PRELIMINARY
AIR POLLUTION SURVEY
OF
ASBESTOS
A LITERATURE REVIEW
U. S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE
Public Health Service
Consumer Protection and Environmental Health Service
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PREFACE
This document represents a preliminary literature review which is being used as a basis for
further evaluation, both internally by the National Air Pollution Control Administration
(NAPCA) and by contractors. This document further delineates present knowledge of the
subject pollutant, excluding any specific conclusions based on this knowledge.
This series of reports was made available through a NAPCA contractual agreement with
Litton Industries. Preliminary surveys include all material reported by Litton Industries as
a result of the subject literature review. Except for section 7 (Summary and Conclusions),
which is undergoing further evaluation, the survey contains all information as reported by
Litton Industries. The complete survey, including section 7 (Summary and Conclusions)
is available from:
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PRELIMINARY
AIR POLLUTION SURVEY
OF
ASBESTOS
A LITERATURE REVIEW
Ralph J. Sullivan
Yanis C. Athanassiadis
Litton Systems, Incorporated
Environmental Systems Division
Prepared under Contract No. PH 22-68-25
U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE
Public Health Service
Consumer Protection and Environmental Health Service
National Air Pollution Control Administration
Raleigh, North Carolina
October 1969
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The APTD series of reports is issued by the National Air Pollution Control
Administration to report technical data of interest to a limited reader-
ship. Copies of APTD reports may be obtained upon reciuest, as supplies
permit, from the Office of Technical Information and Publications, National
Air Pollution Control Administration, U.S. Department of Health, Education,
and Welfare, 1033 Wade Avenue, Raleigh, North Carolina 27605.
National Air Pollution Control Administration Publication No. APTD 69-27
11
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FOR EWORD
As the concern for air quality grows, so does the con-
cern over the less ubiquitous but potentially harmful contarrii—
nants that are in our atmosphere. Thirty such pollutants have
been identified, and available information has been summarized
in a series of reports describing their sources, distribution,
effects, and control technology for their abatement.
A total of 27 reports have been prepared covering the
30 pollutants. These reports were developed under contract
for the National Air Pollution Control Administration (NAPCA) by
Litton Systems, Inc. The complete listing is as follows:
Aeroallergens (pollens)
Aldehydes (includes acrolein
and formaldehyde)
Ammonia
Arsenic and Its Compounds
Asbestos
Barium and Its Compounds
Beryllium and Its Compounds
Biological Aerosols
(microorganisms)
Boron and Its Compounds
Cadmium and Its Compounds
Chlorine Gas
Chromium and Its Compounds
(includes chromic acid)
Ethylene
Hydrochloric Acid
Hydrogen Sulfide
Iron and Its Compounds
Manganese and Its Compounds
Mercury and Its Compounds
Nickel and Its Compounds
Odorous Compounds
Organic Carcinogens
Pesticides
Phosphorus and Its Compounds
Radioactive Substances
Selenium and Its Compounds
Vanadium and Its Compounds
Zinc and Its Compounds
These reports represent current state—of—the—art
literature reviews supplemented by discussions with selected
knowledgeable individuals both within and outside the Federal
Government. They do not however presume to be a synthesis of
available information but rather a summary without an attempt
to interpret or reconcile conflicting data. The reports are
111
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necessarily limited in their discussion of health effects for
some pollutants to descriptions of occupational health expo-
sures and animal laboratory studies since only a few epidemic—
logic studies were available.
Initially these reports were generally intended as
internal documents within NAPCA to provide a basis for sound
decision—making on program guidance for future research
activities and to allow ranking of future activities relating
to the development of criteria and control technology docu—
ments. However, it is apparent that these reports may also
be of significant value to many others in air pollution control,
such as State or local air pollution control officials, as a
library of information on which to base informed decisions on
pollutants to be controlled in their geographic areas. Addi-
tionally, these reports may stimulate scientific investigators
to pursue research in needed areas. They also provide for the
interested citizen readily available information about a given
pollutant. Therefore, they are being given wide distribution
with the assumption that they will be used with full knowledge
of their value and limitations.
This series of reports was compiled and prepared by the
Litton personnel listed below:
Ralph J. Sullivan
Quade R. Stahl, Ph.D.
Norman L. Durocher
Yanis C. Athanassiadis
Sydney Miner
Harold Finkeistein, Ph.D.
Douglas A. Olsen, PhOD.
James L. Haynes
iv
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The NAPCA project officer for the contract was Ronald C.
Campbell, assisted by Dr. Emanuel Landau and Gerald Chapman.
Appreciation is expressed to the many individuals both
outs ide and within NAPCA who provided information and reviewed
draft copies of these reports. Appreciation is also expressed
to the NAPCA Office of Technical Information and Publications
for their support in providing a significant portion of the
technical literature.
V
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ABSTRACT
Inhalation of asbestos may cause asbestosis, pleural or
peritoneal mesothelioma, or lung cancer. Mesothelioma is a
rare form of cancer which occurs frequently in asbestos
workers. All three of these diseases are fatal once they become
established. The dose necessary to produce asbestosis has been
estimated to be 50 to 60 million particles per cubic foot—years.
No information is available on the dose necessary to induce
cancer. Random autopsies of lungs have shown “asbestos bodies”
in the lungs of one—fourth to one—half of samples from urban
populations. Thus, the apparent air pollution by asbestos
reaches a large number of people.
Animals have been shown to develop asbestosis and cancer
after exposure to asbestos.
No information has been found on the effects of asbestos
air pollution on plants or materials.
The likely sources of asbestos air pollution are uses of
the asbestos products in the construction industry and asbestos
mines and factories. Observations in Finland and Russia indi-
cate that asbestos does pollute air near mines and factories.
However, no measurements were reported of the concentration of
asbestos near likely sources in the United States. A concentra-
tion in urban air of 600 to 6,000 particles per cubic meter has
been estimated.
Bag filters have been used in factories to control
v ii
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asbestos emissions; the cost of this type of control in a
British factory was approximately 27.5 percent of the total capital
cost and about 7 percent of the operating cost. No information
has been found on the costs of damage resulting from asbestos
air pollution.
No satisfactory analytical method is available to
determine asbestos in the atmosphere.
viii
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LIST OF TABLES
1. Deaths of Asbestos Insulation Workers in New York,
1963—67 • • . . . . . . 16
2. Distribution of “Asbestos (Ferruginous) Bodies” in
Lungs in Pittsburgh . . . . . . . . 20
3. Type and Number of Tun rs Induced by Intrapleural
Inoculation of S.P.F. Rats with Asbestos . . . . . 22
4. Dust Counts in Asbestos Mines and Mills in South
Africa, 1947 29
5. Cancer of the Lung Among Asbestos Workers 62
6. “Asbestos Bodies” in Consecutive or Random
Autopsies 64
7. Composition and Properties of Asbestos . . . . . . 66
8. World Production of Asbestos . . . . 69
9. The Production and Apparent Consumption of Asbestos
in the United States . . . . 71
10. Regional Distribution of Asbestos Mining and
Processing . . . . . . . . . . . . . . 72
11. Asbestos Mines in the United States, 1966 . . . . 73
12. Apparent Asbestos Consumption, 1965 . . . . . . . . 74
13. Proportion of Asbestos in Various Asbestos Products 75
14. Quantity and Value of Asbestos Input by Industry,
1963 . . . . . . . . . . . . . . . . . . . . . . . 75
15. Population Groups with Occupational and Environmental
Exposure to Asbestos 76
16. Asbestos Control Equipment 77
17. Analysis of Asbestos and Asbestos Products Exports
and Imports . . . . . . . . . 78
18. Selected Statistics for the Asbestos I4anufacturing
Industry 79
ix
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LIST OF TABLES (Continued)
19. Selected Statistics for the Asbestos Products In—
dustr r . . . . . . . . . . . . . . . . . . . . . . 80
20. Asbestos Uses . a a a • • • • . . . 81
21. 1967 List of Manufactured Asbestos Products . . . 84
22. Asbestos Product Manufacturing Plants, 1963 . . . 86
23. Penetration of Fibers Through Nasal Hairs . . . . 93
24. Particle-Mass Relationship of Asbestos as a Function
ofFiberLength . . . . . . . . . . . . . . . . . 93
LIST OF FIGURES
1. Comparison of Trends in World Production and U.S.
Consumption of Unmanufactured Asbestos . . . . . . . 30
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CONTENTS
FOREWORD
ABSTRACT
1. INTRODUCTION. 1
2 . EFFECTS . . . . . . . 3
2.1 Effects on Humans . 3
2.1.1 Asbestosis . . . . . . . . . . . . . . . 4
2.1.2 Pleural Calcification and Plaques . . . 6
2.1.3 Cancer . . . . . . . . . . . . . . . . . 7
2.1.3.1 Cancer of the Lung 7
2.1.3.2 Mesothelioina of the Pleura and
Peritoneum . . . 11
2.1.3.3 Other Cancers . . . . . . . . . 15
2.1.3.4 Synergism . . . . . . 15
2.1.4 “Asbestos Bodies” . . . . . . . . . . . 17
2.2 Effects on Animals . . . . . . . . . . . . . . 20
2.2.1 Commercial and Domestic Animals . . . . 20
2.2.2 ExperimentalAnimals. . . . . . . . . . 21
2.3 Effects on Plants 24
2.4 Effects on Materials . . . . . 24
2.5 Environmental Air Standards . . . . . 24
3. SOURCES 26
3.1 NaturalOccurrence 26
3 . 1 . 1 Me s . . . . . . . . . . . . . . . . . 26
3.2 Production Sources . . . . 29
3.3 Product Sources . . . . . . . . . . . . . . . . 31
3.4 Environmental Air Concentrations . . . . . . . 33
4 . ABA,T E ’4ENT . . . . . . . . . . . . . . . . . . . . . 3 5
5. ECONOMICS . . . . . . . . . . . . . . . . . . . . . 37
6. METHODS OF ANALYSIS 38
R ‘ERENCES . . . . . . . . . . . . . . . . . . . . 41
2-\PPENDIX . . . . . . . . . . . . . . . . . . . . . . 61
APPENDIX B . . . . .
xi
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1. INTRODUCTION
Asbestos is a general name given to a variety of useful
fibrous minerals. The value of asbestos ensues from the
indestructible nature of products fabricated from the various
grades of mineral fibers. The major asbestos minerals are
chrysotile, crocidolite, amosite, and anthophyllite, while
tremolite and actinolite are considerably less important.
Over 90 percent of the asbestos is chrysotile. The United
States uses about one—fourth of the world production of this
substance, practically all imported from Canada and Africa.
Inhalation of asbestos dust has long been recognized as
161,165
an industrial hazard. Early in this century, exposure
to high concentrations of the fibrous dust was causally
associated with asbestosis. In 1935, evidence began to
accumulate that cancer of the lung is also associated with
inhalation of asbestos. 55 More recently, certain rare cancers,
pleural mesotheliomas and peritoneal mesotheliomas, have been
associated with inhalation of asbestos fibers by asbestos
workers. 176 Heirnann 92 states that “The finding of several
such rare tumors in any given group makes that group suspect
of having special and distinct environmental characteristics,
in this case, exposure to asbestos dust.”
Nonoccupational environmental exposure to asbestos was
found as early as 1927 when Haddow 81 reported finding so-
called “asbestos bodies” in the lungs of a person living near
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an asbestos factory. Since then, several investiga-
tors’ 21 ’ 175 ’ 186 ’ 202 ’ 226 have reported finding neighborhood
cases. The subject of nonoccupational environmental exposure
to asbestos assumed a new dimension beginning with the re-
ports of Thomson and his colleagues. 213216 After examining
the lungs in consecutive autopsies, they found that approxi-
mately one-fourth of the populations in both Capetown, South
Africa, and Miami, Fla., have “asbestos bodies” in their
lungs. Other investigators have confirmed that one—fourth
to one—half of the population in Pittsburgh, 42 San Francisco, 43
Milan, 67 Glasgow, 188 blew York, 195 Montreal, 7 Jerusalem, 184
167 82 ,,
Finland, and Sweden have asbestos bodies” in their lungs.
These findings indicate that either these asbestos particles
or other particles that resemble asbestos in many ways 1 in-
cluding the way in which the body reacts to them, are being
inhaled either with the ambient urban air or through direct
exposure to asbestos.
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2. EFFECTS
2.1 Effects on Humans
Asbestosis (a diffuse pulmonary fibrosis), pleural
calcification, pleural plaques, lung cancer, arid pleural and
peritoneal mesotheliomas can result from exposure to
asbestos. Asbestos bodies are commonly found in the lungs of
persons exhibiting these complications. Diagnosis of any of
these or finding “asbestos bodies” in the lungs signifies the
need to review the case history for previous asbestos exposure.
Surveys of people living or working near asbestos mines and
factories have revealed that many nonoccupational cases of
asbestosis and mesothelioma have occurred either from the
polluted air or from asbestos carried home on the workers’
175, 176,178
clothing. However, in many cases no exposure to
asbestos can be established.
The fate of the asbestos fiber once it is inhaled* and
deposited in the lung is still questionable. The short fibers,
<0.5 in length, have been pathologically ignored, probably
because they are much too narrow to be visible under a light
microscope. The longer fibers which are encrusted in an iron—
bearing protein (asbestos bodies) become easily visible.
228 172
Wagner and Skidmore and Morris et al have shown that
rats which have inhaled asbestos lose the asbestos (probably
the short fibers) from their lungs. The biological half—life
*A discussion on respirable fibers is presented in
Appendix B (page 92).
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for asbestos appears to be 20 to 90 days, depending on the
mineral type. Some of the fibers are removed by phagocytosis
to the lymph nodes.
2.1.1 Asbestosis
Among asbestos workers, evidence of pulmonary asbestosis
is common. This condition results in a diffuse fibrosis,
usually in the lower lobes of the lung. Pulmonary asbestosis
has been called a monosymptomatic disease, with dyspnea as the
main complaint. 197 The British Occupational Hygiene Society 136
has reported that basal rales are the first symptoms of asbes—
tosis.
Asbestosis usually develops after long exposure to high
concentrations of asbestos dust. The risk varies directly with
the length of exposure and the dust concentration. Following
continued exposure to high concentrations of dust, asbestosis
may develop fully in 7 to 9 years and may cause death as early
as 13 years from onset of exposure. The common exposure period
before recognition of asbestosis (as observed among asbestos
workers) is 20 to 40 years, with death following about 2 to 10
years later. Once established, asbestosis progresses even after
the exposure to dust ceases: illness or death can occur long
after exposure to concentrations not producing immediate effects. 197
The prolonged latency period between exposure and the
first signs of asbestosis makes it difficult to establish dose—
time relationships. Cooper 43 suggested that a time—weighted
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average concentration of asbestos fibers of 5 mppcf* is too
high. He cites Wells’ 234 idea that multiplying average counts
by years of exposure provides a rough guide to the total dose
allowable. After 50 to 60-mppcf—years, workers began to show
evidence of asbestosis. At an average concentration of 5
mppcf, this total allowable dose would be reached in 10 to 12
years. Unfortunately, dust concentrations have been infre-
quently reported and measurements have been hampered by the
153 191
varied nature of the sources. Marr and Selikoff et al.
have reported that insulation workers are exposed to dust
concentrations below 5 mppcf, yet have exhibited a high
prevalence of asbestosis. Thus, Cooper’s argument is
strengthened.
In 1946, there were about 700 cases of asbestosis in
Germany among a total of approximately 8,000 employees in the
108 235
asbestos industry. Wegelius found 125 cases of asbestosis
of the lung in X—ray examinations of 476 asbestos workers in
one company in Finland. Of 132 asbestos workers examined by
Bohme, 26 29 percent showed X—ray evidence of asbestosis. The
occurrence of asbestosis in members of this worker group rose
with the duration of the employment: 5 percent in workers
exposed to asbestos for less than 3 years; 56 percent for those
employed for 5 to 10 years, and 79 percent for those with over
10 years’ exposure. A similar morbidity of 80 percent among
*5 million particles per cubic foot based on total dust
count and 8—hour--day, 40—hour—week exposure.
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English asbestos workers with over 20 years of employment was
165 177
reported by Merewether and Price in 1930. Noro noted
that the incidence of asbestosis was 65 percent in 167 asbestos
197
workers studied by X—ray. Selikoff j. investigated
1,522 asbestos insulation workers in the New York—New Jersey
metropolitan area. Among 392 individuals examined more than
20 years from the onset of exposure, X—ray evidence of asbestosis
was found in 339. In half of these, the asbestosis was moderate
or extensive. In individuals with less than 20 years of exposure,
radiological evidence of asbestosis was less frequent and when
present, was much less likely to be extensive.
