Asbestos Draft Risk Evaluation


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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
EPA Document # EPA-740-R1-8012
March 2020
Office of Chemical Safety and
Pollution Prevention
v>EPA
United States
Environmental Protection Agency
Draft Risk Evaluation for
Asbestos
March 2020
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31	TABLE OF CONTENTS
32	ABBREVIATIONS	15
33	EXECUTIVE SUMMARY	17
34	1 INTRODUCTION	28
35	1.1 Physical and Chemical Properties and Environmental Fate	31
36	1.2 Uses and Production Volume	33
37	1.3 Regulatory and Assessment History	33
38	1.4 Scope of the Evaluation	35
39	1.4.1 Refinement of Asbestos Fiber Type Considered in this Risk Evaluation	35
40	1.4.2 Refinement of Evaluation of Releases to Surface Water	36
41	1.4.3 Conditions of Use Included in the Risk Evaluation	36
42	1.4.4 Conceptual Models	40
43	1.5 Systematic Review	43
44	1.5.1 Data and Information Collection	43
45	1.5.2 Data Evaluation	50
46	1.5.3 Data Integration	50
47	2 EXPOSURES	51
48	2.1 Fate and Transport	51
49	2.2 Releases to Water	52
50	2.2.1 Water Release Assessment Approach and Methodology	52
51	2.2.2 Water Releases Reported by Conditions of Use	53
52	2.2.2.1 Processing and Industrial Use of Asbestos Diaphragms in Chlor-alkali Industry	53
53	2.2.2.2 Processing Asbestos-Containing Sheet Gaskets	54
54	2.2.2.3 Industrial Use of Sheet Gaskets at Chemical Production Plants	54
55	2.2.2.4 Industrial Use and Disposal of Asbestos-Containing Brake Blocks in Oil Industry	54
56	2.2.2.5 Commercial Use, Consumer Use, and Disposal of Aftermarket Automotive Asbestos-
57	Containing Brakes/Linings, Other Vehicle Friction Products, and Other Asbestos-Containing
58	Gaskets	55
59	2.2.3 Summary of Water Releases and Exposures	55
60	2.3 Human Exposures	55
61	2.3.1 Occupational Exposures	56
62	2.3,1.1 Occupational Exposures Approach and Methodology	57
63	2.3.1.2 Consideration of Engineering Controls and Personal Protective Equipment	57
64	2.3.1.3 Chlor-Alkali Industry	60
65	2.3.1.3.1 Process Description - Asbestos Diaphragms	60
66	2.3.1.3.2 Worker Activities - Asbestos Diaphragms	64
67	2.3.1.3.3 Number of Sites and Potentially Exposed Workers - Asbestos Diaphragms	65
68	2.3.1.3.4 Occupational Inhalation Exposures - Asbestos Diaphragms	66
69	2.3.1.3.5 Exposure Results for Use in Risk Evaluation	68
70	2.3.1.3.6 Data Assumptions, Uncertainties and Level of Confidence	70
71	2.3.1.4 Sheet Gaskets	70
72	2.3.1.4.1 Process Description - Sheet Gasket Stamping	71
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2.3.1.4.2	Worker Activities - Cutting of Asbestos-containing Sheet Gaskets	74
2.3.1.4.3	Number of Sites and Potentially Exposed Workers - Sheet Gasket Stamping	74
2.3.1.4.4	Occupational Inhalation Exposure Results - Sheet Gasket Stamping	75
2.3.1.4.5	Exposure Data for Use in Risk Evaluation - Sheet Gasket Stamping	76
2.3.1.4.6	Data Assumptions, Uncertainties and Confidence Level	77
2.3.1.5	Use of Gaskets in Chemical Production	78
2.3.1.5.1	Process Description - Sheet Gasket Use	78
2.3.1.5.2	Worker Activities - Sheet Gasket Use	79
2.3.1.5.3	Number of Sites and Potentially Exposed Workers - Sheet Gasket Use	79
2.3.1.5.4	Occupational Inhalation Exposures - Sheet Gasket Use	79
2.3.1.5.5	Exposure Results for Use in Risk Evaluation - Sheet Gasket Use	80
2.3.1.5.6	Data Assumptions, Uncertainties and Level of Confidence	81
2.3.1.6	Oil Field Brake Blocks	82
2.3.1.6.1	Process Description - Oil Field Brake Blocks	82
2.3.1.6.2	Worker Activities - Oil Field Brake Blocks	84
2.3.1.6.3	Number of Sites and Potentially Exposed Workers - Oil Field Brake Blocks	84
2.3.1.6.4	Occupational Inhalation Exposures - Oil Field Brake Blocks	85
2.3.1.6.5	Exposure Results for Use in Risk Evaluation - Oil Field Brake Blocks	85
2.3.1.6.6	Data Assumptions, Uncertainties and Level of Confidence	86
2.3.1.7	Aftermarket Automotive Brakes/Linings and Clutches	87
2.3.1.7.1	Process Description - Aftermarket Automotive Brakes/Linings and Clutches	87
2.3.1.7.2	Worker Activities - Aftermarket Automotive Brakes/Linings and Clutches	90
2.3.1.7.3	Number of Sites and Potentially Exposed Workers - Aftermarket Automotive
Brakes/Linings and Clutches	92
2.3.1.7.4	Occupational Inhalation Exposures - Aftermarket Automotive Brakes/Linings and
Clutches	92
2.3.1.7.5	Exposure Data for Use in Risk Evaluation - Aftermarket Auto Brakes/Linings and
Clutches	94
2.3.1.7.6	Data Assumptions, Uncertainties and Level of Confidence	95
2.3.1.8	Other Vehicle Friction Products	96
2.3.1.8.1	Installing New Brakes on New Cars for Export Only	96
2.3.1.8.2	Use of Brakes/Frictional Products for a Single, Larg Transport Vehicle (NASA
Super-Guppy)	97
2.3.1.9	Other Gaskets-Utility Vehicles (UTVs)	100
2.3.1.9.1	Process Description - UTV Gasket installation/Servicing	100
2.3.1.9.2	Worker Activities - UTV Gasket Installation/Servicing	101
2.3.1.9.3	Number of Sites and Potentially Exposed Workers - UTV Gasket
Installation/Servicing	101
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111	2.3.1.9.4 Occupational Inhalation Exposures for Use in Risk Evaluation - UTV Gasket
112	Installation/Servicing	103
113	2.3.1.9.5 Data Assumptions, Uncertainties and Level of Confidence	105
114	2,3,1,10 Summary of Inhalation Occupational Exposure Assessment	106
115	2.3.2 Consumer Exposures	107
116	2,3,2,1 Consumer Inhalation Exposures of Do-It-Yourself (DIY) Mechanics During Brake
117	Repair: Approach and Methodology	108
118	2.3.2.1.1 Consumer Exposure Results - Do-It-Yourself (DIY) Mechanics During Brake Repair
119		110
120	2.3.2.1.2 Exposure Data for Use in Risk Evaluation - Do-It-Yourself (DIY) Mechanics During
121	Brake Repair	112
122	2.3.2.1.3 Exposure Estimates for DIY Brake Repair/Replacement Scenario	115
123	2.3.2.1.4 Data Assumptions, Uncertainties and Level of Confidence	115
124	2,3,2,2 Consumer Exposures Approach and Methodology - DIY Gaskets in UTVs	117
125	2.3.2.2.1 Consumer Inhalation Exposures - DIY Gaskets in UTVs	120
126	2.3.2.2.2 Exposure Estimates for DIY UTV Exhaust System Gasket Removal/Replacement
127	Scenario	120
128	2.3.2.2.3 Data Assumptions, Uncertainties and Level of Confidence	121
129	2,3,2,3 Summary of Inhalation Data Supporting the Consumer Exposure Assessment	122
130	2.3.3 Potentially Exposed or Susceptible Subpopulations	123
131	3 HAZARDS (EFFECTS)	125
132	3.1 Environmental Hazards	125
133	3.1.1 Approach and Methodology	125
134	3.1.2 Hazard Identification - Toxicity to Aquatic Organisms	125
135	3.1.3 Weight of Scientific Evidence	126
136	3.1.4 Summary of Environmental Hazard	128
137	3.2 Human Health Hazards	128
138	3.2.1 Approach and Methodology	128
139	3.2.2 Hazard Identification	130
140	3.2.3 Cancer Hazards	131
141	3.2,3,1 Mode of Actiton (MOA) considerations for asbestos	131
142	3.2.4 Derivation of a Chrysotile Asbestos Inhalation Unit Risk	132
143	3,2,4,1 Derivation of a Chrysotile Asbestos Inhalation Unit Risk	132
144	3.2.4.2 Rationale for Asbestos-Specific Data Evaluation Criteria	132
145	3.2.4.3 Additional considerations for final selection of studies for exposure-response	134
146	3.2.4.4 Statistical Methodology	136
147	3.2.4.4.1 Cancer Risk Models	136
148	3.2.4.4.2 Derivation of Potency Factors	138
149	3.3.4.4.3 Extrapolation from Workers to the general population to derive inhalation unit risk
150	138
151	3.2.4.4.4 Life-Table Analysis and Derivation of Inhalation Unit Risk	139
152	3.2.4.5 Study Descriptions and Model Fitting Results	140
153	3.2.4.6 Summary of Results of North and South Carolina Cohorts	150
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3.2.4.6.1 Combining Lung Cancer Unit Risk and Mesothelioma Unit Risk	151
3.2.4.7	Inhalation Unit Risk Derivation	152
3.2.4.7.1 Selecting the Preferred Model Forms for Lung Cancer	153
3.2.4.8	Biases in the Cancer Risk Values	154
3.2.4.9	Selection of the final IUR for Chrysotile Asbestos	155
3.2.5 Potentially Exposed or Susceptible Subpopulations	155
4 RISK CHARACTERIZATION	156
4.1	Environmental Risk	156
4.2	Human Health Ri sk	157
4.2.1	Risk Estimation Approach	157
4.2.2	Risk Estimation for Workers: Cancer Effects Following Less than Lifetime Inhalation
Exposures by Conditions of Use	162
4.2.2.1	Risk Estimation for Cancer Effects Following Chronic Inhalation Exposures for Chlor-
alkali Industry	163
4.2.2.2	Risk Estimation for Cancer Effects Following Chronic Inhalation Exposures for Sheet
Gasket Stamping	167
4.2.2.3	Risk Estimation for Cancer Effects Following Chronic Inhalation Exposures for Sheet
Gasket Use in Chemical Production	170
4.2.2.4	Risk Estimation for Cancer Effects Following Chronic Inhalation Exposures for Oilfield
Brake Blocks	171
4.2.2.5	Risk Estimation for Cancer Effects Following Chronic Inhalation Exposures for
Aftermarket Auto Brakes and Clutches	173
4.2.2.6	Risk Estimation for Cancer Effects Following Chronic Exposures for Other Vehicle
Friction Products	176
4.2.2.7	Risk Estimation for Cancer Effects Following Inhalation Exposures for Gasket
Installation/Servicing in UTVs	180
4.2.2.8. Summary of Risk Estimates for Cancer Effects for Occupational Inhalation Exposure
Scenarios for All COUs	181
4.2.3	Risk Estimation for Consumers: Cancer Effects by Conditions of Use	183
4.2.3.1	Risk Estimation for Cancer Effects Following Episodic Inhalation Exposures for DIY
Brake Repair/Replacement	183
4.2.3.2	Risk Estimation for Cancer Effects following Episodic Inhalation Exposures for UTV
Gasket Repair/replacement	189
4.2.3.3	Summary of Consumer and Bystander Risk Estimates by COU for Cancer Effects
Following Inhalation Exposures	191
4.3	Assumptions and Key Sources of Uncertainty	193
4.3.1	Key Assumptions and Uncertainties in the Uses of Asbestos in the U.S	193
4.3.2	Key Assumptions and Uncertainties in the Environmental (Aquatic) Assessment	194
4.3.3	Key Assumptions and Uncertainties in the Occupational Exposure Assessment	194
4.3.4	Key Assumptions and Uncertainties in the Consumer Exposure Assessment	195
4.3.5	Key Assumptions and Uncertainties in the Human Health IUR Derivation	197
4.3.6	Key Assumptions and Uncertainties in the Cancer Risk Values	198
4.3.7	Confidence in the Human Health Risk Estimations	199
4.4	Other Risk-Related Considerations	206
4.4.1	Potentially Exposed or Susceptible Subpopulations	206
4.4.2	Aggregate and Sentinel Exposures	207
4.5	Risk Conclusions	207
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201	4,5.1 Environmental Risk Conclusions	207
202	4.5.2 Human Health Risk Conclusions to Workers	208
203	4.5.3 Human Health Risk Conclusions to Consumers	210
204	5 RISK DETERMINATION	213
205	5.1 Unreasonable Risk	213
206	5.1.1 Overview	213
207	5.1.2 Risks to Human Health	214
208	5.1,2,1 Determining Cancer Risks	214
209	5.1.3 Determining Environmental Risk	215
210	5.2 Risk Determination for Chrysotile Asbestos	215
211	5.2.1 Occupational Processing and Use of Chrysotile Asbestos	219
212	5.2.2 Consumer Uses of Chrysotile Asbestos	227
213	5.3 Risk Determination for Five other Asbestiform Varieties	232
214	6 REFERENCES	233
215	7 APPENDICES	245
216	Appendix A Regulatory History	245
217	A.l Federal Laws and Regulations												.245
218	A.2 State Laws and Regulations														.....248
219	A.3 International Laws and Regulations.							249
220	Appendix B List of Supplemental Documents	250
221	Appendix C Conditions of Use Supplementary Information	251
222	Appendix D Releases and Exposure to the Environment Supplementary Information	252
223	Appendix E Ecological Data Extraction Tables	258
224	Appendix F Environmental Fate Data Extraction Table	263
225	Appendix G SAS Codes for Estimating Ki, and Km from Grouped Data	269
226	Appendix H BEIRIV Equations for Life Table Analysis	275
227	Appendix I SAS Code for Life Table Analysis	277
228	Appendix J Results of Modeling for IUR Derivation	294
229	Appendix K Less Than Lifetime (or Partial lifetime) IUR	297
230	Appendix L Sensitivity Analysis of Exposures for DIY/Bystander Episodic Exposure Scenarios
231	299
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234	LIST OF TABLES
235	Table 1-1. Physical and Chemical Properties of Asbestos Fiber Typesa	32
236	Table 1-2. Assessment History of Asbestos	34
237	Table 1-3. Categories Determined Not to be Conditions of Use After Problem Formulation	37
238	Table 1-4. Categories of Conditions of Use Included in this Risk Evaluation	38
239	Table 2-1. EPA OW Six Year Review Cycle Data for Asbestos in Drinking Water, 1998-2011	 53
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Table 2-2. Crosswalk of Conditions of Use and Occupational and Consumer Scenarios Assessed in the
Risk Evaluation 55
Table 2-3. Assigned Protection Factors for Respirators in OSHA Standard 29 CFR 1910.134eg 58
Table 2-4. 30-min Short-Term PBZ Sample Summary* 67
Table 2-5. Full-Shift* PBZ Sample Summary 67
Table 2-6. Summary of PBZ Sampling Data for All Other Durations 67
Table 2-7 Summary of ACC Short-Term PBZ Sampling Data by Exposure Group (samples from 2001 to
2016) 68
Table 2-8 Summary of Asbestos Exposures During Processing and Use in the Chlor-Alkali Industry
Used in EPA's Risk Evaluation 69
Table 2-9. Short-Term PBZ Asbestos Sampling Results (EHM, 2013) 76
Table 2-10 Summary of Asbestos Exposures During Sheet Gasket Stamping Used in EPA's Risk
Evaluation 77
Table 2-11. Summary of Asbestos Exposures During Sheet Gasket Use Used in EPA's Risk Evaluation
81
Table 2-12. Summary of Total Establishments in Relevant Industries and Potentially Exposed Workers
and ONUs for Oilfield Brake Blocks 84
Table 2-13. Summary of Asbestos Exposures During Use in Brake Blocks for EPA's Risk Evaluation 86
Table 2-14. PBZ Asbestos Concentrations Measured by OSHA for Workers at Automotive Repair,
Services, and Parking Facilities 93
Table 2-15. Summary of Asbestos Exposures During Replacement of Aftermarket Automotive Parts
Used in EPA's Risk Evaluation 94
Table 2-16. Other Vehicle Friction Products Exposure Levels (from Aftermarket Automotive Parts
exposure levels) 96
Table 2-17. Number of Other Motor Vehicle Dealers 101
Table 2-18. Number of ATV and Watercraft Dealers in NAICS 44128 102
Table 2-19. Estimated Number of UTV Dealers 102
Table 2-20. Selected Mechanics and Repair Technicians in NAICS 4412 (Other Motor Vehicle Dealers)
102
Table 2-21. Number of Employees per Establishment in NAICS 4412 in Relevant Occupations 103
Table 2-22. Estimated Number of Sites and Employees for UTV Engine Repair 103
Table 2-23. UTV Gasket Installation/Servicing Exposure Levels for EPA's Risk Evaluation 104
Table 2-24. Summary of Occupational Inhalation Exposures 106
Table 2-25. Summary of Studies Satisfying Conditions/Factors for Use in Consumer DIY Brake
Exposure Scenario 110
Table 2-26. Exposure concentrations from Blake (2003) and Sheehy (1989) studies to the DIY user
during various activities 112
Table 2-27. Estimated Exposure Concentration for DIY Consumer User and Bystander 113
Table 2-28. DIY Brake/Repair Replacement - Exposure Levels for EPA's Risk Evaluation 115
Table 2-29. Summary of Studies Satisfying Factors Applied to Identified Literature 117
Table 2-30. Summary Results of Asbestos Exposures in Gasket Repair Studies 118
Table 2-31. Estimated Exposure Concentrations for UTV Gasket Repair/Replacement Scenario - DIY
Mechanic and Bystander 120
Table 2-32. Summary of Consumer Inhalation Exposures 122
Table 2-33. Percentage of Employed Persons by Age, Sex, and Industry Sector (2017 and 2018 worker
demographics from BLS) 124
Table 2-34. Percentage of Employed Adolescents by Industry Sector (2017 and 2018 worker
demographics from BLS) 125
Table 3-1. Environmental Hazard Characterization of Asbestos 127
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Table 3-2. Study Cohort, Individual studies and Study Quality of Commercial Chrysotile Asbestos
Reviewed for Assessment of Lung Cancer and Mesothelioma Risks 135
Table 3-3. Model Fitting Results for the South Carolina Cohort 142
Table 3-4. Model Fitting Results for the North Carolina Cohort 144
Table 3-5. Model Fitting Results for the Chongqing China Cohort 146
Table 3-6. Model Fitting Results for the Quebec, Canada Cohort 148
Table 3-7. Model Fitting Results for the Qinghai, China Cohort 149
Table 3-8. Comparison of Lifetime Units Risks of Lung Cancer by Industry 149
Table 3-9. Cohorts and Preferred Statistical Models for SC and NC Cohorts 150
Table 3-10. Addressing Underascertainment of Mesothelioma 151
Table 3-11. Range of Estimates of Estimated Central Unit Risks and IURs for North and South Carolina
Cohorts 152
Table 3-12. Estimated Central Unit Risks and IURs for North and South Carolina Cohorts and Preferred
Models for Lung Cancer and Mesothelioma 154
Table 3-13. Estimates of Selected Central Risk and IUR for Chrysotile Asbestos 155
Table 4-1. Use Scenarios and Populations of Interest for Cancer Endpoints for Assessing
Occupational Risks Following Inhalation Exposures to Chrysotile Asbestos 160
Table 4-2. Use Scenarios and Populations of Interest for Cancer Endpoints for Assessing
Consumer Risks Following Inhalation Exposures to Chrysotile Asbestos 160
Table 4-3. Reported Respirator Use by COU for Asbestos Occupational Exposures 161
Table 4-4. Excess Lifetime Cancer Risk for Chlor-alkali Industry Full Shift Workers and ONUs
(Personal Samples) before consideration of PPE and any relevant APF 163
Table 4-5. Excess Lifetime Cancer Risk for Chlor-alkali Industry Workers (Short-Term Personal
Samples from Table 2-4, 8-hour full shift) before consideration of PPE and any relevant
APF 164
Table 4-6. Excess Lifetime Cancer Risk for Chlor-alkali Industry Full Shift Workers and ONUs (from
Table 4-4) after consideration of PPE with APF=10 for all workers (excluding ONUs)165
Table 4-7. Excess Lifetime Cancer Risk for Chlor-alkali Industry Full Shift Workers and ONUs (from
Table 4-4) after consideration of PPE with APF=25 for all workers (excluding ONUs) 165
Table 4-8. Excess Lifetime Cancer Risk for Chlor-alkali Industry Short-Term Personal Samples (from
Table 4-5) after consideration of PPE with APF=25 for short-term workers for 0.5 hours
(excluding ONUs) 166
Table 4-9. Excess Lifetime Cancer Risk for Chlor-alkali Industry Short-Term Personal Samples (from
Table 4-5) after consideration of PPE and with APF=10 for full-shift workers and with
APF=25 for short-term workers (excluding ONUs) 166
Excess Lifetime Cancer Risk for Chlor-alkali Industry Short-Term Personal Samples (from
Table 4-5) after consideration of PPE and with APF=25 for full-shift workers and with
APF=25 for short-term workers (excluding ONUs) 167
Excess Lifetime Cancer Risk for Sheet Gasket Stamping Full Shift Workers and ONUs
(from Table 2-10, Personal Samples) before consideration of PPE and any relevant APF
167
Excess Lifetime Cancer Risk for Sheet Gasket Stamping Short-term Exposures within an 8-
hour Full Shift (from Table 2-10, Personal Samples) before consideration of PPE and any
relevant APF 168
Excess Lifetime Cancer Risk for Sheet Gasket Stamping Full Shift Workers and ONUs
(from Table 4-11) after consideration of PPE using an APF=10 (excluding ONUs) 169
Excess Lifetime Cancer Risk for Sheet Gasket Stamping Full Shift Workers and ONUs
(from Table 4-11) after consideration of PPE using an APF=25 (excluding ONUs) 169
Table 4-10.
Table 4-11.
Table 4-12.
Table 4-13.
Table 4-14.
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Table 4-15. Excess Lifetime Cancer Risk for Sheet Gasket Stamping Short-term Exposures within an 8-
hour Full Shift (from Table 4-12) after consideration of PPE using an APF=10 for both
full-shift and short-term exposures (excluding ONUs)	169
Table 4-16. Excess Lifetime Cancer Risk for Sheet Gasket Stamping Short-term Exposures within an 8-
hour Full Shift (from Table 4-12) after consideration of PPE using an APF=25 for both
full-shift and short-term exposures (excluding ONUs)	170
Table 4-17. Excess Lifetime Cancer Risk for Sheet Gasket Use in Chemical Production (using data from
titanium dioxide production), 8-hour TWA (from Table 2-11., Personal Samples) before
consideration of PPE and any relevant APF	170
Table 4-18. Excess Lifetime Cancer Risk for Sheet Gasket Use in Chemical Production, 8-hour TWA
(from Table 4-6) after consideration of PPE using the APF=10 reflecting the current use
of respirators (excluding ONUs)	171
Table 4-19. Excess Lifetime Cancer Risk for Sheet Gasket Use in Chemical Production, 8-hour TWA
(from Table 4-6) after consideration of PPE using an APF=25 (excluding ONUs)	171
Table 4-20. Excess Lifetime Cancer Risk for Oil Field Brake Block Use, 8-hour TWA (from Table 2-13
before consideration of PPE and any relevant APF	172
Table 4-21. Excess Lifetime Cancer Risk for Oil Field Brake Block Use, 8-hour TWA (from Table 4-20)
after consideration of PPE using an APF=10 (excluding ONUs)	172
Table 4-22. Excess Lifetime Cancer Risk for Oil Field Brake Block Use, 8-hour TWA (from Table 4-20)
after consideration of PPE using an APF=25 (excluding ONUs)	172
Table 4-23. Excess Lifetime Cancer Risk for Repairing or Replacing Aftermarket Auto Brakes and
Clutches in an Occupational Setting, 8-hour TWA Exposure (from Table 2-15.) before
consideration of PPE and any relevant APF	173
Table 4-24. Excess Lifetime Cancer Risk for Repairing or Replacing Aftermarket Auto Brakes and
Clutches in an Occupational Setting, Short-term Exposures Within an 8-hour Full Shift
(from Table 2-15.) before consideration of PPE and any relevant APF	174
Table 4-25. Excess Lifetime Cancer Risk for Repairing or Replacing Aftermarket Auto Brakes and
Clutches in an Occupational Setting, 8-hour TWA Exposure (from Table 4-23) after
consideration of PPE with APF=10 (excluding ONUs)	174
Table 4-26. Excess Lifetime Cancer Risk for Repairing or Replacing Aftermarket Auto Brakes and
Clutches in an Occupational Setting, 8-hour TWA Exposure (from Table 4-23) after
consideration of PPE with APF=25 (excluding ONUs)	175
Table 4-27. Excess Lifetime Cancer Risk for Repairing or Replacing Aftermarket Auto Brakes and
Clutches in an Occupational Setting, Short-term Exposures Within an 8-hour Full Shift
(from Table 4-24) after consideration of PPE with APF=10 (excluding ONUs)	175
Table 4-28. Excess Lifetime Cancer Risk for Repairing or Replacing Aftermarket Auto Brakes and
Clutches in an Occupational Setting, Short-term Exposures Within an 8-hour Full Shift
(from Table 4-24) after consideration of PPE with APF=25 (excluding ONUs)	175
Table 4-29. Excess Lifetime Cancer Risk for Installing Brakes and Clutches in Exported Cars in an
Occupational Setting, 8-hour TWA Exposure (from Table 2-15) before consideration of
PPE and any relevant APF	176
Table 4-30. Excess Lifetime Cancer Risk for Installing Brakes and Clutches in Exported Cars in an
Occupational Setting, Short-term Exposures Within an 8-hour Full Shift (from Table
2-15.) before consideration of PPE and any relevant APF	177
Table 4-31. Excess Lifetime Cancer Risk for Installing Brakes and Clutches in Exported Cars in an
Occupational Setting, 8-hour TWA Exposure (from Table 4-29) after consideration of
PPE with APF=10 (excluding ONUs)	178
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Table 4-32. Excess Lifetime Cancer Risk for Installing Brakes and Clutches in Exported Cars in an
Occupational Setting, 8-hour TWA Exposure (from Table 4-29.) after consideration of
PPE with APF=25 (excluding ONUs)	178
Table 4-33. Excess Lifetime Cancer Risk for Installing Brakes and Clutches in Exported Cars in an
Occupational Setting, Short-term Exposures Within an 8-hour Full Shift (from Table 4-
30) after consideration of PPE with APF=10 (excluding ONUs)	178
Table 4-34. Excess Lifetime Cancer Risk for Installing Brakes and Clutches in Exported Cars in an
Occupational Setting, Short-term Exposures Within an 8-hour Full Shift (from Table 4-
30) after consideration of PPE with APF=25 (excluding ONUs)	179
Table 4-35. Excess Lifetime Cancer Risk for UTV Gasket Installation/Servicing in an Occupational
Setting, 8-hour TWA Exposure (from Table 2-23.) before consideration of PPE and any
relevant APF	180
Table 4-36. Excess Lifetime Cancer Risk for UTV Gasket Installation/Servicing in an Occupational
Setting, 8-hour TWA Exposure (from Table 4-35) after consideration of PPE with
APF=10 (excluding ONUs)	181
Table 4-37. Excess Lifetime Cancer Risk for UTV Gasket Installation/Servicing in an Occupational
Setting, 8-hour TWA Exposure (from Table 4-35) after consideration of PPE with
API; 25 (excluding ONUs)	181
Table 4-38. Summary of Risk Estimates for Inhalation Exposures to Workers and ONUs by COU .... 181
Table 4-39. Excess Lifetime Cancer Risk for Indoor DIY Brake/Repair Replacement with Compressed
Air Use for Consumers and Bystanders (exposures from Table 2-32 without a reduction
factor) with Exposures at 30% of 3-hour User Concentrations between Brake/Repair
Replacement (Consumers 1 hour/day spent in garage; Bystanders 1 hour/day)	185
Table 4-40. Excess Lifetime Cancer Risk for Indoor DIY Brake/Repair Replacement with Compressed
Air Use for Consumers for 20 year duration (exposures from Table 2-32 without a
reduction factor) with Exposures at 30% of 3-hour User Concentrations between
Brake/Repair Replacement (Consumers 1 hour/day spent in garage)	186
Table 4-41. Excess Lifetime Cancer Risk for Indoor DIY Brake/Repair Replacement with Compressed
Air Use for Consumers and Bystanders (exposures from Table 2-32 without a reduction
factor) with Exposures at 30% of 3-hour User Concentrations between Brake/Repair
Replacement (Consumers 8 hours/day spent in garage; Bystanders 1 hour/day)	186
Table 4-42. Risk Estimate using one brake change at age 16 years with 10 years further exposure.
Excess Lifetime Cancer Risk for Indoor DIY Brake/Repair Replacement with
Compressed Air Use for Consumers and Bystanders (exposures from Table 2-32 without
a reduction factor) (Consumers 1 hour/day spent in garage; Bystanders 1 hour/day).... 187
Table 4-43. Excess Lifetime Cancer Risk for Outdoor DIY Brake/repair Replacement for Consumers
and Bystanders (5 minutes per day in driveway) (from Table 2-32 with a reduction factor
of 10)	188
Table 4-44. Excess Lifetime Cancer Risk for Outdoor DIY Brake/Repair Replacement for Consumers
and Bystanders (30 minutes per day in driveway) (from Table 2-32 with a reduction
factor of 10)	188
Table 4-45. Risk Estimate using one UTV gasket change at age 16 years with 10 years further exposure.
Excess Lifetime Cancer Risk for Indoor DIY UTV gasket change for Consumers and
Bystanders (exposures from Table 2-32 without a reduction factor) (Consumers 1
hour/day spent in garage; Bystanders 1 hour/day)	189
Table 4-46. Excess Lifetime Cancer Risk for Indoor DIY UTV Gasket /Repair Replacement for
Consumers and Bystanders (exposures from Table 2-32) (Users 1 hour/day spent in
garage; Bystanders 1 hour/day)	190
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Table 4-47. Excess Lifetime Cancer Risk for Indoor DIY Gasket/Repair Replacement for Consumers
and Bystanders (exposures from Table 2-32) (Consumers 8 hours/day spent in garage;
Bystanders 1 hour/day) 190
Table 4-48. Summary of Risk Estimates for Inhalation Exposures to Consumers and Bystanders by COU
(Cancer benchmark is 10-6) 192
Table 4-49. Ratios of risks for alternative exposure scenarios using scenario-specific partial lifetime
IURs from Appendix K by age at first exposure and duration of exposure compared to
baseline occupational exposure scenarios (baseline scenario: first exposure at 16 years for
40 years duration) 199
Table 4-50. Ratios of risks for alternative exposure scenarios using scenario-specific partial lifetime
IURs from Appendix K by age at first exposure and duration of exposure compared to
baseline consumer DIY exposure scenarios (baseline scenario: first exposure at 16 years
for 62 years duration) 200
Table 4-51. Ratios of risks for alternative exposure scenarios using scenario-specific partial lifetime
IURs from Appendix K by age at first exposure and duration of exposure compared to
baseline consumer bystander exposure scenarios (baseline scenario: first exposure at 0
years for 78 years duration) 201
Table 4-52. Results of Sensitivity Analysis of Exposure Assumptions for Consumer DIY/Bystander
Episodic Exposure Scenarios 201
Table 4-53. Time Spent (minutes/day) in Garage, Doers Only (Taken from Table 16-16 in EFH, 2011)
203
Table 4-54. Summary of Estimated Number of Exposed Workers and DIY Consumers21 205
Table 4-55. Summary of Risk Estimates for Inhalation Exposures to Workers and ONUs by COU
(Cancer benchmark is 10"4) 208
Table 4-56. Summary of Risk Estimates for Inhalation Exposures to Consumers and Bystanders by COU
(Cancer benchmark is 10"6) 211
Table 5-1. Risk Determination for Chrysotile Asbestos: Processing and Industrial Use of Asbestos
Diaphragms in Chlor-alkali Industry (refer to section 4.2.2.1 for the risk characterization)
219
Table 5-2. Risk Determination for Chrysotile Asbestos: Processing Asbestos-Containing Sheet Gaskets
(refer to section 4.2.2.2 for the risk characterization) 221
Table 5-3. Risk Determination for Chrysotile Asbestos: Industrial Use of Asbestos-Containing Sheet
Gaskets in Chemical Production 223
Table 5-4. Risk Determination for Chrysotile Asbestos: Industrial Use and Disposal of Asbestos-
Containing Brake Blocks in Oil Industry (refer to section 4.2.2.4 for the risk
characterization) 224
Table 5-5. Risk Determination for Chrysotile Asbestos: Commercial Use and Disposal of Aftermarket
Automotive Asbestos-Containing Brakes/Linings and Other Vehicle Friction Products
225
Table 5-6. Risk Determination for Chrysotile Asbestos: Commercial Use and Disposal of Other
Asbestos-Containing Gaskets 226
Table 5-7. Risk Determination for Chrysotile Asbestos: Consumer Use and Disposal of Aftermarket
Automotive Asbestos-Containing Brakes/Linings 228
Table 5-8. Risk Determination for Chrysotile Asbestos: Consumer Use and Disposal of Other Asbestos-
Containing Gaskets 230
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LIST OF FIGURES
Figure 1-1. Asbestos Life Cycle Diagram 39
Figure 1-2. Asbestos Conceptual Model for Industrial and Commercial Activities and Uses: Potential
Exposures and Hazards 41
Figure 1-3. Asbestos Conceptual Model for Consumer Activities and Uses: Potential Exposures and
Hazards 42
Figure 1-4. Key/Supporting Data Sources for Environmental Fate 46
Figure 1-5. Key/Supporting Data Sources for Engineering Releases and Occupational Exposure 47
Figure 1-6. Key/Supporting Data Sources for Consumer and Environmental Exposure 48
Figure 1-7. Key /Supporting Data Sources for Environmental Hazard 49
Figure 1-8. Key/Supporting Data Sources for Human Health Hazard 50
Figure 2-1. Closeup of a Chrysotile Diaphragm Outside of the Electrolytic Cell Photograph courtesy of
the American Chemistry Council 60
Figure 2-2. Process Flow Diagram of an Asbestos Handling System and Slurry Mix Tank Image
Courtesy of the American Chemistry Council 62
Figure 2-3. Electrolytic Cell Construction 63
Figure 2-4. Typical Gasket Assembly 71
Figure 2-5. Asbestos-Containing Stamping Operation 72
Figure 2-6. Rule Blade for Stamping Machine 72
Figure 2-7. Asbestos Warning Label on Finished Gasket Product 73
Figure 2-8. Photographs of Typical Oil Field Drawworks 83
Figure 2-9. Illustrations of brake assembly components: (a) a brake lining designed to be used with an
internal drum brake and (b) a brake pad designed for use with a disc brake 88
Figure 2-10. Schematic of a clutch assembly. The clutch disc is made of friction material, which may
contain asbestos 90
Figure 2-11. NASA Super Guppy Turbine Aircraft 97
Figure 2-12. Brakes for NASA Super Guppy Turbine Aircraft 98
Figure 2-13. Ventilated Walk-in Booth Where Brakes Pads Are Replaced 99
Figure 3-1. EPA Approach to Hazard Identification, Data Integration, and Dose-Response Analysis for
Asbestos 129
LIST OF APPENDIX TABLES
TableAPX D-l. Summary of Asbestos TRI Production-Related Waste Managed from 2015-2018 (lbs)
253
Table APX D-2. Summary of Asbestos TRI Releases to the Environment from 2015-2018 (lbs) 254
Table APX E-l. Summary Table On-topic Aquatic Toxicity Studies That Were Evaluated for
Chrysotile Asbestos 258
Table_APX F-l. Other Fate Endpoints Study Summary for Asbestos 263
Table_APX F-2. Hydrolysis Study Summary for Asbestos 265
Table_APX F-3. Aquatic Bioconcentration Study Summary for Asbestos 267
TableApx K-l. (LTL) Chrysotile Asbestos Inhalation Unit Risk Values for Less Than Lifetime
Condition of Use 297
Table Apx L-l. Excess Lifetime Cancer Risk for Indoor DIY Brake/Repair Replacement with
Compressed Air Use for Consumers for 20 year duration (exposures from Table 2-32
without a reduction factor) (Consumers 1 hour/day spent in garage) 299
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TableApx
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L-2. Ratios of risk for alternative exposure scenarios compared to DIY User and Bystander
exposure scenario assuming DIY User is first exposed at age 16 years for 62 years
duration and DIY Bystander is exposed from age 0-78 years	300
L-3. Sensitivity Analysis #1: Summary of Risk Estimates for Inhalation Exposures to
Consumers and Bystanders by COU (Cancer benchmark is 10"6) Comparing the Baseline
Exposure Scenario from Table 4-45 with Risks Assuming DIY Users Are Exposed From
Age 16-36 years and Bystanders Are Exposed Age 0-20 years	301
L-4. Sensitivity Analysis #2: Summary of Risk Estimates for Inhalation Exposures to
Consumers and Bystanders by COU (Cancer benchmark is 10"6) Comparing the Baseline
Exposure Scenario from Table 4-45 with Risks Assuming DIY Users Are Exposed From
Age 20-60 years and Bystanders Are Exposed Age 0-40 years	303
L-5. Sensitivity Analysis #3: Summary of Risk Estimates for Inhalation Exposures to
Consumers and Bystanders by COU (Cancer benchmark is 10"6) Comparing the Baseline
Exposure Scenario from Table 4-45 with Risks Assuming DIY Users Are Exposed From
Age 20-40 years and Bystanders Are Exposed Age 0-20 years	304
L-6. Sensitivity Analysis #4: Summary of Risk Estimates for Inhalation Exposures to
Consumers and Bystanders by COU (Cancer benchmark is 10"6) Comparing the Baseline
Exposure Scenario from Table 4-45 with Risks Assuming DIY Users Are Exposed From
Age 30-70 years and Bystanders Are Exposed Age 0-40 years	307
L-7. Sensitivity Analysis #5: Summary of Risk Estimates for Inhalation Exposures to
Consumers and Bystanders by COU (Cancer benchmark is 10"6) Comparing the Baseline
Exposure Scenario from Table 4-45 with Risks Assuming DIY Users Are Exposed From
Age 30-50 years and Bystanders Are Exposed Age 0-20 years	309
L-8: Results of 24 Sensitivity Analysis of Exposure Assumptions for Consumer
DIY/Bystander Episodic Exposure Scenarios	310

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ACKNOWLEDGEMENTS
This report was developed by the United States Environmental Protection Agency (U.S. EPA), Office of
Chemical Safety and Pollution Prevention (OCSPP), Office of Pollution Prevention and Toxics (OPPT).
Acknowledgements
The OPPT Assessment Team gratefully acknowledges participation and/or input from Intra-agency
reviewers that included multiple offices within EPA, Inter-agency reviewers that included multiple
Federal agencies, and assistance from EPA contractors GDIT (Contract No. CIO-SP3,
HHSN316201200013W), ERG (Contract No. EP-W-12-006), Versar (Contract No. EP-W-17-006), ICF
(Contract No. EPC14001) and SRC (Contract No. EP-W-12-003). EPA also acknowledges the
contributions of technical experts from EPA's Office of Research and Development and epidemiologists
subcontracted to SRC who contributed to the development of the IUR.
Docket
Supporting information can be found in public docket: EPA-H( f-2016-0736.
Disclaimer
Reference herein to any specific commercial products, process or service by trade name, trademark,
manufacturer or otherwise does not constitute or imply its endorsement, recommendation or favoring by
the United States Government.
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ABBREVIATIONS
ABPO
1989 Asbestos Ban and Phase Out Rule
ACC
American Chemistry Council
ADC
Average Daily Concentration
AHERA
Asbestos Hazard Emergency Response Act
ASHAA
Asbestos School Hazard Abatement Act
ASHARA
Asbestos School Hazard Abatement Reauthorization Act
AT SDR
Agency for Toxic Substances and Disease Registry
CAA
Clean Air Act
CASRN
Chemical Abstracts Service Registry Number
CBI
Confidential Business Information
CDR
Chemical Data Reporting
CERCLA
Comprehensive Environmental Response, Compensation and Liability Act
COU
Condition of Use
CPSC
Consumer Product Safety Commission
CWA
Clean Water Act
DIY
Do-It-Yourself
EG
Effluent Guideline
ELCR
Excess Lifetime Cancer Risk
EMP
Elongated Mineral Particle
EPA
Environmental Protection Agency
EPCRA
Emergency Planning and Community Right-to-Know Act
EU
European Union
FDA
Food and Drug Administration
f/cc
Fibers per cubic centimeter
FHSA
Federal Hazardous Substance Act
g
Gram(s)
HAP
Hazardous Air Pollutant
HEPA
High-Efficiency Particulate Air
HTS
Harmonized Tariff Schedule
IARC
International Agency for Research on Cancer
IRIS
Integrated Risk Information System
IUR
Inhalation Unit Risk
Ki
Lung cancer potency factor
Km
Mesothelioma potency factor
LADC
Lifetime Average Daily Concentration
lb
Pound
LTL
Less Than Lifetime
LOEC
Lowest Observable Effect Concentration
MAP
Model Accreditation Plan
MCLG
Maximum Contaminant Level Goal
|im
Micrometers
MFL
Million Fibers per Liter
mppcf
million particles per cubic foot of air
mg
Milligram(s)
MPa
Megapascal
MSHA
Mine Safety and Health Administration
mV
Millivolt
NAICS
North American Industry Classification System
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ND
Non-detects (value is < analytical detection limit)
NEI
National Emissions Inventory
NESHAP
National Emission Standard for Hazardous Air Pollutants
NIH
National Institutes of Health
NIOSH
National Institute for Occupational Safety and Health
NPL
National Priorities List
NTP
National Toxicology Program
OCSPP
Office of Chemical Safety and Pollution Prevention
OEM
Original Equipment Manufacturer
ONU
Occupational Non-User
OPPT
Office of Pollution Prevention and Toxics
OSHA
Occupational Safety and Health Administration
PCM
Phase Contrast Microscopy
PECO
Population, Exposure, Comparator and Outcome
PEL
Permissible Exposure Limit
PESO
Pathways/Processes, Exposure, Setting and Outcomes
PF
Problem Formulation
POD
Point of Departure
POTW
Publicly Owned Treatment Works
PPE
Personal Protective Equipment
ppm
Part(s) per Million
RCRA
Resource Conservation and Recovery Act
RA
Risk Assessment
RESO
Receptors, Exposure, Setting/Scenario and Outcomes
RfC
Reference Concentration
RIA
Regulatory Impact Analysis
RR
Relative Risk
SDS
Safety Data Sheet
SDWA
Safe Drinking Water Act
SNUN
Significant New Use Notice
SNUR
Significant New Use Rule
TSFE
Time Since First Exposure
TCCR
Transparent, Clear, Consistent, and Reasonable
TEM
Transmission Electron Microscopy
TRI
Toxics Release Inventory
TSCA
Toxic Substances Control Act
TURA
Toxics Use Reduction Act
TWA
Time Weighted Average
U.S.
United States
USGS
United States Geological Survey
UTV
Utility vehicle
WHO
World Health Organization
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EXECUTIVE SUMMARY
This draft risk evaluation for asbestos was performed in accordance with the Frank R. Lautenberg
Chemical Safety for the 21st Century Act and is being disseminated for public comment and peer
review. The Frank R. Lautenberg Chemical Safety for the 21st Century Act amended the Toxic
Substances Control Act (TSCA), the Nation's primary chemicals management law, in June 2016. As per
EPA's final rule, Procedures for Chemical Risk Evaluation Under the Amended Toxic Substances
Control Act (82 FR 33726), EPA is taking comment on this draft and will also obtain peer review on this
draft risk evaluation for asbestos. All conclusions, findings, and determinations in this document are
preliminary and subject to comment. The final risk evaluation may change in response to public
comments received on the draft risk evaluation and/or in response to peer review, which itself may be
informed by public comments. The preliminary conclusions, findings, and determinations in this draft
risk evaluation are for the purposes of identifying whether asbestos presents unreasonable risk or no
unreasonable risk under the conditions of use, in accordance with TSCA section 6, and are not intended
to represent any findings under TSCA section 7.
TSCA § 26(h) and (i) require EPA to use scientific information, technical procedures, measures,
methods, protocols, methodologies and models consistent with the best available science and to base its
decisions on the weight of the scientific evidence. To meet these TSCA § 26 science standards, EPA
used the TSCA systematic review process described in the Application of Systematic Review in TSCA
Risk Evaluations document ( 018a). The data collection, evaluation, and integration stages of
the systematic review process are used to develop the exposure, fate and hazard assessments for risk
evaluations.
Asbestos is subject to federal and state regulations and reporting requirements. Asbestos is reportable to
the Toxics Release Inventory (TRI) under Section 313 of the Emergency Planning and Community
Right-to-Know Act (EPCRA) but is only reportable in the friable form at concentration levels of 0.1%
or greater. It is designated a Hazardous Air Pollutant (HAP) under the Clean Air Act (CAA), and is a
hazardous substance under the Comprehensive Environmental Response, Compensation and Liability
Act (CERCLA). Asbestos is subject to National Primary Drinking Water Regulations (NPDWR) under
the Safe Drinking Water Act (SDWA) and designated as a toxic pollutant under the Clean Water Act
(CWA) and as such is subject to effluent limitations. Under TSCA, EPA has promulgated several
regulations for asbestos, including the Asbestos Ban and Phase Out rule of 1989, which was then largely
vacated in 1991, and under the Asbestos Hazard Emergency Response Act (AHERA), which requires
inspection of schools for asbestos. On April 25, 2019, EPA finalized an Asbestos Significant New Use
Rule (SNUR) under TSCA Section 5 that prohibits manufacture (including import) or processing of
discontinued uses of asbestos from restarting without EPA having an opportunity to evaluate each
intended use for risks to health and the environment and to take any necessary regulatory action, which
may include a prohibition.
Asbestos has not been mined or otherwise produced in the U.S. since 2002. Although there are several
known types of asbestos, the only form of asbestos known to be imported, processed, or distributed for
use in the United States at the posting of this draft risk evaluation is chrysotile. Raw chrysotile asbestos
currently imported into the U.S. is used exclusively by the chlor-alkali industry. Based on 2019 data, the
total amount of raw asbestos imported into the U.S. was 750 metric tons. EPA has also identified the
importation of asbestos-containing products; however, the import volumes of those products are not
fully known. The asbestos-containing products that EPA has identified as being imported and used are
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sheet gaskets, brake blocks, aftermarket automotive brakes/linings, other vehicle friction products, and
other gaskets. In this draft risk evaluation, EPA evaluated the following categories of conditions of use
(COU) for chrysotile asbestos: manufacturing; processing; distribution in commerce; occupational and
consumer uses; and disposal.
Approach
EPA used reasonably available information (defined in 40 CFR 702.33 as "information that EPA
possesses, or can reasonably obtain and synthesize for use in risk evaluations, considering the deadlines
for completing the evaluation "), in a fit-for-purpose approach, to develop a risk evaluation that relies on
the best available science and is based on the weight of the scientific evidence. EPA used previous
analyses as a starting point for identifying key and supporting studies to inform the exposure, fate, and
hazard assessments. EPA also evaluated other studies published since the publication of previous
analyses. EPA reviewed the information and evaluated the quality of the methods and reporting of
results of the individual studies using the evaluation strategies described in Application of Systematic
Review in TSCA Risk Evaluations (U.S. EPA. 2018a).
During development of this risk evaluation, the only fiber type of asbestos that EPA identified as
imported, processed, or distributed under the COUs in the United States is chrysotile, the serpentine
variety. Chrysotile is the prevailing form of asbestos currently mined worldwide, and so it is assumed
that a majority of commercially available products fabricated overseas are made with chrysotile. Any
asbestos being imported into the U.S. in articles is believed to be chrysotile. The other five forms of
asbestos are now subject to a SNUR as described previously1.
EPA evaluated the following categories of COU of chrysotile asbestos in this draft risk evaluation:
manufacturing; processing; distribution in commerce; occupational and consumer uses; and disposal for
the following COUs: use of diaphragms in the chlor-alkali industry, sheet gaskets in chemical
production facilities, oilfield brake blocks, aftermarket automotive brakes/linings, other vehicle friction
products, and other gaskets. EPA continues to review the recent court decision in Safer Chemicals
Healthy Families v. EPA, Nos. 17-72260 et al. (9th Cir. 2019), and this draft risk evaluation does not
reflect consideration of any legacy uses and associated disposal for chrysotile asbestos or other asbestos
fiber types as a result of that decision. EPA intends to consider legacy uses and associated disposal in a
supplemental scope document and supplemental risk evaluation.
In the problem, formulation ( 018d) (PF), EPA identified the conditions of use and presented
three conceptual models and an analysis plan for this draft risk evaluation. These have been carried into
the draft risk evaluation where EPA has quantitatively evaluated the risk to human health using
monitoring data submitted by industry and found in the scientific literature through systematic review
for the COUs (identified in Section 1.4.3 of this draft risk evaluation). During the PF phase of the Risk
Evaluation, EPA was still in the process of identifying potential asbestos water releases for the TSCA
1 This requires notification to, and review by, the Agency should any person wish to pursue manufacturing, importing, or
processing crocidolite (riebeckite), amosite (cummingtonite-grunerite), anthophyllite, tremolite or actinolite (either in raw
form or as part of articles) for any use (40 CFR 721.11095). Therefore, under the final asbestos SNUR, EPA will be made
aware of manufacturing, importing, or processing for any intended use of crocidolite (riebeckite), amosite (cummingtonite-
grunerite), anthophyllite, tremolite or actinolite (either in raw form or as part of articles). If EPA finds upon review of the
Significant New Use Notice (SNUN) that the significant new use presents or may present an unreasonable risk (or if there is
insufficient information to permit a reasoned evaluation of the health and environmental effects of the significant new use),
then EPA would take action under TSCA section 5(e) or (f) to the extent necessary to protect against unreasonable risk.
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COUs to determine the need to evaluate risk to aquatic and sediment-dwelling organisms. After the PF
was released, EPA continued to search EPA databases as well as the literature and attempted to contact
industries to shed light on potential releases to water. The reasonably available information indicated
that there were minimal or no surface water releases of asbestos associated with the COUs in this draft
risk evaluation.
EPA evaluated exposures (inhalation only) to asbestos in occupational and consumer settings to
estimate risk of health hazard (cancer only) for the COUs in this draft risk evaluation. In occupational
settings, EPA evaluated inhalation exposures to workers and occupational non-users, or ONUs. EPA
used inhalation monitoring data submitted by industry and literature sources, where reasonably
available and that met TSCA systematic review data evaluation criteria, to estimate potential inhalation
exposures. In consumer settings, EPA evaluated inhalation exposures to both consumers (Do-it-
Yourselfers or DIY mechanics) and bystanders and used estimated inhalation exposures, from literature
sources where reasonably available and that met data evaluation criteria, to estimate potential
exposures using a range of user durations. These analyses are described in Section 2.3 of this draft risk
evaluation.
EPA evaluated reasonably available information for human health hazards and identified hazard
endpoints for cancer. EPA used the Framework for Human Health Risk Assessment to Inform Decision
Making ( ) to evaluate, extract, and integrate asbestos' dose-response information. EPA
evaluated the large database of health effects associated with asbestos exposure cited in numerous U.S.
and international data sources. Many authorities have established that there are causal associations
between asbestos exposures and cancer fNTP. 2016; I ARC. 2012; ATSDR. 200 M. \\\\ 1988b;
I ARC. 1987; U.S. EPA. 1986; I ARC. 19771
Given the well-established carcinogenicity of asbestos for cancer, EPA, in its PF document, decided to
limit the scope of its systematic review to cancer and to inhalation exposures with the goal of updating,
or reaffirming, the existing 1988 EPA inhalation unit risk (IUR) for general asbestos (U.S. EPA.
1988b). Therefore, the literature was reviewed to determine whether a new IUR needed to be
developed. The IUR for asbestos developed in 1988 was based on 14 epidemiologic studies that
included occupational exposure to chrysotile, amosite, or mixed-mineral exposures [chrysotile, amosite,
crocidolite]. However, EPA's research to identify COUs indicated that only chrysotile asbestos is
currently being imported in the raw form or imported in products. In addition, most studies of
populations exposed only to chrysotile provide the most informative data for the purpose of developing
the TSCA risk estimates for the COUs for asbestos in this document. EPA will consider legacy uses
and associated disposal in subsequent supplemental documents.
As stated in Section 3.2, epidemiological studies on mesothelioma and lung cancer in cohorts of workers
using chrysotile in commerce were identified that could inform the estimation of an exposure-response
function allowing for the derivation of a chrysotile asbestos IUR. EPA could not find any recent risk
values in the literature for chrysotile asbestos since the IRIS IUR value was the result of contemporary
data from the 1980s.
EPA derived the chrysotile IUR based on review of the epidemiology literature describing occupational
cohorts exposed to commercial chrysotile that provided adequate data for the assessment of lung cancer
and mesothelioma risks. EPA developed data evaluation criteria specifically to assess the quality of
epidemiology studies of asbestos and lung cancer and mesothelioma. The study domains of exposure,
outcome, study participation, potential confounding, and analysis were further tailored to the specific
needs of evaluating asbestos studies for their potential to provide information on the exposure-response
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relationship between asbestos exposure and mortality from lung cancer and from mesothelioma. In terms
of evaluating exposure information, asbestos is unique among these first 10 TSCA chemicals
undergoing risk evaluation as it is a fiber and has a long history of different exposure assessment
methodologies. For mesothelioma, this assessment is also unique with respect to the impact of the
timing of exposure relative to the cancer outcome as the time since first exposure plays a dominant role
in modeling risk. The most relevant exposures for understanding mesothelioma risk were those that
occurred decades prior to the onset of mesothelioma and subsequent mesothelioma mortality.
Cancer potency values were either extracted from published epidemiology studies or derived from the
data within those studies. Once the cancer potency values were obtained, they were adjusted for
differences in air volumes between workers and other populations so that those values can be applied
to the U.S. population as a whole in standard EPA life-table analyses. The life-table methodology
allows the estimation of an exposure concentration associated with a specific extra risk of cancer
mortality caused by chrysotile asbestos. According to standard practice, the lifetime unit risks for lung
cancer and mesothelioma were estimated separately and then statistically combined to yield the cancer
inhalation unit risk. Less-than-lifetime or partial lifetime unit risks were also derived for a range
of exposure scenarios based on different ages of first exposure and different durations of exposure
(e.g., 20 years old and 40 years of exposure).
Risk Characterization
Environmental Risk: Based on the reasonably available information in the published literature,
provided by industries using asbestos, and reported in EPA databases, there is minimal or no releases
of asbestos to surface water associated with the COUs that EPA is evaluating in this risk evaluation.
Thus, EPA believes there is low or no potential for environmental risk to aquatic or sediment-dwelling
receptors from the COUs included in this risk evaluation because water releases associated with the
COUs are not expected and were not identified. Terrestrial pathways, including biosolids, were
excluded from risk evaluation at the PF stage.
Human Health Risks: EPA identified cancer risks from inhalation exposure to chrysotile asbestos.
For workers and ONUs, EPA estimated cancer risk from inhalation exposures to asbestos using IUR
values and exposures for each COU. EPA estimated risks using several occupational exposure
scenarios related to the central and high-end estimates of exposure without the use of personal
protective equipment (PPE), and with potential PPE for workers using asbestos. Industry submissions
indicated that some workers used respirators for certain tasks, but not others, while other workers used
ineffective respirators (sheet gasket stampers using N95 respirators is not protective based on OSHA
regulations). Although hypothetical respirator usage with an applied protection factor (APF) of 10 and
25 was calculated for all COUs, actual respirator use was limited to an APF of 10 (the use of sheet
gaskets) and APFs of 10 and 25, in some cases, for chlor-alkali diaphragm use. No other APFs were
indicated for any other COU. For asbestos, nominal APFs (e.g., 25) may not be achieved for all PPE
users. More information on respiratory protection, including EPA's approach regarding the
occupational exposure scenarios for asbestos, is in Section 2.3.1.2.
For workers, cancer risks in excess of the benchmark of 1 death per 10,000 (or 1 x 10"4) were indicated
for all conditions of use under high-end and central tendency exposure scenarios when PPE was not
used. With the hypothetical use of PPE at APF of 10 (except for chlor-alkali processing and use and
sheet gasket use), most risks were reduced for central tendency estimates but still persisted for sheet
gasket stamping, auto brake replacement, other vehicle friction products and utility vehicle (UTV use
and disposal) gasket replacement for high-end exposure estimates (both 8-hour and short-term
durations). Although not expected to be worn given the reasonably available information, when PPE
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with an APF of 25 was applied, risk was still indicated only for the high-end, short term exposure
scenario for the auto brakes and other vehicle friction products. EPA's estimates for worker risks for
each occupational scenario are presented by each COU in Section 4.2.2 and summarized in Table 4-38.
For ONUs, cancer risks in excess of the benchmark of 1 death per 10,000 (or 1 x 10"4) were indicated for
both central tendency and high-end exposures for sheet gasket use (in chemical production) and UTV
gasket replacement. In addition, cancer risks for ONUs were indicated for high-end exposures only for
chlor-alkali, sheet gasket stamping, and auto brakes. ONUs were not assumed to be using PPE to reduce
exposures to asbestos used in their vicinity. EPA's estimates for ONU risks for each occupational
exposure scenario are presented by each COU in Section 4.2.2 and summarized in Table 4-38.
For consumers (Do-it-Yourselfers, or DIY) and bystanders of consumer use, EPA estimated cancer
risks resulting from inhalation exposures with a range of user durations, described in detail in Section
4.2.3. EPA assumed that consumers or bystanders would not use PPE.
For consumers and bystanders, cancer risks in excess of the benchmark of 1 death per 1,000,000 (or 1
x 10"6) were indicated for most COUs for consumer exposure scenarios. Risks were indicated for all
high-end exposures for both consumers and bystanders for brake and UTV gasket indoor scenarios;
and the high-end consumer outdoor scenarios (for 30-minute exposures). EPA's estimates for
consumer and bystander risks for each consumer use exposure scenario are presented in Section 4.2.3
and summarized in Table 4-48.
Uncertainties. Uncertainties have been identified and discussed after each section in this risk
evaluation. In addition, Section 4.3 summarizes the major assumptions and key uncertainties by major
topic: uses of asbestos, occupational exposure, consumer exposure, envioronmental risk, IUR
derivation, cancer risk value and human health risk estimates.
Beginning with the February, 2017 request for information on uses of asbestos (see 1 tblic
Meeting) and followed by both the Scope document (June ( )) and Problem Formulation (June
(2018d)), EPA has refined its understanding of the current conditions of use of asbestos in the U.S.
Chrysotile asbestos is the only fiber type imported, processed, or distributed in commerce for use in
2019. All the raw asbestos imported into the U.S. is used by the chlor-alkali industry for use in asbestos
diaphragms. The remaining COUs are for articles that contain chrysotile asbestos and EPA received
voluntary acknowledgement from a handful of industries that fall under these COU categories.
Therefore, EPA evaluated manufacturing, processing, distribution in commerce, occupational and
consumer uses, and disposal of chrysotile asbestos in this draft risk evaluation.
By finalizing the asbestos SNUR on April 25, 2019 to include manufacturing (including import) or
processing discontinued uses not already banned under TSCA, EPA is highly certain that manufacturing
(including import), processing, or distribution of asbestos is not intended, known or reasonably foreseen
beyond the six product categories in this risk evaluation. EPA will consider legacy uses and associated
disposal in subsequent supplemental documents.
For occupational exposures, the number of chlor-alkali plants in the U.S. is known and therefore the
number of workers potentially exposed is fairly certain. The number of workers potentially exposed for
other COUs is less certain. Only two workers were identified for stamping sheet gaskets, and two Ti02
manufacturing facilities were identified in the U.S. who use asbestos-containing gaskets. However, EPA
is not certain if asbestos-containing sheet gaskets are used in other industries and to what extent. For the
other COUs, no estimates of the number of potentially exposed workers were submitted to EPA by
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industry or its representatives, so estimates were used and were based on market estimates for that work
category; but with no information on the market share for asbestos containing products. Therefore,
numbers of workers potentially exposed were estimated and, based on the COU, these estimations have
a range of uncertainty from low (chlor-alkali) to high (sheet gasket use, oilfield brake blocks,
aftermarket automotive brakes/linings, other vehicle friction products and other gaskets).
Exposures for ONUs can vary substantially. Most data sources do not sufficiently describe the proximity
of these employees to the exposure source. As such, exposure levels for the ONU category will vary
depending on the work activity. It is unknown whether these uncertainties overestimate or underestimate
exposures.
A review of resonably available literature for consumer exposure estimates related to brake
repair/replacement activities by a DIY consumer was limited and no information for consumer exposure
estimates related to UTV exhaust system gasket repair/replacement activities was found. This absence of
scenario-specific exposure information required EPA to use surrogate monitoring data from
occupational studies to evaluate consumer risk resulting from exposure to asbestos during these two
activities. The surrogate occupational studies tended to be based on older studies that may or may not
reflect current DIY consumer activities, including best practices for removing asbestos containing
materials. In addition, EPA is uncertain about the number of asbestos containing brakes that are being
purchased online and installed in cars (classic cars or new cars) or gaskets that are being replaced in
UTVs.
After the PF was released, EPA continued to search EPA databases and all publicly available literature
and contact industries to shed light on potential releases to water from the COUs in this risk evaluation
for the purpose of evaluating risk to aquatic or sediment-dwelling organisms. EPA found minimal or no
releases of asbestos to surface water associated with the COUs in this risk evaluation. In addition, there
are no reported releases of asbestos to water from TRI. EPA views the uncertainty that this introduces as
low.
A specific IUR was developed in this risk evaluation for combined mesothelioma and lung cancer
following exposure to chrysotile asbestos. There is evidence that other cancer endpoints may also be
associated with exposure to the commercial forms of asbestos. IARC concluded that there was sufficient
evidence in humans that commercial asbestos (chrysotile, crocidolite, amosite, tremolite, actinolite, and
anthophyllite) was causally associated with lung cancer and mesothelioma, as well as cancer of the
larynx and the ovary. The lack of sufficient numbers of workers to estimate risks of ovarian and
laryngeal cancer is a downward bias leading to lower IUR estimates in an overall cancer health
assessment; however, the selected IUR was chosen to compensate for this bias (See Section 3.2.4).
The endpoint for both mesothelioma and lung cancer was mortality, not incidence. Incidence data are
not available for any of the cohorts. Nevertheless, mortality rates approximate incidence rates for
cancers such as lung cancer and mesothelioma because the survival time between cancer incidence and
cancer mortality is short. Therefore, while the absolute rates of lung cancer mortality may underestimate
the rates of lung cancer incidence, the uncertainty for lung cancer is low. For mesothelioma, the median
length of survival with mesothelioma is less than 1 year for males, with less than 20% surviving after 2-
years and less than 6% surviving after 5-years. Because the mesothelioma model is absolute risk, this
leads to an under-ascertainment on mesothelioma risk, however, the selected IUR was chosen to
compensate this bias (See Section 3.2.4)
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Epidemiologic studies are observational and as such are potentially subject to confounding and selection
biases. Most of the studies of asbestos exposed workers did not have information to control for cigarette
smoking, which is an important risk factor for lung cancer in the general population. However, the bias
related to this failure to control for smoking is believed to be small. It is unlikely that smoking rates
among workers in the chosen epidemiology studies differed substantially enough with respect to their
cumulative chrysotile exposures to induce important confounding in risk estimates for lung cancer (see
Section 4.3.7). Mesothelioma is not related to smoking and thus smoking could not be a confounder for
mesothelioma.
Depending on the variations in the exposure profile of the workers/occupational non-users and
consumers/bystanders, risks could be under- or over-estimated for all COUs. The estimates for extra
cancer risk were based on the EPA-derived IUR for chrysotile asbestos. The occupational exposure
assessment made standard assumptions of 240 days per year, 8 hours per day over 40 years starting at
age 16 years. This assumes the workers and ONUs are regularly exposed until age 56. If a worker
changes jobs during their career and are no longer exposed to asbestos, this may overestimate exposures.
However, if the worker stays employed after age 56, it would underestimate exposures.
Potentially Exposed Susceptible Subpopulations (PESS): TSCA § 6(b)(4) requires that EPA conduct a
risk evaluation to "determine whether a chemical substance presents an unreasonable risk of injury to
health or the environment, without consideration of cost or other non-risk factors, including an
unreasonable risk to a potentially exposed or susceptible subpopulation identified as relevant to the risk
evaluation by the Administrator, under the conditions of use. " TSCA § 3(12) states that "the term
'potentially exposed or susceptible subpopulation' means a group of individuals within the general
population identified by the Administrator who, due to either greater susceptibility or greater exposure,
may be at greater risk than the general population of adverse health effects from exposure to a chemical
substance or mixture, such as infants, children, pregnant women, workers, or the elderly. "
EPA identified certain human subpopulations who may be more susceptible to exposure to asbestos than
others. Workers exposed to asbestos in workplace air, especially if they work directly with asbestos, are
most susceptible to the health effects associated with asbestos. Although it is clear that the health risks
from asbestos exposure increase with heavier exposure and longer exposure time, investigators have
found asbestos-related diseases in individuals with only brief exposures. Generally, those who develop
asbestos-related diseases could show no signs of illness for decades after exposure.
A source of variability in susceptibility between people is smoking history or the degree of exposure to
other risk factors with which asbestos interacts. In addition, the long-term retention of asbestos fibers in
the lung and the long latency period for the onset of asbestos-related respiratory diseases suggest that
individuals exposed earlier in life may be at greater risk to the eventual development of respiratory
problems than those exposed later in life (ATSDR. 2001a). There is also some evidence of genetic
predisposition for mesothelioma related to having a germ line mutation in BAP1 (Testa et at. 2011).
Cancer risks were indicated for all the worker COUs and most of the consumer/bystander COUs. In
addition, several subpopulations (e.g., smokers, genetically predisposed individuals, workers who
change their own asbestos-containing brakes) may be more susceptible than others to health effects
resulting from exposure to asbestos. These conditions are discussed in more detail for potentially
exposed or susceptible subpopulations and aggregate exposures in Section 4.4 and Section 4.5.
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Aggregate and Sentinel Exposures: Section 6(b)(4)(F)(ii) of TSCA requires the EPA, as a part of the risk
evaluation, to describe whether aggregate or sentinel exposures under the conditions of use were
considered and the basis for their consideration. The EPA has defined aggregate exposure as "the
combined exposures to an individual from a single chemical substance across multiple routes and
across multiple pathways (40 CFR § 702.33)." Exposures to asbestos were evaluated by the inhalation
route only. Inhalation and oral exposures could occur simultaneously for workers and consumers. EPA
chose not to employ simple additivity of exposure pathways at this time within a COU since the most
critical exposure pathway is inhalation and the target being assessed is combined lung cancer and
mesothelioma.
Aggregate exposures for asbestos were not assessed by all routes of exposure, since only inhalation
exposure was evaluated in the RE. Pathways of exposure were also not combined in this RE. EPA
recognizes that it is possible that workers exposed to asbestos might also be exposed as consumers (by
changing asbestos-containing brakes at home).
The EPA defines sentinel exposure as "the exposure to a single chemical substance that represents the
plausible upper bound of exposure relative to all other exposures within a broad category of similar or
related exposures (40 CFR § 702.33)." In this risk evaluation, the EPA considered sentinel exposure the
highest exposure given the details of the COU and the potential exposure scenarios. EPA considered
sentinel exposures by considering risks to populations who may have upper bound (e.g., high-end, high
intensities of use) exposures
Risk Determination
In each risk evaluation under TSCA section 6(b), EPA determines whether a chemical substance
presents an unreasonable risk of injury to health or the environment, under the conditions of use. The
determination does not consider costs or other non-risk factors. In making this determination, EPA
considers relevant risk-related factors, including, but not limited to: the effects of the chemical substance
on health and human exposure to such substance under the conditions of use (including cancer and non-
cancer risks); the effects of the chemical substance on the environment and environmental exposure
under the COU; the population exposed (including any potentially exposed or susceptible
subpopulations); the severity of hazard (including the nature of the hazard, the irreversibility of the
hazard); and uncertainties. EPA also takes into consideration the Agency's confidence in the data used
in the risk estimate. This includes an evaluation of the strengths, limitations, and uncertainties associated
with the information used to inform the risk estimate and the risk characterization. The rationale for the
risk determination is discussed in Section 5.2.
Environmental Risk: As described in the problem formulation (U.S. EPA. 2.018d). other Agency
regulations adequately assess and effectively manage exposures from asbestos releases to terrestrial
pathways, including biosolids, for terrestrial organisms. After the PF was released, EPA continued to
search EPA databases as well as the literature and contacted industries to shed light on potential releases
of asbestos to water from the TSCA COUs. Based on the reasonably available information in the
published literature, provided by industries using asbestos, and reported in EPA databases, there is
minimal or no releases of asbestos to surface water associated with the COUs in this risk evaluation.
Therefore, EPA concludes there is no unreasonable risk to aquatic or sediment-dwelling environmental
organisms. Details are provided in Section 4.1.
Risk of Injury to Health: EPA's determination of unreasonable risk for specific COUs of asbestos listed
below are based on health risks to workers, occupational non-users, consumers, or bystanders from
consumer use. The health effect driver for EPA's determination of unreasonable risk is cancer from
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inhalation exposure. As described below, risks to the general population were not relevant for these
conditions of use.
There are physical-chemical characteristics that are unique to asbestos, such as insolubility in water,
suspension and duration in air, transportability, the friable nature of asbestos-containing products, which
attribute to the potential for asbestos fibers to be released, settled, and to again become airborne under
the conditions of use (re-entrainment). Also unique to asbestos is the impact of the timing of exposure
relative to the cancer outcome; the most relevant exposures for understanding cancer risk were those that
occurred decades prior to the onset of cancer and subsequent cancer mortality. In addition to the cancer
benchmark, the physical-chemical properties and exposure considerations are important factors in
considering risk of injury to health. To account for the exposures for ONUs and, in certain cases
bystanders, EPA derived a distribution of exposure values for calculating the risk for cancer by using
area monitoring data (i.e., fixed location air monitoring results) where available for certain conditions of
use and when appropriate applied exposure reduction factors, using data from published literature (see
Sections 2.3.1 and 2.3.2 for details on ONU and bystander methods, respectively). The risk
determination for each COU in this risk evaluation considers both central tendency and high-end risk
estimates for workers, ONUs, consumers and bystanders. Where relevant EPA considered PPE for
workers. For many of the COUs both the central tendency and high-end risk estimates exceed the risk
benchmark for each of the exposed populations evaluated. However, the risk benchmarks do not serve as
a bright line for making risk determinations and other relevant risk-related factors were considered. In
particular there are severe and irreversible health effects associated with asbestos inhalation exposures
and fibers can become airborne again and available for exposure, which resulted in EPA focusing on the
high-end risk estimates rather than central tendency risk estimates to be most protective of workers,
ONUs, consumers, and bystanders. Additionally, EPA's confidence in the data used in the risk estimate
is considered.
Risk to the General Population: General population exposures to chrysotile asbestos may occur from
industrial and/or commercial uses; industrial releases to air, water or land; and other conditions of use.
As part of the PF for asbestos, EPA found those exposure pathways are covered under the jurisdiction of
other environmental statutes, administered by EPA, which adequately assess and effectively manage
those exposures, i.e., CAA, SDWA, CWA, and RCRA. EPA believes that the TSCA risk evaluation
should focus on those exposure pathways associated with TSCA uses that are not subject to the
regulatory regimes discussed above because these pathways are likely to represent the greatest areas of
concern to EPA for unmanaged risks. Therefore, EPA did not evaluate hazards or exposures to the
general population in this risk evaluation, and there is no risk determination for the general population.
Risk to Workers: The conditions of use of asbestos that present an unreasonable risk to workers include
processing and industrial use of asbestos-containing diaphragms, processing and industrial use of
asbestos-containing sheet gaskets and industrial use of asbestos-containing brake blocks, aftermarket
automotive asbestos-containing brakes/linings, other vehicle friction products, and other asbestos-
containing gaskets. A full description of EPA's determination for each condition of use is in Section 5.2.
Risk to Occupational Non-Users (ONUs): EPA determined that the conditions of use that present
unreasonable risks for ONUs include processing and industrial use of asbestos-containing diaphragms,
processing and industrial use of asbestos-containing sheet gaskets and industrial use of asbestos-
containing brake blocks, aftermarket automotive asbestos-containing brakes/linings, other vehicle
friction products, and other asbestos-containing gaskets. A full description of EPA's determination for
each condition of use is in Section 5.2.
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1088
1089	Risk to Consumers: For consumers, EPA determined that the conditions of use that present an
1090	unreasonable risk are use of aftermarket automotive asbestos-containing brakes/linings and other
1091	asbestos-containing gaskets. A full description of EPA's determination for each condition of use is in
1092	Section 5.2.
1093
1094	Risk to Bystanders (from consumer uses): EPA determined that the conditions of use that present an
1095	unreasonable risk to bystanders are use of aftermarket automotive asbestos-containing brakes/linings
1096	and other asbestos-containing gaskets. A full description of EPA's determination for each condition of
1097	use is in Section 5.2.
1098
1099	Summary of risk determinations:
1100	EPA has preliminarily determined that there are no conditions of use presenting an unreasonable risk to
1101	environmental receptors (see details in Section 5.1).
1102	EPA has preliminarily determined that the following conditions of use of asbestos present an
1103	unreasonable risk of injury to health to workers (including, in some cases, occupational non-users) or to
1104	consumers (including, in some cases, bystanders). The details of these determinations are presented in
1105	Section 5.2.2
1106
Omipsilioiiiil C onditions of I so 1 h:il Present ;in I nrensonsihle Kisk to 11e:i11 li
•	Processing and Industrial use of Asbestos Diaphragms in Chlor-alkali Industry
•	Processing and Industrial Use of Asbestos-Containing Sheet Gaskets in Chemical Production
•	Industrial Use and Disposal of Asbestos-Containing Brake Blocks in Oil Industry
•	Commercial Use and Disposal of Aftermarket Automotive Asbestos-Containing
Brakes/Linings
•	Commercial Use and Disposal of Other Vehicle Friction Products
•	Commercial Use and Disposal of Other Asbestos-Containing Gaskets
1107
Consumer I ses sind Disposal tlisit Present sin I nresisonnhle Kisk to llesilth
•	Aftermarket Automotive Asbestos-Containing Brakes/Linings
•	Other Asbestos-Containing Gaskets
1108
1109	EPA has determined that the following conditions of use of asbestos do not present an unreasonable risk
1110	of injury to health. The details of these determinations are presented in section 5.2.
1111
1112
1113
2 Although EPA has identified both industrial and commercial uses here for purposes of distinguishing scenarios in this
analysis, the Agency interprets the authority over "any manner or method of commercial use" under TSCA section 6(a)(5) to
reach both.
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Conditions of I so llisil Do Not Present ;i 11 I nrensonnhle Kisk to 11e:i11h
•	Import of asbestos and asbestos-containing products
•	Distribution of asbestos-containing products
•	Disposal of asbestos-containing sheet gaskets processed and/or used in chemical production
•	Import, use, distribution and disposal of asbestos-containing brakes for the specialized and
large National Aeronautics and Space Administration (NASA) transport plane ("Super Guppy")
1114
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1 INTRODUCTION
This document presents the draft risk evaluation for asbestos under the Frank R. Lautenberg Chemical
Safety for the 21st Century Act which amended the Toxic Substances Control Act, the Nation's primary
chemicals management law, in June 2016.
EPA published the scope of the risk evaluation for asbestos (	) in June 2017, and the
problem formulation in June 2018 (	)18d). which represented the analytical phase of risk
evaluation in which "the purpose for the assessment is articulated, the problem is defined, and a plan for
analyzing and characterizing risk is determined" as described in Section 2.2 of the Framework for
Human Health Risk Assessment to Inform Decision Matins. EPA has received information and
comments specific to individual chemicals and of a more general nature relating to various aspects of the
risk evaluation process, technical issues, and the regulatory and statutory requirements. EPA has
considered comments and information received at each step in the process and factored in the
information and comments as the Agency deemed appropriate and relevant including comments on the
published problem formulation for asbestos. Thus, in addition to any new comments on the draft risk
evaluation, the public should re-submit or clearly identify at this point any previously filed comments,
modified as appropriate, that are relevant to this risk evaluation and that the submitter feels have not
been addressed. EPA does not intend to further respond to comments submitted prior to the publication
of this draft risk evaluation unless they are clearly identified in comments on this draft risk evaluation.
As per EPA's final rule, Procedures for Chemical Risk Evaluation Under the Amended Toxic
Substances Control Act (82 Fed. Reg. 33726 (July 20, 2017)), this draft risk evaluation will be subject to
both public comment and peer review. EPA is providing 60 days for public comment on this draft risk
evaluation, including the submission of any additional information that might be relevant to the science
underlying the risk evaluation and the outcome of the systematic review associated with asbestos. This
satisfies TSCA (15 U.S.C. 2605(b)(4)(H)), which requires EPA to provide public notice and an
opportunity for comment on a draft risk evaluation prior to publishing a final risk evaluation.
Peer review will be conducted in accordance with EPA's regulatory procedures for chemical risk
evaluations, including using the EPA. Peer Review Handbook and other methods consistent with Section
26 of TSCA (See 40 CFR 702.45). As explained in the Risk Evaluation Rule (82 Fed. Reg. 33726 (July
20, 2017)), the purpose of peer review is for the independent review of the science underlying the risk
assessment. Peer review will therefore address aspects of the underlying science as outlined in the
charge to the peer review panel such as hazard assessment, assessment of dose-response, exposure
assessment, and risk characterization. EPA believes peer reviewers will be most effective in this role if
they receive the benefit of public comments on draft risk evaluations prior to peer review. For this
reason, and consistent with standard Agency practice, the public comment period will precede peer
review on this draft risk evaluation. The final risk evaluation may change in response to public
comments received on the draft risk evaluation and/or in response to peer review, which itself may be
informed by public comments. EPA will respond to public and peer review comments received on the
draft risk evaluation and will explain changes made to the draft risk evaluation for asbestos in response
to those comments in the final risk evaluation.
The PF identified the conditions of use (COUs) and presented three conceptual models and an analysis
plan. Based on EPA's analysis of the COU, physical-chemical and fate properties, environmental
releases, and exposure pathways, the PF preliminarily concluded that further analysis was necessary for
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exposure pathways to workers, consumers, and surface water, based on a qualitative assessment of the
physical-chemical properties and fate of asbestos in the environment. However, during development of
the PF, EPA was still in the process of identifying potential asbestos water releases for the COUs. After
the PF was released, EPA continued to search EPA databases as well as the literature and either engaged
in a dialogue with industries or reached out for a dialogue to shed light on potential releases to water.
The reasonably available information indicated that there were surface water releases of asbestos;
however, not all releases are subject to reporting (e.g., effluent guidelines) or are applicable (e.g.,
friability). Based on the reasonably available information in the published literature, provided by
industries using asbestos, and reported in EPA databases, there is minimal or no releases of asbestos to
surface water associated with the COUs in this risk evaluation. Therefore, EPA concludes there is no
unreasonable risk to aquatic or sediment-dwelling environmental organisms (See Section 4.1).
Asbestos has been regulated by various Offices of EPA for years. The risk evaluation (RE) for asbestos
has posed some unique challenges to OPPT. Unlike the other nine chemicals that are part of the "First
10" risk evaluations under the Lautenberg Act of 2016, asbestos is a naturally occurring fiber, which
poses its own set of issues, including defining: (1) the COU (by asbestos fiber type); (2) the appropriate
inhalation unit risk (IUR) value to use for the hazard/dose-response process; and (3) the appropriate
exposure assessment measures.
The COUs in this draft risk evaluation for asbestos are limited to only a few categories of ongoing uses,
and chrysotile is the only type of asbestos fiber identified for these COUs3. Ongoing uses of asbestos in
the U.S. were difficult to identify despite using an extensive list of resources. To determine the COU of
asbestos and inversely, activities that do not qualify as COUs, EPA conducted extensive research and
outreach. EPA identified activities that include import of raw asbestos, used solely in the chlor-alkali
industry, and import and use of asbestos-containing products. The COUs included in this draft risk
evaluation that EPA considers to be known, intended, or reasonably foreseen are the manufacture/
import, use, distribution and disposal of asbestos diaphragms, sheet gaskets, other gaskets, oilfield brake
blocks, aftermarket automotive brakes/linings, and other vehicle friction products and the processing of
asbestos diaphragms and sheet gaskets. Some of these COUs are very specialized. Since the PF, three
uses were removed from the scope of the RE based on further investigation (see Section 1.4.3); these
uses include woven products, cement products, and packings (from "gaskets and packings"). EPA
determined that there is no evidence to support that asbestos-containing woven products, cement
products, or packings are COUs of asbestos. These three uses were added to the Significant New Use
Rule (SNUR) for asbestos (40 CFR 721.11095). The Asbestos SNUR is an Agency action
complementary to this risk evaluation and taken under TSCA section 5 to prohibit any manufacturing
(including import) or processing for discontinued uses of asbestos from restarting without EPA having
an opportunity to evaluate them to determine risks to health or the environment and take any necessary
regulatory action, which may include a prohibition. The final asbestos SNUR ensures that any
manufacturing (including import) and processing for all discontinued uses and types of asbestos that are
not already banned are restricted from re-entering the U.S. marketplace without notification to EPA and
review and any necessary regulatory action by the Agency. Thus, should any person wish to
3 Please note that EPA continues to review the recent court decision in Safer Chemicals Healthy Families v. EPA, Nos. 17-
72260 et al. (9th Cir. 2019). This draft risk evaluation does not reflect consideration of legacy uses and associated disposal as
a result of that decision. EPA is still seeking public comment on and peer review of this version, however. EPA intends to
consider legacy uses and associated disposal in a supplemental scope document and supplemental risk evaluation.
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manufacture, import, or process asbestos for an activity that is not a COU identified in this document or
subject to an existing ban, then EPA would review the risk of the activity associated with such a use in
accordance with TSCA section 5.
During the investigation of the COUs, EPA also determined that asbestos is no longer mined in the U.S.,
and that only chrysotile asbestos is being imported. The other five forms of asbestos identified for this
risk evaluation, including crocidolite (riebeckite), amosite (cummingtonite-grunerite), anthophyllite,
tremolite or actinolite, are no longer manufactured, imported, or processed in the United States and are
also now subject to the SNUR. After EPA confirmed that chrysotile asbestos is the only type of asbestos
still being imported into the U.S. either in raw form or in products, EPA developed a chrysotile IUR4 to
be used in the RE. The IUR for asbestos developed in 1988 was based on 14 epidemiologic studies that
included occupational exposure to chrysotile, amosite, or mixed-mineral exposures (chrysotile, amosite,
crocidolite). As a naturally occurring mineral, chrysotile can co-occur with other minerals, including
amphibole forms of asbestos. Trace amounts of these minerals may remain in chrysotile as it is used in
commerce. This commercial chrysotile, rather than theoretically "pure" chrysotile, is therefore the
substance of concern for this assessment. The epidemiologic studies available for risk evaluation all
include populations exposed to commercial chrysotile asbestos, which may contain small, but variable
amounts of amphibole asbestos. Because the only form of asbestos imported, processed, or distributed
for use in the United States today is chrysotile, studies of populations exposed only to chrysotile provide
the most informative data for the purpose of updating the TSCA risk estimates for the COUs for
asbestos in this document. EPA will consider legacy uses and associated disposal in subsequent
supplemental documents.
Related to the focus on chrysotile asbestos is the method of identifying asbestos in studies used to
develop the IUR. The IUR is based on fiber counts made by phase contrast microscopy (PCM) and
should not be applied directly to measurements made by other analytical techniques. PCM
measurements made in occupational environments were used in the studies used to support the
derivation of the chrysotile IUR. PCM detects only fibers longer than 5 |im and >0.4 |im in diameter,
while transmission electron microscopy (TEM), often found in environmental monitoring
measurements, can detect much smaller fibers. In developing a PCM-based IUR in this risk evaluation,
several TEM papers modeling risk of lung cancer were found, but because there was no TEM-based
modeling of mesothelioma mortality, TEM data could not be used to derive a TEM-based IUR.
EPA stated in the PF that the asbestos RE would focus on epidemiological data on lung cancer and
mesothelioma. The 1988 IUR identified asbestos as a carcinogen causing both lung cancer and
mesothelioma from inhalation exposures and derived a unit risk to address both cancers (for all TSCA
Title II fiber types - see Section 1.1). EPA is not aware of any other chrysotile-specific IUR for the
asbestos types included in this RE or any other risk-based values having been estimated for other types
of cancer for asbestos by either EPA or other government agencies. For the derivation of a chrysotile
asbestos IUR, epidemiological studies on mesothelioma and lung cancer in cohorts of workers using
chrysotile in commerce were identified to inform the estimation of an exposure-response function. Over
24,000 studies were initially identified for consideration during the Systematic Review process to
determine whether the IUR needed to be updated. This large number of studies posed its own unique
challenges, including development of data quality review standards specific to asbestos.
4 Inhalation Unit risk (IUR) is typically defined as a plausible upper bound on the estimate of cancer risk per ng/m3 air
breathed for 70 years. For asbestos, the IUR is expressed as cancer risk per fibers/cc (in units of the fibers as measured by
PCM).
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EPA derived an IUR for chrysotile asbestos using five epidemiological study cohorts analyzing lung
cancer and mesothelioma. EPA derived cancer-specific unit risks using lifetables. Different modeling
choices and combinations of cancer-specific unit risks yielded candidate IUR values ranging from 0.08
to 0.33 per f/cc, indicating low model-based uncertainty. The IUR chosen is 0.16 per f/cc and it was
applied to the COUs to calculate lifetime risks for workers and consumers.
EPA estimated risks for workers, occupational non-users (ONUs), consumers (do-it-yourself [DIY]
mechanics) and bystanders for the COUs identified. Inhalation exposure scenarios were used to estimate
risks for cancer based on the EPA-derived IUR for chrysotile asbestos. This assessment is unique with
respect to the timing of exposure relative to the cancer outcome as the time since first exposure plays a
dominant role in modeling risk. Occupational exposures assumed 240 days/year for 8-hour workdays for
40 years starting at 16 years old; with other starting ages and exposure durations also presented.
Occupational exposures for chlor-alkali and sheet gasket workers and ONUs were based on monitoring
data supplied by companies performing the work. Consumer exposures were based on study data
provided in the literature for gasket replacement and brakes. Consumer exposures assumed that DIY
mechanics for both COUs changed brakes or gaskets once every three years (the task taking three hours)
over a lifetime and that exposures lingered between the episodic exposures.
In this draft risk evaluation, Section 1 presents the basic physical-chemical characteristics of asbestos, as
well as a background on regulatory history, COUs, and conceptual models, with particular emphasis on
any changes since the publication of the PF. This section also includes a discussion of the systematic
review process utilized in this draft risk evaluation. Section 2 provides a discussion and analysis of the
exposures, both health and environmental, that can be expected based on the COUs for asbestos. Section
3 discusses environmental and health hazards of asbestos. Section 4 presents the risk characterization,
where EPA integrates and assesses reasonably available information on health and environmental
hazards and exposures, as required by TSCA (15 U.S.C. 2605(b)(4)(F)). This section also includes a
discussion of any uncertainties and how they impact the draft risk evaluation. Section 5presents EPA's
proposed determination of whether the chemical presents an unreasonable risk under the COU, as
required under TSCA (15 U.S.C. 2605(b)(4)).
1.1 Physical and Chemical Properties and Environmental Fate
Asbestos is a "generic commercial designation for a group of naturally occurring mineral silicate fibers
of the serpentine and amphibole series" (I ARC.: ). The Chemical Abstract Service (CAS) definition
of asbestos is "a grayish, non-combustible fibrous material. It consists primarily of impure magnesium
silicate minerals." The general CAS Registry Number (CASRN) of asbestos is 1332-21-4; this is the
only asbestos CASRN on the TSCA Inventory. However, other CASRNs are available for specific fiber
types.
TSCA Title II (added to TSCA in 1986), Section 202 defines asbestos as the "asbestiform varieties of
six fiber types - chrysotile (serpentine), crocidolite (riebeckite), amosite (cummingtonite-grunerite),
anthophyllite, tremolite or actinolite." The latter five fiber types are amphibole varieties. In the Problem
Formulation of the Risk Evaluation for Asbestos (EP A-HQ-OPPT-2016-0736-0131) (U.S. EPA. 2018d).
physical and chemical properties of all six fiber types were presented. As discussed in more detail in
Section 1.4, this risk evaluation has focused on chrysotile given EPA's knowledge of the COUs of
asbestos, and EPA will consider legacy uses and associated disposal in subsequent supplemental
documents. Table 1-1. lists the physical/chemical properties for the six fiber types of asbestos. As with
all silicate minerals, the basic building blocks of asbestos fibers are silicate tetrahedra [Si04]4" where
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1292	four oxygen atoms are covalently bound to the central silicon. These tetrahedra occur as sheets [Si40io]
1293	in chrysotile. In the case of chrysotile, an octahedral brucite layer having the formula [Mg604(0H)8] is
1294	intercalated between each silicate tetrahedral sheet.
1295
1296		Table 1-1. Physical and Chemical Properties of Asbestos Fiber Typesa	

