Document wKq9DMG2JdKxK7qBRBnMb3jxQ

FILE NAME Brakes BRK DATE 2005 DOC BRK151 DOCUMENT DESCRIPTION Letter to the Editor American Journal of Industrial Medicine RE Asbestos in Brakes Exposure and Risk of Disease With Response from Author AMERICAN JOURNAL OF INDUSTRIAL MEDICINE 276-277 2005 Letter to the Editor RE Asbestos in Brakes Exposure and Risk of Disease To the Editor We read with interest the recent article by Richard A. Lemen entitled Asbestos in brakes Exposure and risk of disease Lemen 2004 However we were disappointed that Dr. Lemen omitted a number of key references that bear on this important issue With respect to the decomposition of asbestos in brakes Dr. Lemen refers to the studies by Lynch 1968 Williams and Muhlbaier 1982 and Rohl et al 1976 but fails to reference the more recent study by Langer regarding the reduction of the biological potential of chrysotile asbestos arising from conditions of service on brake pads Langer 2003 Instrumentation required to identify and measure degree of alteration of free fiber was not used by Rohl and colleagues 1976 or by the other investigators in their respective studies Although Rohl et al 1976 detected some forsterite in brake drum dust no further analysis was attempted to determine if the individual fibers released from brake pads had suffered physical or thermal degradation The ray diffraction analyses given characterized the fiber in binder particulates unaltered as well as free fiber in a range of physical states Regarding the putative toxicity of short fibers Dr. Lemen quotes JMG Davis study on brake dust Davis and Coniam 1973 but fails to quote Dr. Davis's extensive work that failed to demonstrate the pathogenicity of fibers less than 5 ...min length Davis et al 1986 Davis and Jones 1988 Furthermore Dr. Lemen omits the study by Berman et al 1995 which reanalyzed Davis data and concluded that fibers less than 10 ...min length are not pathogenic In addition he references three studies by McDonald et al 1989 but omits the study by these authors which analyzed human lung tissue samples and concluded that fibers less than 8 ...min length did not contribute to the development of mesothelioma With respect to exposure assessment of asbestos in brakes Dr. Lemen quotes a variety of studies but fails to quote the extensive review of this subject by Paustenbach et al 2003 The evidence regarding excess mesothelioma among brake workers deserves special attention Dr. Lemen quotes a letter by Otto Wong but fails to quote the analysis by Dr. Wong that found an overall relative risk of mesothelioma among auto mechanics of 0.90 with a 95 confidence interval of 0.66-1.23 Wong 2001 Dr. Lemen also quotes the study by Roggli et al 2002 but omits the authors conclusions regarding mesothelioma and brake mechanics or their separate study of lung fiber burden analyses in brake mechanics Butnor et al 2003 Dr. Lemen also refers to the Australia Mesothelioma Surveillance Program which is not a formal epidemiologic study Unfortunately Dr. Lemen's article does not provide the reader with a balanced view of the available evidence We would urge those interested in this area not to draw con- clusions regarding exposure to brake dust and mesothelioma risk before reading these additional sources Victor L. Roggli MD Duke University Medical Center Durham North Carolina Arthur M. Langer PhD Professor and Deputy Executive Officer PhD Program in Earth and Environmental Sciences Graduate School and University Center City University of New York New York New York Correspondence to Victor L. Roggli Professor of Pathology Duke University Medical Center Durham NC mail roggl002@rogl02@mc.dukme cro.ggdl0u02k@mec..dueked.eudu Accepted 1 June 2004 DOI 10 1002 20129 Published online in Wiley InterScience www.interscience.wiley.com REFERENCES Berman DW Crump KS Chatfield EJ Davis JM Jones AD 1995. The sizes shapes and mineralogy of asbestos structures that induce lung tumors or mesothelioma in HAN rats following inhalation Risk Analysis 181 195 '2005 Wiley Inc. Letter to the Editor 277 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 325 330 Davis JMG Coniam SW 1973. Experimental studies on the effects of heated chrysotile asbestos and automobile brake lining dust injected into the body cavities of mice Exp Mol Path 339 353 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 Davis JM Addison J Bolton RE Donaldson K Jones AD Smith T. 1986. The pathogenicity of long versus short fibre samples of amosite asbestos administered to rats by inhalation and intraperitoneal injection Br J Exp Pathol 415- 430 Langer AM 2003. Reduction of the biological potential of chrysotile asbestos arising from conditions of service on brake pads Reg Toxicol Pharmacol 71-77 Lemen RA 2004. Asbestos in brakes Exposure and risk of disease Am J Ind Med 229 237 Lynch JR 1968. Brake lining decomposition products J Air Pollut Cont Assoc 824 McDonald JC Armstrong B Case B Doell D McCaughey WT McDonald AD Sebastien P. 1989. Mesothelioma and asbestos fiber type Evidence from lung tissue analyses Cancer 63 1544-1547 Paustenbach DJ Richter RO Finley BL Sheehan PJ 2003. An evaluation of the historical exposures of mechanics to asbestos in brake dust Appl Occup Environ Hyg 786-804 Roggli VL Sharma A Butnor KJ Sporn T Vollmer RT 2002. Malig- nant mesothelioma