United States
Environmental Protection
Agencv
of Water
Regulations ana Standard!
Cntena ana Standards Division
Washington DC 20460
EPA 440 5-80-022
Octooer 980
Ambient
Water Quality
Criteria for
Asbestos
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AMBIENT WATER QUALITY CRITERIA FOR
ASBESTOS
Prepared By
U.S. ENVIRONMENTAL PROTECTION AGENCY
Office of Water Regulations and Standards
Criteria and Standards Division
Washington, O.C.
Office of Research and Development
Environmental Criteria and Assessment Office
Cincinnati, Ohio
Carcinogen Assessment Group
Washington, D.C.
Environmental Research Laboratories
Corvalis, Oregon
Ouluth, Minnesota
Gulf Breeze, Florida
Narragansett, Rhode Island
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DISCLAIMER
This report has bttn reviewed by the Environmental Criteria and
Asstssatnt Office, U.S. Environmental Protection Agency, and approved
for publication. Mention of trade names or commercial products does not
constitute endorsement or recommendation for use.
AVAILABILITY NOTICE
This document 1s available to the public through the National
Technical Information Service, (NTIS), Springfield, Virginia 22161.
ii
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FOREWORD
Section 304 (a)(l) of the Clean Water Act of 1977 (P.L. 95-217),
requires the Administrator of the Environmental Protection Agency to
publish criteria for water quality accurately reflecting the latest
scientific knowledge on the kind and extent of all identifiable effects
on health and welfare which may be expected from the presence of
pollutants in any body of water, including ground water. Proposed water
quality criteria for the 65 toxic pollutants listed under section 307
(a)(l) of the Clean Water Act were developed and a notice of their
availability was published for public comment on March 15, 1979 (44 FR
15926), July 25, 1979 (44 FR 43660), and October 1, 1979 (44 FR 56628).
This document is a revision of those proposed criteria based upon a
consideration of comments received from other Federal Agencies, State
agencies, special interest groups, and individual scientists. The
criteria contained in this document replace any previously published EPA
criteria for the 65 pollutants. This criterion document is also
published in satisifaction of paragraph 11 of the Settlement Agreement
in Natural Resources Defense Counci 1. et. alI..vs. Train, 8 ERC 2120
(D.O.C. 1976), modified, 12 ERC 1833 (D.D.C. 1979).
The term "water quality criteria" is used in two sections of the
Clean Water Act, section 304 (a)(l) and section 303 (c)(2). The term has
a different program impact in each section. In section 304, the term
represents a non-regulatory, scientific assessment of ecological ef-
fects. The criteria presented in this publication are such scientific
assessments. Such water quality criteria associated with specific
stream uses when adopted as State water quality standards under section
303 become enforceable maximum acceptable levels of a pollutant in
ambient waters. The water quality criteria adopted in the State water
quality standards could have the same numerical limits as the criteria
developed under section 304. However, in many situations States may want
to adjust water quality criteria developed under section 304 to reflect
local environmental conditions and human exposure patterns before
incorporation into water quality standards. It is not until their
adoption as part of the State water quality standards that the criteria
become regulatory.
Guidelines to assist the States in the modification of criteria
presented in this document, in the development of water quality
standards, and in other water-related programs of this Agency, are being
developed by EPA.
STEVEN SCHATZOW
Deputy Assistant Administrator
Office of Water Regulations and Standards
111
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ACKNOWLEDGEMENTS
Aauatic uife Toxicology
William A. Brungs, ERL-Narraaansett
'J.S. Environmental Protaction Agency
John H. Gentile, ESL-'Jarrasarse*-*.
U.S. Environmental Protecticr -z~z'Z
Marmalian Toxicology and Human Health Effects:
William Nicholson (author)
Mt. Sinai School of Medicine
Oebdas Mukerjee (doc. mgr.) ECAO-C1n
U.S. Environmental Protection Agency
Bonnie Smith (doc. mgr.) ECAO-C1n
U.S. Environmental Protection Agency
Gary Chapman, ERL-CorvalHs
U.S. Environmental Protection Agency
W. Clark Cooper
Michael Flaherty
U.S. Environmental Protection Agency
Thomas J.Haley
National Center for Toxicologlcal Res.
Si Ouk Lee, BCAO-C1n
U.S. Environmental Protection Agency
Steven 0. Lutkenhoff, ECAO-C1n
U.S. Environmental Protection Agency
James Mlllette, HERL-Cin
U.S. Environmental Protection Agency
James Rowt, OTS
U.S. Environmental Protection Agency
Steven Bayard. CAG
U.S. Environmental Protection Agsncy
Roy E. Albert, CAG*
U.S. Environmental Protection Agency
Robert Bruce, ECAO-RTP
U.S. Environmental Protection Agency
Robert Carton, OTS
U.S. Environmental Protection Agency
Patrick Durkin
Syracuse Research Corp.
Alfred Garvin
University of Cincinnati
Phillip M. Cook, ERL-Duljth
U.S. Environmental Protection Agency
Richard Lemen
National Inst. for Occupational Safety
and Health
Gary S. Logsdon, MERL-Cin
U.S. Environmental Protection Agency
Charles Poreli, OTS
U.S. Environmental Protection Agency
Jerry F.Stara, ECAO-Cin
U.S. Environmental Protection Agency
Technical Support Services Staff: D.J. Reisman, M.A. Garlough, 3.L. Zwayer,
P.A. Daunt, K.S. Edwards, T.A. Scandura, A.T. Pressley, C.A. Cooper,
M.M. Oenessefi.
Clerical Staff: C.A. Haynes, S.J. Faehr, L.A. Wade. 0. Oones, B.J. Sordicks,
B.J. Quesnell, C. Russom, 8. Gardiner.
*CAG Participating members: Elizabeth I. Anderson, Larry Anderson, Ralph Arnicar,
Steven Sayari, Cavid L. Bayliss, Chao W. Chan, John R. Fowie III, Bernard Haser
Charallnaayya Hlremath, Chang S. Lao, Robert McGaughy, Jeffrey Rosenblatt,
Dharm V. Singh, and To^d W. Thorslund.
1v
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TABLE OF CONTENTS
Page
~r' ter i 3 Summary
Introduction A-l
Aquatic Life Toxicology 3-1
Effects 8-1
Summary 8-1
Criteria 8-1
References 8-2
Mammalian Toxicology and Human Health Effects C-l
Introduction C-l
Exposure C-l
Analytical Techniques C-l
Ingestion from Water C-13
Ingestion from Food C-19
Exposure from Drugs C-20
Inhalation C-?0
Pharmacokinetics C-28
Absorption and Distribution C-29
Excretion C-32
Effects C-32
Acute, Subacute, and Chronic Toxicity C-32
Teratogenicity C-39
Mutagenicity C-3fl
Carcinogenicity-Animal Data C-*0
Carcinogenicity-Human Data C-6Q
Synergism and/or Antagonism C-90
Fiber Size Considerations C-94
Criterion Formulation C-97
Existing Standards and Guidelines C-97
Current Levels of Exposure C-98
Special Groups at Risk C-99
Basis and Derivation of Criteria C-100
References C-115
Appendix I C-139
Appendix II C-HO
Appendix III C-l«l
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CRITERIA DOCUMENT
ASBESTOS
CRITERIA
Aquatic Life
NO freshwater organisms have been tested with any asbestiform mineral
and no statement can be made concerning acute or chronic toxicity
No saltwater organisms have been tested with any asbestifomi mineral and
no statement can be made concerning acute or chronic toxicity.
Human Health
For the maximum protection of human health froa the ootential
carcinogenic effects of exposure to asbestos through ingestion of water and
contaminated aquatic organisms, the ambient water concentration should be
zens. The estimated levels which would result 1n increased lifetime cancer
risks of 10"5, 10"6, and 10'7 are 300,000 Mbers/1, 30,000 *ibers/l,
and 3,000 fibers/1, respectively. Estimates for cons««ption of aquatic
organisms only, excluding the consumption of water cannot &« Md«.
VI
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INTRODUCTION
Asbestos is a broad term appliea to numerous fiorous -nineral silicates
composed of silicon, oxygen, hydrogen, and metal cations such as sodium,
magnesium, calcium, or iron. There are two major groups of asbestos, ser-
pentine (chrysotile) and ampMbole. Chrysotile is the major type of asbes-
tos used in the manufacture of asbestos products. These products include
asbestos cement pipe, flooring products, paper products (e.g., padding),
friction materials (e.g., brake linings and clutch facings), roofing pro-
ducts, and coating and patching compounds. In 1975, the total consumption
of asbestos in the U.S. was 550,900 metric tons.
Of the 243,527 metric tons of asbestos discharged to the environment,
98.3 percent was discharged to land, 1.5 percent to air, and 0.2 percent to
water. Solid waste disposal by consumers was the single largest contribu-
tion to total discharges. Although no process water is used in dry mining
of asbestos ore, there is the potential for runoff from asbestos waste-tail-
ings, wetmining, and iron ore mining. Mining operations can also contribute
substantially to asbestos concentrations in water via air and solid waste
contamination. In addition to mining and Industrial discharges of asbestos,
asbestos fibers, wMch are believed to be the result of rock outcropplngs,
are found 1n rivers and streams.
The chemical composition of different asbestos fibers varies widely and
typical formulas art presented in Table 1 (U.S. EPA, 1976). It should be
noted that the values obtained from actual chemical analysis of the various
fibers also may differ slightly from the typical formulas. Although chryso-
tlle 1s considered to be a distinct mineral, the five amphibole minerals are
each varieties of other minerals (Zoltai and Stout, 1976). These minerals
differ from each other both chemically and physically with the exception that
A-l
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TABLE 1
Typical Formulas for Asbestos Fiber?
1. Serpentines ChrysotHe
2. Atnphlboles Amoslte
Oocldollte
AnthophylUte
TremolUe
Act1nol1te
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they all contain silicon and all form *;;ers wren crashed. Good duality
asbestos will form fibers with ^igner raf cs of lengtn to *iatn than poorer
grades.
'he basic crystal form of the amphibole funerals is less complicated
than for chrysotile. The basic structure consists of a double silica chain
fSi^O^) that is paired back -to-back with a layer of hydrated cations
between the chains (Speil and Leineweber, 1969).
Some typical physical properties of three different mineral forms are
presented in Table 2 (Gaze, 1965).
Asbestos minerals, despite a relatively high fusion temperature, are
completely decomposed at temperatures of 1,000'C. Both the dehydnjxylation
temperature and decomposition temperature increase with increased MgO con-
tent among the various amphibole species (Speil and Leineweber, 1969).
The solubility product constants for various chrysotile fibers range
from 1.0 x 10 to 3 x 10" . Most materials have a negative surface
charge in aqueous systems. However, since chrysotile has a positive (*)
charge, it will attract, or be attracted to, most dispersed materials. The
highly reactive surface of asbestos causes many surface reactions which are
intermediate between simple absorption and a true chemical reaction. The
absorption of various materials on the surface of chrysotile supports the
premise that the polar surface of chrysotile has a greater affinity for
polar molecules (e.g., h^O.NHj) than for nonpolar molecules (Speil and
leineweber, 1969).
Of all the asbestos minerals, chrysotile is the most susceptible to
acid attack. It is almost completely destroyed within 1 hour in 1 N HC1 at
95*C. Amphibole fibers are much more resistant to mineral acids (Undell,
1972).
A-3
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TABLE 2
Typical Physical Properties of Chrysotile (White Asbestos),
Oocidolite (Blue Asbestos), and AmosUe*
Units ChrysotHe
(white asbestos)
Approximate
d1a«wter of micron 0.01
smallest fibers
Specific - 2.55
gravity
Average
tensile lb/1nch2 3.5 x 105
strength
Modulus of Ib/1nch2 23.5 x 10*
elasticity
Ooddollte Amosite
(blue asbestos)
0.08 0.1
3.37 3.45
5 x 105 1.75 x 1Q5
27.0 x 10* 23.5 x left
^Source: Gaze, 1965
A-4
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The resistance of the asbestos fibers to attack by reagents other than
acid is excellent up to temperatures of approximately 100'C with r3pia
deterioration observed at higher temperatures. Chrysotile is completely
decomposed in concentrated KOH at 200*C. In general, organic acids have a
tendency to react slowly with chrysotile (Speil and leineveber, 1969).
A-5
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REFERENCES
Gaze, P. 1965. The physical and molecular structure of asbestos. Ann.
N.V. Acad. Sci. 132: 23.
Linden, K.V. 1972. Biological effects of asbestos. Int. Agency Res. Can-
cer, Lyon, France.
Spell, S. and J.P. Leine*eber. 1969. Asbestos minerals in modern technol-
ogy. Environ. Res. 2: 166.
U.S. EPA. 1976. Asbestos: A review of selected literature through 1973
relating to environmental exposure and health effects. EPA-560/2-76-001.
U.S. Environ. Prot. Agency, Washington, O.C.
Zoltai, T. and J.H. Stout. 1976. Conwents on asbestlfomi and fibrous min-
eral fragments relative to Reserve Mining Co. taconite deposits. Prepared
for Minnesota Pollut. Control Agency.
A-6
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Aquatic Life Toxicology
EFFECTS
vo appropriate data on the effects of asbestos on aauatic organisms are
available at this time. Therefore, no freshwater or saltwater criterion can
be derived for asbestos. However, microscopic inorganic particles, analyzed
by transmission electron microscopy, have been detected in fish tissues
(Batterman and Cook, 1980). Tissue samples obtained from a river with known
chrysotlle asbestos contamination and lake trout, brook trout, and channel
catfish exposed to Lake Superior water contaminated with amphibole fibers
have been found to contain mineral fibers identical to those in the water.
Muscle tissue concentrations are about one-twelfth of the average water con-
centrations (by volume) but liver and kidney fiber concentrations are 500
times greater than muscle tissue concentrations.
Summary
The only available data for asbestos and freshwater organisms results
from field studies in which chrysotHe and amphibole fibers have Seen found
in tissues of fish collected front freshwater with known concentrations of
these mineral fibers.
No data are available for saltwater organisms.
CRITERIA
No freshwater organisms have been tested with any asbestiform mineral,
and no statement can be made concerning acute or chronic toxicity.
No saltwater organisms have been tested with any asbestiform mineral,
and no statement can be made concerning acute or chronic toxidty.
B-l
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REFERENCES
Batterman, A. R. and P. M. Cook. 1980. A method for the determination of
mineral fibers in fish tissues. Paper to be presented at the 13th Ann.
Meeting of the Minnesota Chapter of the American Fisheries Society.
8-2
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ASBESTOS
Mamma1ian Toxicology and Human Healti Effects
Estimating a risk 'actor for ingestion of asbestos presents significant
difficulties. Although gastrointestinal cancer has been linked to occupa-
tional exposures in several groups of workers, no definitive data exist on
the effects of direct ingestion of asbestos, either in animals or ^umans.
Further, only limited information exists on air exposure levels for those
human studies shoving excess risk of gastrointestinal cancer and peritoneal
mesothelloma. Nevertheless, the most valuable data on risk are those from
human Inhalation exposures, and these will form the primary basis for t 31-0-
jected criterion.
This document 1s not an exhaustive review of all asbestos literature
are all important papers mentioned herein. However, the papers selectto
deemed relevant for estimating dose-response relationships.
EXPOSURE
Analytical Techniques
For the purposes of this document asbestos is defined to be cn
cn>c1dol1te, fibrous cumni1ngtonite-gru/ier1te Including amosltt,
tremoHte, fibrous actlnoUte, and fibrous anthophylllte. The fibrosity of
the above minerals 1s ascertained on a microscopic level with fiber
to be particles with an aspect ratio of 3 to 1 or greater. This
will apply to f1b«r$ of all sizes. Because of the impossibility of «-t'ii'n
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The analytical tec^niiues for the measurement of asbestos minerals ?n
air or water samples collected in occupational or general environment a1 cir-
cumstances are time-consuming, and the results are often mgnly variable.
No single method is suitable for all monitoring circumstances. Techniques
appropriate for monitoring workplace exposures are unreliable when used to
evaluate the much lower environmental concentrations of asbestos, such as
those found in water, largely because of the presence of ouantities of other
inorganic and organic material. Electron microscopic methods used for envi-
ronmental monitoring are difficult to perform and costly. Reproducible re-
sults can be obtained in experienced laboratories 1f standardized techniques
are utilized, careful duality control 1s maintained, and oeHod1c interla-
boratory comoarison of results 1s made. With careful analysis of water,
interlaboratory precision can achieve relative standard deviations of 30 to
65 percent (Anderson and Long, 1980; Chopra, 1978), but without standardiza-
tion intralaboratory variability can be as great as a factor of ten, and in-
terlaboratory variability can exceed two orders of magnitude (Brown, et al.
1976).
Environmental—Water: Considerable effort has taken place in recent
years to standardize technlaues for the ouantHatlon of «i«era! fibers in
water. All work to date has utilized electron mlcroscooy. 1>« presence of
numerous diatom splcules and other nonasbestos fibers in water and the great
difficulty of unlouely Identifying mineral species or classes by optical
microscopy would appear to preclude the use of optical «icrotcocy for even
the ouant1tat1on of large asbestos fibers 1n water, wit* electron micro-
scopy, however, relatively few experimental problems r*Mi«, a*»d reproduci-
ble results can be obtained by experienced laboratories. The disadvantage
of this method 1s the cost and time of analysis and the Halted availability
of laboratories for the analysis of samples.
C-2
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The U.S. EPA has proposed an interim -nethod ^or the analysis of asbestos
in water 'Anderson and Long, 1980). Crom a I-',-ter sample, 50 to 500 nl is
filtered through 0.1 micron polycarbonate 'Nudepore) filter. A portion of
the filter is placed on an electron microscope grid and dissolved sy the
Jaffe wick method and scanned by transmission electron microscopy at 10,000
to 20,000 magnification. Prior to dissolution, the flat polycarbonate fil-
ters are coated with carbon which serves to enmesh the collected material
and to reduce losses during dissolution of the filter material by chloro-
form. Twenty grid squares or 100 fibers are counted. The Identification of
fiber type is by morphology for chrysotile and by selected area electron
diffraction for amphiboles. No attempt is made to determine the amphibole
mineral species. If necessary, this can be done using energy-dispersive
X-ray analysis of each fiber. All individual fibers (length greater than
three times width), irrespective of length are counted in the grid squares
scanned. The fibe^t in large clumps, though, are not counted individually.
For surveillance of large numbers of water systems, the procedures serve to
identify those with significant quantities of asbestos present. For water
systems with high concentrations of suspended solids, the collected material
and filter can be ashed 1n an activated oxygen furnace, the remaining mate-
rial resuspended, ultrasonifled, and reflltered.
The sensitivity of procedure this 1s such as to be able to detect about
250,000 fibers/liter (f/1) or less In most drinking water systems without
the need for the ashing and resuspension step. Most municipal water systems
contain less than 1 mgf\ of suspended solids, and thus 200 ml of water can
be filtered through a 10 cm filter for analysis. The counting of 20 grid
squares as prescribed above, scans 1.3 x 10 cm2 of filter. In this
area typical background counts are less than two fibers. Thus, eigbt fibers
C-3
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counted would establish a detectable level in a given water sample. With
200 ml of water sampled, this corresponds to 250,000 f/1. In water system
Caving less suspended solids the lower limit of detection is proportionally
lower, with systems containing more suspended material, similar detection
limits can be achieved following the ashing procedure.
A previously used technique of condensation-washing of cellulose acetate
Millipore filter pieces on carbon-coated grids using acetone can result in
significant losses unless extreme care is taken. Carbon coating of the M11-
11 pore filter is ineffective in enmeshing the fibers because many of them
are trapped deep within the interstices of the membrane filter. Condensa-
tion of acetone on the grid can result in the formation of poois of solvent
on the filter which wash away fibers. Losses as great as 80 percent have
been reported using this technique {Chatfield, et al. 1978; Seaman and File,
1976; Chopra, 1978).
Eighteen analytics! laboratories participated in an African Society for
Testing and Materials (ASTM) Task Group study of the measurement of amphi -
bole and chrysotile fibers in water. Table 1 lists the data on the interli-
boratory precision that has been obtained by this group In the analysis of
both ehrysotlle and amphibole fibers. The Task Group concluded:
The transmission electron microscope 1s the best basic instru-
ment for the analysis, particularly when it 1s equipped with se-
lected area electron diffraction and energy-dispersive spectrescopy
capabilities. The man fiber concentrations by different groups
aortt within a factor of two. The interlaboratory rtproduc1b111ty
of 50 percent can be expected in relatively clean water samples
unless the concentration is low. In samples with high concentra-
tions of Interfering solids, the precision will not be as good.
When applied on a broad scale there are variable and significant
losses associated with the condensation-washing of staples contain-
ing amphibole. The losses are low and less variable when condensa-
tion-washing is used to prepare samples containing chrysotile
(Chopra, 1978).