2.1.2 Pleural Calcification and Plagues
Pleural calcification resulting from exposure to asbestos
120
is usually bilateral and affects the parietal pleura.
193
Selikoff stated that bilateral pleural calcification involving
the diaphragm is diagnostic of asbestosis. This pleural calci—
117
fication can be readily identified by X—ray.
Kiviluotol2O discovered 499 cases of pleural calcifica-
tion during a community X—ray survey of 6,312 adults in the
Kuusjari commune in Finland. In Ilomantsi commune he found no
such calcification among 7,101 adults. He observed that the
Kuusjari commune contained an asbestos mine and suggested that
these people had been subject to a localized environmental
asbestos expc ure. This investigator’ 21 also observed 77 cases
of pleural plaques out of 35,000 routine chest X—rays. The
case histories of these 77 revealed that 52 had previous
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exposure to asbestos either in the home or in their occupations,
where they handled asbestos products. Of the other 25 persons,
16 were questioned and no previous asbestos exposure could be
ascertained. Raunio 186 continued the study Sand found 1,516
adult cases of pleural calcification from 633,201 X—rays taken
in 13 Finnish towns and 106 rural conununes. In Tuusniemi
commune, where an asbestos quarry is located, pleural calcifi-
cation was found in 9 percent of the population; in urban
populations it was found in 0.7 percent of the people; and in
rural areas calcifications were found in only 7 out of 265,273
people examined (0.002 percent). However, Meurman - 67 found
the pleural plaques were common (39.3 percent of his cases)
in all Finland.
Approximately 2.8 percent of the agricultural workers
in Czechoslovakia 105 and Bulgaria 238 have also been shown to
have appreciable pleural calcification. In Bulgaria the soils
worked by the farmers contained asbestos; even stone fences
were made of outcrops of anthophyllite mineral. However, in
Czechoslovakia no asbestos or known exposure to asbestos was
found. After examining children living in the city of Asbest
in the Soviet Union, Bobyleva etal. 24 ’ 25 concluded that they
were suffering from impaired health caused by air pollution
from asbestos plants.
2.1.3 Cancer
2.1.3.1 Cancer of the Lung
The most common complication of asbestosis is cancer of
the lung. However, cancer of the lung apparently induced by
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asbestos may appear unaccompanied by asbestosis.
The association of lung cancer with exposure to asbestos
dust has been the subject of many investigations in the second
quarter of this century. In 1935, Lynch and Smith’ 49 in the
United States described lung cancer found during autopsy of a
patient with asbestosis. According to Hornburger t s data, 101
over a 20—year period eight cases of asbestosis were found in
4,137 autopsies at the medical school of Yale University. Of
these eight asbestosis cases, four were associated with lung
cancer (50 percent). In contrast, lung cancer was found in
only two (12 percent) of 17 cases of silicosis.
Lynch and Cannon 147 in 1949 found lung cancer in only
three cases (7.5 percent) of 40 patients with asbestosis.
Gloyne 71 in 1951 reported that according to autopsy data for
the London Hospital of chest Diseases, lung cancer was observed
in 14 percent of the 121 patients with asbestosis, but in only
6.9 percent of those with silicosis.
Usually, the lung cancer incidence in men is four to six
times higher than in women, but among patients with asbestosis
it is only twice as high for men. This has been confirmed by
Bohlig, Jacob, and Kalliabis. 29 They note that among women
working in the asbestos industry, lung cancer is observed at
an earlier age than among the rest of the population. In his
review, Behrens 19 reported 44 cases of lung cancer (14 percent)
in 309 autopsies of patients with asbestosis. After examining
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the data of various authors, Isselbacher et al. 111 reported
that of 603 persons with asbestosis, lung cancer was found in
83 (13.8 percent) at autopsy. Hueper 108 and Do11 record an
even higher percentage (15 percent). Doll emphasizes that the
majority of those who died had worked under conditions of high
dust content in the air.
Braun and Truan 33 found lung cancer in 12 (three cases
were not conclusive) of 187 workers in the Canadian asbestos
industry who had died. Boehme 26 reported 74 patients with
asbestosis; lung cancer was found in six of these. The
average age of the patients was 53; the average period from
the beginning of work to death was 28 years. Kea1 114 points
out that of 30 patients with asbestosis, 14 (47 percent) died
of lung cancer and 10 from carcinoma of the peritoneum or
ovaries.
Some additional statistics on the association of lung
cancer with asbestos workers are listed in Table 5 in the
Appendix.
Cancer of the lung produced by asbestos needs further
study. The latent period between exposure and evidence of
carcinoma may be even longer than for asbestosis. Nothing is
known about the dose—time relationship. Cases of lung cancer
have been observed when only a very short exposure or no
exposure to asbestos was known. Furthermore, the low number
of “asbestos bodies” observed in one—fourth to one—half of the
urban population may be sufficient to cause cancer. Because
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the long “asbestos bodies” remain in the lungs, a person who
has inhaled asbestos may carry the potential (for the rest of
his life) to develop carcinoma of the lung. Moreover, it has
not been determined whether more than one fiber is necessary
to induce a malignant tumor. Cox 42 has suggested that the
probability of cancer induction is proportional to the nunther
of asbestos fibers, number of susceptible cells, the concen-
tration of carcino ens on the fibers, and the time from
exposure.
Why asbestos is carcinogenic is not clearly understood.
At least three hypotheses have been advanced;
(1) That the fibers act as a physical irritant which
after 20 to 30 years of constant irritation induces a tumor.
(2) That the fibers contain small amounts of carcinogens——
such as benzo(a)pyrene, nickel, and chromium——which are eluted
from the fibers by the serum in the lungs. These carcinogens
then produce the cancer. Harington and Roe 88 have shown that
(a) chrysotile contains little or no benzo(a)pyrene, but about
100 ig of chromium per g of fiber and 5,000 ig of nickel per g
of fiber; (b) crocidolite contains 0.2 to 24 ig of benzo(a)pyrene
per 100 g of fiber and negligible amounts of nickel and chromium;
and (c) amosite contains 0.2 to 2.4 -ig of benzo(a)pyrene per 100
g of fiber, 100 iLg of nickel per g of fiber and 15 J g of
chromium per g of fiber (see Appendix B, page 92). The
authors have not only shown that these agents can be dissolved
in the lung serum, but also that airborne fibers can adsorb
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carcinogens present in the air. In studies of the adsorption
of benzo(a)pyrene by asbestos, chrysotile adsorbed 100 percent
of benzo(a)pyrene from solution after 48 hours at 37°C,
compared with 40 percent for crocidolite and 10 percent for
amosite. Harington and Roe suggest that these carcinogens
can be adsorbed on airborne fibers. Thus, the fibers become
a transporting vehicle to carry a concentrated quantity of
carcinogens into the lung.
(3) That the fibers accumulate in the lung and are
immobilized as “asbestos bodies” which disintegrate after 20
to 40 years. The resulting free particles cause asbestosis
or carcinoma of the lung.
In addition, Hammond 83 has suggested that asbestos is
a cocarcinogen; i.e., it increases the cancer—producing poten-
tial of small amounts of some other agent. In a study of
asbestos workers, he and his colleagues 199 found cancer of the
lung only in cigarette smokers. The number of deaths attributed
to cancer of the lung was eight times higher in asbestos workers
who smoked cigarettes than in smokers who were not exposed to
asbestos (see Section 2.1.3.4).
2.1.3.2 Mesothelioma of the Pleura and Peritoneum
Primary tumors of the pleura and peritoneum are so rare
that for years they were considered to be pathologic curiosi-
ties. In 1960 the first large series of cases of diffuse
229
mesothelioma were reported by Wagner et al. in South Africa.
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226
In trying to explain this mysterious epidemic, Wagner,
noting that “asbestos bodies’ were found in the lungs of some
of their patients, obtained detailed life histories of these
patients. By 1960, he was able to establish an association
with exposure to the Cape of Good Hope asbestos fields, or the
industrial use of asbestos, in 32 of 33 patients with histolog-
ically proved pleural inesothelioma. The majority of these
patients had not actually worked with asbestos but had lived
in the vicinity of the mines and mills, and some had left these
areas of exposure as young children. The average period between
exposure and development of the tumor was 20 to 40 years. By
226
1962, Wagner had diagnosed a total of 87 pleural and two
peritoneal mesotheliomas. In only two cases was it impossible
to establish a history of exposure to asbestos dust. of these
87 cases, 12 had been industrially exposed and the remainder
had been environmentally exposed from living in the vicinity
of the mills and dumps. This association between mesothelioma
and asbestosis became even more intriguing when i 1955, Bonser
30 described a series of 72 autopsies on patients with
asbestosis in which four cases of peritoneal mesothelioma were
found. Subsequently, Mancuso and Coulter 152 found five
peritoneal mesotheliomas in 1,495 asbestos workers, and
Hourihane,’ 02 upon reviewing the necropsy files of the London
Hospital from 1917 to 1962, found 34 cases of mesothelioma,
half of the pleura and the other half of the peritoneum. All
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of these patients had pulmonary asbestosis, even though in a
few there was no history of exposure to the asbestos dust. In
a subsequent study 103 Houril-iane found 74 cases of mesothelioma
in a London hospital over a 10—year period.
Borow et 3l report that in two years they observed
11 cases of mesothelioma during surgery in New Jersey. These
cases, added to six others previously diagnosed by them, totaled
17 cases of mesothelioma, eight of which were peritoneal and
nine pleural. They suggest that the high prevalence of these
rare tumors in New Jersey can be explained by its close proxim-
ity to a major asbestos mill, where a large percentage of all
the asbestos fiber mined in North America is converted to
coi iercial use.
In an attempt to determine whether mesothelioma of the
serosal surfaces was related in any way to asbestos exposure
in the United States, Selikoff l98 studied 307 consecutive
deaths among asbestos insulation workers in the Northeastern
United States. They found 10 deaths caused by four pleural
and six peritoneal mesotheliomas. In addition, these workers
had a high death rate attributed to cancer of the stomach,
colon, and rectum. Of the 307 deaths, 40.4 percent were
attributed to cancer, 5.5 percent to asbestosis, and 54.1
percent to other causes. In a second study, the investigators
reviewed 26 consecutive autopsies of patients with asbestosis,
and found four mesotheliomas of the pleura and three of the
peritoneum.
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A series of 83 patients from the London Hospital with
a diagnosis of mesothelioma (confirmed by necropsy or biopsy)
were studied by Newhouse and Thompson 176 for possible exposure
to asbestos. The series consisted of 41 men and 42 women; 27
of the patients had peritoneal and 56 pleural tumors. Although
the earliest death recorded from this group was in 1917, only
10 patients died before 1950, while 40 (48 percent) died
between 1960 and 1964. In 76 of the 83 cases, full occupational
and residential histories were obtained. Forty patients (52.6
percent) had a history of occupational exposure to asbestos or
of domestic exposure (living in the house with an asbestos
worker). In comparison, only 11.8 percent (9 of 76) of the
patients from the same hospital suffering from other diseases
had previous exposure to asbestos. There was also evidence
that neighborhood exposures may be important. Among those in
this study with no history of occupational or domestic expo-
sures to asbestos, 30.6 percent of the mesothelioma patients
and 7.6 percent of the inpatients with other diseases lived
within half a mile of an asbestos factory. Of the 31 patients
with occupational exposures to asbestos, only 10 held jobs
scheduled under the British Asbestos Regulations of 1931. The
interval between first exposure and the development of the
terminal illness from mesothelioma ranged between 16 and 55
years. The duration of exposure varied widely, ranging from
two months to over 50 years. In 47 patients in this mesothelioma
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15
series, lung tissue or sputum was available for examination.
In 30 (62.5 percent), either asbestosis or the presence of
asbestos bodies was noted.
Mesothelioma is now considered a frequent cause of
death among asbestos workers. No attempt has been made to
summarize the reports of mesothelioma, since they appear
almost weekly in the current literature. So far, however,
there appear to be few Cases among the general population.
Selikoff 198 reviewed 31,652 deaths among the general popula-
tion of over 1,048,183 in the United States and found only
three cases of mesothelioma. Moreover, he 195 points out that
asbestos is not the only cause of mesothelioma: it has also
224 107
been produced by silica and polyurethane.
2.1.3.3 Other Cancers
Extrapulmonary cancer has also been noted as a cause
of death among asbestos workers. Kogan et , •132 in 1966
reported 14 cases (31.1 percent), 11 women and 3 men. Four of
the women died of uterine cancer, two of intestinal cancer, two
of breast cancer, arid one of liver cancer. among the men, one
died of stomach cancer, another of cancer of the urinary bladder,
and a third of cancer of the prostate. Other cases of extra—
pulmonary cancer have been cited in Section 2.1.3.2.
2.1.3.4 Synergism
While the exact cause of lung cancer or pleural peritoneal
mesothelioma induced by asbestos is not known, air pollution by
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16
other pollutants may accelerate the morbidity. One form of
air pollution which is easily studied in individuals is smoking.
Selikoff et al. 199 recently studied the mortality of 370
asbestos insulation workers. In this group 24 men died of
lung cancer and all had a history of smoking. (See Table 1
below.) This rate was eight times greater than the expected
mortality rate, with age and smoking habits taken into account.
TABLE 1
DEATHS OF ASBESTOS INSULATION
WORKERS IN NE ’! YORK, 1963_67l99
(By Smoking Habits)
Smoking Habits
No. of
Casesa
Observed
Deaths
Expected
Deaths
Never smoked regularly
48
0
0.05
History of pipe, cigar—
smoking only
39
0
0.13
History of regular b
cigarette smoking
283
24
2.98
Total
370
24
3.16
aAll with more than 20 years from Onset of exposure.
bIncludes cigarette smokers who also smoked pipes or
cigars.
The blue asbestos, crocidolite, from South Africa is
believed by many 53 ’ 79 ’ 136 ” 40 ’ 209 to be much more carcinogenic
than the other minerals of asbestos. Studies in Finland’
indicate that anthophyllite also produces cancer. Wagner, 226
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17
Smith 206 and recently Godwin and Jagatic? 3 reported
that they had induced mesothelioma in mice using chrysotile.
76, 78,98—100,113,172,225,228
Moreover, animal experiments have
demonstrated that pulmonary complications occur with crocidolite,
chrysotile, amosite, and anthophyllite. Some investigators
believe that the fiber is not the carcinogenic agent, but
rather the vehicle on which the carcinogens are carried to the
target tissue. As stated earlier, chrysotile contains the
most nickel and chromium of all asbestos minerals, while
crocidolite contains the most benzo(a)pyrene. 8789 ” 59 All
three of these impurities in asbestos are suspected of being
carcinogenic. This knowledge, together with results which
indicate carcinogens can be adsorbed from urban air or tobacco
smoke, indicate that there may be no necessity to distinguish
urban asbestos dust by mineral types.
2.1.4 “ Asbestos Bodies ”
As stated earlier, the recent finding of “asbestos
bodies” in one—fourth to one—half of the urban population
(see Table 6 in the Appendix) has added new impetus to the
examination of asbestos as a general air pollutant.
An “asbestos body” has been defined as “an elongated
golden or reddish—brown structure usually with clubbed ends;
the shaft, which often shows a segmented or beaded appearance,
is usually straight, but sometimes curvilinear with a tendency
toward symmetry; usually it is from 3 to 5 .i in diameter and
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18
20 to 100 t in length. The coating contains iron demonstrable
by Perle’s stain (Prussian blue reaction), and probably
composed of ferritin or ferritin—like material; it may cover
the structure completely, masking the central fiber from direct
view, or may be incomplete in the central portion of the shaft
or in the interstices of the body, revealing an expanse of
220
naked fiber.
There is no doubt that the “asbestos bodies” formed in
the lungs of the asbestos workers contain asbestos. Stumphius
and Meyer 21 ° have investigated the composition of the “kernel”
in the “asbestos bodies” removed from deceased shipyard
workers (an occupational group with only indirect exposure).
They found by electron microscopy and X—ray microanalyses that
the “asbestos bodies” did indeed contain some minerals of
asbestos. Out of 27 fibers, 17 were classified as serpentine
(possibly chrysotile) and 10 as amphibole (possibly crocidolite).
