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AIR POLLUTION ASPECTS
OF
ASBESTOS
Prepared for the
National Air Pollution Control Administration
Consumer Protection & Environmental Health Service
Department of Health, Education, and Welfare
(Contract No. PH-22-68-25)
Compiled by Ralph J. Sullivan
and Yanis C. Athanassiadis
Litton Systems, Inc.
Environmental Systems Division
7300 Pearl Street
Bethesda, Maryland 20014
September 1969
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FOREWORD
As the concern for air quality grows, so does the con-
cern over the less ubiquitous but potentially harmful contami-
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) Ethylene
Aldehydes (includes acrolein Hydrochloric Acid
and formaldehyde) Hydrogen Sulfide
Ammonia Iron and Its Compounds
Arsenic and Its Compounds Manganese and Its Compounds
Asbestos Mercury and its Compounds
Barium and Its Compounds Nickel and Its Compounds
Beryllium and Its Compounds Odorous Compounds
Biological Aerosols Organic Carcinogens
(microorganisms) Pesticides
Boron and Its Compounds Phosphorus and Its Compounds
Cadmium and Its Compounds Radioactive Substances
Chlorine Gas Selenium and Its Compounds
Chromium and Its Compounds Vanadium and Its Compounds
(includes chromic acid) 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
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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
f
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.
i
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 Finkelstein, Ph.D.
Douglas A. Olsen, Ph0D.
James L. Haynes
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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
outside 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.
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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-
i
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
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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.
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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 Mesothelioma 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 Experimental Animals 21
2.3 Effects on P-lants 24
2.4 Effects on Materials 24
2.5 Environmental Air Standards 24
3. SOURCES 26
3.1 Natural Occurrence 26
3.1.1 Mines 26
3.2 Production Sources 29
3.3 Product Sources 31
3.4 Environmental Air Concentrations . 33
4. ABATEMENT 35
5. ECONOMICS 37
6. METHODS OF ANALYSIS . 38
7- SUMMARY AND CONCLUSIONS . 40
REFERENCES 43
APPENDIX A 63
APPENDIX B 92
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LIST OF FIGURES
1. Comparison of Trends in World Production and U.S.
Consumption of Unmanufactured Asbestos 30
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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 Tumors 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 ..... 63
6. "Asbestos Bodies" in Consecutive o» Random
Autopsies ..................... 65
7. Composition and Properties of Asbestos ...... 67
8. World Production of Asbestos ........... 70
9. The Production and Apparent Consumption of Asbestos
in the United States .......... ..... 72
10. Regional Distribution of Asbestos Mining and
Processing .................... 73
11. Asbestos Mines in the United States, 1966 ..... 74
12. Apparent Asbestos Consumption, 1965 ........ 75
13. Proportion of Asbestos in Various Asbestos Products 76
14. Quantity and Value of Asbestos Input by Industry,
1963 ....................... 76
15. Population Groups with Occupational and Environmental
Exposure to Asbestos ............... 77
16. Asbestos Control Equipment ......... ... 78
17. Analysis of Asbestos and Asbestos Products Exports
and Imports .................... 79
18. Selected Statistics for the Asbestos Manufacturing
Industry ..................... 8°
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LIST OP TABLES (Continued)
19. Selected Statistics for the Asbestos Products In-
dustry 81
20. Asbestos Uses 82
21. 1967 List of Manufactured Asbestos Products ... 85
22. Asbestos Product Manufacturing Plants, 1963 ... 87
23. Penetration of Fibers Through Nasal Hairs .... 93
24. Particle-Mass Relationship of Asbestos as a Function
of Fiber Length 93
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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. More recently, certain rare cancers,
pleural mesotheliomas and peritoneal mesotheliomas, have been
associated with inhalation of asbestos fibers by asbestos
1 -j /• g2
workers. Heimann 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
81
found as early as 1927 when Haddow 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-
tors121'175'186'202'226 have reported finding neighborhood
cases. The subject of nonoccupational environmental exposure
to asbestos assumed a new dimension beginning with the re-
— ^ i £
ports of Thomson and his colleagues. 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
40 43
to one-half of the population in Pittsburgh, * San Francisco,
Milan, Glasgow, New York, Montreal, Jerusalem,
167 R5
Finland, and Sweden have "asbestos bodies14 in their lungs.
These findings indicate that either these asbestos particles
or other particles that resemble asbestos in many ways, 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, and 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 M- 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. The British Occupational Hygiene Society
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
i
years later. Once established, asbestosis progresses even after
the exposure to dust ceasess illness or death can occur long
after exposure to concentrations not producing immediate effects. 3/
The prolonged latency period between exposure and the
first signs of asbestosis makes it difficult to establish dose-
43
time relationships. Cooper suggested that a time-weighted
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average concentration of asbestos fibers of 5 mppcf* is too
234
high. He cites Wells' 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
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
26
Bohme, 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 years1 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
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 et al. 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 Pleura! Calcification and Plaques
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-
fication can be readily identified by X-ray.
120
Kiviluoto 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
121
asbestos exposure. This investigator 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. Raunio186 continued the study and found 1,516
adult cases of pleural calcification from 633,201 X-rays taken
in 13 Finnish towns and 106 rural communes. 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, Meurman167 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^05 an(j Bulgaria238 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 e_t a.1,. 24,25 concluded that they
were suffering from impaired health caused by air pollution
from asbestos plants.
2.1.3 Cane er
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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8
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
149
quarter of this century. In 1935, Lynch and Smith in the
United States described lung cancer found during autopsy of a
patient with asbestosis. According to Homburger's data,
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.
147
Lynch and Cannon in 1949 found lung cancer in only
three cases (7.5 percent) of 40 patients with asbestosis.
Gloyne 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
OQ
Bohlig, Jacob, and Kalliabis. 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
19
review, Behrens reported 44 cases of lung cancer (14 percent)
in 309 autopsies of patients with asbestosis. After examining
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9
the data of various authors, Isselbacher et al. reported
that of 603 persons with asbestosis, lung cancer was found in
83 (13.8 percent) at autopsy. Hueper and Doll 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.
