Document NeQ8Va7y5BjZ7yJ6rNj0eDdRQ

y; j vv v m ' w i ; whc/ i^/ > w f ' J-PC& HER FUNG .* CHICAGO, OCT. /5j H71 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- * . .. I ' 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 was seen in 1935. l\vo cases of lung cancer were found in individuals having asbestosis. This portent was grimly verified in FMSI 06459 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. . * -. " . 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 School of Medicine. He has followed since January 1, 1943 the 632 . ; *9 ' 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 and boilers in apartment, office building and individual plants. Some of the material they use 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 tho lung, trachea and pleura where only six or soven wero oxpoctod; 12 diod of asbestosis although nono__ _ FMSI 06460 should have died; three times as many died of cancer of the G. I. tract as were expected. ' Results of continued observation of the group through June 30, 1971 are shown in Tables II and III. They represent a catastrophe. Over half .1 ' of the deaths were from some form of cancer or asbestosis. Nearly 40% could be termed "occupational" deaths. . ; Iri these latter data, special reference should be made to the high death rate from mesothelioma. Twenty-seven cases of this, as yet, in i' .' curable disease woro Boon. A diffvise concoj^ of the lining of the 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. Two 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 asbestos exposure and cigarette smoking in the incidence of lung cancer. Ily 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 Ib nearly ten times the number ex- FMSI 06461 pected in an 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 smoke run more than 90 times the risk of dying of lung cancer than men who neither smoke cigarettes nor work with asbestos. . liiese 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 swareness 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. . . Evidence is accumulating that mesothelioma is rapidly increasing among men who worked in tho vicinity of asbostos application. Recall, that mesothelioma is virtually nonexistent in people who have 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, welders*, carpenters, or painters, all of whom only wonked 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 ' survey of the material in the pathology departments of Scottish hospitals and medical schools from the years^l950 through 1967.- An investigation of the occupational background of these cases revealed a strong association FMSI 06462 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. ,. 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 exposui'es 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. 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 ' . With asbestos, 31 of the 76 cases having had documented occupational . 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 studies, 9 of the London mesotheliomas were in family members, as were 3 of the 46 Pennsylvania cases. FMSI 06463 Unfortunately, thfcse 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 a potential risk of cancer, at exposures much below occupational ones. Obviously, additional research and continued surveillance are highly desirable. 1 Let us now turn to specific items in your 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 other means. _ * To verify that such fireproofing oporntJ.ons 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 thev Department of Air Resources of New York City. The resultB demonstrated that spray fireproofing con indeed con- FMSI 06464 tribute significantly to asbestos air pollution. ' Up to 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 I to be a small amount, it could represent more than 10 million minute . fibers of asbestos. Moreover, the large clumps of asbestos-containing material covering the sidewalk serve as a continuing source to be dispersed by pasSersby. As I mentioned earlier, lacking a dosef-response relationship, we .