Chrysoiile
Amosile
Crocidolik-
A six-si i form
Tivmolile
A six-si i form
Anihophylliic
. \ six-si i form
Aclinolile
1 !ssailml
composition
\lg silicak
with some
water
Iv, \lg
silicate
\ii. Iv
silicate with
some water
( a. \lg
silicate with
some water
\lg silicak
with iron
( a. \lg, Iv
silicate with
some water
Color
White, gray,
green,
yellowish
Ash gray,
greenish or
brown
Lavender,
blue, greenish
Gray-white,
greenish,
yellowish,
bluish
Grayish white,
also brown-
gray or green
Greenish
Luster
Silky
Vitreous to
pearly
Silky to dull
Silky
Vitreous to
pearly
Silky
Surface areab'
(m2/g)
13.5-22.4
2.25-7.10
4.62-14.80
No data
No data
No data
Hardness (Mohs)
2.5-4.0
5.5-6.0
4.0
5.5
5.5-6.0
6.0
Specific gravity
2.4-2.6
3.1-3.25
3.2-3.3
2.9-3.2
2.85-3.1
3.0-3.2
Optical
properties
Biaxial
positive
parallel
extinction
Biaxial
positive
parallel
extinction
Biaxial
extinction
inclined
Biaxial
negative
extinction
inclined
Biaxial positive
extinction
parallel
Biaxial
negative
extinction
inclined
Refractive index
1.50-1.55
1.64
1.7
pleochroic
1.61
1.61
1.63 weakly
pleochroic
Flexibility
High
Good
Good
Poor,
generally
brittle
Poor
Poor
Texture
Silky, soft to
harsh
Coarse but
somewhat
pliable
Soft to harsh
Generally
harsh,
sometimes
soft
Harsh
Harsh
Spinnability
Very good
Fair
Fair
Generally
poor, some
are spinnable
Poor
Poor
Tensile strength
(MPa)
550-690
(80,000-
100,000
lb/in2)
110-620
(16,000-
90,000 lb/in2)
690-2100
(100,000-
300,000
lb/in2)
7-60 (1,000-
8,000 lb/in2)
<30
(< 4,000 lb/in2)
<7 (< 1,000
lb/in2)
Fiber size,
median true
diameter (|_im )c
0.06®
0.26
0.09
No data
No data
No data
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('hrysolile
Amosile
Ciocidolilc
. \ six-si i Ibim
Ti'cmolile
. \ six-si i form
Anlhopln Ilik-
Aslx-slilbim
Aclinolilc
Fiber size,
median true
length (|_im)d
U.55
2.53
1.16
No data
No data
No data
Resistance to:
Acids
Weak,
undergoes
fairly rapid
attack
Fair, slowly
attacked
Fair
Fair
Fair
Fair
Bases
Very good
Good
Good
Good
Very good
Fair
Zeta potential
(mV)d
+13.6 to+54
-20 to -40
-32
No data
No data
No data
Decomposition
temperature (°C)
600-850
600-900
400-900
950-1,040
No data
No data
aBadollet (1951)
b Addison et a I. (.1.966)
0 Hwang (1.983)
d Virta (20.1.1)
e The reported values for diameter and length are median values. As reported in Virta (20.1.1). "Industrial chrysotile fibers
are aggregates.. .that usually exhibit diameters from 0.1 to lOOjun: their lengths range from a fraction of a millimeter to
several centimeters, although most chrysotile fibers used are < 1 cm."
1.2 Uses and Production Volume
The only form of asbestos manufactured (including imported), processed, or distributed for use in the
United States today is chrysotile. The United States Geological Survey (USGS) estimated that 750
metric tons of raw chrysotile asbestos were imported into the U.S. in 2018 (USGS. 2019). This raw
asbestos is used exclusively by the chlor-alkali industry and imported amounts tend to range between
300 and 800 metric tons during a given year (USGS. 2019).
In addition to the use of raw imported chrysotile asbestos by the chlor-alkali industry, EPA is also aware
of imported asbestos-containing products; however, the import volumes of those products are not fully
known. The asbestos-containing products that EPA has identified as being imported and used are sheet
gaskets, brake blocks, aftermarket automotive brakes/linings, other vehicle friction products, and other
gaskets. More information about the uses of asbestos and EPA's methodology for identifying COUs is
provided in Section 1.4.1 of this document. EPA will consider legacy uses and associated disposal in
subsequent supplemental documents.
1.3 Regulatory and Assessment History
EPA conducted a search of existing domestic and international laws, regulations and assessments
pertaining to asbestos. EPA compiled this summary from data available from federal, state, international
and other government sources, as cited in 7Appendix A. EPA evaluated and considered the impact of at
least some of these existing laws and regulations to determine what, if any further analysis might be
necessary as part of the risk evaluation. Consideration of the nexus between these regulations and the
TSCA COU evaluated in this risk evaluation were developed and described in the PF document.
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Federal Laws and Regulations
Asbestos is subject to federal statutes or regulations, other than TSCA, that are implemented by other
offices within EPA and/or other federal agencies/departments. A summary of federal laws, regulations
and implementing authorities is provided in Appendix A.l.
State Laws and Regulations
Asbestos is subject to statutes or regulations implemented by state agencies or departments. A summary
of state laws, regulations and implementing authorities is provided in Appendix A.2.
Laws and Regulations in Other Countries and International Treaties or Agreements
Asbestos is subject to statutes or regulations in countries other than the United States and/or
international treaties and/or agreements. A summary of these laws, regulations, treaties and/or
agreements is provided in Appendix A.3.
Table 1-2. Assessment History of Asbestos provides assessments related to asbestos conducted by other
EPA Programs and other organizations. Depending on the source, these assessments may include
information on COU, hazards, exposures and potentially exposed or susceptible subpopulations.
Table 1-2. Assessment History of Asbestos
Authoring Organization
Assessment
EPA assessments
EPA, Integrated Risk Information System (IRIS)
IRIS Assessment on Asbestos (1988b)
EPA, Integrated Risk Information System (IRIS)
IRIS Assessment on Libbv Amphibole Asbestos
(2014c)
EPA, Region 8
Site-Wide Baseline Ecological Risk Assessment
Libbv Asbestos Suoerfund Site. Libbv Montana
( )
EPA, Drinking Water Criteria Document
\ S I-'!1 \ <"!] inking Water Criteria Document for
Asbestos (1985)
EPA, Ambient Water Quality Criteria for Asbestos
Asbestos: Ambient Water Oualitv Criteria (1980)
EPA, Final Rule (40 CFR Part 763)
Asbestos; Manufacture. Importation. Processing
and Distribution in Commerce Prohibitions (1989)
EPA, Asbestos Modeling Study
Final Report; Asbestos Modeling Study (U.S.
EPA. 1988a)
EPA, Asbestos Exposure Assessment
Revised Report to support 988)
EPA, Nonoccupational Exposure Report
Revised Draft Report, Nonoccupational Asbestos
Exposure (Vers 7)
EPA, Airborne Asbestos Health Assessment
Update
Support document for NESHAP review (1986)
Other U.S.-based organizations
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Authoring Organization
Assessment
National Institute for Occupational Safety and
Health (NIOSH)
Asbestos Fibers and Other Elongate Mineral
Particles: State of the Science and Roadmat) for
Research (2 )
Agency for Toxic Substances and Disease Registry
(AT SDR)
Toxicologieal Profile for Asbestos (2001a)
National Toxicology Program (NTP)
Report on Carcinogens. Fourteenth. Edition (2016)
CA Office of Environmental Health Hazard
Assessment (OEHHA), Pesticide and
Environmental Toxicology Section
Public Health Goal for Asbestos in Drinking
Water (2003)
International
International Agency for Research on Cancer
(IARC)
IARC Monographs on the Evaluation of
Carcinogenic Risks to Human nic. Metals.
Fibres, and Dusts. Asbestos (Chrvsotile. Amosite.
Crocidolite. Tremolite. Actinolite. and
Anthoohvllite) (2012)
World Health Organization (WHO)
World Health Organization (WHO) Chrvsotile
Asbestos (2014)
1.4 Scope of the Evaluation
1.4.1 Refinement of Asbestos Fiber Type Considered in this Risk Evaluation
During risk evaluation, EPA determined that the only form of asbestos manufactured (including
imported), processed, or distributed for use in the United States today is chrysotile. The other five forms
of asbestos are no longer manufactured, imported, or processed in the United States and are now subject
to a significant new use rule (SNUR) that requires notification of and review by the Agency should any
person wish to pursue manufacturing, importing, or processing crocidolite (riebeckite), amosite
(cummingtonite-grunerite), anthophyllite, tremolite or actinolite (either in raw form or as part of articles)
for any use (40 CFR 721.11095). Therefore, under the final asbestos SNUR, EPA will be made aware of
manufacturing, importing, or processing for any intended use of the other forms of asbestos. If EPA
finds upon review of the Significant New Use Notice (SNUN) that the significant new use presents or
may present an unreasonable risk (or if there is insufficient information to permit a reasoned evaluation
of the health and environmental effects of the significant new use), then EPA would take action under
TSCA section 5(e) or (f) to the extent necessary to protect against unreasonable risk.
Data from USGS indicates that the asbestos being imported for chlor-alkali plants is all chrysotile. Virta
(2006) notes that when South Africa closed its amosite and crocidolite mines (in 1992 and 1997
respectively), worldwide production of amosite and crocidolite ceased. Virta (2006) concluded that
almost all of the world's production of asbestos is chrysotile and that "[sjmall amounts, probably less
than a few thousand tons, of actinolite, anthophyllite, and tremolite asbestos are produced for local use
in countries such as India, Pakistan, and Turkey."
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Chrysotile is the prevailing form of asbestos currently mined worldwide, therefore, commercially
available products fabricated overseas are made with chrysotile. Any asbestos being imported into the
U.S. in articles for the COUs EPA has identified is believed to be chrysotile. Based on EPA's
determination that chrysotile is the only form of asbestos imported into the U.S. as both raw form and as
contained in articles, EPA is performing a quantitative evaluation for chrysotile asbestos only in this risk
evaluation. EPA will consider legacy uses and associated disposal in subsequent supplemental
documents.
1.4.2 Refinement of Evaluation of Releases to Surface Water
EPA did not evaluate the risk to aquatic species from exposure to surface water in its PF. During the PF
phase of the Risk Evaluation, EPA was still in the process of identifying potential asbestos water
releases for the TSCA COUs. After the PF was released, EPA continued to search EPA databases as
well as the literature and attempted to contact industries to shed light on potential releases to water. The
available information indicated that there were surface water releases of asbestos; however, not all
releases are subject to reporting (e.g., effluent guidelines) or are applicable (e.g., friability). Based on the
reasonably available information in the published literature, provided by industries using asbestos, and
reported in EPA databases, there is minimal or no releases of asbestos to surface water associated with
the COUs that EPA is evaluating in this risk evaluation (see Appendix D).
1.4.3 Conditions of Use Included in the Risk Evaluation
TSCA § 3(4) defines the COU as "the circumstances, as determined by the Administrator, under which
a chemical substance is intended, known, or reasonably foreseen to be manufactured, processed,
distributed in commerce, used, or disposed of." Throughout the scoping ( ), PF (2018d), and risk
evaluation stages, EPA identified and verified the uses of asbestos.
To determine the COU of asbestos and inversely, activities that do not qualify as COU, EPA conducted
extensive research and outreach. This included EPA's review of published literature and online
databases including the most recent data available from EPA's Chemical Data Reporting program
(CDR), Safety Data Sheets (SDSs), the U.S. Geological Survey's Mineral Commodities Summary and
Minerals Yearbook, the U.S. International Trade Commission's DataWeb and government and
commercial trade databases. EPA also reviewed company websites of potential manufacturers,
importers, distributors, retailers, or other users of asbestos. EPA also received comments on the Scope of
the Risk Evaluation for Asbestos (EPA-HQ-OPPT-2016-0736-0086, 2017c ) that were used to inform
the COU. In addition, prior to the June 2017 publication of the scope document, EPA convened
meetings with companies, industry groups, chemical users, and other stakeholders to aid in identifying
COU and verifying COU identified by EPA.
EPA has removed from the risk evaluation any activities that EPA has concluded do not constitute COU
- for example, because EPA has insufficient information to find certain activities are circumstances
under which the chemical is actually "intended, known, or reasonably foreseen to be manufactured,
processed, distributed in commerce, used or disposed of."
Since the PF document was published in June 2018 (U.S. EPA. 2018d\ EPA has further refined the
COU of asbestos for risk evaluation. The activities that EPA has determined are not COU in this
document are packings, woven products, and cement products. Asbestos "packings" are listed under a
broader category of "gaskets, packings, and seals" and more detailed data revealed that only imported
gaskets, not packings, contain asbestos. EPA concluded that "woven and knitted fabrics," which are
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reported in USGS's 2016 Minerals Yearbook under Harmonized Tariff Schedule (HTS) code
6812.99.0004 are misreported (see Appendix C for further explanation). Upon further review, EPA
determined that woven products are not a COU but are precursors to asbestos-containing products or
physical attributes of the asbestos. EPA contacted potential foreign exporters of asbestos woven
products and asbestos cement products, and these foreign companies informed EPA that they do not
have customers in the United States ( 2018b. c). The Agency has not found any evidence to
suggest that woven products (other than those that are already covered under a distinct COU such as
brake blocks used in draw works) or cement products imported into the United States contain asbestos.
Furthermore, EPA discussed the use of asbestos in cement pipe with a trade organization, who indicated
that domestic production, importation, or distribution for such a use is neither known to be currently
ongoing nor foreseeable (A.WWA. 2019). Based on outreach activity and lack of evidence, EPA does
not believe asbestos packings, asbestos woven products (that are not already covered under a separate
and ongoing COU), or asbestos cement products are COU of asbestos in the United States, and
therefore, packings, woven products, and cement products are no longer under consideration for this risk
evaluation and are now subject to the asbestos SNUR under TSCA section 5. Table 1-3. represents the
activities that have been removed from the scope of the risk evaluation since the PF document was
published in June 2018. EPA will consider legacy uses and associated disposal in subsequent
supplemental documents.
Table 1-3. Categories Determined Not to be Conditions of Use After Problem Formulation
Product Category
Kxamplc
Asbestos Cement Products
Cement pipe
Asbestos Woven Products
Imported Textiles
Asbestos Packings
Dynamic or mechanical seals
EPA has verified that U.S. automotive manufacturers are not installing asbestos brakes on new cars for
domestic distribution or use. Therefore, this use will only be evaluated in occupational settings for one
use that EPA identified for cars that are manufactured with asbestos-containing brakes in the U.S. but
are exported and not sold in the U.S. However, removing and installing asbestos brakes in older vehicles
by both professional mechanics and DIY consumers will be evaluated (see Table 1-4. below). The only
use that was identified for the "other gaskets" category was for a specific utility vehicle (UTV) that has
an asbestos-containing gasket in its exhaust system.
Based on the above discussion, the COUs that are included in this risk evaluation are described in Table
1-4.
The life cycle diagram is presented in Figure 1-1.
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Table 1-4. Categories of Conditions of Use Included in this Risk Evaluation
Product Category
r.xamplc
Asbestos Diaphragms
Chlor-alkali Industry
Sheet Gaskets
Chemical Production
Oilfield Brake Blocks
Oil Industry
Aftermarket Automotive Brakes/Linings
Foreign aftermarket brakes sold online
Other Vehicle Friction Products
Brakes installed in exported cars
Other Gaskets
Utility Vehicles
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PROCESSING	INDUSTRIAL, COMMERCIAL, CONSUMER USES
RELEASES and WASTE DISPOSAL
Manufacture
(Non-U S Mining) -
fpo"1 Sa'.v	s;
75 J! letr c Tons
\ZC QU£€Sj
Import (Contained
within Imported
Products)
Asbestos-Containing
Diaphragms
(Chloralkali Industry)
Use 75C Mrtr c Tons
(IS s'-tesi
Asbestos-Containing
Diaphragms
Oilfield Brake Blocks
Aftermarket Auto Brakes/
Linings
Other Gasket*
Other Vehicle Friction
Products
Asbestos Sheets
(Stamping/Cutting)
Asbestos-Containing Sheet
Gaskets
Emissions to Air
Wastewater
Liquid Wastes
Solid Wastes
See ftppendix D for Environmental
Releases and Wastes
Az The level of detail if tie Me tyc^e diagram,
trier* is 10 a-stinciion Between
jnOv stnaiVterv lerwti,- cois-jmer uses. The
conceptual mece>s "naketnisQiffereni'atsoa
1449
1450	Figure 1-1. Asbestos Life Cycle Diagram
1451	The life cycle diagram depicts the COUs that have been assessed in this risk evaluation. It has been updated to reflect the removal from the PF
1452	of woven products, cement products, and packing (see Section 1.4.3) as well as using the 2018 import volume of raw asbestos.
1453
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1454	1.4.4 Conceptual Models
1455	The conceptual models have been modified to reflect the refined COUs of asbestos described in Section
1456	1.4.1. Figure 1-2. and Figure 1-3 present the conceptual models for industrial and commercial uses and
1457	consumer uses, respectively. The asbestos conceptual model for environmental releases and wastes from
1458	the refined COUs was removed and is discussed in Releases and Exposure to the Environment
1459	Supplementary Information Appendix D since it is not being considered in the RE. This was discussed
1460	in the Introduction and further discussed in Section 1.4.3.
1461
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1462
1463
INDUSTRIAL AMD COMMERCIAL
ACTIVITIES/USES
EXPOSURE PATHWAY
EXPOSURE ROUTE
RECEPTORS8
HAZARDS
0° * e'd brake tj.ccks
Afte-r'Si i--ef veh c e
Biases•! n igs
Othe< Vsh v- e c'
P'OflUC^S
Occupations
t*~ i Useti.
Outdoor/indoor Air
Wastt-larch' ng
"reamw and D.sposai
Asbestos Lcr?t3"'"> n«
D apl' regrv-s
Hazards PotentiaMy Aswxteted with
Asbestos Exposure
See Section 3.2
:rs tc 'A a^tsi ais*
lOu*o »va,te
1464
1465	Figure 1-2. Asbestos Conceptual Model for Industrial and Commercial Activities and Uses: Potential Exposures and Hazards
1466	The conceptual model presents the exposure pathways, exposure routes and hazards to human receptors from industrial and commercial
1467	activities and uses of asbestos.
1468	a Receptors include PESS.
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EXPOSURE PATHWAY6	EXPOSURE ROUTE	RECEPTORS
HAZARDS
Consumers,
Bystanders
Indoor/Outdoor Air
Censure Hand- ngof
D.spesa and Waste
Hazards -or^nt af-v Associated with
Asbestos £\posu-fr
5ee Sect on 5 I
1469
1470	Figure 1-3. Asbestos Conceptual Model for Consumer Activities and Uses: Potential Exposures and Hazards
1471	aWoven products were removed from this model after the PF was published. Upon further review, EPA determined that woven products are
1472	not a COU but are precursors to asbestos-containing products or physical attributes of the asbestos. Utility vehicle gaskets were added during
1473	RE.
1474	bProducts may be used during indoor and outdoor activities.
1475	cReceptors include PES S.
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1.5 Systematic Review
TSCA requires EPA to use scientific information, technical procedures, measures, methods, protocols,
methodologies and models consistent with the best available science and base decisions under Section 6
on the weight of scientific evidence. Within the TSCA risk evaluation context, the weight of the
scientific evidence is defined as "a systematic review method, applied in a manner suited to the nature of
the evidence or decision, that uses a pre-established protocol to comprehensively, objectively,
transparently, and consistently identify and evaluate each stream of evidence, including strengths,
limitations, and relevance of each study and to integrate evidence as necessary and appropriate based
upon strengths, limitations, and relevance" (40 C.F.R. 702.33).
To meet the TSCA science standards, EPA used the TSCA systematic review process described in the
Application of Systematic Review in TSCA Risk Evaluations document (U.S. EPA. 2018a). The process
complements the risk evaluation process in that the data collection, data evaluation and data integration
stages of the systematic review process are used to develop the exposure and hazard assessments based
on reasonably available information. EPA defines "reasonably available information" to mean
information that EPA possesses, or can reasonably obtain and synthesize for use in risk evaluations,
considering the deadlines for completing the evaluation (40 CFR 702.33).
EPA is implementing systematic review methods and approaches within the regulatory context of the
amended TSCA. Although EPA will make an effort to adopt as many best practices as practicable from
the systematic review community, EPA expects modifications to the process to ensure that the
identification, screening, evaluation and integration of data and information can support timely
regulatory decision making under the aggressive timelines of the statute.
1.5.1 Data and Information Collection
EPA planned and conducted a comprehensive literature search based on key words related to the
different discipline-specific evidence supporting this risk evaluation (e.g., environmental fate and
transport; engineering releases and occupational exposure; exposure to general population, consumers
and environmental exposure, and environmental and human health hazard). EPA then developed and
applied inclusion and exclusion criteria during the title and abstract screening to identify information
potentially relevant for the risk evaluation process. The literature and screening strategy as specifically
applied to asbestos is described in the Strategy for Conducting Literature Searches for Asbestos:
Supplemental Document to the TSCA Scope Document (EP A.-H.Q-OPPT-2016-0736). and the results of
the title and abstract screening process were published in the Asbestos (CASRN1332-21-4)
Bibliography: Supplemental File for the TSCA Scope Document, EP A-HQ-OPPT-2016-0736) ("US.
EPA. 2017b).
For studies determined to be on-topic (or relevant) after title and abstract screening, EPA conducted a
full text screening to further exclude references that were not relevant to the risk evaluation. Screening
decisions were made based on eligibility criteria documented in the form of the populations, exposures,
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comparators, and outcomes (PECO) framework or a modified framework.5 Data sources that met the
criteria were carried forward to the data evaluation stage. The inclusion and exclusion criteria for full
text screening for asbestos are available in Appendix D of the Problem Formulation of the Risk
Evaluation for Asbestos (U.S. EPA. 2018d).
Although EPA conducted a comprehensive search and screening process as described above, EPA made
the decision to leverage the literature published in previous assessments6 when identifying relevant key
and supporting data7 and information for developing the asbestos risk evaluation. This is discussed in the
Strategy for Conducting literature Searches for Asbestos: Supplemental Document to the JSC-A Scope
Document (EPA-HQ-Q 56). In general, many of the key and supporting data sources were
identified in the comprehensive Asbestos Bibliography: Supplemental File for the TSCA Scope
Document (U.S. EPA. 2017a. b). However, there were instances during the releases and occupational
exposure data search for which EPA missed relevant references that were not captured in the initial
categorization of the on-topic references. EPA found additional relevant data and information using
backward reference searching, which is a technique that will be included in future search strategies. This
issue is discussed in Section 4 of the Application of Systematic Review for TSCA Risk Evaluations (U.S.
EPA. 2018a). Other relevant key and supporting references were identified through targeted
supplemental searches to support the analytical approaches and methods in the asbestos risk evaluation
(e.g., to locate specific information for exposure modeling) or to identify new data and information
published after the date limits of the initial search.
EPA used previous chemical assessments to quickly identify relevant key and supporting information as
a pragmatic approach to expedite the quality evaluation of the data sources, but many of those data
sources were already captured in the comprehensive literature search as explained above. EPA also
considered newer information on asbestos not taken into account by previous EPA chemical assessments
as described in the Strategy for Conducting Literature Searches for Asbestos: Supplemental Document
to the TSCA Scope Document (EPA-I- ). EPA then evaluated the relevance and
quality of the key and supporting data sources, as well as newer information, instead of reviewing all the
underlying published information on asbestos. A comprehensive evaluation of all of the data and
information ever published for a substance such as asbestos would be extremely labor intensive and
could not be achieved considering the deadlines specified in TSCA Section 6(b)(4)(G) for conducting
risk evaluations.
This pragmatic approach allowed EPA to maximize the scientific and analytical efforts of other
regulatory and non-regulatory agencies by accepting, for the most part, the relevant scientific knowledge
gathered and analyzed by others except for influential information sources that may have an impact on
the weight of the scientific evidence and ultimately the risk findings. The influential information (i.e.,
key/supporting) came from a smaller pool of sources subject to the rigor of the TSCA systematic review
5 A PESO statement was used during the full text screening of environmental fate and transport data sources. PESO stands for
Pathways and Processes, Exposure, Setting or Scenario, and Outcomes. A RESO statement was used during the full text
screening of the engineering and occupational exposure literature. RESO stands for Receptors, Exposure, Setting or
Scenario, and Outcomes.
6 Examples of existing assessments are EPA's chemical assessments (e.g., previous work plan risk assessments, problem
formulation documents), ATSDR's Toxicological Profiles, EPA's IRIS assessments and ECHA's dossiers. This is described
in more detail in the Strategy for Conducting Literature Searches for Asbestos: Supplemental File for the TSCA Scope
1 Key and supporting data and information are those that support key analyses, arguments, and/or conclusions in the risk
evaluation.
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process to ensure that the risk evaluation used the best available science and the weight of the scientific
evidence.
Figure 1-4 to Figure 1-8 depict the literature flow diagrams illustrating the results of this process for
each scientific discipline-specific evidence supporting the draft risk evaluation. Each diagram provides
the total number of references at the start of each systematic review stage (i.e., data search, data
screening, data evaluation, data extraction/data integration) and those excluded based on criteria guiding
the screening and data quality evaluation decisions.
EPA bypassed the data screening step for data sources that were highly relevant to the draft risk
evaluation and moved these sources directly to the data quality evaluation step, as described above.
These data sources are depicted as "key/supporting data sources" in the literature flow diagrams. Note
that the number of "key/supporting data sources" were excluded from the total count during the data
screening stage and added, for the most part, to the data evaluation stages depending on the discipline-
specific evidence. The exception was the releases and occupational exposure data sources that were
subject to a combined data extraction and evaluation step as shown in Figure 1-5.
EPA did not have a previous, recent risk assessment of asbestos on which to build; therefore, initially
the Systematic Review included a very large number of papers for all areas. Initially, studies were
limited to those published after 1987, containing at least one of the six fiber types identified under
TSCA. In addition, only observational human studies were searched for the health hazard assessment.
The risk evaluation was further refined to identify studies pertaining to only mesothelioma and lung
cancer as health outcomes, as well as studies containing information specific to chrysotile asbestos only.
As the process for the risk evaluation proceeded, more data became available and the systematic review
was refined. This included exposure and engineering citations, e.g., correspondences with industry,
considered to be on-topic and used to inform the likelihood of exposure. The nature of these documents
is such that the current framework as outlined in the Application of Systematic Review in TSCA Risk
Evaluations ( 18a) is not well suited for the review of these types of references. And as
such, these references, were handled on a case by case basis and are cited in the references section of
this document.
Information for fate assessment for the first 10 chemical risk evaluations considered the physical
chemical properties of the chemical and environmental endpoints. For the first 10 chemicals, EPA
assessed chemical fate as defined by traditional fate endpoints, for example, solubility, partitioning
coefficients, biodegradation and bioaccumulation - properties that do not apply to asbestos minerals. As
such, there were few discipline-specific papers identified in the fate systematic review of asbestos
literature (Figure 1-4).
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Figure 1-4. Key/Supporting Data Sources for Environmental Fate
Note 1: Literature search results for the environmental fate of asbestos yielded 7,698 studies. Of these
studies 7,687 were determined to be off-topic or they did not meet screening criteria (such as non-primary
source data or lacking quantitative fate data). The remaining studies entered full text screening for the
determination of relevance to the risk evaluation. There were three key and/or supporting data sources
identified, the primary literature cited in these sources were passed directly to data evaluation. One
primary study was deemed unacceptable based on the evaluation criteria for fate and transport studies and
the remaining 10 primary studies were carried forward to data extraction/data integration according to
Appendix F in Application of Systematic Review for TSCA Risk Evaluations (U.S. EPA. 2018a'). The data
evaluation and data extraction files are provided in Appendix F in this draft RE.
Note 2: Data sources identified relevant to physical-chemical properties were not included in this
literature flow diagram. The data quality evaluation of physical-chemical properties studies can be found
in the supplemental document, Data Quality Evaluation of Physical-Chemical Properties Studies ("U.S.
EPA., 20190 and the extracted data are presented in Table 1-1.
Data Search Results (n=7,698)
*Key/Supporting
Data Sources (n=3)
Data Screening (n=7,698)
Data Evaluation (n=ll)
Data Extraction/Data Integration (n=10)
Excluded References
(n=7,687)
Excluded: Ref that are
unacceptable based on the
evaluation criteria (n=l)
*These are key and supporting studies from existing assessments (e.g., EPA IRIS assessments, ATSDR assessments, ECHA
dossiers) that were considered highly relevant for the TSCA risk evaluation. These studies bypassed the data screening
step and primary references cited therein were passed directly to the data evaluation step.
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Figure 1-5. Key/Supporting Data Sources for Engineering Releases and Occupational Exposure
Note: Literature search results for environmental release and occupational exposure yielded 10,031 data
sources. Of these data sources, 114 were determined to be relevant for the risk evaluation through the data
screening process. These relevant data sources were entered into the data extraction/evaluation phase. After
data extraction/evaluation, EPA identified several data gaps and performed a supplemental, targeted search
to fill these gaps (e.g., to locate information needed for exposure modeling). The supplemental search
yielded six relevant data sources that bypassed the data screening step and were evaluated and extracted in
accordance with Appendix D in Application of Systematic Review for TSCA Risk Evaluations (U.S. EPA.
2018a). Of the 120 sources from which data were extracted and evaluated, 39 sources only contained data
that were rated as unacceptable based on serious flaws detected during the evaluation. Of the 81 sources
forwarded for data integration, data from 42 sources were integrated, and 39 sources contained data that
were not integrated (e.g., lower quality data that were not needed due to the existence of higher quality data,
data for release media that were removed from scope after data collection). The data evaluation and data
extraction files are provided as separate files (See Appendix B in this draft RE).
n=114
Data Extraction/Date Evaluation (n-120)
Excluded References (n=9,S17)
Data Seatch Results m-10,O31i
Excluded: Ret that are
unacceptable based on
evaluation criteria (n=39)
Data Integration {n=42)
Data Screening (n-10,031)
"The quality of data in these sources {n=39J were acceptable for risk assessment purposes, but they we-re ultimately
excluded from further consideration based* on EPft's integration approach for environmental release and occupational
exposure datafinformafion. EPA's approach uses a hierarchy of preferences that §uicie decisions about what types of
ctata/information are included for further analysis, synthesis and integration into the environmental release and
occupational exposure assessments. EPA prefers using data with tie highest rated quality among those in the higher
level of the hierarchy of preferences (i.e., data> modeling > occupational exposure limits or release limits). If warranted.
EPA may use data/information of lower rated quality as supportive evidence in the environmental release and
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Figure 1-6. Key/Supporting Data Sources for Consumer and Environmental Exposure
Note: Literature search results for consumer and environmental exposure yielded 1,509 data sources. Of
these data sources, 84 made it through data screening and into data evaluation. These data sources were
then evaluated based on a set of metrics to determine overall relevancy and quality of each data source.
The data evaluation stage excluded an additional 56 data sources based on unacceptability under data
evaluation criteria (6), not considered a primary source of data, no extractable data, or overall low
relevancy to the COUs evaluated (50). The remaining 28 data sources that made it to data evaluation had
data extracted for use within the risk evaluation. The data evaluation and data extraction files are provided
as separate files (See Appendix B in this draft RE).
Data Search Results
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Figure 1-7. Key /Supporting Data Sources for Environmental Hazard
Note: The environmental hazard data sources were identified through literature searches and screening
strategies using the ECOTOX Standing Operating Procedures. Additional details can be found in the
Strategy for Conducting Literature Searches for Asbestos: Supplemental Document to the TSCA Scope
Document, (EP A-HQ-OPPT-2016-0736"). During PF, EPA made refinements to the conceptual models
resulting in the elimination of the terrestrial exposure pathways. Thus, environmental hazard data sources
on terrestrial organisms were determined to be out of scope and excluded from data quality evaluation.
The data evaluation file is provided as a separate file (See Appendix B in this draft RE).
Key/Supportini
Studies
(n = 0)
Excluded References due to
ECOTOX Criteria
(n =48)
Excluded References due to
ECOTOX Criteria
(n = 2976)
Data Extraction I Data Integration (n « 4)
Data Evaluation (n = 10)
Full Text Screening (n = 58)
Excluded References that are
unacceptable based
on evaluation criteria and/or are
out of scope
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Figure 1-8. Key/Supporting Data Sources for Human Health Hazard
Note: Studies were restricted to only mesothelioma and lung cancer as health outcomes, and further
restricted to studies containing information specific to chrysotile asbestos only. The data evaluation and
data extraction files are provided as separate files (See Appendix B in this draft RE).
jrces
Key/supporting data
sources
(n = 3 data sources)
Excluded References
= 24,012 data sources)
Date Search Results |n = 24,050 data sources)
Excluded: Ref that are
unacceptable based on
evaluation criteria {n = 0 cotiorts)
Data Extraction/Data Integration
{n = 2:6 data sources [7 cohorts])
Data Evaluation
frt = 26 data sources |7 cohorts])
Data Screening
(n = 24,036 data sources)
1.5.2 Data Evaluation
During the data evaluation stage, EPA assessed the quality of the data sources using the evaluation
strategies and criteria described in the Application of Systematic Review in TSCA Risk Evaluations (U.S.
E 18a), For the data sources that passed full-text screening, EPA evaluated their quality and each
data source received an overall confidence of high, medium, low or unacceptable.
For evaluation of human health hazard studies, the quality criteria presented for epidemiologic studies in
the Application of Systematic Review in TSCA Risk Evaluations (U. S jjf 2018a) were tailored to meet
the specific needs of asbestos studies and to determine the studies' potential to provide information on
the exposure-response relationship between asbestos exposure and mortality from lung cancer and from
mesothelioma (Section 3.2.3.1). The results of the data quality evaluations are summarized in the
Supplemental File. Supplemental files (see Appendix B) also provide details of the data evaluations
including individual metric scores and the overall study score for each data source.
1.5.3 Data Integration
Data integration includes analysis, synthesis and integration of information for the risk evaluation.
During data integration, EPA considers quality, consistency, relevancy, coherence and biological
plausibility to make final conclusions regarding the weight of the scientific evidence. As stated in the
Application of Systematic Review in TSCA Risk Evaluations (i__S ,018a). data integration
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involves transparently discussing the significant issues, strengths, and limitations as well as the
uncertainties of the reasonably available information and the major points of interpretation (
2018e) EPA defines "reasonably available information" to mean information that EPA possesses, or can
reasonably obtain and synthesize for use in risk evaluations, considering the deadlines for completing
the evaluation (Procedures for Chemical Risk Evaluation Under the Amended Toxic Substances Control
Act (82 FR 33726)).
EPA used previous assessments (see Table 1-2. Assessment History of Asbestos ) to identify key and
supporting information and then analyzed and synthesized available lines of evidence regarding
asbestos' chemical properties, environmental fate and transport properties, and its potential for exposure
and hazard. EPA's analysis also considered recent data sources that were not considered in the previous
assessments (as explained in Section 1.5.1 of this document), as well as reasonably available
information on potentially exposed or susceptible subpopulations.
2 EXPOSURES
For TSCA exposure assessments, EPA evaluated exposures and releases to the environment resulting
from the conditions of use applicable to asbestos. Post-release pathways and routes were described to
characterize the relationship or connection between the conditions of use for asbestos (Section 1.4.1) and
the exposure to human receptors, including potentially exposed or susceptible subpopulations (PESS)
and ecological receptors. EPA considered, where relevant, the duration, intensity (concentration),
frequency and number of exposures in characterizing exposures to asbestos.
2.1 Fate and Transport
Asbestos is a persistent mineral fiber that can be found in soils, sediments, lofted in air and windblown
dust, surface water, ground water and biota (ATSDR. 2< ). Asbestos fibers are largely chemically and
biologically inert in the environment. They may undergo minor physical changes, such as changes in
fiber length or leaching of surface minerals, but do not react or dissolve in most environmental
conditions (Favero-Longo et ai. 2005; Gronow. 1987; Schreier et ai. 1987; Choi and Smith. 1972.).
The reasonably available data/information on the environmental fate of asbestos is found in Appendix F.
Those data are summarized below.
Chrysotile asbestos forms stable suspensions in water; surface minerals may leach into solution, but the
underlying silicate structure remains unchanged at neutral pH (Gronow. 1987; Bales and Morgan. 1985;
Choi and Smith. 1972). Small asbestos fibers (<1 |im) remain suspended in air and water for significant
periods of time and may be transported over long distances (Jaenicke. 1980). Asbestos fibers will
eventually settle to sediments and soil, and movement therein may occur via erosion, runoff or
mechanical resuspension (wind-blown dust, vehicle traffic, etc.) (ATSDR. 2001b).
Limited information is available on the bioconcentration or bioaccumulation of asbestos. Aqueous
exposure to chrysotile asbestos (104-108 fibers/liter) results in embedding of fibers in the tissues of
aquatic organisms (Bel anger et at... 1990; Bel anger et at.. 1986c; Bel anger et at.. 1986a. b). In controlled
laboratory experiments, asbestos had a negligible bioconcentration factor (BCF slightly greater than 1)
(Belanger et at.. 1987). Asbestos is not expected to bioaccumulate in food webs (ATSDR. 2 ).
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Asbestos may be released to the environment through industrial or commercial activities, such as
processing raw asbestos, fabricating/processing asbestos containing products, or the lofting of friable
asbestos during use, disturbance and disposal of asbestos containing products.
2.2 Releases to Water
2.2.1 Water Release Assessment Approach and Methodology
The environmental exposure characterization focuses on aquatic releases of asbestos from facilities that
manufacture, process, or use asbestos under industrial and/or commercial COUs included in this
document. To characterize environmental exposure, EPA assessed point estimate exposures derived
from measured concentrations of asbestos in surface water in the United States. Measured surface water
concentrations were obtained from EPA's Water Quality Exchange (WQX) using the Water Quality
Portal (WQP) tool, which is the nation's largest source of water quality monitoring data and includes
results from EPA's STORage and RETrieval (STORET) Data Warehouse, the United States Geological
Service (USGS) National Water Information System (NWIS), and other federal, state, and tribal sources.
A literature search was also conducted to identify other peer-reviewed or authoritative gray sources of
measured surface water concentrations in the United States, but no data were found.
As discussed in the PF document, because the drinking water exposure pathway for asbestos is currently
addressed in the Safe Drinking Water Act (SDWA) regulatory analytical process for public water
systems, this pathway (drinking water for human health) will not be evaluated in this draft RE. The
Office of Water does not have an ambient water quality criterion for asbestos for aquatic life. Thus,
potential releases from industrial and commercial activities associated with the TSCA COUs included
this document to surface water were considered in this draft RE. However, identifying or estimating
asbestos concentrations in water to evaluate risk to environmental receptors has been challenging.
During the PF phase of the RE, EPA was still in the process of identifying potential asbestos water
releases for the TSCA COUs. After the PF was released, EPA continued to search other sources of data
including TRI data, EPA environmental and compliance monitoring databases, including permits,
industry responses to EPA questions, and other EPA databases. Details of these investigations are
included in Appendix D and summarized below.
TRI reports (Table APX D-2) show that there were zero pounds of friable asbestos reported as released
to water via surface water discharges in 2018. In addition, TRI reports zero pounds of friable asbestos
transferred off-site to publicly owned treatment works (POTWs) or to non-POTW facilities for the
purpose of wastewater treatment. The vast majority of friable asbestos waste management was disposal
to hazardous waste landfills and to non-hazardous waste landfills.
EPA issues Effluent Limitations Guidelines and Pretreatment Standards, which are national regulatory
standards for industrial wastewater discharges to surface waters and POTWs (municipal sewage
treatment plants). EPA issues these guidelines for categories of existing sources and new sources under
Title III of the Clean Water Act (CWA). The standards are technology-based (i.e., they are based on the
performance of treatment and control technologies); they are not based on risk or impacts upon
receiving waters (see Industrial Effluent Guidelines for more information). For most operations covered
by effluent guidelines and standards for the asbestos manufacturing point source category (40 CFR 427),
the discharge of all pollutants is prohibited. For certain asbestos manufacturing operations, the effluent
guidelines establish limits on the allowable levels of total suspended solids (TSS), pH, or chemical
oxygen demand (COD). The regulations do not establish specific limits for asbestos from those
operations where discharges are allowed. Thus, without the requirement to measure asbestos
concentrations in effluent, estimating asbestos levels in effluent or receiving waters is challenging.
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EPA investigated industry sector, facility, operational, and permit information regulated by NPDES
(National Pollutant Discharge Elimination System) under the CWA to identify any permit limits,
monitoring and reporting requirements, and any discharge provisions related to asbestos. The CWA
prohibits point source pollutant discharges into waters of the United States unless specifically authorized
under the Act, for example through a permit under section 402 (by EPA or an authorized state) that
establishes conditions for discharge. Available data were accessed through EPA's Envirofacts and
Enforcement and Compliance History Online (ECHO) systems to identify any evidence of asbestos
discharge pertaining to the COUs being evaluated herein. EPA found that no asbestos discharges
pertaining to the COUs were reported, and no specific asbestos violations were reported. None of the
industrial permits pertaining to the COUs (i.e., chlor-alkali and sheet gasket facilities) had requirements
to monitor asbestos. No violation of TSS standards or pH standards were reported.
EPA reports asbestos levels in drinking water from compliance monitoring data from 1998 through 2011
in two separate six year review cycles (see Table 2-1). However; these data cannot be traced to a
specific COU in this draft risk evaluation. In addition, the data are from public water supplies and most
likely represent samples from finished drinking water (i.e., tap water) or some other representation that
may not reflect the environment in which ecological organisms exist. For these two reasons, these data
may not be relevant in assessing the environmental release pathway.
Table 2-1. EPA OW Six Year Review Cycle Data for Asbestos in Drinking Water, 1998-2011
Re\iew Cycle
Number of Systems
Sampled
Number of Systems with
Detections Minimum
Reporting l.e\el (MRI.of
o 2 Mil.)
Number of Systems with
Detections the MCI. of 7
Mil.
1998-2005
8,278
268 (3.2%)
14 (<0.2%)
2006-2011
5,785
214(3.7%)
8 (<0.1%)
2.2,2 Water Releases Reported by Conditions of Use
2.2.2,1 Processing and Industrial Use of Asbestos Diaphragms in Chlor-alkali
Industry
As noted in the PF, EPA staff visited two separate chlor-alkali facilities in March of 2017 to better
understand how asbestos is used, managed and disposed of. The American Chemistry Council (ACC)
provided a process description of on-site wastewater treatment methods employed by chlor-alkali
facilities to manage and treat wastewater based on their NPDES permits. Some companies in the chlor-
alkali industry are known to collect all used diaphragms, hydroblast the asbestos off the screen on which
the diaphragm is formed, and filter press the asbestos-containing wastewater. This water in these cases is
collected to a sump, agitated, and transferred to a filter press. The filter press contains multiple filter
plates with polypropylene filter elements (8 to 100 |im pore size). After solids separation, the filters are
removed to large sacks for disposal to a landfill that accepts asbestos-containing waste per federal and
state asbestos disposal regulations. The effluent is filtered again and discharged to the facility's
wastewater collection and treatment system (See Attachment B in ACC Submission). Asbestos releases
from chlor-alkali facility treatment systems to surface water and POTWs are not known. While the
treatment technologies employed would be expected to capture asbestos solids, the precise treatment
efficiency is not known. Chlor-alkali facilities are not required to monitor effluents for asbestos releases,
and EPA's broader research into this COU did not find asbestos water release data.
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Another data source considered for asbestos water releases from chlor-alkali facilities was the TRI.
According to the TRI reporting requirements, industrial facilities are required to disclose asbestos waste
management practices and releases only for the portion of asbestos that is friable. TRI reporting is not
required for other forms of asbestos (e.g., non-friable asbestos, asbestos in aqueous solutions) (U.S.
EPA. 2017e). Consistent with this qualification in the TRI reporting requirements, no chlor-alkali
facilities reported asbestos surface water discharges to TRI in reporting year 2018. All chlor-alkali
facilities reported zero surface water discharges and zero off-site transfers for wastewater treatment.
2.2.2.2 Processing Asbestos-Containing Sheet Gaskets
Based on reasonably available process information provided during an EPA site visit, sheet gasket
stamping occurs in a warehouse setting with stamping machines (Branham email(s) and observations
during August 2, 2018 plant visit to Gulfport, MS) (Branham. 2018). The warehouse has no industrial
wastewater or water systems, except for potable uses. Housekeeping practices used in relevant work
areas at the facility EPA visited included a weekly "wipe-down" of equipment (e.g., machine presses,
dies) and workstations (e.g., table tops) with damp rags, which were disposed of with asbestos-
containing gasket scraps. This waste was double bagged, sealed, labeled as asbestos, placed in special
container, and disposed in a landfill permitted to accept asbestos wastes. This company has two sites and
does not report to TRI for friable asbestos and does not have NPDES permits.
EPA attempted to identify other companies that fabricate asbestos-containing sheet gaskets in the United
States but could not locate any. Therefore, it is not known how many sites fabricate imported sheet
gaskets containing asbestos in the United States. If other companies stamp gaskets in the same way that
EPA observed at one facility, it could then be assumed that there will not be water releases. However, it
is not possible to rule out incidental releases of asbestos fibers in wastewater at other fabrication
facilities if different methods are used, but any amounts of release cannot be quantified.
2.2.2.3 Industrial Use of Sheet Gaskets at Chemical Production Plants
Based on reasonably available process information for the titanium dioxide (Ti02) production facility—
the example used in this draft RE for chemical production plants—described by ACC (ACC. 2017b) and
EPA knowledge of the titanium manufacturing process, the purpose of the gasket is to seal equipment
components. The information indicates that after maintenance workers remove a gasket from a flange,
he or she will double-bag and seal the gasket and label the bag "asbestos," and place it in special
containers for disposal in a landfill permitted to accept asbestos wastes. It appears that there are no water
releases during use of asbestos gaskets or disposal, and water is not used as an exposure control method;
therefore, releases to water are not anticipated. However, it is not possible to rule out incidental releases
of asbestos fibers in wastewater at other facilities if different methods are used, but any amounts of
release cannot be quantified.
2.2.2.4 Industrial Use and Disposal of Asbestos-Containing Brake Blocks in Oil
Industry
EPA attempted to evaluate potential water releases of asbestos from use in oil field brake blocks. EPA
found no reasonably available data or publications documenting asbestos releases from the use of oil
field brake blocks to water. The only relevant information obtained was an industry contact's remark
that workers wash down drawworks before removing used brake blocks and installing new ones (Popik.
2.018) - a comment that suggests some asbestos fibers may be released into water during this practice.
The TRI reporting requirements do not apply to the three NAICS codes believed to best represent the
industries that use oil field brake blocks. No other reasonably available data, such as relevant sampling
data, publications, or other quantitative insights were found to inform the release assessment. The
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reasonably available information currently available for this COU is insufficient for deriving water
release estimates.
Regarding solid waste, used brake blocks are replaced when worn down to 0.375-inch thickness at any
point. Because the remaining portions of the used blocks still contain asbestos, they will be handed as
solid waste and are likely handled similarly to used asbestos-containing sheet gaskets: bagged and sent
to landfills permitted to accept asbestos waste. The SDS obtained for asbestos-containing brake blocks
includes waste disposal. It suggests associated waste should be sent to landfills (Stewart & Stevenson.
2000). While these brake blocks are generally considered non-friable when intact, it is unclear if the
asbestos in the used brake blocks is friable or remains non-friable.
2.2.2.5 Commercial Use, Consumer Use, and Disposal of Aftermarket Automotive
Asbestos-Containing Brakes/Linings, Other Vehicle Friction Products, and Other
Asbestos-Containing Gaskets
EPA determined that water releases for aftermarket asbestos-containing automotive parts (brakes,
clutches, gaskets, utility vehicle (UTV) gaskets) do not involve the use of water during the removal and
clean up. EPA has not identified peer-reviewed publications that measure water releases of asbestos
associated with processing, using, or disposing of aftermarket automotive products.
2.2.3 Summary of Water Releases and Exposures
During the PF phase of the RE, EPA was still in the process of identifying potential asbestos water
releases for the TSCA COUs in this document. After the PF was released, EPA continued to search EPA
databases as well as the literature and attempted to contact industries to shed light on potential releases
to water. Very little information was located that indicated that there were surface water releases of
asbestos; however, not all releases are subject to reporting (e.g., effluent guidelines) or are applicable
(e.g., friability). Based on the reasonably available information in the published literature, provided by
industries using asbestos, and reported in EPA databases, there is minmal or no releases of asbestos to
surface water associated with the COUs that EPA is evaluating in this risk evaluation.
2.3 Human Exposures
EPA evaluated both occupational and consumer scenarios for each COU. The following table provides a
description of the COUs and the scenario (occupational or consumer) evaluated in this RE.
Table 2-2. Crosswalk of Conditions of Use and Occupational and Consumer Scenarios Assessed in
the Risk Evaluation
COU
Scenario
Form of asbestos
Diaphragms for Chlor-Alkali
Industry (Processing and Use)
Occupational
Imported raw asbestos (used to fabricate
diaphragms)
Brake Block Use (Use)
Occupational
Imported article
Sheet Gaskets
Stamping (Processing)
Occupational
Imported sheets
Sheet Gaskets
In chemical production (Use)
Occupational
Gaskets imported or purchased in US
Brakes
Installation in exported cars (Use)
Occupational
Imported brakes
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COU
Scenario
Form of asbestos
Brakes
Repair/replacement (Use and
Disposal)
Occupational (repair
shops)
Imported brakes
Brakes
Repair/replacement (Use and
Disposal)
Consumer (DIY)
Imported (Internet purchase)
UTV Gaskets
Manufacture UTV in US (Use
and Disposal)
Occupational
Imported gaskets
UTV Gaskets
Repair/replacement (Use and
Disposal)
Occupational (repair
shops)
Imported gaskets
UTV Gaskets
Repair/replacement (Use and
Disposal)
Consumer (DIY)
Imported gaskets
2.3.1 Occupational Exposures
For the purposes of this assessment, EPA considered occupational exposure of the total workforce of
exposed users and non-users, which include, but are not limited to, male and female workers of
reproductive age who are >16 years of age. This section summarizes the key occupational acute and
chronic inhalation exposure concentrations for asbestos.
EPA only evaluated inhalation exposures to workers and occupational non-users (ONUs) in association
with asbestos manufacturing, import, processing, distribution and use in industrial applications and
products in the Risk Evaluation. The physical condition of asbestos is an important factor when
considering the potential human pathways of exposure. Several of the asbestos-containing products
identified as COUs of asbestos are not friable as intact products; however, non-friable asbestos can be
made friable due to physical and chemical wear and normal use of asbestos-containing products.
Exposures to asbestos can potentially occur via all routes; however, EPA anticipates that the most likely
exposure route is inhalation for workers and ONUs. ONUs do not directly handle asbestos or asbestos-
containing products but are present during their work time in an area where asbestos or an asbestos-
containing product is or may be present.
Where available, EPA used inhalation monitoring data from industry, trade associations, or the public
literature. For each COU, EPA separately evaluates exposures for workers and ONUs. A primary
difference between workers and ONUs is that workers may handle chemical substances and have direct
contact with chemicals, while ONUs are working in the general vicinity but do not handle the chemical
substance. Examples of ONUs include supervisors/managers, and maintenance and janitorial workers
who might access the work area but do not perform tasks directly with asbestos or asbestos containing
products. For inhalation exposure, in cases where no ONU sampling data are available, EPA typically
assumes that ONU inhalation exposure is comparable to area monitoring results that may be available or
assumes that ONU exposure is likely lower than workers.
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Components of the Occupational Exposure Assessment
The occupational exposure assessment of each COU comprises the following components:
• Process Description: A description of the COU, including the role of asbestos in the use;
process vessels, equipment, and tools used during the COU; and descriptions of the worker
activities, including an assessment for potential points of worker exposure.
• Worker Activities: Activities in which workers may be potentially exposed to asbestos.
• Number of Sites and Potentially Exposed Workers: Estimated number of sites that use
asbestos for the given COU; estimated number of workers, including ONUs, who could
potentially be exposed to asbestos for the given COU.
• Occupational Inhalation Exposure Results: EPA used exposure monitoring data provided by
industry, when it was available, to assess occupational inhalation exposures. EPA also
considered worker exposure monitoring data published in the peer-reviewed literature. In all
cases, EPA synthesized the reasonably available information and considered limitations
associated with each data set. Later in this section, EPA reports central tendency and high-end
estimates for exposure distribution derived for workers and for ONUs for each COU and
acknowledges the limitations associated with these exposure estimates.
• Inhalation Exposure Results for Use in the Risk Evaluation: Central tendency and high-end
estimates of inhalation exposure to workers and ONUs.
2,3,1 J Occupational Exposures Approach and Methodology
EPA reviewed reasonably available information from OSHA, NIOSH, the peer-reviewed literature,
industries using asbestos or asbestos-containing products, and trade associations that represent this
industry (e.g., ACC) to identify relevant occupational inhalation exposure data. Quantitative data
obtained during Systematic Review were used to build appropriate exposure scenarios when monitoring
data were not reasonably available to develop exposure estimates. For uses with limited available
exposure data the assessment used similar occupational data and best professional judgment to estimate
exposures. In these cases, EPA used assumptions to evaluate risk.
General Inhalation Exposures Approach and Methodology
EPA provided occupational exposure results for each COU that were representative of central tendency
estimates and high-end estimates when possible. A central tendency estimate was assumed to be
representative of occupational exposures in the center of the distribution for a given COU. EPA's
preference was to use the 50th percentile of the distribution of inhalation exposure data as the central
tendency. In cases where other approaches were used, the text describes the rationale for doing so. EPA
provided high-end estimates at the 95th percentile. If the 95th percentile was not available, or if the full
distribution was not known and the preferred statistics were not available, EPA used a reported
maximum value or other bounding estimate to represent the high-end estimate.
2,3.1.2 Consideration of Engineering Controls and Personal Protective Equipment
OSHA requires employers utilize the hierarchy of controls to address hazardous exposures in the
workplace. The hierarchy of controls prioritizes the most effective measures to address exposure; the
first of which is to eliminate or substitute the harmful chemical (e.g., use a different process, substitute
with a less hazardous material), thereby preventing or reducing exposure potential. Following
elimination and substitution, the hierarchy prioritizes engineering controls to isolate employees from the
hazard, followed by administrative controls, or changes in work practices to reduce exposure potential
(e.g., source enclosure, local exhaust ventilation systems, temperature). Administrative controls are
policies and procedures instituted and overseen by the employer to protect worker exposures. As the last
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means of control, the use of personal protective equipment (PPE) (e.g., respirators, gloves) is required,
when the other control measures cannot reduce workplace exposure to an acceptable level.
Respiratory Protection and OSHA Standards
OSHA has standards that are applicable to occupational exposure to asbestos including the Respiratory
Protection Standard (29 CFR § 1910.134); and the Asbestos Standard (29 CFR § 1910.1001). Both
standards have multiple provisions that are highlighted below.
OSHA's 29 CFR § 1910.134 requires employers to perform a hazard assessment to determine what
hazardous exposures exist, if any, and how to mitigate such exposures. The occupational hazard
assessment is the basis for the implementation of control measures. Certain industries address
workplace hazards by implementing engineering and administrative control measures. When these
measures do not fully mitigate the hazard, respiratory protection may be used. Respirator selection
provisions are provided in § 1910.134(d) and require that appropriate respirators be selected based on
the respiratory hazard(s) to which the worker will be exposed and workplace and user factors that affect
respirator performance and reliability. Assigned protection factors (APFs) are provided in Table 1 under
§ 1910.134(d)(3)(i)(A) (see below in Table 2-3.). APFs refer to the level of respiratory protection that a
respirator or class of respirators is expected to provide to employees when the employer implements a
continuing, effective respiratory protection program.
Table 2-3. Assigned Protection Factors for Respirators in OSHA Standard 29 CFR 1910.134eg
Type of Uespiralor1-h
Quarter
Mask
Half Mask
lull
Kacepiece
Helmet/
Mood
Loose-filling
I'acepiece
1. Air-Purifying Respirator
5
10 c
50

2. Powered Air-Purifying
Respirator (PAPR)

50
1,000
25/1,000 d
25
3. Supplied-Air Respirator (SAR) or Airline Respirator
• Demand mode

10f
50

• Continuous flow mode

50 f
1,000
25/1,000 d
25
• Pressure-demand or other
positive-pressure mode

50 f
1,000

4. Self-Contained Breathing Apparatus (SCBA)
• Demand mode

10f
50
50

• Pressure-demand or other
positive-pressure mode (e.g.,
open/closed circuit)

10,000
10,000

a Employers may select respirators assigned for use in higher workplace concentrations of a hazardous substance for use at
lower concentrations of that substance, or when required respirator use is independent of concentration.
b The assigned protection factors are only effective when the employer implements a continuing, effective respirator program
as required by 29 CFR § 1910.134, including training, fit testing, maintenance, and use requirements.
0 This APF category includes filtering facepieces and half masks with elastomeric facepieces.
dThe employer must have evidence provided by the respirator manufacturer that testing of these respirators demonstrates
performance at a level of protection of 1,000 or greater to receive an APF of 1,000. This level of performance can best be
demonstrated by performing a workplace protection factor (WPF) or simulated workplace protection factor (SWPF) study or
equivalent testing. Absent such testing, all other PAPRs and SARs with helmets/hoods are to be treated as loose-fitting
facepiece respirators and receive an APF of 25.
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e These APFs do not apply to respirators used solely for escape. For escape respirators used in association with specific
substances covered by 29 CFR § 1910 subpart Z, employers must refer to the appropriate substance-specific standards in that
subpart. Escape respirators for other IDLH atmospheres are specified by 29 CFR § 1910.134(d)(2)(ii).
f These respirators are not common.
g Respirators with bolded APFs satisfy the OSHA requirements for asbestos and an appropriate respirator should be selected
based on the air concentration. Filtering facepiece respirators do not satisfy OSHA requirements for protection against
asbestos fiber.
OSHA's 29 CFR § 1910.1001 (g)(2)(ii), however, is specific to asbestos and states that employers must -
when the employee chooses to use a powered air-purifying respirator (PAPR), and it provides adequate
protection to the employee - provide an employee with a tight-fitting PAPR instead of a negative
pressure respirator selected according to § 1910.1001(g)(3). In addition, OSHA 1910.1001(g)(3) states
that employers must not select or use filtering facepiece respirators for protection against asbestos fibers.
Therefore, filtering facepieces (N95), quarter masks, helmets, hoods, and loose fitting facepieces should
not be used. OSHA's 29 CFR § 1910.1001(g)(3)(ii) also indicates that high-efficiency particulate air
(HEPA) filters for PAPR and non-powered air-purifying respirators should be provided.
APFs are intended to guide the selection of an appropriate class of respirators to protect workers after a
substance is determined to be hazardous, after an occupational exposure limit is established, and only
when the occupational exposure limit is exceeded after feasible engineering, work practice, and
administrative controls have been put in place. For asbestos, the employee permissible exposure limit
(PEL) is O.lfibers per cubic centimeter (f/cc) as an 8-hour, time-weighted average (TWA) and/or the
excursion limit of l.Of/cc averaged over a sampling period of 30 minutes.
Using the OSHA PEL for asbestos of 0.1 f/cc, a half-mask negative pressure HEPA filtered facepiece
(when fitted properly) can provide protection in atmospheres with up to 1.0 f/cc [0.1 f/cc multiplied by
the APF of 10],
Only the respirator types and corresponding APFs bolded in Table 2-3. meet the OSHA requirements
for asbestos. The specific respiratory protection required in any situation is selected based on air
monitoring data. OSHA specifies that the Maximum Use Concentration (MUC) be calculated to assess
respirator selection. The MUC is the maximum amount of asbestos that a respirator can handle from
which an employee can be expected to be protected when wearing a respirator. The APF of the
respirator or class of respirators is the amount of protection that it provides the worker compared to not
wearing a respirator. The permissible exposure limit for asbestos (0.1 f/cc) sets the threshold for
respirator requirements. The MUC can be determined mathematically by multiplying the APF specified
for a respirator by the OSHA PEL, short-term exposure limit, or ceiling limit.
The APFs are not assumed to be interchangeable for any COU, any workplace, or any worker. The use
of a respirator would not necessarily resolve inhalation exposures since it cannot be assumed that
employers implement comprehensive respiratory protection programs for their employees. Table 2-3.
can be used as a guide to show the protectiveness of each category of respirator. Based on the APFs
specifically identified for asbestos and presented in Table 2-3, inhalation exposures may be reduced by a
factor of 10 to 10,000 assuming employers institute a comprehensive respiratory protection program.
However, for asbestos, nominal APFs in Table 2-3 may not be achieved for all PPE users (Riala and
Riipinen. 1998). investigated performance of respirators and HEPA units in 21 different exposure
abatement scenarios; most involved very high exposures not consistent with COUs identified in this RE.
However, for three abatement scenarios, exposure concentrations were below 1 f/cc, which is relevant to
the COUs in this draft risk evaluation. In the three scenarios, actual APFs were reported as 50, 5, and 4.
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The strength of this publication is the reporting of asbestos samples inside the mask, use of worker's
own protection equipment, and measurement in different real work conditions. The results demonstrate
that while some workers have protection above nominal APF, some workers have protection below
nominal APF, so even with every worker wearing respirator, some of these workers would not be
protected.
2.3X3 Chlor-Alkali Industry
This section reviews the presence of chrysotile asbestos in semi-permeable diaphragms used in the
chlor-alkali industry and evaluates the potential for worker exposure to asbestos.
2.3.1.3.1 Process Description - Asbestos Diaphragms
Asbestos (raw chrysotile) is used in the chlor-alkali industry for the fabrication of semi-permeable
diaphragms, which are used in the production of chlorine and sodium hydroxide (caustic soda). The
incorporation of asbestos is vital because it is chemically inert and able to effectively separate the anode
and cathode chemicals in electrolytic cells (USGS, 2017). Figure 2-1. below shows a typical diaphragm
after it has been formed.
Figure 2-1. Closeup of a Chrysotile Diaphragm Outside of the Electrolytic Cell
Photograph courtesy of the American Chemistry Council
Chlor-alkali industry representatives have stated that three companies own a total of 15 chlor-alkali
facilities in the United States that use asbestos-containing semi-permeable diaphragms onsite. Some of
these facilities fabricate diaphragms onsite from asbestos, and other facilities receive fabricated
diaphragms from other chlor-alkali facilities and send them back when the diaphragms reach the end of
service life. EPA does not expect exposures to occur when handling fabricated diaphragms. Based on
information provided by ACC, the management of asbestos in the chlor-alkali industry is performed in a
closely controlled process from its entry into a port in the United States through all subsequent uses.
ACC reports that engineering controls, PPE, employee training, medical surveillance, and personal
monitoring are all used to monitor and mitigate worker exposures (ACC submission, see Enclosure C).
The remainder of this section is based on a description of the chlor-alkali diaphragm manufacturing
process and associated asbestos controls. ACC provided this information to EPA, and it is included in
the docket fACC Submission). Unless otherwise specified, all process details presented in the following
paragraphs are based on this docket submission. In addition, in 2017 EPA engineers conducted site visits
to two chlor-alkali facilities. During these site visits, the observations by EPA engineers' confirmed
details of the process descriptions provided by industry and described below. Other citations are
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included in the following paragraphs only for specific details not covered in the main docket reference
(EP A-HO-OPPT-2016-0763-0052Y
After arriving at the plant, the shipping container with raw asbestos is inspected, and any damaged
containers are shipped back to the sender. Port and warehouse workers manage and remediate any
damaged containers in conformance with OSHA's asbestos standard for general industry, which
includes requirements for PPE and respiratory protection (as described above in Section 2.3.1.2).
Asbestos within the containers is sealed in bags, and workers' first task after opening the containers is to
inspect bags for leaks. If bags are broken or loose asbestos is evident, the area is controlled to prevent
accidental exposure, the bags are repaired, and the location is barricaded and treated as an area requiring
cleanup; workers involved in this activity wear PPE and use respiratory protection, per requirements in
OSHA's asbestos standard. Plastic-wrapped pallets are labeled per OSHA's hazard communication and
asbestos standards. Any loose asbestos from punctured bags inside the container is collected using
HEPA-filtered vacuum cleaners or wetted with water and cleaned up before unloading can proceed.
Damaged bags are repaired or placed in appropriately labeled, heavy-duty plastic bags. Workers not
involved in cleanup are prohibited from entering the area until cleanup is complete. When moving the
asbestos bags into storage locations, care is taken to ensure that bags are not punctured, and personnel
moving the bags wear specific PPE, including respirators. Storage areas are isolated, enclosed, labeled,
secured and routinely inspected. Any area or surface with evidence of asbestos is cleaned by a HEPA-
filtered vacuum or wetted and cleaned up by trained employees wearing PPE.
To create asbestos-containing diaphragm cells, sealed bags of asbestos are opened, and the asbestos is
transferred to a mixing tank. At some plants, this process is fully automated and enclosed, in which the
sealed bags of asbestos are placed on a belt conveyor. The conveyor transfers the sealed bag to an
enclosure above a mixing vessel. Mechanical knives cut open the bag, and the asbestos and bag
remnants fall via a chute into the mixing vessel. In other cases, opening of the sealed bags takes place in
glove boxes. Empty bags are placed into closed and labeled waste containers, either through a port in the
glove box or during the automated process. The glove boxes are sealed containers with gloves built into
the side walls, which allow workers to manipulate objects inside while preventing any exposure from
occurring. Glove boxes also allow workers to open sealed bags and transfer asbestos to a mixing tank
via a closed system maintained under vacuum.
Once in the mixing vessel, the raw asbestos used to create a diaphragm is blended with a liquid solution
of weak caustic soda and salt, thus forming a chrysotile asbestos slurry. Modifiers (e.g., Halar®,
Teflon®) are added to the slurry. Figure 2-2. shows a process flow diagram of an example glove-box-
based asbestos handling system and slurry mix tank.
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Representative Asbestos Handling Process Flow Diagram
PRE
FILTER
HEPA
FILTER
INLET
AIR
CHAMBER
NC
BLOWER
H20
ADDITIVE
ADDITIVE
MIX
CHAMBER
HEPA
FILTER
GLOVE BOX
WEIGH SCALE
GLOVE BOX
WASTE
BAG
LIQUOR
ADDITION
SLURRY
TANK
ASBESTOS CLEAN ROOM
OVERFLOW TO
CELL RENEWAL
WASH WATER SUMP
ASBESTOS HANDLING SYSTEM
Figure 2-2. Process Flow Diagram of an Asbestos Handling System and Slurry Mix Tank Image
Courtesy of the American Chemistry Council
Source: EPA-HQ-QPPT-2016-0736-0106
The chrysotile asbestos slurry is deposited onto a metallic screen or perforated plate to form the
diaphragm, using a vacuum to evenly apply the slurry across the screen or plate. The diaphragm is
drained to remove unbound (free) water and then placed in an oven to dry and harden the asbestos. The
modifiers sinter and fuse to the asbestos, the asbestos fuses to the screen or plate, and the asbestos
becomes non-friable. After cooling, the diaphragm is installed in the electrolytic cell.
The amount of asbestos used for each diaphragm ranges from 50 to 250 pounds (depending on cell size)
and a typical chlor-alkali facility will use about 5 to 25 tons of raw asbestos per year. Industry
representatives stated during meetings with EPA that a standard-sized manufacturing cell has a surface
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area of 70 m2 and each cell typically has 20 chrysotile asbestos diaphragms within it, although cell sizes
vary EPA Preliminary Information).
The chlor-alkali chemical production process involves the separation of the sodium and chloride atoms
of salt in saltwater (brine) via electricity to produce sodium hydroxide (caustic soda), hydrogen, and
chlorine. This reaction occurs in an electrolytic cell. The cell contains two compartments separated by a
semi-permeable diaphragm, which is made mostly of chrysotile asbestos. The diaphragm prevents the
reaction of the caustic soda with the chlorine and allows for the separation of both materials for further
processing.
The cell will typically operate for one to three years before it must be replaced due to a loss of
conductivity. Many factors can determine the life of a cell, including the brine quality and the cell size.
During the March 2017 site visit, EPA learned that at least one facility bags and discards the whole
diaphragm apparatus. However, other chlor-alkali facilities reuse parts of the electrolytic cell, including
the screen or plate on which the chrysotile diaphragm was formed. The spent asbestos diaphragm is not
reusable and must be hydroblasted off the screen in a cleaning bay (remaining in a wet state) in order for
the screen to be reused. The excess water used during this process is filtered prior to discharge to the
facility's wastewater collection and treatment system. The filtered waste is placed into containers,
sealed, and sent to a landfill that accepts asbestos-containing waste per federal and state asbestos
disposal regulations EPA Preliminary Information). Figure 2-3. illustrates components and construction
of an electrolytic cell.
Top Gasket
Diaphragm
Cathode
Anodes
Babe Cover
Base Assembly
Figure 2-3. Electrolytic Cell Construction
Image courtesy of the American Chemistry Council
Source: (See Enclosure B)
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2.3.1.3.2 Worker Activities - Asbestos Diaphragms
Workers may be potentially exposed to asbestos during various activities associated with constructing,
using, and deconstructing asbestos diaphragms, including:
• Inspecting or handling broken bags
• Remediating loose asbestos inside the shipping container
• Opening the bag and handling raw asbestos
• Preparing the diaphragm using asbestos slurry
• Installing the diaphragm in an electrolytic cell (assembly)
• Maintaining the electrolytic cells
• Removing, dismantling, and hydroblasting diaphragms
Based on information provided by industry, when receiving and unloading bags at the facility, workers
may be protected through the use of PPE, including respiratory protection (e.g., half-mask respirator
with HEPA filters), work gloves, and disposable particulate suits (See Enclosure C).
As noted previously, some facilities have fully automated and enclosed systems for transferring sealed
bags of asbestos to mixing vessels. However, some chlor-alkali facilities transfer materials to a glovebox
for weighing operations, during which workers typically wear PAPRs, gloves, and disposable particulate
suits (See Enclosure C). The specific practices for loading dry asbestos from 40-kg bags into the
glovebox have not been provided to EPA and likely vary depending on the facility and the glovebox
configuration. While some gloveboxes are designed to form a seal with drum-sized product containers,
others may require open handling to load the material from the bulk bag into the glovebox.
Slurry preparation involves enclosed processes and wet methods, which minimize airborne exposure
potential. Because this is a wet process, workers typically wear gloves and boots with disposable
particulate suits, but do not wear respirators even though the short-term (15-minute sampling time)
ambient air concentrations were reported to be 0.02 fibers/cc at 50th percentile and as high as 0.04
fibers/cc (See Enclosure C).
For preparing diaphragms, wet asbestos slurry is deposited onto diaphragm screens. One facility stated
that the wetted diaphragms are vacuum-dried before being placed in ovens to set (Axiall-W estlake.
2017). While forming the diaphragms, workers typically wear gloves and boots with disposable
particulate suits but do not wear respirators even though the short-term (15-minute sampling time)
ambient air concentrations were reported to be 0.0125 fibers/cc at 50th percentile and as high as 0.1
fibers/cc which is the OSHA PEL (See Enclosure C).
For cell assembly, the asbestos contained in the diaphragm is reported to be non-friable (See Enclosure
C), thereby eliminating exposure potential. Workers typically wear impermeable gloves and boots but
do not wear respirators (See Enclosure C). Following cell assembly, the diaphragm is inspected and then
joined with other parts to complete the electrolytic cell. The short-term (15-minute sampling time)
ambient air concentrations for this process were reported to be as high as 0.154 f/cc (See Enclosure €).
Once the diaphragm is in the cell for use in the electrolytic chlor-alkali production process, asbestos
exposure from the diaphragms is not expected to occur because the cells are sealed throughout
production.
Chlor-alkali facilities use different practices for handling used diaphragms. Some facilities recondition
their own diaphragms; some facilities send their used diaphragms to other facilities for reconditioning;
and other facilities dispose of used diaphragms and do not recondition them. At the facilities that do
perform reconditioning, worker cell repair activities involve disassembling cells and then hydroblasting
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diaphragms to remove the asbestos coating. For disassembly, workers typically wear impermeable
gloves, boots, goggles, and disposable particulate suits but do not wear respirators even though the short
term (15-minute sampling time) ambient air concentrations were reported to be 0.016 fibers/cc at 50th
percentile and as high as 0.45 fibers/cc (See Enclosure €). For hydroblasting, workers wear a supplied
air respirator hood, a waterproof suit, impermeable gloves, and boots (See Enclosure C). This activity
occurs in blasting rooms, and workers (while wearing PPE) may be present in these rooms during
hydroblasting activity (Axiall-Westlake. 2017).
For one site EPA visited, the hydroblasting itself was not enclosed but was conducted in a dedicated
area. The asbestos handling area (slurry mixing, oven, diaphragm disassembly, and hydroblasting area)
was walled off on three sides with a series of giant pull down doors. The fourth side wall did not extend
to the ceiling. The layout of such areas may be different at other sites.
Wastewater from hydroblasting is filter pressed to remove asbestos before discharge from the facility.
Workers who perform this task typically wear impermeable gloves, boots, and disposable particulate
suits but do not wear respirators even though the short term (15-minute sampling time) ambient air
concentrations were reported to be 0.0275 fibers/cc at 50th percentile and as high as 0.2 fibers/cc (See
Enclosur ,. Filters with filter cakes are then removed from the plate press and bagged for disposal.
Additionally, two specific practices are expected to minimize workers' asbestos exposures while
completing this disposal activity: (1) all workers who handle wastes wear PPE, including respirators
(PAPR) and (2) workers wet solid waste before double-bagging the waste, sealing it, and placing it in
roll-off containers for eventual transfer to an asbestos landfill (H_ \ I I.Q-QPPT-201> 0'> ] 0478) .
2.3.1.3.3 Number of Sites and Potentially Exposed Workers - Asbestos
Diaphragms
During a meeting with EPA in January 2017, industry representatives stated that in the United States,
three companies own a total of 15 chlor-alkali plants that continue to fabricate and use asbestos
(chry soti 1 e )-contai ni ng semipermeable diaphragms on site (EPA-HO-OPPT-2016-0736-0069). These
three companies are Olin Corporation, Occidental Chemical Corporation, and Westlake Corporation. A
fourth company, Axiall Corporation, previously operated chlor-alkali facilities in the United States, but
Westlake Corporation acquired this company in 2016. Throughout this section, the companies are
referred to as Olin, Occidental, and Axiall-Westlake, with the latter referring to chlor-alkali facilities
currently owned by Westlake, which includes some facilities that were previously owned by Axiall.
To confirm this facility count, EPA reviewed two other data sources. First, EPA reviewed Chemical
Data Reporting (CDR) data. Only Olin and Axiall-Westlake reported importing asbestos in 2015. Each
company reported using asbestos at fewer than 10 sites. Second, EPA reviewed the 2017 TRI data and
identified a total of 11 facilities reporting information on friable asbestos: three Olin facilities; one
Axiall-Westlake facility; and seven Occidental facilities. However, it is possible that some of the
existing chlor-alkali facilities did not have asbestos usage characteristics that would have triggered TRI
reporting. These two data sources are consistent with the finding that 15 chlor-alkali facilities fabricate
or use asbestos-containing diaphragms onsite.
In 2016 CDR, Olin reported a total of at least 25 and fewer than 50 workers who are likely exposed to
asbestos across all of the company's chlor-alkali facilities, and Axiall-Westlake reported a total of at
least 50 and fewer than 100 workers who are likely exposed to asbestos across all of the company's
chlor-alkali facilities. This results in an estimate of at least 75 (25 plus 50) and fewer than 148 (49 plus
99) workers likely exposed, although this estimate does not include Occidental facilities. As noted
previously, Occidental facilities did not report to CDR.
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ACC has indicated that approximately 100 workers nationwide in the chlor-alkali industry perform daily
tasks working with and handling dry asbestos. ACC's estimate is within the range derived from 2016
CDR and includes Occidental facilities.
Regarding potential ONU exposure, EPA considered the fact that area restrictions and other safety
precautions adopted by the chlor-alkali industry help ensure that no ONU (other than directly exposed
workers) are near the asbestos diaphragm fabrication processes and use (EPA-HQ-OPPT-2016-0763-
0052). However, EPA's observations during site visits suggest that asbestos exposure might occur to
workers outside these processes. Additionally, some ONUs (e.g., janitorial staff) may work near the
asbestos diaphragm fabrication processes. For purposes of this assessment, EPA assumes an equal
number of ONUs (100) may be exposed to asbestos released from diaphragm fabrication processes and
use.
2.3.1.3.4 Occupational Inhalation Exposures - Asbestos Diaphragms
To identify relevant occupational inhalation exposure data, EPA reviewed reasonably available
information from OSHA, NIOSH, the peer-reviewed literature, the chlor-alkali industry, and trade
associations that represent this industry (e.g., ACC).
Analysis of Exposed Workers
EPA first considered the 2011 to 2016 nationwide exposure data provided by OSHA and the history of
NIOSH Health Hazard evaluations (HHEs). The OSHA data did not include any observations from the
chlor-alkali NAICS codes (i.e., 325181 for 2011 and 325180 for 2012 to 2016). Of the NIOSH HHEs
reviewed, only two were conducted at chlor-alkali facilities, but these evaluations focused on chlorine
and mercury exposures, not asbestos exposure. One NIOSH HHE considered a facility that received
disassembled diaphragms for servicing (Afeumdo et at.. 1994). NIOSH found that the anodes contained
80 to 90 percent chrysotile asbestos, but the settled dusts from the electrode-servicing facility did not
have detectable asbestos. The quantitation limit for the dust sampling was not specified. Finally, the
peer-reviewed literature did not include recent quantitative reports of worker asbestos exposures in the
chlor-alkali industry.
To assess occupational inhalation exposures, EPA used exposure monitoring data provided by industry.
Data were provided by the three companies that currently use asbestos in the United States chlor-alkali
industry. Occidental provided exposure monitoring data for six facilities for 1996 to 2016 ;idental
Data, see Volume 2); Axiall-Westlake provided data for 2016 from a single facility (Axiall Attachments
1 and 2); and Olin provided data for 2012 to 2019 from three chlor-alkali facilities and a fourth facility
that reprocesses anodes (Olin Corp. 2017). ACC also provided data for 1996 to 2016 £A ;a). The
data that ACC provided were collected at the same chlor-alkali facilities referenced above, and some of
the data provided by ACC may include duplicates with the data provided by the individual companies.
This section focuses on PBZ data for asbestos workers.
The following tables summarize occupational exposure results of different exposure durations for the
fabrication, use, and disposal of asbestos diaphragms in the chlor-alkali industry. The exposure durations
considered are full-shift samples, 30-minute average samples, and additional samples of other durations.
The tables summarize 1,378 sampling results based on the combined PBZ samples from Axiall-
Westlake, Occidental, Olin, and ACC. Axiall-Westlake, Occidental, and Olin provided a numerical
sample duration for each sample. For these two data sets (i.e., the combined set from three companies
and the ACC data), EPA designated samples with durations between 420 and 680 minutes as "full-shift,
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samples," as these durations characterize workers with either 8-hour or 10-hour shifts. The data provided
by ACC did not include numerical sample durations. Rather, the ACC data had sample duration
descriptions of either "short-term sample" or "full-shift sample," which EPA assumes refers to 30-
minute and 8-hour average observations, respectively. EPA assumes ACC's sample data were PBZ
samples, though this was not clear from the documentation provided.
For samples with results less than the limit of detection (LOD) or limit of quantitation (LOQ), surrogate
values were used based on statistical analysis guidelines for occupational exposure data that were
developed for EPA ( 94). These guidelines call for replacing non-detects with the LOD or
LOQ divided by two or divided by the square root of two, depending on the skewness of the data
distributions. However, at least half of the samples for every sample averaging time considered were
measured concentrations above the detection limit. As a result, the 50th and 95th percentile
concentrations were sensitive only to the magnitude of the measured concentrations and not the strategy
used for non-detect replacement.
Table 2-4 and Table 2-5 provide both full-shift and short-term sample summaries. Table 2-6 summarizes
PBZ data for all other sampling durations, and Table 2-7 summarizes all short-term samples by exposure
group, with additional breakdown by task.
Table 2-4. 30-min Short-Term PBZ Sample Summary*
Sample
Dale Range of
Number of
.Maximum
50|li Percentile
95th Percentile
Type
Samples
Samples
Result (l'/oo)
(l'/oo)
(l'/oo)
PBZ
2004 to 2017
384
2 2**
0.032
0.35
*Data from Olin, Occidental and ACC
**Note: The maximum concentration in this table (11 fibers/cc) was originally reported as being an "atypical result." The
employer in question required respirator use until re-sampling was performed. The follow-up sample found an exposure
concentration (0.019 fibers/cc) more than 500 times lower.
Table 2-5. Full-Shift* PBZ Sample Summary
Sample
Typo
Dale Range of
Samples
Number of
Samples
.Maximum
Result (I'/cc)
50th Percentile
(l/oo)
95th Percentile
(f/cc)
PBZ
1996 to 2017
650
0.41
0.0060
0.050
* Includes both 8-hr and 10-hr TWA sample results.

Table 2-6. Summary of PBZ Sampling Data for All Other Durat
ions
Sample
Type
Date Range of
Samples
Number of
Samples
.Maximum
Result (I'/ee)
50"' Percentile
(I'/cc)
95"' Percentile
(f/cc)
PBZ
2004 to 2019
344
0.91
0.029
0.260
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Table 2-7 Summary of ACC Short-Term PBZ Sampling Data by Exposure Group (samples from
2001 to 20]
16)
Kxposurc Group / Task Namc(s)
Number
of
Samples
.Maximum
Result
(l/cc)
501 It
Percentile
(I'/CC)
95th
Percentile
(l/cc)
Asbestos Unloading/Transport
8
0.12
0.01
0.09865
Glovebox Weighing and Asbestos
Handling
150
1.7
0.0295
0.44
Asbestos Slurry *
5
0.04
0.02
0.036
Depositing *
27
0.1
0.0125
0.0601
Cell Assembly *
31
0.077
0.012
0.0645
Cell Disassembly *
49
0.45
0.016
0.0732
Filter Press *
36
0.2
0.0275
0.1315
Hydroblasting
20
0.51
0.14
0.453
* Task-specific PPE does not incluc
e respirators (See Enclosure C)
Analysis of ONUs
At chlor-alkali facilities, ONU exposures to asbestos are expected to be limited because most asbestos
handling areas are likely designated regulated areas pursuant to the OSHA asbestos standard, with
access restricted to employees with adequate personal protective equipment. However, EPA considered
the possibility of ONU exposure when employees not engaged in asbestos-related activities work near or
pass through the regulated areas and may be exposed to asbestos fibers released into the workplace.
These employees may include maintenance and janitorial staffs.
EPA considered area monitoring data (i.e., fixed location air monitoring results) as an indicator of this
exposure potential. Across the four sampling data sets provided by industry, only the data provided by
01 in included area sampling results (Olin Corp. 2017). The area monitoring data from Olin's Alabama,
Arkansas, and Louisiana facilities include 15 full-shift asbestos samples collected at fixed locations. The
asbestos concentration levels are reported as either 0.004 fibers/cc [N= 11] or 0.008 fibers/cc [N=4],
EPA has reason to believe these are all non-detect observations. The notes fields in the sample results
identified as 0.008 fibers/cc state "detection limit was 0.008 fibers/cc." The data that Olin provided for
its fourth (Texas) facility do not clearly distinguish whether measurements are area samples or personal
breathing zone samples.
As true exposure values below any limit of detection (LOD) are distributed from zero to the limit of
detection, the value of the detection level represents the high end of the distribution of the observations
below LOD. To estimate the central tendency, EPA used the mean of the values which was 0.005
fibers/cc and divided by 2 for a central tendency exposure estimate of 0.0025 fibers/cc. The high-end
exposure estimate of <0.008 fibers/cc is the higher of the two reported LODs. These values will be used
to represent ONU full-shift TWA exposure distribution values in this draft risk evaluation.
2.3.1.3.5 Exposure Results for Use in Risk Evaluation
Table 2-8 presents asbestos exposure data that EPA used in the risk evaluation for workers and ONUs in
the chlor-alkali industry. EPA's basis for selecting the data points appears after the table.
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Table 2-8 Summary of Asbestos Exposures During Processing and Use in the Chlor-Alkali
Industry Used in EPA's Risk Evaluation
Occupational
Kxposure Scenario
Workers
Central
Tendency
lligh-end
(95,h
percentile)
Kxposurc
Confidence
Rating
Lcycls (I'ihe
OMs
Central
Tendency
rs/cc)
lligh-end
Confidence
Uating
Producing,
handling, and
disposing of
asbestos
diaphragms: full-
shift TWA
exposure
0.0060
0.050
High
0.0025
0.008
Medium
Producing,
handling, and
disposing of
asbestos
diaphragms: short-
term TWA
exposure (30 mins)
0.032
0.35
High
—
—
—
"—" indicates no data reported
The data in Table 2-8 provide a summary of exposure values among workers and ONUs who produce,
handle, and dispose of asbestos diaphragms at chlor-alkali facilities. These data represent a complex mix
of worker activities with varying asbestos exposure levels. It should be noted that not all activities
include use of respirators (Table 2-7). The data points in Table 2-8 were compiled as follows (details
presented in Supplemental File: Occupational Exposure Calculations (Chlor-Alkali) (U.S. EPA. 2019b):
• Table 2-8 lists the full-shift TWA exposure levels that EPA used in this risk evaluation. The
central tendency value for workers (0.0050 fibers/cc) is the median value of the exposure
samples provided by Olin, Occidental and ACC, while the high-end value (0.036 fibers/cc) is the
calculated 95th percentile (see Table 2-5).
• For ONU exposure estimates area samples were used. Two chlor-alkali facilities provided a total
of 15 area samples which were all below the limit of detection (LOD). There were two different
detection limits in the two submissions. As true exposure values below any limit of detection are
distributed from zero to the limit of detection, the value of the detection level represents the high
end of the distribution of the observations below LOD. Central tendency exposure concentrations
were calculated by using one-half the detection limit for individual samples; and the high-end
concentration is assumed to be the highest detection limit provided.
• The central tendency short-term TWA exposure value for workers was based on short-term (30-
minute) sampling data provided by industry. The value in Table 2-5 (0.032 fibers/cc) is the
median value of all 30-minute personal samples submitted. The high-end short-term TWA
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exposure value for workers (0.35 fibers/cc) is the calculated 95th percentile value for the
compiled industry short-term exposure data. These values are based on all employee tasks
combined. Refer to Table 2-7 for specific employee tasks (e.g., asbestos handling, filter press
operation) with higher short-term exposure levels.
2.3.1.3.6 Data Assumptions, Uncertainties and Level of Confidence
The exposure data shown in Table 2-8 are based monitoring results from the chlor-alkali industry.
Worker exposure sampling data are available from all three companies (i.e., Occidental, Olin, Axiall-
Westlake) that currently operate the entire inventory of chlor-alkali facilities nationwide and the overall
confidence ratings from systematic review for these data were all rated high. Tables 4 through 7
summarize more than 1,000 individual exposure sampling results, which represent extensive coverage of
the estimated 100 directly exposed workers. Each company submission of monitoring data includes a
variety of worker activities. Therefore, this collection of monitoring data likely captures the variability
in exposures across the different chlor-alkali sites and likely captures the variability in exposures during
normal operations within a single site.
EPA notes several limitations with these data:
• the data provided by Axiall-Westlake, Occidental, and Olin represent worker exposures for the
individual companies. However, the data provided by ACC may include duplicates with the data
provided by the three companies. The extent of duplicate entries is not known and cannot be
assessed from the information provided; and
• the monitoring data capture all of the chlor-alkali facilities that use asbestos. However, it is
uncertain if certain high-exposure activities are captured in this dataset, such as exposures when
cleaning spilled asbestos within a container from damaged bags.
EPA used the data for the risk evaluation because of the large number of samples, both full shift and
short term, and the range of worker activities that will likely capture the variability in exposures.
EPA considered the quality and uncertainties of the data to determine a level of confidence for the
assessed inhalation exposures for this COU. The primary strength of this assessment is the use of
monitoring data from all the sites, which is the highest approach of the inhalation exposure assessment
approach hierarchy. Based on these strengths and limitations of the data, the overall confidence for
EPA's assessment of occupational inhalation exposures for this scenario is high.
Based on these strengths and limitations of the data, the overall confidence for the worker 8-hr TWA
and short-term data is high.
For the ONU data - which were all non-detectable area samples - there is medium confidence for this
set of data.
2,3,1,4 Sheet Gaskets
This section describes how asbestos-containing rubberized sheeting is processed into gaskets.
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2.3.1.4.1 Process Description - Sheet Gasket Stamping
Gaskets are commonly used in industry to form leakproof seals between fixed components (e.g., pipes).
Figure 2-4. shows an asbestos-containing gasket and depicts a typical gasket installation for pipe fittings.
While many asbestos-free gaskets are commercially available and widely used, asbestos-containing
gaskets continue to be the material of choice for industrial applications where gasket material is exposed
to extreme conditions such as titanium dioxide manufacturing (e.g., high temperature, high pressure,
presence of chlorine). Based on correspondence from ACC, gaskets made from non-asbestos materials
reportedly do not provide an adequate seal under these extreme conditions (ACC. 2018).
Gasket
Figure 2-4. Typical Gasket Assembly
From left to right: photograph of a gasket; illustration of a flange before gasket installation; and
illustration of a pipe and flange connection after gasket installation.
Photograph taken by EPA; Illustrations from Wikipedia.
One known company in the United States (Branham Corporation) processes (or fabricates) gaskets from
asbestos-containing aibberized sheeting. This stamping activity occurs at two Branham facilities: one in
Gulfport, Mississippi and the other in Calvert City, Kentucky. Branham imports the sheeting from a
Chinese supplier, and the sheets contain 80 percent (minimum) chrysotile asbestos encapsulated in 20
percent styrene-butadiene rubber (EPA-HQ-QPPT-2016-0736-0067). Branham supplies its finished non-
friable asbestos-containing gaskets to several customers, primarily chemical manufacturing facilities in
the United States and abroad (see Section 2.3.1.5). It is unknown if other U.S. companies import
asbestos-containing sheet material to stamp gaskets.
EPA communicated with industry to understand how Branham typically processes gaskets from
asbestos-containing sheeting. This communication includes an October 2017 meeting between EPA and
industry representatives, written communications submitted by industry representatives and ACC, and
an August 2018 EPA site visit to the Branham gasket stamping facility in Gulfport Mississippi. An
overview of the manufacturing process follows.
Rolls of imported asbestos-containing rubberized sheeting are transported inside bolt-locked, sealed
containers from the port of entry to the Branham facilities. Branham then stores these rolls in the
original inner plastic film wrapping until use. Incoming sheets are typically 1/16-inch thick and weigh
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0.6167 pounds per square foot (ACC, 2018). Branham employees stamp and cut gaskets to customer
size specifications in a production area. Various other operations occur simultaneously at the Branham
facilities to include stamping of non-asbestos gaskets using similar stamping machines. These other
operations occur approximately 20 feet away from the stamping machines used to make asbestos-
containing gaskets (EHM. 2013). As noted later in this section, EPA considers the workers supporting
other nearby operations to be ONUs for this risk evaluation.
At the Branham facility visited by EPA, workers used three stamping machines to cut the imported
asbestos-containing sheets into desired sizes. The facility reportedly does not saw gasket material
(Branham. 2018). and EPA did not see evidence of this practice during its site visit. The stamping
machines can be adjusted to make products of varying diameters, from 4 inches to 4 feet. Figure 2-5.
shows a worker wearing a face mask while operating one of the stamping machines, which uses round
headed dies attached to a blade. Blades are not removed from the dies, and the dies are seldom "re-
ruled" (where the rule blade would be pressed back into the wooden die frame).
Figure 2-5. Asbestos-Containing Stamping Operation
Photographs courtesy of Branham Corporation and used with Branham's permission
Figure 2-6. shows a photograph of the rul e blade, which is approximately 0.010 inches thick.
Figure 2-6. Rule Blade for Stamping Machine
Photographs courtesy of Branham Corporation and used with Branham's permission
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After stamping the sheet, workers place the finished gasket in individual 6-mm thick resealable bags.
These are double-bagged with a warning label and ultimately placed in a container for shipping to
customers. Figure 2-7. shows the warning label that Bran ham applies to asbestos-containing gasket
products.

C°HTAIHs ASRen

Figure 2-7. Asbestos Warning Label on Finished Gasket Product
Photograph taken by EPA and used with Branham's permission
An important consideration for worker exposure is the extent to which sheet gasket stamping releases
asbestos-containing fibers, dusts and particles. Industry representatives have informed EPA that the
stamping process creates no visible dust, due in part to the fact that the asbestos fibers are non-friable
and encapsulated in rubberized sheet material (ACC. 2018). This statement is consistent with EPA's
observations during the site visit, in which no significant dust accumulations were observed on or near
Branham's stamping machines. However, EPA's observations are based on a single, announced site
visit. More importantly, sampling data reviewed for this operation do indicate the presence of airborne
asbestos. This suggests that the stamping releases some asbestos into the workplace air.
The principal cleanup activity during the stamping operation is collection of unused asbestos-containing
scrap sheeting, also referred to by the facility as "lattice drops." Workers manually collect this material
and place it in 6-mm thick polyethylene bags, which are then sealed in rigid containers and shipped to
the following landfills permitted to receive asbestos-containing waste (ACC. 2018):
• Asbestos-containing waste from Branham's Kentucky facility are transported by Branham to the
Waste Path Sanitary Landfill at 1637 Shar-Cal Road, Calvert City, Kentucky.
• Asbestos-containing waste from Branham's Mississippi facility are transported by Team Waste
to the MacLand Disposal Center at 11300 Highway 63, Moss Point, Mississippi.
No surface wipe sampling data are available to characterize the extent of settled dust and asbestos fibers
present during this operation. The Branham facilities informed EPA that they do not use water,
including to wash away scrap or other debris or perform wet mopping, and EPA confirmed this during
the site visit. Once per week, however, workers use a damp cloth to wipe down the stamping machine
area. Spent cloths from this wiping are bagged and placed in the same rigid containers with the unused
scrap material for eventual disposal.
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2.3.1.4.2 Worker Activities - Cutting of Asbestos-containing Sheet Gaskets
Worker activities most relevant to potential asbestos exposure include receiving asbestos-containing
rubber sheeting, processing gaskets by stamping, packaging finished gaskets for shipment, and
collecting asbestos containing scrap waste.
The amount of time that workers conduct cutting asbestos-containing sheets varies with production
demand and other factors. EPA received one month of worker activity data for Branham's Mississippi
facility, and these data indicated that, in May 2018, the worker spent no more than 70 minutes per day
processing asbestos-containing gaskets (Branham. 2018). Branham informed EPA that the worker at the
Kentucky facility perform asbestos-containing gasket stamping activity two to three days per week
(Branham. 2018). The worker exposure levels from the Kentucky facility will be used in this draft risk
evaluation because Branham officials informed EPA that they do not anticipate considerable increases
or decreases in production demand for asbestos-containing sheet gaskets.
Information on worker PPE use was based on photographs provided by Branham, information in facility
documents, and observations that EPA made during its site visit. When handling and stamping asbestos-
containing sheeting and when collecting scraps for disposal, the worker wears safety glasses, gloves, and
N95 disposable facepiece masks, consistent with Branham procedures (ACC. 2017a). A 2013 industrial
hygiene evaluation performed by consultants from Environmental Health Management (EHM)
concluded that measured asbestos exposures at Branham's Kentucky facility were not high enough to
require respiratory protection (EHM.: ); however, the worker uses the N95 masks to comply with
Branham procedures.
2.3.1.4.3 Number of Sites and Potentially Exposed Workers - Sheet Gasket
Stamping
Branham operates two facilities that process asbestos-containing gaskets, with one worker at each
facility who stamps the asbestos-containing sheet gaskets. During its site visit to one facility, EPA
observed that stamping of asbestos-containing sheeting occurs in a 5,500 square foot open floor area.
Other employees work in this open space, typically at least 20 feet away from where asbestos-containing
gaskets are processed. EPA considers these other employees to be ONUs. The facility also included a
fully-enclosed air-conditioned office space, where other employees worked.
EPA received slightly varying estimates of the number of workers at Branham's facilities and the
specific locations where they work (ACC. 2018; Branham. 2018). Based on these estimates, EPA
assumes that both facilities have one worker who processes asbestos-containing gaskets, two workers
who process other non-asbestos containing gaskets in the same open floor area (and are considered to be
ONUs), and at least two workers in the office space. Therefore, EPA assumes that asbestos-containing
gasket stamping at this company (i.e., at both facilities combined) includes two directly exposed workers
and four ONUs.
These estimates are based on the one company known to stamp asbestos-containing sheet gaskets. It is
unknown if other U.S. companies perform this same stamping activity. EPA attempted to identify other
companies that cut/stamp asbestos-containing sheet gaskets in the United States but could not locate
any. Therefore, it is not known how many sites cut or stamp imported asbestos-containing sheet gaskets.
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2.3.1.4.4 Occupational Inhalation Exposure Results - Sheet Gasket Stamping
To identify relevant occupational inhalation exposure data, EPA reviewed reasonably available
information from OSHA, NIOSH, the published literature, and industry. All research steps are
documented below, with more detailed discussion on the most relevant data source, which EPA
determined was the monitoring results conducted at a Branham facility.
EPA first considered the 2011 to 2016 nationwide exposure data provided by OSHA and the history of
NIOSH HHEs, but neither resource included exposure data relevant to stamping of asbestos-containing
sheet gaskets. For instance, the OSHA data did not include any asbestos results for the gasket
manufacturing NAICS code 339991.
EPA also considered the published literature on asbestos exposures associated with sheet gasket
stamping. This search identified two studies that presented original worker exposure monitoring data.
One was a 1998 study of sheet gasket production in Bulgaria (Strokova et at.. 1998). However, the study
lacked specific details on worker activities and the sampling and analysis method used, and the overall
representativeness of 20-year old processing activities in Bulgaria to today's operations is unclear. The
other was a 2000 publication as part of litigation support that examined exposures in a simulated work
environment (Fowler. 20001 but this more recent study involved cutting gasket material with a
conventional woodworking bandsaw - a practice that likely generates elevated asbestos exposures and is
not representative of Branham's stamping operations.
EPA determined that a worker exposure monitoring study conducted at one of the Branham facilities
provides the most relevant data for this COU. Branham hired EHM consultants to conduct this study,
which involved a day of PBZ monitoring at the Kentucky facility in December 2012. The EHM
consultants measured PBZ concentrations for one worker - the worker who operated the stamping
machine to process asbestos-containing gaskets - and issued a final report of results in 2013 (EHM.
2013). The EHM consultants measured worker inhalation exposures associated with a typical day of
processing asbestos-containing gaskets and reported that samples were collected "during work periods
when the maximum fiber concentrations were expected to occur" (EHM. 2013). The EHM consultants
did not measure or characterize ONU exposures, although EPA believes that two ONUs are present at
each Branham facility where asbestos-containing sheet gaskets are processed.
The EHM consultants measured worker inhalation exposure during asbestos-containing gasket stamping
operations. Ten short-term samples, all approximately 30 minutes in duration, were collected from one
worker throughout an 8-hour shift. Samples were analyzed by PCM following NIOSH Method 7400.
The short-term exposures ranged from 0.008 fibers/cc to 0.059 fibers/cc. Table 2-9. lists the individual
measurement results and corresponding sample durations. Based on the short-term results, the EHM
consultants calculated an 8-hour TWA exposure of 0.014 fibers/cc, which assumed no exposure during
periods without sampling. (Note: The periods without sampling appear to be the worker's break and
lunch, when exposure would be expected to be zero.)
The EHM consultants' study report includes a data summary table, which indicates that the primary
worker activity covered during the sampling was "cutting gaskets" (i.e., operation of the stamping
machines); however, the EHM consultants also acknowledged that the worker who was monitored
collected scrap material while PBZ sampling occurred (EHM. 2013). EPA infers from the document that
the sampling represents conditions during a typical workday and covers multiple worker activities.
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Table 2-9. Short-Term PBZ Asbestos Sampling Results (EHM. 201
Duration (minutes)
Result (fihers/ee)
30
0.059
27
0.031
36
0.020
32
0.026
29
0.028
35
0.010
40
0.018
29
0.008
30
0.008
25
0.033
2.3.1.4.5 Exposure Data for Use in Risk Evaluation - Sheet Gasket Stamping
Table 2-10 presents the worker and ONU exposure concentrations that EPA used in this risk evaluation.
The following assumptions were made in compiling these data:
• The central tendency 8-hour TWA exposure value reported for workers (0.014 fibers/cc) was
taken from the single calculated value from the personal exposure monitoring study of a
Branham worker (EHM. 2013). The calculated value was derived from the ten sampling points
shown in Table 2-9., assuming no exposure occurred when sampling was not conducted.
• The high-end 8-hour TWA exposure value for workers (0.059 fibers/cc) is an estimate, and this
full-shift exposure level was not actually observed. This estimate assumes the highest measured
short-term exposure of the gasket stamping worker could persist for an entire day.
• The central tendency short-term exposure value for workers (0.024 fibers/cc) is the arithmetic
mean of the ten short-term measurements reported in the EHM study report on the Branham
worker (EHM. 2013V
• The high-end short-term exposure value for workers (0.059 fibers/cc) is the highest measured
short-term exposure of the Branham worker. This exposure value occurred during a 30-minute
sample (EHM.: ).
Table 2-10 presents the asbestos exposure data that EPA used in this draft risk evaluation for evaluating
risks to workers and ONUs for the COU of processing asbestos-containing sheet gaskets. Given the
small number of sampling data points available to EPA, only central tendency and high-end estimates
are presented and other statistics for the distribution are not calculated.
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Table 2-10 Summary of Asbestos Exposures During Sheet Gasket Stamping Used in EPA's Risk
Evaluation
Occupational Kxposure
Scenario
l-uN-Shil'l Kxposures (fibers/cc)
Workers
OMs
(on (nil
Tendency
High-
end
Confidence
Ualing
Central
Tendency
lligh-
end
Confidence
Ualing
SIkvI gasket stamping S-lir
TWA exposure
0.014
0.059
Medium
0.0024
0.010
Medium
Sheet gasket stamping:
Short-term exposures
(approximate 30-minute
duration)
0.024
0.059
Medium
0.0042
0.010
Medium
ONU Exposures
EPA did not identify any ONU exposure measurements for this COU. However, the literature includes
"bystander" exposure studies that EPA could use to estimate ONU exposures. Specifically, one
publication (Mangold et at.. 2006) measured "bystander" exposure during asbestos-containing gasket
removal. The "bystander" locations in this study were between 5 and 10 feet from the gasket removal
activity, and asbestos concentrations were between 2.5 and 9 times lower than those measured for the
worker. Based on these observations, EPA assumes that ONU exposures for this COU are a factor of
5.75 (i.e., the midpoint between 2.5 and 9) lower than the directly exposed workers. This concentration
reduction factor falls within the range of those reported for other asbestos COUs.
2.3.1.4.6 Data Assumptions, Uncertainties and Confidence Level
The exposure data shown in Table 2-10 are based on 10 PBZ samples collected from one worker
performing sheet gasket stamping on a single day at a single facility. EPA used the data from this study
for the risk evaluation because it was the only study available that provided direct observations for
asbestos-containing sheet gasket stamping operations in the United States. EPA considered the quality
and uncertainties of the data to determine a level of confidence for the assessed inhalation exposures for
this COU. The primary strength of this assessment is the use of monitoring data, which is the highest
approach of the inhalation exposure assessment approach hierarchy. The overall confidence rating from
systematic review for these data was high. These monitoring data were provided to EPA by a single
company that processes asbestos-containing sheet gaskets with data representing one of its two facilities
However, it is not known how many companies and facilities in total process asbestos-containing sheet
gaskets in the United States. Therefore, EPA is uncertain if these monitoring data are representative of
the entire U.S. population of workers that are potentially exposed during asbestos-containing sheet
gasket processing. The monitoring data were sampled throughout the day of the worker performing the
sheet gasket stamping; therefore, these data likely capture the variability in exposures across the various
sheet gasket stamping activities. However, it is uncertain if the single sampling day is representative of
that facility's sheet gasket stamping days throughout the year.
Based on these strengths and limitations of the data, the overall confidence for EPA's assessment of
occupational inhalation exposures for this scenario is medium.
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2,3.1.5 Use of Gaskets in Chemical Production
2.3.1.5.1 Process Description - Sheet Gasket Use
Asbestos-containing gaskets are used primarily in industrial applications with extreme operating
conditions, such as high temperatures, high pressures, and the presence of chlorine or other corrosive
substances. Such extreme production conditions are found in many chemical manufacturing and
processing operations. These include: the manufacture of titanium dioxide and chlorinated
hydrocarbons; polymerization reactions involving chlorinated monomers; and steam cracking at
petrochemical facilities. EPA has attempted to identify all industrial uses of asbestos-containing gaskets,
but the primary use known to the Agency is among titanium dioxide manufacturing facilities.
EPA communicated with the titanium dioxide industry to understand typical industrial uses of asbestos-
containing gaskets. This communication includes an October 2017 meeting between EPA and industry
representatives and written communications submitted by industry representatives and ACC. An
overview of asbestos-containing gasket use in the titanium dioxide manufacturing industry follows.
Branham supplies asbestos-containing gaskets to at least four titanium dioxide manufacturing facilities
worldwide. Two are Chemours facilities located in DeLisle, Mississippi and New Johnsonville,
Tennessee; and the other two are located outside the United States (Mingis. 2018). The manufacture of
titanium dioxide occurs at process temperatures greater than 1,850 degrees Fahrenheit and pressures of
approximately 50 pounds per square inch, and it involves multiple chemicals, including chlorine,
toluene, and titanium tetrachloride (ACC. 2017b). Equipment, process vessels, and piping require
durable gasket material to contain these chemicals during operation. The Chemours facilities use the
Branham products - sheet gaskets composed of 80 percent (minimum) chrysotile asbestos, fully
encapsulated in styrene-butadiene rubber - to create tight chemical containment seals for these process
components (ACC. 2017b). One of these facilities reports replacing approximately 4,000 asbestos-
containing gaskets of various sizes per year, but any given year's usage depends on many factors (e.g.,
the number of major turnarounds) (ACC. 2017b).
Installed gaskets typically remain in operation anywhere from a few weeks to three years; the time-
frame before being replaced is largely dependent upon the temperature and pressure conditions (ACC.
2018). whether due to detected leaks or as part of a routine maintenance campaign. Used asbestos-
containing gaskets are handled as regulated non-hazardous material. Specifically, they are immediately
bagged after removal from process equipment and then placed in containers designated for asbestos-
containing waste. Containerized waste (volume not known) from both Chemours domestic titanium
dioxide manufacturing facilities is eventually sent to the following landfills, which are permitted to
receive asbestos-containing waste (ACC. ):
• Asbestos-containing waste from Chemours' Tennessee facility is transported to the West
Camden Sanitary Landfill at 2410 Highway 70 West, Camden, Tennessee.
• Asbestos-containing waste from Chemours' Mississippi facility is transported to the Waste
Management Pecan Grove Landfill at 9685 Firetower Road, Pass Christian, Mississippi.
Though Chemours has an active program to replace asbestos-containing gaskets with asbestos-free
alternatives and this program has resulted in considerable decreases in asbestos-containing gasket use
(EPA-HQ-OPPT-2016-0736-0067). gaskets formulated from non-friable chrysotile asbestos-containing
sheeting continue to be the only product proven capable of withstanding certain extreme operating
conditions and therefore provide a greater degree of process safety and integrity than unproven
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alternatives according to industry (ACC, 2017b). A single titanium dioxide manufacturer can have
approximately 4,000 gaskets of various sizes distributed throughout the plant which are periodically
replaced during facility shutdowns.
2.3.1.5.2 Worker Activities - Sheet Gasket Use
Worker activities most relevant to asbestos exposure include receiving new gaskets, removing old
gaskets, bagging old gaskets for disposal, and inserting replacement gaskets into flanges and other
process equipment. Asbestos-containing gaskets are received and stored in individual resealable 6-mm
thick plastic bags. Trained maintenance workers wear leather gloves when handling the gaskets for
insertion into a flange. When removing old gaskets for replacement, trained maintenance workers wear
respiratory protection—either an airline respirator or cartridge respirator with P-100 HEP A filters,
although the APF for this respiratory protection was not specified (ACC.! ). Respiratory protection
is used during this task to protect workers in cases where the originally non-friable asbestos in the
gaskets has become friable over the service life (ACC. 2017a).
2.3.1.5.3 Number of Sites and Potentially Exposed Workers - Sheet Gasket
Use
As noted previously, EPA is aware of two Chemours titanium dioxide manufacturing facilities that use
asbestos-containing gaskets in the United States. However, no estimates of the number of potentially
exposed workers were submitted to EPA by industry or its representatives. As gaskets are replaced
during plant shutdowns, this potential number would be low as some workers would be off site during
the shutdown.
To estimate the number of potentially exposed workers and ONUs at these two facilities, EPA
considered 2016 data from the Bureau of Labor Statistics for the NAICS code 325180 (Other Basic
Inorganic Chemical Manufacturing). These data suggest an industry-wide aggregate average of 25
directly exposed workers per facility and 13 ONUs per facility. EPA therefore estimates that the two
Chemours facilities combined have approximately 50 directly exposed workers and 26 ONUs.
These estimates are based on the one company known to use asbestos-containing gaskets at its titanium
dioxide manufacturing facilities. Other titanium dioxide manufacturing plants that operate under similar
conditions in the United States are thought to use asbestos-containing gaskets to prevent chlorine leaks,
but EPA does not have information to confirm this (Mingis. 2018).
2.3.1.5.4 Occupational Inhalation Exposures - Sheet Gasket Use
To identify relevant occupational inhalation exposure data, EPA reviewed reasonably available
information from OSHA, NIOSH, the published literature, and industry. All research steps are
documented below, with more detailed discussion on the most relevant data source, which EPA
determined was the monitoring results submitted by ACC for a Chemours titanium dioxide
manufacturing facility.
EPA first considered the 2011 to 2016 nationwide exposure data provided by OSHA and the history of
NIOSH HHEs, but neither resource included asbestos exposure data for the titanium dioxide
manufacturing industry.
EPA also considered the published literature on worker asbestos exposure attributed to gasket removal.
This search did not identify publications that specifically addressed asbestos-containing gasket use in the
titanium dioxide manufacturing industry. However, two peer-reviewed publications measured worker
exposures of gasket removal in settings like those expected for this industry:
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• One publication was a 1996 study of maintenance workers who removed braided gaskets and
sheet gaskets at a chemical plant in the Netherlands (Spence and Rocchi. 1996). The study
considered two types of sheet gasket removal activity: gaskets that could be easily removed with
a putty knife without breaking, and gaskets that required more intensive means (and longer
durations) for removal. Among the data for sheet gasket removal, the highest worker exposure
concentration—with asbestos presence confirmed by TEM analysis—was 0.02 fibers/cc for a
141-minute sample. A slightly higher result was reported in a different sample, but TEM analysis
of that sample found no detectable asbestos. The overall representativeness of a study more than
20 years old to today's operations is unclear.
• The other publication was a 2006 study that used a simulated work environment to characterize
worker and ONU exposure associated with gasket removal onboard a naval ship or at an onshore
site (Mangold et al. 2006). The simulations considered various gasket removal scenarios (e.g.,
manual removal from flanges, removal requiring use of a knife, removal requiring use of power
wire brushes). The 8-hour TWA PBZ exposures that were not conducted on marine vessels and
therefore considered most relevant to the sheet gasket removal ranged from 0.005 to 0.023
fibers/cc. The representativeness of these simulations to an industrial setting is unclear.
However, the study provides useful insights on the relative amounts of asbestos exposure
between workers and ONUs. The simulated gasket removal scenarios with detected fibers
suggested that exposure levels decreased by a factor of 2.5 to 9 between the gasket removal site
and the "area/bystander" locations, approximately 5 to 10 feet away.
Other peer-reviewed publications were identified and evaluated but not considered in this assessment
because they pertained to heavy-duty equipment (Boelter et al.. 2011). a maritime setting with confined
spaces (Madl et al.. 2014). and braided packing (Boelter et al.. 2002).
EPA determined that worker exposure data submitted by ACC for one of the Chemours titanium dioxide
manufacturing facilities provide the most relevant data for this COU. ACC stated that only trained
Chemours mechanics remove asbestos-containing gaskets, and they use respiratory protection when
doing so (either an atmosphere-supplying respirator or an air-purifying respirator) (ACC. 2017a).
According to the information provided to EPA, 34 worker exposure samples have been collected since
2009 during removal of asbestos-containing gaskets, but the number of workers that were evaluated is
not known (based on discussions with Chemours during a visit to EPA in October 2017). The samples
evidently were collected to assess compliance with OSHA occupational exposure limits, suggesting that
they were analyzed using PCM. Asbestos levels in these samples ranged from 0.0026 to 0.094 fibers/cc,
with an average of 0.026 fibers/cc (ACC. 2017a). The documentation provided for these sampling
events does not indicate the sampling duration or the amount of time that workers performed gasket
removal activity, nor were the raw data provided.
2.3.1.5.5 Exposure Results for Use in Risk Evaluation - Sheet Gasket Use
Table 2-11. presents the worker exposure concentrations that EPA is using in this risk evaluation for use
of asbestos-containing gaskets at titanium dioxide manufacturing facilities. The following assumptions
were made in compiling these data:
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• The central tendency 8-hour TWA exposure value for workers (0.026 fibers/cc) is based on the
average asbestos exposure measurement reported for gasket removal at titanium dioxide
manufacturing facilities (ACC. 2017a). Though the supporting documentation does not specify
sample duration, EPA assumes, based on discussions with Chemours, the average reported
concentration can occur throughout an entire 8-hour shift (e.g., for workers removing gaskets
throughout a day during a maintenance campaign).
• The high-end 8-hour TWA exposure value for workers (0.094 fibers/cc) is based on the highest
exposure measurement reported for gasket removal activity at titanium dioxide manufacturing
facilities (ACC. 2017a). Again, the sample duration for this measurement was not provided and
so this concentration represents a high-end by extrapolating the value to represent an entire shift.
• Because the documentation for the 34 worker exposure samples does not include sample
duration, EPA cannot assume the central tendency and high-end values apply to short-term
exposures. More specifically, if the original data were for full-shift exposures, then assuming
those data points apply to short-term durations would understate these exposures. Therefore,
EPA has determined that no reasonably available data are available for evaluating worker short-
term exposures for this COU.
Table 2-11. Summary of Asbestos Exposures During Sheet Gasket Use Used in EPA's Risk
Evaluation
Occupational
Kxposure Scenario

