Document gE5jnGv4JY6JBqdB79vn373J9

ASBESTOS AIR POLLUTION IN URBAN AREAS I.J. Selikoff, M.D., W.J. Nicholson, Ph.D. and A.M. Laager, Ph.D. INTRODUCTION Early in the 1960s, the problem of asbestos disease was disseminated from the occupational area into the general environment. Three germinal observations were responsible for this. First, Kiviluoto reported finding 499 cases of parietal pleural calcification among 6,312 residents of a rural county in Finland.^ This came very much as a surprise, since the type of calcification observed had previously been described primarily in asbestos workers,2 usually more than 20 or 30 years after starting work;3 yet the cases were not among asbestos workers, but among farmers and farmers' wives. The asbestos link was, however, there - the county did have an asbestos mine. The natural supposition was that asbestos air pollution from the mine was responsible, a presumption that was strengthened when the specific type of asbestos produced by the mine (anthpohyllite) was found in the air up to 50 Km away,4 and asbestos bodies were demonstrated in the lungs of cattle grazing in the nearby fields.1' The same year (1960) saw a second worrisome communication. Vagner5 reported 47 cases of pleural mesothelioma in a part of South Africa important for asbestos mining. He unearthed potential asbestos contact for most of the patients two or more decades before, in many instances merely the result of living in the general area or by chance contact in a family setting. While pleural mesothelioma had previously been attributed to asoestos exposure,6 the strength of this association had not been appreciated. More pertinent, was the demonstration that it could result from other than occupational exposure. Amplification was soon added. Newhouse7 studied all mesotheliomas at the London Hospital. She confirmed the close association with asbestos, 31 of the 76 cases having had occupational exposure. She also confirmed the importance of non-occupational contact: of the 45 Who had not worked with the material, 9 had lived in the households of asbestos workers and 11 had lived decades before, within one-half mile of an asbestos plant! Lieben and Pistawka reported similar findings in Pennsylvania.8 What appeared to be a strong link in the chain of evidence for environmental asbestos disease was the report in 1963 by Thomson9 that asbestos bodies were canmonly to be found in the lungs of people in the general population of Capetown. He expressed a drop of lung tissue fluid onto a slide, as if preparing a smear for malaria examination, examined it by optical microscopy, and in one-quarter of 500 consecutive autopsies, found structures apparently identical with those seen in asbestos workers' lungs. But these were not asbestos workers - they had been ordinary citizens of this large city. Thomson concluded that they had inhaled Presented by I.J. Selikoff, 11.D., at the AlIA's Air Pollution Medical Research Conference on October 6, 1970, in New Orleans. Doctor Selikoff is Professor of Medicine and Professor of Community Medicine, Mount Sinai School of Medicine of the City University of New York and Director of Environmental Sciences Laboratory Mount Sinai School of Medicine. CHEV BB nnntiii "Tr l/o. asbestos in the course of their urban living, from the many asbestos products about them. With knowledge of what exposure to these fibers could do under industrial circumstances as a background, and with Wagner's observations as an example, he suggested that we were now faced with a "modern urban hazard ' and predicted that asbestos-associated neoplasms would rival cigarette-induced lung cancer in the future. It should be noted right off that Thomson's prediction is an extrapolation. It is a wide step from occupational exposure, with large numbers of asbestos bodies, to community contamination, with as a rule far fewer bodies, particularly with little knowledge of a dose-disease response relationship. Too, the particles described had the appearance of those seen in asbestos workers, but some uncer tainty existed that these necessarily had an asbestos core,10 especially since it had been known for 30 years that such bodies could be found after exposure to other fibers as well.11 Despite these caveats, the three reports, taken together, posed a problem that is now very much with us. Occupational asbestos exposure may be associated with serious risk; for example, among asbestos insulation workers in the New York metropolitan area at this time, approximately one in 5 deaths is due to lung cancer, one in ten is due to mesothilloma, one in ten to gastro-intestinal cancer and one in ten to asbestosis and cor pulmonale.1,2*'1'4 These men have been exposed to amounts of asbestos surely greater than those in the community gener ally, and we would not expect their risk to be duplicated in the general popula tion. But is part of their risk disseminated, with the dusts from their work? What sort of dose-response curve are we dealing with? Is there a threshold which once crossed leads to serious neoplasia hazard? An hypothesis could be formu lated that such a threshold includes very little asbestos (since small amounts may still reflect billions of fibers and/or fibrils), that asbestos workers pass it early in their careers. Such an hypothesis, or variations on it, would fit clinical observations made in the last several years. Neoplasms - lung cancer as well as pleural and peritoneal mesothelioma - occur in excess even jmang asbestos workers with little or no radiological evidence of asbestosis. It is now apparent that exposures insufficient to cause asbestosis may still produce neoplasia. The spread of this separation is not established, but is recognized by recent appreciation that while lower dust levels in industry may prevent much asbestosis, such levels will not necessarily prevent cancer.15 It is not now known how low a threshold must be to prevent asbestos-associated neoplasms, if such a threshold indeed exists. ASBESTOS IN LUNGS It thus became important to know whether asbestos truly was a common con taminant of urban dwellers' lung. The demonstration that "asbestos