AxelrodMarc1977

CALIFORNIA STATE UNIVERSITY, NORTHRIDGE
A BUILDING SURVEY
FOR ASBESTOS FALLOUT
A thesis submitted in partial satisfaction of the
requirements for the degree of Master of Science in
Health Science,
Environmental and Occupational Health
by
Marc Harry Axelrod
June 1977
The Thesis of Marc Harry Axelrod is approved:
Steve Zuieback
Meier Schneider
Dennis Kelly, Committee Chairman
CALIFORNIA STATE UNIVERSITY, NORTHRIDGE
ii
ABSTRACT
A BUILDING SURVEY
FOR ASBESTOS FALLOUT
by
Marc Harry Axelrod
Master of Science in Health Science,
Environmental and Occupational Health
A modern sixteen-story office building was surveyed
to determine if erosion of spray asbestos fibres from the
cementitious surface of the air plenum chambers was
contaminating the building air supply system, subjecting the
occupants to a potential hazard.
The NIOSH approved method
of collection and analysis was utilized.
This'consisted of
collecting· the fibres· on a membrane filter, dissolving the
filter on a glass slide, and then counting the fibres
utilizing phase microscopy.
Fibre concentrations were found
to be extremely low and most probably reflect the general
ambient level in the urban environmen·t, as two nearby
buildings that did not incorporate asbestos-based building
materials had comparable levels.
These extremely low levels.
do not appear to be biologically significant.
iii
TABLE OF CONTENTS
TITLE PAGE . . . .
i
SIGNATURE PAGE . •
ii
ABSTRACT.
.
. iii
I
INTRODUCTION.
.
3
II
HEALTH EFFECTS OF ASBESTOS . .
4
Asbestosis . .
4
Respiratory .
.
. . .
Mesothelioma.
.. .
5
9
Risks to General Populations . .
11
III
THE RECOMMENDED STANDARD.
IV
ASBESTOS IN BUILDINGS
16
19
Literature Review .
20
Discussion.
v
.
.
24
MATERIALS AND METHODS
27
Sampling Procedure . .
27
Analysis Procedure . .
29
Estimation of Error .
30
VI
ASSESSMENT OF CITY HALL EAST.
32
VII
SURVEY RESULTS . . . .
35
Airborne Fibre Levels in City Hall . .
35
Discussion and Conclusion .
35
Recommendations
37
38
REFERENCES . . . .
Prima.ry Sources .
38
Secondary Sources
42
APPENDIX.
.
.
.
.
.
.
.
45
.
iv
I
INTRODUCTION
New Jersey School officials closed down eight
schools in suburban Howell township because a pediatrician
had declared that a 13-year-old suffered chronic respiratory
illness caused by asbestos used on some of the school's
:ceilings.
These facts, reported by the Los Angeles Times,
January 5, 1977, are particularly disturbing when one
considers that there are tens of thousands of buildings,
public a::1d semi-public, all over the United States, that
have been sprayed with asbestos-based materials.
Asbestos is a fibrous material found in many
geological formations and it is one of the most valuable and
versatile materials extracted from the earth's surface.
It
is utilized in many products, such as the spray coating on
the New Jersey school ceilings where it provided fireproofing and improved acoustics.
There are seven varieties
of asbestos, all hydrated mineral silicates incombustible in
air and separable into filaments.
Chrysotile (3Mg0"2Si02"
2H 2 0) is the most widely used asbestos type and forms 90% of
the world's output.
The other types are amosite,
crocidolite, tremolite, anthrophyllite, actinolite, and
amphibole.
While this researcher concentrated his efforts on
the possible contamination in one particular building, it
must be emphasized tha·t the possibility of contamination
1
2
·-·
exists in a large number of buildings.
Reitze (1972) states
that the first use of asbestos containing spray materials
for fireproofing buildings was in 1958 and by 1970 well over
half of all large multi-storied office buildings constructed.
in this country were sprayed with an asbestos containing
material.
Through damage or erosion it is possible that
small quantities of asbestos fibres find their way into the
breathing zones of the millions of people who occupy these
buildings during their working day.
This present study was undertaken to ascertain the
possibility of asbestos contamination in the air of a modern.
office building, Los Angeles City Hall East.
Contamination
was suspected because an asbestos containing material was
sprayed on the steel infrastructure of the building and in
the air plenums for fireproofing.
To test this possibility
the building was inspected and the air was sampled for
asbestos fibres.
The results of this survey were compared
with the results from two nearby buildings; City Hall and
City Hall South.
A visual inspection concluded that these
nearby buildings did not incorporate asbestos containing
materials.
The possibility of asbestos exposure to the
inhabitants of this building provided the impetus for this
study.
Inhalation of asbestos fibres can lead to a number
of diseases such as asbestosis, cancer of the lung, and
mesothelioma.
This association betv1een asbestos exposure
_q,:n<i._.disE:ass:. ha._s___p_~_em~VJ§l.l ___~?_t~J?_lj__§h§..;l_a!]._c:1__~~-1.b._)?_~---~~~rr~l~!l~_c:l____ _
3
in the subsequent chapters.
A survey of each of these buildings will be an
enormous undertaking, requiring the commitment of a great
number of people, resources, and time.
This study is
intended as a contribution to this growing area of concern,
in hopes that its findings may help insure the health and
safety of these buildings' occupants.
Hypothesis
The levels of asbestos fibres in the air of Los
Angeles City Hall East do not exceed the present thresholdlimit-value.
@
•
II
HEALTH EFFECTS OF ASBESTOS
The health effects associated with the inhalation of
asbestos fibres are well established and documented.
What
follows is a concise description of the health effects and
the published studies which contributed to their understanding.
Asbestosis
Asbestosis is a consistent pathological change in the
lung, characterized by interstitial, septal, peribronchiolar
or perivascular fibrosis which is eventually visualized by
radiography (ACGIH-AIHA Aerosol Hazards Evaluation Committee,
1975).
It is accompanied by the formation of intra-alveolar
ferruginous bodies.
Sufferers show reduced pulmonary and
vital functions as indicated by forced vital capacity and
forced expiratory volume in one second.
Selikoff (1965)
reports that dyspnea is the main complaint.
Wright (1969)
emphasizes that the term "asbestosis" has recently been
corrupted to include such manifestations as pleural
thickening, pleural plaques, and even the simple presence of
ferruginous bodies.
These inclusions blur the conception of
the disease.
The first reported association between asbestos
exposure and diffuse pulmonary fibrosis was by Murray (1907) .
Cooke (1927), who reported fibrosis of the lung due to
4
5
inhalation of asbestos dust, was another pioneer.
Merewether and Price (1930) demonstrated that asbestosis was.
a threat to the workers in the asbestos textile trade.
Lanza (1938) showed that once established, usually 20-40
years after the first exposure, asbestosis progresses even
after the exposures have ceased.
The manufacturers of asbestos containing products
began to take substantial measures to reduce the concentrations of airborne fibres after the work of Merewether and
Price.
The report of Sayers and Dressen (1939) further
stimulated the introduction of corrective measures, and until
quite recently, served as a guide in establishing thresholdlimit-values for asbestos containing environments.
It should be emphasized that asbestosis is still an
appreciable occupational hazard.
Scansetti (1975), in a
recent study, has found asbestosis in asbestos cement
workers.
Respiratory Cancer
One of the most serious diseases associated with
occupational exposure is respiratory cancer.
Before
examining case studies and epidemiological evidence in this
regard, it is necessary to discuss the environmental
induction of cancer.
Jones and Grendon (1975) propose a theory for the
production of environmental cancers.
