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MlPLAINT'IFF'S EXHIBIT
Im ~-U\\ 4 il I x i i i a i u i -
Case Reports.
Cos* R Cate 1:
of chest
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Floor Tile Installation as a Source of Asbestos Exposure'"
it. Thei dust ex
area of
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RAYMOND L MURPHY, BARRY W. LEVINE, FAIQ J. AL BAZZAZ,4 JOHN J. LYNCH, and WILUAM A. BURGESS
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SUMMARY __
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(. proved hemop again c Thei
Asphalt or vinyl-asbestos floor tile contains fifteen to twenty-five per cent asbestos, but the numeral
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fibers are firmly embedded in the binding material. Installation of these tiles would, therefore,
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seem to be an unlikely source of a hazardous dust exposure. Case reports of two installers of floor
pleura
tile, one with biopsy-proved mesothelioma and another with extensive pleural calcifications are
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presented. Doth workers had frequently sanded asphalt and vinyl tile floors prior to installation
sangui
of new floor covering. An investigation of the work process revealed that under simulated condi-
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lions of work, asbestos dust concentrations as large as U fibers per ml were found in air samples
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passed through membrane filters worn by a person engaged in sanding vinyl asbestos. Character-
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istic asbestos libers were seen in electron photomicrographs of these samples. These findings sug-
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gest that before the tile sanding procedure is performed adequate respiratory protection should
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be provided or alternate, available installation methods should be used.
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Introduction
floor tile, one with biopsy-proved mesotheli-
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of thi
Asphalt or vinyl-asbestos floor tile contains oma and the other with extensive pleural
thelic
15 to 25 per cent asbestos; however, the mineral fibers are firmly embedded in the
calcifications who had no other known exposure to asbestos. These workers had fre-
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Case ferret
binding material (1). Installation of these quently sanded asphalt and vinyl tile floors
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norm
tiles would, therefore, seem to be an unlike before installation of new floor covering. In
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ly source of hazardous dust exposure. Re cently the writers studied two installers of
(Received for publication November 2), 1970)
this report, these cases and the results of an investigation of exposure to asbestos during tile sanding arc presented.
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From 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.
- Supported in part hy (J.S. Public Health Service (.rant F0'j Al :,,,(l).ril and Environmental Center (.rant F.S-IHHXI2.
a Requests for reprints should be addressed to Dr. Ravmond L. H. Murphy, Department of Physiology. Harvard School of Public Health. Wi5 Huntington Avenue, Boston, Massachusetts (KM 15.
t Researclt Fellow in Medicine. Massachusetts General Hospital amt Harvard Medical School. Supported hy National Institutes of Health con tract PH-ISfiT-l-MJ.
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AMERICAN RKVIHV OF RESPIRATORY DISEASE. VOI.OME 101. Ml
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FLOOR TILE INSTALLATION AS SOURCE OF ASBESTOS EXPOSURE
577
t 1 1 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
I area of a shipyard from 1945 to 1947 repairing
I gyroscopes. From 17 to SO yean of age, he had
i smoked one package of cigarettes per day. Four months before nis present admission an
I illness developed with left anterior chest pain
I
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 diest roentgenogram revealed a left
pleural effusion without calcifications.
A thoracentesis yielded 2.000 ml of sero-
sanguincous fluid that contained 3,400 leuko
cytes per mm3, predominately mononuclear cells,
134,000 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 diest 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 dimbing 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.
1'hysical examination revealed a well devel
oped, plethoric while man. The anteroposterior diameter of the diest was increased, and line, scanned, crepitant, inspiiatory rales were noted at the liases liilalrrally. Marked tliihhing of the liugeis was piescnl.
A t liesi iirt*iiigeii<stiaiu (Jigiiiv I) sliowi-d a
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Fig. 1. Posteroanterior chest roentgenogram re vealing extensive pleural ealdheation. pleural thickening, and pulmonary hbrosis.
dense placquc of ealdheation in the left pleural space and sheetlike caldhcatioru in the pleura on tlie right. Dense caldfications were seen on both diaphragmatic pleural surfaces. The dia phragms were flattened.
