&EPA
           United States
           Environmental Protection
           Agency
           Office of Pesticides
           and Toxic Substances
           Washington, DC 20460
EPA-560/12-80-003
October 1980
           Toxic Substances
Support Document
Asbestos - Containing
Materials in Schools

Health Effects and
Magnitude of Exposure

Proposed Rule, Section 6
Toxic Substances Control Act

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                                 EPA  560/12-80-003








                    Support Document



                   for Proposed Rule  on



Friable Asbestos-Containing Materials  in School Buildings
         HEALTH  EFFECTS AND MAGNITUDE OF EXPOSURE
                       October 1980
             Office  of  Testing  and Evaluation



        Office of Pesticides and Toxic Substances



           U.S.  Environmental Protection  Agency



                  Washington, DC   20460

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When promulgating a rule  concerning  a  chemical
substance or mixture under the Toxic Substances
Control Act  (TSCA), the Administrator  is  required
to publish a statement on the effects  of  that
substance on health and the magnitude  of  exposure
of human beings to that substance.   This  document
is a preliminary statement of these  findings  in
support of the rule "Friable Asbestos-Containing
Materials in Schools Proposed Identification  and
Notification."  It is a draft and  is released for
comment on its technical merit and policy
implication.

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                             CONTENTS



  I.   INTRODUCTION 	1



 II.   USE AND PRESENCE OF FRIABLE ASBESTOS-CONTAINING



      MATERIALS IN SCHOOLS  	2



       A.  Uses of Friable  Asbestos-Containing Materials  in



           Building Construction  	3



       B.  Presence of Friable Asbestos-Containing



           Materials in Schools	6



       C.  Number of Persons Exposed to Asbestos  in



           Schools 	12



       D.  Remaining Years  of Use for School Buildings



           	14



III.   ASSESSMENT OF RISK FROM ASBESTOS IN SCHOOLS  	15



       A.  Introduction 	15



       B.  Hazard Assessment 	17



            1.  Introduction	17



            2.  Health Hazards of Asbestos Exposure  	19



                 a.  Lung Cancer  	19



                 b.  Pleural and Peritoneal Mesothelioma  ...22



                 c.  Other  Cancers  	30



                 d.  Asbestosis 	32



                 e.  Summary and Conclusions 	43



            3.  Factors that Modify  the Risk of Asbestos-



                Induced Disease 	44



                 a.  Smoking 	44



                 b.  Age 	51



                 c.  Fiber  Size and  Type  	53


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                 d.   Summary  and  Conclusions  	55



      C.  Exposure  Assessment  	56



           1.  Asbestos  Dispersion  Mechanisms  	....58



           2.  Estimate  of Prevalent  Exposures	59



           3.  Description of  Peak  Exposures  	69



      D.  Risk Assessment  	70



           1.  Procedure for Estimating  Risks of



               Premature Death 	70



                 a.   Outline  of the  Risk  Estimation



                     Procedure  	70



                 b.   Selection  of  the  Underlying Study	72



                 c.   Asbestos Exposure  Among  the Insulation



                     Workers  	*	74



                 d.   Increased  Risk  Among the  Asbestos



                     Insulation Workers 	*	79



                 e.   Asbestos Exposure  in Schools  	82



                 f.   Selection  of  the  Extrapolation



                     Method	84



           2.  Risk  Estimates  for School Building



               Occupants	89



IV.  IDENTIFICATION  OF FRIABLE ASBESTOS-CONTAINING



     MATERIALS IN SCHOOLS  	94



      A.  Introduction 	94



      B.  Sampling  	95



      C.  Analysis  	96



 V.  CONTROL OF  ASBESTOS IN  SCHOOLS 	98



VI.  REFERENCES  	103
                              -ii-

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I.  INTRODUCTION

    Exposure to asbestos fibers can  lead  to  numerous  serious  and

irreversible diseases.  Certain building  materials  in  common  use

can release asbestos  fibers  into  the  atmosphere.   In  particular,

friable asbestos-containing  materials have been  found  to  release

fibers in concentrations which, if inhaled,  are  sufficient  to

increase the risk of  developing such  diseases.   Some  3,000,000

students and 250,000  teachers and other staff  regularly use

public school buildings which contain friable  asbestos-containing

materials and which may contain such  levels  of contamination.

    The Agency has determined that exposure  to asbestos in  school

buildings poses a significant hazard  to public health.  This

determination is based on the following considerations:


    (1)  the extent of use of friable asbestos-containing
         materials in schools,

    (2)  the number of diseases which epidemiologic studies have
         shown to be  caused  by exposure to asbestos,

    (3)  the evidence of elevated airborne concentrations of
         asbestos in  schools and other buildings where friable
         asbestos-containing materials are present, and

    (4)  an estimate  of the  degree of risk posed by these
         elevated concentrations.


    In addition, information on the  identification of  friable

asbestos-containing materials and control measures  that can be

taken to reduce the release  of and consequent  exposure to

asbestos fibers are presented.
                               -1-

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11• USE AND PRESENCE OF  FRIABLE  ASBESTOS-CONTAINING MATERIALS  IN
    SCHOOLS
    Asbestos  is a general  term for a group of  naturally  occurring
hydrated mineral silicates that  separate  into  fibers.  Asbestos
minerals used commercially include: chrysotile, amosite,
crocidolite,  tremolite asbestos, actinolite asbestos,  and
anthophyllite asbestos.
    Chrysotile is a serpentine mineral consisting of  "layers"  of
Si04 linked by Mg ions.  The other five minerals are  amphiboles,
which consist of "chains" of Si04 linked  laterally by Ca,  Mg,  Fe,
or Na ions.
    Asbestos minerals have properties which make them common
construction materials throughout the world.   The construction
industry used more than  half of  the 725,000 metric tons  of
asbestos consumed in the U.S. in 1976.  Asbestos is
incombustible, which makes it a  good thermal and electrical
insulator, and it has high tensile strength and moderate to good
chemical resistance (Levine 1978).  Its fibrous form  adds
cohesive strength to some materials.  Asbestos fibers may  be
packed, woven, or sprayed.
    Asbestos-containing  materials can be  friable; i.e.,  easily
crumbled or pulverized.  They may also be bound in a  firm  matrix
such as cement or organic resins, however, and can be hard and
resistant to damage.
                               -2-

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    A.   Uses of Friable Asbestos-Containing  Materials  in



         Building Construction



    Asbestos is used  in buildings as a  spray- or  trowel-applied



coating to building surfaces to retard  fire,  deaden  sound,  or



decorate; it is also  used  in lagging on boilers and  pipes,  and  in



cement products, plasters, vinyl tile,  and miscellaneous products



such as lab table tops and ventilation  hoods.  Asbestos-



containing sprayed- or trowelled-on materials were first used  in



the U.S. in 1935, when the material was found to  be  suitable for



acoustical purposes and for decorative  finishes in public



buildings.  In the 1950's, one of the most significant  advances



in the construction industry was the replacement  of  concrete with



asbestos to protect structural steel against  fire.   Structural



steel must be insulated to ensure that  it does not become  soft,



bend, and collaspe during  a fire.  The  replacement of concrete by



asbestos greatly reduced the weight and bulk  of large buildings



(Sawyer 1979).



    The amount of asbestos in the mixtures used in these



applications varies widely.  From 1% to 80% or more  of  asbestos,



usually chrysotile or amosite or a mixture of the two,  were



combined with other fibers (including cellulose,  mineral wool, or



fiberglass), and cement or resinous binders.   Table  1 shows the



results of analyses of a variety of sprayed-  or trowelled-on



asbestos samples from schools in the U.S.  (Battelle  1980).



Nicholson et al. (1978a) reported similar concentrations for



schools in New Jersey.  (Paint present  in  these samples may have



been applied at the time of spraying or during subsequent



maintenance operations.)



                               -3-

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Table V Site Sample Results from Battelle Bulk Sample
                  (Continued)
Sample No.
15-01A

01B

QIC

01D

03A

03B

16-01B

02A

02B

02C

02D

03A


03B

04A

04B

17-01A


01B


02A


02B



Location
Hall
water damage
Hall
water damage
Hall

Hall





Hall

Hall
wet damage
Hall
wet damage
Hall

Hall

Music room


Music room

Cafeteria

Cafeteria

Classroom


Classroom


Art room


Art room



Chrysotile Amosite
(%) (%)
90

80

50

40

20

5 40

5

0

5

10

10

10


10

5

5

0


0


0


0



Anthophyllite Other fibers
(%)
2% min.
wool


30% min.
wool
30% min.
wool
20% min.
wool
30% min.
wool


20% min.
wool




50% fiber-
glass
10% fiber-
glass

10% fiber-
glass
10% fiber-
glass
10% fiber-
glass













Nonfiber materials
5% calcite
3% opaque
10% gypsum, 5% glass.
5% opaque
10% gypsum, 5% glass.
5% opaque
20% gypsum
5% glass, 5% opaque
40% gypsum.
10% glass, 10% opaque
20% calcite
5% glass, opaque
50% opaque, 50% calcite.
40% opaque, 5% cotton
20% calcite
60% opaque
45% calcite.
50% opaque
50% calcite,
40% opaque
30% calcite.
50% opaque
25% calcite.
5% opaque.
5% cotton
40% calcite.
40% opaque
35% calcite.
10% opaque
35% calcite,
60% opaque
60% wood.
20% gypsum
10% opaque
60% wood,
20% gypsum
20% opaque
70% wood
20% gypsum,
10% opaque
60% wood.
20% gypsum.
20% opaque.
50% wood
Sample appearance
Fibrous





Fibrous



Fibrous



Granular



Granular

Chunky-
granular
Granular




Granular



Fibrous





Fibrous


Fibrous



                           -4-

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    In the U.S.,  two principal  methods  have  been used to apply



formulations of mineral  fibers,  including  asbestos,  for building



construction applications.   In  one  method, dry fibrous material



was pumped through a 2-  to  4-in.  hose.   The  hose conveyed the dry



material to a nozzle at  the  actual  site of application.  As the



dry material left the  nozzle,  it  passed through the  focus of a



ring of fine water jets.  The mixing  took  place at the focal



point, approximately 4 to 8  in.  from  the end of the  nozzle (Reitz



1972).  The mixture was  directed  against the building surface



from a distance of about 2  ft,  and  depths  of application ranged



up to 3 in.  The  material applied by  this  method often was



fibrous in nature, rather than  compact  and granular.   A coat of



resin or paint frequently was incorporated to increase the



cohesiveness of the final coating.



    In the second process,  the  material was  premixed  with water



in a hopper, and  the resulting  slurry was  pumped to  a nozzle and



sprayed on the surface (Reitze  et al. 1972).   This usually



resulted in a less fibrous,  more  compact material  being



applied.  The depth of application  generally did not  exceed 1 in.



(Barnes 1976).



    Material that was  trowelled-on  had  essentially the same



composition as the sprayed-on materials, and it too  was premixed



with water.  This material  probably formed the densest, hardest



coating of the three types.  The  depth  of  application usually did



not exceed a fraction of an  inch.



    Asbestos also was applied to  pipes  and boilers in several



ways.  In some instances, a  wet slurry  similar to  the above
                               -5-

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material was sprayed or  trowelled on.   In others, a blanket



consisting principally of woven asbestos fibers was wrapped



around the pipe and secured with plaster, tape, or a  sprayed-on



binder.



    In 1973, EPA banned  the use of spray-applied asbestos-



containing material as insulation in buildings to prevent



widespread contamination of the environment during spraying  (EPA



1973).  EPA amended this regulation in  1975 to include  asbestos-



containing pipe lagging, regardless of  the method of  application



(EPA 1975).  EPA extended this ban in 1978, ban to all  uses  of



sprayed-on asbestos (EPA 1978).  EPA also regulated the methods



of removing asbestos from a building and disposing of the wastes



generated by removal (EPA 1973).  These regulations apply to



"friable asbestos material," which is defined as material "that



contains more than 1 percent asbestos by weight and that can be



crumbled, pulverized, or reduced to powder, when dry, by hand



pressure." For the purposes of regulating the spraying  process,



EPA defined "asbestos-containing" as containing >1% asbestos in



bulk.  Thus, the regulation does not preclude the use of



materials contaminated by small amounts of asbestos (_
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    Table 2 shows the results, as of  April  1980,  of  an EPA survey



of school districts regarding  friable  asbestos-containing



materials.  EPA mailed a guidance manual which  included a  survey



form to school districts across the Nation  in May, 1979.   A copy



of the survey form follows Table 2.



    768 school districts containing 7,378 public  schools  (about



8% of the nation's total) responded to the  survey.   Of the 6,422



schools in these districts which were  built or  renovated between



1945 and 1973, 5,797 were inspected.   1,916, or 33%  of the



inspected schools that responded were  identified  as  having



friable asbestos-containing materials.



    Although school districts  across  the country  returned  forms,



districts in 7 States responded and less than 2%  of  the districts



in 22 of the remaining States  responded  (Table  3).



    EPA has preliminarily estimated that 8,545  public  schools



have friable asbestos-containing materials.  These estimates are



based on the survey responses  and follow-up contacts with  the



reporting school districts, contacts  with school  districts that



did not respond to the survey, and data  supplied  by  New York



City's program on asbestos in  schools.
                               — 7 —

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                                        Table 2. U.S. Environmental Protection Agency, Office of Pesticides and Toxic Substances Asbestos Survey Report by School District
#SCH.
•PA Reuion IN DIST.
1 45

II 69
HI 3,307

IV 184

V 540

VI 828

VII 187

VIII 261

IX 755

X 1,202

National 7,378
Totals
BLT/REN
45-78
32

62
3,180

64

466

675

94

199

670

980

6.422

#SCH.
INSP.
42

72
2.666

89

418

588

147

195

612

968

5,797

USING
PLM
10

10
357

14

106

70

22

13

53

94

749

W/ ASB/
DATE
10

4
1,574

11

53

33

33

14

79

105

1,916

•^fj- pf*l j
fT~ outi.
EXPOSED
PROB.
7

a
267

9

20

15

21

10

36

43

436

SO. FT.
EXPOSED
ASBESTOS
9.500

7,073
2,414.320

125.290

327,911

356,562

844,697

1,399,991

286,677

528,970

6,295,991

j^CHILD
EXPOS.
501

560
102,113

1.434

9,279

8,402

8.624

2.590

5.721

58.923

198,147

#sa FT
REMOVE/COST



671,953
12.512,089
41,480
6,940,000
128,370
887.885
51,190
1,876,600


1,405
1,982,250
112,920
543.566
143,157
576,566
1,150.475
25,318,956
j^SO. FT.
ENCAP/COST
1,200
2,250
1,000
721,527
6.508,988


63.840
1,009.200
269,317
25,353,650
281,500
65,000
123,800
610,000
15,200
1.400,400
142,248
866,400
1,619,632
35,815,888
#=SQ. FT.
ENCLS/COST
5,000
19,000

100,435
7,155,785


10
100
125,000
125,000
13,000

116,640
5,317.000


5.244
2,875
365,329
12.619.760
#SQ. FT.
DEFER/INSP.
4,500

6,073
1,172,854

87,720

362.100

106,291

13,500

30,347


27,300
386.968

2,197.653

Note: See the following "Asbestos Survey Report". EPA Form 7710-29 (3-79), for full text of questions 4 through 12.
                                                                                           -8-

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                                     U.S.  ENVIRONMENTAL PROTECTION AGENCY
                                          ASBESTOS SURVEY REPORT
                                           (Survey of Activities to Control
                                  Asbestos-— Containing Materials in School Buildings)
                                                                                  Form Approved
                                                                                  OMB No. 158-R-0165
                                                           GENERAL
This information is collected under the authority of the Toxic Substances Control Act, Sections 6 and 8-  EPA is compiling information
on the progress of State and local programs to control exposure  to asbestos— containing materials in schools.  This form  should be used
to periodically report information concerning the asbestos control activities in your school  district. To obtain more forms, call this
toll— free number  800—424—9065 or in the Washington, D.C. area, call 554—1404.  Data collected in this survey will be  subject to the
provisions  of the Freedom of Information Act ( 5 U.S.C. 552).
                                                   MAILING INSTRUCTIONS
MAIL ONE COPY TO: The EPA Regional Asbestos Coordinator
                      for your Region.  (For names and addresses
                      see reverse side.)
                                              ALSO, please mail a copy to your official State asbestos program
                                              contact (for name and address, call this  toll—free number:  800—
                                              424-9065 or if in the Washington, D.C. area, call 554-1404),
                                                       IDENTIFICATION
1. SCHOOL DISTRICT INFORMATION
                                            2.  PERSON TO CONTACT REGARDING THIS REPORT
                 DIS TR 1C 1
                                            NAME (last, first, & miaale initial)
 CITY OR COUNTY
                                                      JOR TT'LE
 5 T A T £.
                           z:P CODE
                                             • E 1- £ F *•
                                                                                            DATE fmo.. "Q
                                                                                                       By, & ve
                                                     SPECIFIC QUESTIONS
3. Has the school district submitted an EPA Asbestos Survey
   Report before?
           , YES
                            NO
                      ID UNKNOWN
                                               4.  How many schools  in the district were built or renovated
                                                  between 1945 and 197S;

                                              NUMBER OF "SCHOOLS" —  — —  — — —  —  — ——  —  —  —
 5.  As of	(mo./yr.), how many schools in the district
    have been inspected for the presence of friable asbestos—
    containing materials? rN-M-E-0- ScH3oLS	
                                               6. How many schools had bulk sample sona I y zed for a sbestos with
                                                  the EPA recommended technique of Polarized Light Microscopy'
                                              N"UMBE"R OF "SCHOOLS"            ~          — -—       —
 7,  Ac nf,
.(mo./yr. of
    analysis) for how many schools
    in the district was  friable ma-
    terial analyzed as containing
    asbestos?
                  8. (a) In how many schools was friable asbestos—containing material determined to present
                         an exposure problem?
                     (b) Approximately how many square feet of this material were found?
                     (c) Estimate the number of children per school year exposed to this material.  (Multiply
                         the percent of children exposed by the total number  of enrollifl students,  e.g., An
                         exposure problem in five classrooms may involve 15%.ol the total population of 700
                         students; 15% x 700 equals 105 students exposed.)
                     (d) Have the names of the  children been recorded and retained for future reference?
                                                                                   ~~|d. NAM
NUMBER OF SCHOOLS
                                   a.  NO. OF SCHOOLS
1
                                                            SQUARE FEET
                                                                                 c. NO. OF CHILDREN
                                                                                                          NAMES RECORDED