But what about the so—called “asbestos bodies” in the lungs of
the general population? While these “asbestos bodies” probably
contain some asbestos, there is no experimental evidence to
date which shows what fractions contain asbestos or whether
they contain any asbestos at all. 79 ’ 194 This subject is
currently being debated by several investigators. 53 ’ 79 ’ 209 In
fact, some object to the use of the term “asbestos bodies” and
prefer to call them “ferruginous bodies.” Moreover, Gross
79
et al. have shown that “ferruginous bodies”—which appear
identical under the microscope to those formed from asbestos—
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19
can be produced from ceramic aluminium silicate, glass fibers,
and silicon carbide fibers. However, Thomson 215 claims that
a skilled pathologist can tell the difference. This contro-
versy should soon be resolved, since both Gross 53 and Selikoff 194
are investigating the composition of the central fiber with
the electron microprobe.
Generalized contamination with fibrous material is
evidenced by the figures in Table 6 in the Appendix. Two other
obvious conclusions are that “asbestos bodies” are found more
frequently in older people than in younger, and more frequently
in men than in women.
In none of the aforementioned studies has there been
any quantitative count of “asbestos bodies” in the lungs of
the general public. In most studies, “asbestos bodies” found were
scanty, although in some instances the bodies were numerous. 214
In most of the investigations, the method of Thomson 214 was
used (smears taken from basal lobes of the lung were examined
and the asbestos bodies counted). Since only about one—half—
millionth of a lung is examined, the finding of only one asbestos
particle may be extrapolated to mean that perhaps a half-million
fibers are present in the lung. 214 In one recent study in
Pittsburgh, Utidjian et al. 22 o made an attempt to quantify their
results. In this study 98 percent of the 100 lungs examined
contained “asbestos bodies” (“ferruginous bodies”). The results
are given in Table 2. For comparison they suggested that if
those cases with only one “asbestos body” were ignored, then
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20
47 percent of the lungs examined contained two or more bodies,
(20.5 percent of the women and 60.7 percent of the men).
This 47 percent is in substantial agreement with the compar-
able 41 percent reported by Cauna 4 ° (see Table 6 in the Appendix)
for residents of Pittsburgh.
TABLE 2
DISTRIBUTION OF “ASBESTOS (FERRuGIN0us) BODIES”
IN LUNGS IN PITTSBURGH 22 °
No. of Mean Fibers/Unit Distribution
Sex Cases Age of Lung ( Percent )
Men 1 89 0 2
21 62 1 37
15 64 2—5 27
19 70 >5 34
Total 56 65 100
Women 2 29 0 5
29 57 1 66
8 68 2—5 18
5 64 >5 11
Total 44 60 100
2.2 Effects on Animals
2.2.1 Commercial and fl mestic Animals
Kiviluoto 121 reported finding some asbestos bodies in
201
a cow near an asbestos mine. In 1931, Shuster reported
finding extensive pulmonary fibrosis in a dog kept for ratting
in an asbestos factory. The lungs of the dog also contained
some asbestos fibers but no asbestos bodies were found.
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21
Peacock and Peacock 182 have studied the effect of
asbestos on white leghorn fowl. They tried dusting the birds
with asbestos but found that the fibers did not penetrate far
into the lung. When the fibers were injected into the lumen
of the air sac, an immediate inflammatory reaction occurred,
macrophages appeared and engulfed the fibers, and giant cell
formation was observed. Four of the 17 chickens examined
developed tumors: of the six injected with crocidolite, two
developed tumors; of the 10 injected with amosite, only one
developed a tumor; and one chicken injected with an unidenti-
fied variety of asbestos also developed a tumor.
2.2.2 Experimental Animals
Studies with experimental animals have shown that
asbestos can induce fibrosis (asbestosis), cancer of the lung, and
mesothelioma and can form “asbestos bodies.”
Wagner 234 described experiments with rats in which 600
animals were exposed to various minerals of asbestos. The
results are given in Table 3.
Gross and De Treville 76 made the following observations
in studies on rats, hamsters, and guinea pigs. In rats that
have inhaled high concentrations (86,000 1g/m 3 ) of chrysotile
asbestos fibers for only a few months, minimal fibrotic
lesions can be observed in the lungs of all animals. However,
this form of asbestosis in rats is nonprogressive. In hamsters
that have inhaled chrysotile dust, a fibrosis develops which is
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TABLE 3
TYPE AND NUMBER OF TUMORS IN] JCED BY INTRAPL JRAL
INOCULATION OF S.P.F. RATS WITH ASBESTOS 2
Asbestos
Min ra1s
Animals
Exposed
Animals
Died
Misc.
Norimalig.
Misc.
Tumors
Reticulum—cell
Sarcomas
Mesotheliomas
Croc. 1 a
100
19
5
1
1
12
Croc.
100
10
4
6
Arnosite
100
4
1
1
2
Chrysotile
100
25
5
2
18
Silica
100
11
1
1
2
7
Saline
Total
100
5
2
1
2
600
— 74
18
3
8
45
a
Crocidolite from
b
Crocidolite with
Northwest Cape, South Africa.
oil extracted from it.
t’J
NJ
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23
progressive; “asbestos bodies” are also formed. In guinea
pigs, the inhalation of chrysotile dust produces fibrotic
lesions similar to those observed in rats. The data indicate
that the minimum time to produce asbestosis in rats and guinea
pigs is 60 to 120 hours at an asbestos dust concentration of
86,000 1g/m 3 . The investigators think the time required is
shorter for hamsters.
228
Wagner and Skidmore have shown that asbestos dust
tends to accumulate in the alveoli arising directly from the
respiratory bronchioles of rats. They also investigated the
elimination of asbestos from the lungs as discussed in Section
2.1. Gross and De Treville 76 also observed a decrease in fiber
content as the time from end of exposure increased.
Holt et al. 98 suggest from their observations on rats
that fibrotic lesions in the lungs are caused by asbestos
fibers (chrysotile) which are less than 3 p. long. Longer
fibers are stored in the lungs as “asbestos bodies;” shorter
fibers are removed from the lungs by phagocytosis. After
some years, the larger fibers disintegrate, producing a large
number of small particles. These small particles are then
phagocytosed and produce fibrosis. They also suggest that
asbestos is only fibrogenic when it is ingested by phagocytes.
Holt j 100 exposed guinea pigs to asbestos dust.
After 14 days of exposure to dust, bronchiolitis was observed;
after 21 days the damage was very severe, and “asbestos bodies”
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24
were observed along with asbestos fibers. After 226 days the
lungs of animals dusted for more ti-ian 1,000 hours over a 78—
day period developed a wide—spread, progressive fibrosis with
only a few asbestos fibers and “asbestos bodies” present in
the lung tissue. The experimenters concluded that asbestos
fibers too small to be seen under the microscope will produce
asbestosis.
In order to evaluate the possible distribution of
194,195
asbestos within New York City, Selikoff is now examining
the lungs of rats found in the city for asbestos fibers.
In a similar investigation carried out in South Africa,
wild animals captured near an asbestos mine were examined.
However, the small number of “asbestos bodies” found in them
precluded any conclusions. 234
2.3 Effects on Plants
No information has been found in the literature on the
effects of asbestos air pollution on plants.
2.4 Effects on Materials
No information has been found in the literature on the
effects of asbestos air pollution on materials.
2.5 Environmental Standards
Both the American Conference of Governmental Industrial
Hygienists 218 and the American Industrial Hygiene Associa-
tion ° have recommended an industrial threshold limit value
for asbestos dust of 5,000,000 particles per cubic foot
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25
(5 mppcf),based on total dust count and on an B—hour day, 40-
hour week. This value was recommended by Dreessen etal. 56
after a study of 541 employees in three textile plants using
chrysotile. Only three doubtful cases of asbestosis were
found in those exposed to dust concentrations of less than 5
mppcf, whereas numerous cases were found above 5 mppcf.
136
Recently, the British Occupational Hygiene Society
published its standards for chrysotile. The Society has
recommended a maximum accumulated exposure of 2.8 mppcf—years
(108 particle—years per rn 3 ). For example, maximum doses of
0.056 mppcf—years (2 x io6 particle—years/rn 3 ) for 50 years,
0.112 mppcf—years (4 x io6 particle—years/rn 3 ) for 25 years,
or 0.28 mppcf—years (10 particle—years/rn 3 ) for 10 years are
recommended. They have also recommended that dustiness be
designated by categories according to the following scheme:
Concentration Averaged
Over 3 Months
Dust Category ( Million Particles/rn 3 )
Negligible 0—0.4
Low .5—1.9
Medium 2.0—10
High Over 10.0
Only fibers longer than 5.0 i in length with a 3:1
length—to—breadth ratio are counted.
With these standards the risk of asbestosis maybe
reduced to 1 percent; that is, 1 percent of the workers exposed
to a dose of io8 particle—years/rn 3 would contract asbestosis.
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26
3. SOURCES
3.1 Natural Occurrence
Asbestos is a broad term embracing several fibrous
minerals. The minerals are divided into two groups: (1)
Pyroxenes—chrysotile; (2) Axnphiboles—crocidolite, amosite,
tremolite, actinolite, and anthophyllite. Properties of these
minerals are listed in Table 7 of the Appendix.
Asbestos probably occurs in nearly every country in the
world, but only a few of the deposits are commercially
valuable. Over 90 percent of the world asbestos production is
chrysotile, and Canada is the major source of this mineral for
the United States. 93 Table 8 in the Appendix lists the world
production. From these figures an estimate of known free—
world deposits is possible.
It is noteworthy that some soils near asbestos mines
contain considerable quantities of asbestos. In Finland,
farmers working these high—asbestos—content soils have been
observed to suffer from asbestosis) 20
3.1.1 Mines
The mining of asbestos in the United States has in-
creased 180 percent in the last 10 years. (See Table 9 in th€
Appendix.) This mining may constitute a source of air
pollution. A high percentage of the increase in domestic
production has been credited to California producers, who
accounted for 65 percent of the total output in 1966. Four
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27
companies produced chrysotile asbestos fiber: Atlas Minerals
Corp. and Coalinga Asbestos Co., Fresno County; Pacific
Asbestos Corp., Calaveras County; and Union Carbide Corp.,
San Benito County. The latter company processed the crude
material in a plant at King City, Monterey County, whereas
the other producers operated plants near the mine sites. 171
Amphibole asbestos was mined by Powhatan Mining Co.
near Burrisville, Yancey County, N.C. Their output increased
171
66 percent during 1966.
There are four chrysotile mines in Arizona in the Salt
River Valley near Globe. Since these mines are underground,
only the waste needs to be considered in connection with air
pollution (other than the possible pollution from transporting
the mineral). Nearly all of the output from these mines was
used in the Cement industry to manufacture asbestos cement and
building products: 28 percent was classified as filter fiber
and 2 percent as spinning grade; the rest consisted of sand
and waste, floats, or other short fibers. Jacquays Mining Corp.
operated the Regal and Chrysotile Mines and shipped the ore to
a company mill at Globe after hand-sorting the chrysotile.
Western Asbestos Manufacturing Co. operated the Phillips Mine,
171
and the Metal Asbestos Corp. the Lucky Seven Mine.
In Vermont, the Vermont Asbestos Mines Division of the
Ruberoid Co. quarried and processed chrysotile near Lowell in
Orleans County. Twenty—four grades were produced for spinning,
cement stock, paper stock, and other uses. Some waste rock
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28
171
was used for roadstone.
Data on these mines are summarized in Tables 10 and 11
in the Appendix.
Other deposits of asbestos have been found in Georgia
and Maryland.
Although no measurements have been made of the asbestos
air pollution from mining in the United States, some evidence
of the extent of pollution can be drawn from measurements and
observations in foreign countries. The extent of air pollution
from an asbestos mine in Finland was studied by Laamanen, Noro,
and Raunio) 33 They found asbestos dust at distances up to
50 km from the mines, including dust—fall rates ranging from
1.52 g/lOO m 2 /month at 4 km to 34.6 g/l0O m 2 /month at 0.5 km.
They concluded that asbestos dust is disseminated from mining
and milling areas rather extensively and that the degree of
pollution varies according to the distance from the mine or
mill and the prevailing winds.
Schepers 234 described the dust from asbestos mines and
mills in South Africa as dust which “rolled through like a
morning mist,” producing “itching skins caused by asbestos
adhering to our clothes. Even the food at the local hotel was
gritty with dust.”
Sluis—Cremer 202 reports dust counts in asbestos mines
and mills of South Africa as listed in Table 4. He pointed out
that living quarters near the mines were polluted with asbestos
and that the main source of pollution was airborne asbestos
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29
blown off dumps and roads made from the mine tailings.
TABLE 4
DUST COUNTS IN ASBESTOS MINES AND
MILLS IN SOUTH AFRICA, 1947202
Location
Dust Count, mppcf (mppm 3 )
Mines
Mill
-
Northwest Cape Province
Transvaal
2.8—24 (100—840)
2.3—6.5 (80—228)
10—55 (360—1920)
4.6—20 (162—720)
3.2 Production Sources
World production of asbestos during the period 1956 to
1967 increased at the average rate of approximately 13 percent
per year. Figure 1 shows that the world production nearly
tripled during the period 1945 to 1965, while United States
consumption only doubled during the same period. However,
during the period 1956 to 1967, domestic apparent consumption
fluctuated between 665,000 and 813,000 short tons per year and
may be leveling off as substitute materials (such as fiberglass
and plastics) provide competition.
The relative importance of the various industrial uses
of asbestos is given in Table 12 in the Appendix. It is seen
that the highest input of asbestos occurs in the asbestos
cement, floor tile, asbestos paper products, and asbestos
textile industries. The proportions of asbestos used in
various products are shown in Tables 13 and 14 in the Appendix.
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30
Thousands of Short Tons
U.S. WORLD
CONS. PROD.
900 3,500
800 3,000
700 2,500
600 2,000
500 1,500
400 1,000
1945
I I I
1955 1960
1965
Comparison of Trends in World Production and U.S.
Consumption of Unmanufactured Asbestos’ 70 ” 71
FIGURE 1
1970
U. S. CONSUMPTION
WORLD PRODUCTION
1950
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31
of the 78,056 short tons of domestic production in 1965,
66 percent were produced in California and 31 percent* in
Vermont, amounting to 97 percent of the total production.
This 97 percent was produced and processed in five counties. 17 °
More than 50 percent of the 124 plants comprising the asbestos
products industry were located (in 1963) in the States of
California, New Jersey, Illinois, Pennsylvania, and Texas, in
decreasing order. 41
Bobyleva 24,25 have shown that the air can be
polluted by asbestos from plants manufacturing asbestos products.
This asbestos may be carried in the air for distances of 25 to
50 miles. In a study of asbestos air pollution from three
plants in the U.S.S.R.., they found that at a distance of 3 km
from the plant, the dust concentration ranged from 0 to 6,000
ig/m 3 ; at 1.0—1.5 km it was 3,000—33,000 ig/m 3 ; and at 0.5 km
it was 6,000 to 34,000 ig/m 3 .
In the United States some attempts 206 have been made to
determine the concentration of asbestos near asbestos factories,
but the asbestos content of the atmosphere was masked by the
other dusts. Asbestos fibers were detected, but a quantitative
count was not possible.
3.3 Product Sources
I
The uses of asbestos are numerous. Some products which
use asbestos are the following: asbestos cement which may be
* trapo1ated .
-------
applied as mortar or plaster, or sprayed on walls; insulating
materials for the covering of pipes, ducts, boilers, cables,
and conduits; siding shingles, roofing shingles, tiles, flat
and corrugated sheets, wallboard, clapboard, and automobile
undercoating; threads, yarns, wicks, cords, tapes, cloths,
sheets, and blankets; friction materials, brake linings, clutch
facings, gaskets, and lagging cloths; and asphalt tiles,
plastics, and similar materials) 08
Abrasion of brake linings and clutch facings has been
suggested as a primary source of asbestos air pollution.
13 145
Ayer and Lynch have examined the emissions from brakes on
automobiles and found that the fiber is destroyed by the heat
of friction. Asbestos crystalline structures are also destroyed
and are recognizable only by the chemical composition.
Newhouse and Thompson 175 have reported one case of mesothelioma
in a mechanic.
The existence of a wide potential for direct or in —
direct occupational exposure has been cited 32 ’ 34 ”° 8 ’ 12 ° as a
possible explanation for the frequent occurrence of “asbestos
bodies” in the general public. Asbestos is now used in more
than 3,000 products. Most people working in the construction
and demolition of buildings come into contact with asbestos.
Electricians and homeowners strip asbestos insulation off wires;
the carpenter saws asbestos boards and often pounds the asbestos—
insulated furnace ducts to make them fit. As a result, the air
around a construction site is contaminated with asbestos fibers,
-------
33
and the foreman, carpenter, painter, plumber, or new occupants
all breathe this dust. In most homes, the owner will at some
time handle these asbestos products during normal home main—
tenarice. A large number of workers in other industries are
similarly exposed. Some of these are listed in Table 15 in
the Appendix.