First,there is an
alteration
of ----cellular
function
by the carcinogen, followed
--------- ------------------------------ -------------- ----~------
---~
--~
--~------------------------~-----~--------
6
-
by reinforcing interaction by proximal altered cells.
These
interactions are responsible for the relationship between
dose and time of cancer appearance.
Next, organ changes
produced by these cellular alterations reach a level at
which they cause failure of those tissue organizing systems
which normally prevent cancer development.
The failure of
the cancer suppressing mechanism extends from the organ of
origin to the entire body.
Finally, uncontrolled growth
results in death from the malignancy or from intervening
secondary causes.
How asbestos induces changes in cellular function is
not completely understood.
Gross (1967) suggested that the
presence of trace metals plays a role, and later (1973)
found evidence that the locus of pathogenicity resides in
the asbestos fibre's polyfilamentous
structure~
Selikoff
(1968) offers strong·evidence that the carcinogenic role of
asbestos is solely that of a cocarcinogen.
Lung tumors,
according to Reeves (1976), seem to depend on the absorptive
capacity of asbestos fibres, allowing other carcinogens
(heavy metals, polycyclic hydrocarbons, cigarette smoke) to
attain a critical focal concentration.
Although the biochemical role of asbestos in
carcinogenisis is as mysterious as the disease itself, its
association with respiratory cancer in an occupational
context is the subject of a.great body of published accounts.
An association between asbestos and pulmonary
g~!"~-~J!gma __"?_~-~---.:!= ~-!"~.!;.- __ £~_g_9_g11_.t_z ~-?:..c_l2Y'-_l.1.1!1S:b: __<?-_I19-_ ~ J:Il}:_i::Q___LlJ.l~_)__
.____ _
7
Merewether (1949) demonstrated bronchogenic cancer in 13% of
the asbestosis victims in the textile trade.
Despite these
early findings, it was not until fairly recently that an
association with cancer was recognized.
Doll (1955) conducted the first epidemiological
study which indicated increased mortality from lung cancer
in asbestos workers.
Braun (1958) found a slightly elevated
risk of lung cancer in asbestos miners, and Dunn (1960)
found an elevated risk of lung cancer in California asbestos
insulators.
In 1961, the Journal of the American Medical
Association stated that "in the American literature there is
no evidence that there is a relationship between asbestos
and lung cancer."
Evidence was provided shortly thereafter
by Mancuso (1963) who found a relative risk (the ratio of
the incidence rate of those exposed to the incidence of
those not exposed) of respiratory cancer more than three
times greater than expected in asbestos workers.
Shortly
thereafter Selikoff (1964) published data suggesting that
insulation workers had nearly ten times the risk of dying of
·lung cancer than the average American man.
Enterline (1965)
found elevated risks of respiratory cancer among asbestos
products workers.
Asbestos insulators in San Francisco were
found to have elevated risks of lung cancer by Cooper (1968).
Subsequent studies and follow-ups by McDonald (1971) on
asbestos miners; Enterline (1973) on retired asbestos
. 2 .:f9 <1J_1c_ t~.... WQ.ft~ :r:_~_i___w~_gQIJ.~E___ L1~.1-~_L_2!:l: ___I!§!l_U_f a_c:_t:~E.E:!.E_~__2_~--~!_Ci_l<:~----
8
linings and textiles; and Selikoff (1973) on manufacturers
and applicators of asbestos insulation have all reported
elevated relative risks of respiratory cancer ranging from
1.4 to 8.2 times higher than normal.
Enterline (1976) in reviewing many of these studies,
points out a number of shortcomings.
These studies generally
suffer from the lack of information regarding first
exposures, the supplementing of death certificates with
other information in study populations (but not in control
populations), improper groups, lack of exposure data, overlapping exposure and follow up periods in dose response
studies, and failure to adjust for competing causes of
.death.
Despite these pitfalls there has been great progress
in knowledge about the health effects of asbestos.
Some information relating exposure dose to health
effect has accumulated.
Knox (1968) in a continuation of
the study by Doll (1955) showed that the incidence of lung
cancer decreases with progressively smaller total exposures
to asbestos.
Newhouse (1969), also in an asbestos textile
population, reported no increase in incidence of
bronchogenic cancer in a low to moderately exposed group,
whereas in a heavily exposed group the incidence increased
eightfold.
In a series of studies, Mancuso and El-Attar
( 19 6 7) suggested tha·t cancer risk is lower with lower
asbestos exposures.
These observations infer a dose
relationship between bronchogenic cancer and whatever effect
~~l?~_stos fi_!:>E_es___~_9Y.~_J_:f!__~tf3 ___~_9_~§.9:t:.~~~
(l~r:~-~e_!:'--~~-§-~)___·-------~"
9
Mesothelioma
Mesothelioma is a rare cancer of the pleural and
peritoneal membranes, so rare that it is not separately
coded in the International Classification of Causes of
Death.
Only three cases were reported among 31,652 cancer
deaths in a 1959-62 study (Selikoff, 1965).
particularly insidious asbestos-related
It is a
di~ease
because its
latent period has been reported in the literature to be
anywhere between
20~30
years.
Weiss (1953) was the first to suggest a relationship
between mesothelioma and asbestos exposure.
Wagner (1960)
reported 33 cases of pleural mesothelioma occurring after
exposure to crocidolite in the Northwest Cape Province South
Africa.
Many of these individuals had never worked with
asbestos.
Their exposure was associated with living near
asbestos mines, mills, or roadways along which asbestos
fibre was transported.
Newhouse and Thompson (1965),in a
review of 76 cases of mesothelioma in the London Hospital,
found that roughly half were former employees of an asbestos
products manufacturing facility.
Eleven lived within one-
half mile of the asbestos factory and nine lived with
workmen employed in the factory.
Champion (1971) reported
two cases, one of which was exposed from the fibre-laden
workclothes of his father.
Animal studies by Stanton (1972) and Wagner (1973)
indicate that the development of mesothelioma with asbestos
I
•
10
exposure may not be due to its chemical composition, but
rather to its morphology.
The carcinogenicity of these
fibres appear to be related to the structural shapes of the
materials rather than to physiochemical properties.
Reeves
(1976) suggests that mesothelial tumors might arise in
response to mechanical irritation by fibres which may become
lodged during lympathic spread.
The pleura and peritoneum
are subject to constant respiratory movement and are
therefore vulnerable.
Selikoff (1965), in a review of the problem at that
time, concluded that mesothelioma must be added to the risks,
of asbestos inhalation, and join lung cancer and possibly
cancer of the stomach and colon as significant complications
of such exposures.
His own studies of i·nsulation workers
showed 22 deaths from mesothelioma among 532 asbestos
workers who were exposed to mixed asbestos insulation
materials.
Bruckman (1975) points out that a serious implication exists in the risk of developing mesothelioma from
non-occupational exposures.
While current cases are most
likely associated with exposures twenty, thirty, or forty
years ago when world consumption of asbestos was only
500,000 tons per year; neoplasms associated with today's
annual production of over 4,000,000 tons will not be evident
until the 1990's.
The etiological relationship between asbestos
,,
'
11
the evidence is not complete.
The literature is weak in
terms of information regarding exposure values, fibre
variety and size, and extent of occupational exposure.
Risks to General Populations
Evidence has recently accumulated that some
researchers, notably Thomson (1963, 1965) and Selikoff
(1967, 1972), interpret as indicating a health risk to the
general (non-occupationally exposed) public from exposures
to ambient background asbestos contamination of urban and
rural air.
