Document 373n6NapgNoXVKyeeQrxKjR0y

FILE NAME: Talc (TALC) DATE: 1973 DOC#: TALC107 DOCUMENT DESCRIPTION: Journal Article - A Study of Workers Exposed to Asbestiform Minerals in Commercial Talc Manufacture en viro nm ental research 6, 132-143 (1 9 7 3 ) A Study of Workers Exposed to Asbestiform Minerals in Commercial Talc Manufacture M. K leinfeld, J. Messite, and A. M. L ancer ` n IZ I n i Sl i te D, ePZ Z Z nt f Labor Division of Industrial Hygiene, M kt Z-eW ^r0023 nd EnviTnmental Sciences Laboratory, Mount Sinai School of Medicine, New York, New York 10029 Received April 10, 1972 A clinical and environmental study was made of a m-n.m nf no i j omponents and the findings were compared with a control group. The data showed that m spite of a mean exposure of 16.2 yr with a ranee of 11 99 nnl t workers exposed to commercial talc dust showed V contol T " ' The nly significa,lt T ere n ce behveen t a l f workers and console nT ber f people having dyspnea and its severity. The authors onsideied both the element of smoking and the exposure to commercial talc as ggravatmg factors which accounted for the dyspnea. The findings of the 39 workers L " : u i t lpt n' / o,h r ps " "" f Z Z i t '" t m the present study were compared to those obtained from 35 workers studied earlier t Inn tthhee klattiter bgroup MthdeergerCweas faesXiPgn SifUicreantflythinecrgeraosuepd opfre3v3alewnacse aopfpprenceiuambloycognreioasteesr' t is possible that commercial talc containing tremolite and anthophyllite as maior fibrous constmients may be less fibrogenic than chrysotile or a m o s l T t h e d e 3 or dust exposure present m this study. nhalation o! ff 'hcl hr"ysotiilfe ' aTnd/or" amphdibifoFleeieanslbetystpoess odfus*ts* in* coMncekntmratiothnast present m some industrial environments, can produce pulmonary fibrosis ( 1 )' Disabling pneumoconiosis may occur after inhalation of an asbestos dust after E ?^ ed tTM 6 f!'m onset of exposure, up to 20 years or more (15). Morns ei al (2) m a study have reported that chrysotile produced less plumo- nary fibrosis than amosite or crocidolite when comparable concenbSiom of these asbestos minerals were inhaled. These investigators have attributed thl lesser pathogenicity of chrysotile to the ability of the lungs to eliminate it more rapidly than amosite or crocidolite. Recent data on anthophyllite exposure indi cates the fiber to be both a fibrogen (16) and a carcinogen (17) M e Z n i (3) has suggested that pleural plaques and calcification seem to occur more f ! l v among people exposed to anthophyllite, but whether one type of asbestos is moie pathogenic than another still remains to be established. The difficultytises due to the influences of fiber size, other minerals and cofactors present in the in fib S USS, Vlgham (5) cites Selikoff.as having stated that differences in fibrogemcity may exist even between different sources of the same type of YYo?uunng? S((66)lXsshhoowmennotaldiiyfff;erbensecreVsatini nt*heinfitbllreogSeuninicearePsipgonWse tobyfoHuorltt,vpMesilhofa uasdtos, namely, chrysotile, crocidolite, amosite, and anthophyllite. Oi^the other 132 Copyright 1973 by Academic Press, Inc. All rights of reproduction in any form reserved. . v fe.tfe'i5i,mUkmLa. - COM M ERCIAL TALC M ANUFACTURE 133 hand, Parazzi, Pcrnis, Secchi, and Vigliani (7) have shown that crocidolite pro duces a more marked cytotoxic action on guinea pig macrophages than does ehrysotile. Schnitzel- and Pundsack (8) in an earlier study observed that chrysotile fibers produce a marked hemolytic effect on suspension of washed sheep erythrocytes whereas crocidolite, amosite, tremolite, and anthophyllite produced negligible hemolytic effects. In a more recent study (personal communication to A.M .L.), the same authors found that the relative surface areas of ehrysotile versus the amphibole group were among the major factors in determining whether or not the materials were potentially capable of producing hemolytic effects. Although the various authors cited above have shown different responses' to different types of asbestos, their results do