

PR 1 1,542 0 0 91 0 1,633 0 1,633 

RI 3 5 23 0 1,072 477 28 1,549 1,577 

SC 36 27,220 51,763 0 1,313,342 678,479 1,263,992 806,812 2,070,803 

SD 2 1,057 36 0 731,856 0 681,949 51,000 732,949 

TN 24 64,154 106,884 0 4,653,790 334 4,240,684 584,478 4,825,162 

TX 48 158,316 67,044 0 16,122,300 3,011,576 16,164,215 3,195,022 19,359,236 

UT 9 5,422 100 0 3,661,314 3,902 3,510,292 160,446 3,670,738 

VA 28 25,919 26,448 0 2,006,961 189,025 1,704,517 543,836 2,248,353 

VT 1 250 5 0 0 28,667 250 28,672 28,922 

WA 11 1,318 3,118 0 2,274,705 42 2,119,156 160,027 2,279,183 

WI 30 37,077 20,145 0 890,567 1,023,144 342,849 1,628,084 1,970,933 

WV 20 75,248 18,436 0 5,243,526 78,000 4,479,752 935,458 5,415,210 

WY 7 68,528 3,229 0 7,343,092 0 6,751,399 663,450 7,414,849 

Total 1,007 2,156,511 1,471,972 5,951 210,011,467 9,052,963 174,499,278 48,199,586 222,698,864 

a

The TRI data should be used with caution since only certain types of facilities are required to report. This is not an 

exhaustive list. Data are rounded to nearest whole number.
 b

Data in TRI are maximum amounts released by each facility.
 c

Post office state abbreviations are used. 

d

Number of reporting facilities.
 e

The sum of fugitive and point source releases are included in releases to air by a given facility. f

Surface water discharges, waste water treatment-(metals only), and publicly owned treatment works (POTWs) (metal 

and metal compounds). 

g

Class I wells, Class II-V wells, and underground injection. 

h

Resource Conservation and Recovery Act (RCRA) subtitle C landfills; other on-site landfills, land treatment, surface 

impoundments, other land disposal, other landfills. i

Storage only, solidification/stabilization (metals only), other off-site management, transfers to waste broker for 

disposal, unknown 

j

The sum of all releases of the chemical to air, land, water, and underground injection wells. k

Total amount of chemical transferred off-site, including to POTWs. 

RF = reporting facilities; UI = underground injection 

Source: TRI04 2006 (Data are from 2004) 
BARIUM AND BARIUM COMPOUNDS 114 

6. POTENTIAL FOR HUMAN EXPOSURE 

entrainment of soil and rock dust into the air (Schroeder 1970). In addition, coal ash, containing widely 

variable amounts of barium, is also a source of airborne barium particulates (Miner 1969a; Schroeder 

1970). In 1969, an estimated 18% of the total U.S. barium emissions to the atmosphere resulted from the 

processing of barite ore, and more than 28% of the total was estimated to be from the production of 

barium chemicals. The manufacture of various end products (e.g., drilling well muds, and glass, paint, 

and rubber products) and the combustion of coal were estimated to account for an additional 23 and 26% 

of the total barium emissions for 1969, respectively (Davis 1972). 

Estimates of barium releases from individual industrial processes are available for particulate emissions 

from the drying and calcining of barium compounds and for fugitive dust emissions during the processing 

of barite ore. Soluble barium compounds (unspecified) are emitted as particulates from barium chemical 

dryers and calciners to the atmosphere during the processing of barium carbonate, barium chloride, and 

barium hydroxide (Reznik and Toy 1978). Uncontrolled particulate emissions of soluble barium 

compounds from chemical dryers and calciners during barium processing operations may range from 

0.04 to 10 g/kg of final product. Controlled particulate emissions are less than 0.25 g/kg of final product. 

Based on an uncontrolled emission factor of 5 g/kg and a controlled emission factor of 0.25 g/kg, total 

particulate emissions from the drying and calcining of barium carbonate, barium chloride, and barium 

hydroxide are estimated to be 160 metric tons (352,800 pounds) per year (Reznik and Toy 1978). 

Fugitive dust emissions occur during processing (grinding and mixing) of barite ore and may also occur 

during the loading of bulk product of various barium compounds into railroad hopper cars (Reznik and 

Toy 1978). Based on an emission factor of 1 g/kg, total emissions of fugitive dust from the domestic 

barium chemicals industry during the grinding of barite ore have been estimated to be approximately 

90 metric tons (198,450 pounds) per year (Reznik and Toy 1978). Other particulate emissions from the 

industrial production of barium compounds include an estimated 820 metric tons (1.8 million pounds) per 

year from uncontrolled kilns during the processing of barite ore and 8 metric tons (17,640 pounds) per 

year from black ash (i.e., barium sulfide) rotary kilns during the production of barium hydroxide (Reznik 

and Toy 1978). Electric utilities that burn bituminous coal emit a small fraction of the barium contained 

in coal into the air. For example, it is estimated that 830 pounds/year of barium are released to air from a 

650 megawatt (MW) plant, in comparison to 270,000 pounds/year released as ash to land-based waste 

sites (Rubin 1999). 

The use of barium in the form of organometallic compounds as a smoke suppressant in diesel fuels results 

in the release of solids to the atmosphere (Miner 1969a; Ng and Patterson 1982; Schroeder 1970). The 
BARIUM AND BARIUM COMPOUNDS 115 

6. POTENTIAL FOR HUMAN EXPOSURE 

maximum concentration of soluble barium in exhaust gases containing barium-based smoke suppressants 

released from test diesel engines and operating diesel vehicles is estimated to be 12,000 μg/m3

, when the 

barium concentration in the diesel fuel is 0.075% by weight and 25% of the exhausted barium (at a 

sampling point 10 feet from the engine and upstream from the muffler) is soluble (Golothan 1967). Thus, 

1 L of this exhaust gas contains an estimated 12 μg soluble barium or 48 μg total barium (Schroeder 

1970). However, recent legislation requiring the use of low-sulfur fuel in diesel engines has eliminated 

the need for barium as a sulfur-scavenging additive and, therefore, has greatly reduced the emissions of 

barium from diesel engine exhaust (Schauer et al. 1999; Winkler 2002). 

6.2.2 Water 

Estimated combined releases of 1.48 million pounds (674 metric tons) of barium (0.01 million pounds) 

and barium compounds (1.47 million pounds) to surface water from 1,107 domestic manufacturing and 

processing facilities in 2004, accounted for about 0.64% of the estimated total environmental releases 

from facilities required to report to the TRI (TRI04 2006). 

The primary source of naturally occurring barium in drinking water results from the leaching and eroding 

of sedimentary rocks into groundwater (Kojola et al. 1978). Although barium occurs naturally in most 

surface water bodies (i.e., approximately 99% of those examined) (DOI 1970), releases of barium to 

surface waters from natural sources are much lower than those to groundwater (Kojola et al. 1978). 

About 80% of the barium produced is used as barite to make high-density oil and gas well drilling muds, 

and during offshore drilling operations there are periodic discharges of drilling wastes in the form of 

cuttings and muds into the ocean (Ng and Patterson 1982). For example, in the Santa Barbara Channel 

region, about 10% of the muds used are lost into the ocean (Ng and Patterson 1982). Operations 

involving three drilling platforms in the Santa Maria Basin off the coast of central California released 

approximately 1.8x106 kg of barium to the ocean in discharged muds, cuttings, and waste water from 

1986 to 1994 (Phillips et al. 1998). The use of barium in offshore drilling operations may increase 

barium pollution, especially in coastal sediments (Ng and Patterson 1982). 

6.2.3 Soil 

Estimated combined releases of 216 million pounds (98,095 metric tons) of barium (5.81 million pounds) 

and barium compounds (210 million pounds) to soils from 1,107 domestic manufacturing and processing 

facilities in 2004, accounted for about 93.7% of the estimated total environmental releases from facilities 
 

BARIUM AND BARIUM COMPOUNDS 116 

6. POTENTIAL FOR HUMAN EXPOSURE 

required to report to the TRI (TRI04 2006). An additional combined total of 0.023 million pounds 

(10 metric tons) from barium (0.017 million pounds) and barium compounds (0.006 million pounds), 

constituting about 0.01% of the total environmental emissions, were released via underground injection 

(TRI04 2006). These releases are summarized in Tables 6-1 and 6-2. 

The process of drilling for crude oil and natural gas generates waste drilling fluids or muds, which are 

often disposed of by land farming. Most of these fluids are water based and contain barite and other 

metal salts. Thus, barium may be introduced into soils as the result of land farming these slurried reserve 

pit wastes (Bates 1988). 

The use of barium fluorosilicate and carbonate as insecticides (Beliles 1979; Meister 2004) might also 

contribute to the presence of barium in agricultural soils. 

Barium has been detected with a positive geometric mean concentration of 100.5 ppm in soil samples 

from approximately 52% of the hazardous waste sites that have had samples analyzed by the CLP 

(CLPSD 1989). Note that these data from the CLPSD represent frequency of occurrence and 

concentration data for NPL sites only. 

6.3 ENVIRONMENTAL FATE 

6.3.1 Transport and Partitioning 

Most barium released to the environment from industrial sources is in forms that do not become widely 

dispersed (Ng and Patterson 1982). In the atmosphere, barium is likely to be present in particulate form 

(EPA 1984). Although chemical reactions may cause changes in speciation of barium in air, the main 

mechanisms for the removal of barium compounds from the atmosphere are likely to be wet and dry 

deposition (EPA 1984). 

In aquatic media, barium is likely to precipitate out of solution as an insoluble salt (i.e., as BaSO4 or 

BaCO3). Waterborne barium may also adsorb to suspended particulate matter through the formation of 

ion pairs with natural anions such as bicarbonate or sulfate in the matter (Bodek et al. 1988; EPA 1984; 

Giusti et al. 1993; Lagas et al. 1984; Tanizaki et al. 1992). Precipitation of barium sulfate salts is 

accelerated when rivers enter the ocean because of the high sulfate content (905 mg/L) in the ocean 

(Bowen 1966; WHO 2001). It is estimated that only 0.006% of the total barium input into oceans from 

freshwater sources remains in solution (Chow et al. 1978; WHO 2001). Sedimentation of suspended 
BARIUM AND BARIUM COMPOUNDS 117 

6. POTENTIAL FOR HUMAN EXPOSURE 

solids removes a large portion of the barium content from surface waters (Benes et al. 1983). There is 

evidence to suggest that the precipitation of barium from the surface of fresh and marine waters occurs, in 

part, as the result of the barite crystal formation in microorganisms (González-Muñoz et al. 2003). 

Barium in sediments is found largely in the form of barium sulfate (barite). Coarse silt sediment in a 

turbulent environment will often grind and cleave the barium sulfate from the sediment particles leaving a 

buildup of dense barites (Merefield 1987). Estimated soil:water distribution coefficients (Kd) (i.e., the 

ratio of the quantity of barium sorbed per gram of sorbent to the concentration of barium remaining in 

solution at equilibrium) range from 200 to 2,800 for sediments and sandy loam soils (DOE 1984; Rai et 

al. 1984). 

The uptake of barium by fish and marine organisms is also an important removal mechanism (Bowen 

1966; Schroeder 1970). Barium levels in sea water range from 2 to 63 μg/L with a mean concentration of 

about 13 μg/L (Bowen 1979). Barium was found to bioconcentrate in marine plants by a factor of 400– 

4,000 times the level present in the water (Bowen 1966). Bioconcentration factors in marine animals, 

plankton, and brown algae of 100, 120, and 260, respectively, have been reported (Schroeder 1970). In 

freshwater, a bioconcentration factor of 129 was estimated in fish where the barium in water was 

0.07 mg/L (Hope et al. 1996). 

Barium added to soils (e.g., from the land farming of waste drilling muds) may either be taken up by 

vegetation or transported through soil with precipitation (Bates 1988). Relative to the amount of barium 

found in soils, little is typically bioconcentrated by plants (Schroeder 1970). For example, a 

bioconcentration factor of 0.4 has been estimated for plants in a Virginia floodplain with a barium soil 

concentration of 104.2 mg/kg (Hope et al. 1996). However, there are some plants, such as legumes, 

forage plants, Brazil nuts, and mushrooms that accumulate barium (Aruguete et al. 1998; IPCS 1991; 

WHO 2001). Bioconcentration factors from 2 to 20 have been reported for tomatoes and soybeans (WHO 

2001). 

Barium is not very mobile in most soil systems, due to the formation of water-insoluble salts and an 

inability of the barium ion to form soluble complexes with fulvic and humic acids (WHO 2001). The rate 

of transportation of barium in soil is dependent on the characteristics of the soil material. Soil properties 

that influence the transportation of barium to groundwater are cation exchange capacity, calcium 

carbonate (CaCO3) content and pH. In soil with a high cation exchange capacity (e.g., fine textured 

mineral soils or soils with high organic matter content), barium mobility will be limited by adsorption 

(Bates 1988; Kabata-Pendias and Pendias 1984). High CaCO3 content limits mobility by precipitation of 
 

 

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6. POTENTIAL FOR HUMAN EXPOSURE 

the element as BaCO3 (Lagas et al. 1984). Barium will also precipitate as barium sulfate in the presence 

of sulfate ions (Bodek et al. 1988; Lagas et al. 1984). Barium is more mobile and is more likely to be 

leached from soils in the presence of chloride due to the high solubility of barium chloride as compared to 

other chemical forms of barium (Bates 1988; Lagas et al. 1984). Barium may become more mobile in 

soils under acid conditions as barium in water-insoluble salts, such as barium sulfate and carbonate, 

becomes more soluble (WHO 2001). Barium complexes with fatty acids (e.g., in acidic landfill leachate) 

will be much more mobile in the soil due to the lower charge of these complexes and subsequent 

reduction in adsorption capacity (Lagas et al. 1984). 

Barium mobility in soil is reduced by the precipitation of barium carbonate and sulfate. Humic and fulvic 

acid have not been found to increase the mobility of barium (EPA 1984). 

6.3.2 Transformation and Degradation 

6.3.2.1 Air 

Elemental barium undergoes oxidation in air and is oxidized readily in moist air (Boffito 2002; EPA 

1983; Kresse et al. 2007; Kunesh 1978). The residence time of barium in the atmosphere may be several 

days, depending on the size of the particulate formed, the chemical nature of the particulate, and 

environmental factors such as rainfall (EPA 1984; WHO 2001). 

6.3.2.2 Water 

Under natural conditions, barium will form compounds in the +2 oxidation state. Barium does not 

hydrolyze appreciably except in highly alkaline environments (i.e., at pH levels ≥10) (Bodek et al. 1988). 

Appreciable levels of barium sulfate occur because natural water often contains high sulfate 

concentrations, especially ocean water. Since the solubility of barium sulfate is low, only trace amounts 

of barium dissolve in surface water (Bodek et al. 1988; NAS 1977). At pH levels of 9.3 or below, barium 

sulfate may limit barium concentrations in natural waters (Bodek et al. 1988). The solubility of barium 

- sulfate increases considerably in the presence of chloride (Cl-

) and other anions (e.g., NO3 and CO3

-2), 

and at pH levels of 9.3 or below, the barium ion (Ba2+) is the dominant species (Bodek et al. 1988; NAS 

1977). The Ba2+ ion is stable under the pH-Eh range of natural systems. However, natural and treated 

waters usually contain sufficient sulfate so that a barium ion concentration of more than 1,000– 
BARIUM AND BARIUM COMPOUNDS 119 

6. POTENTIAL FOR HUMAN EXPOSURE 

1,500 μg/L cannot be maintained in solution (EPA 1983; Hem 1959; Lagas et al. 1984; McCabe et al. 

1970). 

As pH levels increase above 9.3 and in the presence of carbonate, barium carbonate becomes the 

dominant species (Bodek et al. 1988; Singer 1974). Barium carbonate also exhibits fast precipitation 

kinetics and very low solubility and in alkaline environments limits the soluble barium concentration 

(Faust and Aly 1981; Hem 1959; Rai et al. 1984; Singer 1974). Barium forms salts of low solubility with 

arsenate, chromate, fluoride, oxalate, and phosphate ions (Bodek et al. 1988; EPA 1983; Kunesh 1978). 

The chloride, hydroxide, and nitrate of barium are water-soluble (Bodek et al. 1988; EPA 1983; 

Kirkpatrick 1978) and are frequently detected in aqueous environments (Rai et al. 1984). 

Barium also forms complexes with natural organics in water (e.g., fatty acids in acidic landfill leachates) 

to a limited extent (Lagas et al. 1984; Morel 1983; Rai et al. 1984). 

6.3.2.3 Sediment and Soil 

Barium reacts with metal oxides and hydroxides in soil and is subsequently adsorbed onto soil 

particulates (Hem 1959; Rai et al. 1984). Adsorption onto metal oxides in soils and sediments probably 

acts as a control over the concentration of barium in natural waters (Bodek et al. 1988). Under typical 

environmental conditions, barium displaces other adsorbed alkaline earth metals from MnO2, SiO2, and 

TiO2 (Rai et al. 1984). However, barium is displaced from Al2O3 by other alkaline earth metals (Rai et al. 

1984). The ionic radius of the barium 2+ ion, its typical oxidation state, makes isomorphous substitution 

possible only with strontium, and generally not with the other members of the alkaline earth elements 

(Kirkpatrick 1978). Among the other elements that occur with barium in nature, substitution is common 

only with potassium but not with the smaller ions of sodium, iron, manganese, aluminum, and silicon 

(Kirkpatrick 1978). 

Barium is also adsorbed onto soil and subsoil through electrostatic interactions (Bodek et al. 1988; Singer 

1974). The cation exchange capacity of the sorbent largely controls the retention of barium in soils 

(Bodek et al. 1988). Barium is strongly adsorbed by clay minerals (Kabata-Pendias and Pendias 1984; 

Lagas et al. 1984). 
BARIUM AND BARIUM COMPOUNDS 120 

6. POTENTIAL FOR HUMAN EXPOSURE 

Barium can also form salts with acetate, nitrate, chloride, and hydroxide ions in soil. The mobility of 

barium in soils increases upon formation of these water soluble salts (Bodek et al. 1988). In general, the 

solubility of barium compounds increases with decreasing pH. 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 

Reliable evaluation of the potential for human exposure to barium depends in part on the reliability of 

supporting analytical data from environmental samples and biological specimens. Concentrations of 

barium in unpolluted atmospheres and in pristine surface waters are often so low as to be near the limits 

of current analytical methods. In reviewing data on barium levels monitored or estimated in the 

environment, it should also be noted that the amount of chemical identified analytically is not necessarily 

equivalent to the amount that is bioavailable. The analytical methods available for monitoring barium in 

a variety of environmental media are detailed in Chapter 7. 

6.4.1 Air 

The concentration of barium in ambient air is estimated to be <0.05 μg/m3

 (IPCS 1991). Airborne barium 

likely exists as the carbonate or sulfate salts and is carried on particulate matter that results as a 

consequence of natural processes (e.g., suspension of soil dust) or anthropogenic activities (e.g., 

combustion process, mining and calcining of barium ores) (WHO 2001). However, there is no apparent 

correlation between the degree of industrialization and barium concentrations in ambient air (Winkler 

2002). Particulate matter from diesel exhaust was once a source of barium in ambient air. However, 

barium emissions from diesel engines has been greatly diminished to near zero emissions with the current 

use of low-sulfur diesel fuels, which do not require the addition of barium as a sulfur-scavenging agent 

(Hildemann et al. 1991; Schauer et al. 1999; Shahin et al. 2000; Winkler 2002). 

Tabor and Warren (1958) report urban and suburban air concentrations of barium ranging from <0.005 to 

1.5 μg/m3

. In another study of barium concentrations in ambient air, values ranged from 0.0015 to 

0.95 mg/m3

 (EPA 1984). No distinct pattern related to industrialization appeared in the results reported 

on 754 samples from 18 cities and four suburban areas in the United States. For example, in Houston, 

Texas and its suburbs, 76% of the samples contained barium at levels ranging from 0.005 to 1.5 μg/m3

, 

whereas in Fort Worth, Texas, 66% of the samples had values <0.005 μg/m3

 (Tabor and Warren 1958). 

Another compilation of atmospheric data shows barium concentrations in urban atmospheres of North 

America ranging from 2x10-4 to 2.8x10-2 

μg/m3 with a mean concentration of 1.2x10-2 μg/m3 (Bowen 
BARIUM AND BARIUM COMPOUNDS 121 

6. POTENTIAL FOR HUMAN EXPOSURE 

1979). In contrast, barium levels in samples from the South Pole and northern Norway were 1.6x10-5 and 

7.3x19-4 

μg/m3, respectively (Bowen 1979). Mean barium concentrations in background air collected 

between April and October 2002 on the campus of the University of Birmingham, United Kingdom, were 

0.32 and 1.4 ng/m3

 in the <0.5 and 3.0–7.2 μm particular matter fractions, respectively (Birmili et al. 

2006). 

Maximum ground-level barium concentrations (as soluble compounds) associated with uncontrolled 

atmospheric particulate emissions from chemical dryers and calciners at barium-processing plants have 

been estimated (using dispersion modeling) to range from 1.3 to 330 μg/m3

 over a 24-hour averaging time 

at locations along facility boundaries (i.e., away from the source of emission) (Reznik and Toy 1978). 

Barium has been measured in dust samples taken from 49 residences in Ottawa, Canada. Mean and 

median concentrations of 405.56 and 222.22 mg barium/kg dust, respectively, were measured within a 

sub-fraction of the dust samples where the particulate sizes ranged from 100 to 250 μm (Butte and 

Heinzow 2002; Rasmussen et al. 2001). 

Barium has been measured in rain and snow collected near Claremont, New Hampshire in 1996–1997 

(Feng et al. 2000). Barium concentrations in rain ranged from 0.22 to 0.84 μg/L with a mean 

concentration of 0.39 μg/L. In snow, barium concentrations ranged from 0.64 to 7.44 μg/L with a mean 

concentration of 1.5 μg/L. 

Barium has been detected in air samples collected at 24 of the 798 hazardous waste sites where barium 

has been detected in some environmental medium (HazDat 2006). The HazDat information includes data 

from both NPL and other Superfund sites. Concentrations of barium in air ranged from 0.015 to 

327,000,000 μg/m3

 in 16 onsite (HazDat 2006). In comparison, concentrations of barium in air ranged 

from 0.0135 to 561,000,000 μg/m3

 in 12 offsite samples (HazDat 2006). 

6.4.2 Water 

Barium has been found in almost all raw surface waters and public drinking water supplies sampled (i.e., 

approximately 99%) (Kopp 1969) at concentrations ranging from ≤5 to 15,000 μg/L with mean 

concentrations generally on the order of 10–60 μg/L (Barnett et al. 1969; Bowen 1979; DOI 1970; Durfor 

and Becker 1964; Durum and Haffty 1961; Elinder and Zenz 1994; EPA 2005c; Kopp 1969; Longerich et 

al. 1991; McCabe et al. 1970; Neal et al. 1996; Saleh and Wilson 1999; Tuovinen et al. 1980). Barium 
BARIUM AND BARIUM COMPOUNDS 122 

6. POTENTIAL FOR HUMAN EXPOSURE 

concentrations are lowest (mean value of 15 μg/L) in the drainage basins of the western Great Lakes and 

highest (mean value of 90 μg/L) in the southwestern drainage basins of the lower Mississippi Valley 

(EPA 2005c). Barium concentrations in the shallow aquifer below Denver, Colorado, have been reported 

to range from 18 to 594 μg/L with a median value of 104 μg/L (Bruce and McMahon 1996). Barium 

concentrations in most drinking water supplies are <200 μg/L with a mean concentration of 28.6 μg/L 

(EPA 2005c). In California, mean and median values of 302 and 160 μg/L, respectively, were measured 

for barium concentrations in drinking water supplies (Storm 1994). 

Barium concentrations in groundwater supplies have been known to exceed EPA's maximum contaminant 

level (MCL) of 2.0 mg/L (2,000 μg/L) (EPA 2002a); this may be due to leaching and erosion of barium 

from sedimentary rocks (Calabrese 1977; Kojola et al. 1978). For example, community water supplies 

from deep rock and drift wells in northeastern Illinois have been found to have barium concentrations 

ranging from 1,100 to 10,000 μg/L (Calabrese 1977). Many communities in Kentucky, Pennsylvania, and 

New Mexico have drinking water where the barium content is up to ten times higher than the MCL (EPA 

2005c). Water samples taken from groundwater wells in Texas that are within 750 m of brine injection, 

dry, or plugged gas/oil wells contain barium ranging in concentration from 1.2 to 2,300 μg/L (Hudak and 

Wachal 2001). 

A mean concentration of 167 μg/L for barium was measured in influent streams of a public waste water 

treatment plant in Melbourne, Australia (Wilkie et al. 1996). The amount of barium in the influent 

streams could not be accounted for based on the mean concentrations of barium in domestic water 

supplies (20 μg/L) or domestic sewage (38 μg/L). Instead, it is likely that the barium unaccounted for in 

the influent stream is the result of barium carried in effluents from industries that are discharged into the 

catchment area of the treatment plant. 

Barium has also been found in sea water at concentrations ranging from 2 to 63 μg/L with a mean 

concentration of 13 μg/L (Bowen 1979). 

Barium has been detected in surface water and groundwater samples collected at 257 and 561 of the 

798 hazardous waste sites, respectively, where barium has been detected in some environmental medium 

(HazDat 2006). The HazDat information includes data from both NPL and other Superfund sites. 

Maximum concentrations of barium in surface water (lakes, streams, ponds, etc.) ranged from 0.33 to 

18,100,000 μg/L in 77 onsite samples (HazDat 2006). In comparison, maximum concentrations of 

barium in surface water (lakes, streams, ponds, etc.) ranged from 10 to 73,8000 μg/L in 112 offsite 
BARIUM AND BARIUM COMPOUNDS 123 

6. POTENTIAL FOR HUMAN EXPOSURE 

samples (HazDat 2006). The maximum concentrations of barium in groundwater ranged from 0.064 to 

2,100,000 μg/L in 442 onsite samples (HazDat 2006). In comparison, maximum concentrations of 

barium in groundwater ranged from 0.05 to 803,000 μg/L in 260 offsite samples (HazDat 2006). 

6.4.3 Sediment and Soil 

Barium is relatively abundant in the earth's crust and is found in most soils at concentrations (Table 6-3) 

ranging from about 15 to 3,500 ppm (dry weight) and mean values ranging between 265 and 835 ppm, 

depending on soil type (EPA 1995a; Kabata-Pendias and Pendias 1984; Lide 2005; Zenz et al. 1994). 

The barium content in cultivated and uncultivated soil samples collected during a number of field studies 

ranged from 15 to 1,000 ppm (mean concentration of 300 ppm) for B horizon soils (subsurface soils) in 

the eastern United States and from 70 to 5,000 ppm (mean concentration of 560 ppm) for B horizon soils 

in the western United States (Bowen 1979; Schroeder 1970; Shacklette and Boerngen 1984). Barium 

content ranged from 150 to 1,500 ppm for surface horizon soils collected in Colorado (mean 

concentration of 550 ppm) (Connor and Shacklette 1975). Soil samples (0–6 inch depth) taken from three 

New England cities, Boston, Providence and Springfield, were reported to have mean barium 

concentrations of 53.95, 45.29 and 45.17 mg/kg, respectively, and upper 95% interval values of 66.25, 

59.43, and 51.03 mg/kg, respectively (Bradley et al. 1994). Soil samples were obtained from areas that 

were not influenced by industrial activity, such as along roads and sidewalks, parks and open lots, and 

may account for why the mean values for barium concentration were well below a mean value of 

420 mg/kg for the United States. 

