Document 9JRq1Meq4QVRaD62aYn5n8OBR

PLAINTIFF'S EXHIBIT f South Miami \ HealthSystem IA FENCOlO, M.O., F.fLC.P.(C), FCCP Chief, Division of Pulmonary medicine South Miami Hosphtm. 200 $wrihwt 7it4 S*st( Miami, Florida JJ141 Tataphona: (SOS) 66243117 FscslmSs: (305) 6624314 24 hr amerjaney; (305) 551-4611 Mr. Olllo Harton, Hawkint & Parnell 4000 Suntrust Plaza 303 Peachtree Street, N.E. Atlanta, GA 30308-3243 Re: Asbeatoa containing electrical wire Oat*: 09/30/81 Dear Mr. Harton. I have reviewed a series of Industrie! hygiene studies regarding asbestos containing electrical wire. From my perspective as an occupational pulmonary medicine specialist, i am pleased to submit the following opinions. 1, Maxim Engineer*! 1990 On 12/03/00 Maxim Engineers, Inc. a Oallat, Texas engineering consultation firm, released a report titled Industrial Hygiene Exposure Dot* Simulation Study, An Evaluation of Airborne Asbtstoa Concentrations Associated With Asbestos* Containing Electrical Wire Stripping Operations, Project No. D963. The Maxim Engineers report was prepared under the supervision of Kyle Dotson, a certified industrial hygienist, for Ericcson, Inc The stated puposa of the study "was to evaluate the airborne concentration of asbestos fiber* to which n electrician employee might bo oxposod while stripping asbestos containing insulation off of electrical wire." The test chamber that was constructed for this study and the expenmenta! technique were described in detail in in# body of the report. The Maxim Engineers report provided three important findings: 1. The observed 8 hour time weighted average (TV/A) worker exposure, based on breathing zone sampling, was 0.012 fiber/cc by phase contrast microscopy (PCM NtOSH 7400 method). 2. The general workroom (lest chamber 10 x 10 x 8 feet) airborne asbesj fiber concentration was 0.008 fiber/cc. I.A. Felngold, M.D., F.R.C.P.(C), FCCP Narrative Report Re: Asbestos containing alactrlcil wire To: Mr. Olle Harton, Hawkins and Pamell Date: 0940-9* Page:2 3. The "area percent" of 4 different wire* tested ranged from 25-40% chrysolite asbestos. There was no detection of woddolite or amosite. The Maxim Engineering study concluded : The sample results Indicate that airborne concentrations of asbestos fibers in the electricians' breathing zone ware well below workplace employee exposure standards established fa asbestos by the Occupational Safety and Health Administration (OSHA) and the American Conference of Governmental Industrial Hygienists (ACGIH). Additionally, the sample results of the general workroom air indicate airborne concentrations of esbestoe fibers were tees than the current post-abatement final clearance "clean air standard established for public and private schools by the Environmental Protection Agency (EPA). ~ 2. Penn Environmental Health Company, 1991 On 03/04/91 the Peat Environmental Health company of Pittsburgh released a report titled The Measurement of Aibeitoa Fibers Released From Electric Wires Coated With Asbestos-Containing Insulation. This report was conducted for Mr. Theodore Goldberg of the legal firm Goldberg, Henderson & Goldberg of Pittsburgh. The staled purpose of the study was "to determine whether asbestos fibers are released upon working with tha wire*." Four samples of coated electric wire were studied. A somewhat different experimental approach was used, In comparison to tha testing method of Maxim Engineers. Fa the Penn Environmental study, wire stripping was performed Inside a lest chamber 30" x 1(T x 15". Samples of the wire were subjected to bending, twisting, cutting and stripping. The Penn Environmental Health report provided two important findings: 1. Tha airborne asbestos fiber concentration was On two tests) 0.002$ fiber/ce and 0.0073 fiber/oc. An 8 fwur TWA wee not calculated. 2. Chrysolite was the only fiber type detected. I.A. Felngold, M.D., F.R.C.P.(C), FCCP Nsrrstlve Report R: Asbestos containing electrical wire To: Mr. Olio Harton, Hawkins and Pemell Dele; 09-30-90 Page: 3 3, Vittorio K. Argento, Ph.D., Environmental Engineering Service*, Inc., 1992 On 01*10-92 Vittorio K. Argento, Ph.D., P.E. (Environmental Engineering Servleee, Inc.) of Duncanville, Texas released a report titled Asbestos Fiber Release Study Nevy Cable at the request of Erlccson Radio Systems, Inc. The slated purpose of the report >31 to evaluate the airborne concentration of asbestos fibers that would exist in the breathing zone of an electrician employee due to cutting, stripping and manipulating asbestos Insulated Navy csbls." Dr. Argento presented a detailed description of "two inch diameter navy cable" and two different kinds of "one inch diameter navy cable * These wires contained 20% chrysolite asbestos In a waxy matrix. The study technique was very similtr to the Maxim Engineers study described above and was conducted inside a 10 x 10 x 8 ft test chamber. This report by Dr. Argento revealed: 1. The observed worker exposure, based on breathing zone sampling, was 0 034 structures (transmission electron microscopy) /ee equal to or greater than 5 micron fn Tength forThe one inch wire. ' ............ .. 2. Ths obisrvsd worktr exposure, based on breathing zone sampling, was 0.01 structures (transmission electron microscopy) /cc equal to or greater than 5 micron In length for ths two inch wire. 3. The percent (Tweight) of the different wires tested was 20% chrysotile asbestos. Thar* was no detection of crocldoiite or amesite. Ths chrysolite asbestos was Impregnated in a waxy resin. The above described study prepared by Vittorio K. Argento, Ph.D concluded: The results of the airborne asbestos fiber counting, using the most current analytical techniques and sampling methodology, show that airborne concentrations of asbestos fibers In the electrician's breathing zone were well below the allowable worker exposure standards established for asbestos by the Occupational Safety and Health Administration (OSHA). The airboma fiber concentrations were even further below Ihe maximum worker exposure levels recommended by the American Conference of Governmental Industrial Hygienists (ACGtH). -- 4? I.A. Felngold, M.D., F.R.C.P.