33
Braun and Truan found lung cancer in 12 (three cases
were not conclusive) of 187 workers in the Canadian asbestos
96
industry who had died. Boehme 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
114
the beginning of work to death was 28 years. Keal 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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10
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 has suggested that the
probability of cancer induction is proportional to the number
of asbestos fibers/ number of susceptible cells, the concen-
tration of carcinogens on the fibers/ and the time from
expo sure.
Why asbestos is carcinogenic is not clearly understood.
At least three hypotheses have been advanced5
(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
DP
then produce the cancer. Harington and Roe have shown that
(a) chrysotile contains little or no benzo(a)pyrene, but about
100 |ag of chromium per g of fiber and 5,000 |ag of nickel per g
of fiber; (b) crocidolite contains 0.2 to 24 jag 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 Hg of benzo(a)pyrene per 100
g of fiber, 100 |-ig of nickel per g of fiber and 15 ug 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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11
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.
83
In addition, Hammond 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
199
asbestos workers, he and his colleagues 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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12
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 mesothelioma. 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
OOfi
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 in 1955, Bonser
30
et al. described a series of 72 autopsies on patients with
asbestosis in. which four cases of peritoneal mesothelioma were
152
found. Subsequently, Mancuso and Coulter found five
peritoneal mesotheliomas in 1,495 asbestos workers, and
102
Hourihane, 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
-------
13
of these patients had pulmonary asbestosis, even though in a
few there was no history of exposure to the asbestos dust. In
103
a subsequent study Hourihane found 74 cases of mesothelioma
in a London hospital over a 10-year period.
31
Borow et al. 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
commercial use.
In an attempt to determine whether mesothelioma of the
serosal surfaces was related in any way to asbestos exposure
198
in the United States, Selikoff et al. 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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14
A series of 83 patients from the London Hospital with
a diagnosis of mesothelioma (confirmed by necropsy or biopsy)
176
were studied by Newhouse and Thompson 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.
198
Selikoff reviewed, 31,652 deaths among the general popula-
tion of over 1,048,183 in the United States and found only
195
three cases of mesothelioma. Moreover, he 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
132
of death among asbestos workers. Kogan et al. in 1966
reported 14 cases (31.1 percent), 11 women and 3 men. Pour of
the women died of uterine cancer, two of intestinal cancer, two
of breast cancer, and 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 Svnergism
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.
1 QQ
Selikoff et al.. " 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 OP ASBESTOS INSULATION
WORKERS IN NEW YORK, 1963-67199
(By smoking Habits)
Smokina Habits
No. of
Cases3
Observed
Deaths
Expected
Deaths
Never smoked regularly 48 0 0.05
History of pipe, cigar-
smoking only 39 0 0.13
History of regular .
cigarette smoking 283 24 2.98
Total 370 24 3.16
aAll with more than 20 years from onset of exposure
1
cigars
Includes cigarette smokers who also smoked pipes or
The blue asbestos, crocidolite, from South Africa is
believed by many53'79'136'140'209 to be much more carcinogenic
167
than the other minerals of asbestos. Studies in Finland
226
indicate that anthophyllite also produces cancer. Wagner,
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17
Smith et al., and recently Godwin and Jagatic, reported
that they had induced mesothelioma in mice using chrysotile.
..Moreover, animal experiments76'78'98-100'113'172'225'228 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
87 8Q 1 'iQ
crocidolite contains the most benzo(a)pyrene. °?,±->? A11
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 body1' 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 M. in diameter and
-------
18
20 to 100 |Ji 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
naked fiber.
There is no doubt that the "asbestos bodies" formed in
the lungs of the asbestos workers contain asbestos. Stumphius
210
and Meyer 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
7Q 1 Q4
they contain any asbestos at all. /y'J-yi* This subject xs
CO "7Q 7QO
currently being debated by several investigators.30''y'*^y 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—
-------
19
can be produced from ceramic aluminium silicate, glass fibers,
915
and silicon carbide fibers. However, Thomson claims that
a skilled pathologist can tell the difference. This contro-
co 194
versy should soon be resolved, since both Gross and Selikoff
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
214
scanty, although in some instances the bodies were numerous.
214
In most of the investigations, the method of Thomson 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. In one recent study in
220
Pittsburgh, Utidjian et al.. 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
-------
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-
40
able 41 percent reported by Cauna (see Table 6 in the Appendix)
for residents of Pittsburgh.
TABLE 2
DISTRIBUTION OF "ASBESTOS (FERRUGINOUS) BODIES1'
IN LUNGS IN PITTSBURGH220
Sex
Men
-
Total
Women
Total
No. of
Cases
1
21
15
19
56
2
29
8
5
44
Mean
Aqe
89
62
64
70
65
29
57
68
64
60
Fibers/Unit
of Lunq
0
1
2-5
>5
0
1
2-5
>5
Distribution
(Percent)
2
37
27
34
100
5
66
18
11
100
2.2 Effects on Animals
2.2.1 Commercial and Domestic Animals
121
Kiviluoto 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.
-------
21
182
Peacock and Peacock 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."
234
Wagner described experiments with rats in which 600
animals were exposed to various minerals of asbestos. The
results are given in Table 3.
7fi
Gross and De Treville made the following observations
in studies on rats, hamsters, and guinea pigs. In rats that
have inhaled high concentrations (86,000 i-ig/m3) 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
-------
TABLE 3
TYPE AND NUMBER OF TUMORS INDUCED BY INTRAPLEURAL
INOCULATION OP S.P.F. RATS WITH ASBESTOS234
Asbestos
Minerals
Croc . Ia
Croc. IIb
Amosite
Chrysotile
Silica
Saline
Total
Animals
Exposed
100
100
100
100
100
100
600
Animals
Died
19
10
4
25
11
5
74
Misc.
Nonmaliq.
5
4
1
5
1
2
18
Misc.