bodies" were to be regularly found at autopsy in msny cities of the world16 confirmed Thomson's finding, but did not settle the question. There remained the nagging doubt that the cores were necessarily asbestos, an insecurity perpetuated by the technical difficulties involved in analyzing such cores.17 In recent months, the impasse has been resolved by avoiding the detour of asbestos bodies, with the direct search for asbestos fibers and fibrils.18 In vestigation of 3,000 consecutive autopsies in New York had shown that asbestos bodies were common; optical microscopic examination of 175u x 1cm2 of lung tissue CHEV BB 0003112 .3. in each of these cases showed ssbestos bodies in 1,449 (48.3%) (Table I). It is likely that, had a greater volume of tissue been submitted for study, asbestos bodies would have been found in all the cases, except perhaps the infants and very young children. The same examination showed that, in addition to coated particles ("asbestos bodies"), uncoated inorganic fibers were also readily seen. Fibers thicker than l.Ou were almost universally to be found; most of these nre as yet still unidenti fied although some were diatom fragments, glass fibers or phytollths. We were more concerned, however, with thinner fibers - less than l.Ou in diameter - since these would be more consistent with chrysotlle, the asbestos variety making up 95% of the asbestos used in the United States. Such thin fibers were also coonon ly present, being found in 1,038 of the 3,000 cases, and tending to vary with the number of asbestos bodies (Table 2). The critical infoxmation was obtained by examining, in 28 of the 3,000 cases a very small portion of lung (conservatively estimated at 10"6) by a technique which allowed qualitative analysis,17 with the appreciation that the unique morphology of chrysotlle allows its specific identification by high magnification electron microscopy. Chrysotlle fibers and/or fibrils were found in every specimen. (Figures 1,2). In 4 of the 28, background contamination could conceivably have been responsible for the findings. In 24 of the 28, the number found was greater than background counts could explain (Table 3). The morphological appearance and other charact eristics of these fibers and fibrils and recorded elsewhere.19 It is evident that chrysotlle asbestos is a common contaminant of the lungs of New York City residents at this time. Similar electron microscopic observations have been recorded in London,90 where not only was chrysotlle asbestos found in almost 80 percent of cases, but it was noted to be the most common and most abun dant of all fibers detected. The question inherent in Thomson's observations in 1963 "is chrysotlle as bestos commonly found in the lungs of urban dwellers at this time?" has now been answered. Yes, unequivocally." RELATION OF ASBESTOS LUNG BURDEN TO ENVIRONMENTAL ASBESTOS DISEASE There are few data at this time that would allow Judgement of the significance of the asbestos we have found in lung tissue of urban residents. Whether or not the amounts present as the result of other than occupational exposure are associated with frequent risk of disease is not known. In part, this is a reflection of the paucity of data concerning the asbestos content of lungs in general, indluding those of asbestos workers. Such data as are available suggest that the amount in lungs of the latter is quite small, ranging fran 0.6 to 0.001 percent of lung weight.2122 it would be expected to be even lower in those not occupationally exposed. No information is at hand concerning the asbestos content of the lungs among Wagner's cases, or Newhouse's or those of other cases with environmental disease.23*24 Nor is there quantitative information concerning the asbestos content of the lung in individuals in the general population without asbestos stigmata. This is rather urgently needed, with age, sex, residence and occupational exposure taken into account. :hev bb 1003113 -4 Studies now In progress in our Laboratory and elsewhere25 indicate that suitable quantitative techniques for estimating asbestos lung content will be feasible and that fairly accurate estimates - approximating an order .of magni tude - are to be anticipated in the future. ASBESTOS AIR POLLUTION It is probably an entirely Justified concept that the asbestos found in urban dwellers' lung is derived from the inhalation of air contaminated with these fibers. Very little is known, however, of the conditions of such contam ination and facile assumptions should be avoided at this time. Previous Epidemiologic Observations An example of where an "obvious" explanation might also be inaccurate may be found in the assumptions adopted to explain Kiviluoto's observations. It seemed natural to expect that the demonstrable anthophyllite asbestos air pollu tion from the mine and mill was etiologically related to the equally demonstrable asbestotic pleural calcification in the population living about that point source. It turns out, however, that this may not be the entire explanation, and that in timate contact with local asbestos bearing rocks including those used in building houses, saunas, barns and the like might also play a role.25 Indeed, the latter association better explains almost identical epidemio logical findings in Bulgaria, where, again, pleural calcification was found in a rural population. In this district, too, an asbestos mine was being worked but it was an underground mine and had opened only in 1943, too recently for its dis charges to confidently be expected to have had the effect noted (the lapsed period between initial exposure and evidence of pleural calcification is 20, 30, 40 or more years). As in Finland, the local'field rocks have a high asbestos content and are used for various structures by the farming population, which then may have intimate contact with what is shed from them. More important, perhaps, the soils tilled by these farmers can be demonstrated to have asbestos fiber (anthophyllite) content. The importance of this observation was emphasized by the discovery that those farmers working plots without asbestos soil contamination had little