United States
              Environmental Protection
              Agency
              Office of Health and
              Environmental Assessment
              Washington DC 20460
EPA/60O/8-84/O26F
November 1987
&EPA
              Research and Development
Health Assessment
Document for
Beryllium

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                                   EPA/600/8-84/026F
                                   November 1987
   Assessment Document
     for  Beryllium
 U.S. ENVIRONMENTAL PROTECTION AGENCY
    Office of Research and Development
Office of Health and Environmental Assessment
 Environmental Criteria and Assessment Office
 Research Triangle Park, North Carolina 27711

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                                  DISCLAIMER
     This document  has  been reviewed in accordance with the U.S.  Environmental
Protection Agency's peer ;and administrative review policies  and  approved for
presentation and publication.   Mention of trade names  or  commercial  products
does not constitute endorsement or recommendation for use.

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                               TABLE OF CONTENTS
LIST OF TABLES	.	     vi
LIST OF FIGURES	..........."	     viii
PREFACE	     ix
ABSTRACT		-.	     x
AUTHORS, REVIEWERS, AND CONTRIBUTORS		     xi

I.  INTRODUCTION	     1-1

2.  SUMMARY AND CONCLUSIONS 	.-	     2-1
    2.1  BACKGROUND INFORMATION 	     2-1
    2.2  BERYLLIUM METABOLISM	     2-1
    2.3  BERYLLIUM TOXICOLOGY 	 	     2-2
         2.3.1   Subcellular and Cellular Aspects of Beryllium
                 Toxicity	     2-2
         2.3.2   Pulmonary and Systemic Toxicity of Beryllium in
                 Man and Animal s 	     2-3
         2.3.3   Dermatological Effects of Beryllium Exposure 	     2-5
         2.3.4   Teratogenic and Reproductive Effects of Beryllium
                 Exposure 	     2-5
    2.4  MUTAGENIC EFFECTS OF BERYLLIUM EXPOSURE 	     2-5
    2.5  CARCINOGENIC EFFECTS OF BERYLLIUM EXPOSURE	     2-6
         2.5.1   Animal Studies	     2-6
         2.5.2   Human Studies	     2-7
         2.5.3   Qualitative Carcinogenicity Conclusions	     2-7 "
    2.6  HUMAN HEALTH RISK ASSESSMENT OF BERYLLIUM 	     2-8
         2.6.1   Exposure Aspects 	     2-8
         2.6.2   Relevant Health Effects	     2-8
         2.6.3   Dose-Effect and Dose-Response Relationships of
                 Beryllium	     2-9
         2.6.4   Populations at Risk	     2-12

3.  BERYLLIUM BACKGROUND INFORMATION 		     3-1
    3.1  GEOCHEMICAL AND INDUSTRIAL BACKGROUND 	     3-1
         3.1.1   Geochemistry of Beryllium		*	     3-1
         3.1.2   Production and Consumption of Beryllium Ore	     3-3
         3.1.3.  Industrial Uses of Beryllium	     3-3
    3.2  CHEMICAL AND PHYSICAL PROPERTIES OF BERYLLIUM 	     3-5
    3.3  SAMPLING AND ANALYSIS TECHNIQUES FOR BERYLLIUM 	     3-6
    3.4  ATMOSPHERIC EMISSIONS, TRANSFORMATION, AND DEPOSITION 	     3-7
    3.5  ENVIRONMENTAL CONCENTRATIONS OF BERYLLIUM 	     3-12
         3.5.1   Ambient Air	•.	     3-12
         3.5.2   Soils .and Natural Waters	     3-12
    3.6  PATHWAYS TO HUMAN CONSUMPTION '	     3-20.

4.  BERYLLIUM METABOLISM IN MAN AND ANIMALS	     4-1
    4.1  ROUTES.OF BERYLLIUM ABSORPTION 	     4-1
         4.1.1   Beryllium Absorption by Inhalation 	     4-1
         4.1.2   Gastrointestinal Absorption of Beryllium 	     4-3

                                      iii

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                                                                          Paqe
                         TABLE OF CONTENTS  (continued)
          4.1.3    Percutaneous  Absorption  of Beryllium  	     4-4
          4.1.4    Transplacental  Transfer  of Beryllium  	              4-4
    4.2   TRANSPORT AND  DEPOSITION  OF  BERYLLIUM IN  MAN  AND
          EXPERIMENTAL ANIMALS  	                      4-4
    4.3   EXCRETION OF BERYLLIUM  IN MAN  AND  ANIMALS	     4-5

5.  BERYLLIUM TOXICOLOGY  .,	                 5-1
    5.1   ACUTE  EFFECTS  OF .BERYLLIUM EXPOSURE IN MAN AND ANIMALS  	     5-1
          5.1.1    Human  Studies	     5-1
          5.1.2    Animal Studies  	                   5-2
    5.2   CHRONIC  EFFECTS  OF  BERYLLIUM EXPOSURE IN  MAN  AND ANIMALS  ...     5-2
          5.2.1    Respiratory and Systemic Effects  of Beryllium 	     5-2
                  5.2.1.1  Human  Studies 	     5-2
                  5.2.1.2  Animal Studies	     5-13
          5.2.2    Teratogenic and Reproductive  Effects  of Beryllium  ..     5-17
                  5.2.2.1  Human  Studies 	     5-17
                  5.2.2.2  Animal Studies	     5-17

6.  MUTAGENIC EFFECTS OF  BERYLLIUM 	                        6-1
    6.1   GENE MUTATIONS IN BACTERIA AND YEAST	     6-1
          6.1.1    Salmonella  Assay  	     6-1
          6.1.2    Host-Mediated Assay  	     6-3
          6.1.3    Escherichia col i  WP2 Assay	     6-3
    6.2   GENE MUTATIONS IN CULTURED MAMMALIAN  CELLS 	     6-3
    6.3   CHROMOSOMAL ABERRATIONS	               6-5
    6.4   SISTER CHROMATID EXCHANGES 	     6-7
    6.5   OTHER TESTS OF GENOTOXIC  POTENTIAL  	     6-7
          6.5.1    The Rec Assay	     6-7
          6.5.2    Pol Assay	     6-8
          6.5.3    Hepatocyte  Primary Culture/DNA Repair Test	     6-8
          6.5.4    Berylliurn-Induced  DNA Cell  Binding	     6-9
          6.5.5    Mitotic Recombination in Yeast 	     6-9
          6.5.6    Biochemical Evidence of .Genotoxicity	     6-9
          6.5.7    Mutagenicity  Studies in Whole Animals 	     6-10

7.  CARCINOGENIC  EFFECTS OF  BERYLLIUM 	    7-1
    7.1  ANIMAL STUDIES 	    7-1
         7.1.1    Inhalation  Studies 	    7-1
         7.1.2    Intratracheal  Injection Studies	    7-8
         7.1.3    Intravenous Injection .Studies 	    7-10
         7.1.4    Intramedullary Injection Studies  	    7-17
         7.1.5    Intracutaneous Injection Studies  	    7-17
         7.1.6   The Percutaneous Route of Exposure 	.•	    7-18
         7.1.7   Dietary Route of Exposure	    7-18
         7.1.8   Tumor Type, Species Specificity, Carcinogenic
                  Forms,  and Dose-Response 	    7-19
                 7.1.8.1  Tumor Type and Proof of Malignancy	    7-19
                 7.1.8.2  Species Specificity and Immunobiology 	    7-20
                                      IV

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                        TABLE OF CONTENTS  (continued)
                 7.1.8.3  Carcinogenic Forms and Dose-Response
                          Relationships 	
         7.1.9   Summary of Animal Studies 	
    7.2  EPIDEMIOLOGIC STUDIES	
         7.2.1   Bayliss et al. (1971)	
         7.2.2   Bayliss and Lainhart (1972, unpublished) 	
         7.2.3   Bayliss and Wagoner (1977, unpublished) 	
         7.2.4   Wagoner et al. (1980)	
         7.2.5   Infante et al. (1980) 	
         7.2.6   Mancuso and El-Attar (1969)	
         7.2.7   Mancuso (1970)	
         7.2.8   Mancuso (1979) 	
         7.2.9   Mancuso (1980) 	
         7.2.10  Summary of Epidemiologic Studies 	
    7.3  QUANTITATIVE ESTIMATION
         7.3.1   Procedures for the Determination of Unit Risk 	
                 7.3.1.1  Low-Dose Extrapolation Model 	
                 7.3.1.2  Selection of Data	
                 7.3.1.3  Calculation of Human Equivalent Dosages ..
                          7.3.1.3.1  Inhalation Exposure 	
                 7.3.1.4  Calculation of the Unit Risk from Animal
                          Studi es	
                          7.3.1.4.1  Adjustments for Less Than Life
                                     Span Duration of Experiment ...
                 7.3.1.5  Model for Estimation of Unit Risk Based
                          on Human Data 	
         7.3.2   Estimation of the Carcinogenic Risk of Beryllium ..
                 7.3.2.1  Calculation of the Carcinogenic Potency
                          of Beryllium on the Basis of Animal  Data  .
                 7.3.2.2  Calculation of the Carcinogenic Potency
                          of Beryllium on the Basis of Human Data ..
                          7.3.2.2.1  Information on. Exposure Levels
                          7.3.2.2.2  Information on Excess Risk 	
                          7.3.2.2.3  Risk Calculation on the Basis
                                     of Human Data 	
                 7.3.2.3  Risk Due to Exposure to 1 ug/m3 of
                          Beryl 1iurn in Air	
                 Comparison of Potency With Other Compounds 	
                 Summary of Quantitative Assessment	
     7.3.3
     7.3.4
7.4  SUMMARY
     7.4.1   Qualitative Summary
     7.4.2   Quantitative Summary
7.5  CONCLUSIONS 	
8.  REFERENCES
APPENDIX - Analysis of Incidence Data with Time-dependent
                 Dose Pattern 	
7-21
7-23
7-27
7-27
7-28
7-29
7-30
7-40
7-43
7-44
7-45
7-48
7-51
7-54
7-57
7-57
7-60
7-60
7-61

7-62

7-63

7-63
7-65

7-68

7-74
7-75
7-75

7-76

7-76
7-80
7-80
7-87
7-87
7-89
7-93

8-1
                                                                     A-l

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                                LIST OF TABLES
Number
                                                                          Page
  3-1    Global Production and U.S. Consumption of Beryllium Ore 	     3-2
  3-2    Industrial Uses of Beryllium Products 	     3-4
  3-3    Physical Properties of Beryllium and Related Metals 	     3-6
  3-4    Natural and Anthropogenic Emissions of Beryllium	     3-8
  3-5    Concentrations of Beryllium in Urban Atmospheres 	     3-13
  3-6    Potential Human Consumption of Beryllium from Normal
         Sources in a Typical Residential.Environment 	     3-22

  5-1    Beryl 1ium Registry Cases, 1959 	     5-4
  5-2    Time from Last Exposure to First Symptom in the BCR,  1959 ...     5-4
  5-3    Changes of Latency from 1922 to Present in Occupational
         Beryl!iosis Cases 	     5-7
  5-4    Symptoms of Chronic Beryl 1 ium Disease	"    5-7
  5-5    Signs of Chronic Beryllium Disease 	     5-8
  5-6    Comparison of 1971 and 1974 Data of Workers Surveyed  in
         Beryllium Extraction and Processing Plants 		     5-11
  5-7    Comparison of 1971 and 1974 Arterial Blood Gas Results  	     5-11

  6-1    Mutagenicity Testing of Beryllium:   Gene Mutations  in
         Bacteria and in Yeast	     6-2
  6-2    Mutagenicity Testing of Beryllium:   Gene Mutations
         in Mammalian Cells In Vitro		     6-4
  6-3    Mutagenicity Testing of Beryllium:   Mammalian In Vitro
         Cytogenetics Tests 	     6-6

  7-1    Pulmonary Carcinoma from Inhalation Exposure to Beryllium ...     7-3
  7-2    Pulmonary Carcinoma from Exposure  to Beryllium Via
         Intratracheal  Insti11ation 	     7-9
  7-3    Beryllium Alloys -- Lung Neoplasms  	     7-11
  7-4    Lung Tumor Incidence in Rats Among  BeO,  As203 and Control
         Groups 	,	j	     7-12
  7-5    Histological  Classification of Lung Tumors and Other
         Pathological  Changes 	     7-12
  7-6    Osteogenic Sarcomas in Rabbits 	     7-14
  7-7    Osteosarcoma from Beryl 1i urn	     7-15
  7-8    Carcinogenicity of Beryl 1ium Compounds  	     7-24
  7-9    Percentage Distribution of Beryllium-Exposed Workers  and
         of Age-Adjusted U.S.  White Male Population by Cigarette
         Smoking Status	     7-32
  7-10    Lung Cancer Mortality Ratios for Males,  by Current  Number
         of Cigarettes  Smoked per Day,  from  Prospective Studies 	     7-33
  7-11    Observed and Expected Deaths Due to Lung Cancer According to
         Duration of Employment and Time Since Onset of Employment
         Among White Males Employed Sometime During January  1942
         Through December 1967 in a Beryllium Production Facility
         and Followed Through 1975 	     7-36
  7-12    Industries in  the Lorain Area 1942-1948	     7-48
                                      VI

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                          LIST OF TABLES (continued)
Number
Page
  7-13   Comparison of Study Cohorts and Subcohorts of Two
         Beryllium Companies	     7-52
  7-14   Problems with Beryllium Cohort Studies	     7-55
  7-15   Dose-Response from Inhalation Studies with Beryllium
         Salts on Animals and the Corresponding Potency (Slope)
         Estimations		     7-69
  7-16   Beryllium Oxide Dose-Response from Three Inhalation and
         Five Intratracheal Instillation Studies on Animals and the
         Corresponding Potency (Slope) Estimates 	     7-72
  7-17   Upper-Bound Cancer Potency Estimates Calculated Under
         Various Assumptions	     7-77
  7-18   Relative Carcinogenic Potencies Among 59 Chemicals
         Evaluated by the Carcinogen Assessment Group as Suspect
         Human Carci nogens	     7-82

  A-l    Time-to-Death Data	     A-2

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                              LIST OF FIGURES
Figure
3-1

Pathways of Environmental Beryllium Concentrations
Leading to Potential Human Exposure 	
Page
3-21
5-1    Latency of Occupational Berylliosis According to Year of
       First Exposure	      5-6

7-1    Pulmonary Tumor Incidence in Female Rats, 1965-1967 	      7-5
7-2    Histogram Representing the Frequency Distribution of the
       Potency Indices of 59 Suspect Carcinogens Evaluated by
       the Carcinogen Assessment Group 	      7-81
                                   vi n

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                                    PREFACE
     The  Office  of Health and Environmental  Assessment,  in consultation with
other  Agency  and non- Agency scientists, has prepared this health assessment to
serve  as  a "source document" for Agency-wide use.   Specifically, this document
was prepared  at  the request  of the Office of  Air Quality  Planning and Standards.
     In the  development of this assessment document, the scientific literature
.has been  inventoried, key studies have been evaluated, and summary/conclusions
have been prepared such that the  toxicity  of beryllium  is qualitatively and
where  possible,  quantitatively,  identified.  Literature  on beryllium has been
collected and reviewed up to January,  1986;  general  information pertaining to
the calculation  of unit risk values is complete through April, 1987.   Observed
effect levels and dose-response relationships are discussed where  appropriate
in  order  to  place significant health  responses  in perspective with observed
environmental  levels.

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                                   ABSTRACT
     The chemical  and geochemical  properties of beryllium  resemble  those  of
aluminum, zinc, and  magnesium.   This resemblance is primarily due to  similar
ionic potentials which facilitate covalent bonding.   The three most common  forms
of  beryllium in  industrial  emissions are  the  metal,  the  oxide,  and the
hydroxide.
     The main routes of beryllium intake for man and animals are  inhalation and
ingestion.   While the absorption of ingested beryllium is probably quite  small,
the chemical properties of beryllium are such that inhaled beryllium has  a  long
retention time in the lungs and, thus, a greater potential for absorption.   The
tissue distribution  of  absorbed beryllium is characterized  by depositions  pri-
marily in the skeleton where the biological half-time is fairly long.
     The lung  is  the critical  organ of both acute and  chronic non-carcinogenic
effects.  However, unlike;most other metals, the lung effects caused by chronic
exposure to beryllium may be combined with systemic effects, of which one common
factor  may  be hypersensitization.   Certain beryllium compounds  have  shown
carcinogenic  activity in various  experimental  animals by various routes  of
exposure, but  not by ingestion per  se.   Epidemiologic  studies are  inadequate
to  demonstrate or refute ;a human carcinogenicity potential.   In  terms of  the
weight  of evidence for carcinogenicity, beryllium is judged to be in Group B2
signifying  that the  animal  evidence for carcinogenicity is  sufficient  and  that
beryllium and its compounds are regarded as probably carcinogenic for humans.

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                     AUTHORS, REVIEWERS, AND CONTRIBUTORS
Authors
The authors of this document are:

Mr. David L Bayliss
Carcinogen Assessment Group
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Washington, D.C.

Dr. Chao W. Chen
Carcinogen Assessment Group
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Washington, D.C.

Dr. Vincent James Cogliano
Carcinogen Assessment Group
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Washington, D.C.

Dr. Margaret M. L. Chu
Reproductive Effects Assessment Group
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Washington, D.C.

Dr. Robert Eli as
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Research Triangle Park, North Carolina

Dr. David Jacobson-Kram
Reproductive Effects Assessment Group
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Washington, D.C.

Dr. Kantharajapura S.  Lavappa
U.S. Food and Drug Administration
Washington, D.C.
(formerly of the Reproductive Effects Assessment Group,
Office of Health and Environmental Assessment)
                                      XI

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 Dr.  William E.  Pep«lko
 Carcinogen Assessment Group
 Office of Health and Environmental  Assessment
 U.S.  Environmental  Protection Agency
 Washington, D.C.

 Dr.  Magnus Piscator
 Karolinska Institute
 Stockholm, Sweden

 Dr.  Andrew L.  Reeves
 Wayne State University
 Detroit,  Michigan

 Dr.  Carol  Sakai
 Reproductive Effects Assessment  Group
 Office of Health  and Environmental  Assessment
 U.S.  Environmental  Protection Agency
 Washington,  D.C.

 Project Manager:

 Ms.  Donna J.  Sivulka'     !           '     '
 Environmental Criteria and  Assessment Office
 Office of Health  and Environmental  Assessment
 U.S.  Environmental  Protection Agency
 Research  Triangle Park, North Carolina

 Special assistance  to  the 'project manager was provided by:

 Ms. Darcy  Campbell
 Environmental Criteria and  Assessment Office
 Office of  Health and Environmental  Assessment
 U.S.  Environmental  Protection Agency
 Research Triangle Park, North Carolina

 Reviewers  and Contributors

The carcinogenicity  chapter was  reviewed by the Carcinogen Assessment Group
 (CAG)  of the Office  of Health  and Environmental Assessment, U.S. Environmental
 Protection Agency.   Participating members of the CAG were:

Steven Bayard, Ph.D.
Robert P.  Beliles, Ph.D
William H. Farland,  Ph.D (Director)
Herman J.  Gibb, B.S.,  M.P.H.
Charalingayya B.  Hiremath, Ph.D
James W. Holder,  Ph.D
Aparna M.  Koppikar, M.D., D.P.H., D.I.H.
Robert McGaughy,  Ph.D.
Charles H. Ris, M.S.,  P.E.
Dharm V. Singh, D.V.M., Ph.D.
                                      xn

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The following individuals reviewed earlier drafts of this document and submitted
valuable comments at a public workshop:

Dr. Frank D'ltri
Michigan State University
East Lansing, Michigan

Dr. Philip Enter!ine
University of Pittsburgh
Pittsburgh, Pennsylvania

Dr. Jean French
Centers for Disease Control
Atlanta, Georgia

Dr. Richard Henderson
Health Sciences Consultants
Osterville, Massachusetts

Dr. Marshall Johnson
Thomas Jefferson Medical College
Philadelphia, Pennsylvania

Dr. Magnus Piscator
Karolinska Institute
Stockholm, Sweden

Dr. Neil Roth
Roth and Associates
Rockville, Maryland

Dr. Flo Ryer, formerly with  the
Exposure Assessment Group
Office of  Health and  Environmental Assessment
U.S. Environmental Protection  Agency
Washington,  D.C.

Dr. Carl Shy
University of North Carolina
Chapel Hill, North Carolina

Dr. Vincent  Simmon
Genex  Corporation
Gaithersburg, Maryland

Dr.  F. William  Sunderman,  Jr.
University of Connecticut
 Farmington,  Connecticut

Dr.  J.  Jaroslav Vostal
General  Motors  Research Laboratory
Warren,  Michigan

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 Dr.  John  Wood
 University  of Minnesota
 Navarre,  Minnesota
                             SCIENCE  ADVISORY  BOARD
     This document was  independently  peer-reviewed  in public  session by the
Metals Subcommittee  of  the  Environmental  Health  Committee,  Environmental
Protection Agency Science Advisory  Board.  The following were members of that
Committee:

Chairman, Metals Subcommittee

Dr. Bernard Weiss, Professor, Division of Toxicology, P.O.  Box RBB, University
     of Rochester, School of Medicine, Rochester, New York  14642

Executive Secretary

Dr. Daniel Byrd, III, Science Advisory Board, A-101F, U.S.  Environmental
     Protection Agency, Washington, D.C.  20460

Members

Dr. Thomas W. Clarkson, Professor and Head, Division of Toxicology, University
     of Rochester, School of Medicine, P.O. Box  RBB, Rochester, New York  14642

Dr. Gary Diamond, Assistant Professor of  Pharmacology, University of Rochester,
     School of Medicine, P.O. Pharmacology, Rochester, New York  14642

Dr. Edward F. Ferrand, Assistant Commissioner for Science and Technology,
     New York City Department of Environmental Protection, 51 Astor Place,
     New York, New York  10003

Dr. Robert Goyer, Deputy Director, National Institute of Environmental  Health
     Sciences, P.O.  Box 12233, Research Triangle Park, North Carolina  27709

Dr. Marvin Kuschner, Dean, School of Medicine, Health Science Center, Level 4,
     State University of New York, Stony Brook, New York  11794

Dr. Gunter Oberdoerster, Associate Professor, Radiation Biology and Biophysics
     Division, University of Rochester, School of Medicine, 400 Elmwood
     Avenue, Rochester, New York  14642

Dr. F.  William Sunderman, Jr., Professor of Laboratory Medicine and Pharmacology
     and Head of Department ,of Laboratory Medicine, University of Connecticut
     Health Center,  Room C 2021, Farmington,  Connecticut  06032

Dr. Ronald Wyzga (Vice-Chair), Electric Power Research Institute, 3412  Hillview
     Avenue, P.O.  Box 1041,  iPalo Alto, California  94303
                                      xiv

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In addition, there were several Agency and non-Agency scientists who also con-
tributed valuable information and/or constructive criticism to interim drafts
of this report.  Of specific note were the contributions of:  Jack Behm, Richard
Chamber!in, Thomas J. Concannoh, John Cope!and, Bernie Greenspan, Si Duk Lee,
Brian MacMahon, Robert J. McCunney, Vlasta Molak, Ray Morrison, Om Mukheja,
Charles Nauman, Martin B. Powers, Otto Preuss, Scott Voorhees, and Elizabeth K.
Weisburger.


Technical Assistance

Project management, editing, production, word processing, and workshop from
Northrop Services, Inc., under contract to the Environmental Criteria and
Assessment Office, Office of Health and Environmental Assessment:


Ms. Barbara Best-Nichols
Mr. John Bennett
Ms. Ivra Bunn
Ms. Linda Cooper
Dr. Susan Dakin
Ms. Terri Driver
Mr. Chip Duke
Ms. Anita Flintall
Ms. Kathryn Flynn
Ms. Miriam Gattis
Ms. Lorrie Godley
Ms. Tami Jones
Ms. Varetta Powell
Ms. Jane Thompson
Ms. Patricia Tierney

Word  processing  and  other technical  assistance at  the Office  of  Health  and
Environmental  Assessment:

Ms. Linda  Bailey
Ms. Frances P. Bradow
Mr. Doug Fennel 1
Mr. Allen  Hoyt
Ms. Barbara Kearney
Ms. Theresa Konoza
Ms.  Emily  Lee
Ms. Marie  Pfaff
Ms.  Diane  Ray
Ms.  Judy Theisen
Ms.  Donna  Wicker
                                       xv

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Reference support from Systems Research and Development Corporation, under
contract to the Environmental Criteria and Assessment Office, Office of Health
and Environmental Assessment:

Ms. Susan McDonald
Ms. Deborah Staves
Ms. Sherry Stubbs
Mr. Robert Terry
Ms. Mary Williamson
                                     xvn

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                               1.   INTRODUCTION
     This report  evaluates  the effects  of beryllium on human  health,  with
particular emphasis on those  effects  which are of most concern to the general
U.S. population.   It is organized into chapters that present in a logical  order
those aspects  of beryllium that relate  directly  to human  health risk.  The
chapters include: an  executive  summary (Chapter 2); background information on
the chemical and environmental aspects of beryllium, including levels of beryl-
lium in  media  with  which U.S. populations may  come into contact (Chapter  3);
beryllium metabolism, where absorption, biotransformation,  tissue distribution,
and  excretion  of beryllium are discussed with  reference  to the  element's
toxicity (Chapter 4);  beryllium toxicology,  where the  various  acute,  subacute,
and  chronic health effects of  beryllium  in man and  animals  are reviewed
(Chapter 5); beryllium mutagenesis,  in which the  ability of beryllium to  cause
gene mutations,  chromosomal  aberrations,  and sister-chromatid  exchanges  is
discussed  (Chapter 6); and information on  beryllium  carcinogenesis, which
includes a  discussion of selected dose-effect and dose-response relationships
(Chapter 7).
     This report is not intended to be an exhaustive review of all the beryl-
lium  literature, but is focused instead  upon those data thought to  be most
relevant to  human health risk assessment.  Literature on beryllium was  collected
and reviewed up  to  January, 1986.  General information pertaining to  the calcu-
lation  of unit risk values was  reviewed  up to April, 1987.   In view of  the  fact
that this  document is to provide  a  basis for making decisions  regarding the
regulation  of  beryllium as a hazardous  air  pollutant under the  pertinent  sec-
tions  of the  Clean Air Act,  particular  emphasis is placed on those  health
effects associated with exposure to  airborne beryllium.  Health effects asso-
ciated  with the ingestion of beryllium or with  exposure via other routes are
also discussed,  providing a  basis for possible use of this document  for multi-
media risk  assessment purposes.  The  background information provided  on sources,
 emissions,  and ambient concentrations of beryllium in  various  media  is presented
                                       1-1

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to  provide  a general perspective for  viewing  the health-effects evaluations
contained in later chapters of the document.  More detailed exposure assessments
will be prepared separately for use in subsequent EPA reports regarding regula-
tory decisions on beryllium.
                                     1-2

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                          2.   SUMMARY AND CONCLUSIONS
2.1  BACKGROUND INFORMATION
     The industrial use of beryllium has increased tenfold in the last 40 years.
Despite this fact,  increases  in the environmental concentrations of beryllium
have not been  detected.   Atmospheric beryllium is primarily  derived  from the
combustion of coal.
     Contamination of  the  environment occurs almost  entirely  by the deposition
of beryllium from  the  air.  Beryllium  from  the  atmosphere eventually reaches
the soil or  sediments, where it is probably retained in the relatively insol-
uble form  of  beryllium oxide.   Since the time of the industrial revolution,  it
is likely  that no  more than 0.1 ug  Be/g has been added to the surface of the
soil,  which  has a natural .beryllium  concentration of 0.6 ug/g.  Distributed
evenly  throughout  the  soil column, beryllium derived from the atmosphere could
account for  not more than one  percent of the total  soil beryllium.  Allowing
for greater  mobility of atmospheric beryllium in  soil than natural beryllium,
it is possible  that  10 to  50 percent of the .beryllium in plants  and animals may
be of anthropogenic  origin..
     The typical American  adult usually takes in 400 to  450 ng  Be/day, of which
50 to  90  percent comes from food  and  beverages.   Some of  this  beryllium  found
in food may be derived from the  atmosphere; however, aside  from primary and
secondary  occupational settings,  air  or dust has  little impact on  total  human
intake.
 2.2  BERYLLIUM METABOLISM
      Inhalation and ingestion are  the  main routes  of beryllium intake  for  man
 and animals.   Percutaneous absorption is insignificant.
      Due to  the  specific  chemical  properties of  beryllium  compounds,  even
 primarily soluble beryllium compounds  are  partly transformed to more insoluble
 forms in  the lungs.   This can result  in long retention times  in  the  lungs
                                       2-1

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 following  exposure to all types  of  beryllium compounds.   Like other particu-
 lates,  dose and particle size  are critical  factors  that determine the deposi-
 tion  and clearance of inhaled beryllium particles.  Of the deposited beryllium
 that  is absorbed,  part will be rapidly excreted and part will  be  stored in
 bone.   Beryllium  is  also ;transferred  to  regional  lymph  nodes.   Beryllium
 transferred  from the lungs to  the gastrointestinal  tract  is mainly eliminated
 in the  feces with  only a  minor  portion  being absorbed.
     There are  no  quantitative  data  on  absorption  of beryllium from the gastro-
 intestinal  tract  in  humans,  but several  animal  studies  indicate  that  the
 absorption  of  ingested beryllium is less than one percent.  The absorption of
 beryllium  through  intact skin  is very  small, as beryllium is tightly bound in
 the epidermis.
     Absorbed  beryllium  will  enter  the  blood,  but there are no data on  the
 partitioning of beryllium between plasma and erythrocytes.   In  plasma,  there
 are limited  data to suggest that, at  normally  occurring levels  of beryllium,
 the main binding is to various plasma proteins.   In animal experiments,  it has
 been shown that  large doses of  injected  beryllium are found in aggregates bound
 to phosphate.  The smaller the  dose, the more beryllium will be in the diffusi-
 ble form.   The  data are  insufficient to permit  an estimate of the levels of
 beryllium normally occurring in blood or plasma.
     Absorbed beryllium  is  deposited in the  skeleton, with  other  organs  con-
 taining  only very  low levels.   In the  liver,  beryllium  seems  to be  preferen-
 tially  taken up by.lysosomes.   There are not enough data to  permit  any defini-
 tive conclusions about the distribution and amounts of beryllium normally pre-
 sent in the human body.   However, total body burden  is probably less than 50 |jg.
     Based on animal studies,  beryllium appears to have a long biological  half-
time, caused mainly by its retention in bone.  The half-time in soft tissues is
relatively short, except  in the lung.
     Beryllium  seems  to  be normally  excreted in  small  amounts  in urine, normal
 levels probably  being only a  few nanograms  per  liter.   Animal  data indicate
that some excretion occurs by way of the gastrointestinal tract.
2.3  BERYLLIUM TOXICOLOGY
2.3.1  Subcellular and Cellular Aspects of Beryllium Toxicity
     It is  not  well  known in  what form or through which mechanism beryllium  is
bound to tissue.  Beryllium can  bind to lymphocyte membranes,  which may  explain
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the sensitizing properties  of  the  metal.   A  number  of  reports  describe  various
iji vivo  and iji vitro effects  of beryllium compounds on enzymes,  especially
alkaline phosphatase,  to which  beryllium  can  bind.  Effects on protein  and
nucleic acid metabolism  have been  shown  in many experimental  studies; however,
the doses  in these  studies have been large and parenterally administered.
Because such administrative routes have  less practical application to humans,
the data from  these  studies have limited utility in advancing  an  understanding
of human effects,  which  are mainly on the lung.  Beryllium particles retained
in the  lung are  found in the  macrophages, and the  understanding  of how these
and other pulmonary cells.metabolize beryllium is probably of most relevance to
the understanding of chronic beryllium disease.
     An important  aspect of beryllium toxicology is that  beryllium can cause
hypersensitivity which is essentially cell-mediated.  There are species  differ-
ences;  humans  and guinea  pigs can be sensitized to beryllium,  whereas the
present data indicate  that no  such mechanism  exists for the rat.  There are
also strain differences  among  guinea pigs indicating that a genetic component
may be  operative.   Patch tests  have been used to detect beryllium hypersensi-
tivity  in  humans,  but these tests are no longer used since they were shown to
cause a  reactivation of  latent  beryllium disease.  Presently, the lymphoblast
transformation test  is regarded as the most useful  test to detect hypersensi-
tivity to beryllium.

2.3.2  Pulmonary and Systemic Toxicity of Beryllium in Man and Animals
     There  are no data  indicating that  moderate beryllium exposure  by oral
administration causes  any  local  or systemic  effects  in humans  or animals.
Respiratory effects, occasionally combined with  systemic  effects,  constitute
the major  health  concern of beryllium exposure, with hypersensitization likely
playing  an important  role  in  the  manifestation of the systemic effects.
Respiratory effects  may  occur  as either a nonspecific acute disease or as a
more specific  chronic beryllium  disease.
     The most  acutely toxic beryllium compounds are probably beryllium oxides
fired at low temperatures,  e.g.  500°C, and some  salts, such as the fluoride and
the sulfate.   The latter forms-  of beryllium are acidic, and part of the toxic
reactions  caused  by  these compounds may  be due  to the  acidity of the particles.
                                                                            o
Acute  effects  have  generally  occurred at  concentrations above 100 |jg  Be/m .
The main  feature  of such effects  is  a chemical pneumonitis which may lead to
                                       2-3

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 pulmonary  edema and even death.  In animal experiments, concentrations of more
            O
 than  1 mg/m  have generally been needed to produce acute effects, but effects
 have  been  reported at lower levels of exposure.  In most cases, the acute dis-
 ease  will  regress, but it may  take several weeks or months before recovery is
 complete.   If there is no further excessive exposure to beryllium, it is gen-
 erally  believed that acute disease will not lead to chronic beryllium disease.
 The amount initially deposited during  acute exposure and an individual's pre-
 disposition  are probably the main factors  leading to later sequelae.
      Acute  beryllium poisoning was quite  common  in  the 1940s, but since the
 present  standards  were established in  1949, the  number of new cases  reported
 has been relatively  small.
      Chronic  beryllium disease occurred as an  epidemic in the  1940s,  which  led
 to the  establishment of the "Beryllium Case Registry"  (BCR),  a file for all
 cases of acute and chronic beryllium disease.   Chronic beryllium disease is
 characterized  by  dyspnea,  cough,  and weight loss.  It  is sometimes associated
 with  systemic  effects  in the form of granulomas  in the skin and muscles, as
 well  as  effects on calcium metabolism.   There  are  many similarities  between
 chronic  beryllium  disease and  sarcoidosis,  but in sarcoidosis the systemic
 effects are  much  more prominent.   In most cases of chronic beryllium disease,
 there are  only lung effects  without  systemic  involvement.   Pathologically,  the
 disease is  a granulomatous interstitial pneumonitis in which eventually there
 may be  fibrosis,   emphysema?  and  also  cor pulmonale.   Deaths  from chronic
 beryllium  disease  are often due  to  cor pulmonale.   A  long  latency  time is
 typical; sometimes  there  may be more than 20 years  between  last  exposure and
 the diagnosis of the disease.
      It has  been  very  difficult to establish the  levels  of beryllium in air
 that  may cause the disease.   One reason for this difficulty is that  exposure
data  have  not  always been obtainable.   Another factor is that hypersensitiza-
tion  may cause the occurrence  of the disease  in people with  relatively  low
exposures,  whereas in nonsensitized people with much higher exposures  there  may
be no effects.  Diagnosis of the disease is obtained by X-ray examinations,  but
vital  capacity  may decrease  before roentgenological changes are seen.  Hyper-
sensitization can be detected by the lymphoblast transformation test.
     There  are limited data  on levels  of  beryllium  found in lung tissue in
cases of acute and chronic .beryllium disease,  and these data do not allow for
conclusions about dose-effect relationships.
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     New cases of chronic beryllium disease are still  being reported due to the
fact that, in  some  instances,  the occupational standards  have been exceeded.
In industries where the average exposure generally has been below 2 ug/m ,  there
have been very few new cases of chronic beryllium disease.
     There have  also  been  a large number of "neighborhood" cases of beryllium
disease.  Neighborhood  cases are  those in which  chronic  beryllium disease
occurs  in people living in the  vicinity of beryllium-emitting plants.   The air
concentrations of beryllium in such areas at the time when the disease occurred
have probably  been  around  0.1  ug/m3,  but considerable exposure via dust trans-
ferred  to  homes on workclothes  likely  contributed to the occurrence of the
disease.  No  new "neighborhood" cases of beryllium disease have  occurred since
standards of 0.01 ug/m3 were  set for  the ambient air and the  practice of
washing workers'  clothes in the plants was initiated.  Presently, ambient air
                                 2
levels  are generally below 1 ng/m  .

2.3.3   Dermatological Effects of Beryllium  Exposure
     Contact  dermatitis and some  other dermatological effects  of beryllium
have  been documented in occupationally  exposed persons, but there are  no  data
indicating  that such reactions  have  occurred, or may occur, in the  general
population.

2.3.4   Teratogenic  and  Reproductive Effects of Beryllium Exposure
      Available information on  the  teratogenic  or  reproductive effects of beryl-
lium  exposure is limited  to three animal  studies.  The information from these
studies is  not  sufficient  to  determine whether  beryllium compounds have  the
potential  to  produce  adverse   reproductive or teratogenic effects.   Further
studies are  needed in this area.
 2.4  MUTAGENIC EFFECTS OF BERYLLIUM EXPOSURE
      Beryllium has  been tested for  its  ability to cause gene mutations  in
 Salmonella typhlmurlum,  Escherichia  col 1,  yeast,  cultured human lymphocytes,
 and Syrian hamster embryo cells; DNA damage in Escherichia coli;  and unscheduled
 DNA syntheses in rat hepatocytes.
      Beryllium sulfate  and  beryllium chloride have been  shown to  be  nonmuta-
 genic in  all  bacterial  and yeast gene mutation assays.   However,  this  may  be
                                       2-5

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due to the fact that bacterial and yeast systems generally are not sensitive to
metal  mutagens.   In contrast,  gene mutation  studies in cultured mammalian
cells, Chinese  hamster V79 cells, and  Chinese  hamster ovary (CHO) cells have
yielded  positive  mutagenic  responses  of beryllium.   Similarly,  chromosomal
aberration and  sister-chromatid  exchange studies in cultured human lymphocytes
and Syrian  hamster embryo  cell's have  also resulted  in  positive mutagenic
responses of beryllium.   In  DNA damage and repair  assays,  beryllium was
negative  in  pol,  rat  hepatocyte,  and mitotic recombination  assays,  but was
weakly positive in  the rec assay.  Based  on available information,  beryllium
appears to have the potential to cause mutations.
2.5  CARCINOGENIC EFFECTS OF BERYLLIUM EXPOSURE
2.5.1  Animal Studies
     Experimental beryllium  carcinogenesis  has been induced by intravenous or
intramedullary injection  of  rabbits and by inhalation  exposure  or by intra-
tracheal injection of rats and monkeys.  With one possible exception, beryllium
carcinogenesis has  not  been  induced by ingestion.   Carcinogenic  responses  have
been induced  by  a variety of forms  of beryllium including beryllium sulfate,
phosphate,  oxide,  and  beryl  ore.   The carcinogenic  evidence   in  mice
(intravenously injected or exposed via inhalation) and guinea pigs and hamsters
(exposed via inhalation) is equivocal.
     Osteosarcomas  are  the predominant  types  of tumors induced  in  rabbits.
These tumors  are  highly invasive, metastasize readily, and  are  judged to be
histologically similar  to human  osteosarcomas.   In  rats,  pulmonary adenomas
and/or  carcinomas  of questionable  malignancy  have  been  obtained, although
pathological end points have not been well documented in many cases.
     Although, individually, many of the reported animal  studies have method-
ological and reporting limitations compared to current standards  for bioassays,
collectively  the  studies provide reasonable  evidence  for carcinogenicity.
Responses have been  noted in multiple species at  multiple sites  and,  in  some
cases,  afford evidence of a dose response.  On this basis, using EPA Guidelines
for Carcinogen Risk Assessment  (U.S.  EPA,  1986)  to classify  the weight of  evi-
dence  for carcinogenicity :in  experimental animals,  there is "sufficient"
evidence to conclude that beryllium is carcinogenic in animals.   Since positive
responses were seen for a variety of beryllium compounds,  all forms of beryllium
are considered to be carcinogenic.
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2.5.2  Human Studies
     Epidemiclogic studies provide equivocal conclusions on the carcinogenicity
of beryllium and beryllium compounds.  Early epidemiologic studies of beryllium
exposed workers  (see IARC,  1972,  1980; Bayliss  et al., 1971; Bayliss  and
Lainhart,  1972) do not report positive evidence for increased cancer incidence^
However, recent studies do report a significantly increased risk of lung cancer
in exposed workers.  The absence of beryllium exposure levels and a demonstrated
concern about  possible confounding  factors within the  workplace make  the
reported positive correlations between 'beryl 1iurn exposure and increased risk of
cancer difficult  to  substantiate.   This relegates the reported  statistically
significant increases of lung cancer to, at best, an elevated incidence that is
not  statistically significant.   Because of these  limitations, the  EPA (U.S.
EPA, 1986) considers the available epidemiologic evidence to be "inadequate" to
support or  refute the existence of a carcinogenic  hazard for humans  exposed to
beryllium.
     This designation  of  the epidemiologic data as "inadequate"  differs from
that of the International  Agency for Research on Cancer (IARC, 1980) which con-
cluded that the epidemiologic data provides "limited" evidence for the carcino-
genicity of beryllium.  In the  EPA evaluation,  more recent  unpublished tabula-
tions and analysis of the earlier study cohorts that  correct for  errors in  the
data base and the National Institute for Occupational Safety and Health (NIOSH)
Life-Table program were included.   Use of this newer data provides a basis to
change the weight-of-evidence conclusion for the human data.

