Document G5kLLdgzeRgpep0oqkXyBVaBq

FILE NAME: RT Vanderbilt (RTV) DATE: 2007 May 4 DOC#: RTV078 DOCUMENT DESCRIPTION: Comments by Richard A. Lemen - Public Hearing Asbestos and Other Mineral Fibers with Attachments Comments by Richard A. Lemen, Ph.D. Public Hearing on Asbestos and Other Mineral Fibers: A Roadmap for Scientific Research -M ay 4, 2007 - I would like to commend NIOSH on their Draft Roadmap for Scientific Research on Asbestos and Other Mineral Fibers released in February 2007. Im portant issues are addressed in this docum ent and NIOSH has set forth a good agenda to address them. I would like to make some personal observations before I go into specifics about issues in the NIOSH Roadmap. First, I encourage NIOSH to evaluate all data input it receives with full disclosure of the source. I am here today as in my role as Co chairm an of the Science Advisory Board of the Asbestos Disease Awareness Organization (ABA#), a non-profit asbestos victims advocacy organization. I also testify on behalf of plaintiffs in asbestos litigation. I am also an Adjunct Professor with the Department of Occupational and Environmental Health of the Robbins School of Public Health of Emory University in Atlanta. I am here today at my own expense. I would hope all who testify here today will disclose their own affiliations and potential conflicts of interest and who is supporting their attendance here today. Since the passage of the OSHAct of 1970, NIOSH has been the leader in prevention methodologies for asbestos-related health issues. The first criteria document from the newly formed NIOSH of 1971, was on asbestos, after NIOSHs first Director Dr. M arcus Key had sent a letter to OSHA stating the inadequacy of OSHAs new start-up standard for asbestos, based on the then ACGIH TLV. Dr. Key recommended an immediate lowering to 2 fibers/cc. NIOSH was the first Federal agency, in its 1976 Revised Criteria Document, to call for a ban on asbestos. NIOSH has m aintained this position to the present while suggesting in the interim th a t the only reliable and practical analytical method, at that time, was 0.1 Statement o f Dr. RA Lernen on NIOSH Asbestos Roadmap 2 fiber/cc using the NIOSH Phase Contrast Method (PCM) 7400 asbestos analytical method. Unfortunately chrysotile cannot be seen in the light microscope when it occurs in the fibril form and th u s most chrysotile is not counted in an air sample using a NIOSH 7400 .count scheme-diameter resolution of approximately 0.25 microns since m ost individual "fibrils" of crocidolite and chrysotile are 0.02-0.05 microns in diameter. OSHA describes the advantages and disadvantages of the Phase C ontrast Microscope (PCM) as can be seen in the footnote.*1234 This is something NIOSH suggests it intends to address in the new Roadmap. NIOSH's new Roadmap represents its continued leadership role in occupational safety and health by addressing asbestosrelated issues needing clarification and further elucidating a n d /o r addressing questions still unresolved. By so doing NIOSH is fulfilling its congressionally m andated role under the Occupational Safety and Health AcCMf$1970. NIOSH should not back away from including all respirable asbestiform fibrous minerals, including cleavage fragments 1 Rules and regulations-Dept Labor-OSHA 29 CFR Parts 1910, 1915, 1926Occupational Exposure to Asbestos- Final rule-Aug 10, 1994 59FR4096 "1.3 Advantages and Disadvantages There are four main advantages of PCM over other methods: (1) The technique is specific for fibers. Phase contrast is a fiber counting technique which excludes non-fibrous particles from the analysis. (2) The technique is inexpensive and does not require specialized knowledge to y out the analysis for total fiber counts, (3) The analysis is quick and can be performed on-site for rapid determination of air concentrations of asbestos fibers. (4) The technique has continuity with historical epidemiological studies so that estimates of expected disease can be inferred from long-term determination of asbestos exposures. 41066 The main disadvantage of PCM is that it does not positively identify asbestos fibers. Other fibers which are not asbestos may be included in the count unless differential counting is preformed. This requires a great deal of experience to adequately differentiate asbestos from non-asbestos fibers. Positive identification of asbestos must be performed by polarized light or electron microscopy techniques. A further disadvantage of PCM is that the smallest visible fibers are about 0.2pm in diameter while the finest asbestos fibers may be as small as 0.02pm in diameter. For some exposures, substantially more fibers may be present than are actually counted." ? -\ Statement o f Dr. RA Lemen on NIOSH Asbestos Roadmap 3 which appear to be in a fibrous habit and th u s fitting the asbestos definition by light microscopy and that are clearly respirable2 dusts. This should only be changed if there exist irrefutable data, both hum an and animal, showing the safety of any such fibrous mineral being excluded since the only difference of these entities from the structures of the same mineral in true asbestiform habit is the structural morphology with all other characteristics being the same. NIOSH should develop valid methodologies to sample for all size fibers, including those less than 5 um in length, now not addressed by OSHA regulatory standards. Both animal and hum an data support such an inclusion as can be seen by the . attached Appendix - l.3 * NIOSH should address and refine their current surveillance of fiber-related diseases. For example it is well known th at the National Cancer Institutes