Tumors
1
1
1
3
Reticulum— cell
Sarcomas
1
1
2
2
2
8
Mesothelioraas
12
6
2
18
7
45
Crocidolite from Northwest Cape, South Africa,
Crocidolite with oil extracted from it.
to
to
-------
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 ug/m3. 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
76
2.1. Gross and De Treville also observed a decrease in fiber
content -as the time from end of exposure increased.
98
Holt et al. suggest from their observations on rats
that fibrotic lesions in the lungs are caused by asbestos
fibers (chrysotile) which are less than 3 M. 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 et al. 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"
-------
24
were observed along with asbestos fibers. After 226 days the
lungs of animals dusted for more than 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.^^
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
1 ~ _tfmiimilllll^^^^^
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
218
Hygienists 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
-------
25
(5 mppcf), based on total dust count and on an 8-hour day, 40-
hour week. This value was recommended by Dreessen et al.
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
Q O
(10 particle-years per m ). For example, maximum doses of
6 Q
0.056 mppcf-years (2 x 10 particle-years/m) for 50 years,
fi o
0.112 mppcf-years (4 x 10 particle-years/m ) for 25 years,
or 0.28 mppcf-years (10 particle-years/m^) 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/m3)
Negligible 0-0.4
Low .5-1.9
Medium 2.0-10
High Over 10.0
Only fibers longer than 5.0 |a in length with a 3:1
length-to-breadth ratio are counted.
With these standards the risk of asbestosis may be
reduced to 1 percent; that is, 1 percent of the workers exposed
to a dose of 10 particle-years/m 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) Amphiboles—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
93
the United States. Table 8 in the Appendix lists the world
production. Prom 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
120
observed to suffer from asbestosis.
i
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 the
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. Pour
-------
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.
Amphibole asbestos was mined by Powhatan Mining Co.
near Burnsville, Yancey County, N.C. Their output increased
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
-------
28
A * X
was used for roads-tone.
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,
133
and Raunio. They found asbestos dust at distances up to
50 km from the mines, including dust-fall rates ranging from
•? 2
1.52 g/100 nr/month at 4 km to 34.6 g/100 m /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.
234
Schepers 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 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
-------
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
Northwest Cape Province
Transvaal
Dust Count, mppcf (mppnr*)
Mines
2.8-24 (100-840)
2.3-6.5 (80-228)
Mill
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.
-------
30
Thousands of Short Tons
U.S. WORLD
CONS. PROD.
900
800
700
600
500
400
3,500
3,000
2,500
2,000
1,500
1,000
U.S. CONSUMPTION
1945
1950 1955
WORLD PRODUCTION
1960 1965
1970
FIGURE 1
Comparison of Trends in World Production and U.S.
Consumption of Unmanufactured Asbestos '
-------
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.
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.^
' ?4 75
Bobyleva et. al.."6*' 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
Hg/m3. at 1.0-1.5 km it was 3,000-33,000 ug/m3; and at 0.5 km
it was 6,000 to 34,000 |ag/ms.
?06
In the United States some attempts 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
The uses of asbestos are numerous. Some products which
use asbestos are the following: asbestos cement which may be
*Extrapolated.
-------
32
applied as mortar or plaster, or sprayed on walls; insulating
materials for the covering of pipes, dacts, 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,
108
plastics, and similar materials.
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 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 2''' 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-
tenance. 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" 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
195
have a high exposure to asbestos. 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
195
working on the job with people handling asbestos.
3.4 Environmental Air Concentrations
Only one estimate of the environmental air concentrations
of asbestos in the United States was found. Smith and Tabor206 have
roughly estimated that urban air in the vicinity of heavily
3
traveled streets contains 600 to 6,000 particles/m . They
indicate that the validity of these values is highly suspect
because the methods available for the determination of asbestos
-------
34
are inadequate at the concentrations found in the urban air,
-------
35
4. ABATEMENT
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. 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 fireproof ing 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-
34
tion sites.
-------
36
No information has been found on the abatement methods
used in United States asbestos mines and in asbestos mills
near the mines.
-------
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
95
industry in Britain, show that the dust extraction equipment
1
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.
-------
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 |a
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
205
Control Administration.
*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.
-------
39
Modern analytical methods and instrumentation used in
the asbestos industry are listed below:
Microscopic particle counting of samples on membrane
filters1'2'14'15'57'97'136'187
Thermal precipitators1'2,97,136,187
impingers1'2'14'15'136'187
Royco particle counter1'2'136'187
Mass concentration methods1'14'136'187
Microsieving116
1 1 Ft
Digestion-1--1-0
Column chromatography of organics adsorbed on the
surface116
X-ray diffraction14'46'47'116
Low-temperature ashing116
Atomic adsorption spectrophotometry14'116
11 f\
Electron microprobe^ °
Neutron activation116
Owens jet counter1'2
Konimeter1'2
-------
40
7. SUMMARY AND CONCLUSIONS
Asbestos is an air pollutant which carries with it the
potential for a national or worldwide epidemic of lung cancer
or mesothelioma of the pleura or peritoneum. Asbestos bodies
have been observed in random autopsies of one-fourth to one-
half of the population of Pittsburgh, Miami, and San Francisco
and will probably be found in the people of every large city.
Although asbestos has been shown to produce asbestosis, lung
cancer, and mesothelioma in asbestos workers, the relationship
between "asbestos bodies" and cancer or asbestosis has not
been determined.
The latent period required to develop asbestosis, lung
cancer, or mesothelioma is 20 to 40 years, and the exposure
required to cause asbestosis has been estimated to be 50 to
60 mppcf-years. No such exposure relationship has been es-
tablished between asbestos and lung cancer or mesothelioma.
Asbestosis, lung cancer.- and mesothelioma are all diseases
which, once established, progress even after exposure to dust
ceases.
Experiments with animals have shown that animals may
develop asbestosis or cancer after inhaling asbestos.
No information has been found on the effects of asbestos
air pollution on either plants or materials.
The likely sources of air pollution appear to be the
vast number of asbestos products used in our modern society,
particularly in the building industry. Mines, factories, and
-------
41
shipping yards may also constitute pollution sources.
