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Characterization of asbestos exposure among automotive mechanics servicing and handling asbestos-containing materials

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Title:
Characterization of asbestos exposure among automotive mechanics servicing and handling asbestos-containing materials
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Book
Language:
English
Creator:
Dotson, Gary Scott
Publisher:
University of South Florida
Place of Publication:
Tampa, Fla
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Subjects / Keywords:
Occupational risk analysis
Vehicles
Friction materials
Seam sealant
Gaskets
Dissertations, Academic -- Public Health -- Doctoral -- USF
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bibliography   ( marcgt )
theses   ( marcgt )
non-fiction   ( marcgt )

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Summary:
ABSTRACT: The historic use of asbestos-containing materials during the manufacturing of automobiles has resulted in a perception of an increased risk of asbestos-related pulmonary diseases within mechanics. This study was conducted to assess the potential asbestos exposures mechanics encounter while servicing vehicles assembled with parts containing asbestos, in addition to compare the cumulative lifetime asbestos exposures for different maintenance activities against theorical threshold exposures for asbestosis, lung cancer and mesothelioma. Exposure data were assembled from four independent exposure assessments performed to elucidate the airborne asbestos levels generated during the removal and replacement of brakes, gaskets, clutches and seam sealants containing asbestos. The phase contrast microscopy (PCM) and phase contrast microscopy equivalent (PCME) fiber concentrations for personal samples and air sampled identified to contain asbestos fibers through Transmission Electro n Microscopy (TEM) analysis were applied to calculate the cumulative lifetime asbestos exposures. This index of exposure was compared to no-effect exposure thresholds identified through an extensive literature review for the selected pulmonary diseases. The results of this study indicate that mechanics encounter PCM fiber concentrations approximately 10 to 100 times lower than the current Occupational Safety Health Administration (OSHA) Permissible Limit Exposure (PEL) of 0.1 fibers per cubic centimeter (f/cc). Additionally, the cumulative lifetime asbestos exposures ranged from < 1 fiber-year/cubic centimeter of air (f-yr/cc) to 2.0 f-yr/cc, and did not exceed the no-effect exposure thresholds for asbestosis, lung cancer and mesothelioma. The findings of this study provide additional support to previously published epidemiologic investigations and exposure assessments against an increased risk of asbestos-related disease within mechanics historically employed to service vehiclescontaining asbestos fibers.
Thesis:
Dissertation (Ph.D.)--University of South Florida, 2006.
Bibliography:
Includes bibliographical references.
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System Details:
Mode of access: World Wide Web.
Statement of Responsibility:
by Gary Scott Dotson.
General Note:
Title from PDF of title page.
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Document formatted into pages; contains 153 pages.
General Note:
Includes vita.

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aleph - 001798431
oclc - 162106021
usfldc doi - E14-SFE0001643
usfldc handle - e14.1643
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ABSTRACT: The historic use of asbestos-containing materials during the manufacturing of automobiles has resulted in a perception of an increased risk of asbestos-related pulmonary diseases within mechanics. This study was conducted to assess the potential asbestos exposures mechanics encounter while servicing vehicles assembled with parts containing asbestos, in addition to compare the cumulative lifetime asbestos exposures for different maintenance activities against theorical threshold exposures for asbestosis, lung cancer and mesothelioma. Exposure data were assembled from four independent exposure assessments performed to elucidate the airborne asbestos levels generated during the removal and replacement of brakes, gaskets, clutches and seam sealants containing asbestos. The phase contrast microscopy (PCM) and phase contrast microscopy equivalent (PCME) fiber concentrations for personal samples and air sampled identified to contain asbestos fibers through Transmission Electro n Microscopy (TEM) analysis were applied to calculate the cumulative lifetime asbestos exposures. This index of exposure was compared to no-effect exposure thresholds identified through an extensive literature review for the selected pulmonary diseases. The results of this study indicate that mechanics encounter PCM fiber concentrations approximately 10 to 100 times lower than the current Occupational Safety Health Administration (OSHA) Permissible Limit Exposure (PEL) of 0.1 fibers per cubic centimeter (f/cc). Additionally, the cumulative lifetime asbestos exposures ranged from < 1 fiber-year/cubic centimeter of air (f-yr/cc) to 2.0 f-yr/cc, and did not exceed the no-effect exposure thresholds for asbestosis, lung cancer and mesothelioma. The findings of this study provide additional support to previously published epidemiologic investigations and exposure assessments against an increased risk of asbestos-related disease within mechanics historically employed to service vehiclescontaining asbestos fibers.
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Charaterization of Asbestos Exposure Among Automotive Mechanics Servicing and Handling Asbestos-Containing Materials by Gary Scott Dotson A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy Department of Environmental and Occupational Health College of Public Health University of South Florida Major Professor: Raymond D. Harbison, Ph.D. Steve Mlynarek, Ph.D. Ira Richards, Ph.D. Yiliang Zhu, Ph.D. Date of Approval: July 07, 2006 Keywords: occupational risk analysis, vehicles friction materials, seam sealant, gaskets Copyright 2006, Gary Scott Dotson

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DEDICATIONS To those that supported and believed in me, I thank you. To those that did not, I thank you even more.

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ACKNOWLEDGEMENTS Support for this project came from the Ce nter for Environmenta l/Occupational Risk Analysis and Management, in addition to Clayton Group Services. All funding and exposure data associated with this stu dy were provided by these organizations. Specials thanks should be offered to Mr Charles Blake and Dr. Raymond Harbison. Without both of their wisdom and guidance, this dissertation w ould not have been possible. I would like to express my sincer e gratitude and appreciation to Dr. Harbison for providing me with the opportuni ty to work at the Center for Environmental/Occupational Risk Analysis and Management, and acting as my mentor on matters relating to academics and all other things of importance. Additional acknowledgment goes to Dr. Thom as Truncale for acting as Chairperson during the Dissertation Defense.

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i TABLE OF CONTENTS List of Tables iv List of Figures vii List of Acronyms and Abbreviations ix Abstract xi Chapter 1.0 Introduction 1 Chapter 2.0 Literature Review 5 2.1 Asbestos and Occupational Health Risk 5 2.1.1 Fiber Type 6 2.1.2 Fiber Size 7 2.1.3 Intensity of Exposure 8 2.2 Asbestos-Related Diseases 9 2.2.1 Asbestosis 9 2.2.2 Lung Cancer 12 2.2.3 Mesothelioma 14 2.3 Automotive Parts and Compone nts Containing Asbestos 15 2.3.1 Asbestos-Containing Friction Materials 16 2.3.2 Asbestos-Containing Gaskets 16 2.3.3 Asbestos-Containing Sealants 17 2.4 Summary of Epidemiological Studies 17 2.5 Exposure Assessments of Automotive Asbestos-Containing Materials 27 2.5.1 Asbestos-Containing Brakes 28 2.5.2 Asbestos-Containing Gaskets 32 2.5.3 Asbestos-Containing Sealants 34 2.6 Summary 35 Chapter 3.0 Methods 37 3.1 Assembly and Evaluation of Exposure Data 37 3.2 Exposure Assessment I: Asbestos-Containing Gaskets 41 3.2.1 Test Location and Environmental Setting 41 3.2.2 Test Vehicles 42 3.2.3 Mechanic’s Activities, Equipment and Tasks 44 3.2.4 Air Sampling and Analysis 49 3.2.5 Bulk Sampling and Analysis 52

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ii 3.3 Exposure Assessment II: Asbestos-Containing Seam Sealant 53 3.3.1 Test Location and Environmental Setting 53 3.3.2 Test Vehicles 54 3.3.3 Mechanic’s Activities, Equipment and Tasks 54 3.3.4 Air Sampling and Analysis 57 3.3.5 Bulk Sampling and Analysis 58 3.4 Exposure Assessment III: Asbestos-Containing Clutches 59 3.4.1 Test Location and Environmental Setting 59 3.4.2 Test Vehicle 61 3.4.3 Mechanic’s Activities, Equipment and Tasks 62 3.4.4 Air Sampling and Analysis 66 3.4.5 Bulk Sampling and Analysis 68 3.5 Exposure Assessment IV: Asbestos-Containing Brakes 68 3.5.1 Test Location and Environmental Setting 68 3.5.2 Test Vehicles 69 3.5.3 Mechanic’s Activities, Equipment and Tasks 70 3.5.4 Air Sampling and Analysis 71 3.6 Statistical Analysis 72 3.7 Risk Analysis 75 3.7.1 No-Effect Exposure Thres holds for Asbestos-Related Diseases 76 3.7.2 Estimation of the Cumulative Lifetime Asbestos Exposure 82 3.7.3 Determination of Risk 83 Chapter 4.0 Results 85 4.1 Gasket Exposure Assessment 85 4.1.1 Individual Test Sessions 85 4.1.2 Personal Air Samples 88 4.1.3 Samples Identified to Contain Asbestos 90 4.1.4 Bulk Sample Analysis of Removed Automotive Gaskets 92 4.2 Seam Sealant Exposure Assessment 93 4.2.1 Area Air Samples 93 4.2.2 Personal Air Samples 94 4.2.3 Air Samples Containing Asbestos 95 4.2.4 Transmission Electron Micrograph of Air Samples 97 4.2.5 Bulk Sample Analysis of Seam Sealant 98 4.3 Clutch Exposure Assessment 99 4.3.1 Area Air Samples 99 4.3.2 Personal Air Samples 101 4.3.3 Air Samples Containing Asbestos Fibers 102 4.3.4 Bulk Samples of Clutch Material and Debris 103 4.4 Brake Exposure Assessment 104 4.4.1 Area Air Samples 105 4.4.2 Personal Air Samples 107 4.5 Cumulative Lifetime Asbestos Exposure 108

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iii Chapter 5.0 Discussion 116 Chapter 6.0 Conclusion 130 References 134 Appendix A: Quality Evaluation of Exposure Data 146 About the Author End Pages

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iv LIST OF TABLES Table 1: Summary of Reviewed Epidemiological Studies 26 Table 2: Summary of Epidemiological Studies of Case-Control and Cohort Study Designs 27 Table 3: Summary of Exposure Assessmen ts Associated with the Servicing of Automotive Asbestos-Contain ing Brakes Components 32 Table 4: Summary of Exposure Assessments Associated with the Removal of Automotive Asbest os-Containing Gaskets 34 Table 5: Guidelines Used to Evaluate Data for Inclusion in to Risk Analysis 38 Table 6: Definitions of the Core Information Used for Assembled Exposure Data 39 Table 7: Framework Used to Evaluate the Completeness of the Core Information 39 Table 8: Make and Model of Vehicles and Engines Used in Gasket Tests 43 Table 9: Activities Associated with the Removal and Replacement of Asbestos-Containing Gaskets 46 Table 10: Location of Area Samples within Service Facility 51 Table 11: Computational Formula Used to Determine Phase Contrast Microscopy Equivalent (PCME) 52 Table 12: Description of Test Vehicles Used in Seam Sealant Assessment 55 Table 13: Locations of Seam Sealan t Bulk Sampling on Test Vehicles 59 Table 14: Work Activities Perf ormed during Clutch Removal 63 Table 15: Work Activities Perfor med during Clutch Installation 63 Table 16: Locations of Area Air Samp les during Clutch Exposure Assessment 67 Table 17: Tasks Performed during the Servicing of Asbestos Brakes 71

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v Table 18: Location of Area Ai r Samples during Brake Study 72 Table 19: No-Effect Exposure Threshol ds for Asbestos-Related Diseases 81 Table 20: Cumulative Lifetime Asbestos Exposure Matrix 83 Table 21: PCM Fiber Concentrations fo r the Individual Gasket Test Sessions 86 Table 22: Area Fiber Concentrations for the Complete Disassembly and Reassembly of Engines Containi ng Asbestos Gaskets 87 Table 23: Mean Area Air Fiber Concentr ations Relative to Sampling Location 88 Table 24: Personal Air Samples Co llected during the Gasket Study 89 Table 25: Personal PCM and PCME Fiber Concentrations for the Complete Disassembly and Reassembly of En gines Containing Asbestos Gaskets 90 Table 26: Air Samples Containing Asbestos Fibers Collected during Gasket Study 91 Table 27: Average PCM and PCME Fibe r Concentrations for Air Samples Containing Asbestos Fibers 92 Table 28: Asbestos and Non-Asbestos Components of Removed Gaskets 93 Table 29: Average TEM Asbestos Concentrations for Area Air Samples Collected During Seam Sealant Removal 94 Table 30: Average PCM and PCME Concentrations for Personal Air Samples 95 Table 31: All Air Samples Containing Asbestos Fiber Collected during the Removal of Seam Sealant 96 Table 32: Average PCM and PCME Fibe r Concentrations for Air Samples Containing Asbestos 97 Table 33: Bulk Sample Analysis of Seam Sealant Material 99 Table 34: Individual Area Air Sample s Collected during Clutch Study 100 Table 35: Area Air Samples Collected during Clutch Study 101 Table 36: Individual Personal Air Samp les Collected during Clutch Study 102

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vi Table 37: Air Samples Containing Asbestos Fibers Collected during Clutch Study 103 Table 38: Bulk Sample Analysis of Clutch Materials and Residue 104 Table 39: Individual Test Sessi ons Conducted during Brake Study 105 Table 40: Area Air Samples Collected Less than 3 Meters from Test Vehicles 106 Table 41: Indoor Background and Work Bench Area Air Samples 106 Table 42: Personal Air Samples Collected during Brake Study 108 Table 43: Summary of the Annual Average 8-HR Daily Exposures, Cumulative Lifetime Asbestos Exposures and 95% Upper Confidence Limits Obtained From Personal Air Samples 110 Table 44: Summary of the Annual Average 8-HR Daily Exposures, Cumulative Lifetime Asbestos Exposures and 95 % Upper Confidence Limits Obtained from Air Samples Identified to Contain Asbestos through TEM during the Gasket, Seam Sealant, Clutch and Brake Exposure Assessments 113 Table A-1: Quality Evaluation of Exposure Data from Gasket Test 149 Table A-2: Quality Evaluation of Expos ure Data from Seam Sealant Test 150 Table A-3: Quality Evaluation of E xposure Data from Clutch Test 151 Table A-4: Quality Evaluation of Exposure Data from Brake Test 152

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vii LIST OF FIGURES Figure 1: Automotive Servicing Facility Used during Gasket Test 43 Figure 2: Mechanic at Workbench Cl eaning Intake Manifold Mating Surface Using Powered Rotary Wire Brush 47 Figure 3: Mechanic at Bench Using Putty Knife and Mallet to Remove Intake Manifold Gasket Remnants 47 Figure 4: Mechanic Cleaning Manifold in Parts Washer 48 Figure 5: Mechanic Using Air Powered Ro tary Wire Brush to Clean Dry Engine Block Upper Surface 48 Figure 6: Mechanic Installing Intake Manifold to Engine 49 Figure 7: Mechanic Wearing Two Pers onal Samplers during the Cleaning of Intake Manifold with a Rotary Brush 50 Figure 8: Automotive Repair Facility Used During Seam Sealant Test 54 Figure 9: Demonstration of Seam Sealant Removal and Area Air Sample Placement 57 Figure 10: Illustration of Facility Used during Clutch Assessment 61 Figure 11: 1967 Kaiser J eep 1.25 Ton Pickup Truck 62 Figure 12: Removal of the G ear Shifter and Floor Plate 65 Figure 13: Removal of Clutch Disc from Test Vehicle 65 Figure 14: Automotive Service Facility Used during Brake Exposure Assessment 70 Figure 15: Distribution of All Area Air Samples Collected during Gasket Exposure Assessment 86

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viii Figure 16: Distribution of PCM Fiber Concentrations Obtained from Personal Air Samples Collected during Gasket Study 89 Figure 17: Distribution of All Air Samples Identified Via TEM to Contain Asbestos Fibers during the Removal of Gaskets 92 Figure 18: Transmission El ectron Micrograph of Chryso tile Fibers Suspended in Asphalt-Based Seam Sealant 98 Figure 19: Distributi on of the Area Air Samples to the OSHA PEL 101 Figure 20: Cumulative Lifetime Asbestos Exposures based on PCM and PCME Fiber Concentrations Associated with Personal Air Samples Collected during the Gasket, Clutch and Brake Exposure Assessments 111 Figure 21: Cumulative Lifetime Asbe stos Exposures based on PCM Fiber Concentrations Associated with Al l Air Samples Identified to Contain Asbestos through TEM from the Gasket, Seam Sealant, Clutch and Brake Exposure Assessments 114 Figure 22: Cumulative Lifetime Asbest os Exposures based on PCME Fiber Concentrations Associated with All Air Samples Identified to Contain Asbestos through TEM from the Gasket, Seam Sealant, Clutch and Brake Exposure Assessments 115

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ix LIST OF ACROYNMS AND ABBERVATIONS Agency for Toxic Substance and Disease Registry ATSDR Asbestos Containing Materials ACMs Automobile Service Excellence ASE Confidence Interval CI Environmental Protection Agency EPA Feet ft Fibers per Cubic Centimeter f/cc Fibers per Cubic Centimeter per Year f-yr/cc Level of Detection LOD Micron m Millimeters mm Mixed Cellulose Ester membrane filter MCE filter National Institute of Occupational Safety and Health NIOSH Occupational Safety and H ealth Administration OSHA Permissible Exposure Limit PEL Phase Contrast Microscopy PCM Phase Contrast Microscopy Equivalent PCME Polarized Light Microscopy PLM Recommended Exposure Limit REL

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x Scanning Electron Microscopy SEM Square Feet ft2 Standard Operating Procedures SOP Time Weighted Average TWA Transmission Electron Microscopy TEM United States US Upper Confidence Limit UCL

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xi Characterization of Asbestos Exposure Among Automotive Mechanics Servicing and Handling Asbestos Containing Materials Gary Scott Dotson ABSTRACT The historic use of asbe stos-containing materials during the manufacturing of automobiles has resulted in a perception of an increased risk of asbestos-related pulmonary diseases within mechanics. This study was conducted to assess the potential asbestos exposures mechanics encounter whil e servicing vehicles assembled with parts containing asbestos, in addition to compare the cumulative lifetime asbestos exposures for different maintenance activ ities against theorical thres hold exposures for asbestosis, lung cancer and mesothelioma. Exposure data were assembled from four independent exposure assessments performed to elucidate the airborne asbestos levels generated during the removal and replacement of brakes, gaskets, clutches and seam sealants containing asbestos. The phase contrast microscopy (PCM) and phase contrast microscopy equivalent (PCME) fiber con centrations for personal samples and air sampled identified to contain asbestos fi bers through Transmission Electron Microscopy (TEM) analysis were applied to calculate the cumulative lifetime asbestos exposures. This index of exposure was compared to noeffect exposure thres holds identified through an extensive literature review for the selected pulmonary diseases. The results of this study indicate that mechanics encounter PCM fiber concentrations approximately 10 to

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xii 100 times lower than the current Occupationa l Safety Health Administration (OSHA) Permissible Limit Exposure (PEL) of 0.1 fibers per cubic centimeter (f/cc). Additionally, the cumulative lifetime asbestos exposures ra nged from <1 fiber-year/cubic centimeter of air (f-yr/cc) to 2.0 f-yr/cc, and did not ex ceed the no-effect exposure thresholds for asbestosis, lung cancer and mesothelioma Th e findings of this study provide additional support to previously published epidemiologi c investigations and exposure assessments against an increased risk of asbestos-rela ted disease within mechanics historically employed to service vehicles containing asbestos fibers.

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1 CHAPTER 1.0 INTRODUCTION Mechanics employed in the automotive repair industry represent a large occupational cohort perceived to be at elevated risk of asbestos-related diseases including lung cancer and mesothelioma, due to the historic use of asbestos-containing materials during the manufacturing of passenger vehicles and light-d uty trucks. Asbestos fibers emitted from brake linings have been investigated as po ssible environmental a nd occupational health risks since the 1960s [1]. It is es timated that approximately 150,000 to 900,000 mechanics and garage workers in the United Stated (US) were potentially exposed to asbestos through the handling and servicing of automotive parts containing asbestos [2,3]. Epidemiological studies investigating automotive mech anics consistently report no association between asbestos exposure and increased risks of lung cancer and mesothelioma [4-8]. Despite these findings, the presence of asbestos in the workplace and the potential for fibers to be lib erated during the maintenance of vehicles has given rise to the perception of increased risk of as bestos-related diseas es among professional mechanics [9, 10]. Exposure assessments designed to characteri ze the asbestos concentrations produced during the maintenance of automotive ACMs rep eatedly report airborne asbestos levels

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2 below the current Occupational Safety and H ealth Administration’s (OSHA) Permissible Exposure Limit (PEL) of 0.1 fibers per cubi c centimeter (f/cc), and indicate that mechanics are exposed to extremely low leve ls of airborne asbe stos fibers [1,11-18] These findings provide support to the epidem iological studies agai nst an association between worker asbestos exposure in the auto motive repair industry and elevated risks of asbestos-related diseases. Asbestos-containing parts found in vehicles include friction materials, gaskets and undercoating materials. Each component re presents an independent point source of asbestos exposure, and constitutes a unique workplace hazard for professional automotive mechanics. The majority of epidemiological studies and exposure assessments investigating asbestos expos ure among mechanics focus primarily on the repair and replacement of brake and brake components [1, 4-8, 12-15]. This is attributed to the large volume of brake changes performed annually, the number of mechanics involved in this form of automotive servicing and the high con centrations of asbest os found within the matrix of brake components. Other parts, such as gaskets, seam sealants and clutches, have not received the same level of atten tion. The absence of exposure data for the various asbestos-containing automotive parts prevent the further analysis of risk for mechanics potentially exposed to asbestos dur ing the maintenance of vehicles containing ACMs. Inhalation exposure to asbestos is cumulativ e in nature with the lungs’ fiber burden increasing with time. For this reason, expos ure is frequently expressed in terms of

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3 concentration over time, or more specifical ly Phase Contrast Mi croscopy (PCM) fiberyears per cubic centimeter (f-yr/ cc) [19]. The development of asbestos-related diseases is generally associated with annual average e xposures of 0.125 to 30 f-yr/cc or cumulative exposures between 5 to 1,200 f-yr/cc [19]. A qualitative risk analysis was implemented to determine if mechanics are at increased risk of asbestos-related diseases due to asbe stos exposure associated with the se rvicing of asbestos-containing parts and components. This was accomplished in three distinct steps: 1) Characterization of the asbestos fiber concentrations generated during the servicing and handling of automotive gaskets, seam sealants, clutches and brakes containing asbestos, 2) Calc ulation of the cumulative lif etime asbestos exposure for mechanics based on the asbestos concentra tions reported in the assembled exposure database and 3) Comparison of the estimated cumulative lifetime as bestos exposure to no-effect exposure thresholds for asbestosis, lung cancer and mesothelioma identified within published literature [20-26]. An elevat ed risk of asbestos-r elated diseases was determined if the cumulative lifetime asbestos exposure exceeded the threshold doses. The objectives of this study were to: 1. Characterize the airborne asbestos concen trations generated during the servicing and handling of automotive asbestos-contai ning gaskets, seam sealants, clutches and brakes.

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4 2. Determine the cumulative lifetime asbestos exposure for mechanics employed to perform maintenance on asbest os-containing gaskets, seam sealants, clutches and brakes. 3. Compare the estimated cumulative lifetime asbestos exposure to no-effect exposure thresholds for asbestosis, lung can cer and mesothelioma to determine if mechanics are at increased risk of developing the diseases. The hypotheses for this study were: 1. Airborne asbestos concentrations observ ed during the maintenance of asbestoscontaining gaskets, seam sealants, clutches and brakes do not exceed the current OSHA PEL of 0.1 f/cc. 2. The cumulative lifetime asbestos exposure estimated for mechanics engaged in the servicing and handling of automotive asbestos-containing materials does not exceed the no-effect exposure thresholds id entified in the literature for asbestosis, lung cancer and mesothelioma.

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5 CHAPTER 2.0 LITERATURE REVIEW 2.1 Asbestos and Occupa tional Health Risk Asbestos is a general term applied to a fam ily of naturally occurri ng hydrated silicates. The identifying characteristic of this minera logical group is the abil ity to be separated into individual fibers, or structures with one dimension significantly larger than the other two [27]. Asbestos fibers exhi bit physical and chemical prope rties including resistance to thermal and chemical degradation, high tensile strength and durability [28]. Despite being classified into the same mineralogica l family, variations in the physiochemical properties of the individual asbestos species affect their fibrogenic and carcinogenic potentials [29]. The inhalation of asbestos fibers has been recognized to cause numerous pulmonary disorders in human and animal studies [30]. Multiple exposure conditions, including fiber type, fiber size and magnitude of exposure, dire ctly affect th e onset of the different respiratory diseases. In 1993, Wong st ated that these factors must be described and defined to establish a causal relationshi p between occupational asbestos exposure and cancers [31].