                                                                                                              YES    3' N0
Questions 9 through 11  refer to the friable asbestos—containing material that presents an exposure problem in Question K.
 9.  (a) Approximately how many square feet of this material have
       been or will be removed?
    (b) What is the estimated total cost of removal?
 a. SQUARE FEET
            ~|

             1
                                 COST;  $
                                              10. (a) Approximately how many square feet of this material have
                                                     been or wil! be encapsuloted?
                                                  (b) What is the estimated total cost of encapsulation?
                                                                a. SQUARE FEET
                                     1
                                                                                                COST:  S
11.  (a) Approximately how many square feet of this material have
       been or will be enclosed?
    (b) What is the estimated total cost of enclosure?
                                              12.  (a) For approximately how many square feet of asbestos
                                                      containing material was action deferred?
                                                  (b) Will this material be inspected periodically to de-
                                                      termine if an exposure problem exists?
 a. SQUARE  FEET
            "T

             |
                                                               a. SQUARE FEET
                                 COST:  $
1
                                       b.  PERIODIC INSPECTION

                                               G YES   D NO
13. What is the source of funding for the asbestos control
    activities in  your district?
                                              14.  When did for vcilh the asbestos  control activities in the
                                                  district begin and end?
                                                                                              TENDING YEAR"
 FUNDING SOURCE
                                                                BEGINNING YEAR
                                                          COMMENTS
EPA Form 7710-29 (3-79).
                                                               -9-

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REGIONAL OFFICES
Region 1
Mr. Paul Heffernan
Asbestos Coordinator
Air & Hazardous Materials Div.
Pest. &. Toxic Substances Br.
EPA Region 1
JFK Federal Bids.
Boston, MA 02203
(617) 223-0585

Region 2
Mr. Marcus Kantz
Asbestos Coordinator
EPA Region II
Room 802
26 Federal Plaza
New York. NY  10007
(212) 264-9538

Region 3
Mr. Fran Dougherty
Asbestos Coordinator
EPA Region III
Curtis Building
Sixth & Walnut  Streets
Philadelphia. PA 19106
(215) 597-8683

Region 4
Mr. Dwight Brown
Asbestos Coordinator
EPA Region IV
345 Courtland Street
Atlanta, GA 30308
(404) 881-3864

Region 5
Dr. Lyman Condie
Asbestos Coordinator
EPA Region V
230 S. Dearborn St.
Chicago. IL 60604
(312) 353-2291
Region 6
Dr. Norman Dyer
Asbestos Coordinator
EPA Region VI
First Internat'l Bide.
1201 Elm Street
Dallas, TX 75270
(214) 767-2734

Region 7
Mr. Wolfgang Brandner
Asbestos Coordinator
EPA Region VII
324 East 11 Street
Room  1500
Kansas City, MO 64106
(816) 374-3036

Region 8
Mr. Ralph Larsen
Asbestos Coordinator
EPA Region VIII
1860 Lincoln Street
Denver, CO 80295
(303) 837-3926

Region 9
Mr. John Yim
Asbestos Coordinator
EPA Region IX
215 Fremont Street
San Francisco. CA 94105
(415) 556-3352

Region 10
Ms. Margo Partridge
Asbestos Coordinator
EPA Region X
1200 Sixth Avenue
Seattle, WA 98101
(206) 442-5560
                                         -10-

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Table 3. Respondents to EPA Survey for Asbestos-Containing Materials in Schools
                           (As of April 25, 1980)
State
Alaska
Alabama
Arkansas
Arizona
California
Colorado
Connecticut
Delaware
Florida
Georgia
Hawaii
Idaho
Illinois
Indiana
Iowa
Kansas
Kentucky-
Louisiana
Maine
Maryland
Massachusetts
Michigan
Minnesota
Mississippi
Missouri
Montana
No.
of forms
returned
2
0
0
122
11
3
3
8
1
1
0
6
5
0
3
3
1
4
1
0
2
44
4
3
6
3
Percentage of
total districts
that responded
3.9
0
0
57.8
1.0
1.7
1.8
50.0
1.5
0.5
0
5.2
0.5
0
0.7
0.9
0.5
6.0
0.7
0
0.8
7.6
0.9
1.9
1.1
0.5
State
Nebraska
Nevada
New Hampshire
New Jersey
New Mexico
New York
North Carolina
North Dakota
Ohio
Oklahoma
Oregon
Pennsylvania
Rhode Island
South Carolina
South Dakota
Tennessee
Texas
Utah
Vermont
Virginia
Washington
Washington, D.C.
(citywide)
West Virginia
Wisconsin
Wyoming
No.
of forms
returned
7
5
1
1
44
18
3
24
6
6
14
134
0
1
5
2
22
4
0
85
119
1

25
2
3
Percentage of
total districts
that responded
2.0
29.4
0.2
0.2
5.0
2.5
2.0
7.8
1.0
1.0
25.9
26.6
0
1.1
2.6
1.3
10.0
10.0
0
63.0
39.3
100.0

45.5
0.5
6.1

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    The data for major school jurisdictions which reported



inspection results for large portions of their schools compare



favorably with the estimates.  New York City reported that  180  of



the 1,735 city schools inspected had sprayed-on friable asbestos-



containing material in general use areas or 10.4% of the city



schools.  A 1978 statewide survey of 326 schools in Rhode Island



revealed that 24 (8%) had sprayed-on asbestos material.  In nine



schools some degree of deterioration was noted (Faich 1980).



Massachusetts' Special Commission on Asbestos in Schools and



Public Buildings reported that walk-through surveys had been



conducted in all 1,432 public schools in the State which were



built or renovated between 1946 and 1972.  178 schools, 12%, were



identified as containing "sprayed-on asbestos" (Commonwealth of



Massachusetts 1978).



    Several factors, in addition to the low response rate in some



States, affect the validity of the estimates.  First, the



analysis is based on a small sample with a large response from



one geographic area (EPA Region III).  Second, this sample  is not



random, and it may reflect a bias due to the use of information



from early respondents to the survey.



    C.   Number of Persons Exposed to Asbestos in Schools



    Throughout the country, an estimated 3,000,000 students and



250,000 teachers, administrators, and other staff, including



approximately 23,000 janitorial and maintenance workers are



potentially exposed to airborne asbestos from friable asbestos-



containing materials in public schools during the school year.



An additional unknown number of persons may be exposed in private



schools.



                               -12-

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    The number of exposed students was  estimated  from  information



contained in responses to the Agency's  survey  of  school  districts



regarding friable asbestos-containing materials.   The  survey  form



included question 8(c):  "Estimate the  number  of  children  per



school year exposed to this  (friable asbestos-containing)



material."  Respondents were instructed  to consider whether only



a portion of the school's population used the  area in  which



friable asbestos-containing materials were found  and to  estimate



the "exposed" population accordingly (see survey  form).



    Adjustments were made to this data  base by contacting



responding school districts, reviewing  data from  New York  City,



and contacting school districts which did not  respond  to



determine whether the response to the survey was  biased.



    To complete the analysis, the sample school districts  were



clustered by metropolitan code (inner,city, suburban,  rural), EPA



region, number of schools in the district, and number  of students



per district.  Survey results were then extrapolated to  the



aggregate of public school districts to  estimate  the total number



of students using areas likely to lead  to exposure.



    The number of exposed teachers was  estimated  on the  basis of



National Center for Education Statistics data  that, nationwide,



there is approximately 1 teacher per 20  students.   Finally, the



number of exposed janitorial and maintenance workers was



estimated on the basis of the assumption that  there are



approximately two such staff persons for each  of  the 8,545 public



schools with friable asbestos-containing materials.
                               -13-

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    D.   Remaining Years of Use for School Buildings

    School buildings are built to last  for about  50 years,

although during the late 1950's and the 1960's, slightly  shorter

lifetimes were expected.  The 50-year estimate  is a rule  of

thumb; no studies have been found that  statistically or otherwise

validate this approximation (Gardner 1980).

    The schools most likely to have friable  asbestos-containing

materials were built between  1945 and 1973.  Using the 50-year

lifetime estimate, a school built in 1945 would have a remaining

life of 15 years, one built in 1973 a life of 43 years.   If  the

construction of the 8,545 schools with  friable  asbestos-

containing materials was equally distributed among the years 1945

to 1973, the average expected remaining life would be 29  years.

Factors that affect this estimated average are:

    (1)  spraying of asbestos was most  popular  in the late 1950's
         and in the 1960's;

    (2)  more schools were built during the  1950's and 1960's,  to
         accommodate the postwar baby boom,  than during 1945-
         1950;

    (3)  schools built in the 1950's and 1960's may not be
         expected  to last as long as those  built earlier or
         later;

    (4)  many schools are being closed  across the nation
         because  of declining enrollment.

    The first two factors would increase the expected average

remaining life of schools; the last two would reduce it.  In view

of the lack of definitive information on these  factors as applied

specifically to schools with  friable asbestos-containing

materials, an average remaining life of 30 years  has been chosen.
                               -14-

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III.     ASSESSMENT OF RISK FROM  ASBESTOS  IN  SCHOOLS



         A.   Introduction



    Friable asbestos-containing materials  that  have been  used  in



the construction of a large number of  schools release  asbestos



fibers, and the Agency believes that occupants  of  these schools



incur risks of developing diseases caused  by  exposure  to  such



airborne fibers.



    This section assesses the risks of adverse  health  effects and



premature deaths from exposures to asbestos in  schools.   In



making this assessment,  it was necessary to identify the  health



hazards of asbestos exposure  (Part B), to  estimate the amount of



asbestos to which occupants of schools are being or will  be



exposed, and to estimate the  length of time and the number of



occupants who are and will be exposed  (Part C).  This



information, in turn, was used to estimate the  number  of  people



expected to die from asbestos-caused diseases as a result of



exposure to "prevalent"  (average) levels of asbestos in schools



(Part D), if all asbestos materials currently in the schools



remain in place until the buildings are no longer  used.



    The application of asbestos materials  by  spraying  produces a



friable coating.  The fact that asbestos fibers may be released



from these coatings was  recognized as  early as  1969  (Byrom,



Hodgson, and Helms, 1969), which  led to considerable concern that



asbestos-caused diseases may  develop in occupants  of buildings



containing the coatings  (Reitze et al. 1972).   Investigators



found that fiber levels  in these  buildings varied  widely  because



of a combination of many factors  (Nicholson et  al. 1978a,
                               -15-

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Sebastian et al. 1979a).  The wide variation  of  asbestos



concentrations in time  and space means  that no single  measurement



can determine prevalent levels -of asbestos fibers  (Nicholson et



al. 1978a).  Studies do show, however,  that levels  in  buildings



containing friable asbestos materials can frequently be very high



("peak" levels; see Table 13, Part C).  Exposure to these  levels



and to lower, prevalent levels are predicted, as shown in  Part D,



to result in a considerable number of premature  deaths among



occupants of schools.



    An evaluation of the risk requires  combining estimates of



asbestos concentrations in the buildings, the risk of  disease due



to a given exposure, the number of people exposed, and the



duration of exposure.   The accuracy of  the risk  evaluation is



limited, however, because all of the available data are on a



small number of areas sampled in a small number  of buildings or



on the risk of asbestos-induced disease in only  a  few



populations.  This limitation is dealt  with in two ways:  (1)  in



most cases, reasonable  assumptions are  made about  how  well the



sampling data apply to  possible situations in schools  and  the



validity of these assumptions is discussed; (2)  when reasonable



assumptions cannot be made, cases are presented  that give  the



lowest or highest reasonable estimate of risk.   The accuracy of



the risk estimates is defined in both of these ways.



    Three sets of reasonable assumptions are  made  that give low,



medium, and high estimates of the risk  of mortality from  exposure



to the prevalent concentration of asbestos in schools. These



estimates indicate that no fewer than 100 and no more  than 7,000
                               -16-

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premature., deaths will be caused by exposure  to  prevalent  levels



of asbestos in schools if no controls are  instituted.   Additional



premature deaths caused by short-term exposures  to  "peak"  levels



of asbestos also are very likely  to occur.   However,  as explained



in Part D, the number of these additional  deaths  as well  as



morbidity due to cancer and asbestosis cannot be  estimated



quantitatively.



    B.   Hazard Assessment



         1.   Introduction



    The first step  in assessing risk from  asbestos  in schools  is



to identify the adverse health effects arising  from human



exposure to asbestos.  The evidence comes  primarily from



epidemiologic research.  Persons  exposed to  asbestos  were  found



in these studies to be at increased risk of  developing  specific



diseases, thereby implicating the diseases as hazards of  asbestos



exposure.  Indications of dose-response relationships in  the



studies support these findings.



    The use of epidemiologic research to identify a disease as a



hazard of asbestos exposure requires consideration  of four major



criteria: bias, confounding, chance, and biologic plausibility



(Cole 1979).  The proper design of studies and  analysis of



results to avoid misleading interpretation due  to bias and



confounding are explained in detail in many  epidemiologic



textbooks (e.g., MacMahon and Pugh 1970).  The  probability that



apparent associations between asbestos exposure  and specific



diseases might be due to chance alone is distinguished by the



application of standard statistical tests.   In  this assessment,



it is considered biologically plausible that asbestos exposure





                               -17-

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can increase the risk of cancer at a given anatomic  site  if



inhaled or ingested fibers can reach that site.



    Epidemiologic studies may demonstrate dose-response relation-



ships (increasing risk with increasing level of exposure)  for



asbestos-induced diseases in various degrees of detail.   Many



studies group exposure into only a small number of categories



(e.g., "high," "medium," or "low").  These studies provide



"qualitative" evidence of dose-response relationships  and  are



briefly summarized.  Other studies contain sufficiently detailed



exposure data to examine in more detail the shape of dose-



response curves within the range of observed exposures.



    Part 2 below, identifies the following diseases  on the basis



of epidemiologic reasearch as hazards of asbestos exposure:  lung



cancer; pleural and peritoneal mesothelioma; cancers of the



larynx, oral cavity, esophagus, stomach, colon, and  kidney;  and



asbestosis.



    The next step in the assessment is to identify factors that



influence the degree of risk posed by asbestos exposure.   In Part



3, smoking, age, and fiber type and size are discussed as



possible factors that modify the degree of risk.  As shown in



Part  3, the increase in lung cancer risk among smokers exposed  to



asbestos is greater than the sum of the separate  increases



produced by asbestos exposure alone and smoking alone.  Smoking



also may increase the risk of developing asbestosis.   Because



children have a greater remaining life span than  adults,  they may



have a greater likelihood of developing asbestos-induced



diseases.  The overall influence of other age-related  risk



factors, however, is difficult to assess.  All types of asbestos





                               -18-

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present in schools have  been  shown  to  be  hazardous,  and

differences in fiber size and  type  are  not  likely to affect the

risk assessment substantially.

         2.   Health Hazards  of  Asbestos  Exposure

              a.   Lung  Cancer

    Epidemiologic studies demonstrate  clearly  that the  risk of

lung cancer is increased by exposure  to asbestos  (e.g.,  Doll

1955, Selikoff et al.  1964, Peto et al. 1977,  Newhouse  and  Berry

1979).  Several studies  show  qualitatively  that the  greater the

exposure, the greater  the increase  in  risk  (Table 4).   In

addition, the authors  of two  studies of respiratory  cancer

mortality (predominantly due  to  cancers of  the  lung)  among

asbestos workers have  drawn linear  non-threshold  dose-response

curves to summarize  their data  (Figure  1) .1/1  According  to  this

curve, all asbestos  exposures,  even those of very brief  duration

or very low intensities, intensities,  increase  risk  of  cancer.
I/  Figures 1 and 2 are presented  simply  to  demonstrate  the  shape
    of the dose-response relationships  in  the  two  studies.   These
    and similar dose-response  curves  appearing  in  this report
    should not be compared directly to  each  other,  because
    substantial differences exist  among study  designs,
    measurement techniques, and exposure  conditions.   For
    instance, asbestos concentrations  in  Figures 1A and  IB were
    measured with the same type of instrument  (midget  impinger),
    but the method does not distinguish asbestos particles from
    other particles.  Thus, the apparent  difference in slope
    between the two curves could have  resulted  from a  higher
    fraction of asbestos particles in  samples  taken in the
    asbestos products factory  (Figure  IB)  than  in  samples  taken
    in the mining and milling  facility  (Figure  IB).
                               -19-

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                               Table 4.  Studies Showing Qualitative Dose-Response Relationships
                                 Between Asbestos Exposure and Increased Risk of Lung Cancer
                   Reference
                                  Type of asbestos
                         Type of exposure
                          Measure of exposure
to
o
Newhouse and Berry (1979)
Hobbsetal. (1979)
Meurman et al. (1979)
Wagoner et al. (1973)
Mancuso and El-Attar (1967)
Selikoff and Hammond (1975)
Nicholson et al. (1978b)
Hughes and Weill (1979)
Mixed
Australian crocidolite
Anthophyllite
Primarily chrysotile
Primarily chrysotile
Amosite
Primarily chrysotile
Mixed
Factory work
Mining and Milling
Mining and milling
Factory work
Factory work
Factory work
Factory work
Factory work
Intensity and duration
Duration
Intensity
Duration
Duration
Duration
Intensity
Cumulative exposure

-------
I
to
    ra

    v>
    01
   <- w
    oc
                 x through 1966

                 o through 1975
          0
500
1000
1500
                             Cumulative exposure"

                (million particles per cubic foot x years)



         Source: Adapted from McDonald and Liddell (1979).
                                  0)


                                  !
                                  0)
                                  oc
                         10



                          9



                          8



                          7



                          6



                          5



                          4



                          3



                          2



                          1



                          0
                                                                                -  B
                                                        0   100  200   300  400  500  600  700  800  900  1000


                                                                        Cumulative exposure


                                                              (million particles per cubic foot x years)



                                                       Source: Adapted from Henderson and Enterline (1979).
         aRelative risk is the mortality rate in an exposed group divided by the rate in a comparison group.