not justify drawing firm conclusions as to the relative pathogenicity of the different types of asbestos. The present study deals with a group of 39 individuals who were exposed to commercial talc dust with tremolite and anthophyllite as its major fibrous com ponent. The purpose of the study was to (a ) correlate the environmental exposure with the clinical and roentgenographic findings in order to obtain information on a dose-response relationship among workers, all of whom had relatively long term occupational exposure to commercial talc; and (b ) obtain additional data on the composition and morphology of the commercial talc dusts. MATERIALS AND METHODS All of the workers in the study group were exposed to commercial talc for 10 or more yr. Each worker underwent a clinical evaluation which included a de tailed occupational history, a physical examination and chest roentgenogram. A similar evaluation was made of 41 workers who lived in the same area as the talc workers and who were of the same sex and mean age and range but who had had no occupational dust exposure in their working environment. Tire 41 workers served as a control group. Dyspnea was graded using a modification of Fletcher's criteria (9 ). Only four of the five grades categorized by Fletcher were adopted for this study. The criteria for a positive smoking history was smoking of 20 or more cigarettes per day for a minimum of 5 yr. In addition to the clinical and roentgenographic examinations, air samples were taken in both the workers' breathing zones and general air at various loca tions where the mining and milling of tremolite talc took place. Total particle counts as well as fiber counts were determined. The dust was collected by means of a midget impinger and the samples were taken at a rate of 0.1 cpm for 10 min according to the Public Health Service method (10). Several 10-min samples were taken during the individuals work day to obtain results representative of a given worker's actual exposure. Particles were counted using the light field low-power method. The fibers were collected on a millipore filter and concentra tions were determined using phase contrast illumination at 400 X . The mineral nature of 16 talc samples from New York State was determined. These samples represented talc specimens obtained at different mining and milling operations, as well as the finished product. Techniques of analysis included polarized light microscopy, transmission electron microscopy with selected area diffraction, x-ray diffraction, and electron microprobe analysis. 134 KLEINFELD, M ESSITE, AND LANGER TABLE 1 C linical and E nvironmental D ata of E xposed and Control Group Study group Control P No. Age (yr) mean range Exposure (yr) mean range Radiologic findings compatible with pneumoconioses Clinical findings Cough Dyspnea Lung crepitations Clubbing Positive smoking history 39 45.9 34-75 16.2 11-22 1 (2.6%) 10 (25.65) 9 (23.1%) 2 (5.1%) 0 (0.0%) 19 (48.7%) 41 48.8 32-71 0 (0.0%) 0 (0.0% 0 (0.0%) 5 (12.2%) 3 (7.3%) 3 (7.3%) 0 (0.0%) 19 (46.3%) N.S. N.S. N.S. <0.05 N.S. N.S. N.S. FINDINGS Clinical. A summary of the clinical and environmental data of the 39 indi viduals in the study group as compared to the control group is shown in Table 1. Data showing the relationships of dyspnea and cough to age, smoking and dura tion of exposure are given in Table 2. The characteristics for each grade are given in Table 2. Table 3 summarizes the mean dust concentrations obtained for specific years between 1954 and 1970. Fiber counts were made only in 1970 as shown in Table 3. Comparative environmental, clinical and chest roentgeno- TABLE 2 R elationships of D yspnea and Cough to Age, S moking and D uration of E xposure in the S tudy Group Case number 1 2 3 4 . 