2.5.3  Qualitative Carcinogenicity Conclusions
     Using the  EPA weight-of-evidence criteria for evaluating both  human and
animal evidence,  beryllium is most appropriately classified in Group B2, indi-
cating that, on the strength of animal  studies, beryllium should  be  considered
a probable  human  carcinogen.  This category  is  reserved for chemicals having
"sufficient" evidence  for carcinogenicity  in animal  studies  and  "inadequate"
evidence in human  studies.   In this particular case, the animal evidence demon-
strates that  all  beryllium  species should  be  regarded as  probably being
carcinogenic for  humans.
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2.6  HUMAN HEALTH RISK ASSESSMENT OF BERYLLIUM
2.6.1  Exposure Aspects
     In the general  U.S.  population,  the  dietary  intake  of  beryllium  is  proba-
bly less than  1 ug a day, and  due  to its chemical  properties,  very little  is
available in the gut for absorption.  Approximately half of the absorbed beryl-
lium enters the skeleton.
     For most people, the daily amount of beryllium inhaled is only a  few nano-
grams.  However,  it  is  likely that  much of this is  retained in  the lungs.   The
available data  indicate that the beryllium lung  burden  in  the average adult
ranges from 1  to 10 ug.  Since beryllium occurs in cigarettes, it is  possible
that smokers will  inhale  and retain more beryllium than nonsmokers.   Unfortu-
nately, the  data on  beryllium concentrations in  mainstream smoke are,  at
present, uncertain.

2.6.2  Relevant Health Effects
     Occupational exposure to various beryllium compounds has been associated
with acute respiratory  disease and  chronic beryllium disease  (in the form  of
granulomatous interstitial pneumonitis).   Some systemic  effects have  also been
noted and a  hypersensitization component  probably plays  a  major role in the
manifestation of  these  effects.   In the  past, chronic  beryllium disease was
found  in  members of  the  general population  living near beryllium-emitting
plants, but past exposures  were relatively high compared to present levels  of
beryllium in  the ambient air.   Contaminated  workclothes  brought home  for
washing contributed  to  these exposures.    No  "neighborhood"  cases  of  chronic
beryllium disease have been reported in the past several years.
     Numerous animal  studies  have been performed to determine  whether or not
beryllium and  beryllium-containing  substances are carcinogenic.   Although some
of these studies have limitations,  the overall evidence from animal  studies
should be classified as "sufficient" using EPA Guidelines for Carcinogen Risk
Assessment (U.S.  EPA,  1986).   IARC  (1980) has also concluded that the evidence
from animal studies is "sufficient."  Human studies on beryllium carcinogenicity
have deficiencies  that  limit,any definitive conclusion  that a true association
between beryllium exposure and cancer exists.  Nevertheless, it is possible that
a portion of  the excess cancer  risks  reported in these studies may,  in fact,
be due  to  beryllium exposure.  Although  IARC  concluded  that beryllium and  its
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compounds should be  classified  as having "limited" human evidence of carcino-
genicity, the U.S.  Environmental Protection Agency's Carcinogen Assessment Group
(CAG) has concluded that the human evidence is "inadequate."

2.6.3  Dose-Effect and Dose-Response Relationships of Beryllium
     As previously stated,  beryllium can act upon the lung in  two ways,  either
through a direct toxic effect on pulmonary  tissue or through  hypersensitiza-
tion.  Even  if  reliable and detailed exposure data  were available, it would
still be difficult to establish dose-effect and dose-response relationships due
to  this  hypersensitization factor.   No adverse  effects  have  been noted in
                                     3
industries complying with  the 2 ug/m  standard set by the Occupational Safety
and  Health  Administration  (OSHA);  therefore,  it appears that this  level  of
beryllium in  air provides  good protection with regard to respiratory effects.
It  is  unknown whether  exposures to  the maximum  permissible  peak standard
        3
(25 ug/m ) can cause delayed effects.
     From available  data,  the CAG has discussed  the estimation of carcinogenic
unit risks  for  inhalation exposure to  beryllium.   The quantitative aspect of
carcinogen risk assessment  is included  here because it may be of  use in setting
regulatory priorities  and  in evaluating the adequacy of technology-based con-
trols and other aspects of  the  regulatory decision-making process.  However, the
methodologic  uncertainties  associated with estimating cancer risks to humans at
low  levels  of exposure should  be recognized.  The linear extrapolation proce-
dures  used  (see Section 7.3) typically  provide a rough  but plausible estimate
of  the  upper limit of risk—that is, it is not likely that the true risk would
be much  higher than  the estimated risk,  but  it could  be  considerably lower.  In
the  case of  beryllium,  due  to the uncertainty introduced by specific character-
istics of the data base which may be  best thought of  as  affecting the confidence
in  the  upper-limit estimates,  the  unit risk estimates presented below may be
most appropriately viewed  as  sensitivity analyses.  These  risk estimates  should
not be regarded,  therefore, as  accurate representations of true  cancer  risks.
The estimates presented may, however, be factored into regulatory decisions to
the extent  that the concept  of upper-limit  risks and sensitivity analyses  are
found  to be  useful.
     Both  animal  and human studies  have been used to examine  the carcinogenic
potency  of beryllium.  For quantitative risk assessment purposes  the animal
data present some difficult  analytical  problems  because of weaknesses in the
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 design and  the  reporting of the studies.  Despite the weaknesses of the indi-
 vidual studies,  however,  there is little doubt  that beryllium induces cancer
 in laboratory animals.                         :
      An additional difficulty in the use of animal data for quantitative assess-
 ment is due to  the fact that, not only did many of the animal studies utilize
 different forms of beryllium than those commonly present in the ambient environ-
 ment, but the carcinogenic  response  varied with  the  beryllium compound used.
 Moreover,  the form most common  in  ambient air is beryllium oxide  and,  although
 all  the animal  studies were: deficient  in  some respects,  the  ones  utilizing
 beryllium  oxide were more deficient,  as a group,  than those utilizing beryllium
 salts.   Nevertheless,  it was  felt  that the quantitative analysis  should focus
 upon the form of beryllium humans are most likely to be exposed to.
      While  the  available beryllium  oxide  studies were individually weak, a
 correlation  of estimates from  several  data sets  would be  expected to increase
 confidence in the results.  Potency  factors were thus calculated  using data
 from eight beryllium  oxide  animal  studies.   The  results were  reasonably con-
 sistent and  the geometric mean  of  all  eight  potency  factors  was  2.1 x 10~3/
 (MS/rn ), which agreed quite  well  with the potency factor derived from the human
 epidemiologic data.
      The question of  beryllium potency  by  ingestion is highly  uncertain  and
 debatable  due to  the equivocal or negative  results  from  ingestion studies.
 From  a weight-of-evidence point of view, the  potential for human  carcinogeni-
 city  by this route cannot be dismissed.  For  practical purposes,  however, the
 potency of beryllium  via ingestion  must  be considered  as largely unknown.
      Even  though the  epidemiologic  studies have been  judged to  be  qualitatively
 inadequate to assess  the potential  of carcinogenicity  for humans,  these  studies
 can be analyzed to determine the  largest plausible risk that is  consistent with
 the  available epidemiologic  data.  This upper bound is a risk estimate and can
 be used to evaluate the  reasonableness of estimates derived  from animal  studies.
 Information  from the  epidemiologic study by  Wagoner  et al. (1980) and the
 industrial  hygiene  reviews  by  NIOSH (1972) and Eisenbud and Lisson (1983) have
been  combined to  estimate a plausible upper bound for incremental cancer risk
associated with  exposure to  air contaminated with beryllium oxide.   The epide-
miologic data, while  being useful for estimating the cancer potency of beryl-
lium,  nevertheless,   also  has   interpretative   limitations  because  of  the
uncertainties regarding  exposure  levels.  In the  occupational  exposure studies
upon which the  risk analysis is  based,  the  narrowest range  for median exposure
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that could be  obtained on the basis of available information was 100 to 1,000
(jg/m .   Furthermore, an assumption was made that the ratio of exposure duration
to years at  risk ranged from 0.25  to  1.0.   The geometric mean  of the potency
                                                       -3      3
factors derived using these assumptions equals 2.4 x 10  /((jg/m ).
     The unit  risks  from the beryllium oxide animal data sets are best viewed
as demonstrating  a  consistency  of response, as opposed to a collection of in-
dividually reliable  upper-bound risk  values.   Within  the consistency range,
sensitivity  is  shown relating to the  beryllium species tested, and for beryl-
lium oxide, perhaps  to firing temperature.  Because of the need to assume expo-
sure levels, the risk estimate  derived from the human  epidemiology data is,  in
effect, also the result of a sensitivity analysis which shows a consistency  of
response.
     With  these  noted caveats,  the CAG feels that a recommendation for a spe-
cific  upper-bound estimate of risk is warranted,  even though it does evolve
from less than ideal data, in order to provide a crude measure of the potential
for public health impact if, in fact, beryllium is assumed to be a human car-
cinogen.   Taken  together,  the notable comparability of  the  animal  and human
based  estimates  for beryllium oxide encourages one to  consider these estimates
as being of  some  utility.  Given the correlation of animal and human  estimates,
                                                                         3
the upper-bound  incremental  lifetime cancer risk  associated  with 1 ug/m  of
                                                                    -3
beryllium oxide,  after rounding to one significant figure, is 2 x 10  .
     There are two  types  of uncertainty  associated  with this  value,  one
involving  the  typical  concern about upper-limit values  (i.e. the true risk  is
not  likely to  be higher  than  this value  and  may be lower) and a second
uncertainty  relating to the use of dosimetry assumptions in the risk modelling
which  may  result in either an over-  or  underestimation of the  recommended
upper-limit  value.   The  utility  of the beryllium  oxide risk value  in risk
management analysis  should be judged with these uncertainties in mind.   Hence,
whereas  one  might use these estimates to screen for a possible public hazard,
one should exercise much greater caution in using these  values for. an assess-
ment of  individual cancer  risk.  If the form of beryllium present includes more
than a small fraction of  beryllium salts,  then the beryllium oxide risk value
may underestimate the upper limit and the animal based estimates for beryllium
sulfate  or other salts  should be  used.   These estimates  have  the typical
upper-limit  uncertainty  relating to the true risk.  The  incremental upper-limit
          -3      3
of  2  x 10  /(pg/m ) places beryl!
carcinogens  evaluated  by the CAG.
of 2 x  10   /(pg/m  )  places  beryllium  oxide  in  the  third quartile of  59  suspect
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2.6.4  Populations at Risk
     In terms  of exposure,  persons engaged in  handling  beryllium in occupa-
tional environments  obviously comprise  individuals  .at  highest  risk.   With
regard to  the  population at large,  there may  be a small  risk for people  living
near beryllium-emitting industries.  However,  the risk for such individuals may
not be from ambient air levels of beryllium, but rather from beryllium-contami-
nated dust within  the household.   There are no data that allow an estimate of
the number of  people that may be at such risk, but it is reasonable to assume
that it is a very small group.  It should be noted that no new "neighborhood"
cases of beryllium disease have been reported since the 1940s.
                                     2-12

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                     3.   BERYLLIUM BACKGROUND INFORMATION
3.1  GEOCHEMICAL AND INDUSTRIAL BACKGROUND
3.1.1  Geochemistry of Beryllium
     Average crustal rock  contains  about  2.8 ug  Be/g  (Mason,  1966),  but beryl-
lium also  occurs in more  concentrated forms  as a component of over  forty
different minerals.  Granites  are  enriched by 15 to 20 ug Be/g.   It is likely
that most beryllium  minerals were  formed  during  the cooling of granitic magmas
(Beus,  1966).  The  element was excluded during  the early cooling  stages  and
accumulated  in the  crystallization products formed during the final stages,
commonly in  association with  quartz.   The most  highly enriched deposits of
beryllium are in pegmatitic intrusions.
     Only two beryllium  minerals are  of current  economic  importance, beryl and
bertrandite.   Beryl, an  aluminosilicate (Be-AlpSigOg),  is mined  largely in the
USSR, Brazil, and  the  People's Republic of China;  smaller amounts  are  produced
in several other countries (Table  3-1).  Formed  by pegmatite processes,  beryl
is 5- to 11-percent beryllium  oxide and,   in its purest gem-quality form,  is
treasured as  the green  or blue emerald.   Until  the  late  1960s, the common
technique for separating beryl from associated r.ock was to crush the rock and
hand pick  the mineral  crystals.   By  1969, mechanical  flotation separation
techniques were developed,  and a second mineral, bertrandite [Be.SipO^OJ-Op],
became economically  important  (Anonymous,  1980).  Bertrandite occurs  as very
tiny silicate granules  that have a beryllium oxide concentration of less  than
one percent.  The  only active  commercial  deposit of bertrandite  in the United
States is at  Spor  Mountain, Utah.   This domestic source supplies about 85 per-
cent of the  beryllium  ore  consumed in the United States;  the  rest  is imported,
either as beryl  or bertrandite, as  listed  in Table 3-1 (Kramer,  1984).
     Beryllium was  discovered  by Vauquelin in 1798.  The element was isolated
in metallic  form in 1828 by Woehler, and  perhaps independently that same  year
by Bussy (Beus,  1966).   Beryllium is a light-grey, low-density metal with  a
                                      3-1

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      TABLE 3-1.   GLOBAL PRODUCTION  AND  U.S.  CONSUMPTION OF  BERYLLIUM ORE
                                 (METRIC TONS)
Country
Argenti na
Brazil
Madagascar
Mozambique
: 1948
45
1617
8
73
People's Republic of China (1) (4).
Portugal
Rwanda
U.S.S.R.
United States (2)
Zimbabwe
Other Countries (3)
World production
U.S. consumption
(1) Estimated from U.S.
(2) Includes bertrandite
9
40
(4)
82
—
257
2131
1787
imports.
ore, calculated as
1968
593
2078
—
95
(4)
128
149
1197
152
88
2088
6568
8384

equivalent
1980
31
550
10
20
580
19
108
1814
6756
9
""•"
9897
7717

to beryl
1985
15
1497
50
6
93
10
50
1905
5204
50
_ «
8880
7126

containing
         BeO.
(3)  Includes Australia, French Morocco, India, South-West Africa,  and Spain
     in 1948,  and Australia, India, Kenya, Malagasy Republic and Uganda in
     1968.   These countries are no longer a significant part of global beryl-
     lium production.
(4)  Data not available, not included in total.
(--) No production or less than 0.5 tons.

Source:  U.S.  Bureau of Mines (1950); Whitman (1970); Kramer (1984).

high melting  point,  exceptional  resistance to corrosion,  and  the  capacity  to
absorb heat.   In  the United States, beryllium ore is processed at Delta, Utah
by Brush Wellman, Inc.
     Although  beryllium was isolated as a metal in 1828, it was not until the
1930s  that beryllium-copper alloys  came into widespread use.   Deposits of
beryl  known  for ,gem production were the first to be exploited.   In  the USSR,
geochemical  techniques  for locating beryl deposits  by chemical  anomalies in
surrounding rock  formations were used  for some  time,  but had little success
(Goldschmidt  and  Peters, 1932).
                                       3-2

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3.1.2  Production and Consumption of Beryllium Ore
     From the  ore,  beryllium is extracted  as  the hydroxide, from which  all
forms of the metal  and its alloys can  be made.   The most useful  products are
beryllium metal, beryllium  oxide,  and beryllium-copper alloys.   Its  stiffness-
to-weight ratio and  high  thermal  conductivity make  beryllium metal  useful  in
the aerospace  industry.   In the electronics industry, beryllium oxide is used
to dissipate heat away from thermally sensitive components.  Beryllium-copper
alloys, which  provide  a combination  of strength, electrical conductivity, and
resistance to stress relaxation, are us*ed extensively for electrical/electronic
switches, sockets,  and connectors.   The alloys  are  also nonmagnetic.   Other
beryllium alloys are especially valuable for their resistance to oxidation or
corrosion and  have  been used in the production of dental prostheses (New!and,
1982).
     From 1930 to 1969,  deposits  of beryl  remained  the sole source  of beryl-
lium.   The consumption of beryllium increased 600-percent between 1948 and 1968
(Table 3-1), a rate  that was ten times that of any other common metal  (Knapp,
1971).   During this  period,  the nuclear power industry joined  the aerospace
and electronics  industries  as  a  consumer of beryllium  products  (Anonymous,
1980).   Two  countries, the  USSR  and the United  States,  became the primary
consumers of beryllium ore and producers of beryllium products.
     After the production of bertrandite became  economically feasible in  1969,
its production in the  United States  rose to the equivalent of about 6000 tons
of beryl by  1981.   From the  domestic production of 5204 equivalent tons  of
beryl  ore, the use  of  existing  stocks,  and  the  import of 1493 actual tons,  the
United States  consumed about 287 tons of contained  beryllium in 1985, of  which
about 54 tons were exported as finished or unfinished products.

3.1.3 Industrial Uses of Beryllium
     About 10  percent  of the domestic  beryllium hydroxide is  used in the
production of  pure  beryllium metal  in sheet, rod,  or wire  form.   Since 1979,
Brush Wellman, Inc.  has been the only  free-world producer  of beryllium metal
(Anonymous,  1980).  The metal  is  milled to desired specifications at the user
facility, producing beryllium dust and  scrap in  the  vicinity of machine shops.
Because of the high  cost  of the metal,  efficient recovery and recycling of the
metal  are a high priority.
                                      3-3

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     About 15 percent of the raw beryllium hydroxide is consumed in the produc-
tion of beryllium  oxide  (beryllia).   It is used in the production of ceramics
that have  excellent thermal  conductivity,  especially at  high temperatures
(Table 3-2).  These  products  make good electrical  insulators  and have a  high
resistance to thermal  shock.   The high  melting point  permits  the  use  of beryl-
lium oxide in rocket nozzles and thermocouple tubing.

               TABLE 3-2.  INDUSTRIAL USES OF BERYLLIUM PRODUCTS
                                Beryllium Metal
Aircraft disc brakes
Navigational systems
X-ray transmission windows
Space vehicle optics and
  instruments
Ai rcraft/satel1i te structures
Missile parts
                                Beryllium Oxide
High-technology ceramics
Electronic heat sinks
Electrical insulators
Microwave oven components
Gyroscopes
                               Beryllium Alloys
Spri ngs                  ,
Electrical connectors and relays
Pivots, wheels and pinions
Plastic injection molds
Nuclear reactor neutron
  reflectors
Fuel containers
Precision instruments
Rocket propel!ants
Heat shields
Mirrors
Nuclear weapons

Military vehicle armor
Rocket nozzles
Crucibles
Thermocouple tubing
Laser structural components

Precision instruments
Aircraft engine parts
Submarine cable housings
Non-sparking tools
                                      3-4

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     The remaining 75  percent of beryllium hydroxide is  used in  the  production
of alloys, primarily beryllium-copper alloys.   As a general rule, two percent
beryllium  in  a copper  alloy with  a  mixture of  other metals  can markedly
increase the strength,  endurance, and hardness of the alloy.  Most applications
for beryllium  alloys are  in the electronic  field,  although specialized uses
such as  springs,  wheels,  and pinions serve  an  indispensable industrial  func-
tion.    Cabot  Corporation  (formerly  Kawecki-Berylcp,  Inc.)  at Reading,
Pennsylvania and  Brush Wellman  at ETmbre, Ohio  are  the  major producers of
beryllium alloys in .the United States.
3.2  CHEMICAL AND PHYSICAL PROPERTIES OF BERYLLIUM
     The chemical and physical properties of beryllium resemble those of alumi-
num, zinc, and  magnesium (Table  3-3).   Chemical  similarities  are  due primarily
to similar ionic  potentials,  which facilitate  covalent bonding (Novoselova  and
Batsanova, 1969).
     The properties  of  beryllium are often considered  in  the context of the
three most  common forms  of  potential  industrial emissions:   the metal,  the
oxide and the hydroxide.  In certain occupations, beryllium halides may also be
important, but these cases are too few to merit extended discussion.
     Beryllium is extracted from ores as the hydroxide and shipped in this form
to commercial processing plants  (Anonymous,  1980).   The most  common concentra-
tion process  involves  the leaching  of  20-mesh particles with  sulfuric  acid
followed  by  hydroxylation with  di-2-ethylhexylphosphate in  kerosene.   The
beryllium hydroxide salt is then collected by filtration.  The process recovers
about 80 percent of the beryllium found in low-grade bertrandite ore.
     From beryl,  beryllium may be extracted by  the  Sawyer-Kjellgren process;
the ore  is melted at 1625°C and cooled quickly with water to form a beryllium
glass.   The  glass is dried and  ground  to  200-mesh  powder, then leached with
sulfuric acid.   Sodium  hydroxide is used to convert the sulfate  to beryllium
hydroxide.  This process is also about 80-percent efficient but can not be used
to extract the small amounts of beryllium in bertrandite ore.
     A third  process,  the Copaux-Kawecki process, uses sodium ferric fluoride
to extract beryllium from low-grade, fine-grained bertrandite  ores  at a 90-
percent  efficiency.  This process is no  longer used in the United  States or
Europe, due to its expense and the toxicity of beryllium fluoride.  Indeed,  the
                                      3-5

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         TABLE 3-3..  PHYSICAL PROPERTIES OF BERYLLIUM AND  RELATED METALS
                                    Be
Zn
Mg
 Metal

 Atomic  number
 Atomic  weight
 Atomic  radius
 Valence      0
 Ionic radius  A
 Density 25  °C
 Melting point °C
 Boiling point °C
 Thermal  conductivity 100°
 Electrical  resistivity
   (u°nm • cm  @ 20°C)

 Oxide

 Formula
 Molecular weight
 Density
 Melting point °C
 Boiling point °C
 Thermal  conductivity 725°C
4
9.012
1.40
2+
.35
1.85
1283
2970
.401
4.31
13
26.98
1.82
3+
.51
2.7
660.4
2467
.573
2.65
30
65.38
1.53
2+
.74
7.14
419.58
907
1.12
5.916
12
24.31
1.72
2+
.66
1.74
648.8
1107
.376
4.45
BeO
25.01
3.008
2530
3900
.111
A1203
101.96
3.965
2072
2980

ZnO
81.37
5.606
1975
—

MgO
40.31
3.58
2852
3600

(cal/sec • cm2 • °C/cm)
Hydroxide
Formula
Molecular weight
Density
Solubility moles/liter
Decomposes to oxide °C


Be(OH)2
43.01

0.8 x 10"4
250-300


A1(OH)3
78.00
2.42

300


Zn(OH)2
99.38
3.053

125


Mg(OH)2
58.33
2.36

350
first medical  report  of beryl!iosis in 1933  can  be attributed to  exposure to

beryllium fluoride at an extraction plant (Weber and Engelhardt, 1933).
3.3  SAMPLING AND ANALYSIS TECHNIQUES'FOR BERYLLIUM

     Beryllium occurs  in ienvironmental  samples  at concentrations  of  about 0.01
            2
to 0.1  ng/m  in  air, 0.05 to  0.1  ug/g  in dust, 0.01 to  1.0  ng/g in surface

waters, 0.3 to 6.0  ug/g in soil, and 0.01 ug/g in biological  materials.   Some

plants, such  as  hickory, may  accumulate beryllium as much as  1  ug/g  dry weight

(Newland, 1982).   Two  techniques,  gas chromatography (GC) (Ross  and Sievers,
                                      3-6

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1972)  and  atomic absorption  spectroscopy (AAS)  (Owens  and Gladney,  1975),
appear  to  offer the  best combination of sensitivity and  sample  handling
efficiency.  However, colorimetry,  fluorometry,  and emission spectrometry are
also occasionally used.
     Environmental samples analyzed  by atomic absorption spectroscopy and gas
chromatography require pretreatment  to remove interfering  substances and  in-
crease  sensitivity.   At  high  concentrations (500 ug/g), aluminum  and silicon
interfere  with  beryllium analysis by  AAS.   Separation of  these elements  is
achieved by chelation and extraction with an organic  solvent.   The limit of
detection  for the  flame  method of AAS is 2 to 10 ng/ml, and 0.1 ng/ml for the
fTameless method.  Air samples of a few cubic meters must be concentrated after
extraction to a  liquid  volume of less than 1 ml to enter the detection  range.
                                                                     o
The high-volume  sampler,  which collects   in the range of 1.1 to 1.7 m/min, is
more desirable than  either  a low-volume  sampler  or  a  cascade  impactor,  which
                   3
collect at 0.001 m /min.  Normal  concentrations  of  dust, water,  and biological
materials  are all  at or below the detection  limits  of flame!ess AAS, so that
preconcentration by wet digestion is necessary.
     Using gas  chromatography,  Ross and  Sievers  (1972)  reported a detection
                                              o
limit  for  beryllium  in  air  of about 0.04 ng/m , making this method marginally
acceptable for small   sample sizes.  Extensive chemical  digestion and extraction
are required, however.
     Standard reference  materials  are  available  for  each method  in the  form of
fly ash, coal,  orchard  leaves, and bovine  liver.   Beryllium values for these
standard sources have been reported by Owens and Gladney (1975).
3.4  ATMOSPHERIC EMISSIONS, TRANSFORMATION, AND DEPOSITION
     Although there  is  little evidence for significant emissions of beryllium
to the atmosphere during ore production, emissions could be significant without
existing regulations.   The  20 percent of beryllium  lost  as  waste during  pro-
cessing (in  the  form of the hydroxide or the  fluoride)  could also represent an
environmental problem.   Any potential effects from  these  sources  of exposure
would  be  locally confined  to-the  sole  ore-processing plant in  the  United
States, operated by Brush Wellman at  Delta, Utah.  -
     Emission of  beryllium  from non-metallurgical  processes  (coal  and fuel  oil
combustion) accounts for 99 percent of U.S. emissions (Table 3-4).  The average
                                      3-7

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         TABLE 3-4.  NATURAL AND ANTHROPOGENIC EMISSIONS OF BERYLLIUM
Sources
of
Emissions
Natural
Windblown dust
Volcanic particles
Total
Anthropogenic
Coal combustion
Fuel oil
Beryllium ore processing
Total
Total U.S.
Production
(106 t/yr)
8.2
0.41

640
148
0.008b
Emission
Factor
(g/t)
0.6
0.6

0.28
0.048
37. 5b
Emission
(t/yr)
5
0.2
5.2

180
7.1
0.3
187.4
aUnits are in metric tons.
 the emission factor of 37.5 is hypothetical.

concentration of beryllium  in  coal  is between 1.8 and 2.2 ug/g.   In 1984, the
United States burned  790  x  10   metric tons  of coal.   Had  emission  control  mea-
sures for  other  pollutants  not been  used,  1300  tons  of beryllium would have
been emitted,  an amount that  is  far  greater than the  0.3  tons  lost during
beryllium  ore processing.   However, there  is  evidence  that emission control
measures capture 70 to 90 percent  of  beryllium  in  the  fly ash.    The  actual
efficiency  of  beryllium retention  during coal  combustion  is a subject  of
controversy and  a  source  of confusion in several published reports.  Phillips
(1973) presented data  that  suggested  86 percent of the beryllium in coal is
released to the  atmosphere.  Gladney  and Owens (1976) concluded  that less  than
4 percent  escapes.  Henry (1979)  suggested  that less than  1 percent escapes,
but could  not account for 35  percent  of the beryllium  in mass-balance esti-
mates.   The following calculations may explain this discrepancy.
     All three authors  use  a  form  of  a  mass-balance  calculation in which  the
concentration of beryllium  in  the coal  and  the  fly ash is  either  measured or
assumed.   Since  beryllium output  is presumed  to be confined to  captured fly
                                      3-8

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ash and emitted  stack gases,  that fraction of the coal input not found in the
fly ash is  considered as emitted to the  atmosphere.   Neither  Phillips  (1973)
nor Gladney and  Owens (1976)  knew the actual  mass  of the ash produced.   In
both cases, they reported ash content published  elsewhere  in  the  literature.
Phillips measured  a  beryllium content of the  coal  (2.5  ug/g)  and of the ash
(5.0 ug/g), ar|d  assumed an ash content of  7 percent to  calculate  the  emitted
fraction as:
                         2.5 ug/g - (0.07)(5 ug/g) = 0 86
                                  2.5 ug/g
     Gladney and  Owens  (1976) assumed an ash  content  of 12 percent,  which is
near the  upper range of the 7 to 14 percent normally found in coal.   They mea-
sured  a coal  beryllium  content of  1.89  and  an  ash beryllium  content of
15.3 ug/g-  The calculated percent loss would  be:
                         1.89 ug/g - (0.12)(15.3 ug/g) _ Q Q285
                                   1.89 ug/g
     Both  calculations  are extremely sensitive to  the  assumed ash content of
 coal.   Using the range of 7  to  14 percent, the data of Phillips would show
 beryllium  losses of 72 to 86 percent, and  the data of Gladney and Owens, 0 to
 43 percent.   It  is  also possible that errors of analysis were made in measuring
 the  beryllium concentration of coal and ash.  Coal and ash from the same plant
 that Phillips investigated were reported by the Southwest  Energy Federal Task
 Force  (1972) to contain 0.43 and 7 ug Be/g, respectively.   However, these con-
 centrations  cannot  be considered typical because in the  range of  7 to 14 percent
 ash, these data  would yield  a percent beryllium loss of  less than zero.  If the
 average beryllium content of western coal  (1  ug/g) is  used with the Phillips
 data,  the  loss  to the atmosphere ranges  from 30 to 65 percent.
      Henry (1979) made similar measurements of coal and ash.  Sixty-five per-
 cent of the beryllium  was accounted for in the  ash.   However,   measurements
 of beryllium at  the precipitation  outlet and  in the stack did not  account  for
 the remainder of the beryllium.
      Although the data range from  0 to 86  percent, it seems reasonable to con-
 clude that between  10 and 30 percent of the beryllium  in coal  is  emitted to the
 atmosphere  during  the  coal combustion process.   While  not all   coal burning
                                       3-9

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 racilities control emissions as well as power plants, the following calculation
 is a conservative estimate of total beryllium emissions from coal in the United
 States during 1984.

   790 x 106 t coal/yr x 1.4 g Be/t coal x (0.2 ± 0.1) = 220 ± 110 t Be/yr
                                            efficiency
     Emissions  from  oil-burning facilities may be calculated from the average
beryllium  concentrations  of fuel  oil  (Anderson, 1973),  an  assumed loss of
                                           o
40 percent, and a consumption  of 1.1 x  10  tons residual oil  per year.   From
this calculation,  it appears that 7.1 tons of beryllium  are emitted from this
source.
     Although no  data exist, it is  likely that  less than 0.5 percent of the
contained  beryllium  is emitted during the post-ore  production metallurgical
processes, adding  a  maximum of 0.12 tons/year to  the atmosphere.   Therefore,
187 tons/year would  seem  to be a reasonable estimate for anthropogenic beryl-
lium emissions  from the United States.   An estimate by Flinn and Reimers (1974)
that coal  combustion accounts  for 88 percent of the total beryllium emissions
was probably  conservative ;and  could perhaps  be  revised upward  to  95 percent or
higher.
     Assuming a residence time of 10 days,  an  effective stratospheric volume
            -J C  O
of 2.3 x  10  m ,  and stationary air mass above  the  United States,  this  amount
of  beryllium could  account for  an average  atmospheric concentration  of
         3
0.22 ng/m .   Because  of the dispersion caused by moving global  air masses,  the
actual air concentrations are about one-third this value.
     Because  most  atmospheric  beryllium  is derived from coal combustion,  it is
likely that  its chemical  form  would be beryllium oxide.   Conversion to ionized
salts is possible, but has not been reported.  Gladney and Owens (1976) studied
the particle size distribution of stack emissions and reported that most beryl-
lium is found on particles smaller than  1 urn.   Particles of this size remain
aloft for about ten days.
     Removal  of beryllium from the atmosphere is  by wet and dry deposition.
The rate of dry deposition; of aerosol particles is a function of particle size,
windspeed, and  surface roughness.  The actual deposition  rate for beryllium has
not been measured, but can be estimated by analogy to other elements.  Davidson
et al. (1982) described the relationship between concentration of particles in
                                     3-10

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air, particle  size,  and surface roughness. For vegetation surfaces, a reason-
able deposition velocity would be 0.25 cm/sec.  Assuming an average air concen-
                      3
tration of 0.1 ng Be/m  in air, 0.002 ng of beryllium would be removed from the
atmosphere per square centimeter of actual surface area.
     Kwapulinski and Pastuszka (1983) have determined that in Poland, emissions
of  beryllium appear  to be in balance with deposition.  They applied the solu-
tion of  the  Reynolds mass-balance model  described by Astarita et al.  (1979)  to
the deposition  of  beryllium as a function of air concentration.   The coeffi-
cient  of deposition, K-,, was found  to  be constant during rainy  periods  and
linearly  correlated  with windspeed during dry periods.   This  report confirms
that beryllium is removed from the atmosphere by both wet and dry deposition  in
a  manner similar to metals on particles  of comparable  size  distribution.
Values for 1C,  have not yet been  measured  in the United  States.   Because  K^
varies regionally  with surface roughness and windspeed, calculations based on
metals associated  with particles  of comparable size are an acceptable substi-
tution.
     Concentrations  of  beryllium  in precipitation have not been reported in the
United States.  Assuming that half of the beryllium emitted into the atmosphere
returns  to earth  as  wet precipitation, the average concentration of beryllium
in  rain  or snow is expected to be 0.01 ng/g.   This value  is below the detection
limit  for most analytical techniques.   In a  report from Australia, the actual
concentration  of  beryllium in rain was reported  to  average 0.07 ng/g (Meehan
and Smythe, 1967).
     Beryllium  oxide is very insoluble and would not be mobilized in soil or
surface  water  at  normal environmental  pH  ranges  of  4 to 8.   If  this is the
chemical  form  of  beryllium at the time  of deposition, the compound would not
move easily  along grazing food chains, but  would instead be confined to soil
and sediment.  If,  however, significant amounts of beryllium are converted to
chloride-, sulfate-, or nitrate-salts  during atmospheric transport, solubility
upon deposition would be greatly enhanced and mobility within ecosystems could
be facilitated.   Beryllium is classified as  a fast-exchange metal, which means
that  it  could potentially interfere with  the transport of nutritive metals,
such as  calcium,  into eukaryotic cells (Wood and Wang, 1983).  There is a need
for research into the effects of pH on the mobility of beryllium in ecosystems
and its  subsequent  effects on plants  and animals.   Some of the toxic effects
                                      3-11

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 of beryllium on  natural  populations of plants  and animals are reviewed by
 Brown  (1979).
3.5  ENVIRONMENTAL CONCENTRATIONS OF BERYLLIUM
3.5.1  Ambient Air
     Beryllium is measured :at many of the stations  in the SLAMS (State and Local
Air Monitoring  Stations) and NAMS (National Air Monitoring Stations) networks.
The data  are available from the AIRS (Aerometric Information Retrieval  System).
data base which supercedes SAROAD (Storage  and Retrieval of Aerometric Data) and
is maintained by the  U.S.  Environmental  Protection Agency.   The detection
limit  for  most  of these analyses is 0.03 ng/m3,  except those using AAS  (Atomic
Absorption  Spectroscopy),  where  the  detection  limit  is  0.2 ng/m3.   The
systematic  difference  between  the two methods (Table  3-5)  cannot be readily
explained and has  not been addressed in the literature.  However, most values
                           3
are well  below  the 10 ng/m  standard set by the U.S. Environmental Protection
Agency (U.S.  EPA,  1973).  Only those annual averages  that exceeded 0.1 ng/m3
during 1981-86  are  shown in Table 3-5.   Some  of these annual  averages  do not
have the  required  number and distribution  of  reported 24-hour values to meet
the statistical criteria for summarization, but they  do  reflect  the general
pattern of air concentrations of beryllium.

