Document M4B7Z8d02DKgroRJb1Q7JYJJL

PLAINTIFF'S EXHIBIT AN ASSESSMENT OF THE RISK OF HEALTH EFFECTS RESULTING FROM THE USE OF MOBIL PRODUCTS BEARING THE NAME "DUM DUM" WITH AN UPDATE OF SCIENTIFIC KNOWLEDGE TO 1999. GRAHAM W GIBBS MSc PhD LRSC ROH Safety Health Environment International Consultants Corp Suite 101, 38, Athabasca Avenue, Devon, Alberta, Canada, T9G 1G2 FEBRUARY 2000 MOB-HarrisMaster 00233 PREFACE In June 1992,1 issued a report entitled "An assessment of the risk of health effects resulting from the use ofMobil Products bearing the name "Dum Dum". The report was prepared at the request of Mr Thomas Campion, Shanley & Fisher, Morristown, New Jersey. The task undertaken was to prepare a document which evaluated the risk of asbestos-related disease for persons using Dum Dum products. This current report contains information updating that original report to take account of the scientific literature since the original report was prepared. Ms Julia Kingsley Evans and/or other legal counsel acting for Mobil provided no specific direction concerning the scientific aspects of the report. The Preface in the original report was as follows: This report was prepared at the request of Mr Thomas Campion, Shanley & Fisher, Morristown, New Jersey. The task undertaken was to prepare a document which evaluated the risk of asbestos-related disease for persons using Dum Dum products. Mr Campion provided no specific direction other than the report should advise " whether, on the basis of the available scientific evidence, the encapsulated asbestos in the products caused injury in the application or removal process." MOB-HarrisMaster 00234 REPORT ORGANIZATION The report guides the reader through a logical sequence of steps, critically evaluating the factors which determine the occurrence of health effects in workers exposed to "asbestos" fibres. These factors are then examined in making an assessment of the risks for persons using "Dum Dum" products. For convenience, technical terms and abbreviations are provided as footnotes on the pages where they occur. When more detail is required to support a particular evaluative step, this is provided in an appendix to the report. The various sections of the report are numbered according to subject matter. The studies to which references are made in the report are listed in alphabetical and date order in the BIBLIOGRAPHY. In order to facilitate reading this updated report, the original report layout and content have been retained. Information updating the report has been added at the end of each section and additional sections added when necessary. For convenience, references to the updated information have been incorporated into the original BIBLIOGRAPHY.. MOB-HarrisMaster 00235 Ill TABLE OF CONTENTS SECTION PAGE PREFACE............... ,.......................................................................................................................... i REPORT ORGANIZATION..............................................................................................................ii 1.0 OBJECTIVES..................................................................................................................................1 2.0 "DUM DUM" TERMINOLOGY.................................................................................................. 2 3.0 BACKGROUND............................................................................................................................. 2 3.1 SCOPE ............................................................................................................................... 2 3.2 PERIOD OVER WHICH PRODUCTS WERE SOLD...................................................3 4.0 THE ASBESTOS MINERALS.................................................................................................... 3 4.1 CHRYSOTILE (WHITE ASBESTOS) .......................................................................... 3 4.2 THE AMPHIBOLES............................................ 4 4.2.1 Crocidolite (Blue Asbestos)........................................................................ 4 4.2.2 Amosite (Brown Asbestos) ........................................................................ 6 4.2.3 Anthophyllite................................................................................................ 6 4.2.4 Tremolite and Actinolite...............................................................................6 5.0 THE DUM DUM PRODUCTS...................................................................................................7 5.1 GENERAL CHARACTERISTICS ................................................................................. 7 5.2 THE SPECIFIC PRODUCTS ...................................................................................... 8 6.0 OCCUPATIONALLY RELATED DISEASES......................................................................... 10 7.0 DISEASES ASSOCIATED WITH ASBESTOS EXPOSURE................................................. 13 7.1 MESOTHELIOMA .. ..................................................................................................... 14 7.1.1 Occurrence ................................................................................................. 14 7.1.2 Diagnosis..................................................................................................... 14 7.1.3 Survival........................................................................................................16 7.1.4 Etiological Factors...................................................................................... 16 7.1.4.1 Agent ................................................................................ 17 7.1.4.2 Asbestos Fibre Type ........................................................18 7.1.4.3 Other Fibres .................... 32 7.1.4.4 Ionizing Radiation............................................................35 7.1.4.5 Other Chemicals ..............................................................38 7.1.4.6 Other Factors .................................................................. 38 7.2 MECHANISTIC CONSIDERATIONS ......................................................................42 MOB-HarrisMaster 00236 IV 7.3 LEVEL OF EXPOSURE.......................................... .................................................46 7.3.1 Neighbourhood Exposure ....................................................................... 49 7.3.2 Household Exposure................................................................................. 51 7.4 LATENCY .....................................................................................................................52 8.0 ASBESTOSIS ................................................................................................................................ 55 8.1 DEFINITION AND DIAGNOSIS................................................................................. 55 8.1.1 Radiological Changes................................................................................. 57 8.1.2 Breathlessness................................................... ...................................... 58 8.1.3 Lung Function Changes............................................................................. 59 8.1.4 Clinical observations ................................................................................. 59 8.1.5 Mechanistic considerations.............................................................. -.... 59 9.0 LUNG CANCER........................................................................................................................... 61 9.1 LUNG CANCER RISK, TYPE OF ASBESTOS AND OCCUPATION....................61 9.2 SMOKING .......................................................................................................................71 9.3 OTHER FACTORS ......................................................................................74 10.0 GASTROINTESTINAL CANCER.......................................................................................... 78 11.0 OTHER CANCERS .................................................................................................................. 79 12.0 TALC . ...................................................................................................................................... 79 13.0 ASSESSING HAZARD AND RISKS......................................................................................80 13.1 PARTICLE SIZE & SHAPE........................................................................................ 80 13.1.1 Aerodynamic behaviour, respirability and deposition .......................... 81 13.1.2 Role of particle size in particle removal from the lung........................ 82 13.1.3 Particle solubility...................................................................................... 83 14.0 RISKS OF HEALTH EFFECTS FROM WORKING WITH DUM DUM .......................... 83 14.1 CHARACTERISTICS AND PROPERTIES OF AIRBORNE ASBESTOS DUSTS FROM DUM DUM .............................................................................................84 14.1.1 Asbestos fibre types..................................................................................84 14.1.2 Sizes of airborne fibres............................................................................. 85 14.1.3 Asbestos exposure of workers applying and removing Dum Dum products........................................................................................ 88 14.1.3.1 Levels of exposure ........................................................90 14.1.3.2 Duration of exposure................................................... 101 15.0 THRESHOLD LIMIT VALUES AND LEGAL EXPOSURE LIMITS.............................102 MOB-HarrisMaster 00237 V 16.0 RISKS OF HEALTH EFFECTS FOR USERS OF DUM DUM PRODUCTS . . 102 16.1 RADIOLOGICAL CHANGES ...................... 106 16.2 LUNG CANCER..........................................................................................................107 16.3 MESOTHELIOMA RISKS.........................................................................................114 16.4 COMPARISONS..........................................................................................................117 17.0 CONCLUSIONS.................................................................................................................... 121 BIBLIOGRAPHY............................................................................................................................ 123 MOB-HarrisMaster 00238 TABLE OF CONTENTS vi SECTION FIGURES PAGE FIGURE 1 THE ASBESTOS MINERALS .............................................................................................. 4 FIGURE 2 ELECTRON MICROGRAPHS OF CROCIDOLITE, AMOSITE, ANTHOPHYLLITE AND CHRYSOTILE AT THE SAME MAGNIFICATION (x 1700)3'4............................ 5 FIGURE 3 EXPOSURE - RESPONSE RELATIONSHIPS FOR VARIOUS OCCUPATIONAL GROUPS (AFTER MCDONALD 1984).......................................... 64 FIGURE 4 - THE USE OF NAIL HOLE FILLER -............................................................................. 93 FIGURE 5 OSHA PERMISSIBLE EXPOSURE LIMITS, ACGEH TLVS FOR CHRYSOTILE ASBESTOS AND THE CONCENTRATION OF ASBESTOS STRUCTURES ASSOCIATED WITH THE APPLICATION AND REMOVAL OF DUMDUM PRODUCTS ............................................................................................. 104 FIGURE U1 OSHA PERMISSIBLE EXPOSURE LIMITS, ACGIH TLVS FOR CHRYSOTILE ASBESTOS AND THE CONCENTRATION OF ASBESTOS STRUCTURES ASSOCIATED WITH THE APPLICATION AND REMOVAL OF DUM DUM PRODUCTS ................................................................................................................................................. 105 MOB-HarrisMaster 00239 TABLE 1. TABLE 2. TABLE 3. TABLE 4. T.ABLE 5. T.ABLE 6a. TABLE OF CONTENTS TABLES ' vu PAGE MESOTHELIOMA IN VARIOUS COHORTS - AMPHIBOLE ONLY - BLUE ASBESTOS ....:...................................................................................................................19 MESOTHELIOMA IN VARIOUS COHORTS - AMPHIBOLE ONLY - AMOSITE ASBESTOS ...................................................................................................................................... 19 MESOTHELIOMA IN VARIOUS COHORTS - MIXED FIBRE - AMPHIBOLE & CHRYSOTILE 20........................................................................'................................................................................................................................................................................................................... MESOTHELIOMA IN VARIOUS COHORTS - TREMOLITE ONLY 21................................................................................................................................................................................................................................................................................................ MESOTHELIOMA IN VARIOUS COHORTS - CHRYSOTILE ONLY - ........................................................................................................... 21 MESOTHELIOMA IN CHRYSOTILE MINERS & MILLERS AND BLUE ASBESTOS GAS MASK WORKERS...................................... 23 MOB-HarrisMaster 00240 J TABLE 6b. TABLE 7. TABLE Ul. TABLE U2. TABLE U3 TABLE U4. TABLE U5. vrn MESOTHELIOMA IN MILITARY (BLUE) & CIVILIAN (CHRYSOTTLE) GAS MASK WORKERS ...................................................24 MESOTHELIOMA RISK INCREMENTS PER FIBRE PER MICROGRAM................................................................................................... 25 MESOTHELIOMA IN VARIOUS COHORTS - AMPHIBOLE ONLY - BLUE ASBESTOS ..............................................................................................................................28 MESOTHELIOMA IN VARIOUS COHORTS - AMPHIBOLE ONLY - AMOSITE ASBESTOS ........................................ :................................................................................... 29 MESOTHELIOMA IN VARIOUS COHORTS - MIXED FIBRE - AMPHIBOLE & CHRYSOTTLE .............................................................................................................................. 30 MESOTHELIOMA IN VARIOUS COHORTS -CHRYSOTTLE ONLY ............................. '................................................................................................31 MESOTHELIOMA IN ANTHOPHYLLITE COHORTS ANTHOPHYLLITE ONLY - 31 MOB-HarrisMaster 00241 IX TABLE U6. TABLE U7. TABLE U8. TABLE 8. TABLE 9. TABLE 10. TABLE U9: TABLE U10 MESOTHELIOMA OCCURENCES IN PERSONS RECEIVING THERAPEUTIC RADIATION TREATMENT ............................................................................................................................. 36 THOROTRAST 37 BIOPERSISTENCE OF CROCIDOLITE 44 MESOTHELIOMA -EVIDENCE OF EXPOSURE-RESPONSE................. 47 MESOTHELIOMA ODDS RATIOS IN RELATION TO LUNG TISSUE FIBRE CONTENTS RE-CALCULATED FROM VARIOUS STUDIES BY BERRY................48 THE OBSERVED & EXPECTED NUMBERS OF DEATHS FROM LUNG CANCER BY FIBRE TYPE AND INDUSTRY SECTOR33 63 DEATHS FROM LUNG CANCER IN RELATION TO EXPOSURE ACCUMULATED TO AGE 55 IN QUEBEC CHRYSOTILE MINERS & MILLERS. ....................................................................... ;................................................... 65 NUMBER OF OBSERVED AND SMRS BY DURATION OF EXPOSURE FOR MINERS OF THE BALANGERO MINE ITALY .............................................................................................................................. 65 MOB-HarrisMaster 00242 TABLE UU. RELATIONSHIP BETWEEN ASBESTOSIS AND LUNG CANCER .... 68 TABLE II. EFFECTS OF SMOKING & ASBESTOS EXPOSURE ON LUNG CANCER RISKS .............................................................................................................................. 71 TABLE 12. EFFECTS OF SMOKING & ASBESTOS EXPOSURE ON LUNG CANCER RISKS ..............................................................................................................................72 TABLE U12. COMPARISON OF LUNG CANCER DEATH RATES BETWEEN CPS-1 AND CPS-11 FOR MALES OF ALL RACES WITH REVALENT CANCERS INCLUDED ................................................................................................................................ 73 TABLEU13 ODDS RATIOS* BETWEEN CIGARETTE SMOKING AND LUNG CANER FOR EVER-SMOKERS AND FOR SUBGROUPS DEFINED BY CUMULATIVE AMOUNT SMOKED, BY TWO CONTROL GROUPS .............................................................................................................................. 74 TABLE 13. CHEMICALS LISTED AS CONFIRMED (Al) OR SUSPECTED CARCINOGENS (A2) BY ACGEH A!..................................................... 75 TABLE U14. CHEMICALS LISTED AS CONFIRMED (Al) OR SUSPECTED CARCINOGENS (A2) BY ACGIH ............................................................................................................................... 76 MOB-HarrisMaster 00243 xi TABLE U15. ESTIMATES OF CONTRIBUTIONS TO LUNG CANCER RISK BY LATENCY PERIOD BASED ON INSULATION WORKER DATA. ............................................................................................................................. 78 TABLE 14. CONCENTRATIONS OF AIRBORNE STRUCTURES DURING THE APPLICATION AN.......................................................................................... 87 TABLE U16. CONCENTRATIONS OF AIRBORNE STRUCTURESDURING THE APPLICATION AN............................................................................................ 89 TABLE 15. FIBRE CONCENTRATIONS ASSOCIATED WITH THE SPRAY APPLICATION OF ASBESTOS CONTAINING PETROLEUM BASED COATING PRODUCTS...................................................................... 96 TABLE 16. MAXIMUM POSSIBLE DURATIONS OF EXPOSURE AND MAXIMUM CUMULATIVE EXPOSURES OF WORKERS APPLYING DUM DUM PRODUCTS MARKETED BY MOBIL ................................................................................103 T.ABLE 17. LIFETIME RISK VALLES FOR SELECTED SITUATIONS............. US TABLEU17 EXAMPLES OF RISKS REPORTED BY DR JOHN PALING. 120 MOB-HarrisMaster 00244 PLATE 1. PLATE 2. PLATE 3. PLATE 4. PLATE 5. PLATE 6. PLATE 7. PLATE 8. PLATE 9. PLATE 10. PLATE 11. TABLE OF CONTENTS ALL PLATES FOLLOW PAGE 85. XII SURFACE OF DUM DUM MASONOC TO SHOW ENCAPSULATION (SEM) BROKEN CROSS-SECTION OF CHIMNEY DUM DUM SHOWING HOW FIBRES ARE ENCAPSULATED. (SEM) CLUMP OF FIBRES SHOWING ENCAPSULATION. PRODUCT CHIMNEY DUM DUM (SEM). FREE CHRYSOTILE FIBRES AT THE SAME MAGNIFICATION AS FIGURE 1. SAMPLE PREPARED IN SAME LABORATORY AS FIGURE I FREE CHRYSOTILE FIBRES AT THE SAME MAGNIFICATION AS FIGURE 2. SAMPLE PREPARED IN SAME LABORATORY AS FIGURE 2 FREE CHRYSOTILE FIBRES AT THE SAME MAGNIFICATION AS FIGURE 3. SAMPLE PREPARED IN SAME LABORATORY AS FIGURE 3 AIRBORNE ASBESTOS STRUCTURES - DUM DUM MASONOC REMOVAL EXPERIMENT. AIRBORNE ASBESTOS STRUCTURES - DUM DUM MASONOC APPLICATION EXPERIMENT AIRBORNE ASBESTOS STRUCTURES - DUM DUM MASONOC APPLICATION EXPERIMENT AIRBORNE ASBESTOS STRUCTURES - CHIMNEY DUM DUM APPLICATION EXPERIMENT. AIRBORNE ASBESTOS STRUCTURES - CHIMNEY DUM DUM APPLICATION EXPERIMENT. MOB-HamsMaster 00245 xiii PLATE 12. PLATE 13. AIRBORNE ASBESTOS STRUCTURES - HI-HEAT DUM DUM REMOVAL EXPERIMENT. AIRBORNE ASBESTOS STRUCTURES - HI-HEAT DUM DUM REMOVAL EXPERIMENT. TABLE OF CONTENTS CONT PLATE 14. PLATE 15. PLATE 16. PLATE 17. AIRBORNE ASBESTOS STRUCTURES - HI-HEAT DUM DUM APPLICATION EXPERIMENT. AIRBORNE ASBESTOS STRUCTURES - HI-HEAT DUM DUM REMOVAL EXPERIMENT. AIRBORNE ASBESTOS STRUCTURES - HI-HEAT DUM DUM REMOVAL EXPERIMENT. AIRBORNE ASBESTOS STRUCTURES - HI-HEAT DUM DUM REMOVAL EXPERIMENT MOB-HarrisMaster 00246 Kj/ an assessment of the risk of HEALTH EFFECTS RESULTING FROM THE USE OF MOBIL PRODUCTS BEARING THE NAME "DUM DUM" WITH AN UPDATE OF SCIENTIFIC KNOWLEDGE TO 1999. Dr. GRAHAM W GIBBS Safety Health Environment International Consultants Corp 1.0 OBJECTIVES The objectives of the original June 1992 report were: to describe a systematic approach which might be applied in evaluating whether the "asbestos" used in certain "Dum Dum" products has, or might reasonably be expected, to have caused adverse health effects in persons who applied or removed the products. b. to apply this approach in critically evaluating the available scientific evidence ' concerning the health risks for workers applying or removing products bearing the name "Dum Dum". The purpose of this updated report remains as originally stated. However, as this report incorporates information which has appeared in the scientific literature since the original report was prepared it also examines whether the scientific literature published between the early 1990s and 1999 has changed the conclusions recorded in the 1992 report. Those conclusions were: It is highly improbable that the levels of asbestos exposure by persons using Dum Dum products continuously over a 20 year period would be adequate to give rise to detectable "radiological changes" compatible with asbestosis. It is highly improbable that the levels of asbestos exposure by persons using Dum Dum products continuously over a 20 year period would be adequate to produce detectable increases in lung cancer or primary malignant mesothelioma death rates. The risks of mesothelioma, lung cancer and lung fibrosis associated with the use of the Dum Dum Products are so low that other sources of exposure and other MOB-HarrisMaster 00247 factors deserve a much higher priority for consideration in determining the etiology of cancers or radiological changes. 2.0 "DUM DUM" TERMINOLOGY This report addresses "DUM DUM" products manufactured and marketed by Mobil. While preparing this report, it was found that a product known as "Red Dum Dum Boiler Putty" was currently being manufactured by "The Presco Co. Ltd", Mississauga, Ontario. In a telephone conversation, Mr R.C. Smith of that company informed me that this product has been manufactured by them since at least 1935 and probably earlier. The most recent Material Safety Data Sheet (MSDS) for the "Presco" product (APPENDIX A) does not report the presence of asbestos, although an earlier MSDS for a "Dum Dum Hi-Temp Boiler Putty" (date unknown - APPENDIX B) did note asbestos as a constituent. "Red Dum Dum Boiler Putty" product was not, as far as I could ascertain, ever produced by Mobil. The products discussed in this report will be restricted to those produced and/or marketed by Mobil. UPDATE: There has been no change in the nomenclature applied to these products. 3.0 BACKGROUND 3.1 SCOPE This report was prepared in response to the question posed by Mr Thomas F. Campion, Shaniey & Fisher, Morristown, New Jersey. Referring to Dum Dum products he asked ".... whether the encapsulated1 asbestos in Mobil's products caused an injury to those who applied it or removed it." The report specifically targets the risks for persons working with the manufactured products as marketed by Mobil and does not include an assessment of health risks for workers involved in manufacturing the products or handling raw materials used in their manufacture. "Working with" has been defined as applying, removing and disposing of the products. UPDATE: There is no change in the broad scope of the report. ^Encapsulated denote* the eadoue ofthe isbosto* by substance* which cover or form a seal over the individual or bundles of fibres fcrnmn a mast in which the fibres are now an integral part of the whole and no longer five isbesto* fibres. MOB-HarrisMaster 00248 3 3.2 PERIOD OVER WHICH PRODUCTS WERE SOLD In 1963, Mobil acquired the paints and coatings business of the Martin-Marietta Corporation and began to manufacture and sell coatings products which contained small amounts of encapsulated asbestos. Several ofthese products were discontinued at various dates between 1963 and 1980, with the asbestos containing materials being totally discontinued by the end of 1980. This report, while drawing on information gathered outside this time-frame, addresses only products produced and sold in the period 1963-1980. UPDATE: There has been no information forthcoming since the preparation ofthe original report to indicate any modification to the time period 1963 - 1980. 4.0 THE ASBESTOS MINERALS Asbestos is not a single substance. In later sections of this report, it will be seen that there are clear differences in the risk of asbestos-related diseases associated with exposure to the different fibrous minerals referred to as "asbestos". That they should pose different levels of risk should not be surprising as each of the "fibre types" has its own distinct chemical, mineralogical and physical characteristics. Asbestos is a generic term applied to the naturally occurring hydrated fibrous silicates. There are six main varieties (FIGURE 1). Four of them, chrysotile, amosite, crocidolite and anthophyllite have been of commercial importance. Differences in the general appearance of these minerals under the electron microscope are shown in FIGURE 2. UPDATE: While there have been advances in understanding the importance of potential contaminants in commercially produced chrysotile asbestos, there has been no new information that would change the very general descriptions of the asbestos minerals given in sections 4.0 - 4.24. While the medical literature has given more attention to specific fibre types, the generic term "asbestos" is still widely used and in most instances the medical literature is still very imprecise in respect to mineral terminology. 4.1 CHRYSOTILE (WHITE ASBESTOS) Chrysotile is an hydrated magnesium silicate and a member of the serpentine group of minerals. It usually occurs as white flexible fibres and is sometimes referred io as "white asbestos". The main asbestos fibre type referred to in this report will be "CHRYSOTILE" as chrysotile was the MOB-HarrisMaster 00249 5 FIGURE 2 ELECTRON MICROGRAPHS OF CROCEDOLITE, AMOSITE, ANTHOPHYLLITE AND CHRYSOTILE AT THE SAME MAGNIFICATION (x 1700)3'4 CROCIDOLITE AMOSITE 10 jtni acuta ofthe fibrea were: crocidoliic: Nonh-Wcaicm Cepe Prowvoe. South Airica; emoeite: Ttanavaal. South Africa; anthophyQiia: Finland; chtyaotil**: Canada. * Soot (be sngbt amphibole fibres (crocidoUte; athopyiyHrt) ip e^wtrtf ir> th* curty chiysotile fibres; tht relative erda* ofmagnitude of tbs inwtoi of dv ud tbs lowjtuHinai cf(bo chxysodlo fibres and the small diameter of the ultimate fibril (approx 0.03um) (TanbreB 1973).The dimensions of fibra air conventionally erpmed in micrometres (jim). Ijtm * l x lO^m. MOB-HarrisMaster 00250 6 In order to avoid confusion in the use of mineralogical terms, the term used throughout this text to identify crocidolite, the mineral mined in South Africa and Australia, wall be "BLUE ASBESTOS" UPDATE: The production in South Africa has ceased. 4.2.2 Amosite (Brown Asbestos) Amosite is a brown-grey or white fibre mined in South Africa. UPDATE: The production of amosite in South Africa has ceased. 4.2.3 Anthophyllite Anthophyllite is a white fibre which was mined mainly in Finland and has had limited application commercially. 4.2.4 Tremolite and Actinolite Tremolite and actinolite are two minerals in a series of minerals in which the iron/magnesium ratio determines the mineral name. Tremolite is not of direct commercial importance at this time However, tremolite has become quite important in understanding the health risks associated with chrysotiie asbestos as tremolite would appear to occur in extremely small amounts in some chrysotiie deposits. When Quebec chrysotiie miners and millers have inhaled mine and mill dusts, tremolite fibres appear to have been preferentially concentrated in their lungs. Some chrysotiie miners in Quebec have been found to have as much tremolite as chrysotiie in their lungs at autopsy ('Rowlands et al 19821 Tremolite can be a contaminant ofvermiculite and talc. Mesotheliomas have been reported :n vermiculite miners (McDonald et al 1986a), and in talc miners (Vianna et al 1981). This has led :o an hypothesis, increasingly supported by scientific research results, that the tremolite fibre contamination of chrysotiie may explain the occasional occurrence of mesothelioma in workers in the Quebec chrysotiie mines and mills. Talc was used in some of the Dum Dum products. Some talcs have tremolite associated with them. It should be emphasized that not all talcs contain tremolite and not all tremolite is asbestiform. Whether or not talcs used by Mobil prior to the mid 1970's were contaminated by asbestiform tremolite is not known. However, after that time, Mobil stipulated that only tremolite-free talcs be purchased for use in the Dum Dum product line. MOB-HarrisMaster 00251 UPDATE: In view of the importance of asbestiform tremolite, it should be noted that while fibrous tremolite is a potential contaminant in some chrysotile deposits, it is not a contaminant of all commercial chrysotile. The tremolite in the Quebec chrysotile mines is associated with mineralogical alterations in the rock usually close to igneous intrusive rocks (Williams-Jones 1999; Gibbs 1999). The fibrous tremolite was not in the ore body but in other rocks occurring in the mine. Tremolite fibres occur at very high concentrations in the lungs of some Quebec chrysotile miners [McDonald et al 1997). 5.0 THE DUM DUM PRODUCTS UPDATE: There have been no changes to the list of Dum Dum Products considered in this report or in the compositional data for these Dum Dum products. 5.1 GENERAL CHARACTERISTICS A list ofDum Dum products is provided in Appendix C. For convenience, they have been classified according to their application, asbestos content and period over which they were manufactured. The applications were. * Filling nail holes * General purpose caulking * High temperature caulking * Exterior masonry coatings * Chimney coatings The shared characteristics of "Dum Dum" products were that they were designed to..... * harden only at the surface so that they could be painted. * remain pliable underneath the surface during application and throughout the product lifetime to expand and contract with the building * bridge cracks and flaws in the surfaces to which applied * in most cases have a weatherproof exterior. * reseal automatically if the surface were cracked because the exposed sub-surface material would reform a new coating. The products were sold in a form ready for use and the components were thoroughly mixed in oils MOB-HarrisMaster 00252 so that the products were essentially ofputty consistency making it unlikely that they would produce any dusts or respirable aerosols during use. 5.2 THE SPECIFIC PRODUCTS Brief descriptions of the products taken from product literature, product labels and material safety data sheets provided by Mobil follow.... A. Dum Dum Nail Hole A number of nail hole products were manufactured until 1973, the only-differences between the various products were in the additives used to produce different colours (See APPENDIX Cl). This material was of putty-like consistency, for knife application to fill nail holes in pre-finished wood. B. Caulking Compounds A number of products were manufactured and marketed as caulking materials (See APPENDIX C2). The Mobil Chemical Product Data sheet for "DUM DUM Calking, 46-F-5" shows that this product was a mixture of pigment and asbestos fibre in a vegetable oil vehicle (Mobil 1976a). At 24C its viscosity was described as putty and would build one inch (1") on the vertical without slumping. The label for this particular product was clearly marked "For industrial use only. Do not use around a household or dwelling" (Mobil 1976a; Mobil 1970a). The product label indicated that "Dum Dum Calking" was designed for all conventional exterior caulking work, with flexibility to withstand building stresses, settling and shrinkage. It was described as an oil based caulking compound for glazing and filling operations by knife or gun for joints or cracks (Mobil 1976b). The product was clearly under oil as instructions to stir it, if oil had risen to the top, were provided. The surface was reported to "skin" in 18 hours and could be painted in 24 hours. C. High temperature Caulking compounds The high temperature caulking materials are described in APPENDIX C3. There appear to have been two such products. "Hi-Heat Dum Dum, 46-F-7" was marketed from 1964 through October 1980. A Material Safety Data Sheet dated September 26 1980 states that this product was at that time "asbestos-free" (Mobil 1980). Hi- Heat Dum Dum is described in the Mobil product literature as a heavy semi-plastic fibred coating which acts as a joint sealer and pliable gasket for boilers, furnaces and dry kilns. It retains its elasticity at constant heat up to I75C and at intermittent heat to 350C (Mobil 19XXa)3. Its viscosity at 24C was described as mastic (Mobil 1976c)-. The product after application could be painted over after 24 hours (Mobil 1970b). This product contained chrysotile asbestos and talc in a linseed oil blend (Chamberlain 1991). "Dum Dum Armorcote, 46-J-9" was a specially compounded heavy bodied product containing asphalt, reinforcing pigment and high boiling point hydrocarbons. It was resistant to fumes, moisture and sustained temperatures to 300T. It was used to protect and increase the efficiency of brick boiler settings, as a dry kiln liner and in similar refractory applications (Mobil 19XXb; Mobil 1973a). Its viscosity at 24C was described as a putty (Mobil 1976d). D. Masonry Coatings The "95 series DUM DUM Masonoc" was marketed from 1964 to 1979 and contained not less than 10 and not more than 15% chrysotile asbestos. Its viscosity was mastic and while forming a "skin" in 1 hour the under surface remained pliable (Mobil 1976e). The product was described as a heavy bodied coating of mastic consistency designed for "hi build" application for filling and bridging cracks and crevices, with application by special brush or heavy duty mastic spray equipment (Mobil 19XXc). The product was noted to be used in applications for the waterproofing and restoration of exterior masonry and for the protection of steel surfaces and for industrial use only (Mobil 1971a; Mobil 1976e). E. Chimney Coatings The "97 Series Chimney Dum Dum" was marketed in the period 1964-1979. The product was a mixture containing chrysotile asbestos fibre (4-5%) and color fast pigments in a resinated vegetable 011 (Mobil I976f, Mobil 1970c). According to the product literature, "Chimney Dum Dum" provides "the same outstanding protective and waterproofing qualities as the 95 Series Masonoc except that it has been formulated for use on concrete chimneys where additional heat resistance up to 210F may be required" (Mobil 1976g). The viscosity is described as mastic. Although the surface "skins" in 4-6 hours, the product was designed so that the under-surface remained pliable (Mobil 1976f). F. Primers Literature relating to the use of "Dum Dum Masonoc" recommended that the surface be prepared with primers. Examples of primers for use with the "Dum Dum Masonoc 95 series" were "Masonoc Primer, 47-W-21" and "Masonoc Primer,47-B-l". There were others which differed in colour but with essentially the same constituents except for the pigment. The 47-W-l product was described *The dote 19XX hi* been used is references when the product fiieruure etisa but is undated. MOB-HarrisMaster 00254 10 as "a normal paint like material to be used beneath the Masonoc coating on all types of masonry surfaces to seal off and eliminate surface porosity" (Mobil 1976h). A primer recommended for use with the Chimney Dum Dum was "Chimney Dum Dum Primer 38-V-5". Commercial asbestos was not a component in the formulation of these primers (Chamberlain 1991). Hence, these primers will not be considered further. 6.0 OCCUPATIONALLY RELATED DISEASES Occupational diseases result from exposures at work and are essentially of three types. The first is a disease which occurs very rarely in the general population. When a few cases occur in a working population in relation to a specific occupational exposure this is sufficient to raise a suspicion that the disease is occupational in origin. However, there are often factors other than occupation which are common to the cases and working population. Thus the observation of a clustering of cases of a rare disease should signal the need to seek confirmatory data. This usually involves an independent epidemiological study. An example is primary malignant mesothelioma. The second type of occupational disease occurs quite commonly in the general population. In this situation it becomes necessary to determine whether the disease occurs more frequently in the workers exposed to a specific agent than in workers ofthe same age, sex, socio-economic status, etc. who are not so exposed. This is the situation in regard to linking health effects such as lung cancer to asbestos exposure. In such instances, several different agents may independently be associated with the disease. They may also interact to increase or decrease risks. The third type of occupational disease is one where the disease has been established as occurring in occupationally exposed persons or is so defined. Such a disease is classical silicosis which occurs in persons exposed to high levels of respirable crystalline silica dust, often over relatively long periods of time. These are conditions which are typically encountered occupationally. The key factors which determine whether or not a worker contracts or is identified with a dust related disease are as follows: i. The characteristics and properties of the dust. ii. The concentrations of the respirable dust to which the worker is exposed, iii Duration of exposure to the airborne dust. iv. Partem of exposure. MOB-HamsMaster 00255 v. Period since first exposure to time that the worker is examined for health effects. vi. Personal habits of the worker which might directly or indirectly: a. influence the risk of occurrence of a dust related disease(s) or health effect(s) or influence the course of the disease (eg: smoking). b. produce a disease indistinguishable from that produced by the dust. vii. Individual personal characteristics or pre-disposing conditions which might directly or indirectly influence the occurrence or course of a disease in that worker. There are several essential considerations in determining the link between exposure and disease in both groups and in individuals. First, the presence ofthe disease or health effect must be clearly defined and demonstrated. Second, it must make mechanistic sense for the disease to be associated with the agents or dusts to which the individual or group are exposed. Third, the nature and level ofthe dust exposure must be appropriate to explaining the nature of the disease or health effect and frequency with which it occurs. Fourth, other agents or factors known to be associated with, give rise to, or influence the occurrence or course of the disease must be evaluated. In the following sections, these are examined in relation to the diseases associated with the various asbestos minerals. UPDATE: The types of occupationally related diseases and the factors responsible for them remain as described above. In relation to asbestos, the same diseases have been emphasized (mesothelioma, lung cancer and asbestosis). However, over the past 10 years, there has been an increasing tendency to classify exposures as occupational, paraoccupational, domestic, building and environmental. This has been stimulated by increased concern about the risks for occupants and workers in buildings (Harvard 1988, HEI-AR 1991; Browne 1994); the finding that mesotheliomas were occurring more frequently in workers outside of the conventional production and manufacturing sectors (Peto et al 1999; Hodgson et al 1997; Hutchings et al 1996; Albin et al 1999; Peto et al 1995) and continued reports of spousal or familial mesotheliomas. As it has been claimed that an increasing number of persons working periodically with asbestos or in the vicinity of asbestos workers are at an increased risk of asbestos-related diseases, this new nomenclature has been introduced. General definitions seem to be as follows: Occupational exposure refers to exposure which occurs while working directly with asbestos. MOB-HarrisMaster 00256 12 Para-occupational exposure refers to the exposure ofworkers through the work of others. It normally results from working in the vicinity of workers applying or removing insulation products. Domestic exposure (and sometimes para-occupational exposure) has been used to refer to exposure in the home as a result of workers bringing work clothes home after working in asbestos producing, manufacturing, or using occupations. Such exposures can potentially be important for household members, especially spouses and children. While measurements of exposure are few, the fact that domestic exposures can be relatively high has been confirmed by fibre lung burden measurements (Gibbs et al 1990) and by measurements made in the homes of workers (Nicholson 1980). Neighbourhood exposure refers to exposures resulting from living in the vicinity of a factory or other source of airborne asbestos. Building exposure refers to exposure resulting from living or working in a building containing asbestos. In a properly maintained building containing chrysotile asbestos the average building resident is not at any practically detectable increased risk of mesothelioma, lung cancer or asbestosis. 0=8/ Environmental exposure refers to exposure resulting from the natural background of fibres in the environment. Handyman exposure refers to the occasional exposure of maintenance personnel or handymen ' to asbestos by working directly with asbestos products. While the above terms are widely used, such categorisation of exposures is not, in my view, appropriate as low exposures can occur in occupational settings and high exposures can occur under para-occupational circumstances. There have been no major changes in the science underlying the importance of the factors (i vii) noted in the original June 1992 report. However, the increasing emphasis on genetics in the mid-1990's is leading to an increased understanding of the genetic parameters affected by chemical exposures and of the genetic factors that might put persons at greater risk of certain diseases. The possibility that different genetic alterations occur in the same tumour as the result of different environmental insults has been suggested. Such factors may become important parameters to consider in the future, but are not yet at a point where they can be addressed from an epidemiological standpoint. MOB-HarrisMaster 00257 13 7.0 DISEASES ASSOCIATED WITH ASBESTOS EXPOSURE The diseases or health effects which are frequently studied in relation to asbestos exposure are.....asbestosis4, lung cancer and mesothelioma. Other diseases such as gastrointestinal cancer, cancer of the larynx, cancer of the ovary as well as cancers of other sites remain controversial. UPDATE: There has been no change in the main diseases (ie. lung cancer, mesothelioma and asbestosis) studied for their relationship to exposure to the various asbestos minerals. IPCS (1998) in addressing other diseases stated: "There has been considerable unresolved controversy regarding the possible carcinogenic effect of asbestos on the larynx, kidney and gastrointestinal tract. Moreover there is little evidence that permits an assessment of chrysotile in particular as a risk factor for these cancers. In four of the cohorts exposed almost exclusively to chrysotile, data were presented on SMRs for laryngeal cancer (Hughes et al 1987; Piolatto et al 1990; McDonald et al 1993, Dement et al 1994). Non-significant excesses were observed in some ofthe studies. It is not possible to draw conclusions about the association with laryngal cancer because confounding may play an important role in creating associations. Where examined, laryngeal cancer was strongly associated with cigarette smoking (McDonald et al 1993) and alcohol consumption (Piolatto et al 1990)." IPCS (1998) also pointed out that because kidney cancer is rare, cohort studies have limited statistical power to detect even moderate excesses. Referring to McDonald et al (1993) they noted that there was no overall excess of kidney cancer in Quebec miners and millers although some increases occurred in subgroups stratified by mine and exposure but the number of cases "precludes meaningfully interpretation". In an asbestos cement production plant (chrysotile) Hughes et al (1987) reported an SMR of225 for kidney cancer based on only 4 cases but the SMR from lung cancer was only 117. IPCS (1998) also mentioned that there were no data on kidney cancer risks reported in other chrysotile worker chohorts. In predominantly chrysotile exposed cohorts no consistent evidence of excess mortality from stomach or colorectal cancer and no systematic relation between gastric cancer and exposure in the Quebec chrysotile mining cohort (McDonald et al 1993) was noted. See also Liddell et al (1997). Asbestoca the leaning of (he tung oaue naoinnj from exposure 10 normally hi(fc cocceauioone of Mbcaot minersb over miny yean. MOB-HarrisMaster 00258 14 7.1 MESOTHELIOMA 7.1.1 Occurrence The tumour occurs on the pleura and peritoneum, membranes that surround the lung and line the thoracic and abdominal cavities. The pathological and clinical characteristics of mesotheliomas are now described in standard texts (Hunter 1987; Parkes 1975). UPDATE: Mesothelioma descriptions now appear in almost all standard medical texts (eg: Parkes 1994; Watson in Peckham et al 1995; Churg and Green 1998; Roggli et al (1994). 7.1.2 Diagnosis Kannerstein etaj (1979) drew attention to the difficulties of diagnosing this tumour and the value of "mesothelioma panels" to review cases. They noted that due to the "pathologic overlap with other neoplasms... there is scarcely another variety of tumour which is so ill-defined and which admits of so much doubt as to its true nature". Microscopically the tumour shows considerable variation and the appearance varies from tumour to tumour making accurate diagnosis difficult. Parkes (1975) notes that the diagnosis has either been by biopsy alone or at autopsy. He states that diagnosis made by biopsy alone is not reliable. The difficulties noted above are exemplified in the study by McDonald et al (1973). Six pathologists reviewed 119 of 165 cases reported as primary malignant mesothelial tumours between 1960 and 1968 in a Canadian national survey. Based on histologic observations only, the panel was in favour of the diagnosis in 50% of cases, uncertain in 14% and against in 36%. This illustrates the tendency at that time to "over diagnose mesothelioma". In the United Kingdom, Greenberg & Davies (1974) reported that of 413 notifications of mesotheliomas: 76 were "definitely not" mesotheliomas when reviewed; 35 of these 76 had been identified as mesothelioma on the death certificate. In a quite recent study of 78 autopsied cases in Canada, pathological review resulted in 33 (42%) being considered as definite mesotheliomas, 25 (32%) probable, 7 (9%) possible, 4 (5%) doubtful but 9 could not be classified because of inadequate tissue samples (McDonald et al 1989). While it is likely that the tendency is towards being more rigorous in diagnosis, diagnosis is difficult and must be based on stringent standards of post mortem examination (Parkes 1975). Review by panels of pathologists is now the accepted method of obtaining agreement on such cases. The early cases identified by Wagner etal (1960) were referred as having tuberculosis. More recently the possibility was raised that some of the women with "cancer ofthe ovary" who worked with blue MOB-HarrisMaster 00259 15 asbestos (crocidolite) while making military gas masks may have had mesotheliomas (Acheson et al 1982). The existence of benign mesothelioma must also be considered. For example, Daya & McCaughey (1990) reported 22 cases (18 women) ofwell differentiated papillary mesothelioma of the peritoneum (WDPMP) which they described, for practical purposes, as benign. The cause of these tumours is not known7. This further illustrates diagnostic complexity. UPDATE: The 1992 report drew attention to the considerable difficulties in diagnosis. This still appears to be a problem. As Wang (1996) stated: "After a century of debate and more than 3 decades of intense epidemiological, clinical and morphological studies, a specific and definitive diagnostic method of mesothelioma still eludes detection". Referring to McCaughey et al (1991) who reported on North American mesothelioma diagnosis, Wang notes: "Discrepancy in scoring among members is common, especially when only haematoxylin-eosin stained slides are available and the clinical history and gross findings inadequate. Similar observer variations appear to persist even when the results of electron (EM) microscopy and immimo-histochemistry are available for analysis". This is extremely important as diagnoses are sometimes made by pathologists who see very few cases, and diagnosis are sometimes based only on biopsies. A major segment ofthe recent literature on mesothelioma is devoted to differentiating between lung cancer and mesothelioma and proposed methods of improving diagnosis (eg: Dejmek 1996; Nash et al 1999; Attanoos & Gibbs 1997; Churg & Green 1998; Colt 1997). An example ofa diagnostic/classification problem was described in Denmark where an unexpectedly large number of peritoneal mesotheliomas in women was reported to the Danish Cancer Registry during the year 1960 - 1985. A review found that only 37% were verified mesotheliomas and 33% possible mesotheliomas. Misclassification of other cancers was the reason for the peritoneal mesothelioma excess (Nielsen etal 1994). Bias in reporting is also very important. For example a bias in reporting was identified in Sweden where asbestos exposure was found in 93% of cases reported to the Swedish Register ofReported Occupational Diseases while only 47% ofthe unreported cases had an asbestos exposure (Andersson & Toren 1995). While other registries report that mesothelioma reporting is good or complete, not ail have undergone such a review. As noted in the 1992 report, the presence of a disease or health effect must be clearly defined and demonstrated before any search for etiology is undertaken. The potential for a major problem with diagnosis exists when the fact or claim of asbestos exposure, regardless of the type or level of exposure is used as a criterion for diagnosis. Perhaps equally important is the fact that other potential ?Ih their report they noted that although diffloc mifgnxm mcsotbe&oma a a highly maKg&aat cancer, there an other mnotheSal neoplasms that are less aggressive or are benign. They letted mulusywc meaothc&orea, adenomatoid tumour and Tustogcncocafly contentious* localized fibrous mesothelioma as ntl1 as WDPMP. MOB-HarrisMaster 00260 16 etiologies are ignored. In Scandinavia, mesotheliomas have been reported in persons immigrating from the area of Turkey where mesothelioma rates are high (Ozesmi et al 1990). 7.1.3 Survival In view of the high fatality rate with this tumour and short survival times, cases with very long survival times should be examined critically to ensure that the diagnosis is correct. UPDATE: In 1992, Ribak & Selikoff (1992) reported on the survival of 457 consecutive cases of pleural and peritoneal mesothelioma occurring among 17,800 asbestos insulation workers followed January 1, 1967 to January 1, 1987. The mean survival time from initial presentation of pleural mesothelioma to death was 11.4 months compared to 7.4 months for those with peritoneal mesothelioma. This difference in survival was statistically significant. For pleural mesotheliomas only 1 case (0.7%) survived 36 months from initial symptoms to death. For peritoneal mesotheliomas only 1 case (0.4%) survived more than 36 months. Various treatment modalities were compared. They concluded that "no effective therapy is available yet." While many new treatment regimes have been introduced and tested in the 1990's, this conclusion appears sadly to be as valid today as in 1992. 7.1.4 Etiological Factors Etiological factors refer to those factors which are associated with a disease and which may explain its occurrence. It is now well accepted that several factors are important in the occurrence of primary malignant mesothelioma. These fit well with the factors identified in Section 6.0 as essential in assessing the risk of occupationally related diseases':* * agent * level of exposure * duration of exposure * period since first exposure to diagnosis * other factors UPDATE: No changes. MOB-HarrisMaster 00261 17 7.1.4.1 Agent Non-pulmonary pleural tumours have been reported in the literature for more than 100 years. However it would appear that the first formal link between primary malignant mesothelial tumours and an environmental factor was in 1959 when Dr. Christopher Wagner first diagnosed primary malignant mesotheliomas in persons living and/or working in the blue asbestos mines of South Africa (Wagner et al 1960). Since that time there has been considerable research carried out and some findings are now well established....... * The majority of mesotheliomas in workers to date, have been shown to be associated with exposure to asbestos particularly to the amphibole fibres - blue asbestos, amosite and tremolite. This high proportion of mesotheliomas linked to asbestos exposure may, in part, be the result of biasses in reporting because major efforts have been directed at confirming asbestos associations, not at identifying other etiological factors. In spite of this... * In about 25-30% ofmesothelioma cases, a clear history of asbestos exposure has not been established. While this may reflect differences in the methods used to establish exposure, those reporting this proportion appear to be reasonably confident that not all mesotheliomas are asbestos related. * Mesothelioma risks have been shown to be increased in persons exposed to a mineral other than asbestos, specifically a fibrous zeolite known as erionite (Baris et al 1987). Mesotheliomas have also been produced in experimental animals by fibres other than asbestos and zeolites.* * Fibre length, diameter, durability and biopersistence play important roles in a fibre's potential to induce mesothelioma, pulmonary fibrosis and pulmonary tumours in experimental systems. * The tumour occurs in both sexes. * The tumour risk appears to be unrelated to smoking * Mesothelioma has a long "latency" with periods between first exposure and tumour detection of generally 20-40 years or more. UPDATE: In spite of another decade of research and an increased emphasis on tissue analyses to confirm exposure, there still remains a substantial proportion of mesothelioma cases in which asbestos exposure has not been established. A number of other causes for mesothelioma appear to be increasingly plausible and the possibility that other agents might play a role in asbestos related mesotheliomas is now receiving serious consideration. MOB-HarrisMaster 00262 Spirtas et al (1994) reported that the proportion of pleural mesotheliomas in men attributable to asbestos exposure was 88%. The attributable risk for peritoneal mesothelioma in men was 58%. For both sites combbed the attributable risk b women was 23%. Some caution is needed b bterpretbg the results ofvarious studies as the findbgs will vary with the likelihood of exposure to asbestos by the study population. Yates et al (1996) reported that among 272 mesotheliomas, 87% had documented asbestos exposure, while in the remabder, no asbestos exposure or asbestos bodies were found. Thus in South East England, most cases were asbestos related. There were no clinical differences between those b which asbestos exposure was established and those where it was not. It now appears that between 10 and 25% ofmesotheliomas occur where an asbestos etiology cannot be confirmed, although even b 1989, there were 33% of mesotheliomas at one urban centre where there was no historic evidence of asbestos exposure (Shepherd et al 1989). The occurrence of mesotheliomas in childhood and the existence of the stable background rate of mesothelioma b women in most countries suggest that non-asbestos etiologies exist. This is consistent with the multiple etiologies of cancer b general. Clearly the key question of whether or not there are non-asbestos related mesotheliomas or mesotheliomas at low levels of exposure must relate to the agents, exposure and dose. A recent review by HHlerdal (1999) illustrates one opinion on this complex question of background rates and low level exposure. Another view is expressed by McDonald & McDonald (1996). 