5 6 7 8 9 Years Age exposure 45 14 36 19 45 15 53 15 45 20 49 20 58 14 50 19 55 15 Dyspnea grade" 1 1 1 1 4 1 2 4 1 Cough Productive 0 Productive6 Productive6 Productive 0 Productive Productive 0 Smoking + 0 0 + + + 0 + 0 No. packs cigarettes/ day 1 1 2 1.5 2 ** Years 25 30 20 18 31 * Four grades of dyspnea, a modification of Fletcher's grading (7), were used: Grade 1--able to walk normally without breathlessness on the level, but breathless on hurrying or climbing slight hills; Grade 2--able to keep on walking at own, slower than average pace on the level; Grade 3-- forced to stop for breath when walking at own slow pace on the level; and Grade 4--breathless on slightest exertion such as washing or undressing. 6 Morning only. COM M ERCIAL TALC MANUFACTURE 135 TABLE 3 E nvironmental D ata Obtained at Various M ine and M ill Operations - Mean dust counts (mppcf) Fiber count (fiber > 5 /tm/ml) 1954 1958 1963 1964 1969 1970 1970 Mine Drilling Dragline loading Tramming & mucking Primary crushing Hoist loading " Mill Secondary crushing Grinding (Wheeler mills) Grinding (Hardinge mills) Bagging Palletizing Bulk loading Direct R.I1. car loading of bags 5 5 13 7 7 10 29 11 2 26 23 IS 13 48 70 140 14 12 23 8 10 15 13 5 3 18 14 4 7 25 15 5 9 40 25 109 39 31 12 13 11 19 8 48 10 6 10 62 8 16 22 260 . 29 13 30 33 30 27 8 TABLE 4 D ata in P resent P lant C ompared to Another P lant S tudied P reviously Present plant Comparative study plant study P Environmental data" (mppcf) Mining Drilling Mucking Milling Crushing Milling Bagging R.R. car and truck load Workers examined Number in group Age (yr) mean range Exposure (yi) mean range Radiographic findings compatible with pneumoconioses Clinical findings Cough Dyspnea Lung crepitations Clubbing Smokers 6 20 15 13 16 6S 39 45.9 34-75 16.2 11-22 1 (2.6%) 10 (25.6%) 10 (25.6%) 2 (5.1%) 0 19 (48.7%) 182 31 117 60 106 77 35 49.1 29-67 17.4 11-22 12 (34.3%) 10 (40.0%) 22 (62.9%) 8 (22.9%) 7 (20.0%) 23 (65.7%) N.S. N.S. . <0.01 N.S. <0.01 <0.05 N.S. The dust count data represent mean dust concentrations over 20-yr periods. 136 KLEINFELD, M ESSITE, AND LANGER TABLE 5 C omparative D ust Counts and F iber C ounts in the T wo P lants Present plant, data Comparative plant data - obtained in 1970 obtained in 1969 Dust count Fiber count Dust count Fiber count (mppcf) (fibers > 5 / m/ml) (mppcf) (fibers > 5 inn/ml) Mine . Drilling 7 8 16 371 Dragline loading 10 11 -- -- Tramming & mucking 11 22 2 62 Primary crushing 48 260 -- -- Hoist loading 14 29 -- -- Mill Secondary crushing 13 13 19 112 Grinding (Wheeler) 19 30 21 S4 Grinding (Hardinge) 8 33 -- -- Bagging 8 30 12 135 Palletizing 6 27 -- -- Bulk loading 10 s -- -- R.R. car and truck -- -- 70 198 loading (--) Not done. graphic data compiled frojy a previous study made 6 yr earlier in another talc mining and milling plant l^ m e same regional area are shown in Table 4. Table 5 shows the comparative dust and fiber counts in the two plants; the counts in the present plant study were taken in 1970 and those at the comparative plant were taken in 1969. A flow sheet of the mining and milling operations in the plant most recently studied is shown in Fig. 1. Mineral analysis of talc samples. Optical, x-ray, electron microscopic and elec tron microprobe examination of the talc samples taken from the plant studied most recently indicated that the true mineral talc, as defined mineralogically, is only one of many mineral components in the materials mined, milled and sold as commercial talc and that it is present as either a major or minor component. The asbestiform minerals tremolite and anthophyllite may constitute major frac tions of commercial talc. Figures 2, 3 and 4 show the various constituents of the dust samples as viewed under plane polarized light (Fig. 2) and electron micros copy (Figs. 3 an d 4). DISCUSSION - A correlation of the clinical and environmental findings noted in Table 1 shows that in spite of a mean exposure of 16.2 yr with a range of 11-22, only one indi vidual showed a chest roentgenogram consistent with pneumoconiosis. This oc curred in a 75-yr-old individual who had a nonproductive cough, Grade 1 dyspnea and who worked as a janitor for 11 yr. Although the absence of positive roentgenographic shadows does not conclusively exclude the presence of pneumoconiosis COM MERCIAL TALC MANUFACTURE 137 I d r i l l in g MUCKING OR DRAGLINE LOADING TRAMMING PRIMARY CRUSHING Underground