3.5.2  Soils and Natural Waters
     Shacklette et al.  (1971)  reported a geometric mean of 0.6 ug Be/g  in soil
for 847 samples taken from sites distributed evenly across the United States.
Only 12 percent of the samples exceeded 1.5 ug/g.   The soils  were sampled at a
depth  of  20 cm.  These results  are  lower than  those of previous  geochemical
surveys conducted by  Vinogradov (1960), Hawkes and Webb  (1962),  and Mitchell
(1964), each  of whom  reported a mean of 6.0 ug/g.  The differences may be due
to limitations in analytical techniques.  The 0.6 ug/g value is more consistent
with the average crustal value of 2r8 ug/g  reported by Mason (1966).
     Values for beryllium in surface waters range from 0.01 to 1.0 ng/g (Bowen,
1979).   The  lowest value (0.01 ng/g) was reported by Meehan and Smythe (1967)
in Australia.   These concentrations  are in the same  range  as the expected
concentration of beryllium in precipitation (0.01 ng/g) discussed above.  The
                                     3-12

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beryllium  concentration  in seawater was reported to be 0,0005 ng/g by Merrill
et  al.  (1960)  and 0.0056 ng/g by Bowen (1979).   there are no available reports
of  beryllium concentrations in groundwater.
3.6  PATHWAYS TO HUMAN CONSUMPTION
     Humans  may be exposed to  beryllium through air, food, water,  and  dust
(Figure  3-1).   In this  section, beryllium concentrations are  estimated  for
typical  environments  not exposed to extraordinary sources of beryllium.   These
values are combined with the consumption rates of air, food, water, and dust to
estimate the typical total daily intake of beryllium.
                                                    o
     A likely  average concentration of 0.08 ng Be/m  in  a residential  environ-
ment can be projected from data collected from monitoring stations.  Values are
undoubtedly  influenced  by the  distance and location of  monitoring  stations
from beryllium  sources,  and  whether indoor or outdoor, filtered or unfiltered
air is sampled.  Only limited data on the beryllium content of foods are avail-
able.  Meehan  and Smythe  (1967) analyzed  a  few foods  from Australia and
reported values  from  0.05 to 0.15 ng/g  fresh  weight.  The reported  values  of
beryllium in drinking water  range from 0.01 to  1.2 ng/g, with an average of
0.2 ng/g. There  are  no reports of beryllium in  household dust, but if it is
assumed that such dust originates solely from the atmosphere having a beryllium
                          o
concentration of 0.1  ng/m ,  and that the air/dust ratio  is 600,  then household
dust would contain 60 ng Be/g.
     The average American  adult inhales 20 m  of air/day and consumes 1200 g
of food  and  1500 g of water and beverages (Pennington, 1983).  The daily con-
sumption of dust is not well  established, but a conservative estimate of 0.02 g
is made  here  for the  purpose of illustration.  The typical  American  adult con-
sumes  423  ng/day of beryllium, most  of which  comes from food  and beverages
(Table 3-6).   It is  apparent  that  air or dust derived  from air has little
impact on  the total  intake  of  beryllium.   This overall  determination  is
extremely sensitive  to  the  average concentration  of beryllium  in food  and
water, which accounts for 99.3 percent of total daily consumption of beryllium.
Variation in these  numbers can be expected,  depending on the types of food and
beverages consumed and  the atmospheric contribution to  the  beryllium concen-
trations of food and beverages.
                                     3-20

-------
              INDUSTRIAL
               EMISSIONS
                                                                SURFACE AND
                                                               GROUND WATER
                                                                  DRINKING
                                                                   WATER
Figure 3-1. Pathways of environmental beryllium concentrations leading to potential human exposure.
                                     3-21

-------
            TABLE 3-6.  POTENTIAL HUMAN CONSUMPTION OF BERYLLIUM FROM
               NORMAL SOURCES IN A TYPICAL RESIDENTIAL ENVIRONMENT

Air
Food
Water
Dust

Environmental
Concentration
0.08 ng/m3
0.1 ng/g
0.2 ng/g
60.0 ng/g

Total Daily
Human
Intake
20.0 m3
1200 g
1500 g
0.02 g
Total
Consumption
1.6 ng/day
120
300
1.2
422.8
Percent of
Total Daily
Consumption
0.4
28.4
70.9
0.3

      Daily consumption from extraordinary  sources,  such as occupational  expo-
 sures or secondary occupational  exposure  e.g.,  a non-worker's exposure  to  a
 worker's clothes, may increase  the  relative contribution of air and  dust to
 overall  beryllium exposure. At  2 Mg Be/m3  (the current occupational standard),
 a  worker's exposure for an 8-hour shift would increase to more than 13,000 ng/
 day.   Dust of beryllium metal  or metal  oxide consumed at a  daily rate  of  0.02 g
 (including dust consumed during the working shift and dust carried home on the
 clothing of the worker), could  add  2,000,000 ng beryllium to the total daily
 consumption.   There is also the  possibility that certain individuals  might be
 exposed  to beryllium from implanted dental  prostheses.   Although the  leaching
 of  nickel  and chromium from alloys  used  in prostheses has been reported, no
 studies  on  the  leaching of beryllium are available.
      Consumption  of beryllium  from cigarette smoking was discussed by Zorn and
 Diem  (1974).   They found ah average of 630 ng Be/cigarette and an average of
 35 ng  Be/cigarette in  the inhaled smoke.    Based  on  these findings, a person
 smoking  a pack of twenty cigarettes per  day would  inhale about 700  ng  of
 beryllium,  which  is nearly  twice the  daily consumption  from other sources.
 Unfortunately,  details in  this study are lacking.   The  origin  of  the  tobacco
was not  given,  and the relationship  between the  beryllium concentration of the
 tobacco and the smoke was very weak.
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                  4.  BERYLLIUM METABOLISM IN MAN AND ANIMALS
4.1  ROUTES OF BERYLLIUM ABSORPTION
4.1.1  Beryllium Absorption by Inhalation
     There are  no  data on the absorption of inhaled beryllium in humans.   How-
ever,  it  can be expected that the dose, size,  and solubility of beryllium
particles will  be  important factors in determining the rates of absorption and
clearance.
     Beryllium  has  been  found in the  lungs  of  persons without known occupa-
tional exposure to  the metal.  Cholak (1959) analyzed 70 lungs from unexposed
individuals and reported  an average concentration  of  3.3 |jg Be/kg dry  weight
(range: 0.1-19.8 ug/kg).   Meehan  and Smythe (1967) reported  a mean beryllium
level  of  1.3  ug/kg  wet weight (range: 0.3-2.0 ug/kg)  in  four human lungs (a
value  which corresponds  to about 6 ug/kg dry weight).   Sumino et al.  (1975)
analyzed  beryllium  in  the lungs of 12 Japanese  subjects  and found concentra-
tions  of  up  to  30  |jg/kg wet  weight.   It should be kept in mind that smoking
habits were not taken into account in any of these studies.   In addition, it is
difficult to  validate  such data,  as well  as other data on beryllium in  tissues
or body fluids, since  no interlaboratory or quality control studies have been
conducted and no reference samples  for beryllium in tissues or body fluids are
available.  The highest  value recorded by Cholak (20 ug Be/kg dry weight) has
been used to  denote an upper normal  level  of  beryllium in human lung tissue
(Hasan and Kazemi,  1974).
     Animal  studies  have  shown that rats exposed  to  beryllium sulfate  at an
                                     o
average beryllium content of 35 ug/m  .for  7 hours a day, 5 days a week, for
72 weeks,  reached a plateau in lung beryllium concentrations of about 13.5 |jg
after  36  weeks  of  exposure.   A plateau in the tracheobronchial lymph nodes was
also reached  at that time.   After exposure  was  terminated,  pulmonary beryllium
was  initially eliminated  with a  half-time  of two weeks,  followed by a  much
slower elimination rate (Reeves et al., 1967; Reeves and Vorwald, 1967).
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     In studies of the distribution of radioactive beryllium compounds adminis-
tered by  intratracheal  injection,  Kuznetsov  et  al.  (1974)  reported  a  half-time
of 20 days  in  rats  given  a single  injection  of  beryllium chloride,  whereas Van
Cleave and Kaylor (1955) reported that beryllium citrate was rapidly eliminated
in rats.  Longer  observation  periods in rats, however, suggest a half-time of
about 325 days  after inhalation of beryllium  oxide  (Sanders  et al., 1975,
1978).  Reanalysis  of the latter data showed that there was an initial clear-
ance of*30 percent of the deposited beryllium at a half-time of 2.5 days, while
the rest was cleared much more slowly at  a  half-time of 833 days  (Rhoads and
Sanders,  1985).   About  25  percent of the beryllium  cleared from  the lungs
during the slow phase was translocated to regional lymph nodes  (Sanders et al.,
1978).
     Hart et al.  (1984) exposed 20 rats for one hour to beryllium oxide fired
                                                                q
at 560°C.  The  average  concentration of beryllium was  447 ug/m ,  and 90 per-
cent of the particles had a mean diameter of 1 urn or less.   The beryllium oxide
contained a trace of carrier-free   Be.   Four animals were killed at 2.5 hours
and at  2,  5,  12, and 21  days after exposure.    Lungs  were  lavaged and the
beryllium content was determined in the lavage  fluid and  in the lung tissue.
In the  lung tissue,  about 200  ng of beryllium was  found 2.5 hours  after
exposure.  This amount  remained constant over  the following weeks.   In con-
trast,  the amount of beryllium in  the lavage fluid  decreased  from 280 ng to
16 ng in  three  weeks.   The lavage fluid contained free alveolar cells (mainly
macrophages).
     It is not  known in detail how beryllium is retained in the lungs.  It is
likely  that soluble beryllium compounds  are  transformed to insoluble  complexes
with, for instance,  phosphate, when the  beryllium concentration reaches a cer-
tain  level  (Reeves  and  Vorwald, 1967).   Beryllium particles in the insoluble
state are apt  to be taken up  by macrophages  as  demonstrated ijn vitro  (Hart and
Pittman,  1980).   At high  ui vitro  and iji  vivo  exposures,  beryllium has been
shown to  be very toxic  to  alveolar macrophages (Camner et al., 1974; Sanders
et al., 1975;  Hart  et al., 1984).   Robinson  et  al.  (1968)  exposed two dogs for
20 minutes to  a mixture of beryllium oxide,  beryllium fluoride and beryllium
                                         o
chloride  (average concentration 115 mg/m ).   The dogs were killed after three
years.  The average beryllium concentration  in  the-lungs was 3.9 and  5.5 mg/kg
wet weight.   Beryllium  deposits were seen in  the  interstitial tissue where they
were  in the lysosomes of histiocytes.
                                      4-2

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     Zorn et al.  (1977) exposed  rats  and guinea pigs  to  beryllium sulfate
aerosol (with  Be  added as  the  chloride)  for  a  period of three  hours.  Animals
(number not  given) were killed  at  the end of  3  hours  and then from 20  to
408 hours, thereafter.   The  total  amount of beryllium  inhaled  was  less  than
3 mg of which  10  ng was  Be.  At the  end of the exposure, about 5 ng of the
isotope was  retained  and about 0.5 ng was  found  in  excreta.  Of the  retained
amount of  Be,  about  67 percent was in  the lungs and  15  percent was in  the
skeleton, indicating  a  rapid initial  clearance.  After 408  hours  (17 days),
about  80  percent  of  the total  body burden of   Be  was  in the  skeleton  and
approximately 18 percent was in the lungs.  Less than one percent of  Be was in
other  organs.   During the  first four days,   Be  was  cleared from the lungs with
a half-time  of about  24 hours.   This was followed by a  slower clearance  with a
half-time of several  weeks.   Unfortunately, the  lack of detailed information
precludes a thorough  evaluation of this study.

4.1.2  Gastrointestinal  Absorption of Beryllium
     There are  no  data on the absorption  of  ingested beryllium compounds in
humans.   Animal  experiments, however,  generally  indicate  that  less than one
percent of ingested beryllium is absorbed (Hyslop et al. , 1943;  Crowley et al. ,
1949;  Furchner et  al.,  1973).   The latter  two  studies  were done using tracer
amounts of  Be.
     Reeves  (1965) gave two groups  of  rats, four in each group, beryllium sul-
fate in  drinking water.  The average  daily intake  was  about 6.6 ug Be in one
group  and 66.6 jjg Be in the other.  One rat  in each group was  killed after  6,
12,  18,  and 24 weeks of exposure.   Reeves found that 60 to 90  percent of the
ingested  beryllium was  eliminated in the feces, indicating that an appreciable
amount was  absorbed.   However, the skeletal uptake of beryllium in both groups
of  rats  was nearly  the same,  averaging 1.49 yg in the low-dose  group  and
1.19 |jg  in the high-dose group.  This suggests either that  gastrointestinal
absorption  was much  less in the high exposure group or that the uptake in bone
was  independent of absorbed dose.  If it is assumed that 50 percent of gastro-
 intestinally absorbed beryllium goes  to  the  skeleton and  that the biological
 half-time in the  skeleton is 100 to 1000 days, the daily absorbed amount would
 be  less  than 50 ng (or  less  than 1  percent of the low oral  daily dose).
                                       4-3

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     In  reporting  the study,  Reeves  (1965) concluded  that due to the  low
solubility of  beryllium  in intestinal  fluid, it was precipitated as the phos-
phate and was  not,  therefore, available for absorption.  Reeves surmised that
most of the beryllium found in the body was absorbed from the stomach.
     In contrast to  Reeves'  study, Morgareidge et al.  (1977,  abstract)  found
that uptake  in bone  was  dose-dependent.   They  exposed rats  orally  to beryllium
as the sulfate at  concentrations of 5, 50, and 500 mg/kg for up to two years.
Unfortunately, no quantitative data are given in the abstract of this study.

4.1.3  Percutaneous Absorption of Beryllium
     There are no  data on skin absorption  in  humans.   Tracer  studies  in rats
have shown  that small  amounts of beryllium may  be absorbed from  the  tail
(Petzow and  Zorn,  1974).   Belman (1969) reported that ionic beryllium applied
to the skin  will  bind to epidermal constituents,  mainly alkaline phosphatase.
However,  the  chemical  properties  of beryllium in any of its different forms
make it unlikely that significant absorption can occur through skin.

4.1.4  Transplacental Transfer of Beryllium
     In a study by Bencko et al.  (1979),  the soluble salt of beryllium,  Bed,,,
was evaluated  for  its ability to  penetrate the placenta and reach  the  fetus  of
mice.  Radio!abeled   BeCl2,   injected  into the caudal vein  of  7 to 9  mice,
crossed  the  placenta and was  deposited in various  organs of the  fetus  (see
Chapter 5 for  a detailed discussion of this study).
     No other  data are available on placenta! transfer of beryllium.
4.2  TRANSPORT AND DEPOSITION OF BERYLLIUM IN MAN AND EXPERIMENTAL ANIMALS
     Ingestion studies  on  animals  have shown that beryllium absorbed from the
gastrointestinal tract  accumulates  mainly in the skeleton.   In  soft tissues,
the highest  concentrations have been found in the liver (Reeves, 1965; Mullen
et al.,,  1972).   Similar results have  been obtained in injection  studies  on
animals  (Mullen et al., 1972; Hard et al., 1977).  In the case of the injection
studies, the physiochemical  state  of the injected compound determines the main
site  of  deposition:   soluble  beryllium rapidly distributes to the skeleton,
whereas  colloidal  forms go mainly to the liver  (Klemperer et al., 1952).   In
rat  blood,  large doses of injected  beryllium tend to aggregate and bind to
                                      4-4

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phosphate, whereas  small  doses  remain largely in a diffusible  form (Vacher  and
Stoner, 1968a,b).   At  low doses of beryllium, the main binding in human blood .
was reported  to  be  the prealbumin and a-globulin fractions of plasma (Stiefel
et al., 1980).  Recent data indicate that there is a binding site for beryllium
in the lymphocyte membrane (Skilleter and Price, 1984).
     Witschi  and Aldridge (1968)  found that less than 10 percent of an intra-
venous dose of beryllium, sulfate in rats was in the liver 24 hours after dosing
(dose range:  0.75-15 (jg  Be/kg b.w.).  In  contrast,  more  than 25 percent was
found in  the  liver  following the administration  of  doses  of 63 (jg/kg  b.w.  or
higher.   With  increasing  dose,  comparatively more beryllium was located in  the
nuclear fraction and  less in the supernatant  of subcellular fractions of rat
liver.  At  the lowest  dose (0.75  pg), the  light mitochondria!  fraction had  the
highest amount of  beryllium, and  some evidence was presented  for beryllium
being located  in  the  lysosomes.  Further evidence  for a role  of lysosomes  in
the hepatic accumulation  of beryllium was  presented by Skilleter  and Price
(1979).
     There  are  few  data on beryllium  levels  in  humans.  Analysis of tissues
from people occupational.ly exposed to beryllium showed that, generally, concen-
trations were highest in bone,   liver, and kidney (Tepper et al., 1961).  Meehan
and Smythe  (1967) reported that in the brain,  kidney, spleen,  liver,  muscle,
and heart,  concentrations were  generally less than  1  pg/kg wet weight.  How-
ever,  in  one  bone  sample the concentration was 2 pg/kg, and in five vertebrae
the mean  was 3.6 pg/kg.   The form  in which beryllium is  stored  in bone is
presently unknown.
4.3  EXCRETION OF BERYLLIUM IN MAN AND ANIMALS
     In rats given intravenous injections of tracer doses of  Be, 15 percent of
the dose was  excreted in urine by day 1 and 64 percent was excreted by day 64
(Crowley et al.,  1949).   In mice,  monkeys,  and dogs,  urinary excretion was  the
main  route  of beryllium  elimination  during the first days  after  parenteral
dosing  (Furchner  et  al.,  1973).  These researchers  found  that only later did
elimination by the  gastrointestinal  tract equal  that  of  urinary excretion.   In
early  studies,  Scott et  al.  (1950)  discovered that  increasing the dose in
experimental  animals resulted in a relatively  lower  urinary excretion rate.
Biliary excretion seems  to play  only a minor role in  total  beryllium excretion
(Cikrt and Bencko, 1975).
                                      4-5

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     With  oral  dosing, Reeves (1965)  found  that less than one percent of the
 administered dose was  excreted in  urine  of rats.
     Quantitative data on the excretion of beryllium in humans are scarce.   In
 one  study  of persons  not exposed  to an  occupational  source of beryllium, very
 small  amounts  (<0.1 |jg Be/1), as measured by emission spectroscopy, were found
 in the urine (Lieben  et al.,. 1966).   Much  higher values (averages of 0.9 pg
 Be/1)  were reported in two other  studies, one of 120 people from California
 (Grewal and  Kearns, 1977) and another of 20 individuals from Germany (Stiefel
 et  al., 1980).   In the  latter two  studies,  flameless atomic  absorption
 spectroscopy was  used  to  measure the  beryllium concentrations.   Thus,  the
 differences observed between these two studies and that of Lieben et al.  (1966)
 may have been due to the different analytical methods used.
     Since human dietary intake of beryllium is  low, and animal studies suggest
 that gastrointestinal  absorption would also be low, the total human body burden
 of beryllium is  likely to be such that only a few nanograms would be excreted
 daily.   Based on  the limited data reported  by Meehan and Smythe (1967), the
 soft tissue burden of  an adult is likely to be less than 20 ng and the skeletal
burden about-30 ug.
     Presently,  there are no estimates of the biological half-time of beryllium
 in humans.   However, in dogs, mice, rats, and monkeys, the long-term biological
half-times of beryllium after injection have been estimated at 1270, 1210,  890,
and 770 days, respectively  (Furchner et al., 1973).   Some circumstantial evi-
dence suggests  that the half-time in human bone is likely to be many years.
                                      4-6

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                           5.   BERYLLIUM TOXICOLOGY
     This chapter  reviews the  nonmutagenic  and noncarcinogenic  effects of
beryllium.   Because  of the  volume of  information  available regarding  the
mutagenic and carcinogenic  effects of beryllium, these topics  are  dealt with
specifically in Chapters 6 and 7.

5.1  ACUTE EFFECTS OF BERYLLIUM EXPOSURE IN MAN AND ANIMALS
5.1.1  Human Studies
     Acute  lung  disease  from  excessive exposure to beryllium  compounds was
first reported in Europe during the 1930s.  The first case in the United States
was reported in 1943 (Van Ordstrand et al., 1943).   In the 1940s, many hundreds
of cases occurred,  but with today's improved working conditions, acute beryl-
lium poisoning is rare.
     Acute  lung  disease can be caused by inhalation of soluble beryllium com-
pounds, such as  the fluoride with acidic pH or the low-fired beryllium oxide.
The reported symptoms  have been nonspecific, with chemical pneumonitis as the
most severe manifestation (Freiman and Hardy,  1970;  Reeves,  1979).   In a study
of  six fatal  cases,  Freiman and  Hardy  (1970)  reported  that death occurred
between 17  days  and 10 weeks after exposure.  Interstitial edema and cellular
infiltration dominated the histological tissue analyses.  The  beryllium con-
centrations in the lung ranged  from 4 to 1800 ug/kg.  It was not stated whether
the analyses were based on wet  or  dry weight.
     In most cases  of  acute poisoning,  recovery is slow, taking several weeks
or  months  (Reeves,  1979).  In  the U.S.  Beryllium  Case Registry (BCR), a file
on  reported cases of  acute and chronic beryllium  disease, 215 cases of acute
poisoning were  registered up to 1967  (Freiman  and Hardy, 1970).   Since 1967,
an  additional nine cases  have been reported  (Eisenbud and  Lisson, 1983).
     The  fact  that there still  is some occupational  risk for acute beryllium
disease  is  shown by recent  case  reports by Hooper (1981) and  Lockey  and co-
workers  (1983).   Hooper describes a case of an 18-year-old sandblaster exposed
                                       5-1

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 during grinding to dyes  containing a copper-beryllium alloy.   The man developed
 acute  respiratory disease, which  was  diagnosed  as  interstitial  pneumonitis by
 an  open lung biopsy performed  six. days after exposure.  Beryllium concentra-
 tions  in the lung  tissue  were  28 ng/kg dry weight.   In  the  report by Lockey
 and co-workers, acute chemical pneumonitis  in a. dental laboratory technician
 was attributed  to the  casting and grinding  of dental  bridges  containing nickel-
 beryllium alloys.
     Contact  dermatitis  caused by exposure  of skin to soluble beryllium salts
 has also been described  (Van Ordstrand et al., 1945).

 5.1.2   Animal Studies
     Acute  chemical pneumonitis  has been  produced  in a variety of animals
 exposed to  beryllium as a sulfate or  fluoride (Stokinger et  al., 1950).   Some
 insoluble  compounds, especially  low-fired  beryllium  oxide,  have also caused
 acute  effects  in rats (Hall  et al., 1950).   The  concentrations needed to  cause
 acute  effects have  generally been  on the order of several mg/m3.
     Injection  of beryllium  compounds can  cause acute liver  damage  (Aldridge
 etal., 1949; Cheng, 1956)..
5.2  CHRONIC EFFECTS OF BERYLLIUM EXPOSURE IN MAN AND ANIMALS
5.2.1  Respiratory and Systemic Effects of Beryllium
5.2.1.1  Human Studies.   Hardy and Tabershaw (1946) were  the  first to report
chronic lung disease  caused by beryllium.  They  presented data on 17 persons
employed in  the  fluorescent lamp manufacturing  industry.   The main symptoms
noted were dyspnea  on exertion, cough, arid weight  loss.   In most cases, the
symptoms first  appeared  months or  even years after exposure.   The  patients
were generally younger than  30 years of age  and the majority  were  women.
X-rays showed  that  an early sign of  chronic  beryllium poisoning was  a  fine
diffuse granularity in  the lungs.   In the second stage,  a diffuse reticular
pattern was  seen, while in the third stage,  distinct nodules appeared.  After
generally less than two years of illness, five  deaths  occurred among the  17
persons.   Though disability persisted in most cases, some recovery was  noted
in two cases.  Postmortem examination of the lungs  from  one person showed a
granulomatous inflammation  characterized  by  central  and eccentrically located
giant cells  of the  foreign!body type  in  the  alveoli.   Infiltration of plasma
cells and lymphocytes was also noted.
                                      5-2

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      This  pioneer, study by  Hardy and Tabershaw led  to  further occupational
 studies,  which  have been documented  in  papers by Hardy  (1980)  and Eisenbud
 (1982).   In  addition,  there  have been reports  on  "neighborhood cases," i.e.
 beryllium  disease  in persons  living in  the  vicinity of beryllium-emitting
 plants.  In these cases, exposure was not only to beryllium in ambient air, but
 also to  contaminated clothing  brought  into  the  house from  occupationally
 exposed members  of the  household (Eisenbud  et al.,  1949).   At least three
 children,   ages  7 to 14  years,  were counted  among such  cases (Hall et al.,
 1959).
      These and other findings  led to the adoption of beryllium standards  for
 both industrial  and ambient  environments.   A Threshold Limit  Value (TLV)  of
 2  ug/m  was  set as an average for an  8-hour occupational  exposure;  the maximum
 permissible peak (not to exceed more than one  30-minute  period) was set  at
 25 ug/m .   For the  ambient environment,  a level  of  0.01 ug/m3  was proposed.  It
 should  be  noted  that  the 2 ug/m3 standard was  not based on actual dose-response
 relationships.   As  stated by Eisenbud (1982), the  standard was  based  on the
 molar toxicity of beryllium  in  relation  to  some heavy metals  such as lead  and
 mercury, which have TLVs  around  100  ug/m3.
      While these proposed standards  seemed to  prevent  acute  poisoning,  many new
 cases of chronic beryllium disease  appeared mainly as a  result of heavy  expo-
 sures during  the period  from 1940 to  1946.  This led  to the foundation of  the
 Beryllium  Case Registry  (BCR) in 1952.  The BCR  was intended to serve as  a  file
 for  all cases  of acute and chronic beryllium disease,  from which  information  on
 the  development  and clinical  manifestations  of beryllium disease  could be
 obtained.   Since  1978,  the BCR  has  been  maintained by the National Institute
 for  Occupational Safety and Health.
      Throughout the years,  many scientific reports  have relied on the informa-
 tion  found in the  BCR.   In 1959, Hall  et al. presented  data  on 601 cases
 (Table 5-1).   The authors noted that most acute cases  occurred in males.   How-
 ever, in later reports  the number of  cases  of chronic disease increased and
 currently  number more than 600.    In contrast,  only  a  few additional cases  of
 acute disease  have  been  reported.  It should  be noted that 28 of  the  acute
 cases in Table 5-1  were  also  classified  as chronic.  Between 1966 and 1974, 74
 new  cases  of  beryllium  disease  were reported to the BCR, of which 36 had been
exposed after 1949 (Hasan and Kazemi, 1974).
                                      5-3

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Acute
Chronic
TABLE 5-1.
Men
227
191'
BERYLLIUM REGISTRY CASES, 1959
Women Total
20 247 (39%)
191 382 (61%)

Dead
15 ( 6%)
121 (31%)
Source:  Hall et al. (1959).
    TABLE 5-2.  TIME FROM LAST EXPOSURE TO FIRST SYMPTOM3 IN THE BCR, 1959
Time
Less than 1 month
1 month to 1 year
1-5 years
5-10 years
More than 10 years

Cases of beryllium disease
126
27
89
56
12
310
%
41
9
29
18
4

 Maximum was 15 years.
Source:  Hall et al. (1959).

     Chronic beryllium  disease  often appears many years after  exposure  ends.
In more than  20 percent of the  cases recorded in the BCR before 1959,  the  time
since  last  exposure was  greater than 5  years,  the maximum being 15  years
(Table 5-2).  There  has  been some overlap between  acute and chronic disease,
but generally the  disease has been  registered as chronic if it  has lasted  more
than one year.
     The latest  report  contains 897 cases, 10 of which have been added  since
1978  (U.S.  Centers  for  Disease Control,  1983).   Eisenbud  and  Lisson  (1983)
reported on 888  cases,  but noted that they knew  of  45 other chronic cases  that
had not yet been included in the BCR.  Therefore, the total number of  cases of
beryllium disease in this country may exceed 900.
     Of the 888  cases  reported  by Eisenbud and Lisson, 224 were classified as
acute.  This  number is  smaller than  the  one given  in  Table  5-1,  but  as
mentioned earlier, 28 acute cases in that table were also classified  as chronic.
The chronic cases  were  reported to be 622,  leaving 42 cases unaccounted.  Of
the 622 cases,  557 occurred in  individuals occupationally  exposed to beryllium
                                      5-4

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and 65 occurred  among members  of the general  populace.   Of the latter,  42 were
attributed to ambient air exposure and 23 to dust exposure in the home.
     The majority  of  the occupational cases cited by Eisenbud and Lisson were
from the fluorescent  lamp (319) or beryllium extraction (101) industries.  In
62 percent of  the  cases, dates for  first  exposure  and onset of disease were
available.    Figure  5-1 shows that up to 40 years  may elapse between initial
exposure and onset of  disease.    There is  some suggestion,  however,  that
latency  times  may  be declining in recent years  (Table  5-3).   Eisenbud and
Lisson urged caution  when interpreting these data,  as  a rough correspondence
between  the  maximum  latency time and  number of years  elapsed  since first
exposure must  exist.   It could be argued,  for  instance, that among  the more
recent members  of  the cohort, not enough  time  has passed for them to develop
the disease.
     Some  of the common symptoms of  chronic  beryllium disease noted from the
BCR are  shown  in Table  5-4  (Hall et  a!.,  1959).  These  symptoms confirm those
reported earlier by Hardy and Tabershaw (1946).   Table  5-5 shows some of the
signs  of chronic beryllium disease.   The  cardiovascular signs can be attribu-
ted to cor pulmonale, which is a sequela of the severe forms of chronic beryl-
lium  disease.   There are also  signs  that  may be  seen as pure  systemic  effects
of beryllium exposure.
     An  extensive description of chronic  beryllium disease was presented  by
Stoeckle  et  al.  (1969).  In their report,  clinical findings and the  results of
treatment  were presented.   In another  paper  by Freiman and Hardy (1970), the
pulmonary  pathology  was presented.   Data were given for  60 patients with
chronic  beryllium  disease  who had  been  investigated at  the Massachusetts
General  Hospital  between  1944  and  1966.    Patients  came from  different
 industries and exposure  levels were  unknown.   Consequently, the data cannot be
 used  for dose-response  analyses.  However, valuable  information can  be derived
 from  the clinical  findings  and the diagnostic problems  noted during  the examina-
 tion  of these patients.   In  addition  to the  pulmonary effects, there was
 further evidence  for extrapulmonary signs  of  beryllium  disease.    In some
 patients,  granulomas were found in muscle  or skin.
      Some of the  features  of chronic beryllium disease are  similar to those
 seen  in sarcoidosis.   In the paper by Stoeckle  et al.,  as well as in an earlier
 paper by Israel and Sones (1959), the differentiation of these two diseases is
                                       5-5

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         5-6

-------
            TABLE 5-3.   CHANGES OF LATENCY FROM 1922 TO PRESENT IN
                        OCCUPATIONAL BERYLLIOSIS CASES3
Period of First
Exposure
1922-1981
1922-1937
1938-1949
1950-1959
1960-1981

No. of Cases
347
33
264
32
18
Latency, in
Mean
11
16
9.8
9.6
6.6
years
Range
1-41
4-40
1-39
1-25
1-13
aCases were included only if both dates of first exposure and diagnosis of
 first symptoms were known.

Source:  Eisenbud and Lisson (1983).
               TABLE 5-4.  SYMPTOMS OF CHRONIC BERYLLIUM DISEASE
Symptom
Dyspnea
on exertion
at rest
Weight loss
> 10%
< 10%
Cough
nonproductive
productive
Fatigue
Chest pain
Anorexi a
Weakness
Percent
69
17
46
15
45
33
34
31
26
17
Source: Hall et al. (1959).
                                      5-7

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                 TABLE 5-5.   SIGNS  OF  CHRONIC  BERYLLIUM  DISEASE*
Sign
Chest signs
Cyanosis
Clubbing
Hepatomegaly !
Splenomegaly
Complications
Cardiac failure
Renal stone
Pneumothorax
Percent
43
42
31
5
3
17
10
12
 Signs attributable to cardiac failure are not included.
Source:  Hall et al. (1959).

discussed.  One  distinguishing  characteristic between the diseases is the con-
siderably greater  systemic involvement in sarcoidosis, as  noted  in more than
80 percent of the  sarcoidosis cases.  X-rays of  the  lungs, however, may show
very similar pictures of the two conditions.
     Among laboratory  findings  in cases of beryllium  disease,  hypercalcemia,
hypercalcuria, stone formation,  and osteosclerosis have been noticed (Stoeckle
et al., 1969), as has hyperuricemia (Kelley et al., 1969).
     In addition to studies based on the BCR, there have also been some studies
within industrial  populations.   Balmes and co-workers (1984) reported on four
cases of suspected chronic beryllium disease in a group of workers exposed to
beryllium released  from  melted  scrap metals.   Hogberg and Rajs  (1980) reported
granulomatous myocarditis  as  the cause of death  in two individuals who were
occupationally exposed to beryllium.
                          i
     Wagoner et  al.  (1980) conducted  a  more  extensive mortality study  on  a
cohort of 3055 workers exposed  to beryllium in a plant in Pennsylvania.  (See
Section 7.2 for  detailed  discussion of lung cancer within the cohort.)  Among
causes of death other than lung cancer, there was a significant excess of heart
disease (396 observed  versus  349 expected) and respiratory disease other than
influenza and pneumonia  (31 observed versus 18.7  expected).   It is  conceivable
that some of the cardiac deaths  were, in fact, caused by cor pulmonale secondary
                                      5-8

-------
to beryllium disease.   There are no data to indicate that beryllium exposure fay
inhalation has a direct effect on the cardiovascular'system.
     These data can be compared to a mortality study by Infante et al.  (1980)
on 421 white  males  listed in the  BCR  during  the  period of 1952 through  1975.
Heart disease was stated  to be the  cause  of  death  in  31 of  these  cases  (29.9
were expected).   Respiratory disease other than influenza and pneumonia was the
cause of  death  in  52  cases (only 1.6 were expected).   It should be noted that
both the  Wagoner and  Infante  studies  should be  viewed  with caution  due to
various deficiencies  in  study  design  and analysis.  These  deficiencies  are
discussed in greater detail in Section 7.2.
     Results  of  studies  on respiratory function have  been presented by  Andrews
et  al.  (1969),  Kanarek et al.  (1973), and Sprince et al.  (1978).  Andrews
et al.  performed lung  function tests  (vital capacity and FEV-^) on 41 patients
registered  in the BCR as having  chronic  beryllium disease.   In  only two
patients  were the  test results normal; 16  out of the 41 patients had airway
obstruction.
     The  studies by  Kanarek et al.  (1973) and  Sprince et al. (1978) were per-
formed on workers  employed in beryllium extraction and  processing plants.   In
the  first study,  214  employees were examined.  They had been exposed for 1  to
14 years,  and exposure had started after recommended occupational  standards  had
been  set.  It  was  known, however,  that the  recommended standards of 2 and
25  ug/m^  for  8-hour and short-term exposures, respectively,  had been exceeded.
In  some  areas of the plants, peak exposures were above 1 mg/m  .  Lung function
tests  including FVC,   FEV-^ and gas exchange were performed.   Among the 31 sub-
jects with X-ray abnormalities  of  the  lung, 11 had  hypoxemia at rest, but these
subjects  were also heavy  smokers.   In this study,  there was no control group
and it is  difficult,  therefore,  to establish whether  smoking or  beryllium
caused the effects.  However,  lung biopsies were  performed in two  subjects,  and
 in  one of these cases a  diffuse granulomatous reaction, typical of beryllium
 exposure, was found.   The beryllium content  of the lung was elevated in both
 cases.   It is  noteworthy that  the case with the granulomatous reaction had a
 much lower beryllium concentration in the  lung than did the  case without tissue
 changes.
      A follow-up was  made three  years later on these workers (Sprince  et al.,
 1978).    Occupational  exposure  levels  had  been  reduced  due to engineering
 changes,   and peak  concentrations were now  less than 25 jjg/m .   For  some
                                       5-9

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 operations,  peak concentrations were less than 2 |jg/m3.   Workers who had parti-
 cipated in 1971 and  had not changed smoking  habits were studied  (Table  5-6).
 There were no major  differences between  the results from the two  examinations,
 but as  seen  in Table 5-7,  there  had  been some improvement of  hypoxemia as
 indicated by the results of the Pa02 determinations.   In the 13  persons  who had
 clearly demonstrated hypoxemia   02 in  1971,  there was a  highly  significant
 rise  in   02 by 1974 (average  rise of 19 mm Hg).  Among the 98 workers who had
 a normal   02 in 1971,  the average increase was 4.1 mm.   Of the  31 subjects who
 had X-ray abnormalities in .1971,  9 now showed normal X-ray  readings.   These
 findings  indicate that  some minor  effects  might be reversible  in beryllium-
 exposed workers  if exposure is reduced.  A new follow-up was conducted in 1977
 and reported  briefly  (Sprince  et al.,  1979).   The  improvement in Pa02  remained,
 and there was a tendency towards normalization of lung X-rays.   It is obvious,
 however,  that due  to  long  latency  times,  longer follow-ups  are necessary  before
 any final  conclusions can  be made  with  regard  to prognosis.
      In a recent British  study, Cotes  et al.  (1983) presented data on workers
 exposed to beryllium compounds, mainly  beryllium  oxide.   The plant in which
 these  workers had been employed started operation in 1952.   The first study of
 these  workers was made  in  1963 when 130 men  out  of a group of 146, who had
 worked  for more  than 6 months, were examined.   Chest X-rays were taken,  and in
 all but one case,  pulmonary function was  measured  by a set  of respiratory func-
 tion  tests.   Airborne beryllium had been measured during  the years  1952 to
 1960,  but it is  unclear whether any measurements had been made  since 1960.   In
 a  total  of 3401 samples taken, only 20 exceeded the 25 |jg/m3 limit  and 318
                    3
 exceeded  the  2 |jg/m  limit.  Concentrations were presented as geometric  means,
 and in both  1952  and 1960  these  concentrations were never  above 2 ug/m3.
                                                Q
 Generally, concentrations  were far below 1 pg/m .  The  1963 study found six
 cases of definite  or suspected  beryllium  disease.
     In a  follow-up in 1973, 106 of the original 130 workers were  examined.   In
 another  follow-up  in  1977, only 8 men from the 1973 group  and one  ex-employee
were examined, but to this  new  group were added 24 employees and 14 ex-employees
 employed  since 1963.   The same tests were  performed  on  these subjects.   The
 follow-up  studies  did not find any  new  cases  of beryllium disease.  However,
 after the  1977 study, two  further  cases  were  added.   Both were men who  had
worked  since  1952.   There were also two  cases of acute beryllium pneumonitis,
 and these  two men were  among  a group  of 17 who were  deemed to  have had the
 highest exposures.  Both of these cases were normal in the  1963 study.
                                     5-10

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       TABLE 5-6.  COMPARISON OF 1971 AND 1974 DATA OF WORKERS SURVEYED IN BERYLLIUM
                             EXTRACTION AND PROCESSING PLANTS3
Workers
Smokers
Ex-smokers
Nonsmokers

Total
Year
1971
1974
1971
1974
1971
1974
1971
1974
No.
55
55
36
36
20
20
111
111
Age
(years)
40.9
43.9
43.3
.46.3
43.4
46.4
42.1
45.1
Ciga-
rette-
Pack-
years
23
27
25
25
0
0
23.5
26.2
Length of
Employ-
ment
(years)
10.2
13.2
10.6
13.6
10.9
13.9
10.4
13.4
FEVj. (%
predicted)
92.9
90.4
97.9
97.7
105.3
102.4
96.7
95.1
FVC (%
predicted)
96.6
95.2
97.8
101.. 2
98.6
102.5
97.3
98.5
PEFR (%
predicted)
96.9.
91. 3b
100. 0_
94. 8C
104.7
99.2
99.3.
93. 8a
 FEVj = 1-sec forced expiratory volume; FVC = forced vital capacity; PEFR = peak
 expiratory flow rate.   Results are mean values.
bp <0.02
cp = 0.02
dp <0.01
Source:  Sprince et al.  (1978).
            TABLE 5-7.   COMPARISON OF 1971 AND 1974 ARTERIAL BLOOD GAS RESULTS
                                                                              .a
Workers
Smokers
Ex- smokers
Nonsmokers
Total
aPa~ = arterial Pn
U2 U
",, yn m
Year
1971
1974
1971
1974
1971
1974
1971
1974

No.
55
. 55
36
36
20
20
111
111
= arterial P»0
Pao
(mm Hg)
90.9.
96. lb
89.1.
95. 7b
93.4
100. 2C
90.8.
96. 8b
Results are mean
Paco2
(mm Hg)
38.0.
35. lb
37.9.
36. lb
38.0
36.3
38.0,
35. 7b
values.
pH
7.42
7.42
7.42
7.42
7.43.
7.41b
7.43
7.42C

 p
cp <0.05
Source:  Sprince et al. (1978).
                                         5-11

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      After  adjusting for age,  smoking,  and  other factors,  the respiratory
 function tests showed that exposure was related only to vital capacity.  In the
 1963 study, a significant negative correlation between estimated total exposure
 to beryllium and lung compliance was shown in a subgroup of 19 workers from the
 slip-casting bay.   Comparison between data  from  1963 and 1973 showed only
 changes that  could be ascribed to  personal  factors.   The conclusion  of the
 authors was that respiratory function studies generally could not detect beryl-
 lium disease before  radiographic  changes appeared.  Decreases  in  lung function
 were only  observed in cases with clear  X-ray changes.   However, Preuss and
 Oster (1980) have  noted  that changes in vital capacity may occur long before
 X-ray changes  appear.
      As mentioned  above,  chronic beryllium  disease differs  from some other
 occupational lung diseases in  that  it has  a  systemic  component.   The systemic
 involvement suggests  that  there  is  also an  immunological component  to  the
 disease,  and that hypersensitivity can explain some of the findings in chronic
 beryllium  disease.
      In 1951,  Curtis developed a patch test which was found to be positive for
 most cases of dermatitis and skin granuloma caused by beryllium.  In addition,
 it  was positive in many  cases of lung disease caused  by  beryllium  (Curtis,
 1959; Nishimura, 1966).   However,  the patch test could also initiate  the devel-
 opment  of  skin reactions or  pulmonary disease  in people exposed to beryllium,
 but  who had not had  previous  symptoms of respiratory illness (Sneddon, 1955;
 Stoeckle et  al., 1969; Rees,  1979; Cotes et al., 1983).
     These  early  studies  Ted to attempts to  develop other tests suitable for
 studying hypersensitivity to  beryllium.   Of these,  the lymphocyte transforma-
 tion  test  has been  the most  useful  (Deodhar  et  al.,  1973;  Williams and
 Williams,  1982a,b,  1983).   This test gave a  positive  response in 16  patients
with established chronic  beryllium disease, whereas it was negative  in 10 sub-
 jects with  suspected  disease.   Only two  positive  responses were reported among
117  healthy  beryllium workers (Williams and Williams, 1983).   Similar  results
 have also  been  reported by Van Ordstrand  (1984).   It is  not clear, however,  if
a positive  test  in  an otherwise healthy worker really  indicates that such  an
 individual  is at a higher risk Tor getting pulmonary disease.
     Rom et al.  (1983) conducted a three-year prospective study to evaluate the
relationship between  lymphocyte transformation and beryllium  exposure.  The
average beryllium exposure;levels  ranged  from 7.18 ug/m3 in 1979 to  less than
                                     5-12

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1 ng/m  from 1980  to  1982.   Of  11 workers  with  a  positive  test in  1979,  8  were
negative in 1982.  A possible reason for this change may have been the decrease
in exposure levels.
     In an area  in Czechoslovakia where coal with a high beryllium content is
burned, Bencko  et al. (1980) studied  immunoglobulins and autoantibodies  in
workers in a power plant and in  people  living  in the vicinity of the plant.
The  average  concentration  of  beryllium in  the town was  estimated to  be
80 ng/m3, which  is 8  times higher than the suggested standard for ambient air
in the United  States.   In both  the workers and general public,  levels of
immunoglobulins  IgG and  IgA and concentrations  of autoantibodies were elevated
compared to a  control group not exposed to beryllium.  The workers had higher
                                             o
exposure than the  town dwellers (up to 8 |jg/m ), and they also had cons-iderably
higher  levels  of  IgM than either the town  residents or the control  group.
Since  many factors can contribute to  increases  in  immunoglobulin  levels,  the
significance of  these findings  is not clear.
5.2.1.2  Animal  Studies.   There have been a large number of animal studies on
the  acute  and  chronic effects  of beryllium exposure by  air.   Much  of  the early
work  in  the  1940s and 1950s has  been  described by Vorwald et al. (1966).   A
large  number of the rat studies were performed by Vorwald and co-workers, but
many  were  never fully reported.  The  main information  source continues to be
the  1966 review  by Vorwald  et al.
      In one study, rats were exposed to beryllium sulfate aerosol  in concentra-
tions  ranging from 2.8 to  194 ug/m3 of air.  The exposures were usually given 7
hours  a day,  for  1 to 560  days.  It was stated that  exposure  to 2.8 ug/m  did
not  produce  any specific  inflammatory abnormalities, whereas  21 ug/m  caused
significant  inflammatory changes in some  long-surviving rats.  At 42 pg/m ,
chronic  pneumonitis  was  produced, while an  exposure  level of  194  ug/m  caused
acute beryllium disease.   While  the main  finding of this study was  that  the
 low-exposure  group had  a  high  incidence  of pulmonary  cancer (see Section
                                           O
7.1.8.3),  in  the  group exposed to  42  ug/m , microscopic examination of lung
tissue showed  alveolar changes with a large increase in the number of macro-
phages.   With  longer exposure, diffuse pneumonitis  and focal granulomatous
 lesions became  increasingly prominent,  typically  occurring  in  patches.
      Schepers  et al.  (1957) exposed rats  to beryllium  sulfate at an  average
                                       O
 concentration  of  beryllium  of  35 ug/m .   In one experiment,  115  animals were
 exposed for six months;  the number of controls was  139.   In  this study,  46
                                      5-13