pleural calcification, whereas farmers working soil with anthophyllite readily showed the radiological changes.28 It may be that similar explanations will became available for the finding of endemic pleural calcification in some rural areas of Czecho slovakia.29*35 Technical Factors At first glance, it seems somewhat surprising that so few data are avail able concerning the asbestos content of ambient air, especially since so much is known regarding the asbestos content of air within the work place. Perhaps the best explanation is that once the factory gates are passed, a whole new set of technical problems is encountered and sampling procedures, analytical approaches and measuring methods useful for industrial controls are no longer applicable. Fiber Identification Under industrial circumstances, there is usually no problem in knowing ex actly what is being measured, since the materials being used are either well characterized or can be readily analyzed. Thus, whatever fibers are seen can be confidently labelled as "chrysotile," "crocidolite", "amosite", "fibrous glass", etc. CHEV BB i\nnti 11 -5- If these same fibers were to be seen in s randan sample, especially if they are small, our confidence disappears. All that can be said is that inor ganic fibers are present. Even then, if these fibers were found in very large numbers, identification could be readily accomplished by such mass techniques as x-ray diffraction; but when they occur singly or randomly scattered in small numbers, these techniques are no longer applicable and readily available alter nate approaches such as polarized light microscopy, hardly have the same defini tive assurance. While it is true that analytical attach on single fibers is still possible, these approaches (including electron microprobe analyses, electron diffraction and electron microscopy) are time consuming and often restricted by the size of the particle available for analyses. (See below). Our own experi ence suggests that reticence is usually warranted when identifying single small fibers in-ambient air samples, unless extended techniques are used. Particles and Fibers There has long been an anomaly in particle counting for asbestos threshold levels. In the United States, a threshold level was proposed in 1938 for occu pational exposure to asbestos, based upon experiences necessarily limited to that point.31 The recommendation reflected the instrumental restrictions of the times and were based upon counting of "particles" by optical microscopy. It was recognized that such particles could either be fibrous or non-fibrous and that the proportion could vary widely according to the materials used, process studied, etc. Since the presumption is that only the fibers are responsible for the biological effect, such analytical dilution is hardly acceptable at this time and current approaches to industrial threshold limit values are based entirely on fiber count. But even here, the matter is not so easily disposed of, since the admixture of particles and fibers often includes surface interactions among them. Figures 3 and 4 show particles of clay and a diatom collected near a con struction site during sampling by our Laboratory. By light microscopy these would be categorized as "particles." Yet'by electron microscopy it was found that numerous fibers (fibrils) were attached to the surface of the particles (opposite surface charges!). In such circumstances, any biological effect of the fibers could be incorrectly attributed to the particles. The question of size and magnification are critical. Fiber-fibril Each asbestos fiber variety is quite different chemically, physically, structurally and morphologically.32 Chrysotile seems unique in its tendency to physical instability tinder a number of circumstances. The chrysotile "fiber" is not a unit whole byt is rather composed of a large number of individual fibrils, each from 30QA-400A (Figure 5). These unit fibrils cannot be seen with the optical microscope. The intact chrysotile fiber can be seen. Under industrial circum stances, this dichotomy is understood. It is recognized that when a population of fibers is counted, "invisible" fibrils are also present,33 but that the opti cally visible fibers reflect, in varying proportions under different circumstances, the total chrysotile population, even though there be but one fiber for a very large number of fibrils. Also, with proximity to the industrial source, many fibers are still present, not having been subjected to influences which could result in their separation into fibrils. In the ambient air, however, very little is known about the proportion of fibers to fibrils. The matter is of some importance, since not only must number be categorized as fiber and fibril, but the surface area and potential biological effect might be quite different with the same total chrysotile mass, with different percentage fibrillation. Once again, we retuzn to the problem of ultramicroscopic CHEV BB -6 size, since the proportion of fibers to fibrils cannot be determined without the electron microscope. Size It may be seen from the foregoing that a critical factor in studying asbestos air pollution is the utilization of techniques which will measure very small particles. It is unlikely that approaches which do not include the electron microscope will be effective. Indeed, one might add that high magnification electron microscopy will be needed, including magnifications of at least 20,000X (direct) and probably over 30,000X. While optical microscopy may be suitable as a guide for occupational asbestos exposure, it has insurmountable inadequacies in studying asbestos pollution of the ambient air. In addition to the fine diameter of the fibrils, it has been our experience that many of them are quite,short, as well. We have observed chrysotile fibrils with lengths less than lOOOA'in many instances; when these are enmeshed in samp ling debris, not only is high magnification electron microscopy necessary, but visual scanning may be inadequate, and Inferior to photographic recording.17 It may be worth noting that such small particles .are at present subject to