It is necessary to investigate this interpreta-
tion since contamination levels of asbestos fallout in
buildings may approximate urban contamination levels.
In the previous section, some studies were presented
that indicated that mesothelioma has occurred in
occupationally exposed populations and some marginally
exposed individuals.
Can these studies of specific popula-
tions be extrapolated to the point where an increased risk
of mesothelioma is predicted in general populations?
The
roles played by fibre types, the possibilities of
cocarcinogenesis, dosage level and fibre shape and size are
so far from being clear in specialized occupational settings
"as to give little assurance that they can be transferred
in any meaningful way to the non-occupational related or
general public populations" (1ivright, 1969).
The significance of the "curious bodies," tiny,
._i:r-qt:l_-:-:_s:~J.._o:r:~<i__ E_?_~~~~- f?_~~~ __ j._n__:f:h~___l~!?:_SI_~ __<?_f __ ~s_9-~~-i:_?_~-~?r~-~:J:"-~'--
12
first described by Murray (1906), is also open to various
interpretations.
Gloyne (1929) described asbestos bodies
and stated that their formation was the result of a tissue
reaction to a foreign body as a benign irritant.
Many
studies have since appeared indicating their presence at
autopsy of former urban dwellers.
Thomson (1963) reported
asbestos bodies in 30% of men and 20% of women in Cape Town
South Africa.
Cauan (1965) reported finds of 47% and 34%
respectively in adults who had no known connection with an
asbestos industry.
Angivel and Thurbeck (1966) found a
57% incidence of asbestos bodies in men and a 34% incidence
in women who lived in Montreal.
Meurman (1966) found an
overall prevalence of 70% in the urban element of a regional
survey in Finland.
Utidjian, et al.
(1968} report
ferruginous bodies in 99% of men and 96.5% of women in a
similar study.
Selikoff (1972) found asbestos bodies in
48.3% of 3,000 consecutive autopsies.
Ghadgavan and Koss
(1976) found 91.1% of their Baltimore necropsy population
harbored asbestos bodies in their lungs.
The biological
importance of this finding, the authors said, is certain
and speculative.
Utidjian suggests that asbestos bodies
are found in proportion to the intensiveness of the search.
That the above studies have defined the bodies in
morphologically similar terms is undeniable.
That asbestos
is responsible for and exists at the cores of all the bodies
cannot be uncritically accepted.
Crally (1968) lists at
. . J~~~t. ___t:we_~i::Y__f!!~-~~~~!_--~~-]:)_s_t_~Il:~~~---!:~~!:- ar_~
-~2-?E~--~E_!l_Ci t:tE~·-----
13
that ~may be widely disseminated in the environment of the
general public and that produce bodies of identical
appearance, although Meurman (1966) believes that bodies in
longitudinal fission visible by light microscopy are almost
certainly asbestos.
Gross (1968) suggested the term
"ferruginous body" unless the central core can be positively
identified, which Selikoff (1972) attempted with electron
microscopy in a small percentage of his samples.
Granted the presence of ferruginous or possibly
asbestos, bodies in these populations, are they evidence of
a potential hazard?
Botham and Holt's studies (1968) with
animals have suggested that once a fibre is coated it is no
longer pathogenic and that only uncoated fibres produce
pathological effects.
Utidjian's (1968) conclusion is that
there is no evidence that the presence of ferruginous or
asbestos bodies in the lungs of non-occupationally exposed
individuals in urban industrial communities is making any
contribution to pulmonary disease, either inflamatory or
neoplastic.
A recent study seems to support this conclusion.
Breedin and Buss (1976) found no apparent difference in the
incidence or quantity of ferruginous bodies in the lungs of
a group with various pulmonary neoplasms and a randomly
selected group.
Attention has been focused on another phenomenon
said to be the result of past exposure to asbestos fibre.
Pleural plaques, with or without calcification, are a matter
·-
of------·-·-considerable
interest. Extensive plaque
formation in-------- --·.
---- -----·- ------------------------------------------ -----------·-- ----~
---~---------------------------
~-------·--------
14
populations living· iri regions where asbestos· is ·mined or··
used have been reported by Kiviluoto (1960) and Raunia
(1966) in Finland, Rous (1970) in Czechoslovakia and
Burlikov (1970) in Bulgaria.
What is the significance of these findings?
Wright
(1969) points out that the plaques have limited predictability in marking previous asbestos exposure since the
plaques have other causes and their absence does not preelude asbestos exposure.
The two largest concentrations of
pleural plaques, in Finland (Raunia, 1966) and Quebec
(Timbrell, 1969), show no related excessive frequencies of
respiratory cancer or mesothelioma (McDonald, 1974).
The
ACGIH-AIHA (1975) observes that even large calcified plaques
have little effect on respiratory function.
Some researchers are disturbed at the presence of
background levels of fibres in communities with no asbestos
mines or manufacturing operations.
Holt and Young (1973)
report that asbestos fibres have been found in London,
Reading, Rochdale, Prague, Pilson, Johannesburg and
Reyjavik.
In Rochdale, the only one of these cities with
important asbestos industry, Richards and Badami (1971),
have determined an upper limit of 100 nanograms per cubic
meter (ng/m 3 ).
Selikoff (1972) reports chrysotile content
in ambient air around New York City and vicinities, as well
as in Philadelphia, Ridgewood, and Port Allegany ranging
from 10 to 100 ng/m 3 .
These sources point out that the
0
_(lspes:t9?_J9J.1!19 __i_~ __1.1?11.~JJ_y_~_!l__t:i))_Fi~--~_orgt_, ___~!_Q_Q_Q____..l\.___~:t:'___ ~Y:~~l:~l:"
15
in length.
Gross (1974) has concluded that the patho-
genicity of short fibres
negligible.
(less than five microns) is
There is no evidence that these ambient levels
have resulted in a single neoplasm.
This author is in agreement with Wright (1969) who
states "that the risk to the general public posed by the
mostly intermittent exposure to low concentrations of
asbestos likely to be present in the ambient air has been
exaggerated beyond the limits imposed by the known facts."
However, the goal should always be to reduce the exposure
levels of known carcinogens as low as possible.
@ •
III
THE RECOMMENDED STANDARD
A new OSHA standard went into effect on July 1,
1976.
It changed the June 1972 standard, which limited
worker exposure to an eight-hour time-weighted average (TWA)
of five asbestos fibres longer than 5 micrometers per cubic
centimeter (f/cm 3 ) of air, to an eight-hour TWA of 2 f/cm 3 .
This includes a ceiling limit of 10f/cm
minute period.
3
for any fifteen-
An eight-hour average exposure value of
1 f/cm 3 means that a worker breathing 15 liters per minute
for eight hours inhales some 10
and Bouhuys, 1971).
7
fibres every workday (Gee.
The standard also includes
reco~~enda-
tions for environmental monitoring, medical surveillance,
labeling, personal protection equipment and clothing,
employee appraisal, and record-keeping requirements.
The standard has been criticized on several grounds.
The criticisms are that it was designed primarily to prevent
asbestosis and not cancer, that the epidemiological studies
upon which it was based contained too little data on
exposure values, and that the environmental data that was
collected was obtained through a variety of techniques and
expressed in terms other than f/cm 3 .
There is also a
general lack of data that would define a threshold for
carcinogenic substances, other than zero, which would
assu~e
prevention of mesothelioma in all workers.
As
asbestos associated diseases have long latent periods,
16
17
----
twenty years or more, Gee and Bouhuys (1971) believe that
a more sweeping decision on the control of asbestos must be
made now, on the basis of "reasonable probability" rather
than after a delay for a more precise definition of doseresponse relations.
