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Effects of Asbestiform Fibers on Human Health This chapter begins with a discussion of the types of evidence that researchers generally use in determining causes of disease. It then pro~ldes information on biodispositlon of fibers and on diseases associated with exposure to asbestos. A discussion of health consequences that have been associated with nonoccupational exposure of humane to asbestos and other asbestiform fibers is followed by a description of occupational epidemiological studies. NATURE OF EVIDENCE Three lines of evidence--clinical, epidemiological, and laboratory- are considered when determining whether a particular environmental agent may cause adverse effects on human health. For asbestos, as for most hazardous environmental agents, the first evidence of health effects was provided by clinical observations. Physicians observed that individual or clusters of cases of pneumoconiosis,} lung cancer, and finally mesothelioma were associated with exposure to asbestos. Paeumoconiosis was the first health effect to be associated with asbestos. In 1907 Dr. Montague Murray reported his observations of such disease in a man who had worked in a carding room at an asbestos plant in England (Murray, 1907~. In 1924, Cooke wrote that "medical men in areas where asbestos is manufactured have long suspected the dust to be the cause of chronic bronchitis and fibrosis....- (Cooke, 19241. Numerous other reports followed. Other types of paeumoconioses, such as silicosis, were also known at that time, so asbestosis, the fibrotic disease caused by asbestos, was not an entirely new type of disease. However, mesothelioma was sufficiently rare that its connection with asbestos was not accepted until 1960 (Wagner, 1960~. Clinical observations led to the hypothesis that asbestos caused the observed disease. Epidemlologists then conducted studies to ascertain whether the hypothesis was true. The association was eventually Pneumoconiosis is the pathological reaction of tissue to the inhalation and accumulation of dust in the lunge. 97 . ..

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98 established primarily through cohort studies, in which the rate of disease occurrence in an exposed group is compared with the rate in a group not exposed to the material of concern (Do1l, 1955; McDonald and McDor - ~d, 1981; Selikoff and Hammond, 1979~. In laboratory studies, asbestos was administered to avowals to determine whether pathological effects similar to those found in humans could be induced. These experiments followed the methodology established in the Scientific study of infectious agents as causes of disease--a methodology later extended to the investigation of noninfectious agenda. However, performing the experiments and interpreting the results are more complicated for diseases with long latency periods. The laboratory studies demonstrated that asbestos could cause rung cancer and mesotheliomas in animals. Fibrotic reactions, however, usually differed somewhat from the lesions observed in humans with asbestosis. This difference could be attributed to variation among species and in the nature and amount of fibers (Wagner, 1960~. Each of the three kinds of data have strengths and weaknesses. The clinician distinguishes the observed disease from similar conditions and considers the possible links to environmental and other factors. Thus the clinical contribution to understanding lies primarily in the definition of clinical entities and in suggesting possible etiological factors. Erroneous conclusions may be drawn--or new insights gained--if an atypical group of cases comes to a particular clinician's attention. Difficulties may also arise if the observed effects are confused with other syndromes with similar signs and symptoms. Misinterpretation may also occur because of the usual reliance at this stage on nonquantitative methods of assessing the relationship to environmental circumstances. The epidemiological approach results in the quantification of risk for a defined health effect associated with exposure to particular environmental circumstances. During the application of this method, two types of errors are commonly made: (~) the findings are generalized too far beyond the population and circumstances studied and (2) there is a failure to adequately take into account the presence of other factors that may be involved in addition to, or instead of, the major factor being examined. In laboratory experiments in animals, the investigator has the great advantage of being able to exercise control over the conditions of observation, rather than having to rely on observations of natural phenomena as in most nonintervention clinical and epidemiological studies. Also, the laboratory investigator can make more detailed observations over time, thereby increasing the potential for ascertaining the mechanism or steps by which the agent exerts its effect. On the other hand, inference from one species to another carries some uncertainty. There is also uncertainty in extrapolating from laboratory observations to the exposures and resulting effects experienced by humans. Furthermore, laboratory animals are usually exposed to one agent, whereas humans are exposed to many.