identification by their morphological characteristics only; structural and mic rochemical analysis by electron microprobe or electron diffraction study has many difficulties. It may be hoped that instrumental advances will remedy this situation (greatly improved microprobe definition can be anticipated, for ex ample). Turkevich's "World of Fine Particles"34 is surely with us! Quantitation Under industrial circumstances, again, there is little difficulty in es timating the quantity of asbestos in a given sample of air. From this, the sur face area of the fibers can be estimated or directly measured by nitrogen absorp tion or other techniques. It is even possible to conceiye of gravimetric methods, rather than the more laborious counting of fibers. Quantitation is much more difficult in ambient air samples and, in our experience, only approximations can presently be obtained. Current Approaches to Asbestos Air Sampling With the foregoing factors in mind the absence of published lnfoxmation on asbestos levels in urban ambient air may be appreciated. Few air monitoring agencies have had available the technical equipment for the examination of ultramicroscopic asbestos fibrils. Moreover, even those fibers seen by optical micro scopy in air samples required elaborate techniques (such as electron diffraction or microprobe analysis) for positive identification. Present approaches to quantitating asbestos levels in ambient air, using ultramicroscopic techniques, have sought two objectives. First, to obtain a measure of the mass of asbestos per unit air volume at various locations in urban centers and later, for comparison purposes, in more rural areas. This would provide a stable estimate, since fiber size distributions change as sampling is undertaken at different distances from asbestos emission sources. In such cir cumstances, equal numbers of fibers can represent significantly different amounts. CHEVBB 0003116 7 - by weight, of asbestos. Moreover, It Is not currently known how strongly bio logical effect is dependent on fiber size. This being so, a measure by mass or weight may be more conservative for the establishment of air quality criteria and standards, as the biological effect of a sample dominated by large fibers may be overestimated. Second, fiber size distribution is important. At the moment, to obtain such a distribution at each sampled site is time consuming, and the presence of other material and existing transfer and sampling methods may distort the ob served fiber distribution. However, experiences in current studies suggest that these problems can be overcome and that complete fiber size distributions will be obtained at selected sites in the near future. Sample Preparation In our studies, air samples were collected on membrane filters having an effective pore size of either 0.8 or 1.2 microns. (Millipore AA or RA filters were used). While this pore size is larger than the largest dimension of sane asbestos fibrils, it has been found that the surface charge properties of the filter and the asbestos, as well as the circuitous path through the filter, allow virtually complete collection of all asbestos material. Both high volume samplers capable of drawing 40 cubic feet per minute through an 8" x 10" filter and small battery operated personnel monitoring samp lers with a capactiy of 2 liters per minute through 8 cm2, were found effective in sample collection. Portions of each collected sample were ashed in an act ivated oxygen asher which oxidized the membrane filter and all organic or car bonaceous material in the sample.35 The residue, consisting mostly of fly ash and mineral matter, was dispersed on a microscope slide by grinding in a solution of 1% nitrocellulose in amyl acetate for 2 to 5 minutes. Upon evaporation of the amyl acetate, the dispersal was scanned for uniformity by optical microscopy and a representative area chosen for transfer to an electron microscope grid for scanning. During this procedure, those chrysotlle fiber bundles present are broken into their elementary fibril fora. The grid so prepared of the dispersed chrysotile is scanned at 42,000X in an electron microscope. Typically, six grids are prepared of each sample and three 100 by 100 micron squares of each grid scanned. The mass of asbestos is obtained by measuring the volume of asbestos per grid square and multiplying by the appropriate density. Figure 6 shows several isolated fibrils in an ambient air sample as seen by electron microscopy. Usually only single fibrils, if any, are observed in the microscopic field. However, as one samples near sources of asbestos, more large fiber bundles are present in the initial sample. As these are dispersed during sample pre paration, occasionally same groups of fibrils remain intact. Such a group is shown in Figure 7. The presence of these bundles, or even localized fibril clumps, gives rise to a variation between samples greater than one would expect from statistical considerations alone. However, the scanning of many grid squares serves to average their effect. Results of Initial Investigations Table 4 gives the ranges of values for ambient air levels measured at various sites in New York City. These samples were taken at selected locations of the sampling network of New York City's Department of Air Resources. The sites were all located on public buildings distant from any known significant source of :hev bb iaa-* 8 ' asbestos. While preliminary in nature, the samples from Manhattan tended to be higher than those from other boroughs. Lowest values were usually from sites most distant from densely populated business areas (Staten Island). While amounts ranging from approximately 10 to 100 x 10"9 grams per cubic meter of sampled air may appear to be exceedingly small quantities of asbestos, it is well to recall that chrysotile asbestos easily fragments into ultimate fibrils 300A to 40ol in diameter and often 2000A or smaller in length. Thus, 10~9 grams of chrysotile asbestos could represent a million fibrils. That Manhattan has higher levels of asbestos that other boroughs is to be expected, as greater use of asbestos in building