(C), FCCP Narrative Report Re: Aabestoa containing electrical wire To: Mr. Olle Harton, Hawkins and Parnell Date: Q9-30-99 Pigt; 4 4. MVA, Inc., 1992 On 12/06/92 MVA, Inc. of Norcross, Georgia released a report titled Report of RtjulU: MVA0410, Studies to Determine Asbestos Fiber Release During Cutting and Stripping of Wire Cablet at the request of Richard F. Scruggs, PA of Pascagoula, Mississippi. The stated purpose of the study was to "determine under controlled conditions, the levels of esbostos, if any, which might be released Into the air when asbestos-containing wire cable is cut and stripped and what might be re-tuspended into the air when sweeping the dust released during the cuttings." Testing methods similar to the techniques described In the above studies were utilized within test chambers 4 x 8 x 5 ft. Four different wire cables produced by General Cable, Phelps Dodge, U.$. Steel Corporation and General Ceble Corporation were studied. Again, similar to the methods of the previously described studies, the test electricians were fitted with double personal air sampling devices. Area air samples were also taken after "aggressive disturbance" by area sweeping. The MVA report did not give time weighted averages. A range of PCM and TEM results was Qiven but the report noted that "The limits of detection vary with the volume of air collected. The detection limits ror the cutting and stripping experiments were less than 0.1 f/cc." The MVA report found that: 1. "PCM values cf airborne fibers greater than 0 pm were not significantly over the detection limits Airing cutting and stripping of wire cables." 2. The levels detected (by PCM) during sweeping were limited by small collected volumes. In an experiments in which 25 liters were collected the observed level was <.1 t/cc and In an experiment In which 30 liters were collected the leva! was <.08 f/cc. 3. Chrysotila was the only fiber type detected. The MVA study concluded: PCM values cfaibocne fibers greater than 5 pm were not significantly over the detection limits during cutting end stripping of wire cable*. Similar 'i I.A. Felngold, M.D., F.R.C.P.(C), FCCP Nsrratlve Riport Page:6 R: Asbestos containing electrical wire To: Mr. Olle Barton, Hawkins and Parnell Dete: 09-30-9# results were found for asbestos liber* >5 pm In the TEM analyses, however, concentrations of asbestos fibers of all sizes in the air were Increased over background air levels during the cutting and stripping of the wire cables containing asbestos. S. M. Douglas Mueller, 6CM, 1999 On 02/05/93 a report was submitted by M. Douglas Mueller, a certified Industrial hygienist and EPA certified building inspector to Gallagher & Kennedy, PA of Phoenix, Arizona. The report was titled Test Chamber Studies on Shipboard Electrical Cable Handling Operations, 8CM Project No. 064554*0101. The stated purpose of the study was "to ascertain if airborne fibers or asbestos structures were being gonorotod during normal marine electrician tasks that would be adverse to the health of the marine electricians i performing those activities," Five different shipboard electrical cables were studied. The cables had been in service on U.S. naval ships for many years. It was possible to determine that these cables had been manufactured by Anaconda Wire and Cable Company. Phelps Dodge Copper Products Corporation, Colly#r Insulated Wire Company, General Cable Corporation and General Electric Company. The studies were conducted Inside test chambers 10 x 10 x 10 IUn dimension. A marine electrician performed the study tasks including cutting, stripping, manipulating and dooming. As in the previously described studies, breathing zone air samples were obtained during wire manipulation end stripping work performed by the test electrician, in addition, work area samples were also obtained. The results are given In table 3 of this study. The results were not averaged snd no attempt was made to give a TWA Resuite werrstated for both PCM and TEM. The study revealed: 1. The observed worker exposure, based on breathing zone sampling, ranged from <0.01 I7ce or structures (transmission electron microscopy) /cclo 0.045 f/cc or structures (transmission electron microscopy) foe with most of the values in the undetectable or vary low range. 2. The observed work tree exposure was very lew, ranging from <0.003 to 0.02 with most of the values in the undetectable or extremely tow range. ) LA. Felngold, M.D., F.RX.P.(C). FCCP Nsrretlve Report Re: Asbestos containing electrical wire To: Mr. Olio Harton, Hawkins and Parnell Date: 09-30-99 Page: e 3. By TEM, all identified structures were chrysotile. The Mueller study concluded At no time did the airborne fiber or airborne asbestos structure levels approach or exceed the prescribed OSHA Action level (Al) of 0.1 f/cc or the Permissible Exposure Level (PEL) of 0.2 f/oc. Thus, it can be concluded that, based on the studies conducted to date and assuming the cables tested to be representative of shipboard electrical cables that (here would be no exceedances of tha OSHA AL or PEL during normal marine electrician tasks associated with shipboard electrical cable. 