* ' cannot state that environmental exposure levels from this practice are certain to produce disease. However, it is hard to imagine factory 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, the space between tho false room coiling and the under side of the fldo<r above, which has been sprayed with asbestos,,serves os o 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 Hew York City., we have not been \ `' . allowed to analyze the air in buildings that has been in direct contact FMSI 06465 with asbestos-containing Insulation. . Finally, this spray procedure leaves a legacy of potential risk to future generations. Ihe 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 will be followed but we have no such assurance at this.time. . Unfortunately, safe procedures developed for the spray application ^of asbestos-containing materials have not been 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. - . Moreover, because of uncertain knowledge of the health effects of ex posure to mineral fibers other than asbestos, i't 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 I 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, with proper procedures,.even asbestos cement con be applied with minimal release of fiber. FMSI 06466 9 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. For 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, even 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. . Since bag 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. . ' ., ( 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 on inspector they could pay for adequate air analysis by electron microscopy. - FMSI 06467 I enclose in Tabid 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 occunence and from the fiber size distribution on high .I samples, it appears that the contribution of some specific source is important in these high levels. 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 thpt 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 snfoty is demonstrated tho uso of nsboBtos.,.." In summary, your regulations in general are excellent, your intent is proper, and I am pleased to support you. FMSI 06468 Table I if Observed and Expected Number of Deaths Among 632 Asbestos Workers Exposed to Asbestos Dust 20 Years or Longer, 1^43-1962 . .... Cause of Death , `Years . 1943 1948- " 1953 ' 1947 1552 1957 . . Total, 1958-. 1943 1962 . 1962 Total, -all causes....'.................... Observed (asbestos workers) Expected (US whito males).. . Total cancer, all sites.............. Observed (asbestos workers) Expected (US white males... 28 39.7 " *m 54 50.8 i ' . '85 * 56.6 13 .17 5.7' 8*1. 26 13.0 88 54.4 255 203.5 39' 9.7 95 ; 36.5 Cancer of lung and pleura.,,. Observed (asbestos workers) Expected (US white males).. .6 . 0.8 Cancer of stomach, colon and V* 'rectum........................................................ Observed (asbestos workers) Expected (US white males).. ^ 4 2- 8 1.4 13 2.0 18 ' ..2.4 4" 2.5 \\\ - -7 .. ' .. 2.6 14 , 2.3 45 6.6 29 9.4 Cancer of all other sites com bined........................................................... Observed (asbestos workers) Expected (US white males).. 3 "5 . 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. .. 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. .` . $ * / . 4 * FMSI 06469 t Table n */ Expected and observed deaths among 370 asbestos insulation workers, Jan. 1, 19S3 - June 30, 1971, II I ill i . 54 ' ] (1 4 ! ' .. ' t: . ! it : i1i - * ti : ; ! j ' v. Observed Expected 'deaths '* deaths* Total cancer (all sites) ' : 92 . is. 1 Cancer of lung, pleura, trachea, bronchus V 47 ' `4.5 Lung'cancer ' '% . -. * : ' ' Pleural mesothelioma . Peritoneal mesothelioma '43 " 1 . V, ' Vi ... ,.*`4' '/ `i . 19 , i- *4* *+ .. + ... Cancer of stomach, colon and rectum. ;.. ;. . 12 3.0 Cancer all other sites ; . : .':v", 14 . 7.6 ; Asbestosis - ' '.. * ' . ; ' 20 . *. \ .* ' * .. .. 1 1 j' . ' ' All other causes /./. ' . ' ' Total deaths- ' . /, .. .. ' " 51. a, . '1.63 .. *\ , 63.5 . 7S.6 ' ^Expected deaths are based upon ago -specific rates for U.S. . white males in 1957. Smoking habits are disregarded. . -i-Unitcd States data not available but figure should bo only V slightly less than 4.5. ' . : . ^United States data not availablo'lbut these are rare .causes . of death in general population. ' ; ' 41* ...' : y'-`" !'* *: ii .*..**:,* V * . . \; * . ' ` . ;!..v"' ' *\ **.- * , /,, * . , ; * '/ ` ; ' _ I * ..*" V*. *. . * 1 ' ' ` . *.;**v 'y': f'('`*V'.. . `^ ' ' . ' ' ' | * ft l. M < *./. ... -y.. i ./',* ' ... *. ,'* . 1 '* *'.'* ** ' * .* . * * . ' *.. , **,.* ' I ; . I . . ; ( * ' i ' % * *"* . 1 f , i* '. 'I ! *.\v ' '*. ' v . I * FMSI 06470 Table III Mortality experience of 632 members of IAHFIAW, Locals 12 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 if : ' Number 85 7 20 ( 40 36 Per Cent 20.0 1.6 4.8 9.3 8.4 32 205 425 7.7 48.2 100.0 Table IV ' Asbestos Air Levels in United States Cities 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 s' 50-99 .. _ 61 103 12 ,8 2 1 " FMSI 06471