-------
  animals  died during  exposure and  17 were  killed  at the end of  exposure.
  Fifty-two  rats  were then transferred to  normal  air and observed for up to 18
  additional  months.   The  cause of  death  during  exposure was mainly pleural
  pericarditis  with a tendency  to  chronic  pneumonitis.   No bacteria were iso-
  lated, but the  authors concluded that the response was caused by  infection,
  since  sulfathiazole had a beneficial  effect.  In further experiments, similar
  exposures  were  given,  but no  rats  died during exposure or up to nine months
  afterward.  Among the  findings after  six  months  of exposure were: adenomas;
  foam-cell  clusters; focal mural  infiltration; lobular  septa!-cell  prolifera-
 tions; peribronchial, alveolar-wall epithelialization, and granulomatosis.
      In a study by  Reeves et al. (1967), 150 rats (with an equal number of con-
 trols) were exposed to beryllium sulfate at a mean concentration of 34 ug/m3.
 Exposure was  for 72 weeks,  7 hours a  day,  5  days  a week.   Control of  the
 exposure concentrations was  poor (the standard deviation  of  the mean  level was
 24 ug/m ).   Every month,  three male and three  female  rats from the  exposed and
 control groups were killed.   Among  the findings  were progressive  increases  in
 lung weight in the  exposed  animals.  At the end  of the experiment, the  lung
 weights of exposed  animals  were,  on «an average, more than four times greater
 than those  of controls.  Histological  examination  showed inflammatory  and
 proliferative  changes.   Also,  clusters  of  macrophages in the alveolar spaces
 were a common finding.   Granulomatosis  and  fibrosis  were only occasionally
 seen.   The proliferative changes  ultimately  led to  the generation of tumors in
 all  of the  exposed animals (43/43) (see Section 7.1.1).
     Wagner et al. (1969) exposed two groups of 60  rats to the beryllium ores,
 beryl  and bertrandite,  for up to  17  months  at a concentration  of 15  mg/m3. This
 dose corresponded to 210 pg  Be/m3 as  bertrandite  and 620 ug Be/m3  as beryl.
 Exposure was generally for 6 hours  a  day,  5 days  a week.   A very large inci-
 dence  of  lung tumors was  reported among rats  exposed to  beryl  (see Section
 7.1.1).  Among the  nonmalignant  changes,  clusters of dust-laden macrophages
were seen.  Granulomas were seen  in  lungs from  bertrandite-exposed rats.
     Sanders et al.  (1975) exposed  rats to beryllium oxide particles calcined
at 1000°C.   Single exposures to beryllium  oxide were  given  through the nose
only.  Exposure time ranged from 30  to  180 minutes,  and concentrations of beryl-
 lium were  from 1 mg to 100 mg/m .   The  single  exposures resulted in chronic
changes characterized by the appearance of foamy  macrophages  and  some  granulo-
matous  lesions.   A  significant depression  of  alveolar  clearance was  also
observed.
                                     5-14

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     Other studies have  examined  the effects of beryllium exposure on monkeys
(Schepers, 1964; Vorwald  et  al.,  1966;  Wagner et al . ,  1969;  Conradi  et al . ,
1971),  dogs  (Robinson et  al . ,  1968; Conradi  et al.,  1971),  guinea  pigs
(Policard, 1950; Reeves et al . ,  1971, 1972) and hamsters (Wagner et al . , 1969).
     Vorwald et al. (1966) exposed  monkeys to intermittent daily  administra-
                                                              3
tions of  beryllium sulfate  (average concentration  of 35 ug/m ) for  several
months.    Some  monkeys were  given intratracheal instillations  of  beryllium
oxide.  Both routes of administration led  to typical  chronic  beryllium disease
with pneumonitis and granulomatosis.
     Schepers (1964)  exposed three  groups  of monkeys,  four  in  each group, to
aerosols  of beryllium fluoride,  beryllium  sulfate,  and beryllium phosphate in
                                3
concentrations of about 200 MQ/m  beryllium.  In another experiment, two groups
of monkeys,  four animals  in each, were given  higher  concentrations  of the
beryllium  phosphate,  containing about 1140  and 8380 jjg Be/m ,  respectively.
Exposure was  for 1  or 2 weeks in  the  animals  exposed to the  fluoride  and
sulfate, and  from  3  to 30 days in the groups exposed to the phosphate.  After
exposure ceased, the  animals were kept in normal air for different periods of
time.
     There were  signs of initial  general  toxicity,  in  the form  of anorexia, in
the exposed animals.   Dyspnea, one of the typical signs of human chronic beryl-
lium disease,  developed rapidly in the animals exposed to fluoride and to the
high beryllium phosphate  concentrations.   Mortality was 100 percent  in the
animals  exposed  to  the two highest beryllium phosphate concentrations.  Exami-
nation  of  lungs from animals who  either  died during the experiment  or  were
killed  showed pulmonary edema and congestion, mainly in the animals exposed to
beryllium  fluoride or to the highest concentration of beryllium phosphate.  Cor
pulmonale  was also  a common finding.  The histological picture was similar to
that seen  in  other animals and humans.  Notable were pigment-filled macrophages
and  invasion  of  plasma  cells in the alveoli.
     Wagner  et al .  (1969) exposed 2  groups  of 12 squirrel  monkeys  (Saimiri
sciurea)  for  23 months to  beryl  dust (620 ug Be/m )  and  bertrandite dust
(210 ug Be/m3).   Exposure was generally for six hours a day, five days a week.
While  exposure to both ores resulted  in  aggregates  of  dust-laden  macrophages,
lymphocytes,  and plasma cells  near respiratory bronchioles, no other marked
changes were  seen compared to the  controls.
                                      5-15

-------
      The effects  of  beryllium oxide calcined at 1400°C  were  studied by Conradi
 et al.  (1971).  Five  monkeys  received inhalation exposures with  concentrations
 varying between 3.3 and 4.4 mg Be/m3.  Exposure was for 30 minutes at 3 monthly
 intervals.   After two years follow-up,  histological  examinations  were  negative
 and no  other differences .were  noted between controls and exposed animals.
      Conradi et al.  (1971) studied six dogs exposed in the same way as  the mon-
 keys.   No pathological changes were observed.
      Robinson et al.  (1968) exposed two dogs for 20 minutes  to rocket  exhaust
 products  containing mixtures of beryllium oxide, beryllium fluoride, and beryl-
 lium chloride at  average  concentrations  of 115  mg beryllium/m3.   The dogs were
 observed  for a period of three years and were then  killed.   Immediately after
 exposure  the dogs had some acute symptoms, but  during  the rest  of the study
 they remained clinically healthy.   Histological  examination of the lungs showed
 small foci  of granulomatous inflammation scattered throughout the  lungs of both
 dogs.   Beryllium deposits were also  found in the lungs.  The average beryllium
 content of  the lungs  of  these  dogs  was 3.9 and 5.5 mg/kg wet  weight.
     Granulomatosis  has  also  been  shown  in  guinea pigs exposed to  beryllium
 oxide dust  (Policard, 1950; Chiappino  et al.,  1969).   In the guinea pig,  it
 is  possible to produce beryllium sensitivity, and this is thought to have some
 protective  effect  against the  development of pulmonary disease (Reeves  et al.,
 1971; Reeves et al.,  1972).   Barna et al. (1981) studied two  strains of guinea
 pigs given  intratracheal injections  of  10 mg of beryllium oxide.   All  of the
 animals in  one strain  developed granulomatous  lung disease, whereas  the  animals
 in  the  other  strain  did  not,  indicating genetic differences  in  beryllium
 sensitivity.  The  latter animals also showed  negative  skin tests and lymphocyte
 transformation tests,  whereas  positive reactions were seen in the group with
 the  lung  reactions.   Administration of the immunosuppressive drug prednisone
 had a beneficial effect on the animals with lung  disease.  However, this effect
 lasted  only as long as treatment continued.   Further studies by  Barna  et al.
 (1984a,b) have  confirmed these findings.  Barna  and  co-workers  observed that
beryllium exerted  a more  direct toxic  effect on alveolar macrophages in
nonsensitized animals.
     Wagner  et al.  (1969)  exposed two groups of hamsters,  48 animals in each
group, for 17 months to beryl  and bertrandite dust under the  same exposure con-
ditions previously described above  for rats  and  squirrel  monkeys.   After six
months  of'exposure,  the bertrandite-exposed  animals  had a few granulomatous
                                     5-16

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lesions in the lungs, and in both groups there were some atypical cell prolifer-
ations.
     It is  noteworthy that  rats,  in the various  studies  showing differing
degrees of  granulomatosis,  have not  developed beryllium  hypersensitivity
(Reeves, 1978).
     There have also  been  some  experimental  studies  of  chronic,  oral  beryllium
exposure.   In some  early studies (Guyatt et  al.,  1933;  Jacobson,  1933;  Kay  and
Skill, 1934), rickets  was  produced in young  animals  by giving  large  doses  of
beryllium carbonate  (0.1-0.5 percent;  1000-5000 mg/kg food).   This effect has
since been regarded as an indirect result of the binding of phosphate to beryl-
lium in the gut and, consequently, phosphorus depletion in the body.
     Schroeder and Mitchener (1975a,b) gave rats and mice beryllium in drinking
water  at  a concentration  of 5 mg/1  for lifetime duration.  No  consistent
differences were  noticed between exposed animals  and controls  with regard  to
weight or  life  span.   In a two-year  feeding study,  Morgareidge et al.  (1977,
abstract)  fed rats dietary concentrations of 5,  50, and 500 mg  Be/kg.   The
highest dose  level  resulted in  a slight decrease  in weight.  Specific details
about  the results were not reported.
     A large  number  of  studies have  been conducted on beryllium compounds
injected  into animals.   Some of these are mentioned in Section 7.1 on experi-
mental  carcinogenicity.   Some  of  these studies have also  been  presented in
earlier documents  on beryllium, especially with regard to the effect of beryl-
lium  on  enzymes (Drury et al.,  1978).   However,  these  injection studies are
less  relevant than  inhalation or ingestion studies for  understanding  the  action
of  beryllium  in humans.

5.2.2  Teratogenic  and Reproductive  Effects  of  Beryllium
5.2.2.1   Human  Studies.  There  are  no  known  studies  on  the  possible teratogenic
and reproductive  effects of  beryllium  in humans.
5.2.2.2   Animal Studies.   Very  few  studies have investigated  the  teratogenic or
reproductive  effects of beryllium  in  animals.  Only three  such  studies  exist:
one that evaluates the  behavior of the offspring of mice  exposed to  beryllium
 sulfate during pregnancy (Tsujii and  Hoshishima,  1979),  one that deals  with
 the ability of beryllium  chloride  to penetrate the placenta (Bencko et al.,
 1979), and another concerned with  the effects of  beryllium chloride on develop-
 ing chick embryos (Puzanova et al.,  1978).
                                      5-17

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      Hoshishima et al.  (1978)  presented a brief abstract and,  later,  a more
 extensive report (Tsujii and Hoshishima,  1979) on the effects of trace  amounts
 of beryllium  injected into pregnant CFW  strain  mice.   Six  female mice were
 exposed to 22 compounds  of metals,  including BeS04 (140  ng/mouse/day).   The
 mice  received intraperitoneal  injections  (0.1  ml)  11 times during pregnancy.
 The  injections were given  once daily for  three consecutive days and then every
 other day for an additional  eight treatments.  The  gestational  days of treat-
 ment  were not reported.   In this  study,  beryllium (140 ng/day  or ~5 ug/kg/b.w.)
 produced the following differences  in  the offspring of  the metal-exposed dams
 as compared to the offspring from a control group:  delayed response  in head
 turning in a geotaxis test,  acceleration  in a straight-walking test,  delayed
 (for  a moment) bar-holding  response, and  acceleration  of bar holding (for 60
 seconds).
      In a study by Bencko et al.  (1979), the soluble salt of beryllium, BeCl2,
 was evaluated for its ability  to  penetrate the placenta and reach the fetus.
 Radio!abelled  BeCl2  was injected into  the caudal  vein  of seven to nine  ICR
 SPF mice and  was  administered in three different  time  periods: (1) before
 copulation  (group A), (2)  the  7th day  of  gestation (group  B),  and (3) the
 14th  day of gestation (group C).  The  animals  were sacrificed on  the  18th to
 19th  day of  pregnancy and the radioactivity associated with  the  fetal and
 maternal  compartments  was  evaluated.   In  group  C,  higher levels  of radio-
 activity  were associated with the fetuses  than were  associated with fetuses of
 other  exposure periods (group A,  0.0002 ug 7Be/g fetus; group  B,  0.0002 ug
 Be/g  fetus;  and  group C, 0.0013  ug  7Be/g fetus).  The  amount  of radioactivity
 in the various organs  of the fetus  was  generally not  influenced by beryllium
 exposure  except in  the spleen and liver.   The  amount  of  Be penetrating the
 spleen  was  decreased,  while in  the liver it was increased when 7BeCl was given
 on the 14th day of pregnancy.
     Puzanova  et  al.  (1978)! conducted studies on the effects  of beryllium on
the development of  chick embryos.   BeCl2  (300 to 0.00003 ug dissolved in 3 ul
twice-distilled water) was  injected subgerminally  into chick  embryos  (10
embryos per  dose) on the second day  of  embryogenesis.  After a 24-hour incuba-
tion,  the eggs were opened and stained with 0.1 percent neutral red so that the
distance between the origin of the vitelline arteries and the caudal tip of the
body could be measured.  In a second part of this experiment,  the same doses of
                                     5-18

-------
BeC"U  were admin-istered  subgerminaVly to  two-day-old embryos  and intra-
amniotically to three-  and four-day-old embryos.  The  surviving embryos  were
examined after the 6th day of incubation.
     In the first part of the experiment, it was found that 300 ug BeCl2 killed
all  of the embryos,  whereas 0.3 ug  was not lethal  to any.   Doses of 0.003 ug
and  less had no observable effects on the development of the embryos.  When the
eggs were  treated on day two, the most common malformation was  caudal regres-
sion,  open abdominal cavity,  and  ectopia cordis.  When administered  on  the
fourth day,  exencephalia,  mandibular malformation,  and malformations described
as  the "straitjacket syndrome" were reported.   It  is not known,  however,  if
these  types  of teratogenic effects  in  chick embryos  are reflective  of effects
that might occur in humans.   Additional  studies would have to  be done using
mammals to determine whether  beryllium  has  teratogenic  potential.
     Considered collectively, current  data are  not  sufficient to  determine
whether beryllium compounds have the potential to produce adverse reproductive
 or teratogenic effects.  It  should  be  noted that the  studies discussed above
 were not  designed to specifically  investigate  the effects  of beryllium compounds
 on reproduction or  the developing conceptus.  Further  studies in  this area are
 desirable.
                                       5-19

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-------
                      6.   MUTAGENIC EFFECTS OF BERYLLIUM
     Beryllium has been  tested  for  its  ability  to  cause genetic  damage  in  both
prokaryotic and  eukaryotic organisms.  The prokaryotic studies  include gene
mutations  and  DMA damage  in  bacteria.   The eukaryotic studies  include DNA
damage and gene mutations in yeast and cultured mammalian cells,  and studies of
chromosomal aberrations  and  sister-chromatid  exchanges in mammalian cells  |n
vitro.  The available  literature indicates that beryllium has  the potential  to
cause gene mutations, chromosomal aberrations, and sister-chromatid exchange in
cultured mammalian somatic cells.
6.1  GENE MUTATIONS IN BACTERIA AND YEAST
     The  studies  on beryllium-induced gene mutations in bacteria and yeast are
summarized  in Table 6-1.

6.1.1   Salmonella Assay
     Beryllium  has been tested for  its  ability to cause reverse mutations in
Salmonella  typhimurium  (Simmon, 1979a; Rosenkranz  and  Poirier,  1979).
     Simmon (1979a) found  that beryllium sulfate was not mutagenic  in  Salmonella
strains TA1535,  TA1536, TA1537,  TA98,  and TA100.   Agar-incorporation  assay,
with and without  S-9 metabolic activation, was employed.   The  highest concen-
tration of  beryllium  sulfate tested was  250 pg/plate  (12.5  M9 Be).   No mutagenic
 response was obtained in any of the above strains.
      Beryllium sulfate  was also not mutagenic in Salmonella typhimurium strains
 TA1535 and  TA1538,  both  in  the  presence and absence of the S-9  activation
 system (Rosenkranz and Poirier,  1979).   The two  concentrations of the test
 compound used were 25 ijg/plate-and 250 jjg/plate.   No significant differences in
 the mutation frequencies  between the experimental and the control  plates  were
 noted.
                                       6-1

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6.1.2  Host-Mediated Assay
     Negative mutagenic  response of  beryllium  sulfate was  obtained  in the
host-mediated assay  (Simmon  et al.,  1979).   Several procedures were used.   In
all procedures the  tester strain was  injected intraperitoneally and the beryl-
lium sulfate was given orally or by intramuscular injection.   Four hours later,
the Salmonella or Saccharomyces tester strain was recovered from the peritoneal
cavity and  plated  to determine the number of mutants (Salmonella) or recombi-
nants (Saccharomyces) and the number of recovered microorganisms.  Simultaneous
experiments were conducted with control (untreated) mice.   Using 25 mg/kg given
intramuscularly, beryllium sulfate was not  mutagenic with tester strain TA1530
or TA1538.   Using  1200 mg/kg given orally,  beryllium sulfate was not  mutagenic
in TA1535  and did  not significantly  increase the  recombination frequency in
S. cerevisiae D3.

6.1.3  Escherichia coli WP2 Assay
     A  negative  mutagenic response  in the  Escherichia coli  WP2 system was
obtained  with beryllium  concentrations  ranging from  0.1 to  10 umol/plate
(10.5-105 ug  Be/plate)  (Ishizawa, 1979).   These results should not be taken as
proof,  however,  that beryllium is not mutagenic.   The standard test system may
be  insensitive  for the detection of  metal mutagens because of the large amount
of  magnesium salts,  citrate, and phosphate  in  the rtiinimal medium  (McCann et
al.,  1975).   Bacteria appear to  be selective in  which metal  ions  are  inter-
nalized.   More research  is  needed to select a suitable  strain of bacteria
to  detect metal-induced mutagenesis in these prokaryotic  systems.
 6.2   GENE  MUTATIONS  IN  CULTURED MAMMALIAN  CELLS
      The  ability of  various beryllium compounds to  cause  gene mutations in
 cultured  mammalian cells  has  been investigated by Miyaki  et  al.  (1979) and
 Hsie et al.  (1979a,b)  (Table 6-2).
      Miyaki  et al.  (1979) demonstrated the induction of 8-azaguanine-resistant
 mutants by  beryllium  chloride in the Chinese  hamster  V79  cells.   Beryllium
 chloride  at concentrations  of 2  and 3 mM (18 and 27 pg Be/ml,  respectively)
 induced 35.01 ± 1.4 and 36.5 ± 1.7  mutant colonies  per 10  survivors.  These
 values were approximately six times higher than the  control value of 5.8 ±0.8
 colonies  per 106 survivors.  The  cell  survival  rates  were 56.9 percent at 2  mM
                                       6-3

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concentration and 39.4  percent at 3 mM.  Analysis of mutant colonies revealed
that  they  were deficient  in the enzyme hypoxanthine guanine  phosphoribosyl
transferase (HGPRT)  activity indicating that the mutation had occurred at the
HGPRT locus.
     Hsie  et  al.  (1979a,b)  also reported that beryllium sulfate  induced  8-
azaguanine-resistant mutants  in  Chinese hamster ovary (CHO) cells.,  However,
they  did not  provide details about the concentrations  of the test compound and
the number of mutants induced per 10  survivors.
     These  studies  indicate  that  beryflium has  the  ability  to  cause  gene
mutations  in cultured mammalian  cells.
6.3  CHROMOSOMAL ABERRATIONS
     Beryllium  sulfate was tested for  its  clastogenic potential  in cultured
human  lymphocytes  and Syrian hamster embryo  cells  (Larramendy et al., 1981)
(Table 6-3).   Cultured human  lymphocytes  (24-hours old)  were exposed to a
single concentration,  2.82 x 10~5M (0.25 ug Be/ml), of beryllium sulfate, and
chromosome  preparations were made 48 hours after the  treatment.  A minimum of
200  metaphases  were scored for chromosomal aberrations.   In cultures treated
with beryllium, there  were 19  cells  (9.5 percent) with chromosomal, aberrations,
or  0.10  ±0.02 aberration  per metaphase.   In the  nontreated control  cells,
only 3 cells (1.5 percent) had chromosomal aberrations.   This sixfold increase
in  the  aberration frequency  clearly  indicates  that  beryllium sulfate  is
clastogenic in  cultured human lymphocytes.   A  beryllium  concentration  of
2.82 x 10~5M was  selected because it  induced  a maximum  number  of sister-
chromatid exchanges in human lymphocytes in another experiment reported by the
same authors (see  Section 6.4).
      In  the Syrian hamster embryo cells  the  results were even more dramatic.
This same concentration  of beryllium  sulfate induced  aberrations  in  38 out  of
200  cells (19 percent) 24 hours after  the  treatment.   The  number  of aberrations
per  metaphase was  0.12 ± 0.03.   In  control  cells,  only 3 cells (1.5 percent)
 had  aberrations,  or  0.01 ± 0.01  aberration  per cell.   In  these  studies,
 chromosomal gaps were  also  considered  as  aberrations.  Even  if the gaps were
 not included as true  aberrations, the  aberration frequency was still far above
 the control level, indicating that  beryllium sulfate  has  clastogenic potential
 in cultured mammalian cells.
                                       6-5

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6.4  SISTER CHROMATID EXCHANGES
     Larramendy et al. (1981) also studied the potential of beryllium to induce
sister chromatid  exchanges  (Table 6-3).   Both cultured human  lymphocytes  and
Syrian hamster embryo cells were used in these studies.
     After 24 hours of cultivation, lymphocytes were exposed to increasing con-
centrations of  beryllium  sulfate (0.05, 0.125, and 0.25 (jg Be/ml) followed by
10 |jg BrdUrd/ml medium.  Cultures were incubated for an additional 48 hours and
chromosome preparations  were made and  stained for sister-chromatid exchange
analysis.  At  least  30 metaphases were  scored for each concentration of the
test compound.  The background sister-chromatid exchange level was 11.30 ± 0.60.
According  to  these  investigators,  there was  a dose-dependent increase  in
sister-chromatid  exchanges,  i.e.  17.75 ± 1.10, 18.15 ± 1.79,  and 20.70 ± 1.01,
respectively, for the above concentrations.
     In  the  Syrian  hamster embryo cells, the  same concentrations of beryllium
sulfate  induced 16.75 ± 1.52,  18.40 ± 1.49, and 20.50 ± 0.98  sister-chromatid
exchanges.  The background sister-chromatid exchange frequency was 1-1.55 ± 0.84.
The  sister-chromatid exchange assay has been  extensively  used in mutagenicity
testing  because of its sensitivity to many chemicals.
     The authors stated  that the results  of the sister-chromatid exchange
studies  in human lymphocytes and Syrian hamster  embryo cells demonstrated a
dose-response  relationship.   However,  in these studies, the  increase was  less
than  twofold  and fell within a  plateau  region.  Thus,  the dose-response rela-
tionship suggested  by the authors may be somewhat tenuous.  Further experimen-
tation to  confirm the study  results  are  advisable.
 6.5  OTHER TESTS OF GENOTOXIC POTENTIAL
 6.5.1  The Rec Assay
      Kanematsu et al.  (1980)  found that beryllium sulfate was weakly mutagenic
 in the rec  assay.   Bacillus  subtil is strains H17 (rec+)  and M75 (rec  )  were
 streaked onto agar  plates.   An aqueous solution (0.05 ml) of 0.01 M  (4.5 [jg
 Be/plate) beryllium sulfate  was  added to a filter paper disk (10-mm diameter)
 placed on the  plates  at the starting point  of  the  streak.   Plates were  first
 cold  incubated  (4°C)  for  24 hours  and then  incubated at 37°C  overnight.
 Inhibition  of  growth  due to DNA damage was measured in both the wild-type H17
 (rec+)  and the  sensitive-type (rec")  strains.  The  difference in growth
                                       6-7

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 inhibition between the  wild-type strain and the  sensitive  strain was 4 mm,
 which  was considered to  indicate  a weak mutagenic response.  Similar results
 were also obtained by Kada et al.  (1980).

 6.5.2   Pol Assay
     Beryllium  was tested for mutagenicity  in  the pol  assay using Escherichia
 coli  (Rosenkranz  and Poirier, 1979;  Rosenkranz and Leifer,  1980).  This assay
 is  based on  the fact  that cells deficient in  DNA repair mechanisms are more
 sensitive than  normal cells  to  the growth-inhibiting properties of mutagenic
 agents.   Escherichia  coli strains pol A   (normal) and pol  A~ (DNA polymerase
 I-deficient)  were grown  on agar  plates,  and  filter  disks   impregnated with
 250 ug  of beryllium sulfate were  placed  in  the middle of each agar plate and
 incubated at  37°C for 7  to  12 hours.   Experiments were conducted both in the
 presence  and  absence  of an  S-9  activation system.  There was no difference in
 the diameter  of the zones of growth in  either strain.  Positive and negative
 controls were used for comparison.   The shortcomings  of this assay are that (1)
 conclusions can be drawn  only when measurable zones of growth inhibition occur;
 (2) it  is possible that  the  test  chemical  may not be  able  to  penetrate  the
 test organisms; and (3) insufficient diffusion of chemicals from the disk can
 occur because of low solubility  or large molecular size.

 6.5.3  Hepatocyte  Primary  Culture/DNA Repair Test
     DNA  damage and repair, as  reflected by unscheduled DNA synthesis (incor-
 poration  of  tritiated  thymidine),  was  examined for  beryllium  sulfate  by
Williams  et al.  (1982).   Rat primary hepatocyte cultures were exposed to 0.1,
 1, and  10 mg/ml  of beryllium sulfate with 10 p;Ci/ml of tritiated thymidine and
 incubated  for 18  to 20 hours.   Following incubation,  autoradiographs of cells
were prepared.  A  minimum of 20 nuclei was counted for each concentration and
the uptake of  radioactive label was measured as grain counts in each nucleus.
The compound  was   considered  positive when  the  nuclear grain count was five
grains  per nucleus above  the control value.   The compound was  considered
negative  in the assay if the  nuclear grain  count was less  than  five  at  the
highest nontoxic dose.   Cytotoxicity was determined  by the  morphology of the
cells.   According  to  the authors,  beryllium  sulfate did not  induce a  statisti-
cally greater grain count at any  of the  concentrations.   Benzo(a)pyrene  was
employed as a positive compound.
                                      6-8

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6.5.4  Beryl!iurn-Induced DNA Cell Binding
     Kubinski et al.  (1981)  reported that beryllium  induces  DNA  protein  com-
plexes (adducts) that  can  be measured.   Escherichia  coli  cells  and Ehrlich
ascitis cells  were exposed  to  radioactive  DNA in the presence of 30 uM  of
beryllium.  Methyl  methanesulfonate  (MMS) was  used as a  positive  control.   The
negative control consisted of cells  only and radioactive DNA.  The radioactive
DNA  bound  to cell  membrane  proteins  was measured, and,   like MMS,  beryllium
induced positive results.  However,  the significance of beryllium-induced DNA
binding to  cell membranes is not clear  in  terms  of its ability  to  induce
mutations.

6.5.5  Mitotic Recombination In Yeast
     Beryllium  sulfate did  not  induce  mitotic recombination  in   the  yeast
Saccharomyces cerevisiae D3  (Simmon, 1979b).   The S. cerevisiae  strain DS is a
heterozygote with mutations  in ade 2 and his 8 of chromosome XV.   When grown on
a medium  containing adenine, cells  homozygous  for  the ade 2 mutation produce a
red  pigment.   These homozygous mutants  can  be  generated  from the  heterozygotes
by mitotic  recombination  induced by mutagenic compounds.  A single concentra-
                                                                  c
tion  (0.5 percent)  of  beryllium induced 10 mutant .colonies per 10  survivors,
                                                                  5
while  in  the control  the mutant frequency  was 6  colonies  per 10 .   In the
mitotic recombination  assay, there  must be a threefold increase in the mutant
frequency of experimental over the control in order to be considered a positive
mutagenic response.  The negative mutagenic response of beryllium may be due to
an inability of beryllium to penetrate yeast cells.

6.5.6  Biochemical  Evidence  of Genotoxicity
     Several  iji  vitro  experiments of the genotoxic potential  of beryllium have
been reported.  In  one study, jm vitro exposure of rat liver cells to beryllium
resulted  in its binding  to  phosphorylated non-histone  proteins  (Parker  and
Stevens,  1979).   Perry et al. (1982) found  that exposure of cultured rat  hepa-
tosomal  cells to beryllium  reduced  the  glucocorticoid  induction  of tyrosine
transaminase  activity.   In  a DNA fidelity assay,  beryllium increased the mis-
incorporation  of  nucleotide  bases in the daughter strand of DNA  synthesized
TJQ vitro  from polynucleotide templates  (Zakour et-al.,  1981).   Beryllium has
also been investigated for its effects on the  transcription of calf thymus DNA
and  phage T» DNA by RNA polymerase (from E.  coli)  under controlled conditions.
                                      6-9

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Beryllium  inhibited overall  transcription but  increased RNA chain initiation,
indicating  the interaction of the metal with the DMA template (Niyogi et a!.,
1981).

6.5.7  Mutagenicity Studies in Whole Animals
     Information  on the mutagenicity of beryllium  compounds  in  whole animal
organisms,  such  as Drosophila and mammals,  is not available in the literature.
Such studies would be highly valuable for assessing the jin vivo effects of beryl-
lium compounds,  in particular to learn  whether or not they induce mutations  in
germ cells.  Metals  such as  cadmium  and methyl  mercury have been  implicated  in
the induction of aneuploidy (numerical chromosomal aberrations) in female rodent
germ cells.  Aneuploidy is generally induced as a result of malfunctioning of
the spindle apparatus.   Such  studies  with beryllium  compounds would yield
valuable information.
                                    6-10

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                     7.   CARCINOGENIC EFFECTS OF BERYLLIUM
     The purpose of  this  section is to evaluate the carcinogenic potential of
beryllium, and oh the assumption that beryllium is a human carcinogen, to esti-
mate its potency relative to  other  known  carcinogens,  as  well  as  its  impact  on
human health.
     The estimation of the carcinogenic potential of beryllium relies on animal
bioassays and epidemiological  studies.   However, studies on the mutagenicity,
DNA interaction, and metabolism of  beryllium are also  important for  the quali-
tative and quantitative assessment  of its carcinogenicity.   Because  the latter
are specifically dealt with elsewhere in this document, this section focuses on
animal and epidemiological studies as well as the dose-response (i.e., quantita-
tive) aspects of beryllium carcinogenicity.   Summary and conclusions sections
highlight the most significant aspects of beryllium carcinogenicity.
7.1  ANIMAL STUDIES
     Numerous animal  studies  have been performed to determine  whether or not
beryllium  and beryllium-containing substances  are carcinogenic.   In  these
studies,  metallic beryllium,  salts  of beryllium,  and beryllium-containing
alloys and  ores  were administered by various routes.   In the discussions that
follow, the studies are grouped according to the route of administration.
7.1.1  Inhalation Studies
     The  first  report of  pulmonary tumors  after  exposure to  beryllium  by
inhalation  was  made by  Vorwald (1953).   Four  of  8 female rats exposed  to
beryllium sulfate  (BeS04)  aerosol  (at 33 |jg Be/m3, 7 hrs/d, 5.5 d/wk) for one
year  developed  primary  pulmonary  adenocarcinomas.   The rate was 80  percent
(4/5)  for animals  necropsied after 420 days of exposure.  This study was pre-
sented in a paper read  before  a meeting  of the American Cancer Society, but
was  never published; an abstract  of  the  presentation was printed  two  years
later  (Vorwald et al., 1955).
                                      7-1

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      Schepers  et al. (1957)  updated  the  Vorwald  study  to  include  115  rats, 78
 of which survived to planned necropsy.   Tumors were  counted  after the animals-
 had been expo'sed for 6  months to beryllium sulfate aerosol followed by up to
 18 months  in normal  air.  The total number of tumors (76) -- not the number of
 tumor-bearing  animals  — was  counted.  Eight  histologic variants  of neoplasms
 were observed.   Intrathoracic nietastases were also noted,  and  transplantation
 was successful  in several  cases.   No  lung'tumors  were reported  among controls.
      During  the late 1950s and early  1960s, both  Schepers  and Vorwald  continued
 their experiments.   Unfortunately, because these studies were never published,
 details  are  often lacking, although some  of the results have been  alluded to in
 subsequent  reviews  (Schepers, 1961; Vorwald et al., 1966).  It can be surmised
 that Schepers  observed 35 to  60  tumors in 170 rats (21 to  35 percent)  exposed
 to beryllium phosphate at  a concentration of 32 to 35 ug Be/m3, and 7  tumors in
 40 animals  (17.5 percent)  at  227 ug Be/m3.   After  exposure to  beryllium
 fluoride, he obtained a  tumor rate of 10  to 20 in 200 animals (5 to 10  percent)
                     o
 exposed  to  9 ug Be/m .   With zinc beryllium manganese silicate (ZnBeMnSiOg),  a
 fluorescent  phosphor in  use  at that  time,  the tumor rate was 4 to 20  in 220
 animals  (2  to  9 percent) exposed to  0.85 to  1.25 mg Be/m3 (Table 7-1).   No
 tumors were  observed in  similarly exposed rabbits or guinea pigs.
      In  all  but one of  his  inhalation experiments, Vorwald  exposed  rats  to
 beryllium sulfate aerosol at  concentrations ranging from 2.8 to 180 ug  Be/m  at
 exposure schedules of 3  to 24 months.  In one experiment, beryllium oxide was
               o
 used at  9  mg/m  (temperature of firing not given).   Pulmonary lesions  believed
 to be adenocarcinomas  were found  in all  groups at frequencies ranging  from 20
 to 100 percent.  Weak correlations were  observed between tumor rate and expo-
 sure concentrations, and between tumor rate and  exposure  length (Table 7-1).
 No metastases were observed,  and  serial homotransplants were unsuccessful.
      Reeves  et  al.  (1967) exposed 150 Sprague  Dawley rats  of  both  sexes and an
 equal number of controls to  beryllium sulfate aerosol,  with  a mean particle
 diameter of  0.2 u,  at a mean  concentration of 34.25  ± 23.66 ug Be/m3'for 35
 hours a week.   Sacrifices were conducted  quarterly.   The first lung tumors were
 seen  at  9  months,  and by  13;months  all  43 animals necropsied  had pulmonary
 adenocarcinomas.  Similar results were reported by Reeves and Deitch (1969) two
years later  for another  animal group.   In the  latter study, 225 female Charles
 River  CD rats  of various  ages were  exposed (35  hrs/wk) to 35.66  ± 13.77  ug
     o
 Be/m with a mean particle size of 0.21 urn (Figure 7-1).  Five groups were
                                      7-2

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TABLE 7-1.   PULMONARY CARCINOMA FROM INHALATION EXPOSURE TO  BERYLLIUM
Atmospheric
concentration
Compound Species pg/m3 as Be
BeS04 Rats 33-35
33-35
32-35
55
180
18
18
18
. 18
1.8-2.0
1.8-2.0
1.8-2.0
21-42
2.8
34
36
36
36
36
36
Monkeys 35-200
38.8
Weekly
exposure
ti me
(hours)
33-38
33-38
44
33-38
33-38
33-38
33-38
33-38
33-38
33-38
33-38
33-38
33-38 ,
33-38
35
35
35
35
35
35
42
15
Duration
of
exposure
(months)
12-14
13-18
6-9
3-18
12
3-22
8-21
9-24
11-16
8-21
9-24
13-16
18
18
13
3
6
9
12
18
8
36+
Incidence
of
pulmonary
carcinoma
4 in 8
17 in 17
58 in 136
55 in 74
11 in 27
72 in 103
31 in 63
47 in 90
9 in 21
25 in 50
43 in 95
3 in 15
Almost all
13 in 21
43 in 43
19 in 22
.33 in 33
15 in 15
21 in 21
13 in 15
0 in 4
8 in 11
Reference
Vorwald (1953)
Vorwald et al . (1955)
Schepers et al. (1957)
Vorwald (1962)
Vorwald (1962)
Vorwald (1962)
Vorwald (1962)
Vorwald (1962)
Vorwald (1962)
Vorwald (1962)
Vorwald (1962)
Vorwald (1962)
Vorwald et al. (1966)
Vorwald et al. (1966)
Reeves et al. (1967)
Reeves and Dei ten
(1969)
Reeves and Deitch
(1969)
Reeves and Deitch
(1969)
Reeves and Deitch
(1969)
Reeves and Deitch
(1969)
Schepers (1964)
Vorwald (1968)
                                     (continued on the following page)
                               7-3

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                                    ' TABLE 7-1.   (continued)
Compound
BeS04
BeHP04
BeF2
ZnBeHnSi03
Beryl ore
Betrandite
ore
Weekly
Atmospheric exposure
concentration time
Species ug/m3 as Be (hours)
Guinea pigs

Rats
Monkeys
Rats
Monkeys
Rats
Rabbits
Guinea pigs
Rats
Hamsters
Monkeys
Rats
Hamsters
Monkeys
35
36 ;
3.7-30.4
-15
32-35
227
200
1100
8300
9
180
700
700
700
620
620
620
210
210
210
NR
35
35
35
NR
NR
42
42
42
NR
42
NR
NR
NR
30
30
30
30
30
30
Duration
of
exposure
(months)
12
12
18-24
18-24
1-12
1-12
8
8
8
6-15
8 •
9
24
22
17+ .
17+
17+
17+
17+
17+
Incidence
of
pulmonary
carcinoma
0
2 in 20
0 in 58
0 in 110
35-60 in
170a
7 in 40a
0 in 4
1 in 4
0 in 4
10-12 in
200
0 in 4
4-20 in
220a
0
. 0
18 in 19
0 in 48
0 in 12
0 in 30-60
0 in 48
0 in 12
Reference
Schepers (1961)
Schepers (1971)
Reeves et al. (1972)
Reeves (1976)
Schepers (1961)
Schepers (1961)
Schepers (1964)
Schepers (1964)
Schepers (1964)
Schepers (1961)
Schepers (1964)
Schepers (1961)
Schepers (1961)
Schepers (1961)
Wagner et al. (1969)
Wagner et al. (1969)
Wagner et al . (1969)
Wagner et al. (1969)
Wagner et al . (1969)
Wagner et al. (1969)
 Number of tumors per number of animals exposed.
 NR:   Not reported.
Source:  Adapted from Reeves (1978).
                                           7-4

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 exposed for 800 hours, two groups  for  1600  hours, and one group for 2400 hours.
 It was found that  tumor  yield depended not on length of exposure  but  on age at
 exposure.   Rats exposed  at an early age for  only 3  months had essentially  the
 same tumor frequency  (19/22;  86 percent) as rats exposed for the  full 18 months
 (13/15;  86 percent),  whereas  rats  receiving the 3-month exposure  later  in  life
 had substantially  reduced tumor  counts  (3-10/20-25;   15  to 40  percent).
 Generally,  an incubation time  of  at least  9 months  after commencement of expo-
 sure was required  to produce  actual  tumors.   Epithelial hyperplasia of the
 alveolar  surfaces  commenced after  about  1  month, progressed  to metaplasia by 5
 to 6 months, and to  anaplasia by 7 to 8 months.  In guinea pigs, 18 months of
 exposure  (35 hrs/wk)  to three  different concentrations of beryllium sulfate  (3.7
 ±  1.5  ug Be/m3, 16.6  ± 8.7 ug Be/m3, and 30.4  ± 10.7 |jg Be/m3) produced only
 alveolar  hyperp1 asia/metaplasia (associated with diffuse interstitial  pneumoni-
 tis)  in 23  of  144  animals.   No tumors were seen.   The  rate of hyperplasia/
 metaplasia  in unexposed controls was  3/55 (Reeves et  a!., 1971, 1972;  Reeves and
 Krivanek, 1974).  Schepers (1971)  reported  the occurrence of  lung  tumors in  2 of
 20  guinea pigs  exposed to beryllium sulfate (at 36 ug Be/m3,  35 hrs/wk)  for one
year. : While these  results are suggestive of a positive effect when compared to
 the  very  low background  incidence  of tumors in  guinea pigs,  very  little detail
was given in the report to reach definitive  conclusions.
     Sanders  et al. (1978) exposed female  Wistar  rats  to aerosols of medium-
 fired (1000°C)  beryllium  oxide, with a mass median  diameter of 1.1 ± 0.17  urn.
A  single  nose-only  exposure of 30  to  180 minutes duration was used.   Exposure
concentrations  were not  reported,  but  initial alveolar  deposition of beryllium
for  three exposure groups  averaged 0.9 ± 0.3 ug, 16.0  ± 15.0 ug  and  57.0  ±
17.0 ug.  The animals were held from 625 to 661 days.  Of the animals  surviving
to termination,  no  tumors were seen in 50 controls,  30  low-dose, or 43 medium-
dose rats.  One of  29  rats in  the high-dose group developed an adenocarcinoma.
     Wagner et al.   (1969) exposed Charles River CD rats, Golden Syrian hamsters,
and squirrel  monkeys  (Saimiri  sciurea)  to aerosols  of beryl  ore  and bertrandite
ore at what was then regarded  as  the "nuisance limit" for all dusts (15  mg/m ).
At this particle concentration, the beryllium content of the aerosols was  620
                2
and 210 ug  Be/m  for  beryl and bertrandite,  respectively.  The  geometric mean
diameter for  bertrandite  was  0.27 |j (a 2.4) and  for  beryl  was 0.64 u  (a 2.5).
Exposure was  for 6 hours/day,  5  days/week,  for  17 months.   Of the 19  rats
exposed-,to  beryl dust, 18 had  bronchiolar  or  alveolar cell tumors,  7  of which
                                       7-6

-------
were  judged to  be adenomas,  9 adenocarcinomas,  and  2 epidermoid  tumors.
Metastases were  not observed,  and transplants were not attempted.  No indispu-
table tumors were  found in either hamsters or squirrel  monkeys exposed to beryl
dust, although  atypical  proliferations were seen in the hamsters which,  accord-
ing  to  the authors, "could be considered  alveolar cell tumors except for their
size."   There  were no  indisputable  tumors in any  of  the  animals exposed to
bertrandite dust.   However,  granulomatous lesions were seen in each species  and
"atypical' proliferations"  of the cells lining the respiratory bronchioles and
alveoli were seen  in the rats and hamsters.
     Schepers  (1964)  found that among  20  female  rhesus monkeys  (Macaca mulata)
exposed  for eight  months,  6 hours/day, by  inhalation to  beryllium  sulfate
(BeSOJ,  beryllium phosphate (BeHP04), or beryllium fluoride (BeF2) (concentra-
tions  ranging  from 0.035 to 8.3 mg Be/m ; particle size not reported), only one
animal  had a small (3  mm)  pulmonary neoplasm which appeared to be an alveolar
carcinoma.   The animal  was exposed to beryllium phosphate at a concentration of
1.1  mg Be/m3.   The tumor  was  discovered  on day  82  of  exposure; however, its
association  with the beryllium  exposure was  judged uncertain.  Unfortunately,
the  eight-month exposure period  used  in  the  study was  probably  insufficient to
induce  lung cancer in any  of the monkeys.
      Vorwald  (1968) reported  the outcome  of a  chamber  study  using  rhesus
monkeys,  about 18  months  of age,  exposed to beryllium sulfate  (particle size
not  reported)  at a mean atmospheric  concentration of 38.8  (jg Be/m .   The  animals
were exposed for  6 hours/day,  5 days/week initially,  but  exposures were  inter-
mittent with fewer exposures as the  animals aged.  The average exposure  time for
the  duration of the experiment was  15 hours/week.   The animals  were  held for a
 lifetime.  Four animals,  two  males  and two females, died within  six months  of
 the  start of  exposure.  Three additional  females died after  approximately  one
 to  four  years.   None  of  these  seven  animals developed  lung tumors.   The
 remaining 9 animals survived  approximately 6 to  10 years.   Three of the four
 surviving females and all  five of the males developed pulmonary tumors.
      The pathology varied  among animals.   In some monkeys,  the  tumor  was in the
 nature of  a gross mass, predominantly situated in either the hilar area, or in
 the more peripheral  portions  of  the  lung.   In  other  cases,  small  and large
 tumors were scattered  irregularly throughout the pulmonary region.   The histo-
 pathology was  generally very  anaplastic,  but various  adenomatous patterns often
 predominated  among areas  with epidermal   characteristics.   Extensive metastases
                                        7-7

-------
 to the mediastinal lymph nodes were seen, and in some animals there were metas-
 tases to the bone, liver,  and adrenals.   No control animals were kept in this
 experiment.
      Dutra et al. (1951) exposed 5, 6, and 8 rabbits to beryllium oxide aerosol
 (degree of firing unidentified)  at  1,  6,  and  30  mg  Be/m3  (mean particle diameter
 0.235 u),  respectively,  on a 25-hour-per-week schedule for 9 to 13 months.   One
                                          o
 rabbit in the group exposed  to  6 mg Be/m  developed osteosarcoma of the pubic
 bone,  with extension into  the contiguous musculature.   Scattered tumors which
 were  judged to be metastases  of  the osteogenic sarcoma were seen in the lungs
 and spleen.   The  lungs also exhibited  extensive  emphysema,  interstitial fibrosis,
 and  lymphocytic  infiltration.   Rabbits  in the  other groups  remained  free  of
 malignancies.