0. Clayton Environmental Consultants, Inc., 1994 On 01/31/94 a report was submitted by Clayton Environmental Consultants, Inc. of Edison, New Jersey to the legal firm of Lowenstein, Sandler, Kohl, Fisher & Boylsa The report was titled Industrial Hygiene Assessment Limited to the Evaluation of Asbestos Fibers Released During Wire Stripping of Rockbestos Cable. The Clayton report duplicated "the workplace exposure of the licensed electrician to airborne fibers, including asbestos" by stripping end cutting 3 different kinds of wire over 2-hour periods within tsst chambers. Clayton analyzed the cables for their content tnd collected personal sir samples from the electrician cutting the cade. Personal and area sample analysis was performed using PCM and TEM. Bulk wire analysis was performed using polarized light microscopy (PLM). Consistent with the above described earlier studies, the Clayton study found: 1. Personal and area air samples analyzed by PCM were et or below 0.01 tfee. 2. Persona! and area air samples analyzed by TEM were at or below 0.069 structures/cc. 3. The insulation (not Including embedded wire) of two of the kinds of wire I.A. Felngold, M.D., F.R.C.P.(C), FCCP Narrative Report Re: Asbestos containing electrical wlrt To; Mr. Olio Barton, Hawkins and Parnell Date: 09*40-86 i Page; 7 contained 20% chrysolite esbestoa end the third wire contained 50% chrysotila asbestos. There was no amosfte or crocidolite detected. The Clayton report concluded The results of the testing show that the electrician's exposure to airborne asbestos fiber concentrations was wall below the current OSKA standards." Summary of engineering reports Six separate studies of asbestos containing electrical wire were conducted by industrial hygiene and engineering consultants between 1990 and 1994. The methodology of each } of the six studies was presented in detail and was very similar. Within specially constructed test chambers, experienced electricians perfumed tasks identical to the kind of work done in the past in the construction of ships and buildings. Wre stripping and similar activities were conducted continuously during sampling periods, producing "worst case scenario" measurement, rather than an 8 hour TWA Phase contrast microscopy and transmission electron microscopy wars used to analyze personal air zont, work ares and bulk wirs samples. Although conducted by different consultants, with analysis performed In different laboratories in different cities end using wire produced by different manufacturers, the results of these studies were remarkably consistent activities such as tripping, bending, breaking and cutting asbestos insulated electrical wire produce* minimal airborne asbestos dust with worst case (not TWA) exposures an order of magnitude teas than the 1986 OSHA' peak exposure limit (PEL) of 0.2 (fee. The results were also lower than the more recent 1994 OSHAa PEL of 0.1 f/oc. All of th# asbestos insulated wire was found to contain chrysolite with no detection of any amphibote fibers. . In summa7, working with asbestos insufatad electrical wire results in very low dose chrysotile exposure, m the rest ct true report t consider the implications of such exposure. Low dote asbestos exposure and the rtak of aebeatoale in general, the risk of pneumoconiosis increases with increasing intensity end duretion of ) exposure to dust Tote! or cumuletive exposure is the product of exposure multiplied by vc t I' t l! r i r r v i1 I c L t' )e T I.A. Felngold, M.O., F.R.C.P.(C), FCCP Narrative Report Re: Asbestos containing eteclrleel wire To; Mr, OHe Harton, Hawkins and Parnell Data; 0140-M Page: 6 duration of exposure and Is typically represented in 'fiber/ml-years*. For example, a man who has worked In an environment where the average duet count was 2 fibere/ml lor 10 years has a total exposure * 2 x 10 or 20 flber/ml-years. Most individuals with some asbestos exposure do not develop asbestosis.1 Residents of chrysotile asbestos mining towns had an increased lung burden of asbestos fibers but no increased incidence of asbestosis.4 In the peel, asbestos insulators and ether workers with hands-on asbestos exposure were heavily exposed, often to levels In excess of 10 f/mi. Asbestosis was common In such workers; nevertheless, only a few studies attempted to establish a dose-relationship in asbestos workers because of the difficulty encountered in retrospectively eetablithing reliable airborne occupational asbestos levels. In 1975 Weill ef at* reported on a large scale study of 859 workers employed In two New Orte8n$ asbestos cement factories. Weill suggested that diffusa asbestosis would not likely occur in workers who had a cumulative work exposure of lest than 200 f/mf-yeere. In 1979 Berry et el* reported on a study of 197 asbestos workers employed after 1950 for an average of 16 years. Berry estimated that the average annual exposure was 5 f/ml-yr and the cumulative exposure was 94 f/ml-yrs. The overall prevalence of `possible asbestosis* (as determined by two physicians) was 6.6H but the prevalence of the dlsoese fell to zero below a cumulative lifetime work exposure of 10 f/ml-yrs. tn 1962 Ftnkelstein7 reported on his study of 201 workers at an amosite asbestos-cement factory who were first exposed to asbestos dust prior to 1980 and who had been employed for at least 15 years. Using 'limited* air sampling deta, Flnkelstein calculated an 18 year fiber exposure and the cumulative probability of being certified by the Ontario Workers1 Compensation Board as having asbestosis. hinkeistein reported that among heavily exposed workers with an astimatad cumulative occupational exposure of 200-249 f/ml* years the probability of asbestosis was 90H, in contrast to workers with a 50 f/ml-yr history for whom the probability was 10H end workers with e tow exposure of 10 f/ml-yrs who had an asbestosis probability of 1% of isss. in 1983 the British Occupational Hygiene Society1 (BOHS) updatsd Berry's 1979 report I.A. Fetngold, M.D., F.R.C.P.