Although only a few of these people work in the asbestos
industry, all may have inhaled sufficient asbestos to show
“asbestos bodies t ’ upon autopsy. The hazard is there, but how
great is the hazard? It will be necessary to obtain quantita-
tive concentration data to delineate its seriousness.
From the above discussion it may be concluded that
approximately 100,000 asbestos workers in the United States
have a high exposure to asbestos. 195 An additional 3.5 million
construction workers—carpenters, welders, electricians, masons,
plumbers, steamfitters, tile setters, etc.—are indirectly
exposed,either by themselves handling asbestos products or by
working on the job with people handling asbestos. 195
3.4 Environmental Air Concentrations
Only one estimate of the environmental air concentrations
of asbestos in the United States was found. Smith and Tabor 206 have
roughly estimated that urban air in the vicinity of heavily
traveled streets contains 600 to 6,000 particles/rn 3 . They
indicate that the validity of these values is highly suspect
because the methods available for the determination of asbestos
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34
are inadequate at the concentrations found in the urban air.
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35
4. ABAT EMENT
The asbestos industries in the United States have
developed elaborate ventilation systems to prevent high dust
13, 95
concentrations which might be inhaled by the workers.
This dusty air is passed from the ventilators through fabric
sleeve filters and then discharged to the atmosphere. The
asbestos fibers are easily filtered out since the fibers form
a mat which becomes an absolute filter. 1 In addition to the
ventilation system, it has been necessary to carry out some
operations (such as spinning and weaving) as wet processes to
eliminate dust. As a result, the pollution from factories is
minimal. Attempts to measure concentrations in the vicinity
of an asbestos plant have proved futile with present analytical
methods.
Pollution during the transportation of asbestos has
been controlled by enclosing the material in plastic—coated
bags.
Although the most common procedure used to suppress
dust emission is wetting of the material, it is unfortunately
not desirable to wet a large number of asbestos products.
In New York, insulators are required to enclose the
area when asbestos fireproofing is blown onto steel frames, but
even this does not prevent pollution. Asbestos fibers are
reported to be a common occurrence in the air around construc-
tion sites. 34
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36
No information has been found on the abatement methods
used in United States asbestos mines and in asbestos mills
near the mines.
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37
5. ECONOMICS
No information has been found in the literature on the
damage costs or economic losses due to the effects of asbestos
air pollution on humans, animals, plants, or materials. However,
a large fraction of the people in the United States have been
exposed to asbestos, including the following:
(1) approximately 100,000 workers using asbestos in
their occupations,
(2) approximately 3,500,000 construction workers ex-
posed indirectly to asbestos as they work with
asbestos products or near those who handle
asbestos products,
(3) approximately 50,000,000 Americans who possibly
have “asbestos bodies” in their lungs.
No attempt has been made to assess the cost of health
impairment for these people. Workmen’s compensation laws for
234
dust diseases are in effect in most States.
No information has been found on the cost of the present
and future abatement of air pollution by asbestos in this country.
The data in Table 16 in the Appendix, which refer to the asbestos
industry in Britain, 95 show that the dust extraction equipment
cost alone, for a given size and type of plant, amounts to 27.5
percent of the total capital cost and approximately 7 percent
of the operating cost of that plant. The type of control
equipment used is primarily designed to meet government speci-
fications relating to occupational health standards.
Data on the production and consumption of asbestos are
presented in Section 3.
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38
6. METHODS OF ANALYSIS
1,2,206
Of the methods presently being used to count
dust samples in the asbestos industry,* none is applicable to
atmospheric asbestos air pollution. There are at present no
proven satisfactory methods for the collection, detection,
and identification of asbestos fibers in the 0.1 to 5.0 u
range in ambient air. Satisfactory sampling can probably be
accomplished by use of a membrane filter—pump system. The
major difficulty lies in the problem of identifying a very
few asbestos fibers in the presence of relatively large num-
bers of a wide variety of other inorganic particulate matter
found in the same air. Attempts to determine the asbestos
content of urban air have revealed the need for development
of new methods. Battelle Memorial Institute is currently
developing one such method for the National Air Pollution
Control Administration. 205
*In all the asbestos monitoring methods used, microscopic
counting of the fibrous particles is necessary to determine the
proportion of fibrous material, and even then it is not known
what fraction of the fibers are asbestos. Counting of fibers
by eye under the microscope is tedious and difficult. If the
number of fibers is less than 1 percent (<5 wt%) of total dust,
the other dust masks the fibers, and quantitative results cannot
be obtained.
In parts of the asbestos industry where the asbestos—to—
dust ratio is high (>5 wt%), it is often possible to determine
the asbestos content indirectly. 136 For example, if the pro-
portion of asbestos in the airborne dust was known by microscopic
count for a given sampling location, the concentration (at least
the order of magnitude) could then be inferred from a simple
measurement of the concentration of the total dust.
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39
Modern analytical methods arid instrumentation used in
the asbestos industry are listed below:
Microscopic particle counting of samples on membrane
filters 1 ’ 2,14,15,57, 97,136,187
Thermal precipitators 1 ’ 2 ’ 97 ’ 136 ’ 187
Impingers ” 2 ’ 4 ’ 15 ’ 136,187
Royco particle counter 1 ’ 2 ’ 136 ’ - 87
Mass concentration methods 1 ’ 14 ” 36 ’’ 87
Microsieving 116
Digestion 116
Column chromatography of organics adsorbed on the
surf ace 116
X—ray diffraction 14 ’ 46 ’ 47 ’ 116
Low—temperature ashing 116
Atomic adsorption spectrophotometry 14 ’ 116
Electron microprobe 116
Neutron activation 116
Owens jet counter ” 2
2
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41
REFERENCES
1. Addingley, C. G., Dust Measurement and 1 nitoring in the
Asbestos Industry, Ann. N.Y. Acad. Sci. 132:298 (1965).
2. Addingley, C. G., Asbestos Dust arid Its Measurement,
Ann. Occup. Hyg . (London) 9:73 (1966).
3. Allen, G. L., F. H. Viets, and L. C. McCabe, Control of
Metallurgical and Mineral Dusts and Fumes in Los Angeles
County, California, U.S. Bur. Mines Inform. Circ. 7627
(1952). -
4. Anderson, D. 0., The Effects of Air Contamination on
Health: A Review. Part II, Can. Med. Assoc. J . 97:585
(1967).
5. Anderson, J., and F. A. Campagne, Asbestosis and Carcinoma
of the Lung, Arch. Environ. Health 1:27 (1960).
6. Anderson, W. A. D., Synopsis of Pathology , 5th ed.,
(St. Louis: MDsby, p. 429, 1960).
7. Anjilvel, L., and W. M. Thuribeck, The Incidence of
Asbestos Bodies in the Lungs at Random Necropsies in
Montreal, Can. Med. Assoc. J . 95:1179 (1966).
8. Annual Report of Chief Inspector of Factories for the
Year 1955 (London: Her Majesty’s Stationery Office,
p. 206, 1956).
9. Asbestos and Cancer, Can. Med. Assoc. J . 92:1020 (1965).
10. Asheroft, T., Asbestos Bodies, Brit. Med. J . 2:637 (1968).
11. Ashcroft, T.., Asbestos Bodies in Routine Necropsies on
Tyneside: A Pathological and Social Study, Brit. Med .
J. 19:614 (1968).
12. The Association of Exposure to Asbestos Dust and Cancer,
Ann. Occup. Hyg . (London) 8:267 (1965).
13. Ayer, H., and W. S. Lainhart, personal communication
(Oct. 1968).
14. Ayer, H. E., and J. R. Lynch, Motes and Fibers in the Air
of Asbestos Processing Plants and Hygienic Criteria for
Airborne Asbestos, Proc. Intern. Symp. Inhaled Particles
Vppours, II , Cambridge, Eng., p. 511 (1967).
-------
42
15. Ayer, H. E., J. R. Lynch, and J. H. Fanney, A Comparison
of Impinger and Membrane Filter Techniques for Evaluating
Air Samples in Asbestos Plant, Ann. N.Y. Acad . Sd. 132:
274 (1965).
16. Bader, M. E., R. A. Bader, A. S. Tierstein, and I. J.
Seli]coff, Pulmonary Function in Asbestosis: Serial Tests
in a Long—Term Prospective Study, AXmn.N.Y. Acad. Sci. 132 :
391 (1965).
17. Badollet, M. S ., and w. A. Gantt, Preparation of Asbestos
Fibers for Experimental Use, Ann. N.Y. Acad. Sd . 132:451
(1965).
18. Baizer, J. L.,and W. C. Cooper, The Work Environment of
Insulating W3rkers, Am. md. Hyg. Assoc . J. 29(3):222
(1968).
19. Behrens, W., Jr., The Clinical Picture and Pathology of
Asbestosis, Unffallmed. Berufskr . 45:129 (1952).
23. Berger, H., Asbestos_Fundamenta , Translated from Gerrn n
by R. E. Oesper. (New York: Chemical Publishing Co.,
1963).
21. Berkley, C. J., J. C’nurg, I. J. Seli]coff, and W. E. Smith,
The Detection and Localization of Mineral Fibers in
Tissue, Ann. N.Y. Acad. Sd. 132:48 (1965).
22. Billings, C. E., L. H. Levenbaum, C. Kurker, Jr., E. C.
Hickey, and L. Silverman, Further Investigations of the
Continuous Slag Wood Filter, J. Air Pollution Control Assoc .
8(1):53 (May 1958).
23. Blesovsky, A., The Folded Lung After Asbestos Exposure,
Brit. J.Diseases Chest 60(1):19 (1968).
24. Bobyleva, A. T., R. M. Bukhartseva, S. E. Lovtsova, and
M. S. Sadilova, Dust Concentration in Residential Districts
of Asbest City and the Effect on the Children s Health,
Gigiena i Sanit . 23(11):9 (1958). Translated from Russian
by B. S. Levine, U.S.S.R. Literature on Air Pollution and
Related Occupational Diseases 4:251 (1960).
25. Bobyleva, A. T., et al , The Amount of Dust in Residential
Districts of the City of Asbest and Its Effect on Children’s
Health, Arch. Environ. Health 2:727 (1961).
26. Boehme, A., Asbestose und Lungencarcinom, Arch. Gewerbepath
Gewerbehy . 17:384 (1959).
-------
43
27. Bohlig, H., Radiological Classification of Pulmonary
Asbestosis, Ann . N.Y._Acad. Sci. 132:333 (1965).
23. Bohlig, H., Krankheitserscheinungen nach Asbeststaubin—
halatiori, Zentr.Arbeitsmed.Arbeitsschutz 16(12):353 (1965).
29. Bohlig, H., G. Jacob, and 13. Kalliabis, Mortality and
Pathology of Lung Cancer with Asbestosis, Unffallnied .
Berufskr. 52:64 (1959).
30. Bonser, G. M., J. S. Faulds, and N. J. Stewart, Occupa-
tional Cancer of Urinary Bladder in Dyestuffs Operations
and of Lung in Asbestos Textile Workers and Iron Ore
Mines, Am. J. Olin . Pathol. 25:126 (1955).
31. Borow, M., A. Conston, L. L. Livornese, and N. Schalet,
Mesothelioma and its Association with Asbestos, J.Am.
Med._Assoc. 201(8):587 (Aug. 1967).
32. Bo qles, 0., Asbestos—A Materials Survey, U.S. Bur. Mines
Inform. Circ. 7880 (1959).
33. Braun, D. C., and T. D. Truan, Epideni±ological Study of
Lung Cancer in Asbestos Miners, Arch. md. Health 17:
63.4 (1958).
34. Brodeur, P., The Magic Mineral, New Yorker:117 (Oct. 12,
1968).
35. Buchanan.. W. D., Asbestos arid Primary Intrathoracic
Neoplasms, Arm. N.Y. Acad . Sd. 132:507 (1965).
36. Campbell, J., Asbestosis, Part I, P nnsy1vania Bureau of
Industrial S tandards , S lal Bull. (1934).
37. Campbell, W. N., Pleural Mesotheliomas, Arn.J. Pathol .
26:473 (1950).
33. Caplan, A., J. C. Gilson, K. F. W . Hinson, J. C. McVittie,
and J. C. Wagner, A Preliminary Study of Observer Varia-
tion in the Classification of Radiographs of Asbestos-
E cposed Wor)cers and the Relation of Pathology and X-Ray
Appearances (Part II of Radiological and Pathological
Correlations in Asbestosis in the Republic of South
Africa and the United Kingdom), Ann. N.Y. Acad. Sci .
132:379 (1965).
39. Cartier, P., Abstract of Discussion, md. Hyc . 5:262
(1952).
-------
44
40. Cauna, D., R. S. Totten, and P. Gross, As:bestos Bodies
in Human Lungs at Autopsy, J. Am. Med. Assoc . 192(5):111
(1965).
41. 1963 Census of Manufacturers, U.S Bur. of Census Pubi .
MC63(1) (1964).
42. Churg, J., S. Rosen, and S. Moolten, Histological Charac-
teristics of Mesothelioma Associated with Asbestos, Ann.
N.Y. Acad. Sci. 132:614 (1965).
43. Cooper, W. C., Asbestos as Hazard to Health, Arch. Environ.
Health 15:285 (1961).
44. Cordova, 3. F.., H. Tesluk, and K. Kundtson, Asbestosis and
Carcinoma of the Lung, Cancer 15:1181 (1962).
45. Cox, E. F., University of Maryland, Baltimore, Md., per-
sonal communication (Sept. 1968).
46. Crable, 3. V., Quantitative Determination of Chrysotile,
Amosite and Crocidolite by X-ray Diffraction, Am. Inch
Hyg. Assoc. 3. , 27:293 (1966).
47. Crable, 3. V.., and M. 3. Knott, Quantitative X-ray Dif-
fraction Analysis of Crocidolite and Aznosite in Bulk
or Settled Dust Samples, Am. md. . Hyg. Assoc. 3 . (5):
449 (1966).
48. Cralley, L. 3., R. G. Keenan, and 3. R. Lynch, Exposure to
Metals in the Manufacture of Asbestos Textile Products,
Am. md. Hyg. Assoc. J . 28:452 (1967).
49. Cralley, L. 3., R. G. Keenan, 3. R. Lynch, and W. S.
Lainhart, Source and Identification of Respirable Fibers,
Ani. md. Hyg. Assoc. 3 . 29:129 (1968).
50. Cuthbert, 3., Die Gefahren des Asbest fuer die Ailgemein—
heit, Muench. Med. Wochschr. 109:1369 (1967).
51. Davis, 3. M. G., Electron Microscope Studies of Asbestosis
in Man and Animals, Ann. N.Y. Acad. Sc!. 132:98 (1965).
52. Davis, 3. N. G., The Effects of Chrysotile Asbestos Dust
on Lung Macrophages Maintained in Organ Culture. An
Electron Microscope Study, Brit. 3. Exp. Pathol . (4):
379 (1967).
53. deTreville, R. T. p., p. Gross, and 3. M. G. Davis,
Asbestos Bodies and Their Bioeffects, 3. Am. Med. Assoc .
203(13):l143 (1968).
-------
45
54. Documentation of Threshold Limit Values, American Con-
ference of Governmental Industrial Hygienists, Committee
on Threshold Limit Values, Cincinnati, Ohio (1962).
55. Doll, R., Mortality from Lung Cancer in Asbestos Workers,
Brit. J. md. Med . 12:81 (1955).
56. Dreessen, W. C., et al. , A Study of Asbestosis in the
Asbestos Textile Industry, U.S. Public Health Serv. Bull.
241 (1938).
57. Edwards, G. H., and J. R. Lynch, The Method Used by the
U.S. Public Health Service for Enumeration of Asbestos
Dust on Membrane Filters, Ann. Occup. Hyg . II(1):1 (1968).
58. Elmes, P. C., The Epidemiology and Clinical Features of
Asbestosis and Related Diseases, Postgrad. Med . 42:623
(1966).
59. Elmes, P. C., and 0. L. Wade, Relationship Between Expo-
sure to Asbestos and Pleural Malignancy in Belfast,
Ann. N.Y. Acad. Sci. 132:549 (Dec. 1965).
60. Elmes, P. C., W. T. E. McCaughey, and 0. L. Wade, Diffuse
Mesothelionia of the Pleura and Asbestos, Brit. Med. J .
1:350 (1965).
61. Enterline, P. E., &,rta1ity Among Asbestos Products Workers
in the United States, Ann. N.Y. Acad. Sci. 132:156 (1965).