construction takes place in that borough. Curing the past 10 years it has been common practice to spray fireproofing material containing from 10 to 30% asbestos, onto girders, spandrels and decking of high-rise office buildings. Often inadequate precautions were taken by contractors to contain the spray material and extensive "snowfalls" of asbestos containing material took place over wide spread areas of Manhattan. This practice was of such obvious concern that the New York City Department of Air Resources instituted stringent regulations controlling the procedure in May, 1970.36 Table 5 records findings on several days at various sites in lower Manhattan near buildings under construction. Data were obtained prior to the implementation of New York City's regulations. During the two days on which data were obtained sites 1 and 4 were downwind from a spray source, 3 and 5 were upwind from any source, and 2 was 45 from one source and upwind from others. The data in New York are being supplemented by measurements in other urban and more rural areas. Initial data are shown in Table 6. The sampling locations in Philadelphia were near sites where spraying was taking place but after the issuance of control regulations. These data are preliminary. They serve to establish that, at least in theareas sampled, there is a background of chrysotile contamination of the ambient air and that this is considerably higher about construction sites in urban areas. Much more information will be required, however, before reliable estimates can be made concerning quantitative levels of such contamination. EPIDEMIOLOGICAL PERSPECTIVES Environmental Disease The occurrence of asbestos pollution of urban air is now established. What has not been defined, however, are the dimensions of disease which may be associ ated with this pollution. Indeed, it is hardly proper to speak of "asbestos air pollution" in general terms. There are different sets of circumstances in which such pollution can occur, varying in intensity, intimacy and duration of exposure. For example, the pollution which might exist about a shipyard or an asbestos mill can hardly be equated with that in the ambient air of an urban community. It would be well, at least until much more is known of the dose-disease response relationship, to separate each type of asbestos air pollution, in the study of associated disease. CHEVBB 0003118 9- Lapsed Period A problem common to all types of asbestos air pollution is the Ions lapsed period between onset of exposure and appearance of disease. In general, this is 20, 30, 40 or more years insofar as neoplasia is concerned. There are variations, of course. It may be that intensity of exposure is one such variable; others could include fiber variety, fiber size, competitive risk of asbestoais37 co-factors as cigarette smoking,13 trace elements, and perhaps other concomitant air pollutants. Defined Populations It should be recognized that the different kinds of asbestos air pollution are not limited to well separated compartments. Exposure to general community asbestos air pollution may be overwhelmed by indirect occupational exposure, in the case of a construction workman.. Similarly, the asbestos inhaled by virtue of family contact in the household of an insulation worker could hardly be attri buted to the scant asbestos fibrils in the air of a rural community in which that employee happened to live. Such permutations are common and may be misleading unless identified. When considering neighborhood air pollution about an asbestos plant (30 years ago: since it would be these people with whose fate we would now be concerned) it is well to remember that, at least in the 1930s and 1940s, people who worked in a plant tended to live near it. Thus, the population about a plant being studied would have to be well characterized, to identify those with direct occupational exposure, before the effects of neighborhood contamination could be evaluated. Other examples could be given. The construction industry, for Instance, employs over 4,000,000 men in the United States. They live in all areas, in all types of communities. Asbestos disease among them may not be entirely the result of asbestos air pollution in those communities. Special circumstances have also occurred. During World War II, shipyard employment rose rapidly in the United States, with close to 1,750,000 people engaged in ship building and repair at peak periods. These people, or at least those still alive, are now reaching 30 years from onset of shipyard employment and such asbestos disease as they might have as a consequence of asbestos exposure during their shipyard working days, will now be seen. Yet few of them are still employed as shipyard workers, so that unless this previous employment history is extracted, current disease could be improperly attributed to asbestos air pollution of various other sorts. Stigmata of Asbestos-Associated Disease The matter is further complicated by consideration of what is meant by disease caused by asbestos air pollution. Most of our current concepts are de rived from the experiences of occupationally exposed workmen. While the same kind of disease can be seen in people not occupationally exposed, its attribution is much more difficult. It is complicated, moreover, by the necessity for sepa rating those effects of asbestos which may be present but which do not actually constitute ill health, from those effects which should be categorized as disease. Pleural plaques and pleural calcification, for example, are often associated with no disability, even when impressively extensive on roentgenogrsms.lt3 The same could be said for the mere demonstration of asbestos fibers and asbestos bodies in lung and for scattered areas of minimal fibrosis associated with the asbestos fibers in the lung. CHEV BB 0003119 10- Neoplasia is a different matter. Here, there is considerable -concern. Those neoplasms which have been found associated with occupational asbestos exposure have included bronchogenic carcinoma, pleural mesothelioma, peritoneal mesothelioma. Gastrointestinal cancer, oro-pbaryngeal neoplasms14 and other