7.1.4.2Asbestos Fibre Type The differences b the risk ofmesothelioma for workers exposed to different asbestos fibre types are quite marked. These risks will be described for the various fibre types and then compared. a. Blue Asbestos TABLE 1 shows the mesothelioma experience of persons who were occupationally exposed to blue asbestos. It is clear from these results that mesothelioma is strongly associated with workbg with blue asbestos and that the risks for workers b occupations where this material has been used can be very high. b. Amosite Amosite has been implicated b mesothelioma as an important cause of death b a US amosite factory (Seidman et al 1979) and b a British amosite factory (Acheson et al 1984). See TABLE 2. c. Mixed fibre exposures The pattern ofmesothelioma mortality b workers exposed to mixtures of amphiboles and chrysotile are very similar to those among amphibole only exposed workers. See TABLE 3. MOB-HarrisMaster 00263 - ' ) w eZ&v ^ 19 TABLE 1. MESOTHELIOMA IN VARIOUS COHORTS - AMPHIBOLE ONLY -BLUE ASBESTOS - a. Gas mask filter manufacture - Canada McDonald & McDonald (1978) Total Cohort 199 Dead 56 Mesothelioma 9 (16.1%)* b. Gas mask filter manufacture - UK Acheson et al (1982) Total Cohort 757 Dead 219 Mesothelioma 5(2.3%) c. Mining Blue Asbestos - Australia Hobbs et al (19801 Total Cohort 6200 Dead 526 Mesothelioma 17(3.2%) TABLE 2. MESOTHELIOMA IN VARIOUS COHORTS - AMPHIBOLE ONLY - AMOSITE ASBESTOS - a. Amosite factory - US Seidmanet al ('19791 Total Cohort 820 . Dead 528 Mesothelioma 14 (2.7%) b. Amosite factory - UK Acheson et al (1984) Total Cohort 5969 Dead 422 Mesothelioma 5(1.2%) As used in tables 15, parentheses represent percentage ofdeaths due to mesotheEcjoa - MOB-HarrisMaster 00264 TABLE 3. MESOTHELIOMA IN VARIOUS COHORTS - MIXED FIBRE - AMPHIBOLE & CHRYSOTELE - a. Insulation workers - NY - New Jersey Selikoffet al (1979a) Total Cohort 632 Dead 478 Mesothelioma 38 (7.9%) :o b. Insulation workers - US & Canada Selikoffet al (1979a) Total Cohort 17800 Dead 2271 Mesothelioma 175 (7.7%) c. Dockyards - UK Rossiter & Coles (1980) Total Cohort 6292 Dead 1043 Mesothelioma 31 (3.0%) d.Insulators in shipyards - USA Selikoff et_al (1979b) Total Cohort 440 Dead 79 Mesothelioma 8(10.1%) e. Asbestos factory workers in London - UK Newhouse & Berry (1979) Total Cohort M 4600 F 992 Dead 775 225 Mesothelioma 46( 5.9%) 21( 9.3%) d. Tremolite Fibrous tremolite has been implicated in the occurrence of mesothelioma in vermiculite miners where tremolite is a contaminant of the vermiculite (McDonald et al'(1986a) and Amandus & Wheeler (1987). See TABLE 4. Mesotheliomas have also been reported in talc miners where the talc contained asbestiform tremolite. MOB-HarrisMaster 00265 TABLE 4. MESOTHELIOMA IN VARIOUS COHORTS - TREMOLTTE ONLY - a. Vermicuiite mining - USA McDonald et al (1986a) Total Cohort 406. Dead 165 Mesothelioma 4 (2.4%)9 b. Vermicuiite mining - USA Amandus & Wheeler (1987) Total Cohort 575 Dead 161 Mesothelioma e. Chrysotile Mesothelioma has been relatively rarely described in pure chrysotile exposed workers. See TABLE 5. As noted earlier, the finding oftremolite fibres in high concentrations in the lungs of some Quebec chrysotile miners and millers (Rowlands et al 1982) has led to the hypothesis that the tremolite contamination of chrysotile may explain the increased mesothelioma risk in that mining and milling industry. TABLE 5. MESOTHELIOMA IN VARIOUS COHORTS - CHRYSOTILE ONLY - a. Chrysotile miners & millers McDonald et al (1980) Total Cohort 11379 Dead 4547 Mesothelioma 11 iO.24%)10 MOB-HarrisMaster 00266 TABLE 5 (CONT.) MESOTHELIOMA IN VARIOUS COHORTS - CHRYSOTTLE ONLY - b. Chrysotile miners & millers Rubino et al (1979) Total Cohort 900 Dead 332 Mesothelioma 1 (0.3%)" c. Chrysotile miners & millers Nicholson et al (1979) Total Cohort12 544 Dead 178 Mesothelioma 1 (0.56%) d. Chrysotile products factory Weiss (1977) Total Cohort 264 Dead 66 Mesothelioma 0 (-) e. Asbestos cement plant Thomas et al (1982) Total Cohort 1970 Dead 351 Mesothelioma 013 f. Chrysotile textile plant McDonald et al (1983a) Total Cohort 25-13 Dead 863 Mesothelioma 1 (0.1%)W * * \ot supported b' wstologicai examination. ''Conors comprised men with at least 20 yean seniority. J There were 2 mesothelioma exposed to blue asbestos (pre 1936) but 0 in those exposed to chrysotile only. 4 There was one pemoneai mcsothehoim with no autopsy. MOB-HarrisMaster 00267 TABLE 5 (CONT.) MESOTHELIOMA IN VARIOUS COHORTS - CHRYSOTILE ONLY - g. Friction materials manufacture - USA McDonald et al (1984) Total Cohort 3641 Dead 1267 Mesothelioma 0(-) 23 h. Friction materials manufacture - UK Newhouse & Sullivan (1989) Total Cohort 13450 Dead 2577 Mesothelioma 215 f. Comparisons of risks The occurrence of 9 mesotheliomas among 56 deaths of crocidolite gas mask workers (16.1%) and 11 among 4,247 deaths of chrysotile miners (0.26%) illustrate clear differences in the mesothelioma risk posed by these two fibres (McDonald & McDonald 1978). See TABLE 6a. This difference and the strong association between blue asbestos and mesothelioma is paralleled by observations in several other studies. TABLE 6a. MESOTHELIOMA IN CHRYSOTILE MINERS & MILLERS AND BLUE ASBESTOS GAS MASK WORKERS McDonald & McDonald (1978) Blue Asbestos Gas Mask Chrysotile Miners Filter Workers & Millers Total Cohort 199 (55% male) Dead 56 Mesothelioma 9(16.1%) 11,379(96% male) 4,247(since 1935) 11(0.26%)16 MOB-HarrisMaster 00268 In the study of workers manufacturing civilian gas masks using chrysotile asbestos there were no mesothelioma that could be linked to the chrysotile exposures. At the plant manufacturing military gas masks using blue asbestos 2.3% ofthe deaths were due to this cancer (Acheson et al 1982). See TABLE 6b. TABLE 6b. MESOTHELIOMA IN MILITARY (BLUE) & CIVILIAN (CHRYSOTILE) GAS MASK WORKERS Acheson et al (1982) Blue Asbestos Gas Mask Chrysotile Gas Mask Filter Workers Filter Workers Total Cohort Dead Mesothelioma 757 219 5(2.3%) 570 177 l17 * The mesothelioma experience of insulation workers11 has been considerably worse than that of chrysotile miners and millers, chrysotile textile workers, friction manufacturing workers and other chrysotile-only exposed populations which makes it likely that their mesotheliomas are not linked to their chrysotile exposure. Amosite has been implicated in mesothelioma as an important cause of death in an amosite factory in the US (Seidman et al 1979), with 14 of 528 amosite worker deaths (2.7%). It seems most probable that the mesothelioma experience of amosite and insulation workers is explained by their exposure to amphibole fibres. This association between amphibole fibre exposure and mesothelioma has been further supported by several case-control studies in which the lung fibre contents of mesothelioma cases and controls have been determined. In a recent study in Canada, lung tissues from 78 mesothelioma cases and matched "referents"19 *were analyzed (McDonald et al 1989). The different fibre types were classified by length (greater than or equal to 8um and less than 8 um). More than one type of fibre and both long and short fibres were found in the lung tissue from some individuals. Despite the fact that concentrations of short fibres were highly correlated with the concentrations of long ones "analyses in which both short and long fibre concentrations were entered simultaneously into risk models showed likelihoods barely increased from those for long fibres alone indicating that short fibres were not significantly associated with excess risk, after accounting for the effect of long fibres". 17 Tha cmc was abo considered to hive bees exposed to blue asbesux et soother factory. These wu also an exeat number ofpersons with cancer ofthe ovary at the blue fibre plwL These were considered by the author* to pocnbly be additional mesotheliomas. IS Insulation worker*, in general have usually worked with chiysotilt and amodte and certainly in many cotrtfirics with blue asbestos. 19 Person* fiom dr sane autopsy regny who dd not die ofnufignmey or respiniovy disease bur who were ofthe same age. sec, date of death, and for whom the same type of tmue ( paraffin block, or wet) was available. MOB-HarrisMaster 00269 25 When the possible confounding effect ofmore than one fibre type in the lung was taken into account through the use of multivariate methods, risk increments were derived. See TABLE 7.21 TABLE 7. MESOTHELIOMA RISK INCREMENTS PER FIBRE PER MICROGRAM /MCDONALD ETAL 1989) Fibre Lone Fibres (>8um) Risk Increment Risk(%) (95% CD20 Attributable' Amphiboles(afi) 32.1 (8, 120) 68 Amosite 93.7 (20, 500) 28 Crocidolite 24.9 (1.4, 120) 10 Tremolite 69.7 ( 9,300) 30 Talc/Anthophyllite 1.8 ( <0, 50) 2 Chrysotile <0 ( <0, 8) - Short Fibres /<8um) Amphiboles (all) 0.7 (0.1,3) 55 Amosite 13.5 (0, 980) 20 Crocidolite . 1.6 (0,110) 13 Tremolite 0.6 (0,3) 18 Talc/Anthophyllite 0.2 (0, 17) 6 Chrysotile 0.02 (<0, 0.2) 6 20 9SH CL " Confidence Irttcrvili. The lower Emit tt shown on the Itft end the upper limit on the right. This means that the true value of the risk increment lies within these confidence intervals unless s on in twenty mischance has oef'tfTcd. 21 Attributable risk ts the proportion ofcases occurring in the total population which can be explained by the risk factor. MOB-HarrisMaster 00270 26 The "increment in relative risk" is the slope ofthe line expressing the relationship between the relative risk ofmesothelioma and the number of fibres per microgram of dry lung tissue. It should be noted that the confidence intervals for the 4 amphibole fibres are wide and differences between them were no more than could be accounted for by chance (p >0.10). The much lower risk for chrysotile could not be accounted for by chance (p <0.001). The attributable risk suggests that perhaps 30% of the mesotheliomas were attributable to tremolite exposure. AH the mesothelioma from the Quebec mines and mills (9 cases) were among these. A similar study was conducted in Australia, but controls were taken from only one hospital and not matched (Rogers et al 1991). The greatest risk of mesothelioma in Australia was associated with crocidolite fibres >10 urn in length but that study claimed a significant contribution by short chrysotile fibres. Recognising that hospitals are often catchment areas for the industries in their district, the use of "control" tissues from one single centre in a national study may be a serious design flaw. A second important factor is that the large numbers of short chrysotile fibres may reflect recent exposures to this fibre type. Chrysotile is also well recognised to be removed from the lung over time (Davis 1991) and this may have prompted Rogers et al to note the difficulty of assessing the risks of chrysotile alone due to the almost universal exposure to both chrysotile and amphiboles. Although the levels of exposure ofthe various occupational groups described in this section have not been as well defined as one might like, the experience ofworkers using different fibre types have been so different that it is clearly inappropriate to extrapolate from the mesothelioma experience of persons working with one fibre type to another. Thus, in this report, only the experience of persons exposed to the asbestos fibre types likely to be found in Dum Dum products will be used in assessing the risk associated with these products. UPDATE: By 1992, differences in the risk of mesothelioma for workers exposed to different asbestos fibre types were quite marked and there have been no studies since to contradict this conclusion. Indeed, the difference between the mesothelioma producing potential of commercial chrysotile exposure and amphibole fibre exposure was clearly defined at a meeting of experts in 1994 (See Gibbs et al 1994). However, in the 1990s there were several reviews claiming that the risk of mesothelioma was the same for chrysotile and the amphiboles, that chrysotile under all circumstances caused mesothelioma or that the widespread use of chrysotile made it responsible for most of the mesotheliomas occuring in the world. In this section, this debate will be critiqued and new information concerning the mesothelioma risks associated with the various asbestos fibre types which has been published over the past decade will be summarized. In almost all instances these claims include mesotheliomas where exposure has been to amphibole as well as chrysotile. The Amphibole Hypothesis. Since 1990 there have been several articles claiming that chrysotile is responsible for mesothelioma occurrences. One such paper is that by Stayner et al (1996). Cullen (1996) also wrote on this subject. Both received critical comment from Wagner (1997) who first linked mesothelioma to MOB-HarrisMaster 00271 27 crocidolite asbestos exposure in 1959. He stated very clearly that; "The vast majority of mesotheliomas are associated with exposure to crocidolite asbestos..... No mesotheliomas have been shown to have occurred in chrysotile exposed workers unless the exposure has been intense and for more than 20 years. In addition there must be tremolite contamination of the chrysotile". Langer and Nolan (1997), pointed out evidence which supported Wagnefs contention. Mossman and Gee (1997) pointed out that both the articles by Stayner et al and Cullen did not include recent data and noticed errors in Stayner et ai's claim that the carcinogenicity of crocidolite was based primarily on in-vitro studies. While Stayner et al (1996) accepted that there was a difference in the mesothelioma producing potential of amphibole and chrysotile fibres, their literature review on chrysotile was incomplete, selective, contained errors and failed to reflect the observations of the original researchers. A second paper was published by Smith et al (1996). This article included a number of technically incorrect statements, errors and omissions. By only including studies in which high mesothelioma risks were reported, they were able to exclude from consideration those industries where risks were not reported because no cases had occurred, namely the chrysotile using industries. In fact their "evidence" was based on industries involving mixed exposures to amphibole and chrysotile. In making broad generalisations, they ignored the feet that not all chrysotile is contaminated with fibrous tremolite. They ignored the feet that exposure level is important. They also ignored the fact that the likelihood of downstream users being exposed to fibrous tremolite in chrysotile is extremely low if not nil. The inference was made that because most of the world's asbestos is chrysotile, most of the world's mesotheliomas are chrysotile related. This does not automatically equate. Most, if not all asbestos-related mesothelioma cases have had amphibole or mixed fibre exposures. Liddell (1997) commenting on the paper by Smith et al summed it up: "Therefore, these 16 studies which, by the definition of a low mesothelioma PMR included every one of those cohorts exposed to chrysotile alone, were ignored. Further comment is surely unnecessary- although a great deal more would be Killy justified." A review by McDonald and McDonald (1996) provides a rather different and more rational interpretation of the world's literature on mesothelioma. Two other papers claiming that chrysotile is responsible for mesotheliomas were published by Nicholson and Landrigan (1994) and Nicholson and Rafin (1995). The articles depend on their assertion that amphibole exposures did not occur in the USA prior to about the mid 1930s. Evidence which I have gathered concerning the importation, mining and use of amphibole fibres in the USA prior to 1940 demonstrates that there was ample opportunity for workers to be exposed to amphiboles well prior to 1935. Those exposures included amosite, crocidolite and anthophyliite. The fallacy in the argument used by Nicholson and colleagues is perpetuated by Smith et al (1996), Stayner etal (1996) and others later - ie: that a little amphibole usage is not important. The work of Koyhama and Suzuki (1991) which shows commercial amphibole fibres in the lungs of all the US insulation workers studied by them, raises serious doubts about any claims of non-amphibole related mesotheliomas in US insulation workers. MOB-HarrisMaster 00272 28 Amosne was also found in the lungs of all insulation workers in a study by Langer & Nolan (1998). Crocidolite was present in the lungs of 13% of insulation workers and 38.3% of shipyard workers. Crocidolite and amosite are not minerals commonly found in high concentration in the lungs of the general population. Since the 1992 report, some studies ofthe mortality experience of asbestos exposed workers have been updated and new studies have been reported. The following section incorporates this new and updated information a. Blue Asbestos TABLE U1 shows the mesothelioma experience of persons who were occupationally exposed to blue asbestos. It is even clearer now, that mesothelioma is strongly associated with exposure to blue asbestos. TABLE Ul. MESOTHELIOMA IN VARIOUS COHORTS - AMPHIBOLE ONLY - BLUE ASBESTOS - ua. Mining Blue Asbestos - Australia Berry G (1991) Total Cohort 6258 Dead 983 Mesothelioma 84 (8.5%) ub. Mining Blue Asbestos - Australia de Klerk et al (T9931 Total Cohort 1106 Dead 193 Mesothelioma 12(6.2%) * Bat evidence * 17 pletnL uc. Mining Blue Asbestos - South Africa Sluis-Cremer et al (1992) Total Cohort 3430 Dead 423 Mesothelioma 20*(4.7%) MOB-HarrisMaster 00273 29 TABLE U1 (CONT). MESOTHELIOMA IN VARIOUS COHORTS - AMPH3BOLE ONLY - BLUE ASBESTOS - ud. Blue Asbestos Cigarette filter Production Talcott et et al (1989) Total Cohort 35 Dead 28 Mesothelioma 5*(17.8%) * t pleural, 4 peritoneal. Another Australian study was reported by Musk et al (1992) with 6505 men in the cohort and 32 mesotheliomas but the number of deaths was not dear. However, information on this Wittenoon cohort has been adequately described by the other Australian authors. b. Amosite Amosite has been directly implicated in mesothelioma as an important cause of mesothelioma in the US amosite factory reported by Seidman etal 1979, in a British amosite factory (Acheson et al 1984), and now by further studies in Texas (Levin etal 1998) and in South Africa (Sluis-Cremer et al 1992). See TABLE U2. TABLE U2. MESOTHELIOMA IN VARIOUS COHORTS - AMPHIBOLE ONLY - AMOSITE ASBESTOS - ua. Mining Amosite Asbestos - South Africa Sluis-Cremer et al (1992) Total Cohort 3212 Dead 648 Mesothelioma 4 (0.6%) ub. Amosite factory - Tyler Texas - US Levin et al (1998) Total Cohort 1130 Dead 315 Mesothelioma 6** (1.9%) 4 pleural and 2 pentoneaL 17% of peraons with more than 10 yon from first exposure. In an experiment with Baboons, 5 out of 12 developed malignant diffuse mesothelioma, three peritoneal, and two pleural after exposure to amosite at 1100-1200 free for up to 898 days (Webster etal 1993). MOB-HarrisMaster 00274 c. Mixed asbestos fibre exposures TABLE U3. MESOTHELIOMA IN VARIOUS COHORTS - MIXED FIBRE - AMPHIBOLE & CHRYSOTILE - ua.Insulators in shipyards - Sweden Jarvholm& Sanden (1998) Total Cohort 248 Dead 86 Mesothelioma 7 (8.1%) @ AD pcrixoacil ub. Insulation workers - US & Canada Selikoff & Seidman (1991) Total Cohort 17800 Dead 4951 Mesothelioma 458 (9.3%)# 30 estzmate. Pleural mcsotbctiomas 173. Peritoneal msoiheKoniM 215. d. Tremolite While there have been many studies of fibre burden, there do not appear to have been any new occupational cohort studies. e. Chrysotile There have been claims ofmesothelioma resulting from chrysotile only exposures in the former East Germany (Sturm et al 1994). I met with these researchers and discussed these cases. The cases were examined at one central laboratory but there were no tissue analyses for fibre type. The denominator for these cases is not well known. There was some blue asbestos used in some parts of Germany in insulation materials although most of their asbestos came from Russia. Without tissue analyses to verify the exposures ofthe "chrysotile only" exposed persons, this study cannot be interpreted. I was informed that because of the amalgamation of the two Germany's, no further work would be done on this question. Only 1 probable mesothelioma was reported from Zimbabwe chrysotile mining operations as of 1991. It appears that there was no autopsy (Cullen & Baloyi 1991). Elmes (1994) reported that:"The chrysotile mines in the Transvaal, Swaziland and Zimbabwe appear to have exposed large numbers of workers to high levels of of pure chrysotile ... and yet there have been very few cases of lung cancer let alone mesotheliomas among the miners and mine mill workers (Webster, personal communication 1993; Baloyi, this workshop)." MOB-HarrisMaster 00275 TABLE U4. MESOTHELIOMA IN VARIOUS COHORTS - CHRYSOTILE ONLY - ua. Chrysotile miners & millers McDonald et al (1997) Total Cohort 9780 T 5041 A 4031 F 708 Dead 8009 4125 3331 553 Mesothelioma 38 (0.47%) 25 (0.61%) 8 (0.2%) 5 (0.9%) F is j hoary when ereddoKln & xnotite were mod CM of aboot 11,000 men bora 1*91 - 1920 ia the anginal cohort, 9710 turvived into 1936. ub. Chrysotile textile plant Dement et al (1994) Total Cohort 3022 Dead 1259 Mesothelioma 2(0.16%) @ Sebuttea et al (1919) and Cue and Dufrcmc (1999) showed that some workers h this eohott had axnphiboie fibers m their lungs uc. Mining chrysotile -Italy Piolatto (1990) Total Cohort 1058 Dead 427 Mesothelioma 2 (0.46%) @ At the Medichon Symposium m Vienna (1999) Dr GmbgySurittcriand reported that amptnbolc fibres had been milled at this reme. f. Anthophyllite TABLE U5. MESOTHELIOMA IN ANTHOPHYLLITE COHORTS . - ANTHOPHYLLITE ONLY - Anthophyllite miners -Finland Kaijalainen et al (1994) *3 pleural and 1 peritoneal Total Cohort 999 Dead 503 Mesothelioma 4* (0.8%) MOB-HarfisMaster 00276 TABLE U5. (CONT.) MESOTHELIOMA IN ANTHOPHYLLITE COHORTS - ANTHOPHYLLITE ONLY - Anthophyllite miners -Finland Meurman et al (1994) 32 Total Cohort Dead 735 137 Mesothelioma 4* (2.9%) * 3 pleural and 1 peritoneal f. Comparisons of risks The evidence from all the new and updated studies, listed above, is consistent with the risk of mesothelioma being associated with amphibole exposures. When "chrysotile only" workers have been reported, they have been exposed to very high concentrations and tremolite has been present (eg: Quebec miners and millers). There have been cases of mesothelioma in which only chrysotile has been found in tissues, but usually these laboratories have not studied referent cases and issues concerning the representativity of the tissue analyzed and likelihood that the fibres reflect recent exposures have not been adequately addressed. There has continued to be a consistent association between amphibole asbestos exposure and mesothelioma based on tissue burden studies. 7.1.4.3 Other Fibres a. Zeolites: Evidence that fibres other than asbestos may be related to mesothelioma in humans is found in Turkey, where, in several small villages, the rates of mesothelioma are vety high. Research concentrated in this area has shown that the most likely etiological factor is exposure to the fibrous zeolite, erionite, which occurs in the rock of that area (Baris et al 1987). This zeolite was shown to produce high rates of mesotheliomas in experimental animals (Wagner et al 1985). b. Man-Made Mineral Fibres: Certain of these fibres have the characteristics, size and durability that are widely accepted as making them candidates for the production of mesothelioma and experiments in animals have been reviewed by Hesterberg 1991a. Indeed, it is possible to produce mesothelioma in experimental animals by inoculation with a wide variety of naturally occurring and man-made mineral fibres (Monchaux et al 1985; Stanton 1973; Stanton & Layard 1978; Pott et al 1980; Pott et al 1987). Recent animal experiments in which animals inhaled ceramic fibres by a nose only route, yielded a high percentage of mesotheliomas (Hesterberg 1991b). To date, no excess of mesothelioma has been reported in any occupational groups producing man-made mineral fibres. MOB-HarrisMaster 00277 33 c. Biogenic Fibres: The possibility that organically produced fibres might be related to mesothelioma was raised by observations ofmesothelioma in sugar cane workers in India (Das et al 1976) where after burning the cane, there remain long silica fibres (Newman 1983). McDonald and McDonald (1991) note that there is support for this observation with the observed higher than expected rates of mesothelioma in the sugar producing areas ofLouisiana (Rothchild and Mulvey 1982) and in sugar refinery workers in Sweden, although there, asbestos exposure may also have been involved (Steinbeck et al 1983; Malker et al 1983). UPDATE: In spite of considerable research, it still appears that some 10-25% of mesotheliomas occur in which an asbestos exposure cannot be ascertained. As noted earlier, the reasons for these other mesotheliomas continues to be a subject of scientific debate. Evidence for spontaneous and non asbestos etiologies include the experience with erionite in Turkey (see below), spontaneous mesothelioma occurrence in children the occurrence of malignant pleural mesotheliomas before the industrial exploitation of asbestos at the end of the last century. There has also been an increasing number of other possible etiological factors identified including biogenic silica fibres in sugar cane, ionising radiation, and pleural scars following empyema or therapeutic pneumothorax (Hubbard 1997). a. Zeolites: In the previous report it was stated that there was evidence that fibres other than asbestos were associated with the occurrence ofmesothelioma in Turkey, where, in several small villages, the rates of mesothelioma were extremely high when the population was exposed to fibrous erionite. Since then, Baris et al (1996) have further reported on the experience in 3 villages in the Cappadocian region of Central Anatolia, Karain, Tuzkoy and Sarihidir. They found that between 1970 and 1994 there were 305 deaths in Karain, 177 (58%) were cancer related including 150 (49.2%) malignant pleural mesothelioma and seven (2.3%) peritoneal mesothelioma. Between 1980 and 1994, there were 519 deaths in the other two villages, with 257 cancer related with 120 malignant pleural mesotheliomas and 64 malignant peritoneal mesotheliomas. These rates ofmesothelioma exceed even those associated with crocidolite gas mask work. Survival in the Turkish cases has been 13.52 months for erionite-associated pleural mesothelioma compared to 21.6 months for asbestos associated mesothelioma (Selcuk et al 1992). However, Ribak and Selikoff (1992) reported shorter survival periods for asbestos related mesotheliomas (see 7.1.3). Evidence that cases originating in Turkey can turn up in other countries may be very important. As noted elsewhere in this report, among 150 immigrants to Stockholm from this region of Turkey, there were, by 1985, 7 cases of malignant mesothelioma in still, very young people (Ozesmi et al 1990). As noted in the 1992 report, erionite has been shown to produce very high rates of mesothelioma in experimental animals (Wagner etal 1985). The erionite fibres used in those experiments were MOB-HarrisMaster 00278 cy 34 from Rome Oregon. More recent data, while confirming the carcinogenic potential of erionite using fibres from Pine Valley, Nevada did not produce the same high rates of mesothelioma (Fraire et al 1997). Caution is needed in interpreting these findings as the physico-chemical properties, in particular, differences in size distributions have been found to be critical in other circumstances where differences in fibre carcinogenicity have been identified. b. Man-Made Mineral Fibres: In 1992 it was reported that certain ofthe man-made or synthetic fibres have the characteristics, size and durability that are widely accepted as making them candidates for the production of mesothelioma. The statement that no excess of mesothelioma has been reported in any occupational group producing synthetic mineral fibres appears to be still valid in 1999. However, it must be remembered that the cohorts have been production workers where exposures have been extremely low. Boffetta et al (1997) in a study of 22,002 production workers with 4521 deaths found 5 deaths from pleural mesothelioma. This is a PMR of 0.1%. They note that this may not represent an excess. Overall they did find a possibly increased lung cancer risk in rock and slag wool workers. There were 2 cases ofmesothelioma with more than 12 years of employment in rock and slag wool production [PMR = 0.16] and 1 in glass wool production [PMR = 0.06%] with 25 years of employment. The lung cancer risk for rock and slag wool workers increased with time since first exposure and with duration of exposure. They concluded: "These results are not sufficient to conclude that the increased lung cancer risk is the result of exposure to rock/slag wool; however, insofar as respirable fibres were an important component of the ambient pollution of the working environment, they may have contributed to the increased risk." A Case-control study is now underway to eliminate possible "confounders". In a US Study (Marsh et al 1996), only 1 mesothelioma was reported in cohort of 443 workers from one factory with 237 deaths, but none among a larger cohort of 3035 workers with 781 deaths. Cohorts of refractory ceramic fibre workers are small, have had low exposure and it is probabiy premature to see mesotheliomas in these cohorts even if there were a risk. It should be noted that there are many different types of synthetic vitreous and ceramic fibre. c. Biogenic Fibres: The possibility that biogenically produced fibres might be related to mesothelioma is still under investigation. Bhatt et al (1991) using fibres from the surfaces of the grains of P. canariensis failed to produce mesotheliomas experimentally. However, in rats injected intra-peritoneally with the carcinogen 15,16- dihydro-ll-methylcyclopent(a)phenantren-17-one (11-methyl 17-ketone), silica fibres implanted on the pleura induced mesotheliomas indicating that they can act as promoters. MOB-HarrisMaster 00279 35 To date, epidemiological investigations have not produced any firm evidence of a relationship between biogenic fibre exposure and mesothelioma. In Hawaii, there was no statistically significant excess risk of mesothelioma in sugarcane workers (OR = 1.3; 95%CI = 0.4-3.8). Studies have not identified any sugarcane workers who developed mesothelioma and worked in jobs where high exposure levels to biogenic silica fibres had been measured (Sinks et al 1994). In Florida, Brooks et al (1992) found a slight but non significant increased risk of lung cancer and one mesothelioma case and no controls who worked in the sugarcane industry. Maltoni and colleagues (1995) reported 12 cases of mesothelioma in sugar refinery workers but concluded that they were exposed to asbestos. 7.1.4.4 Ionizing Radiation The possibility that ionising radiation may be responsible for isolated cases of malignant mesothelioma has been noted in the literature (Stock et al 1979; Pelnar 1988). UPDATE: In the 1992 report, the possibility that ionizing radiation may be responsible for isolated cases of malignant mesothelioma was noted. Since then, there have been several reports addressing the question of radiation effects. These are summarized below: Therapeutic radiation There have been several case repons and case series reported since 1990 which suggest a link between therapeutic radiation and both localized benign and malignant mesothelioma. See TABLE U6. There have now been many pleural and peritoneal mesotheliomas reported after radiotherapy for Hodgkin's disease, testicular carcinoma, cervical cancer, Wilms tumour and breast carcinoma as well as after radiation treatment for nonmalignant disease. There have also been mesothelioma reported after Thorotrast exposure. The time interval between irradiation and mesothelioma has ranged from a few years to 35 years or more. Radiation has been shown to be carcinogenic to the pleura and peritoneum and animal studies suggest a possible interaction with asbestos in inducing mesothelioma. All the human evidence is from case reports except for the study by Neugut et al (1997) which did not find a statistically significant relationship between radiation treatment and mesothelioma, although the relative risk was 1.56. Carvazza (1996) noted that post-irradiation malignant mesothelioma show an approximately equal male:female ratio and average age at diagnosis of 45 which contrasts with the male predominance and older mean age seen in asbestos-related mesotheliomas. Thorotrast The results of various thorotrast studies are summarized in the TABLE U7. MOB-HarrisMaster 00280 TABLE U6. MESOTHELIOMA OCCURENCES IN PERSONS RECEIVING THERAPEUTIC RADIATION TREATMENT 36 REFERENCE Lcrman et al 1991 Pappoetal f 19971 Cavazza et al (1996) Hoffinan et al (1994) Weissman et al (1996) Neugat etaj (1997) Shannon et al (1995) CASE DESCRIPTION ASBESTOS EXPOSURE Malignant pleural mesothelioma in a woman 20 years after radiotherapy for Hodgkin's disease. Sought but none found. 3 mesotheliomas after childhood treatment. 1 Hodgkin's disease. Interval between treatment and secondary cancer* 11 years. Sought but none found. 8 cases with mesothelioma at sites ofradiotherapy for a prior tumour. Mean age at diagnosis * 45 years (range 22-78 years). Average interval between radiotherapy and mesothelioma was 21 years (range 11-29). 6 cases were treated for Hodgkin's disease and 2 for breast cancer. They also reviewed 27 previously reported cases ofpost-irradiation malignant mesotheliomas of the pleura and peritoneum. Sought - none found in 4, unknown in 4. A mesothelioma occured after radiation therapy for Hodgkin's disease. Interval between treatment and mesothelioma was 9 years. Sought -none found. 4 cases following radiation treatment ofHodgkin's disease. Mean interval 15 years. Sought - none found. 250 ferruginous bodies found in tissue from one case. Retrospective cohort study of 251,750 women with breast cancer. The overall estimated relative risk of malignant pleural mesothelioma after treatment was 1.56 (95% Cl 0.18-5.63). No cases found in Hodgkin's disease treated patients. No specific information available. Retrospective random review of 1000 irradiated breast cancer cases3 cases ofmalignant pleural mesothelioma reported after thoracic irradiation Persons with history compatible with asbestos exposure excluded from review. MOB-HarrisMaster 00281 REFERENCE Falohero et al (1996) Hill eLM (1997) 37 CASE DESCRIPTION Case ofmalignant pleural mesothelioma after mantle radiotherapy for Hodgkin's disease. Interval 17 years. Case report ofbenign localized pleural mesothelioma in a woman following adjuvant radiation of breast and axillary region. ASBESTOS EXPOSURE Sought - none found. Not mentioned. TABLE U7. THOROTRAST Nationality German (Ishikawa et al 1995) Danish (Andersson et al 1995) Japanese (Ishikawa et al 1995) Stev et al (1995) Thorotrast Exposed Control 9/2241 (5 pleural and 4 peritoneal). 0/1575 The risk for malignant mesothelioma reached 2.5% based on 7 cases, with an actuarial risk of7-8% for patients receiving 20 mi ofThorotrast A possible gradient was found between Thorotrast and malignant mesothelioma. 1/258 (peritoneal). Combined plcuro-peritoneal and retroperitoneal malignances were five fold more Sequent (1.1%) than in the controls (0.2%). 0/1630 Case report - peritoneal mesothelioma in a 63 year old male. Andersson (1995) notes that for malignant mesothelioma, the risk has been demonstrated to be elevated in the Danish, Japanese, and the German Studies. Plutonium Sanders (1992) showed that pleural mesothelioma was infrequent following deposition of 23sPu02 in the lung or pleura of rats with 5 tumours in 2105 rats. In a previous study, 4 tumours in 527 rats were found. The risk of pleural mesothelioma was not significantly increased by intrapleural injection of 30kflq 239Puo2, but a much higher incidence was found following intraperitoneal injection of 239Pu02 considered to be due to aggregation of particles. It was argued that these findings fit with pleural particle clearance limiting the a-irradiation. In a postmortem research study using the United States Transuranium and Uranium Registries, there MOB'HarrisMaster 00282 38 were 6 mesotheliomas in the first 260 deaths (in a biased seif selected cohort). Five of the 6 cases were known to have had potential for asbestos exposure. One was a uranium miner with no asbestos exposure. There was no apparent relationship with internal or external dose and mesothelioma (Gold and Kathren 1998). The authors caution against drawing conclusions, recognising the fact that the original cohort was voluntary. Atomic Bomb . A case of mesothelioma has been reported in a man who developed mesothelioma of the left hemithorax 50 years after the atomic bomb was dropped on Nagasaki in 1945 (Mizuki et al (1997). An asbestos exposure cannot be ruled out. Overall Radiation While the case reports and anecdotal evidence are strong, the link between radiation and mesothelioma cannot be accepted as proven on present evidence. On the other hand, the data are highly suggestive of an association for some types ofradiation exposure so a link cannot be dismissed without additional carefully controlled studies which are negative. 7.1.4.5 Other Chemicals While the evidence from experimental animals has shown that certain chemicals and drugs can induce mesothelioma (Kurakawa et al 1983; Okada et al 1989) there is, to date, no systematic evidence of such effects in humans. Beryllium has also been suggested (Oels etal 1971). UPDATE: A review ofPotassium Bromate by Kurokawa et al (1990) showed statistically significant increases in peritoneal mesotheliomas in male F344 rats given 500 ppm of postassium bromate in drinking water for various periods. Donna et al (1991) showed that 2, 6-Dichloronbenzonitrile (Dichlobenil), a principle in a commercial herbicide, both by intraperitoneal and subcutanesous routes induced a significant increase in tumours including a small number of mesotheliomas. 7.1.4.6 Other Factors a. Smoking: Smoking does not appear to increase the risk of mesothelioma. b. Diet: A recent case-control study has suggested that a low vegetable diet might influence mesothelioma occurrence (Schiffman et al 1988). MOB-HarrisMaster 00283 c. Genetic Predisposition: It has been suggested that certain familial cases in which siblings or parents and children in the same family get mesothelioma might be genetically linked (Risberg et al 1980; Martennsson et al 1984). The early childhood cases may fit this category. In practice, however, the close interaction of genetic and environmental factors makes it very difficult to separate them. d. Viruses In his review of non-asbestos mesothelioma, Peterson et al (1984) noted that an avian virus had been shown to induce mesotheliomas in chickens which were similar to those in mammals. To date, there is no comparable human evidence. e. Non-asbestos exposed mesothelioma cases There is a certain consistency in the epidemiological literature that clear evidence of asbestos exposure cannot be established for 25-30% of cases. Peterson et al (1984) have reviewed this problem and quote a range (0-87%) without documented asbestos exposure. In most countries where women have not been a major part of the workforce, the rates of mesothelioma in women have remained reasonably constant at the 1-2 per million population "background" rate. These might represent genetically controlled or background environmentally induced rates (Hirsch et al 1982; McDonald & McDonald 1986; Huncharek 1989; Peto et al 1981). UPDATE: a. Smoking: There is still no evidence to suggest that smoking is important. The possibility that certain cigarettes with a crocidolite filter could have a role has neither been demonstrated nor ruled out. b. Diet: A Vitamin A based cancer prevention program (P-carotene or retinol) has been carried out on former crocidolite miners in Australia. Program participants had signifanctly lower mortality than nonparticipants, but the rates ofthe two groups converged with time (Musk et al 1998). The relative rate ofmesothelioma in those on retinol compared to P-carotene was 0.24 (95% Cl, 0.07 - 0.86), a significantly lower rate of mesothelioma (deKlerk et al 1998). c. Genetic Predisposition: While genetic predisposition continues to be suggested, the difficulties of separating environmental from genetic effects remain. However, this may be changed with the ongoing rapid developments in genetics. MOB-HarrisMaster 00284 d. Viruses In the 1992 report the review of non-asbestos mesothelioma by Peterson et a] (1984) was mentioned noting that an avian virus had been shown to induce mesotheliomas in chickens which were similar to those in mammals. More recently England etal (1991) inoculated chickens with a v-src-positive DNA fragments and found a peritoneal based tumour which was diffuse mesothelioma. An important development since 1992 has been the finding of fragments of the DNA from SV40 in mesothelioma tissues. SV40 is a virus which contaminated some of the polio vaccines used in the late 1950's early 1960's. The finding of SV40-like DNA sequences in human mesotheliomas (Carbone et al 1994) and the induction of mesotheliomas in hamsters by injection ofwild type SV40 into the pleura or peritoneum (Cicala eta! 1993) raised the possibility that the SV40 virus might act as an independent carcinogen or co-carcinogen with asbestos. When the SV40 was injected in the pleural space, pericardial and pleural tumours identified as mesotheliomas were observed in 100 percent of Syrian hamsters. To date, there is as yet no comparable evidence in humans. Since the early 1990's, SV40 DNA sequences have been reported in a substantial portion of British mesotheliomas (Gibbs et al 1998; Pepper et al 1996; Stenton 1997), in 5 of 7 asbestos associated mesotheliomas in New Zealand (Mayall et al 1999) but in none of the non-asbestos associated mesotheliomas. Pepper et al (1996) suggested that vaccination with live SV40 through contaminated polio vaccines given between 1959 and 1961 might be a factor in the continuing rise in the incidence of malignant mesothelioma in some countries. HIrvonen et al (1999) failed to find SV40 in Finnish mesothelioma specimens. This may be related to the fact that the Finnish poliovaccines were not contaminated with SV40 or other presently unknown factors (Carbone et al 1999). In Belgium, the SV40 Ltag-like DNA sequences were found, but they did not detect nuclear expression of the viral oncoprotein which they concluded made a pathogenic role of SV40-tag in mesothelioma carcinogenesis questionable (Dhaene et al 1999). However, they intend to repeat their study. In France, Galateau-Salle (1998) reported sequences related to SV40 Large T antigen (Tag) in 28.6% of bronchopulmonary carcinomas, 47.6% of mesotheliomas and 16% of cases with non-neoplastic and pulmonary disease. While the difference between pulmonary cancer and mesothelioma findings were not significant, the difference between mesotheliomas and non-malignant cases was statistically significant. Testa et al (1998) reported on the results of a multi-institutional study which confirmed the presence and expression of Simian Virus 40 in human mesotheliomas with 10 of 12 (83 %) of human mesotheliomas tested revealing SV40 sequences and SV40 large T antigen expression. Electron MOB-HarrisMaster 00285 '^ ^'0 41 microscopy demonstrated variable amounts of asbestos fibres in 5 (71%) of 7 lung tissues available for analysis. Based on their work it has been suggested that the tumerogenic potential of SV40 Tag in some human mesotheliomas may arise from its ability to interact with and thereby inactivate several tumour and/or growth suppressive proteins in cooperation with asbestos fibres in inducing pleural mesotheliomas (Mutti et al 1998b, Matker et al 1998). Stenton (1997) concluded that there is circumstantial evidence which suggests that SV40 may act as a cofactor with asbestos in inducing human mesotheliomas. The source of the SV40 human infections has not been completely identified even though the administration from 1957-1965 of SV40 contaminated coat or vaccine is highly suspected (Pass et al 1996; Mutti et al 1998a). Mutti et al (1998a) reported that horizontal infection by sexual transmission has also been hypothesized. To date, only one epidemiological study has been undertaken (Strickler et al 1998). They carried out a retrospective cohort study using data from the Surveillance Epidemiology and End Results program (1973-1993) and the Connecticut Cancer registry (1950-1969) as well as national mortality statistics (1947-1973). They assumed that the cohorts who were likely to have received SV40 contaminated polio virus vaccine as infants were bom in 1956 through 1962. Those who received it as children were bom in 1947 through 1952. They assumed that persons bom 1964 through 1969 would not have received the vaccine. After more than 30 years of follow-up Strickler et al concluded that exposure to SV40 contaminated polio virus vaccine was not associated with a significant increase in mesothelioma rates. This study did not take into account exposure to asbestos. The Relative risks for the cohort exposed as infants was 3.0 (95% Cl - 0.67-13.11) and as children was 2.45 (95% Cl 0.50=12.03). However they recommended that as the exposed cohorts mature it is important to continue monitoring cancer risks, noting that the birth cohorts studied had not yet reached the age at which most mesotheliomas occur "resulting in few cases (71) and imprecise estimates of risk". In a very recent paper, Carbone et al (1999) summarized the molecular and epidemiological issues. The current situation was sumarized as follows: - SV40 was introduced into a significant portion of the human population between 1955 and 1963 through polio vaccines and adenovaccines contaminated with the virus. By 1961, 80-90% of all US children under the age of 20 had received at least one polio vaccination potentially contaminated with SV40. During the 9 year distribution, it is estimated that 98 million people, children and adults may have been injected with an SV contaminated vaccine in the US. In 1960, Sweet & Hillman demonstrated that SV40 contaminated both the Salk and Sabin poliovaccines which were prepared in the kidneys of rhesus monkeys. MOB-HarrisMaster 00286 - In 1962, Eddy et al showed that rhesus monkey cells when injected into hamsters caused sarcomas. By 1964, SV40 had been shown to be capable of infecting and transforming hamster, rodent and human cells and were capable of human growth when injected subcutaneously in terminally ill human volunteers. Short term studies and one long term epidemiological study of 1073 children (up to 19 years offollow-up) did not suggest that the virus was oncogenic in humans. (A 22 year follow-up study in Germany involving mainly oral polio vaccine was also negative). In the study by Strickler, direct exposure should not be considered as the only source of SV40 infection as it appears that the virus can infect and spread in human populations. Clearly there is adequate information to question a role for SV40 in the occurrence of mesothelioma. However, it is premature to reach any conclusions as to whether SV40 has caused mesothelioma in asbestos exposed or non-asbestos exposed persons. However a role for the SV40 virus in mesothelioma causation in humans cannot, on present evidence, be ruled out. e.Non asbestos exposed mesothelioma cases The data remain consistent, that in most countries where women have not been a major part of the workforce, the rates of mesothelioma in women have remained reasonably constant at the 1-2 per . million population "background" rate. This was discussed in Section 7.1.4.1. 7.2 MECHANISTIC CONSIDERATIONS Experimental work in animals and other biological systems are consistent with fibre length and diameter being important in both the ability of fibres to produce experimental fibrosis and to produce mesothelial tumours when introduced directly to the pleural surface. Experiments where "long" asbestos fibres were placed on the pleura, produced mesothelioma from all fibre types (Wagner & Berry 1973; Stanton 1973), but experience in humans has shown no clear high risk of mesothelioma for workers exposed to chrysotile asbestos fibres. While the reasons for such differences remain conjecture, a convincing argument is that in experimental animals, with a lifespan of approximately 2 years, the lung protection / removal mechanisms have less than 2 years over which to act. Thus if solubility of the fibre or removal mechanisms are important in reducing the number offibres at a site, the time over which these mechanisms can act is truncated. Although the processes of tumour development occur within the lifetime of the animal, exposure levels in animals tend to be high and might further impede fibre removal mechanisms. Moreover, experiments where fibres are placed directly on the pleura exclude consideration of the mechanisms impeding MOB-HarrisMaster 00287 43 fibres from reaching the pleura under normal circumstances. In humans, time frames are measured in tens ofyears, which provides the fibres with the opportunity to be dissolved or removed from the lung. In spite of the apparent difference between the human and animal experience, experimental data are never-the-less useful because they provide a possible mechanistic perspective on the importance of fibre shape and.dimensions. Studies by Stanton & Wrench (1972); Stanton (1973), Stanton et a! (1977) and Stanton & Layard (1978) showed that fibres greater than 8um in length and less than 0.25 um in diameter had a higher probability of producing tumours than did shorter and larger diameter fibres. They also demonstrated that reducing the length of fibres by pulverization decreases the carcinogenicity as far as mesotheliai tumour production is concerned. They concluded that pulverized blue asbestos of length less than 1.25-3.75 um could be discounted in mesothelioma production. Demonstrating that glass fibres and aluminium oxide fibres produced mesothelioma when in contact with the pleura suggested that mesotheliai tumour carcinogenicity was linked primarily to length, diameter and, possibly, durability. UPDATE: Reaching the pleura: The mechanism by which fibres reach the pleura (Nishimura & Broaddus 1998) or even whether they need to reach the pleura is still not known. A possibly important finding was the identification of "black spots" on the parietal pleura which contained anthracotic pigment and high concentrations of amphibole fibres compared to normal pleura fBoutinetal 19961. They suggested that this could explain why the parietal pleura is the target for plaques and mesothelioma Fibre size: The British Health & Safety Executive (Meldrum 1996) concluded that there is good evidence that longer fibres are more toxic than equal masses of shorter fibres of the same composition. They noted that results from intraperitoneal (IP) and inhalation studies in rats with long and short fibre amosite suggests that short fibres (<5um) pose little if any concern for disease development at any site. Donaldson & Golyasnya (1995) showed that chromosomal abnormalities were caused by long fibres but not by short ones. They concluded that fibres with length of at least 10 to 15 micrometres are necessary to induce disease in the pulmonary parenchyma, but shorter fibres in the region of 8 to 10 micrometres can in their view cause mesothelioma. It appears that short fibres of chrysotile have been reported on the pleura or in tumours on the pleura. This finding has little relevance, as it is not known whether the fibres arrived before or after tumour MOB-HarrisMaster 00288 growth was initiated and the evidence shows that short fibres do not induce mesotheliomas. 44 Biopersistence: Fibre biopersistence is an important parameter in the evaluation of the fibrogenicity and carcinogenicity offibres. It is now well established that the removal of fibres from the lung involves two phases. The first, is the rapid phase involving macrophage clearance of fibres from the lung. In this phase, fibre length seems to be the most important parameter. A second phase involves the removal of the longer fibres from the lung. In this phase, fibre length and fibre durability or dissolution are dominant. It has been shown that when biopersistence is measured in rats following the inhalation of synthetic mineral fibres, clearance of the size range greater than 5 pm in length (WHO fibres), fails to differentiate between the different fibre types. However, when the bioperistence of fibres longer than 20pm is examined, differences in the behaviour of the fibres become very apparent (Bernstein 1995,1996). In the rat, there was an important difference in the removal of long fibres >20pm compared to short ones (<20 pm). Measurement of the biopersistence of man-made fibres is easier than for the asbestos minerals, in particular chrysotile, as the latter breaks into fibrils increasing the fibre number concentration with time. An important factor in such experiments is the length distribution of the originally deposited fibres. The half-times in days for crocidolite of various fibre length in rats (Bernstein et al 1996) has been reported in TABLE U8: TABLE U8. BIOPERSISTENCE OF CROCIDOLITE L<5um T'-:-l Th-2 w-Th 2.7 430 172 Half-times for Crocidolite in days Fibre Length L5-20um________ L>20um Tk-1 TVi-2 w-TVS Tk-1 TVi-2 w-T'/j 1 442 262 1.9 806 536 l * hiif-ozne Ost clearance phase; T*-2 half-time daw clearance phase; W-Ttt half-tsaa combined weighted clearance. As far as chrysotile is concerned. Coin eyd (1992; 1994) reported that fibres longer than 16pm were cleared slowly, ifat alL They estimated, a pulmonary retention half-time for fibres longer than 16pm of 114 days. They did not see transportation of chrysotile fibres from the central regions of the lung toward the sub-pleural regions. Caution is needed in interpreting these findings as the size of a rat macrophage is less than that in humans and a rat's life span is considerably less. Oberdorster (1994) noted that fibres up to 8pm in length were cleared very rapidly with pulmonary retention times MOB-HarrisMaster 00289 45 ranging 8-30 days. He concluded that dissolution is a very important clearance mechanism in the rapid disappearance of pulmonary chrysotile fibres. Assuming that all mammals behave similarly, Oberdorster (1996), ignoring sequestration of fibres, estimated that the overall retention half-time for chrysotile in a primate would be about 105 days. Searl (1997) also found the rapid removal of short chrysotile fibres in rats but retention of long fibres. Unfortunately in none of these experiments were the fibres retained in the lung tissue analyzed to determine if they were tremoiite not chrysotile fibres. However, Wagner (1974), when he looked, did find tremoiite in the lungs of exposed animals. Churg & Wright (1994) noted that very little information is available on actual fibre clearance rates from human lungs. They indicated that for amosite and crocidolite, the estimated clearance half times are measured in years to decades whereas the data that exist suggest that the vast majority of chrysotile fibres are cleared within months although some fibres may be sequestered and cleared very slowly. Short Coalinga amphibole free chrysotile fibres were found not to produce fibrosis or tumours and to have low biopersistence (Hgren and Chatfield 1997, 1998a, 1998b). That study produced no mesotheliomas. Recently, an experiment was conducted with "pure" chrysotile from Brazil. The same method as used in synthetic mineral fibre tests was used. The study found that fibres longer than 20pm chrysotile had a half-time of about 1 1/3 days (Bernstein 1999). It is known that the solubility of fibres depends on whether they are inside or outside the cells as the ph differs. In vitro experiments of fibre durability have been undertaken to see if in-vitro fibre durability predicts biopersistence which it seemed to do for sue synthetic mineral fibres and amosite fibres longer than 20pm (Searl et al 1999). McDonald (1998) noted that a small number of well controlled studies using lung burden analyses have shown that amphibole fibres differ from chrysotile in as far as being more durable and having greater biopersistence in lung tissue. - Boffetta (1994) concluded that there are few data available concerning biopersistence in humans. He notes that studies analyzing asbestos lung burden in workers following cessation of exposure suggest a decreasing concentration over time that is independent of duration of exposure. However, the data in his paper suggests that this finding applies more closely to Canadian miners and Norwegian asbestos cement workers than to amosite workers. A review ofthe situation for man-made fibres concluded:" Intraperitoneal injection studies showed clear dose-response relationships with many fibres and differences between their carcinogenic potency. These results support the concept that the durability of fibres in the body is an important factor in the production of fibre-related cancer" (Pott & Roller 1996). MOB-HamsMaster 00290 46 In summary, the data are all consistent with long biopersistent fibres being considerably more important in disease causation than short or non-biopersistent fibres. Tissue burden The importance of tissue burden studies has been outlined by Becklake & Case (1994). McDonald (1998) concludes that research over the past forty years, demonstrates with increasing clarity that amphibole asbestos fibres-crocidolite, amosite and tremolite are more carcinogenic than chrysotile. It is evident that without tissue analyses, potentially important exposures would go undetected. This is very important in the search for etiology. For example, a Jewelry worker with a mesothelioma was assumed to have been exposed to chrysotile only until it was found through tissue analysis that he was exposed to amosite (Kern et al 1992). Gibbs eLll (1994) demonstrated the importance of tissue analyses for confirming past exposure. There are numerous reports describing the tissue content of fibres in cases occupationally exposed to asbestos and in cases of asbestosis, lung cancer, and mesothelioma (Nolan et al 1994, Paoletti et al 1993; Langer & Nolan 1994; Murai & Kittagawa 1992; Tossavainen et al 1994; Sakai et al 1993; Dufresne et al 1995; Roggii 1995). The importance oftissue analyses in establishing etiology depends on the use of appropriate controls or referents. For example workers are likely to have in their lungs, the fibres to which they are exposed, regardless of whether or not those fibres are related to health outcome. Inferences about association can only be made when the exposures of cases are compared to those of referents of similar age and circumstance who do not have mesothelioma or the other dieseases under investigation (McDonald 1994). Many studies have reported ferruginous body concentrations in lung tissues. Criteria for evaluating tissue and ferruginous body burden study results have been reported (Helsinki Criteria Document 1997; Gibbs 1993). LTICC samples. Frank (1995) claims that a study of the UICC chrysotile asbestos used in many animal experiments did not contain any tremolite. In fact tremolite was only found in the Quebec mines and mills by analysis of the fibres present in the lungs ofminers. Few investigators have examined the fibre types in the lungs of the experimental animals after exposure. 