62. Enterline, P. E., and M. A. Kendrick, Asbestos—Dust
Exposure at Various Levels and Mortality, Arch. Environ.
Health 15:181 (1967).
63. Exposure to Asbestos and Malignancy, London Clin. Med.J .
7(1):10 (1966).
64. Freundlich, I. M., and R. R. Greening, Aslestosis and
Associated Medical Problems, Radiolo y89(2):224 (1967).
65. Gardner, L. V., and D. E. Cumings, Inhalation of Asbestos
Dust: Its Effect Upon Primary Tuberculosis Infection,
J. md. Hyg . 13:65 (1931).
66. Gaze, R., The Physical and Molecular Structure of Asbestos,
Ann. N.Y. Acad. Sci. 132:23 (1965).
67. Ghezzi, I., G. Molteni, and U. Puccetti, Asbestos Bodies
in the Lungs of Inhabitants of Milan, Med. Lavoro (Milan)
59(3):223 (1967).
-------
46
68. Gilson, J. C., Problems and Perspectives: The Changing
Hazards of Exposure to Asbestos, Ann. N.Y. Acad. Sd.
132:696 (1965).
69. Gloyne, S. R., The Formation of the Asbestosis Body in
the Lung, Tubercle 12:399 (1931).
70. Gloyne, S. R., The Asbestosis Body, Lancet 1:1351 (1932).
71. Gloyne, S. R., Pneumoconiosis: A Histological Survey of
Necropsy Material in 1205 Cases, Lancet 1:810 (1951).
72. Godwin, N. C., Diffuse Mesotheliomas with Comment on Their
Relation to Localized Fibrous Mesotheliornas, Cancer 10:298
(1957).
73. Godwin, M. C., and G. Jagatic, Asbestos and Mesothelioma
J. Am. Med. Assoc . 204(11):1009 (1968).
74. Gold, C., and J. Cuthbert, Asbestos—A Hazard to the
Community, Public Health (London) 80(6):261 (1966).
75. Gough, J., Differential Diagnosis in the Pathology of
Asbestosis, Ann. N.Y. Acad. Sci. 132:368 (1965).
76. Gross, P.., and R. P. P. deTreville, Experimental Asbestosis.
Studies on the Progressiveness of the Pulmonary Fibrosis
Caused by Chrysotile Dust, ch. Environ. Hea1 i j (5) :638
(1967).
77. Gross, P., and B. Talker, Dust Particles in Lung Sections
(Some ] sbtes on Methods of Their visualization), Arch.
Environ. Health 12(2):213 (1966).
78. Gross, P., L. J. Cralley, and R. T. P. deTreville,
Asbestos Bodies: Their Nonspecificity, Am. md. Hyg.
Assoc. J . 28:541 (1967).
79. Gross, P., R. T. P. deTreville, L. J. Cralley, and J. M.
G. Davis, Pulmonary Ferruginous Bodies, Arch. PatI p .
85:539 (1968).
80. Gross, P., R. T. P. deTreville, E. B. Tolker, M. Kaschak,
and M. A. Balykak, Experimental Asbestosis, Arch. Environ.
Health 15(3):638 (1967).
81. Haddow, A. C., Report of Annual Meeting of British Medical
Association, Manchester, 1929, Lancet 2:2330 (1929).
-------
47
82. Haegerstrand, I., L. Meurman, and B. Delund, Asbestos
Bodies in the Lungs and Mesotheliorna, Acta Pathol.
Microbiol. Scand . 72:177 (1968).
83. Hammond, E., Statement to U.S. Senate, Hearings Before
Subcommjttee on Air and Water Pollution of the Committee
on Public Works, United States Senate, 90th Congress,
2nd Session on Air Quality Criteria, Air Pollution—i 968
Part 2 (July 29—31, 1968).
84. Hammond, E. C., I. J. Selikoff, and J. Churg, Neoplasia
Among Insulation Workers in the United States with Special
Reference to Intra—Abdominal Neoplasia, Ann. N.Y. Acad.
Sci. 132:519 (1965).
85. Handbook of Asbestos Textiles , 2nd ed., Asbestos Textiles
Institute, Philadelphia, Pa. (1967).
86. Hardy, H. L., Asbestos Related Disease, Mi. J. Med. Sci .
250(4):49 (1965).
87. Harington, J. S., Chemical Studies of Asbestos, Ann. N.Y.
Acad. Sci. 132:31 (1965).
88. Harington, J. S., and F. J. C. Roe, Studies of Carcinogenesis
of Asbestosis Fibers and Their Natural Oils, Ann. N.Y.
Acad. Sci. 132:439 (1965).
89. Harington, J. S., and M. Smith, Studies of Hydrocarbons on
Mineral Dusts: The Elution of 3,4-Benzopyrene and Oils
from Asbestos and Coal Dusts by Serum, Arch. Environ.
Health 8(3):453 (1964).
90. Harries, P. G., Asbestos Hazards in Naval Dockyard,
Ann. Occupational Hyg . II(2):135 (1968).
91. Health Hazards of Some Newer Processes Used in Construction,
md. Hyg. News pt . 4:1 (1961).
92. Heimann, H., Status of Air Pollution Health Research,
1966, Arch. Environ. Health 14:488 (1967).
93. Hendry, N. W., The Geology, Occurrences, and Major Uses
of Asbestos, Ann. N.Y. Acad. Sci. 132:12 (1965).
94. High Temperature Bag Filter Development (Final Report) .
(Cambridge, Mass.: Arthur D. Little, 1959).
95. Hills, D. W., Economics of Dust Control, Ann. N.Y. Acad.
Sci. 132:322 (1965).
-------
48
96. Hinson, K. F. W., Cancer of the Lungs and Other Diseases
After Exposure to Asbestos Dust, Brit. J. Diseases Chest
(London) 49:121 (1965).
97. Holmes, S., Developments in Dust Sampling and Counting
Techniques in the Asbestos Industry, Ann. N.Y. Acad. Sd .
132:288 (1965).
98. Holt, P. F., J. Mills, and D. K. Young, The Early Effects
of Chrysotile Asbestos Dust on the Rat Lung, J. Pathol.
Bacteriol . 87:15 (1964).
99. Holt, P. F., J. Mills, and D. K. Young, Experimental Asbes-
tosis with Four Types of Fibers: Importance of Small
Particles, Ann. NY. Acad. Sci. 132:87 (1965).
100. Holt, P. F., J. Mills, and D. K. Young, Experimental
Asbestos in the Guinea—Pig, J. Pathol. Bacteriol . (London)
92(1):185 (1966).
101. Homburger, F., The Co—Incidence of Primary Carcinoma of
the Lung in Pulmonary Asbestosis, Am. J. Pathol . :797
(1943).
102. Hourihane, D. O’B., The Pathology of Mesotheliomata and an
Analysis of Their Association with Asbestos Exposure,
Thorax 19:268 (1964).
103. Hourihane, D. O’B., A Biopsy Series of Mesotheliomata, and
Attempts to Identify Asbestos Within Some of the Tumors,
Ann. N.Y. Acad. Sci. 132:647 (1965).
104. Hourihane, D. O’B., L. Lessof, and P. C. Richardson,
Hyaline and Calcified Pleural Plaques as an Index of
Exposure to Asbestos—A Study of Radiological and Patho-
logical Features of 100 Cases with a Consideration of
Epidemiology, Brit. Med. J . 1:1069 (1966).
105. Hrome]c, J,, The Mass Incidence of Characteristical Pleural
Changes in Citizens of the Western Part of the Former
Jilalava Region, Rozhledy Tuberk . 22:405 (1962).
106. Hueper, W. C., Carcinogens in the Human Environment, Arch.
Pathol . 71:237 (1961).
107. Hueper, W. C., Cancer Indu ction by Polyurethane and
Polysilicone Plastics, J.. Natl. ..Cancer _ Inst . l0O5
(1964).
-------
49
108. Hueper, W. C., Occupational and No -Occupationa1 Exposure
to Asbestos. IV. Human Exposure to Asbestos: Community
Studies, an _ n. N.Y. Acad. Sd . 132:184 (1965).
109. Hunt, R., Routine Lung Function Studies on 830 Employees
in an Asbestos Processing Factory, Ann . N.Y._Acad.Sci.
132:406 (1965).
110. Hygienic Guides Committee, Asbestos, Am. md. Hyg. Assoc .
3. 19:161 (1958).
111. Isselbacher, K. J., H. Klaus, and H. L. Hardy, Asbestosis
and Bronchogenic Carcinoma, J.Am. Med. Assoc . 15:721
(1953).
112. Jacob, G., and M. Anspach, Pulmonary Neoplasis Among
Dresden Asbestos Wor)cers, Ann. N.Y. Acad. Sd. 132:536
(1965).
113. Jagatic, M., M. E. Rubnitz, M. C. Godwin, and R. W.
W3iskopf, Tissue Response to Intraperitoneal Asbestos
with Preliminary Report of Acute Toxicity of Asbestos
in Mice, Preprint (1967).
114. Keal, E. E., Asbestosis and Abdominal Neoplasms, Lancet
2:1210 (1960).
115. Keane, W. T., and M. R. Zavon, Occupational Hazards of
Pipe Insulators, Arch. Environ. Hea1t L3_:171 (1966).
116. Keenan, R. G., and R. E. Kupel, Modern Techniques for
Evaluating Mixed Environmental E cposures to Fibrous and
Particulate Dusts in the Asbestos Industry, Preprint.
U.S. Public Health Service, National Center for Urban
and Industrial Health, Cincinnati, Ohio (1968).
117. Kendall, B., and M. Caplin, Pleural Calcification,
Brit. J. Diseases _ Chest (London) 61:126 (1967).
118. Kennedy, M. C. S., and R. Routledge, Investigation of a
Minor Asbestos Hazard, Brit. J.Ind. Med . (London) 24:
232 (1967).
119. Kesting, A. M., Dust Measurement in Plants with Asbestos
Processing Machinery, Staub (English Transi.) 26(1O):14
(1966).
120. Kiviluoto, R., Pleural Calcification as a Roentgenologic
Sign of Non-Occupational Endemic Anthophyllite-Asbestosis,
Acta Radiol. Suppi. 1, 194 (1960).
-------
50
121. Kiviluoto, R., Pleural Plaques and Asbestos: Further
Observations on Endemic and Other Non—Occupational Asbes-
tosis, Ann. N.Y. Acad. Sd. 132:235 (1965).
122. Kleinfeld, M., Pleural Calcification as a Sign of Sill—
catosis, Am. J. Med. Sci . 251:125 (1966).
123. Kleinfeld, M., J. Messite, and 0. Kooyman, Mortality
Experience in a Group of Asbestos Workers, Arch. Environ.
H a1th 15(2):177 (1967).
124. Kleinfeld, M., J. Messite, 0. Kooyrnan, and J. Saifaty,
Effect of Asbestos Dust Inhalation on Lung Function,
Arch. Environ. Health 12:741 (1966).
125. Kleinfeld, M., J. Messite, 0. Kooyman, and M. H. Zaki,
Mortality Among Talc Miners arid Millers in New York State,
Arch. Environ. Health 14(5):663 (1967).
126. Kiosterkotter, V. W., Studies of Animals Experimentally
Infected with Silicosis Through Inhalation of Amorphous
and SilIcic Acid, Arch. Hyg. Baicteriol . l0(6):542 (1966).
127. Knox, J. F., R. S. Doll, and I. D. Hill, Oohort Analyeis
of Changes in Incidence of Bronchial Carcinoma in a
Textile Asbestos Factory, Ann. N.Y. Acad. Sci. 132:526
(1965).
128. Kogan, F. M., Asbestos Dust and Lung Cancer, Gigienai
Sanit. ( Hygiene and Sanitation ) 29(7):96 (1964).
129. Kogan , F. N., and A. P. Dorinovslcaya , Effect of Asbestos
and Serpentine Dusts on Pulmonary Tissue Culture, Gigiena
i Sanit. ( Hygiene and Sanitation ) 31(4-6):37 (1966).
130. Kogan, F. N., and S. Yu. Troits]cii, Hygienic Assessment of
Measures for Dust Control at Asb3stos—Dressing Factories,
Gi iena i Sanit. ( Hygiene and Sanitationj 31(4-6) :453
(1966).
131. Kogan, F. 14., A. A. Gerasimen]co, and G. T. Bunimovich,
The Occurrence of Certain Immunobiological Changes in
Asbestosis, Giq enaiSanit. ( Hygiene and Sanitation )
30(5):184 (1965).
132. Kogan, F. M., S. Yu. Troitskii, and M. R. Gulevskaya,
Carcinogenic Effect of Asbestos Dust, Gigierial Sanit.
( Hygiene and Sanitation ) 31(8):218 (1966).
-------
51
133. Laamanen, A., L. Noro, and V. Raunio, Observations on
Atmospheric Air Pollution Caused by Asbestos, Ann. N.Y.
Acad . Sci. 132:240 (1965).
134. LaBelle, C. W., and H. Brieger, “Patterns and Mechanisms
in the Elimination of Dust from the Lung,” Proceedings of the
International Symposium on Inhaled Particles Vapours, Oxford,
Eng., 1960, P. 356 (1961).
135. Laboya, T. T., “Study of the Particle Size Distribution of
Dust by the Microscopy Method,” in Methods of Studying
Industrial Dust and the Incidence of Pneumoconioses , A. A.
Letavet, and Ye. V. Khu]thrina, Eds. Clearinghouse for
Federal Scientific and Technical Information, Washington,
D.C., Joint Publications Research Service, TT 66—30952,
p. 39 (1966).
136. Lane, R. E., et al., Hygiene Standards for Chrysotile
Asbestos Dust, Ann. Occup. Hyg . II(2):47 (1968).
137. Lanza, A. J., Silicosis and Asbestosis (New York, London,
Toronto: Oxford Univ. Press, 1938).
138. Lanza, A. J., Asbestosis. Presented at the 4th Conference
of the McIntyre Research Foundation on Silicosis held in
Quebec (Jan. 1952).
139. Lanza, A. J., The Pneumoconiosis (New York: Grune &
Stratton, 1963).
140. Lewinsohn, H. C., Asbestos Bodies, Brit. Med. J . 2:120
(1968).
141. Lieben, J., Malignancies in Asbestos Workers, Arch.
Environ. Health 13(5):6l9 (Nov. 1966).
142. Lieben, J., and H. Pistawka, Mesothelioma and Asbestos
Exposure, Arch. Environ. Health 14:559 (1967).
143. Low, M. J. D., Pressure Effects on Hydrogen Chemisorption
on Zinc Oxide, J. Am. Chem. Soc . 87(1):7 (1965).
144. Lower Schuyl]cill Valley Air Pollution Survey, Pennsylvania
Dept. of Health, Harrisburg (Oct. 1966).
145. Lynch, J. R., Brake Lining Demonstration Products. Pre-
sented at the Engineers Round Table, 30th Annual Meeting,
American Conference of Governmental Industrial Hygienists,
St. Louis, Mo. (May 12, 1968).
-------
52
146. Lynch, 3. B., and H. E. Ayer, Measurement of Dust Expo—
sures in the Asbestos Textile Industry, Am md . Hyg.
Assoc. 3 . 27(5):431(1966).
147. Lynch, K. N., and W. N. Cannon, Asbestosis: VI. Analysis
of 40 Necropsied Cases, Brit. J. md. Ned . 14:874 (1949).
148. Lynch, K. N., and W. A. Smith, Asbestosis Bodies in Sputum
and Lung, 3. Am. Med. Assoc . 95:659 (1930).
149. Lynch, K. M., and W. A. Smith, Pulmonary Asbestosis: Car-
cinoma of Lung in Asbesto-Silicosis, Am. 3. Cancer 24:56
(1935).
150. Macnab, G., and 3. S. flarington, Hemolytic Activity of
Asbestos and Other Mineral Dusts, Nature 214:522 (1967).
151. Mader, P. P.,, and E. S. Mills, Contaminant Control in Space
Cabins: Approach and Results, Aerospace Med . 38(8):822
(1967).
152. Mancuso, I. F., and E. 3. Coulter, Methodology in Indus-
trial Health Studies, Envjro . Health 6:210 (1963).
153. Marr, W. T., Asbestos Exposure During Naval Vessel Over-
haul, Am. md. Hyg. Assoc. 3 . 25:264 (1964).
154. Martens, A. E., and 3. D. Keller, An Instrument for Sizing
and Counting Airborne Particles, Am. md. Hyg. Assoc. 3 .
:257 (1968).
155. McCaughey, W. T. E., Primary Tumors of the Pleura, J. Pathol.
Bacteriol . 76:517 (1958).