neoplasms are also under investigation, but more data are needed before their association can be considered fintly established. There has been the problem of identifying neoplasms associated with en vironmental asbestos exposure against the background of random neoplasms of the same kind, not due to asbestos exposure, bang cancer, for example, is highly associated with cigarette smoking and the added influence of environmental asbestos exposure is not easy to define. There is an advantage in studying mesothelioma, since evidence suggests that, apart from asbestos exposure, it has been a fairly uncommon disease. Yet even here more data are needed. It would be good to know, for example, exactly what the incidence of mesothelioma has been in the past 70 years, during decades in which the neoplasm was often not considered by pathologists. Too, it would be useful to have information on the percentage of mesothelioma which occurs other than with asbestos exposure. With such refinements, we will be able to use mesothelioma as an accurate index of asbestos disease under various environmental conditions. Sources and Control Sources for asbestos air pollution can be looked at in two ways. First, they can be identified and measured without reference to exposed populations. Epidemiological attention may then be attracted to these "contamination sources in search of disease." Alternatively, sources for asbestos air pollution can be studied in relation to their potential for exposure of human populations. Both approaches are hampered by inadequate information at this time of the relative significance of peak exposures compared to constant background contam ination. There are clinical experiences which Indicate that heavy exposure for brief periods (days, weeks, months), with retention of the inhaled fibers for the rest of the individual's lifetime, may carry serious disease potential. Therefore, intermittent high peak exposures may carry an unusual risk, especially when added to the cumulative retention associated with background pollution over long periods of time. Adequate information is needed concerning the natural history of asbestos air pollution, including persistence, variations with meteorological conditions and ultimate fate. Asbestos fibers, being mineral, may persist in the environment for long periods. It is not known, however, if this is so, or to what extent attrition occurs by a variety of physical processes. We have found amosite asbestos fibers in the settled dust and in the household air, within homes which had been occupied IS years before by workmen of an amosite factory. Similarly, both settled dust and ambient air in a construction workman's heme contained chrysotile fibers at levels beyond those usually observed as background. Neighbor hood contamination from factory sources may also be associated with long per sistence of the mineral fibers. In preliminary studies, we have found this to ` be true of both superficial soil contamination and settled dust on attic rafters, in such neighborhoods. It is apparent that information concerning persistence and fate of asbestos air pollution would be important, if only as a background to the evaluation of air levels from current emission sources. CHEV BB -11- Natural Sources of Asbestos Air Pollution It is likely that same sir contamination occurs from natural sources. Serpentine rock outcroppings occur in many parts of the United States and other countries. Studies in our laboratories suggest that, on an ultramlcroscopic level, serpentine very frequently contains same fibrous mineral components, which are properly classified as chrysotile. In addition, some outcroppings contain frank chrysotile veins. Such chrysotile-containlng rocks are widely distributed, although not necessarily in commercial concentrations. It may be of interest to recollect that the original sources for chrysotile asbestos used by the company which later became the Johns-Manville Corporation, were in small deposits on Staten Island, in New York City. Such surface deposits have long been known to geologists and are sometimes used as a guide in their explorations. The tale is told of fortuitous forest fires initiated by lightning in the 1860's in Quebec, resulting in clearing of brush overgrowth. This uncovered surface chrysotile-bearing serpentine formations, leading to the discovery of the valuable Quebec chrysotile fields. Abrasion and weathering of such surface formations may be accompanied by release of chrysotile fibers into the surrounding air. It is expected that this has occurred. It is not known, however, whether this adds a measurable burden to the ambient air, but it should be considered as one source in the evaluation of ambient air levels. It is apparent that quantitative studies in this regard would be helpful; we are investigating the chrysotile content of ice core samples, accurately dated for many years past, in one study. Other approaches would be useful, and can be designed. Soil contamination has already been mentioned (see above) and epidemiological data have been collected Indicating that human exposure from this source can pro duce pleural changes.27*28 Wider dissemination from this source is also possible, and should be investigated. Parenthetically, ground waters coursing through asbestos-bearing rock formations may be expected to became contaminated by random fibers, and water from such sources could contain occasional fibers, without in voking the necessity for asbestos air pollution. Industrial and Commercial Sources Although natural sources for asbestos air pollution should be considered, it is likely that they add but an infinitesimal amount to the asbestos air bur den in urban areas. Host.is derived from commercial and Industrial sources. Here, emission-source inventories can be prepared and would include transport and storage of raw fiber supplies, manufacture of the many useful asbestos-containing products, transport and end-use of these products, and their weathering and ulti mate disposal as waste. The relative contribution would vary with the type of product. In general, the potential for pollution varies with the degree of fix ation of the fiber in the product. Under circumstances in which asbestos is loose or the material friable (asbestos cements, insulation materials, etc.) the like lihood of fibers becoming airborne is greater; conversely, where the fibers are more or less bound in the product's matrix, the likelihood la considerably de creased (asbestos cement materials, asbestos containing plastics, etc.). The spectrum of this variation requires detailed study, since control efforts will be guided by the findings. 