Document jGeLaNJ2DNXn0KeJxz4DB9j9
>/?. id, J, /Y/CHoLSO// T^STiiTiOHY XPCB H0PRJ/M& CHICAGO, OCT, /S, HU
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Thank you very much for the opportunity to appear in support of
your regulations controlling the use and production of asbestos materi
als and spray insulation.
For purposes of identification, my name is William J, Nicholson.
I am Assistant Professor of Community Medicine at the Mount Sinai
School of Medicine of the City University of New York. As a physicist,
I-have served as coordinator of several projects undertaken by the
Environmental Sciences Laboratory of Mount Sinai to evaluate the ef-
fects of asbestos exposure. These include an industrial hygiene re
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search program designed to identify and control asbestos hazards in
the insulation industry, the development of analytical techniques for
the quantitation of asbestos in ambient air, and a study of asbestos
air pollution in New York City and throughout the United States. Addi
tionally, I am engaged in several epidemiological studies of disease as
sociated with occupation or environmental exposures to various substances.
Two of these studies involve the effects of asbestos on defined popula
tions. The Justification is strong for controlling the use of asbestos on
basis of the health effects produced by its use in the past. The evidence that heavy occupational exposure to asbestos is associated with pulmonary
disease dates from 1900 when massive fibrosis was found at post mortem
in the lungs of a man who was the last survivor of a group of 10 men who
worked since 1886 in the carding room of an asbestos textile mill.
Cases of asbestos-induced scarring of the lungs, asbestosis, were seen '
with increasing frequency in subsequent years as the use of asbestos in
creased. However, a hint of additional disease risk from occupational
asbestos exposure v/as seen in 1935, Two cases of lung cancer were foimd
in individuals having asbestosis. This portent was grimly verified in
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later studies. In 1947, the Chief Inspector of Factories in Britain
found lung cancer in 13 per cent of deaths in which asbestosis was
present.
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To bring us ..up to date, 70 years after the first knowledge of as
bestos disease, and to-complete the picture of occupational risk from
exposure to asbestos, let me present some data obtained by Dr, Irving J,
Selikoff, Director of the Environmental Sciences Laboratory, Mount Sinai
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School of Medicine. He has followed since January 1, 1943 the 632
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members of the New York and New Jersey Locals of the asbestos workers
union, the International Association of Heat and Frost Insulators and
Asbestos Workers. These men apply the insulation to high temperature
pipes Bnd boilers in apartment, office building and individual plants. Some of the material they v.ce contains a small amount, of asbestos -- 7
to 15 per cent, usually. Often it contains none. In comparison to the
factory exposures during early decades of this century, their exposures
are relatively light. Knowing their ages in 1943 and using standard tables, it was poss
ible to calculate the expected mortality experience of these 632 workers.
This was done by Dr. E. Cuyler Hammond, Chief Epidemiologist of the Ameri
can Cancer Society, and the results, along with those actually seen,
are given in Table I for the years 1943 through 1962, . From all causes, 203 deaths were expected of those who had worked
20 years. In fact, there were 255. More than 50 men who died should not have died. Looking at the table;-we can see the causes of these "excess'death": 45 died of cancer of the lung, trachea and pleura where
only six or eoven wero oxpoctod; 12 diod of o'sbostosis although nono^ ^ _
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should have died; three times as many died of cancer of the G. I. tract
as were expected,
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Results of continued observation of the group through June 30, 1971
are shown in Tables II and III, They represent a catastrophe. Over half
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of the deaths were' from some form of cancer or asbestosis. Nearly 40%
could be termed "occupational" deaths.
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i- In these latter data, special reference should be made to the high
death rate from mesothelioma. Twenty-seven cases of this, os yet, in
curable disease woro soon, A diffuse cancojj of the lining of tho chost
or abdomen, it is so rare that it has yet to be separately classified in
the International Classification of Causes of Death. Its occurrence
in the general population may be so infrequent as to cause only one death ' .
in 10,000. Here, it was the cause of death in one of every 16 individu
als. Moreover, in other studies, its appearance in -increased amounts
has always been associated with asbestos exposure,
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TVo other aspects of the research by Doctor Selikoff are important.
The first is the evidence of the long lapsed period between onset of
asbestos exposure and the incidence of disease. Lung cancer usually
appears between 20 and 40 years after first exposure to asbestos, and
mesothelioma most often after a 35-year lapsed period.