156. McCaughey, W. T. E., Exposure to Asbestos Dust and Diffuse
Pleural Mesotheliomas, Brit. Med. 3 . 2:1397 (1962).
157. McCaughey, W. T. E., Criteria for Diagnosis of Diffuse
Mesothelial Tumors, Ann. N.Y. Acad. Sci. 132:603 (1965).
158. McCrone, W. C., and R. Draftz, The Importance of Thinking
Small, Heating, Pjping, Air CQflditioning 1) :126 (1966).
159. McFee, I). R., and R. Tye, Adsorption of Proteins on Dusts
Related to the Pneumoconioses: Selectivity, 3. Occupational
Med . (Ottawa) 7(6):269 (1965).
160. McVjttie, 3. C., Asbestosis in Great Britain, Ann. N.Y.
Acad. Sci. 132:128 (1965).
-------
53
161. Merewether, E. R. A., The Occurrence of Pulmonary Fibrous
and Other Pulmonary Affections in Asbestos Workers, J. md.
Hyg . 12:239 (1930).
162. Merewether, E. R. A., A Memorandum on Asbestos, Tubercie
15:69 (1933—34).
163. Merewether, E. R. A., Annual Report of the Chief Inspector
of Factories for the Year 1947, vol. 79 (London: Her
Majesty’s Stationery Office, 1947).
164. Merewether, E. R. A., Annual Report of the Chief Inspector
of Factories for the Year 1955, vol. 206 (London: Her
Majesty’s Stationery Office, 1955).
165. Merewether, E. R. A., and C. W. Price, Effects of Asbestos
Dust on Lungs and Dust Suppression (London: Her Majesty t s
Stationery Office, 1930).
166. Meukin, V., Role of Inflammation in Carcinogenesis, Brit.
Med. J . 1:1586 (1960).
167. Meurman, L., Asbestos Bodies and Pleural Plaques in a
Finnish Series of Autopsy Cases, Acta Path. Microbiol.
Scand. Suppi. 181 (1966).
168. Mikov, M. I., Asbestosis in Employees of the “Korlace”
Asbestos and Separating Works, Text in Serbo—Croatian,
Archiv. Hig. Rada Toksikol . (Yugoslavia) 17:63 (1966).
169. Miller, L. , W. E. Smith, and S. W. Berliner, Tests for
Effect of Asbestos on Benzo(a)Pyrene Carcinogenesis in the
Respiratory Tract, Ann. N.Y. Acad. Sci. 132:489 (1965).
170. 1 Linera1s Yearbook, Vol. I—lI, Metals, Minerals, and Fuels ,
U.S. Govt. Printing Office, Washington, D.C. (1948-1966).
171. Minerals Yearbook, Vol. III, Area Reports: Domestic ,
Bureau of Mines, U.S. Govt. Printing Office, Washington,
D.C. (1948—1966).
172. Morris, T. G., W. H. Roberts, R. E. Silverman, J. W.
Skidmore, J. C. Wagner, and G. W. Cook, “Comparison of Dust
Retention in Specific Pathogen Free and Standard Rats,” Pro-
ceedings of the International Symposium on Inhaled Particles
Vapours, II, Cambridge, Eng. 1965, p. 205 (1967).
173. Nagelschrnidt, G., Some Observations of the Dust Content and
Composition in Lungs with AsbeStoSis, Made During Work on
Coal Miners’ PneumoconiosiS, Ann. N.Y. Acad. Sd. 132:64
(1965).
-------
54
174. Nakamura, I., Clinical arid Pathological Studies of Pul—
rnonary Asbestosis, J. Nara Med. Assoc . 18(4):455 (1967).
175. Newhouse, M. L., and H. Thompson, Epidemiology of
Mesothelial Tumors in the London Area, Ann. N.Y. Acad.
Sd. 132:579 (1965).
176. Newhouse, M. L., and H. Thompson, Mesotheliorna of Pleura
and Peritoneum Following Exposure to Asbestos in the
London Area, Brit. J. md. Med . (London) 22(4) :261
(1965).
177. Noro, L.,Histology of Asbestosis, Acta Pathol. Microbiol.
Scand . 23:53 (1946).
178. Noro, L., Occupational and “Non—Occupational” Asbestosis
in Finland, Am. md. Hyg. Assoc. 3 . 29:196 (1968).
179. Nutt, A.. and J. S. Harington, The Reaction of Reduced
Glutathione with Quartz Powder and with Associated Iron
and Copper, Med. Lavoro (Milan) 55(3):176 (1964).
180. Owen, W. G., Mesothelial Tumors and Exposure to Asbestos
Dust, Ann. N.Y. Acad. Sd. 132:674 (1965).
181. Parkersburg, West Virgini —Marietta Ohio, Air Pollution
Abatement Activity, U.S. Public Health Serv. (March 1967).
182. Peacock, P. R., and A. Peacock, Asbestos—Induced Tumors
in White Leghorn Fowls, Ann. N .Y. Acad. Sci. 132:501
(1965).
183. Pernis, E. C., C. Vigliani, arid I. J. Selikoff, Rheumatoid
Factor in Serum of Individuals Exposed to Asbestos, Ann.
N.Y. Acad.Sci. 132:112 (1965).
184. Polliack, A., and M. J. Sacks, Prevalence of Asbestos
Bodies in Basal Lung Smears, Israel J. Of Med. Sciences
(2) (1968).
185. Radczewski, 0. E., The Significance of Fine Mineral
Particles in Nature arid Technology, Staub (English
Transi.) 27(5):1 (1967).
186. Raunio, V., Occurrence of Unusual Pleural Calcification
in Finland, Ann. Med. Internae Fenniae Suppl. 47 ,
55:61 (1966).
-------
55
187. Roach, S. A., Measurement of Airborne Asbestos Dust by
Instruments Measuring Different Parameters, Ann. N.Y.
Acad. Sc!. 132:306 (1965).
188. Roberts, G. H., Asbestos Bodies in Lungs at Necropsy,
J. Clinical Pathol . 20:570 (1967).
189. Sano, T., Pathology and Patl-iogenesis of Pneunioconiosis,
Acta Pathol. Japon (Tokyo) 13(3):77 (1963).
190. Sayers, R. R., and W. C. Dreessen, Asbestosis, Pm. J.
Public Health 29:205 (1939).
191. Schall, B. L., Present Threshold Limit Value in the U.S.A.
for Asbestos Dust: A Critique, Ann. N.Y. Acad. Sci. 132 :
316 (1965).
192. Selecting Fabrics for Filtration and Dust. Cn11i ’rtinn
TF w York: J. P. Stevens & Co., Synthetic Industrial
Fabric Dept., 1966).
193. Selikoff, I. J., The Occurrence of Pleural Calcification
Among Asbestos Insulation Workers, Ann. N.Y. Acad. Sc! .
132:351 (1965) .
194. Seljkoff, I. J., personal communication (Oct. 1968).
195. Selikoff, I. J., and E. C. Hammond, Community Effects of
Non—Occupational Environmental Asbestos Expo sure, Am.J.
Public Health , j9):l658 (1968).
196. Selikoff, I. J., J. Churg, and E. C. Hammond, Asbestos
Exposure and Neoplasia, J. Am. Med. Assoc. 188:22 (1964).
197. Selikoff, I. J., 3. Chury, and E. C. Hammond, The
Occurrence of Asbestosis Among Insulation Workers in the
United States, Ann. N.Y. Acad. Sc!. 132:139 (1965).
198. Selikoff, I. J., 3. Churg, and E. C. Hammond, Relation
Between Exposure to Asbestos and Mesotbelioma, New Engi.
J. Med. 272:560 (1965).
199. Selikoff, I. J., H. C. Hammond, and 3. Churg, Asbestos
Exposure, Smoking, and Neoplasia, 3. Am. Med. Assoc. 204 :
106 (1968).
200. Selikoff, I. 3.., R. A. Bader, M. B. Bader, J. Churg, and
B. C. Hammond, Asbestosis and Neoplasia, Am. 3. Med . 42:
487 (1967).
201. Shuster, N. H., Pulmonary Asbestosis in a Dog, 3. Pathol.
Bacteriol . 34:751 (1931).
-------
56
202. Sluis—Crerner, G. K., Asbestos in South Africa— -- rtain
Geographical and Environmental Considerations, Ann. N.Y.
Acad. Sci. 132:215 (1965).
203. Siuls—Cremer, G. K., and C. P1. Theron, A Proposed
Radiological Classification of 4sbestosis (Part I of
Radiological and Pathological Correlations in Asbestosis
in the Republic of South Africa and the United Kingdom),
Ann. N.Y. Acad. Sci. 132:373 (1965).
204. Smith, K. W., “Pulmonary Disability in Asbestos Workers,”
in j ps f the McIntyre Saran a c Conference on
0 G. W. H. Schepe rs, Ed.
(Chicago: A.M.A. p. l96 1955).
205. Smith, K. W., Trends in the Health of the Asbestos Worker,
Ann. N.Y. Acad. Sci. 132:685 (1965).
206. Smith, R., and E. Tabor, personal corrununication (Sept.
1968).
207. Smith, W. E., L. Miller, R. E. Elsasser, and D. D. Hubert,
Tests for Carcinogenicity of Asbestos, Ann. N.Y. Acad.
Sci. 132:456 (1965).
208. Smither, W. J., Secular Changes in Asbestosis in an Asbestos
Factory, Ann. N.Y. Acad. Sci. 132:166 (1965).
209. Smither, W. J., Asbestos Bodies, Brit. Med. J . 2:51
(1968).
210. Stumphius, J.., and P. B. Meyer, Asbestos Bodies and
Mescthelioma, Ann. _ Oçcup. Hyg . 11:283 (1968).
211. Szymczykiewicz, K., The Mesenteric Test as a Method of
Evaluation of Harmful Effects of Industrial Dust, Med.
Pracy (Lodz, Poland) 15(4):221 (1964).
212. Tanaka, S., and J. Lieben, Community Chest X—rays for
Pneumoconiosis Prevention, Arch. Environ. Health 12:
10 (1966).
213. Thomson, J. G., Exposure to Asbestos Dust and Diffuse Pleural
Mesotheliomas, Brit. Med. J . 1:123 (1963).
214. Thomson, J. G., Asbestos arid the Urban Dweller, Ann.
N.Y. Acad. Sd. 132:196 (1965).
-------
57
215. Thomson, J. G., and W. M. Graves, Asbestos As an Urban
Air Contaminant, Arch. Pathol . 81(5):458 (1966).
216. Thomson, J. C., R. 0. C. Kasthula, and R. R. MacDonald,
Asbestos as a Modern Urban Hazard, S. African Med. J .
37:77 (1963).
217. Thomson, M. L., A. M. Peizer, and W. J. Srnither, The
Discriminant Value of Pulmonary Function Tests in
Asbestosis, Ann. N.Y. Acad. Sci. 132:421 (1965).
218. Threshold Limit Values for 1967. Adopted at the 29th
Annual Meeting of the American Conference of Governmental
Industrial Hygienists, Chicago, Ill. (May 1-2, 1967).
219. Timbrell, V., The Inhalation of Fibrous Dusts, Ann. N.Y.
Acad. Sci. 132:421 (1965).
220. Utidjian, N. D., P. Gross, and R. T. P. deTreville,
Ferruginous Bodies in Human Lungs, Arch. Environ. Health
17:327 (1968).
221. Vasil’eva, A. A.., and N. D. Manita, Carboxyhemoglobin in
the Blood of Persons Directing City Traffic, Gigiena I
Sanit . 25(12):77 (1960), Translated by B. S. Levine, U.S.S.R.
Literature on Air Pollution and Related Occupational
Diseases 7:290 (1962).
222. Vigliani, E. C., G. Mottura, and P. Marazana, Association
of Pulmonary Tumors with Asbestosis in Piedmont and Lombardy,
Ann. N.Y. Acad. Sci.132:558 (1965).
223. Vorwald, A. J., T. N. Durkam, and P. C. Pratt, Experimental
Studies of Asbestosis, Arch. md. Hyg. Occup. Med . 3:1
(1951).
224. Wagner, J. C., Experimental Production of Mesothelial
Tumors of the Pleura by Implantation of Dusts in Laboratory
Animals, Nature 196(4850) :180 (1962).
225. Wagner, J. C., Asbestosis in Experimental Animals, Brit.
J. md. Med . 20:1 (1963).
226. Wagner, J. C., Epidemiology of Diffuse Nesothelial Tumors.
Evidence of an Association from Studies in South Africa
and the United Kingdom, Ann. N.Y. Acad. Sci . 2:575
(1965).
-------
58
227. Wagner, J. C., The Sequelae of Exposure to Asbestos Dust,
Ann. N.Y. Acad. Sd. 132:691 (1965).
228. Wagner, J. C., and J. W. Skic3.more, Asbestos Dust Deposi-
tion and Retention in Rats, Ann. N.Y. Acad. Sc 132:77
(1965).
229. Wagner, T. C., C. A. Sleggs, and P. Marchand, Diffuse
Pleural Mesotheliorna and Asbestos Exposure in North
Western Cape Province, Brit. J. md. Med . 17:260 (1960).
230. Walter, E., Evaluation and Assessment of Dust Measure-
merits in Asbestos Plants of the Textile Industry, Staub
(English Trarisi.) (Dusseldorf) (1O):16 (1966).
231. Warren, S., Survey of Some Current British and European
Studies of Occupational Tumor Problems, Occup. Med .
5:249 (1948).
232. Webster, I., Mesotheliomatous Tumors in South Africa:
Pathology and Experimental Pathology, Ann. N.Y. Acad.
Sci. 132:623 (1965).
233. Wegelius, C., Changes in the Lungs in 126 Cases of
Asbestosis Observed in Finland, Acta Radial . 28:139 (1947).
234. Whipple, H. E., Biological Effects of Asbestos, Ann.
N.Y. Acad. Sd. 132 (1965).
235. Wickert, K., So 3 Determination in Dust-Laden and Dust-
Free Combustion Gases, Text in German. Erdoel Kohie
(Hamburg) 2Q (8):568 (1967).
236. Windom, H., J. Griffin, and E. D. Goldbert, Talc in
Atmospheric Dusts, Environ. Sc4. _ Tech . j (ll):923 (1967).
237. Wood, W. B., and S. R. Gloyne, Pulmonary Asbestosis,
Lancet 1:445 (1930).
238. Zolov, C., T. Bourilikov, and L. Baladjoa, Pleural
Asbestos in Agricultural Workers, Environ. Res . 1(3):
287 (1967).
-------
59
OTHER REFERENCES
Asbestos (Philadelphia: Secretarial Service, 1968).
Asbestos Cement Quarterly (New York: Asbestos Cement Products
Assoc., 1968).
The Asbestos Mining Industry (Ottawa: Bureau of Statistics,
1968).
The Asbestos Products Industry (Ottawa: Bureau of Statistics,
1968).
Bankoff, E., The Canadian Asbestos Industry (Toronto: General
Research Associates, p. 41, 1958).
Berger, H., Asbestos Fundamentals , Translated from the German
(New York: Chemical Publishing Company, 1963).
Berger, H., Asbestos with Plastics arid Rubber (New York:
Chemical Publishing Company, 1966).
Bowles, 0., The Asbestos Industry, U.S. Bur. Mines Bulletin 552
(1959).
Monthly Report——Asbestos Production in Canada (Ottawa: Bureau
of Statistics, 1968).
