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EPA Document# EPA-740-D-24-008
July 2024
Office of Chemical Safety and
Pollution Prevention
SEPA
United States
Environmental Protection Agency
Draft Risk Evaluation for 1,1-Dichloroethane
CASRN 75-34-3
ch3
CI—
CI
July 2024
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TABLE OF CONTENTS
ACKNOWLEDGEMENTS 23
EXECUTIVE SUMMARY 25
1 INTRODUCTION 28
1.1 Scope of the Risk Evaluation 28
1.1.1 Life Cycle and Production Volume 28
1.1.2 Conditions of Use Included in the Draft Risk Evaluation 31
1.1.2.1 Conceptual Models 32
1.1.3 Populations Assessed 36
1.1.3.1 Potentially Exposed or Susceptible Subpopulations 36
1.2 Systematic Review 37
1.3 Organization of the Risk Evaluation 38
2 CHEMISTRY AND FATE AND TRANSPORT OF 1,1-DICHLOROETHANE 40
2.1 Physical and Chemical Properties 40
2.2 Environmental Fate and Transport 41
2.2.1 Fate and Transport Approach and Methodology 43
2.2.2 Summary of Fate and Transport Assessment 44
2.2.3 Weight of Scientific Evidence Conclusions for Fate and Transport 47
2.2.3.1 Strengths, Limitations, Assumptions, and Key Sources of Uncertainty for the Fate and
Transport Assessment 47
3 RELEASES AND CONCENTRATIONS OF 1,1-DICHLOROETHANE IN THE
ENVIRONMENT 49
3.1 Approach and Methodology 49
3.1.1 Industrial and Commercial 49
3.1.1.1 Identify and Describe OES 50
3.1.1.2 Collect Facility Release Data from Data Sources 52
3.1.1.2.1 Toxic Release Inventory (TRI) 52
3.1.1.2.2 Discharge Monitoring Reports (DMR) 53
3.1.1.2.3 National Emissions Inventory (NEI) 54
3.1.1.2.4 Systematic Review 55
3.1.1.2.5 National Response Center and DOT Hazmat 55
3.1.1.3 Map Facility Release Data to OES 56
3.1.1.3.1 Mapping TRI Release Data to an OES 56
3.1.1.3.2 Mapping DMR Release Data 56
3.1.1.3.3 Mapping NEI Release Data 57
3.1.1.3.4 Mapping Systematic Review Data 57
3.1.1.4 Fill in Gaps with Modeling to Estimate Releases for OES with No Data 57
3.1.1.5 Estimate the Number of Release Days per Year for Facilities in the OES 58
3.2 Environmental Releases 59
3.2.1 Industrial and Commercial Releases 59
3.2.1.1 Number of Facilities with 1,1-Dichloroethane Emissions 60
3.2.1.2 Environmental Releases by Geographic Location 61
3.2.1.3 Environmental Releases by Media of Release 62
3.2.1.4 Environmental Releases by OES 63
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3,2.2 Weight of Scientific Evidence Conclusions for the Estimates of Environmental Releases
from Industrial and Commercial Sources 66
3.3 Concentrations of 1,1-Dichloroethane in the Environment 70
3.3.1 Ambient Air Pathway 71
3.3.1.1 Measured Concentrations in Ambient Air 71
3.3.1.2 EPA Modeled Concentrations in Ambient Air and Air Deposition
(IIO AC/AERMOD) 72
3.3.1.2.1 Ambient Air: Multi-Year Methodology IIO AC 74
3.3.1.2.2 Ambient Air: Multi-Year Methodology AERMOD TRI 74
3.3.1.2.3 Ambient Air: Multi-Year Methodology AERMOD NEI 81
3.3.1.2.4 Population Analysis 83
3.3.2 Indoor Air Pathway 83
3.3.2.1 Measured Concentrations in Indoor Air 83
3.3.2.2 Modeled Concentrations in Indoor Air 83
3.3.3 Surface Water Pathway 84
3.3.3.1 Measured Concentrations in Surface Water 85
3.3.3.2 Modeled Concentrations in Surface Water 87
3.3.3.2.1 Surface Water Modeling Methodology 87
3.3.3.2.2 Surface Water Modeling Results 89
3.3.3.2.3 Model Estimates from Point Source Calculator (PSC) 92
3.3.3.3 Measured Concentrations in Benthic Pore Water and Sediment 93
3.3.3.4 Modeled Concentrations in Benthic Pore Water and Sediment 93
3.3.3.4.1 Benthic Pore Water and Sediment Modeling Methodology 93
3.3.3.4.2 Benthic Pore Water and Sediment Modeling Results 94
3.3.3.5 Measured Concentrations in Drinking Water 95
3.3.3.6 Modeled Concentrations in Drinking Water 96
3.3.3.6.1 Drinking Water Modeling Methodology 96
3.3.3.6.2 Drinking Water Modeling Results 96
3.3.4 Land Pathway (Soils, Groundwater, and Biosolids) 98
3.3.4.1 Air Deposition to Soil 98
3.3.4.2 Measured Concentrations in Groundwater 99
3.3.4.2.1 Ambient Groundwater Monitoring 99
3.3.4.2.2 Measured Concentrations in Groundwater Sourced Drinking Water 101
3.3.4.3 Modeled Concentrations in Groundwater 101
3.3.4.3.1 Disposal to Landfills and Method to Model Groundwater Concentrations 102
3.3.4.3.2 Summary of Disposal to Landfills and Groundwater Concentrations 104
3.3.4.4 Measured Concentrations in Biosolids and Sludge 104
3.3.4.5 Modeled Concentrations in Groundwater Resulting from Land Application of
Biosolids 105
3.3.4.6 Modeled Concentrations in Wastewater Treatment Plant Sludge 105
3.3.4.6.1 Modeled Concentrations of 1,1-Dichloroethane in Soil Receiving Biosolids 105
3.3.4.6.2 Modeled Concentrations of 1,1-Dichloroethane in Soil Pore Water Receiving
Biosolids 106
3.3.5 Weight of Scientific Evidence Conclusions for Environmental Concentrations 106
3.3.5.1 Strengths, Limitations, and Sources of Uncertainty in Assessment Results for
Monitored and Modeled Concentrations 106
4 ENVIRONMENTAL RISK ASSESSMENT 114
4.1 Environmental Exposures 114
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4.1.1 Approach and Methodology 114
4.1.2 Exposures to Aquatic Species 115
4.1.2.1 Measured Concentrations in Aquatic Species 115
4.1.2.2 Calculated Concentrations in Aquatic Species 115
4.1.3 Exposures to Terrestrial Species 116
4.1.3.1 Measured Concentrations in the Terrestrial Environment 116
4.1.3.2 Modeled Concentrations in the Terrestrial Environment 116
4.1.4 Trophic Transfer Exposure 117
4.1.4.1 Trophic Transfer (Wildlife) 117
4.1.4.2 Trophic Transfer (Dietary Exposure) 118
4.1.5 Weight of Scientific Evidence Conclusions for Environmental Exposures 122
4.1.5.1 Strengths, Limitations, Assumptions, and Key Sources of Uncertainty for the
Environmental Exposure Assessment 122
4.1.5.2 Trophic Transfer Confidence 123
4.2 Environmental Hazards 127
4.2.1 Approach and Methodology 127
4.2.2 Aquatic Species Hazard 128
4.2.3 Terrestrial Species Hazard 135
4.2.4 Weight of Scientific Evidence Conclusions for Environmental Hazards 138
4.2.4.1 Strengths, Limitations, Assumptions, and Key Sources of Uncertainty for the
Environmental Hazard Assessment 138
4.2.5 Environmental Hazard Thresholds 140
4.2.5.1 Aquatic Species COCs 140
4.2.5.2 Terrestrial Species Hazard Values 142
4.3 Environmental Risk Characterization 145
4.3.1 Risk Characterization Approach 146
4.3.1.1 Risk Characterization Approach for Trophic Transfer 149
4.3.2 Risk Characterization for Aquatic Receptors 150
4.3.3 Risk Characterization for Terrestrial Organisms 161
4.3.4 Risk Characterization Based on Trophic Transfer in the Environment 163
4.3.5 Overall Confidence and Remaining Uncertainties Confidence in Environmental Risk
Characterization 168
4.3.5.1 Risk Characterization Confidence 168
4.3.6 Summary of Environmental Risk Characterization 170
5 HUMAN HEALTH RISK ASSESSMENT 176
5.1 Human Exposures 176
5.1.1 Occupational Exposures 176
5.1.1.1 Approach and Methodology 177
5.1.1.1.1 Identify and Describe Occupational Exposure Scenarios to Assess 178
5.1.1.1.2 Estimate Inhalation Exposure for OES Using 1,1-Dichloroethane Inhalation
Monitoring Data 180
5.1.1.1.3 Estimate Inhalation Exposure for OES Using Surrogate Monitoring Data 183
5.1.1.1.4 Approaches for Estimating Inhalation Exposure for Remaining OESs and ONU
Exposures 184
5.1.1.1.5 Estimate Dermal Exposure to 1,1-Dichloroethane 185
5.1.1.1.6 Estimate the Number of Workers and Occupational Non-users Potentially
Exposed 189
5.1.1.2 Estimates of Occupational Exposure (ppm) and Dermal Exposure (mg/day) 190
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5.1.1.3 Weight of Scientific Evidence for the Estimates of Occupational Exposures from
Industrial and Commercial Sources
5.1.2 General Population Exposures
5.1.2.1 Approach and Methodol ogy
5.1.2.1.1 General Population Exposure Scenarios
5.1.2.2 Summary of Inhalation Exposure Assessment
5.1.2.2.1 Ambient Air Exposure
5.1.2.2.2 Indoor Air Exposure
5.1.2.2.3 Populations in Proximity to Air Emissions
5.1.2.3 Summary of Dermal Exposure Assessment
5.1.2.3.1 Incidental Dermal Exposure from Swimming
5.1.2.4 Summary of Oral Exposure Assessment
5.1.2.4.1 Drinking Water Exposure
5.1.2.4.2 Fish Ingestion Exposure
5.1.2.4.3 Incidental Oral Ingestion from Swimming
5.1.2.4.4 Incidental Oral Ingestion from Soil (Biosolids)
5.1.2.4.5 Incidental Oral Ingestion from Soil (Air Deposition)
5.1.2.5 Weight of Scientific Evidence Conclusions for General Population Exposure
5.1.2.5.1 Strengths, Limitations, Assumptions, and Key Sources of Uncertainty for the
General Population Exposure Assessment
5.1.3 Aggregate Exposure Scenarios
5.1.4 Sentinel Exposures
5.2 Human Health Hazard
5.2.1 Approach and Methodol ogy
5.2.1.1 Identification and Evaluation of 1,1 -Dichloroethane Hazard Data
5.2.1.2 1,1-Dichloroethane Data Gaps
5.2.1.2.1 Non-cancer Data Gaps
5.2.1.2.2 Cancer Data Gaps
5.2.1.3 Identification of an Analog and the Use of Read-Across from 1,2-Dichloroethane
Hazard Data
5.2.1.3.1 Structural Similarity
5.2.1.3.2 Physical and Chemical Similarities
5.2.1.3.3 Metabolic Similarities
5.2.1.3.4 Toxicological Similarity - Cancer
5.2.1.3.5 Toxicological Similarity - Non-cancer
5.2.1.3.6 Read-Across Conclusions
5.2.1.4 Identification and Evaluation of 1,2-Dichloroethane Hazard Data
5.2.1.5 Structure of the Human Health Hazard Assessment
5.2.2 Toxicokinetics Summary
5.2.2.1 1,1-Dichloroethane
5.2.2.2 1,2-Dichloroethane
5.2.3 Non-cancer Hazard Identification and Evidence Integration
5.2.3.1 Critical Human Health Hazard Outcomes
5.2.3.1.1 Renal Toxicity
5.2.3.1.2 Immunological/Hematological
5.2.3.1.3 Neurol ogi cal/B ehavi oral
5.2.3.1.4 Reproductive/Developmental
5.2.3.1.5 Hepatic
5.2.3.1.6 Nutritional/Metabolic
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5.2.3.1.7 Respiratory
5.2.3.1.8 Mortality
5.2.4 Genotoxicity Hazard Identification and Evidence Integration
5.2.5 Cancer Hazard Identification, Mode of Action (MOA) Summary and Evidence
Integration
5.2.5.1 Cancer Hazard Identification and Evidence Integration
5.2.5.1.1 Human Evidence
5.2.5.1.2 Animal Evidence
5.2.5.2 Mode of Action (MOA) Summary
5.2.5.3 Weight of Scientific Evidence
5.2.6 Dose-Response Assessment
5.2.6.1 Selection of Studies and Endpoints for Non-cancer Toxicity
5.2.6.1.1 Uncertainty Factors Used for Non-cancer Endpoints
5.2.6.1.2 Non-cancer PODs for Acute Exposures
5.2.6.1.3 Non-cancer PODs for Short-Term/Subchronic Exposures
5.2.6.1.4 Non-cancer PODs for Chronic Exposures
5.2.6.2 Endpoint Derivation for Carcinogenic Dose-Response Assessment
5.2.6.3 PODs for Non-cancer and Cancer Human Health Hazard Endpoints
5.2.6.4 Human Health Hazard Values Used by Other Agencies
5.2.7 Weight of Scientific Evidence Conclusions for Human Health Hazard
5.2.7.1 Overall Confidence - Strengths, Limitations, Assumptions, and Key Sources of
Uncertainty in the Human Health Hazard Assessment
5.2.7.2 Hazard Considerations for Aggregate Exposure
5.3 Human Health Risk Characterization
5.3.1 Risk Characterization Approach
5.3.1.1 Estimation of Non-cancer Risks
5.3.1.2 Estimation of Cancer Risks
5.3.2 Risk Characterization for Potentially Exposed or Susceptible Subpopulations
5.3.3 Human Health Risk Characterization
5.3.3.1 Risk Estimates for Workers and ONUs
5.3.3.1.1 Acute Risk
5.3.3.1.2 Short-Term Subchronic Risk
5.3.3.1.3 Chronic Non-cancer Risk
5.3.3.1.4 Cancer Risk
5.3.3.1.5 Occupational Exposure Summary by OES
5.3.3.2 Risk Estimates for the General Population
5.3.3.2.1 Inhalation Exposure Risk
5.3.3.2.2 Land Use Analysis
5.3.3.2.3 Dermal Exposures
5.3.3.2.4 Oral Exposures
5.3.3.2.5 Summary of Risk Estimates for General Population
5.3.4 Risk Characterization of Aggregate and Sentinel Exposures
5.3.5 Overall Confidence and Remaining Uncertainties in Human Health Risk
Characterization
5.3.5.1 Occupational Risk Estimates
5.3.5.2 General Population Risk Estimates
5.3.5.3 Hazard Values
UNREASONABLE RISK DETERMINATION
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6.1 Unreasonable Risk to Human Health 355
6.1.1 Populations and Exposures EPA Assessed to Determine Unreasonable Risk to Human
Health 355
6.1.2 Summary of Unreasonable Risks to Human Health 356
6.1.3 Basis for EPA's Determination of Unreasonable Risk to Human Health 356
6.1.4 Unreasonable Risk in Occupational Settings 357
6.1.5 Unreasonable Risk to the General Population 358
6.2 Unreasonable Risk to the Environment 360
6.2.1 Populations and Exposures EPA Assessed to Determine Unreasonable Risk to the
Environment 360
6.2.2 Summary of Unreasonable Risks to the Environment 360
6.2.3 Basis for EPA's Determination of Unreasonable Risk of Injury to the Environment 360
6.3 Additional Information Regarding the Basis for the Unreasonable Risk Determination 361
6.3.1 Additional Information about COUs Characterized Qualitatively 361
REFERENCES 366
APPENDICES 394
Appendix A ABBREVIATIONS, ACRONYMS, AND GLOSSARY OF SELECT TERMS 394
A. 1 Key Abbreviations and Acronyms 394
A.2 Glossary of Select Terms 397
Appendix B REGULATORY AND ASSESSMENT HISTORY 399
B.l Federal Laws and Regulations 399
B.2 State Laws and Regulations 403
B.3 International Laws and Regulations 404
B.4 Assessment History 404
Appendix C LIST OF SUPPLEMENTAL DOCUMENTS 407
Appendix D PHYSICAL AND CHEMICAL PROPERTIES AND FATE AND TRANSPORT
DETAILS 411
D. 1 Physical and Chemical Properties 411
D.2 Fate and Transport 421
D. 2.1 Approach and Methodol ogy 421
D.2.1.1 EPI Suite™ Model Inputs 421
D.2.1.2 Fugacity Modeling 421
D. 2.1.3 Evi dence Integrati on 422
D.2.2 Air and Atmosphere 424
D.2.2.1 Key Sources of Uncertainty in the Fate Assessment for Air and the Atmosphere 425
D.2.3 Aquatic Environments 425
D.2.3.1 Surface Water 425
D.2.3.2 Sediments 426
D.2.3.3 Key Sources of Uncertainty in the Fate Assessment for Aquatic Environments 427
D.2.4 Terrestrial Environments 427
D.2.4.1 Soil 427
D.2.4.2 Groundwater 430
D.2.4.3 Landfills 431
D.2.4.4 Biosolids 432
D.2.4.5 Key Sources of Uncertainty in the Fate Assessment for Terrestrial Environments 434
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D.2.5 Persistence Potential
D.2.5.1 Destruction and Removal Efficiency
D.2.5.2 Removal in Wastewater Treatment
D.2.5.3 Key Sources of Uncertainty in the Persistence Assessment
D.2.6 Bioaccumulation Potential
D.2.6.1 Key Sources of Uncertainty in the Bioaccumulation Assessment
D.3 Measured Data in Literature for Environmental Media
D. 3.1 Exampl e Tornado PI ot
D.3.2 Ambient Air
D. 3.3 Drinki ng Water
D. 3.4 Groundwater
D.3.5 Indoor Air
D.3.6 Soil and Soil-Water Leachate
D. 3.7 Surface Water
D.3.8 Wastewater
Appendix E AIR EXPOSURE PATHWAY
E. 1 Modeling Approach for Estimating Concentrations of 1,1-Dichloroethane in Air and
Deposition to Land and Water
E. 1.1 Multi-year Analysis Methodology IIOAC
E.1.1.1 Model
E.l.1.2 Releases
E.l.1.3 Exposure Scenarios
E. 1.2 Multi-year Analysis Methodology AERMOD (TRI or NEI)
E. 1.2.1 Model
E.l.2.2 Releases
E.l.2.3 Exposure Scenarios
E. 1.2.4 Meteorological Data
E. 1.2.5 Urban/Rural Designations
E. 1.2.6 Physical Source Specifications for TRI Release Facilities and Alternative Release
Estimates
E. 1.2.7 Temporal Emission Patterns
E.l.2.8 Emission Rates
E. 1.2.9 Deposition Parameters
E. 1.2.10 Other Model Settings
E. 1.2.11 Ambient Air Exposure Concentration Outputs
E. 1.2.12 Physical Source Specifications: NEI Release Facilities
E.2 Inhalation Exposure Estimates for Fenceline Communities
E.3 Land Use Analysis
E.4 Aggregate Analysis across TRI Facilities
E.5 Ambient Air Exposure to Population Evaluation
Appendix F SURFACE WATER CONCENTRATIONS
F. 1 Surface Water Monitoring Data
F. 1.1 Monitoring Data Retrieval and Processing
F.2 Surface Water Concentration Modeling
F.2.1 Hydrologic Flow Data Assimilation
F.2.2 Facility-Specific Release Modeling
F.2.3 Modeling at Drinking Water Intakes
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353 Appendix G GROUNDWATER CONCENTRATIONS 480
354 G. 1 Groundwater Monitoring Data 480
355 G. 1.1 Monitoring Data Retrieval and Processing 480
356 Appendix H DRINKING WATER EXPOSURE ESTIMATES 481
357 H. 1 Surface Water Sources of Drinking Water 482
358 H.2 Groundwater Sources of Drinking Water 482
359 H.3 Removal through Drinking Water Treatment 483
360 Appendix I ECOLOGICAL EXPOSURE ESTIMATES 484
361 1.1 The Point Source Calculator 484
362 1.1.1 Description of the Point Source Calculator 484
363 1.1.2 Point Source Calculator Input Parameters 484
364 1.1.3 Water Column, Pore Water, and Benthic Sediment Results 486
365 1.2 Concentrations in Biota and Associated Dietary Exposure Estimates 487
366 Appendix J ANALOG SELECTION FOR READ-ACROSS 494
367 J.l Analog Selection for Environmental Hazard 494
368 J. 1.1 Structural Similarity 494
369 J. 1.2 Physical, Chemical, and Environmental Fate and Transport Similarity 495
370 J.1.3 Toxicological Similarity 497
371 J.1.4 Analog Data Availability 500
372 J.2 Analog Selection for Human Health Hazard 500
373 J.2.1 Structural Similarity 501
374 J.2.2 Physical and Chemical Similarity 502
375 J.2.3 Metabolic Similarities 503
376 J.2.4 Toxicological Similarity - Non-cancer 505
377 J.2.5 Toxicological Similarity - Cancer 506
378 J.2.6 Read-Across Utilized in Other Program Offices 508
379 J.2.7 Read-Across Conclusions 510
380 Appendix K ENVIRONMENTAL HAZARD DETAILS 511
381 K. 1 Approach and Methodology 511
382 K.2 Hazard Identification 511
383 K.2.1 Aquatic Hazard Data 511
384 K.2.1.1 Web-Based Interspecies Correlation Estimation (Web-ICE) 511
385 K.2.1.2 Species Sensitivity Distribution (SSD) 515
386 K.2.1.3 Dose-Response Curve Fit Methods 518
387 K.2.2 Terrestrial Hazard Data 520
388 K. 2.3 Evi dence Integrati on 522
389 K.2.3.1 Weight of Scientific Evidence 523
390 K.2.3.2 Data Integration Considerations Applied to Aquatic and Terrestrial Hazard
391 Representing the 1,1,-Dichloroethane Environmental Hazard Database 527
392 Appendix L ENVIRONMENTAL RISK DETAILS 532
393 L. 1 Risk Estimation for Aquatic Receptors 532
394 L.2 Risk Estimation for Terrestrial Receptors 532
395 L.3 Trophic Transfer Analysis Results 533
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Appendix M HUMAN HEALTH HAZARD DETAILS 537
M.l Toxicokinetics 537
M.l.l Absorption 537
M.l. 1.1 1,1-Dichloroethane 537
M.l. 1.2 1,2-Dichloroethane 537
M.l.2 Distribution 539
M.l.2.1 1,1-Dichloroethane 539
M.l.2.2 1,2-Dichloroethane 540
M.l.3 Metabolism 541
M.l. 3.1 1,1-Dichloroethane 541
M.l. 3.2 1,2-Dichloroethane 543
M.l.4 Elimination 545
M.l.4.1 1,1-Dichloroethane 545
M.l.4.2 1,2-Dichloroethane 545
M.2 Non-cancer Dose-Response Assessment 547
M.2.1 Non-cancer Dose-Response Assessment for 1,1-Dichloroethane 547
M.2.2 Non-cancer Dose-Response Assessment for 1,2-Dichloroethane 553
M.2.3 Non-cancer PODs for Acute Exposures for 1,1-Dichloroethane 569
M.2.4 Non-cancer PODs for Short/Intermediate-Term Exposures for 1,1-Dichloroethane 569
M.2.5 Non-cancer PODs for Chronic Exposures for 1,1-Dichloroethane 570
M.2.6 Non-cancer PODs for Acute Exposures for 1,2-Dichloroethane 572
M.2.7 Non-cancer PODs for Short/Intermediate-Term Exposures for 1,2-Dichloroethane 574
M.2.8 Non-cancer PODs for Chronic Exposures for 1,2-Dichloroethane 576
M.3 Equations 576
M.3.1 Equations 576
M.3.1.1 Air Concentration Unit Conversion 577
M.3.1.2 Adjustment for Continuous Exposure 577
M.3.1.3 Calculation of HEDs and HECs from Animal PODs 577
M.3.1.4 Cancer Inhalation Unit Risk 579
M.3.1.5 Conversion of Continuous PODs to Worker PODs 580
M.4 Summary of Continuous and Worker Non-cancer PODs 580
M.5 Evidence Integration Tables for Non-cancer for 1,1-Dichloroethane 582
M.6 Evidence Integration Tables for Non-cancer for 1,2-Dichloroethane 594
M.7 Mutagenicity and Cancer 625
M. 7.1 1,1 -Di chl oroethane 625
M.7.1.1 Evidence Integration Table for Cancer for 1,1-Dichloroethane 629
M.7.2 1,2-Dichloroethane 634
M.7.2.1 Evidence Integration Tables for Cancer for 1,2-Dichloroethane 639
M.8 Cancer Dose-Response Assessment (Read-Across from 1,2-Dichloroethane) 654
M.8.1 Summary of Continuous and Worker PODs 656
Appendix N DRAFT OCCUPATIONAL EXPOSURE VALUE DERIVATION 658
N.l Draft Occupational Exposure Value Calculations 659
N.2 Summary of Air Sampling Analytical Methods Identified 662
Appendix O 1,1-DICHLOROETHANE CONDITIONS OF USE 663
0.1 Additions and Name Changes to Conditions of Use Based on Updated 2020 CDR Reported
Data and Stakeholder Engagement 663
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0.2 Consolidation and Other Changes to Conditions of Use Table 663
0.3 Descriptions of 1,1-Dichloroethane Conditions of Use 663
0.3.1 Manufacturing 663
0.3.1.1 Domestic Manufacturing 663
0.3.2 Processing - As a Reactant 663
0.3.2.1 Intermediate in All Other Basic Organic Chemical Manufacture 663
0.3.2.2 Intermediate in All Other Chemical Product and Preparation Manufacturing 664
0.3.2.3 Repackaging 664
0.3.2.4 Recycling 664
0.3.3 Distribution in Commerce 664
0.3.4 Commercial Use in Laboratory Chemicals 664
0.3.5 Disposal 664
LIST OF TABLES
Table 1-1. Categories and Subcategories of Use and Corresponding Exposure Scenario in the Risk
Evaluation for 1,1-Dichloroethane 31
Table 2-1. Physical and Chemical Properties of 1,1-Dichloroethane 40
Table 2-2 Environmental Fate Characteristics of 1,1-Dichloroethane 43
Table 3-1. Crosswalk of Conditions of Use to Occupational Exposure Scenarios Assessed 51
Table 3-2. Description of the Function of 1,1-Dichloroethane for Each OES 52
Table 3-3. Generic Estimates of Number of Operating Days per Year for Each OES 59
Table 3-4. Number of Sites with 1,1-Dichloroethane Environmental Releases 60
Table 3-5. Average Annual Environmental Release Estimates by Media of Release 63
Table 3-6. Summary of EPA's Annual and Daily Release Estimates for Each OES 64
Table 3-7. Summary of Weight of Scientific Evidence Ratings for Environmental Release Estimates by
OES 67
Table 3-8. Summary of Selected Statistics of 1,1-Dichloroethane Ambient Air Concentrations ([j,g/m3)
from EPA Ambient Monitoring Technology Information Center 72
Table 3-9. Summary of Select Statistics for the 95th Percentile Annual Average Concentrations for 1,1-
Dichloroethane Releases Reported to TRI 77
Table 3-10. Summary of Select Statistics for the 95th Percentile Daily Average Air Deposition Rates for
1,1-Dichloroethane Releases Reported to TRI 78
Table 3-11. Summary of Select Statistics for the 95th Percentile Annual Average Air Deposition Rates
for 1,1-Dichloroethane Releases Reported to TRI 79
Table 3-12. Summary of Maximum 95th Percentile Annual Average Concentrations for 1,1-
Dichloroethane for Commercial Use as a Laboratory Chemical, and Processing -
Repackaging for Laboratory Chemicals OESs for the 95th Percentile Production Volume
80
Table 3-13. Summary of Select Statistics for the 95th Percentile Estimated Annual Average
Concentrations for 1,1-Dichloroethane Releases Reported to NEI 82
Table 3-14. Summary of Select Statistics for the 95th Percentile Estimated Annual Average Indoor Air
Concentrations for 1,1- Dichloroethane Releases Reported to TRI 84
Table 3-15. Results from the Point Source Calculator, Showing Facility Release Information, 7Q10
Flow Values, and Modeled Chronic Surface Water (Water Column) Concentrations that
Exceed the Water Column Acute Coc (7,898 (J,g/L) and Chronic CoC (93 (J,g/L) for
Ecological Species Exposure 92
Table 3-16. Results from the Point Source Calculator, Showing the Highest 95th Percentile Daily
Average Air Deposition Rate for OES Manufacturing and Modeled Surface Water (Water
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Column) Concentrations for a 1-Day Acute and 21-Day Chronic Scenario for Ecological
Species Exposure 10 m from Releasing Facility of TRI-Reported Fugitive Emissions... 93
Table 3-17. Results from the Point Source Calculator, Showing the Highest 95th Percentile Daily
Average Air Deposition Rate per OES, and Modeled Benthic Pore Water and Sediment
Concentrations for a 1-Day Acute and 21-Day Chronic Scenario for Ecological Species
Exposure 95
Table 3-18. Modeled 30Q5 Concentrations of 1,1-Dichloroethane in Drinking Water at PWSs within
250 km Downstream of a Facility Release Site, Changes in Hydrologic Flow between the
Release Site and PWS Intake Location, as Well as the Population Served by the PWS.. 98
Table 3-19. Soil Catchment and Soil Catchment Pore Water Concentrations Estimated from 95th
Percentile Maximum Daily Air Deposition Rates 10 m from Facility for 1,1-
Dichloroethane Releases Reported to TRI 99
Table 3-20. Estimated Groundwater Concentrations (mg/L) of 1,1-Dichloroethane Found in Wells
within 1 Mile of a Disposal Facility Determined by the DRAS Model 102
Table 3-21. Soil and Soil Pore Water Concentrations Estimated from Annual Application of Biosolids
106
Table 3-22. Comparison of 1,1-Dichloroethane AERMOD Modeled Concentrations for a TRI Facility
with 1,1-Dichloroethane Ambient Air Monitoring Data from Six AMTIC Monitoring
Sites within 10 km of the Facility from 2015 to 2020 109
Table 3-23. Confidence and Weight of Scientific Evidence per OES for 1,1-Dichlorethane Concentration
in Media 112
Table 4-1. Terms and Values Used to Assess Potential Trophic Transfer of 1,1-Dichloroethane for
Terrestrial and Semi-Aquatic Receptors 119
Table 4-2. 1,1-Dichloroethane Evidence Table Summarizing Overall Confidence Derived for Trophic
Transfer (Dietary) 126
Table 4-3. Aquatic Organisms Environmental Hazard Studies for 1,1-Dichloroethane, Supplemented
with 1,2-Dichloropropane and/or 1,1,2-Trichloroethane Data as Analogs 133
Table 4-4. Terrestrial Organisms Environmental Hazard Studies Used for 1,1-Dichloroethane 137
Table 4-5. 1,1-Dichloroethane Evidence Table Summarizing the Overall Confidence Derived from
Hazard Thresholds 139
Table 4-6. Environmental Hazard Thresholds for Aquatic Environmental Toxicity 142
Table 4-7. Environmental Hazard Thresholds for Terrestrial Environmental Toxicity 144
Table 4-8. Environmental Risk Quotients (RQs) by COU for Aquatic Organisms with 1,1-
Dichloroethane Surface Water Concentration (|ig/L) Modeled by PSC 154
Table 4-9. Environmental Risk Quotients (RQs) by COU for Aquatic Non-vascular Plants with 1,1-
Dichloroethane Surface Water Concentration (|ig/L) Modeled by PSC 156
Table 4-10. Environmental Risk Quotients (RQs) by COU for Aquatic Organisms with 1,1-
Dichloroethane Benthic Pore Water Concentration (|ig/L) Modeled by PSC 157
Table 4-11. Environmental Risk Quotients (RQs) by COU for Aquatic Organisms with 1,1-
Dichloroethane Sediment Concentration (|ig/kg) Modeled by PSC 159
Table 4-12. Calculated Risk Quotients (RQs) For Terrestrial Plants Based on Modeled Air Deposition of
1,1-Dichloroethane to Soil from Reported or Modeled Fugitive Emissions 162
Table 4-13. Calculated Risk Quotients (RQs) For Terrestrial Plants Based on 1,1-Dichloroethane Soil
Pore Water Concentrations (|ig/L) as Calculated Using Modeled Biosolid Land
Application Data 163
Table 4-14. Risk Quotients (RQs) for Screening Level Trophic Transfer of 1,1-Dichloroethane from Air
Deposition in Insectivorous Terrestrial Ecosystems Using EPA's Wildlife Risk Model for
Eco-SSLs 165
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Table 4-15. Risk Quotients (RQs) for Screening Level Trophic Transfer of 1,1-Dichloroethane from Air
Deposition in Herbivorous Terrestrial Ecosystems Using EPA's Wildlife Risk Model for
Eco-SSLs 165
Table 4-16. Risk Quotients (RQs) for Screening Level Trophic Transfer of 1,1-Dichloroethane from
Biosolid Land Application in Insectivorous Terrestrial Ecosystems Using EPA's Wildlife
Risk Model for Eco-SSLs 166
Table 4-17. Risk Quotients (RQs) for Screening Level Trophic Transfer of 1,1-Dichloroethane from
Biosolid Land Application in Herbivorous Terrestrial Ecosystems Using EPA's Wildlife
Risk Model for Eco-SSLs 166
Table 4-18. Risk Quotient (RQ) Based on Potential Trophic Transfer of 1,1-Dichloroethane from Fish to
American Mink (Mustela vison) as a Model Aquatic Predator Using EPA's Wildlife Risk
Model for Eco-SSLs 167
Table 4-19. Risk Quotient (RQ) Based on Potential Trophic Transfer of 1,1-Dichloroethane from
Crayfish to American Mink (Mustela vison) as a Model Aquatic Predator Using EPA's
Wildlife Risk Model for Eco-SSLs 167
Table 4-20. Evidence Table Summarizing Overall Confidence for Environmental Risk Characterization
169
Table 4-21. COUs and Corresponding Environmental Risk for Aquatic Receptors Exposed to 1,1-
Dichloroethane in Surface Water, Benthic Pore Water, and Sediment 172
Table 4-22. COUs and Corresponding Environmental Risk for Terrestrial Receptors Exposed to 1,1-
Dichloroethane in Soil Pore Water (Plants) and Trophic Transfer 174
Table 5-1. Data and Approaches for Assessing Occupational Exposures to 1,1-Dichloroethane 178
Table 5-2. Similar Exposure Groups (SEGs) for 1,1-Dichloroethane 179
Table 5-3. Summary of Manufacturing Inhalation Exposures to 1,1-Dichloroethane 181
Table 5-4. Worker Activities Associated with the Five Highest Sampling Results 181
Table 5-5. Summary of Processing as a Reactive Intermediate Inhalation Exposure Estimates 182
Table 5-6. Summary of Commercial Use as a Laboratory Chemical Inhalation Exposure Estimates... 182
Table 5-7. Summary of Approaches for the Occupational Exposure Scenarios Using 1,1-Dichloroethane
Monitoring Data 183
Table 5-8. Summary of General Waste Handling, Treatment, and Disposal Inhalation Exposure
Estimates 184
Table 5-9. Summary of Waste Handling, Treatment, and Disposal (POTW) Inhalation Exposure
Estimates 184
Table 5-10. Approach for the Occupational Exposure Scenarios Using Surrogate Monitoring Data.... 184