7.3 LEVEL OF EXPOSURE There is epidemiological evidence that the risk ofmesothelioma is dose related (Newhouse et al 1985 and Newhouse & Berry 1979). See TABLE 8. In studies where exposure has not been quantitative, duration of employment has often been used as a surrogate. For example, in the British textile MOB-HarrisMaster 00291 47 industry there was no case of mesothelioma in men with less than 6 years of employment (Peto et al 1985) compared to 33 such cases where individuals were exposed for more than 6 years with 23 of the cases exposed for 20 years or more. The existence ofexposure-response relationships has been strengthened by measurements of fibres in tissues where progressive increases in relative risk have been observed with increasing fibre content. TABLE 8. MESOTHELIOMA -EVIDENCE OF EXPOSURE-RESPONSE. Newhouse & Berry (1979)" Exposure category Number of cases Rate / 100.000 s.vrs23 Low- Moderate" <2 4 >2 7 33 93 Severe" <2 >2 16 19 104 243 Rogers etal (1991) found relative risks to increase more rapidly with concentrations of fibre in lung tissue greater than 3 x 10s fibres /g by light microscopy and 10s-10" fibres /g by transmission electron microscopy. Rogers etal (1991) used data from various studies, evaluated by Berry to illustrate how the risk of mesothelioma increased with the concentration of fibres in lung tissue. He did this by calculating odds ratios13 which are shown in TABLE 9. These show that when the odds of mesothelioma occurrence is set at 1 for concentrations of less than 10s fibres/g of tissue, the odds of mesothelioma occurring for concentrations greater than 10s fibres/g of lung tissue are consistently greater than 1. This shows that the risk of mesothelioma increases with increasing exposure.* 1 ~Dau shown for men only. a.yn Subject or pesoa yean of etpoture. 1*The catryrics ofeqxxure <2 and >2 represent leu than or more than 2 yean of eqxxure. The *lcw-<nodcr*te* exposure category was "probably 5-10 fibrea/ml The 'severe* exposure category included conccatnaotu which before 1945 avenged 20 fibrta/mi or higher. 25An 'odds ratio* is the ratio ofthe 'odds* ofdisease occurrence as (he cqsneed sod noa-etposed xubgrtjpe. MOB-HarrisMaster 00292 TABLE 9. MESOTHELIOMA ODDS RATIOS IN RELATION TO LUNG TISSUE FIBRE CONTENTS RE-CALCULATED FROM VARIOUS STUDIES BY BERRY From Rogers et al (1991) Concentration26 < 106fibres/g Berry et al 198927 *cr.a 1 Concentration >l06fibres/g 3.8 (1.8- 8.0) Berry et al 19892* cr.a 1 7.4 (3.5-16.0) Mowe et al 1985 1 8.5(2.3-31.0) 48 In the Quebec chrysotile mines and mills the relative risk of mesothelioma increased with cumulative exposure. The case with the lowest cumulative exposure had 8.8 years of employment at a concentration of6.7 fibres/ml (Liddell 1989). The mesotheliomas in the Quebec chrysotile mines and mills were also highly correlated with the concentrations of tremolite >8um long in their lungs as described earlier in this report (McDonald et al 1989). UPDATE: There has been no new evidence to suggest that mesothelioma risk is not exposure dependent. Roggli (1995) found a significant correlation between duration of exposure and asbestos bodies as measured by light microscopy and between the duration of exposure and total uncoated fibres of 5 pm or longer as well as commercial amphiboles as determined by scanning electron microscopy. In a US series of mesotheliomas, Dodson et al (1997) found that 46 of 55 individuals with a pathological diagnosis ofmesothelioma had ferruginous bodies at concentrations of more than 1000 per gram dry lung tissue. The majority ofthe cores contained amosite. Roggli et al 11993) identified amosite in 81 percent of cases which accounted for 58 percent of all fibres of five micrometres or greater in length Hughes & Weill (1994) pointed out, quite correctly, that by not including controls, the Roggli et al study cannot be used to deduce the relative importance or potencies of different fibre types. *6 < means less Dun or equal to stated value; > mains mote than stated value. 27 recalculated data from McDonald et il 1912. It recalculated data from Wiener et al 1912. MOB-HarrisMaster 00293 49 In a study of asbestos cement workers, exposed to chrysotile asbestos and small amounts of amphibole, the exposed workers with mesothelioma had a significantly higher total content of asbestos fibres in their lungs than those without mesothelioma who in turn had higher concentrations than controls. Chiysotile was the major type offibre identified. However the difference between the various groups (exposed with mesotheliomas, exposed without mesotheliomas and controls) was most pronounced for the amphibole fibre (62, 4.7, 0.15 fig) especially crocidolite (54, 1.8, <0.001 fig) but were evident also for tremolite (2.9, <0.001, <0.001 fig) and anthophyllite (1.7, <0.001, <0,001 fig). For arnosite, there was no statistically significant difference between the lung burdens from workers with and without mesothelioma. Fibrosis was correlated with tremolite but not with chrysotile in the lungs. (Albin et al 1990) Churg et al (1993) determined the fibre content of the lungs of 94 long-term chrysotile miners & millers from the region of Thetford Mines. They found that mesothelioma, airway fibrosis, and asbestosis were strongly associated with a high tremolite fibre concentration, whereas pleural plaques and carcinoma of the lung showed no relationship to tremolite burden. It is important to point out that in the Quebec chrysotile mining industry there was no case of mesothelioma in men employed for less than 2 years. Studies of fibre in the tissues of the general population case control series have consistently shown higher amphibole concentrations in the lungs of mesothelioma cases compared to controls. 7.3.1 Neighbourhood Exposure Another possible indirect measure of exposure is distance from a source. In this regard, the absence ofhigh rates of mesothelioma in persons living near asbestos factories would be supportive of zero or very low risks at low levels of exposure, neighbourhood exposures being presumably less than those in the workplace. In fact, the only evidence of neighbourhood exposure increasing risk has been in cases where large quantities of blue asbestos was involved ("Wagner et al 1960, Newhouse et al 1985). Other studies in Canada and the USA have not shown such an association (McDonald & McDonald 1980; Hammond etal 1979a). These latter studies were concerned with chrysotile and arnosite respectively. Quebec chrysotile mining and milling communities were included in the mesothelioma survey conducted by McDonald & McDonald (1980). There, even in the 1970's, airborne fibre concentrations29 ranged 160-11000 ng/m3 . These concentrations were orders of magnitude greater than the 0.1-100 ng/m3,reported in other rural and urban areas (Gibbs et al 1980). While subject to many errors, the mean fibre concentrations at the "dustiest" site in these communities as measured by phase contrast microscopy was about 0.015 fibres/ml30. 'Hie ecocentnaoni wav determined uainf mncirinon deem nderoecopy. Because fibres an durupttd <n the preparation procedure, coocauntions an "^p*1***"*00 * aaas ***** M ntta** One o* Ixl0*g. 30 TWi tie mean value far tf* taufr of Id umpia counted uaiog two dfferaf pfeue central membrane filter mounttJf *ad counting methods (NIOSH and BOHS) and 4 comm. The main aoureca of error mv parade qvqiap which wouM likely k*d to qpdqnrimirioo of fibrv conccagiaon and lack offibre diffcrcaaittoq which would overeanufia the concentration. MOB-HarrisMaster 00294 50 UPDATE: An understanding of the possible impact of neighbourhood exposures is not possible without an understanding of background rates of mesothelioma. Background rates of mesothelioma McDonald and McDonald (1993,1996) have reviewed this question. They provided as evidence for the existence of background rates: 1. High rates of mesothelioma have occurred in certain villages in Turkey related to the natural occurrence of fibrous erionite. 2. Deposits offibrous erionite are widespread on the earth and there is some suggestion of erionite related cases in proximity to deposits in the Rocky Mountains States of North America (Enterline and Henderson 1987). 3. The occurrence of mesothelioma in childhood unless the usual latency with asbestos related cases is shorter in childhood (Fraire et al 1988). 4. In tissue burden studies there have been a certain proportion of mesothelioma cases that cannot be attributed to asbestos exposure. 5. Backward extrapolation of trends to before the divergence in rates between men and women occurred indicates a mortality rates of about 1 to 2 per million population per annum in both sexes. 6. There are studies where there remains a low mesothelioma rate after exclusion of occupationally related cases. 7. There were mesotheliomas diagnosed prior to the commercial exploitation of asbestos. Neighbourhood exposure .As reported before, the only evidence ofneighbourhood exposures increasing mesothelioma risk has been where large quantities of blue asbestos was involved. Further evidence of risks for residents possibly confounded by domestic exposures, has been reported in the blue asbestos mining town of Wittenoom Australia (Hansen et al 1993, 1998). The possibility of environmental exposure could not be excluded in five cases of mesothelioma, who did not have occupational exposure, four of whom lived within one half mile of a factory in Leeds using blue asbestos to manufacture asbestos mattresses for the insulation of steam boilers (Arblaster et al 1995). In another UK study in Calderdale, neighbourhood exposure cases again associated with MOB-HarrisMaster 00295 crocidolite were also identified (Edward et al 1996). Mesotheliomas have been reported in persons possibly exposed to a natural background of fibres throughout childhood with tremolite fibres considered most likely to be responsible (Rey et al 1993). In Greece malignant mesotheliomas have occurred in persons using a material containing tremolite to white wash buildings. (Constantopoulos et al 1991; Sakellariou et al 1996). A study in Italy claims an excess of mesothelioma in persons living near a crocidolite using factory, but that study did not take adequate account ofother possible occupational exposures (Magnani et al 1991; Browne 1991). In a study of persons living in Manville, New Jersey where a major asbestos manufacturing facility which used chrysotile and amphibole asbestos was located. Berry (1997) suggests an increased rate of mesothelioma in residents due to past exposures to asbestos. However the possibility of other occupational exposures has not been adequately taken into account to conclude that the mesotheliomas are environmentally induced. A study of persons living in the vicinity of chrysotile asbestos mines and mills in the province of Quebec Canada has been reported (Camus et al 1998). Seven pleural cancers were reported. It is not known whether these were mesotheliomas or if they were, whether they had occupational exposure. Churg (1998) observed high concentrations of amosite and crocidolite asbestos in the lungs from three women, from this region, who died ofmesothelioma between 1983 and 1988. They had not worked in the mines and mills but had worked in an asbestos bag repair operation. This suggests that other exposures are important. Case (1998) noted that this mortality rate (seven cases) could be entirely explained by a few cases among women in the area who had occupational exposure to amphiboles in the manufacture of gas masks, the repair of burlap bags which contained imported fibre and possibly in one case, tremolite exposure brought home on a miner's clothes. He reported that seven such women received workers' compensation in Quebec during the period of the study by Camus et al. In view of the experience of miners and millers exposed in the community as well as being exposed to concentrations many orders of magnitude above that of the general population this seems to be the most logical explanation for these cases. In summary there have been no studies indicating an increase in the risk of environmentally induced mesothelioma for persons living in the vicinity of chrysotile only using plants. 7.3.2 Household Exposure There have been instances where it appears that household exposure from living with a person who is occupationally exposed to asbestos may have been involved in increases in mesothelioma risks, with cases in case-control studies reporting more domestic contact than controls. (McDonald & McDonald 1980; Vianna & Polan 1978; Lieben & Pistawa 1967). The studies by McDonald & McDonald (1980) involved chrysotile (and tremolite contamination if present), other mine dusts and dusts from a factory where blue asbestos was also used. Fibre types MOB-HarrisMaster 00296 l' - ^ 52 were not identified by Vianna & Polan (1978) but the occupations ofhousehold contacts included, brake-lining worker, pipe fitter, heat insulation worker, heat electric-wire worker, elevator insulation worker and electric wire insulation worker. Lieben & Pistawa (1967) noted that the asbestos fibre types to which mesothelioma cases may have been exposed by family contacts in the three cases were: chrysotile and amosite; an unidentified fibre used in an insulation plant; and, unidentified fibres used in insulation work in a shipyard. The levels offibre exposures associated with the household contacts were not described in any ofthe reports. However radiological changes similar to those found in asbestos workers have been described in persons living in the same household as amosite asbestos workers (Anderson et al 1979). Such radiological changes in workers have usually involved long term exposures at levels in excess of occupational exposure limits of 1-2 fibres per ml. Thus, it is likely that past household exposures, may have been quite high. UPDATE: Valic and Beritic-Stahujak (1993) drew attention to the feet that Nicholson et al (1980) had measured concentrations in the homes ofminers and non-miners in a chrysotile mining community. On a mass basis they found that concentrations were much higher in the former, where 61% of samples were between 100 and 2,000 ng/m3 compared to the latter (32, 45 and 65 ng/m3). While there continue to be cases of domestic exposure reported (eg: Schneider et al 1996), there are no findings which alter the view that household exposures were high. The fact that mesothelioma incidence in females in North America and Western Europe has shown little or no increase during the last 20 to 30 years suggests that neither household or environmental exposures have increased mesothelioma risks significantly. IPCS (1998) reported "In several casecontrol studies reviewed therein "(Referring to an earlier IPCS Criteria Document 53)," there were more mesothelioma cases with household exposure than in controls, after exclusion of occupation. However for most of these investigations, it is not possible to distinguish the form of asbestos to which household contacts were exposed on the basis of the information included in the published reports". It is clear that this is very important as shown in Quebec. 7.4 LATENCY There was no mesothelioma death in the Quebec chrysotile mines and mills below 20 years from first exposure (McDonald 1980). Peto (1980) found no mesotheliomas in the British textile industry under 20 years from first exposure. While the latter used predominantly chrysotile, some amphibole (blue asbestos) was used at the plant. Overall, the literature would appear to support the statement by Browne (1983) that in asbestos related cases the onset of the illness is usually 35-40 years after first exposure, rarely less than 20 years and perhaps never less than 15 years. MOB-HarrisMaster 00297 53 UPDATE: The Helsinki criteria document (Consensus report 1997) states that: "a minimum of 10 years from first exposure is required to attribute the mesothelioma to asbestos exposure, though in most cases the latency is longer (e.g. on the order of30 to 40 years). In the Quebec chrysotile mining and milling industry there was only 1 case with a period from first exposure to death of less than 30 years and the latency period ranged up to 60 years (McDonald et al 1997). In 1992, Lanphear & Buncher (1992) reviewed 21 articles that documented the latency periods for 1690 malignant mesothelioma. Of these 1105 (65%) fulfilled strict histologic and exposure criteria. Of these, 99% had a latency of more than 15 years, 96% had a latent period of at least 20 years. They calculated that the probability ofa mesothelioma occurring within a decade ofthe first exposure was 0.0000, 10-14 years after first exposure was 0.0045, between 15 and 19 years was 0.0317 and after more than 20 years from first exposure was 0.9638. The estimated median latent period was at least 32 years after initial exposure. They did not analyze the results by fibre type or distinguish between pleural and peritoneal tumours. As was pointed out by Peto et al (1982) and discussed later in this report, the major predictor of risk ofmesothelioma appears to be period from first exposure. Mathematically, this can be expressed as p = b.t" where p = incidence in any one year, b is a constant, t is time since first exposure and k is an exponential between 3 and 4. Morgan (1991) argued that this could be used to work backwards from disease to probable cause. Based on this argument and assuming that exposure to asbestos is the cause of the mesothelioma, he adapted the model to P0 + SPi=1 where p0= background ifit is assumed that the disease in this instance is caused by asbestos, and not background, the model becomes fiR-1 - kk where p; = tl /E\ t As an example of an application, Morgan considered a former insulator with mesothelioma diagnosed in 1988, who was exposed to asbestos from 1942 through 1944 and again in 1950. The table provides the data that allows the conclusion that for this person there was an 84.4% likelihood that his 1942 through 1944 job caused the disease, and a 15.6% likelihood for the 1950 exposure. MOB-HarrisMaster 00298 Exposure 1942 1943 1944 1950 Total Probability ofEach Year as Cause Time (t)* t33 46 660,165 45 611,285 44 565,047 38 338,254 2,174,751 Casual Probability riVEt3-3 .303 .281 .260 .156 54 * t = time in years since first exposure. The causal probability = tj3,5 t; 3,5 . Using this relationship, the causal likelihoods could be calculated. Peto showed that this equation (actually t4) was approximately correct for exposure durations ofup to 10 years. While the model is appealing it has several weaknesses. It assumes that asbestos exposure is the cause and does not take fibre type or exposure levels or industry sector into account. A residence time model used by Hughes was described later in the 1992 report in which Incidence I at time t = KC (t3-2 - (t-d)3-2) where t = time since first exposure and d = duration of exposure, C is the concentration and K is a constant depending on the process. Various models approximating a cubic model have been employed in various studies. It was noted by Hillerdahl (1999) that even in the most heavily exposed cohorts only a proportion ofthe cohort dies ofmesothelioma so the formula is not applicable in all cases. Berry (1995) refined this model in which the increase in risk with time is attenuated by a factor representing a decline in risk corresponding to elimination of asbestos from the lungs. He further introduced a lag period to allow the tumour time to develop. This was shown to apply in experiments in which rats were inoculated with fibres. The new formula became: I = ce'(t-w)k where I = incidence, c=cumuiative exposure, z = elimination rate, t = time since first exposure, w=lag period and k is a constant. Berry applied this formula to residents and visitors to the Wittenoom crocidolite mining area. With the elimination factor, incidence was relatively stable from 40-60 years after first exposure in contrast to the risks without fibre elimination. It assumes a linear non-threshold model. The lifetime risks of mesothelioma based on this model for residents estimated to be exposed continuously for 10 years to 0.001 frml from age 25 was 9/million. This was an estimate for crocidolite. The estimate for visitors exposed for I week at O.Olfrml at age 20 was 0.27 - 1.6 per million. Ifthere is a background of2 per million per year, the lifetime risk is about 140 or 200 according to HEI-AR (1991). MOB-HarrisMaster 00299 55 If chrysotile itself can cause mesotheliomas in humans, its potency is at least l/40th of that of crocidolite and may be zero. Extrapolating for Dum Dum, the lifetime risk for persons exposed continuously for 10 years to chrysotile at 0.001 fee from age 25 would be 9/40 per million = 0.225/million at most. 8.0 ASBESTOSIS 8.1 DEFINITION AND DIAGNOSIS The definitions applied to asbestosis are many and highly variable although Harber & Smitherman (1991) found that over the last decade there was "stability of the criteria for asbestosis case definitions". As damage to the tissues (fibrosis or scarring) can only strictly be observed at autopsy or biopsy, asbestosis should be a pathological diagnosis. In practice, the observation of signs and symptoms in life are used for "clinical diagnosis". Thus, "asbestosis" is usually a clinical term applied to fibrosis ofthe lungs which has been caused by asbestos. The diagnosis is a clinical opinion which takes into account a variety of observations such as changes on the chest radiograph, worker complaints of breathlessness, crepitations (noises in the lungs), certain lung function deficits and evidence of asbestos exposure. The simple knowledge that the person being examined has been exposed to asbestos is likely to introduce a bias into a clinical diagnosis. There is probably little disagreement in the literature that high grades of certain radiological abnormalities reflecting scarring of the lung, combined with certain characteristic symptoms, pulmonary function deficits and clear evidence oflong term exposure to high levels of asbestos might be called "asbestosis". However, minor radiological abnormalities or lung function changes may or may not be indicative of"asbestosis". The application ofnewer techniques in diagnosis, such as CAT and High Resolution CAT scans, positive gallium scans, exercise and other tests, has not improved the situation because the relationship between these techniques and the currently more accepted definitions of clinical asbestosis remains unclear. It is for these reasons that the term "asbestosis" is rarely used in epidemiological studies. In most epidemiological studies the frequency of changes on a chest radiograph or frequency of symptoms etc., are treated independently and examined in relation to exposure. In some studies, combinations ofchanges to define asbestosis have been used but this definition has been for study purposes only. UPDATE: Browne (1994) reports that even in the 1990's, accurate statistics on the incidence and prevalence of asbestosis are bedeviled by problems of definition ofboth disease and exposure. Browne describes the parameters used to "diagnose" asbestosis for epidemiological purposes as radiographic change MOB-HarrisMaster 00300 56 (measured by ILO subcategories), pulmonaiy function deficits and presence of basal crackles. He points out that asbestosis possesses no pathognomonic, clinical, physiological or radiological features. Hence, given evidence of "occupational asbestos exposure" the diagnosis of asbestosis rests upon ft.<tfahlishing clinical features and excluding diffuse interstitial pulmonary fibrosis due to other causes or diseases. Ferruginous bodies and/or radiological evidence of pleural plaques may support the likelihood of exposure but do not establish the existence of asbestosis. The Helsinki document (Criteria document 1997) reports that the chest radiograph is still the basic tool for identifying asbestos related diseases such as asbestosis, pleural abnormalities, lung cancer and mesothelioma. They note that the limitations ofthe chest radiograph in the detection of asbestosis and asbestos associated pleural abnormalities are widely recognized and that computed tomography (CT) and high-resolution computed tomography (HRCT) can facilitate the detection of asbestosis and asbestos related pleural abnormalities but were not recommended as screening tools. They suggested that analysis oflung tissue for asbestos fibres and asbestos bodies could provide data to supplement the occupational history. Some of the advantages and limitations of various methods of examining the pleura have been described by Muller (1993) and several others. For clinical purposes the Helsinki Criteria document recommended that to identify persons with a high probability of past exposure to asbestos the results of tissue burden study results should be: Aj "Over 0.1 million amphibole fibres (>5um in length per gram of dry lung tissue as measured by electron microscopy in a qualified laboratory OR, Over 1000 asbestos bodies per gram of dry tissue (100 asbestos bodies per gram ofwet lung tissue) OR Over 1 asbestos body per milliliter by bronchoalveolar lavage as measured by light microscopy in a qualified laboratory." It was recommended that each laboratory establish its own reference values and that efforts be made to standardize the fibre burden analytical methods used by different laboratories. The Helsinki document recommended that the term "pleural asbestosis" not be used and recognised that pleural plaques are often asymptomatic and without clinically important findings. These conclusions are not unlike those of a workshop in Japan in 1991 (Gibbs et al 1993) where it was concluded that: "The finding ofa lung parenchymal content ofgreater than 1000 ferruginous bodies/g dry lung is highly suggestive ofoccupational exposure to asbestos, as long as the value is obtained with standard methods in a laboratory with experience in the application ofthe technique." MOB-HarrisMaster 00301 57 The possibility that idiopathic pulmonary fibrosis cases might occur in asbestos-exposed workers has been reported (Gaensler et al 1991). 8.1.1 Radiological Changes The chest radiograph may show changes. These include: lung markings which obscure the normal lung appearance; pleural thickening; pleural calcification; and possibly changes to the cardiac outline. These changes can be graded and an internationally agreed classification system exists for the reading of radiographs known as the ILO/UC Classification. Interpreting these readings is not straightforward for the following reasons: * There is almost always significant variation between even "expert" readers in terms of the existence or degree of radiological change. It is for this reason that scientific studies involve the review of films by multiple readers. An idea ofthe effect that this might have has been reported by Parker et al (1989). They reported that an initial reading of 566 radiographs found 30% of films to be classified as positive for pleural change. However, only 4% were considered positive by at least 2 out of 3 readers from a NIOSH panel reading radiographs under blind conditions31. * Readings by a single reader, especially when they have knowledge of exposure and other clinical information may be quite unreliable from the standpoint of obtaining objective information on which to establish etiological factors. * Some radiological changes such as pleural calcification may be quite marked but have little or no importance in producing respiratory disability. * As the radiological changes become less pronounced, there can be serious difficulties in the interpretation of results. Readings of the radiographs of persons with and without asbestos exposure may reveal the same types and degrees of abnormality. It is for this reason that, before reaching conclusions that there is a disease or indicator of a health effect in a group of workers, it is necessary to know that the frequency and degree of change is greater in those exposed than in a comparable group of non-exposed workers or that the degree ofchange and the incidence of such changes relate to exposure levels. * Becklake (1991) notes that while the presence of small irregular opacities are usuallyconsidered important in the diagnosis of asbestosis (Canadian Thoracic Society 1979; American Thoracic Society 1986; Council report 1984) they are nonspecific for this condition "'Blind* means without information on ige, occupation, exposures, other clinical information etc MOB-HarrisMaster 00302 58 Fibrosis may be the resuh of exposure to other agents or to pathophysiological processes. Moreover, there is evidence that milder grades ofradiological abnormality may be related to smoking or enhanced in asbestos exposed smokers (Hnizdo and Sluis-Cremer 1988; Rosenstock et al 1988; Lilis et al 1986; Weiss 1984; Blanc & Gamsu 1988; Blanc & Gamsu 1989; Weiss 1991). UPDATE: While there have been no major changes in the nature ofradiological changes, the issue concerning the importance of pleural plaques remains. The relationship between pleural and parenchymal changes and lung cancer are discussed elsewhere. (See Section 9.1). Pleural plaques Sanden & Jarvholm (1991) did not find pleural plaques to be associated with mesothelioma in a prospective cohort study of3893 insulation workers. Likewise in Canada definite pleural calcification was not associated with malignant mesotheliomas in the Quebec chrysotile miners (McDonald et al 1997). This absence of an association was originally noted by Gibbs (1972) and observed in Greece by Contantopoulos et al (1992). On the other hand, Hillerdal (1993, 1994) in a general population study in Sweden, reported that pleural plaques without asbestosis were associated with a slightly increased risk oflung cancer. However, in that study the fibre types and exposure levels were not known. The SMR for men with asbestosis was 2.3 and for men without asbestosis was 1.4. A study of residents in Japan suggested that the prevalence of pleural plaques was associated with an increased concentration of anthophyllite fibres in the lung (Murai et al 1997). This is consistent with the findings many years ago of endemic pleural plaques associated with anthophylite exposure in Finland. Endemic pleural calcification has been reported too in Metsovo in North-west Greece, where persons white washed their homes with a material made from white rocks composed of tremolite fibres (Sakeilariou et al 1996). Areas were identified in other parts ofGreece where similar materials containing tremolite were used as whitewash. Malignant pleural mesothelimoas have occured in some of these areas (Constantopoulos etal 1991). 8.1.2 Breathlessness While breathlessness relates well to cumulative exposure in asbestos exposed workers, the symptom alone is non-specific. UPDATE: There have been no significant additions to the literature. MOB-HarrisMaster 00303 59 8.1.3 Lung Function Changes While certain changes may correlate well with cumulative exposure to asbestos, not all tests are equally predictive. Some changes are completely non-specific and are influenced by other factors such as smoking, age, race etc. UPDATE: Symptoms and pulmonary function as measures of morbidity were reviewed by Becklake (1994). 8.1.4 Clinical observations These are rarely used in epidemiological studies because ofobserver variation. However, certain well standardized observations may be useful (eg; presence of "rales" or "crepitations")32. In epidemiological studies the frequencies of certain measured outcomes in exposed workers are compared to those in non-exposed workers. The relationships between observations and levels of dust/fibre exposure are also examined to determine if the rate of adverse outcomes increases sensibly with exposure. UPDATE: There have been no significant additions to the literature. 8.1.5 Mechanistic considerations In studies offibre size in relation to fibrosis of the lung in experimental animais, Wright & Kuschner (1977) found that short fibres (glass and blue asbestos) less than 10 um in length did not produce lung fibrosis but that the long fibres did. The explanation for this would appear to be the removal of these shorter fibres from the lung. This and removal of chrysotile through solubility may also explain the observations by McDonald et al (1989) ofdifferent dose-response (radiographic outcome) curves for tremolite and chrysotile. LTDATE- The major new information available since 1990 relates to the importance ofbiopersistence which was discussed earlier. "RjJcs were proposed u one of the more sensow indicator* of `ubcitous* when the British Occupational standard for asbestos was published (BOHS 1968). MOB -HarrisMaster 00304 The fundamental finding is that the parameters which distinguish man-made fibres in terms of their carcinogenicity are fibre length, and fibre biopersistence. The dimension of fibres which distinguish the fibres on the basis ofbiopersistence are much longer than 5 pm (ie: > about 20 pm). Churg et al (1990), based on tissue analyses of amosite exposed workers found that fibrosis grade was positively correlated with amosite concentration and negatively with mean fibre length parameters including fibre length, surface area and mass. When fibrosis grade vs. fibre burden was examined for amosite, chtysotile and tremolite, the relationships were statistically different. These findings indicate that the amosite concentrations like chrysotile and tremolite concentrations are closely and directly related to fibrosis at the local lung level. The concentration comparison data indicates that fibre for fibre amosite is more fibrogenic than chrysotile or tremolite and that the tremolite is more fibrogenic than chrysotile. The apparent inconsistency in the results from these tissue analyses and the results from the animal studies which show that long fibres are more fibrogenic and carcinogenic than short fibres might be explained in several ways. Timbrell has suggested that fibrotic lungs retain more fibres than do nonfibrotic lungs. The bulk ofairborne fibres are short fibres therefore the use of mean or median length may not accurately reflect the existence of potent very long fibres. In addition as long fibres break apart they are likely to increase the number of short fibres. Certainly in humans, short fibres are unlikely to be important generators of fibrosis because populations exposed to enormous numbers ofshort chrysotile fibres (eg: in mining and milling) do not show higher rates of asbestosis than those in industries where longer fibres are used (eg: in textiles). Dufresne etal. (1996) found that lung cancers in workers with and without asbestosis from Asbestos Township had equal concentrations of retained fibres in the lungs but that those with lung cancer showed a tendency to a higher length to diameter ratio of amphiboles. They also had a 29 percent higher average cumulative smoking index. They found that the geometric means (GM) concentrations were higher in cases than in the controls for chrysotile fibres 5 to 10 pm long in patients with asbestosis with or without lung cancer, for tremolite fibres 5 to 10 pm long in all patients; for crocidolite talc or anthophyllite fibres 5 to 10 pm long in patients with mesothelioma; for chrysotile and tremolite fibres greater or equal to 10 pm in length in patients with asbestosis; and crocidolite, talc or anthophyllite fibres longer than 10 pm in patients with mesothelioma. Green etal (1997] studying textile workers reported a significant positive correlation between lifetime human exposure to asbestos and total lung burden of asbestos fibres. Fibrosis was correlated with both exposure to asbestos and concentration of asbestos fibres in the lung. The concentration of tremolite fibres in the lung provided a better estimate oflung fibrosis than did the concentration of chrysotile. Mechanisms in the pathogenesis of asbestosis have been reviewed by Mossman and Churg (1998], MOB-HarrisMaster 00305 61 9.0 LUNG CANCER The occurrence of lung cancer in certain age groups is not uncommon due to past smoking habits. In North America, almost one quarter of all cancer deaths are due to lung cancer. The American Cancer Society Statistical report for 1978 (American Cancer Society 1978) reported the eventual risk ofdying of lung cancer for white males 20 years of age in 1970 as 5.07%. Thus in a cohort of 100,000 men, approximately 5070 deaths from lung cancer would be predicted to occur if men were followed from age 20 to death. Hughes (1989) noted a lifetime risk in 1982 of approximately 0.07 for a man dying of lung cancer. At this rate, approximately 7000 lung cancer deaths would be expected over the lifetime of a cohort of 100,000 men. While the estimates of "background " may differ somewhat depending on the method of calculation and assumptions made, the numbers are quite large and it is against this background that the risks of lung cancer from asbestos exposure must be measured. The normal variation in background rates can make it very difficult to detect small increases in risk. UPDATE: Carcinoma ofthe lung associated with asbestos exposure has been reviewed in some detail by Churg (1993). The mortality of the Quebec chrysotile miners has now been followed up to the point where more than 80% of the cohort has died. The findings from these studies are discussed in the following sections ofthis report. An important new study is that ofCamus etal (1998). They found no measurable excess risk of lung cancer mortality among women in two chrysotile asbestos-mining regions. These studies included estimates of exposure. The authors concluded that the EPA's model overestimated the risk of chrysotile asbestos-related lung cancer by a factor of at least 10. 9.1 LUNG CANCER RISK, TYPE OF ASBESTOS AND OCCUPATION As noted in the discussion ofmesothelioma, differentiating between asbestos fibre types is important because there is good evidence that different fibres pose different levels of health risk. These differences in risk not only exist between mesothelioma and fibre type, but also between lung cancer and fibre type. Although lung cancer differences are not as striking as for mesothelioma, they are worthy of consideration. Hughes (1991) recently compiled the observed and expected numbers of deaths from lung cancer for various occupational groups, using only deaths 20 years after hire or when data were not available. MOB-HarrisMaster 00306 62 10 years after hire. The results of combining these, by fibre type and industry sectors in which more than one fibre type is represented, are shown in TABLE 10. In all industry sectors, the risks of lung cancer are lower for chrysotile only exposed persons than for those with mixed or amphibole only exposures. The lung cancer risk in the chrysotile textile industry is substantially greater than in the other chrysotile exposed occupations. Since differences in the exposure levels for persons in the various studies reflected in table 10 were not taken into account, the validity of adding the studies together might be questioned. However, this problem is somewhat eliminated in FIGURE 3, where lung cancer risks in different industry sectors can be compared for the "same" levels of cumulative exposure37. These risks range from not detectable in the friction materials manufacturing industry, to risks in textile workers, which are approximately 50 times greater than those in Quebec chrysotile miners and millers (McDonald et al 1983 a). The reason for lung cancer risks being so much higher in textile plants is not yet known. It is hypothesized that it may be related to other materials used in the textile manufacturing process such as mineral oils which were sprayed on the fibres (Sebastien et al 1989). The possibility that the proportion ofvery long fibres in the airborne dust may be responsible still needs further investigation. This difference in risk of lung cancer is not explained on the basis of the tremolite content of the airborne dust (Sebastien et al 1989). to* \r\) In the case of the asbestos textile industry where chrysotile has been the main fibre type used, lung cancer risks may be elevated but mesotheliomas are rare or absent. Thus, in ail chrysotile industry sectors, mesothelioma occurs rarely or is absent. In many studies, persons have been exposed to more than one fibre type. The health experience of these workers may not be directly relevant in considering the possible risk to workers using Dum Dum products where only chrysotile was used. The clear difference in the lung cancer experience of workers in the chrysotile textile industry compared to that of workers in other chrysotile industries suggests that there is something special about that industry. Extrapolation of.the high risks from that industry to the Dum Dum product industry is unlikely to be appropriate, except to err on the side of overestimating risks. UPDATE: Mining and Milling Industry Mortality The updated experience of Quebec chrysotile miners and millers has been reported in a number of papers (McDonald et al 1993; McDonald et al 1997; Liddell et al 1997, 1998). Liddell et al (1997) reported the mortality for 9780 Quebec miners and millers followed from 1935 through 1992. The results (TABLE U9) showed no discemable association between chrysotile exposure and SMR below 300 mpcf.y (roughly 1000 f/cc-yrs). However, higher exposures led to excess mortality from lung MOB-HarrisMaster 00307 \V 63 cancer. At higher levels of exposure, the risk increased with cumulative exposure. The effect of cigarette smoking was far more deleterious as the SMR for' a 20+ cigarette per day smoker was 4.6 times higher than that of a non-smoker. '. TABLE 10. THE OBSERVED & EXPECTED NUMBERS OF DEATHS FROM LUNG CANCER BY FIBRE TYPE AND INDUSTRY SECTOR" Modified from Hughes (1991). FIBRE TYPE INDUSTRY CHRYSOTILE M .MIXED." AMPHIBOLES" Mining & Milling Gas Mask Insulation K?) Misc. Manufacturing Asbestos Cement Textiles TOTAL O E O/E 239 192.7 1.24 6 4.8 1.25 4 4.3 0.93 58 56.3 1.03 94 55.6 1.69 401 313.7 1.28 O E O/E 397 93.7 4.24 77 72.4 2.71 351 225.1 1.56 342 188.9 1.81 167 536.1 2.18 O E O/E 91 34.5 2.64 *> * 15.8 2.09 84 17.5 4.80 208 67.8 3.07 This table hai been reproduced with tome modification from dial prevented by Hughe* (1991). The fiction product* industry wu ebmiiuicd from the original ^cnplanm bfra mr t had no"meted* or araphibote* eqiavaiau for companion. The totals reflect this change. The table has otherwise retained the claudication used by Hughe* although it is noted that Hughe* included as 'chryiotfle texhle*. the plant studied by Robinson &jJ (1979). While this plant used mainly chrysoole. varying quanaoes of amoste and blue aibcsto* were also used. ^"*3ased on the following publications... McDonaldgjJ(1980);Rubinoail(1979); Acheson sui (1912); Wets* (1977); Thomas eyj (1982); Ohlson iHognedt (I95); Gardner Ul(1986); McDonald ct si (1983a); Robmson ctal (1979). ^Based on the following publications.. SeUkoffsUi (1979); McDonald sul (1913b); Enterimesul (1917); Petofljl (1983); Hughe* ct al (1987* Newhousc Ul (1985); Afbm jLii (1984); Riffin ajl (1989); Fmkektm (1914); Afie^Psdcn Vaflcron (1915); Laquet sLll (1910); ^Based on the following publications- Armstrong snl(l9SI); Jones gjl (1910); McDonald A McDonald (1911); Acheion flj| (1984); Sddman et al (1916) MOB-HarrisMaster 00308 FIGURE 3 EXPOSURE - RESPONSE RELATIONSHIPS FOR VARIOUS OCCUPATIONAL GROUPS (AFTER MCDONALD 1984) 64 Jlciuivt riu Cuodsnc apmia arc the Mm of th* produca ofexposure level and duonoo ofexposure over a working Ufgnmg and an ctpreaaod in cooccatnaoo-ycan. Tb* Cfimana uot tnprfrrfs* to cnlboQS of parricia/eubic foot Prior to tho lata 1960% dust enw^htnnqf a (forth America wen meaosed oamg a known m ds Thi \sd udiy ii (be mesabma filter phase corunat macroscopic to which *'~^*+'*r**j**** b% ffporTfd in fibccsfcc* Then cu%n(F2GlJR3)wercccoaucscdumgfh6ccpaunmajwuijui&aKd&thaarig(ajiitudiei.Ifclosures wcrcetpraaedBfibn^ce-yetnlbe axce would have changed but (be overall pancra of differrocca in risks xa the different industry sooon would rcauhtlbe units, fibra/ml (J7ml) and fibne/cc m(I7cc) an treated lynocymouaiy. MOB-HarrisMaster 00309 66 When the Quebec chrysotile miners' lung cancer and mesothelioma experience was examined in a case-referent study by the geographic area in which mines were located, the following was found: Miners in a Central area (A) had a statistically significant excess of lung cancer and of mesothelioma (ORs 1.98 and 2.55 respectively). The odds-ratios for the peripheral area (B) were not significant (1.09 and 1.11 respectively). The Likelihood ratio comparing the two areas for lung cancer was 8.25 (or p < 0.004 for lung cancer). The rates ofmesothelioma in the two areas were statistically significantly different (p = 0.03). The time weighted exposure of the referents in areas A and B for lung cancer were 15.1 and 20.7 mpcfrespectively, and for mesothelioma were 17.4 and 16.3 mpcf respectively. Thus the effect was not due to differences in levels of exposure. The tremolite content of the lungs ofworkers employed in the central area were much higher than those in the periferal area. Thus, the results indicate that mesothelioma and lung cancer risks in chrysotile miners are related to the fibrous tremolite and not to the chrysotile exposure (McDonald & McDonald 1997). Textile Lung Cancer Risks Since 1990, attempts have been made to better understand the reasons for the high cancer risks in the textile industry. Several hypotheses have been proposed including chrysotile fibre length, amphibole fibre length, amphibole exposure and oils. Gibbs (1997, 1999) raised the possibility that long amphibole fibres may be responsibile for the difference between the miners and textile industry lung cancer risks. He pointed out that based on the limited data from the study of fibre in tissues from miners and textile workers by Sebastien et al (1989) that the percentage oftremolite fibres longer than 20 um was 11 times greater in the lungs of textile workers than in the lungs ofminers. The size distributions ofthe chrysotile fibres were only slightly different. Recent analyses oflung tissue by Case and Dufresne (1999) confirm the earlier findings of Sebastien et al (1989) that the hmgs ofalmost 40% ofthe textile workers' lungs examined contained crocidolite and amosite. More importantly, these studies showed that the amphibole fibres in the lungs oftextile workers were longer. Thus it seems quite plausible that the excess risk in this industry may be due to long amphibole fibres. MOB-HarrisMaster 00311 67 Dement (1991; 1998) examined the question of oil use as a factor in explaining the high lung cancer risk in textiles. He concluded that only a modest reduction (at most) in the slope occurred after controlling for mineral oil exposures. He considered the possible role of longer, thinner, more carcinogenic fibres in textile as a plausible explanation needing further investigation. Scientific opinions differ on whether oils are still to be considered a factor. Luna cancer risk estimates Based on his studies Dement estimated that the lung cancer risk increment per fibre/cc-year was 0.031 (Dement et al (1994). The slope reported by Lash et al (1997) was very similar (0.028) based on these same data. The slope derived from the Quebec chrysotile mining data published by McDonald et al (1993) was 0.0002. The lung cancer risk estimates reported by Lash et al (1997) who reviewed the various exposureresponse studies for chrysotile are discussed in section 16.2. They re-calculated slopes for studies in which exposure response data existed. Differences between the risks in different industry sectors are clear. Lash claims that between sector differences are greater than the between fibre-type differences. However, it is most probable that there are major between fibre-type differences within individual Industrial sectors. An example of such a difference is the difference in the mesothelioma risks between chrysotile and blue asbestos in gas mask workers. Thresholds of risk. Over the past 10 years there has been growing acceptance of the possibility that a real or at least practical threshold exists. Meldrum (1996) in an HSE report stated: "However, the balance of toxicological evidence does not support the no-threshold model for asbestos-induced lung cancer." Others have also examined this concept. While proving the negative is impossible, the evidence is certainly compatible with such a concept or at least non-linearity, with, for practical purposes undetectable risks at low exposures. Hgren & Browne (1991) examined the evidence for a threshold in animals and humans and the question was examined specifically for chrysotile by Browne & Gibbs (1998). Using Quebec chrysotile mining data, Vacek (1997) found a threshold effect using a linear relative risk model and found exposure intensity to be a better fit than cumulative exposure. However, Stayner et al (1997) applying models to textile data did riot find support for a threshold type of response. In view of two studies now which show that a substantial faction of the textile workforce was exposed to amphibole fibres, this study should no longer be considered a pure chrysotile cohort. MOB-HarrisMaster 00312 68 Asbestosis and Luna Cancer In the 1990's significant scientific discussion has centred on the relationship between asbestosis and lung cancer with views expressed in favour and against asbestosis, pathological or radiological being an essential pre-cursor (Churg 1993, Hughes & Weill 1991; Weill 1994; Jones ct al 1996; Weiss 1999; Abraham JL 1994; Roggli et al 1994; Egilman and Reinert 1996; Wilkinson et al 1995; Banks et al 1999; and Case & Dufresne 1997). While authors have invoked animal studies, case reports and anecdotes to support their contentions, the answer to the question must come from epidemiological studies. There are to date only three specifically designed to answer this question The first showed that the lung cancer risk 20 years after hire was not increased in the absence ofparenchymal changes of 1/0 or greater. The study involved 839 men examined in a cross-sectional morbidity study in 1969 (Hughes and Weill 1991; Weill 1994; and Jones et al 1996). This study was strong in the sense that the authors had quantitative exposure estimates for each individual based on measurements in the industry and the study was based only on workers who had radiological changes on entering the study. This study also found no relationship between pleural changes and lung cancer. A criticism leveled at the study was principally its statistical power. Sluis-Cremer (1991) examined the relationship between asbestosis as diagnosed at autopsy and lung cancer. He was able to take into account age, smoking, residence time and cumulative exposure to amphibole asbestos in fibres/ml-years. The most significant predictor oflung cancer was the presence of asbestosis with an improvement in the likelihood chi-square of 30.1. The study results are shown in Table Ull. TABLE Ull. RELATIONSHIP BETWEEN ASBESTOSIS AND LUNG CANCER (FROM SLUIS-CREMER 1991) Asbestosis No of persons Expected Cancer SPMR diagnosed at necropsy Cancer as on death certificate SPMR None 302 12.4 11 88.7 8 64.5 Slight 69 3.6 15 416.7 11 305.6 Moderate- 28 1.6 9 pronounced 562.5 6 375.0 In the third study (Wilkinson et al 1995), occupational histories and smoking histories were obtained from 271 patients with a confirmed diagnosis of primary lung cancer and 678 referents. Workers were assigned to definite or probable exposure to asbestos more than 15 years before diagnosis. The extent of fibrosis was read by three readers. A previous reader blanked out changes such as tumour mass or lymphadenopathy using a silhouette over no more than two quadrants. These authors MOB-HarrisMaster 00313 concluded that their results did not suggest that radiological evidence of fibrosis was a prerequisite for asbestos-related lung cancer. The many weaknesses ofthis study were pointed out by Browne (1994); Weill et al (1995) and Weiss (1995). Jones et al (1996) reviewed the whole field and also identified weaknesses in the study by Wilkinson et al (1995). In contrast to the studies by SluisCremer and Hughes and Weill in which well defined populations, personal quantitative exposures were available and biases largely avoided, the evidence from the Wilkinson study must be interpreted in terms of its weaknesses. Jones et al presented their evidence for asbestosis being a pre-cursor of lung cancer as follows: In a series of post-mortem lung specimens from patients with asbestos and silicosis there were 13.2% and 1.3% oflung cancers respectively. In the study by Doll (1955), all lung cancer cases had asbestosis. Kipen et al (1987) reported that of 138 cases of lung cancer in insulation workers, all had histological evidence of lung fibrosis and 85% also had radiographic evidence of fibrosis. If all the lung cancer cases in insulation workers have asbestosis, then all the excess lung cancer must be in persons with asbestosis. Newhouse and Wagner reported moderate or severe histological asbestosis in necropsy specimens of confirmed lung cancer cases in ex-workers in an asbestos factory. Excess lung cancer deaths in populations exposed to asbestos generally start at about the same cumulative exposure levels as those at which asbestosis begins to appear. The Hughes & Weill study was prospective, had individual smoking and exposure information and radiologic status at outset of observation. The excess risk of lung cancer was restricted to workers with radiographic evidence of asbestosis, a finding consistent with the view that asbestos is a lung carcinogen because of its fibrogenicity. Sluis-Cremer & Bezeuidenhout found histological asbestos was significantly associated with the presence of bronchial cancer. Increased risks of lung cancer have been reported in studies in which fibrosis has resulted from factors other than asbestos (ie: idiopathic pulmonary fibrosis) Based on their analysis they concluded that "While the issue of whether asbestos is a necessary precursor to asbestos-attributable lung cancer cannot at this time be considered settled, the weight of the available evidence strongly supports this proposition". MOB-HarrisMaster 00314 70 They also noted: Lung fibrosis ofmany causes - known and unknown - is associated with an increased risk of lung cancer. The much discussed synergism between asbestos exposure and smoking found in mortality studies of insulation workers turns out to be a synergism involving asbestosis not just asbestos exposure. The site of.origin and cell type ofa lung cancer are not regarded as reliable indicators of causation (or non-causation) by asbestos. In asbestos inhalation experiments, animals develop excess lung tumours only when lung fibrosis is produced. Pleural plaques have not proved to be a reliable marker for an increased risk of lung cancer. The Helsinki report (Criteria document 1997) states that in their view "Heavy exposure in the absence of radiologically diagnosed asbestosis, is sufficient to increase the risk oflung cancer". They note that asbestosis is an "indicator of high exposure". Further they suggest that "Asbestosis may also contribute some additional risk of lung cancer beyond that conferred by asbestos exposure alone. Asbestosis diagnosed clinically, radiologically (including HRCT, or histologically can be used to attribute a substantial causal or contributory role to asbestos for an associated lung cancer". Pleural plaques alone were not considered indicative of adequate exposure to attribute lung cancer. In this case, a history of substantial asbestos exposure or high tissue burden of fibres should be required. Unfortunately different studies still use different definitions of asbestosis. The relevance of the debate concerning lung cancer and asbestosis to Dum Dum exposures is two fold: If radiological changes are predictors of risk, the levels of exposure associated with Dum Dum products even with a lifetime of continuous use (say 20 years at 0.01 ficc) is still more than two orders of magnitude beiow that at which one might begin to be able to discern any change radiologically. Therefore there can be no doubt that working with Dum Dum cannot increase lung cancer risk if radiologically defined asbestosis is a pre-cursor to lung cancer Asbestosis occurs as a result of long and high exposures. In fact, Dum Dum workers are never exposed to high fibre concentrations. If pathological changes are predictors of risk, it is still highly improbable that at these levels of exposure even pathological changes compatible with asbestosis would occur. MOB-HarrisMaster 00315 71 As smoking and other exposures can give rise to parenchymal fibrosis, the level of chrysotile exposure associated with working with Dum Dum is such that it is highly improbable that any pathological change, even in a worker continuously with Dum Dum for 20 years is due to any Dum Dum related exposure. It is clear that in the absence ofany parenchymal radiological changes consistent with asbestosis, the likelihood that a lung cancer is asbestos related, if not nil, must be extremely small. Therefore at cumulative lifetime exposure levels such as those associated with the use of Dum Dum the risk of lung cancer may in fact be zero and for practical purposes is zero. 9.2 SMOKING It is important to consider the magnitude ofthe risk of lung cancer associated with smoking. TABLE 11 modified from Hammond et al (1979), clearly indicates the importance of smoking. The asbestos workers were insulation workers and the "control" population was the 73763 men in the Cancer Society's prospective cancer prevention study. The risk of lung cancer for non-smoking asbestos insulation workers is 5 times that of non-smoking, non-asbestos exposed workers. The risk of lung cancer for asbestos exposed insulation workers who smoke is 53.24 which is more than 10 times that of non-smoking, asbestos exposed insulation workers. This effect of smoking is termed "multiplicative" because smoking multiplies the risk posed by the asbestos exposure. McDonald (1984) showed that effects were more additive than multiplicative in chrysotile mine and mill workers as shown in TABLE 12. The risk of lung cancer for chrysotile miners and millers who are heavily exposed non-smokers is 6.9 times that of the non-smoking miner or miller with little exposure. The risk of lung cancer for the heavily exposed but moderate smoker is 12.8 times that of the "little" exposed non-smoker. Thus, moderate smoking almost doubles the risk so it is not possible to say whether the risk is simply the sum of the individual risks of heavy exposure (6.9) plus the risk of moderate smoking (6.3) or a risk of 6.9 multiplied by 2. These risks might be considered to be "additive" as opposed to multiplicative. TABLE 11. EFFECTS OF SMOKING & ASBESTOS EXPOSURE ON LUNG CANCER RISKS Group Control Asbestos Control Asbestos Asbestos insulation workers Hammond et al 1979 Exposure to Asbestos History Cigarette Smoking? Death Rate /100000' No No Yes No No Yes Yes Yes 11.3 58.4 122.6 601.6 Mortality" Ratio 1.00 5.17 10.85 53.24 *Mortiirty ra&oa the nio of deiih me relative tdtraeqMcdxm'aaoldncpopulitioa. MOB-HarrisMaster 00316 TABLE 12. EFFECTS OF SMOKING & ASBESTOS EXPOSURE ON LUNG CANCER RISKS Quebec chrvsotile miners & millers39 McDonald 1984 Asbestos Exposure Non Smokers Moderate Smokers Heavy Smokers Little 1 6.3 11.8 Moderate40 Heavy41 2.0 6.9 7.5 12.8 13.3 25.0 *Thec <re ntb relurv to tfao rak for ooD-cmokznf wcrtoi wah cxpout. *Modercle expocure is csssoli&ve ecpocure of 30*300 mpcf*yn imanabrnci to Age 45. "Harvy expocure is cmnuktrvo exposure greater this 300 mpefyn accumulated to age 45. Smoking habits must be taken into account in study design or in interpreting findings. It might be noted that for both chrysotile miners and millers and insulation workers the risk of lung cancer is increased more by smoking than by asbestos exposure. For example, the risk of lungcancer for moderate smokers with little asbestos exposure in the chrysotile mining & milling industry is more than 6 times that ofnon-smokers with the same exposure while moderate asbestos exposure increases the risk for a non-smoker twofold. In insulation workers, the lung cancer risk in non-smoking, asbestos exposed workers is 5 times that ofnon-smokers who are not asbestos exposed whereas the risk for workers who smoke but are not exposed to asbestos, is almost 11 times that ofnon-smokers who are not asbestos exposed. See TABLES 11 & 12. UPDATE: There have been several developments concerning smoking in recent years. The American Cancer Society follow-up study has shown that there was a major increase in the risk of lung cancer associated with cigarette smoking between the eariier study (CPS1) and the more recent study (CPS II).