SEER data base underreports ' mesotheliom a.4 NIOSH should continue its Respiratory Disease Surveillance System and should assure that other NIOSH surveillance systems become more comprehensive and inclusive, and analysis should not relying solely on Proportionate Mortality/Morbidity Analysis (PMR) for determining mortality or incidence data, as this type analysis underreports low incidence and rare diseases, albeit important diseases i.e. mesothelioma. , NIOSH should also determine how m uch of background mesothelioma and other asbestos-related diseases are related to increased consum ption of asbestos within any reference populations used for control comparison and th u s adjust expected rates accordingly in order to determine the true risk of asbestos-related diseases. Evidence suggests as 2 Dement J M, Zumwalde RD, Gambel JF, Fellner W, DeMeo MJ, Brown DP, Wagoner JK, 1980. Occupational exposure to talc containing asbestos-Morbidity, Mortality, and environmental studies of miners and millers. NIOSH Technical Report-DHEW (NIOSH) Publication No. 80-115, Feb.34 3 See Appendix 1 - Short Fibers, Richard A. Lemen, Ph.D. 4 See Appendix 2 - Mesothelioma Surveillance, Richard A. Lemen, Ph.D. . Statement of Dr. RA Lemen on NIOSH Asbestos Roadmap 4 consumption of asbestos has gone up so have background rates of asbestos-related diseases.5 NIOSH should review the epidemiology literature on all fibrous materials, not ju st those related to the currently regulated asbestiform fiber types. Such research should address all respirable fiber types and all size param eters, including short respirable fibers. Since biopersistence h as been used as a surrogate by identifying lung fiber burden as a critical factor in causation, toxicological studies should evaluate whether external airborne concentrations are representative of the fiber concentrations and morphologies once the fibers have been inhaled into the lung. Data suggest that the breathing zone samples of chrysotile may not represent the actual fiber burden of chrysotile fibers in the lung as they break apart from fiber bundles and multiply once within the lung, while the amphiboles do not.6 This is im portant as it means a higher dose of chrysotile in the lung as well as higher rate of translocation of chrysotile from the lung. Because dose plays a significant role in the toxicity of chrysotile as compared to amphiboles such findings would be important in determining the actual role of chrysotile in asbestos-related diseases such as mesothelioma. This translocation of chrysotile asbestos indicates a more specific role for chrysotile in the etiology of mesothelioma. Mesotheliomas develop in the pleura, peritoneum and other serosal surfaces of the body. It is universally accepted that chrysotile is a cause of cancer in the lung and migrates to and is concentrated in the pleura7. Since 5 See Appendix 3 - Mesothelioma Background, Richard A. Lemen, Ph.D. 6 Bellman B, Muhle H, Pott F, Konig H, Kloppeel H, Spumy K, 1987. Persistence of man-made fibers (MMF) and asbestos in rat lungs. Annals of Occup Hyg, 31: 693-709. 7 Suzuki, Y. & Kohyama, N., 1991. Translocation of Inhaled Asbestos Fibers from the Lung to Other Tissues. Am J Ind Med, Vol. 19, p. 701-704; Kohyama, N. & Suzuki, Y., 1991. Analysis of asbestos fibers in lung parenchyma, pleural plaques, and mesothelioma tissues of North American insulation workers. Ann N Y Acad Sci, Vol. 643, p. 27-52; Suzuki, Y., Yuen, S., Ashley, R. & Calderaro, A., 1998. Asbestos fibers and human malignant mesothelioma. Advances in the Prevention of Occupational Respiratory Diseases, Eds. Chiyotani, K., Hosoda, Y., & Aizawa, Y., Elsevier Science Statement of Dr. RA Lemen on NIOSH Asbestos Roadmap 5 chrysotile is carcinogenic and is present in high concentrations in the pleura where the mesothelioma is induced, it is biologically plausible that it causes or contributes to cause mesothelioma. This is also shown by many mechanistic and molecular studies that indicate how chrysotile may cause mesothelioma. Fiber penetration can rearrange the cytoskeletal apparatus of the cell and this could indicate an interaction between the chrysotile fibers and the normal mitotic process, since giant multinucleated cells are formed. These studies indicate that chrysotile penetrates the cell, enters the nucleus and induces abnormal chromosome formations in dividing cells.8 Some of these abnormalities include the deletion of the P53 gene th at controls cell growth.9 Additional research should include evaluation of the synergistic effects between amphibole a n d "serpentine fiber exposures, since it is highly unlikely that uncontaminated serpentine exposures exist in occupational and environmental settings. To date such findings have suggested such a synergistic action between the mixed fiber types.10*It has been suggested by some th at the fibrous tremolite contamination of chrysotile, usually less than 1%, is the cause of mesothelioma B.V., p.709 and Sebastien, P., Janson, X., Gaudichet, A., Hirsch, A. & Bignon, J., 1980. Asbestos retention in human respiratory tissues: comparative meas urements in lung parenchyma and in parietal pleura. IARC Sci Pub, Vol. 30, p. 237-246; Dodson RF, Graef R, Shepherd S, O'Sullivan M, Levin J, 2005. Asbestos burden in cases of mesothelioma from individuals from various regions of the United States. Ultrastruct Pathol. Sep-Oct;29(5):415-33. 8 Malomi, W., Loai, F., Falchi, M., and Donnelli, G., 1990. On the mechanism of cell internalization of chrysotile fibers: An immunocytochemical and ultrastructural study. Environmental Research, Vol. 52, No. 2, pages 164-177. 