(C), FCCP Narrative Report Rr, Asbe etoe containing electrical wire To; Mr. ONe Harlon, Hawkins and Parnell Date: OS-50-96 Page: 9 with a study on 295 men who ware employed after 1950 and who had a total of at (east 10 years of asbestos exposure by 1976. The BOHS committee established 7 abnormal radiological end clinical alter!* for the diagnosis of asbestos!* and reported that tho probability of at least one of these criteria occurring was 7% In workers who hed a cumulative asbestos exposure of 50 f/ml-yr end was !es than 2*A In workers who had a lifetime exposure of only 25 f/ml-yre. In 1984 the Ontario Royal Commission on Mattert of Health and Safety Arising from the Use of Asbestos in Ontario* (Canada) summarized the evidence pertaining to a dose* response relationship for the development or asbestosia by stating: ... our assessment of the evidence finds us in agreement with Dr. Finketetefn's comment [in testimony to the Royal Commission on 07/28/91) that there is probably an effective threshold below which clinical ssbestosis may be unlikely to occur,, although there -may be"occasional cases developing in very susceptible individuals. At tow levels of occupational exposure to asbestos the fibrotic*pfOcess in the lungs, H indeed it can be initialed, will not llkaty progress to the point of clinical manifestation or even the mildest discomfort On the basis of the available date, our beat judgement as to the lifetime occupational exposura to asbestos at which the fibrotic process cannot advance is in the range of 25 f/cc-yrs and below. In 1985 Doll and Peto'* accepted the same cumulative dose threshold In an Important report prepared for the British government. Further support of the often-quoted Ontario Royal Commission report was published in 1990 by Huang11 who studied tha dose-response relationship for osbosto* exposure in a chrysotile product factory for which exposure data had bean available for many years, in that report, the threshold for 1% prevalence of ssbestosis at the factory was 22 fiber/mi yeert. In 1991 Browne1* theorised that fibrogenesis only predominates when the fiber burden is "excessive." A threshold effect was thorefore "implied." The effects of macrophage mediators on the surrounding tissues depend on the quantity released. Macrophages are modulating agents capable of I.A. Fungoid, M.D., F.R.C.P,{C), FCCP Narrative Report Re: Asbestos containing electrical wire To: Mr. Olle Harton, Hawkins and Parnell Date; 9-30S9 Pags: 10 producing fibrinolysis and fibrogenesis, and fibrogenetia will only predominate when the fiber burden 1$ excessive. A threshold effect is there* (ore implied in this fibrinolysis-fibrocenesis balance... Quinlan19 also demonstrated dose-related cellular responses. Fibrogenic reactions were observed only for high concentrations of asbestos: Differential ceil counts revested a dose-related infiltration of neutrophils that preceded elevations in gene expression. Noutrophil infiltration into lung end focal lesions of fibrosis as well as increased levels of hydroxyprollne were observed only at high concentrations of asbestos. These results indicate that high airborne concentrations of asbestos eause molecular chanpet in lung that may be related to antioxidant defense and the triggering of cell proliferation, t feature of esbestosis and lung cancer. Aebeatosla at a biological threshold for an Increased risk of lung cancer in 1947 the British Annual Report fif Jbfi Chief Inspector of Factories noted that 'Thirty one cases of carcinoma of lungs and pisura ware found at autopsy of 235 cases of Asbestosis.14 Commenting on this report, a 1949 editorial in the Journal of the American Medical Association11 observed that *... the available evidence shows that the occurrence of cancer of the lung is related to pulmonary asbestosis and is not moraly a posslbla sequela of exposure to asbestos dust In 1855 Dot!19 reported that of 113 men who worked for at least 20 years with asbestos, 11 developed King cancer compared to an expected Incidence of 0.8. Doll observed: All the cases of lung cancer were confirmed histologically and alt were associated with the presence of asbestosis. The landmark 1979 study by Hammond, Selikoff and Setdmen17 attempted to define the relative risks of lung cancer in a group of 17,800 asbestos insulators. Hammond et al I.A. Fungoid, M.D., F.R.C.P.(C), FCCP NanratlYt Report Re: Asbestoa containing electrics! wire To: Mr. Oils Harton, Hawkln* and Parnell Det#: 01-30-90 Pig#: 11 quoted a lung cancer inddenca of 11.3/100,000/year for non-smokers and 122.6/100,000/year tor smokers who had not worked with asbestos. Of the 17,800 insulators studied. 891 claimed to have been nonsmokers and 4 died of lung cancer, resulting In a corrected Incidence of 58.4/100,000/year. The rest of the group studied by Hammond et el were considered cigarcito smokers and they were found to,have an Incidence of lung cancer of $01.6/100,000/year. Unfortunately, the 1979 Hammond report did not identify the sub-cohort that had asbestosls. Subsequent analysis of lung cancer cases derived from the original 17,800 cases published by Kipen et al (including Selikoff)1* revealed that ait of the patients who died of lung cancer also had pathological evidence of asbestos!