8-hr TWA Kxposurc Levels (fibers/cc)

Workers

OMs

(on (ml
Tendency
lligh-end
Confidence
Killing
(cnl nil
Tendency
lligh-end
Confidence
Rating
Shccl uaskel use K-
hr TWA exposure
0.026
0.094
Medium
0.005
0.016
Medium
ONU Exposures
As noted previously, one study (Mangold et at.. 2006) measured "bystander" exposure during asbestos-
containing gasket removal. The bystander locations were between 5 and 10 feet from the gasket removal
activity, and concentrations were between 2.5 and 9 times lower than those measured for the worker.
Based on these observations, EPA assumes that ONU exposures for this COU are a factor of 5.75 (i.e.,
the midpoint between 2.5 and 9) lower than the directly exposed workers. This factor is based on a study
that evaluated exposures in an enclosed setting and therefore may overstate ONU exposures for gasket
removal activity in outdoor environments. ONUs may include other maintenance workers, operators,
and supervisors.
2.3.1.5.6 Data Assumptions, Uncertainties and Level of Confidence
The exposure data shown in Table 2-11. are based on observations from a single reference that presents
worker exposure monitoring data for a single company, and documentation for this study is incomplete.
EPA estimates that using the 34 direct observations for gasket removal workers likely offers the most
representative account of actual exposures, rather than relying on data from the published literature
taken from other settings. Moreover, the central tendency concentration shown in Table 2-11. is higher
than results from the relevant literature that EPA reviewed., suggesting that the data source considered
(ACC. 2017a) does not understate exposures.
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EPA considered the quality and uncertainties of the data to determine a level of confidence for the
assessed inhalation exposures for this COU. The primary strength of this assessment is the use of
monitoring data, which is the highest approach of the inhalation exposure assessment approach
hierarchy. The overall confidence rating from systematic review for these data was rated medium. These
monitoring data were provided to EPA by industry and represent actual measurements made during
asbestos-containing sheet gasket removal at a titanium dioxide manufacturing facility in the United
States. However, the total number of facilities using asbestos-containing sheet gaskets in the United
States is not known, and EPA could not determine if the industry-provided monitoring data are
representative of all U.S. facilities that use asbestos-containing sheet gaskets. The monitoring data were
collected from 2009 through 2017; therefore, the data likely capture temporal variability in the facility's
operations.
Based on these strengths and limitations of the data, the overall confidence for EPA's assessment of
occupational inhalation exposures for this scenario is medium.
2.3.1.6 Oil Field Brake Blocks
This section reviews the presence of chrysotile asbestos in oil field brake blocks and evaluates the
potential for worker exposure to asbestos during use.
2.3.1.6.1 Process Description - Oil Field Brake Blocks
The rotary drilling rig of an oil well uses a drawworks hoisting machine to raise and lower the traveling
blocks during drilling. The drawworks is a permanently installed component of a mobile drilling rig
package, which can be either "trailerized" or self-propelled. Therefore, there is no on-site assembly of
the drawworks. Except for initial fabrication and assembly prior to installation on a new rig, the
drawworks is not set or installed in an enclosed building (Popik. 2018).
The drawworks consists of a large-diameter steel spool, a motor, a main brake, a reduction gear, and an
auxiliary brake. The drawworks reels the drilling line over the traveling block in a controlled fashion.
This causes the traveling block and its hoisted load to be lowered into or raised out of the wellbore
(Schlumberger. 2018). The drawworks components are fully enclosed in a metal housing. The brake
blocks, which ride between an inner brake flange and an outer metal brake band, are not exposed during
operation of the drawworks (Popik. 2.018).
The brake of the drawworks hoisting machine is an essential component that is engaged when no motion
of the traveling block is desired. The main brake can have several different designs, such as a friction
band brake, a disc brake, or a modified clutch. The brake blocks are a component of the braking system
(Schlumberger. 2.018). According to product specification sheets, asbestos-containing brake blocks are
most often used on large drilling drawworks and contain a wire backing for added strength. They are
more resistant than full-metallic blocks, with good flexibility and a favorable coefficient of friction. The
asbestos allows for heat dissipation and the woven structure provides firmness and controlled density of
the brake block. Workers in the oilfield industry operate a drilling rig's brakes in an outdoor
environment and must periodically replace spent brake blocks (Popik. 2018).
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Figure 2-8. Photographs of Typical Oil Field Drawworks
Photograph courtesy of Stewart & Stevenson and used with Stewart & Stevenson's permission
Drawworks can have either one or two drums, with each drum usually containing two bands, and each
band usually containing 10 brake blocks, resulting in a total of 20 to 40 brake blocks per drawworks.
The configuration can vary depending on the size of the drawworks. An industry contact specified brake
block dimensions of 8 to 12 inches wide by 12 inches long by 0.75 to 1.125 inches thick and weighing
six to seven pounds per block. The percent asbestos composition of the brake blocks is unknown (Popik.
2018).
Brake blocks do not require maintenance other than replacement when worn down to a 0.375-inch
thickness at any point in the block. The brake blocks typically last between 2 and 3 years under daily
operation of the drawworks. Due to the heterogeneous pressure distribution inherent in the mechanics of
the brake band design, the brake blocks wear differently depending on their position within the band.
However, efforts are made to equalize the tapering pressure distribution by grading the brake block
material in order to achieve a more uniform friction at all points along the brake band. (Popik. 2018).
The brake blocks are enclosed in the drawworks, so it is not necessary to clean off brake dust under
normal operations. The drawworks is washed down prior to removal and installation of brake blocks—a
task that could lead to water releases of asbestos dust. Brake block servicing typically takes place
outdoors or in a large service bay inside a shop (Popik. 2018).
EPA obtained a safety data sheet (SDS) from Stewart & Stevenson Power Products, LLC for "chrysotile
woven oilfield brake blocks, chrysotile woven plugs, and chrysotile molded oilfield brake blocks." The
SDS recommends avoiding drilling, sanding, grinding, or sawing without adequate dust suppression
procedures to minimize air releases and inhalation of asbestos fibers from the brake blocks. The SDS
recommends protective gloves, dust goggles, and protective clothing. The SDS also specifies that used
brake block waste should be sent to landfills (Stewart & Stevenson. 2000).
At least one U.S. company imports and distributes non-metallic, asbestos-woven brake blocks used in
the drawworks of drilling rigs. Although the company no longer fabricates brake blocks using asbestos,
the company confirmed that it imports asbestos-containing brake blocks on behalf of some clients for
use in the oilfield industry. It is unclear if any other companies fabricate or import asbestos-containing
brake blocks, or how widespread the continued use of asbestos brake blocks is in oilfield equipment.
However, EPA understands from communications with industry that the use of asbestos brake blocks
has decreased significantly over time and continues to decline (Popik. 2018).
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3014 2.3.1.6.2 Worker Activities - Oil Field Brake Blocks
3015 Worker activities include receipt of asbestos-containing brake blocks, removing old brake blocks,
3016 bagging old brake blocks for disposal, and installing new brake blocks into drawworks machinery. The
3017 activities that may result in asbestos exposure include installing and servicing brake blocks (which may
3018 also expose workers in the vicinity). Additionally, workers at the drawworks may be exposed to asbestos
3019 fibers that are released as the brake blocks wear down over time. EPA has not identified PPE and
3020 industrial hygiene practices specific to workers removing and installing asbestos-containing brake
3021 blocks.
3022 2.3.1.6.3 Number of Sites and Potentially Exposed Workers - Oil Field Brake
3023 Blocks
3024 EPA identified one U.S. facility that imports asbestos-containing brake blocks CPopik. ). It is
3025 unknown how many other facilities import asbestos-containing brake blocks. It is also unknown how
3026 many customers receive brake blocks from the sole facility identified by EPA. Unlike some of the other
3027 COUs, the lack of any information on oilfield brake block COU necessitated the use of other established
3028 methods to estimate the number of potentially exposed workers.
3029
3030 To estimate the number of potentially exposed workers, EPA used 2016 Occupational Employment
3031 Statistics data from the Bureau of Labor Statistics (BLS) and 2015 data from the U.S. Census' Statistics
3032 of U.S. Businesses. EPA used BLS and Census data for three NAICS codes: 211111, Crude Petroleum
3033 and Natural Gas Extraction; 213111, Drilling Oil and Gas Wells; and 213112, Support Activities for Oil
3034 and Gas Operations. Table 2-13 summarizes the total establishments, potentially exposed workers, and
3035 ONUs in these industries. EPA does not have an estimate of the number of establishments in these
3036 industries that use asbestos-containing brake blocks. Therefore, EPA presents these results as bounding
3037 estimates of the number of establishments and potentially exposed workers and ONUs.
3038
3039 For each of the three NAICS codes evaluated, Table 2-12. presents EPA's estimates of industry-wide
3040 aggregate averages of directly exposed workers per site and ONUs per site. EPA estimates an upper
3041 bound of 21,670 sites, 61,695 directly exposed workers, and 66,108 ONUs.
3042
3043
3044 Table 2-12. Summary of Total Establishments in Relevant Industries and Potentially Exposed
3045 Workers and ONUs for Oilfield Brake Blocks
NAICS
Codes
NAICS
Description
Toi;il (I-.mire Indusln Sector)
Workers «illi Kclc\;inl Occiipiilions
Toiiil
linns
Tohil
I'lsliihlish-
mcnls
Tohil
I'.iliplovccs
A\ cniiic
I'.mplovccs
per
I'lsliihlish-
I11CIII
Workers in
Relet ;inl
Occupa-
tions
Occup;i-
(ioinil Non-
l scrs
W orkers
per Sile
ONI s
per
Sile
211111
Crude
Petroleum
and Natural
Gas
Extraction
6,270
7,477
124,847
17
15,380
32,704
2
4
213111
Drilling Oil
and Gas
Wells
1,973
2,313
89,471
39
10,256
7,397
4
3
213112
Support
Activities
for Oil and
9,591
11,880
314,589
26
36,059
26,007
3
2
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NAICS
Codes
NAICS
Description
Toi;il (I-.mire Indnsln Seelor)
Workers «illi Kele\;inl Occiipiilions
Toi;il
linns
Toliil
I'lsliihlish-
IlK'lKS
Tool
1-1 nip lot ees
A\ er;i}»e
r.iiiploM'os
per
I'lsliihlish-
nienl
Workers in
Relet iinl
Oeeu pil-
lions
()cciip;i-
lioiiiil Non-
l sers
W orkcrs
per Sile
ONI s
per
Sile

Gas
Operations

All NAICS
17,834
21,670
528,907
27
61,695
66,108
3
3
3046 2.3.1.6.4 Occupational Inhalation Exposures - Oil Field Brake Blocks
3047 EPA did not identify any studies that contain exposure data related to asbestos-containing brake blocks
3048 but did identify one published study that contains limited air sampling data for asbestos-containing brake
3049 bands (Stein svag et al. 2007). In the absence of any other exposure data, the limited data provided in
3050 this study were used to estimate exposures to workers from brake block installation, servicing, and
3051 removal. The study references stationary samples of asbestos fibers taken in 1988 from the drilling floor
3052 at an unnamed facility in Norway's offshore petroleum industry. Use of asbestos was generally banned
3053 in Norway in late 1984, but asbestos brake bands were used in the drilling drawworks on some
3054 installations until 1991. The study notes: ".. .the design of the drilling area might have led to migration
3055 of fibers from the brake bands into the drilling cabin or down one floor to the shale shaker area"
3056 ("Steinsvag et al.. 2007).
3057
3058 Stationary samples were taken at two locations: "above brake drum" and "other samples, brake dust."
3059 Reported arithmetic mean concentrations of asbestos fibers for both locations were 0.03 and 0.02
3060 fibers/cc, respectively. However, because the publication does not indicate what activities workers
3061 performed during sample collection, no inferences can be made regarding whether the results pertain to
3062 brake installation, removal, servicing, or repair. The study involved an unknown number of
3063 measurements made over an unknown duration of time. While the study does not identify the sample
3064 collection methods or the fiber counting algorithms, some text suggests that the presence of asbestos in
3065 the samples was confirmed by electron microscope. The study reports the following additional details
3066 about the asbestos content of the brake lining: "The composition of the brake lining was: 41% asbestos,
3067 28% rayon and cotton, 21% binding agent, 9% brass chip" (Steinsvag et al... 2007).
3068
3069 The sample measurements were made over an unknown duration of time, and EPA is assuming
3070 measurements are representative of an 8-hr TWA. EPA assumes the measurements taken above the
3071 brake drum are most relevant to worker exposures, as workers are likely to work nearest the brakes, such
3072 as operating a brake handle to control the speed of the drawworks or replacing the brake blocks. EPA
3073 assumes the other brake dust samples are relevant to ONU exposures as their exact sampling location is
3074 not specified but the arithmetic mean concentration is lower than that of the samples taken above the
3075 brake drum. Since these two results are both arithmetic means, EPA assumed the values were 0.03 and
3076 0.02 fibers/cc for 8-hour TWA, for workers and ONUs, respectively. This study was rated "low" in
3077 systematic review (Steinsvag et al.. 2007).
3078
3079 2.3.1.6.5 Exposure Results for Use in Risk Evaluation - Oil Field Brake
3080 Blocks
3081 The information available to EPA confirms that some brake blocks used in domestic oilfields contain
3082 asbestos, as demonstrated by an SDS provided by a supplier. It is reasonable to assume that wear of the
3083 brake blocks over time will release some asbestos fibers to the workplace air. However, the magnitude
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of these releases and resulting worker exposure levels is not known. In an effort to provide a risk
estimate for this COU, the exposure scenario described in the previous section will be used. Table 2-13
presents the exposure data used for the risk estimates for brake block usage.
Table 2-13. Summary of Asbestos Exposures During Use in Brake Blocks for EPA's Risk
Evaluation
Occupational Kxposure Scenario
8-hr TWA Kxposurc Levels (fibcrs/cc)
Workers
OMs
(on (nil
Tendency
Confidence
Rating
Central
Tendency
Confidence
Rating
Brake Blocks:
8-hr TWA exposure
0.03
Low
0.02
Low
ONU Exposures
EPA has not identified specific data on potential ONU inhalation exposures from brake block use. It is
assumed that ONUs do not directly handle brake blocks and drawworks machineries, and it is also
assumed that drawworks are always used and serviced outdoors close to oil wells. Given the limited
information identified above, the lower of the two reported values in the Norway study will be used to
represent ONU exposures for this COU.
2.3.1.6.6 Data Assumptions, Uncertainties and Level of Confidence
The extent of brake block usage and associated worker exposures are highly uncertain. EPA was not
able to identify the volume of imported asbestos-containing brake blocks, the number of brake blocks
used nationwide, nor the number of workers exposed as a result of installation, removal, and disposal
activities. Further, the study reviewed in this section examined asbestos exposures in 1988 in Norway's
offshore petroleum industry and is of unknown relevance to today's use of oil field brake blocks in the
United States. No other data for brake blocks could be located.
EPA considered the quality and uncertainties of the data to determine a level of confidence for the
assessed inhalation exposures for this condition of use. The primary strength of this assessment is the
use of monitoring data, which is the highest approach of the inhalation exposure assessment approach
hierarchy. However, the monitoring data are limited a single offshore oil platform in Norway in 1988. It
is unknown if these data capture current-day U.S. oil field or offshore platform operations. It is also
unknown if the monitoring data capture the variabilities in the day-to-day operations of the single
offshore platform sampled in the study.
Based on these strengths and limitations of the data, the overall confidence for EPA's assessment of
occupational inhalation exposures for this scenario is low.
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2.3.1.7 Aftermarket Automotive Brakes/Linings and Clutches
The use of asbestos in automotive parts has decreased dramatically in the last 30-40 years. Several
decades ago, virtually all vehicles had at least some asbestos-containing components. Currently,
information indicates asbestos containing automobile components are used in a single vehicle which is
manufactured domestically, but only exported and sold outside of the United States. However, the
potential remains for some older vehicles to have asbestos-containing parts and for foreign-made
aftermarket parts that contain asbestos to be imported and installed by consumers in cars when replacing
brakes or clutches.
EPA is aware of one car manufacturer that imports asbestos-containing automotive friction products for
new vehicles, but those vehicles are then exported and not sold in the United States. This COU is
categorized as "other vehicle friction products" in Table 1-4. of Section 1.4.2 of this risk evaluation.
This section reviews the presence of chrysotile asbestos in aftermarket automotive parts and evaluates
the potential for worker exposure to asbestos. The section focuses on asbestos in light-duty passenger
vehicles, including cars, trucks, and vans.
Note that for occupational exposure for this COU, the use of compressed air as a work practice will not
be considered because, in addition to the EPA current best practice guidance (EPA-747-F-04-004). there
is a provision in the OSHA Asbestos Standard: 29 CFR § 1910.1001(f)(l)(ix): Compressed air shall not
be used to remove asbestos or materials containing asbestos unless the compressed air is used in
conjunction with a ventilation system which effectively captures the dust cloud created by the
compressed air.
2.3.1.7.1 Process Description - Aftermarket Automotive Brakes/Linings and
Clutches
Based on the long history of the use of asbestos in automobile parts, and because aftermarket automotive
parts may still be available for purchase, the Agency believes this COU is still ongoing. Over the past
few decades, automobile weights, driving speeds, safety standards, and applicable environmental
regulations have changed considerably. These and other factors have led to changes in materials of
choice for automobile parts. Asbestos was previously a component of many automobile parts, including
brakes, clutches, gaskets, seam sealants, and exhaust systems (Blake et ai. 2008; kohl et at... 1976); and
older model vehicles still in operation may have various asbestos-containing parts. Additionally,
aftermarket automotive parts made from asbestos can be purchased from online retailers, and it is
possible that such products exist in older stockpiles. This section focuses on asbestos in brakes/linings
and clutches because repairs for these parts - and hence potential occupational exposure to asbestos - are
more likely than repairs for other vehicle components that were known to previously contain asbestos
(e.g., seam sealants). For the purpose of this risk evaluation, EPA generally refers to brakes in the
following sections, but this term also includes brake linings, brake pads, and clutches.
Automobile Brakes
Chrysotile asbestos fibers offer many properties (e.g., heat resistance, flexibility, good tensile strength)
that are desired for brake linings and brake pads (Paustenbach et at... 2004). New automobiles
manufactured in the United States had brake assemblies with asbestos-containing components. For
instance, NIOSH reported in the late 1980s that friction materials in drum brakes typically contained 40
to 50 percent asbestos by weight (OSlj \ 2006). Other researchers reported that some brake components
during these years contained as much as 73 percent asbestos, by weight (Blake et at.. 2003).
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The two primary types of automobile brakes are drum brakes and disc brakes, and chrysotile asbestos
has been found both in linings for drum brake assemblies and pads in disc brake assemblies (see Figure
2-9.). Drum brakes were more prevalent than disc brakes in older vehicles. When the vehicle operator
engages drum brakes, the brake shoes (which contain friction materials) contact the rotating brake drum,
and this contact slows the vehicle. Disc brakes are much more common today than drum brakes, and
they function by applying brake pads (which contain friction materials) to the surface of the revolving
brake disc, and this contact slows the vehicle. Since the mid-1990s, material and design improvements
have led to most cars being manufactured with disc brakes, effectively phasing out drum brakes in
passenger automobiles (Richter et al.. 2009).
Figure 2-9. Illustrations of brake assembly components: (a) a brake lining designed to be used
with an internal drum brake and (b) a brake pad designed for use with a disc brake.
Source: (Paustenbach et al.. 2004).
Rotor
Brake
Lining
Shoe
Shoe
Brake
Pad
Use of asbestos-containing braking systems began to decline in the 1970s due to many factors, including
toxicity concerns, rising insurance costs, regulatory scrutiny, challenges associated with disposing of
asbestos-containing waste, and availability of asbestos-free substitutes (Paustenbach et al.. 2004). In
1989, EPA issued a final rule that banned the manufacturing and importing of many asbestos-containing
products, including automobile brake pads and linings (Federal Register, 1989). While the court
overturned most of this ban in 1991, many manufacturers had already begun to phase out asbestos-
containing materials and develop alternatives, including the non-asbestos organic fibers that are almost
universally used in automobile brake assemblies today (Paustenbach et al.. 2004). By 2000, domestic
manufacturers had eliminated asbestos from virtually all brake assemblies in automobiles (Paustenbach
et al.. 2004). EPA is not aware of any automobile manufacturers that currently use asbestos products in
brake assemblies for U.S. vehicles. In fact, the Agency received verification from five major vehicle
manufacturers that asbestos-containing automotive parts are no longer used and import data has been
misreported under the wrong Harmonized Tariff Schedule (HTS) code. However, the Agency knows of
at least one company that imports asbestos-containing friction products for use in cars assembled in the
U.S., but those vehicles are exported for sale and are not sold domestically. The COU identified for this
scenario is specified as "other vehicle friction products" in Table 1-34, and the exposure values are
based on aftermarket auto brakes (see Section 2.3.1.8).
The history of asbestos in aftermarket brake products has followed a similar pattern. For decades,
asbestos was found in various aftermarket brake replacement parts (e.g., pads, linings, and shoes); but
the same factors listed in the previous paragraph led to a significant decline in the use of asbestos in
aftermarket vehicle friction products. Nonetheless, the literature indicates that asbestos-containing
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replacement brake materials continued to be available from parts suppliers into the 2000s; researchers
were able to purchase these materials in 2008 from a vintage auto parts facility (Madl et at... 2008).
Today, individual consumers can find aftermarket automotive products marketed as containing asbestos
through online retailers.
In more recent years, state laws and regulations have limited sales of asbestos-containing aftermarket
brake parts, even among existing stockpiles. In 2010, for instance, the state of Washington passed its
"Better Brakes Law," which prohibits manufacturers, retailers, wholesalers, and distributors from selling
brake friction material that contains more than 0.1 percent asbestiform fibers (Washington State. 2010).
In the same year, the state of California passed legislation with similar requirements. The not-to-exceed
limit of 0.1 percent asbestiform fibers in aftermarket brake parts now essentially extends nationwide,
due to a memorandum of understanding between EPA and multiple industry stakeholders (e.g., Motor
and Equipment Manufacturers Association, Automotive Aftermarket Suppliers Association, Brake
Manufacturers Council) (U.S. EPA. 2015).
Despite this trend, asbestos in automotive parts is not banned at the federal level, and foreign suppliers
face no restrictions (other than those currently in place in the states of California and Washington) when
selling asbestos-containing brake products to business establishments and individuals in the United
States. The Motor and Equipment Manufacturers Association informed EPA that approximately $2.2
million of asbestos-containing brake materials were imported into the United States in 2014 (MEMA,
2.016). In 2018, the U.S. Geological Survey indicated that "an unknown quantity of asbestos was
imported within manufactured products," such as brake linings (LISGS. 2019).
Based on this context, asbestos is currently found in automobile brakes in the United States due to two
reasons: (1) vehicles on the road may have asbestos-containing brakes, whether from original
manufacturers (primarily for older and vintage vehicles) or aftermarket parts; and (2) vehicles may have
new asbestos-containing brakes installed by establishments or individuals that use certain imported
products.
Automobile Clutches
In a manual transmission automobile, which currently accounts for less than 5 percent of automobiles
sold in the United States, the clutch transfers power generated by the engine to the drive train. The
schematic in Figure 2-10. shows a typical clutch assembly. Because it lies at the interface between two
rotating metallic surfaces, the clutch disc typically contains friction materials. Decades ago, the friction
material of choice was chrysotile asbestos, which previously accounted for between 30 and 60 percent of
the friction material in clutch discs (Jiang et ai. 2008).
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Transmission
Clutch Disc
Pressure Plate Flywheel Engine
Figure 2-10. Schematic of a clutch assembly. The clutch disc is made of friction material, which
may contain asbestos.
Source: (Jiang et al.. 2008).
Consistent with the history for brakes, friction materials in clutches moved from asbestos-containing to
asbestos-free designs over recent decades. By the 1980s, automobile manufacturers began using various
asbestos-free substitutes in clutch assemblies (Jiang et al.. 2008); and by 2000, most automobiles in the
United States were no longer made with asbestos-containing clutches (Cohen and Van Orden, 2008).
However, aftermarket clutch parts may contain asbestos. As evidence of this, Jiang et al. (2008) reported
purchasing 27 boxes of asbestos-containing clutch discs that had been stockpiled at a parts warehouse
(Jiang et al.. 2008). suggesting that stockpiles of previously manufactured asbestos-containing clutch
assemblies could be available.
Asbestos-containing aftermarket clutches may be found as imports from foreign suppliers, although the
extent to which this occurs is not known. No barriers currently exist to these imports, as asbestos in
automotive clutches is not banned at the federal level and the brake laws passed in 2010 in the state of
California and the state of Washington do not apply to clutches.
2.3.1.7.2 Worker Activities - Aftermarket Automotive Brakes/Linings and
Clutches
This section describes worker activities for repair and replacement of both brakes and clutches,
including the types of dust control measures that are typically used. For both types of parts, asbestos
exposure may occur during removal and disposal of used parts, while cleaning the assemblies, and
during handling and installation of new parts.
Automobile Brake Repair and Replacement
For both drum brakes and disc brakes, maintenance, repair, inspection, and replacement jobs typically
involve several basic steps. Workers first need access to the brake assembly, which is typically
accomplished by elevating the vehicle and removing the wheel. They then remove dust and debris from
the brake apparatus using methods described below. Replacement or repair of parts follows, during
which workers use various mechanical means to remove old parts and install new ones.
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Two critical issues for exposure assessment are the work practices used to remove dust and debris from
the brake assembly and the asbestos content of this material:
1. Work practices for automobile brake repair have changed considerably over the years. In the
1970s, use of compressed air to clean brake surfaces was commonplace (RoM et ai. 1976).
While effective at quickly preparing surfaces for repair, this practice caused brake dust and other
material to become airborne, leading to potential asbestos exposures among workers and ONUs.
The practice also caused asbestos-containing dust to settle at locations throughout the workplace,
which became a source of future exposure.
Concerns about asbestos exposure during brake repair led NIOSH to perform a series of
industrial hygiene evaluations in the late 1980s to investigate the effectiveness of different dust
control strategies. Based on the results of these studies and other factors, OSHA amended its
asbestos standard in 1994 to require workers performing brake repair and replacement tasks to
control dusts (Federal Register, 1994). OSHA's standard established acceptable work practices
for brake and clutch repair, with the extent of controls depending on the number of jobs
performed per week. Examples of acceptable work practices for brake dust removal include: use
of a negative pressure enclosure equipped with a HEPA-filtered vacuum, use of low-pressure wet
cleaning methods, and use of wet wipe methods (Federal Register, 1994). This regulation is an
important consideration for interpreting worker exposure studies because observed exposure
levels prior to promulgation of OSHA's amended asbestos standard may not be representative of
exposures at establishments that currently comply with OSHA requirements.
2. The second important consideration for exposure assessment is the asbestos content in brake
dust. Due to the high friction environment in vehicle braking, asbestos fibers in the brake
material degrade both chemically and physically. While brake linings and pads at installation
may contain between 40 and 50 percent chrysotile asbestos (i.e., fibers longer than 5
micrometers) (OSHA. 2006). brake dust is largely made up of particles and fibrous structures
less than 5 micrometers in length, which would no longer be measured as asbestos by PCM. In
1989, NIOSH reviewed brake dust sampling data and concluded "the vast majority of samples"
reviewed contained less than 5 percent asbestos (OSHA. 2006). Other researchers have reported
lower values, indicating that brake dust typically contains less than 1 percent asbestos
(Paustenbach et ai. 2003). This wearing and degradation of asbestos in brake parts must be
considered when assessing worker exposures.
The amount of time that workers repair and replace automobile brakes depends on many factors. The
literature suggests that a typical "brake job" for a single vehicle takes between 1 and 2 hours
(Paustenbach et ai. 2003). While most automotive mechanics perform various repair tasks, some
specialized mechanics work exclusively on brakes. The literature also suggests that the number of brake
repair jobs performed by automotive service technicians and mechanics range from 2 to 40 per week
(Madl et ai. 2008).
Automobile Clutch Repair and Replacement
Repairing and replacing asbestos-containing clutch assemblies could also result in asbestos exposure.
Workers typically elevate vehicles to access the clutch assembly, remove dust and debris, and perform
repair and replacement tasks accordingly. Like asbestos in brakes, asbestos in clutch discs degrades with
use. (Cohen and Van Orden. 2008) evaluated clutch assemblies from a vehicle salvage yard and found
that clutch plates, on average, contained 43 percent asbestos, while the dust and debris in clutch
housings, on average, contained 0.1 percent asbestos (Cohen and Van Orden. 2008).
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However, clutch repair and replacement differ from brake work in two important ways. First, clutches
generally do not need to be repaired as frequently. By estimates made in 2008, clutches typically last
three times longer than brake linings (Cohen and Van Orden. 2008). Second, a common clutch repair
method is to remove and replace the entire clutch assembly, rather than replacing the clutch disc
component (Cohen and Van Orden. 2008). These two factors likely result in clutch repair asbestos
exposures being lower than comparable brake repair asbestos exposures.
2.3.1.7.3 Number of Sites and Potentially Exposed Workers - Aftermarket
Automotive Brakes/Linings and Clutches
EPA considered several data sources when estimating the number of workers directly exposed to
asbestos when working with aftermarket automotive products. In the late 1980s, NIOSH conducted a
series of industrial hygiene surveys on brake repair facilities, and the Agency estimated that 155,000
brake mechanics and garage workers in the United States were potentially exposed to asbestos (OSHA.
2.006). In 1994, OSHA estimated as part of its updated asbestos rulemaking that 676,000 workers
performed automotive repair activities, and these workers were found in 329,000 establishments (i.e.,
approximately two workers per establishment) (Federal Register, 1994). EPA considers the best current
estimate of this worker population to be from the Bureau of Labor Statistics, which estimates that
749,900 workers in the United States were employed as automotive service technicians and mechanics
in 2016 (U.S. BLS. ). This includes workers at automotive repair and maintenance shops,
automobile dealers, gasoline stations, and automotive parts and accessories stores.
ONU exposures associated with automotive repair work are expected to occur because automotive repair
and maintenance tasks often take place in large open bays with multiple concurrent activities. EPA did
not locate published estimates for the number of ONUs for this COU. However, consistent with the
industry profile statistics from OSHA's 1994 rulemaking, EPA assumes that automotive repair
establishments, on average, have two workers who perform automotive repair activities. Accordingly,
EPA estimates that this COU has 749,900 ONUs.
2.3.1.7.4 Occupational Inhalation Exposures - Aftermarket Automotive
Brakes/Linings and Clutches
To identify relevant occupational inhalation exposure data, EPA reviewed reasonably available
information from OSHA, NIOSH, and other literature. All research steps are documented below, with
more detailed discussion on the most relevant data sources, which EPA determined to be the post-1980
studies conducted by NIOSH and the post-1980 publications in the peer-reviewed literature.
Automobile Brake Repair and Replacement
EPA first considered worker exposure data from OSHA compliance inspections. EPA reviewed data that
OSHA provided for 2011 to 2016 inspections, but these data did not include any PBZ asbestos
measurements for the automotive repair and maintenance industry. For additional insights into OSHA
sampling results, EPA considered the findings published by Cowan et al. (2015). These authors
summarized OSHA workplace compliance measurements from 1984 to 2011, which included 394 PBZ
samples obtained from workers at automotive repair, services, and parking facilities (Cowan et al..
2015). Because the samples were taken for compliance purposes, all measurements were presumably
made using OSHA-approved methods (i.e., PCM analyses of filters). Table 2-14. summarizes these data,
which suggest that asbestos exposures for this COU decreased from the mid-1980s to 2011.
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Table 2-14. PBZ Asbestos Concentrations Measured by OSHA for Workers at Automotive Repair,
Services, and Parking Facilities

.Number of
Number of
Uange of Delected
l ime l-'rame
Number of
Samples
Samples Non-
Deled for
Samples with
Detected
Asbestos
Concentrations

Asbestos
Asbestos
(fibers/cc)
1984-1989
274
241
33
0.0031 -35.6
1990-1999
101
101
0
N/A
2000-2009
17
17
0
N/A
2010-2011
2
2
0
N/A
Total
394
361
33
0.0031 -35.6
Notes: Data from (Cowan et at.. 2015).
Data are personal breathing zone (PBZ) concentrations of unknown duration.
EPA then considered relevant NIOSH publications, focusing on those published since 1980, because
earlier publications evaluated work practices (e.g., compressed air blowdown of brake dust) that are no
longer permitted. Specifically, EPA considered five NIOSH in-depth survey reports published in 1987
and 1988 (Cooper et at.. 1988. 1987; Godbev et al. 1987; Sheehy etaL 1987a; Sheehv et at, 1987b)
and a 1989 NIOSH publication that reviewed these findings (OSHA. 2.006). The NIOSH studies
investigated PBZ asbestos exposures among workers who employed various dust removal methods
while servicing brakes. These methods included use of vacuum enclosures, HEPA-filtered vacuums, wet
brushing, and aerosol sprays. In three of the NIOSH studies, the average (arithmetic mean) asbestos
concentration over the 2-hour duration of brake repair jobs was below the detection limit (0.004
fibers/cc). The other two studies reported average (arithmetic mean) asbestos concentrations over the
brake job duration of 0.006 fibers/cc and 0.007 fibers/cc. NIOSH's summary of the five studies
concluded that "exposures can be minimal" provided workers use proper dust control methods (OSHA.
2.0061
EPA also considered the published literature on asbestos exposures associated with automobile brake
repair. This review focused on post-1980 publications that reported original asbestos PBZ measurements
for business establishments in the United States. Three publications met these criteria (all were given a
high rating in the data evaluation; see supplemental file (U.S. EPA. 2019D):
• The first study was published in 2003, but it evaluated asbestos exposure for brake repair jobs
conducted on vehicles with model years 1965-1968. The study considered work practices
commonly used during the 1960s, such as compressed air blowdowns and arc grinding and
sanding of surfaces (Blake et al... 2003). PBZ samples were collected during seven test runs, and
measured asbestos concentrations ranged from 0.0146 fibers/cc to 0.4368 fibers/cc, with the
highest level observed during arc grinding operations. This range of measurements was for
sample durations ranging from 30 minutes to 107 minutes. These observations were considered
in the occupational exposure evaluation even though they likely represent an upper-bound
estimate of today's exposures.
• The second study, conducted in 2008, measured worker asbestos exposure during the unpacking
and repacking of boxes of asbestos-containing brake pads and brake shoes (Madl et al.. 2008).
The asbestos-containing brake materials were originally manufactured for 1970-era automobiles,
and the authors obtained the materials from vintage parts suppliers and repair facilities. The
study evaluated how exposure varied with several parameters, including type of brake material
(e.g., drum, shoe) and worker activity (e.g., packing, unpacking, cleaning). The range of personal
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breathing zone concentrations observed across 70 short-term samples was 0.032 fibers/cc to
0.836 fibers/cc, with the highest exposure associated with unpacking and packing 16 boxes of
asbestos-containing brake pads over approximately 30 minutes. EPA used bystander
measurements from this study to assess ONU exposures for this COU.
• The third study examined asbestos exposures during brake repair operations, considering various
worker activities (Weir et al. 2001). EPA did not use this study's measurements in the
occupational exposure evaluation because the publication lacked details necessary for a thorough
review. For instance, this study (in contrast to all others considered) did not report on the
complete data set, the time-weighted average exposure values did not include an exposure
duration, and the TEM metrics were qualitative and vague. For these and other reasons, the study
was considered for contextual information, but not quantitatively in the exposure assessment.
Automobile Clutch Repair and Replacement
EPA considered the same automotive brake repair and replacement information sources when assessing
asbestos exposure during automobile clutch repair and replacement but did not identify relevant data
from OSHA monitoring data or NIOSH publications. EPA identified three peer-reviewed publications
(Blake et al.. 2008; Cohen and Van Orden. 2008; Jiang et al.. 2008) that measured worker asbestos
exposure during automotive clutch repair. Though the clutch repair data are limited in comparison to
brake repair exposure data, the three studies suggest that worker asbestos exposure while repairing or
replacing asbestos-containing clutches are lower than corresponding exposures for brake repair and
replacement activity. As noted earlier, EPA used the available brake repair data as its basis for deriving
exposure estimates for the entire COU of working with aftermarket automotive parts.
2.3.1.7.5 Exposure Data for Use in Risk Evaluation - Aftermarket Auto
Brakes/Linings and Clutches
Table 2-15. presents the asbestos exposure data that EPA used in the risk evaluation for working with
asbestos-containing aftermarket automotive parts. EPA's basis for selecting the data points appears after
the table.
Table 2-15. Summary of Asbestos Exposures During Replacement of Aftermarket Automotive
Parts Used in EPA's Risk Evaluation

Kxposure Levels (fibers/cc)
Occupational
Workers
OMs
Kxposure Scenario
(on (nil
Tendency
High-end
Confidence
Rating
(cnl nil
Tendency
High-end
Confidence
Rating
Repairing or replacing
brakes with asbestos-

Medium

Medium
containing aftermarket
0.006
0.094

0.0007
0.011

automotive parts: 8-hour

TWA exposure

Repairing or replacing
brakes with asbestos-

Medium

Medium
containing aftermarket
0.006
0.836

0.0007
0.100

automotive parts: short-

term exposure

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Worker Exposures
• The central tendency short-term TWA exposure value for workers is based on the seven studies
found to include relevant measurements (Madl et at.. 2008; Blake et at.. 2003; Cooper et at..
1988. 1987; Godbev etal. 1987; Sheehv et A i^7a; Sheehv ^ .1 l - 7b). For each study,
EPA identified the central tendency short-term exposure, which was either reported by the
authors or inferred from the range of data points, and the value in Table 2-15. (0.006 fibers/cc) is
the median of those central tendencies. Most of the studies selected for review do not present 8-
hour TWA exposure values. They instead typically report "brake job TWA exposures"—or
exposures that occur over the duration of a single brake repair activity. EPA selected a central
tendency 8-hour TWA exposure value for workers (0.006 fibers/cc) by assuming the median
short-term exposure level could persist for an entire workday. This is a reasonable assumption
for full-time brake repair mechanics, who may conduct 40 brake repair jobs per week, and a
protective assumption for automotive mechanics who do not repair brakes throughout their
shifts.
• The high-end short-term TWA exposure value for workers (0.836 fibers/cc) is the highest short-
term personal breathing zone observation among the seven studies that met the review criteria
(Madl et at.. 2008). The high-end 8-hour exposure value for workers (0.094 fibers/cc) is based on
a study (Blake et at.. 2003) that used arc grinding during brake repair with no exposure controls,
which is a representation of a high-end exposure scenario of today's work practices.
ONU Exposures
EPA has not identified data on potential ONU inhalation exposures from after-market auto brake
scenarios. ONUs do not directly handle brakes and the ONU exposure estimates in Table 2-15. were
generated by assuming that asbestos concentrations decreased by a factor of 8.4 between the worker
location and the ONU location. EPA derived this reduction factor from a publication (Madl et at.. 2008)
that had concurrent worker and bystander exposure measurements where the bystander was
approximately 5 feet from the worker. The value of 8.4 is the average concentration reduction across
four concurrent sampling events.
2.3.1.7.6 Data Assumptions, Uncertainties and Level of Confidence
The universe of automotive repair establishments in the United States is expected to have large
variability in the determinants of exposure to asbestos during brake repair. These exposure determinants
include, but are not limited to, vehicle age, type of brake assembly (disc vs. drum), asbestos content of
used and replacement parts, dust control measures used, number of vehicles serviced per day, and
duration of individual repair jobs. It is uncertain if the studies EPA cited for exposure data fully capture
the distribution of determinants of exposure of current automotive brake jobs, and some of the studies
reviewed for this draft risk evaluation are based on practices that are not widely used today.
PCM-based personal exposure measurement in an automotive repair facility may overstate asbestos
exposures, which some studies have demonstrated through TEM analyses of filter samples (Blake et at..
2003; Weir et at... 2001). PCM measurements are based entirely on dimensional criteria and do not
confirm the presence of asbestos, as can be done through supplemental analyses by TEM or another
confirmatory method. Automotive repair facilities involve many machining operations that can release
non-asbestos airborne fibers, such as cellulose fibers from brushes and metal and plastic fragments from
body repair (Blake et at.. 2008).
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EPA considered the quality and uncertainties of the data to determine a level of confidence for the
assessed inhalation exposures for this condition of use. The primary strength of this assessment is the
use of monitoring data, which is the highest approach of the inhalation exposure assessment approach
hierarchy. The overall confidence ratings from systematic review for these data were high. The
monitoring data were all collected from U.S.-based vehicular maintenance and repair shops. While these
studies were conducted after the implementation of the OSHA rule, many of the studies were conducted
in the late 1980s and may not be representative of current operations.
Based on these strengths and limitations of the data, the overall confidence for EPA's assessment of
occupational inhalation exposures for this scenario is medium.
2.3,1,8 Other Vehicle Friction Products
While EPA has verified that U.S. automotive manufacturers are not installing asbestos brakes on new
cars for domestic distribution, EPA has identified a company that is importing asbestos-containing
brakes and installing them in their cars in the United States. These cars are exported and not sold
domestically.
In addition, there is a limited use of asbestos-containing brakes for a special, large transport plane (the
"Super-Guppy") by the National Aeronautics and Space Administration (NASA) that EPA has recently
learned about. In this public draft risk evaluation, EPA is providing preliminary information for public
input and the information is provided in a brief format.
2.3.1.8.1 Installing New Brakes on New Cars for Export Only
EPA did not identify any studies that contain exposure data related to installation of asbestos-containing
brakes from an Original Equipment Manufacturer (OEM). As a result, the exposure assessment
approach used for the aftermarket automotive brakes/linings and clutches described in Section 2.3.1.7
was also used for this COU and is reported here in Table 2-16.
Most, if not all, of the literature that EPA reviewed pertained to servicing vehicles that were already
equipped with asbestos-containing brakes and clutches; requiring the removal of asbestos-containing
parts and installing non-asbestos-containing replacement parts. When removing an asbestos-containing
part, one of the main sources of exposure is the dust and debris that must be removed from the brake
housing, which is not the case for installing OEM asbestos-containing components on new vehicles.
Therefore, the aftermarket auto brakes/linings and clutches exposure value used to assess this COU may
be an overestimate. The actual exposure for OEM installation is likely to be lower.
Table 2-16. Other Vehicle Friction Products Exposure Levels (from Aftermarket Automotive
Occupational
l-.xposure
Scenario

Kxposurc 1.
e\ els (fihers/cc)

Workers
OMs
Central
Tendency
Nigh-end
Confidence
Ualing
Cent nil
Tendency
Nigh-end
Confidence
Ualing
Installing brakes

with asbestos-

containing
automotive parts:
0.006
0.094
Low
0.0007
0.011
Low
8-hour TWA

exposure

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Installing brakes
with asbestos-
containing
automotive parts:
short-term
exposure
0.006
0.836
Low
0.0007
0.100
Low
Data Assumptions. Uncertainties and Level of Confidence
The assumptions and uncertainties described above under Section 2.3.1.7 apply here. In addition, the
procedure for installing asbestos containing brakes/friction products into a new vehicle does not involve
removing of old asbestos-containing brakes/friction products. Thus, the actual exposure is likely to be
much lower than estimated here.
Based on these strengths and limitations of the underlying data described above and in Section 2.3.1.7,
the overall confidence for EPA's assessment of occupational inhalation exposures for this scenario is
low.
2.3.1.8.2 Use of Brakes/Frictional Products for a Single, Larg Transport
Vehicle (NASA Super-Guppy)
This section evaluates asbestos exposures associated with brake block replacement for the Super Guppy
Turbine (SGT) aircraft, which is operated by the National Aeronautics and Space Administration
(NASA). The SGT aircraft (Figure 2-11) is a specialty cargo plane that transports oversized equipment,
and it is considered a mission-critical vehicle (NASA. 2020b). The aircraft brake blocks contain
chrysotile asbestos, and this section evaluates potential worker exposures associated with servicing the
brakes. All observations in this section are based on information provided by NASA.
Figure 2-11. NASA Super Guppy Turbine Aircraft
Photograph courtesy of NASA
Aircraft and Brake Description
Only one SGT aircraft is in operation today, and NASA acquired it in 1997. The SGT aircraft averages
approximately 100 flights per year (NASA. 2020a). When not in use, it is hangered at the NASA
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Aircraft Operating Division's (AOD) El Paso Forward Operating Location in El Paso, Texas. This is
also where the aircraft is serviced (NASA 2020b).
The SGT aircraft has eight landing gear systems, and each system has 32 brake blocks. The individual
blocks (Figure 2-12) contain 43 percent chrysotile asbestos; and they are 4 inches long, 4 inches wide,
and 1 inch thick ( -IASA, 2020b). Each brake block weighs approximately 12.5 ounces.
Figure 2-12. Brakes for NASA Super Guppy Turbine Aircraft
Photograph courtesy of NASA
Worker Activities
Replacing asbestos-containing brake blocks is the principal worker activity potentially associated with
asbestos exposure, and this task is performed by four certified technicians. According to NASA, the
brake blocks are not replaced due to excessive wear; rather, they are typically replaced because they
have become separated from the brake system or because they have become covered with hydraulic
fluid or other substances (NASA, 2020a). This is an important observation, because in EPA's judgment,
worn brake blocks would be more likely to contain dusts to which workers would be exposed.
In materials provided to EPA, NASA described the process by which workers replace brake blocks. This
process begins by removing the brakes from the landing gear. To do so, the SGT aircraft is raised at the
axle pads, and the landing gear is opened to allow workers access to the individual brake systems. The
workers remove the brakes from the aircraft and clean the brakes at an outdoor wash facility.
The certified technicians then take the breaks into a ventilated walk-in booth (Figure 2-13), which is
where brake block replacement occurs. According to a NASA job hazard analysis, workers use wet
methods to control release of asbestos dust during this task (NASA. 2020a). The workers use spray
bottles containing a soap-water mixture to keep exposed surfaces damp when replacing brake blocks.
Waste dusts generated during this activity are collected using a high-efficiency particulate air vacuum;
and all asbestos-containing wastes, including vacuumed waste, are double-bagged (NASA Occupational
Flealth. 2020) and disposed of according to waste management regulations for asbestos (NASA. 2020b).
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Figure 2-13. Ventilated Walk-in Booth Where Brakes Pads Are Replaced
Photograph courtesy of NASA
The four certified technicians for SGT aircraft brake replacement receive annual training on asbestos.
The training course addresses asbestos health hazards, work practices to reduce generation of airborne
asbestos dust, and information on how PPE can reduce exposures (NASA Occupational Health. 2020).
The training also indicates that brake replacement workers who follow proper methods for controlling
asbestos dust releases are not required to use respiratory protection (NASA Occupational Health. 2020).
Respirator usage is also not required because measured exposures were below applicable occupational
exposure limits (NASA 2020a). Despite respiratory protection not being required, NASA informed
EPA that some certified technicians choose to use half mask air-purifying respirator with P-100
particulate filters when replacing brake blocks (NASA 2020a).
Brake pad replacement for the one SGT aircraft occurs infrequently, approximately four times per year
(NASA 2020a). According to NASA, the four certified technicians who service the aircraft spend
approximately 12 hours per year replacing brake pads.
Number of Sites and Potentially Exposed Workers
Brake pad replacement for the SGT aircraft occurs at only one site nationwide: a NASA facility located
in El Paso, Texas (NASA. 2020b).
Over the course of a year, only four certified technicians at this location perform brake pad replacement;
and one or two of these technicians will perform individual brake pad replacements (NASA, 2020b).
Because the brake replacement work occurs in a ventilated walk-in booth, asbestos fibers likely are not
released into the general workspace where ONUs may be exposed.
Therefore, for this conditi on of use, EPA assumes four workers may be exposed, and no ONUs are
exposed.
Worker Inhalation Exposures
EPA's estimate of occupational inhalation exposures for this condition of use are based on five worker
exposure samples that NASA collected in 2014 (NASA. 2020a). The sampling was conducted according
to NIOSH Method 7400, and asbestos was not found above the detection limit in any of the samples.
EPA estimated worker exposure levels for the risk evaluation as follows:
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¦ Three of the five sampling results that NASA provided were labeled as "8-hour TWA"
observations, and EPA considered these to be representative of full shift exposures. The three
results for this exposure duration were: <0.003 fibers/cc, <0.006 fibers/cc, and <0.0089 fibers/cc
(NASA. 2.02.0a). To calculate the central tendency for full shift exposure, EPA replaced the three
observations with one-half the detection limit and calculated the arithmetic mean of those three
value. By this approach, EPA calculated a central tendency concentration of <0.003 fibers/cc.
For the high-end full shift exposure estimate, EPA used the highest detection limit across the
three samples.
¦ Two of the five sampling results that NASA provided were labeled as being evaluated for "30-
minute excursion limits"; and EPA considered these to be representative of short-term exposures.
The two results, based on sampling durations of 30 and 35 minutes, were: <0.044 fibers/cc and
<0.045 fibers/cc. Following the same approach that was used for full shift exposures, EPA
estimated a central tendency short-term exposure of <0.022 fibers/cc and a high-end short-term
exposure of <0.045 fibers/cc.
Based on these assumptions, EPA will use these exposure values in this risk evaluaton:
Full Shift: Central Tendency - <0.003 f/cc
Full Shift: High-End - <0.0089 f/cc
Short-Term: Central Tendency - <0.022 f/cc
Short-Term: High-End - <0.045 f/cc
EPA assigned a confidence rating of "high" for these exposure data. This rating was based on the fact
that monitoring data are available from the one site where this condition of use occurs. Further,
replacement of SGT aircraft brake blocks occurs approximately 12 hours per year, and the five available
sampling events spanned more than 4 hours. Therefore, the available data, which were collected using
an appropriate NIOSH method, represent almost one-third of the worker activity over an entire calendar
year. The spatial and temporal coverage of these data are greater than those for any other condition of
use in this risk evaluation.
ONI I Inhalation Exposures
As noted previously, EPA assumes no ONU exposures occur, because the worker activity with the
highest likelihood of releasing asbestos occurs in a walk-in ventilated booth, where ONUs are not
present.
2,3,1,9 Other Gaskets-Utility Vehicles (UTVs)
2.3.1.9.1 Process Description - UTV Gasket installation/Servicing
EPA has identified the use of asbestos-containing gaskets in the exhaust system of a specific type of
utility vehicle available for purchase in the United States. This COU is identified as "other gaskets" in
Table 1-4. of Section 1.4.2. It is known that these UTVs are manufactured in the United States, so EPA
expects that there is potential for exposures to workers who install the gaskets during assembly and
workers who may repair these vehicles.
To derive occupational exposure values for this risk evaluation, EPA is drawing on a review of several
studies in the literature which characterize exposure scenarios from asbestos-containing gasket
replacement in different types of vehicles.
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2.3.1.9.2 Worker Activities - UTV Gasket Installation/Servicing
The UTV manufacturers receive the pre-cut gaskets which are then installed during manufacture of the
UTV. The gaskets may be removed during servicing of the exhaust system.
Thirty studies relating to gasket repair/replacement were identified and reviewed as part of the
systematic review process for the consumer exposure scenario (see Section 2.3.2.2); resulting in
identifying three studies as being relevant to gasket installation and replacement in vehicles (see Table
2-29).
2.3.1.9.3 Number of Sites and Potentially Exposed Workers - UTV Gasket
Installation/Servicing
EPA estimated the number of UTV service technicians and mechanics potentially exposed to asbestos
by assuming that asbestos-containing gaskets are most likely to be replaced at UTV dealerships that sell
these vehicles.8 However, no NAICS codes are specific to UTV dealers. These establishments are
classified under the 4-digit NAICS 4412, "Other Motor Vehicle Dealers." Table 2-17. lists the specific
industries included in that 4-digit NAICS. The industry most relevant to UTV dealers is the 7-digit
NAICS code 4412281, "Motorcycle, ATV, and personal watercraft dealers." The 2012 Economic
Census reports 6,999 establishments in this industry.
Table 2-17. Number of Other Motor Vehicle Dealers
2012 NAICS code
2012 NAICS Code Description
Number of
Kslahlishmcnls
4412
Other motor vehicle dealers
14,249
44121
Recreational vehicle dealers
2,605
441222
Boat dealers
4,645
441228
Motorcycle, ATV, and all other motor vehicle dealers
6,999
4412281
Motorcycle, ATV, and personal watercraft dealers
5,098
4412282
All other motor vehicle dealers
1,901
Source: (U.S. Census Bureau., 2016a).
The Economic Census also reports the product and service line statistics for retail establishments down
to the 6-digit NAICS code level. Product and service code 20593 represents "All-terrain vehicles
(ATVs) and personal watercraft." Out of the 6,999 establishments in the 6-digit NAICS code 441228,
Table 2-18. shows that 2,989 of them deal in ATVs and personal watercraft. For purposes of this
assessment, EPA assumes that approximately half of them (1,500 establishments, see Table 2-18.) sell
and repair UTVs and ATVs, and that the other half specialize in personal watercraft.
8 While UTV owners may have their vehicles serviced at repair and maintenance shops that are not part of dealerships, the
total number of sites and workers exposed may not necessarily change from the estimates in this analysis. More vehicles
being repaired in other types of repair shops would mean fewer vehicles being repaired (and fewer workers exposed) in
dealerships. This analysis simplifies the estimates by assuming that engine repairs all occur at dealerships.
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Table 2-18. Number of ATV and Watercraft Dealers in NA
ICS 44128
2012 NAICS
Code
2012 NAICS Code
Description
Products
and
Services
Code
Products and
Services Code
Description
Number of
Establishments
441228
Motorcycle, ATV,
and all other motor
vehicle dealers
20593
All-terrain vehicles
(ATVs) & personal
watercraft
2,989
Source: ("U.S. Census Bureau, 2016b).
Table 2-19. Estimated Number of UTV Dealers

Description
Number of Establishments
Estimated number of dealerships repairing and maintaining
UTVs/ATVs
1,500
The next step in estimating potentially exposed workers is to determine the number of workers engaged
in UTV repairs. This number had to be estimated because the Bureau of Labor Statistics does not
provide employment data by occupation forNAICS 4412281 and because Standard Occupational
Classification (SOC) codes are not specific to workers engaged in UTV repairs. Reasonably available
information to estimate potentially exposed workers is SOCs at the 4-digitNAICS level (NAICS 4412),
which includes dealers in recreational vehicles, boats, motorcycles and ATVs. Table 2-20. presents
SOCs that reflect the types of workers that may repair engines and identifies 41,930 workers in relevant
occupations in NAICS 4412.9
Table 2-20. Selected Mechanics and Repair Technicians in NAICS 4412 (Other Motor Vehicle
Dealers)
Occupation (SOC code)
I'liiiploymcnl
First-Line Supervisors of Mechanics, Installers, and Repairers (491011)
4,140
Aircraft Mechanics and Service Technicians (493011)
120
Automotive Service Technicians and Mechanics (493023)
3,360
Motorboat Mechanics and Service Technicians (493051)
9,800
Motorcycle Mechanics (493052)
13,250
9 This count excludes occupations in NAICS 4412 that are less likely to engage in engine repair involving gaskets similar to
those found in UTVs. Thus, Table 4 does not include occupations such as Electrical and Electronic Equipment Mechanics,
Installers, and Repairers (SOC 492000), Automotive Body and Related Repairers (SOC 493021), Mobile Heavy Equipment
Mechanics, Except Engines (SOC 493042), Tire Repairers and Changers (SOC 493093) and Outdoor Power Equipment and
Other Small Engine Mechanics (SOC 493053). The latter covers workers who repair items such as lawn mowers, chain saws,
golf carts, and mobility scooters, which do not generally have engines similar to UTVs.
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Occupation (SOC code)
Kmploymcnt
Recreational Vehicle Service Technicians (493092)
11,260
Total
41,930
Source: (U.S. BLS. 2019).
Based on the estimates for NAICS 4412 in Table 2-17. and Table 2-20., Table 2-21. calculates that
across all entities in NAICS 4412, approximately 3 employees per dealership engage in occupations
potentially relevant to UTV repairs.
Table 2-21. Number of Employees per Establishment in NAICS 4412 in Relevant Occupations
Number of other motor vehicle dealers (NAICS 4412) (see Table 2-17.)
14,429
establishments
Number of mechanics and repair technicians in NAICS 4412 that may repair
engines in recreational vehicles, boats, motorcycles, ATVs, etc. (see Table
2-20.)
41,930 employees
Estimated average number of employees per establishment that may
repair motor vehicle engines (calculated as 41,930 divided by 14,429)
~3 employees per
establishment
Assuming that the average number of mechanic and service technicians across NAICS 4412 is
applicable to NAICS 4412281, Table 2-22. combines the estimate of 1,500 dealerships repairing and
maintaining UTVs/ATVs from Table 2-19. Estimated Number of UTV Dealers with the estimated
average of 3 employees per establishment from Table 2-21. to generate an estimate of 4,500 total
employees that may repair UTV engines.
Table 2-22. Estimated Number of Sites and Employees for UTV Engine Repair
Description
Number of
establishments
Estimated number of dealerships repairing and maintaining L TVs ATYs (see
Table 2-19. Estimated Number of UTV Dealers)
1,500
Estimated average number of employees per establishment that may repair
motor vehicle engines (see Table 2-21.)
3
Estimated total number of employees that may repair UTV
4,500
2.3.1.9.4 Occupational Inhalation Exposures for Use in Risk Evaluation - UTV
Gasket Installation/Servicing
No information from OSHA, NIOSH, or the scientific literature was available on occupational
exposures to asbestos associated with installing and servicing gaskets in UTVs. EPA therefore
considered studies of similar worker exposure scenarios to use as a surrogate. Multiple publications (see
Section 2.3.2.2) report on occupational exposures associated with installing and servicing gaskets in
automobiles. However, EPA located only one study (Paustenbach et al. 2006) that examined exposures
associated with replacing vehicle exhaust systems, which is the UTV component where asbestos-
containing gaskets are found. Therefore, EPA based its occupational inhalation exposure assessment for
UTV gasket installation and servicing on this study.
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Worker Exposures
EPA's estimate of occupational inhalation exposures is based on a 2006 study fPaustenbach et at..
2.006). in which workers at a muffler shop removed exhaust systems from 16 vehicles. The vehicle
model years ranged from 1946 to 1970; and 12 of the 16 vehicles were found to have asbestos in some
combination of the mufflers, manifold gaskets, and exhaust pipe gaskets. The measured asbestos content
in these components ranged from 9.5 to 80.1 percent, with only chrysotile asbestos fibers detected.
The study considered multiple types of exhaust system projects, including removal of different
combinations of mufflers, exhaust pipes, and exhaust manifolds and conversion from single to dual
exhaust systems. The time needed to remove an exhaust system and install a new one lasted up to 4
hours, but workers reportedly spent less than one minute handling or coming into contact with gaskets.
All jobs were performed indoors at the muffler shop, with service bay doors closed, and no other vehicle
repair work occurring at the same time.
Personal breathing zone measurements were taken using sampling materials consistent with NIOSH
Method 7400. Overall, 23 valid personal breathing zone samples were collected from mechanics and
tested with PCM. Some additional samples were taken, but they were overloaded with particulate
material and could not be analyzed. Among the 23 valid samples, 17 were non-detect for asbestos by
PCM analysis; and 6 samples contained asbestos at concentrations up to 0.0505 fibers/cc. The TEM
analyses identified asbestos fibers in 7 of the sampling filters.
Overall, based on the PCM analysis of the 23 valid samples, the study authors reported an average
worker asbestos concentration of 0.024 fibers/cc and a maximum concentration of 0.066 fibers/cc.
(Note: 1) The authors reported an average "PCM-adjusted" concentration that is 18 percent lower than
the un-adjusted result. The adjustment accounts for the amount of fibers confirmed by TEM as being
asbestos. 2) This appears to be a detection level 0.132 f/cc divided by two, contrary to more standard
division by square root of two (approximately 1.4), thus underestimating the maximum concentration.
The average and maximum concentrations pertain to the times when sampling occurred, and sampling
durations ranged from 9 to 65 minutes. The study authors calculated an 8-hour TWA exposure
concentration of 0.01 fibers/cc, based on a worker performing four exhaust system removal tasks in one
shift.
EPA used the personal breathing zone (PBZ) values for the worker as follows: the last row in Table 2-30
shows the maximum concentration calculated from the information within the study (Paustenbaeh et at..
2.006) as the high-end estimated concentration for the worker and the mean concentration calculated
from the information within the study as the central tendency concentration (see Table 2-23 below).
Table 2-23. UTV Gasket Installation/Servicing Exposure Levels for EPA's Risk Evaluation
Occupational
Kxposure
Scenario
S-hr TWA Kxposure l.e\els (fibers/cc)
Asbestos \\ orkcr
OM
Central
Tendency
High-end
Confidence
Killing
Central
Tendency
High-
end
Confidence
Rating
UTV
0.024
0.066
Medium
0.005
0.015
Medium
ONU Exposures
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The same publication (Paustenbach et ai. 2006) includes area sampling results that EPA found
appropriate for ONU exposures (rather than what the paper defines as a bystander). These samples were
collected at breathing zone height at locations near the ends of the muffler shop bays where the exhaust
system work was performed. The area sample durations ranged from 25 to 80 minutes, and these
samples were collected during exhaust system work. Overall, 21 area samples from these locations were
analyzed by PCM; and 16 of these samples were non-detects for asbestos. Among the PCM data from
this subset of area samples, the authors report that the average asbestos concentration was 0.005
fibers/cc and the maximum asbestos concentration was 0.015 fibers/cc. The study authors did not report
8-hour TWA concentrations for the area sample locations. EPA used these average and maximum
asbestos concentrations to characterize ONU exposures.
2.3.1.9.5 Data Assumptions, Uncertainties and Level of Confidence
A principal assumption made in this assessment is that worker asbestos exposures for removing
automobile exhaust systems are representative of worker asbestos exposures associated with installing
and servicing gaskets found in UTV exhaust systems. Further, this assessment assumes that data from
one publication (Paustenbach et at.. 2006) are representative of exposures for this condition of use.
However, the job activities and exposure scenarios considered in the publication differ from the UTV-
related exposures in at least two ways.
First, the publication used in this analysis (Paustenbach et at... 2006) considered older automobiles. This
focus was intentional, because newer vehicles generally do not have asbestos-containing exhaust
systems. However, all vehicles considered in the study were more than 35 years old at the time the
research was published. According to the study, the highest concentrations of asbestos in the removed
gasket was 35.5 to 48.9 percent. It is unclear if the asbestos content in the automobile exhaust systems
from pre-1970 automobiles are representative of the asbestos content in today's UTV exhaust systems.
Second, because the study considered vintage automobiles that presumably contained older parts, it is
likely that the asbestos-containing gaskets in the exhaust systems had worn down with use and time.
These older gaskets presumably would be more prone to release fibrous asbestos into the air, as
compared to newer gaskets (which typically are pre-formed with the asbestos encapsulated in a binding
agent or some other matrix) (Paustenbach et at.. 2006). Therefore, the asbestos concentrations measured
during the study may overstate the concentrations that might occur during UTV exhaust system
servicing.
Additionally, EPA identified two sources of uncertainty pertaining to the data analysis. One pertains to
the uncertainties associated with non-detect observations. For the average worker exposure
concentration, 74 percent of the samples were non-detects; and the study authors replaced these
observations with one-half the detection limit when calculating average concentrations (instead of more
standard division by square root of 2, approximately 1.4). Similarly, for the area sampling results used
for ONU exposures, 76 percent of the samples were non-detects.
Moreover, five of the personal breathing zone samples collected from mechanics had filters overloaded
with particulate, and these samples were not analyzed. The authors noted that the overloaded filters may
have resulted from particulate matter released while mechanics used torches to cut and weld exhaust
pipes; but EPA cannot rule out the possibility that these overloaded filters might have contained elevated
levels of asbestos.
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3840 Based on these strengths and limitations of the data, the overall confidence for EPA's assessment of
3841 occupational inhalation exposures for this scenario is medium.
3842
3843 2.3.1,10 Summary of Inhalation Occupational Exposure Assessment
3844 Table 2-24. summarizes the inhalation exposure estimates for all occupational exposure scenarios.
3845 Where statistics can be calculated, the central tendency estimate represents the 50th percentile exposure
3846 level of the available data set, and the high-end estimate represents the 95th percentile exposure level.
3847 The central tendency and high exposures for ONU are derived separately from workers, often by using a
3848 reduction factor. See the footnotes for an explanation of the concentrations used for each COU.
3849
3850 Table 2-24. Summary of Occupational Inhalation Exposures
Condition of
I se
Duration
Type
n
Central
Tendency
YA Kxposures. fih
(soo loot noles)
Nigh-end
ers/cc
Con fidcncc
Rating
Diaphragms for
Chlor-Alkali
Industry
(Processing and
Use)
Full Shift
Worker
0.0060 (a)
0.036 (a)
High
ONU
0.0025 (b)
<0.008 (b)
High
Short-term
Worker
0.032 (a)
0.35 (a)
Medium
ONU
No data
No data
-
Sheet gaskets -
stamping
(Processing)
Full Shift
Worker
0.014(c)
0.059 (c)
Medium
ONU
0.0024 (d)
0.010 (d)
Medium
Short-term
Worker
0.024 (c)
0.059 (c)
Medium
ONU
0.0042 (d)
0.010 (d)
Medium
Sheet gaskets -
use
Full Shift
Worker
0.026 (e)
0.094 (e)
Medium
ONU
0.005 (d)
0.016 (d)
Medium
Short-term
Worker
No data
No data
-
ONU
No data
No data
-
Oilfield brake
blocks - Use
Full Shift
Worker
0.03 (f)
No data
Low
ONU
0.02 (f)
No data
Low
Short-term
Worker
No data
No data
-
ONU
No data
No data
-
Aftermarket
automotive
brakes/linings,
clutches (Use
and Disposal)
Full Shift
Worker
0.006 (g)
0.094 (g)
Medium
ONU
0.0007 (h)
0.011 (h)
Medium
Short-term
Worker
0.006 (g)
0.836 (g)
Medium
ONU
0.0007 (h)
0.100 (h)
Medium
Other Vehicle
Friction Products
Full Shift
Worker
0.006 (g)
0.094 (g)
Medium
ONU
0.0007 (h)
0.011 (h)
Medium
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Condition of
I sc
(brakes installed
in exported cars)
(Use)
Dursilion
Type
n
Ccnl nil
Tendency
YA Kxposurcs. I'ih
(see loot notes)
lligli-cnd
crs/cc
Con lldence
Killing
Short-term
Worker
0.006 (g)
0.836 (g)
Medium
ONU
0.0007 (h)
0.100 (h)
Medium
Other gaskets -
UTVs (Ue and
Disposal)
Full Shift
Worker
0.024 (i)
0.066 (i)
Low
ONU
0.005 (i)
0.015 (i)
Low
Short-term
Worker
No data
No data
-
ONU
No data
No data
-
(a) Chronic exposure concentrations for the chlor-alkali industry are based on worker exposure monitoring data. Central
tendency concentrations are 50th percentile values and high-end concentrations are 95th percentile values.
(b) Short-term exposure concentrations for the chlor-alkali industry are based on area monitoring data. Central tendency
concentrations are 50th percentile values and high-end concentrations are 95th percentile values.
(c) Concentrations for sheet gasket stampers are based on worker exposure monitoring data (10 samples). For chronic
exposures, central tendency is the single full-shift TWA data point available; and high-end assumes the highest
observed short-term exposure persists over an entire shift. For short-term exposures, central tendency is the median
concentration observed, and high-end is the highest concentration observed.
(d) Concentrations for ONUs at sheet gasket stamping facilities and sheet gasket use facilities were estimated by EPA
using a concentration-decay factor for bystander exposures derived from the literature.
(e) Concentrations for sheet gasket use are based on descriptive statistics provided to EPA of 34 worker exposure
monitoring samples. The central tendency concentration is the arithmetic mean and the high-end concentration is the
highest measured value.
(f) Concentrations for oil field brake blocks are based on two data points—arithmetic mean exposure for different
worker activities—reported in the scientific literature.
(g) Concentrations for aftermarket automotive parts are based on worker exposure monitoring data documented in seven
studies. For chronic exposures, the central tendency concentration is the median of the arithmetic mean exposure
values reported across the seven studies; and the high-end concentration is the highest TWA exposure concentration
reported. For short-term exposures, the same data set was used but data were summarized for individual
observations, not the full-shift TWA values.
(h) Concentrations for ONUs at auto repair facilities were estimated by EPA using a concentration-decay factor for
bystander exposures derived from the literature, based on studies of this industry.
(i) Asbestos air measurements from Paustenbach et al., (2006'): Removal and replacement of exhaust system gaskets
from vehicles manufactured before 1974 with original and old exhaust systems.
2.3.2 Consumer Exposures
This section summarizes the data used for estimating consumer inhalation exposures to asbestos for two
potential do-it-yourself (DIY) scenarios: (1) brake repair/replacement and (2) gasket repair/replacement
in Utility Vehicles (UTVs). Specifically, the brake repair/replacement scenario involves repair or
installation of imported aftermarket brake pads (disc brakes) or brake shoes (drum brakes) containing
asbestos. The gasket repair/replacement in the UTV scenario involves removal or installation of
aftermarket gaskets for UTV exhaust systems containing asbestos. Inhalation exposures are evaluated
for both the individual doing the repair/replacement work and a potential bystander observing the work
within the immediate area. For each scenario, it is assumed that consumers and bystanders will not be
wearing any personal protective equipment. The number of consumers impacted by these COUs is
unknown because the number of products containing asbestos for these COUs is unknown.
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Dermal exposures are not assessed for consumers in this draft risk evaluation. The basis for excluding
this route is the expected state of asbestos being only solid/fiber phase. While asbestos may deposit on
open/unprotected skin, it will not absorb into the body through the protective outer skin layers.
Therefore, a dermal dose resulting from dermal exposure is not expected.
EPA has found no reasonably available information to suggest that asbestos-containing brakes are
manufactured in the United States, and based on stakeholder outreach, the Agency does not believe that
any domestic car manufacturer installs asbestos-containing brakes in new cars sold domestically.10
However, consumers can purchase asbestos-containing brakes as an aftermarket replacement part for
cars as well as asbestos containing gaskets for UTV exhaust systems.
The DIY consumer brake assessment and UTV gasket replacement assessment rely on qualitative and
quantitative data obtained during the data extraction and integration phase of Systematic Review to build
appropriate exposure scenarios and develop quantitative exposure estimates using personal inhalation
monitoring data in both the personal breathing zone and the immediate area of the work. The literature
search resulted in very little information specific to consumer exposures, thus the consumer assessment
relies heavily on the review of occupational data, and best professional judgment. Many of the studies in
existing literature are older (dating back to late 1970s). When possible, EPA used the most recent studies
available and also considered data quality and adequacy of the data. Targeted literature searches were
conducted as appropriate to augment the initial data obtained and to identify supplemental information
such as activity patterns and exposure factors specific to consumers.
2.3.2,1 Consumer Inhalation Exposures of Do-It-Yourself (DIY) Mechanics During
Brake Repair: Approach and Methodology
This consumer assessment addresses potential scenarios in which a DIY consumer installs, repairs or
replaces existing automobile brakes with imported aftermarket brake pads or shoes containing asbestos;
including brake linings and clutches. While peer-reviewed literature indicates much of the asbestos
brake pad or shoe use has been phased out and the majority of existing cars on the road do not have
asbestos brakes (Finlev et at. 2007). asbestos-containing brakes and shoes can still be purchased in the
United States. This scenario evaluates potential consumer inhalation exposure to asbestos during
removal of the old brakes or shoes containing asbestos, cleaning of the brake housing, shoes, and wheel
assembly, as well as installation and grinding of the newly installed brakes or shoes containing asbestos.
Brake repair and replacement typically involve several basic steps. For both drum brakes and disc
brakes, the first step is to access the brake assembly by elevating the vehicle and removing the wheel.
The next step is to remove the old brake pads or shoes followed by cleaning the brake apparatus using
various cleaning equipment such as dry or wet brush, wet rag, brake cleaning fluid, or compressed air.
Although EPA does not recommend the work practice of blowing brakes with compressed air (U.S.
37), there is insufficient information indicating such practice has been fully discontinued by the
consumer. After the brake apparatus is cleaned, new pads or shoes are installed. In some situations,
installation of new pads may require additional work such as brake shoe arc grinding. This additional
work may be more likely when consumers are working on vintage vehicles and brake shoes do not fit
exactly inside the brake drum.
10 EPA is aware of one car manufacturer who imports asbestos-containing automotive friction products for new vehicles, but
those vehicles are then exported and not sold in the United States.
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Systematic review of the reasonably available literature on brake repair and replacement resulted in
insufficient inhalation personal/area monitoring studies specifically for DIY consumer brake repair.
Therefore, the DIY brake repair/replacement exposure assessment uses surrogate monitoring data from
occupational brake repair studies. EPA recognizes that brake repair/replacement by a professional
mechanic may involve the use of different equipment and procedures. Consumer exposure during DIY
brake repair is expected to differ from occupational brake repair in four ways ("Versar. 1987): (1)
consumers generally do not have a fully equipped professional garage to perform auto repairs (in some
cases, the repairs would occur in an enclosed garage); (2) consumers would not wear respirators,
mitigate dust emissions, or have available the professional equipment found in commercial repair shops;
(3) consumers have limited experience, and thus the time required to make repairs would be longer; and
(4) consumers are unlikely to perform more than one brake job per year and it was assumed that only
one consumer would perform the task of replacing asbestos brakes or shoes. Considering the expected
differences between brake repair/replacement work conducted by a professional mechanic and a DIY
consumer, EPA identified several factors to consider during the systematic review process for using
professional mechanic information as a surrogate for the DIY consumer. The goal was to examine the
activity patterns monitored in the various occupational studies and only select those studies which are
expected to represent a DIY consumer scenario.
Specifically, EPA only considered activity patterns within the various occupational studies
representative of expected DIY consumer activity patterns and work practices. EPA also considered only
those studies with information related to typical passenger vehicles (automobiles, light duty trucks,
mini-vans, or similar vehicle types); it is not expected that a typical DIY consumer would perform brake
repair/replacement work on heavy duty trucks, tractor trailers, airplanes, or buses. Furthermore,
consideration was given to reasonably available literature which had monitoring data in the personal
breathing zone of the potential DIY consumer and area monitoring within a garage. Lastly, EPA
considered those studies where the work was performed without localized or area engineering controls
as it is unlikely a DIY consumer will have such controls (e.g., capture hoods, roof vents, industrial
exhaust fans baghouses, etc.) within their residential garage.
The following assumptions are used to assess consumer inhalation exposure to asbestos during DIY
brake repairs:
• Location: EPA presents an indoor and an outdoor scenario for brake repair and
replacement work. The indoor scenario assumes the DIY brake repair/replacement is
performed in the consumer's residential garage with the garage door closed. It also
assumes the additional work associated with this brake work is arc grinding and occurs
within the garage with the garage door closed. The outdoor scenario assumes the DIY
brake repair/replacement work is performed in the consumer's residential driveway. It
also assumes the additional work associated with this brake work is brake filing and
occurs in the residential driveway.
• Duration of Activity: Available literature indicates a typical "brake job" for a
professional brake mechanic for a single vehicle takes between one and two hours
(Paustenbach et at. 2003). No data were found in existing literature on the length of
time needed for a DIY consumer to perform a brake job. EPA assumes a consumer
DIY brake repair/replacement event could take twice as long as a professional
mechanic, or about three hours (double the mean of time found in the literature for
professional mechanics).
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• Cleaning methods: EPA assumes, for the indoor scenario, a consumer may use
compressed air to clean brake assemblies since it was historically utilized, is still
readily available to consumers (canned air or air compressor systems), and nothing
prohibits consumers from using compressed air. EPA assumes, for the outdoor
scenario, a consumer does not use compressed air.
• Possible additional work during repair/installation of brakes: EPA assumes a consumer
may perform additional work on brakes, like arc grinding, hand filing, or hand sanding
of brake pads as part of the brake repair/replacement work. EPA assumes the
consumer performs arc grinding for the indoor scenario and assumes the consumer
performs hand filing for the outdoor scenario. Concentrations resulting from brake
work including this additional work is utilized as the high-end estimate for consumer
exposure. The central tendency is based on changing out brakes only with no
additional work.
• Frequency of brake repair jobs: EPA assumes the average consumer performs a single
brake repair/replacement job about once every three years. Brakes in cars and small
trucks are estimated to require replacement approximately every 35,000 to 60,000
miles (Advance Auto Parts, website accessed on November 12, 2018). The three-year
timeline is derived by assuming the need to replace brakes every 35,000 miles, and an
average number of annual miles driven per driver in the United States of 13,476
miles/year ( 2018). This can vary if the consumer has more than one car or
works on vintage cars and that same consumer does all of the brake repair/replacement
work for all cars they own.
• Brake type: EPA assumes exposure to asbestos is similar during the replacement of
disc brake pads and drum brake shoes.
2.3.2.1.1 Consumer Exposure Results - Do-It-Yourself (DIY) Mechanics
During Brake Repair
Utilizing the factors and the assumptions discussed above, EPA identified five relevant studies which
could be applied to the expected DIY consumer brake repair/replacement scenario. These references as
well as the data quality scores are provided in the following table:
Table 2-25. Summary of Studies Satisfying Conditions/Factors for Use in Consumer DIY Brake
Exposure Scenario
Reference
Occupational
Kxposures?
('oiisumcr/DlY
Kxposures?
Data Quality Ualing (Score)
CSheehv etaL 1989)
Yes
Yes
Medium (1.7)
(Blake et al.„ 2003)
Yes
No
Medium (1.8)
(Paustenbach et ai„ 2003)
Yes
No
High (1.0)
(Yeung et al„ 1999)
Yes
No
Medium (2.0)
(Kakooei et )
Yes
No
Medium (2.0)
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Monitoring data from two of the five studies ((Sheefay et at.. 1989) and (Blake et at.. 2003)) were used to
evaluate consumer inhalation exposure to asbestos resulting from brake repair/replacement work. These
studies were U.S. studies which used standard sampling and analysis methods (including both PCM and
TEM analyses) for asbestos. (Sheefay et at.. 1989) provided DIY consumer exposure data for work
conducted outdoors (although limited to two samples). Although professional mechanics were
conducting the brake repair/replacement work in the (Blake et at.. 2003) study, the work practices
utilized by the professional mechanics were comparable to a DIY consumer in that neither engineering
controls nor personal protective equipment were used. The third U.S. study (Paustenbach et at.. 2003)
was a supplemental study used to inform the length of time it takes a DIY consumer to complete brake
repair/replacement work. The final two studies were non-U.S. studies. (Yeiroa et at.. 1999) was a
secondary study and did not provide supplemental/raw data. Additionally, all breathing zone and area
samples from this study were below the PCM detection limits. (Kakooei et at.. 2011) had a limited
description of the exposure scenario and therefore may not be representative of the expected DIY
consumer activity. Neither of these non-US studies will be further described in this risk evaluation.
A brief summary of the two monitoring studies used for this evaluation is provided below.
(Sheehy et at.. 1989) measured air concentrations during servicing of rear brakes on a full-size van. The
work was performed outdoors, on a drive-way, by a DIY consumer. The DIY consumer wet the drum
brake with a spray can solvent to dissolve accumulated grease and dirt. The mechanic then used a garden
hose to flush the surfaces with water. The duration of the monitoring activity was not provided.
(Stake et at.. 2003) measured air concentrations in the personal breathing zone of professional
mechanics performing brake repair/replacement work. (Blake et at.. 2003) evaluated asbestos exposure
for brake repair jobs conducted on passenger vehicles from model years 1965-1968. The study sought to
use tools and practices common to the mid-1960s for cleaning, repairing, and replacing the brakes. In six
separate tests, brake shoe change-outs were conducted on all four wheels of a car which had already
been fitted with new asbestos containing brake shoes and then driven for 1,400 miles prior to the
monitoring. The monitoring began with driving the test car into the service bay and ended upon return
from a test drive after the brake-change out. The total brake change-out monitoring period was 85 to 103
minutes in duration. In general, all tests involved removing the wheel and tire assemblies, followed by
the brake drum. The drum was then placed on the concrete floor creating a shock which broke loose the
brake dust. Each brake assembly was then blown out using compressed shop air. For two baseline tests,
no additional manipulation of the brake shoes (such as filing, sanding, or arc grinding) was conducted.
The remaining four tests involved additional manipulation of the brake shoes as follows:
1) arc grinding of the new shoes to precisely match each shoes' radius to that of its companion
brake drum (n = 2), and
2) sanding to bevel the edges and remove the outermost wear surfaces on each shoe (n=l), and 3)
filing to bevel the square edges of the shoe friction material prior to installation (n=l).
These activities encompassed approximately 12.5 minutes, 4.1 minutes, and 9.7 minutes of the
monitoring period, respectively. An additional test was conducted during cleaning only (sweeping) for a
total of 30 minutes by the mechanic after four brake change test runs. The tests were conducted in a
former automobile repair facility (7 bays, volume of 2,000 m3) with the overhead garage doors closed.
An exhaust fan equipped with a filter was installed 16 meters away from the brake changing area and
operated during all brake changes to ventilate the building. However, smoke testing showed no air
movements toward the exhaust fans suction beyond 8 meters from the fan. PCM and TEM analyses
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were conducted on all samples except for the seventh test; which was cleaning the work area after all
brake changes were complete and for which only PCM analysis was conducted.
(Blake et ai. 2003) included area sampling collected from seven locations within the building during
each test run, including four samples within 3 meters of the vehicle, one sample within 3 meters of the
arc grinding station, and two samples >3 meters from the automobile. Background samples were not
collected.
2.3.2.1.2 Exposure Data for Use in Risk Evaluation - Do-It-Yourself (DIY)
Mechanics During Brake Repair
Consumer inhalation exposure to asbestos for the DIY brake repair/replacement scenario was assessed
for both the consumer user (individual doing the brake repair/replacement work) and a bystander
(individual observing the brake work or present within the garage during the brake work). Consumer
inhalation exposure was evaluated for two conditions for the consumer user and bystander.
1) All brake work conducted indoors
2) All brake work conducted outdoors
The monitoring data extracted from the (Blake et at.. 2003) and (Sheehy et ai. 1989) studies are
presented in Table 2-26. A discussion of this information follows Table 2-26.
Table 2-26. Exposure concentrations from Blake (2003) and Sheehy (1989) studies to the DIY user
during various activities
Siiidv
\cii\ ii\
1 )iii';iik>n
( \iiilviiIi';iIkiii (lilvi's cc)
1 Avalion
( Diilidence kainiu

(hours)
PBZ
<3 m from auto

(Blake et al.
Brake shoe
removal/
replacement
1.5
0.0217
0.00027
Indoors
Medium
2003)
1.4
0.0672
0.0258
Indoors
Medium
Filing brakes
1.7
0.0376
0.0282
Indoors
Medium
Hand sanding
Brakes
1.6
0.0776
0.0133
Indoors
Medium
Arc-grinding
Brakes
1.7
0.4368
0.0296
Indoors
Medium
1.6
0.2005
0.0276
Indoors
Medium
Cleaning
facility
0.5
0.0146
0.0069
Indoors
Medium
aTTiwr
Brake shoe
removal/
replacement
Unknowna
0.007
Not monitoredb
Outdoors
Medium
a No monitoring duration was provided within the study.
b This study did not include outdoor area monitoring which could be applied to the bystander
For purposes of utilizing the information provided in Table 2-26 within this evaluation, EPA applied the
personal breathing zone (PBZ) values to the DIY consumer user for the indoor and outdoor scenarios
under the assumption that hands on work would result in exposure within the PBZ of the individual.
EPA assumes exposure to asbestos resulting from brake repair/replacement work occurs for the entire
three-hour period it takes the DIY consumer to conduct the work.
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EPA applied the area monitoring data obtained less than 3 meters from the automobile for the DIY
bystander for the indoor scenario under the assumption that the bystander could be an observer closely
watching the work being performed, an individual learning how to do brake repair/replacement work, or
even a child within the garage while the brake work is being performed. EPA assumes the bystander
remains within 3 meters of the automobile on which the work is being done for the entire three-hour
period it takes for the DIY consumer to conduct the work.
EPA evaluated consumer bystander exposure for the DIY brake outdoor scenario by applying a
reduction factor of 10 to the PBZ value measured outdoors for the consumer user. The reduction factor
of 10 was chosen based on a comparison between the PBZ and the < 3meter from automobile values
measured indoors across all activities identified in the study data utilized from Blake (a ratio of 6.5). The
ratio of 6.5 was rounded up to 10, to account for an additional reduction in concentration to which a
bystander may be exposed in the outdoor space based on the high air exchange rates and volume in the
outdoor11.
Table 2-27 provides a summary of the data utilized for this evaluation.
Table 2-27. Estimated Exposure Concentration for DIY Consumer User and Bystander
Condition of I so
I'lMilllilll
im
(cm ml
1 cndcno
(1 Consumer 1-1
I scr
llilih-cnd
xposmv (once
(Vnli'iil
Tcndcno
nlmlion (I'/cc)
sliiiulcr
lli
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measured during brake repair/replacement activities only (no additional work like grinding/filing) and
do include the use of compressed air. However, compressed air was only used to blow out residual dust
from brake drums after the majority of residual dust is broken out by placing the brakes on the floor with
a shock to knock off loose material. While the use of compressed air is not a recommended practice, no
reasonably available information was found that surveyed actual cleaning methods used or preferred by
DIY consumers for this scenario. EPA therefore utilized these values to evaluate consumer inhalation
exposure with the understanding that they may represent a more conservative exposure concentration
value.
Outdoor Scenario
EPA utilized the personal breathing zone concentration from the (Blake et at. 2003) study obtained
during filing of brakes for the high-end exposure concentration for the consumer user under the outdoor
scenario. Although this value was obtained in an indoor environment it is a potential additional work
activity that could also be performed outside. Additionally, even though it is outdoors, it is expected that
filing work would entail the consumer user's personal breathing zone to be very close to the brakes
being filed and therefore high air exchange rates and outdoor volumes would not be expected to have a
considerable impact on the exposure during such work.
EPA used the average monitored outdoor concentration measured in the personal breathing zone from
the (Sheehy et ai. 1989) study to represent the central tendency value for the consumer user under the
outdoor scenario. The (Sheehy et at.. 1989) study is the only study identified through the systematic
review process which included PBZ monitoring data for a DIY consumer user during outdoor brake
repair/replacement work. The duration of the monitoring in (Sheehy et ai. 1989) was not specified for
the outdoor work, EPA assumes monitoring occurred for the entire expected duration for the DIY
consumer user to complete the work. As the study describes, the DIY consumer user utilized various
wetting techniques on the brakes to clean grease, dirt, and flush the surface of the drums. Considering
these methods were utilized, EPA assumes compressed air was not used for the outdoor scenario.
Bystander
Indoor Scenario
EPA utilized the (Blake et ai. 2003) area sampling data obtained within three meters from the
automobile on which the work is being performed to represent exposure concentrations for the bystander
under the indoor scenario. These values are expected to be representative of bystander exposure under
the assumptions described above in that individuals who may remain within the garage during brake
repair/replacement work would be in close quarters within a typical consumer garage for the entire
three-hour period. The high-end value utilized was the highest area concentration monitored within three
meters from the automobile. This value occurred during arc-grinding of the brake shoe. The central
tendency value utilized was the average of the two area sampling concentrations monitored within three
meters from the automobile during brake shoe removal/replacement activities.
Outdoor Scenario:
There were no area monitoring data for the outdoor work in (Sheehy et ai. 1989) which could be
representative of potential bystander exposure. As a surrogate, EPA used the analysis of reduction
factors (RFs) based on available data for the gasket ONU exposure scenario. Those data showed people
5-10 feet away from the user had measured values from 2.5 to 9-fold lower than the exposure levels
measured for the user. For that COU, EPA used the mean of 5.75 as the RF; which was in the range of
RFs from other COUs. Because there were no such measured data available to estimate an RF for
outdoor DIY brake work, EPA selected an RF of 10 that was greater than the range of RFs for other
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COUs, but still allowed evaluation of potential bystander exposure in an outdoor scenario even though
such exposure is expected to be low due to high air exchange rates and the volume of the outdoor space.
EPA therefore applied a reduction factor of 10 to the data utilized for consumer users to represent the
concentration to which the bystander is exposed under the outdoor scenario. This reduction factor was
applied to both the central tendency and high-end estimates to represent potential exposure of the
bystander.
2.3.2.1.3 Exposure Estimates for DIY Brake Repair/Replacement Scenario
EPA assessed chronic exposures for the DIY brake repair/replacement scenarios based on the exposure
concentrations, assumptions, and exposure conditions described above. Because reasonably available
information was not found to characterize exposure frequencies and lifetime durations, EPA made the
following assumptions:
• Exposure frequency of 3 hours on 1 day every 3 years or 0.04 days per year. This considers car
maintenance recommendations that brakes be replaced every 35,000 miles, and the average
annual miles driven per driver in the United States is 13,476 miles/year ( ).
• Exposure duration of 62 years. This assumes exposure for a DIY consumer user starts at 16 years
old and continues through the average adult lifetime (78 years). EPA also used a range of
exposures (for both age at first exposure and duration of exposure); these are further described in
Section 4.2.3 of the Risk Characterization.
Table 2-28. DIY Brake/Repair Replacement - Exposure Levels for EPA's Risk Evaluation
Condition of I so

l-lxposinv ('onccnl ml ions
( (inlidcncc Killing
l filler
( on I nil
Tendeno
s/cc)
lliiih-r.nd
Aftermarket automotive parts - brakes (Indoor)
DIY User
0.0445
0.4368
Medium
Bystander
0.0130
0.0296
Medium
Aftermarket automotive parts - brakes (outdoors)
DIY User
0.007
0.0376
Medium
Bystander
0.0007
0.0038
Medium-Low
2.3.2.1.4 Data Assumptions, Uncertainties and Level of Confidence
Due to lack of reasonably available information on DIY consumer exposures, the consumer assessment
relies on reasonably available occupational data obtained under certain conditions expected to be more
representative of a DIY consumer user scenario (no engineering controls, no PPE, residential garage).
However, the studies utilized have uncertainties associated with the location where the work was done.
In (Blake et ai. 2003). worker exposures were measured at a former automobile repair facility which
had an industrial sized and filtered exhaust fan unit to ventilate the building during testing while all
doors were closed. A residential garage is not expected to have a filtered exhaust fan installed and
operating during DIY consumer brake repair/replacement activities. While this presents some
uncertainty, the study ( ce et ai. 2003) performed smoke testing and found that air movement was
limited to within eight meters of the installed and operating exhaust fan. Based on this testing, it is
reasonable to assume that the existence of the exhaust fan would have limited effect on the measured
concentrations within the PBZ of the DIY consumer and limited effect on the measured concentrations
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at the area monitors which were within three meters of the automobile being worked on because both
locations (automobile and area monitoring stations) were more than eight meters from the exhaust fan.
The volume of a former automobile repair facility is considerably larger than a typical residential garage
and will have different air exchange rates. While this could raise some uncertainties related to the
applicability of the measured data to a DIY consumer user environment, the locations of the
measurements utilized for this evaluation minimize that uncertainty. The PBZ values are very near the
work area and should not be affected by the facility volume or air exchange rates. The area samples
utilized for bystander estimates were obtained within three meters from the automobile on which the
work was being done, so while affected more by volume and air exchange rates, the effects should be
limited as air movement appeared to be minimal based on the smoke testing conducted in the (Blake et
at.. 2.003) study.
There is some uncertainty associated with the assumed length of time the brake repair/replacement work
takes. EPA assumes it takes a DIY consumer user about three hours to complete brake
repair/replacement work. This is two times as long as a professional mechanic. While it is expected to
take a DIY consumer longer, it is also expected DIY consumer users who do their own brake
repair/replacement work would, over time, develop some expertise in completing the work as they
continue to do it every three years.
There is also some uncertainty associated with the assumption that a bystander would remain within
three meters from the automobile on which the brake repair/replacement work is being conducted for the
entire three-hour period EPA assumes it takes the consumer user to complete the work. However,
considering a residential garage with the door closed is relatively close quarters for car repair work, it is
likely anyone observing (or learning) the brake repair/replacement work would not be able to stay much
farther away from the car than three meters. Remaining within the garage for the entire three hours also
has some uncertainty, although it is expected anyone observing (or learning) the brake
repair/replacement work would remain for the entire duration of the work or would not be able to
observe (or learn) the task.
The assumptions and uncertainties associated with a consumer's use of compressed air to clean brake
drums/pads are discussed above. While industry practices have drifted away from the use of compressed
air to clean brake drums/pads, no reasonably available information was found in the literature indicating
consumers have discontinued such work practices. To consider potential consumer exposure to asbestos
resulting from brake repair/replacement activities, EPA uses data which included use of compressed air.
However, EPA recognizes this may be a more conservative estimate because use of compressed air
typically could cause considerable dust/fibers to become airborne if it is the only method used. The
(Blake et ai. 2003) study notes that compressed air was used to clean residual dust from brake drums,
but it was only used after "shocking" dust free by placing the brake drums on the ground to knock dust
free. As a result, the bulk of the dust would be on the ground and a limited portion would be removed
through the use of compressed air.
EPA has an overall medium confidence rating for the literature, studies, and data utilized for the
Consumer DIY Brake Repair/Replacement COU. This is based on the existence of monitoring data in
both the personal breathing zone and area sampling associated directly with brake repair/replacement
activities. The studies utilized are also representative of expected consumer working conditions for a
DIY consumer. Both factors would indicate a high confidence in the studies and data used. However,
since the data utilized is based on a professional mechanic performing the brake repair/replacement
work rather than a DIY consumer, the overall confidence is medium.
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EPA has an overall medium confidence rating for the exposure results associated with the consumer
user under the Consumer DIY Brake Repair/Replacement COU for both indoor and outdoor work. This
is based on the use of direct monitored personal breathing zone data for the individual doing the work in
an indoor and outdoor location.
EPA has an overall medium confidence rating for the exposure results associated with the bystander
indoor location under the Consumer DIY Brake Repair/Replacement Scenario. This is based on the
existence of area monitoring data obtained in the immediate vicinity of the brake repair/replacement
work in an indoor location which is representative of where a bystander may reside during brake
repair/replacement work within a residential garage.
EPA has an overall medium-low confidence rating for exposure results associated the bystander
outdoor location under the Consumer DIY Brake Repair/Replacement Scenario. This is based on the
absence of area monitoring data in an outdoor work location resulting in the need to apply an adjustment
factor to estimate bystander exposure concentrations.
2.3.2.2 Consumer Exposures Approach and Methodology - DIY Gaskets in UTVs
This exposure assessment looks at a potential consumer exposure scenario where a DIY consumer
removes, cleans, handles, and replaces gaskets associated with exhaust systems on UTVs which may
contain asbestos. This scenario falls under the "other gaskets" COU in Table 1-4 of this draft risk
evaluation. Asbestos exposure is estimated for the DIY consumer user (the individual performing the
gasket repair work) as well as a bystander who may observe the gasket work. This scenario also assumes
all the work is conducted indoors (within a garage) and both the consumer and bystander remain in the
garage for the entirety of the work.
There was no reasonably available information found in the published literature related to DIY
consumer exhaust system gasket repair/replacement activities on UTVs. As a result, EPA expanded the
search to include information on occupational gasket repair/replacement for automobiles and identified
several studies with relevant information. The gasket repair/replacement scenario relies on monitored
values obtained in an occupational setting and considers only those environments and working
conditions that may be representative of a DIY consumer user scenario.
Thirty studies relating to gasket repair/replacement were identified and reviewed as part of the
systematic review process for exposure. These studies were compared against a series of criteria to
evaluate how representative the studies are for DIY consumer exhaust system gasket repair/replacement
activity. The first two criteria involved identifying whether the studies were automotive in nature and
whether there was enough information about automotive gaskets within the study. EPA also focused on
primary sources of data and not secondary or supplemental sources. The final criterion was to review the
studies to ensure they were consistent with an expected DIY consumer scenario of removal, cleaning,
and replacing gaskets. For example, studies involving machining or processing of gaskets were not
considered as it is unlikely a DIY consumer gasket repair/replacement activity would involve machining
and gasket processing. When compared to these criteria, three of the thirty studies were fully evaluated;
a 2006 study by Blake (Blake et at.. 2006). a 2005 study by Liukonen (YLiukonen and Weir. 2005). and a
2006 study by Paustenbach (Paustenbach et at.. 2006). as shown in Table 2-29.
Table 2-29. Summary of Studies Satisfying Factors Applied to Identified Literature
Reference
Occupational
Consumer
Data Quality Rating (Score)
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(Blake et al.„ 2006)
Yes
No
Medium (2.1)
(Liukonen and Weir. 2.005)
Yes
No
Medium (2.0)
(Paustenbach et al.. 2006)
Yes
No
Medium (1.7)
The (Blake et ai. 2006) study measured worker asbestos exposure during automotive gasket
removal/replacement in vintage car engines. The (Liukonen and Weir. 2.005) study measured worker
asbestos exposure during automotive gasket removal/replacement on medium duty diesel engines. The
(Paustenbach et at... 2006) study measured worker asbestos exposure during gasket removal/replacement
on automobile exhaust systems of vintage cars (ca. 1945-1975). All three studies were conducted in the
United States and used air sampling methods in compliance with NIOSH methods 7400 and 7402 for
PCM and TEM, respectively. All three studies demonstrate that the highest exposure to asbestos occurs
during removal of old gaskets and cleaning of the area where the gasket was removed. All three studies
received a medium-quality rating through EPA's systematic review data evaluation process.
Relevant data from each of the three studies identified in Table 2-29 were extracted. Extracted data
included vehicle or engine type, sampling duration, sample size, exposure concentrations, and units of
measurement. The extracted data were transcribed into Microsoft Excel for further analysis to calculate
minimum, maximum, and mean concentrations by study, activity type, and sample type. All the
extracted data and calculated values are included in Supplemental File: Consumer Exposure
Calculations ( a). All analysis and calculations for the three studies were performed
based on the raw data rather than summary data provided by each study due to differences in the
summary methodologies across the studies. For non-detectable samples reported within a study at their
respective sensitivity limits, statistics were calculated based on the full sensitivity value for that sample.
For non-detectable samples reported within a study below their respective sensitivity limits, statistics
were calculated based on one-half the sensitivity limit for that sample. For non-detectable samples
reports at levels greater than their respective sensitivity limits, statistics were calculated based on one-
half the reported non-detectable value. Table 2-30 summarizes the data based on the methodologies
described here.
Table 2-30. Summary Results of Asbestos Exposures in Gasket Repair Studies
Sliuh
l-lngine Work
Sample T\ |V
Sample
Si/e
\ir Sample 1)
Non-
Deleelable
Samples
¦la
Mean
Sample
Duration
(Minnies)
Aii* Sani|
(
Minimum
tie Coneenlr
l"ibers/ee)
Maximum
.ilions
Mean
( unl'irienee
Kaling
(Blake et al.. 2006)
28
14
140
0.002
0.027
0.007
Medium
Engine Dissembly
15
4
128
0.003
0.027
0.009
Medium
Area
9
2
135
0.003
0.008
0.005
Medium
Personal
6
2
117
0.007
0.027
0.015
Medium
Engine Reassembly
13
10
153
0.002
0.008
0.003
Medium
Area
9
9
154
0.002
0.008
0.003
Medium
Personal
4
1
153
0.003
0.008
0.005
Medium
(Liukonen and Weir. 2005)