Geometric mean concentrations of barium in sediments taken from 16 sampling sites along the southern 

shore of Lake Ontario and southeastern shore of Lake Erie ranged from 6.0 to 143.6 μg/g (dry weight) 

(Lowe and Day 2002). Thirteen of the 16 sites had mean barium concentrations that exceeded EPA’s 

guidelines (20–60 μg barium/g dry weight) for defining moderately polluted harbor sediments for this 

metal. However, these concentrations are lower than the mean barium concentration of 482.1 μg/g in 

sediments collected from Lake Pontchartrain near New Orleans, Louisiana (USGS 2002c). The barium 

content in total suspended solids collected from the Mississippi River before it enters Lake Pontchartrain 

was 599 μg/g. 

Barium concentrations in sediments near offshore drilling platforms are typically higher than unaffected 

sediments. Surficial and suspended sediments collected within 500 m of a drilling platform in the Santa 

Maria Basin offshore of central California contained barium at concentrations of 923 and 736 mg/kg dry 
BARIUM AND BARIUM COMPOUNDS 124 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-3. Concentrations of Barium in Surface Soils of the United Statesa,b 

Concentrationc 

Soil Mean Range 

Sandy and lithosols on sandstone 400 20–1,500 

Light loamy soils 555 70–1,000 

Loess and soils on silt deposits 675 200–1,500 

Clay and clay loamy soils 535 150–1,500 

Alluvial soils 660 200–1,500 

Soils over granite and gneisses 785 300–1,500 

Soils over volcanic rocks 770 500–1,500 

Soils over limestones and calcareous rocks 520 150–1,500 

Soils on glacial till and drift 765 300–1,500 

Light desert soils 835 300–2,000 

Silty prairie soils 765 200–1,500 

Chernozems and dark prairie soils 595 100–1,000 

Organic light soils 265 10–700 

Forest soils 505 150–2,000 

Various soils 560 70–3,000 

Mean concentration in Earth’s crustd 500 — 

Mean concentration in Earth’s cruste 425 — 

a

Data obtained from Kabata-Pendias and Pendias (1984) unless indicated otherwise

b

Data are for whole soil profiles 

c

Concentrations expressed as ppm dry weight

d

Zenz et al. 1994 

e

Lide 2000 

Source: Adapted from EPA 1995a 
BARIUM AND BARIUM COMPOUNDS 125 

6. POTENTIAL FOR HUMAN EXPOSURE 

weight, respectively (Phillips et al. 1998). These values were higher (although not statistically 

significant) than the values of 869 and 687 mg/kg dry weight measured in surficial and suspended 

sediments, respectively, collected at a distance of 1,000 meters from the platform and are similar to the 

predrilling concentrations of barium in these sediments. In other California coastal sediments, for 

example the Southern California Bight, barium concentrations range from 145 to 1,259 ppm with an 

average of 720 ppm (Chow et al. 1978). Median barium concentration ranges in sediments from the lake 

system in Chiapas, Mexico were 54.4–121.2 and 50.3–155.3 μg/g dry weight in three lakes during the dry 

(June 2002) and rainy (September 2000) seasons, respectively (Pascual-Barrera et al. 2004). This lake 

system is an area of petroleum extraction and processing. Barium concentrations ranging from 180 to 

2,800 μg/g dry weight (mean 729 μg/g dry weight) were reported in surface sediments (<63 μm fraction) 

collected in April 2002 from eight stations in Izmit Bay, Turkey (Pekey 2006). 

Barium has been detected in soil and sediment samples collected at 369 and 260 of the 798 hazardous 

waste sites, respectively, where barium has been detected in some environmental medium (HazDat 2006). 

The HazDat information includes data from both NPL and other Superfund sites. Maximum 

concentrations of barium in soil (topsoil, <3 inches depth) ranged from 1.59 to 13,000 ppm in 84 onsite 

samples (HazDat 2006). In comparison, maximum concentrations of barium in soil (topsoil, <3 inches 

depth) ranged from 3 to 54,700 ppm in 28 offsite samples (HazDat 2006). Maximum concentrations of 

barium in sediment (lakes, streams, ponds, etc.) ranged from 13.1 to 17,600 ppm in 36 onsite samples 

(HazDat 2006). In comparison, maximum concentrations of barium in sediment (lakes, streams, ponds, 

etc.) ranged from 0.156 to 26,400 ppm in 92 offsite samples (HazDat 2006). 

6.4.4 Other Environmental Media 

Barium occurs in many foods at generally low levels (Table 6-4). In the Canadian Total Diet Study, the 

concentrations of barium were found to be less than 4 ppm (4,000 ng/g) in a variety of foods (Health 

Canada 2005). However, Brazil nuts have notably high concentrations of barium (3,000–4,000 ppm) 

(Beliles 1979). Some plants bioconcentrate barium from the soil (Beliles 1979; Reeves 1979; Schroeder 

1970). The barium content in corn samples from Georgia, Missouri, and Wisconsin collected during a 

number of field studies ranged from 5 to 150 ppm with mean concentrations ranging from 15 to 54 ppm 

(Connor and Shacklette 1975). The barium content in other cultivated plants (e.g., lima beans, cabbage, 

soybeans, and tomatoes) from Georgia, Missouri, and Wisconsin ranged from 7 to 1,500 ppm with mean 

concentrations in various plants ranging between 38 and 450 ppm. The highest levels occurred in 
BARIUM AND BARIUM COMPOUNDS 126 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-4. Concentrations of Barium in Food Obtained from the Canadian Total 

Diet Study Between 1993 and 1999
 

Concentration (ng/g) 

Food Categories Averagea Rangeb 

Milk 71.22 67.96–73.24 

Dairy produce (ice cream, yogurt, cheese, cream) 332.37 70.61–962.93c 

Meats (beef, pork veal, lamb, organ meats) 131.82 12.06–237.57 

Eggs 456.69 456.69 

Poultry (chicken, turkey) 52.53 52.53 

Fish (marine, fresh water, canned) and shellfish 137.28 36.17–481.34 

Soups (meat, cream, tomato, dehydrated) 130.01 119.66–154.53 

Breads, cereals, pasta, rice, pastries (cake, pies) 891.16 45.86–3,840.40d 

Vegetables 425.69 47.99–2,282.23e 

Fruits 570.33 57.62–3,750.03f 

Oils, fats, butter 32.45 20.67–53.08 

Candy, syrups, jams, gelatin, puddings, honey, sugar 300.60 4.86–903.07g 

Peanut butter and peanuts 2,919.11 2,919.11 

Beverages (beer, wine, coffee, tea, soft drinks, tap water) 70.94 13.05–151.82 

Baby foods and formula 196.46 46.98–481.85 

Frozen entrees 457.76 393.57–594.11 

Processed foods (pizza, burgers, French fries, hot dog, etc.) 516.96 278.43–864.58 

a

Values represent the average barium concentration in the foods covered under the individual food categories. 

b

Values represent the range of average concentrations of the food items covered under the individual food
 

categories. 

c

The highest barium concentrations were found in unprocessed cheeses (962.93 ng/g). 

d

The highest barium concentrations were found in wheat and bran cereals (3,840.40 ng/g), whole wheat bread 

(1,494.06 ng/g), muffins (1,434.30 ng/g), and cookies (1,029.13 ng/g). e

The highest barium concentrations were found in beets (2,282.23 ng/g) and carrots (1,309.25 ng/g). f

The highest barium concentrations were found in raspberries (3,750.03 ng/g) and strawberries (1,176.48 ng/g). 

g

The highest barium concentrations were found in chocolate candy bars (903.07 ng/g). 

Source: Health Canada (2005) 
BARIUM AND BARIUM COMPOUNDS 127 

6. POTENTIAL FOR HUMAN EXPOSURE 

cabbage from Georgia and soybeans from Missouri and the lowest levels occurring in Georgia tomatoes 

(Connor and Shacklette 1975). 

Grippo et al. (2006) measured various metal concentrations in dietary supplements purchased from 

random local vendors in the Little Rock, Arkansas area between 2002 and 2003. Barium concentrations 

in botanicals were 0.0200 and 15.4 ng/g in samples of milk thistle and kava kava, respectively. Barium 

concentrations in ephedra-containing supplements were 0.0400 and 93.3 ng/g in Virgin Earth and 

Xenadrine RFA-1, respectively. The authors noted that all metals measured in this study were detected at 

concentrations below toxic levels or physiological limits for daily intake, where such limits have been 

identified (Grippo et al. 2006). 

The Wyoming Game and Fish Department collected game fish during the 2000–2001 season to survey the 

state’s fisheries for metal contamination. Ninety-six fish composites (fillets) were collected, representing 

11 species, from 28 lakes and reservoirs across Wyoming. In this study, barium concentrations were at or 

below the method detection limit of 0.05 mg/kg (Dailey et al. 2005). Mean barium concentrations 

ranging from 0.057 to 0.255 mg/kg wet weight were reported in muscle tissue of five species of sturgeons 

collected from the Caspian Sea (Pourang et al. 2005). 

Barium is also found in anaerobic sewage sludge at concentrations ranging from 100 to 9,000 ppm (mean 

concentration of 800 ppm) and in aerobic sewage sludge at concentrations ranging from 100 to 300 ppm 

(mean concentration of 200 ppm) (Sommers 1977). 

Barium concentrations in leachates from municipal landfills range from 0.11 to 9,220 μg/L (EPA 1990, 

1991; Roy 1994). 

Barium concentrations in fertilizers and soil amendments range from <0.2 to 669 μg/g mean (Raven and 

Loeppert 1997). The highest levels are in tilemsi phosphate rock (669 μg/g), austenite (408 μg/g), 

milorganite (165 μg/g), manure (153 μg/g), and compost (131 μg/g). There is some concern that 

continued use of fertilizers and soil amendments, which contain high amounts of barium and other metals, 

may result in an accumulation of barium in agricultural soils. The accumulation of barium in soils that is 

due to the continued use of fertilizers and soil amendments and the potential for increased content of 

barium in agricultural products and potential harm to the environment have not yet been assessed (Raven 

and Loeppert 1997). 
BARIUM AND BARIUM COMPOUNDS 128 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE 

The primary routes of exposure of humans to barium are consumption of food and water and inhalation of 

ambient air (ICRP 1974; Reeves 1979; WHO 2001). Based on compliance monitoring data from the 

Federal Reporting Data System (FRDS), of the approximately 214 million people in the United States 

who are connected to a public water supply, it is estimated that about 150,000 people are exposed to 

barium concentrations greater than EPA's MCL of 2.0 mg/L (2,000 μg/L) (EPA 2002a). However, since 

94% of all samples collected from public water supplies of the 100 largest cities in the United States had 

barium concentrations <100 μg/L (Durfor and Becker 1964), it is likely that most of the people connected 

to a public water supply receive drinking water with barium concentrations below the MCL. In a survey 

of drinking water from residences in EPA Region V (Indiana, Illinois, Michigan, Minnesota, Ohio, and 

Wisconsin) taken from the National Human Exposure Assessment Survey (NHEXAS) in 1995, an 

average barium concentration of 30 μg/L was obtained, with a 90th percentile value of 77 μg/L (Thomas et 

al. 1999). Assuming an average adult drinking water consumption rate of 2 L/day and that barium is 

present at concentrations of 30 μg/L, the average adult daily intake of barium through the consumption of 

drinking water would be 60 μg/day (0.86 μg/kg/day for a 70-kg adult). However, the International 

Commission for Radiation Protection (ICRP) estimates that the gastrointestinal absorption of barium is 

<5% (ICRP 1973). 

The International Commission on Radiological Protection (ICRP 1974) has estimated that intake of 

barium through inhalation ranges from 0.09 to 26 μg/day. Based on reported urban air concentrations for 

barium (<0.005–1.5 μg/m3

) (Tabor and Warren 1958) and assuming an average adult ventilation rate of 

20 m3

/day (EPA 1989), the calculated daily respiratory intake of barium ranges from <0.1 to 30 μg, which 

is comparable to the ICRP estimated intake range above. Based on the 8-hour time-weighted average 

threshold limit value (TLV) in workplace air of 500 μg/m3

 (ACGIH 2004), and assuming an 8-hour 

inhalation of 10 m3

 of air, a daily barium workplace intake of 5,000 μg can be calculated. NAS (1977) 

estimated that 75% of inhaled barium could be absorbed into the bloodstream if soluble barium salts were 

involved. 

Since average ground level concentrations of an emission vary with the distance from the emission point, 

the population around a source site will be exposed to differing emission levels. Using an average 

population density of 27 persons/km2

 (based on actual population data from areas surrounding barium 

production and processing plants), it has been estimated that approximately 0–886 persons within an area 

of up to 32.8 km2

 around a source site could be exposed to soluble barium compound concentrations of 
BARIUM AND BARIUM COMPOUNDS 129 

6. POTENTIAL FOR HUMAN EXPOSURE 

>1.67 μg/m3 in ambient air (Reznik and Toy 1978). Assuming that the average adult daily ventilation rate 

is 20 m3

 (EPA 1989), breathing these ambient air barium concentrations would result in daily respiratory 

intakes of >32 μg. No other correlations have been established between barium concentrations in air and 

geographical areas or land-use types. 

The day-to-day intake of barium is likely to vary with the quantity and types of food ingested since the 

barium content in foods varies widely (Schroeder 1970). Based on consumption of food and beverages in 

long-term balance studies of four individuals, daily barium intake was estimated to range from 650 to 

1,770 μg/day, or from 9.30 to 25.3 μg/kg body weight/day based on an adult weight of 70 kg (Tipton et al. 

1966, 1969). Assuming an estimated average barium intake of 60 μg/day from drinking water that is 

based on the barium concentrations in drinking water obtained in the NHEXAS EPA Region V study 

(Thomas et al. 1999) and a consumption of 2 L of water per day, the barium intake from the consumption 

of non-drinking water dietary sources alone would range from 590 to 1,710 μg/day. Thus, food is 

typically the primary source of barium exposure for the general population. Gastrointestinal absorption of 

barium from food was reported to be approximately 6% (ranging from 1 to 15%) (ICRP 1974). However, 

reevaluation of this ICRP data and the data from other studies (Harrison et al. 1956; LeRoy et al. 1966); 

Tipton et al. 1969, Schroeder et al. 1972) using the methods of re-estimating barium absorption, which are 

based on current information of systemic kinetics of barium (Leggett 1992), suggest that gastrointestinal 

absorption of barium may be higher, generally ranging between 7 and 30% and could be as high as 95% 

in some individuals. 

In the Canadian Total Diet Study (TDS) of 1993–1999, the average barium intake in individuals surveyed 

was found to be highest in young children (Health Canada 2005). The average barium intake ranged from 

20.760 to 25.251 μg/kg body weight/day for children ages 0–4 years old (Table 6-5). For individuals 

older than 4 years, the average barium intake decreased for both males and females with increasing age to 

values of 9.704 (20–39 years) and 7.839 (>65 years) μg/kg body weight/day in males and 8.418 (20– 

39 years) and 7.546 (>65 years) μg/kg body weight) in females. The average daily barium intakes from 

the Canadian TDS for males and females of all ages (8.817 μg/kg body weight/day) is in reasonable 

agreement with the low end of the daily intake range for barium of 9.30 μg/kg body weight/day 

determined by Tipton et al. (1966, 1969). 

Mean daily balances (excluding loss via hair and sweat) determined from long-term balance studies of 

four adult subjects ranged from a negative balance of 800 μg to a positive balance of 890 μg (Tipton et 

al. 1966, 1969). Based on data from these studies, Schroeder (1970) estimated that human daily intake 
BARIUM AND BARIUM COMPOUNDS 130 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-5. Average Dietary Intake of Barium in Different Age/Sex Groups from 

the Canadian Total Diet Study (1993–1999) 

Sex Age Intakea 

Male and female 0–1 months 20.760 

Male and female 2–3 months 23.350 

Male and female 4–6 months 21.414 

Male and female 7–9 months 21.213 

Male and female 10–12 months 22.823 

Male and female 1–4 years 25.251 

Male and female 5–11 years 18.741 

Male 12–19 years 11.759 

Male 20–39 years 9.704 

Male 40–64 years 8.976 

Male ≥65 years 7.839 

Female 12–19 years 9.280 

Female 20–39 years 8.418 

Female 40–64 years 7.855 

Female ≥65 years 7.546 

Male and female All ages 8.817 

a

micrograms barium per kilogram body weight per day 

Source: Health Canada (2005) 
BARIUM AND BARIUM COMPOUNDS 131 

6. POTENTIAL FOR HUMAN EXPOSURE 

from food (1,160 μg), water (80 μg), and air (10 μg) would be approximately 1,250 μg, and that loss from 

urine (180 μg), feces (1,010 μg) and other sources (e.g., sweat and hair) (85 μg) would be 1,275 μg. 

Using these latter estimates of barium intake and loss, a negative barium balance of 25 μg would occur. 

According to ICRP, the average daily intake of barium from food and fluids (750 μg) and ambient air 

(0.09–26 μg) ranges from 750 to 776 μg. In addition, ICRP (1974) estimated that approximately 825 μg 

of barium is lost daily through the urine (50 μg), feces (690 μg), sweat (10 μg), and hair (75 μg). These 

intake and loss estimates indicate a negative daily balance of up to 75 μg. However, these negative daily 

balance values of 25 and 75 μg are not significant. Also, it is not expected that a negative daily balance 

would maintain a total body content of barium for a 70-kg adult of 22,000 μg, a value that was estimated 

from a study of barium content in major human organs and tissues (ICRP 1974; Schroeder et al. 1972). 

Ninety-three percent of this barium was found in bone and connective tissue. The remaining 7% of 

barium exists largely in fat, skin, and lungs. 

Barium content in the human population has been determined in urine and major organs and tissues in 

more current studies. Barium concentrations in urine for the United States population aged 6 years and 

older were measured in the Third National Health and Nutrition Examination Survey (NHANES). The 

geometric mean (95% confidence interval) for the creatinine-adjusted levels of barium in urines for all 

ages was 1.44 (1.31–1.58) μg per gram of creatinine (CDC 2005). Within age groups, the geometric 

means for the barium concentration in urine decreased as a function of age, from 2.20 μg per gram of 

creatinine (6–11 years) to 1.45 μg per gram of creatinine (12–19 years) and 1.37 μg per gram of creatinine 

(20 years and older). The geometric mean concentration of barium in females (1.59 μg per gram of 

creatinine) was slightly higher than in males (1.30 μg per gram of creatinine). As a function of ethnicity, 

non-Hispanic whites had the highest geometric mean barium concentrations (1.62 μg per gram of 

creatinine) followed by Mexican Americans (1.18 μg per gram of creatinine) and non-Hispanic African 

Americans (0.891 μg per gram of creatinine). A median urinary concentration of 1,146 ng/L (range 295– 

5,250 ng/L) was reported in urine of 50 healthy individuals, aged 20–68 years, in central Italy (Alimonti 

et al. 2005). 

Occupational exposure to barium primarily occurs in workers and miners who inhale barium sulfate (or 

the ore, barite) and barium carbonate dust during the mining of barite and the manufacturing and 

processing (e.g., mixing, grinding, and loading) of barium compounds (Beliles 1979; Reznik and Toy 

1978; Schroeder 1970). Inhalation exposure to barium is also known to occur for industrial welders, 

especially those using barium-containing stick electrodes and self-shielded flux core wires, and those 
BARIUM AND BARIUM COMPOUNDS 132 

6. POTENTIAL FOR HUMAN EXPOSURE 

working in ceramic factories (Ramakrishna et al. 1996; Roig-Navarro et al. 1997; WHO 2001; Zschiesche 

et al. 1992). 

Data from a workplace survey, the National Occupational Exposure Survey (NOES), conducted by 

NIOSH from 1980 to 1983, estimated the number of workers potentially exposed to various chemicals in 

the workplace in 1980 (NIOSH 1989a), including a separate tally of female workers. The data for barium 

and barium compounds included in the survey are summarized in Table 6-6. The NOES database does 

not contain information on the frequency, concentration, or duration of exposure of workers to any of the 

chemicals listed therein. This is a survey that provides only estimates of the number of workers 

potentially exposed to chemicals in the workplace. 

6.6 EXPOSURES OF CHILDREN 

This section focuses on exposures from conception to maturity at 18 years in humans. Differences from 

adults in susceptibility to hazardous substances are discussed in Section 3.7, Children’s Susceptibility. 

Children are not small adults. A child’s exposure may differ from an adult’s exposure in many ways. 

Children drink more fluids, eat more food, breathe more air per kilogram of body weight, and have a 

larger skin surface in proportion to their body volume. A child’s diet often differs from that of adults. 

The developing human’s source of nutrition changes with age: from placental nourishment to breast milk 

or formula to the diet of older children who eat more of certain types of foods than adults. A child’s 

behavior and lifestyle also influence exposure. Children crawl on the floor, put things in their mouths, 

sometimes eat inappropriate things (such as dirt or paint chips), and spend more time outdoors. Children 

also are closer to the ground, and they do not use the judgment of adults to avoid hazards (NRC 1993). 

The main exposures of children to barium are expected to occur mainly from the diet or by dermal contact 

with barium-containing dust, with minor exposures through barium in air. Data on the daily intake of 

barium in the total diet of children in the United States were not located in the available literature. 

However, the average daily intake of barium in children has been determined in a Canadian Total Diet 

Study (1993–1999), showing that children ages 0–48 months have the highest barium intake through their 

diet in comparison to older children (>4 years) and adults (Health Canada 2005). The average barium 

intake in young male and female children increased from 20.760 for infants (0–1 month) to 25.251 μg/kg 

body weight/day for children ages 1–4 years (Table 6-5). For older children (>4 years), there is a 

continual decrease in the average daily barium intake, with values of 18.741 μg/kg body weight/day for 
BARIUM AND BARIUM COMPOUNDS 133 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-6. Number of Workers Potentially Exposed to Barium and Barium 

Compounds 

Total workers (female 

Chemical Number of plants workers) 

Barium 815 10,308 (3,598) 

Barium carbonate 4,494 61,019 (6,889) 

Barium chloride 4,293 57,767 (15,249) 

Barium hydroxide 1,423 35,351 (12,208) 

Barium oxide (BaO2) 46 511 (325) 

Barium nitrate 353 9,625 (2,699) 

Barium sulfate 20,089 305,887 (83,800) 

Barium sulfide 7 7 (0) 

Chromic acid (H2CrO4), barium salt (1:1) 20 3,546 (1,984) 

Source: NIOSH 1989a 
BARIUM AND BARIUM COMPOUNDS 134 

6. POTENTIAL FOR HUMAN EXPOSURE 

individuals aged 5–11 years and then down to 11.759 μg/kg body weight/day for males and 9.280 μg/kg 

body weight/day for females aged 12–19 years. It is expected that the data obtained from the Canadian 

Total Diet Study will reasonably approximate the daily barium intake for children living in the United 

States. It is estimated that for children in the United States, the barium intake through drinking water will 

range between 36 and 60 μg/day. This estimate is based on an average concentration of 30 μg barium/L 

in drinking water within the United States (Thomas et al. 1999) and the consumption of 1.2–2.0 L 

water/day. A factor to be taken into account is that fractional intestinal absorption of metals in young 

children, as in young mammals, may be higher than in adults (Foulkes and Bergman 1993). Dermal 

contact with barium in household dust is not expected to result in uptake of barium through the skin. Oral 

intake of barium through hand-to-mouth exposures to barium-containing dust is likely to occur. 

However, it is not known how much barium is taken in through this route of exposure. There is also the 

potential of oral intake of barium through the licking or ingestion of crayons or water colors, but it is not 

known how much barium is ingested or how much is bioavailable (Rastogi and Pritzl 1996). 

Dietary intake of barium in 3-month-old infants has been given by Biego et al. (1998) for exclusive 

consumption of various types of milk. The average barium intake from the consumption of breast milk 

only was determined to be 4 μg/day. Barium intake increases with exclusive consumption of bottled milk 

(39 μg/day), evaporated milk (42 μg/day), formula (44 μg/day), and dried milk (59 μg/day). The highest 

average intake of barium occurred with exclusive consumption of soya milk (91 μg/day). These intakes 

are based on an average daily intake of milk of 700 mL. 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 

The general population is commonly exposed to barium primarily through ingestion of drinking water and 

consumption of food and beverages. However, certain populations face greater than average exposures to 

this element due to environmental sources, such as drinking water (EPA 1987). High levels of barium 

have been reported in groundwater from deep rock and drift wells in several communities in northeastern 

Illinois (Brenniman et al. 1981; Calabrese 1977) where barium is a naturally occurring geochemical 

pollutant found almost exclusively in the Cambrian-Ordovician Aquifer (Gilkeson et al. 1978). Other 

populations that might receive increased exposure to barium are consumers of crops grown on soils that 

have been used for the land farming of waste oil-well drilling muds (Bates 1988). Individuals who work 

at or live near barium mining, manufacturing, or processing plants might inhale higher ambient air 

concentrations or increased amounts of fugitive dust containing barium particulates. Populations living in 

the vicinity of the NPL sites known to be contaminated with barium may also be exposed to higher than 
 

BARIUM AND BARIUM COMPOUNDS 135 

6. POTENTIAL FOR HUMAN EXPOSURE 

background levels of the compound through contact with contaminated waste site media or barium in 

offsite air or water. Barium has been measured in air, surface water, and groundwater collected offsite of 

some NPL sites (HazDat 2006). No information was found regarding the sizes of these populations or 

their intake levels of barium. 

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 barium is available. Where adequate information is not 

available, ATSDR, in conjunction with NTP, is required to assure the initiation of a program of research 

designed to determine the health effects (and techniques for developing methods to determine such health 

effects) of barium. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 

6.8.1 Identification of Data Needs 

Physical and Chemical Properties. The physical and chemical properties of metallic barium and 

its inorganic compounds have been well characterized (Boffito 2002; CHRIS Manual 2005; Dibello et al. 

2003; DOT 2004; Genter 2001; HSDB 2007; Kresse et al. 2007; Lewis 1997; Lide 2005; NIOSH/OSHA 

1978; NIOSH 1999; Budavari et al. 2001; OHM/TADS 1989; Parmeggiani 1983; Perry and Chilton 1973; 

RTECS 2007; Lewis 2000; Stokinger 1981; Weast 1989). Physical and chemical properties of organic 

compounds of barium have not been comprehensively examined probably due to the limited extent of 

formation of these compounds. However, further study of the properties of these compounds would help 

in understanding their role in the environmental fate and transport of barium, particularly at hazardous 

waste sites where high levels of organic contaminants might be present. 

Production, Import/Export, Use, Release, and Disposal. According to the Emergency 

Planning and Community Right-to-Know Act of 1986, 42 U.S.C. Section 11023, industries are required 

to submit substance release and off-site transfer information to the EPA. The TRI, which contains this 
 

 

BARIUM AND BARIUM COMPOUNDS 136 

6. POTENTIAL FOR HUMAN EXPOSURE 

information for 2004, became available in May of 2006. This database is updated yearly and should 

provide a list of industrial production facilities and emissions. 

Because barium compounds occur naturally and are widely used in oil well drilling muds, in steel, rubber 

and plastic products, glass and ceramics, chemical, and pyrotechnics industries, in insecticides, and as a 

smoke suppressant in diesel fuels (Bodek et al. 1988; Dibello et al. 2003; ILO 1983; Kirkpatrick 1985; 

Meister 2004; Stokinger 1981; Venugopal and Luckey 1978; WHO 2001; Worthing 1987), the potential 

for human exposure to these compounds, such as through ingestion of food and water or inhalation of 

ambient air, is substantial. Recent data on production volumes and import and export of barite and some 

barium compounds (e.g., barium chloride, barium carbonate, barium hydroxide, and barium oxide) are 

available (USGS 2006). In addition, only limited information on disposal of barium compounds was 

available (HSDB 2007; IPCS 1991; NIOSH/OSHA 1978). Additional information on production, import, 

export, and disposal would be useful in assessing the potential for the release of, and exposure to, barium 

compounds. 