*. In 1980 Liddell and McDonald19 reported a study of Quebec chrysolite asbestos miners. Liddell and McDonald Identified 118 lung cancer deaths which represented an excess of 52 deaths over predicted. Of 49 men whose last chest x-ray was rated as normal by the ILO system, the SMR for lung cancer was not elevated at 1.08; however, of the remaining miners whose x-rays were abnormal (and who presumably had asbestosls) the SMR for lung cancer was 3.5. Liddell and McDonald commented: . . . most, but not necessarily all, cases of lung cancer attributable to chrysotlle exposure in mining and milling probably have small parenchymal opacities before death. In 1981 Berry39 reported on a study of asbestos workers who were certified by British Pneumoconiosis Medical Panels as haying asbestosls. Derry observed that the standardized mortality ratio (SMR} for lung cancer Increased from 9.1 for men classified as 10% disabled to 25 for men with 50% disability. These finding# suggest an increasing nsklof lung cancer with increasing degrees of asbestosls. tn 1989 Sluls-Cremer and Bezuldenhout31 reported an autopsy study of 399 former amphibole asbestos miners in South Africa. Thirty-five cases of lung cancer were Identified on autopsy. Of the 399 patients, 302 were found to hay* no pathological evidence of asbestosis, 69 had "slight" asbestosls and 28 had moderate to severe asbestosls. tn the group of 302 without asbestosls. the authors calculated that 12.4 lung cancers were expected (based on smoking habits) but only 11 were observed for an SMR of 887. Of the 69 patients with slight asbestosis. 3.6 lung cancers were expected but 15 i.A. Fetngold, M.D., F.R.C.P.(C), FCCP Narrative Report Rt: Asbestos containing eteetrfcal wtre To: Mr, Oil* K&rton, Hawkins snd Parnell Date: Ot*3O-90 Pag*: 12 were observed resulting In en SMR of 4.16. Among the 28 patient! who were demonstrated to nave moderate or severe asbestos!* on autopsy, 1.6 lung cancers were expected but 8 were observed for an SMR of 5.63. The authors concluded: The SPMR for both the 35 cases proved by necropsy and the 25 cases' certified as bronchial cancer on the death certificate show no excess bronchial cancer in the group without esbestosls whereas there it an excess In those with asbestos!*. The excess increases with the aevority of the esbestosls found at necropsy. In conclusion this study suggests that asbestos caused bronchia! cancer it almost always associated with some degree of histologically demonstrable asbestosis. Sluis-Cremer and Bezuidenhout also observed that tn the absence of esbestosls at necropsy a bronohlsl cancer In man exposed to asbestos It unlikely to be due to asbestos. In 1991 Hughes and Weill*1 described o study of all 839 workers employed In two New Orleans asbestos cement factories in 1969. By 1983 154 of the 839 men had died and death certificates of 153 of these men were available. X-rays on alt of the men were interpreted by three prominent radiologists using the ILO system. The authors observed: Among workers with no x-ray film abnormalities in 1969, the lung cancer risk was not raised (five mesotheliomas, however, wen found). For the long term workers In this group, there were six lung cancers compared with 5.8 expected. By contrast among those with small opacities, profusion % 1/0, there were around seven excess malignancies, ell of them due to lung cancer; lha lung coneor risk was tignifJeanUy raised (0v 2.1; p0.001) and significantly different from the risk In long term workers without abnormalities (p0.0l, likelihood ratio test). I.A. Felngold, M.D., F.R.C.P.(C), FCCP - Narrative Report Ra: Asbestos containing atectrlcal wire To; Mr. Olio Harton, HawkJns and Pamall Dat#; 09-30*98 Page: 13 HuQhes and Weill commented that: The current stud/ is the latest in an emerging body of evidence supporting the view (hat asbestos is a lung carcinogen because of Its ability to causa lung fibrosis..,. Because detectable asbestosis is not likely to result from current occupational and general environmental exposures, the prevention of the effect of exposure on lung fibrosis is likely also to prevent the excess risk of lung cancer-- Finally, these data may provide further evidence to support the common practice of attributing lung cancer to exposure to asbestos only if asbestosis Is also present; otherwise, these tumors are, in most part, due (o cigarette smoking. Almost all cases of lung cancer, including those wnich occur in asbestos workers, are related to cigarette smoking. Of tha 35 lung cancer cases described in 1989 by SluisCremer and Bexuidenhout, 33 were current or ex-smokers. Of the 29 cases of lung cancer described in 1991 by Hughes and Wa.1, all were smokers. A1991 study published by tha Edinburgh Lung Career Group0 reviewed 3,070 patients who developed lung cancer from 1981-1985 drawn from a population canter of 950,000. Of tha 3,070 lung cancer patients, only 74 (2%) were lifelong non-smokers. Slopping smoking at any ag# significantly reduces the subsequent risk of lung cancer, but does not reduce that risk to tha level experienced by never-amokera.*4 The persisting risk Is most likely significantly greater for former heavy smokers than for former moderate or light smokers. To summarize the above: Asbestos workers who smoke cigarettes and have asbestosis are st significantly greator risk of developing lung cancer than other SmOKeD Who do not have asbestosis. in contrast, asbestos workers who do not have asbestosis experience Hie seme risk of lung cancer at non-asbestos workers who smoke (or smokad) tha same amount In 1991 editorial in tha British Journal of Industrial Medicine, Kevin Browne* presents the possible explanations for the difference in lung cancer risk experienced by workers who have or do not have asbestosis. Browne reviewed the Calmi hypothesis of mutagenesis, originally presented in the Journal Nature in 1975* and tha evidence that asbestos, I.A. Felngold, M.O., F.R.C.P.