Above Ground HOIST LOADING SCREENING SECONDARY CRUSHING DRYI NG HARDINGE SCREENING I GRINDING OR W HEELER M ILLS II---------------------- ------------------------- BAGGING P A LLE T IZIN G BULK LOADING RR CAR OR TRUCK LOADING RR CAR OR TRUCK LOADING- F ig. 1. Flow chart of commercial talc mining and milling operations in the plant studied. in the other individuals who had positive clinical findings, it makes the presence of pneumoconiosis less likely. Usually the criteria for asbestotic pneumoconiosis is a history of prolonged exposure coupled with positive roentgenographic shadows and a restrictive breathing disorder. When the clinical data on the workers was compared with the control group (Table 1), there was no appreci able difference in the presence of cough or lung crepitations, the only difference being in the number of people with dyspnea and its severity. In the control group there were three individuals who had dyspnea which was categorized as Grade 1. Of the nine individuals in the study group with dyspnea, six showed Grade 1, one showed Grade 2 and two showed Grade 4. Of the two with Grade 4 dyspnea, one was a cardiac who had sustained a myocardial infarction and the other had pulmonary emphysema prior to his employment. These two individuals were heavy smokers, one having smoked two packs daily for over 20 yr and the other two packs daily for a period of 31 yr. Hence, the element of smoking must be included as an important etiologic factor. Although the dyspnea in these two individuals was not primarily related to their occupational exposure, it may very well have been that their prolonged exposure to the commercial talc dust acted as an additional causal element. By and large, as shown in Table 2, there was no good correlation between dyspnea and cough when related to age, smoking habits and duration of exposure. In order to obtain some information on the dose-response relationship, it was 138 KLEINFELD, M ESSITE, AXD LA X GEE F ig. 2. Talc samples as viewed in plane polarized light. All magnifications are as shown in (F)'. Sample (A), a primary crushing area; (B ), drilling area; (C ), mill; (D ), talc "N200L"; (E ), talc N200 ; (F ), talc "N300." These samples represent materials from source to end- product. In addition to the mineral species, rock fragments were observed in the first three samples. ~ possible to compare a group of 35 individuals of the plant studied earlier ( Table 4) who were of the same age and range and who had a similar mean duration of exposure as well as r a n g e b u t w h o se d e g r e e of e x p o su re in te r m s of to ta l par ticle counts was appreciably greater than those in the plant recently studied as shown in Tables 4 and 5. As would be expected, the group exposed to higher dust concentrations and fiber counts showed a significantly increased prevalence f .sjjSwtittSiU* SiS*> COM M ERCIAL TALC MANUFACTURE 139 F ig. 3. Amphibole fibers present in talc. This sample was examined for amphibole fibers and electron diffraction patterns obtained on selected fibers (3A; insert 3A). The structural array is clearly different than that obtained on talc fibers. 3B shows the presence of talc fibers (T F ), amphibole fibers and fragments (A ), and the presence of talc aggregate grains (TA). 3C shows a chrysotile (C ) fibril and an amphibole (A) fiber admixed in the talc. of positive chest roentgenographic findings consistent with pneumoconiosis as well as more positive clinical findings. In both talc plants there was no correlation between the fiber count and mean dust counts indicating the desirability of utilizing both total particle concentra- 140 KLEINFELD, M ESSITE, AND LANGER F ig. 4. Talc aggregate grains as viewed with transmission electron microscopy. These grains are apparently intergrowths of true talc, talc fibers, serpentine minerals and after frag ments, and amphibole fibers and fragments. (A) These grains appear to survive the milling operations as entities. Particles making up the grain may range from several thousand to several hundred angstroms in size. ( B ) ' tion as