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6 2.1.1 Fiber Type The individual species of asbestos are divi ded into two distinct groups, serpentine and amphiboles, based on variations in their chemi cal and physical characteristics. Chrysotile fibers, the sole member of the serpentine as bestos group, represent approximately 95% of all asbestos used commercially within the US [32]. Research has demonstrated that serpentine fibers are relativ ely sensitive to thermal and chemical degradation [33]. Exposure to acidic environments, such as the interior of the lungs, have been demonstrated to leach magnesium from chry sotile asbestos causing the dissolution of fibers approximately 0.5 microns (m) in le ngth in a short period of time (<2 months) [34]. Bernstein theorized that the removal of the magnesium from serpentine asbestos is due to the orientation of the metal being locat ed on the outside of the curled chrysotile structure [35]. In comparison, the magne sium component of amphibole asbestos is locked within the internal structure of the fibers which limits the contact of the metal with the acidic environment of th e lungs [35]. The location of the magnesium component of amphibole asbestos enables the fi bers to be more stable than serpentine asbestos allowing them to persist for decades within the lungs [36]. Additional evidence from animal studies has demonstrated the fracturing of chry sotile fibers laterally into shorter segments of fibers makes them capable of being engulfed and removed by macrophages [36]. Amphibole fibers tend to fragment longitudinally into thinner fibers of the same relative length as the original fibers and remain too long to be phagocytized [36]. Previous studies have identified additional va riations within the chemical composition of the individual fiber species [35, 37, 38]. Amphibole fibers have molecular structures

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7 comprised approximately of 25 to 36% iron by we ight [37]. Chrysotile asbestos contains little iron (<5%) [38]. Iron is a transition metal capable of participating in redox reactions within the body capable of gene rating free radicals a nd other reactive oxygen species (ROS) [39-41]. ROS are theorized to act as mediators of asbestos-induced toxicity within numerous pulmonary cells including macrophages, epithelial cells, mesothelial cells and endothelial cells [39] The concentration of iron within the individual asbestos fiber sp ecies may directly result in the different fibrogenic and carcinogenic properties. A causal association between increased risks of asbestos-related can cer and inhalation of high concentrations of amphibole fibers has been established through multiple epidemiological studies [42-46]. In contra st, there has been considerable debate regarding the carcinogenicity of chrysotile fibers [ 42, 44, 47-50]. The conflicting findings have given rise to the “amphibole theory” or the belief that only amphibole fibers, such as crocidolite, amosite and trem olite, are capable of acting as carcinogens due to their physical and chemical properties [51]. Serpentine fibers, which vary significantly from amphiboles, are theorized to lack this abil ity and primarily represent a risk factor for the development of non-malignant pulmonary diseases, including fibrosis and pleura plaques [29, 31]. 2.1.2 Fiber Size Stanton’s theory states that the pathogenesi s of asbestos-related di seases is partially influenced by the physical dimensions of asbe stos fibers [52]. The two primary factors

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8 affected by the physical characteristics of as bestos fibers are 1) deposition within the lungs and 2) clearance. The length and diamet er of fibers dictate their ability to be deposited within the lungs, and subsequently affect the onset of malignant and benign diseases [53, 54]. Research has demonstrated that fibers with diam eters less than 3 m are respirable, while fibers greater than 3 m in diameter generally are incapable of entering the lungs [55]. An additional factor influenced by fiber di mensions is the ability of macrophages to engulf and clear particulate matter from the lung or pleura. Fibers too large for macrophages to phagocytize persist in the lungs and frequently become protein-coated asbestos bodies or migrate through the interstiti al space to the pleura [53]. Fibers longer than 10 m are not easily phagocytized, and tend to remain in the lower respiratory tract or penetrate the pleura membrane [54]. Th e fiber dimensions most commonly associated with the onset of asbestosis, lung cancer and mesothelioma are discussed in greater detail in Section 2.2. 2.1.3 Intensity of Exposure Development of asbestos-related diseases is directly influenced by the magnitude of asbestos exposure [31]. Asbestosis, lung cancer and mesothelioma have been conclusively linked to frequent exposures to high concentrations of airborne asbestos fibers [22, 25, 56]. An association between lo w level asbestos exposures in occupational and environmental settings is highly debated [57-59]. The current scientific consensus states that elevated rates of asbestos-induced fibrosis and cancers in occupational cohorts

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9 is caused by exposure to frequent high levels of airborne asbestos for multiple years or extremely high exposures for short periods [22, 24, 25]. No conclusive link between exposure to low levels of asbestos and risk of malignant or benign lung diseases has been established. 2.2 Asbestos-Related Diseases Asbestos is a recognized occupational heal th hazard. Inhalation of the naturally occurring fibers primarily affects the lungs a nd pleura of exposed wo rkers, and is linked to three distinct occupational diseases: 1) as bestosis, 2) lung cancer and 3) mesothelioma [60]. The following section reviews the pa thology and epidemiology of the asbestosrelated diseases. 2.2.1 Asbestosis Asbestosis is a bilateral diffuse interstit ial fibrosis of the pulmonary parenchyma associated with chronic high-level asbest os exposure [22, 25, 61]. The pathophysiology of asbestosis is a chronic inflammatory re sponse accompanied by collagen and scar tissue formation in the lungs [27, 32]. Problems arise during the diagnosis of asbestosis due to the difficulties in distinguishing between idi opathic interstitial fi brosis and asbestosinduced fibrosis. Mossman and Churg re ported, “The clinic al, physiologic, and radiological findings of asbestos is are not in any way specific, and they can be seen in diffuse interstitial fibrosis of other causes particularly usual interstitial pneumonia (idiopathic interstitial fibrosis), except that patients with as bestosis always have a history of heavy occupational as bestos exposure...”[22].

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10 The presence of asbestos in the alveolar region of the lungs activates alveolar macrophages that attempt to phagocytize fi bers. Damaged and activated macrophages release cytokines and growth f actors that subsequently result in cytotoxic oxidation [32]. Lesions caused by persistent assaults from chemical mediators, free radicals and the continued presence of asbestos fibers result in the production of collagen and fibrous tissues [30, 62]. The long term effects of asbestosis are reducti on in surface area, flexibility and gas exchange cap ability across the surface of aff ected alveoli. Individuals diagnosed with this form of pneumoconios is experience dyspnea and dry cough that progressively worsens with further exposures to asbestos or ot her agents, such as cigarette smoke [63]. Detection of asbestos fibers, or protein-coated fibers known as asbestos bodies, in the lungs, in addition to the thickening of the visceral pleura, or honeycombing of the lower zones of the lungs provide additional support for diagnosis of the disease [30, 64]. Epidemiological evidence suggests that the deve lopment of asbestosis requires repetitive exposure to high levels of air borne asbestos (25-100 f/cc) for many years or exposure to extremely high asbestos concentrations (> 100 f/cc) for short durations [22, 25, 65-67]. Studies have consistently concluded that exposure to high concentrations of both serpentine and amphibole fiber types have the potential to cause asbe stosis [25, 68]. The onset of the pulmonary fibrosis disease is di rectly related to the magnitude and duration of exposure to asbestos fibers with the la tency period for the illness ranging between 15

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11 to 40 years [20, 22, 25]. Diagnosis in extr eme cases has occurred within approximately five years of initial asbestos exposure [22, 25]. The broad range of latency periods reported in epidemiological studies, in addition to the lack of evidence of the diseas e resulting from low level asbe stos exposures, indicate the existence of a threshold dose below which asbe stosis is not observed [22, 24]. Support of an exposure-response relationship between as bestos exposure and pulmonary diseases comes from previous studies investigating non-occupational asbestos exposures within the general population. Asbestos fibers are an ubiquitous com ponent of ambient air. The ATSDR has reported that ambient concentration of asbestos fibers in urban areas range between 3 x 10-6 to 3 x 10-4 PCM f/cc [19]. No increased ri sk of asbestos-related diseases in the general population exposed to asbestos from environmental sources [24]. These findings indicate that the cumulative exposure to asbestos fibers associated with nonoccupational sources remain re latively low and does not increase the probability of inducing the onset of asbestos -related diseases [24]. Environmental studies have consistently reported no increase risk of diseases from the inhalation of low levels of airborne asbestos, and provide additional evid ence to the existence of a threshold dose below which asbestos-relat ed diseases do not occur The dimensions of the fibers associated with the development of as bestosis have been investigated. Lippman proposed that the pul monary fibrotic dis ease was most commonly caused by fibers longer than 2 m and thicker than 0.15 m [53]. Other studies have indicated that fibe rs approximately 5 m in length are primarily responsible for

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12 asbestosis [53]. Conflicting resu lts indicate that the most seve re cases of asbestosis occur in cases with average fiber lengths less than 5 m [69]. Although the exact length of asbestos fibers associated with the developm ent of asbestosis has not been elucidated, currently available evidence indicated that fi bers ranging from 2 to 5 m in length are responsible for the onset of the pulmonary disease. 2.2.2 Lung Cancer Carcinoma of the lungs is one of the most common forms of cancer diagnosed in the US [56]. Increased rates of lung cancer have b een reported in occupa tional cohorts exposed to high concentrations of asbestos fibers [ 56, 70]. Asbestos-related cancers have been documented in all zones of the lung with tu mors being predominantly adenocarcinomas, but bronchogenic carcinomas are also common [61, 62]. Three main hypothesis regarding the associat ion between asbestos exposure and lung cancer have been purposed: 1) asbestos-related lung carcinomas occur only in the presence of asbestosis, 2) the dose of asbestos is the predominant ri sk factor for lung cancer development and 3) all asbestos exposures potentially increase the risk of lung carcinoma with no threshold existing between asbestos exposure and onset of disease [71]. Attemp ts to elucidate the association between asbestosis and lung can cer have consistently yielded conflicting results. Several studies have stated that the risk for l ung cancer occurs only in the presence of asbestosis [4, 72-75]. Other st udies have concluded th at asbestosis is not required as a precursor of lung cancer, instea d that a dose-response relationships exists between asbestos exposure and onset of th e disease [76-79]. No consensus of the relationship between asbestosis and lung cancer currently exist. Despite the lack of

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13 understanding between asbestos exposure, as bestosis and lung cancer, what remains clear is that workers exposed to high concentr ations of asbestos are at increased risk of lung cancer either directly from the inhala tion of the fibers or the progression of asbestosis. As in asbestosis, the time of onset of the disease is dependent on the magnitude and duration of asbestos exposure. The latency period for asbestos-related lung cancer has been estimated to be 15 to 40 years [24]. The link between exposure to all asbestos fibe r types and increased rates of lung cancer has not been consistently reported. Amphiboles fibers, such as crocidolite and amosite, are more potent carcinogens than serpentine fibers [29]. Several studies support this claim, and report increased rates of lung cancer in occupational cohorts exposed primarily to amphibole fibers [42, 43, 45, 46]. Investigations of workers predominantly exposed to chrysotile fibers have reported inconsistent findings [44, 49]. Epidemiological evidence is currently able to establish a causal relationship between exposure to amphibole fibers and lung cancer in occupa tional cohorts, but is inconsistent in demonstrating a similar link for chrysotile fibers. Fibers longer than 10 m in length and thicker than 0.15 m are most commonly associated with asbestos-related lung cancer [53]. Studies of the fiber burden of lung tissue consistently identify fibers with sim ilar dimensions [55, 80]. Smaller fibers are removed through phagocytosis and are generally not associated with the onset of lung carcinomas [55, 80].

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14 2.2.3 Mesothelioma Mesothelioma is an extremely rare progres sive malignant carcinoma of the pleura and peritoneal linings associated with occupatio nal asbestos exposure [30, 81]. The National Cancer Institute (NCI) reported that the a nnual incidence rate of the disease among US white males is approximately 10 per million [ 82, 83]. The specific mechanism of action that induces the onset of the disease is unknown, but it is believed that many genetic alterations are involved in the initiation and progression of mesothelioma [63, 84-86]. The presence of asbestos initiates a chroni c inflammatory response resulting in pleura lesions and plaques through a pe rsistent cycle of repair a nd damage. Contact between asbestos fibers and mesothelial cells s timulate the activation of macrophages that subsequently attempt to phagocytize the partic ulate matter [63]. Cytokines released from the macrophages have been documented to resu lt in the generation of hydroxyl radicals and superoxides which potentially cause DNA damage in the form of strand breaks and deletions [22, 63, 84, 87]. Asbestos–related ge notoxicity directly alters the phenotypic expression of tumor suppressant genes, and oncogenes indirectly change the pathways that relate to cell pr oliferation and apoptosis [63, 84, 86]. This process results in the progression of the injuries and the eventual on set of the mesothelioma in extreme cases. The latency period for mesothelioma ranges from 15-40 years [81, 88]. Epidemiological investigations have demonstrated an associ ation between mesothelioma and exposure to amphibole fibers, more specifically crocid olite and amosite [2 3, 29, 89]. Studies attempting to determine the carcinogenicity of chrysotile fibers have reported no elevated risk of mesothelioma in workers exposed ex clusively to chrysotile [47, 90-93]. Increased

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15 rates of mesothelioma in certain occupa tional cohorts exposed predominantly to serpentine fibers have also been published [ 48]. It has been proposed that these observed cases of mesothelioma were not caused by ch rysotile fibers, but instead by tremolite fibers, which are frequently identified in chrysotile samples as a contaminant [97]. Hodgson and Darnton calculated the specific risk of mesothelioma between the three major commercial asbestos types, chrysotil e, amosite and crocidolite, as 1:100:500, respectively [23]. These results, in conjugation with other stud ies’ findings, indicate that any increase of mesothelioma associated with chrysotile fibers is minimal in comparison to amphibole fibers. Additionally, Albin et al. stated mesothelioma is a disease primarily associated with the inhalati on of amphibole fibers [21]. Stanton’s theory states th at fibers greater than 8 m in length and less than 0.25 m in width are commonly linked to the developmen t of mesothelioma [5 2]. More recently conducted studies have identif ied fibers approximately 5 m in length and thinner than 0.1 m in width in tissue samples [53, 80]. Fibers in the range of 5-8 m in length and 0.10-0.25 m in thickness are most commonly associ ated with the onset of malignant tumors. 2.3 Automotive Parts and Components Containing Asbestos The automotive industry historic ally used vast quantities of ACMs during the assembly of passenger cars and light-dut y trucks. The relative abund ance of asbestos made it a readily available and an inexpensive fibrous material source. Additional benefits of asbestos use were its physical and chemi cal properties, which allowed for automotive

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16 parts and components to with stand the stressors produced by the operation of modern vehicles. Three primary groups of automotiv e parts were produced with asbestos: 1) friction materials, 2) gask ets and 3) sealants [94]. 2.3.1 Asbestos-Containing Friction Materials Asbestos fibers have been used as a compone nt of friction products since the early 1900s because of their thermal stability, high fric tion level and durability [94]. An estimated 43,700 metric tons of asbestos were used to manufacture friction materials in 1980 [94]. This broad group of ACMs includes brake lini ngs, disc brake pads and clutches which respectively represent 58.9 %, 6.9% and 33% of produced friction materials [95]. Chrysotile fibers have been predominantly us ed in friction products, and account for 1070% of their total weight [ 95]. Asbestos-containing fricti on materials, primarily brake linings, have been identified as a potentia l occupational health hazard since the 1960s, and have previously been revi ewed in great detail [1]. Th e perception that fibers are liberated from the brake matrix during brak ing, in addition to the servicing of these components, has given rise to allegations of in creased risk of asbestos-related diseases in automotive mechanics. 2.3.2 Asbestos-Containing Gaskets Asbestos-containing gaskets have been used in internal combustion engines as interfaces between solid components and to prevent leak age. The asbestos content of gasket material provides additional flexibility, dur ability and resistance against thermal and chemical degradation. Estimates state appr oximately 9% of all asbestos consumed

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17 annually before 1980 was used to manufacture beater additional (beater-add) gaskets, which have been used primarily in the automotive industry [94]. Made through a continuous paper-making process, beater-a dd gaskets are found in numerous parts and components including carburetors, manifolds, transmissions, exhaust systems and engine heads [93]. Commercial grade beater-add gask ets contain 60-80% chry sotile fibers [94]. Liberation of asbestos fibers during normal ga sket removal and handling is suspected to be small because the fibers are locked in th e gasket matrix [94, 96]. Installation of new beater add gaskets is also believed to release limited quantities of as bestos fibers due to the gasket being precut and spra yed with adhesive sealant [94]. 2.3.3 Asbestos-Containing Sealants Asbestos has been used as filler in as phalt-based automotive undercoating and seam sealant. These products are primarily applied to the undercarriage of vehicles to prevent rusting and inhibit road nois e. Ninety-eight percent of asbestos consumed in the production of asphalt-based undercoating are chry sotile fibers, and constitute less than 10% of the total volume of the material [ 94]. Application and removal of asbestoscontaining sealants are considered relatively sa fe due to the affinity asbestos fibers have for petro-based chemicals. Asbestos fibers directly bind with th e asphalt component of the sealants, and become suspended in the matr ix [94]. Liberation of independent fibers is believed to be limited, and does not re present an occupational health hazard.

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18 2.4 Summary of Epidemiological Studies Twelve epidemiological studies of various study designs that eval uated the risk of asbestos-related cancers in mechanics exposed to asbestos duri ng the servicing of automotive parts containing asbestos have been identified and reviewed. The majority of theses studies focus primarily on workers employed to perform maintenance on brakes and brake components. Tables 1 and 2 cont ain a summary of the epidemiologic studies reviewed within this section. McDonald and McDonald assembled all fata l cases of malignant tumors in Canada between the years 1960 and 1972, in additi on to all fatal cas es of malignant mesothelioma in the United States in 1972, to conduct a case-contro l study designed to elucidate the occupational risk of mesothelioma for multiple industries [4]. The comparison group weas comprised of i ndividuals diagnosed with nonpulmonary malignant tumors from the same hospitals fr om which the cases we re identified[4]. A total of 480 cases and an equa l number of controls were id entified and placed into a specific occupational group based on work hi stories. The relative risk for garage mechanics was calculated at 0.90 (95% Confid ence Interval (CI) 0.39-2.13) [4]. Other occupational cohort’s relative risk range d between 2.6-46.0 [4]. The significant difference between the risks reported for ga rage mechanics and insulators strongly indicates that the mere presence of ACMs in the workplace is inadequate evidence for the establishment of a relationship between poten tial workplace exposures to asbestos and increased rates of malignant mesothelioma [4]. Additional factors, such as intensity of exposure and fiber type, must be assessed to establish a causa l relationship [31].

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19 Teta et al. identified all cases of malignant mesothelioma and other primary malignant pleura tumors reported to the Connectic ut Tumor Registry from 1955 through 1977 to determine high-risk occupations and industries [97]. All subjects that were over 30 years of age at death or diagnosis were us ed for this case-control study with a case to control ratio of 1:3 [ 97]. A total of 220 ma le subjects were chosen from the largest Veteran Administration hospital in the state. Controls were randomly selected from the Connecticut Tumor Registry for the same time period as the cases. Information, including demographics, medical recorders, occupational and exposure histories, were obtained for each test subject who was assigne d a three-digit industrial and occupational code based on the 1970 US Census. The attributab le risk of asbestos exposure for each job code was calculated. Several occupationa l cohorts, such as carpenters and plumbers, were identified to be at a two to fourfold in creased risk. For mechanics, the calculated relative risk was 0.65 (95% CI 0.08-5.53) i ndicating that workers employed in the automotive repair industry are not at increased risk of asbestos-related diseases [97]. Hansen conducted a cohort study of mechanics to determine if increased risk of ischemic heart disease and specific malignant neoplas ms existed within the occupational cohort [98]. The study participants were followed fo r ten years, and were compared to another cohort of skilled workers who were not expos ed to petrochemicals or asbestos. The standard mortality rate (SMR) for all can cers in mechanics was 115 (95% CI: 97-136) [98]. The SMR reported for carcinoma of the bronchus and lungs was 101 (95% CI: 72137) [98]. No SMR was provided for pleura mesothelioma. The results for this study

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20 indicate that mechanic s are not at increased risk of lung cancer. Woitwitz and Rodelsperger reported an incr ease in the incidence of mesothelioma among German mechanics exposed to asbestos [99 ]. This study was based on case reports, and did not provide a description of the size of the population of mechanics at risk or risk estimates for these individuals [5]. Inferen ce of causality cannot be based solely on case reports due to the lack of a comparison group. A follow-up study was conducted to address the original studies weaknesses and to complete the assessment for car mechanics. It was concluded that any evidence of a risk of mesothelioma associated with brake work or employment as a car mechanic did not exist or it was undetectable [100]. A total of 208 mesothelioma cases iden tified from 1975 to 1980 in the Los Angeles County Surveillance Program, the New Yo rk Cancer Registry and 39 Veterans Administration hospitals were evaluated to de termine occupational c ohort at risk of the pulmonary disease [101]. Controls for th is study were chosen from death records obtained from the State of New York and Lo s Angeles County. Referents were matched to controls for date of birth, race, sex, year of death and county of residence or hospital [7]. The next of kin of all study particip ants were interviewed to ascertain general information about previous exposure to asbest os, in addition to nine specific activities associated with potential asbestos exposure including history of performing brake repairs, furnace servicing, building demolition, plumbi ng, installing insulation, production of textiles or paper products [7]. A relative ri sk of 1.0 (95% CI: 0.6-1.6) was determined among individuals historically employed to pe rform brake installation and repair [101].

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21 Pezzotto et al. identified occupational cohorts in Argentine at increased risk of lung cancer through a case-control study [102]. A total of 367 cases diagnosed with lung cancer were matched against controls. Th e referent group was comprised of patients admitted to the same hospital as cases. Age-matched controls were individuals admitted for non-smoking related diseases including trau matic conditions, urol ogical diseases, and other illnesses. All study participants were divided into 16 occupational cohorts based on interviews and work histories. Additionall y, the participants were divided into three categories based on smoking habits. The odds ratios for mechanics were determined to be 1.3 (95% CI 0.7-2.4) for all lung carcinom as, 1.8 (95% CI 0.9-4.2) for squamous cell and 1.1 (95% CI 0.5-2.7) for adenocarcinoma [102]. The results of this study provide additional support against a relationship between asbestos exposure during the servicing of automobiles assembled with ACMs and increased rates of cancer. The Institute of Epidemiology and Clinical Research in Spain conducted a case-control study to evaluate the asso ciation between occupational asbestos exposure and mesothelioma [103]. Test subjects were recruited from residents of the Spanish provinces of Barcelona and Cadiz. Indivi duals identified through hospital records to have been recently diagnosed with pleura me sothelioma were selected as cases [103]. Two groups of controls were selected for this study [103]. The first referent group consisted of a random sample of the population which was used to determine the age, sex and municipality of residence for the control series. Patients with the same age and sex distribution were then selected from th e participating hospita ls [103]. The study

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22 population consisted of 132 c onfirmed mesothelioma cases and 257 matched controls. A complete occupational history was obtained fo r each study participan t, and reviewed by a panel of industrial hygienist that estimated asbestos exposur e. A probability score based on the occupational history and exposure esti mate was assigned to each test subject ranging from 1 (possible exposure) to 4 (sure exposure) [103]. J obs with an average score greater than 1 (>1) were considered at in creased risk of exposure to asbestos [103]. The relative risk for mechanics was determin ed to be 0.62 (CI 95% 0.17-2.25) [5]. Based on this estimate, no increased risk of mesothelioma among Spanish mechanics was determined. In 2001, a meta-analysis of six previously published case-control studies was conducted to determine the relative risk of malignant mesothelioma for automotive mechanics [5]. The original studies consistently reported a lack of an asso ciation between employment in the automotive repair indust ry and increased ri sk of mesothelioma. Approximately 1,500 malignant mesothelioma cases were assemble d from the six case-control studies and a relative risk of 0.90 (95% CI 0.66-1.23) was calculated [5]. The author concluded that the meta-analysis clearly demonstrates that automotive mechanics are not at increased risk of mesothelioma as a result of expos ure to asbestos during the maintenance of friction materials [5]. This study provided extensive evidence ag ainst an association between historical employment in the automo tive repair industry and increased asbestosrelated mesothelioma. Goodman et al. conducted a meta-analysis to evaluate the risks of lung cancer and

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23 mesothelioma among mechanics potentially exposed to asbe stos during the maintenance of brakes [6]. Published epidemiological st udies investigating rate s of asbestos-related cancers were identified and categorized by the authors based on their quality and applicability. The re lative risk for mesothelioma for studies belonging to the highest quality tier was 0.81 (95% CI 0.52-1.28) [6]. This group was determined to be at statistically significant increas ed rate of lung cancer, but when adjusted for smoking the relative risk estimate was 1.09 (95% CI 0.921.28) [6]. These findings indicate that mechanics are not at increased risk of me sothelioma from asbestos exposure while servicing asbestos-containing brakes. Hessel et al. conducted a casecontrol study to determine th e risk of mesothelioma associated with brake work [7]. Study part icipants were identifi ed through the National Cancer Institute’s database and divided into eight indepe ndent occupational groups. The authors decided that white males with genera lly reliable work hist ories represented the most appropriative study popul ation. Two independent assess ments were conducted. The first analysis compared cases that conducted brake work either occupationally or nonoccupationally against controls that did not conduct any form of brake work. A second analysis was conducted to disti nguish occupational from nonoccupational brake work. The odds ratios for mesothelioma among insulators and shipbuilders were 3.38 (95% CI 2.20-5.17) and (6.04 95% CI 3.74-9.75), respectively [7]. For individuals potentially exposed to asbestos during e ither occupational or nonoccupational brake work, no increased risk of mesothelioma wa s reported [7]. The odds ratio for workers performing brake work exclusively was 0.74 (95% CI 0.35-1.54) [7].