9 Levresse, Renier, Fleury-Feith, Levy, Moritz, Vivo, Pilatte, Jaurand, 1997. Analysis of Cell Cycle Disruptions in Cultures of Rat Pleural Mesothelial Cells Exposed to Asbestos Fibers. Am J Respir Cell Mol Biol, 17: 660-671. 10 Nicholson WJ, Landrigan PJ, 1994. The carcinogenicity of chrysotile asbestos, In : The Identification and Control of Environmental and Occupational Diseases : Asbestos and Cancer. Eds. M Mehlman, A Upton: Princeton Scientific Publishing Co., Inc. Vol XXII; Acheson ED, Gardner MJ, 1979. Mesothelioma and exposure to mixtures of chrysotile and amphibole asbestos. Statement o f Dr. RA Lernen on NIOSH Asbestos Roadmap 6 among predominately chrysotile exposed persons.11 New evaluation of the South Charleston chrysotile exposed population of textile workers has confirmed a dose-response relationship between asbestosis and lung cncer.12 This is im portant as entities suggesting th at chrysotile is the "safe asbestos" base their conclusions on only one outcome, that being mesothelioma. While it is generally recognized that chrysotile on a dose-by-dose basis is less potent than the amphiboles in producing mesothelioma; however, this does not appear the case for other asbestos-induced disease. Therefore, future NIOSH research should continue to look at other asbestos-induced diseases when determining recommended regulatory actions for the prevention of asbestos-related diseases. The current OSHA regulations govern exposure to entities defined in the regulations as asbestos; however, formations that contain tremolite asbestos also have tremolite cleavage fragments. Thus, ju st because the cleavage fragments are not covered under the current OSHA regulations, as regulated fibers does not mean that they are biologically inactive. The em phasis of the fiber pathogenicity being related to the fact that any asbestos structure is a fiber is only one explanation of how it causes disease. The fact is th at the non asbestiform cleavage fragment is an analog of the fibrous asbestos structure and is chemically made of the same composition. The complexity of asbestos induced lung disease/injuiy includes a wide array of issues other than ju s t physical features (Kamp and Wiseman, 1999).13 Next I will provide some data which may shed some light on the arguments for including a broad fiber definition when it 11 McDonald J.C., McDonald AD, Chrysotile, Tremolite and Mesothelioma. Letter published in Science, 10 Feb 1995, Vol. 267:775 12 Hein MJ, Stayner L, Lehman E, Dement JM, 2007. Follow-up study of chrysotile textile workers : cohort mortality and exposure-response. Occup Environ Med (published online 20 Apr. 2007), 031005. 13 Kamp DW, Weitzman SA, 1999. The molecular basis of asbestos induced lung injury. Thorax. 54:638-652 Statement of Dr. RA Lemen on NIOSH Asbestos Roadmap 7 comes to m aterials contam inated with asbestos. As former Deputy and Acting Director of NIOSH I know the agency has been dealing with the issue of talc contaminated with fibrous asbestos for many years. Researchers found among miners and millers from two counties in Northern New York eight talc miners identified as having mesothelioma and now Hull, Abraham and Case (2002) have added five new cases.14 Rohl and Langer (1974) have stated "Talc because of its composition, conditions of formation and geological occurrence, is frequently contam inated with asbestos fibers."15 The data, however, support earlier studies that indicate that talc miners and millers experience excess parenchymal fibrosis and pleural changes. The data also suggest that individuals in the paper industry and construction trades may be at risk.16 Dement et al., in 1980 found from one mine and mill, reported by the company to be producing non asbestiform talc, air samples of 5 fibers/cc as time weighted average (TWA) in six job categories containing 48% mineral talc, 37-59% tremolite, 4.5-15% anthophyllite, and 10-15% serpentine, lizardite, antigorite. Thus the TWA exposures to asbestiform amphiboles (anthophyllite and tremolite) were found to be in excess of the present U.S. Occupational Safety and Health (OSHA) and Mine Safety and Health Administration (MSHA) occupational exposure standards and th at in many mine and mill operations more th an 90 percent of the total airborne fibers were less th an 5jum in length. They found asbestiform tremolite, anthophyllite and in a couple of samples chrysotile and found they were fibers when using analytical transmition 14 Hull MJ, Abraham JL, Case BW, 2002. Mesothelioma among workers in asbestiform fiber-bearing talc mines in New York State Ann Occ Hyg, 46, (Supplement 1): 132-135 13 Rohl AN, Langer AM, 1974. Identification and quantitation of asbestos in talc. E n v Health Perspectives, Dec., 9; 95-,109 16Fitzgerald EF, Stark AD, Vianna N, Hwang S-A, 1991. Exposure to asbestiform minerals and radiographic chest abnormalities in a talc mining region of upstate New York. Archives of Environmental Health. May/Jun, 46 (3); 151-154. Statement o f Dr. RA Lernen on NIOSH Asbestos Roadmap 8 electron microscope (ATEM) as well as Phase contrast microscope (PCM) and not cleavage fragm ents.17 I would subm it for the record today some correspondence you may not be aware of dealing with this issue. These data show how Johns-M anville analysis determ ined th at R.T. Vanderbilt's talc products contain tremolite, chrysotile, and anthophyllite and that CP talc's contain up to 30% tremolite and that because of this Johns-M anville determ ined the necessity for labeling such fibrous containing talc's as containing asbestos. I recommend th at NIOSH m aintain its position th a t all fibrous asbestiform minerals and that all other minerals or materials