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99 Ultimately, the determination of a causal relationship between exposure to an environmental agent and a health effect is a Judgment based on careful evaluation of evidence. Guidelines for making such causal inferences have been suggested and generally adopted. For example, Koch's postulates for infectious agents constituted a powerful and widely accepted framework for Judging laboratory evidence to determine whether a particular microbiological agent is responsible for a certain disease. No such guidelines have been generally established for noninfectious agents. Perhaps the closest approximation is provided by the frequently cited criteria adopted by the Surgeon General's Advisory Committee on Smoking and Health (1964~: - The causal significance of an association is a matter of judgment which goes beyond any statement of statistical probability. To judge or evaluate the causal significance of the association between the attribute or agent and the disease, or effect upon health, a renumber of criteria must be utilized, no one of which is an all-sufficient basis for judgment. These criteria include: (a) The consistency of the association [with diverse methods and among multiple studies] (b) The strength of the association [ratio of rates among those exposed to rates among those not exposed ~ (c) The specificity of the association [precision with which one component of the associated pair can be used to predict the other ~ (d) The temporal relationship of the association [i.e., which comes first, the agent or the disease] (e) The coherence of the association [with the natural history and biology of the disease] The more of these criteria tat are met and the stronger the evidence related to them, the more likely it is that a causal relationship exists. As another example, Hackney and Lit (1979) have updated Koch's postulates and applied them to environmental toxicology. ID evaluating relationships between exposure to hazardous environmental agents and adverse health effects, it is useful to proceed beyond identifying and confirming the hazard to quantifying the risks under various conditions. In a recent publication of the National Research Council (1983b), the authors noted that the steps of risk assessment involve (~) identification of a toxic agent and its effects, (2) determine Lion of dose-response relationships, (3) determiD.ation of the extent of exposure, and finally (4) determination of risk. . - ..

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100 In some situations, it is difficult to identify the effects of an agent because a given disease, such as lung cancer, may be caused by a variety of agents. mus, exposure to cigarette smoke, asbestos, certain chromates, ionizing radiation, some chemicals, and possibly other agents may all increase the chance that a person will develop lung cancer. By contrast, for infectious diseases such as typhoid fever or tuberculosis, the microorganism is the specific and only cause, although not everyone infected by the organism gets the disease. For most cancers, there is some chance that an individual will get the disease even with no known exposure to an identified cause. In comparing the risk of developing the disease in an exposed person to the risk for an unexposed person, it is often crucial and difficult to determine the existence and value of a 'background" rate for the disease. A background rate is the rate of occurrence of a disease with no association, or no known association, with the agents being considered. Exposure to an agent such as asbestos may then increase this background rate. For example, some lung cancer occurs in the absence of cigarette smoking or exposure to asbestos. In the absence of exposure to asbestos, cigarette smoking increases the chance of getting lung cancer (compared with nonsmokers) up to a factor of about 10, varying with the number of c igarettes smoked (U. S. Department of Health, Education, and Welfare, 1979~. Asbestos exposure among insulation workers who do not smoke cigarettes increases the risk for lung cancer up to about 5 times (Harmond et al., 1979~. Together, the cigarette smoking and asbestos exposure appear to produce a multiplicative effect, i.e., the lung cancer rate is inc reased up to 50-fold above background . Expressing the relationship as an absolute risk, rather than as a re let ive risk, may provide informal ion about the magnitude of the pub 1 ic health problem. If a relatively small risk is increased 10-fold, the resulting public health problem may still be much smaller than would result from doubling a larger risk. For example, the risk for coronary heart disease among smokers is about 1.6 times greater than the risk for nonsmokers, as contracted with a lO-fold increase in risk for lung cancer among smokers compared with nonsmokers. However, cigarette smoking causes more deaths from coronary heart disease than it toes from lung cancer, because the base line "background" risk for heart disease is much higher than for lung cancer. BIODISPOSITION OF FIBERS - In this section the co~nmittee briefly describes how asbestiform fibers enter the body, the properties of fibers that are important in cellular injury, and factors affecting durability of fibers after deposition and interaction with cells. Figure 5-l shows the anatomy of the respiratory tract ant the individual cell types ins olved in asbestos-associated diseased. The pathological effects of asbestos begin