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24 Laden et al. critically assessed all ep idemiological studies of lung cancer and mesothelioma risk among male automotive mechanics [8]. A total of forty-nine studies were reviewed, and represent thousands of cas es of diseases, in addition to hundreds of thousands of workers potentially exposed to as bestos [8]. Due to the vast number of study designs reported in this review, no attemp t was made to calculate new estimates for asbestos-related diseases. The authors conc luded no increase risk of lung cancer or mesothelioma was identified w ithin the occupationa l cohort when the individual studies where examined in an aggregate and consiste nt pattern, and that ev idence of asbestos exposure concentrations capable of acting as a carcinogen, were not identified in reviewed industrial hygiene survey s of brake repair work [8]. A comprehensive review of multiple epidem iological studies and exposure assessments associated with potential occupational and non-occupational exposure to asbestos from brake linings and pads was pe rformed [15]. The data coll ected for this study indicated that brake mechanics were not exposed to Time Weighted Average (TWA) concentrations above the occupational exposure limits (OEL), and that no increase risk of mesothelioma, asbestosis or lung cancer in th is cohort could be attr ibuted to asbestos exposure [15]. Additional evidence against increased rates of asbestos-related diseases was reported within 20 epidemiological studi es investigating workers employed in the friction product manufacturing industry. No incr eased rates of diseases were observed in these occupational cohorts that had documented exposur e to chrysotile fiber concentrations 10 to 50 times greater than those of brake mechanics [15].

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25 The twelve reviewed epidemiological inves tigations represent a broad range of study designs conducted internationally to determine the risk of as bestos-related diseases in mechanics. The results of these studies consis tently indicate that mechanics are not at an increased risk of asbestos-related cancers due to the inhalation of asbestos fibers liberated during the servicing of automotive ACMs.

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26 Table 1: Summary of Reviewed Epidemiological Studies Author Study Design Description & Purpose Results McDonald (1980) Case-Control Purpose of the study was to determine occupational cohorts at risk of mesothelioma. Relative Risk (RR) of mesothelioma for mechanics: 0.90 (95% CI 0.39-2.13) Teta (1983) Case-Control Designed to elucidate high-risk occupations and industries. RR of mesothelioma for mechanics: 0.65 (95% CI 0.08-5.53) Hansen (1989) Cohort Intent of study was to determine if a cohort of mechanics followed for 10 years were at increased risk of ischemic heart disease and specific malignant neoplasms. Standard mortality rate (SMR) for mechanics for all cancers: 115 (95% CI: 97-136); SMR for carcinoma of the bronchus and lungs: 101 (95% CI: 72-137). Woitwitz (1991 & 1994) Case Series Investigates a perceived increased rate of mesothelioma in German mechanics exposed to asbestos. No risk estimate reported due to lack of comparison group; Study reevaluated in 1994 and no increased risk of mesothelioma identified Spirtas (1994) Case-Control Study designed to determine occupations at risk of mesothelioma. RR of mesothelioma for mechanics brake servicing: 1.0 (95% CI: 0.6-1.6) Pezzeto (1999) Case-Control Study designed to determine occupational cohorts at increased risk of lung cancer from exposure to asbestos. Odds Ratios of lung cancer for mechanics: 1.3 (95% CI 0.7-2.4) for all lung carcinomas,1.8 (95% CI 0.9-4.2) for squamous cell, 1.1 (95% CI 0.5-2.7) for adenocarcinoma. Agudo (2000) Case-Control Study conducted to evaluate the association between occupational asbestos exposure and mesothelioma in specific worker groups. RR of mesothelioma for mechanics: 0.62 (CI 95% 0.17-2.25) Wong (2001) Meta-Analysis Six previously published casecontrol studies were assembled to conduct a meta-analysis to determine the risk of mesothelioma for mechanics engaged in the servicing of asbestos-containing brake parts. RR of mesothelioma for mechanics: 0.90 (95% CI 0.66-1.23) Goodman (2004) Meta-Analysis Epidemiological studies were evaluated and assembled into a meta-analysis to determine the risks of asbestos-related cancers among mechanics. RR for mesothelioma: 0.81 (95% CI 0.52-1.28) RR for lung cancer when adjusted for smoking: 1.09 (95% CI 0.92-1.28) Hessel (2004) Case-Control Study conducted to elucidate the risk of mesothelioma in workers performing removal and replacement of asbestoscontaining brakes. RR for mesothelioma: 0.74 (95% CI 0.35-1.54) Laden (2004) Review of Published Epidemiological Studies Forty-nine studies investigating the risk of asbestos-related cancers in mechanics were critically reviewed. No risk ratios were provided, authors concluded that when the literature is reviewed in a consistent pattern no increased risk of lung cancer or mesothelioma was identified for mechanics. Paustenbach (2004) Review of Published Epidemiological Studies and Exposure Assessments Comprehensive review of published literature investigating occupational and nonoccupational exposure to asbestos during the servicing of brake components. No risk ratios provided, but authors concluded that no increased risk of asbestos-cancer was identified based on the exposure assessments and epidemiological studies.

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27 Table 2: Summary of Epidemiological Studi es of Case-Control and Cohort Designs Author Year Design Exposure definition Sources of Cases Comparison Group McDonald 1980 Case-Control Garage workers Hospital Recorders Non-pulmonary cancers Teta 1983 Case-Control Automobile repairs, related services Connecticut Tumor Registry Connecticut decedents Hansen 1989 Cohort Repair of motor vehicles Danish Cancer Registry All other occupations combined Woitwitz 1994 Case-Control Motor vehicle repair workers Not Specified Lung resection patients and population controls Spirtas 1994 Case-Control Occupations at risk of asbestosrelated cancer New York Cancer Registry, Los Angeles County Cancer Surveillance Program, Veteran Administration Hospitals Deaths from causes other cancer, respiratory disease or violence Pezzeto 1999 Case-Control Occupations at risk of asbestosrelated cancer Argentine Hospital Records Patients with nonsmoking related diseases including traumatic conditions, urological diseases, and other illnesses Agudo 2000 Case-Control Mechanics, motor vehicles Hospital Recorders Patients with nonasbestos-related conditions Hessel 2004 Case-Control Mechanics performing brake work National Cancer Institute database Deaths from causes other cancer, respiratory disease or violence 2.5 Exposure Assessments of Automoti ve Asbestos-Containing Materials The literature review of pub lished and governmental documen ts yielded several studies that directly or indirectly assessed the air borne asbestos levels associated with the servicing and handling of automotive ACMs. From these studies, only the exposure assessments that characterized asbestos con centrations during the removal or replacement of ACMs using standard workplace practices were summarized. Other studies that evaluated control methods designed to preven t asbestos liberation are not presented in this review because their findings do not represent conditions experienced by automotive

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28 mechanics under normal work conditions. Tables 3 and 4 provide summaries of all studies discussed in this section. 2.5.1 Asbestos-Containing Brakes Plato et al. constructed a predictive model base d on data from international literature and quantitative asbestos measurements performed from 1976-1988 in Swedish car repair workshops to calculate cumulative asbestos exposure from friction materials [109]. Additionally, five lung functi on variables were assessed to characterize exposureresponse relationships. It was concluded that the aver age cumulative exposure was estimated to be 2.6 f-yr/cc indicating that mechanics are exposed to a relatively low overall asbestos exposure [104]. No signi ficant reduction in lung function was observed within mechanics exposed to low level asbestos associated with the maintenance of brakes and clutches [104]. A study was conducted in Australia in 1996 to ev aluate the concentrations of chrysotile fibers mechanic are exposed to during the ma intenance of vehicles assembled with ACMs [12]. Three primary operations were examined : 1) servicing of friction materials, 2) brake bonding and 3) gasket processing. Nine automotive service facilities were utilized in this assessment, and a total of 68 air sa mples were collected. Transmission Electron Microscopy (TEM) analyses of the samples revealed a range of <0.01-0.07 chrysotile fibers per cubic centimeter (c-f/cc) [12]. Th e authors note that the majority of fibers identified in these samples were foresterite, a non-asbestiform silicate mineral produced when chrysotile fibers are exposed to high temperatures [12]. Fiber concentrations

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29 reported in this study were well below th e OSHA PEL and the current Australian occupational exposure limit for chrysotile fibers of 1.0 f/cc. Weir et al. conducted an exposure assessment ai med at determining the airborne asbestos concentrations and total particulate matter associated with the replacement of brake drums and the arc grinding of asbestos brak e pads [13]. Brake drum inspections and replacements were performed on three vehi cles using standard workplace practices, which included test sessions where compressed air was used to remove accumulated dust. The second phase of the study investigated the le vels of total dust and asbestos generated during the arc grinding of asbestos-contai ning brake pads. An unspecified Scanning Electron Microscopy (SEM)/Transmission Electron Microscopy (TEM) method was utilized for bulk sample analyses of collect ed dust samples. The majority of samples contained nonfibrous material with little, if any, asbestos or non-as bestos fibers being detected. This supports the theory that asbe stos fibers are broken down or changed into nonfibrous materials by the mechanical and thermal stressors placed on the brake pads during normal braking operations. Results from this section of the study indicate that mechanics are exposed to quantities of as bestos fibers that are below current Occupational Exposure Limits [13]. The second phase of the study focused on the airborne asbestos levels li berated during arc grinding of asbestos brake pads. Two different methods were applied for the arc grinding. The first method followed the manufacturer’s recommendations for use of the grinding equipment, while the second technique was performed at a quicker ra te and did not follow the manufacturer’s directions. The PCM TWA concentration for personal samples was 0.03 f/cc with the

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30 TEM analysis reporting a few bundles longer than 5 m [13]. The highest PCM TWA observed in area samples was 0.02 f/cc [13]. Th e authors concluded that limited, if any, quantities of chrysotile fibers are liberated wh en the equipment is used in a manner that is consistent with the manufacturer’s operating instructions [13]. Blake et al. performed an exposure assessment aimed at elucidating the airborne asbestos fibers generated during the maintenance of asbestos-containing brakes [14]. Four identical automobiles were fitted with repla cement asbestos brake shoes and driven for a prescribed distance to produce wear on the ne w brake components. Six independent test sessions were conducted in which one of the following tasks were performed: 1) the repair and replacement of brake shoes, 2) filing of new replacement asbestos-containing shoes for installation purposes, 3) sanding of new shoes to remove the outermost wear surfaces or 4) arc grinding of new shoes to match companion brake drum’s circumstance [14]. Standard workplace practices were applied to ensure that the study was representative of conditions normally encount ered by mechanics during the servicing of brakes. Personal and area air samples were collected and subsequently analyzed via NIOSH Method 7400 (PCM) and Method 7402 (TEM). Additionally, bulk samples of the brake were analyzed using EPA Method 600 [Polarized Light Microscopy (PLM)]. The average PCM TWA fibers levels reported during the six test se ssions ranged from 0.0069 to 0.0450 f/cc [14]. The authors conclu ded that replacement of asbestoscontaining automotive brake shoes, including blowing, filing and sanding, did not result in asbestos concentrations above the OSHA PEL. Additional information about the study design and results about this exposure assessment can be located in Section 3.5

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31 Ten previously published asbestos monitoring studies were identified and assembled to characterize retrospective asbe stos exposures for brake mechanics under various working conditions [1]. A total of 162 8-HR Ti me Weighted Average (TWA) asbestos concentrations from the late 1960s to 2003 where identified from the ten original studies. Airborne asbestos levels were evaluated and compared based on the location and time period of sampling, servicing methodology and type of vehicle receiving brake maintenance [1]. Analysis of a subset of 141 samples collected dur ing the servicing of light trucks and automobiles between 1968 and 1996 reported an average TWA of 0.05 f/cc with a range of 0.004 to 0.28 f/cc [1]. Fi ber concentrations corre lated to maintenance activities performed in the late 1980s and 1990s were signi ficantly lower than levels observed in samples collected in the 1970s a nd early 1980s [1]. The overall 8-HR TWA for all samples (n-162) was 0.04 f/cc [1]. The findings from the historical assessment of asbestos levels during the servic ing and repair of brakes conc luded that airborne asbestos concentrations were consistently below the current OSHA PEL, in addition to enforceable standards in the 1970s through 1990s [1]. The concentration of airborne asbestos experienced by mechanics were 10-100 times lower than exposure levels reported in workers involved in the ma nufacturing of friction products [1].

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32 Table 3: Summary of Exposure Assessmen ts Associated with the Servicing of Automotive Asbestos-Containing Brake Components Author Task Studied Study Design Results Plato (1995) Servicing of Friction Materials Predictive Model Average cumulative exposure estimated to be 2.6 f-yr/cc Yeung (1996) 1. Brake Servicing 2. Brake Bonding 3. Gasket Processing Industrial Hygiene Survey Chrysotile fiber concentrations ranged <0.01-0.07 f/cc Weir (2001) 1. Brake Drum Replacement 2. Arc Grinding of Brake Shoes Workplace Simulation Using Actual Work Practice, Conditions and Setting Fiber concentrations during the replacement of brake drums ranged 0.05-0.9 PCM f/cc Highest PCM TWA observed during arc grinding was 0.03 f/cc Blake (2003) 1. Brake Shoe Repair and Replacement 2. Filing of New Brake Shoes 3. Sanding of New Brake Shoes 4. Arc Grinding of New Brake Shoes Workplace Simulation Using Actual Work Practice, Conditions and Setting Average PCM fibers levels ranged from 0.0069 to 0.0450 f/cc during all workplace activities Paustenbach (2003) Brake Maintenance Historical Analysis of Published Data Fiber concentrations ranged from of 0.004 to 0.28 PCM f/cc 2.5.2 Asbestos-Containing Gaskets Liukonen and Weir assessed asbestos concen trations during the dismantling and cleaning of a medium-duty diesel e ngine containing asbestos ga skets (2005). Bulk sample analyses established the presence of asbestos fibers within 28 of the 33 removed gaskets in concentrations ranging from 15-70% [16]. Only one area sample (n = 29) collected

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33 during this test was above the limit of det ection (LOD) indicating th at the potential for fibers to be liberated is almo st nonexistence [16]. Airborne le vels of asbestos fibers were reported to be approximately 10% of the OSHA PEL [16].. Paustenbach et al. evaluated the exposure to asbestos dur ing the removal of automotive exhaust systems containing asbestos gaskets [17]. This study was designed to simulate the work and conditions associated with 1950s through 1970s. A total of 16 pre-1974 vehicles were identified to contain their original exhaust system s. Two professional mechanics removed the exhaust systems, and extracted the exhaust gaskets and linings. Twelve of the removed gaskets contained ch rysotile fibers betw een 9.5 to 80.1% [17]. Only 28% of the personal samples analyzed by TEM were identified to contain asbestos fibers. The authors concluded that mechanic s are exposed to an 8-Hour (8-HR) TWA of 0.01 f/cc when performing gasket removal usin g standard workplace practices common to the mid to late 20th century [17].

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34 Table 4: Summary of Exposure Assessmen ts Associated with the Removal of Automotive Asbestos-Containing Gaskets Author Task Studied Study Design Results Liukonen and Weir (2005) 1. Disassembly of medium duty diesel engine 2. Removal of asbestos-containing gaskets Workplace Simulation Using Actual Work Practice, Conditions and Setting Over 90% of reported PCM concentrations were below the LOD Observed asbestos concentrations were approximately 10% of current OSHA PEL Paustenbach (2005) Removal of exhaust gaskets Workplace Simulation Using Actual Work Practice, Conditions and Setting Asbestos was detected in only 28% of samples analyzed through TEM The 8-HRTWA for mechanics removing exhaust gaskets using standard workplace practices from the 1950s1970s was 0.01 f/cc 2.5.3 Asbestos-Containing Sealants Mechanics involved with the restoration of vi ntage or wrecked vehicles routinely must remove undercoating and seam sealant to perform additional body work or frame alignment. Commonly used methods to rem ove the coatings include hand scrapping and the use of pneumatic chisels. Despite the po tential for asbestos fibers to be liberated during both techniques, no studies investigating the airborne asbestos concentrations generated during the removal of these produc ts were identified dur ing the literature review.

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35 2.6 Summary Asbestos is a generic term referring to a group of silicate fibrous minerals used historically in the production of commercial products. Differences in the physical and chemical composition of the various fiber types result in disparit y in their ability to act as a carcinogen. Other factors, including fibe r dimensions, exposure concentration and duration of exposure, attribute to the onset of asbestos-relat ed diseases. Asbestosis, lung cancer and mesothelioma are the three di seases most commonly associated with occupational exposure to asbestos. Dose-re sponse relationships have been theorized between asbestos exposure and the development of these diseases. Cumulative lifetime asbestos exposure exceeding the no-effect e xposure thresholds discussed in Section 2.2 for asbestosis, lung cancer and mesothelioma are believed to increase the risk of these diseases. The historic use of asbestos-containing mate rials during the assembly of automobiles has resulted in allegations of elevated risk s of lung cancer and mesothelioma within automotive mechanics. Numerous epidemiological studies have consistently concluded that no increased risk of asbestos-related cancers exist within workers historically employed to service asbestos -containing automotive compone nts (Table 1). Exposure assessments have provided additional suppor t against a relations hip by repeatedly reporting airborne asbestos levels belo w the OSHA PEL during the servicing and handling of asbestos-containing brakes and gaskets (Tables 2 and 3). No epidemiological studies addressing the risk of asbestos-related diseases asso ciated with the maintenance of automotive components beyond asbestos-cont aining brakes were identified during the

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36 literature search. The absence of epidemio logical data, in addition, to limited exposure data for automotive ACMs has allowed for th e proliferation of the perception of an increased risk of lung cancer and mesothelioma in automotive mechanics.

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37 CHAPTER 3.0 METHODS 3.1 Assembly and Evaluation of Exposure Data The data set utilized in th is study consisted of exposure data assembled from four independent exposure assessments conducte d to characterize the asbestos fiber concentration generated duri ng the servicing of specific automotive ACMs. Concerns regarding the use of previously existing data include fragmented information, data with limited external validity, a nd researcher bias or poor study designs [105-107]. As previously existing data sour ces are frequently used in the risk assessment process, several methods have been developed to eval uate the quality of existing exposure data [106-108]. Inclusion of the collected exposure data in to the current study occurred only after an evaluation of its quality based on methodologi es adapted from multiple studies [105-107, 109]. Table 5 provides a summary of the compon ents assessed in the analysis of quality of the collected exposure data. Raw data, fi eld notes and calibration records for sampling instrumentation were obtained from the orig inal researchers, and evaluated for quality, consistency and applicability to the purpose of the current study. Multiple interviews were held with the original research team responsible for the collection of the exposure

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38 data. These conversations were aimed at obtaining information beyond what was contained in the field notes, raw data and other records asso ciated with the four exposure assessments. Table 5: Guidelines Used to Evaluate Data for Inclusion into Risk Analysis 1. Evaluation of the Completeness of Data 2. Clear Definement of the Original Purpose of Study 3. Study Design 4. Air Sampling Strategy 5. Analysis Methodology 6. Consistency with Other Studies (Comparison of the analysis meth odologies, averaging times, study design) 7. Applicability to Current Study Appraisal of the completeness of exposure data was the first step in evaluating the quality of the assembled exposure data. Table 6 defines the core information utilized to determine the completeness of the exposure da ta. The framework adapted to ensure that the exposure data, including the original fiel d notes, raw data and laboratory reports, in addition to instrumentation and calibration reco rds, were complete and capable of being applied for the purpose of the current study is illustrated in Table 7 [107, 108].

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39 Table 6: Definitions of the Core Inform ation Used for Assembled Exposure Data* Core Information Category Definition Workplace Description of the work area in which the worker's activities are carried out. Study Protocol Clear definement of the original purpose and approach used to collect exposure data. Measurement Strategy The air sampling approach used to obtain the quantitative exposure measurements. Measurement Procedure The methodology utilized for collection and analysis of air samples including storage, chain-of-custody and transportation. Results The quantitative airborne concentration of chemical agent in the workplace. *Adapted from [108]. Table 7: Framework Used to Evaluate the Completeness of the Core Information* Core Information Evaluated Components Good Quality Moderate Quality Poor Quality Workplace Description of the work area Study Protocol Definement of the Original Purpose Definement of the Sampling Strategy Measurement Strategy Type of survey (representative, worstcase, other) Measurement Procedure Sampling Date Sample ID Sampling Device Type of sample Sampling Time Sampling Duration Exposure Duration Analytical Methods Instrumentation Calibration Recorders Results Measured Concentration Units Used Sample Status *Adapted from [107,108].

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40 The completeness of the core information was based on three quality le vels defined as 1) Good, 2) Moderate or 3) Poor. These para meters have been adapted from previous studies [107,108] and are defined as: 1) Good : All core information was present. 2) Moderate : Information was available for evaluation with some aspects about the variability and precision of the data remaining undefined. 3) Poor : A minimum level of information wa s available providing a fragmented assessment of the conditions and setti ng under which the data was collected. Data were deemed unacceptable, or incomplete, if one or more of the evaluated components could not be classified at the minimal quality level of poor [107]. This framework is a qualitative technique designe d to establish the completeness of the individual data sets for inclusion into th e current study based on the rankings the core information received and the res earcher’s professional judgment. The final step of the quality evaluation of the exposure data consisted of comparing the methodologies, sampling strategies and results of the studies to ensure consistency and applicability towards the current risk analys is. Sections 3.2 thr ough 3.4 provide in-depth descriptions of the unpublished studies a ssembled for the current study. The peerreviewed exposure assessment has been re viewed in Section 3.5, in addition to a summary of the results being located in Sect ion 2.5.1. The core information defined and evaluated in Tables 5 and 6 have served as the focal points for these reviews to ensure that the independent studies use compatib le study designs, sampling strategies and

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41 analytical techniques. The summaries of th e individual exposure assessments have been based on the original field notes, raw data a nd laboratory reports, instrumentation and calibration records, in addition to interviews w ith original researchers. The results of the quality and completeness evaluation of the exposure data are located in Appendix A. 3.2 Exposure Assessment I: Asbestos-Containing Gaskets The purpose of this assessment was to evalua te the airborne asbestos levels generated during the removal and replacement of asbestos -containing gaskets. This investigation was conducted by staff of Clayton Group Services in 1998 and has been publication as of July 2006 in Regulatory Toxicology and Pharmacology [18]. The following section describes the design and execution of the st udy including the setting of the assessment, sampling strategy and activities performed by the mechanic. 3.2.1 Test Location and Environmental Setting This assessment was conducted in a fully e quipped and functioning automobile service facility located in Detroit, Michigan. The specific workspace used for this testing was a 2-bay automotive service garage with rollup doors on both ends of each bay. Interior dimensions of the service garage measured 37.5 feet (ft) by 29-f t with exposed roof decking at 17.8-ft. The general layout of this garage is shown in Fi gure 1. The north wall of this garage angled into a hallway that lead to offices a nd the main shops located to the north. Barriers and isolation de vices were not utilized to s eal the test area from this section of the service facility due to its distance from the act ual test area and to aid in maintaining standard environmental conditions. Area air samples were collected in this

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42 region of the facility to establish the absence of dust migration from external sources. A warehouse used for storage purposes was located adjacent to the north wall of the garage. Existing materials and equipment were left insi de the automotive service facility and the connecting hallway during the te sting. This included, but is not limited to, the parts bins, used tires, compressed gas bottles, trash receptac les, tire inflation sa fety cage and to two fully functional hydraulically op erated automobile lifts. Vehicles receiving service entered from the west side and exite d from the east side or vice versa. The ventilation system located within the 2bay automotive service garage was shutdown during the three days of testing. Testing wa s performed in an unventilated facility to facilitate a “worst case” scen ario. Also, the rollup door s remained closed during each test session. The four rollup doors were opened between test sessions to remove airborne particulates generated during the previous test sessions. 3.2.2 Test Vehicles Vintage automobiles utilized in this experi ment were selected based on 1) the likelihood of encountering asbestos-containing gaskets an d, 2) the availability of new replacement asbestos-containing engine gaskets. The tested vehi cles included a 1974 Chevrolet Malibu, 1978 Chevrolet pickup truck and a Ford 390 cubic inch V-8 engine. Table 8 contains a brief description of the vehicl es and engines utiliz ed in this study.