C-4
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TABLE 1
Interlaboratory Precision Obtained in the Analysis of Water
Samples for Chrysotlle and Amphibole Minerals*
Sample
Type
v ~
Chrysotlle
Chrysotlle
Chrysotlle
Chrysotile
Chrysotile
ChrysotHe
Ainphibole
A/npMbole
Amphibole
NUiwber of
Laboratories
Reporting
10
9
11
9
9
3
11
4
14
Mean Fiber
Concentration
(106 fibers of
all sizes/1)
877
119
59
31
28
25
139
95
36
Relative
Standard
Deviation
of Analysis (X)
35
43
41
65
32
35
50
52
66
'Source: Anderson and Long, 1980 (see also Chopra, 1978)
C-5
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Environmental--Air: As with water, the analysis of ambient air samples
by ooti'cal techniques introduces significant difficulties. First, the quan-
tity of asbestos in ambient air is only a small fraction of the total aero-
sol. This aerosol contains large quantities of organic and mineral material
of various origins, including many fibers other than asbestos. Therefore,
enumeration of fibers collected in ambient air may have little relevance to
the asbestos material present. In one instance, a comparison of 25 ambient
air samoles collected in buildings, some of which were contaminated with
asbestos, showed no correspondence between concentrations of fibers longer
than 5 um, as determined using optical microscopic techniques, and the total
mass of asbestos present, quantitated by electron microscopic methods (Nich-
olson, et al. 1975). Here, using the National Institute for Occupational
Safety and Health (NIOSH) technique, no fiber concentrations measured ex-
ceeded 0.03 f/ml, and contributions to the measured filter concentration
from other than asbestos fibers were felt to be significant. A review (Dug-
gan and Culley, 1978) of the results of the analysis of six side-by-slde am-
bient air samples by nine laboratories also highlighted the difficulty of
using optical microscopy at low asbestos concentrations. They found that
intralaboratory variability could exceed a factor of 10 and the results be-
tween laboratories could differ by a factor of 100. The possibility exists
that optical techniques using petrographic, polarized light Microscopes or
d1sp«rs1on staining techniques could produce better results. This has not
been Investigated, however.
A variety of techniques, each of which utilizes electron microscopy,
have been developed for the analysis of asbestos in the aablent air. At the
present time, there is less agreement on an Ideal method for air analysis
than for water analysis. Two general electron microscopic techniques are
C-6
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utilized ftx the analysis. ?ne invc'ves tne collection o* astestcs on ~9<'-
ulose acetate 'Mi 11 ioore ) or oo'ycareonate filters >' Vuc 'epore : ''SamuOa, et
al. 1978) ard its subseauent trans'e-- to elect-on iicrosccce gnds. r3>-
samples collected on cellulose acetate filters, the filter and col'ectea
material are ashed, the ash suspended in water, and the suspension filtered
through a polycarbonate filter. Such filters are then processed using tech-
niques similar to those used for water and previously discussed (see Water
section). Although not well studied, the use of flat-surfaced polycar-
bonate filters in field situations may lead to losses of particles prior to
sample preparation for analysis.
Direct transfer techniques have other limitations. Ambient aerosols are
made up of agglomerates of particles with asbestos fiber? attached to a
variety of other material. Chrysotile asbestos, for example, with a posi-
tive surface charge, readily adheres to any of the large number of nega-
tively charged particles, such as clays, in the ambient air. Without dis-
persal, these agglomerations can result in the asbestos being obscured when
viewed by an electron microscope. Further, agglomeration can occur on the
filter during the long collection times required to quantltate low concen-
trations. In many cases, these agglomerates, which usually are of respir-
able size, contribute the most to the mass of the sample. Also, they may
occur so infrequently that a statistically reliable measure of their quan-
tity 1s difficult to obtain. To obviate these difficulties, techniques have
been developed 1n which collected material and filter are ashed in a low-
temperature, activated oxygen furnace. The resulting residue is dispersed
by physical means, either through the application of ultrasonic energy or
grinding, and is enmeshed 1n a nitrocellulose or collodlan film for mounting
on electron microscope grids or is reflltered through a polycarbonate fil-
C-7
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ter. Suc^ "i-jb-out" methods also involve losses and, as with washing tech-
niques, roaj
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sufficient to establish if they are organic or mineral in origin. in
general, when the principle fiber in an aerosol is known to be asbestos,
this presents no problem. However, in some occupational circumstances, as
with the use of insulation materials, fibers of various origins are present
in the same material, and this can result in overestimates of the actual
asbestos concentrations.
The adoption of a 5 win cutoff for the length of fibers enumerated was
imposed by the limitations of light microscopy. It has long been known that
fibers longer than 5 u/n and visible by phase contrast microscopy represent
only a small fraction of the total number of asbestos fibers in the air
(Lynch, et al. 1970). This would present no problem were fiber size distri-
butions similar 1n different circumstances. However, such is not the case.
It has been shown, using electron microscopy, that when chrysotile asbestos
concentrations in different exposure circumstances are enumerated, the frac-
tion greater than 5 urn may vary by I0-fo1d (from 0.4 percent of the total
number of fibers present to approximately 5.0 percent). When amphibole
varieties of asbestos are also considered, the fraction counted can vary
more than 100-fold (Nicholson, et al. 1972). Thus, we do not have an accu-
rate yardstick for the quantitatlon of asbestos air concentration in the
workplace. This do«s not present serious problems when monitoring for stan-
dard compliance but complicates comparisons of health effects between vari-
ous Industrial processes such as mining, manufacturing, and end-product use.
It also complicates extrapolations of dose-response relationships determined
in occupational circumstances to lower concentrations of asbestos measured
in the general environment by other techniques. Nevertheless, when assess-
ing exposure in a defined asbestos aerosol, the precision of optical methods
C-9
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can be good. NlOSH (1976) Has estimated that a coefficient of variation of
about 20 percent can be achieved in the assessment of asbestos concentra-
tions greater than 0.1 f/ml.
Although fiber counts have been utilized for the assessment of occupa-
tional asbestos exposure since 1966, in prior years other methods, usually
involving total particle counts (fibrous and nonflbrous), were utilized.
Some attempts have been made to relate these earlier counts to present day
fiber concentrations (Lynch and Ay«r, 1966). However, these have been found
to depend strongly on the particular asbestos use process, and no universal
conversion factor is available that would relate total particle concentra-
tions 1n a given circumstance with asbestos fiber counts. It 1s unfortunate
that earlier data have limited relevance, since the disease experience that
we are seeing today is the result of exposures that took place 20, 30, or
more years previously when work conditions may have been considerably dif-
ferent from those currently existing. Thus, dose-response relationships are
tenuous and can only be approximate, based upon current data.
IntercompaHson of Techniques: All data, scant as they are, that relate
asbestos disease to exposure are derived from studies of workers exposed in
occupational environments. In th«se studies, concentrations of fibers long-
er than 5 urn w«r« determined using optical microscopy or w«re estimated from
optical microscopic measurements of total particulate matter. On the other
hand, all current low-level environmental assessments utilize electron
microscopic techniques which are not comparable to those used 1n the work-
place since optical techniques do not provide data on the number of fibers
less than 5 urn in length. To extrapolate dose-response data obtained in
studies of working groups to environmental exposures, 1t 1s necessary to
establish the relationship between optical fiber counts and mass or total
fiber number determined by electron microscopy.
C-10
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Recent studies nave attempted to relate optical fiber counts :'f;cers > 5
um) and TEM counts fall EM-countable fibers}. An interlaboratory comoarison
of optical versus EM counts of chrysotile fibers suggested an average '•e'a-
tionshlp between optical counts and TEM counts of 1:1000 ('«iner an: Cas-
sette, 1979). The samples studied included air samples from six D'arts 'one
asbestos -cement, one brake lining, two treating mills, and two texti'e
plants). Lower ratios are expected for amphibole fibers. An ana'ys-s :y
the U.S. EPA (Personal communication, J. Millette) relating optical Mser
counts of fibers longer than 5 u"> to total fiber counts by transmission
electron microscopy gave a ratio of 400 for six samples of asbestos ceiling
insulation material (which, however, may contain fibers other than asoestcs
and were not actual air samples). Other data by Wallingford (1978)
3 ratio as low as 15 for EM count to optical counts.
Sosse data exist that relate optical fiber counts (longer than 5
the total mass of asbestos as determined by electron microscopic
or by other weight determinations of collected airborne asbestos
These are listed in Table 2 and provide crude estimates of a
factor relating fiber concentrations (f/m!) to airborne asbestos
(ug/m )• The proposed standards for asbestos in Great Britain 5y :•>«
British Occupational Hygiene Society (BOHS) stated that a "respiraoi**
of 0.12 mq asbtstos/ii3 was equivalent to 2 f/ml (BOHS, 1968). It •«*
stated how this relationship was determined. However, if it were fro*
nesium determinations in an aerosol, the weight determination woo id :<<•)/
be high because of the presence of other nonfibrous, magnesium-contjinmq
compounds in the aerosol. Such was the case in the work of Lynch, «t *i.
(1970), and their values for the conversion factor are undoubtedly overesti-
mates. The data of RoM, et al. (1976) are likely to be underestimates
C-ll
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TABIE ?
Measured Relationships Between Optical Fiber Counts and Mass of Airborne Chrysotile
Fiber* Mass Conversion Factors
Counts Concentration
Sampling Situation (f
/•O (ng/*3) M9/*3 or M9 103f/mg
f/.l 106f
Textile factory
BOHS (1968)
(weight vs. fiber count) 2
Air chamber monitoring
Davis, et al. (1978) 1,950
120
10,000
60 16
5 200
Monitoring brake repair work
Rohl. et al. (1976)
(€.M. mass vs. fiber count)
TeittU mill
Friction products off.
0.1 to 4.7
(7 samples)
0.1 to 6.6
L>nc*i. «t al. (1970)
0.7 to 24»
mean - 6
150C
45C
170
6.7
13.9
22.5
*A11 fiber counts used phase-contrast microscopy and enumerated fibers longer than 5 M«-
^Conversion factor may be low due to losses In E.M. processing.
^Conversion factor may be high because of overestimate of asbestos mass on the basis of total magnesium.
C-12
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because of possible losses ''n the dete^^t- ;n :- -*<; :, - --•• - -•;-:-
scopy. No data exist on tre C'-ocedu'-es used to ~et5'~ •-? :-e - = :: ;-" :-'-./-
sotPe in the data presented Dy Davis, et a". ''197?'.
'He range of 5 to 15Q for the conversion factor- '•elating -asi ::"cer>tra -
tion to ootical fiber concentration is great, and any average Ji'^* :er-;ea
from it has a large uncertainty. However, for the ouroose c* ^x:'-.;c'ati"g
to low mass concentrations from fiber count, the geomef-: -ean, 30
ug/m^/f/ml, of the above range of conversion factors wil< se .sed. 'he
accuracy of this value is felt to be no more than a factor of 5 ^nd tnis
uncertainty severely limits any extrapolation in which it is jsed. .'n the
case of amosite, the data of Davis, et al. (1978) suggest that a :crve-sion
factor of 18 is appropriate. However, since this data yielded 'ever :~ryso-
tlle values than all other chrysotile estimates, it may a's; :e " _••* for
amosite.
Ingestlon from Water
Asbestos is cormonly found in domestic water supplies. Sacpies •'•cm 365
cities have been collected and analyzed by electron microscopy :y :^e j.S.
EPA. Of these, 45 percent had detectable levels of asbestos, jsuaKy of the
chrysotlle variety (Mlllette, 1979). Table 3 lists the distribution of the
concentrations of these samples.
Earlier, asbestos had b«en reported in a variety of Canadian water sup-
plies (Cunningham and Pontefract, 1971). These waters were found to contain
from 2.0 to 172.7 x 106 fibers/1. (In this subsection fibers will denote
all EM-countable fibers. Irrespective of length). Two U.S. river systems
were also reported to contain chrysotile at average levels of from 0.3 to
1.5 ug/1 (Nicholson and Pundsack, 1973). Other reports include that of ,
-------
TABLE 3
Distribution of Reported Asbestos Concentrations in
Drinking Hater from 365 Cities in 43 States,
Puerto R1co, and the District of Columbia*
Asbestos Concentration
(106 fibers/ 1)
Below detectable limits^
Not statistically significant
Less than 1
1-10
Greater than 10
Total
Number of
Cities
110
90
90
34
J!
365
Percentage
of Samples
30.1
24.6
24.6
9.3
11.2
99.8
4M1llette, 1979
bFor these analyses average detectable limits were 5 x 105 fibers/1.
However, significant variations occurred In some instances due to the
presence of nonasbestos fibers.
C-14
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During 1973, large amounts of asoestos-'Hke fioers of amphibole minerals
found in the waters of Lake Superior, the soiree of drinking water for
Ouluth, Minnesota, and other cities (Cook, et al. 1974, 1976; Nicholson,
1974). ciber concentrations during normal lake conditions ranged from 20 x
10^ to 75 x 10^ f/1 and from about 5 to 30 ug/1 in terms of mass
fNicholson, 1974). During storm conditions amphibole fiber concentrations
as high as 600 x 10° f/1 were observed (Cook, et al. 1976). Filtration
plants now used in Ouluth maintain fiber concentrations below 0.1 x 10
f/1 (Mlllette, 1979).
Certain U.S. water systems currently have high levels of asbestos as a
result of serpentine or amphibole deposits in their watersheds. These
include Everett, Washington, with concentrations of chrysotile above 10
f/1; Seattle, with from 1 to 10 x 106 f/1; and San Francisco, with chryso-
tile concentrations about 10 f/1 in some systems (Mlllette, 1979; Cooper,
et al. 1978).
Under certain conditions, asbestos-cement (A/C) pipe may also contribute
asbestos to municipal water supplies. Asbestos fiber concentrations in A/C
pipe distribution system were found to be as high as 38 x 10 chrysotile
and 4 x 106 amphibole fibers/1 in one Florida city; 17 x 106 1n another
Florida town; and 47 x IQ6 f/1 1n a Kentucky A/C pipe system. Water at
the end of a little-used A/C p1p« line 1n Massachusetts contained as much as
480 x 1C6 chrysotlle f/1 (Mlllette, 1976). Many of the A/C pipe systems
in Connecticut have be«n sampled and analyzed (Craun, et al. 1977). The
majority of samples taken after transit through A/C pipe showed concentra-
tions under 1 x 10 f/1, and only one sample was over 10 x 10 f/1.
While there are an estimated 200,000 miles of A/C pipe now 1n use in the
United States, 1t Is apparent that not all A/C pipe sheds fibers. If the
C-15
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wate>- ;s nonaggressive the pipe does not erode and contribute fibers to the
water (Hallenbeck, et al. 1978).
A study (Buelow, et al. 1980) of 10 A/C pioe systems showed that fibers
we«-e added to the water by the A/C pipes of the 5 systems with aggressive
water (Aggressiveness Index <10.0) and little effect was seen in the non-
aqgressive systems. In two systems the pipe was eroded to a depth of 0.3
cm, in one case in a period of only 5 years. In this system fiber counts as
high as 550 x 10 f/1 were measured in the distribution network versus
800,000 at the well source. In a third system high concentrations at a dead
end sample were attributed to debris from tapping and drilling of pipes 1n
the network.
Sampling of representative water utilities throughout the United States
has indicated that over half of the samples had water which was moderately
aggressive and 16.5 percent had very aggressive water (Table 4) (Mlllette,
et al. 1979b). Water supplies in both the very aggressive and moderately
aggressive categories are potentially capable of eroding asbestos-cement
pipe (i.e., 68.5 percent of U.S. water systems) although the very aggressive
waters could be expected to result 1n the contribution of nwch higher fiber
concentrations.
Host data on asbestos 1n water are expressed 1n terms of fiber concen-
trations, enumerating fibers of all sizes using appropriate electron micro -
scope techniques. Some estimates exist (Mlllette, 1979) relating chrysotile
fiber concentrations to mass concentrations. Because the number-to-mass
relationship 1s highly dependent on average fiber length and diameter,
knowledge of the source of the fibers 1n the water 1s Important in determin-
ing a conversion factor. Some average conversion factors are listed in
Table 5.
C-16
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TABLE 4
Representative Average Water Utility Aggressiveness Indices3
Highly aggressive^ 16.5 percent
Moderately aggressive^ 52.0 percent
Nonaggress1ved 31.5 percent
, et al. 1979b
^Highly aggressive: pH * logio(AH)<10.0
^Moderately aggressive: pH * log (AH) • 10.0 - 12.0
dNon«ggress1ve: p« * log (AH)>12.0
where A - total alkalinity In mg/1, CaCOj
H • calclcM hardness as mg/1, CaC03
C-17
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TABLE 5
Relationship of Total Fiber Counts by Electron Microscopy and
Mass of Chrysotlle Asbestos 1n Water*
Fiber Source
Average Mass In ug
of 106 Fibers of All Lengths
Natural erosion of serpentine rock
(shorter fibrils)
A/C pipe (longer fibers)
Contributions from commercial dump
site runoff and untreated discharge
(more fiber bundles)
0.002
0.01
0.05
'Source: MUlette, 1979
C-18
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Similar information on the relationship of fiber count and .mass .^as seen
oublished by Kay (1973), whose data suggest that 10 fibers corresooncs to
from 2 x 1C"4 to 2 x 10 ug in water systems. Data on asbestos
concentrations from erosion of fibers from A/C cooling tower panels indicate
that the mass of 106 fibers is from 0.01 to 0.2 ug (Lewis, 1977).
Based on the aforementioned data, it is concluded that the majority
faooroximately 95 percent) of water consumers in the United States are ex-
posed to asbestos fiber concentrations of less than 10 f/1. In a few
areas people are exposed to concentrations between 1 and 10 million f/1 with
intermittent exposures over 100 million f/1. There 1s at least one area
where continuous exposure 1s over 100 million f/1. Persons using asbestos-
cement pipe in areas where the water 1s nonaggressive or is treated to pre-
vent corrosion are generally not additionally exposed. In areas of aggres-
sive water, however, the consumer may be exposed to added asbestos fiber
concentrations of from fewer than 1 million to over 100 million fibers per
liter, depending on factors such as length of pipe, flow rate, and mineral
content of the water.
The mass concentrations of chrysotHe asbestos in the water of cities
with less than 106 f/1 are likely to be less than 0.01 ug/1, corresponding
to a daily Intake of less than 0.02 ug. However, 1n areas with significant
contamination, whether from natural sources, man's activities, or erosion
from A/C pipes, the Intake of asbestos from water sources can exceed 2
ug/day.
Ingestlon fnxii Food
There are scant data on the contribution of food products to population
asbestos exposure. Cunningham and Pontefract (1971) showed that various
beers and wines could contain Quantities of asbestos fibers similar to those
C-19
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found 1n water systems (106 to 10 f/1). The source of this contamina-
tion could be from natural water sources or from the erosion of asbestos
fibers from filters used to purify the product. Asbestos filters are cur-
rently used for the purification of beverages and a variety of other food
products, but little data exist on possible fiber contamination from such
sources. Contamlnation of drinking water by fibrous glass and other synthe-
tic fibers used 1n cartridge filters has been measured at concentrations in
excess of 109 f/1 (Cook, et al. 1978).
Exposure from Drugs
Erosion of chrysotlle from asbestos filters, used to purify parenteral
dnjgs, has been documented (Nicholson, et al. 1972). Contamination levels
up to 1 ug/dose were noted in approximately one-third of drugs tested, Indi-
cating that filter erosion can be significant. Because of these findings,
the use of asbestos filters for drug purification, without subsequent clean-
up, has been prohibited by the Food and Drug Administration (41 FR 16933).
Inhalation
General Population Exposures: Asbestos of the chrysotHe variety has
been found to be a ubiquitous contaminant of ambient urban air. A study of
187 quarterly composite samples collected in 48 U.S. cities from 1969 to
1970 showed chrysotlle asbestos to be present in virtually all metropolitan
areas (Nicholson, 1971a; Nicholson and Pundsack, 1973). Table 6 lists the
distribution of values obtained 1n that study. Each represents an average
of from five to seven 244iour samples and thus averages over possible peak
concentrations which could occur periodically or randomly. A second set of
ambient air analyses 1s also shown for comparison (U.S. EPA, 1974). These
studies utilized different analytical techniques but the results agree well.
In both studies, 98.5 percent of the 244iour samples had chrysotlle asbestos
C-20
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TABLE 6
Distribution of 24-Hour Chrysotlle Asbestos
Concentrations in the Ambient Air of U.S. Cities*
Electron Microscopic Analysis
Mount Sinai
School of Med1c1n«
Battelle
Memorial Institute
Asbestos
Concentration
(ng/«3)
less than
1.0
2.0
5.0
10.0
20.0
50.0
100.0
Hunter
of
samples
61
119
164
176
184
185
187
Percentage
of
samples
32.6
63.6
87.7
94.2
98.5
99.0
100.0
Number
of
samples
27
60
102
124
125
127
127
Percentage
of
samples
21.3
47.2
90.1
}7.6
)8.5
100. 0
100.0
'Source: Nicholson, 1974; U.S. EPA, 1974
C-21
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concentrations of ^ess than 20 ng/m3. Of the three samples greater than
20 ng/-n^ analyzed 3y the Mount Sinai School of Medicine, one was in a citv
having a major shioyard and another in a city that had four brake manufac-
turing facilities. Thus, these samples may include a contribution from a
specific source in addition to that of the general ambient air.