contaminated with fibrous asbestos be treated as hazardous. Finally when NIOSH conducts or contracts out epidemiology studies strict criteria m ust be followed to assure the best quality studies possible. These criteria should include, but not be limited to such areas as: 1 - Determine actual exposure to the fibrous material and not allow dilution of any finding because non -exposed were included in the cohort non-exposed; 2 - Allow sufficient size of the study population to assure sufficient power to detect adverse effects if they exist; 3 - Conduct sufficient follow-up to assure th at at least 95% of the cohort is traced and th at vital statu s is known and evaluated; 4 - Allow sufficient latency to determine if adverse effects do develop, this is im portant since known traditional latency periods may be extended due to lower level cumulative exposures; 17 Dement J M, Zumwalde RD, Gambel JF, Fellner W, DeMeo MJ, B ro w n DP, W ag o n er JK, 1980. Occupational exposure to talc containing asbestos-Morbidity, Mortality, and environmental studies of miners and millers. NIOSH Technical Report-DHEW (NIOSH) Publication No. 80-115, Feb. Statement of Dr. RA Lemen on NIOSH Asbestos Roadmap 9 5 - Identify and account for any possible confounders or co-factors th a t may skew or alter the outcome of the study; and 6 - If case-control analyses are conducted make sure that all m atched controls are selected so that confounding or co-factors will not skew the outcome, including securing adequate occupational histories to rule out other causative agents or p ast occupational exposures. Last, I would encourage NIOSH support the Ban Asbestos Act introduced by Sen. Murray to ban all commercial uses and importation of asbestos. I would also add my assistance should NIOSH need it as I have had an intimate role in NIOSH asbestos research and policy recommendations dating since the agencies inception and until my retirement in 1996. Statement of Dr. RA Lemen on NIOSH Asbestos Roadmap 10 Appendix 1 Short Asbestos Fibers Richard A. Lemen, Ph.D. EPA reported th a t m illions of asb esto s fibers can be released during brake and clutch servicing and th at such asbestos can linger around the garage long after brake jobs are done and can be breathed in by everyone inside the garage w hich can present a hazard for m onths or years. G rinding of u sed brake block linings h as been shown to release u p to 7 million fibers per cubic m eter and beveling new linings up to 72 million fibers an d even light grinding of th e new linings u p to 4.8 fib ers.18 It h as also been reported th at during this decomposition process the majority of fibers th a t rem ain are of sm all diam eter as well as below 5 m icron in len g th 19 a n d th u s a re less h arm fu l.20 . Any assum ption th at short fibers, less than 5 micron in length, are not hazardous cannot be justified based on the available science. Because the analytical m ethod of choice, for regulatory purposes, h as been the 18 USEPA, 1986. Guidance for Preventing Asbestos Disease Among Auto Mechanics. United States Environmental Protection Agency. EPA-560-OPTS-86-002, June. 19 Rohl, AN, Langer, AM, Wolff, MS & Weisman, I, 1976. Asbestos exposure during brake lining maintenance and repair. Environ Research, Vol. 12, p. 110; Sheehy, J. W., Cooper, T. C., O'Brien, D. M., McGlothlin, J. D., & Froehlich, P. A., 1989. Control of Asbestos Exposure During Brake Drum Service. National Institute for Occupational Safety and Health, Public Health Service, Centers for Disease Control, U. S. Department of Health and Human Services, August; & Yeung, P, Patience, K, Apthorpe, L, & Willcocks, D, 1999. An Australian study to evaluate worker exposure to chrysotile in the automotice service industry. Appl Occup Environ Hyg, Vol. 14, No. 7, July, p. 448. 20 Hatch, D, 1970. Possible alternatives to asbestos as a friction material. Ann Occup Hyg, vol. 13, p. 25. Statement of Dr. RA Lemen on NIOSH Asbestos Roadmap 11 p h a se c o n tra st m ethod [PCM] w hich c o u n ts only fibers g rea ter th a n 5 um in length, epidemiology studies therefore have been forced to com pare doses in their cohorts only to fibers g reater th an 5 pm in length and capable of being seen based on diam eter of the fiber. The later point is m ost critical since the majority of chrysotile released from brake com ponents are fibrils (0.02-0.05pm) an d thus not resolvable by light m icroscopy reg ard less of length. It m u s t be noted th a t the PCM analytical m ethod w as chosen based on its ability to count fibers only a n d n o t on a h e a lth effect b a sis.21 While PCM h a s been the international regulatory m ethod for analysis, it is n o t able to detect thin diam eter fibers [<0.2pm in diam eter]. The evidence su g g ests th a t PCM m ay underestim ate exposures and the health risks as found in the analysis of 21 "The first decision made concerned that part of the dust spectrum which should be counted and it was agreed that only fibers or fiber bundles having a minimum length of 5 microns and a maximum of 100 microns should be counted, the definition of a fiber being arbitrarily taken as a particle whose length was at least three times it diameter. This decision was taken in the light of evidence to the effect that the particle size distribution or spectrum of an asbestos dust cloud was reasonably constant over a wide range of textile processes, although later work has suggested that this might not be strictly true" This decision represent the conclusions made for use of the Thermal Precipitator Method in collecting asbestos-containing dust and when the Membrane Filter Technique came into use, the basis