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43 Table 8: Make and Model of Vehicles and Engines Used in the Gasket Tests Automobile/Engine Description of Engines 1974 Chevrolet Malibu Small Block Engine, 350 Cubic Inch V-8 1978 Chevrolet Pickup In-line Engine, 250 Cubic Inch 6 Cylinder Ford Thunderbird 390 Cubic Inch V-8 (Loose Engine) Figure 1: Automotive Servicing Fa cility Used During Gasket Test *Numerical values represen t locations of area samples and correspond with Table 10 Lift Workbench Parts Cleaner Warehouse Offices & Shops Warehouse Roll up Doors Outdoors Ceiling Height 17’9” Engine Test Vehicle 3 6 5 1 9 4 2 7 8 Outdoors Roll up Doors Air Compressor

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44 3.2.3 Mechanic’s Activities, Equipment and Tasks The professional automotive mechanic was Automobile Service Excellence (ASE) certified, and was instructed to perform ga sket removals or installations using his standard operating procedures (SOP). For th is reason, he was allowe d to select all tools and equipment to ensure limited interference w ith his job practices. Tools utilized during this experiment included wrenches, screwdri vers, scrapers and hammers, in addition to pneumatic powered ratchets for the remova l of bolts and nuts. The mechanic was directed to wear a normal work uniform to further ensure that cumbersome or uncomfortable garments would not interfere with his normal activities or habits. Five individual test sessions were conducted to assess the levels of airborne asbestos fiber generated during the servicing and handling of asbestos-containing gaskets. Three test sessions focused first on the disassembling of an engine and the removal of gasket remnants from engine receiving surfaces a nd loose parts. The two remaining test sessions involved the installment of new as bestos-containing gasket s and reassembly of the engine. Table 9 summarizes the indi vidual activities perf ormed during testing. During the gasket removal test sessions, the mechanic first removed all engine components that covered or otherwise held th e target gaskets. Many of these gaskets came off intact leaving gasket residue on the metal mating surface. Bulk samples of the removed gaskets were obtained for subseque nt analysis. The mechanic next scraped away gasket residue using a wide blade putty knife, sometimes assisted with a rubber hammer. Loose parts, such as engine head s and manifolds, were next immersed into a

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45 water bath cleaner and washed using an Arm & Hammer brand Aqua Works Cold Cleaning Solution, before being burnished using a rotary 1-inch knot type wire end brush. The end brush was powered by a hand held drill motor operated from 90 PSI line pressure. To aid in the gask et and other residue removal process, the mechanic sprayed the parts with a non-chlorine containing solv ent dispersed from an aerosol spray can. This solvent contained; xylen es, aliphatic petroleum distillates, and acetone, with a compressed carbon dioxide propellant. When cleaning the surfaces of fixed, nontransportable parts such as e ngine blocks, the mechanic u tilized scraping, powered wire brushing and solvent spray, however no aqueous wash occurred with the fixed parts. This process continued until all gasket remnants were removed from the loose parts and engine block. Reassembly of the engines and installation of new asbestos-containing gaskets occurred in two test sessions. The mechanic chose to initially apply an adhesive glue strip to previously cleaned receiving surfaces on the en gine block. This step ensured that the new gaskets would be securely held in place as the loose engine components were reattached. New asbestos-containing gasket s were laid on the engine receiving surface and the respective engine part was lowered in to place. Bolts and other fasteners were tightened to secure a seal. The mechanic was responsible for cleaning th e work area after each test session. When conducting cleanups, the mechanic utilized a hand held straw broom, a push broom and a dust pan. Debris on the work surfaces and floor was swept up and disposed of into

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46 available trash containers. Air sampling continued during this time period and ended after the mechanic was satisfied with the condi tions of the garage and work area. Figures 2 through 6 demonstrate tasks performed by mechanic. Table 9: Activities Associated with the Removal and Replacement of AsbestosContaining Gaskets Task Description Engine Disassembly and Removal of Asbestos-Containing Gaskets 1. Vehicle/Engine moved into service facility 2. Vehicle placed on rack 3. Engine partially disassembled 4. Gaskets removed 5. Dry scrape and brushing of engine receiving surfaces to remove gasket remnants 6. Loose engine components placed in water bath; washing of parts 7. Rotary brush to remove gasket remnants Engine Reassembly and Installation of Asbestos-Containing Gaskets 1. Placement of adhesive on engine receiving surfaces 2. Placement of gasket into position 3. Placement of loose engine components 4. Fasteners tightened; loose parts secured to engine block Cleanup of Service Facility 1. Sweeping of all debris into dust pan 2. Placement of debris into trash bin

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47 Figure 2: Mechanic at Workbench Cleaning Intake Manifold Mating Surface Using Powered Rotary Wire Brush Figure 3: Mechanic at Bench Using Putty Knife and Mallet to Remove Intake Manifold Gasket Remnants

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48 Figure 4: Mechanic Cleaning Manifold in Parts Washer Figure 5: Mechanic Using Air Powered Ro tary Wire Brush to Clean Dry Engine Block Upper Surface

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49 Figure 6: Mechanic Installing Intake Manifold to Engine 3.2.4 Air Sampling and Analysis Personal and area samples were collected to estimate the exposure the mechanic and hypothetical bystanders would enc ounter during the previously described work activities. The equipment utilized for collecting persona l samples consisted of battery powered portable air pumps Ametek Model 1 that drew air at metered flowrates, nominally 2.0 to 2.4 liters per minute (lpm), through 25-mm diam eter, cassette mounted, mixed cellulose ester (MCE) membrane filters. The cassettes were placed within the mechanic’s breathing zone. Figure 7 illustrates placement of personal air samples. The filters which were placed atop the mechanics right shoulde r were of 0.8 micron (m) pore size, while those placed atop his left shoulde r were of 0.45 m pore size.

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50 Figure 7: Mechanic Wearing Two Personal Sa mplers during Cleaning of Intake Manifold with a Rotary Brush Area samples were collected using line ope rated vacuum pumps, Gast Manufacturing, Inc., at metered flowrates nominally 10 lpm. These pumps drew air through 25 millimeter (mm) diameter cassettes with 0.45 m pore size mixed cellulose ester (MCE) membrane filters. The flowrates for all air sampling systems were measured and documented prior to and after completion of each test. A primary standard flow calibrator, Bios Internationa l Model DC-1 was used for these airflow measurements. Nine indoor area air samples (n = 9) were collected during eac h test session at breathing zone heights (5-ft above floor) either bei ng supported by portable stands or the test vehicles. Area samples were located; on either si de of the test vehicles (or engine), at the four corners of the test gara ge, on the work bench used for wire brush cleaning and down the connecting hallway. These samples were pl aced at distances rang ing from 0 to up to 50-ft from the test vehicle. Table 10 summa ries the location of ar ea samples during each test session. Area samples locations are represented on Figure 1.

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51 Table 10: Location of Area Samples within Service Facility Sample Number Location 1 Southeast corner (SE Corne r); 22 Feet SE of Vehicle 2 Southwest corner (SW Corne r); 19 Feet SW of Vehicle 3 Northwest corner (NW Corne r); 15 Feet NW of Vehicle 4 Northeast corner (NE Corn er);18 Feet NE of Vehicle 5 Intermediate Hallway; 30 Feet NE of Vehicle 6 Distant Hallway; 50 NE of Vehicle 7 Driver's Side Fender 8 Passenger's Side Fender 9 Work Bench; 9 Feet S of Vehicle Sample approximate locations are represented on Figure 1. Samples were analyzed using Phase Cont rast Microscopy (PCM) and Transmission Electron Microscopy (TEM). The PCM analysis followed the National Institute of Occupational Safety and Health (NIOSH ) Method 7400 [110], which counts fibrous particles exhibiting a three to one length to width ratio of asbe stos and non-asbestos origins. Additionally, the optical limitations of the phase contract microscope restrict its resolution capabilities to fibers wider than 0.25 micrometer (m). NIOSH Method 7400 counts fibers 5m and longer. Use of this method satisfies the requirements of the OSHA standards for measuring asbestos. PCM analysis of air samples counts all fibrous structures including non-asbestos fibers that meet the dimensional criteria. There ex ists the potential for such analysis to yield airborne fiber concentration data which exceeds the actual airborne asbestos concentration. In settings, such as automob ile repair shops, cellulose fibers, long thin metal fragments from power brushing activit ies and cotton fibers often appear in air

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52 samples taken during work of the type that is the subject of this res earch. For this reason, additional analysis of air samples was performed using TEM, following NIOSH Method 7402 [111]. This analytical method measures fibers 5m or longer and wider than 0.25m, and allows development of an asbestos -to-total fiber ratio. This ratio is then multiplied by the airborne fiber concentration generated using the PCM analysis, yielding an asbestos fiber count known as Phase Cont rast Microscopy Equiva lent (PCME). This asbestos fiber count may be used for comparison against occupational exposure limits (OEL) such as the OSHA PEL or NIOSH R ecommended Exposure Limits (REL). Table 11 illustrates the calculation of PCME based on the PCM and TEM results. Table 11: Computational Formula Used to Determine Phase Contrast Microscopy Equivalent (PCME) Part 1: Asbestos Fiber Ratio = (No. of Asbestos Fibers Counted by TEM) (Total No. of Fibers Counted by TEM) Part 2: PCME = PCM Fiber Concentration (f/cc) Asbe stos Ratio PCME = Estimated Asbestos Fiber Concentration (f/cc) 3.2.5 Bulk Sampling and Analysis Asbestos contained in gaskets was determ ined by Polarized Light Microscopy (PLM) using the Environmental Protection Agency (EPA) Method 600/R93/116 [112]. PLM is capable of identifying the individual component s of a sample and estimating their relative concentration within the samp le’s matrix. Additionally, th e specificity of the method allows for the differentiation of the indi vidual serpentine and amphibole fibers.

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53 3.3 Exposure Assessment II: Asbestos-Containing Seam Sealant The original purpose of this exposure asse ssment was to characterize the asbestos concentrations associated w ith the removal of asbestos-c ontaining seam sealants using hand tools and a pneumatic chisel. This study was conducted by staff of Clayton Group Services in 2002, and is an unpublished investigation. The following section outlines the methodology utilized to characterize the asbe stos levels during the removal process 3.3.1 Test Location and Environmental Setting Removal of asbestos-conta ining seam sealant was pe rformed in an operational automotive repair facility located in Ypsilant i, Michigan. The three bay garage was 60 ft by 80 ft with a 15-ft open ceiling. An office space located along the north wall occupied approximately 25% of the floor space within the service facility. Outside doors were located beside the office on the north and east walls. On the dates of assessment, the facility had an unpainted concre te floor and cinder block wall s, in addition to a painted metal deck roof with exposed st eel structures. The test area was not pneumatically sealed from the remaining sections of the service f acility. Figure 8 illustra tes the basic layout of the automotive repair facility. All external entrances, including the three ro llup doors that provided access to the individual bays, remained closed during each test session. The automotive service facility did not contain a ventilation system and relied on natural ventilation for removal of contaminants. The absence of mechanic al and natural ventilation allowed for the

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54 assessment of “worse case” conditions for a mechanic engaged in the servicing of vehicles assembled with asbestos-containing seam sealants. Figure 8: Automotive Repair Facili ty Used During Seam Sealant Test 3.3.2 Test Vehicles Two automobiles were identified that contained asbestos seam sealant prior to the start of testing. Both vehicles were 1967 Ford Musta ngs, one a coupe, while the other a fastback. These vehicles are representative of unitized body, or unibody, automobiles manufactured in the 1960s through 1970s with asbestos-containing seam sealant. Table 12 provides additional information and desc ription of the test automobiles. 80 fee t 60 fee t Rollu p Doors NorthMustang Coupe Mustang Fastback Spare Jack Stand External Doo r Location of Indoor Background Area Sample External Doo r External Doo r Office

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55 Table 12: Description of Test Vehicl es Used in Seam Sealant Assessment Make and Model Description of Automobile 1967 Ford Mustang Coupe (VIN 7R01C102182) 1967 Ford Mustang Fastback (VIN 7F02C105118) 3.3.3 Mechanic’s Activities, Equipment and Tasks Two methods of removing the asphalt-bas ed undercoating material were performed during this study. The first technique i nvolved the mechanic manually scrapping the seam sealant from the wheel wells with a ha nd scrapper. The second manner applied for removing undercoating material from the test vehicles relied on the use of a handheld pneumatic chisel. Each process was believed to have the potential to liberate varying levels of particulate matter from the seam s ealant. Test sessions were conducted using both methods to assess the airborne asbestos concentrations the mechanic was exposed to during the manual and mechanical removal of asbestos-containing seam sealant. The professional mechanic that performed all work activities for this study was a former Ford Motor Company employee who specia lized in the development of repair methodology and the restoration of vintage vehi cles. He was instructed to execute the servicing of the test vehicl es using his standard workpl ace practices. This included allowing the automotive mechanic to wear his normal work uniform, select all tools, in addition to the specific workplace procedures app lied for the removal of seam sealant. Before testing commenced, the tw o cars and test area were prepared to ensure an accurate assessment of the airborne asbestos levels generated during the removal of asbestos-

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56 containing seam sealant from the wheel wells. This began with the movement of the vehicles through the rollup doors into the gara ge bays. The automobiles were positioned on jack stands, raised and the wheels were removed to provide access to the seam sealant material. To prevent the lib eration of asbestos fibers from asbestos-containing brake components, the wheel hubs, which included the brake assembly, were covered with plastic disposal bags. Additionally, the au tomotive service facility was cleaned and inspected to prevent the aerolization of fi bers from alternative asbestos sources. A total of fourteen individual test sessions were conducted to assess the airborne asbestos levels generated during the removal of asbe stos-containing seam sealant. Four wheel wells from the Mustang Coupe and three wheel wells from the Mustang Fastback underwent testing during this assessment. E ach wheel well was subjected to two rounds of testing. In the first test series, the mechanic removed the undercoating with a hand scrapper. The subsequent test session involve d the application of the pneumatic chisel to take off seam sealant at an alternative site in the same wheel well. Removal of the undercoating material occurred in 15-minute test intervals. The mechanic performed eight, 15-minute-duration removal exercises on the Mustang Coupe (two at each of four wheel wells), and one 15-minute-duration remo val exercise on the Mustang Fastback on the first day of testing. The five additiona l 15-minute-duration removal exercises were performed on the Mustang Fastback the following day. All outside doors remained closed during ea ch test session. Following each 15-minute sampling period, the bay and pedestrian doors were opened for approximately 30 minutes

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57 to facilitate the “airing-out” of the automo tive service facility. Additional activities performed during the clean-up phase included the removal of debris, the wet-mopping of the floor and the repositioning of ai r sampling locations when necessary. 3.3.4 Air Sampling and Analysis Personal and area samples were collected during each 15-minute seam sealant removal exercise. This included five fixed-loca tion area air samples forming a 5 feet (ft) perimeter around the removal ac tivity, one area air sample a pproximately 50 feet away from the activity and one personal air sample placed on the mechanic’s shoulder. All area samples were suspended from portable stands and were placed approximately at breathing-zone height. Area air sample lo cations are noted on Figure 8. Figure 9 illustrates the placement of the air samples lo cated within 5 ft of the work activity. Figure 9: Demonstration of Seam Sealant Removal and Area Air Sample Placement *Arrows indicate the locations of area samples during test session

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58 Personal and area air samples used line opera ted electric air-sampling pumps that drew air at flowrates between 12 to 15 liters per minute (lpm) through cassettes containing 0.8 micrometer pore size, 25 millimeter (mm) diameter, MCE filters. Each pump was checked for calibration with a primary calibration standard before and after each 15minute sample collection period. NIOSH Method 7402 (TEM) was used to analyze a ll air samples (n = 98 ) collected in this study [111]. In samples identified to contain asbestos fibers (n =19), further analysis was conducted following NIOSH Method 7400 [110]. Fiber concentrations obtained from PCM represent total fiber leve ls because the analytical me thod is unable to distinguish between asbestiform and non-asbestiform fibers For this reason, PCME has also been calculated to estimate the airborne asbestos concentration mechanics encounter while removing automotive seam sealant. Calculation of this value is discussed in Section 3.2.4 and illustrated in Table 10. Additional in sight into NIOSH Methods 7400 and 7402 can be found in Section 3.2.4. 3.3.5 Bulk Sampling and Analysis Bulk samples of the seam sealant were collected from multiple locations on the two test vehicles using a hand tool to sc rape seam sealant into separa te self-sealing plastic bags. A total of 13 bulk samples of seam sealant we re obtained from the test vehicles. The samples were analyzed using the Chatfiel d TEM Method which is a full-quantitative TEM bulk sample analytical technique capable of determining the type and

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59 concentrations of asbestos within a sample [113]. Table 12 identifies the locations where bulk samples were collected on the two test vehicles. Table 13: Locations of Seam Sealan t Bulk Sampling on Test Vehicles Test Vehicle Sample Location 1967 Ford Mustang Coupe Front left wheel well Front right wheel well Left rear wheel well Interior Passenger’s side floor Interior Driver's side floor Right side of trunk Underside of car; Drivers side 1967 Ford Mustang Fastback Front left wheel well Front right wheel well Engine compartment, right seam seal Trunk; right side Engine compartment, right side thin layer 3.4 Exposure Assessment III: Asbestos-Containing Clutches The purpose of this evaluation was to ascertain the asbestos concentrations associated with the removal and installation of auto motive asbestos-containing clutches. The following section provides a detailed description of this section of th e study including the setting of the assessment, sampling strategy and activities performe d by the mechanic. This study is an unpublished i nvestigation that was conducte d in 2006 by staff of Clayton Group Services, in addition to the author of the current study. 3.4.1 Test Location and Environmental Setting Figure 10 illustrates the facility utilized during the clutch re moval and installation of an asbestos-containing automotive clutch. This build ing located in Benton, Kentucky

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60 measured 40 ft by 32 ft with a 10 ft drop cei ling. It was constructed in 1999 for the intended purpose of storing anti que tractors, in addition to acting as a metal work shop on limited occasions. Prior to testing, no automotive mainte nance activities had been performed in this facility. No ventilati on system or air conditioning unit was located within the building. Isolation barrier devices, in the form of plastic sheets, were placed over shelves located along the entire West wall of the facility to pr event the migration of dust from this area. The storage facility c ontained two sliding doors approximately 16 ft in length located at the North and South ends of the facility, and one external pedestrian door placed in the Southwest corner. All porta ls of entry were maintained closed during the individual test sessions and were opene d for approximately 90 minutes between the two individual test sessions to facilitate the airing out of the complex. Air hoses connected to an external ai r compressor located in a ne ighboring complex were brought into the building through the South sliding do or. This unit was used for blow outs, in addition to charge pneumatic tools.

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61 Figure 10: Illustration of Facili ty Used during Clutch Assessment *Numerical values represent locations of area samples and correspond with Table 16 3.4.2 Test Vehicle The test vehicle used for this exposure asse ssment was a 1967 Kaiser Jeep (Federal Stock Number: 2320-921-6365) assembled with an American Motor Company in-line six cylinder engine and a four speed manual tr ansmission. This 1.25 ton four wheel truck originally used for military purposes was id entified through an extensive search and contained its original asbe stos-containing clutch. At the time of the exposure assessment, the vehicle’s mileage was doc umented at approximately 13,000. The owner was able to confirm the low mileage and provi ded a complete history of the Kaiser Jeep after being removed from military usage. Fi gure 11 is a photograph of the test vehicle. Stora g e Area 40’ 32’ North 1 2 3 4 19’2” Test Vehicles External Door North Sliding Door South Sliding Door Location of Background Samples Collected Prior to Testing

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62 Figure 11: 1967 Kaiser J eep 1.25 Ton Pickup Truck 3.4.3 Mechanic’s Activities, Equipment and Tasks An automotive mechanic with approximatel y 20 years of professional experience was hired to perform all work activities involve d with the removal and replacement of the asbestos-containing clutch from the Kaiser Je ep. He was instructed to perform all work based on his standard operating procedures including the selection of the methodology used to perform the maintenance activitie s and equipment. Tools utilized by the mechanic included, but was not limited to, a pneumatic impact wrench, screwdrivers, scrapers and hammers. Work coveralls we re provided during testing to limit the generation of non-asbestos fibers from th e mechanic’s clothing. Additionally, the mechanic was outfitted with a harness that was used to connect the personal sampling pumps.

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63 The workplace simulation was divided into tw o test sessions 1) detachment of the transmission and removal of the clutch and 2) installation of replacement asbestos clutch and reattachment of transmission. Tables 14 and 15 summarize the work activities the professional mechanic performed during the removal and installa tion of the clutch, respectively. Table 14: Work Activities Perf ormed during Clutch Removal Task Description Transmission Detachment and Removal of Clutch 1. Disassembly of the top of the transmission housing including removal of the gear shifter and transmission pan. 2. Removal of drive shaft and crossbars to provide access to the bell housing. 3. Disconnection of the transmission. 4. Placement of transmission and bottleneck jacks. 5. Transmission lowered and moved back. 6. Bell housing opened. 7. Pressure plate, clutch forks and housing removed. 8. Removal of the clutch disc from clutch housing. 9. Detachment of linkage rods from bell housing. Table 15: Work Activities Perfor med during Clutch Installation Task Description Installation of Clutch and Reattachment of Transmission 1. Replacement clutch removed from packing and placed beneath test vehicle. 2. Clutch placed within housing with a centering pilot. 3. Slide transmission up to the clutch disk. 4. Reconnect clutch fork fingers. 5. Slide transmission connected via bolts to the bell housing. 6. Transmission cross member reattached. 7. Front and rear drives installed. 8. Linkage and gear box shift lid reattached. 9. Clutch adjusted. 10. Floor plate and gear shift reinstalled and adjusted.

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64 The duration of the clutch removal test session was approximately 130 minutes and began with the removal of the gear shifter, floor plate and other parts found within the cab of the truck. This activity facilitated ac cess to the top of the transmission, in addition to allowing the mechanic to perform a blowout to prevent debris from falling into the transmission. Figure 12 illustrate s the removal of the gear shif ter and floor plating. Parts, including the drive shaft and crossbars, that inhibited admission to the clutch and bell housings were removed with the use of the pne umatic impact wrench and hammer. Due to the design of the vehicle, the mechanic wa s forced to disconnect the transmission from the vehicle to gain complete access to th e bell housing. Transmission and hydraulic bottleneck jacks were set into place, and th e transmission was lowered and moved back. The bell housing was opened allowing removal of the clutch housing, pressure plate and clutch forks. The clutch disc was pulled aw ay from the flywheel and out of its housing. During the disassembly of the drive train and removal of the cl utch, the mechanic randomly performed blowouts to prevent debr is from falling into the transmission. Figure 13 demonstrates the clutch disc bei ng disconnected and pulled from the vehicle. The test session ended with the linkage rods being detach ed from the bell housing. During the break period between the two test sessions, the bell housing and clutch were sprayed and cleaned with th e aid of a non-chlorinated so lvent, NAPA 4800, and prepared for reinstallation into the test vehicle. An original replacement asbe stos-containing clutch was not available for installation into the test vehicle due to the age of the Kaiser Jeep. To replicate the handling of a new clutch, a su rrogate clutch disc was identified and used for this experiment. The substitute part wa s a Sachs/Borg and Beck manual clutch (PAT

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65 2.227.558-2.448.879) originally designed for Porsche racing cars. The external packing containing the clutch was marked with a Eu ropean Asbestos Warning which provided evidence of the presence of asbe stos within the automotive part. Figure 12: Removal of the Ge ar Shifter and Floor Plate *Arrows show the location of the gear shifter and transmission pan Figure 13: Removal of the Clut ch Disc from Test Vehicle *Arrows show the location of the clutch disc

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66 Installation of the new clutch and reassembly of the transmission lasted approximately 190 minutes. The test session bega n with the removal of the ne w asbestos clutch from its packing and placement on the floor beside the dr iver’s side door. The mechanic installed the clutch within the vehicle and utilized a centering pilot to ensure proper placement within its housing. Parts, including the pr essure plate, clutch forks and housing, in addition to the bell housing were attached and the transmission was slid forward for reconnection. The transmission cross members and drives were installed followed by the linkage and gear box shift lid. Th is test session finished with the reattachment of the gear shifter and floor plate within the cab of the test vehicle. 3.4.4 Air Sampling and Analysis Personal and area air samples were collected to assess the asbestos fiber concentration generated during the removal and installation of an asbestos-containing clutch from the 1967 Kaiser Jeep pickup truck. All pumps used during the two sessions were calibrated before and after testing with a Bios International Model DC1. Area air samples (n = 4) suspended at approximately breathing-zone he ight from fixed-loca tion portable stands were placed at varying distances from the Kaiser Jeep. Table 16 provides the actual locations where area samples were placed duri ng the two test sessions that comprise the clutch exposure assessment. Area air sample s used line operated electric air-sampling pumps that drew air at flow rates between 7 to 10 lpm th rough cassettes containing 0.8 micrometer pore size, 25 mm diameter, MCE filters.