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Epiglottis Ail Visceral _ Pleura Parietal _ Pleura Alveol i- ~ Figure 5 101 ~ Esophagus Trachea- /~\\ \ Peritoneal Cavity ~ Diaphragm I Cavity Pharynx Main Bronchus See Figure 5-1B Pleural Cavity (the pleura consists of the membrane enveloping the lungs and lining e chest cavity) FIGURE 5-1A. Routes of inhalation and ingestion of asbeseifonm fibers are shown by small arrows. Mesothelial cells line the outside of the lungs ant the pleural and peritoneal cavities. Interaction of asbestos with these cells can result in either pleural or peritoneal me~othelioma. Adapted from Wagner, 1980.

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102 niacin Granule Epi~elium Connemive Tissue so Tr;chea ~ #! ~ ~ . ~ ~' at , Macrophap~]'il~l' Ciiia~e~ Cell it} ., ~ ~ 4~/ I '~/)j?.2 torus ,~ ,,,.,~";'1.~}' ~ ".., FIGURE 5-1B. Cells of the bronchus, or large airways, leading from the trachea. The epithelial cell layer conalats of ciliated cells, mucin-secreting goblet cells, and basal cells. the interaction of asbestos with the epithelium and with macrophages is be' ieved to be related to the onset of asbestos-related diseases. Epithelial cells are the target for most lung cancer, whereas the macrophages serve as intermediary cells. In'.rss't.~t Soace Alveo'at Ep''bel~um FlUed Layer ~ \ my, Surtactent I\ Layer ~\ ALVEOLUS D'ffuslon ~- ~ Cao~ll.rV Basement / l~kmDrane / ~CapellarY Entlot~l,um l.\ {~: of CAPILLARY} ~ FIGURE 5-1C. . _ . . i. Dittus~on'/ot ~ |Carbon Dioxide /f, L ~/~ Cells of the alveoli, where gas exchange occurs. Interac- tion of asbestos with fibroblasts within the interstitial space can result in fibrosis, whereas interaction of asbestos with alveolar epithelial cells can give rise to lung cancer. (Drawing from Guyton, 1971.) r ..

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103 when fibers are inhaled and ingested. Subsequently, they are deposited either in the respiratory tract or in the gastrointestinal tract. Fibers can then interact with resident cells and eventually move to the pleura and various organs. The mechanisms by which fibers reach the peritoneum are not known. Fiber Deposition Various factors influence the deposition of inhaled particles in the respiratory tract. When nonfibrous compact dust particles are inhaled, the ones greater than about 5 Am in diameter are generally trapped in the nasal passages before reaching the respiratory system (Walton, 1982~. However, inhaled fibers align parallel to the airways and act as spheres of approximately "equivalent" diameter (Gross, 1931; Timbrell et al., 1970), where the equivalent or aerodynamic diameter of a particle is defined as the diameter of a sphere with a density of 1 g/cm3 that has the same falling speed as the particle. There is no sharp cutoff of particle sizes determining their deposition site (Brain and Valberg, 1974). The aerodynamic diameter of fibers depends primarily on the diameter. For fibers with aspect ratios greater than about 10:1, it is only slightly affected by length (Timbrell, 1965~. From his experiments in rats, Timbrell (1965) found that the aerodynamic diameter of fibers was about 3 times the actual diameter of the fibers. Fibers with diameters greater than about 3 Am would be very unlikely to reach the alveoli. The sizes of inhaled and deposited fibers have been compared. Morgan et al. (1979) showed the relationship between median aerodynamic diameter and alveolar deposition in rats using a variety of fibers. Hammad et al. (1982) experimented with retention of sized glass fibers in lungs of rats and found that fibers less than 1 Am in diameter accounted for most of the fibers retained (Figure 5-2~. Although the count median length of fibers in the aerosol inhaled by the rats was 13 ~m, the count median length fo''nd in lungs was 7 Am; for actual (as opposed to aerodynamic) diameters, the respective values were 1.2 Am and 0.5 ~m. They also found that length played some role. Timbrell (1982) compared the sizes of fibers found in the air of an anthophyllite mine and mill with the sizes of fibers found in the lungs of three adult workers. Both the configuration and dimension of asbestiform fibers determine where they impact after inhalation. Because the curlier chrysotile fiber has a relatively large cross-sectional area, its chance for interception in the airways is greater. Hence, these fibers are more likely to deposit in larger bronchioles (Morgan et al., 1973), whereas thin, rodlike fibers are carried peripherally to the terminal airways and alveoli (Timbrell, 1965; Timbrell et al., 1970; Wagner et al., 1974~.