for the method referred to as the PCM method, it was determined that the 5 micron in length would remain the standard as `The filter on the other hand, having a pore size in the region of 0.45 micron, would appear to be quite adequate for trapping fibers in the length range 5-100 microns." While it was thought th e Membrane Filter T ech n iq u e would be more rep resen tative in assessing the "true health hazard to which an operative is subjected" it did not rely upon knowledge that fibers less than 5 micron in length had been shown harmless. Holmes S, 1965. Developments in dust sampling and counting techniques in the asbestos industry. Ann NYA Sciences: 132(1); 288-297. Statement of Dr. RA Lemen on NIOSH Asbestos Roadmap 12 brake resid u e,22 a n d b ecau se of th is, it h a s been suggested th a t tran sm issio n electron m icroscopy [TEM] sh o u ld be a n a d ju n c t to PCM. S tan to n and W rench (1972)23 a n d S ta n to n et al. (1981)24 found th a t the longer, thinner fibers were more carcinogenic, but could not identify a precise fiber length th a t did not dem onstrate biological activity. It m ust be kept in m ind th at Dr. S tanton h as never said long fibers are bad and short fibers are good. In fact, he appreciated that a large num ber of short fibers, individually of low tum orogenic probability, m ight be more h a zard o u s th a n fewer long fibers, individually of high probability.25 Studies have also found th at the m ajority of asbestos fibers in lung and msothlial tissues were shorter than 5 pm in length, thus indicating the ability of the sh o rter fibers to reach the tum or site, rem ain there, and therefore th e ir role in th e etiology of disease is im plicated.26 R esearch has found in typical occupational environm ents fibers shorter than 5 pm 22 Yeung, P, patience, K, Apthorpe, L, & Willcocks, D, 1999. An Australian study to evaluate worker exposure to chrysotile in the automotice service industry. Appl Occup Environ Hyg, Vol. 14, No. 7, July, p. 448. 23 Stanton, M.F., and Wrench, C., 1972. Mechanisms of mesothelioma induction with asbestos and fibrous glass. J. Natl. Cancer Inst., Vol. 48, p. 797. 24 Stanton, MF, Laynard, M, Tegeris, A, et al. 1981. Relation of particle dimension to carcinogenicity in amphibole asbestoses and other fibrous minerals. JNCI, Vol. 67, No. 5, November, p. 965. 25 Greenberg, M, 1984. S Fibers. Am J Indust Med, Vol. 5, p. 421-422 & Personal correspondence from Dr. Morris Greenberg, 23 May 2003. 26 S u z u k i, Y. 8s Y u en , S R ., 2 0 0 2 . A sb e sto s fib ers c o n tr ib u tin g to th e in d u c tio n o f h u m a n malignant mesothelioma. Ann NY Acad Sci, Vol. 982. pp. 160-176 8s Dodson, RF, O'Sullivan, MF, Brooks, DR 8s Bruce, JR, 2001. Asbestos content of omentum and mesentery in nonoccupationally exposed individuals. Tox Indust Health, Vol. 17, p. 138. Statement of Dr. RA Lemen on NIOSH Asbestos Roadmap 13 in length o u tn u m b e r th e longer fibers by a factor of 10 or m ore.27 S horter fibers m ust be studied in more depth and they should not be disregarded especially w hen clearan ce is reta rd ed .28 T h a t chrysotile fibers tend to spit longitudinally a s well as partially dissolve, resulting in sh o rter fibers w ithin the lung, w as rep o rted in a review of several articles.29 Davis et al., 1986, 1988 and the Berm an et al., 1995 reanalysis.of the Davis data and the McDonald et al., 1989 papers exam ine both the toxicity or lack th ereo f for sh o rt fibers.30 The Davis p a p ers show that: 1) long fibers produced 6 tim es more fibrosis and 3 tim es more tum ors than th e sh o rt fiber p re p a ra tio n s after inhalation; 2) injection "stu d ies, a t the highest dose levels 25 mg, found little difference in the n u m bers of tum ors produced by both long and short-fibre chrysotile, while a t lower levels there w as a significant difference between the long and short-fibre p re p a ra tio n s w ith the longer fibers being m ore carcinogenic; 3) the m ean 27 Dement, JM & Wallingford, KM, 1990. Comparison of phase contrast and electron microscopic methods for evaluation of occupational asbestos exposures. Applied Occ Env Hyg, Vol. 5, p. 242. 28 Oberdorster, G, 2001. Fiber characteristics, environmental and host factors as determinants of asbestos toxicity. 2001 Asbestos Health Effects Conference, May 24 25, Oakland, CA, U. S. Environmental Protection Agency. - 29 Dement, JM & Brown,'DP, 1993. Cohort mortality and case-control studies of white male chrysotile asbestos textile workers. J Occup Med Toxic, Vol. 2, No. 4, p. 355. 30 Davis JM, Addison J, Bolton RE, et al. 1986. The pathogenicity of long versus short fibre samples of amosite asbestos administered to rats by inhalation and intraperitoneal injection. Br J Exp Pathol 67: 415-430; Davis JM, Jones AD. 1988. Comparisons of the pathogenicity of long and short fibres of chrysotile asbestos in rats. Br J Exp Pathol 69: 717-737; Berman DW, Crump KS, Chatfield EJ et al. 1986. The sizes, shapes, and mineralogy o f asbestos structures that induce lung tumors or mesothelioma in AF/HAN rats following inhalation. Risk Analysis 15: 181-195; & McDonald JC, Armstrong B, Case B et al. 1989. Mesothelioma and asbestos fiber type: Evidence from lung tissue analyses. Cancer 63: 1544-1547. Statement o f Dr. RA Lemen on NIOSH Asbestos Roadmap 14 tum or induction period was longer for the short-fibre preparation in producing m esotheliom as a t both the 25m g and 2.5m g dose level and the au th o rs conclude "...would probably have been seen with the 0.25m g dose if the short-fibre chiysotile had produced any m esotheliom as at this level."; a n d 4) th e a u th o rs sta te th