(See TABLE U12). A study of smokers in Quebec Canada by Siemiatycki et al (1994) has shown that lung cancer risk increases considerably with cumulative exposure to cigarettes. The magnitude of this increase in risk is shown in TABLE U13. Thus smoking is a very important parameter. This is especially important because studies of friction product manufacturing workers exposed to low levels of chrysotile (Berry & Newhouse 1983, Newhouse & Sullivan 1989, Berry 1994) did not show any increase in lung cancer risk. As those workers would have included smokers, there is clearly no evidence of synergistic effects at these levels of exposure (at least adequate for any risk to be detected). MOB-HarrisMaster 00317 73 McDonald et al (1993) reported on the mortality from 1976 to 1988 of the 1891-1920 birth cohort of Quebec chrysotile miners and millers and examined the relationship between exposure and cigarettes smoking. They showed that the asbestos effect is greater for the non-smoker than for the smokers or ex-smokers. The authors examined the relationship between lung cancer and smoking which showed standardized mortality ratios for lung cancer of0.47 for nonsmokers; 0.67 for ex-smokers, 1.09 for those smoking less than 20 cigarettes per day and 2.41 for those smoking 20 + cigarettes per day. This increase in lung cancer risk from nonsmokers to a 20 + cigarettes per day smoker is about five fold. The overall asbestos effect was only 1.13 being highest for the non-smoker 1.65 and lowest for the greater than 20 + cigarette per day smoker (0.90). They concluded that the interaction between cigarette smoking and asbestos was "less than multiplicative and far from simple". TABLE U12. COMPARISON OF LUNG CANCER DEATH RATES BETWEEN CPS-1 AND CPS-11 FOR MALES OF ALL RACES WITH PREVALENT CANCERS INCLUDED ( Data from the Smoking and Tobacco Control Monograph, Appendix 4 provided by CDC) Lung Cancer Death Rates for Males of AH Races, 20 Cigarettes Per Day, Duration Fixed at Entry into the Study, 5+ Deaths in Cell CPS-1 Rates Duration Age 30-34 35-39 40-44 45-49 50-54 64.5 154.7 55-59 122.8 127.4 149.9 60-64 220.7 269.5 312.6 65-69 330.2 449.5 70-74 304.1 75-79 CPS-11 Rates Duration Age 30-34 35-39 40-44 45-49 50-54 100.0 107.4 55-59 101.3 225.9 289.5 60-64 139.9 323.9 440.5 65-69 550.5 583.7 563.2 70-74 722.9 551.9 75-79 2:,225.5 Lung Cancer Death Rates for Males of All Races, 40 Cigarettes Per Day, Duration Fixed at Entry into the Study, 5+ Deaths in Cell CPS-1 Rates Duration Age 30-34 35-39 40-44 45-49 50-54 67.8 55-59 136.1 189.8 327.1 60-64 319.7 478.6 374.6 65-69 803.5 785.7 70-74 CPS-11 Rates Duration Aee 30-34 35-39 40-44 45-49 50-54 188 174.4 55-59 161.5 235.2 354.8 60-64 540.7 526.0 404.4 65-69 811.1 851.7 836.6 70-74 1,380.3 1,356.2 Note: Rues n presented for ill cells with five or men hots cancer deaths. Ptrson*yesrs of obsovadon sad deaths accrue m the age group that an individual was m ir (he year of followup (age advance) but accrue to the duration category at the time of entry to the study (duration fixed). Key: CPS~Caaccr Prevention Study. MOB-HarrisMaster 00318 74 TABLE U13. ODDS RATIOS* BETWEEN CIGARETTE SMOKING AND LUNG CANER, FOR EVER-SMOKERS AND FOR SUBGROUPS DEFINED BY CUMULATIVE AMOUNT SMOKED, BY TWO CONTROL GROUPS (from Siemialycki et al 1994). ORi: Adjusted for tgr, ORJ: also adjusted for socioeoooocnic sums and ethnic group; ORj: also adjusted for a priori occupational confounders; OR4: also adjusted for daU*based occupational coefounderr, 95% Cl - 95% confidence interval for ORa Control Group and Smokine Status Cancer controls Nonsmoker Ever-smoker Cigarette-years 1-500 501-1,000 1,001-1,500 a 1,501 Number of Number of Odds Ratios Cases Controls Q&i QS2 OR3 OR* 13 336 844 1,371 1.0 1.0 1.0 1.0 14.7 13.1 14.1 15.8 60 350 209 463 248 324 327 234 4.3 4.1 4.4 4.9 10/7 10.0 10.7 12.3 20.1 17.8 19.1 21.3 34.6 30.5 33.0 37/5 95% Cl for OR* 8.7-29.1 2.6-9.4 6.6-22.6 11.5-39.5 20.2-69.5 Population controls Nonsmoker Ever-smoker Cigarette-years 1-500 501-1,000 1,001-1,500 >1,501 13 844 60 209 248 327 105 428 101 143 111 73 1.0. 1.0 1.0 1.0 16.1 14.7 15.0 17.3 9.2-32.5 4.8 4.6 4.7 5.4 11.6 10.8 11.3 12.8 20.4 19.0 19.6 23.0 37.2 34.7 35.6 42.2 2.7-10.8 6.6-24.7 11.8-45.0 21.4-83.2 9.3 OTHER FACTORS It is well established that agents other than asbestos and cigarette smoking are associated with increased risks of lung cancer. Some of the chemicals listed as confirmed or suspected human carcinogens by the American Conference ofGovernmental Industrial Hygienists are shown in TABLE 13. Many of these have the lung as a possible site for the cancer. Workers may encounter one or more of these as part of their work, hobbies or even by virtue of where they live. Elsewhere in the literature, materials such as man made mineral fibres, silica, herbicides and cadmium among others are mentioned as possibly increasing the risk of lung cancer (Hunter 1987). The radioactive gas radon and radon daughters, which can be present in homes in some parts ofthe country, has been well established as increasing lung cancer risk in uranium and certain other underground mining industries. These are just a few ofthe other factors which need consideration in evaluating lung cancer aetiology. MOB-HarrisMaster 00319 TABLE 13. CHEMICALS LISTED AS CONFIRMED (Al) OR SUSPECTED CARCINOGENS (A2) BY ACGIH AJ. 4-AMINODIPHENYL BIS-CHLOROMETHYL ETHER HEXAVALENT CHROMIUM COMPOUNDS BETA-NAPHTHYLAMINE 4-NITRODIPHENYL ZINC CHROMATES BENZIDINE CHROMATE PROCESSING (CHROMATE) COAL TAR PITCH VOLATILES NICKEL SULPHIDE ROASTING VINYL CHLORIDE 75 A2 ACRYLAMIDE ACRYLONITRILE ARSENIC TRIOXIDE PRODUCTION BENZENE BENZO(A)PYRNE BERYLLIUM & COMPOUNDS 1,3 BUTADIENE CHLOROMETHYL METHYL ETHER CHRYSENE 3.3' -DICHLOROBENZIDINE DIMETHYL CARBAMOYL CHLORIDE 1,1- DIMETHYL HYDRAZINE DIMETHYL SULPHATE ETHYLENE DIBROMIDE ETHYLENE OXIDE FORMALDEHYDE HEXACHLOROBUTADEENE HEXAMETHYL PHOSPHORAMIDE LEAD CHROMATE METHYLENE CHLORIDE METHYLENE BIS (2-CHLOROANILINE) 4,4'METHYLENE DIANILINE METHYL HYDRAZINE METHYL IODIDE NITROPROPANE N-NITROSODIMETHYLAMINE N-PHENYL-BETA-NAPTHYLAMINE PHENYLHYDRAZINE PROPANE SULTONE BETA-PROPIOLACTONE PROPYLENE IMINE O-TOLIDINE O-TOLUIDINE P-TOLUIDINE VINYL BROMIDE VINYL CYCLOHEXANE DIOXIDE UPDATE: In the 1992 report it was noted that it was well established that agents other than asbestos and cigarette smoking are associated with increased risks of lung cancer. Other chemical substances Some of the chemicals listed as confirmed or suspected human carcinogens by the American Conference of Governmental Industrial Hygienists were shown in TABLE 13, many of which had the lung as a possible site for the cancer. This table has now been updated (TABLE U14). There are several new lists ofsubstances classified as carcinogens which might be consulted to identify possible MOB-HarrisMaster 00320 76 carginogenic exposures. IARC, as of Nov 1998 listed 75 Group 1 chemicals, mixtures or exposure circumstances classified as carcinogenic to humans, 59 probably carcinogenic, and 227 possibly carcinogenic. The National Toxicology Program - Management status reports are produced from NTP Chemtrack system and identify carcinogenic substances. There is still scientific debate concerning the carcinogenicity of some of the substances on these lists. TABLE U14. CHEMICALS LISTED AS CONFIRMED (Al) OR SUSPECTED CARCINOGENS (A2) BY ACGIH AL 4-AVONODIPHENYL ASBESTOS BENZIDINE BIS-CHLOROMETHYL ETHER CHROMIUM HEXAVALENT CHROMIUM COMPOUNDS NICKEL NICKEL SULFIDE ROASTING VINYL CHLORIDE ZINC CHROMATES ARSENIC BENZENE BERYLLIUM CHROMATE PROCESSING (CHROMATE) COAL TAR PITCH VOLATILES p NAPHTHYLAMINE NICKEL SUBSULPHIDE URANIUM WOOD DUST A2 ACRYLONITRILE BENZ(A)ANTHRACENE BENZO(A)PYRENE 1.5 BUTADIENE CALCIUM CHROMATE CHLOROMETHYL METHYL ETHER 1.4 DICHLORO-2-BUTENE ETHYLENE OXIDE LEAD CHROMATE 4-NITRODIPHENYL SULFURIC ACID VINYL FLOURIDE ANTIMONY TRIOXIDE BENZO(B)FLUORANTHENE BENZOTRICHLORIDE CADMIUM CARBON TETRACHLORIDE DIAZOMETHANE DIMETHYL CARBAMOYL CHLORIDE FORMALDEHYDE 4,4'-METHYLENE BIS STRONTIUM CHROMATE VINYL BROMIDE Radon In the 1992 report, the radioactive gas radon and radon daughters were noted as substances which could be present in homes in some pans of the country. It was also noted that radon and radon daughters had been well established as increasing lung cancer risk in uranium and certain other underground mining industries. Since that time, there have been several studies ofhomes, some of which have claimed or reported an increased risk and others reporting that they did not find any MOB-HarrisMaster 00321 77 l - y increased risk (Samet 1992; Chaffey & Bowie 1994; Auvinen et al 1996; Letoumeau et al 1994; Pershagen et al 1994; Lubin & Steindorf 1995; Leenhouts 1999). Environmental Tobacco Smoke fETSl In the 1990's, a debate centred around the risk of lung cancer for persons exposed to sidestream or environmental tobacco smoke (ETS). In a review, Woodward& McMichael (1991) concluded there was an increased risk. Fonthom et al (1994) in 5 metropolitan areas of the US found an increased risk for non-smoking women. A recent international multicenter study found "weak evidence" of a doseresponse relationship between the risk of lung cancer and spousal and workplace ETS (Boffetta et al 1998). Other publications offer other opinions (Lee & Forey 1999; Denson 1999). Lung Cancer Latency The point at which a cancer process is initiated is not known and depends on the actual mechanism by which the cancer occurs. If epidemiological studies have shown a link between exposure and the occurrence of lung cancer then some indication of the exposures which might have,potential to contribute to risk can be inferred from the data For example, Mustacchi (1996) argues that because insulation workers exposed less than 15 years before death did not show a statistically significant excess mortality from lung cancer, -,.J while all longer categories of latency did, the latency for lung cancer (at least in insulation workers) most probably exceeds 15 years. On this basis, any exposures occurring in the last 15 years before death are unlikely to have contributed to the occurrence of the cancer or death. He goes on to argue that exposures in the period prior to the last 15 years should be considered cumulative contributors' to a decedent's fully materialized risk of 100% (ie: in the case of an individual who died with lung cancer). Based on the risks of dying from lung cancer in the various periods (TABLE U15) and cumulating all those risks he estimated the proportionate contributions to risk. Unfortunately, a serious limitation ofthe insulation worker's study is that level of exposure or nature of exposure was not taken into account. There is ample evidence that these are important. The calculations cannot be applied to industrial sectors where there is no human evidence of an increased lung cancer risk. While the application of this latency concept for risk apportionment is appealing it would only be a reasonable way of apportioning risk if the level and nature of exposure and other factors are taken into account and if there is epidemiological evidence that at these latencies there is a detectable increase in lung cancer risk in workers with that type and level of exposure. This is not the case with some chrysotile cohorts such as friction product manufacturing workers. Mustacchi (1996) attempts to overcome the issue of exposure level using the experience of amosite factory workers where he argues that the latency shortens with increasing cumulative exposure and that at 50f-y/ml the risk falls below that suffered by the insulation workers. Therefore it would be MOB-HarrisMaster 00322 reasonable to consider as unlikely an asbestos etiology for lung cancer developing in less than 15-19 yean in an individual with a cumulative exposure of25-49 f-y/ml or occurring in less than 20-24 years in the presence of a cumulative exposure of 6-24 f-y/ml or in less than 25-29 years when the cumulative exposure is less than 6 f-yr/ml. TABLE U1S. ESTIMATES OF CONTRIBUTIONS TO LUNG CANCER RISK BY LATENCY PERIOD BASED ON INSULATION WORKER DATA. LATENCY <15 15-19 20-24 25-29 30-34 TOTAL RISK/100000PERSON/YEAR 64.5 147.6 340.5 679.0 1230.6 PROPORTIONATE CONTRIBUTION % 0 5.2 12.0 27.7 55.1 10.0 GASTROINTESTINAL CANCER Selikoff et al (1964), in a study of insulation workers, reported that there was an excess of gastrointestinal cancer. As mentioned earlier these workers were most likely exposed to mixed chrysotile/amphibole fibres. Since that time there have been a number of cohorts studied where an excess of gastrointestinal cancer has been claimed and others where the results have been negative. The epidemiological studies have not shown consistent excesses of gastrointestinal cancers of specific sites. Thus, there is still controversy over whether gastrointestinal cancer risks are increased. Edelman(1988) reassessed the results of32 published cohort studies and he concluded that "asbestos workers are not at an increased risk of gastrointestinal cancer". .As will be shown later in this report, the levels of exposure to fibres from "Durr. Dum" are such that gastrointestinal cancer risks do not require further consideration. UPDATE: Liddell (1994) reporting on mortality in chrysotile miners concluded, "There is no evidence that the risk of stomach cancer is adversely affected by exposure to chrysotile; and there is no evidence of increased risk of other abdominal malignancies". .An excess of GI cancer has been reported in insulation workers who have been exposed to chrysotile and amphibole fibres (Selikoff & Seidman 1991). MOB-HarrisMaster 00323 79 11.0 OTHER CANCERS The question of whether laryngeal cancers are associated with exposure to the various asbestos minerals is doubtful but still debated. Liddell (1991) in reviewing previous evidence opined that" the evidence on the link between exposure to asbestos and laryngeal cancer has failed to satisfy accepted criteria for causation". He noted that the Industrial Injury Advisory Council (UK) had recently recommended that, on the balance of the evidence, cancer of the larynx should not be added to the schedule of prescribed diseases in respect of occupations involving exposure to asbestos. There have been studies ofwomen working with blue asbestos where an excess of cancer of the ovary has been reported (Acheson et al 1982). Whether these were cancers of the ovary or mesothelioma remains unclear, as does the possibility of an association between asbestos and cancers of this site. There have been claims in the literature that cancers of other sites, such as the kidney, might be associated with asbestos exposure, but the cases appear to be isolated. My review of the evidence concerning kidney cancer indicates that if there is an increased risk, it is not associated with chrysotile. UPDATE: There has been no information to change the situation as stated in 1992 and elsewhere in this report. 12.0 TALC Although chrysotile was the only commercial asbestos used in the Dum Dum products, some contained talc. Talc, under some circumstances, has been shown to be contaminated with asbestiform tremolite, anthophyllite and chrysotile. Contaminants of the talc will be encapsulated in the Dum Dum products in the same way as the talc, chrysotile asbestos and other constituents. None-the-iess, talc and the possibility of tremolite contaminants will be considered for completeness. Talcs do not always contain tremolite, much less asbestiform tremolite or other asbestos fibres. After the mid-I970's Mobil purchased only tremolite free talc for use in its Dum Dum products. This does not mean that the talc before that time contained asbestiform tremolite but provides assurance that it did not, after that time. The presence of tremolite does not necessarily mean the presence of asbestiform tremolite. There is considerable debate concerning the importance of cleavage fragments of tremolite. However as will be seen later in this report, the very low dust concentrations associated with applying or removing Dum Dum compounds do not make lung fibrosis from the asbestos minerals or tremolite contamination of talc a viable consideration. MOB-HarrisMaster 00324 UPDATE: There has been no information to change the situation as stated in 1992. 80 13.0 ASSESSING HAZARD AND RISKS In an earlier section it was noted that one of the key factors in the initiation of a disease process was "the characteristics and properties ofthe dust to which the worker is exposed." In this section, characteristics other than fibre type will be considered. The characteristics and properties of a dust which are important in determining its potential to produce a health effect include: a. Particle size, shape and particle density (number of grams/cubic centimetre of the particle). These determine the aerodynamic behaviour and respirability ofthe dust, as well as whether and where the panicle deposits in the respiratory system. b. Panicle size, particle shape and solubility. These determine whether and how long the deposited particle remains at the site of deposition or whether it is removed from the lung. c. Chemistry and mineralogy. These determine the likely reactivity of the dust in the lung or system. d. The toxicity or potential for the dust to produce adverse health effects. e. Associated contaminants which might, in their own right, have the potential to cause health effects or influence the dust effects. UPDATE: No new information. 13.1 PARTICLE SIZE & SHAPE The size, shape and density ofparticles are extremely important in determining whether they get into the lung, and if they do, how well lung defense mechanisms can remove them. The ability of fibres to experimentally induce disease is also size dependent. UPDATE: No new information. MOB-HarrisMaster 00325 81 13.1.1 Aerodynamic behaviour, respirability and deposition Panicles of significance from the standpoint of evaluating the health effects of asbestos, are those suspended in air (collectively known as aerosols) which may be inhaled. Airborne particulates may range in size from molecular dimensions up to about 100 pm in diameter42. The rate at which spherical particles settle out in air is governed by Stokes' Law. This relates the terminal settling velocity of a particle (rate at which it falls in the air) to its density and radius as it falls in non-turbulent air. The aerodynamic diameter is the diameter of a sphere of unit density which has the same terminal settling velocity as the particle of interest. As most dust clouds are made up of particles with a wide range of sizes and densities, it is convenient to consider particles equivalent if they exhibit the same settling rates which are defined by the aerodynamic diameter mentioned above. The physical dimensions of particles are important as they determine the aerodynamics of the particle, its ability to enter the respiratory tract and its behaviour in the respiratory system after deposition. Particles are deposited in the lung by essentially four mechanisms, gravitational settlement, inertial impaction. Brownian movement43 and interception. Particles which can penetrate deep into the alveolar region of the lung are defined as "respirable". Timbrell (1965, 1970, 1973); Timbrell & Skidmore (1971) and Timbrell et al (1970) studied the aerodynamic behaviour of fibres and the relationships between fibre and non-fibrous particle aerodynamic behaviour by measuring particle and fibre deposition rates. They were able to show that length of the fibre was of little importance in determining fibre deposition rates but that, aerodynamically, fibre diameter was extremely important. Based on these relationships and assuming that the upper limit of the diameter of a spherical particle of unit density reaching the lung alveolar region is 10pm, then the expected upper limit of the diameter of asbestos fibres penetrating to the alveolar region would be approximately 3.5um. .Assuming that they are straight, differences in the aerodynamic behaviour of fibres of different types are governed by their fibre densities and their diameter size distributions. The sizes of compact particles found in the alveolar or gas exchange region of the lung are generally 10 pm or less in diameter. On the other hand, fibres of lengths exceeding 100 pm can be found deep in the lung at autopsy. This fits with the lesser importance of length in explaining aerodynamic behaviour. ~iun micrometre or one millionth of > metre and if the standard unit used in describing the size* of small piracies. ^Biuwnun movement means that panicles are moved about m the lung air by bombardment by gas molecules. In this way they get close to surfaces and deposit. Fibre deposition in the lung is governed by essentially the same mechanisms is for spherical particle deposition. MOB-HarrisMaster 00326 82 Interception as a mechanism for fibre deposition in the respiratory airways is very important. Timbrell (1965) showed that there was a definite tendency for fibres longer than 5 pm to align in laminar air flow. He also showed that asymmetry led to a lower rate of alignment which is important because it means that curly fibres or those with adhering particles have a lower chance of penetrating deep into the lung. Timbrell (Davies 1970) suggested that curliness was an important factor in explaining the apparent lower risks ofhealth effects associated with chrysotile asbestos. Using UICC chrysotile fibre samples44 and glass fibres of various shapes, he was able to show a significant reduction in the penetration into the alveolar regions of the lung of curly compared to straight fibres. In a person who breathes through the nose, long fibres, curly fibres and fibres with adhering panicles are likely to be trapped in the nose and to be removed by sneezing or by blowing the nose. If a person breathes through the mouth, the larger airborne fibres, normally trapped in the nose, are deposited by impaction in the upper part of the respiratory system. Whether breathed through the nose or mouth, fibres are rapidly transferred to the mouth, swallowed and excreted. UPDATE: There has been no new information to change the information provided. The importance of aerodynamics, size and shape was reviewed by Lippmann (1994). 13.1.2 Role of particle size in particle removal from the lung The moment that either inert or toxic particles are deposited in the lung, mechanisms to remove them come into play. These can be divided into those that depend on ciliary action and those that act in the non-ciliated regions of the lung. As in everyday life, particles and fibres which are deposited on the tracheobronchial part of the respiratory system are transported by mucociliary action upwards to be swallowed. This method of particle removal can be hindered by damage to the cilia, as through the effects of cigarette smoking, with clearance of particles severely impaired (Cohen et al 1979). If particles are deposited more deeply in the lung, one ofthe most rapid removal mechanisms involves recruitable macrophages (phagocytic cells contained in the alveolar surface epithelium). A particle is engulfed by the macrophage or phagocyte which moves the particle towards the ciliary escalator for removal. Phagocytes may also serve to render the particles incapable of injuring or irritating the tissues. Panicle size and shape are important in clearance from the alveolar surface because shape and dimension may hinder phagocytosis. Allison (1973) examined the limit to the size of particles that W UICC ** (he Iittmavrul Union Against Cancer and under their mipiccs special tcnpka were prepared for use in animal experiment* around the world. There were 2 cnryiodk unties, cne from "Rhode*** and nether from Canada. The liner wu mrnure of fibres from varioua mill* m Quebec. There were also samples of amotue *nd cToadohic front South Africa and of aathophyQite from Finland. MOB-HarrisMaster 00327 S3 could be ingested by phagocytes, using fractions of chrysotile and blue asbestos containing high and low percentages ofshort and long fibres. Independently of fibre type, the short fibres (<5 pm) were rapidly and completely taken up by the phagocytes; fibres longer than 20 pm were never completely taken up; and fibres of length 5-20 pm were sometimes completely ingested. The observation that short (less than 5 pm) fibres are readily removed from the lung has been reported many times in the literature. UPDATE: Bioperistence is very important and has been discussed elsewhere in this report. 13.1.3 Particle solubility Particle solubility is important in assessing health risks. In the case of chrysotile it has been well established that its outer magnesium layer makes it possible for body fluids to dissolve or leach out magnesium. The chrysotile structure is thus steadily dissolved and at a much greater rate than for the amphibole asbestos minerals (Morgan & Cralley 1973). Thus, increased solubility over the amphiboles may be another factor in the decreased retention of chrysotile in the lung. UPDATE: Particle durability is very important and has been discussed elsewhere in this report. 14.0 RISKS OF HEALTH EFFECTS FROM WORKING WITH DUM DUM In section 6.0 it was noted that the risk of disease was related to the following.... i. The characteristics and properties of the dust to which the worker is exposed. ii. The concentrations of the respirable fraction of the dust to which the worker is exposed. iii. Duration of exposure to the airborne dust. iv. Pattern of exposure. v Period since first exposure to time that the worker is examined for health effects. vi. Personal habits of the worker which might directly or indirectly: a. influence the risk of occurrence of a dust related disease(s) or health effect(s) or influence the course of the disease. MOB-HarrisMaster 00328 b. produce a disease indistinguishable from that produced by the dust. 84 vii. Individual personal characteristics or pre-disposing conditions which might directly or indirectly influence the occurrence or course of a disease in that worker. In the following sections the information available for Dum Dum products will be systematically applied in the assessment of the health risks for persons using Dum Dum products. 14.1 CHARACTERISTICS AND PROPERTIES OF AIRBORNE ASBESTOS DUSTS FROM DUM DUM 14.1.1 Asbestos fibre types Earlier in this report it was noted that chrysotile was the only commercial asbestos fibre used in the Dum Dum products. It was also noted that talc was used in some ofthe products. In order to ensure that risks are not in any way underestimated, products will be considered to fit into 4 separate categories. CATEGORY A: Products which contained neither commercial asbestos nor talc. Products in this category include - Chimney Dum Dum Primer CATEGORY B: Products which contained only chrysotile but no talc. Products in this category include - Chimney Dum Dum - Nail Hole Dum Dum - Dum Dum Masonoc - Dum Dum Armorcote CATEGORY C: Products which contained no commercial asbestos as part of their formulations but contained talc. There is no information on whether tremolite was present in the talcs used. Two scenarios can be envisaged. i Products containing no asbestos - This is assured after the mid-1970's when the talc used was tremolite free. It may always have been tremolite free. 2. Products containing some tremolite by virtue of use of talc containing asbestiform tremolite. This is an assumption for which there is no direct evidence. A product in this category is - Dum Dum Masonoc Primer CATEGORY D. Products which contained chrysotile asbestos as part of their formulations plus talc. MOB-HarrisMaster 00329 85 Two scenarios can be envisaged. 1. Product containing chrysotiie only. This can be assured after the mid 197Q's when the talc used was tremoiite free. It may have always been tremolite free. 2. Product containing chrysotiie plus tremolite by virtue of the use of talc containing asbestiform tremolite. .This is an assumption for which there is no direct evidence. Products in this category include - Hi -Heat Dum Dum UPDATE: There has been no new information since 1992 to change the products or their categorization. 14.1.2 Sizes of airborne fibres The composition and size distribution ofthe fibres to which a worker might be exposed are rarely the same as those of the bulk material with which he or she may be working. This is because panicles of different sizes may have different compositions and because size, shape and density determine whether particles, dispersed in air, remain airborne. In the case of Dum Dum products, the commercial grade of chrysotiie fibre used was short (grade 7) (Chamberlain 1991). The production process called for this fibre to undergo several stages of intimate mixing with various resins and oils as well as other inorganic materials and solvents. Thus the product was quite unlike the free asbestos used in its production. Dum Dum products are of putty or mastic consistency. Scanning electron images45 show how the surface of the Dum Dum product forms to encapsulate the fibre and this is evident in the removed product (PLATE 1). This binding of fibres to the matrix and to other fibres is seen in the broken cross-section of a piece of Chimney Dum Dum (PLATE 2) and in the surface clump (PLATE 3). The latter clump of fibres is about 20um in diameter and non-respirable. For comparison, scanning electron images of free chrysotiie at the same magnifications are shown in PLATES 4-5 The difference between the encaspulated and non-encapsulated fibre is quite evident. The material after application dries with a hard surface. A sample of the Hi-Heat Dum Dum after removal, which was dark in colour, was provided to me by Dr Peters (1991). This sample when broken, was still moist and putty-like under the surface layer. There were no overtly visible fibres in the surface of the specimen. While much thinner, fragments of the "dried" Dum Dum Masonoc and Chimney Dum Dum were still very pliable. It is clear at both the macroscopic and electron microscopic level that the asbestos is encapsulated and not likely to give rise to high concentrations of fibres during use or removal of the product. The micrographs were nude svxiUble to me courtesy of Dr E.T. Peten of Arthur D. LmJc Inc.,C*mbridge Misuchuuetis. MOB-HarrisMaster 00330 I' l.A T H MOB-HarrisMaster 00331 MOB-HarrisMaster 00332 iM .A iii . u k o k h n ru o s s -s iic rn o N o f c ih m n h y d u m d u m s h o w in g n o w I'ln m -S ARH I*N ('AI\SUI.ATI*:n. (SHM) MOB-HarrisMaster 00334 PI | . A |( T il I i k'I.l l ; -' I K Ii S li A C M l I IK 'l.l Y S O T II-li i I'K Iil'AK M IM Ii Iil). IN S S A A T M T Ii ill- SAMIi MAGNIFICATION I A IK )KA I(,)R Y AS I'lG U R i; AS I. MOB-HarrisMaster 00335 MOB -HarrisM aster 00336 PLATI2 6 FREE CHRYSOT1LE FIBRES A T THE SAME MAGNIFICATION AS FIGURE 3. SAMPLE PREPARED IN SAME UVBORATORY AS FIGURE 3 PLATE 7. AIRBORNE ASBESTOS STRUCTURES - DUM DUM MASONOC REMOVAL experiment. MOB-HarrisMaster 00337 PLATE 8. AIRBORNE ASBESTOS STRUCTURES - DUM DUM MASONOC .APPLICATION EXPERIMENT. MOB-HarrisMaster 00338 PLATE 9. .AIRBORNE ASBESTOS STRUCTURES - DUM DUM MASONOC APPLICATION EXPERIMENT. MOB-HarrisMaster 00339 .J PLATE 10. AIRBORNE ASBESTOS STRUCTURES - CHIMNEY DUM DUM APPLICATION EXPERIMENT. MOB-HairisMaster 00340 PLATE 11. .AIRBORNE ASBESTOS STRUCTURES - CHIMNEY DUM DUM APPLICATION EXPERIMENT. MOB-HarrisMaster 00341 4 PLATE 12. AIRBORNE ASBESTOS STRUCTURES - CHIMNEY DUM DUM .APPLICATION EXPERIMENT. MOB-HarrisMaster 00342 <8* PLATE 13. .AIRBORNE ASBESTOS STRUCTURES - HI-HEAT DUM DUM REMOV.AL EXPERIMENT. MOB-HarrisMaster 00343 PLATE 14. AIRBORNE ASBESTOS STRUCTURES - HI-HEAT DUM DUM REMOVAL EXPERIMENT MOB-HarrisMaster 00344 PLATE 15. AIRBORNE ASBESTOS STRUCTURES - HI-HEAT DUM DUM REMOVAL EXPERIMENT. MOB-HarrisMaster 00345 w & PLATE 16. AIRBORNE ASBESTOS STRUCTURES - HI-HEAT DUM DUM REMOVAL EXPERIMENT. MOB-HarrisMaster 00346 PLATE IT. .AIRBORNE ASBESTOS STRUCTURES - HI-HEAT DUM DUM REMO\'AL EXPERIMENT. MOB-HarrisMaster 00347 86 From a health effects standpoint, it is the airborne respirable fibres which are important. Dr E.T. Peters (1990, 1991) performed a series oftests with three Dura Dum products, measuring the concentrations of asbestos structures (fibres, bundles, clusters and matrix)46 associated with the trowelled on, spray application and removal ofthe products. Counts of airborne fibre were made using transmission electron microscopy. Chimney Dum Dum was applied to bricks, Dum Dum Masonoc was applied to concrete and Hi Heat Dum Dum was applied to steel sheets; each such product was then removed. As will be described later, the concentrations rarely exceeded the minimum detection limit for the experiments (0.01 asbestos structures/ml). Thus, there were few airborne asbestos structures to examine. Dr Peters provided me with the raw data concerning the dimensions ofthe structures in the airborne dust samples collected and analyzed by him (Peters 1991). a. Dum Dum Masonoc The dimensions ofasbestos structures associated with ten application and removal experiments of this product are shown in APPENDIX Dl. The concentrations measured in these experiments are summarized in TABLE 14. The total number of structures observed in all the Dum Dum Masonoc experiments was 20. Ofthe 20 observed structures, 3 would not have been visible by light optical microscopy (limit of visibility is approx 0.23 pm) and another had a diameter well exceeding 3 pm and would not be respirable. Thus 3 ofthese structures would not have been counted under the rules for counting fibres for compliance with the US OSHA standard47. These fibres have been removed and concentrations recalculated to reflect the concentrations that would have been reported under OSHA rules. These concentrations are ictentified as "PCM Equivalents". See TABLE 14 Based on transmission electron micrographs provided by Dr Peters (1991), the structures observed during the application of this product tended to be bundles offibres with adhering particles rather than individual fibres (See PLATES 7-8). Similar results were seen during removal (See PLATE 9). Such adhering particles were, in some cases, quite large and could possibly have rendered these fibres non-respirable.. w Or Peten ccimdered an asbestos structure to have a length to breadth ratio of3:1 or p-eato and a length of 5pm or more. The OSHA regulations (Appendix A to 763.12I-EPA/OSHA Reference Method-Mandatory - Federal Register 52 No 36-37 February 25 1917 page 5629) require that 'fibre* counts be made by potttiw phaae eoonet microscope* at *toul magraficadoo of approximately 400 X* and counting "only fibre equal to or longer than 5 fiucromeaaa* and countstg * al ptLie* aa ashrstne that have a length to width ratio (aspect ratio) of3:1 or greater*. The method also require* that the microscope used not be able a re*ohcthc&vac&oc*6 A 7ccthsHS phmsdxfitzxr slide. The width of the smallest ridge 7 0.25pm. The assumption of a limit ofviability of 0.23um still allows for the inchmoa ofsame fibres that would not be cotmted by the OSHA method. This mean* that the eooecmndoftt that would have boa annriirM with oat of thii product, had they been determined using phaae contrast fight optical microscopy, 2* teqoaedfiypea*mngcorap&ice with the OSHA p'lmjaHr closure Emit, would hive been much lower, these 'OSHA* equivalent concentrations are recalculated and shown m TABLE 14. ^ <- MOB-HarrisMaster 00348 87 TABLE 14. CONCENTRATIONS OF AIRBORNE STRUCTURES DURING THE APPLICATION AND REMOVAL OF VARIOUS Dum Dum PRODUCTS IN A SERIES OF EXPERIMENTS BY ARTHUR D LITTLE INC. (BASED ON DATA PROVIDED BY PETERS 1991) PRODUCTHi- Heat Dum Dum PROCESS TEM** CONCN s/cc Application 1 <0.01 2 <0.01 Removal Replicate Removal Removal 1 1 2 3 <0.01 <0.01 <0.01 0.01 PCM" EQurv. f/cc <0.01 <0.01 <0.01 <0.01 <0.01 0.01 Dum Dum Masonoc Application IP A Application 2P A 0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 Chimney Dum Dum b. Chimney Dum Dum. Removal IP <0.01 Replicate IP <0.01 Removal 1A <0.01 Removal 2p <0.01 Replicate 2p <0.01 Removal 2A <0.01 Application IP Replicate IP Application A Removal IP Removal IP Removal IP 0.088 0.024 0.024 <0.01 <0.01 <0.01 - <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 0.02 <0.01 <0.01 <0.01 <0.01 <0.01 The dimensions of fibres in the samples collected during the application and removal of this product are shown in APPENDIX D-2. The concentrations measured in these experiments are shown in TABLE 14. TEM * Traramarion dectrem microscopy. Concottmaons are repotted u tmxotres/cc(i/cc). s/cc number ofstructures meeting (he 'ubcfioi structure* definition per l cc of dr. 49 PCM-EQUIV Phise Contrast Microscopic (PCM) equivalent concmtnaoQ. This concentration reproots the concentration (hit would hive been reported hid the filter been counted using phase contrast microscopy and OSHA counting rules. The structures c*ptnfM by transmssion electron microcopy arc considered to be asbestos fibre. TtaK OSHA-oquivikRf fibres are ccnadexed to be those longer than 5pm in length with diameters greater than of0.23pm Conccnratiotti arc expressed in fibrca'ec in fine with the practice m the OSHA standard to ecpnas concentration* in Bbra/cc (f7cc). MOB-HarrisMaster 00349 88 The vast majority ofthe structures observed in the airborne samples taken during tests ofthis product were short and thin. In fact, the majority offibres observed had diameters less than would be visible by light optical microscopy (PLATES 10-12). The relatively high proportion offibres of5-6pm length would suggest that fibres from this product would be dealt with relatively efficiently by macrophages as part ofthe lung protective mechanism if they were to enter and be deposited in the lung (Allison 1973). Combining the size distributions of all the fibres recorded in the Chimney Dum Dum experiment, 37 of the 45 had diameters of 0.2 pm or less (78.7%) and would not be visible by light optical microscopy. This has an important effect on the concentration relative to the OSHA permissible exposure limit. See TABLE 14. c. Hi-Heat Dum Dum The dimensions offibres in the samples collected during the application and removal ofthis product are shown in APPENDIX D-3. The concentrations measured in these experiments are shown in TABLE 14. There were only 11 structures observed in the whole series of experiments with Hi- Heat Dum Dum, ^5^ 1 during product application and 10 during the 3 removal experiments with replicate. While a few ofthe structures observed in samples during removal of the Hi-heat Dum Dum appeared as relatively straight "fibres" (PLATE 13-14), others were quite bent or had large adhering particles which would influence their respirability. PLATES 15-17. None ofthese fibres had diameters less than 0.23 pm,. so all would be visible by phase contrast optical microscopy. UPDATE: There has been no new information since 1992 to change the information on the sizes of airborne fibres. The results as presented in the final reports by Arthur D Little Inc (1992) are shown in TABLE U16. 14.1.3 Asbestos exposure ofworkers applying and removing Dum Dum products UPDATE: The reports describing the production test procedures used by AD. Little are given in Appendix UI. MOB-HarrisMaster 00350 89 TABLE 1716. CONCENTRATIONS OF AIRBORNE STRUCTURES DURING THE APPLICATION AND REMOVAL OF VARIOUS DUM DUM PRODUCTS IN A SERIES OF EXPERIMENTS BY ARTHUR D LITTLE INC. (FROM REPORTS BY ARTHUR D. LITTLE INC (1992). TEM4* PRODUCT PROCESS CONCN s/cc Hi-Heat Dum Dum Application 1 <0.01 2 <0.01 Removal 1 <0.01 Replicate 1 <0.01 Removal 2 <0.01 Removal 3 0.01 Dum Dum Masonoc Application IP 0.01 A <0.01 Application 2P <0.01 A <0.01 Removal Replicate Removal Removal Replicate Removal IP <0.01 IP <0.01 1A <0.01 2p <0.01 2p <0.01 2A <0.01 Chimney Dum Dum Application Replicate Application Removal Removal Removal IP 0.088 IP 0.024 A 0.024 IP <0.01 IP <0.01 IP <0.01 PCM4*9 EQUIV. f7cc <0.01 <0.01 <0.01 <0.01 <0.01 0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 0.02 <0.01 <0.01 <0.01 <0.01 <0.01 TEM " Tansnaaion electron microscopy. Coocaunsoss are reported a xtrucmre*/cc(i/cc). i/cc " number ofstructures meeting the `asbestos structure* definition per I ce of sir. 49 PCM-EQLTV Phase Conoui Microscopic (PCM) equivalent crnrrnrmioc. This concentration represents the concentration that would have been reported had the filter been counted using phase contras txsomcopy sod OSKA couwing rules. The structuree counted by trannmsson electron microcopy are considered to be asbestc* 6brea There OSHA-oquivslcnt fibres are eooadered to be there longer than 5pm m length with diameien greater than of0.23pm Concentrations ire expressed in fibrcs/cc in Kne with the practice in the OSHA standard to eeprere concentra&ORs a fibrcVcc (Pcc). MOB-IIarrisMaster 00351 90 14.1.3.1 Levels of exposure Hodgson (1985), reviewing alternatives to asbestos, noted "Mastics and sealants based on pitch and asbestos are used in coating applications where felts are inappropriate........ In these materials, asbestos imparts the property whereby the mixture remains in a consistent state. Mastics and sealants are marketed in sealed tins and the components must not settle or separate. If the mastic is to be applied to a vertical or sloping surface it must not run or sag, and again this is prevented by the presence ofasbestos..... At present it would appear that asbestos based mastics and sealants have not been superseded by any wholly viable and workable alternative." Cogley et al (1982), in a report on asbestos in commercial and industrial use, described the composition ofasbestos roofing products, coatings and paints and bituminous coatings as virtually all using grade 7 fibre. He noted " The asbestos fibres are thought to be completely bound by all ofthese additives in the final product". In describing the primary manufacture ofsealants mixed with asphalt, tar and solvents or other additives, they noted " shortly after mixing, the asbestos fibre is bound by the asphalt and upon completion of mixing, the asbestos is considered completely bound in the asphalt with little chance of fibre dust exposure." In discussing the release of fibres from wastes, weathering, corrosion, wear and scrap through demolition, they state "...In nearly all of these losses the asbestos fibres should be completely encased in the bituminous binder. Consequently, only small quantities offree fibre are likely to be released" The Consumer Products Safety Commission under the product "Mastic" noted "Since asbestos as an additive reduces embrittlement, the danger of free fibre exposure appears limited" (CPSC 1978). In the guidelines for assessment and abatement of asbestos containing materials in buildings, nonfriable materials are defined as "matrix-bonded composite products" prepared by mixing fibres with various bonding agents such as starch, glue, plastics, cements and asphalt. The degree of bonding of asbestos fibres within the composite material or the fibre's immobilization covers a wide range. Caulking putties and mastics are described as non-friable (NBS 1983). As the fibres in Dum Dum are coated with oleoresinous substances and by design will adhere to other panicles, they will if rendered airborne, tend towards being far less respirable than free fibres encountered in the industries where health risks have been assessed. Crucial to the potential of the product to pose a risk ofhealth effects is the airborne respirable fibre concentration. In the following subsections, the potential for generating airborne asbestos fibre concentrations and the order ofmagnitude ofthe concentrations are discussed. The various products under consideration are applied in a viscous "putty-like" state with the asbestos fibres and other components intimately mixed into a matrix. MOB-HarrisMaster 00352 91 Let us consider the various products in the categories described in section 14.1.1. CATEGORY A. (Chimney Dum Dum Primer) There will be no asbestos exposure as the product does not contain asbestos minerals. CATEGORY B. (Nail Hole Dum Dum; Chimney Dum Dum, Dum Dum Masonoc, Dum Dum Armorcote) i. Nail Hole Dum Dum. As far as could be determined, measurements of exposure to chiysotile asbestos when using this product do not appear to have been described in the literature. However the following is known or can be deduced; The potential for a worker to be exposed to chiysotile asbestos fibre from this product is limited by the asbestos content ofthe product (only 2% chrysotile). * The product is putty-like in consistency which will not readily give rise to aerosols of free fibre or any dust. * The product is applied as a solid encapsulated material and physically pressed into a nail hole. The method to set nails in wood is well known and described in readily available manuals (Readers' Digest 1973). As shown in FIGURE 4, the nail is countersunk below the surface of the wood by placing a "nail set" of slightly smaller dimension than the nail head onto it. The nail is driven in such away as to sink the head below the surface ofthe wood. It is the small space above the nail head which would be filled with the "Dum Dum Nail Hole." In order to avoid damage to the wood surface, this would be pressed into the hole and the surface left flat or level with the wood surface. As the material is a putty-like consistency with the fibre mixed within the "putty", it would be virtually impossible for the applicator to be exposed to fibres during this work. The time taken to fill a hole might be measured in seconds. As the "Dum Dum Nail Hole" would be applied to make the surface ofthe filler level with the wood, sanding would not be necessary and the surface could be painted or varnished further sealing in any asbestos. The nail hole fillers were produced in colours to match the wood colour and texture ofpre-finished woods so that there is only a very remote possibility that the surface containing this filler would ever be sanded. In the event that the surface of the wood was sanded, the surface area of the Dum Dum exposed would be extremely small and the depth of any sanding would be minimal, as the purpose of a nail hole filler is to just cover the head ofnails. As the asbestos content ofthe filler was only 2%, it would be virtually impossible even with aggressive sanding for workers MOB-HarrisMaster 00353 to begin to approach a fraction of the asbestos exposure limits in effect in the USA even today. * The quantity of"Nail Hole Dum Dum" used on a single board would be extremely small. As the product was recessed in the wood on which the product was used, it is difficult to identify even hypothetical situations under which it could give rise to any measurable exposures for persons disposing ofthe wood after its useful life. * It is not known when this product was first manufactured, but it was not manufactured or marketed after 1973. Overall, it is difficult to conceive of any situation under which "Dum Dum Nail Hole" might have been used, where the concentrations of respirable free asbestos fibres would be measurable above background levels by either conventional phase contrast microscopy or electron microscopy. Support for a conclusion that chrysotile asbestos fibre exposure when using Dum Dum Nail Hole would be virtually zero is found in the very low levels of fibre exposure associated with the application of similarly encapsulated Dum Dum products described later in this section. ii. Dum Dum Masonoc. The 95 series Dum Dum Masonoc contained 12-15% asbestos and was a heavy bodied coating of mastic consistency designed for high build application for filling and bridging of cracks and crevices with application by special brush or heavy duty mastic spray equipment. There are several reasons to conclude that during the normal application of this product the exposures would be extremely low if not zero: * The product is of a putty consistency which will not make it easy to generate an airborne dust or aerosol. * The products are typically applied in the open air as the masonry coatings are designed and recommended only for exterior use. * It is recommended that if there is an enclosed area in which the product is used, an air supplied respirator be used. For example the label for "Dum Dum Masonoc Soft White 95W-9" dated 4-73 states... "............... Use adequate ventilation. Wear an air supplied mask to avoid breathing concentrated fumes in enclosed areas. Keep container closed..........." Air supplied respirators provide total protection from solvent and fibre exposure as the air is completely separate from that in the immediate work area. MOB-HarrisMaster 00354 a, 93 FIGURE 4 - THE USE OF NAIL HOLE FILLER From Readers Digest (1973) "J MOB-HarrtsMaster 00355 94 * Measurements ofthe concentrations of airborne asbestos structures during application and removal ofDum Dum Masonoc were all very low. (TABLE 14). Using the highest concentrations measured, the concentrations were all still less than 0.01 asbestos structures/cc. At 0.01 structures /cc, this represents less than l/20th ofthe present OSHA permissible exposure limit of0.2 fibres/cc and l/500th ofthe permissible exposure limit when the product was being widely used in commerce in the early 1970's. SEE APPENDIX E. iii. Chimney Dum Dum The 97 Series Chimney Dum Dum provides "the same outstanding protective and waterproofing qualities as the 95 Series Masonoc except that it has been formulated for use on concrete chimneys where additional heat resistance up to 210F may be required". The exposures associated with the application and removal ofthis product were likely to be low for the following reasons: As with the previous Dum Dum products. Chimney Dum Dum was of a putty consistency which would make it difficult to generate an airborne respirable dust or aerosol. The product was usually applied in the open air as the chimney coatings were designed and recommended only for exterior use. The same recommendation as appeared in chemical product data for the Dum Dum Masonoc 95 Series appeared in the literature concerning Chimney Dum Dum 97 Series in 1976 (Mobil 1976E, 1976F). This recommended that, ifthere was an enclosed area in which the product was used, an air supplied respirator be used. Air supplied respirators provide total protection as the air to be breathed comes from a completely separate supply of air from that in the immediate work area. I f the recommendation by Mobil was properly followed, this would make it impossible for the worker to be exposed to any asbestos. The results of the tests carried out by Arthur D Little Inc. (Peters 1990,1991) showed that the concentrations associated with the application and removal of this product were low. TABLE 14. Indeed, after adjusting the concentrations for fibres that would not be risible by light microscopy, the concentrations were less than O.Olfrcc in all cases but one, which gave 0.02f/cc. A replicate of that measurement in a second-test carried out while applying the product gave results of<0.01 free and it is reasonable to conclude that the fibre concentration associated with the use of this product is generally less than O.Olfrcc. Even when the total transmission electron microscopic fibre counts were considered, the highest concentration recorded was still low (0.088frcc), and well below the current OSHA standard based on phase contrast light optical microscopic fibre counts. Under normal conditions of application and removal of this product, the concentrations offibres to MOB-HarrisMaster 00356 95 which workers would have been exposed would have been less than one twentieth (l/20th) of the present OSHA permissible exposure limit and less than one five hundredth (l/500th) ofthe OSHA standard in effect or ACGIH recommended TLV in the early 1970's (5 fibres/cc). iv Armorcote Dum Dum This product is asphalt based. Petroleum based products which primarily included asphalt and tar based sealants were studied by Anderson et al (1982) in a report to EPA They noted that the petroleum sealants contained 5-30% asbestos (primarily chrysotile) and 55-80% asphalt. They noted that other petroleum derivatives added to achieve proper consistency included naphtha, mineral spirits and lighter weight solvents. Other ingredients including rust proofing chemicals, pigments, heat reflecting powdered metals such as aluminium, emulsifiers, resins and clay fillers, were also present in those products. Of special interest in the EPA study was that airborne fibre concentration measurements were collected for a variety of different materials and operations. The operations monitored varied from spraying cutback asphalt containing 5.8 - 7.7% asbestos on a roof surface to sand blasting a 2.1% asbestos content high performance exterior resin coating from a steel tank. The airborne fibre concentrations measured in the period 1974-1976 did not exceed 0.6f7ml for any of the asphalt tests. The results ofthose tests are shown in TABLE 15. The duration ofthe activity or sampling times were recorded only in the cutback asphalt spraying and lasted approximately 6-7 hours. It is important to note that all these activities are carried on out of doors and not in confined spaces. The EPA report noted that there is no secondary processing necessary ofthe product and that the fibre releasability was classified as "low". The CPSC, while noting that the product is designed to form a watertight seal for the roofs of industrial plants, warehouses and other flat roofs, concluded under their scenario for fibre release.... "Roof coatings are formulated to remain somewhat flexible, therefore fibre release during abrasion or demolition is not likely". This conclusion is consistent with the conclusion reached in the EPA report in which fibre concentrations reported were very low. Although only ranges were reported in the report by Anderson et al (1982), means and medians were probably ofthe same order ofmagnitude as determined for the Dum Dum materials tested by Peters (1990, 1991). A clear indication exists that these encapsulated products give rise to, at most, extremely low fibre exposure levels for workers. The findings are also consistent in that the fibre concentrations during removal are very low. While measurements made during the application and removal of Armorcote Dum Dum products were not available, there is good support for concluding that exposure to asbestos during application and removal of the product would be very remote. MOB-HarrisMaster 00357 96 Reasons for such a conclusion might be sumarized as follows: * The product was ofa consistency that would make it difficult to generate respirable dusts or aerosols. * The product was applied in the open air as it was designed and recommended only for exterior use. * Measurements made in several US States have provided consistent evidence that the concentrations ofairborne fibres recorded during the spraying of chrysotile-containing asphalt products and during the removal of such products are very low. TABLE 15. FIBRE CONCENTRATIONS ASSOCIATED WITH THE SPRAY APPLICATION OF ASBESTOS CONTAINING PETROLEUM - BASED COATING PRODUCTS (Summarized from Anderson et al 19S2) PRODUCT ACTIVITY CONCN ` TIME fi'cc mins DATE OF TEST Cut back asphalt Spraying 0.003-0.15 342-432 1974 Asphalt-emulsion Spraying Built-up roofing Tear-off o' l d 0.01 - 0.3 NR50 NR 1974,76 1974 Tear-off & Replace 0.0 - 0.3 NR 1974,76 Spraying 0.0 - 0.6 NR 1974,75,76 * There was a strong recommendation on the labels of containers of Dum Dum Armorcote Black 46-J-9 dated 4-73 stating.. "............. Use adequate ventilation. Wear an air supplied mask to avoid breathing concentrated fumes in enclosed areas. Keep container closed..........." If followed, this recommendation would make it impossible for such workers to be exposed to any asbestos even if any respirable fibres were rendered airborne. ... 