The world production of asbestos has approximately
doubled over the past 10 to 12 years, whereas the domestic
consumption has apparently remained relatively constant.
These results indicate that while the asbestos air pollution
problem of the world may be increasing, the air pollution
potential in the United States has remained relatively un-
changed. The increase in the number of lung cancer or mesotheli-
oma cases reported in the current literature may be due to
increases in asbestos use that occurred 20 to 40 years ago.
Moreover, the effects of the asbestos being inhaled today may
not be reflected in the general health of the population until
the 1990's or the next century.
The number of people exposed to asbestos has been esti-
mated to be 100,000 asbestos workers, 3.5 million people working
in areas where asbestos is handled in ways which emit small
quantities of dust, and 50 to 100 million people who have
breathed or will breathe enough fibers to show positive "asbestos
bodies" at autopsy.
No measurements have been made of the concentration of
asbestos in urban air. A single estimate of 600 to 6,000
particles per cubic meter has been reported.
Bag filters are used to control asbestos in the exhaust
gases from asbestos factories. Wetting the asbestos or its
products has also been used to keep the dust from becoming
airborne. The cost of abatement equipment in a British factory
-------
42
amounted to 27.5 percent of the total factory cost and
approximately 7 percent of the operating cost. Similar data
on the costs of abatement or economic losses due to asbestos
air pollution in the United States were not found.
No satisfactory method is available to determine the
asbestos content at the concentration found in the ambient air.
One method is presently under development.
Based on the material presented in this report, further
studies are suggested in the following areas:
(1) Identification of the fibers in the lungs of
deceased members of the general public should be completed.
(Two studies are in progress.)
(2) The relationship between these "asbestos bodies'1
and lung cancer or mesothelioma should be determined.
(3) The time-concentration relationship between inhala-
tion of asbestos fibers and lung cancer and mesothelioma should
be determined.
(4) Methods must be developed to determine the asbestos
concentration in air. (One method is under development.)
(5) The concentrations of asbestos fibers in urban air,
near mines and factories, and in the vicinity of building
construction and demolition should be measured.
(6) The methods and cost of control of asbestos emission
from mines, construction or demolition sites, and other normal
uses should be determined.
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43
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57
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61
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-------
APPENDIX A
-------
APPENDIX
TABLE 5
CANCER OP THE LUNG AMONG ASBESTOS WORKERS
43
Place
United Kingdom
United Kingdom
United Kingdom
United Kingdom
Quebec
Pennsylvania
New York &
New Jersey
Population Studied
Reported deaths from
asbestos
Cases of asbestosis in
1,247 autopsies with
pneumoconiosis
Asbestos textile workers,
industry areas , 20 years '
or more exposure
Reported deaths from
asbestosis
Chrysotile miners and
mill workers with over
5 years ' employment
Workers in asbestos
products plant employed
in 1938-39, aged 25-64
Insulating workers, over
20 years ' union membership
No. of
Workers
235
121
113
365
5,958
1,495
632
Years
Followed
1924-1947
1922-1953
1924-1955
1950-1955
1940-1960
1932-1962
No. With
Lung
Cancer
31/235
(13.1%)
17/121
11/39
deaths
65/365
(17.8%)
9/187
deaths
19/186
deaths
45/255
deaths
Comparison
Groups
Silicotics
(1.32%)
Silicotics
(6.9%)
0.8
Expected
en-
Expected
5.61
Expected
6.6
Expected
(continued)
u>
-------
APPENDIX
TABLE 5
CANCER OF THE LUNG AMONG ASBESTOS WORKERS (Continued)
Place
California
Dresden
United States
United Kingdom
Bulgaria
New York
Pennsylvania
Population Studied
Insulating workers,
mixed, 15 years in
trade, aged 35-64
All asbestos trade
mixed exposures
Asbestos textile workers
employed in 1948-1951,
aged 15-64
Reported deaths from
asbestosis
Agricultural workers near
an asbestos mine
Asbestos insulators em-
ployed more than 15
years, aged 40-80
Asbestos textile and
friction workers
No. of
Workers
529
2,636
2,833
584
3,325
152
68
Years
Followed
1954-1957
1924-1963
1951-1963
1924-1963
1962
1945-1965
1957-1962
No. With
Lung
Cancer
10/41
deaths
34/150
deaths
24/285
deaths
146/584
(25%)
155/3325
asbestosis
18/46
deaths
13/68
deaths
Comparison
Groups
2.8
Expected
11.4
Expected
11.9
Expected
3.1
Expected
-------
APPENDIX
TABLE 6
"ASBESTOS BODIES" IN CONSECUTIVE OR RANDOM AUTOPSIES
Location
Capetown
Miami
Pittsburgh
Milan
Tyneside
Jerusalem
Glasgow
Finland
Sweden
Total
Cases
500
500
100
100
311
100
100
264
34
%
Posi-
tive
26.4
27.2
41
51
20.3
26
23
57.6
35.3
% Positive by Aqe*
<24
.5
(4.3)
0
0
(0)
0
(0)
r"«M
0
1.5
(57)
0
25-34
2.4
(25.6)
0
5
(83)
(<
0.3
(25)
(14)
0
3.0
(57)
0
35-44
4.4
(28.4)
1
(16.1)
5
(46)
3
(14)
1.6
(19.2)
t W «ff
>){<-
0
3.8
(71)
0
45-54
4.6
(22.4)
3.4
(23)
3
(38)
— -i >)
2.9
(17.3)
1
(12)
8.7
(55)
0
55-64
7.4
(31.6)
5.6
(27.2)
13
(54)
30
(60)
4.8
(18.5)
. 7—5>«.