          In Study A, the comparison group is the group of least exposed workers. In Study B, it is the general

          population.

         ^Unitsfor cumulative exposure are not directly comparable among studies. See footnote on page 22.
         Figure 1. Dose-response Curves for Respiratory Cancer Mortality in Two Groups of Asbestos Workers.

                  A, Chrysotile miners and millers; B, retired asbestos production and maintenance workers.

-------
The increases are directly proportional  to  cumulative

o V^OMV-O 2/  This curve, and  its  use  in  predicting  risk increases
GXpOSl-lirG •

predicting risk increases at  low  exposure  levels,  is  discussed in

greater detail below  in Part  D.l.f.

    Direct evidence of elevated lung  cancer risk following low

cumulative asbestos exposure  is provided by a  study of  asbestos

production workers  (Seidman et al.  1979).  In this  study,  men with

less than 3 months  of employment  had  a lung cancer  mortality rate

more than two times higher than that  expected  from  general

population rates.   EPA has estimated  that  the  average  exposure

level  in  the plant  was 40,000,000  f/m3  (EPA 1979a).   Thus, an

increase  in lung cancer risk  was  detected  epidemiologically

following a cumulative exposure of  less  than 10,000,000

f-yr/m3.  Although  it was achieved  by relatively short-term

exposure  to high concentrations,  this is the lowest level of

cumulative asbestos exposure  shown  epidemiologically  to lead to

increased lung cancer risk.

              b.    Pleural and Peritoneal  Mesothelioma

    Malignant mesothelioma is an  extremely  rare  type  of cancer

that appears as a thick, diffuse  mass inside any of the serous

membranes (mesothelia) that line  body cavities.  '   Considerable
2/   Cumulative  exposure  is  calculated  by  multiplying  the average
     concentration of asbestos  in  the air  by  the  duration of
     exposure.   When concentration is measured  in fibers per cubic
     meter of air and duration  is  measured in years,  the units for
     cumulative  exposure  are  fiber-years/cubic  meter  (f-yr/nr).
 /  There  is a benign  form  of mesothelioma  (Taryle et al.
    1976).  This discussion concerns  only  the  malignant form.


                               -22-

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epidemiologic research  (e.g., Wagner  et  al.  1960,  Mancuso and



Coulter 1963, Selikoff  et  al. 1965, Newhouse  and  Thompson 1965,



Ashcroft and Heppleston 1970, Puntoni et al.  1976)  has  shown  that



exposure to asbestos can produce  mesothelioma at  two  sites:  the



pleura, the serous membrane  that  surrounds  the lungs  and



separates them from the thorax; and the  peritoneum, the  serous



membrane that surrounds the  abdominal organs  and  lines  the



abdominal and pelvic cavities.



    Neither pleural nor peritoneal mesothelioma can be  treated



effectively, and both are  nearly  always  fatal (Taryle et  al.



1976, Kovarik 1976, Saijo  et al.  1978).   One-half  of  all  patients



die during the first year  after diagnosis, and  few patients



survive longer than 2 years  (e.g., Whitwell and Rawcliffe 1971,



Rubino et al. 1972, Lumley 1976).



    As in the case of lung cancer, a  number of  epidemiologic



studies qualitatively demonstrate dose-response relationships



between occupational asbestos exposure and  the  risk of



mesothelioma (Table 5).  In  addition,  Hobbs and colleagues (1979)



found that the incidence of  pleural mesothelioma  among  Australian



crocidolite miners and  millers  increased in direct proportion to



increasing duration of  exposure.  The linear  trend  and  the



occurrence of mesothelioma among  the  workers  in this  study who



were exposed most briefly  (<3 months)  are reasonably  compatible



with a linear nonthreshold dose-response relationship  (See Part



D.l.f) .
                               -23-

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                                       Table 5. Studies Showing Qualitative Dose-Response Relationships


                                Between Asbestos Exposure and Occurrence of Pleural and Peritoneal Mesothelioma
Reference
McDonald
ISlewhouse
etal. (1970)
and Berry (1979)
Hobbsetal. (1979)
Selikoff (1
I977)
Type of asbestos
Chrysotile
Mixed
Crocidolite
Amosite
Anatomic site
Pleura
Pleura/peritoneum
combined
Pleura
Pleura/peritoneum
Measure of exposure
Cumulative exposure
Duration and
Intensity
Duration
intensity


                                                                        separately
i
to

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    Pleural and peritoneal mesothelioma are considered  "marker



diseases" for asbestos exposure.  A marker disease  is one  that  is



often, if not always, caused by a particular agent.  In all  cases



of pleural and peritoneal mesothelioma, extremely rare  types of



cancer, there have been very strong suspicions that exposure to



asbestos was the cause.  In fact, as discussed below, close



examination of individual case histories of mesothelioma patients



usually provides evidence of some identifiable exposure to



asbestos above ambient levels, even if only of brief duration or



low intensity.



    It is estimated  that "apparently complete" case history



information reveals  some source of asbestos exposure above



ambient levels for 85%-90% of all mesothelioma patients (Wagner



et al. 1971).  For some patients, however, "apparently complete"



information is actually incomplete.  Milne (1976) discovered that



the last known occupations recorded on death certificates



misleadingly indicated an absence of asbestos exposure  for 66% of



a series of mesothelioma patients later found, when their case



histories were traced more diligently, to have been exposed.



McEwen and colleagues (1971) found that the hospital records of



55% of another series of patients did not contain information on



the asbestos exposures that these patients had,  in  fact,



experienced.  In addition, mesothelioma patients who, during



personal interviews, were unable to recall experiencing any



asbestos exposure were later found to have asbestos fibers in



sections of their lung tissue taken at autopsy (Chen and Mottet



1978, Hourihane 1964).  These studies strongly imply that



significantly more than 90% of all persons with mesothelioma have





                               -25-

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been exposed- to asbestos above the ambient outdoor  exposure



levels experienced by most urban dwellers  (Selikoff and  Lee



1978).  Ambient exposure levels in urban and  rural  air may have



been responsible for a substantial proportion of  the <10%



remaining cases.  It is, therefore, reasonable  to presume  that



all cases of mesothelioma in persons who have had previous



asbestos exposure are the result of that exposure.



    Given the status of pleural and peritoneal  mesothelioma  as



marker diseases for asbestos exposure, the many well-documented



cases that have followed extremely brief exposure to high



concentrations of asbestos or long-term exposure  to low



concentrations provide evidence that risk is  increased at  these



low levels of cumulative exposure.  Table 6 lists a few  of the



cases of mesothelioma that have followed brief  or low-intensity



asbestos exposure both inside and outside the workplace.   Table  7-



lists 48 cases of mesothelioma that have occurred in persons



sharing homes with asbestos workers.  Table 8 lists 144



mesotheliomas that have occurred in persons who resided  within a



mile of an asbestos products factory, mine, or  shipyard  and  who



had no other known asbestos exposure.  These  case histories



provide evidence that very brief or low-intensity exposure to



asbestos can cause mesothelioma.
                               -26-

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             Table 6. Mesothelioma Occurring After Brief or Low-Intensity Asbestos Exposure
            Reference
   Anatomic site and nature of exposure
Lieben and Pistawka (1967)
McDonald et al. (1970)
Borowetal. (1973)
Newhouse (1973)
Greenberg and  Lloyd Davies (1974)
Nurminen (1975)


Jones etal. (1976)



Aruland Holt (1977)


Bruckman et al. (1977)

Wiiiiwell et al. (1977)


Cochrane and Webster (1978)


Seidman etal. (1979)
1 pleural; helped replace plaster board
during extensive remodeling of his house

1 pleural; mixed and applied asbestos insulation
to boilers in home for "a few hours"

1 pleural; recycled asbestos filters in a brewery

1 pleural; sawed pipe coverings at home

1 (site unspecified); handled asbestos  sheet
and pipe in a hardware store

2 pleural; stock boys in asbestos products
factory for 10 and 18 months, respectively

1 peritoneal; played on an  asbestos factory
waste pile as a child

1 (site unspecified); relined and refitted clutches
and brakes  as hobby.

1 (site unspecified); lived in a house largely
composed of asbestos sheeting

1 (site unspecified); worked on and lived adjacent
to a chicken farm with asbestos-cement buildings

1 (site unspecified)); sawed asbestos-cement
sheets for 1 day to construct two sheds

1 pleural; did repair work on own house and
handled asbestos boards

1 (site unspecified); inspector at a gas mask
assembly plant, did not handle asbestos pads
used in assembly of masks

1 pleural; resided near an asbestos products
factory for  2 years

1 (site unspecified); toll collector

2 pleural; filled gas mask cannisters with
crocidolite for 6 months

1 pleural; jeweller, occasionally cut
sections from a roll of asbestos textile

1 pleural and 1 peritoneal; worked in an
amosite products factory for less than
9 months
                                              -27-

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                                                Table 7.  Mesothelioma Occurring in Persons
                                                 Sharing Households with Asbestos Workers
                                                                                         No. of
                                             Reference                                mesotheliomas


                                     Anderson et al. (1976)                                  37a

                                     Vianna and Polan (1978)                                7

                                     Hobbsetal. (1979)                                     2

                                     Edge and Choudhury (1978)                             1

                                     Main et al. (1974)                                       1
                                                                                   Total  48
(sj                                ••••^••••••••••••••••••••••••••^•••••••••i    I         |
oo
 1                                     a Total includes cases reviewed from reports other than those listed.

-------
                                                  Table 8.  Mesothelioma Occurring in Persons

                                                Residing Near Point Sources of Asbestos Emissions
                                                  Reference                       No. of mesolheliomas



                                        Main et al. (1974)                                  105a

                                        Cochrane and Webster (1978)                         13

                                        Wagner et al.  (1960)                                  13

                                        Borowetal. (1973)                                  2

,                                       Greenberg and Lloyd Davies (1974)                    10
K>
*f                                       Arul and Holt (1977)                                 1
                                                                                  Total  144
                                      aTotal includes cases reviewed from reports other than those listed.

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         c.    Other Cancers



    The scientific evidence reported below supports  the



identification of cancers of the larynx, oral cavity, esophagus/



stomach, colon, and kidney as hazards of asbestos exposure.



    Three cohort studies of asbestos workers  (Newhouse and Berry



1979, Selikoff et al. 1979a, Rubino et al. 1979) and  two  case-



control studies (Stell and McGill 1973, Morgan and Shettigara



1976) found increases in the risk of larynx cancer following



exposure to asbestos.  In one of the studies  (Rubino  et al.



1979), the risk increased with increasing cumulative  asbestos



exposure, an indication of a possible dose-response  relationship.



    The rates of mortality due to cancers of  the esophagus and



oral cavity the latter comprised of the (buccal cavity and



pharynx) were elevated in a group of 17,800 asbestos  insulation



workers, compared with the rates in a group of other  blue-collar



workers (Hammond et al. 1979, Selikoff et al. 1979a).  These



cancers, like cancer of the larynx, have been shown  to be related



to cigarette smoking (Hammond 1966).  To allow for this



association, Hammond and colleagues (1979) accounted  for  the



smoking habits of the insulation workers and  the comparison



group.



    The asbestos insulation workers had higher stomach cancer



mortality rates than the comparison group (Hammond et al.



1979).  In addition, stomach cancer rates were elevated in a



group of amosite production workers (Selikoff and Hammond



1975).  In the latter group, the risk of stomach cancer increased



with duration of asbestos exposure, an indication of  a possible



dose-response relationship.






                               -30-

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    A clear excess risk of colon  cancer was  reported  in  a  group



of 632 asbestos insulation workers  in New York and New Jersey



(Selikoff 1977a) .  Mortality .rates  for cancers of the colon  and



rectum combined were significantly  elevated  among the larger



group of 17,800 asbestos  insulation workers  (Hammond  et  al.  1979)



and among the amosite  factory workers  (Selikoff  and Hammond



1975).  Because the results for rectal cancer were not reported



separately in the latter  two studies, only cancer of  the colon



can be said to be a hazard of asbestos exposure  at this  time.



    The large group of asbestos insulation workers also



experienced an increase in kidney cancer mortality (Hammond  et



al. 1979).  This epidemiologic finding and the corroboration lent



by an experiment in which an excess of kidney cancer  was seen in



rats fed ground, paper-based beverage filters containing 53%



chrysotile asbestos (Gibel et. al 1976) lead to  the conclusion



that kidney cancer should be considered a hazard of asbestos



exposure.



    Inhaled asbestos can  be expected to reach each of the



anatomic sites at which increased risks of cancer were shown in



the epidemiologic studies discussed above.   The  process  of



respiratory clearance  results in  exposure of the larynx, oral



cavity, esophagus, stomach and colon to inhaled  asbestos
                               -31-

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fibers 4//  Exposure of the kidneys was  shown  directly  when

chrysotile asbestos was found in the kidneys  of  rats  (Cunningham

et al. 1977) and a baboon  (Hallenbeck and  Patel-Mandlik 1978)

that had been fed the fibers.  Indirect evidence  that  the  kidneys

become exposed was provided by the detection  of  fibers in  the

urine of persons who drank water contaminated  with  the fibers

(Cook and Olson 1979).

              d.   Asbestosis

    Exposure to airborne asbestos produces  a  chronic  non-

cancerous disease of the lungs that, in its severest  form  is

called asbestosis.  As implied by its name, the  disease is caused

solely by exposure to asbestos.  It  is  characterized  by a

hardening and thickening of lung tissue that  is  called

fibrosis.  The rigidity produced by  this process  restricts the

normal movement of the lungs.  Asbestosis  is  irreversible  and

there is no effective treatment  (Becklake  1976,  Selikoff and Lee

1978).   In advanced stages, the  disease can be fatal.   In  a study

of mortality among asbestos textile  workers employed  under

extremely dusty conditions (Doll 1955), 63% of the  death

certificates listed noncancerous respiratory  disease  in

conjunction with asbestosis as the cause of death.
4/  The airways of the lungs are  lined  with  a  layer of mucus that
    is moved along by cilia, hairlike structures  attached to the
    free surface of the cells on  the  airway  surfaces.   Inhaled
    particles that become embedded  in the  mucus  eventually are
    cleared to the oral cavity, where they are swallowed or
    expectorated.
                               -32-

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    Asbestosis is a progressive disease  that has various degrees

of severity (Berry and Lewinsohn 1979).  Asbestos exposure can

continue to cause damage  to  the lungs even after direct exposure

has ceased (Becklake et al.  1979).  Symptoms likely  to prompt an

exposed individual to seek medical care, such as loss of breath

or a bluish discoloration of the skin,£/ do not aPPear until wel1

after severe oxygen deprivation has occurred (Harries 1973, Robin

1979).  In order to detect progressing asbestosis (i.e., the less

severe stages of the disease), exposed individuals must be

examined for clinical and diagnostic signs.

    Most often, medical examinations of  persons exposed to

asbestos include chest x-rays and a physical examination that

includes a determination  of  the presence or absence  of

crepitations, the abnormal lung sounds that are characteristic of

asbestosis (Leathart 1968, Forgacs 1967, 1969).  Unlike lung

function tests, which are conducted less frequently, crepitations

and abnormal x-ray findings  do not indicate directly that health

is impaired.  Instead, they  show that the disease process has

begun.  For example, persons with crepitations have  a high

probability of suffering  later decrements in lung function (Berry

et al. 1979).  Often, persons with lung  damage visible on x-rays

already have impaired lung function (Jodoin et al. 1971, Selikoff

and Lee 1978).  Abnormal  x-ray findings  also indicate that a

person is at high risk of subsequently developing more severe.
5/  This discoloration-(called cyanosis)  is due  to  an  excessive
    concentration of nonoxygenated hemoglobin  in  the blood.
                               -13-

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stages of asbestosis.  For instance, Liddell  (1979) found  that
asbestos miners and millers with lung damage  detectable on  x-rays
later experienced an asbestosis mortality rate nine times  greater
than that experienced by workers with normal  x-rays.
Consequently, although some researchers reserve  the term
"asbestosis" for advanced stages of the disease  [e.g.,  "clinical"
asbestosis  (Murphy et al. 1971) or "certified" asbestosis
(McVittie 1965)], crepitations, x-rays findings  of lung damage,
and measurements indicating decreased lung function are each
considered  signs of asbestosis in the following  discussion.
    A large number of occupational studies have  used  the various
measures of asbestosis to demonstrate dose-response
relationships.  The studies in Table 9 show qualitatively  that
the risk of asbestosis rises with increasing  asbestos exposure.
McDonald and colleagues (1979) described the  dose-response  curve
for asbestosis mortality among Canadian chrysotile miners  and
millers as  a linear relationship (Figure 2),  although they
cautioned against extrapolation to very low exposure  levels.  An
earlier study of x-ray-detectable lung damage among South  African
crocidolite miners and millers (Sluis-Cremer  and duToit 1973) is
consistent  with this finding (Figure 3), as is a very recent
study of asbestos textile workers in the United  Kingdom  (Berry
and Lewinsohn 1979).  Data from the latter study are  used  in
Figure 4 to draw dose-response curves for three  stages  of
asbestosis  (crepitations, "possible" asbestosis, and  "certified"
asbestosis).
                               -34-

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                                       Table 9.  Studies Showing Qualitative Dose-Response Relationships

                                         Between Asbestos Exposure and Various Measures of Asbestosis
Ln
I
Reference
Selikoff and Hammond (1975)
Nicholson et al. (1979b)
Hobbs etal. (1979)
Lacquet (1979)
Selikoff (1977b)
Selikoff et al. (1979b)
Selikoff (1977c)
Sluis-Cremer and duToit (1973)
Baselga-Monte and Segarra (1978)
Harf etal. (1979)
Ayer and Burg (1978)
Type of
asbestos
Amosite
Primarily chrysotile
Australian crocidolite
Mixed
Chrysotile
Mixed
Primarily chrysotile
Amosite and crocidolite
Mixed
Mixed
Mixed
Type of
exposure
Factory Work
Factory Work
Mining and milling
Factory work
Mining and milling
Shipyard work
Insulation work
Mining and milling
Factory work
Spray application
Factory work
Measure of
exposure
Duration
Intensity
Duration
Cumulative
exposure
Duration and
intensity
Duration from
exposure onset
Duration from
exposure onset
Cumulative
exposure
Mean cumulative
exposure
Duration
Duration
Measure of
asbestosis
Mortality
Mortality
Incidence
Incidence
X-ray changes
X-ray changes
X-ray changes
X-ray changes
X-ray changes
Decreased vital
capacity
Decreased forced
vital capacity

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             90
             80
             70
             60
             50
       v    40
        0)

       CC
             30
u>
cr>
             20
             10
                            100
200           300           400           500           600



 Cumulative exposure" (million particles per cubic foot x years)
700
_J

 800
                        Source: McDonald, as reported Acheson and Gardner (1979).
                         aSlope determined by the formula, slope =

                         "Units for cumulative exposure are not directly comparable among studies. See footnote on page 22.