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104 , _ ~ ._ , '1 1 ,1 1 E ._ C) - ~_ . I I I 1 1 - _ CD to (WH) NAZIS 8381d 14 - 1 l ] O tD ~O O O - o o Cut Cat _ - _ CO ~ (wow NAZIS H381d ~D o o o 1 . c LU o ~ as - UJ <: LO ~ Z I tn J z Ul _ I _ a _ 1 1 1 1 _ C ~ a, - l O CD ~ O o o C~ C~ (WH) ~ZIS B381d - LU o N ~ - C] UJ ~n Z cn ~n O L~ z UJ CC e C) 0 o x - CO - - e E C' e Ct 5: o rl C' CL ~ E o o s" C~ 1 C,

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105 In addition to diameter and shape, factors such as changes in breathing rate, individual anatomic variat ions , smoking, and the presence of bronchitis or lung disease also influence both the extent and site of fiber deposition in humans (Brain and Valberg, 1979; Sanchis en al., 1971). Studies in animals have demonstrated that most deposited fibers are removed from the respiratory tract within a few days. However, at least a quarter of the initial burden remains 1 month later (Evans et al., 1973; Muggenburg et al., 1981~. Since much of the inhaled asbestos is not readily cleared, pulmonary tissue burden in humans may be a useful index of exposure. Attempts have been made to quantify the amount of fibers and ferruginous bodies in human and animal lungs in order to reach a better understanding of the mechanism of action of the fibers. In addition to pulmonary or other tissues, sputum and ravage samples have been stud fed ~ Di Menza, 1980 ~ . Analyses of lung tissue samples from humans indicate that heavily exposed workers can be distinguished from those lightly exposed or from controls. Sebase fen et al. (1977) reported that the number of fibers/cm3 of lung sample, as seen by the light microscope, was approximately 106 for a heavily exposed group, 103 for lightly exposed workers, and 102 for controls. Early researchers discovered the presence of asbestos bodies as well as asbestos fibers in pulmonary tissues of exposed workers, especially in those with asbestosis ~ Cooke, 1927, 1929; Cooke and Hill, 1930; Gloyne, 1929; Sebastien et al., 1979~. Asbestos bodies are asbestos fibers coated with an iron-protein material that is readily visible with a light micro- scope. The coating, which is produced by macrophages (Suzuki and Churg, 1969), seems to prevent the fiber from interacting with cells as effectively as uncoated fibers. Because the coating may also be found on other types of fibers, the term ferruginous body is now often used instead of asbestos body. There are many reports of ferruginous bodies counted under various circumstances (Sebastian et al., 1979), but the pathological significance of these bodies is unclear. Asbestos bodies form with greater efficiency on varieties of amphibole asbestos than on chrysotile (Pooley, 1972~. Because the vast majority of deposited fibers are not converted to ferruginous bodies, the presence of these bodies reflects past exposure in only a very limited way. Electron microscope observations have provided detailed information on the deposition of fibers in animal and human tissues (Lange r et al., 1973; Pooley, 1972~. Chrysotile seems to degrade or be removed In Vito more readily than the amphiboles (Lange r et al., 1972a, b; Wagner et al. , 1974, 1982 ; Rowlands, 1983) . Fibers found in tissue samples obtained from the general population tend to be shorter in length and diameter than those found in workers (Larger et al., 1971; Pooley en al., 1970~. Fibers have also been detected in extrapulmonary tissues from both humans and animals. (For reviews, see Sebastien et al ., 1979 and Cook, 1983) . -