50NR Not recorded. Phxae central microscopy wn axsumed in tbe original report. Monitoring mi done a several US States. MOB-HarrisMaster 00358 In summary, the levels of exposure for persons using or removing Armorcote Dum Dum products might reasonably be expected to range from zero (if proper procedures are followed) to average workplace concentrations, certainly below 0.1 fibre/cc and most probably below 0.01 fibres/cc. CATEGORY C (Dum Dum Masonoc Primer) After the mid-1970's, there would have been no asbestos exposure as the product does not contain commercial asbestos and any talc would then be tremolite fibre free. Ifany tremolite was present, prior to that time, it would be as a minor contaminant ofthe talc. As talc represents about 20 % of this product, a 1% tremolite content in the talc would represent only 0.2% ofthe product. The product is applied as an ordinary paint and is unlikely to give rise to respirable fibre aerosols during applicatioa After application it is covered by the Dum Dum Masonoc which has already been shown not to give rise to significant fibre exposures. CATEGORY D The asbestos contents ofthe Dum Dum caulking products were in the range 2-13% Product data (Mobil 1976) notes that the materials are present in vegetable oil and that at 24C the caulking has a viscosity of "putty". It skinned over in 18 hours and could be painted with conventional paints in 24 hours. The caulking products were applied using a caulking gun, trowel or knife. It is evident that the consistency of this product and its application is such that exposure to fibres during application is virtually impossible. The effectiveness of "encapsulation " in reducing asbestos fibre release was reported by Strassburg (1981) who found that when handling graphite, silicone or teflon-treated asbestos packs there was so little dust production that changeover from asbestos to substitute materials was not required. The only situation where exposure to asbestos could occur, would be ifthe user attempted to thicken the caulking by mixing more asbestos into the caulking material. It is evident that under such circumstances the potential would exist for exposure to the free asbestos before mixing but the quantities ofasbestos involved would be small, the time adding the fibre short, the occasion rare and lifetime exposures insignificant when compared to those of occupational groups where increased health risks have been demonstrated. As far as can be ascertained Mobil did not supply raw asbestos to add to their product. As with regular putty, the Dum Dum caulking materials are oil based and designed so that the surface hardens but the underlying product remains in a putty state. In their review of asbestos use in consumer products for the US Consumer Product Safety Commission, Kearney Management Consultants (CPSC 1978) noted that caulking compounds contained 0.5-1% asbestos, somewhat less than in commercial products. The purpose ofthe asbestos appears to be to "lend viscosity and retains by absorption the oils which insure ductility, thus preventing cracking" . Their scenario for fibre release involved hardening ofthe compounds through weathering and loss of oils. They postulated MOB-HarrisMaster 00359 98 that cracking and embrittlement may result and fibres might then be released during removal ofthe brittle putty. Their opinions about the release of fibres were not supported by measurements and appear to be contradicted by the measurements made with H3- Heat Dum Dum. First & Love (1982) carried out measurements ofairborne asbestos dust in a factory manufacturing a high asbestos content caulking compound (putty tape) over a 17 month period in 1979-81. The product was manufactured by kneading asbestos fibres into a mixture ofmastic materials. Pertinent to the products under study in this report are the comments by the authors who when referring to the conclusion of the mixing period when the charge was dropped from an open hatch onto a pallet stated.... "By this point in the process, all ofthe asbestos and talc has become thoroughly incorporated into a sticky non-dusting plastic mass and release ofasbestos fibres is no longer possible" Concentrations offibres were determined using the methods recommended by NIOSH. The exposure ofthe shipping and receiving room worker as measured using a personal sampler was 0.007 f/cc, on the extruder 0.003 fi'cc, on the batchmaker 0 - 0.047 f7cc and in all areas ofthe plant at least an order of magnitude below the then proposed standard of 0.5 fi'cc. This would likely be similar to the materials sold under the name " Dum Dum" caulking and exposures associated with the use of the Dum Dum caulking materials might be closer to those ofthe extruder (0.003 fibres/cc) if measurable. The information available on HI-Heat Dum Dum from the experiment by Peters (1990) is more likely to be relevant to the low temperature materials and fit well with the very low concentrations measured during caulking manufacture. See TABLE 14. i. Hi-Heat Dum Dum High temperature resinous caulking materials of putty-like consistency are used in sealing joints and crevices on furnaces and boilers to prevent heat loss. One such product, Hi-Heat Dum Dum, is described as a mastic at 24C. According to product literature, it was designed to remain pliable and withstand expansion and contraction associated with intermittent use. The product consisted of a linseed oil-base vehicle (resin) containing various solid fillers, including clay and chrysotile asbestos added for its resiliency and bridging properties. The fibre concentrations associated with the application and removal ofthe material were determined in a special test carried out for Mobil by Arthur D Little (Peters 1990). In the experiment, steel panels were coated and heated to accelerate aging. Subsequently the product was removed from these panels by scraping in three separate 80 minute experiments. During application and removal the concentrations as determined by transmission electron microscopic counts of structures were 0.01 structures/cc or less, the limit ofdetection ofthe technique applied. The results are shown in TABLE 14.' A reasonable conclusion based on the above results, is that there is insignificant occupational exposure to free asbestos fibres during the application and removal ofHi-Heat Dum Dum. MOB-HarrisMaster 00360 99 Based on the fact that this product was exposed to heat (225-250F for 18 days), increasing its possibility of drying out, results might be expected to provide an upper estimate ofthe fibre release during removal. Oil based materials which are not so heated would be expected, because ofthe low vapour pressures ofvegetable oils, to remain in a semi solid state throughout their lives. It is clear that fibre exposures from the use or removal of this product are extremely low, with all "OSHA" fibre concentrations less than 0.01 fibres/cc which is l/20th of the present OSHA permissible exposure level of 0.2 fibres/cc. ii. Heating & Ventilating "Dum Dum". A product known as " Heating and Ventilating Dum Dum" (46-X-9) was produced in the period 1964-1969. This material was recommended specifically for sealingjoints of air ducts in heating and air conditioning systems. The product would have been unlikely to be subjected to high temperatures and so would readily retain its semi-solid state. Experience with all the Dum Dum products tested suggest that they have the same basic characteristics of being associated with low or undetectable levels offibre release. As it would be highly unlikely that such a material would have been applied, other than using a caulking gun or trowel, exposures associated with its use would be anticipated to be similar to other trowelled on products - very low. This product would be expected to be associated with low or undectectable fibre concentrations during removal also. UPDATE: Court decision concerning regulations governing roofing sealants and coatings. In the original report, in 1992, some analogies were made between the Dum Dum products and asbestos fibres bound in asphalt. Since that time, the OSHA regulations governing asphalt roofing mastics were challenged and the rules overturned. The Federal Reporter reports that on July 21 1997, the Asbestos Information Association ofNorth America (AIA/NA) petitioned the Court for review of a final rule promulgated by the Occupational Safety & Health Administration (OSHA). The facts relevant to AIA/NA's claim were as follows: During the manufacturing process, solid asphalt is liquified by dissolving it in paint thinner, resulting in a thin black syrup. Enough chrysotile or powdered asbestos is mixed into the syrup to make a stiff paste that can be used, for example to seal the crack around a chimney. When the solvent evaporates, the asphalt becomes a tough leather-like film that shuts out water. Roof coatings are manufactured in the same way, except that they have a thinner consistency so that they can be applied with a brush. The position taken by AIA/NA was that "the manufacturing process encapsulates the fibres in asphalt so that they cannot become airborne and workers cannot inhale or swallow the fibres inadvertently. MOB-HarrisMaster 00361 100 There is no evidence in the record that these products have ever been found to cause any worker exposure to asbestos. AIA/NA therefore objects to OSHA's regulations requiring warning labels on the products, notification to building owners when the products are installed and work practice requirements that increase the cost ofremoval". The record review by the Court confirmed that: "there was no evidence in the record that asbestos fibres can ever escape from roofing sealants and become airborne; in feet the evidence in the record indicates that they cannot." Neither OSHA. nor the AFL-CIO seriously disputed this assertion. The argument was made by OSHA and the AFL-CIO that it is not possible to distinguish roofing coating from built-up roofing for purposes of asbestos regulations because "other" kinds ofroofing materials break down due to weathering. ' The decision ofthe Court was: " We grant review and vacate the Agency's shipyard and construction standards in so far as they regulate asphalt roof coatings and sealants which contain asbestos." "We hold that, because ofthe lack of substantial evidence in the record, the challenged regulations are invalid as to asbestos containing asphalt coatings and sealants." This decision is fully supportive of arguments made in the original report concerning certain similarities between roofing sealants and Dum Dum products. For example: The scientific evidence leaves little if any doubt that in the case of the Dum Dum products described in the report, the asbestos fibres are encapsulated. This is the situation with asphalt roof coatings and sealants. Fibres in Dum Dum are coated with oleoresinous substances which do not "dry out". This renders the chance of releasing free asbestos fibres as low if not lower than that of asphalt coatings and sealants. Measurements made during the spraying of asphalt asbestos coatings (Table 14 of original report) and application ofDum Dum products show the concentration of fibre structures to be, if anything lower for the Dum Dum (Table 16 of original report) than for the asphalt product. The 8 hour time weighted average elongated structure exposures of roofers during removal of asbestos roofing products ranged from not detectable ND to 0.036 free (Emission Standards & Engineering Division 1990). The elongated structure concentrations during removal ofDum Dum were 0.01 free or less. MOB-HarrisMaster 00362 101 The asbestos regulation was challenged by AIA/NA because asbestos roof sealants and coatings are still manufactured. Dum Dum products performed some of the same functions as the sealants (eg: cracks around chimneys) but are no longer sold. Based on the available evidence, it is reasonable to conclude that ifthe asbestos containing Dum Dum products were still sold today (in 1999), they would also now be exempt from OSHA regulatory requirements. Clearly, like asphalt sealants, they would result in little or no exposure to free asbestos fibres in a form or at a concentration adequate to pose any practically measurable level ofhealth risk for workers. The conclusions regarding levels of exposure associated with the use of the various Dum Dum products are unchanged. 14.1.3.2Duration of exposure The total exposure ofa worker over his/her lifetime is often expressed as a cumulative exposure. This is the sum ofthe products ofconcentration and duration of exposure over a working lifetime. In this equation some consideration must be given to the number ofhours worked per day with the product. The nature ofthe products and the most probable users (construction workers) make it unlikely that workers would work continuously with the product day after day. A possible exception might be Dum Dum Nail Filler which may have been used in prefabricated house manufacture where a worker might work all day filling nail holes. The period ofexposure and hence maximum cumulative exposure possible for a worker from working with Mobil-supplied Dum Dum products would be limited by the period over which the products were on the market. Making the following assumptions. * The worker was exposed for the total period over which Mobil sold the product. * The worker worked 8 hours/day applying or removing Dum Dum products. * The average exposure levels associated with the use/removal ofthe various products were less than or equal to 0.01 fibres /ml. * No air supplied respirator was used. The maximum durations of exposure and maximum possible cumulative exposures are shown in TABLE 16. UPDATE: There are no changes to the possible exposure periods. MOB-HarrisMaster 00363 102 15.0 THRESHOLD LIMIT VALUES AND LEGAL EXPOSURE LIMITS The American Conference ofGovernmental Industrial Hygienists (ACGIH) is an organisation which has reviewed and published annually a list of Threshold Limit Values. These have been adopted as guidelines or even legal standards in many countries. They refer to "airborne concentrations of substances and represent conditions under which it is believed that nearly all workers may be repeatedly exposed day after day without adverse effect." The levels have changed with time and values for the asbestos minerals are shown in Appendix E. Legal standards for the workplace in the US have been set by the Occupational Safety and Health Administration. They have also changed permissible exposure limits over the years and values are shown in Appendix F. It appears from the experimental test results that it would have been virtually impossible for workers using Dum Dum products to be exposed to concentrations which exceeded the standards in effect to protect health at the time that the material was used and would not, even during removal of the product, give rise to exposures that would exceed present day exposure limits (FIGURE 5). UPDATE: TLVs for the asbestos minerals updated to 1999 are shown in Appendix UE. Legal standards for the workplace in the US have been set by the Occupational Safety and Health Administration. They have also changed permissible exposure limits. Values updated to 1999 are shown in Appendix UF. Based on the test results it would have been impossible for workers using Dum Dum products to be exposed to concentrations which exceeded the standards in effect to protect health at the time that the material was used and would not, even during removal ofthe product, give rise to exposures that would exceed even the Threshold Limit Values or legal standard in existence in 1999 (FIGURE Ul). 16.0 RISKS OF HEALTH EFFECTS FOR USERS OF DUM DUM PRODUCTS There can be several ways of determining whether the risks faced by workers using Dum Dum products were unreasonable or unwarranted. The first makes direct comparisons of the levels of exposure of the workers with the occupational exposure standards31-that have been established for the substance under consideration. This was done in section 15.0. See FIGURE 551 51 Occupaitorul oqpcxurcs6oid*fd or Erma are generally set by Governments to provide protection for workers within the confines ofsodxl scccptibUiiy at any point in time. MOB-HarrisMaster 00364 103 Another approach is to estimate the risks ofdisease for persons at their measured or assessed levels of exposure and to situate these risks in relation to other day-to-day risks or risks faced by nonexposed persons. In the following sections such risks are assessed. TABLE 16. MAXIMUM POSSIBLE DURATIONS OF EXPOSURE AND MAXIMUM CUMULATIVE EXPOSURES OF WORKERS APPLYING DUM DUM PRODUCTS MARKETED BY MOBIL PRODUCT YEARS YEARS CONCN51 CUM.EXP32 OF EXP. No. Fee (fibres/cc-yrs) Dum Dum Armorcote 64-79 15 0.01 0.15 Chimney Dum Dum 64-79 15 0.01 0.15 Dum Dum Masonoc 64-79 15 0.01 0.15 Heating & vent ilating Dum Dum 64-69 6 0.01 0.06 Dum Dum Calk 64-69 5 0.01 0.05 Dum Dum Nail Hole 64-73 10 0.01 0.10 Hi Heat Dum Dum 64-80 16 0.01 0.16 Workers using Dum Dum products studied in this report have either not been exposed at all (if air supplied respirators were used) or were exposed to extremely low concentrations, orders of magnitude less than the prevailing standards. This would infer that they were protected at levels deemed safe at the time. UPDATE: There have been no developments that change this section, other than the lower Occupational Exposure Limit which is still not exceeded. * his bom a^tffnedduf the maanura PCMeqt*v*kconcflnsadcx*m TABLE 24 (which were modified iron the concentrations expressed in stntctura/cc measured by Peters (1990. 1991)) applied throughout the period ofexposure. -. ^Cumulative exposure has been expressed in fibresfec-yeari. Under OSHA counting rules all particles meeting the definition ofa fibre arc counted as asbestos fibres and concentration expressed as fibres/cc which is synonymous with fibres/mL MOB-HarrfsMaster 00365 104 FIGURES OSHA PERMISSIBLE EXPOSURE LIMITS, ACGIH TLV'S FOR CHRYSOTILE ASBESTOS AND THE CONCENTRATION OF ASBESTOS STRUCTURES ASSOCIATED WITH THE APPLICATION AND REMOVAL OF DUM DUM PRODUCTS AGENCY OR ORGANIZATION AND YEAR STANDARD WAS IN PLACE FOR CHRYSOTILE ASBESTOS T.Va * Tune weighted average exposure (Shrs). < TLV Threshold Limit Value Permissible exposure limit MOB-HarrisMaster 00366 105 FIGURE U1 OSHA PERMISSIBLE EXPOSURE LIMITS, ACGIH TLV'S FOR CHRYSOTILE ASBESTOS AND THE CONCENTRATION OF ASBESTOS STRUCTURES ASSOCIATED WITH THE APPLICATION AND REMOVAL OF DUM DUM PRODUCTS OSHA1971*4" ACGIH 1980s*-11 ACGIH 1991s*-11 OSHA19881*1* OSHA 1994s*-1* AGENCY OS. ORGANIZATION AND YEAR STANDARD WAS IN PLACE FOR CHRYSOTILE ASBESTOS Tm Mtcttil tnr^i enut :vn< 7L* Ttrcsnkl Lmi V wm MOB-HarrisMaster 00367 106 16.1 RADIOLOGICAL CHANGES As mentioned earlier in this report, epidemiological studies are rarely based on clinical diagnoses so the true incidence of "asbestosis" is rarely known. More often radiological changes, pulmonary function or clinical signs are assessed and examined in relation to various indices ofexposure. There have been several such studies which, in the absence of studies ofDum Dum workers, might be useful in assessing risks. These include a study ofworkers exposed to tremolite, which permits an estimation to be made of the effect of exposure if the talc in certain of the Dura Dum products contained tremolite and studies ofchrysotile asbestos miners and millers because they were exposed to chrysotile. An idea ofthe order ofmagnitude oftremolite exposures associated with radiological changes was reported in a radiological survey ofvermiculite miners (McDonald et al 1986b). This study included workers who had left the company as well as current employees, eliminating to a large extent a common criticism ofcross-sectional studies where only healthy workers are examined. They showed that age, smoking and exposure levels contributed to the observed prevalence of radiological change.. The relationship between cumulative exposure and the prevalence of pleural changes was statistically less strong than for small opacities. Estimates, as is usual in such studies, are associated with uncertainties because population size, exposure estimates, reading errors, age, smoking and other environmental variables also contribute to radiological change. However, using dose-response relationships, they estimated that by retirement age, the increase in prevalence of small opacities greater than 1/0 using the ELO-UC classification lay between 5 and 10% for workers with 100 fi'cc-years of exposure to tremolite.57 There have been at least 4 studies of Quebec chrysotile miners and millers which have provided factors for radiological prevalence. Increases in prevalence per 100 fibre/ml-years of cumulative exposure been identified as 0.2% (Liddell et al 1982); 0.6 (Rossiter et al 1972) and 4% (McDonald et al 1984). The higher value in the latter study probably relates to the inclusion ofcurrent and past employees in the survey. McDonald et al (1986b) noted that no radiological change would be detectable at an average concentration of 0.1 tremolite fibres/cc for 40 years (cumulative exposure of 4 fibre/ml-years) because the variation and errors associated with radiology would be considerably greater than any expected level of risk. 57A andy at die me mine by cxhcr mveagsoi gju: uraeKhat torcantata (Amsutus ct al 1987b). McDonald cl a!0986b) concluded dial Amandua et al (I987a.b) may have underestimated risk* because the IBS men m their study woe an current employees. MOB-HarrisMaster 00368 107 The upper limit of cumulative exposures associated with the application of Dum Dum products r-almlatffH above was 0.16 fibre/cc-yrs. Ifit was assumed that a worker worked 40 years applying and removing Dum Dum products full time, the maximum total cumulative exposure would be 40 X 0.01 f/cc which is 0.4 fibre/cc-years, which is one tenth of the cumulative exposure level at which McDonald et al (1986b) reported that no radiological change due to asbestos exposure would be detectable. In fact, the probability of detecting changes in workers today as a result of work with Dum Dum would be even less for several reasons: a. The exposure-response relationships used in the above calculations were based on the experience oftremolite exposed workers. Workers who used Dum Dum may not have been exposed to tremolite at all. The rates of radiological change resulting from chrysotile exposures are 1.25 to 2.5 times lower than those for tremolite. b. By 1992, a worker starting to use Mobil marketed Dum Dum in 1964, ifworking full time on applying and removing it, could only have aquired 28 years ofexposure. This would result in a cumulative exposure of0.28 fibres/cc-years whereas 40 years was used in the calculation. c. As regulations requiring respiratory protection for persons involved in removing asbestos, have been in place for several years, exposure during removal will have been less than 28 years. d. It is highly improbable that a worker would work full time, 8 hours/day for 28 years applying or removing only Dum Dum products. Any lesser duration of exposure reduces the risk of radiological change further. In conclusion, at levels ofcumulative exposure associated with the use and removal of the Dum Dum products in this report, radiological changes would not be detectable even after 40 or more years of full time work with them. UPDATE: There have been no developments that change the conclusion ofthis section. 16.2 LUNG CANCER Information on lung cancer risks in relation to levels of exposure are available for a number of cohorts. The risks vary quite considerably between different occupational groups as shown in FIG 3. There have been no studies ofpersons who have spent their working lives with Dum Dum products; indeed, such groups are not likely to exist. On the other hand, construction workers and others who are likely to have used Dum Dum products are exposed to asbestos fibres from other sources. Thus, MOB-HarrisMaster 00369 108 data do not exist to directly derive risk estimates and it is necessary to extrapolate from the experience ofother groups to the experience ofworkers using Dum Dum products. This is far from ideal as we need to choose the occupational group whose lung cancer experience will be used to estimate lung cancer risks for workers using Dum Dum. In order to arrive at risk estimates it has been necessary to make some assumptions. Because the only commercial asbestos fibre type used in Dum Dum products was chrysotile and because it is possible that for some years some ofthe Dum Dum products may have contained asbestiform tremolite in talc, the lung cancer experience in three industrial situations will be used in assessing risks for the Dum Dum products. - a. the chrysotile textile industry which has been the chrysotile sector associated with the highest levels oflung cancer risk. b. the tremolite exposure in vermiculite mining. c. the chrysotile mining & milling industry which has been associated with a low risk/unit exposure. The use ofthe first two studies will lead to overestimates ofrisk. Lung cancer risks in the chrysotile , textile industry are considerably greater than in any other chrysotile industry, as are the risks from tremolite exposure; tremolite was only a minor constituent of the airborne dust and over a limited time period, ifit was present at all. Because the exposure-response relationships for lung cancer have been developed in industries where exposures have been orders ofmagnitude higher than those associated with working with Dum Dum products, it is necessary to extrapolate from these high doses to levels of exposure where the shape ofthe relationship is not known. For these estimates,it has been assumed that the exposure-response relationships are linear and pass through zero. This is a convenient model However, it is unlikely that the line passes lineariy through zero. Some suggest that a threshold exists below which no effect occurs. There is also a body ofopinion that asbestos related lung cancers do not occur in the absence of "fibrosis" and, recently, evidence was presented that this may be the situation (Hughes & Weill 1991). As "fibrosis" may not occur in persons with veiy low exposures, the assumption of a threshold for lung cancer may be valid. It was shown earlier that the level of exposure anticipated from using Dum Dum products is a small fraction of those at which any radiological change could be detected, one of the markers used in the clinical diagnosis of asbestosis. Ifwe assume a working lifetime ofcontinuous exposure to Dum Dum of 20 years (4 more years than the period over which Dum Dum products were marketed by Mobil) and a concentration of 0.01 fibres/cc associated with the use and removal of Dum Dum products, the total lifetime cumulative fibre exposure due to working with this product would be at most 20 x 0.01 = 0.20 fibre/ml-years. -*s This figure is likely to be a gross overestimate of cumulative exposure for several reasons: MOB-HarrisMaster 00370 ; -'I ~V 109 * The PCM Equivalent concentrations in only 2 out of 22 tests reached or exceeded a concentration of 0.01 structure/ml. The values were 0.01 and 0.02 respectively and a replicate ofthe second measurement resulted in a concentration of less than 0.01. * Workers would rarely be expected to work with a Dum Dum product continuously for 8 hours per day every day for 20 years. * Some ofthe products were identified for exterior use only and/or others were recommended to be used with an air supplied respirator, thereby eliminating asbestos exposure. The number ofobserved deaths (O) from lung cancer in a working population = the number expected (E) in the workforce without asbestos exposure + the additional number due to the asbestos exposure. O = E + E(y) x C C = cumulative lifetime exposure and y is the increase in risk per unit fibre/cc-year of cumulative exposure. As discussed above, the cumulative exposure for workers working 20 years at a concentration of 0.01f7cc = 0.20 f/cc-years. If we assume that y = 0.0158 the relationship becomes.... O = E + E(0.01)xC Let us further assume a cohort of 1000 men are involved in applying and removing Dum Dum products for a total of 20 years each and calculate the risks in a variety ofways. a. The crude annual death rate from cancer ofthe lung, trachea and bronchus in the period 1985-87 in the USA was 75/100,000. Thus ifthe average life expectancy for working men in the 1000 man cohort were 74, the number of deaths expected over the 74 year period would be 55.50. O = 55.50 + 55.50 (0.01)x(0.20) = 55.50-0.11 There would be 0.11 lung cancers found in the cohort in addition to the number expected at US death rates. If we assume that exposure started at age 20 there would be 54 years of life expectancy left when the 1000 men started work with the Dum Dum Hence the number of additional lung cancer deaths per annum due to exposure would be 0.11/54 = 0.002/annum.* *Tha 0.01 s baaed on the eaamtied imwe ia risk wsh crtraofite of IS for each fibre/ml-ycar of exposure (McDonald etal 1986a).This u about the same aj determined by Hughes gjJ (1987) for on asbestos cement plant and by McDonald QjI (1983a), McDonald ct il (1983b) and Peto et il (1983) for textile plants. The use of a 0.01 figure will represent an upper Emit ofrisk, the risk based on other chrysotfle dose-response curves being between perhaps l/5th and l/50th or more ofthis value. MOB-HarrisMaster 00371 110 b. Ifthe above calculation is carried out using the eventual probability ofdeveloping lung cancer for a person of20 years ofage based on the cancer statistics for .1970 (American Cancer Society 1978), the expected number of deaths from lung cancer would be 1000 x 5.07 = 50.70 O = 50.70 + 50.70 (0.01)x(0.20) = 50.70 + 0.10 This would translate into 0.0019 additional lung cancer deaths /annum in the cohort. c. A third method is to use the fractional increases in risk /unit exposure calculated by Nicholson (1986). He determined the fractional increases in lung cancer risks per fibre/ml-year of exposure (KJ, along with adjustments for possible biases, estimates of statistical variation and uncertainties associated with exposure estimates in various studies. He used a KL of 0.01 in calculating lifetime risks for persons with 0.01 frcc-yrs of exposure. He calculated, where smoking habits were not considered, that the lifetime risk for men with an age at first exposure of 20 and with 20 years of exposure was 59.5/100,000. As this reflects exposures for 24 hours/day it must be divided by 4.2 to bring the rate back to that for an 8 hr /day exposure which yields a risk of 14.2 /100.000. For a cohort of 1000 men this would be 0.14/1000. This would mean an additional 0.0026 lung cancer deaths per annum in the cohort for a life expectancy of 74. d. Calculations by Doll and Peto (1985) quoted in the Nicholson (1986) report gave a lifetime risk of 25.2/100,000 for men exposed 35 years from age 20 at a concentration of O.Olf/ml. Assuming linearity, this would mean a risk ofabout 14.4/100,000 for men exposed 20 years from age 20 at 0.01 fibres/ml. This is 0.14/1000. Thus, there is considerable consistency in the estimates of risk, all life-time risks being in the range 0.10-0.14/1000 or 0.0019 -0.0026 additional lung cancers due to exposure each year in a cohort of 1000 men. These figures are already small compared to other risks. See TABLE 17. Exposure in the exposure-response curves on which risks for occupational groups are derived, are based on phase contrast microscopic (PCM) fibre counts. This is why the PCM-equivalent values have been used. However, even if we were to use the mean of the three highest concentrations recorded by transmission electron microscopy, in the experiments by Arthur D. Little Inc (0.045 fibres/cc), there would still be less than 1 death predicted as due to asbestos exposure in the cohort of 1000 men. There will be approximately 50 lung cancer deaths due to other factors. In practice, these risks will be considerably lower because the values used to calculate risk were the same or similar to those for the textile industry which carried risks much greater than for any other chiysotile industry sectors. The slopes of the lines from various dose-response relationships for chrysotile can range as high as two order ofmagnitude. McDonald, et al (1983a) has estimated that the risk in the chrysotile tortile industry sector are 50 times those in chrysotile mining and milling. The ratio of the KL values for predominantly chrysotile'textiles and chrysotile mining and milling calculated by Nicholson(1986) was 20. MOB-HarrisMaster 00372 Ill Ifthe non-textile risks for chiysatile exposure were considered, as is probably more appropriate, the annual increase in the rate oflung cancer due to asbestos exposure from the product based on mining and milling experience would be at most an average of0.00013 hing cancer deaths /annum in a cohort of 1000 men. This has assumed 20 years continuous exposure which is extremely unlikely, so actual risks are smaller still. While calculations based on estimated increases in risk per unit exposure developed using different assumptions may provide slightly different risk estimates, the order ofmagnitude ofthe calculated risks at this concentration are in fact very similar, all are very low and in practice not detectable. An increased risk of lung cancer was not detected at levels of exposure several fold greater than these, in the friction materials manufacturing industry with a workforce of 13,460 persons (Newhouse and Sullivan 1989). UPDATE: Lash etal (1997) carried out a meta-analysis ofthe relation between cumulative exposure to asbestos and relative risk oflung cancer. They assumed linear relationships and there were other assumptions made in order to cany out the meta-analysis. They reported that estimates ofthe study specific doseresponse coefficient (Klti) ranged from zero to 42 x 10*3 ml/fibre-year. Under the fixed effect model, a maximum likelihood estimate (MLE) ofthe summary measure ofthe coefficient (IQ) equal to 0.42 x 10'3 (95% confidence intervals (95% Cl) = 0.221 to 0.69 x 10 `3 ) ml/fibre-years was obtained. Thus under a fixed effects model, the estimate ofIQ by Lash et al was 24-fold lower than OSHA's (ie: the value reported by Nicholson of 10 x 10'3 noted in calculation c. above). Under the random effects model implemented because there was substantial heterogeneity in the estimates ofK and zero dose intercepts (Aj), (the model that they preferred), a MLE of IQ = 2.6 x 10'3 (95% Cl 0.65 to 7.4 x 10'3) was found. The potency ] was fourfold lower than calculated by the US Occupational Safety and Health Administration (OSHA). The reported values for the various "chrysotile only" cohorts summarized by Lash et al are listed below. In fact, all the textile cohorts had some amphibole fiber exposure, some substantial. Chrvsotile textiles; Dement et al (1994) IQ= 24 x 10'3 (95% Cl = 11 - 48 x 10'3) (A= 1.32) MOB-HarrisMaster 00373 112 Dement ct al (1983) Kj= 28 x 10'3 (95% Cl = 8.4 - 90 x 10'3) (A= 1.56) McDonald et al 11983) Kj= 42 x I O'3 (95% Cl = 15 - 120 x 10`3) (A= 1.09) Peto et al H985) Ki= 4.1 x 10`3 (95% Cl = 0.8 - 9.8 x W3) (A= 1.09) McDonald etal(1982) K~ 36 x 1 O'3 (95% Cl = 13 - 110 x 10) (A= 0.53) Friction products McDonald et al (1984) Kj= 0 (95% Cl = 0 - 3 x 10`3) (A= 1.6) It should be noted that the study by Berry & Newhouse which also did not have a slope different from zero (ie: Kj = 0) was not included in the study. Mining & milling Piolatto et al (1990) K;= 0.2 x 10-3 (95% Cl = 0 - 3 x 10'3) (a= i.oi; Liddell et al 119771 K~ 0.5 x 1 O'3 (95% Cl = 0.2 - 0.9 x 1 O'3) (A= 0.76) MOB-HarrisMaster 00374 McDonald sL! (1980) Ki= 0.5 x 10 (95% Cl - 0.2 - 0.9 x 10'3) (A= 0.96) McDonald et al (1993) 0.2 x 10*3 (95% Cl = 0.1 - 0.4 x 10'3) (A=1.22) The effect of applying either ofthe new estimates (ie: 0.0026 or 0.00042) instead of0.01 would be to reduce the risks based on Nicholson (1986) in the 1992 report even further. When the mining and milling slope noted by Lash etal was applied using the mining risks ofMcDonald et al (1993), which probably represent the closest to pure commericial chiysotile exposure; Eu-AiO+KudyJejj Ku*0. Cg population boodctpocfrf numbrrofdecks firmlucg coocr. dg * cuzzsilaav* cxpomxe. tEg * oumbcx ofdcs&s from hog eneer eepooed underthe model foroqpcmre a study j. A,* fitted tntmet ocnrqyixting to tfac reUave risk ofluog ameer caccg the cohort t zero exposure. Kq * mama* apotency d the cod&eea rcUm* aaauUavt axpcmxt to asbestos to re!tiv risk ofluoy aoccr in study h Assume that the crude lung cancer rate in the US is 757100,000 and that there are 1000 men with a life expectancy of74. The number ofdeaths over the 74 year period would be 55.5 (ie: 75/100,000 x 74). Ifwe assume that these men were continuously exposed at 0.01 free for 8 hours per day for 20 years. The expected number of deaths E = 1.22 (1 + 0.2 x 10-3 x 0.01 x 20) E = 1.22 (1 + 0.2 x 10'3 x 0.01 x 20) 55.5 The excess lung cancer deaths = 1.22 (0.2 x I0'3x 0.20) 55.5 = 2.7 x 10*3 Thus 0.0027 men would die oflung cancer in a population of 1000 workers exposed to chiysotile from Dum Dum for 20 years at an assumed concentration of 0.01 fibre/ml. The fibre concentration is in fact less than this. This is a lifetime risk of 0.0000027 or 2.7/million. In fart the risk will be even lower than this. In conclusion, the more recent data, show that as reported in the 1992 report, the lung cancer risks for workers working with Dum Dum are extremely low and possibly zero. Based on their study of lung cancer in women residents living near chiysotile mines Camus et al (1998) reported that the EPA overestimated lung cancer risks associated with chiysotile 10 fold. They found an SMR of0.99 (95% Cl = 0.78 -1.25) ie: no increased risk oflung cancer at cumulative exposure of less than 25 fibres-year/ml. MOB-HarrisMaster 00375 114 As noted In the 1992 report, the studies by Newhouse and Sullivan found no increased risk oflung cancer in friction product manufacturing workers and that cohort included workers with cumulative exposures as high as 356 frcc-years. Also the Kj value for the other friction product plant was reported by Lash et al (1997) as zero. 16.3 MESOTHELIOMA RISKS The factors which may be involved in mesothelioma causation were described in an earlier section. The characteristics of the Dum Dum products were also described. Ifwe examine these in relation to the likely use ofthe Dum Dum products, the following would appear to be the situation. * The asbestos used in Dum Dum is chrysotile. There is general agreement in the scientific literature that the risks ofmesothelioma for workers exposed to chrysotile are considerably less than those for workers exposed to amphibole fibres. The mesothelioma risk may not be due to chrysotile but to amphibole contaminants associated with certain chrysotile fibre occurrences. * The concentrations as measured using Hi-Heat Dum Dum were 0.01 asbestos structures/cc or less. As in the case of lung cancer, it is necessary to extrapolate from risks at high levels of exposure in industries where the mesothelioma exposure data exist in order to quantify risks at low dose levels. Unlike the lung cancer situation, mesothelioma is a rare disease and reliable background rates to calculate the expected numbers of deaths from this cause are not available. The incidence of the disease is therefore calculated using a model based on observations in a number of studies. This model assumes that incidence rates increase as a power ofthe time since exposure began, that incidence is proportional to concentration and includes duration of exposure based on multi-stage carcinogenicity. The model used by Hughes (1989) can be expressed mathematically as... Incidence ofMesothelioma at time t = KC where t>d C = concentration; t = time since exposure began; d = duration of exposure Hughes proposed that while there was considerable variability in the estimates of K from various studies "for mixed asbestos exposures, the median value of 0.2x104 provides a reasonable estimate" ofK (Hughes & Weill 1986). This value would take account of any tremolite contamination in the talc and has been used here to provide an upper estimate ofrisk. Hughes (1989) calculated, using lifetable methods, that for a cohort of 100,000 men exposed 20 years to 0.00117ml starting at age 20 there would be 0.9 mesothelioma deaths by age 80. Ifthese values MOB-HarrisMaster 00376 115 are expressed in terms ofthe number of deaths that would be seen in a cohort of 1000 workers exposed for 20 years at O.OlfZml there would be about 0.09 deaths. This, over 60 years would be an average of 0.0015 mesothelioma deaths per annum in the 1000 man cohort. Hughes used a factor offive to calculate the number ofmesotheliomas that would be associated with chrysotile exposures39. Under this scenario there would be 0.018 deaths from mesothelioma if 1000 men were followed from age 20 until 80 years of age. The levels ofexposure ofworkers who worked with Dum Dum products are so low that one would not expect to see a single mesothelioma related to work with Dum Dum in a cohort of 50,000 workers working full time with the products for 20 years. UPDATE: It is now almost certain that workers in the Quebec chrysotile mining cohort did not get their mesotheliomas as a result of chrysotile exposure but through amphibole fibre exposures. Based on the latest mining data there were at most 38 mesothelioma deaths (several of them not mining related) in about 10,000 workers and 8000 deaths followed from 1935-1993 (ie almost a lifetime for all cohort members). Some ofthese mesothelioma diagnoses are also questionable, so the number of mesotheliomas may be less. No case of mesothelioma had less than 2 years of employment in the Quebec asbestos mines and mills. It is known that exposures were extremely high in the past (100s offibres/cc). Based on the data from McDonald & McDonald (1997) the average exposure of mesothelioma referents was 17.4 mppcfin the central area ofThetford Mines where most ofthe risk was found. On this basis, ifwe assume 20 years ofexposure and a particle to fibre conversion factor of3:1, this would be about 1000 f/cc-years. Workers exposed to Dum Dum products for 20 years continuously would have had lifetime exposures ofless than 0.2 fibre/cc-years. If the risk is linearly related to cumulative exposure, this would mean that the proportional mortality from mesothelioma in workers using Dum Dum products would be 38/8000 :x 0.2/1000 = 0.00000095 = 0.95/million deaths. This is a lifetime risk which is a tiny fraction of the lifetime risk due to the background risk of mesothelioma of about 2 per million population per annum or 140 per million. As it appears that the mesotheliomas in the Quebec cohort are related to crocidolite (in the factory) and tremolite exposure (in the mine and mills) the risk would be lower still. - - -- 59 This assumes (hat any moothe&onus in chzysoole exposed populations are due to the chrysotile exposure which may not be the cue. MOB-HarrisMaster 00377 117 16.4 COMPARISONS In order to understand statements ofrisk, it is useful to place them in the perspective of risks faced on a daily basis. One way to do this is to express risks as an annual rate or lifetime risks/100,000 persons as has been done by Commins (1985). See TABLE 17. In the previous section (16.3), it was found that, assuming a chrysotile only exposure, the number of fMthi due to mesothelioma among 1000 Dum Dum workers exposed to O.Olf/ml for 20 years and followed from age 20 to age 80 was 0.018. This assessed risk of death from mesothelioma could be expressed as a balance of lifetime risk of about 1.8/100,000 which is less than the lifetime risk ofbeing struck by lightning. It must be remembered that calculations of risk have assumed a conservative linear extrapolation through zero. It is probable that at very low concentrations, risks cease to be linear as clearance and other mechanisms cannot be overwhelmed and can act effectively to protect cells. A less conservative view which may be correct is that their exists a threshold of exposure below which no effects occur. In practice, this threshold exists because at such low risks, the risk becomes undetectable epidemiologically or experimentally. The assessed risk ofdeath from lung cancer was expressed as an increase in the annual average death rate from lung cancer which, for the same exposure scenario as for mesothelioma, resulted in an annual average death rate increase for men of 0.10 -0.26/100,000. This is equivalent to a balance of lifetime increase in risk of 5.4 to 14/100,000. This is a very low risk and much lower than the risk of cancer from x-rays or dying in a transcontinental airline crash. In considering whether an individual who has worked with Dum Dum might have a cancer related to that exposure, it is necessary to recognise that the risk associated with the asbestos exposure due to that product is so low that almost all other identified non-asbestos and societal factors pose considerably greater risks oflung cancer and are the more likely etiological factors. If we compare the exposure of someone using Dum Dum full time for 20 years, with the exposure of mesothelioma cases in the Quebec chrysotile mining and milling industry, we find: that the lowest lifetime cumulative exposure of a mesothelioma case in the Quebec chrysotile mining and milling industry was 59 fibre/ml years (6.7 fibres/ml for 8.8 years). A person exposed to Dum Dum at the concentrations determined during the use ofthe Hi-Heat product would need to work at least 5,900 years to achieve this exposure. MOB-HarrisMaster 00378 118 TABLE 17. LIFETIME RISK VALUES FOR SELECTED SITUATIONS Commins (1985) Selected risk situations, mainly U.S. data Lifetime risk per 100,000 EXTRA HIGH RISK Smoking (all causes ofdeath) Smoking (cancer only) 21,900 8,800 HIGH RISK Motor Vehicle, U.SA 1975 (deaths) 1,600 ELEVATED RISK Frequent airline passenger (deaths) Cirrhosis of liver, moderate drinker Motor Accidents, pedestrians U.S.A 1975 (deaths) Skiing 40 hours per year (deaths) 73 0 290 290 220 MODERATE RISK Light drinker, one beer per day (cancer) Drowning deaths,all recreational causes Air Pollution U.S.A Benzo(a) pyrene cancer Natural Background radiation, sea level (cancer) Frequent airline passenger, cosmic rays cancer 150 140 110 110 110 LOW RISK Home accidents, U.S.A.1975 (deaths) Cycling (deaths) Person sharing a room with a smoker (cancer) Diagnostic x-rays U.S.A (cancer) Risk level where few would commit own resources to reduce risk; Royal Society, London (1983) 88 75 75 75 70 VERY LOW RISK Person living in brick building, additional natural radiation (cancer) Vaccination for small pox, per occasion (death) One transcontinental air flight/year (death) Saccharin, average USA consumption (cancer) Risk level where few would consider action necessary, unless clear causal links with consumer products. Royal Society, London 1983 35 22 22 15 7 EXTREMELY LOW "RARE EVENT" RISK One transcontinental air flight per year, natural radiation (cancer) Lightning Hurricane deaths Charcoal Broiled steak,one per week Environmental asbestos risk," 1985, (cancer)(around 1 per 100,000 or lower) "Acceptable" risk: World health Organization for drinking water, 1984, (cancer) (Further control not justified, Royal Society, London 1983 4 3 3 3 1 1 0.7 60 Excludes possible effects ofsmokxnc. MOB-HarrisMaster 00379 UPDATE: Cigarette gmnlring risks can put into perspective the order ofmagnitude oflung cancer risk from Dum Dum. Based on Siemiatycki etal (1994), a person smoking 20 cigarettes per day (ie: 1 pack) for 40 years would have a cumulative smoking history of 800 cigarette years (or 40 pack years). Their risk ofdying with lung cancer would be 13.2 times that ofa non-smoker. The annual death rate ofa non-smoker based on the British physicians study was 10/100,000 and for a person smoking 14-24 cigarettes per day was 127/100,000 (Doll and Peto 1976). This was based on rates derived from the 1950's and 1960's. The CPS II rate for a 50-60 year old man smoking 20 cigarettes/day for 40-44 years is 323.9/100,000. The CPS II rate for 55-59 year old male never smokers is 5.3/100,000. The additional risk ofdying from lung cancer for a worker, even ifcontinuously exposed to chiysotile from Dum Dum for 20 years was calculated to be 2.7 per million as a lifetime risk which is on average 0.04 per million annual risk or a tiny fraction ofthe usual risk for a non-smoker dying oflung cancer. Given the nature of the product, no worker would work with it continuously for 20 years, or even a small fraction ofthat, so risks would be even less. Dr John Paling (1992) has introduced the "Paling Perspective scale" and has described risks on this scale. Some ofthe risks reported by Dr Paling are shown in TABLE U17. It can be seen that the risks of cancer associated with working with Dum Dum are below those that EPA regulates and at a level that FDA considers too low to be of concern and well below that associated with eating a peanut butter sandwich each day for a year. It should be noted that as the Quebec cohort has now been followed up for many more years, it is not known whether 59 fibres/cc-years is still the lowest exposure ofa mesothelioma case in that industry as an updated exposure has not been published. However that comparison is not needed to conclude that the risks ofworking with Dum Dum are well below those where Governmental action is taken to reduce the risk. This is intrinsically recognised by the decision to eliminate regulatory controls on asphalt products which fall into a very similar category to the Dum Dum products. MOB-HarrisMaster 00380 TABLE U17 EXAMPLES OF RISKS REPORTED BY DR JOHN PALING. 