Document OEqa2MR4LBQe70ge5BwNnNgjL

FILE NAME: Flooring (FLR) DATE: 1971 DOC#: FLR008 DOCUMENT DESCRIPTION: Journal Article - Case Reports: Floor Tile Installation as a Source of Asbestos Exposure - American Review of Respiratory Disease Case Reports Floor Tile Installation as a Source of Asbestos Exposure' 3 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, R e cently the writers studied two installers of (Received jor publication November 23, 1910) 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 F02-AI-39054 and Environmental Center Grant ES-00002. 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. a 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. 576 AMERICAN REVIEW OF RESPIRATORY DISEASE, VOLUME 104, 1971 TI.O O R TII.F. IN STALLATION AS SOURCE <)) ASBESTOS EXPOSURE. r>77 Case Reports Case I: A 44-year-old man was admit led because o chest pain of one week's duration. He bad worked from 194R 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 nondnsty area of a shipyard from 1945 to 1947 repairing gyroscopes. From 17 to 30 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 Tales were noted at the bases bilaterally. Marked clubbing of the fingers was present. A chest roentgenogram' (figure 1) showed a Fig. 1. Posteroantcrior chest roentgenogram re vealing extensive pleural calcification, pleural thickening, and pulmonary fibrosis. dense placque of calcification in the left pleural space and shectlike 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 (54 peT 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 pre dicted. I)usl. 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 air changes per hour. An operator wearing a respira tor sanded the tile for approximately 20 minutes using a conventional belt sander 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 Tate of 3.6 liter per min. Fibers longer than 5 i 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 1.2 fibers and 1.3 fibers per mi of air, respectively. These concentrations are below the recently revised threshold limit value 578 M URPHY, LEVINE. AL BA77.AZ. LYNCH, AND BURGESS Fig. 2. Electron photomicrograph of a replicated membrane filter showing asbestos fibers. of 5 fibers per ml (3) 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 scries of samples on grids for electron microscopy. These fibers met the criteria proposed for asbes tos by Gross and associates (4) (figure 3). 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. T h e first patient had typical clinical, 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). T h e 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 th at air borne asbestos particles are generated during sanding of FLOOR TII.F. INSTAI.T.ATION A s SOURitF. OF ASItF.STOS K X I'OS[!RF. 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 employment in gyroscope repair did not in volve work in engineering spaces, it is un likely that he was exposed to asbestos dust. Nonoccupational exposure to asbestos or mesothelioma unrelated to asbestos cannot be excluded. Significant asbestos exposure was also im plicated in the second patient who had ex tensive bilateral pleural calcifications. Selikoff 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 seems clear because the patient had no his tory of pulmonary infection or trauma and 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 the lungs (9). The patient exhibited most of these findings and had rto 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 30 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 environm ent suggest that before the tile sanding procedure is performed ade- 580 M URPH Y , LV.VINE. A!. BA7.ZAZ, I.YNt'.H, AN1> RURCKSS quaie rcspiratory protection or an altrnate installation method sliould be u.sed. The association between installation of tile and asbesto,s-rclated diseasc suggests tbat epidem iologic, environmental, and el inira1 inves tigation of tile installcrs be tomlueted. In addition, practicing physicians slvould be alertcd to the possibility of asbestos-rclated illness in this occupation. AckUowledgments The writers are gratcful