The standard includes a provision that the minimum
countable fibre size be five micrometers in length.
Ruby
and Buchan (1974) believe that the absence of available
clinical and environmental data concerning size distributions of asbestos fibres make it unscientific to permit the
institution of any minimum fibre size as a criteria.
A TWA of zero would have a major impact on the
operations and expenses of the asbestos industry.
also be unnecessary.
It may
Jones and Grendon (1974) maintain that
low dose exposure of carcinogens may be virtually without
risk because the expected life span of those exposed is
exceeded by the time necessary for low concentrations of
altered cells to develop into cancers.
But how low is low?
This is a question which at
least two researchers have addressed.
Bruckman and Rubino
(1975) propose a standard of 30 ng/m 3 which they feel is not
unreasonable even though they estimate it is one-thousandth
of the current OSHA standard.
Even the most stringent standards are only as good
as they are enforced.
The carcinogenic nature of asbestos
requires the most diligent control no
matter what the
18
standard.
Industry should seek to control any sources of
environmental contamination to the maximum extent, the
overriding concern being the health of those exposed,
especially the workers.
Because of recent developments of clinical data on
the carcinogenicity of asbestos, a proposed revision of the
OSHA standard was published in the Federal Register in
October, 1975 (Job Safety and Health, 1976).
It would
reduce the TWA to .5 f/cm 3 and reduce the ceiling limit
3
value to 5 f/cm .
February 9, 1976, was the last date to
file public comments.
Since that time, NIOSH has proposed
to OSHA to lower the TWA to .1 f/cm 3 and the ceiling value
to .5 f/cm 3 , according to the Journal of Environmental
Health (January-February, 1977).
IV
ASBESTOS IN BUILDINGS
According to Reitze, et al.
(1972), the use of
sprayed asbestos-containing insulation was developed in
Britain in 1932 and was introduced in the United States in
1935.
Sprayed asbestos-fibre containing materials have four
major uses in the construction industry:
thermal insulation,
accoustical and decorative purposes, condensation control
(because of the unique wicking effect of asbestos fibres)
and fireproofing.
spray application.
Asbestos also increases lubricity in
Its use as fireproofing in City Hall
East is the major concern of this present investigation.
Since 1950, when Underwriters Laboratories approved
asbestos-containing spray insulation for fireproofing, its
use has steadily increased.
In 1968 over 40,000 tons of
this material was used for this purpose, and by 1970 over
half of all large multi-story buildings made use of this
agent in their construction.
The method of application determines in part the
extent to which the asbestos may become a hazard.
In the
dry method, the dry material is agitated and blown by hose
to a nozzle which directs the material through a stream of
water jets.
In the wet method, the material is premixed
with water and the resulting slurry is sprayed on the
surface to be coated.
type -matrix-
The dry method produces a fibrous
that---is-cons-iderably-more~friable,_
19
-and-therefore
20
more likely to cause air contamination than the wet method
which produces a harder, cementitious coating.
The Environmental Protection Agency banned the use
of products that contain greater than 1% asbestos in 1973
because of dangers to workers involved with its manufacture,
mixing and application.
Selikoff (1972) also points out
that the application process caused widespread contamination
of urban centers.
But possible environmental exposures to
asbestos may still occur.
Spray asbestos fibres from the
surface of the coated areas may erode and contaminate the
building air supply system.
There is also the potential
environmental contamination that may result from future
alterations and eventual demolition of such buildings.
Literature Review
Byrom, Hodgson and Holmes (1969) conducted a survey
in Great Britain of asbestos contamination in typical
situations where asbestos-based building materials were used.
This survey included over sixty buildings.
In over 90% of
the buildings, the asbestos concentrations did not exceed
.04 f/cm 3 (one-tenth the level regarded as acceptable for
occupational exposure in Great Britain at that time).
Also,
more than 40% of the concentrations were of. the same order
as the levels in buildings where no asbestos had been used.
The researchers concluded that the buildings were not likely
to constitute a hazard to the health of their occupants.
21
.
-
Lumley, Harries and O'Kelly (1971)
surveyed a
different type of building in Great Britain:
storehouses
insulated with crocidolite and amosite asbestos sprays.
Crocidolite insulated storehouses had fibre counts ranging
from .26 f/cm 3 during periods of no activity to a mean high
of 11.29 f/cm
3
when there was a great deal of activity
(disturbing fallen asbestos on boxes on the floor) .
In
storehouses insulated with amosite asbestos the mean
concentrations ranged from 1.9 f/cm 3 (no activity) to a high
of 350 f/cm 3 when ·the unprotected sprayed material was
brushed.
These researchers concluded that the sprayed
asbestos insulation constituted a potential hazard to the
building occupants.
They recommended sealing the insulation
and protecting the sealed insulation from damage.
The hazards of sprayed crocidolite asbestos
insulation on the steelwork of a small boiler compressor·
house was described by Lee and Smith (1974).
The asbestos
surfaces were friable and small areas of damage, from
leaning ladders on the insulation, were noted.
During work
periods, the researchers found a mean contamination level of
.18 f/cm 3 .
The vibration from machinery on the upper floor
was considered to be a prime cause for the contamination
observed.
A lower count of .06 f/cm 3 resulted when the
plant was not operating.
It was decided to seal the exposed
surfaces of the insulation with a self-setting gypsum-based
composition with a layer of hessian scrim between coats for
:r:-~j.nf9 rcem~ni:
._____A.f t gr:__g.~yi-_D:g_c_i:~_Q_ ___c_o a_~s_'?£_p <3:_~~-:t:_ --~'§_:t::.<: _____
22
applied.
The workers wore protective dust respirators and
protective clothing, which were removed in special changing
rooms during this sealing operation.
Other protection
included a vacuum cleaner for the clothes, polythene bags
for soiled clothes, and the use of warning notices and a
security guard.
After the sealant was applied, fibre counts
during work periods were very low;
.04 f/cm 3 .
Workers in
the area were informed of the need to prevent future damage
of the sealant and
perma~ent
warning notices were posted.
Sawyer (1975) described the problems of asbestos
contamination in the Yale Art and Architecture Building.
Soon after the sprayed application of a mixture containing
25% asbestos fibres on the building's ceiling, the exposed
and friable surface began gradual disintegration.
Mainte-
nance and engineering activity necessitated direct contact
with the ceiling and subsequent fibre release.
Sawyer
concluded that the contamination occurred in three general
modes:
persistent low level fallout resulted in a mean
count of .02 f/cm 3 ; occasional high intensity concentrations, 15.54 f/cm 3 , resulted from direct contact; repeated
re-entrainment and dispersal from surfaces where the dust
had settled ranged from .02 f/cm
3
during general activity
to 4.02 f/cm 3 during custodial dry dusting.
The decision
was reached to remove the insulation and the building was
evacuated.
Special precautions to pro·tect the workers and
23
These precautions included half-face mechanical filter
respirators, pre-spraying the ceiling with a mixture of
water and a surfactant to prevent dust formation, shielding
working spaces with polyethylene sheets, decontamination
rooms, and the sealing of the removed insulation material
into air-tight drums for dispersal.
The contamination
during this work sequence ranged from 6.45 f/cm 3 during the
gross clean-up to .00 f/cm
3
during the final wet mopping.
Post removal sampling resulted in fibre levels in the
building that equaled city background levels:
Nicholson, Rohl and Weisman (1976)
3
. 00 f/ em .
investigated
asbestos contamination of building air supply systems in
nineteen modern office buildings.
Their results are diffi-
cult to compare with previous studies because of different
analytical techniques.
