Document ExQ4BvprLEw2onrbmzOOyQrR

Case Reports Floor Tile Installation as a Source of Asbestos Exposure"' RAYMOND L MURPHY, BARRY W. LEVINE, FAIQ J. AL BAZZAZ,4 JOHN J. LYNCH, and WILLIAM A. BURGESS SUMMARY_______________________ Asphalt or vinyl-asbestos floor tile contains fifteen to twenty-five per cent asbestos, but the numeral fibers are firmly embedded in the binding material. Installation of these tiles would, therefore, seem to be an unlikely source of a hazardous dust exposure. Case reports of two installers of floor tile, one with biopsy-proved mesothelioma and another with extensive pleural calcifications are presented. Both workers had frequently sanded asphalt and vinyl tile floors prior to installation of new floor covering. An investigation of the work process revealed that under simulated condi tions of work, asbestos dust concentrations as large as 1.3 fibers per ml were found in air samples passed through membrane filters worn by a person engaged in sanding vinyl asbestos. Character istic asbestos fibers were seen in electron photomicrographs of these samples. These findings sug gest that before the tile sanding procedure is performed adequate respiratory protection should be provided or alternate, available installation methods should be used. Introduction Asphalt or vinyl-asbestos floor tile contains 15 to 25 per cent asbestos; however, the mineral fibers are firmly embedded in the binding material (1). Installation of these tiles would, therefore, seem to be an unlike ly source of hazardous dust exposure. Re cently the writers studied two installers of (Received for publication November 23, 1970) floor tile, one with biopsy-proved mesotheli oma and the other with extensive pleural calcifications who had no other known ex posure to asbestos. These workers had fre quently sanded asphalt and vinyl tile floors before installation of new floor covering. In this report, these cases and the results of an investigation of exposure to asbestos during tile sanding are presented. iFrom the Medical Services, Massachusetts General Hospital and Department of Medicine, Harvard Medical School; and the Departments of Environmental Health Services and Physiol ogy, Harvard School of Public Health, Boston, Massachusetts. 2 Supported in part by U.S. Public Health Service Grant E02-A1-39054 and Environmental Center Grant ES-00002. 8 Requests for reprints should be addressed to Dr. Raymond L. H. Murphy, Department of Physiology, Harvard School of Public Health, 665 Huntington Avenue, Boston, Massachusetts 02115. 4 Research Fellow in Medicine, Massachusetts General Hospital and Harvard Medical School. Supported by National Institutes of Health con tract PH-4367-1443. 575 AMERICAN REVIEW OF RESPIRATORY DISEASE, VOLUME 104, 1971 FLOOR TILE INSTALLATION AS SOURCE OF ASBESTOS EXPOSURE 577 Case Reports Case I: A 44-year-old man was admitted because of chest pain of one week's duration. He had worked from 1948 to 1967 as a floor tile installer and routinely sanded old tile before resurfacing it. There was no history of other occupational dust exposure. He had worked in a nondusty area of a shipyard from 1945 to 1947 repairing gyroscopes. From 17 to SO years of age. he had smoked one package of cigarettes per day. Four months before his present admission an illness developed with left anterior chest pain and hemoptysis. On admission to another hospi tal, a left pleural effusion was noted. He was treated with penicillin and was discharged im proved. One week before his current admission, hemoptysis and severe, pleuritic, left chest pain again developed. There were dullness and decreased breath sounds over the left lower chest. No friction rub was heard. A chest roentgenogram revealed a left pleural effusion without calcifications. A thoracentesis yielded 2,000 ml of serosanguineous fluid that contained 3,400 leuko cytes per mm3, predominately mononuclear cells, 154,000 erythrocytes per mm3, and no polymor phonuclear leukocytes. The glucose concentra tion was 25 g per 100 ml; the concurrent blood glucose was 80 mg per 100 ml. Total protein con centration of the fluid was 4.8 g per 100 ml. No asbestos bodies were seen, and cytologic exami nation of the cells in the fluid suggested malig nancy. Histologic examination of a needle biopsy of the pleura showed malignant papillary meso-. thelioma. Case 2\ A 61-year-old floor tile installer was re ferred to the pulmonary clinic because of an ab normal chest roentgenogram taken during a routine periodic medical evaluation. The patient had worked for the past 30 years installing asphalt and vinyl tile. There was no history of other occupational dust exposure, chest trauma, pneumonia, or hemoptysis. He complained of mild dyspnea on climbing two flights of stairs, but denied orthopnea, pa roxysmal nocturnal dyspnea, and ankle edema. He had smoked one package of cigarettes per day for the past 45 years. Physical examination revealed a well devel oped, plethoric