Table 5-11. Summary of Processing - Repackaging Inhalation Exposure Estimates 185
Table 5-12. Approach for the Occupational Exposure Scenarios Using Modeling 185
Table 5-13. Summary of Dermal Model Input Values 187
Table 5-14. Comparison of Dermal Exposure Values 188
Table 5-15. Dermal Potential Dose Rate Estimates 189
Table 5-16. Total Number of Workers and ONUs Potentially Exposed to 1,1-Dichloroethane for Each
OES 190
Table 5-17. Summary of Assessment Methods for Each Occupational Exposure Scenario 191
Table 5-18. Summary of Inhalation and Dermal Exposure Estimates for Each OES 192
Table 5-19. Weight of Scientific Evidence Conclusions for the Inhalation Exposure Assessment 194
Table 5-20. Lifetime Average Daily Concentrations Estimated within 10,000 m of 1,1-Dichloroethane
TRI Releases to Air 205
Table 5-21. Lifetime Average Daily Concentrations Estimated within 10,000 m of 1,1-Dichloroethane
Releases to Air Reported to NEI 205
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Table 5-22. Lifetime Average Daily Concentrations Estimated within 10,000 m of 1,1-Dichloroethane
Releases to Air for the Commercial Use as a Laboratory Chemical, and Processing -
Repackaging for Laboratory Chemicals OESs, for the 95th Percentile Production Volume
206
Table 5-23. Indoor Air Lifetime Average Daily Concentrations (LADCs) Estimated within 1,000 m of
1,1-Dichloroethane Releases to Air Reported to TRI 207
Table 5-24. Population Density Estimates within 1,000 m of a Subset of AERMOD TRI Air Release
Sites that Reflect High-End Exposures 208
Table 5-25. Population Density Estimates by Age Groups within 1,000 m of the Subset of AERMOD
TRI Air Release Sites 209
Table 5-26. Population Density by Race and Ethnicity Expressed as a Percentage of the Total Population
within 1,000 m of the Subset of AERMOD TRI Release Sites 210
Table 5-27. Median Household Income, Population Density, and Poverty Status for Populations within
1,000 m of the Subset AERMOD TRI Release Sites 210
Table 5-28. Highest Modeled Incidental Dermal (Swimming) Doses for all COUs, for Adults, Youth,
and Children 213
Table 5-29. Highest Drinking Water Exposures from Surface Water Releases 214
Table 5-30. Summary of Fish Ingestion Exposures 216
Table 5-31. Summary of Incidental Oral Exposures from Swimming 218
Table 5-32. Modeled Exposure to 1,1-Dichloroethane in Land Applied Biosolids for Children 220
Table 5-33. Modeled Soil Ingestion Doses for the Processing as a Reactant OES, for Children 222
Table 5-34. Weight of Scientific Evidence (WOSE) Conclusions for General Population Exposure
Assessments 225
Table 5-35. Structural Similarity of 1-1 Dichloroethane Compared to Other Chlorinated Solvents 235
Table 5-36. Comparison of 1,1-Dichloroethane and 1,2-Dichloroethane for Physical and Chemical
Properties Relevant to Human Health Hazard 236
Table 5-37. Qualitative Comparison of Cancer Findings for 1,1-Dichloroethane compared to 1,2-
Dichloroethane 237
Table 5-38. Comparison of Cancer Study Findings for 1,1-Dichloroethane and 1,2-Dichloroethane... 237
Table 5-39. OncoLogic Carcinogenic Potential Results for 1,1-Dichloroethane and 1,2-Dichloroethane
238
Table 5-40. Qualitative Comparison of Non-cancer Findings between 1,1-Dichloroethane and 1,2-
Dichloroethane 238
Table 5-41. Common Hazards and Properties of 1,1-Dichloroethane and 1,2-Dichloroethane 239
Table 5-42. Acute Oral Non-cancer POD-Endpoint Selection Table 266
Table 5-43. Acute Inhalation Non-cancer POD-Endpoint Selection Table 268
Table 5-44. Short-Term/Subchronic Oral Non-cancer POD-Endpoint Selection Table 275
Table 5-45. Short-Term/Subchronic Inhalation Non-cancer POD-Endpoint Selection Table 278
Table 5-46. Chronic Oral Non-cancer POD-Endpoint Selection Table 283
Table 5-47. Chronic Inhalation Non-cancer POD-Endpoint Selection Table 286
Table 5-48. IUR Estimates for Tumor Data from Nagano et al. (2006) Study of 1,2-Dichloroethane
Using Linear Low-Dose Extrapolation Approach 291
Table 5-49. PODs and Toxicity Values Used to Estimate Non-cancer Risks for Acute Exposure
Scenarios 295
Table 5-50. PODs and Toxicity Values Used to Estimate Non-cancer Risks for Short-Term Exposure
Scenarios 296
Table 5-51. PODs and Toxicity Values Used to Estimate Non-cancer Risks for Chronic Exposure
Scenarios 298
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Table 5-52. Cancer PODs for 1,1-Dichloroethane Lifetime Exposure Scenarios - Read-Across from 1,2-
Dichloroethane Data 300
Table 5-53. Non-Cancer Human Health Hazard Values Used by Other Agencies and EPA Offices.... 302
Table 5-54. Confidence Summary for Human Health Hazard Assessment 314
Table 5-55. Exposure Scenarios, Populations of Interest, and Hazard Values 316
Table 5-56. Summary of PESS Categories in the Draft Risk Evaluation and Remaining Sources of
Uncertainty 319
Table 5-57. Parameter Values for Calculating Exposure Estimates 322
Table 5-58. Summary of Occupational Inhalation Exposure Metrics 327
Table 5-59. Summary of Occupational Dermal Exposure Metrics 328
Table 5-60. Occupational Risk Summary Table 329
Table 5-61. Inhalation Lifetime Cancer Risks within 1 km of TRI Air Releases Based on 95th Percentile
Modeled Ambient Air Exposure Concentrations 336
Table 5-62. Inhalation Lifetime Cancer Risks within 1 km of NEI Air Releases Based on 95th Percentile
Modeled Ambient Air Exposure Concentrations 337
Table 5-63. Inhalation Lifetime Cancer Risks within 1 km of TRI Air Releases Based on 50th Percentile
Modeled Ambient Air Exposure Concentrations 338
Table 5-64. Inhalation Lifetime Cancer Risks within 1 km of NEI Air Releases Based on 50th Percentile
Modeled Ambient Air Exposure Concentrations 339
Table 5-65. Inhalation Lifetime Cancer Risks within 1 km of TRI Air Releases 340
Table 5-66. Inhalation Lifetime Cancer Risks within 1 km of NEI Air Releases 340
Table 5-67. Inhalation Lifetime Cancer Risks within 1 km of Air Releases Based on 95th Percentile
Modeled Exposure Concentrations for the Commercial Use as a Laboratory Chemical,
and Processing - Repackaging for Laboratory Chemicals OESs 341
Table 5-68. IIOAC Indoor Air Inhalation Lifetime Cancer Risks within 1 km of TRI Air Releases Based
on 95th Percentile Modeled Exposure Concentrations 341
Table 5-69. IIOAC Indoor Air Inhalation Lifetime Cancer Risks within 1 km of TRI Air Releases Based
on 50th Percentile Modeled Exposure Concentrations 342
Table 5-70. General Population Risk Summary 345
Table 5-71. Overall Confidence for Acute, Short-Term, and Chronic Human Health Non-cancer Risk
Characterization for COUs Resulting in Risks 352
Table 5-72. Overall Confidence for Lifetime Human Health Cancer Risk Characterization for COUs
Resulting in Risks 353
Table 6-1. Supporting Basis for the Draft Unreasonable Risk Determination for Human Health 363
Table 6-2. Supporting Basis for the Draft Unreasonable Risk Determination for the Environment 365
LIST OF FIGURES
Figure 1-1. TSCA Existing Chemical Risk Evaluation Process 28
Figure 1-2. 1,1-Dichloroethane Life Cycle Diagram 30
Figure 1-3. 1,1-Dichloroethane Conceptual Model for Industrial and Commercial Activities and Uses:
Potential Exposure and Hazards 33
Figure 1-4. 1,1-Dichloroethane Conceptual Model for Environmental Releases and Wastes: General
Population Exposures and Hazards 34
Figure 1-5. 1,1-Dichloroethane Conceptual Model for Environmental Releases and Wastes: Ecological
Exposures and Hazards 35
Figure 1-6. Populations Assessed in this Draft Risk Evaluation for 1,1-Dichloroethane 36
Figure 1-7. Diagram of the Systematic Review Process 38
Figure 2-1. Transport, Partitioning, and Degradation of 1,1-Dichloroethane in the Environment 45
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Figure 3-1. Overview of EPA's Approach to Estimate Releases for Each OES 50
Figure 3-2. Overview of EPA's Approach to Map Facility Release Data to OES 56
Figure 3-3. 1,1-Dichlorothane Annual Releases to Air as Reported by TRI, 2015-2020 61
Figure 3-4. 1,1-Dichloroethane Annual Releases to Air as Reported by NEI, 2014 and 2017 62
Figure 3-5. Concentrations of 1,1-Dichloroethane (|ig/m3) in the Vapor/Gas Fraction of Ambient Air
from U.S.-Based and International Studies, 2005-2017 71
Figure 3-6. Brief Description of Methodologies and Analyses Used to Estimate Air Concentrations and
Exposures 73
Figure 3-7. Concentrations of 1,1-Dichloroethane (|ig/m3) in the Vapor/Gas Fraction in Indoor Air,
from U.S.-Based and International Studies, 1992-2017 83
Figure 3-8. Locations of 1,1-Dichloroethane Measured in Ambient Surface Waters Obtained from the
WQP, 2015-2020 86
Figure 3-9. National Distribution of 1,1-Dichloroethane Concentrations Measured in Ambient Surface
Waters from Surface Waters Obtained from the WQP, 2015-2020 86
Figure 3-10. Concentrations of 1,1-Dichloroethane (|i/L) in Surface Water from U.S.-Based and
International Studies, 1984-2005 87
Figure 3-11. Locations of Modeled Estimates of 1,1-Dichloroethane Concentration from Facility
Releases to Ambient Surface Waters, 2015-2020 90
Figure 3-12. Distribution of Highest Facility Annual Releases of 1,1-Dichloroethane to their Receiving
Water Body between 2015-2020 91
Figure 3-13. Distribution of Surface Water Concentrations of 1,1-Dichloroethane Modeled from the
Highest Annual Facility Releases between 2015-2020 for a One Operating Day Per Year
Scenario 91
Figure 3-14. Concentrations of 1,1-Dichloroethane (|i/L) in Drinking Water from a U.S.-Based Study,
2002-2012 96
Figure 3-15. Distribution of Drinking Water Concentrations of 1,1-Dichloroethane Modeled from the
Highest Annual Facility Releases between 2015-2022 for a One Operating Day per Year
Scenario 97
Figure 3-16. Locations of 1,1-Dichloroethane Measured in Groundwater Monitoring Wells Acquired
from the WQP, 2015-2020 100
Figure 3-17. Distribution of 1,1-Dichloroethane Concentrations from Groundwater Monitoring Wells (N
= 14,483) Acquired from the Water Quality Portal, 2015-2020 100
Figure 3-18. Concentrations of 1,1-Dichloroethane (|i/L) in Groundwater from U.S.-Based and
International Studies, 1984-2005 101
Figure 3-19. Concentrations of 1,1-Dichloroethane (|ig/L) in the Soil-Water Leachate from U.S.-Based
Studies for Locations near Facility Releases, 1984-1993 101
Figure 3-20. Location of TRI Facility (TRI ID 42029WSTLK2468I, Yellow Dot) and AMTIC
Monitoring Sites within 10 km of the TRI Facility (Green Dots) 109
Figure 4-1. Trophic Transfer of 1,1-Dichloroethane in Aquatic and Terrestrial Ecosystems 122
Figure 4-2. Mammalian TRV Derivation for 1,1-Dichloroethane 143
Figure 5-1. Overview of EPA's Approach to Estimate Occupational Exposures for 1,1-Dichloroethane
177
Figure 5-2. Potential Human Exposure Pathways to 1,1-Dichloroethane for the General Population... 198
Figure 5-3. Overview of General Population Exposure Assessment for 1,1-Dichloroethane 200
Figure 5-4. Modeled Exposure Points for Finite Distance Rings for Ambient Air Modeling (AERMOD)
201
Figure 5-5. Modeled Exposure Point Locations for Area Distance for Ambient Air Modeling
(AERMOD) 202
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Figure 5-6. EPA Approach to Hazard Identification, Evidence Integration, and Dose-Response Analysis
for Human Health Hazard 230
Figure 5-7. Hepatocellular Carcinoma Dose Response in Mice for Oral Exposure to 1,2-Dichloroethane
MP (1978) 293
LIST OF APPENDIX TABLES
Table_Apx B-l. Federal Laws and Regulations 399
Table_Apx B-2. State Laws and Regulations 403
Table_Apx B-3. International Laws and Regulations 404
Table_Apx B-4. Assessment History of 1,1-Dichloroethane 404
TableApx D-l. Inputs and Results or Level III Fugacity Modeling for 1,1-Dichloroethane 422
TableApx D-2. First Order Biodegradation Rate Constants for 1,1-Dichloroethane 430
Table Apx D-3. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (|ig/m3)
Levels in the Vapor/Gas Fraction of Ambient Air from U.S.-Based and International
Studies, 2005-2017 439
Table Apx D-4. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (|ig/L)
Levels in Drinking Water from a U.S.-Based Study, 2002-2012 440
TableApx D-5. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (|ig/L)
Levels in Groundwater from U.S.-Based and International Studies, 1984-2005 441
Table Apx D-6. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (|ig/m3)
Levels in the Vapor/Gas Fraction in Indoor Air, from U.S.-Based and International
Studies, 1992-2017 442
Table Apx D-7. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (|ig/m3)
Levels in the Vapor/Gas Fraction of Soil, from International Studies, 2012-2014 442
Table Apx D-8. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (|ig/L)
Levels in the Soil-Water Leachate from U.S.-Based Studies for Locations near Facility
Releases, 1984-1993 443
Table Apx D-9. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (|ig/L)
Levels in Surface Water from U.S.-Based and International Studies, 1984-2005 444
Table Apx D-10. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (|ig/L)
Levels in Wastewater Untreated Effluent from U.S.-Based Studies, 1981-1984 444
TableApx D-l 1. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (|ig/m3)
Levels in Wastewater in Raw Influent U.S.-Based Study in 1993 445
Table Apx E-l. Assumptions for Intraday Emission-Release Duration 452
Table_Apx E-2. Assumptions for Inter-day Emission-Release Pattern 453
Table Apx E-3. Assumptions for Intraday Emission-Release Duration 453
Table_Apx E-4. Assumptions for Inter-day Emission-Release Pattern 454
Table_Apx E-5. Settings for Gaseous Deposition 455
Table Apx E-6. Description of Daily or Period Average and Air Concentration Statistics 458
Table Apx E-7. Procedures for Replacing Values Missing, Equal to Zero, or Out of Normal Bounds for
Physical Source Parameters for NEI Sources 460
Table Apx E-8. Summary of the General Population Exposures Expected near Facilities Where TRI
Modeled Air Concentrations Indicated Risk for 1,1-Dichloroethane 462
Table_Apx E-9. Summary of Aggregate Analysis for TRI Facilities 464
Table Apx E-10. Facilities Reporting TRI Emission Included in General Population Characterization
469
Table Apx 1-1. 1,1-Dichloroethane Chemical-Specific PSC Input Parameters 485
Table Apx 1-2. 1,1-Dichloroethane PSC Mass Release Schedule for an Acute Exposure Scenario 486
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TableApx 1-3. 1,1-Dichloroethane PSC Mass Release Schedule for a Chronic Exposure Scenario.... 486
TableApx 1-4. Meteorologic and Hydrologic PSC Input Parameters 486
Table Apx 1-5. 1,1-Dichloroethane Fish Concentrations Calculated from PSC-Modeled Industrial and
Commercial 1,1-Dichloroethane Releases 487
Table Apx 1-6. 1,1-Dichloroethane Crayfish Concentrations Calculated from PSC-Modeled Industrial
and Commercial 1,1-Dichloroethane Releases 488
Table Apx 1-7. Dietary Exposure Estimates Using EPAs Wildlife Risk Model for Eco-SSLs for
Screening Level Trophic Transfer of 1,1-Dichloroethane to the American Mink from
Consumption of Fish 489
Table Apx 1-8. Dietary Exposure Estimates Using EPAs Wildlife Risk Model for Eco-SSLs for
Screening Level Trophic Transfer of 1,1-Dichloroethane to the American Mink from
Consumption of Crayfish 490
Table Apx 1-9. 1,1-Dichloroethane Trifolium sp. and Earthworm Concentrations Calculated from
AERMOD Modeled Industrial and Commercial Releases Reported to TRI 491
Table Apx 1-10. 1,1-Dichloroethane Trifolium sp. and Earthworm Concentrations Calculated from Land
Application of 1,1-Dichloroethane in Biosolids 491
Table Apx 1-11. Dietary Exposure Estimates Using EPAs Wildlife Risk Model for Eco-SSLs for
Screening Level Trophic Transfer of 1,1-Dichloroethane to the Short-Tailed Shrew that
Could Result from Air Deposition to Soil for 1,1-Dichloroethane Releases Reported to
TRI 492
Table Apx 1-12. Dietary Exposure Estimates Using EPAs Wildlife Risk Model for Eco-SSLs for
Screening Level Trophic Transfer of 1,1-Dichloroethane to the Meadow Vole that Could
Result from Air Deposition to Soil for 1,1-Dichloroethane Releases Reported to TRI. 492
Table Apx 1-13. Dietary Exposure Estimates Using EPAs Wildlife Risk Model for Eco-SSLs for
Screening Level Trophic Transfer of 1,1-Dichloroethane to the Short-Tailed Shrew that
Could Result from Land Application of Biosolids 493
Table Apx 1-14. Dietary Exposure Estimates Using EPAs Wildlife Risk Model for Eco-SSLs for
Screening Level Trophic Transfer of 1,1-Dichloroethane to the Meadow Vole that Could
Result from Land Application of Biosolids 493
Table Apx J-l. Structural Similarity between 1,1-Dichloroethane and Analog Candidates 1,2-
Dichloropropane, 1,1,2-Trichloroethane, and 1,2-Dichloroethane 495
Table Apx J-2. Comparison of 1,1-Dichloroethane and Analog Candidates 1,2-Dichloropropane, 1,1,2-
Trichloroethane, and 1,2-Dichloroethane for Several Physical and Chemical and
Environmental Fate Properties Relevant to Water, Sediment, and Soil 496
Table Apx J-3. ECOSAR Acute (LC50, EC50) and Chronic (ChV) Toxicity Predictions for 1,1-
Dichloroethane and Analog Candidates 1,2-Dichloropropane, 1,1,2-Trichloroethane, and
1,2-Dichloroethane for Aquatic and Terrestrial Taxa 498
Table Apx J-4. Empirical Acute (EC50, LC50) and Chronic (ChV) Hazard Comparison for Various
Aquatic Species Exposed to 1,1-Dichloroethane or Analogs 1,2-Dichloropropane and
1,1,2-Trichloroethane 499
Table Apx J-5. Comparison of Predicted and Empirical Toxicities for Various Aquatic Taxa Exposed to
1.1-Dichloroethane, 1,2-Dichloropropane, and 1,1,2-Trichloroethane 500
Table Apx J-6. Structural Similarity between 1,1-Dichloroethane and Other Chlorinated Solvents.... 502
Table Apx J-7. Comparison of 1,1-Dichloroethane and 1,2-Dichloroethane for Several Physical and
Chemical Properties Relevant to Human Health Hazard 503
Table Apx J-8. Qualitative Comparison of Common Non-cancer Findings between 505
Table Apx J-9. Qualitative Comparison of Common Cancer Findings between 1,1-Dichloroethane and
1.2-Dichloroethan e 506
Table Apx J-10. 1,1-Dichloroethane and 1,2-Dichloroethane Common Chronic Study Findings11 507
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TableApx J-ll. 1,1-Dichloroethane and 1,2-Dichloroethane Oncologic Results 508
TableApx J-12. 1,1-Dichloroethane and 1,2-Dichloroethane Precursor Events 508
Table Apx J-13. 1,1-Dichloroethane Cancer Slope Factors across EPA Offices/Programs 508
Table Apx J-14. 1,2-Dichloroethane Cancer Slope Factors across EPA Offices/Programs 509
TableApx J-15. Summary of Hazards and Chemical Properties for 1,1-Dichloroethane and 1,2-
Dichloroethane 510
Table Apx K-l. Empirical and Web-ICE Predicted Species that Met Model Selection Criteria 513
Table Apx K-2. Considerations that Inform Evaluations of the Strength of the Evidence within an
Evidence Stream (i.e., Apical Endpoints, Mechanistic, or Field Studies) 525
Table Apx L-l. Risk Quotients for Screening Level Trophic Transfer of 1,1-Dichloroethane that Could
Result from Air Deposition (1,1-Dichloroethane Releases Reported to TRI) in
Insectivorous Terrestrial Ecosystems Using EPA's Wildlife Risk Model for Eco-SSLs533
Table Apx L-2. Risk Quotients for Screening Level Trophic Transfer of 1,1-Dichloroethane Which
Could Result from Air Deposition (1,1-Dichloroethane Releases Reported to TRI) in
Herbivorous Terrestrial Ecosystems Using EPA's Wildlife Risk Model for Eco-SSLs 534
Table Apx L-3. Risk Quotients Based on Potential Trophic Transfer of 1,1-Dichloroethane from Fish to
American Mink (Mustela vison) as a Model Aquatic Predator Using EPA's Wildlife Risk
Model for Eco-SSLs 535
Table Apx L-4. Highest Risk Quotients Based on Potential Trophic Transfer of 1,1-Dichloroethane
from Crayfish to American Mink (Mustela vison) as a Model Aquatic Predator Using
EPA's Wildlife Risk Model for Eco-SSLs 536
Table Apx M-l. 1,2-Dichloroethane Partition Coefficients Steady State Estimates 539
Table_Apx M-2. 1,1-Dichloroethane Partition Coefficients 540
Table Apx M-3. Tissue Levels and Time to Peak Tissue Level in Rats Exposed to 1,2-Dichloroethane
by Gavage in Corn Oil 540
Table Apx M-4. Tissue Levels and Time to Peak Tissue Level in Rats Exposed by Inhalation to 1,2-
Dichloroethane for 6 Hours 541
Table_Apx M-5. 1,2-Dichloroethane Tissue:Air Partition Coefficients 541
Table Apx M-6. Estimates of Metabolic Parameters for 1,1-Dichloroethane Obtained from Gas Uptake
Experiments in Male F344 Rats 543
Table Apx M-7. Studies Not Considered Suitable for PODs for 1,1-Dichloroethane 548
Table Apx M-8. Summary of Studies Considered for Non-cancer Dose-Response Assessment of 1,1-
Dichloroethane 549
Table Apx M-9. Summary of Candidate Non-cancer Oral PODs for 1,1-Dichloroethane 550
Table Apx M-10. Summary of Candidate Non-cancer Inhalation PODs for 1,1-Dichloroethane 551
Table Apx M-l 1. Oral Studies Not Considered Suitable for PODs for 1,2-Dichloroethane 553
Table Apx M-12. Inhalation Studies Not Considered Suitable for PODs for 1,2-Dichloroethane 555
Table Apx M-13. Dermal Studies Not Considered Suitable for PODs for 1,2-Dichloroethane 557
Table Apx M-14. Summary of Studies Considered for Non-cancer, Dose-Response Assessment of 1,2-
Dichloroethane 557
Table Apx M-15. Summary of Candidate Acute, Non-cancer, Oral PODs for 1,2-Dichloroethane 560
Table Apx M-16. Summary of Candidate Short-Term/Intermediate, Non-cancer, Oral PODs for 1,2-
Dichloroethane 561
Table Apx M-17. Summary of Candidate Acute, Non-cancer, Inhalation PODs for 1,2-Dichloroethane
563
Table Apx M-l 8. Summary of Candidate Short-Term/Intermediate, Non-cancer, Inhalation PODs for
1,2-Dichloroethane 566
Table Apx M-19. Summary of Candidate Chronic, Non-cancer, Inhalation PODs for 1,2-Dichloroethane
568
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Table_Apx M-20. Dosing Regimen in (NCI, 1978) Chronic Mouse Study 571
TableApx M-21. Relative Kidney Weights in Male Mice Exposed to 1,2-Dichloroethane Once by
Gavage 572
Table Apx M-22. Incidence of Nasal Lesions in Male and Female Rats (Combined) Exposed to 1,2-
Dichloroethane for 8 Hours 573
TableApx M-23. Antibody-Forming Cells per Spleen in Male Mice Exposed to 1,2-Dichloroethane by
Daily Gavage for 14 Days 574
Table Apx M-24. Sperm Concentration in Male Mice Exposed to 1,2-Dichloroethane for 4 Weeks... 575
TableApx M-25. Summary of Non-cancer PODs for 1,1-Dichloroethane (Read-Across from 581
Table Apx M-26. Evidence Integration Table for Reproductive/Developmental Effects 582
Table_Apx M-27. Evidence Integration Table for Renal Effects 585
Table_Apx M-28. Evidence Integration Table for Hepatic Effects 587
Table_Apx M-29. Evidence Integration Table for Nutritional/Metabolic Effects 589
Table_Apx M-30. Evidence Integration Table for Mortality 591
Table_Apx M-31. Evidence Integration Table for Neurological Effects 593
Table Apx M-32. 1,2-Dichloroethane Evidence Integration Table for Reproductive/Developmental
Effects 594
Table Apx M-33. 1,2-Dichloroethane Evidence Integration Table for Renal Effects 600
Table Apx M-34. 1,2-Dichloroethane Evidence Integration Table for Hepatic Effects 604
Table Apx M-3 5. 1,2-Dichloroethane Evidence Integration Table for Immune/Hematological Effects
610
Table Apx M-36. 1,2-Dichloroethane Evidence Integration Table for Neurological/Behavioral Effects
613
Table Apx M-37. 1,2-Dichloroethane Evidence Integration Table for Respiratory Tract Effects 617
Table Apx M-3 8. 1,2-Dichloroethane Evidence Integration Table for Nutritional/Metabolic Effects .619
Table Apx M-39. 1,2-Dichloroethane Evidence Integration Table for Mortality 622
Table_Apx M-40. In Vitro Genotoxicity Tests of 1,1-Dichloroethane 625
Table Apx M-41. In Vivo Genotoxicity Studies of 1,1-Dichloroethane 626
Table Apx M-42. Binding of 14C-1,1-Dichloroethane to DNA (pmol/mg) after Intraperitoneal Exposure
628
Table_Apx M-43. Evidence Integration Table for Cancer 629
Table Apx M-44. 1,1-Dichloroethane Cancer Evidence Integration Table Based on Read-Across from
1,2-Dichloroethane 639
Table Apx M-45. IUR Estimates for Tumor Data from Nagano et al. (2006) Study of 1,2-
Dichloroethane Using Linear Low-Dose Extrapolation Approach 655
Table Apx M-46. Summary of Cancer PODs for 1,1-Dichloroethane (Read-Across from 1,2-
Dichloroethane) 657
Table Apx N-l. Limit of LOD and LOQ Summary for Air Sampling Analytical Methods Identified. 662
Table Apx O-l. Subcategory Editing from the Final Scope Document to the Draft Risk Evaluation.. 663
LIST OF APPENDIX FIGURES
FigureApx D-l. Physical-Chemical Property Data for 1,1-Dichloroethane under Standard Conditions
412
Figure Apx D-2. Boiling Point of 1,1-Dichloroethane as a Function of Pressure 414
Figure Apx D-3. Density of 1,1-Dichloroethane as a Function of Temperature 415
Figure Apx D-4. Vapor Pressure of 1,1-Dichloroethane as a Function of Temperature 416
FigureApx D-5. Water Solubility of 1,1-Dichloroethane as aFunction of Temperature 417
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FigureApx D-6. Octanol/Water Partition Coefficient (log Kow) of 1,1-Dichloroethane as a Function of
Temperature 418
Figure Apx D-7. Henry's Law Constant of 1,1-Dichloroethane as a Function of Temperature 419
Figure Apx D-8. Viscosity of 1,1-Dichloroethane as a Function of Temperature 420
Figure_Apx D-9. Example Tornado Plot 437
Figure Apx D-10. Concentrations of 1,1-Dichloroethane (|ig/m3) in the Vapor/Gas Fraction of Ambient
Air from U.S.-Based and International Studies, 2005-2017 438
Figure Apx D-l 1. Concentrations of 1,1-Dichloroethane (|i/L) in Drinking Water from a U.S.-Based
Study, 2002-2012 439
Figure Apx D-12. Concentrations of 1,1-Dichloroethane (|i/L) in Groundwater from U.S.-Based and
International Studies, 1984-2005 440
Figure Apx D-13. Concentrations of 1,1-Dichloroethane (|ig/m3) in the Vapor/Gas Fraction in Indoor
Air, from U.S.-Based and International Studies, 1992-2017 442
Figure Apx D-14. Concentrations of 1,1-Dichloroethane (|ig/m3) in the Vapor/Gas Fraction of Soil,
from International Studies, 2012-2014 442
Figure Apx D-15. Concentrations of 1,1-Dichloroethane (|ig/L) in the Soil-Water Leachate from U.S.-
Based Studies for Locations near Facility Releases, 1984-1993 443
Figure Apx D-16. Concentrations of 1,1-Dichloroethane (|i/L) in Surface Water from U.S.-Based and
International Studies, 1984-2005 443
Figure Apx D-17. Concentrations of 1,1-Dichloroethane (|i/L) in Wastewater Untreated Effluent from
U.S.-Based Studies, 1981-1984 444
Figure Apx D-18. Concentrations of 1,1-Dichloroethane (|ig/m3) in Wastewater in Raw Influent U.S.-
Based Study in 1993 445
Figure Apx E-l. Brief Description of Methodologies and Analyses Used to Estimate Air Concentrations
and Exposures 446
Figure Apx E-2. Modeled Exposure Points for Finite Distance Rings for Ambient Air Modeling
(AERMOD) 449
Figure Apx E-3. Modeled Exposure Point Locations for Area Distance for Ambient Air Modeling
(AERMOD) 450
Figure Apx E-4 Cuticular Resistance as a Function of Vapor Pressure 456
Figure Apx E-5. Example of Group of Air Releasing Facilities with Overlapping 10 km Buffers for
Aggregate Air Risk Screening 463
Figure_Apx E-6. Map of Aggregated Air Facilities, Group 1 465
Figure_Apx E-7. Map of Aggregated Air Facilities, Group 2 465
Figure_Apx E-8. Map of Aggregated Air Facilities, Group 3 466
Figure_Apx E-9. Map of Aggregated Air Facilities, Group 4 466
Figure Apx E-10. Flowchart Illustrating the Conceptual Design and Approach Taken for this Evaluation
468
Figure Apx F-l. Generic Schematic of Hypothetical Release Point with Surface Water Intakes for
Drinking Water Systems Located Downstream 478
Figure Apx J-l. Proposed Metabolic Scheme for 1,1-Dichloroethane (McCall et al., 1983) 503
Figure Apx J-2. Proposed Metabolic Scheme for 1,2-Dichloroethane (IPCS, 1995) 504
Figure Apx J-3. Hepatocellular Carcinomas Dose Response in Mice for 1,2-Dichloroethane 507
Figure Apx K-l. SSD Toolbox Interface Showing HC05s and P Values for Each Distribution Using
Maximum Likelihood Fitting Method Using 1,2-Dichloropropane's Acute Aquatic
Hazard Data (Etterson, 2020a) 516
Figure Apx K-2. AICc for the Six Distribution Options in the SSD Toolbox for 1,2-Dichloropropane
Acute Aquatic Hazard Data (Etterson, 2020a) 517
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FigureApx K-3. Q-Q plot of 1,2-Dichloropropane Acute Aquatic Hazard Data with the Gumbel
Distribution (Etterson, 2020a) 517
Figure Apx K-4. SSD Distribution for 1,2-Dichloropropane Acute Hazard Data (Etterson, 2020a).... 518
Figure Apx K-5. Log-Logistic Curve Fit to 96-Hour Abnormal Swimming Behavior Data from
(Mitsubishi Chemical Medience Corporation, 2009b) for Oryzicis latipes Exposed to 1,1-
Dichloroethane 519
Figure Apx K-6. Log-logistic Curve Fit to Hatching Percent Data from Ophryotrocha labronica
Exposed to 1,1,2-Trichloroethane (Rosenberg et al., 1975) 520
Figure_Apx K-7. TRV Flow Chart 522
Figure Apx M-l. Proposed Metabolic Scheme for 1,1-Dichloroethane (McCall et al., 1983) 542
Figure Apx M-2. Proposed Metabolic Scheme for 1,2-Dichloroethane (IPCS, 1995) 544
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ACKNOWLEDGEMENTS
The Assessment Team gratefully acknowledges the participation, input, and review comments from U.S.
Environmental Protection Agency (EPA or the Agency) OPPT and OCSPP senior managers and science
advisors as well as assistance from EPA contractors Abt Global (Contract No. EP-W-16-009); ICF
(Contract No. 68HERC23D0007); ERG (Contract No. 68HERD20A0002; 68HERC21D0003); and SRC
(Contract No. 68HERH19D0022; 68HERH19F0213).