The vital capadty 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 diifusing capacity was 60 per cent of pre dicted.
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 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 nut to determine the exposure to asbestos filters. Two personal samplers worn by the opera tor collected air samples oil membrane filters at an average sampling rate of 3.6 liter per min. Fibers longer than 5 u with an aspect ratio great er Ilian 3 were counted under phase contrast microscopy by the technique of Edwards anil l.yucli (2). Dust concentrations fur these two parallel samples were 1.2 fillers and 13 fibers per ml of air. respect ivclv. These concentrations arc Ik-Iow the nr roily revised tlirrshohl limit value
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578
MURPHY. LEVINE. AL BAZZAZ. LYNCH. AND BURGESS
Fig. !!. Electron photomicrograph of a replicated membrane tiller showing asbestos libers.
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 os marine insulation installation and tearout. Discrete libers were evident and were easily counted. Characteristic asbestos fibers arc shown in the electron photomicrograph of a replicated meinhninefilter sample (figure!!).
During the sanding operation, a poinl-to-plane electrostatic precipitator was used to collect a series of samples on grids for electron microscopy. 1 hese 111mts hot I lie criteria proposed for asbes tos by (.ross aiul .issueiaii-s (I; (figure .'I). The
mils of ihc fillers had profiles iliaractcri/ed by sleplike interruption^, and tibul bundles were
easily seen. Fibers were clumped together within the matrix of the tile material.
Discuuion Both of the tile installers had diseases known to be associated with exposure to asbestos.
The first patient had typical clinical, rocntgenographic aiul pathologic findings ot pleural mesothelioma. Epidemiologic inves tigations of cases of mesothelioma have shown asbestos exposure in more than 40 per cent (5, (i). The incidence of mesothelioma in the general imputation is (ram I in 1.000 to I in 10.1100 deaths (7). Because the pres ent .studies revealed that airborne asbestos panicles ate generated during sanding ot
tile, a cau cmplt volve likely None mcioi be :
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FLOOR TILE INSTALLATION AS SOURCE OF ASBESTOS EXFOSURE
579
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bnown "'Vstos. - -I clinical, "--'.uings of 'oric invesioma have hua -10 per
Glioma t 1.000
pres- asbestos .nding of
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 unreiatea 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 he considered to be due to asbestos exposure (8). The causal relationship seems clear because the patient had no his tory of pulmonary infection or trauma and bail a known ex|>osure to asbestos. It was more difficult, however, to- assess die 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 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 50 years. Because this industry is the second largest consumer
of this mineral in tlic United Slates, the po tential hazard is significant if the current method ol 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-
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580
MURPHY. LEVINE. AL BAZZAZ. LYNCH. AND BURGESS
quaie respiratory protection or an alternate installation method should be used. The as
troubles pneumoconiotiques. Les rapports medicaux de deux ouvrien installeurs de carTclagc.
Aspergilloi
sociation between installation of tile and l'un souSrant de mesotheliome confirmc a la bi-
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.
opsie. et l'autre Otant porteur de calcification pleuralcs sont presentO iti. Ces deux ouvrien avaient souvent sable des carreiages d'aspltaltc ou de vinyl-asbeste au papier de verse, avant d'installer des nouveaux carrcaux. L'incitlcnude ces cas a incili & une investigation du pn>etdi. En reertant les conditions de travail, ik>
'
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GEORGE A. S P. M. HUGGIN
concentrations de poussicre d'amiante ilun
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Acknowledgments
niveau aussi elevO que 1J fibres par ml ont pu
The writers are grateful to Mr. Lloyd Shoenliach for the extensive electron microscopy car ried out during this study and to Dr. Heinrich Brtigsch for reviewing the manuscript
RESUMED--------------------------------------------------------
Instalacidu tie baldosas para el piso como una fiicnte de exposition a asbestos
El asfalto o la baldosa para cl piso de vinilo-asItcstos contienc de 15 a 25 por ciento de asbestos, pero las libras numerates estan lirmamentc incrustadas en cl material de ligamiento. La instalacion de estas baldosas, por consiguiente. no parcccria scr una fitente peligrosa de exposi tion al polvo. Se presentan los casos de 2 instaiadores de baldosas para el piso, uno con mi mesotelioma comprobado por biopsia y el otro con calcilicacioncs pleuralcs extensas. Estos trabajadotes habian lijado frccucntcmcnte baldosas el piso de asfalto y de viuilo antes de instalar los nuevos pisos. La ocurrcntia de estos casos llevO a una iuvcsiigacidu del proceso de trabajo. llajo condicioncs de trabajo simuladas. se cncontraron concentrationes de polvo de aslicstos tan alias como 1.3 fibras por ml cn mucstras de airc en nitres de membrana que Uevaba ptiesta una per sona envudta cn lijar los asbestos de vinilo. Fibras de asbestos caractcrislicas de estas mttestras fueron vistas en fotomicrOgtafos electr6nicos. Estos hallazgos sugieren qite antes ilel privceso de lijar sc llcvc a cabo. se deberia usar una protection respiratoria adccuada o usar otros metotlos tie insulation al alcancc.