white man. The anteroposterior diameter of the chest was increased, and fine, scattered, crepitant, inspiratory rales were noted at the bases bilaterally. Marked clubbing of the fingers was present. . A chest roentgenogram (figure 1) showed a Fig. I. Posteroanterior chest roentgenogram re vealing extensive pleural calcification, pleural thickening, and pulmonary fibrosis. dense placque of calcification in the left pleural space and sheetlike calcifications in the pleura on the right. Dense calcifications were seen on both diaphragmatic pleural surfaces. The dia phragms were flattened. The vital capacity was 64 per cent of predicted with a one-second forced expiratory volume of 65 per cent of the total. Arterial oxygen tension at rest was 71 mm Hg. The single breath pulmo nary diffusing capacity was 60 per cent of predieted. Dust Exposure To simulate normal work practice, samples of vinyl tile were laid on a plywood sheet using tile cement. This sheet was placed inside a room ap proximately 10 feet wide, 12 feet long, and 7 feet high that was exhausted at a rate of four aitchanges per hour. An operator wearing a respira tor sanded the tile for approximately 20 minutes using a conventional belt sandcr with a coarse grit. During the work period, air sampling was car ried out to determine the exposure to asbestos fibers. Two personal samplers worn by the opera tor collected air samples on membrane filters at an average sampling rate of 3.6 liter per min. Fibers longer than 5 ft with an aspect ratio great er than 3 were counted under phase contrast microscopy by the technique of Edwards and Lynch (2). Dust concentrations for these two parallel samples were 12 fibers and 1.3 fibers per ml of air, respectively. These concentrations are below the recently revised threshold limit value 578 MURPHY. LEVINE. AL BAZZAZ. LYNCH. AND BURGESS of 5 fibers per ml (5) but do represent significant exposures. Under other work conditions; the threshold limit value could be exceeded. The fields of these membrane filters examined under phase microscopy were consistent with those seen in samples collected in other asbestos operations such as marine insulation installation and tearout. Discrete fibers were evident and were easily counted. Characteristic asbestos fibers are shown in the electron photomicrograph of a replicated membrane filter sample (figure 2). During the sanding operation, a point-to-plane electrostatic precipitator was used to collect a series of samples on grids for electron microscopy. These fibers met the criteria proposed for asbes tos by Gross and associates (4) (figure S). The ends of the fibers had profiles characterized by steplike interruptions, and fibril bundles were easily seen. Fibers were clumped together within the matrix of the tile material. Discussion Both of the tile installers had diseases known to be associated with exposure to asbestos. . The first patient had typical dinical, roentgenographic and pathologic findings of pleural mesothelioma. Epidemiologic inves tigations of cases of mesothelioma have shown asbestos exposure in more than 40 per cent (5, 6). The incidence of mesothelioma in the general population is from 1 in 1,000 to 1 in 10,000 deaths (7). Because the pres ent studies revealed that airbo-.r.t' asbestos particles are generated during sanding of FLOOR TILE INSTALLATION AS SOURCE OF ASBESTOS EXPOSURE 579 Fig. 3. Air-borne asbestos fibers collected by electrostatic precipitator. ; tile, asbestos must be strongly considered as . a cause of the patient's illness. Because his j employment in gyroscope repair did not in' volve work in engineering spaces, it is un| likely thai he was exposed to asbestos dust. Konoccupational exposure to asbestos or mesothelioma unrelated to asbestos cannot | be excluded. ? Significant asbestos exposure was also im plicated in the second patient who had extensive bilateral pleural calcifications. Seli- f koff found 150 cases of pleural calcification ' in 1,117 installation workers and concluded ' that in the absence of a history of chest infec tion or trauma, bilateral pleural calcification can usually be considered to be due to as| bestos exposure (8). The causal relationship f seems clear because the patient had no hisi- tory of pulmonary' infection or trauma and t had a known exposure to asbestos. It was { more difficult, however, to assess the extent of underlying pulmonary asbestosis in this worker. The commonly described clinical manifestations of this disease include dysp nea, basilar rales, clubbing of the fingers, de creased vital capacity, abnormal diffusing capacity, decreased compliance, hypoxemia, and characteristic radiographic changes in die lungs (9). The patient exhibited most of these findings and had no evidence of heart disease, other systemic disorder, or oc cupational exposure. It is likely, therefore, that he had at least minimal pulmonary as bestosis as well as pleural disease. Asbestos tile has been installed on