a t th e alteration of the short-fibre chrysotile produced by ball-milling is subject to a level of crystal dam age w hich is sufficient to m ake resu lts difficult to in terp ret in relation to hazards resulting from short fibres produced during the m anufacture of asbestos products or during the subsequent usage of these materials. B erm an et al., 1995, u sin g 'a risk analysis model of their choice choose to elim inate all fibres less th an 5 pm in length as "S tru ctu res <5 pm in length do n o t appear to m ake any contribution to lung tum or risk." Such an assum ption is unw arranted given the conclusions of the Davis et al. papers along w ith the other data, discussed in this appendix, showing toxicity for the short asbestos-fibers. McDonald et al., 1989 exam ined 78 cases of m esotheliom a from autopsy between 1980 through 1984 with m atched referents to evaluate the lung burden of long vs. short fibers, concluded th at the role of short-fibers w as nil. Looking only a t lung burden analysis for chiysotile short-fibers is not the only way nor is it the m ost appropriate analysis to determ ine the role or body burden of either chrysotile or short-fibers, as they are cleared from the lung rapidly com pared to longer non-chiysotile fibers. Statement o f Dr. RA Lemen on NIOSH Asbestos Roadmap 15 This sam e criticism is applicable to th e B utnor et al.,31 an aly sis of 10 cases of m esotheliom a among brake exposed workers where analysis was only made of lung tissue. B u tn o r et al. also d ism iss the `h it-a n d -ru n ' hypothesis for chrysotile as `flim sy' and h av in g no solid scientific su p p o rt and cite H esterberg et al., 1994, 1995, 1996 stu d ie s,32 of m an -m ad e vitreous fibers, a s their proof for this contention. While there is clear proof of the longer biopersistence for am phibole asb esto s, the lack of su ch biopersistence of o ther fibers, as show n in the H esterberg et al papers, provide support to the contrary, and are an indication th a t pathogenicity of a fiber is dependent upon more than sim ply the dose, dim ension, and the durability of the fibers found with in th e lung. It is also im p o rtan t to note th a t chrysotile asbestos produced fibrosis, lung tum ors and mesothelioma in rats after 'inhalation stu d ies as show n in the Research and C onsulting Company (RCC) stu d ies cited in th e H esterberg et al., 1995 paper. * 31 Butnor KJ, Sporn TA, Roggli VL. 2003. Exposure to brake dust and malignant mesothelioma: A study of 10 cases with mineral fiber analyses. Ann Occup Hyg 47: 325-330. 32 Hesterberg TW, Miiler WC, Mast R, McConnell EE, Bernstein DM & AndersonR. 1994. Relationship between lung biopersistence and biological effects of man-made vitreous fibers after chronic inhalation in rats. Env Health Perspect 102{S); 133137;Hesterberg TW, Mller WC, Thevenaaz P, & Anderson R. 1995. Chronci inhalation studies of man-made vitreous fibres: Characterization of fibres in the exposure aerosol and lungs. Ann Occup Hyg 39 (5): 637-653%Hesterberg TW, Mller WC, Musselman RP, Kamstrup RD, Hamilton RD &Thevenaz P. 1996. Biopersistence of man-made vitreous fibers and crocidolite asbestos in the rat lung following inhalation. Fund Appl Toxico 29: 267-279. Statement o f Dr. RA Lemen on NIOSH Asbestos Roadmap 16 Appendix - 2 Mesothelioma Surveillance Richard A. Lemen, Ph.D. Two recent papers have concluded the beginning of a decrease in m esotheliom a ra te s in the U nited S ta te s.33 T heir d a ta an aly se s bring to the fore additional questions ab o u t the reliability of surveillance d ata for m esotheliom a based solely on death certificate analysis or m ortality data w ithout pathological confirm ation of m esotheliom a. SEER d ata, for exam ple, prior to th e im plem entation of the ICD 10 codes are inaccu rate a n d u n d e re stim a te th e tru e incidence of m esotheliom a in th e U.S.34 The new IC D -10 codes for m esotheliom a are C 45.0 for p leural an d C45.1 for p eritoneal.35 Before the new ICD-10 codes w ent into effect in 1999 the reporting based on incidence d ata w as likely underreported and th u s analysis using such d ata.is likely to have underreported the incidence of mesothelioma. In some cases, SEER d ata reported only 12% of the m esotheliom a c a se s were accurately reported a n d even w ith th e new ICD 10 codes it is e stim ated th a t only ab o u t 80% will be d etected through SEER data, indicating th a t m esotheliom a reporting will still be 33 Price B & Ware A, 2004. Mesothelioma trends in the United States: An update based on surveillance, epidemiology, and end results program data for 1973 through 2003 & 34 Pinheiro GA, Antao VCS, Bang KM & Attfield MD, 2004. Malignant mesothelioma surveillance: A comparison oflCD 10 mortalaity data with SEER incidence data in nine areas of the United States. Int J Occup Environ Health: 10; 251-255. 