RESUME
L.'installation ill's tarrtiages: source il'exposition a I'amiaiiii:
I ts taiieaiix iras|ihalie on dime coinltinaison le tmvl et diislicstc tiintieiineiii tie 15 it 25 poiirteiit I'.iiniaiilc. inais It's liliri > siitil iiiliim-mcnt
ctre mesurOe dans Fair ambiant. Les mcsurcs furent determinee cn faisant passer des endiantillons d'air sur un papier iiltrO fixe sur un travaillcur en train de sablcr des tuiles de vinylasbeste. Des photomicrographies de ces prelevcment ont montrO qu'il s'agissait de fibres amiantc caracteristiqucs. En consequence, nous ilcvons appliquer. une proteaion respiratoirc sullisantc lors du sablage de tuiles oil choisir un autre procfdi d'installation.
References 1. Hendry, N. W.: The geology, occurrences.
and major uses of asbestos, Ann. N. Y. Acad. Sti.. 1965.1)2,20.
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 membranc filter, Amer. Occup. Hyg., 1968, 11, 1-
3. Committee on Threshold Limit Values: Threshold Limit Values for 1970, Am. Conf. of Cov. 1ml. Hyg.. Cincinnati, 1967.
4. Gross. P,, de Trcville. R. T. P.. and Haller, M. N.: Asbestos versus nonasbestos libers. ultra-microscopic criteria. Arch. Environ. Health (Chicago). 1970.20,571.
5. Neivhoiisc. M. I... and Thompson, II.: 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.. McCaughcy, VV. T. E.. and Wade. O. L.: DifTuse mesothelioma of the pleura anil asbestos, Brit. Med. J.. 1965. I350.
7. Sclikoir, J. J., Clung, J., and Hammond. E. C.: Relation between asbestos exposure anil ucoplasia. New Eng. J. Med., 1965. 272, 560.
6. Seliknlf, J. J.: The occurrence of pleural calci fication among aslicstos insulation workers, Ann. N. Y. Acad. Sci.. 1965.1 >?,35l. TIiiii|koii. M. 1... 1'clrer. A-M.. and Sniilher. W. |.: The discriiuiiiant value of pulmonary
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SUMMARY___
Aspergillom two yean c amphoterio the appears to these pat
introduction Of tire three aspergillosis di ciates (1), the perhaps the eathe fungus grt destruction, u> characteristic t the diagnosis r
These fungoccur in any to tissue desrt Pulmonary till cavity format sarcoidosis (3
[Received in rc
I From the I Center for DI: Mental lU-dt: Service. . i and W.-r.'i.-. inini-irv: -n Term,-, i i ' Tt-mit--rc.
- Iletpir . 'o L)r. IT.-:
t' Wi-sf .lot', .
tiers a I'agml >UK'1111 utaitl. I.inslullalinn tie ten
function tests tu asbcslosis, Aun. N. Y. Aiad.
rain-jus pataii tltmt nut* stmtie iiupiobalile tie
Su.. 1965.112. 121.
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