(C), FCCP Narrative Report Re: Asbestos containing electrical wire To: Mr. Cite Harton, Hawklna and Parnell Date: 0t40`99 PflQ*: 14 .., is not e mutagen, and attempts to establish a mechanism whereby it can directly produce malignant transiormation in bronchial epithelium or meaothetium have either failed completely or have required unrealistic In vitro conditions. Browne observed that A consensus exists that asbestosis (diffuse interstitial pulmonary fibrosis. DiPF) results from the effect of mediators released by lung macrophagee after incomplete phagocytosis.... The effects of macrophego modtotora on the surrounding tissues depends on the quantity released. Macrophagee are modulating agents capable of producing fibrinolysis end fibrogenesis, and fibrogenesis wilt only predominate when the fiber burden is excessive. Powerful evidence that no additional carcinogenic action specific to asbestos is needed comes from studies of DIPF from other causes, in cryptogenic fibrosing alveolitis the histological picture may be indistinguishable from asbestosis apart from the absence of excess asbestos bodiis or fibers, end patients suffering from this disease, or from DIPF secondary to other systemic diseases, show greatly increased incidence of lung cancer... .... if the carcinogens In cigarette smoke have caused DNA damage to large numbers of lung epithelial calls, chronic proliferation of some of these cells will more readily result in the expression of malignancy than from both mechanisms independently. Asbestos is then acting as a classical promoter on Initiated calls.... in summary, asbestos workers who smoke and who develop asbestosis are at Increased risk for the development of lung cancer because: (a) cigarette smoke is primary carcinogen or Induced which stimulatee mutations (l.e. malignant transformation of DNA) in bronchial epithelial ceils; (b) chronic proliferation of pulmonary calls associated with pulmonary fibrosis increases the likelihood (hat mutated ceils will produce a malignant tumor; and (c) pulmonary fibrosis disrupts the lung'* natural protective mechanisms which normally limit the proliferation of mutated ceils. - (.A. Felngotd, M.O., F.R.C.P.(C|, FCCP . Narrative Report Re: Asbestos containing electrical wire To: Mr. Olio Horton, Hawkins and Pamtll Date: 09*30-88 Pag#;15 Pulmonary parenchymal atbettot fiber burden and risk of lung canctr Greenberg and Roggli" have expressed agreement with the above described relationship between asbeslosis and lung cancer but suggested that the simple presence of an elevated tissue asbestos burden (without associated asbeslosis) might also be enough to Increase the risk of tung cancer: ... the weight of the evidence at this time seams to Indicate that, In an asbestos worker with carcinoma of tha lung who also smokes cigarettes, asbestosie must be present clinically or histologically (or Mere should ef least be a tissue asbestos content within the range of values observed in patients with asbestosis) (emphasis added] In order to assign substantial contributing role to asbestos in the causation of the lung cancer. Roggli, Pratt and Brody3* reviewed. 5 reports of tissue asbestos content In asbestosis. In at! 5 reports the median uncoated fiber count exceeded (usually by a oonsiderabit amount) 1x10* fibers per gram of dry lung tissue. Roggli at a! suggested that 1x10* fibers is a threshold tissue burden for the development of asbestosis. Roggli further reported that the mean uncoated fiber count In 7(5 patients who had pathologies! evidence of asbestosis was 3.3 x 10* fibers per gram of dry lung tissue. Roggli et al also reported on a study of 143 patients who had been exposed to asbestos and who developed lung cancer. All but 6 were cigarette smokars or ax-smokers. Among the 48 patients who had pulmonary parenchymal asbestosie the mean asbestos fiber count was 3.07 x 10* fibers per gram of dry lung tissue. Roggli29 reported that of 76 patients who had asbestosis, the mean asbestos body count was 378,000 per gram dry tung. Roggl. Greenberg and Pratt** reported that of 48 patients who had asbestosis and lung cancer, the metn asbestos body count was 334,000 bodies per gram dry tung. Asbestos fiber type and mesothelioma Wegner was the first to report In 1900*' of the association between asbestos exposure and the development of mesothelioma. Wagner suggested that it was only 'Cape Western T - -- 4* 1 -} y I.A. Felngold, M.D., F.R.C.P.(C), FCCP Narrative Report Re: Asbestos containing electrical wire To; Mr. OH Harton, Hawkins and Parnell Date; 09*30*96 Page; 16 Blue* or crocidolit asbestos that was the cause of mesothelioma. In 1965 Selikoff* noted: This remarkable concentration of cases In one area of South Africa was explained by the hypothesis that mesothelioma was the result of exposure to one special type of asbestos (crocidollta).... Despite this finding. Selikoff suggested that.. mesothelioma may not necessarily be a problem of only one kind of asbestos (crocidollta)... .* but in 1965 Sluis-Cremef* reported on a methodical search for mesothelioma cases outside of the South African North West Cape Province croddollle mining area and concluded that there were no casea from the amcslle mines of the Transvaal Province. It was not until 1972 that Selikoff, Hammond and Chorg* demonstrated that amosite was a cause of mesothelioma. In 198Q Selfcoff, Seidman and Hammond* reported on a further study of amosite factory workers. Selikoff et el noted that ________ In 1941, with the encouragement of the U S. Navy, a factory was established in Paterson. New Jersey, to manufacture asbestos products for the armed forces for Industrial uses. We have ascertained that amosite asbestos was used almost exclusively (wifc very email amounts of chrysotile asbestos also being used). Amosite was specified by the U.S. and other navies for the construction of war ships. Sheers and Coles (HM Naval Base, Devooport, England)* noted Two major developments since 1944: * (1) the very extensive use of crocidolite for environmental insulation and fire protection from 1944 to 1963, and (2) the large Increase in the amount of amosite used for machinery insulation between 1950 and 1961 An earlier report by Harries* described the same kind of amosite use in British shipyards. In 1962 McDonald* reported on e study of asbestos textile workers exposed to chrysotile, amosite and crocidoille. The authors noted that: T I.A. Felngold, M.O., F.R.C.P.