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Engine Dissembly
29
26
53
0.004
0.060
0.018
Medium
Area
10
10
58
0.004
0.059
0.016
Medium
Observer
3
3
43
0.004
0.057
0.026
Medium
Outdoor
2
2
112
0.006
0.006
0.006
Medium
Personal
14
11
44
0.011
0.060
0.019
Medium
fPaustenbach et al. 2006)

Engine Dissembly
94
61
39
0.002
0.066
0.014
Medium
Area
22
15
46
0.002
0.015
0.005
Medium
Bystander
44
29
40
0.004
0.030
0.012
Medium
Personal
28
17
32
0.006
0.066
0.024
Medium
After review and consideration of all the information within each of the three studies, EPA used the
fPaustenbach et at.. 2006) study to evaluate DIY consumer exposure to asbestos resulting from
removal/replacement of exhaust system gaskets for this risk assessment. This study was used because it
was specific to exhaust system work involving asbestos-containing gaskets. It also includes information
applicable to a DIY consumer user (the individual[s] doing the gasket work) and the bystander (the
individuals] observing the gasket work).
The fPaustenbach et at.. 2006) study was conducted in two phases in Santa Rosa, CA during 2004 at an
operational muffler shop that has been open since 1974 and specializes in exhaust repair work. The
repair facility was about 101 feet by 48 feet with five service bay doors. The vehicles studied were
located near the center of the garage. During the study, the bay doors were closed, and no heating, air
condition, or ventilation systems were used.
The (Paustenbach et at.. 2006) study looked at 16 vehicles manufactured before 1974 with original or
old exhaust systems likely to have asbestos containing gaskets at either the flanges of the muffler system
or the manifold of the engine where the exhaust system connects. The study looked at four different
types of muffler work: 1) removal of exhaust system up to the flange; 2) removal of exhaust system
including manifold gaskets; 3) conversion from single to dual exhaust system; and 4) removal of muffler
system up to the manifold with installation of an asbestos donut gasket. Two mechanics performed the
exhaust repair work and neither mechanic wore respiratory protection. The mechanics removed the
gaskets with either their fingers or by prying with a screwdriver, and any residual gasket material was
scraped off with the screwdriver or pulled off by hand.
All airborne samples were collected using MCE filters consistent with NIOSH method 7400. Personal
breathing zone air samples were collected from the right and left lapel of the mechanic, and area air
samples were collected at four locations about four feet from the vehicle. Background and ambient air
samples were also collected both indoors and outdoors. A total of 134 air samples were collected, but
some samples could not be analyzed due to overloaded filters. Other samples were excluded because
they were taken during work on vehicles with non-asbestos gaskets. Ultimately, 82 air samples (23
personal, 38 area, and 21 background) were analyzed by PCM, and 88 air samples (25 personal, 41 area,
and 22 background) were analyzed by TEM. Samples below the analytical sensitivity limit were
included in the statistical analysis by substituting a value of one-half the sensitivity limit.
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2.3.2.2.1 Consumer Inhalation Exposures - DIY Gaskets in UTVs
Consumer inhalation exposure to asbestos for the DIY exhaust system gasket removal/replacement
scenario was assessed for both the DIY consumer user (individual doing the exhaust system gasket
removal/replacement work) and a bystander (individual observing the exhaust system gasket
removal/replacement work within the garage).
DIY Consumer User
EPA used the PBZ values from (Paustenbach et ai. 2006) identified in Table 2-30 for the DIY consumer
user. The maximum concentration was used as the high-end estimated concentration for the consumer
user and the mean concentration was used as the central tendency concentration.
EPA used the bystander values from (Paustenbach et al.. 2006) identified in Table 2-30 for the DIY
consumer bystander.The bystander values from (Paustenbach et al.. 2006) represent monitoring within
four feet of the automobile on which the exhaust system work was being performed. The maximum
concentration from Table 2-30 was utilized as the high-end estimated concentration for the consumer
bystander and the mean concentration was utilized as the central tendency concentration.
2.3.2.2.2 Exposure Estimates for DIY UTV Exhaust System Gasket
Removal/Replacement Scenario
EPA assessed exposures for the DIY UTV exhaust system gasket removal/replacement scenario based
on the exposure concentrations, assumptions, and exposure conditions described above. There was no
reasonably available information found within the literature providing specific information about the
length of time it would take for a DIY consumer to complete an exhaust system gasket
removal/replacement activity on a UTV. The studies from which data was extracted have sample periods
ranging from 32 minutes to 154 minutes to complete various gasket work for a professional mechanic
(assuming the sampling time within these studies was equal to the time it took to complete the gasket
work). Therefore, EPA assumes, for this evaluation, the exhaust system work would take the DIY
consumer three hours to complete which is approximately two times the average sample periods across
the studies extracted.
There was no reasonably available information found within the literature providing specific information
about the frequency of gasket change-out and it is expected that frequency can vary depending on the
location of the gasket and the number of gaskets needing change-out at any one time. The exhaust
system gasket on the engine manifold may be exposed to more extreme temperature fluctuations than
one on the muffler and therefore experience more wear and tear requiring replacement more frequently.
EPA assumes, for this evaluation, one or more gaskets will be replaced once every three years.
Exposure durations were assumed to be 62 years. This assumes exposure for the DIY consumer user
starts at 16 years old and continues through the average adult lifetime of 78 years. Table 2-31 provides a
summary of the data utilized for this evaluation.
Table 2-31. Estimated Exposure Concentrations for UTV Gasket Repair/Replacement Scenario -
DIY Mechanic and Bystander
Condilion of I si*
Tj |)0
I'1\|)iimiiv C onceii I r;i I ions I-'Mkts/it
Confidence
Killing

Central Tendency 1 Hij>h-cnd

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UTV gasket
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(Paustenbach et al. 2006)
DIY
Consumer
0.024
0.066
Medium
Bystander
0.012
0.030
Medium
2.3.2.2.3 Data Assumptions, Uncertainties and Level of Confidence
There were no reasonably available information identified through systematic review providing
consumer specific monitoring for UTV exhaust system gasket repair/replacement activities. Therefore,
this evaluation utilized published monitoring data obtained in an occupational setting of professional
mechanics, as a surrogate for estimating consumer exposures associated with UTV gasket
removal/replacement activities. There is some uncertainty associated with the use of data from an
occupational setting for a consumer environment due to differences in building volumes, air exchange
rates, available engineering controls, and the potential use of PPE. As part of the literature review, EPA
considered these differences and utilized reasonably available information representative of the expected
consumer environment. The (Paustenbach et ai. 2006) study was conducted in an occupational setting,
but no engineering controls were utilized. Additionally, no additional heating, ventilation, and air
condition systems were utilized during the study. The monitored values used were the PBZ data which
are not expected to be impacted by differences in the ventilation rates, work area volume, or air
exchange rates. Similarly, the area monitoring data utilized for bystander exposure were obtained four
feet from the automobile on which the work was being performed where differences in the ventilation
rates, work area volume, or air exchange rates should have minimal effect on the concentrations to
which the bystander is exposed.
There is some uncertainty associated with the use of an automobile exhaust system gasket
repair/replacement activity as a surrogate for UTV exhaust system gasket repair/replacement activity
due to expected differences in the gasket size, shape, and location. UTV engines and exhaust systems
are expected to be smaller than a full automobile engine and exhaust system, therefore the use of an
automobile exhaust system gasket repair may slightly overestimate exposure to the consumer. At the
same time, the smaller engine and exhaust system of a UTV could make it more difficult to access the
gaskets and clean the surfaces where the gaskets adhere therefore increasing the time needed to clean
and time of exposure resulting from cleaning the surfaces which could underestimate consumer
exposure.
There is some uncertainty associated with the assumption that UTV exhaust system gasket
repair/replacement activities would take a consumer a full three hours to complete. An internet search
revealed some videos suggesting gasket replacement would take a DIY consumer 30 minutes to
complete. This value mirrors the sampling time-frames within the (Paustenbach et at.. 2006) study.
However, the time needed for a DIY consumer to complete a full UTV exhaust system gasket
repair/replacement activity can vary depending on several factors including location of gaskets, number
of gaskets, size of gasket, and adherence of the gasket and residual material once the system is opened
up and the gasket is removed.
There is some uncertainty associated with the assumption that UTV exhaust system gasket
repair/replacement activities would be necessary and performed by a consumer once every three years.
A general internet search ("google") did not identify how often certain gaskets associated with the
exhaust systems of UTVs would last or need to be replaced. Some information was found on ATV
Maintenance including repacking the exhaust silencer of ATVs annually on machines that are frequently
used or every few years on machines used seasonally. Other information found online suggested
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whenever you do exhaust system maintenance, you should also replace gaskets to ensure an ongoing
effective seal for safety and efficiency.
There is some uncertainty associated with the assumption that an individual would be associated with
using an UTV for the entire average adult lifetime of 78 years beginning at 16 years of age. It is possible
certain individuals may be involved with UTV work prior to 16 years of age. While older individuals
may not be associated with their personal UTV and related gasket work up to age 78, they may provide
assistance on gasket work or perhaps change from a consumer "user" to a consumer "bystander".
The EPA has an overall medium confidence rating for the literature, studies, and data utilized for the
Consumer DIY UTV Exhaust System Gasket Repair/Replacement COU. This is based on the existence
of monitoring data in both the personal breathing zone and area sampling associated directly with gasket
repair/replacement activities. The studies utilized are also representative of expected consumer working
conditions for a DIY consumer. Both factors would indicate a high confidence in the studies and data
used. However, since the data utilized is based on a professional mechanic performing the brake
repair/replacement work rather than a DIY consumer, the overall confidence is medium.
The EPA has an overall medium confidence rating for the exposure results associated with the consumer
user and bystander under the Consumer DIY Exhuast System Gasket Repair/Replacement COU. This is
based on the use of direct monitored personal breathing zone data for the individual doing the work and
the existence of area monitoring data obtained in the immediate vicinity of the gasket repair/replacement
work in an indoor location which is representative of where a bystander may reside during gasket
repair/replacement work within a residential garage.
2,3,2.3 Summary of Inhalation Data Supporting the Consumer Exposure
Assessment
Table 2-32 contains a summary of the consumer inhalation exposure data used to calculate the risk
estimates in Section 4.2.3.
Table 2-32. Summary of Consumer Inhalation Exposures
Condition of I se
Duration
Type
Kxposure
1"
Central
Tendency
Concentrations,
hers/cc
lligh-end
Confidence
Rating
Brakes
Repair/Replacement
(Indoors)
3 hours
once
every 3
years
DIY
Consumer
0.0445
0.4368
Medium
Bystander
0.0130
0.0296
Medium
Brakes
Repair/Replacement
(Outdoors)
3 hours
once
every 3
years
DIY
Consumer
0.007
0.0376
Medium
Bystander
0.0007
0.0038
Medium-Low
UTV gasket
Repair/replacement
3 hours
once
every 3
years
DIY
Consumer
0.024
0.066
Medium
Bystander
0.012
0.030
Medium
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2.3.3 Potentially Exposed or Susceptible Subpopulations
TSCA requires that a risk evaluation "determine whether a chemical substance presents an unreasonable
risk of injury to health or the environment, without consideration of cost or other non-risk vactors,
including an unreasonable risk to a potentially exposed or susceptible subpopulation identified as
relevant to the risk evaluation by the Administrator, under the conditions of use." TSCA § 3(12) states
that "the term 'potentially exposed or susceptible subpopulation' means a group of individuals within
the general population identified by the Administrator who, due to either greater susceptibility or greater
exposure, may be at greater risk than the general population of adverse health effects from exposure to a
chemical substance or mixture, such as infants, children, pregnant women, workers, or the elderly."
During problem formulation (U.S. EPA. 2018d). EPA identified potentially exposed and susceptible
subpopulations for further analysis during the development and refinement of the life cycle, conceptual
models, exposure scenarios, and analysis plan. In this section, EPA addresses the potentially exposed or
susceptible subpopulations identified as relevant based on greater exposure. EPA addresses the
subpopulations identified as relevant based on greater susceptibility in Section 3.2.5
In developing the draft risk evaluation, the EPA analyzed the reasonably available information to
ascertain whether some human receptor groups may have greater exposure than the general population
to the hazard posed by asbestos. Exposures of asbestos would would be expected to be higher amongst
groups living near facilities covered under the COUs in this draft risk evaluation, groups with asbestos-
containing products in their homes, workers who use asbestos as part of their work, and groups who
have higher age and route specific intake rates compared to the general population.
Of the human receptors identified in the previous sections, EPA identifies the following as potentially
exposed or susceptible subpopulations due to their greater exposure to asbestos and considered them in
the risk evaluation:
• Workers and occupational non-users for the COUs in this draft risk evaluation (chlor-alkali,
sheet gaskets, oilfield brake blocks, aftermarket automotive brakes and linings, other
frictional products and other gaskets [UTVs]). EPA reviewed monitoring data found in
published literature and submitted by industry including both personal exposure monitoring
data (direct exposure) and area monitoring data (indirect exposures). Exposure estimates
were developed for users (males and female workers of reproductive age) exposed to
asbestos as well as non-users or workers exposed to asbestos indirectly by being in the same
work area of the building. Also, adolescents and female workers of reproductive age (>16 to
less than 50 years old) were also considered as a potentially exposed or susceptible
subpopulations
• Consumers and bystanders associated with consumer (DIY) use. Asbestos has been identified
as being used in products (aftermarket automotive brakes and linings and other gaskets in
UTVs) available to consumers; however, only some individuals within the general population
may use these products (i.e., DIYers or DIY mechanics). Therefore, those who do use these
products are a potentially exposed or susceptible subpopulation due to greater exposure.
• Other groups of individuals within the general population who may experience greater
exposures due to their proximity to conditions of use identified in Section 1.4.3 that result in
releases to the environment and subsequent exposures (e.g., individuals who live or work
near manufacturing, processing, use or disposal sites).
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For occupational exposures, EPA assessed exposures to workers and ONUs for the asbestos COUs.
Table 2-33 presents the percentage of employed workers and ONUs who may be susceptible
subpopulations within select industry sectors relevant to the asbestos COUs. The percentages were
calculated using Current Population Survey (CPS) data for 2017. CPS is a monthly survey of households
conducted by the Bureau of Census for the Bureau of Labor Statistics and provides a comprehensive
body of data on the labor force characteristics. Statistics for the following subpopulations of workers and
ONUs are provided: adolescents, adult men and women. As shown in Table 2-33, men make up the
majority of the workforce in the asbestos COUs. In other sectors, women (including those of
reproductive age and elderly women) make up a larger portion of wholesale and retail trade.
Table 2-33. Percentage of Employed Persons by Age, Sex, and Industry Sector (2017 and 2018
worker demographics from BLS)
Age (iroup
Sex
Mining,
quarrying, and
oil and gas
extraction
.Manufacturing
W holesale and
retail trade

Oilfield lirake
Block
Chlor-Alkali:
(iasket stamping:
(iaskct use in
chemical plants
Auto brake:
I TV
Adolescent
(16-19 years)
Male
0.4%
0.8%
3.0%
Female
0.0%
0.4%
3.2%
Adults
(20-54 years)
Male
68.2%
52.9%
42.8%
Female
9.2%
22.2%
35.4%
Elderly (55+)
Male
19.4%
17.5%
12.3%
Female
3.3%
7.3%
9.6%
Manufacturing - The Manufacturing sector comprises establishments engaged in the mechanical,
physical, or chemical transformation of materials, substances, or components into new products.
Establishments in the sector are often described as plants, factories, or mills. For asbestos, this sector
covers the COUs that occur in an industrial setting, including processing and using chlor-alkali
diaphragms, gasket stamping, and gasket use in chemical plants.
Wholesale and retail trade - The wholesale trade sector comprises establishments engaged in
wholesaling merchandise, generally without transformation, and rendering services incidental to the sale
of merchandise. Wholesalers normally operate from a warehouse or office. This sector likely covers
facilities that are engaged in the handling of imported asbestos-containing articles (i.e., aftermarket
automotive parts, other vehicle friction products and other gaskets.
Adolescents, or persons between 16 and 19 years in age, are generally a small part of the total
workforce. Table 2-34 presents further breakdown on the percentage of employed adolescents by
industry subsectors. As shown in the table, they comprise less than 2 percent of the workforce, with the
exception of wholesale and retail trade subsector where asbestos may be used in UTV gaskets and auto
brakes.
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Table 2-34. Percentage of Employed Adolescents by Industry Sector (2017 and 2018 worker
demographics from BLS)
Sector
cor
Adolescents
(16-19 years)
Mining, quarrying, and uil
and gas extraction
Oilfield Brake Block
0.89%
Manufacturing
Chlor-Alkali;
Gasket cut;
Gasket use in chemical plants
1.50%
Wholesale and retail trade
Auto brake;
UTV
6.13%
For consumer exposures, EPA assessed exposures to users and bystanders. EPA assumes, for this
evaluation, consumer users are male or female adults (greater than 16 years of age). Bystanders could be
any age group ranging from infants to adults.
3 HAZARDS (Effects)
3.1 Environmental Hazards
3.1.1 Approach and Methodology
EPA conducted comprehensive searches for data on the environmental hazards of asbestos, as described
in Strategy for Conducting Literature Searches for Asbestos: Supplemental File for the TSCA Scope
Document (TEPA-HO-OPP' 36-0083).
Only the on-topic references listed in the Ecological Hazard Literature Search Results were considered
as potentially relevant data/information sources for this risk evaluation. Inclusion criteria were used to
screen the results of the ECOTOX literature search (as explained in the Strategy for Conducting
Literature Searches for Asbestos: Supplemental File for the TSCA Scope Document). Since the
terrestrial pathways, including biosolids, were eliminated in the PF, EPA only reviewed the aquatic
information sources following problem formulation using the data quality review evaluation metrics and
the rating criteria described in the Application of Systematic Review in TSCA Risk Evaluations (US.
EPA, 2018a). Data from the evaluated literature are summarized below and in Table 3-1. in a
supplemental file ( 2019d) and in Appendix E (data extraction table). Following the data
quality evaluation, EPA determined that of the six on-topic aquatic toxicity studies, four of these studies
were acceptable for use in risk assessment while the two on-topic aquatic plants studies were rated as
unacceptable based on the evaluation strategies described in (\l ^ I'P \ 2018a). The studies rated as
unacceptable were not used in this risk evaluation. EPA also identified the following documents sources
of environmental hazard data for asbestos: 45 FR 793 18, 1980; ATSDR (2001a); U.S. EPA. (2014c);
I r j * \ < 2014b); WH' * I I), I ARC (2012) and Site-Wide Baseline Ecological Risk Assessment,
Libby Asbestos Superfund Site, Libby Montana (U.S. EPA. 2.014b).
3.1.2 Hazard Identification - Toxicity to Aquatic Organisms
Reasonably available information indicated that the hazards from chronic exposure to fish and aquatic
invertebrates following exposure to asbestos at concentrations ranging from 104- 108 fibers/L (which is
equivalent to 0.01 - 100 Million Fibers/Liter (MFL)) resulted in significant effects to development and
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reproduction. Sublethal effects were observed following acute and chronic exposure to asbestos at
concentrations lower than 0.01 MFL; for example, reduction in siphoning abilities in clams. As
summarized below and in Appendix TableAPX E-l: On-topic Aquatic Toxicity Studies Evaluated for
Chrysotile Asbestos, four citations were determined to be acceptable in quality and relevance for this
risk evaluation. All four citations received a rating of high quality following the data quality evaluation
process.
Belanger (1986c) exposed larval coho salmon (Oncorhynchus kisutch) and juvenile green sunfish
(Lepomis cyanellus) to chrysotile asbestos at concentrations that were environmentally relevant during
the time of the study and reported behavioral and pathological stress caused by chrysotile asbestos. No
treatment related increases in mortality were detected. Coho were exposed for 40 days at 3.0 MFL and
86 days at 1.5 MFL, while sunfish were exposed for 52 days at 3 MFL and 67 days at 1.5 MFL.
According to the study, coho larvae exposed to 1.5 MFL were significantly more susceptible to an
anesthetic stress test, becoming ataxic and losing equilibrium faster than control fish. Juvenile green
sunfish developed behavioral stress effects in the presence of 1.5 and 3.0 MFL. Specifically, the coho
and green sunfish exposed to 3.0 MFL had sublethal effects, which include the following: epidermal
hypertrophy superimposed on hyperplasia, necrotic epidermis, lateral line degradation, and lesions near
the branchial region. Lateral line abnormalities were associated with a loss of the ability to maintain
normal orientation in the water column.
In addition, Belanger (1986b) and Belanger (1986a) investigated the effects of chrysotile asbestos
exposure on larval, juvenile, and adult Asiatic clams (Corbicula sp.). Exposure to 0.01 MFL caused a
significant reduction in release of larva by brooding adults as well as increased mortality in larvae.
Reduced siphoning activity and fiber accumulation in clams were observed in the absence of food after
96-hr of exposure to 0.0001 and 0.1 MFL chrysotile asbestos, respectively (Belanger et at.. 1986b).
Sublethal and reproductive effects observed following 30 days of exposure to 0.0001 to < 100 MFL
chrysotile include the following: 1) fiber accumulation in gill and visceral tissues, 2) decreased
siphoning activity and shell growth of adult clams, 3) decreased siphoning activity, shell growth, and
weight gain of juveniles, 4) reduction of larva releases, and 5) larva mortality.
Lastly, Belanger (1990) studied the effects of chrysotile asbestos at concentrations of 0, 0.0001, 0.01, 1,
100 or 10,000 MFL on all life stages of Japanese Medaka (Oryzias latipes), including egg development,
hatchability, and survival; reduction in growth of larval to juvenile fish; reproduction performance; and
larval mortality. Eggs were exposed to chrysotile until hatching for 13-21 days, larvae-juvenile fish were
exposed to chrysotile for 13 weeks, and juvenile-adult fish were exposed to chrysotile for 5 months.
Asbestos did not substantially impair egg development, hatchability or survival. At concentrations of 1
MFL or higher, hatching of eggs was delayed, larval Medaka experienced growth reduction, and fish
developed thickened epidermal tissue. Juvenile fish exposed to 10,000 MFL suffered 98% mortality by
42 days and 100% mortality by 56 days.
For additional perspective on understanding the environmental hazard of asbestos materials, EPA
considered other related documents on asbestos. For example, EPA Region 8 reviewed the same data by
Belanger et al. discussed above for the Libby Superfund Site ecological risk assessment (U.S. EPA.
2014b) and considered the data adequate for asbestos in general, but not relevant for the Libby site
specifically.
3.1.3 Weight of Scientific Evidence
During the data integration stage of systematic review EPA analyzed, synthesized, and integrated the
reasonably available information into Table 3.1. This involved weighing scientific evidence for quality
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and relevance, using a weight of scientific evidence (WoE) approach, as defined in 40 CFR 702.33, and
noted in TSCA 26(i) (UAEPA^20|8a).
During data evaluation, EPA reviewed on-topic environmental hazard studies for data quality and
assigned studies an overall quality level of high, medium, or low based on the TSCA criteria described
in the Application of Systematic Review in TSCA Risk Evaluations ( i). While integrating
environmental hazard data for asbestos, EPA gave more weight to relevant information that were
assigned an overall quality level of high or medium.
The ten on-topic ecotoxicity studies for asbestos included data from aquatic organisms (i.e., vertebrates,
invertebrates, and plants) and terrestrial species (i.e., fungi and plants). Following the data quality
evaluation, EPA determined that four on-topic aquatic vertebrate and invertebrate studies were
acceptable while the two on-topic aquatic plants studies were unacceptable based on the evaluation
strategies described in the Application of Systematic Review in TSCA Risk Evaluations (U.S. EPA.
2018a). Since the terrestrial pathways were eliminated in the PF, EPA excluded three studies on
terrestrial species as terrestrial exposures were not expected under the COUs for asbestos. One
amphibian study was excluded from further review and considered out of scope because it was not
conducted on chrysotile asbestos. Ultimately the four aquatic toxicity studies were rated high in quality
and used to characterize the adverse effects of chrysotile asbestos to aquatic vertebrate and invertebrate
organisms from chronic exposure, as summarized in Table 3-1. Any information that EPA assigned an
overall quality of unacceptable was not used. The gray literature EPA identified for asbestos had
minimal or no information about environmental hazards and were consequently not used. EPA
determined that data and information were relevant based on whether they had biological,
physical/chemical, and environmental relevance ( ):
• Biological relevance: correspondence among the taxa, life stages, and processes measured or
observed and the assessment endpoint.
• Physical/chemical relevance: correspondence between the chemical or physical agent tested and
the chemical or physical agent constituting the stressor of concern.
• Environmental relevance: correspondence between test conditions and conditions in the
environment.
Table 3-1
. Environmental Hazard
""haracterization of Asbestos
Duration
l osl Organism
I'.iulpoini
II a/a I'd
Value
I nil
l-IIVcl I'lndpoinlis)
References
Aquatic Organisms
Acute
Aquatic
invertebrates
96-hr LOEC
0.0001-100
MFLd
Reduction in siphoning activity;
Fiber accumulation
Belaneer ef al.
(1986b) (High)
Chronic
Fish
13-86 day
NOECa
0.01-1.5
MFL
Behavioral stress (e.g., aberrant
swimming and loss of
equilibrium); Egg development,
hatchability, and survival;
Growth; Mortality
Belaneer et al.
(1990) (Hieh);
Belaneer et al.
(1986c) (Hiah):
13-86 day
LOECb
1-3
Aquatic
invertebrates
30-day LOEC
0.0001-100
MFL
Reduction in siphoning activity;
Number of larvae released;
Alterations of gill tissues; Fiber
accumulation in tissues;
Growth; Mortality
Belaneer et al.
(1986b) (High);
Belaneer et al.
(1986a) (Hieh)
'NOEC. No Observable Effect Concentration.
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bLOEC, Lowest Observable Effect Concentration.
"Values in the tables were reported by the study authors and combined in ranges (min to max) from different effect endpoints. The
values of the NOEC and LOEC can overlap because they may be based on different effect endpoints. For example, fish NOEC =1.5
MFL was based on behavioral stress (e.g., aberrant swimming and loss of equilibrium) and fish LOEC = 1 MFL was based on
significant reduction in growth of larval individuals. See Table APX E-l for more details.
dMFL, Million Fibers/Liter.
"Data quality evaluation scores for each citation are in the parenthesis.
3.1.4 Summary of Environmental Hazard
A review of the high-quality aquatic vertebrate and invertebrate studies indicated that chronic exposure
to waterborne chrysotile asbestos at a concentration range of 104-108 fibers/L, which is equivalent to
0.01 to 100 MFL, may result in reproductive, growth and/or sublethal effects to fish and clams. In
addition, acute exposure of waterborne chrysotile asbestos at a concentration range of 102-108 fibers/L to
clams demonstrated reduced siphoning activity.
3.2 Human Health Hazards
Many authorities have established that there are causal associations between asbestos exposures and
lung cancer and mesotheliomas CNTP. 2016; I ARC. 2012; AT SDR. 2001a; U.S. EPA. 1988b; IARC.
1987; U.S. EPA. 1986; IARC. 1977). Although asbestos is also associated with other types of cancers,
there are no Inhalation Unit Risk (IUR) values available for these other cancers. Given the well-
established carcinogenicity of asbestos for lung cancer and mesothelioma, EPA, in its PF document,
decided to limit the scope of its systematic review to these two specific cancers and to inhalation
exposures with the goal of updating, or reaffirming, the existing EPA IUR for general asbestos (U.S.
EPA. 1988b). As explained in Section 1.4.1, EPA has determined that the asbestos fiber associated with
the COUs in this draft risk evaluation is chrysotile. Thus, this draft risk evaluation uses the EPA-derived
chrysotile IUR described in Section 3.2.4 to calculate risk estimates.
3.2.1 Approach and Methodology
EPA used the approach described in Figure 3-1 to evaluate, extract and integrate asbestos human health
hazard and dose-response information. This approach is based on the Application of Systematic Review
in TSCA Risk Evaluations (U.S. EPA. 2018a) and the Framework for Human Health Risk Assessment to
Inform Decision Making (\ c. \ V \ _V i 1
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Systematic
Review
Stage
Oatpot of rbe (/
-.teiurrtic
R« lev,
Stage

tjam integration

ffisk
Am**
ibi.i r.\ aiuatioa
M-texl
appfv we-ekteroissed dat
juatty
to assess the eoefetes
k-.-v .!!\d ,-up;>orr.v:ij:
idfnhhvJ i:-:--' tou;
..i> '•"'Oil a
itadfej
P*
dtaaatn of:
Hazard ID
Confirm potential
hazards identified
during
scoping/problem
formulation
Analysts
Dose-
Response;
Selection of
PODs;
IUR Derivation
ly

Sttmuiarv
of Swings
• O-ritatb. rf
creative ass\imptk>ns
Cancer sisk
/"
/ estimates a»d
discussion of
arious
considerations
"Sections 4.2 and /
4.3)
Stud"/ Qualrt]
Nummar, Table
(Data quality
lafaiigs and
namencal scored
tAppenckx B)
Data
Sismniaue-. Jot
Ad*erse
tudpoints
Nanatrve b
IUR derivation
V (Sections 3.2.4}
^ (Appwnda Bv /
Spl noii
Figure 3-1. EPA Approach to Hazard Identification, Data Integration, and Dose-Response
Analysis for Asbestos
In the PF document, it was stated that the asbestos RE would focus on epidemiological inhalation data
on lung cancer and mesothelioma for all TSCA Title II fiber types, just as stated in the 1988 EPA IRIS
Assessment on Asbestos (U.S. EPA. 1988b). This was based on the large database on the health effects
associated with asbestos exposure which has been cited in numerous U.S. and international data sources.
These data sources included, but were not limited to, EPA IRIS Assessment IRIS Assessment on
Asbestos 0988b). IRIS Assessment on Libbv Amphibole Asbestos (2014c). National Toxicology
Program (NTP) Report on Carcinogens. Fourteenth Edition (2016). NIOSH Asbestos Fibers and Other
Elongate Mineral Particles: State of the Science and Roadman for Research ( ), ATSDR
Toxicological Profile for Asbestos (2001a). IARC Monographs on the Evaluation of Carcinogenic Risks
to Humans. Arsenic. Metals. Fibres, and Dusts. Asbestos (Chrvsotile. Amosite. Crocidolite. Tremolite.
(20141 P~S ( ' ^ " " 8 ' _
EPA conducted comprehensive searches for reasonably available information on health hazards of
asbestos, as described in Strategy for Conducting Literature Searches for Asbestos: Supplemental File
for the TSCA Scope Document (EPA-HQ-OPPT-2016-0736). The relevant studies were evaluated using
the data quality criteria in the Application of Systemic Review in TSCA Risk Evaluations document (U.S.
EPA. 2018a). The process and results of this systematic review are available in a supplemental
document (see Systematic Review Supplemental File: Data Quality Evaluation and Data Extraction of
Human Health Hazard Studies).
This EPA human health hazard assessment consists of hazard identification and dose-response
assessment as described in EPA's Framework for Human Health Risk Assessment to Inform Decision
Making (U.S. EPA. 2014a). Hazards were identified from consensus documents. EPA integrated
epidemiological studies of asbestos with other readily available information to select the data to use for
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dose-response assessment. Dose-response modeling was performed for the hazard endpoints with
adequate study quality and acceptable data sets.
After publication of the PF document, EPA determined that only chrysotile asbestos is still imported into
the U.S. either in raw form or in products; the other five forms of asbestos have neither known, intended,
nor reasonably foreseen manufacture, import, processing, or distribution. EPA will consider legacy uses
and associated disposal in subsequent supplemental documents. Therefore, for this document, in order to
inform the estimation of an exposure-response function allowing for the derivation of a chrysotile
asbestos IUR, EPA identified epidemiological studies on mesothelioma and lung cancer in cohorts of
workers using chrysotile in commerce. To identify studies with the potential to be used to derive an
inhalation unit risk (IUR), EPA also screened and evaluated new studies that were published since the
EPA IRIS assessment conducted in 1988.
The new literature was screened against inclusion criteria in the PECO statement, and the literature was
further screened to identify only hazard studies with inhalation exposure to chrysotile asbestos. Cohort
data deemed as "key" was entered directly into the data evaluation step based on its relevance to the risk
evaluation. The relevant (e.g., useful for dose-response for the derivation of the IUR) study cohorts were
further evaluated using the data quality criteria for human studies. Only epidemiological hazard studies
by inhalation and only chrysotile asbestos exposures were included.
EPA developed unique data quality criteria for epidemiological studies on asbestos exposure and
mesothelioma and lung cancer (see Systematic Review Supplemental File: Data Quality Evaluation and
Data Extraction of Human Health Hazard Studies). EPA considered studies of low, medium, or high
confidence for dose-response analysis for the derivation of the IUR. Information that was rated
unacceptable was not included in the risk evaluation ( 318a). The Systematic Review
Supplemental File: Data Quality Evaluation and Data Extraction of Human Health Hazard Studies
presents the data quality information on human health hazard endpoints (cancer) for all acceptable
studies (with low, medium, or high scores). See section 3.2.4.
Following the data quality evaluation, EPA extracted a summary of data from each relevant cohort. In
the last step, the strengths and limitations of the data among the cohorts of acceptable quality were
evaluated for each cancer endpoint and a weight-of-the-scientific evidence narrative was developed.
Data for either mesothelioma or lung cancer was modeled to determine the dose-response relationship.
Finally, the results were summarized, and the uncertainties were presented. The process is described in
Section 3.2.4.
Section 3.2.4.3 describes the epidemiological studies chosen for the derivation of the IUR for chrysotile
asbestos.
3.2.2 Hazard Identification
Asbestos has an existing EPA IRIS Assessment, an ATSDR Toxicological Profile, and many other U.S.
and international assessments (see Section 1.3); hence, many of the hazards of asbestos have been
previously compiled and reviewed. Most of the information in these assessments is based on inhalation
exposures to human populations. Only inhalation exposures in humans are evaluated in the risk
evaluation of asbestos. EPA identified key and supporting studies from previous peer reviewed
assessments and new studies published since 1988 and evaluated them against the data quality criteria
developed for asbestos. The evaluation criteria were tailored to meet the specific needs of asbestos
studies and to determine the studies' potential to provide information on the exposure-response
relationship between asbestos exposure and mortality from lung cancer and from mesothelioma.
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During scoping and PF, EPA reviewed the existing EPA IRIS health assessments to ascertain the
established health hazards and any known toxicity values. EPA had previously, in the IRIS assessment
on asbestos (U S. l^88b). identified asbestos as a carcinogen causing both lung cancer and
mesothelioma from inhalation exposures and derived an IUR to address both cancers. No toxicity values
or IURs have yet been estimated for other cancers that have been identified by the International Agency
for Research on Cancer (IARC) and other government agencies. Given the well-established
carcinogenicity of asbestos for lung cancer and mesothelioma, EPA, in its PF document, had decided to
limit the scope of its systematic review to these two specific cancers and to inhalation exposures with
the goal of updating, or reaffirming, the existing unit risk. As explained in Section 1.4, the only COUs of
asbestos or asbestos containing products assessed in this risk evaluation are for chrysotile asbestos.
Thus, an IUR value for chrysotile asbestos only was developed. EPA will consider legacy uses and
associated disposal in subsequent supplemental documents.
3.2.3 Cancer Hazards
Many authorities have established that there are causal associations between asbestos exposures and
lung cancer and mesotheliomas in humans based on epidemiologic studies (NTP. 2016; IARC. 2012;
ATSDR. 2001a; U.S. EPA. 1988b; IARC. 1987; U.S. EPA. 1986; IARC. 1977V EPA also noted in the
scope that there is a causal association between exposure to asbestos and cancer of the larynx and cancer
of the ovary (IARC. 2012). and that there is also suggestive evidence of a positive association between
asbestos and cancer of the pharynx (IARC. 2012; NRC. 2.006). stomach (IARC. 2012; ATSDR. 2001a)
and colorectum CNTP. 2.016; IARC. 2012.; NRC. 2006; ATSDR. 2.001a; NRC. 1983; U.S. EPA. 1980).
In addition, the scope document reported increases in lung cancer mortality in both workers and
residents exposed to various asbestos fiber types, including chrysotile, as well as fiber mixtures (IARC.
2.012). Mesotheliomas, tumors arising from the thin membranes that line the chest (thoracic) and
abdominal cavities and surround internal organs, are relatively rare in the general population, but are
often observed in populations of asbestos workers. All types of asbestos fibers have been reported to
cause mesothelioma - including chrysotile asbestos (IARC. 2012; U.S. EPA. 1988b. 1986).
During PF. EPA reviewed the existing EPA IRIS health assessments (U.S. EPA, ' M , s 88b) to
ascertain the established health hazards and any known toxicity values. EPA had previously (
1988b. 1986) identified asbestos as a carcinogen causing both lung cancer and mesothelioma and
derived a unit risk based on epidemiologic studies to address both cancers. The U.S. Institute of
Medicine (IQM. 2006) and the International Agency for Research on Cancer (IARC. 2012) have
evaluated the evidence for causation of cancers of the pharynx, larynx, esophagus, stomach, colon, and
rectum, and IARC has evaluated the evidence for cancer of the ovary. Both the U.S. Institute of
Medicine and IARC concluded that asbestos causes laryngeal cancer and IARC concluded that asbestos
causes ovarian cancer. No toxicity values or IURs have yet been estimated for either laryngeal or
ovarian cancers.
3.2.3.1 Mode of Actiton (MOA) considerations for asbestos
As stated in IRIS Assessment on Libbv Amphibole Asbestos (2014c) for asbestos in general,
International Agency for Research on Cancer (IARC) has proposed a mechanism for the carcinogenicity
of asbestos fibers [see Figure 4-2 in (IARC. 2012)1. Asbestos fibers lead to oxidant production through
interactions with macrophages and through hydroxyl radical generation from surface iron. Inhaled fibers
that are phagocytosed by macrophages may be cleared or lead to frustrated phagocytosis, which results
in macrophage activation, release of oxidants, and increased inflammatory response, in part due to
inflammasome activation. Free radicals may also be released by interaction with the iron on the surface
of fibers. Increased oxidant production may result in epithelial cell injury, including DNA damage.
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Frustrated phagocytosis may also lead to impaired clearance of fibers, with fibers being available for
translocation to other sites (e.g., pleura). Mineral fibers may also lead to direct genotoxicity by
interfering with the mitotic spindle and leading to chromosomal aberrations. Asbestos exposure also
leads to the activation of intracellular signaling pathways, which in turn may result in increased cellular
proliferation, decreased DNA damage repair, and activation of oncogenes. Research on various types of
mineral fibers supports a complex mechanism involving multiple biologic responses following exposure
to asbestos (i.e., genotoxicity, chronic inflammation/cytotoxicity leading to oxidant release, and cellular
proliferation) in the carcinogenic response to mineral fibers [see Figure 4-2, ("IARC. )].
3.2.4 Derivation of a Chrysotile Asbestos Inhalation Unit Risk
3.2.4.1 Derivation of a Chrysotile Asbestos Inhalation Unit Risk
As stated in Section 3.2.3, epidemiological studies on mesothelioma and lung cancer in cohorts of
workers using chrysotile in commerce were identified that could inform the estimation of an exposure-
response function allowing for the derivation of a chrysotile asbestos IUR. In addition, EPA could not
find any recent risk numbers in the literature for the types of asbestos regulated under TSCA since the
IRIS IUR12 value, which had been developed in the 1980s. Thus, rather than update or reaffirm the
existing IUR for general asbestos, EPA developed a chrysotile-specific IUR in this risk evaluation.
EPA did not have a previous, recent risk assessment of asbestos on which to build; therefore, the
literature was reviewed to determine whether a new IUR needed to be developed. As the RE process
progressed, several decisions were made that refined and narrowed the scope of the RE. It was
determined during PF that the RE would focus on epidemiologic data on mesothelioma and lung cancer
by the inhalation route. The existing EPA IUR for asbestos was developed in 1988 was based on 14
epidemiologic studies that included occupational exposure to chrysotile, amosite, or mixed-mineral
exposures (chrysotile, amosite, crocidolite). However, EPA's research to identify COUs indicated that
only chrysotile asbestos is currently being imported in the raw form or imported in products. The other
five forms of asbestos identified for this risk evaluation are no longer manufactured, imported,
processed, or distributed in the United States. This commercial chrysotile is therefore the substance of
concern for this quantitative assessment and thus EPA sought to derive an IUR specific to chrysotile
asbestos. The epidemiologic studies available for risk assessment all include populations exposed to
commercial chrysotile asbestos, which may contain small, but variable amounts of amphibole asbestos.
Because chrysotile is the only form of asbestos in the United States with COUs in this document, studies
of populations exposed only to chrysotile provide the most informative data for the purpose of
developing the TSCA risk estimates for the COUs for chrysotile asbestos. EPA will consider legacy uses
and associated disposal in subsequent supplemental documents.
3.2.4.2 Rationale for Asbestos-Specific Data Evaluation Criteria
For the first 10 TSCA REs, a general set of study evaluation criteria was developed. These data
evaluation criteria were not tailored to any specific exposure or outcome. In the PF step of the asbestos
assessment, it was accepted that exposure to asbestos was a known cause of lung cancer and
mesothelioma, and that the purpose of the systematic review would be the identification of studies which
12 Inhalation Unit risk (IUR) is typically defined as a plausible upper bound on the estimate of cancer risk per |ig/m3 air
breathed for 70 years. For asbestos, IUR is expressed as cancer risk per fibers/cc (in units of the fibers as measured by PCM).
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could inform the estimation of an exposure-response function allowing for the derivation of an asbestos
inhalation unit risk for lung cancer and mesothelioma combined. The study domains of exposure,
outcome, study participation, potential confounding, and analysis were further tailored to the specific
needs of evaluating asbestos studies for their potential to provide information on the exposure-response
relationship between asbestos exposure and mortality from lung cancer and from mesothelioma (
).
In terms of evaluating exposure z'nformation, asbestos is unique among these first 10 TSCA chemicals as
it is a fiber and has a long history of different exposure assessment methodologies. For mesothelioma,
this assessment is also unique with respect to the impact of the timing of exposure relative to the cancer
outcome as the time since first exposure plays a dominant role in modeling risk. The most relevant
exposures for understanding mesothelioma risk were those that occurred decades prior to the onset of
cancer and subsequent cancer mortality. Asbestos measurement methodologies have changed over those
decades, from early measurement of total dust particles measured in units of million particles per cubic
foot of air (mppcf) by samplers called midget impingers to fibers per milliliter (f/ml), or the equivalent
fibers per cubic centimeter (f/cc), where fiber samples were collected on membrane filters and the fiber
count per volume of air was measured by analyzing the filters using phase contrast microscopy (PCM).
In several studies encompassing several decades of asbestos exposures, matched samples from midget
impingers and membrane filters were compared to derive job- (or location-) specific factors allowing for
the conversion of earlier midget impinger measurements to estimate PCM measurement of asbestos air
concentrations. While some studies were able to provide these factors for specific locations and jobs,
other studies were only able to derive one factor for all jobs and locations. The use of such data has
allowed asbestos researchers to investigate the risk of asbestos and successfully model lung cancer and
mesothelioma mortality over several decades of evaluation (U.S. EPA. 2.014c. 1988b. 1986). Thus, the
general exposure evaluation criteria were adjusted to be specific to exposure assessment methodologies
such as midget impingers and PCM with attention to the use of job-exposure-matrices (JEMs) to
reconstruct workers' exposure histories and the reporting of key metrics needed to derive exposure-
response functions for lung cancer and mesothelioma.
In terms of evaluating the quality of outcome information, lung cancer is relatively straightforward to
evaluate as an outcome. Specific International Classification of Disease (ICD) codes for lung cancer
have existed for the entire time period of the studies evaluated here making it possible to identify cases
from mortality databases. On the other hand, there was no diagnostic code for mesothelioma in the
International Classification of Diseases prior to the introduction of the 10th revision (ICD-10) which was
not implemented in United States until 1999. Before ICD-10, individual researchers employed different
strategies (e.g., had to go beyond ICD codes and generally searched original death certificates for
mention of mesothelioma, considered certain ICD rubrics). Thus, the general outcome evaluation criteria
were adjusted to be specific to mesothelioma and outcome ascertainment strategies.
Mesothelioma is a very rare cancer. As noted by U.S. EPA (2014c). the "Centers for Disease Control
and Prevention estimated the death rate from mesothelioma, using 1999 to 2005 data, as approximately
23.2 per million per year in males and 5.1 per million per year in females (CDC. 2009)." While
extremely rare, the overwhelmingly dominant cause of mesothelioma is asbestos exposure (Tossavainen.
1997) making the observance of mesothelioma in a population a very specific indicator for asbestos
exposure. It is critical to understand that the prevailing risk model for mesothelioma models is an
absolute risk model of mesothelioma mortality which assumes there is no risk at zero exposure (U.S.
EPA. 1986; Peto et al.. 1982; Peto. 1978). This use of an absolute risk model differs from is in stark
contrast to the standard use of a relative risk model for lung and other cancers. For the relative risk
model, the risk of lung cancer in an asbestos exposed population multiplies a background risk in an
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unexposed population. Thus, an important consideration of study quality is the evaluation of that
comparison population. However, for mesothelioma, no comparison population is needed to estimate the
absolute risk among people exposed to asbestos, and therefore the criteria in the study participation
domain (that include comparison population) were adjusted for mesothelioma.
In terms of evaluating potential confounding, the generic potential confounding section was adapted to
recognize that there are both direct and indirect methods for controlling for some confounders. -
specifically, that methodologies that involve internal comparisons within a working population may
indirectly control for smoking and other factors assuming when these factors do not vary with asbestos
exposure concentrations in the workplace. In contrast, mesothelioma is much simpler to evaluate for
potential confounding as diagnostic X-ray contrast medium "Thorotrasf'and external beam
radiotherapy are the only other known risk factors for mesothelioma, and this rare exposure these are
unlikely to be a confounder. because these are rare procedures are not routinely done on healthy
workers, screening programs typically x-ray all workers - regardless of their cumulative asbestos
exposure.
In terms of analysis, the evaluation criteria were needed to be adapted for both mesothelioma and lung
cancer. For mesothelioma, the Peto model (Peto et at.. 1982; Peto. 1978) was traditionally used for
summary data published in the literature (U.S. EPA. 1986) rather than raw individual-level data, so
studies were considered acceptable that only reported sufficient information to fit modeling using the
Peto model by the authors or the presentation of sufficient information to fit the Peto model post hoc
was considered acceptable. For lung cancer, a wider selection of statistical models was acceptable, with
the preference generally given to modeling that used individual data in the analysis. Grouped data
modeling will also be reported but would be carried forward to the summary only if no individual data
modeling were available.
3.2.4.3 Additional considerations for final selection of studies for exposure-response
As shown in Figure 1-8, EPA's literature search identified more than 24,000 studies, but for the final
data evaluation 26 papers covering seven cohorts were identified, and these cohorts are listed in Table
3-2.
In reviewing these available studies, EPA distinguished between studies of exposure settings where only
commercial chrysotile was used or where workers exposed only to commercial chrysotile could be
identified, and situations where chrysotile was used in combinations with amphibole asbestos forms and
the available information does not allow exposures to chrysotile and amphibole forms to be separated.
Studies in the latter group were judged to be uninformative with respect to the cancer risks from
exposure to commercial chrysotile and were excluded from further consideration (e.g., Slovenia cohort:
Dodic et al., (2007; 2.003).
All the studies determined to be informative for lung cancer and mesothelioma analysis were based on
observation of historical occupational cohorts. Some cohorts have been the subject of multiple
publications; in these cases, only data from the publication with the longest follow-up for each cohort or
the most relevant exposure-response data were used unless otherwise specified.
Studies were deemed informative for lung cancer risk assessment if either the relative risk of lung cancer
per unit of cumulative chrysotile exposure in fibers per cc-year (f/cc-yrs) from fitting log-linear or
additive relative risk models or the data needed to fit such models as described below were available.
The group of Balangero, Italy cohort studies including Pira et al.,(2009) was excluded for lack of results
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from models using a continuous measure of exposure. Studies that presented lung cancer risks only in
relation to impinger total dust exposure were excluded from consideration unless they provided at least a
data-based, study-specific factor for converting concentrations from mppcf to f/cc.
EPA identified studies of five independent occupational cohorts exposed only to commercial chrysotile
that provided adequate data for assessment of lung cancer risks: asbestos textile manufacturing workers
in North Carolina and South Carolina, USA (Loomis et at.. 2009; Hein et at.. 2007) and Chongqing,
China (Dene et at..: ) and chrysotile miners in Quebec, Canada (Liddell et at.. 1997). and Qinghai,
China (201 I; Wang et at.. 201 Jh). A pooled analysis of the two U.S. studies (NC and SC) asbestos
textile cohorts (Elliott et at.. 2012) also provides informative data. In addition, Berman and Crump
(2008) provide informative risk estimates for the Quebec miner cohort based on modeling dose-response
data that were not available in the original study.
Studies were considered informative for mesothelioma risk assessment if risk estimates from fitting the
EPA mesothelioma model to individual-level data or data needed to fit the model as described below
were available. None of the original publications reported risk estimates from fitting the Peto model.
However, Berman & Crump (2008) provide risk estimates for the Quebec miners from analyses of
original, individual-level data (Liddell et at.. 1997) and for South Carolina from analysis of grouped data
(Hein et ai. 2007). Comparable risk estimates were generated for North Carolina textile workers
(Loomis et at.. 2009) using tabulated mesothelioma data (Loomis et ai. 2019). Data needed to fit Peto
mesothelioma model have not been published for any other cohort exposed to chrysotile only.
Table 3-2. Study Cohort, Individual studies and Study Quality of Commercial Chrysotile Asbestos
Reviewed for Assessment of Lung Cancer and Mesothelioma Risks
Study Cohort
Author, Year
HERO ID
Study Quality**

( 'man and Crump. 2008)
626405

( >wn et al. 1994)
3081832

(Cole et al.. 2013)
3078261

(Dement et al.. 1983b)
67

(Dement et al.. 1994)
3081766
Lung Cancer
South
Carolina, US
(IVment and Brown. 1994)
3081783
1.6 High
(Edwards et al.. 2014)
3078061

(<'ihott^ it .'i'l)
1247861
Mesothelioma

(Hein et al.. 2007)
709498
1.7 Medium

(Loomis et al.. )
1257856

(SRC. 2019c)
5080236

(Stavner et al.. 1997)
3081241

(Stavner et al.. 2008)
2604140

Qinghai,
(Wane et al.. 2012)
2572504
Lung Cancer
1.6 High
China - miners
(Wane et al.. 2013b)
2548289

(Wane et al.. 2014)
2538846
Balangero,
(Piolatto et al.. 1990)
3082492

Italy*
(Pira et al.. 2.009)
2592425

(Pira et al.. )
5060134

(Rubino et *.)! tr*"9)
178

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Si udv Cohort
Author. Year
III.UO II)
Study Quality""
North
(Herman and Crump. 2008)
626405

Carolina, US
( nent et aL 2008)
626406
Lung Cancer
1.7 Medium

O-' Utott et aL 2012)
1247861

(Loomis et aL 2009)
3079232

(Loomis et aL )
2225695
Mesothelioma
1.5 High

(Loomis et aL )
1257856

(Loomis et aL )
5160027

(SRC. 2.019a)
5080241

Salonit
CDodic Fikfak. 2003)
3080279

Anhovo,
Slovenia*
( die Fikfak et aL 2007)
3079664

Quebec,
( 'man and Crump. 2008)
626405

Canada
(\nbbs and Lachan > C .)
3580825
Lung Cancer
Low (professional
judgement)

0 indell et ,'ii )
3081408

(1 tudell et a! It!'}8)
3081200

(Liddell and Armstrong. 2002)
3080504

(Mcdonald et aL 1993a)
3081910
Mesothelioma

(Mcdonald et aL 1993b)
3081911
Medium (professional

(SRC. 2019b)
5080232
judgement)

(Vacek. 1998)
3081118

Chongqing,
(Courtice et aL 2016)
3520560

China -
(Dei )
2573093

asbestos
(Wane et aL 2014)
2538846
Lung Cancer
1.4 High
products
factory
including
textiles
(Yano et aL 2001)
3080569
* Cohorts from Italy and Slovenia are not considered further (see text above the table)
** Detailed information on Study quality is in Systematic Review Supplemental File: Data Quality
Evaluation and Data Extraction of Human Health Hazard Studies
3.2.4.4 Statistical Methodology
The first step towards deriving a cancer unit risk for risk estimation is to identify potency factors for
lung cancer and mesothelioma. Cancer potency values are either extracted from published epidemiology
studies or derived from the data within those studies. Once the cancer potency values have been
obtained, they are adjusted for differences in air volumes between workers and other populations. Those
adjusted values can be applied to the U.S. population as a whole in the standard EPA life-table analyses.
These life-table analyses allow for the estimation of an exposure concentration associated with a specific
extra risk of cancer mortality caused by asbestos. The unit risks for lung cancer and mesothelioma are
estimated separately and then combined to yield the cancer inhalation unit risk.
3.2.4.4.1 Cancer Risk Models
A cancer risk model predicts the probability of cancer in an individual with a specified history of
exposure to a cancer-causing agent. In the case of inhalation exposure to asbestos, the cancer effects of
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chief concern are lung cancer and mesothelioma, and exposure history is the product of the level and
timing of the asbestos exposure. The most common model forms are described below.
Lung Cancer
For lung cancer, the risk for grouped data from epidemiologic studies from exposure to asbestos is
usually quantified using a linear relative risk model of the following form (Herman and Crump. 2008;
U.S. EPA. 1988b. 1986V
RR = a (1 + CE Kl)
where:
RR = Relative risk of lung cancer
CE = Cumulative exposure to asbestos (f/cc-yrs), equals the product of exposure
concentration (f/cc) and the duration of exposure (years). In many publications, exposure estimates are
"lagged" to exclude recent exposures, since lung cancer effects usually take at least 10 years to become
apparent. In this case, cumulative exposure is indicated as CE10 to represent the 10-year lag period.
Kl = Lung cancer potency factor (f/cc-yrs)"1.
a = The ratio of baseline (unexposed) risk in the study population compared to the
reference population. If the reference population is well-matched to the study population, a is usually
assumed to be constant=l and is not treated as a fitting parameter. If the general population is used as
the reference population, then a may be different from 1 and is treated as a fitting parameter.
A re-parametrization with a = exp (J3o) is called the linear relative rate model. For epidemiologic studies
where, individual data analysis was conducted, other models have been used for modeling lung cancer.
These include both linear relative rate model (e.g., (Hein et al. 2007)). the Cox proportional hazard
model (e.g., ( ; Wang et al.. 2014) and other log-linear relative rate models (e.g., (Elliott
et al.. 2012; Loom is et al.. 2009). Results from all these model types were considered to be informative
in estimating the lung cancer potency factor (Kl) and were carried forward for further consideration.
Mesothelioma
For mesothelioma, the risk model is usually an absolute risk model that gives the risk of death from
mesothelioma in an individual following exposure to asbestos that is a function of the concentration and
length of time since first exposure. The model form (originally proposed by (Peto et al.. 1982; Peto.
1978) and subsequently used by others, including U.S. EPA (1986) and Berman and Crump (2008)) is:
Im = C Km Q
where:
Im
C
Km
Q
exposure, as follows:
Rate of mesothelioma (cases per person year)
Concentration of asbestos (f/cc)
Mesothelioma potency factor (f/cc-yrs3)"1
A cubic function of the time since first exposure (TSFE) and the duration (d) of
for TSFE <10 Q = 0
for 10d + 10 Q = (TSFE - 10)3 - (TSFE - 10 - d)3
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3.2.4.4.2 Derivation of Potency Factors
Values for the cancer potency factors (Kl and Km in the equations above) are derived by fitting a risk
model to available exposure-response data from epidemiological studies of workers exposed to asbestos.
Fitting is performed using the method of Maximum Likelihood Estimation (MLE), assuming that the
observed number of cases in a group is a random variable described by the Poisson distribution.
In general, the preferred model for fitting utilizes individual-level observations. This allows for the
exposure metric to be treated as a continuous variable, and also allows for the inclusion of categorical
covariates of potential interest such as gender, calendar interval, race, and birth cohort. When the
individual data are not available, then the data for individuals may be grouped according to a key
exposure metric (CE10 for lung cancer, TSFE for mesothelioma), and the mid-point of the range for
each model parameter is usually used in the fitting. In cases where the upper bound of the highest
exposure category was not reported in the publication, the value for the upper bound was assumed to be
the maximum exposure reported in the publication.
In cases where study authors reported a potency factor derived using an appropriate model, that value
was retained for consideration. In cases where the authors did not report a potency factor derived by an
appropriate method, EPA estimated the potency factor by fitting a model to grouped data, if they were
reported. EPA fitting was performed using SAS. Appendix G provides the SAS codes that were
employed. As a quality check, calculations were also performed using Microsoft Excel. Both methods
yielded the same results to 3 or more significant figures.
When the potency factors were estimated by the study authors, EPA relied upon the confidence bounds
reported by the authors. These were generally Wald-type bounds. Because, the inhalation unit risk (see
below) is derived from the one-sided 95th% upper bound (which is equivalent to the upper bound of the
two-sided 90th% upper bound), if the authors reported a two-side 95% confidence interval (i.e., from the
2.5th to the 97.5th bounds), EPA estimated the two-sided 90% confidence interval by back calculating the
5th and 95th confidence bounds, assuming a normal distribution.
When EPA performed the fitting, 90% two-sided confidence bounds around the potency factors were
derived using the profile likelihood method. In this method, the 100(l-a) confidence interval is
computed by finding the two values of the potency factor that yield a log-likelihood result that is equal
to the maximum log-likelihood minus 0,5-%2( l-a, 1), i.e., central chi-square distribution with one degree
of freedom and confidence level 1-a. For a 90% confidence interval, this is equal to the maximum log-
likelihood minus 1.353.
3.3.4.4.3 Extrapolation from Workers to the general population to
derive inhalation unit risk
Because EPA defines the cancer inhalation unit risk for asbestos as an estimate of the increased cancer
risk from inhalation exposure to a concentration of 1 f/cc for a lifetime13, and the cancer potency factors
are derived by fitting risk models to exposure-response data based on workers, it is necessary to adjust
the worker-based potency factors to derive values that are applicable to an individual with a different
13 Note that the lifetime inhalation unit risk is then applied to specific environmental exposure scenarios applicable to current
asbestos uses; for specific worker exposure scenarios, the extrapolation factor described may not be applied.
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exposure pattern (e.g., a resident with continuous exposure). The extrapolation is based on the
assumption that the ratio of the risk of cancer in one population compared to another (both exposed to
the same level of asbestos in air) is related to the ratio of the amount of asbestos-contaminated air that is
inhaled per unit time (e.g., per year).
For workers, EPA assumes a breathing rate of 10 m3 of air per 8-hour work day (U.S. EPA. 2009). If
workplace exposure is assumed to occur 240 workdays/year, the volume of air inhaled in a year is
calculated as follows:
Volume Inhaled (worker) =10 m3/workday • 240 workdays/yr = 2,400 m3/yr
For a resident, EPA usually assumes a breathing rate of 20 nrVday ( >09). If exposure is
assumed to be continuous (24 hours per day, 365 days per year), the volume inhaled in a year is
calculated as follows:
Volume Inhaled (resident) = 20 m3/day • 365 days/yr = 7,300 m3/yr
In this case, the extrapolation factor from worker to resident is:
Extrapolation factor = 7,300 / 2,400 = 3.042
In the tables below (Section 3.2.4.5), the potencies are shown as calculated from epidemiological
studies, and the worker to other populations extrapolation factor is applied in the life-table analyses so
that the unit risks and IUR incorporate that extrapolation factor.
3.2.4.4.4 Life-Table Analysis and Derivation of Inhalation Unit Risk
Potency factors are not analogous to lifetime unit risks or cancer slope factors, and do not directly
predict the excess risk of lung cancer or mesothelioma in an exposed individual. Rather, the potency
factors are used in lifetable analyses for lung cancer and mesothelioma to predict the risk of dying as a
result of the exposure in a specified year of life. However, it is important to recognize that cancer risk in
a particular year of life is conditional on the assumption that the individual is alive at the start of the
year. Consequently, the risk of dying of an asbestos-related cancer within a specified year of life is
calculated as the product of two terms: the probability of being alive at the start of the year and the
probability of dying of the asbestos exposure within the specified year. The lifetime risk is then the sum
of all the yearly risks. This procedure is performed to calculate the lifetime risk both for an unexposed
individual (Ro) and for an individual with exposure to asbestos (Rx).
"Extra risk" for cancer is a calculation of risk which adjusts for background incidence rates of the same
type of cancer, by estimating risk at a specified exposure level only among the fraction of the population
not expected to develop the cancer due to background causes, and is calculated as follows (U.S. EPA...
2012V
Extra Risk = (Rx - Ro) / (1 - Ro)
For mesothelioma, because background risk (Ro) is assumed to be zero, extra risk is the same as absolute
risk (Rx).
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The unit risk is risk of incident cancer14 per unit asbestos concentration (fiber/cc) in inhaled air. The unit
risk is calculated by using life table analysis to find the exposure concentration (EC) that yields a 1%
(0.01) extra risk of cancer. The 1% value is referred to as the Benchmark Response (BMR). This value
is used because it represents a cancer response level that is near the low end of the observable range
(U.S. EPA. 2012.). Given the EC at 1% extra risk (ECoi), the unit risk is the slope of a linear exposure-
response line from the origin through the ECoi:
Unit risk = 0.01 / ECoi
A unit risk value may be calculated based on both the best estimate and the 95% upper confidence
bound (UB) on the potency factor. The value based on the upper 95% confidence bound is normally
used for decision-making, since it corresponds to a lower 5% confidence bound (LB) on the exposure
level yielding 1% extra risk (LECoi). Inhalation unit risk is derived by statistically combining risks of
lung cancer and mesothelioma. This procedure is described below in the section on combining unit risks.
Life table calculations require as input the all-cause and cause-specific mortality rates for the general
population in each year of life. The all-cause mortality data were obtained from the National Vital
Statistics Report Vol 66 No 3 Table 1 (2017). which provides data from the U.S. population in 2013.
Lung-cancer mortality rates were obtained by downloading 2016 mortality data for malignant neoplasms
of trachea, bronchus and lung (ICD-10 C33-C34) from CDC Wonder (http://wonder.cdc.gov/ucd-
icdlQ.html). Because cause-specific mortality rates were given for 5-year intervals, the cause-specific
rate for each 5-year interval was applied to each age within the interval. For mesothelioma, the mortality
rate in the absence of asbestos exposure was assumed to be zero.
The detailed equations for calculating lifetime excess cancer risk for a specified exposure concentration
in the presence of competing risks are based on the approach used by NRC (1988) for evaluating lung
cancer risks from radon. The equations are detailed in Appendix H. The SAS code for lung cancer life
table analysis was provided to EPA by NIOSH15 and was adapted for use by a) entering the mortality
data noted above, b) adding an equation to compute extra risk, and c) adding a macro to solve for the
EC. The SAS code for mesothelioma was created by inserting user-defined equations for the
mesothelioma risk model into the NIOSH code. The SAS codes for performing the mesothelioma and
lung cancer life table calculations are provided in Appendix I. As a quality check, life table calculations
were also performed using Microsoft Excel. Both methods yielded the same results to 3 or more
significant figures.
3.2.4.5 Study Descriptions and Model Fitting Results
The asbestos exposure data and exposure assessment methods in studies of the Charleston, South
Carolina textile plant (Elliott et at.. 2012: Hein et at.. 2007) are exceptionally detailed compared to most
asbestos studies. The methods used were innovative at the time, a large number of exposure
measurements cover the relevant study period, and detailed process and work history information were
available and utilized in estimating exposures. The exposure data used in studies of North Carolina
plants (Loomis et at.. 2019: Elliott et at..: ) are also high quality. The methods were similar to those
developed for the studies of the South Carolina plant. However, relative to the South Carolina study, the
14IUR is for incident cancer, but the data available from epidemiology studies are only in terms of mortality (see Section
3.2.4.8)
15 Beta Version. SAS 30NOV18, provided by Randall Smith, National Institute for Occupational Safety & Health.
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number of exposure measurements is smaller, and the historical process and work-history data are less
detailed. Nevertheless, the exposure data are of higher quality than those utilized in other studies of
occupational cohorts exposed to chrysotile. For both U.S. textile cohorts, the exposure assessment
methods and results have been published in full detail.
Studies of the asbestos products factory in Chongqing, China (Courtice et at.. 2016; Wang et ai. 2013b;
Deng et at.. 2012; Yano et at... 2001) provide informative data on a cohort that has not been included in
previous risk assessments. The methods used to estimate worker exposures for exposure-response
analyses appear to have emulated those used in the U.S. textile-industry studies. Nevertheless,
confidence in the exposure data is lower because exposure measurements were made only in later years
in the study period, the number of measurements is small, and the methodology is not reported in detail.
Information about the assessment of exposures for the Quebec asbestos mining and milling cohorts is
presented in several papers (Liddell ant! \mtstrong. 2002; 1998; Vacei Liddell et at.. 1997;
1993a; 1980a; Mcdonald et at.. 1980b). but the reports are lacking important details and are sometimes
in conflict. Nevertheless, it is evident that exposure measurements do not cover the entire study period.
The number of measurements is not consistently reported but appears to be smaller than for either of the
U.S. textile cohorts, while the number of distinct jobs was larger. Moreover, all the reported
measurements were of total dust, rather than fibers. Some reports have suggested or used a conversion
factor, but the use of single factor for all operations is likely to introduce substantial exposure
misclassification since the relationship between total dust and fiber counts has been shown to vary
considerably by process.
Fewer details are available about the assessment of exposures for studies of chrysotile miners in China
(2014; 2013b; Wang et at.. 2012). Although workshop- and job title-specific fiber concentrations were
estimated in the study in China, these estimates were based on a small number of paired samples and
important details of the exposure assessment are not available. The quality of the exposure data is
therefore difficult to judge.
Cohorts are listed in order of the quality of exposure assessment with the highest quality cohorts first.
The cohorts from SC and NC were judged to have the highest quality exposure assessment and only
those results were carried forward for consideration on the cancer-specific unit risks and the overall
IUR. For the rest of the cohorts, results of modeling are reported, but not carried forward.
South Carolina asbestos textile plant [carried forward for unit risk derivation]
Mortality in a cohort of workers at an asbestos textile plant in Charleston, South Carolina, USA has been
reported in several papers (Elliott et at.. 2012; 2008; Hein et at... 2007; Stavner et at.. 1997; Brown et at..
1994; 1994; Dement et at.. 1983a). Workers employed for at least one month between 1940 and 1965
were included; the cohort originally included only white men but was later expanded to include non-
whites and women.
The Charleston plant produced asbestos textiles from raw chrysotile fibers imported from Canada
(Quebec and British Columbia) and Rhodesia (now Zimbabwe). Purchased crocidolite yarns were also
woven in a small separate operation for about 25 years, but crocidolite was never carded or spun on site
(Dement |). The total amount of crocidolite handled was 0.03% of the amount of asbestos
processed annually (Dement et at.. 1994).
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Methods and results of exposure assessment for this cohort were published in detail by Dement et al.,
(1983b) and summarized in subsequent publications (e.g., (Hein et al.. 2007)). Engineering controls for
dust levels were introduced in the plant beginning in the 1930s and the facility was believed to represent
the best practice in the industry at the time (Dement et a 5b). Estimates of individual exposure
were based on 5952 industrial hygiene air samples between 1930 and 1975. All samples before 1965
were obtained by midget impinger; both impinger and membrane filter samplers were used from 1965
until 1971, and afterward only membrane filter samplers were used. Phase-contrast microscopy (PCM)
was used in conjunction with membrane filter sampling to estimate concentrations of fibers >5|im in
length. Further details of historical fiber counting rules are not reported, but fibers <0.25 |im in diameter
cannot be visualized by PCM and are normally not counted. Paired and concurrent samples by both
methods were used to estimate job and operation-specific conversion factors from mppcf to f/cc. One
hundred and twenty paired samples were collected in 1965 and 986 concurrent samples were collected
during 1968-1971. Statistical analysis of the data indicated no significant trends in fiber/dust ratios over
time and no significant differences among operations, except for preparation. Consequently, conversion
factors of 8 PCM f/cc per mppcf for preparation and 3 PCM f/cc per mppcf for all other operations were
adopted for further analysis. Fiber concentrations were estimated for 9 departments and 4 job categories
by linear regression, accounting for time-related changes in process and dust control. Individual
cumulative exposures were estimated by linking this job-exposure-matrix to detailed occupational
histories for each worker.
The most up to date data for lung cancer and mesothelioma in the cohort were reported by Hein et al.
(2007) based on follow-up of 3072 workers through 2001; 198 deaths from lung cancer and 3 deaths
from mesothelioma were observed. Quantitative exposure-response relationships for lung cancer were
estimated by Poisson regression modeling using a linear relative rate form. Cumulative chrysotile
exposure in f/cc-yrs was lagged by 10 years and entered as a continuous variable with sex, race and age
as covariates. Elliott et al. ( ) performed a similar analysis, except some members of the cohort were
excluded to improve comparability with a cohort of textile workers from North Carolina (see below).
Hein et al. (2007) did not report exposure-response analysis or detailed data for mesothelioma in the
Charleston cohort. All death certificates for deaths before ICD-10 in 1999 were investigated (Hein,
personal communication) for mention of mesothelioma (3 deaths), no mesothelioma deaths after 1999
were observed. Berman & Crump (2008) estimated Km for the cohort from analyses of the original data
obtained from the study investigators (see Table 3-3).
Table 3-3 Model Fitting Results for the Sout
l Carolina Cohort

Exposure

Concent rat ion

K nd point
Source
la hie in
original
publica-
tion
Potency Eactor
associated with
IJMK (1%
Extra Kisk)
(f/cc)
Lifetime In it
Kisk (per f/cc)

Mil.
95%
ECoi
1 .EC mi
Mil.
95%

IB
Mil.
5% I.I!
IB

Hein et al. (2007)
linear
Table 5
1.98E-02
2.80E-02
7.15E-2
5.06E-2
1.40E-01
1.98E-01
Lung Cancer
EPA modeling of Hein

et al. (2007) grouped
Table 3
1.73E-02
2.22E-02
8.19E-2
6.38E-2
1.22E-1
1.57E-1

data linear

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Elliott et al. (2012)
linear
Table 2
2.35E-02
3.54E-02
6.03E-2
4.00E-2
1.66E-1
2.50E-1

Elliott et al. (2012)
exponential
Table 2
5.13E-03
6.36E-03
2.44E-1
1.97E-1
4.09E-2
5.07E-2
Mesothelioma
Berman and Crump
(2008) based on Hein
et al. (2007)
Table 4
1.5E-09
3.3E-09
4.0E-1
1.8E-1
2.5E-2
5.5E-2
1) Details for the modeling for lung cancer are provided in Appendix G, Section 1. Details for the modeling of
mesothelioma is provided in Berman and Crump (20081
2) In EPA modeling of Hein et al. (20071 grouped data, alpha= 1 and upper bound on the highest exposure interval was
assumed 699.8 f/cc (the maximum exposure reported in the publication).
3) In calculations involving Elliott et al. (2012). the 95% upper bound on potency factor was calculated from the
reported 97.5% upper bound as described above.
4) Berman and Crump (2008) reported mesothelioma potency number (KM) with 2 significant digits.
Selection of the results from the South Carolina cohort
As discussed above, for lung cancer, the modeling of individual data is preferred so results from Hein et
al. (2.007) as well as two results of Elliott et al. (2012) were carried forward for further consideration.
For mesothelioma, only the results of modeling of the South Carolina cohort data by Berman and Crump
(2008) are available, and those are will be carried forward for the unit risk derivation.
North Carolina asbestos textile plants [carriedforward for unit risk derivation]
Loom is et al. (2019; 2009) reported on mortality in a cohort of workers in four North Carolina asbestos
textile mills that had not been studied previously. Three of the plants were operationally similar to the
South Carolina plant, but did not have equivalent exposure controls. They produced yarns and woven
goods from raw chrysotile fibers, mostly imported from Canada. A fourth, smaller plant produced
several asbestos products using only purchased yarns. The latter plant lacked adequate exposure data
and was included in comparisons of cohort mortality to the general population, but not in exposure-
response analyses for lung cancer or mesothelioma. One of the three larger plants also carded, twisted
and wove amosite fibers in a separate facility for 13 years (Loomis et al.. 2009). Quantitative data on the
amounts of amosite used are not available. However, the operation was isolated from general production
and no amosite fibers were found in TEM analysis of archived samples from that plant or any other
(Elliott et al. 2012).
Workers employed at least 1 day between 1950 and 1973 were enumerated from company records: 5770
workers (3975 men and 1795 women) and files of state and national health agencies were included and
followed for vital status through 2003. Causes of death were coded to the ICD revision in force at the
time of death. All conditions mentioned on the death certificate, including intermediate causes and other
significant conditions were coded. Death certificate data were examined for any mention of
mesothelioma and for ICD codes often applied to mesothelioma before a specific code for mesothelioma
was introduced in 1999. Only one worker in the cohort, who did not develop lung cancer or
mesothelioma, had a history of employment in the operation where amosite had been used.
Exposure assessment methods and results are described by Dement et al. (2009). The approach was
similar to that used in South Carolina (Dement et al. 1983b) with updated statistical methods. Asbestos
fiber concentrations were estimated from 3420 air samples taken from 1935 to 1986. Sampling until
1964 was by impinger; membrane filter sampling was introduced in 1964 and both methods were used
until 1971, with only membrane filter sampling thereafter. Fibers longer than 5 |im captured on
membrane filters were counted by PCM to estimate concentrations; further details of historical fiber
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counting rules are not available. Paired and concurrent samples by both methods were used to estimate
plant-, operation- and period-specific factors for converting dust to PCM-equivalent fiber
concentrations. Fiber/dust ratios did not change significantly over time, so plant- and operation-specific
conversion factors (range 1.6 (95% CI 0.4-2-8) fibers/mppcf to 8.0 (95% CI 7.4-8.7) fibers/mppcf) were
used for further analysis. Fiber concentration data were analyzed using multivariable mixed models to
estimate average concentrations by plant, department, job and time period. The operation and job
categories of the job-exposure matrix were similar to those developed for South Carolina (2009; Dement
et ai. 1983a). These estimates were linked to individual work history records to estimate average and
cumulative exposure to asbestos fibers for each worker. Detailed job titles within departments were
missing for 27% of workers, mostly short-term; in these cases, exposure was estimated using the plant,
period and department average (Loomis et at.. 2009). For years prior to 1935, when no exposure
measurements and few work history records were available, exposures were assumed to have been equal
to those in 1935, before dust controls were implemented.
In total, 277 deaths from lung cancer occurred during follow-up. Exposure-response analyses for lung
cancer included 3803 workers in production jobs in 3 of the 4 study plants and 181 lung cancer deaths.
Data were analyzed using conventional log-linear Poisson regression models adjusted for age, sex, race,
decade of follow-up and birth cohort. Results were reported as relative rates per 100 f/cc-yrs with
exposure lags of 0 to 30 years (Loomis et at. 2009).
Elliott et al. (2.012) also evaluated exposure-response relationships for lung cancer in the North Carolina
cohort using Poisson regression with both log-linear and additive relative rate model forms. Models
were adjusted for age, sex, race, calendar period and birth cohort. Results were reported per 100 f/cc-yrs
of cumulative fiber exposure with lags of 0, 10 or 20 years.
During the follow-up of the North Carolina cohort, four deaths were coded to mesothelioma according
to the ICD-10, and, prior to the implementation of ICD-10, four deaths coded as cancer of the pleura and
one death coded as cancer of the peritoneum were observed (2.019; Loomis et ai. 2009). Because
Loomis et al. (2.019) reported only pleural cancers before ICD-10, EPA modeled the exposure-response
for mesothelioma using data from 1999 onward when ICD-10 was in use (see Table 3-4).
Table 3-4. Model Fitting Results for the North Carolina Cohort
K nd point
Source
Table in
original
publica-
tion
Potency
Ml.l.
l-'actor
95%
IB
Kxp<
Conccii
associat
li.MH
Kxlra
(f7
IX Ml
Mil.
>sure
(ration
cri with
(1 %
Kisk)
cc)
I.I ( mi
5% 1.1!
l.ilelin
Kisk (|i
Mil.
le I nil
er l'/cc)
95%
IB
Lung Cancer
l-llioii el ill ( )
linear
Table 2
1.20L-3
2.71L-3
1.180
5.23L-1
8.47L-3
1.91L-2
Elliott et al. (2012)
exponential
Table 2
9.53E-4
1.40E-3
1.32
8.95E-1
7.60E-3
1.12E-2
Loomis et al. (2009)
exponential
Table 6
1.01E-3
1.47E-3
1.24
8.53E-1
8.06E-3
1.17E-2
EPA modeling of
Loomis et al. (2009)
grouped data linear
Table 5
8.08E-4
1.31E-3
1.75
1.08
5.71E-3
9.25E-3
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Mesothelioma
EPA modeling of
Loomis et al. (2019)
Table Sib
2.44E-9
5.04E-9
2.45E-1
1.19E-1
4.08E-2
8.42E-2
1) Details for the modeling are provided in Appendix G, Section 2.
2) In EPA modeling of the Loomis et al. (2009) lung cancer grouped data, alpha= 1 and the upper bound on the
highest exposure interval was assumed 2,194 f/cc (the maximum exposure reported in the publication).
3) In calculations involving Loomis et al. (2009) and Elliott et al. (20.1.2) lung cancer modeling, the 95% upper
bound on potency factor was calculated from the reported 97.5% upper bound as described above.
4) In EPA modeling of the Loomis et al. (20.1.9) mesothelioma data, the two top TSFE groups were combined by
adding cases and person-years; TSFE, concentration and duration were calculated by averaging person-year-
weighted results for both groups.
Selection of the results from the North Carolina Cohort
As discussed above, for lung cancer, the modeling of individual data is preferred so results from Loomis
et al. (2009) as well as two results of Elliott et al. (2012.) are carried forward for further consideration.
The mesothelioma results from the Loomis et al. (2019) sub-cohort of workers that were evaluated with
ICD-10 are carried forward for unit risk derivation.
Chongqing, China, asbestos products factory
An initial report on mortality among workers at a plant in Chongqing, China, that produced a variety of
asbestos products was published by Yano et al. (2001). A fixed cohort of 515 men employed at least one
year and active as of 1 January 1972 was established and followed for mortality using plant records.
Women were not included in the original cohort as none were hired before 1970. Further analyses based
on extended follow-up were reported in subsequent papers (Courtice et al.. 2016; Wane et al.. 201 Jb;
Deng et al.. ^ ). The 2008 follow-up of the cohort added 279 women employed between 1970 and
1972 (Wang et al.; ).
The Chongqing plant opened in 1939 and expanded in the 1950s; a range of asbestos products, including
textiles, friction materials, rubber-impregnated goods and cement were produced (Yano et al.. 2001).
The plant is reported to have used chrysotile asbestos from two mines in Sichuan Province; amphibole
contamination in bulk samples from these mines assessed by transmission electron microscopy (TEM)
was found to be below the limit of detection (LOD <0.001%, (Courtice et al.. 2016; Yano et al.. 2001).
An independent study of commercial chrysotile extracted from six mines in China reported tremolite
content of 0.002 to 0.312% by weight (Tossavainen et al.. 2001). but it is not clear whether these mines
supplied chrysotile to the Chongqing factory.
Deng et al. (. ) reported on the methods of exposure assessment. Fiber concentrations for four
operations (raw materials processing, textile carding and spinning, textile weaving and maintenance, and
rubber and cement production) were estimated from 556 area measurements taken every 4 years from
1970 to 2006. Only total dust was measured before 1999, while paired measurements of dust and fibers
were taken subsequently. A total of 223 measurements of fiber concentration by PCM were available.
Paired dust and fiber samples from 1999-2006 were used to estimate dust to PCM fiber-equivalent
concentrations for the 1970-1994 using an approach similar to that of Dement et al. (2009) and the
estimated and measured concentrations were combined for analysis; however, no details were reported
on what operations and jobs these estimates represent. Individual cumulative fiber exposures were
estimated from the concentration data and the duration of employment in each area of the plant. Work
histories were reported to have been stable with few job changes (Dene et al.. 2012).
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Exposure-response data for lung cancer in the Chongqing cohort have been reported in several papers.
Deng et al.(2012) analyzed data for 586 men and women followed to 2006 and reported quantitative risk
estimates for cumulative chrysotile exposure obtained by fitting log-linear and additive relative rate
models with adjustment for age, smoking and calendar period. Wang et al. (2.014) published additional
analyses of the same study population but truncated the follow-up period from 1981 to 2006 to make it
more comparable with a study of Chinese asbestos miners (described below). The vital status of this
cohort was updated to 2008 and an analysis including follow-up from 1972 to 2008 was published by
Courtice et al. (2016). The latter papers provide quantitative risk estimates from internal analyses with
log-linear relative rate models. Papers on the Chongqing cohort provide informative exposure-response
information in units of f/cc-years from Cox or Poisson regression analyses. However, there is potential
for misclassification of exposures due to the relatively small number of exposure measurements, the lack
of fiber measurements before 1999 and use of area rather than personal sampling (Deng et al.. 2012.).
Fitting results from Deng et al. (2012) are provided in Table 3-5.
Table 3-5. Model Fitting Results for the Chongqing China Cohort

Kxposure

('onccnl ration

la hie in
Polencv l-'aclor
associated with
Lil'dime I nil
Kndpoinl
Source
original
publica-
li.MU (1%
Kxlra Kisk)
Kisk (per l'/cc)

tion

(l'/cc)

MM.
95%
IB
IX Ml
mi.i:
I.I ( mi
5% 1.1!
Mil.
95%
IB
Lung
Cancer
Deng et al. ( )
exponential
Table 3
2.08E-3
3.02E-3
6.03E-1
4.15E-1
1.66E-2
2.41E-2

Deng et al. ( )
Linear
Table 3
4.21E-3
4.56E-3
3.36E-1
3.11E-1
2.97E-2
3.22E-2
Details for the modeling are provided in Deng et al. (20.1.21
Data for mesothelioma were reported for follow-up through 2008 of the expanded cohort including
women (Wane et al.. 2013b). Three deaths coded as mesothelioma according to the I CD-10 (2 among
men and 1 among women) were recognized and only SMRs were reported separately for men and
women (Wane et al.. 2013b). Data on the exposure levels of the mesothelioma cases are not available,
however, so model fitting was not possible. No other analyses of mesothelioma have been reported for
the Chongqing cohort.
Quebec, Canada asbestos mines and mills [not carriedforward]
Data from studies of miners, millers and asbestos products factory workers at several facilities in
Quebec, Canada are reported in multiple publications (Liddell and Armstrong. 2002; 1998; Vacek. 1998;
Liddell et al.. 1997; 1993a; 1980a; Mcdonald et al.. 1980b). The earliest publication, McDonald et al.
(1980b). included 1 1,379 miners and millers from Quebec, Canada who were born between 1891 and
1920 and had worked for at least a month in the mines and mills and were followed to 1975. Additional
findings based on follow-up of the cohort to 1988 were reported by McDonald et al. (1993 a). and further
extended to 1992 by Liddell et al. (1997). Trace amounts of tremolite have been reported in samples
from the Canadian mines (IARC, i ), with the amounts varying between mines (Liddell et al.. 1997).
The most detailed description of exposure assessment methods used in the Quebec studies is given by
Gibbs and Lachance (1972). Additional details and updates are given in later publications (e.g., (Liddell
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et at.. 1997; Mcdonald et al. 1980b)). Total dust concentrations (in mppcf) were estimated using midget
impinger measurements taken from 1948 to 1966 (Gibbs and Lachance. 1972). Several different figures
are reported for the total number of dust measurements used to estimate exposures: Gibbs and Lachance
(GibbsandLachan.ee. 1972) reported 3096; McDonald et al. (1980b) reported "well over 4000," and
McDonald et al. (1980a) reported 10,205. Annual dust concentrations for 5783 unique jobs were
assigned according a 13-point scale with categories of 0.5, 2, 7, 12, 17, 22, 27, 32, 37, 42, 47, 70 and
140 mppcf. The authors describe the categories as "approximating to the mean", but the methods of
analyzing the exposure measurements and developing the categories are not reported. Different
approaches were used to estimate exposures in earlier and later years when dust data were judged to be
inadequate; exposures in years before 1948 were reportedly estimated by expert assessment based on
interviews with workers and company personnel, while those after 1966 were estimated by extrapolation
from the previously measured levels (Liddett et al.. 1997). Cumulative dust exposure (in mppef-years)
for each worker was estimated from the assigned dust concentrations and individual work histories;
estimated exposures in years before 1938 were multiplied by 1.65 to account for longer work weeks at
that time (Liddell et al.. 1997). Fibers reportedly accounted for 8-15% of total dust (Gibbs and
Lachance. 1972). Most exposure-response analyses for the cohort were reported relative to cumulative
dust exposure in mppcf. However, in a case-control study of lung cancer, McDonald et al. (1980a)
adopted an overall conversion factor of 3.14 f/cc per mppcf, citing 11,819 fiber measurements (methods
of measurement and analysis not described), "unfortunately with little overlap" with the dust data. In
another publication, McDonald et al. (1980b) suggested fiber concentrations per cc would be between 1
and 7 per mppcf. Liddell et al. (1984) subsequently reported conversion factors ranging from 3.44 to
3.67 f/cc per mppcf. Gibbs (1994) reported a 95% confidence interval of 0.58(D)0 68 to 55.7(D)0 68, where
D is the dust concentration measured by impinger, for the ratio of fibers to dust (units not specified).
Gibbs and Lachance (1972.). reported that the correlation between midget impinger and membrane filter
counts (0.32) was poor and suggested that "no single conversion factor was justified". Berman (2010)
performed an analysis of dust samples from the Quebec mines and found that one third of the PCM
structures samples in the dust were not asbestos, and that about one third of structures counted by PCM
were also counted by TEM. These findings along with the uncertainties concerning what is an
appropriate conversion factor raise significant concerns about the accuracy of the f/cc estimates of
exposure from the Quebec studies.
Most analyses of the Quebec cohort compared workers' mortality to the general population using SMRs
(e.g., (Liddell et al.. 1997; 1993a; Mcdonald et al. 1980b). Liddell et al. (1998) conducted a nested case-
control study of lung cancer in a subset of workers at the mines and mills that were included in the
previous cohort studies and workers from an asbestos products factory. Subsequent publications by
Vacek et al. (1998). and Liddell and Armstrong (2002) presented more detailed analyses on a subset of
the cohort to examine the role of intensity and timing of exposure, and of potential effect modification
by cigarette smoking. All exposure-response analyses of lung cancer in the Quebec studies utilized total
dust exposure expressed in mppcf. Estimates of Kl or analogous additive relative risk measures have not
been reported for these studies.
Liddell et al. (1997) reported 38 cases of mesothelioma in the last follow-up through 1992. The same
publication also reported that mesothelioma as a cause of death was almost unknown in Quebec until
1960, which was more than 40 years after start of the cohort's exposure. Because of that, the method of
ascertainment for mesothelioma for the cohort was considered to be insufficient because it did not
include likely mesothelioma deaths and mesothelioma results are not reported in a way to allow for
derivations of Km for the cohort once mesothelioma reporting in Quebec became reliable.
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Berman and Crump (2008) estimated Ki for the Quebec cohort from analyses of original data obtained
from the study investigators. A single conversion factor for all operations of 3.14 fibers/cc per mppcf
was assumed in this analysis. Results are presented in Table 3-6.
Table 3-6. Model Fitting Results for the Quebec, Canada Cohort
Knilpoint
Source
Table in
original
publication
I'olcnc)
mm:
I'actor
«>5%
I li
K\p<
Con con
associal
IIMR (1
Risk)
i:c,,,
mm:
)Sll IV
(ration
eil w itli
Vn Kxtra
(f/cc)
I.IX
5% US
Li let in
Risk (p
mm:
le I nit
er f/cc)
«>5%
I li
Lung
Cancer
Berman and Crump
(2008) modeling of
grouped data linear
Table B1
2.9E-4
4.10E-4
4.88
3.45
2.05E-3
2.90E-3
1. Details for the modeling are provided in Berman and Crump (2008).
2. In Berman and Crump (2008) modeling of the grouped data, alpha= 1.15 was fitted.
Qinghai, China asbestos mine [not carried forward]
Wang et al. (JO 14; 2013a; 201 J) reported findings from exposure-response analyses of a cohort of 1539
workers at a chrysotile mine in Qinghai Province, China who were on the registry January 1, 1981 and
had been employed for at least one year. The cohort was followed for vital status from 1981 to 2006.
The mine opened in 1958 (no closing date reported) and produced commercial chrysotile with no
detectable tremolite content (LOD 0.1%, (Wang et al. 2012)). Total dust concentrations in the mine
were measured periodically between 1984 and 1995 by area sampling in fixed locations (Wane et al..
2012). Sampling was performed according to Chinese national standards. The number of measurements
during this period is not reported. An additional 28 measurements were taken in 2006 in 8 different
workshops. Dust concentrations in mg/m3 were converted to f/cc using a linear regression model based
on 35 paired measurements taken in 1991. Fiber concentrations were estimated by workshop and job
title for the period 1984-2006, apparently using a single conversion factor. The estimation methods are
not described in detail in English-language publications, but further details may be available in Chinese-
language publications referenced by Wang et al. (2013a; 2012). but not reviewed here. As recognized by
the authors (Wane et al.. 2013a). there is potential for exposure measurement error due to the conversion
from mppcf to f/cc-yrs which was based on 35 paired samples that were collected in only one year, for
an unspecified number of operations.
Wang et al. ( ) report estimates of SMRs and standardized rate ratios (SRRs) for lung cancer by
categorical levels of f/cc-yrs, stratified by smoking status. EPA used these combined data for smokers
and non-smokers to estimate a value and confidence interval for Kl based on the linear relative risk
model.
Wang et al. (2014) presented rate ratios for categorical and continuous exposure variables using log-
linear Cox proportional hazards models adjusted for age and smoking. The findings from the Cox model
are useful for risk assessment in that asbestos exposure is modeled as a continuous variable using
individual level data, which generally provides a more statistically powerful examination of exposure-
response relationships than a grouped analysis. Furthermore, the Cox PH analyses by Wang et al. (2014)
adjusted for smoking, whereas the earlier SMR and SRR analyses (Wane et al.. 2013a) did not. Fitting
results are shown in Table 3-7.
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No data on mesothelioma have been reported for the Qinghai mining cohort.
Table 3-7. Model Fitting Results for the Qinghai, China Cohort

Exposure

Concentration

Lndpoint
Source
Table in
original
Publication
Potency l-'actor
associated with
IJMK (1 %
Extra Kisk)
(f/cc)
Lifetime In it
Kisk (per f/cc)