(21)
4
(22)
20.0
(64)
11.7
(80)
65-74
7.4
(28.0)
9.2
(30.6)
8
(40)
7.7
(28.9)
i n
(30)
11
(32)
16.7
(58.7)
14.7
(25)
>75
90
(31.9)
6
(30)
18
(66)
2.9
(15)
- V
... .>)
7
(19)
3.8
(34.5)
18.8
(43)
Sex
% Positive*
Female
7.8
(20)
8
(20.4)
16
(34)
16
(44)
4.2
(13)
10
(29.1)
0
(0)
23.9
(54.3)
14.7
(38)
Male
18.6
(30.4)
19.2
(31.6)
25
(47)
35
(54)
16.1
(25.5)
16
(22.2)
23
(37)
33.7
(60)
20.6
(33)
Year
of
Study
1960
1961
1964
1966
1967
1967
1967
1966
1966
Refer-
ence
214,216
214,216
40
67
11
184
188
167
82
(continued)
-------
APPENDIX
TABLE 6
"ASBESTOS BODIES" IN CONSECUTIVE OR RANDOM AUTOPSIES (Continued)
Location
Johannesburg
San Francisco
Belfast
London
Montreal
New York
.Total
Cases
200
50
100
355
%
Posi-
tive
39.2
42
20
6
48
50.5
% Positive bv Aqe*
<24
25-34
«•-
35-44
3 >
(30)
45-54
•tfiJ R
(50)
55-64
65-74
^ 07
(50)
>75
% Positive*
Female
16
(36)
3.9
(29.8)
Male
32
(57)
46.5
(53.7)
Year
of
Studv
1965
1966
1965
1964
1966
1966
Refer-
ence
234
43
60
102
7
195
*Numbers in parenthesis represent percentage of group-age or sex.
-------
APPENDIX
TABLE 7
COMPOSITION AND PROPERTIES OP ASBESTOS MINERALS
66
Approximate Formula
Percentage of Manor Components
Silica SiO2
Alumina A12O3
Ferrous Oxide FeO
Ferric Oxide Pe2O3
Manganous Oxide MnO
Calcium Oxide CaO
Magnesium Oxide MgO
Sodium Oxide Na2O
Potassium Oxide K2O
Carbon Dioxide CO2
Water of Crystallization H2O
Chrysqtile
3MgO-2Si02'2H20
40.3
0.7
1.0
1.5
0.2
42.4
0.2
13.7
Crocidolite
Na2O-3FeOFe2O-
8SiO2-H2O
51.4
20.3
17.5
0.1
0.8
1.4
6.2
0.4
1.9
Amosite
1.5 MgO-5.5FeO-
8SiO2'H2O
49.3
40.9
0.4
0.7
0.4
5.7
0.2
0.3
0.2
1.9
(continued)
-------
APPENDIX
TABLE 7
COMPOSITION AND PROPERTIES OF ASBESTOS MINERALS (Continued)
Approximate Formula
Trace Organic Impurities
Oil-wax (mg/100 g fiber)
Benzo ( a )pyr ene
(ua/100 a fiber)
Trace Inorganic Impurities
(ug/g fiber)
Pb
Sn
Ga
Bi
V
Mo
Cu
Ti
Ag
Hi
Zv
Co
Mn
Cr
Chrvsotile
3MgO-2Si02-2H20
4-7.6
none detected
2
<5
<2
<5
50
<2
35
50
<0.2
5,000
(1,000-14,000)
<200
<5 (<100)
130 (400-500)
1,000 (400-900)
Crocidolite
Na20-3FeOFe20-
8SiO2 'H2O
4-200
0.2-24
5
<5
<2
<5
<2
<2
7
50
0.2
<10
«100)
700
<5 (<100)
180 (200)
20 (<100)
Amosite
1.5 MgO-5.5FeO-
8SiO2 *H2O
4-20
0.2-2.4
20
<5
2
<5
<2
<2
7
300
0.2
1,000
(<100)
1,000
<5 (<100)
7,000 (7,900)
150 (<100)
00
(continued)
-------
APPENDIX
TABLE 7
COMPOSITION AND PROPERTIES OP ASBESTOS MINERALS (Continued)
Approximate Formula
Radioactive Contaminants
(liUc/g fiber)
K40
Th238
Ra226
Chrvsotile Crocidolite Amosite
0.14 0.02 0.55
<0 . 01 0 . 05
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"
Harsh to soft
Very high
Very good
Poor
Fair
Good
V to 6"
Coarse but pliable
Fair
Good
Good
Fair
CTi
-------
APPENDIX
TABLE 8
WORLD PRODUCTION OF ASBESTOS
(Short Tons)
170
Location
1962
1963
1964
1965
1966
b,e
North America
Canada (sales)
United States
(shipments)
1,215,814
53,190
South America
Argentina 203
Bolivia (exports) . . 56
Brazil 4,900a
Europe
Austria 503
Bulgaria . 1,323C
Finland^ 10,869
France 28,034C
Greece
Italy 60,860
Portugal
U.S.S.R. ....... 710,000a'c
Yugoslavia 7,401
Africa
Botswana ....... 2,375
Kenya 212
Mozambique 370
Rhodesia, Southern . . 142,195°
South Africa 221,302
Swaziland ...... 32,830
United Arab Republic . 606
1,275,530 1,420,769
66,396 101,092
365
10
l,440f
638
1,323C
10,201
26,094C
74
63,016
29
755,000a'c
9,074
2,368
78
142,254°
205,744
33,350
192
542
7
l,430a'c'f
1,433G
11,611
24,289C
65a
75,573
810,000a'c
9,280
2,161
204
153,450
215,592
39,862
1,739
1,387,555 1,479,281
118,275 125,928
243C
3
1,204
1,433
13,307
7,506C
85a
79,214
53C
865,000
10,585
888
136
176,149°
240,752
40,884
3,225
24 Oc
4
1,820
1,430*
13,250
7,720a
85a
90,464
10
925,000a
8,411
880a
73
175,000a
276,597
36,142
2,057
(continued)
-------
APPENDIX
TABLE 8
WORLD PRODUCTION OF ASBESTOS (Continued)
(Short Tons)
Location
Asia
Cyprus
India
Japan
Korea , South ....
Philippines
Turkey
Oceania
Australia
New Zealand
World Total3 . . .