(C), FCCP Narrative Report Re: Asbestos containing electrical wire To: Mr. Olle Harton, Hawkins and Parnell Date: 09-50-U Page:17 The much greater risk of mesothelioma from exposure to proceises in which even quite smelt quantities of amphiboies were used wet also confirmed. In 1984 McDonald* reported that long teun follow up of a large cohort of men who were exposed only to chrysotite did not reveal any cases of mesothelioma 'consistent with a much lower risk of (his tumor with chrysotile than with amphiboies.* In 1989 Newhouse and Sullivan*5 described a long term follow up of men who had worked in a factory that produced friction materials (principally brakes). The factory used chrysotile asbestos except for certain specific contracts. Alt of the mesothelioma cates were attributed to croddoilte exposure. in 1989 Wamock*1 reported on the lung tissue fiber burdens of workers In a shipyard in the Scteno County area of California who developed mesothelioma. The median fiber burden for all types of amphiboies was 2.7 million f/g dry lung. Wamock noted that amotite was the most prevalent fiber type. In 1992 an important study was published by Begin* who identified a total of 4$ oases of mesothelioma in former Quebec chrysotile asbestos mine and mill workers. Begin noted: The present study documents an increasing incidence of oases of malignant mesothelioma in chrysotile miner* and millers of the Eastern Townships of Quebec, with 49 cases in the last 23 years, and a rate of 2.5 cases per yetr in the last 10 years In the primary Industry.... _E tn their report, Begin at ai also noted that* In the past, these cancer cases among Quebec chrysotile miners and millers were considered to be likely attributable to amphibote contamination of the worksite and/or of the mineral ore... Nonetheless, eases of mesothelioma in Quebec miners have been documented where chrysotite fibers were the only fibers in lung tissue. Begin noted evidence for a significant difference in the (remoiile contamination of chrysotile ore mined h the two main Quebec asbestos centers, the towns of Asbestos and I.A. Felngold, M.D., F.R.C.P.(C), FCCP Narrative Report Rt: Asbestoa containing electrical wlra To: Mr. Olla Harton, Hawkins and Parnell Data: 0J-30-96 Pag#; 16 Thetford Mines, but the incidence of mesothelioma was proportional to the work force and not related to residence in one of the two areas. Our data suggest that some of the cases of malignant mesothelioma In Quebec chrysolite miners and milters may not be necessarily attributable to amphibole and could be chrysoUleinduced. In 1993 Churg et ai reported on the fiber burdens in the lungs of 94 tong term chrysotile asbestos miners fromThetford Mines, Quebec. In the patients who hed mesothelioma, the chrysotile fiber burdens were very targe, with a mean of 34 million f/g dry lung. The tremolite burdens in the mesothelioma cases were even greater, 160 million f/g dry lung. Churg et ai concluded: ... in this population of heavily exposed chrysotile miners and milters; the presence of airways fibrosis and asbestosfs and, probably, mesothelioma reflects high tremolite burden. Whether chrysotile fibers themselves play a role in disease induction remains uncertain. In a subsequent report, Churg and Vedal" reported on a study of 144 shipyard workers and insulators from Oregon Washington state and British Columbia. Churg and Vedal stated: Our results show clearly that, despite known historic exposure to amotile and chrysotile, amoslte is by far the predominant residual fiber, and there .are correlations between amosite measures and disease. Chrysolite was present Inconstantly and In relatively small amounts, and no corralatlons were found between chrysotile measures and disease. Churg and Vedat also commented on the issue of tremotila contamination of chrysotile: Wa have proposed elsewhere that tremolite, which is a natural minor constituent of chrysotile ora, might serve as substitute marked for chrysotBe, and that tremoflte rather than chrysotile may actually be the agent responsible for 'chrysotlle-induced* mesothelioma.... t.A. Feingold, M.D., F.R-C.P.(C), FCCP . Narrative Report R: Asbestos containing electrical wlra To: Mr. Olio Harton, HawKIna and Parnell Date; O9-30-W Page:19 Becklake* provided an in-depth editorial comment of Churg and Vedal'f study. Professor Becklake noted that: ... the major contribution of the two studies of Churg and associates reviewed here Is in adding further weight to the already substantial body of evidence concerning differentia! disease-generating potential for different asbestos fiber types. Although the facts of differentia) clearance of chrysotile are acknowledged in both papers, we believe ths authors are right to conclude that 'there are major differences in the relationship of fiber concentration and disease for chryaotite and tremolite compared with amosite or crocidoiite.