 7.1.2   Intratracheal Injection Studies
      Intratracheal administration of beryllium  compounds was used as a substi-
 tute  for inhalation in experiments  by Vorwald (1950, 1953,  1968), Van Cleave and
 Kaylor  (1955),  Spencer et al. (1965),  Kuznetsov et al.  (1974),  Ishinishi  et al.
 (1980),  and Groth et al. (1980).   The  fate  and effects  of beryllium compounds
 deposited  by intratracheal  injection are not necessarily the same as those for
 identical  compounds deposited by inhalation.   Intratracheal injection produces
 an unnatural  deposition  pattern  in the lungs and  permits the entry of larger
 particles  that  normally  would be filtered out  in  the  upper respiratory  tract.
 Dusts,  therefore, frequently  show  longer pulmonary half-times  after intra-
 tracheal injection than after inhalation.
     Vorwald  (1953) found  one lung tumor among  eight  female rats after  intra-
 tracheal injection of  338 pg beryllium (as beryllium oxide)  and one "sarcoma"
 among  eight male rats  (site  unidentified) after  intratracheal  injection of
 33.8 ug beryllium as  sulfate  (Table 7-2).  The  induction of  lung cancer with
 intrathoracic metastases  in rhesus monkeys following intrabronchial  injection
and/or  bronchomural implantation  of "pure" beryllium oxide (firing temperature
 unknown) has  been mentioned in a review,  but without reference to any original
publication (Vorwald et al., 1966).
     Groth et al.  (1980)  intratrachealTy  injected rats with dusts of beryllium
metal,  passivated beryllium metal  (with  <1 percent chromium),  and various
beryllium alloys, as well  as  beryllium hydroxide.   Lung  tumors  were observed
after injection of beryllium metal,  passivated beryllium metal,  and a
                                       7-8

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 beryllium-aluminum alloy  (containing 62  percent  beryllium),  but  not  after
 injection of other beryllium  alloys in which the beryllium concentration was
 less than  four percent.   The injection of  beryllium hydroxide into 25 rats
 yielded 13 cases  of  neoplasia,  of which  six were judged  to  be adenomas and
 seven adenocarcinomas (Table  7-3).   The  remaining animals had various  degrees
 of metaplasia,  which were  regarded  as precancerous  lesions.   Several  of the
 tumors  were successfully  transplanted.
      The most detailed studies  of intratracheal  injections of beryllium were
 reported by Spencer et al.  (1965, 1968,  1972).   High-fired (1600°C), medium-
 fired (1100°C),  and  low-fired  (500°C) specimens of beryllium oxide  were injected
 into rats.   The rates of  pulmonary  adenocarcinomas were 3/28,  3/19,  and 23/45
 (11,  16, and 51 percent)  in the three groups, respectively.    None were seen
 in controls.
      Ishinishi  et al.  (1980)  intratracheally injected 30 male Wistar rats  with
 beryllium  oxide (calcined at  900°C)  in  15 weekly doses of 1 mg each.   Of 29
 animals  examined 1.5 years  later, six  (21 percent)  had lung  tumors,  i.e.  one
 squamous cell  carcinoma,  one adenocarcinoma, three adenomas,  and one malignant
 lymphoma.   The  adenomas  had "strong  histological  architectures [of]  suspected
 malignancy" (Tables 7-4 and  7-5).  The malignant lymphoma was found not  only in
 the  lung,  but also in the hilar lymph nodes and in the abdominal cavity, with
 the  primary site remaining  undetermined.  Six extrapulmonary  lymphosarcomas,
 fibrosarcomas,  or  other  tumors were  found in  further injected animals  but  in
 only  one of the 16 control animals.   The frequency of clearly malignant  primary
 pulmonary tumors in this experiment was 2/29, or 7 percent.

 7.1.3  Intravenous Injection Studies
      In  1946,  Gardner and Heslington,  in  a  search to find the  cause of an
 "unusual incidence of pulmonary  sarcoid" in the fluorescent light tube industry,
 injected zinc beryllium silicate  (ZnBeSiOg) into rabbits.   They found osteosar-
 comas of the  long bones  in all  seven animals which survived the treatment for
 seven or more months.  Because  this  was  the first instance of  experimental
 carcinogenesis by  an  inorganic substance,  it evoked great  interest.   Beryllium
was clearly implicated as the causative agent because zinc oxide, zinc silicate,
 or silicic  acid  did  not cause  osteosarcomas  in a  second set of  trials,  whereas
 beryllium oxide  (firing temperature  unknown) did.   Guinea pigs and rats, when
 similarly treated with both zinc beryllium silicate and beryllium oxide, failed
                                     7-10

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to respond.  The  dose  of beryllium within the two compounds injected (beryllium
oxide and  zinc beryllium silicate) was  360 and 60 mg, respectively, and was
given in 20 divided doses during a 6-week period.
     This  basic  experiment was  repeated many times by several  investigators
(Tables 7-6 and 7-7).  Cloudman et al. (1949) produced osteosarcomas in four out
of five  rabbits  receiving a total dose  of 17 mg beryllium (as zinc beryllium
silicate).   Mice  were  also injected with  "some"  tumors  being produced  (counts
not stated).   In  this  experiment,  "substantially 100 percent beryllium  oxide by
spectrographic standards"  (degree  of firing  not stated, total dose 1.54-390 mg
beryllium) produced no tumors.  Nash (1950) produced five cases of osteosarcomas
in 28  rabbits injected  with zinc  beryllium  silicate  phosphor.   The minimum
effective  dose appeared  to be 200 mg zinc beryllium silicate (12 mg beryllium).
Dutra and  Largent  (1950)  produced osteosarcomas  in rabbits  with  both zinc
beryllium  silicate  (2/3) and beryllium  oxide (6/6),  and  reported a successful
transplant  in  the anterior chamber of the eye of a guinea pig.   Barnes et  al.
(1950) produced  six cases of osteosarcomas among 17 rabbits  injected with zinc
beryllium  silicate  and one case of osteosarcoma among 11 rabbits injected with
beryllium  silicate.   The tumors were multicentric  in  origin, and blood-borne
metastases  were  common.    Hoagland et al.  (1950) injected  rabbits  with two
samples  of zinc  beryllium silicate phosphor,  containing 2.3 and 14 percent
beryllium  oxide,  and  produced  osteosarcomas in 3/6 and  3/4 rabbits,  respec-
tively.  With uncompounded  beryllium oxide,,  the  tumor rate  was  1/8.   The
osteosarcomas  appeared to be highly  invasive,  but could not  be transplanted.
Beryllium  phosphate  produced  no  tumors.
     Araki  et al.  (1954) injected 35  rabbits with zinc beryllium  manganese
silicate,  zinc beryllium silicate, or beryllium phosphate.   The rate of osteo-
sarcoma  formation was 6/24,  2/7,  and 2/4  in the  three groups,  respectively.
There were no tumors  among  three  rabbits injected with beryllium oxide (firing
temperature unstated)  or  among two  uninjected controls.  There was  also  a
primary  thyroid  tumor in the  group  injected  with  zinc  beryllium manganese
silicate.   Liver cirrhosis and splenic  fibrosis were also observed.  Transplant
experiments were  all negative.
      Several  experiments  reported from the  Mayo  Foundation confirmed the
carcinogenic  effects of  intravenous beryllium on bone  (Janes et  al., 1954,  1956;
Kelly et al.,  1961).   Twenty-two of 31  rabbits receiving  zinc beryllium silicate
 (total  dose 12 mg Be) developed osteosarcomas.  New bone formation was  observed
 in the  medullary cavities of the long bones before the malignant changes became
                                      7-13

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-------
apparent.   Of particular  interest  was the observation of splenic atrophy only
in those  animals which  developed  bone tumors.   Following  splenectomy,  the
incidence of  bone tumor  or  new bone formation in the medullary cavity  was
100 percent, whereas the  incidence of these  developments  in non-splenectomized
rabbits receiving identical  doses  of beryllium  was  only 50 percent.   The
results suggest  that a well-functioning spleen may serve  as protection against
beryllium carcinogenesis  in the  rabbit.   Tibial  chondrosarcomas  were  also
produced, and successful  transplants to the anterior chambers  of the eyes  of
rabbits were performed (Higgins et al., 1964).

7,1.4  Intramedullary  Injection Studies
     Beryllium oxide or zinc beryllium silicate  was  directly  introduced into
the medullary cavity  of bones of rabbits by Yamaguchi (1963),  Tapp (1969),  and
Fodor  (1977).    Osteosarcomas,  chondrosarcomas,  and  presarcomatous changes
(irregular  bone  formation)  were observed.   In  the Yamaguchi study, twenty  to
30 injections (20 mg  beryllium oxide per injection) gave the highest frequency
of tumor  formation (11 of 13 animals).  The tumors developed directly from  the
medullary bone,  and were sometimes  preceded by fibrosis.   Tumors  metastasized
to the liver, kidney,  lymph  nodes,  and particularly the lung.  Tumors developed
in 9 of 16  animals  receiving 11 to 20 injections  and  1 of 14 animals  given  1  to
10 injections.

7.1.5  Intracutaneous  Injection Studies
     Neither  the  intracutaneous  injection  of  beryllium sulfate, nor  the
accidental  introduction  of  insoluble  beryllium  compounds  (beryllium oxide,
beryllium phosphate,  beryllium-containing fluorescent phosphors)  into the  skin
 have  been  found to produce tumors  (Van  Ordstrand et al.,  1945;  Reeves  and
 Krivanek,  1974).  The  lesions that were produced were cutaneous  granulomas, or,
 in the case of  extensive injury, necrotizing granulomatous  ulcerations.
      In  the immunotoxicologic  experiments of  Reeves  et al.  (1971,  1972)  beryl-
 lium sulfate was  administered  intracutaneously in doses  of 5 yg beryllium, but
 there was  no evidence that measurable amounts of beryllium left  the sites of
 administration.
                                      7-17

-------
 7.1.6  The  Percutaneous  Route  of Exposure
      No neoplasms have been observed  following percutaneous administration of.
 beryllium compounds  in any  species.  However,  eczematous contact dermatitis has
 been  noted  in humans who have worked  with  soluble compounds of beryllium (Van.
 Ordstrand et a!., 1945).  Curtis (1951) studied the allergic etiology of these
 reactions and developed  a beryllium patch test.  In 1955, Sneddon reported that
 a  patient with  a positive beryllium patch-test developed a sarcoid-like granu-
 loma  at the test site.   Granulomatous ulcerations  followed if insoluble beryl-
 lium  compounds  became imbedded  in the skin.   Using  pigs,  Dutra et al.  (1951)
 were  able to produce beryllium-induced cutaneous  granulomas that resembled  the
 human  lesions.   There is no record that any of these lesions underwent malig-
 nant degeneration.   The  fact that no neoplasms were observed could be explained
 by the  virtual impenetrability of intact skin  by beryllium  (see Section 4.1.3).

 7.1.7   Dietary Route  of  Exposure
     With one  exception, no .known  neoplasms  have  been observed  following
 beryllium exposure by the dietary route in  any species.  Guyatt et  al.  (1933),
 Jacobson (1933),  and Kay and  Skill (1934)  produced  rickets in  young rats fed
 beryllium carbonate  at  0.1  to 0.5 percent  dietary  level.   This result  is
 attributable to  the  precipitation  of beryllium phosphate  in the  intestine,
 leading  to  phosphate deprivation.   Using  similar dietary  concentrations of
 beryllium,  Sols  and  Dierssen  (1951)   observed a decrease  in the intestinal
 absorption  of glucose, which has been  attributed to  the  inhibition  of alkaline
 phosphatase  (Du  Bois et  al.,  1949).    At  intake  levels of 0.16 to  5  ppm
 beryllium sulfate in the diet, no toxic effects of any kind were found (Reeves,
 1965; Schroeder and Mitchener, 1975a,b).
     In a study  by Morgareidge et al.  (1977,  abstract),  a  significant increase
 in reticulum cell sarcomas  were  found  in male  rats exposed  to 5  or  50,  but  not
500 ppm beryllium in the diet.  The lack of  response  at the high dose, the
 lack of response  in  earlier studies using much greater doses,  and the results
of intravenous injection studies showing  beryllium accumulation in  the bones
along with  induction of  osteosarcomas, but no tumors at other  sites, render
the results  highly equivocal.
     If insoluble beryllium dusts (beryllium, beryllium alloys,  beryllium oxide,
beryllium phosphate,  or  beryllium ores) are ingested, the  bulk  of  these sub-
 stances will  pass through the gastrointestinal tract  unabsorbed.   Depending
                                     7-18

-------
on the  size  of the particles, and,  in  the case of beryllium  oxide,  on the
firing temperature, a minor proportion of these dusts could become dissolved in
gastric juices,  and traces  of the  resultant  beryllium chloride  could be
absorbed from  the stomach.  Upon  entry  into  the intestine,  any dissolved
beryllium  would become  precipitated again, mainly  as beryllium  phosphate
(Reeves, 1965).
     In most mammalian  species,  alimentary absorption of  soluble beryllium
salts [beryllium fluoride (BeFg),  beryllium chloride (BeCl2), beryllium sulfate
(BeSO.), and beryllium nitrate (Be[N03]2«)] is minor.   Researchers have observed
that 80 percent or more  of an oral beryllium intake of 0.6 to 6.6 ug/day passes
unabsorbed through  the gastrointestinal  tract of rats (Reeves, 1965; Furchner
et al., 1973;  Schroeder and Mitchener,  1975a,b).  Upon  entering the alkaline
milieu  of  the  intestine, beryllium  forms  a precipitate  that is excreted with
the  feces.   There is some evidence  that increasing  the intake concentration
does not  increase the amount absorbed from the intestine because the latter is
governed by  the solubility of the intestinal  precipitates  rather than by the
total amount of beryllium present.

7.1.8   Tumor Type, Species Specificitya  Carcinogenic Forms, and Dose-Response
7.1.8.1 Tumor Type  and  Proof of Malignancy.   Pulmonary neoplasms  found in  rats
after  beryllium exposure have been  classified as  adenocarcinomas, showing  a
predominantly  alveolar pattern.   Reeves et al.  (1967) distinguished  four his-
tological  variants,  including focal  columnar, focal squamous,  focal  vacuolar,
and  focal  mucigenous.   Schepers  et al.  (1957)  distinguished several  more,
including  some adenomas judged to be  nonmalignant.   Wagner et al. (1969) and
Groth  et  al.  (1980) found that about  half of the tumors  they produced with
beryllium  were benign  adenomas.   The diagnosis of pathological  lesions is
complicated, and requires special expertise.   The histological differentiation
between adenomas and adenocarcinomas is  not  always  well defined and may also
have species-related peculiarities,  so  that different conclusions on the same
specimen  may  sometimes  be reached by  pathologists.   This is  especially  true
when pathologists have  been trained in  human  rather than  veterinary medicine.
 It is  also  noteworthy  that  neoplasia  in the lungs of rats was  invariably
associated with the purulent lesions of chronic murine pneumonia, which itself
was  exacerbated by inhalation  of  the acidic beryllium  sulfate aerosol.
                                      7-19

-------
     Metastases,  as  well  as successful transplants, were  claimed  by Schepers-
et al.  (1957).   In the rat experiments of  Vorwald,  neither was claimed, but
later  reports  have been ambiguous on  these  points  (Vorwald et al.,  1966;  see
also Lesser,  1977).   In the monkey experiments of Vorwald (1968),  which lacked
controls, extensive  metastases  to the mediastinal lymph nodes and  sometimes to
the bones,  liver, and adrenals were  reported.   Groth  et al.  (1980)  performed
successful  transplants in  experiments  with intratracheal  administration  of
beryllium metal  and  beryllium alloy, but metastasis to the mediastinal lymph
node was observed  in only one animal.
     The nature  of the neoplasms produced by the intravenous or intramedullary
administration of  beryllium in rabbits is much more certain.  The osteosarcomal
or chondrosarcomal character  of these neoplasms  has not been challenged,  and
metastases  to  all  parts of the body  have  been observed.  Transplant results
have been equivocal,  however.   Successful transplants to the anterior chamber
of the eye were reported by Dutra and Largent (1950) and Higgins et al.  (1964),
whereas  failure  with  transplants was  expressly admitted by Hoagland et al.
(1950) and  Araki  et  al. (1954).  It is possible that the degree of malignancy
of the bone tumors depends on the type of compound used in the injection.
7.1.8.2  Species Specificity and Immunobiology.  Pulmonary tumors were produced
after  inhalation  exposure  and sometimes after intratracheal injection in rats
(Vorwald, 1953;  Vorwald et al., 1955; Schepers  et  al., 1957;  Schepers, 1961;
Vorwald et  al.,  1966;  Reeves  et al.,  1967;  Reeves  and Deitch, 1969; Spencer
et al., 1965, 1968, 1972; Wagner et al., 1969; Groth et al., 1980;  Ishinishi et
al., 1980) and in monkeys (Schepers, 1964; Vorwald et al., 1966; Vorwald,  1968;
but see Wagner et al., 1969 for negative evidence).  No pulmonary tumors were
produced in rabbits (Vorwald,  1950).  The evidence for hamsters (Wagner et al.,
1969), and  guinea pigs (Vorwald,  1950; Schepers, 1961,  1971;  Reeves et al.,
1972), while generally negative,  was suggestive of a  positive  effect in some
cases.
     Bone tumors  were  produced  by intravenous or intramedullary injection  in
rabbits (Gardner  and  Heslington,  1946;  Dutra and Largent,  1950;  Barnes  et  al.,
1950;   Hoagland et al., 1950;  Araki et al.,  1954;  Janes et al., 1954,  1956;
Kelly  et al.,  1961;  Yamaguchi,  1963; Higgins et al.,  1964; Tapp, 1969;  Fodor,
1977).   The single report  claiming  osteosarcomas in  mice (Cloudman et al.,
1949)   needs  confirmation,  as  does  the report of osteosarcomas  in rabbits after
inhalation exposure  (Dutra  et al.,  1951).  Bone  tumors  were not observed in
rats or guinea pigs.
                                     7-20

-------
     It would appear  from these  data that (1)  pulmonary tumors  can  be  obtained
with beryllium  in  rats  and in monkeys, possibly  in hamsters  and guinea pigs,
but not  in  rabbits,  and (2) that bone tumors can  be obtained  with beryllium  in
rabbits  and  perhaps  in  mice, but not  in  rats or guinea pigs.   The negative
evidence with guinea pigs involves  both the intravenous injection (Gardner and
Heslington,  1946; Vorwald,  1950) and inhalation (Schepers, 1961;  Reeves et al.,
1972)  of beryllium at levels that were definitely  carcinogenic  in  rabbits and
rats,  respectively.   However, in  the  later inhalation studies of Schepers
(1971),  there was  suggestive  evidence  for the  induction of lung  cancer in guinea
pigs.
     This apparent species specificity, which  might operate with other types of
carcinogenesis  as  well  (guinea  pigs  are  generally  regarded as  poor models for
cancer induction), has  remained  largely unexplored.  It is certainly noteworthy
that  guinea pigs develop  cutaneous  hypersensitivity to beryllium,  whereas rats
do not (Reeves, 1978).   In rabbits,  the spleen has  been found to be involved in
the neoplastic  response  to  intravenous  beryllium.  Gardner  and Heslington
 (1946)  observed prompt splenic  atrophy  in  beryllium-injected  rabbits, while
 Janes et al. (1954)  found that  splenic  atrophy  afflicted only those  animals
 that developed the osteosarcomas.   In later work, Janes et al.  (1956)  increased
 the yield of osteosarcomas in beryllium-injected rabbits twofold by performing
 splenectomy. These  studies suggest  that some form of  cellular immunity,  with
 immunocompetent cells  arising from  the  spleen, may be a factor  in determining
 whether  beryllium  is  neoplastic.   Various  species,  or perhaps individual
 members of  a species, may have  resistance to  beryllium-induced  cancer according
 to their immunocompetence.
 7.1.8.3 Carcinogenic  Forms  and Dose-Response Relationships.  There is insuffi-
 cient evidence to  implicate any  specific chemical form of  beryllium as  the
 exclusive  carcinogenic entity.   Ionic beryllium changes to beryllium hydroxide
 upon  inhalation,  and  both  forms have  caused pulmonary tumors  in rats when
 inhaled (ionic beryllium) or   injected  intratracheally (beryllium hydroxide)
  (Vorwald,   1953;  Schepers et al.,   1957;  Reeves  et al., 1967;  Groth  et al.,
 1980).   There  is reason  to believe that  beryllium hydroxide  particles  can
  change to a much  less  soluble crystalline form upon aging  (Gilbert and Garrett,
  1956).   Beryllium  oxide, when directly introduced into the  lungs of rats,
  showed a remarkable pattern of carcinogenicity, clearly indicating that  firing
                                       7-21

-------
 temperature had a.definite  influence on the tumor yield  and -that only "low-
 fired" (500°C) beryllium  oxide  was highly carcinogenic (Spencer et al., 1968,
 1972).  Sanders  et  al. (1978)  observed  only one lung tumor among  184 rats
 exposed to "medium-fired" (1000°C) beryllium oxide.   Frequently,  no tumors are
 obtained with beryllium oxide;  however,  in early studies,  the type of  beryllium
 oxide to which the animals were exposed was  not  generally identified  (Cloudman
 et al., 1949; Dutra  and Largent,  1950;  Hoagland et  al.,  1950;  Araki  et al.,
 1954; Vorwald et  al., 1966).
      Experiments  attempting  to  establish a  dose-response relationship with
 intravenous beryllium are limited.   Nash  (1950)  suggested 12 mg beryllium per
 rabbit was the minimum  effective  total  dose  to produce osteosarcomas.   In the
 experiments of Hoagland et al.  (1950), the frequency  of osteosarcomas  increased
 from  50 to 75 percent as beryllium oxide content of a  fluorescent phosphor was
 increased  from 2.3 to 14 percent.   Barnes  et  al.  (1950) could increase the rate
 of rabbit osteosarcomas from 4/14 (29 percent) to 2/3  (67 percent) by doubling
 the dose of intravenous  zinc  beryllium silicate from  7.5 to 15 mg.   However, in
 the  inhalation experiment of Dutra et al. (1951) and in  the intramedullary
 experiments of Yamaguchi (1963), no  clear-cut  relation between  dose and  tumor
 yield was  found.
      Vorwald  et  al.  (1966),   citing results of  their own unpublished studies,
 claimed  that "almost  100  percent  of  a large number  of rats" developed lung
 cancer after 18  months of exposure to 42 or 21 ug Be/m3 (as  sulfate).  After
 exposure to 2.8  ug Be/m   (as sulfate), their reported rate of lung cancer was
 13/21 (62  percent).   These figures came  under considerable scrutiny during the
 beryllium  hearings at the  Occupational  Safety  and  Health   Administration
 (Lesser,  1977).    It  was  pointed  out that these experiments were  poorly
 controlled  and that  the exposure data of 2.8 ug  Be/m3  deserved  no confidence.
Wagner et  al.  (1969)  obtained  pulmonary tumors  in  rats with  beryl  ore
 (beryllium  content 4.14 percent)  but not  with bertrandite  ore (beryllium
 content 1.4 percent).  Similarly, Groth et al.  (1980)  obtained pulmonary tumors
with  beryllium metal, beryllium  hydroxide, and  a  beryllium-aluminum alloy, with
beryllium content ranging from 62 to  100 percent.  They obtained no tumors with
other  alloys,  ranging in beryllium content from  2.2 to 40 percent.  Thus, the
evidence points to the existence of  a definable  dose-response relationship in
experimental beryllium carcinogenesis.
                                     7-22

-------
     Reeves (1978) examined this  relationship  by the probit method.  For the
induction of osteosarcomas in  rabbits  following intravenous injection of zinc
beryllium  silicate,  the median effective total  dose  per animal  was 11.0 mg
beryllium.  The dose-response  curve  intersected the 1 percent incidence level
at 3.8  mg,  the 0.1 percent incidence  level  at 2.7 mg, and the  0.01  percent
incidence  level at  2.0  mg.   For the induction of pulmonary carcinoma in rats
after inhalation of beryllium sulfate (a 35-hr/wk chamber exposure lasting 3 or
more months),  the  median effective concentration was  18.0  pg  Be/m ,  and the
curve intersected  the  1 percent incidence level at 12.0 H9  Be/m  ,  the 0.1 per-
cent incidence level  at 10.5  M9 Be/m3, and the 0.01 percent incidence level  at
9.0 |jg  Be/m3.   Obviously,  these  estimates are subject to  considerable
uncertainty.

7.1.9   Summary of Animal Studies
     The  results  of the studies that  have  been reviewed in this  section are
summarized in  Table  7-8.
     Tumors have  been  successfully  induced by  intravenous or intramedullary
injection of  beryllium  into  rabbits and,  possibly,  mice,  and by inhalation
exposure  or intratracheal injection into rats, monkeys, and possibly  guinea
pigs.   With one possible exception, attempts  to induce tumorigenesis  by the
dietary route  have  proven unsuccessful.   This failure to induce tumors is
probably attributable  to minimal  absorption resulting from  the precipitation of
beryllium compounds in  the intestine.  Guinea pigs and  hamsters appear  to have
a low  degree  of  susceptibility  to  beryllium  carcinogenesis.   This  species
 specificity appears to be connected  with immunocompetence.
      In  rabbits,  osteosarcomas and  chondrosarcomas  have been obtained.  The
 tumors  are highly  invasive  and metastasize  readily, but transplant  with
 variable  success.   They have  been  judged  to be histologically  similar to
 corresponding human tumors.   In rats,  pulmonary adenomas and/or adenocarcinomas
 have been  obtained.   The tumors are  less  invasive,  and their metastatic and
 transplant potential are variable.  They appear to be histologically associated
 with the purulent lesions of chronic murine pneumonia.
      There  *s some evidence  that the  cardnogenicity of beryllium oxides  is
  inversely related to  their  firing  temperature,  w.ith only the "low-fired"
  (500°C)  variety  presenting  a  substantial hazard.   Limited dose-response
  evidence indicates  that approximately 2.0  mg  beryllium  (as beryllium oxide) is
                                       7-23

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the minimum intravenous  dose  for production of osteosarcomas  in  rabbits, ami
approximately 10 pg  Be/m3  (as sulfate)  is  the  minimum atmospheric  concentration
for the production of adenocarcinomas in rats.
     Although some  studies involving beryllium clearly  have limitations, the
combined data,  using EPA's Guidelines for  Carcinogen Risk Assessment (U.S.  EPA,
1986)  to classify weight  of  evidence  for carcinogenicity  in experimental
animals, suggest there  is  "sufficient evidence" to conclude that beryllium and
beryllium compounds  are carcinogenic  in animals.

7.2  EPIDEMIOLOGIC STUDIES
7.2.1  Bayliss  et al. (1971)
     The first  in  a series of government-sponsored studies of cancer in workers
exposed  to beryllium was  conducted  by  Bayliss et  al.  (1971).   This cohort
mortality  study consisted  originally of 10,356 former and current employees of
the  beryllium-processing  industry (the  Brush Beryllium Company of Ohio,
presently  Brush Wellman, Inc. and  Kawecki-Berylco  Industries  of Pennsylvania,
presently  Cabot Corporation).   Some 2153  workers  were  excluded  because of
 insufficient  data.   Records  consisted only of names of  workers and  approximate
years  of employment of workers employed at the Brush  Beryl!iurn. Company prior to
 1942.   Company employment records provided no additional  information despite an
 intensive  search.  These lists were prepared  by a former Brush Beryllium Company
 physician,  now deceased.   After further  removal  of 1130 females, the cohort
 totaled 6818 males.   In this group, 777  members  died during  the period from
 January 1, 1942 to  the cutoff  date,  December 31, 1967.  This was  less  than
 the 842.4 expected  deaths  based upon U.S. male death rates—a shortfall  attri-
 butable to the "healthy worker effect."  No elevated risk of lung cancer (Inter-
 national Classification of  Diseases  [ICD] 160-164)  was evident  overall (36
 observed versus 34.06  expected).   No significant excess risk  of  lung cancer was
 found to exist in  relation to  length of  employment, beginning date of employ-
 ment, or  kind  of  employment  (office versus production), nor  were significant
 risks of other forms of cancer evident from these data.
      This study suffers from several deficiencies.  Over 2000 individuals had to
 be  eliminated  from  the cohort because birth  date, race, and sex were not avail-
 able.  The authors  indicated that this reduction in  the  size  of the  study neces-
 sitated  the  elimination  of  some 251 deaths, and  represented a  loss of over
 20  percent of  the cohort  and 25 percent of the known deaths,  a circumstance that
 had the potential for  introducing considerable bias into the  results.
                                        7-27

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      A second major problem with the study is the fact that the authors did not
 analyze the data according to  length  of time since initial employment  in the
 industry. The lack  of  such  an analysis meant  that  questions dealing with latency
 could not be  addressed.
      A third  deficiency  is  that the populations  of several different plants were
 combined  into one  cohort for  the  study.   As a result, the study  failed to
 consider the  many potential differences of exposure levels at different plants.
 Individuals were studied in groups according to beginning date and duration of
 employment, despite the  fact that their  exposure histories may have been totally
 dissimilar.
      For the  above-cited reasons,  this study is not adequate for the evaluation
 of cancer mortality in beryllium-exposed workers.

 7.2.2   Bayliss and Lainhart (1972, unpublished)
      In an  attempt  to  remedy the deficiencies  of  the  1971 study, Bayliss and
 Lainhart (1972),  in  an unpublished report presented at the American Industrial
 Hygiene Association meeting on  May 18,  1972,  narrowed  the  scope  of  the original
 study  by focusing only on data  from Kawecki-Berylco Industries (KBI) which had
 seemingly complete  employment  records  for two locations in Pennsylvania.  This
 change effectively reduced the size of the cohort to some 3795 white males while
 retaining the  same  starting and cutoff dates  as were used  in the  earlier study.
 In the 1972 study, Bayliss and Lainhart  found that 601 members of the cohort had
 died,  compared to 599.9  expected deaths based on period- and age-specific U.S.
white  male  death rates.   Again, no  significant  excess  of unusual  mortality  from
 any cause was  evident.   For lung cancer (ICD 160-164) overall, 25  deaths were
 observed versus  23.69  expected.   Even  when latency was considered,  no signifi-
 cant  excess risk of lung cancer was apparent after  a  lapse of 15 years from
 initial exposure, at which  time 14 deaths were observed versus 13.28 expected.
 In addition,  no  significant risks were  apparent in  relation to  intensity of
exposure, duration of exposure,  or beginning date of employment.
     The Bayliss  and Lainhart (1972) study was criticized by Bayliss and Wagoner
 (1977)  in a third version of the study,  which was  submitted to the Occupational
Safety  and  Health Administration  (OSHA) as part  of the beryllium  standards
development process.   In this  criticism,  the 1972  study  was said  to have
multiple limitations, among which  were the following:   (1) the study  included
clerical and  administrative workers who presumably had not been exposed to
                                      7-28

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beryllium;  (2)  the data were obtained  from  industrial  representatives,  which
precluded an independent assessment of plant employment files to ensure that all
potentially  exposed workers were included;  and  (3)  the study did  not assess
latency  20  or  more  years after initial employment,  although  it did examine
mortality after a 15-year lapse.

7.2.3  Bayliss  and Wagoner  (1977, unpublished)
     In  the third  attempt  to  remedy  the  deficiencies of  the two previous
studies,  Bayliss  and -Wagoner (1977) reduced the  size of the cohort to include
workers  employed at only one plant site of KBI.  This particular  plant site
in  Pennsylvania was considered  to  be  the  best choice for  a cohort mortality
study  for the following reasons:  (1) this plant had, according to the authors,
the  most complete and detailed set of personnel records of any of the companies
and  sites examined; (2) it had been in continuous operation producing beryllium
prior  to 1940,  thus,  allowing an analysis  of latent  effects; and (3)  it  provided
a large group  of  employees from which valid inferences could  be made.   Other
plant  sites were deficient in  one  or more  of these respects.   The cohort  was
composed of 3070 white  males who were followed until January  1, 1976.   Vital
status was  unknown  for  only 80 members of  the  cohort  (3  percent), and these
 individuals were  considered to be  alive  until the study's cutoff  period.
Altogether, 884  deaths  were observed,  compared to  829.41 expected (based on
 period- and age-specific U.S.  white male  death rates).  A significant  excess
 of  lung cancer  was noted (ICD 162-163),  with 46  cases  observed  versus
 33.33.expected (p  <0.05).   A significant  excess of  heart disease was  also  noted
 (399  observed  versus  335.15 expected, p <0.05), as was a significant excess of
 nonmalignant respiratory disease  (32  observed versus 19.02 expected, p <0.01).
 Irrespective of  duration  of employment, a significant  excess  was noted  in  bron-
 chogenic cancer following  a lapse of 25 or more years since initial employment.
       In this study, the authors discussed for the first time the impact of ciga-
 rette smoking  as a possible confounding agent contributing to the excess risk of
 lung  cancer.   An examination of the  results  of a cross-sectional  health exam-
  ination  survey conducted at the plant  by the U.S.  Public Health Service (PHS)
  in  1968 revealed  some  differences in  the  cigarette-smoking  patterns of the
  surveyed employees,  compared to smoking patterns in the United  States as a whole
  (determined from a health  interview  survey conducted  by  the PHS  from  1964 to
  1965).   A greater percentage  of heavy smokers was  indicated  in the  1968 survey
                                        7-29

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 as  compared with national data (21.4 versus 15.3 percent).  However, Wagoner et
 al.  (1980)  later dismissed the  results  as  a  possible  cause of the  increased risk
 of  bronchogenic cancer and other  diseases in  the  study  cohort.  Dismissing the
 role of cigarette smoking as a contributing cause of the excess  risk of lung
 cancer  may  have been premature  for several reasons.   First, the smoking patterns
 of  the  379 current employees surveyed  in  1968 were probably not  the  same  as
 those of the entire cohort of 3795, which  included both  current and past workers
 employed as early as 1942.  Second, the first national  reports of smoking as a
 cause of lung cancer were published in  1964  and were  accompanied by a great deal
 of  media attention.   By 1968,  intense  media coverage dealing with the health
 consequences  of smoking  probably  produced a  diminution of  cigarette  smoking
 among various  subgroups of the population in  the 4-year interim period between
 surveys.   Furthermore,  while  the 1968  survey  at the plant did speak of current
 cigarette-smoking  patterns,  the  issue of prior  cigarette smoking  was  not
 addressed,  nor  was the  issue of pipe or cigar  smoking.   Additional criticisms of
 the  Bayliss and Wagoner (1977)  study,  as well  as  the final version of  the study
 (Wagoner et al., 1980), follow.