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106 Fiber burden in the lung parenchyma ( the body of the lung) may be different from that in the parietal pleura (the pleura lining the chest cavity) as shown in a study of 29 persons, most of whom had pleural asbestosis (Sebastian et al., 1979~. The parenchymal samples had both amphibole and chrysotile fibers. Their average length was 4.9 ~m; 15% of them were longer than ~ Am. The pleural samples were predominantly chrysotile fiber, with an average length of 2.3 Am; 2X of these fibers were longer than 8 Am. Thus, short chrysotile fibers tended to predominate in the parietal pleura. Most studies of fibers in human tissues have been conducted in workers known to have been exposed to asbestos (Churg, 1983a). However, there have been some studies of the amounts and types of fibers in the general population (Churg, 1983b; Churg and Warnock, 1980~. Churg (1983b) examined mineral fibers2 in the pulmonary tissues of 20 patients with no known occupational exposure to asbestos. He reported 13 types or groups of minerals, other than asbestos, including silica, talc, and attapulgite . More than 85: of the part ic les counted, and al 1 of the a~ctapulgite particles, were less than 5 Am long. Clearance and Transport Several mechanisms are involved in clearing fibrous materials from the lung. These include removal by the beating of ciliated cells and secretion of mucin (i.e., mucociliary clearance), transport by alveolar macrophages to regional lymph nodes and distal sites (Lippmann en al., 1980; Morgan et al., 1978, 1982), uptake by epithelial cells that line the airways and alveoli (Mossman et al., 1977; Suzuki, 1974), and direct translocation of fibers between ep~thelial cells to the interstitium and the pleura. The physical properties (i.e., length and cross-sectional dimensions) of fibers appear to determine the mechanisms of cellular interaction and transport. For example, short fibers with fine diameters can be translocated within cells, whereas longer fibers (approximately 20 Am long) are not completely engulfed by macrophages and are cleared ineffectively (Morgan et al., 1978~. Incomplete mucociliary clearance might result from discont~nuities in the mucus layer or hypersecretion, a situation observed in people who smoke or have infections. Alternatively, toxic irritants such as cigarette smoke cause dysfunction and loss of ciliated ant secretory cells that line the airways (Sanchis _ al., 1971~. Clearance of asbestos from the gastrointestinal tract is less well understood, although it has been reported that fibers cross the mucosa of 2The materials detected did not necessarily have the characteristics of asbestiform fibers. -

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107 the stomach and intestines (Cook, 1983; Westiake et al., 1965~. Fibers have been detected in urine and feces (Muggenburg et al., 1981~. When injected into the femoral vein of pregnant rats, chrysotile crosses the placenta and has been observed in fetal liver and lung (Cunningham and Pontefract, 19743. CLINICAL ASPECTS OF "BESTOS-"SOCIATED DISHES l m e four major asbestos-related diseases or changes are: (1) lung cancer; (2) mesothelioma; (3) pulmonary asbestosis; and (4) pleural plaques or diffuse thickening, calcifications, and effusion. Some other cancers may also be related to asbestos exposure (Selikoff et al.. 1979~. Lung cancer and mesothelioma are typically fatal cancers. Therefore, the degrees of severity are generally not relevant. Pulmonary asbestosis and the pleural changes noted above are nonmalignant pathological conditions that may range from mild to severe. They are usually related to the amount (intensity and duration) of exposure that the individual has experienced. Although lung cancer can usually be diagnosed with reasonable certainty, menothelioma and asbestonis are often more difficult to identify. For example, by the time a tumor is observed in a patient with mesothelioma, it may be difficult to ascertain both cell type and tissue of origin. For asbestosis, there is no complete agreement as to what constitutes a definitive diagnosis, especially for milder cases. These diagnostic uncertainties present difficulties to those analyzing results of epidemiological studies and determining incidence rates. Inhalation is the major route by which asbestiform fibers enter the body. They may also enter the digestive tract via ingested material such as water or drugs or via asbestos-containing secretions from the lung airways that are brought up into the mouth and then swallowed (Bouhuys, 1974; Langer et al., 1979; Selikoff and Lee, 1978~. _ ~ Necessary AsSumptioD8 Used in Determining Health Effects In the absence of adequate data on the health effects of low-level and nonoccupational exposure, certain assumptions must be made in order to predict and identify possible health effects. One assumption is that clinical manifestations in nonoccupational and occupational illness will be similar in kind but not necessarily in extent or degree. In cases of lung carcinoma and mesothelioma, malignancy is usually the cause of death. Both the time from exposure to onset of symptoms and the rate of progression from time of diagnosis are assumed to be similar in nonoccupational and occupational disease. ..