Special acknowledgement is given for the contributions of technical experts from EPA ORD-CESER
Randall Ross and David Burden; ORD-CCTE-CCED-CCCB Tony Williams; OCSPP-OPPT-DGMPD-
TAIB-TAIS1 Andrea Hindman; and ORD-CPHEA-CPAD-TEABC, Jonathan Phillip Kaiser - for their
joint efforts.
The Existing Chemicals Risk Evaluation Division (ECRAD) has received input from senior scientists
and technical experts from EPA's OCSPP and across the Agency. Specifically, ECRAD has received
input from the OCSPP Senior Science Advisors, OCSPP's Science Policy Council, and through the
intra-agency review process. The areas of analysis contained in this draft risk evaluation reflect some of
the revisions received throughout the review process and during scientific deliberations; however, there
are some significant aspects of the draft 1,1-dichloroethane risk evaluation and the draft 1,2-
dichloroethane human health hazard assessment technical support document for which there is not
agreement between ECRAD and senior scientists and technical experts. In accordance with EPA's
Scientific Integrity Policy (https://www.epa.gov/scientific-integrity/epas-scientific-integrity-policy), the
areas of scientific disagreement are described in relevant charge questions and are intended to guide the
scientific peer review by the TSCA Science Advisory Committee on Chemicals (SACC). EPA is
requesting the SACC provide input on these science issues—including the differences of scientific
opinion—which relate specifically to 1,1-dichloroethane and 1,2-dichloroethane but also more broadly
in the application of risk assessment practices and use of existing EPA and internally accepted guidance
documents.
Docket
Supporting information can be found in public docket, Docket ID EPA-HQ-OPPT-2018-0426.
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.
Authors: Janet Burris (Risk Assessment Lead), Seema Schappelle (Branch Supervisor), Clara Hull
(Risk Determination Lead), Aderonke Adegbule, Katherine Anitole, Albana Bega, Jennifer Brennan,
Craig Connolly, Andrea Hindman, Lauren Housley, Jonathan Kaiser, Ryan Klein, William Irwin, David
Lynch, Greg Macek, Andrew Middleton, Nerija Orentas, Christina Robichaud, Ali Shohatee, Kelley
Stanfield, Nicholas Suek, and Catherine Taylor
Contributors: Sarah Au, Tyler Amrine, Brian Barone, Joshua Booth, Nicholas Castaneda, Jone
Corrales, Kellie Fay, Rebecca Feldman, Janine Fetke, Patricia Fontenot, Ross Geredien, Bryan Groza,
Annie Jacob, Keith Jacobs, June Kang, Grace Kaupas, Virginia Lee, Yadi Lopez, Matt Lloyd, Benjamin
Kunstman , Edward Lo, Bryan Lobar, Kiet Ly, Rony Arauz Melendez, Bethany Masten, Azah Abdalla
Mohamed, Brianne Raccor, Simon Regenold, Anthony Rufka, Abhilash Sasidharan, Cory Strope, David
Turk, Leora Vegosen, Kevin Vuilleumier, Jason Wight, William Wimbish, Joel Wolf, and Eva Wong
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1032 Technical Support: Mark Gibson, Hillary Hollinger, S. Xiah Kragie, and Houbao Li
1033
1034 This draft risk evaluation was reviewed and cleared for release by OPPT and OCSPP leadership.
1035
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EXECUTIVE SUMMARY
EPA has evaluated 1,1-dichloroethane under the Toxic Substances Control Act (TSCA). In this draft risk
evaluation, EPA preliminarily finds that 1,1-dichloroethane presents an unreasonable risk of
injury to human health and the environment. The human health risks are to workers in facilities
making or using 1,1-dichloroethane, and the risks to the environment are to invertebrates (such as
worms and small crustaceans) and algae in water bodies into which 1,1-dichloroethane may be released.
In December 2019, EPA designated 1,1-dichloroethane as a high-priority substance for TSCA
evaluation and in August 2020 released the final scope of the risk evaluation. This draft risk evaluation
assesses human health risk to workers, including occupational non-users (ONUs), the general
population, and the environment. No consumer or bystander exposures were assessed because no
consumer conditions of use (COUs) were identified. Nor were any commercial or consumer products or
articles containing 1,1-dichloroethane identified or assessed in this draft risk evaluation.
1,1-Dichloroethane is manufactured in the United States and used as an industrial and commercial
solvent and to make many different substances, including other chlorinated solvents that have broad
industrial applications. Relatively small amounts of 1,1-dichloroethane support commercial uses in
laboratory research. 1,1-Dichloroethane is not imported, and the reported total production volume in
2020 was between 100 million and 1 billion pounds for just two corporations located in the southern
United States. (To protect proprietary information, production volumes are often reported to EPA in
ranges.) The Agency has evaluated 1,1-dichloroethane across its conditions of use ranging from
manufacture to disposal.
1,1-Dichloroethane is a colorless oily liquid with a chloroform- or ether-like odor and is volatile,
meaning it evaporates rapidly at ambient temperatures. 1,1-Dichloroethane is soluble in water and can
evaporate into the air in hours or days, depending on environmental conditions. However, due to its
water solubility, continuous releases to water from industrial facilities that make or use 1,1-
dichloroethane will partition between water and air, with a portion of the substance remaining in water.
Given the relatively low quantity directly released to water, surface water will generally not be an
important source of exposure other than direct releases of 1,1-dichloroethane into deep, slower-moving
or stagnant surface waters. 1,1-Dichloroethane is not expected to accumulate in soil and sediment.
Nonetheless, 1,1-dichloroethane is persistent in the environment and only slowly degrades over months
and years if it gets in air, water, soil, and sediment. Estimated bioconcentration and bioaccumulation
factors indicate that 1,1-dichloroethane is not likely to bioaccumulate in aquatic or terrestrial organisms.
Unreasonable Risk to Human Health
EPA evaluated reasonably available information for human health hazards from 1,1-dicloroethane and
did not find adequate human health data for this draft risk evaluation. For this reason, the Agency used
hazard data for the isomer 1,2-dichloroethane because of its structural, physical, chemical, metabolic,
cancer and non-cancer toxicological similarity as the best available candidate to provide analogous
human health data for this draft risk evaluation. The data shows that exposure to 1,1-dichloroethane may
increase the risk of kidney and other cancers, as well as harmful, non-cancer renal, nasal, immune
system, and reproductive effects. EPA evaluated the risks to people experiencing these effects at work,
in the home, in fenceline communities (residences in proximity to facilities releasing 1,1-dichloroethane
to ambient air), and by eating fish taken from waters into which 1,1-dichloroethane was released. When
determining the unreasonable risk of 1,1-dichloroethane to human health, in addition to workers, EPA
also accounted for other potentially exposed and susceptible subpopulations (PESS), which included:
infants exposed to drinking water during formula bottle feeding, subsistence and tribal fishers, pregnant
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women and people of reproductive age, individuals with compromised immune systems or neurological
disorders, workers, people with the aldehyde dehydrogenase-2 mutation which is more likely in people
of Asian descent, lifestyle factors such as smoking cigarettes or secondhand smoke, and fenceline
communities.
Workers with the greatest potential for exposure to 1,1-dichloroethane are those who work directly with
the chemical in environments where 1,1-dichloroethane is manufactured or used in processing or
disposal.
EPA evaluated exposures to the general population associated with (1) breathing the ambient air where
1,1-dichloroethane was released from facilities; and (2) ingesting drinking water, surface water, or soil
from 1,1-dichloroethane disposed to land (i.e., direct disposal to landfills or land-applied biosolids from
public wastewater treatment works treating 1,1-dichloroethane-containing wastewater). The Agency did
not identify unreasonable risk to the general population. EPA also evaluated subsistence fishers and did
not find unreasonable risk.
EPA's assessment preliminarily shows unreasonable risks of cancer and noncancer health effects
from the 1,1-dichloroethane COUs to workers. For workers there are certain activities where acute,
short-term/sub chronic, chronic, and lifetime exposures to 1,1-dichloroethane—especially from contact
with skin—contribute to unreasonable risk. Outside the work environment, EPA did not identify risks of
injury to the general population, including PESS, which would contribute to the preliminary
unreasonable risk determination for 1,1-dichloroethane.
Unreasonable Risk to the Environment
EPA assessed 1,1-dichloroethane exposures to the environment through the manufacturing, processing,
use, or disposal of 1,1-dichloroethane, including when the chemical leaches out or is released to water.
Exposure to aquatic species was evaluated through surface water and sediment; exposure to terrestrial
species was evaluated through soil, surface water, and sediment. EPA's assessment preliminarily
determined that chronic exposure to 1,1-dichloroethane contributes to the unreasonable risk to
aquatic species, including invertebrates and algae, from the manufacturing, processing, and
disposal of 1,1-dichloroethane. The Agency preliminarily determined that there is no unreasonable risk
of injury to aquatic and terrestrial species from acute exposures to 1,1-dichloroethane.
Considerations and Next Steps
Eight COUs were evaluated for 1,1-dichloroethane. EPA preliminarily determined that the following
seven COUs contribute to the unreasonable risk from 1,1-dichloroethane:
• Manufacturing (domestic manufacture);
• Processing as a reactant as an intermediate in all other basic organic chemical manufacturing;
• Processing as a reactant as an intermediate in all other chemical product and preparation
manufacturing;
• Processing: repackaging;
• Processing: recycling;
• Commercial use in laboratory chemicals; and
• Disposal.
EPA preliminarily determined that the distribution in commerce COU does not contribute to the
unreasonable risk.
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Additional Note
ECRAD has received input from senior scientists and technical experts from EPA's Office of Chemical
Safety and Pollution Prevention (OCSPP) and across EPA. Specifically, ECRAD has received input
from the OCSPP Senior Science Advisors, OCSPP's Science Policy Council, and through the intra-
agency review process. The areas of analysis contained in this risk evaluation reflect some of the
revisions received throughout the review process and during scientific deliberations; however, there are
some significant aspects of the draft 1,1-dichloroethane risk evaluation and the draft 1,2-dichloroethane
human health hazard assessment technical support document for which there is not agreement between
ECRAD and senior scientists and technical experts. In accordance with EPA's Scientific Integrity
Policy, the areas of scientific disagreement are described in relevant charge questions and are intended
to guide the scientific peer review by the TSCA Science Advisory Committee on Chemicals (SACC).
EPA is requesting the SACC provide input on these science issues—including the differences of
scientific opinion—which relate specifically to 1,1-dichloroethane and 1,2-dichloroethane but also more
broadly in the application of risk assessment practices and use of existing EPA and internally accepted
guidance documents.
This draft risk evaluation has been released for public comment and will undergo independent, expert
scientific peer review. After considering input from the public and peer reviewers EPA will issue a final
1,1-dichloroethane risk evaluation. If in the final risk evaluation the Agency determines that 1,1-
dichloroethane presents unreasonable risk to human health or the environment, EPA will initiate
regulatory action to mitigate those risks.
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1 INTRODUCTION
EPA has evaluated 1,1-dichloroethane under the Toxic Substances Control Act (TSCA). 1,1-
Dichloroethane is a colorless, oily liquid with a chloroform4ike odor, which is primarily used in organic
chemical manufacturing. Section 1.1 provides production volume, life cycle diagram (LCD), conditions
of use (COUs), and conceptual models used for 1,1-dichloroethane; Section 1.2 includes an overview of
the systematic review process; and Section 1.3 presents the organization of this draft risk evaluation.
Figure 1-1 describes the major inputs, phases, and outputs/components of the TSCA risk evaluation
process, from scoping to releasing the final risk evaluation.
Inputs
Existing Laws, Regulations,
and Assessments
Use Document
Public Comments
Public Comments on
Draft Scope Document
Analysis Plan
Testing Results
Data Evaluation Process
Data Integration
Public Comments on
Draft RE
Peer Review Comments
on Draft RE
Phase
4
Draft Scope
Document
Final Scope
Document
J}
Outputs
Conditions of use, exposure, hazardsand
potentially exposed or susceptible
subpopulations(PESS)
Analysis of conditions of use
Lifecycle Diagram
• Initial Conceptual Models
• Industrial/Commercial uses
• Environmental releases
• Preliminary analysis plan
i>
£
Draft Risk
| \
Final Risk
Evaluation
1
Evaluation
Refined Conceptual
Models
Refined Analysis Plan
V7
\7
Draft Risk
Determination
Final Risk
Determination
—
V7
Risk Management
Process
Figure 1-1. TSCA Existing Chemical Risk Evaluation Process
1.1 Scope of the Risk Evaluation
EPA evaluated risk to human and environmental populations for 1,1-dichloroethane. Specifically, for
human populations, EPA evaluated risk to (1) workers and occupational non-users (ONUs) via
inhalation routes; (2) workers via dermal routes; and (3) the general population, including potentially
exposed and susceptible subpopulations (e.g., pregnant women, bottle-fed infants, immuno-
compromised peoples), via oral, dermal, and inhalation routes. For environmental populations, EPA
evaluated risk to aquatic species via water and sediment and to terrestrial species via air, water,
sediment, and soil pathways leading to dietary and direct ingestion exposure.
1.1.1 Life Cycle and Production Volume
The LCD shown in Figure 1-2 depicts the COUs that are within the scope of the draft risk evaluation
during various life cycle stages, including manufacturing, processing, use (industrial, commercial),
distribution and disposal. The LCD has been updated since it was presented in the Final Scope of the
Risk Evaluation for 1,1-Dichloroethane CASRN 75-34-3 (U.S. EPA. 2020) to include the processing
activity of repackaging for distribution of 1,1-dichloroethane for use as a laboratory chemical. The
information in the LCD is grouped according to the Chemical Data Reporting (CDR) processing codes
and use categories (including functional use codes for industrial uses and product categories for
industrial and commercial uses). The CDR Rule under TSCA requires U.S. manufacturers (including
importers) to provide EPA with information on the chemicals they manufacture or import into the
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United States. EPA collects CDR data approximately every 4 years with the latest collections occurring
in 2006, 2012, 2016, and 2020.
The production volume reported in the final scope document was between 100 million and 1 billion
pounds, based on total production volume of 1,1-dichloroethane in 2015 from the 2016 CDR reporting
period. The range did not change in the latest 2020 CDR data (the reported total production volume in
2020 was between 100 million and 1 billion pounds). Production volume is described here as a range to
protect production volumes that were claimed as confidential business information (CBI). For the 2016
CDR cycle, data collected per chemical included the company name, volume of each chemical
manufactured/imported, the number of workers at each site, and information on whether the chemical is
used in the commercial, industrial, and/or consumer sector(s).
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MANUFACTURE PROCESSING INDUSTRIAL & COMMERCIAL USES WASTE DISPOSAL
1194 Figure 1-2. 1,1-Dichloroethane Ljfe Cycle Diagram
1195 11 See (U.S. EPA. 2020) for additional details on 1,1 -dichloroethane uses.
1196 The production volumes shown are for reporting year 2015 from the 2016 CDR reporting period (U.S. EPA. 2016b).
1197 The activities of loading 1,1-dichloroethane product into transport containers and unloading at receiving sites as well as repackaging into smaller
1198 containers are considered part of Distribution in Commerce and these are assessed under those OES. Cleanup of accidents/spills that may occur during
1199 transport are not within the scope of this Risk Evaluation.
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Descriptions of the industrial and commercial use categories identified from the 2016 and 2020 CDR are
included in the LCD (Figure 1-2)(U.S. EPA. 2016b). The descriptions provide a brief overview of the
use category. The Draft RiskEvaluation for 1,1-Dichloroethane - Supplemental Information File:
Environmental Releases and Occupational Exposure Assessment (U.S. EPA. 2024e) contains more
detailed descriptions (e.g., process descriptions, worker activities, process flow diagrams, equipment
illustrations) for each manufacture, processing, use, and disposal category.
1.1.2 Conditions of Use Included in the Draft Risk Evaluation
The Final Scope of the Risk Evaluation for 1,1-Dichloroethane CASRN 75-34-3 (U.S. EPA. 2020)
identified and described the life cycle stages, categories and subcategories that comprise COUs that EPA
planned to consider in the risk evaluation. The COUs included in this draft risk evaluation are reflected
in the LCD (Figure 1-2) and conceptual models (Section 1.1.2.1). These COUs are evaluated for acute,
short-term, chronic, and lifetime exposures, as applicable based on reasonably available exposure and
hazard data as well as the relevant study populations for each. Table 1-1 below presents all COUs for
1,1-dichloroethane. No consumer uses were identified and therefore, none were evaluated in the 1,1-
dichloroethane risk evaluation. In this draft risk evaluation, EPA added the COU processing -
repackaging to account for the repackaging for distribution of 1,1-dichloroethane for use as a laboratory
chemical.
Table 1-1. Categories and Subcategories of Use and Corresponding Exposure Scenario in the Risk
Evaluation for 1,1-Dichloroethane
Life Cycle
Stage"
Category6
Subcategoryc
Reference(s)
Manufacture
Domestic
manufacturing
Domestic manufacturing
U.S. EPA (2016b) U.S. EPA (2016b)
Processing
As a reactant
Intermediate in all other basic organic
chemical manufacture
U.S. EPA (2016b) KEML (2008);
(U.S. EPA. 2017b)
Intermediate in all other chemical
product and preparation manufacturing
U.S. EPA (2016b)
Repackaging
Repackaging
(Siema-Aldrich. 2020)
Recycling
Recycling
U.S. EPA (2016b)
Distribution
Distribution in
commerce
Distribution in commerce
Use Document. EPA-HO-OPPT-2016-
0735-0003: U.S. EPA (2016b): U.S.
EPA (2014b)
Commercial
Other use
Laboratory chemicals
(Sigma-Aldrich. 2020)
Disposal
Disposal
Disposal
KEML (2008)
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Life Cycle
Stage"
Category6
Subcategoryc
Reference(s)
11 Life Cycle Stage Use Definitions (40 CFR § 711.3)
- "Industrial use" means use at a site at which one or more chemicals or mixtures are manufactured (including
imported) or processed.
- "Commercial use" means the use of a chemical or a mixture containing a chemical (including as part of an
article) in a commercial enterprise providing saleable goods or services.
Although EPA has identified both industrial and commercial uses here for purposes of distinguishing scenarios in
this document, the Agency interprets the authority over "any manner or method of commercial use" under TSCA
section 6(a)(5) to reach both.
h These categories of COUs appear in the LCD, reflect CDR codes, and broadly represent COUs of 1,1-
dichloroethane in industrial and/or commercial settings.
c These subcategories reflect more specific COUs of 1,1-dichloroethane.
- The manufacture of 1,1-dichloroethane as an unintentional byproduct during the manufacture of 1,2-
dichloroethane (CASRN 107-06-2) (EPA-HQ-OPPT-2018-0426-0027) is not included in this draft risk evaluation
but will be addressed it in the draft risk evaluation for 1,2-dichloroethane.
- In this draft risk evaluation, EPA added the condition of use processing - repackaging to account for the
repackaging for distribution of 1,1-dichloroethane.
- The presence of 1,1-dichloroethane in produced water from hydraulic fracturing is included in the disposal
COU.
1.1.2.1 Conceptual Models
The conceptual model in Figure 1-3 presents the exposure pathways, exposure routes and hazards to
human populations from industrial and commercial activities and uses of 1,1-dichloroethane, Figure 1-4
presents general population exposure pathways and hazards for environmental releases and wastes, and
Figure 1-5 presents the conceptual model for ecological exposures and hazards from environmental
releases and wastes. For general population, only acute, chronic and lifetime exposure scenarios were
assessed as exposures resulted from the facility releases that were averaged over annual operating days.
The conceptual model depicted in Figure 2-15 of the 2020 Final Scope document has been updated in
Figure 1-4 and Figure 1-5 to reflect the exposure pathways, exposure routes, and hazards to human and
ecological receptors, respectively, from environmental releases and wastes from industrial and
commercial uses of 1,1-dichloroethane that EPA considered in the draft risk evaluation. Section 2.6.3.1
of the 2020 Final Scope stated that EPA would not consider certain exposure pathways and risks that are
addressed or could in the future be addressed by other EPA-administered statutes and regulatory
programs. As explained in the preamble to the final rule, Procedures for Chemical Risk Evaluation
Under the Toxic Substances Control Act (89 FR 37028, 37033-34, May 3, 2024), EPA no longer
interprets the law to authorize exclusion of such exposure pathways from the scope of TSCA risk
evaluations. Accordingly, consistent with that final rule (to be codified at 40 CFR 702.39(d)(9)), the
Draft Risk Evaluation for 1,1-Dichloroethane does not exclude exposure pathways from ambient air,
drinking water, onsite releases to land disposal and soil, as described in Section 2.6.3.1 of the 2020 Final
Scope.
The exposure pathways depicted in Figure 1-4 are based on data EPA compiled on the presence of 1,1-
dichloroethane in environmental media as well as physical chemical properties that predict the fate and
transport and partitioning of 1,1-dichloroethane in the environment. As presented in detail in Section
3.3, monitoring data from EPA databases as well as peer-reviewed literature confirm 1,1-dichloroethane
presence in most environmental media. For example, facilities releasing 1,1-dichloroethane into ambient
air, surface water and landfills have reported these releases to EPA via the Toxics Release Inventory and
monitoring data of effluent containing 1,1-dichloroethane released to surface receiving waters is
reported via Discharge Monitoring Reports. Publicly-owned water treatment systems report receiving
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INDUSTRIAL AND EXPOSURE PATHWAY EXPOSURE ROUTE POPULATION EFFECTS
C OMMERC IAL ACTIVITIES / USES
Figure 1-3.1,1-Dichloroethane Conceptual Model for Industrial and Commercial Activities and
Uses: Potential Exposure and Hazards
11 See Table 1-1 for categories and subcategories of COUs.
h Fugitive air emissions are those that are not stack emissions and include fugitive equipment leaks from valves,
pump seals, flanges, compressors, sampling connections and open-ended lines; evaporative losses from surface
impoundment and spills; and releases from building ventilation systems.
c Exposure may occur through mists that deposit in the upper respiratory tract however, based on physical
chemical properties, mists of 1,1-dichloroethane will likely be rapidly absorbed in the respiratory tract or
evaporate and were evaluated as an inhalation exposure.
''Population includes potentially exposed or susceptible subpopulations such as infants exposed to drinking water
from public drinking water treatment systems during formula bottle feeding, subsistence and tribal fishers,
pregnant women and people of reproductive age, individuals with compromised immune systems or neurological
disorders, workers, people with the aldehyde dehydrogenase-2 mutation which is more likely in people of Asian
descent, lifestyle factors such as smoking cigarettes or secondhand smoke, and fenceline communities who live
near facilities that emit 1,1-dichloroethane.
influent containing 1,1-dichloroethane and therefore may have wet biosolids that still contain 1,1-
dichloroethane.
Surface water and groundwater monitoring data from the Water Quality Portal presents detected levels
of 1,1-dichloroethane and UCMR3 data from some public drinking water systems also detected 1,1-
dichloroethane in finished drinking water. Thus, monitoring data provides evidence of the presence of
1,1-dichloroethane in water which given the water solubility of 1,1-dichloroethane does not easily
evaporate from water without agitation.
Lastly, 1,1-dichloroethane concentrations are found in a number of air monitoring programs such as that
reported via the EPA Ambient Monitoring Technology Information Center (AMTIC). Ambient air
concentrations of 1,1-dichloroethane are mostly associated with industrial facility releases of 1,1-
dichloroethane.
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RELEASES AND WASTES FROM INDUSTRIAL/
COMMERCIAL / CONSUMER USES
EXPOSURE PATHWAYS
EXPOSURE ROUTES
POPULATIONS
HAZARDS
Wastewater or
Liquid Wastes
Solid Wastes
Liquid Wastes
Industrial Pre-
—~ Treatment or
Industrial WWT
Indirect discharge
~ _
Water, Sedin
Biosolids
Hazardous and
—~ Municipal Waste
Landfill
Hazardous and
—~ Municipal Waste
Incinerators
Off-site Waste
Recycling, Other
Treatment
Hazards Potentially
Associated with
Acute and/or Chronic
Exposures
Emissions to Air
Figure 1-4.1,1-Dichloroethane Conceptual Model for Environmental Releases and Wastes: General Population Exposures and
Hazards
The conceptual model presents the exposure pathways, exposure routes, and hazards to human populations from environmental releases and wastes from
industrial and commercial uses of 1,1-dichloroethane.
11 Industrial wastewater or liquid wastes may be treated on-site and then released to surface water (direct discharge), or pre-treated and released to a
publicly owned treatment works (POTW) (indirect discharge).
h General population includes potentially exposed or susceptible subpopulations such as infants exposed to drinking water from public drinking water
treatment systems during formula bottle feeding; subsistence and tribal fishers; pregnant women and people of reproductive age; individuals with
compromised immune systems or neurological disorders; workers; people with the aldehyde dehydrogenase-2 mutation, which is more likely in people of
Asian descent; lifestyle factors such as smoking cigarettes or secondhand smoke; and fenceline communities who live near facilities that emit 1,1-
dichloroethane.
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RELEASES AND WASTES FROM INDUSTRIAL
COMMERCIAL USES
EXPOSURE PATHWAYS
EXPOSURE ROUTES
RECEPTORS
HAZARDS
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Figure 1-5. 1,1-Diehloroethane Conceptual Model for Environmental Releases and Wastes: Ecological Exposures and Hazards
" Industrial wastewater or liquid wastes may be treated on-site and released to surface water (direct discharge) or pre-treated and released to POTW
(indirect discharge).
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_M.3 Populations Assessed
Based on the conceptual models presented in Section 1.1.3.1, Figure 1-6 presents the human populations
and ecological receptors assessed in this draft risk evaluation. EPA evaluated risk to human populations
and environmental receptors for 1,1-dichloroethane. Specifically, for human populations, EPA evaluated
risk to (1) workers via inhalation and dermal exposure routes; (2) occupational non-users (ONUs)
workers via inhalation routes; and (3) the general population via oral, dermal, and inhalation routes. For
environmental receptors, EPA evaluated risk to aquatic species via water and sediment as well as
terrestrial species via air, water, sediment, and soil leading to dietary and direct ingestion exposure.
Figure 1-6. Populations Assessed in this Draft Risk Evaluation for 1,1-Dichloroethane
1.1.3.1 Potentially Exposed or Susceptible Subpopulations
TSCA section 6(b)(4)(A) requires that risk evaluations "determine whether a chemical substance
presents an unreasonable risk of injury to health or the environment, without consideration of costs 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 section 3(12) states that "the term 'potentially exposed or susceptible subpopulation''
[PESS] 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."
Evaluation of the qualitative and quantitative evidence for PESS begins as part of the systematic review
process. Any available relevant published studies and other data are identified from a broad literature
search strategy across several databases, focused only on the chemical name (including synonyms and
trade names) with no additional search limits. This broad search process is described in the Draft
Systematic Review Protocol Supporting TSCA Risk Evaluations for Chemical Substances (U.S. EPA.
2021b) (also referred to as "2021 Draft Systematic Review Protocol"; see Section 1.2). When adequate
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and complete, evidence related to PESS informs the derivation of exposure estimates and human health
hazard endpoints/values that are protective of those potentially exposed or susceptible subpopulations.
PESS factors can influence the selection of relevant exposure pathways, the sensitivity of derived hazard
values, the identification of human subpopulations, and the discussion of uncertainties throughout the
assessment. Factors that may contribute to increased exposure or biological susceptibility to a chemical
include lifestage; pre-existing disease; lifestyle activities (e.g., smoking, physical activity); occupational
and consumer exposures, including workers and occupational non-users; consumers and other
bystanders; physical space and geography (e.g., communities living in proximity to facilities releasing
1,1-dichloroethane to air); social, economic and other demographics; nutrition; genetics; unique
activities (e.g., subsistence fishing); tribal and/or other cultural practices; aggregate exposures; and other
chemical and non-chemical stressors.
EPA considered whether each of the PESS factors was addressed by the risk evaluation, including
discussion of any remaining uncertainties, as identified evidence enabled. For the 1,1-dichloroethane
draft risk evaluation, EPA integrated and assessed available information on hazards and exposures for
the conditions of use of 1,1-dichloroethane, including information relevant to specific risks of injury to
PESS. In addition to workers, PESS subpopulations identified as relevant include infants exposed to
drinking water during formula bottle feeding, subsistence and Tribal fishers, pregnant women and
people of reproductive age, individuals with compromised immune systems or neurological disorders,
workers, people with the aldehyde dehydrogenase-2 mutation which is more likely in people of Asian
descent, lifestyle factors such as smoking cigarettes or secondhand smoke, and communities who live
near facilities that emit 1,1-dichloroethane (see Risk Characterization for Potentially Exposed or
Susceptible Subpopulations, Section 5.3.2).
1.2 Systematic Review
EPA/OPPT applies systematic review principles in the development of risk evaluations under the
amended TSCA. Section 26(h) of 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.
To meet the TSC A section 26(h) science standards, EPA used the TSC A systematic review process
described in the 2021 Draft Systematic Review Protocol (U.S. EPA. 2021b) and the Draft Risk
Evaluation for 1,1-Dichloroethane - Systematic Review Protocol (U.S. EPA. 2024t) (hereafter "7,7-
Dichloroethane Systematic Review ProtocoF). Systematic review supports the risk evaluation in that
data searching, screening, evaluation, extraction, and evidence integration 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).
The systematic review process is briefly described in Figure 1-7 below. More detail regarding these
steps is provided in the 2021 Draft Systematic Review Protocol (U.S. EPA. 2021b) and the 1,1-
Dichloroethane Systematic Review Protocol (U.S. EPA. 2024t). The latter provides additional
information on the steps in the systematic review process, including literature inventory trees and
evidence maps for each discipline (e.g., human health hazard) containing results of the literature search
and screening as well as sections summarizing data evaluation, extraction, and evidence integration.
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• Based on the
approach
described in the
Literature
Search Strategy
documents.
Data Search
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• Title/abstractand
full-text screening
based on pre-
defined
inclusion/exclusion
criteria.
~
Data Screen
•jg)
• Evaluateand
document the
quality of studies
based on pre-
defined criteria.
Data
Evaluation
~ —
~ —
~ —
Figure 1-7. Diagram of the Systematic Review Process
• Extract relevant
information based
on pre-defined
templates.
Data
Extraction
=1
1
• Evaluate results
both within and
across evidence
streams to develop
weight of the
scientific evidence
conclusions.
Evidence I /\
Integration \J V,
EPA reviewed reasonably available information, defined in 40 CFR 702.33, 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 scientific evidence in accordance with TSCA sections 6 and 26. EPA reviewed reasonably available
information and evaluated the quality of the methods and reporting of results of the individual studies
using the evaluation strategies described in the 2021 Draft Systematic Review Protocol (U.S. EPA.
2021b) and the 1,1-Dichloroethane Systematic Review Protocol (U.S. EPA. 2024t).
EPA also identified key assessments conducted by other EPA programs and other U.S. and international
organizations. Depending on the source, these assessments may include information on COUs (or the
equivalent), hazards, exposures, and PESS. Some of the most pertinent assessments that were consulted
for 1,1-dichloroethane include the following:
• U.S. EPA 2006 Provisional Peer Reviewed Toxicity Values for lJ-Dichloroetham; CASRN 75-
34-3
• U.S. EPA 2009 Provisional Peer Reviewed Toxicity Values for 1,2-Dichloroetham; CASRN 107-
06-2
• U.S. EPA Integrated Risk Information System (IRIS) Chemical Assessment 1990 1,1-
Dichloroethane: CASRN 75-34-3
• U.S. Department of Human Health Services, Public Health Service, Agency for Toxic
Substances and Disease Registry (ATSDR) 2015 ToxicolosicalProfile for 1,1-Dichloroethane
(also called 2015 ATSDR Tox Profile)
• California Environmental Protection Agency, Office of Environmental Health Hazard
Assessment (OEHHA) 2003 Public Health Goals for Chemicals in Drinking Water: 1,1-
Dichloroethane in Drinking Water
• California Environmental Protection Agency, OEHHA 2006 Public Health Goals for 1,2-
Dichloroethane in Drinking Water and 2005 update memorandum
1.3 Organization of the Risk Evaluation
This draft risk evaluation for 1,1-dichloroethane includes five additional major sections and a total of 14
appendices:
• Section 2 summarizes basic physical-chemical characteristics as well as the fate and transport of
1,1-dichloroethane.
• Section 3 includes an overview of releases and concentrations of 1,1-dichloroethane in the
environment.
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• Section 4 provides a discussion and analysis of the environmental risk assessment, including the
environmental exposure, hazard, and risk characterization based on the COUs for 1,1-
dichloroethane.
• Section 5 presents the human health risk assessment, including the exposure, hazard, and risk
characterization based on the COUs. Section 5 also includes a discussion of potentially exposed
or susceptible subpopulations (PESS) based on both greater exposure and susceptibility, as well
as a description of aggregate and sentinel exposures.
• Section 6 presents EPA's proposed determination of whether the chemical presents an
unreasonable risk to human health or the environment under the assessed COUs.
Appendix A provides a list of abbreviations and acronyms as well a glossary of select terms used
throughout this draft risk evaluation. Appendix B provides a brief summary of the federal, state, and
international regulatory history of 1,1-dichloroethane. Appendix C lists all separate supplemental
documents associated with this draft risk evaluation, which can be accessed through hyperlinks included
in the references.
All subsequent appendices (Appendix D through Appendix N) and supplemental documents listed in
Appendix C include more detailed analysis and explanations than are provided in this draft risk
evaluation for 1,1-dichloroethane.
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2 CHEMISTRY AND FATE AND TRANSPORT OF 1,1-
DICHLOROETHANE
Physical and chemical properties determine the behavior and characteristics of a chemical that inform its
conditions of use, environmental fate and transport, potential toxicity, exposure pathways, routes, and
hazards. Environmental fate includes environmental partitioning, accumulation, degradation, and
transformation processes. Transformation or degradation occur through reaction of the chemical in the
environment. Environmental transport is the movement of the chemical within and between
environmental media. Thus, understanding the environmental fate of 1,1-dichloroethane informs the
determination of the specific exposure pathways and potential human and environmental receptors that
EPA considered in this draft risk evaluation.