Environmental Fate. The partitioning of barium in environmental media is influenced by the specific 

form of the compound and such site-specific conditions as pH and cation exchange capacity (Bates 1988; 

Bodek et al. 1988; Bowen 1966; Giusti et al. 1993; Kabata-Pendias and Pendias 1984; Lagas et al. 1984; 

Tanizaki et al. 1992). Upon release to the environment, barium is most likely to partition to soils and 

sediments (Chow et al. 1978; DOE 1984; Rai et al. 1984; WHO 2001). Barium is transported in the 

atmosphere, surface waters, soil runoff, and groundwater. In surface waters and soils, barium may ionize 

and form various salts depending on the pH and the availability of anions (Bates 1988; Bodek et al. 1988; 

Bowen 1966; Kabata-Pendias and Pendias 1984; Lagas et al. 1984; WHO 2001). Additional information 

on the transport and transformation of barium in the atmosphere would be useful in developing a more 

complete understanding of the environmental fate of barium compounds. 

Bioavailability from Environmental Media. Barium is absorbed following ingestion (Chou and 

Chin 1943; Cuddihy and Griffith 1972; McCauley and Washington 1983; Taylor et al. 1962) and 

inhalation (Cuddihy and Ozog 1973b). The bioavailability of barium from air, water, and food has been 

examined rather extensively in animals (Chou and Chin 1943; Cuddihy and Griffith 1972; McCauley and 

Washington 1983; Taylor et al. 1962) and humans (Tipton et al. 1969). However, bioavailability from 

soil has not been studied. Since soil is an important repository for barium, information on barium 

absorption from ingested soil would be useful in developing an understanding of the potential for 

exposure following ingestion of contaminated soils, particularly at hazardous waste sites. 
BARIUM AND BARIUM COMPOUNDS 137 

6. POTENTIAL FOR HUMAN EXPOSURE 

Food Chain Bioaccumulation. There is information that barium bioconcentrates in certain plants 

and aquatic organisms (Aruguete et al. 1998; Bowen 1966; Hope et al. 1996; IPCS 1991; Schroeder 1970; 

WHO 2001). However, the extent to which plants bioconcentrate barium from soil or to which uptake 

occurs in terrestrial animals is not well characterized. Further studies on the bioconcentration of barium 

by plants and terrestrial animals and on the biomagnification of barium in terrestrial and aquatic food 

chains would be useful to better characterize the environmental fate of barium and define the importance 

of food chain accumulation as a source of human exposure. 

Exposure Levels in Environmental Media. Reliable monitoring data for the levels of barium in 

contaminated media at hazardous waste sites are needed so that the information obtained on levels of 

barium in the environment can be used in combination with the known body burden of barium to assess 

the potential risk of adverse health effects in populations living in the vicinity of hazardous waste sites. 

The need for additional information on the relationship between barium exposure and levels of barium 

achieved in vivo is essential if such concentrations are to be used as biomonitors of exposure. 

Barium has been detected in the atmosphere (Bowen 1979; EPA 1984; Hildemann et al. 1991; IPCS 

1991; Schauer et al. 1999; Shahin et al. 2000; WHO 2001; Winkler 2002), surface water (Barnett et al. 

1969; Bowen 1979; DOI 1970; Durfor and Becker 1964; Durum and Haffty 1961; Elinder and Zenz 

1994; EPA 2005c; Kopp 1969; Longerich et al. 1991; McCabe et al. 1970; Neal et al. 1996; Saleh and 

Wilson 1999; Tuovinen et al. 1980), groundwater (Bruce and McMahon 1996; Calabrese 1977; Hudak 

and Wachal 2001; Kojola et al. 1978), soils (Bowen 1979; Bradley et al. 1994; EPA 1995a; KabataPendias and Pendias 1984; Lide 2005; Schroeder 1970; Shacklette and Boerngen 1984; Zenz et al. 1994), 

and foodstuffs (Beliles 1979; Connor and Shacklette 1975; Health Canada 2005; Schroeder 1970). There 

are reliable data to characterize the potential for human exposure via intake of drinking water (Durfor and 

Becker 1964; Hadjimarkos 1967; Thomas et al. 1999), and foods (Health Canada 2005; Tipton et al. 

1966, 1969). Recent data on barium levels in plants and ambient air, soils, and groundwater, particularly 

from hazardous waste sites, would be useful in helping to develop a more complete understanding of the 

potential for human exposure. 

Exposure Levels in Humans. Barium can be detected in blood, urine, feces, and biological tissues 

(CDC 2001, 2003; Mauras and Allain 1979; Schramel 1988; Shiraishi et al. 1987). However, there are no 

data correlating barium levels in tissues and fluids with exposure levels. Recent biomonitoring data exist 

for the U.S. general population (CDC 2005), although there are limited monitoring data for occupational 
BARIUM AND BARIUM COMPOUNDS 138 

6. POTENTIAL FOR HUMAN EXPOSURE 

exposure and for populations living near hazardous waste sites. This information is necessary for 

assessing the need to conduct health studies on these populations. 

Exposures of Children. Child health data needs relating to susceptibility are discussed in 

Section 3.12.2, Identification of Data Needs: Children’s Susceptibility. 

Data on the exposure of children in the United States to barium are very limited. It is expected that the 

largest exposure to barium will be through the diet. Therefore, market basket surveys or total diet studies 

similar to those conducted by the U.S. Food and Drug Administration would be useful for providing data 

on typical levels of exposure via dietary intake for children in the United States. Data are available for 

barium intake in Canadian children obtained from a 1993–1999 total diet study (Health Canada 2005) and 

in a separate study (Biego et al. 1998) in infants (3 months old) from the exclusive consumption of breast 

milk and other types of milk. 

Exposure Registries. No exposure registries for barium were located. This substance is not 

currently one of the compounds for which a sub-registry has been established in the National Exposure 

Registry. The substance will be considered in the future when chemical selection is made for subregistries to be established. The information that is amassed in the National Exposure Registry facilitates 

the epidemiological research needed to assess adverse health outcomes that may be related to exposure to 

this substance. 

6.8.2 Ongoing Studies 

Three ongoing studies concerning the fate/transport of barium and measurement of barium in 

environmental media were identified in the Federal Research in Progress database (FEDRIP 2005). 

These studies are summarized in Table 6-7. No other pertinent ongoing studies were identified. 
BARIUM AND BARIUM COMPOUNDS 139 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-7. Ongoing Studies on Environmental Fate and the Potential for Human 

Exposure to Barium and Barium Compounds 

Investigator Affiliation Research description Sponsor 

Batiza, R Oregon State University The proposed research will attempt to NSF 

quantify the cold seep barite contribution to 

the marine sediment record by first 

quantifying the cold seep barite (an 

important carrier of barium) contribution to 

barium and radon fluxes within the San 

Clemente basin and then, secondly, 

quantify the effects of this source on the 

chemical signature of barite in the basin 

sediments. 

Naehr, TM; Texas A&M University Acquisition of a basic powder x-ray NSF 

MacDonald, IR Corpus Christi difractometer system for qualitative and 

quantitative phase analysis in studies of 

(1) geologic materials to enhance research 

into the formation of diagenetic barite and 

silicate minerals in sediments from the 

Peruvian Continental Margin, (2) the 

authigenic seafloor deposits at sites of 

active submarine fluid expulsion in the Gulf 

of Mexico region to elucidate the geochemical environment at these sites, and 

(3) barium and other metals in soil and 

sediment samples. 

Odom, JW Auburn University Develop analytical techniques for total and Hatch 

plant-available forms of barium and other 

metals in soils and for total analysis of 

these metals in plant material; determine 

the normal occurrence of both total and 

extractable forms of these elements in 

selected soil profiles; and ascertain the 

availability of soil test calibration data and 

soil test procedures for these elements. 

NSF = National Science Foundation 

Source: FEDRIP 2005 
BARIUM AND BARIUM COMPOUNDS 140 

6. POTENTIAL FOR HUMAN EXPOSURE 

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BARIUM AND BARIUM COMPOUNDS 141 

7. ANALYTICAL METHODS 

The purpose of this chapter is to describe the analytical methods that are available for detecting, 

measuring, and/or monitoring barium, its metabolites, and other biomarkers of exposure and effect to 

barium. 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 

Inductively coupled plasma-atomic emission spectrometry (ICP-AES) has been used for measuring low 

levels of barium in the blood, urine, and bones of humans and animals (Mauras and Allain 1979; 

Schramel 1988; Shiraishi et al. 1987) (see Table 7-1). In general, biological samples are nebulized and 

the resulting aerosol is transported to the plasma torch. Atomic-line emission spectra are produced by the 

inductively coupled plasma for specific element and the intensities of the lines (bands) are monitored by a 

photomultiplier tube. A line emission at 455.50 nm was observed for barium (Mauras and Allain 1979; 

Oppenheimer et al. 1984). Detection limits of 0.25 μg barium/L of urine, 0.6 μg barium/L of blood, and 

0.0005 μg of barium per gram of bone were achieved (Mauras and Allain 1979; Shiraishi et al. 1987). 

Advantages of ICP-AES technique include moderate costs, fairly rapid analysis time, and high sensitivity 

(Mauras and Allain 1979; Oppenheimer et al. 1984). The presence of spectral interferences is a 

disadvantage of ICP-AES technique. These interferences are caused when a sample contains elements or 

compounds that have analytical emission lines (bands) that overlap the line chosen for the analyte. Boric 

acid or sodium borate (at a concentration of >100 mg boron/L of sample) was reported to interfere with 

the line emission spectra of barium at 455.50 nm (Mauras and Allain 1979). 

Neutron activation analysis (NAA) technique has also been used for determining low levels of barium in 

human blood (Olehy et al. 1966). This technique is based on the interaction of the nuclei of individual 

barium atoms with neutron irradiation, resulting in the emission of x-rays (photons). Detection limits of 

7 μg barium/L of erythrocyte and 66 μg barium/L of plasma were obtained (Olehy et al. 1966). The 

advantages of the NAA technique include minimal sample preparation and the fact that destruction of the 
BARIUM AND BARIUM COMPOUNDS 142 

7. ANALYTICAL METHODS 

Table 7-1. Analytical Methods for Determining Barium in Biological Materials 

Preparation Analytical Sample Percent 

Sample matrix method method detection limit recovery Reference 

Urine and blood Dilute sample with ICP-AES 0.25 μg/L (urine); 3–7% Mauras and 

demineralized water, 0.6 μg/L (blood) coefficient of Allain 1979 

introduce into the variation 

plasma and analyze 

Urine Dilute sample with ICP-AES 0.2 μg/L No data Schramel 

demineralized water, 1988 

introduce into the 

plasma and analyze 

Erythrocyte and Ash sample, digest NAA 7 μg/L 28.5% RSD Olehy et al. 

plasma with acid and (erythrocyte); (erythrocyte) 1966 

irradiate 66 μg/L (plasma) 7.6% RSD 

(plasma) 

Biological tissues Digest sample in Gravimetry No data No data Borchardt et 

acid; precipitate as al. 1961 

the sulfate and 

analyze 

Visceral materials Ash sample and AES No data 86.8–130.5% Baisane et al. 

(intestine, analyze 1979 

stomach, liver, 

spleen, and 

kidney) 

Fetus bones Ash sample and ICP-AES 0.0005 μg/g 0.5% RSD Shiraishi et al. 

digest with acid 1987 

AES = atomic emission spectroscopy; ICP-AES = inductively coupled plasma-atomic emission spectrometry; 

NAA = neutron activation analysis; RSD = relative standard deviation 
 

BARIUM AND BARIUM COMPOUNDS 143 

7. ANALYTICAL METHODS 

sample is not needed to conduct the analysis. Disadvantages of this technique include its high costs and a 

nuclear reactor may not be readily available to many laboratories. 

Gravimetric and spectrometric techniques have also been described for quantifying barium in tissues. 

Borchardt et al. (1961) measured barium in tissues gravimetrically following digestion of 15–20 grams of 

sample in a 2:1 (by volume) mixture of sulfuric and nitric acids. The barium in the samples was 

precipitated out as the sulfate, dried, and weighed. No limits of detection were given. Recovery of 

barium from acid-digested tissues can be impaired when organic ions react with barium and interfere with 

the formation of the barium sulfate precipitate. However, Borchardt et al. (1961) reported that no such 

interferences were observed in their assay and that complete recovery of barium from the sample was 

obtained. In another method, Baisane et al. (1979) used atomic emission spectroscopy to measure barium 

in visceral material. The method required ashing of tissue samples by heating with a burner or a muffle 

furnace and then fusing the ash with graphite and lithium carbonate. The barium in the fused ash was 

quantified by using an electric arc as an excitation source and monitoring the barium emission at 2,335 Å. 

Limits of detection were not given, but recoveries ranged from 86.8 to 130.5%. 

7.2 ENVIRONMENTAL SAMPLES 

Atomic absorption spectroscopy (AAS) is the most prevalent analytical technique for measuring low 

levels of barium in air, water, waste water, geological materials (calcium carbonate), unused lubricating 

oil, and diagnostic meals containing barium sulfate (see Table 7-2). 

Samples may be prepared for AAS in a variety of ways (EPA 1974, 1994a, 1994b, 1996; Hui-Ming and 

Yao-Han 1984; Johnson et al. 1983; Murata and Noguchi 1974; Pierce and Brown 1977; Renshaw 1973; 

Sharp and Knevel 1971; Sugiyama et al. 1984). Acid digestion with nitric acid is the most common 

method of preparation. Sample dilution with nitric acid or other agents to solubilize barium from the 

matrix can also be employed. If the concentration of barium in the dissolved sample is very low, 

preconcentration techniques such as chelation or extraction may be employed. 

Flame atomic absorption spectroscopy (FAAS) (Methods 208.1 and 7080) and graphite furnace atomic 

absorption spectroscopy (GFAAS) (Methods 208.2 and 7081) are the techniques recommended by the 

Office of Solid Waste and Emergency Response of EPA for determining ppb (μg/L) levels of barium in 

water and waste water (EPA 1974, 1979, 1992, 1994a, 1994b). Parts-per-trillion (sub μg/L) levels of 

barium in seawater and freshwater have been detected by GFAAS (Epstein and Zander 1979; Roe and Froelich 
BARIUM AND BARIUM COMPOUNDS 144 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining Barium in Environmental Samples 

Sample Analytical Sample Percent 

matrix Preparation method method detection limit recovery Reference 

Air Collect sample on FAAS 2 μg per sample 102% NIOSH 1994 

cellulose membrane and (Method 7056) 

extract with hot acid; 

evaporate extract to 

dryness and dissolve 

residue in acid 

Air Collect sample on ICP-AES 0.005 μg per 97.7– NIOSH 2003 

cellulose or PVC sample 102.4% (Method 7300) 

membrane; extract with 

hot acid and evaporate at 

150 °C to near dryness; 

dissolve residue in acid 

Water Reflux with addition of ICP-MS 0.8 μg/L 95% EPA 1994a 

HNO3 and HCl; filter (Method 200.8) 

Reflux with addition of ICP-AES 1 μg/L 92% EPA 1994b 

HNO3 and HCl; filter (Method 200.7) 

Acidify with HNO3; filter FAAS 100 μg/L 94% EPA 1974 

(Method 208.1) 

Reflux with addition of FAAS 33.5–132 μg/L 104.5– ASTM 2000 

HNO3 and HCl (working range) 106.9% (Method D4382) 

(33.5 μg/L) 

Acidify sample and pass FAAS 3 μg/L 11.6% Pierce and 

through ion-exchange RSD Brown 1977 

resin 

Pass sample through ion- FAES μg/L levels No data Johnson et al. 

exchange resin 1983 

Extract sample with FAAS 5 μg/L No data Edelbeck and 

buffered HFA solution West 1970 

 No data GFAAS 7 μg/L 90–110% Fagioli et al. 

1988 

Inject sample directly into GFAAS 0.6 μg/L 13% RSD Roe and 

graphite furnace (seawater); Froelich 1984 

0.2 μg/L 

(freshwater) 

Seawater and Acidify and inject DCAP-AES 10–20 mg/L 108.8% ASTM 1999 

brackish (working range) (10 mg/L) (Method D3986) 

water 

Water and Digest sample and FAAS, 100 μg/L (FAAS); 94–113% EPA 1974, 

waste water evaporate to dryness; GFAAS 2 μg/L (GFAAS) (FAAS); 1979, 1992, 

dissolve residue in acid 96–102% 1994 (Methods 

(GFAAS) 208.1, 208.2, 

7080, and 7081) 

Industrial Digest sample; mix with XFS 290 μg/L (in 5.1% RSD Murata and 

waste water cation-exchange resin; 500 mL samples) Noguchi 1974 

dry and analyze 
BARIUM AND BARIUM COMPOUNDS 145 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining Barium in Environmental Samples 

Sample Analytical Sample Percent 

matrix Preparation method method detection limit recovery Reference 

Unused Dissolve sample in FAAS No data No data Holding and 

lubricating oil 2-methyl- Rowson 1975 

propan-2-ol:toluene (3:2); 

add potassium 

naphthenate solution 

Rocks and Precipitate barium from FAAS Low μg/g levels 118% Bano 1973 

minerals sample; dissolve in 

(calcium ammoniacal solution of 

carbonate) EDTA 

Soil Digest sample in HNO3 GFAAS 0.2 μg/g dry 96% EPA 1978, 1996 

and H2O2, filter, dilute with weight (Methods 3050B 

acid and 208.2) 

Sediment, Digest sample in a ICP-MS 0.15 ppm 96–102% USGS 2002a 

soil, rocks mixture of HCl, HNO3, and (Method T20) 

HClO4 by heating to 

dryness; resuspend 

residue in HNO3 and H2O2 

and heat; cool and dilute 

in 1% HNO3 

Sediment, Digest sample in a ICP-AES 0.3 ppm 95–106% USGS 2002b 

rocks, plants mixture of HF, HNO3, and (Methods E011 

HClO4 by heating to and T01) 

dryness; resuspend 

residue in HClO4 and heat 

to dryness; resuspend in 

aqua regia, dilute with 

1% HNO3, and reheat 

Food, Homogenize sample; ICP-AES 0.03 mg/kg (food) 86–94% EPA 1995b 

beverage microwave digestion of 0.004 mg/kg (food) 

sample in HNO3; (beverage) 86–92% 

centrifuge (beverage) 

Diagnostic Add sample to EDTA FAAS No data 98.6– Sharp and 

meals solution and warm 102.5% Knevel 1971 

containing 

barium sulfate 

Compound Prepare solution of Scintillation No data No data Larsen 1973 

formulation 

(Ba14CO3

) 

sample in EDTA and 

count 

spectrometry 

Ba14CO3 = radiolabeled barium carbonate; DCAP-AES = direct-current argon plasma-atomic emission spectroscopy; 

EDTA = ethylenediamine tetraacetic acid; FAAS = flame atomic absorption spectroscopy; FAES = flame atomic 

emission spectroscopy; GFAAS = graphite furnace atomic absorption spectroscopy; HCl = hydrochloric acid; 

HClO4 = perchloric acid; HF = hydrofluoric acid; HFA = hexafluoroacetylacetone; HNO3 = nitric acid; 

H2O2 = hydrogen peroxide; ICP-AES = inductively coupled plasma-atomic emission spectroscopy; 

ICP-MS = inductively coupled plasma-mass spectrometry; PVC = polyvinyl chloride; RSD = relative standard 

deviation; XFS = x-ray fluorescence spectroscopy
 
BARIUM AND BARIUM COMPOUNDS 146 

7. ANALYTICAL METHODS 

1984). The advantages that GFAAS and FAAS techniques offer are that they are sensitive techniques, 

use relatively simple and inexpensive instrumentation, and have high accuracy and precision. In addition, 

GFAAS technique requires a small amount of sample and is more sensitive than FAAS methodology for 

determining barium in aqueous media (Edelbeck and West 1970; Oppenheimer et al. 1984). 

FAAS (Method 7056) is the technique recommended by NIOSH for detecting soluble barium compounds 

in air (NIOSH 1994). AAS has also been employed for detecting barium in air at 20 ppb (Miner 1969a). 

Other analytical techniques that have been employed for measuring barium and its compounds in 

environmental media include x-ray fluorescence spectroscopy (XFS), neutron activation analysis (NAA), 

direct current argon plasma-atomic emission spectroscopy (DCAP-AES), inductively coupled plasmamass spectrometry (ICP-MS), inductively coupled plasma-atomic emission spectroscopy (ICP-AES), 

scintillation spectroscopy, and spectrography (Boothe and James 1985; Landis and Coons 1954; Larsen 

1973; Murata and Noguchi 1974; Oppenheimer et al. 1984). XFS and NAA methods are less sensitive 

than other available analytical methods for measuring barium in environmental media. Scintillation 

spectroscopy and spectrography are less commonly used to measure barium in the environment relative to 

other analytical methods. ICP-MS and ICP-AES offer low detection sensitivities that are typically at the 

ppb level and are becoming more routinely used for analysis of samples with complex mixtures of metals 

and metal complexes. For example, ICP-AES (Method 7300) is a technique recommended by NIOSH for 

analyzing soluble barium compounds in air with a limit of detection of 0.005 μg per sample 

(approximately 0.005 μg/m3

), which is 400 times less than the detection limit for another NIOSH method 

(7056) that uses FAAS as the technique to quantify barium in air (NIOSH 1994, 2003). ICP-AES 

(Methods E011 and T01) and ICP-MS (Method T20) are recommended by the U.S. Geological Survey 

(USGS) for measuring the barium content in sediments and rocks (USGS 2002a, 2002b). ICP-AES is 

also used to quantify barium and other trace metals in food and beverages with minimum detection limits 

of 0.004–0.3 mg/kg (ppm) and recoveries of 86–94% (EPA 1995b). ICP-MS is a useful technique for 

isotopic analysis of barium to determine sources of environmental emissions of barium compounds. 

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 barium is available. Where adequate information is not 

available, ATSDR, in conjunction with NTP, is required to assure the initiation of a program of research 
BARIUM AND BARIUM COMPOUNDS 147 

7. ANALYTICAL METHODS 

designed to determine the health effects (and techniques for developing methods to determine such health 

effects) of barium. 

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. 

Exposure. Several methods are available for measuring biomarkers of exposure. ICP-AES is the 

analytical method used for measuring barium in blood, urine and bone of humans and animals at ppt (sub 

μg/L) levels (Mauras and Allain 1979; Schramel 1988; Shiraishi et al. 1987). NAA technique has also 

been employed for measuring barium in blood of humans and animals at ppb (μg/L) levels (Olehy et al. 

1966). These techniques are sensitive for measuring background levels of barium in the population. 

However, information is needed on whether data collected using these techniques can be used to correlate 

the levels of barium in biological tissues and fluids with exposure levels. 

Effect. At present, no biomarkers of effect are available for barium. There are no data to indicate 

whether a biomarker, if available, would be preferred over chemical analysis for monitoring effects from 

long- and short-term exposure to barium. 

Methods for Determining Parent Compounds and Degradation Products in Environmental 

Media. GFAAS and FAAS are the most widely used analytical techniques for measuring barium and 

its compounds in air (NIOSH 1987), water (ASTM 2000; Edelbeck and West 1970; EPA 1974, 1994a, 

1994b; Fagioli et al. 1988; Johnson et al. 1983; Pierce and Brown 1977; Roe and Froelich 1984), seawater 

and brackish water (ASTM 1999), waste water (EPA 1974, 1979, 1992, 1994b), rocks and minerals 

(Bano 1973), unused lubricating oil (Holding and Rowson 1975), soil (EPA 1978, 1996), and diagnostic 

meals (Sharp and Knevel 1971). The media of most concern for potential human exposure to barium is 

water. GFAAS and FAAS techniques are sensitive for measuring background levels of barium in 

aqueous media (Epstein and Zander 1979; Roe and Froelich 1984). However, it is not known whether 
 

BARIUM AND BARIUM COMPOUNDS 148 

7. ANALYTICAL METHODS 

these techniques are sensitive for measuring levels of barium at which health effects might begin to occur. 

FAAS and GFAAS are the methods (Methods 208.1, 208.2, 7080, and 7081) recommended by EPA for 

detecting ppb levels of barium in water and waste water (EPA 1974, 1979, 1992, 1994c). GFAAS has 

also been employed to detect ppt levels of barium in aqueous media (Epstein and Zander 1979; Roe and 

Froelich 1984). ICP-MS and ICP-AES quantitative methods are increasing in use for routine analysis of 

barium at ppb levels and are capable of ppt levels of detection when ion chromatographic and other 

prepurification methods are used in sample preparation and analysis. Therefore, analytical methods are 

available that are sufficiently specific and sensitive to measure barium in the environment, and no data 

needs have been identified at this time. 

7.3.2 Ongoing Studies 

No ongoing studies regarding techniques for measuring and determining barium in biological and 

environmental samples were located. 
BARIUM AND BARIUM COMPOUNDS 149 

8. REGULATIONS AND ADVISORIES 

The international and national regulations and guidelines regarding barium and barium compounds in air, 

water, and other media are summarized in Table 8-1. 

ATSDR has derived an intermediate-duration oral MRL of 0.2 mg barium/kg/day for barium. This MRL 

is based on a NOAEL of 65 mg barium/kg/day and a LOAEL of 115 mg barium/kg/day for increased 

kidney weight in female rats (NTP 1994) and an uncertainty factor of 100 (10 to account for animal to 

human extrapolation, and 10 for human variability) and modifying factor of 3 to account for the lack of an 

adequate developmental toxicity study 

ATSDR has derived a chronic-duration oral MRL of 0.2 mg barium/kg/day for barium. The MRL is 

based on a BMDL05 of 61 mg barium/kg/day for nephropathy in male mice (NTP 1994) and an 

uncertainty factor of 100 (10 to account for animal to human extrapolation and 10 for human variability) 

and modifying factor of 3 to account for the lack of an adequate developmental toxicity study. 

EPA (IRIS 2006) has derived an oral reference dose (RfD) for barium of 0.2 mg/kg/day, based on a 

BMDL05 of 63 mg/kg/day for nephropathy in male mice (NTP 1994) and an uncertainty factor of 300 

(10 to account for animal to human extrapolation, 10 for human variability, and 3 for database 

deficiencies, particularly the lack of a two-generation reproductive toxicity study and an adequate 

investigation of developmental toxicity). EPA (IRIS 2006) has not recommended an inhalation reference 

concentration (RfC) for barium at this time. 