 7.2.4  Wagoner  et al. (1980)
     Wagoner et al.  (1980)  slightly reduced the  cohort  of Bayliss and Wagoner
 (1977)  to  a smaller cohort mortality study  of 3055  white males employed some
 time  between  January 1,  1942 and  December 31, 1967,  in the  same beryllium-
 processing  facility.  This version of the  study did not  differ markedly from the
 Bayliss and Wagoner (1977) study except in minor respects.  Thirteen persons who
 had  been included in the earlier  cohort were  found  to be salespersons who  had
 never appeared  in the  plant;  thus, they  were removed  from the cohort.  In
 addition, three individuals who were  nonwhite  and therefore  also  ineligible  for
 inclusion were  removed.   One individual with a definite  diagnosis of lung cancer
 but  questionable employment  credentials  was  added.   The results  showed  a
 significantly high  risk of  lung cancer (47 observed versus  34.29 expected,
p <0.05) for those  individuals  followed until  December  31,  1975.   This  excess
extended to members  of  the cohort  followed for more  than 24 years  since  initial
employment  (20  observed versus  10.79  expected, p  <0.01).  When  the analysis was
confined to those whose initial  employment occurred  prior to  1950, but who were
 followed for 15 years  or more from date of initial employment,  a significantly
 high  risk  of lung  cancer was  apparent (34  observed  versus 22.46 expected,
                                      7-30

-------
p <0.05).   For those whose initial employment occurred after 1950, 4 deaths from
lung cancer were  observed versus  2.4 expected.   The  authors  concluded  that this
excessive risk of lung cancer "could not be related to an effect of age, chance,
self-selection", study group  selection,  exposure to other agents  in  the study
facility, or place of residence."
     This study has received severe criticism from several sources:  an internal
Centers for  Disease Control  (CDC)  Review Committee appointed  to investigate
defects tn  the study,  several  professional epidemiologists  (MacMahon,  1978,
1979; Roth, 1983), and also one of the study's coauthors (Bayliss, 1980).  These
researchers criticized Wagoner et al. for inadequately discussing all qualifiers
that might explain any of the significant findings of the study.
     The cohort  studied by Wagoner  et al.  (1980) was composed of workers at the
facility who  had  been employed prior to December 31, 1967,  based on  the facili-
ty's employment records and the results of a 1968 cross-sectional medical  survey
of  the  plant.   The cohort excluded  employees  who were not directly  engaged in
the  extraction,  processing,  or fabrication of beryllium, or in on-site adminis-
trative, maintenance,  or support activities.   The  numbers  of expected deaths
used  in the  study were based on U.S.  white male death rates  that  had been
generated  by  an analytic life table program designed by the  National  Institute
for  Occupational  Safety and Health (NIOSH).   As a basis for these calculations,
the  program  used actual U.S. deaths recorded by cause, age, race, sex, and year
through 1967,  together with census  population  data  from 1941 to  1967.  These
data  were  provided by  the Bureau of the Census  and the National Center  for
Health  Statistics.  Unfortunately,  at the time of  this  study and subsequent
studies on beryllium, cause of  death  information was not available from these
agencies on  a year-to-year basis after 1967.  As a result, the NIOSH life-table
program could not generate death  rates  during this  period without certain
assumptions.   In order to estimate  expected deaths  during  the period  from 1968
through 1975,  death rates were  assumed by  the  authors  to be  unchanged  from those
generated  by  the  NIOSH  life-table program  for  the period from 1965 through 1967.
The result was that  for  causes  of death with  declining death rates,  expected
 deaths  were overestimated, with  a  resultant underestimate  of risk.  Similarly,
 for those  causes  with  increasing death rates during the interval studied, ex-
 pected deaths  were underestimated, with a  resultant  upward risk bias, which
 was the case  for all  of the lung cancer risk calculations  made by the authors.
 After  this problem had been corrected by the  inclusion of actual lung cancer
                                       7-31

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 mortality data  for  the  period in question, expected  lung  cancer deaths were
 recomputed  by Bayliss (1980) prior  to  the Wagoner et al. (1980) publication.
 The  result was  an  increase  from 34.29 to 38.2 expected lung cancer deaths, or an
 excess  of 11 percent.   This correction in  itself was  enough to  eliminate the
 statistical  significance calculated by Wagoner et al. in their  overall  lung
 cancer  tabulation.   With respect to latency, the risk of lung cancer remained
 significant  in  the subgroup of the cohort that was observed for 25 years or more
 after initial  employment (20 observed versus 13.36 expected, p s 0.05).  These
 corrections  have been confirmed  by Richard Monson  (MacMahon, 1978,  1979),
 following a  reanalysis  of the NIOSH data  tapes  in an  independent Monson life-
 table program at Harvard University.
     In attempting to  assess the impact of  cigarette  smoking on the  risk of
developing lung  cancer  in this cohort,  Axelson's  method  (1978) was  applied to
the  meager  cigarette smoking  data  that were available  from Wagoner  et al
(Table 7-9).
     n        ?;   PERCENTAGE DISTRIBUTION OF BERYLLIUM-EXPOSED WORKERS AND
     OF AGE-ADJUSTED U.S.  WHITE MALE POPULATION BY CIGARETTE SMOKING STATUS
Cigarette
Smoking Status
Never smoked
Former smokers
Current smokers
<1 pack a day
>1 pack a day
Beryllium Production
Workers (%)
27.2
22.4
50.4
29.0
21.4
U.S. Population3
(%)
24.7
20.5
54.7
39.4
15.3
 National Center for Health Statistics (1967).
Source:  Wagoner et al. (1980).

     The problems  with these  data have been discussed in the earlier critique
of the Bayliss and Wagoner (1977, unpublished) paper.  However, in the interest
of adjusting  the  expected lung cancer deaths by the contribution due to ciga-
rette smoking, one must first assume as valid the risks of lung cancer by level
of smoking  that are given  in the American Cancer Society's  25  State Study
(Hammond, 1966).  These data are given in Table 7-10.
                                     7-32

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    TABLE 7-10.  LUNG CANCER MORTALITY RATIOS FOR MALES, BY CURRENT NUMBER
            OF CIGARETTES SMOKED PER DAY, FROM PROSPECTIVE STUDIES
American Cancer Society
25- State Study
Nonsmokers
Moderate
Heavy
Cigarettes Smoked
per Day
0
1-9
10-19
20-39
40+
Mortality
Ratio
1.00
4.62
8.62
14.69
18.77
Source:  Hammond (1966).

     Next, a number  of  different assumptions about the  data  must be made in
order to  produce  a range of estimates that  will  presumably include the best
estimate of the contribution due to smoking.   Four calculations were done based
on varying the  assumptions  as  follows:  for the first calculation, the former
smokers were grouped with  the  nonsmokers, and the lower risk ratios were used
(i.e., 4.62 and 14.69);  second,  the  former smokers were  again  grouped  with  the
nonsmokers, but the higher risk ratios were used (i.e., 8.62 and 18.77)'; third,
the former smokers were  grouped with the moderate smokers, and the lower risk
ratios were  used; and for  the fourth calculation, .the  former smokers were
grouped with  the  moderate  smokers,  and  the  higher  risk ratios were  used.
Using  this  method, the increase  in  expected lung cancer deaths ranges  from
4.1 to .9.8 percent.  This procedure is described below.
Let I  = the incidence in the comparison population (U.S.  males),
     g
         I  = the incidence in any nonsmoking population,
R.J, R

Pi> P
                 and R3 = the relative risks in nonsmokers, moderate smokers,
                          and heavy smokers, respectively, and
                 anc' PS = tne percentage of the population who are nonsmokers,
                          moderate smokers, and heavy smokers, respectively.
Then, the incidence of lung cancer in the comparison population is:
V + (R2
                                     V + (R3
                                                               V
                                     7-33

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Similarly,  if  I   = the incidence of lung cancer in the plant study population
and  IQ)  Rp R2,  and RS are  the same as above, but  p^  p2,  and p- are the
percentages of the plant  population who are nonsmokers, moderate smokers,  and
heavy smokers, respectively,' then the  incidence of lung cancer  in  the plant or
study population is:
V
                                   (R
                                                               V
and finally,  the  contribution to the increase (or  decrease)  in  the expected
deaths is  the ratio  of  I  to I
                                     Hence,  (I/In)  *  (expected lung cancer
                                                 y
deaths) is the adjustment due to the confounder cigarette smoking.
     When  the calculation  is  completed  which produces  the  least change
(+4.1 percent) in  the expected lung cancer deaths in the 25+  latent category,
the new adjusted expected number of lung cancer deaths is
                             13.36 x 1.041 = 13.91

which when  compared with 20  observed  deaths in this latent category  is  no
longer statistically significant.   Repeating this calculation and assuming the
highest effect (i.e., +9.8 percent), the number of expected deaths  is

                             13.36 x 1.098 = 14.67

which, also, is not statistically significant.
     A number  of  assumptions  must be made in order to apply this crude method
to adjust for  the contribution  to lung cancer due to  cigarette smoking.  These
are outlined below:

     1.    Smoking  levels  in Table 7-9  are similar to those  of  the  entire
          cohort.    This  is  not  necessarily  true.   Although most  former
          employees  began work  prior   to  1950, a  smaller  proportion  of
          those current  workers  in  1967  who  participated  in the  smoking
          survey  began work  prior  to 1950.   Smoking  among  blue-collar
          employees was thought to be greater in the 1940s.
                                     7-34

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    2.   Smoking levels  at the plant in 1968 are similar to those of the
         United  States  in  1964.   The  survey  on smoking  in  the  U.S.
         population was  completed  in 1964 at about the  same time as the
         release  of  the report on smoking  and  health  by  the Surgeon
         General,  while  the  survey of the plant  was  completed in 1968.
         The   ensuing national  publicity  engendered  by  the  Surgeon
         General's report  helped to produce a reduction in smoking levels
         in the  U.S.  population,  and probably  in  this plant, during the
         three-year  period from 1964* to 1968.   Therefore,  these levels
         are  not strictly comparable because of a lack of concurrence of
         the  two events.
    3.   In each smoking category  (heavy, moderate, and nonsmoking), the
         age   distributions  are similar.   This  is  not  necessarily the
         case.   It was  impossible  to  age-adjust the  plant population in
         each smoking category to the U.S.  male population in the same
         smoking category  because of  the lack  of  age-specific smoking
         data in each category of  both populations.
    4.   The  assignment of  persons into  specific smoking categories by
         quantity  smoked assumes that  such persons always  belonged to the
         category  to  which  they  were classified.   This may  not be the
         case in  either  population.   No time factor could  be used to
         classify  persons as to  the  category  of smoking  to which they
         were assigned,  since such information  was not available.

Unfortunately, these  estimates are  by necessity based  on the only data availa-
ble to the U.S.  Environmental Protection Agency's Carcinogen Assessment  Group
(CAG).  Table  7-11, which  is  adapted from the Wagoner  et al.  (1980) study, has
been  corrected to  eliminate  the 11-percent underestimate of  expected  deaths
caused by the failure to  use the appropriate  lung cancer death rates  in  the com-
parison population and has been adjusted upward another 4.1  percent (minimum
effect) to account  for the smoking contribution based on the information pro-
vided in Table 7-9.   One ineligible lung cancer  death has been removed from
the observed deaths.
                                     7-35

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    TABLE  7-11.   OBSERVED  AND  EXPECTED  DEATHS  DUE TO  LUNG CANCER ACCORDING TO
      DURATION OF EMPLOYMENT AND TIME SINCE ONSET OF  EMPLOYMENT AMONG WHITE
      MALES  EMPLOYED  SOMETIME  DURING JANUARY 1942 THROUGH DECEMBER 1967  IN
      A BERYLLIUM PRODUCTION  FACILITY  AND FOLLOWED THROUGH 1975 (REVISED)
Interval Since Ons

Duration of employment (years)3'
;et <5 years
of Employment (yrs) obs.
<15
15-24
>25
Total
7
15
17
39
vs. exp.
8.88
13.44
12.00
34.32
>5 years
obs. vs.
1
3
3
7
exp.
1.76
3.15
2.67
7.58
Total
obs.
8
18
20
46
vs. exp.
10.64
16.59
14.67
41.90
 Employment histories were ascertained only through 1967.
 No comparison is statistically significant at p <0.05; obs. = observed,
 exp. = expected.

     Wagoner  et  al.  found 875 deaths  in  their cohort.  The vital  status  of
79 members of the cohort remained unknown as of December 31, 1975. The authors'
assumption was that  these individuals would be counted as alive until the end
of the  study,  and that because of their  added person-years,  any  finding of in-
creased cause-specific  mortality  would tend to be underestimated.   Actually,
these 79  individuals  represented  only two percent  of  the total cohort,  and any
additional person-years  included  from the time when they were  last  known to be
alive would have  added little to the number of expected deaths.   Furthermore,
given the intense scrutiny afforded this population in determining vital status
by both Wagoner  and Mancuso  in their own  studies of the  same workers, and  con-
sidering the fact that these researchers shared information on newly found lung
cancer deaths, it  is  questionable whether any additional  lung cancers  would
have been found  either- in the 79 individuals  with unknown vital  status  or in
the 15 known dead for whom causes of death were not known by the  cutoff date of
the study.  The  latter number was  reduced  to ten  in  subsequent  tabulations
after information on causes of death was  located for  five individuals (Bayliss,
1980).   None of these was lung cancer.
     Additional factors that could have contributed to the finding of an excess
risk of lung cancer in Wagoner et al. (1980) are as follows:
                                     7-36

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     (1)  One lung cancer victim was added to the cohort based on a single 4 by
7 inch  personnel  card that listed the same day (June 1,  1945) as the  "starting
date" and "release date" in the plant.  In actuality, the individual,  according
to company sources, never reported for work because a preemployment chest X-ray
revealed a  lung  abnormality.   The company paid  him  for  the time he was  being
examined, which is why his name and social security number appeared on a social
security earnings  report.   Bayliss excluded him from his original  cohort based
on the  information on the same personnel record that said "did not pass chest
X-ray."
     (2)  In  a  supplemental  summation on the  epidemiology  of beryllium with
respect to the proposed occupational safety and health standard for exposure to
beryllium (January 13,  1978;  prepared by Roth  and submitted by Brush  Wellman),
it is  stated  that 295 white males, who  were employed at the Reading  plant  of
Kawecki-Berylco Industries  (KBI)  in jobs similar or identical to those of the
Wagoner et al. cohort,  were not included in the study cohort.  Of that group,
the report  states  that 199 employees  had a known vital status:   181 were alive
and 18 were deceased  by the close of  the  study period.   Roth's post hearing
statement indicated that the inclusion of these additional employees would have
increased the cohort by about ten percent.
     (3)  In  researching  the medical  files of the  47 lung cancer victims,
Bayliss, one  of  the coauthors,  discovered that 23 files  contained information
to the  effect that the individuals in question were  smokers.   In addition,  the
company from  which the cohort was derived provided data indicating that 36 of
the 47  lung  cancer victims (77 percent)  smoked  cigarettes.   These data were
based  on  a company-sponsored survey  by  Hooper-Holmes and reported in a KBI
interoffice  memorandum (Butler,  1977).    Bayliss  determined  that of  the
47 cases, a total  of  42,  or nearly 90 percent,  smoked cigarettes,  based on a
combination  of smoking  information  gathered  by  the  company and  smoking
information from  the  medical  files.   If  this information is accurate,  it could
indicate the  presence of  a confounding  effect  due  to  cigarette smoking.
Bayliss  further  established that  one of the remaining  five  cases  died  from
another cause  of  death.   This victim actually died from a glioblastoma multi-
forme  (astrocytoma)  of the  brain,  according to medical  data.   However,  his
death  certificate incorrectly listed  lung  cancer as an underlying cause of
death.  If the 47  cases are reduced to 46, then 91 percent smoked cigarettes.
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     (4)  An inadequate  discussion  was presented on the confounding effects  of
exposure to  potential carcinogens  prior  to and following employment  in  the
beryllium industry.   These  factors  are especially important since the authors
maintained that only short-term employees were affected.  Evidence from employ-
ment records, medical files, questionnaires administered during the 1968 NIOSH-
sponsored medical  survey of  the plant,  and  death  certificates indicated a
distinct possibility  that these factors are  significant  in  the cohort under
study (Bayliss, 1980).
     Another problem  with the Wagoner et al.  (1980)  study,  as stated by the
authors, is  that  the expected deaths were overestimated by 19 percent because
of the  use  of death rates  for  white males  in the  United  States  as a whole,
rather  than  those  for Berks County, Pennsylvania, where the  plant was located.
This statement  was based on a comparison  by Mason and McKay  (1973) of the 1950
to 1969 age-adjusted lung cancer death rate  for white males in Berks County,
Pennsylvania, with that  of'the 1950 to 1969  age-adjusted lung cancer rate for
white males  in  the United States.   This reference by Wagoner et al.  to "lower"
Berks County rates as a  justification for the position  that the expected deaths
based on national  rates  are overestimated, has  been criticized by Roth (1983)
as well as  by  Bayliss (1980).   Bayliss cited the  fact that the periods of
observation  were  different, i.e.  the Mason data covered the period from 1950
through 1969, while those of Wagoner et al. (1980)  covered the period from 1942
through 1975.   Bayliss  also pointed out  that to derive reliable county death
rates  from  the existing data would  be extremely difficult to  do with any
confidence.   Roth criticized the  use of Berks County  rates  as not being
reflective of greatly elevated  lung cancer  death rates  for the City of  Reading,
which  they  maintained  were  12 percent  higher  than  the  national rates.
According to Roth (1983), 46 percent  of  the  workers employed by the plant in
1968 resided within the city limits,  whereas only 34 percent of Berks County
residents (1970)  resided within the city.  Therefore,  death rates calculated
for  Berks  County  should be weighted  toward the relatively  higher City of
Reading rates.   This adjustment would have the effect of generating comparison
lung cancer rates that  are perhaps greater than U.S.  rates  and,  consequently,
would increase  the number of  estimated expected deaths.
     Wagoner et al. (1980) also claimed  to have noted an unusual histopatho-
logic  distribution of cell types in 27 of  the  47 lung cancer  deaths  for  which
pathologic  specimens could be  obtained.  Adenocarcinomas  were noted in  8  of
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25 individuals  (32  percent)  histologically confirmed  to  have  died  from
bronchogenic  carcinoma  (Smith and Suzuki, 1980).  Wagoner  et  al.  apparently
disregarded the  conclusion  of Smith and Suzuki that "the prevalence of histo-
pathologic  cell  types  of  bronchogenic  carcinomas among beryllium-exposed
workers could not be  presently defined."  Smith and  Suzuki  attributed their
conclusion  to the  fact that  there  was  "an inadequate response rate for  the
submission  of pathology specimens for review," since  tissue specimens  were not
available for 20 (43  percent) of the total  number of lung cancers.  Wagoner
et al.,  however, citing data from earlier studies (Haenszel  et  al.,  1962;
Axtell et al.,  1976)  to the  effect that the frequency of adenocarcinomas in
U.S. white  males was  15 or 16 percent,  concluded that a significant "shift"  of
histologic  cell  types  was apparent in lung cancer deaths in beryllium  workers.
However, an internal  NIOSH memorandum (Smith,  1978)  stated that  more  recent
data by  Vincent et  al. (1977)  indicated that  a shift in the  prevalences of
histopathological cell  types  of lung cancer in  the general population over time
has  led  to  an increase in  the prevalence  of adenocarcinoma to 24 percent, and
therefore the prevalence  of  adenocarcinomas  in  the  lung  cancer  deaths  of
beryllium workers  is  not  significantly  different  from that expected.   Smith
suggested  in  his memorandum  that  any  mention by  Wagoner  et al.  of  the
histopathological examination of lung tumor specimens that does not take  into
consideration the  unrepresentative nature of  the  specimens  should be  deleted
from the paper.
     To  summarize,  it appears that  the  authors of the Wagoner et  al.  (1980)
study  tended to exaggerate the  risk of  lung cancer in a population of workers
potentially exposed to  beryllium,  and underemphasized or did not discuss  suffi-
ciently  the shortcomings of  the  study.   The net effect was to turn a "non-
significant  association"  of   lung  cancer with beryllium exposure into  a
questionable "significant  association."   Despite  the study's  problems,  there
still  remains  a possibility  that the elevated risk  of  lung cancer reported
therein  was  due in part  to beryllium exposure, and although the CAG considers
the study  inadequate to assess the  risk of lung cancer from exposure to beryl-
 lium at this time,  it recommends  further refinement and follow-up of this
 cohort to  determine  if the  reported increase associated  with  lung cancer
 becomes  statistically significant.
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7.2.5  Infante et al. (1980)
     In  a  companion paper by Infante et al.  (1980),  which appeared in the same
journal  as  the  Wagoner et al. (1980) study, lung cancer mortality was studied
by  the retrospective cohort  method in  white  males  for whom data  had been
entered  into the Beryllium  Case Registry (BCR) with diagnoses  of  beryllium
disease.  A person was judged to have beryllium disease and thus to be eligible
for  inclusion into  the  BCR if  three  or more  (two  were  mandatory) of the
following five criteria were met (Hasan and Kazemi, 1974).

     Mandatory -- (1)  Establishment  of  significant  beryllium  exposure
                       based on sound epidemiologic history.
                  (2)  Objective  evidence  of   lower  respiratory  tract
                       disease  and  a  clinical  course  consistent  with
                       beryllium disease.
     Mandatory — (3)  Chest  X-ray  films  with  radiologic  evidence  of
                       interstitial fibronodular disease.
                  (4)  Evidence of  restrictive  or obstructive defect with
                       diminished, carbon monoxide  diffusing capacity by
                       physiologic studies of lung function.
                  (5)  1 - Pathologic  changes,  consistent  with  beryllium
                           disease on examination of lung tissue.
                       2 - Presence of beryllium in lung tissue or thorac-
                           ic lymph nodes.

At the time  of  the studies, close  to  900 individuals had been  entered  into
the  BCR,  based  on  evidence  of nonmalignant respiratory  disease  objectively
determined by appropriate and established medical procedures (Mullan, 1983).
     According to Mull an (1983),  the criteria listed above are characterized by
high sensitivity but low specificity.   Hence,  while they are able to identify
cases of actual  beryllium disease,  they can also lead to  the  inclusion of non-
beryllium disease cases, in particular, cases of sarcoidosis.
     Infante et al.  (1980) eliminated from their cohort all nonwhite and female
subjects  because of  their lack of "statistical sensitivity."   They also
eliminated all subjects  who  were deceased at the  time  of the BCR entry.   The
authors maintained  that  this  constraint was necessary in order to ensure that
no  bias  would result  from the "selective referral  of  individuals  with the
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outcome still under investigation", i.e.  individuals with lung cancer.   The use
of the above  procedure,  however,  raises the question that such a self-imposed
constraint may  not have  prevented the "selective  referral"  of  lung cancer
victims prior to their deaths.  This possible effect might have been eliminated
if the above-referenced limitation had been applied to such cases as well.   Or,
alternatively,  it  should perhaps  have been assumed that  no  potential  bias
existed,  and that all BCR cases added posthumously should have been retained.
     Altogether, Infante  et  al.  (1980)  included in their study cohort  only
421 members  of  the BCR,  less than  50  percent  of the total.   Of these,  vital
status could not be determined for 64 (15 percent), while 139 (33 percent)  were
found to  have died by December 31, 1975.  In this latter group,  the causes of
death could  not be ascertained for 15 individuals.   These were  placed in  an
"undetermined  cause of  death"  category.  The  authors ceased accumulating
person-years  on  the group of 64 with  unknown vital  status  at  the time each was
last  known to be alive instead of  to  the end of the  study.   This procedure
served to  slightly reduce expected mortality in  every cause  category.   This
reduction was  offset,  however,  by the fact that no potential  deaths that might
have  occurred up to the cutoff date were included.  With the intense scrutiny
given the  issue of lung cancer and beryllium by Infante and the many research
investigators  who  have worked  with the  BCR since  its inception  (including
Wagoner, Bayliss,  and Mancuso), it  is questionable whether any of the 15 deaths
from  undetermined  causes,  or any of the  64  cases with unknown vital status,
were  lung  cancer deaths.   Hence,  it is probable that the estimated lung cancer
risk  is somewhat overestimated by this procedure.
      Additionally,  since  the same National  Institute  for  Occupational  Safety
and Health  (NIOSH) life-table program that  was  used to calculate  lung  cancer
deaths in  the Wagoner et al. study was the method used to derive expected  lung
cancer deaths in the Infante et al. study, it was subject to  the same  problems
as mentioned previously,  i.e. an 11-percent deficit in the calculated  expected
lung  cancer deaths.   If  it is  assumed that this  distortion  is  of the same
magnitude  as that described  in the discussion of the Wagoner et  al.  (1980)
study, the SMR of the Infante  et al.  (1980) study would  also be  inflated  by
11 percent.
      As  expected,   Infante  et al.  (1980)  found a significantly high excess
risk  of  "nonneoplastic"  respiratory  disease  (52  observed  deaths versus
3.17  expected).   In terms  of total  cancer,  19 deaths were observed versus
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 12.41 expected.   With  respect  to lung  cancer,  6 deaths occurred more than
 15 years  after the onset of beryllium exposure versus 2.81 expected (p <0.05).-
 If the expected  deaths  are  adjusted  upwards  by 11 percent to compensate for the
 overestimate  produced by the NIOSH life-table program, the  results are 6 deaths
 versus 3.12 expected  (p >0.05).
      Infante  et al.  divided  their  cohort  on the  basis of "acute" versus
 "chronic"  beryllium  disease.   Subjects  were considered "acute"  if the BCR
 records indicated a  diagnosis  of chemical  bronchitis,  pneumonitis,  or other
 acute respiratory  illness at time of  entry  into the registry.   Subjects  were ^
 called "chronic" if BCR records indicated a diagnosis of pulmonary fibrosis or
 some  recognized  chronic lung condition at time of entry  into the registry.  All
 other cases,  if they could not be designated as chronic, were considered by
 Infante et al. to be  acute  if the onset of the disease occurred within one year
 of initial  exposure.    These  definitions should  not be confused  with the
 medically accepted definitions  of acute and  chronic  beryllium disease, in which
 cases  of  beryllium  disease lasting  one year or less are termed "acute," while
 those  lasting longer  than one  year are termed "chronic." The  authors  found no
 significant lung cancer, not  even an excess in  their "chronic"  respiratory
 disease group of 198  persons (1 observed death versus 1.38 expected).  However,
 in  their  "acute" respiratory disease group, they found 6 observed lung cancer
 deaths  versus 1.91 expected  (p <0.05),  and in   the interval  of  more than
 15 years  since  initial   onset  of beryllium  exposure, 5  observed lung  cancer
 deaths  were found  versus 1.56  expected (p <0.05).   These  findings,  however,
 suffer  from the  same  problems  previously discussed  regarding  the  NIOSH life-
 table  program and must  therefore be  regarded as  questionable with respect  to
 their implications.
     The possibility  cannot be discounted that cigarette smoking may have con-
 tributed to an  excess risk in  the Infante et  al. (1980) study, despite the
 authors' claim that cigarette  smoking  is  unlikely to have played a role in  the
marginally increased  lung cancer risk they found.   Although the criteria for
 inclusion in the BCR have been  undergoing revision to improve their sensitivity
and specificity since the Registry's  inception in 1952,  it is possible that, in
the early years  of  the  Registry,  the criteria could  have allowed the inclusion
of  individuals with respiratory disease  either brought  on  or  exacerbated  by
cigarette smoking.   Such individuals  would then have been likely candidates  for
selection into the  BCR.   Of the seven lung  cancer cases discussed by  Infante
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et al.  (1980),-six were  admitted to the hospitals  for  treatment  before  1955,
and one  was  admitted  in 1964.   The  ability to detect subtle  radiographic
changes  consistent  with  a  diagnosis of  beryllium disease was relatively
undeveloped in the early 1950s.  Given  current  practices  in the interpretation
of X-rays and  pulmonary  function data,  such a  misdiagnosis would be  unlikely
today.                        •
     Any one of  the  factors referred to above  could  have been of sufficient
magnitude to produce  a significant excess lung cancer risk in the group under
study.   The authors'  treatment  of these confounders serves to exaggerate this
risk without  presenting  any compensating negatives.  It  appears  likely that
correcting or  controlling the  influence of two or more of these factors could
reduce  the  estimated  risk  calculated to nonsignificance.  The findings of
Infante  et  al.  (1980) are  thus  seen to be, at best, only suggestive of an
increased risk of lung cancer from exposure to beryllium.

7.2.6  Mancuso and El-Attar (1969)
•>    The  first in a  series of  four epidemiologic studies of  mortality in
workers  exposed  to  beryllium was conducted  by  Mancuso  and El-Attar (1969) on
the  same study population used  in the Bayliss and Wagoner studies.  The names
and  social  security  numbers  of individuals  who  made up  the cohort  in the
Mancuso  and El-Attar  study,  however, were  derived from quarterly earnings
reports  provided by  the Social  Security Administration.   Quarterly earnings
reports  on  every employee of a  given company covered by  social  security  are
filed  four  times a year by all  companies included under  the Social  Security
Act.   These reports  generally  consist  of  lists  of  names,  social security
numbers,  dates of birth, and reported  earnings during the quarters for which
filing is done.  With  respect  to  beryllium,  Mancuso and El-Attar obtained
quarterly earnings  reports for both companies studied by Bayliss et al. (1971)
and  Wagoner et al.  (1980), but limited their study to the period of employment
from 1937 to  1948.    Altogether, they  identified 3685  white males from two
beryllium plants.   Only  729 white  males were found to have  died through  the
year 1966.   Included  in this  group were 31 lung  cancers  (ICD  162-163).   The
authors contrasted  internally  generated age-,  plant-,  and period-specific  death
 rates  by cause with internally generated age-specific death rates by  cause from
 an "industrial control."  Unfortunately, because  of the small  numbers involved,
 the authors  did not include any employees  aged  55 or over.    The  industrial
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 cohort used for purposes  of comparison  was  not  identified.   The  729  deaths were
 distributed into 160 narrow subcategories, based on four broad age groups, two
 companies,  four periods of time,  and  five broad death categories.   Internal
 death  rates were computed in each subcategory.   Because the numbers from which
 these  internal  rates were derived are so small  (in some instances nonexistent)
 from one subcategory to another,  the comparisons with  20 rates  generated from
 the  industrial  control  are shaky  at best and appear to vary considerably.  No
 trends  are  evident.   No significance tests were  done.   The data  are open to
 interpretation.  The authors themselves conclude, based on their analysis, that
 their  data  are "severely limited" with respect to  answering the  question of
 carcinogenic risk.

 7.2.7  Mancuso  (1970)
     In  a second study of the  same  cohort,  Mancuso (1970)  added  duration of
 employment  as  a variable^ and divided the cohort into  a 1937 to  1944 component
 and a  1945  to 1948 component,  by  dates of initial employment.  Both subgroups
 were followed  until  1967, and  internal death rates  were  computed based on a
 technique the  author  termed "the  generation cohort  method."  Each cohort  was
 classified  into  10-year age groups,  beginning  with  1940.   An average annual
 mortality rate was calculated  by  age  as  of 1940.   Age adjustment was done
 through the direct method, using the 1950 standard million as a base population
 (presumably  the U.S.  1950  standard  million, although  the  author does  not
 specifically identify his comparison population).   Comparisons were internal  by
 gradient of  exposure  as defined by duration of employment  and by  evidence of
 prior chemical respiratory disease.
     A higher  rate of lung cancer was noted by the author among workers whose
 first employment occurred  during the period 1937  to  1944  in  age  category 25 to
 64, and who were employed for five or fewer quarters (99.9 per 100,000) compared
 to those employed  six  quarters or longer  (33.2 per  100,000) based on 16 and
4 lung cancers,  respectively.   In  one  company,  the author also found a higher
 rate of  lung cancer  among a group  of workers with histories of  chemical
 respiratory illness than  ,in  those  who did  not have this condition.   During the
1940 to  1948 period,  142 white males with respiratory illness were identified
 in this plant.   Out of a total of 35 deaths occurring in this group,  6 were due
to lung  cancer.  Based  on these 6 lung cancers,  an  age-adjusted lung cancer
death rate  of  284.3  per 100,000 was calculated,  compared  to an  age-adjusted
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rate of 77.7 per 100,000 (based on 9 lung cancer deaths) in the total cohort of
this company's workers  employed from 1937 to 1948.   These calculations  were
confined to  individuals  who were in the  25  to  64 age group in the year  1940.
For  some  unknown reason, the  author  neglected  to include  the  15 to 24  age
group.   Had he done so, the lung cancer death rate in individuals without prior
respiratory  illness would  have increased by the  addition  of two lung cancer
deaths,  leaving  the rate  unchanged in  those  with respiratory  illness  and
narrowing the  difference between the two rates.   No  significance  tests  were
done,  and,  as noted by the author, the  observations were based upon small
numbers.
     Although  Mancuso  (1970)  found elevated risks in  these groups,  the results
are  subject  to considerable variability.   Mancuso criticized his own study for
several  alleged  deficiencies.  Some of  these  criticisms seem inappropriate,
while  others appear valid for this study and also for later studies  by Mancuso
on  this  same population.  The deficiencies,  according to Mancuso,  consisted of
"the marked influence  of  labor turnover on duration of employment, perhaps
induced  by  the presence of respiratory  disease;  the  inability to define the
specific populations by department, process, or  by type or form of beryllium
exposure; the  presence of competing causes  of  death; and  the  shortness of the
period of  observation."  Other potential problems with  these  data,  which were
not mentioned  by the author,  are  a lack of consideration  of  the effects  of
smoking  and the effects of exposure to potential  carcinogens in other jobs the
workers  may have had before  and  after  their exposure to beryllium,  since the
suggested  increase appeared only in "short-term employees."  This is discussed
further  in  a  later description of the study (Mancuso,  1979).   The author's
conclusion  that  prior  chemical respiratory  illness influenced the  subsequent
development of lung cancer among beryllium workers may be  somewhat overstated,
in  view of  the many limitations of the  study.

7.2.8   Mancuso (1979)
     In a third update, Mancuso  (1979)  conducted a cohort mortality study in
which  he divided the  cohort  into two  subgroups,  each consisting of  former and
current employees  of the two  beryllium  manufacturing  companies.  Employees were
 included in the study  if  they had worked at any time  during  the period from
 1942  to 1948.   The original  source  documents, from  which  names and  social
 security numbers  were derived to  form the cohort,  consisted of quarterly
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earnings  reports 'submitted to the Social  Security Administration.   The Ohio
cohort  consisted  of  1222 white males,  of which  334  were deceased.   The
Pennsylvania cohort  consisted of 2044 white males, of  which 787 were deceased,
A life-table analysis was performed by  NIOSH,  utilizing  U.S.  white male  age-
and  period-specific  rates  (5-year  age groupings) to  generate  expected lung
cancer  deaths  (ICD  162, 163) through  1974 for the Ohio cohort,  and through
1975 for  the  Pennsylvania cohort.   An excess  risk of  lung cancer appeared  in
the  Ohio  employees  after  a  lapse  of 15 years  from the  onset  of employment
(22 observed  versus  9.9  expected,  p <0.01).   The same was  true  for  the
Pennsylvania employees  (36 observed versus 22.0 expected,  p <0.01)  following a
similar latent  period.   The author noted  that  this  risk occurred to workers
with less  than  one year's duration of employment in the  industry.   No signifi-
cant excess risk was noted in workers of  either plant who were employed for
more than  five  years in the  industry.   The author concluded on the basis of
this study  and  the  Wagoner et al.  (1980)  study that  "there is evidence that
beryllium causes cancer in man."
     Several questions  must  be  considered before  these  conclusions can be
accepted as valid.   These data, although derived from  social security quarterly
earnings reports and not from personnel records,  are  not independent of the
data set  utilized in the Wagoner et al.  (1980) study.   Both sets of data were
analyzed through the use of the  NIOSH life-table program.   The expected deaths
generated  in both studies are subject to the same influences  introduced by  the
use of the same life-table program, and by the  use of  the same comparison rates
(U.S. white male  lung cancer rates).  In  addition,  the  extensive cooperation
between Mancuso (at the University of Pittsburgh) and Wagoner (at NIOSH) in the
search  for  causes of death in the  respective cohorts for study, contributed to
the  inclusion of  lung cancer deaths  known  to  one but  not  the  other in both
studies.  As mentioned  previously,  because of the use  of the  NIOSH  life tables
in the Mancuso study, the calculation of expected lung cancer deaths was on the
low  side  (approximately 11 percent)  because of the same  artifact involving  the
calculation of  lung  cancer rates for which the Wagoner et al.  (1980) study  was
criticized.  Hence,  these results  should not be considered independent of the
results of the Wagoner study.
     Another problem  with this cohort is the use of social security quarterly
earnings reports to constitute a cohort of potentially exposed employees. These
files, for the most part,  are limited with  respect to  the data available.  Only
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the fun name,  social  security number, and amount  paid  into the system each
quarter of any  given year are provided, and  only  for covered employees.   An
examination  of  microfilm records  of the  reports  maintained by the  Social
Security Administration  shows  that there  is  no  possibility of determining from
the  reports  what jobs these  individuals  performed for the  companies,  where
their  job  stations  were  located,  whether their  jobs were  on or  off  the
premises,  or whether they  had actually been exposed  to  beryllium, or even
precisely  when  during the three-month period they actually started work.   And,
of course, these records give  no information on workers who were not covered by
the  Act.   Furthermore,  in the period prior to 1942, the social security system
was  in the process  of being  established,  and tremendous logistic problems in
setting  up the system were being  encountered during this time.   Because  the
system was not fully functional until  1942,  millions of employees throughout
the  country  did not get  social  security numbers until after that  date.   Large
numbers  of employees refused  to join the  system because  they considered  it  to
be  "welfare,"  and  many  more  simply reported their social  security  numbers
inaccurately if at  all when applying for work.  Thus,  questions remain  concern-
ing  the validity of this cohort.
      Another difficulty  with  the Mancuso (1979)  study,  as with his earlier
 studies,   is  a  lack of discussion of  other  exposures  these workers may have
 received.   The author observed  that the  main effect (lung cancer) occurred  in
 short-term  employees  more  than 15  years after  initial  employment.    These
 workers had an opportunity to be exposed to other potential carcinogens at jobs
 they  may  have  held prior to  or  immediately  following  their short  employment in
 the beryllium  industry.  This is  a distinct  possibility  because the  beryllium-
 manufacturing  companies  are  located in or near heavily  industrialized  areas of
 Ohio  (Cleveland, Toledo)  and Pennsylvania (Reading).  Roth (1983) reports the
 presence  of several industries in  the Lorain, Ohio area in the  period  from
 1942  to 1948 that conceivably could  have provided an opportunity for short-
 term  employees to  receive exposure  to potential carcinogens (Table 7-12).
       Another serious omission of  the  Mancuso (1979) study  is the  lack  of  a  dis-
 cussion of  the effect of cigarette smoking  on the target  organ  of interest,
 i.e.  the  lung.  With respect  to-the question of smoking,  it would  appear  likely
 that  since  there was considerable  overlap  between this study and the Wagoner
 study,  it is probable that most of the lung cancer victims in the Pennsylvania
 cohort of the  Mancuso study  were  smokers.   Hence,  it  is  possible  that  cigarette
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              TABLE 7-12.  INDUSTRIES IN THE LORAIN AREA 1942-1948
    Company
      Operations
Approx. No. Employees
 National Tube
 (now U.S. Steel)
 Thew Shovel
 Lorain Products

 American Crucible

 Iron Ore Ship Dock
Foundry, rolling, extruding,
 coke ovens
Foundry, machining, fabricating
Electrical conductors,
 fabricating, nonferrous foundry
Structural steel parts, machining,
 fabricating, foundry
Unloading-ore
       12,000

        2,000
          500

          200
 Source:  Roth (1983).

 smoking  contributed to the  increased risk of lung cancer in the Pennsylvania
 cohort.   No information was  provided in the Ohio portion of the Mancuso study
 regarding the  smoking influence,  an exposure of  considerable importance  in  lung
 cancer.   The findings of  significant excesses of lung cancer  in both plants
 must be  seen as  limited  because  of the  inadequate consideration of  the con-
 founding effects  of  these two likely exposures,  the  problem with  the NIOSH
 life-table programs,  and  the inadequate nature  of social security quarterly
 earnings reports  in defining  an occupationally-exposed cohort for study.