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67 Table 16: Locations of Area Air Sa mples during Clutch Exposure Assessment Sample Number Location 1 Passenger Side; 4' East of Vehicle 2 Driver Side; 3' 5" West of Vehicle 3 Front of Vehicle; 6' 8" South of Vehicle 4 Rear of Vehicle;18 F eet North of Vehicle Sample approximate locations are represented on Figure 11 The mechanic was outfitted with a body ha rness to accommodate the wearing of two battery powered portable air pumps Ametek Model 1 utilized to collect personal samples. These pumps were calibrated with a primary standard device with metered flowrates, nominally 2.0 to 2.5 lpm, through 25-mm diameter, cassette mounted, 0.8 micrometer pore size MCE filters. Cassettes were placed within the worker’s breathing zone on each shoulder. Additional samples we re collected to test compliance with the OSHA PEL 30 minute excursion limit for asbestos of 1.0 f/cc [11]. The first sample was collected at the end of the test session associ ated with the removal of the clutch, while the second excursion limit sample was collected at the start of the installation of the replacement clutch. These sampling periods were determined based on professional judgment and the highest likelihood of en countering airborne asbestos fibers. All samples collected during this study were analyzed by NIOSH Methods 7400 (PCM) and 7402 (TEM) to establish airborne fiber conc entration associated with the removal and installation of automotive clutches containi ng asbestos [110, 111]. The results of these two analytical techniques were combined to calculate the PCME fiber concentration for all air samples. Table 10 found in Section 3.2.5 provides additional information for the calculation of the PCME based on the re sults of NIOSH Methods 7400 and 7402.

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68 3.4.5 Bulk Sampling and Analysis Bulk samples (n = 3) were collected to confir m the presence of asbest os within the clutch removed from the test vehicle. The first sample was obtained from the clutch by drilling small holes into the sides of the disc. An additional bulk sample consisted of dust scraped from the seams of the clutch facing. The final sample was debris removed from the bell-housing that encased the clutch disc. All bulk samples were analyzed by PL M based on EPA Method 600/R-93/116 [112]. This method, which has been previously discussed in section 3.2.5, is capable of identifying non-asbestos and asbe stos fibrous materials, the i ndividual species of asbestos found within a bulk sample and provide an estim ated concentration for each material. 3.5 Exposure Assessment IV: Asbestos-Containing Brakes The purpose of this study was to characterize the airborne asbestos fiber concentrations generated during the removal and replacement of asbestos-containing brake components. This investigation was conducted by staff of Clayton Group Services in 2001, and has been previously published in Regulatory Toxicology and Pharmacology [14]. Additional information about this exposure assessment can be found in Section 2.6.1 or from the published article [14]. 3.5.1 Test Location and Environmental Setting The brake study was conducted in a former auto mobile repair facility located in New Kensington, PA approximately 2000 cubic meters in total volume. Figure 14 has been

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69 adapted from the original i llustration provided in the publis hed study [14]. Offices were located on the north side of the facility with the designated te st area being located throughout the remaining garage. Ventilation smoke tests indicated that the air flow within the facility was extremely low, and allowed for the assessment to be conducted under worst-case scenarios. Additional means utilized to control the ventilation rates included the closing of all external and internal ports of entry. 3.5.2 Test Vehicles Four Chevrolet Impalas manufactured be tween 1965 through 1968 were used in this study. These vehicles were chosen based on their high sales volumes and the brake system specifications common to cars manufact ured in the mid-1960s [14]. The cars had duel servo style drum brakes that contain tw o different brake shoes on each wheel. Prior to testing, each vehicle was equipped with ne w chrysotile-containing asbestos brakes and driven on a prescribed road course for approxi mately 1,400 miles. The test vehicles were subjected to the road course to simulate the normal wear brakes expe rience and facilitate the potential generation of brake dust.

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70 Figure 14: Automotive Service Faci lity Used during the Brake Exposure Assessment 3.5.3 Mechanic’s Activities, Equipment and Tasks A total of six test sessions were conducte d to assess the airbor ne asbestos levels generated during the servicing of asbestos-cont aining brakes. Two of the sessions served as baseline tests with the m echanic being instructed to remove and replace the brake shoes only. In the other test sessions, the mechanic performed additional acivities including the sanding, arc grinding and beve ling of replacement asbestos brakes for extend periods. These tasks were evaluated to determine the effects on airborne asbestos concentrations. Table 17 is a summary of the tasks conducted during each test session. The methods and tools used to perform the brake replacements were selected by the mechanics. Standard workplace practices a ssociated with the 1960s were applied to ensure that the study was representative of conditions normally encountered by mechanics during the servicing of brakes a nd brake components during this time period. Location of Area Samples Garage Rollup Doors Offices Arc Grinding Bench Test Vehicles Filtered Exhaust Fan Unit Air Compressor

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71 Among the techniques applied during the test sessions, the mechanic performed multiple “blowouts” with compressed air, in addition to placi ng the brake drum on the floor of the service facility. The impact of the drum be ing set on the floor was believed to aid in cleaning the brake components by loosening the surface build up and dust [14]. Table 17: Tasks Performed during the S ervicing of Asbestos-Containing Brakes Task Description Preparation of Test Vehicles 1. Mechanic removed old brakes and installed new replacement chrysotile-containing shoes. 2. Vehicles driven for approximately 1,400 miles on road course to stimulate normal wear on shoes. 3. Vehicles positioned on lift in service facility and asbestos-containing brakes removed. Test 1 Removal and replacement of brakes shoe s with no additional manipulation of brake shoes. Test 2 Brake shoes were filed to bevel the squa re edges to prepare the friction material for installation. Test 3 Sanding of new brake shoes to bevel the edges and the outermost wear surfaces on each shoe. Test 4 Arc grinding of new shoes to match the radius of the brake component with the brake drum. Test 5 Repeat of Test 1. Test 6 Brake shoes grinding, repeat of Test 4. 3.5.4 Air Sampling and Analysis All air samples collected during the exposur e assessment followed the guidelines stated within NIOSH Methods 7400 (PCM) and 7402 (TEM) [110, 111]. Area air samples were collected at seven sites within the Automo tive Service Facility. Table 18 summaries the specific locations were these samples were take n. Gast vacuum pumps were calibrated at 5 L/min or less with a primary calibration de vice to ensure limited variation during the duration of the test sessions. Additionally, the stationary area samp les were placed at breathing zone height. All air-sampling pumps were calibrated prior to and after the end

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72 of each sampling day using a primary flow calibrator and a bubble generator. Table 18: Locations of the Area Air Samples during Brake Study Location of Sample Number of Samples 3 meters (m) from test vehicle 4 1.5 m from each wall of the servi ce bays (background samples) 2 3 meters (m) from work bench 1 Personal air samples were collected during th e total test session, which included the time period between the moving of the vehicle in to the service facility through the post completion repair drive. Cassettes mounted with 37-mm MCE membra ne filters with 0.8 m pore size were mounted within the breath ing zone of the mechanic. The battery powered pumps utilized for collection of the personal air samples were calibrated at flow rates of 3 L/min or less. 3.6 Statistical Analysis Airborne asbestos concentrations for the individual exposure assessments have been summarized in terms of descriptive statisti cs. The means and standard deviations for personal and area air samples have been calcu lated, in addition to the specific tasks conducted in each exposure assessment. With in toxicological and industrial hygiene investigations, these statistics are the most commonly used de scriptors for data sets [114]. The exposure data assembled from the four i ndependent exposure assessment utilized in this study were collected using a non -random sampling methodology designed to characterize the “worst-case” exposure or highest potential exposure workers are

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73 expected to experience during a specific task or set of conditions. It is assumed that if no sample collected under “worst-case” conditi ons exceeds the occupational exposure limit then the workers are not excessively exposed to the chemical agent being investigated [115]. Approximately 28% and 88% of the air sample s collected during the gasket and clutch exposure assessments were reported at or below the LOD, which for NIOSH Methods 7400 and 7402, are dependent on the number of fibers and optical fields counted, in addition to the volume of sampled air. Thes e values are unusable fo r statistical purposes and must be addressed to minimize data censorship [114]. Multiple techniques have been developed to minimize the censorship of data due to samples reported at the LOD [114, 116-118]. These methods include, but are no t limited to, 1) the replacement of the unusable censored data with values derived from the LOD and 2) extrapolation of the left-hand tail of the di stribution [118]. In 2001, Glass and Gray evaluated these me thods to determine which was the most appropriate in assessing hist orical exposure to benzene in the Australian Petroleum Industry. The researchers assemb led a total of 36 independent data sets ranging in sample size from less than 10 to several hundred data points [118]. The mean exposures calculated by the first two methods, replacement of the values with either half of the detection limit (LOD/2) or the LOD divided by the square root of 2 [LOD/(SQRT 2)], resulted in limited differences (less than 5 %) in most cases [118]. The means varied by 20% or greater only in data sets with 90% of the samples being reported at the LOD

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74 [118]. These techniques are independent of the distribution and are slightly biased, but considered by the authors reliable for estimati ng the reliable exposure estimates. The last method, extrapolation of the left-hand tail of the distribution, al so known as Cohen’s method, is dependent on the distribution of the data set, and can estimate summary statistics in the presence of heavily censor ed data sets as long as the underlying data distribution is known [118]. This methodology is not commonly applied in industrial hygiene investigations due to its cumberso me and complex nature [118]. The means calculated by the Cohen’s method were substa ntially greater then the means estimated using the two previously desc ribed techniques [118]. The aut hors credited the differences to a deviation of the data from a simple log-normal distribution, in part due to the presence of high outliers [118]. Glass a nd Gray conclude that among these three techniques of addressing the LOD, Cohen’s method resulted in erratic and unreliable estimates, while the use of the half limit of detection was most appropriate [118]. For this study, three set of values were assess ed and compared to ev aluate the effects of the different methods on the summary statisti cs. This included the 1) use of the upper limits of the LOD as the actual exposure valu e, 2) replacement of the unusable values with (LOD/2) and 3) replacement of the censo red data with the [LOD/SQRT (2)]. The statistics calculated from the three methods were compared, and it was determined that application of values obtained from eith er use of the (LOD/2) or [LOD/SQRT(2)] produced means that ranged from 8 to 13% lo wer than the estimates associated with the use of the upper limit values. Application of the LOD within the data sets resulted in slightly exaggerated exposure concentrations that are considered conservative in nature

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75 [118]. Helsel reported that the overestimation of the summary statistics by this method is approximately 10%, and is inconsequential [116] It was decided that the conservative estimates produced by the use of the upper limit values in place of the LOD would be used in the current study. 3.7 Risk Analysis Risk analysis is defined as a procedure th at characterizes the likelihood of potential adverse health effects resulting from exposur e to a hazardous agent. In this study, a qualitative risk analysis was developed and implemented to determine if mechanics were at increased risk of asbestos-related diseas es associated with th e servicing and handling of automotive parts containing asbestos. This methodology is based on the following assumptions: 1. Risk (R) is proportional to the toxicity of asbestos (T) multiplied by the exposure concentration (E), or R = T* E. 2. The toxicity (T) for asbestos represents a static value, while intensity of exposure (E) is dynamic. 3. A no-effect exposure threshold, or exposure levels below which risk of disease is not expected, for asbestosis, lung cancer and mesothelioma exists. 4. That risk of asbestos-related diseases is elucidated by directly comparing calculated cumulative lifetime asbestos exposures to theoretical no-effect exposure thresholds found within published literature. 5. An increased risk is identified for automotive mechanics if the estimated cumulative lifetime asbestos exposure exceeded the theorical exposure thresholds

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76 for the selected asbestos related diseases. This process is comprised of three distinct steps which are discussed in detail in the following sections. The prescribed steps of this risk analysis technique are: 1. Identification of the no-effect exposure th resholds for asbestosis, lung cancer and mesothelioma from published literature. 2. Calculation of the cumula tive lifetime asbestos e xposures for mechanics. 3. Comparison of these values to determine if mechanics are at increased risk of asbestos-related diseases. 3.7.1 No-Effect Exposure Thresholds for Asbestos-Related Diseases One of the primary assumptions of this risk an alysis is that the development of asbestosinduced diseases occurs only after the cumulative exposure to asbestos exceeds theorical exposure thresholds. There ha s been a long standing debate about the exposure-response relationship between inhalation of asbestos fibers and increased risk of asbestos-related diseases, including lung cancer and mesoth elioma [10, 19, 49, 69, 70]. Epidemiologic evidence appears polari zed between the existence of th resholds, or level of exposure below which a biological response is not observed, and linear non-th reshold relationships associated with asbestos exposure [63]. In part this is due to the in ability to identify the specific mechanism of action responsible of the induction and promo tion of the various non-malignant asbestos-related pulmonary di seases, lung cancer and mesothelioma. What is currently understood is that once inha led the presence of the fibrous minerals within the lungs results in a series of ev ents including the activation of macrophages,

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77 physical damage to pulmonary tissue and th e production of free radicals [19, 20, 22, 30, 32, 39, 62, 63]. For a more in-depth discussion of these events, please review Chapter 2. A potential consequence of these factors is the induction of a ch ronic inflammatory response. This continuous cycle of damage a nd repair is believed to be associated with potential alterations of the phenotypic expre ssion of numerous genes responsible for the regulation of cell proliferati on and apoptosis [63, 84, 86]. Despite the failure to identify the exact mech anism of action responsible for the onset of asbestosis, lung cancer and mesoth elioma, sufficient evidence is currently available that indicates that the chronic infl ammatory response associated with these diseases may not occur until a threshold is exceeded [19, 20, 22, 30, 32, 39]. Although this view is not shared by the entire scientific community, the theory of a no-effect exposure threshold for asbestos-induced pulmonary diseases is both biologically plau sible and supported by numerous epidemiologic studies [ 21, 23, 65-67, 119-124]. Several additional investigations provide summaries of theorical thresholds for asbe stosis, lung cancer and mesothelioma [22, 24, 63, 124-126]. These publica tions have been reviewed to identify no-effect exposure thresholds for asbestosis, lung cancer and mesothelioma that have been applied in the current qua litative risk analysis process to determine if mechanics are at increased risk of asbestos-related dis eases. The following paragraphs summaries the results of the literature review. A threshold for asbestosis is less controvers ial than for lung cancer and mesothelioma. Governmental agencies, such as the EPA, have based risk assessment for non-

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78 carcinogenic health outcomes, including non-malignant asbestos-induced pulmonary diseases, on the concept of threshold doses The exposure-response relationship between asbestos exposure and the development of th e interstitial pulmonary fibrosis has been reported to be non-linear with the risk of the disease decreasing with a reduction in cumulative exposure [69]. A review of publishe d literature resulted in the identification of several studies that report a no observable adverse effect level (NOAEL) for asbestosis (65-67). This no-effect expos ure threshold has been report ed to range from 25 to 100 fibers-years per cubic centimet er (f-yr/cc) [22, 25, 65-67]. It should be noted that only a small percentage of individuals exposed to as bestos concentrations in this range develop asbestosis indicating that additional unidentifi ed factors may play a role in the onset of the pulmonary diseases [22, 63]. The Helsin ki Criteria, a document that summaries the findings of the International Expert Meeting on Asbestos, As bestosis and Cancer, states that cumulative exposures within this ra nge represent a reasonable threshold for asbestosis [125]. Unlike non-malignant pulmonary diseases, the existence of a threshold dose for lung cancer is highly debated. In a review of epidemiological studies investigating various occupational cohorts exposed to asbestos fi bers, Browne stated “The data…show that every industrial group of asbest os workers with adequate da ta on individual duration and intensity of exposure provides some eviden ce of a threshold of cumulative exposure below which the risk of lung cancer does not appear to be raised. The evidence of a threshold is also supported by one well doc umented study giving duration of exposure only, and by several studies s howing no increase in lung cance r risks despite the presence

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79 of low levels of other asbestos related dis eases” [126]. No observable adverse effect levels for lung cancer have been repo rted between 25 and 3,200 f-yr/cc within epidemiologic studies [124]. Additionally, es tablishment of a dose-response relationship between asbestos exposure and lung cancer has been difficult, but is reported by numerous investigations at cumulative exposure between 25 to 100 f-yr/cc [24, 60, 126, 127]. The exposure range, in part, is base d on the Helsinki Criteria. This document states that at this level of cumulative exposur e, the relative risk of lung caner is estimated to increase 0.5-4% for each fiber-year per cubi c centimeter of air (f -yr/cc) [125]. At the upper boundary of this range, a cumulative exposur e of 25 f-yr/cc is estim ated to result in a risk of 2-fold [125]. A clearly defined exposure-response relati onship between chrysotile asbestos and mesothelioma has not been established and is highly debated [29]. Studies attempting to determine the risk of asbestos-related di seases in occupational cohorts exposed to chrysotile fibers report e xposure to amphibole fibers as a potential confounder [124, 128130]. Amphiboles, such as tremolite, are co mmonly found in varying concentrations as contaminants of chrysotile ore [129, 130]. Hodgson and Darnton pr esented evidence of increased risk of mesothelioma with expos ures to amphibole fibers below 0.1 f-yr/cc [23]. In comparison, no significant increase of risk for mesothelioma was reported for chrysotile fiber exposures in a similar exposur e concentration [23]. Any elevated risk of disease reported in occupati onal cohorts exposed to chrysotile fibers may be due to amphibole fiber contaminants instead of the serp entine asbestos. Although the specific relationship between exposure to chrysotile fibers and mesothelioma is unknown, the risk

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80 of the pleura disease associated with chrysotile fibers is insignificant when compared to amphibole fibers. Pierce and Finley reviewed published literatur e to identify studies that reported NOAEL for mesothelioma associated with exposure to mesothelioma [124]. From their analysis of the currently available data, it was dete rmined that the no-effect exposure threshold ranged from 15 to 1,599 f-yr/cc [124]. Thes e studies were further reviewed and compared to the results of additional epidemiologic investigations [21, 23, 119, 122, 123]. It was determined that the NOAEL reported by Albin et al. of 15 f-yr/cc represented a plausible threshold for meso thelioma [21]. The following paragraph provides greater detail on this study. Albin et al. investigated as bestos exposures among Swedish cement workers [21]. The authors determined that the relative risk for workers with cumulative exposures to asbestos ranging from 15-39 f-yr/cc and >40 f-yr/cc were 21.2 (95% CI 2.5-178) and 22.8 (95% CI 2.4-212), respectively [21]. For cement workers with cumulative lifetime exposures below 15 f-yr/cc, the relative risk was 1.9 (95% CI 0.2-21.3) [21]. The exposure estimates were based on 12,196 person-y ears. It should be noted that this occupational cohort was not exclusively exposed to serpentine asbest os. Albin et al. stated that cement products primarily c ontain chrysotile fibers supplemented with crocidolite and amosite [21]. Additionally, contamination by tremolite was also suspected. Exposures to low level amphibol e fibers within workers diagnosed with mesothelioma may be responsible for the onset of the pleura cancer instead of chrysotile

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81 asbestos [21]. Although potential exposure to amphibole fibers may contribute to the number of cases of mesothelioma reported in this study, what remains clear is that when workers received cumulative lifetime e xposures above 15 f-yr /cc the risk of mesothelioma potentially increases. Table 19 summaries the no-effect exposure thre sholds for the selected asbestos-related diseases, in addition to the sp ecific asbestos types that are associated with the cumulative exposure concentrations. The no-effect e xposure thresholds identified for asbestosrelated diseases associated with chrysotile fibers are likely to offer a conservative estimate due to the inability of the reviewed studies to control for the presence of amphibole fiber within the workplace, in addition to the previous employment of test subjects in trades associated with exposure to amphibole fibers. Another factor that have resulted in the overestimation of the thresh olds is the failure to control for smoking. Burdof and Swuste offer support for this statem ent by reporting that at 25 f-yr/cc at least half of the cases of lung cancer attributed to asbestos e xposure would actually be caused by cigarette smoking and other risk factors [60]. The values us ed in this risk analysis represent plausible expo sure estimates supported by published literature. Table 19: No-Effect Exposure Thresholds for Asbestos-Related Diseases Disease Fiber Type Threshold Dose (f-yr/cc) References Asbestosis Amphibole, Chrysotile 25-100 [20,25] Lung Cancer Amphibole, Chrysotile 25-100 [24, 60, 126, 127] Mesothelioma Chrysotile 15 [21]

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82 3.7.2 Estimation of the Cumulative Lifetime Asbestos Exposure Calculation of the cumulativ e lifetime asbestos exposure is based on methodologies adapted from published studies [131, 132]. This value is an index of exposure that estimates the aggregate asbestos fiber concentr ation over time and is expressed in units of f-yr/cc [19]. The cumulative lifetime asbe stos exposures for automotive mechanics calculated in the current study are based on the following assumptions: 1. Cumulative lifetime asbestos exposure is equal to the annual average eight-hour (8-HR) daily exposure multiplied by th e duration of exposure in years [132]. 2. The average exposure intensity applied w ithin the estimation of the cumulative lifetime exposure for mechanics is base d on the mean fiber concentrations observed within the 1) personal air sample s and 2) all air samples identified to contain asbestos through TEM. 3. The annual average 8-HR daily exposure is equivalent to an 8-HR occupational exposure for 250 days per year [19]. 4. The annual average 8-HR daily exposure is the same for all workers [133]. 5. The annual average 8-HR daily exposu re is constant over time [133]. 6. The duration of exposure e quals 45 years [134]. The previously described parameters have been utilized to construct the matrix found in Table 20. The hypothetical exposure profile was developed based on Price and Ware [125]. Two sets of cumulative lifetime asbe stos exposures have been calculated based on 1) the personal air samples collected duri ng the individual exposure assessments and 2)

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83 all air samples (personal and area) collected within the individual tests identified to contain asbestos fibers. Among the postulate s previously described, a working lifetime of 45 years was applied as the duration of exposure within the estimation of the cumulative lifetime asbestos exposures. The use of this value was based on risk assessment practices and guideline s commonly utilized by OSHA [134]. Table 20: Cumulative Lifetime Asbestos Exposure Matrix Activity Duration (Years) Average Exposure Intensity (f/cc)a Hours per day Days per year Annual Average 8-HR Daily Exposure (f/cc) Cumulative Lifetime Exposure (f-yr/cc)b Gasket Complete 45 8 250 Removal 45 8 250 Installation 45 8 250 Seam Sealant 45 8 250 Manual Removal 45 8 250 Pneumatic Removal 45 8 250 Clutch Complete 45 8 250 Removal 45 8 250 Installation 45 8 250 Brakes 45 8 250 Removal and Replacement 45 8 250 Filing 45 8 250 Sanding 45 8 250 Arc Grinding 45 8 250 a (f/cc) = Fibers/cubic centimeter of air; b (f-yr/cc)= Fibers-years per cubic centimeter of air 3.7.3 Determination of Risk The qualitative risk analysis implemented in this study has been designed to determine if mechanics are at increased risk of asbestos-related diseases without the calculation of a risk estimate. Risk of asbestosis, lung can cer and mesothelioma is based on the direct comparison of the cumulative lifetime asbestos exposures to the no-effect exposure

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84 thresholds identified within published lit erature for asbestosis, lung cancer and mesothelioma. Increased risk was declared if the estimated lifetime exposures exceeded the threshold levels of the selected asbest os-induced pulmonary diso rders. A potential shortcoming of this technique is the inability to compare a quantify risk level against the EPA or OSHA accept risk standards of 1 in 1,000,000 or 1 in 10,000, respectfully.

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85 CHAPTER 4.0 RESULTS 4.1 Gasket Exposure Assessment 4.1.1 Individual Test Sessions A summary of the area airborne fiber levels generated during the removal and installment of asbestos-containing gaskets is presente d in Table 21. Duri ng the three sessions associated with the disassembly of the test engines, the length of the simulations ranged from 132-157 minutes. Installation of replacement gaskets in the Ford engine and Chevrolet Malibu required 122 minutes and 150 minutes, respectively. Approximately 23% (n = 10) of the area samples were belo w the analytical LOD for PCM. The highest mean PCM fiber concentration was 0.0069 f/cc, and occurred duri ng the removal of gaskets from the Chevrolet Malibu. The relatio nship of the individual area samples to the OSHA PEL is illustrated in Fi gure 15. All area samples (n = 43) were approximately 100 times lower than the current PEL of 0.1 f/cc.