2.1 Physical and Chemical Properties
EPA gathered and evaluated physical and chemical property data and information according to the
process described in the Draft Systematic Review Protocol Supporting TSCA Risk Evaluations for
Chemical Substances (U.S. EPA. 2021b). During the evaluation of 1,1-dichloroethane, EPA considered
both measured and estimated physical and chemical property data and information for 1,1-
dichloroethane summarized in Table 2-1, as applicable. Information on the fully extracted dataset is
available in the supplemental file Systematic Review of Data Quality Evaluation and Data Extraction
Information for Physical and Chemical Properties (U.S. EPA. 2024z).
1,1-dichloroethane is a colorless oily liquid with a chloroform- or ether-like odor (Government of
Canada. 2021; NLM. 2018; NIOSH. 2007). It is soluble in water and is miscible in most organic
solvents (NCBI. 2020a; NLM. 2018). With a vapor pressure of 228 mm Hg at 25 °C and a boiling point
of 57.3 °C, 1,1-dichloroethane is a highly volatile organic compound (VOC) (Elsevier. 2019; Dreher et
al.. 2014; O'Neil. 2013; RIVM. 2007). The physical and chemical properties of 1,1-dichloroethane are
listed in Table 2-1 and a detailed discussion is provided in Appendix D.
Table 2-1. Physical and Chemical Properties of 1,1-Dichloroethane
Property
Selected Value(s)
Reference(s)
Overall
Quality
Determination
Molecular formula
C2H4CI2
N/A
N/A
Molecular weight
98.95 g/mol
N/A
N/A
Physical form
Colorless oily liquid with
a chloroform- or ether-
like odor
(Government of Canada, 2021;
NLM. 2018; NIOSH. 2007)
High
Melting point
-96.93 °C
(NLM. 2018)
High
Boiling point
57.3 °C
(O'Neil. 2013)
High
Density
1.1757 at 20 °C
(O'Neil. 2013)
High
Vapor pressure
228 mm Hg at 25 °C
(Rumble, 2018b)
High
Vapor density
3.44 (air = 1 g/cm3)
(NCBI. 2020b)
High
Water solubility
5040 mg/L at 25 °C
(NLM. 2018)
High
Octanol/water partition
coefficient (log Kow)
1.79 at 25 °C
(Elsevier, 2019)
High
Henry's Law constant
0.00562 atm m3/mol at
24 °C
(NLM. 2018)
High
Flash point
-12 °C
(Dreher et al., 2014)
High
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Property
Selected Value(s)
Reference(s)
Overall
Quality
Determination
Autoflammability
458 °C
(Rumble, 2018b)
High
Viscosity
0.464 cP at 25 °C
(Rumble, 2018c)
High
Refractive index
1.4164
(Rumble, 2018a)
High
Dielectric constant
10.9 at 20 °C
flNLM. 2018)
High
Heat of evaporation
30.8 kJ/mL at 25 °C
(Dreher et al., 2014)
High
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1,1-Dichloroethane _ Environmental Fate and Transport (Section 2.2)
Key Points:
EPA evaluated the reasonably available environmental fate and transport information for 1,1-
dichloroethane. The following are key points from EPA's evaluation:
• Environmental Distribution:
o 1,1-Dichloroethane is a volatile liquid that evaporates rapidly at ambient temperature. Under the
COUs, environmental releases are expected to partition primarily to air with lesser amounts to
water, sediment, and soil.
• Fate and Transport in Air:
o 1,1-Dichloroethane released to air is expected to primarily remain in air due to its greater
propensity to partition into air than into water (Henry's Law constant of 0.00562 atm-m3/mol).
o In air, 1,1-dichloroethane will react with -OH radicals with a reported half-life of 39 days and
may be subject to transport and wet and dry deposition,
o Given the relatively large quantities of 1,1-dichloroethane released to air under the COUs, and
the relatively long half-life, air is expected to be an important medium for exposure.
• Fate and Transport in Soil:
o 1,1-Dichloroethane released to soil may be subject to volatilization to air, biodegradation,
runoff to surface waters, and infiltration to groundwater,
o Due to its low affinity for soil organic matter (log organic carbon: water partition coefficient
1.48), migration through soil to groundwater will be largely unhindered,
o Biodegradation in soil will generally occur slowly with half-lives ranging from months to years,
o Given the expected low soil concentrations resulting from releases to land under the COUs use,
soil is not expected to be an important medium for exposure to 1,1-dichloroethane.
• Fate and Transport in Surface Water and Sediment:
o In surface water, 1,1-dichloroethane will be subject to volatilization and slow biodegradation as
well as advection, dispersion, and dilution,
o Due to its relatively high-water solubility (5,040 mg/L), continuous releases of 1,1-
dichloroethane to deeper, slower moving surface water will result in a portion of the release
remaining in water.
o In sediment, 1,1-dichloroethane will generally biodegrade with half-lives ranging from months
to years.
o Given the relatively low quantity directly released to water under the COUs—coupled with the
effects of volatilization, dilution, advection, and dispersion—surface water will generally not be
an important medium for exposure. However, exceptions could include sustained direct releases
of 1,1-dichloroethane into deep, slower moving, or stagnant surface waters.
• Fate and Transport in Groundwater:
o Biodegradation of 1,1-dichloroethane in groundwater generally occurs slowly with half-lives
ranging from months to years,
o Releases of 1,1-dichloroethane to land under the COUs use could migrate over a period of time
to groundwater. Modeled groundwater concentrations suggest groundwater will generally not
be an important medium for exposure,
o 1,1 -dichloroethane can be produced as a product in the anaerobic biodegradation of 1,1,1 -
trichloroethane in groundwater, potentially contributing to 1,1-dichloroethane concentrations.
• Persistence and Bioaccumulation:
o 1,1-Dichloroethane meets criteria for persistence but not criteria to be classified as persistent
and bioaccumulative based on estimated bioconcentration factor (BCF)/bioaccumulation factor
(BAF) values of less than 1,000. With low bioconcentration/bioaccumulation potential, fish
ingestion and trophic transfer are not expected to be important pathways.
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2.2.1 Fate and Transport Approach and Methodology
Reasonably available environmental fate data—including biodegradation rates, removal during
wastewater treatment, volatilization from lakes and rivers, and organic carbon: water partition
coefficient (Koc)—are among selected parameters for use in the current risk evaluation. In assessing the
environmental fate and transport of 1,1-dichloroethane EPA considered the full range of results from
sources that were rated high confidence. Data evaluation information and information on the full
extracted dataset is available in the supplemental file Data Quality Evaluation and Data Extraction
Information for Environmental Fate and Transport (U.S. EPA. 2024x). Other fate estimates were based
on modeling results from EPI Suite™ (U.S. EPA. 2012c). a predictive tool for physical/chemical and
environmental fate properties. Information regarding the model inputs is available in Appendix D.2.1.1.
EPI Suite™ was reviewed by the EPA Science Advisory Board (SAB. 2007). and the individual models
that comprise EPI Suite™ have been peer reviewed through publication in technical journals. Citations
for the supporting manuscripts are available in the EPI Suite help files.
In addition, methods for estimation of BCF/BAF developed by EPA's Office of Water for the
establishment of Ambient Water Criteria for the Protection of Human Health (U.S. EPA. 2003 c) are also
presented for comparison to EPI Suite estimations. Details are presented in Appendix D.2.6
Table 2-2 provides selected environmental fate data that EPA considered while assessing the fate of 1,1-
dichloroethane. The data were updated after publication of the final scope document with additional
information identified through the systematic review process and supplemental literature searches.
Table 2-2 Environmental Fate Characteristics of 1,1-Dfchloroethane
Property or Endpoint
Value"
Reference
Overall
Quality
Determination
Indirect photodegradation
t 'A = 39 days (based on 12-hour day;
1.5E06 OH/cm3from OH rate constant of
2.74E-13 cm3/ molecule second at 25 °C)
(U.S. EPA. 2012c)
High
Direct photodegradation
Not expected to be susceptible to direct
photolysis by sunlight because 1,1-
dichloroethane does not contain
chromophores that absorb at wavelengths
>290 nm
(NCBI. 2020b)
Medium
Hydrolysis half-life
t '/2 = 61.3 years at 25 °C and pH 7
(Jeffers et al.. 1989)
High
Aerobic biodegradation water
up to 91% in 7 days after extensive
acclimation
(Tabak et al.. 1981)
High
Anaerobic biodegradation
Anaerobic sludge
31% in 25 days
(Van Eekert et al..
1999)
High
Anaerobic biodegradation
t Vi = 1.5-6.9 years
(Huff et al.. 2000)
High
t Vi =115 days
(Washington and
Cameron, 2001)
Medium
Bioconcentration factor
(BCF)
7 (estimated)
(U.S. EPA. 2012c)
High
Bioaccumulation factor
(BAF)
6.8 (estimated)
(U.S. EPA. 2012c)
High
Organic carbon:water
partition coefficient (log Koc)
1.48
(Poole and Poole.
1999)
High
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Property or Endpoint
Value"
Reference
Overall
Quality
Determination
Removal in wastewater
treatment
33-100%
(U.S. EPA. 1982)
High
11 Measured unless otherwise noted
b Information was estimated using EPI Suite™ (U.S. EPA. 2012c)
2.2.2 Summary of Fate and Transport Assessment
1,1-Dichloroethane is a volatile liquid that evaporates rapidly at ambient temperature (Rumble. 2018b).
Estimated half-lives for volatilization from water range from hours to days depending on environmental
conditions. Under the COUs, based on its physical and chemical properties, environmental releases of
1,1-dichloroethane are expected to partition primarily to air with lesser amounts to water, sediment and
soil. Figure 2-1 graphically depicts the relative major and minor partitioning and transport pathways
predicted for 1,1-dichloroethane between and within environmental media. Environmental releases of
1,1-dichloroethane reported to the Toxics Release Inventory (TRI), and the National Emissions
Inventory (NEI) between 2015 and 2020, indicate most releases are to air. Based on the reported release
data, environmental partitioning modeling predicts that approximately 85 percent mass distribution will
remain in air, 15 percent in water, and less than one percent in soil and sediment. See Appendix D.2.1.2
Fugacity Modeling for further discussion.
In air 1,1-dichloroethane will react with hydroxyl (-OH) radicals with a half-life of 39 days (U.S. EPA.
2012c) and may be subject to transport and wet and dry deposition. Because the highest releases of 1,1-
dichloroethane are to air, and those releases are expected to remain in air, it is expected to be an
important transport medium and inhalation is expected to be an important exposure pathway. The
presence of 1,1-dichloroethane in ambient air is confirmed by 2015 to 2020 monitoring data from the
AMTIC ambient air monitoring archive, which shows national annual average concentrations ranging
from 8.0xl0~2 to 0.13 [^g/m3 (Section 3.3.1). The fate of 1,1-dichloroethane in air is further discussed in
Appendix D.2.2 and inhalation exposure further discussed in Section 5.1.2.2.1.
In surface water, 1,1-dichloroethane will be subject to volatilization to air (due to its relatively high
Henry's Law constant), and biodegradation in anaerobic water. Partitioning from water to sediment is
not expected to be an important process based on its low organic carbon:water partition coefficient (log
Koc = 1.48 (Poole and Poole. 1999). Due to its relatively high water solubility (5,040 mg/L) (NLM.
2018). continuous releases of 1,1-dichloroethane to water will result in a portion of the release
remaining in water. Environmental releases to water and wastewater treatment plants are relatively low
and distributed across multiple sites (see Section 3.2). Water Quality Portal (WQP) (NWOMC. 2022)
concentrations of 1,1-dichloroethane measured in ambient surface waters from 2015 to 2020 ranged
from 0 to 2 (J,g/L, with a median concentration of 0.25 [j,g/L and a 95th percentile concentration of 0.5
[j,g/L. The fate of 1,1-dichloroethane in water is further discussed in Appendix D.2.3.1, environmental
aquatic exposure in Section 3.3.3, and human exposure in Section 5.1.2.4.
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Figure Legend
~ Negligible Partitioning/transportation
*¦ Low/slow
» Moderate I I Transformation/degradation
High/fast/strong I Wastewater facility
indirect/direct discharge
Figure 2-1. Transport, Partitioning, and Degradation of 1,1-Dichloroethane in the Environment"
11 The diagram depicts the distribution (grey arrows), transport and partitioning (black arrows) as well as the
transformation and degradation (white arrows) of 1,1-dichloroethane in the environment. The width of the arrow
is a qualitative indication of the likelihood that the indicated partitioning will occur or the rate at which the
indicated degradation will occur (i.e., wider arrows indicate more likely partitioning or more rapid degradation).
1,1-Dichloroethane will not partition strongly to sediment based on its low measured organic
carbon:water partition coefficient (log Koc 1.48 (Poole and Poole. 1999). 1,1-Dichloroethane in
sediment is expected to biodegrade slowly with half-lives of months to greater than months ( lamonts et
al.. 2009). (Simsir et al.. 2017). No monitoring data were found for exposure of humans and biota to 1,1-
dichloroethane via sediment. Relatively low levels of 1,1-dichloroethane in water and low partitioning to
sediment suggests low levels of 1,1-dichloroethane would be found in sediment. The fate of 1,1-
dichloroethane in sediment is further discussed in Appendix D.2.3.2 and environmental benthic
exposure in Section 3.3.3.4.
Releases of 1,1-dichloroethane to land may be subject to volatilization to air, runoff to surface waters,
and due to its low affinity for soil organic matter, (log Koc 1.48 (Poole and Poole. 1999). migration
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through soil to groundwater. Biodegradation in soil will generally occur slowly, with half4ives ranging
from months to years (U.S. EPA. 2013a). No monitoring data were found for exposure of humans and
biota to 1,1-dichloroethane via soil. The releases of 1,1-dichloroethane to land (TRI2015 to 2020
average 1 kg/year, EPA estimated releases less than 22,682 kg/year to Hazardous Waste Landfills) under
the conditions of use will be subject to the effects of dilution, advection, and dispersion. The fate of 1,1-
dichloroethane in soil is further discussed in Appendix D.2.4.1, environmental terrestrial exposure in
Section 4.1.3, and general population exposure in Section 5.1.2.4.5.
In groundwater, 1,1-dichloroethane will have a low affinity for organic matter based on its measured
organic carbon: water partition coefficient of 31 and will not significantly sorb to suspended solids in
groundwater. 1,1-Dichloroethane has a reported hydrolysis half-life of approximately 61 years (Jeffers et
al.. 1989); therefore, losses of 1,1-dichloroethane from groundwater will most likely be due to
biodegradation. Biodegradation half-lives are generally on the order of months to years under anaerobic
conditions that favor biological reductive dechlorination. Half-lives can also differ markedly within a
groundwater plume. (Wiedemeier et al.. 1999) for example, report half-lives for cis-l,2-dichloroethylene
(cis-l,2-DCE) that are more than an order of magnitude higher in one portion of a plume than in another
portion of the same plume. There may be cases where no biodegradation takes place. (Wilson et al..
1983) reported no biodegradation in unamended aquifer sediments containing 1,1-dichloroethane after
16 weeks of incubation under aerobic conditions. This indicates that 1,1-dichloroethane entering a
pristine oxic aquifer setting may conceivably be recalcitrant to biodegradation. The limited data
available in the literature makes this difficult to assess. There are no recent studies showing aerobic
biodegradation of 1,1-dichloroethane. There are no studies showing aerobic biodegradation of 1,1-
dichloroethane in simple mineral culture media. (Tabak et al.. 1981) reported biodegradation in
laboratory experiments, but this was most likely co-metabolic degradation supported by aerobic
degradation of the yeast extract or digester solids in their reaction mix.
(Wiedemeier et al.. 1999) describes three types of biodegradation behavior for chlorinated solvents:
Type 1, where anaerobic biodegradation is supported by an anthropogenic electron donor such as
landfill leachate or a fuel spill; Type II, where anaerobic biodegradation is supported by natural electron
donors such as buried soils or aquifer sediment with high organic matter; and Type III, where the supply
of electron donor is inadequate, and the chlorinated organic is not biodegraded. This suggests that if a
release of 1,1-dichloroethane is not accompanied by landfill leachate or other source of electron donor it
may not biodegrade.
Monitoring data confirm the presence of 1,1-dichloroethane in groundwater. 1,1-Dichloroethane
concentrations from groundwater monitoring wells retrieved from the Water Quality Portal (NWOMC.
2022) for the years 2015 to 2020 ranged from 0 to 650 [j,g/L (see Appendix 6.3.1G.1). Groundwater and
soil-water leachate concentration data collected through EPA's systematic review of published literature
reported ranges from not detected to 1,900 [j,g/L in 400 samples collected between 1984 and 2005 in the
United States. UCMR 3 monitoring data for 1,1-dichloroethane found in finished drinking water from
404 public water sources across 16 states that draw primarily from groundwater sources indicated a
maximum concentration of 1.6 (J,g/L, indicating that 1,1-dichloroethane in finished drinking water
derived from groundwater was measured in relatively low amounts across the nation between 2013 to
2015 (U.S. EPA. 2021c). Modeled groundwater concentrations of 1,1-dichloroethane resulting from
migration of its releases to soil suggest groundwater will generally not be an important medium for
exposure. However, 1,1-dichloroethane does frequently occur in anaerobic groundwater as a
biodegradation product of the compound 1,1,1-trichloroethane. The fate of 1,1-dichloroethane in
groundwater is further discussed in Appendix D.2.4.2. 1,1-Dichloroethane groundwater concentrations
are further discussed in Appendix G.
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Minor amounts of 1,1-Dichloroethane in wastewater undergoing biological wastewater treatment may be
removed by processes including sorption to wastewater solids. No recent data were found on 1,1-
dichloroethane concentrations in biosolids. However, the 1988 National Sewage Sludge Survey sampled
208 representative POTWs for a list of substances including 1,1-dichloroethane. 1,1-Dichloroethane had
a zero percent detection frequency. As discussed in Appendix D.2.5.2, less than 1 percent of 1,1-
dichloroethane is expected to be removed by sorption in biological wastewater treatment based on its
Koc value of 31. 1,1-Dichloroethane removed by sorption to wastewater solids may enter the
environment if the solids are land applied following treatment to meet standards (biosolids application).
Due to low sorption of 1,1-dichloroethane to solids and the low amounts of 1,1-dichloroethane
undergoing wastewater treatment (see Section 3.2 for details), land application of biosolids from 1,1-
dichloroethane wastewater treatment is not expected to be a significant exposure pathway. However,
specific POTW facilities reporting 1,1-dichloroethane releases could land apply biosolids containing
1,1-dichloroethane. Thus, land application of biosolids was further considered for general population
and environmental terrestrial exposures. The fate of 1,1-dichloroethane in biosolids is further discussed
in Appendix D.2.5.2, environmental terrestrial exposure to biosolids in Section 3.3.4.6.1, and general
population exposure in Section 5.1.2.4.4.
1,1-Dichloroethane does not meet the criteria to be classified as persistent and bioaccumulative (U.S.
EPA. 1999). Although 1,1-dichloroethane is expected to have half-lives exceeding 2 months in some
environmental compartments, it does not meet bioconcentration/bioaccumulation criteria based on
estimated BCF/BAF values of less than 1,000 (U.S. EPA. 2012c). With low
bioconcentration/bioaccumulation potential, fish ingestion and trophic transfer are not expected to be
important pathways. The bioconcentration of 1,1-dichloroethane in in fish is further discussed in
Appendix D.2.6, trophic transfer of 1,1-dichloroethane in Section 4.1.4, and general population exposure
through fish ingestion in Section 5.1.2.4.2 (see also Figure 2-1 above).
2.2.3 Weight of Scientific Evidence Conclusions for Fate and Transport
2.2.3.1 Strengths, Limitations, Assumptions, and Key Sources of Uncertainty for the
Fate and Transport Assessment
The weight of scientific evidence supporting the fate and transport assessment is based on the strengths,
limitations, and uncertainties associated with the fate and transport studies evaluated within and outside
systematic review. The judgment is summarized using confidence descriptors: robust, moderate, slight,
or indeterminate confidence descriptors. This approach is consistent with the Draft Systematic Review
Protocol Supporting TSCA Risk Evaluations for Chemical Substances (U.S. EPA. 2021b).
The weight of scientific evidence regarding fate and transport as reported in high-moderate quality
studies, identified both through systematic review and outside of systematic review, give robust to
moderate confidence that 1,1-dichloroethane
• will not undergo direct photolysis (Appendix D.2.2);
• will not appreciably partition to organic carbon in particulate matter in the air (Appendix D.2.2);
• will exist in the gas phase (Appendix D.2.2);
• will undergo slow indirect photolysis (Appendix D.2.2);
• will not undergo hydrolysis at environmental pH and temperature (Appendix D.2.3);
• will undergo slow or negligible biodegradation in water under aerobic conditions (Appendix
D.2.3.1);
• will undergo slow biodegradation to form chloroethane in soil and sediment under anaerobic
conditions (Appendix D.2.3.1);
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• will volatilize from surface water and moist soil (Appendixes D.2.3.1 and D.2.4.1);
• will not appreciably partition to organic carbon in sediment and soil thus has the potential to
migrate to groundwater (Appendixes D.2.3.2 and D.2.4.1);
• is not bioaccumulative in fish (Appendix D.2.6);
• will be removed in wastewater treatment by volatilization with a very low fraction adsorbed onto
sludge (Appendix D.2.5.2);
• is minimally removed in conventional drinking water treatment but may be highly removed by
certain other treatment technologies (activated carbon adsorption and packed tower aeration)
(Appendix H.3);
• is not expected to undergo long-range transport (LRT) relative to LRT benchmark chemicals
(Appendixes D.2.2); and
• can be formed under environmental conditions by the anaerobic biodegradation of 1,1,1 -
trichloroethane (Appendix D.2.4.1).
There is limited evidence on the aerobic biodegradation of 1,1-dichloroethane in water under
environmental conditions. The single study identified was a laboratory study that employed extensive
efforts to develop microbial populations capable of biodegrading 1,1-dichloroethane. As such,
extrapolating rates of biodegradation observed in the laboratory study to environmental biodegradation
rates is highly uncertain (Appendix D.2.3.1). A detailed discussion of strengths, limitations,
assumptions, and key sources of uncertainty for the fate and transport assessment of 1,1-dichloroethane
is available in Appendix D.2.
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3 RELEASES AND CONCENTRATIONS OF 1,1-
DICHLOROETHANE IN THE ENVIRONMENT
EPA estimated environmental releases of 1,1-dichloroethane that are discussed in Sections 3.1 and 3.2.
Section 3.1 describes the approach and methodology for estimating releases. Section 3.2 presents
estimates of environmental releases by geographic location, media of release, and by OES. This section
also includes an evaluation of the weight of scientific evidence for the environmental releases. Section
3.3 presents the approach, methodology for estimating environmental concentrations, and the estimates
of environmental concentrations that result from environmental releases of 1,1-dichloroethane.
3.1 Approach and Methodology
The assessment of environmental releases for 1,1-dichloroethane focuses on releases from industrial and
commercial sources.
3.1.1 Industrial and Commercial
1,1-Dichloroethane is a TRI-reportable substance effective January 1, 1994. It is (1) included on EPA's
initial list of hazardous air pollutants (HAPs) under the Clean Air Act (CAA), (2) a designated toxic
pollutant under the Clean Water Act (CWA), and (3) currently not subject to National Primary Drinking
Water Regulations (NPDWR) under the Safe Drinking Water Act (SDWA).
As mentioned in Section 1.1.1, the total production volume (PV) of 1,1-dichloroethane in 2015 from the
2016 CDR reporting period was between 100 million and 1 billion lb. This range did not change in the
2020 CDR reporting period. Due to a lack of information, EPA was not able to identify the percentage
of the PV that goes toward processing as a reactive intermediate or commercial use as a laboratory
chemical. The Agency assumes that a high percentage of the PV is used for processing as a reactive
intermediate, and a small percentage of the PV is used for commercial use as a laboratory chemical.
EPA's approach for estimating releases is illustrated in Figure 3-1 below.
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Identify and describe
Occupational Exposure
Scenarios (OES)
Section 3.1.1.1
Collect annual facility
release data from
programmatic databases
(TRI, DMR, NEI)
Section 3.1.1.2
Map release
data to OES
Section 3.1.1.3
Fill in gaps with
release modeling
Section 3.1.1.4
Estimate days/yr
of release for
facilities in OES
Section 3.1.1.5
Results: Environmental
releases - geographical
location, media of
release, OES release
estimates
Section 3.2.1
Figure 3-1. Overview of EPA's Approach to Estimate Releases for Each OES
The following Sections (3.1.1.1 through 3.1.1.5) provide information on this approach. A more detailed
description of occupational exposures and environmental releases is available in the Draft Risk
Evaluation for 1,1-Dichloroethane - Supplemental Information File: Environmental Releases and
Occupational Exposure Assessment (U.S. EPA. 2024e).
3.1.1.1 Identify and Describe OES
COUs are the unique combinations of Lifestyle Stage, Category, and Subcategory that EPA developed
and are presented in Table 1-1 of this draft risk evaluation. EPA has identified eight COUs in Table 3-1.
An OES was identified for each COU with the exception of processing as a reactive intermediate where
three COUs were combined into one OES due to expected similarities in release and exposure potential.
Table 3-1 also lists the seven OESs that EPA assessed for 1,1-dichloroethane.
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1687 Table 3-1. Crosswalk of Conditions of Use to Occupational Exposure Scenarios Assessed
Condition of Use
OES
Life Cycle
Stage
Category"
Subcategory6
Manufacturing
Domestic
manufacturing
Domestic manufacturing
Manufacturing17
Processing
As a reactant
Intermediate in all other basic
organic chemical manufacturing
Processing as a reactive
intermediate
As a reactant
Intermediate in all other chemical
product and preparation
manufacturing
Recycling
Recycling
Processing -
repackaging
Processing - repackaging
Processing - repackaging
Distribution in
Commerce
Distribution in
commerce
Distribution in commerce
Distribution in commerce''
Commercial Use
Other use
Laboratory chemicals
Commercial use as a
laboratory chemical
Disposal
Disposal
Disposal
General waste handling,
treatment, and disposal
Waste handling, treatment,
and disposal (POTW)
Waste handling, treatment,
and disposal (remediation)
11 These categories of COUs reflect CDR codes and broadly represent COUs for 1,1-dichloroethane in industrial
and/or commercial settings.
h These subcategories reflect more specific uses of 1,1-dichloroethane.
c 1,1-Dichloroethane manufactured as a byproduct during the manufacture of 1,2-dichloroethane will be assessed in
the draft risk evaluation for 1,2-dichoroethane.
d EPA considers the activities of loading and unloading of chemical product part of distribution in commerce. These
activities were assessed as part of the OES of Manufacturing, processing as a reactive intermediate, processing -
repackaging, and commercial use in laboratory chemicals. EPA's current approach for quantitively assessing releases
and exposures for the remaining aspects of distribution in commerce consists of searching DOT and NRC data for
incident reports pertaining to 1,1-dichloroethane distribution.
1688
1689 After identifying the OES that will be assessed, the next step was to describe the function of 1,1-
1690 dichloroethane within each OES (Table 3-2). This would be utilized in mapping release data to an OES
1691 as well as in applying release modeling approaches.
1692
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Table 3-2. Description of the Function of 1,1-Dichloroethane for Each PES
OES
Role/Function of 1,1-Dichloroethane
Manufacturing
1,1-Dichloroethane may be produced by chlorination of ethane or
chloroethane, addition of hydrogen chloride to acetylene or vinyl chloride, or
oxychlorination with hydrogen chloride. Additionally, 1,1-dichloroethane is
manufactured as a byproduct or impurity during the intentional manufacturing
of 1.2-dichloroethane (NCBI. 2020a; Dreher et al.. 2014).
Processing as a reactive
intermediate
1,1-Dichloroethane is used as an intermediate in the production of other
chemicals, primarily 1.1.1-trichloroethane (Dreher et al.. 2014; RIVM. 2007;
U.S. EPA. 2000a). Additionally. EPA assumes that waste streams containing
1,1-dichloroethane may be recycled on-site and then re-introduced into the
facility's process waste stream or recycled as a feedstock to be used in the
manufacture of other chemicals.
Processing - repackaging
A portion of the 1,1-dichloroethane manufactured is expected to be repackaged
into smaller containers for commercial laboratory use.
Distribution in commerce
1,1-Dichloroethane is expected to be distributed in commerce for processing as
a reactive intermediate and commercial laboratory use. EPA expects 1,1-
dichloroethane to be transported from manufacturing sites to downstream
processing and repackaging sites.
Commercial use as a laboratory
chemical
1,1-Dichloroethane is used as a laboratory reference standard domestically for
instrument calibration and analytical method validation (Siema-Aldrich. 2020).
Waste handling, treatment, and
disposal
Each of the OES may generate waste streams of 1,1-dichloroethane that are
collected and transported to third-party sites for disposal or treatment, and
these cases are assessed under this OES.
3.1.1.2 Collect Facility Release Data from Data Sources
Sections 3.1.1.2.1 through 3.1.1.2.5 describe sources of facility-specific release data for 1,1-
dichloroethane and the methods used to collect the data from TRI, Discharge Monitoring Reports
(DMRs), and the NEI. To help evaluate trends in releases, release data was collected for multiple years
from these data sources. The results of the systematic review are also a potential source of release data
as described in Section 3.1.1.3.4.
When evaluating releases during distribution in commerce of 1,1-dichloroethane, EPA considered
National Response Center (NRC) data and Department of Transportation (DOT) Hazmat Incident
Report Search Tool data during the 2015 to 2020 timeframe (NRC. 2009) (DOT Hazmat Incident Report
Data) as described in Section 3.1.1.2.5.
3.1.1.2.1 Toxic Release Inventory (TRI)
The TRI database includes facility-specific information on disposal and other releases of 1,1-
dichloroethane to air, water, and land (U.S. EPA. 2022f). The release data is reported in lbs/year. EPA
downloaded available water, air, and land release data from TRI for six reporting years from 2015
through 2020:
• Air emissions in TRI are reported separately for stack air and fugitive air and occur on-site at the
facility. From 2015 to 2020, 23 facilities reported air emissions of 1,1-dichloroethane, and there
were 98 total reports.
• Water releases in TRI include both reports of annual direct discharges to surface water and
annual indirect discharges to off-site POTWs and wastewater treatment (WWT) facilities. Four
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facilities reported water releases of 1,1-dichloroethane, with a total of nine reports over the 6
years that were assessed.
• Land releases in TRI provide the type of release media for a particular facility, as well as how
the chemical is managed through recycling, energy recovery, or treatment. Two facilities
reported land releases of 1,1-dichloroethane to RCRA Subtitle C landfills and other non-site
landfills respectively, and there were six non-zero reports over the 6 years assessed.
EPA obtained 2015 to 2020 TRI data for 1,1-dichloroethane from EPA's Basic Plus Data Files. EPA
followed a similar approach to estimate air, water, and land releases. The Agency used the reported
annual releases directly as reported in TRI. EPA then divided the annual releases over the number of
estimated operating days (as discussed in Section 3.1.1.5) to obtain daily average release estimates. EPA
presents the release data as high-end and central tendency estimates, as discussed in Section 3.2.1.
Release estimates are separated by stack and fugitive air emissions, surface water discharges, and land
releases.
A facility is required to report to TRI if it has 10 or more full-time employees; is included in an
applicable North American Industry Classification System (NAICS) code; and manufactures, processes,
or uses specific chemicals in quantities greater than specified thresholds.1 Facilities provide on-site
release information using readily available data (including monitoring data) collected pursuant to other
provisions of law, or, where such data are not readily available, "reasonable estimates" of the amounts
released.
For each release quantity reported, TRI filers select a "basis of estimate" code to indicate the principal
method used to determine the release quantity. TRI provides six basis of estimate codes, which in no
particular order, are continuous monitoring, periodic monitoring, mass balance calculations, published
emission factors, site-specific emission factors, and engineering calculations/best engineering judgment.
For facilities that use a TRI chemical in multiple operations, the filer may use a combination of methods
to calculate the overall release quantity. In such cases, TRI instructs the facility to enter the basis of
estimate code for the method that corresponds to the largest portion of the reported release quantity.2
Additional details on the basis for the reported release estimate (e.g., calculations, underlying
assumptions) are not reported in TRI.
For further discussion of water, air, and land emission data collection and estimation from TRI, refer to
the Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Environmental
Releases and Occupational Exposure Assessment (U.S. EPA. 2024e).
3.1.1.2.2 Discharge Monitoring Reports (DMR)
DMRs include facility-specific information on releases of 1,1-dichloroethane to water. Under the CWA,
EPA regulates the discharge of pollutants into receiving waters through the National Pollutant Discharge
Elimination System (NPDES). ANPDES permit authorizes discharging facilities to discharge pollutants
up to specified limits and requires facilities to monitor their discharges and report the results to EPA and
the state regulatory agency in DMRs. EPA makes these reported data publicly available via EPA's
Enforcement and Compliance History Online (ECHO) system and EPA's Water Pollutant Loading Tool
(Loading Tool). The data collected is annual release data for a given reporting year.
1 See https://www.epa.gov/toxics-release-inventorv-tri-program/tri-tlireshold-screening-tool.
2 See TRI Program Guidance on EPA's GuideME website under Reporting Forms and Instructions, Section 5. Quantity of the
Toxic Chemical Entering Each Enviromnental Medium On-Site (Form R).
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EPA downloaded DMR data from reporting years 2015 through 2020 (U.S. EPA. 2022c) using ECHO
system and the Loading Tool. Over the 6 reporting years, 79 facilities reported water releases in DMR
for 1,1-dichloroethane with a total of 219 reports.
Where available, EPA used DMR data to estimate annual wastewater discharges, average daily
wastewater discharges, and high-end daily wastewater discharges. For DMR, annual discharges are
automatically calculated by the Loading Tool based on the sum of the discharges associated with each
monitoring period in DMR. Monitoring periods in DMR are set by each facility's NPDES permit and
can vary between facilities. Typical monitoring periods in DMR include monthly, bimonthly, quarterly,
biannual, and annual reporting.
In instances where a facility reports a period's monitoring results as below the limit of detection (LOD)
(also referred to as a non-detect or ND) for a pollutant, the Loading Tool applies a hybrid method to
estimate the wastewater discharge for the period. The hybrid method sets the values to half of the LOD
if there was at least one detected value in the facility's DMRs in a calendar year. If all values were less
than the LOD in a calendar year, the annual load is set to zero. EPA included emissions below the LOD
in the release estimates. To estimate daily discharges, EPA divided the annual discharges over the
number of estimated operating days (as discussed in Section 3.1.1.5). In some cases, the same facility
reported water releases to both TRI and DMR for a given reporting year. EPA presented data from both
sources for the water release assessment.