Mil.
95%
ECoi
MX m.
Ml.l.
95%

IB
Mil.
5% LIS
I IS
Lung
Cancer
EPA modeling of
Wang et al. (2013a)
grouped data linear
Tables 5
and 6
2.16E-2
6.47E-2
6.56E-2
2.19E-2
1.53E-1
4.57E-1
Wang et al. (2014)
exponential
Table 3
1.82E-3
2.63E-3
6.89E-1
4.77E-1
1.45E-2
2.10E-2
1) Details for the modeling are provided in Appendix I, Section 3.
2) In EPA modeling of the Wang et al. (2013a) grouped data, alpha was fitted (1.21) and the upper bound on the
highest exposure interval was assumed 1097 f/cc (the maximum exposure reported in Wang et al. (20.1.4) for this
cohort). The data in Tables 5 and 6 were combined in modeling.
3) In calculations involving Wang et al. (20.1.4) results of lung cancer modeling, the reported hazard ratio at
exposure level of 100 f/cc-yrs was 1 and it was used to calculate the potency factor as follows: potency factor =
In (1.2)/100.
Cancer risk ranges by Industry
Historically, it has been proposed in the asbestos literature, that cancer risks may differ by industry (e.g.,
U.S. EPA (1986). Berman and Crump (2008) and references therein). While lifetime unit risks of
mesothelioma are derived only from the two cohorts (the NC and SC textiles cohorts), the lifetime unit
risks of lung cancer are available from both those two-cohorts and from two other cohorts (Quebec,
Canada; Qinghai, China) and that allows comparison of lung cancer risks by industry (textile vs.
mining); one remaining cohort included multiple industries and was not included in the comparison
(Chongqing, China). Because there are only two cohorts in each industry category, only a rough
comparison is possible by looking at range of risks for each industry. Results are in Table 3-8 below. It
is clear that the range of risks in each cell is very wide; however, this limited data indicates that among
these cohorts exposed only to chrysotile asbestos, the lifetime unit risks of lung cancer are not different
between textile and mining industries.
Table 3-8. Comparison of Lifetime Units Risks of Lung Cancer by Industry
Industry
Lifeli
Mil.
lie unit risks of lung cancer
95% I IS
Textiles
7.60E-3 - 1.66E-1
1.17E-2 - 2.50E-1
Mining
2.05E-3 - 1.53E-1
2.90E-3 - 4.57E-1
Textiles cohorts (Loomis et al. 2009: Hein et al. 2007): Mining cohorts (Quebec, Canada; Qinghai, China). The cohort from
Chongqing, China was not included here, but those values are intermediate and would not change the ranges provided here.
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3.2.4.6 Summary of Results of North and South Carolina Cohorts
As discussed above, the cohorts from NC and SC, and the models based on individual-level data are
listed in the Table 3-9 below.
Table 3-9. Cohorts and Preferred Statistical Models for SC and NC Cohorts
Cohort
Knilpoinl
Source
Potency Tjictor
Kxposure
Concentration
associated with
liMR (1% Extra
Risk) (f/cc)
Lifetime I nit Risk
(per f/cc)
mm:
*>5%
I li
IX „i
mm:
MX
5% Mi
mm:
«>5% I li
South
Carolina
Lung Cancer
Hein et al. (2007)
linear
1.98E-2
2.80E-2
7.15E-2
5.06E-2
1.40E-1
1.98E-1
Elliott et al. (2012)
linear
2.35E-2
3.54E-2
6.03E-2
4.00E-2
1.66E-1
2.50E-1
Elliott et al. (2012)
exponential
5.13E-3
6.36E-3
2.44E-1
1.97E-1
4.09E-2
5.07E-2
Mesothelioma
Berman and Crump
(2008) based on
Hein et al. (2007)
1.5E-9
3.3E-9
4.0E-1
1.8E-1
2.5E-2
5.5E-2
North
Carolina
Lung Cancer
Elliott et al. (2012)
linear
1.20E-3
2.71E-3
1.18
5.23E-1
8.47E-3
1.91E-2
Elliott et al. (2012.)
exponential
9.53E-4
1.40E-3
1.32
8.95E-1
7.60E-3
1.12E-2
Loomis et al.
(2.009)
exponential
1.01E-3
1.47E-3
1.24
8.53E-1
8.06E-3
1.17E-2
Mesothelioma
EPA modeling of
Loomis et al.
2.44E-9
5.04E-9
2.45E-1
1.19E-1
4.08E-2
8.42E-2
Addressing underascertainment of mesothelioma
Unlike for lung cancer, where the relative risk model is used, the model used for mesothelioma is an
absolute risk model. For mesothelioma, the undercounting of cases (underascertainment) is a particular
concern given the limitations of the ICD classification systems used prior to 1999. In practical terms,
this means that some true occurrences of mortality due to mesothelioma are missed on death certificates
and in almost all administrative databases such as the National Death Index. Even after the introduction
of a special ICD code for mesothelioma with the introduction of ICD-10 in 1999, detection rates were
still imperfect (Camidee et al.. 2.006; Pinheiro et at.. 2004). and the reported numbers of cases typically
reflect an undercount of the true number (note that the North Carolina cohort was updated in 2003, soon
after the introduction of ICD-10). The undercounts are explained by the diagnostic difficulty of
mesothelioma, both because of its rarity, variety of clinical presentations, and complexity of cytological
confirmation. For example, primary diagnosis of pleural mesothelioma is by chest exam and pleural
effusion, but the latter is absent in 10-30% of pleural mesothelioma cases (e.g., (Ismail-Khan et al..
2006).
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There is no single or set of morphological criteria that are entirely specific for mesothelioma (Whitaker.
2000). Peritoneal mesothelioma diagnosis is challenging to differentiate between mesothelioma and
ovarian or peritoneal serous carcinoma, with these tumors have a common histogenesis, may be difficult
to differentiate morphologically and co-express many of the diagnostic markers (Davidson. 201I). To
account for various sources of underascertainment of mesothelioma deaths, U.S. EPA (2 ),
following Kopylev et al. (2011). developed a multiplier of risk for mesothelioma deaths before and after
introduction of ICD-10. Although this procedure was developed based on the Libby Worker cohort, the
problematic diagnostic issues described above are agnostic to the fiber type exposure. The developed
multiplier (!.' ^ l'P \ JO I is 1.39 with confidence interval (0.80, 2.17). Table 3-10 shows the
mesothelioma unit risks adjusted for underascertainment.
Table 3-10. Addressing Underascertainment of Mesothelioma
Cohort
Source
Mesothelioma
I nil risk
(per l'/cc)
Mesothelioma
I B unit risk
(per l'/cc)
Adjusted
.Mesothelioma
1 nit Kisk
(per l'/cc)
Adjusted
.Mesothelioma
IT! risk
(per l'/cc)
South
Carolina
Berman and Crump
(2.008) based on
Hein et al. (2007)
2.5E-2
5.5E-2
3.48E-2
7.65E-2
North
Carolina
EPA modeling of
Loomis et al. (2019)
4.08E-2
8.42E-2
5.67E-2
1.17E-1
3.2.4.6.1 Combining Lung Cancer Unit Risk and Mesothelioma Unit
Risk
Once the cancer-specific lifetime unit risks are obtained, the two are then combined. It is important to
note that this estimate of overall potency describes the risk of mortality from cancer at either of the
considered sites and is not just the risk of an individual developing both cancers concurrently. Because
each of the unit risks is itself an upper bound estimate, summing such upper bound estimates across
mesothelioma and lung cancer mortality is likely to overpredict the upper bound on combined risk.
Therefore, following the recommendations of the Guidelines for Carcinogen Risk Assessment (U.S.
35), a statistically appropriate upper bound on combined risk was derived as described below.
Because the estimated risks for mesothelioma and lung cancer mortality were derived using maximum
likelihood estimation, it follows from statistical theory that each of these estimates of risk is
approximately normally distributed. For independent normal random variables, a standard deviation for
a sum is easily derived from individual standard deviations, which are estimated from confidence
intervals: standard deviation = (upper bound - central estimate) ^ Z0.95, where Z0.95 is a standard normal
quantile equal to 1.645. For normal random variables, the standard deviation of a sum is the square root
of the sum of the squares of individual standard deviations. It is important to mention here that
assumption of independence above is a theoretical assumption, but U.S. EPA (2.014c) conducted an
empirical evaluation and found that the assumption of independence in this case does not introduce
substantial error.
In order to combine the unit risks, first obtain an estimate of the standard deviation (SD) of the sum of
the individual unit risks as:
SD = V [ [(UB LC - CE LC) - 1,645]2 + [(UB M - CE M) - 1.645 ]2]
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Where,
UB - upper bound unit risk; CE - central estimate of unit risk; LC - lung cancer
M - mesothelioma
Then, the combined central estimate of risk (CCE) of mortality from either mesothelioma or lung cancer
is CCE = (CE LC + CE M) per fiber/cc, and the combined IUR is CCE + SD x 1.645 per fiber/cc.
3.2.4.7 Inhalation Unit Risk Derivation
To illustrate the range of estimates in the estimates of the IUR, central risks and upper bounds for the
combined IUR for South and North Carolina cohorts are presented in Table 3-10.
Table 3-11. Range of Estimates of Estimated Central Unit Risks and IURs for North and South
Carolina Cohorts
l.ung
Cancer
Source
Central
1 nil
Uisk
1 .ting
Cancer
I pper
lion nd
1 nil
Uisk
l.iing
Cancer
Mesothelioma
Source
Central
I nil
Uisk
Meso
I pper
lion nd
I nil Uisk
Meso
Combined
(cnl nil
I nil Uisk
(Lung
Cancer +
Meso)
Lifetime
Cancer 11 U
(per I7cc)
South Carolina Colum
Hein et al.
(2007)
Linear
1.40E-1
1.98E-1
Berman and
Crump (2008)
based on Hein
et al. (2007)
3.48E-2
7.65E-2
0.175
0.25
Elliott et al.
(: )
Linear
1.66E-1
2.50E-1
Berman and
Crump (2008)
based on Hein
et al. (2007)
3.48E-2
7.65E-2
0.201
0.29
Elliott et al.
(: )
Exponential
4.09E-2
5.07E-2
Berman and
Crump (2008)
based on Hein
et al ( )
3.48E-2
7.65E-2
0.076
0.12
North Carolina Cohort
Elliott el al.
(2012)
Linear
8.47E-3
1.91E-2
LPA modeling
of Loomis et al.
(2019)
5.67E-2
1.17E-1
0.065
0.13
Elliott et al.
(: )
Exponential
7.60E-3
1.12E-2
EPA modeling
of Loomis et al.
(2019)
5.67E-2
1.17E-1
0.064
0.12
Loomis et
al. (2.009)
l-\ponential
8.06E-3
1.17E-2
EPA modeling
of Loomis et al.
( )
5.67E-2
1.17E-1
0.065
0.13
Combinations of South and North Carolina Cohorts hum and mesothelioma unit risks
SC Hein et
al. (2007)
Linear
1.40E-1
1.98E-1
NC EPA
modeling of
Loomis et al.
(2019)
5.67E-2
1.17E-1
0.197
0.28
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l.uil"
Csincer
Source
Cenlrsil
1 nil
Uisk
l.uii"
Csincer
I pper
lion nd

Cenlrsil
I pper
Combined
Cenlrsil
Lifetime
Csincer 11 U
(per f/cc)
1 nil
Uisk
1 .ling
Mesothelioma
Source
I nil
Uisk
Meso
lion nd
I nil Uisk
Meso
I nil Uisk
(Lung
Csincer +

Csincer

Meso)

SC Elliott

NC EPA

et al.
(2012)
1.66E-1
2.50E-1
modeling of
Loomis et al.
5.67E-2
1.17E-1
0.223
0.33
Linear

0 )

SC Elliott

NC EPA

et al.
(: )
4.09E-2
5.07E-2
modeling of
Loomis et al.
5.67E-2
1.17E-1
0.098
0.16
Exponential

(2019)

NC Elliott

SC Berman and

et al.
(: )
8.47E-3
1.91E-2
Crump (2008)
based on Hein
3.48E-2
7.65E-2
0.043
0.09
Linear

et al. (2007)

NC Elliott

SC Berman and

et al.
(: )
7.60E-3
1.12E-2
Crump (2008)
based on Hein
3.48E-2
7.65E-2
0.042
0.08
Exponential

et al. (2007)

NC Loomis

SC Berman and

et al.
(2009)
8.06E-3
1.17E-2
Crump (2008)
based on Hein
3.48E-2
7.65E-2
0.043
0.08
Exponential

et al. (2007)

The values of the estimated IURs range from 0.08 per f/cc to 0.33 per f/cc. There is about a four-fold
difference between lowest and highest IUR estimates - a very low range of model uncertainty in risk
assessment.
3.2.4.7.1 Selecting the Preferred Model Forms for Lung Cancer
Between the linear relative rate and exponential model forms for lung cancer mortality in both SC and
NC cohorts, the exponential models clearly fit better (Elliott et at.. ). Table 2 of that publication
shows that the standard model fit metric, called the Akaike Information Criterion (AIC; smaller values
indicate better fit), for the SC exponential model was 2656.96 and for the SC linear model was 3039.5.
For the NC exponential model, the AIC was 2020.53 compared to 2327.1 for the linear model (Elliott et
at.. 2012). When AlC-based comparisons are made, differences in AIC within 2 AIC units are generally
considered to be indistinguishable with respect to model fit; models with AIC 10 units higher than the
best model "have either essentially no support, and might be omitted from further consideration, or at
least those models fail to explain some substantial explainable variation in the data" (Burnham and
Anderson. 2002). For lung cancer in both South Carolina and North Carolina, the fit of the exponential
models is hundreds of AIC units lower than the linear relative rate models. Such differences in AIC
clearly differentiate the quality of the model fit, and although the linear model (which is the traditional
EPA model and is used for lung cancer modeling in asbestos assessment ( 58b) is shown in
the Table 3-11 for comparison, only the exponential models-based risks for lung cancer are used in the
final IUR derivation. For the results from North Carolina, there were two candidate exponential models
(Elliott et at.. 2012; Loom is et at.. 2009). Both used Poisson regression and controlled for the same set
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of covariates, but the Loomis et al. (2009) publication reported on 181 lung cancer deaths while Elliot et
al.(2012) reported on 159 lung cancer deaths. Only the North Carolina lung cancer results from Loomis
et al. (2009) were further advanced in the IUR derivation.
Limiting the results in Table 3-6 to lung cancer results based on the better fitting exponential models
yielded four combinations that were essentially equivalent in terms of statistical fit and study quality
(Table 3-7).
Table 3-12. Estimated Central Unit Risks and IURs for North and South Carolina Cohorts and
Preferred Models for Lung Cancer and Mes<
l.iing
Cancer
Source
Central
I nil
Uisk
l.ung
Cancer
I pper
Bound
1 nil
Uisk
l.ung
Cancer
Mesothelioma
Source
Central
I nit
Uisk
Meso
I pper
liound
In it
Uisk
Meso
Com hined
Central
1 nit Uisk
(l-uiig
Cancer +
Meso)
Lifetime
Cancer 11 U
(per I7cc)
SC Elliott
et al.
(: )
Exponential
4.09E-2
5.07E-2
SC Berman and
Crump (2008)
based on Hein
et al. (2007)
3.48E-2
7.65E-2
0.076
0.12
NC Loomis
et al.
(2009)
Exponential
8.06E-3
1.17E-2
NC EPA
modeling of
Loomis et al.
(2019)
5.67E-2
1.17E-1
0.065
0.13
SC Elliott
et al.
(2012)
Exponential
4.09E-2
5.07E-2
NC EPA
modeling of
Loomis et al.
(2019)
5.67E-2
1.17E-1
0.098
0.16
NC Loomis
et al.
(2009)
Exponential
8.06E-3
1.17E-2
SC Berman and
Crump (2008)
based on Hein
et al. (2007)
3.48E-2
7.65E-2
0.043
0.08
None of these combinations of IUR estimates account for two important biases - each of which
underestimates the true risk of incident cancer associated with exposure to chrysotile asbestos.
3.2.4.8 Biases in the Cancer Risk Values
Bias in use of mortality data
The endpoint studied for both mesothelioma and lung cancer was mortality, not cancer incidence.
Cancer incidence data are not available for any of the chrysotile asbestos cohorts. According to the
National Cancer Institute's Surveillance Epidemiology and End Results (SEER) data on cancer
incidence, mortality, and survival (Howlader et al.. 2013). the median length of survival for lung cancer
is less than 1 year, with 2-year survival for males about 25% and 5-year survival for males about 17%.
For lung cancer, any bias would be expected to be low because the cancer slope factor (Kl) is estimated
based upon the relative risk. For mesothelioma, the median length of survival with mesothelioma is less
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than 1 year, with 2-year survival for males about 20%, and 5-year survival for males about 6%. Thus,
because the cancer slope factor (Km) is based on the absolute risk, any missed incident cases of
mesothelioma will necessarily underestimate the total mesothelioma risk associated with chrysotile
asbestos and in the absolute risk model even one incident case close to the follow-up date and missed in
follow-up will increase the risk estimate.
Bias in assessing of mortality corresponding to other cancer endpoints
There is evidence that other cancer endpoints may also be associated with exposure to the commercial
forms of asbestos. IARC concluded that there was sufficient evidence in humans that commercial
asbestos (chrysotile, crocidolite, amosite, tremolite, actinolite, and anthophyllite) was causally
associated with lung cancer and mesothelioma, as well as cancer of the larynx and the ovary (Strait' et
at.. 2009). EPA lacked quantitative estimates of the risks of cancers of the larynx and the ovary from
chrysotile asbestos. While the additional risks from ovarian and laryngeal cancer are likely to be smaller
than the risks of lung cancer and mesothelioma, failing to account for those risks in the IUR necessarily
underestimates the total cancer risk associated with chrysotile asbestos.
3.2.4.9 Selection of the final IUR for Chrysotile Asbestos
Due to the downward biases described above, the largest IUR (0.16 per f/cc) was selected from the four
combinations that were essentially equivalent in terms of statistical fit and study quality in Table 3-8.
This largest estimate was most likely to cover the total risk of incident cancers.
Table 3-13. Estimates of Selected Central Risk and IUR for Chrysotile Asbestos
l.uil"
Cancer
Source
Central
I nil
Uisk
l.llllg
Cancer
I pper
Bound
I nil
Uisk
1 .ting
Cancer
Mesothelioma
Source
Ccnl nil
I nil
Uisk
Meso
I pper
lion nd
I nil
Uisk
Meso
Coin billed
Ccnlral
I nil Uisk
(1 .ling
Cancer +
Meso)
Lifetime 11 U
(per f/cc)
SC Elliott et
al. (2012)
Exponential
4.09E-2
5.07E-2
NC EPA
modeling of
Loomis et al.
(2019)
5.67E-2
1.17E-1
0.098
0.16
The definition of the IUR is for a lifetime of exposure. For the estimation of lifetime risks for each condition of use, the
partial lifetime (or less than lifetime) IUR has been calculated using the lifetable approach and values for different
combination of age of first exposure and duration of exposures are presented in Appendix J.
Uncertainties in the cancer risk values are presented in Section 4.3.7.
3.2.5 Potentially Exposed or Susceptible Subpopulations
TSCA requires that a risk evaluation "determine whether a chemical substance presents an unreasonable
risk of injury to health or the environment, without consideration of cost or other non-risk vactors,
including an unreasonable risk to a potentially exposed or susceptible subpopulation identified as
relevant to the risk evaluation by the Administrator, under the conditions of use." TSCA § 3(12) states
that "the term 'potentially exposed or susceptible subpopulation' means a group of individuals within
the general population identified by the Administrator who, due to either greater susceptibility or greater
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exposure, may be at greater risk than the general population of adverse health effects from exposure to a
chemical substance or mixture, such as infants, children, pregnant women, workers, or the elderly."
During problem formulation (U.S. EPA. 2018d). EPA identified potentially exposed and susceptible
subpopulations for further analysis during the development and refinement of the life cycle, conceptual
models, exposure scenarios, and analysis plan. In this section, EPA addresses the potentially exposed or
susceptible subpopulations identified as relevant based on greater susceptibility. EPA addresses the
subpopulations identified as relevant based on greater exposure in Section 2.3.3.
Factors affecting susceptibility examined in the available studies on asbestos include lifestage, gender,
genetic polymorphisms and lifestyle factors. There is some evidence of genetic predisposition for
mesothelioma related to having a germ line mutation in BAP1 (Testa et at.. 2011). Cigarette smoking in
an important risk factor for lung cancer in the general population. In addition, lifestage is important
relative to when the first exposure occurs. The long-term retention of asbestos fibers in the lung and the
long latency period for the onset of asbestos-related respiratory diseases suggest that individuals
exposed earlier in life may be at greater risk to the eventual development of respiratory problems than
those exposed later in life (AT SDR. 2001a). Appendix J of this RE illustrates this point in the IUR
values for less than lifetime COUs. For example, the IUR for a one-year old child first exposed to
chrysotile asbestos for 40 years is 1.31 E-l while the IUR for a 20-year old first exposed to asbestos for
40 years is 5.4 E-2.
4 RISK CHARACTERIZATION
4.1 Environmental Risk
EPA made refinements to the conceptual models during the PF that resulted in the elimination of the
terrestrial exposure, including biosolids, pathways. Thus, environmental hazard data sources on
terrestrial organisms were determined to be out of scope and excluded from data quality evaluation and
further consideration in the risk evaluation process.
In the PF, EPA identified the need to better determine whether there were releases to surface water and
sediments from the COUs in this risk evaluation and whether risk estimates for aquatic (including
sediment-dwelling) organisms should be included in the risk evaluation. Thus, reasonably available
environmental hazard data/information on aquatic toxicity was carried through the systematic review
process (data evaluation, data extraction and data integration).
EPA reviewed reasonably available information on environmental hazards posed by chrysotile asbestos.
A total of four on-topic and in scope environmental hazard studies were identified for chrysotile
asbestos and were determined to have acceptable data quality with overall high data quality (7Appendix
E). In addition, the Systematic Review Supplemental File: Asbestos Data Quality Evaluation of
Environmental Hazard Studies presents details of the data evaluations for each study, including scores
for each metric and the overall study score. These laboratory studies indicated reproductive,
development, and sublethal effects at a concentration range of 104-108 fibers/L, which is equivalent to
0.01 to 100 MFL, to aquatic environmental receptors following chronic exposure to chrysotile asbestos.
On the exposure side of the equation, Table 2-1 presents asbestos monitoring results from the last two
six-year Office of Water sampling programs (encompassing 1998 through 2011). Results of the next six-
year review cycle is anticipated to be completed in 2023. The data show a low number of samples
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(approximately 3.5% of over 14,000 samples over a 12-year period) above the reported minimum
reporting limit (MRL) of 0.2 MFL. This exposure value is within the range of hazard values reported to
have effects on aquatic organisms (0.01 to 100 MFL). EPA believes there is low or no potential for
environmental risk to aquatic or sediment-dwelling receptors from the COUs included in this risk
evaluation because water releases associated with the COUs are not expected and were not identified.
Also, after the PF was released, EPA was still in the process of identifying potential asbestos water
releases for the TSCA COUs. EPA continued to search EPA databases as well as the literature and
engaged in a dialogue with industries and reached out for a dialogue to shed light on potential releases to
water. The available information indicated that there were surface water releases of asbestos; however,
not all releases are subject to reporting (e.g., effluent guidelines) or are applicable (e.g., friability). Based
on the reasonably available information in the published literature, provided by industries using
asbestos, and reported in EPA databases, there is little to no evidence of releases of asbestos to surface
water associated with the COUs that EPA is evaluating in this risk evaluation. Therefore, EPA
concludes there is low or no risk to aquatic or sediment-dwelling organisms. In addition, terrestrial
pathways, including biosolids, were excluded from analysis at the PF stage.
4.2 Human Health Risk
4.2,1 Risk Estimation Approach
EPA usually estimates extra cancer risks for repeated exposures to a chemical using an equation where
Risk = Human Exposure (e.g., LADC) x IUR. Then estimates of extra cancer risks would be interpreted as
the incremental probability of an individual developing cancer over a lifetime as a result of exposure to
the potential carcinogen (i.e., incremental or extra individual lifetime cancer risk).
However, as discussed in Section 3.2, this assessment is unique with respect to the impact of the timing
of exposure relative to the cancer outcome as the time since first exposure plays a dominant role in
modeling risk. The most relevant exposures for understanding mesothelioma risk were those that
occurred decades prior to the onset of cancer and subsequent cancer mortality. For this reason, EPA has
used a less than lifetime exposure calculation.
The general equation for estimating cancer risks for less than lifetime exposure from inhalation of
asbestos, from the Office of Land and Emergency Management Framework for Investigating Asbestos-
contaminated Superfund Sites (U.S. EPA. 2008). is:
ELCR = EPC • TWF • IURltl
where:
ELCR= Excess Lifetime Cancer Risk, the risk of developing cancer as a
consequence of the site-related exposure
EPC = Exposure Point Concentration, the concentration of asbestos fibers in air
(f/cc) for the specific activity being assessed
IURltl = Less than lifetime Inhalation Unit Risk per f/cc
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[For example: the notation for the less than lifetime IUR could start at age 16 with 40
years duration IUR(i6,40). Values for different combination of starting age and duration
can be found in TableApx K-l in Appendix K.
TWF = Time Weighting Factor, this factor accounts for less-than-continuous
exposure during a one-year exposure16, and is given by:
Tyyp — \ExPosure time (hours per dayjj I"Exposure frequency (days per year)!
L 24 hours J L 365 days J
The general equation above can be extended for more complex exposure scenarios by computing the
time-weighted-average exposure of multiple exposures (e.g., for 30-minute task samples within a full 8-
hour shift). Similarly, when multiple exposures may each have different risks, those may be added
together (e.g., for episodic exposures during and between DIY brake work).
There are three points to emphasize in the application of the general equation:
1. The EPC must be expressed in the same units as the IUR for chrysotile asbestos. The units of
concentration employed in this risk evaluation are f/cc as measured by phase contrast microscopy17.
2. The concentration-response functions on which the chrysotile asbestos IUR is based varies as a
function of time since first exposure. Consequently, estimates of cancer risk depend not only on
exposure concentration, frequency and duration, but also on age at first exposure. Therefore, it is
essential to use an IUR value that matches the exposure period of interest (specifically the age of first
exposure and the duration of exposure).
3. When exposures of full-shift occupational workers are to be evaluated, the TWF should be adjusted to
account for differences in inhalation volumes between workers and non-workers. As noted in Appendix
G, EPA assumes workers breath 10 m3 air during an 8-hour shift and non-workers breath 20 m3 in 24
hours. The hourly ratio of those breathing volumes is the volumetric adjustment factor for workers
(V(worker)) [(10/8) / (20/24) = 1.5], Thus, for workers, the formula, ELCR = EPC • TWF • IURltl, is
extended as ELCR = EPC • TWF • V • IURltl.
TWF (worker) = (8 hours / 24 hours) • (240 days / 365 days) = 0.2192, and
V (worker) 1.5
If the worker began work at age 16 years and worked for 40 years, the appropriate unit risk
factor for cancer risk of chrysotile asbestos (taken from Table Apx K-l (Less Than Lifetime (or
Partial lifetime) IUR) in Appendix K) would be:
IUR(16,40) = 0.0707 per f/cc
16 See U.S. EPA (1.994) and Part F update to RAGS inhalation guidance (TJ.S. EPA. 2009).
17 PCM-equivalent (PCMe) concentrations measured using TEM could also be used.
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Based on these two factors, the excess lifetime cancer risk would be computed as:
ELCR = EPC in f/cc • 0.2192 • 1.5 • (0.0707 per f/cc)
BOX 4-1
IUR values for other combinations of age at first exposure and duration of exposure can be
found in Table Apx K-l: Less Than Lifetime (or Partial lifetime) IUR and in Appendix L:
Sensitivity Analysis of Exposures for DIY/Bystander Scenarios
For example:
• First exposure at age 16 with 62 years exposure: IUR(i6,62) = 0.0768 per f/cc
• First exposure at age 16 with 40 years exposure: IUR(i6,40) = 0.0707 per f/cc
• First exposure at age 16 with 20 years exposure: IUR(i6,20) = 0.0499 per f/cc
• First exposure at age 0 with 78 years exposure: IUR(o,78) =0.16 per f/cc
The use scenarios and populations of interest for cancer risk estimation for partial lifetime chronic
exposures are presented in Table 4-1.
EPA provided occupational exposure results representative of central tendency conditions and high-end
conditions. A central tendency was assumed to be representative of occupational exposures in the center
of the distribution for a given condition of use. EPA used the 50th percentile (median), mean (arithmetic
or geometric), mode, or midpoint values of a distribution as representative of the central tendency
scenario. EPA's preference was to provide the 50th percentile of the distribution. However, if the full
distribution was not known, EPA assumed that the mean, mode, or midpoint of the distribution
represented the central tendency depending on the statistics available for the distribution. EPA provided
high-end results at the 95th percentile. If the 95th percentile was not available, or if the full distribution
was not known and the preferred statistics were not available, EPA estimated a maximum or bounding
estimate in lieu of the high-end. Refer to Table 2-24. and Table 2-25 for occupational and consumer
exposures.
EPA received occupational monitoring data for some of the uses (chlor-alkali and sheet gaskets) and
those data were used to estimate risks. For the other COUs, EPA used monitoring information from the
reasonably available information. Risks for both workers and ONUs were estimated when data were
reasonably available. Cancer risk was calculated for the central and high-end exposure estimates. Excess
cancer risks were expressed as number of cancer cases per 10,000 (or 1 x 10"4).
It was assumed that the exposure frequency (i.e., the amount of days per year for workers or occupational
non-users exposed to asbestos) was 240 days per year and the occupational exposure started at age 16
years with a duration of 40 years. EPA typically uses a benchmark cancer risk level of lxlO"4 for
workers/ONUs and lxlO"6 for consumers/bystanders for determining the acceptability of the cancer risk
in a population. For consumers (DIY and bystanders; see Section 4.2.3.1), the exposure frequency
assumed was 62 years, assuming exposure starting at 16 years old and continuing through their lifetime
(78 years). Exposure frequency was also based on data from the EPA Exposure Factors Handbook (U.S.
EPA. 2011) for exposure to chrysotile asbestos resulting from the COUs. As noted in Box 4-1, other
age/duration assumptions may be made.
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Table 4-1. Use Scenarios and Populations of Interest for Cancer Endpoints for Assessing
Populations and Toxicolo<>ical Approach
Occupational I se Scenarios of Asbestos
Population of Interest and Exposure
Scenario:
Users
Adult and youth workers (>16 years old) exposed to chrysotile
asbestos 8 hours/day for 240 days/year for working 40 years
Population of Interest and Exposure
Scenario:
Occupational Non-Users (ONUs)
Adults and youths of both sexes (>16 years old) indirectly
exposed to chrysotile asbestos while being in the same building
during product use.

Cancer Health Effects: Lung Cancer/Mesothelioma

Chrysotile Asbestos Cancer IUR (see Section 3.2.4)
• Lifetime Inhalation Unit Risk per f/cc (from Table 3-
13)
o Mesothelioma or Lung Cancer,
o 0.16 per f/cc
• Less than Lifetime Inhalation Unit Risk oer f/cc
(IURltl)
o Uses values from life tables for different
combination of starting age of exposure and
duration (see Table APX-K-1)
Uses a Time Weighting Factor, this factor accounts for less-than-
continuous exposure during a one-year exposure
Health Effects of Concern,
Concentration and Time Duration
Notes:
Adult workers (>16 years old) include both healthy female and male workers.
Table 4-2. Use Scenarios and Populations of Interest for Cancer Endpoints for Assessing
Consumer Risks Following Inhalation Exposures to Chrysotile Asbestos
Populations and Toxicolo^ical
Approach
I se Scenarios of Asbestos
Population of Interest and Exposure
Scenario: Users (or Do-It-Yourselfers;
DIY)
Consumer Users:
Adults and youths of both sexes (>16 years old) exposed to
chrysotile asbestos
Population of Interest and Exposure
Scenario: Bystanders
Individuals of any age indirectly exposed to chrysotile asbestos
while being in the same work area of the garage as the consumer
Health Effects of Concern,
Concentration and Time Duration
Cancer Health Effects:
Lung Cancer/Mesothelioma
Chrysotile Asbestos Cancer IUR (see Section 3.2.4)
• Lifetime Inhalation Unit Risk per f/cc (from Table 3-13)
o Mesothelioma or Lung Cancer,
o 0.16 per f/cc
• Less than Lifetime Inhalation Unit Risk oer f/cc (IURi ti
o Uses values from life tables for different
combination of starting age of exposure and
duration (see Table APX-J-1)
Uses a Time Weighting Factor, this factor accounts for less-than-
continuous exposure during a one-year exposure
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Populations and To\icoloi>ical
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1 so Scenarios of Asbestos
18
Re-entrainment of asbestos can occur indoors in a garage. Both users and bystanders can be exposed.
Reported Respirator Use by COU
EPA evaluated inhalation exposure for workers and consumers using personal monitoring data either
from industry or journal articles. Respirators may be used when effective engineering controls are not
feasible as per OSHA's 29 CFR § 1910.134(a). The knowledge of the range of respirator APFs is
intended to assist employers in selecting the appropriate type of respirator that could provide a level of
protection needed for a specific exposure scenario. EPA received information from industry on certain
COUs that specified the types of respirators currently being used. This information is summarized in
Table 4-3. The APF EPA suggests be applied for this risk calculation is provided in bold (based on the
discussion in Section 2.3.1.2). When no respirator usage was provided or it was deemed inadequate for
the COU, EPA provided a hypothetical APF. It is important to note that based on published evidence for
asbestos (see Section 2.3.1.2), nominal APF may not be achieved for all respirator users.
Table 4-3. Reported Respirator Use by COU for Asbestos Occupational Exposures
Condition of
I so
Monitoring
Data?
Respirator I so Text
API- for Risk
Calculation
Chlor-alkali
Yes,
provided by
industry
(EPA-HQ-
OPPT-2016-
0736-0052,
Enclosure C)
Workers engaged in the most hazardous
activities (e.g., those with the highest likelihood
of encountering airborne asbestos fibers) use
respiratory protection. Examples include
workers who: handle bags of asbestos; clean up
spilled material; operate glove boxes; and
perform hydroblasting of spent diaphragms. The
types of respirator used range from half-face
air-purifying respirators to supplied air
respirator hoods, depending on the nature of the
work.
Half-face air-
purifying APF of 10
Supplied air
respirator hoods APF
of 25 for specific
tasks3
APF to use for the
risk calculation: 10
to 25
Sheet gasket
stamping
Yes,
provided by
industry
Workers wear N95 filtering facepiece masks. A
site-specific industrial hygiene evaluation
determined that asbestos exposures were not
high enough to require employee respirator use.
(Note: the EPA risk estimates indicate that these
workers should be wearing appropriate
respirators, which is not an N95 mask. See
footnote 1).
Half mask with
N951
Hypothetical APF
to use for the risk
calculation: 10 to 25
Sheet gasket use
(Chemical
Production)
Yes,
provided by
industry
When replacing or servicing asbestos-
containing sheet gaskets, workers in the
titanium dioxide industry wear respirators,
either airline respirators or cartridge respirators
with P-100 HEP A filters.
Cartridge respirators
with P-100 HEP A
filters APF 10
Airline respirators:
APF 10
18 Settled Asbestos Dust Sampling and Analysis 1st Edition Steve M. Hays, James R. Millette CRC Press 1994
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Condition of
I se
.Monitoring
Data?
Respirator I se Text
API- for Risk
Calculation

APF to use for the
risk calculation: 10
Oilfield brake
blocks
Yes, from
the
literature
No information is reasonably available on
respirator use for this COU.
Hypothetical APF
to use for the risk
calculation: 10 to 25
Aftermarket
automotive
brakes and
clutches
Yes,
provided in
literature
An unknown amount of respirator use occurs
among these workers. OSHA's asbestos
standard requires establishments to use control
methods to ensure that exposures are below
permissible exposure limits. OSHA has also
reported: "Respiratory protection is not required
during brake and clutch jobs where the control
methods described below are used" (OSHA,
2006). Nonetheless, some respirator use among
workers in this industry is expected.
Hypothetical APF
to use for the risk
calculation: 10 to 25
Other gasket
vehicle friction
product (UTV)
No2
No information is reasonably available on
respirator use for this COU, but worker
activities are expected to be similar to those for
aftermarket automotive brakes and clutches.
Hypothetical APF
to use for the risk
calculation: 10 to 25
1 OSHA Asbestos Standard 1910.1001 states that negative pressure and filtering masks should not be used for asbestos
exposure. The N95 is a negative pressure mask.
2 EPA is using worker exposure data from the sheet gasket replacement in the chemical manufacturing industry as a surrogate
for the exposures that may occur when workers service UTV friction products.
Source: (OSHA. 2006). Asbestos-Automotive Brake and Clutch Repair Work: Safety and Health Information Bulletin. SHIB
07-26-06. Available online at: https://www.osha.gov/dts/shib/shib072606.html.
2 See Table 2-7.
As determined in the problem formulation and again in Section 3.2.2, exposures to asbestos were
evaluated for the inhalation route only. Inhalation and dermal exposures are assumed to occur
simultaneously for workers and consumers. EPA chose not to employ simple additivity of exposure
pathways at this time within a condition of use because of the uncertainties present in the current
exposure estimation procedures and this may lead to an underestimate of exposure.
4.2.2 Risk Estimation for Workers: Cancer Effects Following Less than Lifetime
Inhalation Exposures by Conditions of Use
Table 4-38 summarizes the risk estimates for inhalation exposures for all occupational exposure
scenarios for asbestos evaluated in this RE. EPA typically uses a benchmark cancer risk level of lxlO"4
for workers/ONUs for determining the acceptability of the cancer risk in a worker population. Risk
estimates that exceed the benchmark (i.e., cancer risks greater than the cancer risk benchmark) are
shaded and in bold.
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For all COUs that were assessed, there were risks to workers without respirators as personal protective
equipment (PPE) for both central and high-end exposure estimates; including those scenarios for which
short-term exposure concentrations were available to include in the analysis. When PPE were applied
(some known, some hypothetical), risks were not exceeded for some COUs (chlor-alkali and oilfield
brake blocks) but they were exceeded for others (sheet gasket stamping - central and high-end, short-
term exposure estimates; sheet gasket use - high-end exposure estimate; aftermarket auto brakes and
other vehicle friction products - high-end and high-end short-term exposure estimates; and other gaskets
[UTV] - high-end exposure estimates). Industry submissions indicated no use of respirators (sheet
gasket stampers using N95 respirators is not protective based on OSHA regulations), or respirators with
an APF of 10 or 25 (chlor-alkali) and an APF of 10 (gasket use). It is important to note that based on
published evidence for asbestos (see Section 2.3.1.2), nominal APF may not be achieved for all
respirator users.
ONUs were not assumed to use PPE and results show some COUs with cancer risk exceedances for both
central and high-end exposure estimates (sheet gasket use and other gasket s [UTV]). For all other
COUs, at least one of the ONU scenarios exceeded the cancer risk benchmark. Thus, exceedances were
observed for ONUs in every COU.
4,2.2.1 Risk Estimation for Cancer Effects Following Chronic Inhalation Exposures
for Chlor-alkali Industry
Exposure data from the chlor-alkali industry were presented for two sampling durations (full shift and
short-term) in Table 4-4. and Table 4-5., respectively (taken from Table 2-8). Short term samples were
assumed to be approximately 30 minutes in duration. Data on exposure at central tendency (median) and
the high-end (95th percentile) are presented along with the Excess Lifetime Cancer Risk (ELCR) for
each exposure distribution.
Table 4-4. Excess Lifetime Cancer Risk for Chlor-alkali Industry Full Shift Workers and ONUs
(Personal Samples) before consideration of PPE and any relevant APF
Occupational
Exposure Scenario
Exposure Levels (fibers/cc)
ELCR (40 yr exposure starting at age 16
years)
Asbestos Worker
ONU19
Asbestos Worker
ONU
Central
Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Producing, handling,
and disposing of
asbestos diaphragms:
Full shift exposure
0.005
0.036
< 0.0025
<0.008
1.2 E-4
8.4 E-4
5.8 E-5
1.9 E-4
Asbestos Workers: ELCR (Central Tendency) 0.005 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
Asbestos Workers: ELCR (High-end) = 0.036 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
ONU: ELCR (Central Tendency) 0.0025 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
ONU: ELCR (High-end> = 0.008 f/cc • 0.2192 • 1.5 • 0.0707 per f/cc
19 Excel file "Chlor-Alkali - Summary of Area Sampling Data (7-5-2019).xlsx list 15 area samples from Olin. Eleven area
samples from one facility all have exposure concentrations of exactly 0.004 f/cc with no mention of detection limit; four area
samples from another facility have exposure concentration of exactly 0.008 f/cc and these four samples are labeled 'Detection
limit was 0.008f/cc\" For the purposes of estimating risks, the sampling values of 0.004 f/cc are used as the measure of
central tendency of ONU exposure and the values of 0.008 f/cc at the detection limit are used to represent the high-end of
ONU exposure.
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Table 4-4. presents the inhalation cancer risk estimates for chlor-alkali workers and ONUs exposed to
asbestos. The exposure values in Table 4-4. were based on monitoring data from 3 chlor-alkali
companies. For asbestos workers, the benchmark cancer risk estimate of lxlO"4 was exceeded for both
high-end and central tendency exposure estimates. For ONUs, the cancer benchmark was exceeded for
the high-end exposure value. Estimates exceeding the benchmark are bolded and shaded in pink.
OSHA Standard Number 1910.1001(c)(2) for asbestos describes the 30-minute excursion limit. "The
employer shall ensure that no employee is exposed to an airborne concentration of asbestos in excess of
1.0 fiber per cubic centimeter of air (1 f/cc) as averaged over a sampling period of thirty (30) minutes as
determined by the method prescribed in Appendix A to this section, or by an equivalent method." Table
2-4 reports 30-minute short-term personal exposures. As these exposures may not represent chronic
exposures, risk estimates were not calculated based on these sample values in isolation. However,
workers exposed to these short-term exposure concentrations are likely to be exposed to chrysotile
asbestos at other times during their full-shift period. As these short-term exposure concentrations exceed
the full shift exposure concentrations, averaging the 30-minutes values into a full 8-hour shift would
result in an increased 8-hour TWA exposure concentration with increased risks. Table 4-5 uses 30
minutes as the short-term exposure concentration averaged with 7.5 hours at the full shift exposure
concentration. The 30-minute values are provided for asbestos workers at the central tendency and at the
high-end, but risks are not calculated just for them. The revised 8-hour TWA for a full shift containing
one 30-minute exposure value per day is provided along with the risk associated with that revised full-
shift exposure value.
There are no short-term values for ONUs, presumably because the short-term sampling is specifically
limited to asbestos workers.
Table 4-5. Excess Lifetime Cancer Risk for Chlor-alkali Industry Workers (Short-Term Personal
Samples from Table 2-4, 8-hour full shift) before consideration of PPE and any relevant APF
Occupational
Exposure Scenario
Exposure Levels (fibers/cc)
ELCR (40 yr exposure starting at age
16 years)
Asbestos Worker
ONU
Asbestos Worker
ONU
Central Tendency
High-end
Central
Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Producing, handling,
and disposing of
asbestos diaphragms:
Short-term exposures
(exactly 30-minutes);
and 30-minute short
term samples within a
full shift)*.
30 min value: 0.026
8-hr TWA: 0.0063*
0.35
0.056**
N/A
N/A
N/A
N/A
1.5 E-4
1.3 E-3
—
...
* This 8-hour TWA includes the 30-minute short-term exposure within an 8-hour full shift and is calculated as follows:
{[(0.5 hour) • (0.026 f/cc) + (7.5 hours) • (0.005 f/cc from Table 4-2)]/8 hours}=0.0063 f/cc
** This 8-hour TWA includes the 30-minute short-term exposure within an 8-hour full shift and is calculated as follows:
{[(0.5 hour) • (0.35 f/cc) + (7.5 hours) • (0.036 f/cc from Table 4-2)]/8 hours}=0.056 f/cc.
ELCR (Central Tendency) {[(0.5 hour) •EPC(30mmute> + (7.5 hours) • EPQfuiishifti] / 8 hours}. • 0.2192 • 1.5 • 0.0707.
ELCR (High-end) = {[(0.5 hour) • EPCoominutei + (7.5 hours) • EPC(fuii shift >] / 8 hours} • 0.2192 • 1.5 • 0.0707.
ELCR (Central Tendency) {[(0.5 hour) • 0.026 + (7.5 hours) • 0.005] / 8 hours}. • 0.2192 • 1.5 • 0.0707.
ELCR (High-end) {[(0.5 hour) • 0.35 + (7.5 hours) • 0.036] / 8 hours} • 0.2192 • 1.5 '0.0707.
The results in Table 4-5 show that when a 30-minute high exposure short-term exposure concentration
is included as part of a full shift exposure estimation, the result is that workers are likely exposed at
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6001 higher concentrations than other full-shift workers who are not exposed to short-term exposures
6002 monitored for OSHA compliance, thereby posing an even higher excess lifetime cancer risk. Note that
6003 this will be true regardless of the frequency at which they may be exposed to those 30-minute short-term
6004 sample values within the 8-hour TWA, as the inclusion of high 30-minute exposures will always be
6005 higher than the standard full-shift TWA.
6006
6007 Applying APFs to Data from Both Full Shift Work and Short-Term Work
6008 ELCRs for chlor-alkali workers that assumes that they will be wearing PPE with APFs of 10 and 25 for
6009 8-hour TWAs and various combinations of 30 minutes and 7.5 hour exposures are presented in Table
6010 4-6, Table 4-7, Table 4-8, Table 4-9 and Table 4-10.
6011
6012 Table 4-6. Excess Lifetime Cancer Risk for Chlor-alkali Industry Full Shift Workers and ONUs
6013 (from Table 4-4) after consideration of PPE with APF=10 for all workers (excluding ONUs)
Occupational Kxposure Scenario

Asbestos Worker
Central
Tendency
1 li«h-
end
Producing, handling, and disposing of asbestos diaphragms: Full shift
exposure
1.2 E-5
8.4 E-5
6014
6015
6016 Table 4-7. Excess Lifetime Cancer Risk for Chlor-alkali Industry Full Shift Workers and ONUs
6017 (from Table 4-4) after consideration of PPE with APF=25 for all workers (excluding ONUs)
Occupational Exposure Scenario
KI.CU (40 \ r exposure starting at a«e
16 years)
Asbestos Worker
Central Tendency
lligh-end
Producing, handling, and disposing of asbestos diaphragms:
Full shift exposure
4.8 E-6
3.4 E-5
6018
6019 Table 4-6 and Table 4-7 show the risk estimates when an APF of 10 or 25 is applied to all full shift
6020 worker exposures. In both scenarios, the risk estimates for the workers are below the benchmark of 10"4
6021 (1 E-4). Since the assumption is that ONUs do not wear respirators, application of APFs do not apply
6022 and so their risk estimates do not change (i.e., the benchmark cancer risk estimate of lxlO"4 was
6023 exceeded for ONUs for high-end exposures). Table 4-3. indicated the respirators that ACC reported to
6024 EPA are currently used by chlor-alkali workers and both APF of 10 and 25 are used depending on the
6025 activity being performed. It is not clear whether the workers monitored for either short-term or full shift
6026 exposures were wearing respirators at the time of the collection of air samples.
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Table 4-8. Excess Lifetime Cancer Risk for Chlor-alkali Industry Short-Term Personal Samples
(from Table 4-5) after consideration of PPE with APF=25 for short-term workers for 0.5 hours
Occupational Exposure Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central
Tendency
High-end
Producing, handling, and disposing
of asbestos diaphragms: Short-term
exposures (exactly 30-minutes); and
30-minute short term samples within
a full shift)
1.1 E-4
8.1 E-4
The central risks for 7.5 hours at 0.005 f/cc with no APF were calculated and added to the 0.5 hour risk at 0.026 f/cc and
APF=25 and then the sum divided by 8 hours. The high-end risks for 7.5 hours at 0.005 f/cc were calculated and added to the
0.5 hour risk at 0.35 f/cc and APF=25 and then sum divided by 8 hours.
Central: Risk for 7.5 hours = 0.005 f/cc • 0.2192 • 1.5 • 0.0707 = 1.2 E-4
Risk for 0.5 hours = 0.026 f/cc • 0.2192 • 1.5 • 0.0707 / (APF of 25) = 2.4 E-5
Risk for 8 hours = [7.5 • 1.2 E-4 + 0.5 • 2.4 E-5]/8 = 1.1 E-4
High-end: Risk for 7.5 hours = 0.036 f/cc • 0.2192 • 1.5 • 0.0707 = 8.4 E-4
Risk for 0.5 hours = 0.35 f/cc • 0.2192 • 1.5 • 0.0707 / (APF of 25) = 3.3 E-4
Risk for 8 hours = [7.5 • 8.4 E-4 + 0.5 • 3.3 E-4]/8 = 8.1 E-4
Table 4-9. Excess Lifetime Cancer Risk for Chlor-alkali Industry Short-Term Personal Samples
(from Table 4-5) after consideration of PPE and with APF=10 for full-shift workers and with
Occupational Exposure Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central
Tendency
High-end
Producing, handling, and disposing
of asbestos diaphragms: Short-term
exposures (exactly 30-minutes); and
30-minute short term samples within
a full shift).
1.3 E-5
9.9 E-5
The central risks for 7.5 hours at 0.005 f/cc and APF=10 were calculated and added to the 0.5 risk at 0.026 f/cc and
APF=25 and then sum divided by 8 hours. The high-end risks for 7.5 hours at 0.005 f/cc and APF=10 were
calculated and added to the 0.5 risk at 0.026 f/cc and APF=25 and then sum divided by 8 hours.
Central : Risk for 7.5 hours = 0.005 f/cc • 0.2192 • 1.5 • 0.0707 / (APF of 10) = 1.2 E-5
Risk for 0.5 hours = 0.026 f/cc • 0.2192 • 1.5 • 0.0707 / (APF of 25) = 2.4 E-5
Risk for 8 hours = [7.5 • 1.2 E-5 + 0.5 • 2.4 E-5]/8 = 1.3 E-5
High-end: Risk for 7.5 hours = 0.036 f/cc • 0.2192 • 1.5 • 0.0707 / (APF of 10) = 8.4 E-5
Risk for 0.5 hours = 0.35 f/cc • 0.2192 • 1.5 • 0.0707 / (APF of 25) = 3.3 E-4
Risk for 8 hours = [7.5 • 8.4 E-5 + 0.5 • 3.3 E-4]/8 = 9.9 E-5
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Table 4-10. Excess Lifetime Cancer Risk for Chlor-alkali Industry Short-Term Personal Samples
(from Table 4-5) after consideration of PPE and with APF=25 for full-shift workers and with
Occupational Kxposure Scenario
KI.CU (40 yr exposure starling al age 16
years)
Asbestos Worker
Central
Tendency
lligh-end
Producing, handling, and disposing ofaslx-slos
diaphragms: Short-term exposures (exactly 30-
minutes); and 30-minute short term samples within
a full shift).
6.0 E-6
5.2 E-5
Here the method is simply to divide the risks in Table 4-5 by 25:
Central Risk from Table 4-5 = 1.5E-4/25 = 6.0E-6
High Risk from Table 4-5 = 1.3E-3/25 = 5.2E-5
Table 4-8, Table 4-9, and Table 4-10 present the ELCR for short-term exposures for chlor-alkali
workers. The three scenarios represented are: (1) APF of 25 for short-term (30-minute exposure) and no
APF for 7.5 hours; (2) APF of 25 for short-term exposures and APF of 10 for the remaining 7.5 hours;
and (3) APF of 25 for both short-term and remaining 7.5 hours. The central tendency and high-end risk
estimates exceeded the benchmark for workers in only the first of the three scenarios presented. None of
the other combinations of APFs exceeded the benchmark. Note that APFs do not apply to ONU
scenarios.
4,2,2,2 Risk Estimation for Cancer Effects Following Chronic Inhalation Exposures
for Sheet Gasket Stamping
Table 4-11 presents the ELCRs for workers stamping gaskets from sheets, using exposure data from two
sampling durations (8-hour full shift; 30 minute short-term). The central tendency and high-end
exposure values are presented along with the ELCR for each exposure distribution in Table 4-11 and
Table 4-12. The exposure levels (personal samples) for full shift workers are from Table 2-10 The high-
end 8-hour TWA exposure value for workers (0.059 fibers/cc) is an estimate, and this full-shift exposure
level was not actually observed. This estimate assumes the highest measured short-term exposure of the
gasket stamping worker could persist for an entire day.
Table 4-11. Excess Lifetime Cancer Risk for Sheet Gasket Stamping Full Shift Workers and
Oeenpiilioiiiil
r.xpnsiMY
Scenario
i:\posiiro l.e\els (libers/eel
I'.I.CU (4(1 jr exposure s(;u (iuii ill ii»e
K» \eiirs)
Asbestos \\ orker
OM
Asbestos Worker
OM
( oil(nil Tendency
lli»h-
OII(l
( cn(nil
Teii(lene\
lli»h-
011(1
( en (nil
1 eii(lene\
lli»h-
end
( en (nil
1 eii(lene\
1 lich-
en (1
Sheet gasket
stamping: 8-hr
TWA exposure
0.014
0.059
0.0024
O.ulu
3.3 E-4
1.4 1.-3
5.6L-5
2.3 1.-4
Asbestos Workers: ELCR (central Tendency) = 0.014 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
Asbestos Workers: ELCR (High-end) = 0.059 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
ONU: ELCR (Central Tendency)
0.0024 f/cc • 0.2192 • 1.5 • 0.0707 per f/cc
ONU: ELCR (High-end) 0.01 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
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Table 4-11. presents the inhalation cancer risk estimates for workers stamping asbestos-containing sheet
gaskets and for ONUs exposed to asbestos. For asbestos workers, the benchmark cancer risk estimate of
lxlO"4 was exceeded for both central tendency and high-end exposure estimates. For ONUs, the cancer
benchmark was exceeded for the high-end exposure values. Estimates exceeding the benchmark are
shaded in pink and bolded.
Table 4-12 presents the inhalation cancer risk estimates for workers stamping sheet gaskets and for
ONUs exposed to asbestos, using an averaging of short-term exposures (assuming 30 minutes) and full
shift exposures (7.5 hours per day of the full shift TWA exposure) based on monitoring data. The central
tendency short-term exposure value for workers (0.024 fibers/cc) is the arithmetic mean of ten short-
term measurements reported in a study of one worker at a company that stamps sheet gaskets containing
asbestos. The high-end short-term exposure value for workers (0.059 fibers/cc) is the highest measured
short-term exposure value from the available monitoring data. This exposure value occurred during a
30-minute sample.
Table 4-12. Excess Lifetime Cancer Risk for Sheet Gasket Stamping Short-term Exposures within
an 8-hour Full Shift (from Table 2-10, Personal Samples) before consideration of PPE and any
relevant APF
Occupational
Exposure Scenario
Exposure Levels (Fibers/cc)
ELCR (40 yr exposure starting at age
16 years)
Asbestos Worker
ONU
Asbestos Worker
ONU
Central Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Sheet gasket
stamping: Short-
term exposures
(~30- minute; and
~30-minute short
term samples within
a full shift)*.
30 min value: 0.024
8-hr TWA: 0.015*
0.059
0.059*
0.0042
0.0025*
0.010
0.010*
3.5 E-4
1.4 E-3
5.6 E-5
2.3 E-4
* Short-term exposures are assumed to be 30 minutes in duration. For the purposes of risk estimation, short term exposures
are averaged with full shift exposure by assuming 30 minutes per day of short-term exposure with an additional 7.5 hours per
day of the full shift TWA exposure.
ELCR = {[(0.5 hour)*EPC(30mmute, + (7.5 hours)* EPC(Fuii shift,] / 8 hours} • 0.2192 • 1.5 • 0.0707.
Asbestos Worker: ELCR (Central Tendency) {[(0.5 hour)*0.024 + (7.5 hours)* 0.014] / 8 hours} • 0.2192 • 1.5 • 0.0707.
Asbestos Worker: ELCR,High-end, = {[(0.5 hour)*0.059 + (7.5 hours)* 0.059] / 8 hours} • 0.2192 • 1.5 • 0.0707.
For asbestos workers, the benchmark cancer risk estimate of lxlO"4 was exceeded for both central
tendency and high-end exposure estimates. For ONUs, the cancer benchmark was exceeded for the high-
end exposure values. Estimates exceeding the benchmark are shaded in pink and bolded.
Applying APFs to Data from Both Full Shift Work and Short-Term Work
ELCRs for workers who stamp sheet gaskets using PPE with hypothetical APFs of 10 and 25 applied for
8-hour TWAs and various combinations of 30 minutes and 7.5 hour exposures are presented in Table
4-13, Table 4-14., Table 4-15, and Table 4-16.
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Table 4-13. Excess Lifetime Cancer Risk for Sheet Gasket Stamping Full Shift Workers and
ONUs (from Table 4-11) after consideral
tion of PPE using an APF=10 (excluding ONUs)
Occupational Exposure Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Sheet gasket stamping: 8-hr TWA exposure
3.3 E-5
1.4 E-4
Table 4-14. Excess Lifetime Cancer Risk for Sheet Gasket Stamping Full Shift Workers and
ONUs (from Table 4-11) after consideration of PPE using an APF=25 (excluding ONUs)
Occupational Exposure Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Sheet gasket stamping: 8-hr TWA
exposure
1.3 E-5
5.6 E-5
For full shift worker scenarios, the benchmark cancer risk estimate of lxlO"4 was exceeded for workers
with high-end exposures when a hypothetical APF of 10 was applied; all other worker scenarios were
below the benchmark (central tendency for hypothetical APFs of 10 and 25 and high-end exposures with
an APF of 25. Since the assumption is that ONUs do not wear respirators, application of APFs do not
apply and so their risk estimates do not change (i.e., the benchmark cancer risk estimate of lxlO 4 was
exceeded for ONUs for high-end exposures).
Table 4-15. Excess Lifetime Cancer Risk for Sheet Gasket Stamping Short-term Exposures within
an 8-hour Full Shift (from Table 4-12) after consideration of PPE using an APF=10 for both full-
shift and short-term exposures (excluding ONUs)
Occupational Exposure
Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Sheet gasket stamping: Short-
term exposures
3.5 E-5
1.4 E-4
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Table 4-16. Excess Lifetime Cancer Risk for Sheet Gasket Stamping Short-term Exposures within
an 8-hour Full Shift (from Table 4-12) after consideration of PPE using an APF=25 for both full-
Occupational Kxposure Scenario
KI.C'U (40 yr exposure starling al age 16 years)
Asbestos Worker
Central Tendency
lligh-end
Sheet gasket stamping: Short-term
exposures
1.4 E-5
5.6 E-5
Tables 4-15 and 4-16 present the ELCR for short-term exposures for sheet gasket stamping workers. The
two scenarios represented are (all hypothetical applications of an APF): (1) APF of 10 for short-term
(30-minute exposure) and an APF of 10 for 7.5 hours; and (2) APF of 25 for both short-term and
remaining 7.5 hours. The central tendency and high-end risk estimates exceeded the benchmark for
workers in only the first of scenario presented. None of the other combinations of hypothetical APFs
exceeded the benchmark. And again, APFs do not apply to ONU scenarios.
4,2,2.3 Risk Estimation for Cancer Effects Following Chronic Inhalation Exposures
for Sheet Gasket Use in Chemical Production
Exposure data from sheet gasket use (replacing gaskets) - using titanium dioxide production as an
example - were presented for 8-hour full shift exposures in Table 2-11. These data are based on reports
from ACC for gasket removal/replacement at titanium dioxide facilities. The 8-hour TWA exposures
assume that the workers removed gaskets throughout the day during maintenance. Data on the exposure
at the central and high-end estimates are presented along with the ELCR for each exposure distribution
in Table 4-6. The high-end value for 8-hr TWA worker exposure (0.094) is based on the highest
exposure measurement (see Section 2.3.1.4.5). No data are available for evaluating worker short-term
exposures for this COU (see 2.3.1.4.5).
Table 4-17. Excess Lifetime Cancer Risk for Sheet Gasket Use in Chemical Production (using data
from titanium dioxide production), 8-hour TWA (from Table 2-11., Personal Samples) before
consideration of PPE and any relevant APF
()cciipiilion;il
r.xposure l.o\ols (I'ihors/ec)
l.l.( R(40>
r exposure sdirlinii ;il
liio l(> xe;irs)
I'ApoSIII'C
Scoii ;i ritt
Asbestos Worker
ONI
Ashcslos Worker
OM
('enlrsil
1 lich-
( en 1 nil
1 Hull-
(cnlriil
lli^h-end
( enlnil
lli^h-end

TcihIciio
en (1
Tondonex
end
1 endeno
Tendcnex
Sheet gasket use:
8-hr TWA
0.026
0.094
0.005
0.016
6.0 1.-4
2.2 1.-3
1.2 1.-4
J."7 1.-4
exposure

Asbestos Workers: ELCR (Central Tendency) 0.026 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
Asbestos Workers: ELCR (High-end) = 0.094 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
ONU: ELCR (Central Tendency) 0.005 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
ONU: ELCR (High-end) = 0.016 f/cc • 0.2192 • 1.5 • 0.0707 per f/cc
Table 4-17. presents the inhalation cancer risk estimates based on data for workers replacing sheet
gaskets in titanium dioxide production and for ONUs exposed to asbestos. For asbestos workers, the
benchmark cancer risk estimate of lxlO"4 was exceeded for both central tendency and high-end exposure
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estimates. For ONUs, the cancer benchmark was also exceeded for both the central tendency and the
high-end exposure values. Estimates exceeding the benchmark are shaded in pink and bolded.
Applying APFs
ELCRs for workers who repair/replace sheet gaskets and ONUs exposed to asbestos using PPE with
hypothetical APFs of 10 and 25 applied for 8-hour TWAs are presented in Table 4-18. and Table 4-19.
Based on data received from ACC, the current APF used for these activities is 10.
Table 4-18. Excess Lifetime Cancer Risk for Sheet Gasket Use in Chemical Production, 8-hour
TWA (from Table 4-6) after consideration of PPE using the APF=10 reflecting the current use of
respirators (excluding ONUs)
Occupational Exposure
Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Sheet gasket use: 8-hr
TWA exposure
6.0 E-5
2.2 E-4
Table 4-19. Excess Lifetime Cancer Risk for Sheet Gasket Use in Chemical Production, 8-hour
TWA (from Table 4-6) after consideration of PPE using an APF=25 (excluding ONUs)
Occupational Exposure Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central
Tendency
High-end
Sheet gasket use: 8-hr TWA exposure
2.4 E-5
8.8 E-5
In both scenarios, the risk estimates for the workers are below the benchmark of lxlO"4 for the central
tendency risk estimate and it exceeds the benchmark when a hypothetical APF of 10 is used for the high-
end scenario; but not when the APF of 25 is applied to the high-end scenario. As shown in Table 4-3.,
ACC reported that titanium dioxide sheet gasket workers use respirators with an APF of 10. Since the
assumption is that ONUs do not wear respirators, application of APFs do not apply and so their risk
estimates do not change. Estimates exceeding the benchmark are shaded in pink and bolded.
4.2.2.4 Risk Estimation for Cancer Effects Following Chronic Inhalation Exposures
for Oilfield Brake Blocks
Qualitatively, the information available to EPA confirms that some brake blocks used in domestic
oilfields contain asbestos, as demonstrated by a safety data sheet provided by a supplier. It is reasonable
to assume that wear of the brake blocks over time will release some asbestos fibers to the air. However,
the magnitude of these releases and resulting worker exposure levels are not known. Only 1 study on
brake blocks was located and used to estimate exposures. In an effort to provide a risk estimate for this
activity, estimated exposures from Table 2-13 were used to represent the central tendencies of exposures
for workers and ONUs; there is no estimate for high-end exposures. More information on the limitations
of these data is provided in Section 2.3.1.5.3.
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Table 4-20. Excess Lifetime Cancer Risk for Oil Field Brake Block Use, 8-hour TWA (from Table
2-13 before consideration of PPE and any relevant APF
Occupational
Exposure
Scenario
Exposure Levels (Fibers/cc)
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
ONU
Asbestos Worker
ONU
Central
Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-end
Central
Tendency
High-end
Brake Block use:
8-hr TWA
exposure
0.03
...
0.02
...
7.0 E-4
...
4.6 E-4
...
Asbestos Workers: ELCR (Central Tendency) 0.03 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
ONU: ELCR (Central Tendency) 0.02 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
Table 4-20. presents the inhalation cancer risk estimates for workers around brake block use and for
ONUs exposed to asbestos. For workers and ONUs, the benchmark cancer risk estimate of lxlO"4 was
exceeded for central tendency. No high-end exposures were available for this activity. Estimates
exceeding the benchmark are shaded in pink and bolded.
Applying APFs
ELCRs for workers who work near oil field brake blocks exposed to asbestos using PPE with
hypothetical APFs of 10 and 25 applied for 8-hour TWAs are presented in Table 4-21. and Table 4-22..
Table 4-21. Excess Lifetime Cancer Risk for Oil Field Brake Block Use, 8-hour TWA (from Table
4-20) after consideration of PPE using an APF=10 (excluding ONUs)
Occupational Exposure
Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Brake Block use: 8-hr TWA
exposure
7.0 E-5
—
Table 4-22. Excess Lifetime Cancer Risk for Oil Field Brake Block Use, 8-hour TWA (from Table
4-20) after consideration of PPE using an APF=25 (excluding ONUs)
Occupational Exposure
Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central
Tendency
High-end
Brake Block use: 8-hr TWA
exposure
2.8 E-5
—
In both scenarios, the risk estimates for the workers using either the hypothetical APF of 10 or 25 are
below the benchmark of 1 E-4. Since the assumption is that ONUs do not wear respirators, application
of APFs do not apply and so their risk estimates do not change.
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4.2.2.5 Risk Estimation for Cancer Effects Following Chronic Inhalation Exposures
for Aftermarket Auto Brakes and Clutches
Exposure data from aftermarket auto brakes and clutches were presented for two sampling durations (8-
hour TWA and short-term) in Table 2-15. The exposure levels are based on an 8-hour TWA from Table
2-15., which are based on 7 studies found in the literature. ELCRs for short-term data from Table 2-15.
are also presented.
Table 4-23. Excess Lifetime Cancer Risk for Repairing or Replacing Aftermarket Auto Brakes
and Clutches in an Occupational Setting, 8-hour TWA Exposure (from Table 2-15.) before
consideration of PPE and any relevant APF
Occupational
Exposure Scenario
Exposure Levels (Fibers/cc)
ELCR (40 yr exposure starting at age 16
years)
Asbestos Worker
ONU
Asbestos Worker
ONU
Central Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Repairing or
replacing brakes with
asbestos-containing
aftermarket
0.006
0.094
0.0007
0.011
1.4 E-4
2.2 E-3
1.6 E-5
2.6 E-4
automotive parts: 8-
hour TWA exposure

Asbestos Workers: ELCR (Central Tendency) 0.006 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
Asbestos Workers: ELCR (High-end) = 0.094 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
ONU: ELCR (Central Tendency) 0.0007 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
ONU: ELCR (High-end) 0.011 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
Table 4-23. presents the inhalation cancer risk estimates for workers repairing and replacing auto brakes
and clutches and for ONUs exposed to asbestos. For workers, the benchmark cancer risk estimate of
lxlO"4 was exceeded for central tendency and high-end. For ONUs, the cancer benchmark was exceeded
for the high-end only. Estimates exceeding the benchmark are shaded in pink and bolded.
Table 4-24. presents the inhalation cancer risk estimates for workers repairing or replacing aftermarket
auto brakes and clutches and for ONUs exposed to asbestos, using an averaging of short-term exposures
(assuming 30 minutes per day) and full shift exposures (7.5 hours per day of the full shift TWA
exposure) based on 7 studies located in the literature. For asbestos workers, the benchmark cancer risk
estimate of lxlO"4 was exceeded for both central tendency and high-end exposure estimates. For ONUs,
the cancer benchmark was exceeded for the high-end exposure values. Estimates exceeding the
benchmark are shaded in pink and bolded.
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Table 4-24. Excess Lifetime Cancer Risk for Repairing or Replacing Aftermarket Auto Brakes
and Clutches in an Occupational Setting, Short-term Exposures Within an 8-hour Full Shift (from
Table 2-15.) before consideration of PPE and any relevant APF
Occupational
Exposure Scenario
Exposure Levels (Fibers/cc)
ELCR (40 yr exposure starting at age 16
years)
Asbestos Worker
ONU
Asbestos Worker
ONU
Central Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Repairing or
replacing brakes with
asbestos-containing
aftermarket
automotive parts:
short-term exposure
(~30- minute; and
~30-minute short
term samples within a
full shift)*.
30 min value: 0.006
8-hr TWA: 0.006*
0.836
0.140*
0.0007
0.0007*
0.100
0.011*
1.4 E-4
3.3 E-3
1.6 E-5
2.6 E-4
* Short-term exposures are assumed to be 30 minutes in duration. For the purposes of risk estimation, short term exposures
are averaged with full shift exposure by assuming 30 minutes per day of short-term exposure with an additional 7.5 hours per
day of the full shift TWA exposure.
ELCR = {[(0.5 hour)*EPC(30mmute, + (7.5 hours)* EPC,Fuii shift,] / 8 hours}. • 0.2192 • 1.5 • 0.0707.
Asbestos Worker: ELCR (Central Tendency) = {[(0.5 hour)*EPC(30mmute, + (7.5 hours)* EPC(Fuii shift,] / 8 hours} • 0.2192 • 1.5 •
0.0707.
Asbestos Worker: ELCR (High-end, = {[(0.5 hour)*EPC(30mmute, + (7.5 hours)* EPQfuii shift,] / 8 hours} • 0.2192 • 1.5 • 0.0707.
Asbestos Worker: ELCR (Central Tendency) = {[(0.5 hour)*0.006 + (7.5 hours)* 0.006] / 8 hours} • 0.2192 • 1.5 • 0.0707.
Asbestos Worker: ELCR (High-end) = {[(0.5 hour)*0.836 + (7.5 hours)* 0.094] / 8 hours} • 0.2192 • 1.5 • 0.0707.
ONU: ELCR (Central Tendency) = {[(0.5 hour)*0.0007 + (7.5 hours)* 0.0007] / 8 hours} • 0.2192 • 1.5 • 0.0707.
ONU: ELCR (High-end) = {[(0.5 hour)*0.1 + (7.5 hours)* 0.011] / 8 hours} • 0.2192 • 1.5 • 0.0707.
/
Applying APFs to Data from Both Full Shift Work and Short-Term Work
ELCRs for workers who repair/replace auto brakes and clutches exposed to asbestos using PPE with
hypothetical APFs of 10 and 25 applied for 8-hour TWAs and various combinations of 30 minutes and
7.5 hour exposures are presented in: Table 4-26., Table 4-27., Table 4-27 and Table 4-28.
Table 4-25. Excess Lifetime Cancer Risk for Repairing or Replacing Aftermarket Auto Brakes
and Clutches in an Occupational Setting, 8-hour TWA Exposure (from Table 4-23) after
consideration of PPE with APF=10 (excluding ONUs)
Occupational Exposure
Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Repairing or replacing brakes
with asbestos-containing
aftermarket automotive parts: 8-
hour TWA exposure
1.4 E-5
2.2 E-4
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Table 4-26. Excess Lifetime Cancer Risk for Repairing or Replacing Aftermarket Auto Brakes
and Clutches in an Occupational Setting, 8-hour TWA Exposure (from Table 4-24.) after
consideration of PPE with APF=25 (excluding ONUs)
Occupational Exposure
Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Repairing or replacing brakes
with asbestos-containing
aftermarket automotive parts: 8-
hour TWA exposure
5.6 E-6
8.8 E-5
For asbestos workers wearing a hypothetical respirator at APF 10, the benchmark cancer risk estimate of
lxlO"4 was exceeded for high-end exposure estimates; all other scenarios (hypothetical APF of 10 for
central tendency and hypothetical APF of 25 for both central and high-end exposures) had risk estimates
below the benchmark. Since the assumption is that ONUs do not wear respirators, application of APFs
do not apply and so their risk estimates do not change. Estimates exceeding the benchmark are shaded in
pink and bolded.
Table 4-27. Excess Lifetime Cancer Risk for Repairing or Replacing Aftermarket Auto Brakes
and Clutches in an Occupational Setting, Short-term Exposures Within an 8-hour Full Shift (from
Table 4-24) after consideration of PPE with APF=10 (excluding ONUs)
Occupational Exposure Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Repairing or replacing brakes with
asbestos-containing aftermarket
automotive parts: short-term
exposure
1.4 E-5
3.3 E-4
Table 4-28. Excess Lifetime Cancer Risk for Repairing or Replacing Aftermarket Auto Brakes
and Clutches in an Occupational Setting, Short-term Exposures Within an 8-hour Full Shift (from
Table 4-24) after consideration of PPE with APF=25 (excluding ONUs)
Occupational Exposure Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Repairing or replacing brakes with asbestos-
containing aftermarket automotive parts:
short-term exposure
5.6 E-6
1.3 E-4
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6335
6336
6337
6338
6339
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Table 4-27. and Table 4-28. display the ELCRs for short-term exposures for workers repairing or
replacing auto brakes and using hypothetical APFs of 10 and 25. For asbestos workers exposed to
asbestos, the benchmark cancer risk estimate of lxlO"4 was exceeded for high-end exposures, but not
central tendency exposures, after consideration of both hypothetical APF 10 and APF 25. Estimates
exceeding the benchmark are shaded in pink and bolded. And again, APFs do not apply to ONU
scenarios.
4.2,2.6 Risk Estimation for Cancer Effects Following Chronic Exposures for Other
Vehicle Friction Products
As discussed in Section 2.3.1.8, EPA is using the exposure estimates for aftermarket auto brakes and
clutches for the other vehicle friction products COU. Therefore, the risk estimates will mimic those for
the aftermarket auto brakes scenarios. Exposure data from aftermarket auto brakes and clutches were
presented for two sampling durations (8-hour TWA and short-term) in Table 2-15. The exposure levels
are based on an 8-hour TWA from Table 2-15., which are based on 7 studies found in the literature.
ELCRs for short-term data from Table 2-15. are also presented.
In addition, as noted in Section 2.3.1.8, there is a limited use of asbestos-containing brakes for a special,
large transport plane (the "Super-Guppy") by the National Aeronautics and Space Administration
(NASA) that EPA has recently learned about. In this public draft risk evaluation, EPA is providing
preliminary information for public input and the information is provided in a brief format.
Table 4-29. Excess Lifetime Cancer Risk for Installing Brakes and Clutches in Exported Cars in
an Occupational Setting, 8-hour TWA Exposure (from Table 2-15.) before consideration of PPE
and any relevant APF
Occupational
Exposure Scenario
Exposure Levels (Fibers/cc)
ELCR (40 yr exposure starting at age 16
years)
Asbestos Worker
ONU
Asbestos Worker
ONU
Central Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Installing brakes with
asbestos-containing
automotive parts: 8-
hour TWA exposure
0.006
0.094
0.0007
0.011
1.4 E-4
2.2 E-3
1.6 E-5
2.6 E-4
Asbestos Workers: ELCR (Central Tendency) 0.006 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
Asbestos Workers: ELCR (High-end) = 0.094 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
ONU: ELCR (Central Tendency) 0.0007 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
ONU: ELCR ,High-end>= 0.011 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
Table 4-23. presents the inhalation cancer risk estimates for workers repairing and replacing auto brakes
and clutches and for ONUs exposed to asbestos. For workers, the benchmark cancer risk estimate of
lxlO"4 was exceeded for central tendency and high-end. For ONUs, the cancer benchmark was exceeded
for the high-end only. Estimates exceeding the benchmark are shaded in pink and bolded.
Page 176 of 310
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6351
6352
6353
6354
6355
6356
6357
6358
6359
6360
6361
6362
6363
6364
6365
6366
6367
6368
6369
6370
6371
6372
6373
6374
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6376
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Table 4-30. Excess Lifetime Cancer Risk for Installing Brakes and Clutches in Exported Cars in
an Occupational Setting, Short-term Exposures Within an 8-hour Full Shift (from Table 2-15.)
Occupational
Exposure Scenario
Exposure Levels (Fibers/cc)
ELCR (40 yr exposure starting at age 16
years)
Asbestos Worker
ONU
Asbestos Worker
ONU
Central Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Central
Tendency
High-
end
Repairing or
replacing brakes with
asbestos-containing
aftermarket
automotive parts:
short-term exposure
(~30- minute; and
~30-minute short
term samples within a
full shift)*.
30 min value: 0.006
8-hr TWA: 0.006*
0.836
0.140*
0.0007
0.0007*
0.100
0.011*
1.4 E-4
3.3 E-3
1.6 E-5
2.6 E-4
* Short-term exposures are assumed to be 30 minutes in duration. For the purposes of risk estimation, short term exposures
are averaged with full shift exposure by assuming 30 minutes per day of short-term exposure with an additional 7.5 hours per
day of the full shift TWA exposure. ELCR = {[(0.5 hour)*EPC(30minute> + (7.5 hours)* EPC(fuii shift >] / 8 hours}. • 0.2192 • 1.5
• 0.0673.
Asbestos Worker: ELCR (Central Tendency)
{[(0.5 hour)*EPC(30mmute, + (7.5 hours)* EPC(Fuiisua,] / 8 hours} • 0.2192 • 1.5 •
0.0707.
Asbestos Worker: ELCR (High-end>= {[(0.5 hour)*EPC(3o minute i + (7.5 hours)* EPC(fu1i shift J / 8 hours} • 0.2192 • 1.5 • 0.0707.
Asbestos Worker: ELCR (Central Tendency) {[(0.5 hour)*0.006 + (7.5 hours)*0.006] / 8 hours} • 0.2192 • 1.5 • 0.0707.
Asbestos Worker: ELCR (High-end>= {[(0.5 hour)*0.836 + (7.5 hours)*0.094 / 8 hours} • 0.2192 • 1.5 • 0.0707
Table 4-24. presents the inhalation cancer risk estimates for workers repairing or replacing aftermarket
auto brakes and clutches and for ONUs exposed to asbestos, using an averaging of short-term exposures
(assuming 30 minutes per day) and full shift exposures (7.5 hours per day of the full shift TWA
exposure) based on 7 studies located in the literature. For asbestos workers, the benchmark cancer risk
estimate of lxlO"4 was exceeded for both central tendency and high-end exposure estimates. For ONUs,
the cancer benchmark was exceeded for the high-end exposure values. Estimates exceeding the
benchmark are shaded in pink and bolded.
Applying APFs to Data from Both Full Shift Work and Short-Term Work
ELCRs for workers who repair/replace auto brakes and clutches exposed to asbestos using PPE with
hypothetical APFs of 10 and 25 applied for 8-hour TWAs and various combinations of 30 minutes and
7.5 hour exposures are presented in Table 4-26., Table 4-27. Table 4-33 and Table 4-28.
Page 177 of 310
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Table 4-31. Excess Lifetime Cancer Risk for Installing Brakes and Clutches in Exported Cars in
an Occupational Setting, 8-hour TWA Exposure (from Table 4-29) after consideration of PPE
Occupational Exposure
Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Installing brakes with asbestos-
containing automotive parts: 8-
hour TWA exposure
1.4 E-5
2.2 E-4
Table 4-32. Excess Lifetime Cancer Risk for Installing Brakes and Clutches in Exported Cars in
an Occupational Setting, 8-hour TWA Exposure (from Table 4-24.) after consideration of PPE
with APF=25 (excluding ONUs)
Occupational Exposure Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Installing brakes with asbestos-
containing aftermarket automotive
parts: 8-hour TWA exposure
5.6 E-6
8.8 E-5
For asbestos workers wearing a hypothetical respirator at APF 10, the benchmark cancer risk estimate of
lxlO"4 was exceeded for high-end exposure estimates; all other scenarios (hypothetical APF of 10 for
central tendency and hypothetical APF of 25 for both central and high-end exposures) had risk estimates
below the benchmark. Since the assumption is that ONUs do not wear respirators, application of APFs
do not apply and so their risk estimates do not change. Estimates exceeding the benchmark are shaded in
pink and bolded.
Table 4-33. Excess Lifetime Cancer Risk for Installing Brakes and Clutches in Exported Cars in
an Occupational Setting, Short-term Exposures Within an 8-hour Full Shift (from Table 4-30)
after consideration of PPE with APF=10 (excluding ONUs)
Occupational Exposure
Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Installing brakes with asbestos-
containing aftermarket
automotive parts: short-term
exposure
1.4 E-5
3.3 E-4
Page 178 of 310
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6405
6406
6407
6408
6409
6410
6411
6412
6413
6414
6415
6416
6417
6418
6419
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Table 4-34. Excess Lifetime Cancer Risk for Installing Brakes and Clutches in Exported Cars in
an Occupational Setting, Short-term Exposures Within an 8-hour Full Shift (from Table 4-30)
Occupational Exposure Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
Installing brakes with asbestos-
containing aftermarket automotive
parts: short-term exposure
5.6 E-6
1.3 E-4
Table 4-27. and Table 4-28. display the ELCRs for short-term exposures for workers repairing or
replacing auto brakes and using hypothetical APFs of 10 and 25. For asbestos workers exposed to
asbestos, the benchmark cancer risk estimate of lxlO"4 was exceeded for high-end exposures, but not
central tendency exposures, after consideration of both hypothetical APF 10 and APF 25. Estimates
exceeding the benchmark are shaded in pink and bolded. And again, APFs do not apply to ONU
scenarios.
Other Vehicle Friction Product - Preliminary Risk Estimates for the NASA Large Transport Plane
The following exposure values have been estimated for this use (see Section 2.3.1.8):
Full Shift: Central Tendency - <0.003 f/cc
Full Shift: High-End - <0.0089 f/cc
Short-Term: Central Tendency - <0.022 f/cc
Short-Term: High-End - <0.045 f/cc
Given this information, and assuming 12 hours of brake changes every year starting at age 26 years with
20 years exposure, the Excess Lifetime Cancer Risk for Super Guppy Brake/Repair Replacement for
Workers is20:
20FULL SHIFT:
TWFuSER Brakes (2-hours on 4 days every year) = (3.3 llOUrS / 24 llOUrS) • (3.6 dayS / 365 days) = 0.001356
IUR(26,20)=0.0318
User: ELCR (Central Tendency)
0.003 f/cc • 0.001356 • 1.5 • 0.0318 per f/cc
User: ELCR (High-end) 0.0089 f/cc» 0.001356 * 1.5 • 0.0318 perf/cc
SHORT TERM:
Central Tendency Exposure includes the 30-ininute short-term exposure within each 3.3 hour brake change as follows:
{[(0.5 hour) • (0.022 f/cc) + (2.8 hours) • (0.002 f/cc from Section 2.3.18)]/3.3 hours}=0.005 f/cc
High End Exposure includes the 30-minute short-term exposure within each 3.3 hour brake change as follows:
{[(0.5 hour) • (0.045 f/cc) + (2.8 hours) • (0.0089 f/cc from Section 2.3.1.8])3.3 hours}=0.014 f/cc
Page 179 of 310
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6421
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6423
6424
6425
6426
6427
6428
6429
6430
6431
6432
6433
6434
6435
6436
6437
6438
6439
6440
6441
6442
6443
6444
6445
6446
6447
6448
6449
6450
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Full Shift: Central Tendency - 1.9 E-7
Full Shift: High-End - 5.8 E-7
Short-Term: Central Tendency - 3.2 E-7
Short-Term: High-End - 9.1 E-7
4.2.2.7 Risk Estimation for Cancer Effects Following Inhalation Exposures for
Gasket Installation/Servicing in UTVs
Multiple publications (see Section 2.3.2.2) report on occupational exposures associated with installing
and servicing gaskets in automobiles. The exposure data used for this COU are presented in Table 2-23.
Data on the exposure at the central and high-end estimates are presented along with the ELCR for each
exposure distribution in Table 4-35.
Table 4-35. Excess Lifetime Cancer Risk for UTV Gasket Installation/Servicing in an Occupational
Setting, 8-hour TWA Exposure (from Table 2-23.) before consideration of PPE and any relevant
APF
Occupational Exposure
Scenario
Exposure Levels (Fibers/cc)
ELCR (40 yr exposure starting at age 16
years)
Asbestos Worker
ONU
Asbestos Worker
ONU
Central
High-
Central
High-
Central
High-
Central
High-

Tendency
end
Tendency
end
Tendency
end
Tendency
end
UTV (based on gasket
repair/replacement in
vehicles: 8-hr TWA
0.024
0.066
0.005
0.015
5.6 E-4
1.5 E-3
1.2 E-4
3.5 E-4
exposure)

Asbestos Workers: ELCR (central Tendency) = 0.024 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
Asbestos Workers: ELCR (High-end> = 0.066 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
ONU: ELCR (Central Tendency) 0.005 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
ONU: ELCR (High-end) 0.015 f/cc • 0.2192 • 1.5 • 0.0707 perf/cc
Table 4-35. presents the inhalation cancer risk estimates for workers installing and/or servicing gaskets
in utility vehicles and for ONUs exposed to asbestos. For both workers and ONUs, the benchmark
cancer risk estimate of lxlO"4 was exceeded for both central tendency and high-end exposures. Estimates
exceeding the benchmark are shaded in pink and bolded.
Applying APFs
ELCRs for workers who install/service gaskets in UTVs exposed to asbestos using PPE with
hypothetical APFs of 10 and 25 applied for 8-hour TWAs are presented in Table 4-36. and Table 4-37.
TWFuserBrakes = (3.3 hours / 24 hours) • (3.6 days / 365 days) = 0.001356
IUR(26,20)=0.0318
Worker: ELCR (Central Tendency)
0.005 f/cc • 0.001356 • 1.5 • 0.0318 perf/cc
Worker: ELCR (High-end> = 0.014 f/cc • 0.001356 • 1.5 • 0.0318 per f/cc
Page 180 of 310
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6457
6458
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6460
6461
6462
6463
6464
6465
6466
6467
6468
6469
6470
6471
6472
6473
6474
6475
6476
6477
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Table 4-36. Excess Lifetime Cancer Risk for UTV Gasket Installation/Servicing in an
Occupational Setting, 8-hour TWA Exposure (from Table 4-35) after consideration of PPE with
Occupational Exposure Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
UTV (based on gasket
repair/replacement in vehicles: 8-hr
TWA exposure)
5.6 E-5
1.5 E-4
Table 4-37. Excess Lifetime Cancer Risk for UTV Gasket Installation/Servicing in an
Occupational Setting, 8-hour TWA Exposure (from Table 4-35) after consideration of PPE with
APF=25 (excluding ONUs)
Occupational Exposure Scenario
ELCR (40 yr exposure starting at age 16 years)
Asbestos Worker
Central Tendency
High-end
UTV (based on sheet gasket use in
chemical production: 8-hr TWA exposure)
2.2 E-5
6.0 E-5
For asbestos workers using respirators with a hypothetical APF of 10, the benchmark cancer risk
estimate of lxlO 4 was exceeded for the high-end exposure estimate; all other scenarios (hypothetical
APF of 10 for central tendency and hypothetical APF of 25 for both central and high-end exposures) had
risk estimates below the benchmark. Since the assumption is that ONUs do not wear respirators,
application of APFs do not apply and so their risk estimates do not change. Estimates exceeding the
benchmark are shaded in pink and bolded.
4.2.2.8.Summary of Risk Estimates for Cancer Effects for Occupational Inhalation
Exposure Scenarios for All COUs
Table 4-38 summarizes the risk estimates for inhalation exposures for all occupational exposure
scenarios for asbestos evaluated in this RE. EPA typically uses a benchmark cancer risk level of 1x10
for workers/ONUs for determining the acceptability of the cancer risk in a worker population. Risk
estimates that exceed the benchmark (i.e., cancer risks greater than the cancer risk benchmark) are
shaded and in bold.
Table 4-38. Summary of Risk Estimates for Inhalation Exposures to Workers and ONUs by CPU
-4
cou
Population
Exposure Duration and
Level
Cancer Risk
Estimates (before
applying PPE)
Cancer Risk
Estimates (with
APF=10C)
Cancer Risk
Estimates (with
APF=25C)

Worker
Central Tendency (8-hr)
1.2 E-4
1.2 E-5
4.8 E-6
Page 181 of 310
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Diaphragms for
chlor-alkali
industry
Section 4.2.2.1.