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154 Hilt, J. W., C. E. Rossiter, and D. W. Fode. 1982. A pilot respiratory study of cancers in a MUFF plant in the United Kingdom. Presented at the Biological Effects of Man-Made Mineral Fibers, Occupational Health Conference, WHO~E]JRO, Copenhagen, April 20, 1982 . World Health Organization. Hobbs, M. S. T., S . D. Woodward , B. Murphy , A. W. Musk, and J. E. Elder. 1980. me incidence of pneumoconiosia, mesothelioma and other respiratory cancer in men engaged in mining and milling crocidolite in western Australia. Pp. 615-625 in J. C. Wagner, ed. Biological Effects of Mineral Fibres. Vol. 2. IARC Scientific Pub. No. 30. International Agency for Research on Cancer, Lyon. Hughes, J., and H. Weill. 1980. Lung cancer risk associated with manufacture of asbestos~cement products. Pp. 627-635 in J. C. Wagner, ed. Biological Effects of Mineral Fibres. Vol. 2. LARC Scientific Pub. No. 30. International Agency for Research on Cancer, Lyon. International Labour Office. 1980. International classification of radiographs of the pneumoconioses; Occupational Safety and Health Series XX. International Labour Office, Geneva, Switzerland. Irwig, L. M., R. S. J. DuToit, G. K. Sluis-Cremer, A. Solomon, R. G. Thomas, P. P. H. Hamel, I. Webster, and T. Hastie. 1979. Risk of anbestosis in crocidolite and amosite mines in South Africa. Ann. N.Y. Acad. Sci. 330:34-52. Ives, J. C., P. A. Buffler, and S. D. Greenberg. 1983. Environmental associations and histopathologic patterns of carcinoma of the lung: The challenge and dilemma in epidemiologic studies. Am. Rev. Resp. Dis. 128:195-209. Jaurand, M. C., J. Bignon, P. Sebastier`, and J. Goni. 1979. Leaching of chrysotile asbestos in human lungs. Correlation with in vitro studies using rabbit alveolar macrophages. Environ. Res. 14:245-254. Jones, R. N., J. E. Diem, H. Glindmeyer, H. Weill, and J. C. Gilson. 198Oa. Progression of asbestos radiographic abnormalities: Relationships to estimates of dust exposure and annual decline in lung function. Pp. 537-543 in J. T. Wagner, ed. Biological Effects of Mineral Fibres. Vol. 2. LARC Scientific Pub. No. 30. ~terDationa1 Agency for Research on Cancer, Lyon. Jone ~ , J. S. . P ., F . D . Pooley , G . W . Sawle , R. J . Madeley , P . G . Smith , G. Berry, B. K. Wignall, and A. Aggarwal. l980b. The consequences of exposure to asbestos dust in a wartime gawk factory. Pp. 637-653 in J. C. Wagner, ed. Biological Effects of Mineral Fibres, Vol. 2. LARC Scientific Pub. No. 30. International Agency for Research on Cancer, Lyon. Kanarek, M. S., P. M. Conforti , L. A. Jackson, R. C. Cooper, and J. C. Hurchio. 1980. Asbestos in drinking water and cancer incidence in the San Francisco Bay Area. Am. J. Epidemiol. 112:54-72. Ranneratein, M., and J. Churg. 1972. Pathology of carcinoma of the lung associated with asbestos exposure. Cancer 30:14-21. Kanoeratein, M., J. Churg, and W. T. E. McCaughey. 1978. "bestos and mesothelioma: A re~rlew. Pathol. Ann. 13:~-129.