120 RISKS/100,000 , 0.1-100 0.1 0.18 0.4 1.0 8 10 10 1000 10,000 CATEGORY Homebase Homebase Homebase Homebase Homebase Homebase Rapidly increasing risk Rapidly increasing risk Risk massive RISKS WITH WHICH WE ARE AT HOME US EPA regulates so that risks fall in or below this range. US Food & Drug Administration point belowwhich anyrisk from a food additive is considered too small to be ofconcern. Risk ofdrowning in tub this year. Risk ofresident being killed by crashing airplane. Extra risk ofcancer from eating peanut butter every day for 1 year. Extra risk from living in Denver compared to New York for 1 year. Risk of mother dying in birth of single child. Risk ofdeath from accidents at home in one year. Risk ofbeing murdered in the US. Risk of highway death from 50 yrs of driving. Risk of dying from cancer-smoking 1 pack ofcigarettes per day for 30 years. Vj MOB-HarrisMaster 00381 121 17.0 CONCLUSIONS * It is highly improbable that the levels of asbestos exposure by persons using Dum Dum products continuously over a 20 year period would be adequate to give rise to detectable "radiological changes" compatible with asbestosis. * It is highly improbable that the levels of asbestos exposure by persons using Dum Dum products continuously over a 20 year period would be adequate to produce detectable increases in lung cancer or primary malignant mesothelioma death rates. * The risk ofmesothelioma, lung cancer and lung fibrosis associated with the use ofthe Dum Dum Products are so low that other sources of exposure and other factors deserve a much higher priority for consideration in determining the etiology of cancers or radiological changes. The basis for these conclusions is as follows: * It is extremely improbable that workers could be exposed to significant levels of asbestos fibres during the normal application and removal of Nail Hole Dum Dum, Dum Dum Masonoc, Hi-Heat Dum Dum, Chimney Dum Dum, Dum Dum Calking or Dum Dum Armorcote and it is likely that the same applies to other similar Dum Dum products. - The products are putty like and generally applied outside. - Mobil product literature recommends that workers use air supplied respirators during application to protect themselves from solvent exposures in enclosed areas. This would totally eliminate even the potential for exposure during application of the products so labelled. - Air measurements using personal and area samples made during the application and removal of Dum Dum Masonoc, Chimney Dum Dum and Hi-Heat Dum Dum have shown very low concentrations of "fibrous" structures (0.01 structures/cc or less). - These concentrations are almost all less than 0.01 asbestos structures/cc, low even when all structures visible by transmission electron microscope are considered. - Measured concentrations are consistent with the literature concerning low concentrations associated with the production and use of similar products. MOB-HarrisMaster 00382 122 * Concentrations, when expressed in terms to assess their compliance with OSHA permissible exposure limits, show them to be approximately 1/1 Oth - 1/20 th ofthe present standard of 0.2 fibres/cc and as much as l/500th ofthe OHSA standard of 5 fibres/cc in effect in the early 1970's when the products were in use. Thus, workers have not been exposed at levels which would put them at a level of risk above that determined to be acceptable to the US Government. * In the absence ofstudies of "Dum Dum" product applicators and removers, risks have been estimated using assumptions which would tend to overestimate risk. Assuming daily exposure for 8 hours for 40 years at the maximum measured airborne fibre concentrations associated with the use ofHi-Heat Dum Dum, Chimney Dum Dum and Dum Dum Masonoc (<0.01 fibres/cc), even very minor radiological changes would not be detectable. Forty (40) years is more than twice the time that Mobil has marketed the product, and it will not be possible for a person to achieve.this exposure before the year 2003. * The risk oflung cancer at the levels of exposure associated with the application and removal of the Dum Dum products over 20 years may be 0 and at most classifiable as an extremely low or rare event. Even after 20 years of continuous exposure, at levels determined by laboratory tests of the product, the risk is considerably less than that calculated for sharing a room with a smoker. * The risk of mesothelioma for workers spending 20 years applying and removing Dum Dum products tested by AD Little and Dum Dum products giving rise to the same levels of exposure is less than the lifetime risk ofbeing struck by lightning. UPDATE: There has been no new information since 1990 to change these conclusions. Rather, the most recent data reinforces them. 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Woodward A & McMichael (1991) Passive smoking and cancer risk: the nature and uses of epidemiological evidence. European J Cancer 22 1472-1479. Wright GW & Kushner M (1977) The influence of varying lengths ofglass and asbestos fibres on tissue response in guinea pigs In: Inhaled Particles IV (Ed: Walton H) Pergamon Press, Oxford pp 455-474 Yates DH, Corrin B, Stidolph PN, Browne K (1996) Malignant mesothelioma in south east England: clinicopathological experience of 272 cases. Thorax 52 507-512 MOB-HarrisMaster 00425 ----------------------- . APPENDICES _ : A. MSDS FOR RED DUM DUM BOILER PUTTY B. MSDS FOR DUM DUM HIGH TEMP BOILER PUTTY C. DUM DUM PRODUCT LISTS Cl. DUM DUM NAIL HOLE PRODUCTS C2. CAULKING PRODUCTS C3. CAULKING PRODUCTS-HIGH TEMPERATURE CAULKINGS C4. OTHER DUM DUM PRODUCTS D. SIZE OF FIBRES OBSERVED IN AIRBORNE "DUST" SAMPLES Dl. SIZES OF "ASBESTOS STRUCTURES" IN AIRBORNE DUST SAMPLES COLLECTED DURING THE TESTING OF DUM DUM MASONOC D2. SIZES OF "ASBESTOS STRUCTURES" IN AIRBORNE DUST SAMPLES COLLECTED DURING THE TESTING OF CHIMNEY DUM DUM D3. SIZES OF "ASBESTOS STRUCTURES" IN AIRBORNE DUST SAMPLES COLLECTED DURING THE TESTING OF H3-HEAT DUM DUM E. TLV'S 1946-1991 UE. THRESHOLD LIMIT VALUES (TLV'S) ESTABLISHED BY THE GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH) F. FEDERAL REGULATORY PROGRAM - OSHA UF. FEDERAL REGULATORY PROGRAM OSHA REVISED AND UPDATED TO INCLUDE 1971-1999 G. DUM DUM PRODUCT LABELS H. DUM DUM PRODUCT DATA UL REPORTS FROM ARTHUR D. LITTLE INC. MOB-HarrisMaster 00426 APPENDIX A MOB-HarrisMaster 00427  i" 'I ' ` MATERIAL HEALTH AND SAFETY. .DATA SH&lSSf-' L. ' A* '' VToduct' Red `Dua :. Boiler Putty . ' . .. ' * -/Ghemica1 Fmrnda '...- ' . *: :v- ' ' / r *wi55 - *" <-*', * --Vrt^,'<sC. l/O Y '.J-:* Other Names _ . Manufacturer.^-- Name r The Fresco Co..' Ltd. . . - Address 6345 Netherharf'Rd., Missis-saufea/ Ont. L5T 1B8 Emergency PhoneNo. (415) 6j<J-8282 . ' Name of Contact R. c. Smith ' '-Ml II. COMPONENTS- : th'emlcallngredlents Soybean Oil, Binding Oil, PetrQfiii 100, Petrofin 0. Red Oxide-.! pigment, .Crushed Limestone,' Nyfal 300, (talc Filler) >. IJicalite ; powdered filler, Hedmanite Hi-Tepip: earth filler, Varsol, Trapes .of Qlearate, Fatty Acid Oil, .Cobalt - trace, Exkin,- Tre .'vS (Include any chemicals listed In the ACG1H TLV Booklet or Ontario Government Regulation) III. Route HEALTH HAZARD INFORMATION . Effects(Includeboth immediate andlonc-texm effects) INHALATION None Non Hazardous '*. EYE CONTACT Wash eyes with, cold water* '.Vi SKIN CONTACT None. N on-hazardous, : * '-*Vr SKIN ABSORPTION Q Insignificant. Non-hazardous INGESTION IV: ...c 1 caulking type mastic. If ingested,, see"Doctor^ Ingestion to be avoided. ' -Hit' ''V* . 'hArSDLltfc PRECAUTIONS None known.- * *1 * * * . '** * H'. *.i^ (Include recommendations for personal protecllve_equ!pmen{ tnd controls) IHOUiTRIAU ACCIDENT FREVtNTION ASSOCIATION sJjU/} jid FLOOR. 1 BLOOn ST. CAST. TORONTO. ONT. U4W 3C* ,v j:? MOB-HarrisMaster 00428 VIII. STORAGE INSTRUCTIONS l No. s"pecial reqt uirements .. - ; IX. L______1 ADDITIONAL INFORMATION ; - , Dale- Stgned l . ' *'- *.f)*,* -->'ft* : ^71 . i / . ir MOB-HarrisMaster 00429 APPENDIX B MOB-HarrisMaster 00430 MS0 S Canadian Centre for Occupational Health and Safety *" IDENTIFICATION ** RECORD HUMBER LANGUAGE PROOUCT NAME(S) 47412 ENGLISH Dun Dun Hi Temp. Boiler Putty *** MANUFACTURER INFORMATION ** MANUFACTURER AOORESS EMERGENCY TELEPHONE NO.(S) ESSENTIAL INFORMATION : The Presco Co Ltd : 6345 Netherhart Road Unit 7 Mississauga Ontario Canada L5T IBB Telephone: 416-670-8282 : 416-670-3282 : For further information please contact R.C. Smith *** MATERIAL SAFETY DATA *** MATERIAL HEALTH AND SAFETY DATA SHEET SS===SSSKS3=S3S3=SSSS3S3=ttSS3S3lSSSSSHS=31Sr31|XIS3S33SS333=S3SS3S:53==3 I. S==OSSSeK3M33SS3tSS3B5313:30Sn5S85aSSS33=3:33XSZS33t333a3S3S3SSSSSS3C33CS=SC3333:r=S Product Dun Dun Hi Temp. Boiler Putty Chemical Formula Other Names II. COMPONENTS 3335333333333333--3333333333333333353333333533333--3 Chemical Ingredients Soybean Oil, Binding Oil, Petrofin 100, Petrofin 0, Red Oxide Pigment, Crushed Limestone, Nytal 300 Talc Filler, Dicalite Powdered Filler, Asbestos, Varsol. Traces of Clearate, Fatty Acid Oil, Cobalt, exkin. (Include any chemicals listed in the ACGIH TLV Booklet or Ontario Government Regulation) SSS3SXS32S8SSS8S33SSS3SSXSSIt3Sa3SS3SS3SS3XSSSSSS33;SS9SSSS33S3;23S33S<3S3SS [It. HEALTH HAZARD INFORMATION :38SMssa333SBics33assis3nzaitas3*s*i33MSsssssscisssassss=aax*=sss3 ROUTE EFFECTS (INCLUDE BOTH IMMEDIATE AND LONG-TERM EFFECTS) INHALATION C ] Hone Non-hazardous. EYE CONTACT C ) Wash Eyes with cold water. If inflamed, SKIN CONTACT C I Hone Non-hazardous. SKIN ABSORPTION C ) Insignificant Non-hazardous INGESTION C 1 This product is a caulking type mastic. Doctor. Ingestion to be avoided. 35553353S5X333XSS3S33S33333333353533133355533XX3533333S353333: contact Ooctor. If ingested, see S3SSS333SSSSSSSS MOB-HarrisMaster 00431 tv. HAWOUNG PRECAUTIONS None known (Include recommendations for personal protective equipment and controls) saaasasaiasafUMMaatsaaanamaamtasttiMstnaistsmaisMataxsasssnsaasn V. FIRE AND EXPLOSION OATA nuisasinnussiluumPimumiiaMiuxsuitssnmuiminiluilHun Boiling Point Nil Flashpoint Nil Flammable Limits Dries out at 550 deg F LEL UEL REACTIVITY STABLE CX] UNSTABLE C ] (List conditions to avoid) None known HAZARDOUS DECOMPOSITION PRODUCTS (List) Non* INCOMPATABILITY (List materials to avoid) Hone known EMERGENCY AND FIRE FIGHTING PROCEDURE Hon flaomable =gg:3^..aa.T-i.ggarg.awttggw*aa*..aageag..simja.ttgggs=g33tsss3s VI. SPILLAGE CLEAN-UP AND WASTE DISPOSAL PROCEDURE auvsKtiiinsxasinuniHxmxzsaEMuanmimMaiisxMlnssxisssaxsussxxi Non spillable No special waste disposal required. =XXSS3Slt=XXESX=SSaa3SUE3tlS3l3SX3XX3gISSax33SlS=HEXXSXXKtXaiXSSSX8S3SSS3K:=S VII. first aid ZX33333333383333X333S33XIX3X3X:333333333IE33Z33&X33333EX3S3XXX33X33E33333 INHALATION EYES SKIN INGESTION Hot required Wash eyes with water. Not required See Doctor. 333*2S33S33333a33aS8SS3SXS3S3XX33*3SS3X*3:*SXX3SS33a3X338S38233Xa3333S3S3338X VIII. STORAGE INSTRUCTIONS 33ssHsasss3ssss3st3sasK3ss*X3stsstssa*siasuiaa3333S3ssss3Sss3sx3sasaisas No special requirements 33333333X383333383333X333 33SS352 33&SS833338333383S333333333X333X33333X338333333 IX. ADDITIONAl INFORMATION 33333338X333333333383333333333333333X3332833833333333333X3333333238333333333333 Date Signed MOB-HarrisMaster 00432 APPENDIX C MOB-HarrisMaster 00433 APPENDIX Cl DUM DUM NAIL HOLE PRODUCTS. The date ofinitial production was unknown. The reported year of cessation of marketing of this product was 1973. Nail Hole Dum Dum products had various designations. 77-739 Dum Dum Nail Hole Dark Walnut Asbestos 2% Start Stop 1973 Trade Name Dum Dum Nail Hole Dark Walnut. G-H Number 3720-599-LX32 77-171 Dum Dum Nail Hole Natural Walnut Asbestos 2% Start Stop 1973 Trade Name Dum Dum Nail Hole Natural Walnut G-H Number 3721-199-LX115 77-539 Dum Dum Nail Hole Lt Luan Asbestos 2% Stop 1973 Trade Name Dum Dum Nail Hole Lt Luan G-H Number 3720-499-LX203. Dum Dum Nail Hole Walnut Asbestos 2% Start Stop 1973 Trade Name Dum Dum Nail Hole Walnut G-H Number 3721-499-LX405. 171 Dum Dum Nail Hole White Asbestos 2% Stan Stop 1973 Trade Name Dum Dum Nail Hole White G-H Number 3720-110. MOB-HarrisMaster 00434 739 Dum Dum Nail Hole Dark Walnut Asbestos 2% Start Stop 1973 Trade Name Dum Dum Nail Hole Dark Walnut G-H Number 3 721-499-LX406 77-740 Dum Dum Nail Hole Allspice Asbestos . 2% Start Stop 1973 Trade Name Dum Dum Nail Hole Allspice G-H Number 3721-499-LX247. 742 Dum Dum Nail Hole Natural Walnut Asbestos 2% Start Stop 1973 Trade Name Dum Dum Nail Hole Natural Walnut G-H Number 3721-499-LX315 569-W-1379 Dum Dum Nail Hole Bone White Asbestos 2% Start Stop 1973 Trade Name Dum Dum Nail Hole Bone White G-H Number 3721-1 Dum Dum Travertine White1 Asbestos 2% Start Stop 1973 Trade Name Dum Dum Travertine White G-H-Number 3 721 -199-LX2 76 Mahagony Dum Dum2 Asbestos 2% Stan Stop 1973 Trade Name Mahogany Dum Dum G-H Number 3721-399-LX313 MOB-HarrisMaster 00435 Dum Dum Super White3 Asbestos 2% Start Stop 1973 Trade Name Dum Dum Super White G-H Number 3720-110. U4 These Dum Dum products eontaincd.2*/* asbestos and are probably NaJI Hole products, but this Is unconfirmed. MOB-HarrisMaster 00436 APPENDIX C2 CAULKING PRODUCTS CODE PRODUCT NAME ASB YR YR . DESCRIPTION % START DISC. 46-F-3 Dum Dum Calk Gun-Grade Natural 46-F-6 Dum Dum Calk 46-W-3 Dum Dum Calk Non shrink Off White 46-W-4 Dum Dum nonCartridge Calk Non shrink Off White. 46-W-5 Dum Dum Cartridge Calk Non Shrink Off white 46-F-5 Dum Dum Caulk Natural 46-X-9 Heating and Ventilating Dum Dum Aibcjioj content not known 10% 1964 Aul969 10% 1964 1969 U4 1964 Aul969 A Caulking of putty consistency for application by caulking gun Same as 46-F-3 but supplied in unspouted cartridges Similar to 46-F-3 but offwhite colour U 1964 Jal968 Same as 46-W-3 but supplied in unspouted cartridges U 1964 1969 Same as 46-W-3 but supplied in nozzle type cartridges 2-3% 1964 Jal979 A calking compound of putty consistency used for glazing and filling applications by putty knife and calking gun. U 1964 Aul969 A caulking material for sealing joints on air ducts in heating and air conditioning systems. A heavy putty- type consistency, . for knife or trowel application MOB-HarrisMaster 00437 APPENDIX C3 CAULKING PRODUCTS HIGH TEMPERATURE CAULKINGS CODE PRODUCT NAME ASB YR YR % START DISC. DESCRIPTION 46-F-7 Hi-Heat Dum Dum 10-13 1964 Jal980 A caulking of mastic consistency used for sealing joints and crevices on furnaces and boilers applicable only with caulking gun,trowel,special DumDum brush or heavy duty mastic spray equipment. 46-J-9 Annorcote Dum Dum 5-6 1964 JaI979 A heavy bodied product for refractory' application by trowel. MOB-HarrisMaster 00438 APPENDIX C4 OTHER DUM DUM PRODUCTS CODE PRODUCT NAME ASB YR . YR . DESCRIPTION % START DISC. 95 Series Dum Dum Masonoc 12-15 1964 1969 A heavy-bodied coating of mastic consistency designed for hi-build application and for bridging cracks and crevices with application by trowel, special brush or heavy-duty mastic spray equipment. 97 Series Chimney Dum Dum 4-5 1964 1979 A heavy-bodied coating of mastic consistency ' designed for hi-build application for filling and bridging cracks and and surface sealing of concrete chimneys with application by trowel, special brush or heavy-duty mastic spray equipment. MOB-HarrisMaster 00439 APPENDIX D MOB-HarrisMaster 00440 APPENDIX D1 SIZES OF "ASBESTOS STRUCTURES" IN AIRBORNE DUST SAMPLES COLLECTED DURING THE TESTING OF DUM DUM MASONOC BY ARTHUR D LITTLE (PETERS 1991). PRODUCT APPLICATION DIAMETERS 0.1 0.15 0.2 0.25 0.3 0.4 0.5+ L 5.0-5.9 E 6.0-6.9 N 7.0-7.9 G 8.0-8.9 T 9.0-9.9 H 10 + TOTAL I 2 *> J 12 1 2 1 17 2 13 * Includes 1 fibre of diameter = 6um. TOTAL J 1 *> J 1 10 18 PRODUCT REMOVAL DIAMETERS 0.1 0.15 0.2 0.25 0.3 0.4 0.5+ L 5.0-5.9 E 6.0-6.9 N 7.0-7.9 G 8.0-8.9 T 9.0-9.9 H 10+ 2 TOTAL 2 TOTAL 2 2 MOB-HarrisMaster 00441 APPENDIX D2 SIZES OF "ASBESTOS STRUCTURES" IN AIRBORNE DUST SAMPLES COLLECTED DURING THE TESTING OF CHIMNEY DUM DUM BY ARTHUR D LITTLE (PETERS 1991). PRODUCT APPLICATION DIAMETERS 0.1 0.15 0.2 0.25 0.3 0.4 0.5+ L 5.0-5.9 E 6.0-6.9 N 1.0-13 G 8.0-8.9 T 9.0-9.9 H 10 + 915 1 2 42 '1 1 11 241 2 11 13 TOTAL 17 1 18 2 4 1 TOTAL 16 9 1 4 4 43 PRODUCT REMOVAL DIAMETERS 0.1 0.15 0.2 0.25 0.3 0.4 0.5+ TOTAL L 5.0-5.9 E 6.0-6.9 N 7.0-7.9 G 8.0-8.9 T 9.0-9.9 H 10+ 1 12 TOTAL 1 12 MOB-HarrisMaster 00442 APPENDIX D3 SIZES OF "ASBESTOS STRUCTURES" IN AIRBORNE DUST SAMPLES COLLECTED DURING THE TESTING OF HI-HEAT DUM DUM BY ARTHUR D LITTLE (PETERS 1991). PRODUCT APPLICATION DIAMETERS 0.1 0.15 0.2 0.25 0.3 0.4 0.5+ L 5.0-5.9 E 6.0-6.9 N 7.0-7.9 G 8.0-8.9 T 9.0-9.9 H 10 + 1 TOTAL 1 TOTAL 1 1 PRODUCT REMOVAL DIAMETERS 0.1 0.15 0.2 0.25 0.3 0.4 0.5+ L 5.0-5.9 E 6.0-6.9 N 7.0-7.9 G 8.0-8.9 T 9.0-9.9 H 10 2 1 16 TOTAL 28 TOTAL 2 1 7 10 MOB-HarrisMaster 00443 APPENDIX E MOB-HarrisMaster 00444 APPENDIX E THRESHOLD LIMIT VALUES (TLV'S) ESTABLISHED BY THE AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH) 1946-1991 M.P.P.C.F.= Million Particles per Cubic Foot of air as measured using midget impinger sampler and standard light field count Fibres/cc measured using phase contrast light optical microscopy.Fibres longer than 5um with aspect ratios greater than 3:1 YEAR SUBSTANCE 1946 Asbestos 1947 1948 1949 1950 1951 1952 1953 1956 1957 1958 1959 1960 1961 1962 1963 1964 1965 1966 Tremolite 1967 1968 Intended change.. * Asbestos not listed CONCENTRATION TLV M.P.P.C.F Fibres/cc 5 5 * * * 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 2 12 + MOB-HarrisMaster 00445 TABLE cont. YEAR SUBSTANCE CONCENTRATION TLV M.P.P.C.F Fibres/cc 1969 .? 1970 Asbestos,all types 5 Intended change............ Talc (fibrous) USE ASBESTOS LIMIT 5 +$ 1971 Asbestos.all types Intended change Talc (fibrous) USE ASBESTOS LIMIT Tremolite SEE TALC FIBROUS s+m 1972 Asbestos.all types Intended change........... Tremolite SEE TALC FIBROUS Talc (fibrous) USE ASBESTOS LIMIT 5 +$# Ala 1973 Asbestos,all forms 5 +@# Ala Talc (fibrous) USE ASBESTOS LIMIT 1974 Asbestos.all forms Tremolite,SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5+@# Ala 1975 Asbestos.all forms Tremolite,SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 +@# Ala 1976 Asbestos.all forms Tremolite,SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 +@# Ala 1977 Asbestos.all forms Tremolite, SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 +@# Ala MOB-HarrisMaster 00446 TABLE cont. YEAR SUBSTANCE CONCENTRATION TLV Fibres/cc 1978 Asbestos,all forms 5 +@# Ala Tremolite.SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 1979 Asbestos,all forms 5 +# Ala % Tremolite,SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 1980 Asbestos Amosite 0.5 Chrysotile 2.0 Crocidolite 0.2 Other Forms 2.0 Talc (fibrous) USE ASBESTOS LIMIT Ala +# Ala +# Ala +# Ala+# 1981 Asbestos Amosite Chrysotile 0.5 2.0 Crocidolite 0.2 Other Forms 2.0 Talc (fibrous) USE ASBESTOS LIMIT- Ala +# Ala +# Ala +# Ala +# - 1982 Asbestos Amosite (12172-73-5) 0.5 Chrysotile (12001-29-5) 2.0 Crocidolite (12001-28-4) 0.2 Other Forms 2.0 Talc (fibrous) USE ASBESTOS LIMIT Ala+# AIa+# Ala+# Ala +# 1983 Asbestos Amosite (12172-73-5) 0.5 Chrysotile (12001-29-5) 2.0 Crocidolite (12001-28-4) 0.2 Other Forms 2.0 Talc (fibrous) USE ASBESTOS LIMIT .Ala +# Ala+# Ala +# Ala +# MOB-HarrisMaster 00447 TABLE cont. YEAR SUBSTANCE CONCENTRATION TLV Fibres/cc 1984 Asbestos Amosite (12172-73-5) 0.5 Chrysotile (12001-29-5) 2.0 Crocidolite (12001-28-4) 0.2 Other Forms 2.0 Talc (fibrous) USE ASBESTOS LIMIT Ala +# Ala+# Ala +# Ala +# Asbestos Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 Alax# 2.0 Ala x# 0.2 Alax# 2.0 Alax# Talc (containing asbestos fibres)- USE ASBESTOS TLV. However,should not exceed 2mg/m3 respirable dust. 1986 Asbestos Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms Talc (containing asbestos fibres) 0.5 Alax# 2.0 Alax# 0.2 Ala x# 2.0 Ala x# USE ASBESTOS TLV-TWA.However,should not exceed 2mg/m3 respirable dust. 1987 Asbestos .Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms Talc (containing asbestos fibres) 0.5 Ala x# 2.0 Ala x# 0.2 Ala x# 2.0 Ala x# USE ASBESTOS TLV_TWA.However,should not exceed 2mg/m3 respirable dust. MOB-HarrisMaster 00448 TABLE cont. YEAR SUBSTANCE CONCENTRATION TLV Fibres/cc 1988 Asbestos Amosite (12172-73-5) Chiysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 Ala x#*k 2.0 Ala x#*k 0.2 Ala x#*k 2.0 Alax#*k 1989 Asbestos Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 Ala x#*k 2.0 Ala x#*k 0.2 Ala x#*k 2.0 Ala x#*k 1990 Asbestos Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 Ala x#*k 2.0 Ala x#*k 0.2 Ala x#*k 2.0 Ala x#*k 1991 Asbestos Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 Ala x#*k 2.0 Ala x#*k 0.2 Ala x#*k 2.0 Ala x#*k In 1991 ACGEH gave "notice of intended change" with a proposed TLV =0.2 fibres/cc for all forms of asbestos EXPLANATION OF NOTES TLV Threshold Limit Value TWA Time weighted average Fibres/cc >5um in length x Fibres/cc longer than 5um and with an aspect ratio equal or greater than 3:1 @ A more stringent TLV for crocidolite may be required MOB-HamsMaster 00449 # As determined by the membrane filter method at 400-450 x magnification (4mm objective) phase contrast illumination. ^sr $ Concentrations 5 fibres/ml but not to exceed 10,may be permitted for 15-minute periods each hour up to 5 times daily. Ala Human Carcinogens.Substances or substances associated with industrial processes,recognised to have carcinogenic or cocarcinogenic potential with an assigned TLV % Cigarette smoking can enhance the incidence ofrespiratory cancers from this or others of these substances or processes. * Substance identified by other sources as a suspected or confirmed human carcinogen k Substance for which OSHA and/or NIOSH has a permissible exposure limit (PEL) or a recommended exposure limit (REL) lower than the TLV. \) MOB-HarrisMaster 00450 APPENDIX UE MOB-HarrisMaster 00451 APPENDIX UE THRESHOLD LIMIT VALUES (TLV'S) ESTABLISHED BY THE AMERICAN CONFERENCE OF GOVERNMENTAL INDUSTRIAL HYGIENISTS (ACGIH) REVISED AND UPDATED TO INCLUDE THE PERIOD 1946-1999 DEFINITIONS M.P.P.C.F.= Fibres/cc = Fibre = Million Particles per Cubic Foot of air as measured using impinger samplers and standard light field count. Number of fibers per cubic centimeter of air as measured using phase contrast light optical microscopy and designated fiber definitions. Fibre counts were determined using the membrane filter method at 400-450X magnification [4mm objective] phase contrast illumination. The definition of a fibre used in the TLV is a fibre longer than 5um with aspect ratio equal to or greater than 3:1. THRESHOLD LIMIT VALUES (TLVS) BY YEAR YEAR SUBSTANCE CONCENTRATION TLV M.P.P.C.F Fibres/cc 1946 1947 1948 1949 1950 1951 1952 1953 1956 1957 1958 1959 1960 Asbestos .5 5 * * 5 5 5 5 5 5 '5 5 MOB-HarrisMaster 00452 TABLE cont. YEAR SUBSTANCE 1961 1962 1963 1964 1965 1966 Tremolite 1967 Tremolite 1968 Tremolite Intended change 1969 1970 Asbestos, all types Intended change Talc (fibrous) USE ASBESTOS LIMIT Tremolite SEE ASBESTOS 1971 Asbestos, all types Intended change Talc (fibrous) USE ASBESTOS LIMIT Tremolite SEE TALC FIBROUS. 1972 Asbestos, all types Intended change Tremolite SEE TALC FIBROUS Talc (fibrous) USE ASBESTOS LIMIT 1973 Asbestos, all forms Intended change Talc (fibrous) USE ASBESTOS LIMIT (A more stringent TLV for crocidolite may be required) CONCENTRATION TLV M.P.P.C.F Fibres/cc 5 5 5 5 5 5 5 5 5 5 2 12 + .? 5 5 +S 5 +#$ 5 +S# Ala 5 +@# Ala MOB-HarrisMaster 00453 1974 Asbestos, all forms Tremolite, SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 1975 Asbestos, all forms 5' Tremolite, SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMITTABLE cont. 1976 Asbestos, all forms Tremolite, SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 1977 Asbestos, all forms Tremolite, SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 1978 Asbestos, all forms Intended change Amosite Chrysotile Tremolite Crocidolite Other Forms Tremolite, SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 0.5 2.0 0.5 0.2 2.0 1979 Asbestos, all forms Intended change Amosite Chrysotile Tremolite Crocidolite Other Forms Talc {fibrous} Tremolite,SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 0.5 2.0 0.5 0.2 2.0 0.5 19S0 Asbestos .Amosite Chrysotile Crocidolite Other Forms Talc (fibrous) USE ASBESTOS LIMIT 0.5 2.0 0.2 2.0 +@# Ala +@# Ala +@# Ala +@# Ala +@# Ala Ala +# Ala+# Ala+# Ala+# Ala +# +# Ala % Ala +# Ala+# Ala +# Ala +# Ala +# Ala +# Ala +# Ala +# Ala+# MOB-HarrisMaster 00454 1974 Asbestos, all forms Tremolite, SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 1975 Asbestos, all forms 5' Tremolite, SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMITTABLE cont. 1976 Asbestos, all forms Tremolite, SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 1977 Asbestos, all forms Tremolite, SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 1978 Asbestos, all forms Intended change Amosite Chrysotile Tremolite Crocidolite Other Forms Tremolite, SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 0.5 2.0 0.5 0.2 2.0 1979 Asbestos, all forms Intended change Amosite Chrysotile Tremolite Crocidolite Other Forms Talc {fibrous} - Tremolite,SEE ASBESTOS Talc (fibrous) USE ASBESTOS LIMIT 5 0.5 2.0 0.5 0.2 2.0 0.5 19S0 Asbestos Amosite Chrysotile Crocidolite Other Forms Talc (fibrous) USE ASBESTOS LIMIT 0.5 2.0 0.2 .2.0 +@# Ala +@# Ala +@# Ala +@# Ala +@# Ala Ala +# Ala +# Ala+# Ala+# Ala+# . +# Ala % Ala+# Ala+# Ala +# Ala+ Ala+# Ala +# Ala +# Ala +# Ala+# MOB-HarrisMaster 00455 YEAR SUBSTANCE CONCENTRATION TLV M.P.P.C.F Fibres/cc 1986 Asbestos Amosite (12172-73-5) 0.5 Alax# Chrysotile (12001-29-5) 2.0 Ala x# Crocidolite (12001-28-4) 0.2 Alax# Other Forms 2.0 Ala x# Talc (containing asbestos fibres) USE ASBESTOS TLV-TWA. However, should not exceed 2mg/m3 respirable dust. 1987 Asbestos Amosite (12172-73-5) 0.5 Alx# Chrysotile (12001-29-5) Crocidolite (12001-28-4) 2.0 Al x# 0.2 Alx# Other Forms 2.0 Alx# Talc (containing asbestos fibres) USE ASBESTOS TLV_TWA. However, should not exceed 2mg/m3 respirable dust. 1988 Asbestos Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 Al x#*k 2.0 Al x#*k 0.2 Alx#*k 2.0 Al x#*k 1989 Asbestos Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 Al x#*k 2.0 Alx#*k 0.2 Al x#*k 2.0 Al x#*k 1990 Asbestos .Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 Al x#*k 2.0 .Al x#*k 0.2 Al x#*k 2.0 Al x#*k Comments MOB-HarrisMaster 00456 YEAR SUBSTANCE CONCENTRATION TLV M.P.P.C.F Fibres/cc 1986 Asbestos Amosite (12172-73-5) 0.5 Alax# Chiysotile (12001-29-5) Crocidolite (12001-28-4) 2.0 Alax# 0.2 Alax# Other Forms 2.0 Alax# Talc (containing asbestos fibres) USE ASBESTOS TLV-TWA. However, should not exceed 2mg/m3 respirable dust. 1987 Asbestos Amosite (12172-73-5) Chiysotile (12001-29-5) 0.5 Alx# 2.0 A1 x# Crocidolite (12001-28-4) 0.2 A1 x# Other Forms 2.0 Alx# Talc (containing asbestos fibres) USE ASBESTOS TLV_TWA. However, should not exceed 2mg/m3 respirable dust. 1988 Asbestos Amosite (12172-73-5) Chiysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 A1 x#*k 2.0 A1x#*k 0.2 A1x#*k 2.0 Alx#*k 1989 Asbestos Amosite (12172-73-5) Chiysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 A1x#*k 2.0 Alx#*k 0.2 Alx#*k 2.0 A1x#*k 1990 Asbestos Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 Alx#*k 2.0 AIx#*k 0.2 Aix#*k 2.0 Alx#*k Comments MOB-HarrisMaster 00457 TABLE cont. YEAR SUBSTANCE CONCENTRATION TLV M.P.P.C.F Fibres/cc Comments 1995 Asbestos. Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 A1 x#*k 2.0 A1 x#*k 0.2 Alx#*k 2.0 A1 x#*k Notice ofintended change for "Asbestos, ail forms [1332-21-4]" to 0.2f/cc for fibres longer than 5um and with an aspect ratio equal to or greater than 3:1 as determined by the membrane filter method at 400-450X magnification (4 mm objective) phase contrast illumination. 1996 Asbestos Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 Alx#*k 2.0 Alx#*k 0.2 Alx#*k 2.0 Alx#*k Notice of intended change for "Asbestos, all forms [1332-21-4]" to 0.2fi'cc for fibres longer than 5um and with an aspect ratio equal to or greater than 3:1 as determined by the membrane filter method at 400-450X magnification (4 mm objective) phase contrast illumination. 1997 Asbestos .Amosite (12172-73-5) Chrysotile (12001-29-5) Crocidolite (12001-28-4) Other Forms 0.5 A1 x#*k 2.0 A1 x#*k 0.2 A1 x#*k 2.0 A1 x#*k Notice of intended change for "Asbestos, all forms [1332-21-4]" to O.If'cc for fibres longer than Sum and with an aspect ratio equal to or greater than 3:1 as determined by the membrane filter method at 400-450 x magnification (4 mm objective) phase contrast illumination. 199S Asbestos, all forms (1332-21-4) 0.1 A1 xs Critical effects. asbestosis; cancer. 1999 Asbestos, all forms (1332-21-4) 0.1 A1 x# Critical effects. asbestosis; cancer. MOB-HarrisMaster 00458 EXPLANATION OF NOTES TLV Threshold Limit Value TWA Time weighted average + Fibres/ml >5um in length x Fibres/cc longer than 5um and with an aspect ratio equal or greater than 3:1 @ A more stringent TLV for crocidolite may be required # As determined by the membrane filter method at 400-450 x magnification (4 mm objective) phase contrast illumination. $ Concentrations 5 fibres/mi but not to exceed 10, may be permitted for 15-minute periods each hour up to 5 times daily. % Cigarette smoking can enhance the incidence ofrespiratory cancers from this or others of these substances or processes. * Substance identified by other sources as a suspected or confirmed human carcinogen k Substance for which OSHA and/or NIOSH has a permissible exposure limit (PEL) or a recommended exposure limit (REL) lower than the TLV. Ala Human Carcinogens. Substances or substances associated with industrial processes, recognised to have carcinogenic or cocarcinogenic potential with an assigned TLV A1 1987, 1988 Confirmed Human carcinogen 1989, 1990 Confirmed human carcinogens: Substances, or substances associated with industrial processes, recognized to have carcinogenic potentiai. :99I Confirmed human carcinogens: Substances, or substances associated with industrial processes, recognized to have carcinogenic potentiai Intended change to Confirmed human carcinogen: The agent is carcinogenic to humans based on the weight of evidence from epidemiologic studies of or convincing clinical evidence in exposed humans. MOB-HarrisMaster 00459 EXPLANATION OF NOTES cont. A1 1992, 1993,1994, 1995, 1996, 1997, Confirmed human carcinogen: The agent is carcinogenic to humans based on the weight of evidence from epidemiologic studies of or convincing clinical evidence in exposed humans. 1998, 1999 Confirmed human carcinogen: The agent is carcinogenic to humansbased on the weight of evidence from epidemiologic studies. MOB-HarrisMaster 00460 APPENDIX F MOB-HarrisMaster 00461 DATE 29.05.71 12.07.71 7.06.72 09.10.75 07.76 04.11.83 03.84 APPENDIX F federal regulatory program OSHA 1971-1988 RULE PEL of 12 f7cc over 8 hour time weighted average (TWA) Section 6(a) ofthe OSH Act codified at 29 U.S.C.S 655 (a) (36 FR 10466) (29 C.F.R.Part 1910) PEL of 5 flee over 8 hour time weighted average (TWA) and peak exposure of 10 fleeas Emergency Temporary Standard (36 FR 234207) (29 CJF.RJPart 1910.93a) New Final rule-PEL of 5 flee over 8 hour time weighted average (TWA).To be lowered to 2flee in 1976 (37 FR 11318) (29 C.F.RPart 1910) Proposed Rule PEL of 0.5 flee over 8 hour time weighted average (TWA).Ceiling limit of 5f/cc for 15 minutes (1980)-withdrawn. (40 FR 47652) PEL of 2ficc as 8 hour time weighted average became effective as in 1972 final rule (29 CFR 1910.1001) Emergency temporary Standard (ETS) of 0.5 fi'cc as 8 hour time weighted average. 1983 ETS Overturned MOB-HanisMaster 00462 TABLE cont. DATE RULE 10.04.84 Proposed rule - PEL to be lowered to 0.5 or 0.2 f7cc as time weighted average. (49 FR 14116) 12.07.85 EPA Proposed rule Immediately effective to extend OSHA provisions to state and local workers. (50 C.F.R.28530) 25.04.86 EPA Final Rule-extends OSHA protections to state & local workers. (51 FR 15722) (40 C.F.RPart 763,Subpart G) 20.06.86 PEL lowered to 0.2f/cc as 8 hour time weighted average. (Final Rules 51FR 22612) (29 C.F.KPart 1910, Subpart Z and 29 C.F.RJPart 1926,subpart D) 17.10.86 Partial Stay of 20.06.86 standards as they applied to non asbestiform tremolite.anthophyllite and actinolite pending further review and rule making. (51 FR 37002) 25.02.87 EPA Final Rule-Revised rule extended current OSHA requirements to state local workers involved in abatement and lifted repair exemption for projects 3 feet or less. (52 FR 5618) (40 C.F.RPart 763,Subpart G) 14.09.88 Amendment - excursion limit of 1 ftcc over a 30 minute period added to cover employees involved in jobs with irregular peak whose total exposure may not reach 0.2 f/cc as time weighted average over an 8 hour exposure period. (53 FR 35610) (29 C.F.R.Part 1910,Subpart Z aiid 29 C.F.R. 1926,Subpart D). APPENDIX UF MOB-HarrisMaster 00464 APPENDIX UF FEDERAL REGULATORY PROGRAM OSHA REVISED AND UPDATED TO INCLUDE THE PERIOD 1971-1999 DATE 05.29.71 07.12.71 06.07.72 10.09.75 07.XX.76 11.04.83 RULE PEL of12 f/cc over 8 hour time weighted average (TWA) Section 6(a) ofthe OSH Act codified at 29 U.S.C.S 655 (a) (36 FR 10466) (29 C.F.R.Part 1910) PEL of 5 f7cc over 8 hour time weighted average (TWA) and peak exposure of 10 f7cc as Emergency Temporary Standard (36 FR 234207) (29 C.F.KPart 1910.93a) New Final rule - PEL of 5 flee over 8 hour time weighted average (TWA). To be lowered to 2flce in 1976. Ceiling limit of lOf/cc. (37 FR 11318) (29 CJF.RJPart 1910) Proposed Rule - PEL of 0.5 flee over 8 hour time weighted average (TWA).Ceiling limit of 5f7cc for 15 minutes.Applied to all industries except construction. (In 1980) - withdrawn. (40 FR 47652) PEL of 2f'cc as 8 hour time weighted average became effective as in 19~2 final rule (29 CFR 1910.1001) Emergency Temporary Standard (ETS) of 0.5 f/ce as 8 hour time weighted average. (48 FR 51096) MOB-HarrisMaster 00465 TABLE cont. DATE 03.XX.84 04.10.84 07.12.85 04.25.86 06.17.86 06.20.86 07.21.86 10.17.86 C: 25.87 RULE 1983 ETS - Overturned by US Circuit Court ofAppeals for the Fifth Circuit. Proposed rule - PEL to be lowered to 0.5 or 0.2 f/cc as time weighted average. (49 FR 14116) EPA Proposed rule Immediately effective to extend OSHA provisions to State and local workers. (50 C.F.R.28530) EPA Final Rule-extends OSHA protections to state & local workers. (51 FR 15722) (40 C.F.R.Part 763,Subpart G) Two revised standards issued, one governing exposure to asbestos in general industry and the other applying to construction workplaces [06.20.86], PEL lowered to 0.2f7cc as 8 hour time weighted average. (Final Rules 51FR 22612) (29 C.F.R.Part 1910,Subpart Z and 29 C.F.RPart 1926,subpart D) Revised standards amended OSHA's previous asbestos standard issued in 1972. The 1986 standard explicitly applied to non-asbestiform tremolite, actinolite and anthophyllite Partial Stay of 06.20.86 standards as they applied to non asbestiform tremolite. anthophyllite and actinolite pending further review and rule making. (51 FR 37002) EPA Final Rule-Revised rule extended current OSHA requirements to state local workers involved in abatement and lifted repair exemption for projects 3 feet or less. (52 FR 5618) (40 C.F.R.Part 763,Subpart G) MOB-HarrisMaster 00466 TABLE cont. DATE RULE 09.14.88 Amendment - excursion limit of 1 f7cc over a 30 minute period added to cover employees involved in jobs with irregular peak whose total exposure may not reach 0.2 f/cc as time weighted average over an 8 hour exposure period. (53 FR 35610) (29 C.F.RPart 1910,Subpart Z and 29 C.F.R. 1926,Subpan D). 10.11.94 Final Rule - The final standards amended the standards issued June 17 1986 (51 FR 22612, 29FR 1910.1001, June 20 1986) for occupationa 1 exposure in general industry and in the construction industry. They also include a separate standard covering asbestos exposure in the shipyard (29 CFR 1915.1001). PEL (TWA) = 0.1 f7cc for all asbesos work in all industries. (59 FR 40964). 07.01.98 I Revisions - Safety & Health regulations for construction. PEL (TWA) = 0.1 Fee as an 8 hour time weighted average. Excursion limit = 1 Fee as averaged over 30 minutes. (29 CFR Ch XW 7-1-98 Edition Part 1926). 07.01.98 Revisions - Occupational Safety & Health Standards. PEL (TWA) = 0.1 Fee as an 8 hour time weighted average. Excursion limit = 1 Fee as averaged over 30 minutes. (29 CFR Ch XVH 7-1-98 Edition Part 1910). MOB-HarrisMaster 00467 APPENDIX G MOB-HarrisMaster 00468 Mobil 1970a r'" E..... rr r L MOB-HarrisMaster 00469 i iL ilu > tu i l , J iih A il d f i l i t i l i i MI lllfa L iJ l Mobil Chemical Company MOB-HarrisMaster 00470 Mobil 1970b 00471 MOB-HarrisMaster 00472 i i I i I J I I -1I < .1 1 1 < '-1 1 I % J 1 Mobil Chlemical Company /to co K H j oMir/ncN UAHtEHXMCE MOHr. ic x rro</K X MKACHCirO.itM.HooOoSotOAUOWJ aIMnqICcNUr 3 a w x aiuw. c x ir ttrxn J Mobil 1970c r <CaD: t-n t-- LU iiunUutiamwsv.v;iiui*.*.w {5^Hj,*`Vl ******* jvylv.v.v.vjnilmuiiium; : WMjjj}J,uutvw.V4^rf.'41?.<i ?| i ; ------- KSlVlVAV.wuiuiv.v;."; tuY/fwiit^m>*>\u?\Vtu\VA'A*.v- 1111* r ^,.., jYiTTT;:*' 5 % 0~ 1e c : j S . zC. cow J d i / n >* j j I-'*= l\ > 5 -> Z <D i *aJ- Sjl lilt -r itz I a - f ^rr l5 ic s; ;: so 1% 1s 17 i ****** a-a- 9 J3: > til!!. oOOf<H<AJ .V;;;.v.v^Tmiituii:u i *m"TiY*77j77r ~:: vtr. i*iiv.-.*> MOB-HarrisMaster 00473 Mobil Chemical Company i MOB-HarrisMaster 00474 Mobil Mobil 1971a MOB-HarrisMaster 00475 '('tMimtii!" \ .....v .V.*. ""i,******'f ................... HltlWV.W :7Vt 11t(? t... * `'i **.*****t; >*^VwV.v.VyV//iMiMTftty.v/AV4 _ ;'?;'}`jjjii-'*'-'* tiffiffiti'i.Vmi>i/.v.*.\ i ^^jv^yAww^mtiijv.wrMi^WAJJJltWFwVVfyw.v^itti >,.inw/wwinniutn,.^ miuwHwj vmwWtl .'.v;.';:i:v.'Avriiii(v.wN(iM{ii(ffr/M "li)<t>wvwAv:/.niw'i>! iVum** WWIWtWWIQ1 I'1vMtiVViVmti'iiiic .V.V.V.V.V.Illlltlllli I tiUiJi MOB-HarrisMaster 00476 Mobil Chemical Company noon iy/^a MOB-HanisMaster 00477 M o b il C h o m ic c il C o m p a n y MOB-HarrisMaster 00478 APPENDIX H MOB-HarrisMaster 00479 Mobil 1976a M@bH Chemical Prodtct Data NOVEMBER 1.1971 / Print* in U.SA. Thit supersedes ellprevioos publications. Aiwiyi consult your Mobil representative lor latest information and recommendations for Mobil Produett. DUM DUM*CALK!NG CONFORMS WITH AIR POLLUTION RULES AND REGULATIONS 46"F"5 COLOR FINISH VEHICLE TYPE PIGMENT TYPE SOLVENT TYPE Natural Low Sheen Vegetable oil lnrt pigment and Atbanot Fibre Nona FLASH POINT. MINIMUM % SOLIDS BY VOLUME Nonflammable 100% COVERAGE (THEORETICAL) VISCOSITY AT 75*F. (24*CJ AVERAGE DRY TIME AT7S*F. /24*C/ RECOMMENOED THINNER Size of joint 1 /#** x 1/8"-- 1230 Lineal Faat pargallon 1 /4" x 1/4"- M0 Lineal Faat par gallon 3/8" x 3/8"-- 135 Lineal Feat par gallon 1/2" x 1/2"- 77 Lineal Faat par gallon The actual coverage will be leti, depending on application ticnnicut, joc conditions and type of surface to be coatad. Putty Skins over in 18 hours -- Paint over after 2* nourt with conventional coating: If material stiffens in cold weather add up to 1 cup linseed oil per 5 gallons of calking. Use Thinner 7-T-38 for eiearvuo. RESISTANCE TO Fumes -- Very Good Moisture - Excellent Expansion & Contraction -- Very Good Cracking - Very Good Dry Heat - To 2S0*F./12f*C./ RECOMMENOED PRIMER STEEL GALVANIZED WOOO MASONRY None None Exterior First Coater 17-W-4 or Exterior Primer White 1 7-W-S Misonoe Primer :7W-21 or Exterior Latex Paint 79-W-9 APPLICATION Calking Gun Glazing Knife Will build I" on vertical without tlumping CAUTION Store in warm area in cold weather. MOB-HarrisMaster 00480 Mcbii Chemlcar PradiC i Data DUM DUM'CALKING 46-F-5 PREPARATION: Surface mutt be eln, dry snd free of utt Loom Mint, mortar. or crumbling Butty should be removed. All masonry cracks and mortar joints should ba naked dear.. "Deep cracks and openings should b* packed Mith oakum or fibre glass to about 3/8" of surfac*. Prim* sara surfaces prior to application of Calk. APPLICATION: If oil has. risen to tht top. stir thoroughly <mo the pigment matter. Apply with a calking gun or tool worn; as heavy a bead as possible. Apply in a manner assuring full contact on aides snd bottom of bead. Luvt a well rounded bead on the outside. When a smoothed bead it required for appearance, dip tool in water to tiiminat* nicking. To prevent skin forming whan net in use, pour s liberal amount of water over the unused compound and keep container tightly sated. Pour off water before r*. using. NOTICE: This product is for industrial use only and is not intended or suitable for use in or around a household or dwelling. i l "C " me -~W V ">Mn MS * IMIim IMi aaii aw91c#4a*iM#v*i# sw'A*****M#*r(M*lM* 9*r ## mut ** > hMIfNMUr rtf ffwtyttt Addl INV AA#r;/I -rsrewwyTO ift*Mf T#*Mreatr*oMftscri m mmI*W**g<d*i*ml *iteMmMmri#fair iw*y MVS tm wt* tfwO/SCUMS ii; 9^1* Anr iwtt.WOMrO Mrt**t fic'VlmCk*TASjuTVmm**rnrwrurmmm Arcr-rt*MOttwCif iCftr*cjrCMWff 0--e4C*4ccp#ac9*iat "i ; l I r *i 1: : (IWflfi 8ft*OiM r MIMW VMI nnw*t ia ia# fegsw IMl !* f**/ yiKTI #*** *f i**lMdiU|l<rt M*W rmgr rMM* mr #ewcn r rurr mg <f iPg/M m mmii *** *' iMtf M f w* o*r d?i fc'TS. t ngf a# MVMMII M MM| f CrU|iA^>li flPMfll 9*4*9* <*49*9* 4M l>IMr M MM8IM If ***** v* W^gf 0'OOvCM l hr*; *** *tair ii a ftiwmii **r imi hri wm m>< *m or mm <op '****# it ornp oi fr^i m imk* f atiM di 'miomm cm'i "i jMobil Chemical Company MAINTENANCE 4 MARINE COATINGS DEPARTMENT Edison, New Jersey 08817 ~.0. 3ox 20 / Tel: (201) 287-2626 I**umont_ Teiaa 77704 = .0.3o* 3^31 / Tel: (713) 635-5324 T-anfcskee. Illinois 60901 Los Angeles Area / Azusa. California 91702 1004 West Tenth Slreet / Tel: (213) 334-8251 Louisville, Kentucky 40210 (Railroad Costings) 1630 West Hill Slreet / Tel: (502) 774-4411 ?*rtt O'OrfwCfT iito v>'40'f Ire*" C MOB-HafrisMaster 00481 Mobil 1976b NOVEMBER. 197* / Printed in USX ( Thus SUperSeOeS all previous Duolicxlionj. Ajwivt eorwjti rout Mcoii recvesentalive ler latest mtormalicn arid reconvneneations ter Moot) Predvcn. PH . :7.1 ii'vTx5i S'OUM DUM CAULK / 46-F-5 An oil based caulking compound recommended for glazing and tilling operations by knile or gun lor joints and cracks where movement is not a critical (actor. Recommended specifically for use with 95 Series Masonoc. Excellent adhesion to previously primed sur faces and can be overcoated with conventional finishes - after 24 hours. nil / CHIMNEY DUM DUM / 97 Series Chimney Dum Dum provides the same outstanding pro tective and waterproofing qualities as the 95 Series spiSdS Masonoc, except that it has been formulated lor use on concrete chimneys where additional heat resistance up itsr-tcw-ntry ClfMM oI*T IM*U M I7.f4l Ait 4*4uaW: C/itm*r Owm Ovm tuft Sait Wfiiia Uw.| M4 w.w-i lmrn4tlAA4t Ortn^c to 210*F. is required. v/hI-HEAT DUM OUM / 46-F-7 A heavy semi-plastic fibred coating, which acts as a DUM DUM MASONOC / 95 Secies joint sealer and pliable gasket (or boilers, furnaces and dry kilns. Improves boiler efficiency by preventing heat Masonoc is a. heavy bodied textured coating designed as less. Retains its elasticity at constant heat up to 175* a weather seat, waterproofing, and restoration coating and intermittent heat to 350*. May be used as a complete tor ait types of masonry structures. Pliability and eias* cover to eliminate excess fuel consumption and can be ticity allow for building movement without cracking ot painted over in 24 hours. the coating white a tough outer skin provides protection (or normal usage. Its high build qualities permit hairline f cracks to be bridged and sealed, and surface irregulari- "DUM DUM ARMORCOTE / 46-J-9 ties to be filled and uniformed. Masonoc also provides line protection tor steel with its high film build and impermeability. Its excellent sur face wetting properties recommend use of this material m areas that cannot be cleaned too well, where there are numerous angles and edges to protect, or when a single coat application is all that can be provided. A specially compounded, heavy bodied product con taining asphalt, reinforcing pigment and high boiling hydrocarbons. Resistant to fumes, moisture, and sus tained temperatures up to 300`F. Used to protect and increase the elliciency of brick boiler settings. May be applied to boilers even while they are in operation. CHIMNEY DUM DUM PRIMER I 38-V-5 A clear 100 percent solid neat resistant penetrating primer designed lor application to masonry surfaces be neath Chimney Dum Dum Coatings. MASONOC PRIMER / 47-W-21 Masonoc primer is a normal paint like material wnicr. is to be used beneath the Masonoc coating on alt types ot masonry surfaces to seal off and eliminate surface porosity. 3nl proauct descriptions s/a given lor the purpose al tacilitxting selection. Always reler to the individual Moeil Chernies. Product Dais Sheets let funner specific product recommendations ana use instructions. I /a# rwwwjrung ot ttt. mtotmoitati eotustnoa Ar*w, aoei -a, .atuiitm. . Or uooU inel -y proava or Oracu a free uom pai.tu mttr^rtnorr I cmimi ot pwfl AMTy nor cofUMwf* Um Qfmwig of 4 pngor *y difgnf Ot Wo*W or my Ultra potTf Mao*/ IllvAtl rio UcMtfy for 4fty Wmg*> *<v w/vc/inwr / otrf arena vto oi u*o pfOOoGL MoOrf wirrfut tfui *1 orodvctt moottno tooctltCAtrom iriom. Uo*i OtSCLAJUS ML QTmEA j NAflAAMTJfJ rUin$iot/*4prodwCJ1.4*0/SCLA/USAH **AAax7/5 ALATJMG TO 7/A APPUCATXQN.oxprm* or no* (Os tS*CtlAHTAHUTT f*f!TMSS /orpOtUQytOtOofOOOo. ftoco*pt OtOfOO'sCMtO"* MOOeJ) CA#*'<JCe1M'eX 0mUOr*COrt*l4u4 OCOOOttncm 0/ U*0 ('mi 0/ thu w%rr4/wy. covri/y ptoo*uoru ot Ow/csui# o*0**1 n*wfrtH*/sa*ng. in tr> 4f *rc iofi citejnoot\ ottftor roottoo uo praavett ot rc'im* tr%o noto (n*i WooJ preowet* OohmotoO 4ro O/MOAC/ficbieon. WooM Ugof) cno-c* ot onm ot /* owoti i/u Oo Swyn *o* '"*07- ***** yf*cor no otrotrmttonoos Oo luoto tor consoQv+nuoi 04Agt. **coot mu0/4/ #s i*4ttry a monooxmO Oy U Uo*t */ ool**or jygdbcrc 4i tgtooC timot *~ooior ot a $t rootonootf 00*0 10 00 to. 0*r Mom mott not 0# i*00/0 l* toilvfo to oohwr on nmo mnon mo istiyro a berund r44*0A4tt corvee/ Mobil Chemical Company Edison, New Jersey 03817 P.O. Box 250 / Tel: (201) 287-2626 Beaumont, Texa* 77704 P.O. Box 3431 / Tel: (713) 835-S324 MAINTENANCE i MARINE COATINGS DEPARTMENT Los Angeles Area ! Azusa, California 91702 1004 West Tenth Street / Tel: (213) 334-8251 Louisville, Kentucky 40210 (Railro 1630 West Hill Street / Tel: (502) 7 MOB-HarrisMaster 00482 Mobil 1976c Mobil Chemical Product Data NOVEMBER 1,1971 / Print* in U.SA. THis supersedes til prrviout publication!.' Always eomult your Mobil representative for latest information and recommendations for Mobil Product!. HI-HEAT DUM DUM* CONFORMS WITH AIR POLLUTION RULES ANO REGULATIONS _ ^0"r* / COLOR FINISH Natural Gray j Low . VEHICLE TYPE | Linseed Oil Bland PIGMENT TYPE SOLVENT TYPE J lnrti and Aio rot F>bra Aiionatic nvdrocaroont PLASH POINT, MINIMUM ! \ SOLIOS BY VOLUME \ RECOMMENDED DRY FILM (pr coat) II2F (44*C.i PMC 8SX 1/16-3/J2 inch (1.6-2.4 mm) | COVERAGE (THEORETICAL! 1 \ VISCOSITY AT 75*F. (2**C.l ! AVERAGE DRY TIME at 75*F./2<*C./ t recommendeo thinner 11 square laat oar gallon (0.27 mi/1) par 1/8" (3.2 mm) dry. Tha actual coverage will ba lais. depending on aoplicanon technique, job condition! and type of surface to ba eoatad. Mattie Skim in ISHourt. Paint ovar altar 24 Hourt witn conventional eoatmgs. Nona -- Uia at package consistency Claan-uo -- uta Thinner 7-T-38 i RESISTANCE TO 1 Fumei -- Good Moiittare - Vary Good Ory Haat -- to 3SOF. (177*0.) Intermittent. To 175 F. (73*C.) Suitaintd ; RECOMMENDED USE Boilers. Furnactx. Kilns, etc., at joint seal, pliable gasket ana for overall application during installation and repair. j APPLICATION Calking gun. trowel, orush or toray For foray -- Heavy duty mesne aauipment 5-1 pump With Surge control Oinks 7E2 gun or OaVilbtsi M8C 516 witn 3/8" Noziit and fluid tip. Brush -- Special Gum Gum Brush. MOB-HarrisMaster 00483 Mcbil Chemical Produ . Data rll-KSAT DUWI DUM*46-F-7 Ni.Hjjt Qum Oum ii recommended lor use on furnecei, soixrt. :int end similar installations. It is specially blended :a remain si.able end will withstand the expansion end oanrastion Developed by intermittent use. i-ii-Heat Sum Oum can be used at e iomt sealer end Pliable raifcr: *sr. ooiler settings. at a calkin} material lor crackt and srcken mortar lointi. or lor application overall on the unit. Surtaet should oe dean and ory. For masonry use. all cracxs tno-jid oe rakeo dean and any previously applied Qlk or autty removed, then till with Hi.Hcat Oum Oum. On oett results will be had if metal it at normal temperature at time of aooiication. WARNING: VAPOR HARMFUL CAUSES IRRI TATION. combustible, contains - organic SOL VENTS. Avoid bresthin} vapor. Avoid contact with eyes, skin, and elothing. Keep away from heat and open flame. Wash thoroughly after handling. Use with adeouete ventila tion. Wear an air supplied mask to avoid breathing concern- trated vaoors m enclosed areas. Keep container dosed. FIRST AIO: If inhaled, remove to fresh air. If not breath- mg give artificial respiration, preferably mouth-to-moutn. Call a physician. In esse of contiet, immediately flusn eves with plenty of water for at least 15 mmutts. Call a onvsician. j ! S ! NOTICE: "hit product it for industrial use only and is not mtenoed 3' suitable lor use m or around a household or *'* I* *1 & iRfVaiS H"f<eRB MBI %} C&MtMwl* 4 3e MOfb* 'OCwCf O' IVOCfll 1 -9* '* *** t*4.~\ < gr*. MTTY mm wtl O 9 !<) <** O* CK 4*9 SUv*"* I "0 *#*** *9* ^ *0* 49 4*>to mm tfiRfiiii o' r*# orwmMS Uom* 1 iH4i ,n o*oa*cu ip#i<>cjf+*t *< t#ii *v tmom voa-c Z*SCl^***& ALL Va .Uwm-A/. :f.:f*C**AwM|/^rrI rn FMf&Siof OOnKiM*' Ov'moit *(,,ATt9:'*9C?%e0:s*i-r**4o**tlCf*ftO** **t0r0>* OP ***a**o**? er,vf*i CWf *0* 'M--10 f..t 9e.-.j,,4m9 oommort mm* iwK mmvtooo ortft * **e #** * ** ior 'MtaCift o#****c3 ** "ioo*i*<**+* oe.* 4- *1 .i-f eiU*#f^R BfMbtll f **9 Ow;*oit m,.ce ***>?* i*0 *<* O** ##*! SO** t--er ~ 44--* . >WS C^CWlRCtl W <** *m CONwM.g, 9~wi f acS* **? --#*00 ?r to**' ** it looimmom* mw *oomto o*r* s# oo p* >*'*>w o or~*** o* --* -- UhVi * "*' OsrCM * *i* *#*** e^fo* Mobil Chemical Company / MAINTENANCE A MARINE COATINGS DEPARTMENT Edison, New Jersey 0S817 .0. 5=1 250 / Tel: (201) 2B7-262S .eaumont. Tens 77704 j ?.0. Sox 3*31 / Tel: (713) 235-5324 Kankakee. Illinois 60901 1 90s Norm Greenwood Av-enut .' Tel: ($15) 532-556* Los Angeles Are* / Azusa. Calilornia 9*. 732 * "4 '.-.esi Tef.n Street ' Tel. (212 33-S-S251 Louisville. Kentucky c22:0 (Sa :r;j; Ccai-ngs.' "33 v.'es: Hit" S:ree'. "i i5C2l TTi~c: I ^ aaac.u *a >o< lav -am * -a* -'.'a i-ar * --.)C v '.V.-co MOB-HarrisMaster 00484 Mobil 1976d Ufobil Chemical Product Data NOVEMBER 1. 197* / Printed in U.S.A. *- t iu'St'itdt ill orroout publications. ..jvi consult your Mobil r*pr*ntati 'or Hint information mo recommendations for Mobil Products. DUM DUM*ARMORCOTE ZOMtORMS WITH AIR POLLUTION RULES ANO REGULATIONS Jm 46-J-9 COLOR FINISH | Slack 1 Low Sheen ' vehicle type PIGMENT TYPE ; SOLVENT TYPE FLASH POINT, MINIMUM ; Mocifito aspnalt - ; inert pigments and atstitoi fibrt j Aiionatie hydrocarbons 30SF .77*CJ PMC ! V. SOLIOS BY VOLUME 1 62% j RECOMMENDED DRY FILM(oereoat) j 1/16 to 1/8 men*! II.S to 3.2mm) COVERAGE (THEORETICAL) j IS wuar* lot otr gallon 10.* m2/l) at 1/16 inch 11.6 mm) dry. Tht actual coverage will be lets. depending on application ticnniqu*. job conditions i and tyot of surface to b* coated. VISCOSITY AT 75*F. (24*C.l j Putty AVERAGE DRYTIME AT75*P. l7d*C./ j Surface tkm m 1-2 houri Set! uo m 2* hours RECOMMENDED THINNER Uj* Thinner 7-T-33 for eiean-uo only RESISTANCE TO APPLICATION j Fumei - Very Good Moisture - Excellent i Dry Heat - To 300* F. (l*9aC.I i i Trowel MOB-HarrisMaster 00485 Mcbil Chemicol Prodt .1 Data DUM DUM*ARMORCOTE 46-J-9 Armorcott it J bland of specially Mlactid bitumens to ' provide a low coat resilient material for refractory applies- :>oni. Uiad at a combat* eover. Armorcott forms an air tight tniald which offers tubttantial fuel savings by elimi nating air leaks. It < eteccially useful around and at a gasketing matarial far boilar settings. ' Because Armoreott'is moitturt and fuma rfsittant it lands naif :o all tvoat of environments including interior of dry I aims wntrt cracks and coral allow haat lou and tampersj tuft fiuciuanoni. Armoreota may ba aeoiiad ue to 1/8 men duck and will aosoro expansion and contraction. It will pravant rtitmtegration of Dlastar, mortar, conerate. brick, tilt and ctmtnt bioek. PREPARATION -- Surfaea mutt bt claan and dry. Remove all loota mortar or brick oartielat by wire brusnmg. Ootn mortar |omti and cracks ovar 1/8 inert should bt rakad and filled with quick drying Portland Ctmtnt and allowad to stt hard. NOTICE: This product it for industrial usa only and is not intended or suitable tor ua in or around a household or dwelling. | WARNING: IFLAMMABLE, vapor harmful CAUSES IRRITATION. CONTAINS - ORGANIC SOL- ! VENTS. Keep away from haat, toarks. and open llama, i Avoid breathing vapor. Avoid contact with tyes, skin, and j clothing. Wash thoroughly after handling. Ust with aoe-" ) auatt ventilation. Wear an air supplied mask to avoid breathing concentrated vapors in enclosed areas. Keep con- j tainer elosad. FIRST AlO: If inhaled, remove to fresh air. if i not breathing give artificial respiration, preferably mouth- to-moutn. Call a physician. In cast of contact, immadiattiy \ flush eves with oltnty of watar for at least IS minutes. Call j a ohysieian. i I i I I r*v IA* *iwm4**m M**4*+* an t***l*'eelf * 0* MOM mil Jpy OtCV+Ct o' Z'&w\ *## "O'* 3d'#'* '"-'* Cfdipni * fMf mr --> * wwid^a m* frvedij o* c <* **<09* *** w*' 0* *dooeir d*# m<*-* .He-,*i *o **o......... #etr #? *> 4f'|N| rJI . 3/QOwCrS -*#i "t toc>'-Cdt>op*i 'l **' "#" 0SC-*fc,, 'S Z * ***<tAwric$4i.A?'NC *0 *-,M+*0vC*Tt0* t* --c- vS o-:-''-"-rs : OfO'wett"o*,*oo**C'9*,*<d'Cad`*9`.* . o' ) 9 mai Mdrftwg, TT^trr rf^r-rr t* fy--t^ftr rm *we**i/d*c.** *** #*#'' **4t '**&* * 9*90*90 o#* #*#c c.~ i3#c 'Cdo^ ** :c- aft if .ft | |r M* V00WCO p #**** Jw/Cfiild 0'>C# #0' d'9 0* C*9 C# 9* >"* CP r^*# J ***" ? J.rf't tS-d '#*"#OV MaOd we* A# IPCfd^8K*<99 MW> P* 9W^S#m9<* 4> Cd*d09l #CdO' d ..dft-A'r J *#*#< C# -- ? #* ;*00c:i <9*--0 *^9> *4 el f f|||>Wlih> M Ivf Ufri |P|if o fOf# '0> `P"e'r *C OP<<ep' '"f `V 1 3*e~* *- -C-* C3'"C | Mobil Chemical Company / MAINTENANCE VAF NC CT - ' '-u S r==iFT/ = `.- I Edison, New Jeriey 05817 ' ? 0. Bo* 250 / Tel: (2011 257-2625 iaaument. Teas* 7770* P.O. Box 3*31 I Tel: (713) 535-532* Kankakee, Illinois S0901 901 North Greenwood Avenue / Tel: (8l5i 533-5561 Los Angeles Area / Ausa. Calilemu ?' '15 .-.esiTe-.-.r3:-rv "t: c Louisville. Kentucky :55'3 -i - ilZzi'-'i 53: v.-es; - - S::ee- Ts- 5CI "i a.:-- fz fis pr <: * '*"* * '. . * ' r j :d C. ;*c*p JdC ^r. : 5 ' * * * * MOB-HarrisMaster 00486 Mobil 1976e Mobil Chemical Product Data NOVEMBER 1.1B7B / Printed in U.SA. Thu suoerwdei *H brevious publications; Always consult your Mobil recresantative for latest information and rtcommandations for Mobil Products. DUM DUM MASONOC CONFORMS WITH AIR POLLUTION RULES ANO REGULATIONS 95 SERIES 1 FINISH : VEHICLE TYPE ' Low tmn Resinated Vegetable Oils | PIGMENT TYPE j SOLVENT TYPE j FLASH POINT, MINIMUM Titanium Oioxida -- Color oigmtnts -- Asbestos Fibri Aliphatic hydrocarbons 10S*F. (41*C.) PMC %SOLIOS BY VOLUME ! RECOMMENDED ORY FILM <pr coat) | COVERAGE (THEORETICAL) 42% dtpanding on color 25 mils (S2Sutn1 674 squari feet par gallon (1S.S m^Atr) par dry mil (25umj average, dtpanding on color. Tha actual coverage will ba lass, dtpanding on application technique, job conditions and type of surfaca to ba coated. 1 VISCOSITY AT 7S*F. (24*C.) i AVERAGE DRY TIME AT7S*F. (24*C.l Mastic Skint over in 1 hour -- Undar surface remain* pliable | RECOMMENDED THINNER 1 1 RESISTANCE TO RECOMMENDED PRIMER STEEL GALVANIZED WOOD MASONRY APPLICATION ! NOTE . CAUTION Do not thin for aopiieation - In cold weather store in warm arias before use. For dean-up ust Thinner 7T-38. Dry Heat -- To 150*F. (S5*Cf Weather extremes -- Excellent Chemical Fumes -- Exctllent Moisture -- Excellent Salt Air -- Exctllent None required None required Not recommended 47-W-21 Masonoc Primer | Hu*y duty lOriv -- Trowel - Spci*i brusft. CONVENTIONAL SPRAY (Suggested Equipment) Hsvy duty masuc equipment. 10:1 sums. V' 1.0. fluid not*. Sinks 7E2 gun (45 x 3/8F notzltl and DeVilbiss MBC SIS gun iM3-78 | c*0 'A") h*vt given good rtsultt. Approximate linings - oumo ortsuri Z3 | 01). atomizing pntturi 70 pti. i CfJCkj in (ici of 1/32" (0.8 mmf snouW first & csulkaa witn Oum Dum Calking Compound. Do not ust pn glazed brick without zpnsulting Mobil rroresentative. MOB-HarrisMaster 00487 Mobil Chemical Produ . Data DUM DUM MASONOC95 SERIES | Oum Oum Masonoc i* I heavily bodied. ttktured coning I aesirtd for uu in ni-build applications for the waterproof- ing mo restoration of txterior masonry tnd for the orotic non of (tit/ surfaces. PREPARATION: Old masonry surfaces should bo prepared by on it cleaning or other suitable methods to remove dust. Oirt. surface contaminants'. and loot* particles. Any walling conotti, loost -morur. and unsound masonry must be I ramovtd and the iwrfaci rtoairad and brought to level as | natoed. Portland eamtnt catches must b ailowid to curt and thin niutraliaid prior to overrating. ! Prime all ban masonry surface with a coat of Masonoc Primtr 47.W-21. Oo not aooiy mori orimir than is rinded to seal tht surface. Allow primer an overnight dry and then fill all cracks with suitable caulking material prior to toe New masonry surfaces must be allowed to curt for a suffi cient length of time to reduce alkalinity. A minimum of 30 oays time it rtouirtd with at least 6 months desired.* i Steel surfaces should be Cleaned by blasting or wire brush ing. Oum Oum Masonoc may be aoplied directly to the bare ttael if desired, or over a suitable Mobil steel primer. NOTICE: This product is lor industrial use only end is not intended or suitable for use in or around a household or dwelling. , WARNING: VAPOR HARMPUL. CAUSES IRRl. TATION. COMBUSTIBLE. CONTAINS - ORGANIC SOL VENTS. Avoid breaming vapor. Avoid contact with tvts. skin, and clothing. Keep away from heat and open liai-.e. Wash thoroughly after handling. Use with adequate ventila tion. Wear an air suooiitd mask to avoid breathing concen trated vapors in enclosed areas. Keep conoiner dosed. FIRST AIO: If inhaled, ra move to fresh air. If not breath ing give artificial resoiration, priferably mouth-to-mouth. Call a ohvticun. In case of contact, immediately flush ayes with plenty of water for at least IS minutes. Call a onvsician. I i "** ,1 in* m lit n *wew am cexeiuvw t frr waa* */vsi v >-<> 0~3'VCI1 i * wiv-v .i>--1---- i / <v uvemrw m v mmum u> fravaty a ivn> aw *"r eaia-i ' --ao* a *<* vm n-'-v* -a */. w-1 ----way a--r wae we mw0 saaa -- rr Meat --aivi taa# -n aedueii <vi -- oae>iai-a"i -*<- ./ i#*t -a '.ai OfCCUAias i.iC*-f* .aj>A,T)f},,n,,aaaa>aa>ai.aaeSCWSatLa<ejvtin<t^;we to rf*r*u<P*r/or arj'as* o--oCiuPwOo<*ai w> -./.-..asa -- --laraivns-.-mt *aca-aiaaoac:saMawie*a<*iCunni0--i.oeo"iin/a accaaio-ea s* me v---i a '>i waav. laeiefymMwe a awesvasa areas raMwiwy i- >a nr m*i va> iwi i-ui aacc:i oa--a<ae ai-iaec-cai-a- "sa --.1 ji .is sore essntee aweerveaaee we aeeaesa a lere i-a shic-sk a<a i-a-aa/ ii-c wean eno-ea - o-s 3---asa /r-rao-as sraa ee lwva-i io-v J'-vo weov a vea eg swiwr--a as ee ueere a te-iHvr-ivi a*--rgai treea --to**/ ss >ewr it -la-ca/ac ev *- "oa --/ aeoMC.