Using their 1986 guidelines, EPA has determined that barium is not classifiable as a human carcinogen 

and has assigned it the cancer classification, Group D (IRIS 2006). Using their recent guidelines, EPA 

determined that barium is considered not likely to be carcinogenic to humans following oral exposure and 

its carcinogenic potential cannot be determined following inhalation exposure (IRIS 2006). 
BARIUM AND BARIUM COMPOUNDS 150 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Barium and 

Barium Compounds 

Agency Description Information Reference 

INTERNATIONAL 

Guidelines: 

IARC Carcinogenicity classification No data IARC 2004 

WHO Air quality guidelines No data WHO 2000 

Drinking water quality guidelines 0.7 mg/L WHO 2004 

NATIONAL 

Regulations and Guidelines: 

a. Air 

ACGIH TLV (TWA) ACGIH 2004 

Barium and soluble compounds 0.5 mg/m3
 

(as Ba) 

Barium sulfate 10 mg/m3
 

NIOSH REL (TWA) NIOSH 2005a, 

Barium chloridea

 0.5 mg/m3 2005b 

Barium sulfate 10 mg/m3

 (total) 

5.0 mg/m3

 (respiratory) 

IDLH
 

Barium chloride 50 mg/m3
 

Barium sulfate No data 

OSHA PEL (8-hour TWA) for general industry OSHA 2005c 

Barium, soluble compounds (as Ba) 0.5 mg/m3 29 CFR 1910.1000 

Barium sulfate 15 mg/m3

 (total dust) 

5.0 mg/m3

 (respirable 

fraction) 

PEL (8-hour TWA) for construction OSHA 2005b 

industry 29 CFR 1926.55 

Barium, soluble compounds (as Ba) 0.5 mg/m3 

PEL (8-hour TWA) for shipyard OSHA 2005a 

industry 29 CFR 1915.1000 

Barium, soluble compounds (as Ba) 0.5 mg/m3 

Barium sulfate 15 mg/m3

 (total dust) 

5.0 mg/m3

 (respirable 

fraction) 

b. Water 

EPA Drinking water standards and health EPA 2004 

advisories 

1-day health advisory for a 10-kg 0.7 mg/L 

child 

10-day health advisory for a 10-kg 0.7 mg/L 

child 
BARIUM AND BARIUM COMPOUNDS 151 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Barium and 

Barium Compounds 

Agency Description Information Reference 

NATIONAL (cont.) 

National primary drinking water EPA 2002a 

standards
 

MCLG 2.0 mg/L 

MCL 2.0 mg/L 

Reportable quantities of hazardous 10 pounds EPA 2005b 

substances (barium cyanide) 40 CFR 117.3 

designated pursuant to Section 311 of 

the Clean Water Act 

Water quality criteria for human health EPA 2002b 

consumption of: 

Water + organism 1.0 mg/L 

Organism only No data 

c. Food 

FDA Bottled drinking water 2.0 mg/L FDA 2004 

21 CFR 165.110 

d. Other 

 ACGIH Carcinogenicity classification A4b

 ACGIH 2004

 EPA Carcinogenicity classification Group Dc IRIS 2006 

RfC Not recommended at this 

time 

RfD 0.2 mg/kg/day 

NTP Carcinogenicity classification No data NTP 2005 

a

The REL also applies to other soluble barium compounds (as Ba) except barium sulfate. b

A4: not classifiable as a human carcinogen 

c

Group D: not classifiable as to human carcinogenicity 

ACGIH = American Conference of Governmental Industrial Hygienists; CFR = Code of Federal Regulations; 

DWEL = drinking water equivalent level; EPA = Environmental Protection Agency; FDA = Food and Drug 

Administration; IARC = International Agency for Research on Cancer; IDLH = immediately dangerous to life or health; 

MCL = maximum contaminant level; MCLG = maximum contaminant level goal; NIOSH = National Institute for 

Occupational Safety and Health; NTP = National Toxicology Program; OSHA = Occupational Safety and Health 

Administration; PEL = permissible exposure limit; REL = recommended exposure limit; RfC = inhalation reference 

concentration; RfD = oral reference dose; TLV = threshold limit values; TWA = time-weighted average; WHO = World 

Health Organization 
BARIUM AND BARIUM COMPOUNDS 152 

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BARIUM AND BARIUM COMPOUNDS 153 

9. REFERENCES 

ACGIH. 2004. Threshold limit values for chemical substances and physical agents and biological 

exposure indices. Cincinnati, OH: American Conference of Governmental Industrial Hygienists. 

Adinolfi M. 1985. The development of the human blood-CSF-brain barrier. Dev Med Child Neurol 

27:532-537. 

Adlercreutz H. 1995. Phytoestrogens: Epidemiology and a possible role in cancer protection. Environ 

Health Perspect Suppl 103(7):103-112. 

Agency for Toxic Substances and Disease Registry. 1989. Decision guide for identifying substancespecific data needs related to toxicological profiles; Notice. Atlanta, GA: Agency for Toxic Substances 

and Disease Registry, Division of Toxicology. Fed Regist 54(174):37618-37634. 

Agency for Toxic Substances and Disease Registry. 1990a. Health assessment for Tex Tin Corporation, 

National Priorities List Site, Texas City, Texas, Region 6. CERCLIS No. TXD062113329. Atlanta, GA: 

Agency for Toxic Substances and Disease Registry. PB90250440. 

Agency for Toxic Substances and Disease Registry. 1990b. Biomarkers of organ damage or dysfunction 

for the renal, hepatobiliary, and immune systems. Subcommittee on Biomarkers of Organ Damage and 

Dysfunction. Atlanta, GA: Agency for Toxic Substances and Disease Registry. 

Alimonti A, Forte G, Spezia S, et al. 2005. Uncertainty of inductively coupled plasma mass 

spectrometry based measurements: An application to the analysis of urinary barium, cesium, antimony, 

and tungsten. Rapid Comm Mass Spectrom 19:3131-3138. 

Alcalde AI, Ilundain A. 1988. The effect of BaCl2 on intestinal sugar transport in the rat in vitro. Rev 

Esp Fisiol 44:147-150. 

Altman PL, Dittmer DS. 1974. Biological handbooks: Biology data book. Vol. III. 2nd ed. Bethesda, 

MD: Federation of American Societies for Experimental Biology, 1987-2008, 2041. 

Andersen ME, Krishnan K. 1994. Relating in vitro to in vivo exposures with physiologically based tissue 

dosimetry and tissue response models. In: Salem H, ed. Animal test alternatives: Refinement, 

reduction, replacement. New York: Marcel Dekker, Inc., 9-25. 

Andersen ME, Clewell HJ III, Gargas ML, et al. 1987. Physiologically based pharmacokinetics and the 

risk assessment process for methylene chloride. Toxicol Appl Pharmacol 87:185-205. 

Antonio A, Rocha e Silva M, Yashuda Y. 1973. The tachyphylactic effect of barium on intestinal 

smooth muscle. Arch Int Pharmacodyn Ther 204:260-267. 

Aruguete DM, Aldstadt JH III, Mueller GM. 1998. Accumulation of several heavy metals and 

lanthanides in mushrooms (Agaricales) from the Chicago region. Sci Total Environ 224:43-56. 

*Not cited in text 
BARIUM AND BARIUM COMPOUNDS 154 

9. REFERENCES 

ASTM. 1999. Standard test method for barium in brines, seawater, and brackish water by direct-current 

argon plasma atomic emission spectroscopy. Annual Book of ASTM Standards. West Conshohocken, 

PA: American Society for Testing and Materials, 395-397. 

ASTM. 2000. Standard test method for barium in water, atomic absorption spectrophotometry, graphite 

furnace. Annual book of ASTM standards. West Conshohocken, PA: American Society for Testing and 

Materials, 432-434. 

Ault B, Evans RH, Francis AA, et al. 1980. Selective depression of excitatory amino-acid induced 

depolarizations by magnesium ions in isolated spinal cord preparations. J Physiol 307:413-428. 

Ayre JE. 1966. Human cell-dysplasia following barium. Ind Med Surg 35:393-399. 

Bahlmann H, Lindwall R, Persson H. 2005. Acute barium nitrate intoxication treated by hemodialysis. 

Acta Anaesthesiol Scand 49:110-112. 

Baisane SO, Chincholkar VS, Mattoo BN. 1979. Spectrographic determination of barium in biological 

material. Forensic Sci Int 12:127-129. 

Bano FJ. 1973. The determination of trace amounts of barium in calcium carbonate by atomicabsorption spectrophotometry. Analyst 98:655-658. 

Barnes DG, Dourson M. 1988. Reference dose (RfD): Description and use in health risk assessments. 

Regul Toxicol Pharmacol 8(4):471-486. 

Barnett PR, Skougstad MW, Miller KJ. 1969. Chemical characterization of a public water supply. J Am 

Water Works Assoc 61:61-67. 

Bates MH. 1988. Land farming of reserve pit fluids and sludges: Fates of selected contaminants. Water 

Res 22:793-797. 

Bauer GCH, Carlsson A, Lindquist B. 1956. A comparative study on the metabolism of 140Ba and 45Ca 

in rats. Biochem J 63:535-542. 

Bauer GCH, Carlsson A, Lindquist B. 1957. Metabolism of 140Ba in man. Acta Orthop Scand 26:241­

254. 

Beliles RP. 1979. The lesser metals. In: Oehme FW, ed. Hazardous and toxic substances. Vol. 2. 

Toxicity of heavy metals in the environment. Parts 1 and 2. New York, NY: Marcel Dekker, Inc., 547­

615. 

Benes P, Sebesta F, Sedlacek J, et al. 1983. Particulate forms of radium and barium in uranium mine 

waste waters and receiving river waters. Water Res 17:619-624. 

Berger GS. 1994. Epidemiology of endometriosis. In: Berger GS, ed. Endometriosis: Advanced 

management and surgical techniques. New York, NY: Springer-Verlag, 3-7. 

Berggren PO, Andersson T, Hellman B. 1983. The interaction between barium and calcium in β-cellrich pancreatic islets. Biomed Res 4:129-137. 
BARIUM AND BARIUM COMPOUNDS 155 

9. REFERENCES 

Biego GH, Joyeux M, Hartemann P, et al. 1998. Determination of mineral contents in different kinds of 

milk and estimation of dietary intake in infants. Food Addit Contam 15(7):775-781. 

Birmili W, Allen AG, Bary F, et al. 2006. Trace metal concentrations and water solubility in sizefractionated atmospheric particles and influence of road traffic. Environ Sci Technol 40:1144-1153. 

Bodek I, Lyman WJ, Reehl WF, et al, eds. 1988. Environmental inorganic chemistry: Properties, 

processes, and estimation methods. New York, NY: Pergamon Press, 7.3.1-7.3-4, B2-B7, B11-B13, 

B17-B18. 

Boffito C. 2002. Barium. In: Kirk-Othmer encyclopedia of chemical technology. John Wiley & Sons. 

Boothe PN, James WD. 1985. Neutron activation analysis of barium in marine sediments from the north 

central Gulf of Mexico. J Trace Microprobe Tech 3:377-399. 

Borchardt P, Dindial W, Mettenleiter M. 1961. A rapid semimicromethod for the determination of 

phosphorus and barium in biologic preparations. Clin Chem 7:264-267. 

Borzelleca JF, Condie LW Jr, Egle JL Jr. 1988. Short-term toxicity (one- and ten-day gavage) of barium 

chloride in male and female rats. J Am Coll Toxicol 7:675-685. 

Boullin DJ. 1965. Effect of divalent ions on release of 3

H-noradrenaline by sympathetic nerve 

stimulation. J Physiol 183:76P-77P. 

Boullin DJ. 1967. The action of extracellular cations on the release of the sympathetic transmitter from 

peripheral nerves. J Physiol 189:85-99. 

Bowen HJM, ed. 1966. Trace elements in biochemistry. New York, NY: Academic Press, Inc., 16, 19, 

31, 39, 68, 70, 72, 75-76, 81, 84, 105, 129, 140, 151, 176, 

Bowen HJM. 1979. Environmental chemistry of the elements. New York, NY: Academic Press, Inc. 

Boyd EM, Abel M. 1966. The acute toxicity of barium sulfate administered intragastrically. Can Med 

Assoc J 94:849-853. 

Bradley LJ, Magee BH, Allen SL. 1994. Background levels of polycyclic aromatic hydrocarbons (PAH) 

and selected metals in New England urban soils. J Soil Contam 3:349-361. 

Brenniman GR, Levy PS. 1985. Epidemiological study of barium in Illinois drinking water supplies. In: 

Calabrese EJ, Tuthill RW, Condie L, eds. Inorganics in water and cardiovascular disease. Princeton, NJ: 

Princeton Scientific Publishing Co., 231-240. 

Brenniman GR, Kojola WH, Levy PS, et al. 1979a. Health effects of human exposure to barium in 

drinking water. Cincinnati, Ohio: U.S. Environmental Protection Agency, Office of Research and 

Development, Health Effects Research Laboratory. EPA600179003. PB292268. 

Brenniman GR, Kojola WH, Levy PS, et al. 1981. High barium levels in public drinking water and its 

association with elevated blood pressure. Arch Environ Health 36:28-32. 

Brenniman GR, Namekata T, Kojola WH, et al. 1979b. Cardiovascular disease death rates in 

communities with elevated levels of barium in drinking water. Environ Res 20:318-324. 
BARIUM AND BARIUM COMPOUNDS 156 

9. REFERENCES 

Breuing EP, Kaminskas R, Kobashi YL, et al. 1987. Effects of sodium and calcium concentrations on 

the barium chloride-induced electrical and contractile responses of the guinea-pig vas deferens. Braz J 

Med Biol Res 20:231-242. 

Bronstein AC, Currance PL, eds. 1988. Emergency care for hazardous materials exposure. St. Louis, 

MO: CV Mosby Company, 66, 127-128. 

Bruce BW, McMahon PB. 1996. Shallow ground-water quality beneath a major urban center: Denver, 

Colorado, USA. J Hydrol 186:129-151. 

Budavari S, O'Neil MJ, Smith A, et al., eds. 2001. Barium. The Merck index: An encyclopedia of 

chemicals, drugs, and biologicals. Whitehouse Station, NJ: Merck and Co., Inc, 168-172. 

Butte W, Heinzow B. 2002. Pollutants in house dust as indicators of indoor contamination. Rev Environ 

Contam Toxicol 175:1-46. 

Calabrese EJ. 1977. Excessive barium and radium-226 in Illinois drinking water. J Environ Health 

39:366-369. 

CDC. 2001. National report on human exposure to environmental chemicals. Atlanta, GA: Centers for 

Disease Control and Prevention. 

CDC. 2003. Second national report on human exposure to environmental chemicals. Atlanta, GA: 

Department of Health and Human Services, Centers for Disease Control and Prevention. NCEH Pub. No. 

02-0716. 

CDC. 2005. Third national report on human exposure to environmental chemicals. Atlanta, GA: 

Department of Health and Human Services, Centers for Disease Control and Prevention. NCEH Pub. No. 

05-0570. 

Cember H, Watson JA, Novak ME. 1961. The influence of radioactivity and lung burden on the 

pulmonary clearance rate of barium sulfate. Am Ind Hyg Assoc J 22:27-32. 

ChemIDplus. 2007. ChemIDplus. Bethesda, MD: U.S. National Library of Medicine. 

http://sis.nlm.nih.gov/chemical.html. May 11, 2007. 

CHRIS Manual. 2005. Barium. Chemical Hazards Response Information System. 

http://www.chrismanual.com/findform.idc. May 20, 2005. 

Chou C, Chin YC. 1943. The absorption, fate and concentration in serum of barium in acute 

experimental poisoning. Chinese Med J 61:313-322. 

Chow TJ, Earl JL, Reed JH, et al. 1978. Barium content of marine sediments near drilling sites: A 

potential pollutant indicator. Mar Pollut Bull 9:97-99. 

Clement JG. 1981. BaCl2-induced contractions in the guinea pig ileum longitudinal muscle: Role of 

presynaptic release of neurotransmitters and Ca2+ translocation in the postsynaptic membrane. Can J 

Physiol Pharmacol 59:541-547. 
BARIUM AND BARIUM COMPOUNDS 157 

9. REFERENCES 

Clewell HJ III, Andersen ME. 1985. Risk assessment extrapolations and physiological modeling. 

Toxicol Ind Health 1(4):111-131. 

Connor JJ, Shacklette HT. 1975. Background geochemistry of some rocks, soils, plants, and vegetables 

in the conterminous United States. U.S. Geological Survey Professional Paper. Washington, DC: U.S. 

Government Printing Office. 574-F. 

Cove JKJ, Snyder RN. 1974. Fatal barium intravasation during barium enema. Radiology 112:9-10. 

Cuddihy RG, Griffith WC. 1972. A biological model describing tissue distribution and whole-body 

retention of barium and lanthanum in beagle dogs after inhalation and gavage. Health Phys 23:621-633. 

Cuddihy RG, Ozog JA. 1973b. Nasal absorption of CsCl, SrCl2, BaCl2 and CeCl3 in Syrian hamsters. 

Health Phys 25:219-224. 

Cuddihy RG, Hall RP, Griffith WC. 1974. Inhalation exposures to barium aerosols: Physical, chemical, 

and mathematical analysis. Health Phys 26:405-416. 

Cullen RT, Tran CL, Buchanan D, et al. 2000. Inhalation of poorly soluble particles. I. Differences in 

inflammatory response and clearance during exposure. Inhal Toxicol 12:1089-1111. 

Dailey R, Raisbeck MF, Siemion R, et al. 2005. Trace metals in Wyoming fish. Bull Environ Contam 

Toxicol 74:1078-1083. 

Das NC, Singh V. 1970. Unusual type of cardiac arrest: Case report. Armed Forces Med J India 

26:344-352. 

Davis WE. 1972. National inventory of sources and emissions. Barium, boron, copper, selenium, and 

zinc 1969 - Barium section 1. Research Triangle Park, NC: U.S. Environmental Protection Agency, 

Office of Air Programs. Contract #68020100. PB210676. 

Delfino G, Amerini S, Mugelli A. 1988. Barium cardiotoxicity: Relationship between ultrastructural 

damage and mechanical effects. Toxicol In Vitro 2:49-55. 

Dencker L, Nilsson A, Ronnback C, et al. 1976. Uptake and retention of 133Ba and 133Ba-140La in mouse 

tissues. Acta Radiol 15:273-287. 

Deng JF, Jan IS, Cheng HS. 1991. The essential role of a poison center in handling an outbreak of 

barium carbonate poisoning. Vet Hum Toxicol 33(2):173-175. 

de Zwart IM, Griffioen G, Shaw MP, et al. 2001. Barium enema and endoscopy for the detection of 

colorectal neoplasia: Sensitivity, specificity, complications and its determinants. Clin Radiol 56(5):401­

409. 

Dibello PM, Manganaro JL, Aguinaldo ER, et al. 2003. Barium compounds: Barium sulfide. In: KirkOthmer encyclopedia of chemical technology. John Wiley & Sons, Inc., 1-3. 

Diengott D, Rozsa O, Levy N, et al. 1964. Hypokalemia in barium poisoning. Lancet 2:343-344. 

Dietz DD, Elwell MR, Davis WE, et al. 1992. Subchronic toxicity of barium chloride dihydrate 

administered to rats and mice in the drinking water. Fundam Appl Toxicol 19:527-537. 
BARIUM AND BARIUM COMPOUNDS 158 

9. REFERENCES 

DOE. 1984. A review and analysis of parameters for assessing transport of environmentally released 

radionucleotides through agriculture. Oak Ridge, TN: U.S. Department of Energy by Oak Ridge 

National Laboratory, ORNL-5786. 

DOI. 1970. Trace metals in waters of the United States. A five-year summary of trace metals in rivers 

and lakes of the United States (Oct 1, 1962-Sept 30, 1967). Cincinnati, OH: U.S. Department of Interior, 

Federal Water Pollution Control Administration, Division of Pollution Surveillance. 

Doig AT. 1976. Baritosis: A benign pneumoconiosis. Thorax 31:30-39. 

Domanski T, Trojanowska B. 1980. Studies on metabolic kinetics of lead and alkaline earth elements 

(Ca, Ba). Acta Physiol Pol 31:439-447. 

Domanski T, Liniecki J, Witkowska D. 1969. Kinetics of calcium, strontium, barium, and radium in rats. 

In: Mays CW, Jee WSS, Lloyd RD, et al., eds. Delayed effects of bone-seeking radionuclides. Salt Lake 

City, UT: University of Utah Press, 79-94. 

DOT. 2004. Emergency response guidebook. Department of Transportation, Office of Hazardous 

Materials Safety. http://hazmat.dot.gov/pubs/erg/psn_b.htm. May 20, 2005. 

Douglas WW, Rubin RP. 1964a. The effects of alkaline earths and other divalent cations on adrenal 

medullary secretion. J Physiol 175:231-241. 

Doull J, Klaassen CD, Amdur MD, eds. 1980. Casarett and Doull's toxicology. 2nd ed. New York, NY: 

MacMillan Publishing Co., 438, 466. 

Downs JCU, Milling D, Nichols CA. 1995. Suicidal ingestion of barium-sulfide-containing shaving 

powder. Am J Forensic Med Pathol 16(1):56-61. 

Dreisbach RH, Robertson WO, eds. 1987. Handbook of poisoning: Prevention, diagnosis & treatment. 

12th ed. Norwalk, CT: Appleton & Lange, 119-120. 

Durfor CN, Becker E. 1964. Public water supplies of the 100 largest cities in the United States, 1962. 

U.S. Department of the Interior, U.S. Geological Survey. Washington, DC: U.S. Government Printing 

Office. Water-Supply 1812. 

Durum WH, Haffty J. 1961. Occurrence of minor elements in water. Washington, DC: U.S. 

Department of the Interior, U.S. Geological Survey:1-11. 

Ebeigbe AB, Aloamaka CP. 1987. Mechanism of contractile action of barium ion on rat aortic smooth 

muscle. Can J Physiol Pharmacol 65:2454-2458. 

Edel J, Di Nucci A, Sabbioni E, et al. 1991. Biliary excretion of barium in the rat. Biol Trace Elem Res 

30:267-276. 

Edelbeck L, West PW. 1970. Determination of trace concentrations of barium extracted from aqueous 

systems. Anal Chim Acta 52:447-453. 
BARIUM AND BARIUM COMPOUNDS 159 

9. REFERENCES 

Ehara T, Inazawa M. 1980. Calcium-dependent slow action potentials in potassium-depolarized guineapig ventricular myocardium enhanced by barium ion. Naunyn-Schmiedebergs Arch Pharmacol 315:47­

54. 

Elinder C-G, Zenz C. 1994. Other metals and their compounds. Occup Med 46:595-616. 

Ellenhorn MJ, Barceloux G, eds. 1988. Medical toxicology: Diagnosis and treatment of human 

poisoning. New York, NY: Elsevier, 1017. 

Ellsasser JC, Farnham JE, Marshall JH. 1969. Comparative kinetics and autoradiography of 45Ca and 

133Ba in ten-year-old beagle dogs. J Bone Joint Surg 51A:1397-1412. 

Elwood PC, Abernethy M, Morton M. 1974. Mortality in adults and trace elements in water. Lancet 

1470-1472. 

EPA. 1974. Method 208.1. National Environmental Methods Index. U.S. Environmental Protection 

Agency. http://www.epa.gov/nerl/. April 01, 2005. 

EPA. 1978. Method 208.2. Barium (AA, furnace technique) Washington, DC: U.S. Environmental 

Protection Agency. Code of Federal Regulations. 40 CFR 116.4. 

EPA. 1979. Method 208.2. Atomic absorption, furnace technique. Methods for chemical analysis of 

water and wastes. Washington, DC: U.S. Environmental Protection Agency. EPA600479020, 78-79. 

EPA. 1983. Reportable quantity for barium. Environmental Criteria and Assessment Office, Cincinnati, 

OH. Washington, DC: U.S. Environmental Protection Agency, Office of Solid Waste and Emergency 

Response. 

EPA. 1984. Health effects assessment for barium. Washington, DC: U.S. Environmental Protection 

Agency, Office of Solid Waste and Emergency Response. EPA540186021. 

EPA. 1987. Drinking water health criteria document on barium (final draft). Washington, DC: U.S. 

Environmental Protection Agency, Office of Drinking Water, Criteria and Standards Division. TR-832­

892. PB91142869. 

EPA. 1989. Exposure factors handbook. Washington, DC: U.S. Environmental Protection Agency, 

Office of Health and Environmental Assessment. EPA600889043. 

EPA. 1990. Interim methods for development of inhalation reference concentrations. Washington, DC: 

U.S. Environmental Protection Agency, Office of Health and Environmental Assessment, Office of 

Research and Development, Environmental Criteria and Assessment Office. EPA600890066A. 

EPA. 1991. National pretreatment program: Report to Congress. Washington, DC: U.S. Environmental 

Protection Agency. 21W4004. 

EPA. 1992. Method 7081. Barium (Atomic absorption, furnace technique) Washington, DC: U.S. 

Environmental Protection Agency. 

EPA. 1994a. Method 200.8. National environmental methods index. U.S. Environmental Protection 

Agency. http://www.epa.gov/nerl/. April 01, 2005. 
 

BARIUM AND BARIUM COMPOUNDS 160 

9. REFERENCES 

EPA. 1994b. Method 200.7. National environmental methods index. U.S. Environmental Protection 

Agency. http://www.epa.gov/nerl/. April 01, 2005. 

EPA. 1994c. Method 7080A. Barium (Atomic absorption, direct aspiration). U.S. Environmental 

Protection Agency. http://www.epa.gov/sw-846/pdfs/7080a.pdf. November 9, 2007. 

EPA. 1995a. Determination of background concentrations of inorganics in soils and sediments at 

hazardous waste sites. Washington, DC: U.S. Environmental Protection Agency. EPA540S96500. 

EPA. 1995b. SOP 102: Determination of barium, copper, manganese, vanadium, and zinc in NHEXAS 

food or beverage composites by graphite furnace atomic absorption spectrometry. Compendium of 

methods for analysis of trace metals in dietary samples using Total Diet Study procedures. National 

Human Exposure Assessment Survey (NHEXAS). Arizona study: Quality systems and implementation 

plan for human exposure assessment. Tucson, AZ: U.S. Environmental Protection Agency. 

EPA. 1996. Method 3050B. Acid digestion of sediments, sludges, and soils. In: Environmental 

Monitoring Method Index (CD-ROM): EPA's official database of analytical methods for regulated 

substances. Rockville, MD: Government Institutes. 

EPA. 1997. Special report on environmental endocrine disruption: An effects assessment and analysis. 

Washington, DC: U.S. Environmental Protection Agency, Risk Assessment Forum. EPA630R96012. 

EPA. 2002a. National primary drinking water regulations. Washington, DC: Office of Ground Water 

and Drinking Water, U.S. Environmental Protection Agency. EPA816F02013. 

http://www.epa.gov/safewater/mcl.html. February 15, 2005. 

EPA. 2002b. National recommended water quality criteria. Washington, DC: Office of Water, Office of 

Science and Technology, U.S. Environmental Protection Agency. EPA822R02047. 

http://www.epa.gov/waterscience/pc/revcom.pdf. February 15, 2005. 

EPA. 2004. Drinking water standards and health advisories. Washington, DC: Office of Water, U.S. 

Environmental Protection Agency. EPA822R04005. 

http://www.epa.gov/waterscience/drinking/standards/dwstandards.pdf. February 15, 2005. 

*EPA. 2005a. Designated as hazardous substances in accordance with Section 311(b)(2)(A) of the Clean 

Water Act. Washington, DC: U.S. Environmental Protection Agency. Code of Federal Regulations 40 

CFR 116.4. http://www.epa.gov/ttn/atw/orig189.html. February 15, 2005. 

EPA. 2005b. Reportable quantities of hazardous substances designated pursuant to Section 311 of the 

Clean Water Act. Washington, DC: U.S. Environmental Protection Agency. 40 CFR 117.3. 

http://www.epa.gov/epacfr40/chapt-I.info/chi-toc.htm. February 16, 2005. 

EPA. 2005c. Technical factsheet on: Barium. Ground water and drinking water. Washington, DC: 

U.S. Environmental Protection Agency. 

EPA. 2005d. Toxic chemical release inventory reporting forms and instructions: Revised 2004 version. 