Similar data with the same range of mass concentrations have recently
been reported from France, providing evidence of the presence of chrysotile
in the ambient air of Paris (Sebastlen, et al. 1976).
In a study of the ambient air of New York City, in which samples were
taken during daytime working hours, values higher than those mentioned above
were obtained (Nicholson, et al. 1971). These were 6- to 8-hour samples
collected between 8:00 A.M. and 5:00 P.M., and they reflect what could be
intermittently higher concentrations from construction activities or automo-
bile usage during those hours compared to nighttime periods for example.
Table 7 records the chrysotile content of 22 sample* collected in the 5
boroughs of New vork. It should be noted that the samples analyzed in all
of the studies discussed above were taken during a period •*»•« fireprooflng
highrise buildings by spraying asbestos-containing materials was permitted.
The practice was especially common 1n New York City. While no sampling sta-
tion was known to be located adjacent to an active construction site, unusu-
ally high levels could nevertheless have resulted from the procedure.
To determine 1f construction activities could indeed be a significant
source of chrysotile fiber in the ambient air, 6- to 8-N>gr daytime sampling
was conducted in lower Manhattan In 1969 near sites wftere titensive spraying
of asbestos -containing fireprooflng material was taking place. Table 8
shows the results of this sampling and demonstrates that sprajr flreproofing
C-22
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TABLE 7
ChrysotHe Content of A/*1ent Air in
New York City by Borough
(6- to 8-Hour Daytime Samples)*
Sampling
Locations
Manhattan
Brooklyn
Bronx
Queens
Staten Island
Number of
Samples
7
3
4
4
4
Asbestos
10-9 g,
Range
3-65
6-39
2-25
3-13
5-14
air level in
'm3 (ng/rr»3)
Average
30
19
12
9
3
'Source: Nicholson, et a1-. 1971
C-23
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TABLE 8
Chrysotlle A1r Levels Hear Spray Fireproof1ng Sites 1n New York City
(6- to 8-Hour Daytime Samples)*
Sampling
Locations (distance from site)
1/8
1/4
1/2
- 1/4 mile
- 1/2 mile
- 1 mile
Number of
Samples
11
6
5
Asbestos air level
10-9 g/m3 (ng/ra3)
Range
9 - 375
8 - 54
3.5 - 36
Average
60
25
18
The above concentrations reflect both downwind and upwind saMplIng locations,
*Source: Nicholson, et al. 1971
C-24
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did contribute significantly to asbestos a^ sol ijfcn. In sone instances,
chrysotile asbestos levels approximately ICC ti.^es t.he concentrations typi-
cally found in ambient ai*- were ooservec.
Asbestos contamination has also been documented oy analysis of samples
collected within buildings. In a study of 116 samples collected in or near
19 buildings (primarily office) in 5 U.S. cities, average chrysotile air
concentrations ranged from 2.5 ng/m to 200 ng/m , with individual mea-
surements from 0 to 800 ng/m (Nicholson, et al. 1975). For the outside
air, the variation for the average concentration at a given site extended
from 0 to 48 ng/m . Buildings in which a loose asbestos fireproof ing
material was applied to the structural steel surfaces had evidence of sig-
nificant asbestos contamination. Also, schools in which similar material
had been applied have been found to be seriously contaminated. Optical
fiber counts exceeding 2 f/ml in a library and other areas of student use
were observed during activities which disturbed loose asbestos (Sawyer,
1977; Nicholson, et al. 1978). Ambient air chrysotile concentrations in
schools, 1n absence of any disturbance of the asbestos ranged up to 2,000
^ (Nicholson, et al. 1978; Sebastien, et al. 1976). Finally, analysis
of the air of asbestos workers homes indicate that chrysotile concentra-
tions as high as 5,000 ng/m can be encountered (Nicholson, et al. 1978).
Figure 1 summarizes the ranges of chrysotile concentrations in the van -
ety of environmental and occupational circumstances discussed above. The
concentration ranges are only approximate and in most cases are limited be-
cause of the Halted nuwtoer of samples taken in given circumstances. Exten-
sion to higher and lower concentrations would be expected with the avail-
ability of more data.
C-25
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S«*H»f CtrcMlMM
!»->
ChrytolIU Air C(MC««lr«t to»
(-V-1)
100 IQl 10?
Up
74-JMMT
i- U
lwt «tr
Vicinity
U 191?
Air of
tvUI prlw
n of «*teitoi nerkari
lnttrl«rt of sdM«l
Occult I
|(H
10*
FlttftC I
Air CMc«n(r«l Iwu •( CfcrrsotlU Atkcttot
So-rct: NldMlM*. «t •!. I
C-J«
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the fate of the asbestos in inspired air is only approximately
known, it appeals that eventually more than half the asbestos inhaled will
be swallowed 'see Effects section). Assuming that an individual breathes 10
m3 in 24 hours, most ambient air levels of chrysotile (1 to 10 ng/m3)
result in exposures to the gastrointestinal tract of from 0.01 to 0.05
ug/day of asbestos, although, in some circumstances, inhalation could pro-
duce gastrointestinal exposures exceeding 0.1 vg/day. These exposures are
to be compared with those from water ingestlon which lead to daily intakes
of less than 0.02 ug (see Ingestlon from Water section). Though the data of
Tables 3 and 6 are not related to the same population bases, it would appear
that inhalation can give rise to exposures at least equal to that of direct
ingestion for most of the population of the United States.
Only after 1966 has occupational monitoring attempted to quantify asbes-
tos exposures by fiber counting technloues. Since then, considerable data
have accumulated on occupational exposure of workers to asbestos. A large
compilation of such data 1s Included 1n the 1972 Asbestos Criteria Document
fNlOSH, 1972). Levels during the period from 1966 through 1971 were gener-
ally under lOf (f>5w«)/ml, although concentrations exceeding 100 f/ml were
observed, particularly 1n two plants producing amosltt Insulation materials
and in uncontrolled textile mills. Data on earlier exposures are lacking
although SOM estimates have been made of Insulation•workers' exposure
fNicholson, 1976) and factory environments (BOHS, 1968; Nevnouse and Berry,
1979). Although average exposures of 10 to 40 f/1 are likely to have pre-
vailed, peak or localized exposures 1n excess of 100 f/1 would have been
encountered often by SOM Individuals.
For purposes of estimating dose-response relationships, those data that
are available for given work environments will be discussed 1n conjunction
with the measured health effects.
C-27
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PHARMACOKINETICS
and Q
Ingestion: A key Question in the evaluation of cancer risk associatea
with the ingestion of asbestos in water is whether microscopic fibers under
normal alimentary canal conditions can migrate through the gastrointestinal
mucosa. Such movement of fibers could enable their residence in bowel wall
or, following hematogenous or lymphatic transport, the peritoneum and other
organ tissues. This has been well answered by the work of Carter and Taylor
(1980) who denwnstrated the presence of amphlbole fibers, characteristic of
those in Ouluth, M1nn. drinking water, in tissue samples of liver, Jejunum,
and lung of deceased Ouluth residents. Among 96 tissue specimens of 32
Ouluth residents amphibole fibers were found in 60, with concentrations
ranging from 3 x 10 to 16 x l(r fibers of all sizes/gram of tissue.
Amph'bole fibers were found 1n only 2 of 61 tissue specimens of 21 control
subjects deceased 1n Houston, Texas and St. Paul, M1nn. As air sampling
gave no evidence of amphibole air contamination in Ouluth, the authors
attribute the highly significant evidence (p <0.001) of tissue contamination
to transmucosal uptake of fibers Ingested by drinking Mphlbole contaminated
Ouluth water.
Some studies of tissues of animals that had Ingested fibers report no
evidence of fiber transport through the gastrointestinal lining (Gross, et
al. 1974). These results, however, have been called Into question on the
basis of the 1nsens1t1v1ty of the assay technique used (Cooper and Cooper,
1978). Evidence for such movement 1s reported 1n other studies (Cunningham
and Pontefract, 1973). Cunningham, et al. (1977) observed chrysotlle fibers
in the blood and tissues of rats which previously were fed a diet of one
percent chrysotfle asbestos for six weeks. West lake, et al. (1965) Identi-
-------
fied chrysotile fibers in the colon mucosa of rats fed chrysotile asbestos.
Scanning electron micrographs have revealed large amosite asbestos fibers
penetrating epithelial cells of rat jejunal mucosa tissue (Storeygard and
Brown, 1977). Kidney cortex tissue of neonate baboon fed chrysoti'e for
nine days was found to contain a statistically significant (p « 0.005) ex-
cess of chrysotile fibers compared to kidney cortex tissue from an unexposed
neonate baboon (Pate! Mandlik and Hallenbeck, 1978). Cunningham and Ponte-
fract (197«) observed passage of chrysotlle fibers from the blood across the
placenta to the fetus.
Ingest 1 on of small particles other than asbestos has also resulted in
the subsequent observation of particle accumulation 1n tissues of animals.
Mice that drank water suspensions of 2 vm diameter latex spheres for two
months were found to have the latex particles accumulated in macrophages in
intestinal Peyer's patches (LeFevre, et al. 1978). Latex particles of 0.22
u/n were reported to migrate from rat stomachs to lymphatics of the mucosa
and also to liver and kidney tissues (Sanders and Ashworth, 1960). Much
larger particles of silica, opal phytoTiths from plants, are observed in
digested mesenterlc lymph node and kidney tissue from sheep which eat cereal
chaff and grains (Hottlt. 1977).
Evidence for the human Intestinal uptake ("persorptlon") of particles as
large as 75 u* 1s provided by the observation of starch granules in blood
only minutes after 1ngest1on (Volkhelwer, 1974). Sleep, smoking, and caf-
feine are reported to Increase the number of starch particles in the blood.
Dyed cellulose particles are also Identified in human blood and urine fol-
lowing ingestlon of specially stained plant food (Schrelber 1974). The cel-
lulose fibers are found in urine several weeks after Ingestlon. Langer
(1974) found asbestos fibers 1n extrapulmonary organ tissues of asbestos
C-29
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workers, although fewer than in lung and pleura tissue, and more fibers ir
kidney than in liver, pancreas, adrenal, or spleen tissue.
Human urine sediment examined by transmission electron microscopy may
contain amphibole fibers which originate from ingestion of drinking water
contaminated with these mineral fibers (Cook and Olson, 1979). Ingestion of
filtered water results in eventual disappearance of amphibole fibers from
urine. These observations provide direct evidence for the passage of min-
eral fibers through the human gastrointestinal mucosa under normal alimen-
tary canal conditions. Measured concentrations of ampMbole fibers elimi
nated in urine represent approximately 1 x 10 of the number of fibers
ingested with drinking water. To the extent that some fibers are perma-
nently retained by the body or eliminated by other routes after passage
across the gastrointestinal wall, the urine concentrations are an underesti
mate of ingested fiber absorption.
Inhalation: Inhalation of asbestos dust 1s accompanied by ingestion of
many fibers cleared from the respiratory tract by mucoclHary action. The
occurrence of peritoneal mesotheHoma, excess gastrointestinal tract can-
cers, and possibly cancers at other nonr«p1ratory tract sites could result
from migration of fibers through th« gastrointestinal mucosa. Additionally,
fibers may reach organs 1n the ptHtonwl cavity by transdlaphragroatlc
migration or Iywpn*t1c-nematogenous transport. How«ver, this would likely
be a very small contribution compared to transmucosal migration following
ingestion. The amount of inhaled asbestos which 1s eventually ingested is
important for an assessment of cancer risk based on the excess gastrointes-
tinal cancer observed for occupational exposures (se« Effects section).
whether inspired asbestos fibers will be deposited 1n the lung depends
strongly upon their diameter. Timbrel! (1965) has shown that a fiber, inde-
C-30
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pendent of Us length, behaves aerodynamica' ",y li
-------
and clearance in the respiratory tract were followed. At the conclus'cr of
the inhalation, the distribution in various organ systems was determined.
the results are shown in Table 9. As can be seen, rapid clearance from the
upper respiratory tract occurs with up to two-thirds of the fibers being
swallowed and found in the gastrointestinal tract. Long term respiratory
tract clearance or drainage via the lymphatics leads to additional dissemi-
nation.
Other data on the deposition and retention of Inhaled asbestos have been
reported by Hagner, et al. (1974). Figure 2 shows the dust content of rat
lungs following exposures to different asbestos varieties. As can be seen,
the chrysotlle content of the lung do«s not build up «s significantly as
that of the ampMboles for similar exposure circumstances. This Is likely
the result of some dissolution of chrysotHe by body fluids.
Excretion
Host inhaled or directly Ingested asbestos particles *Mch pass through
the gastrointestinal tract are excreted 1n feces (Cunnin^a», tt al. 1976).
As mentioned previously, some fibers are absorbed by the gastrointestinal
tract and are eventually eliminated through the urinary tract (Cook and
Olson, 1979).
EFFECTS
Acute. Subacute. and Chronic Toxlclty
Acute effects are of Uttle consequence 1n the inhalation exposure of
Individuals to high concentrations of asbestos dust. SOB* temporary breath-
ing difficulty has been reported by workers In various clrcumtances, but
such discomfort has not limited employment 1n the Industry.
Short-term effects have been described 1n a recent study by Harliss, et
al. (1978) who found airflow abnormalities 1n 17 of 23 individuals examined
C-32
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TABLE 9
Distribution of Fiber at the Termination of Exposure
(X of Total Deposited)*.&
Fiber
Chrysotlle A
ChrysotHe 8
Amoslte
Croddollte
AnthophyTMte
Fluoramphlbole
Nasal
Passages'*
9 * 3
8 + 2
6 + 1
8 + 3
7 * 2
3 * 2
Esophagus
2 * 1
2 * 1
2 * 1
2 * 1
2 + 1
1 + 1
SI Tract
51 * 9
54 * 5
57 * 4
51 * 9
61+8
67 + 5
Lower
Respiratory
Tract
38 + 8
36 + 4
35 + 5
39 + 5
30 + 8
29 + 4
aMorgan, et al. 1975
bMean and SO
C-33
-------
Weight of dust
-n lungs (mg)
15-
10-
5-
0-1
Aftv rtmovtI
— -^^ from txposun
*"• •
Amphibolm
Timt (months)
10000 20000
BLOOD (ppm)
30000
FIGURE 2
Mean Wtlght of Oust 1n Lungs of Rats 1n Relation to Oose and Time
Source: Wagner, et al. 1974
C-34
-------
1.5 and 8.0 months following a relatively intense five-month exsosure to
asbestos. Of the 17, 12 were nonsmokers or current light or ex-light smok-
ers 'less than 10-oack years). The obstructive abnormalities were usual'/
present in measurements both of one minute forced expiratory volume and of
closing volume determinations.
Although human data on Initial changes are unavailable, Holt, et al.
(1964) described early (14-day) local inflamatory lesions found in the ter-
minal bronchioles of rats following inhalation of asbestos fibers. These
consisted of muK1 nucleated giant cells, lymphocytes and fibroblasts. Pro-
gressive flbrosls followed within a few weeks of the first exposure to dust.
(These early alterations 1n animals may be related to the early human find-
ings above). Davis, et al. (1978) described similar early lesions in rats
consisting of a proliferation of macrophages and cell debris in the terminal
bronchioles and alveolae.
Jacobs, et al. (1978) fed rats 0.5 mg or 50 mg of chrysotile daily for l
week or 14 months and subsequently examined gastrointestinal tract tissue by
light and electron microscopy. No effects were noted in esophagus, stomach,
or cecuffl tissue but structural changes 1n the ileum were seen, particularly
of the v1ll1. Considerable cellular debris was present by light microscopy
in the Ileum, colon, and rectum tissue. The electron microscopic data con-
firmed that of light microscopy and Indicated the observed changes were con-
sistent with a Mineral-Induced cytotoxiclty.
A single oral administration of from 5 to 100 mg/kg of chrysotile to
rats has produced a subsequent Increase 1n thym1d1ne 1n the stomach, duo-
denum, and jejunum (Anucher, et al. 1975). This suggests that an immediate
response of cellular proliferation and ONA synthesis may be stimulated by
chrysotile 1ngest1on.
C-35
-------
The long-term disease entity, asbestosis, resulting from the inhalation
of asbestos fibers is a chronic, progressive pneumoconiosis. It is charac-
terized by fibrosis of the lung parenchyma, usually radiologically evident
after 10 years from first exposure, although changes can occur earlier fol-
lowing more severe exposures. Shortness of breath is the primary symptom;
cough is less common; and signs such as rales, f1ng«r clubbing, and, in
later stages of the disease, weight loss appear In a proportion of cases.
The disease was first reported 7 decades ago (Murray, 1907) and has occurred
freouently among workers occupationally exposed to the fiber in ensuing
years. Characteristic X-ray changes are small, Irregular opacities, usually
in the lower and middle lung fields, often, accompanied by evidence of pleu-
ral fibrosis or thickening, and/or pleural calcification. Both the visceral
and, more commonly, parietal pleura may be Involved. The mechanism of
action and translocation of asbestos fibers to the parietal pleura is uncer-
tain; both direct migration (K1v1luoto, 1960) or transport via lymphatics
fTaskinen, et al. 1973) have been suggested.
Currently, 50 to 80 percent of individual* in occupational groups with
exposures beginning more than 20 years earlier have been found to have ab-
normal X-rays. These Include asbestos Insulation workers (S«l1koff, et al.
1965), miners and millers (Mount Sinai, 1976) and asbestos factory employees
(lewlnsohn, 1972). In many circumstances the disease progresses following
cessation of exposure; in a group employed in an asbestos factory for vari-
ous periods of time between 1941 and 1954, X-riy changes were observed years
following exposure in individuals having exposures as short as one week
(Personal communication, I.J. Sellkoff).
Restrictive pulmonary dysfunction Is also seen with asbestos exposures
and may be accompanied by diffuslonal defects or airway obstruction (Bader,
C-36
-------
et al. 1961). In the early stages of asoestosis, there is limited correla-
tion between physiologic parameters, such as lung function tests. _ater,
X-ray changes and the lung function deficits are iiore highly correlated, 2ut
sti11 incompletely so.
The above chronic effects are common among occupational groups directly
exposed to asbestos fibers. They also, however, extend to those employed in
other trades working near the application or removal of asbestos. Among
workers other than Insulators employed at a shipyard for longer than 15
years, 48 percent were found to have abnormal X-rays (Selikoff, et al.
1979b). Similar data were obtained in a study of maintenance personnel in a
chemical plant (1111s and Sellkoff, 1979). Even family contacts (wives,
children, etc.) of workers can be affected. Anderson, et al. (1976) have
shown that 36 percent of 626 family contacts of workers employed some time
between 1941 and 1954 at an asbestos insulation manufacturing facility had
X-ray abnormalities years later characteristic of asbestos exposure.
In addition to disease and disablement during life, asbestosis has ac-
counted for a large proportion of deaths among workers. The first reports
of the disease (Auribault, 1906; Murray, 1907) described complete eradica-
tion of working groups. Much improvement in dust control has taken place in
the industry since the turn of the century, but even recently those exposed
in extremely dusty envlrofMltntS, Such as textile mills, may have as much 4S
40 percent of th«1r deaths attributable to this cause 'Nicholson, 197S).
Groups with lesssr exposures for 20 or more years, such as in mining and
milling (Mount Sinai, 1976) or insulation work (Selikoff, et al. 1979a) may
have from 5 percent to 20 percent of their deaths frosa pneumoconiosis. All
varieties of asbestos apptsr equally capable of producing asbestosis, in
both man (Irwlg. et al, 1979) and animals (Wagner, ft al. 1974)', In groups
C-37
-------
exposed at lower concentrations sjci as t^e 'ami lies of workers, tne-e -s
less incaoacitat ion, and death *-om asbestosis ^as not been reported.
Ext-a-ouHonary chronic ejects recocted include "asbestos corns" f*-^~
the oenetration of asbestos fibers into the skin and t^ei" incorporation in
dermal layers, and instances of Caolan's syndrome (rheumatoid pneumoconio-
s1s). No chronic, nonmalignant gastrointestinal effects are reported.
Teratogenicity
No data exist on the presence or absence of teratogenic effects from the
inhalation or ingestlon of asbestos, although transplacental transfer of
asbestos has been reported (Pontefract and Cunningham, 1973; Cunningham and
Pontefract, 1974)
Mutagenicity
In a preliminary study chromosomal aberrations were seen in Chinese ham-
ster cells cultured in a medium containing 0.01 mg/ml of either cnrysotile
or crocidollte (Slncock and Seabrlght, 1975). No chromosomal aberrations
were seen in culture with coarse glass fibers or with control media. A more
extensive series of experiments by Sincock (1977), using several chrysotile
and croddollte samples, showed that both positive transformation of
morphology and positive genetic responses result from t*« passive inclusion
of asbestos In culture media of CHO-K1 Chinese hamster cells. Very fine
fibrous glass produced the same abnormalities, but chemically leached
asb«stos f1b«rs produced fewer abnormalities than those untreated. The
principal results are shown in Table 10.