-i *i *'*w I*--es i-i aa ere /vrrsnai eete ease su weev s/-*u -a* oe *ae *a >iwr - ee**va c- '*w* /-# /*.-w/t -t e-rv vs /aaso*aa/a ce-'-a Mobil Chemical Company I maintenance & masinE CCaTinGS DEPARTMENT Edison, New Jersey 08617 P 0. Box 250 / Tel: (201) 2S7-2S2S Beaumont. Texas 77704 P 0. Box 3431 / Tel: (713) 535'-5324 Kankakee. Illinois 50901 901 North Greenwood Avenue / Tel: (815) 933-556' Los Angeles Area / Arusa. Calilornia 91*02 Tenth Street ' Tel (2121 334-6251 Louisville. Kentucky :32'C [Ra-l'cao Coatings) '533 ..$: hhi Street ' 7: (CZ. *74-4411 '-nr z-ii*cr. *-ir *.< *-<r "a-- 7? rro/>*"tf/7o'o"'e. C<-** i:;:.-s r: s--:* Ua*t. : 3C*nr. **-ce MOB-HairisMaster 00488 Mobil 1976f Mobil Chemical Product Data NOVEMBER t.197* / Print* in U.S.A. Thu supersedes ill previous publications; Always consult your Mobil representative for latest informition and recommendation* for Mobil Product!. CHIMNEY DUM DUM CONFORMS WITH AIR POLLUTION RULES AND REGULATIONS 97 SERIES ! FINISH Medium gloss i VEHICLE TYPE Resinated Vegetaolt Oils PIGMENT TYPE 1 1 SOLVENT TYPE i FLASH POINT, MINIMUM } % SOLIDS BY VOLUME j RECOMMENDED DRY FILM (or co*ii i................... COVERAGE (THEORETICAL) Titanium Dioxide. Asbestos Fibre. Mica plus color fast pigments. Aliphatic nydrocarbons ioi*f. na*cj pmc 63% avaraga. daoanding on color 25 mils (S2Sum) 1010 souara fact par gallon (24.! m^Avi par dry mil (25p/n/ avaraga, depending on color. The actual coverage wiil be las, daoanding on aooiication technique, job conditions and type of surface to ba ooatad. i VISCOSITY AT 75*F. (24*C.) Mastic AVERAGE DRYTIME AT75*F. (24*C.i Surface skin 4-6 hrs. Under surface remains piiabli. j RECOMMENOEO THINNER ' RES1STANCETO i 1 RECOMMENDED PRIMER APPLICATION Oo not thin for application. Use 7-7-38 for elaan-uo. Moisture -- Exctllsnt Chemical Fumes -- Very Good Ory Heat -- To 210*F. (99*C. 1 constant surface temperature. Chimney Oum Oum Primer 38-V-5 Brush -- Spray CONVENTIONAL SPRAY (Suggest* Eouipmant) Heavy duty mastic equipment, 10:1 pump, 1** I.D. fluid hose. Sinks 7E2 gun (45 x 378F nozzle) and DeVilbiss MBC SIS gun |MB*78 cap VI nave given good results. Approximate settings -- pump prassura 40 pti. atomuing pressure 70 osi. NOTE CAUTION On stacks that art in part-tima usa, looly thin orgsn coats of Chimney Oum Oum to aoprox. 10 mils (250um) wet total. Normal heavy coats couie be damaged by rain collection on the interior of the stack. NEW CONCRETE MUST WEATHER A MINIMUM OF 3 MONTHS BEFORE COATINGI MEMBRANE CURING AGENTS MUST BE COMPLETELY WEATHEREO OR OTHERWISE REMOVED BEFORE COATING. MOB-HarrisMaster 00489 Mcbll Chemical Prodv t Data CHIMNEY DUM DUM97 SERIES ! Chimney Oum Own it * rugged heavy coating far the NOTICE: This product is for industrial use only and is not exterior of mimneyt that provides flexible weatherproof intandtd or suitable lor use in or around a housano>0 or orottaion. It fills end bridges heirline creaks with a flexible dwelling. costing under s tougn outer ikin. Should the leathery skin become freetured. the soft under film will harden on con WARNING:tact with sir. May os soohed without completely cooling i stack. vapor harmful, causes irri ' LININGS MUST BE INSPECTED FOR INTEGRITY ANO FREEDOM FROM AIR LEAKS. tation. COMBUSTIBLE. CONTAINS - ORGANIC SOL VENTS. Avoid breaming vigor. Avoid contact witn eyes, skin, and clothing. Kttp away from heat and ooen flame. PREPARATION: Must be clean and dry. Surface should be Wash thoroughly after handling. Use with adequatt ventiia- . i thorougnly wire brushed to remove dirt, grease, toot and tion. Wtar an air supplied mask to avoid breathing eonctn. old coating. Cracks larger than hairline up to V' wide fraud vapors in andostd artat. Keep container dosed. mould be raked, cleaned out and crimed with 38-V-5 FIRST AID: If inhaled, remove to fresh sir. If not breath Chimney Oum Oum Primer and filled with Calk. Fill larger ing give artificial respiration, preferably mouth-io-meutn. cracks witn quick-setting cement. New etment patches Call a physician, in ossa of contact, immediately flush eves should be treated to neutralise alkali content. Prime entire with plenty of water for at least IS minuttt. Call a ohvn- surface witn 33-V-5 Chimney Oum Oum' Primer. cun. j i iII 'e#**ifwf a* ih* *mrmm aai A *>"* * *** mrt Mr mm m mhiumi tmm f**m**i 9* <*> *<< MaM agrtgAft 1**1 .ft iie* ov ***** * #** a'Mwcr v 9*ac*u '*** >*** mi i*r s #* & 4** ** r*# iMCtf<4P0*| ***tw ***** der^i m .* Me* 0*SC*>*wS 1 vhamMamTiIS *HaT:hC TO A*+\.tC*tiO* ttorfii r^w***C >*CtyD*<C of o ACMAMTAMKJTr***riTMtlH*a+n,c+4t tw/Mif Kf. :+ocwcu !/*** 1 C CM^t acc*&*#c* a* .* 1'*'"'1 0< ** MfTtWIfc # IM WM f* * *v+*er Af -- i .ft *** Tfi<w mmt pan It mm > an an /#<** * awe**!* ****## #** i*n l*d SfOTuCn ' f*#<** "Oe-* e**< a' * o r-vif i*H'ii im n K** to-e '"*** MOM * m M UCdOUMm M M0| >#r flCff* wt*ff 49 *M**r **ddM tv -** ##' C' JCwC'l d fM*e| *t%*l*4 4*m *$ fMMMvM I* M M HIM JfM< M 40f| f**vV l M**** C f.f*# e*r* /* * ** ftilO'O* CC^"0 Mobil Chemical Company / MAINTENANCE 4 MARINE COATINGS DEPARTMENT j Edison, New Jersey 09817 P.O. Boa 250 / Tel: (201) 287-2626 Beaumont. Teats 77704 P 0. Boa 3431 / Tel: (713) 835-5324 Kankakee. (Ilinoia 60901 901 North Greenwood Avenue / Tel- (8tS) 933-5561 Los Angeles Area / Azusa. California 91702 ;34 west T.-.:h S:r**t / Tel- (213) 334-2251 Louisville. Kentucky 4C21C (Railroad Ceilings) :53Q West hull Siree: Tef (S02) 774-4411 fl-ooverr #-to ......sir *'-* 0>/r. -vu-a.-Tawo C.-.e. fayorj. Coimt-i See 4.--o C-rv eo MOB-HamsMaster 00490 (Mobil 1976g NOVEMBER. 1971 / Primed in U-SX C This tuocrsoes alt previous publications. aj~v* consult your MoOil representative lor latest intormation and recommendations lor Mobil Products. / m f DUM DUM CAULK / 46-F-5 An oil based caulking compound recommended lor glazing and tilling operations by knile or gun lor joints and cracks wnere movement is not a critical factor. Recommended specifically lor use with 95 Series Masonoc. Excellent adhesion to previously primed sur faces and can be overcoated with conventional finishes alter 24 hours. CHIMNEY DUM DUM / 97 Series / Chimney Dum Dum provides the same outstanding pro tective and waterproofing qualities as the 95 Series Masqnoc, except that it has been formulated for use on concrete chimneys where additional heat resistance up Son Worr tS-C-u Atao aaiia*i: tun ts-c-io Oum Oum fTVJ lm#rfi4tl4Ai O'**** a* to 210'F. is required. *7>W-t v/HI-HEAT DUM DUM / 46-F-7 A heavy semi-plastic fibred coating, which acts as a DUM DUM MASONOC 1 95 Series Masonoc is a heavy bodied textured coating designed as a weather seal, waterproofing,-and restoration coating lor all types of masonry structures. Pliability and elas ticity allow lor building movement without cracking of the coating while a tough outer skin provides protection joint sealer and pliable gasket.for boilers, furnaces and dry kilns. Improves boiler efficiency by preventing heat less. Retains its elasticity at constant heat up to 175' and intermittent heat to 350*. May be used is a complete cover to eliminate excess fuel consumption and can be painted over in 24 hours. lor normal usage. Its high build qualities permit hairline f cracks lo be bridged and sealed, and surface irregulaarirsi- vDDUM DUM ARMORCOTE / 46-J-9 ties to be filled and uniformed. A specially compounded, heavy bodied product con Masonoc also provides fine protection lor steel with taining asphalt, reinforcing pigment and high boiling its high film build and impermeability. Its excellent sur face wetting properties recommend use ol this material >n areas that cannot be cleaned too well, where there are numerous angles and edges to protect, or when a hydrocarbons. Resistant to fumes, moisture, and sus tained temperatures up to 300*F. Used to protect and increase the efficiency of brick boiler settings. May be applied to boilers even while they are in operation. single coat application is all that can be provided. CHIMNEY DUM DUM PRIMER / 3B-V-5 a clear 100 percent solid neat resistant penetrating ormer designed lor application to masonry surfaces be neath Chimney Dum Oum Coatings. MASONOC PRIMER t 47-W-21 . Masonoc primer is a normal paint like material whicn is io be used beneath the Masonoc coating on ail types ol masonry surfaces to seal of! and eliminate surface porosity. Bud product oescription* are given lor the purpose ol facilitating selection. Always refer to the individual Mobil Chemical Product Data Sheets tor further specific product recommendations and use instructions. rn /wrnijit.ng w m* tniotmolten conianwd noiottt a001 net conalilma a 'aiamii,wi or 1*00*1 mar toy prepuce or procoaa * Iroo Item oalam tnirmeomont ot *nr e-uro piny nor oomt a corutuvit mt 0/4*11*9 qi iictm# *notr tny ptttnt of mom cx #ny trurc OtfTy. Woof 4i*w/r*4 a# l*b*hty tot any wif/m?*- /< owf ot tn \j*9 of f ptaavcL. wstrmnti m#t m evoowett mmsi m# t0#cif<C4f'O'W moren * tB for tntm. moo) 0f5COJ**S A(,C OThA **45 rusting tom*proOucto*ncQtSCmiuSAUl mAAANTiS *EVkTlHG TO TnlA APPLICATION. mSDtma or tmpiiod.INCiUDING out not itmtitO (o \ & u PChahTA91UTT tnaflTNS5 lor otfhcyttt ev/oa*#. A#c#<0f of p/ooverx i/m woodi Cf>#m*cjiCotm0*Ovii*o/*COrt4Hiuf*4 *cctpt*npt at tnt t*mi ol inn n*rf9nty, eonittry proni*tt9l of pw/CA4l QtQtr% noivtlRtlintfifty in in# #v#nf Iftjf Mo>l hf>Ct thtt proOwCtl OtUrtttO #/ Off*f09Cif<C4len. WooM wli 41 it lots onettuort. tnntr two**cm fn# proOven or >fiwr< in# p^entit ones internal. *no WoO*i\ CP&ct ot on* ot tntit ttmtOit* inf) om S vytl tof# wood --*u wo#r no c*rcvnut*ncf O* i40f# >o* CO"Ma/*i4i 04mp#x. wtetot intoltt i fiJODiry a m*n0*i#o Or *** uoO) m*U Othvtr otccvcit t tttO >'<* -^oiir 4| if n /ion40*r 10 00 10. Owl wqcw tn*u not Ot i*4o*t lor f4ifwr# lo o#f<#/ ^ nm# wfion mo Itilort a Otfpnc ill /#4ton0/ conicof. Mobil Chemical Company j MAINTENANCE k MARINE COATINGS DEPARTMENT Edison, New Jersey 08817 P.O. Box 250 / Tel: (201) 287-2626 Beaumont. Texai 77704 P.O. Box 3431 / Tel: (713) 83S-S324 Los Angeles Area / Azusa, California 91702 1004 west Tenth Street / Tel: (213) 334-8251 Louisville, Kentucky 40210 (Railroad Coatings) 1630 West Hill Slreet / Tel: (S02) 774-4 MOB-HarrisMaster 00491 Mobil 1976h NOVEMBER. 1976 / Printed in U.S.A. This suoeneoes all orewous puoiications. r ajwsvh consult your Mood representative lor latest inlormation and recommendations lor Mooil ProduCS. s DUM DUM CAULK / 46-F-S An oil based caulking compound recommended lor glazing and filling operations by knife or gun tor joints and cracks where movement is not a critical factor. Recommended specifically tor use with 95 Series Masonoc. Excellent adhesion to previously primed sur faces and can be overcoated with conventional finishes after 24 hours. Son ivory is-C*n Oioy IM.Uon Lc_ wft ts-c*to J 1J.W.I ml CHIMNEY DUM DUM / 97 Series Chimney Dum Dum provides the same outstanding pro tective and waterproofing qualities as the 95 Series Masonoc, except that it has been formulated for use on concrete chimneys where additional heat resistance up to 210'F. is required. All! tvAiUOkc Chmooy Owm OvM INY.J imtrnotioAOl u/Ht-HEAT DUM DUM / 46-F-7 A heavy semi-plastic fibred coating, which acts as a DUM OUM MASONOC / 35 Series Masonoc is a heavy bodied textured coating designed as a weather seal, waterproofing, and restoration coating tor all types of masonry structures. Pliability and elas ticity allow for building movement without cracking of me coating while a tough outer skin provides protection joint sealer and pliable gasket for boilers, furnaces and dry kilns. Improves boiler efficiency by preventing heat less. Retains its elasticity at constant heat up to 175' and intermittent heat to 350'. May be used as a complete cover to eliminate excess fuel consumption and can ce painted over in 24 hours. for normal usage. Its high build qualities permit hairline / cracks to be bridgjed a, nd seated, and surface irregulari- V*0DUM DUM ARMORCOTE / 46-J-9 ties to be filled and uniformed. Masonoc also provides fine protection lor steel with its high lilm build and impermeability. Its excellent sur face wetting properties recommend use of this material in areas that cannot be cleaned too well, where there are numerous angles and edges to protect, or when a single coat application is all that can be provided. A specially compounded, heavy bodied product con taining asphalt, reinforcing pigment and high boiling hydrocarbons. Resistant to fumes, moisture, and sus tained temperatures up to 300*F. Used to protect and increase the efficiency of brick boiler settings. May ce applied to boilers even while they are in operation. ! MASONOC PRIMER / 47-W-21 ] CHIMNEY DUM OUM PRIMER / 38-V-5 Masonoc primer is a normal paint like material wmc.n .$ 1 A clear TOO percent solid heat resistant penetrating to be used beneath the Masonoc coating on ai: types primer designed for application to masonry surlaces be- masonry surlaces to seal olf and eliminate surface neatn Chimney Dum Dum Coatings. porosity. 3'<ei product descriptions are given lor the purpose or Itcilitaring selection. Always refer to me individual Mcsil Cnemica. Product Data Sheets lor lunner spccihc product recommendations and use instructions. lutnttmng qI ma tniaftnation eonurivd Aaram eoas not confute* a ftvaltnwitfi Or udoi mat any groavct or erocaia <4 Iraa from paiam tnitingamana i ; claims or anf emu oanr nor doof it eomnivia too otsnunf of a f<ansa vnoar any oat ant or upoa or any trwrd pome Uorvl assumoi no UaOJny tot any atltnon f mni -scAsvraiiia Owl or mo v*a or maproowCL arooi marrams mar III oroevcis maol ina loacrlicafiam arieli it laBlennaffl. arooil OfSCLAIUS ALL OTtiEfi ; i MAAANTres ilaiin0iomaoroaucil.an<lOISCLAIuSAU~AAAMTIS "ELAT/mG TO 7>rf!A APPLICATION, aaoraa O' imoriao.INCLUOrNC Out not amrtao la,, j tartani,aiol uEACHAN7ABIUTT anoftTNESS lor oantootat o-rooaa. Aoeoior or proaucll Horn u OO.JS Coamacs I Coatflays Pnrismrveorulifulas accaosanea or ma I i lattai oi im worramr. connary or--isiom or ourenasa otoarx not--mitanetno. In ma a-am mat at00-11`IVJI mat oroowcts Oon-atoO ara oll'iooctloattcn. Wool I -at at its iota oiscralion. aisnor raoraca mw otooucn or laiww ma pwcnaaa cu.c# moroor. aU M0O1I4 CAOCa or orw or maaa tamooiol tnatl On Boyaex sola tatnaoy Hocat --u ynaat no etteumatanema Oa Aaola lor coAsaouamial aamagal. ascaol insofar as haottily 4 tnanoaloO Or la-- UoOtl mJl oaltaar oroducis ai ma| apraae fimas .i-aolar aa i( is taaionaoty aosa 10 00 10. Owl atooa tnalt not oa liaola lev taiiuta to oaimar on nma rnan tailura is ooyono ill taaionaota coaimst \ I j Mobil Chemical Company / MAINTENANCE i. MARINE COATINGS DEPARTMENT Edison, New Jersey 08317 P.O. Box 250 / Tel: (201) 287-2626 Beaumont, Texes 77704 P.O. Box 3-431 / Tel: (713) 835-S324 Los Angeles Area / Azusa, California 91702 1004 West Tentn Street / Tel: (213) 334-8251 Louisville, Kentucky 40210 (Railroad Coatings) 1630 West Hill Street / Tel: (502) 7 MOB-HairisMaster 00492 Mobil 1980 MATERIAL SAFETY DATA SHEET 7^ If PEP 9/26/80 FOR COATINGS. RESINS ANO RELATED MATERIALS |AggfOvvU$ 0p*rtmnt ol LAOOt sni*lly ' to O$HA20l Section I --UUCTUWRSNAM6 THE qIbs0ji_HOMANS COMPANY streetaoohess 1755 Enterprise Pkwy\ Twinsburg, OHcity.state.amozipcooe NPCA 1 44087 216/425--3255mercencytelephone no. roouctclass AX-2789-H "manufacturers cooe identification T8AO NAM ASBESTOS FIBRE-FREE MOBIL 46F7 Section III - PHYSICAL DATA :.l:ncrahoe Mineral Spirits 310F. vapor DENSITY j yvl -g *vifl I Sv*PCAATtCN AT IyyIslower than etmeb eaCc*Tvolatile S'* VCLOMC <viC-t =a i .5 'nan a.a Section IV - FIRE AND EXPLOSION HAZARD DATA Combustible it' > jlSniNG MEDIA p.ASi" point Closed Cup 105 F. mintmum C09 . Dry Chemical , Foam `'--Aw ii anO EXPLOSION ha^aOOS jCau ?;oe pfChTinG pOCOuACS Contains solvent, water not effective. MOB-HamsMaster 00493 Section V - HEALTH HAZARD DATA 'j old limit value See Section II. =.'*??. s op overexposure Inhalation - possible dizziness, light headedness. MERGENCE anO PiRST aiQ PROCEDURES See physician. Flush with water. STABILITY UNSTABLE KT1 stable N CO M aTaBILI T Y l MJ,>< ID OhI| A2AOOuS OeCOMPQSTiOM PRODUCTS Section VI - REACTIVITY DATA conditionsroAvoio Sources of` ignition. x;aBDCuS POLYMERIZATION OnOITiQnS TO avOIO I [ WAY OCCUR |"XX WILL NOT OCCUR Section VII - SPILL OR LEAK PROCEDURES TPS TO ae taken in case MATERIA!, is RELEASED on SPillCO Contain 'spill. Remove all sources of ignition. Scoop up and return to container. E Disposal method Place in trash or use for landfill according to regulations. J * ON Section VIII - SPECIAL PROTECTION INFORMATION .f.-_.r,CN Not normally required. - = s.=. es Net normally; if r.eedec, _se :u:;er glf.es. r i on Not normally. * "-= asCTSiTivS cC'-'iPWENT Section IX - SPECIAL PRECAUTIONS = :I-ir:CNS 'C 3 TaXn in anCi,inG anO STORING Keep away from open flame. Z* - ~ sb:;ajTiOnS Store in accordance to N'FPA. State and local regulations. *>\*K'A MOB-HarrisMaster 00494 Mobil 19xxa 00495 * PANORAMA COATINGS / 12 Sorias MOBILTONE LATEX FLAT WALL FINISH / 77 ' A complete line of attractive colors, designed to provide This Vinyl Latex is a flat, interior finish that pr: the "modern look" for all types of industrial installations. uniformity of color and sheen... rapid drying ... e These materials are formulated primarily for service in application. Wide range of attractive colors ms the industrial environments to combine weather durabil ideal for use on walls, ceilings and woodwork. ity, resistance to mildly corrosive exposures, with good film build and ease of application with all generally used . methods. They provide excellent color retention and' HI-HEAT DUM DUM / 4S-F-7 appearance throughout a long service life. , This material acts.as a joint sealer and pliable c STAINLESS STEEL PAINTS for boilers, furnaces and dry kilns. It improves " v-'j efficiency by preventing heat loss. Retains its ela -23>, J Stainless steel pigmented coatings in both one coat high I build quality and finish coat materials for previously primed surfaces. Provide excellent durability and steel/ at constant heat up to 175* and intermittent heat tc A heavy semi-plastic fibred coating, It can be u: a complete cover to eliminate excess fuel consur protection. [; and can be painted over in 24 hours. MOO11 19xxb Mob.] Chemical Protective Coatings Products Catalog MOB-HanisMaster 00497 urn Dum Products : ..v OUM MASONOC / 95 Series CHIMNEY DUM DUM / 97 Series jsc.nsc is a heavy bodied textured coating de: t.-.-eo as a weather seal, waterproofing, and resto- c - coating for ail types of masonry structures. : -c t;r/ana elasticity allow for building movement cracking of tne coating while a tough outer * crevices orotection for normal usage. Its high . <c qualities permit hairline cracks to be bridged r: sealed, and surface irregularities to be filled r: .mformed. `asenoc also provides fine protection for steel --. :s high film build and impermeability. Its ex.: e*.t surface wetting properties recommend use .* t. s material in areas that cannot be cleaned too where mere are numerous angles and edges ". protect. or when a single coat application is all : ran be provided. Chimney Dum Dum provides the same outstanding protective and waterproofing qualities as the 95 Series Masonoc. except that it has been formulated for use on concrete chimneys where additional heat resistance up to 210*F. is required. Ht-HEAT DUM DUM / 46-F-7 A heavy semi-plastic fibred coating, which acts as a joint sealer and pliable gasket for boilers, fur naces and dry kilns. Improves boiler efficiency by preventing heat loss. Retains its elasticity at con stant heat up to 175* and intermittent heat to 3S0*. May be used as a complete cover to eliminate ex cess tuet consumption and can be painted over in 24 hours. CUM DUM ARMORCOTE / 46-J-9 I -if.'NEY DUM DUM PRIMER / 38-V-5 A specially compounded, heavy bodied product - :'e ar fOO percent solid heat resistant penetrating ' containing asohalt. reinforcing pigment and hign : -e."designed for application to masonry sur- boiling nydrocarbons. Resistant to fumes, moisture, beneath Chimney Oum Dum Coatings. and sustained temperatures up to 300*F. Used to ! . v. DUM CAULK / 4S-F-5 o cased caulking compound recommenced lor : .~.~g and filling operations by knife or gun lor *:s ar.d cracks wnere movement is not a critical .--toRecommended specifically for use with 95 j-.-ii-s Masonoc. Excellent adhesion to previously : -ned surfaces and can be overcoated witn convTirnal finishes after 24 hours. protect and increase the efficiency of brick poiler settings. May be applied to boilers even wnile tr.ey are in operation. MASONOC PRtMER / 47-W-21 Masonoc primer is a normal paint like material which is to be used beneath the Masonoc coating on all types of masonry surfaces to seal off ana eliminate surface porosity. -LRYLIC LATEX CALK / 46-W-6 : Latex Calk 46-W-S is a hign quality caiking material cesigneo 'cr use around wincows. cccrs. -gs, wall board joints or similar openings that recuire sealing, it -s particularly effective for mor.r ,c its and (or filling masonry cracks. Acrylic Latex Calk exhibits excellent weatnerabihty. dexib-v.y ;: g poC adhesion to wood, masonry, glass and metal. 'i-MTTTE / 46-X-lO -.'i.-.e is a pipe thread compound for sea..eg (o.r.:s .* o'S. caps, i'c . to prevent air and liquid les-s i ec in a semi-paste consistency. Jomt.te wu: never 'tree.", and a-cv'SCiSjCm.-ngyears later with ease :c' use on joints m steam, gas. water, arc air serv.; Can oe usee on rotao'e water lines Not ?;- r""eided for use on gasoline or soiver.i .nes MOB-HarrisMaster 00498 Mobil I9xxc fV!ob,,] Chemical Protective Coatings Products Catalog . ~r-r-rr7- ttpm& - *7 h .* r' t. ' p r: - rf/,- L *i , V \J3~3 L :._ -*r. '\v'i --^ r`- jp.'^ T 9 v 1 $[^4 'f fEvii -ii Vv- '"" - > V *1 M si MOB-HarrisMaster 00499 Zum Dum Products : ..v DUM MASONOC / 95 Series CHIMNEY DUM DUM / 97 Series isr-noc is a heavy bodied textured coating de- Chimney Oum Dum provides the same outstanding : 2 as a weather seal, waterproofing, and resto- protective and waterproofing qualities as the 95 v c coating lor all types of masonry structures. Series Masonoc. except that it has been formulated : iz tirv and elasticity allow for building movement lor use on concrete chimneys where additional heat r jt cracking ol the coating while a tough outer resistance up to 210`F. is required. * provides orotection for normal usage. Its high . -c dualities permit hairline cracks to be bridged HI-HEAT DUM DUM / 46-F-7 : railed, and surface irregularities to be filled A heavy semi-plastic fibred coating, which acts as : ..iilormed. asenoe also provides fine protection for steel - :s high film build and impermeability. Its ex* r-.t surface wetting properties recommend use r - s material in areas that cannot be cleaned too . where there are numerous angles and edges " :*2te:t, or when a single coat application is all :: can be provided. a joint sealer and pliable gasket for boilers, fur naces and dry kilns. Improves boiler efficiency by preventing heat loss. Retains its elasticity at con stant heat up-to 175' and intermittent heat to 350*. May be used as a complete cover to eliminate ex cess fuel consumption and can be painted over in 24 hours. I CUM DUM ARMORCOTE / 4&-J-9 : -:i.' NcY DUM DUM PRIMER / 38-V-5 . A specially compounded, heavy bodied product -r >00 percent solid heat resistant penetrating containing asohalt. reinforcing pigment and hign : ~s."cesigned for application to. masonry sur* boiling hydrocarbons. Resistant to fumes, moisture, ytss beneath Chimney Dum Oum Coatings. and sustained temperatures up to 300*F. Used to : . V OUM CAULK / 4S-F-5 = C-seC caulking compound recommended for : .c -g and filling operations by knife or gun lor protect and increase the efficiency of brick boiler settings. May be apoiied to boilers even wnile they are in operation. "3 and cracks where movement is not a critical MASONOC PRIMER / 47-W-21 ..to*. Recommended specifically for use with 95 ir'ies l.'.asonoc. Excellent adhesion to previously i me-a surfaces and can be overcoated with con* tirnal finishes after 24 hours. Masonoc primer is a normal paint like material whicn is to be used beneath the Masonoc coating on all types of masonry surfaces to seal off ane eliminate surface porosity. --RrLIC LATEX CALK / 46-W-o 2 Latex Calk 46-W-6 is a hign quality calking material designed `or use around wincows, doers. .-.n.-gs, wall board joints or similar openings mat recuire sealing, n >s particularly effective lor nor,c rts and lor filling masonry cracks. Acrylic Latex Calk exhions excellent weatnerabiliiy. nexio-v.y :: c ood adhesion to wood, masonry, glass and metal. A -:-N--iTc / 46-X-10 is a pipe thread ccmpounc for sas.-ng ,c.n;s _*.p_s. caps. e*c . to prevent air and liquid isa-.s i.c : ic in a semi-paste consistency. Jomt.te n: never - order, ano a.-c*s disjoining years later wo ease :c* use on joints m steam, gas. water, arq air service Can pe used on potaoie water lines. Not *?cIndia for use on gasoline or soiveri res MOB-HarrisMaster 00500 APPENDIX UI MOB-HarrisMaster 00501 Evaluation of Asbestos Release from Exterior Masonry Weatherproofing Mastic During Application and Removal By Arthur D. Little, Inc. Acorn Park Cambridge, MA 02140-2390 1992 Reference No. 65191 A t+hir O I.H+lo MOB-HarrisMaster 00502 Product Background From the mid-1960's through the 1970's, Mobil Chemical Company manufactured and sold a line of mastic-type protective coatings under the name Dum Dum Products. Dum Dum Masonoc/Series 95 was a restoration product for weatherproofing masonry structures. The Mobil Chemical Product Catalog states: "Dum Dum Masonoc/95 Series Masonoc is a heavy bodied textured coating designed as a weather seal, waterproofing, and restoration coating for all types of masonry structures. Pliability and elasticity allow for building movement without cracking of the coating while a tough outer skins provides protection for normal usage. Its high build qualities permit hairline cracks to be bridged and sealed, and surface ixregulaxides to be filled and uniformed. Masonoc also provides fine protection for steel with its high film build and impermeability. Its excellent surface wetting properties recommend use of this material in areas that cannot be cleaned too well, where there are numerous angles and edges to protect,, or when a single coat applicadon is ail that can be provided." Masonoc consists of a rtsinated vegetable oil vehicle with about 22% solid fillers (by weight), including titanium dioxide, the chrysodle form of asbestos and various coloring pigments; the total solids content is 42 peicent by volume. After application, Masonoc skins over in 1 hour, but the undersurface remains pliable* to allow for expansion and contraction. The Mobil Chemical Product Data Sheet for Dum Dum Masonoc claims excellent resistance to dry heat (to 150F), weather extremes, chemical fumes, moisture and salt air. Product Testing During Application and Removal Three 5 gallon pails of Dum Dum Masonoc (soft white 95-W-9) were obtained from an electric utility seeking information on product disposal. A sample was rairen from one pail, about a third full, and ashed at 500C. Microscopic analysis of this ash confirmed the presence of the chrysotile form of asbestos. The other two pails were intact with no visible signs of having been opened; After thorough mixing and being satisfied that the product viscosity was in the range of a mastic, these two pails of Masonoc were used for application and removal experiments. This work was conducted at our facilities in compliance with United Stares and Massachusetts rules and regulations applying to asbestos and in accordance with an approved Arthur D. Little, Inc. Health and Safety Plan. A test plan was developed to simulate typical work practices for product application and removal1. In addition, a sampling and analysis protocol was developed to* 'Although intended for exterior use, this product was tested in an interior (controlled) environment. ArtfurD Little MOB-HarrisMaster 00503 Sample No. 072701 072702 072703 072704 111406 111407 111403 050104 050107 050105 Table 1 Asbestos Exposures During Application and Removal of Dum Dum Masonoc Description Sample Type Exposure (s/cc)4 First Application First Appiicanon Second Appiicanon Second Appiicanon First Removal Hist Removal (replicate) First Removal Second Removal Second Removal (replicate) Second Removal Personal Area Personal Area Personal Personal Area Personal Personal Area 0.01 <d).01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 <0.01 Conclusions The conclusions reached in this study are as fallows: After thorough mixing, the obtained pails of Dum Dum Masonoc, confirmed to contain-chrysodie asbestos; were smooth and of consistency. Application to concrete panels required heavy duty nwine spray apparatus. After aging at 150F for 42 days and arirfidnnai periods of 67 and 168 days at ambient condidons. the product was observed to be pliable and elastic when depressed with a tooL Results of worker exposure measurements during appiicanon ?nd removal of Dum Dum Masonoc in a controlled environment did not the minimum detection limit of 0.01 structures/cc. Based upon the above results, occupational exposure to airborne asbestos fibers during the appiicanon or removal of Dum Dum Masonoc is virtually non-existent.* *Asbestos structures per unit volume of air. Aftfur D little MOB-HarrisMaster 00504 quantify the extent to which asbestos structures" may be released during the experimental application and removal activities. This protocol was designed so that ail applicable NTOSH antLEPA requirements for analysis by transmission, electron microscopy were met or exceeded. The minimum detection limit for the analytical protocol was 0.01 strucmres/cc3. To evaluate the release of asbestos during product application and removal, concrete panels 4 feet by 2-1/2. feet by 1-1/2 inch were prepared, in wooden frames and cured far 42 days. The panels were then each ^*"-1 with Masonoc Primer 47-W-21, "a clear 100 percent solid heat resistant penetrating primer", dried overnight and then coated with. Dum Dum. Masonoc. using a Sinks 7E2 spray gun and 2 gallon pressure pot. to a rhidmess of approximately 30-40 mifc Approximately 15 panels were coated during each of two 80 minute application experiments. Personal exposure and area air urnptes were collected during both experiments. The area, sample was located about 10 feet from the worker (sprayer) at an elevation of 5 feet. After product application, the coated panels were stacked (with spacers), allowed to dry for 24 hours and were then moved to an oven and exposed to flowing dry air at 150F (the rrarimnm irmmrrwnded use temperature) far 42 days to accelerate the aging process fallowed by an addidonal 67 days at ambient ennHirinnt- After aging, the product was found to be pliable and elastic when pressed with a screwdriver blade. A product removal experiment was performed using a putty knife and scraper. Eight panels were nvpr qn apprnT-m-mn-ty go minute period liming which personal samples were collected. After a further ambient aging period of 168 days (a total of 278 days after application), anr} again observing the product to be pliable and elastic, a second replicate removal experiment was performed on tea oaneis. The collected filter samples from these experiments were prepared and analyzed by ransmission eiecnon microscopy. The results of these analyses are given in Table I. These results may be overstated compared to actual exposures which would occur in an open air environment. As such, they are considered to represent a "worst case" condition. 'Asbestos structures arc denned herein as parades fum or more in exient that satisfy the counting guidelines given in 40 CFR Part 763 Asbestos-Containing Materials in Schools. Appendix A. Figure 5 (Federal Register 52 (210) October 30. 1987. 41866-41867). Structures include fibers, bundles, clumps anri matrix. OSHA rggniatri exposure to nbess. which are defined as "a particulate form of asbestos, semolina. amhapn'ylliie or aednoiite. 5" micrometers or longer, with a length-todiameier rario of at least 3 to 1" (29 CFR 1910.1001) 3The minimum detection limit (MDL) for this experiment is the concentration where occupational exposure cannot be differentiated from general background. Arthn-D Little MOB-HarrisMaster 00505 Resiliency of Mobil Hi-Heat Dum Dum after High Temperature Exposure By Arthur D. Litrie, Inc. Acorn Park Cambridge, MA 02140-2390 1992 Reference No. 65191 ArfcKir O Little MOB-HarrisMaster 00506 Product Background High temperature resinous materials of mastic (putty-like) consistency are used in sealing joints and crevices on furnaces and boilers to prevent heat loss. Mobil Chemical Company manufactured and sold such a caulking product from the mid-1960s through the 1970s called Hi-Hear Dum Dum. This product. No. 46-F-7, consisted of a linseed oil-base vehicle (resin) containing various solid fillets, including clay and the chrysodle variety of asbestos (added for its resiliency and bridging properties). The Mobil Chemical Products Catalog provides the following description: "Hi-Heat Dum Dum/46-F-7, a heavy semi-plastic fibred coating, which acts as a joint sealer and pliable gasket for boilers, furnaces and dry kilns. Improves boiler efficiency by preventing heat loss. Retains its elasticity at consistent heat up to 175 and intermittent heat to 350. May be used as a complete cover to eliminate excess fuei consumption and can be painted over in 24 hours." The purpose of a joint or crevice sealant is to bridge gaps between the furnace enclosure and attachments (doors, ports, flanges, etc.). This requires a product that is pliable and resilient (i.e., withstands shock without permanently deforming, tearing, rupturing or pulling away from the furnace surface), and does not degrade over time by becoming friable. The resinous formulation of Hi-Heat Dum Dum provides these properties and also effectively encapsulates the asbestos component, preventing its release. Purpose of the Evaluation The objective of the thermal exposure experiments was to determine the useful service life 'of Hi-Heat Dum Dum for temperatures within and above the recommended service temperature range described in the product literature. Product Testing Experiments and Results Approximately 30 gallons of 46-F-7 Hi-Heat Dum Dum was remanufactured, as observed by Arthur D. Little, Inc. staff who provided chain-of-custody transmittal to our facility. Approximately one pint was used for the tests described herein. The aging experiments were conducted by filling steel fixtures with Dum Dum and placing the fixtures into ovens at different temperatures. The fixtures, consisting of a steel ring spoeweided to a piece of sheet steel, provided for a one inch diameter and three different thicknesses of the material - 0.062 inches. 0.125 inches and 0.187 inches. Fifteen fixtures of each thickness were prepared for a total of 45 fixtures, individually numbered by stamping. Each fixture was taxed on an analytical balance (scale) that measured the weight to 0.0001 grams. The fixtures were then filled with the Dum Dum product, reweighed to determine che a_~l~._ n i (o MOB-HarrisMaster 00507 weight of the- Dura Dura in the fixture and placed into ovens in triplicate at temperatures of: 175. 250. 350, 425 and 500 F. Tne three replicate samples ai each thickness represented a total of nine samples at each temperature. At times of 22. 46, 70. 93.5. 133.5, 400.5 and 763 hours, the samples were removed from the ovens, allowed to cool to room temperature and again weighed. The percent change from initial weights are provided in Table 1. All of the samples underwent a change in the original natural gray color after aging. The colors ranged from a darker gray (175F) to chocolate brown (250F) to dark brown (350F) to black (425F and 500F). During the initial hearing of the 500F samples, smoke was emitted from the oven leading us to believe that the solvent within the sample ignited and burned. The surface of the 500F samples became swollen and expanded out of the fixture in a spherical shape. This occurred to a lesser extent for the 425F samples. The samples also exhibited surface hardening. To determine any product brittleness or friability,' we tested the flexibility of five samples aged for 763 hours by a bending experiment. For this purpose, a test sample was cut from the fixture such that there would be no interference from the fixture on the bend experiment. The tests were done using a three point bend fixture on an Instron 1332 mechanical testing machine with a 1000 pound load ceiL A schematic representation of the bend condition is shown in Figure 1. Crosshead displacement control was used with a displacement rate of 0.1 inchestainute. The applied load and the crosshead displacement was continuously recorded. Test events such as the onset of surface cracking were noted. The experimental results of the bend tests are given in Table 2. Discussion Hi-Hcat Dum Dum contains about 10 percent by weight mineral spirits, to provide a suitable viscosity for application, and a linseed oil blend as the vehicle which may have some .volatiles: the solids content is stated as 85 percent by volume. Loss in weight of Hi-Heat Dum Dum exposed to eievaied temperatures occurs by evaporation of the soivent and oxidation (ablation) of the resinous vehicle. To estimate the useful life of the product, defined as retention of flexibility as demonstrated by a strain of 1 percent, the observed loss in initial weight as a result of furnace aging experiments is plotted in Figure 2, where the averages for three thicknesses tested are pooled. After 22 hours of high temperature exposure, much of the solvent has evaporated, more so as the exposure temperature increases. For longer exposures at elevated temperature, the 175. 250 and 350F exposures demonstrate a linear change in weight loss when plotted against the logarithm of exposure rime. The samples aged at 350F for 763 hours still exhibit a 1 percent strain in bending (Table 2). having lost 12.5 percent of initial weight, representing essentially all of the non-solids content of Hi-Heat Dum Dum. From the data, product life at a sustained temperature of 250F is conservatively estimated at more than 10 years. Arthur D Lrttle MOB-HarrisMaster 00508 Exposures of Hi-Heat Dum Dum at temperatures greater than 350F results in rapid degradation due to both very rapid evaporation of the solvent and oxidadon of the resin. Further, exposure of this product to sustained temperatures of 350F couid result in product life as short as one month. Accordingly, the use of this product under conditions where it is exposed to consistent heat of up to 175F and intermittent heat of up to 350F is considered prudent. Conclusions , The conclusions reached in this study are as follows: Hi*Heai Dum Dum survives constant heating to 250F and intermittent heating to 350F and behaves as described in the product literature. Heating the Dum Dum above 350F causes rapid loss in weight and probable failure of the product. After 763 hours of aging at 250 and 350F. the product can be strained by one to one and a half percent, demonstrating that it has retained elasticity. Based upon extrapolation of the data. Hi-Heat Dum Dum is expected to retain its elasticity for more than 10 yean when used in accordance with the manufacturers recommendations. Arthir D Lrrtle MOB-HarrisMaster 00509 Temp. (F) 22 Thickness = 0.063" 175 8.90 250 9.47 350 9.91 425 10.96 500 14.60 Thickness = 0.125" 175. 7.86 250 8.88 350 10.24 425 11.04 500 15.08 Thickness = 0.183" 175 250 350 1 425 ; 500 6.25 7.79 9.68 11.21 14.15 Table 1 Hi-Heat Dum Dum: Percent Weight Loss (Average of 3 Samples) Time Cumulative Hours at Temperature 46 70.5 93.5 133.5 400.5 8.95 9.50 10.67 11.73 18.39 8.87 9.55 10.91 12.07 21.36 8.87 937 11.00 12.34 23.98 8.94 9.65 11.39 12.74 28.47 9.52 9.93 12.10 14.65 40.41 8.92 9.51 10.86 11.55 17.35 9.27 9.71 11.02 12.17 22.28 9.43 9.73 11.1312.80 24.98 8.94 9.65 11.39 1174 28.47 9.52 9.93 12.10 14.65 40.41 7.79 9.21 10.50 11.70 ' 16.87 832 9.71 10.75 \4n mmmi 19.41 8.90 9.82 10.90 12.68 21.75 9.31 10.13 10.05 10.27 11.15 11.90 13.94 16.42 24.22 I 37.88 I ! i 763 8.99 9.75 1118 16.11 45.53 9.79 9.95 1110 18.98 45.24 ! 1 j ! 1 ! 10.00 10.27 13.31 18.28 .30 ! ; ; : j I rr+<o MOB-HarrisMaster 00510 Table 2 Hi-Heat Dum Dum: Flexibility after 763 Hours at Temperature Angle of Deflection walUpiC Thickness (inches) Aging Temp. (F) Crack Starts Fully at One End Cracked Percent Strain 37 0.125 27 0.187 33 0.062 8 0.125 28 0.187 250 250 350 350 350* 10 16 1.7 4 11 1.2 4 10 1.1 5 10 1.1 N/A M/A N/A Material separated from steel holder. /IrfcJhir s? Lnrtle MOB-HatrisMaster 00511 Figure 1 Schematic of Bend Test Conditions and Bend Angle Calculations y \ Crosshead Displacement SinS = CL5 (1.760) a=180-2 0 rr+la MOB-HarrisMaster 00512 MOB-HarrisMaster 00513 J \ rHiirnlittle 1,000 Tima at tamparatura (hour*) 10,000 100,000 1,000.000 Evaluation of Asbestos Release from Hi-Heat Dum Dum Caulking During Application and Removal By Arthur D. Little. Inc. Acom Park Cambridge, MA 02140-2390 1992 Reference No. 65191 Arthir D Little MOB-HarrisMaster 00514 Product Background High temperature resinous caulking materials of mastic (putty-like) consistency are used in sealing joints and crevices on furnaces and boilers to prevent heat loss. Mobil Chemical Company manufactured and sold such a caulking product from the mid-1960s through the 1970s called Hi-Heat Dum Dum. This product. No. 46-F-7, consisted of a linseed oil-base vehicle (resin) containing various solid fillers, including clay and the chrysodle variety of asbestos (added for its resiliency and bridging properties). The Mobil Chemical Products Catalog provides the following descripdon: "Hi-Heat Dum Dum/46-F-7. a heavy semi-plastic fibred coating, which acts as a joint sealer and pliable gasket for boilers, furnaces and dry kilns. Improves boiler efficiency by preventing heat loss. Retains its elasticity at consistent heat up to 175 and intermittent heat to 350. May be used as a complete cover to eliminate excess fuel consumption and can be painted over in 24 hours." The purpose of a joint or crevice sealant is to bridge gaps between the furnace enclosure and attachments (doors, ports, flanges, etc.). This requires a product that is pliable and resilient (Le., withstands shock without permanently deforming, tearing, rupturing or pulling away from the furnace surface), and does not degrade over rime by becoming friable1. The resinous formulation of Hi-Heat Dum Dum provides these properties and also effectively encapsulates the asbestos component, preventing its release. Product Testing During Application and Removal Hi-Heat Dum Dum was tested by Arthur D. Little, Inc. to determine if asbestos was released during application or removal. Approximately 30 gallons of 46-F-7 Hi-Heat Dum Dum was remanufactured, as observed by Arthur D. Little. Inc. staff who' provided chain-of-custody transmittal to our facility. Experiments (described below) were conduced at our facilities in compliance with ail current United Stares and Massachusetts rules and regulations relating to asbestos and in accordance with an approved Arthur D. Little, Inc. Health and Safety Plan. .An application and removal pian was developed to simulate typical work practices. In addition, a sampling and analysis protocol was developed to quantify the exent to which asbestos structures are released during the experimental application and* 'The U.S. Environmental Protection Agency defines friable as "capable of being crumbled, pulverized, or reduced to powder by hand pressure". Arthir D Little MOB-HarrisMaster 00515 removal activities2. This protocol was designed so that all applicable NIOSH and EPA requirements for analysis by transmission electron microscopy were met or exceeded. The minimum detection limit for the analytical protocol was 0.01 fibers/cc3. To evaluate the release of asbestos during product application and removal, steel panels (1/32 inch thick 1040 steel, cleaned and degreased, measuring about 2 1/2x3 1/2 feet) were coated by troweling at an estimated thickness of 1/8" (and feathered at the panel edges).. Approximately 15 panels were coated during each of two 80minute application experiments. Personal exposure samples were collected during both experiments. After product application, the Hi-Heat Dum Dum was heated to accelerate the aging process4. The neutral gray of the as-applied coating changed in color to a chocolate brown (225-250F for 20 days). After aging, product removal experiments were conducted using a putty knife and scraper. Although the thicker, centrally coated area of each panel was very pliable and quite easily removed, the feathered edge regions were somewhat harder and required substantial mechanical effort to scrape down to the bare metal. Approximately 10 panels were cleaned in each of three, separate 80-tninute experiments during which personal filter samples were collected. The personal filter samples were prepared and analyzed by transmission electron microscopy. The results of these analyses are given in Table 1. 2Asbesios structures are defined herein as panicles 5pm or more in extent that satisfy the counting guidelines given in 40 CFR Part 763 Asbestos-Containing Materials in Schools. Appendix A, Figure 5 (Federal Register 52 (210) October 30, 1987, 41866-41867). Structures include fibers, bundles, clumps and matrix. OSHA regulates exposure to fibers, which are defined as "a paniculate form of asbestos, urmolite. anthophyllite or actinolite, 5 micrometers or longer, with a length to diameter ratio of at least 3 to. 1" (29 CFR 1910.1001). The minimum detection limit (MDL) for this experiment is the concentration where occupational exposure can not be differentiated from general background. '`During preliminary laboratory furnace experiments with coaxed steel coupons, we observed that the product discolored from a neutral grey to a dark chocolate brown after one day ai 350F and to a mMinm brown after four days at 265F. Even after these exposures to temperatures which exceeded the recommended continuous use temperature, the product remained pliable and gummy when probed with a screwdriver. Therefore, although the product was designed for a continuous temperature of 175F. a treatment of two weeks to dry, flowing air at 250F was chosen to not only accelerate aging but also to account for intermittent temperatures greater than 175F. The actual conditions of exposure were 225-250F for 18 to 23 days. Arthir D Little MOB-HarrisMaster 00516 Table 1 Asbestos Exposures During Application and Removal of Hi-Heat Dum Dum: Personal Samples Analyzed by Transmission Electron Microscopy Sample No. 042504 042604 051703 051705 052203 052207 Description First Application Second Application First Removal First Removal (replicate) Second Removal Third Removal Exposure (s/cc)s <0.01 <0.01 <0.01 <0.01 <0.01 0.01 Conclusions The conclusions reached in this study are as follows: The Hi-Heat Dum Dum that was tested was found to be non-fiiable and provided encapsulation of asbestos during application and removal experiments. Exposure of the product to 225-250F for 18 to 23 days changes its color from a neutral gray to a chocoiare brown, indicating modincadon of the resin. Even so, the product was elastic and pliable except at the feathered, thin edges where it was hardened but not friable. Results of worker exposure measurements during use of Hi-Heat Dum Dum did not exceed the minimum detection limit of 0.01 asbestos strucrmes/cc in rither product application or product removal experiments. Based upon the above results, occupational exposure to airborne asbestos fibers during.the application or removal of Hi-Heat Dum Dum is virtually non-existent. 5Exposure represents asbestos structures per unit-volume of air. Artfur D Little MOB-HarrisMaster 00517 Evaluation of Asbestos Release from Chimney Weatherproofing Mastic During Application and Removal By Arthur D. Little, Inc. Acorn Park Cambridge, MA 02140-2390 1992 Reference No. 65191 Arthir D Little MOB-HarrisMaster 00518 Product Background From the mid-1960's through the I970's, Mobil Chemical Company manufactured and sold a line of masdc-type protective coatings under the name Dum Dum Products. Chimney Oum Dum was a protective and waterproofing coating specially formulated for use on concrete and brick chimneys where heat resistance up to 210? is required. The Mobil Chemical Product Catalog states: "Chimney Dum Dum/97 Series Chimney Dum Dum is a rugged heavy coating for the exterior of chimneys that provides flexible weatherproof protection. It fills and bridges hairline cracks with a flexible coating under a tough outer skin. Should the leathery skin become fractured, the soft under film will harden on contact with air. May be applied without completely cooling stack." Chimney Dum Dum consists of a resinated vegetable oil vehicle, containing 41% pigments, including titanium dioxide, mica and the chrysolite form of asbestos; the total solids content is 63%. Application is by brush, or more typically, by spray. At 7SF, the surface skins over in 4-6 hours, and the under surface remains pliable. Resistance to chemical fumes and moisture is very good to excellent and the product is resistant to constant dry heat at 210F. Product Testing During Application and Removal To determine if asbestos is released during the application or removal of Chimney Dum Dum, approximately 18 gallons of the product was prepared on the basis of the formula master and mixing instructions provided by Mobil. The oil base resin was no longer commercially available, and a special batch was prepared for us by McWhorter Corp. All other components were obtained commercially. The product was mad* with a Myers n-rirw in 6 gallon batches which were subsequently combined, blended and stored in 5 gallon pails. The prepared product was observed to be smooth and uniform in appearance and of mastic consistency. This work, as well as subsequent application and removal experiments, was conducted at our facilities in rompiiancw with all current United States and Massachusetts rules and regulations relating to asbestos and in accordance with an approved Arthur D. Little, Inc. Health and Safety Plan. A test plan was developed to simulate typical work practices for product application and removal1. In addition, a samoiing and analysis protocol was developed to 1Although intended for exterior use, this product was tested in an intenor (controlled) environment. ArtfurD Little MOB-HarrisMaster 00519 quantify the extent to which asbestos structures2 may be released during the experimental appiicadon and removal acdvides. This protocol was designed so that all applicable NIOSH and.EPA requirements for analysis by transmission election microscopy were met or exceeded. The minimum detecdon limit for the analytical protocol was 0.01 smtctures/cc3. To evaluate the release of asbestos during product application and removal, ten concrete panels and twelve facing brick panels with concaved mortar joints, both sets four feet by two and one-half feet by one and one-half inches, prepared about one year earlier, were primed (Chimney Dum Dum Primer 38-V-5 equivalent), dried overnight and spray coated with Chimney Dum Dum at an estimated coating thickness of 30-40 mils using a Binks 2 gallon pressure pot with follower and a 7E2 spray gun. The coating operation required 55 minutes during which personal and area air samples were taken. The area sample was about ten feet firm the spray site at an elevation of 5 feet After an ambient cure of 24 hours during which the coating skinned over, the panels were aged for 14 days at 200-210F and eight days at ambient. The purpose of the furnace treatment was to accelerate the natural aging process. After the elapsed 23 days of aging, the product was hardened at the surface yet pliable and elastic when depressed with a screwdriver blade. Product removal was carried out on eight brick panels and six concrete panels over 88 minutes during which personal and area Biter samples were collected. The collected filter samples from these experiments were prepared and analyzed by transmission electron microscopy. The results of these analyses are given in Table 1. These results may be overstated compared to actual exposures which would occur in an open air environment. As such, they are considered to represent a "worst case" condition. ^Asbestos structures are defined herein as particles 5pm or more in extent that satisfy the counting guidelines given in 40 CFR Pan 763 Asbestos-Containing Materials in Schools, Appendix A, Figure 5 (Federal Register 52 (210) October 30, 1987, 41866-41867). Structures include fibers, bundles, clumps and matrix. OSHA regulates exposure to fibers, which are defined as "a particulate form of asbestos, aemolite. antfaophylliie or acunoiite, 5 micrometers or longer, with a Iength-todiameter ratio of at least 3 to 1" (29 CFR 1910.1001). 3The minimum detection limit (MDL) for this experiment is the concentranon where occupational exposure cannot be differentiated from general background. Arthir D Little MOB-HarrisMaster 00520 Sample No. 052802 052803 052805 062001 062002 062003 Table 1 Asbestos Exposures During Application and Removal of Chimney Dum Dum Description Sample Type Exposure (s/cc)4 Application Application Application Removal Removal Removal Personal Personal (replicate) Area Personal Personal (replicate) Area 0.088 0.024 0.024 <0.01 <0.01 <0.01 j | ! Conclusions The conclusions reached in this srudy are as follows: Remanufacrured Chimney Dum Dum was smooch and uniform with mastic like consistency. Application to brick and concrete panels required heavy duty mastic spray apparatus. After 23 days of aging (14 days at 200210F), the product was skinned over but pliable and elastic when depressed with a tool. Results of worker exposure measurements during application of Chimney Dum Dum in a controlled environment were below the current OSHA action level*3. Results of worker exposure measurements during removal of Chimney Dum Dum in a controlled environment did not exceed the minimum detection iimii of 0.01 strucmres/cc. Based upon the above resuits, mere is insignificant occupational exposure to airborne fibers during the application of Chimney Dum Dum and virtually no exposure.to airborne asbestos fibers during the removal of this product. 4Asbestos structures per unit volume of air. The structures observed were fibers (.or fibers and bundles.- corresponding to the EPA definidon). 3OSHA defines action level as "an airborne- concentration of asbestos, tremolite. amhnphyllite, actinolite, or a combination of these minerals, of 0.1 fiber per cubic centimeter (f7cc) of air calculated as an eight (8) hour time weighted average" (29 CFR 1910.1001, promulgated June 20, 1986). ArtHir D Little MOB-HarrisMaster 00521 W^Jemorandum from T. E. ALLEN. M. D. `* NEW YORK. N. Y. D.u_________1_3__A__u!g_u_s_t__1_9_7_3__ Dr. H.H. Golz API Dr. Allen has asked me to send the attached to you for your information. Joan DiGangi Dr. Allen's Secretary MOB-HarrisMaster 00522 Memo to File As noted in a memorandum dated 11 July 1973, a meeting was arranged, following an invitation from Dr. Irving Selikoff, to meet with him at the Mt. Sinai Medical Center. Attending the meeting were: Dr. Harry Hermann - Associate of Dr. Selikoff - NY Dr. W. Nicholson - Associate- of Dr. Selikoff - NY Dr. N.Roberts - Assoc. Medical Director, Exxon Corp.-NY Dr. M. Goldman - Ass'-t. Medical Director, Exxon Corp.-NY Dr. H.A. Sinclaire- Assoc. Medical Director, Mobil-NY Dr. T.E. Allen - Medical Director, Mobil-NY The purpose of the meeting was to present findings that Dr. Selikoff had made following examination of a group of represented Mobil employees (Paulsboro Refinery) on the request of the union at Paulsboro. In addition. Dr. Selikoff hoped that, on discussion of these findings, the group might be able to advise him whether such findings might be considered typical and usual of an average refinery population. The meeting lasted approximately two and one half hours and consisted principally of a presentation of asbestosis as an occupational illness, with major points of same being illustrated by x-rays, statistics, and data gathered on the Mobil population examined. No list of examinees was given, and, at no time, was any data or x-ray identified by a specific name. Initially, Dr. Selikoff gave a brief discussion of the disease, asbestosis. In this coverage, he covered the highlights of work being done here and in U.K. He mentioned historical work done in shipyards in USA and U.K. He made it clear that, during the discussions, he would be talking in terms of "insulators, brick workers, etc. in user companies," rather than in terms of "factory workers(where asbestos products, piping, etc. are made such as Johns Manville, etc.). In spite of this, he pointed out that if exposure to asbestos fibers in insulators was enough to produce malignancy, the great exposure normally experienced in factory employees was "excess exposure" as far as cancer was concerned. Graphically shown, this would be as follows: Exposure (Yrs. & Service) FACTORY WORKERS' exposure m/z/mi/w/mur ; Cancer production level 'TinaaeQ area represents `-wastea" area ox exposure) Dr. Selikoff pointed out that the typical x-ray findings in a case of asbestosis were:1 1) General thickened pleura (the pleura is the thin', transparent covering of the lungs) 2) Pleural plaques (a concentration of thickening of the pleura in certain specific areas) 3) Reticular fibrosis (intensified marking throughout lung tissue, particularly in lower lung fields producing "ground glass" appearance. MOB-HarrisMaster 00523 4) A shaggy appearance to the heart outline. 