Section 313 of the Emergency Planning and Community Right-to-Know Act (Title III of the Superfund 

Amendments and Reauthorization Act of 1986). U.S. Environmental Protection Agency. Office of 

Environmental Information. EPA260B05001. 
 

 

BARIUM AND BARIUM COMPOUNDS 161 

9. REFERENCES 

Epstein MS, Zander AT. 1979. Direct determination of barium in sea and estuarine water by graphite 

furnace atomic spectrometry. Anal Chem 51:915-918. 

Essing H-G, Buhlmeyer G, Valentin H, et al. 1976. [Exclusion of disturbances to health from long years 

of exposure to barium carbonate in the production of steatite ceramics.] Arbeitsmedizin Sozialmedizin 

Praventivmedizin 11:299-302. (German) 

Fagioli F, Locatelli C, Lanciotti E, et al. 1988. Determination of barium in bottled drinking water by 

graphite furnace atomic absorption spectrometry. Anal Lett 21:2107-2116. 

Faust SD, Aly OM. 1981. Chemistry of natural waters. Ann Arbor, MI: Ann Arbor Science Publishers. 

FDA. 2004. Beverages. Bottled water. Washington, DC: Food and Drug Administration. Code of 

Federal Regulations 21 CFR 165.110. 

http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/CFRSearch.cfm. February 15, 2005. 

FEDRIP. 2005. Barium. Federal Research in Progress database. Springfield, VA: National Technical 

Information Service. April 01, 2005. 

FEDRIP. 2006. Barium. Federal Research in Progress database. Springfield, VA: National Technical 

Information Service. October 26, 2006. 

Feng X, Melander AP, Klaue B. 2000. Contribution of municipal waste incineration to trace metal 

deposition on the vicinity. Water Air Soil Pollut 119:295-316. 

Fomon SJ. 1966. Body composition of the infant: Part I: The male reference infant. In: Falkner F, ed. 

Human development. Philadelphia, PA: WB Saunders, 239-246. 

Fomon SJ, Haschke F, Ziegler EE, et al. 1982. Body composition of reference children from birth to age 

10 years. Am J Clin Nutr 35(Suppl 5):1169-1175. 

Foster PR, Elharrar V, Zipes DP. 1977. Accelerated ventricular escapes induced in the intact dog by 

barium, strontium and calcium. J Pharmacol Exp Ther 200:373-383. 

Foulkes EC, Bergman D. 1993. Inorganic mercury absorption in mature and immature rat jejunum: 

Transcellular and intercellular pathways in vivo and in everted sacs. Toxicol Appl Pharmacol 120:89-95. 

Genter MB. 2001. Magnesium, calcium, strontium, barium, and radium: Barium. In: Bingham E, 

Cohrssen B, Powell CH, eds. Patty's toxicology. John Wiley & Sons, Inc. 

Gilkeson RH, Specht SA, Cartwright K, et al. 1978. Geologic studies to identify the source for high 

level of radium and barium in Illinois ground-water supplies: A preliminary report. Illinois State 

Geological Survey and Illinois State Water Survey. Urbana, IL: University of Illinois, Water Resources 

Center. UILU-WRC-78-0135. 

Giusti L, Yang Y-L, Hewitt CN, et al. 1993. The solubility and partitioning of atmospherically derived 

trace metals in artificial and natural waters. Atmos Environ 27A(10):1567-1578. 

Giwercman A, Carlsen E, Keiding N, et al. 1993. Evidence for increasing incidence of abnormalities of 

the human testis: A review. Environ Health Perspect Suppl 101(2):65-71. 
 

 

 

 

BARIUM AND BARIUM COMPOUNDS 162 

9. REFERENCES 

Golothan DW. 1967. Diesel engine exhaust smoke: The influence of fuel properties and the effects of 

using barium-containing fuel additive. Society of Automotive Engineers. S.A.E.-670092, 616-640. 

González-Muñoz MT, Fernández-Luque B, Martínez-Ruiz F, et al. 2003. Precipitation of barite by 

Myxococcus xanthus: Possible implications for the biogeochemical cycle of barium. Appl Environ 

Microbiol 69(9):5722-5725. 

Gore DJ, Patrick G. 1982. A quantitative study of the penetration of insoluble particles into the tissue of 

the conducting airways. Ann Occup Hyg 26:149-161. 

Gould DB, Sorrell MR, Lupariello AD. 1973. Barium sulfide poisoning: Some factors contributing to 

survival. Arch Intern Med 132:891-894. 

Greengard P, Straub RW. 1959. Restoration by barium of action potentials in sodium-deprived 

mammalian B and C fibers. J Physiol 145:562-569. 

Grippo AA, Hamilton B, Hannigan R, et al. 2006. Metal content of ephedra-containing dietary 

supplements and select botanicals. Am J Health-Syst Pharm 63:635-644. 

Guzelian PS, Henry CJ, Olin SS, eds. 1992. Similarities and differences between children and adults: 

Implications for risk assessment. Washington, DC: International Life Sciences Institute Press. 

Haddad LM, Winchester JF, eds. 1990. Clinical management of poisoning and drug overdose. 2nd ed. 

Philadelphia, PA: WB Saunders Company, 1129. 

Hadjimarkos DM. 1967. Effect of trace elements in drinking water on dental caries. J Pediatr 70:967­

969. 

Hampel CA, Hawley GG, eds. 1973. The encyclopedia of chemistry. 3rd ed. New York, NY: Van 

Nostrand Reinhold Company, 125-127. 

Harrison GE, Carr TEF, Sutton A, et al. 1966. Plasma concentration and excretion of calcium-47, 

strontium-85, barium-133, and radium-223 following successive intravenous doses to a healthy man. 

Nature 209:526-527. 

Harrison GE, Raymond WHA, Tretheway HC. 1956. The estimation of barium and strontium in 

biological materials by activation analysis with special reference to the turnover of strontium in man. 

Proceedings of the international conference on the peaceful uses of atomic energy. Vol. 11. Biological 

effects of radiation. New York, NY: United Nations, 156-159. 

Harrison GE, Carr TEF, Sutton A. 1967. Distribution of radioactive calcium, strontium, barium and 

radium following intravenous injection into a healthy man. Int J Radiat Biol 13(3):235-247. 

Hawley GG, ed. 1977. The condensed chemical dictionary. 9th ed. New York, NY: Van Nostrand 

Reinhold Co., 105-110. 

Hawley GG, ed. 1981. The condensed chemical dictionary. 10th ed. New York, NY: Van Nostrand 

Reinhold Company, 105-110. 

Hayes WJ Jr. 1982. Pesticides studied in man. Baltimore, MD: Williams and Wilkins Co. 
BARIUM AND BARIUM COMPOUNDS 163 

9. REFERENCES 

HazDat. 2006. HazDat database: ATSDR’s Hazardous Substance Release and Health Effects Database. 

Atlanta, GA: Agency for Toxic Substances and Disease Registry. www.atsdr.cdc.gov/hazdat.html. 

December 21, 2006. 

Health Canada. 2005. Canadian total diet study. Ottawa, Ontario: Health Canada. http://www.hcsc.gc.ca/food-aliment/cs-ipc/fr-ra/e_tds.html. August 02, 2005. 

Hem JD. 1959. Study and interpretation of the chemical characteristics of natural water. U.S. 

Geological Survey sampling data. Washington, DC: U.S. Government Printing Office. Water Supply 

Paper 1473. 

Hicks R, Caldas LQA, Dare PRM, et al. 1986. Cardiotoxic and bronchoconstrictor effects of industrial 

metal fumes containing barium. Archives of Toxicology, Suppl 9. Toxic interfaces of neurones, smoke 

and genes. Secaucus, NJ: Springer-Verlag New York, Inc. 

Hildemann LM, Markowski GR, Cass GR. 1991. Chemical composition of emissions from urban 

sources of fine organic aerosol. Environ Sci Technol 25:744-759. 

Hiraoka M, Ikeda K, Sano T. 1980. The mechanism of barium-induced automaticity in ventricular 

muscle fibers. Adv Myocardiol 1:255-266. 

Hoel DG, Davis DL, Miller AB, et al. 1992. Trends in cancer mortality in 15 industrialized countries, 

1969-1986. J Natl Cancer Inst 84(5):313-320. 

Holding ST, Rowson JJ. 1975. The determination of barium in unused lubricating oils by means of 

atomic-absorption spectrophotometry. Analyst 100:465-470. 

Hope B, Loy C, Miller P. 1996. Uptake and trophic transfer of barium in a terrestrial ecosystem. Bull 

Environ Contam Toxicol 56:683-689. 

HSDB. 2007. Hazardous Substances Data Bank. Bethesda, MD: National Library of Medicine, 

National Toxicology Information Program. http://toxnet.nlm.nih.gov/. May 8, 2007. 

Hudak PF, Wachal DJ. 2001. Effects of brine injection wells, dry holes, and plugged oil/gas wells on 

chloride, bromide, and barium concentrations in the Gulf Coast Aquifer, southeast Texas, USA. Environ 

Int 26(7-8):497-503. 

Hui-Ming H, Yao-Han L. 1984. Determination of trace Na, K, Ba, and Li by graphite furnace atomic 

emission spectrometry. Spectrochim Acta 39B:493-499. 

Huston J Jr, Wallach DP, Cunningham GJ. 1952. Pulmonary reaction to barium sulfate in rats. AMA 

Archive Pathol 54:430-438. 

IARC. 2004. Overall evaluations of carcinogenicity to humans: As evaluated in IARC Monographs 

volumes 1-82 (at total of 900 agents, mixtures and exposures) Lyon, France: International Agency for 

Research on Cancer. http://www-cie.iarc.fr/monoeval/crthall.html. February 15, 2005. 

ICRP. 1973. International Commission on Radiological Protection. Alkaline earth metabolism in adult 

man. Health Phys 24:125-221. 
 

 

BARIUM AND BARIUM COMPOUNDS 164 

9. REFERENCES 

ICRP. 1974. International Commission on Radiological Protection. Report of the task group on 

reference man. New York, NY: Pergamon Press. 

ICRP. 1993. Age-dependent doses to members of the public from intake of radionuclides: Part 2. 

Ingestion dose coefficients. IRCP publication 67.23(3/4). New York, NY: Pergamon Press. 

ILO. 1983. Barium and compounds. In: Parmeggiani L, ed. International Labour Office encyclopedia 

of occupational health and safety. Volume I and II. Geneva, Switzerland: International Labour Office, 

242-244. 

IPCS. 1991. Barium: Health and safety guide. Health and Safety Guide No. 46. International 

Programme on Chemical Safety. 

IRIS. 2006. Barium. Washington, DC: Integrated Risk Information System. U.S. Environmental 

Protection Agency. http://www.epa.gov/iris/subst/. February 05, 2006. 

Jaklinski A, Maj J, Przegalinski E. 1967. Experimental studies on barium poisoning. J Forensic Med 

14:13-15. 

Jha SK, Kumar R, Verma BS. 1993. A case of barium carbonate poisoning. J Assoc Physicians India 

41(11):750-751. 

Johanson CE. 1980. Permeability and vascularity of the developing brain: Cerebellum vs cerebral 

cortex. Brain Res 190(1):3-16. 

Johnson KE, Yerhoff FW, Robinson J, et al. 1983. Determination of barium at ng ml-1 levels by flame 

emission spectrometry after ion-exchange separation from 1000-fold amounts of calcium. Anal Chim 

Acta 149:129-135. 

Joseph EZ. 1985. Chemical safety data guide. Washington, DC: Bureau of National Affairs, Inc. 

Jourdan S, Bertoni M, Sergio P, et al. 2001. Suicidal poisoning with barium chloride. Forensic Sci Int 

119(2):263-265. 

Kabata-Pendias A, Pendias H. 1984. Trace elements in soils and plants. Boca Raton, FL: CRC Press, 

Inc. 

Kanematsu N, Hara M, Kada T. 1980. Rec assay and mutagenicity studies on metal compounds. Mutat 

Res 77:109-116. 

Karaki H, Ikeda M, Urakawa N. 1967. Effects of external calcium and some metabolic inhibitors on 

barium-induced tension changes in guinea pig taenia coli. Jpn J Pharmacol 17:603-612. 

Kay S. 1954. Tissue reaction to barium sulfate contrast medium. AMA Arch Pathol 57:279-284. 

Kirkpatrick T. 1978. Barium compounds. In: Grayson M, Eckroth D, eds. Kirk-Othmer encyclopedia 

of chemical technology. Vol. 3, 3rd ed. New York, NY: John Wiley and Sons, 463-479. 

Kirkpatrick T. 1985. Barium compounds. In: Grayson M, Eckroth D, eds. Kirk-Othmer concise 

encyclopedia of chemical technology. New York, NY: John Wiley and Sons, 147-148. 
 

BARIUM AND BARIUM COMPOUNDS 165 

9. REFERENCES 

Koch M, Appoloni O, Haufroid V, et al. 2003. Acute barium intoxication and hemodiafiltration. J 

Toxicol Clin Toxicol 41(4):363-367. 

Kojola WH, Brenniman GR, Carnow BW. 1978. A review of environmental characteristics and health 

effects of barium in public water supplies. Rev Environ Health 3:79-95. 

Komori M, Nishio K, Kitada M, et al. 1990. Fetus-specific expression of a form of cytochrome P-450 in 

human livers. Biochemistry 29(18):4430-4433. 

Kopp JF. 1969. The occurrence of trace elements in water. In: Hemphill DD, ed. Proceedings of the 

third annual conference on trace substances in environmental health. Columbia, MO: University of 

Missouri, 59-73. 

Kopp SJ, Perry HM Jr, Feliksik JM, et al. 1985. Cardiovascular dysfunction and hypersensitivity to 

sodium pentobarbital induced by chronic barium chloride ingestion. Toxicol Appl Pharmacol 77:303­

314. 

Korman EF, Ward JF, Myers LS Jr. 1978. Toxic effects of metals on DNA synthesis. In: Mahlum DD, 

ed. Developmental toxicology of energy related pollutants, proceedings of the 17th annual Hanford 

biology symposium, Washington, DC, October 17-19, 1977. Battelle Memorial Institute: Division of 

Biomedical and Environmental Research, Department of Energy, and Pacific Northwest Laboratories, 

384-395. 

Kramer HJ, Gonick HC, Lu E. 1986. In vitro inhibition of Na-K-ATPase by trace metals: Relation to 

renal and cardiovascular damage. Nephron 44:329-336. 

Kresse R, Baudis U, Jager P, et al. 2007. Barium and barium compounds. In: Ullmann's Encyclopedia 

of Industrial Chemistry. Wiley-VCH Verlag GmbH & Co. kGaA. 

http://www.mrw.interscience.wiley.com/emrw/9783527306732/ueic/article/a03_325/current/pdf. 

November 15, 2007. 

Krishnan K, Andersen ME. 1994. Physiologically based pharmacokinetic modeling in toxicology. In: 

Hayes AW, ed. Principles and methods of toxicology. 3rd ed. New York, NY: Raven Press, Ltd., 

149-188. 

Krishnan K, Andersen ME, Clewell HJ III, et al. 1994. Physiologically based pharmacokinetic modeling 

of chemical mixtures. In: Yang RSH, ed. Toxicology of chemical mixtures: Case studies, mechanisms, 

and novel approaches. San Diego, CA: Academic Press, 399-437. 

Kunesh CJ. 1978. Barium. In: Grayson M, Eckroth D, eds. Kirk-Othmer encyclopedia of chemical 

technology. Vol. 3, 3rd ed. New York, NY: John Wiley and Sons, 457-463. 

Kunesh CJ. 1985. Barium. In: Grayson M, Eckroth D, eds. Kirk-Othmer concise encyclopedia of 

chemical technology. New York, NY: John Wiley and Sons, 146-147. 

Lagas P, Loch JPG, Bom CM, et al. 1984. The behavior of barium in a landfill and the underlying soil. 

Water, Air, Soil Pollut 22:121-129. 

Landis FP, Coons MC. 1954. A rapid spectrographic method for the determination of beryllium in air 

dust. Appl Spectroscopy 8:71-75. 
BARIUM AND BARIUM COMPOUNDS 166 

9. REFERENCES 

Larsen PO. 1973. A convenient method for liquid scintillation counting of barium carbonate-14C. Int J 

Appl Radiat Isot 24:612-613. 

Leeder JS, Kearns GL. 1997. Pharmcogenetics in pediatrics: Implications for practice. Pediatr Clin 

North Am 44(1):55-77. 

Leggett RW. 1992. Fractional absorption of ingested barium in adult humans. Health Phys
 

62(6):556-561. 

Lengemann FW. 1959. The site of action of lactose in the enhancement of calcium utilization. J Nutr 

69:23-27. 

LeRoy GV, Rust JH, Hasterlik RJ. 1966. The consequences of ingestion by man of real and simulated 

fallout. Health Phys 12:449-473. 

Leung H-W. 1993. Physiologically-based pharmacokinetic modelling. In: Ballentyne B, Marrs T, 

Turner P, eds. General and applied toxicology. Vol. 1. New York, NY: Stockton Press, 153-164. 

Lewi Z, Bar-Khayim Y. 1964. Food-poisoning from barium carbonate. Lancet 342-343. 

Lewis RJ. 1997. Hawley's condensed chemical dictionary. 13th ed. New York, NY: John Wiley & 

Sons, 111-117. 

Lewis RJ. 2000. In: Lewis RJ, eds. Sax's dangerous properties of industrial materials. 10th ed. New 

York: John Wiley & Sons, Inc, 343-351. 

Lide DR. 2000. Barium. CRC handbook of chemistry and physics. New York, NY: CRC Press, 4-45, 

4-46, 14-14. 

Lide DR. 2005. CRC handbook of chemistry and physics. New York, NY: CRC Press, 4-50, 4-51, 

14-17. 

Lin Y. 1996. Radiopaques. Kirk-Othmer encyclopedia of chemical technology. John Wiley & Sons. 

Liniecki J. 1971. Kinetics of calcium, strontium, barium and radium in rabbits. Health Phys 21:367-376. 

Livingston, AL. 1978. Forage plant estrogens. J Toxicol Environ Health 4(2-3):301-324. 

Longerich HP, Friel JK, Fraser C, et al. 1991. Analysis of drinking water of mothers of neural tube 

defect infants and of normal for 14 selected trace elements by inductively coupled plasma-mass 

spectrometry (ICP-MS) Can J Appl Spectrosc 36(1):15-21. 

Losee FL, Cutress TW, Brown R. 1974. Natural elements of the periodic table in human dental enamel. 

Caries Res 8:123-134. 

Lowe TP, Day DD. 2002. Metal concentrations in zebra mussels and sediments from embayments and 

riverine environments of eastern Lake Erie, southern Lake Ontario, and the Niagara River. Arch Environ 

Contam Toxicol 43:301-308. 

Mattila MJ, Anyos K, Puisto EL. 1986. Cardiotoxic actions of doxepin and barium chloride in conscious 

rabbits. Arch Toxicol 9 (Suppl):205-208. 
 

 

 

BARIUM AND BARIUM COMPOUNDS 167 

9. REFERENCES 

Mauras Y, Allain P. 1979. [Determination of barium in water and biological fluids by emission 

spectrometry with an indirectively-coupled plasma.] Anal Chim Acta 110:271-277. (French) 

Mayr U, Butsch A, Schneider S. 1992. Validation of two in vitro test systems for estrogenic activities 

with zearalenone, phytoestrogens and cereal extracts. Toxicology 74(2-3):135-149. 

McCabe LJ, Symons JM, Lee RD, et al. 1970. Survey of community water supply systems. J Am Water 

Works Assoc 62:670-687. 

McCauley PT, Washington IS. 1983. Barium bioavailability as the chloride, sulfate or carbonate salt in 

the rat. Drug Chem Toxicol 6:209-217. 

McCauley PT, Douglas BH, Laurie RD, et al. 1985. Investigations into the effect of drinking water 

barium on rats. Adv Mod Environ Toxicol, Inorg Drinking Water Cardiovasc Dis 9:197-210. 

McNally WD. 1925. Two deaths from the administration of barium salts. J Am Med Assoc 84:1805­

1807. 

Meister RT, ed. 2004. Crop protection handbook. Willoughby, OH: Meister Media Worldwide, 

C71-C72. 

Merefield JR. 1987. Ten years of barium build-up in the Teign. Mar Pollut Bull 18:220-222. 

Miller RG, Featherstone JDB, Curzon MEJ, et al. 1985. Barium in teeth as indicator of body burden. 

Adv Mod Environ Toxicol 9:211-219. 

Miner S. 1969a. Air pollution aspects of barium and its compounds. Bethesda, MD: Litton Systems, 

Inc Contract No. Ph-22-68-25, 69. 

Miner S. 1969b. Preliminary air pollution survey of barium and its compounds: A literature review. 

Raleigh, NC: U.S. Department of Health, Education and Welfare, Public Health Service, Consumer 

Protection and Environmental Health Service, Consumer Air Pollution and Control Administration. 

Report No. APTD 69-28. 

Mishra SK, Das PK, Sanyal AK. 1988. Barium-induced contraction of rat vas deferens in calcium-free 

solution. Arch Int Pharmacodyn Ther 294:85-98. 

Monaco M, Dominici R, Barisano P, et al. 1990. Mutagen activity of barium chloride in Salmonella 

typhimurium. Med Lav 81:54-64. 

Monaco M, Dominici R, Barisano P, et al. 1991. Valutazione della presunta attivita mutagena del bario 

nitrato. Med Lav 82(5):439-445. 

Morel FMM. 1983. Principles of aquatic chemistry. New York, NY: John Wiley and Sons. 

Morrow PE, Gibb FR, Davies H, et al. 1968. Dust removal from the lung parenchyma: An investigation 

of clearance stimulants. Toxicol Appl Pharmacol 12:372-396. 

Morrow PE, Gibb FR, Johnson L. 1964. Clearance of insoluble dust from the lower respiratory tract. 

Health Phys 10:543-555. 
 

 

BARIUM AND BARIUM COMPOUNDS 168 

9. REFERENCES 

Morselli PL, Franco-Morselli R, Bossi L. 1980. Clinical pharmacokinetics in newborns and infants: 

Age-related differences and therapeutic implications. Clin Pharmacokin 5(6):485-527. 

Morton W. 1945. Poisoning by barium carbonate. Lancet 2:738-739. 

Morton MS, Elwood PC, Abernethy M. 1976. Trace elements in water and congenital malformations of 

the central nervous system in South Wales. Brit J Prev Soc Med 30:36-39. 

Munch DF, Comer HT, Downey JM. 1980. Barium contracture: A model for systole. Am J Physiol 

239:H438-H442. 

Murata M, Noguchi M. 1974. An ion exchanger-epoxy resin pelletization method for sample preparation 

in x-ray fluorescence analysis. Anal Chim Acta 71:295-302. 

Nakazato Y, Onoda Y. 1980. Barium and strontium can substitute for calcium in noradrenaline output 

induced by excess potassium in the guinea-pig. J Physiol 305:59-71. 

NAS. 1977. Drinking water and health. Vol. 1. National Academy of Sciences. Washington, DC: 

National Academy Press, 205-305. 

NAS. 1982. Drinking water and health. Vol. 4. Washington, DC: National Academy of Sciences. 

National Academy Press, 167-170. 

NAS/NRC. 1989. Report of the oversight committee. In: Biologic markers in reproductive toxicology. 

Washington, DC: National Academy of Sciences, National Research Council, National Academy Press. 

Neal C, Smith CJ, Jeffery HA, et al. 1996. Trace element concentrations in the major rivers entering the 

Humber estuary, NE England. J Hydrol 182:37-64. 

Newman J. 1998. Radiographic and endoscopic evaluation of the upper GI tract. Radiol Technol 

69(3):213-226. 

Newton D, Ancill AK, Naylor KE, et al. 2001. Long-term retention of injected barium-133 in man. 

Radiat Prot Dosim 97(3):231-240. 

Newton D, Harrison GE, Kang C, et al. 1991. Metabolism of injected barium in six healthy men. Health 

Phys 61(2):191-201. 

Newton D, Rundo J, Harrison GE. 1977. The retention of alkaline earth elements in man, with special 

reference to barium. Health Phys 33:45-53. 

Ng A, Patterson CC. 1982. Changes of lead and barium with time in California offshore basin 

sediments. Geochim Cosmochim Acta 46:2307-2321. 

NIOSH. 1987. Method 7056. Barium, soluble compounds. National Institute for Occupational Safety 

and Health. http://www.cdc.gov/niosh/nmam/. May 20, 2005. 

NIOSH. 1989. National occupational exposure survey. Cincinnati, OH: National Occupational Safety 

and Health. 
 

BARIUM AND BARIUM COMPOUNDS 169 

9. REFERENCES 

NIOSH. 1994. Method 7056. Barium, soluble compounds. NIOSH manual of analytical methods. 4th 

edition. National Institute for Occupational Safety and Health. 

http://www.cdc.gov/niosh/nmam/pdfs/7056.pdf. August 02, 2005. 

NIOSH. 1999. International Chemical Safety Cards (ICSCs). U.S. National Version. National Institute 

for Occupational Safety and Health. http://www.cdc.gov/niosh/ipcs/nicstart.html. May 7, 2007. 

NIOSH. 2003. Method 7300. Elements by ICP (nitric/perchloric acid ashing). NIOSH manual of 

analytical methods (NMAM). 4th edition. Cincinnati, OH: National Institute for Occupational Safety 

and Health. 

NIOSH. 2005a. Barium chloride. NIOSH pocket guide to chemical hazards. Atlanta, GA: National 

Institute for Occupational Safety and Health, Centers for Disease Control and Prevention. 

http://www.cdc.gov/niosh/npg/npgdname.html. February 15, 2004. 

NIOSH. 2005b. Barium sulfate. NIOSH pocket guide to chemical hazards. Atlanta, GA: National 

Institute for Occupational Safety and Health, Centers for Disease Control and Prevention. 

http://www.cdc.gov/niosh/npg/npgdname.html. February 15, 2004. 

NIOSH/OSHA. 1978. Occupational health guidelines for chemical hazards: Soluble barium compounds 

(as barium). National Institute for Occupational Safety and Health, Occupational Safety and Health 

Administration. 

Nishioka H. 1975. Mutagenic activities of metal compounds in bacteria. Mutat Res 31:185-189. 

NRC. 1993. Pesticides in the diets of infants and children. Washington, DC: National Research 

Council. National Academy Press. 

NRC. 1995. Nutrient requirements of laboratory animals. Washington, DC: National Research Council. 

National Academy Press. http://www.nap.edu/books/0309051266/html/. May 20, 2005. 

NTP. 1994. Toxicology and carcinogenesis studies of barium chloride dihydrate -(CAS No. 10326-27-9) 

in F344/N rats and B6C3F1 mice. National Toxicology Program. TR432. 

NTP. 2005. Report on carcinogens. 11th ed. Research Triangle Park, NC: U.S. Department of Health 

and Human Services, Public Health Service, National Toxicology Program. http://ntpserver.niehs.nih.gov/ntp/roc/toc11.html. May 15, 2005. 

Ogen S, Rosenbluth S, Eisenberg A. 1967. Food poisoning due to barium carbonate in sausage. Isr J 

Med Sci 3:565-568. 

OHM/TADS. 1989. Oil and Hazardous Materials Technical Assistance Data System (database). 

Chemical Information Systems. 

Olehy DA, Schmitt RA, Bethard WF. 1966. Neutron activation analysis of magnesium, calcium, 

strontium, barium, manganese, cobalt, copper, zinc, sodium, and potassium in human erythrocytes and 

plasma. J Nucl Med 6:917-927. 