                         Figure 2. Dose-response Curve for.Asbestosis Mortality in a Group of Chrysolite Miners and Millers.

-------
 I
LO
-J
 I
§>
03

nj
13
en
c
J3

D)
_C


o
         ro
             GO
             50
             40
             30
     20

§
             10
              0
                            1,000
                                   2,000
3,000
4,000
5,000
6,000
7,000
8,000
                                        Cumulative exposure (long-fiber equivalents per cubic centimeter x years)*1


                       Source:  Sluis-Cremer and duToit (1973).


                         aSlope determined by the formula, slope = 2 xy/Sx .

                          Converted by the authors from concentrations measured in million particles per cubic foot x years.  Units for

                          cumulative exposure are not directly comparable among studies. See footnote on page 22.
                         Figure 3.  Dose-response Curve for X-ray Signs of Asbestos in a Group of South African Miners and Millers of

                                  Amosite and Crocidolite.

-------
       80
       60
       40
       20
               slope =  0.26a
  CD
  c
  o
  a>
  a
  §
        2
  I
  8
  I
  u
0 U
                   50      100       150      200       250
                                                        O L
                             Cumulative exposure (f-yr/crrr)


               B
               slope = 0.0213
                                                         300
50       100      150      200      250
          Cumulative exposure (f-yr/cm^) b
                                                        300
              slope = 0.0096a
                  50      100       150      200       250
                          Cumulative exposure (f-yr/cm^)'3
                                                        300
         Source:  Berry, as reported in Acheson and Gardner (1979).

         aSlopes determined by the formula, slope = ^ xy / £ x^.
          Units for cumulative exposure are not directly comparable among studies
           See footnote on page 22.

Figure 4.  Dose-response Curves for (A) Crepitations, (B) Possible Asbestosis and
        (C) Certified Asbestosis in a Group of Asbestos Textile Workers
                                    -38-

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Possible  asbestosis  represents  a  judgment  by  the  factory  medical



officer,  based  on  periodic  physical  examinations  and  x-rays,  that



the disease  has progressed  to  the  extent that a worker  should



move  to a  less  dusty job.   The  diagnosis of certified asbestosis



qualifies  a  patient  for  workmen's  compensation (McVittie  1965).



Without extrapolation, the  curves  in Figure 4 show  the  following



annual incidence rates of asbestosis for workers  with previous



cumulative exposure  of approximately



25 f-yr/cm3:



    certified asbestosis    2  cases/10,000 workers/year



    possible asbestosis      5  cases/10,000 workers/year



    crepitations            65  cases/10,000 workers/year.



This  represents the  lowest  level of  cumulative asbestos exposure



at which  severe forms of asbestosis  have been detected.



    These  studies  of  dose-response relationships  imply  that the



risk  of asbestosis is proportional to  cumulative  asbestos



exposure.  Because the curves do not demonstrate  a  "no-adverse-



effect level" of exposure,  signs of  asbestosis may  well result



from  exposure levels  lower  than those  present in  the asbestos



factories, mines,  and mills  that were  studied.



    The above implication is borne out by  the results of  studies



that  show  that  signs  of  less severe  stages of asbestosis  can



occur in individuals  exposed to asbestos outside  the workplace.



The most important results  are  those reported by  Anderson and co-



workers (1979),  who  found a  high prevalence of lung abnormalities



on the x-rays of children and other  persons living  in the  same



households as asbestos workers  (Table  10).  Persons sharing
                               -39-

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                                               Table 10. Lung Abnormalities Detected on X-rays
                                              of Persons Sharing Households with Asbestos Workers
                                              Group
                             No. of persons
                               examined
              No. of x-rays with
           one or more abnormality
O
I
Controls
All household contacts
  Sons and daughters only
 <.! year of exposure only
325
679
375
192
 15 (4.6%)
239 (35.2%)a
109 (29.1%)a
 47 (24.5%)a
                                Source: Anderson et al. (1979)
                                Probability that the difference from control value resulted by chance alone is less
                                 than 0.001 (Two-tailed chi square test. See Fleiss 1973).

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households  for  less  than  1  year  with  persons  actively employed  as


asbestos workers  had  a  percentage  of  abnormalities  five  times


higher  than  that  of  controls.  The asbestos concentrations  in


these homes  are not  known,  but they are  presumed  to have  been


many times  lower  than those to which  the workers  were exposed at


their places of employment.  Thus,  persons sharing  households for


less than 1  year  with persons actively employed as  asbestos


workers had  very  low  levels of cumulative exposure.


    Another  recently  reported study concerns  office workers  whose


only known  asbestos  exposure was  from sprayed-on  insulation


materials in office  buildings in  Paris (Awad  et al.  1979).   These


individuals  received  medical examinations that  included  a


determination of  the  presence of  "crackling rales"


(crepitations).   Of  office  workers employed for 10  or more years


in building  areas with  "low protection"  but no' "specific


exposure,"  only 0.4%  had  crepitations.   The prevalence was three


times higher  (1.3%)  among workers  whoiwere present  during
                        t

construction of the  building but  who, at the  time of the  survey,


worked  in buildings  free  of asbestos  contamination.   The  highest


prevalence  (2.5%)  was. found among  employees having  direct contact


with "ceilings, sheaths,  cupboards, etc." coated  with asbestos-


containing materials.   These results  are no reported completely


and, because of the  small number  of persons with  crepitations,


cannot be ruled out  the possibility that these  findings  should be


attributed  to chance.   Nevertheless,  if  validated,  they  will form


the first direct  evidence of asbestosis  among  occupants  of


buildings that, like  many school  buildings in the United  States,


were constructed  with sprayed-on  asbestos-containing materials.




                               -41-

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    In South Africa, Sluis-Cremer and duToit  (1979) found  lung



abnormalities characteristic of asbestos exposure  (e.g., pleural



calcification) on the x-rays of nonworkers residing near asbestos



mines.  The prevalence increased with duration of  residence  in



the area, another demonstration of a dose-response relationship.



    The three studies of nonoccupational exposure  cited above



support the inference from occupational dose-response  curves that



lung damage characteristic of asbestosis can  occur in  persons



exposed to asbestos concentrations lower than those in



occupational settings.  The two best sources  of  information  for



predicting whether signs of asbestosis can result  from asbestos



exposure levels found in schools would be the findings among



household contacts of asbestos workers (Table 10)  and  the  dose-



response curves in Figure 4.  Unfortunately,  the absence of  data



on asbestos concentrations in workers' homes  prevents  a direct



comparison with the situation in schools.  The lowest  level  of



cumulative exposure actually measured in Figure  4  (25  f-yr/cm  )



is approximately 100 times the highest estimate  for adults



employed in school buildings (using a conversion factor of 1



f/cm3 = 33,000 ng/m3; see Table 18).  [Unlike the  assessment of



cancer risks, in which extrapolation is warranted  by the current



scientific understanding of carcinogenic processes and by



regulatory policy, an extrapolation of asbestosis  risks over two



orders of magnitude of cumulative exposure may be  unduly



speculative.]  Some noncancerous lung damage  probably  will result



from asbestos exposure in schools, but the extent  of damage



cannot be predicted with a reasonable degree  of  confidence.
                               -42-

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              e.    Summary  and  conclusions



    Epidemiologic research  has  identified cancers of  the  lung,



pleura, peritoneum,  larynx, oral  cavity, esophagus, stomach,



colon and kidney as  hazards of  asbestos exposure.   Inhalation of



asbestos also produces  the  non-cancerous lung disease



asbestosis.  Dose-response  relationships (increasing  risk



correlated with increasing  asbestos exposure) have  been shown or



suggested for cancer of  the lung,  larynx, and stomach, pleural



and peritoneal mesothelioma, and  asbestosis.  Two studies of



respiratory cancer  among  asbestos workers provide results



compatible with linear  nonthreshold dose-response curves.



    These dose-response  studies imply  that  asbestos exposure can



increase the risk of cancer at  lower exposure levels  than those



studied.  This expectation  is supported by  evidence of adverse



health effects resulting  from relatively low levels of asbestos



exposure.  Increased lung cancer  risk  has been observed among



workers exposed to  asbestos for the equivalent of 5 years at the



current workplace standard  of 2,000,000 f/m3.  Mesothelioma, a



"marker disease" for asbestos exposure, has occurred  in persons



with exposures as brief  as  1 or 2 days and  in persons with  steady



exposures as low as  those found in the homes of asbestos  workers



and in neighborhoods around asbestos mines, products  factories,



and shipyards.  X-ray signs of  asbestosis have been detected



among persons sharing households  with  actively employed asbestos



workers for less than a  year.   Linear  nonthreshold  dose-response



curves predict that  asbestos exposure  in schools will produce



adverse health effects  (see Part  D).   This  prediction is
                               -43-

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consistent with the occupational dose-response  curves  and  with



the observation of increased risks of disease at exposure  levels



lower than those found in the workplace.



    Part B 3, below, identifies factors  that  influence  the degree



of increased risk posed by asbestos exposure.   Part  D,  estimates



risks of cancer mortality expected to result  from  exposure to



asbestos in school buildings.



         3.   Factors that Modify the Risk of Asbestos-Induced



              Disease



              a.   Smoking



    The major factor affecting the risk  of asbestos-induced lung



cancer, other than the intensity and duration of asbestos



exposure,  is the smoking habits of exposed individuals.



Although,  as shown below, asbestos exposure alone  and  cigarette



smoking alone can each cause lung cancer in humans,  the  combined



effects of cigarette smoking and asbestos exposure produce an



increase in lung cancer risk that is greater  than  the  sum  of the



increases  produced by the two agents independently.   In  one



study, a group of 283 asbestos insulation workers  who  smoked had



a  lung cancer mortality rate approximately 90 times  greater than



the rate they would have had if they had been neither  smokers nor



asbestos workers (Selikoff et al. 1968).  In  a  more  recent study



of 17,800  asbestos  insulation workers, the rate was  50-60  times



greater  (Hammond et al. 1979).  As discussed  below,  this latter



study also showed that the combined effect of smoking  and



asbestos exposure exceeded the sum of their separate effects, an



indication that the effects of asbestos  and smoking  interact or



modify one another  in some way.



                               -44-

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    In the earlier  study of  asbestos  insulation  workers  (Selikoff



et al. 1968), there were no  lung  cancer deaths among  87



nonsmokers.  This study prompted  speculation  that  asbestos  might



increase lung cancer risk only  in  smokers  (Cole  and Goldman 1975,



Hoffmann and Wynder 1976).   The current evidence,  however,  shows



that asbestos exposure  induces  lung cancer  in smokers  and



nonsmokers alike.   The  recent study by Hammond and colleagues



(1979), found a  fivefold increase  in  the risk of lung  cancer



among 891 nonsmoking asbestos insulation workers.  Because  it



covered a larger group  of nonsmoking  workers  over  a longer



follow-up period, the study  of  Hammond et  al. had  a higher



probability of detecting an  increase  in risk  than  the  earlier



study.  Asbestos exposure, therefore, increases  lung  cancer risk



even in the absence of  cigarette  smoking (Selikoff and Hammond



1979).



    In the study by Hammond  et  al., the asbestos workers who



smoked cigarettes could have avoided  about  the same increase in



lung cancer risk if they had not  been asbestos workers as they



could have if they  had  not been smokers.   In  1978, Selikoff



supplied EPA with a set of unpublished data from this  study that



enables estimates to be made of the proportion of  lung cancer



deaths among the cigarette-smoking asbestos workers that can be



attributed to smoking alone, asbestos alone,  interaction of the



effects of asbestos and smoking,  and  unknown  factors  (Table 11).



Estimates were made of  the number  of  deaths that could be



expected among the  smoking asbestos workers if they had  been



neither smokers nor asbestos workers  (£•]_),  if they had smoked  but
                               -45-

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                   Table 11.  Observed and Expected Lung Cancer Deaths > 20 Years from

                         Onset of Exposure in a Group of Asbestos Workers with
                                    a History of Cigarette Smoking.
   Lung cancer deaths                                                                No. of deaths3


   Observed (0)                                                                      305

   Expected on the basis of:

       Nonsmoking non-asbestos workers (E^)                                            4.4
       Smoking non-asbestos workers (Eo)                                              57.5
       Nonsmoking asbestos workers (Eg)                                               35.0

   Attributable to:
       Factors other than smoking or asbestos (E-j)                                        4.4 (  1.4%)
       Smoking alone (E2 -  EJ                                                      53.1(17.4%)
       Asbestos alone (Eg - E^J                                                       30.6 (10.0%)
       Asbestos/smoking interaction (0-[E1  + (E2 - E^  + (Eg-E-,)])               216.9(71.1%)


Source: Unpublished data supplied to EPA by Selikoff (1978)

       aThe most recently published results from this study (Selikoff et al. 1979a, Hammond et al. 1979) report
        0 = 306, E.J = 4.7; E2 and Eg were not reported. We are requesting updated figures for 0, E*. Eo, and Eo
       from these researchers.

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had not been exposed  to  asbestos  (E2),  and  if  they had  never
smoked but had been exposed  to  asbestos (E3).   For Elf  the  lung
cancer mortality rates of  a  group  of  nonsmoking non-asbestos
workers from a large  study (Hammond 1966) sponsored by  the
American Cancer Society  (ACS) were used.  For  E2,  the rates for
smokers in the ACS study were used.   The  rates of  the nonsmoking
colleagues of the smoking  asbestos insulaton workers were  used  to
derive E-j.
    The results, summarized  in  Figure 5,  are nearly identical  to
the estimates derived by Lloyd  (1979)  using  published data  from
the same study and a  different  method of  derivation.  Less  than
2% of the lung cancer deaths among the  cigarette-smoking asbestos
workers were attributable  to causes other than smoking  and
asbestos exposure; over  70%  were  the  result  of some sort of
interaction between the  effects of the  two  agents.  The most
important implication is that approximately  81% of the  lung
cancer deaths could have been prevented if  none of the  men  had
been asbestos workers and  about 88% could have been prevented  if
none had been smokers.   Thus, from a  preventive standpoint, the
impacts of smoking and asbestos exposure  on  lung cancer risk were
approximately equal in this  group of  workers.
                               -47-

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co
I
                                                           Smoking
                                                           alone
                                                           (17.4%)
                                                                            Asbestos
                                                                            alone
                                                                            (10.0%)
                                                      Asbestos-smoking
                                                         interaction
                                                           (71.1%)
                                                                                           Unknown factors
                                                                                              (1.4%)
                          Figure 5. Proportions of Lung Cancer Deaths Attributable to Known and Unknown
                                   Factors in a Group of Cigarette-smoking Asbestos Workers

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    Smoking may also be  an  important  factor  in  increasing  an
individual's susceptibility  to  asbestosis.   Although  asbestosis
occurs in persons who  smoke  and in  those  who do not smoke,  (e.g,
      et al. 1979, Hammond et al  1979), Frank (1979)  reported
that asbestos  insulation workers  with a history of cigarette
smoking had an asbestosis mortality rate  2.9 times higher  than
that of workers who had  never smoked  regularly.   In addition,
several morbidity studies have  found  that clinical and  diagnostic
signs of asbestosis in asbestos workers are  more prevalent  among
smokers than nonsmokers  (Langlands  et al.  1971,  Weiss 1971, Weiss
and Theodos 1978, Harries et al.  1975, Ayer  and Burg  1978,
Mitchell et al. 1978,  Rossiter  and^  Berry  1978,  Berry  et al.
1979).
    Because none of these morbidity studies  included  a  comparison
group of persons who smoked, but  who  had  not been occupationally
exposed to asbestos, the "polyvalent" (Becklake 1973) or
nonspecific nature of  many of the diagnostic signs of asbestosis
(i.e., signs that can  be produced either  by  smoking or  by
exposure to asbestos)  could  not be  taken  into account.
Consequently,  the mortality  study (Frank  1979)  provides the
strongest evidence that  smokers are at greater  risk of  asbestosis
than nonsmokers under  similar conditions  of  asbestos  exposure.
    Data from  this mortality study  also suggest that  there  may be
a greater risk of pleural mesothelioma among cigarette  smokers
exposed to asbestos than among  nonsmokers similarly exposed
(Selikoff 1977a).  As  shown  in  Table  12,  the rate of  pleural
mesothelioma mortality among the  smokers  was more than  twice  the
                               -49-

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                    Table 12. Mesothelioma Mortality Rates in a Group of

                       Asbestos Insulation Workers, by Smoking History
                                                   Mesothelioma deaths/10,000 person- years
       Smoking history
                                                    Pleural                 Peritoneal
    Never smoked regularly                             1.6                     7.1

    Cigarettes                                          3.8                     7.3

    Pipe or cigar                                       9.7                    11.3

    Unknown                                          2.5                     3.7



Source: Selikoff (1977a).