to Mr. I.loyd Shocnbach fov t.lie extensivo electrn mitroscopy carried ont dnring this sludy and to Dr. Hcinrich BrUgscli Cor reviewing (he manuseript. R E S U M E N ______________________________________ Instalacin de baldosas para el piso romo tina fuente de exposicin a asbestos El asfalto o la baldosa para el piso de viudo-as bestos contiene de 15 a 25 por ciento de asbestos, pero las libras numerales estn firmamento in crustadas en el material de ligamiento. I.a in stalacin de estas baldosas, por consiguiente, no parecera ser una fuente peligrosa de exposi cin al polvo. Se presentan los casos de 2 instala dores de baldosas para el piso, uno con un mesotclioma comprobado por biopsia y el otro con calcificaciones pleurales extensas. Estos trabaja dores haban lijado frecuentemente baldosas el piso de asfalto y de vinilo antes de instalar los nuevos pisos. La ocurrencia de estos casos llev a una investigacin del proceso de trabajo. Bajo condiciones de trabajo simuladas, se encontraron concentraciones de polvo de asbestos tan altas como 1.3 libras por mi en muestras de aire en filtros de membrana que llevaba puesta una per sona envuelta en lijar los asbestos de vinilo. Fibras de asbestos caractersticas de estas mues tras fueron vistas en fotomicrgrafos electrni cos. Estos hallazgos sugieren que antes del pro ceso de lijar se lleve a cabo, se debera usar una proteccin respiratoria adecuada o usar otros mtodos de instalacin al alcance. R E S U M E _______________________________________ L'installation des carrelages: source d 'exposition I'amiante Les carreaux d 'asphalte ou d'une combinaison de vinyl et d'asbeste contiennent de 15 25 pourcent d 'amiante, mais les fibres sont intimement lies l'agent agglutinant. I.'installation de ces carreaux parait done une source improbable de troubles pneumoconiotiques. Les rapports mdi caux de deux ouvriers installeurs de carrelage, l'un 'souffrant de msothliome confirm la b i opsie. et l'antre tant porteur de calcification pleurales sont prsent ici. Tes deux ouvriers avaient souvent sabl des carrelages d'asphalte ou de vinyl-asbeste au papier de verre, avant (l'installer des nouveaux carreaux. L'incidence de ces cas a incit une investigation du pro cd. En recrant les conditions de travail, des concentrations de poussire d'amiante d'un niveau aussi lev cpie 1.3 libres par ml ont pu tre mesure dans l'air ambiant. I.cs mesures furent dtermine en faisant passer des c h a n tillons d'ait sur un papier filtr fix sur mi travailleur en train de sabler des miles de vinylasbeste. Des photomicrographies de ces prlve ment ont montr qu'il s'agissait de fibres amiante caractristiques. F.u consequence, nous (levons appliquer une protection respiratoire suliisanle lors du sablage de tuiles o choisit un mile pro cd (l'installai ion. References 1. Hendry, N. W.: The geology, occurrences, and major uses of asbestos, Ann. N. Y. Acad. Sci., 1965. 132, 20. 2. Edwards, J. II., and Lynch J. R.: The meth od used by the U. S. Public Health .Service for enumeration of asbestos dust on mem brane filler. Amer. Occup. Hyg., 1068, .//, 1. 3. Committee, on Threshold Limit Values: Threshold Limit Values for 1970, Am. Conf. of Gov. Ind. Hyg., Cincinnati, 1907. 4. Cross, I'., de Treville, R. T. 1'., ami Hal ler, M. N.: Asbestos versus nonasbestos libers, ultra-microscopic criteria, Arch. Environ. Health (Chicago), 1970,20,571. 5. Ncwhotise, M. I,., and Thompson, 11.: Mesothelioma of the pleura and peritoneum following exposure to asbestos in the London area, Brit. J. Industr. Med., 1905,22, 261. 6. Elmers, P. C., McCaughey, W. T. F... and Wade, O. L.: Diffuse mesothelioma of the pleura and asbestos, Brit. Med. J., 1905, !, 350. 7. Selikofl, J. J., Cliurg, J., and Hammond, E. C.: Relation between asbestos exposure and neoplasia, New Eng. J. Med., 1965, 272, 560. 8. Selikoff, J. J.: The occur)cnee of pleural calci fication among asbestos insulation workers, Ann. N. Y. Acad. Sci., 1965,132, 351. 9. Thompson, M. L., Pclzer, A-M., and Smither, W. J.: The discriminant value of pulmonary function tests in asbestosis, Ann. N. Y. Acad. Sci., 1965, 132, 421.