The second aspect is the strong synergism found between ssbestos
exposure and cigarette smoking in the Incidence of lung cancer. By
personal interview in 1962, the smoking habits of 370 of the 632 men were
established. By following the mortality experience of these 370 men, a*
special risk of cigarette smoking was established. From January 1, 1963
through February 1, 1971, in 283 -men with a history of cigarette smoking,
40 lung cancers were observed. This is nearly ten times the number ex--
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pected in on equivalent cigarette smoking population. In 87 non-smokers,
only one lung cancer was seen. Thus, it is not asbestos alone, or cigarette smoking alone, but the combination of the two that produced
these grim data. In fact, it is calculated that asbestos workers who I.
smoke run more than 90 times the risk of dying of lung cancer than men
who neither smoke cigarettes nor work with asbestos.
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iTiese data I have presented to you were from occupational exposures to asbestos. At most, 200,000 men and women in the United States have such exposures. Hopefully, 70 years after the first awareness of asbestos,
disease, working conditions will be improved to reduce their risk of dis ease. But were this the only risk of asbestos exposure, it would not be germane to the regulations under consideration here. Unfortunately, in recent years the evidence has accumulated that the problem of as bestos disease has disseminated from the occupational area into the
general environment.
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Evidence is accumulating that mesothelioma is rapidly increasing
among men who worked in the vicinity of asbostos application. Recall,
that mesothelioma is virtually nonexistent in people who hove had no exposure to asbestos. In Holland, 22 cases were found during a 6-year
period in workers of the de Shelde shipyard. These cases occurred, however, not in asbestos workers, but in members of other trades, weldersj
carpenters, or painters, all of whom only wouked in an area where as
bestos insulation was applied or removed. Similar data have appeared
from Great Britain. Here, 80 cases of mesothelioma were found in a
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Burvey of the material in the pathology departments of Scottish hospitals
and medical schools from the yearp,1950 through 1967.- An investigation
of the occupational background of these cases revealed a strong association
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with shipbuilding.or marine work. Here again, however, the cases were
not often found in insulators but in other trades working near the
application or removal of asbestos. A further disconcerting feature
of the Scottish data is the rapid rise in the rate of occurrence of
I mesothelioma; 51 of the 80 cases were seen in the years 1964-67, ap
proximately 30 years after the extensive shipbuilding undertaken during
World War II.
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The spectrum of disease associated with asbestos now extends even
to environmental exposures. In 1960, Wagner, Sleggs and Marchand des
cribed 47 cases of mesothelioma found during a four-year period in the
northern Cape province of South Africa, an area with extensive crocido-
lite asbestos mines. None were seen in the neighboring Transvaal Province
or in 10,000 autopsy cases of workers who had died with known exposures
to silica. Of the 47 cases, approximately half were found to have had
either industrial or mining exposures to asbestos. Virtually all of the
remaining cases were in individuals who simply lived or worked in the
vicinity of the asbestos mines or mills.
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Confirmation of the possibility of environmental asbestos-associated
disease soon appeared. Newhouse and Thompson reviewed all mesothelioma
cases at the London Hospital. They corroborated the close association
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with asbestos, 31 of the 76 cases having had documented occupational
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exposure. Of the remainder, 11 had lived, decades before, within one--half
mile of an asbestos factory. A similar distribution of cases was found by
Lieben and Pistawka in Pennsylvania. One insidious form of indirect '
asbestos exposure is that of families of asbestos workers. In the previ
ously mentioned studios, 9 of the London mesotheliomas were in family
members, as were 3 of the 46 Pennsylvania cases. .
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Unfortunately, thbse data on the Incidence of mesothelioma from
' environmental or Indirect occupational exposure to asbestos are severely limited. The exposures in question took place beginning 20, 30, 40 or
more years ago. No knowledge exists of the associated asbestos dust
I exposure levels. Thus, we have no dose-response information on low-
level asbestos exposure. We only have knowledge.of n potential risk of
cancer, at exposures much below occupational ones. Obviously, additional
research and continued surveillance are highly desirable.
' Let us nbw turn to specific items in youf regulations. Firstly, the I
general requirements of Section 2 are excellent, particularly with regard
to responsibility and education. We find a great problem to be the
ignorance of a potential hazard among marginal users of asbestos. Such
ignorance can easily result in lax procedures.
Secondly, the banning of asbestos in spray insulation is entirely
appropriate. In New York City we have found this to be a major contribu
tor to ambient air asbestos levels. For the past 10 years, during which
spray fireproofing came to be extensively used, it was not uncommon to
see extensive snowfalls of asbestos-containing material over widespread
areas of New York and other metropolitan centers. In some cases, the
fireproofing was even done with no attempt to enclose the spray area by
tarpaulins or othor moans.