35 World Health Organization, 1992. ICD-10 International Statistical Classification of Diseases and Related Health Problems Tenth Revision: 1; 201. ' Statement of Dr. RA Lemen on NIOSH Asbestos Roadmap 17 problem atic b u t m u c h less so th a n in th e p a s t.36 The new ICD 10 codes have only been in existence for the p a st 5 years and any trends based on this d a ta are u n w a rra n te d a t th is tim e an d it will be m any years until a more accurate picture can be seen a s to m esotheliom a tren d s within the U.S. It is im p o rtan t th a t NIOSH a d d re ss this 20% u n d erreporting gag a s suggested even w ith th e intro d u ctio n of th e new IC D -10 codes a n d w ithin the SEER reporting system. Since it has been generally reported th a t the incidence of m esotheliom a in women is m uch less associated with asbestos exposure, Steenland et al.37 suggest th a t if take-hom e a sb e s to s exposure were considered the attributable risks m ay rise to aro u n d 90%. Price and Ware (2004) unjustly suggest th a t because the female lifetime m esotheliom a risk across birth cohorts has remained constant this supports a threshold exposure for m esotheliom a, w hich is yet to be show n and no epidemiological stu d y to date h a s been able to dem onstrate such a threshold. T rends in m esotheliom a are on the rise in m any countries and a large m ulticentric study on m alignant pleural m esotheliom a and non-occupational exposures to asbestos projects th at low-doses from the home and general environm ent may carry a m easurable risk of 36 Pinheiro GA, Antao VCS, Bang KM & Attfield MD, 2004. Malignant mesothelioma su rveillance: A c o m p a r iso n of ICD 10 m o rta la ity d a ta w ith SEER in c id e n c e d a ta m nine areas of the United States. Int J Occup Environ Health: 10; 251-255. 37 Steenland K, Burnett C, Lalich N, Ward E & Hurrell J, 2003. Dying for work: The magnitude of US mortality from selected causes of death associated with occupation. 43; 461-482. " Statement of Dr. RA Lemen on NIOSH Asbestos Roadmap 18 m esotheliom a over the n ex t few d e ca d es.38 The findings of this m ulticentric stu d y have direct im plications to the risk of m esotheliom a from exposures to asbestos am ong en d -product u se r of asbestoscontaining products, e.g. brake m echanics, as their exposures have generally been of a lower m agnitude th at those encountered by the various highly exposed and predom inately studied trades including insulators, construction workers, and pipefitters. 38 Magnani C, Agudo A, Gonzalez CA et al., 2000. Multicentric study on malignant pleural mesothelioma and non-occupational exposure to asbestos. Br J Cancer: 83(1); 104-111. Statement of Dr. RA Lemen on NIOSH Asbestos Roadmap 19 Appendix - 3 Mesothelioma Background Rates Dr. Richard A. Lemen Two recent p ap ers have concluded the beginning of a decrease in m esotheliom a ra te s in the U nited S ta te s.39 T heir d a ta an aly ses bring to the fore additional q u estio n s a b o u t the reliability of cohort studies based solely on m ortality d ata, w ithout pathological confirm ation for m esotheliom a. SEER d a ta for exam ple prior to the im plem entation of the ICD 10 codes are m ost likely in accu rate a n d m o st likely u n d erestim ate the true incidence of m esotheliom a in the U.S. T rends in m esotheliom a are on the rise in m an y c o u n tries an d a large m ulticentric stfcu d y on' m alignant pleural m esotheliom a and non-occupational exposures to asbestos projects that low-doses from the home and general environment m ay carry a m ea su ra b le risk of m esotheliom a over the next few d ecades.40 The findings of th is m u lticen tric stu d y have direct implications to the risk of m esotheliom a from exposures to asbestos among brake m echanics as their exposures have generally been of a lower m agnitude th at those encountered by the various highly'exposed 39 Price B & Ware A, 2004. Mesothelioma trends in the United States: An update based on surveillance, epidemiology, and end results program data for 1973 through 2003 & 40 Magnani C, Agudo A, Gonzalez CA et al., 2000. Multicentric study on malignant pleural mesothelioma and non-occupational exposure to asbestos. Br J Cancer: 83(1); 104-111. . Statement of Dr. RA Lemen on NIOSH Asbestos Roadmap 20 and predom inately studied trades including insulators, construction workers, and pipefitters. The new ICD-10 codes for m esotheliom a are C45.0 for pleural and C45.1 for p eritoneal.41 Since it h a s been generally reported th a t the incidence of m esotheliom a in wom en is m uch less associated with asbestos exposure, S teen lan d et al.42 su g g est th a t if take-hom e a sb esto s exposure were considered the a ttrib u tab le risks may rise to around 90%. Price and W are (2004} u n ju stly su g g est th a t because the fem ale lifetime mesotheliom a risk across birth cohorts has remained constant this su p p o rts a threshold exposure for m esotheliom a, which is yet to be show n and no epidem iological stu d y to date h a s been able to dem onstrate such a threshold. Before the new ICD-10 codes went into effect in 1999 the reporting based on incidence d a ta w as likely underreported and th u s analysis using such d ata is likely to have underreported the incidence of m esotheliom a. In some cases only 12% of the m esotheliom a cases were accurately reported and even with the new ICD 10 codes it is estim ated th a t only about 80% will be detected th rough SEER d ata, indicating th at m ortality d a ta will still be 41 World Health Organization, 1992. ICD-10 International Statistical Classification of Diseases and Related Health Problems Tenth Revision; 1;'201. 42 Steenland K, Burnett C, Lalich N, Ward E & Hurrell J, 2003. Dying for work: The magnitude of US mortality from selected causes of death associated with occupation. 43; 461-482. Statement o f Dr. RA Lemen on NIOSH Asbestos Roadmap 21 problem atic b u t m u ch less so th a n in th e p a s t.43 The new ICD 10 codes have only been in existence for the p ast 5 years and any trends based on th is d a ta are u n w a rra n te d an d it will be m any years until an accu rate picture can be seen as to the real m esotheliom a trends within the U.S. 3 Pinheiro GA, Antao VCS, Bang KM & Attfield MD, 2004. Malignant mesothelioma surveillance: A comparison of ICD 10 mortalaity data with SEER incidence data in nine areas of the United States. Int J Occup Environ Health: 10; 251-255. P . L e in e w e b e r '/1-04 .