5) " Blunting or even complete obliteration of the area where the diaphragm touches the rib area. It was emphasized that the above findings were typical of but not pathog nomonic (specifically distinctive or diagnostic) of asbestosis. These findings, along with an extensive work or exposure history, can be considered diagnostic. One does not necessarily need to have positive pulmonary function tests to clinch the diagnosis. The development of asbestosis need not produce death in any person sufficiently exposed, but, there is developed in cases of asbestosis susceptibility to lung cancer, and even to mesothelioma, a specific type of malignancy. In regard to Mobil's employee group at Paulsboro, Dr. Selikoff stated he was requested by the "union" there to examine a group of represented employees. This group of employees was presented by the union to Dr. Selikoff who did not have a voice in the choice and he had no previous knowledge of the examinees' medical, work or social history. .He stated emphatically that, as a result, the study was a biased one, but he could not state whether it was biased in favor of a sick,-average or well group. The only point on which there was certainty was that all examinees had had at least 20 years of work in the refinery. On several occasions, the size of the examined group was stated to be 137, this is not quite accurate because only 118 were examined. The remaining 19 were those employees who, at an earlier date, had been seen only for a chest x-ray and chest examination and, on whom, the union re quested the company x-rays be forwarded to Dr. Selikoff at his Pate rsom, N.J. office. Dr. Selikoff handed out six sheets showing in graph form some of the findings resulting from his examination of. the 118 employees. (It should be noted.that the examinations were done by a team of 9 people from Mt. Sinai Medical Center who, with the aid of mobile x-ray unit, completed these examinations during one week-end.) After the charts were handed out, discussion was so continuous that it was not possible to examine these charts thoroughly. Constant re ferences were made to the charts, however, during the discussion. On the days following the conference, when the undersigned was able to thoroughly, review these charts, it was evident that there were many errors in calculation, as well as some ambiguity in reporting the population studied and the results found in same. A call vas made to Dr. Selikoff*s office and some corrections were offered via the phone, and others were made by sending revised charts to replace those in question. Attached are copies of the revised tables issued to us at the meeting. Table VI was not given-at the meeting. It was included in a later mailing to the under signed. General comments on the tables, which are self-explanatory, include the. following. It will be immediately obvious from Table I that the medical review was not restricted to "active" employees as was first thought. We are told by Dr. Selikoffs office that the breakdown of the 137 examinees is as MOB-HarrisMaster -2- 00524 follows: annuitants "active" employees "active" employees 13 10S (full medical review) 19 (partial medical review) The 19 employees listed above were employees (no annuitants) who were seen at an earlier date by Dr. Se'likoff and on whom only a chest examination and a chest x-ray were done. This was the group of employees on whom the union requested their company x-rays to be sent to Dr. Selikoff. We are not aware in which group, i.e. service, the 13 annuitants fall. We can assume they may be in the 30-39 and 40-49 because it is in this group that ages in excess of normal retirement age are listed. It is possible that some might be in the first service category, 20-29 yrs., if they re tired at an age younger -than 65 years. The remaining tables are self-explainatory but indicate, among other things, that 1) none of the cases in this series showing classic signs of asbestosis are "serious" cases. There is no doubt that, in x-ray films shown to us (some taken in the mobile unit - some previously in the group of 19) there are some x-ray signs indicative of asbestosis. Unfortunately, we were not given the names of the patients represented in the x-rays shown as samples. Dr. Selikoff feels, from his bang experience, that x-rays alone (if not correlated with pulmonary function tests, etc.) tend to "unread" the time picture of ' asbestosis. 2) Clinical-findings such as bronchitis and positive x-ray findings and pulmonary function tests are higher in "smokers" than "non'smokers" and higher in "ex smokers" than in the group which has no smoking history. 3) A high percentage of this group are "no hisotry of smoking" (28%) and "ex smokers" (39%) making a total group of "non smokers" - 67%. 4) The study is unique in one aspect. With the expected exposure of this group of employees to firebrick, there is no_indication of silicosis. Firebrick is about 85% quartz in composition. We are not prepared, at this time, to dispute or confirm Table VI- It is interesting to note that cancer of the lung in this group studied is recorded as 0.8%. The national average of cancer of the lung (males) is 3+%. Probably the most revealing and appropriate chart is Table VII. This shows that of all the categories of workers represented in the study, that of the insulators, masons and bricklayers (13), 81% show positive signs of both pleural and parenchymal involvement of asbestos exposure. This is markedlv MOB-HarrisMaster 00525 higher than the findings in all other occupations represented. Again, it was stated by Dr. Selikoff that although asbestosis is unquestionably established as a diagnosis, these do not represent presently "serious" cases. Attached with the statistical tables is a copy of the recording form used in the analysis of x-rays of patients whose occupation might make them liable to pneumoconioses (chronic fibrous reaction in the lungs to the inhalation of any type of dust) such as asbestos, iron dust, cloth fibers, and silica. It. should be noticed that this form and its legend is the official classification established by the I.L.O., and generally accepted as a classification by most pulmonary and occupational health specialists. Dr. Selikoff feels that, in an ideal program of preventive health,, workers with 20 years or more exposure in jobs involving insulating materials, fire brick and masonary cement, chest x-rays should be done every three months. He also thinks many other preventive procedures to protect their respiratory systems should be instituted. Thus, he advocates the administration of flu vaccine each year for such a group. Above all, he urges all workers to stop smoking. % Dr. Selikoff was most professional in his conduct during this session. At no time did he mention the company's name and only, as identification of location of the worker studied, was the name Paulsboro used. Furthermore, he feels that the union is unaware of "99% of the great work done by the company medical department." "They only see and talk about the bad things when they happen." He cited a common union complaint that "our men -naturally are sick breathing in that contaminated r.ir- at the refinery every working day." He quickly referred again to Table V showing that chronic bronchitis, if the union complaint had merit, would be appearing in all represented employees, when actually his statistics show it occurs primarily and predominaely in the "smokers." He urged consideration of a joint management - union study of the asbestos.' workers (those who have been exposed during their work life) in at least five refineries, among which should be included the "best" (as far as modem, but not recent construction) and the "worse." Thus assumes more than one company would be so involved. The whole research project should be jointly sponsored developed and each side totally aware of the progress from planning through completion stages. Such a study can be done by any one of many agencies. There is no doubt that it could be done by the federal government - through the agency of NIOSH. If done by them, he feels it would be a fair, well done and complete study. However, NXOSH could and would probably look at such a project only once and not on a continuing basis, and this type of study needs at least a 20-30 year follow-*up since* this can be the "incubation" period of asbestosis. The study could be done completely by any outside agency, such as an academic group or a private research group. Needless to say, choice of the group would -have to be mutually agreeable. MOB-HarrisMaster -4- 00526 The ideal project, in Dr. Selikoff's opinion, is one planned with, guided and supervised by capable outside experts, but with all the examinations, x-rays, lab. work done by the company inolant medical department. He feels this is the only source of ongoing interested medical supervision available to the men. He does feel that, in Paulsboro's case, it may well take a gigantic effort to get the union and management to mutually trust each other in such an under taking. He does not feel that it is impossible, and he feels every effort should be made to accomplish this goal. Again, he pointed out that, in the general male population of the USA, there is a 3-4% death rate due to lung cancer. Admittedly, there are multiple etiological factors in development of lung cancer. However, if and when lung cancer occurs in a company worker ex posed to such materials as asbestos, the first and most obvious conclusion is that this is due to a carcinogenic material in the work environment. This is difficult to combat, and admittedly, can be unfair to managements. Research and careful clinical follow-up can establish data that could remove the haziness as to responsibility in all such cases. In summation, Dr. Selikoff presented findings to the group in a most pro fessional and non spectacular fashion. He admitted repeatedly the group studied is an ideal one in many respects. A more ideal study, jointly sponsored by management and union, should be undertaken. Mobil is not the only petroleum company with this problem (cases in Texaco were cited). Dr. Selikoff did not pretend to be an expert on refinery health since he has never had an opportunity to visit a refinery. No commitment was made to him as to follow up to his presentation or suggestions.. After the close of the meeting, Dr. Selikoff was asked if he would explain his relationship to either OCAW or independent unions in the petroleum industry. He answered that he has no contract with OCAW or any union. OCAW and independent unions have and do request the Mt. Sinai Medical School - Department of En vironmental Medicine to do projects for them as indicated in this study of some Paulsboro employees. He emphasized his commitment is not unilateral, and both the school and he, as an individual, are free at any time to consider research or consultant capacities with any agency, management, union or government. -5- MOB-HarrisMaster 00527 Age d is trib u tio n o f by years since fLi3r7s tr c fl ex dhD hdD U o f-C eq o to CO CO to CO CO GO CD > < a U o f. >> 3 U cn Oc Oa 0 ho 3 d U ho < h .2 o to O CD r1i CO CiD o E-- f r-4 *** GO GO 0) to ** CD to to *-< c ^ CP ID V* oVi V? ^ O u c: 0> N t O) n lO* t r4 t- 03 t CiO 0c > O K o n o CO n tc Z o3O 3K H C S3 C3 03 2. CV1J nii m b* o o 3CO*l *tUut 03 CO Q rrii a c MOB-HarrisMaster 00528 Table II Work Activities of 137 Production and Maintenance Employees Type of Work Active "Clean Work" (Docks, Case-Can, Auto Shop) "Dusty" Production Work (Bead Plant, Filter Dept.) Fume Exposure (All other production units) Mixed Fumes and Dust "Clean" Maintenance (Carpenters, Machinists, Electricians, etc.) High Asbestos Exposure (Insulators, Masons, and Bricklayers) Other Maintenance (Pipefitters, Welders, and Boilermakers) 10 5 28 6 21 13 41 Retirees 1 7 2 3 Totals 124 13 X-ray changes *0 CO uOf JaQ> co *0 ou ce uo VCO e tn cs Vcs} ec 3c > o eo 0 Os Xcs1s < MOB-HarrisMaster 00530 Pulm onary fu n c tio n a b n o rm a litie s in re la tio n to X -ray chances unci sm old lift MOB-HarrisMaster 00531 Length o f Number e x p o s u re . o f ai Smokers ( E x-sm o ke rs a N o n -sm o ke rs MOB-HamsMaster 00532 T a b ic w H O 5 5 u > co *4 G o ocoo a a>ou MOB-HarrisMaster 00533 Table VI History' of previous center in 118 refinery workers Cancer Skin Kurber | of cases 2 ' 1.6% Bladder 2 1.6% Colon 1 ' 0.% Abdcninal 1 O.S% Lung 1 ' O.S% Total 7 6% MOB-HanisMaster 00534 X -ra y n o s u lta o f R o fin o ry P ro d u c tio . .md Maintenance) Entployoea >a o r- n n -r rs m co. a 3O P. N S CM O > CM \ a &o H \ r-i o. r-< r-l tO \ CM to 00 m OB 1? CM to to CO n an tn hH h \o to -w os & ao o J3 o CO >Q/ 4o4 3 u o *c < o M o c c d d V o & 0) H o US >* o cs H -O r CD 4j4d H a* 44 O a da aQ ab 4o4 os l-< . a3 fc. r-* (4 CD d 4^ J3 44 g O K. Hc Ho N<-T 44 o 0) o W0 3 3 o u U* a H n sd 2 T0d 44 iX4 os3 *C Q CO \ *a4 a jz m dcs a e c d SZ^ 4o4 ap4 ^e4 b0) 4b4 rt 44 C OQ) r-l C d ac. w 0o-+ p u d O w - 44 os -- 4a04 rb H N * m b Q> c CJ H o O Cl dc b O e o Jtf . OS b 44 b E c*4 rt 4C4J 44 b HCJ b H M O ao O-- CL -3 44 C. Oa CD d o 03 B rt b 2 0) * d>s 03 b b 4O4 a4 rt b HQ 3OS *c C' *4 d MOB-HarrisMaster 00535 *5 ue I 30u 1 uo aaca IVIBONM ENTAL SCIENCES LABOJlA'. X 'Bli' IISIT S IN A I S C H O O L O F M E D IC IN E O F T H E C IT Y U N IV E R S IT Y O F N E W Y O R K a a i i E e= ew Cl _E 4 I* *y)emoranelu.m from T. E. ALLEN. M. D. NEW YORK. N. Y. Dm,_______ 9 July 1973_______ Do Dr. H.H. Golz Mr. 3.M. McNemey As promised during our telephone conversation. T.E. Allen, M.D. MOB-HarrisMaster 00537 28 June 1973 Memo for File This, morning. Dr. Irving Selikoff of Mt. Sinai Medical Center, called me. For the record, the undersigned has never talked or met with Dr. Selikoff at any time previously and the telephone call was unsolicited. Dr. Selikoff stated that,- at an earlier date, at the union's request, he had examined approximately 18 employees from the Paulsboro Refinery. The employees for this examination' had been selected by the union and general physical ex aminations with laboratory and x-ray procedures were carried out. About six months ago, again at the union's request, Dr. Selikoff examined approximately 118 employees. These examinations were done during a week-end. Although it was not stated specifically, it was my understanding that the ex aminations were done by Dr. Selikoff and staff and not necessarily that each ex amination was done by Dr. Selikoff himself. Furthermore, Dr. Selikoff stated that the 118. employees were "volunteers" and thus represented "a potentially biased population." If he were doing a more scientific study. Dr. Selikoff would have picked his population of examinees at random. .All individuals examined in the group of 118 were people with 20 or more years service with Mobil. The population generally represented those employees working with insulation, bricklayers, and general urrlrty workers employed m the area where insulating materials might have been present but the population was not necessarily restricted to those who have direct and/or constant exposure to insulating materials. In short, the population represented not young people and not people with "very little" exposure to insulating materials. The results of these examinations to date have shown that in slightly less than 50% of the total x-ray findings indicating a marked reticular fibrosis (a classic finding in asbestosis cases). No case was found to be of a "very severe type." Three were considered to be Grade II-2 and two cases were Grade II-l. These gradations are made in accordance with the ILO Classifications of pulmonary fibrosis as seen in cases of asbestosis. Dr. Selikoff's team also made other findings which have not yet been completely tallied. Such findings would have included notations of pulmonary function, finger-clubbing, cigarette smoking, etc., and their relationship to signs of asbestosis. Dr. Selikoff readily admitted that on several occasions during the conversation, that his population was not a random sample, but more or less a selected sample. He is, however, concerned at the percentage of cases, i.e. five cases out of approximately 50. At this point, he stated that with these findings in mind, he is wondering whether Paulsboro is unique with these findings because it is an "old" refinery and/or because it has an "old" population. If the answer to these questions is "no," are the findings here in Paulsboro typical of any refinery in the petroleum in dustry, particularly with any age group and service group similar to that of Paulsboro. Realizing that there is much to be duscussed on this general subject, he thought it best to call me and asked if I would meet with him for discussions on the subject. He was planning also' to call Dr. Norbert Roberts, Associate MOB-HarrisMaster 00538 Medical Director, Exxon Corporation, since he knows Dr. Roberts and does not know any other petroleum company medical directors. He realizes that Dr. Roberts, having never worked in a refinery might not be intimately acquainted with these subjects. He thought if this is so that Dr. Roberts might refer him to a Medical Director of Exxon's domestic operation or to one of Exxonls refinery physicians experienced in this area. He felt that if such discussions were held all of us would tend to gain. He added if this information he has already gathered were given to the union without the benefit of discussion with petroleum medico representatives, the union might press the matter in a manner that might not be ideal for anybody. iiiA/ju Theodore E. Allen, M.D. MOB-HarrisMaster 00539 Evaluation of Asbestos Release from Boiler Caulking During Application and Removal Arthur D. little, Inc. Acorn Park Cambridge,-MA 02140 Jane 1990 C-65191 MOB-HamsMaster 00540 Product Background High temperature resinous caulking materials of masne (puny-like) consistency tie used in sealing jama and devices ^ boilers to prevent heat loss. Mobil Chemical Company manufactured and sold snch a pxodna from the mid-1960s through the 1970s called Hi-Heat Dum Dum. This consisted of a linseed ail-base vehicle (resin) containing various Na_46-F-7, SllerfT including clay and the chrysorile variety of asbestos (added far its resiliency and bridging properties). The Mobil Chemical Products Catalog provides the following description: "Hi-Heat Dmn Dum/46-F7. a heavy.jemi-plaiac fibred coating, which acts as a joint sealer and pliable gasket for boikn, furnaces and dry kilns. Improves boiler efficiency by pxevearing beat loss. Retains its elasticity at consistent heat up to 175* and intermittent heat to 350*. May be used as a cooaplete cover to eliminate excess fuel consumption and can be painted over in 24 hours." The purpose of a joint or crevice sealant is to bridge gaps between the furnace enclosure and attachments (doors, ports, flanges, etc.). This requires a prodna that is pliable and resilient (Le^ withstands shock without permanently deforming, tearing, rupturing or pulling away from the furume surface), and does not degrade over time by becoming finable1. Tire resinous formulation of Hi-Heat Dum Don provides these properties and also effectively encapsulates the asbestos component, preventing its release. Product Testing During Application and Removal Hi-Heat Dum Dum was tested by Arthur D. Little, fag- to dfftrrming if asbestos was released during application or removal. Approximately 30 gallons of 46-F-7 Hi-Heat Dum Dum was remanufaemred. as observed by Arthur D. Little, Inc. who provided chain-of-cnssody transmital to our facility. Experiments (described below) were conducted at our facilities in with all current United Stares and Massachusetts rules and regulations rearing to asbestos and in accordance wife an approved Arthur D. Little, Inc. Health and Safety Flan. A test protocol was developed to simulate typical work practices far prodna application and removal. Since these experiments involved an asbestos containing product, preeansoos were taken so feat ntp-rimMuwi and fee nhfant environment were fully protend from any potential release of asbestos fibers. A sampling and, analysis protocol was developed to quantify fee nrm to which asbestos fibers may 1The U.S. Environmental Pmwiinn Agency friable u "capable of being crumbled, pulverized, or reduced to powder by band pressure". be released dating the cxpcriracaal application and removal activities2. This protocol was rictignrri so that all applicable OSHA. NIOSH and EPA xequae&Ksts wexe taet or wrcrarird. The minimum detection limit far the analytical protocol was 0.01 fiben/cc3. To evaluate the release of asbestos during product application and removal, steel panels (1/32 inch thick 1040 steel, cleaned and degreased, measuring about 21/2x3 1/2 feet) were coated by troweling at an estimated thickness of 1/8" (and feathered at the panel edges). Approximately 15 panels wexe coated during each of two 80minute application experiments. Personal exposure samples were collected during both fXpwimgnn, After product application, the Hi-Heat Dum Dum was heated to accelerate the natural aging process. During preliminary laboratory furnace experiments with coated steel coupons, we observed that the product discolored horn a neutxal grey to a dark chocolate brown after one day at 350"F and to a medium blown after four days at 265"F, indicaring chemical modification of foe resin by rmAaiirm Even after these exposures to temperatures which exceeded foe fw-nmnwifM continuous use temperature, foe product remained pliable and gummy when probed with a screwdriver. Although foe product was for a continuous temperature of 175*F, a treatment of two weeks to dry, flowing air at 250*F was chosen to not only accelerate aging but also to account for intermittent temperatures greater than 175*F. After accelerated aging (actual conditions were 225-250*F for 18 to 23 days), product removal experiments were conducted using a putty knife and scraper. Although foe thicker, centrally coated area of each panel was very pliable and quite easily removed, foe feathered edge regions were sootewhat harder and required substantial mechanical effort to scrape down to foe bare metaL Approximately 10 panels were cleaned in each of three, separate 80-minuin experiments during winch personal samples were collected. The personal filter wexe prepared and analyzed by transmission electron microscopy. The results of these analyses are given in Table 1. 1Fiber is defined as a panicle 5pm or mare in length with substantially and an aspect ratio (length to width) of three or nxse. sides 3Tbe rninimnm detection limit (MDL) is the i*nnwiiiTrinw where occupational exposure can not be differentiated from general background. MOB-HarrisMaster 00542 Tahiti Asbestos Exposures During Application and Removal of HMteat Dum Dum: Personal Samples Analyzed by Transmission Electron Microscopy Satnole No. 042504 042604 051703 051705 052203 052207 Description First Application Second Application First Removal First Removal (replicate) Second Removal Third Removal Exposure (s/cc)4 <0.01 <0.01 <0.01 <0.01 <0.01 0.01 Conclusions The conclusions reached in this study ire as follows: Hi-Hear Dum Dum is non-friable and provides encapsulation of asbestos during application and removal experiments. Exposure of die product to 225-25CTF far 18 days changes its color from a natural gray to a chocolate brown, indicating oxidation of the resin (overheating). Even so, the product was elasrie and pliable except at the feathered, thin edges where it was hardened but not friable. Results of worker exposure measurements during use of Hi-Heat Dum Dum did not exceed the minimum detection Hmir of 0.01 asbestos scrucares/cc in cither product application or product removal experiments. Based upon the above results, there is no potential far occupational exposure to free asbestos fibers during die application, removal or other use of Hi-Heai ^Exposure represents asbestos structures per TMit volume of air. Structures include fibers, bundles (an arrangement of parallel fibers that touch), clusters (an arrangement of random fibers that touch) and warn* (a fiber or fibers embedded in a paniculate). A /friQ-WarricMnster 00543 Appendix A Photographs DocnP1*011 Hi-Heat Dam Dam as Applied and Aged at Ambient Temperance far 20 Days. Hi-Heat Dam Dam as Applied and Aged at 2252507 for 20 Days. MOB-HarrisMaster 00544 MOB-HarrisMaster 00545 Exhibit No. STATE OF-MASSACHUSETTS COUNTY OF MIDDLESEX, SS. AFFIDAVIT I, Edward T. Peters, being duly sworn according to law, hereby depose and says as follows: 1. I am a senior staff scientist in the Materials and Applied Physics Unit of die Prodact Technology Section of Arthur D. Lisle, Incorporated, Cambridge, Massachusetts. I have been a staff scientist at Arthur D. Little. Inc. since-1969. 2. Arthur D. Little, Incorporated, is a research firm experienced in the physical, structural and chemical characterization of materials. 3. I received undergraduate degrees from DePauw and Purdue Universities, a Mister of Science degree from the University of Wisconsin and the degree of Doctor of Science in Metallurgy from the Massachusetts Institute of Technology. 4. I served as a member of the faculty in the Department of Metallurgical Engineering at the University of Wisconsin from 1958 to 1959. 5. From 1963 until 1969 I was employed by ManLabs Incorporated, in Cambridge, Massachusetts. At ManLabs, I specialized in the structural and physical cbaracsrizarion of materials. 6. I am Registered PwfewinMt gnprwr in rh fww nf Mmn-tiiiww, member nf the American Society far Metals and the American Industrial Hygiene Association. 7. While as Arthur D. Little, Inc., I have been responsible far several laboratory bared programs designed to evaluate and characterize oaaterials as well as corporate responsibility far technical studies relating to asbestos. ni: MOB-HarrisMaster 00547 .8 I have written seven! papers on rimes on the subject. etw^c Piiwtwi u ^eil as h"wto 9. Arthur D. Little, Iu&, was reamed by Mobil Oil Corporation to test an asbestos- containing product known as Hi-Hear Dum Dum to evaluate any occupational exposure during product application or removal. 10. The attached report describes the results of a study carried out under my direction to evaluate personal exposure to asbestos in working with Hi-Heat Dum Dum. The report accurately sets forth the methodology of die smdy and the conclusions I reached as a result of the experiments performed. Sworn and subscribed to, before me, this 19th day of June, 1990. . Edward T. Petea Elaine M. Kenney Notary Public MOB-HamsMaster 00548 Evaluation of Asbestos Release from Chimney Weatherproofing Mastic During Application and Removal By Arthur D. Little, Inc. ' Acorn Park Cambridge, MA 02140-2390 1992 Reference No. 65191 Aa+hir D Little MOB-HarrisMaster 00549 Product Background From the mid-1960's through the- 1970's, Mobil Chemical Company manufactured and sold a line of masdc-type protective coatings under the name Dum Dum Products. Chimney Dum Dum was a protective and waterproofing coating specially formulated for use on concrete and brick chimneys where heat resistance up to 210F is required. The Mobil Chemical Product Catalog states: "Chimney Dum Dum/97 Series Chimney Dum Dim is a rugged heavy coating for the exterior of chimneys that provides flexible weatherproof protection. It fills and bridges hairline cracks with a flexible coating unrigr a tough outer skin. Should the leathery skin become fractured, the soft qntier film will harden on contact with air. May be applied without completely cooling stack." Chimney Dum Dum consists of a resinxred vegetable oil vehicle, containing 41% pigments, including titanium dioxide, .mica and the chrysotile form of asbestos; die total solids content is 63%. Application is by brush, or mote typically, by spray. At 75F, the surface skim over in 4-6 hours, and the under surface remains pliable. Resistance to chemical fumes and moisture is very good to excellent and the product is resistant to constant dry heat at 210F. Product Testing During Application and Removal To determine if asbestos is released during the application or removal of Chimney Dum Dum, approximately 18 gallons of the product was prepared on die basis of the formula master and muting instructions provided by Mobil. The oil base resin was no longer commercially tviulabfe, and a special batch was prepared for us by McWhorter Cap. All other components were obtained commercially. The product was made with a Myers mixer in 6 gallon batches which were subsequently combined, blended and stared in 5 gallon pails. The prepared product was observed to be smooth and uniform in appearance and of mastic consistency. This work, as well as subsequent application and removal experiments, was conducted at our facilities in compliance with all current United States and Massachusetts roles tod regulations relating to asbestos and in accordance with an approved Arthur D. Little,Inc. Health and Safety Flan. A test plan was developed to simulate typical work practices for product application and removal1. In addition, a sampling and analysis protocol was developed to 1Although intended for exterior use, this product was tested in an interior (controlled) environment. ArthirD Little MOB-HarrisMaster 00550 quantify the extent to which asbestos structures* may be released during the experimental application and removal activities. This protocol was designed so that all applicable NIOSH and EPA requirements for analysis by transmission electron microscopy were met or exceeded. The minimum detection limit for the analytical protocol was 0.01 structures/cc23. To evaluate the release of asbestos during product application and removal, ten concrete panels and twelve facing brick panels with concaved mortar joints, both sets four feet by two and one-half feet by one and one-half inches, prepared about one year earlier, were primed (Chimney Dum Dum Primer 38-V-5 equivalent), dried overnight and spray with Chimney Dum Dum at an estimated coating thickness of 30-40 mils using a Binks 2 gallon pressure pot with follower and a 7E2 spray gun. The coaxing operation required 55 minutes doing which personal and area air samples were The area sample was about ten feet from the spray site at an elevation of 5 feet. After an ambient cure of 24 hours (hiring which the coating skinned over, the panels were aged for 14 days at 200-210F'and eight days at ambient. The purpose of the furnace treatment was to accelerate the natural aging process. After the elapsed 23 days of aging, the product was hardened at the surface yet pliable and elastic when depressed with a screwdriver blade. Product removal was carried out on eight brick panels and six concrete panels over 88 minutes during which personal and area filter samples were collected. The collected filter samples horn these experiments were prepared and analyzed by transmission electron microscopy. The results of these analyses are given in Table 1. These results may be overstated compared to actual exposures which would occur in an open air environment. As such, they are considered to represent a "worst case" condition. 2Axbestos structures are defined herein as panicles 5pm or mare in extent that satisfy the counting guidelines given in 40 CFR Pan 763 Asbestos-Containing Materials in Schools, Appendix A, Figure 5 (Federal Register 2 (210) October 30, 1987,41866-41867). Structures include fibers, bundles, dumps and matrix. OSHA regulates exposure to fibers, which are defined as "a paniculate form of asbestos, tremolite, amhophyliite or acrinolite, 5 micrometers or longer, with a length-todiameter ratio of at least 3 to 1" (29 CFR 1910.1001). ^The minimum detection limit (MDL) for this experiment is he concentration where occupational exposure cannot be differentiated from general background. ArtfurD Little MOB-HarrisMaster 00551 Sample No. 052802 052803 052805 062001 062002 062003 Table 1 Asbestos Exposures During Application and . Removal of Chimney Dum Dum Description Sample Type . Exposure (s/cc) Application Application Application Removal Removal Removal Personal Personal (replicate) Area Personal Personal (replicate) Area 0.088 0.024 0.024 <0.01 <0.01 <0.01 Conclusions The conclusions reached in this study are as follows: Remanufacnrred Chimney Dum Dum was smooth and uniform with masdcIikc consistency. . Application to brick and concrete panels required heavy duty mastic spray apparatus. After 23 days of aging (14 days at 200-210F), the product was skinned over but. pliable and elastic when depressed with a tooL Results of worker exposure measurements during application of Chimney Dum Dum in a controlled environment were below the current OSHA action level45. Results of worker exposure measurements during removal of Chimney Dum Dum in a controlled environment did not exceed the minimum detection limit of 0.01 structures/cc. Based upon the above results, there is insignificant occupational exposure to airborne fibers during the application of Chimney Dum Dum and virtually no exposure to airborne asbestos fibers during die removal of this product 4Asbestos structures per unit volume of air. The structures observed were fibers (or fibers and bundles, conesponding to the EPA definition). 5OSHA defines action level as "an airborne concentration of asbestos, tremolite, amhophyllite, acrinohte, at a combination of these miwmi*, of 0.1 fiber per cubic centimeter (f/cc) of air calculated as an right (8) hour time weighted average" (29 CFR 1910.1001, promulgated June 20, 1986). Rak,.niMU MOB-HarrisMaster 00552 Evaluation of Asbestos Release from Hi-Heat Dum Dum Caulking During Application and Removal By Arthur D. little, Inc. Acorn Park Cambridge, MA 02140-2390 1992 Reference No. 65191 A*+hir D Little MOB-HarrisMaster 00553 Table 1 Asbestos Exposures During Application and Removal of Hl-Heat Dum Dum: Personal Samples Analyzed by Transmission Electron Microscopy Sample No. 042504 042604 051703 051705 052203 052207 Description First Application Second Application First Removal First Removal (replicate) Second Removal Third Removal Exposure (s/cc)5 <0.01 <0.01 <0.01 <0.01 <0.01 0.01 Conclusions The conclusions reached in this study are as follows: The Hi-Hcat Dum Dum that was tested was found to be non-friable and provided encapsulation of asbestos during application and removal experiments. Exposure of the product to 225-250F for 18 to 23 days changes its color from a neutral gray to a chocolate brown, indicating modification of the resin. Even so, the product was elastic and pliable except at die feathered, thin edges where it was hardened but not friable. Results of worker exposure measurements during use of Hi-Heai Dum Dum did not exceed the minimum detection limit of 0.01 asbestos structures/cc in thgr product application or product removal experiments. Based upon the above results, occupational exposure to airborne asbestos fibers riming the application or removal of Hi-Heai Dum Dum is virtually non-existent. sExposure represents asbestos structures per unit volume of air. ArtHir D Little MOB-HarrisMaster 00554 Product Background High temperature resinous caulking materials of mastic (puny-like) consistency are used in sealing joints and crevices on furnaces and boilers to prevent heat loss. Mobil rhgTnjgai Company manufactured and sold such a caulking product from the mid-1960s through the 1970s called Hi-Heat Dum Dum. This product. No. 46-F-7, rrmtiweri of a oil-base vehicle (resin) containing various solid fillers, inrfwWng clay and the chrysodle variety of asbestos (added for its resiliency and bridging properties). The Mobil Chemical Products Catalog provides the following description: "Hi-Heat Dum Pum/46-F-7. a heavy semi-plastic fibred coating, which acts as a joint sealer and pliable gasket for boilers, furnaces and dry Inins, Improves boiler efficiency by preventing heat loss. Retains its elasticity at consistent hear up to 175 and intermittent heat to 350. May be used as a complete cover to eliminate excess fuel consumption and can be painted over in 24 hours." The purpose of a joint or crevice sealant is to bridge gaps between the furnace enclosure and attachments (doors, ports, flanges, etc.). This requires a product that is pliable and resilient (Le., withstands shock without permanently deforming, tearing, rupturing or pulling away from the furnace surface), and does not degrade over by becoming friable1. The resinous formulation of Hi-Heat Dum Dum provides three properties and also effectively encapsulates the asbestos component preventing its release. Product Testing During Application and Removal Hi-Heat Dum Dum was tested by Arthur D. Little, Inc. to determine if asbestos was released during application or removaL Approximately 30 gallons of 46-F-7 Hi-Heat Dum Dum was remanufactured, as observed by Arthur D. Little, Inc. staff who' provided chain-of-custody transmittal to our facility. Experiments (described below) were conducted at our facilities in compliance with all current United States and Massachusetts rules and regulations relating to asbestos and in accordance with an approved Arthur D. Little, Inc. Health and Safety Plan. An application and removal plan was developed to simulate typical work practices. In addition, a sampling and analysis protocol was developed to quantify the extent to which asbestos structures' are released during the experimental application and 'The U.S. Environmental Protection Agency defines friable as "capable of being crumbled, pulverized, or reduced to powder by hand pressure". it *! n i s*+Ia MOB-HarrisMaster 00555 removal activities2. This protocol was designed so that all applicable NIOSH and EPA requirements for analysis by transmission electron microscopy were met or excrttded. The minimum detection limit for the analytical protocol was 0.01 fibeis/cc3. To evaluate the release of asbestos during product application and removal, steel panels (1/32 inch thick 1040 steel cleaned and'degreased, measuring about 2 1/2x3 1/2 feet) were coated by troweling at an estimated thickness of 1/S" (and feathered at the panel edges). Approximately 15 panels were coated during each of two 80minute application experiments. Personal exposure samples were collected during both experiments. After product application, the Hi-Heat Dum Dum was heated to accelerate the aging process4. The neutral gray of the as-applied coating changed in color to a chocolate brown (225-250F for 20 days). After aging, product removal experiments were conducted using a putty knife and scraper. Although the thicker, centrally coated area of each panel was very pliable and quite easily removed, the feathered edge regions were somewhat harder and required substantial mechanical effort to scrape down to the bare metal. Approximately 10 panels were cleaned in each of three, separate 80-minute experiments during which personal filter samples were collected. The personal filter samples were prepared and analyzed by transmission electron microscopy. The results of these analyses are given in Table 1. 2Asbestos structures are defined herein as particles 5pm or mare in extent that satisfy the counting guidelines given in 40 CFR Part 763 Asbestos-Containing - Materials in Schools, Appendix A, Figure 5 (Federal Register 52 (210) October 30, 1987, 41866-41867). Structures include fibers, bundles, dumps and matrix. OSHA regulates exposure to fibers, which are defined as "a paniculate form of asbestos, tremolite, anthophyllite or actinolite, 5 micrometers or longer, with a length to diameter ratio of at least 3 to 1" (29 CFR 1910.1001). hhe minimum detection limit (MDL) for this experiment is the concentration where occupational exposure can not be differentiated from general background. ^Curing preliminary laboratory furnace experiments with coated steel coupons, we observed that the product discolored from a neutral grey to a dark chocolate brown after one day at 350F and to a medium brown after four days at 265F. Even after these exposures to temperatures which exceeded the recommrnried continuous use temperature, the product remained pliable and gummy when probed with a screwdriver. Therefore, although the product was designed far a continuous temperature of 175F, a treatment of two weeks to dry, flowing air at 250F was chosen to not only accelerate aging but also to account for intermittent temperatures greater than 175F. The actual conditions of exposure were 225-250F for 18 to 23 days. H^Lknl m MOB-HarrisMaster 00556 f Evaluation of Asbestos Release from Exterior Masonry Weatherproofing Mastic During Application and Removal By Arthur D. Little, Inc. Acorn Park Cambridge, MA 02140*2390 1992 Reference No. 65191 ArfhirnUHlll MOB-HarrisMaster 00557 Produet Background From the mid-1960's through the 1970's, Mobil Chemical Company manufactured and sold a line of mastic-type protective coatings under the name Dum Dum Products. Dum Dum Masonoc/Scries 95 was a restoration product for weatherproofing masonry structures. The Mobil Chemical Product Catalog stares: "Dum Dum Masonoc/95 Series Masonoc is a heavy bodied textured coating designed as a weather seal, waterproofing, and restoration coating for all types of masonry structures. Pliability and elasticity allow for building movement without cracking of the coating while a tough outer skins provides protection far normal usage. Its high build qualities permit hairline cracks to be bridged and sealed, and surface irregularities to be filled and uniformed. Masonoc also provides fine protection for steel with its high film build and impermeability. Its excellent surface wetting properties recommend use of this material in areas that cannot be damed too well, where there are numerous angles and edges to protect,, or when a single coat application is all that can be provided." Masonoc consists of a resinated vegetable oil vehicle with about 22% solid fillers (by weight), including titanium dioxide, the chrysotile form of asbestos and various coloring pigments; the total solids content is 42 percent by volume. After application, Masonoc skins over in 1 hour, but the undersurface remains to allow for expansion and contraction. The Mobil Chemical Product Data Sheet for Dum Dum Masonoc claims excellent resistance to dry heat (to 150F), weather extremes, chemical fumes, moisture and salt air. Product Testing During Application and Removal Three 5 gallon pails of Dum Dum Masonoc (soft white 95-W-9) were obtained from an electric utility seeking information on product disposal. A sample was taken from one pail, about a third full, and ashed at 500C. Microscopic analysis of this ash confirmed the presence of the chrysotile form of asbestos. The other two pails were intact with no visible signs of having been opened. After thorough mixing and being satisfied that the product viscosity was in the range of a mastic, these two pails of Masonoc were used far application and removal experiments. This work was conducted at our facilities in compliance with United Stares and Massachusetts rules and regulations applying to asbestos and in accordance with an approved Arthur D. Little, Inc. Health and Safety Plan. A test plan was developed to simulate typical work practices far product application and removal1. In addition, a sampling and analysis protocol was developed to ^though intended for exterior use, this product was tested in an interior (controlled) environment ArthirD Little MOB-HarrisMaster 00558 t quantify tfae to which asbesms structures2 may be released daring the grperimenal application and removal activities. This protocol was designed so that all ppiir?hte NIOSH and_EPA requirements for analysis by transmission. eleoron microscopy were met or exceeded. The minimum detection limit for the analytical protocol was 0.01 strucmres/cc3. To evaluate the release of asbestos during product application and removal, concrete pangfo 4 feet by 2-1/2 feet by 1-1/2 inch were prepaled, in wooden frames and cured for 42 days. The panels woe then each coated with Masonoc Primer 47-W-21, "a clear 100 percent solid hear resistant penetrating primer", dried overnight and then coaxed with Dum Dum Masonoc. using a Binks 7E2 spray gun and 2 gallon pressure pot, to a of approximately 30-40 mils. Approximately IS panels were coated during each of two 80 minute application experiments. Personal exposure and area air woe collected during both experiments. The area simple was located about 10 feet from die worker (sprayer) at an elevation of 5 feet. After product application, the coated panels were (with spacers), allowed to dry for 24 hours and were then moved to an oven and exposed to flowing dry air at L50*F (the uaximnm recommended use tempsamxe) for 42 days to accelerate the aging process followed by an additional 67 days at ambient conditions. Afar aging, the product was found to be pliable and elastic when pressed with a screwdriver blade. A product removal experiment was performed using a putty knife and scraper. Eight panels were cleaned over an.approxhnaieiy 80 minute period during which personal samples were collected. After a further ambient aging period of 168 days (a total of 278 days after application), and again observing tfae product to be pliable and elastic, a second replicate removal experiment was performed on ten pmmf* The collected filler samples from these experiments were prepared and analyzed by transmission electron microscopy.. The results of these analyses axe given in Table 1. These results may be overstated compared to actual exposures which would occur in an open air environment. As such, they are considered to represent a "wont case" condition. 2Asbestos structures are defined herein as panicles 5pm or more in extent that satisfy the counting guidelines given in 40 CFR Part 763 Ah>mt.f,nimtTimg Materials in Schools. Appendix A, Figure 5 (Federal Register . (210) October 30, 1987, 41866-41867). Structures include fibers, bundles, eimnpa and matrix. OSHA regulates cxpusuie to fibers, which are as "a particulate farm of asbestos, gemoiite. anrhophyllite or arrinolite. 5 micrometers or longer, with a length-to- diameter rario of at least 3 to 1" (29 CFR 1910.1001). Y 3The minimum detection limit (MDL) for this experiment is the concentration where occupational exposure cannot be differentiated from general background. ArthirDLrttle MOB-HarrisMaster 00559 Sample No. 072701 072702 072703 072704 111406 111407 111403 050104 050107 050105 Table 1 Asbestos Exposures During Application and Removal of Dum Dum Masonod Description Sample Type Exposure (s/cc)4 Hm Application First Application AppiiCttiOtt Second Application First Removal First Removal (replicate) First Removal Second Removal Second Removal (replicate) Second Removal Personal Area Personal Area Personal Personal Area Personal Personal Area 0.01 <001 <001 <001 <0.01 <0.01 <001 <0.01 <0.01 <0.01 Conclusions Hie conclusions reached in this study are as follows: * After thorough mixing, the obtained pails of Dum Dum Masanoc, cnnfiiinMi to contain- chrysodle asbestos, were smooth and of TTtT'f* consistency. * Application to concrete panels required heavy duty spray apparatus. * After aging at 150F for 42 days and additional periods of 67 and 168 days at ambient conditions, the product was observed to be pliable and when depressed with a tooL * Results of worker exposure during application and removal of Dum Dum Masoned in a controlled environment did not exceed the mimnunn detection limit of 0.01 stiucnnes/cc. * Baaed upon the above results, occupational exposure to airborne asbestos fibers during the application or removal of Dum Dum Masonod is virtually 4Asbestos structures per unit volume of air. Aftha'D Little MOB-HarrisMaster 00560 Resiliency of Mobil Hi-Hcat Dum Dum after High Temperature Exposure By Arthur D. Little, Inc. Acorn Park Cambridge, MA 02140-2390 1992 Reference No. 65191 MOB-HarrisMaster 00561 Product Background High temperature resinous materials of mastic (putty-like) consistency are used in sealing joints and crevices on furnaces and boilers to prevent heat loss. Mobil Chemical Company manufactured and sold such a caulking product from the mid-1960s through the 1970s called Hi-Heat Dum Dum. This product. No. 46-F-7, consisted of a linseed oil-base vehicle (resin) containing various solid fillers, including clay and the chrysodle variety of asbestos (added for its resiliency and bridging properties). The Mobil Chemical Products Catalog provides the following description: "Hi-Heat Dum Dum/46-F-7, a heavy semi-plastic fibred coating, which acts as a joint sealer and pliable gasket for boilers, furnaces and dry kilns. Improves boiler efficiency by preventing heat loss. Retains its elasticity at consistent heat up to 175 and intermittent heat to 350. May be used as a complete cover to gHtninaia excess fuel consumption and can be painted over in 24 hours." The purpose of a joint or crevice sealant is to bridge gaps between the furnace enclosure and attachments (doors, pons, flanges, etc.). This requires a product that is pliable and resilient (i.e., withstands shock without permanently deforming, tearing, rupturing or pulling away from die furnace surface), and does not degrade over time by becoming fixable. The resinous formulation of Hi-Heat Dum Dum provides these properties and also effectively encapsulates the asbestos component, preventing its release. Purpose of the Evaluation The objective of the thermal exposure experiments was to determine the useful service life of Hi-Heat Dum Dum for temperatures within and above the recommended service temperature range described in the product literature. Product Testing Experiments and Results Approximately 30 gallons of 46-F-7 Hi-Heat Dum Dum was remanufactured, as observed by Arthur D. Little, Inc. staff who provided chain-of-custody transmittal to our facility. Approximately one pint was used for the tests described herein. The aging experiments were conducted by filling steel fixtures with Dum Dum and placing the fixtures into ovens at different temperatures. The fixtures, consisting of a steel ring spotwelded to a piece of sheet steel, provided for a one inch diameter and three different thicknesses of the material - 0.062 inches, 0.125 inches and 0.187 inches. Fifteen fixtures of each thickness were prepared for a total of 45 fixtures, individually numbered by stamping. Each fixture was tared on an analytical balance (scale) that measured the weight to 0.0001 grams. The fixtures were then filled with the Dum Dum product, reweighed to determine the h **hir A I ittip MOB-HarrisMaster 00562 weight of the Dum Dum in the fixture and placed into ovens in triplicate at temperatures of: 175, 250. 350. 425 and 500 F. The three replicate samples at each thickness represented a total of nine samples at each temperature. At times of 22, 46, 70, 93.5, 133-5, 400.5 and 763 hours, the samples were removed from the ovens, allowed to cool to room temperature and again weighed. The percent change from initial weights are provided in Table 1. All of the samples underwent a change in the original natural gray color after aging. The colors ranged from a darker gray (175F) to chocolate brown (250F) to dark brown (350F) to black (425F and 500*7). During the initial heating of die 500F samples, smoke was emitted from the oven leading us to believe that die solvent within the sample ignited and burned. The surface of the 500F samples became swollen and expanded out of the fixture in a spherical shape. This occurred to a lesser extent for the 425F samples. The samples also exhibited surface hardening.' To determine any product brittleness or friability,' we tested the flexibility of five samples aged for 763 hours by a bending experiment. For this purpose, a test sample was cut from the fixture such that there would be no interference from the fixture on the bend experiment. The tests were done using a three point bend fixture on an Instron 1332 mechanical testing machine with a 1000 pound load celL A schematic representation of the bend condition is shown in Figure 1. Crosshead displacement control was used with a displacement rate of 0.1 inches/minute. The applied load and the crosshead displacement was continuously recorded. Test events such as the onset of surface cracking were noted. The experimental results of the bend tests are given in Table 2. Discussion Hi-Hear Dum Dum contains about 10 percent by weight mineral spirits, to provide a suitable' viscosity for application, and a linseed oil blend as the vehicle which may have some volatiles; the solids content is stated as 85 percent by volume. Loss in weight of Hi-Heat Dum Dum exposed to elevated temperatures occurs by evaporation of die solvent and oxidation (ablation) of the resinous vehicle. To estimate the useful life of the product, defined as retention of flexibility as demonstrated by a strain of 1 percent, the observed loss in initial weight as a result of furnace aging experiments is plotted in Figure 2, where the averages for three thicknesses tested are pooled. After 22 hours of high temperature exposure, much of the solvent has evaporated, mote so as the exposure temperature increases. For longer exposures at elevated temperature, the 175, 250 and 350F exposures demonstrate a linear change in weight loss when plotted against the logarithm of exposure time. The samples aged at 350F for 763 hours still exhibit a 1 percent strain in bending (Table 2), having lost 12^ percent of initial weight, representing essentially all of the non-solids content of Hi-Heat Dum Dum. From the data, product life at a sustained temperature of 250F is conservatively estimated at more than 10 years. MOB-HarrisMaster 00563 Exposures of Hi-Heat Dum Dum at temperatures greater than 350F results in rapid degradation due to both very rapid evaporation of the solvent and oxidation of the resin. Further, exposure of this product to sustained temperatures of 350F could result in product life as short as one month. Accordingly, the use of this product under conditions where it is exposed to consistent heat of up to 175F and intermittent heat of up to 350F is considered prudent. Conclusions The conclusions reached in this study are as follows: Hi-Heat Dum Dum survives constant heating to 250F and intermittent hearing to 350F and behaves as described in the product literature. Hearing the Dum Dum above 350F causes rapid loss in weight and. probable failure of the product After 763 hours of aging at 250 and 350F, the product can be strained by one to one and a half percent demonstrating that it has retained elasticity. Based upon extrapolation of the data. Hi-Heat Dum Dum is expected to retain its elasticity for more than 10 years when used in accordance with the manufacturers recommendations. Artiiir D Little MOB-HarrisMaster 00564 Temp. (8F) 22 Thickness = 0.063" 175 8.90 250 9.47 350 9.91 425 10.96 500 14.60 Thickness = 0.125" 175 7.86 250 8.88 350 10.24 425 11.04 500 15.08 Thickness = 0.183" 175 625 250 7.79 350 9.68 425 1121 500 14.15 Table 1 Hi-Heat Dum Dum: Percent Weight Loss (Average of 3 Samples) Time Cumulative Hours at Temperature 46 70.5 93.5 1332 4002 8.95 9.50 10.67 11.73 18.39 8.87 925 10.91 12.07 21.36 8.87 9S7 11.00 12.34 23.98 8.94 9.65 1129 12.74 28.47 922 9.93 12.10 14.65 40.41 8.92 9.51 10.86 11.55 17.35 927 9.71 11.02 12.17 2228 9.43 9.73 11.13 12.80 24.98 8.94 9.65 11.39 12.74 28.47 922 9.93 12.10 14.65 40.41 7.79 921 10.50 11.70 16.87 8.52 9.71 10.75 1225 19.41 8.90 9.82 10.90 12.68' 21.75 921 10.05 11.15 13.94 2422 10.13 1027 11.90 16.42 37.88 763 8.99 9.75 12.18 16.11 4523 9.79 9.95 12.10 18.98 4524 10.00 1027 1321 1828 44.30 n I M>lo MOB-HanisMaster 00565 Table 2 Hi-Heat Dum Dam: Flexibility after 763 Hours at Temperature Angie of Deflection Sample Thickness (inches) Aging Temp. (F) Crack Starts Fully at One End Cracked Percent Strain 37 0.125 27 0.187 33 0.062 8 0.125 28 0.187 250 250 350 350 350* 10 16 1.7 4 11 12 ' 4 10 1.1 5. 10 1.1 N/A N/A N/A * Material separated from steel holder. IVi+Kir D little MOB-HairisMaster 00566 Figure 1 Schematic of Bend Test Conditions and Bend Angie Calculations Crosshead Displacement Sm B = 0.5(1.760) a = 180-2 B MOB-HarrisMaster 00567 I S A, Tim * at tamparatur* (hour*) (%) MOf ) A-il__ _ n I Min Jt 5s N 39 c MOB-HarrisMaster 00568