well as fiber counts when one correlates the environmental and clinical data. Table 3 shows the lack of correlation between the two indices in the present plant studied. There is at present no conclusive data that it is the fiber per se which is solely responsible for producing both the fibrotic and malignant changes. In addition, the effect of periodic exposures of short duration to high concentra tions of fibers and particles or peak concentrations needs further study and clari- COM MERCIAL TALC MANUFACTURE 141 fication. One should therefore, consider the particle concentration, fiber count and theii peak values in establishing threshold limit values. Furthermore, the nature of the samples analyzed indicates that fiber counts of aerosols may not provide a true picture of exposure to asbestiform minerals because the fiber counts include talc fibers but exclude many small asbestos fibers and "aggre gate fibers which may contain substantial amounts of asbestiform minerals (Fig. 4). Suzuki and Churg (11) have suggested that it is the submicroscopic fibers that are responsible for most of the biologic effects produced by asbestos. Othei investigators (6, 12) have also pointed out that the fine dust particles below 1 /m in length may be just as damaging as dust containing both large and small particles. In a recent paper by Murphy and associates (13) on workers exposed to chronic low concentrations of asbestos dust in ship construction wherein the as bestos used was principally chrysotile and amosite, the authors reported that they did not find any evidence of asbestosis in persons with less than ten years of cumulative exposure. No information on peak exposures was given. The pe riodic peak exposures may be the more important factor relating to the fibrogenic effect. These authors, however, observed that there was a progressive increase 1^ prevalence of asbestotic pneumoconiosis with the years of exposure there after. In terms of time weighted averages, Murphy and associates (13) found no asbestosis in men exposed less than 60 mppcf-years. Although it is difficult to compare their work with the present study, it does nevertheless appear that while an appreciable number of workers in the present study exceeded the 60 mppcf-years, they did not show any evidence of pneumoconiosis, as determined by the criteria of Murphy and associates. It is possible that, in terms of a fibro genic response, tiemolite and anthophyllite are less pathogenic than chrysotile or amosite at the degrees and intensity of dust exposures present in this study. In terms of the present findings, the data are not sufficiently conclusive for \ carcinogenicity for it has been shown that the occurrence of malignancy requires I a longer elapsed time from onset of exposure. Since the start of its operations, the longest exposure in the plant studied was only 22 yr and the occurrence of malignancy from commercial talcs containing tremolite and anthophyllite in ad dition to talc has not infrequently required a longer duration or a greater elapsed time from initial exposure as was shown in an earlier study (14). None of the insulation workers studied by Selikoff and Hammond (15) died from carcinoma of the lung, mesothelial tumors or asbestosis before 20 years had elapsed since first exposure. To date, no instances of malignancy have occurred in any of the workers exposed exclusively to commercial talc at the plant studied. SUMMARY AND CONCLUSIONS A clinical and environmental study was made of a group of 39 workers exposed to commercial talc dust, of which tremolite and anthophyllite were the major fibrous components. The clinical findings were compared to those obtained from a control group. The data showed that in spite of a mean exposure of 16.2 yr with a range of 11-22, only one of the workers exposed to commercial talc dust showed a chest roentgenogram consistent with pneumoconiosis. When the clinical 142 KLEINFELD, M ESSITE, AND LANGER data on the workers was compared with the control group, the only significant difference was in the number of people having dyspnea and