For further discussion on the collection of DMR data, refer to Draft Risk Evaluation for 1,1-
Dichloroethane - Supplemental Information File: Environmental Releases and Occupational Exposure
Assessment (U.S. EPA. 2024e).
3.1.1.2.3 National Emissions Inventory (NEI)
NEI was established to track emissions of Criteria Air Pollutants (CAPs)3 and CAP precursors and assist
with National Ambient Air Quality Standard (NAAQS) compliance under CAA. 1,1-Dichloroethane is
on EPA's initial list of HAPs under the CAA.4 Air emissions data for the NEI are collected at the state,
local, and tribal (SLT or S/L/T) level.5 SLT air agencies then submit these data to EPA through the
Emissions Inventory System (EIS). In addition to CAP data, many SLT air agencies voluntarily submit
data for pollutants on EPA's list of HAPs. EPA uses the data collected from SLT air agencies, in
conjunction with supplemental HAP data, to build the NEI. EPA releases an updated NEI every 3 years.
For this draft risk evaluation, 1,1-dichloroethane, NEI emissions data was collected for point sources
and area or nonpoint sources. Point sources are stationary sources of air emissions from facilities with
operating permits under Title V of the CAA, also called "major sources." Point source facilities include
large energy and industrial sites and are reported at the emission unit6 and release point-level.7 As
documented in the Technical Support Document for the 2017 NEI,
For point sources (in general, large facilities), emissions are inventoried at a process-level within
a facility. The point data are collected from S/L/T air agencies and the EPA emissions programs
including the TRI, the Acid Rain Program, and Maximum Achievable Control Technology
1 The CAA requires EPA to set National Ambient Air Quality Standards (NAAQS) for five CAPs: ground-level ozone (O3),
particulate matter (PM), carbon monoxide (CO), lead (Pb), sulfur dioxide (SO2), and nitrogen dioxide (NO2).
4 See EPA's initial list of HAPs and subsequent modifications.
5 See EPA Air Emissions Reporting Requirements (AERR).
6 Defined as any activity at a stationary source that emits or lias the potential to emit a regulated air pollutant.
7 Defined as the point from which air emissions from one or more processes are released into the atmosphere (e.g., a stack).
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(MACT) standards development. For nonpoint sources (typically smaller, yet pervasive sources)
and mobile sources8 (both onroad and nonroad), emissions are given as county totals.9
Area or nonpoint sources are stationary sources that do not qualify as major sources. The nonpoint data
are reported at the county-level and include emissions from smaller facilities as well as agricultural
emissions, construction dust, and open burning. Industrial and commercial/institutional fuel combustion,
gasoline distribution, oil and gas production and extraction, publicly owned treatment works, and
solvent emissions may be reported in the point or nonpoint source categories depending upon source
size.10
EPA downloaded NEI data from reporting years 2014 and 2017, which were the most recent datasets
available at the time of this evaluation. In 2017, there were 2,111 facilities that reported point source air
emissions of 1,1-dichloroethane to NEI and 5,136 point source reports, and 13,527 area source reports.
In 2014, there were 2,111 facilities that reported point source air emissions to NEI, 4,192 total reports,
and 13,269 area source reports.
Where available, EPA used NEI data to estimate annual and average daily fugitive and stack air
emissions. Facility-level annual emissions are available for major sources in NEI. EPA then divided the
annual stack and fugitive emissions over the number of estimated operating days (as discussed in
Section 3.1.1.5) to develop daily release estimates. In some cases, the same facility reported air releases
to both TRI and NEI for a given reporting year. EPA presented data from both sources for the air release
assessment.
See the Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Environmental
Releases and Occupational Exposure Assessment (U.S. EPA. 2024e) for additional information on
obtaining NEI data.
3.1.1.2.4 Systematic Review
EPA conducted a systematic review of the literature to supplement release data of 1,1-dichloroethane
from DMR, TRI, and NEI. The systematic review process is briefly described in Section 1.2. More
detail regarding these steps is provided in the Draft Risk Evaluation for 1,1-Dichloroethane -
Supplemental Information File: Environmental Releases and Occupational Exposure Assessment (U.S.
EPA. 2024e). Upon review of the literature, EPA did not identify release data pertaining to 1,1-
dichloroethane.
3.1.1.2.5 National Response Center and DOT Hazmat
Section 103 of the Comprehensive Environmental Response, Compensation, and Liability Act
(CERCLA) requires the person in charge of a vessel or an onshore or offshore facility to immediately
notify the National Response Center (NRC) when a CERCLA hazardous substance is released at or
above the reportable quantity (RQ) in any 24-hour period, unless the release is federally permitted (40
CFR 302). The NRC is an emergency call center maintained and operated by the U.S. Coast Guard that
fields initial reports for pollution and railroad incidents. Information reported to the NRC is available on
the NRC website. The DOT Hazmat Incident Report Data uses submissions from Hazardous Materials
8 Note that the NEI provides data for marine vessel and railroad sources at the sub-county, "polygon" shape-level. "For
wildfires and prescribed burning, the data are compiled as day-specific, coordinate-specific (similar to point) events in the
"event" portion of the inventory, and these emission estimates are further stratified by smoldering and flaming components
(Section 1.2 of EPA's Technical Support Document forthe 2017 NEI)."
9 See Section 1.2 of EPA's Technical Support Document forthe 2017 NEI.
111 See EPA's 2017 National Emissions Inventory: January 2021 Updated Release, Technical Support Document.
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Incident Reports (DOT Form F 5800.1 [01/2004]) that are required to be reported within 30 days of the
discovery of an incident (49 CFR 171).
EPA reviewed NRC data and DOT data for the 2015 to 2020 calendar years for incident reports
pertaining to distribution of 1,1-dichloroethane (NRC. 2009) (DOT Hazmat Incident Report Data). EPA
did not identify reported releases for 1,1-dichloroethane during distribution of the chemical.
3.1.1.3 Map Facility Release Data to PES
EPA developed the OES to group processes or applications with similar sources of release that occur at
industrial and commercial workplaces within the scope of the risk evaluation. There are data available in
each of these data sources that can be utilized to map the facility to an OES. The full details of the
methodology for mapping facilities from EPA reporting programs is described in the Draft Risk
Evaluation for 1,1-Dichloroethane - Supplemental Information File: Environmental Releases and
Occupational Exposure Assessment (U.S. EPA. 2024e). In brief, mapping consists of using facility
reported industry sectors (typically reported as either North American Industry Classification System
[NAICS] or Standard Industrial Classification [SIC] codes), and chemical activity, processing, and use
information to assign the most likely OES to each facility. A brief overview of the mapping process is
shown in Figure 3-2. Mapping results, as well as the associated release data, are provided in Draft Risk
Evaluation for 1,1-Dichloroethane - Supplemental Information File: Environmental Releases and
Occupational Exposure Assessment (U.S. EPA. 2024e).
Figure 3-2. Overview of EPA's Approach to Map Facility Release Data to OES
3.1.1.3.1 Mapping TRI Release Data to an OES
TRI provides facility-specific information such as name, address, and other facility identification
information. However, TRI does not include descriptive information on the activity of the chemical at
the facility. There is information in the TRI that can be utilized to map the facility to a particular OES.
For example, the Olin Blue Cube Facility in Freeport, Texas, reported releases of 1,1-dichloroethane to
TRI. The facility reported a TRI use code that indicates 1,1-dichloroethane is processed as a reactant at
the facility. Using the provided use code, EPA mapped the facility to the Processing as a reactive
intermediate OES.
In some cases, there are multiple TRI uses reported by a given facility. To determine the OES for these
facilities, EPA used the 2020 CDR, NAICS codes, and internet searches to determine the type of
products and operations at the facility. Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental
Information File: Environmental Releases and Occupational Exposure Assessment (U.S. EPA. 2024e)
for further discussion on mapping TRI data to an OES.
3.1.1.3.2 Mapping DMR Release Data
DMR provides facility-specific information such as name, address, and other facility identification
information. However, DMR does not include descriptive information on the activity of the chemical at
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the facility, and unlike the TRI mapping, DMR facilities do not include any use/sub-use codes. There is
information in the DMR that can be utilized to map the facility to a particular OES.
For example, Amcol Health and Beauty Solutions, Inc. reported water discharges of 1,1-dichloroethane
to DMR. For a particular facility in DMR, the report will include a SIC code. The SIC code provided for
this facility is 8731 - Commercial Physical and Biological Research. EPA mapped the facility to the
Commercial use as a laboratory chemical OES based on the reported SIC code. In some cases, EPA
assigned the OES by reviewing 2020 CDR for 1,1-dichloroethane (U.S. EPA. 2020a) or conducting an
internet search of the types of products and operations at the facility.
3.1.1.3.3 Mapping NEI Release Data
NEI provides facility-specific information, such as name, address, site description, and other facility
identification information. Additionally, there is information in NEI that can be used to assign a facility
to a particular OES. For example, the Northwest Tennessee Disposal Corporation reported air emissions
of 1,1-dichloroethane to NEI. According to NEI reporting, the facility is included in the waste disposal
sector. The Source Classification Codes (SCC) also indicate waste disposal operations at the facility.
Based on the sector and SCC, EPA mapped the facility to Waste handling, treatment, and disposal. In
some cases, EPA assigned an OES using NAICS codes or conducting an internet search of the types of
products and operations at the facility.
3.1.1.3.4 Mapping Systematic Review Data
EPA did not identify release data pertaining to 1,1-dichloroethane from systematic review data.
3.1.1.4 Fill in Gaps with Modeling to Estimate Releases for OES with No Data
Generally, EPA performs modeling to estimate releases when
• releases are expected for an OES but TRI, DMR, and/or NEI data or release data from
Systematic Review are not available; or
• the Agency determines that the facility release data collected do not capture the entirety of
environmental releases for an OES.
Standard models that have been previously developed by EPA are used to estimate releases. The models
include loss fraction models as well as models for estimating chemical vapor generation rates. If EPA
determines that an existing model does not capture the entirely of releases for a given scenario, a new
model may be developed.
EPA modeled releases for two OESs: Processing - repackaging as well as the Commercial use as a
laboratory chemical. The Agency modeled releases for both scenarios because the facility release data
collected does not capture the entirety of environmental releases. For the Repackaging OES, although
EPA identified three relevant facilities in DMR, the release estimates reported by those facilities were
below the LOD and there were no releases reported to air and land media.
For the Laboratory chemicals OES, EPA identified four relevant facilities in DMR and NEI. One of the
facilities reported a release estimate that was below the LOD in DMR. Additionally, there were no
releases reported to land media for this OES. Because EPA determined that the data from these four
facilities was not sufficient to capture the entirety of releases for this OES, the Agency modeled releases.
Additionally, EPA identified the following GS that are applicable to the OES: The July 2022 Chemical
Repackaging - Generic Scenario for Estimating Occupational Exposures and Environmental Releases
(U.S. EPA. 2023 c) and Use of Laboratory Chemicals - Generic Scenario for Estimating Occupational
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Exposures and Environmental Releases (U.S. EPA. 2023 c). Both GSs list standard models that are
applicable to the release scenarios. For both scenarios, EPA used the following approach to obtain high-
end and central tendency release estimates:
1. Identify release sources and media of release for the OES.
2. Identify model input parameters from relevant literature sources, Generic Scenarios (GSs), or
Emission Scenario Document (ESDs). Model input parameters include the estimated number of
sites, container size, mass fractions, and 1,1-dichloroethane's physical properties. If a range of
input values is available for an input parameter, determine the associated distribution of input
values.
3. Identify model equations based on standard models from relevant GS or ESDs.
4. Conduct a Monte Carlo simulation to calculate the total 1,1-dichloroethane release (by
environmental media) across all release sources during each iteration of the simulation.
5. Select the 50th percentile and 95th percentile values to estimate the central tendency and high-
end releases, respectively.
EPA performed a Monte Carlo simulation to variability in the model input parameters. The simulation
used the Latin hypercube sampling method in @Risk Industrial Edition, Version 7.0.0, which generates
a sample of possible values. The Agency performed the model at 100,000 iterations to capture a broad
range of possible input values. The model generates statistics, and any desired percentile may be
selected. EPA selected the 50th percentile and 95th percentile to estimate releases.
Detailed descriptions of the model approaches used for each OES, model equations, input parameter
values and associated distributions are provided both in Section 3.3 and th e Draft Risk Evaluation for
1,1-Dichloroethane - Supplemental Information File: Environmental Releases and Occupational
Exposure Assessment (U.S. EPA. 2024e). Additionally, input parameters and modeling results are
provided in Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Laboratory
Chemical Occupational Exposure and Environmental Release Modeling Results (U.S. EPA. 2024h) and
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Repackaging
Occupational Exposure and Environmental Release Modeling Results (U.S. EPA. 2024i).
3.1.1.5 Estimate the Number of Release Days per Year for Facilities in the OES
EPA's general approach is to estimate both an annual (kg/site-year) and a daily (kg/site-day) release rate
for a facility. Data on the number of release days for a facility are not available from data sources such
as DMR and TRI. As a surrogate, EPA uses generic estimates of the number of operating days
(days/year) for facilities in each OES as presented in Table 3-3.
Table 3-3 lists generic estimates of the number of operating days/year for a facility in the OES for the
1,1-dichloroethane release assessment. A daily release rate for a facility with TRI data, for example, can
be estimated by using the annual facility release from TRI and dividing it by the number of operating
days/yr. The annual release and average daily release of 1,1-dichloroethane can be utilized in evaluating
potential environmental concentrations, as discussed in Section 3.3. See DraftRiskEvaluation for 1,1-
Dichloroethane - Supplemental Information File: Environmental Releases and Occupational Exposure
Assessment (U.S. EPA. 2024e) for further discussion on the methodologies used to estimate the number
of operating days. Additionally, see Section 3.3 for assumptions of release days applied to exposure
modeling.
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Table 3-3. Generic Estimates of Number of Operating Days per Year for Each PES
OES
Operating Days
(days/year)
Basis
Manufacturing
350
For the manufacture of the large-PV solvents, EPA
assumes 350 days/year for release frequency. This
assumes the plant runs 7 days/week and 50 weeks/year
(with 2 weeks down for turnaround) and assumes that the
plant is always producing the chemical.
Processing as a reactive
intermediate
350
1,1-Dichloroethane is largely used to manufacture other
commodity chemicals, such as 1,1,1-trichloroethane,
which will likely occur year-round. Therefore, EPA
assumes 350 days/year for release frequency.
Processing - repackaging
260
The Julv 2022 Chemical Repackaging GS (U.S. EPA.
2023c) estimates a default of 260 operatina davs/vear per
the U.S. Bureau of Labor Statistics Occupational
Employment Statistics (BLS OES) data (US BLS, 2020).
Commercial use as a laboratory
chemical
260
The Draft GS on Use of Laboratory Chemicals (U.S.
EPA. 2023c) estimates a default of 260 operatina
days/year per the BLS OES data (US BLS, 2020).
General waste handling,
treatment, and disposal
250
It is unlikely that non-POTW waste handling, treatment,
and disposal facilities use 1,1-dichloroethane every day;
therefore, EPA assumes 250 days/year (5 days/week, 50
weeks/year).
Waste handling, treatment, and
disposal (POTW)
365
POTWs are expected to operate continuously over 365
days/year; therefore, 365 days/year should be used.
Waste handling, treatment, and
disposal (remediation)
365
Remediate sites are expected to operate continuously
over 365 days/year; therefore, 365 days/year should be
used.
3.2 Environmental Releases
Estimates of releases for 1,1-dichloroethane in this section are from industrial and commercial sources.
3.2.1 Industrial and Commercial Releases
This section provides results of EPA's 1,1-dichloroethane environmental release analysis. Although data
on the percentage is not available, EPA assumes that a high percentage of the production volume for
1,1-dichloroethane is reactive intermediate use where 1,1-dichloroethane would be reacted to make
another chemical and therefore the 1,1-dichloroethane would be consumed and not available at that
point for environmental release.
EPA developed environmental release information by estimating and summarizing the following:
• number of facilities with 1,1-dichloroethane environmental releases,
• facility releases according to geographic location,
• releases according to media of release, and
• releases per OES facility.
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3.2.1.1 Number of Facilities with 1,1-Dichloroethane Emissions
EPA compiled the number of facilities reporting 1,1-dichloroethane releases from TRI, NEI, and DMR.
Each programmatic database provides facility-specific release information. DMR data provides annual
effluent measured or monitored concentrations of 1,1-dichloroethane into receiving water bodies as well
as other NPDES permit information. TRI provides both facility-specific annual water release as well as
air emissions and land disposal quantities and NEI provides facility's unit-specific annual ambient air
release estimates. For the Processing - repackaging OES and Commercial use as a laboratory chemical
OES, the number of sites were estimated as part of the release modeling. The number of facilities is
presented by OES and shown in Table 3-4.
Table 3-4. Number of Sites with 1,1-Dichloroethane Environmental Releases
OES
Number of Sites from Programmatic Databases
Number of Sites
Estimated
During Release
Modeling
DMR"
TRI
NEI
Unique Sites6
Manufacturing
1
9
10
10
-
Processing as a reactive
intermediate
58
6
32
90
-
Processing - repackaging
3
-
-
3
2
Commercial use as a
laboratory chemical
2
-
2
4
43-138
General waste handling,
treatment, and disposal
22
8
650
672
—
Waste handling, treatment,
and disposal (POTW)
125
-
-
125
-
Waste handling, treatment,
and disposal (remediation)
42
—
—
42
—
Natural gas fired
reciprocating engines
—
—
1,380
1,380
—
Facilities not mapped to an
OES
68
—
35
103
—
11 Includes sites in DMR that reported releases of 1,1-dichloroethane below the limit of detection.
h Due to the nature of DMR/TRI/NEI reporting, some facilities appear in multiple programmatic databases.
EPA expects that the major contributor to the large number of landfills sites in NEI reporting 1,1-
dichloroethane in the air emissions must be sources other than 1,1-dichloroethane COUs of
Manufacture, Processing, and Commercial Use. The 2015 ATSDR Tox Profile (AT SDR. 2015) states
that emissions of 1,1-dichloroethane in landfills come from the anaerobic decomposition of the organic
material in the landfill; decomposition of 1,1,1-trichloroethane forms 1,1-dichloroethane as a major
product. 1,1-Dichloroethane has a presence in landfills, either by direct disposal of 1,1-dichloroethane or
decomposition of 1,1,1-trichloroethane. However, it is unclear how much 1,1,1-trichloroethane is
disposed to landfills and how much 1,1-dichloroethane is generated.
Sites were mapped to "Natural gas fired reciprocating engines" in NEI due to sites that reported 1,1-
dichloroethane emissions during natural gas combustion. However, upon further review, these 1,1-
dichloroethane emissions were likely due to the use of an AP-42 natural gas-fired reciprocating engine
emissions factor, which was not based on quantitative measurements of 1,1-dichloroethane, but non-
detects. Therefore, EPA does not believe there are actual 1,1-dichloroethane emissions from these NEI
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sites. It should be noted that the number of records in NEI may differ from the number of sites, as
multiple records may exist for a single site.
Facilities were not mapped to an OES in cases where information on the 1,1-dichloroethane use at the
site was not available. These sites do not fit in any of the 1,1-dichloroethane OES since they are mainly
tire manufacturing, pulp and paper, and alloy production.
3.2.1.2 Environmental Releases by Geographic Location
This section provides mapping of the location of facilities reporting air emissions of 1,1-dichloroethane
from TRI and NEI respectively. Ambient air releases as reported by TRI from reporting years 2015 to
2020 are presented below in Figure 3-3.
Tribal Lands
1,1-DCA Air Facilities
Max Annual Total Release Range (Ib/yr)
° <10
o >10 to 100
© >100 to 1,000
® >1,000 to 10,000
• >10,000 to 17,600
Figure 3-3. 1,1-Dichlorothane Annual Releases to Air as Reported by TRI, 2015-2020
Note: Some symbols for individual years may overlap and obscure annual releases at each site.
Alaska, American Samoa, Guam, Hawaii, N. Mariana Islands, Puerto Rico, and the U.S. Virgin
Islands are not shown as there are no known releases for these territories reported to TRI.
Ambient air releases as reported by NEI from reporting years 2014 and 2017 are presented below in
Figure 3-4.
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&& Tribal Lands
NEI Facilities Releasing 1,1-DCA
(Excluding Landfills and Fuel Uses)
Total Annual Release (Ib/yr)
o 0-50
o 50 - 300
O 300 - 600
• 600 - 1300
• 1300 - 2600
Figure 3-4. 1,1-Dichloroethane Annual Releases to Air as Reported by NEI, 2014 and 2017
3.2.1.3 Environmental Releases by Media of Release
EPA compiled the annual environmental releases by air, water, and disposal media as presented in Table
3-5. The data used to compile the release estimates from TRI and DMR are from reporting years 2015 to
2020, and the data from NEI are from reporting years 2014 and 2017. The release estimates are
presented by media of release. NEI releases from natural gas fired reciprocating engines and landfills are
not included in Table 3-5. However, TRI reported disposal of 1,1-dichloroethane to landfills are
included in subsequent land/soil/groundwater estimates.
EPA estimated the releases by media by summing annual releases that were reported directly by
facilities from the programmatic databases and then averaging across the corresponding number of years
of release. For example, for fugitive air releases, EPA averaged the total yearly releases from 2015 to
2020 TRI and 2014 and 2017 NEI to develop an average annual release estimate. The yearly fugitive
releases from 2015 to 2020 TRI are as follows: 2,565 kg/year, 2,238 kg/year, 2,260 kg/year, 2,662
kg/year, 1,990 kg/year, and 4,000 kg/year. The fugitive releases from 2014 and 2017 NEI are 38,576
kg/year, and 37,879 kg/year, respectively. The average annual fugitive release estimate from 2015 to
2020 TRI and 2014 and 2017 NEI data is 11,521 kg/year.
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Table 3-5. Average Annual Environmental Release Estimates by Media of
Release
Media of
Release"
Subcategory6
Average Annual Release
Estimate (kg/yr)
Sources
Air
Fugitive Air (Data)
11,521
TRI/NEI
Stack Air (Data)
3,505
TRI/NEI
Fugitive or Stack Air (Modeled
Release Estimates)
<777
Environmental Release
Modeling
Water
Surface Water
1,052
TRI/DMR
Disposal
Land (Data)
1.0
TRI
1,1-Dichloroethane sent to a
Hazardous Waste Landfill or to
Incineration for combustion of the
waste stream
<22,682c
Environmental Release
Modeling
11 These categories broadly represent the media of release for 1,1-dichloroethane in industrial and/or commercial
settings.
h These subcategories reflect more specific releases of 1,1-dichloroethane.
c 97% of the hazardous waste landfill or incineration releases are from the Commercial use as a laboratory chemical
OES. 1,1-Dichloroethane is included on the list of hazardous wastes pursuant to RCRA section 3001 (40 CFR 261.33)
as a listed waste on the list; therefore, EPA assumed all disposal for the scenario would be to hazardous waste landfill
or incineration.
3.2.1.4 Environmental Releases by PES
EPA compiled the annual and daily release estimates by OES as presented in Table 3-6. The release
estimates are also separated by release media (e.g., surface water, fugitive air, stack air, etc.). Annual
release estimates were reported directly by facilities in TRI, DMR, and NEI. The facility release data
were then mapped to an OES as discussed in Section 3.1.1.3. Annual fugitive air and stack air release
data was provided by TRI and NEI, surface water discharge release data was provided by TRI and
DMR, and land release data was provided by TRI.
For example, one site was mapped to the Manufacturing OES that reported land releases to TRI. The site
reported land releases for reporting years 2015 to 2017 and 2019 to 2020, with the following release
values: 2.3, 1.5 kg/year, 1.4 kg/year, 0.4 kg/year, and 0.2 kg/year. EPA then selected the 50th and 95th
percentile land release estimates for this site which are presented in Table 3-6 (1.4 kg/site-year and 2.1
kg/site-year, respectively). EPA then divided the annual release estimate by the estimated number of
release days as discussed in Section 3.1.1.5, which is 350 days/year for the Manufacturing OES. The
50th and 95th percentile daily land releases for the Manufacturing OES are 3.9x 10 3 kg/day and
6,Ox 10 3 kg/day, respectively.
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2064 Table 3-6. Summary of EPA's Annual and Daily Release Estimates for Each PES
OES
Estimated Annual Release
(kg/site-year)
Type of Discharge,6 Air
Emission^ or Transfer for
Disposal
Estimated Daily Release
(kg/sitc-day)'
Number of
Facilities^
Source(s)
Central
Tendency
High-End17
Central
Tendency
High-End
Manufacturing
1.6
1,299
Surface water
4.7E-03
3.7
3
TRI/DMR
8.4
2,184
Fugitive air
2.4E-02
6.2
8
TRI
34
74
Fugitive air
9.5E-02
0.20
4
NEI
45
499
Stack air
0.13
1.4
9
TRI
33
Stack air
9.1E-02
1
NEI
1.4
2.1
Land
3.9E-03
6.0E-03
1
TRI
Processing as a
reactive intermediate
3.8E-03
7.5E-02
Surface water
1.1E-05
2.1E-04
60
TRI/DMR
2.3
155
Fugitive air
1.0E-02
0.44
5
TRI
4.1
327
Fugitive air
1.2E-02
0.93
16
NEI
14
610
Stack air
4.0E-02
1.7
4
TRI
3.8
526
Stack air
1.1E-02
1.5
23
NEI
0.45
Land
1.3E-02
1
TRI
Processing -
repackaging
1.7E-02
0.40
Surface Water
5.0E-05
1.1E-03
3
DMR
11
19
Fugitive or stack air
0.24
0.46
2 generic
sites
Environmental
release modeling
275
320
Hazardous landfill or incineration
6.0
9.4
Commercial use as a
laboratory chemical
1.1E-03
9.4E-03
Surface water
4.3E-06
3.7E-05
2
DMR
3.4
6.2
Fugitive air
9.5E-03
1.7E-02
2
NEI
2.0E-03
2.0E-03
Stack air
7.9E-06
7.9E-06
2
NEI
17
32
Fugitive or stack air
7.2E-02
0.14
43-138
generic sites
Environmental
release modeling
504
882
Hazardous landfill or incineration
2.2
3.7
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OES
Estimated Annual Release
(kg/site-year)
Type of Discharge,6 Air
Emission/ or Transfer for
Disposal"
Estimated Daily Release
(kg/site-day)''
Number of
Facilities^
Source(s)
Central
Tendency
High-End11
Central
Tendency
High-End
General waste
handling, treatment,
and disposal
9.3E-04
6.0E-03
Surface water
3.7E-06
2.4E-05
22
TRI/DMR
0.63
7.3
Fugitive air
2.5E-03
2.9E-02
7
TRI
34
202
Fugitive air
0.14
0.81
575
NEI
1.8E-02
0.82
Stack air
7.3E-05
3.3E-03
8
TRI
2.5
134
Stack air
1.0E-02
0.54
153
NEI
Waste handling,
treatment, and
disposal (POTW)
5.1E-03
8.9E-02
Surface water
1.4E-05
2.4E-04
126
DMR
Waste handling,
treatment, and
disposal
(remediation)
2.9E-04
8.5E-03
Surface water
8.0E-07
2.3E-05
42
DMR
Distribution in
commerce
N/Ae
" "High-end" are defined as 95th percentile releases
h Direct discharge to surface water; indirect discharge to non-POTW; indirect discharge to POTW
"Emissions via fugitive air; stack air; or treatment via incineration
d Transfer to surface impoundment, land application, or landfills
e Where available, EPA used peer-reviewed literature (e.g., GSs or ESDs to provide a basis to estimate the number of release days of 1,1-dichloroethane within a COU).
' EPA reviewed NRC data and DOT data for the 2015-2020 calendar vears for incident reoorts Dcrtainina to distribution of 1.1 -dichloroethane (NRC. 2009) (DOT
Hazmat Incident Report Data). EPA did not identify reported releases for 1,1-dichloroethane during distribution of the chemical.
2065
2066
2067
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3.2.2 Weight of Scientific Evidence Conclusions for the Estimates of Environmental
Releases from Industrial and Commercial Sources
EPA develops a conclusion on the weight of scientific evidence supporting the environmental release
estimates based on the strengths, limitations, and uncertainties associated with the environmental release
estimates. The conclusion is summarized using confidence descriptors: robust, moderate, slight, or
indeterminate. EPA considers factors that increase or decrease the strength of the evidence supporting
the release estimate—including quality of the data/information, applicability of the release data to the
COU (including considerations of temporal relevance, locational relevance) and the representativeness
of the estimate for the whole industry.
EPA uses descriptors of robust, moderate, slight, or indeterminant, according to EPA's Draft
Application of Systematic Review in TSCA Risk Evaluations (U.S. EPA. 2021b). For example, a
conclusion of moderate weight of scientific evidence is appropriate where there is measured release data
from a limited number of sources such that there is a limited number of data points that may not cover
most or all of the sites within the COU. A conclusion of slight weight of scientific evidence is
appropriate where there is limited information that does not sufficiently cover all sites within the COU,
and the assumptions and uncertainties are not fully known or documented. See Application of Systematic
Review in TSCA Risk Evaluations (U.S. EPA. 2021b) for additional information on weight of scientific
evidence conclusions.
TRI and DMR databases had data quality ratings of medium, and NEI had a high data quality rating.
However, the Variability and Uncertainty data quality metric was determined to be low for all three
databases. Modeled data had data quality ratings of medium. For releases that used GS/ESDs, the weight
of scientific conclusion was moderate when used in tandem with Monte Carlo modeling (Processing -
repackaging, commercial use as a laboratory chemicals). Table 3-7 summarizes EPA's overall weight of
scientific evidence conclusions for its release estimates for each of the assessed OES.
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2094 Table 3-7. Summary of Weight of Scientific Evidence Ratings for Environmental Release Estimates by PES
OES
Weight of Scientific
Evidence Conclusion
Weight of Scientific Evidence Conclusion
Manufacturing
Moderate to Robust
Water releases are assessed using reported releases from 2015-2020 TRI and DMR. The primary strength of
TRI data is that TRI compiles the best readily available release data for all reporting facilities. The primary
limitation is that the water release assessment is based on three reporting sites, and EPA did not have
additional sources to estimate water releases from this OES. Based on other reporting databases (CDR, NEI,
etc.), there are seven additional manufacturing sites that are not accounted for in this assessment.
Air releases are assessed using reported releases from 2015-2020 TRI, and 2014 and 2017 NEI. A strength of
NEI data is that NEI captures additional sources that are not included in TRI due to reporting thresholds.
Factors that decrease the overall confidence for this OES include the uncertainty in the accuracy of reported
releases, and the limitations in representativeness to all sites because TRI and NEI may not capture all
relevant sites. Additionally, EPA made assumptions on the number of operating days to estimate daily
releases.
Land releases are assessed using reported releases from 2015-2020 TRI. The primary limitation is that the
land releases assessment is based on one reporting site, and EPA did not have additional sources to estimate
land releases from this OES. Based on other reporting databases (CDR, DMR, NEI, etc.), nine additional
manufacturing sites are not accounted for in this assessment.
Based on this information, EPA has concluded that the weight of scientific evidence for this assessment is
moderate to robust and provides a plausible estimate of releases in consideration of the strengths and
limitations of reasonably available data.
Processing as a
reactive intermediate
Moderate to Robust
Water releases are assessed using reported releases from 2015-2020 TRI and DMR, which both have a
medium overall data quality determination from the systematic review process. The primary strength of TRI
data is that TRI compiles the best readily available release data for all reporting facilities. The water release
assessment is based on 60 reporting sites. Based on other reporting databases (CDR, NEI, etc.), 30 additional
sites are not accounted for in this assessment.
Air releases are assessed using reported releases from 2015-2020 TRI, and 2014 and 2017 NEI. A strength of
NEI data is that NEI captures additional sources that are not included in TRI due to reporting thresholds.
Factors that decrease the overall confidence for this OES include the uncertainty in the accuracy of reported
releases, and the limitations in representativeness to all sites because TRI and NEI may not capture all
relevant sites.
Land releases are assessed using reported releases from 2015-2020 TRI. The primary limitation is that the
land release assessment is based on one reporting site, and EPA did not have additional sources to estimate
land releases from this OES. Based on other reporting databases (CDR, DMR, NEI, etc.), 89 additional sites
are not accounted for in this assessment.
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OES
Weight of Scientific
Evidence Conclusion
Weight of Scientific Evidence Conclusion
Based on this information, EPA has concluded that the weight of scientific evidence for this assessment is
moderate to robust and provides a plausible estimate of releases in consideration of the strengths and
limitations of reasonably available data.
Processing -
repackaging
Moderate to Robust
All facility release data were below the limit of detection, therefore, EPA assessed releases to the using the
assumptions and values from the Julv 2022 Chemical Repackaging GS (U.S. EPA. 2023c). which the
systematic review process rated medium for data quality. EPA used EPA/OPPT models combined with
Monte Carlo modeling to estimate releases to the environment, with media of release assessed using
assumptions from the ESD and EPA/OPPT models. EPA believes a strength of the Monte Carlo modeling
approach is that variation in model input values and a range of potential releases values is more likely than a
discrete value to capture actual releases at sites. EPA lacks 1,1-dichloroethane facility production volume
data and number of importing/repackaging sites; therefore, throughput estimates are based on CDR reporting
thresholds with an overall release using a hypothetical scenario of two facilities.
Based on this information, EPA has concluded that the weight of scientific evidence for this assessment is
moderate to robust and provides a plausible estimate of releases in consideration of the strengths and
limitations of reasonably available data.
Commercial use as a
laboratory chemical
Moderate
EPA identified four facilities reporting water and air releases of 1,1-dichloroethane, However, EPA
determined this data is not sufficient to capture the entirety of environmental releases for this scenario.
Therefore, releases to the environment are assessed using the Draft GS on the Use of Laboratory Chemicals,
which has a high data quality ratine from the systematic review process (U.S. EPA. 2023c). EPA used
EPA/OPPT models combined with Monte Carlo modeling to estimate releases to the environment, with
media of release assessed using assumptions from the ESD and EPA/OPPT models. EPA assumed that the
media of release for disposal of laboratory waste is to hazardous waste landfill or incineration. EPA believes
a strength of the Monte Carlo modeling approach is that variation in model input values and a range of
potential releases values is more likely than a discrete value to capture actual releases at sites. EPA believes
the primary limitation to be the uncertainty in the representativeness of values toward the true distribution of
potential releases. In addition, EPA lacks 1,1-dichloroethane laboratory chemical throughput data and
number of laboratories; therefore, number of laboratories and throughput estimates are based on stock
solution throughputs from the Draft GS on the Use of Laboratory Chemicals and on CDR reporting
thresholds.