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86 Table 21: PCM Fiber Concentrations fo r the Individual Gasket Test Sessions Test Vehicle/Engine Session Description na Duration (Minutes) Mean PCM b Concentration (f/cc)c Mean PCME d Concentration (f/cc) 1 Chevrolet Malibu Engine disassembly; gaskets removed 8 151 0.0069 0.0040 2 Chevrolet Malibu Engine reassembly; gaskets installed 8 157 0.0037 0.0000 3 Chevrolet Pickup Truck Engine disassembly; gaskets removed 9 132 0.0002 0.0000 4 Ford 390 Engine Engine disassembly; gaskets removed 9 122 0.0042 0.0004 5 Ford 390 Engine Engine reassembly; gaskets installed 9 150 0.0008 0.0000 a (n) = sample number; b (PCM)= Phase Contrast Microscopy; c (f/cc) = Fiber/cubic centimeter of air; d(PCME)= Phase Contrast Microscopy Equivalent Figure 15: Distribution of All Area Air Samples Collected during Gasket Exposure Assessment 0.000 0.001 0.010 0.100 1.000 1611162126313641 OSHA PEL Area Air SamplePCM Fiber Concentration (f/cc) Table 22 provides a summary of the mean PC M and PCME fiber concentrations for the test sessions associated with removal and in stallation of gaskets within the Chevrolet

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87 Malibu and the Ford 390 Engine. The test sess ion concerned with th e removal of gaskets from the Chevrolet Pickup Truck was remove d from this listing because no companion session was conducted in which replacement gask ets were installed within the engine. When observed as a continuous test, the disa ssembly and reassembly of the Malibu and Ford engine required approximately 308 a nd 272 minutes, respectively. The area air samples collected during the entire Malibu test yielded a PCM fiber concentration of 0.0053 f/cc, while the Ford test resulted in a PCM fiber concentration of 0.0025 f/cc. Table 22: Area Fiber Concentrations for the Complete Disassembly and Reassembly of Engines Containing Asbestos Gaskets Vehicle/Engine Task Duration (min)a nb Mean PCMc (f/cc)d SDe Mean PCMEf(f/cc) SD Chevrolet Malibu Removal and replacement of asbestoscontaining gaskets 308 16 0.0053 0.0027 0.0020 0.0027 Ford 390 Engine Removal and replacement of asbestoscontaining gaskets 272 18 0.0025 0.0021 0.0002 0.0008 a (min) = minutes; b(n) = sample number; c (PCM) = Phase Contrast Microscopy; d (f/cc) = Fibers/cubic centimeter of air; e (SD) = standard deviation; f (PCME) = Phase Contrast Microscopy Equivalent Among the nine area sampling locations, only slight variations in the fiber concentrations were observed throughout the automotive se rvice facility during the removal and replacement of asbestos-containing gaskets. The highest fiber c oncentrations observed during the removal of gaskets fr om the three test vehicles di d not occur in the immediate test area. Background levels of fibers ranged from 8-HR TWA of 0.0005-0.0015 f/cc. A summary of the mean fiber levels relative to sampling location is provided in Table 23.

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88 Table 23: Mean Area Air Fiber Concentrations Relative to Sampling Location Task Location Mean PCM a (f/cc) b Mean PCM 8-HR TWA c (f/cc) Gasket Removal Bench 0.0069 0.0019 Driver Side 0.0028 0.0005 Passenger Side 0.0049 0.0013 Northeast Corner 0.0035 0.001 Northwest Corner 0.0061 0.002 Southeast Corner 0.0062 0.0018 Southwest Corner 0.0078 0.0022 Distant Hallway 0.0049 0.0013 Intermediate Hallway 0.0051 0.0015 Gasket Installment Bench 0.0021 0.0036 Driver Side 0.0023 0.0007 Passenger Side 0.0078 0.0024 Northeast Corner 0.0019 0.0006 Northwest Corner 0.0036 0.0011 Southeast Corner 0.003 0.0009 Southwest Corner 0.0023 0.0007 Distant Hallway 0.0015 0.0005 Intermediate Hallway 0.0015 0.0005 a (PCM) = Phase Contrast Microscopy; b (f/cc) = Fibers/cubic centimeter of air; c (8-HR TWA) = Average Eight Hour Time Weighted; Indicates location with one or more samples reported below the LOD 4.1.2 Personal Air Samples A descriptive summary of the individual pers onal air samples colle cted during the five test sessions is presented in Ta ble 24. Fifty percent (n = 5) of the samples were reported below the analytical level of detection. Add itionally, only 3 samples were identified to contain asbestos fibers through TEM analysis. Within these sa mples, the highest asbestos fiber ratio was 56%. The mean PCM and PCME fiber concentrations for all personal air samples were 0.0123 and 0.0027, respectively. Th e values are approximately 10 to 100 times lower than the current OSHA PEL. Figure 16 illustrates the distribution of the PCM fiber concentration for the personal air samples.

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89 Table 24: Personal Air Samples Collected during Gasket Study Test Session Description Location Time (min)a Volume (L) b PCM c (f/cc) d Asbestos Fiber Ratio e PCME f (f/cc) 1 Gaskets removalChevrolet Malibu Left Shoulder 141 320 0.023 0.381 0.0088 1 Gaskets removalChevrolet Malibu Right Shoulder 140 348 0.027 0.556 0.0150 2 Gaskets installationChevrolet Malibu Left Shoulder 156 345 0.0058 0 0 2 Gaskets installationChevrolet Malibu Right Shoulder 155 371 0.005 g 0 0 3 Gaskets removalChevrolet Truck Left Shoulder 124 242 0.012 0 0 3 Gaskets removalChevrolet Truck Right Shoulder 60 131 0.01g 0 0 4 Gaskets removalFord 390 Engine Left Shoulder 119 285 0.007 g 0 0 4 Gaskets removalFord 390 Engine Right Shoulder 119 262 0.01 0.333 0.0033 5 Gaskets installationFord 390 Engine Left Shoulder 151 335 0.0032 g 0 0 5 Gaskets installationFord 390 Engine Right Shoulder 151 371 0.005 g 0 0 a (min) = minutes; b (L) = Liters; c (PCM) = Phase Contrast Microscopy; d (f/cc) = Fibers/cubic centimeter of air; e (8-HR TWA) = Eight Hour Time Weighted Average; e Asbestos Fiber Ratio is defined as the nu mber of asbestos fibers detected via Transmission Electron Microscopy ( TEM) divided by the total number of all fibers detected via TEM; f (PCME) = Phase Contrast Microscopy Equivalent; g Indicates samples below the LOD Figure 16: Distribution of PCM Fiber Con centrations Obtained from Personal Air Samples Collected during Gasket Study 0.001 0.01 0.1 1 12345678910 Personal Air SamplesPCM Fiber Cocnentration (f/cc) OSHA PEL

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90 The mean PCM and PCME fiber concentrations were determined for the test sessions associated with the Chevrolet Malibu and Ford 390 engines. This step has been taken to evaluate the mechanic’s personal exposure during both the disassembly and reassembly of automotive engines containing asbestos ga skets. Table 25 provi des a summary of the results. As in the area air samples, the PCM fiber concentration associated with the Chevrolet Malibu engine were almost triple the fiber levels detected during the maintenance of the Ford engine. The PCM fiber concentration for the Malibu and Ford tests were 0.0152 and 0.0063, respectively. Th ese values are approximately 10 to 100 times lower than the current OSHA PEL of 0.1 f/cc. Table 25: Personal PCM and PCME Fib er Concentrations for the Complete Disassembly and Reassembly of Engi nes Containing Asbestos Gaskets Vehicle/Engine Task Duration (min)a n b Mean PCMc (f/cc)d SDe Mean PCMEf (f/cc) SD Chevrolet Malibu Removal and replacement of asbestoscontaining gaskets 308 4 0.0152 0.0114 0.0045 0.0032 Ford 390 Engine Removal and replacement of asbestoscontaining gaskets 272 4 0.0063 0.0029 0.0017 0.0006 a (min) = minutes; b(n) = sample number; c (PCM) = Phase Contrast Microscopy; d (f/cc) = fibers/cubic centimeter of air; e (SD) = standard deviation; f (PCME) = Phase Contrast Microscopy Equivalent 4.1.3 Samples Identified to Contain Asbestos Approximately 21% (n = 11) of all samples were determined through TEM analysis to contain chrysotile fibers. A summary of the i ndividual samples is presented in Table 26.

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91 The majority of the samples determined to c ontain asbestos fibers were collected during the removal of gaskets from the 1974 Chevro let Malibu. Asbestos fibers were not detected in samples associated with the inst allation of new asbestos -containing gaskets or during removal of gaskets from the Chevrolet Pickup Truck. Table 27 provides descriptive statistics for these samples. The average PCM and PCME concentrations were 0.0106 and 0.0057 f/cc, respectively. It should be noted no amphibole fibers were identified within any sample. Figure 17 illustrates the distribution of these samples in comparison to the OSHA PEL. Table 26: Air Samples Containing Asbest os Fibers Collected during Gasket Study Task Type Location PCMa (f/cc)b Asbestos Fiber Ratio c PCMEd (f/cc) Engine disassembly; gasket removedFord engine Personal Right Shoulder 0.01 0.333 0.0033 Engine disassembly; gasket removedFord engine Area Southwest Corner 0.0052 0.7 0.0036 Engine disassembly; gasket removedChevrolet Malibu Personal Right Shoulder 0.027 0.56 0.0151 Engine disassembly; gasket removedChevrolet Malibu Area Southeast Corner 0.0082 0.4 0.0033 Engine disassembly; gasket removedChevrolet Malibu Area Southwest Corner 0.01 0.83 0.0083 Engine disassembly; gasket removedChevrolet Malibu Area Northwest Corner 0.0083 0.49 0.0041 Engine disassembly; gasket removedChevrolet Malibu Area Driver Side 0.003 0.76 0.0023 Engine disassembly; gasket removedChevrolet Malibu Area Bench 0.0094 0.6 0.0056 Engine disassembly; gasket removedChevrolet Malibu Area Northeast Corner 0.0044 0.76 0.0033 Engine disassembly; gasket removedChevrolet Malibu Area Hall Intermediate 0.0083 0.65 0.0054 Engine disassembly; gasket removedChevrolet Malibu Personal Left Shoulder 0.023 0.38 0.0087 a (PCM)= Phase Contrast Microscopy; b (f/cc) = Fibers/cubic centimeter of air; c Asbestos Fiber Ratio is defined as the number of asbestos fibers detected via Transmission Electron Microscopy (TEM) divided by the total number of all fibers detected via TEM; d (PCME) = Phase Contrast Microscopy Equivalent

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92 Table 27: Average PCM and PCME Fi ber Concentrations for Air Samples Containing Asbestos Sample Type n a Mean PCM b(f/cc) c SD d Mean PCME e (f/cc) SD Personal 3 0.02 0.0089 0.0091 0.0059 All 8 0.0071 0.0025 0.0045 0.0019 Area 11 0.0106 0.0075 0.0057 0.0038 a(n) = sample number; b (PCM)= Phase Contrast Microscopy; c(f/cc) = Fibers/cubic centimeter of air; d (SD) = Standard Deviation; e(PCME) = Phase Contrast Microscopy Equivalent Figure 17: Distribution of Al l Air Samples Identified Vi a TEM to Contain Asbestos Fibers during the Removal of Gaskets 0.001 0.01 0.1 1 0123456789101112 PCM PCME OSHA PEL Air SamplesFiber Concentration (f/cc) 4.1.4 Bulk Sample Analysis of Removed Automotive Gaskets Bulk sample analysis of the removed gasket s was performed to provi de evidence of the presence of asbestos fibers in the gaskets a nd the workplace. A total of nine gaskets were removed from the three test engines, a nd analyzed via Polarized Light Microscopy (PLM). The results and the descriptions of the gaskets can be found in Table 28. Asbestos concentrations ranged from 0 to 75% of the gasket matrices with five of the gaskets identified to contain mo re than 70% asbestos. Amphibole asbestos fibers were

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93 not identified in any of the samples, but chry sotile fibers were present in six of the removed gaskets. Non-asbestos fibrous materi als, including cellulose fibers and fibrous glass, were present in all gaskets except the donut gasket removed from the Chevrolet Malibu. Table 28: Asbestos and Non-Asbest os Components of Removed Gaskets Gasket Description Asbestos Content Non-Asbestos Fibrous Materials 390 Ford Exhaust Manifold Gasket 70% Ch rysotile Cellulose Fiber; Fibrous Glass 390 Ford Intake Manifold Gasket 70% Chrysotile Cellulose Fiber 390 Ford Head Gasket 70% Chrysotile Cellulose Fiber 1978 Chevy Head Gasket 70% Chrysotile Cellulose Fiber Thermostat Gasket None Detected Cellulose Fiber 1978 Chevrolet Carburetor Space 14% Chrysotile Cellulose Fiber Exhaust Donut None Detect ed No Fibers Detected 350 Chevrolet V-8 Intake Gasket 75% Chrysotile Cellulose Fiber 350 Chevrolet V-8 Carburetor Gasket None Detected Cellulose Fiber; Fibrous Glass 4.2 Seam Sealant Exposure Assessment 4.2.1 Area Air Samples Prior to testing, three area air samples we re collected to assess the initial fiber concentration within the automotive service f acility. Airborne fibe r levels ranged from 0.0011 to 0.0013 TEM f/cc. A summary of the area air samples collected during the removal of asbestos-containing seam sealer can be located in Table 29. All background samples (n = 14) collected during the individua l test sessions were below the analytical LOD. The average TEM background asbest os concentration obs erved within these samples was 0.0037 f/cc. Within area samples lo cated approximately 5 feet from the test vehicle, 84% (n = 59) of the samples were below the analytical LOD. No noticeable

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94 difference could be observed between the fibe r levels generated dur ing the removal of seam sealer with the hand scrape r versus the pneumatic chisel. Table 29: Average TEM Asbestos Concentr ations for Area Air Samples Collected during Seam Sealant Removal Description and Location na Number of Samples Below the LODb Mean TEMc Asbestos Concentration (f/cc)d Indoor background air samples 14 14 (100 %) 0.0037 Area samples within 5 feet of test vehicle 70 59 (84 %) 0.0054 a(n)= sample number; b(LOD)= Level of Detection; c(TEM) =Transmission Electron Microscopy; d (f/cc) = fibers/cubic centimeter of air 4.2.2 Personal Air Samples Seventy-two percent (n = 10) of the persona l samples collected during this simulation were below the LOD for TEM. The mean asbestos concentration for personal air samples collected during the hand scrapping a nd pneumatic chipping of the sealant were 0.0061 and 0.0059 f/cc, respectively. Table 30 summ arizes the asbestos levels detected by TEM within the personal air samples. Results are presented as TEM asbestos concentrations for both manual and pneumatic techniques.

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95 Table 30: Average TEM Asbestos Concen trations for Personal Air Samples Description na Samples Below the LODb Mean TEMc Asbestos Concentration (f/cc)d Personal samples collected during hand scrapping of seam sealer 7 6 (86 %) 0.0061 Personal samples collected during pneumatic chipping of seam sealer 7 4 (66 %) 0.0059 All personal samples 14 10 (72 %) 0.006 a(n)= sample number; b(LOD)= Level of Detection; c(TEM) =Transmission Electron Microscopy; d (f/cc) = fibers/cubic centimeter of air 4.2.3 Air Samples Containing Asbestos Among all air samples (n = 98), approximately 20 % (n = 19) of the samples were determined through TEM to contain chrysotile asbestos. Table 31 provides a description of the individual samples including air volum e, PCM and PCME fiber concentrations and asbestos fiber ratio determined via NIOSH Method 7402 (TEM). The majority of air samples identified to contain asbestos fibers we re collected within 5 feet of the test area during the pneumatic chipping of seam seal ant. The highest PCM and PCME fibers concentration observed with in these samples were 0.046 and 0.012, respectively. No amphibole fibers were detected within the air samples. Table 32 summarize the mean PCM and PCME fiber concentrations for pe rsonal, area and all air samples collected during the 14 test sessions.

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96 Table 31: All Air Samples Containing Asbestos Fibers Collected during the Removal of Seam Sealant Volume PCMb Asbestos PCMEe Type of Sample Task (L)a (f/cc)c Fiber Ratiod (f/cc) Area Sample (5 feet) Pneumatic chipping 219 0.046 0.25 0.012 Area Sample (5 feet) Pneumatic chipping 204 0.039 0.182 0.0071 Area Sample (5 feet) Pneumatic chipping 207 0.029 0.235 0.0068 Area Sample (5 feet) Manual scrapping 207 0.0024 0 0 Area Sample (5 feet) Manual scrapping 212 0.011 0 0 Area Sample (5 feet) Manual scrapping 213 0.016 0 0 Area Sample (5 feet) Manual scrapping 210 0.017 0.167 0.0028 Area Sample (5 feet) Pneumatic chipping 213 0.02 0 0 Area Sample (5 feet) Pneumatic chipping 198 0.015 0 0 Area Sample (5 feet) Pneumatic chipping 204 0.0074 0 0 Area Sample (5 feet) Pneumatic chipping 202 0.025 0.455 0.011 Area Sample (5 feet) Pneumatic chipping 207 0.014 0.5 0.007 Area Sample (5 feet) Manual scrapping 207 0.018 0 0 Area Sample (5 feet) Pneumatic chipping 207 0.017 0 0 Area Sample (5 feet) Pneumatic chipping 204 0.028 0.3 0.0084 Area Sample (5 feet) Pneumatic chipping 207 0.029 0.2 0.0058 Personal Sample Pneumatic chipping 224 0.065 0.226 0.015 Personal Sample Pneumatic chipping 240 0.056 0.33 0.019 Personal Sample Manual scrapping 188 0.025 0.25 0.0063 a(L) = Liters; b(PCM)= Phase Contrast Microscopy; c (f/cc) = Fibers/cubic centimeter of air; d Asbestos Fiber Ratio is defined as the number of asbestos fibers detected via Transmission Electron Microscopy (TEM) divided by the to tal number of all fibers detected via TEM; e (PCME) = Phase Contrast Microscopy Equivalent

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97 Table 32: Average PCM and PCME Fiber Concentrations for Air Samples Containing Asbestos Sample Type na Mean PCMb (f/cc)c SDd Range Mean PCMEe (f/cc) SD Range Personal 3 0.0487 0.0210 0.025-0.065 0.0134 0.0065 0.0063-0.019 Area: Pneumatic Chipping 11 0.0245 0.0114 0.0074-0.0046 0.0053 0.0046 0-0.0084 Area: Manual Scrapping 5 0.0129 0.0064 0.0024-0.018 0.0006 0.0013 0-0.0028 All Area Samples 16 0.0209 0.0113 0.0024-0.018 0.0038 0.0044 0-0.0084 All Air Samples Identified to Contain Asbestos Fibers 19 0.0253 0.0163 0.0024-0.065 0.0053 0.0058 0-0.0084 a (sample number); b(PCM)= Phase Contrast Microscopy; c (f/cc) = Fibers/cubic centimeter of air; d(SD) = Standard Deviation; e (PCME) = Phase Contrast Microscopy Equivalent 4.2.4 Transmission Electron Micrograph of Air Samples Figure 18 is a transmission electron microgra ph of area air samples collected during the seam sealant exposure assessment. The im age exhibits chrysotile asbestos fibers suspended within the asphalt-based seam seal ant material liberated during the pneumatic chipping of the undercoating. The photo demons trates that the asbe stos fibers are not generated independently, but rema in within the matrix of the seam sealant reflecting the affinity between asbestos and hydrocarbons [93].

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98 Figure 18: Transmission Electron Micrograp h of Chrysotile Fibers Suspended in Asphalt-Based Seam Sealant 4.2.5 Bulk Analysis of Seam Sealant Bulk samples of seam sealant were collected on the test vehicles in several locations including wheel wells, engine compartment, trunk and underpinning. In total, 13 samples were collected and analyzed through TEM to ensure the presence and concentration of asbestos within the seam sealant. Asbestos concentrations ranged from 5.9 to 28 % with the highest concentration being found in the Mustang Coupe’s trunk. No amphibole asbestos species were detected within thes e samples. Table 33 describes the collection locations and asbestos concentr ations associated with each bulk sample of seam sealer.

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99 Table 33: Bulk Sample Analys is of Seam Sealant Material Test Vehicle Location Asbestos Content (%) Mustang Coupe Front left wheel well 16 (VIN: 7R01C102182) Front right wheel well 12 Left rear wheel well 19 Interior Passenger’s side floor 5.9 Interior Driver’s side floor 7.6 Right side of trunk 28 Underside of car on Driver’s side 11 Mustang Fastback Trunk, Right side 20 (VIN: 7F02C105118) Trunk, left side 17 Front left wheel well 6.7 Front right wheel well 18 Engine compartment, right side seam 19 Engine compartment, right side thin layer 5.6 4.3 Clutch Exposure Assessment 4.3.1 Area Air Samples Eight area air samples were collected during th e removal and installation of an asbestoscontaining clutch in a Kais er Jeep. Table 34 provides the PCM and PCME fiber concentrations for the individual area sample s, in addition to the locations where each was collected. The average fiber PCM fiber concentration observed during the removal of the clutch was 0.0122 f/cc. No asbestos fibe rs were identified in these samples. The mean PCM fiber concentration corresponding to the installation of the substitute clutch and reassembly of the transmission was 0.018 f/cc. Unlike the samples collected during the removal of the clutch, two of the area air samples were determined through TEM to contain chrysotile fibers in concentrations of 4.5 and 5.6 %. The estimated PCME fiber concentration for these samples were 0.0009 and 0.0011 f/cc. Figure 19 illustrates the

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100 area air samples distribution. When compar ed to the current occupational exposure limits, the fiber concentrations were appr oximately 100 times lower than the OSHA PEL of 0.1 f/cc. The PCM and PCME fiber concen tration for all area samples (n = 8) were 0.015 and 0.0003 f/cc, respectively. In comparison to the OSHA PEL of 0.1 f/cc, the PCME fiber concentration, which is based on the level of asbestos found at the sample median, was almost 1000 times lower. Table 35 provides additional statistics of the area air samples. The combined duration of the two test sessions was 321 minutes, and yielded a mean PCM fiber concentration of 0.0151 f/cc. The 8-Hr PCM TWA for removal and replacement of the as bestos clutch was 0.004 f/cc. Table 34: Individual Area Air Samp les Collected during Clutch Study Test Session Work Activity Location Duration (min) a Volume (L) b PCMc (f/cc) d Asbestos Fiber Ratioe PCMEf (f/cc) 1 Clutch Removal Passenger 127 1289 0.011 0 0.0000 1 Clutch Removal Driver 127 1263 0.0099 0 0.0000 1 Clutch Removal Front 127 1274 0.022 0 0.0000 1 Clutch Removal Rear 127 1266 0.0057 0 0.0000 2 Clutch Installation Front 194 1946 0.019 0.056 0.0011 2 Clutch Installation Passenger 194 1969 0.017 0 0.0000 2 Clutch Installation Rear 194 1934 0.015 0 0.0000 2 Clutch Installation Driver 194 1929 0.021 0.045 0.0009 a(min) = minutes; b(L) = liters; c (PCM) = Phase Contrast Microscopy; d (f/cc)= fibers/ cubic centimeter of air; e Asbestos Fiber Ratio is defined as the number of asbestos fibers detected via Transmission Electron Microscopy (TEM) divided by the total number of all fibers detected via TEM; f (PCME) = Phase Contrast Microscopy Equivalent

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101 Figure 19: Distribution of Area Air Sa mples in Comparison to the OSHA PEL 0.001 0.01 0.1 1 012345678 OSHA PEL Area Air SamplesPCM Fiber Concentration (f/cc) Table 35: Area Air Samples Co llected during the Clutch Study Work Activity n Duration (min)a Mean PCMb (f/cc)c Mean PCM 8-HR TWAd (f/cc) Mean PCMEe (f/cc) Mean PCME 8-HR TWA (f/cc) Clutch Removal 4 127 0.0122 0.0032 0 0 Clutch Installation 4 194 0.018 0.0048 0.0005 0.0002 Clutch Removal and Installation 8 321 0.0151 0.004 0.0003 0.0001 a(min) = minutes; b(PCM) = Phase Contrast Microscopy; c (f/cc) = fibers/cubic centimeter of air; d(TWA) = Time Weighted Average; e (PCME) = Phase Contrast Microscopy Equivalent 4.3.2 Personal Air Samples Table 36 summaries the individual fiber concen trations and asbestos content found within the personal samples collected during the two tests sessions. The average PCM and PCME fiber concentration for all pers onal samples (n = 4) were 0.039 and 0.0014, respectively. Chrysotile fibers were de tected only in samples collected during the installation of the replacement clutch. The asbestos concentr ation for these samples (n = 2) were 3.3 and 6.9%. No personal air sample exceeded the OSHA PEL.