Chamberlain and Tarmy (1977) tested UICC asbestos samples of chrysotile,
amosHe, anthopnylllte, and samples of superfine chrysotile on several
strains of £. coll and S. typMmurlum bacterial systems in wMcn mutageni-
city to exogenous materials appears to correlate well with animal carcino-
C-39
-------
IAM.i 10
ffftctt of Dl ' (treat Iro«bM«U on
of CHO-KI - CMiwse Newter Cells*
Polyplotot
C«Us «IUt frtewrtt
IKnffT ttMeVTlM 1 1 1 f m\
Percent •bworWil keryotypo*
folyplottfi
Colls with rrMMtf
Other ttmnMlitlot
Percent ohftonMl cells
•This t*le suMMflm the prim
tram oodl cultwro. C«to«orles
CSiryi»-
tllo
21
13
33
NM*slo»
Ckryto-
Illo 4
13
13
10
M
clpol results ref
of «e«Mtlc 4o»M
Chryso-
t lie •
n
14
9
M
•»4MtM
Chryso-
tllo •
Loodiorf
b
0
0
'
acted !• Slncoci
ie nere M»t outu«
CwitdlM UICC UICC
Chryso- Croc loo- Mtho-
Ille b
21
II
IS
J4
f«»dt« C
Chryso
tile •
I
2b
9
U
42
(I9/;). Results
My eicluslve.
lite
2b
10
29
39
k»»dta
Chryse
til* h
e*ched
10
0
4
14
•ore
•hylllto
2
10
9
S4
• UICC
Croc 1*1-
lite
I
?4
14
28
&;
obl«lned uslNf 48-hour
UICC
14
Ib
1)
26
UICC
Croc leo-
llte
Hilled
6
9
3
Ib
exposure;
110
J
0
0
41
6I4SS
110
4
0
0
b
100 cells were
Cunlrol
Control
4
U
U
-------
gemc test data. Several positive and negative controls were used in al'
experiments. No mutagenicity was observed in any of the bacterial strains.
"he authors aoint out that prokaryotic cells (bacteria) do not pnagocytize
the fibers as do eukaryotic cells, such as macrophages.
Cardnogenicity - Animal Data
Ingestion: Limited data exist on the cardnogenlcity of asbestos admin-
istered by ingestion. With the exception of an abstract which reported
negative data from 12 animals, published 1n 1967 (Bonser and Clayson, 1967),
no reports were extant on the effects of Ingested asbestos until the finding
of large amounts of cumm1ngton1te-gruneHte fibers In Lake Superior and the
drinking water of Duluth, M1nn. focused attention on the problem. As an
outgrowth of the Reserve Mining Company trial 1n which the federal govern-
ment sought abatement of the Lake Superior pollution, two compilations from
four laboratories were made of studies which showed negative results on the
ingestion of asbestos.
Smith (1973) reported results of feeding 45 hamsters 1 percent chryso-
tile or amosite in their diet. A neoplasm of the mesentry of the colon was
found, which was discounted because no fibers were Identified In the tumor;
no details were given concerning how the fibers were sought. The actual
dosage of asbestos was not given, nor were other relevant experimental
details provided. However, the finding of fibers In tumor tissue would be
unlikely and, as these tumors are rare 1n hamsters, this result cannot be
dismissed out of hand.
Gross, et al. (1974) reported the results of a series of feeding experi -
ments with chrysotlle and croddollte. The data w«re the unpublished re-
sults o various experiments conducted over the previous 10 years by three
C-40
-------
laboratories. All available data on these exDeriments are lasted m "ao'e
11. The data are flawed for several reasons. The numbers in each experi-
mental group were small, the doses administered limited, and significant
information on experimental procedures lacking. Also, systematic histo'ogi-
cal examination, which was of most significance, was done on only 53 of
over 200 animals.
Wagner, et al. (1977a) fed groups of 32 rats 100 milligrams per day of
chrysotHe or talc in malted milk for 100 days over a 6-flwnth period of
time. A small decrease 1n survival time was observed in the two study
groups: 614 and 518 days versus 641 for the controls. Two gastric leiomyo-
sarconus were observed, one in each exposure group. Interpretation of the
results of this experiment, too, is difficult because of the small numoer of
animals in experimental groups.
As an outgrowth of concern for the use of asbestos filters in the puri-
fication of wine products and the possible effects of erosion of asbestos
fibers from those filters into the final product, a study was undertaken in
which asbestos filtered material was fed to rats (Gibel, et al. 1976).
Twelve malignant tumors developed in experimental animals, including four
kidney tumors. NO tumors of this site were found 1n control groups. This
observation of renal cancer takes on significance In light of the finding of
an elevated risk of -kidney cancer among asbestos insulation workers
(Sellkoff, et al. 1979a) and a high excretion of asbestos fiber in the urine
of humans drinking fiber-contaminated water (Cook and Olson, 1979).
However, this report provides only limited experimental detail, and the
filter material was composed of sulfated cellulose and a condensation resin
1n addition to 52.6 percent chrysotlle asbestos. The presence of other
substances confounds the study 1n relation to asbestos carcinogenicity.
C-41
-------
IAME ||
ry •» (ipcrtaMits CM Uw frfcctt «f Or* I
on of AtWitot
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far luaorv
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C-4J
-------
UflU II (continued)
y of f after toenti on tkc Effects of Oral Ineestto* of Asbestos
Ante*) Seectei
S -laboratory*
rats
Jl Utslar
Srf rati
11 Mttter
Sff ratt
34 Mtitar
Vf rati
14 Mtstar
Srf ratt
» Millar
?« MUtar
Sff ratt
74 Mtitar
Sff ratt
Material
cwatrel
SSSi
o.n-o.«i
croc Idol He U
kvtUr 0.71 -
0.41 a)Utare
..uJTila 1"
control (»«ittor)
•U Caoe
croc late) Ite
croc I4o lite In
•titter (0.21 to
0.4IJ
control
Oosaoe **'
Croitp et al.
control
10 *f weekly
for U weoks
for U weeks
10 tM weekly
for It weeks
control
10 •) weekly
for U weeks
10 M weekly
for fa weeks
control
trMri"*
. |IW«)
S
31 test
•a few*
33 less
•a few*
34 less
•a few*
(247)
JS less
•a few*
28 less
•a few*
(?47»
flndlnps A«vr«o« ^ur
•o«« s*ci Utced
1 breast carclnoeMS nut Bitted
•one nut st«tv«l
1 IjMphOtU no) staled
3 « tst carclnotMS not stated
1 Utah serca-M
no«e not sl*lc
-------
ry of
IAWC 11 (COMtlMttd)
u «M tto iffecu or om iofe«tio« or
Antail S0tclM Htlorlal fc>tafi
^^ MHlolttorod
CtMMln^i
10 Ml* Mlttar It dtryMtlU*
rat»
10 Mlo MttUr ca»lr*l
raU
40 Ml* Utstar It c*ryMtlU Mt fl«M>
nli
40 m»\» MUtMr control
ratt
-war *.,isrt«,
... .t .1. (l«/M
^kld^y
1 oorltOMoal
1 lyaofcoM
1 rtoroscrcomi
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Average Sur
vlval Mae
not given
not given
not given
not given
C-44
-------
Cunningham, et al. (1977) conducted two limited 'eed^ng studies of
-/istar "ats. One percent chrysotile asbestos with Mve Descent com o''
added to rat c^o* diet and *ed to groups of 10 aro 10 rats -i two seoarjte
experiments. In the first study, six of seven surviving animals *ere *:LPC
with tumors whereas only one malignancy was observed in eight controls !see
Table 11). No gastrointestinal tumors were seen, but two of the treated
group tumors were kidney nephroblastomas• I" the second larger study, 11
tumors each were observed in treated and control groups of 40 animals. ~*o
of the malignancies 1n the asbestos-fed group were of the gastrointestinal
tract and one of the control group was a nephroblastoma, lessening the sig-
nificance of the finding of this tumor 1n the other treated group. With the
limited number of animals in this study, the evidence for carcinogenicity of
asbestos (by feeding) is inconclusive.
Currently, a very large feeding experiment is being conducted under the
auspices of the National Institute of Environmental Health Sciences
(NIEHS). Results, however, are not anticipated until late 1980. Meanwhile,
all previously reported experiments on Ingested asbestos, whether positive
or negative, have significant limitations. To extrapolate such data to man
for use as a criteria for a standard would not be appropriate.
Inhalation: Although lung cancer was suggested as being causally re-
lated to human asbestos exposure 1n case reports in 1935 (Lynch and Smith,
1935; Gloyne, 1935). strongly Indicated to be so in 1947 (Merewether, 1947),
and uneoulvocally associated In a cohort study by Doll (1955), no positive
animal data of consequence were forthcoming until 1967 when Gross, et al.
(1967) showed that lung cancer could be produced by asbestos inhalation
exposure. An early experiment of Nordmann and Sorge (1941) described two
lung tumors in 10 of 100 mice surviving 240 days following exposure to high
C-45
-------
concentrations of chrysotile. This work, however, was called into auesticr
by Smith, et al. (1965) on the basis of the tistology of the nalignancies.
Lynch, et al. (1957) exposed AC/F, hybrid mice to commercial chrysofi le anc
observed a higher incidence of pulmonary adenomas in exposed animals, 45.7
percent (58/127), compared to controls, 36.0 percent (80/222). No malignant
tumors were reported, and the Increase of adenomas was not significant at
the 0.05 level.
The first unequivocal data showing a relationship between asbestos inha-
''atlon and malignancy was that of Gross, et al. (1967) who observed carcino-
mas in rats exposed to a mean concentration of 86 mq/m chrysotlle for 30
hours/week from the age of six weeks. Of 72 rats surviving for 16 months or
longer, 19 developed adenocarcinomas, 4 developed squamous cell carcinomas,
and 1, a mesothelioma. NO malignant tumors were found in 39 control ani-
mals. A search was made for primaries at oth* sites which could have
Tietastasized. None were found. These and other data are summarized in
Table 12.
Peeves, et al. (1971) found 2 squamous cell carcinomas in 31 rats sacri-
ficed after 2 years following exposure to about 48 mg/nr of crocldoHte.
No malignant tumors were reported 1n rabbits, guinea pigs, hamsters, or in
animals exposed to similar concentrations of chrysotlle or amoslte. No
details of th« pathological examinations were given.
In a later study (Reeves, et al. 1974), malignant tumors developed in 5
to 14 percent of the rats surviving 18 months. Lung cancer and mcsothelioma
were produced by exposures to amosite and chrysotlle and lung cancer by cro-
ddollte inhalation. Again, significant experimental details were lacking;
information on survival times and times of sacrifice would have been useful.
Available details of the exposures and results are given in Table 13. While
C-46
-------
IMtE 12
y of (ipcrlBMtt on the Effect* of laluUtlM of Asfettot
IW •*)• Hkllt
rit»
55 Mlt i*IU
r«ts
ItoUrlil
chryMttU «IU/
MltiMMt •.« ml
tetrtUKBMl
& MrCMt MM
c«« trait
Ml
ft
MlMlt [XM
for luaort
troiy. «* «»• 11*7)
47-144
(MM c-c
M ••/•>) for
JOhrt/KM*
control
39
17
4 t••••nut-cell
1 MMUMltOM
• l»*
ur iu
l M
not «v«ll«l>le
not *v«ll*ble
?0t r«tt
IM fulM* plfi
cWy»»tl)e.
lU. MMl
crocl«toMtt
48«?
up
yri
tt «l. (19/1)
itot
? t^u«Mt«it-ce 11
CWClMMt U 11
MllMlt fro* Crotl-
tfollU
no \nlormtlIon
periodic i*(
rl( ic*i were
•ide
r«tt
100 Mice
>?
100 («(•*•• plgt
dtrytotlle,
••Oitte. *nd
croc IdolIte
ieeyet. et *l.
lor 170 r»ti
It hrs/»eck up lit aerbllv
to ? yrs 10 «lce
30 r*M)lti
4) 9ul»e< plgi
? In vice (See l«ble 13)
no lnloi»«liuii
pe«
Mir If uei
C-47
-------
\2 (continued)
y «f (iMrtaetiti
dtY"> versus
754 to 80 1 «
controls.
M>l
C»ntl»
affected by
e«posure.
not
iacr liked at
?« Mntht
C-4«
-------
IMlf 13
E«B«rla**t«l laktlttton C*rci«og»»««lt«
Clp»SUT« Ittt M4CC
Mm* MUr»
Fltar (•«/•>) ('/•!)
CHryuttllt 47. ff M
Mot It* M.t «M
CrocttellU 50.2 I.IOS
Cootrolt
*%lL *l«r«l l«r» Mi.,1^ M.ll9n*nl lu«rs
41 1 IM* M»l»«ry 1» none
I lUM (^MMHHl-Ctll
CWClMMI
1 •lourtl •MoUclloM
4t 2 Blcwtl •tsoUtclloMf 17 none
44 1 WIMOMI-C*)) 18 ? p*ptll*ry
1 «4NOC*rclMMM of bronchus
1 •a»ll|*ry c«rclMHM -
til or UM IIMI
b MOJM 6 1 DAplllAry
lift IlKMM Of
bronchus
. tt *l
»»bciUt IMS COM*(M»I»4 by
ratio) »y ll^it «lcr«tco»y.
•lll(«t, »fiw wMU» O.on to 1.82X o( the tlrboriM MSI "«» of fibrous Morphology (3:
C-4»
-------
the relative carcinogenicity of the fiber types was similar, it was notec
that the fibrogenic potential of chrysotile, which had been substantial'/
reduced in length and possibly altered danger, et al. 1978) by milling, was
much less than that of the amphiboles. These results were also discussed --
a later paper by Reeves (1976).
In an extensive series of experiments, Wagner, et al. (1974) exposed
groups of Wlstar SPF rats to the five UICC asbestos samples at concentra-
tions from 10 to 15 mg/m for times ranging from 1 day to 24 months. For
all exposure times there were 50 adenocardnomas, 40 squamous-cell carcino-
mas, and 11 mesothellomas produced. None appeared prior to 300 days from
first exposure. Considerable experimental detail 1s provided in the paper.
The sianificant data are presented 1n Tables 14 and 15. These tumor? follow
a reasonably good linear relationship for exposure times of three months or
greater. The incidence in the 1-day exposure group, however, is consider-
ably greater than expected. It was noted that exposure had a limited effect
on length of life. Average survival times varied from 669 to 857 days for
exposed animals versus 754 to 803 days for controls. The development of
asbestosls was also documented. The Incidence of lung cancer was found to
be greater in animals surviving 600 days. There were 17 lung tumors, 6 in
animals with no evidence of asbestosls and 11 in rats with minimal or slight
asbestoslj. Cancers at extraptilmonary sites were also listed. Seven malig-
nancies of ovary and 8 of male genitourinary organs were observed in groups
of approximately 350 rats. None were observed 1n groups of 60 male and fe-
male controls. Incidence of malignancy at other sites was little different
from that of controls. If controls are Included from other experiments in
which ovarian and genitourinary tumors were present, the comparative inci-
C-50
-------
TABLE 14
Number of Rats with Lung Tumors or Mesothel1omas After Exposure
to Various Forms of Asbestos Through Inhalation*
Form of Asbestos
Amos He
Anthophylllte
Croddollte
ChrysotHe
(Canadian)
OirysotHe
( Rhodes 1 an)
None
No. of
Animals
146
145
141
137
144
126
Adenocarclnomas
5
3
7
11
19
0
Squamous-cell
Carcinomas
6
a
9
6
11
0
Mesothel lorna
1
2
4
4
0
0
*Source: Wagner, et al. 1974
C-51
-------
TABLE is
Numbers of Rats with Lung Tumors or Mesotheliomas After Various
Lengths of Exposure to Various Forms of Asbestos Through Inhalation*
Length of
Exposure
None
1 day
3 months
6 months
12 months
24 months
No. of
Animals
126
219
180
90
129
95
No. with Lung
Carcinomas
0
3b
8
7
35
37
No. with Pleural
Mesothe11o«as
0
2c
1
0
6
2
X of Animals
with Tumors
0.0
2.3
5.0
7.8
31.8
41.0
'Wagner, et al. 1974
b2 exposed to chrysotile and 1 to crocidollte
cl exposed to amoslte and one to crocidollte
C-52
-------
dence in the exposure groups he^e 'acks significance. No data *ere pro-
vided, however, on the variation of tumor incidence at extrapoLnonary sites
with asbestos dosage.
Wagner, et al. f!977a) also compared effects of inhalation of a super.
fine chrysotile to a pure, nonfibrous talc. One adenocarcinoma was found in
24 rats exposed to 10.8 mg/m3 of chrysotile for 37.5 hours/week for 12
months.
Finally, 1n a study similar to Wagner's, Davis, et al. (1978) exposed
rats to 2.0 or 10.0 mg/nr of chrysotlle, croddolite, and amosite (equiva-
lent to from 430 to 1950 f/ml). Adeno- and squamous cell carcinomas were
observed in chrysotlle exposures, but not with croc1dol1te or amosite fsee
Table 16). One pltural mesothelloma was observed with croddolite exposure,
and extrapulmonary neoplasms Included a peritoneal mesothelioma. A rela-
tively large number of peritoneal connective tissue malignancies were also
observed, including a lelomyofibroma on the wall of the small intestine.
The significance of these tumors 1s speculative, however.
As discussed in the Pharmacokinetics section, inhalation exposures
result in concomitant gastrointestinal exposures from the asbestos that is
swallowed after clearance from the bronchial tret. While all inhalation
experiments focused on thoracic tumors, those of Wagner, et al. (1974),
Davis, et al. (1978) and, te a limited extent, Gross, et al. (1967) also
included a search for tumors at extrathoracic sites. A limited number of
these were found, but no association can be made with asbestos exposure.
One aspect of the Inhalation experiments that 1s noteworthy is the sig-
nificant number of pulmonary neoplasms that can be produced 1n the rat by
Inhalation as compared to other species (Reeves, et al. 1971, 1974). This
points to the variability of species response to asbestos and the need for
C-53
-------
TABLE 16
Experimental Inhalation Carc1nogenes1s in Rats*
Exposure
Mass Fiber
(mg/m3) (f>5u/«l)
Chrysotile 10
Chrysotile 2
Amoslte 10
Crocidollte 10
Crocidollte 5
Control
1.950
390
550
860
430
Nunber of
Animals Malignant Tumors
Examined
40
42
43
40
43
20
6 adenocarcinomas
2 squamous-cell carcinomas
1 squamous-cell carcinoma
1 peritoneal mesothelloma
none
none
1 pleural mesothel
none
1oma
*Source: Davis, et al. 1978
C-54
-------
an appropriate model before extrapolations to -nan can be naae *ctn
dence. """he absence of significant gastrointestinal malignancy frcm i
exposure in animals, in contrast to that found in numans, Tiay 5e the
of the use of inappropriate animal models.
Intrapleural Administration: Evidence tnat intrapleural administration
of asbestos would result in mesothelioma was forthcoming in 1970 when Donna
(1970) produced mesotheliomas in Sprague-Oawley rats treated with a single
dose of 67 mg of chrysotile, amosite, or crocidolite. Reeves, et al. (1971)
produced mesothellal tumors in rats (1 of 3 with crocidolite and 2 of 12
with chrysotile) by Intrapleural injection of 10 mg of asbestos. Two of 13
rabbits injected with 16 mg of crocidolite developed mesotheliomas.
Stanton and Wrench (1972), in a series of experiments, demonstrated that
major commercial varieties of asbestos, as well as various other fibers,
produced mesotheliomas in as many as 75 percent of animals into which mate-
rial had been surgically implanted. Extension of these experiments were re-
ported in 1973 (Stanton, 1973). These results are summarized in Table 17.
The authors concluded that the carcinogenicity of asbestos and other fibers
is strongly related to their physical size, those fibers of a diameter less
than 3 urn being carcinogenic and those of a larger diameter not carcino-
genic. Further, samples treated by grinding in a ball mill to produce
shorter length fibers were less likely to produce tumors. While the authors
attributed the reduced carcinogenicity to a shorter fiber length, the ques-
tion has been raised as to the effect of the destruction of crystallinity
and perhaps other changes 1n the fibers occasioned by the extensive ball
milling danger, et al. 1978).
Another comprehensive set of experiments was conducted by Wagner (Wag-
ner, et al. 1973, 1977b). He, too, has produced mesothelioma from intra-
C-55
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TABLE 17
Oose-response Data Concerning the Effects of Intrapleural
Implantation of Asbestos and Other Fibers in Rats*
UICC-SRAS
CroddoHte
Hand-cobbed
Virgin
Croc1dol1te
Special South African
croc 1 do lite
Partially pulverized
crocfdoHte
UICC-SRAS
UICC-SRAS
chrysotlle
Coarse
fibrous glass
Glass wool
Fine AAA fibrous glass
3wM dlantttr
uncoattd
coattd
Dose
(mg)
1
2
10
20
40
1
20
40
40
40
40
40
40
40
40
40
No. of Rats
with
Mesotheliomas
2
5
11
12
14
4
10
18
15
3
15
15
1
1
3
5
Total no.
of rats
25
23
27
25
23
30
24
27
20
25
25
26
24
25
26
28
X of Rats
with
Tumors
8
22
41
48
61
13
42
67
75
32
60
58
4
4
12
18
*Sourct: Stanton and Hrtnch, 1972
C-56
-------
pleural administration of asbestos to CD rfistar -?ts
strong dose-response relationship. Cables 13 3nd 19
3y1»v and Shabad (1973) and Shabad, et al. (1974) rv»r, ».5
not borne out 1n the experiments described abov<» iy ^gner, et a1. (!>'• -.<•
-Stanton and Wrench (1972).