-------
rate  among  the  nonsmokers.   (There is no evidence that smoking,



by  itself,  can  cause  pleural mesothelioma.)   In contrast,  the



peritoneal  mesothelioma mortality rates were very similar  for



both  cigarette  smokers and  nonsmokers.   The  rates in Table 12



were  not  adjusted  for age or duration of asbestos exposure,  but



they  suggest  that  reevaluation of the conclusion that pleural



mesotheliomas "occur  with equal frequency among smoking and



nonsmoking  asbestos workers" (IARC 1977) would  be worthwhile.



The high  mortality rates from both pleural  and  peritoneal



mesothelioma  among workers  who smoked only  pipes or cigars are



also  worthy of  note.   Unpublished data supplied to EPA by



Selikoff  in 1978  indicate that this small group of workers also



had a very  high asbestosis  mortality rate.   Although the possible



effect of smoking  on  the risk of pleural mesothelioma should  be



explored, it  is not likely  that this effect  (if any)  will  be



found  to  be nearly as large as the effect of smoking on the  risk



of  asbestos-induced lung cancer.



          b.   Age



    The highly  active nature of school children and their



physical  characteristics generate concern that,  under similar



circumstances,  their  degree of actual exposure  to asbestos may be



greater than  that  of  adults (Kane 1976).   Because children



generally are more active than adults,  they  have a higher



breathing rate.  They also  inhale relatively more often through



the mouth than  through the  nose.   Consequently,  more fibers  would



be inhaled  and  fewer  would  be trapped by the nasal hairs and



mucosa.   Young  children are shorter than adults and their  mouths
                               -51-

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and noses are closer to the floor.  Therefore,  they are  likely  to



inhale higher concentrations of dust that  is  stirred  up  from  the



floor.  Children also have a -greater remaining  life span,  during



which the chronic effects of asbestos exposure  can become



manifest.



    It has also been suggested that children  may  be more



biologically susceptible than adults to carcinogens,  including



asbestos (Kotin 1977, Wasserman et al. 1979).   Kotin  (1976)



stated that "...in the induction of cancer, it  is the very young



that  is always the most susceptible."  Other  observers (Doll



1962, Cole 1977), hold the issue to be far  from settled.   Kotin



(1979) reflected the uncertainty by observing more recently that



"special biological susceptibility has not  been demonstrated"  for



children exposed to asbestos.



    One epidemiologic study and one experiment  with rodents shed



some  light on this question with regard to  pleural mesothelioma.



After examining the incidence of this cancer  in an epidemiologic



study of a group of asbestos textile workers, Peto (1979)  stated



that  "the incidence 30 years after first exposure appears  to  be



much  the same irrespective of age at first  exposure."  The



incidence rates were not provided in his report;  nevertheless,  if



the annual incidence is not affected by age at  first  exposure,



then  persons exposed earlier in life experience higher lifetime



risk.  Consistent results were reported in  the  experiment  with



rodents by Berry and Wagner  (1976), who injected  crocidolite  into



the pleurae of two groups of rats:  one at  age  2  months  and the



other at age 10 months.  In the group exposed at  the  earlier  age,
                               -52-

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40% developed mesothelioma;  in  the  latter  group,  the  incidence
was only 19%  (0.005 < p  <  0.01,  two-tailed  chi  square  test).
    Neither of these studies  could  evaluate  the age-dependent
decline in the respiratory clearance  of  fibers  that occurs  in
humans, at least among smokers  (Cohen et al.  1979), and  possibly
among nonsmokers (Wanner 1977)  as well.  This decline  in
clearance capacity might greatly increase  the proportion of
inhaled fibers that reach  the pleura.  Therefore,  the  possibility
cannot be ruled out that pleural tissue  in  young  persons may  be
more susceptible but, because of the  relatively unimpaired
respiratory clearance in these  individuals,  less  severely exposed
than pleural  tissue in older  persons.
    The two studies discussed above apply  solely  to pleural
mesothelioma, which is only one of  the hazards  of  asbestos
exposure.  The empirical relationship of age  at first  exposure to
the risk of other asbestos-induced  diseases  remains an unexplored
subject.
              c.   Fiber size and type
    A great deal of research  and discussion  has been devoted  to
possible variations in risk posed by  durable  fibers differing in
size and chemical composition.   Because  these factors  are not
expected to play a major role in the  assessment of risks due  to
asbestos exposure in schools  (see part d,  Summary and
Conclusions,  below), they  are treated only  briefly here.
    The primary research relating fiber  size  to carcinogenic
potency applies only to  pleural mesothelioma, and  it  involves the
direct injection or implantation of fibers  into the pleurae of
                               -53-

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rats.  These studies strongly suggest  that  fibers  of  certain



sizes are more potent in producing mesothelioma  than  other-sized



fibers of identical or different chemical composition (Stanton



and Layard 1978? Stanton 1973; Stanton  et al.  1977;  Smith et al.



1969; Wagner et al. 1970, 1973 and 1977; Smith and Hubert



1974).  As a whole, this research indicates  that fibers  less than



1.5 microns in diameter and between 5  and 60 microns  long,



regardless of chemical composition, are  likely to  be  more



carcinogenic in the pleura than shorter  or  wider fibers.   The



evidence is not sufficient, however, to  label  fibers  with



dimensions falling outside this range  (especially  short,  thin



fibers) noncarcinogenic.



     Fiber size also helps to determine  the  ability of inhaled



fibers to reach the pleura.  Because the airways of  the  lung



diminish in size as they branch outward, longer  fibers are  more



likely to become deposited on the ciliated  surfaces  of the  upper



airways than shorter fibers  (Dement and  Harris 1979). This early



interception of longer fibers may account for  the  autopsy finding



of a  higher percentage of longer fibers  in  the lung  tissue  than



in the surrounding pleura among persons  with asbestos-related



disease  (Sebastien et al. 1979b).  Additionally, longer  fibers



are  less readily cleared from the lung  than  shorter  fibers,



especially from the alveoli: the small,  saclike  pouches  that



terminate the airways of the lungs  (Morgan  1979).   Thus,  fiber



size  is an important factor  in the transport of  inhaled  fibers.



     Evidence of variation in toxicity  according  to the chemical



composition of asbestos fibers is less firm.   There are  some
                               -54-

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indications of slight differences  in  toxicity among  the various



types of asbestos  (Acheson and Gardner 1979), but these



differences may result  in part from the different fiber size



characteristics of the  asbestos types.



    There is no evidence that the  fiber size distributions  to



which the epidemiologically  studied insulation workers were



exposed differed substantially from the distribution of sizes of



fibers released from asbestos materials in  schools.  In addition,



all asbestos fiber types found in  schools  (e.g., chrysotile,



amosite, crocidolite) are carcinogenic.  Consequently, separate



consideration of the health  effects of the  individual



mineralogical types or  fiber sizes of asbestos in this assessment



is not warranted.



              d.   Summary and conclusions



    Smoking greatly increases the  risk of asbestos-induced  lung



cancer.  Although  asbestos causes  lung cancer in both nonsmokers



and smokers, smokers exposed to asbestos have a greater risk of



developing this disease than would be expected by adding  the



separate effects of smoking  and asbestos exposure.   Smokers also



may be at a higher risk of asbestosis than  nonsmokers with



similar asbestos exposure.   Current data on the possible



influence of smoking on the  risk of asbestos-induced pleural



mesothelioma are not persuasive one way or  the other.  In



estimating the risk of  lung  cancer from exposure to  asbestos in



schools, smokers and nonsmokers will  be considered separately



when appropriate data become available from the insulation



workers study.  Current evidence indicates  that most of the
                               -55-

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increase in lung cancer risk among a group of  smokers



occupationally exposed to asbestos could have  been  prevented



either by their never having been exposed to asbestos  or by their



never having smoked.



    Although children may be more susceptible  to  the effects  of



asbestos exposure than adults, little firm evidence is available



to determine the differences in risk.  The longer remaining life



expectancy of children compared with that of adults is the  only



factor that can be  incorporated into quantitative risk estimates.



    Experimental evidence strongly suggests that  fibers of



certain sizes that  reach the pleura, regardless of  chemical



composition, are more potent in producing mesothelioma than



fibers of other sizes.  The use of data from a study of asbestos



insulation workers  for quantitative risk estimates  (see Section



III, Part D) should avoid any major uncertainties that might



otherwise have been presented by this finding.  Because there are



no data indicating  that the fiber types or sizes  to which the



insulation workers  were exposed were substantially  different  from



those present in schools, the types and sizes  in  both  settings



will be assumed to  be similar.



    C.   Exposure Assessment



    This section assesses the amount of asbestos  that  inhabitants



of schools containing friable asbestos materials  are being



exposed to by applying current data on airborne asbestos



concentrations in various types of buildings to the situation in



schools.  The results are a quantitative estimate of exposures to



the "prevalent" level of asbestos in schools and  a  qualitative
                               -56-

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description of exposures  to  "peak"  levels.   A description  of  the



methods used to make the  quantitative estimates  and a  discussion



of how closely the estimates apply  to schools are  included.



    The prevalent concentration of  airborne  asbestos fibers is



the one present most of the  time  in areas of activity  in



buildings.  Peak concentrations are  those resulting from specific



activities such as damage to or repair of asbestos-containing



materials, and they generally  are high,  localized, and of  short



duration.  For our purposes, prevalent levels are  those



determined by monitoring  areas and  taking measurements of



asbestos  concentrations over long periods of time, and peak



levels are determined  by  taking measurements of  concentrations



resulting from specific activities  over  short periods  of time.



    Because area monitoring  data  are the only consistent data



currently available on concentrations of airborne  asbestos fibers



in buildings and because  these data are  not  likely to  include



peak concentrations systematically,  only exposure  to prevalent



levels of asbestos in  schools  can be estimated quantitatively.



The area  monitoring data  do  not include  peak concentrations



systematically for two reasons: (1)  peak releases  occur



sporadically;  (2) peak concentrations are limited  to very  small



areas.  Only if continuous area monitoring were  being  conducted



at the same time as and very near a specific peak  release  would



the monitoring data reflect  peak  exposure concentrations.  In



addition, the possible mechanisms by which asbestos is dispersed



in buildings also preclude a quantitative estimate of  exposures



at peak levels, as explained below.
                               -57-

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         1.    Asbestos Dispersion Mechanisms



    The concentration of airborne asbestos fibers  is  determined



by how quickly fibers enter the air and by how quickly  they  are



removed.  In buildings containing friable asbestos-containing



materials, fibers can be released from these materials  and enter



the air in several ways (Sebastien et al. 1978, Nicholson et al.



1978a, Sawyer and Spooner 1978).  Mechanisms of fiber release



such as disturbance of the building materials by air  currents



will release fibers over a wide area and thus an elevate the



prevalent concentration.  Other mechanisms of release such as



cutting the materials will release a large amount  of  fibers



locally and over a short period of time and, thus, cause peak



fiber concentrations (up to several thousand times higher than



prevalent concentrations).  In addition, fibers that  have been



removed from the air by settling or by impacting on surfaces



(i.e., desks, light fixtures, and floors) can be resuspended in



air either diffusely or in the form of peak releases  by



activities such as dusting, sweeping, maintenance  work, etc.



    Fibers released during peak episodes eventually become widely



dispersed, and are either removed slowly (over periods  of hours



to days) from the air by settling or impacting on  surfaces or are



removed when ventilation exchanges indoor and outdoor air.   This



wide dispersion also elevates the prevalent concentration.   Table



13 gives airborne asbestos fiber concentrations that  were



measured in various buildings (Sawyer and Spooner  1978).  The



measurements include those of peak concentrations  produced by the



peak release of fibers directly from asbestos materials (for
                               -58-

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example, 2f, g, and h in Table 13) and as a result of



resuspension (for example, 2c, d, e, i, and j  in Table 13).



         2.   Estimate of Prevalent Exposures



    The prevalent exposure levels in schools containing  friable



asbestos materials were estimated by averaging the asbestos



concentrations measured in various buildings.  The exposure



estimates were based on data  from a study by Sebastien et al.



(1978) of several buildings  in Paris.  These data, which are



given in Table 14, were not  taken in a way which would represent



the contribution of peak episodes of exposure.  The choice of



which specific measurements  of asbestos concentration within a



building to use in exposure  estimates depended on certain



assumptions as to what the measurements would  represent.  Three



different assumptions were made  to give three  different  estimates



of prevalent exposure  (Table  15) that are applicable to  all



buildings containing accessible  friable asbestos materials.  A



discussion of how these different assumptions  apply to exposure



in schools and why the data  of Sebastien et al. (1978) were used



to make these estimates is given below-
                               -59-

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Table 13. Optical Microscope Analysis of Airborne Asbestos Fiber Concentrations in Various Buildings
      Sampling conditions or situation
Mean counts   No. of     Standard
  (f/cm^)    samples     deviation
     1. University dormitory, UCLA.
          Exposed friable surfaces, 98% amosite.
          General student activities

     2. Art and Architecture Building, Yale
          University. Exposed friable ceilings,
          20% chrysotile.

       a.    Ambient air. City of New Haven
       Fallout
       b.   Quiet conditions

       Contact
     0.1
     0.00
     0.02
12


15
      Source:  Sawyer and Sponner (1978)

      aNanograms/cubic meter. Determined by electron microscope.

                                          -60-
           0-0.8
           (range)
0.00


0.02
c. Cleaning, moving :,ooks in stack area
d, Relsmping light fixtures
e. Removing ceiling section
f. Installing track light
g. Installing hanging lights
h. Installing partition
Reentrainment
i. Custodians sweeping, dry
j. Dusting, "dry
k. Proximal to cleaning (bystander exposure)
General Activity
3. Office buildings. Eastern Connecticut Exposed
friable ceilings, 5 - 30% chrysotile.
Custodial activities, heavy dusting
4. Private homes, Connecticut
Remaining pipe lagging (dry)
amosite and chrysotile asbestos
5. Laundry: contaminated clothing, chrysotile

6. Office building, Connecticut Exposed sprayed.
• ceiling, 18% chrysotile.
Routine activity

Under asbestos ceiling
Remote from asbestos ceiling
7. Urban grammar school. New Haven. Exposed
ceiling, 15% chrysotile asbestos.
Custodial activity: sweeping, vacuuming

8. Apartment building, New Jersey; heavy
housekeeping. Tremolite and chrysotile
9. Office buildings. New York City
Asbestos in ventilation systems

Quiet conditions and rountine activity
15.5
1.4
17.7
7.7
1.1
3.1

1.6
4.0
0.3
0.2


2.8


4.1
0.4



79a

99a
40a


6438


296a

2.5-2008


3
2
3
6
5
4

5
6
— •
36


8


8
12



3

2
1


2


1




6.7
0.1
8.2
2.9
0.8
1.1

0.7
1.3
0.3
0.1


1.6


,1.8-5.8
(range)
0.1-1.2
(range)


40-110
(range)




186-1,100
(range)



0-800
(range)


-------
                        Table 14. Measurements of Asbestos Concentrations in Several
                   Paris Buildings Used to Estimate Prevalent Exposure Levels of Asbestos
Building8
Ground floor of
research building "A"*
Rooms in research
building "A"
"B" hangar
"C"
"H"
"K" railroad
station (open walls)
at rr
"O"
Sampling sites
Parking lots,
laus, workshops
Libraries, labs
workshops
Workshops
Dining room
Labs, workshops
Parking lot
(open walls)
Mail room
Laboratory
Mean cone.
(ng/m3)
215
55
70
29
23
16
20
38
Max. cone.
(ng/m3)
750
630
490
29
130
24
34
62
Individual samples
(ng/m3)
751,518.19,2,0.6,0.
630,460,420,225,106,
48,46,37,31,28,15,15
14,13,9,7,6,6,(21 measurements
less than 5 ng/m3)
492,65.30,24,7,6,5,2,1
28.8
134.23,14,12,11,6,5,2,1
24,12,11
34,18,17,12
62,13
Source: Sebastien et al. 1979.
Designations are those used by the authors.

-------
        Table 15. Estimated Prevalent Exposure Levels of Asbestos
  (Applicable to all buildings containing exposed friable asbestos materials)
          Assumptions used in                         Predicted concn.
           making estimates
   I.  Mean for a building represents
        the prevalent level                                    58

 II.   Maximum for a building
        represents the prevalent level                         270

III.   Average of the few highest
        concentrations for all buildings
        represents the prevalent level                         500

-------
    Estimate I  is  the mean of  the mean  asbestos  concentration  in



each building  (the mean of column 3,  Table  14).   For  each



building, this  estimate gives  equal weight  to  each measurement of



the airborne fiber concentrations but overall  Estimate  I gives



greater weight  to  individual measurements  in buildings  where many



measurments were taken  (e.g. building A).   An  accurate  estimate



of population  exposure  would require  that each measurement  be



weighted according to the number of people  exposed at that



concentration.  Estimate I approximates  this by  using the mean of



the means rather than the mean of all measurements.   The



measurements listed  in  Table 14 were  made  in areas where



activities similar to school activities  take place, and,



therefore, they represent the  asbestos  concentrations that  occur



in activity areas  in schools.  However,  they are  not  accurately



weighted according to the distribution  of school  populations.



    Estimate II in Table 15 is the mean  of  the maximum



concentrations  of  asbestos measured in  each building  (the mean of



column 4, Table 14).  The Agency believes this estimate gives



more weight to  areas of maximum human activity because  it is



likely that areas  where the maximum asbestos concentrations are



measured are areas of maximum  activity.  This  hypothesis is



supported by data  which show that human  activity  can  increase



airborne asbestos  concentrations by 50  to 200  times (Sebastien et



al. 1979a).  The major  limit to using estimate II is  that there



is no way to verify  that the highest  measurements were  obtained



in the areas of greatest human activity.  The  overall average



exposure to asbestos in buildings containing exposed  friable



asbestos materials is likely to be between  estimates  I  and  II.