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To vorify that such firoproofing oporotjLons woro a significant
source of respirable asbestos fiber, air sampling: was conducted in lower
Manhattan about construction sit where extensive spraying of asbestos-
containing- fireproofing was taking place. This work was done by our
Laboratory in conjunction with thevDepartment of Air Resources of New York
City. The results demonstrated that spray fireproofing can indeed con-
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ii tribute significantly to asbestos air pollution.
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Up to J mile away, levels exceeding 0.1 micrograms per cubic meter
were observed, which exceeds by 100 times background levels found in urban
areas distant from construction sites. While 0.1 micrograms may appear .
to be a small amount, it could represent more than 10 million minute
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fibers of asbestos. Moreover, the large clumps of asbestos-containing
material covering the sidewalk serve as a continuing source to be dispersed
by passersby.
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As I mentioned earlier, lacking a doserresponse relationship, we
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cannot state that environmental exposure levels from this practice are
certain to produce disease. However, it is hard to imagine factory
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emissions, even 40 years ago, being more 'excessive. Since the extensive
spraying of asbestos-containing fireproofing material has only existed
in the construction industry for the last 10 years, disease caused by
the exposure resulting from this practice is 10 or 20 years away. How
ever, continuing the uncontrolled spraying practices of the past decade
in the face of the mounting evidence of risk to all metropolitan residents
would be playing asbestos roulette with the lives of millions of people.
This method of fire protection for high rise buildings presents an
additional, continuing risk to the occupants of those buildings. Often,
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the space between the false room coiling and the under side of the fldoc
above, which Has been sprayed with asbestos,,sorves as a return plenum
for the air supply.system. After filtration, inadequate to remove most as
bestos fibers that may have eroded into the air stream, this return air is
recirculated throughout the building. The magnitude of this problem has
yet to be defined. Until recently in New York City., we have not been
allowed to analyze the air in buildings that has been in direct contact
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with asbestos-containing insulation.
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Finally, this spray procedure leaves a legacy of potential risk to
future generations. The lifetime of modern office buildings is short
and the procedures for the safe future demolition of buildings that could
I contain more than 100 tons of asbestos as fifeproofing have yet to be
devloped. Perhaps these procedures will be found and perhaps they v/ill
be followed but we have no such assurance at this.time.
. Unfortunatelyt safe procedures developed for the spray application
o. f asbestos-containing materials have not bIee n followed either voluntarily or under control regulations by contractors. Because of this failure
and because alternative procedures or materials are available, action
banning this use of asbestos is indeed appropriate. .
Mox*eover, because of uncertain knowledge of the health effects of ex
posure to mineral fibers other than asteslus, it is entirely appropriate
that strict control be exercised over other spraying of such substitute
materials. While some forms of "mineral wool" and other mineral fibers
have been in use since the 1930s there are still no definitive studies on exposed populations that would, at this time, provide assurance that
respirable mineral fibers, other than asbestos, are biologically inert in
humans. In the absence of such assurace, caution is warranted and 1
support, in its entirety, Section 3 of your regulations.
On the other Items, in Section 4, you might wish to add a qualifying
statement that when there is potential release of asbestos to the air,
a special enclosure shall, be used. Many asbestos products used in con
struction can be Installed with no release of fiber. Asbestos-vinyl floor
tile is one example. In fact, wi.th proper procedures,.even.asbestos
cement can be applied with minimal release of fiber.
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I cannot emphasize too strongly the need for stringent controls
during demolition. Those listed here may not be adequate and close sur veillance should be maintained to verify their adequacy. Tor example, I
am not sure that any asbestos should be transported via chutes to trucks. 'I
It is hard to imagine that the debris would be completely wetted. In reference to Section 6 A, I would like to raise some of the problems
assocated with air monitoring which.may be severe. In ambient air samples,
it is difficult, and often impossible, to identify asbestos fibers by
optical microscopy alone. There are many birefringent fibers with a simi
lar appearance. Even the sampling of stacks containing only asbestos has its problems.' Such sampling does not evaluate any emissions from
windows, room exhausts or uncontrolled sources. Moreover, the use of
optical microscopy can misestimate actual concentrations, evqn assuming
accurate counting of all fibers longer than 5 microns. Often as many as
100 times more fibers shorter than 5 microns may be present. If those
counted were a constant fraction of the total present, this would be no
problem. However, such is not the case. In different uses of chrysotile
we have found the ratio of the number of fibers longer than 5 microns to
the total number to vary from 1/250 to 1/20.
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houses have a size dependent efficiency, the results obtained by optical
analysis may be misleading and not comparable to other samples analyzed
by similar means.