Their membrane filter samples were
ashed, weighed, examined by electron microscopy, and
reported in nanograms per cubic meter.
The researchers
decided that a building could be considered contaminated
when the average level inside the building was at least
three times greater and 10 ng/m 3 higher than concentrations
measured outside in the ambient environment.
Four buildings
fireproofed with a fibrous asbestos spray were found to be
contaminated.
Several additional investigators have conducted
unpublished surveys regarding this same problem.
Notani
(personal communication, l976)surveyed a number of buildings
for the -··-·Los
Angeles County
Personnel --Department,Occupational
----- ---- ·----··-··-··
---------------------- --- ·-··-··-------- ··--------- -.. -- --------------- ---
----·--
--- -·-
-~-----·---
-
·---------------------~--
-~--
------~-------
-~-
24
Health Division. The Long Beach Courthouse and the Los
Angeles Sheriff's Crime Lab were the most notable buildings
where contamination was found.
Fibre levels in the Crime
Lab ranged from 1.7 - 2.2 f/cm 3 (Zuieback, personal
communication, 1977).
Where contamination was evident,
vinyl acrylic polymer paint was applied on the asbestos
surfaces as a sealant.
Brown (personal communication, 1976) recommended
removal of the asbestos containing ceiling of a UCLA
dormitory at a cost of $800,000.
During the process he
utilized the wetting technique he later recommended to
Sawyer.
Young (1972) reported on the contamination of a
Wyoming school building.
Since then, recent newspaper
accounts have reported concern with asbestos ceilings in
school buildings in New Jersey (Los Angeles Times, 1977) and
California (Los Angeles Times, 1977).
The California State
Department of Health is also conducting a survey of
buildings incorporating asbestos-based materials (Los
Angeles Times, 1977) .
Discussion
Many of the studies reviewed here have used
different methods of monitoring and analysis.
While a
direct comparison of fibre counts is not possible, it is
clear that certain factors are associated with asbestos
contamination in buildings.
25
In all circumstances where significant con·tamination
has occurred, direct visible damage to the sprayed material
was evident.
Damage from maintenance or engineering
activities or vibrations from nearby machinery operations
contribute to shaking the fibres loose.
Contamination is
also more likely from products, such as fibrous spray
insulation, in which the fibre is loosely bound as opposed
to products in which the fibre is more firmly bound.
Where contamination is found, corrective action
should be taken.
This may be complete removal of the
material, with appropriate safeguards to workers and
surrounding areas, or appropriate sealing of the material.
A word concerning sealant is appropriate.
Heslep
(1972) notes that many areas of a building that may be
coated with asbestos materials are subject to cutting,
fitting, adjusting and various other maintenance activities
in which the integrity of any sealant may be jeopardized.
He maintains that there is no known sealant that would
preclude the erosion of asbestos fibres under all these
various conditions.
The use of a sealant with "soft"
deteriorating asbestos coatings may even accelerate
deterioration as it adds weight to an already weakened
material.
It is also evident that considerable contamina-
tion will occur when and if these buildings are demolished.
Nicholson, et al.
(1976)
found no evidence for
asbestos contamination in cementitious spray fireproofing.
~ :r:~cl§ ~ce 1 J:to~§.VE? :Lr __ §Ug_ge_s_t~ _th_Cl:1::__ i:h~---~p~ S:~f~<==---~J:?.YiEC?.!1-1Tl~!1i:._? ___ _
26
should be inspected and monitored in order to verify that no
hazard exists for the building occupants.
It was therefore
decided to monitor and analyze City Hall East for possible
asbestos fallout with procedures recommended by NIOSH.
v
MATERIALS AND METHODS
The United States Public Health Service has
established sampling and evaluation procedures for
determining airborne asbestos dust exposures.
Sampling and
Evaluating Airborne Asbestos Dust, NIOSH's training manual
(1973), served as the guide during the course of this
investigation.
The approved procedure is to collect the
fibres on a membrane filter, dissolve the filter on a glass
slide, and then count the fibres under a microscope.
Sampling Procedure
The first step in the procedure was the calibration
of a portable rotameter:
Brooks, type 1355 OlCIFAN.
The
rotameter was calibrated using the standard bubble burette
method, in which the travel of a soap bubble through the
burette serves as a primary standard to compare to the
reading on the rotameter.
A rotameter was selected as a
field calibration instrument because of its portability and
convenience.
The rotameter was calibrated with the entire
sampling apparatus in sequence.
The sampling train con-
sisted of approved MSA portable pumps, models G and Si
1/4" inner diameter rubber tubing; and a 37 mm Millipore
field monitor, type MAWP 037AO filter, approved by NIOSH
for monitoring airborne asbestos fibres, assembled and ready
- -- - - -
--
-·---- ----
~-----------------------------~---------------~-----·------
27
------------
------------------~------~---------·---------·
28
to use.
Once the rotameter was calibrated and the sampling
pump batteries charged, actual sampling in City Hall East
was begun.
To collect samples in the building occupants'
breathing zones, special wooden stands were constructed to
hold the pump and maintain the field monitor at 5'6" above
the floor.
Each pump with completed sampling train, was set at
just over 2 lpm with the rotameter.
It was anticipated that
the flow rate would drop due to battery discharge and
indeed this was the case.
Each pump and monitor, open-face
down, were placed on the stand and sampling commenced.
Initial flow rate and starting time were noted.
After the sampling period was completed, the rotameter was again connected to determine the final flow rate.
The pump was then shut off; the monitor removed, plugged,
taped and labeled.
Sampling times ranged from 334 minutes
to 461 minutes, with the average time being 388 minutes.
These long sampling times were necessary because of the
anticipated low concentrations of fibres.
The initial and
final flow rates were averaged and then multiplied times
total minutes to determine total liters sampled.
average flow rate was 2 lpm.
The
The labeled monitors were
placed exposed side up in a plastic foam-lined box.
When
monitoring was completed the filters were brought to the
Environmental Health Sciences Laboratory at CSUN for
microscopic analysis.
29
Analysis Procedure
The filters were prepared for analysis in the
following manner.
Using a scalpel, a pie-wedge
approximating one-eighth of the filter surface was cut from
each filter.
It was then placed sample side up, using a
pair of fine-tipped tweezers, on a l"x3" microscope slide,
previously prepared with a small amount of mounting solution.
The mounting solution consisted of dimethyl pthalate and
diethyl oxalate (mixed in equal proportions) plus .05 gm/ml
of clean filter material for proper viscosity.
A number
one and one-half cover slip was placed on the filter-media
combination and lightly pressed until it made contact with
the dissolving filter.
The slide was then labeled and set
aside for fifteen minutes to clear.
The microscope used for analysis was a Swift model
M-1000 series,· steroscopic compound microscope.
It was
adjusted for phase contrast microscopy and Koehler illumination.
A Parton reticle was placed inside one of the eye-
pieces and calibrated with a stage micrometer.
The filter
samples were examined under 400X magnification.
When counting and sizing the particles, random fields
were selected from the wedge tip to the circumference of the
filter sample, ·a field being the left half of the Por-ton
reticle.
It was necessary to count 100 consecutive field
areas, as the fibre concentration was low.
casette was counted.
One wedge per
I
'
30
The following rules were followed in counting the
fibres.
Only fibres greater than 5 microns and with an
aspect ratio equal or greater than 3:1 were counted.
fibres inside the field area were counted.
Only
These included
fibres which crossed two pre-selected adjacent sides of the
field, and had one end inside the field area.