Intratracheal Injection: Intratracheal injection has been >jsed to 5-> /
the combined effect of administration of chrysotile with benzo(a)pyren* -
--ats or hamster? (see Synergism and/or Antagonism). In rats given t~'--e
-^oses of 2 mg chrysotile fShabad, et al. 1974) or hamsters given 12 -ng -f
chrysotile (Smith, et al. 1970) no lung tumors were observed. However, t e
coadmlnlstratlon of benzo(a)pyrene did result in lunq tumors.
IntrapeMtoneal Administration: IntrapeHtoneal injections of 20 mg of
croddolUe or chrysotile produced three peritoneal mesoth«l1omas in 13
Charles River CO rats. Twenty mg of amosite produced no tumors in a group
of 11 (MiUonl and Annoscla, 1974). They also injected 25 mg of crocldoHte
into 50 male and 50 female 17 -week -old Sprague-Oawley rats and observed 31
mesothellal tumors In males and 34 1n females.
In an extensive series of experiments, Pott and FriedMchs (1972) *nd
Pott, et al. (1976) produced peritoneal mesothel iomas in mice and rats in-
C-57
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TABLE ia
Percentage of Rats Developing Mesotheliomas After
Intrapleural Administration of Various Materials4
Material Percent of Rats
with Mesothellomas
SFA enrysotlle (superfine 66
Canadian sample)
UICC croddolUe 61
UICC amoslte 36
UICC anthophyllUe 34
UICC chrysotHe (Canadian) 30
UICC chrysotlle (Rhodeslan) 19
Fine glass fiber (cod* 100),
median diameter. 0.12 UJR 12
Ceramic fiber, diameter.
0.5-1 u«b 10
Glass ponder 3
Coarse glass fiber (code 110),
dlnMttr, 1,3 >^i 0
, et al. i9/7fa
, et al. 1973
058
-------
TABLE 19
Dose-flesponse Data Following Intrapleural
Administration of Asbestos to Rats*
Material
SFA chrysotHe
Croddollte
Oose
(ing)
0.5
1
2
4
8
0.5
1
2
4
8
No. of Rats with
Mesothelloma
1
3
5
4
8
1
0
3
2
5
Total no.
of Rats
12
11
12
12
12
11
12
12
13
11
X of Pats
with Tumors
3
27
42
23
62
9
0
25
15
45
'Source: Wagner, et al. 1973
C-59
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•v-'.e- • ."'-•'• '•'ar-iet'es of aseestos and other fibrous nate-
T"?. -f- " ?'own in TaDle 20. Using experiments with
i?*--:r-eu'a 20--.r r.--.: ' ;r.. tie malignant response was altered by ball-
m-l'i-g fibe- ; fo - -ours. The rate of tumor production was reduced from
55 ne-rent to ";. PP"'?^ and the time from onset of exposure to first tumor
wds lengthened f-om 323 to AGO days following administration of four doses
of 25 me of UK" Rr.odes'^an ch.-ysot1le. In the case of the ball-milled
'ibe1-, ^\ percent w^re e-r-^er! to be smaller than 3 w«, 93 percent less
than 1 um> ane" 60 pe^rent less than 0.3 um.
A strn.-ic. ccnc 'usio". >»M>- ca,: be a.-a^n from the above exptrliwntal data
• i that id-^^-) amere M,- . vgrcate- than 3 iiffl) art significantly less
carcinogenic t'lan fine" ric»-s. The origin of the r«ductd carc1nogen1c1ty
o' sno-ter, Si '-rii^d fibe-s *v less clear as th« rtl«t1v« contributions
of snorte1* fit;- "i5.iqtri a,- s1 >e ^c^e-dent effects, fnjw Intrapleural
or intraperi tones.. awiiirn strati CM IL ' their cardnog«n1 city must be
demonstrated at a ^evel 100 t1me^ >eis before their contribution can be
neglected.
Carclnoqenlcity - Human Data
The modern history of asbestos disease dates fro* th« turn of the cen-
tury, when two reports were published documenting uncontrolled conditions 1n
asbestos textile factories. One, the testimony of H. Montague *jrray (1907)
-------
IABU ?0
Iu«ors In *bdo»tii »nd/or IKor«x After Utrtpertlonetl Injection of GUss fibers. Crocldollte, or CurumJua In
Rust
GUss fibers
m 104
GUss fibers
MM 104
Glass fibers
MM 104
Croclitollte
CortlMiuB
IIICC Rhodes Ian
chrysolite
IIIU Rhodes Ian
IIICC Rhodes Un
chrysotl le
Ilirr Rhodes IM
rhrysott le
IllCf Rhode 1 1 *n
chrysotlle
IIICC Rhodeslan
•111*4
P*ly*nrUUe
fom^> lote
f t
f 10
f 7 i ?5
f 2
9 ? • ?S
f ?
f 6.?S
f 25
f 4 . ?S
f 3 • ?«.
s.c.
f 4 « K
f 3 « ?S
Effective
IKtMcte4
73
77
77
N
37
37
35
31
33
33
37
34
No of fry*
lefore First
IUHOT
471
no
194
452
545
431
343
?76
3?3
449
400
?s;
Average
Survival Tlae
of R«tl Kith
luoors (days
after Injection)
703
63?
3.7
761
799
6SI
SOI
419
361
449
S09
34H
Rats lu
• Ith
(percent) i t 3
?7.4 17 3
S3.? 36 4
/I. 4 47 6 I
38. S 1? 3
8.1 I
16.? 4 i
77.1 ?4 J
BO. 6 21 ? 1
S4.S Ib t
3.0 1
3?. 4 9 3
/b.b ?4 2
I 1
C-61
-------
In
IA«tl 20 (continued)
Ihorti Alter lntr«per| I one* I Injection ol Gl*ss fibers, trot Idol He. or tormidua in Ha
flusl
fl»SS finer*
s • s in*
£|*M fibers
S • S l(ft
Gliss libers
S « S 106
Gypsua
hentllte
Act Inn lite
nlottte
Xr«i;.».>
"•SLKn
Pec toll U
S«nl4liw>
Ulc
•un (control)
•Source: Pott
hf
f \imnr 1 ynes *
For.*
f
I
r
i
i
9
9
9
»
9
0
9
•nd Frl
. qr.n
re: I
int.
,
10
4 « ?S
4 • ?S
4 i ?S
4 i ?S
4 « ?S
4 « ?S
4 « ?S
4 « ?S
4 » ?S
4 • ?S
4 K 7»l
e<«r|chs. 197?;
ul*r
Mp^olnelloM;
iff II* A,er*9e H.ts
OUiecled lefore First ol *«ls •!(»« IUMTS
••It luaor IUBOTS (d«ys (percent 1 \ j
•Her Injection)
34 69? 69? ?.9 1
36 3SO 530 ll.l ? ?
3? I9/ 3?S 71.9 ?0 1
35 579 M3 K »
34 ?49 315 M.5 17 8
39
37
34
18
40 S69 S69 <-.b
39 S79 S79 ?.t |
36 5R7 587 ? 8 1
7?
Pott, et •) 1976
? Spindle cell ^ art ami, ) Puly* cell SOCOBJ; 4 l*rclcwMu; S Meticuli« ci>ll ia-
I* t
-------
at a hearing concerning compensation, described severe pulmonary fibrosis
found at autopsy in 1900 in the last survivor of a group of 10 workers first
employed 14 years previously in a carding room. The second was the descrip-
tion by Auribault (1906) of deaths during the early years of operation of an
asbestos weaving mill established at Conde-sur-Noireau, France, in 1890.
During this period 50 men died, including 16 of 17 recruited from a cotton
textile mill previously owned by the factory director.
With time, however, the spectrum of diseases associated with asbestos
exposure continued to expand. In 1935 two clinical reports were published
on lung cancer 1n asbestos workers who had died with evidence of pulmonary
fibrosis (Lynch and Smith, 1935; Gloyne, 1935). While such reports were not
sufficient to causally relate asbestos exposure to the lung cancer, the pos-
sibility was raised. In 1947 it was confirmed by substantial data which
showed that 13 percent of a group of individuals who died with asbestosis in
Great Britain also had brorchogenic carcinoma (Merewether, 1947). Mesothe-
lioma, a rare tumor of the lining of the abdomen or chest, was first de-
scribed in an asbestos worker in 1953 (Weiss, 1953) subsequently found to be
frequently associated with potential asbestos exposure (Wagner, et al.
1960), and unequivocally related to such exposure in 1965 (Newhouse and
Thomson, 1965). Gastrointestinal cancer also was found to be in excess
among asbestos Insulation workers in the United States (Sell It off, et al.
1964).
Currently, all major comnerdal asbestos varieties, chrysotile, amoslte,
and crocidolite, have been found to produce a significant Incidence of
asbestos-related disease among workers occupatlonally exposed in mining and
milling, in manufacturing, and In the use of materials containing the fiber,
The predominant route of exposure has been Inhalation, although some asbes-
C-63
-------
tos may be swallowed directly or after being brought up from the respiratory
tract. Not only has asbestos disease been found among individuals exposed
to t^e fiber directly as a result of excessive work exposures in decades
oast, out asbestos-associated cancer has also been identified, albeit less
frequently, among those with inhalation exposures of lesser intensity, in-
cluding those who had worked near the application or removal of asbestos
material, those with history of residing in the vicinity of asbestos plants,
and those who had lived in the household of an asbestos worker.
Water Ingestlon: Five studies have considered the relation of asbestos
ingested in drinking water to gastrointestinal cancer. As an outgrowth of
the contamination of Lake Superior by fibrous material 1n the tailings of an
iron ore processing plant, tte mortality of the population of Duluth was
compared with that of Minnesota and Hennapin County (Minneapolis) for quin-
auenia to 1969 (Mason, et al. 1974). The relative death rates for digestive
cancer, lung ca*ncer, and all neoplasm were elevated from 16 to 49 percent.
However, with the exception of colon/rectal cancer, which was highly e'le-
vated, no trends with time or consistency between male and female were
dearly dlscemable. Because of this, Mason, et al. (1974) concluded that
additional followup was necessary to determine 1f a hazard exists. Levy, et
al. (1976) conducted a similar study with equivalent results. However, the
short follow-up from the earliest possible exposure (1956) would make it
unlikely that any positive result would be found. Furthermore, while the
Reserve plant began production 1n 1956, current discharge levels did not
begin until 1967 when a major plant expansion took place.
A study by Harrington, et al. (1978) reviewed malignancy In the Connec-
ticut Tumor Registry from 1935 to 1973 to see If a correlation existed be-
tween the use of asbestos cemeit (A/C) pipe for public water supply and the
C-64
-------
incidence of gastrointestinal cancer. No association was found between the
age-adjusted, sex-specific incidence data for stomach, colon, and rectal
cancer and the use of A/C pipe. While some water supplies reported A/C pipe
that was 45 years old in 1975, the majority (66 percent) of the population
studied received water through A/C pipes that were only 25 years old. While
the majority (56 percent) of A/C pipe systems In Connecticut have water
which is considered aggressive under the AWWA Standard for A/C transmission
and pressure pipe, fiber counts done on over 100 A/C p1p« systems 1n Con-
necticut showed 98 percent to be under 10 f/1 (J. Mlllette. personal com-
municatlon).
A report published for the University of California analyzed the 1969-
1971 cancer incidence from 721 census tracts of the five Bay Area Counties
along with the chrysotHe asbestos fiber concentrations 1n the drinking
water (Cooper, et al. 1978). For the census tracts the chry$ot1l« asbestos
fiber counts ranged from below detectable limits to 36 x 10 fibers per
liter.
The University of California Investigators grouped the census tracts on
a gradient of low-to-high asbestos counts and found significant
dose-response gradients for the Incidence of several cancers. Statistically
significant positive trends were noted for white male lung and stomach
cancer and white female gall bladder, esophageal, and peritoneal cancer.
The census tracts were cross-classified using both asbestos count and tract
soc1oeconoa1c status Indicators of medium family Income and medium school
years completed. The positive dose-response effect between cancer Incidence
of certain sites and asbestos counts appeared to be independent of the
effect of socio-economic status. The fact that the significant results are
not restricted to one body site 1s not surprising considering the knowledge
-------
that asbestos fibers are probably transported throughout the body, "or ex-
ample, one study using rats has found that ingested fibers are deposited in
the lung. (Cunningham, «t al. 1977). An extension of this study 'Cooper,
et al. 1979) using six years of data showed a statistically significant as-
sociation between asbestos levels In the San Francisco Bay area drinking
water and cancers of the digestive tract.
A study by H1gle (1977) compared the cancer mortality 1n two areas of
Canada with probable high concentrations of asbestos in drinking water with
an area presumably having low concentrations. Only one published asbestos
concentration 1s provided. Five values are listed from a personal communi-
cation with no details given on the sampling and analytical methods uti-
lized. No data are provided to substantiate the assumed exposures of all of
the "probably low exposure" group and five of the seven "possible high expo-
sure" municipalities. The mortality experience was compared with that ex-
pected from Quebec rates, although for some sites it 1s known that the rural
counties have lower cancer rates than Quebec, the rates of which are domi -
nated by the urban center, Montreal. For example, the lung cancer rate of
the rural counties near the asbestos mines 1s only two-thirds that of Quebec
(McDonald, et al. 1971). Elevated rates for cancer of the stomach, colon,
and rectum were seen among "high exposure" males (46 observed vs. 38.4 ex-
pected), "possible high exposure" females (103 vs. 91.3) and "probably low
exposure" females (311 vs. 270.3). The rates for the other two male and one
female groups were about 5 percent less than expected. In addition to the
absense of sampling data on exposure, the small number of deaths observed
seriously Units the study. For example, this document estimates that a
10"^ risk of death from asbestos 1ngest1on may occur from exposures to
400,000 f/1. If there were no population migration Into or from the highly
C-66
-------
exposed areas and everyone deceased in those municipalities were exposed for
a lifetime to the concentrations indicated, the above criteria level would
predict about ten excess deaths among the approximately 1,000 that occurred
over the observation time of this study.
Insulation Application and Removal: A large study by Selikoff, et al.
(1979a) best demonstrates the full spectrum of disease from asbestos expo-
sure. They studied the mortality experience of 17,800 asbestos insulation
workers from January l, 1967 through December 31, 1976. These workers were
exposed primarily to chrysotile prior to 1940, and to a mixture of chryso-
tile and amosite subsequently. No croddollte 1s known to have been used 1n
U.S. insulation material (Selikoff, et al. 1970). In this group, 2,271
deaths have occurred, and their analysis provides important insights into
the nature of asbestos disease. Table 21 lists the expected and observed
deaths by cause, and includes data on tumors less frequently found. Lung
tumors are common and account for about 20 percent of the deaths; 8 percent
are from mesothelioma of the pleura or peritoneum. Additionally, though,
cancer of the gastrointestinal tract is significantly elevated; so, too, are
cancer of the larynx, pharynx, and buccal cavity, and renal tumors. Other
tumors are also increased, but not to a statistically significant degree for
an Individual site. Comparing the deaths from cancer and asbestosls in this
group with those expected 1n the general population, more than 40 percent of
the deaths among Insulators can be attributed to their occupational exposure
to asbestos fiber.
Table 21 lists the observed deaths as categorized on death certificates
and as determined after a review of all autopsy and medical records (BE).
The use of deaths characterized by the best available medical evidence for
risk analysis is appropriate when one considers diseases that are virtually
C-67
-------
TABLE 21
Deaths Amonq 17,300 Asbestos Insulation
in the Jnited States and Canada
January 1, 1967 - January 1, 1977O
Number of
Man -fears
Underlying Cause of Death
Total deaths, all causes
Total cancer, all sites
Cancer of lung
Pleura! mesothelioma
Peritoneal mesothelioma
Mesothelioma, n.o.s.
Cancer of esophagus
Cancer of stomach
Cancer of co Ion -rectum
Cancer of larynx
Cancer of pharynx, buccal
Cancer of kidney
Deaths of less common
malignant neoplasms
Pancreas
Liver, biliary passages
Bladder
Testes
Prostate
Leukemia
Lymphoma
Skin
Brain
All other cancer
Nonlnftctlous pulmonary
diseases total
Asb**tos1s
All other causes
Men: 17,800
of Observati
Expected
1,658.9
319.7
105.6
c
c
c
7.1
14.2
38.1
4.7
10.1
8.1
17.5
7.2
9.1
1.9
20.4
13.1
20.1
6.6
10.4
25.5
59.0
c
1,280.2
on: 166,853
Observed
(BE) (
2,271 2,
995
486
63
112
0
18
22
59
11
21
19
23
5
9
2
30
15
19
12
14
55
212
168
1,064 1,
DC)
271
922
429
25
24
55
18
18
58
9
16
18
49
19
/
1
23
15
16
8
17
92
188
7?
161
"atio
fBE)
1.37
3.11
4.60
..
2.53
1.54
1.55
2.34
2.08
2.36
1.32
0.7Q
D.99
1.47
1.15
0.95
1.82
1.35
2.16
3.59
--
0.83
3/e
'DC)
1.37
2.88
4.06
_ _
2.53
1.26
1.52
1.91
1.59
2.23
2.81
2.65
0.77
--
1.37
1.15
0.80
1.22
1.63
3.61
3.19
--
0.91
'SeHkoff, et al. 1979i
^Expected deaths are based upon white m«1e age specific mortality data of
th« U.S. National Center for Health Statistics for 1967-1975 and extrapola
tlon to 1976.
cRates are not available, but th«se have been rare causes of death in the
general population.
BE: Best evidence. Number of deaths categorized after review of 5est
available information (autoosy, surgical, clinical)
DC: Number of deaths as recorded from death certificate information only.
C-68
-------
absent in the general population {asbestosis and mesothelioma). Since meso-
thel ioma is not a cornnon cause of death in other than asbestos-exposed indi-
viduals, its misdiagnosis on the death certificates of general population
has little significance. However, as it is a major cause of death of asbes-
tos-exposed workers, its proper diagnosis is necessary in order to evaluate
the extent of occupational disease. Moreover, were 1t not to be properly
characterized one would conclude that cancers of the liver and pancreas were
elevated from asbestos exposure. Thus, one would have to consider excesses
at these sites (as inlsdiagnosed on death certificates) rather than mesotne-
lioma in evaluating abdominal cancers. Otherwise, the use of best evidence
rather than death certificate information 1s a minor factor 1n the evalua-
tion of gastrointestinal cancer. For example, among cancers of the esopha-
gus, stomach, colon, and rectum 1n 2,271 consecutive deaths in Insulation
workers, 112 were listed at these sites on death certificates. Best evi-
dence indicated that 118 occurred. This difference would have little effect
upon the calculation of gastrointestinal cancer. On the other hand, peri-
toneal mesothel 1oma per se was specified 1n only 24 deaths where best evi-
dence indicated 112 occurred from this disease. The difference was largely
made up from overdlagnosed cancer of the pancreas (26 cases), cancer of the
liver (14 cases), and from 55 mesotheHomas unspecified as to site.
The large number of deaths allows an analysis to be wade of the onset of
effects as related to time from first exposure. Figure 3 depicts the excess
asbestos-related lung cancers and mesothel1oma$ according to time from onset
of exposure. It 1s seen that an Important rise 1n bronchogenlc carcinoma
occurs only after 25 years and mesothel1oma and asbestosis after 30 years.
This long-lapsed period 1s seen In Individuals exposed continuously to rela-
tively high concentrations of asbestos. At lower exposures, longer periods
C-69
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120
100
80
60
20
10
20
TIME ntOM ONSET
OF
30
EZPOSU1Z
40
(TEAM)
FIGURE 3
The Excess, Asbestos-related Mortality Ratts for Lung Cancer and
MtsothtHoM According to T1w from Onset of Asbestos Olstast
Source: S«Hkoff, tt al. 1979a
MtSOthtllOM
m lung cancer
070
-------
exposure onset to tumor development would be expected ana, thus, stud-
ies that do not provide adeauate 'ollow-up can be .TITS leading.
Among other groups of insulation workers, high rates of cancer, particu-
larly bronchogenic carcinoma and pleura! or peritoneal mesothelioma, have
been reported by Selikoff (1976). In this study 632 New York and New Jersey
insulation workers, 20 or more years from onset of exposure were observed
from January 1, 1943 through December 31, 1974. Of these, fewer than 300
individuals were Included In the larger study of 17,800 insulation workers.
With a much longer observation period, even more severe effects were seen.
Similarly, a study by Elmes and Simpson (1971, 1977) in the United Kingdom
portrays a more severe mortality experience, particularly for lung cancer
over a period of time, 1940-1975.