* Although the medicsl literature published since 1980 reflects significant controversy, (not presented here, but see Roggti* and the multiple responses in the literature such as Hughes and WeRl^) at this timo thore i etrong scientific support for the following conclusions about mesothelioma: 1. Without an amphibote contaminant, chryaotite is unlikely to be a causa of malignant mesothelioma. 2. In terms of mesothelioma inducing potency, the different forms of asbestos can be rated as: erocidofite 0 amosite o tremolite 0 ?chryoti!e 3. In terms of frequency, amosite represents the cause of most mesothelioma cases in the United Slates. Amosite exposure wes typical of World Wtr It era shipyard work. 4. Where chrysotile has been associated with mesothelioma, the majority of cases hsvs probably been caused by tremolite contamination of chrysotile ore. 5. Since tremolite Is a minor contaminant of chrysotile ore, very large chrysotile exposures are necessary before mesothelioma can occur. As noted above. In 1993 Churg et a! reported that the mean chrysotile fiber burdens in asbestos miners who developed mesothelioma were enormous - 34 mltlion f/g dry lung and that the tremolite burdens were even greater. 1 `) ) I,A. Felngoid, M.D., F.R.C.P.(C), FCCP Narrative Report Re: Asbettoi containing electrical wire To: Mr, OUe Harton, Hawklna and Pamell Date; 0-3Q*M Page; 20 Conclusion* rrom the medical literature The medical literature presented above provides strong, consistent, rational evidence for the following conclusions: 1. There is a threshold of exposure below which diffuse Interstitial pulmonary esbestosls does not occur. That threshold is in the range of 25-50 f/mlyeers. Compliance with the peak exposure limit (PEL) of 0.2 ffee 8 hour time weighted average sot by the United States Occupational Safety and Health Administration in 1986 makes it impossible to acomulate a lifetime occupational exposure >2b t/mi-yrs even after 40 years of employment 2. The risk of bronchogenic carcinoma is increased in asbestos workers who._________ smoke cigarettes and have pulmonary parenchymal asbostosls. The rltk of lung cancer in asbestos workers who do not have esbestosls Is related to amount of cigarette smoking and is unrelated to asbestos exposure. Thus, iha development of pulmonary parenchymal asbestosis Is a necessary, biological threshold below which an increase In the risk of lung cancer it not observed. 3. , Evidence for e lifetime threshold of asbestos exposure below which there is no increased risk of mesothelioma was not presented in this report. The risk of mesothelioma It much more closely related to elapsed time since first exposure than to dosau but the literature does suggest a threshold of exposure below which the risk of mesothelioma is extremely low or non* existent4* * " Asbestos fiber type is of greater significance lhan threshold fiber burden. The weight of the medical evidence strongly indicates that chrysotife exposure alone does not increase the risk of mesothelioma. The "one fiber* theory ve. biological plausibility Some medical experts have suggested that any exposure to asbestos fibers contributes to the development of asbestos-related diseases. Such experts ergj* that for an asbestos insulator who has accumulated, for example, a moderate fibrogenic asbestos burden of T I.A. Felngold, M.O., F.R.C.P.{C), FCCP Narrative Report Rs: Asbestos containing electricil wire To: Mr. Oil Harton, Hawkins and Parnell Oat*; 09*30*96 Psge:21 100 f/ml-yrs, exposure to'even one asbestos fiber contributed In a meaningful way to his eventual development of asbestosls and, possibly, lung canoer. According to this view, exposure to the minute quantities of asbestos released during the manipulation of asbestos insulated electrical wiring would be significant However, the medicat literature presented above reveals that such 'one fiber* theories are scientifically incorrect. A considerable asbestos fiber burden must be accumulated before there Is any risk of asbestosls. The average amount of asbestos in the lungs of patients who have asbestosls is in excess of 9,000,000 fibers per gram of dry lung. Thus, patients who have asbestosls have accumulated hundreds of millions of asbestos fibers during their occupational lifetime. Exposure to chrysotite asbestos within the limits (PEL*) established by OSHA In 1994 (or 1986) cannot result In a sufficient pulmonary asbestos tissue burden to result In asbestosls. Work with asbestos insulated electrical cable can, in "worst case* scenarios, result in asbestos exposure 10 to 20 limes lower than the OSHA peak exposure limits. In conclusion, It Is my opinion to a reasonable degree of medical certainty, that work with asbestos Insulated electrical cable cannot result in dangerous asbestos fiber exposure. Electricians working with such cable cannot, in a lifetime, accumulate a significant pulmonary asbestos burden If an Individual worker who has other occupational asbestos exposure develops asbestosis, the exposure to asbestos fibers from insulated cable does not represent a biologically significant contribution to Ns disease. 8ecaus* asbestoeis cannot result from the level of asbestos exposure associated with asbestos-insulated cable, such exposure cannot result In lung cancer. Exposure to chrysotfie asbestos from asbestos-insulated cable cannot result in mesothelioma. 1A Felngold, M.D., F.R.C.P.(C), FCCP - s- I.A. Felngotd, M.D., P.R.C.P.tC), FCCP . Narrativs Report Re: Asbestos containing electrical wire To: Mr. Olle Harton, Hawklnt and Parnell Date: 0900*96 Pago: 22 Bibliography 1. Department of Labor. Occupational Safety and Health Administration: Occupational exposure to asbestos; final rule. Federal Register 51:22612, 06-20-66. 2. Department of Labor. 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