and occupational exposure to asbestos A clinico- pathological correlation of 1445 cases Ultrastruct Pathol 55 65 Rohl AN Langer AM Wolff MS Weisman I. 1976. Asbestos exposure during brake lining maintenance and repair Env Res 110-128 Williams RL Muhlbaier JL 1982. Asbestos brake emissions Env Res 70-82 Wong O. 2001. Malignant mesothelioma and asbestos exposure among auto mechanics Appraisal of scientific evidence Reg Toxicol Pharmacol 170 177 AMERICAN JOURNAL OF INDUSTRIAL MEDICINE 278-280 2005 Letter to the Editor Reply to Victor L. Roggli and Arthur M. Langer To the Editor am happy to see that my article on Asbestos and Brakes has generated interest to this often estimated risk Dr. Roggli and Dr. Langer suggest several articles were not recognized in my paper which if they had been included would allow a more complete analysis of the risks or lack thereof to workers exposed to containing brake dust Dr. Langer's paper Langer 2003 dealing with the reduction of the biological potential of chrysotile asbestos offers a position in contrast to that discussed in my paper however his analysis analysis does support the necessity for continued vigilance to protect brake repair workers especially in new brake applications Dr. Langer's analysis purports the elimination of the biological potential of chrysotile because of its transformation into the supposed innocuous degradation product of chrysotile fosterite a substance my paper points out lacks suitable analysis to determine its term effects and while some chrysotile does convert to fosterite the evidence other than Dr. Langer's paper has not been consistent Dr. Langer contends that hrysotile biological activity is thereby greatly reduced and can become virtually nil hundreds of degrees below the olivine transformation temperature This is not supported by the data presented in my paper nor by a follow paper by Rohl et al 1977 which is in fact a follow of the Rohl et al 1976 analysis which Dr. Langer contends was never done that concludes by using the transmission electron microscopy TEM that ost of the chrysotile retained is characteristic morphology without significant alteration and selected area electron diffraction patterns obtained on representative fibers demonstrated the preservation of crystal structure as well Dr Lemen is retired Surgeon General USPHS and retired Deputy Director and Acting Director NIOSH and has testified as a plaintiff's expert in brake exposure cases Correspondence to Richard A Lemen 241 Rose Ridge Court Canton GA 30115 mail richard@richard@alemn.orrg raiclhearmd@eranle.meon.rorgg Accepted 1 June 2004 DOI 10 1002 20130. Published online in Wiley InterScience www.interscience.wiley.com ww.interscience.wiley.com Dr. Roggli and Dr. Langer suggests my paper lacks objectivity in that it does not review the Davis et al 1986 Davis and Jones 1988 or Berman et al 1986 reanalysis of the Davis data nor the McDonald et al 1989 papers concerning the lack of toxicity for short fibers First the Davis papers do not conclude a lack of toxicity for fibers shorter than 5 ...min length What the Davis papers do show is that 1 long fibers produced six times more fibrosis and three times more tumors than the short preparations after inhalation 2 injection studies at the highest dose levels 25 mg found little difference in the number of tumors produced by both long- and short chrysotile while at lower levels there was a significant difference between the long and short preparations with the longer fibers being more carcinogenic 3 the mean tumor induction period was longer for the short preparation in producing meso- theliomas at both the 25 mg and 2.5 mg dose level and the authors conclude would probably have been seen with the 0.25 mg dose if the short chrysotile had produced any mesotheliomas at this level and 4 the authors state that the alteration of the short chrysotile produced by milling is subject to a level of crystal damage which is sufficient to make results difficult to interpret in relation to hazards resulting from short fibers produced during the manufacture of asbestos products or during the subsequent usage of these materials Berman et al 1986 using a risk analysis model of their choice simply choose to eliminate all fibers less than 5 ...min length as Structures < ...min length do not appear to make any contribution to lung tumor risk Their support for this assumption is unwarranted given the conclusions of the Davis et al papers and the scientific evidence to date McDonald et al 1989 examined 78 cases of meso- thelioma from autopsy between 1980 through 1984 with matched referents to evaluate the lung burden of long versus short fibers concluding that the role of fibers was nil As I stated in my paper looking only at lung burden analysis for chrysotile fibers may not be the most appropriate analysis to determine the role of either chrysotile or fibers as they are cleared from the lung rapidly '2005 Wiley Inc. Letter to the Editor 279 compared to longer chrysotile fibers This same criticism is applicable to the Butnor et al 2003 analysis of ten cases of mesothelioma among brake exposed workers where analysis was only of lung tissue Butnor et al 2003 dismiss the and hypothesis for chrysotile as flimsy and having no solid scientific support and cite Hesterberg et al 1994 1995 