3HEV BB 1003121 -12- Such analyses night well be focused, at the outset. In the construction industry. Approximately two-thirds of the asbestos used in the United States is used in construction products. Ship building and repair, and waste disposal of asbestos products are important areas for study. Spraying of asbestos-con taining mineral fiber insulation has already been mentioned. Factory Missions are an obvious - and controllable - difficulty. Housekeeping in all asbestos using facilities may turn out to be a knotty problem, and ultimately associated with much asbestos air pollution. Our experiences suggest that much education on appropriate methods for containing asbestos in commercial use will be neces sary; here, the asbestos industry has both important responsibility and oppor tunity. CHEV BB 0003122 REFERENCES 1. Kiviluoto, R. Pleural calcification as roentgenologic sign of nonoccupational endemic anthophylllte - asbestosis. Acta Radiol. Suppl. 194 pp 1-67, 1960. 2. Jacob, G. and Bohlig, H. Roentgenological complications in pulmonary asbestosis. Fortschr. Roentgenstr. 83:515-525, 1955. 3. Selikoff, I. J. The occurrence of pleural calcification among asbestos insulation workers. Ann. N.Y. Acad. Sc. 132:35-367, 1965. 4. Laamanen, A., Koro, L. and Raunio, V. Observations on atmospheric air pollution caused by asbestos. Ann. N.Y. Acad. Sc. 132:240-245, 1965. 5. Wagner, J.C., Sleggs, C.A. and Marchand, F. Diffuse pleural mesothe lioma and asbestos exposure in North Western Cape Province. Brit. J. Indust. Med. 17:260-271, 1960. 6. Weiss, A. Pleurakrebs bei lungenasbestose, in vivo morphologisch geSichert. Medizinische p.93, 1953. 7. Newhouse, M.L. and Thompson, H. Mesothelioma of pleura and peritoneum following exposure to asbestos in the London area. Brit. J. Indust. Med. 22:261-269, 1965. 8. Lieben, J. and Pistawka, H. Mesothelioma and asbestos exposure. Arch. Envir. Health 14:559-563, 1967. 9. Thomson, J.G., Kaschula, R.O.C. and MacDonald, R.R. Asbestos as a modern urban hazard. South Afr. Med. J. 7:77-81, 1963. 10. Gross, P., Cralley, L.J. and deTrevllle, R.T.P. Asbestos bodies: their nonspecificity. Amer. Indust. Byg. Assoc. J. 28:541-542, 1967. 11. Williams, E. "Curious bodies" found in the lungs of coal-workers. Lancet 2:541-542, 1934. 12. Selikoff, I.J., Churg, J. and Hammond, E.C. Asbestos exposure and neoplasia. J.A.M.A. 188:22-26, 1964. 13. Selikoff, I.J., E.C. Hammond and. Churg, J. Asbestos exposure, smoking, and neoplasia. J.A.M.A. 204:106-112, 1968. 14. Selikoff, I.J., Hammond, E.C. and Churg, J. Mortality experiences of asbestos insulation workers, 19415-1968. Proc. Int. Coni. Pneumoconiosis, Johannesburg, 1969. In press. 15. Lane, R.E., et al Hygiene standard lor chrysotlle asbestos dust. Ann. Occup. Hyg. 11:47-49, 1968. 16. Selikoff, I.J. and Hammond, E.C. environmental asbestos exposure. 1968. Community effects of non-occupatlonal Amer. J. Pub. Health 58:1658-1666, CHEVBB 0003123 4- 17. Laager, A.K., Selikoff, Z.J. and Saatre A. Chrysotile asbestos in the lungs of persons in New York City. Arch. Envlr. Health. In press. 18. Longer, A.K., Baden, V., Hammond, E.C. and Selikoff, I.J. Inorganic fibers, including chrysotile, in lungs at autopsy: preliminary report. Proc. Third Int. Symp. Inhaled Particles, London, 1970. In press. 19. Larger, A.M. and Mackler, A.D. Morphology of chrysotile asbestos fibrils: electron microscopic observations. Aaer. Mineralogist. To be published. 20. Fooley, F.D., Oldham, P.D., Dm, Chang-Byun and Vagner, J.C. The detection of asbestos in tissues. Proc. Inti. Coni. Pneumoconiosis, Johannesburg, 1969. In press. 21. Sundius, N. and Bygden, A. Der staubinhalt einer asbestosis-lungen and die beschaflenheit der sogenaxmter asbestosis - korperchen. Arch. Gewerbepath. 8:26-80, 1938. 22. Beattie, J. and Knox, J.F. Studies of mineral content and particle size distribution in the lungs of asbestos textile workers. In: Inhaled Particles and Vapours, Ed. C.N. Davies, Pergamon, New York, 1961, 419-433. 23. Bohlig, H., Dabbert, A.F., Dalquen, P., Hain, E. and Hinz, I. Epidemiology of malignant mesothelioma in Hamburg. Envlr. Res. press. In 24. Borow, M., Conston, A., Livomese, L.L. and Schalet, H. Mesothelioma and its association with asbestosis. J.A.M.A. 201:587-591, 1967. 25. Pooley, F.D. Personal Communication, July, 1970. 26. Raunio, V. Occurrence of unusual pleural calcification in Finland. Studies on atmospheric pollution caused by asbestos. Ann. Med. Intern. Fenniae 5S:Suppl. 47 pp.61, 1966. 27. Zolov, C., Bourilkov, T. and Babadjov, L. Pleural asbestosis in agricultural workers. Envir. Res. 1:287-292, 1967. 28. Burilkov, T. and Nichailova, L. Asbestos content of the soil and endemic pleural asbestosis. Envlr. Res. In press. 29. Hromek, J. The mass Incidence of characteristic pleural changes in citizens of the western part of the former Jihlava region. Rozhl. V. Tuberk. 22:405-414, 1962. 30. Rous, V. and Studeny, J. Aetiology of pleural plaques.Thorax 25(3): 270-284, 1970. 31. Dreessen, W.C., Dal1avalle, J.M., Edwards, T.I., Miller, J.V. and Sayers, R.R. with Eason, H.F. and Trice, M.F. A study of asbestosis in the asbestos textile industry. Pub. Hlth. Bull. # 241, August 1938, Washington, D.C. CHEV bb 3 32. Spiel, S. and Leineweber, J.P. Asbestos alnerals la sodsrn technology. Envir. Bs. 2(3):166-206, 1969. 33. Lynch, J.R. and Ayer, E.E. Measurewent of asbestos exposure. J. Occ. Med. 10:21-24, 1968. 34. Turkerich, J. The world of fine particles, Aamr. Sci. 47:97-119, 1959. 35. Berkley, C., Churg, J., Sellkoff, Z.J. and Snith, W.K. The detection and localization of alneral fibers in tissue. .Inn. H.Y. Acad. Sc. 132:48-63, 1965. 