1962
100,000
22,391
1,865
15,407
1,333
1,037
525
709
18,416
457
2,655,000C
1963
110,000
19,962
3,038C
18,210
2,120
421
604
408
13,374
439
2,760,000C
1964
130,000
13,755
3,710C
17,979
1,402
586
526
1,291
13,545
3,050,000C
1965
140,000
17,622°
4,989
16,451°
1,710C
883
1,376
11,647
3,140,000C
1966b'S
140,000
24,449
7,646
17,067
687
721
1,258
13,472
3,350,000
aEstimated.
Preliminary.
c
Revised.
Asbestos 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.
^Includes asbestos flour.
-------
APPENDIX
72
TABLE 9
THE PRODUCTION AND APPARENT CONSUMPTION
OF ASBESTOS IN THE UNITED STATES41'170'171
Quant d
Year
1967
1966
1965
1964
1963
1962
1961
1960
1959
1958
1957
1956
1955
1950
1945
1940
1935
Production
123,190
125,928
118,275
101,092
66,396
53,190
52 , 814
45,223
45,459
43,979
43,653
41,312
50,431
.ties
in Short Tons
Imports
645,
726,
719,
739,
667,
675,
616,
669,
713,
644,
682,
689,
716,
110
459
559
361
860
953
529
945
047
331
732
910
480
Values (X
Exports Consumption
47,
46,
43,
27,
10,
2,
3,
5,
4,
3,
2,
2,
7,
1,000)
710 720,580
996 805,391
126 794,708
147 813,
044 724,
949 726,
799 (665,
525 709,
461 754,
026 685,
893 723,
950 782,
001 759,
727,
378,
270,
170,
306
212
194
440)
193
045
284
492
272
910
002
030
000
000
Exports
Year
1967
1966
1965
1964
1963
1962
1961
1960
1959
1958
1957
1956
Production
$11
11
10
8
5
4
4
4
4
5
4
4
4
,100
,056
,162
,143
,108
,677
,347
,231
,391
,127
,918
,742
,534
Imports
$66
73
70
72
61
64
(63
63
65
58
60
61
59
,000
,100
,457
,973
,739
,112
,000)
,345
,006
,314
,104
,939
,339
Asbestos
$6
5
5
3
1
1
,030
,763
,294
,199
,304
598
759
857
793
424
350"
375
,497
Asbestos Products
$21,963
19,139
16,288
16,267
14,274
13,233
15,223
14,181
12,464
-------
APPENDIX
TABLE 10
REGIONAL DISTRIBUTION OP ASBESTOS MINING AND PROCESSING
(Ranking and Production)
170,171
Rank
1
2
3
4
State
1960
Vt.
Ariz.
N.C.
Calif.
1964
Calif.
Vt.
Ariz.
N.C.
1966
Calif.
Vt.
Ariz.
N.C.
Quantity. (Short Tons)
1964
55,041
*
*
*
(55,041)
1965
74,587
*
3,469
*
(78,056)
1966
81,671
*
*
*
(81,671)
Value (X 1,000)
1964
$4,419
*
*
*
(4,419)
1965
$6,177
*
441
*
(6,177)
1966
$6,945
*
*
*
(6,945)
*Data withheld to avoid disclosure of producer's confidential information to
the Bureau of Mines.
00
-------
APPENDIX
TABLE 11
ASBESTOS MINES IN THE UNITED STATES, 1966
170
State
California .
/
Vermont
Arizona
North Carolina
Mineral
Chrysotile
Chrysotile
Chrysotile
Chrysotile
Chrysotile
Chrysotile
Chrysotile
Chrysotile
Crocidolite
Production
Rank*
1
2
3
4
1
1
2
3
1
Name of Producer
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?
LeTourneau Asbestos Corp.a
Powhatan Mining Co.
Location — Coun v or City of
Mine
Fresno County
Fresno County
Ca laveras
County
San Benito
County
Nap a
Orleans County
(Lowell)
Salt River
Valley
(North of
Globe)
Yancey County
tBurnsville)
Processing Plant
Near Mine
Near Mine
Near Mine
Monterey County
(King City)
fRanlced by production only within the State.
**Not in operation during previous years.
-------
75
APPENDIX
TABLE 12
APPARENT ASBESTOS CONSUMPTION, 1965170
(In Thousands of Short Tons)
Use
Asbestos Industry Production
Mining and Processing
Asbestos in Products
Textiles
Cement
Friction Materials
Asbestos Paper
Floor Tile
Paints, Roof Coating, Caulks
Plastics
Miscellaneous
Total Products
World97
66
2,190
111
220
307
85
21
221
3,221
United States*
78
17
548
28
55
77
21
5
55
806
*Based on 25% of world consumption.
-------
76
APPENDIX
TABLE 13
PROPORTION OF ASBESTOS IN VARIOUS ASBESTOS PRODUCTS170
Product
Percent.
Asbestos*
Asbestos textiles
Asbestos cement
Friction materials and gaskets
Asbestos paper and products
Floor tile
Other asbestos products
80-100
15-90b
30-80
80-90
10-30
c
U.D.
aChrysotile asbestos is used unless otherwise stated.
^15% to 90% chrysotile, with some materials containing as
much as 85% amosite and small amounts of crocidolite and antho-
phyllite.
GThese products contain undetermined quantities of
chrysotile, tremolite, actinolite, and anthophyllite.
TABLE 14
QUANTITY AND VALUE OF ASBESTOS INPUT BY INDUSTRY 1963170
Product
Asbestos textiles
Asbestos cement
Friction materials
and gaskets
Paper and products
Floor tile
Paint and coating
fillers
Plastics
Other
Total
Quantity
Short
Tons (000)
66
2,190
111
220
307
85
21
220.7
3,220.7
Fraction
of Total
0.02
0.68
0.04
0.07
0.09
0.02
0.01
0.07
1.00
Value
$(000,000)
26.4
328.5
11.1
19.8
13.2
3.7
9.2
19.7
423.3
Fraction
of Total
0.06
0.78
0.03
0.05
0.03
0.01
0.04
1.00
-------
77
APPENDIX
TABLE 15
POPULATION GROUPS WITH OCCUPATIONAL AND ENVIRONMENTAL
EXPOSURE TO ASBESTOS108
Occupational Groups
Nonoccupational 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
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
-------
78
APPENDIX
TABLE 16
ASBESTOS CONTROL EQUIPMENT95
Cost Data
Asbestos Textile Industry3
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 Mines*5
Dust extraction equipment
Total capital cost (TCC) ~ $ 360,000
(TCC/TCC of plant) x 100 ~ 27.5%
Operating cost (per year) ~ $ 195,000
Specif ications
Asbestos Textile Industry3
Volume of dust-containing air
extracted from textile machines 1,000,000 ft /min or
700 ft^/min/operative
Quantity of asbestos dust filtered
per year (at above rate) 700 tons or
2.8 tons/working 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.