Some data on exposure of U.S. insulation workers exist. These have been
reviewed by vicholson (1976) and are summarized in Table 22. Estimates of
past average exposures were made on the basis of current measurements by
four laboratories of fiber concentrations during work activities thought to
be typical of those of past years and information on product composition and
usage. Time-weighted average concentrations of 10 to 15 f > 5 urn/ml and 15
to 20 f > 5 urn/ml were suggested for commercial construction and marine
worir, respectively. It was noted that, while these average concentrations
were not extraordinary, peak concentrations could often be very high and
exceed 100 f/wl. At Lyon, 1n 1972, Cooper and Mledema (1973) reported,
"peak concentrations may be high for brief periods, while time-weighted
averages are often deceptively low." To the extent possible these high
exposures were taken Into account and the time-weighted average exposure was
largely due to peak exposures. This averaging and the extrapolation to ear-
lier years introduce uncertainties in the estimate. However, the above
C-71
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TABLE 22
Summary of Average Asbestos A1r Concentrations during Insulation Work
Average
Fiber Concentration f/wl
Light and Heavy
Research Group Construction Marine Work
Average concentrations of fibers longer than 5 u« evaluated by
membrane filter techniques and phase-contrast microscopy
Nicholson (1971b) 6.3
Balzer and Cooper (1968) 2.7
Cooper and Balzer (1968) 6.6
Ferris, et al. (1971) 2.9
Harries (1971a,b) 8.9
Average concentrations of all visible fibers counted
with a konlmeter and bright-field microscopy
Hirphy, et al. (1971) 8.0
Fleischer, et al. (194«) 30-40
Estimates of past exposure based on current rne»brane-fliter data
Nicholson (1976) 10-15
C-72
-------
:""e-«e v ted average exoosures are fe't to be accurate witnin a 'actor of
•>c. "-•: 's suggested by the good agreement among the exposure estimates
anc ^e*s.-e-ents of four different laboratories and by the good agreement of
'nsularc"- :cse-resoonse data with that of other groups.
Factory ;.roloytnent: An early study of workers from an asbestos products
factory (Mancjsco and Coulter, 1963) showed a significant excess in total
Tiortality, wit- important contributions to excess death rates from asbesto-
sis, cance" uf *ne lung, bronchus, and trachea, and neoplasms of the diges-
tive orq?ns a"? peritoneum. In this latter group of deaths, an important
'actor wei Zt- '..-;.tal mesothelioma. While in excess, increases in cancer of
the esro^c'j? str-v'ch, colon, and rectum did not have statistical signifi-
cance, "hern - 3 consistent increase in the mortality rate with increas-
ing lengf o* ^-Tloyfnent in the asbestos industry for all causes of death
ano especially *cr malignant neoplasms and asbestosis.
Additional stuc-.es of factory employees (Enterline, et al. 1972; Hender-
sor. and cnteriine, 1979) focused upon a group of retirees from several
slants T* 3 -mjor asoestos products manufacturing company. It shows a simi-
lar oattern of mortality. Table 23 lists standard mortality rates (SMRs) by
cause in two time periods. The usual asbestos cancers and asbestosis are
seen as significant causes of death. Here, too, a correlation was found be-
tween total dust exposure and excess mortality for both malignant and non-
malignant disease. Table 24 lists the data for lung cancer and shows a lin-
ear relationship with exposure.
These authors (Enterline and Henderson, 1973) suggested earlier that
crocidolite may have a higher carcinogenic potential (for lung) than amoslte
or chrysotiie. The later analysis (Henderson and Enterline, 1979) shows
that individuals in the textile departments of the company (chrysotiie only)
C-73
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TABIE 23
Observed Deaths and '.jMRs for Selected Causes of Death by
Period of Follow-
Digestive (150-159)
Respiratory (162-163)
All other cancers
Stroke (330=334)
H«»rt disease (400-441)
Peso1r«tory disease
(470-527)
Pneomocon1o$1s and
pulmonary f1bro$1s
(523-525)
Asbestos is (523.2)
All other causes
Death certificates
net located
Observed
Deaths
781
173
55
63
55
74
321
68
31
19
113
32
SMR
120.4
159.0
137.8
270.4
120.6
96.4
106,5
173.0
— ^
--
92.5
—
1941-1969
Observed
Deaths
616
138
46
49
43
48
269
54
25
16
96
11
SMR
115.8
154.5
136.1
270.7
115.0
76.7
108,4
178.2
..
—
94.6
--
1970-1973
Observed
Deaths
165
35
9
14
12
26
52
14
6
3
17
21
SMR
141.6
179.5
147. 5
269.2
146.3
183.1
97,7
155.6
„
--
82.5
--
'Henderson and Enter11ne, 1979
bOlsease code
-------
TABLE 24
Lung Cancer Mortality Rates According to Oust Exposure*
Cumulative Oust Exposurt
(mppcfb - years)
<125 197.9
125 - 149 180.0
250 - 499 327.6
500 - 749 450.0
750 777.8
*H«nd«rson and Enterline, 1979
bM1H1on particles per cubic foot
C-75
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have a love'' lung cancer $MR than those in the oioe ceoart-ent :"
and crocidolite) for eaual dust exposures. However, no c:nc'js-cns ::^'c ---
drawn from an analysis of the Tiorta'ity --ates of ai' '"d^v^^'s exccsed, ~-
not exposed, to crocidol i te. Since the 'ollow-jo of this icoulation :eca°
only after the cohort member;; reached age 65, survivor ejects rcay oe of
importance. For example, those individuals who smoke cigarettes jnd are
thus at higher risk for lung cancer may be preferentially excluded by virtue
of death before age 65 because of smoking-associated disease such as •nyocar-
dlal infarction. Further, the limited number of mesotheliomas (5 of 781
deaths) found 1n the latest followup of this group could be due to the high
incidence of mesothelloma at age 50 to 65, 30 to 45 years from onset of
first employwwnt (see Figure 3). Mortality data *ere correlated with esti-
mates of previous dust concentrations 1n terms of millions :f ^articles per
cubic meter of air (mppcf). No information was provided :n possible fioer
concentrations.
A study of the largest factory of the company studied by -nterl^ne, et
al. (197?), but not limited to retirees, shows a consideraoly different Tier -
tality pattern (Nicholson, 1976; Nicholson, et a1. 1980bv. A-' 58? -••
nance and production employees on January I, 1959, who --• • • •-•;: ---
at least 20 years earlier were followed through 1976. In this group, <^74
dea^s occurred, whereas 188.19 were expected. Fourteen pleural and 12
p«rlton««l ««sothel1om«s accounted for nearly 10 percent of the deaths, most
occurring b«for« ag« 65. A strong correlation with estimated dust exposure
was st«n 1n dtaths 'row ^stouls, but not with the asbestos-related malig-
nancies. Gastrointestinal canc«r was especially high in the lowest of four
dust categories (11 observed versus 3.15 expected) and only elevated slight-
ly In the higher exposure categories. In the hlgnest dust category, the
C-76
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textile miV, carcsr was not dramatically increased, but 40 percent of the
deaths were from asbestosis. Individuals in this department tended to die
of nonmalignant disease before reaching the age of greatest risk for cancer.
A study by Wei 11, et al. (1979) of two asbestos cement product facili-
ties has also been published. Here, the mortality experience of 5,645 em-
ployees was followed for at least 20 years. It shows excess mortality for
lung cancer in the highest exposed groups but deficits of death from all
causes (as great as 40 percent) in all categories. Of the group 3,354 (68
percent) were employed for less than 2 years. Thus, exposures were limited
for the majority of the cohort members. Further, as most of the followup
involved observations prior to 25 years from first exposure (18,117 person-
years at risk <25 years from initial exposures versus 5,910 person-years >25
years), there was limited risk from asbestos disease in the group. Of most
consequence, however, 25 percent of the cohort was untraced and all untraced
were considered alive. This could explain the large mortality deficits in
all categories other than lung cancer and invalidates the study for any use
in establishing dose-response relationship.
A final significant U.S. factory study Is that of Seldman, et al. (1979)
which extends an earlier study (Sellkoff, et al. 1972) and documents the
experience of workers exposed only to amoslte asbestos in the production of
insulation materials, primarily for use aboard naval vessels. Overall mor-
tality shows patterns similar to other heavily exposed groups, with 594
deaths observed versus 363.62 expected. Lung cancer was more than five
times the number expected, and 16 deaths from mesothelloma occurred, of
particular Importance 1n this study 1s the finding that Individuals employed
for periods less than 6 months had significant excess of lung cancer (Table
25). Gastrointestinal cancer was also elevated for those with exposures of
C-77
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TABLE 25
Expected and Observed Deaths from Lung Cancer and Cancer of
the Esophagus, Stomach, Colon, and Rectum in Worker?
Exposed to AtnosUe Asbestos
(Followed 5 to 35 Years after Employment from 1941 to 1945}*
Length of
Employment
1 mo
1 mo
2 mo
3-5 mo
6-11 mo
1 yr
2* yrs
Total
Lung Cancer
Expected
1.6
2.5
2.4
4.2
3.2
2.6
6.0
22.5
Observed
4
6
3
9
12
15
11
93
GI Cancer
Expected
1.4
2.4
2.6
4.2
3.2
2.5
6.4
22.7
Observed
2
2
3
3
1
5
7
28
'Source: Seldman, et al. 1979
C-78
-------
less than 6 months (15 observed versus 10.6 expected), but the difference
did not have statistical significance. Further, there was not an increasing
risk with time of employment as in the case with lung cancer.
Some data exist that would indicate the air concentrations of asbestos
to which workers in a factory, which operated in Paterson, New Jersey, from
19*1 through 1954, were exposed. Following cessation of operations there,
two similar plants were opened elsewhere, using the same equipment and
manufacturing the same product with the same materials. As in the Paterson
factory, dust control was inadequate in the newer plants. These continued
operation through 1971 in one case and 1975 in the second. During 1967,
1970, and 1971 asbestos fiber concentrations in the plants were measured by
the National Institute for Occupational Safety and Health (NIOSH, 1972), and
the results are presented in Table 26. The overall arithmetic average expo-
sure was 34.9 f/ml with a range from about 20 to 80. Using 40 f/ml, as an
estimate of the fiber count in the Paterson factory, one calculates the
average dose received by those employed for less than 6 months to bt no nore
than 120 f/ml -months, the same dose as would be received by a worker em-
ployed 20 years at an exposure of 0.5 f/ml. Of significance, also, Is that
the mesothe11oma risk is less than that of insulators (3 percent versus 7
percent). Since times from onset of exposure to amosite are comparable for
each group, the presence of amosite in insulation materials cannot explain
the high rate of mesothelioma among insulators.
In Great Britain, a well-studied factory population (Doll, 1955; Knox,
et al. 1968) provides useful information because of the availability of
environmental Information. The mortality experience of this group has bt«n
recently updated fPeto, et al. 1977). Workers exposed prior to 1933 (before
dust concentrations were significantly reduced) had a marked excess of lung
C-79
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'ABLE 26
Asbestos Fiber Concentrations in ""wo Amosite Insulation
Production Facilities3^
Operation
Mixing
Forming
Finishing
Inspection
and Packing
Miscellaneous
Operation
Mixing
Forming
Curing
Finishing
Inspection
and Packing
Miscellaneous
Mean
107.0
98.9
32.2
13.3
Mean
163.0
33.3
2.5
44.6
16.7
ASBESTOS
1967
No. of
Samples
3
12
4
2
ASBESTOS
1967
No. Of
Samples
5
13
1
3
7
INSULATION
Mean
27.7
24.1
16.3
13.0
21.0
INSULATION
Mean
36.2
25.7
31.0
34.8
17.9
13.8
PLANT Y
1970
NO. Of
Samples
2
13
2
8
14
PLANT X
1970
NO. Of
Samples
3
3
1
4
3
2
Mean
46.3
25.2
15.0
11.0
2.7
Mean
74.4
50.6
14.4
39.5
22.8
16.6
1971
NO. Of
Samples
7
32
17
19
5
1971
NO. Of
Samples
11
39
5
26
15
24
«NIO», 1972
samples expressed as f > 5
C-80
-------
cancer (25 observed versus *.63 expected). Other cancers were elevated, but
not so greatly. Of significance, however, individuals employed after 1933,
and even after January, 1951, were found to have an excess risk of lung can-
cer. These data were analyzed by Peto (1978) in relation to measured and
estimated fiber concentrations. Exposures averaged about 10 f/ml after 1933
and were virtually exclusively chrysotile. Using a linear dose-response
relationship for lung cancer and pleural mesothelioma, he estimated that a 2
f/ml exposure for 50 years would cause approximately 10 percent of male
asbestos workers to die from asbestos-related disease. It should be noted
that data available for analysis were very limited and the estimate was
based on extremely small numbers (14 deaths from lung cancer, 4 from meso-
thel ioma, and 17 from nonmalignant respiratory disease). Furthermore, few
individuals in the cohort were more than 35 years from onset of exposure and
at a period of hiohest risk from asbestos disease.
Another factory population has been extensively studied (Newhouse, 1969;
Newhouse, et al. 1972; Newhouse and Berry, 1976, 1979). Exposures were to
chrysotile, crocidollte, and amosite. Table 27 lists the mortality experi-
ence of both men and women according to estimates of fiber exposure (no
details are provided as to the method of estimation) (Newhouse and Berry
1979). Lung cancer, gastrointestinal cancer, and mesothelloma are signifi-
cantly elevated In the long-term (>2 years) or severe exposure groups. It
has been estimated (Newhouse and Berry, 1976) that as much as 11 percent of
this entire group will d1t of pleural or peritoneal mesothelioma. Among fe-
male workers, cancer of the breast and cancer of the ovary were significant-
ly higher (p . 0.05).
Mining and Milling: Thre« studies exist showing mortality patterns in
the mining and milling of pure chrysotlle asbestos. A series of studies
C-81
-------
TABLE 27
Mortality Experience of Male and Fenale Factory Workers*
No. of
Exposed Males
884
554
937
Low to Moderate (5-10 f/al)
Cause of
Death
All causes
Cancer of lung and
pleura (ICO 162
61 cancer
(ICO 150-158)
Other cancers
Chr. resp.
disease
<2 yrs
0 E
118(4) 118.0
17(3) 11.01
10 9.0
6 7.4
19 17.5
>2 yrs
0
89(7)
16(1)
9(4)
8(1)
16
E
95.3
9.0
7.3
5.8
14.7
<2 yrs
0
162<*(16)
31^(6)
20C(6)
16C(3)
20(1)
512
Severe (20* f/ml)
E
122.2
12.8
9.5
7.9
17.6
>2 yrs
0
176
-------
TABLE 21 (continued)
Mortality Experience of Male and Feaale Factory Workers*
No. of
Exposed Females
Cause of
Death
All causes
Cancer of lung and
pleura
(ICO 162-163)
Gl cancer
(ICO 150-158)
Other cancers
Chr. resp.
disease
98
Low to Moderate
(5-10 f/«l)
0 E
34b(l ) 22.0
3D(1) 0.5
3 1.9
4 3.2
3 2.3
3%
Severe
<2 yrs
0 E
88C(13) 65.6
15^(7) 1.9
14^(4) 5.7
16(2) 11.9
6 6.8
199
(20* f/«l)
>2 yrs
0
78<*(7)
2ld(4)
9C(2)
16
-------
(McDonald and Liddell, 1979; *cDonald, et a1. 1971, 1980) of 10,939 na'e
Canadian mine and mill employees show excess mortality, particularly of :re
respiratory system. Table 25 lists the mortality for those individuals ' i
the cohort that achieved 20 or more years from first employment. Standard
mortality ratios were calculated from the expected number of deaths in the
province of Quebec. The risk of death from lung cancer increases linearly
with dust 1nd£jt with no evidence of a threshold [relative risk • 1 * 0.0014
(mppcf-years)]. The mortality for esophogeal and stomach cancers shows a
strong relationship with dust index, but that of colonrectal cancer does
not. Pleural mesothelioma was a cause of 11 deaths to 1975. The use of
Quebec mortality statistics may underestimate the actual risk as the
earliest report by McDonald (McDonald, et al. 1971) stated that lung cancer
mortality 1n the five counties near the asbestos mines was only two-thirds
of the province as a whole, the rates of which would be dominated by the
urban center Montreal. The effect of urban-rural difference on the rates
of cancer at ottner sites is not known. Additionally, it is not stated in
th«> publication how the 10 percent of the cohort that was untraced was
treated. All data on exposure are given in terms of millions of particles
p«r cubic foot (mppcf). While earlier work described the difficulties of
converting particle counts to f/1 (Glbbs and LaChance, 1974), it 1s now sug-
gested that a conversion factor between 1 and 5 f/m per mppcf may be appro-
priate (McDonald, et al. 1980).
A Soviet study of the health effects of chrysotile mining and milling is
that of Kogan, et al. (1972). Overall excess mortality of cancer of the
respiratory or digestive tract wis seen, particularly in the groups aged 50
years or older (and presumably 3d or more years fn* first exposure). Among
these, stoMCh cancer mortality in male miners 1s Increased 2.5 times and
C-84
-------
IMU ?8
Out I fipoiwc tmd fertility In Cfcrysotlle Hitting. I9IO-7S
0*«ths. by CMIIC. In KeUtton to OurUlo* of Service*
CMIt* Of tt«U
All CMttat
PlMMWCWllMlt
NillflHWt Ma»l*MB:
L««f
fSaafcafM Md ttamdl
LarjM
OtlMr
Mtart 4lMMt
•at.tr.tary t4*Mrc«lMl.
OtlMr ratfitr.tary
C*r*r..Mc»l.r
AcclAMt.
All aUar kMM C«MUS
C.WM IWt kMMI
(•ft 981 arc ralla* «f tfaal
•SMrct: NcBMiaM. at •!.
Nr
•
886
1
47
17
22
N
67
170
7
»
w
S7
1M
M
tks •taarwai
1980
y Start
(
SMI
I.W
US
•.•7
l.tt
!.*«•
1.12
1.06
8.62
O.M
•.M
t.U
I.U
—
* U UWM\!!M
(
0
.29
3
29
IS
11
12
S
2SI
7
44
49
M
M
14
acui M
Short
SMt
1.09
5.00
0.83
1.27
0.67
0.92
l!fM
1.02
0.09
1.S2
1.1?
1.32
1.07
—
Mars or aw*
hnlt af ••)•
ICDfUl
Ne4l<
(S - .
0
679
?
SO
18
23
14
1
48
287
71
n
so
37
94
11
•rt*r flrtt <
•arUllty In
of Servtct
M tOM
SM
1.15
1.19
1.37
l!l«
1.04
0.14
I.I)
I.IS
?.6>
0.71
1.13
1.18
1.05
—
Malay
QHokai
0
1.098
36
104
SO
71
4
424
22
59
•2
56
13?
8
•ml. accyrrtnf **
sm
1.07
34.6?
1.61
1.47
0.62
0.90
0.78
1.08
0.97
I.S6
1.12
I.U
0.96
0.8S
—
rtaa. I9SI-7S;
Coltort
U
3.?9I
4?
730
130
b/
U
1,332
57
156
?43
183
450
69
( Igures under
SMM
1.09
33.55
0.78
0.98
1.07
1.09
1.04
1.39
0.99
1.07
1.17
0.98
held
C-85
-------
that of female workers by 3.6 times. The corresponding increases *:•- -?'-a"e
and male mill workers are 4.3 and 19.9 times expected. Addit^cna1'y, --:as-
tinal cancer is elevated among ;ne 50* year group 4.3 times 'or -ta'e mners,
5.9 times for female miners and 14.3 for women mill employees. 'Jnfortunate -
ly, data on the number of deaths are not provided. NO cases of -lesotne'- oma
are reported.
Anthophyllite mining has al;io been found to produce a high MSK of bron-
chogenlc carcinoma (Meunnan, et al. 1974). In a study of miners exoosed to
fibers of cum»1ngton1te-grunerite ore series (in which amosite is for-neal,
G111am, et al. (1976) reported excess malignant respiratory disease '10
observed versus 2.7 expected) at an average air concentration of 0.25 ml.
No cohort mortality studies exist for the mining or milling of crocido-
lite or amosite.