-------
APPENDIX A
-------
APPENDIX A
TABLE 5
CANCER OF THE LUNG AMONG ASBESTOS DRKERS
43
No. With
No. of
Years
Lung
Comparison
Place
Population Studied
Workers
Followed
Cancer
Groups
United Kingdom
Reported deaths fzom
asbestos
235
1924—1947
31/235
(13.1%)
SilicotiCS
(1.32%)
United Kingdom
Cases of asbestosis in
1,247 autopsies with
pneumoconiosis
121
17/121
Silicotics
(6.9%)
United Kingdom
Asbestos textile workers,
industry areas, 20 years’
or more exposure
113
1922—1953
11/39
deaths
0.8
Expected
United Kingdom
Reported deaths from
asbestosis
365
1924—1955
65/365
(17.8%)
Quebec
Chrysotile miners and
mill workers with over
5 years’ employment
5,958
1950—1955
9/187
deaths
6+
Expected
Pennsylvania
Workers in asbestos
products plant employed
in 1938—39, aged 25—64
1,495
1940—1960
19/186
deaths
5.61
Expected
New York &
Insulating workers, over
632
1932—1962
45/255
6.6
New Jersey
20 years’ union membership
deaths
Expected
(continued)
r’)
-------
APPENDIX A
TABLE 5
CANCER OF THE LUNG AMONG ASBESTOS WORKERS (Continued)
Place
Population Studied
No. of
Workers
Years
Followed
No. With
Lung
Cancer
Comparison
Groups
California
Insulating workers,
mixed, 15 years in
trade, aged 35—64
529
1954—1957
10/41
deaths
2.8
Expected
Dresden
All asbestos trade
mixed exposures
2,636
1924—1963
34/150
deaths
11.4
Expected
United States
Asbestos textile workers
employed in 1948—1951,
aged 15—64
2,833
1951—1963
24/285
deaths
11.9
Expected
United Kingdom
Reported deaths from
asbestosis
584
1924—1963
146/584
(25%)
Bulgaria
Agricultural workers near
an asbestos mine
3,325
1962
155/3325
asbestosis
New York
Asbestos insulators em—
ployed more than 15
years, aged 40—80
152
1945—1965
18/46
deaths
3.1
Expected
Pennsylvania
Asbestos textile and
friction workers
68
1957—1962
13/68
deaths
-------
APPENDIX A
TABLE 6
“ASBESTOS BODIES” IN CONSECUTIVE OR RANLXDM AUTOPSIES
Location
•
Total
Cases
%
Posi-
tive
% Positive by Age* -
Sex
% Positive*
Year
of
Study
Refer—
ence
<24
25—34
35—44
45—54
55—64
65—74
>75
Female
Male
Capetown
500
26.4
.5
(4.3)
2.4
(25.6)
4.4
(28.4)
4.6
(22.4)
7.4
(31.6)
7.4
(28.0)
7.8
(20)
18.6
(30.4)
1960
214,216
Miami
500
27.2
0
0
1
(16.1)
3.4
(23)
5.6
(27.2)
9.2
(30.6)
9
(31.9)
8
(20.4)
19.2
(31.6)
1961
214,216
Pittsburgh
100
41
0
(0)
5
(83)
5
(46)
3
(38)
13
(54)
8
(40)
6
(30)
16
(34)
25
(47)
1964
40
Milan
.
100
51
(<—-
3
(14)
— >)
30
(60)
18
(66)
16
(44)
35
(54)
1966
67
Tyrieside
Jerusalem
311
100
20.3
26
0
(0)
<
0.3
(25)
1
(14)
1.6
(19.2)
---- )( -
2.9
(17.3)
4.8
(18.5)
7—>
(21)
7.7
(28.9)
—18
(30)
2.9
(15)
—>)
4.2
(13)
10
(29.1)
16.1
(25.5)
16
(22.2)
1967
1967
11
184
Glasgow
100
23
0
0
0
1
(12)
4
(22)
11
(32)
7
(19)
0
(0)
23
(37)
1967
188
Finland
264
57.6
1.5
(57)
3.0
(57)
3.8
(71)
8.7
(55)
20.0
(64)
16.7
(58.7)
3.8
(34.5)
23.9
(54.3)
33.7
(60)
1966
167
Sweden
34
35.3
0
0
0
0
11.7
(80)
14.7
(25)
18.8
(43)
14.7
(38)
20.6
(33)
1966
82
(continued)
-------
APPENDIX A
TABLE 6
“ASBESTOS BODIES” IN CONSECUTIVE OR RANDOM AUTOPSIES (Continued)
Location
Total
Cases
%
Posi—
tive
Year
of
Study
Refer—
ence
% Positive by Age*
<24 25—34 35—44 45—54 55—64
65—74
>75
Positive
Female Male
Johannesburg
39.2
1965
234
San Francisco
42
1966
43
Belfast
200
20
.
1965
60
London
Montreal
50
100
6
48
<-
—3 ----
(30)
48—
>
<—27—-
(50)
>
16
(36)
32
(57)
1964
1966
102
7
(50)
New York
355
50.5
3.9
(29.8)
46.5
(53.7)
1966
195
*Nurp.bers in parenthesis represent percentage of group—age or sex.
0
-------
APPENDIX A
TABLE 7
COMPOSITION AND PROPERTIES OF ASBESTOS MINERALS 66
Approximate Formula
Qirysotile
Crocidolite
Arnosite
1.5 MgO—5.5FeO—
8S1O 2 H 2 O
Na 2 0—3FeOFe 2 O—
8SiO 2 H 2 O
3MgO—2SiO 2 2H 2 O
Percentage of Malor Components
40.3
51.4
49.3
Silica Si0 2
Alumina A1 2 0 3
0.7
Ferrous Oxide FeO
1.0
20.3
40.9
Ferric Oxide Fe 2 0 3
1.5
17.5
0.4
Mariganous Oxide MnO
0.1
0.7
Calcium Oxide CaO
0.2
0.8
0.4
Magnesium Oxide MgO
42.4
1.4
5.7
Sodium Oxide Na 2 0
6.2
0.2
Potassium Oxide K 2 0
0.3
Carbon Dioxide CO 2
0.2
0.4
0.2
Water of Crystallization H 2 0
13.7
1.9
1.9
(continued)
-------
APPENDIX A
TABLE 7
COMPOSITION AND PROPERTIES OF ASBESTOS MINERALS (Continued)
Approximate Formula
Chrvsoti le
Crocidolite
Na 2 0—3FeOFe 2 O—
8Si0 2 H 2 O
Amosite
1.5 MgO—5.5FeO—
8SiO H 2 O
3MgO-2S1O 2 2H 2 O
Trace Organic Impurities
Oil—wax (mg/100 g fiber)
4—7.6
4—200
4—20
Benzo(a)pyrene
.
(ug/l00 g fiber)
none detected
0.2—24
0.2—2.4
Trace Inorganic Imp ities
( ig/g fiber)
Pb
2
5
20
Sn
<5
<5
<5
Ga
<2
<2
2
Bi
<5
<5
<5
V
50
<2
<2
Mo
<2
<2
<2
Cu
35
7
7
Ti
50
50
300
Ag
<0.2
0.2
0.2
Ni
5,000
(1,000—14,000)
<10
(<100)
1,000
(<100)
Zv
<200
700
1,000
Co
<5 (<100)
<5 (<100)
<5 (<100)
Mn
130 (400—500)
180 (200)
7,000 (7,900)
Cr
1,000 (400—900)
20 (<100)
150 (<100)
(continued)
-------
APPENDIX A
TABLE 7
COMPOSITION AND PROPERTIES OF ASBESTOS MINERALS (Continued)
Approximate
Formula
Chrysotile
Crocidolite
Z ’ mosite
Radioactive
Contaminants
•
( ic/g
fiber)
K 40
0.14
0.02
0.55
Th 238
<0.01
0.05
Ra 226
0.07
0.15
Physical Properties
Flexibility
Length
Texture
Tensile strength
Acid resistance
Heat resistance
Spinnability
Very flexible
Short to 3”
Harsh to silky
Very high
Fairly soluble
Good
Very good
Fair to good
Short to 3$I
Harsh to soft
Very high
Very good
Poor
Fair
Good
¼” to 6”
Coarse but pliable
Fair
Good
Good
Fair
C.’
OD
-------
APPENDIX A
TABLE S
WORLD PRODUCTION OF ASBESTOS 17 °
(Short Tons)
Location 1962 1963 1964 1965 1966 b,e
North AmerIca
Canada (sales) .
United States
(shipments) .
• . 1,215,814 1,275,530
• . 53,190 66,396
1,420, 769
101,092
1,387,555 1,479,281
118,275 125,928
South America
Argentina .
Bolivia (exports)
Brazil • . .
• 203
• 5€
• 4900 a
365
10
1, 440
542 243 c
7 3
1 , 430 a,c,f 1,204
4
1,820
Europe
Austria
Bulgaria
France
Greece
Italy
Portugal
U.S.S.R.
Yugoslavia
Africa
• . • S I •
• . . . . .
503
1, 323
10,869
60,860
7,401
638
l, 32 : 3 C
10,201
26 ,O 94 c
74
63, 016
29
755 , 000 a,c
9,074
l, 433 c
11,611
24, 289
75,573
810 , 000 a,c
9,280
l, 433 c
13, 307
71506 c
85 a
79,214
53 c
865,000
10,585
13,250
85 a
90,464
10
925, 000 a
8,411
Botswana
Kenya
Mozarubique
Rhodesia, Southern
South Africa . . .
Swaziland . . .
United Arab Republic
• . 2,375
• 5 212
370
• l 42 ,l 95 c
• 221,302
• 32,830
• 606
2,368
78
2,161
204
888 880 a
136 73
l42,254’
153,450
176 , 149 c
1751000 a
205,744
215,592
240,752
276,597
33,350
39,862
40,884
36,142
192
1,739
3,225
2,057
(continued)
-------
APPENDIX A
TABLE 8
WORLD PRODUCTION OF ASBESTOS (Continued)
(Short Tons)
Location
1962
1963
1964
1965
1966 b,e
Asia
China
Cyprus . .
India . . .
Japan . . .
. .
. .
. .
•
.
.
•
.
,
•
•
•
.
100,000
22,391
1,865
15,407
110,000
19,962
3 ,O 38 C
18,210
130,000
13,755
3710 C
17,979
140,000
l 7 , 622 c
4,989
16,451°
140,000
24,449
7,646
17,067
Korea, South
.
.
.
.
1,333
2,120
1,402
l,710C
687
Philippines
. .
.
.
.
1,037
421
586
Taiwan
•
•
.
.
525
604
526
883
721
Turkey .
•
.
•
•
709
408
1,291
1,376
1,258
Oceania
Australia .
.
.
.
•
18,416
13,374
13,545
11,647
13,472
New Zealand • .
World Totala
.
.
•
.
•
.
457
439
2655 000°
2760000 c
3050000 C
3,140,000°
3,350,000
a Estimated
bpreiiminary
C Revised.
dAsbestos also is produced in Czechoslovakia, Eritrea, Malagasy, North Korea, and
Rumania. No estimates for these countries are included in the total because production is
believed to be negligible.
eCompiled from data available May 1967.
Bahia only.
g nciuaes asbestos flour.
-------
APPENDIX A
71
TABLE 9
THE PRODUCTION AND APPARENT CONSUMPTION
OF ASBESTOS IN THE UNITED STATES 41 ” 70 ” 7 ’
—— Qu
antities in Short Tons
Year
Production
Imports Exports Consumption
1967
123,190
645,110 47,710 720,580
1966
125,928
726,459 46,996 805,391
1965
118,275
719,559 43,126 794,708
1964
101,092
739,361 27,147 813,306
1963
66,396
667,860 10,044 724,212
1962
53,190
675,953 2,949 726,194
1961
52,814
616,529 3,799 (665,440)
1960
45,223
669,945 5,525 709,193
1959
45,459
713,047 4,461 754,045
1958
43,979
644,331 3,026 685,284
1957
43,653
682,732 2,893 723,492
1956
41,312
689,910 2,950 782,272
1955
50,431
716,480 7,001 759,910
1950
727,002
1945
378,030
1940
270,000
1935
170,000
-
Values (X 1,000)
Year
Production
Exports
Imports Asbestos Asbestos Products
1967
$11,100
$66,000 $6,030
1966
11,056
73,100 5,763 $21,963
1965
10,162
70,457 5,294 19,139
1964
8,143
72,973 3,199 16,288
1963
5,108
61,739 1,304 16,267
1962
4,677
64,112 598 14,274
1961
4,347
(63,000) 759
1960
4,231
63,345 857
1959
4,391
65,006 793
1958
5,127
58,314 424 13,233
1957
4,918
60,104 350 15,223
1956
4,742
61,939 375 14,181
4,534
59,339 1,497 12,464
-------
APPENDIX A
TABLE 10
REGIONAL DISTRIBUTION OF ASBESTOS MINING AND PROCESSING 170 ’ 171
(Ranking and Production)
Rank
Quantity (Short Tons)
Value (X 1,000)
f_.
1
1960
1964
1966
1964
1965
1966
1964
1965
1966
V ..
‘ iif.
Calif.
55,041
—
74,587
81,671
$4,419
$6,177
$6,945
2
Ariz.
Vt.
Vt.
*
*
*
*
*
*
3
N.C.
Ariz.
Ariz.
*
3,469
*
*
441
*
4
Calif.
N.C.
N.C.
*
(55,041)
*
(78,056)
*
(81,671)
*
(4,419)
*
(6,177)
*
(6,945)
*Data withheld to avoid disclosure of producer’s confidential
the Bureau of Mines.
information to
r\.)
-------
APPENDIX A
TABLE 11
ASBESTOS MINES IN THE UNITED STATES, 1966170
Chrysoti le
Chrysotile
Chrysotile
Chrysotile
Chrysotile
Chrysotile
Chrysotile
Chrysotile
1
2
3
4
1
2
3
Atlas Minerals Corp.
Coalinga Asbestos Co.
Pacific Asbestos Corp.
Union Carbide Corp.
b
Ash Bonding Co.
Vermont Asbestos Mines
Div. of Ruberoid Co.
Jacquays Mining Corp.
Western Asbestos Mfg. Co.
Metate Asbestos Corp.
Kyle Asbestos Mines of Ariz.a
LeTourneau Asbestos Corp.a
Fresno County
Fresno County
Ca laveras
County
San Benito
County
Napa
Orleans County
(Lowell)
Salt River
Valley
(North of
Globe)
Near Mine
Near Mine
Near Mine
Monterey County
(King City)
State -
Mineral
Production
Ran]c
Name of
Producer
Location——County
or City
of
Mine
Processing Plant
California
Vermont
Arizona
1
North Carolina Crocidolite
1
aRanked by production only within the State.
bNot in operation during previous years.
Powhatan Mining Co.
Yancey County
t urnsvi11e)
—I
-------
74
APPENDIX A
TABLE 12
APPARENT ASBESTOS CONSUMPTION, 1965170
(In Thousands of Short Tons)
Use
World 97 United States*
Asbestos Industry Production
Mining and Processing
78
Asbestos in Products
Textiles
66
17
Cement
2,
190
548
Friction Materials
111
28
Asbestos Paper
220
55
Floor Tile
307
77
Paints, Roof Coating, Caulks
85
21
Plastics
21
5
Miscellaneous
221
55
Total Products
3,
221
806
*Based on 25% of world consumption.
-------
75
APPENDIX A
TABLE 13
PROPORTION OF ASBESTOS IN VARIOUS ASBESTOS PRODUCTS 17 °
Percenta
Product Asbestos
Asbestos textiles 80—100
Asbestos cement 15—90
Friction materials and gaskets 30—80
Asbestos paper and products 80—90
Floor tile 10—30
Other asbestos products U.D.C
aQ rysotile asbestos is used unless otherwise stated.
to 90% chrysotile, with some materials containing as
much as 85% arnosite and small amounts of crocidolite and antho—
phyllite.
CThese products contain undetermined quantities of
chrysotile, tremolite, actinolite, and anthophyllite.
TABLE 14
QUANTITY AND VALUE OF ASBESTOS INPUT BY INDUSTRY 1963170
Quantity
Value
Short
Fraction
Fraction
Product
Tons(000)
of Total
$jOOQ,000J
of
Total
Asbestos textiles
66
0.02
26.4
0.06
Asbestos cement
2,190
0.68
328.5
0.78
Friction materials
and gaskets
111
0.04
11.1
0.03
Paper arid products
220
0.07
19.8
0.05
Floor tile
307
0.09
13.2
0.03
Paint and coating
fillers
85
0.02
3.7
0.01
Plastics
21
0.01
9.2
Other
220.7
0.07
19.7
0.04
Total
3,220.7
1.00
423.3
1.00
-------
76
APPENDIX A
TABLE 15
POPULATION GROUPS WITH OCCUPATIONAL AND ENVIRONMENTAL
EXPOSURE TO ASBESTOS 108
Occupational Groups
Asbestos rock miners,
loaders, truckers, crushers,
millers, asbestos spinners,
weavers, electrical appli-
ance and wire manufacturers,
masons, carpenters, heating
equipment workers, rubber
workers, shingle and tile
manufacturers, building
material manufacturers,
filtering material manufac-
turers, molders of asbestos
products, asbestos—asphalt
makers, putty manufacturers,
asbestos cement makers,
asbestos paper, cardboard
and brake—lining producers,
asbestos felt insulation
workers, asbestos sound insu-
lation workers, asbestos insu-
lators, pipe coverers, asbes-
tos tube wrappers, asbestos
cork insulation workers, con-
struction workers, automobile
makers, garage attendants
Nonoccupational Groups
Residents in vicinity of
asbestos processing and tex-
tile mills inhaling plant
effluents polluted with
asbestos dust, and indivi-
duals living and working along
roads on which asbestos is
trucked; residents in the
vicinity of asbestos mines;
residents in vicinity of
building construction and
demolition, inhabitants of
homes or offices with asbes-
tos acoustical tile
-------
77
APPENDIX A
TABLE 16
ASBESTOS CONTROL EQUIPMENT 95
Cost Data
Asbestos Textile Industrya
Dust extraction equipment
Total capital cost (fixed) $1,500,000
Operating cost per year $ 250,000
Operating cost/labor cost 7 %
Operating cost/total cost 2.7%
conversion
Asbestos Minesb
Dust extraction equipment
Total capital cost (TCC) $ 360,000
(TCC/TcC of plant) x 100 27.5%
Operating cost (per year) $ 195,000
Specifications
Asbestos Textile Industrya
Volume of dust—containing air
extracted from textile machines 1,000,000 ft 3 /min or
700 ft 3 /min/operative
Quantity of asbestos dust filtered
per year (at above rate) 700 tons or
2.8 tons/worlcing day
Asbestos Mines
Total installed horsepower 796
part used to generate air for
dust removal 230 (29%)
Total air needed (for aspiration
and dust removal) per pound of 3
fiber produced 1,350 ft
aFigures apply to the Turner Bros. Asbestos Co. plant at
Rochdale, England.
bFigures apply to the Cape Asbestos Co. at Penge in the
Transvaal. The most modern mill (in Canada), which is 10 times
larger, needs only about half the quantity of air stated (using
gravity instead of air—swept mills and horizontal transportation
of ore).