                               -63-

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    Estimate III in Table 15  is  the mean  of  the  four  highest


maxima in column 4 of Table 14  (750,  630,  490, and  130  ng/m3).


Estimate III may account for  the  future deterioration of  friable


asbestos materials now in place.  Sebastien  et al.(1978),


describe the sites where the  value used in estimate III were


obtained as areas where asbestos  materials have  deteriorated.   In


the future, friable asbestos  materials that  are  now in  place


likely will deteriorate through  damage or  be  subjected  to


maintenance activities such as cutting and drilling.   The


assumptions in using estimate III to  predict  future exposure are


that deteriorated material is responsible  for the few highest


measured levels, that all materials eventually will deteriorate,


and that when materials do deteriorate, they  will cause


significantly high prevalent  asbestos concentrations.   There are


insufficient data to document these assumptions.


    These three estimates lead to the conclusion that the  current


average exposure to asbestos  in  buildings  containing  accessible



friable asbestos materials^  is  not li^ly to be less than 58

    3                               n
ng/m , it may be as high as 270  ng/irr, and,  in the  future,  it may


become as high as 500 ng/m .  Of  course,  these are  estimates of


exposure to the prevalent concentration.   Peak exposures  add


significantly to the overall  exposure of  specific groups of


people.  For example, as shown  in Part D,  janitors  can  easily be


exposed to an average level of asbestos fibers that is  more than


twice the prevalent level.
6/  Materials not enclosed by a  solid partition  such  as  a

    suspended, or false, ceiling.
                               -64-

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    The estimates 'are based  on  data  from  the  Sebastien  et al.



(1978) study because this  study meets  the  following  three



criteria:  (1) applicability  of  the data  to exposure  in  schools;



(2) consistency, reliability, and accuracy of  the  measuring and



sampling techniques; and  (3)  adequate  data on  "control"



buildings.  The  study meets  these three  criteria because:   (1)



the areas  and materials studied are  similar to those  in  U.S.



schools (see discussion below);  (2)  the measurements  were made by



transmission electron microscopy  (the  only technique  which is



accurate for environmental sampling  at low concentrations - see



below), the measurements  were checked  by  statistical  quality



control techniques, and the  samples  were  taken over relatively



long time  periods (5 days);  and (3)  comparisons were  made with



outdoor air and  with a significant number  of buildings that did



not contain asbestos materials.   Data  on  asbestos  concentrations



in U.S. buildings from a.  study  (Nicholson  et al. 1978a)  that did



not meet these criteria were carefully assessed and used  to



verify that the  results of the  Sebastien  et al. study are



consistent with  data for  U.S. buildings  (Logue 1980).



    The specific data selected  from  the  study  of Sebastien et al



represent  the exposure situation  in  U.S.  schools.  These  data are



measurements of  asbestos  concentrations  in buildings  with



accessible friable asbestos  materials.   Enclosure  of  the  material



(for example, with a suspended  ceiling) may greatly reduce



exposure, and different enclosures will  have different effects.



Too little data  are available to  determine whether the types of
                               -65-

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enclosures in the buildings sampled by Sebastien  et  al.  are



similar to those in U.S. schools.  Therefore, exposure  estimates



are too high for buildings in which enclosed or covered  asbestos



materials are present.



    Friable materials were selected for  the estimates because



they represent the materials of greatest concern.



    Asbestos levels in buildings containing friable  asbestos



materials are significantly greater than asbestos  levels  in



buildings which do not contain asbestos  surface materials.   A



statistical study (Levy, 1980) showed that there  is  less  than  a



5% probability that chance alone caused  this difference.



Therefore the Agency concludes that the  presence  of  friable



asbestos caused the difference.  In addition to elevated



prevalent exposure in these buildings, peak exposures are  likely



to be  frequent when friable materials are present  because  these



materials are easily damaged.



    The selection of friable materials for the estimates  does  not



mean that non-friable materials do not make a significant



contribution to both prevalent and peak  asbestos  exposures.  The



statistical study cited above, however,  shows that there  are



insufficient data at this time to say whether the  observed



elevation of asbestos concentration in buildings  containing  non-



friable asbestos materials (see Table 16) is caused  by  the



presence of these materials or due to chance alone.  Peak



exposures from non-friable asbestos materials can  also  occur if
                               -66-

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en
-j
 I
                    Table 16.  Comparison of Mean and Maximum Levels of Airborne Asbestos in Buildings Containing

                                             Friable and Nonfriable Asbestos Materials3'0
Buildings containing friable
Buildingb
Mean concen.
materials
Max. concen.
airborne asbestos . airborne asbestos

A-G
A-St
B
E
H
K
L
O
A-Ct
C
D
(ng/m3)
220
55
70
29
23
16
20
20
13
0.1/
3.0
(ng/m3)
750
630
490
29
130
24
34
62
28
0.2
5
Building
Buildingb
containing nonfriable materials
Mean concen.
airborne asbestos

F
T
S
G
1
J
P
Q
R


(ng/m3)
19
21
0.1
1.7
0.4
3.2
3.2
0.83
8.6


Max concen.
airborne asbestos
(ng/m3)
40
68
0.1
2.8
2.1
7.1
7.1
1.3
12


                   Source: Sebastien et al. (1978)

                   aAII asbestos measurements in buildings without asbestos-containing materials were less than 5 ng/m3.

                   ^Building notations are those of Sebastien et al.

                   GBoth enclosed and exposed asbestos-containing materials are included in this table.

-------
they are cut or drilled.  However, such materials are  far  less



susceptible to damage than are friable materials.



    The application of estimates based on various types  of  French



buildings to U.S. schools is possible, because  (1)  the materials



containing asbestos and, as shown by comparing  Table 1 and  Table



14, the uses of areas in the French buildings are the  same  as



those in U.S. schools; and (2) the French data  on asbestos  levels



in rooms with friable materials are not statistically different



from comparable data  (Nicholson et al. 1978a) for U.S. buildings



(Logue 1980).  Asbestos-containing materials in France and  the



United States are also similar in that the French processes for



applying these materials (Sebastien et al. 1978) are similar to



the processes used in the United States (cf. Section II  of  this



document).  In both cases, "friable" coatings are produced  by



mixing the asbestos with binders after the material leaves  the



spray nozzle.  In addition, both French and United  States data



reveal that most of the airborne fibers detected are chrysotile



and that the accessible asbestos material is located in  similar



places.



    The use of transmission electron microscopy techniques  is



necessary for the identification and measurement of asbestos



fibers outside of the workplace.  The optical microscopy



techniques, especially the phase contrast microscopy technique



recommended for use in the workplace (HEW 1976), are not suitable



for measurement of low airborne asbestos concentrations  in



buildings because the phase contrast technique  cannot distinguish



between asbestos and many other fibers and, because the
                               -68-

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measurement accuracy is limited by the  small  number of  fibers

counted (HEW 1976).  At low fiber concentrations a larger

proportion of the  fibers will be non-asbestos  fibers  and,  thus,

the ability to distinguish asbestos  fibers  from other fibers

becomes important.  For this reason,  transmission electron

microscopy, supplemented when necessary with  electron diffraction

to specifically identify asbestos, is the only tool suitable for

measuring airborne asbestos concentrations  outside of the

workplace. —L~

3.  Description of Peak Exposures

    Significant "peak" releases of asbestos fibers will occur and

cause the total exposure of an individual to  be higher  than the

estimated prevalent asbestos concentration.   Students,  teachers,

and school administrators will only  occasionally encounter peak

exposures.  Janitors, custodians, and maintenance workers  will

encounter them more frequently.  Available  data are insufficient

to estimate the frequency with which either group would encounter

peak exposures.
?/  Because both asbestos and  non-asbestos  fibers  are  counted,
    measurements made by phase contrast microscopy are expected
    to be higher than those made by  electron microscopy.  This  is
    found in the results of Byron, Hodson and Holms,  (1969).
    They measured  fiber concentrations in schools  (and other)
    buildings by the phase contrast  microscopy  technique  and
    found that 11  of 18 schools with sprayed asbestos  had
    concentrations greater than .005 fibers/cm  .   This
    corresponds to (using 30 fibers/ng as the conversion) to
    about 200 ng/ra  which is much higher than what Sebastien et
    al. (1978) found by electron microscopy (see Table 14).
                               -69-

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    Peak exposures occur during episodes of damage  to  friable



asbestos materials, repair or renovations  involving  the



materials, cleaning operations in buildings that contain  the



materials, or maintenance work performed in spaces  that enclose



the materials (e.g., in crawl spaces over  false ceilings).  Peak



exposures that occur during damage episodes will affect all



occupants, including students, teachers, and school



administrators; in general, however, maintenance, janitorial,  and



custodial personnel will experience peak exposures  most



frequently.  The total exposure of these groups to  asbestos may



be much greater than their exposure to  the prevalent level.



    D.   Risk Assessment



         1.   Procedure for Estimating  Risks of Premature Death



              a.   Outline of the Risk  Estimation Procedure.



    The number of people expected to die prematurely from



exposure to asbestos in school buildings can be predicted within



limits from available epidemiologic data.  The initial step in



the risk assessment procedure is to choose the most  appropriate



epidemiologic study or studies to serve as the basis for making



the estimates.  The key criteria are that  a study contain a



quantitative characterization of cumulative asbestos exposure  and



that  the study population exhibit an increase in risk  of



premature death following asbestos exposure.  A statistical model



of the relationship between cumulative  asbestos exposure and



subsequent increases in risk  (dose-response model)  is  then



established.  The cumulative  asbestos exposure of the  building



occupants is estimated using  the prevalent asbestos
                               -70-

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concentrations  (see Part C above),  the number of persons  likely



to be exposed and the probable duration of exposure  for those



persons.  Combining the exposure estimates with the  dose-response



model allows risk estimates to be expressed as the number of



premature deaths expected to occur.   In this analysis, such



estimates are made for each of three  groups of school occupants:



students, teachers and administrative staff, and custodians and



maintenance workers.  Because of the  necessary assumptions and



uncertainties in quantitative risk  assessment, three risk



estimates will  be presented for each  group: the minimum, maximum,



and most reasonable predictions of  the increases in  carcinogenic



risk expected to result from asbestos exposure in schools.



    Although asbestos exposure in schools likely will also



produce signs of asbestosis that are  not severe enough to result



in death, this  risk cannot be estimated quantitatively with



currently available data (see Section III, Part B above).  In



addition, available mortality studies do not reflect the



increased incidence of cancer because some cancers (e.g., larynx



cancer) frequently are treated with success.  These  necessary



omissions lead  to underestimates of the risk of developing



nonfatal asbestosis and treatable cancers.  This risk assessment



is further restricted to a consideration only of exposure to



prevalent levels of asbestos in schools.  Increased  risks



resulting from  exposure to peak levels have not been included in



the overall risk estimate because the frequency of these



exposures is unknown.
                               -71-

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              b.   Selection of the Underlying  Study.



    The epidemiologic study selected to be the  basis  for  making



quantitative estimates of the risk of premature death  from



exposure to asbestos in schools is a large study of asbestos



insulation workers reported most recently by Hammond  et al.



(1979) and Selikoff et al. (1979a).  In the original  report of



mortality among these workers, the men were described  as



"building trades insulation workers" who were chosen  for  their



"asbestos exposure of limited extent and intensity" (Selikoff et



al. 1964).



    The data that will be used from this ongoing study concern



12,051 men who were employed in asbestos insulation work  for at



least 10 years  (Hammond et al. 1979, Selikoff et al.  1979a).  The



results for this group are restricted to the time commencing at



the 20th year after each worker's first exposure, each worker's



20th year since first exposure.  The diseases caused  by asbestos



exposure appear after an induction period— a minimum  length of



time following  initial exposure that must elapse before risk



begins to increase.  In this study and in others (Peto 1978,



Berry et al. 1979, Seidman et al. 1979), the minimum  induction



period for mortality from asbestos-induced diseases generally has



been reported to be 10-20 years.  The use of data that cover only



the period that starts >2Q years following first exposure allows



for the induction of asbestos-induced tumors.   The results,



therefore, pertain only to the time subsequent  to each worker's



20th anniversary of employment, the time at which he  was  at



increased risk of dying from the diseases that  are hazards  of



asbestos exposure.



                               -72-

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    The mortality experience of the 12,051 workers was  observed

during the 10-year period from January 1, 1967,  to December  31,

1976 (the "follow-up period").  As each of these workers was

actively employed on January 1, 1967, and had reached the  20-year

point from initial exposure at some time before  the end of the

follow-up period, each worker was exposed to asbestos for  at

least 10 years.  Workers who had reached the 20-year mark  prior

to January 1, 1967, were traced throughout the follow-up period

(i.e., they entered observation on January 1, 1967).  Those  who

reached the 20-year mark at some time during the follow-up period

were followed only from that point on (i.e., they entered

observation on the date of the 20th anniversary of employment).

The reported increases in risk, therefore, took place >2Q years

from initial exposure among 12,051 workers, each of whom

previously had been exposed to asbestos for at least 10 years.

    In addition to allowing for cancer induction by providing

data restricted to the period that starts X20 years from first

exposure, the asbestos insulation workers study has a number of

attributes that make it uniquely suitable as a basis for

quantitative risk estimation.  No other study combines  all of

these useful attributes:

    0    The sample of 12,051 workers surviving >2Q years  from
         first exposure is very large, minimizing the probability
         of chance results.

    0    Reasonable estimates of the average asbestos
         concentrations to which insulation workers were exposed
         are available (see Part c below).

    0    Each of the diseases identified as hazards of  asbestos
         exposure was investigated and was found to be  in  excess
         (see Table 17 below).
                               -73-

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    0    The death certificates were assiduously verified with
         supplemental information (e.g., autopsy reports,
         histological specimens) in 86% of the deaths (Selikoff
         et al.  1979a), leading to a greatly improved detection
         of frequently misdiagnosed mesotheliomas (Newhouse and
         Wagner  1969, Selikoff et al. 1979a).

    0    A highly appropriate control group was used, for which
         smoking-specific results are available (Hammond 1966).

    0    The material to which the insulation workers were
         exposed (commercial asbestos, primarily chrysotile) was
         very similar and, in some instances, identical to the
         asbestos present in school buildings.

              c.   Asbestos Exposure Among the Insulation

                   Workers.

    The measure  of exposure that will be used in this risk

assessment is "cumulative exposure"—the product of the average

asbestos concentration (in this study, it is expressed as

nanograms per cubic meter of air, ng/itr) times the number of

years of exposure to this concentration.  Therefore, cumulative

exposure, which  is expressed here in units of ng-yr/m ,

incorporates the intensity and duration of exposure into a single

measure.  This system of measuring exposure has the disadvantage

of assuming implicitly that brief, high-intensity exposure is

equivalent to extended, low-intensity exposure.  For instance, a

person exposed to 100 ng/m3 for 10 years and a person exposed to

1,000 ng/m  for  1 year would both be assigned cumulative exposure

values of 1,000  ng-yr/m .  The influence of this assumption on

the risk estimates for cancer mortality under the linear

nonthreshold dose-response curve will be discussed later.

    During the 1940's and 1950's, when the insulation workers in

the underlying study received the- bulk of the asbestos exposure

responsible for  risk increases observed during the follow-up


                               -74-

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period (1967-1976), airborne asbestos concentrations  in  the  work



environment probably were higher  than the concentrations  measured



in more recent years.  Because  reliable monitoring  data  are  not



available for the earlier period, approximations must  be  made  on



the basis of the recent measurements and  in  light of changing



work practices and conditions.  Nicholson (1976) reviewed  several



monitoring studies and concluded  that "the overall  time-weighted



average exposure of United  States asbestos  [insulation] workers



in the late 1960's was less than  3  f/ml"  (3,000,000 f/m3).   This



estimate, made under the assumption that  insulation workers  in



the late 1960's worked with asbestos-containing materials  only



half of the time, agrees closely  with the figure of 4,200,000



f/nr derived by  the National Institute for Occupational Safety



and Health (NIOSH 1972) for full  time asbestos insulation  work.



Consequently, 3,000,000 f/m3 represents the  lowest  reasonable



estimate of the  average asbestos  concentration to which workers



in the underlying study were exposed.



    Nicholson (1976) also found that, during the late  1960's,



"work practices were virtually  identical  to  those of the  past,



and ...few controls of significance were  in  use."   Nevertheless,



he identified two major changes in  the conditions of  insulation



work over the years.  First, workers in the  1940's  and 1950's



were in contact more often  with insulation containing  asbestos,



as opposed to insulation containing fibrous  glass and  other



materials that recently have become more  popular.   Second,  the



asbestos content of insulation materials  containing asbestos



declined by as much as one-half over the  period  ranging  from the
                               -75-

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1940's and 1950's to the late 1960's.  These  factors helped  lead



Nicholson (1976)  to state that "insulators' average exposures  in



the United States during the past  years could have ranged  from 10



to 15 f/ml" (10,000,000-15,000,000 f/m3).  Therefore,  15,000,000



f/m3 is the highest reasonable estimate of the average exposure



level or the asbestos insulation workers.



    The most reasonable estimate lies between 3,000,000 and



15,000,000 f/m3.   If it is assumed that insulation workers in  the



late 1960's handled asbestos one-half of the  time, that previous



workers handled asbestos three-fourths of the time (a  50%



increase), and that older insulation materials containing



asbestos had twice the asbestos content of newer asbestos-



containing materials, the recent average exposure level



(3,000,000 f/m3)  can be multiplied by a factor of 3 to yield an



estimate of the earlier concentration.  This conversion yields a



"most reasonable" estimate of approximately 9,000,000  f/m  for



the average asbestos concentration to which the workers in the



underlying study were exposed.