The asbestos fibre concentration was calculated
from the following formula:
(AFC - BAFC)
(Filter Area)
(Field Area)
(Volume)
(1000)
c =
C
=
AFC
BAFC
Concentration in f/cm 3
=
Average fibre count for 100 field areas
=
Background average fibre count of blank filter
Filter Area
Field Area
=
=
855 mm
2
Area of counting field,
.0031 mm
2
Volume = Volume of air sampled in liters
Estimation of Error
The joint ACGIH-AIHA Aerosol Hazards Evaluation
Committee (1975) estimates a potential error of + 30% for
sampling results.
This includes such sources of error as
sampling flow rate calibration, error in measuring the area
of the sample field and error in measuring the area of the
viewing field.
Significant error is also associated with microscopy
and variations between counters.
Oritz, Ettinger and
Fairchild (1975), in a study comparing count data from
31
several counters at a single facility, report a coefficient
of variation of + 20% with maximum individual variations of
+ 50%.
An additional limitation in this technique is the
absence of a convenient absolute method for readily
identifying asbestos by phase contrast microscopy (NIOSH,
1973).
It is not possible, therefore, to conclude positively
that all countable fibres are indeed asbestos.
VI
ASSESSMENT OF CITY HALL EAST
Los Angeles City Hall East was designed by the
architectural firm of Stanton and Stockwell, who completed
their plans in 1969.
The construction firm of Montgomery
Ross Fisher was contracted to build the structure.
Construction commenced in 1971, and city employees moved
into the building in 1974.
This investigation is primarily concerned with the
erosion into the building's air supply system of asbestos
fibres from the spray-lined plenum spaces in the building.
To fully appreciate the potential problem it is necessary to
describe the building's air supply system.
The air enters the building through openings on the
11th floor.
There it goes through a media-type filter of
high density fiberglass and a Farr HP gauze-backed paper
filter for capturing fine dust.
The air is supplied to
occupied areas throughout the entire 16-story structure by
fans on the 11th floor, which drive the air through sheet
metal ducts.
Return air, however, is not ducted and passes through
a plenum space formed by the hung ceiling of the room and
the underside of the floor above.
It is then carried back
to the fan room through centrally located ducts where it is
discharged.
On hot days, above 80°F, the air is not dis-
:tr(3?_P__ aj,:r.:__.:tnc1______________ .
chCl.:r:ged,_}:)ut_:t:'_a~tJ:ler~is_mi;~E;!d_w:Lth_2Q_!5___
32
33
recirculated through the building.
The steelwork and plenum spaces in City Hall East
have been sprayed with Zonolite Monokote #2, a registered
trademark of Grace Construction Products.
Monokote adds
fire resistance to steel, concrete and other surface
structures.
It is an example of the materials that are
supplied as sprayed slurries, commonly known as
cementitious sprays, that often contain gypsum, Portland
cement, vermiculite and 5-30% chrysotile asbestos fibre
(Reitze, et al., 1972).
Although the asbestos fibres in
this product are not loosely bound, the possibility of
erosion of the fibres into the breathing zone of the
building occupants exists.
Additionally, maintenance
activities within the plenum space can damage the coating
and contribute to contamination.
This study concerns
itself with the ambient levels of fibre present in
breathing zones throughout the building.
To test the possibility of contamination, 10 samples
.of indoor air were obtained by the NIOSH prescribed method,
and analyzed for asbestos fibres to obtain concentration
data.
Six of these samples were taken in office areas on
the lst, 4th, 7th, 8th, 11th and 13th floors.
In addition,
4 samples were taken in the fan room on the 11th floor to
sample the return air most recently in contact with the
spray material.
'I'he fan room did not have a hung ceiling,
and the fireproofing was exposed for inspection.
There was
~?TI\e __ <:tart1a g ~---"t:~- -~_1:~~--<::-~~t:j_I?: <:r _ ~~-~---"'=-~ _m~~~ t-~-~~n~e___~i:-~'1 i-t:~~-~ ,
VII
SURVEY RESULTS
The filter samples were examined in the laboratory
on January 20-27, 1977.
The low concentrations of fibres
in the air of the office buildings resulted in a low
average of fibres per viewing field:
.07.
The background
count on the blank filter was .00 f/cm 3 .
Airborne Fibre Levels in City Hall Buildings
Asbestos fibre levels in the three buildings were as
follows:
BUILDING
N
SD
City Hall East
.028
10
.027
City Hall
.024
2
.071
City Hall South
.016
2
.056
Discussion and Conclusion
The OSHA standard for asbestos, effective July 1,
1976, and through the time period of this survey, is
2.0 f/cm 3 TWA and 10.0 f/cm
15-minute period.
3
maximum excursion for any
The OSHA standards used in this study do
not represent definite pathological benchmarks, but are used
for comparison and as guidelines.
The standard t-test was used to establish the
significance of the survey findings when compared to the
OSHA standard.
Comparison of building levels and the OSHA
35
36
--
standard yielded a significance test of p less than .001.
It can therefore be concluded that the contamination level present in City Hall East is statistically
insignificant when compared to the OSHA standard.
These
very low concentrations are not likely to be of long term
biological significance.
Comparison with the two nearby
buildings which did not incorporate asbestos-based materials
in their construction suggest that all three values
represent a general ambient level of fibre concentration in
downtown Los Angeles.
To test this interpretation, sampling was conducted
on March 25, 1977, using the previously described techniques
and equipment.
Air samples were simultaneously obtained
from the 11th floor fan room in City Hall East and from the
outside ambient air near the 11th floor fan intake and at
street level.
The results were as follows:
FIBRE CONCENTRATION (f/cm 3 )
SOURCE
Inside, 11th floor fan room
.028
Outside, 11th floor
.021
Street level
. 031
This data tends to support the interpretation that the fibre
concentrations inside the buildings reflect a general
ambient level of fibre concentration in downtown Los Angeles.
The hypothesis stated in the Introduction is hereby
accepted:
No significant levels of asbestos fibres were
found in City Hall East.
37
Recommendations
Because occupants in the office building are in no
danger of exposure to harmful asbestos fibre levels, sealant
or removal is not recommended.
But the possibility exists
that maintenance or engineering personnel engaged in
activities that include modifying, brushing against, or
cutting and removing parts of the fireproofing coating may
be in danger of exposure to intermittently high levels of
asbestos fibres.
Although quantification of this problem is
beyond the scope of this study, these personnel should be
informed of the nature of the problem before they contact
the coating and should take proper precautions.
These
precautions might include the wearing of proper particulatefilter respirators, changing and bagging their clothes, and
preventing the spread of the fibres to other areas by proper
and thorough clean-up of debris, which should also be bagged
and disposed of.
Permanent reminders, in the form of
warning signs, are recommended for the exposed spray areas
in the fan room on the 11th floor.
REFERENCES
Primary Sources
ACGIH-AIHA Aerosol Hazards Evaluation Committee.
Background
Documentation on Evaluation of Occupational Exposure
to Airborne Asbestos.
American Industrial Hygiene
Association Journal, 91-103, February, 1975.
Brown, R.
Personal communication concerning asbestos
contamination in a U.C.L.A. dormitory.
U.C.L.A.
Health and Safety Department, 1976.
Bruckman, L., R. A. Rubino.
"Asbestos:
Rationale Behind a
Proposed Air Quality Standard," Journal of the Air
Pollution Control Association, 25:1207-1215, 1975.
Bryon, J.D., A. A. Hodgson, S. Holmes.
"A Dust Survey
Carried Out in Buildings Incorporating AsbestosBased Material in Their Construction," Annals of
Occupational Hygiene, 12:141-145, 1969.