 7.2.9  Mancuso  (1980)
     In  the  fourth update  to  his  study of workers  potentially exposed to  beryl-
 lium in  two beryllium-manufacturing facilities,  Mancuso (1980)  found statisti-
 cally  significant elevated risks of  lung cancer in 3685 white  males employed
 during the period from 1937  to 1948  and followed until the end of  1976, when
 contrasted with viscose  rayon workers.   The  beryllium cohort,  as  mentioned
 earlier,  was derived  from quarterly  earnings reports filed with the Social
 Security  Administration  by the two companies.   The only  new addition to this
 latest update  was the introduction of a new  comparison  population,  that of
 viscose  rayon workers.   The source or location  of these  workers, however,  is
 not  mentioned by  the  author, who states  that the "viscose rayon cohort" was
 derived  from one  company's "complete" file  of microfilmed  employment data  on
 employees  first hired  during the period  from  1938 to  1948  and  followed  until
 1976 (a  period  which  began one year later than that of the beryllium cohort).
The origin and description of this group of workers is inadequately discussed.
                                     7-48

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     Lung cancer mortality  experience  in the beryllium cohort was  contrasted
with that expected,  based on rates specific to age and duration of employment
generated from the  mortality experience of the viscose rayon worker cohort.
Rates were based either on the total group  of  employees  in  the  viscose  rayon
industry, or on employees with permanent assignments to  only one department,
according to the author.   Presumably,  those who moved  from  one  department  to
another  were  excluded  from  the  lung cancer death rate calculations  in  the
second  method.   No  rationale  is presented  by  the author  to  explain why
mortality in  beryllium workers  should  be contrasted  with  expected  deaths
derived  in these two separate ways.  However, the net result was two separate
sets of  expected lung cancer rates  that differed considerably from  each  other.
Mancuso  observed 80  lung cancer deaths  in his  beryllium  cohort of employees
from the two  companies combined,  as compared to 57.06  expected  deaths based on
the former set  of  derived rates and 50.63 expected deaths based on the latter
subset  of  employees working their  entire  time  in  only one  department.   The
author did not  compare his beryllium workers on the basis of time since onset
of employment, but  did contrast them by duration  of  employment.  He found a
statistically significant excess  risk  of lung cancer  in employees who had been
employed for one year or less, and  also in employees who  had been employed  for
four or more years by the beryllium companies.  No basis was given for choosing
four years of  total  employment as the  point  at  which  short-term workers  should
be  separated  from  long-term  workers.   In his  earlier  versions, the author
utilized different  durations  of employment,  i.e.   five  quarters  (1  1/4 years)
and five-year duration  of employment categories.
     An  interesting  omission  from  this study  is  any consideration  of  the
effects  of latency  according to duration of employment.   It  seems unusual that
a discussion  of  this topic was not included by Mancuso, since the major  output
of the  NIOSH  life-table program, which  was  utilized  by Mancuso, is a set of
tabulations by  time  since onset of employment.  Lung cancers diagnosed within
ten years of initial  exposure probably were not a consequence of that exposure.
Furthermore,  the  designation  "duration of  employment"  is   not  necessarily
uninterrupted  continuous employment.   In  reality, what  is  meant  is "total
employment", that  is periods of time when the  employee was not  exposed or  not
actually working.  Layoffs and terminations, sickness, vacations, and leaves of
absence  between  initial employment and final day  of employment  are  not counted
by  the  NIOSH  life-table program in the category  "duration of  employment."
                                     7-49

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 Therefore, it is  possible  that included in the observed deaths are the deaths
 of individuals who  had  worked only a few  days  for the  companies and who died
 from lung cancer  20 years  later,  as well  as  individuals  who worked for the
 companies for several years  continuously,  but who died within  five years  of
 initial  employment.
      Additionally, the viscose rayon cohort  appears  to have been  a somewhat
 younger  population by age  at hire than  was the beryllium  cohort (47.2  percent
 in the  viscose  rayon  cohort were under  age  25 when  hired, compared to the
 beryllium cohort in which 38.4 percent were under age 25 when hired).   Whether
 or not the author  adjusted  for age differences is  questionable.   Indeed, at the
 Peer Review Workshop on  the Health Assessment  Document  for Beryllium (U.S. EPA,
 1983)  sponsored  by the U.S. Environmental Protection Agency, an epidemiologist
 from NIOSH, Dr. Jean  French, expressed  concern that the age adjustment in
 Mancuso's comparison of expected mortality based on viscose rayon workers with
 that of  actual  mortality from Mancuso's  beryllium cohort was  "inadequate"
 (Dakin,  1984).   Dr.  French  reported that NIOSH  reanalyzed the data and found
 serious  problems  with Mancuso's analysis.  Efforts to  resolve this issue have
 not been successful  through official NIOSH channels.   Unsuccessful  attempts  to
 obtain  the results  of the   analysis  from NIOSH  have made it difficult to
 determine the magnitude  of  impact  of the  required adjustment on  risk estimates.
 Since the viscose  rayon cohort was younger than the  beryllium cohort,  the net
 impact  of an adjustment would  be  to decrease the gap  between  observed lung
 cancer deaths  based  on the  beryllium cohort  and expected deaths based  on  the
 viscose  rayon cohort.
     Another problem concerns the  acquisition of cause-of-death data.   Some
 4.3 percent of the  reported deceased members  of the  viscose  rayon cohort
 remained  without a cause of death, compared to only 1.5 percent of the beryl-
 lium cohort.   This could potentially lead  to  a greater underestimate of lung
 cancer  in the  viscose rayon  cohort  compared  to the beryllium cohort if the
 causes of death in these two groups were fairly evenly distributed.
     As  in the  earlier studies by the same author, a further difficulty with
 this study is  its  lack of discussion of  the confounding effects  of  smoking and
 its disregard  of potential  exposures received not only while working for the
 beryllium  companies, but also in jobs prior and subsequent to employment in the
beryllium  industry.   This represents a  particular problem  because a  large
majority  of this cohort  worked for less  than  one year.   Because the towns  in
                                     7-50

-------
which the beryllium  companies  were located were considerably  industrialized,
work in  these  industries  could potentially have produced  exposures  to other
known or  suspected  carcinogens.   As an example, one of the major employers in
the  Lorain,  Ohio  area in the period  from  1942 to 1948 was the National Tube
Company  (now U.S.  Steel),  whose operations involved extensive  exposure to coke
ovens.  Nothing is revealed in the study of the origin or makeup of the viscose
rayon cohort.  What  is known about its location comes from the Wagoner et al.
.(1980) study in  which the authors stated  that Mancuso's viscose rayon cohort
was  located  in the vicinity of the beryllium companies.
     Furthermore,  since  both cohorts  utilized the NIOSH life-table program,
both suffer  from the previously discussed  11-percent underestimation of expected
lung cancer  deaths.
     In  conclusion,  despite the author's certainty  regarding the existence of  a
causal relationship  between beryllium exposure and lung cancer,  the evidence
presented in this study is  not convincing  because  of the many  limitations of the
study, as described  above.  Hence  it would appear  that the study is at best only
suggestive of  an  increased  risk of lung cancer due  to exposure to beryllium.

7.2.10   Summary of Epidemiologic Studies
     Although  several  studies claim a statistically significant excess risk of
lung cancer  in individuals exposed to beryllium, all of the studies cited have
deficiencies that limit  any definitive conclusion that a true association
exists.   Support for a finding  of an excess  risk  of lung  cancer in beryllium-
exposed  persons  consists  of evidence  from  cohort mortality  studies  of  two
companies (Table 7-13) and one cohort mortality study of cases admitted to the
Beryllium Case Registry.  None of these studies can be  said to be independent,
 since all are studies of  basically  the  same groups of workers.   Extensive
 cooperation  existed between the authors  of  all of these studies, even to the
 extent of running all  cohorts through a NIOSH computer-based  life-table program
 known to produce an 11-percent underestimate  of expected lung cancer  deaths at
 the time.   This  problem has  since  been  remedied.   Furthermore, the  authors
 could not adequately address the confounding effects of smoking or of exposures
 received during prior and  subsequent employment in other non-beryllium indus-
 tries in the  area  known  to produce potential  carcinogens  (especially  in  beryl-
 lium workers  with  short-term employment).  Problems in the design and conduct
 of the studies further weaken the strength of the findings.   There appeared to
                                      7-51

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 be a  tendency on the part of the authors to overemphasize the positive nature
 of their  results and minimize the contribution of qualifying factors.  A list
 of these  problems  is presented in Table 7-14.   If  the errors  detailed in the
 preceding paragraphs were  corrected  and proper consideration given to address-
 ing the  problems described above, the  finding of a significant excess  risk
 would probably  no  longer be apparent, although the possibility, nevertheless,
 remains that  a portion  of the remaining  excess lung  cancer  risk may  be
 partially due to beryllium exposure.
      The International Agency  for Research  on  Cancer  (IARC)  has concluded that
 beryllium and its  compounds  should  be classified as "limited"  with respect  to
 the human epidemiologic  evidence of  carcinogenicity.   This can  be  explained by
 the fact that IARC uses  only published information to  weigh the carcinogenic
 evidence for  any given  substance.   In the  case of beryllium, more  recent
 tabulations  and analyses of  the major study cohorts than those found in the
 published  reports  were  available  to  CAG.   These tabulations  included some
 corrections  to the data  base and were prepared using the more accurate updated
 NIOSH  life-table program.  Thus, based upon  the analysis of this newer informa-
 tion,  CAG  regards the epidemiologic  evidence of beryllium carcinogenicity in
 beryllium-exposed workers as, inadequate.
7.3  QUANTITATIVE  ESTIMATION
     This  quantitative section deals only with estimation of the unit risk for
beryllium  as a  potential  carcinogen  in  air, and  compares  the potency of
beryllium  to other carcinogens that  have  been  evaluated by the CAG.  In the
Ambient  Water Quality  Criteria Document for Beryllium,  (U.S.  EPA,  1980)  an
upper-limit  potency estimate  for ingestion was derived  from the Schroeder and
Mitchener  (1975a)  drinking water  study.   The  value derived  in  the water
document may have  been overly conservative,  however, since negative results  at
much  greater doses  have been  obtained, in earlier  studies.   In the  only
ingestion study  in which a significant tumor  response was reported (Morgareidge
et a!.,  1977, abstract),  the  results were  considered  to be  equivocal  for
reasons discussed in Section 7.1.7.  Moreover, this study was only published in
abstract form.   Because no study  is  available  in which  tumor  induction was
definitively  shown,  a  potency estimate for beryllium  via the  ingestion  route
was not derived  in this document.
                                     7-54

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                      TABLE 7-14.   PROBLEMS WITH BERYLLIUM COHORT STUDIES
Bayliss et al.  (1971)
Bayliss and Lainhart (1972)
Bayliss"and Wagoner (1977)
        and
Wagoner et al. (1980)
Mancuso and El-Attar (1969)
Mancuso (1970)
 Mancuso  (1979)
 Mancuso  (1980)
A.   Loss of 2000 individuals because of insufficient data.
B.   No latency considerations.
C.   Combined study populations of several plants from two
    companies.

A.   Includes clerical and administrative personnel with no
    exposure.
B.   No independent assessment plant employment files.
C.   Latency after 20 years not assessed.

A.   Cigarette smoking a possible confounder.
B.   Underestimate of expected lung cancer deaths in
    comparison population by 11 percent.
C.   Inclusion of 1 lung cancer victim who did not fit
    definition for inclusion.
D.   Loss of 295 individuals from study cohort.
E.   Exposure to potential carcinogens prior and post
    beryllium employment.

A.   Unidentified comparison population.
B.   Internal rates based on small numbers.
C.   Tremendous variability and impossible to test
    significance.
D.   .No smoking consideration as possible confounder.

A.   Internal  rates based on small numbers.
B.   Inappropriate comparison  (age group  15-24 left out of
    comparison).
C.   No consideration of smoking as a possible confounder.
D.   No consideration of latency.
E.   Exposure  to potential carcinogens prior and post
    beryllium employment.

A,  Underestimate of expected  lung cancer deaths  in
    comparison population by  11 percent.
B.  No consideration of smoking as a possible confounder.
C.  Incomplete delineation  of  cohort from use of  Social
    Security Quarterly Earnings reports.
D.  Exposure to potential carcinogens prior and post
    beryllium employment.

A.  No consideration of  latent effects.
B.  Probable lack of age  adjustment.
C.  No  consideration of  effects of  smoking.
D.  No  description  of  origin or makeup  of comparison
    cohort except for  age.
E.  Underestimate of expected lung  cancer deaths
     in  comparison population by 11  percent.
                                           7-55

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      The  unit risk for an air pollutant is defined as the incremental  lifetime
 cancer  risk to humans from daily exposure to a concentration of 1 jjg/m3 of the
 pollutant  in  air by inhalation.  The  unit  risk estimate for beryllium repre-
 sents an  extrapolation below the dose  range  of experimental data.  There is
 currently  no  solid scientific basis for any  mathematical  extrapolation model
 that relates  exposure to  cancer risk  at the extremely low concentrations,
 including  the unit concentration  given above,  that  must be dealt with  in
 evaluating  environmental hazards.   For practical reasons, the correspondingly
 low levels  of risk cannot  be measured  directly either by animal  experiments  or
 by epidemiologic  studies.   Low-dose extrapolation  must,  therefore, be  based  on
 current understanding of the mechanisms of carcinogenesis.
      At the present time,  the  dominant view of the  carcinogenic  process
 involves the  concept that  most  cancer-causing agents  also cause  irreversible
 damage  to DNA.   This position is based in  part  on the fact  that  a very large
 proportion of agents that  cause  cancer  are  also  mutagenic.   There  is reason  to
 expect  that a quanta!  response characteristic of mutagenesis  is  associated with
 a  linear (at low doses) nonthreshold dose-response  relationship.   Indeed,  there
 is substantial evidence from  mutagenicity studies with both  ionizing radiation
 and a wide  variety  of  chemicals that this  type  of dose-response model  is the
 appropriate one to  use.  This is particularly true at  the lower  end  of the
 dose-response  curve; at high  doses, there can be an upward curvature,  probably
 reflecting  the effects of multistage processes on the mutagenic response.   The
 linear  (at low doses)  nonthreshold  dose-response relationship is  also  consis-
 tent  with the relatively  few epidemiologic studies  of cancer responses  to
 specific agents  that contain  enough  information to make the evaluation  possible
 (e.g.,  radiation-induced leukemia,  breast  and thyroid cancer,  skin cancer
 induced by arsenic  in drinking water, liver  cancer induced by aflatoxins in the
 diet).   Some supporting evidence also exists from animal experiments  (e.g. the
 initiation  stage of the two-stage carcinogenesis model  in rat liver and mouse
 skin).
     Because its  scientific basis,  although  limited,  is the best of any of the
 current  mathematical extrapolation models,  the  nonthreshold  model,  which is
 linear at  low  doses, has been adopted as the primary  basis  for  risk extrapola-
 tion to  low levels of the  dose-response relationship.   The  risk  estimates  made
with such  a  model should be regarded as conservative,  representing a plausible
 upper limit  for  the risk,  i.e. the  true risk is  not  likely to be  higher than
the estimate, but it could be  lower.
                                     7-56

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     For several reasons, the  unit risk estimate based on animal  bioassays is
only an approximate  indication  of the absolute risk in populations exposed to
known carcinogen concentrations.   First,  there are important species differ-
ences in uptake, metabolism, and  organ  distribution and  elimination of carcin-
ogens, as well as species differences in target-site susceptibility,  immunolog-
ical responses,  hormone  function,  dietary factors, and  disease.   Second,  the
concept of equivalent  doses  for humans as compared to animals on a mg/surface
area basis is  virtually  without experimental verification with respect to the
carcinogenic  response.   Finally,  genetic constitution,  diet, living  environ-
ment, activity patterns, and other  cultural  factors  are quite varied among
different human populations.
     The unit  risk estimate can give a rough indication of the relative potency
of  a  given agent as compared with other  carcinogens.   Such  estimates are,  of
course, more  reliable  when  the comparisons are  based  on studies  in which the
test species,  strain, sex, and routes of exposure are similar.
     The quantitative  aspect  of carcinogen risk assessment  is  addressed here
because of its possible  value in  the  regulatory decision-making process, for
example,  in  setting regulatory  priorities,   evaluating, the adequacy  of
technology-based controls, and so forth.  However, the imprecision of presently
available technology for estimating cancer risks  to  humans  at  low levels of
exposure  should be  recognized.  At best,  the linear-extrapolation model  used
here  provides  a rough but plausible estimate  of the upper limit of risk—that
is, with this  model  it is not likely that true risk would be much more than the
estimated  risk, but it  could be  considerably lower.   The  risk estimates
presented in  subsequent  sections  should not be regarded, therefore, as accurate
representations of the true cancer risks, even when the exposures involved are
accurately  defined.   The estimates presented  may,  however,  be factored  into
regulatory decisions to  the extent that  the  concept  of upper-risk limits  is
found to be  useful.

7.3.1 Procedures  for  the Determination  of Unit  Risk
7.3.1.1   Low-Dose Extrapolation Model.   Two  dose-response  models, which  are
derivatives  of the  theory of multistage  carcinogenesis, are  used  to  calculate
the unit risk of beryllium on  the basis  of animal  data.   The  selection of these
two models is  dictated  by the  nature of the  data  available  for  quantitative
risk assessment.  The first model,  a multistage model  that  allows for a time-
                                      7-57

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 dependent  dose pattern, was developed  by Crump and Howe (1984), and uses the
 theory  of multistage  carcinogenesis developed by  Armitage  and Doll (1961).
 The Armitage-Doll multistage model  assumes  that a cell  is capable of generating
a  neoplasm when it has  undergone  k changes  in  a  certain  order.   The 'rate,
       ,th

of the iul change  is  assumed  to  be  linearly  related  to  D(t),  the  dose  at  age  t,
i.e.  r.j  = a.j + b..D(t), where a.,  is  the  background rate,  and  b. is  the propor-
tionality  constant for the dose.  It can be  shown  that the probability of
cancer by age t is given by
                            P(t) = 1 - exp  [-H(t)]
 where
H(t) =  J
                           {Ca
                                           [(ak + bRD(uk)]} dur..duk
is the cumulative incidence rate by time t.
     When H(t)  or  the risk of cancer is small, P(t) is approximately equal to
H(t).  When  only one stage is dose-related, all proportionality constants are
zero except for the proportionality constant for the dose- related stage.
     This model  will  be applied to the data in Reeves and Deitch (1969) where
the dose  D(t)  is constant for t in an interval [s.,, s^]  and is zero elsewhere.
Under this particular exposure pattern and the assumption  that only a single
stage is dose-related, the term H(t) can be written as the sum of two . components
H1(t) and Hg(t)  where H-^t) = 3-!^  •  a2 . . .  ak tk/k!  represents the  background
cumulative incidence  and H2(t) is the incremental cumulative incidence due to
exposure.  Three special  cases of FL which are often used to interpret a given
set of data are given below.
H2(t) =
                )
           k!a.
                    x
                       0
                       (t -
                                                                 t < s.
s-, < t <
                         (t - Sl)  - (t - s2)
if the first stage is affected (t = 1),
                                     7-58

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H2(t)  =
  db-L(na1-)
            k!a
               k-1
          Ckt "  (k "
         (k-l)s2]
                                              .k-1
                                                 [kt -
if the penultimate stage is affected (r = k - 1), and
                                                                   t <
                                                                   s, < t <
H2(t) =
db,(7ia.)     tk
—±5——  x  L
  k! a.
' s
                                                                        '1

                                                                        t
                         2     1   ... .                                2 ~

 if the  last  stage  is  affected  (r = k).

      A  computer  program, ADOLL1-83,  has  been  developed by Crump and Howe  (1984)
 to implement the computational aspect of the  model.   In this  program, the model
 is generalized to  include  tumor  induction time I  by replacing the time factor t
 by  t-I.  The best-fit model is identified as the one that  has  the maximum
 likelihood  among various models with  different numbers of stages  and the stage
 affected by the  exposure.
      The second model  used  to calculate the  carcinogenic potency of beryllium
 is  the  one-hit model  with  zero background rate.   This model  is used because all
 the  experiments, except that  of Reeves and  Dei ten  (1969),  had only one data
 point and did not have a control group.  The slope,  b,  of the one-hit model,
 P(d) = 1 -  exp(-bxd), is calculated by the formula

                                b = [-Ln(l-P)]/d

 Since  the  background rate is zero, the least-square estimate  b,  as  calculated
 above,  is also  a maximum-likelihood estimate.
                                       7-59

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 7-3.1.2  Selection of Data.  For some  chemicals,  several  studies  in different
 animal  species, strains, and sexes,  each run at several  doses  and different
 routes  of exposure, are  available.   A choice must be made as to which of the
 data sets from several  studies  to  use in the model.   It  may  also be appropriate
 to correct  for metabolism differences  between  species and  for absorption
 factors via  different routes  of  administration.   The  procedures used  in
 evaluating these data are  consistent with  the approach of making  a maximum-
 likelihood risk estimate.   They are as  follows:

      1.    The  tumor incidence data are  separated  according  to organ sites or
 tumor types.   The  set of  data (i.e.,  dose and tumor incidence) used in the model
 is the  set where the incidence is significantly higher  statistically than the
 control  for at least one test dose level and/or where the tumor incidence rate
 shows a statistically significant trend  with respect to dose  level.' The data
 set that gives the highest estimate  of the  lifetime carcinogenic risk, q*  is
 selected in most cases.   However, efforts  are made  to exclude data sets  that
 produce spuriously high  risk estimates  because of a  small number  of animals.
 That  is,  if  two sets of data show a similar  dose-response  relationship, and one
 has  a very small sample size,  the set of data having  the larger sample size  is
 selected for calculating the carcinogenic potency.
      2.     If  there are two or  more  data sets of comparable  size  that are
 identical  with respect  to species,  strain,  sex,  and tumor sites, the geometric
 mean  of q*,  estimated from each of these data sets,  is  used for risk assess-
 ment.  The geometric mean of numbers Ap Ap,  ..., A ,  is defined as

                            f&  v A  v     v  A \1/IU
                            V.*«1  " ••o " • • • AMI
                              12          m

     3.    If two or more  significant tumor  sites  are observed  in the same
 study,  and  if  the  data are available, the number of animals with at  least one
 of  the  specific tumor  sites under consideration is used as  incidence data in
 the model.

7.3.1.3   Calculation of Human Equivalent Dosages.   Following  the suggestion of
Mantel  and  Schneiderman  (1975), it is assumed that mg/surface area/day is an
equivalent dose  between  species unless adequate evidence  is  presented to the
                                     7-60

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contrary.   Since, to a close approximation, the surface area is proportional to
the two-thirds power  of  the weight,  as  would be  the  case  for  a perfect  sphere,
the exposure in mg/day per two-thirds power of the weight is also considered to
be  equivalent  exposure.   In  an animal experiment,  this  equivalent dose is
computed in the following manner.
 Let
      L  =  duration  of  experiment
      e
      1   = duration  of exposure
       e
      m = average dose per day in mg during administration of the agent (i.e.
          during le),  and
      W = average weight of the experimental animal during the exposure period.
 Then, the lifetime exposure is
                                  d =
  73131   inhalation exposure.   Often it is  necessary to convert given expo-
  sures  into mg/day.  When exposure  is  via inhalation, the calculation of dose
  can be considered for two cases.   In the first case the carcinogen is a poorly
  water-soluble gas which reaches  equilibrium  between the  air breathed and the
  body compartments.  After equilibrium  is  reached,  the uptake of such gases  is
  expected to  be proportional  to  the metabolic rate, which is itself  a function
  of surface area  and  is  thus not limited by the respiratory exchange rate.   In
  the second case,  in  which the carcinogen  is  in the form  of  either a  completely
  water-soluble gas, or an  aerosol,  uptake is  respiration  limited.   This  form
  will  be considered  here.   For aerosols, the  dose  in mg/day can be expressed
  as-   m  =  I x C x de, where  I equals the respiratory exchange rate  in m /day, C
  equals  mg/m3 of  the agent,   and  de equals  the deposition fraction.   Particle
  clearance  rates  may also influence the bioavailable dose, but such  information
  is seldom available  for  the same types of  particles  in  both  humans  and
  laboratory animals.
                                        7-61

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      The  inhalation  rates,  I, for various  species  can be calculated from the
 observations of  the  Federation of American Societies  for Experimental Biology
 (FASEB, 1974)  that  25-g mice breathe 34.5  liters/day  and 113-g rats breathe
 105 liters/day.   For mice and rats  of  other weights,  W  (in  kilograms),  the
 surface area proportionality  can be used to find breathing rates in m3/day as
 follows:

                     For mice, I = 0.0345 (W/0.025)2/3 m3/day

                     For rats, I = 0.105 (W/0.113)273 m3/day

 Respiratory values  for most  other  laboratory species are  also  reported  by
 the Federation of American Societies  for  Experimental Biology (1974).   For
 humans,  the value of  20  m /day* is  adopted as a  standard breathing rate
 (International  Commission on  Radiological  Protection,  1977).  The equivalent
 human  concentration  [Ch] can be derived from the experimental air concentration
 by the following  formula    ;

where  a and h refer  to  animals and humans, respectively.  An  adjustment for
deposition  efficiency can also be  made  if adequate data are available.  The
equivalent  human dose can be determined  by
                                  d -
                                        W
7.3.1.4  Calculation of the Unit Risk from Animal Studies.  The risk associated
with d mg/kg   /day is obtained from GLOBAL86 (Howe et a!., 1986), and for most
cases  of interest to  risk assessment,  can  be  adequately  approximated by
P(d) = 1 - exp (-q*d).  A "unit risk" in units X is simply the risk correspond-
ing to an exposure of X = 1.  This value is estimated by finding the number of
*From "Recommendation of the International Commission on Radiological Protec-
 tion," page 9.  The average breathing rate is 107 cm3 per 8-hour workday and
 2 x 107 cm3 in 24 hours.

                                     7-62

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ing/kg2'3/day that corresponds to one unit of X, and substituting this value into
                                                                      2
the above  relationship.   Thus,  for example, if X  is  in units  of [ig/m  in the
                                     1/o     --3      O/3
air, then  for  case 1, d = 0.29  x 70 '   x 10   mg/kg   /day, and for case 2,
                ^
d = 1, when ug/m  is the unit used to compute parameters in animal experiments.
     Note  that  an  equivalent method of calculating unit risk  would be  to use
mg/kg for the animal exposures, and then to increase the j
cient by an amount
                                                          -th
                        polynomial  coeffi-
                         (wh/wa)
                                J/3
j = 1, 2,
k,
and to use mg/kg equivalents for the unit risk values.
7.3.1.4.1  Adjustments  for  less than life span duration  of  experiment.   If the
duration of experiment  L  is less than the natural life  span of the test animal
L, the slope q?, or more generally the exponent g(d),  is  increased by multiply-
ing by  a factor (L/L )3.   We  assume  that if the average dose d is continued,
the age-specific  rate of cancer will continue to  increase  as a constant func-
tion  of  the background rate.  The  age-specific  rates for  humans  increase at
least by the second power of the age and often by a considerably higher power,
as demonstrated by Doll  (1971).  Thus, it is  expected that  the cumulative  tumor
rate  would  increase by  at least the third power of age.   Using this fact,  it  is
assumed  that the  slope  q*, or more generally the exponent g(d),  would also
increase by at least the third power of age.  As a result, if the slope q£ [or
g(d)] is calculated at  age L  , it  is expected that  if the  experiment  had  been
continued  for the full life span L at the given average  exposure, the slope  qj
 [or g(d)] would have  been  increased by at least  (i-/Le) .
      This  adjustment is conceptually consistent  with the proportional hazard
model proposed by Cox  (1972)  and the time-to-tumor  model considered by Daffer
 et al.  (1980), where the probability of cancer by age t  and at dose d  is given
 by

                         P(d,t) =  1  -  exp [-f(t)  x g(d)]

 7.3.1.5  Model for Estimation of Unit Risk Based on Human Data.    If human epi-
 demiologic studies and sufficiently  valid.exposure'information are available
 for  a compound,  they are always used in  some way.   If they show a carcinogenic
 effect, the data  are analyzed to give an estimate of the linear dependence of
 cancer  rates  on  lifetime  average  dose,  which is  equivalent to the factor BH-
                                      7-63

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 If they show no carcinogenic effect when positive animal evidence is available,
 then  it  is  assumed that a  risk  does  exist,  but it is smaller than  could have'
 been  observed  in  the epidemiologic study.  An upper limit to the cancer inci-
 dence  is  calculated,  assuming hypothetically that the true incidence is below
 the level of  detection in the cohort  studied,  which  is  determined  largely  by
 the cohort  size.   Whenever  possible,  human  data are  used  in preference to
 animal bioassay data.
      Very little  information exists that  permits extrapolation  from  high-
 exposure occupational  studies to exposures at low environmental  levels.   How-
 ever,   if  a  number of simplifying assumptions  are made,  it is possible to
 construct a crude  dose-response  model  whose  parameters can  be estimated  using
 vital  statistics,  epidemiologic  studies,  and  estimates of worker  exposures.
      In human studies, the  response  is measured in terms of the  relative risk
 of the exposed cohort of  individuals as  compared with the control group.  The
 mathematical  model employed  for  low-dose extrapolation assumes that for low
 exposures  the  lifetime probability of death from cancer,  PQ,  may  be  represented
 by the linear  equation

                           :        po =  A  +  V

 where  A is the lifetime probability in the absence of  the agent, and x is the
 average lifetime  exposure  to environmental levels  in  units  such  as  ppm.   The
 factor BH  is the  increased  probability of cancer associated  with each  unit
 increase of x, the  agent in air.
     If it  is  assumed that R, the relative risk of cancer for exposed workers
 as compared  to  the general  population,  is independent  of length of exposure  or
 age at exposure,  and  depends only upon average  lifetime exposure, it follows
 that
                                    A +
x2)
                                       A + BH xl
or
                             RP0 = A + BH
                                     7-64

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where x, = lifetime average daily exposure to the agent for the general popula-
tion, x? =  lifetime average daily exposure  to  the agent in the occupational
setting, and PQ = lifetime probability of dying of cancer with no or negligible
exposure.
     Substituting PQ = A + BH (x-^ and rearranging gives

                               BH = PQ (R - l)/x2
To  use  this  model, estimates of  R  and x,, must be obtained from epidemiologic
studies.  The  value PQ is derived by means of the life-table methodology fron
the  age-  and cause-specific death rates  for  the general  population found in
U.S. vital statistics tables.
7.3.2  Estimation of the Carcinogenic Risk of Beryllium
     In  extrapolating  from  animal  data, the  equivalent human  dose  may be
influenced  by a  variety  of factors.   An  important variable for inhalation
studies  is  measurement (or  estimation) of  ventilation.   Since it has  been
shown  that  ventilatory exchange  rates  generally  vary with  metabolic  rate
(McMahon  et al.,  1977), it  could  be assumed that human and animal  equivalent
concentrations  are the same.  As  described  in Section 7.3.1.3.1, however, a
more  conservative approach  is  made.  Resting values  are  used  for  estimated
animal  respiration,  while 20 m /day is  assumed  for humans, a rate well above
resting  values.   Based on this method,  the  human equivalent concentration is
only  38 percent that of a 350 gram  rat.  Such a method is reasonable, however,
           Q
since  20 m  /day is based upon normal 24-hour  activity levels.   Animal  inhala-
tion  exposures,  on the other hand,  are most often conducted during  the time
period when the animals are normally inactive,  or sleeping,  with accompanying
low levels  of respiration.
     The efficiency of  deposition  may  also influence the equivalent  human
dose.   For  most particles in the  respirable size  range the fraction  deposited
in the alveoli  and smaller conducting airways  would be predicted to be  somewhat
less  in rats than  in  humans (Raabe et  al., 1977;  Lippman, 1977; Schlesinger,
1985).   At submicron sizes  the  differences  decrease and may disappear  at very
small  particle sizes.   Among these  studies, deposition varied  greatly within
species due  to  breathing patterns  and experimental  techniques.   For  many
studies, the standard of the means overlapped for  humans  and  rats exposed to
                                      7-65

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 comparable particle sizes.  Due  to the variability in deposition efficiency,
 an adjustment  in  dose based on this variable  was  not incorporated into the
 quantitative assessment of  risk.   As more data become available, however, such
 adjustment should be  carried  out.   Oberdoerster  (personal communication) has
 developed methodology  to adjust for both deposition efficiency and  lung  surface
 area.   This method is  outlined in Section 7.3.2.1.
      Retention  of particles can be an  important factor for determining dose to
 the lung,  since  the  degree of solubilization  and absorption is related to
 residence time.  Humans normally  clear inhaled particulate matter more  slowly
 than  small laboratory animals  and thus might be expected to absorb a greater
 percentage of a deposited dose (Pepelko,  1987)^   Rhoads  and Sanders  (1985),
 however,  reported a clearance  rate  half-time for  beryllium oxide particles in
 rats  of 833 days.   The  slow clearance  rate  suggests that the majority of the
 beryllium is solubilized, absorbed, and  retained  intracellularly in the cells
 lining  the lung,  probably by reaction with macromolecules.  Reeves  and Vorwald
 (1967)  found that following cessation  of exposure to  beryllium sulfate about
 one-half  the pulmonary load was  cleared  within a  few weeks, but the remainder
 tended  to remain  for much longer periods.  They also theorized that the beryl-
 lium  probably became incorporated into the nucleus of certain pulmonary cells.
 Since  clearance is  apparently quite slow  in the rat, it is  doubtful  that
 clearance rate  differences between humans and laboratory animals will result in
 important differences  in the percentage of deposited dose absorbed.
     Finally, consideration should be given to the appropriateness of a surface
 area  versus a  body  weight correction  of inhaled  dose.   Dose corrections
 compensating  for  metabolic rate differences  are largely based  on  the belief
 that a  smaller  animal, with a  correspondingly more rapid metabolic rate, will
 inactivate  or eliminate  potentially harmful   xenobiotics more rapidly.   On the
 other hand,  if  the chemical  requires activation,  and the  rate  limiting step is
 along the activation pathway,  then it may not be correct to adjust dose based
 on  surface area.   If activation is required,  the  relationship  between  exposure
 levels and the  area under the time-concentration curve of the active metabolite
 should be determined.   There is no evidence  to date,  however,  that  beryllium
 requires  activation.
     Some  evidence indicates that beryllium may be  sequestered  in  the cells
 lining the alveoli  and bronchioles and is inactivated, or eliminated  slowly.
According to Vorwald et al. (1966), inhaled beryllium aerosols are precipitated
                                     7-66

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by lung fluids,  but  then  hydrolysis  results  in  a  supply  of  beryllium  ions that
enter the cell  and  react with macromolecules,  possibly  DNA and  RNA.  Vorwald
and Reeves  (1959) found that 85  percent of subcellular beryllium sedimented  in
the nuclear  fraction.   Any conclusions  were  limited since the  actual  localiza-
tion  of  beryllium could  not  be  shown by biochemical means.   Firket  (1953),
however, was  able to identify beryllium histochemically in the  nucleolus, an
organelle made  up of macromolecules  including  RNA.   If  beryllium reacts with
macromolecules  and  no mechanism is available for elimination or deactivation,
then  toxic  dose levels are not  likely  tp  correlate well with  metabolic rate.
Although the data suggest that  beryllium  may  be  bound intracellularly and is
eliminated  very slowly, the evidence is not sufficiently  conclusive to show
that  a dose  adjustment  based  on  metabolic  rate  is not  correct.
      The  direct experimental  evidence  available  to determine if  the rat  is
uniquely  susceptible  to the  carcinogenic effects  of beryllium,  is quite
limited.   While no  definitive positive results  are  available for hamsters,
Wagner  et  al.  (1969)  reported  atypical  proliferations  in animals  of this
species  exposed to  beryl  ore at  beryllium  levels  of 620  ug/m3, a dose producing
tumors  in 18 of 19  rats.  The authors would have  considered these prolifera-
tions to be  bronchoalveolar  tumors  except for their  small  size.  It is quite
possible that  these proliferations  would have progressed to tumors if the
 hamster had a longer life span.
      Although  statistically  significant positive  responses were  not seen  in
 guinea pigs, Schepers  (1971)  reported  the occurrence  of lung  tumors  in  2 of 20
 animals exposed to  beryllium sulfate and in 1 of 30 males  and 1 of 20 females
 exposed to  beryllium oxide.   Since lung  tumors  are  extremely rare  in guinea
 pigs, the  data are indicative of a possibly positive response even  if  exposure
 conditions were not well described and control values were not reported.
      The  only  other species  other than  rats  in which  a  clear-cut response
 occurred  was the  rhesus monkey (Vorwald et al.,  1966; Vorwald,  1968).  No
 tumors were detected in five monkeys  dying of pulmonary disease the first two
 years  of exposure.   Eight of  11  monkeys,  however,  surviving  exposure to
 39 MQ/m3  beryllium, an  average of 15 hours per week,  for greater than two
 years  up  to 10 years, developed lung cancer.  Based on  this one study, monkeys
 appear  to  be as  sensitive to  cancer induction  by beryllium as rats.
      The  data  for hamsters and guinea pigs  is only  suggestive, while  the data
  on  monkeys is based upon one study which lacked controls.   Taken collectively,
                                       7-67

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 however, the  evidence suggests that the  rat  is  not uniquely susceptible to
 lung cancer induction by beryllium.   Moreover, the positive results in monkeys,
 a species  much  closer  phylogenetically  to humans than rats,  increases  the
 likelihood  that  humans may also be susceptible.
 7.3.2.1  Calculation of the Carcinogenic Potency of Beryllium on the Basis  of
 Animal  Data.   Of the  studies available for estimating the carcinogenic risk of
 exposure to beryllium,  the majority used  beryllium salts.   Potency values were
 derived from  seven  inhalation studies with beryllium  sulfate,  and one each
 using beryllium  phosphate land beryllium  fluoride.   This  information is
 presented in Table 7-15.  In order to  provide some comparison among species,
 values  for  guinea pigs  and rhesus monkeys were  determined,  even though the
 guinea  pig  study was poorly documented with only suggestive effects, while the
 monkey  study lacked controls.  Except  for the Reeves and Deitch  (1969) study,
 the  investigations  were conducted at single dose levels.   In  these cases, the
 one-hit  model,  as  described  in  Section 7.3.1.1  is  used  as  the low-dose
 extrapolation  model.   For the  data of  Reeves  and Deitch, the  multistage model
 with  time-dependent  dose patterns is  used as the low dose  extrapolation model.
 The data and calculations  for this study are presented in the  appendix.
      In  all  of these calculations, the equivalent concentrations are derived
 by the  following procedure, using ventilatory values arrived  at as described
 in Section  7.3.1.3.1.   For an experimental exposure concentration of 1 ug/m3,
where 0.224 m  /day  is assumed to be the  volumetric breathing rate for a rat
weighing 0.35  kg, and 20 m /day is assumed for a 70-kg man, the  human equiva-
 lent concentration (ug/m ) satisfies the equation

                    C =  (0.224/20) m3/day x (70/0.35)273 kg

or C  =  0.38 ug/m .   Therefore,  the human equivalent concentration in ug/m3 is
obtained by multiplying  the: experimental  concentration by 0.38.   For a 466-gm
guinea pig  with  a reported daily breathing volume of 0.23  m3 (Spector, 1971),
the human equivalent concentration will  equal 0.32 ug/m3.   For a 2.68-kg
rhesus monkey  with a  reported daily breathing volume of 1.24 m3/day (Spector,
1971), the human equivalent concentration will  equal 0.55 ug/m3.
     The  last  column of  Table  7-15  represents the  carcinogenic  potency  of
beryllium as calculated from each of these studies.  Based  on the equivalent
                                     7-68

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human condmtratlon, using  a  surface area correction  the maximum  likelihood
estimate of  slope  (MLE) varied from 4.3  to  3.7 x 10   for  rats  exposed to
beryllium sulfate.  The most  reliable estimate is 8.1 x 10   derived from the
Reeves and Deitch (1969) study.  Beryllium fluoride and beryllium phosphate are
somewhat less  potent  with MLEs of 1.4 x lO'1 and 3.0 x 10  , respectively.   In
comparing  species,  rhesus  monkeys  were  at  least  as sensitive to beryllium
sulfate as rats, while  guinea  pigs were about an order of magnitude less.
      Because  over  99  percent  of  beryllium emitted into the atmosphere is the
result  of  oil or coal  combustion for electric power generation, the chemical
form present in the ambient environment  is  likely to be beryllium oxide rather
than a beryllium  salt  (see  Section 3.4).   Based upon  the  likelihood that
beryllium  oxide is the primary form of human exposure,  an attempt  was  made to
 derive  a quantitative  estimate of  risk for  this compound.   Unfortunately,  the
 available  studies utilizing beryllium  oxide have  even greater  limitations  than
 those employing beryllium  salts.   These  studies are listed  in Table 7-16  in
 order of decreasing  potency.   The  first  study  listed (Wagner et  al., 1969) was
 well designed  and  conducted.   The animals,  however, were exposed to beryllium
 ore   While  the beryllium is  generally  present as  an oxide, it is conjugated
 with fluorides  and  silicates; thus, altering its physical characteristics and
 possibly  its  potency.   In the next study carried out by Sanders et al.  (1978),
 the  animals were given a single  inhalation exposure.  Only  the  deposited
 amount, but not the concentration or exposure duration, was reported:   Vorwald
 (1962)  exposed several groups of  rats  for  periods of three to twelve months,
 but only reported the total  tumor incidence for all  groups.   The remaining
 five studies  utilized intratracheal  instillation,  which  results in  uneven
 distribution in the  lungs and makes dosimetry estimates  somewhat uncertain.
       Among the inhalation exposures,  the  MLE varied from 7.4  x  10
                                                                     for the
  beryl ore study  to  3.2 x 10'3 for the Vorwald (1962) study.   The MLEs _for the
  intratracheal instillation studies  varied  from 1.7 x 10   to 2.1 x 10   .   In
  this series,  the MLE decreased with increasing firing temperature.   Since the
  solubility  of beryllium oxide decreases with  increasing  firing temperature,
  these  studies point  out  a relationship between solubility  and carcinogenic
  potency  for this compound.   The geometric mean of  the MLEs from all eight
                            This value is in good agreement with the MLE of 2.4 x
studies was 2.1 x 10 '
10'3 derived from human  epidemiological  data.   It is also  in  good agreement
with the  MLE of 3.2 x 10"3 derived from  the  1962 Vorwald study, the only
subchronic or longer inhalation study utilizing beryllium oxide.
                                     7-71

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     Although each of the studies has important limitations, taken collectively
they provide reasonable  evidence that  the  true MLE  is  likely to  be at  least  in
the range of the  MLEs  derived.   Moreover,  since  the geometric mean of  the MLEs
for the eight studies do agree quite well with the MLE derived from human data,
these estimates do  provide support to the quantisation of risk from the human
epidemiology studies.
     In addition to the previously described methods for deriving an equivalent
human  concentration,  an alternate  method has been  proposed by  Oberdoerster
of  the  University of Rochester  (personal  communication).   In  this method,  an
adjusted  human  equivalent  concentration, which takes  into account differences
in  both deposition efficiency and lung  surface area is derived.  As a further
refinement,  concentration  per unit of surface area is estimated separately  for
alveolar  and tracheobronchial regions.
     The  study by  Reeves  and Deitch  (1969), in  which rats were exposed to
beryllium sulfate at  a beryllium concentration  of 35 ug/m , was  used to
demonstrate  this  method.  For a mean  particle  diameter of 0.35 urn, tracheo-
bronchial  deposition was  estimated  to equal one percent  in  rats  versus two
percent in  humans.   Alveolar deposition was estimated to equal ten percent
 in rats versus twenty percent in humans.  The daily volume of air breathed per
 day was assumed to equal  0.20 m3/day  for 300 gm  rats  and 20 m3/day for a 70 kg
 man.   The dose to  the  tracheobronchial  (tb) region in rats then can be  calcu-
 lated to equal

                    .20 m3/day x .01 x 35 ug/m3  = 0.07 ug/day

 The dose to the alveolar (alv) region equals

                    .20 m3/day x .10 x 35 ug/m3 = 0.70 ug/day

 The human equivalent tb concentration equals
 The  human  equivalent alv concentration equals
                            2/3
                    (70/.30)    x   20 mVday x  .20
                                       7-73
OK= 1.13 ug/m'