1996 studies of manmade vitreous fibers as their proof for this contention While there is clear proof of the biopersistence for amphibole asbestos the lack of such biopersistence of other fibers as shown in the Hesterberg et al papers provide support to the contrary that pathogenicity of a fiber is dependent upon more than simply the dose dimension and the durability of the fibers found in the lung Hesterberg et al 1995 It is also of interest that chrysotile asbestos produced fibrosis lung tumors and mesothelioma in rats after inhalation studies as shown in the Research and Consulting Company RCC studies cited in the Hesterberg et al 1995 paper Finally to rely upon the Wong 2001 analysis or the recompilation by Paustenbach et al 2003 for support of the proposition that brake dust exposures pose no mesothelioma risk is weak at the very best Wong 2001 uses a technique analysis to pool data from available epidemiology studies and concludes a lack of causal association between exposure to brakes and mesothelioma First metaanalyses of observational studies present inherent biases such as selection bias and confounding biases as discussed in my paper Secondly analysis is a technique which was first envisioned for evaluating clinical studies where combining results based on individual participation data would be less likely to suffer from such biases and its further application to the analysis of observational studies becomes problematic If the data relied upon for analysis have flaws then the outcome of the analysis will also suffer from the impact of such flaws as will their conclusions As Dr. Wong states in his paper which he attributes to IARC In addition all studies that are judged to be methodologically sound should be consistent with a relative risk of unity for any observed level of exposure to the agent and when considered together should provide a pooled estimate of relative risk which is at or near unity and has a narrow confidence interval due to population size The observational studies selected for analysis by Wong 2001 do not meet this standard and thus are inappropriate for use in pooling their data because of their heterogeneity in several areas including their cohort selection criteria their exposure categories and their varying risks of exposure to asbestos Until such time as methods of controlling heterogencity are developed like those employed in clinical trials analysis of observational epidemiology studies will remain problematic and their conclusions remain unclear as are those purported by Dr. Wong Therefore systematic reviews as done in my paper remain a far superior method to the meaning of observational epidemiology studies where heterogencity issues remain Paustenbach et al 2003 report exposures to asbestos from some 200 historical samples taken of brake dusts which generally show low exposures but do report the occurrence of findings above the current PEL Their findings are of very limited use as they represent only a small fraction of the brake dust exposures encountered That is to say 200 samples among the estimated 5 million repair workers exposed to asbestos in the United States is far less than a representative sample of the spectrum of potential exposures encountered by American workers to containing brake dust What the Paustenbach et al 2003 data show is that asbestos can and is released from brakes and as a result repair workers can be exposed to asbestos Any comparison of this data set to the total universe of exposures to repair workers is a phantom stretch of the imagination In conclusion Dr. Roggli and Dr. Langer have presented no evidence that negated the findings or conclusions of my paper and I thank them for their comments which have helped to strengthen and further affirm my conclusions Finally my paper draws the conclusion that as long as brakes contain asbestos there remains the real threat that workers will be exposed to releases of asbestos which have the potential to cause worker diseases related to exposure from containing brake dusts Richard A. Lemen PhD MSPH REFERENCES Berman DW Crump KS Chatfield EJ Davis JM Jones AD 1986. The sizes shapes and mineralogy of asbestos structures that induce lung tumors or mesothelioma in HAN rats following inhalation Risk Anal 181-195 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 325 330 Davis JM Jones AD 1988. Comparisons of the pathogenicity of long and short fibres of chrysotile asbestos in rats Br J Exp Pathol 717- 737 Davis JM Addison J Bolton RE Donaldson K Jones AD Smith T. 1986. The pathogenicity of long versus short fibre samples of amosite asbestos administered to rats by inhalation and intraperitoneal injection Br J Exp Pathol 415 430 Hesterberg TW Miiler WC Mast R McConnell EE Bernstein DM Anderson R. 1994. Relationship between lung biopersistence and biological effects of made vitreous fibers after chronic inhalation in rats Env Health Perspect 133 137 Hesterberg TW Miiller WC Thevenaaz P Anderson R. 1995. Chronic inhalation studies of made vitreous fibres Characterization of fibres in the exposure aerosol and lungs Ann Occup Hyg 637- 653 Hesterberg TW Miiller WC Musselman RP Kamstrup RD Hamilton RD Thevenaz P. 1996. Biopersistence of made vitreous fibers and crocidolite asbestos in the rat lung following inhalation Fund Appl Tox 267 279