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The only way to accurately asses environmental exposures is by
electron microscopy. Here, however, an analysis may cost $200 - $300 \
and be very time-consuming. You may wish to consider procedural controls
with the requirement of no Visible emissions of asbestos from any building
or site. If the facility inspected questions the judgement of an inspector they could pay for adequate air analysis by electron microscopy.
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I enclose in Tahiti IV data from our work analyzing samples of ambient
' air from nearby 50 U. S. cities. These data show that a background of
some asbestos fiber is found in all cities, but occasional peaks appear.
From this occasional occurence and from the fiber size distribution on high .I
samples, it appears that the contribution of some specific soui-ce is
important in these high levels.
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Finally, one comment on the proposed ban of asbestos in brake .
linings after 1975. The problem here is there is a dearth of information.
We have some very preliminary information thp.t asbestos air levels near ;i
sites of extensive braking may be 3 times higher than background. Since
wind conditions are highly variable, much more analysis of this question
is required. All our data really show is that brakes are not as obvious a problem as asbestos-containing fireprooofing spray in New York City..
Perhaps you may wish to qualify 7 B by the words "Unless evidence of
safoty is demonstrated tho uso of osbostos...."
In summary, your regulations in general are excellent, your intent
is proper, and I am pleased to support you.
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Table I
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Observed and Expected Number of Deaths Among 632 Asbestos Workers Exposed to
Asbestos Dust 20 Years or Longer, lf943-1962
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Cause of Death
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19431947
Years
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1948- " 1953-
1S52
1957 .
19581962 .
Total, 19431962
Total, all causes....'................. Observed (asbestos workers) Expected (US whito males).,
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28 39.7
" 54 '85 1 88
50.8
56,6 ' 54.4
255 203.5
Total cancer, all sites............ Observed (asbestos Workers) Expected (US white males...
Cancer of lung and pleura..,. Observed (asbestos workers) Expected (US white males)..
Cancer of
colon and
: rectum............ ..................................
Observed (asbestos workers)
Expected (US whito males)..
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13 5.7-
17 8*1.
26 13.0
6. 0.8
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8 13 1.4 2.0
39' 9.7
' 95 36.5
18 ,,2.4
45 6.6
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4 ' 4'1 . -7 .. 14 . 2.0 2.5 2.6 2.3
29 9.4
Cancer of all other sites com-
Observed (asbestos workers) ' 3 " 5
Expected (US white males)..
. 2.9
4.2
6' . 8.4
7' 5.0
21 20.5
Asbcstosis......................................... Observed (asbestos workers) 0 1 4 7 . 12
Death rates as reported annually by the U.S. National Office of Vital
Statistics. A five year average is given here for each period.
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Death rates include cancer of lung, bronchus, pleura, mediastinum and
trachea, assigned to international list'code No, 47b-f prior to 1949
and to No. 160-164 thereafter.
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Table n
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inEs>uroleacttieodnawndorkoebrs.se,rveJdand. e_1a,ths.19_6a_3rio-n*c* J.!3u: 7ni 0o 3a_ 0*s,be-1s9_to_7s1.
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Observed "deaths
Expected deaths*
Total cancer (all sites)
: 92 ` .,-.15.1 .
Cancer of lung, pleura, trachea, bronchus 47
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Lung'cancer
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' Pleural mesothelioma
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Peritoneal mesothelioma ,, Cancer of stomach, colon and rectum.
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. 12
3.0
Cancer all other sites Asbostosis
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14 :: 20
. '7.6
- > .+
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All other causes
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51.
63.5 *
Total deaths-
11. ,1.63 .
. 7S.6
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H'Exp'octed deaths are based upon ago -specific rates for U.S.
. white males in 1957. Smoking habits arc disregarded.
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+Unitcd States data not available but figure should bo only
v slightly loss than 1.5. t
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^United States data not availablo'Wt these are rare .causes i
of death in general population. '
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%
x: i,-.: '
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Table III
Mortality experience of 632 members of 1AHFIAW, locals 12 and 32 January 1, 1943 to June 30, 1971
Cause of Death Lung cancer Pleural mesothelioma Peritoneal mesothelioma Gastro-intestinal cancer . All other cancers
Total cancer = 188
Asbestosis All other causes 1/ - :
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Number 85 7
20 ! 40
36
Per Cent 20.0 1.6 4.8 9.3 8.4
32 7.7 205 48.2
425 100.0
Table IV
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Asbestos Air Levels in United States Citiep
Analysis of 187 Quarterly Composite Samples
Asbestos Air Levels (10-9 grams/m3)
Number of Samples With Given Vaule
0.0-0.9 1.0-4.9 5.0-9.9 10. 0-19. 9 20-49 50-99
61 103
12 8 2 1
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