Oppenheimer JA, Eaton AD, Leong LYC, et al. 1984. Multielemental analytical techniques for 

hazardous waste analysis: The state-of-the-art. Las Vegas, NV: U.S. Environmental Protection Agency, 

Office of Research and Development, Environmental Monitoring Systems Laboratory. EPA600484028. 
 

BARIUM AND BARIUM COMPOUNDS 170 

9. REFERENCES 

OSHA. 1982. U.S. Department of Labor, Occupational Safety and Health Administration. Fed Regist 

47:30420-30434. 

OSHA. 1989. U.S. Department of Labor, Occupational Safety and Health Administration. Fed Regist 

54:2920. 

OSHA. 2005a. Air contaminants. Occupational safety and health standards for shipyard employment. 

Washington, DC: U.S. Department of Labor, Occupational Safety and Health Administration. Code of 

Federal Regulations 29 CFR 1915.1000. http://www.osha.gov/comp-links.html. February 15, 2005. 

OSHA. 2005b. Gases, vapors, fumes, dusts, and mists. Safety and health regulations for construction. 

Washington, DC: U.S. Department of Labor, Occupational Safety and Health Administration. Code of 

Federal Regulations 29 CFR 1926.55, Appendix A. http://www.osha.gov/comp-links.html. February 15, 

2005. 

OSHA. 2005c. Limits for air contaminants. Occupational safety and health standards. Washington, DC: 

U.S. Department of Labor, Occupational Safety and Health Administration. Code of Federal Regulations. 

29 CFR 1910.1000. http://www.osha.gov/comp-links.html. February 15, 2005. 

OTA. 1990. Neurotoxicity: Identifying and controlling poisons of the nervous system. Washington, 

DC: Office of Technology Assessment. OTABA438. 

Owen GM, Brozek J. 1966. Influence of age, sex and nutrition on body composition during childhood 

and adolescence. In: Falkner F, ed. Human development. Philadelphia, PA: WB Saunders, 222-238. 

Pascual-Barrera A, Gold-Bouchot G, Ceja-Moreno V, et al. 2004. Heavy metals and hydrocarbons in 

sediments from three lakes from San Miguel, Chiapas, Mexico. Bull Environ Contam Toxicol 

73:762-769. 

Parmeggiani L, ed. 1983. Encyclopedia of occupational health and safety. Prepared under the auspices 

of the International Labour Organization. Vol. II, 3rd ed. Geneva, Switzerland: International Labour 

Office, 242-244. 

Pekey H. 2006. Heavy metal pollution assessment in sediments of the Izmit Bay, Turkey. Environ 

Monit Assess 123(1-3):219-231. 

Perry RH, Chilton CH, eds. 1973. Chemical engineer’s handbook. 5th ed. New York, NY: McGrawHill Book Co., 3-8. 

Perry HM Jr, Kopp SJ, Erlanger MW, et al. 1983. Cardiovascular effects of chronic barium ingestion. 

Trace Subst Environ Health 17:155-164. 

Perry HM Jr, Kopp SJ, Perry EF, et al. 1989. Hypertension and associated cardiovascular abnormalities 

induced by chronic barium feeding. J Toxicol Environ Health 28:373-388. 

Perry HM Jr, Perry EF, Erlanger MW, et al. 1985. Barium-induced hypertension. Adv Mod Environ 

Toxicol, Inorg Drinking Water Cardio Vasc Dis 9:221-229. 

Peyton JC, Borowitz JL. 1978. Effects of Ba2+ and Cd2+ on convulsive electroshock sensitivity and 45Ca 

distribution in brain subcellular fractions in mice. Toxicol Appl Pharmacol 45:95-103. 
 

 

 

BARIUM AND BARIUM COMPOUNDS 171 

9. REFERENCES 

Phelan DM, Hagley SR, Guerin MD. 1984. Is hypokalemia the cause of paralysis in barium poisoning? 

Br Med J 289:882. 

Phillips C, Evans J, Hom W, et al. 1998. Long-term changes in sediment barium inventories associated 

with drilling-related discharges in the Santa Maria Basin, California, USA. Environ Toxicol Chem 

17(9):1653-1661. 

Pierce FD, Brown HR. 1977. A semi-automated technique for the separation and determination of 

barium and strontium in surface waters by ion exchange chromatography and atomic emission 

spectrometry. Anal Lett 10:685-699. 

Pijl MEJ, Chaoui AS, Wahl RL, et al. 2002. Radiology of colorectal cancer. Eur J Cancer 38:887-898. 

Pourang N, Tanabe S, Rezvani S, et al. 2005. Trace elements accumulation in edible tissues of five 

sturgeon species from the Caspian Sea. Environ Monit Assess 100:89-108. 

Preisman L, Davis LW. 1948. Barium compounds. In: Kirk RE, Othmer DF, eds. Kirk-Othmer 

encyclopedia of chemical technology. Vol. 2. New York, NY: Interscience Encyclopedia, Inc., 317. 

Princenthal RA, Lowman R, Zeman RK, et al. 1983. Ureterosigmoidostomy: The development of 

tumors, diagnosis, and pitfalls. Am J Roentgenol 141:77-81. 

Proctor NH, Hughes JP, Fischman ML, eds. 1988. Chemical hazards of the workplace. 2nd ed. 

Philadelphia, PA: JB Lippincott Company, 88-89. 

Rae T. 1977. Tolerance of mouse macrophages in vitro to barium sulfate used in orthopedic bone 

cement. J Biomed Mater Res 11:839-846. 

Rai D, Zachara JM, Schwab AP, et al. 1984. Chemical attenuation rates, coefficients, and constants in 

leachate migration. Vol. I: A critical review. Palo Alto, CA: Electric Power Research Institute, 6-1 to 

6-6. Report EA-3356. 

Ramakrishna VVS, Singh V, Garg AN. 1996. Occupational exposure amongst locomotive shed workers 

and welders using neutron activation analysis of scalp hair. Sci Total Environ 192(3):259-267. 

Rasmussen PE, Subramanian KS, Jessiman BJ. 2001. A multi-element profile of housedust in relation to 

exterior dust and soils in the city of Ottawa, Canada. Sci Total Environ 267:125-140. 

Rastogi SC, Pritzl G. 1996. Migration of some toxic metals from crayons and water colors. Bull 

Environ Contam Toxicol 56:527-533. 

Raven KP, Loeppert RH. 1997. Heavy metals in the environment: Trace element composition of 

fertilizers and soil amendments. J Environ Qual 26:551-557. 

Reeves AL. 1979. Barium. In: Friberg L, Nordberg GF, Vouk VB, eds. Handbook on the toxicology of 

metals. New York, NY: Elsevier/North Holland Biomedical Press, 321-328. 

Reeves AL. 1986. Barium. In: Friberg L, Nordberg GF, Vouk VB, eds. Handbook on the toxicology of 

metals. 2nd ed. New York, NY: Elsevier Science Publishers BV, 84-94. 
 

 

 

BARIUM AND BARIUM COMPOUNDS 172 

9. REFERENCES 

Renshaw GD. 1973. The determination of barium by flameless atomic absorption spectrophotometry 

using a modified graphite tube atomizer. At Absorpt Newsl 12:158-160. 

Reznik RB, Toy HD Jr. 1978. Source assessment: Major barium chemicals. Cincinnati, OH: U.S. 

Environmental Protection Agency. EPA600278004b. 

Riley RF. 1987. Barium. In: Parker SP, ed. McGraw-Hill encyclopedia of science and technology. 

Vol. 2, 6th ed. New York, NY: McGraw-Hill Book Company, 397-399. 

Roe KK, Froelich PN. 1984. Determination of barium in seawater by direct injection graphite furnace 

atomic absorption spectrometry. Anal Chem 56:2724-2726. 

Roig-Navarro AF, Lopez FJ, Serrano R, et al. 1997. An assessment of heavy metals and boron 

contamination in workplace atmospheres from ceramic factories. Sci Total Environ 201:225-234. 

Rossman TG, Molina M, Meyer L, et al. 1991. Performance of 133 compounds in the lambda prophage 

induction endpoint of the Microscreen assay and a comparison with S. typhimurium mutagenicity and 

rodent carcinogenicity assays. Mutat Res 260:349-367. 

Roy WR. 1994. Groundwater contamination from municipal landfills in the USA. In: Adriano DC, 

Iskandar A, Murarka IP, eds. Contamination of groundwaters: Case studies. Northwood: Science 

Reviews, 411-446. 

Roza O, Berman LB. 1971. The pathophysiology of barium: Hypokalemic and cardiovascular effects. J 

Pharmacol Exp Ther 177:433-439. 

RTECS. 2007. Registry of Toxic Effects of Chemical Substances (database). Washington, DC: U.S. 

Department of Health and Human Services, National Institute for Occupational Safety and Health. 

www.cdc.gov/niosh/rtecs/default.html. May 7, 2007. 

Rubin ES. 1999. Toxic releases from power plants. Environ Sci Technol 33:3062-3067. 

Sacchetti G. 1972. Gastric emptying of barium sulfate suspensions in humans: A useful tool for clinical 

investigations. Farmaco Prat 27:80-88. 

Saeki Y, Shibata T, Shiozawa K. 1981. Excitation-contraction coupling in mammalian cardiac muscle 

during Ba2+-induced contracture. Am J Physiol 240:H216-H221. 

Saito Y, Sakai Y, Urakawa N. 1972. Effect of cholinergic drugs and barium on oxygen consumption in 

guinea pig taenia coli. Jpn J Pharmacol 22:653-661. 

Saleh MA, Wilson BL. 1999. Analysis of metal pollutants in the Houston Ship Channel by inductively 

coupled plasma/mass spectrometry. Ecotoxicol Environ Saf 44:113-117. 

Sax NI, Lewis RJ Sr, eds. 1987. Hawley's condensed chemical dictionary. 11th ed. New York, NY: 

Van Nostrand Reinhold Company, 117-122. 

Sax NI, Lewis RJ Sr, eds. 1989. Dangerous properties of industrial materials. Vol. II, 7th ed. New 

York, NY: Van Nostrand Reinhold Company. 
 

 

BARIUM AND BARIUM COMPOUNDS 173 

9. REFERENCES 

Sax NI, Feiner B, Fitzgerald JJ, et al. 1984. Dangerous Properties of Industrial Materials. 6th ed. New 

York, NY: Van Nostrand Reinhold Company. 

Schauer J, Kleeman MJ, Cass GR, et al. 1999. Measurement of emissions from air pollution sources 2 

C1 through C29 organic compounds from medium duty diesel trucks. Environ Sci Technol 33:1578-1587. 

Schott GD, McArdle B. 1974. Barium-induced skeletal muscle paralysis in the rat, and its relation to 

human familial periodic paralysis. J Neurol Neurosurg Psychiatr 37:32-39. 

Schramel P. 1988. ICP and DCP emission spectrometry for trace element analysis in biomedical and 

environmental samples: A review. Spectrochim Acta 43:881-896. 

Schroeder HA. 1970. Barium. Air quality monograph. American Petroleum Institute. Washington, DC: 

Air Quality Monograph No. 70-12. 

Schroeder HA, Kraemer LA. 1974. Cardiovascular mortality, municipal water, and corrosion. Arch 

Environ Health 28:303-311. 

Schroeder HA, Mitchener M. 1975a. Life-term studies in rats: Effects of aluminum, barium, beryllium, 

and tungsten. J Nutr 105:421-427. 

Schroeder HA, Mitchener M. 1975b. Life-term effects of mercury, methyl mercury, and nine other trace 

metals on mice. J Nutr 105:452-453. 

Schroeder HA, Tipton IH, Nason AP. 1972. Trace metals in man: Strontium and barium. J Chronic Dis 

25:491-517. 

Seaton A, Ruckley VA, Addison J, et al. 1986. Silicosis in barium miners. Thorax 41:591-595. 

Segreti A, Vocci FJ, Dewey WL. 1979. Antagonism of barium chloride lethality by atropine and 

naloxone: Analysis by a multivariate logistic model. Toxicol Appl Pharmacol 50:25-30. 

Setchell BP, Waites GMH. 1975. The blood-testis barrier. In: Creep RO, Astwood EB, Geiger SR, eds. 

Handbook of physiology: Endocrinology V. Washington, DC: American Physiological Society. 

Shacklette HT, Boerngen JG. 1984. Element concentrations in soils and other surficial materials of the 

conterminous United States. U.S. Geological Survey Professional Paper. Washington, DC: U.S. 

Government Printing Office. No. 1270. 

Shahin U, Yi SM, Paode RD, et al. 2000. Long-term elemental dry deposition fluxes measured around 

Lake Michigan with an automated dry deposition sampler. Environ Sci Technol 34:1887-1892. 

Shanbaky NM, Emran A, Borowitz JL. 1982. Identification of subcellular organelles involved in Ba2+-

and Cd2+-induced adrenomedullary secretion. Toxicol Appl Pharmacol 62:167-171. 

Shankle R, Keane JR. 1988. Acute paralysis from inhaled barium carbonate. Arch Neurol 45:579-580. 

Sharp RA, Knevel AM. 1971. Analysis of barium in barium sulfate and diagnostic meals containing 

barium sulfate using atomic absorption spectroscopy. J Pharm Sci 60:458-460. 
 

 

BARIUM AND BARIUM COMPOUNDS 174 

9. REFERENCES 

Shephard TS, ed. 1989. Catalog of teratogenic agents. 6th ed. Baltimore, MD: The Johns Hopkins 

University Press, 68. 

Shiraishi K, Kawamura H, Tanaka GI. 1987. Determination of alkaline-earth metals in foetus bones by 

inductively-coupled plasma atomic-emission spectrometry. Talanta 34:823-827. 

Shvydko NS, Il'in LA, Norets TA, et al. 1971. Comparative behavior of Sr89 and Ba140 in skin following 

cutaneous application. Gig Sanit 36:386-390. 

Sill CW, Willis CP. 1966. Determination of radioisotopes of cerium, barium, lanthanum, and neptunium 

after separation by barium sulfate. Anal Chem 38:97-102. 

*Silva SA. 2003. Barium toxicity after exposure to contaminated contrast solution- Gois State, Brazil, 

2003. MMWR Morb Mortal Wkly Rep 52(43):1047-1048. 

Singer PC. 1974. Chemical processes for the removal of trace metals from drinking water. In: Sapoznik 

AR, O'Connor JT, eds. Trace metals in water supplies: Occurrence, significance, and control. Urbana, 

IL: Engineering Publications Office, University of Illinois. 

Sirover MA, Loeb LA. 1976a. Infidelity of DNA synthesis in vitro: Screening for potential metal 

mutagens or carcinogens. Science 194:1434-1436. 

Sirover MA, Loeb LA. 1976b. Metal-induced infidelity during DNA synthesis. Proc Natl Acad Sci 

73:2331-2335. 

Sommers LE. 1977. Chemical composition of sewage sludges and analysis of their potential use as 

fertilizers. J Environ Qual 6:225-232. 

Sora S, Carbone MLA, Pacciatini M, et al. 1986. Disomic and diploid meiotic products induced in 

Saccharomyces cerevisiae by the salts of 27 elements. Mutagenesis 1:21-28. 

Sowden EM. 1958. Trace elements in human tissue: 3. Strontium and barium in non-skeletal tissue. 

Biochem J 70:712-715. 

Sowden EM, Pirie A. 1958. Barium and strontium concentrations in eye tissue. Biochem J 70:716-717. 

Sowden EM, Stitch SR. 1957. Trace elements in human tissue: 2. Estimation of the concentrations of 

stable strontium and barium in human bone. Biochem J 67:104-109. 

Spencer RP, Lange RC, Treves S. 1971. Use of 135mBa and 131Ba as bone scanning agents. J Nucl Med 

12:216-221. 

Spritzer AA, Watson JA. 1964. The measurement of ciliary clearance in the lungs of rats. Health Phys 

10:1093-1097. 

SRI. 2006. Barium. Directory of chemical producers: United States. Menlo Park, CA: SRI Consulting, 

471-472. 

Stewart DW, Hummel RP. 1984. Acute poisoning by a barium chloride burn. J Trauma 24:768-770. 
 

 

 

 

BARIUM AND BARIUM COMPOUNDS 175 

9. REFERENCES 

Stoewsand GS, Anderson JL, Rutzke M, et al. 1988. Deposition of barium in the skeleton of rats fed 

Brazil nuts. Nutr Rep Int 38:259-262. 

Stokinger HE. 1981. Barium, Ba. In: Clayton GD, Clayton FE, eds. Patty's industrial hygiene and 

toxicology, Vol. 2A. 3rd ed. New York, NY: John Wiley and Sons, Inc., 1531-1537. 

Storm DL. 1994. Chemical monitoring of California's public drinking water sources: Public exposures 

and health impacts. In: Wang RGM, ed. Water contamination and health: Integration of exposure 

assessment, toxicology, and risk assessment. New York: Marcel Dekker, Inc., 67-124. 

Sugiyama M, Fujino O, Matsui M. 1984. Determination of barium in sea water by graphite furnace 

atomic absorption spectrometry after preconcentration and separation by solvent extraction. Bunseki 

Kagaku 33:E123-E129. 

Sutton A, Humphreys ER, Shepherd H, et al. 1972. Reduction in the retention of radioactive barium in 

rats following the addition of sodium alginate derivatives to the diet. Int J Radiat Biol 22:297-300. 

Syed IB, Hosain F, Mann NS. 1981. G.I. tract excretion of barium. Am J Proctol Gastroenterol Colon 

Rectal Surg 32:16, 18, 20. 

Tabor EC, Warren WV. 1958. Distribution of certain metals in the atmosphere of some American cities. 

AMA Arch Ind Health 17:145-151. 

Takahashi S, Kubota Y, Sato H, et al. 1993. Retention of 133Ba in the trachea of rabbits, dogs, and 

monkeys following local administration as 133BaSO4 particles. Inhal Toxicol 5:265-273. 

Takahashi S, Patrick G. 1987. Long-term retention of 133Ba in the rat trachea following local 

administration as barium sulfate particles. Radiat Res 110:321-328. 

Talwar KK, Sharma BK. 1979. Myocardial damage due to barium chloride poisoning. Indian Heart J 

31:244-245. 

Tanizaki Y, Shimokawa T, Nakamura M. 1992. Physicochemical speciation of trace elements in river 

waters by size fractionation. Environ Sci Technol 26(7):1433-1444. 

Tarasenko NY, Pronin OA, Silaev AA. 1977. Barium compounds as industrial poisons (an experimental 

study). J Hyg Epidemol Microbiol Immunol 21:361-373. 

Tardiff RG, Robinson M, Ulmer NS. 1980. Subchronic oral toxicity of BaCl2 in rats. J Environ Pathol 

Toxicol 4:267-275. 

Taylor DM, Bligh PH, Duggan MH. 1962. The absorption of calcium, strontium, barium and radium 

from the gastrointestinal tract of the rat. Biochem J 83:25-29. 

Thomas K, Colborn T. 1992. Organochlorine endocrine disruptors in human tissue. In: Colborn T, 

Clement C, eds. Chemically induced alterations in sexual and functional development: The 

wildlife/human connection. Princeton, NJ: Princeton Scientific Publishing, 365-394. 

Thomas KW, Pellizzari ED, Berry MR. 1999. Population-based dietary intakes and tap water 

concentrations for selected elements in the EPA Region V National Human Exposure Assessment Survey 

(NHEXAS). J Expo Anal Environ Epidemiol 9:402-413. 
 

 

 

 

 

BARIUM AND BARIUM COMPOUNDS 176 

9. REFERENCES 

Thomas M, Bowie D, Walker R. 1998. Acute barium intoxication following ingestion of ceramic glaze. 

Postgrad Med J 74(875):545-546. 

Tipton IH, Stewart FL, Dickson J. 1969. Patterns of elemental excretion in long term balance studies. 

Health Phys 16:455-462. 

Tipton IH, Stewart PL, Martin PG. 1966. Trace elements in diets and excreta. Health Phys 

12:1683-1689. 

Toda N. 1970. Barium-induced automaticity in relation to the calcium ions and norepinephrine in the 

rabbit left atrium. Circ Res 27:45-57. 

TRI04. 2006. TRI explorer: Providing access to EPA’s toxics release inventory data. Washington, DC: 

Office of Information Analysis and Access. Office of Environmental Information. U.S. Environmental 

Protection Agency. Toxics Release Inventory. http://www.epa.gov/triexplorer/. August 19, 2006. 

Tuovinen OH, Button KS, Vuorinen CL, et al. 1980. Bacterial, chemical, and mineralogical 

characteristics of tubercles in distribution pipelines. J Am Water Works Assoc 72:626-635. 

USGS. 1985. Barium, atomic absorption spectrometric, direct. Denver, CO: U.S. Geological Survey. 

http://reports.er.usgs.gov/reports. April 16, 2005. 

USGS. 2002a. Chapter I. The determination of forty-two elements in geological materials by 

inductively coupled plasma – mass spectrometry. In: Taggart JE, ed. Analytical methods for chemical 

analysis of geologic and other materials. U.S. Geological Survey. Open File Report 02-223-I, 1-14. 

USGS. 2002b. Chapter G. The determination of forty elements in geological and botanical samples by 

inductively coupled plasma – atomic emission spectrometry. In: Taggart JE, ed. Analytical methods for 

chemical analysis of geologic and other materials. U.S. Geological Survey. Open File Report 02-223-G, 

1-18. 

USGS. 2002c. Sediment database and geochemical assessment of Lake Pontchartrain Basin, Chapter J. 

Manheim, FT, Hayes, L (eds.), Lake Pontchartrain Basin: Bottom sediments and related environmental 

resources: U.S. Geological Survey professional paper 1634. http://pubs.usgs.gov/prof/p1634. September 

19, 2006. 

USGS. 2004. Barite. U.S. Geological Survey minerals yearbook. USGS, 9.1-9.3, Tables 1-7. 

http://minerals.usgs.gov/minerals/pubs/commodity/barite/baritmyb04.pdf. September 12, 2006. 

USGS. 2006. Barite. U.S. Geological Survey, Mineral Commodity Summary. 

http://minerals.usgs.gov/minerals/pubs/commodity/barite/baritmcs06.pfd. September 12, 2006. 

Van Duuren BL, Sivak A, Langseth L, et al. 1968. Initiators and promoters in tobacco carcinogenesis. 

World Conference on smoking and health: Toward a less harmful cigarette. National Cancer Institute 

Monograph 28:173-180. 

Venugopal B, Luckey TD. 1978. Metal toxicity in mammals. 2nd ed. New York, NY: Plenum Press, 

63-67. 
 

 

BARIUM AND BARIUM COMPOUNDS 177 

9. REFERENCES 

Vieira I, Sonnier M, Cresteil T. 1996. Developmental expression of CYP2E1 in the human liver: 

Hypermethylation control of gene expression during the neonatal period. Eur J Biochem 238(2):476-483. 

Volkl H, Greger R, Lang F. 1987. Potassium conductance in straight proximal tubule cells of the mouse. 

Effect of barium, verapamil and quinidine. Biochim Biophys Acta 900:275-281. 

Weast RC, ed. 1989. CRC handbook of chemistry and physics. 70th ed. Boca Raton, Florida: CRC 

Press, Inc., B.73-B.75. 

Weiss G, ed. 1986. Hazardous chemicals data book. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 

144, 146. 

Welch SP, Vocci FJ, Dewey WL. 1983. Antinociceptive and lethal effects of intraventricularly 

administered barium and strontium: Antagonism by atropine sulfate or naloxone hydrochloride. Life Sci 

33:359-364. 

Wells JA, Wood KE. 2001. Acute barium poisoning treated with hemodialysis. Am J Emerg Med 

19(2):175-177. 

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. 

Wetherill SF, Guarino MJ, Cox RW. 1981. Acute renal failure associated with barium chloride 

poisoning. Ann Intern Med 95:187-188. 

WHO. 2000. Air quality guidelines. 2nd ed. Geneva, Switzerland: World Health Organization. 

http://www.euro.who.int/air/Activities/20050104_1. February 15, 2005. 

WHO. 2001. Barium and barium compounds. Geneva, Switzerland: World Health Organization. 

http://www.inchem.org/documents/ehc/ehc/ehc221.htm. April 01, 2005. 

WHO. 2004. Guidelines for drinking-water quality. 3rd ed. Geneva, Switzerland: World Health 

Organization. http://www.who.int/water_sanitation_health/dwq/gdwq3/en/. February 15, 2005. 

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. 

Wilkie PJ, Hatzimihalis G, Koutoufides P, et al. 1996. The contribution of domestic sources to levels of 

key organic and inorganic pollutants in sewage: The case of Melbourne, Australia. Water Sci Technol 

34(3-4):63-70. 

Windholz M, ed. 1976. The Merck index. 9th ed. Rahway, NJ: Merck & Co, Inc., 127-131. 

Windholz M, ed. 1983. The Merck index. 10th ed. Rahway, NJ: Merck & Co, Inc., 965-993. 

Winkler J. 2002. Barium and barium compounds: Barium in the environment. Ullmann's encyclopedia 

of industrial chemistry. John Wiley & Sons, Inc. 

Wones RG, Stadler BL, Frohman LA. 1990. Lack of effect of drinking water barium on cardiovascular 

risk factors. Environ Health Perspect 85:355-359. 
BARIUM AND BARIUM COMPOUNDS 178 

9. REFERENCES 

Worthing CR, ed. 1987. The pesticide manual: A world compendium. 8th ed. Thornton Heath, UK: 

The British Crop Protection Council, 857. 

Yamamura M, Nishi M, Furubayashi H, et al. 1985. Barium peritonitis: Report of a case and review of 

the literature. Dis Colon Rectum 28:347-352. 

Yesilada E. 2001. Genotoxicity testing of some metals in the Drosophila wing somatic mutation and 

recombination test. Bull Environ Contam Toxicol 66(4):464-469. 

Zenz C, Dickerson OB, Horvath EP, eds. 1994. In: Zenz C, Dickerson OB, Horvath EP, eds. 

Occupational medicine. 3rd ed. St Louis: Mosby, 721-722, 747-748. 

Ziegler EE, Edwards BB, Jensen RL, et al. 1978. Absorption and retention of lead by infants. Pediatr 

Res 12(1):29-34. 

Zschiesche W, Schaller K-H, Welte D. 1992. Exposure to soluble barium compounds: An interventional 

study in arc welders. Int Arch Occup Environ Health 64:13-23. 
BARIUM AND BARIUM COMPOUNDS 179 

10. GLOSSARY 

Absorption—The taking up of liquids by solids, or of gases by solids or liquids. 

Acute Exposure—Exposure to a chemical for a duration of 14 days or less, as specified in the 

Toxicological Profiles. 

Adsorption—The adhesion in an extremely thin layer of molecules (as of gases, solutes, or liquids) to the 

surfaces of solid bodies or liquids with which they are in contact. 

Adsorption Coefficient (Koc)—The ratio of the amount of a chemical adsorbed per unit weight of 

organic carbon in the soil or sediment to the concentration of the chemical in solution at equilibrium. 

Adsorption Ratio (Kd)—The amount of a chemical adsorbed by sediment or soil (i.e., the solid phase) 

divided by the amount of chemical in the solution phase, which is in equilibrium with the solid phase, at a 

fixed solid/solution ratio. It is generally expressed in micrograms of chemical sorbed per gram of soil or 

sediment. 

Benchmark Dose (BMD)—Usually defined as the lower confidence limit on the dose that produces a 

specified magnitude of changes in a specified adverse response. For example, a BMD10 would be the 

dose at the 95% lower confidence limit on a 10% response, and the benchmark response (BMR) would be 

10%. The BMD is determined by modeling the dose response curve in the region of the dose response 

relationship where biologically observable data are feasible. 