^Figures 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
TABLE 17
ANALYSIS OF ASBESTOS AND ASBESTOS PRODUCTS EXPORTS AND IMPORTS
170
Short
1965
Crude and spinning fibers
Nonspinning fibers
Waste and refuse
i
1
24
17
,251
,221
,523
Exports
Tons
1966
1,455
28,017
17,218
Re-exports
Dollars
1965
326
3,622
1,323
(000)
1966
325
3,973
1,414
Short
1965
50
81
Tons
1966
176
130
Dollars
1965
10
13
(OOP)
1966
30
21
Total
Gaskets .and packing
Brake lining
Clutch lining (number)
Textiles and yarn
Shingles and clapboard
Asbestos-cement
Sub total
Other products
Total
42,995
46,690 5,271 5,712
131
306 23
2,
If
3,
020,
5,
6,
732
065
864
794
465
101
2,
3,
2,246,
10,
4,
678
630
986
900
010
742
4,
4,
1,
1,
1,
1,
528
728
691
067
096
588
5,
5,
1,
1,
1,
1,
261
236
897
326
797
332
14,698 16,849
4,389 5,058
19,087 21,907
Imports
Short Tons
1 1
5,000 5,000
113 231
5,114 5,232
Dollars (OOP)
1
2
4
37
44
8
52
51
1
2
1
41
45
11
56
1965
1966
1965
1966
Chrysolite
Crude
Spinning/
Textiles
All Other
Total
Crocidolite
Amosite
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
6,319
56,308
70,454
73,100
-------
80
APPENDIX
TABLE 18
SELECTED STATISTICS FOR THE ASBESTOS MANUFACTURING INDUSTRY41
(Employment Size)
Number of
Employees*
1-49
50-99
100-2,499
over 2,500
Total
Number of
Companies
39
6
10
18
73
Number of
Plants
39
6
17
62
124
Number of
Production
Workers
308
231
2,445
12,754
15,738
Value of
Shipments
$ (000)
8,264
4,827
89,131
407,014
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.
-------
81
APPENDIX
TABLE 19
SELECTED STATISTICS FOR THE ASBESTOS PRODUCTS INDUSTRY41
Expenditures (in $000)
New plant and equipment
New structures
New machinery and equipment
Total
Used plant and equipment
Total
1958
2,419
10,418
12,837
428
13,265
1963
2,613
9,768
12,381
1,289
13,670
-------
APPENDIX 82
TABLE 20
ASBESTOS USES85
Textiles:
Varieties used: Chrysotile, crocidolite, and in part
amosite
Yarns and Cordst
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
Sealing 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 rnelters' shields
Slideways in the glass industry
Handles and fire-doors
Auto Parts
Safes
Protective walls
Curtains, etc.
(continued)
-------
APPENDIX 83
TABLE 20 (Continued)
ASBESTOS USES85
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 1ining
Nonwoven: Clutch lining
Transmission lining
(continued)
-------
APPENDIX 84
TABLE 20 (Continued)
ASBESTOS USES85
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)
AsbestosAcid-Resistant Compositions;
Used mostly in chemical industry
-------
85
APPENDIX
TABLE 21
1967 LIST OF MANUFACTURED ASBESTOS PRODUCTS85
Industry and Product Description
Quantity Measure
Miscellaneous Nonmetallic Mineral Products
Asbestos Products
Asbestos Friction Materials
Brake Linings
Woven, containing asbestos yarn,
tape, or cloth
Molded, including all nonwoven types
Clutch facing
Woven, containing asbestos yarn,
tape, or cloth
Molded, including all nonwoven types
Asbestos-Cement Shingles and Clapboard
Siding shingles and clapboard,
including accessories
Roofing shingles
Asphalt Floor Tile
Asphalt floor tile
Vinyl Asbestos Floor Tile
Vinyl asbestos floor tile
Asbestos Textiles and Other Asbestos-
Cement Products
Asbestos textiles
Yarn, cord, and thread
Cloth
Other asbestos textiles, including
roving, lap, wick, rope, tape,
carded fibers, etc.