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155 Kilburn, K. H. 1977. Clearance mechanisms in the respiratory tract. Pp. 243-262 in D. H. K. Lee, H. Falk, and S. D. Murphy, eds. Handbook of Physiology, Section 9: Reactions to Environmental Agents. American Physiological Society, Bethesda, Md. Kiviluoto, R. 1960. Pleural calcification as a roentgenologic sign of non-occupational endemic anthophyllite-asbestos. Acta Radiologica ~(Supplement) 194:~-67. 4, Kiviluoto, R. 1965. Pleural plaques and asbestos: Further observations on endemic and other nonoccupational asbestosis. Ann. N.Y. Acad. Sci. 132:235-239. Kleinfeld M., J. Messite, 0. Kooyman, and M. H. Zaki. 1967. Mortality among talc miners and miners in New York State. Arch. Environ. Health 14:663-667. Kleinfeld, M., J. Messite, and A. J. Langer. 1973. A study of workers exposed to asbestiform minerals in commercial talc manufacture. Eaviron. Res. 6:132-143. Kleinfeld, M., J. Messite, and M. H. Zaki. 1974. Mortal ity experience among talc workers: A follow-up study. J. Occup. Med. 16:345-349. Klingholz, R. 1977. Technology and production of man-made mineral fibres. Ann. Occup. Hyg. 20:153-159. Knox, J. F., S. Holmes, R. Doll, and I. D. Hill. 1968. Mortality from lung cancer and other causes among workers in an asbestos textile factory. Br. J. Ind. Med. 25:293-303. Laamanen, A., L. Noro, and V. Raunio. 1965. Observations on atmospheric pollution caused by asbestos. Ann. N.Y. Acad. Sci. 132:240-254. Langer, A. M., I. J. Selikoff, and A. Sastre. 1971. Chrysotile asbestos `. in the lungs of persons in New York City. Arch. Environ. Health i 22:348. Langer, A. M., I. Rubin, and I. J. Selikoff. 1972a. Chemical characterization of asbestos body uses by electron microprobe analysis. J. Histochem. Cytochem. 20 : 723-734. Ianger, A. M., I. B. Rubin, I. J. Selikoff, and F. D. Pooley. 1972b. Chemical characterization of uncoated asbestos fibers from the lungs - of asbestos workers by electron microprobe analysis. J. Histochem. Cytochem. 20: 735-740. Lange r , A. M., B . S . Ashley , V. Baden , M . S . Berk' ey , E . C . Hammond , A. D. Hackled, C. J. Maggiore, W. J. Nicholson, A. N. Rohl, I. B. Rubin, A. Sastre, and I. J. Selikoff. 1973. Identification of asbestos in human tissues. J. Occup. Med. 15:287-295. Larger, A. M., C. M. Maggiore , W. J. Nicholson, A. N. Rohl, I. B. Rubin, and I. J. Selikoff. 1979. me contamination of Lake Superior with amphibole gangue mineral. Ann. N.Y. Acad. Sci. 330:549-572. Lagger, A. M., A. N. Rohl, I. J. Selikoff, G. E. Hariow, and M. Prinz. 1980. Asbestos as a cofactor in carcinogenesis among atckel-processing workers. Science 209:420-422. Levy, B. S., E. Sigurdson, J. Handel, E. Laudon, and J. Pearson. 1976. Investigating possible effects of asbestos in city water: Surveillance of gastrointestinal cancer incidence in Duluth, Minnesota. Am. J. Epidemlol. 103:362-368. Lewinsohn, H. C. 1972. The medical surveillance on asbestos workers. R. Soc. Health J. 92:69-77.

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