Benchmark Dose Model—A statistical dose-response model applied to either experimental toxicological 

or epidemiological data to calculate a BMD. 

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. 

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. 

Cancer Effect Level (CEL)—The lowest dose of chemical 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. 

Carcinogen—A chemical capable of inducing cancer. 

Case-Control Study—A type of epidemiological study that examines the relationship between a 

particular outcome (disease or condition) and a variety of potential causative agents (such as toxic 

chemicals). In a case-controlled study, a group of people with a specified and well-defined outcome is 

identified and compared to a similar group of people without outcome. 

Case Report—Describes a single individual with a particular disease or exposure. These may suggest 

some potential topics for scientific research, but are not actual research studies. 

Case Series—Describes the experience of a small number of individuals with the same disease or 

exposure. These may suggest potential topics for scientific research, but are not actual research studies. 
BARIUM AND BARIUM COMPOUNDS 180 

10. GLOSSARY 

Ceiling Value—A concentration of a substance that should not be exceeded, even instantaneously. 

Chronic Exposure—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. 

Cross-sectional Study—A type of epidemiological study of a group or groups of people that examines 

the relationship between exposure and outcome to a chemical or to chemicals at one point in time. 

Data Needs—Substance-specific informational needs that if met would reduce the uncertainties of human 

health assessment. 

Developmental Toxicity—The occurrence of adverse effects on the developing organism that may result 

from exposure to a chemical 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. 

Dose-Response Relationship—The quantitative relationship between the amount of exposure to a 

toxicant and the incidence of the adverse effects. 

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 occurs. The terms, as used here, include malformations and variations, altered growth, and in utero 

death. 

Environmental Protection Agency (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. 

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. 

Half-life—A measure of rate for the time required to eliminate one half of a quantity of a chemical from 

the body or environmental media. 

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. 
BARIUM AND BARIUM COMPOUNDS 181 

10. GLOSSARY 

Incidence—The ratio of individuals in a population who develop a specified condition to the total 

number of individuals in that population who could have developed that condition in a specified time 

period. 

Intermediate Exposure—Exposure to a chemical for a duration of 15–364 days, as specified in the 

Toxicological Profiles. 

In Vitro—Isolated from the living organism and artificially maintained, as in a test tube. 

In Vivo—Occurring within the living organism. 

Lethal Concentration(LO) (LCLO)—The lowest concentration of a chemical in air that has been reported 

to have caused death in humans or animals. 

Lethal Concentration(50) (LC50)—A calculated concentration of a chemical in air to which exposure for 

a specific length of time is expected to cause death in 50% of a defined experimental animal population. 

Lethal Dose(LO) (LDLo)—The lowest dose of a chemical introduced by a route other than inhalation that 

has been reported to have caused death in humans or animals. 

Lethal Dose(50) (LD50)—The dose of a chemical that 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. 

Lowest-Observed-Adverse-Effect Level (LOAEL)—The lowest exposure level 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. 

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. 

Minimal Risk Level (MRL)—An estimate of daily human exposure to a hazardous substance that is 

likely to be without an appreciable risk of adverse noncancer health effects over a specified route and 

duration of exposure. 

Modifying Factor (MF)—A value (greater than zero) that is applied to the derivation of a Minimal Risk 

Level (MRL) to reflect additional concerns about the database that are not covered by the uncertainty 

factors. The default value for a MF is 1. 

Morbidity—State of being diseased; morbidity rate is the incidence or prevalence of disease in a specific 

population. 

Mortality—Death; mortality rate is a measure of the number of deaths in a population during a specified 

interval of time. 
BARIUM AND BARIUM COMPOUNDS 182 

10. GLOSSARY 

Mutagen—A substance that causes mutations. A mutation is a change in the DNA sequence of a cell’s 

DNA. Mutations can lead to birth defects, miscarriages, or cancer. 

Necropsy—The gross examination of the organs and tissues of a dead body to determine the cause of 

death or pathological conditions. 

Neurotoxicity—The occurrence of adverse effects on the nervous system following exposure to a 

chemical. 

No-Observed-Adverse-Effect Level (NOAEL)—The dose of a chemical 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. 

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) that 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 OR of greater than 1 is considered to indicate greater risk of disease in the 

exposed group compared to the unexposed group. 

Organophosphate or Organophosphorus Compound—A phosphorus-containing organic compound 

and especially a pesticide that acts by inhibiting cholinesterase. 

Permissible Exposure Limit (PEL)—An Occupational Safety and Health Administration (OSHA) 

allowable exposure level in workplace air averaged over an 8-hour shift of a 40-hour workweek. 

Pesticide—General classification of chemicals specifically developed and produced for use in the control 

of agricultural and public health pests. 

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. 

Pharmacokinetic Model—A set of equations that can be used to describe the time course of a parent 

chemical or metabolite in an animal system. There are two types of pharmacokinetic models: data-based 

and physiologically-based. A data-based model divides the animal system into a series of compartments, 

which, in general, do not represent real, identifiable anatomic regions of the body, whereas the 

physiologically-based model compartments represent real anatomic regions of the body. 

Physiologically Based Pharmacodynamic (PBPD) Model—A type of physiologically based doseresponse model that 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—Comprised of 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 
BARIUM AND BARIUM COMPOUNDS 183 

10. GLOSSARY 

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. 

Prevalence—The number of cases of a disease or condition in a population at one point in time. 

Prospective Study—A type of cohort study in which the pertinent observations are made on events 

occurring after the start of the study. A group is followed over time. 

q1*—The upper-bound estimate of the low-dose slope of the dose-response curve as determined by the 

multistage procedure. The q1* can be used to calculate an estimate of carcinogenic potency, the 

incremental excess cancer risk per unit of exposure (usually μg/L for water, mg/kg/day for food, and 

μg/m3 for air). 

Recommended Exposure Limit (REL)—A National Institute for Occupational Safety and Health 

(NIOSH) time-weighted average (TWA) concentration for up to a 10-hour workday during a 40-hour 

workweek. 

Reference Concentration (RfC)—An estimate (with uncertainty spanning perhaps an order of 

magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) 

that is likely to be without an appreciable risk of deleterious noncancer health effects during a lifetime. 

The inhalation reference concentration is for continuous inhalation exposures and is appropriately 

expressed in units of mg/m3 or ppm. 

Reference Dose (RfD)—An estimate (with uncertainty spanning perhaps an order of magnitude) 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 no-observed-adverse-effect level 

(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. 

Reportable Quantity (RQ)—The quantity of a hazardous substance that is considered reportable under 

the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA). Reportable 

quantities are (1) 1 pound or greater or (2) for selected substances, an amount established by regulation 

either under CERCLA or under Section 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. 

Retrospective Study—A type of cohort study based on a group of persons known to have been exposed 

at some time in the past. Data are collected from routinely recorded events, up to the time the study is 

undertaken. Retrospective studies are limited to causal factors that can be ascertained from existing 

records and/or examining survivors of the cohort. 

Risk—The possibility or chance that some adverse effect will result from a given exposure to a chemical. 
BARIUM AND BARIUM COMPOUNDS 184 

10. GLOSSARY 

Risk Factor—An aspect of personal behavior or lifestyle, an environmental exposure, or an inborn or 

inherited characteristic that is associated with an increased occurrence of disease or other health-related 

event or condition. 

Risk Ratio—The ratio of the risk among persons with specific risk factors compared to the risk among 

persons without risk factors. A risk ratio greater than 1 indicates greater risk of disease in the exposed 

group compared to the unexposed group. 

Short-Term Exposure Limit (STEL)—The American Conference of Governmental Industrial 

Hygienists (ACGIH) 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 Threshold Limit Value-Time Weighted Average (TLV-TWA) may 

not be exceeded. 

Standardized Mortality Ratio (SMR)—A ratio of the observed number of deaths and the expected 

number of deaths in a specific standard population. 

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. 

Teratogen—A chemical that causes structural defects that affect the development of an organism. 

Threshold Limit Value (TLV)—An American Conference of Governmental Industrial Hygienists 

(ACGIH) concentration of a substance to which most workers can be exposed without adverse effect. 

The TLV may be expressed as a Time Weighted Average (TWA), as a Short-Term Exposure Limit 

(STEL), or as a ceiling limit (CL). 

Time-Weighted Average (TWA)—An allowable exposure concentration averaged over a normal 8-hour 

workday or 40-hour workweek. 

Toxic Dose(50) (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. 

Uncertainty Factor (UF)—A factor used in operationally deriving the Minimal Risk Level (MRL) or 

Reference Dose (RfD) or Reference Concentration (RfC) 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 lowestobserved-adverse-effect level (LOAEL) data rather than no-observed-adverse-effect level (NOAEL) data. 

A default for each individual UF is 10; if complete certainty in data exists, a value of 1 can be used; 

however, a reduced UF of 3 may be used on a case-by-case basis, 3 being the approximate logarithmic 

average of 10 and 1. 

Xenobiotic—Any chemical that is foreign to the biological system. 
BARIUM AND BARIUM COMPOUNDS A-1 

APPENDIX A. ATSDR MINIMAL RISK LEVELS AND WORKSHEETS 

The Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) [42 U.S.C. 

9601 et seq.], as amended by the Superfund Amendments and Reauthorization Act (SARA) [Pub. L. 99– 

499], requires that the Agency for Toxic Substances and Disease Registry (ATSDR) develop jointly with 

the U.S. Environmental Protection Agency (EPA), in order of priority, a list of hazardous substances most 

commonly found at facilities on the CERCLA National Priorities List (NPL); prepare toxicological 

profiles for each substance included on the priority list of hazardous substances; and assure the initiation 

of a research program to fill identified data needs associated with the substances. 

The toxicological profiles include an examination, summary, and interpretation of available toxicological 

information and epidemiologic evaluations of a hazardous substance. During the development of 

toxicological profiles, Minimal Risk Levels (MRLs) are derived when reliable and sufficient data exist to 

identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration for a 

given route of exposure. An MRL is an estimate of the daily human exposure to a hazardous substance 

that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration 

of exposure. MRLs are based on noncancer health effects only and are not based on a consideration of 

cancer effects. These substance-specific estimates, which are intended to serve as screening levels, are 

used by ATSDR health assessors to identify contaminants and potential health effects that may be of 

concern at hazardous waste sites. It is important to note that MRLs are not intended to define clean-up or 

action levels. 

MRLs are derived for hazardous substances using the no-observed-adverse-effect level/uncertainty factor 

approach. They are below levels that might cause adverse health effects in the people most sensitive to 

such chemical-induced effects. MRLs are derived for acute (1–14 days), intermediate (15–364 days), and 

chronic (365 days and longer) durations and for the oral and inhalation routes of exposure. Currently, 

MRLs for the dermal route of exposure are not derived because ATSDR has not yet identified a method 

suitable for this route of exposure. MRLs are generally based on the most sensitive chemical-induced end 

point considered to be of relevance to humans. Serious health effects (such as irreparable damage to the 

liver or kidneys, or birth defects) are not used as a basis for establishing MRLs. Exposure to a level 

above the MRL does not mean that adverse health effects will occur. 

MRLs are intended only to serve as a screening tool to help public health professionals decide where to 

look more closely. They may also be viewed as a mechanism to identify those hazardous waste sites that 
BARIUM AND BARIUM COMPOUNDS A-2 

APPENDIX A 

are not expected to cause adverse health effects. Most MRLs contain a degree of uncertainty because of 

the lack of precise toxicological information on the people who might be most sensitive (e.g., infants, 

elderly, nutritionally or immunologically compromised) to the effects of hazardous substances. ATSDR 

uses a conservative (i.e., protective) approach to address this uncertainty consistent with the public health 

principle of prevention. Although human data are preferred, MRLs often must be based on animal studies 

because relevant human studies are lacking. In the absence of evidence to the contrary, ATSDR assumes 

that humans are more sensitive to the effects of hazardous substance than animals and that certain persons 

may be particularly sensitive. Thus, the resulting MRL may be as much as 100-fold below levels that 

have been shown to be nontoxic in laboratory animals. 

Proposed MRLs undergo a rigorous review process: Health Effects/MRL Workgroup reviews within the 

Division of Toxicology and Environmental Medicine, 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 and 

Environmental Medicine, Agency for Toxic Substances and Disease Registry, 1600 Clifton Road NE, 

Mailstop F-32, Atlanta, Georgia 30333. 
BARIUM AND BARIUM COMPOUNDS A-3 

APPENDIX A 

MINIMAL RISK LEVEL (MRL) WORKSHEET 

Chemical Name: Barium, Soluble Salts 

CAS Numbers: 

Date: August 2007 

Profile Status: Final 

Route: [ ] Inhalation [X] Oral 

Duration: [ ] Acute [X] Intermediate [ ] Chronic 

Graph Key: 23 

Species: Rat 

Minimal Risk Level: 0.2 [X] mg/kg/day [ ] ppm 

Reference: NTP. 1994. Toxicology and carcinogenesis studies of barium chloride dihydrate (CAS No. 

10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). Research Triangle Park, NC: 

U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, 

National Toxicology Program. NTP TR 432. 

Experimental design: Groups of 10 male and 10 female F344/N rats were administered 0, 125, 500, 

1,000, 2,000, or 4,000 ppm barium chloride dihydrate in drinking water for 90 days. Using measured 

body weights and water consumption, the investigators estimated the daily barium doses to be 0, 10, 30, 

65, 110, and 200 mg barium/kg/day for males and 0, 10, 35, 65, 115, and 180 mg barium/kg/day for 

females. Neurobehavioral tests (spontaneous motor activity, grip strength, tail flick latency, startle 

response, hindlimb foot splay) were performed prior to exposure and after 45 and 90 days of exposure. 

Cardiovascular testing (heart rate, blood pressure, and electrocardiogram) was conducted prior to 

exposure and after 45 and 91 days of exposure. Organ weights (adrenal gland, brain, heart, liver, kidney, 

lung, testis, thymus), blood analysis for hematological and clinical chemistry (barium, sodium, potassium, 

calcium, and phosphorus levels) alterations, and histological examination of major tissues and organs 

(only in the 200/180 mg/kg/day group) were conducted at termination; kidney, liver, spleen, and thymus 

of male and female rats in the 110/115 mg/kg/day groups and adrenal gland, heart, and salivary gland of 

female rats in the 115 mg/kg/day group were also examined microscopically. 

Effect noted in study and corresponding doses: Exposure-related deaths were observed during the last 

week in 30% of the males and 10% of the females exposed to 200/180 mg barium/kg/day. Significant 

decreases in final body weights were also observed in the 200 mg barium/kg/day males (13% lower than 

controls) and 180 mg barium/kg/day females (8% lower than controls); significant decreases in water 

consumption (approximately 30% lower than controls) were also observed at this dose level. Marginal, 

but statistically significant, decreases in undifferentiated motor activity was observed in all groups of rats 

exposed to barium for 90 days, except females exposed to 115 mg barium/kg/day; no other alterations in 

neurobehavioral performance were observed. No significant alterations in heart rate, blood pressure, or 

EKG readings were observed. Significant increases in serum phosphorus levels were observed in males 

in the 110 and 200 mg barium/kg/day groups and females in the 35, 65, 115, and 180 mg barium/kg/day 

groups; however, the investigators noted that these increases were probably an artifact from hemolysis of 

collected blood samples. Significant increases in absolute and relative kidney weights were observed in 

females exposed to 115 or 180 mg barium/kg/day and increases in relative kidney weights were also 

observed in males at 200 mg barium/kg/day. An increase in relative kidney weight was also observed in 

the females exposed to 65 mg barium/kg/day. The magnitude of the increases in relative kidney weights 

were 7, 14, and 19% in the females exposed to 65, 115, and 180 mg barium/kg/day and 12% in males 

exposed to 200 mg barium/kg/day. ;Minimal to mild, focal to multifocal dilatation of the proximal 

convoluted tubules of the outer medulla and renal cortex was observed in three male and three female rats 

in the 200/180 mg barium/kg/day group. The small increase in relative kidney weight (7%) observed in 
BARIUM AND BARIUM COMPOUNDS A-4 

APPENDIX A 

the female rats exposed to 65 mg barium/kg/day was not considered biologically significant because it is 

not supported by an increase in histological alterations in the kidney at 65 or 115 mg barium/kg/day or in 

rats exposed to 75 mg barium/kg/day for 2 years (NTP 1994). 

Dose and end point used for MRL derivation: The MRL is based on a NOAEL of 65 mg barium/kg/day 

for increased absolute and relative kidney weight. The increased kidney weight was considered an early 

indicator of potentially more serious effects in the kidney. A NOAEL/LOAEL approach was used to 

derive the MRL because none of the available benchmark dose models provided an adequate fit to the 

absolute or relative kidney weight data. 

[X] NOAEL [ ] LOAEL 

Uncertainty Factors used in MRL derivation: 100 

[ ] 10 for use of a LOAEL 

[X] 10 for extrapolation from animals to humans 

[X] 10 for human variability 

Modifying Factor used in MRL derivation: 3 

[X] 3 for database deficiences 

A modifying factor of 3 was included to account for deficiencies in the oral toxicity database, particularly 

the need for an additional developmental toxicity study. Decreases in pup birth weight and a 

nonstatistically significant decrease in live litter size were observed in the offspring of rats exposed to 

180/200 mg Ba/kg/day as barium chloride in drinking water prior to mating (Dietz et al. 1992). Maternal 

body weight gain and water consumption were not reported, thus it is not known if the decreases in pup 

body weight were secondary to maternal toxicity or direct effect on the fetus. No developmental effects 

were observed in mice at the highest dose tested (200 mg Ba/kg/day) (Dietz et al. 1992). One other study 

examined the potential for developmental toxicity in orally exposed animals (Tarasenko et al. 1977). 

However, because the study was poorly reported and no incidence data or statistical analysis were 

presented in the published paper, the reported findings of increased mortality and systemic toxicity in the 

offspring of an unspecified species orally exposed to barium during conception and pregnancy can not be 

adequately evaluated. The Dietz et al. (1992) study was designed to be a mating trial and did not expose 

the animals during gestation; thus, database is lacking an adequate study to evaluate the potential for 

barium to induce developmental effects. 

Was a conversion factor used from ppm in food or water to a mg/body weight dose? No. Doses were 

calculated by the investigators using measured drinking water consumption and body weight data. 

If an inhalation study in animals, list conversion factors used in determining human equivalent dose: Not 

applicable. 

Was a conversion used from intermittent to continuous exposure? Not applicable. 

Other additional studies or pertinent information that lend support to this MRL: There are limited data on 

the toxicity of barium in humans following repeated doses. Wones et al. (1990) found no significant 

alterations in blood pressure or ECG readings, relative to initial baseline measurements in men 

experimentally exposed to up to 0.2 mg barium/kg/day as barium chloride in drinking water for 4 week 

(Wones et al. 1990). These findings are supported by several animal studies that did not find significant 
BARIUM AND BARIUM COMPOUNDS A-5 

APPENDIX A 

alterations in blood pressure or ECG readings in rats exposed to 150–180 mg barium/kg/day in drinking 

water for 13 or 16 weeks, respectively (McCauley et al. 1985; NTP 1994). A study by Perry et al. (1983, 

1985, 1989) found significant increases in blood pressure in rats administered 8.6 or 11 mg barium/kg/day 

as barium chloride in drinking water for 1 or 4 months, respectively. The reason for the differences 

between the results from the Perry et al. (1983, 1985, 1989) study and the NTP (1994) and McCauley et 

al. (1985) studies is not known. It is possible that the diet used in the Perry et al. (1983, 1985, 1989) 

study influenced the results. In this study, the rats were fed a low-mineral diet; the calcium content of the 

rye-based diet was 3.8 mg/kg, which is lower than the concentration recommended for maintenance, 

growth, and reproduction of laboratory rats (NRC 1995b). 

The results of studies by McCauley et al. (1985) and NTP (1994) suggest that the kidney is the most 

sensitive target of toxicity in rats and mice. In the McCauley et al. (1985) study, glomerular alterations 

consisting of fused podocytes and thickening of the capillary basement membrane were found in rats 

exposed to 150 mg barium/kg/day in drinking water for 16 weeks. This lesion was found in 

uninephrectomized Sprague Dawley rats, Dahl salt-sensitive rats, and Dahl salt-resistant rats. In the NTP 

(1994) rat study, significant increases in absolute and relative kidney weights were observed in female 

rats exposed to 115 or 180 mg barium/kg/day and in males exposed to 200 mg barium/kg/day. A 

statistically significant increase in relative kidney weight was also observed in the females exposed to 

65 mg barium/kg/day; however, the increase was small (7%) and was not considered biologically 

significant. At 200 and 180 mg barium/kg/day, minimal to mild dilatation of the proximal renal cortex 

was observed in the males and females, respectively; an increase in mortality (30%) was also observed in 

the males exposed to 200 mg barium/kg/day. In mice, mild to moderate nephropathy (characterized as 

tubule dilatation, regeneration, and atrophy) was observed in 100% of the males exposed to 450 mg 

barium/kg/day and 90% of the females exposed to 495 mg barium/kg/day; no renal lesions were observed 

at the next lowest dose level (205 and 200 mg barium/kg/day in males and females, respectively). Other 

effects observed at the 450/495 mg barium/kg/day dose level included weight loss, spleen and thymus 

atrophy, and increased mortality (60% of the males and 70% of females died after 5 weeks of exposure). 

Other end points that have been examined in rats and mice include neurotoxicity, reproductive toxicity, 

and developmental toxicity. In male and female rats, slight decreases in undifferentiated motor activity 

were observed at 10 mg barium/kg/day and higher. However, with the exception of female rats exposed 

to 200 mg barium/kg/day, the difference between motor activity in the barium-exposed rats and the 

controls was less than 20%; this was not considered to be biologically significant. At 200 mg 

barium/kg/day, the difference was 30%, which was considered to be adverse. No significant alterations 

were found in performance on the remaining neurobehavioral tests (grip strength, tail flick latency, startle 

response, and hindlimb foot splay). In mice, a significant decrease in forelimb grip strength was observed 

in females exposed to 495 mg barium/kg/day; this may have been due to debilitation. No other alterations 

in neurobehavioral performance were found. No effects on reproductive tissues or reproductive 

performance were observed in rats or mice exposed to approximately 200 mg barium/kg/day (Dietz et al. 

1992; NTP 1994). Pre-mating exposure to 180/200 mg barium/kg/day resulted in decreased litter size and 

body weight in rat offspring; the NOAEL for these effects was 110/115 mg barium/kg/day (Dietz et al. 

1992). No developmental effects were observed in mice exposed to 200 mg barium/kg/day (Dietz et al. 

1992). 

Agency Contacts (Chemical Managers): Cassandra Smith and Yee-Wan Stevens 
BARIUM AND BARIUM COMPOUNDS A-6 

APPENDIX A 

MINIMAL RISK LEVEL (MRL) WORKSHEET 

Chemical Name: Barium, Soluble Salts 

CAS Numbers: 

Date: August 2007 

Profile Status: Final 

Route: [ ] Inhalation [X] Oral 

Duration: [ ] Acute [ ] Intermediate [X] Chronic 

Graph Key: 49 

Species: Mouse 

Minimal Risk Level: 0.2 [X] mg barium/kg/day [ ] ppm 

Reference: NTP. 1994. Toxicology and carcinogenesis studies of barium chloride dihydrate (CAS No. 

10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). U.S. Department of Health and 

Human Services, Public Health Service, National Institutes of Health, National Toxicology Program, 

Research Triangle Park, NC. NTP TR 432. 

Experimental design: Groups of 60 male and 60 female B6C3F1 mice were administered 0, 500, 1,250, 

or 2,500 ppm barium chloride dehydrate in drinking water for 2 years. Using measured body weights and 

water consumption, the investigators estimated the daily barium doses to be 0, 30, 75, and 160 mg 

barium/kg/day for males and 0, 40, 90, and 200 mg barium/kg/day for females. Organ weights, blood 

analysis for hematological and clinical chemistry (barium, sodium, potassium, calcium, and phosphorus 

levels, and alanine aminotransferase, creatine kinase, lactate dehydrogenase, and gammaglutamyltransferase activities) alterations (measured after 15 months), and histological examination of 

major tissues and organs were conducted at termination. 

Effect noted in study and corresponding doses: Increased mortality attributed to renal lesions was 

observed in the 160/200 mg/kg/day group. Decreased body weights (<7%) were observed in the bariumexposed mice. The investigators noted that a moderate to marked weight loss was observed in animals 

dying early. No significant alterations in hematology or clinical chemistry parameters were observed. A 

significant increase in the incidence of nephropathy was observed in male and female mice exposed to 

160/200 mg/kg/day. The nephropathy was characterized by extensive regeneration of cortical and 

medullary tubule epithelium, tubule dilatation, hyaline cast formation, multifocal interstitial fibrosis, and 

glomerulosclerosis in some kidneys. The incidence of nephropathy was 1/50, 0/50, 2/48, and 19/50 in the 

males and 0/50, 2/53, 1/50, and 37/50 in the females, respectively. The average severity of the 

nephropathy was 3.6 (moderate to marked) for both the males and females in the 160/200 mg/kg/day 

group. An increased incidence of lymphoid depletion in the spleen and decreased relative and absolute 

spleen were also observed in the 160/200 mg/kg/day group; however, this was attributed to debilitation 

associated with nephropathy rather than a direct effect on the spleen. No significant increases in the 

incidences of neoplasms were observed. 

Dose and end point used for MRL derivation: Benchmark dose analysis of the dose-response data 

(Table A-1) for nephropathy in male and female mice exposed to barium chloride in drinking water for 

2 years (NTP 1994) was conducted. EPA’s Benchmark Dose Software (version 1.3.2) was used to fit 

nine mathematical models to the incidence data. Model fit was judged by the p-values associated with the 

chi-square goodness-of-fit statistic generated by the models and visual inspection of the plot of observed 

and predicted values. As assessed by the chi-square goodness-of-fit test, several models in the software 

provided adequate fits to the data for the incidence of nephropathy in male and female mice (x2

 p-value 

≥0.1). As assessed by lowest Akaike Information Criterion (AIC), the logistic model for the male mouse 
BARIUM AND BARIUM COMPOUNDS A-7 

APPENDIX A 

data and the gamma model for the female mouse data provide the greatest fit. The results of the 

benchmark dose analysis are presented in Table A-2. 