In the above studies of chrysotlle mining and milling, mesotheiicma -as
present to much less a degree than in the following three instances: a fac-
tory using chrysotlle exclusively, (4 percent of 20* year employees) ;'?eto,
1978); the l>--«*t U.S. chrysotlle using facility 10 :ercert! . .:,,_,
et al. 19791 .-r insulation work using chrysotile and amosite (7 percent)
(Sellkoff, et al. 1979a). It appears that as :ne -~::e- are manipulated
through mining, processing,
-------
IA8lf ?9
(Uilrolntett ln«l Cancer In Occuptl loo*I ly C»poit
-------
IMU n (co»tlm*4)
Castro UUtllM I Cutctr U Occur*tlo«4lly €xpot«4 A*fc«iloi Uork«ri
l««rt mt
OkMTVttlMI
IMall (l«79)
"ttttvy
K«tM. «t «i. (i»7?)
fsssU s!!!sri
*•!•••»•
MrUllty
U 74
.{*.,»
Daatks
ficcii
0»»iht
Huobrr of
Per I toneJI
HI HIM MB NIILIW
ISO-ISl
ISO
4)0
1*0
I.WO
none
reported
C-88
-------
Indirect Occupational Asbestos Exposure: In 1968 it was oointed out by
Harries (1968) that shipyard workers other than insulators were at risk from
asbestos disease. Among Devonport Dockyard employees, five cases of meso-
thelioma we>-e found among men who had not been "asbestos workers" but had
followed other trades in the yard. These men presumably had been inadver-
tently exposed to asbestos merely by working in the same shipyard areas
where asbestos had been used. Continuing to follow this group, Harries
later documented 55 cases of mesothelioma in this shipyard alone, only 2 of
which occurred in asbestos workers (Harries, 1976), and 1 of which occurred
in a man who had previously sprayed asbestos. A study of the distribution
of all verified cases of mesothelioma found in Scotland between the years of
1950 and 1967 is also revealing. Of 89 cases available for study, 55 were
in shipyard employees, dockers, or naval personnel. Of the 55, again only 1
was an asbestos insulation worker (McEwen, et al. 1977).
A study by Edge (1976) of men who had worked in a shipyard in Barrow,
England, attempted to establish a risk of low-level asbestos exposure on a
population basis. He selected 235 shipyard workers with pleural plaques but
no parenCnymal fibrOSiS On X-*=ajf, and followed their mortality experience
from 1970 through 1973. Seventy died, 17 of mesothelfoma and 13 fros lung
cancer, 2.6 times greater than expected. However, the relevance of these
data have been called into question by the possibility of bias in the
selection of tht 235 cam (Edge 1979).
The previously mentioned radiological evidence (see1 Indirect Occupa-
tional Asbestos Exposure section) that asbestos concentrations in general
shipyard work (Selikoff, et al. 1979a) or maintenance activities 1« » chemi-
cal factory (L1Hs and Selikoff, 1979) are sufficient to produce f1bro$1$
points to the existence of a widespread carcinogenic problem frow Indirect
asbestos exposures.
C-89
-------
Environmental Asbestos Disease: Wagner, et al. f!960) reviewed *7 cases
of mesothelioma found in the Northwest Caoe 'rovince, South Africa i n :,-e
orevious 5 years. Of this number, roughly naif the cases *ere in peoo'e «nc
had worked with asbestos. Virtually all the rest were in individuals *ro
had, decades before, singly lived or worked in an area of asbestos mining
(one living along a roadway in which asbestos fibers were shipped). This
germinal observation demonstrated that asbestos exposure of limited inten-
sity, often intermittent, could cause mesothelioma. The hazard was further
pointed out by the findings of Newhouse and Thomson (1965), who showed that
mesothelioma could occur among people whose potential asbestos exposure con-
sisted of their having resided near an asbestos factory or in households of
asbestos workers. Twenty of 76 cases from the files of the London Hospital
(1917 to 1964) were the result of such exposure; 31 *er« occupational in
origin, and asbestos exposure w.js not Identified for 25.
Both pleura! and peritoneal mesotheliomas have been found to occur from
environmental asbestos exposure. For example, in the neighborhood and fam-
ily cases documented by Lieben and Pistawka (1967), two of three family con-
tacts and two of eight neighborhood mesotheliomas were peritoneal. In gen-
eral, a greater percentage of environmental mesotheliomas compared to occu-
pational are pleura 1 in origin. This, however, may be the result of a
greater propensity for peritoneal mesotheliomas to be nisdiagnosed. In
occupational circumstances, 40 percent of pleural mesotheliomas were cor-
rectly classified on death certificates versus only 21 percent of peritoneal
nesotheliows (Sellkoff, et al. I979a).
Synergis* and/or Antagonism
Asbestos exposure and cigarette smoking have been found to act syner-
gistically to produce dramatic increases in lung cancer over that from expo-
C-90
-------
-e to either agent alone. In 3 prospective study by Hammond, et al.
'1979^ of 17,500 insulation workers, smoking histories were solicited from
d'1 individuals during 1966 prior to observation. Of 12,051 workers who
oassed the 20-year point since entering the trade before or during the
10-year observation period, January l, 1967 to December 31, 1976, 891 re-
ported they had never smoked, 488 had smoked only a pipe and/or cigars, and
6,841 gave a history of cigarette smoking. No information was available
from the remaining 3,831. Using data of the American Cancer Society (ACS)
on age- and calendar year-specific cancer rates among smokers and nonsmokers
in a prospective study of more than one million people in the United States,
it was possible to make smoking-specific comparisons of the mortality exper-
ience of insulation workers with nonasbestos exposed individuals in the gen-
eral population. Those insulation workers who claimed never to have smoked
cigarettes were found to have an increased risk of death from lung cancer
compared with nonsmokers in the general population, although there were
relatively few deaths, 8 observed versus 1.3 expected. However, among those
with a history of cigarette smoking, the risk was also Increased and Us
effect was large, 268 deaths being recorded versus 4.7 expected. Among non-
cigarette smokers in the general population Table 30 lists the death rates
and mortality ratios of smoking and nonsmoking asbestos workers compared to
the ACS control population. Asbestos exposure appears to multiply the M$k
of death of lung cancer by four to six times, Irrespective of smoking hab-
its. When that risk 1s already high, as in cigarette smokers, the result 1s
catastrophic. An earlier study by Sellkoff, et al. (1968) Indicated that
the risk of death from lung cancer 1n cigarette-smoking asbestos workers was
92 times that among Individuals who were neither exposed to the fiber nor
smoked cigarettes.
C-91
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TABLE 30
Age-Standardized Lung Cancer Death Rates* For Cigarette Smoking and/or
Occupational Exposure to Asbestos Oust Compared with No Smoking and
No Occupational Exposure to Asbestos Oust0
Group
Control
Asbestos workers
Control
Asbestos workers
Exposure
to
Asbestos
NO
*es
NO
Yes
History
Cigarette
Smoking
No
NO
Yes
Yes
Death
Pate
11.3
58.4
122.6
601.6
Mortality
Difference
0.0
+47.1
+111.3
+590.3
Mortality
Ratio
1.00
5.17
10.85
53.24
aRat« p«r 100,000 man-years standardized for age on the distribution of the
man years of all the asbestos workers. Number of lung cancer deaths based
on death certificate Information.
bHawnond, et al. 1979.
cThe central population is a group of 73,763 white, male workers exposed on
th« Job to dust, fumes, vapors, chemicals, or radiation.
C-92
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Cancels of the larynx, pharynx and buccal cavity, and of the esophagus
"'n insulation *orkers zrs also associated with cigarette smoking (Hammond,
et al. 1979). Among 50 deaths due to tumors of these sites, none were among
ncnsmokers and 3 were among individuals who smoked only pipes or cigars.
Mesothelioma of the pleura or peritoneum and cancer of the stomach, colon,
and rectum, however, were unrelated to smoking habits. It 1s worth noting
that in these studies by Selikoff and Hammond over 200 excess deaths
occurred from peritoneal mesothelioma and gastrointestinal cancer (excluding
esophagus) in 2,271 deaths of insulation workers. Were smoking-related lung
cancer not a factor, abdominal cancer deaths would dominate the mortality
experience of this group of asbestos workers.
Other studies have substantiated the synerglstlc effect of cigarette
smoking. Berry, et al. (1972) obtained retrospective smoking histories on a
group of asbestos workers and analyzed their mortality according to smoking
habits over a 10-year period of time. The results indicated that the com-
bined effect of cigarette smoking and asbestos exposure on the development
of lung cancer is multiplicative rather than additive.
Although synergistlc effects have been documented for bronchogenlc car-
cinoma, only cigarette smoking has been Investigated 1n the etiology of
abdominal cancers. The possibility exists, of course, that these tumors too
could have a multiple factor etiology and that other contaminants, Ingested
with asbestos, may potentiate tumor development.
Additionally, some nonmallgnant asbestos effects are related synerglstl-
cally to cigarette smoking. Among a group of factory employees It was found
by Weiss (1971) that evidence of f1bro$1s, as manifest on X-rays, was In-
creased among individuals who smoked cigarettes compared to nonsmokers.
Deaths due to asbestosls appear also to be Increased 1n cigarette smokers
compared to nonsmokers (Hammond, et al. 1979).
c-93
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In animal exoeri-nents, exposure to oe^zola)Dyrono (3°*' anri asbestos •";<•
act synergistical' y • 3ylev and Shabad '1973) reoorted t^at 'ntrjt'-ic"^ •
injections o^ 5 ^g of chrysot'le onto *nici *as absorbed D.1-- -3 :•" :-
(from a benzene suspension) and 2 mg of chrysotile coadmin istered *~tn ; ~>q
3P oroduced malignant tumors -n 29 percent and 54 oercent of -ats, resoec-
tively. Administration of 6 TK; of chrysolite or 5 -nq 3P yielded no tumors.
MHIer, et aT. (1965) found inHratracheal injection of chrysolite with 3P to
increase tumor yield over that of 8P alone while amosite aooeared to nave
1Ittle such effect.
No data exist on antagonistic or prophylatic compounds in Delation to
animal or human disease. In. vitro experiments by Schnitzer, et al. (1971)
have shown that hemolysis of red cells can be inhibited by coating the
fibers with ionic polymers such as carboxymethylcellulose.
Fiber Size Considerations
Experimental systems, particularly those used by Stanton and Wrench
(1972) and Pott, et al. (1976), indicate a significantly reduced carc^o-
genicity of fibers as the length is reduced or the diameter increased. On
the other hand human data sugg««t an important role for small fibers. From
analyses of t1ssu« samples from 29 mesothelioma cases, Sebastien, et al.
(1979) found that larger fibers, often amphiboles, tend to be found in the
lung parenchyma. In contrast, 1n the pleura, the fibers were finer and
shorter and generally chrysotHe. The mean length in pleura was 2.3 um and
that of th« lung 4.9 um. In 20 pleura! samples of 29 autopsy cases in which
asbe«to* fibers were found, chrysotlle was Identified as the only fiber in 3
and only a trace (<1 percent) of amphlboles was found 1n 2 others. In con-
trast, significant percentages of amphlbole fibers (>18 percent) were found
in 26 of 29 lung parenchyma samples from the same cases.
C-94
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In an examination of the mortality of workers in different types of
asbestos industries, significant differences occur that may be related to
fiber size. In amosite and chrysotile mining, few mesotheliomas are seen,
whereas, in manufacturing and end product use, large percentages of deaths
occur from this tumor. For example, chrysotile mining and milling, while
related to a significantly increased risk of death from lung cancer and
asbestosis (McDonald and Liddell, 1979; Nicholson, et al. 1979), has not
been associated with an extraordinary mesothelioma risk. Similarly, amosite
mining and milling does not appear to significantly increase the risk of
mesothelioma, while crocidolite mining and milling does (Webster, 1970). On
the other hand, the manufacture of amosite products is associated with a
significant risk of death from mesothelioma, 3.5 percent of the deaths of
individuals 20 or more years from first employment being from this cause
(Seidman, et al. 1979). Further, insulators who were exposed to chrysotile
and amosite, but never to crocidolite (Selikoff, et al. 1970) have 9 percent
of their deaths, 20-plus years from onset of exposure, from mesothelioma
(Selikoff, et al. 1979a). As neither amosite nor crocidolite can account
for this extraordinary risk, chrysotile must contribute significantly. This
is also borne out by observations of the mortality of workers in a
chrysotile using factory. 4.3 percent of long-term deaths were from
mesothelioma in a facility using 5,000-6,000 tons of chrysotile,
approximately 50 tons of amosite, and less than 4 tons of crocidolite
annually (except for 3 years when 375 tons of amosite were used annually)
(Robinson, et al. 1979).
Much of these differences in risk may be accounted for by the differ-
ences in fiber size distributions in the three work environments rather than
by fiber type. The greatest percentage of longer and thicker fibers would
occur in the work environment of miners and millers. As the asbestos is
C-95
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used in manufacturing processes,, it is broken apart as it is incorporated •-
finished products. During application or removal of insulation products, ':
is further manipulated and the fiber reduced in length and diameter. -s
these smaller fibers can readily be carried to the periphery of the 1ung,
penetrate the visceral pleura and lodge in the visceral or parietal pleura,
they may be of greater importance in the etiology of mesothelioma, even
though longer fibers, once the"e, are more carcinogenic. In the case of
croddollte, fine fiber aerosols are produced even 1n mining and, thus, all
uses of that fiber are associated with mesothelloM.
-------
Existing guidelines and Standards
The cui"-e"t Occupational Safety and Healtn Administration (OSHA) stan-
dard *cr an 3-hoi-r time-weighted average (~WA) occupational exposure to
asbestos is 2 fibers longer than 5 microns in length per mill-Miter of air
(2 f/ml or 2,000,000 f/m ). Peak exposures of up to 10 f/ml are permitted
for no more than 10 minutes (29 CFR 1910.001). This standard has been in
effect since Jjly 1, 1976, when it replaced an earlier one of 5 f/ml (TWA).
In Great Britain, too, a value of 2 f/ml is the accepted level, below which
no controls are recuired (BOHS, 1968); the British standard, in fact, served
as a guide *or the OSHA standard (NIOSH, 1972).
The British standard was developed specifically to prevent asbestosis
among work^g populations; data were felt to be lacking that would allow a
determination cf a standard for cancer (BOHS, 1968). Unfortunately, among
occupational groups, cancer is the primary cause of excess death among work-
ers (see Carcinogenicity section). Three-fourths or more of asbestos-
related deaths a.-e from malignancy. This fact has led OSHA to propose a
lower TWA standa.-d of 0.5 f/ml (500,000 f/m3) (29 CFR 1910.001). The
National Institute for Occupational Safety and Health (NIOSH), 1n thtir Cri-
teria document for the hearings on a new standard, have proposed a vilu« of
0.1 f/ml (NIOSH, 1976). In the discussion of the NIOSH proposal, it »«s
stated that the value was selected on the basis of the sensitivity of ana-
lytical technioues using optical microscopy and that 0.1 f/ml may not ntcts-
sarily protect against cancer. Recognition that no information exists tMt
would define a threshold for asbestos carcinogenesis was also contained in
the preamble to the OSHA proposal. The existing standard in Great Britain
has also been called into Question by Peto (1978), who estimates that aib«s-
C-97
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tos disease may cause the death of 10 percent of workers excosed a: 2 *'.-ni
for a working lifetime. A fiber concentration limit of 1.0 */ml nas recent-
ly been published in Great Britain (Advisory Committee on Ascestcs, 19791.
The existing Federal standard for asbestos emissions into the environ-
ment prohibits "visible emissions" (40 FR 48291). No numerical value was
specified because of difficulty in monitoring ambient air asbestos concen-
trations in the ambient air or 1n stack emissions. (Time-consuming and
expensive electron microscopy 1s often required.) Some local government
agencies, however, may have numerical standards (New vortc, 27 ng/m^ for
example).
Mo standards for asbestos 1n foods or beverages exist even tnougn the
use of filtration of such produces through asbestos filters has been a com-
mon practice 1n past years. Asbestos filtration, however, is prohibited or
limited for human drugs (41 FR 16933).
Current Levels of Exposure
As detailed in the Exposure section, asbestos is a ubiquitous contami-
nant of our air and water. Air concentrations over 24 hours in -netropolitan
areas usually are less than 5 ig/m but can range up to 20 ng/nr. Val-
ues up to 50 ng/«r are found during daytime hours 1n locations where con-
struction activities and traffic can be contributing sources. A significant
fraction of the fibers Inhaled ran be brought up from the respiratory tract
and swallowed. This leads to an 1ngest1on exposure from air sources of up
to 0.1 tig/day, although most of the population exposure 1s fro* 0.01 to 0.05
ug/dty.
Water concentrations of asbestos are usually less than 10 fibers of
all sizes per liter although significantly higher values (10s f/1) have
been found 1n circumstances where water systems have been in contact with
098
-------
asbestiform minerals or where contamination of the water supply exists.
r'ber mass concentrations corresponding to fiber concentrations are usually
less than o.Ol ug/1 but could exceed 1 ug/1. Thus, direct water ingestion
usually leads to exposures of less than 0.02 ug/day.
Clearly, point source pollution can cause both air and water concentra-
tions to exceed the above values. Such Instances are discussed in the
Exposure section.
SoedjJ Groups at Risk
Special groups at risk may Include neonates and children; however, no
data exist on the relative sensitivity to asbestos of Infants and children
undergoing rapid growth. Concern exists because fibers deposited in the
tissues of the young may have an extremely long residence time during which
malignant changes could occur. In addition, risk could be influenced by
differential absorption rates which have not been fully studied at this time.
Individuals on kidney dialysis machines may also be at greater risk as
fluids, potentially contaminated with asbestos fibers can enter the blood
stream directly or, in selected Instances, the peritoneal cavity (peritoneal
dialysis).
Although no synergistlc effects have been identified 1n the etiology of
asbestos-related gastrointestinal cancer, they cannot be ruled out. Thus,
people exposed to other carcinogens, Initiators, or promoters could be at
increased risk.
An increased risk 1s also associated with increased exposure to asbestos
in water 1n municipalities such as San Francisco or Seattle where asbestos
occurs naturally in water, in cities where there 1s an Interaction between
aggressive water and asbestos-cement pipe, or in cities whose water may be
contaminated as a result of asbestos operations. Also, the use of asbestos
C-99
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oroducts for the collection of *ater, such as in cisterns • r,
Virgin Islands or in ^cof '•UP -of*s in tropical areas, increases exposure.
Basis and relation o* Cr
•^s previously discussed, no definitive studies, eitner animal or
exist that would establish risk levels from ingestion o* asaestos fibers.
Those studies published provide both positive and negative data, but all
have methodological limitations. In the case of the "luman studies, these
include observations on only recently exposed individuals, small study
groups, low exposures, population mobility, uncertainty over the effect of
confounding variables, and inappropriate control populations. Animal stud-
ies have usually been conducted with very small numbers of animals, have
lacked proper pathology, used limited doses of asbestos, and poorly defined
the materials ingested.
On the other hand, human studies of workers exposed to airborne asbestos
uneauivocal ly demonstrate an excess risk of gastrointestinal cancer in vir-
tually all croups surveyed. A route of exposure to the gastrointestinal
tract from such exposures is also clear from the fibers cleared from the
lunq and bronchial tract and subsequently swallowed. Jsing information on
airborne exposures to workers, it 1s possible to estimate an approximate
exposure level to the gastrointestinal tract from estimates of airborne
asbestos concentrations. This, however, Involves the use of data having, in
sown casts, significant uncertainties and, thus, the criterion level on
asbestos In water that will produce a specified risk cannot at established
with high precision.
Experimental uncertainties e;t1st as to the air concentrations in fibers
longer than 5 um/ml to which workers were exposed in past years, the conver-
sion of these >5 ud fiber concentrations to concentrations of fibers of all
0100
-------
sizes in air, arc on the size distributions of water and airborne asbestos
sols. Information is also lacking on the Importance of fiber size in the
production of human cancer. On the one hand, longer fibers are more car-
cinogenic in experimental systems although Quantitative data are limited.
On the other hand, smaller fibers appear to more readily cross body barriers
to reach sites of importance for human carcinogenesis. The relative impor-
tance of these two factors cannot be accurately estimated.
A substantial body of data exists which shows Increased incidence of
cancer of the esophagus, stomach, colon, and rectum or peritoneal mesothe-
lioma in humans exposed to asbestos occupatlonally. For several of these
groups, data exist on the approximate airborne fiber concentrations to which
individuals were exposed (see Effects section). These human data will serve
as the primary basis for a standard of asbestos in water. Experimental data
(see Pharmacoklnetics section) indicate that a major fraction of the asbes-
tos deposited in the lungs is subsequently swallowed. In this section, the
dose to the gastrointestinal tract of four occupational groups will be cal-
culated from knowledge of the air concentrations to which the workers were
exposed and the assumption that all the asbestos inhaled subsequently passed
through the gastrointestinal tract and provided the exposure that led to the
observed increase in abdominal cancer. The assumption that all inhaled as-
bestos is ingested is an overestimate but not a significant one. No account
has been taken of the material that a worker nay swallow directly, and this
quantity could be important. The extent to which these factors are offset-
ting cannot bt estimated. Uncertainties exist in the extrapolation of ani -
mal data on clearance to man and in the effect of the aerosol size distribu-
tion on the fraction swallowed. These uncertainties, however, are felt to
be unimportant in comparison to our inability to estimate the quantity of
C-101
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asbestos that might be directly swallowed. If the amount of asbestos
directly ingested is less thar that which remains in the lungs or is c'earoc
from the body by other than ingestion, the estimated criteria level will :e
less stringent. If the directly ingested asbestos is of more importance,
the criteria level will be more stringent.
Table 31 lists the percentage of death from excess gastrointestinal can-
cer and peritoneal mesothelloma in four groups of asbestos workers. Calcu-
lations of these percentages were made using expected numbers of death,
rather than the observed, because the latter 1s often significantly inflated
by Including other asbestos -related deaths (asb«sto$1s, lung cancer, and
pleural mesothel 1oma) .