Asbestos-cement products
Flat sheets and wallboard, all
thicknesses converted to V basis
Corrugated sheets
Pipe, conduits, and ducts, including
pressure pipe
Linear feet
Cubic feet
Thousand pieces
Thousand pieces
Squares
Squares
Thousand square
yards
Thousand square
yards
Pounds
Pounds
Pounds
100 square feet
100 square feet
Short tons
(continued)
-------
APPENDIX
86
TABLE 21 (Continued)
oc
1967 LIST OF MANUFACTURED ASBESTOS PRODUCTS 3
Industry and Product Description
Quantity Measure
Asbestos felts
Roofing-asphalt or tar saturated
Other
Other asbestos and asbestos-cement
products, including millboard 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
Packing (for sealing moving parts)
Asbestos, asbestos-metallic, and
asbestos-rubber
Insulation materials containing
asbestos pipe insulation
Cellular and laminated
85 percent magnesia
Diatomaceous silica, calcium,
silicate, expanded silica, and
asbestos fiber
Other pipe insulation
Block insulation, including sheet
and lagging
85 percent magnesia
Diatomaceous silica, calcium
silicate, expanded silica, and
asbestos fiber
Other block insulation, including
celluar and laminated
All other asbestos insulation
Short Tons
Short Tons
Pounds
Thousand pounds
Linear feet
Linear feet
Linear feet
Linear feet
Thousand
board feet
Thousand
board feet
Thousand
board feet
-------
APPENDIX
87
TABLE 22
ASBESTOS PRODUCT MANUFACTURING PLANTS, 196341
vocation
flew Hampshire
Belknap
Hillsborough
Total
lassachusetts
Essex
Franklin
Middlesex
Suffolk
Worcester
Total
Connecticut
Fairf ield
Hartford
Middlesex
Total
Slew York
Albany
Kings
Orange
Suffolk
Total
Sew Jersey
Bergen
Essex
Hudson
Mercer
Morris
Passaic
Somerset
Union
Total
Total
Plants
1
1
2
1
1
2
2
1
7
3
1
1
5
1
3
1
1
6
1
3
1
2
1
3
4
1
\
16
No. of Plants with Eraplo
1-
19
1
1
2
4
1
1
1
1
2
2
2
1
5
20-
49
1
1
1
1
1
1
2
50-
99
1
1
1
3
1
1
100-
249
1
1
1
1
1
2
3
250-
499
1
1
1
1
2
1
2
1
1
5
lament of
500-
999
1
1
1
1
1,000
or more
1
1
1 (continued)
-------
APPENDIX
88
TABLE 22 (Continued)
ASBESTOS PRODUCT MANUFACTURING PLANTS, 196341
Location
Pennsylvania
Elk
Lancaster
Montgomery
Northampton
Philadelphia Cit}
Potter
Total
Ohio
Cuyahoga
Paulding
Portage
Ross
Total
Indiana
Henry
Huntington
Kosciusko
Lagrange
Lake
Rush
Total
Illinois
Cook
Kankakee
Lake
Will
Total
Michigan
Wayne
Total
Total
Plants
1
1
2
1
3
1 1
9
1
1
1
1
4
1
1
1
1
1
1
6
8
1
4
1
14
1
1
No. of Plants with Employment of
1-
19
2
1
3
1
1
1
1
5
5
1
1
20-
49
1
1
1
1
•^^MWMi
50-
99
1
1
100-
249
1
2
3
1
1
1
3
1
1
2
2
1
3
250-
499
1
1
1
1
2
2
1
1
4
500-
999
1
1
*
1,000
or more
1
1
(continued)
-------
APPENDIX
89
TABLE 22 (Continued)
ASBESTOS PRODUCT MANUFACTURING PLANTS, 196341
jocation
Wisconsin
Milwaukee
Total
Missouri
St . Louis
St. Louis City
Total
Cansas
Barton
Total
Virginia
Essex
Frederick
Norfolk City
•Total
Jorth Carolina
Mecklenburg
Union
Total
South Carolina
Charleston
Marlboro
Total
Georgia
DeKalb
Talbot
troup
Total
Total
Plants
1
1
2
3
5
1
1
1
1
1
3
2
1
3
1
1
2
1
1
1
3
No. of Plants with Emp!
1-
19
1
1
1
1
1
1
1
1
2
1
1
2
20-
49
50-
99
2
2
1
1
1
1
100-
249
2
2
1
1
1
250-
499
1
1
1
1
1
1
ovment of
500-
999
1,000
or more
J— i continued j
-------
APPENDIX
90
TABLE 22 (Continued)
ASBESTOS PRODUCT MANUFACTURING PLANTS, 196341
Location
Florida
Dade
Total
Alabama
Mobile
Total
Mississippi
Hinds
Union
Total
Louisiana
Jefferson
Orleans
Total
Texas
Dallas
EC tor
Grayson
Harris
Hill
Total
California
Alameda
Contra Costa
Los Angeles
Orange
Sacramento
San Benito
San Joaquin
San Mateo
Santa Clara
Total
JNITED STATES
TOTAL
Total
Plants
1
1
1
1
1
1
2
3
3
6
2
1
1
3
1
8
2
1
9
1
1
1
1
1
1
18
124
1-
19
1
1
1
1
2
1
3
1
1
1
1
1
5
40
No,
20-
49
1
1
1
2
3
10
of Plants with Employment of
'56-
99
1
1
1
1
1
3
13
100-
249
1
1
2
1
3
1
2
1
4
4
1
1
6
34
250-
499
1
1
2
1
1
1
1
21
500-
999
4
1,000
or more
2
-------
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?
218
Timbrell has studied the deposition of fibrous
material in the respiratory system. Fibers 50 or even 200 n
long are found in the lungs because the free-falling speed
depends largely on the diameter. Thus, particles less than
3.5 [i (most asbestos particles are less than 0.5 M) 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 M, 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 Society204 as fibers less than 200 M.
long, less than 3.5 [1 in diameter, and having a length-to-
breadth ratio of 3:1. Only the fibers longer than 5 n in
length are counted.
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TABLE 23
PENETRATION OF FIBERS THROUGH NASAL HAIRS218
Length of Fiber
(microns)
0.5
50
100
150
200
250
300
350
% Penetration through Nasal Hairs
1st Stage
100
75
53
31
26
20
17
14
2nd Staqe
100
57
24
10
5
3
2
1
3rd Stacre
100
42
11
3
1
229
Walter 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 [ig contain 5 x 10 particles
of asbestos per |-ig. From this conversion factor the threshold
"limit value for asbestos can be calculated* as approximately
350 |-ig/m (5 mppcf).
TABLE 24
PARTICLE-MASS RELATIONSHIP OF ASBESTOS AS
A FUNCTION OF FIBER LENGTH
Total Concentration^
_ f-**y/ m
Particles*/cirr (approx)
100
200
400
600
100
400
1,000
2,500
Incineration Residue
Ug/nr
(approx)
50-60
200-300
700-800
1,800-2,000
Fiber Length
in Microns
(approx)
< 150
< 500
< 700
<10,000
*Particles counted with a konimeter.
*5 mppcf=177 x 106 p/m3=350 |ag/m3. The concentration
estimated in air is 600-6,000 p/m3=1.2 - 12 x 10~*
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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 (J. and shorter than 200 )a with diameters less than
3.5 H .
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