Based on this information, EPA has concluded that the weight of scientific evidence for this assessment is
moderate and provides a plausible estimate of releases in consideration of the strengths and limitations of
reasonably available data.
General waste
handling, treatment,
and disposal
Moderate to Robust
Water releases for non-POTW sites are assessed using reported releases from 2015-2020 TRI and DMR. The
primary strength of TRI data is that TRI compiles the best readily available release data for all reporting
facilities. For non-POTW sites, the primary limitation is that the water release assessment is based on 22
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OES
Weight of Scientific
Evidence Conclusion
Weight of Scientific Evidence Conclusion
reporting sites, and EPA did not have additional sources to estimate water releases from this OES. Based on
other reporting databases such as NEI, there are additional sites that are not accounted for in this assessment.
Air releases for non-POTW sites are assessed using reported releases from 2015-2020 TRI, and 2014 and
2017 NEI. A strength of NEI data is that NEI captures additional sources that are not included in TRI due to
reporting thresholds. Factors that decrease the confidence for this OES include the uncertainty in the accuracy
of reported releases, and the limitations in representativeness to all sites because TRI and NEI may not
capture all relevant sites. The air release assessment is based on 650 reporting sites. Based on other reporting
databases (CDR and DMR), there are 22 additional non-POTW sites that are not accounted for in this
assessment. Additionally, EPA made assumptions on the number of operating days to estimate daily releases.
EPA found that major sources of air emissions of 1,1-dichloroethane in landfills come from sources other
than 1,1-dichloroethane COUs of Manufacture, processing, and commercial use; specifically, the
decomposition of 1,1,1-trichloroethane. However, it is unclear how much 1,1,1-trichloroethane is disposed to
landfills and how much 1,1-dichloroethane is generated.
Based on this information, EPA has concluded that the weight of scientific evidence for this assessment is
moderate to robust and provides a plausible estimate of releases in consideration of the strengths and
limitations of reasonably available data.
Waste handling,
treatment, and
disposal (POTW)
Moderate to Robust
Water releases for POTW sites are assessed using reported releases from 2015-2020 DMR. A strength of
using DMR data and the Pollutant Loading Tool is that the tool calculates an annual pollutant load by
integrating monitoring period release reports provided to the EPA and extrapolating over the course of the
year. However, this approach assumes average quantities, concentrations, and hydrologic flows for a given
period are representative of other times of the year. The release assessment is based on 126 reporting sites.
Based on other reporting databases (CDR, TRI, etc.), all sites are accounted for in this assessment.
Based on this information, EPA has concluded that the weight of scientific evidence for this assessment is
moderate to robust and provides a plausible estimate of releases in consideration of the strengths and
limitations of reasonably available data.
Waste handling,
treatment, and
disposal
(remediation)
Moderate to Robust
Water releases for remediation sites are assessed using reported releases from 2015-2020 DMR. A strength
of using DMR data and the Pollutant Loading Tool is that the tool calculates an annual pollutant load by
integrating monitoring period release reports provided to the EPA and extrapolating over the course of the
year. However, this approach assumes average quantities, concentrations, and hydrologic flows for a given
period are representative of other times of the year. The release assessment is based on 42 reporting sites.
Based on other reporting databases (CDR, TRI, etc.), all sites are accounted for in this assessment.
Based on this information, EPA has concluded that the weight of scientific evidence for this assessment is
moderate to robust and provides a plausible estimate of releases in consideration of the strengths and
limitations of reasonably available data.
2095
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3.3 Concentrations of 1,1-Dichloroethane in the Environment
1,1-Dichloroethane - Concentrations in the Environment (Section 3.3):
Key Points
EPA evaluated the reasonably available information on concentrations of 1,1-dichloroethane in the
environment, including air, water, and land (soil, biosolids, and groundwater). The key points on
environmental concentrations are summarized in the bullets below:
• For the air pathway, measured data from a variety of locations within and outside of the
United States as well as data obtained from the EPA's ambient air monitoring databases
provided 1,1-dichloroethane concentrations near facilities and locations represent general
population exposure.
o EPA also modeled ambient air concentrations and air deposition from facilities
releasing 1,1-dichloroethane to air. The Agency expects infiltration of ambient air
concentrations of 1,1-dichloroethane may be an important source of 1,1-
dichloroethane to the indoor environment.
• For the water pathway, measured data from a variety of locations (surfaces waters and
groundwaters) within and outside of the United States provided 1,1-dichloroethane
concentrations to understand general occurrence. However, these locations are not typically in
receiving water bodies associated with the facility releases investigated or were not measured
at relevant timeframes. Thus, it remains difficult to use monitoring data to assess general
population exposure and compare with EPA modeled results.
o EPA modeled aqueous concentrations in surface waters and groundwater from
facilities releasing 1,1-dichloroethane directly to a receiving surface water body or
from the disposal to landfill in the case of groundwater.
o The Agency expects that facility releases to surface waters and disposal to landfills
results in concentrations of 1,1-dichloroethane that present an exposure to the general
population, however, these aqueous concentrations are expected to be low even for the
conservative scenarios that were modeled.
The environmental exposure characterization focuses on releases of 1,1-dichloroethane from facilities
that use, manufacture, or process 1,1-dichloroethane under industrial and/or commercial COUs subject
to TSCA regulations as described in Section 3.2.1. To characterize environmental exposure, EPA
assessed point estimate exposures derived from both measured and modeled concentrations of 1,1-
dichloroethane in ambient air, surface water, and groundwater resulting from landfills in the United
States. Measured concentrations of 1,1-dichloroethane in groundwater are presented from monitoring
data and predicted concentrations in soil are noted as a possible source of environmental exposures.
A literature search was also conducted to identify peer-reviewed or gray sources of 1,1-dichloroethane
measured and reported modeled data. The tornado plots and associated tables in Appendix D.3 and in
the Draft RiskEvaluation for 1,1-Dichloroethane - Systematic Review Protocol (U.S. EPA. 2024t) are a
summary of the measured and reported modeled data for the various environmental media. The plots
provide the range of media concentrations in monitoring various studies. The plots show U.S. and non-
U.S. data, fraction (e.g., vapor, gas, particle) and the studies are ordered from top to bottom from newer
to older data. The plots are colored to indicate general population, remote, near facility, and unknown
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population information. An example of a tornedo plot and additional details on the location type such as
near facility, general population, are provided in Appendix D.3.1.
3.3.1 Ambient Air Pathway
EPA searched peer-reviewed literature, gray literature, and databases to obtain concentrations of 1,1-
dichloroethane in ambient air. Section 3.3.1.1 shows the aggregated results of reported measured
concentrations for ambient air found in the peer-reviewed and gray literature from the systematic review
and from the EPA Ambient Monitoring Technology Information Center (AMTIC). Section 3.3.1.2
reports EPA modeled ambient air concentrations and air deposition 1,1-dichloroethane from facility
releases.
3.3.1.1 Measured Concentrations in Ambient Air
Ambient air concentrations of 1,1-dichloroethane were measured in one study in the United States
(Figure 3-5). Logue et al. (2010) reported concentrations of 1,1-dichloroethane in ambient air from non-
detect to 4.Ox 10~2 |ig/m3 at four locations across Pittsburgh, Pennsylvania (two residential areas near
chemical and industrial facilities, one downtown residential area with high traffic, and one residential
area with distant industrial facilities), from 2006 to 2008.
US Vapor/Gas
1255270 - Logue el al., 2010 - US
^¦1 General Population
¦m Near Facility
A Normal Distribution (CT and 90th percentile)
H Non-Dctect
Al
1255270 - Logue et al., 2010 - US
1
NonUS Vapor/Gas
5431563 - Huang et al., 2019 - CN
4
A
2517712 - Marti'et al., 2014 - ES
4 A
2443817 - Ras-Mallorqui et al.. 2007 - ES
*
IOA-4
0.001
0.01 0.1
Concentration (ug/m3)
i
Figure 3-5. Concentrations of 1,1-Dichloroethane (^g/m3) in the Vapor/Gas Fraction of Ambient
Air from U.S.-Based and International Studies, 2005-2017
Additional ambient air concentrations of 1,1-dichloroethane were obtained from the EPA's AMTIC. The
AMTIC archive houses data from 2,800 ambient air monitoring sites across the United States from 1990
to 2020, with 90 percent of the data from the years 2000 to 2020, resulting from the air toxics program.
The air toxics program includes the National Air Toxics Trends Sites (NATTS) Network, Community-
Scale Air Toxics Ambient Monitoring (CSATAM) and Urban Air Toxics Monitoring Program
(UATMP) that monitor for hazardous air pollutants (HAPs), including 1,1-dichloroethane. This data is
reported from federal, state, local, and tribal monitoring networks. AMTIC HAPs monitoring data is
summarized in Table 3-8 for the years 2015 to 2020. These years were selected to be consistent with the
TRI and NEI data used in the modeled ambient air concentrations (Section 3.3.1.2). As shown in Table
3-8, measured concentrations from the AMTIC archive ranged from non-detect to 26 |ig/m3. Since most
of the TRI reporting facilities are either in Texas (seven of 23) or in Louisiana (nine of 23), EPA focused
on AMTIC data in these states. Approximately 25 percent of the monitoring data was reported by the
State of Texas where nearly 99 percent of the samples were considered non-detects. The State of
Louisiana reported approximately eight percent of the monitoring data and about 95 percent of the data
reported were considered non-detects.
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For more information on 1,1-dichloroethane in ambient air monitoring data, see the Draft Risk
Evaluation for 1,1-Dichloroethane - Supplemental Information File: Ambient Monitoring Technology
Information Center (AMTIC), 1,1-Dichloroethane Monitoring Data 2015 to 2020 (U.S. EPA. 2024b).
Table 3-8. Summary of Selected Statistics of 1,1-Dichloroethane Ambient Air Concentrations
Eig/m3) from EPA Ambient Monitoring Technology Information Center
Chemical
Statistics"
Year
2015
2016
2017
2018
2019
2020
1,1 -dichloroethane
Number of
Samples
12,332
11,954
11,849
11,495
10,234
9,581
Percent ND
96.6
93.8
97.4
98.3
98.7
98.0
Minimum6
ND
ND
ND
ND
ND
ND
Mean
8.0E-02
8.5E-02
8.6E-02
0.11
0.12
0.13
Max
7.6
2.0
26
1.2
8.9
6.1
" Approximately 97 percent of the samples were non-detects. For samples with a reported minimum detection limit (MDL), EPA
considered any sample with a concentration below the MDL to be a non-detect. Additionally, for samples with no reported
MDL, EPA considered any sample with a concentration less than or equal to zero to be a non-detect. For calculation of summary
statistics, EPA did not include data points where no concentration was reported. EPA also did not include data points in the
summary statistics where no MDL was reported, and the concentration was less than or equal to zero. For data points where the
concentration was less than the reported MDL, a concentration of half the MDL was used for calculating the mean.
h According to AMTIC's technical euide. NDs are to be reported in AOS as zeroes. Therefore. EPA is unable to distinguish
between ND and zero measured values.
ND - Non-detect.
3.3.1.2 EPA Modeled Concentrations in Ambient Air and Air Deposition
(IIOAC/AERMOD)
EPA developed and applied tiered methodologies and analyses to estimate ambient air concentrations
and air deposition of 1,1-dichloroethane from facility releases. These methodologies and analyses focus
on inhalation exposures to a sub-set of the general population residing nearby facilities reporting 1,1-
dichloroethane releases to TRI and NEI. For purposes of these analyses, EPA focused on a subset of the
general population residing within 10,000 m of a releasing facility. EPA considered multiple years of
data and multiple data sets (TRI and NEI) for this analysis. The methodology and analyses were first
presented in the Draft TSCA Screening Level Approach for Assessing Ambient Air and Water Exposures
to Fenceline Communities referred to here as the "2022 Fenceline Report."11 The specific methodologies
used in this assessment to evaluate general population exposures to 1,1-dichloroethane in air are briefly
described in Figure 3-6 and below. Additional details on the methodologies and the full set of inputs are
provided in Appendix D.3 and in the Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental
Information File: AERMOD Input Specifications (U.S. EPA. 2024a).
11 See 2022 Fenceline Report.
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Figure 3-6. Brief Description of Methodologies and Analyses Used to Estimate Air Concentrations
and Exposures
1,1-dichloroethane ambient air concentrations were modeled using facility releases reported in TRI and
NEI or alternative release estimates where facility specific data were not available. EPA performed a full
analysis using the American Meteorological Society/Environmental Protection Agency Regulatory
Model (AERMOD)12 and EOA's Integrated Indoor/Outdoor Air Calculator (IIOAC).13 EPA used the air
release estimates obtained using the methodology described in Section 3.1 as direct inputs for the
models to estimate exposure concentrations at various distances from a releasing facility. EPA expanded
upon the methods described in the 2022 Fenceline Report by evaluating air deposition and potential
aggregate concentrations from multiple TRI and NEI reporting facilities.
Specifically, to estimate ambient air concentrations of 1,1-dichloroethane from facility releases EPA
used the Ambient Air: Multi-Year Analysis Methodology IIOAC. This analysis relies upon TRI data and
basic model inputs (IIOAC) and evaluates ambient and indoor air concentrations and associated
exposures/risks at three pre-defined distances from a releasing facility to inform whether additional,
more specific, higher-tier analysis may be warranted. For 1,1-dichloroethane, the results of the Ambient
12 See https://www.epa.gOv/scram/air-aualitv-dispersion-modeling-preferred-and-recommended-models#aemiod for more
information.
13 See IIOAC website for more information.
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Air: Multi-Year Methodology IIOAC identified risk estimates above typical Agency benchmarks for
cancer at all distances modeled and for multiple releases (high-end and central tendency). Due to results
of the Ambient Air: Multi-Year Methodology IIOAC EPA conducted a higher-tier analysis (Ambient
Air: Multi-Year Analysis Methodology AERMOD TRI) of all facilities reporting releases of 1,1-
dichloroethane to TRI and NEI.
The Ambient Air: Multi-Year Analysis Methodology AERMOD TRI relies upon TRI data as the
previous tier analysis but uses a higher tier model (AERMOD) and evaluates ambient air concentrations
and associated exposures/risks at eight finite distances and two area distances from each releasing
facility. This tier also evaluates total (wet and dry) deposition concentrations to land and water at each
distance/area distance modeled. For 1,1-dichloroethane, the results of the Ambient Air: Multi-Year
Analysis Methodology AERMOD TRI identified risk estimates above typical Agency benchmarks for
cancer for multiple releases (high-end and central tendency).
The final tier EPA used in this assessment is the Ambient Air: Multi-Year Analysis Methodology
AERMOD NEI. Compared to the previous two tiers of analyses that are facility and scenario specific,
this analysis is process level, site and scenario specific. It includes source specific parameter values used
in modeling like stack parameters (stack height, stack temperature, plume velocity, etc.), and releases of
facilities that may not report to TRI.
3.3.1.2.1 Ambient Air: Multi-Year Methodology IIOAC
The Ambient Air: Multi-Year Methodology IIOAC utilizes EPA's IIOAC model to estimate high-end
(95th percentile) and central tendency (mean) 1,1-dichloroethane exposure concentrations in ambient air
and indoor air at three distances from an emitting facility: 100, 100 to 1,000, and 1,000 m. EPA
considered 6 years of TRI release data (2015 through 2020) for this analysis. The TRI data were used as
direct inputs to the IIOAC. EPA modeled releases reported to TRI considering source attribution
(fugitive and stack releases) for each facility and each year of reported releases. Facilities were
categorized into OESs and later cross-walked to COUs. Indoor air concentrations were calculated by
multiplying the outdoor air concentration by the indoor-outdoor ratio of 0.65 and 1 for the mean and
high-end exposure concentrations, respectively.
The Ambient Air: Multi-Year Methodology IIOAC includes both estimates of exposures as well as
estimates of risks to inform the need, or potential need, for further analysis. For 1,1-dichloroethane, the
results of the Ambient Air: Multi-Year Methodology IIOAC identified risk estimates above typical
Agency benchmarks for cancer at all distances modeled and for multiple releases (high-end and central
tendency). Due to results of the Ambient Air: Multi-Year Methodology IIOAC and the inability to
model gaseous deposition, EPA conducted a higher-tier analysis (AERMOD) of all facilities reporting
releases of 1,1-dichloroethane to TRI and NEI.
The full set of inputs and results of IIOAC are provided in the Draft RiskEvaluation for 1,1-
Dichloroethane - Supplemental Information File: Supplemental Information on IIOAC TRI Exposure
and Risk Analysis (U.S. EPA. 2024p).
3.3.1.2.2 Ambient Air: Multi-Year Methodology AERMOD TRI
The Ambient Air: Multi-Year Methodology AERMOD TRI utilizes AERMOD to estimate 1,1-
dichloroethane concentrations in ambient air and air deposition concentrations to land and water, at eight
finite distances (10, 30, 60, 100, 1,000, 2,500, 5,000, and 10,000 m) and two area distances (30 to 60 m
and 100 to 1,000 m) from an emitting facility (Appendix E. 1.2.3). EPA modeled two different types of
release estimates for 1,1-dichloroethane: (1) facility-specific chemical releases with source attribution
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when TRI data was available, and (2) alternative release estimates representing a generic facility when
TRI data was not available for an OES. When TRI data was available, EPA considered 6 years of release
data (2015 through 2020), and modeled releases reported to TRI considering source attribution (fugitive
and stack releases) for each facility and each year of reported releases as well as an arithmetic average
release for each facility across all reported releases across all years. Not all facilities reported releases
for all six years. Facilities were categorized into OESs and later cross-walked to COUs. Daily and period
average outputs were obtained via modeling, and post-processing scripts were used to extract a variety
of statistics from the modeled concentration distribution, including the 95th (high-end), 50th (central
tendency), and 10th (low-end) percentile 1,1-dichloroethane concentrations at each distance modeled.
A summary of the air concentration ranges estimated using the Ambient Air: Multi-Year Methodology
AERMOD TRI is provided in Table 3-9. The summary includes three OESs and select statistics
(maximum, mean, median, and minimum) calculated from the modeled concentration distributions
within each OES at each distance modeled. The associated range of estimated concentrations is based on
the maximum 95th percentile annual average exposure concentrations for each distance. For the
maximum 95th percentile, range of modeled concentrations varied by as much as four orders of
magnitude between minimum and maximum concentrations across all modeled distances for the
Manufacturing OES, three orders of magnitude for the Processing as a reactive intermediate OES, and
12 orders of magnitude for the General waste handling, treatment, and disposal OES. This occurs
because within each OES there are multiple facilities with varying releases. These varying releases, in
turn, affect the range of estimated exposure concentrations at a given distance. AERMOD modeled
concentrations for the 95th percentile ranged from 0 to 232 |ig/m3 across all modeled distances, with the
maximum modeled concentration being approximately one order of magnitude higher than the
maximum monitored concentration of 26 |ig/m3 from AMTIC (Table 3-8) and approximately four orders
of magnitude higher than the maximum concentration of 4.Ox 10~2 |ig/m3 measured in (Logue et al..
2010).
A summary of the air deposition rate ranges estimated using the Ambient Air: Multi-Year Methodology
AERMOD TRI is provided in Table 3-10 and Table 3-11. The summary includes three OESs and select
statistics (maximum, mean, median, and minimum) calculated from the TRI modeled deposition rates
distributions within each OES at each distance modeled. The associated range of estimated deposition
rates is based on the maximum 95th percentile daily (Table 3-10) and annual (Table 3-11) deposition
rates for each distance.
Table 3-12 provides a summary of the air concentrations estimated using the Ambient Air: Multi-Year
Methodology AERMOD TRI for the Commercial use as a laboratory chemical and Processing -
repackaging OESs where there was no site-specific data available for modeling. The associated range of
estimated concentrations is based on the maximum 95th percentile annual average exposure
concentrations. The ambient air modeled concentrations values are presented for high-end modeled
releases, high-end meteorology (Lake Charles, Louisiana), and both rural and urban settings. The high-
end meteorological station used represents meteorological datasets that tended to provide high-end
concentration estimates relative to the other stations within IIOAC (see Appendix E. 1.2.4). The modeled
results indicate a maximum ambient air concentration of 0.9 |ig/m3 at 10 m from the facility for the
Processing - repackaging OES, 22,680 kg/year production volume, and 95th percentile release estimate
scenario for both rural and urban land category scenarios. For the Commercial use as a laboratory
chemical OES, results indicate a maximum ambient air concentration of 1.5 |ig/m3 at 10 m from the
facility, 22,680 kg/year production volume, and 95th percentile release estimate scenario for both rural
and urban land category scenarios.
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2285 The full inputs and results are presented in the Draft Risk Evaluation for 1,1-Dichloroethane —
2286 Supplemental Information File: Supplemental Information on AERMOD TRI Exposure and Risk
2287 Analysis (U.S. EPA. 2024n) and in the Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental
2288 Information File: Supplemental Information on AERMOD Generic Releases Exposure and Risk Analysis
2289 (U.S. EPA. 20241V
2290
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2291 Table 3-9. Summary of Select Statistics for the 95th Percentile Annual Average Concentrations for 1,1-Dichloroethane Releases
2292 Reported to TRI
OES
# Facilities
Evaluated
in OES
Statistics
95th Percentile Annual Average Concentration (jug/m3) Estimated within 10 to 10,000 m of Releasing Facilities
10 m
30 m
30 to 60 m
60 m
100 m
100 to 1,000 m
1,000 m
2,500 m
5,000 m
10,000 m
Manufacturing
9
Max
2.3E02
9.0E01
6.9E01
3.7E01
1.8E01
2.5
4.1E-01
9.3E-02
3.0E-02
1.0E-02
Mean
2.0E01
8.7
6.1
3.6
1.7
2.4E-01
4.3E-02
1.0E-02
3.5E-03
1.2E-03
Median
6.1E-01
2.9E-01
1.8E-01
1.3E-01
6.2E-02
1.2E-02
3.3E-03
1.3E-03
5.7E-04
2.1E-04
Min
4.0E-02
1.7E-02
1.1E-02
6.5E-03
3.0E-03
3.6E-04
6.4E-05
1.4E-05
4.6E-06
1.5E-06
Processing as a
reactive
intermediate
6
Max
1.5E01
6.4
4.3
2.5
1.2
1.6E-01
2.7E-02
1.3E-02
6.8E-03
2.9E-03
Mean
3.2
1.4
9.7E-01
5.8E-01
3.0E-01
4.9E-02
1.3E-02
5.1E-03
2.3E-03
9.2E-04
Median
2.2E-02
1.0E-02
3.8E-02
5.4E-02
1. IE—01
5.5E-02
1.7E-02
4.5E-03
1.5E-03
4.9E-04
Min
0
0
0
0
0
0
0
0
0
0
General waste
handling,
treatment, and
disposal
8
Max
1.9E01
9.3
6.1
3.9
1.9
1.4E-01
4.8E-02
1.1E-02
3.4E-03
1.1E-03
Mean
8.4E-01
4.0E-01
2.6E-01
1.7E-01
8.2E-02
6.3E-03
2.0E-03
4.4E-04
1.5E-04
4.8E-05
Median
4.1E-02
1.6E-02
1.1E-02
5.7E-03
2.4E-03
3.0E-04
4.9E-05
1.3E-05
4.5E-06
1.5E-06
Min
7.6E-11
6.5E-08
3.6E-07
5.4E-07
9.4E-07
3.1E-07
1.1E-07
4.4E-08
2.4E-08
1.1E-08
2293
2294
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2295
2296
Table 3-10. Summary of Select Statistics for the 95th Percentile Daily Average Air Deposition Rates for 1,1-Dichloroethane Releases
OES
# Facilities
Evaluated
in OES
Statistic
95th Percentile Daily Average Air Deposition Rate (g/m2/day) Estimated within 10 to 10,000 m of Releasing
Facilities
10 m
30 m
30 to 60 m
60 m
100 m
100 to 1,000 m
1,000 m
2,500 m
5,000 m
10,000 m
Manufacturing
9
Max
4.0E-02
3.9E-02
2.2E-02
1.3E-02
5.4E-03
1.8E-04
5.8E-05
1.0E-05
2.9E-06
8.9E-07
Mean
3.3E-03
3.1E-03
1.7E-03
1.1E-03
4.1E-04
1.5E-05
4.6E-06
7.9E-07
2.4E-07
7.7E-08
Median
2.8E-05
2.9E-05
1.7E-05
1.3E-05
1.3E-05
1.7E-06
6.1E-07
7.7E-08
2.1E-08
8.0E-09
Min
1.5E-08
1.3E-08
6.9E-09
4.3E-09
1.7E-09
5.3E-11
1.8E-11
3.4E-12
1. IE—12
3.6E-13
Processing as
a reactive
intermediate
6
Max
8.9E-04
7.9E-04
4.6E-04
2.8E-04
1.2E-04
2.3E-05
9.3E-06
1.6E-06
4.2E-07
1.2E-07
Mean
2.0E-04
2.0E-04
1.2E-04
8.0E-05
5.4E-05
5.9E-06
2.1E-06
3.8E-07
1.1E-07
3.5E-08
Median
9.4E-06
1.3E-05
1.4E-05
3.0E-05
7.5E-05
2.7E-06
8.7E-07
1.4E-07
4.1E-08
1.4E-08
Min
0
0
0
0
0
0
0
0
0
0
General waste
handling,
treatment, and
disposal
8
Max
2.1E-05
2.7E-05
1.6E-05
1.1E-05
4.2E-06
1.3E-07
4.8E-08
7.8E-09
2.4E-09
8.8E-10
Mean
2.9E-06
3.1E-06
1.9E-06
1.2E-06
4.8E-07
1.7E-08
6.2E-09
1.1E-09
3.3E-10
1. IE—10
Median
8.0E-08
4.7E-08
2.3E-08
1.8E-08
2.2E-08
5.2E-10
1.6E-10
3.2E-11
1.0E-11
3.6E-12
Min
2.9E-14
4.7E-12
5.6E-11
1.3E-10
2.2E-10
1.6E-11
4.0E-12
6.5E-13
2.3E-13
8.3E-14
2297
2298
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2299 Table 3-11. Summary of Select Statistics for the 95th Percentile Annual Average Air Deposition Rates for 1,1-Dichloroethane
2300 Releases Reported to TRI
OES
# Facilities
Evaluated
in OES
Statistic
95th Percentile Annual Average Air Deposition Rates (g/m2/year) Estimated within 10 to 10,000 m of Releasing
Facilities
10 m
30 m
30 to 60 m
60 m
100 m
100 to 1,000 m
1,000 m
2,500 m
5,000 m
10,000 m
Manufacturing
9
Max
2.2E01
2.2E01
1.5E01
7.9
3.1
2.2E-01
3.8E-02
7.4E-03
2.3E-03
7.4E-04
Mean
8.5E-01
8.6E-01
6.0E-01
3.1E-01
1.2E-01
9.4E-03
1.7E-03
3.3E-04
1.0E-04
3.3E-05
Median
7.0E-03
6.9E-03
4.9E-03
3.0E-03
2.5E-03
5.3E-04
1.5E-04
3.8E-05
1.3E-05
4.3E-06
Min
1.5E-06
1.3E-06
9.0E-07
4.5E-07
1.8E-07
2.0E-08
3.2E-09
7.4E-10
2.7E-10
1. IE—10
Processing as
a reactive
intermediate
6
Max
4.0E-01
4.5E-01
3.3E-01
2.0E-01
2.2E-01
4.3E-02
1.7E-02
3.5E-03
1.1E-03
3.3E-04
Mean
4.4E-02
5.5E-02
4.2E-02
2.9E-02
2.6E-02
4.3E-03
1.4E-03
3.0E-04
9.0E-05
2.8E-05
Median
2.3E-03
3.3E-03
9.4E-03
1.4E-02
1.8E-02
1.4E-03
3.0E-04
5.7E-05
1.9E-05
5.9E-06
Min
0
0
0
0
0
0
0
0
0
0
General waste
handling,
treatment, and
disposal
8
Max
5.1E-03
7.8E-03
5.6E-03
3.2E-03
1.3E-03
1.1E-04
1.7E-05
3.3E-06
9.9E-07
3.2E-07
Mean
6.1E-04
7.9E-04
5.5E-04
3.2E-04
1.4E-04
1.0E-05
2.0E-06
4.0E-07
1.2E-07
4.2E-08
Median
1.5E-05
1.5E-05
1.0E-05
6.7E-06
4.9E-06
4.6E-07
9.3E-08
2.4E-08
8.0E-09
2.6E-09
Min
5.9E-12
3.2E-09
3.4E-08
7.2E-08
1.2E-07
1.5E-08
3.6E-09
6.7E-10
2.4E-10
1.0E-10
2301
2302
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2303
2304
Table 3-12. Summary of Maximum 95th Percentile Annual Average Concentrations for 1,1-Dichloroethane for Commercial Use as a
OES
Meteorology"
Source
Land
95th Percentile Annual Average Concentration (jug/m3) Estimated within 10 to 10,000 m of Releasing
Facilities
10 m
30 m
30 to
60 m
60 m
100 m
100 to
1,000 m
1,000 m
2,500 m
5,000 m
10,000 m
Processing -
repackaging
High
Stack and
Fugitive
Urban
9.3E-01
2.6E-01
2.1E-01
1.5E-01
1.4E-01
3.8E-02
1.3E-02
3.8E-03
1.3E-03
4.7E-04
High
Stack and
Fugitive
Rural
9.3E-01
2.6E-01
2.0E-01
1.2E-01
1.0E-01
3.4E-02
1.5E-02
4.5E-03
1.9E-03
9.8E-04
Commercial
use as a
laboratory
chemical
High
Stack and
Fugitive
Urban
1.5
4.4E-01
3.9E-01
3.1E-01
3.5E-01
1.0E-01
3.4E-02
1.0E-02
3.7E-03
1.3E-03
High
Stack and
Fugitive
Rural
1.5
4.3E-01
3.5E-01
2.5E-01
2.4E-01
9.0E-02
4.0E-02
1.3E-02
5.1E-03
2.5E-03
" High refers to meteorological conditions from Lake Charles, Louisiana. Since the scenarios are not at real locations, they were modeled using a meteorological station that
represents meteorological datasets that tended to provide high-end concentration estimates relative to the other stations within IIOAC.
2305
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2306
2307
2308
2309
2310
2311
2312
2313
2314
2315
2316
2317
2318
2319
2320
2321
2322
2323
2324
2325
2326
2327
2328
2329
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3.3.1.2.3 Ambient Air: Multi-Year Methodology AERMOD NEI
The Ambient Air: Multi-Year Methodology AERMOD NEI utilizes AERMOD to estimate 1,1-
dichloroethane concentrations in ambient air and air deposition rates to land and water, at eight finite
distances (10, 30, 60, 100, 1,000, 2,500, 5,000, and 10,000 m) and two area distance from an emitting
facility. EPA considered the most recent 2 years of NEI release data (2014 and 2017) for this analysis.
The NEI data was used as direct inputs to the AERMOD. NEI releases were categorized into OESs and
later cross-walked to COUs. Daily and period average outputs were obtained via modeling, and post-
processing scripts were used to extract a variety of statistics from the modeled concentration
distribution, including the 95th (high-end), 50th (central tendency), and 10th (low-end) percentile 1,1-
dichloroethane concentrations at each distance modeled. A summary of the concentration ranges
estimated using the Ambient Air: Multi-Year Methodology AERMOD NEI is provided in Table 3-13.
The summary includes four OESs and select statistics (maximum, mean, median, and minimum)
calculated from the NEI modeled concentration distributions within each OES at each distance modeled.
The associated range of estimated concentrations is based on the maximum 95th percentile annual
average exposure concentrations for each distance. EPA grouped all the NEI releases, currently not
mapped to an OES, in the "Facilities not mapped to an OES" OES (Section 3.2).
Ambient Air: Multi-Year Methodology AERMOD NEI modeled concentrations ranged from 0 to 32
|ig/m3 (Table 3-13) with the maximum modeled concentration being similar to the maximum monitored
concentration of 26 |ig/m3 from AMTIC (Table 3-8), which is approximately an order of magnitude
lower that the AERMOD TRI maximum modeled concentration of 232 |ig/m3 (Section 3.3.1.2.2). Like
the AERMOD TRI, there are many instances where within an OES the range of maximum modeled
concentrations extends across as many as five orders of magnitude across all modeled distances. This
occurs because within each OES there are multiple facilities with varying releases. These varying
releases, in turn, affect the range of estimated exposure concentrations at a given distance.
The full inputs and results are presented in the Draft Risk Evaluation for 1,1-Dichloroethane -
Supplemental Information File: Supplemental Information on AERMOD NEI Exposure and Risk
Analysis (U.S. EPA. 2024m).