Table A-1. Incidence of Nephropathy in Male and Female Mice Exposed to 

Barium Chloride in Drinking Water for 2 Years (NTP 1994) 

Water concentration Dose 

(ppm) (mg barium/kg/day) Incidence 

Males 

0 0 1/50 

500 30 0/50 

1,250 75 2/48 

2,500 160 19/50 

Females 

0 0 0/50 

500 40 2/53 

1,250 90 1/50 

2,500 200 37/50 

Table A-2. Predictions from Models for Doses Associated with 10 and 5% Extra 

Risk for the Incidence of Nephropathy in Male and Female Mice Exposed to 

Barium in Drinking Water for 2 Years (NTP 1994) 

BMD10 BMDL10 BMD5 BMDL5 

Model mg/kg/day mg/kg/day mg/kg/day mg/kg/day x2

 p-value AIC 

Male mice 

Logistic 103.96 87.26 80.06 61.13 0.28 99.34 

Probit 96.13 80.07 71.96 54.66 0.13 100.11 

Log-probita 

99.73 77.90 83.39 59.54 0.31 100.25 

Gammab 

102.31 80.06 84.94 59.65 0.31 100.28 

 Log-logistica 

104.44 80.50 86.43 59.69 0.31 100.32 

 Weibullb 

106.59 81.79 87.63 59.54 0.31 100.35 

 Quantal quadratic 82.83 69.51 57.80 48.5 0.14 101.89 

Multi-stagec 

82.83 69.14 57.80 44.97 0.14 101.89 

 Quantal linear NA NA NA NA 0.0032 111.94 

Female mice 

Gammab 

125.59 101.49 113.96 87.66 0.34 90.89 

Log-probita 

134.85 100.63 125.10 88.39 0.17 92.84 

 Log-logistica 

147.43 101.75 137.35 87.01 0.17 92.84 

 Weibullb 

153.60 102.66 142.51 84.95 0.17 92.84 

 Logistic NA NA NA NA 0.08 92.35 
BARIUM AND BARIUM COMPOUNDS A-8 

APPENDIX A 

Table A-2. Predictions from Models for Doses Associated with 10 and 5% Extra 

Risk for the Incidence of Nephropathy in Male and Female Mice Exposed to 

Barium in Drinking Water for 2 Years (NTP 1994) 

BMD10 BMDL10 BMD5 BMDL5 

Model mg/kg/day mg/kg/day mg/kg/day mg/kg/day x2

 p-value AIC 

Probit NA NA NA NA 0.03 94.03 

 Quantal quadratic NA NA NA NA 0.01 102.21 

Multi-stagec 

NA NA NA NA 0.01 102.21 

 Quantal linear NA NA NA NA 0.00 126.61 

a

slope restricted to >1

b

restrict power ≥1 c

restrict betas ≥0 

degree of polynomial = 2; NA = not applicable 

The BMDL05 for male mice was selected as the point of departure for deriving the chronic-duration oral 

MRL. Data from the male mice were used because they identify a lower BMDL than the female data. 

The predicted 5% incidence approach was selected over the other two approaches as a precaution due to 

the severity of the observed effects (moderate to marked severity nephropathy), which resulted in marked 

weight loss and increased mortality. 

[ ] NOAEL [ ] LOAEL [X] BMDL 

Uncertainty Factors used in MRL derivation: 300 

[ ] 10 for use of a LOAEL 

[X] 10 for extrapolation from animals to humans 

[X] 10 for human variability 

Modifying Factor used in MRL derivation: 3 

[X] 3 for database deficiences 

A modifying factor of 3 was included to account for deficiencies in the oral toxicity database, particularly 

the need for an additional developmental toxicity study. Decreases in pup birth weight and a 

nonstatistically significant decrease in live litter size were observed in the offspring of rats exposed to 

180/200 mg Ba/kg/day as barium chloride in drinking water prior to mating (Dietz et al. 1992). Maternal 

body weight gain and water consumption were not reported, thus it is not known if the decreases in pup 

body weight were secondary to maternal toxicity or direct effect on the fetus. No developmental effects 

were observed in mice at the highest dose tested (200 mg Ba/kg/day) (Dietz et al. 1992). One other study 

examined the potential for developmental toxicity in orally exposed animals (Tarasenko et al. 1977). 

However, because the study was poorly reported and no incidence data or statistical analysis were 

presented in the published paper, the reported findings of increased mortality and systemic toxicity in the 

offspring of an unspecified species orally exposed to barium during conception and pregnancy can not be 

adequately evaluated. The Dietz et al. (1992) study was designed to be a mating trial and did not expose 
BARIUM AND BARIUM COMPOUNDS A-9 

APPENDIX A 

the animals during gestation; thus, database is lacking an adequate study to evaluate the potential for 

barium to induce developmental effects. 

Was a conversion factor used from ppm in food or water to a mg/body weight dose? No. Doses were 

calculated by the investigators using measured drinking water consumption and body weight data. 

Was a conversion used from intermittent to continuous exposure? Not applicable. 

Other additional studies or pertinent information that lend support to this MRL: Several studies have 

examined the toxicity of barium following chronic-duration exposure. Significant increases in blood 

pressure were observed in rats exposed to 0.8 mg barium/kg/day as barium chloride in drinking water for 

16 months (Perry et al. 1983, 1985, 1989); the NOAEL for this effect was 0.17 mg barium/kg/day. At 

higher doses (7.2 mg barium/kg/day), depressed rates of cardiac contraction, reduced cardiac electrical 

conductivity, and decreased cardiac ATP levels were observed. As noted in the discussion of the 

intermediate-duration oral MRL, interpretation of the results of this study is limited due to the low 

mineral diet which may have supplied inadequate levels of calcium. 

No adverse effects were observed in rats exposed to 60 mg barium/kg/day as barium chloride in drinking 

water for 2 years (NTP 1994), 15 mg barium/kg/day to an unspecified barium compound in drinking 

water for 68 weeks (McCauley et al. 1985), or 0.7 mg barium/kg/day as barium acetate in drinking water 

for a lifetime (Schroeder and Mitchener 1975a). In mice exposed to barium chloride in drinking water for 

2 years, marked renal nephropathy was observed at 160 mg barium/kg/day; the increased incidence of 

nephropathy in the next lowest dose group (75 mg barium/kg/day) was not statistically significant. Other 

adverse effects observed at 160 mg barium/kg/day included weight loss and increased mortality. 

The animal data provide suggestive evidence that the kidney is the most sensitive target of toxicity. A 

serious LOAEL of 160 mg barium/kg/day was identified for nephropathy in mice (NTP 1994); the 

NOAEL identified in this study is 75 mg/kg/day. Although no kidney lesions were observed in rats 

exposed to doses as high as 60 mg barium/kg/day (NTP 1994), the doses utilized in the study may not 

have been high enough to cause kidney damage. Biologically significant kidney alterations were 

observed at 115 mg barium/kg/day and higher in rats exposed for an intermediate duration (NTP 1994). 

Agency Contacts (Chemical Managers): Cassandra Smith and Yee-Wan Stevens 
BARIUM AND BARIUM COMPOUNDS A-10 

APPENDIX A 

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BARIUM AND BARIUM COMPOUNDS B-1 

APPENDIX B. USER'S GUIDE 

Chapter 1 

Public Health Statement 

This chapter of the profile is a health effects summary written in non-technical language. Its intended 

audience is the general public, especially people living in the vicinity of a hazardous waste site or 

chemical release. If the Public Health Statement were removed from the rest of the document, it would 

still communicate to the lay public essential information about the chemical. 

The major headings in the Public Health Statement are useful to find specific topics of concern. The 

topics are written in a question and answer format. The answer to each question includes a sentence that 

will direct the reader to chapters in the profile that will provide more information on the given topic. 

Chapter 2 

Relevance to Public Health 

This chapter provides a health effects summary based on evaluations of existing toxicologic, 

epidemiologic, and toxicokinetic information. This summary is designed to present interpretive, weightof-evidence discussions for human health end points by addressing the following questions: 

1.	 What effects are known to occur in humans? 

2. What effects observed in animals are likely to be of concern to humans? 

3. What exposure conditions are likely to be of concern to humans, especially around hazardous 

waste sites? 

The chapter covers end points in the same order that they appear within the Discussion of Health Effects 

by Route of Exposure section, by route (inhalation, oral, and dermal) and within route by effect. Human 

data are presented first, then animal data. Both are organized by duration (acute, intermediate, chronic). 

In vitro data and data from parenteral routes (intramuscular, intravenous, subcutaneous, etc.) are also 

considered in this chapter. 

The carcinogenic potential of the profiled substance is qualitatively evaluated, when appropriate, using 

existing toxicokinetic, genotoxic, and carcinogenic data. ATSDR does not currently assess cancer 

potency or perform cancer risk assessments. Minimal Risk Levels (MRLs) for noncancer end points (if 

derived) and the end points from which they were derived are indicated and discussed. 

Limitations to existing scientific literature that prevent a satisfactory evaluation of the relevance to public 

health are identified in the Chapter 3 Data Needs section. 

Interpretation of Minimal Risk Levels 

Where sufficient toxicologic information is available, ATSDR has derived MRLs for inhalation and oral 

routes of entry at each duration of exposure (acute, intermediate, and chronic). These MRLs are not 

meant to support regulatory action, but to acquaint health professionals with exposure levels at which 

adverse health effects are not expected to occur in humans. 
BARIUM AND BARIUM COMPOUNDS B-2 

APPENDIX B 

MRLs should help physicians and public health officials determine the safety of a community living near 

a chemical emission, given the concentration of a contaminant in air or the estimated daily dose in water. 

MRLs are based largely on toxicological studies in animals and on reports of human occupational 

exposure. 

MRL users should be familiar with the toxicologic information on which the number is based. Chapter 2, 

"Relevance to Public Health," contains basic information known about the substance. Other sections such 

as Chapter 3 Section 3.9, "Interactions with Other Substances,” and Section 3.10, "Populations that are 

Unusually Susceptible" provide important supplemental information. 

MRL users should also understand the MRL derivation methodology. MRLs are derived using a 

modified version of the risk assessment methodology that the Environmental Protection Agency (EPA) 

provides (Barnes and Dourson 1988) to determine reference doses (RfDs) for lifetime exposure. 

To derive an MRL, ATSDR generally selects the most sensitive end point which, in its best judgement, 

represents the most sensitive human health effect for a given exposure route and duration. ATSDR 

cannot make this judgement or derive an MRL unless information (quantitative or qualitative) is available 

for all potential systemic, neurological, and developmental effects. If this information and reliable 

quantitative data on the chosen end point are available, ATSDR derives an MRL using the most sensitive 

species (when information from multiple species is available) with the highest no-observed-adverse-effect 

level (NOAEL) that does not exceed any adverse effect levels. When a NOAEL is not available, a 

lowest-observed-adverse-effect level (LOAEL) can be used to derive an MRL, and an uncertainty factor 

(UF) of 10 must be employed. Additional uncertainty factors of 10 must be used both for human 

variability to protect sensitive subpopulations (people who are most susceptible to the health effects 

caused by the substance) and for interspecies variability (extrapolation from animals to humans). In 

deriving an MRL, these individual uncertainty factors are multiplied together. The product is then 

divided into the inhalation concentration or oral dosage selected from the study. Uncertainty factors used 

in developing a substance-specific MRL are provided in the footnotes of the levels of significant exposure 

(LSE) tables. 

Chapter 3 

Health Effects 

Tables and Figures for Levels of Significant Exposure (LSE) 

Tables and figures are used to summarize health effects and illustrate graphically levels of exposure 

associated with those effects. These levels cover health effects observed at increasing dose 

concentrations and durations, differences in response by species, MRLs to humans for noncancer end 

points, and EPA's estimated range associated with an upper- bound individual lifetime cancer risk of 1 in 

10,000 to 1 in 10,000,000. Use the LSE tables and figures for a quick review of the health effects and to 

locate data for a specific exposure scenario. The LSE tables and figures should always be used in 

conjunction with the text. All entries in these tables and figures represent studies that provide reliable, 

quantitative estimates of NOAELs, LOAELs, or Cancer Effect Levels (CELs). 

The legends presented below demonstrate the application of these tables and figures. Representative 

examples of LSE Table 3-1 and Figure 3-1 are shown. The numbers in the left column of the legends 

correspond to the numbers in the example table and figure. 
BARIUM AND BARIUM COMPOUNDS B-3 

APPENDIX B 

LEGEND 

See Sample LSE Table 3-1 (page B-6) 

(1) Route of Exposure. One of the first considerations when reviewing the toxicity of a substance 

using these tables and figures should be the relevant and appropriate route of exposure. Typically 

when sufficient data exist, three LSE tables and two LSE figures are presented in the document. 

The three LSE tables present data on the three principal routes of exposure, i.e., inhalation, oral, 

and dermal (LSE Tables 3-1, 3-2, and 3-3, respectively). LSE figures are limited to the inhalation 

(LSE Figure 3-1) and oral (LSE Figure 3-2) routes. Not all substances will have data on each 

route of exposure and will not, therefore, have all five of the tables and figures. 

(2) Exposure Period. Three exposure periods—acute (less than 15 days), intermediate (15– 

364 days), and chronic (365 days or more)—are presented within each relevant route of exposure. 

In this example, an inhalation study of intermediate exposure duration is reported. For quick 

reference to health effects occurring from a known length of exposure, locate the applicable 

exposure period within the LSE table and figure. 

(3) Health Effect. The major categories of health effects included in LSE tables and figures are 

death, systemic, immunological, neurological, developmental, reproductive, and cancer. 

NOAELs and LOAELs can be reported in the tables and figures for all effects but cancer. 

Systemic effects are further defined in the "System" column of the LSE table (see key number 

18). 

(4) Key to Figure. Each key number in the LSE table links study information to one or more data 

points using the same key number in the corresponding LSE figure. In this example, the study 

represented by key number 18 has been used to derive a NOAEL and a Less Serious LOAEL 

(also see the two "18r" data points in sample Figure 3-1). 

(5) Species. The test species, whether animal or human, are identified in this column. Chapter 2, 

"Relevance to Public Health," covers the relevance of animal data to human toxicity and 

Section 3.4, "Toxicokinetics," contains any available information on comparative toxicokinetics. 

Although NOAELs and LOAELs are species specific, the levels are extrapolated to equivalent 

human doses to derive an MRL. 

(6) Exposure Frequency/Duration. The duration of the study and the weekly and daily exposure 

regimens are provided in this column. This permits comparison of NOAELs and LOAELs from 

different studies. In this case (key number 18), rats were exposed to “Chemical x” via inhalation 

for 6 hours/day, 5 days/week, for 13 weeks. For a more complete review of the dosing regimen, 

refer to the appropriate sections of the text or the original reference paper (i.e., Nitschke et al. 

1981). 

(7) System. This column further defines the systemic effects. These systems include respiratory, 

cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, and 

dermal/ocular. "Other" refers to any systemic effect (e.g., a decrease in body weight) not covered 

in these systems. In the example of key number 18, one systemic effect (respiratory) was 

investigated. 

(8) NOAEL. A NOAEL is the highest exposure level at which no harmful effects were seen in the 

organ system studied. Key number 18 reports a NOAEL of 3 ppm for the respiratory system, 

which was used to derive an intermediate exposure, inhalation MRL of 0.005 ppm (see 

footnote "b"). 
BARIUM AND BARIUM COMPOUNDS B-4 

APPENDIX B 

(9) LOAEL. A LOAEL is the lowest dose used in the study that caused a harmful health effect. 

LOAELs have been classified into "Less Serious" and "Serious" effects. These distinctions help 

readers identify the levels of exposure at which adverse health effects first appear and the 

gradation of effects with increasing dose. A brief description of the specific end point used to 

quantify the adverse effect accompanies the LOAEL. The respiratory effect reported in key 

number 18 (hyperplasia) is a Less Serious LOAEL of 10 ppm. MRLs are not derived from 

Serious LOAELs. 

(10) Reference. The complete reference citation is given in Chapter 9 of the profile. 

(11) CEL. A CEL is the lowest exposure level associated with the onset of carcinogenesis in 

experimental or epidemiologic studies. CELs are always considered serious effects. The LSE 

tables and figures do not contain NOAELs for cancer, but the text may report doses not causing 

measurable cancer increases. 

(12) Footnotes. Explanations of abbreviations or reference notes for data in the LSE tables are found 

in the footnotes. Footnote "b" indicates that the NOAEL of 3 ppm in key number 18 was used to 

derive an MRL of 0.005 ppm. 

LEGEND 

See Sample Figure 3-1 (page B-7) 

LSE figures graphically illustrate the data presented in the corresponding LSE tables. Figures help the 

reader quickly compare health effects according to exposure concentrations for particular exposure 

periods. 

(13) Exposure Period. The same exposure periods appear as in the LSE table. In this example, health 

effects observed within the acute and intermediate exposure periods are illustrated. 

(14) Health Effect. These are the categories of health effects for which reliable quantitative data 

exists. The same health effects appear in the LSE table. 

(15)	 Levels of Exposure. Concentrations or doses for each health effect in the LSE tables are 

graphically displayed in the LSE figures. Exposure concentration or dose is measured on the log 

scale "y" axis. Inhalation exposure is reported in mg/m3

 or ppm and oral exposure is reported in 

mg/kg/day. 

(16) NOAEL. In this example, the open circle designated 18r identifies a NOAEL critical end point in 

the rat upon which an intermediate inhalation exposure MRL is based. The key number 18 

corresponds to the entry in the LSE table. The dashed descending arrow indicates the 

extrapolation from the exposure level of 3 ppm (see entry 18 in the table) to the MRL of 

0.005 ppm (see footnote "b" in the LSE table). 

(17) CEL. Key number 38m is one of three studies for which CELs were derived. The diamond 

symbol refers to a CEL for the test species-mouse. The number 38 corresponds to the entry in the 

LSE table. 
BARIUM AND BARIUM COMPOUNDS 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. 
3 4 

SAMPLE 

1 → Table 3-1. Levels of Significant Exposure to [Chemical x] – Inhalation 

LOAEL (effect) Exposure 

Key to frequency/ NOAEL Less serious Serious (ppm) 

figurea Species duration System (ppm) (ppm) Re

2 → INTERMEDIATE EXPOSURE 

5 

→ Systemic ↓

18 Rat 

→

CHRONIC EXPOSURE Cancer 38 Rat 39 Rat 40 Mouse 

6↓13 wk 5 d/wk 6 hr/d 18 mo 5 d/wk 7 hr/d 89–104 wk 5 d/wk 6 hr/d 79–103 wk 5 d/wk 6 hr/d 

7 8 9 

↓ ↓ ↓

3b Resp 10 (hyperplasia) 

11 ↓20 (CEL, multiple 

organs) 

10 (CEL, lung tumors, 

nasal tumors) 

10 (CEL, lung tumors, 

hemangiosarcomas) 

10 

↓

NitWoNTNT

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 ex

by an uncertainty factor of 100 (10 for extrapolation from animal to humans, 10 for human variability). 

BARIUM AND BARIUM COMPOUNDS B-8 

APPENDIX B 

This page is intentionally blank. 
BARIUM AND BARIUM COMPOUNDS C-1 

APPENDIX C. ACRONYMS, ABBREVIATIONS, AND SYMBOLS 

ACGIH American Conference of Governmental Industrial Hygienists 

ACOEM American College of Occupational and Environmental Medicine 

ADI acceptable daily intake 

ADME absorption, distribution, metabolism, and excretion 

AED atomic emission detection 

AFID alkali flame ionization detector 

AFOSH Air Force Office of Safety and Health 

ALT alanine aminotransferase 

AML acute myeloid leukemia 

AOAC Association of Official Analytical Chemists 

AOEC Association of Occupational and Environmental Clinics 

AP alkaline phosphatase 

APHA American Public Health Association 

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 

DHEW Department of Health, Education, and Welfare 

DHHS Department of Health and Human Services 

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/Intergovernmental Maritime Dangerous Goods Code 
BARIUM AND BARIUM COMPOUNDS C-2 

APPENDIX C 

DWEL drinking water exposure level 

ECD electron capture detection 

ECG/EKG electrocardiogram 

EEG electroencephalogram 

EEGL Emergency Exposure Guidance Level 

EPA Environmental Protection Agency 

F Fahrenheit 

F1 first-filial generation 

FAO Food and Agricultural Organization of the United Nations 

FDA Food and Drug Administration 

FEMA Federal Emergency Management Agency 

FIFRA Federal Insecticide, Fungicide, and Rodenticide Act 

FPD flame photometric detection 

fpm feet per minute 

FR Federal Register 

FSH follicle stimulating hormone 

g gram 

GC gas chromatography 

gd gestational day 

GLC gas liquid chromatography 

GPC gel permeation chromatography 

HPLC high-performance liquid chromatography 

HRGC high resolution gas chromatography 

HSDB Hazardous Substance Data Bank 

IARC International Agency for Research on Cancer 

IDLH immediately dangerous to life and health 

ILO International Labor Organization 

IRIS Integrated Risk Information System 

Kd adsorption ratio 

kg kilogram 

kkg metric ton 

Koc organic carbon partition coefficient 

Kow octanol-water partition coefficient 

L liter 

LC liquid chromatography 

LC50 lethal concentration, 50% kill 

LCLo lethal concentration, low 

LD50 lethal dose, 50% kill 

LDLo lethal dose, low 

LDH lactic dehydrogenase 

LH luteinizing hormone 

LOAEL lowest-observed-adverse-effect level 

LSE Levels of Significant Exposure 

LT50 lethal time, 50% kill 

m meter 

MA trans,trans-muconic acid 

MAL maximum allowable level 

mCi millicurie 

MCL maximum contaminant level 

MCLG maximum contaminant level goal 

MF modifying factor 
BARIUM AND BARIUM COMPOUNDS C-3 

APPENDIX C 

MFO mixed function oxidase 

mg milligram 

mL milliliter 

mm millimeter 

mmHg millimeters of mercury 

mmol millimole 

mppcf millions of particles per cubic foot 

MRL Minimal Risk Level 

MS mass spectrometry 

NAAQS National Ambient Air Quality Standard 

NAS National Academy of Science 

NATICH National Air Toxics Information Clearinghouse 

NATO North Atlantic Treaty Organization 

NCE normochromatic erythrocytes 

NCEH National Center for Environmental Health 

NCI National Cancer Institute 

ND not detected 

NFPA National Fire Protection Association 

ng nanogram 

NHANES National Health and Nutrition Examination Survey 

NIEHS National Institute of Environmental Health Sciences 

NIOSH National Institute for Occupational Safety and Health 

NIOSHTIC NIOSH's Computerized Information Retrieval System 

NLM National Library of Medicine 

nm nanometer 

nmol nanomole 

NOAEL no-observed-adverse-effect level 

NOES National Occupational Exposure Survey 

NOHS National Occupational Hazard Survey 

NPD nitrogen phosphorus detection 

NPDES National Pollutant Discharge Elimination System 

NPL National Priorities List 

NR not reported 

NRC National Research Council 

NS not specified 

NSPS New Source Performance Standards 

NTIS National Technical Information Service 

NTP National Toxicology Program 

ODW Office of Drinking Water, EPA 

OERR Office of Emergency and Remedial Response, EPA 

OHM/TADS Oil and Hazardous Materials/Technical Assistance Data System 

OPP Office of Pesticide Programs, EPA 

OPPT Office of Pollution Prevention and Toxics, EPA 

OPPTS Office of Prevention, Pesticides and Toxic Substances, EPA 

OR odds ratio 

OSHA Occupational Safety and Health Administration 

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 
BARIUM AND BARIUM COMPOUNDS C-4 

APPENDIX C 

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 

VOC volatile organic compound 

WBC white blood cell 

WHO World Health Organization 
BARIUM AND BARIUM COMPOUNDS C-5 

APPENDIX C 

> greater than ≥ greater than or equal to 

= equal to 

< less than ≤ less than or equal to 

% percent α alpha β beta γ gamma δ delta μm micrometer μg microgram q1 

* cancer slope factor 

– negative 

+ positive 

(+) weakly positive result 

(–) weakly negative result 
BARIUM AND BARIUM COMPOUNDS C-6 

APPENDIX C 

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BARIUM AND BARIUM COMPOUNDS D-1 

APPENDIX D. INDEX 

absorbed dose..............................................................................................................................................72 

adsorbed ....................................................................................................................................................119 

adsorption.......................................................................................................................................... 107, 117 

aerobic.......................................................................................................................................................127 

ambient air ............................................................................................ 9, 120, 128, 129, 131, 134, 136, 137 

anaerobic...................................................................................................................................................127 

atropine .......................................................................................................................................................74 

bioavailability ...........................................................................................................................................136 

bioconcentration factor .............................................................................................................................117 

biomarker .................................................................................................................. 71, 72, 73, 86, 141, 147
 

body weight effects ......................................................................................................................... 25, 52, 57 

breast milk................................................................................................................................. 132, 134, 138 

cancer ............................................................................................................ 4, 5, 10, 26, 56, 58, 70, 83, 149 

carcinogen............................................................................................................................. 11, 83, 149, 151 

carcinogenic .................................................................................................................. 6, 11, 12, 21, 56, 149 

carcinogenicity.................................................................................................................... 5, 11, 56, 83, 151 

carcinomas ..................................................................................................................................................59 

cardiovascular ........................................................................... 10, 14, 17, 27, 48, 57, 73, 74, 75, 81, 82, 85 

cardiovascular effects................................................................................................................ 24, 28, 57, 82 

cation exchange capacity .................................................................................................. 107, 117, 119, 136 

clearance .....................................................................................................................................................61 

death.................................................................................................................. 10, 21, 23, 27, 28, 57, 74, 85
 

deoxyribonucleic acid (see DNA)...............................................................................................................59 

dermal effects.................................................................................................................................. 52, 57, 58 

DNA (see deoxyribonucleic acid)............................................................................................. 59, 60, 72, 83 

drinking water ........................ 1, 3, 6, 7, 9, 10, 11, 14, 15, 16, 17, 18, 26, 27, 28, 48, 49, 50, 51, 52, 53, 54, 

55, 56, 63, 76, 79, 82, 84, 85, 107, 115, 121, 122, 128, 129, 134, 137, 151 

endocrine................................................................................................................................... 23, 57, 68, 69 

fetus....................................................................................................................................................... 69, 84 

fractional absorption ...................................................................................................................................62 

gastrointestinal effects ........................................................................................................ 10, 24, 49, 57, 80
 

general population....................................................................................... 9, 71, 75, 76, 107, 129, 134, 137 

genotoxic............................................................................................................................................... 21, 83 

genotoxicity........................................................................................................................................... 59, 83 

groundwater .......................................................................................... 9, 107, 115, 117, 122, 134, 136, 137 

half-life........................................................................................................................................................71 

hematological effects ............................................................................................................................ 24, 49 

hepatic effects ....................................................................................................................................... 24, 50 

hypokalemia.......................................................................................... 10, 28, 50, 68, 73, 74, 77, 80, 86, 87 

immune system ...........................................................................................................................................84 

immunological .......................................................................................................................... 21, 25, 53, 84 

immunological effects..................................................................................................................... 25, 53, 84 

LD50........................................................................................................................................... 27, 28, 55, 80 

leukemia......................................................................................................................................................56 

lymphoreticular..................................................................................................................................... 53, 84 

Metabolic Effects............................................................................................................................ 25, 52, 58 

milk ........................................................................................................................................... 127, 134, 138 

musculoskeletal effects ................................................................................................................... 24, 49, 50 

neoplastic ....................................................................................................................................................83 
BARIUM AND BARIUM COMPOUNDS D-2 

APPENDIX D 

neurobehavioral............................................................................................................................... 15, 69, 85 

nuclear.......................................................................................................................................................143 

ocular effects......................................................................................................................................... 23, 52 

particulate.......................................................................................... 107, 114, 116, 118, 119, 120, 121, 134 

particulate emissions......................................................................................................................... 114, 121 

pharmacodynamic.......................................................................................................................................65 

pharmacokinetic.................................................................................................................. 64, 65, 67, 70, 74 

renal effects............................................................................................................................... 10, 25, 50, 68 

retention ............................................................................................................................ 61, 63, 71, 74, 119 

sequestered..................................................................................................................................................72 

serum glutamic-oxaloacetic transaminase (see SGOT) ..............................................................................50 

serum glutamic pyruvic transaminase (see SGPT) .....................................................................................50 

SGOT (see serum glutamic-oxaloacetic transaminase) ..............................................................................50 

SGPT (see serum glutamic pyruvic transaminase) .....................................................................................50 

solubility ................................................................................................................... 9, 61, 89, 118, 119, 120 

surface water ................................................................. 3, 107, 115, 117, 118, 120, 121, 122, 135, 136, 137
 

toxicokinetic............................................................................................................ 21, 71, 72, 82, 84, 87, 88 

tumors ................................................................................................................................................... 56, 58 

vapor pressure .............................................................................................................................................95 
BARIUM AND BARIUM COMPOUNDS D-3