    The units  in which the minimum, maximum, and most  likely



average exposure levels are expressed can be converted from



fibers per cubic meter to nanograms per cubic meter.   In a study



conducted for  the Office of Pesticides and Toxic Substances, EPA



(Versar 1980), it was concluded that for insulation work,  a



fiber-to-mass  conversion ratio of  30 f/m3 to  1 ng/m3 is the  best



approximation  if fibers are counted by light microscopy.   This



factor is in general agreement with data on fiber size



distributions  for the asbestos industry as a whole (Dement and

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Harris 1979) and  for  insulation work  in  particular  (Nicholson
1976).  It should be  remembered that  this  conversion  factor  is
rough and currently cannot be  verified because  the  nature  of the
industry has changed.   It is,  however, the  best  available
estimate.
    Conversion of the  three  estimates of average asbestos
exposure for the  insulation  workers studied by  Selikoff's  group
yields the following  estimates:
              maximum          500,000 ng/m3
              most reasonable  300,000 ng/m3
              minimum          100,000 ng/m
    It is important to determine  the  period of  exposure  to these
concentrations that should be  held reponsible for the  increases
in risk detected  during the  observation  period  (1967  through
1976).  Asbestos-induced increases in risk do not appear until
2.10 years after exposure (Peto 1978,  Seidman et  al. 1979), so the
attributable exposure  period for  each worker in  this  risk
assessment ends 10 years prior to the time  the  worker  entered
observation.
         A         B               C                  D
          |<	>|<	10  yr	>|<	10 yr	>|
    Under the approach described  above,  A-B (ending for  most
workers on December 31, 1956)  is  the  period of  attributable
exposure.  C-D is the  follow-up period,  during  which  all exposure
is presumed to be "wasted" in  the sense  that it  is  not
responsible for increases in cancer risk during  the same
period.  B-C is an additional  period  of  time during which
exposure is considered to be "wasted."   If  the  minimum induction

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period for death from asbestos-induced  neoplasms  were  exactly 10



years, the greatest degree of underestimation of  exposure  would



result from the fact that exposure during year  B+l  ended,  not 10



years, but 18 years before year D-l began.  The choice,  however,



of a length of 10 years for the additional  "wasted"  exposure



period (B-C) is a conservative one.  The minimum  induction period



for mesothelioma, for instance, appears to  be closer to  20 years



than to 10 years (Selikoff et al. 1979a).   For  lung  cancer,



Peto's (1978) data show the minimum induction period to  be about



15 years.  If the minimum induction period  for  these diseases



were >20 years, no relevant exposure would  be ignored  by choosing



10 years for the length of period B-C.



    Thus, although a certain degree of exposure relevant to



increased risk during the follow-up period  (C-D)  is  likely to be



ignored under this approach, 10 years for B-C is  considered a



reasonable length in order to optimize three goals:  (1)  to make



use of the published mortality data from the insulation  workers



study; (2) to avoid attributing "wasted" exposure to increased



risk during the follow-up period; and (3) to avoid  labeling



exposure "wasted" that actually contributed to  increased risk



during the follow-up period.  The attributable  exposure  period



for each of the 12,051 workers was his period of  employment



ending 10 years before he entered observation.  The  total  number



of years of relevant exposure for the group divided  by 12,051



yields the average exposure period.   [Note:  We are  requesting



this total from the researchers.  For the time  being,  a  figure of



20 years will be used as the mean attributable  exposure  period in



the calculations.  When the actual value becomes  available, it



will replace the 20-year figure.]



                               -78-

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    It was estimated above  that the average exposure  level  for

the insulation workers was  between 100,000 and 500,000  ng/m3,

with the most reasonable estimate being 300,000 ng/m3.  Over  a

20-year average exposure period, these figures yield  the

following estimates of cumulative exposure:

         maximum            1.0 x 107 ng-yr/m3

         most reasonable    6.0 x 106 ng-yr/m3

         minimum            2.0 x 106 ng-yr/m3

    The three values are estimates of the average cumulative

asbestos exposure of the 12,051 workers at the time 10  years

before observation began.   Many continued to be exposed, but

exposure beyond that point  is not thought to have contributed to

the observed increases in risk.

         d.   Increased Risk Among the Asbestos Insulation

              Workers.

    Following the 20-year induction period, the researchers

compared the observed number of deaths from specific  causes among

the 12,051 workers to the number expected on the basis  of

mortality rates in an appropriate comparison group .__^_  Tne

greater number of observed  than expected deaths indicates

increased risk.  The results for cancer deaths are shown in Table

17.  The use of 95% confidence  intervals for the observed number
8/  The data for the control or comparison  group  were  obtained
    from a large study sponsored by  the American  Cancer  Society
    (Hammond 1966) of the age-, calendar  year-, and  smoking-
    specific experience of white males with at most  a  high  school
    education and a history of occupational exposure to  dust,
    fumes, vapors and gases, excluding farmers.
                               -79-

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          Table 17.  Mortality Data Taken from the Study of 12,051 Asbestos Insulation
                 Workers and Used To Make Quantitative Estimates of Risk from
                                Asbestos Exposure in Schools
Cause of death

Cancer, all asbestos-
related sites
Lung
Pleura
Peritoneum
Larynx, buccal
cavity, pharynx
Esophagus
Kidney
Colon-rectum
Stomach
Expected
deaths (Ej)a

145.8
81.7
0
0
7.5
5.1
8.5
30.5
12.5
Observed
deaths (O,)

692
397
61
109
21
17
15
54
18
95% Confidence
limits5
Lower
641.4
358.9
46.6
89.5
13.0
9.9
8.4
40.6
10.7
Upper
745.6
438.1
78.4
131.5
32.1
27.2
24.7
70.5
28.4
Statistical
significance
level0

< 0.001
<0.001
<0.001
<0.001
< 0.001
<0.001
0.027
<0.001
0.084
Source: Hammond et al. (1979)

al\lumber of observed deaths based on death certificate information only, except for pleural and
 peritoneal mesothelioma. Supplemental information was used for these two cancers.  This
 procedure was recommended by Hammond et al. (1979).

^Method of Bailar and Ederer (1964), assuming a Poisson distribution of observed deaths. Values
 from Documenta Geigy (1970), some by linear interpolation.

cMethod of Bailar and Ederer (1964), assuming a Poisson distribution of observed deaths. One-tailed
 test, values from Molina (1942).

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of deaths  is a way of  accounting  for  the  role  of chance variation



in the results.   In comparisons with  the  expected number of



deaths, the minimum risk estimate  is  provided  by the lower 95%



confidence limit  for observed deaths,  the maximum estimate by the



upper 95% confidence limit  for observed deaths,  and the most



likely risk estimate by the  actual  number of deaths observed.



    The measure of increased risk  most useful  for predicting



premature mortality from asbestos  exposure in  schools  is the



difference between the observed  (   O.j_) and expected (   E.j_)



numbers of deaths from the  cancers  related to  asbestos  exposure



divided by the total number  of deaths  expected from all causes



(ET = 1,148.0)  (Hammond et  al. 1979).  This measure is the



fraction of all expected deaths that  were "in  excess"  because  of



the asbestos exposure.  It  is called  "lifetime risk" (LR)  by the



EPA Carcinogen Assessment Group, Office of Research and



Development, EPA, and  is defined, as follows:   LR= (Oi-Ei)/ET.  If •



the study were carried out  until all  were deceased  (actually,



only 16% of the 12,051 workers died during the observation



period),   (0^-Ej_) would equal the  total number of "excess,"  or



premature deaths.



    In using lifetime  risk,  as defined above,  as the measure of



increased cancer  risk  in this assessment,  certain assumptions



must be made.  First,  it must be assumed  that  the estimate  of



lifetime risk when only 16%  of the  workers have  died will  be the



same when all 12,051 have died.  Second,  it must be assumed that



this estimate of  lifetime risk among  persons exposed as .adults



will be indicative of  the lifetime  experience  of exposed school
                               -81-

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children, who have a greater remaining period of  expected  life



during which the effects of asbestos exposure can become



manifest.  The use of the lifetime risk measure,  therefore,  does



not allow the greater remaining life expectancy of  children  to  be



taken into account and for this reason may underestimate risk.



    The mortality rates for each of the cancer hazards of



asbestos exposure were increased among the insulation workers



(Table 17).  The data for the separate causes of  death can be



combined in order to estimate overall lifetime risk for all



asbestos-induced cancers:



    maximum =      (745.6 - 145.8)/l,148.0 = 0.522



    most reasonable =  (692 - 145.8)/l,148.0   =  0.476



    minimum =      (641.4 - 145.8)/l,148.0 = 0.432



    The results give a most reasonable estimate that the overall



mortality rate was increased by 48% above the expected value by



asbestos-induced deaths from cancer.  (Additional premature



deaths from asbestosis are not included here.)  The  above



lifetime risk estimates will be used to predict the  risks of



mortality from asbestos exposure in schools.



              e.   Asbestos Exposure in Schools



    In Section III, Part C, three prevalent asbestos



concentrations were estimated for school buildings.  Estimates  I



(58 ng/m3) and II (270 ng/m3) were developed to reflect current



concentrations and Estimate III (500 ng/m3) to reflect



concentrations in the future, as the building materials



deteriorate.  The risk assessment concerns exposures over  the



next 30 years.  Consequently, Estimates I and III will be  used  as
                               -82-

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the minimum and maximum future concentrations,  respectively.



Estimate II, although developed as a maximum estimate  of  the



current concentration, will be used as  the most reasonable



estimate of future concentrations.



    Three groups of school building occupants are  considered:



students; teachers and administrative staff; and custodians and



maintenance workers.  It was estimated  in Section  II that



approximately 3,000,000 students, 222,000 teachers and



administrative staff, and 23,000 custodians and maintenance



workers are occupying schools that contain friable asbestos



materials (See Section II above).  These numbers of exposed



school occupants at risk of death from  asbestos-induced cancers



need to be adjusted to reflect the number expected to die before



a minimum period of time from first exposure has elapsed.



Adopting the same 20-year minimum induction period as in the



insulation workers study and assuming that the  average student is



first exposed at age 12 and the average adult school occupant at



age 30, national life tables (NCHS 1978) can be used to estimate



that 2.2% of exposed students and 5.9%  of exposed  adults will die



before 20 years have elapsed from first exposure.  The estimated



number of school occupants at risk, then is 3,000,000 - 2.2% =



2,934,000 persons exposed while attending school,  222,000 - 5.9%



= 208,900 teachers and administrative staff, and 23,000 - 5.9% =



21,600 custodians and maintenance workers.  The average remaining



service time for the buildings is approximately 30 years  (See



Part II above).  Therefore, the average cumulative exposure for



the adult occupants is equal to the prevalent asbestos
                               -83-

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concentration times 30 work years.!/  For students,  it  is  the

prevalent concentration times 15 work years.  These  estimates  are

shown in Table 18.

    The calculations were made under the assumption  that each  of

the current school occupants will be exposed for the entire  30-

year period that the buildings will remain  in service.  Although

this assumption is not technically correct  (as students graduate

and adults leave their positions, others will replace them), as

long as the exposed populations continue to average  3,000,000,

222,000, and 23,000, respectively, the risk estimates will not be

affected.  This is because of the nature of the cumulative

exposure measure  (1,000 ng-yr/m  resulting  from either 10 years

at 100 ng/m  or 1 year at 1,000 ng/m ) and  the linear

nonthreshold dose-response model (cumulative exposure of 1,000

persons to 1,000 ng-yr/m3 yielding the same number of premature

deaths as cumulative exposure of 100 persons to 10,000 ng-yr/m3).

              f.   Selection of the Extrapolation Method

    Once the most suitable epidemiologic study of asbestos

workers has been chosen for the risk assessment, a method must be

selected for using the results of the study to predict  the
9/  A work year is assumed to be made up of 50 weeks at  5 days  a
    week and 8 hours a day.  A school year is assumed to be made
    up of 33 weeks at 5 days a week and 6 hours a day.
    Therefore, 2 school years equal one work-year:

    33 weeks x 5 days x 6 hours = 0.5.
    50 weeks   5 days   8 hours
                               -84-

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00
en
                                          Table 18. Estimates of Cumulative Asbestos Exposure in Schools3
o
Cumulative exposure levels (ng-yr/m ) for:
Population group
Students
Teachers, administrative
staff
Custodians, maintenance
workers
Average
number exposed
2,934,00
208,900
21,600
Minimum
estimate of risk
870
1,740
1,740
Most reasonable
estimate of risk
4,050
8,100
8,100
Maximum
estimate of risk
7,500
15,000
15,000
            aAssuming 30 work years of exposure per adult and 15 work years of exposure per student See discussion on page 92.

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increase in carcinogenic risk that will result from asbestos

exposure in schools.  The prediction is made by extrapolating10/

from the exposure levels experienced by the asbestos  insulation

workers to the lower levels of asbestos to which school occupants

are exposed.  A dose-response curve is developed to describe  the

relationship between cumulative asbestos exposure and subsequent

increases in cancer risk.  From this curve, predictions of

increased risk can be derived that correspond to cumulative

exposure levels lower than those for which epidemiologic data are

available.  Because the empirical relationship of dose to

response at these exposure levels is unknown, criteria must be

established for selecting the most appropriate dose-response

curve.

    Two general types of evidence can be used to show that a

dose-response curve or model is unsuitable:  (1) knowledge of the

biological processes that influence the degree to which inhaled

asbestos increases carcinogenic risk, and  (2) the dose-response

data available from epidemiologic studies or experiments with

laboratory animals.  The first type of information, often called

"pharmacokinetics," includes a carcinogen's "absorption,

distribuiton, reactions with cellular components, and

elimination," as well as its interaction with physiologic
10/ If, as in most risk assessments, it is assumed  that  the  dose-
    response curve passes throught the point corresponding to
    zero exposure and zero increase in risk, the prediction  is
    technically an interpolation.  Nevertheless, the conventional
    term, extrapolation, will be used here.
                               -86-

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mechanisms of activation and detoxification  (Gehring  et  al.



1977).  This kind of information, if available,  can lead  to



inferences about the shape of the dose-response  curve  at  low



doses, including the possibility of a threshold  dose  below which



the risk of cancer would not be increased  (Cornfield  et  al.



1977).  EPA is unaware of information about  the  pharmacokinetics



of asbestos that would enable such inferences  to be drawn.



    The second type of evidence, dose-response data from



epidemiologic and toxicologic studies, is  available for asbestos-



induced carcinogenicity.  Table 19 shows the results of



statistically "fitting" several dose-response models that have



been developed for chemicas carcinogens to data  from two studies:



an epidemiologic study of asbestos workers (Henderson  and



Enterline 1979, see also Figure 1-B) and an  experiment with rats



(Wagner et al. 1974).  By the usual and widely accepted criterion



that a p-value greater than 0.05 or 0.10 indicates an  adequate



fit (Remington and Schork 1970), none of the models can be



dismissed on the basis of these studies.



    Current scientific evidence alone cannot be  used to select



the most appropriate dose-response curve for this extrapolation



because none of the curves in Table 19 can be ruled out on the



basis of pharmacokinetics or available dose-response data.  Of



these curves, however, linear nonthreshold regression  (see, e.g.,



Figure 1) usually provides the highest predictions of  increased



risk and there is no strong scientific reason  to prefer any of
                               -87-

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                                                   Tdble 19. Dose-response Curves Applied to Two Studies of
                                                        Asbestos Exposure and Carcinogenic Response
                                                                                      Goodness-of-fit p-value

                       Dose-response curve       Reference                  Epidemiologic studya>e     Experiment with rats"

                       One-hit                  Brown (1976)                    0.58                         °-08
                       Multi-hit                 Van Ryzin and Rai (1980)         0.42                         °-13
                       Multi-stage (1 stage)       Crump (1980)                    0.58                         O-11
                       Multi-stage (5 stages)      Crump (1980)                    0.53C                        ° °9C
                       Linear regression          Meter and Wasserman              0.87                         0-10
                                                (1974)


                       aHenderson and Enterline (1979)
                       bWagneretal. (1974)

                       cThe results of a Monte Carlo simulation
,                      "The "p" values calculated from the chi-square (X2) statistic are based on the difference
CD                      between the observed (Oj) and the expected (Ej) counts in the ith dose group. The
^°                      degrees of freedom equal number of dose levels-1-(number of parameters estimated).

                                                      X2  = £ (Oj-Ej)2/Ej


                       eln the epidemiologic study, each measure of response concerns a group of people with a
                        unique age distribution; hence, the "background" mortality rates will differ among the
                        groups. To fit models with this type of data, it is necessary  to adjust the observed response
                       to what they would be if there were a common "background" rate. The risk attributable
                        to the carcinogen is calculated from Abbott's equation:

                                                    P = (pdose  ~Pcontro|) / ^1~Pcontrol*

                        The adjustment to common "background" is done by recalculating the observed response,
                       pdose»  as p' dose •  Wnere p' control rePresents tne common "background" rate:

                                                           P  dose = p^~p' control' +  P control

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the dose-response curves  that yield  lower  estimates  of  increased



risk.  Consequently, the  Agency has  chosen to  take the  most



prudent course with respect to public health by  using a linear



nonthreshold dose-response curve to  extrapolate  from the  asbestos



exposure levels experienced by the  insulation  workers to  the



lower levels of asbestos  to which school occupants are  exposed.



         2.   Risk Estimates for School Building Occupants.



    Figures from Tables 17 and 18 and the  preceding  discussion



are summarized in Table 20.  They are arranged in the way that



yields minimum, most reasonable and  maximum estimates of



increased risk for school building occupants.



    When the linear nonthreshold model is  used, calculation of



predicted risk levels is  fairly simple.  For instance,  as shown



in Table 21, the minimum  lifetime cancer risk  for school  children



would be:



    (0.432 x 870 ng-yr/m3)/(1.0 x 107 ng-yr/m3) = 3.8 x 10~5.