Table 32 lists the fiber concentration estimates (s«e Carcinogenicity
section) and an exposure index for each cohort (years of exposure x fiber
concentration). This index will be used to calculate the number and mass of
asbestos fibers ingested during a working lifetime. As the observed mortal-
ity 1s, to a large extent, after 20 years from first exposure, the inter-
mixing of time and exposure does not present significant problems.
The average length of exposure for the insulation workers in the first
group was calculated from data on employment time at entry into the cohort
in 1967. A working lifetime of 40 years was use
-------
TABLE 31
Percentage of Excess Gastrointestinal Cancers and Peritonea) Mesotheliomas
in Four Groups of Asbestos Workers
Exposed Group
Insulation workers*
(chrysotile and Mosfte)
Insulation work erst)
{chrysotile and aaosite)
Factory ewploywentc
(awostte)
Factory eaploynentd
(chrysotile, croc idol ite
and aiMosite)
Factory Retirees*
(chrysotile, croc Idol Ite
and amosite)
Miners and ailler**
(chrysotile)
Nuitoer of Excess
(from Table
Gl Cancer
39.9
(ICO 150-154)
29.4
(ICO 150-154)
10.5
(ICO 150-154)
15.8
(1CD 150-158 ea neso)
14.9
(1CD 150-159)
27.8
(ICO 150-151)
Deaths
29)
Peritoneal
Hesothelioma
112
22
8
35
unknown
but < 5
0
Excess deaths a* a
Expected Percentage of Expecte
Number of Deaths in Cohort
Deaths in
Cohort Gl Per. mesa. To
1,658.9 2.4 6.7 9
305.20 9.6 7.2 16
368.62 2.9 2.2 S
556.0 2.8 6.3 9
648.7 2.3 ? ?
3,019.3 0.9 0 0
a$elikoff, et •!. 1979*
bSelikoff, 1976
, et al. 1979
dNewtiouse and Berry, 1979
^Henderson and Enter line, 1979
fMcDonald, et al. 1980
9.1
C-103
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"ABLE 32
Exposure Indices for Asbestos Worker Groups
Exposed Group
Air Fiber
Concentration
(f/Bll)
Person-weighted Exposure Index
Average Exposure (years x f/mi)
Time (yrs.)
U.S. Insulators
Selikoff, et al. (1979a)
NY/NJ Insulators
Selikoff (1976)
Amos He factory workers
Seidman, et al . (1979)
15 (Tible 22)
15 (Table 22)
40 (Tible 26)
34
40
1.9
510
600
76
British factory workers
Newhouse and
8«rry (1979) 10-30
Factory retirees See note a
Henderson and
Enter!1ne (1979)
Chrysotile miners See note a
and millers
See Table 33
ISO
740
585
*The cumulative exposure Index in f/ml x years was calculated by multiply-
ing a person-weighted exposure index in mppcf x years by 3.
C-104
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TABLE 33
Exposure Estimates for Workers 1n a British Factory*
Exposure Group No. at Risk Exposure (f/»1) Time of Exoosure
Severe <2 years 711 30 20
>2 years 1,333 30 2
Low to Moderate <2 years 503 10 20
>2 years 933 10 2
*Source: Newtiouse and B«rry, 1979
C-105
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The fiber exposures for the studies of McOonald, et al. ;198C) ana -er -
derson and Enterline (1979) were calculated from the estimate of ^
et al. (1980) that 1 Tipocf is equivalent to 3 f/ml. While no data
this suggestion, it appears reasonable and was also used for the factory
exposure circumstances.
The majority of samples analyzed for the EPA to date were characterized
by a concentration of all electron microscopic visible fibers per liter of
water (se« Exposure section). f:urth«r, techniques for the determination of
fiber concentrations (as opposed to mass concentrations') have been pub-
lished as Interim EPA procedures (Anderson and Long, 1980). Thus, a criter-
ion for the concentration of fibers of all sizes in water corresponding to a
1C"5 risk will be calculated directly from the concentrations of fibers
greater than 5 urn measured 1n the occupational circumstances that produced
disease. Unfortunately, the dal:a currently available relating air concen-
trations of fibers longer than 5 urn, counted by optical microscopy, to those
determined by electron microscopy, are extremely limited. These include
those by WalUngford (1978), 1:15; MUlette (personal communication), 1:400;
and Winer and kissett (1979), 1:1,000 and are only for chrysotile asbestos.
Using the geometric mean of 200 for this factor from all available data, a
total fiber concentration corresponding to a 10 risk can be calculated
from the data of Tables 31 and 32. The scant data on the relation between
electron and optical microscopic counts 1s uncertain. The variability
between these three measurements 1s likely the result of losses during the
preparation of specimens for electron microscopy. Thus, the value by wal-
Ungford appears unduly low and Is 1n disagreement with electron microscopic
size distributions showing 1 to 3 percent of fibers 1n chrysotile asbestos
aerosols to be longer than 5 um. With these considerations, the uncertainty
1n the value 200 may be estimated to be a factor of 3.
C-106
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In making the calculation, one tacitly assumes the same fiber size dis-
tribution in water as in occupational air samples. Some data show that
water fiber size distributions vary greatly (Gillette, et al. 1979a,D), and
occupational air distributions have been shown to be so variable that the
fraction of fibers longer than 5 um can range over a factor of 10 depending
on sampling circumstances (Nicholson, et al. 1972). Although sizing of
airborne and waterborne fibers has not been done using the same methods,
qualitatively, water appears to nave fiber distributions with more smaller
fibers than 1n occupational air samples. Experimental studies, previously
discussed, have shown that once in place, longer fibers are more
carcinogenic than shorter ones. However, shorter fibers 'appear to more
easily cross organ barriers and migrate throughout the body, and may, thus,
be of greater importance for some asbestos malignancies, particularly meso-
thelioma (Sebastien, et al. 1979). The extent to which the assumption of
the same fiber size distribution in water as in air will likely yield a con-
servative criteria (from the point of view of health) cannot be estimated.
A detailed calculation of the 70-year lifetime risk from the Injection
of 10 fibers of asbestos per day 1$ given 1n Appendix I. Data of th« oc-
cuoatlonal risk of both gastrointestinal cancer and peritoneal mesothelIonia
were used (Table 31). Account was taken of the fact that occupational expo-
sures took place over a 5-day work week and that the ingestion exposure may
encompass a Hfespan of 70 years. It was assumed that a worker brtath«s at
the rate of 1 m /hr during work exposure for the purpose of calculating
total asbestos Intake per day. Using a linear dose-response relationship
and a specified risk of 10 , the calculated 70-year dally Intake result-
Ing from these calculations are given 1n Table 34. It is not correct to
simply average intake levels (rather than risks) as a single study showing
C-107
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TABLE 34
The Calculated Risk of Death over a 70-Year Lifetime from
Gastrointestinal Cancer and Peritoneal Mesothelioma from
Ingestlon of 1C)6 f/day of Asbestos
Exposure Group Estimated Risk
106 f/day
Sellkoff, et al. (1979a) l.L x 10-5
Sellkoff (1976) 1.7 x 10-5
Newnouse and Berry (1979) 3.1 x 10-5
Henderson and Enter!1n«
(1979) 1.9 x 10-6
McDonald, et al. (19801 9.5 x 10-7
Average 1.24 x 10-5
This average corresponds to a dally Intake of
300,000 fibers for a 10-5 lifetime risk.
0108
-------
w risks could yield an inta-om Seidman, et al. (1979) were not used because it was
exclusively fr^r anosite exposures. While exposure over the last 10 or 20
years of life may not have been of great importance in the generation of
asbestos related cancers, those ingested during the first 10 years may be
much more imoortant than fibers Ingested later, and no consideration was
taken of this possibility in establishing criteria levels. Further, the
occupational exposures from which the criteria were developed utilized
exposures through the lifetime of the populations. Assuming that two liters
of water are ingested per day, this would correspond to a concentration of
^00,000 fibers of all sizes/liter of water.
It is remarkaDle that three long exposure groups had similar exposure
indices. This would suggest that these estimates are indeed reasonable.
The exposure index for the study of Newhouse and Berry may be low, and this
would produce a higher risk estimate. On the other hand, as previously dis-
cussed, the mortality data of Henderson and Enterline (1979) and McDonald,
et al. (1980) may jnderestlmate effects producing lower risk estimates.
A criterion for a mass concentration of asbestos can also be calculated
usinq the conversion value of 30 ug/m3/f/ml derived from the data of Table
2 for predominantly chrysotlle exposures. A value of 150 ug/nr/f/ml for
amoslte appears more appropriate, based on the finding of Davis, et at.
(1978) that amoslte has approximately a three time greater conversion factor
than chrysotlle. A detailed calculation Is given in Appendix II and the
results summarized in Table 35. Assuming that 2 liters of water are ingest-
ed per day, a risk of 10 would be produced from ingesting water contain-
ing 0.05 ug/liter. As mentioned in the "Exposure" section, the variability
0109
-------
TABLE 35
The Calculated Risk of Death over a 70-Year Lifetime
Gastrointestinal Cancsr and Peritoneal Mesothglioma
Ingestlon of 1 ug/day of Asbestos
Exposure Group
Selikoff, et al. (1979a)
Selikoff (1976)
Seldman, et al. (1979)
Newhouse and Berry (1979)
Henderson and Enter line ('..979)
McDonald, et al. (1980)
Average*
Estimated Hisfc
ug asbestos
7.3 x
I. 1 X
5.5 x
2.1 x
1.3 x
5.4 x
3.6 x
10-5
10-4
10-5
io-4
10-5
10-*
10-5
*Th1$ corresponds to a dally Intake of 0.12 ug for a
10-5 lifetime risk.
C-110
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in the data used to convert ootica1 fi3er counts to -nass (factor D in Appen-
dix I", leads to a large uncertainty 'a 'actor of 5) in the above estimate.
Considering chrysotile and depending on the source of the asbestos in
water (see Table 5), 0.05 ug/liter corresponds to from 10 to 25 x 10^
fibers of all lengths per day. Such estimates are considerably higher than
those derived previously and are most likely a reflection of the differences
in the sizes of the fibers found in water, as compared to those found in
air. Because of these uncertainties, high priority should be given to ob-
taining accurate size and mass distribution of typical fibers found 1n dif-
ferent circumstances (air and water) which would allow appropriate conver-
sions to be made between fiber concentrations 1n air and water.
Although positive animal experiments had various experimental limita-
tions, risk estimates were calculated from their data using a modified one
hit model as previously discussed in the Methodology document. The data are
presented in Table 36. Considering the large number of experimental uncer-
tainties, these values provide reasonable support for the concentration
derived from human exposure data.
This document was concerned with the estimation of that concentration of
asbestos in water which will produce a lifetime risk of 1 1n 100,000 1n a
population exposed continuously. The risk estimate was made using a linear
extrapolation from existing human data and would appear to constitute a con-
servative extrapolation. However, 1n the case of asbestos, the risk factor
of 1/100,000 1s not conservative. If we were concerned with intermittent or
localized contamination incidents of some carcinogen that once identified,
could be abated, such a value would have utility. With asbestos, however,
we are concerned with a ubiquitous contaminant in the environment to which
large populations are continuously exposed for decades. Further, the esti-
mated value has a high degree of uncertainty associated with 1t, based upon
the data from which it was derived.
c-111
-------
TABLE 36
Risk Estimates from Animal Experiments*
Estimated 10-5
Effect Dosage (ugAl)
4/42 Kidney carcinomas 3.2
0/49 control
12/42 Malignancies 1.1
2/49 control
*Source: Slbel, et al. 1976
C-U2
-------
Undep the ron;er-t Decree in NRDC v. Train, criteria are to state "recom-
mended maximum permissible concentrations (including where appreciate,
zero) consistent with the protection of aquatic organisms, human health, and
recreational activities." Asbestos is suspected of being a human carcino-
gen. Because there is no recognized safe concentration for a human carcino-
gen, the recommended concentration of asbestos 1n water for maximum protec-
tion of human health is zero.
Because attaining a zero concentration level may be infeasible in some
cases and in order to assist the Agency and states in the possible future
development of water Quality regulations, the concentrations of asbestos
corresponding to several incremental lifetime cancer risk levels have been
estimated. A cancer risk level provides an estimate of the additional inci-
dence of cancer that may be expected in an exposed population. A risk of
10 for example, indicates a probability of 1 additional case of cancer
for every 100,000 people exposed, a risk of 10 indicates 1 additional
case of cancer for every million people exposed, and so forth.
In the Federal Register notice of availability of draft ambient water
quality criteria, EPA stated that it is considering setting criteria at an
interim target risk level of 10"5, 10"6, or 10~7 as shown in the fol-
lowing table.
Exposure Assumption Risk Levels and Corresponding Criteria (1)
10-7 10-6 io-5
2 liters of drinking water
Consumption of fish and
shellfish only
*f - fibers
3,000 f/11
30,000 f/1
No Criterion
300,000 f/1
0113
-------
(1) Calculated by applying a relative HSK epidemiologicai -noce1 :;s
described in the Methodology Document to the human eoidemic'cc'C:i'
data presented in appendix [II. Since the extr-apo lafcn "Cce" 's
linear at low doses, the additional lifetime "is< is directly oro-
oortional to the water concentration. Therefore, water concentra-
tions corresponding to other risk levels can be derived by mult1 -
plying or dividing one of the risk levels and corresponding water
concentrations shown in the table by factors such as 10, 100,
1,000, and so forth.
Concentration levels were derived assuming a lifetime exposure to var- -
ous amounts of asbestos occurring from the consumption of drinking wat«r
only.
Although total exposure information for asbestos is discussed and an
estimate of the contributions from other sources of exposure can be mad«,
this data will not be factored into ambient water quality criteria formula-
tion until additional analysis can be made. The criteria presented, there-
fore, assume an incremental risk from ambient water exposure only.
C-114
-------
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Appendix I
Sample calculation of Ms* per 10 fibers/day Ingested using a linear
dose-response relationship.
16.8 x 10"2 x
600(f/ml) yrs 8 x 106 ml/day
x _L_ x 70 years x I x 10°
200 5
D E F 6
A • Percentage of excess GI cancer and peritoneal mesothell -
oma 1n study group.
B - Exposure Index.
C • Exposure took place for 8 hours and the worker was as-
sumed to breathe 1 nH/hr (io& ml/hr).
D » Conversion from optical counts (/1b«r$ >5 \M) to electron
microscopic counts (all fibers).
E • 70-ytar exposure to water 1s assumed.
F » Exposure was concentrated 1n 5 days rather than 7 days/
G • Calculation 1s for a 70-year risk per 106 fibers/day.
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Sample calculation of risx oer ag of asbestos -ngestec js-ng 3
ear dose-resoonse rela
16.3 x 10-2 x 1 x __ 1 _ x .033 f/*n1 x 70 years x 1
600(f/m1) yrs 8 mT/day Ug/m3 5
A 8 C D E c
A • Percentage of excess GI cancer and oeritoneal
oma in study group.
B - Exoosur* Index.
C - Exposure took place for 3 hours and the worker was as-
sumed to breathe 1 m3/hr.
0 • Conversion of 30 ug/m^ per 1 f/ml of chrysotile (Table
2).
E • 70-year exposure to water is assumed.
F • Exposure was concentrated in 5 days rather than 7 jays/
week.
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Appendix III
Summary and Conclusions Regarding the
Carcinogenicity of Asbestos*
Asbestos is a collective mineralogical term referring to naturally oc-
curring minerals which have crystallzed in the form of masses of long fibers
which can be easily separated. This term also commonly refers to certain
mineral occurrences in which fibrous silicate mineral can be extracted and
used commercially for Insulation, textiles, brake linings, asbestos cement,
construction products, etc. Chrysotlle, the fibrous form of serpentine,
provides over 95 percent of the approximately 900,000 tons of asbestos con-
sumed each year in the United States. The remaining asbestos used consists
of the fibrous amphibole minerals crocidollte, amosite (fibrous grunerite),
and anthophyllite. Fine dusts produced from the mining, milling, manufac-
tuHng, and use of these asbestos minerals contain discreet microscopic,
elongated mineral particles of "fibers" which when Inhaled by man art known
to cause bronchogenic carcinoma and pleural and peritoneal rnesothellOM.
Asbestos particles and other Inorganic fibers introduced Into the pleu-
ra, peritoneum, and trachea of rodents have Induced malignant tumor* 1n
numerous studies reported 1n the literature, limited and contradictory data
exist for the carc1nogtn1c1ty of asbestos administered to animals by Inges-
tlon. One study In wMch asbestos filter material was fed to rats (filbel,
et al. 1976) reports 12 malignant tumors 1n 42 exposed animals versus only 2
liver-cell carcinomas In 49 control animals. Electron microscope analysis
*Th1s summary has been prepared and approved by the Carcinogens Assessment
Group of EPA on June 23, 1979.
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of ani-na1 tissues *or assestcs ideates t-at ""cested *';:e'-s :ai jcc.-u'ate
at T>any sites *o1low'rig nefiatocenQDs cr '/rrat'c trJr'53ort r* ' "cest^c
*
-------
intestinal, and other extrapulmonary cancer as a result of asbestos exposure
suggests that asbestos is likely to be a human carcinogen when ingested.
The water quality criterion for asbestos particles is derived from the
substantial data which exist for the increased incidence of peritoneal meso-
thelioma and gastrointestinal tract cancer in humans exposed occupationally
to asbestos. This derivation assumes that much or all of this increased
disease Incidence 1s caused by fibers Ingested following clearance from the
respiratory tract. Several studies, Including one of 17,800 Insulation
workers, allow the association of approximate airborne fiber concentrations
to which Individuals were exposed with observed excess peritoneal and
gastrointestinal cancer. All of the inhaled asbestos 1s assumed to be even-
tually cleared from the respiratory tract and ingested.
The water concentration, calculated to keep the 1nd1v1dua"! lifetime can-
cer risk below 10 , is 300,000 fibers of all sizes/liter. The corre-
sponding mass concentration for chrysotHe asbestos is approximately 0.05
ug/Hter.
Derivation of the Water Quality Criterion for Asbestos
The criterion for asbestos particles 1n water 1s derived from the sub-
stantial data which exist for the Increased Incidence of peritoneal mesothe-
lioma and gastrointestinal tract cancer in humans exposed occupationally to
asbestos. This derivation assumes that much or all of this Increased dis-
ease Incidence 1s caused by fibers ingested following clearance from the
respiratory tract. Several studies, including one of 17,800 insulation
workers, allow the association of approximate airborne fiber concentrations
to which individuals were exposed with observed excess, peritoneal and
gastrointestinal cancer. All of the inhaled asbestos is assumed to be even
tually cleared from the respiratory tract and Ingested.
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Excess deaths due to peritoneal mesothelioma and gastrointestinal carce--
(I CD 150-158) eaual aocroxinately 12 oercent of the expected njmoer o*
Deaths for asbestos *orkers ^n three different cohorts studied. An average
axoosure index of 430 years x *ibers >5 um/ml is calculated *or t^ese Cork-
ers by multiplying average air fioer concentration estimates by average
years of exposure time.
Since water measurement for asbestos reauires electron microscope analy-
sis for fibers (asbestos particles with length to width ratios _>3.0) of all
sizes, the occupational exposjre index must be converted from fibers >5 urn
(ootlcal m1croscoo«) to fiber«; of all sizes (electron microscope). A ratio
of 200 electron microscope identifiable fibers to one optical microscope
identifiable fiber is used for chrysotile asbestos in workplace air samples.
A much smaller ratio is expected for amphibole fibers.
Assuming a linear dose response, occupational exposure of 5 days/we<»k
and 8m ai1" inhaled/workday, and 70 years for fngestion of drinking water,
the criteriorr is calculated as follows:
(430 f>5 urn/ml -years) (5/7) (200 f/f>5 ufli) (1/70 years)
A B C 0
(106ml/m3) (8m3/day) (10"5/1.2 x 104)
E F G
600,000 fibers of all sizes/day
A • Exposure 1nd«x In years x fibers >5 urn/ml from Selikoff, et al. (1976,
1979a) and Newhouse and Berry (1979)
B • Occupational exposure for 5 days versus 7 days for water exposure.
C - Conversion from optical counts (F >5um) to TEM counts (all fibers) in
fibers/fibers Sum
0 • 70-year exposure 1s assumed for drinking water.
E • Conversion from ml to m3.
-------
P - Occupational exposure for 8 hours while breathing Im3/i hour.
G m A risk of 10 is calculated from data on an average observed risk of
1.2 x 10~* from Selikoff, et al. (1976, 1979a) and Newhouse and Berry
(1979).
Based on these parameters and an average ingestion exposure of 2 liters
of water per day, the water concentration calculated to keep the individual
lifetime cancer risk below 10"5 is 300,000 fibers of all sizes/1. The
corresponding mass concentration for chrysotlle asbestos based on occupa
tlonal data 1s approximately 0.05 ug/1.
•t.i. OOTOMR mmx> omen i**o-o-7*w>!l/>W
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