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102 Table 36: Individual Personal Air Sa mples Collected during Clutch Study Test Session Work Activity Location Duration (min) a Volume (L) b PCM c(f/cc)d Asbestos Fiber Ratio e PCMEf (f/cc) 1 Clutch Removal Right Shoulder 126 282 0.012 0 0 1 Clutch Removal Left Shoulder 126 291 0.021 0 0 2 Clutch Installation Left Shoulder 191 458 0.082 0.033 0.0027 2 Clutch Installation Right Shoulder 191 435 0.041 0.069 0.0028 a(min) = minutes; b(L) = liters; c (PCM) = Phase Contrast Microscopy; d (f/cc)= fibers/cubic centimeter of air; e Asbestos Fiber Ratio is defined as the number of asbestos fibers detected via Transmission Electron Microscopy (TEM) divided by the total number of a ll fibers detected via TEM; f (PCME) = Phase Contrast Microscopy Equivalent Two additional personal samples were coll ected for comparison to the OSHA 30-minute Excursion PEL of 0.1 f/cc for asbestos. The first excursion personal sample was collected during the last 30minutes of the clutch removal. This time period was determined to have the highest likelihood of ge nerating asbestos fibers due to the opening of the bell housing. No asbestos fibers were identified in this sample and the observed PCM fiber concentration was 0.0081 f/cc. A second 30-minute excursion sample was attempted at the start of the installation of the new asbestos clutch, but was not analyzed due to the hose connecting the cassette to the pump becoming disconnected. 4.3.3 Air Samples Containing Asbestos Fibers Approximately 33% (n = 4) of the air samples collected during the two test sessions were determined to contain chrysotile asbestos fibe rs. No asbestos fibe rs were detected in samples collected during the removal of the clutch. Table 37 provides information on the four samples identified to contain asbestos During the handling of the new asbestos-

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103 containing clutch, the fiber c oncentrations observed within personal samples remained well below the current OSHA PEL. The PC ME fiber concentrations for the personal samples containing asbestos were 0.0027 and 0.0028 f/cc. Table 37: Air Samples Containing Asbest os Fibers Collected during Clutch Study Task Sample Type Location Duration (min) a Volume (L) b PCM c(f/cc) d Asbestos Fiber Ratio e PCME f (f/cc) Clutch Installation Area Front 194 1946 0.019 0.056 0.0011 Clutch Installation Area Driver 194 1929 0.021 0.045 0.0009 Clutch Installation Personal Left 191 458 0.082 0.033 0.0027 Clutch Installation Personal Right 191 435 0.041 0.069 0.0028 a(min) = minutes; b(L) = liters; c (PCM) = Phase Contrast Microscopy; d (f/cc)= fibers/cubic centimeter of air; e Asbestos Fiber Ratio is defined as the number of asbestos fibers detected via Transmission Electron Microscopy (TEM) divided by the total number of all fibers detected via TEM; f (PCME) = Phase Contrast Microscopy Equivalent 4.3.4 Bulk Samples of Clutch Material and Debris Table 38 summarizes the findings of the PLM anal ysis of the three bulk samples. Results are presented as the percenta ge of asbestos fibers, non-as bestos fibrous materials and non-fibrous materials. Asbestos fibers were detected in th e clutch disc and dust removed from the disc face in concentrations of 30 and 5%, respectively. No amphibole fibers were detected in these samples. No asbest os fibers were identi fied in the residue removed from the bell housing.

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104 Table 38: Bulk Sample Analysis of Clutch Materials and Residue Sample Asbestos Content Non-Asbestos Fibrous Materials Non-Fibrous Materials Bell Housing Residue NDa 2% Cellulose Binder/Filler Clutch Disc Composition 30% Chrysotile ND Binder/Filler Dust from Clutch Disc Face 5% Ch rysotile 1% Cellulose Binder/Filler a (ND) = None detected 4.4 Brake Exposure Assessment Six test sessions were conducte d to assess the airborne asbe stos levels generated during the removal and replacement of chrysotil e-containing brakes. Table 39 provides a summary of the activities conducted in each sess ion, in addition to the duration of the test session dedicated to the specifi c task and blowout. Test se ssions 1 and 5 were performed to serve as baseline measurements with no additional manipulation to the brake shoes, while the remaining four sess ions examined the affects of filing, sanding and arc grinding on airborne asbestos levels. The three i ndividual tasks, which included sanding, filing and arc grinding, are commonly pe rformed to aid in the shapi ng of brake shoes to match its companion brake drum. The duration of th e various work activities ranged from 4 to 20 minutes. Additionally, the mechanic pe rformed blowouts for intervals up to 46 seconds. These short durations of blowouts are believed to genera te large volumes of airborne asbestos fibers [9].

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105 Table 39: Individual Test Sess ions Conducted during Brake Study Test Test Duration (min) a Task Task Duration (min) Blowout Duration (sec) b 1 92 Repair and replacement of brakes 92 29 2 102 Filing and replacement of brakes 10 46 3 95 Sanding and replacement of brakes 4 34 4 107 Arc grinding and replacement of brakes 20 39 5 85 Repair and replacement of brakes 85 22 6 96 Arc grinding and replacement of brakes 18 22 a(min) = minutes; b(sec) = seconds 4.4.1 Area Air Samples A total of 38 area air samples were collected during the six indepe ndent test sessions focusing on the repair and replacement of asbestos-containing brakes. Among these samples, approximately 64% (n = 24) were collected within 3 me ters of the test vehicle. The remaining 14 samples were either backgr ound samples collected along the external walls or less than 3 meter from the arc we lding bench. Table 40 summarizes the average PCM and PCME fiber concentrations sampled within 3 meters of the test vehicles. Within these samples, the average PCM fi ber levels ranged 0.0027 between 0.0296 f/cc. The two highest PCM fiber concentrati ons of 0.0276 and 0.0296 f/cc were observed during the arc grinding of new replacement brakes containing chrysotile asbestos. Background area samples, in addition to sa mples collected near the grinding bench, reflected similar findings. The highest fibe r concentrations observed in these samples occurred during the arc grinding of brake s hoes. Analysis of these samples by TEM detected only chrysotile fibers. Table 41 revi ews the background fiber levels, in addition to the fiber concentrations dete cted near the grinding bench.

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106 Table 40: Area Air Samples Collected Less than 3 Meters from Test Vehicles Test Task n a Duration (min)b Mean PCMc(f/cc)d Mean PCM TWAe (f/cc) Mean PCMEf (f/cc) Mean PCME TWA (f/cc) 1 Removal and replacement of brake shoes 4 92 0.0027 0.0005 0.0002 0.0000 2 Filing 4 102 0.0282 0.0060 0.0128 0.0027 3 Sanding 4 95 0.0133 0.0026 0.0097 0.0019 4 Arc grinding I 4 107 0.0296 0.0064 0.0266 0.0057 5 Removal and replacement of brake shoes 4 85 0.0258 0.0046 0.0060 0.0011 6 Arc grinding II 4 96 0.0276 0.0055 0.0186 0.0037 a(n) = sample number; b (min) = minutes; c(PCM) = Phase Contra st Microscopy; d (f/cc) = fibers/ cubic centimeter of air; e(TWA) = Time Weighted Average; f(PCME) =Phase Contrast Microscopy Equivalent Table 41: Indoor Background and Work Bench Area Air Samples Test Task Location PCMa (f/cc)b PCMEc (f/cc) 1 Removal and replacement of brake shoes Background d Workbench d 2 Filing Background 0.03 0.0097 Workbench d 3 Sanding Background 0.0113 0.0092 Workbench 0.0142 0.0091 4 Arc grinding I Background 0.0389 0.0389 Workbench 0.0895 0.0828 5 Removal and replacement of brake shoes Background 0.0227 0.0095 Workbench 0.0325 0.0093 6 Arc grinding II Background 0.0265 0.0154 Workbench 0.045 0.0372 a (PCM) = Phase Contrast Microscopy; b (f/cc)= fibers/cubic centimeter of air; c (PCME) = Phase Contrast Microscopy Equivalent; d Indicates samples that were overloaded or not collected

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107 4.4.2 Personal Air Samples The personal air samples collected and anal yzed during the brake exposure assessment are summarized in Table 42. The average PC M and PCME fiber concentrations for all six personal air samples were 0.122 and 0.105 f/ cc, respectively. The asbestos fiber ratios for these samples ranged from 7 to 99 % with the highest concentrations being observed during arc grinding of new shoes. The PCM fiber concentration corresponding to the arc grinding tests were 0.437 and 0.201 f/ cc. Ninety-nine percent of the fibers detected by TEM during the firs t arc grinding test were dete rmined to be chrysotile asbestos, with the remaining 1% being non-asbest os fibers. The duration of this test was 107 minutes with approximatel y 20% of the test being dedicated to arc grinding. The baseline tests resulted in PCM fiber c oncentrations of 0.0217 and 0.0672 f/cc. These values provide evidence that when arc grin ding is not performed fiber liberations is minimal and that the servicing of brake co mponents results in a minimal exposure to asbestos fibers.

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108 Table 42: Personal Air Sample s Collected during Brake Study Test Task Time (min)a Volume (L)b PCMc(f/cc)d PCM TWAe (f/cc) Asbestos Fiber Ratiof PCMEg (f/cc) PCME TWA (f/cc) 1 Removal and replacement of brake shoes 92 282 0.02170.0042 0.76 0.0164 0.0031 2 Filing 102 313 0.03760.008 0.95 0.0356 0.0076 3 Sanding 95 199 0.07760.0154 0.88 0.0684 0.0135 4 Arc grinding I 103 215 0.437 0.0937 0.99 0.436 0.0935 Cleaning 30 67 0.01460.0009 0 0 0 5 Removal and replacement of brake shoes 85 175 0.06720.0119 0.07 0.0048 0.0009 6 Arc grinding I 96 198 0.201 0.0401 0.86 0.173 0.0347 a(min) = minutes; b(L) = liters; c (PCM) = Phase Contrast Microscopy; d (f/cc)= fibers/cubic centimeter of air; e(TWA) = Time Weighted Average; f Asbestos Fiber Ratio is defined as th e number of asbestos fibers detected via Transmission Electron Microscopy (TEM) divided by the total number of all fibers detected via TEM; g (PCME) = Phase Contrast Microscopy Equivalent 4.5 Cumulative Lifetime Asbestos Exposure Two sets of cumulative lifetime asbestos exposures have been estimated for mechanics engaged in the servicing of as bestos-containing automotive parts. These values are point estimates calculated to elucidate the poten tial asbestos exposure mechanics would be expected to experience over a 45-year work ing lifetime. Additionally, these exposure estimates serve as a referen ce value for comparison against theorical no-effect exposure threshold for of asbestos-related diseases. In the first group, the cumulative lifetime asbestos exposures were based on the m ean PCM and PCME fiber concentrations obtained from the personal air samples collect ed during the individua l tasks performed in each assessment. A summary of the cumulative lifetime asbest os exposures for mechanics based on the mean PCM and PCME fiber concentrations from personal air samples can be found in

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109 Table 43. The highest lifetime exposures for bot h sets of estimates were associated with the removal and replacement of chrysotilecontaining brakes. The cumulative lifetime asbestos exposure based on PCM and PCME fiber concentrations were 2.000 and 0.477 f-yr/cc, respectively. These values were based on the personal samples collected during test sessions that focused exclusively on the installation and removal of asbestos brake linings. The mean PCM fiber concentrations for these samples was 0.045 f/cc, which is within the same range of fibe r concentrations reported in previously published exposure assessments [1, 5, 12, 13, 15]. The personal sa mples collected during the other four test sessions conducted during the br ake study were not applied with in this analysis because arc grinding, sanding and filing were performed for extended durations of time that may not be representative of the standard work practices applied by brake mechanics. The second highest cumulative lifetime asbestos e xposure asbestos obser ve in this study was approximately 1.8 f-yr/cc, while all other expos ure estimates were le ss 1 f-yr/cc (< 1 fyr/cc). No exposure estimate exceeded the theorical thresholds for asbestosis, lung cancer and mesothelioma applied within this study. Additionally, when estimated for a 45-year working lifetime, the OSHA PEL of 0.1 f/cc results in a cumulative lifetime asbestos exposure of 4.5 f-yr/cc. The cumu lative lifetime asbestos exposures calculated for mechanics from the PCM fiber concentr ations range from approximately 2 to 10 times lower than the value based on the OS HA PEL. These findings indicate that mechanics servicing these forms of asbestos-containing automotive parts are not at increased risk of asbestos-related diseases. Figure 20 illustrates the distribution of the cumulative lifetime asbestos exposures to the thresholds for asbestosis, lung cancer and mesothelioma.

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110 Table 43: Summary of the Annual Average 8-HR Daily Exposures, Cumulative Lifetime Asbestos Exposures and 95% U pper Confidence Limits Obtained from Personal Air Samples Exposure Source n a Annual Average 8-HR b Daily Exposure (PCM f/cc) c Cumulative Lifetime Exposure (PCM f-yr/cc) d 95% UCLe Annual Average 8-HR Daily Exposure (PCME f/cc) f Cumulative Lifetime Exposure (PCME f-yr/cc) g 95% UCL Gaskets 10 0.010 0.469 0.210 0.002 0.102 0.137 Clutch 4 0.039 1.755 2.229 0.001 0.062 0.114 Brakes 2 0.045 2.000 0.289 0.011 0.477 0.289 a (n) = sample number; b (8-HR) = Eight Hour Daily; c (PCM f/cc) = Phase Contrast Microscopy fibers/cubic centimeter of air; d (PCM f-yr/cc) = Phase Contrast Microscopy fiber-year/cubic centimeter of air; e (UCL) = Upper Confidence Limit; f (PCME f/cc) = Phase Contrast Microscopy Equivalent fiber/cubi c centimeter of air; g (PCME f-yr/cc) = Phase Contra st Microscopy Equivalent fiber-year /cubic centimeter of air

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111 Figure 20: Cumulative Lifetime Asbest os Exposures based on PCM and PCME Fiber Concentrations Associated with P ersonal Air Samples Collected during the Gasket, Clutch and Brake Exposure Assessments Relationship of the estimated cumulative lifeti me asbestos exposure to the theorical no-effect thresholds for asbestosis, lung cancer and mesot helioma based on the mean PCM and PCME fiber concentrations associated wi th personal air samples. a Correspond with theorica l thresholds for lung cancer and asbestosis found in Table 19; b Correspond with theorical thresholds for mesothelioma found in Table 19; The bars above the different cumulative lifetime asbestos exposures represent the 95% Upper Confidence Limit The second series of cumulativ e lifetime asbestos exposures are based on air samples identified through TEM to contain asbestos fi bers. These samples have been chosen to estimate the working lifetime exposure to asbestos for mechanics while servicing

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112 automotive parts containing chrysotile fibers Within the four independent exposure assessments, all area and personal air sample s identified to contain asbestos were averaged to determine the mean PCM and PCME fiber concentrations. Table 44 provides a summary of the cumulative lifetime asbe stos exposures estimated from samples identified to contain asbestos, in addi tion to the 95% UCL and the mean fiber concentrations of these samples. The estima ted exposure values associated with the PCM fiber concentrations ranged from 0.477 to 3.560 f-yr/cc. In comparison, the cumulative lifetime asbestos exposure based on the PCME fiber concentration ranged from 0.266 to 2.179 f-yr/cc. As in the exposure estima tes based on the personal air samples and presented in Table 43, the highest cumulative lif etime asbestos exposures were associated with the removal and replacement of brake li nings containing chrysotile fibers. The cumulative lifetime asbestos exposures base d on air samples identified through TEM to contain asbestos do not exceed the theorized noeffect exposure thresholds for asbestosis, lung cancer or mesothelioma. The highest cumulative lifetime asbestos exposure mechanics experience during the maintena nce of asbestos-containing parts is approximately 4 f-yr/cc. This value is a pproximately 4 to 7 times lower than the noeffect exposure thresholds for the different as bestos-related diseases. In comparison, the lowest cumulative lifetime asbestos expos ure was 0.086 f-yr/cc, and occurred during the servicing of the asbestos-clutch. When compar ed to the threshold limits for the asbestosrelated diseases, this value is between 175 to 300 times lower. These estimated cumulative lifetime asbestos exposures indicate that mechanics are not at increased risk of asbestos-induced pulmonary diseases. Fi gures 21 and 22 illustra te the relationship

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113 between the theorized thresholds for the asbe stos-related diseases and the calculated cumulative lifetime asbestos exposures for automotive mechanics. Table 44: Summary of the Annual Average 8-HR Daily Exposures, Cumulative Lifetime Asbestos Exposures and 95% Upp er Confidence Limits Obtained from Air Samples Identified to Contain Asbestos through TEM during the Gasket, Seam Sealant, Clutch and Brake Exposure Assessments Exposure Source n a Annual Average 8-HR b Daily Exposure (PCM f/cc) c Cumulative Lifetime Exposure (PCM fyr/cc) d 95 % UCL e Annual Average 8HR Daily Exposure (PCME f/cc) f Cumulative Lifetime Exposure (PCME fyr/cc) g 95% UCL Gaskets 11 0.011 h 0.477 0.205 0.003 h 0.256 0.112 Seam Sealant 19 0.025 h 1.136 0.353 0.005 h 0.239 0.126 Clutch 4 0.039 h 1.834 2.094 0.001 h 0.086 0.073 Brakes 39 0.079 h 3.560 1.941 0.048 h 2.179 1.988 a (n) = sample number; b (8-HR) = Eight Hour Daily; c (PCM f/cc) = Phase Contrast Microscopy fibers/cubic centimeter of air; d (PCM f-yr/cc) = Phase Contrast Microscopy fiber-year/cubic centimeter of air; e (UCL) = Upper Confidence Limit; f (PCME f/cc) = Phase Contrast Microscopy Equivalent fiber/cubi c centimeter of air; g (PCME f-yr/cc) = Phase Contra st Microscopy Equivalent fiber-year /cubic centimeter of air; h Values represent averages of all area and personal air samples

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114 Figure 21: Cumulative Lifetime Asbe stos Exposures based on PCM Fiber Concentrations Associated with All Air Samples Identified to Contain Asbestos through TEM from the Gasket, Seam Sealant, Clutch and Brake Exposure Assessments 0.4771.1361.834 3.560 0 5 10 15 20 25 30 012345 Gaskets Seam Sealant Clutch Brakes Cumulative Lifetime Asbestos Exposure(PCM f-yr/cc)No-Effect Exposure Threshold for M esothelioma bNo-Effect Exposure Threshold for Asbestosis and Lung Cancer a Relationship of the estimated cumulative lifeti me asbestos exposure to the theorical no-effect exposure thresholds for asbestosis, lung can cer and mesothelioma based on the mean PCM fiber concentrations associated with all air samples id entified to contain asbestos fiber through TEM. a Correspond with theorical thresholds for lung cancer and asbestosis found in Table 19; b Correspond with theorical thresholds for mesothelioma found in Table 19; The bars above the different cumulative lifetime asbestos exposu res represent the 95% Upper Confidence Limit

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115 Figure 22: Cumulative Lifetime Asbe stos Exposures based on PCME Fiber Concentrations Associated with All Air Samples Identified to Contain Asbestos through TEM from the Gasket, Seam Sealant, Clutch and Brake Exposure Assessments 0.266 0.23850.0855 2.1790 5 10 15 20 25 30 012345 Gaskets Seam Sealant Clutch Brakes No-Effect Exposure Threshold for M esothelioma bNo-Effect Exposure Threshold for Asbestosis anf Lung Cancer aCumulative Lifetime Asbestos Exposur e (PCME f-yr/cc) Relationship of the estimated cumulative lifeti me asbestos exposure to the theorical no-effect exposure thresholds for asbestosis, lung cancer and mesothelioma based on the mean PCME fiber concentrations associated with all air samples id entified to contain asbestos fiber through TEM. a Correspond with theorical thresholds for lung cancer and asbestosis found in Table 19; b Correspond with theorical thresholds for mesothelioma found in Table 19; The bars above the different cumulative lifetime asbestos exposu res represent the 95% Upper Confidence Limit

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116 CHAPTER 5.0 DISCUSSION Establishment of an association between o ccupational asbestos exposure and pulmonary diseases is dependent on the characterization of multiple factors including fiber type and size, in addition to the intensity of exposure [31]. Using these guidelines, and evidence presented in epidemiological investigati ons and previous exposure assessments, mechanics historically employed in the automotiv e repair industry are not at elevated risk of asbestosis, lung cancer or mesothelioma. This statement is supported by the overall findings reported in the current investiga tion, in addition to published studies. Previous investigations have established a causal association between increased risk of lung cancer and mesothelioma within occupa tional cohorts exposed to amphibole fibers [42-46, 51]. Such findings have not been cons istently reported in ep idemiological studies attempting to elucidate the risk of asbest os-related cancers in workers exposed to serpentine fibers. Currently available evid ence indicated that exposure to chrysotile fibers represent a significantly lower risk than amphibole asbestos [46, 93, 94, 98, 135]. Hodgson and Darnton quantified the specific ri sk of mesothelioma between the three major commercial asbestos types, chrysotil e, amosite and crocidolite, as 1:100:500, respectively [23]. In the curre nt study, only chrysotile fibers were detected in the air and

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117 bulk samples collected within the four individual exposur e assessments supporting the belief that amphibole fibers were not used within the manufacturing of automotive ACMs [94, 136]. The absence of tremolite and ot her contaminant amphibole fibers in parts containing asbestos greatly de crease the risks of lung cancer and mesothelioma within automotive mechanics. The risk analysis developed and implemente d in this study was based on the assumption that a threshold exists below which asbestos-related diseases are not expected to occur. These theorical no-effect expos ure thresholds are based on cumulative lifetime exposures due to the ability of asbestos fibers to pers ist and accumulate within human lungs. It is important to note that the view of a threshol d for asbestos-induced pulmonary disease is a highly debated issue that has polarized the sc ientific community. Numerous studies have reported that no threshold dose exists for asbe stos, and that these diseases follow linear dose-response relationships [121]. Traditi onally, governmental agencies, such as the EPA, identify all types of asbestos as know n human carcinogens, and state that there is no level of exposure to the fibrous minerals that does not increas e the risk of cancer. Non-threshold relationships assume that a single fiber could potentially induce a biological response that results in a cell becomi ng cancerous. In part this is do to the lack of chemical-specific data that elucid ates the pharmacokinetics and the mechanism of action responsible for the induction of cancers associated with asbestos fibers. Nonthreshold models are commonly applied due to insufficient animal and epidemiological data capable of directly meas uring the risk at low levels of exposure [137, 138]. For this reason, linear relationships are unable to re liably evaluate the pl ausible upper bound risk

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118 or the actual risk determined by the chemi cal properties of the carcinogen, and may not be biologically plausible [ 139]. Governmental agencies including the EPA, NIOSH and OSHA, have been charged with the responsib ility of protecting pe ople from potentially deleterious exposures to chemicals, such as asbestos, from environmental or occupational sources. A non-threshold, or linear, model is commonl y applied because these organization prescribe to the precautionary principle. For this reason, non-threshold dose-response relationship resu lts in the development of health policies that offers a conservative or overestimated probability th at a substance will produce cancer. This ensures that the majority of the population po tentially exposed to the chemical will be protected from the onset of diseases, but doe s not necessarily repr esent a biologically plausible dose-respons e relationship. The majority of published exposure assessments and workplace simulations investigating asbestos exposure during the maintenance of automotive friction materials have focused principally on brake components [1, 4-8, 1215, 98-104]. No study could be identified that exclusively repo rted the airborne asbestos le vels mechanics encounter while servicing and handling clutches containing chry sotile asbestos. Activities, including arc grinding, sanding and filing the edges of brake sh oes to match the internal dimensions of companion brake drums are frequently required to complete the installation of new brake shoes on a vehicle. New clutches do not requ ire this form of manipulation and can be directly inserted into the ve hicle. For this reason, asbestos exposure for mechanics servicing manual transmissions containing asbest os clutches cannot be extrapolated from

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119 these previous studies due to the signifi cant differences in work activities being performed on the two types of friction materials. Multiple studies have reported increased rates of asbestos-related diseases in workers employed to refurbish asbestos-containing fric tion materials, includ ing clutches [140142]. Individuals performing the restoration of friction materials frequently strip worn brake linings and clutches faces, in add ition to machine grinding the surfaces of refurbished automotive parts [142]. Airborne fiber levels have been reported ranging between 0.025-76.4 f/cc [142]. Th ese activities and workplac e conditions are unique to refurbishing facilitie s and do not occur during the remova l and replacement of asbestosclutches. In contrast, the highest PCM fiber concentration observed during the current study was 0.0022 f/cc. This value is approxima tely 10 times below the lowest fiber level reported in the previous desc ribed studies, and 100 times lower than the current OSHA PEL. Mechanics are exposed to extremely lim ited levels of airborne asbestos during the servicing of automotive clutches containing as bestos using standard operating procedures including blowouts with compressed air. Asbestos fibers were identified in 66% (n = 4) of the air samples associated with the installation and reassembly of the manual tr ansmission. A pattern of exposure can be observed during this test session when the sa mples identified to contain asbestos are compared to the individual activities perf ormed by the mechanic. The area samples located at the front and driver’s side door of the test vehicl e were determined to contain asbestos fibers through TEM. These two monito ring stations were in close proximity to

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120 the location were the mechanic initially ope ned the packing containing the new asbestos replacement. Additionally, both samples were ob tained directly in the path the mechanic utilized to carry the new clutch disc to the test vehicle before placi ng it beneath the truck. Based on these observations, it appears that the greatest potential for exposure to asbestos during the removal and replacement of asbest os-containing automotive clutches lies in the interim between the initial handling of th e new clutch and it being sealed within the bell housing. No additional exposure is expect ed once the clutch is placed in the housing due to it being completely enclosed by the structure. Anderson reported chrysotile fibe r concentrations of <10% within asphalt-based seam sealants and undercoating materi als [94]. TEM analysis of the bulk samples collected during the seam sealant exposure assessment yielded asbestos concentrations ranging from 5.6 to 28%. Despite the relatively hi gh concentration of chrysotile fibers within the seam sealant, the mean asbestos fibe r level for personal samples was 0.006 TEM f/cc with many of the samples reported at or belo w the analytical LOD. These observations indicate that asbestos fibers are not readily liberated duri ng the removal of the sealant material from unibody vehicles. Additionally, no foresterite was identified within any bulk or air samples collected within the four independent exposure assessments. These findings do not support the theory of the breakdo wn of chrysotile asbestos into this form of non-asbestiform hydrated silicat e mineral. The failure to de tect this mineral could be the result of a complete degrada tion of asbestos fibers into particulates outside the range of detection for TEM or beyond the optical limitations of PCM analysis.