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2335
2336
Table 3-13. Summary of Select Statistics for the 95th Percentile Estimated Annual Average Concentrations for 1,1-Dichloroethane
OES
# Releases
Evaluated
in OES
Statistic
Annual Average Concentration (jig/m3) Estimated within 10 to 10,000 m of Releasing Facilities
10
30
30 to 60
60
100
100 to 1,000
1,000
2,500
5,000
10,000
Commercial
use as a
laboratory
chemical
2
Max
3.7E-02
1.2E-02
7.2E-03
4.2E-03
1.9E-03
1.9E-04
3.8E-05
8.2E-06
2.6E-06
8.4E-07
Mean
1.2E-02
3.8E-03
2.4E-03
1.4E-03
6.2E-04
6.4E-05
1.3E-05
2.7E-06
8.7E-07
2.8E-07
Median
1.7E-06
8.1E-07
5.6E-07
3.4E-07
1.7E-07
1.8E-08
4.1E-09
8.9E-10
2.9E-10
9.2E-11
Min
4.2E-07
2.0E-07
1.4E-07
8.4E-08
4.1E-08
4.4E-09
1.0E-09
2.2E-10
7. IE—11
2.3E-11
Manufacturing
9
Max
2.1
6.1
6.1
6.0
5.7
1.0
1.2E-01
2.6E-02
8.3E-03
2.6E-03
Mean
7.0E-01
3.6E-01
3.0E-01
2.2E-01
1.6E-01
3.3E-02
4.7E-03
1.0E-03
3.3E-04
1.1E-04
Median
3.8E-03
3.1E-03
4.2E-03
4.0E-03
2.7E-03
7.1E-04
1.7E-04
4.5E-05
1.7E-05
5.5E-06
Min
-
-
-
-
-
-
-
-
-
-
Processing as a
reactive
intermediate
50
Max
3.2E01
1.2E01
8.2
4.9
2.2
2.7E-01
4.8E-02
1.7E-02
6.7E-03
2.4E-03
Mean
9.9E-01
4.7E-01
3.1E-01
1.9E-01
8.9E-02
1.1E-02
3.0E-03
8.1E-04
3.1E-04
1.2E-04
Median
1.3E-06
2.5E-05
1.7E-04
2.0E-04
4.4E-04
2.3E-04
7.2E-05
2.5E-05
1.1E-05
5.5E-06
Min
-
-
-
-
-
-
-
-
-
-
General waste
handling,
treatment, and
disposal
102
Max
1.3E01
8.2
6.5
4.1
2.1
2.1E-01
5.2E-02
1.1E-02
3.4E-03
1.0E-03
Mean
8.3E-01
3.5E-01
2.5E-01
1.5E-01
7.6E-02
9.8E-03
2.0E-03
4.5E-04
1.5E-04
4.8E-05
Median
3.1E-04
6.3E-04
6.9E-04
5.0E-04
3.3E-04
5.4E-05
1.8E-05
6.5E-06
2.5E-06
9.8E-07
Min
-
-
-
-
-
-
-
-
-
-
Facilities not
mapped to an
OES
57
Max
9.2
3.7
2.8
1.5
7.3E-01
1.2E-01
1.8E-02
3.9E-03
1.3E-03
4.0E-04
Mean
1.3E-01
5.7E-02
4.1E-02
2.3E-02
1.1E-02
1.7E-03
2.9E-04
6.6E-05
2.2E-05
7.6E-06
Median
2.8E-09
2.9E-06
1.7E-05
2.4E-05
3.2E-05
1.4E-05
7.3E-06
2.8E-06
1.2E-06
4.4E-07
Min
-
-
-
-
-
-
-
-
-
-
Details found in: Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Supplemental Information on AERK IOD NEI Exposure and Risk
Analysis (U.S. EPA. 2024m)
Reported in NEI as "0"
2337
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2340
2341
2342
2343
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2346
2347
2348
2349
2350
2351
2352
2353
2354
2355
2356
2357
2358
2359
2360
2361
2362
2363
2364
2365
2366
2367
2368
2369
2370
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3.3.1.2.4 Population Analysis
The Ambient Air: Multi-Year Methodology AERMOD TRI and NEI includes a detailed population
analysis described in Section 5.3.3.2.5 and Appendix E.2. This includes an evaluation of the general
population in terms of characterization of those members of the general population that are considered
PESS (see Section 5.3.2), that are living within 1,000m of TRI releasing facilities - locations with
highest 1,1-dichloroethane ambient air concentrations (see Table 3-12). The analysis also includes an
examination of the environments and community infrastructure surrounding the TRI release sites, such
as residential neighborhoods, parks, schools, childcare centers, places of worship, and hospitals.
3.3.2 Indoor Air Pathway
Concentrations of 1,1-dichloroethane in the indoor environment may be limited to a few sources, the
most likely from outdoor air intrusion to indoor air through heating, ventilation, and air conditioning
systems and open windows. There are no consumer products or articles currently identified containing
and off-gassing 1,1-dichloroethane and thus not anticipated to contribute to indoor 1,1-dichloroethane
concentrations. Also, given the very low estimated groundwater concentrations (see Section 3.3.4.3),
vapor intrusion is not expected to be a source of 1,1-dichloroethane exposures.
3.3.2.1 Measured Concentrations in Indoor Air
Indoor air concentrations of 1,1-dichloroethane were measured in one study in the United States (Figure
3-7). Lindstrom et al. (1995) reported non-detect concentrations of 1,1-dichloroethane in indoor air in 34
homes (conventional single-family homes and townhomes) in the Rocky Mountains, United States
between 1992 (pre-occupancy) and 1993 (during occupancy).
US Vapor/Gas
78782 - Lindstrom et al., 1995 - US
Residential
jg Non-Detect
A Normal Distribution (CT and 90th percentile)
*
NonUS Vapor/Gas
5431563 - Huang et al., 2019 - CN
4 A
5736601 - Li et al., 2019 - CA
0.001
0.01
0.1 1
Concentration (ug/m3)
10
Figure 3-7. Concentrations of 1,1-Dichloroethane (^g/m3) in the Vapor/Gas Fraction in Indoor
Air, from U.S.-Based and International Studies, 1992-2017
3.3.2.2 Modeled Concentrations in Indoor Air
IIOAC calculates a mean and high-end indoor air concentration based on the outdoor/ambient air
concentration and the mean and high-end indoor-outdoor ratios. In IIO AC, the indoor-outdoor ratio of
0.65 is used to calculate indoor air concentrations corresponding to the mean outdoor air concentration
for each potentially exposed population. The indoor-outdoor ratio of 1 is used to calculate the indoor air
concentration corresponding to the 95th percentile of outdoor air concentration of each potentially
exposed population.
IIOAC modeled high-end indoor air concentrations ranged from 9.9><10~8 to 18 |ig/m3 (Table 3-14). The
range of concentrations can vary by as much as six orders of magnitude between minimum and
maximum concentrations. This occurs because within each OES there are multiple facilities with
varying releases. These varying releases, in turn, affect the range of estimated exposure concentrations
at a given distance.
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The full inputs and results of IIOAC are presented in the Draft Risk Evaluation for 1,1-Dichloroethane -
Supplemental Information File: Supplemental Information on IIOAC TRI Exposure and Risk Analysis
(U.S. EPA. 2024pY
Table 3-14. Summary of Select Statistics for the 95th Percentile Estimated Annual Average Indoor
Air Concentral
tions for 1,1- Die
lloroethane Releases Reported to TRI
OES
# Facilities
Evaluated in
OES
Statistic
Annual Average Indoor Air Concentration (jug/m3)
Estimated within 100 to 1,000 m of Releasing Facilities
100 m
100 to 1,000 m
1,000 m
Manufacturing
9
Max
1.8E01
2.0
8.3E-01
Mean
1.5
1.8E-01
7.2E-02
Median
4.1E-02
7.1E-03
3.3E-03
Min
3.2E-03
3.7E-04
1.5E-04
Processing as a
reactive
intermediate
6
Max
9.5E-01
1. IE—01
4.5E-02
Mean
2.1E-01
2.9E-02
1.3E-02
Median
7.9E-02
2.5E-02
1.3E-02
Min
0
0
0
Waste handling,
treatment, and
disposal
8
Max
6.4E-01
7.5E-02
3.0E-02
Mean
2.7E-02
3.1E-03
1.3E-03
Median
3.2E-03
3.8E-04
1.5E-04
Min
5.9E-07
1.9E-07
9.9E-08
3.3.3 Surface Water Pathway
Surface water contamination from 1,1-dichloroethane occurs primarily from the direct discharge of
wastewater from industrial operations and wastewater treatment plants. To understand the possible
exposure scenarios from these ongoing practices, EPA assessed exposures to the general population
from ambient surface waters and drinking water. EPA also evaluated exposures to ecological species
dwelling in the water column and benthic zone of ambient surface waters. These exposures are due to
the release of 1,1-dichloroethane from direct facility discharges to receiving surface waterbodies.
The evaluation of these exposures considered the review of available monitoring data collected from
ambient surface waters and finished drinking water, as well as model results generated by the EPA.
Although EPA identified a robust set of surface and drinking water monitoring data (Section 3.3.3.1),
indicating the presence of 1,1-dichloroethane in both sources of exposure, the timing and location that
samples were collected as a part of these datasets typically do not coincide with locations and
timeframes most relevant to modeled estimates of 1,1-dichloroethane concentrations using available
release information. Therefore, EPA relied primarily on a series of modeling approaches to estimate
concentrations of 1,1-dichloroethane in surface waters near known release locations (Section 3.3.3.2.1)
and at known downstream drinking water intake locations that serve public water systems (PWS). To the
degree possible, the relationship between monitoring and modeled data is further evaluated in Section
3.3.5.
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3.3.3.1 Measured Concentrations in Surface Water
Measured aqueous concentration data for 1,1-dichloroethane in ambient surface water (i.e., collected
from rivers, streams, lakes, and ponds, rather than within industrial operations or drinking water
systems) from across the country, were collected from public databases and peer-reviewed publications.
Measured concentrations of 1,1-dichloroethane in finished (i.e., treated) drinking water as a part of
routine monitoring conducted by PWSs were likewise collected from public databases and peer-
reviewed publications. The methods for retrieving this ambient surface water and PWS monitoring data
are described in detail in Appendix F.
Measured concentrations of 1,1-dichloroethane from surface waters were retrieved from the Water
Quality Portal (WQP) (NWOMC. 2022) to characterize the distribution of 1,1-dichloroethane levels
found in ambient surface water from across the nation, and to provide context for the modeled surface
water concentrations of 1,1-dichloroethane presented in Section 3.3.3.2.2. Measured data were retrieved
irrespective of the reason for sample collection in order to assess trends in the observed concentrations
more broadly. WQP data were downloaded in May 2023 for samples collected between 2015 to 2020,
resulting in 6,274 data points (Figure 3-8 and Figure 3-9). Full details of the retrieval and data
processing steps of ambient surface water monitoring data from the WQP are presented in Appendix F.
WQP concentrations of 1,1-dichloroethane measured in ambient surface waters ranged from the
detection limit to 2 (J,g/L, with a median concentration of 0.25 [j,g/L and a 95th percentile concentration
of 0.5 (J,g/L. Figure 3-8 shows the national spatial distribution of these results, with a strong bias of
samples collected from New Mexico, Louisiana, North Carolina, and New Jersey. In the absence of a
national standardized study of 1,1-dichloroethane in ambient surface water (that would be analogous to
EPA's third Unregulated Contaminant Monitoring Rule [UCMR3] for drinking water), and without
greater national coverage and metadata, it is difficult to characterize the national occurrence of 1,1-
dichloroethane in surface waters. Over-representation of certain states or regions may reflect targeted
sampling campaigns of specific locations expected to have potentially high concentrations of 1,1-
dichloroethane. Conclusions about areas without monitoring data cannot be drawn without further
exploration through modeling. However, for those areas containing sufficient data coverage, it is
apparent that 1,1-dichloroethane is found in relatively low quantities in ambient surface waters.
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Figure 3-8. Locations of 1,1-Dichloroethane Measured in Ambient Surface
Waters Obtained from the WQP, 2015-2020
American Indian, Alaska Native and Native Hawaiian (AIANNH) tribal boundaries are
shaded gray. Note: Alaska, American Samoa, Guam, Hawaii, N. Mariana Islands, Puerto
Rico, and the U.S. Virgin Islands are not shown because they do not contain surface water
monitoring data within the WQP.
Observed t, 1 -OCA Concentration in Surface Water (ug/L)
Figure 3-9. National Distribution of 1,1-Dichloroethane Concentrations
Measured in Ambient Surface Waters from Surface Waters Obtained from
the WQP, 2015-2020
A limited amount of 1,1-dichloroethane concentration data was identified through EPA's systematic
review of published literature. A summary of the individual studies is shown in Figure 3-10. Results
from peer-reviewed studies showed that concentrations of 1,1-dichloroethane ranged from not detected
to 48.7 iig/'L from 155 surface water samples, from near facility release sites or not associated with
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release sites of 1,1-dichloroethane, collected between 1984 and 2005 in three countries: Australia,
United Kingdom, and the United States. Reported detection frequency ranged from 0 to 0.5 (J,g/L. While
these results collected from EPA's systematic review process are few, they do indicate that relatively
high concentrations of 1,1-dichloroethane have been observed in ambient surface waters in years past.
US Not Specified
659873 - Chen et al., 1995 - US
5449639 - Bigsby and Myers, 1989 - US
1335577 - Enwright, 1985 - US
5436115-Roy, 1986-US
| Near Facility
General Population
Non-Detect
*
*
NonUS Not Specified
5438705 - Hunt el al., 2007 - AU
3544475 - Ellis and Rivett, 2007 - GB
0.001
0.1 1
Concentration (ug/L)
Figure 3-10. Concentrations of 1,1-Dichloroethane (^/L) in Surface Water from U.S.-Based and
International Studies, 1984-2005
3.3.3.2 Modeled Concentrations in Surface Water
To assess general population and aquatic ecological species exposures to 1,1-dichloroethane via
industrial releases to surface waters, aqueous concentrations of 1,1-dichloroethane were modeled in the
receiving water bodies of individual facility releases. These estimates reflect the highest potential
aqueous concentrations resulting from reported 1,1-dichloroethane facility discharges.
3.3.3.2.1 Surface Water Modeling Methodology
A full description of the modeling approach to estimate concentrations of 1,1-dichloroethane in surface
waters from direct facility-specific releases can be found in Appendix F.
As described in Section 3.2.1, annual releases of 1,1-dichloroethane to surface waters from regulated
facility discharges were retrieved from the TRI and DMR public data records. To the extent possible,
modeled hydrologic flow data (i.e., stream flow) associated with the facility's receiving water body was
retrieved from the NHDPlus V2.1 dataset (U.S. EPA and U.S.G.S.. 2016). The receiving water body was
identified from NPDES permit information of the releasing facility for the 2015 to 2020 time reporting
period. Detailed methods for the retrieval and processing steps with the flow data are presented in
Appendix F. Surface water (water column) concentrations of 1,1-dichloroethane were calculated for
general population and human health exposures as well as exposure to aquatic ecological species.
Individual Facility Modeling
Individual facility modeling was conducted to estimate concentrations in receiving waterbodies resulting
from the highest facility-specific annual release reported between 2015 through 2020. An exception was
made for the release data of the manufacturing COU facility where the next highest release data which
occurred in 2016 was used in lieu of the highest release data corresponding with a hurricane event in
2020 (U.S. EPA. 2024d). In some cases, a calculated facility effluent hydrologic flow was prioritized
over a modeled NHD receiving water body stream flow value (see Appendix F for more details). This
modeling approach employed the equations used to model releases from facilities in the E-FAST 2014
model (U.S. EPA. 2014a). which is described in Appendix F. Each facility and annual release amount
were applied to a 1-day maximum release scenario, which assumes that the annual release amount
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occurs in a single operation day as well as a scenario in which releases are equal to the facility's OES
operating days (see Table 3-3). The former scenario provides more conservative estimates of resulting
surface water concentrations and are intended to evaluate the full range of possible facility release
patterns based on the best available information. The latter scenario provides a refined analysis and
provides more realistic surface water concentrations for estimating drinking water and fish ingestion
exposure estimates.
Two flow metrics based on NHD hydrologic stream flow or the facility effluent hydrologic flow value
were used to estimate concentrations associate with general population exposure and human health
outcomes: a 30Q5 (the lowest 30-day average flow within a 5-year period) and the harmonic mean flow.
The resulting modeled water column concentrations for each facility release site were used to calculate
exposures related to human dermal contact, oral ingestion, and fish consumption.
The 7Q10 flow metric (the lowest measured 7-day average flow within a 10-year period) was used to
estimate concentrations and exposures to aquatic ecological species. These 7Q10 flow values were also
based on NHD stream flow or a calculated facility effluent flow. Aqueous concentrations of 1,1-
dichloroethane for acute and chronic aquatic ecological exposures were calculated as described in
Appendix F. To estimate concentrations for acute or water column ecological exposure, the highest
annual facility load was divided by one and then paired with the respective receiving water body flow
value, which assumes the annual release occurred in a single operation day. To estimate concentrations
for chronic ecological exposure, the highest annual facility load was divided by 21, which thereby
assumes the annual release occurred in equal daily amounts over the course of 21 consecutive facility
operation days.
The acute (highest 1-day daily) and chronic (highest 21-day daily) concentrations were then compared
with identified concentrations of concern (CoCs) for acute water column ecological exposure (7,898
(j,g/L) and chronic water column ecological exposure (93 (J,g/L). Details that describe how the CoCs
were chosen can be found in Section 4.2.5.1. Facility releases that result in modeled acute and chronic
aqueous concentrations of 1,1-dichloroethane that exceed these water column CoCs formed a new list of
facility releases to re-model estimates of water column concentration using the Point Source Calculator
(PSC). A description of the PSC and modeling steps taken herein can be found in Section 3.3.3.2.3. The
PSC allows for a refined estimation of chemical concentrations in the water column of receiving water
bodies that takes into consideration several key physicochemical and fate properties of the chemical
following its release into surface water (e.g., biological and physical degradation). The PSC is a
preferred model for estimating concentrations of 1,1-dichloroethane for ecological species exposures,
but the model in its present version is impractical to apply for multiple sites without making certain
assumptions surrounding the model's input parameters. Details on the assumptions made can be found
in Section 3.3.3.2.3. After applying PSC, refined estimates of 1,1-dichloroethane concentration in the
water column were again compared with their respective acute and chronic water column CoCs. Those
facility releases with modeled aqueous concentrations that exceed their respective CoC formed a final
list of facility releases. This list was carried through to estimate acute and chronic water column 1,1-
dichloroethane concentrations for the ecological exposure assessment using the PSC. In addition, the
modeled number of days that the concentration exceeds the respective acute or chronic CoC was
calculated by PSC and considered in the ecological exposure evaluation.
Concentrations of 1,1-dichloroethane in surface waters resulting from air deposition were estimated for a
small, slow moving, stream scenario using the PSC. The intention was to estimate aquatic water column
concentrations resulting from air deposition that represent a conservative scenario, appropriate for a tier-
1 style evaluation. The highest 95th percentile daily average air deposition rate and associated
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AERMOD modeled distance for each OES was first identified using the results from Table 3-10. These
air deposition rates were then applied to the following scenario in PSC: constant 365 consecutive days-
on of release (and deposition) that overlaps entirely with a stream having a 200 m2 surface area and 200
m3 volume (40 m length x 5 m width x 1 m depth), and a constant streamflow of 10 m3/day. The same
1,1-dichloroethane physicochemical properties, biogeochemical parameters, and weather file described
in the wastewater discharge analysis was used for the PSC runs. PSC results for the 1- and 21-day
average surface water column concentrations were compared with their respective acute (1-day) and
chronic (21-day) water column CoCs for exposure to aquatic ecological species. The distances between
the facility air release sites (i.e., the TRI coordinates) and the nearest neighboring NHD hydrological
flowlines were estimated using GIS software to inform whether the highest 95th percentile daily average
air deposition rate and associated modeled distance for each OES were reasonably representative to
choose. If the PSC-estimated concentrations exceeded their respective acute or chronic CoC, but the
distance between the facility release site and nearest neighboring NHD flowline was deemed too far
away relative to the AERMOD modeled distance or areal range, a new daily average air deposition rate
was chosen based on the distance between the release site and nearest NHD flowline. PSC was then run
again using the new deposition rate. Results of the air deposition rates and surface water column
concentrations of 1,1-dichloroethane are shown Table 3-16.
3.3.3.2.2 Surface Water Modeling Results
The locations where surface water concentrations of 1,1-dichloroethane were modeled are shown in
Figure 3-11. The annual release amounts used to generate the highest 1-day concentration estimates are
shown in Figure 3-12. The corresponding modeled concentrations of 1,1-dichloroethane for each
individual direct facility release to their respective receiving surface water body or within a calculated
facility effluent flow is summarized in Figure 3-13. These results reflect estimates of the highest
potential 1,1-dichloroethane concentration at the site of facility release into surface water, where the
entire annual release derived from the Pollutant Loading Tool is assumed to occur in a single operation
day. Thus, these estimates reflect a conservative scenario and provide an upper limit of the potential
aqueous concentrations that may have occurred between 2015 and 2020. It is important to note that these
results do not consider aggregate contribution of 1,1-dichloroethane from other sources, including
instances where multiple facility releases combine within the same stream/river network.
The lowest modeled 30Q5-based 1,1-dichloroethane concentrations were near detection limit. The 25th,
50th, 75th, and 95th percentiles of the modeled concentrations were 3.6, 49.6, 194, and 913 (J,g/L,
respectively. A similar distribution of data was found for modeled harmonic mean based 1,1-
dichloroethane concentrations. The highly variable estimates are due to variability in the annual facility
release amounts and the receiving water body or calculated facility effluent hydrologic flow values.
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2570
2571 Figure 3-11. Locations of Modeled Estimates of 1,1-DichIoroethane Concentration from Facility
2572 Releases to Ambient Surface Waters, 2015-2020
2573 AIANNH tribal boundaries are shaded in gray.
2574 Note: Alaska, American Samoa, Guam, Hawaii, N. Mariana Islands, Puerto Rico, and the U.S. Virgin Islands are
2575 not shown because they do not contain surface water monitoring data within the WQP.
2576
&ZP Tribal Lands
Max Annual Surface Water
from DMR Facilities (kg/yr)
o o-io
O 10-50
o 50 -100
® 100 - 500
• 500 - 90,000
2,000
I Kilometers
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35-
30-
25"
1-20-
. 15"
10"
~_
D=l
10 10 10 10 10
Highest Annual 1.1-DCA Pollutant Load to Surface Water between 2015-2020 (kg/yr)
Figure 3-12. Distribution of Highest Facility Annual Releases of 1,1-Dichloroethane to their
Receiving Water Body between 2015-2020
10 10 10 10 10 10
Modeled Max 1-Day 1,1-DCA Surface Water Concentration (ug/L)
Figure 3-13. Distribution of Surface Water Concentrations of 1,1-Dichloroethane Modeled from
the Highest Annual Facility Releases between 2015-2020 for a One Operating Day Per Year
Scenario
Estimates of 30Q5 hydrologic flow used to generate these concentrations.
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3.3.3.2.3 Model Estimates from Point Source Calculator (PSC)
Industrial Releases to Surface Waters
Of the 319 unique sites releasing 1,1-dichloroethane to surface water, 3 and 11 sites had initially
modeled concentrations that exceeded the acute water column CoC (7,898 (J,g/L) and chronic water
column CoC (93 (J,g/L), respectively. However, of these sites, the CA0083721 site was excluded from
further analysis because of a data reporting error. After estimating their water column concentrations
again using the PSC, seven site concentration estimates exceeded the chronic water column CoC (Table
3-15). It is important to note that some low hydrologic flow values were applied to these facility
releases, which increases the concentration estimates.
Table 3-15. Results from the Point Source Calculator, Showing Facility Release Information, 7Q10
Flow Values, and Modeled Chronic Surface Water (Water Column) Concentrations that Exceed
the Water Column Acute Coc (7,898 jig/L) and Chronic CoC (93 jig/L) for Ecological Species
Facility
NPDES ID
21-Day Highest
Release
(kg/day)
7Q10 Flow
(MLD)
Surface Water
Concentration
(Hg/L)
LA0000761
5.788
4.051
1,430
KY0022039
3.881
27.334
143
NE0043371
2.368
10.996
218
TX0119792
1.056
4.656
236
CA0064599
0.243
0.41617
580
OH0143880
0.025
0.073
312
NV0021067
0.019
0.129
139
11 For CA0064599 permit reported plant flow was used to estimate surface water concentrations instead of estimated
receiving water body 7Q10.
Air Deposition to Surface Waters
The PSC-simulated 1-day average concentrations of 1,1-dichloroethane in the water column resulting
from air deposition of 1,1-dichloroethane from TRI-reported fugitive emissions to the small, slow-
moving stream scenario did not exceed the acute water column CoC of 7,898; however, an initial 21-day
average concentration did exceed the chronic water column CoC of 93 [j,g/L for the Manufacturing OES
designation. Under this conservative stream scenario, the air deposition of 1,1-dichloroethane to surface
waters from facilities with a Manufacturing OES may result in exposure levels that pose a concern to
water-column dwelling ecological species. It is important to note, however, that the air deposition rate
for this specific Manufacturing facility applies to a distance of 10 m from the facility release site. EPA
found that the nearest NHD flowline to this facility release site was -340 m away, indicating the
scenario modeled is unrealistic and should be further evaluated. The Agency repeated the PSC run using
the highest p95 daily average air deposition rate at 100 m (-0.003 g/m2/day), which resulted in a 21-day
average water column concentration of 64 [j,g/L that no longer exceeded its respective chronic CoC.
Thus, it is more likely that the air deposition of 1,1-dichloroethane to surface waters results in exposure
levels that do not pose a concern for ecological species dwelling in the water column.
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Table 3-16. Results from the Point Source Calculator, Showing the Highest 95th Percentile Daily
Average Air Deposition Rate for OES Manufacturing and Modeled Surface Water (Water
Column) Concentrations for a 1-Day Acute and 21-Day Chronic Scenario for Ecological Species
OES
Highest p95 Daily Average Air
Deposition (g/m-2/day)
Water Column Concentration
(Hg/L)
21-Day Average
Manufacturing
0.0402
791
Processing as a reagent
0.0402
791
Waste handling, disposal,
treatment, and recycling
0.000114
2.24
3.3.3.3 Measured Concentrations in Benthic Pore Water and Sediment
No relevant data on measured concentrations of 1,1-dichloroethane in ambient aquatic benthic pore
waters or sediments were found in the WQP for the 2015 to 2020 timeframe. Likewise, no relevant
ambient monitoring data on these sample types were collected through EPA's systematic review
process.
3.3.3.4 Modeled Concentrations in Benthic Pore Water and Sediment
To assess exposures of 1,1-dichloroethane via industrial releases to ecological species dwelling in the
aquatic benthic environment, benthic pore water and bulk sediment concentrations at the facility release
sites were modeled using the PSC.
3.3.3.4.1 Benthic Pore Water and Sediment Modeling Methodology
A full description of the modeling approach to estimate concentrations of 1,1-dichloroethane in benthic
pore waters and bulk sediment from facility-specific releases can be found in Appendix F and is briefly
summarized below.
Estimated concentrations of 1,1-dichloroethane in surface waters that reflect acute (assumed 21-day
highest release) and chronic (assumed consecutive releases over the annual operating days, depending
on the COU 250 to 365 days) exposures to ecological species were compared with their identified acute
and chronic CoCs for aquatic ecological species dwelling in the benthic zone (detailed in Section
4.2.5.1). The PSC was applied to those facilities with modeled water column 1,1-dichloroethane
concentrations that exceeded the acute and chronic benthic pore water CoCs.
The 7Q10 flow metric was used to estimate concentrations and exposures for aquatic ecological species.
These 7Q10 flow values were also based on NHD stream flow or the facility effluent flow. Aqueous
concentrations of 1,1-dichloroethane for acute and chronic aquatic ecological exposures were calculated
as described in Appendix F. To estimate concentrations for acute ecological exposure, the highest annual
facility load was paired with the respective receiving water body or prioritized facility hydrologic
effluent 7Q10 flow value, which assumes the entire highest annual release occurred over 21 days. To
estimate concentrations for chronic ecological exposure, the highest annual facility load was divided by
the number of annual operating days and paired with the respective receiving water body or prioritized
facility effluent 7Q10 flow value, which assumes the annual release occurred in equal daily amounts
over the course of 250/365 consecutive days.
Similarly, water column acute (highest 21-day) and chronic (highest over number of facility operating
days-day daily) concentrations were then compared with identified CoCs for acute benthic pore water
(15-day) ecological species exposure (7,898 (J,g/L) and chronic benthic pore water (operating-day)
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ecological species exposure (6,800 (J,g/L). Details that describe how the CoCs were chosen can be found
in Section 4.2.5.1. Facility releases that result in modeled acute and chronic aqueous concentrations of
1,1-dichloroethane that exceed these benthic CoCs formed a new list of facility releases to model
benthic pore water and bulk sediment concentrations using PSC. After applying PSC, estimates of 1,1-
dichloroethane concentration in benthic pore water were compared with the acute and chronic benthic
pore water CoCs. Those facility releases with modeled concentrations that exceed their respective CoC
formed a final list of facility releases and their estimates of acute and chronic benthic pore water 1,1-
dichloroethane concentrations for the ecological exposure assessment. In addition, the modeled number
of days that the concentration exceeds the respective acute or chronic benthic pore water CoC was
calculated by PSC and considered in the ecological exposure evaluation. The list of sites modeled in
PSC to estimate benthic pore water concentrations of 1,1-dichloroethane were also modeled to estimate
benthic sediment concentrations. Benthic sediment concentrations were estimated from consecutive
releases for a 3 5-day operating period. These values were compared with a benthic sediment (3 5-day)
CoC of 2,900 (J,g/kg.
Concentrations of 1,1-dichloroethane in aquatic benthic pore waters and bulk sediments resulting from
air deposition were similarly estimated for a small, slow-moving, stream scenario using the PSC.
Likewise, the intention was to estimate benthic pore water and sediment concentrations resulting from
air deposition that represent a conservative scenario, appropriate for a tier-1 style evaluation, and so the
same approach discussed under the surface water section applies here. The highest 95th percentile daily
average air deposition rate and associated AERMOD modeled distance for each OES was first identified
using the results from Table 3-17. These air deposition rates were then applied to the following scenario
in PSC: constant 365 consecutive days-on of release (and deposition) that overlaps entirely with a
stream having a 200 m2 surface area and 200 m3 volume (40 m length x 5 m width x 1 m depth), and a
constant streamflow of 10 m3/day. The same 1,1-dichloroethane physicochemical properties,
biogeochemical parameters, and weather file described in the wastewater discharge analysis was used
for the PSC runs.
PSC results for the 15- and facility operating-day average benthic pore water concentrations and the 35-
day sediment concentrations were compared with their respective CoCs for exposure to aquatic
ecological species. The distances between the facility air release sites (i.e., the TRI coordinates) and the
nearest neighboring NHD flowlines were estimated using GIS software to help inform whether the
highest 95th percentile daily average air deposition rate and associated modeled distance for each OES
were reasonably representative to choose. If the PSC-estimated concentrations exceeded their respective
acute or chronic CoC, but the distance between the facility release site and nearest neighboring NHD
flowline was deemed too far away relative to the AERMOD modeled distance or areal range, a new
daily average air deposition rate was chosen based on the distance between the release site and nearest
NHD flowline. PSC was then run again with the new deposition rate. Results of the air deposition rates
and benthic pore water and bulk sediment concentrations of 1,1-dichloroethane are shown below in
Table 3-17.
3.3.3.4.2 Benthic Pore Water and Sediment Modeling Results
Industrial Releases to Benthic Pore Waters and Sediment
Of the 319 unique sites releasing 1,1-dichloroethane to surface water, 3 sites had initially modeled
(water column) concentrations that exceeded the acute benthic pore water aquatic CoC (7,898 (J,g/L), but
no sites had modeled concentrations that exceeded the chronic benthic pore water aquatic CoC (6,800
(j,g/L). Similarly, site CA0083721 was excluded from further analysis. After estimating their benthic
porewater concentrations again using the PSC, no PSC-estimated concentrations exceeded the acute
benthic porewater CoC. For the sites that had initially modeled (water column) concentrations that
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exceeded the chronic benthic pore water CoC, the PSC-modeled estimates of their chronic benthic
sediment concentrations did not exceed the benthic chronic sediment CoC (2,900 (J,g/L). Thus, it does
not appear that facility releases of 1,1-dichloroethane to surface waters pose a concern for aquatic
ecological species dwelling in the benthic porewaters and sediment of receiving water bodies.
Air Deposition to Benthic Pore Waters and Sediment
EPA did not find that any PSC-simulated estimates of benthic pore water or sediment concentrations
exceeded their respective aquatic acute and chronic benthic pore water CoCs (7,898 [j,g/L and 6,800
[j,g/L, respectively) or chronic benthic sediment CoC (2,900 (J,g/kg) (Table 3-17). Thus, like the results
for the surface water column, it does not appear that air deposition of 1,1-dichloroethane to surface
waters results in exposure levels that may pose a concern for ecological species dwelling in the benthic
pore waters and sediment.
Table 3-17. Results from the Point Source Calculator, Showing the Highest 95th Percentile Daily
Average Air Deposition Rate per OES, and Modeled Benthic Pore Water and Sediment
Concentrations for a 1-D
»ay Acute and 21-Day Chronic Scenario for Ecological Species Exposure
OES
Highest p95 Daily Average
Air Deposition
(g/m-2/day)
Benthic Pore Water
Concentration (jig/L)
Benthic Sediment
Concentration (jig/kg)
21-Day Average
35-Day Average
Manufacturing
0.000736
12.8
19.9
Processing as a reagent
0.0402
700
1,090
Waste handling, disposal,
treatment, and recycling
0.000114
1.99
3.08
3.3.3.5 Measured Concentrations in Drinking Water
Public Water Systems are regulated under the SDWA to enforce common standards for drinking water
across the country. Although individual primacy agencies, such as state governments, may require
monitoring or impose limits for contaminants beyond those regulated under SDWA, currently there are
no national requirements to routinely monitor or limit 1,1-dichloroethane in finished water from PWSs.
To assess concentrations in surface water known to be distributed as drinking water, monitoring data
collected by PWSs were evaluated. Concentrations of 1,1-dichloroethane found in finished (i.e., treated)
drinking water were collected from the EPA's published UCMR3 dataset, which includes samples
collected between 2013 to 2015. To the extent that it could be determined from the database records,
only those PWSs that draw from surface water as their primary source were included for this
assessment. Similarly, only treated water that was sent to the distribution system were included.
Descriptions of these data retrieval and processing methods are presented in Appendix F.
The UCMR3 dataset was used to gather concentrations of 1,1-dichloroethane found in finished drinking
water from PWSs that draw primarily from surface water sources (U.S. EPA. 2017c). This portion of the
UCMR3 dataset includes 1,785 samples from 407 PWSs across 16 states. The maximum concentration
of 1,1-dichloroethane measured in finished drinking water was 0.28 (J,g/L. These results indicate that
1,1-dichloroethane in finished drinking water from PWSs was measured in relatively low amounts
across the nation between 2013 and 2015.
Two studies that reported concentrations of 1,1-dichloroethane in drinking water for general population
locations were found through EPA's systematic review process (see Figure 3-14). Overall,
concentrations ranged from not detected to 367 |ig/L from 170 samples collected between 2002 and
2012 in the United States.