count less floors during the last SO years. Because this industry is the second largest consumer of this mineral in the United States, the po tential hazard is significant if the current method of sanding these floors continues (1). The clinical findings in these subjects and the results of air sampling in a simulated work environment suggest that before the tile sanding procedure is performed ade 5S0 MURPHY, LEVINE, AL BAZZAZ, LYNCH, AND BURGESS quate respiratory protection or an alternate installation method should be used. The as sociation between installation of tile and asbestos-related disease suggests that epidem iologic, environmental, and clinical inves tigation of tile installers be conducted. In ad dition, practicing physicians should be alerted to the possibility of asbestos-related illness in this occupation. Acknowledgments The writers are grateful to Mr. Lloyd Shoenbach for the extensive electron microscopy car ried out during this study and to Dr. Heinrich Brugsch for reviewing the manuscript. RESUMES------------------------------------------------------- Instalacion de baldosas para el piso como una fuente de exposition a asbestos El asfalto o la baldosa para d piso de vinilo-asbestos contiene de 15 a 25 por ciento de asbestos, pero las ftbras numerates estdn firmamente incrustadas en el material de ligamiento. La instalacidn de estas baldosas, por consiguiente, no pareceria ser una fuente peligrosa de exposi tion al polvo. Se presentan los casos de 2 instaladores de baldosas para el piso, uno con un mesotelioma comprobado por biopsia y el otro con calcificaciones pleurales extensas. Estos trabajadorcs habian lijado frecuentemente baldosas el piso de asfalto y de vinilo antes de instalar los nuevos pisos. La ocurrencia de estos casos llevo a una investigation del proceso de trabajo. Bajo condiciones de trabajo simuladas, se encontraron concentraciones de polvo de asbestos tan altas como 1.3 fibras por ml en muestras de aire en filtros de membrana que llcvaba puesta una per sona envuelta en lijar los asbestos de vinilo. Fibras de asbestos caracteristicas de estas mues tras fueron vistas en fotomicrOgrafos electrOnicos. Estos hallazgos sugieren que antes del pro ceso de lijar se lleve a cabo, se deberia usar una protecciOn rcspiratoria adecuada o usar otros metodos de instalaciOn al alcance. RESUME L'installation des carrelages: source deposi tion a l'amiante Les carreaux d'asphalte ou d une combinaison de vinyl et d'asbeste contiennent de 15 a 25 pourcent d'amiante, mais les fibres sont intimement liees a l'agent agglutinant. L'installation de ces carreaux para it done une source improbable de troubles pneumoconiotiques. Les rapports medicaux de deux ouvriers installeurs de carrelage, 1'un souffrant de mOsotheliome confirme u la biopsie, et l'autre etant porteur de calcification pleurales sont presentO ici. Ces deux ouvriers avaient souvent sabl des carrelages d'asphalte ou de vinyl-asbeste au papier de Terre, avant d'installer des nouveaux carreaux. L'intidence de ces cas a incite 5 une investigation du pre cede En recreant les conditions de travail, des concentrations de poussi&re d'amiante d'un niveau aussi eleve que 1.3 fibres par ml ont pu etre mesuree dans l'air ambiant. Les mesures furent determinee en faisant passer des enchantillons d'air sur un papier filtre fixe sur un travailleur en train de sabler des tuiles de vinylasbeste. Des photomicrographies de ces prelevement ont montrf qu'il s'agissait de fibres amiante caracteristiques. En consequence, nous devons appliquer une protection respiratoire sulfisante lors du sablage de tuiles dii choisir un autre prored^ d'installation. References 1. Hendry, N. W.: The geology, occurrentes, and major uses of asbestos, Ann. N. Y. Acad. Sri., 1965,132, 20. 2. Edwards, J. H., and Lynch J. R.: The meth od used by the U. S. Public Health Service for enumeration of asbestos dust on mem brane filter, Amer. Occup. Hyg., 1968, 11, 1. 3. Committee on Threshold Limit Values: Threshold Limit Values for 1970, Am. Conf. of Gov. Ind. Hyg., Cincinnati, 1967. 4. Gross, P., de Treville, R. T. P,, and Hal ler, M. N.: Asbestos versus nonasbestos fibers, ultra-microscopic criteria. Arch. Environ. Health (Chicago), 1970, 20, 571. 5. Newhouse, M. L., and Thompson, H.: Mesothelioma of the pleura and peritoneum following exposure to asbestos in the London area, Brit. J. Industr. Med., 1965,22,261. 6. Elmers, P. C., McCaughey, W. T. E., and Wade, O. L.: Diffuse mesothelioma of the pleura and asbestos, Brit. Med. J., 1965, 1, 350. 7. Selikoff, J. J., Churg, J., and Hammond. E. C.: Relation between asbestos exposure and neoplasia, New Eng. J. Med., 1965, 272, 560. S. Selikoff, J. J.: The occurrence of pleural calci fication among asbestos insulation workers, Ann. N. Y. Acad. Sri., 1965,132, 351. 9. Thompson, M. 7., Pelzer, A-M., and Smither, W. J.: The discriminant value of pulmonary function tests in asbestosis, Ann. N. Y. Acad. Sci., 1965.772, 421.