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121 During the brake exposure assessment, the hi ghest fiber concentrations were observed within test sessions associated with extensive arc grinding of new asbe stos brakes shoes. Arc grinding is a process that uses an abra sive wheel or belt to shape a brake shoe to precisely match the internal dimensions of its companion brake drum. This process has previously been reported to ge nerate levels of asbestos fi bers between 0.02 to 8.2 f/cc for passenger automobiles [9, 13]. TEM analysis of the personal samples associated during the arc grinding of brake shoes yielded chrysot ile fiber concentrations of 86 and 99%. Additionally, the PCM fiber con centrations for these samples were between 2 and 4 times higher than the current OSHA PEL. Mechanics that performed this activity for extended intervals of time may be at the highest risk of developing asbestos-r elated diseases. The baseline tests conducted with in this exposure assessment yielded much lower fiber concentrations. The results from these se ssions indicate when bl owouts and activities beyond the removal and replacement of brakes are not performed the level of fibers liberated are substantially lower. The PC M fiber concentrations for these two test sessions were approximately 10 to 20 times lower than the levels observed during arc grinding. Previous studies reporting cumulative lifet ime asbestos exposures for mechanics and garage workers have relied on predictive mode ls to estimate exposure values [110, 124]. These studies have utilized va rious models to predict the aggregate lifetime exposure to asbestos mechanics experience [114, 124]. The exposure estimates reported in the previously reported investiga tions range from 0.8 to 2.92 f-yr/cc, and indicate that mechanics are not at increased risk of asbe stos-related diseases [114, 124]. The current

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122 study applied point estimates of exposure obtai ned from actual exposure data to elucidate the aggregate exposure for mechanics servicing automotive friction materials, gaskets and sealants containing asbestos. The cumula tive lifetime asbestos exposures calculated in this study are well below the no-effect exposure thresholds for asbestosis, lung cancer and mesothelioma, in addition to being within the same approximate range of exposures reported in the previous studi es [104, 125]. It should be noted that an association between exposure to chrysotile asbestos and mesothelioma is not supported by epidemiologic evidence. Based on the lack of data for a relationship between inhalation of serpentine fibers and malignant pulmona ry diseases, the findings of this study corroborate previous investigations that report that mechanics are not at increased risk of lung cancer and mesothelioma from the limited exposure to chrysotile asbestos [5, 31]. PCM fiber concentrations are indexes of e xposure that provide an estimate of total airborne fiber levels. PCME fiber concen trations are exposure estimates designed to reflect only the potential asbestos fiber levels. The cumulative lifetime asbestos exposures calculated in the current study were based on the mean PCM and PCME fiber concentrations obtained from the individual e xposure assessments. When compared, the aggregate lifetime exposures yielded results that are significantly difference in many instances. An example of the variations betw een the different sets of calculation can be observed in the cumulative lifetime asbestos exposures for the insta llation of clutches. The cumulative lifetime asbestos exposure based on the PCME fiber concentration was approximately 20 times lower than the exposure value based on the PCM value. Cumulative lifetime asbestos exposure have traditionally been calculated using PCM

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123 fiber concentrations within previously published studi es, in addition to ATSDR documents [19, 104, 125, 132]. This practice may be out dated and resu lt in a significant overestimation of the aggregate exposure an individual may receive from a specific task or environmental condition. Numerous uncertainties may have occurred du ring the individual exposure assessments and analysis of data that may have affected the results of th is study. First, the airborne levels of fibers reported for the individual work activities may have been influenced by the use of certain practices, low fiber density and the statistical met hods used within this study. Additional factors that should be considered includ e the analytical methodology used to analyze the samples. The followi ng paragraphs discuss the potential limitations and shortcomings of this study. Use of the water bath cleaner may have ha d some asbestos fiber suppression effect. Despite the argument that the wetting of loos e parts may potentially prevent the liberation of fibers during the cleaning process and subsequently reduce the concentration of airborne asbestos fibers, the water bath cleaner is commonly us ed in the automotive repair industry and conforms to the study desi gn’s aim of applying actual work practices. Additionally, the water wash pe riods were brief and power wi re brushing was performed without aqueous wash on the engine blocks. For these reasons, the fiber suppression effect attributed to the use of th e water bath cleaner was minimal. A potential shortcoming of this st udy is the ability of the findi ngs to be applied to setting

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124 beyond the conditions under which the exposur e assessments were conducted. Concerns about the external validity of this investig ation include the types of vehicles and number of mechanics used in the test. The first pot ential limitation involved the selection of the vehicles used in the exposure assessments. The staff members of Clayton Group Services and the author of the current investigation atte mpted to use vehicles that were common in the 1960s through 1970s. Although all attempts were made to utilize automobiles and light-duty trucks representati ve of the pre-1980 era, it is logistically and finically infeasible to perform exposure assessments fo r every vehicle produced in the desired time period that were assembled with parts containing chrysotile fibers. Secondly, due to the duration of time that has pasted since these vehicles were originally manufactured, the availability of these cars is extremely limited. For example, only one vehicle, the Kaiser Jeep, was identified after a broad search to contain its original clutch. Additional problems arise in acquiring replacement parts containing asbestos for tests associated with the installation of new ACMs. These re asons have limited the number of vehicles used in the exposure assessments. The second factor that may have affected th e external validity of this study is the selection of the mechanics us ed in the individual exposure assessments. Each mechanic that participated in the various studies wa s a professional who have a minimum of 20 years of experience. The technical skills and techniques applied by these mechanics may not be representative of garage workers w ith limited practice performing the maintenance activities conducted in the differe nt tests. The fiber concen trations generated during the removal and replacement of ACMs by inexperi enced mechanics may vary from the fiber

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125 concentrations observed in this study. For these reasons, the results of this investigation may be applicable primarily to mechanic s employed as professionals and who are experienced Approximately 200 total personal and area air samples were collect ed during the four exposure assessments. When viewed independen tly, the individual data sets ranged from 12 to 98 air samples. Several published exposure assessments and workplace simulations report sample sizes within a similar range [12, 13, 15, 16, 95]. Although these sample numbers are not uncommon within exposure assessments, the sample sizes may have been too small to provide external validit y beyond the current investigation. For this reason, the conclusion of this study that mechan ics are exposed to low levels of airborne asbestos fibers during the servicing of au tomotive ACMs may only be representative of garage workers that experience occupational settings similar to the conditions described in the current study. Additionally, the sm all sample size potentially narrowed the reported variance, which in turn, may have re sulted in an underestima tion of the asbestos concentrations mechanics are exposed to with in this study. Future investigation should attempt to ascertain sample sizes large e nough to increase the st atistical power and decrease the uncertainty associat ed within this type of study. The use of the upper limits of the LOD as the actual exposure value in the calculation of the summary statistics may have resulted in two potential limitations. The first shortcoming is a possible narrowing of the vari ance observed in this investigation. By using conservative values within the estimation of the statistics, the confidence levels

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126 may not truly represent the variance associated within these samples. An analysis was performed to determine the difference in the su mmary statistics associated with the use of (LOD/2) and [LOD/SQRT(2)] against the a pplication of the upper limit. It was determined that the mean fiber concentrations produced by the use of the upper limits for censored data of the LOD were no greater th an 13% higher than the other methods. The variance associated with the application of (LOD/2) and [LOD/SQRT(2)] in place of censored data were approximately 7 to 14% lo wer than the use of the LOD. The overall results of this potential shortcoming may be the underestimation of the variance of the cumulative lifetime asbestos exposures, and the false declaration of no increased risk of asbestos-induced diseases when these exposur e estimates are compared to the no-effect exposure thresholds. The second shortcoming associated with us e of the LOD in the calculation of the exposure concentration is a pot ential underestimation of the ri sk. Epidemiologic studies have demonstrated that when inaccurate or overestimated exposure estimates are applied within the calculation of ri sk the likelihood of underestima ting that risk or missing the adverse health outcome altogeth er is increased [143]. For the current study, the use of the LOD within the calculation of the mean fi ber concentrations was determined to offer conservative exposure estimates. In using th is methodology to address censored data, the results of this study may have resulted in th e underestimating of the risk of asbestosrelated diseases within auto motive mechanics engaged in the servicing of automotive parts containing asbestos. The use of a differing methodology to address censored data, such as the extrapolation of the left-hand tail of the data distribution, may have provided

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127 a more accurate representation of the expos ure values and risk of asbestos-related diseases. The air samples assembled for this study have been analyzed by phase contrast microscopy and transmission electron micr oscopy using NIOSH Methods 7400 and 7402. Criticism of the use of PCM and TEM fo r fiber counting focuses primarily on the exclusion of short (<5m long) and long but thin (<0.25 m wi de) asbestos fibers [9, 10, 144]. The elimination of fibers shorter than 5m in length and 0.25m in diameter is based on the limitations of light microscopy an alyses, which are unable to consistently and accurately count fibers with in this size range [27]. Due to the optical limitations of light microscopy, PCM fiber concentrations ar e considered indexes of exposure that are assumed to be correlated with the fibers res ponsible for the onset of diseases such as lung cancer or mesothelioma [27]. Arguments against the use of NIOSH Methods 7400 and 7402 state that the elimination of the short and thin structures from the data set underestimates the risk that exposed worker s encounter [144]. This theory is not supported by previously published studies and recent committee findings released by the ATSDR report that found limited or no human cancer risk from fibers fitting the previous descriptions [52-54]. The fiber populations excluded fr om counting by NIOSH Methods 7400 (PCM) and 7402 (TEM) are arguably of lim ited significance, and more importantly distracts attention from the real benefit these methods offer. Benefits of the use of data obtained from NIOSH Met hods 7400 and 7402 include direct comparison against established health risk databases, occ upational exposure limits and environmental standards. No such databases exist for the asbestos structure data for short (<5m long)

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128 and long but thin (<0.25 m wide) asbestos fibers. Despite the limitations associated with these analytical and sampling methods, the advantages of their use exceed their disadvantages. Initially, the air samples collected during the removal of seam sealant were analyzed via TEM based on the methodologies outlined in NIOSH Method 7402. PCM was used only on air samples identified to contain asbestos. The established rou tine of performing PCM followed by TEM was not performed because the original purpose of the exposure assessment was to elucidate the asbestos fi ber levels liberated from the removal of chrysotile-containing undercoa ting material. PCM fiber concentrations were only determined for samples identified to contain as bestos fibers after th e initial analysis by TEM. Although the cumulative lif etime asbestos exposure for mechanics engaged in this work activity was estimated based on these sa mples, no exposure values were available from the personal samples. This has prevented the comparison of the cumulative lifetime asbestos exposure based on personal samples between seam sealants and other asbestoscontaining automotive parts evalua ted within the current study. NIOSH Method 7400 recommends fiber loadi ng concentrations at or above 100 fibers/mm2 (f/mm2) to avoid inaccuracies during the counting process [110]. In situations, such as the gasket and seam sealant studies, where airborne fibers concentrations remain low or do not exis t, compliance with the recommendation is difficult. Several techniques have been sugge sted to offset the effects of low fiber densities including decreasing the surface area of the filter or increasing the sampling

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129 flowrates [145]. During each of the individual tests, the range of a pplied flowrates varied from 2 to 12 lpm. The fiber concentrati ons determined through PCM and TEM analyses for samples collected at the different flowrate s did not noticeably diffe r, and indicate the absence of airborne fibers, both asbestos a nd non-asbestos, within the automotive repair facility. The potential error a ssociated with low fiber densit ies has been demonstrated to result in high fiber counts and frequen tly yield overestimated airborne fiber concentrations [145].

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130 CHAPTER 6.0 CONCLUSION Mechanics employed in the automotive repair industry represent a large occupational cohort frequently perceived to be at increase d risks of asbestos-related diseases [9, 10}. Large volumes of ACMs have been historically utilized during the a ssembly of vehicles with each automotive part representing a uni que exposure point source. The current study has been conducted to determine the asbestos exposure mechanics potentially experienced during the servicing of multiple automotive parts containing asbestos, in addition to elucidating if mechanics are at in creased risk of asbestosis, lung cancer and mesothelioma. To date, no published study has provided an es timate of the lifetime asbestos exposure for mechanics associated with parts cont aining asbestos beyond brake components. Future research needs include the elucidati on of the overall cumulative lifetime asbestos exposure for mechanics associated with au tomotive ACMs including friction materials, gaskets and seam sealant. The methodology developed by Plato et al. could potentially serve as a template to estimate the aggreg ate lifetime asbestos exposure for mechanics from all point sources of asbestos within the work environment [104]. The prescribed process includes an exposure matrix and a predictive model described as applying both

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131 additive and multiple components to assess m echanics’ asbestos exposure. Covariates, included within this model, are work ac tivities, equipment, ventilation, workshop descriptions, in addition to exposure intens ity and duration. The exposure matrix and data set would need to be expanded to incl ude information relati ng to parts containing asbestos beyond brake components. Additiona l sources of exposure data would need to be identified either within published literature or previ ously unpublished sources to ensure that the investigation would be repres entative of multiple settings and mechanics, in addition to having an overa ll high external validity. Prior to the current investiga tion, the majority of published l iterature focusing on asbestos exposure within the automotive repair industr y centered primarily on brake components. Little exposure data were available for ch rysotile-containing engi ne gaskets, seam sealants and clutches. This study has provided supplementary exposure data beyond brake parts, in addition to the estimation of the cumulative life time asbestos exposure associated with the servicing of various forms of automotive ACMs. An additional contribution of the current investigation wa s the implementation of a qualitative risk analysis process capable of de termining if mechanics were at increased risk of selected asbestos-related diseases. Four exposure assessments were conducted to provide the exposure data required to calculate the cumulative lifetime asbestos exposures for mechanics engaged in the servicing of gaskets, seam sealant and fricti on materials. These workplace stimulations applied standard operating procedures a nd settings representative of conditions

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132 mechanics historically experien ced when the use of automotive parts containing asbestos were most prevalent. The cumulative lifetim e asbestos exposures were compared against no-effect exposure thresholds for asbestos-related dis eases identified through an extensive literature search. An elevated ri sk of disease was declared if the calculated cumulative lifetime asbestos exposures exceeded the theoretical thresholds. All cumulative lifetime exposur es calculated in the current study were below the noeffect exposure thresholds associated with asbestosis, lung cancer and mesothelioma. The estimated exposure values were within the same approximate range reported in previous studies [110, 137]. Based on these results, mechanics are not at increased risk of asbestos-related diseases due to poten tial asbestos exposures generated during the servicing of automotive parts containing asbestos. Asbestos concentrations observed in the cu rrent study are predominantly lower than the airborne asbestos levels repor ted in previous studies [1, 1215]. When compared to the OSHA PEL, the PCM fiber concentrations observed within the current study were approximately 10 to 100 times lower than 0.1 f/cc. These findings indicate limited fiber liberation during the mainte nance of automotive ACMs us ing standard workplace practices. Overall, the conclusions of this study are: 1. The airborne asbestos levels generate d during the removal and replacement of asbestos-containing gaskets, seam seal ants and friction materials do not exceed

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133 the current OSHA PEL of 0.1 f/cc. 2. The cumulative lifetime asbestos exposures calculated for mechanics servicing automotive asbestos-containing materials do not exceed the no-effect exposure thresholds identified for asbestos is, lung cancer and mesothelioma. 3. This study supports the findings of previ ous epidemiological studies and exposure assessments that report no increased risk of asbestosis, lung cancer and mesothelioma among mechanics performi ng maintenance activities on automotive parts containing asbestos [1, 4-8, 12-15].

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145 130) Rees, D., Phillips, J.I., Garton, E. and P ooley, F.D. (2001). "Asbestos lung fiber concentrations in South African ch rysotile mine workers." Annual of Occupational Hygiene 45 (6): 473-477. 131) Chen, W., Zhu, Z., Attfield, M.D., Chen, B.T., Gao, P., Harrison, J.C., Chen, J. and Wallace, W.E. (2001). “Exposure to silica and silicosis among tin miner in China: Exposure-response analyses a nd risk assessment.” Occupational and Environmental Medicine 58: 31-17. 132) Price, B. and Ware, A. (2005). "Mes othelioma: Risk apportionment among asbestos exposure sources." Risk Analysis 25(4): 937-943. 133) Stewart, P. A. and Herrick, R.F.. (1991) "Issues in performing retrospective exposure assessment." Applied Occupati onal and Environmental Hygiene 6(6): 421-427. 134) Occupational Safety and Health Admini stration (1988). “Occupational Exposure to Asbestos, Tremolite, Anthophyllite and Ac tinolite.” Section 2: Regulatory and Legal Authority Background. http://www.osha.gov/pls/oshaweb/owadisp.show_document?p_table=PREAMBLES&p_id=793. 135) Butnor, K.J., Sporn, T.A. and Roggli, V. L. (2003). “Exposure to brake dust and malignant mesothelioma: A study of 10 cas es with mineral fiber analyses.” Annuals of Occupational H ygiene 47 (4): 325-330. 136) Rodelsperger, K., Jahn, H., Bruckel, B., Ma nke, J., Paur, R. and Woitowitz, H.J. “Asbestos dust exposure during brake repa ir.” American Journal of Industrial Medicine 10 (1): 63-72. 137) Purchase, I.F.H. and Auton, T.R. (1995). “Thresholds in Chemical Carcinogenesis.” Regulatory Toxi cology and Pharmacology 22: 199-205. 138) IRIS. (1992). “EPA's Approach for Asse ssing the Risks Associated with Chronic Exposure to Carcinogens.” (Retrieved on July 11, 2006). U.S. Environmental Protection Agency, Integrated Risk Information System. http://www.epa.gov/iris/carcino.htm 139) Conolly, R.B. (1987). “Cancer and no-cance r risk assessment: Not so s different if you consider mechanism.” Toxicology 102: 179-188. 140) Levin, J.L., O’Sullivan, M., Corn, C.J. and Dodson, R.F. (1995). “An individual with a majority of ferruginous bodies form ed on chrysotile cores.” Archives of Environmental Health 50(6):462-5. 141) Levin, J.L., O’Sullivan, M. and Dodson, R.F. (2003). “Environmental sample correlation with clinical a nd historical data in a friction product exposure.”

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146 Inhalation Toxicology 15 (7): 639-47. 142) Sakai, K., Hisanaga, N., Shibata, E., O no, Y. and Takeuchi, Y. (2006). “Asbestos exposures during reprocessing of automobile brakes and clutches.” International Journal of Occupational and Environmental Health 12 (2): 95-105. 143) Hatch, M. and Thomas D. (1993). “Measurement issues in environmental epidemiology.” Environmental Health Perspective 101 (Supplement 4): 49-57. 144) Atkinson, M.A.L, O’Sullivan, M., Zuber, S., and Dodson, R.F. (2004). “Evaluation of the size and type of fr ee particulates collected from unused asbestos-containing brake co mponents as related to poten tial for respirability.” American Journal of Indust rial Medicine 46: 545-553. 145) Cherrie, J., Jones, A.D. and Johnston, A. M. (1986) “The influence of fiber density on the assessment of fiber concentrati on using the membrane filter method.” American Industrial Hygiene Asso ciation Journal (47) 8: 465-474.

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147 APPENDIX A Quality Evaluation of Exposure Data The purpose of the evaluation was to assess th e quality and completeness of the exposure data assembled from the four independent stud ies. The protocol discussed in Section 3.1 was adapted from multiple published studies [ 105-108]. This technique was designed to address concerns relating to the exposure data including incompleteness, poor external validity, biases and poor study design. In formation examined during the quality evaluation included, but was not limited to, the raw data, field notes and calibration records for sampling instrumentation relati ng to the exposure data. Additionally, multiple interviews with the original research team were conducted to address issues not answered by the quality evaluation. As described in Table 4, the first step in th e quality evaluation was the assessment of the completeness of the exposure data with focus on the Core Information defined in Table 5. The completeness of the core information was based on three quality levels defined as: 1. Good : All core information present. 2. Moderate : Information was available for evaluation with some aspects about the variability and precision of the data remaining undefined.

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148 3. Poor : A minimum level of information wa s available providing a fragmented assessment of the conditions and setting under which the data were collected. Based on the three quality levels, data were deemed unacceptable, or incomplete, if one or more of the evaluated components could not be classified at the minimal quality level of “ poor ” (Tielemans, 2002). Tables A-1 thr ough A-4 provide the results of the assessment of completeness of the data collected during the gasket, seam sealant, clutch and brake studies.

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149 Table A-1: Quality Evaluation of Exposure Data from Gasket Test Core Information Evaluated Components Good Quality Moderate Quality Poor Quality Workplace Description of the work area X Study Protocol Definement of the Original Purpose X Definement of the Sampling Strategy X Measurement Strategy Type of survey (representative, worst-case, other) X Measurement Procedure Sampling Date X Sample ID X Sampling Device X Type of sample X Sampling Time X Sampling Duration X Exposure Duration X Analytical Methods X Instrumentation Calibration Recorders X Results Measured Concentration X Units Used X Sample Status X

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150 Table A-2: Quality Evaluation of Ex posure Data from Seam Sealant Test Core Information Evaluated Components Good Quality Moderate Quality Poor Quality Workplace Description of the work area X Study Protocol Definement of the Original Purpose X Definement of the Sampling Strategy X Measurement Strategy Type of survey (representative, worst-case, other) X Measurement Procedure Sampling Date X Sample ID X Sampling Device X Type of sample X Sampling Time X Sampling Duration X Exposure Duration X Analytical Methods X Instrumentation Calibration Recorders X Results Measured Concentration X Units Used X Sample Status X

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151 Table A-3: Quality Evaluation of Exposure Data from Clutch Test Core Information Evaluated Components Good Quality Moderate Quality Poor Quality Workplace Description of the work area X Study Protocol Definement of the Original Purpose X Definement of the Sampling Strategy X Measurement Strategy Type of survey (representative, worst-case, other) X Measurement Procedure Sampling Date X Sample ID X Sampling Device X Type of sample X Sampling Time X Sampling Duration X Exposure Duration X Analytical Methods X Instrumentation Calibration Recorders X Results Measured Concentration X Units Used X Sample Status X

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152 Table A-4: Quality Evaluation of Exposure Data from Brake Test Core Information Evaluated Components Good Quality Moderate Quality Poor Quality Workplace Description of the work area X Study Protocol Definement of the Original Purpose X Definement of the Sampling Strategy X Measurement Strategy Type of survey (representative, worst-case, other) X Measurement Procedure Sampling Date X Sample ID X Sampling Device X Type of sample X Sampling Time X Sampling Duration X Exposure Duration X Analytical Methods X Instrumentation Calibration Recorders X Results Measured Concentration X Units Used X Sample Status X Each individual set of data was determined to meet the minimal requirements needed to be included in the current study. Among the f our independent data sets, the seam sealant data set was deemed of the poorest quality. This set of exposure data received the rating of “poor” in three different cat egories: 1) Calibration record s, 2) Analytical methods and 3) Units used. In regards to the calibration recorders, the low ranking was bestowed on the data due to the recorders for the samp ling instrumentation appearing “fragmented”. This issue was eliminated through multiple inte rviews with the original research team

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153 that provided additional information about the methodology applied to calibrate the equipment. The second and third grouping receiving a low ranking, the analytical methods and units used, occurred due to th e order in which the different analytical methods were used. All air samples obtained from the gasket, clut ch and brake studies were analyzed by both PCM and TEM. In the cas e of the seam sealant data, the original researchers initially performed TEM analysis only. Within the air samples identified to contain asbestos, approximately 20% (n = 19) of the samples were reanalyzed with PCM. This prevented the calculati on of the cumulative lifetime asbestos exposure based on the personal air samples and establis hment of the PCM fiber concentrations for all samples. The data were included into the current study because a large portion of the samples were analyzed by PCM. In addition, TEM results coul d be used to illustrate potential asbestos levels mechanics encounter while removing seam sealant containing asbestos. Overall, the exposure data from the individua l assessments were determined to be of sufficient quality to meet the needs of the current study. The exposure estimates for the air samples were utilized to determine th e asbestos exposure mechanics received while servicing the four different types of auto motive ACMS and to calculate the cumulative lifetime asbestos exposures.

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ABOUT THE AUTHOR Mr. Gary Scott Dotson is a gra duate of Murray State Univers ity with a B.S. in Biology (2000) and a M.S. in Occupational Safety and Health/Industrial Hygiene (2001). After graduating with his M.S., Mr. Dotson was employed as a Safety Representative by General Motors and Graycor Construction Co mpany. In 2002, Mr. Dotson was accepted into the Ph.D. program in P ublic Health at the Univers ity of South Florida by the Department of Environmental and Occupa tional Health. His degree has focused primarily on toxicology, risk assessment and industrial hygiene. Mr. Dotson has participated in research designed to eluc idate mechanisms induced chemical-induced hepatotoxicity associated with industrial so lvents, toxins and pharmacological agents and aiding the Center’s Director in the daily operations of the center. Additio nal positions held by Mr. Dotson included Primary Instructor and Graduate Teaching Assistant. He was involved with the teaching of graduate level risk assessm ent courses, in addition to undergraduate pathology and basic health courses.