-------
 The alveolar  surface  area for a 300 gm  rat  was  estimated to equal 4453 cm2
 compared with  548,789 cm   for  humans.   Tracheobronchial  surface  area was
 estimated to equal 45.7 cm   in rats compared with 4060 cm2 in humans.  The alv
 surface area to body  weight ratio  is equal to 4453 cm2/0.3 kg or 14,843 cm2/kg
 in the rat and 548,789 cm2/70 kg  or 7040 cm2/kg  in  humans.  The  alveolar  surface
 area per unit  body weight is thus  14,843/7040 or 1.89 times greater in the rat
 while  the tracheobronchial  surface is  2.62 times greater in  the rat  using  the
 same method.   Adjusting for  alv surface area, the human equivalent  concentration
                              o
 equals 1.13/1.89 or 0.60 ug/m .   Adjusting for  relative  tb surface area, the
 human  equivalent concentration equals 1.13/2.62 or  0.43 |jg/m3.
     As can be seen,  the adjusted human concentration based upon estimated
 differences  in deposition efficiency is about half that using standard method-
 ology.   As a result,  an MLE calculated on  this basis would be about doubled.
 Making a further adjustment  to account  for  differences in  relative  lung surface
 will result  in  even smaller  human equivalent  concentrations and  thereby greater
 MLEs.
     The application  of methodology such as  that  illustrated above  has  the
 potential  for  greatly  refining  the quantitative assessment  of risk.  This
 method was not  used for  the development of quantitative  risk  estimates  for
 beryllium because there is still some uncertainty regarding relative deposition
 efficiency  in  laboratory animals  and humans.   Deposition  can  vary considerably
 with breathing  patterns and  with particle size, shape, and density.  It is also
 uncertain  if a higher  concentration over a  small  lung surface area will  result
 in  a greater degree of tumor induction  than the  same  total dose  deposited over
 a larger surface.  As more data become available reducing uncertainty regarding
 deposition efficiency,  methodology  such as  this should be incorporated into the
 quantitative assessment of risk.
 7.3.2.2  Calculation of the  Carcinogenic Potency of Beryllium on the Basis of
 Human Data.  Given the need  to estimate the  cancer risk  of beryllium and the
 uncertainty  inherent in  the  use  of animal  data,  it is desirable to  use  the
 available  human data  in  some way  to  estimate  the carcinogenic  potency  of
 beryllium.   Data from  Wagoner et al.  (1980)  are considered  appropriate  for
 this purpose.  This study is selected because  the cohort consisted of beryllium
workers  employed prior to  1949,  when controls on beryllium in the workplace
began.   The workers'  exposures to beryllium before 1949 were very high.  A 1947
 study reviewed by NIOSH (1972) reported beryllium concentrations in a beryllium
extraction plant in  Pennsylvania  of up  to 8840 MQ/m3.  In more than 50 percent
                                     7-74

-------
of the  determinations  reviewed, beryllium  concentrations were in excess of
100 ug/m3.   According to  NIOSH  (1972),  the  levels  of environmental exposure to
beryllium in the workplace  were markedly reduced  after  control measures were
instituted  in  1949.   In  one  Ohio extraction plant, the beryllium exposure
                                o
levels  were recorded at 2  ug/m or  less during almost  all  of a  seven-year
period.  The  information available  about beryllium exposure  levels  in the
workplace and  the  excess  cancer risk observed among workers  employed  in beryl-
lium production plants is summarized below.
7.3.2.2.1   Information  on exposure levels.   The beryllium  plant  studied by
Wagoner  et  al. (1980)  was  a major  beryllium extraction, processing,  and
fabrication facility located  in Pennsylvania.   The workplace concentrations of
beryllium in various  beryllium  production plants in Pennsylvania  and  Ohio were
found  to be comparable  (Eisenbud and Lisson,  1983).  Based on the NIOSH (1972)
report  described previously,  the lower-bound estimate of the median  exposure
                                O
concentration  exceeded  100  ug/m ,  since more than 50 percent of the determina-
tions  exceeded that level.  According  to Eisenbud and  Lisson  (1983),  it  is
                                 o
likely  that this  value  (100 ug/m  )  is  an underestimation of the actual median
exposure level, in  the workplace,  and thus  should  be considered to be a lower-
bound  estimate of median  level.  Eisenbud and Lisson (1983) stated "...published
studies of  conditions  in the Pennsylvania  production  plant  indicate  that  the
levels  of  exposure prior to installation of  dust controls were comparable  to
conditions  in  the  Ohio plants.   Concentrations  in excess of 1000 ug/m  were
commonly found in  all  three extraction plants during  the late  1940s."  On the
other   hand,  it  is  unlikely  that the  median level could greatly exceed
1000 ug/m3, since  at that  level almost all of  the exposed workers developed
acute  respiratory  diseases (Eisenbud, 1955).  Thus, it  is reasonable to assume
that the median level of  beryllium concentration did not exceed 1000  ug/m .  In
the risk calculation, the median level  of beryllium concentration  is  assumed to
range  from 100 to 1000 ug/m3.  This is the narrowest range for median exposure
that  could  be  obtained  on the basis  of  available information.
7.3.2.2.2   Information on  excess  risk.    Wagoner et al.  (1980) conducted a
cohort study  of 3055 white males  who were initially  employed  in a  plant  in
 Pennsylvania from  1942  to 1967, and  who were followed  to December 30, 1975.  Of
particular interest to  the present risk assessment is  a  subcohort of  workers who
were   initially employed  prior to 1950,  and  who were  followed for at  least
 25 years from the date  of  initial employment.   The elevation  of lung cancer
 mortality was originally shown by Wagoner  et al.  (1980)  to be statistically
                                      7-75

-------
 significant (p <0.05).   However,  the significant  elevation of  lung  cancer
 mortality disappears after making  an  adjustment for differences in cigarette
 smoking between cohort and .control  populations.   For the  subcohort of workers
 who were  followed  at least  25 years since  their initial  employment,  the
 smoking-adjusted expected lung cancer deaths  are  found  to range from  13.91  to
 14.67,  in comparison with the  20  observed lung cancer  deaths.   The relative
 risk estimates are 20/13.91: =  1.44 and  20/14.67 = 1.36, which  are  not statis-
 tically significant (p >0.05).   Although the  epidemiologic study did  not  show
 carcinogenic  effects,  the data can be used to calculate an upper limit of lung
 cancer  risk.
      Assuming  that  the observed cases follow  a Poisson  distribution  and  the
 expected  value is  constant,  the 95  percent confidence limits  for the two
 relative  risk estimates,  1.36 and  1.44,  are  respectively  1.98 and 2.09.  The
 values  1.98 and 2.09 are used to estimate the lifetime lung cancer risk due to
 1 ug/m  of beryllium in air.;
 7.3.2.2.3   Risk calculation on the basis of human data.    To  calculate the
 lifetime  cancer risk  on  the  basis of information  described previously,, the
 median  level  of beryllium exposure must be converted to the "effective" dose,
 through multiplying by a factor of (8/24) x (240/365) x  (f/L),  to reflect  that
 workers were  exposed to beryllium 8 hours/day, 240 days/year, for f years out
 of  a period of  L years at risk (i.e. from the onset of  employment to the
 termination of follow-up).   Two values  of  f/L are used in the  calculation:
 f/L = 1 and f/L = 0.25.  The: use of f/L = 1 would avoid overestimating the risk
 (but  could underestimate the risk)  if the  observation by  Reeves and  Deitch
 (1969)~that tumor  yield depends  not on length of exposure but on age at
 exposure—is valid.  Table 7-17 presents a range  of  cancer potency estimates
 calculated under various assumptions about relative risk estimates and level  of
 exposures.  The  upper-bound  estimate  of the cancer  risk  associated with  1
 ug/m  of  beryllium  ranges from 1.6 x 10~4/(ug/m3)  to 7.2 x 10~3/(ng/m3), with
 a geometric mean  of 2.4 x 10~3/(ug/m3).   Because of the  range of uncertainty,
this number is rounded to 2 x 10~3/(ug/m3).
                                       *j
7.3.2.3  Risk Due to Exposure to 1 ua/m  of Beryllium in Air.  Both  animal and
 human studies  have  been  used  to qualitatively  evaluate the potential for human
carcinogenicity.   For  quantitative risk  assessment purposes, the  available
data  presents  some  difficult analytical  problems.   In  the case of animal
studies, although  several  forms of beryllium were  tested, the  design  and
reporting of many of the  studies were  inferior  by  current  standards, resulting
                                     7-76

-------
              TABLE 7-17.  UPPER-BOUND CANCER POTENCY ESTIMATES
                    CALCULATED UNDER VARIOUS ASSUMPTIONS
Beryllium
concentration
in workplace
(|jg/m3)
100



1000



"Effective"
dose
f/L (yg/m3)
1 21.92

0.25 5.48

1 219.18

0.25 54.79

95 percent
upper-bound
estimate of
relative risk
1.98
2.09
1.98
2.09
1.98
2.09
1.98
2.09
Cancer potency
(ug/m3)-1
1.61 x 10 3
.1.79 x 10"3
6.44 x 10"3
7.16 x 10"3
1.61 x 10"4
1.79 x 10"4
6.44 x 10"4
7.16 x 10"4
a"Effective" dose is calculated by multiplying the beryllium concentration
 in the workplace by the factor (8/24) x (240/365) x (f/L).
bFor a aiven "effective" dose d and a relative risk R, the carcinogenic
 potency is calculated by the formula B = (R-l) x 0.036/d, where 0.036 is
 the estimated lung cancer mortality rate in the U.S. population.

in  a  clear basis for uncertainty  about  the reasonableness of the upper-limit
risk  estimates.   The epidemiologic data, while  being  useful  for analysis of
cancer  incidence, nevertheless, has  interpretive  limitations because of the
uncertainties regarding exposure levels.
      Despite  the uncertainties and weaknesses of  the  individual studies, the
cancer  response  in beryllium exposed animals is very strong and there seems to
be  a pattern of  response which relates  to the  beryllium  specie tested  (i.e.
oxide,  sulfate,  etc.).   The  unit  risks  derived from the  animal data sets are
best viewed as  a sensitivity analysis as opposed to a collection of reasonable
upper-bound risk values.   The  sensitivity  relates to beryllium specie tested
and for beryllium oxide  alone, perhaps  to solubility and firing temperature.
The  epidemiology  based risk  analysis  is also  a  sensitivity  analysis which
 results from the  need  to make fundamental  assumptions about exposure together
 with the use of nonsignificant incidence data in order to derive an upper-limit
 risk  approximation.   Interestingly, the  two distinct  sensitivity analyses
                                      7-77

-------
  (animal  data, human data)  correlate  very closely for beryllium  oxide,  there
  being no human data to  compare to the animal  data  for  beryllium sulfate and
  other beryllium compounds.
       Many of the animal experiments used beryllium salts, a form not likely to
  be  present  either  in  ambient  air or  in occupational  settings.   In mining
  operations,  for  example, the beryllium present in the ore is in the form of an
  oxide,  but may be  bound with  other chemicals as well.   In the extraction
  process,  the primary product, beryllium oxide, is then reduced to the metallic
  form.  In operations such as melting,  pouring, or welding of beryllium,  fumes
  consisting of fine  particles of beryllium  oxide  are produced by condensation
  from  the  vapor phase.   Other sources of  workplace  contamination result  from
 metallic dusts generated by a variety of operations such as crushing, grinding,
 or  cutting  of beryllium-containing material.   For  further details regarding
 industrial processing  of beryllium,  refer to Tepper et al. (1961).  Beryllium
 is most commonly  found in ambient air  as a trace metal component of fly ash
 emitted from coal-burning electric power generating plants.  Since fly ash is a
 combustion product,  the beryllium again is primarily present as the oxide.
      Although all  of the animal studies were deficient  in  some respect, the
 ones  utilizing beryllium oxide were more deficient,  as  a group, than those
 utilizing beryllium salts.  Since  humans  are  likely  to be exposed to beryllium
 as an oxide,  however,  and  since the carcinogenic response was  shown to  vary
 with the form of  beryllium,  the use of beryllium oxide data is considered an
 important  focus in estimating the  cancer  potency.  While the available beryl-
 lium oxide studies  were individually weak, a .correlation  of estimates  from
 several  data  sets would  be expected to increase  confidence  in the results.
 Potency  factors were thus  calculated using data  from  eight beryllium oxide
 animal  studies.   The results were reasonably consistent and the geometric mean
 of all eight potency factors was 2.1 x 10~3/(ug/m3),  which closely agrees with
 the potency factor derived from  the human  epidemiology data.  Although the con-
 fidence levels are still  too  low to  recommend a potency factor and unit risk
 based  on the  animal data, these  estimates, nevertheless, do provide support for
 the potency estimate derived from the human epidemiology data.
     A risk  assessment  based upon human epidemiology  data was calculated  based
on the occupational  exposure study of Wagoner et  al.  (1980).  The narrowest
range  for  median  exposure that  could  be obtained  on the basis  of available
information was 100  to  1000  pg/m3.   The  ratio  of exposure duration to duration
of risk was  assumed to range from  a  minimum of 0.25 to  1.0.
                                     7-78
The geometric

-------
mean of the  range  of potency factors derived  using the above assumptions is
equal to  2.4 x  10~3/(ug/m3).   As  indicated  in the previous section, this
                           ~3      3
number is rounded to 2 x 10  /(ug/m )•
     The CAG  feels  that a recommendation for a specific  upper-bound estimate
of risk  is  warranted,  even though it does evolve from less  than ideal  data,  in
order to provide a crude measure of  the  potential  for a  public health impact
if,  in  fact,  beryllium is a human  carcinogen.   Some of the risk values dis-
cussed "in  the document are  derived from animal data  which  have significant
shortcomings, the  result  being that the estimates taken as  a whole demonstrate
a  sensitivity analysis of reasonableness rather than being a  collection  of
equally  reliable upper-bound values.  In a similar manner, the  risk estimates
derived  from the human data have  inherent  uncertainty because of the need to
                                                                       ) is  in
 assume exposure levels and, thus,  the  risk estimate  of  2  x 10
 effect also the result of a sensitivity analysis.
      Taken together the  notable  comparability  of the animal and human  based
 estimates for beryllium  oxide  encourages  one to consider  these estimates  as
 being of some utility.  Given  the correlation of the  animal and human estimates,
 a value of  2  x 10~3/(ug/m3) is considered to be a useful  approximation  of  the
 upper-limit risk for beryllium oxide.   This can be converted to a  q* value  of  7
 (mg/kg/day)'1 after adjusting  for  a weight of  70  kg  and 20 m3  of air breathed/
 day.  The uncertainty of the beryllium oxide risk value in relation to the  true
 risk  has  two  aspects, one being  the usual  uncertainty which is attributable to
 the  linearized  multistage procedure  in the case  of  animal data or the upper
 limit modelling  of human data (i.e.  the  true  risk is  not likely to be  higher
 and  may be lower).  A second  uncertainty unique to  the  beryllium  data base
 relates  to the  need  to  make  dosimetry assumptions  as a part of  the risk
 modelling  of  the animal   and human data.  The dosimetry influenced uncertainty
 should  be viewed  as  potentially causing either an  overestimation  or under-
 estimation  of the  upper limit.   The  utility  of these risk values  in  risk
 management  analysis should be judged with these uncertainties  in  mind.   Hence,
 whereas one might use these estimates  to  screen  for a  possible public  hazard,
 one should exercise much  greater  caution  in using these  values for  an  assess-
 ment of individual  cancer risk'.
       Since beryllium  salts are more potent,  the higher  unit risk values  derived
  from these studies should be  used  in cases of  potential human  exposure  to  these
  forms of beryllium.  The uncertainties associated with the beryllium salt risk
                                       7-79

-------
 estimates  [especially  beryllium sulfate,  risk value of 0.8/((jg/m3)]  is  the
 typical concern associated  with the upper-limit estimation  from  animal  studies
 (the true  risk  is  not  likely to be higher and may be lower), there being no
 significant dosimetry problems with these data.

 7.3.3  Comparison of Potency With Other Compounds
      One of the uses of  quantitative potency  estimates  is to  compare the  rela-
 tive potencies  of  carcinogens.   Figure  7-2  is a histogram representing  the
 frequency distribution of potency  indices  for 59 suspect carcinogens evaluated
 by the CAG.  The actual  data summarized by the histogram are presented  in  Table
 7-18.   The potency index used,herein was derived from the carcinogenic potency
 of the compound and  is  expressed in terms  of (mmol/kg/day)"1.  Where no human
 data were  available, animal oral studies were  used  in  preference to animal
 inhalation studies, since oral  studies have constituted the majority of animal
 studies.
      The potency index  for beryllium oxide  is  2 x 10+2,  calculated by multiply-
 ing the potency  estimate, 7.0/(mg/kg/day),  and the  molecular weight of  beryllium
 oxide  (25).  This calculation  places the  relative potency of beryllium  oxide in
 the third quartile of the 59  suspect carcinogens evaluated by the CAG.   The
 potency index for  beryllium sulfate is  3  x  10+5 (see Table 7-18), placing
 beryllium  sulfate in the  first quartile.
     The  ranking of relative potency indices  is subject to the uncertainties
 involved  in comparing a  number  of  potency  estimates  for different chemicals,
 based on varying routes of exposure  in different species, by means  of data from
 studies whose quality varies widely.  All of the indices presented  are based on
 estimates  of  low-dose risk,  using  linear extrapolation from the observational
 range.  These indices may not be  appropriate for the comparison of  potencies if
 linearity  does not  exist at  the  low-dose range, or  if comparison  is to  be  made
 at  the  high-dose range.   If the  latter  is  the case,  then an index other than
 the one calculated above  may be more  appropriate.

 7.3.4  Summary of Quantitative Assessment
     Both  animal and  human  data  have been  used to  calculate the  carcinogenic
potency of beryllium.   Many  of the  animal  studies  conducted on beryllium  are
not well documented,  were conducted at single  dose levels,  and in some cases
did not utilize control  groups.  Nevertheless, because positive effects  were
                                     7-80

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                                       7-81

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 seen in multiple species, at multiple sites, and often at very low doses, these
 studies  collectively provide sufficient animal evidence  for carcinogenicity.
 In the present report,  data from  animal  inhalation and intratracheal  studies
 (using rats,  guinea  pigs, or rhesus monkeys exposed to a variety of beryllium
 compounds)  have  been used to calculate  the  upper bounds for the potency  of
 beryllium.  The maximum  likelihood slope estimates, calculated  on the  basis  of
 animal  data,  vary  from  2.1 x 10~4  to 4.3/(|jg/m3),  a range of four orders of
 magnitude.
      The magnitude of the potency  appears  to depend primarily on the beryllium
 compound used in the experiment, although some variability in sensitivity among
 species was also seen with guinea  pigs  responding to a  lesser degree than  rats
 or monkeys.   Among the beryllium  compounds  examined in the  animal studies,
 beryllium oxide is the  least carcinogenically potent,  while beryllium  sulfate
 (BeSO^) is  the most potent.   Solubility appears  to be one factor affecting
 potency.   In the intratracheal  instillation  studies of Spencer et al.  (1968,
 1972),  beryllium oxide calcined at  1100°C and 1600°C was much less potent than
 the  more  soluble form of  beryllium oxide which  was  calcined at  500°C.  If  one
 adopts  the  most  conservative  approach, the  maximum  potency  estimate,
 4.3/(fjg/m ), would  be used to represent  the carcinogenic potential of beryllium
 sulfate.   This potency is  estimated on the  basis of  animal data  (Vorwald  et al.,
 1966) obtained in an experiment in which the level  of  exposure to beryllium
 sulfate was  very similar  to  occupational exposure conditions.  Thus, the high
 potency estimate  is not due  to  the use  of a  particular  low-dose extrapolation
 model.  Since  most  beryllium compounds present in ambient air or the workplace
 environment  are not in the form of beryllium salts,  but are, more likely to be
 the  less  potent beryllium oxide,  use of the sulfate potency estimate  would
 clearly overestimate  the human risk.  The geometric  mean of  2.1 x lO'Vdjg/m3),
 obtained  from  eight animal studies  utilizing beryllium oxide  or beryllium ore
 is considered  to  more accurately represent human  risk  to beryllium  compounds
 present in ambient air.
     Data  from the  epidemiological  study by Wagoner et  al.  (1980)  and the
 industrial hygiene  reviews by NIOSH (1972)  and  Eisenbud and  Lisson (1983) have
been used  to  develop  a cancer risk  estimate  associated with exposure to air
contaminated with beryllium.   Two upper-bound relative risk estimates,  1.98 and
2.09 from  the  human data,  have been used in the calculations.  In recognition
of the  greater uncertainty associated  with  the exposure estimation,  four
                                        7-86

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different "effective" levels  of  exposure that reflect various  uncertainties,
along with two  relative  risk  estimates,  have  been  used in  the present  calcula-
tions.  As a result, eight potency estimates have been calculated, ranging from
1.6 x 10~4/(ug/m3)  to 7.2 x 10~3/(ug/m3),  with the geometric mean of the  eight
                         -3      3
estimates being  2.4  x 10  /(ug/m )
                                       Rounding off this number because of the
level of uncertainty,  the  incremental  life time cancer  risk  (based  upon epide-
miologic data) associated  with  1 ug/m3 of beryllium in the air is thus calcu-
lated to be 2 x 10~3.  This estimate could be considered an upper-bound estimate
of the  cancer  risk because low-dose linearity is assumed in the extrapolation
and  the  95  percent upper-confidence limits of the  relative  risks are used in
the  calculations.   With  these quantitative approaches, the CAG has calculated
two  risk estimates, one  from epidemic!ogic data and one from animal data, for
exposures  to  mainly  oxides of beryllium.   These  rounded  estimates,
2  x  I0"3/(ng/m3)  each, are in complete agreement.  The risk estimates for the
salts  of beryllium (i.e.,  sulfate)  are much higher and are derived from animal
data only.
 7.4  SUMMARY
 7.4.1  Qualitative Summary
      Experimental beryllium carcinogenesis has  been  induced by intravenous or
 intramedullary injection of rabbits, and by inhalation exposure or intratracheal
 instillation of rats and monkeys.
      Osteosarcomas were  induced in rabbits by  intravenous  injection  of zinc
 beryllium silicate (9 studies), beryllium oxide (2 studies), metallic beryllium
 (1  study)  and by  intramedullary  injection of  zinc  beryllium  silicate  and
 beryllium oxide  (1  study each).  Lung tumors  were induced in rats by  intratra-
 cheal  instillation  of beryllium oxide (4 studies), beryllium hydroxide (2 stu-
 dies), metallic  beryllium (2 studies), beryl ore  (1 study) and in monkeys by
 beryllium oxide  (1 study).  Lung tumors were also induced in rats by inhalation
 of  beryllium sulfate (5 studies),  beryllium phosphate, beryllium fluoride, and
 beryl  ore  (1 study each), and  in  monkeys by beryllium sulfate (1 study).  No
 significant neoplastic responses  were observed via  the intracutaneous or per-
 cutaneous  routes,  while the responses via the dietary routes were either nega-
 tive or  equivocal.   This was considered to be due to low absorption efficiency
 resulting  from precipitation of beryllium compounds  in the  small  intestine.
                                          7-87

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      The  beryl 11 urn-induced osteosarcomas in rabbits were  shown to be highly
  invasive  and  to readily metastasize.  They were  judged to be  histologically
  indistinguishable  from  non-beryllium-induced  human osteosarcomas,  although the
  sites may be different.
      As noted above,  positive carcinogenic responses in animals were obtained
  in multiple species and through various routes of exposure.  In studies using
  either  inhalation  or the intravenous injection route,  positive results were
  obtained  in  multiple experiments.   For  several  of  the beryllium  compounds
  tested, such as  beryllium sulfate, significant responses were obtained at low
  dose levels.  Based on  the above  findings, the overall  evidence for  carcino-
 genicity of beryllium  in animals  is  convincing  despite  the limitations of  many
 of the  studies.   According  to  EPA's criteria for evaluating the  weight of
 evidence for carcinogenicity (U.S.  EPA,  1986),  the evidence for  carcinogenicity
 of beryllium in  animals is considered to  be "sufficient".
      Although  several studies (Wagoner et.  al.,  1980;  Mancuso,  1979;  Manusco,
 1980) claim a statistically  significant excess risk of  lung cancer in individ-
 uals  exposed to  beryllium,  all  of the studies  cited have deficiencies that
 limit definitive  conclusions regarding  a  true   carcinogenic association.
 Support for finding an excess risk of lung cancer in beryllium-exposed persons
 consists of evidence from cohort mortality studies of two beryllium production
 facilities.  None of these studies are  independent, as  they are all based  on
 the  same groups  of workers.  Extensive  collaboration  existed  between  the
 authors  of these  studies.  The expected lung cancer deaths  used  in  all of these
 studies  were  based on a  NIOSH computer-based life-table  program known to pro-
 duce  an 11-percent underestimation of expected  lung  cancer deaths.  Further-
 more, the studies did not adequately  address the confounding effects of smoking
 or of exposures  received during prior or  subsequent  employment  in  other non-
 beryllium  industries in  the  area.   Many of these industries  were  known to
 produce  other potential carcinogens.  Problems in  the design and conduct of the
 studies  further  weaken the  strength  of  the findings.  After  correcting  the
 life-table error  and adjusting for some of the  problems described  above,  the
 finding  of a significant  excess risk is no longer  apparent.   While the possibi-
 lity remains that the portion of the reported excess lung cancer risk remaining
 in these studies  may,  in  fact, be  due to  beryllium exposure, the epidemiologic
evidence is, nevertheless,  considered to be "inadequate" according to EPA's
criteria for evaluating the weight of evidence  provided  by epidemiologic data.
                                        7-88

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     Limited testing has  shown  beryllium sulfate and beryllium chloride to be
nonmutagenic in bacterial  and yeast gene mutation assays.   In  contrast,  gene
mutation studies  in  cultured mammalian cells, Chinese hamster  V79  cells,  and
Chinese hamster ovary (CHO) cells have yielded positive mutagenic responses for
beryllium.   Beryllium increased  the infidelity of DNA and  RNA  polymerase in
prokaryotes.  Chromosomal  aberration  and sister chromatid exchange studies in
cultured human  lymphocytes and  Syrian hamster embryo cells have also resulted
in positive mutagenic responses  for  beryllium.   In  DNA damage and  repair
assays, beryllium is negative in the pol, rat hepatocyte, and mitotic recombina-
tion assays but is  weakly positive in the rec assay.   Based on  the  information
available, beryllium appears to have the potential to cause mutations.
     Using  the  EPA  criteria for evaluating the overall weight of evidence for
carcinogenicity in  humans, beryllium  is most appropriately classified as  group
82, a probable human carcinogen.  This category is reserved for those chemicals
having  sufficient evidence  for carcinogenicity  in  animals but  inadequate
evidence in humans.

7.4.2  Quantitative Summary
     Both  animal  and human data are used to  estimate the carcinogenic potency
of beryllium.   Among the animal studies, only  data  from inhalation exposures
or intratracheal  instillation are used because the intravenous or intramedullary
exposure routes are not considered  to be directly  relatable to human  exposures,
and all dietary ingestion  studies yielded negative results.  Many of  the animal
inhalation  studies  for  beryllium are not well  documented,  were conducted at
single-dose levels,  and,  in some  cases,  did not utilize  control  groups.
Collectively,  however,  the studies provide  a reasonable basis  for estimating
potency (at least for beryllium  sulfate  and  beryllium oxide), as exemplified by
the  consistency of response  in  rats.   Data from nine studies  (7  studies of
rats,  1 study of guinea pigs, and 1 study of monkeys) using beryllium sulfate,
phosphate,  and fluoride have been  used  to  calculate the upper bounds for the
carcinogenic  potency of beryllium  salts.   Data  from eight studies with  rats
have  been  used to calculate  the upper bounds for the carcinogenic potency of
beryllium  oxide.   The  upper-bound potency estimates from  the  data based on
                                              3                      ~2      3
exposure  to beryllium sulfate equal 3.6/(ng/m ) in monkeys, 6.5 x 10  /(|jg/m )
in guinea  pigs and  range  from 4.3/(|jg/m3) to 3.7  x lO'Vdjg/m )  in  rats.   Esti-
mates  derived from  responses in rats  exposed to beryllium fluoride  and beryllium
                                         7-89

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  phosphate equal  1.4 x  lO'V^g/m3)  and 3.0  x I0"2/(ug/m3),  respectively.
  Potency estimates derived  from  responses  of rats exposed to  beryllium  oxides
  ranged from 7.4 x 10"2/(|jg/m3) to 2.1 x 10"4/(|jg/in3).
       The magnitude of the potency estimates from animal  data depends to  a large
  extent on the beryllium  compound used in  the experiment,  although some  varia-
  bility in sensitivity among  species  is also seen, with  guinea pigs responding
  to  a  lesser  degree than  rats or monkeys.   Among the  beryllium  compounds
  examined in the animal studies,  beryllium  sulfate (BeS04) is  the  most potent,
  with  beryllium fluoride and beryllium phosphate somewhat less so and beryllium
  oxide  the  least  potent.   There is some indication that the carcinogenic  potency
  of  beryllium oxide varies  with  the  firing temperature.   The  low-temperature
  fired,  more soluble oxides appear somewhat more potent than  those fired at
  higher  temperatures.   If one  adopts an  approach which  selects data from the
 most  sensitive experimental  animal  species and the most potent compound as
 being  representative of  risk to humans,  the  maximum  potency estimate,
 4.3/(ug/m ), would be used to  represent the carcinogenic potential  of beryllium.
 This potency  is  estimated on  the basis of  data from  rats exposed by inhalation
 (Vorwald et  al., 1966).   Since  beryllium  is  most commonly present in  the
 ambient air as  the  oxide, a potency estimate  based  upon the beryllium oxide
 studies  is  considered  to be most  representative of  human  risk.  Due to  the
 individual  weaknesses of  each  of the eight beryllium oxide studies, a potency
 estimate of 2.1 x 10" /(pg/m3) was derived  by calculating the geometric mean  of
 the  individual  potency estimates  from each  of the studies.
      Information from the epidemiologic  studies  by Wagoner et  al.   (1980) and
 the  industrial  hygiene reviews by NIOSH (1972) and Eisenbud  and Lisson (1983)
 have been used to estimate  the cancer  risks associated with  exposure to  work-
 place  air contaminated with beryllium.  Even though the epidemiologic evidence
 does  not demonstrate a  statistically significant causal  association between
 beryllium and  cancer, that does not mean that no risk exists.  The size of the
 study population, the background  risk,  and a variety of other factors limit the
 ability  of  a study to detect  small  risks.   Each study has a level  of sensi-
 tivity,  and the  study  population may be too  small to  show a  statistically
 significant association  if the true risk is below this level.  An  upper-bound
 risk estimate can be calculated from a  non-positive, or even negative, study  to
describe  the study's  level of  sensitivity.   Risk levels below that  upper  bound
are completely  compatible  with the study data.   The upper bound may be  thought
                                        7-90

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of as indicating  the  largest plausible  risk  that  is  consistent with the avail-
able data.  Thus, the epidemiologic studies can be used to estimate a plausible

upper bound for the increased cancer risk from human exposure to beryllium.
     In the Wagoner  et al.  (1980) study,  20 lung cancer deaths  were  observed

in a  cohort  of workers followed for  at least 25  years compared  with  13.91  to
14 67 expected (p <0.lO).   Using the revised estimates of relative  risk  from
this  study,  two upper-bound relative risk estimates,  1.98 and 2.09, have been
used  by the  CAG to calculate the carcinogenic potency of beryllium.   In recog-
nition  of the  greater uncertainty associated with the  exposure estimation,  four
different "effective" levels of exposure  that reflect various  uncertainties,

along with the two relative risk estimates,  have been used in the  present
 calculations.   As a  result, eight  unit risk estimates  have been  calculated,

 ranging from  1.6 x
              .                 to 7.2 x Nf3/(pgV) , with the geometric mean

of the eight estimates being 2.4 x lO^/Cug/m3).   After rounding  to  one  signifi-
cant figure, the  incremental  lifetime  cancer risk associated with 1 ug/m  of

beryllium oxide in  the  air is thus estimated to  be  2 x l
-------
  metal are most commonly  present.   When animals are exposed to beryllium oxide
  or oxide-containing  beryllium ore, the  potency estimates agree  with  those
  derived from human exposures.
       A major uncertainty of the  risk  estimate based on human data comes from
  the derivation of exposure levels  in  the workplace and the temporal  effect  of
  the patterns of exposure.  To account for these uncertainties, the "effective"
  exposure  level  of beryllium is derived in several ways, and the geometric mean
  of different potency  estimates  thus  calculated  is used  to  represent  the
  carcinogenic  potency  of beryllium.
       Another  uncertainty  concerns the use of  potency  values  derived from ex-
  posures  in the workplace environment to  estimate  potency from exposure in
  ambient air.   The  types of sources which emit beryllium to the ambient air are
  limited.   There is little evidence^that ore  production is  a significant source
  of  beryllium emissions.   Metallurgical processing  is  likewise considered an
  insignificant source.   As much as 95 percent of atmospheric beryllium emissions
 are estimated to come from coal-fired electric power plants, with most of the
 remainder resulting from fuel  oil combustion (see Chapter 3).   During coal com-
 bustion beryllium  is  likely emitted as a  relatively insoluble  oxide,  generally
 as a  trace contaminant of fly  ash particles which are  even more  insoluble.   On
 this basis, the potency of  beryllium from this source  would be expected to be
 quite low.  Beryllium emissions  from fuel oil  combustion are  similarly likely
 to occur primarily in the oxide  form.   Experimental evidence  also indicates
 that beryllium in  fly ash has  a  low degree of potency, since  even very high
 concentrations of  fly ash containing other known carcinogens have  failed  to
 induce cancer in laboratory  animals.  On this basis,  it is  unlikely that values
 derived from exposure in  the workplace will  significantly  underestimate  the
 potency of beryllium in ambifent air,  unless soluble  beryllium compounds  such  as
 fluoride,  phosphate, or sulfate are  known  to be present.
     Because  of  the weaknesses  of the  animal  studies upon  which some of the
 carcinogenic  potency estimates  were derived,  these estimates are judged to be
 less reliable  than  those derived from  human occupational exposures.  They do,
 however, provide  support  for the  occupationally-derived estimates.  Despite'
 some  uncertainties  concerning  exposure levels  in  the workplace and possible
 differences in the  forms  of beryllium  found in ambient air compared with the
workplace  environment, the CAG-revised  relative risks from the Wagoner et al.
 (1980) epidemiologic study were considered to be the best choice for estimating
                                        7-92

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the upper-bound  incremental  cancer risk for inhalation exposure to mixtures  of
beryllium compounds  (mostly  beryllium oxide) likely to  be  present in ambient
air.                                                   33
     The  upper-bound incremental  unit risk of  2  x 10  /(ug/m ) results in a
potency  index  of 2 x 10+2, which  places beryllium oxide in the third quartile
of  the 59 suspect  carcinogens evaluated by  the  CAG.
 7.5   CONCLUSIONS
      Using EPA's  Guidelines for Carcinogen Risk Assessment (U.S. EPA, 1986) to
 classify the weight of  evidence  for carcinogenicity in experimental animals,
 there is sufficient evidence to conclude that beryllium and beryllium compounds
 are  carcinogenic  in animals.   This evidence  is  based  upon the induction of
 osteosarcomas and  chondrosarcomas  by  intravenous and intramedullary injection
 in rabbits and upon the induction of lung tumors in rats and monkeys by inhala-
 tion  and intratracheal  instillation.   Although results  were equivocal or
 negative  for  ingestion,  it is believed that  if an  agent is carcinogenic by one
 route  it is  potentially carcinogenic by any  route.  The lack of  a definitive
 response  via  the  ingestion route  is considered most likely due to low absorp-
 tion  efficiency.    Due  to  limitations  in  methodology,  the  epidemiological
 evidence is considered  to  be  "inadequate", even though  significant increases  in
 lung  cancer  were  seen  in  some  epidemiology  studies of occupationally exposed
 persons.
       A potency of 2.4 x 10~3/(ug/m3) was derived from the occupational studies
 involving human exposure to beryllium  compounds  (thought to  be mostly  beryllium
 oxide) commonly present in the workplace.
       The carcinogenic potency of  inhaled beryllium derived from animal studies
 varies with-the  form of beryllium.  Potency  values for beryllium  sulfate ranged
  from 4.3 to 3.7  x lo'V^g/m3) with the most reliable  estimate being 8.1 x 10  ,
 while those derived from studies using beryllium fluoride or phosphate equalled
  1.4 x 10"1 and 3.0 x 10"2/(|jg/m3), respectively.  The  geometric mean of potency
  values  derived from  eight studies utilizing beryllium  oxide  was  2.1 x 10   /
  (Mg/m3).  Since  beryllium oxide is considered to  be  the major form of human
  exposure, this  latter value provides  support  for the occupational^ derived
  potency  of  similar magnitude, even though individual  weaknesses  in  each of  the
  animal  studies argue against the  recommendation  of an animal-only based car-
  cinogenic potency.
                                          7-93

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      Recognizing, that the  carcinogenic potency  of inhaled beryllium varies
 according  to  the form of beryllium present,  an upper-bound incremental  lifetime
 cancer  risk for continuous  inhalation  exposure at 1 ug Be/m3, rounded to one
                                              -• ^
 significant figure,  is estimated  to be  2 x 10   for general  ambient conditions.
 This  presumes that beryllium is  present in  ambient air primarily  in  the oxide
 form.   The upper bound  means that the  actual  unit  risk  is  not likely to be
 higher,  but could  be  lower  than  2 x Iff3.   In addition,  there  is  an  added un-
 certainty  regarding this value in the sense that it may over- or underestimate
 an  upper bound due to assumptions made about dosimetry in the animal  and human
 risk modelling.  This  value  places beryllium oxide  in the  the third quartile of
 59  suspect carcinogens evaluated by the CAG.   It should be cautioned, however,
 that  if compounds  such as beryllium fluoride, phosphate, and sulfate  are known
 to  be present in other than  a small  percentage of total beryllium  in  the ambient
 air,  this  potency  estimate  (2 x  10"3) will  likely  underestimate the  potential
 carcinogenic  risk.   Conversely, since beryllium has  not been shown definitively
 to  induce  neoplasms via oral ingestion in any studies  to date, this potency
 estimate is likely to  overestimate risk by this route.
     The question  of beryllium potency by ingestion is highly uncertain and
 debatable  due to the  equivocal  or negative  results from  ingestion studies.
 From  a  weight-of-evidence point  of view, however,  the potential  for human
 carcinogenicity by  this  route cannot be dismissed.  The Ambient Water Quality
 Criteria Document  for Beryllium  (U.S.  EPA,  1980)  provided an  upper-limit
 potency  estimate based upon  the  negative  oral study of  Schroeder  and  Mitchener
 (1975a).   This 1980 estimate  was even higher than the  inhalation potency
 estimate presented in this  assessment,  thus, casting  much doubt on  its
 reasonableness.  The  lack of  clear-cut tumor  induction,  coupled with  the
demonstrated  very  low beryllium  absorption  in  the  intestinal  tract,  suggests
that the oral  potency could  not be higher than the  inhalation estimate and is
just as likely to be insignificant (i.e.,  close to zero).
                                        7-94

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-------
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                                     8-20

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                                   APPENDIX
          ANALYSIS OF INCIDENCE DATA WITH TIME-DEPENDENT DOSE PATTERN
     Table A-l presents  time-to-death  data with  or without  lung  tumors.  These
data  are  reconstructed from Figure 1  in  Reeves  and Deitch (1969), in which
study animals were  exposed to beryllium by  inhalation  at a concentration of
.35 ug/m3, 35 hours/week, for specific durations during the 24-month observation
period.
      The  computer program  ADOLL1-83,  developed by Crump  and  Howe (1984),  has
been  used to fit these data.   Models  with one to seven stages, and with  one of
the  stages affected by  the dose,  have been calculated.  The  model with the
maximum  likelihood  has been selected as the  best-fitting  model.  The identified
best-fitting model  has six stages, with the fifth stage  dose-affected.  Using
this  model,  the maximum likelihood estimate of  the slope (linear component),
under the assumption of  constant exposure,  is 0.81/ug/m3.   The 95  percent  upper-
confidence limit for the slope is 1.05/ug/m  .
                                          A-l

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                t"

 Exposure period
                         TABLE A-'l.  TIME-TO-DEATH-DATA3
                      Time-to-death
 1.   Control

 2.   14th -  19th
     month

 3.   llth -  16th
     month

 4.   8th  - 13th
     month

 5.   5th  -10th
     month

 6.   2nd  - 8th
     month

7.   8th  - 19th
     month

8.   2nd - 13th
    month
19  , 20 (2), 21  (6),  22" (8),  24" (8)
    (2>,  15,  20 (4), 20,
                                      ,  22~(5), 24~(3),
20"(2), 21"(5), 21+, 22",  22+(3),  24+(9)
13",
            , 20(3),
      ,  24
14", 18", 19" (4), 20+(3),
                                              '  24"(4)'
                                     22~(4),  23",  24+(3)
                                                   ,  22",
                                , 22+(4), 24+(2)
9.  2nd - 19th         16",  18"(4),  19"(2),  20~(5), 20+(3), 21+(3), 2l", 22+


 t  n and t  n indicate, respectively,  the time-to-death with and without
 lung tumor; n is the number of  replications.

 All animals were exposed to beryllium  at  a  concentration of 35 ug/m3, 35
 hours/week.
                                   *U.S. GOVERNMENT PRINTING OFFICE: 1988-5i> 8-1 5^67076
                                        A-2

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