-------
APPENDIX A
TABLE 17
ANALYSIS OF ASBESTOS AND ASBESTOS PRODUCTS EXPORTS AND II 4PORTS 17 °
.
Exports
Re—exports
Short
Tons
Dollars(000)
Short
Tons
Dollars
(000J
1965
1966
1965
1966
1965
1966
1965
1966
Total
42,995
46,690 5,271
5,712 131
306 23 51
Other products
* *
4,389 5,058
* 8 11
Total
19,087 21,907
52 56
Imports
— Short
Tons
Dollars
(000L
1965
1966
1965
1966
Crude and spinning fibers
1,251
1,455
326
325
50
176
10
30
Nonspinning fibers
24,221
28,017
3,622
3,973
81
130
13
21
Waste and refuse
17,523
17,218
1,323
1,414
Gaskets and packing
1,732
2,678
4,528
5,261
1
1
Brake lining
3,065
3,630
4,728
5,236
1
1
2
2
Clutcl’i lining (number)
2,020,864
2,246,986
1,691
1,897
5,000
5,000
4
1
Textiles and yarn
794
900
1,067
1,326
Shingles and clapboard
5,465
10,010
1,096
1,797
113
231
37
41
Asbestos—cement
6,101
4,742
1,588
1,332
Sub total
14,698
16,849
5,114
5,232
44
45
*
Chrysolite
Crude
Spinning/
Textiles
All Other
Total
Crocidolite
Amo site
Total
12,496
17,339
643,149
672,984
21,165
17,042
711,191
6,596
16,839
642,894
666,329
26,995
23,934
716, 258
6,245
55,077
70, 454
6,319
56,308
73,100
*Not available.
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79
APPENDIX A
TABLE 18
SELECTED STATISTICS FOR THE ASBESTOS MANUFACTURING INDUSTRY 41
(Employment Size)
Number of Value of
Number of Number of Number of Production Shipments
Employees* Companies Plants Workers $ (000)
1—49
39
39
308
8,264
50—99
6
6
231
4,827
100—2,499
10
17
2,445
89,131
over 2,500
18
62
12,754
407,014
Total
73
124
15,738
509,236
*The employment size class is determined by the total
company employment in all manufacturing activities in the
U.S., including central offices and auxiliaries serving
manufacturing establishments. All establishments of a
company are therefore included in the same employments size
column regardless of establishment size.
-------
80
APPENDIX A
TABLE 19
SELECTED STATISTICS FOR THE ASBESTOS PRODUCTS INLXJSTRY 41
Expenditures (in $000) 1958 1963
New plant and equipment
New structures 2,419 2,613
New machinery and equipment 10,418 9,768
Total 12,837 12,381
Used plant and equipment 428 1,289
Total 13,265 13,670
-------
APPENDIX A 81
TABLE 20
ASBESTOS USES 85
Textiles :
Varieties used: Chrysotile, crocidolite, and in part
amo site
Yarns and Cords :
Processes: Weaving of yarns and cords
Braiding (interlacing)
Classification of chrysotile fabrics:
Class Quality Code Asbestos content (% )
1 AAAA 75—79.9
2 AAA 80-84.9
3 AA 85—89.9
4 A 90—94.9
5 Underwriters 95—100
Commercial
Seating and Packing Materials :
Packing (woven fabrics)
stuffing for boxes and sleeves
manhole rings, boiler covers
Flat Packing :
Gaskets, flanges (on pipes) and containers
1. Without metal: high pressure gasket sheets (rubber)
2. With metal: material for sealing cylinder heads and
exhausts in motors and combustion engines,
and for sealing compressors and turbines
Asbestos Boards and Papers:
Boards
Filtering and clarifying
Coverings, coatings, casings, and jacketings for all
kinds of surfaces
Manufacturing of welders’ and melters’ shields
Slideways in the glass industry
Handles and fire—doors
Auto Parts
Safes
Protective walls
Curtains, etc.
(continued)
-------
82
APPENDIX A
TABLE 20 (Continued)
ASBESTOS USES 85
Sheets
Inner/outer linings of furnaces and heating vessels,
drying ovens, incubators, heaters, climate—
controlled spaces, etc.
Plates
Insulating buildings against vibrations (aluminum—
asbestos)
Solar—heat reflecting surfaces (70% of solar heat)
Special Asbestos Papers
Filters
Asbestos Cement (10 to 25% asbestos):
Slabs
Corrugated sheets
Pipes
Corrugated tiles for roofs in industry, agriculture, and
dwellings
Planks for platforms in buildings under construction
Balcony canopies
Rain gutters
Interior walls
Ventilating shafts
Air conditioning assemblies
Pressure piping (for underground drinking water
distribution systems, fuel gas, and sewage)
Cooling towers (electricity—generating stations)
Thermal Insulants and Fire—Proofing :
Sprayed asbestos ( insulant in both heating and
refrigeration), sound absorbent (eliminates booming and
improves acoustical properties of walls and ceilings)
Magnesia asbestos (85% magnesia, 15% asbestos) as
thermal insulant for covering pipes
Friction Material :
Woven: Brake lining
Noriwoven: Clutch lining
Transmission lining
(continued)
-------
APPENDIX A 83
TABLE 20 (Continued)
ASBESTOS USES 85
Asbestos Plastics :
Flooring tiles (asbestos—asphalt tiles and, increasingly,
asbestos—polymers of vinyl)
Pressed or molded (thermal insulation and in electrical
machinery)
Resinated asbestos felt (manufacturing of wings and firing
of missiles and expansion cones for nozzles of boost
motors). Other uses in aircraft industry: nozzles for
motor tubes, missile tailpipes, and missile—heat barriers;
fuselages for guided missiles, fuel tanks for fighter
bombers, cabin floors, etc.
Radar (large molded reflectors and scanners)
Asbestos Acid-Resistant Compositions :
Used mostly in chemical industry
-------
84
APPENDIX A
TABLE 21
1967 LIST OF MA 1JFACTURED ASBESTOS PRODUCTS 85
Industry and Product Description Quantity Measure
Miscellaneous Nonmetallic Mineral Products
Asbestos Products
Asbestos Friction Materials
Brake Linings
Woven, containing asbestos yarn,
tape, or cloth Linear feet
Molded, including all nonwoven types Cubic feet
Clutch facing
Woven, containing asbestos yarn,
tape, or cloth Thousand pieces
Molded, including all nonwoven types Thousand pieces
Asbestos—Cement Shingles and Clapboard
Siding shingles and clapboard,
including accessories Squares
Roofing shingles Squares
Asphalt Floor Tile Thousand square
Asphalt floor tile yards
Vinyl Asbestos Floor Tile Thousand square
Vinyl asbestos floor tile yards
Asbestos Textiles and Other Asbestos—
Cement Products
Asbestos textiles
Yarn, cord, and thread Pounds
Cloth Pounds
Other asbestos textiles, including
roving, lap, wick, rope, tape,
carded fibers, etc. Pounds
Asbestos—cement products
Flat sheets and wallboard, all
thicknesses converted to ¼” basis 100 square feet
Corrugated sheets 100 square feet
Pipe, conduits, and ducts, including
pressure pipe Short tons
(continued)
-------
85
APPENDIX A
TABLE 21 (Continued)
1967 LIST OF I’4ANUFACTURED ASBESTOS PROIXJCTS 85
Industry and Product Description Quantity Measure
Asbestos felts
Roofing—asphalt or tar saturated Short Tons
Other Short Tons
Other asbestos and asbestos—cement
products, including rnillboard and
prefabricated housing components
Gaskets and Insulation
Gaskets, All Types
Gaskets (for sealing nonmoving parts)
Asbestos, asbestos—metallic, and
asbestos—rubber
Packing (except leather, rubber, and
metal) and Asbestos Insulations
Asbestos compressed sheet Pounds
Packing (for sealing moving parts)
Asbestos, asbestos—metallic, and
asbestos—rubber Thousand pounds
Insulation materials containing
asbestos pipe insulation
Cellular and laminated Linear feet
85 percent magnesia Linear feet
Diatomaceous silica, calcium,
silicate, expanded silica, and
asbestos fiber Linear feet
Other pipe insulation Linear feet
Block insulation, including sheet
and lagging Thousand
85 percent magnesia board feet
Diatomaceous silica, calcium
silicate, expanded silica, and Thousand
asbestos fiber board feet
Other block insulation, including Thousand
celluar and laminated board feet
All other asbestos insulation
-------
APPENDIX A 86
TABLE 22
ASBESTOS PROtUCT MANUFACTURING PLANTS, 196341
4 ocation
Total
Plants
No. of_Plants with Emplo
ment of
1—
19
20—
49
50—
99
100—
249
250—
499
500—
999
1,
or
000
more
Jew Hampshire
Belknap 1 1
Hilisborough 1
Total 2 1 1
as sachusetts
Essex 1 1
Franklin 1 1
Middlesex 2 1
Suffolk 2 2
Worcester 1 1
Total 7 4 3
onnecticut
Fairfield 3 1 1
Hartford 1 1
Middlesex 1 1
Total 5 1 1 1 1
lew York
Albany 1
Kings 3 1 1 1
Orange 1 1
Suffolk 1 1
Total 6 2 1 2
ew Jersey
Bergen 1 1
Essex 3 2 1
Hudson 1 1
Mercer 2 2
Morris 1 1
Passaic 3 2 1
Somerset 4 2 1
Union 2 1
Total 16 5 2 3 5
(continued)
-------
APPENDIX A 87
TABLE 22 (Continued)
ASBESTOS PRODUCT MANUFACTURING PLANTS, 196341
•
Location
Total
Plants
No. of Plants with_Employment of
1—
19
20—
49
50—
99
100—
249
250—
499
500—
999
1,000
or more
Pennsylvania
Elk 1 1
Lancaster 1
Montgomery 2 2
Northampton 1 1
Philadelphia Cit 3 2 1
Potter 1 1
Total 9 3 1 3 1
Ohio
Cuyahoga 1 1
Paulding 1 i
Portage 1 1
Ross 1 1
Total 4 1 3
Indiana
Henry 1 1
Huntington 1 1
Kosciusko 1 1
Lagrange 1 1
Lake 1 1
Rush 1 1
Total 6 1 1 2 2
Illinois
Cook 8 5 1 2
Kankakee 1 1
Lake 4 2 1
Will 1 1
Total 14 5 1 3 4
Michigan
Wayne 1 1
Total 1 1
(continued)
-------
APPENDIX A 88
TABLE 22 (Continued)
ASBESTOS PRODUCT MANUFACTURING PLANTS, 196341
ocation
Total
Plants
No.
of Plants with_Employment of
1—
19
20—
49
50—
99
100—
249
250—
499
500—
999
1,
or
000
more
rj 5 fl jfl
Milwaukee
Total
issouri
St. Louis
St. Louis City
Total
(an s as
Barton
Total
Tirginia
Essex
Frederick
Norfolk City
Total
forth Carolina
Mecklenburg
Union
Total
;outh Carolina
charleston
Marlboro
Total
4eorgia
DeKaib
Talbot
Troup
Total
2
2
2
2
1
1
1
1
1
1
1
1
2
I
1
2
3
5
1
1
1
1
1
3
2
1
3
1
1
2
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
3
1
1
2
(continued)
-------
TABLE 22 (Continued)
ASBESTOS PRODUCT MANUFACTURING PLANTS, 196341
Location
Total
— Plants
No
of Plants with_Employment of
1—
19
20—
49
50—
99
100—
249
250—
499
500—
999
1,0D0
or more
Florida
Dade 1 1
Total 1 1
Alabama
Mobile 1 1
Total 1 1
4ississippi
Hinds 1 1
Union 1 1
Total 2 1 1
Louisiana
Jefferson 3 2
Orleans 3 1 1
Total 6 1 3 2
rexas
Dallas 2 2
Ector 1 1
Grayson 1 1
Harris 3 2
Hill 1 1
Total S 3 4
alifornia
Alameda 2 1 1
Contra Costa 1 1
Los Angeles 9 1 2 1 4
Orange 1 1
Sacramento 1 1
San Benito 1 1
San Joaquin 1 1
San Mateo 1 1
Santa Clara 1 1
Total 18 5 3 3 6
ThTITED STATES
TOTAL 124 40 10 13 34 21 4 2
APPENDIX A
89
-------
APPENDIX B
-------
92
RESPIRABLE ASBESTOS FIBERS
A number of questions arise regarding respirable
asbestos fibers. What length of fiber is respirable? What
is the particle—to—mass ratio? Should all fibers, whatever
their length or diameter, be counted? If not, can any
instrument be designed to select the right size distribution
in the atmosphere?
Timbrell 219 has studied the deposition of fibrous
material in the respiratory system. Fibers 50 or even 200 ii.
long are found in the lungs because the free—falling speed
depends largely on the diameter. Thus, particles less than
3.5 (most asbestos particles are less than 0.5 p) in
diameter can possibly penetrate deeply into the lung. The
more symmetrical a fiber is, the greater its chance of pene’-
trating. The largest compact particles normally found in the
lung are about 10 I in diameter. Limitation on the lengths
of the fibers which reach pulmonary air spaces is imposed by
the nasal hairs and the small diameters of the respiratory
bronchioles. These limitations are summarized in Table 23.
Respirable fibers have been defined by the British
Occupational Hygiene Society 205 as fibers less than 200 .i
long, less than 35 in diameter, and having a length—to—
breadth ratio of 3:1. Only the fibers longer than 5 i in
length are counted.
-------
TABLE 23
PENETRATION OF FIBERS THROUGH NASAL HAIRS 219
ength of Fiber
(microns)
% Penetration through Nasal Hairs
1st
Stage
2nd Stage
3rd
Sta
0.5
100
100
100
50
75
57
42
100
53
24
11
150
31
10
3
200
26
5
1
250
20
3
300
17
2
350
14
1
Walter 23 ° has investigated the mass of average particles
in the asbestos textile industry (see Table 24). He found
that respirable dust contains approximately 50 percent asbestos
and that 10 particles of dust per ug contain 5 x 10 particles
of asbestos per pig. From this conversion factor the threshold
limit value for asbestos can be calculated.* as approximately
350 g/m 3 (5 mppcf).
TABLE 24
PARTICLE-MASS RELATIONSHIP OF ASBESTOS AS
A FUNCTION OF FIBER LENGTH 229
Total Concentration
g/m 3
Particles*/cm 3 (approx)
Incineration Residue
g/m
- (approx)
Fiber Length
in Microns
(approx)
100
200
400
600
100
400
1,000
2,500
50—60
200—300
700—800
1,800—2,000
< 150
< 500
< 700
<10,000
*partjcles counted with a Iconimeter.
*5 mppcfl77 x io 6 p/m 3 350 ig/m 3 . The con entration
estimated in air is 600—6,000 p/m 3 =l.2 — 12 x 10 g/m 3 .
93
-------
94
Finally, there remains the problem of counting respirable
fibers in ambient air. It appears that a fairly sophisticated
instrument will be required which can (1) separate the other
particles from fibers, (2) identify the asbestos fibers in a
host of other fibers, and (3) count only those fibers longer
than 5 i and shorter than 200 i with diameters less than
3.5 U.
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