High-end (8-hr)
8.4 E-4
8.4 E-5
3.4 E-5
Central Tendency short term
1.5 E-4
1.1 E-4a
1.3 E-5d
6.0 E-6b
High-end short term
1.3 E-3
8.1 E-4a
9.9 E-5d
5.2 E-5b
ONU
Central Tendency (8-hr)
5.8 E-5
N/A
N/A
High-end (8-hr)
1.9 E-4
N/A
N/A
Asbestos Sheets -
Gasket Stamping
Section 4.2.2.2
Worker
Central Tendency (8-hr)
3.3 E-4
3.3 E-5
1.3 E-5
High-end (8-hr)
1.4 E-3
1.4 E-4
5.6 E-5
Central Tendency short term
3.5 E-4
3.5 E-5e
1.4 E-5f
High-end short term
1.4 E-3
1.4 E-4e
5.6 E-5f
ONU
Central Tendency (8-hr)
5.6 E-5
N/A
N/A
High-end (8-hr)
2.3 E-4
N/A
N/A
Central Tendency short term
5.6 E-5
N/A
N/A
High-end short term
2.3 E-4
N/A
N/A
Asbestos Sheet
Gaskets - use
(based on repair/
replacement data
from TiO: industry)
Section 4.2.2.3
Worker
Central Tendency (8-hr)
6.0 E-4
6.0 E-5
2.4 E-5
High-end (8-hr)
2.2 E-3
2.2 E-4
8.8 E-5
ONU
Central Tendency (8-hr)
1.2 E-4
N/A
N/A
High-end (8-hr)
3.7 E-4
N/A
N/A
Oil Field Brake
Blocks
Section 4.2.2.4
Worker
Central Tendency (8-hr)
7.0 E-4
7.0 E-5
2.8 E-5
ONU
Central Tendency (8-hr)
4.6 E-4
N/A
N/A
Aftennarket Auto
Brakes
Section 4.2.2.5
Worker
Central Tendency (8-hr)
1.4 E-4
1.4 E-5
5.6 E-6
High-end (8-hr)
2.2 E-3
2.2 E-4
8.8 E-5
Central Tendency short-term
1.4 E-4
1.4 E-5e
5.6 E-6f
High-end short-term
3.3 E-3
3.3 E-4e
1.3 E-4f
ONU
Central Tendency (8-hr)
1.6 E-5
N/A
N/A
High-end (8-hr)
2.6 E-4
N/A
N/A
Central Tendency short-term
1.6 E-5
N/A
N/A
High-end short-term
2.6 E-4
N/A
N/A
Other Vehicle
Friction Products
Section 4.2.2.6
Worker
Central Tendency (8-hr)
1.4 E-4
1.4 E-5
5.6 E-6
High-end (8-hr)
2.2 E-3
2.2 E-4
8.8 E-5
Central Tendency short term
1.4 E-4
1.4 E-5e
5.6 E-6f
High-end w short term
3.3 E-3
3.3 E-4e
1.3 E-4f
ONU
Central Tendency (8-hr)
1.6 E-5
N/A
N/A
High-end (8-hr)
2.6 E-4
N/A
N/A
Central Tendency short-term
1.6 E-5
N/A
N/A
High-end short-term
2.6 E-4
N/A
N/A
Page 182 of 310
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Other Gaskets -
Utility Vehicles
Section 4.2.2.7
Worker
Central Tendency (8-hr)
5.6 E-4
5.6 E-5
2.2 E-5
High-end (8-hr)
1.5 E-3
1.5 E-4
6.0 E-5
ONU
Central Tendency (8-hr)
1.2 E-4
N/A
N/A
High-end (8-hr)
3.5 E-4
N/A
N/A
6478 N/A: Not Assessed; ONUs are not assumed to wear respirators
6479 aNo APF applied for 7.5 hours, APF of 25 applied for 30 minutes.
6480 bAPF 25 applied for both 30 mins and 7.5 hours
6481 0 As shown in Table 4-3, EPA has information suggesting use of respirators for two COUs (chlor-alkali: APF of 10 or 25; and
6482 sheet gasket use: APF of 10 only). Application of all other APFs is hypothetical.
6483 d APF 25 for 30 minutes, APF 10 for 7.5 hours
6484 e APF 10 for 30 minutes, APF 10 for 7.5 hours
6485 f APF 25 for 30 minutes, APF 25 for 7.5 hours
6486
6487 For workers, cancer risks were indicated for all conditions of use under high-end and central tendency
6488 exposure scenarios when PPE was not used. With the use of PPE at APF of 10, most risks were reduced
6489 but still persisted for chlor-alkali (for both central and high-end estimates when short-term exposures
6490 were considered), sheet gasket stamping (high-end only), sheet gasket use (high-end only), auto brake
6491 replacement (high-end only for 8-hour and high-end estimates when short-term exposures are
6492 considered), and UTV gasket replacement (high-end only). When an APF of 25 was applied, risk was
6493 still indicated for the auto brakes high-end short-term exposure scenario.
6494
6495 For ONUs - in which no PPE is assumed to be worn - the benchmark for risk is exceeded for all high-
6496 end estimates and most central tendency estimates. The exceptions for central tendency exceedances are
6497 for the following COUs: choralkali (8-hour), sheet gasket stamping (8-hour), and auto brake
6498 replacement (8-hour and short-term exposure scenarios).
6499 4.2.3 Risk Estimation for Consumers: Cancer Effects by Conditions of Use
6500
6501 4.2.3.1 Risk Estimation for Cancer Effects Following Episodic Inhalation Exposures
6502 for DIY Brake Repair/Replacement
6503 EPA assessed chronic chrysotile exposures for the DIY (consumer) and bystander brake repair/
6504 replacement scenario based on repeated exposures resulting from recurring episodic exposures from
6505 active use of chrysotile asbestos related to DIY brake-related activities. These activities include
6506 concomitant exposure to chrysotile asbestos fibers which are reasonably anticipated to remain within
6507 indoor and outdoor use facilities. It is well-understood that asbestos fibers in air will settle out in dust
6508 and become re-entrained in air during any changes in air currents or activity within the indoor and
6509 outdoor use facilities. On the other hand, in occupational settings, regular air sampling would capture
6510 both new and old fibers and have industrial hygiene practices in place to reduce exposures.
6511
6512 EPA used the following data on exposure frequency and duration, making assumptions when needed:
6513
6514 • Exposure frequency of active use of chrysotile asbestos related to DIY brake repair and
6515 replacement of 3 hours on 1 day every 3 years or 0.33 days per year. This is based on the
6516 information that brakes are replaced every 35,000 miles, and an average number of miles driven
6517 per year per driver in the U.S. of 13,476 miles/year (U.S. DOT. 2018).
6518
6519 • An estimate assuming a single brake change at age 16 years old is presented.
6520
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6530
6531
6532
6533
6534
6535
6536
6537
6538
6539
6540
6541
6542
6543
6544
6545
6546
6547
6548
6549
6550
6551
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
• Estimates for exposure duration of 62 years and assuming exposure for a DIY mechanic starting
at 16 years old and continuing through their lifetime (78 years) is presented. EPA also did a
sensitivity analyses with different ages at first exposure and different exposure durations (see
7Appendix L and the uncertainties Section 4.3.7).
• Exposure frequency of concomitant exposure to chrysotile asbestos resulting from COUs was
based on data in the EPA Exposure Factor Handbook (U.S. EPA. 201 0. 'Doers' are the
respondents who engage or participated in the activity.21 According to Table 16-16 of the
Handbook, the median time 'Doers' spent in garages is approximately one hour per day. The 95th
percentile of time 'Doers' spent in garages is approximately 8 hours. According to Table 16-57
of the Handbook, the median time spent near outdoor locations is 5 minutes, and the 95th
percentile of time is 30 minutes.
• Over the interval of time between the recurring episodic exposures of active COUs, the fraction
of the exposure concentrations from active use of chrysotile asbestos is unknown, however some
dispersion of fibers can reasonably be expected to occur over time. For example, if 50% of fibers
were removed from garages each year, the concentration at the end of the first year would be
50%, at the end of the second year would 25%, and at the end of the third year would be 13%. In
this example, the mean exposure over the 3-year interval would be approximately 30% of the
active COUs. In order to estimate the chrysotile asbestos concentration over of the interval of
time between the recurring episodic exposures of active COUs in the garages, EPA simply
assumed approximate concentrations of 30% of the active COUs over the 3-year interval. In
order to estimate the chrysotile asbestos concentration over of the interval of time between the
recurring episodic exposures of active COUs in outdoor driveways, EPA simply assumed
approximate concentrations of 2% of the active COUs over the 3-year interval based on 95%
reduction of fibers each year.
• Exposure frequency of bystander exposures are similar to those of active user (i.e., Doers) and
may occur at any age and exposure durations are assumed to continue for a lifetime; with an
upper-bound estimate of 78 years of exposure (i.e., ages 0-78) No reduction factor was applied
for indoor DIY brake work inside residential garages. A reduction factor of 10 was applied for
outdoor DIY brake work22. A sensitivity analysis is presented in Appendix L which includes a
lower-bound estimate for a bystander of 20 years (ages 0-20) (see the uncertainties Section
4.3.7).
Excess lifetime cancer risk for people engaging in DIY brake repair (consumers) and
replacement
o 1
This RE uses the term "consumer" or Do-It-Yourselfer (DIY) or DIY mechanic to refer to the "doer" referenced in the
Exposure Factor Handbook.
22 As explained in Section 2.3.1.2, EPA evaluated consumer bystander exposure for the DIY brake outdoor scenario by
applying a reduction factor of 10 to the PBZ value measured outdoors for the consumer user. The reduction factor of 10 was
chosen based on a comparison between the PBZ and the < 3meter from automobile values measured indoors across all
activities identified in the study data utilized from Blake (a ratio of 6.5). The ratio of 6.5 was rounded up to 10, to account for
an additional reduction in concentration to which a bystander may be exposed in the outdoor space based on the high air
exchange rates and volume in the outdoors.
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ELCRdiy Brakes EPCdiy Brakes * TWFdiy Brakes • IURltl(diy Brakes)
EPCconcomitant Exposures * TWFconcomitant Exposures * IURLTL(Concomitant Exposures)
TWFdiy Brakes (3-hours on 1 day every 3 years) (3/24)*(l/3)*(l/365) = 0.0001142
IURltl(diy Brakes) IUR(i6,62) = 0.0768 per f/cc
TWFConcomitant Exposures (1-hour per day every day) (l/24)*(365/365) = 0.04167
IURLTL(Concomitant Exposures) IUR(16,62) 0.0768 per f/cC
Excess lifetime cancer risk for bystanders to DIY brake repair and replacement
ELCRBystander = EPCBystander to DIY brake work * TWFBystander to DIY brake work * IURLifetime +
EPCBystander to Concomitant Exposures * TWFBystander to Concomitant Exposures * IURLifetime
TWF Bystander to DIY brakes work (3-hours on 1 day every 3 years) (3/24)*(l/3)*(l/365) = 0.0001142
IURLifetime =0.16 per f/cc
TWF Bystander to Concomitant Exposures (1-hour per day every day) (l/24)*(365/365) = 0.04167
Exposure values from Table 2-32 were used to represent indoor brake work (with compressed air) and
are the basis for the exposure levels used in Tables 4-39 through 4-42, EPA then assumed that the
concentration of chrysotile asbestos in the interval between brake work (every 3 years) is 30% of that
during measured active use.
Consumers and bystanders were assumed to spend one hour per day in their garages based on the 50th
percentile estimate in the EPA Exposure Factors Handbook. Based on these assumptions, the consumer
risk estimate was exceeded for central and high-end exposures based on replacing breaks every 3 years
(Table 4-39). Estimates exceeding the benchmark are shaded in pink and bolded.
Tables 4-40 and 4-41 used the alternative assumptions for age at first exposure (16 years old) and
exposure duration (40 years) for the DIY user; and the assumptions for the exposure duration of the
bystander (lifetime). Table 4-41 presents another alternative estimate for both the DIY user (performing
work from ages 16-36, and a bystander being present from ages 0-20) for the one-hour/day scenario (i.e.,
Table 4-40). The risk estimates note that the benchmark is exceeded for both these alternative estimates.
Table 4-39. Excess Lifetime Cancer Risk for Indoor DIY Brake/Repair Replacement with
Compressed Air Use for Consumers and Bystanders (exposures from Table 2-32 without a
reduction factor) with Exposures at 30% of 3-hour User Concentrations between Brake/Repair
Replacement (Consumers 1 hour/day spent in garage; Bystanders 1 hour/day)
Consumer
I'1\|)umiiv Scenario
r.xpoMiiv l.c\ols (libers/cc)
IK K Ki2 \ r oxposii iv
sliirliiiii ill !i«e l(>
\ c;i rs)
i:i.( Kll.ilclimc
exposure)
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE

DIY User
DIY Bystander
DIY User
DIY Bystander
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Aftennarket
automotive parts -
brakes (3-hour
TWA indoors every
3 years with
compressed air)
0.0445
0.4368
0.0130
0.0296
4.3 E-5
4.2 E-4
2.6 E-5
6.0 E-5
TWFConcomitant Exposures (1 hour per day every day) (l/24)*(365/365) = 0.04167
IUR(16,62)=0.0768; IUR(Lifetime)=0.16
DIY User: ELCR (Central Tendency) 0.0445 f/cc • 0.0001142 • 0.0768 perf/cc + 0.0445 • 0.3 • 0.04167 • 0.0768
DIY User: ELCR (High-end> = 0.4368 f/cc • 0.0001142 • 0.0768 per f/cc + 0.4368 • 0.3 • 0.04167 • 0.0768
DIY Bystander: ELCR (central Tendency i = 0.013 f/cc • 0.0001142 • 0.16 perf/cc + 0.013 • 0.3 • 0.04167 • 0.16
DIY Bystander: ELCR (High-end> = 0.0296 f/cc • 0.0001142 • 0.16 perf/cc + 0.0296 • 0.3 • 0.04167 • 0.16
Table 4-40. Excess Lifetime Cancer Risk for Indoor DIY Brake/Repair Replacement with
Compressed Air Use for Consumers for 20 year duration (exposures from Table 2-32 without a
reduction factor) with Exposures at 30% of 3-hour User Concentrations between Brake/Repair
Consumer
Exposure Scenario
Exposure Levels (fibers/cc)
ELCR (20 yr exposure
starting at age 16
years)
ELCR ((20 yr
exposure starting at
age 0 years))
DIY User
DIY Bystander
DIY User
DIY Bystander
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Aftennarket
automotive parts -
brakes (3-hour
TWA indoors every
3 years with
compressed air)
0.0445
0.4368
0.0130
0.0296
2.8 E-5
2.7 E-4
1.7 E-5
3.8 E-5
TWF Concomitant Exposures (1 hour per day every day) (l/24)*(365/365) = 0.04167
IURi6.36F0.0499; IURo,2o,=OT01
DIY User: ELCR (Central Tendency) 0.0445 f/cc • 0.0001142 • 0.0499 perf/cc + 0.0445 • 0.3 • 0.04167 • 0.0499
DIY User: ELCR ,High-end> = 0.4368 f/cc • 0.0001142 • 0.0499 per f/cc + 0.4368 • 0.3 • 0.04167 • 0.0499
DIY Bystander: ELCR (CentralTendency) = 0.013 f/cc • 0.0001142 • 0.101 perf/cc + 0.013 • 0.3 • 0.04167 • 0.101
DIY Bystander: ELCR (High-end> = 0.0296 f/cc • 0.0001142 '0.101 perf/cc + 0.0296 • 0.3 • 0.04167 '0.101
For Table 4-41, users were assumed to spend eight hours per day in their garages based on the 95th
percentile estimate in the EPA Exposure Factors Handbook (Table 16-16 in the Handbook). Bystanders
were assumed to spend one hour per day in their garages. Based on these assumptions, both the
consumer and the bystander risk estimates were exceeded for central tendency and high-end exposures.
Estimates exceeding the benchmark are shaded in pink and bolded.
Table 4-41. Excess Lifetime Cancer Risk for Indoor DIY Brake/Repair Replacement with
Compressed Air Use for Consumers and Bystanders (exposures from Table 2-32 without a
reduction factor) with Exposures at 30% of 3-hour User Concentrations between Brake/Repair
Consumer
Exposure
Scenario
Exposure Levels (Fibers/cc)
ELCR (62 yr exposure
starting at age 16 years)
ELCR (Lifetime
exposure)
DIY User
DIY Bystander
DIY User
DIY Bystander
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE

Central
Tendency
High-
end
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-
end
Aftennarket
automotive parts -
brakes (3-hour
TWA indoors with
compressed air)
0.0445
0.4368
0.0130
0.0296
3.4 E-4
3.4 E-3
2.6 E-5
6.0 E-5
TWFConcomitant Exposures (8 hours per day every day) (8/24)*(365/365) = 0.3333
IUR(16,62)=0.0768; IUR(Lifetime)=0.16
DIY User: ELCR (Central Tendency) 0.0445 f/cc • 0.0001142 • 0.0768 perf/cc + 0.0445 • 0.3 • 0.3333 • 0.0768
DIY User: ELCR (High-end> = 0.4368 f/cc • 0.0001142 • 0.0768 per f/cc + 0.4368 • 0.3 • 0.3333 • 0.0768
DIY Bystander: ELCR (central Tendency i = 0.013 f/cc • 0.0001142 • 0.16 perf/cc + 0.013 • 0.3 • 0.04167 • 0.16
DIY Bystander: ELCR ,High-end> = 0.0296 f/cc • 0.0001142 • 0.16 perf/cc + 0.0296 • 0.3 • 0.04167 • 0.16
In Table 4-42 the assumption is that DIY brake/repair replacement with compressed air is limited to a
single brake change at age 16 years. EPA then assumed that the concentration of chrysotile asbestos
following this COU decreases 50% each year as was assumed in all the indoor exposure scenarios. EPA
then assumed that both the DIYer and the bystander would remain in the house for 10 years. Risks were
determined for the 10-year period by calculating the risk with the appropriate partial lifetime IUR and
re-entrainment exposure over 10 years, averaging 10% of the brake/repair concentrations each year
(total 10-year cumulative exposure is 50% in first year plus 25% in second year is for all practical
purposes equals a limit of one year at the 3-hour concentration divided by 10 years).
Table 4-42. Risk Estimate using one brake change at age 16 years with 10 years further exposure.
Excess Lifetime Cancer Risk for Indoor DIY Brake/Repair Replacement with Compressed Air
Use for Consumers and Bystanders (exposures from Table 2-32 without a reduction factor)
(Consumers 1 hour/day spent in garage; Bystanders 1 hour/day
Consumer
Exposure Scenario
Exposure Levels (fibers/cc)
ELCR (62 yr exposure
starting at age 16
years)
ELCR (Lifetime
exposure)
DIY User
DIY Bystander
DIY User
DIY Bystander
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Aftennarket
automotive parts -
brakes (3-hour
TWA indoors once
at 16 yrs old; with
compressed air)
0.0445
0.4368
0.0130
0.0296
5.6 E-6
5.5 E-5
3.2 E-6
7.3 E-6
TWF Concomitant Exposures (1 hour per day every day) (l/24)*(365/365) = 0.04167
IURi6,io)=0.0300; IUR(o,ior0.0595
DIY User: ELCR (Central Tendency) 0.0445 f/cc • 0.000005524 • 0.0300 per f/cc + 0.0445 • 0.1 • 0.04167 • 0.0300
DIY User: ELCR ,High-end> = 0.4368 f/cc • 0.000005524 • 0.0300 per f/cc + 0.4368 • 0.1 • 0.04167 • 0.0300
DIY Bystander: ELCR (Central Tendency) 0.013 f/cc • 0.000005524 • 0.0595 perf/cc + 0.013 • 0.1 • 0.04167 • 0.0595
DIY Bystander: ELCR ,High-end> = 0.0296 f/cc • 0.000005524 • 0.0595 perf/cc + 0.0296 • 0.1 • 0.04167 • 0.0595
Exposure Levels in Table 4-43 are from Table 2-32 and the assumption is used that the concentration of
chrysotile asbestos in the interval between brake works is 2% of that during measured active use. Users
and bystanders were assumed to spend 5 minutes per day in the driveway each day based on the 50th
percentile estimate in the EPA Exposure Factors Handbook (in Table 16-57 in the Handbook). The
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reduction factor is 10 for bystanders23. The risk estimates for the DIY consumer exceeded the risk
benchmark for the high-end exposure only, whereas the risk estimates were not exceeded for either
scenario for the bystanders.
Table 4-43. Excess Lifetime Cancer Risk for Outdoor DIY Brake/repair Replacement for
Consumers and Bystanders (5 minutes per day in driveway) (from Table 2-32 with a reduction
factor of 10)
Consumer
Exposure Scenario
Exposure Levels (Fibers/cc)
ELCR (62 yr exposure
starting at age 16
years)
ELCR (Lifetime
exposure)
DIY User
DIY Bystander
DIY User
DIY Bystander
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Aftennarket
automotive parts -
brakes (3-hour TWA
outdoors)
0.007
0.0376
0.0007
0.0038
9.9 E-8
5.3 E-7
2.1 E-8
1.1 E-7
TWF Concomitant Exposures (0.0833 hours per day every day) (0.08333/24)*(365/365) = 0.003472
IUR(16,62)=0.0768; IUR(Lifetime)=0.16
DIY User: ELCR (Central Tendency) 0.007 f/cc • 0.0001142 • 0.0768 perf/cc + 0.007 • 0.02 • 0.003472 • 0.0768
DIY User: ELCR ,High-end> = 0.0376 f/cc • 0.0001142 • 0.0768 per f/cc + 0.0376 • 0.02 • 0.003472 • 0.0768
DIY Bystander: ELCR (Central Tendency) 0.0007f/cc • 0.0001142 • 0.16 perf/cc + 0.0007 • 0.02 • 0.003472 • 0.16
DIY Bystander: ELCR ,High-end> = 0.0038 f/cc • 0.0001142 • 0.16 perf/cc + 0.0038 • 0.02 • 0.003472 • 0.16
Table 4-44. Excess Lifetime Cancer Risk for Outdoor DIY Brake/Repair Replacement for
Consumers and Bystanders (30 minutes per day in driveway) (from Table 2-32 with a reduction
factor of 10)
Occupational
Exposure Scenario
Exposure Levels (Fibers/cc)
ELCR (62 yr exposure
starting at age 16
years)
ELCR (Lifetime
exposure)
DIY User
DIY Bystander
DIY User
DIY Bystander
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Aftennarket
automotive parts -
brakes (3-hour TWA
outdoors)
0.007
0.0376
0.0007
0.0038
2.9 E-7
1.5 E-6
5.9 E-8
3.2 E-7
TWF Concomitant Exposures (0.5 hours per day every day) (0.5/24)*(365/365) = 0.02083
IUR(16,62)=0.0768; IURLifetime)=0.16
DIY User: ELCR (Central Tendency) 0.007 f/cc • 0.0001142 • 0.0768 perf/cc + 0.007 • 0.02 • 0.02083 • 0.0768
DIY User: ELCR ,High-end> = 0.0376 f/cc • 0.0001142 • 0.0768 per f/cc + 0.0376 • 0.02 • 0.02083 • 0.0768
DIY Bystander: ELCR (Central Tendency) 0.0007 f/cc • 0.0001142 • 0.16 perf/cc + 0.0007 • 0.02 • 0.02083 • 0.16
23 As explained in Section 2.3.1.2, EPA evaluated consumer bystander exposure for the DIY brake outdoor scenario by
applying a reduction factor of 10 to the PBZ value measured outdoors for the consumer user. The reduction factor of 10 was
chosen based on a comparison between the PBZ and the < 3meter from automobile values measured indoors across all
activities identified in the study data utilized from Blake (a ratio of 6.5). The ratio of 6.5 was rounded up to 10, to account for
an additional reduction in concentration to which a bystander may be exposed in the outdoor space based on the high air
exchange rates and volume in the outdoors.
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DIY Bystander: ELCR (High-end) = 0.0038 f/cc • 0.0001142 • 0.16 perf/cc + 0.0038 • 0.02 • 0.02083 • 0.16
Exposure Levels from Table 2-32 are used in Table 4-44. The assumption that the concentration of
chrysotile asbestos in the interval between brake works is 2% of that during measured active use. Users
and bystanders were assumed to spend 30 minutes per day walking to their cars in the driveway each
day based on the 95th percentile estimate in the EPA Exposure Factors Handbook (in Table 16-57 in the
Handbook). The reduction factor is 10 for bystanders. Neither of the risk estimates for consumers or
bystanders in Table 4-44 exceeded the risk benchmark for central tendency and the DIY user exceeded
for the high-end but the bystander did not.
4,2,3,2 Risk Estimation for Cancer Effects following Episodic Inhalation Exposures
for UTV Gasket Repair/replacement
EPA assessed chrysotile exposures for the DIY (consumer) and bystander UTV gasket
repair/replacement scenario based on aggregated exposures resulting from recurring episodic exposures
from active use of chrysotile asbestos related to DIY brake-related activities. These activities include
concomitant exposure to chrysotile asbestos fibers which are reasonably anticipated to remain within
indoor use facilities. It is well-understood that asbestos fibers in air will settle out in dust and become re-
entrained in air during any changes in air currents or activity indoors. On the other hand, in occupational
settings, regular air sampling would capture both new and old fibers and have industrial hygiene
practices in place to reduce exposures.
For the risk estimations for the UTV gasket COU, EPA used the same data/assumptions identified in
Section 4.2.3.1 for brakes for exposure frequency and duration; with the exception that there is no
outdoor exposure scenario. A sensitivity analysis is presented which includes a lower-bound estimate for
a bystander of 20 years (ages 0-20) (see Appendix L and the uncertainties Section 4.3.7).
In Table 4-45, the assumption is that DIY UTV gasket replacement is limited to a single gasket change
at age 16 years. EPA then assumed that the concentration of chrysotile asbestos in following this COU
decreases 50% each year as was assumed in all the indoor exposure scenarios. EPA then assumed that
both the DIYer and the bystander would remain in the house for 10 years. Risks were determined for the
10-year period by calculating the risk with the appropriate partial lifetime IUR.
Based on these assumptions, the consumer risk estimate was exceeded for high-end exposures based on
a single UTV gasket change and remaining in the house for 10 years (Table 4-45). Estimates exceeding
the benchmark are shaded in pink and bolded.
Table 4-45. Risk Estimate using one UTV gasket change at age 16 years with 10 years further
exposure. Excess Lifetime Cancer Risk for Indoor DIY UTV gasket change for Consumers and
Bystanders (exposures from Table 2-32 without a reduction factor) (Consumers 1 hour/day spent
in garage; Bystanders 1 hour/day)
Consumer
llxposurc Scemirio
l.xposuro l.c\ols (libers/cc)
IK K Ki2 j r exposure
shirliuii id ii»e l(>
\ c;i rs)
i:i.( Kll.ilclimc
exposure)
DIY I ser
DIY li\siiimlcr
DIY I ser
DIY litsiiimliT
(cm nil .... .
... . II luh-ond
1 cmk-no
(Ollll-ill .... .
... . Iliuh-oml
1 cmk-no
(omnil ... . .
... . Ilitih-cud
1 cmk-im
(ciilr;il ... . .
... . Iliuh-ciul
Icmk-no
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Aftennarket

automotive parts -

brakes (3-hour
0.024
0.066
0.012
0.03
4.6 E-7
1.3 E-6
1.7 E-7
9.2 E-7
TWA once.

indoors)

TWFConcomitant Exposures (1 hour per day every day) (l/24)*(365/365) = 0.04167
IUR(i6,io)=0.0300; IUR(0,ior0.0595
DIY User: ELCR (Central Tendency) 0.024 f/cc • 0.000005524 • 0.0300 perf/cc + 0.024 • 0.1 • 0.04167 • 0.0300
DIY User: ELCR ,High-end> = 0.066 f/cc • 0.000005524 • 0.0300 per f/cc + 0.066 • 0.1 • 0.04167 • 0.0300
DIY Bystander: ELCR (Central Tendency) = 0.012 f/cc • 0.000005524 • 0.0595 perf/cc + 0.012 • 0.1 • 0.04167 • 0.0595
DIY Bystander: ELCR (High-end> = 0.03 f/cc • 0.000005524 • 0.0595 perf/cc + 0.03 • 0.1 • 0.04167 • 0.0595
Table 4-46. Excess Lifetime Cancer Risk for Indoor DIY UTV Gasket /Repair Replacement for
Consumers and Bystanders (exposures from Table 2-32) (Users 1 hour/day spent in garage;
Bystanders 1 hour/day)
Consumer
Exposure Scenario
Exposure Levels (Fibers/cc)
ELCR (62 yr exposure
starting at age 16
years)
ELCR (Lifetime
exposure)
DIY User
DIY Bystander
DIY User
DIY Bystander
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Aftennarket UTV
parts - gaskets
(indoors every 3
years)
0.024
0.066
0.012
0.030
2.3 E-5
6.4 E-5
2.4 E-5
6.1 E-5
TWF Concomitant Exposures (1 hour per day every day) (l/24)*(365/365) = 0.04167
IUR(16,62)=0.0768; IURLifetime)=0.16
DIY User: ELCR (Central Tendency) 0.024 f/cc • 0.0001142 • 0.0768 perf/cc + 0.024 • 0.3 • 0.04167 • 0.0768
DIY User: ELCR ,High-end> = 0.066 f/cc • 0.0001142 • 0.0768 perf/cc + 0.066 • 0.3 • 0.04167 • 0.0768
DIY Bystander: ELCR (Central Tendency) 0.012 f/cc • 0.0001142 • 0.16 perf/cc + 0.012 • 0.3 • 0.04167 • 0.16
DIY Bystander: ELCR ,High-end> = 0.030 f/cc • 0.0001142 • 0.16 perf/cc + 0.030 • 0.3 • 0.04167 • 0.16
The exposure values from Table 2-32 were used to estimate ELCRs in Table 4-46 for indoor DIY gasket
repair/replacement (one-hour/day assumption). The assumption is that the concentration of chrysotile
asbestos in the interval between gasket work (every 3 years) is 30% of that during measured active use.
Consumers and bystanders were assumed to spend one hour per day in their garages based on the 50th
percentile estimate in the EPA Exposure Factors Handbook (in Table 16-16 in the Handbook). Based on
these assumptions, both the consumer and the bystander risk estimates were exceeded for central
tendency and high-end exposures. Estimates exceeding the benchmark are shaded in pink and bolded.
Table 4-47. Excess Lifetime Cancer Risk for Indoor DIY Gasket/Repair Replacement for
Consumers and Bystanders (exposures from Table 2-32) (Consumers 8 hours/day spent in garage;
Bystanders 1 hour/day)
Consumer
Exposure
Scenario
Exposure Levels (Fibers/cc)
ELCR (62 yr exposure
starting at age 16 years)
ELCR (Lifetime
exposure)
DIY User
DIY Bystander
DIY User
DIY Bystander
Central
Tendency
High-
end
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-
end
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Aftennarket

automotive parts -
brakes (indoors
0.024
0.066
0.012
0.030
1.8 E-4
5.1 E-4
2.4 E-5
6.1 E-5
every three years)

TWFConcomitant Exposures (8 hours per day every day) (8/24)*(365/365) = 0.3333
IUR(16,62)=0.0768; IUR(Lifetime)=0.16
DIY User: ELCR (Central Tendency)
0.024 f/cc • 0.0001142 • 0.0768 perf/cc + 0.024 • 0.3 • 0.3333 • 0.0768
DIY User: ELCR ,High-end> = 0.066 f/cc • 0.0001142 • 0.0768 perf/cc + 0.066 • 0.3 • 0.3333 • 0.0768
DIY Bystander: ELCR (Central Tendency) 0.012 f/cc • 0.0001142 • 0.16 perf/cc + 0.012 • 0.3 • 0.04167 • 0.16
DIY Bystander: ELCR (High-end> = 0.030 f/cc • 0.0001142 • 0.16 perf/cc + 0.030 • 0.3 • 0.04167 • 0.16
The exposure values from Table 2-32 were used to estimate ELCRs in Table 4-47 for indoor DIY gasket
repair/replacement (eight hours/day assumption). The assumption is that the concentration of chrysotile
asbestos in the interval between replacement is 30% of that during measured active use. Users were
assumed to spend eight hours per day in their garages based on the 95th percentile estimate in the EPA
Exposure Factors Handbook. Bystanders were assumed to spend one hour per day in their garages.
Based on these assumptions, both the consumer and the bystander risk estimates were exceeded for
central tendency and high-end exposures. Estimates exceeding the benchmark are shaded in pink and
bolded.
4.2.3.3 Summary of Consumer and Bystander Risk Estimates by COU for Cancer
Effects Following Inhalation Exposures
Table 4-48 summarizes the risk estimates for inhalation exposures for all consumer exposure scenarios.
Risk estimates that exceed the benchmark (i.e., cancer risks greater than the cancer risk benchmark) are
shaded and in bold.
Ranging from using an estimate for a single brake job at 16 years of age, and estimates for age at first
exposure (16 years old for DIY users and 0 years for bystanders) and exposure duration (62 years for
DIY users and 78 years for bystanders), for all COUs that were assessed, there were risks to consumers
(DIY) and bystanders for all high-end exposures with the following exceptions: outdoor brake repairs (5
minutes/day in the driveway - benchmark not exceeded for high-end for both DIY and bystanders) and
outdoor brake repairs (30 minutes/day in the driveway - benchmark not exceeded for high-end
exposures for the bystander only). In addition, risks were noted for central tendency estimates for all
COUs (brake and UTV gasket repair/replacement) for both consumers (DIY) and bystanders except for
the outdoor exposure scenarios. Outdoor exposure scenarios for brake repair/replacement for 5 minutes
in the driveway was the only scenario that did not exceed the benchmark for consumers (DIY) and
bystanders. For outdoor exposures of 30 minutes/day once every 3 years, there were no exceedances for
either the DIY or bystander for the central tendency exposure scenario.
To evaluate sensitivity to the age at first exposure and exposure duration assumptions, EPA conducted
multiple sensitivity analyses assuming that exposure of DIY users was limited to a single brake change
at age 16 years as well as durations of exposure as short as 20 years with different ages of first exposure.
Section 4.3.7 provides a summary of the detailed analyses in Appendix L. These sensitivity analyses
show that in four of the five scenario pairings different durations and age of first exposure, only one of
24 possible scenarios changed from exceeding the benchmark cancer risk level of lxlO 6 to no
exceedance (DIY user, brake repair outdoors, 30 minutes/ day, high-end only). In the fifth scenario
(Sensitivity Analysis 2), there was no change in any of the 24 scenarios exceeding risk benchmarks. All
analyses are in Appendix L.
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6811 Table 4-48. Summary of Risk Estimates for Inhalation Exposures to Consumers and Bystanders
681 2 by CPU (Cancer benchmark is 10-6)
Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure Duration
and Level
Cancer Risk
Estimates
Imported asbestos
products
Brakes
Repair/replacement
Indoor, compressed air,
once every 3 years for 62
years starting at 16 years,
exposures at 30% of active
used between uses, 1
hour/d in garage
Section 4.2.3.1
DIY
Central Tendency
4.3 E-5
High-end
4.2 E-4
Bystander
Central Tendency
2.6 E-5
High-end
6.0 E-5
Brakes Repair/
replacement
Indoor, compressed air,
once every 3 years for 62
years starting at 16 years,
exposures at 30% of active
used between uses, 8
hours/d in garage
Section 4.2.3.1
DIY
Central Tendency
3.4 E-4
High-end
3.4 E-3
Bystander
Central Tendency
2.6 E-5
High-end
6.0 E-5
Brakes
Repair/replacement
Indoor, compressed air,
once at 16 years, staying in
residence for 10 years, 1
hour/d in garage
Section 4.2.3.1
DIY
Bystander
Central Tendency
5.6 E-6

High End
5.5 E-5
Bystander
Central Tendency
3.0 E-6

High-end
7.1 E-6
Brakes Repair/
replacement
Outdoor, once every 3
years for 62 years starting
at 16 years, exposures at
2% of active used between
uses, 5 min/d in driveway
Section 4.2.3.1
DIY
Central Tendency
9.9 E-8
High-end
5.3 E-7
Bystander
Central Tendency
2.1 E-8
High-end
1.1 E-7
Brakes Repair/
replacement
Outdoor, once every 3
years for 62 years starting
at 16 years, exposures at
2% of active used between
uses, 30 min/d in driveway
Section 4.2.3.1
DIY
Central Tendency
2.9 E-7
High-end
1.5 E-6
Bystander
Central Tendency
5.9 E-8
High-end
3.2 E-7
Imported Asbestos
Products

Gaskets Repair/
replacement in UTVs
Indoor, 1 hour/d, once
every 3 years for 62 years
starting at 16 years
exposures at 30% of active
used between uses, 1
hour/d in garage
Section 4.2.3.2
DIY
Central Tendency
2.3 E-5
High-end
6.4 E-5
Bystander
Central
Tendency
2.4 E-5
High-end
6.1 E-5

Section 4.2.3.2
DIY
Central Tendency
1.8 E-4
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Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure Duration
and Level
Cancer Risk
Estimates

Gaskets Repair/
replacement in UTVs
Indoor, 1 hour/d, once
every 3 years for 62 years

High-end
5.1 E-4

Bystander
Central Tendency
2.4 E-5

starting at 16 years
exposures at 30% of active
used between uses, 8
hour/d in garage

High-end
6.1 E-5

Gasket Repair
Repair/replacement
Section 4.2.3.2
DIY
Central Tendency
3.0 E-6

Indoor, once at 16 years,
staying in residence for 10
years, 1 hour/d in garage

High end
8.3 E-6

Bystander
Central Tendency
3.08 E-6

High-end
7.16 E-6
6813
6814
6815 4.3 Assumptions and Key Sources of Uncertainty
6816
6817 4.3.1 Key Assumptions and Uncertainties in the Uses of Asbestos in the U.S.
6818 EPA researched sources of information to identify the intended, known, or reasonably foreseen asbestos
6819 uses in the U.S. Beginning with the February, 2017 request for information (cite public meeting on Feb
6820 14th) on uses of asbestos and followed by both the Scope document (June (2017c)) and Problem
6821 Formulation (June (2018d)), EPA has refined its understanding of the current conditions of use of
6822 asbestos in the U.S. This has resulted in identifying chrysotile asbestos as the only fiber type
6823 manufactured, imported, processed, or distributed in commerce at this time and under six COU
6824 categories. EPA received voluntary acknowledgement of asbestos import and use from a handful of
6825 industries that fall under these COU categories. Some of the COUs are very specialized, and with the
6826 exception of the chlor-alkali industry, there are many uncertainties with respect to the extent of use, the
6827 number of workers and consumers involved and the exposures that might occur from each activity. For
6828 example, the number of consumers who might change out their brakes on their cars with asbestos-
6829 containing brakes ordered on the Internet or the number of consumers who might change out the
6830 asbestos gaskets in the exhaust system of their UTVs is unknown.
6831
6832 On April 25, 2019, EPA finalized an Asbestos Significant New Use Rule (SNUR) under TSCA section 5
6833 that prohibits any manufacturing (including import) or processing for discontinued uses of asbestos from
6834 restarting without EPA having an opportunity to evaluate each intended use for risks to health and the
6835 environment and to take any necessary regulatory action, which may include a prohibition. By finalizing
6836 the asbestos SNUR to include manufacturing (including import) or processing discontinued uses not
6837 already banned under TSCA, EPA is highly certain that manufacturing (including import), processing,
6838 or distribution of asbestos is not intended, known or reasonably foreseen beyond the 6 product
6839 categories identified herein.
6840
6841 EPA will consider legacy uses and associated disposal in subsequent supplemental documents.
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4.3.2 Key Assumptions and Uncertainties in the Environmental (Aquatic) Assessment
While the EPA has identified reasonably available aquatic toxicity data to characterize the overall
environmental hazards of chrysotile asbestos, there are uncertainties and data limitations regarding the
analysis of environmental hazards of chrysotile asbestos in the aquatic compartment. Limited data are
available to characterize effects caused by acute exposures of chrysotile asbestos to aquatic organisms.
Only one short-term aquatic invertebrate study was identified (Belanger et at.. 1986b). In addition, the
reasonably available data characterizes the effects of chronic exposure to waterborne chrysotile asbestos
in fish and clams. While these species are assumed to be representative for aquatic species, without
additional data to characterize the effects of asbestos to a broader variety of taxa, the broader ecosystem-
level effects of asbestos are uncertain. The range of endpoints reported in the studies across different life
stages meant that a single definitive, representative endpoint could not be determined, and the endpoints
needed to be discussed accordingly. Several of the effects reported by Belanger et al. (e.g., gill tissue
altered, fiber accumulation, and siphoning activity) are not directly related to endpoints like mortality or
reproductive effects and therefore the biological relevance is unclear. Lastly, the effect concentrations
reported in these studies may misrepresent the actual effect concentrations due to the inconsistent
methodologies for determining aquatic exposure concentrations of asbestos measured in different
laboratories.
During development of the PF, EPA was still in the process of identifying potential asbestos water
releases for the COUs. After the PF was released, EPA continued to search EPA databases as well as the
literature and either engaged in a dialogue with industries or reached out for a dialogue to shed light on
potential releases to water. In addition to the Belanger et al. studies, EPA evaluated the following lines
of evidence that suggested there is minimal or no releases of chrysotile asbestos to water: (1) 96% of
-14,000 samples from drinking water sources are below the minimum reporting level of 0.2 MFL and
less than 0.2% are above the MCL of 7 MFL for humans; (2) the source of the asbestos fibers is not
known to be from a TSCA condition of use in this draft risk evaluation; and (3) TRI data have not
shown releases of asbestos to water (Section 2.2.1.). The available information indicated that there were
surface water releases of asbestos; however, not all releases are subject to reporting (e.g., effluent
guidelines) or are applicable (e.g., friability). Based on the reasonably available information in the
published literature, provided by industries using asbestos, and reported in EPA databases, there is
minimal or no releases of asbestos to surface water associated with the COUs that EPA is evaluating in
this risk evaluation. Therefore, EPA concludes there is no unreasonable risk to aquatic or sediment-
dwelling environmental organisms. While this does introduce some uncertainty, EPA views it as low
and has confidence in making a determination of no exposure regarding potential releases to water for
the COUs in this risk evaluation. This conclusion is also based on the information in Section 2.3 in
which, for the major COUs (i.e., chlor-alkali, sheet gasket stamping and sheet gasket use), there is
documentation of collecting asbestos waste for disposal via landfill. In addition, there are no reported
releases of asbestos to water from TRI.
4.3.3 Key Assumptions and Uncertainties in the Occupational Exposure Assessment
The method of identifying asbestos in this RE is based on fiber counts made by phase contrast
microscopy (PCM). PCM measurements made in occupational environments were used both in the
exposure studies and in the studies used to support the derivation of the chrysotile IUR. PCM detects
only fibers longer than 5 |im and >0.4 |im in diameter, while transmission electron microscopy (TEM),
often found in environmental monitoring measurements, can detect much smaller fibers. Most of the
studies used in the RE have reported asbestos concentrations using PCM.
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In general, when enough data were reasonably available, the 95th and 50th percentile exposure
concentrations were calculated using reasonably available data (i.e., the chlor-alkali worker monitoring
data). In other instances, EPA had very little monitoring data available on occupational exposures for
certain COUs (e.g., sheet gasket stamping and brake blocks) or limited exposure monitoring data in the
published literature as well. Where there are few data points available, it is unlikely the results will be
representative of worker exposure across the industry depending on the sample collection location (PBZ
or source zone) and timing of the monitoring.
EPA acknowledges that the reported inhalation exposure concentrations for the industrial scenario uses
may not be representative for the exposures in all companies within that industry. For example, there are
only three chlor-alkali companies who own a total of 15 facilities in the U.S. that use chrysotile
diaphragms, but their operations are different, where some of them hydroblast and reuse their chrysotile
asbestos-containing diaphragms and others replace them. The exposures to workers related to these two
different activities are expected to be different.
EPA also received data from one company that fabricates sheet gaskets and one company that uses sheet
gaskets. These data were used, even though there are limitations, such as the representativeness of
practices in their respective industries.
All the raw chrysotile asbestos imported into the U.S. is used by the chlor-alkali industry for use in
asbestos diaphragms. The number of chlor-alkali plants in the U.S. is known and therefore the number
of workers potentially exposed is fairly certain. In addition, estimates of workers employed in this
industry were provided by the chlor-alkali facilities. However, the number of workers potentially
exposed during other COUs is very limited. Only two workers were identified for stamping sheet
gaskets, and two titanium dioxide manufacturing facilities were identified in the U.S. who use asbestos-
containing gaskets. However, EPA is not certain if asbestos-containing sheet gaskets are used in other
industries and to what extent. For the other COUs, no estimates of the number of potentially exposed
workers were submitted to EPA by industry or its representatives, so estimates were used. Therefore,
numbers of workers potentially exposed were estimated; and these estimates could equally be an over-
estimate or an under-estimate.
Finally, there is uncertainty in how EPA categorized the exposure data. Each PBZ and area data point
was classified as either "worker" or "occupational non-user." The categorizations are based on
descriptions of worker job activity as provided in worker monitoring data, in the literature and EPA's
judgment. In general, PBZ samples were categorized as "worker" and area samples were categorized as
"occupational non-user." Exposure data for ONUs were not available for most scenarios. EPA assumes
that these exposures are expected to be lower than worker exposures, since ONUs do not typically
directly handle asbestos nor are in the immediate proximity of asbestos.
4.3.4 Key Assumptions and Uncertainties in the Consumer Exposure Assessment
Due to lack of specific information on DIY consumer exposures, the consumer assessment relies on
available occupational data obtained under certain environmental conditions expected to be more
representative of a DIY consumer user scenario (no engineering controls, no PPE, residential garage).
However, the studies utilized still have uncertainties associated with the environment where the work
was done. In Blake et al. (2.003). worker exposures were measured at a former automobile repair facility
which had an industrial sized and filtered exhaust fan unit to ventilate the building during testing while
all doors were closed. A residential garage is not expected to have a filtered exhaust fan installed and
operating during DIY consumer brake repair/replacement activities.
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The volume of a former automobile repair facility is considerably larger than a typical residential garage
and will have different air exchange rates. While this could raise some uncertainties related to the
applicability of the measured data to a DIY consumer user environment, the locations of the
measurements utilized for this evaluation minimize that uncertainty.
There is some uncertainty associated with the length of time EPA assumes the brake repair/replacement
work takes. The EPA assumed it takes a DIY consumer user about three hours to complete brake
repair/replacement work. This is two times as long as a professional mechanic. While it is expected to
take a DIY consumer longer, it is also expected DIY consumer users who do their own brake
repair/replacement work would, over time, develop some expertise in completing the work as they
continue to do it every three years.
There is also some uncertainty associated with the assumption that a bystander would remain within
three meters from the automobile on which the brake repair/replacement work is being conducted for the
entire three-hour period EPA assumes it takes the consumer user to complete the work. However,
considering a residential garage with the door closed is relatively close quarters for car repair work, it is
likely anyone observing (or learning) the brake repair/replacement work would not be able to stay much
further away from the car than three meters. Remaining within the garage for the entire three hours also
has some uncertainty, although it is expected anyone observing (or learning) the brake
repair/replacement work would remain for the entire duration of the work or would not be able to
observe (or learn) the task.
While industry practices have drifted away from the use of compressed air to clean brake drums/pads,
no information was found in the literature indicating consumers have discontinued such work practices.
To consider potential consumer exposure to asbestos resulting from brake repair/replacement activities,
EPA uses data which included use of compressed air. However, EPA recognizes this may be a more
conservative estimate because use of compressed air typically could cause considerable dust/fibers to
become airborne if it is the only method used.
There were no data identified through systematic review providing consumer specific monitoring for
UTV exhaust system gasket repair/replacement activities. Therefore, this evaluation utilized published
monitoring data obtained in an occupational setting, by professional mechanics, as a surrogate for
estimating consumer exposures associated with UTV gasket removal/replacement activities. There is
some uncertainty associated with the use of data from an occupational setting for a consumer
environment due to differences in building volumes, air exchange rates, available engineering controls,
and the potential use of PPE. As part of the literature review, EPA considered these differences and
utilized reasonably available information which was representative of the expected consumer
environment.
There is some uncertainty associated with the use of an automobile exhaust system gasket
repair/replacement activity as a surrogate for UTV exhaust system gasket repair/replacement activity
due to expected differences in the gasket size, shape, and location. UTV engines and exhaust systems
are expected to be smaller than a full automobile engine and exhaust system, therefore the use of an
automobile exhaust system gasket repair may slightly overestimate exposure to the consumer. At the
same time, the smaller engine and exhaust system of a UTV could make it more difficult to access the
gaskets and clean the surfaces where the gaskets adhere therefore increasing the time needed to clean
and time of exposure resulting from cleaning the surfaces which could underestimate consumer
exposure.
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There is some uncertainty associated with the assumption that UTV exhaust system gasket
repair/replacement activities would take a consumer a full three hours to complete. While there was no
published information found providing consumer specific lengths of time to complete a full
repair/replacement activity. The time needed for a DIY consumer to complete a full UTV exhaust
system gasket repair/replacement activity can vary depending on several factors including location of
gaskets, number of gaskets, size of gasket, and adherence once the system is opened up and the gasket
removed. Without published information, EPA assumes this work takes about three hours and therefore
utilized the three-hour TWA's to estimate risks for this evaluation.
Finally, EPA has made some assumptions regarding both age at start of exposure and duration of
exposure for both the DIY users and bystanders for both the brake and UTV gasket scenarios. Realizing
there is uncertainty around these assumptions, specifically that they may over-estimate exposures, EPA
developed a sensitivity analysis approach specifically for the consumer exposure/risk analysis (see
appropriate part of Section 4.3.8 below) and also performed a sensitivity analysis using five different
scenarios (Appendix L).
4.3.5 Key Assumptions and Uncertainties in the Human Health IUR Derivation
The analytical method used to measure exposures in the epidemiology studies is important in
understanding and interpreting the results as they were used to develop the IUR. As provided in more
detail in Section 3, the IUR for "current use" asbestos (i.e., chrysotile) is based solely on studies of PCM
measurement as TEM-based risk data are limited in the literature and the available TEM results for
chrysotile lack modeling results for mesothelioma. In TEM studies of NC and SC (Loomis et at.. 2010;
Stavner et at.. 20081 models that fit PCM vs TEM were generally equivalent (about 2 AIC units),
indicating that fit of PCM is similar to the fit of TEM (for these two cohorts), providing confidence in
those PCM measurements for SC and NC. Given that confidence in the PCM data and the large number
of analytical measurements, exposure uncertainty is considered low in the cohorts used for IUR
derivation.
There is evidence that other cancer endpoints may also be associated with exposure to the commercial
forms of asbestos. IARC concluded that there was sufficient evidence in humans that commercial
asbestos (chrysotile, crocidolite, amosite, tremolite, actinolite, and anthophyllite) was causally
associated with lung cancer and mesothelioma, as well as cancer of the larynx and the ovary (Straif et
at.. 2.009). The lack of sufficient numbers of workers to estimate risks of ovarian and laryngeal cancer is
a downward bias leading to lower IUR estimates in an overall cancer health assessment; however, the
selected IUR was chosen to compensate for this bias.
The endpoint for both mesothelioma and lung cancer was mortality, not incidence. Incidence data are
not available for any of the cohorts. Nevertheless, mortality rates approximate incidence rates for
cancers such as lung cancer and mesothelioma because the survival time between cancer incidence and
cancer mortality is short. Therefore, while the absolute rates of lung cancer mortality at follow-up may
underestimate the rates of lung cancer incidence, the uncertainty for lung cancer is low. For
mesothelioma, the median length of survival with mesothelioma is less than 1 year for males, with less
than 20% surviving after 2-years and less than 6% surviving after 5-years. Because the mesothelioma
model is absolute risk, this leads to an under-ascertainment on mesothelioma risk, however, the selected
IUR was chosen to compensate this bias.
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The IUR only characterizes cancer risk. It does not include any risks that may be associated with non-
cancer health effects. Pleural and pulmonary effects from asbestos exposure (e.g., asbestosis and pleural
thickening) are well documented ( 58b), although there is no reference concentration (RfC)
for these non-cancer health effects specifically for chrysotile. During the Problem Formulation step for
TSCA's risk evaluation of asbestos, EPA considered risks of 1 cancer per 1,000,000 people, and at that
level of risk, cancer was considered to be a risk driver for the overall health risk of asbestos. The IRIS
IUR for general asbestos is 0.23 per fiber/cc. The IRIS assessment of Libby amphibole asbestos (U.S.
EPA. 2014b) derived a RfC for non-cancer health effects, and at that concentration (9 E-5 fibers/cc), the
risk of cancer for general asbestos fibers (including chrysotile, actinolite, amosite, anthophyllite,
crocidolite, and tremolite) was 2 E-5 [IUR*RfC = (0.23 per fiber/cc)*(9 E-5 fibers/cc)]. Thus, at a target
risk of 1 cancer per 1,000,000 people (1E-6), the existing EPA general asbestos cancer toxicity value
appeared to be the clear risk driver as meeting that target risk would result in lower non-cancer risks
than at the RfC.
However, in occupational settings, with workers and ONUs exposed in a workplace, EPA considered
risks of cancer per 10,000 people. At this risk level, if the non-cancer effects of chrysotile are similar to
Libby amphibole asbestos, the non-cancer effects of chrysotile are likely to contribute additional risk to
the overall health risk of asbestos beyond the risk of cancer. Thus, the overall health risks of asbestos
based on cancer alone are underestimated.
The POD associated with the only non-cancer toxicity value is 0.026 fibers/cc (
2014b). Although the non-cancer toxicity of chrysotile may be different from Libby amphibole asbestos,
there is uncertainty that the IUR for chrysotile asbestos may not fully encompasses the health risks
associated with chrysotile exposure. Several of the COU-related exposures evaluated for human health
risks in section 4.2 are at or greater than the POD for non-cancer effects associated with exposure to
Libby amphibole asbestos.
4.3.6 Key Assumptions and Uncertainties in the Cancer Risk Values
Although direct comparison of cancer slopes for PCM and TEM fibers is impossible because different
counting rules for these methods result in qualitatively and quantitatively different estimates of asbestos
exposure, comparing the fit of models based on different analytical methods is possible. In TEM studies
of NC and SC (Loomis et at.. 2010; Stavner et at.. 2008). models that fit PCM vs TEM were generally
equivalent (about 2 AIC units), indicating that fit of PCM is similar to the fit of TEM (for these two
cohorts), providing confidence in those PCM measurements for SC and NC, whose data is the basis for
chrysotile IUR.
Another source of uncertainty in the exposure assessment is that early measurements of asbestos fiber
concentrations were based on an exposure assessment method (midget impinger) that estimated the
combined mass of fibers and dust, rather than on counting asbestos fibers. The best available
methodology for conversion of mass measurements to fiber counts is to use paired and concurrent
sampling by both methods to develop factors to convert the mass measurements to estimated fiber
counts for specific operations. There is uncertainty in these conversion factors, but it is minimized in the
studies of SC and NC chrysotile textile workers due to the availability of an extensive database of paired
and concurrent samples and the ability to develop operation-specific conversion factors. Uncertainty in
the estimation of these conversion factors and their application to estimate chrysotile exposures will not
be differential with respect to disease.
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Given the high confidence in the PCM data and the large number of analytical measurements, exposure
uncertainty is overall low in the SC and NC cohorts, as very high-quality exposure estimates are
available for both cohorts. Statistical error in estimating exposure levels is random and not differential
with respect to disease. Therefore, to the extent that such error exists, it is likely to produce either no
bias or bias toward the null under most circumstances (e.g., (Kim, et al. 2011; Armstrong. 1998)).
Epidemiologic studies are observational and as such are potentially subject to confounding and selection
biases. Most of the studies of asbestos exposed workers did not have information to control for cigarette
smoking, which is an important risk factor for lung cancer in the general population. In particular, the
NC and SC studies of textile workers, which were chosen as the most informative studies, did not have
this information. However, the bias related to this inability to control for smoking is believed to be small
because the exposure-response analyses for lung cancer were based on internal comparisons and for both
studies the regression models included birth cohort, thus introducing some control for the changing
smoking rates over time. It is unlikely that smoking rates among workers in these facilities differed
substantially enough with respect to their cumulative chrysotile exposures to induce important
confounding in risk estimates for lung cancer. Mesothelioma is not related to smoking and thus smoking
could not be a confounder for mesothelioma.
For the purpose of combining risks, it is assumed that the unit risks of mesothelioma and lung
cancer mortality are normally distributed. Because risks were derived from a large
epidemiological cohort, this is a reasonable assumption supported by the statistical theory and the
independence assumption has been investigated and found a reasonable assumption (U.S. EPA. 2014c).
4.3.7 Confidence in the Human Health Risk Estimations
Workers/Occupational Non-Users
Depending on the variations in the exposure profile of the workers/occupational non-users, risks could
be under- or over-estimated for all COUs. The estimates for extra cancer risk were based on the EPA-
derived IUR for chrysotile asbestos. The occupational exposure assessment made standard assumptions
of 240 days per year, 8 hours per day over 40 years starting at age 16 years. This assumes the workers
and occupational non-users are regularly exposed until age 56. If a worker changes jobs during their
career and are no longer exposed to asbestos, this may overestimate exposures. However, if the worker
stays employed after age 56, it would underestimate exposures.
The concentration-response functions on which the chrysotile asbestos IUR is based varies as a function
of time since first exposure. Consequently, estimates of cancer risk depend not only on exposure
concentration, frequency and duration, but also on age at first exposure. To approximate the impact of
different assumptions for occupational exposures, Table 4-49 can be used to understand what percentage
of the risk in the baseline occupational exposure scenario remains for different ages at first exposure and
different durations of exposure
Table 4-49. Ratios of risks for alternative exposure scenarios using scenario-specific partial
lifetime IURs from Appendix K by age at first exposure and duration of exposure compared to
baseline occupational exposure scenarios (baseline scenario: first exposure at 16 years for 40 years
duration)
Duration of exposure (years)
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Age at first exposure (years)
20
40
16
0.0499/0.0707 = 0.71
0.0707/0.0707 = 1
20
0.0416/0.0707 = 0.59
0.0591/0.0707 = 0.84
30
0.0267/0.0707 = 0.38
0.0374/0.0707 = 0.53
Other occupational exposure scenario can be evaluated by selecting different values for the age at first
exposure and the duration of exposure from the table of partial lifetime IUR values in Appendix K.
Exposures for ONUs can vary substantially. Most data sources do not sufficiently describe the proximity
of these employees to the exposure source. As such, exposure levels for the ONU category will vary
depending on the work activity. It is unknown whether these uncertainties overestimate or underestimate
exposures.
Cancer risks were indicated for all of the worker COUs and most of the consumer/bystander COUs. If
additional factors were not considered in the RE, such as exposures from other sources (e.g., legacy
asbestos sources), the risks could be underestimated. Legacy asbestos is not evaluated in the RE at this
time, but EPA will consider legacy uses and associated disposal in subsequent supplemental documents.
In addition, several subpopulations (e.g., smokers, genetically predisposed individuals, COU workers
who change their own asbestos-containing brakes, etc.) may be more susceptible than others to health
effects resulting from exposure to asbestos. These conditions are discussed in more detail for potentially
exposed or susceptible subpopulations and aggregate exposures in Section 4.4 and Section 4.5.
Consumer DIY/Bystanders
Similarly, for consumers/bystanders risks could be under- or over-estimated for their COU. Unlike
occupational scenarios, there are no standard assumptions for consumers and bystanders, EPA
conducted sensitivity analyses to evaluate some alternative scenarios for consumers/bystanders as
described below.
For consumers (see Table 4-48) EPA considered age at first exposure of 16 years with duration of
exposure 62 years and for bystanders EPA considered age at first exposure of 0 years with lifetime
duration (78 years). To evaluate sensitivity to these assumptions, EPA conducted multiple sensitivity
analyses assuming that duration of exposure as short as 10 years with different ages of first
exposure. Tables 4-50 and 4-51 below show the different scenarios covered in the sensitivity analysis
and the associated adjustment factor that may be used to calculate a different risk number. In Table 4-50,
DIY exposures with different ages at start of exposure (16, 20 or 30 years old) are paired with different
durations of exposure (20, 40 or 62) and Table 4-51 shows the same for bystanders (age at start is
always zero but the three exposure durations are 20, 40 and 78). All analyses are presented in Appendix
L and show that using the ratios in both Tables 4-49 and 4-50 does not change the overall risk picture in
almost all scenarios (see Table 4-51).
Table 4-50. Ratios of risks for alternative exposure scenarios using scenario-specific partial
lifetime IURs from Appendix K by age at first exposure and duration of exposure compared to
baseline consumer DIY exposure scenarios (baseline scenario: first exposure at 16 years for 62
years duration)
Duration of exposure (years)
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Age at first exposure
(years)
20
40
62
16
0.0499/0.0768 =
0.65
0.0707/0.0768 =0.92
0.0768/0.0768 = 1
20
0.0416/0.0768 =
0.54
0.0591/0.0768 =
0.77
-
30
0.0267/0.0768 =
0.35
0.0374/0.0768 =
0.49
-
Table 4-51. Ratios of risks for alternative exposure scenarios using scenario-specific partial
lifetime IURs from Appendix K by age at first exposure and duration of exposure compared to
baseline consumer bystander exposure scenarios (baseline scenario: first exposure at 0 years for
78 years duration)

Duration of exposure (years)
Age at first exposure
(years)
20
40
78
0
0.101/0.16 = 0.63
0.144/0.16=0.90
0.16/0.16 = 1
Table 4-52 provides a summary of the detailed analyses in Appendix L. These sensitivity analyses show
that in four of the five scenario pairings, only one of 24 possible scenarios changed from exceeding the
benchmark cancer risk level of lxlO 6 to no exceedance (DIY user, brake repair outdoors, 30
minutes/day, high-end only). In the fifth scenario (Sensitivity Analysis 2), there was no change in any of
the 24 scenarios. All analyses are in Appendix L.
Table 4-52. Results of Sensitivity Analysis of Exposure Assumptions for Consumer DIY/Bystander
Episodic Exposure Scenarios
Sensili\ ily
Analysis'
DIY (iiiic ill skirl and
aue al end of duration)
IJy slander (aue al
slarl and aue al end
of duration)
Chanue in Risk
lVoni l-Aceedance
lo No lAccedance
Scenario Afleclcd
Baseline
16-78
0-78
None
17/24 Exceed
Benchmarks
1
16-36
0-20
1/24
DIY user, Brake
repair, 30 min/day,
high-end
2
20-60
0-40
0/24
None
3
20-40
0-40
1/24
DIY user, Brake
repair, 30 min/day,
high-end
4
30-70
0-40
1/24
DIY user, Brake
repair, 30 min/day,
high-end
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5
30-50
0-20
1/24
DIY user, Brake

repair, 30 min/day,

high-end
1 Includes all brake repair/replacement and gasket repair replacement scenarios - a total of 24. See Table 4-45
Assumptions About Bystanders
The EPA Exposure Factors Handbook (2011) provides the risk assessment community with data-derived
values to represent human activities in a variety of settings. For the purposes of this draft risk evaluation,
understanding the amount of time consumers spend in a garage is important to develop an exposure
scenario for DIYers/mechanics who change their own brakes or gaskets and bystanders to those
activities. Table 16-16 in the Handbook, entitled Time Spent (minutes/day) in Various Rooms at Home
and in All Rooms Combined, Doers Only, has a section on time spent in a garage.
The total number of respondents to the survey question on time spent in the garage was 193 and the
minimum and maximum reported times were one minute and 790 minutes (-13 hours). Again, these
respondents are "doers", defined as people who reported being in that location (i.e., the garage). In this
analysis, it was assumed that the 50th percentile would represent a central tendency estimate for being
present in the garage (one hour/day) and the 95th percentile would represent a high-end estimate for
being present in the garage (8 hours).
EPA understands that a bystander in this exposure situation (DIY automotive and UTV repair) is most
likely to be a family member (minor or adult relative) with repeated access to the garage used to repair
vehicles. As a familial bystander, and not a neighbor or someone visiting, EPA considered that these
bystanders would have similar exposures to the garage, and thus to any chrysotile fibers in the same
garage environment as the DIY user. EPA used the same median time of one hour per day as the
bystander's estimated central tendency and the same estimate of high end exposures. EPA noted that the
younger doers appear to spend somewhat more time in the garage (EFH Table 16-16). In the same table
of time spent per day in the garage, some data on doers is shown for ages 1-17 years (children) which
can be aggregated to find the mean time spent in a garage. The mean for these children is 77 minutes per
day based on 22 young doers, which is similar to the one hour median based on all 193 doers. EPA also
noted that male doers had a median of 94 minutes compared to female doers who had a median of 30
minutes per day in the garage. It is possible that familial bystanders are unlike the DIY users and spend
little time in the garage. If this were true, then with little or no time spent in the garage, their risks
would be limited.
Finally, as part of the sensitivity analysis, understanding that a bystander in a doer family may spend
somewhat less time in the garage than the 50th percentile time of one hour (60 minutes/day), Table 4-53
below shows the data available in the Exposure Factors Handbook that present other percentiles broken
down by age and gender. In its original analysis, EPA used 60 minutes/day. If 10 minutes/day were used
for the bystander and in keeping with deriving a risk estimate following a single brake or gasket change
and a time-in-residence of only 10 years, the calculated risk values would be:
At 10 minutes/day in the garage following a single brake change and the next 10 years in the
house, the by-stander risks would be 6.9 E-8 for the central tendency and 1.6 E-7 for the high-
end estimates.
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At 10 minutes/day in the garage following a single UTV gasket change and the next 10 years in
the house, the by-stander risks would be 6.4 E-8 for the central tendency and 1.6 E-7 for the
high-end estimates.
Table 4-53. Time Spent (minutes/day) in Garage, Doers Only (Taken from Table 16-16 in EFH, 2011
(lender mid Age
Percentiles in the Distribution o
'Survev Respondents
Usmgc
5"'
25 th
50 th
75th
95 th
All ages
5
20
60
150
480
Men
10
30
94
183
518
Women
5
15
30
120
240
1-4 yrs old
15
52
100
115
120
5 to 11
10
25
30
120
165
12-17
10
20
51
148
240
Potential Number of Impacted Individuals
Table 4-54 provides an estimate of the number of impacted individuals for both occupational and
consumer exposure scenarios. Some of the estimates have a higher level of confidence than others. For
example, EPA is fairly certain about the number of chlor-alkali workers given the information submitted
by industry. For some of the other COUs, while there may be some knowledge about the potential
number of workers/consumers in a particular COU, there is a lack of information/details on the market
share of asbestos-containing products available to both workers and consumers. This makes it difficult
to assess level of both certainty and confidence estimating the potential number of impacted individuals
using asbestos for the COUs (except for chlor-alkali) in this draft risk evaluation. For ONUs and
bystanders, there is a similar lack of understanding of the potential number of potentially impacted
individuals.
The following text accompanies the estimates presented in Table 4-54:
Chlor-Alkali Workers and ONUs
There is a total of 3,050 employees at the 15 chlor-alkali plants we have identified as using diaphragms;
with approximately 75-148 potentially exposed to asbestos during various activities associated with
constructing, using and deconstructing asbestos diaphragms. Subtracting the 75 to 148 workers
potentially exposed to asbestos results in approximately2,900 to 3,000 other employees who work at the
same or adjoining plant. This is an upper bound estimate of the number of ONUs and only an unknown
subset of these workers may be ONUs. EPA has low certainty in this number because some of these
sites are very large and make different products in different parts of the facility (one site is 1,100 acres
and has 1,300 employees). Thus, this approach may overestimate the number of ONUs for asbestos
diaphragms.
Sheet Gaskets - Stamping (Workers and ONUs)
EPA found only two gasket sampling sites handling asbestos containing sheet gasket; one worker and
two ONUs per site. However, there may be more gasket stamping sites processing asbestos containing
sheet gasket in US. Thus, the uncertainty in this number of impacted individuals is high.
Sheet Gaskets - Use (Workers and ONUs)
The Bureau of Labor Statistics 2016 data for the NAICS code 325180 (Other Basic Inorganic Chemical
Manufacturing) indicates an industry-wide aggregate average of 25 directly exposed workers per facility
and 13 ONUs per facility. The total number of use sites is unknown.
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Oilfield Brake Blocks (Workers and ONUs)
According to 2016 Occupational Employment Statistics data from the Bureau of Labor Statistics (BLS)
and 2015 data from the U.S. Census' Statistics of U.S. Businesses. EPA used BLS and Census data for
three NAICS codes: 211111, Crude Petroleum and Natural Gas Extraction; 213111, Drilling Oil and Gas
Wells; and 213112, Support Activities for Oil and Gas Operations, there are up to 61,695 workers and
66,108 ONU. See Table 2-12 for the breakdown by each category. It is not known how many of these
workers are exposed to asbestos.
Aftermarket Automotic Brakes/Linings/Clutches (Workers and ONUs)
EPA considers the best current estimate of this worker population to be from the Bureau of Labor
Statistics, which estimates that 749,900 workers in the United States were employed as automotive
service technicians and mechanics in 2016 (II ,S. 2019); see Section 2.3.1.7 for more details. This
includes workers at automotive repair and maintenance shops, automobile dealers, gasoline stations, and
automotive parts and accessories stores. ONU exposures associated with automotive repair work are
expected to occur because automotive repair and maintenance tasks often take place in large open bays
with multiple concurrent activities. EPA did not locate published estimates for the number of ONUs for
this COU. However, consistent with the industry profile statistics from OSHA's 1994 rulemaking (see
Section 2.3.1.7), EPA assumes that automotive repair establishments, on average, have two workers who
perform automotive repair activities. Accordingly, EPA estimates that this COU has 749,900 ONUs.
1J TV Sheet Gaskets (Workers and ONUs)
Based on Bureau of Labor Statistics and several assumptions detailed in section 2.3.1.9, EPA estimate
1,500 workers for UTV service technicians and mechanics. It is not known how many of them service
and/or repair UTV with asbestos containing gasket.
Aftermarket Automotic Brakes/Linings/Clutches (Consumers/DIY/Bystanders)
According to the Census's American Community Survey, 108,357,503 occupied housing units have at
least one vehicle available. Of these, 39,472,759 (36%) have one vehicle available, 44,402,282 (41%)
have two vehicles available, and 24,482,462 (23%) have three or more vehicles available.24
According to a 2001 market research study by the Automotive Aftermarket Industry Association ("The
Aftermarket Consumer: Do-it-Yourself or Do-it-For-Me"), nearly half of all U.S. households contain at
least one automotive DIYer.25 While some households may contain more than one automotive DIYer,
EPA assumes that the number of automotive DIYers is 50% of the number of households with an
automobile.
24
American Fact Finder, 2013-2017 American Community Survey 5-Year Estimates, DP04, U.S. Census Bureau.
25 The Auto Channel, AAIA REPORT: Percentage of Auto DIYers Unchanged, 07-03-01.
https://www.theautochannel.com/news/2001/07/03/024549.html
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According to a 2014 online survey of 2,843 consumers conducted by AutoPartsWarehouse.com, 63% of
male DIYers and 35% of female DIYers responded that they replace brake pads. The survey respondents
were 85% male and 15% female.26
Combining this data, (108,357,503 households with at least one vehicle available) x (50% of households
contain an automotive DIYer) x ((85% of DIYers are male) x (63% of male DIYers replace brake pads)
+ (15%) of DIYers are female) x (35% of female DIYers replace brake pads)) = 31,857,106 automotive
DIYers replace brake pads.
EPA estimates that brakes are replaced about once every three years.27 Combining the Census ACS data
on the distribution of vehicles per household; the estimate that 31,857,106 automotive DIYers replace
brake pads; and the estimate that brakes are replaced once every three years, results in an estimate that
that there are approximately 20 million DIY brake jobs per year.
The number of asbestos-containing brakes sold in the aftermarket is not known.
COUs for Which No Estimates May be Made
EPA could develop an reasonable estimate of potentially impacted individuals for two COUs: other
vehicle friction products (workers/ONUs) and UTV gasket replacement/repair (DIY/bystanders).
Table 4-54. Summary of Estimated Number of Exposed Workers and DIY Consumers3.
Condition of I se
Industrial and Commercial
DIY

Workers
OM
Consumer
Bystanders
Asbestos diaphragms - chlor-alkali
75-148
<2900-3000
-
-
Sheet gaskets - stamping
>2
>4
-
-
Sheet gaskets - use
25/facility (no.
of facilities
Unknown)
13/facility (no.
of facilities
Unknown
~
~
Oilfield brake blocks
<61,695 (total;
number exposed
to asbestos
unknown)(c)
<66,108 (total;
number in
vicinity of
asbestos
Unknown(c)

26 Consumers Continue to Embrace DIY Auto Repair, Attempting More Difficult Jobs and Report Saving Big Bucks,
September 30, 2014 by Auto Parts Warehouse
https://www.autopartswarehouse.com/blog/2014/09/consumers-continue-embrace-diy-auto-repair-attempting-difficult-jobs-
report-saving-big-bucks/
27 Brakes in cars and small trucks are estimated to require replacement approximately every 35,000 to 60,000 miles (Advance
Auto Parts, website accessed on November 12, 2018). The three-year timeline is derived by assuming the need to replace
brakes every 35,000 miles, and an average number of annual miles driven per driver in the U.S. of 13,476 miles/year (U.S.
DOT, 2018).
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Aftermarket automotive
brakes/linings, clutches
749,900
749,000
31,857,106
Unknown
Other Vehicle Friction Products
(brakes installed in exported cars)
Unknown
Unknown
-
-
Other gaskets - UTVs
-1500 (total;
number exposed
to asbestos
unknown(d)
Unknown
Unknown
Unknown
a See Text for details.
4.4 Other Risk-Related Considerations
4.4.1 Potentially Exposed or Susceptible Subpopulations
EPA identified workers, ONUs, consumers, and bystanders as potentially exposed populations. EPA
provided risk estimates for workers and ONUs at both central tendency and high-end exposure levels for
most COUs. EPA determined that bystanders may include lifestages of any age.
For inhalation exposures, risk estimates did not differ between genders or across lifestages because both
exposures and inhalation hazard values are expressed as an air concentration. EPA expects that
variability in human physiological factors (e.g., breathing rate, body weight, tidal voume) could affect
the internal delivered concentration or dose of asbestos.
Workers exposed to asbestos in workplace air, especially if they work directly with asbestos, are most
susceptible to the health effects associated with asbestos. Some workers not associated with the COU
may experience higher exposures to asbestos, such as, but not limited to, asbestos removal workers,
firefighters, demolition workers and construction workers (Landrigan et at.. 2004); and these
populations will be considered when EPA evaluates legacy uses in subsequent supplemental documents.
Although it is clear that the health risks from asbestos exposure increase with heavier exposure and
longer exposure time, investigators have found asbestos-related diseases in individuals with only brief
exposures. Generally, those who develop asbestos-related diseases show no signs of illness for a long
time after exposure (ATSDR. 2.001a).
A source of variability in susceptibility between people is smoking history or the degree of exposure to
other risk factors with which asbestos interacts. In addition, the long-term retention of asbestos fibers in
the lung and the long latency period for the onset of asbestos-related respiratory diseases suggest that
individuals exposed earlier in life may be at greater risk to the eventual development of respiratory
problems than those exposed later in life (ATSDR. 2001a). Appendix J of this RE illustrates this point in
the IUR values for less than lifetime COUs. For example, the IUR for a one-year old child first exposed
to chrysotile asbestos for 40 years is 1.31 E-l while the IUR for a 20-year old first exposed to asbestos
for 40 years is 5.4 E-2. Using the central tendency bystander exposure value of 0.032 f/cc, the resulting
risk estimates are 1.7 x E-4 and 7.2 x E-5, respectively. There is also some evidence of genetic
predisposition for mesothelioma related to having a germline mutation in BAP1 (Testa et ai. 2011).
Finally, from an environmental receptor perscpective, although there is evidence of reproductive and
developmental effects in controlled laboratory settings following asbestos exposure to aquatic
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7376
7377
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7380
7381
7382
7383
7384
7385
7386
7387
7388
7389
7390
7391
7392
7393
7394
7395
7396
7397
7398
7399
7400
7401
7402
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organisms. The likelihood these effects would occur in the environment is low due to the lack of
environmental releases of asbestos to surface water from the COUs in this draft risk evaluation.
4.4.2 Aggregate and Sentinel Exposures
Section 2605(b)(4)(F)(ii) of TSCA requires the EPA, as a part of the risk evaluation, to describe whether
aggregate or sentinel exposures under the conditions of use were considered and the basis for their
consideration. The EPA has defined aggregate exposure as "the combined exposures to an individual
from a single chemical substance across multiple routes and across multiple pathways (40 CFR §
702.33)."
Aggregate exposures for asbestos were not assessed by routes of exposure, since only inhalation
exposure was evaluated in the RE. EPA chose not to employ simple additivity of exposure pathways at
this time within a condition of use because of the uncertainties present in the current exposure estimation
procedures. This lack of aggregation may lead to an underestimate of exposure but based on physical
chemical properties the majority of the exposure pathway is believed to be from inhalation exposures.
Pathways of exposure were not combined in this RE. Although it is possible that workers exposed to
asbestos might also be exposed as consumers (e.g., by changing brakes at home), the number of
workers/uses is potentially small. The individual risk estimates already indicate risk; aggregating the
pathways would increase the risk.
In addition, the potential for exposure to legacy asbestos for any populations or subpopulation, due to
activities such as home or building renovations, as well as occupational or consumer exposures
identified in this RE, is possible. Legacy asbestos exposure is not considered in the RE at this time
which could underestimate exposures and thus, risks. This is discussed as an uncertainty in Section 4.3.8
of the RE. EPA will consider legacy uses and associated disposal in subsequent supplemental
documents.
The EPA defines sentinel exposure as "the exposure to a single chemical substance that represents the
plausible upper bound of exposure relative to all other exposures within a broad category of similar or
related exposures (40 CFR § 702.33)." In terms of this risk evaluation, the EPA considered sentinel
exposure the highest exposure given the details of the conditions of use and the potential exposure
scenarios. EPA considered sentinel exposure for asbestos in the form of a high-end level scenario for
occupational exposure resulting from inhalation exposures for each COU; sentinel exposures for
workers are the high-end 8-hour exposures for sheet gasket stamping without any PPE.
4.5 Risk Conclusions
4.5.1 Environmental Risk Conclusions
Based on the reasonably available information in the published literature, provided by industries using
asbestos, and reported in EPA databases, there is minimal or no releases of asbestos to surface water and
sediments associated with the COUs in this risk evaluation. Therefore, EPA concludes there is no
unreasonable risk to aquatic or sediment-dwelling environmental organisms. In addition, terrestrial
pathways, including biosolids, were excluded from analysis at the PF stage.
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7410
7411
7412
7413
7414
7415
7416
7417
7418
7419
7420
7421
7422
7423
7424
7425
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4.5.2 Human Health Risk Conclusions to Workers
Table 4-57 provides a summary of risk estimates for workers and ONUs. For workers in all six COUs
identified in this risk evaluation, cancer risks were exceeded for all central tendency and high-end
exposures (chlor-alkali industry, stamping of sheet gaskets, use of sheet gaskets in the chemical
production industry, oil field brake blocks, aftermarket auto brakes/other vehicle friction products
installation and UTV gasket repair). In addition, for ONUs, cancer risks were exceeded for high-end
exposure estimates in all of the COUs. For central tendency exposure estimates for ONUs, cancer risks
were exceeded for sheet gasket use, oilfield brake block use, and UTV gasket repair.
With the assumed use of respirators as PPE at APF of 10, most risks would be reduced but still persisted
for sheet gasket stamping, sheet gasket use, auto brake replacement, and UTV gasket replacement.
When respirators with an APF of 25 was assumed, risk was still indicated for the auto brakes high-end
short-term exposure scenario only. It is important to note that based on published evidence for asbestos
(see Section 2.3.1.2), nominal APF may not be achieved for all respirator users. ONUs were not
assumed to be using PPE to reduce exposures to asbestos.
Table 4-55. Summary of Risk Estimates for Inhalation Exposures to Workers and ONUs by COU
(Cancer benchmark is 10 4)
Life Cycle
Stage/Category
Subcategory
Occupational
Exposure
Scenario
Popula-
tion
Exposure
Duration
and Level
Cancer Risk
Estimates
(before
applying
PPE)
Cancer
Risk
Estimates
(with
APF=10C)
Cancer Risk
Estimates
(with
APF=25C)

Diaphragms for
chlor-alkali
industry
Section 2.3.1.3
Worker
Central
Tendency
(8-hr)
1.2 E-4
1.2 E-5
4.8 E-6

High-end
(8-hr)
8.4 E-4
8.4 E-5
3.4 E-5

Central
Tendency
short term
1.5 E-4
1.1 E-4a
1.5 E-5d
6.0 E-6b
Import - Raw
asbestos

High-end
short term
1.3 E-3
8.1 E-4a
9.9 E-5d
5.2 E-5b

ONU
Central (8-
hr)
5.8 E-5
N/A
N/A

High (8-hr)
1.9 E-4
N/A
N/A

Central (w/
short-term)
--
N/A
N/A

High (w /
short-term)
--
N/A
N/A

Asbestos Sheets -
Gasket Stamping
Section 2.3.1.4
Worker
Central
Tendency
(8-hr)
3.3 E-4
3.3 E-5
1.3 E-5

High-end
(8-hr)
1.4 E-3
1.4 E-4
5.0 E-5

Central (w/
short-term)
3.5 E-4
3.5 E-5e
1.4 E-5f
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Life Cycle
Stage/Category
Subcategory
Occupational
Exposure
Scenario
Popula-
tion
Exposure
Duration
and Level
Cancer Risk
Estimates
(before
applying
PPE)
Cancer
Risk
Estimates
(with
APF=10C)
Cancer Risk
Estimates
(with
APF=25C)

High (w /
short-term)
1.4 E-3
1.4 E-4e
5.6 E-5f
Import of
asbestos

ONU
Central (8-
hr)
5.6 E-5
N/A
N/A
products

High (8-hr)
2.3 E-4
N/A
N/A

Central (w/
short-term)
5.6 E-5
N/A
N/A

High (w /
short-term)
2.3 E-4
N/A
N/A

Asbestos Sheet
Gaskets - use
(repair/replacement
Section 2.3.1.5
Worker
Central
Tendency
(8-hr)
6.0 E-4
6.0 E-5
2.4 E-5

in TiO: industry)

High-end
(8-hr)
2.2 E-3
2.2 E-4
8.8 E-5

ONU
Central (8-
hr)
1.2 E-4
N/A
N/A

High (8-hr)
3.7 E-4
N/A
N/A

Oil Field Brake
Blocks
Section 2.3.1.6
Worker
Central
Tendency
(8-hr)
7.0 E-4
7.0 E-5
2.8 E-5

ONU
Central
Tendency
(8-hr)
4.6 E-4
N/A
N/A

Aftennarket Auto
Brakes
Section 2.3.1.7
Worker
Central
Tendency
(8-hr)
1.4 E-4
1.4 E-5
5.6 E-6

High-end
(8-hr)
2.2 E-3
2.2 E-4
8.8 E-5

Central (w/
short-term)
1.4 E-4
1.4 E-5e
5.6 E-6f

High (w /
short-term)
3.3 E-3
3.3 E-4e
1.3 E-4f

ONU
Central (8-
hr)
1.6 E-5
N/A
N/A

High (8-hr)
2.6 E-4
N/A
N/A

Central (w/
short-term)
1.6 E-5
N/A
N/A

High (w /
short-term)
2.6 E-4
N/A
N/A
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Life Cycle
Stage/Category
Subcategory
Occupational
Exposure
Scenario
Popula-
tion
Exposure
Duration
and Level
Cancer Risk
Estimates
(before
applying
PPE)
Cancer
Risk
Estimates
(with
APF=10C)
Cancer Risk
Estimates
(with
APF=25C)

Other Vehicle
Friction Products
2.3.1.8
Worker
Central
Tendency
(8-hr)
1.4 E-4
1.4 E-5
5.6 E-6
High-end
(8-hr)
2.2 E-3
2.2 E-4
8.8 E-5
Central (w/
short-term)
1.4 E-4
1.4 E-5e
5.6 E-6f
High (w /
short-term)
3.3 E-3
3.3 E-4e
1.3 E-4f
ONU
Central (8-
hr)
1.6 E-5
N/A
N/A
High (8-hr)
2.6 E-4
N/A
N/A
Central (w/
short-term)
1.6 E-5
N/A
N/A
High (w /
short-term)
2.6 E-4
N/A
N/A
Other Gaskets -
Utility Vehicles
Section 2.3.1.9
Worker
Central
Tendency
(8-hr)
5.6 E-4
5.6 E-5
2.2 E-5
High-end
(8-hr)
1.5 E-3
1.5 E-4
6.0 E-5
ONU
Central (8-
hr)
1.2 E-4
N/A
N/A
High (8-hr)
3.5 E-4
N/A
N/A
7427 N/A: Not Assessed; ONUs are not assumed to wear respirators
7428 aNo APF applied for 7.5 hours, APF of 25 applied for 30 minutes.
7429 bAPF 25 applied for both 30 mins and 7.5 hours
7430 0 As shown in Table 4-3, EPA has information suggesting use of respirators for two COUs (chlor-alkali: APF of 10 or 25; and
7431 sheet gasket use: APF of 10 only). Application of all other APFs is hypothetical.
7432 d APF 25 for 30 minutes, APF 10 for 7.5 hours
7433 e APF 10 for 30 minutes, APF 10 for 7.5 hours
7434 f APF 25 for 30 minutes, APF 25 for 7.5 hours
7435
7436 4.5.3 Human Health Risk Conclusions to Consumers
7437 Table 4-56 provides a summary of risk estimates for consumers and bystanders. Cancer risks were
7438 exceeded for all consumer and bystander UTV gasket replacement exposure scenarios. For consumer
7439 and bystander brake replacement scenarios conducted indoors, cancer risk estimates were exceeded for
7440 both central tendency and high-end exposures. For outdoor scenarios, cancer risks were exceeded
7441 for high-end exposures for 5 minutes/day scenario for DIYers. In addition, cancer risks were exceeded
7442 for both DIYers and bystanders for the 30 minutes/day scenario.
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7443
7444 Table 4-56. Summary of Risk Estimates for Inhalation Exposures to Consumers and Bystanders
by COU
Cancer benchmark is 10~6)
Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure
Duration and
Level
Cancer Risk
Estimates
Imported asbestos
products
Brakes
Repair/replacement
Indoor, compressed air,
once every 3 years for 62
years starting at 16 years,
exposures at 30% of active
used between uses, 1 hour/d
in garage
Section 4.2.3.1
DIY
Central Tendency
4.3 E-5
High-end
4.2 E-4
Bystander
Central Tendency
2.6 E-5
High-end
6.0 E-5
Brakes Repair/ replacement
Indoor, compressed air,
once every 3 years for 62
years starting at 16 years,
exposures at 30% of active
used between uses, 8
hours/d in garage
Section 4.2.3.1
DIY
Central Tendency
3.4 E-4
High-end
3.4 E-3
Bystander
Central Tendency
2.6 E-5
High-end
6.0 E-5
Brakes Repair/ replacement
Outdoor, once every 3
years for 62 years starting
at 16 years, exposures at
2% of active used between
uses, 5 min/d in driveway
Section 4.2.3.1
DIY
Central Tendency
9.9 E-8
High-end
5.3 E-7
Bystander
Central Tendency
2.1 E-8
High-end
1.1 E-7
Brakes Repair/ replacement
Outdoor, once every 3
years for 62 years starting
at 16 years, exposures at
2% of active used between
uses, 30 min/d in driveway
Section 4.2.3.1.
DIY
Central Tendency
2.9 E-7
High-end
1.5 E-6
Bystander
Central Tendency
5.9 E-8
High-end
3.2 E-7
Brakes
Repair/replacement
Indoor, compressed air,
once at 16 years, staying in
residence for 10 years, 1
hour/d in garage
Section 4.2.3.1
DIY
Bystander
Central Tendency
5.6 E-6
High End
5.5 E-5
Bystander
Central Tendency
3.2 E-6
High-end
7.3 E-6
Imported Asbestos
Products
Gaskets Repair/
replacement in UTVs
Indoor, 1 hour/d, once
every 3 years for 62/20
years starting at 16 years
exposures at 30% of active
used between uses, 1 hour/d
in garage
Section 4.3.2.2
DIY
Central Tendency
2.3 E-5
High-end
6.4 E-5
Bystander
Central
Tendency
2.4 E-5
High-end
6.1 E-5
Gaskets Repair/
replacement in UTVs
Section 4.3.2.2
DIY
Central Tendency
1.8 E-4
High-end
5.1 E-4
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Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure
Duration and
Level
Cancer Risk
Estimates

Indoor, 1 hour/d, once
every 3 years for 62 years
starting at 16 years
exposures at 30% of active
used between uses, 8 hour/d
in garage

Bystander
Central Tendency
2.4 E-5
High-end
6.1 E-5
Gasket Repair
Repair/replacement
Indoor, once at 16 years,
staying in residence for 10
years, 1 hour/d in garage
Section 4.2.3.2
DIY
Central Tendency
3.0 E-6
High end
8.3 E-6
Bystander
Central Tendency
3.08 E-6
High-end
7.16 E-6
7446
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7451
7452
7453
7454
7455
7456
7457
7458
7459
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7463
7464
7465
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7467
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7472
7473
7474
7475
7476
7477
7478
7479
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7481
7482
7483
7484
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7487
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5 Risk Determination
5.1 Unreasonable Risk
5.1.1 Overview
In each risk evaluation under TSCA § 6(b), EPA determines whether a chemical substance presents an
unreasonable risk of injury to health or the environment, under the conditions of use. The determination
does not consider costs or other non-risk factors. In making this determination, EPA considers relevant
risk-related factors, including, but not limited to: the effects of the chemical substance on health and
human exposure to such substance under the conditions of use (including cancer and non-cancer risks);
the effects of the chemical substance on the environment and environmental exposure under the
conditions of use; the population exposed (including any potentially exposed or susceptible
subpopulations); the severity of hazard (including the nature of the hazard, the irreversibility of the
hazard); and uncertainties. EPA takes into consideration the Agency's confidence in the data used in the
risk estimate. This includes an evaluation of the strengths, limitations and uncertainties associated with
the information used to inform the risk estimate and the risk characterization. This approach is in
keeping with the Agency's final rule, Procedures for Chemical Risk Evaluation Under the Amended
Toxic Substances Control Act (82 FR 33726).
Under TSCA, conditions of use are defined as the circumstances, as determined by the Administrator,
under which the substance is intended, known, or reasonably foreseen to be manufactured, processed,
distributed in commerce, used, or disposed of (TSCA §3(4)).
An unreasonable risk may be indicated when health risks under the conditions of use are identified by
comparing the estimated risks with the risk benchmarks and where the risks affect the general
population or certain potentially exposed or susceptible subpopulations (PESS), such as consumers. For
other PESS, such as workers, an unreasonable risk may be indicated when risks are not adequately
addressed through expected use of workplace practices and exposure controls, including engineering
controls or use of personal protective equipment (PPE). The risk evaluation for asbestos evaluated the
cancer risk to workers and occupational non-users and consumers and bystanders from inhalation
exposures only, and in this risk determination of asbestos, respirator PPE (where present) and its effect
on mitigating inhalation exposure was considered.
EPA uses the term "indicates unreasonable risk" to show EPA concern that the chemical substance may
have the potential to present unreasonable risk, recognizing that other factors may be considered in
making a determination of presents/does not present unreasonable risk. EPA only assessed cancer
endpoints in the asbestos risk evaluation. For cancer endpoints, EPA uses the term "greater than risk
benchmark" as one indication for the potential of a chemical substance to present unreasonable risk; this
occurs, for example, if the lifetime cancer risk value is 5xl0"2, which is greater than the benchmarks of
lxlO"4 to lxlO"6. Conversely, EPA uses the term "does not indicate unreasonable risk" when EPA does
not have a concern for the potential of the chemical substance to present unreasonable risk. More details
are described below.
The degree of uncertainty surrounding cancer risk is a factor in determining whether or not unreasonable
risk is present. Where uncertainty is low and EPA has high confidence in the hazard and exposure
characterizations (for example, the basis for the characterizations is measured or monitoring data or a
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7495
7496
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7498
7499
7500
7501
7502
7503
7504
7505
7506
7507
7508
7509
7510
7511
7512
7513
7514
7515
7516
7517
7518
7519
7520
7521
7522
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robust model and the hazards identified for risk estimation are relevant for conditions of use), the
Agency has a higher degree of confidence in its risk determination. EPA may also consider other risk
factors, such as severity of endpoint, reversibility of effect, or exposure-related considerations such as
magnitude or number of exposures, in determining that the risks are unreasonable under the conditions
of use. Where EPA has made assumptions in the scientific evaluation and whether or not those
assumptions are protective, will also be a consideration. Additionally, EPA considers the central
tendency and high-end scenarios when determining unreasonable risk. High-end risk estimates (e.g.,
95th percentile) are generally intended to cover individuals or subpopulations with greater exposure, and
central tendency risk estimates are generally estimates of average or typical exposure.
Conversely, EPA may make a no unreasonable risk determination for conditions of use where the
substance's hazard and exposure potential, or where the risk-related factors described previously, lead
EPA to determine that the risks are not unreasonable.
5.1.2 Risks to Human Health
EPA estimates cancer risks by estimating the incremental increase in probability of an individual in an
exposed population developing cancer over a lifetime (excess lifetime cancer risk (ELCR)) following
exposure to the chemical under specified use scenarios. However, for asbestos, EPA used a less than
lifetime exposure calculation because the time of first exposure impacts the cancer outcome (see Section
4.2.1). Standard cancer benchmarks used by EPA and other regulatory agencies are an increased cancer
risk above benchmarks ranging from 1 in 1,000,000 to 1 in 10,000 (i.e., lxlO"6 to lxlO"4 or also denoted
as 1 E-6 to 1 E-4) depending on the subpopulation exposed. Generally, EPA considers benchmarks
ranging from lxlO"6 to lxlO"4 as appropriate for the general population, consumer users, and non-
occupational PES S.28
For the purposes of this risk determination, EPA uses lxlO"6 as the benchmark for consumers (e.g., do-
it-yourself mechanics) and bystanders. In addition, consistent with the 2017 NIOSH guidance,29 EPA
uses lxlO"4 as the benchmark for individuals in industrial and commercial work environments subject to
Occupational Safety and Health Act (OSHA) requirements. It is important to note that lxlO"4 is not a
bright line, and EPA has discretion to make risk determinations based on other benchmarks and
considerations as appropriate. It is also important to note that exposure-related considerations (e.g.,
duration, magnitude, population exposed) can affect EPA's estimates of the ELCR.
5,1.2.1 Determining Cancer Risks
General population: In this risk evaluation for asbestos, EPA did not evaluate hazards or exposures to
the general population. Further, as part of the problem formulation for asbestos, EPA identified exposure
28 As an example, when EPA's Office of Water in 2017 updated the Human Health Benchmarks for Pesticides, the
benchmark for a "theoretical upper-bound excess lifetime cancer risk" from pesticides in drinking water was identified as 1 in
1,000,000 to 1 in 10,000 over a lifetime of exposure (EPA. Human Health Benchmarks for Pesticides: Updated 2017
Technical Document. January 2017. https://www.epa.gov/sites/production/files/2015~10/documents/hh~benchmarks~
techdoc.pdf). Similarly, EPA's approach under the Clean Air Act to evaluate residual risk and to develop standards is a two-
step approach that includes a "presumptive limit on maximum individual lifetime [cancer] risk (MIR) of approximately 1 in
10 thousand" and consideration of whether emissions standards provide an ample margin of safety to protect public health "in
consideration of all health information, including the number of persons at risk levels higher than approximately 1 in 1
million, as well as other relevant factors" (54 FR 38044, 38045, September 14, 1989).
29 NIOSH (20.1.6). Current intelligence bulletin 68: NIOSH chemical carcinogen policy, available at
https://www.cdc.gOv/niosh/docs/2017-100/pdf/2017-100.pdf.
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7529
7530
7531
7532
7533
7534
7535
7536
7537
7538
7539
7540
7541
7542
7543
7544
7545
7546
7547
7548
7549
7550
7551
7552
7553
7554
7555
7556
7557
7558
7559
7560
7561
7562
7563
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pathways under other environmental statutes, administered by EPA, which adequately assess and
effectively manage exposures and for which long-standing regulatory and analytical processes exist, i.e.,
the Clean Air Act (CAA), the Safe Drinking Water Act (SDWA), the Clean Water Act (CWA) and the
Resource Conservation and Recovery Act (RCRA). The Office of Chemical Safety and Pollution
Prevention works closely with the offices within EPA that administer and implement the regulatory
programs under these statutes. EPA believes that the TSCA risk evaluation should focus on those
exposure pathways associated with TSCA uses that are not subject to the regulatory regimes discussed
above because these pathways are likely to represent the greatest areas of concern to EPA. Because
stationary source releases of asbestos to ambient air are adequately assessed and any risks are effectively
managed when under the jurisdiction of the CAA, EPA did not evaluate emission pathways to ambient
air from commercial and industrial stationary sources or associated inhalation exposure of the general
population or terrestrial species in this TSCA evaluation. Based on the reasonably available information
in the published literature, provided by industries using asbestos, and reported in EPA databases, there is
no evidence of releases of asbestos to water associated with the conditions of use that EPA evaluated. As
such, EPA did not evaluate in the risk evaluation the surface water pathway for general population
exposures during or after land application of biosolids. Therefore, EPA did not evaluate hazards or
exposures to the general population in the risk evaluation, and there is no risk determination for the
general population.
5.1.3 Determining Environmental Risk
As explained in this risk evaluation, after PF, EPA did not evaluate ecological receptors. EPA believes
there is low or no potential for environmental risk to aquatic receptors (including sediment-dwelling
organisms) from the COUs included in this risk evaluation because water releases associated with the
COUs are not expected and were not identified. The available information indicated that there were
surface water releases of asbestos; however, not all releases are subject to reporting (e.g., effluent
guidelines) or are applicable (e.g., friability). Based on the reasonably available information in the
published literature, provided by industries using asbestos, and reported in EPA databases, there is
minimal or no releases of asbestos to surface water and sediments associated with the COUs in this risk
evaluation. Therefore, EPA concludes there is no risk to aquatic or sediment-dwelling organisms.
Further, as described in the PF and above for the general population, other Agency regulations
adequately assess and effectively manage exposures to terrestrial organisms from asbestos releases to
terrestrial, including biosolids, pathways. Although EPA assessed the hazards to aquatic and sediment-
dwelling organisms in the risk evaluation, since no exposures exist under the COUs, EPA determined
there is no unreasonable risk for the environment.
5.2 Risk Determination for Chrysotile Asbestos
EPA's determination of unreasonable risk for the conditions of use of chrysotile asbestos is based on
health risks to workers, occupational non-users (exposed to asbestos indirectly by being in the same
work area), consumers, and bystanders (exposed indirectly by being in the same vicinity where
consumer uses are carried out).
As described in sections 4, significant risk were identified for lung cancer and mesothelioma. Section 26
of TSCA requires that EPA make decisions consistent with the "best available science." Section 26 also
requires other scientific considerations including consideration of the "extent of independent
verification" and "weight of the scientific evidence." As described in EPA's framework rule for risk
evaluation [82 FR 33726] weight of the scientific evidence includes consideration of the "strengths,
limitations and relevance of the information." Neither the statute nor the framework rule requires that
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7574
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7600
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7602
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EPA choose the lowest number and EPA believes that public health is best served when EPA relies upon
the highest quality information for which EPA has the greatest confidence.
During risk evaluation, the only fiber type of asbestos that EPA identified as manufactured (including
imported), processed, or distributed under the conditions of use is chrysotile, the serpentine variety.
Chrysotile is the prevailing form of asbestos currently mined worldwide. Therefore, it is reasonable to
assume that commercially available products fabricated overseas are made with chrysotile. Any asbestos
being imported into the U.S. in articles for the conditions of use EPA has identified in this document is
believed to be chrysotile. Based on EPA's determination that chrysotile is the only form of asbestos
imported into the U.S. as both raw form and as contained in articles, EPA performed a quantitative
assessment for chrysotile asbestos. The other five forms of asbestos are no longer manufactured,
imported, or processed in the United States and are now subject to a significant new use rule (SNUR)
that requires notification (via a Significant New Use Notice (SNUN)) of and review by the Agency
should any person wish to pursue manufacturing, importing, or processing crocidolite (riebeckite),
amosite (cummingtonite-grunerite), anthophyllite, tremolite or actinolite (either in raw form or as part of
articles) for any use (40 CFR 721.11095). Under the final asbestos SNUR, EPA will be made aware of
manufacturing, importing, or processing for any intended use of the other forms of asbestos. If EPA
finds upon review of a SNUN that the significant new use presents or may present an unreasonable risk
(or if there is insufficient information to permit a reasoned evaluation of the health and environmental
effects of the significant new use), then EPA would take action under TSCA section 5(e) or (f) to the
extent necessary to protect against unreasonable risk. In this draft risk evaluation, EPA evaluated the
following categories of conditions of use of chrysotile asbestos: manufacturing; processing; distribution
in commerce; occupational and consumer uses; and disposal. EPA will consider any legacy uses and
associated disposal for chrysotile asbestos or other asbestos fiber types in subsequent supplemental
documents.
As explained in the problem formulation document and Section 1.4 of this risk evaluation, EPA did not
evaluate the following: emission pathways to ambient air from commercial and industrial stationary
sources or associated inhalation exposure of the general population or terrestrial species; the drinking
water exposure pathway for asbestos; the human health exposure pathway for asbestos in ambient water;
emissions to ambient air from municipal and industrial waste incineration and energy recovery units; on-
site releases to land that go to underground injection; or on-site releases to land that go to asbestos
National Emission Standards for Hazardous Air Pollutants (NESHAP) (40 CFR part 61, subpart M)
compliant landfills or exposures of the general population (including susceptible populations) or
terrestrial species from such releases.
The risk evaluation for chrysotile asbestos describes the physical-chemical characteristics that are
unique to chrysotile asbestos, such as insolubility in water, suspension and duration in air,
transportability, the friable nature of asbestos-containing products, which attribute to the potential for
asbestos fibers to be released, settled, and to again become airborne under the conditions of use (re-
entrainment30). Also unique to asbestos is the impact of the timing of exposure relative to the cancer
outcome; the most relevant exposures for understanding cancer risk were those that occurred decades
prior to the onset of cancer and subsequent cancer mortality. In addition to the cancer benchmark, the
physical-chemical properties and exposure considerations are important factors in considering risk of
injury to health. To account for the exposures for occupational non-users and, in certain cases
30 Settled Asbestos Dust Sampling and Analysis 1st Edition Steve M. Hays, James R. Millette CRC Press 1994
Page 216 of 310
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7631
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7634
7635
7636
7637
7638
7639
7640
7641
7642
7643
7644
7645
7646
7647
7648
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7650
7651
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7653
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7659
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bystanders, EPA derived a distribution of exposure values for calculating the risk for cancer by using
area monitoring data (i.e., fixed location air monitoring results) where available for certain conditions of
use and when appropriate applied exposure reduction factors when monitoring data was not available,
using data from published literature.
The risk determination for each COU in this risk evaluation considers both central tendency and high-
end risk estimates for workers, ONUs, consumers and bystanders. Where relevant EPA considered PPE
for workers. For many of the COUs both the central tendency and high-end risk estimates exceed the
risk benchmark while some only at the high-end for each of the exposed populations evaluated.
However, the risk benchmarks do not serve as a bright line for making risk determinations and other
relevant risk-related factors and EPA's confidence in the underlying data were considered. In particular,
risks associated with previous asbestos exposures are compounded when airborne asbestos fibers settle
out and again become airborne where they can cause additional exposures and additional risks. The
Agency also considered that the health effects associated with asbestos inhalation exposures are severe
and irreversible. These risk-related factors resulted in EPA focusing on the high-end risk estimates
rather than central tendency risk estimates to be most protective of workers, ONUs, consumers, and
bystanders. Additionally, as discussed in Section 4.5.3, for workers and ONUs exposed in a workplace,
EPA considered extra risks of 1 cancer per 10,000 people. At this risk level (1E-4), if the non-cancer
effects (e.g., asbestosis and pleural thickening) of chrysotile are similar to Libby amphibole asbestos, the
non-cancer effects of chrysotile are likely to contribute additional risk to the overall health risk of
asbestos beyond the risk of cancer. Thus, the overall health risks of asbestos are underestimated based
on cancer alone and support the Agency's focus on using the high-end risk estimates rather than central
tendency risk to be protective of workers and ONUs.
The limited conditions of use of asbestos in conjunction with the extensive regulations safeguarding
against exposures to asbestos helped to focus the scope of the risk evaluation on occupational and
consumer scenarios where chrysotile asbestos in certain uses and products is known, intended, or
reasonably foreseen. EPA did not quantitatively assess each life cycle stage and related exposure
pathways as part of this risk evaluation. Existing EPA regulations and standards adequately assess and
effectively manage exposure pathways to the general population, terrestrial species and chlor-alkali
industry occupational populations (i.e., workers and ONUs) for the asbestos waste pathway (e.g., RCRA
and the asbestos NESHAP. As such, the Agency did not evaluate these pathways.
The risk determinations are organized by conditions of use and displayed in a table format. Presented
first are those life cycle stages where EPA assumes the absence of asbestos exposure, and the conditions
of use that do not present an unreasonable risk are summarized in a table. EPA then presents the
preliminary risk determination for the chrysotile asbestos-containing brakes conditions of use for the
NASA "Super Guppy." Those conditions were determined not to present an unreasonable risk. The risk
determinations for the conditions of use that present an unreasonable risk are depicted in section
5.2.1 (Occupational Processing and Use of Chrysotile Asbestos) and section 5.2.2 (Consumer Uses of
Chrysotile Asbestos). For each of the conditions of use assessed under the asbestos risk evaluation, a
risk determination table is presented based on relevant criteria pertaining to each exposed population
(i.e., health only for either workers, occupational non-users, consumers, or bystanders as indicated in
table headings) is provided and explained below.
Import, Distribution in Commerce and Disposal of Chrysotile Asbestos
EPA assumed the absence of exposure to asbestos at certain life cycle stages. Raw asbestos and
asbestos-containing products are imported into the U.S. in a manner where exposure to asbestos is not
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
anticipated to occur. According to information reasonably available to EPA, raw asbestos is imported in
bags wrapped in plastic where they are contained in securely locked shipping containers. These shipping
containers remain locked until they reach the chlor-alkali plants (Enclosure B: Asbestos Controls in the
Chlor-Alkali Manufacturing Process httos:/Amw.remk$tiom.gov/dbcwnent?D=EPA-HO-OPPT-2Q16-
0736-0052). Asbestos articles (or asbestos-containing products) are assumed to be imported and
distributed in commerce in a non-friable state, enclosed in sealed boxes, where fibers are not expected to
be released.
EPA also assumes the absence of asbestos exposure during the occupational disposal of asbestos sheet
gaskets scraps during gasket stamping and the disposal of spent asbestos gaskets used in chemical
manufacturing plants. This assumption is based on the work practices followed and discussed in section
2.3.1 that prevent the release of asbestos fibers.
Considering these exposure assumptions, EPA finds no unreasonable risk to health or the environment
for the life cycle stages of import and distribution in commerce of asbestos for all the conditions of use.
EPA also finds no unreasonable risk to health or the environment for occupational populations for the
disposal of asbestos sheet gaskets scraps during gasket stamping and the disposal of spent asbestos
gaskets used in chemical manufacturing plants.
In addition, there is a limited use of asbestos-containing brakes (categorized under other vehicle friction
products) for a special, large NASA transport plane (the "Super-Guppy") that EPA recently learned
about. In this public draft risk evaluation, EPA is providing preliminary information for public input and
the information is provided in a brief format (see sections 2.3.1.8.2 and 4.2.2.6).
EPA calculated risk estimates using occupational exposure monitoring data provided by NASA. EPA
assumes 12 hours of brake changes occur every year starting at age 26 years with 20 years exposure.
The Excess Lifetime Cancer Risk for Super Guppy Brake/Repair Replacement for Workers is:
Full Shift (8-hour): Central Tendency - 1.9 E-7
Full Shift (8-hour): High-End - 5.8 E-7
Short Term: Central Tendency - 3.2 E-7
Short Term: High-End -9.1 E-7
Because the risk estimates fall below the benchmark for both the central tendency and high-end and after
considering the engineering controls and work practices in place discussed in section 2.3.1.8.2, EPA
finds these COUs (import/manufacture, distribution, use and disposal) do not present an unreasonable
risk of injury to health.
Conditions of I so llisil Do Not Present ;in Inrensonnhle Kisk to 11e:i11 h or KnvironnienI
• Import of asbestos and asbestos-containing products
• Distribution of asbestos-containing products
• Use of asbestos-containing brakes for a specialized, large NASA transport plane.
• Disposal of asbestos-containing sheet gaskets processed and/or used in the industrial setting and
asbestos-containing brakes for a specialized, large NASA transport plane Distribution of
asbestos-containing products
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
5.2.1 Occupational Processing and Use of Chrysotile Asbestos
EPA identified the following conditions of use where asbestos is processed and/or used in occupational
settings: asbestos diaphragms in chlor-alkali industry, processed asbestos-containing sheet gaskets,
asbestos-containing sheet gaskets in chemical production, asbestos-containing brake blocks in the oil
industry, aftermarket automotive asbestos-containing brakes/ linings and other vehicle friction products
and other asbestos-containing gaskets. OSHA's Respiratory Protection Standard (29 CFR § 1910.134)
requires employers in certain industries to address workplace hazards by implementing engineering
control measures and, if these are not feasible, provide respirators that are applicable and suitable for the
purpose intended. Assigned protection factors (APFs) are provided in Table 1 under §
1910.134(d)(3)(i)(A) (see Table 2-3 of the risk evaluation) and refer to the level of respiratory protection
that a respirator or class of respirators is expected to provide to employees when the employer
implements a continuing, effective respiratory protection program. Where applicable, in the following
tables, EPA provides risk estimates with PPE using APFs derived from information provided by
industry. However, there is some uncertainty in taking this approach as based on published evidence for
asbestos (see Section 2.3.1.2), nominal APF may not be achieved for all respirator users.
Occupational non-users (ONUs) are not expected to wear PPE since they do not directly handle the
chemical substance or articles thereof. Additionally, because ONUs are expected to be physically farther
away from the chemical substance than the workers who handle it, EPA calculated an exposure
reduction factor for ONUs based on the monitoring data (i.e., fixed location air monitoring results)
provided by industry and the information available in the published literature (refer to section 2.3.1.3 of
the risk evaluation).
As explained in section 5.2, EPA considers the high-end risk estimates for workers, occupational non-
users, consumers, and bystanders for this risk determination of asbestos.
Table 5-1. Risk Determination for Chrysotile Asbestos: Processing and Industrial Use of Asbestos
Diaphragms in Chlor-alkali Industry (refer to section 4.2.2.1 for the risk characterization)
Criteria lor Risk
Determination