Cauno, D., E. Totten, P. Gross.
"Asbestos Bodies in Human
Lu.Ylgs at Autopsy," Journal American Medical
Association, 192:371-373, 1965.
Champion, P.
"Two Cases of Malignant Mesothelioma After
Exposure to Asbestos," American Review of Respiratory Disease, 103:821-826, 1971.
Crally, L. J., R. G. Keenan, J. R. Lynch, W. S. Lainhart.
"Source and Identification of Respirable Fibers,"
American Industrial Hygiene Association Journal,
29:129, 1968.
Doll, R.
"~lortali ty From Lung Cancer in Asbestos Workers,"
British Journal of Industrial Medicine, 12:81, 1955.
Enterline, P., P. DeCoufle, V. Henderson.
"Respiratory
Cancer in Relation to Occupational Exposures Among
Retired Asbestos v-Jorkers," British Journal of
Indus·trial Medicine, 30: 162-168, 1973.
Enterline, P.
"Pitfalls in Epidemiological Research: An
Examination of the Asbestos Literature," Journal of
Occupational Medicine, 18:150-156, 1976.
38
39
Federal Register.
Effluent limitations. Guidelines for
Asbestos Manufacturing Point Source Category,
38:208, 1973.
Gee, B., A. Bouhuys.
"Action on Asbestos," The New England
Journal of Medicine, 285:1317-8, 1971.
Gross, P., et al.
"Experimental Asbestosis: The Development of Lung Cancer in Rats with Pulmonary Deposits
of Chrysotile Asbestos Dust," Archives of
Environmental Health, 15:345-352, 1967.
Gross, P.
"Is Short-Fibered Asbestos Dust a Biological
Hazard?" Archives of Environmental Health,
29:115-117, 1974.
Gross, P., R. Harley.
"The Locus of Pathogenicity of
Asbestos Dust: A Theory," Archives of
Environmental Health, 27:240-242.
Heslep, J. M. Letter to Leroy F. Green, State Assembly,
concerning AB 314. Department of Public Health,
Berkeley, California, April 4, 1972.
Holt, P. F., D. K. Young.
"Asbestos Fibre in the Air of
Towns," Atmospheric Environment, 7:481-483, 1973.
Job Safety and Health.
4:12-13, 1976.
Asbestos in the Office Air,
Jones, H. B., A. Grendon.
"Environmental Factors in the
Origin of Cancer and Estimation of the Possible
Hazard to Man," Food and Cosmetic Toxicology,
13:268, 1975.
Journal of the American Medical Association.
and Answers, 176:81, 1961.
Questions
Journal of Environmental Health. New Asbestos Exposure
Limits Proposed by NIOSH, 39:254, 1977.
Knox, J. F., s. Holmes, R. Doll, D. D. Hill.
"Mortality
From Lung Cancer and Other Causes Among Workers
in An Asbestos Textile Factory," British Journal
of Industrial Medicine, 25:293, 1968.
Lee, G. L., D. J. Smith.
"Steelwork Insulated with Sprayed
Crocidolite Asbestos: Controlling a Potential
Hazard," Annals of Occupational Hygiene,
17:49-52, 1974.
Los Angeles Times.
"Schools Ordered to Check for Asbestos
In Buildings," p. 1, column 5, January 19, 1977.
40
Los Angeles Times.
"State to Test Air in Buildings for
Asbestos," p. 3, column 4, January 25, 1977.
Los Angeles Times.
"8 Schools Closed in Probe of Asbestos
in Ceilings," p. 22, column 1, January 5, 1977.
Lumley, K., P. Harries, F. O'Kelly.
"Buildings Insulated
With Sprayed Asbestos: A Potential Hazard,"
Annals of Occupational Hygiene, 14:255-257, 1971.
McDonald, J. C. , et al.
"Mortality in the Chrysotile
Asbestos Mines and Mines of Quebec," Archives of
Environmental Health, 22:61-68, 1971.
McDonald J. C., et al.
"The Health of Chrysotile Asbestos
Mine and Mill Workers of Quebec," Archives of
Environmental Health, 28:61, 1974.
Mancuso, T. F., A. A. El-Attar.
"Mortality Pattern in a
Cohort of Asbestos Workers," Journal of Occupational
Medicine, 9:147-162, 1967.
National Institute for Occupational Safety and Health,
Division of Training.
"Sampling and Evaluating
Airborne Asbestos Dust," U.S. Department of Health,
Education, and Welfare, Public Health Service, 1973.
Newhouse, J. L., H. Thompson.
"Mesothelioma of Pleura and
Peritoneum Following Exposure to Asbestos in the
London Area," British Journal of Industrial
Medicine, 22:261, 1965.
Nicholson, W. J., A. Rohl, I. Weisman.
"Asbestos Contamination of Building Air Supply Systems," The Institute
of Electrical and Electronic Engineers, Inc.,
29-6:1-4, 1976.
Notani, P. Personal communication concerning asbestos
contamination in L.A. County buildings. Occupational
Health and Safety, Los Angeles County, 1976.
Oritz, L. M., H. Ettinger, C. Fairchild.
"Calibration
Standards for Counting Asbestos," American
Industrial Hygiene Association Journal, 36:104-112,
1975.
Reitze, W. B., W. J. Nicholson, D. A. Holaday, I. J.
Selikoff.
"Application of Sprayed Inorganic Fiber
Containing Asbestos: Occupational Health Hazards,"
American Industrial Hygiene Association Journal,
178-191, March, 1972.
Rickards, A.A., D. V. Badami.
"Chrysotile Asbestos in
. TJfban.. _1\,:i.,r.-_, " Natu;e __, -~:34_: 9_3-:_9_4_ ,_ J 97J_.__ ____ _ ___ --------~--
41
Ruby, J. L. , Ruchan, R. M.
"Critique of the Proposed
Standard of the NIOSH Criteria Document on Asbestos,"
Journal of Environmental Health, 37:165-166, 1974.
Sawyer, R. N.
"Yale Art and Architecture Building Asbestos
Contamination: Past, Present, and Future,"
Yale Health Service, Yale University, New Haven,
Connecticut, 1975.
Sayers, R. R., W. C. Dressen.
"Asbestosis," American
Journal of Public Health, 29:205, 1939.
Scanzetti, G., G. C. Coscia, W. Psiani, G. F. Rubino.
"Cement, Asbestos and Cement-Asbestos
Pneunoconioses," Archives of Environmental Health,
30:272-275, 1975.
Selikoff, I. J., J. Churg, E. C. Hammond.
"Asbestos
Exposure and Neoplasia," Journal of the American
Medical Association, 188:22-26, 1964.
Selikoff, I. J., J. Churg, E. C. Hammond. "Relation Between
Exposure to Asbestos and Mesothelioma," The New
England Journal of Medicine, 272:560-565, 1965.
Selikoff, I. J., R. A. Rader, M. E. Rader, J. Churg, E. C.
Hammond. Editorial "Asbestos and Neoplasia, 11
A~erican Journal of Medicine, 42:487, 1967.
Selikoff, I. J., E. C. Hammond, J. Churg.
"Asbestos
Exposure, Smoking, and Neoplasia," Journal of
the American Medical Association, 204:104-110, 1968.
Selikoff, I. J., W. J. Nicholson, A. M. Langer.
"Asbestos
Air Pollution," Archives of Environmental Health,
25:1-13, 1972.
Stanton, M. F., C. Wrench. 11 Mechanism of Mesothelioma
Conduction with Asbestos and Fibrous Glass,"
Journal of the National Cancer Institute,
48:797, 1972.