its severity. Two in dividuals had severe dyspnea. One of the two had a cardiac condition and the other had primary pulmonary disease prior to his employment. Both were heavy smokers for over 20 yr. The authors considered both the element of smoking and the exposure to commercial talc as aggravating factors which accounted for the dyspnea. The findings of the 39 workers in the present study were compared to those obtained from 35 workers studied earlier in another talc plant. Both groups had similar mean durations of exposure to commercial talc but the de gree of exposure of the group of 35 was appreciably greater. In the group pre viously studied there was a significantly increased prevalence of positive roentgenographic findings consistent with pneumoconioses as well as more positive clinical findings. In the present study where the mean exposure was 16.2 yr with a range of 11-22, no instance of malignancy occurred in any of the workers ex posed exclusively to commercial talc. It is possible that commercial talc contain ing tremolite and anthophyllite as major fibrous constituents may be less fibrogenic than chrysotile or amosite at the degrees and duration of dust exposure present in this study. ACKNOWLEDGMENT Dr. Langer wishes to acknowledge support under Career Scientist Award NIEHS 44812. REFERENCES 1. Whipple, H. E. (Ed.) (1965). Biological effects of asbestos, Ann. N. Y. Acad. Set. 132, Art. 1, 87-111. 2. Morris, T. G., Roberts, W. H., Silverton, R. E., Skidmore, J. W., Wagner, J. C., and Cook, G. W. (1965). Comparison of dust retention in specific pathogen-free and standard rats. In "Inhaled Particles and Vapours" (C. N. Davies, Ed.). Pergamon Press, London-Paris, 2, 205. 3. Meurman, L. O. (1968). Pleural fibrocalcific plaques and asbestos exposure. Environ. Res. 2, 30^6. 4. "Asbestos: The Need for and Feasibility of Air Pollution Controls," Committee on Bio logic Effects of Atmospheric Pollutants, Division of Medical Sciences, National Research Council, National Academy of Sciences, Washington, D. C., 1971, 3. 5. Vigliani, E. C. (1968). The fibrogenic response to asbestos. Med. Lavoro 59, 401-410. 6. Holt, P. F., Mills, J., and Yoonc, D. K. (1965). Experimental asbestosis with four types of fibers: importance of small particles. Ann. N. Y. Acad. Sci. 132, 87-97. 7. Parazzi, E., Pernis, B., Secchi, G. C., and Vigliani, E. C. (1968). Studies on in vitro cytotoxicity of asbestos dusts. Med. Lavoro 59, 561-576., 8. "Schnitzer, R. J., and Pundsack, F. L. (1970). Asbestos hemolysis. Environ. Res. 3, 1-13. 9. "Short Questionnaire on Respiratory Symptoms," as approved by the Medical Research Council Committee on the Aetiology of Chronic Bronchitis, Dr. C. M. Fletcher, Chairman, London, 1960. 10. American Conference of Governmental Industrial Hygienists, 1962: Air sampling instru ments (Document B-3-31), Cincinnati, Ohio, 1963. 11. Suzuki, Y., and Churg, J. (1969). Structure and development of the asbestos body. Amer. J. Pathol. 55, 79-91. 12. Davis, J. M. G. (1965). Electron-microscope studies of asbestosis in man and animals. Ann. N. Y. Acad. Sci. 132, 98-111. 13. Murphy, R. L. H., J r., F erris, B. G., Jr., Burgess, W. A., Worcester, J., and Gaensler, if ViMfc ,t. .TiUA-sSMki-'iSu.--- COMMERCIAL TALC MANUFACTURE 143 E. A. (1971). Effects of low concentrations of asbestos. New Eng. J. Med. 285, 1271 1278. 14. Kleinfeld, M., Messite, J., Kooyman, O., and Zaki, M. (1967). Mortality among . talc miners and millers in New York State. Arch. Environ. Health 14, 663-667. 15. Selikoff, I. J., and Hammond, E. C. (1968). Community effects of nonoccupational environmental asbestos exposure. Amer. J. Publ. Health 58, 1658-1666. 16. Ahlman, K., Partanen, T. J., Rintala, E., and WriKERt, M. (1972). Anthophyllite mining and milling as a cause of asbestosis. In Conf. Biol. Effects Asbestos, Lyon, France, 2-6 Oct., 1972, Paper 25. 17. Meurman, L. O., Kivtluoto, R., and Hakama, M. (1972). Mortality and morbidity of employees of anthophyllite asbestos in mines of Finland. In Conf. Biol. Effects Asbestos, Lyon, France, 2-6 Oct., 1972, Paper 31. ,,