Workers
Occupational Non-l sers
Life cycle
Stage
Processing and Industrial Use
Processing and Industrial Use
TSCA Section
6(b)(4)(A)
Unreasonable Risk
Determination
Presents an unreasonable risk of injury to health
(workers and occupational non-users).
Unreasonable Risk
Driver
Cancer resulting from chronic
inhalation exposure
Cancer resulting from chronic inhalation
exposure
Benchmark (Cancer)
10"4 excess cancer risks
10"4 excess cancer risks
Risk Estimates
without PPE
8 hour TWA
1.2 E-4 Central Tendency
8.4 E-4 High-end
Short Term
1.5 E-4 Central Tendency
1.1 E-4 Central Tendencya
8 hour TWA
5.8 E-5 Central Tendency
1.9 E-4 High-end
Short Term
Not available
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Criteriii lor Risk
Delerminiilion

Workers
Omi|):ilion:il Non-l sers

1.3 E-3 High-end
8.1 E-4 High-enda

Risk Estimates with
PPE
APF=10
8 hour TWA
1.2 E-5 Central Tendency
8.4 E-5 High-end
Short Term
1.3 E-5 Central Tendency
9.9 E-5 High-end
APF=25
8 hour TWA
4.8 E-6 Central Tendency
3.4 E-5 High-end
Short Term
6.0 E-6 Central Tendency
5.2 E-5 High-end
Not Assessed; ONUs are not assumed to
wear respirators
Risk Considerations
EPA calculated risk estimates using
occupational exposure monitoring data
provided by industry (Section 2.3.1.3).
Without respiratory PPE the risk
estimates indicate risk (central tendency
and high-end); however, when expected
use of respiratory PPE is considered for
some worker tasks (APF=10 and
APF=25), the risk estimates do not
indicate unreasonable risk (central
tendency and high-end). As depicted in
Table 2-7 and documented by industry13,
of the eight asbestos-related worker
tasks, workers wear respiratory PPE
during three tasks (Asbestos
Unloading/Transport, Glovebox
Weighing and Asbestos Handling, and
Hydroblasting), but do not wear
respiratory PPE during five of the tasks
(Asbestos Slurry, Depositing, Cell
Assembly, Cell Disassembly, and Filter
Press). Although the use of respiratory
PPE during three of the worker tasks
reduces asbestos exposure and overall
risk to workers, respiratory PPE is not
worn throughout an entire 8-hour shift.
The industry data depicted in Table 2-7
indicates workers without respiratory
PPE are exposed to asbestos fibers
EPA calculated risk estimates using area
monitoring data (i.e., fixed location air
monitoring results) provided by industry
(Section 2.3.1.3), which supports EPA's
expectation that ONU inhalation exposures
are lower than inhalation exposures for
workers directly handling asbestos
materials (Table 2-8). There is some
uncertainty in the ONU exposure estimate
because much of the reported area
monitoring data were reported as "less
than" values, which may represent non-
detects. One facility did not clearly
distinguish whether measurements were
area samples or personal breathing zone
samples. EPA considered both the high-end
and central tendency risk estimates in its
determination, and although the high-end
exceeds the cancer risk benchmark of 1x10"
4, both risk estimates are fairly similar.
Based on the benchmarks exceedances and
considering the physical-chemical
properties of asbestos, including the
potential for asbestos fibers to be released,
settled, and to again become airborne
during worker activities, the expected
absence of respiratory PPE, and the severe
and irreversible health effects associated
with asbestos inhalation exposures, these
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Criteria lor Risk
Determination

Workers
Occupational Non-l sers

where the maximum short-term PBZ
samples for three tasks (cell assembly,
cell disassembly and filter press) are in
the range of some tasks, and higher than
one task (Asbestos
unloading/Transport), where respiratory
PPE is used. Considering that
respiratory PPE is not worn for all
worker tasks where occupational
exposure monitoring data indicates the
presence of airborne asbestos fibers, the
potential for released asbestos fibers to
settle and to again become airborne
during worker activities, and
considering the severe and the
irreversible effects associated with
asbestos inhalation exposures, these
conditions of use (for processing and
use) present unreasonable risk to
workers.
conditions of use (for processing and use)
present unreasonable risk to ONUs.
7736 aNo APF applied for 7.5 hours, APF of 25 applied for 30 minutes.
7737 industry provided descriptions of the PPE used in Enclosure C: Overview of Monitoring Data and PPE Requirements
7738 fattps://www. regulations. gov/doeument?D=EPA~HQ~OPPT~2016~0736~00S2
7739
7740
7741 Table 5-2. Risk Determination for Chrysotile Asbestos: Processing Asbestos-Containing Sheet
7742 Gaskets (refer to section 4.2.2.2 for the risk characterization)
(lit or in for Kisk
Determination

Workers
Occupational Non-l sers
Life cycle
Stage
Processing
Processing
TSCA Section
6(b)(4)(A)
Unreasonable Risk
Determination
Presents an unreasonable risk of injury to health
(workers and occupational non-users)
Unreasonable Risk
Driver
Cancer resulting from chronic
inhalation exposure
Cancer resulting from chronic inhalation
exposure
Benchmark (Cancer)
10"4 excess cancer risks
10"4 excess cancer risks
Risk Estimates
without PPE
8-hour TWA
3.3 E-4 Central Tendency
1.4 E-3 High-end
Short Term
3.5 E-4 Central Tendency
8-hour TWA
5.6 E-5 Central Tendency
2.3 E-4 High-end
Short Term
5.6 E-5 Central Tendency
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Crherisi lor Kisk
Detenu million

Workers
OcciipnlioiKil Non-l sers

1.4 E-3 High-end
2.3 E-4 High-end
Risk Estimates with
PPEb
APF = 1
An APF of 1 was assigned to the
respiratory PPE provided to workers
based on industry information b
8-hour TWA
3.3 E-4 Central Tendency
1.4 E-3 High-end
Short Term
3.5 E-4 Central Tendency
1.4 E-3 High-end
Not Assessed; ONUs are not assumed to
wear respirators
Risk Considerations
EPA calculated risk estimates using
occupational exposure monitoring data
provided by industry and in the
published literature (Section 2.3.1.4).
The use of N95 respirators was
reported by industrya to be worn by a
worker cutting gaskets. However, the
OSHA Asbestos Standard 1910.1001
states that such respirators should not
be used to mitigate asbestos exposure.
Thus, the N95 respirator has an
assigned APF=1 due to ineffectiveness
as respiratory PPE for mitigating
asbestos exposure. Absent effective
respiratory PPEb risk estimates for
both central tendency and high-end
exceeds the benchmark of lxlO"4.
Based on the benchmarks exceedances
and considering the physical-chemical
properties of asbestos, including the
potential for asbestos fibers to be
released, settled, and to again become
airborne during worker activities, and
the severe and irreversible health
effects associated with asbestos
inhalation exposures, this condition of
use presents unreasonable risk to
workers.
EPA calculated risk estimates using
monitoring data provided by industry and
in the published literature. ONU
inhalation exposures are expected to be
lower than inhalation exposures for
workers directly handling asbestos
materials and based on exposure
measurements in the published literature
comparing workers to non-workers, EPA
estimated a reduction factor of 5.75 for
ONUs which was applied to the exposure
estimate for workers (Section 2.3.1.3).
Considering the physical-chemical
properties of asbestos including the
potential for asbestos fibers to be
released, settled, and to again become
airborne during worker activities, the
expected absence of respiratory PPE, and
the severe and irreversible health effects
associated with asbestos inhalation
exposures, EPA considered the high-end
risk estimate appropriate for determining
ONU risk. High-end risk estimates
exceed the cancer risk benchmark of
lxlO"4. As such this condition of use
presents unreasonable risk to ONUs.
7743 industry provided description of PPE (ACC. 2017a).
7744 bRisk to workers was calculated using hypothetical respirator PPE of APF=10 and APF=25 in the risk evaluation. However,
7745 the risk estimates based on the hypothetical APF were not used in the risk determination based on industry description of
7746 current respiratory PPE.
7747
7748
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7749 Table 5-3. Risk Determination for Chrysotile Asbestos: Industrial Use of Asbestos-Containing
7750 Sheet Gaskets in Chemical Production
7751 (Titanium Dioxide Example is Representative of this COU; refer to section 4.2.2.3 for the risk
7752 characterization)
Criteria for Risk

Determination
Workers
Occupational Non-l sers
Life cycle
Stage
Industrial Use
Industrial Use
TSCA Section
6(b)(4)(A)
Unreasonable Risk
Determination
Presents an unreasonable risk of injury to health
(workers and occupational non-users)
Unreasonable Risk
Driver
Cancer resulting from chronic
inhalation exposure
Cancer resulting from chronic
inhalation exposure
Benchmark (Cancer)
10"4 excess cancer risks
10"4 excess cancer risks
Risk Estimates
without PPE
8-hour TWA
6.0 E-4 Central Tendency
2.2 E-3 High-end
8-hour TWA
1.2 E-4 Central Tendency
3.7 E-4 High-end

APF=10
Not Assessed; ONUs are not
assumed to wear respirators
Risk Estimates with
current PPEa
8-hour TWA
6.0 E-5 Central Tendency
2.2 E-4 High-end
Risk Considerations
EPA calculated risk estimates using
occupational exposure monitoring
data provided by industry and in the
published literature (Section
2.3.1.5). Based on respiratory PPE
used according to industry21 EPA
also calculated the risk estimates
using an APF of 10; however, even
with PPE and considering the
physical-chemical properties of
asbestos, including the potential for
asbestos fibers to be released,
settled, and to again become
airborne during worker activities
and the severe and irreversible
health effects associated with
asbestos inhalation exposures, high-
end risk estimates for this condition
of use exceed the benchmark of
lxlO"4 and presents unreasonable
risk to workers.
EPA calculated risk estimates using
monitoring data provided by
industry and in the published
literature. Based on exposure
measurements in the published
literature, EPA estimated a
reduction factor of 5.75 for ONUs
(Section 2.3.1.4.). Because asbestos
fibers released during the worker
activities described in Section
2.3.1.5.can settle and again become
airborne where they can be inhaled
by ONUs, EPA considered it
appropriate to use the high-end
estimate when determining ONU
risk. Based on the high-end risk
estimate exceeding the benchmark
of lxlO"4, the expected absence of
respiratory PPE and the severe and
irreversible effects associated with
asbestos inhalation exposures, this
condition of use presents
unreasonable risk to ONUs.
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7753 industry provided description of PPE (ACC. 2017a).
7754
7755
7756
7757 Table 5-4. Risk Determination for Chrysotile Asbestos: Industrial Use and Disposal of Asbestos-
Containing Brake Blocks in Oil Industry (refer to section 4.2.2.4 for the risk characterization
Criteria lor Uisk
Determination

Workers
Occupational Non-l sers
Life cycle
Stage
Industrial Use and Disposal
Industrial Use and Disposal
TSCA Section
6(b)(4)(A)
Unreasonable Risk
Determination
Presents an unreasonable risk of injury to health
(workers and occupational non-users)
Unreasonable Risk
Driver
Cancer resulting from chronic
inhalation exposure
Cancer resulting from chronic
inhalation exposure
Benchmark (Cancer)
10"4 excess cancer risks
10"4 excess cancer risks
Risk Estimates without
PPE
8-hour TWA
7.0 E-4
8 hour-TWA
4.6 E-4
Risk Estimates with
PPE
APF=1
Workers are not assumed to wear
respirators
Not Assessed; ONUs are not
assumed to wear respirators
Risk Considerations
(applies to both
workers and ONUs)
The estimated exposure scenario used in the risk evaluation is based on
one 1988 study of Norway's offshore petroleum industry and relevance
to today's use of oil field brake blocks in the United States is uncertain.
EPA is aware that brake blocks are imported, distributed, and used in the
U.S. although the full extent of use could not be determined. According
to industry21, Drawworks machineries are always used and serviced
outdoors, close to oil wells. Information on processes and worker
activities are insufficient to determine the proximity of ONUs to
workers. ONU inhalation exposures are expected to be lower than
inhalation exposures for workers directly handling asbestos materials.
Although EPA has calculated a single conservative risk estimate for
workers and for ONUs, EPA does not expect routine use of respiratory
PPE. Considering the cancer risk benchmark of 1x10-4 is exceeded and
the severe and irreversible effects associated with asbestos inhalation
exposures, these conditions of use present unreasonable risk for both
workers and ONUs.
7759 a Industry provided data fPopik. 2018)
7760
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7761
7762 Table 5-5. Risk Determination for Chrysotile Asbestos: Commercial Use and Disposal of
7763 Aftermarket Automotive Asbestos-Containing Brakes/Linings and Other Vehicle Friction
7764 Products
7765 (Commercial Mechanic Brake Repair/Replacement is Representative for both COUs; refer to
seci
tion 4.2.2.5 and 4.2.2.6 for the risk characterization)
Criteria lor Kisk
Dclcrminnlion

Workers
Occupational Non-l sers
Life cycle
Stage
Commercial Use
Commercial Use
TSCA Section
6(b)(4)(A)
Unreasonable Risk
Determination
Presents an unreasonable risk of injury to health
(workers and occupational non-users)
Unreasonable Risk
Driver
Cancer resulting from chronic
inhalation exposure
Cancer resulting from chronic
inhalation exposure
Benchmark (Cancer)
10"4 excess cancer risks
10"4 excess cancer risks
Risk Estimates
without PPE
8-hour TWA
1.4 E-4 Central Tendency
2.2 E-3 High-end
Short Term
1.4 E-4 Central Tendency
3.3 E-3 High-end
8-hour TWA
1.6 E-5 Central Tendency
2.6 E-4 High-end
Short Term
1.6 E-5 Central Tendency
2.6 E-4 High-end
Risk Estimates with
PPE
APF = 1
Workers are not assumed to wear
respirators; Respirators only
required by OSHA if PEL
exceeded.
8-hour TWA
1.4 E-4 Central Tendency
2.2 E-3 High-end
Short Term
1.4 E-4 Central Tendency
3.3 E-3 High-end
Not Assessed; ONUs are not
assumed to wear respirators
Risk Considerations
EPA calculated risk estimates based
on data provided in the published
literature and OSHA monitoring
data (Table 2-14). Although OSHA
standards require certain work
practices and engineering controls
to minimize dust, respiratory PPE is
not required unless the permissible
exposure limit (PEL) is exceeded.
With the expected absence of PPE,
the cancer benchmark is exceeded
EPA calculated risk estimates data
provided in the published literature.
ONU inhalation exposures are
expected to be lower than
inhalation exposures for workers.
EPA estimated a reduction factor of
8.4 (Section 2.3.1.7) for ONUs.
Because asbestos fibers released
during the worker activities
described in Section 2.3.1.7.2 can
settle and again become airborne
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Criteria for Kisk
Determination

Workers
Occupational Non-l sers

(for both central tendency and high-
end). Based on the exceedance of
the benchmark of lxlO"4 and
consideration of the severe and
irreversible effects associated with
asbestos inhalation exposures, these
conditions of use present
unreasonable risk to workers.
where they can be inhaled by
ONUs, EPA considered it
appropriate to use the high-end
estimate when determining ONU
risk. Based on the exceedance
(high-end) of the benchmark of
lxlO"4, the expected absence of
respiratory PPE and the potential
severity and irreversible effects
associated with inhalation
exposures to asbestos, these
conditions of use present
unreasonable risk to ONUs.
7767
7768
7769 Table 5-6. Risk Determination for Chrysotile Asbestos: Commercial Use and Disposal of Other
7770 Asbestos-Containing Gaskets
7771 (Commercial Mechanic Gasket Repair/Replacement is Representative for this COU; refer to
7772 section 4.2.2.7 for the risk characterization)
Crilcria for Risk
Determination

Workers
Omipnlionnl Non-l sers
Risk Considerations
EPA calculated risk estimates
using exposure scenarios based on
occupational monitoring data
(breathing zone of workers) for
asbestos-containing gasket
replacement in vehicles. Although,
risk to workers was calculated
using hypothetical respirator PPE
of APF=10 and APF=25, workers
are not expected to wear
respiratory PPE during gasket
repair and replacement in a
commercial setting. Based on the
expected absence of PPE and the
benchmark of lxlO"4 is exceeded
(for both central tendency and
high-end), these conditions of use
present unreasonable risk to
workers.
EPA calculated risk estimates
using exposure scenarios based on
occupational monitoring data
(work area samples in the vicinity
of the workers) for asbestos-
containing gasket replacement in
vehicles. EPA estimated a
reduction factor of 5.75 (Section
2.3.1.9) for ONUs. Due to the
severe and irreversible effects
associated with asbestos
inhalation exposures and that
asbestos fibers released during the
worker activities described in
Section 2.3.1.9 can settle and
again become airborne where they
can be inhaled by ONUs, EPA
considered it appropriate to use
the high-end estimate when
determining ONU risk. Based on
the exceedance of the benchmark
of lxlO"4 (for both central
tendency and high-end), and the
expected absence of respirators,
and the potential severity of effect
associated with inhalation
exposures to asbestos, these
conditions of use present
unreasonable risk to ONUs.
7773
7774
7775 5,2.2 Consumer Uses of Chrysotile Asbestos
7776 The consumer uses of asbestos include aftermarket automotive asbestos-containing brakes/linings, and
7777 other asbestos-containing gaskets. Consumers and bystanders are not assumed to wear respiratory PPE,
7778 therefore, EPA did not assess risk estimates with PPE the conditions of use for these exposed
7779 populations.
7780
7781
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7782 Table 5-7. Risk Determination for Chrysotile Asbestos: Consumer Use and Disposal of
7783 Aftermarket Automotive Asbestos-Containing Brakes/Linings
7784 (Do-it-Yourself Consumer Brake Repair/Replacement is Representative for both COUs; refer to
7785 section 4.2.3.1 for the risk characterization)
Criteria for Kisk
Determination
S
Do-il-'S oursi'lf Mechanic
l>\ slander
Life cycle
Stage
Consumer Use
Consumer Use
TSCA Section
6(b)(4)(A)
Unreasonable Risk
Determination
Presents an unreasonable risk of injury to health
(consumers and bystanders)
Unreasonable Risk
Driver
Cancer resulting from chronic
inhalation exposure
Cancer resulting from chronic inhalation
exposure
Benchmark (Cancer)
10"6 excess cancer risks
10"6 excess cancer risks

Indoor, compressed air
Indoor, compressed air

1 hour/day; once every 3 years for
62 years (starting age 16)
Exposures at 30% of active used
between uses, 1 hour/d in garage
4.3 E-5 Central Tendency
4.2 E-4 High-end
1 hour/day; once every 3 years for 62
years (starting age 16)
Exposures at 30% of active used
between uses, 1 hour/d in garage
2.6 E-5 Central Tendency
6.0 E-5 High-end

Indoor, compressed air
Indoor, compressed air
Risk Estimates
without PPE
8 hour/day; once every 3 years for
62 years (starting age 16)
Exposures at 30% of active used
between uses, 8 hours/d in garage
3.4 E-4 Central Tendency
3.4 E-3 High-end
1 hour/day; once every 3 years for 62
years (starting age 16)
Exposures at 30% of active used
between uses, 8 hours/d in garage
2.6 E-5 Central Tendency
6.0 E-5 High-end
Indoor, compressed air
Indoor, compressed air

Indoor, compressed air, once at 16
years, staying in residence for 10
years, 1 hour/d in garage
5.6 E-6 Central Tendency
5.5 E-5 High-end
Indoor, compressed air, once at 16
years, staying in residence for 10
years, 1 hour/d in garage
3.0 E-6 Central Tendency
7.1 E-6 High-end

Outdoor
Once every 3 years for 62 years
(starting age 16)
Exposures at 2% of active used
between uses, 5 min/d in driveway
9.9 E-8 Central Tendency
5.3 E-7 High-end
Outdoor
Once every 3 years for 62 years
(starting age 16)
Exposures at 2% of active used between
uses, 5 min/d in driveway
2.1 E-8 Central Tendency
1.1 E-7 High-end
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Criteria lor Kisk
Delerm in ill ion
l)o-il-Yoursclf Mechanic
IJ> slander
Outdoor
Once every 3 years for 62 years
(starting age 16)
Exposures at 2% of active used
between uses, 30 min/d in driveway
2.9 E-7 Central Tendency
1.5 E-6 High-end
Outdoor
Once every 3 years for 62 years
(starting age 16)
Exposures at 2% of active used between
uses, 30 min/d in driveway
5.9 E-8 Central Tendency
3.2. E-7 High-end
Risk Estimates with
PPE
Not Assessed; Consumers are not
assumed to wear respiratory PPE
Not Assessed; Bystanders are not
assumed to wear respiratory PPE
Risk Considerations
EPA calculated risk estimates are
based on data provided in the
published literature and surrogate
monitoring data from occupational
brake repair studies. EPA considered
4 different exposure scenarios with
different assumptions on the duration
of exposure, whether indoors in a
garage using compressed air or
outside without compressed air.
Although DIY brake and clutch work
is more likely to occur outdoors, it
may also occur inside a garage.
Additionally, considering that many
DIY mechanics have access to air
compressors, EPA expects that at
least some DIY mechanics may use
compressed air to clean dust from
brakes or clutches and can spend up
to a full day (8 hours) in their garage
and working three hours specifically
on brakes and clutches. Because
asbestos fibers released during the
DIY (consumer) activities described
in Section 2.3.2.1 can settle and again
become airborne where they can be
inhaled by bystanders, EPA
considered it appropriate to use the
high-end estimate when determining
consumer risk. EPA chose a
conservative and protective brake and
clutch repair/replacement exposure
scenario of 3 hours/day once every 3
years inside a garage using
compressed air to account for the
possibility that some DIY mechanics
EPA calculated risk estimates are based
on data provided in the published
literature and surrogate monitoring data
from occupational brake repair studies.
No reduction factor was applied for
indoor DIY brake work inside
residential garages due to the expected
close proximity of bystanders inside a
garage. In the absence of data to
estimate a reduction factor for outdoor
brake work, EPA assumed a reduction
factor of 10 (Section 2.3.2.1). Because
asbestos fibers released during the DIY
(consumer) activities described in
Section 2.3.2.1 can settle and again
become airborne where they can be
inhaled by bystanders, EPA considered
it appropriate to use the high-end
estimate when determining bystander
risk. EPA also chose a conservative and
protective brake repair/replacement
exposure scenario of 3 hours/day while
inside a garage up to 8 hours once every
3 years, using compressed air to account
for the possibility that some bystanders
(e.g., children watching parents) may fit
this exposure scenario. EPA also used a
less conservative brake and clutch
repair/replacement exposure scenario of
once in a lifetime, 1 hour per day, while
inside a garage, using compressed air.
As part of the analysis, EPA made some
assumptions regarding both age at the
start of exposure and the duration of
exposure. Realizing there is uncertainty
around these assumptions, EPA
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Criteria for Uisk
Determination
Do-it-y ourself Mechanic
IJ> slander

may fit this exposure scenario. EPA
also used a less conservative brake
and clutch repair/replacement
exposure scenario of once in a
lifetime, 1 hour per day, while inside
a garage, using compressed air. As
part of the analysis, EPA made some
assumptions regarding both age at the
start of exposure and the duration of
exposure. Realizing there is
uncertainty around these assumptions,
EPA developed a sensitivity analysis
approach specifically for the
consumer exposure/risk analysis (see
Section 4.3.7 and Appendix L.) Under
the chosen indoor exposure scenarios,
the cancer benchmark is exceeded
(both central tendency and high-end),
therefore, these conditions of use
present unreasonable risk to
consumers.
developed a sensitivity analysis
approach specifically for the bystander
exposure/risk analysis (see Section 4.3.7
and Appendix L.) Based on the
exceedance (both central tendency and
high-end) of the benchmark of lxlO"6 for
the chosen indoor exposure scenarios,
the expected absence of respiratory PPE,
and the potential severity of effects
associated with inhalation exposures to
asbestos, these conditions of use present
unreasonable risk to bystanders.
7786
7787
7788 Table 5-8. Risk Determination for Chrysotile Asbestos: Consumer Use and Disposal of Other
7789 Asbestos-Containing Gaskets
7790 (Do-it-Yourself Consumer Gasket Repair/Replacement is Representative for this COU; refer to
7791 section 4.2.3.2 for the risk characterization)
Criteria for Uisk
Determination
Do-il-^ oursclf Mechanic
Bvstander
Life cycle
Stage
Consumer Use
Consumer Use
TSCA Section
6(b)(4)(A)
Unreasonable Risk
Determination
Presents unreasonable risk of injury to health
(consumers and bystanders)
Unreasonable Risk
Driver
Cancer resulting from chronic inhalation
exposure
Cancer resulting from chronic inhalation
exposure
Benchmark (Cancer)
10"6 excess cancer risks
10"6 excess cancer risks
Risk Estimates
without PPE
Indoor
1 hour/day; once every 3 years for 62
years (starting age 16)
Indoor
1 hour/day; once every 3 years for 62
years (starting age 16)
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Criteria lor Risk
Dclerininalion

Do-it-Yourself Mechanic

Exposures at 30% of active used
between uses, 1 hour/d in garage
2.3 E-5 Central Tendency
6.4 E-5 High-end
Exposures at 30% of active used between
uses, 1 hour/d in garage
2.4 E-5 Central Tendency
6.1 E-5 High-end
Indoor
8 hour/day; once every 3 years for 62
years (starting age 16)
Exposures at 30% of active used
between uses, 8 hours/d in garage
1.8 E-4 Central Tendency
5.1 E-4 High-end
Indoor
1 hour/day; once every 3 years for 62
years (starting age 16)
Exposures at 30% of active used between
uses, 8 hours/d in garage
2.4 E-5 Central Tendency
6.1 E-5 High-end
Indoor
1 hour/day, once in a lifetime (at age
16), staying in residence for 10 years
3.0 E-6 Central Tendency
8.3 E-6 High-end
Indoor
1 hour/day, once in a lifetime (at age
16), staying in residence for 10 years
3.08 E-6 Central Tendency
7.16 E-6 High-end
Risk Estimates with
PPE
Not Assessed; Consumers are not
assumed to wear respiratory PPE
Not Assessed; Bystanders are not assumed
to wear respiratory PPE
Risk Considerations
EPA assumed that the duration of gasket
repair activity was 3 hours a day and that
a DIY mechanic is likely to perform one
gasket repair once every 3 years and can
spend up to a full day (8 hours) in their
garage. This scenario assumes all the
work is conducted indoors (within a
garage) and both the consumer and
bystander remain in the garage for the
entirety of the work. EPA presents this
conservative and protective gasket
repair/replacement exposure scenario
approach to account for the possibility
that some DIY mechanics may fit this
exposure scenario. EPA also presents a
less conservative gasket
repair/replacement exposure scenario of
1 hour a day, once in a lifetime gasket
repair/replacement at age 16. EPA made
some assumptions regarding both age at
the start of exposure and the duration of
exposure. Realizing there is uncertainty
around these assumptions, EPA
developed a sensitivity analysis
approach specifically for the consumer
exposure/risk analysis (see Section 4.3.7
EPA assumed that the duration of
bystander exposure was 1 hour a day once
every 3 years. EPA also presents a less
conservative gasket repair/replacement
exposure scenario of 1 hour a day, once in
a lifetime gasket repair/replacement at age
16. EPA made some assumptions
regarding both age at the start of exposure
and the duration of exposure. Realizing
there is uncertainty around these
assumptions, EPA developed a sensitivity
analysis approach specifically for the
consumer exposure/risk analysis (see
Section 4.3.7 and Appendix L.) Due to the
severe and irreversible effects associated
with asbestos inhalation exposures and
that asbestos fibers released during the
DIY activities described in Section 2.3.2.2
can settle and again become airborne
where they can be inhaled by bystanders,
EPA considered it appropriate to use the
high-end estimate when determining
bystander risk. Based on the exceedance
of the benchmark of lxlO"6, at both the
central tendency and high-end estimates
and the expected absence of respiratory
Page 231 of 310
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('rhcrin lor Risk
Dolcriniiiiilion
and Appendix L.) Due to the severe and
irreversible effects associated with
asbestos inhalation exposures and that
asbestos fibers released during the DIY
activities described in Section 2.3.2.2,
can settle and again become airborne
where they can be inhaled EPA
considered it appropriate to use the high-
end estimates when determining
consumer risk. Based on the exceedance
of the benchmark of lxlO"6, at both the
central tendency and high-end estimates
and the expected absence of respiratory
PPE, these conditions of use present
unreasonable risk to consumers.
PPE, these conditions of use present
unreasonable risk to bystanders.
7792
7793 5.3 Risk Determination for Five other Asbestiform Varieties
7794 For the risk evaluation, EPA adopted the TSCA Title II definition of asbestos which includes the
7795 varieties of six fiber types - chrysotile (serpentine), crocidolite (riebeckite), amosite (cummingtonite-
7796 grunerite), anthophyllite, tremolite or actinolite. In this document, EPA only assessed the conditions of
7797 use of chrysotile. EPA will consider legacy uses and associated disposal (which could include the other
7798 five asbestiform varieties) in subsequent supplemental documents.
7799
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7808
7809
7810
7811
7812
7813
7814
7815
7816
7817
7818
7819
7820
7821
7822
7823
7824
7825
7826
7827
7828
7829
7830
7831
7832
7833
7834
7835
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6 REFERENCES
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Courtice, MM; Wang, X; Lin, S; Yu, IT; Berman, DW; Yano, E, (2016). Exposure-response estimate for
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Davidson. B, (2011). The diagnostic and molecular characteristics of malignant mesothelioma and
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2012, EC1244SLLS1. Retrieved from
https://factfinder.census.gov/faces/tableservices/isf/pages/productview.xhtml?pid=ECN 2012
US 44SLLSl&prodType=table
U.S. DOT (U.S. Department of Transportation,). (2018). Average annual miles per driver by age group.
Available online at https://www.fhwa.dot.eov/ohim/onh00/bar8.htm
U.S. EPA. (1980). Ambient water quality criteria for asbestos [EPA Report]. (EPA/440/5-80/022).
Washington, DC. http://nepis,epa,gov7Exe/ZyPURL,cgi?Dockey=00001LP6,txt
U.S. EPA. (1985). Drinking water criteria document for asbestos. (600/X-84/199-1). Cincinnati, OH:
Environmental Criteria and Assessment Office, U.S. Environmental Protection Agency.
U.S. EPA. (1986). Airborne asbestos health assessment update. (EPA/600/8-84/003F). Washington DC:
U.S. Environmental Protection Agency, Environmental Criteria and Assessment.
U.S. EPA. (1988a). Asbestos Modeling Study. Final Report. Report from Versar to EPA. (560/3-88/091).
Washington, D.C.: Office of Toxic Substances.
U.S. EPA. (1988b). IRIS summary for asbestos (CASRN 1332-21-4). Washington, DC: U.S. Environmental
Protection Agency, Integrated Risk Information System.
http://www.epa.eov/iris/subst/0371.htm
U.S. EPA. (1994). Guidelines for Statistical Analysis of Occupational Exposure Data: Final. United States
Environmental Protection Agency :: U.S. EPA.
U.S. EPA. (1998). Guidelines for ecological risk assessment [EPA Report]. (EPA/630/R-95/002F).
Washington, DC: U.S. Environmental Protection Agency, Risk Assessment Forum.
https://www.epa.eov/risk/euidelines-ecoloeical-risk-assessment
U.S. EPA. (2005). Guidelines for carcinogen risk assessment [EPA Report] (pp. 1-166). (EPA/630/P-
03/001F). Washington, DC: U.S. Environmental Protection Agency, Risk Assessment Forum.
http://www2.epa.eov/osa/euidelines-carcinoeen-risk-assessment
U.S. EPA. (2007). Current best practices for preventing asbestos exposure among brake and clutch
repair workers. (EPA-747-F-04-004). https://www.epa.eov/asbestos/current-best-practices-
preventine-asbestos-exposure-among-brake-and-clutch-re pair-workers
U.S. EPA. (2008). Framework for investigating asbestos-contaminated superfund sites (pp. 71). (OSWER
Directive #9200.0-68). Washington, DC: U.S. Environmental Protection Agency, Office of Solid
Waste and Emergency Response.
http://www.epa.eov/superfund/health/contaminants/asbestos/pdfs/framework asbestos eui
dance.pdf
U.S. EPA. (2009). Risk assessment guidance for superfund volume I: Human health evaluation manual
(Part F, supplemental guidance for inhalation risk assessment): Final [EPA Report]. (EPA/540/-R-
070/002). Washington, DC. https://www.epa.eov/nsk/risk~assessment-euidance-superfund~
raes-part-f
U.S. EPA. (2011). Exposure factors handbook: 2011 edition (final) [EPA Report]. (EPA/600/R-090/052F).
Washington, DC: U.S. Environmental Protection Agency, Office of Research and Development,
National Center for Environmental Assessment.
http://cfpub.epa.eov/ncea/cfm/recordisplay.cfm?deid=236252
U.S. EPA. (2014a). Framework for human health risk assessment to inform decision making. Final [EPA
Report]. (EPA/100/R-14/001). Washington, DC: U.S. Environmental Protection, Risk Assessment
Forum, https://www.epa.eov/nsk/framework~human-health-risk~assessment-inform-decision-
makine
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U.S. EPA. (2014b). Site-wide Baseline Ecological Risk Assessment Libby Asbestos Superfund Site.
https://www.epa.gov/sites/production/files/2015~Ql/documents/libby-asbestos-site~wide~
bera~l~9~2Q15.pdf
U.S. EPA. (2014c). Toxicological review of libby amphibole asbestos: In support of summary information
on the Integrated Risk Information System (IRIS) [EPA Report]. (EPA/635/R-11/002F).
Washington, DC: Integrated Risk Information System, National Center for Environmental
Assessment, Office of Research and Development.
https://cfpub.epa.gov/ncea/iris/iris documents/documents/toxreviews/lQ26tr.pdf
U.S. EPA. (2014d). TSCA work plan chemical risk assessment. Trichloroethylene: Degreasing, spot
cleaning and arts & crafts uses. (740-R1-4002). Washington, DC: Environmental Protection
Agency, Office of Chemical Safety and Pollution Prevention.
http://www2.epa.gov/sites/production/files/2015~
09/documents/tce opptworkplanchemra fi 2414.pdf
U.S. EPA. (2015). Memorandum of Understanding on Copper Mitigation in Watersheds and Waterways
between U.S. Environmental Protection Agency and various industry stakeholders.
https://www.epa.gov/sites/production/files/2015~ll/documents/copper brakepads mou.pdf
U.S. EPA. (2017a). 1,4-dioxane (CASRN: 123-91-1) bibliography: Supplemental file for the TSCA Scope
Document [EPA Report], https://www.epa.gov/sites/production/files/2017~
06/documents/14dioxane comp bib.pdf
U.S. EPA. (2017b). Asbestos (CASRN: 1332-21-4) bibliography: Supplemental file for the TSCA scope
document [EPA Report]. Washington, DC. https://www.epa.gov/sites/production/files/2017~
06/documents/abestos comp bib.pdf
U.S. EPA. (2017c). Scope of the risk evaluation for Asbestos [EPA Report]. (EPA-740-R1-7008).
Washington, DC: U.S. EPA, Office of Chemical Safety and Pollution Prevention (OCSPP), Office of
Pollution Prevention and Toxics (OPPT). https://www.epa.gov/sites/production/files/2017~
06/documents/asbestos scope 06~22~17.pdf
U.S. EPA. (2017d). Toxics Release Inventory (TRI), reporting year 2015. Retrieved from
https://www.epa.gov/toxics~release~inventory-tri~program/tri~data~and~tools
U.S. EPA. (2018a). Application of systematic review in TSCA risk evaluations. (740-P1-8001).
Washington, DC: U.S. Environmental Protection Agency, Office of Chemical Safety and Pollution
Prevention, https://www.epa.gov/sites/production/files/2018~
06/documents/final application of sr in tsca 05~31~18.pdf
U.S. EPA. (2018b). Meeting summary: Chemical Use Outreach Phone Call with Mexalit and EPA to
Discuss Asbestos in Products Exported to the United States. Washington, DC.
U.S. EPA. (2018c). Meeting summary: Chemical Use Outreach Phone Call with Textiles Tecnicos and
EPA to Discuss Asbestos in Products Exported to the United States. Washington, DC.
U.S. EPA. (2018d). Problem formulation of the risk evaluation for asbestos. (EPA-740-R1-7018).
Washington, DC: Office of Chemical Safety and Pollution Prevention, United States
Environmental Protection Agency.
U.S. EPA. (2018e). Strategy for assessing data quality in TSCA risk evaluations. Washington DC: U.S.
Environmental Protection Agency, Office of Pollution Prevention and Toxics.
U.S. EPA. (2019a). Draft Risk Evaluation for Asbestos, Supplemental File: Consumer Exposure
Calculations.
U.S. EPA. (2019b). Draft Risk Evaluation for Asbestos, Supplemental File: Occupational Exposure
Calculations (Chlor-Alkali).
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U.S. EPA. (2019c). Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data
Quality Evaluation of Consumer Exposure.
U.S. EPA. (2019d). Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data
Quality Evaluation of Ecological Hazard Studies.
U.S. EPA. (2019e). Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data
Quality Evaluation of Environmental Fate and Transport Studies.
U.S. EPA. (2019f). Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data
Quality Evaluation of Environmental Releases and Occupational Exposure.
U.S. EPA. (2019g). Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data
Quality Evaluation of Environmental Releases and Occupational Exposure Data Common
Sources.
U.S. EPA. (2019h). Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data
Quality Evaluation of Human Health Hazard Studies: Mesothelioma and Lung Cancer Studies.
U.S. EPA. (2019i). Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data
Quality Extraction Tables for Consumer Exposure.
U.S. EPA. (2019j). Draft Risk Evaluation for Asbestos. Systematic Review Supplemental File: Data
Quality Evaluation of Physical-Chemical Properties studies. Washington, D.C.: U.S.
Environmental Protection Agency. Office of Chemical Safety and Pollution Prevention.
USGS. (2017). Mineral commodity summaries 2017. Washington, DC: U.S. Department of the Interior.
https://minerals.usgs.gov/minerals/pubs/mcs/2017/mcs2017.pdf
USGS. (2019). Mineral commodity summaries: Asbestos. USGS.
https://minerals.usgs.gov/minerals/pubs/commoditv/asbestos/mcs-2019-asbes.pdf
Vacek, PM. (1998). Effects of the intensity and timing of asbestos exposure on lung cancer risk at two
mining areas in Quebec. J Occup Environ Med 40: 821-828.
Versar. (1987). Nonoccupational asbestos exposure. Revised Report. Washington, D.C.: U.S.
Environmental Protection Agency.
Virta, R. (2011). Asbestos. In Kirk-Othmer Encyclopedia of Chemical Technology, [online]: John Wiley &
Sons. http://dx.doi.org/10.1002/0471238961.01190205101512Q9.a01.pub3
Virta, RL (2006). Asbestos. In Industrial Minerals & Rocks: Commodities, Markets, and Uses (7th ed.).
U.S.: SME.
Wang. X: Lin. S: Yano, E; Qiu. H; Yu, IT: Tse, L; Lan, ¥'; Wang. M. (2012). Mortality in a Chinese chrysotile
miner cohort. Int Arch Occup Environ Health 85: 405-412. http://dx.doi.org/lQ.10Q7/s00420~
011-0685-9
Wang. X: Lin. S: Yano. E; Yu. IT: Courtice. Christiani, DC. (2014). Exposure-specific lung cancer
risks in Chinese chrysotile textile workers and mining workers. Lung Cancer 85:119-124.
http://dx.doi.Org/10.1016/i.lungcan.2014.Q4.011
Wang. X: Lin ¦. E. (2013a). Cause-specific mortality in a Chinese chrysotile
textile worker cohort. Cancer Sci 104: 245-249. http://dx.doi.org/10.llll/cas.12060
Wang. X: Yano. E; Lih S; nt H; ton V i ^e, LA: Qiu. H; Christiani. DC. (2013b). Cancer mortality in
Chinese chrysotile asbestos miners: exposure-response relationships. PLoS ONE 8: e71899.
http://dx.doi.org/10.1371/iournal.pone.0071899
Washington State. (2010). RCW (Revised Code of Washington) Chapter 70.285: Brake Friction Material.
Washington State. http://app.leg.wa.gov/RCW/default.aspx?cite=70.285.030
Weir. FW; Tokn, ^ ?vi raz, LB. (2001). Characterization of vehicular brake service personnel exposure
to airborne asbestos and particulate. Appl Occup Environ Hyg 16: 1139-1146.
http://dx.doi.org/10.lQ80/104732201274Q2
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Whitaker. D. (2000). The cytology of malignant mesothelioma [Review]. Cytopathology 11:139-151.
http://dx.doi.Org/10.1046/i.1365-2303.2000.00247.x
Whittaker, C: Riu* I" McKernan, L; Dankovic. D; Lentz, T; Macmahon, K: Kuempel, E; Zumwalde, R;
Schui (2016). Current Intelligence Bulletin 68: NIOSH Chemical Carcinogen Policy.
Whittaker, C; Rice, F; Mckernan, L; Dankovic, D; Lentz, T; Macmahon, K; Kuempel, E; Zumwalde,
R; Schulte, P.
WHO. (2014). Chrysotile asbestos. Geneva, Switzerland.
http://www.who.int/ipcs/assessment/public health/chrvsotile asbestos summarv.pdf
Yano, E; Wang. ZM; Wane. XR: Wane. MZ (2001). Cancer mortality among workers exposed to
amphibole-free chrysotile asbestos. Am J Epidemiol 154: 538-543.
Yeung. P; Patience. K: Apthorpe. L; Willcocks. D. (1999). An Australian study to evaluate worker
exposure to chrysotile in the automotive service industry. Appl Occup Environ Hyg 14: 448-457.
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7 APPENDICES
Appendix A Regulatory History
A.l Federal Laws and Regulations
The federal laws and regulations applicable to asbestos are listed along with the regulating agencies
below. States also regulate asbestos through state laws and regulations, which are also listed within this
section.
Toxics Substances Control Act (TSCA), 1976
v- "¦ M ^ sea
The Toxic Substances Control Act of 1976 provides EPA with authority to require reporting, record-
keeping and testing requirements, and restrictions relating to chemical substances and/or mixtures.
Certain substances are generally excluded from TSCA, including, among others, food, drugs, cosmetics
and pesticides.
TSCA addresses the production, importation, use and disposal of specific chemicals including
polvchlorinated biphenyls (PCBsi asbestos, radon and lead-based paint. The Frank R. Lautenberg
Chemical Safety for the 21st Century Act updated TSCA in 2016 https://www.epa.gov/1 aws-
regulations/summary-toxic-substances-control-act.
Asbestos Hazard Emergency Response Act (AHERA), 1986
TSCA. Subchapter II: Asbestos Hazard Emergency Response 15 U.S.C. §2641-2656
Defines asbestos as the asbestiform varieties of— chrysotile (serpentine), crocidolite (riebeckite),
amosite (cummingtonite-grunerite), anthophyllite, tremolite or actinolite.
Requires local education agencies (i.e., school districts) to inspect school buildings for asbestos and
submit asbestos management plans to appropriate state; management plans must be publicly available
and inspectors must be trained and accredited.
Tasked EPA to develop an asbestos Model Accreditation Plan (MAP) for states to establish training
requirements for asbestos professionals who do work in school buildings and also public and
commercial buildings.
Asbestos-Containing Materials in Schools Rule (per AHERA), 1987
40 CFR Part 763. Subp
Requires local education agencies to use trained and accredited asbestos professionals to identify and
manage asbestos-containing building material and perform asbestos response actions (abatements) in
school buildings.
1989 Asbestos: Manufacture, Importation, Processing, and Distribution in Commerce
Prohibitions; Final Rule (also known as Asbestos Ban and Phase-out Rule (Remanded), 1989)
40 CFR Part 763. Subpart 1
Docket ID: OPTS-62Q48E: FRL-3269-8
EPA issued a final rule under Section 6 of Toxic Substances Control Act (TSCA) banning most
asbestos-containing products.
In 1991, this rule was vacated and remanded by the Fifth Circuit Court of Appeals. As a result, most of
the original ban on the manufacture, importation, processing or distribution in commerce for the
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majority of the asbestos-containing products originally covered in the 1989 final rule was overturned.
The following products remain banned by rule under the Toxic Substances Control Act (TSCA):
o Corrugated paper
o Rollboard
o Commercial paper
o Specialty paper
o Flooring felt
In addition, the regulation continues to ban the use of asbestos in products that have not historically
contained asbestos, otherwise referred to as "new uses" of asbestos (Defined by 40 CFR 763.163 as
"commercial uses of asbestos not identified in §763.165 the manufacture, importation or processing of
which would be initiated for the first time after August 25, 1989").
Restrictions on Discontinued Uses of Asbestos; Significant New Use Rule (SNUR), 2019
40 CFR Parts 9 and 721 - Restrictions on Discontinued Uses of Asbestos
Docket ID: EPA-HQ-OPPT-2018-0159; FRL 9991-33
This final rule strengthens the Agency's ability to rigorously review an expansive list of asbestos
products that are no longer on the market before they could be sold again in the United States. Persons
subject to the rule are required to notify EPA at least 90 days before commencing any manufacturing,
importing, or processing of asbestos or asbestos-containing products covered under the rule. These uses
are prohibited until EPA conducts a thorough review of the notice and puts in place any necessary
restrictions or prohibits use.
Other EPA Regulations:
Asbestos Worker Protection Rule, 2000
40 CFR Part 763. Sufap
Extends OSHA standards to public employees in states that do not have an OSHA approved worker
protection plan (about half the country).
Asbestos Information Act, 1988
15 LI.S.C. §2607ffi
Helped to provide transparency and identify the companies making certain types of asbestos-containing
products by requiring manufacturers to report production to the EPA.
Asbestos School Hazard Abatement Act (ASHAA), 1984 and Asbestos School Hazard Abatement
Reauthorization Act (ASHARA), 1990
20 I r I. MM I et sea, and Docket 4* OPTS-62Q48K U69-8
Provided funding for and established an asbestos abatement loan and grant program for school districts
and ASHARA further tasked EPA to update the MAP asbestos worker training requirements.
Emergency Planning and Community Right-to-Know Act (EPCRA), 1986
42 LI.S.C. Chapter 116
Under Section 313, Toxics Release Inventory (TRI), requires reporting of environmental releases of
friable asbestos at a concentration level of 0.1%.
Friable asbestos is designated as a hazardous substance subject to an Emergency Release Notification at
40 CFR §355.40 with a reportable quantity of 1 pound.
Clean Air Act, 1970
42 LI.S.C. §7401 et sea.
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Asbestos is identified as a Hazardous Air Pollutant.
Asbestos National Emission Standardfor Hazardous Air Pollutants (NESHAP), 1973
bpart M of the Clean Air Act
Specifies demolition and renovation work practices involving asbestos in buildings and other facilities
(but excluding residences with 4 or fewer dwelling units single family homes).
Requires building owner/operator notify appropriate state agency of potential asbestos hazard prior to
demoliti on/renovati on.
Banned spray-applied surfacing asbestos-containing material for fireproofing/insulating purposes in
certain applications.
Requires that asbestos-containing waste material from regulated activities be sealed in a leak-tight
container while wet, labeled, and disposed of properly in a landfill qualified to receive asbestos waste.
Clean Water Act (CW.A), 1972
33 LI.S.C. §1251 et sea
Toxic pollutant subject to effluent limitations per Section 1317.
Safe Drinking Water Act (SDWA), 1974
42 LI.S.C. §300f
Asbestos Maximum Contaminant Level Goals (MCLG) 7 million fibers/L (longer than lOum).
Resource Conservation and Recovery Act (RCRA), 1976
42 LI.S.C. §6901 et sea.
40 CFR 239-282
Asbestos is subject to solid waste regulation when discarded; NOT considered a hazardous waste.
Comprehensive Environmental Response, Compensation and Liability Act (CERCLA), 1980
£ ?601 et sea.
40 CFR Part 302.4 - Designation of Hazardous Substances and Reportable Quantities
13 Superfund sites containing asbestos, nine of which are on the National Priorities List (NPL)
Reportable quantity of friable asbestos is one pound.
Other Federal Agencies:
Occupational Safety and Health Administration (OSHA):
Public Li Occupational Safety and Health Act, 1970
Employee permissible exposure limit (PEL) is 0.1 fibers per cubic centimeter (f/cc) as an 8-hour, time-
weighted average (TWA) and/or the excursion limit (1.0 f/cc as a 30-minute TWA).
Asbestos General Standard 29
Asbestos Shipyard Standard
Asbestos Construction Standard 29 CFR 1926
Consumer Product Safety Commission (CPSC): Banned several consumer products. Federal Hazardous
Substances Act (FHSA) "R 1500
Food and Drug Administration (FDA): Prohibits the use of asbestos-containing filters in pharmaceutical
manufacturing, processing and packing. 21 CFR 211.72
Mine Safety and Health Administration (MSHA): follows OSHA's safety standards.
Surface Mines 30 CFR part 56. subpart D
Underground Mines 30 CFR p subpart D
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Department of Transportation
Prescribes the requirements for shipping manifests and transport vehicle placarding applicable to
asbestos rt. 172.
Non-regulatory information of note:
NIOSH conducts related research and monitors asbestos exposure through workplace activities in an
effort to reduce illness and ensure worker health and safety.
A.2 State Laws and Regulations
Pursuant to AHERA, states have adopted through state regulation the EPA's Model Accreditation Plan
(MAP) for asbestos abatement professionals who do work in schools and public and commercial
buildings. Thirty-nine (39) states31 have EPA-approved MAP programs and twelve (12) states32 have
also applied to and received a waiver from EPA to oversee implementation of the Asbestos-Containing
Materials in Schools Rule pursuant to AHERA. States also implement regulations pursuant to the
Asbestos NESHAP regulations or further delegate those oversight responsibilities to local municipal
governments. While federal regulations set national asbestos safety standards, states have the authority
to impose stricter regulations. As an example, many states extend asbestos federal regulations - such as
asbestos remediation by trained and accredited professionals, demolition notification, and asbestos
disposal - to ensure safety in single-family homes. Thirty (30) states33 require firms hired to abate
asbestos in single family homes to be licensed by the state. Nine (9) states34 mandate a combination of
notifications to the state, asbestos inspections, or proper removal of asbestos in single family homes.
Some states have regulations completely independent of the federal regulations. For example, California
and Washington regulate products containing asbestos. Both prohibit use of more than 0.1% of asbestos
in brake pads and require laboratory testing and labeling.
Below is a list of state regulations that are independent of the federal AHERA and NESHAP
requirements that states implement. This may not be an exhaustive list.
California
Asbestos is listed on California's Candidate Chemical List as a carcinogen. Under California's
Propositions 65. businesses are required to warn Californians of the presence and danger of asbestos in
products, home, workplace and environment.
California Brake Friction Material Requirements (Effective 2017)
Division 4.5, California Code of Regulations, Title 22 Chapter 30
31 Alabama, Alaska, Arkansas, California, Colorado, Connecticut, Delaware, Florida, Illinois, Indiana, Kentucky, Louisiana,
Maine, Maryland, Massachusetts, Michigan, Minnesota, Mississippi, Missouri, Montana, Nebraska, New Hampshire, New
Jersey, New York, North Carolina, North Dakota, Oklahoma, Oregon, Pennsylvania, Rhode Island, South Carolina, South
Dakota, Texas, Utah, Vermont, Virginia, Washington, West Virginia, and Wisconsin.
32 Connecticut, Colorado, Illinois, Kentucky, Louisiana, Massachusetts, Maine, New Hampshire, Oklahoma, Rhode Island,
Texas, and Utah.
33 California, Colorado, Connecticut, Delaware, Florida, Georgia, Hawaii, Iowa, Kansas, Maine, Maryland, Massachusetts,
Michigan, Minnesota, Nebraska, Nevada, New Hampshire, New Jersey, New Mexico, New York, North Carolina, North
Dakota, Oregon, Pennsylvania, Utah, Vermont, Virginia, Washington, West Virginia, and Wisconsin.
34 Colorado, Connecticut, Georgia, Maine, Massachusetts, New York, Oregon, Vermont, and West Virginia.
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Sale of any motor vehicle brake friction materials containing more than 0.1% asbestiform fibers by
weight is prohibited. All brake pads for sale in the state of California must be laboratory tested, certified
and labeled by the manufacturer.
Massachusetts
Massachusetts Toxics Use Reduction Act (JURA)
Requires companies in Massachusetts to provide annual pollution reports and to evaluate and implement
pollution prevention plans. Asbestos is included on the Complete List of TLIRA. Chemicals - March
2016.
Minnesota
Toxic Free Kids Act Minn. Ski '01 116.9407
Asbestos is included on the 2.016 Minnesota Chemicals of Hi eh Concern List as a known carcinogen.
New Jersey
New Jersey Right to Know Hazardous Substances
The state of New Jersey identifies hazardous chemicals and products. Asbestos is listed as a known
carcinogen and talc containing asbestos is identified on the Right to Know Hazardous Substances list.
Rhode Island
Rhode Island Air Resources - Air Toxics Air Pollution Control Regulation No. 22
Establishes acceptable ambient air levels for asbestos.
Washington
Better Brakes Law (Effective 2015) Chapter 70.285 RCW Brake Friction Material
Prohibits the sale of brake pads containing more than 0.1% asbestiform fibers (by weight) in the state of
Washington and requires manufacturer certification and package/product labelling.
Requirement to Label Building Materials that Contain Asbesto RCW
Building materials that contain asbestos must be clearly labeled as such by manufacturers, wholesalers,
and distributors.
A.3 International Laws and Regulations
Asbestos is also regulated internationally. Nearly 60 nations have some sort of asbestos ban. The
European Union (EU) will prohibit the use of asbestos in the chlor-alkali industry by 2025 (Regulation
(EC) No 1907/2006 of the European Parliament and of the Council, 18 December 2006).
Canada banned asbestos in 2018
Prohibition of Asbestos and Products Containing Asbestos Regulations: SOR/2018-196
Canada Gazette. Pai 11i, Volume tv' \umber 21
In addition, the Rotterdam Convention is considering adding chrvsotile to Annex III, and the World
Health Organization (WHO) has a global campaign to eliminate asbestos-related diseases (WHO
Resolution 60.26).
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Appendix B List of Supplemental Documents
List of supplemental documents:
Associated Supplemental Systematic Review Data Quality Evaluation and Date Extraction
Documents - Provides additional detail and information on individual study evaluations and
data extractions including criteria nad scoring results.
Physical-Chemical Properties, Fate and Transport
a. Draft Risk Evaluation for Asbestos, , Systematic Review Supplemental File: Data Quality
Evaluation of Physical-Chemical Properties Studies (U.S. EPA. 2019i)
b. Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data
Extraction of Environmental Fate and Transport Studies ( J019e)
Occupational Exposures and Releases
c. Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data Quality
Evaluation of Environmental Releases and Occupational Exposure ( .019f)
d. Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data Quality
Evaluation of Environmental Releases and Occupational Exposure Data Common Sources (US.
H^_2019g)
Consumer and Environmental Exposures
e. Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data Quality
Evaluation of Consumer Exposure ( 019c)
f Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data Quality
Extraction Tables for Consumer Exposure ( E0191)
Environmental Hazard
g. Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data Quality
Evaluation of Ecological Hazard Studies (U.S. EPA. 2019d)
Human Health Hazard
h. Draft Risk Evaluation for Asbestos, Systematic Review Supplemental File: Data Quality
Evaluation of Human Health Hazard Studies: Mesothelioma and Lung Cancer Studies (US.
EPA. 2019b.)
Associated Supplemental Information Documents - Provides additional details and information on
exposure.
Occupational Exposures
i. Draft Risk Evaluation for Asbestos, Supplemental File: Occupational Exposure Calculations
(Chlor-Alkali)] (U.S. EPA. 2.019b)
Consumer Exposures
j. Draft Risk Evaluation for Asbestos, Supplemental File: Consumer Exposure Calculations (U.S.
EPA. 2019a)
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Appendix C Conditions of Use Supplementary Information
EPA identified and verified uses of asbestos throughout the scoping, PF, and risk evaluation stages. As
explained in the PF document, EPA believes that most asbestos imports listed by Harmonized Tariff
Schedule (HTS) code in government and commercial trade databases are likely misreported and are not
ongoing COU. EPA has been working with federal partners to better understand the asbestos-containing
product import information. In coordination with Customs and Border Protection (CBP), EPA has
reviewed available import information for the following asbestos Harmonized Tariff Schedule (HTS)
codes:
2524.90.0045 Chrysotile Milled Fibers, Group 4 And 5 Grades
2524.90.0055 Chrysotile Milled Fibers, Other
6812.92.0000 Asbestos, Fibers, Fabricated, Paper, Millboard and Felt
6812.93.0000 Asbestos, Fiber, Compressed, Jointing, in Sheets or Rolls
6812.99.0003 Asbestos, Fabricated, Cords and String, whether or not Plaited
6812.99.0020 Asbestos, Fibers, Fabricated, Gaskets, Packing and Seals
6812.99.0055 Asbestos, Fibers, Fabricated, Other
6813.20.0010 Asbestos, Mineral Subst, Friction Mat, Brake Lin/Pad, Civil Air
6813.20.0015 Asbestos, Mineral Subst, Friction Mat, Brake Linings And Pads
6813.20.0025 Asbestos, Mineral Subst, Friction Mat, Other
CBP provided import data for the above asbestos HTS codes in CBP's Automated Commercial
Environment (ACE) system, which provided information for 26 companies that reported the import of
asbestos-containing products between 2016 and 2018. EPA contacted these 26 companies in order to
verify the accuracy of the data reported in ACE. Of these 26 companies, 22 companies confirmed that
the HTS codes were incorrectly entered and one company could not be reached. Three companies
confirmed that the HTS codes entered in ACE are correct. EPA received confirmation that the following
asbestos-containing products are imported into the United States:
• Gaskets for use in the exhaust for off-road utility vehicles
o 6812.99.0020 Asbestos, Fibers, Fabricated, Gaskets, Packing and Seals
• Gaskets for sealing pipes and flanges
o 6812.93.0000 Asbestos, Fiber, Compressed, Jointing, in Sheets or Rolls
• Brake linings for use in automobiles that are manufactured and then exported (not sold
domestically)
o 6813.20.0015 Asbestos, Mineral Subst, Friction Mat, Brake Linings And Pads
Regarding the two HTS codes that represent raw chrysotile, one company imported asbestos as waste
but reported it in ACE under the HTS code 2524.90.0055 (Chrysotile Milled Fibers, Other). EPA did not
contact the two facilities that reported under HTS code 2524.90.0045 (Chrysotile Milled Fibers, Group 4
And 5 Grades) because these entries were from a chloralkali company, which has already confirmed
import and use of raw chrysotile.
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Appendix D Releases and Exposure to the Environment
Supplementary Information
Toxics Release Inventory Data
A source of information that EPA considered in evaluating exposure is data reported under the Toxics
Release Inventory (TRI) program. TRI reporting by subject facilities is required by law to provide
information on releases and other waste management activities of Emergency Planning and Community
Right-to-Know Act (EPCRA) Section 313 chemicals (i.e., TRI chemicals) to the public for informed
decision making and to assist the EPA in determining the need for future regulations. Section 313 of
EPCRA and Section 6607 of the Pollution Prevention Act (PPA) require certain facilities to report
release and other waste management quantities of TRI-listed chemicals annually when a reporting
threshold is triggered, but these statutes do not impose any monitoring burden for determining the
quantities.
TRI data are self-reported by the subject facility where some facilities are required to measure or
monitor emission or other waste management quantities due to regulations unrelated to the TRI
Program, or due to company policies. These existing, readily available data are often used by facilities
for TRI reporting purposes. When measured (e.g., monitoring) data are not "readily available," or are
known to be non-representative for TRI reporting purposes, the TRI regulations require that facilities
determine release and other waste management quantities of TRI-listed chemicals by making
"reasonable estimates." Such reasonable estimates include a variety of different approaches ranging
from published or site-specific emission factors (e.g., AP-42), mass balance calculations, or other
engineering estimation methods or best engineering judgement. TRI reports are then submitted directly
to EPA on an annual basis and must be certified by a facility's senior management official that the
quantities reported to TRI are reasonable estimates as required by law.
Under EPCRA Section 313, asbestos (friable) is a TRI-reportable substance effective January 1, 1987.
For TRI reporting, facilities in covered sectors are required to report releases or other waste management
of only the friable form of asbestos, under the general CASRN 1332-21-4. TRI interprets "friable" under
EPCRA Section 313, referring to the physical characteristic of being able to be crumbled, pulverized or
reducible to a powder with hand pressure, and "asbestos" to include the six types of asbestos as defined
under Title II of TSCA35. Facilities are required to report if they are in a covered industrial code or
federal facility and manufacture (including import) or process more than 25,000 pounds of friable
asbestos, or if they otherwise use more than 10,000 pounds of friable asbestos.
35 According to 53FR4519 (VII)C(5), "The listing for asbestos is qualified by the term "friable." This term refers to a physical
characteristic of asbestos. EPA interprets "friable" as being crumbled, pulverized, or reducible to a powder with hand
pressure. Again, only manufacturing, processing, or use of asbestos in the friable form triggers reporting. Similarly, supplier
notification applies only to distribution of friable asbestos."
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Table_APXD-l provides production-related waste management data for friable asbestos reported by
facilities in covered sectors to the TRI program from reporting years 2015 to 201836. This is an updated
table from that reported in the PF document. In reporting year 2018, 43 facilities reported a total of
approximately 32 million pounds of friable asbestos waste managed. Of this total, zero pounds were
recovered for energy or recycled, approximately 46,000 pounds were treated, and over 32 million
pounds were disposed of or otherwise released into the environment.
Table_APX D-2 provides a summary of asbestos TRI releases to the environment for the same
reporting years as Table_APXD-l . There were zero pounds of friable asbestos reported as released to
water via surface water discharges, and a total of 171 pounds of air releases from collective fugitive
and stack air emissions reported in 2018. The vast majority of friable asbestos was disposed of to
Resource Conservation and Recovery Act (RCRA) Subtitle C landfills and to landfills other than
RCRA Subtitle C. Of the 153,947 pounds of friable asbestos reported in 2018 as
"other releases", 90,640 pounds were sent off-site to a waste broker for disposal, 14,760 pounds were
sent off-site for storage only, and 48,547 pounds were sent off-site for other off-site management.
TableAPX D-l. Summary of Asbestos TRI Production-Related Waste Managed from 2015-2018
(lbs)
Year
Nil in ber
of
l-'acilities
Recycling
Knergy
Recovery
Treatment
Releases ll lM
Total
Production
Related
Waste
2015
38
0
0
188,437
33,446,648
33,635,084
2016
40
2
0
31,993
25,971,339
26,003,335
2017
38
0
0
179,814
30,434,703
30,616,517
2018
43
0
0
46,106
32,329,759
32,375,865
Data source: 2015-2018 TRI Data fUndated November 2019) ("U.S. EPA. 2017dV
a Terminology used in these columns may not match the more detailed data element names used in the TRI public data
and analysis access points.
b Does not include releases due to one-time events not associated with production such as remedial actions or
earthquakes.
0 Counts all releases including release quantities transferred and release quantities disposed of by a receiving facility
reporting to TRI.
While production-related waste managed shown in Table_APXD-l. excludes any quantities reported as
catastrophic or one-time releases (TRI section 8 data), release quantities shown in Table_APX D-2
include both production-related and non-routine quantities (TRI section 5 and 6 data) for 2015-2018.
As a result, release quantities may differ slightly and may further reflect differences in TRI calculation
methods for reported release range estimates (U.S. EPA, 2017d).
36 Reporting year 2018 is the most recent TRI data available. Data presented were queried using TRI Explorer and uses the
2018 National Analysis data set (released to the public in November 2019). This dataset includes revisions for the years 1988
to 2018 processed by EPA.
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Tahle_APX D-2. Summary of Asbestos TRT Releases to the Environment from 2015-2018 (lbs)

Air Rclcsiscs

1 .siii(l Dispossil

Ycsir
Nil 111 her
ol'
l-'sicililics
Si sick Air
Rclcsiscs
l"iiiii(i\c
Air
Rclcsiscs
\\ silcr
Rclcsiscs
( Isiss 1
I ndcr-
liround
Injection
RCRA
Suhiiilc
<
IsiiKllills
All oilier
1 .SI 11(1
Dispossil
.1
Oilier
Rclcsiscs •'
Toisil On- siiid OIT-
Silc Dispossil or
Oilier Rclcsiscs 1,1
Totals
2015
38
101
208
0
0
9,623,95
7
24,029,8
20
0
33,654,087

310

33,653,777

Totals
2016
40
178
106
0
0
8,759,57
8
17,826,8
52
0
26,586,715

285

26,586,430

Totals
2017
38
80
67
0
0
6,199,22
4
24,802,7
48
0
31,002,120

147

31,001,972

Totals
2018
43
96
75
0
0
10,599,5
87
21,65
7,453
15
32,411,158

171

32,257,040
3,9
47

Data source: 2015-2018 TRI Data ("Undated November 2019s) (U.S. EPA. 2017d).
a Terminology used in these columns may not match the more detailed data element names used in the TRI public data and analysis access points.
b These release quantities do include releases due to one-time events not associated with production such as remedial actions or earthquakes.
c Counts release quantities once at final disposition, accounting for transfers to other TRI reporting facilities that ultimately dispose of the chemical waste.
The Clean Water Act and the Safe Drinking Water Act
Background (Numeric Criteria and Reportable Levels)
The Clean Water Act (CWA) requires that states adopt numeric criteria for priority pollutants for which
EPA has published recommended criteria under section 304(a). States may adopt criteria that EPA
approves as part of the state's regulatory water quality standards. Once states adopt criteria as water
quality standards, the CWA requires that National Pollutant Discharge Elimination System (NPDES)
discharge permits include effluent limits as stringent as necessary to meet the standards [CWA section
301(b)(1)(C)], If state permit writers determine that permit limits are needed, they will determine the
level of pollutant allowed to ensure protection of the receiving water for a designated use. This is the
process used under the CWA to address risk to human health and aquatic life from exposure to a
pollutant in ambient waters.
EPA develops recommended ambient water quality criteria for pollutants in surface water that are
protective of aquatic life or human health designated uses with specific recommendations on the
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duration and frequency of those concentrations under section 304(a) of the CWA. These criteria are
based on priorities of states and others, and a subset of chemicals are identified as "priority pollutants".
EPA has identified asbestos as a priority pollutant for which a nationally recommended human health
water quality criteria for asbestos of 7 MFL has been developed. EPA has not developed a nationally
recommended water quality criteria for the protection of aquatic life for asbestos, yet EPA may publish
aquatic life criteria for asbestos in the future if it is identified as a priority under the CWA.
EPA's National Primary Drinking Water Regulations (NPDWR), established under the Safe Drinking
Water Act (SDWA), are legally enforceable primary standards and treatment techniques that apply to
public water systems. Primary standards and treatment techniques protect public health by limiting the
levels of contaminants in drinking water. The Maximum Contaminant Level (MCL) for asbestos under
the Safe Drinking Water Act is 7 million fibers per liter, or MFL, for fibers >10 micrometers. EPA has
set this level of protection based on the best available science at the time the NPDWR was promulgated
to prevent potential health problems and considering any limitations in both the feasible treatment
methods to remove a contaminant and availability of analytical methods to reliably measure the
occurrence of the contaminant in water. In the case of asbestos, the MCL was set based entirely on the
health goal since feasible treatment methods and analytical methods were available to achieve the
protective level of 7 MFL. Public water systems are required to sample each entry point into the
distribution system for asbestos at least once every 9 years. Transmission electron microscopy is used
for detection (EPA 800/4-83-043). The detection limit is 0.01 MFL. Here are links to the analytical
standards and the drinking water regulations.
The Phase II Rule, the regulation for asbestos, became effective in 1992. The Safe Drinking Water Act
requires EPA to review the national primary drinking water regulation for each contaminant every six
years and determine if the NPDWR is a candidate for revision, at that time. EPA reviewed asbestos as
part of the Six Year Review and determined that the 7 MFL for asbestos is still protective of human
health.
As discussed in the PF document, because the drinking water exposure pathway for asbestos is currently
addressed in the SDWA regulatory analytical process for public water systems, this pathway (drinking
water for human health) will not be evaluated in this draft RE.
EPA issues Effluent Limitations Guidelines and Pretreatment Standards which are national regulatory
standards for industrial wastewater discharges to surface waters and publicly owned treatment works, or
POTWs (municipal sewage treatment plants). EPA issues Effluent Limitations Guidelines and
Pretreatment Standards for categories of existing sources and new sources under Title III of the Clean
Water Act. The standards are technology-based (i.e., they are based on the performance of treatment and
control technologies); they are not based on risk or impacts upon receiving waters. (See effluent
guidelines).
The Effluent Limitations Guidelines and Pretreatment Standards for the Asbestos Manufacturing Point
Source Category (40 CFR Part 427) do not require that industrial facilities monitor asbestos
concentrations in discharges. Rather, the regulations contain either a zero discharge of pollutants
standard or require that the discharger not exceed a specified release amount of pollutants including total
suspended solids (TSS), chemical oxygen demand (COD) and pH. These guidelines were originally
developed in 1974 and 1975 and were revised in 1995. These guidelines cover legacy uses such as
manufacture of asbestos cement pipe, asbestos cement sheet, roofing, paper, etc. and may not be
particularly useful to the COU of asbestos. Additionally, there are effluent guidelines for the chlor-alkali
industry under 40 CFR Part 415 that cover pollutants such as chlorine, mercury, and lead, but they are
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not specific to asbestos. The EPA Industrial Waste Water Treatment Technology Database does not
currently include any data for asbestos (link to database).
Reasonably Available Data from Water Release Databases and Other Information
EPA investigated industry sector, facility, operational, and permit information regulated by NPDES
under the Clean Water Act to identify any permit limits, monitoring and reporting requirements, and any
discharge provisions related to asbestos and its COU. The Clean Water Act section 402 specifies that
point source pollutant dischargers into waters of the United States must obtain a permit to regulate that
facility's discharge. NPDES permits are issued by states, tribes, or territories that have obtained EPA
approval to issue permits or by EPA Regions in areas without such approval. Effluent limitations serve
as the primary mechanism in NPDES permits for controlling discharges of pollutants to receiving waters
and the NPDES permit data are cataloged into the Integrated Compliance Information System (ICIS) to
track permit compliance and enforcement status. NPDES permittees must then submit Discharge
Monitoring Reports (DMRs) to the appropriate permitting authority on a periodic basis to ensure
compliance with discharge standards for water quality and human health. Note that EPA does not
currently have data available on facilities that indirectly discharge wastewater to POTWs.
Available discharge data and permit information was accessed through EPA's Envirofacts and
Enforcement Compliance History Online (ECHO) database systems. EPA then investigated these data
sources for information pertinent to asbestos COU (chlor-alkali plants, sheet gasket stamping and
titanium dioxide plants) to identify if there is evidence of asbestos discharges or concentrations and/or
violations of their wastewater permits.
ICIS-NPDES information. ICIS-NPDES is an information management system maintained by EPA to
track permit compliance and enforcement status of facilities regulated by the NPDES under the Clean
Water Act. ICIS-NPDES is designed to support the NPDES program at the state, regional, and national
levels, and contains discharge monitoring and permit data from facilities in all point source categories
who discharge directly to receiving streams.
EPA identified pollutant parameter codes in ICIS-NPDES specific to asbestos (such as asbestos, fibrous
asbestos, asbestos (chrysotile), asbestos (amphibole), asbestos fibers (ambiguous asbestos), and non-
chrysotile, non-amphibole asbestos fibers) and identified unique NPDES-permitted facilities, outfalls,
and locations for those asbestos parameters. EPA then cross-checked their identified standard industrial
codes (SIC) with SIC codes associated with the current asbestos users and COU. The results were that
none of these identified SIC codes were associated with current asbestos COU and were not considered
relevant for risk evaluation purposes.
EPA next did a specific NPDES permit search for facilities that may release asbestos (chlor-alkali and
sheet gasket facilities) based on gathered location and addresses for these sites. It was found that most
chlor-alkali facilities do have issued NPDES permits for industrial (major and minor permit status)
operations and for general stormwater and construction stormwater projects. Yet for the identified
permits for these industrial subcategories, none of the NPDES limits/monitoring requirements contained
asbestos or asbestos-related parameters codes or any direct effluent screening information for asbestos.
Based on the analysis, EPA found no current surface water releases of asbestos or exceedances in the
ICIS-NPDES database.
EPA's Water Pollutant Loading Tool. EPA's Water Pollutant Loading Tool calculates pollutant
loadings from NPDES permit and Discharge Monitoring Report (DMR) data from EPA's ICIS-NPDES
for industrial and municipal point source dischargers. Data are available from the year 2007 to the
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present and also include wastewater pollutant discharge data from EPA's Toxics Release Inventory
(TRI). The Loading Tool was transitioned into ECHO to increase user access to data and streamline site
maintenance and EPA retired the legacy site (the Discharge Monitoring Report Loading Tool) on
January 24, 2018. DMR data identifies the permit conditions or limits for each water discharge location,
the actual values, identified by the permittee, for each monitored pollutant that was discharged, and
whether or not the amounts discharged exceeded the permit limits.
DMR was used to help identify facilities with current uses that discharge asbestos to surface water.
Information was obtained from the DMR Pollutant loading tool accessed on December 1, 2017.
Facilities were identified using two different search methods: 1) "EZ Search" which identifies facilities
that submit Discharge Monitoring Reports (DMRs) and 2) "Toxics Release Inventory (TRI) Search"
which identifies facilities that report releases to the TRI. Searches were conducted for the two most
current (and complete) years in the tool: 2015 and 2016 for DMR facilities, and 2014 and 2015 for TRI
facilities.
TRI data indicate no releases of asbestos in 2014 and 2015 (only friable asbestos is subject to reporting).
The DMR database reported just one facility reporting a discharge in 2014 and 2015 (accessed on
December 1, 2017) and this facility has been identified as a mining facility in Duluth, Minnesota. Later,
in a subsequent search (October 10, 2018) this facility was no longer identified on the DMR. The DMR
reported a total of zero pounds released in 2014 and 2015 but did provide maximum and average
effluent concentrations (mg/L) of allowable asbestos. It is assumed that the entry referred to mining
runoff, since asbestos has not been mined or otherwise produced in the United States since 2002. EPA
has currently not identified in the existing literature or through consultation with industry any evidence
of discharge to surface water from DMR or TRI database as to any current uses of asbestos (release
from sheet gaskets, release from working on industrial friction products and/or release from asbestos
diaphragms from chlor-alkali facilities). Based on this database no water dischargers were established.
EPA did a search of the database for the parameter description of asbestos and identified three facilities
reporting actual limit values of discharge of asbestos to surface water. One of facilities was the mining
facility identified earlier on DMR and the other was a quarry. The third was an electric facility. Two
other electric facilities were also reported. These facilities were not directly related to the current uses of
asbestos mentioned earlier.
STORET. STORET refers overall to "STORage and RETrieval", an electronic data system for water
quality monitoring data developed by EPA. Since about 2000, STORET has referred to a local data
management system ("Modernized STORET") as well as data repository ("STORET Data Warehouse")
developed for purposes of assisting data owners to manage data locally and share data nationally. Until
September 2009, the distributed STORET database has been used to compile data at the national level in
the STORET Data Warehouse. As of September 2009, the Water Quality Exchange, or WQX
framework, provides the main mechanism for submitting data to the STORET Data Warehouse.
EPA did not identify in STORET any evidence of discharge to surface water for the COUs of asbestos.
EPA also did not identify in the existing literature or through consultation with industry any evidence of
discharge to surface water.
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Appendix E Ecological Data Extraction Tables
JL JL O
The EPA has reviewed acceptable ecotoxicity studies for Chrysotile Asbestos according to the data
quality evaluation criteria found in the Application of Systematic Review in TSCA Risk Evaluations ("U.S.
18a). The ten "on-topic" ecotoxicity studies for asbestos included data from aquatic organisms
(i.e., vertebrates, invertebrates, and plants) and terrestrial species (i.e., fungi and plants). Following the
data quality evaluation, EPA determined that four "on-topic" aquatic vertebrates and invertebrate studies
were acceptable while the two "on-topic" aquatic plants studies were unacceptable as summarized in the
Table APX E-l below. In the PF, it was determined that the terrestrial exposure pathways, including
biosolids, to environmental receptors was not within the scope of this assessment. As a result, EPA
excluded three studies on terrestrial species from further analysis as terrestrial exposures were not
expected under the conditions of use for asbestos. One amphibian study was excluded from further
review because it was not conducted on chrysotile asbestos. Ultimately four aquatic toxicity studies
were used to characterize the effects of chronic exposure of chrysotile asbestos to aquatic vertebrates
and invertebrates, as summarized in Table 3-1 Environmental Hazard Characterization of Chrysotile
Asbestos.
The results of these ecotoxicity study evaluations can be found in Chrysotile Asbestos (CASRN1332-21-
4) Systematic Review: Supplemental File for the TSCA Risk Evaluation Document. The data quality
evaluation indicated these studies are of high confidence and are used to characterize the environmental
hazards of Chrysotile Asbestos. The results of these studies indicate that there are adverse effects to
aquatic organisms following exposure to chrysotile asbestos.
TableAPX E-l. Summary Table On-topic Aquatic Toxicity Studies That Were Evaluated for
Chrysotile Asbestos.
Species
Freshwater/
Salt Water
Duration
End-
point
Concentration
(s)
(MFL=
Millions of
fibers per
liter)
Effcct(s)
Reference
Data Quality
Evaluation
Rating
Asiatic Clams
Freshwater
30d
LOEC <
10s fibers/L
Gill Tissue Altered
CBelaneer et aL
High
(Corbicula
sp.)

108
fibers/L
(100
MFL)
100 MFL

1986b)

30d
Reproduct
ive LOEC
= 104
fibers/L
(0.01MFL
)
104-108 fibers/L
0.01-100 MFL
Increase in Larvae
mortality/ decrease in
larvae released

96hr-30d
No
mortality
observed;
NOEC
>108
fibers/L
102-108 fibers/L
0.0001-100 MFL
Mortality

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Species
Freshwater/
Salt Water
Duration
End-
point
Concentration
(s)
(MFL=
INIi 1 lions of
fibers per
liter)
Effcct(s)
Reference
Data Quality
Evaluation
Rating

(>100
MFL)

30d
LOEC=
108
fibers/L
(100
MFL)
102-108 fibers/L
0.0001-100 MFL
Growth

30d
NOEC <
108
fibers/L
(<100
MFL)
LOEC =
108
fibers/L
(100
MFL)
102-108 fibers/L
0.0001-100 MFL
Fiber Accumulation

96hr-30d
LOEC =
102
fibers/L
(0.0001
MFL)
102-108 fibers/L
0.0001-100 MFL
Siphoning Activity

Asiatic Clams
(Corbicula
fluminea)
Freshwater
30d
LOEC <
102
fibers/L
(<0.0001
MFL)
102-108 fibers/L
0.0001-100 MFL
Reduction in
siphoning activity
(Belanger et al,
1986a)
High

30d
LOEC <
108
fibers/L
(<100
MFL)
108 fibers/L
100 MFL
Presence of asbestos
in tissues

Coho Salmon
(Onchorhync
hus kisutch)
Saltwater and
freshwater
40-86d
NOEC =
1.5xl06
fibers/L
(1.5
MFL)
LOEC =
3.0xl06
fibers/L
(3 MFL)
1.5xl06 fibers/L,
3.0xl06 fibers/L
1.5 MFL, 3MFL
Behavioral stress
(aberrant swimming,
loss of equilibrium)
Sublethal effects
including: epidermal
hypertrophy
superimposed on
hyperplasia, necrotic
epidermis, lateral line
degradation, and
lesions near the
branchial region
(Belanger et al,,
1986c~l
High
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Species
Freshwater/
Salt Water
Duration
End-
point
Concentration
(s)
(MFL=
INIi 1 lions of
fibers per
liter)
Effcct(s)
Reference
Data Quality
Evaluation
Rating

40-86d
No
significan
t
Mortality;
1.5xl06 fibers/L,
3.0xl06 fibers/L
Mortality

1.5 MFL, 3MFL

NOEC
>3.0xl06
fibers/L

(>3 MFL)

40-86d
No
Significan
t effect;
NOEC
>3.0xl06
fibers/L
(>3 MFL)
1.5x10 6 fibers/L,
3.0xl06 fibers/L
1.5 MFL, 3MFL
Growth

Green
Sunfish
(Lepomis
cyanellus)
Freshwater
52-67d
NOEC
<1.5xl06
fibers/L
(<1.5
MFL)
LOEC =
1.5x10 6
fibers/L
(1.5
MFL)
1.5xl06 fibers/L,
Behavioral stress
(aberrant swimming,
loss of equilibrium)
Sublethal effects
including: epidermal
hypertrophy
superimposed on
hyperplasia, necrotic
epidermis, lateral line
degradation, and
lesions near the
branchial region

40-86d
No
significan
t
Mortality;
1.5xl06 fibers/L,
3.0xl06 fibers/L
Mortality

1.5 MFL, 3MFL

NOEC
>3.0xl06
fibers/L

(3 MFL)

Japanese
Medaka
(Oryzias
latipes)
Saltwater and
freshwater
13-21d
No
significan
t effects;
NOEC
>106
fibers/L
106-1010 fibers/L
1 MFL-10,000
MFL
Egg development,
hatchability, survival.
1990)
High
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Species
Freshwater/
Salt Water
Duration
End-
point
Concentration
(s)
(MFL=
INIi 1 lions of
fibers per
liter)
Effcct(s)
Reference
Data Quality
Evaluation
Rating

(>1 MFL)

28d
LOEC =
106
fibers/L
(1 MFL)
NOEC =
104
fibers/L
(0.01
MFL)
106-1010 fibers/L
1 MFL-10,000
MFL
Significant reduction
in growth of larval
individuals

7w
Not
statisticall
y
analyzed
104-108 fibers/L
0.01-100 MFL
Reproductive
performance (viable
eggs/day, nonviable
eggs/day)

49d
LCioo=10
10 fibers/L
1010 fibers/L
10,000 MFL
100% Larval
mortality

Duckweed
(Lemna
Freshwater
28d
LOEC =
0-5(j.g
0.5-5.0 ng
chrysotile/frond
Decreased # fronds
(2007: Trivedi
et aL 2004)
Unacceptable
gibba)

chrysotile
/frond
0.5-5.0 ng
chrysotile/frond
Decreased Root
length

NOEC <
0-5(j.g
0.5-5.0 [ig
chrysotile/frond
Decreased
Chlorophyll Content

chrysotile
/frond
0.5-5.0 ng
chrysotile/frond
Decreased Carotenoid
content

0.5-5.0 [ig
chrysotile/frond
Decrease in biomass/
frond

0.5-5.0 ng
chrysotile/frond
Decreased Protein
content (mg/g fresh
wt)

0.5-5.0 ng
chrysotile/frond
Decreased Free sugar
(mg/g fresh wt)

0.5-5.0 [ig
chrysotile/frond
Decreased Starch
(mg/g fresh wt)

0.5-5.0 |xg
chrysotile/frond
Decreased
photo synthetic
pigments

0.5-5.0 [ig
chrysotile/frond
Increased lipid
peroxidation

0.5-5.0 |xg
chrysotile/frond
Increased cellular
hydrogen peroxide
levels

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Species
Freshwater/
Salt Water
Duration
End-
point
Concentration
(s)
(MFL=
INIi 1 lions of
fibers per
liter)
Effcct(s)
Reference
Data Quality
Evaluation
Rating

0.5-5.0 |xg
chrysotile/mL
Increase in catalase
activity

8883
8884
8885
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8886 Appendix F Environmental Fate Data Extraction Table
8887
8888 Environmental Fate Study Summary for Asbestos
8889
8890 Table APX F-l. Other Fate Endpoints Study Summary for Asbestos
Sj stem
Siuclj 1 \pe lu'sir)
Results
( OlllllieillS
AITiliiilod
Reference
Diilii Qiinlih
l-'.\iiliiiilion
Results ol-
l-iil 1 Siuclj
Report
Non guideline,
experimental study;
the effect of lichen
colonization on
chrysotile structure
is investigated by
analyzing the
composition of
both colonized and
uncolonized field
samples. The effect
of oxalic acid
exposure on
chrysotile structure
is also investigated
at various
concentrations.
Chrysotile fibers were
incubated in oxalic acid
solutions for 35 days to
observe its effect on
MgO content. Chrysotile
(both uncolonized or
colonized by lichens)
from 3 serpentinite
outcrops and one
asbestos cement roof
were collected.
In the three asbestos outcrops
and asbestos-cement roof,
MgO content (wt %) was
lower by 15-20% in lichen
colonized chrysotile than in
uncolonized chrysotile.
Incubation in 50 mM oxalic
acid transformed chrysotile
fibers into "an amorphous
powdery material, consisting
mainly of pure silica", and
without fibrous nature.
The reviewer
agreed with
this study's
overall quality
level.
(Favero-
Loneo et
a.L 2005)
High
Non guideline,
experimental study;
oxalic acid and
citric acid leaching
of asbestos rich
sediment
Asbestos rich sediment
and a serpentine bedrock
sample underwent
leaching in 0.025 M
oxalic acid and 0.017 M
citric acid. Total
elemental analysis was
performed using
inductively coupled
plasma spectrometry
(ICPS), individual fiber
analysis was done using
energy dispersive x-ray
analysis (EDX) and a
scanning and
transmission electron
microscope (STEM).
ICPS results showed citric
acid was slightly more
effective at removing most
metals from the sediment
samples than oxalic acid;
however, EDX analysis of
individual fibers showed
Mg/Si ratios were reduced
from 0.68-0.69 to 0.07 by
oxalic acid and only to 0.38
by citric acid.
The reviewer
agreed with
this study's
overall quality
level.
(Schreier et
at. 1987)
High
Non-guideline,
experimental study;
decomposition
study of asbestos in
25% acid or caustic
solutions
Chrysotile, crocidolite,
amosite, anthophyllite,
actinolite, and tremolite
asbestos fibers were
dissolved in 25% acid or
NaOH solution
Degradation in 25% HC1,
acetic acid, H3P04, H2S04
and NaOH, respectively was
reported for
Chrysotile (55.69, 23.42,
55.18, 55.75 and 0.99%),
Crocidolite (4.38, 0.91, 4.37,
3.69 and 1.35%), Amosite
Due to limited
information
assessing the
results were
challenging.
(Soeil and
Leineweber.
1969)
Unacceptable
Page 263 of 310
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(12.84, 2.63, 11.67, 11.35 and
6.97%),
Anthophyllite (2.66, 0.60,
3.16, 2.73 and 1.22%),
Actinolite (20.31, 12.28,
20.19, 20.38 and 9.25%) and
Tremolite (4.77, 1.99, 4.99,
4.58 and 1.80%).

8891
8892
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8893 Table APX F-2. Hydrolysis Study Summary for Asbestos
Siiulj Tjpe
(je.ir)
pll
Tempcriiliire
Dui'iilioii
Komi lis
( ommi-ills
AITiliiilod
Reference
Diilii
Qu;ilil>
l-'.\iiliiiilion
Results of
l ull Sluclj
Report
Non-guideline,
experimental
study;
dissolution of
asbestos in water
at various pH
and
temperatures.
7, 7, 7, 9,
and 4 for
experiments
1-5,
respectively
44, 6, 25, 25,
and 25°C for
experiments
1-5,
respectively
170 or
1024
hours
170-hour study results
evaluating Mg removal
from Chrysotile
(proportion of 1 layer):
Experiments 1-4: 0.32-
0.94.
Experiment 5 (pH 4,
25°C): 8.84
170-hour study results
evaluating Si removal
from Chrysotile
(proportion of 1 layer):
Experiments 1-4: 0.5-0.25.
Experiment 5: 5.05.
170-hour study results
evaluating Mg removal
from Crocidolite
(proportion of 1 layer):
Experiments 1-5: 0.42-
1.80.
170-hour study results
evaluating Si removal
from Crocidolite
(proportion of 1 layer):
0.03-0.56.
1024-hour results
(proportion of one layer
removed) for experiment 3
only:
Chrysolite, Mg: 0.94; Si:
0.36 Crocidolite, Mg:
1.42; Si: 0.37
The
reviewer
agreed
with this
study's
overall
quality
level.

High
Non-guideline;
dissolution
study; sample
size, temperature
andpH
evaluated; pH
change over time
compared for
asbestos
minerals,
amosite and
crocidolite and
chrysotile
5.9-6.1
(initial)
5 to 45 °C
20 min;
1000
hours
Rate of dissolution is a
function of surface area
and temperature. Mg2+
may be continuously
liberated from fibers
leaving a silica skeleton.
The rate-controlling step
was determined to be
removal of brucite layer.
Smaller particles liberated
more magnesium
The
reviewer
agreed
with this
study's
overall
quality
level.
(Choi and
Smithy
.1.972)
High
Non guideline;
experimental
study; a particle
Not
reported but
Not reported
but held
constant
3-5 days
Chrysotile in natural water
acquires a negative
surface charge by rapid
The
reviewer
agreed
(Bales and
Morgan.
.1.985)
High
Page 265 of 310
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Siudj T>|K*
(jcsir)
pll
1 ciii|R'r;i(iMV
Diinilion
Komi lis
( oinnioiils
AITiliiilod
KoI'oiviico
Diilii
Qu:ilil>
r.\iiiiiiiiion
Results ol
l ull Sliid>
Kcporl
electrophoresis
apparatus was
used to monitor
absorption
properties of
chrysotile
asbestos aging in
water
held
constant

adsorption of natural
organic matter (<1 day).
Positively charged >Mg-
OH2+ sites are removed by
dissolution in the outer
brucite sheet resulting in
exposure of underlying
>SiO" sites.
with this
study's
overall
quality
level.

8894
8895
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8896 Table APX F-3. Aquatic Bioconcentration Study Summary for Asbestos
Siiulj Tjpe
Ijcsir)
Iniliiil
( i>iiiTiilr;ilioii
Species
Dui'iilioii
Kosu II
( oiiimi-ills
AITiliiilcri
Reference
Diilii
Qu;ili(\
l'.\iiliiiilion
Results of
l ull Siiulj
Report
Non-guideline;
experimental
study; uptake
monitoring of
chrysotile
asbestos in
Coho and
juvenile green
sunfish
1.5><106and
3.0x10s
fibers/L
Coho salmon
(Oncorhynchus
kisutch) and
juvenile green
sunfish
(Lepomis
cyanellus)
Coho
salmon: 86
and 40
days;
Green
sunfish: 67
and 52
days
Asbestos fibers were
found in the asbestos-
treated fish by
transmission
electron microscopy
(TEM); however total
body burdens were
not calculated.
Sunfish lost scales
and had epidermal
tissue erosion.
Asbestos fibers were
not identified in
control or blank
samples.
The
reviewer
agreed
with this
study's
overall
quality
level.
(IB danger
ef al.„
1986c)
High
Non-guideline;
experimental
study; uptake
monitoring of
chrysotile by
Asiatic clams
2.5xl08-
8.8xl09
fibers/L
Asiatic clams
(Corbicula sp.)
96-hours
and 30-
days
Chrysotile asbestos
was detected in clams
at 69.1±17.1
fibers/mg whole body
homogenate after 96
hours of exposure to
108 fibers/L and food.
Chrysotile asbestos
was detected in clams
after 30 days of
exposure to 108
fibers/L at 147.3±52.6
fibers/mg dry weight
gill tissue and
903.7±122.9
fibers/mg dry weight
visceral tissue.
Chrysotile asbestos
was not detected in
clams after 96 hours
at all asbestos
exposure
concentrations tested
with no food.
The
reviewer
agreed
with this
study's
overall
quality
level.
(B elan get'
et at.
1986b)
High
Non-guideline;
experimental
study;
measuring
uptake of
chrysotile
asbestos by
Asiatic clams
0, 104, and 108
fibers/L
Asiatic clams
0Corbicula sp.,
collected in
winter and
summer)
30-days
Fibers were not
detected in clams
from blank control
groups and after
exposure to 104
fiber/L groups for 30
days.
Asbestos
concentration in tissue
after exposure to 108
fiber/L for 30 days
The
reviewer
agreed
with this
study's
overall
quality
level.
(B elan get'
et at.
1986a)
High
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(fibers/mg dry weight
tissue) in winter
samples: Gills:
132.1±36.4; Viscera:
1055.1±235.9 and
summer samples: Gill:
147.5±30.9; Viscera:
1127.4±190.2.