U.S. Department of Health, Education and Welfare, Public
Health Service, Center for Disease Control,
National Institute for Occupational Safety and
Health. Criteria for a Recommended Standard Occupational Exposure to Asbestos, 1972.
"Diffuse Pleural
Wagner, J. C., C. A. Sleggs, P. Marchand.
Mesothelioma and Asbestos Exposure in North Western
Cape Province," British Journal of Industrial
Medicine, 17:260, 1960.
,~.
·-··
-------------------
~---
----
------------------------
-~
42
-
-
-
Wright, G. W.
"Asbestos and Health in 1969," American
Review of Respiratory Disease, 100:4, 467-479, 1969.
Young, K.
"A Silent Pollutant," Health Services World,
September-October, 1972.
Zuieback, S. Personal communication concerning fibre
concentration level in Los Angeles County Sheriff's
Crime Lab. California State University at
Northridge, March, 1977.
Secondary Sources
Angivel, L., W. M. Thurbeck.
"The Incidence of Asbestos
Bodies in the Lungs at Random Autopsies in Montreal,"
Canadian Medical Association Journal, 6:1179-1182,
1966.
Bhagavan, B. S., L. G. Moss.
"Secular Trends in Prevalence
and Concentration of Pulmonary Asbestos Bodies, 1940·
to 1972: A Necropsy Study," Archives of
Pathological Medicine, 100:539-41, 1976.
Betham, S. K., P. E. Holt.
"The Mechanism of Formation of
Asbestos Bodies," Journal of Pathology and
Bacteriology, 96:443-453, 1968.
Braun, D. C., T. D. Truan.
"An Epidemiological Study of
Lung Cancer in Asbestos Miners," American Medical
Association's Archives of Industrial Health,
17:634-653, 1958.
Breedin, P. H., D. H. Buss.
"Ferruginous (Asbestos) Bodies
in the Lungs of Rural Dwellers, Urban Dwellers, and·
Patients with Pulmonary Neoplasms," Sout.h Medical
Journal, 19:401~404, 1976.
Burlikov, R., L. Michailova.
"Asbestos Content of the Soil
and Endemic Pleural Asbestosis," Environmental
Resources, 3:443, 1970.
Cooke, W. E.
"Pulmonary Asbestosis," British Medical
Journal, 2:1024, 1927.
Cooper, W. C., J. L. Balzer.
"Evaluation and Control of
Asbestos Exposures in the Insulating Trade," from
proceedings of a Working Conference on the
Biological Effects of Asbestos, Dresden, Germany,
1968.
43
Dunn, J. E., J. M. Weir.
"Lung Cancer Mortality of Man in
Certain Occupations in California," American Journal
of Public Health, 50:1475-1487, 1960.
Enterline, P.
"Mortality Among Asbestos Products Workers
in the United States," Annals of New York Academy
of Science, 132:156-165, 1965.
Gloyne, S.
"The Presence of the Asbestos Fibre in the
Lesions of Asbestos Workers," Tubercle, 10:404,
1929.
Gross, P. T., P. DeTreville, L. J. Crally, J. M. Davis.
"Pulmonary Ferruginous Bodies," Archives of
Pathology, 85:539, 1969.
Kiviluoto, R.
"Pleural Calcification as Roentgenologic
Sign of Nonoccupational Endemic AnthophyliteAsbestosis," Acta Radial, 194: 1-67, 1960.
Lanza, A. J.
"Silicosis and Asbestos," Oxford University
Press, New York, 1938.
Lynch, K. M., W. A. Smith.
"Carcinoma of the Lung in
Asbesto-Silicosis," American Journal of Cancer,
24:56, 1935.
Mancuso, T. M., E. J. Coulter.
"Methodology in Industrial
Health Studies," Archives of Environmental Health,
6:210-226, 1963.
Merewether, E. T.
"Asbestosis and Carcinoma of the Lung,"
Annual Report of Chief Inspector of Factories for
the Year 1947. Long, His Majesty's Stationary
Office, 79-81, 1949.
Meurman, L.
"Asbestos Bodies and Pleural Plaques in a
Finnish Series of Autopsy Cases," Acta Pathology
and Microbiology of Scandinavia, supp 181, 1966.
Murray, M.
Report of the Departmental Committee on
Compensation for Industrial Disease. C.D. 3495,
3496, HMSO, 1907.
Newhouse, M. L.
"The Mortality of Asbestos Factory Workers,"
proceedings of the National Conference on
Pneumoconiosis, Department of Mines, Republic of
Africa (to be published), 1969.
Raunio, V. "Occurrence of Unusual Pleural Calcification in
Finaldn," Annal of Medicine Intern Finland, 55:61,
1966.
44
Reeves, A. L.
"The Carcinogenic Effect of Inhaled Asbestos
Fibers," The Annals of Clinical Laboratory Science,
6:459-466, 1976.
Rous, V. J. Studeny.
"Aetiology of Pleural Plaques,"
Thorax, 25:270-284, 1970.
Selikoff, I. J. , E. C. Hammond, H. Seidman.
"Cancer Risk
of Insulation Workers in the United States," in
proceedings of IARC Working Group to Review the
Biological Effects of Asbestos, Lyon, France, 1972.
Lyon International Agency for Research on Cancer,
1973.
Thomson, J. G., P. R. Kaschula, R. K. McDonald.
"Asbestos
as a Modern Urban Hazard," South Africa Medical
Journal, 37:77, 1963.
Thomson, J. G.
"Asbestos and the Urban Dweller," Annals of
The New York Academy of Science, 132:196, 1965.
Timbrell, V. "The Inhalation of Fibres," proceedings of the
International Conference on Pneumonconiosis,
Department of Mines, Republic of South Africa
(to be published), 1969.
Wagner, J. C., G. Berry, V. Timbrell.
''Mesothelioma in Rats
with Asbestos and Other Materials," British Journal
of Cancer, 28:173, 1973.
Wagoner, J. K., W. M. Johnson, R. Lemen.
"Malignant and
Non-malignant Respiratory Disease Mortality
Patterns Among Asbestos Production Workers," in
~ongressional Record.
Senate proceedings and
debates of the 93rd Congress, 1st session.
U.S.
Government Printing Office, Washington, D.C.,
Volume 119, part u, March 14, pp. 7828-7830, 1973.
Weis.s, A.
"Pleurakrebs bei Lungenasbestos, in vivo
Morphologisch Geischert," Medizinsihe, p. 93, 1953.
,,
APPENDIX
The raw data concerning fibre counts is as follows:
LOCATION
DATE
LITERS
FIBRE COUNT (f/cm 3 )
1/19/77
CHE-Fan Room
840
.020
1/19/77
CHE-F an Room
858
.047
1/19/77
CHE-Room 800
743
.022
1/19/77
CHE-Room 1330
662
.066
1/19/77
CHE-Room 425
79 2
.031
1/20/77
CHE-Fan Room
851
. 012
1/20/77
CHE-Fan Room
845
.016
l/20/77
CHE-Room 1100
847
.026
1/20/77
CHE-Room 700
783
.021
1/24/77
CHE-Room 100
735
.015
1/24/77
CH-Room 1600
850
.019
1/24/77
CH-Room 500
1014
.029
1/24/77
CHS-Room 103
897
.012
1/24/77
CHS-Room 700
680
.020
3/25/77
CHE-OA 11th floor
780
.021
3/25/77
CHE-Fan Room
858
.028
3/25/77
CHE-OA Street level
787
.031
Key:
CHE
CH
CHS
OA
City Hall East
City Hall
City Hall South
Outside l~ient
'