36. Departsent of Air Resources, City of Xew York. Conissloner*s' Order: In the Matter of Spraying of Asbestos - Containing notarial. May 13, 1970. 37. Jacob, G. and Anspach, M. Pulaonary neoplasia anong Dresden asbestos workers. Ann. K.Y. Acad. Sc. 132:936-548, 1965. 38. Sellkoff, I.J., Bader, R.A., Bader, M.., Churg, J. and Easnond, E.C. Asbestosis and neoplasia. Anor. J. Med. <12:487-496, 1967. :hev bb Illustrations Figure 1 Oirysotile fibrils sepsrated from human lung tissue. Figure 2 Examples (A-G) of the association of ehrysotile fibrils and incompletely digested lung tissue. Figure 3 A clay particle with adsorbed ehrysotile fibrils, in an air sample about a construction site. Figure 4 Adsorption of ehrysotile fibrils onto surface of a diatom. The fibrils would not be seen by optical microscopy. Figure 5 A ehrysotile "fiber," considered a single unit by optical microscopy, is seen composed of Individual fibrils (300&-400A diameter) by electron microscopy. Figure 6 Single, short fibrils collected 3/16 of a mile downwind of a ehrysotile source. Arrowhead indicates position of a clay particle. Figure 7 Group of ehrysotile fibrils in air sample near an asbestos source. Such bundles or clumps are less common in samples at greater distances from emission area. CHE-V BB Table I Asbestos Bndiw in 3.000 conaocutlvc utopiloa, H.Y.C. 1966-1968 *& <1 1-19 20-38 40-38 60-76 04 . Male 2/73 ( 2.8%) 0/7 r o,,o%> 34/102 (33.3%) 318/606 (32.1%) 3SS/997 (55.7%) 106/186 (57.0%) 1013/1971(31.4%) resale 2/93 ( 3.8%) 4/25 ( 16.0%) 19/58 (32.8%) 108/247 (43.7%) 220/491 (44.8%) 83/155 (53.5%) 436/1029(42.4%) Total 4/126 ( 3.2%) 4/32 (12.3%) 53/160 (33.1%) 424/853 (49.7%) 775/1488(52.1%) 189/341 (55.4%) 1448/3000(48.3%) A. Analysis by nt. a 1-19 20-39 40-99 60-79 80*. 0 122 28 107 429 713 152 Asbestos todies 1-4 5-14 15 ' 2 4 53 359 630 156 2 0 0 45 105 40 0 0 0 20 40 3 TOTAL 126 32 160 853 1488 341 . Anilyili by mx. Asbestos Bndlti 0 1-4 5-14 IS*. Male tail* 38 (4S.) 383 (57.6) >02 (40.7) 392 (38.1) 132 (7.7) 40 (3,9) 38 (3.0) 4 (0.4) 1,981 1,194 192 93 TOTAL 1,871 (100.0) 1,029 (100,0) 3,000 Table II Inorganic fibers (optical elcroscopy) in lunia of 3000 conaecutiva autopsies, KYC, 1966-1969. Correlation with aabeatoa bodies. Bodies 0 1-4 8-14 15*. 09 1,168 (59.5%) 705 (35.9%) 76 ( 3.8%) 13 ( 0.66%) 1,962 (65.4) 1-4 332 (38.3%) 424 (49.0%) 89 (10.3%) 20 ( 2.3%) 865 (28.6) 5-14 35 (28.0%) 87 (41.6%) 21 (16.8%) 17 (13.6%) 125 (4.1) 15* 16 (33.3%) 13 (27.1%) 6 (12.5%) 13 (27.1%) 46 (1.6) Asbestos todies 0 1-4 5-14 15*- 0 1.168 (73.3%) 705 (99.0%) 76 (39.6%) 13 (20.6%) Thin inorganic fibers 1-4 5-14 15* 332 (21 .4%) 424 (35.5%) 89 (46.3%) 20 (31.7%) 35 (2.3%) 52 (4.3%) 21(10.9%) 17(27.0%) 16 (1.0%) 13 (1.1%) 6 (3.1%) 13(30.6%) . TOTAL 1,651 (51.7) 1,164 (26.6) 123 ( 6.4) 63 ( 3.1) CHEV BB 0003127 Ittlt SIS Qgyaotlla i 39 Om Otadlad 1 3 3 4 3 Blaafc Qrlda" tateri f Cteyaotftla Fibara Hbrlla m or < f 10-40 51-99 100-300 >901 or < 9 ban vat 11/39 9/M 4/39 3/39 Mala 3 5 1 4 3 hula 1 9 5 0 0 -- CHEV BB 0003128 Sampling Locutions Manhattan Bronx Brooklyn Queens Staten Island Table XT Content of Antalant Air in W.T.C. Prelinlnary Results Asbestos air level in 10***grmas/a3 29-60 25-28 19-22 18-29 11-21 Table V Chrysotile content of R.T.C. air In vicinity of spray fireproofing with asbestos-containing Materials Site 1- Downwind from source 2- 45 from source 3- Upwind from source 4- Downwind from source 5- Upwind from source Asbestos level in 10 49-180 15-30 20 45 20 Table VZ Chrysotile content of air in three selected locations Location Philadelphia, Pa. Ridgewood, H.J. (suburban) * Port Allegany, Pa. Q Asbestos lerel in 10 graas/n 45-100 20 10-30 *We have also found amosite fibers in the air of this eoeananity; a factory using this material is present. :hev bb 1003129 Fig. 1 CHEV BB 0003130  * Fig. 2 CHEVBB 0003131 Fig. 3 1 mu CHEV BB Fig. 5 r 3HEV BB *003133 / i * f. *1 *\ , 1.0 mu Fi*. 6 n 0.4 mu VJT_ 1 CHEVBB nnnil "i/i The following itesis arc suggested when purchasing a phase-contrast microscope for use in evaluating airborne asbestos dust for comparison with the A.C.G.I.ll. Thrcshhold Limit Value (T.L.V.) 1970. 1. Microscope body with a binocular head and a fine focus accuracy of .005 mm. 2. 10X Kuygenian eyepiece (s) 3. Porton reticle 4. Mechanical stage 5. Koehler illumination (preferably built in and having provisions for adjusting light intensity) 6. Abbe condenser with an adjustable iris 7. 40 - 45 X (.65 K.A. at least) Positive (bright field) phase-contrast objective 8. Annular ring condenser diaphragm (corresponding to the objective) 9. Phase ring centering telescope 10. Green filter Note Most manufacturers sell a basic body unit and ' built-in illuminaLion system as a unit. Phase-contrast accessories can usually be purchased as a kit usually consisting of a 10X, 40X and 90X ob jective, an Abbe condenser containing appropriate annular ring diaphragms, a phase ring centering telescope, and a. green filter. It is to the microscopist's advantage to purchase the kit. A list of manufacturers of phase-contrast microscopes is given here to aid in selecting a proper instrument. Bau^-ch and Lomb Scientific Instrument Division' 72624 Bausch Street Rochester, New York 14602 CHEV BB Hacker Instruments Box 646 " West Caldwell, New Jersey 07006 E. Lcitz Inc. Rockleigh, New Jersey 07647 Nikon Inc. Instrument Division Garden City, New York 11530 Olympus Microscopes Micro Optics Company 28165 Greenfield Southfield, Michigan 48075 American Optical Corporation Reichert Prbducts Buffalo, New York 14215 Unitron Instrument Company Microscope Sales Division '66 Needham Street Newton Highlands,Massachusetts 02161 Carl Zeiss 444 Fifth Avenue New York, New York 10018 Additional Information on airborne asbestos dust evaluation is available in the paper, Equipment and Pi-ocodurcs for Mour-tin~ Millioorc Filters and Counting, Asbestos Fibers i>v. khase Contrast Microscopy by S. G. Bayer and R. D. Zumwaloe. 2 Prepared by: Stephen G. Bayer and James S. .Ferguson National Institute for Occupational Safety and Health Division of Training . 1014 Broadway Cincinnati, Ohio 45202 CHEV BB 0003136