Non-guideline;
experimental
study; BCF
determination
of asbestos in
the Asiatic
clam
0, 104, and 108
fibers/L
Asiatic clam
(corbicula sp.)
30 day and
field
exposed
BCF = 0.308 in gill
tissue, 1.89 in viscera
tissue, and 1.91 in
whole clam
homogenates after 30-
days exposure to 108
fibers/L.
Field exposed BCFs =
0.16-0.19 in gills,
64.9-102 in viscera,
1,442-5,222 in whole
clams.
The
reviewer
agreed
with this
study's
overall
quality
level.
(B danger
et al.
1987)
High
Non-guideline;
experimental
study;
chrysotile
asbestos
uptake study in
Japanese
Medaka
5.1±2.8xl06,
7.6±8.1xl08
fibers/L
Japanese
Medaka
(Oryzias
latipes)
13 weeks
After 28 days of
exposure to chrysotile
asbestos at 101CI
fibers/L
concentrations, fish
total body burden was
375.7 fibers/mg. After
3 months of exposure
to chrysotile asbestos
at 108 fibers/L
concentrations, fish
total body burden was
486.4±47.9 fibers/mg.
The
reviewer
agreed
with this
study's
overall
quality
level.
(B danger
ef al.
1990)
High
8897
8898
8899
Page 268 of 310
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8900
8901
8902
8903
8904
8905
8906
8907
8908
8909
8910
8911
8912
8913
8914
8915
8916
8917
8918
8919
8920
8921
8922
8923
8924
8925
8926
8927
8928
8929
8930
8931
8932
8933
8934
8935
8936
8937
8938
8939
8940
8941
8942
8943
8944
8945
8946
8947
8948
8949
8950
8951
8952
8953
8954
8955
8956
8957
8958
8959
8960
8961
8962
8963
8964
8965
8966
8967
8968
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Appendix G SAS Codes for Estimating Kl and Km from
Grouped Data
\S code estimates c l for I uii , n r potency (KL) 'oisson maximum likelihood
ii i :)n (lMLE)f alonq wit l l c in i j n interval (CI) c xi using the likelihood prof
I The basic model is l l I • CE'J i 1 \ )
:ode was created by Rebekha Shaw and Bill Thayer at SRC Inc. This is version 1„0 /*
/*This is where the code begins execution, */
/ * Tin e first step is to create a data table */
data Data_Table;
input CE10_min CE10_max CE10_mid Observed Expected RR;
/ * e n t e r d a t a h e r e * /
datalines;
0 20 10.0 6 5.75 1.04
20 100 60.0 12 2.82 4.25
100 450 275.0 17 1.57 10.82
450 1097 773.5 21 1.23 17.07
/* Enter text strinq to identify data source */
title "Wang et al 2013";
/*model */
proc nlmixed data=Data_Table;
parms KLE2 10; /* KLE2 :::::: KL* 1E + 02. The initia 1 guess is 10. This can be changed if a solution is not
found (unlikely) „ */
Predicted = (1 + CE10 mid*KLE2/10Q) * Expected; / "k equation to ca leu la te predicted number of lung cancer
cases*/
LL=LogPDF ( " POISSON" , Observed, Predicted) ; /*Lourni'' ium Returns the logarithm of a probability
d e i "i s i t y (rn a s s ) f u n c t i o i i. P o i s s o i i d i s t r i b u t i o i ' * /
model Observed ~ general(LL);
estimate 'KLE2' KLE2 ALPHA=0.1;/^generates "Additional Estimates" table in the Results tab with Wald 90%
CI*s*/
predict Predicted out=Predicted alpha=0.1; /*generates SAS data table with predicted values and CI's
t i 11 e d " P r e d i c t e d " * /
ods output FitStatistics = FitStats;
ods output ParameterEstimates = ModelParams;
Proc print data=Predicted;/*Prints the "Predicted" table in the Results tab*/
run;
data _null_;
set Fitstats;
if _n_ =1;
LLTarget = (Value/-2)-1.353;/*calculates LL target needed to run macro PoissonLLBounds*/
call s ymp u t x ('' L L T a r g e t'', L L T a r g e t) ; / * c r e a t e s m a c r o v a r i a b 1 e * /
run;
data _null_;
set ModelParams;
KLMLE = Estimate*le-02; /*\
KLINITLB= E s t i m a t e *1e-0 2/1C;
rn a c r o p o i s s o i i L L B o u n d s * /
KLINITUB= Estimate*le-02*10; /*Ca 1cu1ates 11ie
m a c r o P o i s s o i "i L L B o u n d s * /
call symputx("KLMLE", KLMLE);/*creates macro
call symputx("KLINITLB", KLINITLB);/*creates i
call symputx("KLINITUB", KLINITUB);/*creates
mds*/
1. o w e r b o u n d v a r i a b 1 e K L
gu e s s for th e uppe r bou nd vari ab1e KL
:..,B in
1,B in
Page 269 of 310
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8969 run;
8970
8971 / * T1 'i i s i s 11 'i e rn a c r o w 1 'i i c 1 "i c a 1 c u 1 a t e s 11 "i e 9 0 % c o i "i :f i d e i "i c e i i "i t e r v a 1 u s i i "i q 11 "i e 1 i k e 1 i 1 "i o o d p r o :f i 1 e rn e 11 "i o d - 11
8972 is executed a f ter the MLE soution 1 "ia s beei"i f ound /
8973 %macro PoissonLLBounds(inputData=, KL MLE=, KL Init LB=, KL Init UB=,
8974 conv criterion=, LL tarqet=, max iteration=);
8975 - -
8976 %Let dsid=%sysfunc(open(&inputdata)); * open the input data file;
8977 %Let NumSamples = %sysfunc ( attrn ( &dsid, nobs ) ) ; * qet the number of observations;
8978 %Let rc=%sysfunc(close(&dsid) ) ; * close the data file;
8979
8980 %Do j=l %To 2; * one for upper bound and one for lower bound;
8981
8982 %If %eval(&J=l) %then %Let KL=&KL init LB;
8983 %If %eval(&J=2) %then %Let KL=&KL Init UB;
8984 " "
8985 %Let i=l; * first time throuqh loop;
8986
8987 %Let ConvFactor = 10;
8988 %let ConvRate = %sysevalf(((&KL MLE-&KL)/&KL MLE)/10);
8989
8990 %Let ConvDirect = -1;
8991 / * i 'i e q a t i v e:::::: f r o rn 11 "i e 1 e f t a i "i d p o s i t i v e:::::: f r o m 11 "i e r i q 1 "i t- F o r 1 o w e r b o u n d F t1 "i e i i "i i t i a 1 q u e s s i s 1 e s s 11 "i a i "i
8992 11 "i e t a r q e t L L s o 111 e i i i i t i a 1 v a 1 u e o f c o i i v d i r e c t i s -1 * /
8993
8994 %Let KLAdj ust=%Sysevalf(-1* &ConvDirect* &KL* &ConvRate);
8995
8996 %Do %Until (%sysevalf(&DeltaLL < &conv criterion) OR %sysevalf(&i > &max iteration));
8997
8998 Data tempDataLLBound; Set &InputData;
8999 Predicted = (1 + CE10 Mid * &KL) * Expected;
9000 LL=(LogPDF("POISSON",Observed,Predicted)); * likelihood for each
9001 o b s e r v a t i o i "i;
9002 LL sum+LL;
9003 output;
9004 Run;
9005
9006 Data TempDataLLBound2; Set tempDataLLBound;
9007 If N = &NumSamples;
9008 NumLoops=&i;
9009 thisKL=&KL;
9010 ConvRateVar=&ConvRate;
9011 ConvFactorVar=&ConvFactor;
9012 ConvDirectVar= %eval(SConvDirect);
9013
9014 KLAdj ustVar=(-l*ConvDirectVar)^thisKL^ConvRateVar;
9015 If &ConvDirect=-l then DiffLL=abs(LL sum)-abs(&LL Target);
9016 Else DiffLL=abs(&LL Target)-abs(LL Sum);
9017
9018 /* Test if 1m - dii t i i >>n t h- r > > 11 - i qence. It w li 'hi'' t i>>n
9019 (subtract from cui i' lit ilu- if we r i I'I'Immi 1" t'U' ,) and ci i ill' >'ii ' it ii' ' i it'
9020 (ConvRate) bv a factor ' ''ii I " t-i k /
9021
9022 if DiffLL<0 then
9023 do; / "k i "i e e d t o c 1 "i a i "i q e d i r e c t i o i "i s a i "i d m a k e c o i "i v r a t e m o r e q r a d u a 1 "k /
9024 ConvDirectVar= %eval(-1*&ConvDirect);
9025 ConvRateVar=%sysevalf(&convRate/&ConvFactor);
9026 KLAdj ustVar=(-l*ConvDirectVar)^thisKL^ConvRateVar;
9027 call symput( 'KLAdj ust',KLAdj ustVar);
9028 call symput('ConvDirect',ConvDirectVar);
9029 call symput('convRate',ConvRateVar);
9030 end;
9031 AbsDi ffLL=abs(Di ffLL) ;
9032
9033 call symput( 'DeltaLL',ABsDiffLL);
9034
9035 output;
9036 Run;
9037
9038 Data tempAHOutput; if N =1 then Set TempDataLLBound2; Set tempDataLLBound; Run;
9039
9040 %If %eval(&i=l) %then %do; Data AllOutput; Set tempAHOutput; Run; %end;
9041
9042 %If %eval(&i>l) %then %do; Proc Append base=A110utput data=tempA110utput; Run;
9043 %End;
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
9044
9045 %Let i=%eval(&i+l);
9046
9047 %Let KL=%sysevalf(&KL + &KLAdjust);
9048
9049 %End;
9050
9051 %If %eval(&J=l) %then
9052 %Do;
9053 Data tempoutl; length limit $5; Set TempDataLLBound2; limit='lower';
9054 estimate=thisKL; LogLikelihood=LL sum; loops=numloops; Run;
9055 %End;
9056 % If %eval(&J=2) %then
9057 %Do;
9058 Data tempout2; length limit $5; Set TempDataLLBound2; limit='upper';
9059 estimate=thisKL; LogLikelihood=LL sum; loops=numloops; Run;
9060 %End;
9061 %End;
9062
9063 Data PrntOutput; Set tempoutl tempout2; run;
9064
9065 Proc print data=PrntOutput; var limit estimate LogLikelihood Loops ; Run;
9066
9067 %Mend;
9068
9069 /*run macro PoissonLLBounds*/
9070 ¦sPoissonLLBouncLs ( inputData—Data Table,
9071 KL MLE=&KLMLE,
9072 KL Init LB=&KLINITLB,
9073 KL Init UB=&KLINITUB,
9074 conv criterion=0.001,
9075 LL target=&LLTarget,
9076 max iteration=100);
9077 run;
9078
9079 /11 "i e f o 11 o w i i "i q c o d e c r e a t e s a s u rn rn a r v t a be w i 11 "i t lie M L E K L E a i "i d c o i "i f i d e i "i c e b o un d s /
9080 PROC SQL;
9081 CREATE TABLE WORK.MLEKL AS
9082 SELECT ("MLE KLE") AS Parameter,
9083 (tl.Estimate*le-2) AS Value
9084 FROM WORK.MODELPARAMS tl;
9085 QUIT;
9086
9087 PROC SQL;
9088 CREATE TABLE WORK.LBKLUBKL AS
9089 SELECT (case
9090 when tl.limit="lowerM then "5% LB KL"
9091 else "95% UB KL"
9092 end) AS Parameter,
9093 tl.estimate AS Value
9094 FROM WORK.PRNTOUTPUT tl;
9095 QUIT;
9096
9097 PROC SQL;
9098 CREATE TABLE WORK.Parameter Values AS
9099 SELECT * FROM WORK.MLEKL
9100 OUTER UNION CORR
9101 SELECT * FROM WORK.LBKLUBKL
9102 ;
9103 Quit;
9104
9105 Proc print data=Work.Parameter_values;
9106 run;
9107
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9182
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
/*Th;is SAS code es Lima t.es a value for iik v ;¦ 'I lie I i una potency (KM) using Poisson maximum likelihood estimation (MT.,E), along with the 90% confidence interval (CI)
genera ted using the 1 ikel ihood pr of .11 n n m
This code was created by Rebelcha Shaw a i iu iilh Thayer at SRC Inc.
This is version 1.0*/
/*Th;is is where the code begins execution. */
data Data_Table;
input TSFE_Min TSFE_Max TSFE_Mid Duration Cone PY Obs ;
/'''The values of TST.'T/; Mid and Duration are used to calculate a parameter called Q. * /
if TSFE_Mid=„ then Q =
else if TSFE_Mid<:iQ then Q = q;
else if TSFE_Mid>(lO+duration) then
Q = (TSFE_Mid-10)**3-(TSFE_Mid-10-duration)**3;
else Q =(TSFE_Mid-10)**3;
/'''enter data here. The contents of the columns are as follows:
TST.'T; Min (years)
SFE Max (years)
TST.'T; Mid (years)
Dxir a Li on (yea r s )
Cone (f/cc)
Person Years (PY)
Observed cases(Obs)
*/
20 30 27.7 1.00 6.5 1926 0
30 40 33.9 2.10 8.7 6454 0
40 50 43.1 3.00 14. 6 3558 2
50 72 53.56 5.78 31.4 1080 2
/*enLer Lhe name of Lhe da La set.*/
title "North Carolina Sub Co-hort (1999-2003;4 groups)";
proc nlmixed data= Data_Table;
parms KME8 10; /*KMF8 is egual i" kit u'.iun. The sLarLing guess is 10. This can be changed in Lhe unexpecLed case where a soluLion is not. found*/
Pred = Conc*Q*PY*KME8/le+-0S; /*'",hmi inn in calculaLe pred.ict.ed va.'hies*/
LL=LogPDF (" POISSON", Obs, Pred) ; /¦ i.iugi.'ui.1 i.unct.ion ReLurns Lhe logari t.h.m of a probabiliLy densi t.y (mass) funct.ion. Poisson di sLr ibuLi on is specified.*/
model Obs ~ general(11);
estimate 'KME8' KME8 ALPHA=Q, l ;/* genera t.es "Addi Lional Es Lima Les" t.a.b.le in Lhe ResulLs Lab wi t.h 90% Wald CI's - t.h.ls can be de.Iet.ed if we do not. want. Lhe Wald CIs
displayed in Lhe SAS ouLput. */
predict Pred out=Predicted alpha=0.'l; /*generat.es SAS dat.a t.ab.le wi t.h pred.ict.ed values and CI's Li Lied "Pr edi c: Led"* /
ods output FitStatistics = FitStats;
ods output ParameterEstimates = ModelParaias;
Proc print data=Predicted; / * Pr i n t.s Lhe "Pred.ict.ed" t.ab.le in Lhe ResulLs Lab*/
OPTIONS MPRINT SYMBOLGEN ;/*t.h;is pr.int.s in Lhe log what, value is used for each variable in Lhe macro*/
data _nuH_'
set Fitstats;
if _n_ ='.L ;
LLTarget = (Value/-2) -1 .. 353 ;/* cal c:\i.la t.es T.,T., t.arget. - needed t.o run macro Pol ssonT.,T.,Bounds* /
call syiaputx ( "LLTarget" , LLTarget );/* cr ea t.es macro variable*/
data _null_;
KMMLE = Estimate*le-B; /*:.¦'... i i n:. Mm' km nnr, y.iini' n. ¦! mi . 11 ni; i.w Proc nlmixed - v.n ii.ii.~ji.' r,n nnr, in nn.i' v u Pol ssonLT.,Bounds*.
KMINITLB= Estimate*le-8/in; /' i..'., I r.n JI. • I h" mil n.iJ ¦:. |..i llm lower bound - va v j , 11 .> I ¦¦ KM il.il 1,1' n
KMINI TUB= Estimate*le-S*in; / ' ii J i.. n i. 11 n: ¦ ui" nil mi im i in.' upper bound - va i < .11 > J ¦¦ kii n i I nr. in
call syiaputx ( "KMMLE", KMMLE );/* cr ea t.es macro va r i. ib'l n'1'/
call syiaputx ( "KMINITLB" , KMINITLB ) ;/* cr ea t.es maci" v.-.i < i, ih I ¦¦'/
call syiaputx ("KMINITUB", KMINITUB ) ;/* cr ea t.es mac 7
/*Th;is is Lhe macro which calculat.es Lhe 90% confidence int.erval xis.ing Lhe .1 :i lcel i hood profile met.hod. It. is execuLed aft.er Lhe MI ,!¦; solxU'.ion has been found */
PoissonLLBounds(inputData=, KM_MLE=, KM_Init_LB=, KM_Init_UB=,
conv_criterion=, LL_target=, iaax_iteration=);
Page 272 of 310
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%If % eval(&J=l) % then %Let KM= & KM_i ni t_LB;
%If % eval(&J=2) % then %Let KM= & KM_Ini t_UB;
%Let i=l; * first. Lime through loop;
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
9183 ^ Let ds id—o sy s f Line ( op en ( & inputdat a) ) ; ope? n the It ipu t da La 111 0 ;
9184 %Let NumSaiaples=%sysfunc (attrn( Sdsid, nobs ) ) ; * get the number of: observa l".:i oris,"
9185 %Let rc=%sysfunc(close(&dsid) ) ; * close the data file;
9186
9187
9188
9189 %Do j—i %To 2: * orie for upper benvnd arid orie for lower bound;
9190
9191
9192
9193
9194
9195
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9197
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9199
9200
9201
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9253
9254
9255
9256
9257
%Let ConvFactor = 10;
%let ConvRate = %sysevalf(( (&KM_MLE-&KM)/&KM_MLE)/10);
%Let ConvDirect = -1;
/* nega Live^f 1:0m the left and posi Liv e^f 1: om the right. For lower bound, the initial guess is less than the target T.,1, so the initial value of convdirect is -1 * /
%Let KMAdjust=%Sysevalf(-1* SConvDirect* &KM* SConvRate);
%Do %Until (%sysevalf(SDeltaLL < Sconv_criterion) OR %sysevalf(&i > &max_iteration));
Data tempDataLLBound; Set SlnputData;
E = Cone * Q * PY * &KM;
LL=(LogPDF("POISSON",Obs,E)); * likelihood for each observation;
LL suia+LL;
output;
Run;
Data TempDataLLBound2; Set tempDataLLBound;
If _N_= SNumSaiaples;
NumLoops=&i;
thisKM=&KM;
ConvRateVar=&ConvRate;
ConvFactorVar=&ConvFactor;
ConvDirectVar= %eval(SConvDirect);
KMAdjustVar=(-1*ConvDirectVar)*thisKM*ConvRateVar;
If &ConvDirect=-:i then DiffLL=abs (LL_suia) -abs (&LL_Target) ;
Else DiffLL=abs(&LL_Target)-abs(LL_Sum);
/* Test if we have changed direction on the convergence. If we have, change direction (subtract from current value? if we were adding before,
and decrease the convergence rate (ConvRate) by a factor == ConvT/'a c tor . * /
if DiffLLi) %then %do; Proc Append base=A110utput data=tempA110utput; Run; %End;
%Let i=%eval(&i+l);
%sysevalf(&KM + SKMAdjust);
%If %eval(&J=i) %then
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9284
9285
9286
9287
9288
loops=numloops; Run;
%If %eval(&J=2) %then
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Data tempoutl; length limit $5; Set TempDataLLBound2; lirait=' lower' ; estiraate=thisKM; LogLikelihood=LL ;
Data tempout2; length limit $5; Set TempDataLLBound2; limit='upper'; estimate=thisKM; LogLikelihood=LL ;
loops=numloops; Run;
Data PrntOutput; Set tempoutl tempout2;
Proc print data=PrntOutput; var limit estimate LogLikelihood Loops ; Run;
?o:issonT.,T.,Bounds*/
% PoissonLLBounds ( inputData=Data TaJDle,
KM_MLE= &KMMLE,
KM_Init_LB=&KMINITLB,
KM_Init_UB=&KMINITUB,
conv_criterion=0.001,
LL_target=&LLTarget,
max_iteration=ioo) ;
Page 274 of 310
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9289
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9298
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9300
9301
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9304
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9310
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9317
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9319
9320
9321
9322
9323
9324
9325
9326
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Appendix H BEIRIV Equations for Life Table Analysis
Lung Cancer
Let ei be the calculated excess relative risk of lung cancer in an exposed individual at age i.
Then:
Excess Lifetime Risk = Re/( — ROh
110
ro„=2ro,
i=1
110
Re/( = X Re,
i=1
ht
he
Re, = —^Seu(l-qei)
hei
het = ht (1 + ei)
lie] = //* + hjej
q, = exp(~h* )
qet =exp (-he*)
K-%,
j= 1
i-1
Seu =]JgeJ
j=i
where:
iandj = Year index (1 = year 0-1, 2 = year 1-2, etc.)
ROit = Lifetime risk of lung cancer in the absence of exposure
Reit = Lifetime risk of lung cancer in the presence of exposure
R0i = Risk of lung cancer in the absence of exposure in year i
Rei = Risk of lung cancer the presence of exposure in year i
hi = Lung cancer mortality rate in the absence of exposure in year i
hi* = All-cause mortality rate in the absence of exposure in year i
qi = Probability of surviving year i, all causes acting (no exposure)
qei = Probability of surviving year i, all causes acting (with exposure)
Si,i = Probability of surviving up to start of year i, all causes acting (no exposure)
Sei,i = Probability of surviving up to start of year i, all causes acting (with exposure)
Page 275 of 310
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9327
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9330
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9332
9333
9334
9335
9336
9337
9338
9339
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Mesothelioma
The same basic approach is followed for calculating lifetime risk of mesothelioma, except that the
baseline (un-exposed) risk is so small that it is generally assumed to be zero. Thus, the equations for
calculating lifetime mesothelioma risk are the same as above, except as follows:
mi = risk of mesothelioma in an exposed individual at age i
110
Re;, = X Re,
i=1
Re, =-^Seli(l-qei)
hel
Page 276 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
9340 Appendix I SAS Code for Life Table Analysis
9341 Lung Cancer Lifetable
9342
9343 /*
9344 il it. tin-? ii I iji Inn. iii i i i 11 j i n i nli hi n exposure to asbestos,
9345 u MM, ' I It. t ,l,|, ,o, I,. ¦!!„ I, I , I I = 1 - KL.
9346
9347 T1 "i e b a s i c c o d e :f o r 11"i e 1 i :f e t a b 1 e c a 1 c u 1 a t i o i i s w e r e d e v e 1 o p e d a r . d e d t o E P A
9348 by Randall Smith at NIOSH. The code from NIOSH calculates the ie risk (R0) and the exposed risk
9349 (Rx)
9350 from exposure to an exposure concentration of X Level usinq NIOoii nooel 2: Rx :::::: R0 "k (1 + COEF *
9351 X Level).
9352
9353 El I nodified tlie NI II t I Lows;
9354 1) 'i' ill . 111; 111 .Mid " i >¦1 f 1 uiKi '¦1.111 '¦1'111) i iii. .i i1 i . i 1 i i v d.ii.i tables have been updated
9355 2) tii'.1 r lor a ¦ i¦ i 111(.1 are for the rri.id---po.int of the veari
9356 (n ; , i t i , , ,, ia11 ,t , „ )
9357 3) A - RO) / ( 1 - RO)
9358 4) A i i i in/: i luii vi cids an extra risk of 0.01 (1%).
9359 Tin i i i i i ! i , I I Mil ii 1 ii 1 i il mI M ill unit risk: UR 0.01 / ECU
9360 */
9361 / * „ \Beta Version „ sa s 1 9"] an 00, 2 6"] ul 00, 25oct0.1., 06dec05, SOnovl 8
9362 : :
9363 E x p e r i rn e 111 a 1 v < -1 ¦;: i i. .i n
9364 : */
9365 title "Excess Risks using BEIR IV method to account for competing risks";
9366 title2 "Effects of airborne exposure to asbestos on lung cancer mortality rates";
9367 title3 "under a linear relative rate model ";
9368
9369 /* t
9370 I C o rn p u t e e x c e s s r i s k b v 11"i e B EIR IV rn e 111 o d u s i i i q S A S d a t a s t e p s „ |
9371 i
9372 I Hi 1 i i in nipute th iilt ii i < i t i.
9373 | < th M, th ,, noo of t ,1, Hi h! th u -
9374 i
9375 i
9376 I where
9377 i
9378 i
9379 I ¦; iii.' , v.,' i t ,' ¦¦ i (' 111 t ,. j i ii ut <\«.o re and
9380 i
9381 i i .. i t to.i , t 111, , , i, 11111, t i 11 t i |, i
9382 i
9383 I ' i i mi I nodels of ill i iii i as
9384 1 I a(, Mtrt I II mi 1 i l fied with |
9385 in i A/ork. ( F 1 i )i j ami. 1 |
9386 I III I LIB\ PROG I II , Jill II III ,1 J I II SAS) .
9387 i
9388 IReferenoe; ,
9389 I Hea I i.h K i ;1 i l.adon n I th i Int in I ho it H M ha-
9390 | I I ers i I I II IV) . iimi i i nili til i. Iii )f
9391 | II i ns. II I i 1, I i I ! 1 9 8 8 ) . |
9392 I See c,'.u.K v i ,¦! i iv paqes ui-ijb. I
9393 i i
9394 + USER-SU tJohitJ.) ASSIGNMENTS : +
9395 i
9396 |> ' re assigned usinq "ILET" state-- |
9397 3T X, DURATION, LASTAGE.
9398 i )w.
9399 |> Dirtinq risk are defined
9400 i
9401 >
9402 i
9403 i -
9404 i ,t i i i i j I, i mm,ooo I,, i I, 11 i t i j i i
9405 | lilt Hi I i I 11 t h Hit, tep 'Mil
9406 i
9407 +NOTES: +
9408 I > IDatastep "EX F\ISK" is where the desired risks are computed „ |
9409 i
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9474
9475
9476
9477
9478
9479
9480
9481
9482
9483
9484
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
If the
a modei
rn n H p> 1 p> i
O f
11 "i e L i i "i e a r R e 1. R a t e
r i s k i s o v e r 11'i e
ed at a younqer aqe.
Low, )
+ S A S P r o q r a rn rn e r :
M o d i f i c a t i o 11 s :
2 6 j u 10 0 Fi> e
23ju101
rni th
i Inst„ for Occupationa 1 Sa fety & Hea 1th
, 2 3 j u .12 0 01, 2 5 o c 12 0 01, 18 n o v 2 018
?ctly
iped
a rn a c r o I
i defininq the aqe exposure beqins, )
t o f a c i 1 it it 11111 I t i i I 11 i I i 11 i ii
.l'iiTif i.e. Ml I M I i I 11' I M
concenti 11 i 11 t i i t i i i i I 1 h
/e definin 1 I i i 11 mm 1 I II II nil I
i..th code i 1 1 ii i i 11 ii j i
\re rate mod el„
sk) (
?5oct01
to
3 0nov.l
.ed .
( S R C ) A d d e < w h i c 1'i 11 e r a 11 v e .1 y
\4 until tl'i .ON corresponds to an
(tl'ie point :i r i.11 re i i >\> i )
1M a c r o C ONV E R 4 w o r k s w i 11 'i o i 'i e v a 1 u e f o r 11 'i e e x p o s u r e
variable ^ i „ e „ f wl'ien tl'ie data C Levels includes one record, )
o BE IF 1 i | " > ib'b-' Th i a t <
i-?d but t 1 till i I il ;f
n a d d i t i o n t o i. 111 i. ¦>. i i ¦.
in PART 1, and th<> u;i<
for tl'ie new mac
in a c r o C ON VE RG E B EIR 4 (
,.ow) .
/¦k PART I. USER-SUP
/ *
Model of curnuL
1 =>
v a r i a b ].. e s ) :
1-
Page 278 of 310
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9488
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9501
9502
9503
9504
9505
9506
9507
9508
9509
9510
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9545
9546
9547
9548
9549
9550
9551
9552
9553
9554
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9558
9559
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
R=R(J^ (1+X) ' COEF
| 0 => User Defined & programmed |
| in datastep Ex_Risk below |
| */ %Let Model = 2;
| Cumulative exposure parameter: */ %Let COEF = 0.01;
| Lag or delay between exposure and effect: */ %Let Lag = 10;
| Age exposure begins: */ %Let Agelst_x = 0;
/* Exposure duration (years): */ %Let Duration = 85;
/* Adjust dose from occupational to |
| continuous environmental exposures (Y/N)? */ %Let EnvAdj = Yes;
/* Age to stop accumulating excess risk |
| (supposing rates are available for |
| ages >= &LastAge); otherwise use all of |
| the supplied rate information: */ %Let LastAge =85;
/* */
/* PART II. USER-SUPPLIED ASSIGNMENTS (Datesets AllCause, Cause, X_Levels
data AllCause (label="Unxposeds' age-spec mortalty rates (all)"
drop=Lx rename=(BLx=Lx) );
/ * +
| Input lifetable and calculate the corresponding age-specific |
| (all-causes) mortality rate (AllCause) and conditional survival |
| probability for each year of age (gi) together with |
| the corresponding values of age (Age). I
-I -k /
Label Age = "Age at start of year (Age=i)"
BLx = "Number alive at start of year"
Lx = "Number alive at end of year"
CndPrDth = "Pr[Death before age i+1 | alive at age i]"
gi = "Pr[Survive to age i+1 | Alive at age i]"
AllCause = "Age-spec mortality rate (all causes)";
if _n_=l then input age //// @1 BLx 6;
input Lx 66;
CndPrDth = (BLx - Lx)/BLx;
gi = 1-CndPrDth;
if gi <= 0 then AllCause = le+50;
else AllCause = - log(gi);
if age < &LastAge then output; else STOP;
BLx=Lx;
age+1;
retain age BLx;
cards;
0 = Life-table starting age. (Reguired: Values must begin 4 lines down!
The following are 2016 Life-table values of US population
starting
at birth and
ending at
age 85

(Source:
Nat.Vital Statistics Reports
2017 Vol 66 :
Wo 3, 1
100000
99404
99362
99337
99318
99303
99288
99275
99264
99254
99244
99235
99225
99213
99197
99174
99145
99110
9 9066
99014
98953
98883
98805
98720
98632
98542
98450
98357
98262
98164
98062
97957
97848
97735
97620
97500
97377
97247
97110
96 965
96811
9664 6
96470
96280
96073
95848
95601
95332
95036
94710
94352
93962
93539
93084
92592
92062
91491
90879
90224
89527
88788
88003
87169
86282
85341
84343
83284
82159
80961
79681
78308
76833
75245
73539
71713
69764
67694
65481
63109
60575
57879
55026
52028
48886
45607

data CAUSE (label="Unxposeds' age-cause-spec mortalty rates");
/ * +
| Specify unexposeds' age-specific mortality rates (per year) |
| from specific cause. I
-I -k /
label Age = "Age"
Rate_e5 = "Age,cause-specific rate per 100,000"
Rate = "Age,cause-specific rate per individual";
if _n_ = 1 then input age /* input starting age */
///; /* // => skip next 3 lines */
Page 279 of 310
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9582
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9591
9592
9593
9594
9595
9596
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9598
9599
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9601
9602
9603
9604
9605
9606
9607
9608
9609
9610
9611
9612
9613
9614
9615
9616
9617
9618
9619
9620
9621
9622
9623
9624
9625
9626
9627
9628
9629
9630
9631
9632
9633
9634
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
input Rate_e5 66;
Rate = Rate_e5 * le-5; /* Convert to rate per individual */
if age <= 4
then DO; output; age+1; END;
else DO i = 0,1,2,3,4; /*
if age < &LastAge /*
then output; /*
age+1; /*
/*
/* Fill out into yearly intervals from */
/* inputted five year intervals after age 4*/
*/
*/
*/
END;
cards;
0 = Start age of cause-specific rate (Reguired: Rates begin 3 lines down!)
The following are 2013 ICD10 = 113 death rates per 100,000 for US pop'n starting at birth.
For ages 5 and above, each rate holds for the age thru age+4 years.
Source: CDC Wonder
0.0 0.0 0.0 0.0 0.0
0.0 0.0 0.0 0.1 0.1 0.4 1.2 3.2 9.6 27.1 57.8
90.7 136.6 212.5 277.3 321.2
data X_LEVELS (label= "Exposure levels (e.g., concentrations)" );
/ •k +
| Specify environmental exposure levels I
| and update label for the variable, XLevel, if necessary: |
+ */
/ * +
| BT 3/8/19: Add maxro CONVERGE_BEIR4 which iteratively runs macro |
| BEIR4 until the EXPOSURE_CONCENTRATION corresponds to extra_risk=0.01|
| The intent was to make as few changes to BEIR4 as possible. The data |
| X_LEVELS and variable XLevel are retained but the initial value of |
| XLevel is provided in the call to macro CONVERGE_BEIR4 (the value
| of Xlevel in the cards statement is not used in the calculations. |
+ */
input XLevel 66;
label XLevel= "Asbestos exposure (F/ml)";
cards;
0.0383
%Macro BETR4;
/* March 2019 - BT (SRC): Macro BEIR4 is now called by macro CONVERGE_BEIR4.
*/
/* 23jul01 modification */
/* Enclose the actual calculations and printed results in a macro */
/* to facilitate multiple applications of the algorithm. */
/* PART III. Perform calculations: */
data EX_RISK (label = "Estimated excess risks [Method=BEIR IV]"
/*keep = XLevel Rx ex_risk RskRatio R0 extra_Risk */
rename= (Rx=Risk));
/ * +
| Calculate risk and excess risk for each exposure concentration!
| in work.X_Level by BEIR IV method using information in |
| work.AllCause and work.Cause to define referent population: |
+ */
length XLevel 8.;
label Age =
"Age at start of year (Age=i)"
"Exposure duration midway between i & i+1"
"Cumulative exposure midway betw. i & i+1"
XTime
XDose
R0
Rx
Ex_Risk
RskRatio
"Unexposed's risk"
"Exposed1s risk (Rx)"
"Excess risk (Rx-Ro)"
"Ratio of risks (Rx/Ro)"
hi
hix
"Unexposed's hazard rate at age i"
"Exposed1s hazard rate at age i"
Page 280 of 310
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9652
9653
9654
9655
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9657
9658
9659
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9661
9662
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9666
9667
9668
9669
9670
9671
9672
9673
9674
9675
9676
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9678
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9680
9681
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9687
9688
9689
9690
9691
9692
9693
9694
9695
9696
9697
9698
9699
9700
9701
9702
9703
9704
9705
9706
9707
9708
9709
:eration
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
hstari = "Unexposeds all causes hazard rate(age=i)"
hstarix = "Exposed1s all causes hazard rate(age=i)"
qi = "Pr[Survive to i+1 | Surv. to i,unexposed]"
S li = "Pr[Survive to age=i | unexposed]"
S lix = "Pr[Survive to age=i | exposed]";
/* BT 3/8/19: Caleulation of unexposed s s risk (following DO LOOP) could be omitted from
but may require further changes to BEIR4 (?) *
* e q, ( % i f i:::::: 1 % t h e n % d o; 'k /
if _n_=l then DO;
/* Caleulate unexposed ? s risk (R0) to be retained */
i "k based on equation 2A-21 (pg. 131) of BEIR IV: */
!"k Initialize; "k I S_li = 1; R0 = 0;
DO pointer = 1 to min(n all,n cause) until (age>=&LastAge-l);
set allcause (keep=age AllCause rename=(AllCause=hstari))
point=pointer nobs=n all;
set cause (keep=age Rate rename=(age=ageCause Rate=hi))
point=pointer nobs=n cause;
if Age NE AgeCause then
put "** WARNING: Age values in datasets ALLCAUSE and CAUSE don't conform **"
/ 613 "Rates misaligned on age could give incorrect results"
/ 013 Pointer=
+2 "Age(ALLCAUSE)=" Age +2 "Age(CAUSE)=" AgeCause /;
qi = exp(-hstari);
R0 = R0 + ( hi/hstari 'k S_li * (1-qi) );
S_li = S_li * qi;
END;
END; !"k End of 5 if n =1 then DO; 5 stmt */
retain R0;
/ "k (11 ? i i 1 i 1 i j i i :l"i exposure level "k /
/k i. I l I 1 i |ii ii l ii fog. 132) of BEIR IV */
/ "'• 1: i ) j lm lm i 1 n i .¦) equation 2A-2.1: "'• /
* BT 3/20/19. This version of 4 will work when there is
one in data set x levels -
i wiM.1 v.iiue for xlevel.
T1 'i e D o ].. o o p f o r X ].. e v e J., s i s c o rn rn e i 'i i: e d o u t;
*DO to No of Xs;
"k s e t x .. n t:::::: p o i i "i t X i "i o b s:::::: N o o f X s ; / "k B T 3 / 8 /1 9 : d e t e r m i i "i e s when t o
e i 'i d 11 'i e ].. o o p „ N o b s i s s e t a t c o rn p i i 11 "ii,
s o th e va 1 u e o f n obs i s a va i 1 a b].. e a t fi r s t ru n th rou gh .1. oop -
"j ust one record and one variable (XLevel) in dataset x levels. */
I.. 9: added the next lint to set the exposure
concentration :::::: current va lue of &expc )nc~ "k /
= ^exposure cone;
/ "k Initialize : */ S_lix = 1; Rx = 0;
DO pointer = 1 to min(n all,n cause) until (age>=&LastAge-l) ;
set allcause (keep=age AllCause rename=(AllCause=hstari))
point=pointer nobs=n all;
set cause (keep=Rate rename=(Rate=hi))
point=pointer nobs=n cause;
XTime = min( max(0,(age+0.5-&Agelst_x-&Lag))
, SDuration - 0.5 );
if UpCase("SEnvAdj") = "YES" /* Occupational to Environmental Conversion
*/
then XDose = XLevel
* 365/240 /* Days per year */
* 20/10 !"k Ventilation (L) per day */
* XTime;
ELSE if UpCase ( "&EnvAdj " ) = "NO" /* 30nov2018 ('ELSE') "k /
Page 281 of 310
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9751
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9753
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9759
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9761
9762
9763
9764
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9767
9768
9769
9770
9771
9772
9773
9774
9775
9776
9777
9778
9779
9780
9781
9782
9783
9784
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
then XDose = XLevel^XTime;
else DO; put //"Macro variable ENVADJ incorrectly specified."
/"It should be either YES or NO. Value specified is:
&ENVADJ"
/;
STOP;
END;
hix=.;

if &Model =
1
then
hix =
hi
*
exp(&COEF*XDose);
else
if &Model =
2
then
hix =
hi
*
(1 + SCOEF^XDose);
else
if &Model =
3
then
hix =
hi
+
&COE F^XDos e;
else
if &Model =
4
then
hix =
hi
*
(1 + XDose)* *&COE F;
else
if &Model =
0
then
DO;

hix = -9

99; /'
Cod e
fo.1

i s e r - d e f i i 'i e d rn o d e 1 q c
)es he
END;
hstarix = hstari
+ (hix - hi);
qix = exp(-hstarix);
Rx = Rx + ( hix/hstarix * S lix
S lix = S lix * qix;
output;
i' a t e i s i i i c 1 u d e d i n h s t a r i * /
. i d d i i "i q i i i 111 e e x c e s s * /
> s u r e ( h i x - h i ) q i v e s t h e * /
11. e o f 11 "i e e x p o s e d * "1; /
1-qix ) );
END;
Ex Risk = Rx - R0;* Rx :::::: risk in exposed population;
RskRatio = Rx / R0; "k R0 from cancer;
Extra_risk = Ex_Risk/(1-R0);
/* BT 3/20/19 added ; "k /
call symput('Extra Riskm',Extra Risk);
/*BT 4/24/19 replaced the next line
Diff Ex Risk abs(&ex risk target-Ex Risk); */
Diff Ex Risk = abs(&ex risk tarqet-Extra Risk);
call symput( 'Delta_Ex_Risk',Diff_Ex_Risk);
output;
* E N D; * c o r r e s p o i i d s t o X L e v e 1 s ;
STOP;
run;
%Mend BEIR4;
once),
BT : March 2019; r.M r. 1111<. m . 1 r;: i or the converqence that are used
i i "i 11 "i e iti o d i f i e d v < -1 ¦;: i i. .< 11 i. .i i i 11 e B EIR 4 rn a c r o „
*/
%macro Converqe BEIR4 (init exposure conc=, ex risk tarqet=, conv criterion=, ma;
%Let Delta Ex Risk = 1; * initial hiqh value to make sure loop is run at least once
(i.e., macro BEIR4 is called at least
/* BT 4/15/19; added next line to avoid error durinq compilinq of BEIR4*/
%Let Extra Riskm = 1;
%Let i = l; "k first time throuqh loop;
%Do %Until (%sysevalf(&Delta Ex risk < &conv criterion) OR %sysevalf(&i > &max iteration));
* first time throuqh loop, set expsosure conc=.in.it exposure cone;
%If &i=l %Then
%Do;
%Let exposure conc=&init exposure cone;
%End;
%If &i>l %Then
%Do;
Page 282 of 310
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9791
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9793
9794
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9796
9797
9798
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9800
9801
9802
9803
9804
9805
9806
9807
9808
9809
9810
9811
9812
9813
9814
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9816
9817
9818
9819
9820
9821
9822
9823
9824
9825
9826
9827
9828
9829
9830
9831
9832
9833
9834
9835
9836
9837
9838
9839
9840
9841
9842
9843
9844
9845
9846
9847
9848
9849
9850
9851
9852
9853
9854
9855
9856
9857
9858
9859
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
data tempBEIRCONVERGE;
*BEIR4 has run at least once. Adjust
e x p o s i.i r e c o n c
Extra Riskrn is created in BEIR4
(=Extra Risk);
NumLoops=&i;
thisExposureConc=&exposure cone;
/ * B 'I'1 4 /15 /1 9 : r e p 1 a c e d a 11 o :f 111 e c o i i v e r q e i i c e c o d e w i 111 111 e s a rn e
cod e tl"i a t we u s ed
i i 'i 11 'i e rn e s o c o d e „ * /
numvar=&ex risk target;
denvar=&Extra Riskm;
thisexposureconc = thisexposureconc * (numvar/denvar) ; ^update the
c o i "i c e i "i t r a t i o i i;
call symput('exposure cone',thisexposureconc);
output;
Run;
% E n d; * C o r r e s p o i i d s t o I :f i 1 s t a t e rn e i 11;
%BEIR4;
%Let i=%eval(&i+l);
%End;
%Let EC IPercent = Sexposure cone;
/'J;- f
I Report results if converqence criterion met: I
-+ : 1 */
%If %sysevalf(&Delta Ex risk < &conv criterion) %then %do;
data _null_; /* Modified 2 6--julv-- 0 0 */
pointer=l;
set allcause (keep=age
rename=(age=ageall0)) point=pointer nobs=n all;
set cause (keep=age
rename=(age=ageCs0)) point=pointer nobs=n cause;
pointer=n all;
set allcause (keep=age
rename=(age=agealll)) point=pointer nobs=n all;
pointer=n cause;
set cause (keep=age
rename=(age=ageCsl)) point=pointer nobs=n cause;
Tmp = sum(min(AgeAlll,AgeCsl,(&Lastage-l)),1);
file PRINT;
if ageallG NE ageCsO then DO;
put /"ERROR: The initial age for all-causes rate differs from the"
/" initial age for the cause-specific rate.";
END;
else DO;
put /
"Values of macro variables
used in
this computation: "
//
@3
"Value"
@17
"Macro Var"
029
"Description"
/
@3
it ii
@17
tl
(l
@29

//
03
"SModel "
@17
"MODEL"

029
"1 = Loglinear Relative Rate,"
/

@29
"2 = Linear Relative Rate, "
/

029
"3 = Linear Absolute Rate, "
/

029
"4 = 'Power' Relative Rate, "
/

029
"0 = User defined. "
/
03
"SCoef "
@17
"COEF"

029
"Exposure parameter estimate"
//
83
"&Lag "
@17
"LAG"

02S
"Exposure Lag "
//
03
"&Agelst x"
@17
"AGE1ST
X"
029
"Age exposure begins"
/
@3
"^Duration"
@17
"DURATION"
029
"Duration of exposure"
/
03
"SEnvAdj"
@17
"ENVADJ

029
"Adjust dose from intermittent
/

029
"occupational exposures to "
Page 283 of 310
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9861
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9863
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9869
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9871
9872
9873
9874
9875
9876
9877
9878
9879
9880
9881
9882
9883
9884
9885
9886
9887
9888
9889
9890
9891
9892
9893
9894
9895
9896
9897
9898
9899
9900
9901
9902
9903
9904
9905
9906
9907
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
/ 029 "continuous environmental exposures"
/ @3 " " @17 " " @29 " "
// " "
// @3 "EC1% = " @10 "&EC_1Percent" @25 "(f/ml); Rx = " @39 " SExtra Riskm"
// "
/"The risks are calculated from age " ageallO " up to age " Tmp "."
// ;
if agealll NE ageCsl then
put /"WARNING: The last age for the all-causes rates differs from"
/" the last age for the cause-specific rates, suggesting"
/" the possibility that the rates weren't entered as desired."
/;
END;
Stop;
run;
proc print data=ex risk lab 5;
format risk Ell, ex ri Xlevel El 1.;*RskRatio 6.4;
run;
%End; *end of the If statement that tests if convergence was met;
%Mend Converge_BEIR4;
/* I-
| Marnh 201^: RT (SRC) Added rnaxro CONVERGE BEIR4 which iterativelv |
| until the EXPOSURE CONCENTRATION corresponds to an |
I t\.i r.:i ri.'-a; 11111 (the point of departure [POD]), I
I 11 "1 a d d i t i o 11 t o 111 e p a .1: a rn e t e .1: f o .1: C ONV E R Cv E B EIR 4 r 111 e u s e .1: s 11 o u 1 d a 1 s o |
I review parameters and data that are assigned/entered in Part 1 and |
| Part II (see above) , Parameters for CONVERG5E BEIR4 are defined below |
-I */
title5 " test of converge_BEIR4, based on MLE(Coef)=&COEF and LastAge=&LastAge";
*%BEIR4; ,J;' originally called rnacr BEIR4 directly. Now BEIR4 is called by Converge BEIR4;
%Conve2:g,e_BEIR4 (init exposure conc=l, / "'• initial ex]c :mi 1 111 1 a 1 guess) "'• /
ex_risk_target=Q. 01000000, / ¦' uir lvmiu
-------
9908
9909
9910
9911
9912
9913
9914
9915
9916
9917
9918
9919
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9922
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9926
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9934
9935
9936
9937
9938
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9944
9945
9946
9947
9948
9949
9950
9951
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9955
9956
9957
9958
9959
9960
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9962
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9964
9965
9966
9967
9968
9969
9970
9971
9972
9973
9974
9975
9976
9977
9978
9979
9980
9981
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Mesothelioma Lifetable
This proqrarn calculates the risk of mesothelioma from inhalation exposure to asbestos,
using a lifetable approach. The basic model is Im :::::: C * KM * Q*
T1 c o d e f o r 't I l •? t a b 1 e c a 1 c u 1 a t i o i i s w e r e d e v e 1 o p e d a i i d p r o v i d e d t o E P A
b1 .1 Smith at I I II
For mesothelioma,, calculations are based on NIOSH Model 3; Rx :::::: R0 1 COEF "k X Dose
For mesothelioma,. RQ is assumed to be zero.
El' ^ I "i i i i ^ t 11 11 I' II i i I Lows ;
1 i ti M - "ic (mesothelioma ) mortality data tables have been updated „
2 .ate X Dose :::::: X Level * QF where Q is a function of TSFE and exposure
dm 11 i ' '11 ,
2 Mi u t i 11 11 I n ided to
3 * 1 ma i hi l 11 ) j j j to find
This is referred to as EC„
Tl i to calculate the unit risk; UR :::::: 0.01 / EC
*/
Risk = (Rx - R0) / ( 1 - R0)
;X Level) that yields an extra risk of 1%„
/ * „ \Beta Version „ sa s 1 9"] an 00 F 2 6"] ul 00 F 25oct0.1. F 06dec05 F 30nov.l. 8
Expei:irnenta].. version
*/
title "Excess Risks using BEIR IV method to account for competing risks";
title2 "Effects of airborne exposure to asbestos on mesothelioma mortality rates";
title3 "under a linear absolute rate model .";
f.
Compute excess risk by the BEIR IV method using SAS datasteps.
wh e .1: e
(with Lag)
i.lie 'Ukm i mm i.ip.1 ei i em. of exposure and
iO is the (ii | 11 i i 11 ' i 11 11 l i I i 11 i ;=0 ) .
(Except fo.]' '..'.¦.'CI i. 11 (.1;: i.1 .ire i i n p- m i m i;: >m ige. )
odels o:f i I i 1 i i 1 i i i i 1
/V „ More im 1 i ) i j in j 1 ml i i i wil
Afork. im I l i ! im I
LIB\PROGRAM ^ 11 11 I II Mm. 11 II I SAS),
;.:i doi"
8) .
USER-SUPPLIED ASSIGNMENTS:
+
I
re assigned using "%LET" state- |
dT Xf DURATION, LASTAGE. |
:.)w „ |
o u t i l "i a r i s k a r e d e f i l "i e d I
"i d i v i d u.
f 0 0 C
:.ep
Page 285 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
+NOTES:
Datastep "EX RISK" is wine re tine desired risks are computed.
from
i si or
S A S P r o q r a m m e r : R a 1 n d a 11 S'
Tine Nat' 1
2 6 j u 12 0 0 0.
M o d i f i c a t i o i n s :
26jul00 Fix tine procedure
>0 0.1
Linear Rel. Rate
: is over tine
ft: a younqer aqe.
11 S a f e t y & H e a 111 n
i. r 18nov2 018
•ectiy
nped
a ri'i a c r o
?5oct01
3 0movl
evented tine
1 r a t.. ..1.11 q a 1i a c'
exposures to
* BT (SRC) Added ma-rr
BEIR4 until tine EXl
K01 (tine point of h
/oils wi
. , win en tine
i I l o r \ 11 Mi i i
i 111; o C( m 11 i nil
i I 'xpo; 111
i o r t „
n o f
i r o rn i i n t e r rn i 11 e i n t
is ex ed.
:GE BEIR4 wlnicln iteratively
' E N T R A TI ON c o r r e s p o l n d s t o a l n
[POD]).
record „ )
3EIR4 as possib
h.Mlt t he lilt I , I
3NVERGE BEIR^ (
- |-M I '¦
I 11 h T it I \',
In addition to
in PART 1, and
for tine new mac
macro CONVERGE
d I::., j.. r\ h \ s e e e 11 u u i
.. OW)
PART I. USER-SUPPLIED ASSIGNMENTS
(M a c r o v a r i a b I e s )
f
Page 286 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
/¦>
/¦>
val
/
Model of cumulative exposure effects:
1 => Loglinear Relative rate
R=R0* exp(COEF*X)
2 => Linear Relative rate,
R=R0*(1+C0EF*X)
3 => Absolute rate,
R=RO+COEF*X
4 => Power relative rate
R=R0*(1+X)^COEF
0 => User Defined & programmed
in datastep Ex_Risk below
Cumulative exposure parameter:
feLet Model
feLet COEF
3;
0.000000015;
Lag or delay between exposure and effect: */ %Let Lag
ue is ignired */
| Age exposure begins:
/* Exposure duration (years):
/* Adjust dose from occupational to
| continuous environmental exposures (Y/N)
/* Age to stop accumulating excess risk
| (supposing rates are available for
| ages >= &LastAge); otherwise use all of
| the supplied rate information:
feLet Agelst_x
feLet Duration
10; /* Lag is built into Q, so this
0;
85;
k/ %Let EnvAdj
feLet LastAge
Yes;
35;
/* PART II. USER-SUPPLIED ASSIGNMENTS (Datesets AllCause, Cause, X_Levels
data AllCause
(label="Unxposeds' age-spec mortalty rates
drop=Lx rename=(BLx=Lx) );
(all)
Input lifetable and calculate the corresponding age-specific
(all-causes) mortality rate (AllCause) and conditional survival
probability for each year of age (gi) together with
the corresponding values of age (Age).
Label Age
BLx
Lx
CndPrDth
gi
AllCause
"Age at start of year (Age=i)"
"Number alive at start of year"
"Number alive at end of year"
"Pr[Death before age i+1 | alive at age
"Pr[Survive to age i+1 | Alive at age i]
"Age-spec mortality rate (all causes)";
if _n_=l then input age
input Lx 66;
CndPrDth = (BLx - Lx)/BLx;
§1 BLx
gi = 1-CndPrDth;
if gi <= 0 then AllCause = le+50;
else AllCause = - log(gi)
if a
BLx:
age+
reta
cards;
0
Th
st
(S
100000
99244
98953
98062
96811
94352
88788
78308
57879
ge < &LastAge then output; else STOP;
Lx;
1;
in age BLx;
Life
e foil
arting
ource:
99404
99235
98883
97957
9664 6
93962
88003
76833
55026
table starting age. (Reguired: Values must begin 4 lines down!
owing are 2013 Life-table values of US population
at birth and ending at age 85.
Nat.Vital Statistics Reports 2017 Vol 66 No 3, Table 1)
99362 99337 99318 99303 992E
99275 99264
99225 99213 99197 99174 99145 99110 990£
99254
99014
98805 98720 98632 98542 98450 98357 98262 98164
97848 97735 97620 97500 97377 97247 97110 96965
96470 96280 96073 95848 95601 95332 95036
93539 93084 92592 92062 91491 90879 90224
87169 86282 85341 84343
75245 73539 71713 69764
52028 48886 45607 C
94710
89527
83284 82159 80961 79681
67694 65481 63109 60575
Page 287 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
/¦>
data CAUSE (label=MUnxposeds' age-cause-spec mortalty rates")
Specify unexposeds' age-specific mortality rates (per year)
from specific cause.
label Age = "Age"
Rate_e5 = "Age,cause-specific rate per 100,000"
Rate = "Age,cause-specific rate per individual";
if _n_ = 1 then input age /* input starting age */
///; /* // => skip next 3 lines */
input Rate_e5 66;
Rate
Rate e5
le-5; /* Convert to rate per individual */
if age <= 4
then DO; output; age+1; END;
else DO i = 0,1,2,3,4; /* */
if age < &LastAge /* Fill out into yearly intervals from */
then output; /* inputted five year intervals after age 4*/
age+1; /* */
END;
cards;
0 = Start age of cause-specific rate (Reguired: Rates begin 3 lines down!)
The following are 2013 ICD10 = 113 death rates per 100,000 for US pop'n starting at birth.
For ages 5 and above, each rate holds for the age thru age+4 years.
Source: CDC Wonder
0.0 0.0 0.0 0.0 0.0
0.0 0.0 0.0 0.0 0.0 0.0 0.0 0.0 0.0 0.0 0.0
0.0 0.0 0.0 0.0 0.0
''Exposure levels (e.g., concentrations)
run;
data X_LEVELS (label=
/*
| Specify environmental exposure levels
| and update label for the variable, XLevel, if necessary:
input XLevel 66;
label XLevel= "Asbestos exposure (F/ml)";
cards;
0. 001
%Macro BEIR4;
/* April 2 2019 - BT (SRC): Macro BEIR4 is now called by macro CONVERGE_BEIR4.*/
/* 23jul01 modification */
/* Enclose the actual calculations and printed results in a macro
/* to facilitate multiple applications of the algorithm.
/* PART III. Perform calculations:
data EX_RISK (label = "Estimated excess risks [Method=BEIR IV]"
/*keep = XLevel Rx ex_risk RskRatio */
rename= (Rx=Risk));
/*
| Calculate risk and excess risk for each exposure concentratior
| in work.X_Level by BEIR IV method using information in
| work.AllCause and work.Cause to define referent population:
+
length XLevel 8.;
label Age = "Age at start of year (Age=i)"
XTime = "Exposure duration midway between i & i + 1"
XDose = "Cumulative exposure midway betw. i & i+1"
R0 = "Unexposed's risk"
Rx = "Exposed*s risk (Rx)"
Ex_Risk = "Excess risk (Rx-Ro)"
RskRatio = "Ratio of risks (Rx/Ro)
Page 288 of 310
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10207
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10232
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10234
10235
10236
10237
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10239
10240
10241
10242
10243
10244
10245
10246
10247
10248
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10251
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10254
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10256
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10259
10260
10261
10262
10263
10264
10265
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10269
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10275
10276
10277
10278
10279
10280
10281
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
the
hi = "Unexposed's hazard rate at age i"
hix = "Exposed1s hazard rate at age i"
hstari = "Unexposeds all causes hazard rate(age=i)"
hstarix = "Exposed's all causes hazard rate(age=i)"
gi = "Pr[Survive to i+1 | Surv. to i,unexposed]"
S li = "Pr[Survive to age=i | unexposed]"
S lix = "Pr[Survive to age=i | exposed]"
XLevel = "EC1%";
/* BT 3/8/19: Caleulation of unexposed ? s risk (following DO LOOP) could be omitted from
ira tion
but may renin re iun nrr nnanqes to BEIR4 (?) -
* e . g. , * /
if _n_ 1 I hen IK);
/ "k isk (R0) to be retained "k /
/ * (p g . 131 ) o f B EIR IV: * /
/* Initialize; */ S_li =1; R0 = 0;
DO pointer = 1 to min(n all,n cause) until (age>=&LastAge-l);
set allcause (keep=age AllCause rename=(AllCause=hstari))
point=pointer nobs=n all;
set cause (keep=age Rate rename=(age=ageCause Rate=hi))
point=pointer nobs=n cause;
if Age NE AgeCause then
put "** WARNING: Age values in datasets ALLCAUSE and CAUSE don't conform **"
/ @13 "Rates misaligned on age could give incorrect results"
/ @13 Pointer=
+2 "Age(ALLCAUSE)=" Age +2 "Age(CAUSE)=" AgeCause /;
gi = exp(-hstari);
R0 = R0 + ( hi/hstari * S_li * (1-qi) );
S_li = S_li * qi;
END;
END; /* End of 'if n =1 then DO;s stmt */
retain R0;
/* C i I ¦ ill u. i mm ed ? s risk (Rx) for each exposui I •?! */
/ "k i.i I t i in it - I lii - d on equation 2A-22 (pq. .1.32) t MIR IV "k /
/ "k but i. . nil . ri in a form similar to equaticn ^ M.; */
„ This version of CON'\ will work when there is
m I pc I 1 I t I M
Loop, Nobs is set at ¦ in; i I it i n,
s o th e va.].. u e o f n obs i s a va i.].. a b.].. e a t fi r s t ru n tl"i rou ql"i .].. oop
~j ust one record and one variable (XLevel) in dataset x leve
") f o r X ].. e v e ].. s i s c o rn rn e i 11 e d o u t;
i "i o b s:::::: N o o f X s ; / * B T 3 / 8 /1 9 ; d e t e r rn i i i e s when t o e i i d
xlevel = Sexposure cone;
/ "k Initialize : k / S_lix = 1; Rx = 0;
DO pointer = 1 to min(n all,n cause) until (age>=&LastAge-l);
set allcause (keep=age AllCause rename=(AllCause=hstari))
point=pointer nobs=n all;
set cause (keep=Rate rename=(Rate=hi))
point=pointer nobs=n cause;
/*
X T i rn e :::::: rn i l "i ( rn a x ( 0 F ( a q e + 0 „ 5 - & A q e 1 s t x - & L a q ) )
F &Duration );
Q = . ;
If Aqe < 10 then Q :::::: 0;
Page 289 of 310
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10337
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10349
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
I f A q e ":::::: (X T i rn e ~f 10 ) then Q :::::: ( ( A q e -10 ) * * 3 ) -- ( (10 X T i rn e ) * * 3 ) ;
E1 s e Q :::::: (X T i rn e --10 ) ,J;',J;' 3;
*/
TSFE=.;
If Aqe < &Aqelst_x then TSFE = 0;
Else TSFE = Aqe - &Aqelst_x + 0.5;
d = . ;
If Aqe < &Aqelst_x then d = 0; else
If Aqe >= &Aqelst x + &Duration then d = &Duration - 0.5;
Else d = Aqe-&Aqelst_x + 0.5;
If TSFE < 10 then Q = 0; else
If TSFE >= d + 10 then Q = (TSFE-10) **3-(TSFE-10-d)**3;
Else Q = (TSFE-10)**3;
if UpCase("&EnvAdj") = "YES" /* Occupational
then XDose = XLevel
* 385/240 /* Days
* 20/10 /* Venti
o E i 'i v i r o i 'i rn e i 'i t a 1 C o i "i v e r s i o i "i * /
V
ion (L) per day */
* Q; / ¦¦ i ¦ i ¦in lunq cancer proqramf tl'iis line lias "just
XTirne (instead of Q) */
ELSE if UpCase ( "&EnvAdj " ) = "NO" /* 30nov2018 ('ELSE') */
then XDose = XLevel^XTime;
else DO; put //"Macro variable ENVADJ incorrectly specified."
/"It should be either YES or NO. Value specified is: &ENVADJ"
/;
STOP;
END;
hix=.;
if &Model = 1 then hix = hi * exp(&COEF^XDose); else
if &Model = 2 then hix = hi * (1 + &COEF*XDose); else
if &Model = 3 then hix = hi + &COEF^XDose; else
if &Model = 4 then hix = hi * (1 + XDose)**&COEF; else
if &Model = 0 then DO;
hix = -99999; f "k Code for user-defined model qoes here, "k i
END;
/ * 1 "i i:::::: b a c k q r d r a t e
/* so
/*
/*
exp(-hstarix);
Rx + ( hix/hstarix * S lix * ( 1-qix
S lix * qix;
hstarix = hstari
+ (hix - hi);
qix
Rx
S lix
; i i "i c 1 u d e d i n h s t a r:
at addinq in the excess
from exposure (hix-hi) qives the
total rate of the exposed.
END;
Ex_Risk
k RskRatio
output;
output;
Rx - R0; /* BT
= Rx / R0;
9: was
9 :
Risk
R0;
calculated r:
*/
END;
:l'ie macro variables for risk and difference between the
a i "i d 11 "i e t a r q e t r i s k w e r e rn o v e d f r o rn C o i i v e r q e B EIR 4 t o B EIR 4
call symput('Extra Riskm',Ex Risk);
Diff Ex Risk = abs(&ex risk tarqet-Ex Risk);
call symput( 'Delta_Ex_Risk',Diff_Ex_Risk);
c o r r e s p o i i d s t o X L e v e 1 s ;
STOP;
run;
%Mend BEIR4;
March 2 019;
tl'ie modified
tlie converqence
BEIR^I ma cro .
"iat are used
Page 290 of 310
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%macro Converge BEIR4 (init exposure conc=, ex risk target=, conv
once),
feLet Extra Riskm = 1;
iLet Delta Ex Risk = 1; * initial high value to make sure loop is run at least once
(i „ e „ f macro BEIR4 is called at leas-
iLet i = l; first time through loop;
£Do %Until (%sysevalf(&Delta Ex risk < &conv criterion) OR %sysevalf(&i > &max iteration));
* first time tl'irougl'i loop, set expsosure conc=.in.it exposure cone;
%If &i=l %Then
%Do;
%Let exposure conc=&init exposure cone;
%End;
%If &i>l %Then
%Do;
data tempBEIRCONVERGE;
once „ Ad"] ust exposure cone
(-Ex Risk)*/
c o i 'i c e i 'i t r a t i o i 'i;
/"k BT Marcl'i 201 9 : BEIR4 l'ias run at least
Extra Riskm is created in BEIR4
NumLoops=&i;
t h i s E x p o s u r e C o n c = & e x p o s u r e cone; * s e t e g u a 1 t o c o i 'i c e i 'i t r a t i o i 'i i i 'i
numvar=&ex risk target;
denvar=&Extra Riskm;
thisexposureconc = thisexposureconc * (numvar/denvar) ; 'J;'update the
call symput('exposure cone',thisexposureconc);
output;
Run;
% E n d; * C o r r e s p o i 'i d s t o
%BEIR4;
%Let i=%eval(&i+l);
^End;
iLet EC IPercent = ^exposure cone);
st a terneri t,
Report results if convergence criterion me
'V
ilf %sysevalf(&Delta Ex risk < &conv criterion) %then %do;
data _null_; / "k "Modified 26-july-00 "k /
pointer=l;
set allcause (keep=age
rename=(age=ageallO)) point=pointer nobs=n all;
set cause (keep=age
rename=(age=ageCs0)) point=pointer nobs=n cause;
pointer=n all;
set allcause (keep=age
rename=(age=agealll)) point=pointer nobs=n all;
pointer=n cause;
set cause (keep=age
rename=(age=ageCsl)) point=pointer nobs=n cause;
Page 291 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Tmp = sum(min(AgeAlll,AgeCsl,(&Lastage-l)),1);
file PRINT;
if ageallO NE ageCsO then DO;
put /"ERROR: The initial age
for all-causes rate differs from the"
/"
END;
else DO;
put /
//
/
//
/
/
/
/
initial age for the cause-specific rate.'
"Values of macro variables used in this computation:
'&Extra Riskm"
@3 "Value"
/
/
//
03 "&Model
@17
617
617
''Macro Var"
629
629
629
629
62S
629
629
/
@3
"SCoef "
@17
"COEF"
@29
"Exposure parameter estimate"
II
@3
"SLag "
@17
"LAG"
@29
"Exposure Lag "
//
@3
"&Ageist x"
@17
"AGE1ST X"
@29
"Age exposure begins"
/
03
"^Duration"
@17
"DURATION"
@29
"Duration of exposure"
/
@3
"SEnvAdj"
@17
"ENVADJ"
@29
"Adjust dose from intermittent
Description"
1 = Loglinear Relative Rate,
2 = Linear Relative Rate,
3 = Linear Absolute Rate,
4 = 'Power' Relative Rate,
0 = User defined.
/ 63
629 "occupational exposures to "
629 "continuous environmental exposures"
617 " " 629 "
// 63 "ECl*
//
610
'&EC IPercent"
620
(f/ml); Rx
634
/"The risks are calculated from age " ageallO " up to age
// ;
Tmp
if agealll NE ageCsl then
put /"WARNING: The last age for the all-causes rates differs from"
/" the last age for the cause-specific rates, suggesting"
/" the possibility that the rates weren't entered as desired.
/;
END;
Stop;
run;
proc
run;
£End; *
print data=ex risk label noobs;
format risk Ell. ex risk Ell. Xlevel El 1.;*RskRatio 6.4;
•?nd of the If statement that tests if convergence was met
%Mend Converge_BEIR4;
/ * 11 "i e f o 11 o w i i i q o p t i o i i s a r e f o r d e b u q q i i i q
Options mlogic mprint symbolgen;
out after code is running as expected*/
L.,et LastAqe
1,ET LAG = 10;
:,et MODEL = 3;
l,et COEF = 0,00000001!
April 2019: BT (SRC) Added rnaxro CONv
runs macro BEIR4 until the EXPOSURE
e x t r a r i s k:::::: 0 „ 01 (11 "i e p o i i "i t o f d e p a r 11
w 1 'i i c 1 'i i t e r a t i v e 1 v
i. ON c o r r e s p o i "i d s t o a i "i
Page 292 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
I In addition to i. 11<1 i.¦>¦ i i'¦ 1111<11.<11' u 1 d a 1 so |
I review par a mete 1 and |
I Part II (see at d below |
. j -k j
title5 "based on MLE(Coef)=&COEF and LastAge=&LastAge";
*%BEIR
-------
10528
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10534
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10537
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10541
10542
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Appendix J Results of Modeling for IUR Derivation
Section 1
Hein et al. (2007)
EPA Modeling of Hein et al. (2007) Grouped Lung Cancer Data
Cohort: South Carolina
Citation: Hein et al. 2007
Data: Table 3
CE1D (PCM s/cc-yrs)
Lun<
Cancer Deaths
Min
Max
Mid
Obs
Exp
RR
0
1.5
0.75
34
22.1D
1.54
1.5
5
3.25
33
25.30
1.30
5
15
10
34
21.7D
1.57
15
60
37.5
35
18.80
1.86
60
120
90
37
9.20
4.02
120
699.8
409.9
25
4.7D
5.32

198 101.8 1.94
CE10 (PCM s/cc-yr)
Value
Alpha
KL
AIC
MLE
1.0D
1.73E-02
54.29
UB
1.00
2.22 E-02
-
Page 294 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Section 2
Loomis et al. (2009)
EPA Modeling of Loomis et al. (2009) Grouped Lung Cancer Data
Cohort: North Carolina
Citation Loomis et al 2009
Data: Table 5
CE1Q (PCM s/cc-vrsl
Luna Cancer Deaths
Min
Max
Mid
Obs
Exp
RR
0
2.3
1.15
37
37.00
1.00
2.3
11.5
6.9
37
32.74
1.13
11.5
34.8
23.15
35
22.15
1.58
34.8
152.7
93.75
37
29.6D
1.25
152.7
2194
1173.35
35
18.62
1.88

181 140.1 1.29
3.0
a = 1.0 (fixed)
2.5
KL = 8.08E-04
2.0
1.5
1.0
0.5
0
2D0
400
600
800
1000
1200
14M
CE10 (PCM s/cc-yr)
Value
Alpha
KL
AIC
MLE
1.00
8.08 E-04
35.33
UB
1.00
1.31 E-03
-
Page 295 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Section 3
Wang et al. (2013b)
EPA Modeling of Wang et al. (2013) Grouped Lung Cancer Data
Cohort; Chinese miners
Citation Wang el al. 2
-------
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
10592 Appendix K Less Than Lifetime (or Partial lifetime) IUR
10593 TableApx K-l. (L'l'L) Chrysotile Asbestos Inhalation Unit Risk Values for Less Than Lifetime
10594 Condition of Use
Age at
first
exposure
(years)
Duration of exposure
(years)
10
15
20
25
30
35
40
62
78
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
4.06E-03 3.12E-02 5.95E-02 8.25E-02 1.01E-01 1.15E-01 1.27E-01 1.36E-01 1.44E-01 1.62E-01
3.91E-03 3.00E-02 5.72E-02 7.91E-02 9.67E-02 1.11E-01 1.22E-01 1.31E-01 1.38E-01 1.55E-01
3.78E-03 2.89E-02 5.49E-02 7.59E-02 9.27E-02 1.06E-01 1.17E-01 1.25E-01 1.32E-01 1.48E-01
3.64E-03 2.77E-02 5.27E-02 7.28E-02 8.89E-02 1.02E-01 1.12E-01 1.20E-01 1.26E-01 1.42E-01
3.51E-03 2.66E-02 5.06E-02 6.98E-02 8.51E-02 9.73E-02 1.07E-01 1.15E-01 1.21E-01 1.35E-01
3.39E-03 2.56E-02 4.85E-02 6.69E-02 8.15E-02 9.31E-02 1.02E-01 1.10E-01 1.15E-01 1.30E-01
3.27E-03 2.45E-02 4.65E-02 6.41E-02 7.81E-02 8.91E-02 9.79E-02 1.05E-01 1.10E-01 1.24E-01
3.15E-03 2.35E-02 4.46E-02 6.14E-02 7.47E-02 8.53E-02 9.37E-02 1.00E-01 1.06E-01 1.18E-01
3.04E-03
2.93E-03
2.82E-03
2.72E-03
2.62E-03
2.52E-03
2.43E-03
2.34E-03
2.26E-03
2.17E-03
2.09E-03
2.02E-03
1.94E-03
1.87E-03
1.81E-03
1.74E-03
1.68E-03
1.62E-03
1.57E-03
1.51E-03
1.46E-03
1.41E-03
1.37E-03
1.33E-03
1.28E-03
2.26E-02
2.17E-02
2.08E-02
1.99E-02
1.91E-02
1.82E-02
1.75E-02
1.67E-02
1.60E-02
1.53E-02
1.46E-02
1.40E-02
1.34E-02
1.28E-02
1.22E-02
1.17E-02
1.12E-02
1.07E-02
1.02E-02
9.78E-03
9.36E-03
8.96E-03
8.57E-03
8.21E-03
7.87E-03
4.27E-02
4.09E-02
3.91E-02
3.75E-02
3.59E-02
3.43E-02
3.28E-02
3.14E-02
3.00E-02
2.87E-02
2.74E-02
2.62E-02
2.50E-02
2.39E-02
2.28E-02
2.18E-02
2.08E-02
1.99E-02
1.90E-02
1.82E-02
1.74E-02
1.67E-02
1.59E-02
1.53E-02
1.46E-02
5.87E-02 7.15E-02
5.62E-02 6.84E-02
5.38E-02 6.54E-02
5.15E-02 6.25E-02
4.92E-02 5.98E-02
4.71E-02 5.72E-02
4.50E-02 5.46E-02
4.30E-02 5.22E-02
4.11E-02 4.99E-02
3.93E-02 4.77E-02
3.75E-02 4.55E-02
3.58E-02 4.35E-02
3.42E-02 4.16E-02
3.27E-02 3.97E-02
3.12E-02 3.80E-02
2.99E-02 3.63E-02
2.85E-02 3.47E-02
2.73E-02 3.32E-02
2.61E-02 3.18E-02
2.50E-02 3.04E-02
2.39E-02 2.91E-02
2.29E-02 2.79E-02
2.19E-02 2.67E-02
2.10E-02 2.57E-02
2.01E-02 2.46E-02
Page 297
8.16E-02
7.80E-02
7.46E-02
7.13E-02
6.82E-02
6.52E-02
6.23E-02
5.95E-02
5.69E-02
5.44E-02
5.20E-02
4.97E-02
4.75E-02
4.54E-02
4.34E-02
4.15E-02
3.97E-02
3.80E-02
3.64E-02
3.49E-02
3.34E-02
3.20E-02
3.07E-02
2.94E-02
2.82E-02
of 310
8.96E-02
8.57E-02
8.19E-02
7.83E-02
7.49E-02
7.16E-02
6.84E-02
6.54E-02
6.25E-02
5.98E-02
5.71E-02
5.46E-02
5.22E-02
5.00E-02
4.78E-02
4.57E-02
4.38E-02
4.19E-02
4.01E-02
3.84E-02
3.68E-02
3.53E-02
3.38E-02
3.24E-02
3.10E-02
9.60E-02
9.18E-02
8.78E-02
8.39E-02
8.03E-02
7.67E-02
7.34E-02
7.01E-02
6.71E-02
6.41E-02
6.13E-02
5.86E-02
5.61E-02
5.36E-02
5.13E-02
4.91E-02
4.70E-02
4.50E-02
4.30E-02
4.12E-02
3.94E-02
3.77E-02
3.61E-02
3.45E-02
3.30E-02
1.01E-01
9.67E-02
9.25E-02
8.85E-02
8.46E-02
8.09E-02
7.73E-02
7.39E-02
7.07E-02
6.76E-02
6.46E-02
6.18E-02
5.91E-02
5.65E-02
5.40E-02
5.16E-02
4.94E-02
4.72E-02
4.51E-02
4.30E-02
4.11E-02
3.92E-02
3.74E-02
3.56E-02
3.39E-02
1.64E-
01
1.57E-
01
1.50E-
01
143E-
01
1.37E-
01
1.31E-
01
1.25E-
01
1.19E-
01
1.13E-01
1.08E-01
1.03E-01
9.80E-02
9.34E-02
8.90E-02
8.48E-02
8.07E-02
7.68E-02
7.31E-02
6.96E-02
6.62E-02
6.29E-02
5.99E-02
5.69E-02
5.41E-02
-------
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Age at
first
exposure
(years)
Duration of exposure
(years)
1
10
15
20
25
30
35
40
62
78
33
34
35
36
37
38
39
40
41
42
43
44
45
46
47
48
49
50
51
52
53
54
55
56
57
58
59
60
61
62
63
64
65
66
67
68
69
70
1.25E-03
1.21E-03
1.18E-03
1.14E-03
1.11E-03
1.08E-03
1.06E-03
1.03E-03
1.01E-03
9.81E-04
9.59E-04
9.38E-04
9.16E-04
8.93E-04
8.71E-04
8.50E-04
8.31E-04
8.10E-04
7.87E-04
7.65E-04
7.44E-04
7.24E-04
7.00E-04
6.74E-04
6.49E-04
6.24E-04
6.00E-04
5.71E-04
5.37E-04
5.04E-04
4.72E-04
4.40E-04
4.05E-04
3.67E-04
3.29E-04
2.93E-04
2.58E-04
2.21E-04
7.54E-03
7.23E-03
6.94E-03
6.67E-03
6.41E-03
6.17E-03
5.94E-03
5.72E-03
5.51E-03
5.32E-03
5.13E-03
4.95E-03
4.78E-03
4.62E-03
4.46E-03
4.31E-03
4.16E-03
4.02E-03
3.88E-03
3.74E-03
3.60E-03
3.46E-03
3.31E-03
3.17E-03
3.02E-03
2.86E-03
2.70E-03
2.53E-03
2.36E-03
2.18E-03
2.00E-03
1.81E-03
1.63E-03
1.44E-03
1.25E-03
1.06E-03
8.61E-04
6.53E-04
1.40E-02
1.35E-02
1.29E-02
1.24E-02
1.19E-02
1.15E-02
1.10E-02
1.06E-02
1.02E-02
9.87E-03
9.52E-03
9.18E-03
8.85E-03
8.53E-03
8.23E-03
7.92E-03
7.63E-03
7.34E-03
7.04E-03
6.75E-03
6.44E-03
6.13E-03
5.82E-03
5.49E-03
5.16E-03
4.81E-03
4.46E-03
4.10E-03
3.73E-03
3.36E-03
2.98E-03
2.59E-03
2.20E-03
1.81E-03
1.47E-03
1.16E-03
8.91E-04
6.53E-04
1.93E-02
1.85E-02
1.78E-02
1.71E-02
1.65E-02
1.58E-02
1.52E-02
1.47E-02
1.41E-02
1.36E-02
1.31E-02
1.26E-02
1.21E-02
1.17E-02
1.12E-02
1.07E-02
1.03E-02
9.81E-03
9.33E-03
8.85E-03
8.36E-03
7.86E-03
7.34E-03
6.82E-03
6.29E-03
5.74E-03
5.19E-03
4.62E-03
4.07E-03
3.55E-03
3.07E-03
2.62E-03
2.20E-03
1.81E-03
1.47E-03
1.16E-03
8.91E-04
6.53E-04
2.36E-02
2.27E-02
2.18E-02
2.09E-02
2.01E-02
1.94E-02
1.86E-02
1.79E-02
1.72E-02
1.65E-02
1.59E-02
1.52E-02
1.46E-02
1.39E-02
1.33E-02
1.26E-02
1.20E-02
1.13E-02
1.06E-02
9.94E-03
9.25E-03
8.55E-03
7.84E-03
7.14E-03
6.47E-03
5.82E-03
5.21E-03
4.62E-03
4.07E-03
3.55E-03
3.07E-03
2.62E-03
2.20E-03
2.71E-02
2.60E-02
2.50E-02
2.40E-02
2.30E-02
2.21E-02
2.12E-02
2.03E-02
1.94E-02
1.86E-02
1.77E-02
1.69E-02
1.60E-02
1.52E-02
1.43E-02
1.35E-02
1.26E-02
1.18E-02
1.09E-02
1.01E-02
9.33E-03
8.57E-03
7.84E-03
7.14E-03
6.47E-03
5.82E-03
5.21E-03
4.62E-03
2.97E-02
2.85E-02
2.73E-02
2.61E-02
2.50E-02
2.39E-02
2.28E-02
2.17E-02
2.06E-02
1.96E-02
1.86E-02
1.75E-02
1.65E-02
1.55E-02
1.45E-02
1.36E-02
1.27E-02
1.18E-02
1.09E-02
1.01E-02
9.33E-03
8.57E-03
7.84E-03
3.15E-02
3.01E-02
2.87E-02
2.73E-02
2.60E-02
2.47E-02
2.34E-02
2.21E-02
2.09E-02
1.98E-02
1.86E-02
1.75E-02
1.65E-02
1.55E-02
1.45E-02
1.36E-02
1.27E-02
1.18E-02
3.23E-02
3.07E-02
2.91E-02
2.76E-02
2.61E-02
2.48E-02
2.34E-02
2.21E-02
2.09E-02
1.98E-02
1.86E-02
1.75E-02
1.65E-02
For calculation of Table Apx K-l, the following procedure was used. For each cell of the table, the
lung cancer and mesothelioma partial lifetime risk corresponding to the age at first exposure and
duration of exposure was calculated using selected models for lung cancer and mesothelioma and
Page 298 of 310
-------
10599
10600
10601
10602
10603
10604
10605
10606
10607
10608
10609
10610
10611
10612
10613
10614
10615
10616
10617
10618
10619
10620
10621
10622
10623
10624
10625
10626
10627
10628
10629
10630
10631
10632
10633
10634
10635
10636
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
potency factors from Table 3-9 and 3-10, Then lung cancer and mesothelioma risks were statistically
combined using the same procedure as described in Section 3.2.4.6.
Appendix L Sensitivity Analysis of Exposures for
DIY/Bystander Episodic Exposure Scenarios
As presented in Section 4.3.8, there are some uncertainties pertaining to the assumptions made for
exposure durations for both DIY users and bystanders for the brake repair/replacement scenarios. This
Appendix provides a more detailed analyses using various combinations of age at start of first exposure
and duration of exposure for both the DIYers and the bystanders for both the brake repair/replacement
and the UTV gasket repair/replacement scenarios.
In Table L-l, the assumption is that DIY brake/repair replacement with compressed air begins at age 16
years and continues for 20 years instead of for 62 years.
Here, the unit risk for Users is: IURltl(DIY Brakes) = IUR(16,20) = 0.0499 per f/cc
The unit risk for Bystanders is: IURltl(DIY Bystanders) = IUR(0,20) = 0.101 per f/cc
TableApx L-l. Excess Lifetime Cancer Risk for Indoor DIY Brake/Repair Replacement with
Compressed Air Use for Consumers for 20 year duration (exposures from Table 2-32 without a
reduction factor) (Consumers 1 hour/day spent in garage).
Consumer
Exposure Scenario
Exposure Levels (fibers/cc)
ELCR (20 yr exposure
starting at age 16
years)
ELCR ((20 yr
exposure starting at
age 0 years))
DIY User
DIY Bystander
DIY User
DIY Bystander
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Central
Tendency
High-end
Aftennarket
automotive parts -
brakes (3-hour
TWA indoors every
3 years with
compressed air)
0.0445
0.4368
0.0130
0.0296
2.8 E-5
2.7 E-4
1.7 E-5
3.8 E-5
TWFConcomitant Exposures (1 hour per day every day)
(l/24)*(365/365) = 0.04167
DIY User: ELCR (Central Tendency)
0.0445 f/cc • 0.0001142 • 0.0499 per f/cc + 0.0445 • 0.3 • 0.04167 • 0.0499
DIY User: ELCR (High-end> = 0.4368 f/cc • 0.0001142 • 0.0499 per f/cc + 0.4368 • 0.3 • 0.04167 • 0.0499
DIY Bystander: ELCR (Central Tendency) 0.013 f/cc • 0.0001142 • 0.101 per f/cc + 0.013 • 0.3 • 0.04167 • 0.101
DIY Bystander: ELCR ,High-end> = 0.0296 f/cc • 0.0001142 '0.101 per f/cc + 0.0296 • 0.3 • 0.04167 '0.101
Exposure values from Table 2-32 were used to represent indoor brake work (with compressed air) and
are the basis for the exposure levels used in Table Apx L-l. EPA then assumed that the concentration of
chrysotile asbestos in the interval between brake work (every 3 years) is 30% of that during measured
active use. Consumers were assumed to spend one hour per day in their garages based on the 50th
percentile estimate in the EPA Exposure Factors Handbook. Based on these assumptions, the consumer
risk estimates were exceeded for central tendency and high-end exposures (L-l). Estimates exceeding
the benchmark are shaded in pink and bolded.
Comparing these results with those of Table 4-38, we see that the ratio of the risks for the DIY User
based on 20 years exposure compared to 40 years of exposures is equal to the ratio of the less than
lifetime inhalation unit risks:
Page 299 of 310
-------
10637
10638
10639
10640
10641
10642
10643
10644
10645
10646
10647
10648
10649
10650
10651
10652
10653
10654
10655
10656
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
DIY Users: [IUR(16,20) = 0.0499 per f/cc] / [IUR(16,62) = 0.0768 per f/cc] = 0.65
DIY Users: [20 yr risk (Central) = 2.80 E-5] / [62 yr risk (Central) = 4.31 E-5] = 0.65
DIY Users: [20 yr risk (High) = 2.74 E-4] / [62 yr risk (High) = 4.23 E-4] = 0.65
Similarly for bystanders, the ratio of the risk based on 20 years exposure compared to 62 years exposure
is equal to the ratio of the 20-year less than lifetime risk to the lifetime unit risk:
DIY Bystanders: [IUR(0,20) = 0.101 per f/cc] / [IUR(Lifetime) = 0.16 per f/cc] = 0.63
DIY Bystanders: [20 yr risk (Central) = 1.66 E-5] / [78 yr risk (Central) = 2.62 E-5] = 0.63
DIY Bystanders: [20 yr risk (High) = 3.77 E-5] / [78 yr risk (High) = 5.97 E-5] = 0.63
Using this approach, and relying on the ratios presented in Table 4-49, TableApx L-2provides and
ratios for five different sensitivity pairings.
Table Apx L-2. Ratios of risk for alternative exposure scenarios compared to DIY User and
Bystander exposure scenario assuming DIY User is first exposed at age 16 years for 62 years
duration and DIY Bystander is exposed from age 0-78 years.
Kxposure
scenario

Age at first
exposure
(years)
Duration
(years)
liasclinc
partial
lifetime
11 U
Kxposurc
scenario
partial
lifetime
11 U
Uatio of
risks for
exposure
scenario
Baseline
DIY User
16
62
0.0768
0.0768
1
Bystander
0
78
0.16
0.16
1

Sensitivity
#1
DIY User
16
20
0.0768
0.0499
0.65
Bystander
0
20
0.16
0.101
0.63

Sensitivity
#2
DIY User
20
40
0.0768
0.0591
0.77
Bystander
0
40
0.16
0.144
0.90

Sensitivity
#3
DIY User
20
20
0.0768
0.0416
0.54
Bystander
0
20
0.16
0.101
0.63

Sensitivity
#4
DIY User
30
40
0.0768
0.0374
0.49
Bystander
0
40
0.16
0.144
0.90

Sensitivity
#5
DIY User
30
20
0.073
0.0267
0.37
Bystander
0
20
0.16
0.101
0.63
Page 300 of 310
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10657
10658
10659
10660
10661
10662
10663
10664
10665
10666
10667
PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
TableApx L-3through TableApx L-7 below show the results of applying these ratios to all of the
possible scenarios presented in Table 4-48 using the five sensitivity analyses pairings in Table Apx L-2.
Table Apx L-8 at the end summarizes the results to show how only one of 24 scenarios changes from an
exceedence to no exceedence for four (1, 3, 4, 5) of the five sensitivity analyses (DIY user, Brakes
Repair/ replacement, Outdoor, once every 3 years, 30 min/d in driveway, high-end only).
Table Apx L-3. Sensitivity Analysis #1: Summary of Risk Estimates for Inhalation Exposures to
Consumers and Bystanders by COU (Cancer benchmark is 10~6) Comparing the Baseline
Exposure Scenario from Table 4-45 with Risks Assuming DIY Users Are Exposed From Age 16-36
years and Bystanders Are Exposed Age 0-20 years.
Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure
Duration
and Level
Cancer
Risk
Estimates
(from
Table 4-
45)
Cancer Risk
Estimates
Users age
16-36
(*0.65) and
Bystanders
0-20 (*0.63)
Imported asbestos
products
Brakes
Repair/replacement
Indoor, compressed air,
once every 3 years for
62/20 years starting at
16 years, exposures at
30% of active used
between uses, 1 hour/d
in garage
Section
4.2.3.1
DIY
Central
Tendency
4.3 E-5
2.8 E-5
High-end
4.2 E-4
2.7 E-5
Bystander
Central
Tendency
2.6 E-5
1.6 E-5
High-end
6.0 E-5
3.8 E-5
Brakes Repair/
replacement
Indoor, compressed air,
once every 3 years for
62/20 years starting at
16 years, exposures at
30% of active used
between uses, 8 hours/d
in garage
Section
4.2.3.1
DIY
Central
Tendency
3.4 E-4
2.2 E-4
High-end
3.4 E-3
2.2 E-3
Bystander
Central
Tendency
2.6 E-5
1.6 E-5
High-end
6.0 E-5
3.8 E-5
Brakes Repair/
replacement
Outdoor, once every 3
years for 62/20 years
starting at 16 years,
exposures at 2% of
active used between
uses, 5 min/d in
driveway
Section
4.2.3.1
DIY
Central
Tendency
9.9 E-8
6.4 E-8
High-end
5.3 E-7
3.4 E-7
Bystander
Central
Tendency
2.1 E-8
1.3 E-8
High-end
1.1 E-7
6.9 E-8
Brakes Repair/
replacement
Outdoor, once every 3
years for 62/20 years
starting at 16 years,
exposures at 2% of
active used between
Section
4.2.3.1
DIY
Central
Tendency
2.9 E-7
1.9 E-7
High-end
1.5 E-6
9.8 E-7
Bystander
Central
Tendency
5.9 E-8
3.7 E-8
Page 301 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure
Duration
and Level
Cancer
Risk
Estimates
(from
Table 4-
45)
Cancer Risk
Estimates
Users age
16-36
(*0.65) and
Bystanders
0-20 (*0.63)

uses, 30 min/d in
driveway

High-end
3.2 E-7
2.0 E-7
Imported Asbestos
Products
Gaskets Repair/
replacement in UTVs
Indoor, 1 hour/d, once
every 3 years for 62/20
years starting at 16
years
exposures at 30% of
active used between
uses, 1 hour/d in garage
Section
4.2.3.2
DIY
Central
Tendency
2.3 E-5
1.5 E-5
High-end
6.4 E-5
4.2 E-5
Bystander
Central
Tendency
2.4 E-5
1.5 E-5
High-end
6.1 E-5
3.8 E-5

Gaskets Repair/
replacement in UTVs
Indoor, 1 hour/d, once
every 3 years for 62/20
years starting at 16
years
exposures at 30% of
active used between
uses, 8 hour/d in garage
Section
4.2.3.2
DIY
Central
Tendency
1.8 E-4
1.2 E-4
High-end
5.1 E-4
3.3 E-4
Bystander
Central
Tendency
2.4 E-5
1.5 E-5
High-end
6.1 E-5
3.8 E-5
10668
10669
10670
10671
10672
10673
10674
10675
10676
10677
Page 302 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
10678 TableApx L-4. Sensitivity Analysis #2: Summary of Risk Estimates for Inhalation Exposures to
10679 Consumers and Bystanders by COU (Cancer benchmark is 10~6) Comparing the Baseline
10680 Exposure Scenario from Table 4-45 with Risks Assuming DIY Users Are Exposed From Age 20-60
10681 years and Bystanders Are Exposed Age 0-40 years.
Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure
Duration
and Level
Cancer
Risk
Estimates
(from
Table 4-
45)
Cancer
Risk
Estimates
Users age
20-60
(*0.77) and
Bystanders
0-40 (*0.90)
Imported asbestos
products
Brakes
Repair/replacement
Indoor, compressed
air, once every 3
years for 62/40 years
starting at 16/20
years, exposures at
30% of active used
between uses, 1
hour/d in garage
Section
4.2.3.1
DIY
Central
Tendency
4.3 E-5
3.3 E-5
High-end
4.2 E-4
3.2 E-4
Bystander
Central
Tendency
2.6 E-5
2.3 E-5
High-end
6.0 E-5
5.4 E-5
Brakes Repair/
replacement
Indoor, compressed
air, once every 3
years for 62/40 years
starting at 16/20
years, exposures at
30% of active used
between uses, 8
hours/d in garage
Section
4.2.3.1
DIY
Central
Tendency
3.4 E-4
2.6 E-4
High-end
3.4 E-3
2.6 E-3
Bystander
Central
Tendency
2.6 E-5
2.3 E-5
High-end
6.0 E-5
5.4 E-5
Brakes Repair/
replacement
Outdoor, once every 3
years for 62/40 years
starting at 16/20
years, exposures at
2% of active used
between uses, 5 min/d
in driveway
Section
4.2.3.1
DIY
Central
Tendency
9.9 E-8
7.6 E-8
High-end
5.3 E-7
4.1 E-7
Bystander
Central
Tendency
2.1 E-8
1.9 E-8
High-end
1.1 E-7
9.9 E-8
Brakes Repair/
replacement
Outdoor, once every 3
years for 62/40 years
starting at 16/20
years, exposures at
2% of active used
between uses, 30
min/d in driveway
Section
4.2.3.1
DIY
Central
Tendency
2.9 E-7
2.2 E-7
High-end
1.5 E-6
1.2 E-6
Bystander
Central
Tendency
5.9 E-8
5.3 E-8
High-end
3.2 E-7
2.9 E-7
Imported Asbestos
Products
Gaskets Repair/
replacement in UTVs
Section
4.2.3.2
DIY
Central
Tendency
2.3 E-5
1.8 E-5
High-end
6.4 E-5
4.9 E-5
Page 303 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure
Duration
and Level
Cancer
Risk
Estimates
(from
Table 4-
45)
Cancer
Risk
Estimates
Users age
20-60
(*0.77) and
Bystanders
0-40 (*0.90)

Indoor, 1 hour/d, once
every 3 years for
62/40 years starting at
16/20 years
exposures at 30% of
active used between
uses, 1 hour/d in
garage

Bystander
Central
Tendency
2.4 E-5
2.2 E-5
High-end
6.1 E-5
5.5 E-5

Gaskets Repair/
replacement in UTVs
Indoor, 1 hour/d, once
every 3 years for
62/40 years starting at
16/20 years
exposures at 30% of
active used between
uses, 8 hour/d in
garage
Section
4.2.3.2
DIY
Central
Tendency
1.8 E-4
1.4 E-4
High-end
5.1 E-4
3.9 E-4
Bystander
Central
Tendency
2.4 E-5
2.2 E-5
High-end
6.1 E-5
5.5 E-5
10682
10683
10684 TableApx L-5. Sensitivity Analysis #3: Summary of Risk Estimates for Inhalation Exposures to
10685 Consumers and Bystanders by COU (Cancer benchmark is 10~6) Comparing the Baseline
10686 Exposure Scenario from Table 4-45 with Risks Assuming DIY Users Are Exposed From Age 20-40
10687 years and Bystanders Are Exposed Age 0-20 years.
Life Cycle
Subcategory
Consumer
Population
Exposure
Cancer
Cancer
Stage/Category

Exposure

Duration
Risk
Risk

Scenario

and Level
Estimates
Estimates

(from
Users age

Table 4-
20-40

45)
(*0.54) and

Bystanders

0-20 (*0.63)
Imported asbestos
Brakes
Section
DIY
Central
4.3 E-5
2.3 E-5
products
Repair/replacement
4.2.3.1

Tendency

High-end
4.2 E-4
2.3 E-4
Page 304 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure
Duration
and Level
Cancer
Risk
Estimates
(from
Table 4-
45)
Cancer
Risk
Estimates
Users age
20-40
(*0.54) and
Bystanders
0-20 (*0.63)

Indoor, compressed
air, once every 3
years for 62/20 years
starting at 16/20
years, exposures at
30% of active used
between uses, 1
hour/d in garage

Bystander
Central
Tendency
2.6 E-5
1.6 E-5
High-end
6.0 E-5
3.8 E-5
Brakes Repair/
replacement
Indoor, compressed
air, once every 3
years for 62/20 years
starting at 16/20
years, exposures at
30% of active used
between uses, 8
hours/d in garage
Section
4.2.3.1
DIY
Central
Tendency
3.4 E-4
1.8 E-4
High-end
3.4 E-3
1.8 E-3
Bystander
Central
Tendency
2.6 E-5
1.6 E-5
High-end
6.0 E-5
3.8 E-5
Brakes Repair/
replacement
Outdoor, once every 3
years for 62/20 years
starting at 16/20
years, exposures at
2% of active used
between uses, 5 min/d
in driveway
Section
4.2.3.1
DIY
Central
Tendency
9.9 E-8
5.3 E-8
High-end
5.3 E-7
2.8 E-7
Bystander
Central
Tendency
2.1 E-8
1.3 E-8
High-end
1.1 E-7
6.9 E-8
Brakes Repair/
replacement
Outdoor, once every 3
years for 62/20 years
starting at 16/20
years, exposures at
2% of active used
between uses, 30
min/d in driveway
Section
4.2.3.1
DIY
Central
Tendency
2.9 E-7
1.6 E-7
High-end
1.5 E-6
8.1 E-7
Bystander
Central
Tendency
5.9 E-8
3.7 E-8
High-end
3.2 E-7
2.0 E-7
Imported Asbestos
Products
Gaskets Repair/
replacement in UTVs
Indoor, 1 hour/d, once
every 3 years for
62/20 years starting at
16/20 years
Section
4.2.3.2
DIY
Central
Tendency
2.3 E-5
1.2 E-5
High-end
6.4 E-5
3.5 E-5
Bystander
Central
Tendency
2.4 E-5
1.5 E-5
Page 305 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure
Duration
and Level
Cancer
Risk
Estimates
(from
Table 4-
45)
Cancer
Risk
Estimates
Users age
20-40
(*0.54) and
Bystanders
0-20 (*0.63)

exposures at 30% of
active used between
uses, 1 hour/d in
garage

High-end
6.1 E-5
3.8 E-5

Gaskets Repair/
replacement in UTVs
Indoor, 1 hour/d, once
every 3 years for
62/20 years starting at
16/20 years
exposures at 30% of
active used between
uses, 8 hour/d in
garage
Section
4.2.3.2
DIY
Central
Tendency
1.8 E-4
9.7 E-5
High-end
5.1 E-4
2.8 E-4
Bystander
Central
Tendency
2.4 E-5
1.5 E-5
High-end
6.1 E-5
3.8 E-5
10688
Page 306 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
10689 TableApx L-6. Sensitivity Analysis #4: Summary of Risk Estimates for Inhalation Exposures to
10690 Consumers and Bystanders by COU (Cancer benchmark is 10~6) Comparing the Baseline
10691 Exposure Scenario from Table 4-45 with Risks Assuming DIY Users Are Exposed From Age 30-70
10692 years and Bystanders Are Exposed Age 0-40 years.
Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure
Duration
and Level
Cancer
Risk
Estimates
(from
Table 4-
45)
Cancer
Risk
Estimates
Users age
30-70
(*0.49) and
Bystanders
0-40 (*0.90)
Imported asbestos
products
Brakes
Repair/replacement
Indoor, compressed
air, once every 3
years for 62/40 years
starting at 16/30
years, exposures at
30% of active used
between uses, 1
hour/d in garage
Section
4.2.3.1
DIY
Central
Tendency
4.3 E-5
2.1 E-5
High-end
4.2 E-4
2.1 E-4
Bystander
Central
Tendency
2.6 E-5
2.3 E-5
High-end
6.0 E-5
5.4 E-5
Brakes Repair/
replacement
Indoor, compressed
air, once every 3
years for 62/40 years
starting at 16/30
years, exposures at
30% of active used
between uses, 8
hours/d in garage
Section
4.2.3.1
DIY
Central
Tendency
3.4 E-4
1.7 E-4
High-end
3.4 E-3
1.7 E-3
Bystander
Central
Tendency
2.6 E-5
2.3 E-5
High-end
6.0 E-5
5.4 E-5
Brakes Repair/
replacement
Outdoor, once every 3
years for 62/40 years
starting at 16/30
years, exposures at
2% of active used
between uses, 5 min/d
in driveway
Section
4.2.3.1
DIY
Central
Tendency
9.9 E-8
4.9 E-8
High-end
5.3 E-7
2.6 E-7
Bystander
Central
Tendency
2.1 E-8
1.9 E-8
High-end
1.1 E-7
9.9 E-8
Brakes Repair/
replacement
Outdoor, once every 3
years for 62/40 years
starting at 16/30
years, exposures at
2% of active used
between uses, 30
min/d in driveway
Section
4.2.3.1
DIY
Central
Tendency
2.9 E-7
1.4 E-7
High-end
1.5 E-6
7.4 E-7
Bystander
Central
Tendency
5.9 E-8
53 E-8
High-end
3.2 E-7
2.9 E-7
Imported Asbestos
Products
Gaskets Repair/
replacement in UTVs
Section
4.2.3.2
DIY
Central
Tendency
2.3 E-5
1.1 E-5
High-end
6.4 E-5
3.1 E-5
Page 307 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure
Duration
and Level
Cancer
Risk
Estimates
(from
Table 4-
45)
Cancer
Risk
Estimates
Users age
30-70
(*0.49) and
Bystanders
0-40 (*0.90)

Indoor, 1 hour/d, once
every 3 years for
62/40 years starting at
16/30 years
exposures at 30% of
active used between
uses, 1 hour/d in
garage

Bystander
Central
Tendency
2.4 E-5
2.2 E-5
High-end
6.1 E-5
5.5 E-5

Gaskets Repair/
replacement in UTVs
Indoor, 1 hour/d, once
every 3 years for
62/40 years starting at
16/30 years
exposures at 30% of
active used between
uses, 8 hour/d in
garage
Section
4.2.3.2
DIY
Central
Tendency
1.8 E-4
8.8 E-5
High-end
5.1 E-4
2.5 E-4
Bystander
Central
Tendency
2.4 E-5
2.2 E-5
High-end
6.1 E-5
5.5 E-5
10693
10694
10695
Page 308 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
10696 TableApx L-7. Sensitivity Analysis #5: Summary of Risk Estimates for Inhalation Exposures to
10697 Consumers and Bystanders by COU (Cancer benchmark is 10~6) Comparing the Baseline
10698 Exposure Scenario from Table 4-45 with Risks Assuming DIY Users Are Exposed From Age 30-50
10699 years and Bystanders Are Exposed Age 0-20 years.
Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure
Duration
and Level
Cancer
Risk
Estimates
(from
Table 4-
45)
Cancer
Risk
Estimates
Users age
30-50
(*0.37) and
Bystanders
0-20 (*0.63)
Imported asbestos
products
Brakes
Repair/replacement
Indoor, compressed
air, once every 3
years for 62/20 years
starting at 16/30
years, exposures at
30% of active used
between uses, 1
hour/d in garage
Section
4.2.3.1
DIY
Central
Tendency
4.3 E-5
1.6 E-5
High-end
4.2 E-4
1.6 E-4
Bystander
Central
Tendency
2.6 E-5
1,6 E-5
High-end
6.0 E-5
3.8 E-5
Brakes Repair/
replacement
Indoor, compressed
air, once every 3
years for 62/20 years
starting at 16/30
years, exposures at
30% of active used
between uses, 8
hours/d in garage
Section
4.2.3.1
DIY
Central
Tendency
3.4 E-4
1.3 E-4
High-end
3.4 E-3
1.3 E-3
Bystander
Central
Tendency
2.6 E-5
1.6 E-5
High-end
6.0 E-5
3.8 E-5
Brakes Repair/
replacement
Outdoor, once every 3
years for 62/20 years
starting at 16/30
years, exposures at
2% of active used
between uses, 5 min/d
in driveway
Section
4.2.3.1
DIY
Central
Tendency
9.9 E-8
3.7 E-8
High-end
5.3 E-7
2.0 E-7
Bystander
Central
Tendency
2.1 E-8
1.3 E-8
High-end
1.1 E-7
6.9 E-8
Brakes Repair/
replacement
Outdoor, once every 3
years for 62/20 years
starting at 16/30
years, exposures at
2% of active used
between uses, 30
min/d in driveway
Section
4.2.3.1
DIY
Central
Tendency
2.9 E-7
1.1 E-8
High-end
1.5 E-6
5.6 E-7
Bystander
Central
Tendency
5.9 E-8
3.7 E-8
High-end
3.2 E-7
2.0 E-7
Imported Asbestos
Products
Gaskets Repair/
replacement in UTVs
Section
4.2.3.2
DIY
Central
Tendency
2.3 E-5
8.5 E-6
High-end
6.4 E-5
2.4 E-5
Page 309 of 310
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PEER REVIEW DRAFT. DO NOT CITE OR QUOTE
Life Cycle
Stage/Category
Subcategory
Consumer
Exposure
Scenario
Population
Exposure
Duration
and Level
Cancer
Risk
Estimates
(from
Table 4-
45)
Cancer
Risk
Estimates
Users age
30-50
(*0.37) and
Bystanders
0-20 (*0.63)

Indoor, 1 hour/d, once
every 3 years for
62/20 years starting at
16/30 years
exposures at 30% of
active used between
uses, 1 hour/d in
garage

Bystander
Central
Tendency
2.4 E-5
1.5 E-5
High-end
6.1 E-5
3.8 E-5

Gaskets Repair/
replacement in UTVs
Indoor, 1 hour/d, once
every 3 years for
62/20 years starting at
16/30 years
exposures at 30% of
active used between
uses, 8 hour/d in
garage
Section
4.2.3.2
DIY
Central
Tendency
1.8 E-4
6.7 E-5
High-end
5.1 E-4
1.9 E-4
Bystander
Central
Tendency
2.4 E-5
1.5 E-5
High-end
6.1 E-5
3.8 E-5
10700
10701
10702 TableApx L-8: Results of 24 Sensitivity Analysis of Exposure Assumptions for Consumer
10703
10704
DIY/Bystander Episodic Exposure Scenarios
Sensitivity
Analysis
DIY (age at start and
age at end of duration)
Bystander (age at
start and age at end
of duration)
Change in Risk
from Exceedence
to No Exceedence
Scenario Affected
Baseline
16-78
0-78
None
17/24 Exceed
Benchmarks
1
16-36
0-20
1/24
DIY user. Brake repair,
30 inin/day, high-end
2
20-60
0-40
0/24
None
3
20-40
0-40
1/24
DIY user. Brake repair,
30 inin/day, high-end
4
30-70
0-40
1/24
DIY user. Brake repair,
30 inin/day, high-end
5
30-50
0-20
1/24
DIY user. Brake repair,
30 inin/day, high-end
Page 310 of 310
-------