- :Db1o:; F'brar^; 7 ' ' ` ` ; \ . - ` ` ''. ' `l'-jr/.J*K!\:wt';f'^r2?K>o Copies: R. Lamar 3-05 w: C. :Streib Rf<D Subjoct; PPKR BY C. .S. ;iH0MP'S.G^ '"ASB'STS IN YOUIC FUTURE" . File' Chrono 0^ * P --L eih ew b er /pa . . .:- .-.Attachment ' - V y--* v :.*/.- : v --V'.-ji^v^ w ' , " ;*; :: - -, '-iVS # s S f'Si/Johns-iVlarviSJe To- H- R.. K eefe ~ 2W 0a!e;.-Janu ary 7 , 1975 Fr0i7V R. . S.. Lamar . . >.<ir ,f .v . . *r v Copies: S e e end o f c o r r e sp o n d e n c e Subject: YQpRr&CTKf OF, JANUARY 2 , 1 9 7 5 TO ' V / T KOTlh . " TALC:AND ASBESTOS .1 .can n ot h e lp b u t. f e s l ; that-.aorae a d d i t i o n a l in p u t from R esearch is- needed h ere. Several points-: - . 1 , .The ^.N ational ...Paint., and ;C p a tin g .A ss o c ia tio n " is' sim p ly , a.'-tradfeYor.gani'aa'tio iii.-." >car.r ie -st r fo u le g a l. w e ig h t y . , We';-arei s.u d ll :.boundi-by \thWilav? a'si'a'escrib ed i n OSHA - d ocu m en ts;. . It'.perns 'ltQ-..rne t h a t 3 te n d e r / in h i s l e t t e r o f ib c to b e r 9'/.-L97-4 f; d e s t r o y s :h;is-,ov.ni'.; . ' .. . o r g a n i z a t i o n W; > confh0;io.n'^'it:h'ih.- OSHA-.-i'?. - . '. re&bXyedi':we h a v e -no- c h o ic e ; b u t t o c o m p ly w it h t h e - law a s w r itte n . ' ' ' . . . . 2 ., As I r e a d - t h e NPSCA. B u l l e t i n No. 2 0 , 'I g e t . tv.'o' strong im pressions: ' s . Rather-, th an c l a r i f y i n g t.l - - t t e r s t a t e d r-- th e y o n ly add. t o my coni- . . ' . b . .. Ash'e.stp.s;.is'vndf .'r ea lly .aj-vt-ttos, but it..can - be ' : iyotf:w^rit;-;to;':caai i t y e . g . "cornmhrdial. informa t&o "sho' . n c i s i y i y h a t i _i R.'-s#!l^ahd'rb.i.it e t ' cont a i n -no.tyohl^- . trmorite.,;'but sign/ amiopu/nt s''; f ;;c hry o t i 1 e 'yend :ant:hP^byi:i;i.t;.vas jve lv_ Wv_h..at l i g h t , -, -by f^rthHolili suli' -.ihfohjfia't io n 7 ' R e f e r .t: C R M C -EL S-004702 Memo. O ctob er . 9, . 1 9 7 4 . V-. E.- W olkodoff- t o R . - s . Report No-.. ..4 14-T -33, O ctober 4 , . 1974 ; . M em o.O ctober.-1 0 , 1 9 7 4 K. L.' J a u n a r a js. to R. S- Lamar Mi^no .O ctober 23,. 1974 V. E. W olk od off. t o R. S. Lamar Memo O cto b er .11, 1974 R* S . Lamar t o V. ' E. W olkodoff '#cfehO`t'a7p r o v id e t h i s i' F i n a l l y , t h e f^.i\.-;4fe.stiK,Vi;>mddai\a.nn a t u r e . From "in f o r m a t io n .I have -from K o tin and Fenner , th e r e i s more th a n -a m p le r e a s o n why we sh o u ld la b e l r e g a r d le s s o f . w hat-..the'-law m ig h t .s a y . 'And, t h is - c o u ld " in tim e have a g r e a t d ea i.-.to. do w ith d-M lS1leg l; a s tw e ll a s - i t s -- 'Vv;obligations. . "sense th e .......................... f o r : 'W h ave t o - l e a r n to' Live. w ith ' i t 'in 'a reg a rd less o f hw.d if f ic u lt th is appears. R. - S . .Lamar kjm attachm ent cc:.- v' KOtin - 4N H M J . S o lo n ; . - 4N . ,, M, Fenner - - 4M A. C. F r n k b in er - 5W .P, A'. 'M a r tin so n 2V{ K. K ran ich - - 2W W; C. S t r e i b F ile;- 259-611 ' ; ` f\ i . > '' i >k U L J A. - \\J Y .-Vs > (v- V,-.V ^ * m . km . :# ; `W- m ?l --*i>t : *>'i - 1-V -1 CRMC-ELS-004703 ->*?} Jw v r M '-* : T ` i Uohns-WlaiWilii \ :<r fe .j . j|- Swe risen Frrjtvi, .R-. s. Lamar Copies: .]?_ > 5 . ' Fenner, G- R. Kinzer, fi. R. Keefe, T, E. Remmers, . = i W. .C. Gtroj.b, S,. R .S p c i l . -G* coombs, D, C ' _Subject: Me eting. w i t f e - M / i i z e r '. p e r s o n n e l . a t RiD C e n t e r August' 3 1 , 1 9 7 6 . A s b e s t o s M i n e r a l s ini T a l c and T e s t Methods .We. met w i t h R o b e r t E. Norwood', R e s e a r c h Manager f o r P f i - z e r ' . s i M i n c r a l s , P i g m e n t s , arid'.Metals D i v i s i o n and w i t h H a ro ld D. Stanley', J r .;. Group Leader, T e s t in g . . - : XRD, TEM, SEM,t;. DTfeiTGAV''etc. bu t ;s<sWi^^ upon TEM and XRD; ' '' ` ' .M :0m --.- Tv., - ' R. Si, Lamar. RSL/.imb . ;[ .Vfe'fe:.:Gi'r/-.,; ' life. -&nm ... ' . (CRMC-ELS-004502 ->*?} Jw v r M '-* : T ` i Uohns-WlaiWilii \ :<r fe .j . j|- Swe risen Frrjtvi, .R-. s. Lamar Copies: .]?_ > 5 . ' Fenner, G- R. Kinzer, fi. R. Keefe, T, E. Remmers, . = i W. .C. Gtroj.b, S,. R .S p c i l . -G* coombs, D, C ' _Subject: Me eting. w i t f e - M / i i z e r '. p e r s o n n e l . a t RiD C e n t e r August' 3 1 , 1 9 7 6 . A s b e s t o s M i n e r a l s ini T a l c and T e s t Methods .We. met w i t h R o b e r t E. Norwood', R e s e a r c h Manager f o r P f i - z e r ' . s i M i n c r a l s , P i g m e n t s , arid'.Metals D i v i s i o n and w i t h H a ro ld D. Stanley', Jr. ;. Group Leader, T e s t in g . . - : XRD, TEM, SEM,t;. DTfeiTGAV''etc. bu t ;s<sWi^^ upon TEM and XRD; ' '' ` ' .M :0m --.- Tv., - ' R. Si, Lamar. RSL/.imb . ;[ .Vfe'fe:.:Gi'r/-.,; ' life. -&nm ... ' . (CRMC-ELS-004502 ' . ' '-' ' - " . ' -: - ' F., j , S o lo n , -Jr, Page 2 O c t.. 3 1 , 19.74 . ` ' ' ' ' '" ' - ' . ":-Kcu''-.H->::::*-';'s-^^'/Wy-'- - , - V-.V`. J^s V v< ?$ |- : . . L\y'sr-`J:- \r.. <.yv:>;0 a' .'-LeN-- . >;-. ' y yvfrjfeJaaSl&jislgn^ R.^Pvj.Car.tr .-' ^.^Gyrnri- ' ,': Xj /-* **., .* *** fF r.C '- f * - >. ' , - ' , . V j >,' l fe .' - ' ** :*` --'S ./- v<>j.r:J^v^2>r/ ; fcr&SBeoe ' yy.\\yy:3$?# .., ''r-v^s ' '-'T-V ` - ' *. " / y . .*r . . . ' . ,' *1 . . \; - .vy-fi-. v ; ; - 'm m \ Johns-IVlanvHle &: . F,, J . S o l o n ,. Jr-. S .ts?w; r, p , c rte r' Coptas: F i l e & C . " -- Dato; O c t. 3 1 , 1974 \.-Vrv^-*WB5.r ... r 'WWmi Syblct;- TELEPHONE' CONVERSATION WITH. BOB BACON' P f0TMPply At ak. -phe;.f o i l w ing. , c t i o n s -.in ' th e - s e q u e n c e `^l'xstd-^-'-"->-r-&::v^$s b g1<5v: . - ": ' " ; -;< :"- r^-r . - ..".* , _i ' 1 ' 1.