    Multiplying this figure by the number  of students yields the



minimum estimate of premature deaths:



    (3.8 x 10 ~5) x (2,934,000) = 111.
                               -89-

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I
VO
o
I
                 Table 20. Summary of Cumulative Exposure and Lifetime Risk Estimates To Be Used in

                              Quantitative Risk Assessment of Asbestos Exposure in Schools
Estimates leading to:
Minimum
Population group risk estimate
Insulation workers 1.0 x 10
Students 870
Adult schools occupants 1,740
Insulation workers 43.2
Most reasonable
risk estimate
o
Cumulative exposure (ng-yr/m0):
6.0 x 106
4,050
8.100
Lifetime cancer risk {%}
47.6
Maximum risk
estimate
2.0 x 106
7,500
15,000
52.2

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Table 21. Quantitative Risk Estimates of Mortality from Exposure to Asbestos in Schools



1
M
1


Lifetime risk
o i *• Most
Population group Minimum reasonable
2,934,000 students 3.8 ;< 10~5 3.2 x 10"4
208,900 teachers. R A
administrative staff 7.5 x 10 ° 6.4 x 10"^
21, 600 custodians, R .
maintenance workers 7.5 x 10~° 6.4 x 10~^

Premature deaths
Most
Maximum Minimum reasonable Maximum
2.0 x 10~3 111 960 5,868
3.9 x 10~3 16 142 814
3.9 x 10~3 2 15 84
Totals 129 1,117 6,766

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    The results of this and similar calculations  are  shown  in

Table 21.  A total of approximately 100 to  7,000  premature  deaths

are anticipated to occur as a result of exposure  to prevalent

concentrations of asbestos in schools containing  friable  asbestos

materials over the next 30 years.  The most  reasonable  estimate

is approximately 1,000 premature deaths.  About 90% of  these

premature deaths are expected to occur among persons  exposed as

school children.  The remaining 10% include  teachers, custodians,

and other adult occupants of the buildings.  The  most reasonable

estimates represent extrapolations of approximately four  orders

of magnitude from the exposure levels experienced by  the

insulation workers.

    The risk estimates in Table 21 are subject to further

refinement.  For instance, the influence on  risk  of the greater

remaining life expectancy of children compared with that  of

adults has not yet been incorporated into the assessment.   In

addition, when supplemental information requested from  the

investigators who conducted the insulation workers study  is

supplied, it will alter these estimates to  some degree.   The

information requested is:

    0    the total number of person-years of exposure accumulated
         by the 12,051 workers up to the time 10  years  before
         they entered observation;

    0    the number of person-years of observation and  the  number
         of observed and expected deaths from lung cancer,
         asbestosis, and pleural mesothelioma by  smoking  history;

    0    the number of observed and expected deaths due to  cancer
         of the colon separate from those due to  cancer of  the
         rectum.
                               -92-

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    This additional  information, with  the possible  exception  of



the smoklng-specific data for lung cancer,  is not expected  to



have a major effect on the overall results  of the risk



assessement.  At present, an assumption  is  implicit  that  the



distribution of smoking habits among exposed school  occupants



will be the same as among the insulation workers.



    It is important to emphasize that  the risk estimates  in Table



21 concern only a portion of the total adverse impact on  health



expected to result from asbestos exposure in schools.  The  less-



than-fatal effects of asbestos exposure on  lung function  and  the



number of cases of certain types of cancer  that may  be treated



successfully (e.g., larynx cancer) are not  included  in this



quantitative risk assessment.  The substantial but  unquantifiable



risks resulting from peak exposures also are absent  from  the



assessment.
                               -93-

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IV.   IDENTIFICATION OF FRIABLE ASBESTOS-CONTAINING MATERIALS  IN




     SCHOOLS
    A.   Introduction



    In order to control the release or resuspension of  asbestos



in schools or other types of buildings, it is necessary to



determine whether asbestos is, in fact, present  in the  bulk



building materials.  This determination can be made by  examining



building records and by analyzing samples of the materials.



Records will not establish conclusively that asbestos is not



present in a building, as they may be incomplete or there may



have been a substitution (e.g., of asbestos for  nonasbestos



fibers) of the components in the material that was applied.  The



magnitude of the risks involved makes it necessary to take



additional, more extensive steps such as sampling/analysis to



ensure the accurate identification of friable asbestos-containing



materials.



    To locate friable materials, it is necessary to visually



inspect the steel support beams, columns, ceilings, and walls of



all areas of the school.  Asbestos-containing materials also may



have been applied to hidden areas, such as those above  a



suspended ceiling, and they must be checked.  Inspectors should



direct particular attention to boiler rooms and other equipment



areas, in view of the frequent use of asbestos as insulating



material.



    Procedures for inspecting buildings and taking samples of



friable materials and guidelines for establishing the presence of



asbestos in these materials are described in two recent EPA



publications (EPA 1979b and EPA 1980, respectively).





                               -94-r

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    B.   Sampling
    A sample of friable material can be  obtained  by  penetrating
the depth of the material with a small canister or jar  or  by
dislodging the material with a knife.  An  amount  equal  to  2
tablespoons is sufficient for analysis.  Proper sampling requires
that each sample container be tightly sealed, wiped  clean  with  a
damp cloth, and labeled.  The label should be recorded  by  the
sampler (EPA 1979b).
    Samples must be taken in a manner that will provide a
representative indication of the composition of the  material.
The amount of asbestos in the friable asbestos-containing
materials on a building surface may vary.  If the material is
homogeneous in appearance and was applied  at one  time,  the amount
may not vary greatly over one surface area.  From three to seven
samples may be needed, however, to establish whether asbestos is
present and, if so, the approximate percentage that  is present.
EPA recommends that 3 samples be taken for homogeneous  surfaces
that are up to 1,000 ft , 5 samples for  surfaces  that are between
1,000 and 5,000 ft2, and 7 samples for surfaces that are >5,000
ft2 (EPA 1980) .
    A random selection of sampling sites is necessary to
eliminate the bias that may result from  taking samples  from
convenient locations.  Representative sampling can be achieved  by
extracting material from different places  within  a sampling  area
(close to walls, at joints, etc.).  A more involved  method for
the random selection of sample sites (EPA  1980) involves the use
of a.random number table and a diagram of  the area to be sampled.
                               -95-

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    Friable material is disturbed during the sampling process,
and asbestos fibers, if present, may be released.  Release of  and
consequent human exposure to asbestos can be minimized by  taking
samples when the area is not in use and limiting the number of
persons present, lightly spraying water on the area to be  sampled
to discourage dust formation, holding the sample container away
from the face, and wet cleaning the area if any pieces are
dislodged and fall to the floor.
         C.   Analysis
    Three analytical methods can be used to identify asbestos
fibers in bulk materials.  The first, polarized light microscopy
(PLM), uses the different refractive indices, birefringence, and
other optical crystallographic properties of asbestos minerals to
distinguish them from nonasbestos ones.  PLM also characterizes
and identifies other fibers such as glass fibers and cellulose.
The second method, x-ray diffraction (XRD), uses the unique
diffraction pattern produced when x-rays strike any crystalline
material to identify specific asbestos minerals.  The third,
electron microscopy (EM), uses electron diffraction or energy-
dispersive x-ray analysis to identify asbestos fibers by
examining the structure of individual fibers.
    EPA's Guidance Manual on Asbestos Analytical Programs  (EPA
1980) recommends PLM as the method of choice for determining
asbestos in suspect material and XRD as a backup technique to
confirm the PLM analysis.  Although electron microscopy can be
used, it is not recommended, because only very small quantities
of sample can be analyzed at one time and the analysis of
multiple samples is prohibitively expensive.

                               -96-

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    The EPA Environmental Monitoring Systems Laboratory,  Research



Triangle Park, North Carolina, has prepared and  currently is



field testing interim PLM and XRD analytical protocols  to be



followed in identifying asbestiform minerals in  bulk  samples.



The protocols clarify and refine the guidance originally  offered



in Appendix H of the Guidance Manual.  They have been circulated



to laboratories currently participating  in the Technical



Assistance Program.  An Asbestos Particle Atlas  with  color PLM



photomicrographs has been developed by McCrone Research



Institute.  The Atlas is available from  Ann Arbor Press.



    EPA has identified and complied a list of laboratories that



analyze bulk samples for asbestos using  PLM.  This list is based



in part on the laboratories' successful  participation in  a



proficiency analytical testing program.  A report on  this  testing



program will be available in September,  1980.  Copies of  the list



can be obtained from EPA by calling the  following toll-free



number:  800-344-8571, extension 6892.
                               -97-

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V.  CONTROL OF ASBESTOS IN SCHOOLS

    This section presents information on  the  steps  that  can  be

taken to control exposure to asbestos in  school  buildings  once

friable asbestos-containing materials have  been  identified.

    EPA has published guidance materials  on the  corrective

actions that can be taken in schools and  other buildings if

asbestos-containing materials are found to  be damaged  or

deteriorating.  Long-term solutions to the  release  of  asbestos

fibers from these materials are removal,  encapsulation,  or

enclosure.  Removal eliminates the source of  contamination,

enclosure  (with a barrier such as a suspended or  false ceiling)

reduces the likelihood that incidental contact with the  asbestos-

containing material will occur, and encapsulation  (with  an

effective  sealant) reduces the likelihood that fibers  will be

released into the building environment.

    Exposure to asbestos in buildings also  can be controlled to

some extent by a number of other actions, most of which  are  aimed

at reducing physical contact with asbestos-containing  surfaces.

These actions simply interrupt the process  by which asbestos

fibers enter building air.  Asbestos fibers enter a school

environment from friable asbestos-containing  materials as  a

consequence of:

    (1)  disturbance of the material during maintenance  or
         renovation operations, implementation of the  long-term
         corrective actions described above,  and  vandalism;

    (2)  fallout encouraged by normal activity in the  building;
         and

    (3)  resuspension of settled fibers caused by normal activity
         or custodial dusting or cleaning.
                               -98-

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    Usually, asbestos enters the air as a  result of  physical



contact with asbestos-containing material.  Contact  can  cause



significant amounts of fibers to be released  to the  air,



resulting in airborne concentrations that  frequently exceed



industrial standards (Sawyer 1977).



    Loosely compacted friable materials are more likely  to



release fibers than tightly bound materials.  When a friable



material was brushed by hand to simulate mild damage, fiber



counts as high as 3.8 f/cm3 were measured  as  far away as 10 feet



from the site of the damage (Nicholson et.al. 1978a).  In



contrast, counts of 0.2 f/cm  were noted when a cementitious



material was brushed (Table 17 in Nicholson et.al.).



    Repair, renovation, or maintenance of  buildings  may bring



about the highest airborne concentrations  of airborne fibers,



because these activities disturb asbestos-containing materials



directly.  Sanding or cutting asbestos-containing solid materials



during construction or repair produces the greatest  release of



fibers.  Incidental contact that occurs when other maintenance



chores (e.g., installing a lighting unit)  are performed can lead



to significant release.  In addition, damage to the  material from



vandalism, maintenance work, or, simply, deterioration can



increase the rate of fiber release by fallout (Sawyer 1977).  In



schools, there is the additional opportunity for damage of



friable materials by students.  Whether it is the result of



normal school activity (such as throwing a ball around a



gymnasium) or acts of vandalism, damage caused by students can be



significant.
                               -99-

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    Small amounts of asbestos can fall spontaneously  from



ceilings or walls, building up the airborne  fiber concentration



over time.  Low harmonics and vibrations caused by machinery and



other sources also can increase the release  of fibers.   Once a



wall or ceiling is damaged, it can shed fibers without



significant further disturbance.  These fibers can accumulate



around a room and be continually resuspended any time there  is



movement of the air.  Accumulation of asbestos fibers caused by



fallout can be significant.



    Finally, the resuspension of fibers that have been  released



can continue to cause asbestos exposure.  Cleaning or other



maintenance work or the movement of people through an area can



cause settled fibers to be resuspended.  Suspended ceilings  can



hide the accumulation of fibers until maintenance work  causes the



suspended ceiling to be disturbed; this could result  in the



release of a large amount of fibers to the air (Sawyer  1977).



Custodial services such as sweeping and dusting also  can elevate



fiber levels by disturbing material that has collected  on floors



and other surfaces.  Asbestos fibers tend to stay suspended  in



the air for a long time; for smaller fibers, this time  may be on



the order of days.  When they do settle out, the fibers can



easily be resuspended.  They do not diffuse  as a gas  does;



rather, they tend to be confined to a given  area.



    Exposure to asbestos can be controlled to some extent by



reducing the physical contact of individuals with friable



asbestos-containing materials.  Sawyer reported on the  beneficial



effects of wet cleaning, wet handling during maintenance, and



barrier systems in inhibiting the movement of fibers  in a

-------
building.  The  simple rearrangement of  schedules  so  that  direct



work on asbestos-containing material will occur when  the  building



is not in use and provision of workers  with  respirators also  can



reduce inhalation of asbestos.  Regular wet  cleaning  of building



surfaces can remove accumulated fallout, thus  reducing the



resuspension of asbestos.  Sawyer reported that wet cleaning



reduced fiber concentrations due to custodial  activity from 4.0



f/cm3 (before control) to 0.3 f/cm3.  Wet cleaning is



particularly effective in reducing the  exposure of the person



doing the cleaning.



    General exposures throughout the building  also might  be



reduced somewhat as a result of wet cleaning,  although no studies



have been done  to show the effectiveness of  regular wet cleaning



per se on the building environment.  Unless  care  is taken in



disposing of any fibers collected during either wet or dry



cleaning, fibers will remain available  to be resuspended  in



building air.



    Sawyer reported that during removal operations, wetting bulk



asbestos-containing materials with water containing wetting



agents reduced mean fiber counts to 8.1 f/cm3, compared with the



mean count of 82.2 f/cm3 that was calculated for  dry



conditions.  [Nicholson et al. (1978a)  reported fiber counts of



up to only 1.78 f/cm3 during wet removal of  asbestos-containing



materials in a New Jersey school.]  Sawyer also demonstrated  that



fiber levels dropped more quickly when  wet methods were used.



    The migration of fibers to non-work areas  can be  inhibited  by



barriers.  When removing asbestos in a  New Jersey school,



Nicholson et al. isolated the work area with plastic  barriers.

-------
Fiber counts outside the work area ranged from 0.01 to 0.03



f/cm ,  but counts within the removal area ranged from 0.02



(during wetting) to 1.78 f/cm .



    Vacuum cleaners equipped with high-efficiency particulate



absolute (HEPA) filters can collect asbestos dust.   Sawyer showed



that, whereas dry dusting of shelves and books in a library



raised fiber counts to 4.02 f/cm3, use of HEPA filters raised



counts to only 0.4 f/cm .  Wet wiping the shelves produced a



count of 0.2 f/cm3.  Household and normal industrial vacuums



without HEPA filters cannot collect asbestos fibers.
                              -102-

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                              -108-

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material.  Memorandum  to H. Teitelbaum,  Chemical  Review and
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                              -109-

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                              -110-

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                               -112-

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Sebastian  p,  Gaudichet  A,  Dufour  G,  Bonnaud  G,  Bignon J,  Goni
J.   1978.   Metrological  survey  of  atmospheric  pollution inside
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                              -113-

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Selikoff IJ, Lee DHK.   1978.  Asbestos and disease.   New  York:
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Weiss W.   1971.  Cigarette smoking, asbestos and pulmonary
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                               -116-

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 50272
  REPORT DOCUMENTATION , i-l REPORT NO.
         PAGE          f  EPA 560/12-80-003
4. Title and Subtitle
 Support Document for Proposed Rule on Friable Asbestos-Contain-
 ing Materials  in School Buildings.  Health Effects and Magnitude
 Of Exposure
  7. Authors)
          Charles Pcole,  Health Effects Review division
   Harry Teitolbaum. Aooooanont Division
                                                                         5. Report Date
                                                                         September  1980
                                                                         8. Performing Organization Rept. No.
  . i.ioj.j.j>—.icj.m-u-iaumi—/issosauc
  9. Performing Organization Name and Address
   Chemical Control Division, Office  of Pesticides-and Toxic
     Substances
   401 M Street "S.V.  TS-r794
   Washington,  D.C.  20460
                                                                        10. Project/Task/Work Unit No.
                                                                        11. Contract(C) or Grant(G) No.

                                                                        (C)
                                                                         (G)
                                                                             WE
  12. Sponsoring Organization Name and Address
   U.S. Environment 1 Protection Agency
   401 M Street S.W.
   Washington,  D.C.   20460
                                                                        13. Type of Report & Period Covered
                                                                        Draft  Support Document
                                                                         14.
  15. Supplementary Notes
   Published as  a support document for  a section  6  prcnosed rule on as*^estos-contain:ma
   materi a\s in  schools.
  16. Abstract (Limit: 200 words)
   The Agency has determine! that exposure to asbestos in schorl buildings roses a
   significant  hazard to public health.   Expcusre  to asbestos  fibers can lead to serious
   and irreversible diseases,   liable asbestos-containina materials release asbestos
   fibers into  the ambient environment.   A sizeable proportion of schools contain
   asbestos-containing materials.  In certain conditions these materials release fibers
   in concentrations which pose increased risks of developing  the disease.
 17. Document Analysis  •. Descriptor*
   Schools
   Public Health
   Hazards and Public Health
   Exposure
    b. Identifiers/Open-Ended Terms
   Asbestos
   Exposure Conditions
   Exposure Data
   Exposure Control

    c. COSATI Field/Group
                                  Environments and Exposure
                                  Expousre and Level
                                  Control and  Exposure
                                  Determination and ^vironments
                                  Environments
                                  Exposure Response
                                  Exposure '"ests
                                  Eiber
        ancq Minerals
Asbestos and nust
Asbestos
 18. Availability Statement
   Release unlimited; available from Industry Ass-
   istance Office,  USEPA,  Toll free  800-424-9065
 	           Tn MagVnrvyh-tt-^ EJ54-1404
                                                        19. Security Class (This Report)
                                                         Unclassified	
                                                        20. Security Class (This Page)
                                                                                    21. No. of Pages
                                                                                  22. Price
(See ANSI-Z39.18)
                                         See Instructions on Reverse
                                                                                 OPTIONAL FORM 272 (4-77)
                                                                                 (Formerly NTIS-35)
                                                                                 Department of Commerce

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