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US Not Specified
General Population
V Lognormal Distribution (CT and 90th percentile)
a Non-Detect
5639273 - Landmeyer and Campbell, 2014 - US
^"M
3364193 - Kingsbury el a)., 2008 - US
*
0.001
0.01
0.1 1 10 100
Concentration (ug/L)
1000
Figure 3-14. Concentrations of 1,1-Dichloroethane (^/L) in Drinking Water from a U.S.-Based
Study, 2002-2012
3.3.3.6 Modeled Concentrations in Drinking Water
To assess general population exposures to 1,1-dichloroethane via industrial releases to surface waters,
aqueous concentrations of 1,1-dichloroethane in potential drinking water sources were modeled at PWS
intake locations downstream of known 1,1-dichloroethane release sites. Estimates of 1,1-dichloroethane
concentrations in drinking water account for upstream-to-downstream dilution and were adjusted for
applicable treatment processes that remove of 1,1-dichloroethane in source water.
3.3.3.6.1 Drinking Water Modeling Methodology
To provide more robust estimates of 1,1-dichloroethane concentrations in drinking water, known facility
releases were mapped to drinking water sources using PWS data stored in EPA's Safe Drinking Water
Information System Federal Data Warehouse (U.S. EPA. 2022e). This dataset is updated quarterly, and
the 2nd quarter 2022 version was used for this analysis. Following the mapping, the colocation of and
proximity of facility release sites to PWS drinking water intake locations were evaluated. These drinking
water data are considered sensitive by EPA's Office of Water and are protected from public release.
Geospatial analysis using the NHDPlus V2.1 flowline network was used to determine PWS intake
locations within 250 km downstream of facility 1,1-dichloroethane release sites. Provided a PWS may
have multiple intake locations, concentrations of 1,1-dichlorethane were estimated at the most upstream
intake for a given PWS, thus reflecting a more conservative estimate. Results of surface water
concentrations of 1,1-dichloroethane modeled from the highest annual facility releases between 2015
and 2020 for a 1-operating day per year scenario were adjusted by a dilution factor that was calculated
from the change in hydrologic flow between the facility release site and receiving water body associated
with the identified PWS intake location. The resulting drinking water source concentration was then
adjusted for the removal of 1,1-dichloroethane during the respective PWS treatment processes, if
applicable. It is important to note that multiple facility releases can be upstream of the same PWS intake.
Estimates of 1,1-dichloroethane concentration in finished drinking water were evaluated independently
for each facility-intake linkage. Details of the methodology used for this analysis is provided in
Appendix F.
3.3.3.6.2 Drinking Water Modeling Results
Drinking water concentrations of 1,1-dichloroethane were modeled from the highest annual facility
releases between 2015 to 2020 utilizing a first tier, 1-operating day per year scenario as well as a less
conservative facility operating day release scenario. For the more conservative 1-day release scenario
the drinking water concentrations ranged from below detection limit to 3,365 (J,g/L. The 75th and 95th
percentile of 1,1-dichloroethane concentrations in drinking water were 0.08 and 12.89 (J,g/L. These
results demonstrate that most of the modeled concentrations in drinking water are below 13 [j,g/L for a
conservative, acute, 1-day highest concentration exposure scenario. The distribution of these results is
shown in Figure 3-15. Those facility releases and resulting drinking water concentrations of 1,1-
dichloroethane that comprise the highest top 5 percent of estimates (i.e., are in the 95 to 100 percentile
range) are reported in Table 3-18.
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Table 3-18 shows for each facility release site, the modeled drinking water concentration at the most
upstream intake location of each PWS within 250 km of the release site. Calculated 30Q5 hydrologic
flow values were used to estimate the drinking water concentrations shown in Table 3-18, accounting for
dilution with changes in the flow values between the facility release site and PWS intake location. Those
differences in flow, as well as the distance between the facility release site and PWS intake location
modeled, are included. In addition, the population served for each PWS is shown in Table 3-18. This
table excludes facility CA0083721 because of an error in the 1,1-dichloroethane wastewater discharge
data.
Modeled drinking water concentrations within the high-end top five percent of modeled values ranged
from near detection limit to 382 (J,g/L. Some of the resulting concentrations can be explained in part by
low 30Q5 hydrologic flow values that were applied to their estimation. It is important to note that in the
event the downstream flow value was lower than the upstream flow value, the upstream flow value was
used in the calculation step and so no adjustment to the amount of dilution was applied.
10
10 10 10 10
Modeled 1,1-DCA 30Q5 Drinking Water Concentration (ug/L)
10
Figure 3-15. Distribution of Drinking Water Concentrations of 1,1-Dichloroethane Modeled from
the Highest Annual Facility Releases between 2015-2022 for a One Operating Day per Year
Scenario
Estimates of 30Q5 hydrologic flow were used to generate these concentration estimates. The dashed black line
indicates concentrations at 10 |ig/L.
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Table 3-18. Modeled 30Q5 Concentrations of 1,1-Dichloroethane jn Drinking Water at PWSs
within 250 km Downstream of a Facility Release Site, Changes in Hydrologic Flow between the
Facility
NPDES ID
PWSID
Facility
30Q5 Flow
(MLD)
Intake
30Q5 Flow
(MLD)
30Q5 Drinking Water
Concentration (jig/L)
Population Served
KY0022039
KY0470175
45
214
382
76,326
MI0004057
MI0006101
1.1
0.0
183
9,133
MI0004057
IN5245012
1.1
0.0
183
29,500
CA0048143
CA4210010
20
0.1
183
95,628
CA0048127
CA4210010
12
0.1
183
95,628
CA0022764
CA2110001
43
0.3
91.3
1,445
CA0048194
CA4410010
30
0.1
91.3
87,957
CA0048194
CA2710004
30
0.0
91.3
N/A
CA0048194
CA4000684
30
0.1
91.3
N/A
AZ0020559
AZ0407093
122
0.2
64.8
234,766
AZ0020559
AZ0407096
122
0.2
64.8
135,975
KY0066532
KYI 110054
52
297
55.3
6,165
CA0084271
CA0710003
2.9
0.4
49.5
198,000
MI0044130
MI0006101
7.5
0.0
30.4
9,133
MI0044130
IN5245012
7.5
0.0
30.4
29,500
MI0044130
IN5245020
7.5
0.0
30.4
78,384
3.3.4 Land Pathway (Soils, Groundwater, and Biosolids)
3.3.4.1 Air Deposition to Soil
EPA used AERMOD to estimate air deposition from facility releases and calculate the resulting soil
concentrations near the 1,1-dichloroethane emitting facility. AERMOD modeling methodology is
detailed in Appendix D.3. The highest 95th percentile maximum daily air deposition rates for each OES
generally occurred at 10 m from the facility (Table 3-19). For this reason, 1,1-dichloroethane soil
concentrations which could result from maximum daily air deposition were estimated for each OES at a
distance of 10 m from facility for determining dietary exposure of terrestrial ecological receptors.
Appendix E.1.2.9 presents details and equations and details in estimating 1,1-dichloroethane in soil from
air deposition.
Table 3-19 presents the resulting calculated 95th percentile maximum 1,1-dichloroethane soil
concentrations 10 m from facility corresponding to the applicable exposure scenarios. Across exposure
scenarios, the exposure scenario Manufacturing 1,1-dichloroethane resulted in the highest estimated 1,1-
dichloroethane soil concentrations which could result from air deposition. These 1,1-dichloroethane soil
concentrations which could result from air deposition were then used to estimate soil pore water
concentrations 10 m from facility (Table 3-19) according to the methodology described in Section
3.3.4.6.2.
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Table 3-19. Soil Catchment and Soil Catchment Pore Water Concentrations Estimated from 95th
Percentile Maximum Daily Air Deposition Rates 10 m from Facility for 1,1-Dichloroethane
Releases Reported to TRI
OES
Number of
Facilities
Maximum Daily
Air Deposition
(g/m2/day)"
Soil
Concentrations
(jug/kg)
Soil Pore Water
Concentrations
(Jig/L)
Manufacturing
9
4.02E-02
2.36E02
1.46E02
Processing as a reactive
intermediate
6
8.90E-04
5.24
3.23
Waste Handling,
Treatment and Disposal
(non-POTW)
8
2.10E-05
1.24E-01
7.63E-02
11 Estimated via AERMOD within 10 m of releasing facilities.
To help determine the significance of the air deposition to the groundwater exposure pathway, annual air
deposition loading rates of 1,1-dichloroethane to soil were input to the Pesticide in Water Calculator
(PWC) (U.S. EPA. 202010 model to estimate groundwater concentrations. PWC simulates chemical
substance applications to land surfaces and the chemical substance's subsequent transport to and fate in
water bodies, including surface water bodies as well as simple ground water aquifers. Scenarios with six
sandy soils containing a relatively low fraction of organic carbon and shallow groundwater were
modeled. The loading of 1,1-dichloroethane to the soil surface was estimated by taking the 95th
percentile air deposition rate at 1000 m from the emission source for the largest OES emission
(Processing as a reactive intermediate) and estimating the mass deposited on soil per hectare. From this
loading the model estimated post breakthrough average groundwater concentrations ranging from
approximately 2.7 to 8.0 |ig/L, suggesting that the air deposition to groundwater pathway is not an
important source of general population exposure to 1,1-dichloroethane. No additional analysis of the air
deposition to groundwater pathway was conducted.
3.3.4.2 Measured Concentrations in Groundwater
3.3.4.2.1 Ambient Groundwater Monitoring
Concentrations of 1,1-dichloroethane measured from groundwater monitoring wells are collated by the
National Water Quality Monitoring Council and stored in the WQP (NWOMC. 2022). Groundwater 1,1-
dichloroethane concentration results were acquired between 2015 to 2020 from the WQP. Figure 3-16
shows the spatial distribution of measured concentrations of 1,1-dichloroethane in groundwater across
the contiguous United States. Groundwater was measured at a much higher frequency in Oregon,
Georgia, Minnesota, New York, and New Jersey in comparison to the rest of the states. The distribution
of the groundwater sample concentrations is shown in Figure 3-17. The process for identifying this data
is provided in Appendix G. This analysis is intended to characterize the observed ranges of 1,1-
dichloroethane concentrations in groundwater irrespective of the reasons for sample collection and to
provide context for the modeled groundwater concentrations presented in Section 3.3.4.3.
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Figure 3-16. Locations of 1,1-Dichloroethane Measured in Groundwater Monitoring Wells
Acquired from the WQP, 2015-2020
AIANNH tribal boundaries are shaded in gray.
Note: Alaska, American Samoa, Guam, Hawaii, N. Mariana Islands, Puerto Rico, and the U.S. Virgin
Islands are not shown because they do not contain groundwater monitoring data within the WQP.
Observed 1,1-DCA Concentration in Groundwater (ug/L)
10 10
Observed 1,1 -DCA Concentration in Groundwater (ug«l)
Figure 3-17. Distribution of 1,1-Dichloroethane Concentrations from Groundwater Monitoring
Wells (N = 14,483) Acquired from the Water Quality Portal, 2015-2020
Concentrations of 1,1-dichloroethane in groundwater ranged from 0 to 650 [j,g/L for samples collected
between 2015 and 2020. The 50th and 95th percentile of groundwater concentrations of 1,1-
dichloroethane was 0.25 and 1 (J,g/L. There were 602 groundwater samples with concentrations of 1,1-
dichloroethane that exceeded 1 [j,g/L (Figure 3-17, right inset). For this subset of results greater than 1
[j,g/L, the 50th and 95th percentile was 2.5 and 12 (J,g/L, respectively. There were 33 (-0.3 percent of the
total) groundwater monitoring wells that exceeded 1,1-dichloroethane concentrations of 10 [j,g/L for
samples collected between 2015 to 2020.
A small amount of groundwater and soil-water leachate 1,1-dichloroethane concentration data was
collected through EPA's systematic review of published literature. A summary of the individual studies
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is shown in Figure 3-18 for groundwater data and Figure 3-19 for leachate data. A review of published
literature resulted in nine studies reporting measured concentrations of 1,1-dichloroethane in
groundwater. Concentrations ranged from not detected to 1,900,000 ng/L in 400 samples collected
between 1984 and 2005 in the United States.
US Not Specified
g General Population
Near Facility
V Lognomial Distribution (CT and 9<)th percentile)
jS Non-Detect
3975066 - Hopple el al.. 2009 - US
4912133 - Buszka el al., 2009 - US I
1740826 - Westinghouse Savannah River, 1997 - US
659873 - Chen cl al.. 1995 - US
5438509 - Heck el al„ 1992 - US
5449639 ¦ Bigsby and Myers. 1989 - US
724484 - Sabcl and Clark. 1984 - US
1335577 - Hnwrighi. 1985 - US
5436115 - Roy. 1986 - US
KT
NonUS Not Specified
631540 - Fan et al., 2009 - TW
10**6
10**4
0.01 1 KM)
Concentration (ug/L)
10*4
Figure 3-18. Concentrations of 1,1-Dichloroethane (^/L) in Groundwater from U.S.-Based and
International Studies, 1984-2005
US Wet
Near Facility
A Normal Distribution (CT and 90th percentile)
661846 - Schrab et al., 1993 - US
724484 - Sabel and Clark, 1984 - US
0.001 0.01 0.1
Concentration (ug/L)
Figure 3-19. Concentrations of 1,1-Dichloroethane (jig/L) in the Soil-Water Leachate from U.S.-
Based Studies for Locations near Facility Releases, 1984-1993
3.3.4.2.2 Measured Concentrations in Groundwater Sourced Drinking Water
The UCMR3 dataset was used to gather concentrations of 1,1-dichloroethane found in finished drinking
water from PWSs that draw primarily from groundwater sources. This portion of the UCMR3 dataset
includes 2,539 samples from 404 PWSs across 16 states. The maximum concentration of 1,1-
dichloroethane measured in groundwater sourced finished drinking water was 1.6 (J,g/L. Similar for
surface water derived sources, these results indicate that 1,1-dichloroethane in finished drinking water
derived from groundwater was measured in relatively low amounts across the nation between 2013 to
2015.
3.3.4.3 Modeled Concentrations in Groundwater
EPA found reported releases of 1,1-dichloroethane to land (TRI2015-2020 average 1 kg/year) and used
Generic Scenarios or Emission Scenario Documents to model releases of less than 22,682 kg/year to
Hazardous Waste Landfills under the TSCA COUs. The groundwater concentrations resulting from the
range of expected releases, making the conservative assumption that the releases go to non-hazardous
waste landfills, are predicted to be less than 9.17x 10~4 mg/L (Table 3-20).
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Table 3-20. Estimated Groundwater Concentrations (mg/L) of 1,1-Dichloroethane Found in Wells
within 1 Mile of a Disposal Facility Determined by the DRAS Model
Leachate Concentration
(mg/L)
Loading Rate
0.1 kg/year
1.0 kg/year
10 kg/year
100 kg/year
1,000 kg/year
1.0 E-05
1.11 E— 14
1.06E-13
1.01E-12
9.62E-12
9.17E-11
1.0 E-04
1.11 E— 13
1.06E-12
1.01 E— 11
9.62E-11
9.17E-10
1.0 E-03
1.11 E— 12
1.06E-11
1.01E-10
9.62E-10
9.17E-09
1.0 E-02
1.11 E— 11
1.06E-10
1.01E-09
9.62E-09
9.17E-08
1.0 E-01
1.11 E— 10
1.06E-09
1.01E-08
9.62E-08
9.17E-07
1.0
1.1 IE—09
1.06E-08
1.01E-07
9.62E-07
9.17E-06
10
1.11E-08
1.06E-07
1.01E-06
9.62E-06
9.17E-05
100
1.11E-07
1.06E-06
1.01E-05
9.62E-05
9.17E-04
Concentrations organized by potential loading rates (kg) and potential leachate concentrations (mg /L).
3.3.4.3.1 Disposal to Landfills and Method to Model Groundwater Concentrations
Landfills may have various levels of engineering controls to prevent groundwater contamination. These
can include industrial liners, leachate capturing systems, and routine integration of waste. However,
groundwater contamination from disposal of consumer, commercial, and industrial waste streams
continues to be a prominent issue for many landfills throughout the United States (Li et al.. 2015a; Li et
al.. 2013; Mohr and DiGuiseppi. 2010). This contamination may be attributed to perforations in the
liners, failure of the leachate capturing system, or improper management of the landfills. 1,1-
Dichloroethane can migrate away from landfills in leachate to groundwater. If communities rely on this
groundwater as their primary drinking water source, there is a potential for exposure via ingestion if that
water is contaminated with 1,1-dichloroethane and does not undergo treatment. Depending on the
distance between the landfill and a drinking water well, as well as the potential rate of release of landfill
leachate into groundwater, the concentration of this exposure can vary substantially.
Landfills are regulated under the Resource Conservation and Recovery Act (RCRA). RCRA landfills
can be classified as Subtitle C (hazardous waste landfills) or Subtitle D (municipal solid nonhazardous
waste landfills). Subtitle C establishes a federal program to manage hazardous wastes from "cradle to
grave." The objective of the Subtitle C program is to ensure that hazardous waste is handled in a manner
that protects human health and the environment. When waste generators produce greater than 100 kg per
month of non-acutely hazardous waste, those hazardous wastes, including 1,1-dichloroethane, meeting
the U076 waste code description in 40 CFR 261.33, must be treated to meet the land disposal restriction
levels in 40 CFR part 268 and be disposed in RCRA subtitle C landfills. These disposals are captured
partially through the TRI and are reported for both onsite and offsite facilities. Recent violations of
permits are reported in the footnotes of each table.
Review of state databases does not suggest any readily available evidence of groundwater contamination
near or coinciding with these operations that could affect a drinking water supply. Similar review of the
data available via the WQP suggests that there are no known contaminations from RCRA Subtitle C
Landfills as reported to the TRI program. The absence of groundwater contamination near RCRA
Subtitle C Landfills may be attributed to many of the ongoing engineering controls built into these
facilities as well as active monitoring of groundwater wells around facilities. As a result, EPA did not
assess Subtitle C landfills beyond understanding their permit violations.
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Regulations established under Subtitle D ban open dumping of waste and set minimum federal criteria
for the operation of municipal waste and industrial waste landfills, including design criteria, location
restrictions, financial assurance, corrective action (clean up), and closure requirements. States play a
lead role in implementing these regulations and may set more stringent requirements. National
requirements for Subtitle D landfills are most specific for Municipal Solid Waste (MSW) landfills.
MSW landfills built after 1990 must be constructed with composite liner systems and leachate collection
systems in place. Composite landfill liners consist of a minimum of 2 feet of compacted soil covered by
a flexible membrane liner, which work in concert to create a low hydraulic conductivity barrier and
prevent leachate from being released from the landfill and infiltrating to groundwater. A leachate
collection system typically consists of a layer of higher conductivity material above the composite liner
that funnels leachate to centralized collection points where it is removed from the landfill for treatment
and disposal. Despite these controls, releases may still occur due to imperfections introduced during
construction or that form over time (Li et al.. 2015a; Li et al.. 2013; Mohr and DiGuiseppi. 2010); thus,
groundwater monitoring is required to identify and address any releases before there can be harm to
human health and the environment. RCRA Subtitle D requirements for non-MSW landfills are less
stringent. In particular, nonhazardous industrial landfills and C&D debris landfills do not have specified
national requirements for construction and operation and certain landfills are entirely exempt from
RCRA criteria. Under the Land Disposal Program Flexibility Act of 1996 (Pub.L. 104-119), some
villages in Alaska that dispose of less than 20 tons of municipal solid waste daily (based on an annual
average) may dispose of waste in unlined or clay4ined landfills or waste piles for open burning or
incineration.
There are no known potential sources of 1,1-dichloroethane to Subtitle D landfills. Waste generators that
produce less than 100 kg per month of non-acutely hazardous waste, including 1,1-dichloroethane
meeting the U076 waste code, may dispose of this waste in these landfills. Nonhazardous industrial
wastes also have the potential to contain 1,1-dichloroethane at variable concentrations, but due to its
limited use as a laboratory chemical, concentrations in waste are expected to be low. EPA did not
identify any consumer or commercial products that contain 1,1-dichloroethane; therefore, release of 1,1-
dichloroethane to Subtitle D nonhazardous waste landfills as part of municipal solid waste is expected to
be negligible. In addition, landfilled 1,1-dichloroethane will only reach groundwater from landfills that
do not have an adequate liner and leachate control systems. Based on the previous information, EPA
concludes the potential for exposure to general populations to 1,1-dichloroethane via ingestion of
leachate contaminated groundwater is negligible. To support this conclusion, an assessment was
conducted to evaluate the potential for groundwater contamination by 1,1-dichloroethane in leachate in
the absence of landfill controls.
This assessment was completed using the Hazardous Waste Delisting Risk Assessment Software
(DRAS) (U.S. EPA. 2020h). DRAS was specifically designed to address the Criteria for Listing
Hazardous Waste identified in Title 40 Code of Federal Regulations (40 CFR) Section 261.11(a)(3), a
requirement for evaluating proposed hazardous waste delistings. In this assessment, DRAS is being
utilized to determine potential groundwater concentrations of 1,1-dichloroethane after they have been
disposed of into a non-hazardous waste landfill. The results of this assessment are provided in Table
3-20. Because measured loading rates of 1,1-dichloroethane to individual landfills are unknown,
multiple DRAS runs were conducted which included the estimated ranges of waste loading per site (see
Section 3.3.1.2.3 for loading estimates. The assessment relied on the default values for 1,1-
dichloroethane as the chemical of concern. Lastly, leachate concentrations were estimated for a range of
possibilities until no risk could be identified at the lower end of those concentrations. Because DRAS
calculates a weight-adjusted dilution attenuation factor (DAF) rather than a groundwater concentration,
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a back calculation was used to convert the DAF to a potential concentration that receptors located within
one mile of a landfill might be exposed if the release was not controlled.
3.3.4.3.2 Summary of Disposal to Landfills and Groundwater Concentrations
EPA determined through modeling that groundwater concentration of 1,1-dichloroethane increased with
increasing landfill load rate and increasing leachate concentration. With each progressive iteration of
loading rate or leachate concentration, potential groundwater concentrations increase by an order of
magnitude. When both loading rate and leachate increase by one order of magnitude, potential
groundwater concentration increase by two orders of magnitude. These increases can largely be
attributed to the increasing weight adjusted dilution attenuation factor and are what would be expected
for a chemical substance with 1,1-dichloroethane's physical-chemical properties (water solubility,
Henry's law constant) and fate characteristics (biodegradability, half4ife in groundwater). 1,1-
Dichloroethane migrates in groundwater at approximately the rate of hydraulic flow and can persist with
a half-life of greater than 150 days in anaerobic environments (Adamson et al.. 2014; Mohr and
DiGuiseppi. 2010). Thus, these concentrations are likely to represent the range of exposure
concentrations for individuals living within a 1-mile radius of a poorly managed landfill who rely on
groundwater as their primary source of drinking water.
EPA also determined that the modeled concentrations are within the range of concentrations of 1,1-
dichloroethane found in groundwater monitoring studies. Monitoring data from the WQP dataset
reported 1,1-dichloroethane concentrations in groundwater ranging from near detection limit to 650
[j,g/L. Though the corresponding sites in these monitoring surveys may not be specifically tied to the
disposal of 1,1-dichloroethane to landfills, they provide context for what concentrations may be
expected when contamination occurs. These concentrations support the conclusion that the low
concentrations modeled by EPA are common in groundwater aquifers nationwide.
3.3.4.4 Measured Concentrations in Biosolids and Sludge
Biosolids are a primarily organic solid product produced by wastewater treatment processes that can be
beneficially recycled via land application. The EPA published The Standards for the Use or Disposal of
Sewage Sludge (40 CFR, Part 503) in 1993 to protect public health and the environment from any
reasonably anticipated adverse effects of certain pollutants that might be present in sewage sludge
biosolids. Municipal wastewater treatment systems mainly treat biosolids to ensure pathogen and vector
attraction (e.g., rats) reduction and limits in metals concentrations; however, other chemicals are
monitored as well.
Data regarding 1,1-dichloroethane measured concentrations in biosolids has not been identified in public
databases or published literature particularly for those facilities that treat wastes and report discharges of
1,1-dichloroeethane. EPA did refer to the 1988 Sewage Sludge Survey and found zero percent detection
frequency for 1,1-dichloroethane (see Appendix D.2.4.4). In addition, EPA identified a 2004 published
report by the King County Department of Natural Resources and Parks (King County DNRP),
Wastewater Treatment Division (WTD) characterizing two municipal wastewater treatment facilities
that monitored biosolids for 135 chemicals including 1,1-dichloroethane (King County DNRP. 2004). In
reviewing the 2004 report, EPA concluded that 1,1-dichloroethane is not detected in these biosolids and
in subsequent annual reports, King County DNRP does not list 1,1-dichloroethane levels in biosolids,
which is noted in the report as a chemical that is not detected in biosolids. However, data on the 125
public-owned treatment works (POTWs) (see in Table 3-4), reporting releases of 1,1-dichloroethane and
which generate biosolids that are either disposed or used for land application is not available.
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3.3.4.5 Modeled Concentrations in Groundwater Resulting from Land Application of
Biosolids
Though there is no literature data of 1,1-dichloroethane in biosolids, EPA estimated 1,1-dichloroethane
in biosolids since 125 POTWs treat and release 1,1-dichloroethane to surface water and generate
biosolids in the process.
The Biosolids Tool (BST) (U.S. EPA. 2023 a) was used to assess the importance of the biosolids land
application to groundwater pathway. The BST is a multimedia, multipathway, multireceptor
deterministic, problem formulation, and screening4evel model that can estimate high-end human and
ecological hazards based on potential exposures associated with land application of biosolids or
placement of biosolids in a surface disposal unit. The BST was peer reviewed by the EPA Science
Advisory Board in 2023 (EPA-SAB-24-001). A default annual biosolids land application rate of 1
kg/m2/year and a 1,1-dichloroethane biosolids concentration of 20 mg/kg, estimated using the
SimpleTreat 4.0 wastewater treatment plant model, were used as input to the BST. The model predicted
groundwater concentrations of 3.2 |ig/L suggesting the biosolids land application containing 1,1-
dichloroethane with migration to groundwater is not an important source of general population exposure.
However, soil and pore water exposures to 1,1-dichloroethane from biosolids land application could
occur to ecological species and is presented in the subsequent sections below.
3.3.4.6 Modeled Concentrations in Wastewater Treatment Plant Sludge
Chemical substances in wastewater undergoing biological wastewater treatment may be removed from
the wastewater by processes including biodegradation, sorption to wastewater solids, and volatilization.
As discussed in Appendix D.2.5.2, 1,1-dichloroethane is expected to be removed in wastewater
treatment primarily by volatilization with little removal by biodegradation or sorption to solids.
Chemicals removed by sorption to sewage sludge may enter the environment when sewage sludge is
land applied following treatment to meet standards. The treated solids are known as biosolids.
The removal of a nonbiodegradable neutral organic chemical present in WWTP influent via sorption to
sludge is evaluated by considering its partitioning to sludge organic carbon.
Based on its Koc value of 31, 1,1-dichloroethane is not expected to significantly partition to sewage
sludge. Releases of 1,1-dichloroethane to wastewater treatment are expected to be low and disperse
across many sites, therefore, land application of biosolids containing 1,1-dichloroethane is not expected
to be a significant exposure pathway. To support this conclusion, range-finding estimates were made to
evaluate the concentrations of 1,1-dichloroethane in biosolids, in soil receiving biosolids, and soil pore
water concentrations resulting from biosolids application. Releases from wastewater treatment plants
with DMRs for 1,1-dichloroethane were reviewed to identify those plants discharging the highest
amount of 1,1-dichloroethane annually. The two highest releasing facilities were not chosen due to
errors or uncertainties in their release estimates. The site with the third largest estimated releases of 1,1-
dichloroethane to water was chosen and it was assumed that all biosolids generated at that facility were
land applied over a year at a single site. The releases from the facility were used to back-calculate input
to the SimpleTreat 4.0 wastewater treatment plant model to estimate the concentration of 1,1-
dichloroethane in biosolids. It was also assumed that the modeled site used activated sludge wastewater
treatment and that SimpleTreat 4.0 defaults were a reasonable representation of the activated sludge
treatment at the site. Using this loading data, the model predicted 1,1-dichloroethane concentration in
combined sludge of 20 mg/kg. Details on the procedure are provided in Appendix D.2.4.4.
3.3.4.6.1 Modeled Concentrations of 1,1-Dichloroethane jn Soil Receiving Biosolids
No information on the concentration of 1,1-dichloroethane in soil receiving biosolids was found.
To assess soil concentrations resulting from biosolid applications, EPA relied upon modeling work
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conducted in Canada (EC/HC. 2011). which used Equation 60 of the European Commission Technical
Guidance Document (TGD) (ECBi_2003). The concentration in sludge was set to 20 mg/kg dry weight
based on the combined sludge concentration estimated by SimpleTreat 4.0. Using these assumptions, the
estimated 1,1-dichloroethane soil concentrations after the first year of biosolids application were 29.4
ug/kg in tilled agricultural soil and 58.8 |ig/kg in pastureland. See Section 3.3.4.5 for discussion of the
estimation of biosolids concentrations.
The method assumes complete mixing of the chemical in the volume of soil it is applied to as well as no
losses from transformation, degradation, volatilization, erosion, or leaching to lower soil layers.
Additionally, it is assumed there is no input of 1,1-dichloroethane from atmospheric deposition and there
are no background 1,1-dichloroethane accumulations in the soil.
3.3.4.6.2 Modeled Concentrations of 1,1-Dichloroethane jn Soil Pore Water
Receiving Biosolids
To estimate soil pore water concentrations for 1,1-dichloroethane in soil receiving biosolids for
ecological species' exposures, EPA used a modified version of the equilibrium partitioning (EqP)
equation developed for weakly adsorbing chemicals such as 1,1-dichloroethane and other VOCs. The
modified equation accounts for the contribution of dissolved chemical to the total chemical
concentration in soil or sediment (Fuchsman, 2002). The equation assumes that the adsorption of
chemical to the mineral components of sediment particles is negligible.
Using Equation Apx D-l and estimating Cdissoived from the Kocfor 1,1-dichloroethane assuming a soil
organic carbon fraction (/oc) of 0.02, and a soil solids fraction of 0.5, the estimated pore water
concentrations are 18.2 pg/L in tilled agricultural soil and 36.6 pg/L in pastureland.
Table 3-21. Soil and Soil Pore Water Concentrations Estimated from Annual Application of
Biosolids
Exposure
Scenario
Combined Sludge
Concentration
(jig/kg)
Soil Type
Soil Concentration
(jug/kg)
Soil Pore Water
Concentration
(mg/L)
Waste Handling,
Treatment and
Disposal (POTW)
20,000
Tilled
agricultural
29.2
18.2
Pastureland
58.8
36.6
11 Modeled using SimpleTreat 4.0 wastewater treatment plant model.
3.3.5 Weight of Scientific Evidence Conclusions for Environmental Concentrations
3.3.5.1 Strengths, Limitations, and Sources of Uncertainty in Assessment Results for
Monitored and Modeled Concentrations
According to the Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Protocol (U.S.
EPA. 2024t). the selection of data and information are informed by the hierarchy of preferences, which
considers the use of both measured (monitoring) and estimated (modeled) data. Monitoring data from
both published literature and sampling databases provides strong evidence for the presence of 1,1-
dichloroethane in ambient air, surface water, and groundwater. EPA modeling of TSCA releases also
predicts presence in ambient air and surface water. Fate and physical-chemical properties provide
additional context; that is, high water solubility of 1,1-dichloroethane and low potential for hydrolysis
are factors that strengthen the evidence of 1,1-dichloroethane presence in water and the volatility of 1,1-
dichloroethane and low potential for photolysis provides evidence of its presence in air.
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Ambient and Indoor Air Monitored and Modeled Concentrations
EPA modeled air concentrations from TRI and NEI facility releases. The TRI and NEI data are reported
by facilities and state/county government entities and provide EPA with data on the level of 1,1-
dichloroethane being emitted into ambient air. EPA monitoring of HAPs via the AirToxic monitoring
program provides high quality data for the monitoring location. EPA has high confidence in the air
concentrations estimated from TRI and NEI release data using AERMOD. The Agency has high
confidence in the deposition concentrations estimated to land and water from TRI and NEI release data
using AERMOD. EPA has medium confidence in the air concentrations estimated from TRI release data
using IIOAC.
IIOAC estimates air concentrations at three pre-defined distances (100, 100 to 1,000, and 1,000 m). The
inherent distance limitations of IIOAC do not allow estimation of exposures closer to a facility (<100 m
from the facility) where higher exposures from fugitive releases would be expected. IIOAC uses
meteorological data from 14 pre-defined meteorological stations representing large regions across the
United States. This generalizes the meteorological data used to estimate exposure concentrations where
competing conditions can influence the exposure concentrations modeled upwind and downwind of a
releasing facility. To reduce the uncertainties associated with using regional meteorological data, EPA
conducted a sensitivity analysis of all 14 pre-defined meteorological stations to identify which two
within IIOAC tended to result in a high-end and central tendency estimate of exposure concentrations.
This maintained a more conservative exposure concentration estimate, which is then used in calculations
to estimate risks. This approach adds confidence to the findings by ensuring potential risks would be
captured under a high-end exposure scenario, while also providing insight into potential risks under a
less conservative exposure scenario (central tendency).
Indoor air concentrations within IIOAC are calculated by multiplying the modeled ambient air
concentrations by an indoor-outdoor ratio. In IIOAC, indoor-outdoor ratios of 0.65 and 1 are used for
the mean and high-end ratios, respectively. The indoor-outdoor ratio is influenced by many factors
including the characteristics of the building such as building footprint and architecture, interior sources
or sinks, physical form of the chemical substance (particulate or gas), HVAC system air flow rates, and
activity patterns such as how often are windows and doors opened, how the HVAC system is operated.
However, in many screening models, the indoor-outdoor ratio is set to a value of one, which represents
the upper bound of this ratio if there are no indoor sources, as it is the case for 1,1-dichloroethane.
Indoor air concentrations of 1,1-dichloroethane were measured in one study in the United States
(Lindstrom et al.. 1995) and concentrations were reported as not detected.
AERMOD is an EPA regulatory model and has been thoroughly peer reviewed; therefore, the general
confidence in results from the model is high but relies on the integrity and quality of the inputs used and
interpretation of the results. For the full analysis, EPA used releases reported to the TRI and NEI as
direct inputs to AERMOD. For 1,1-dichloroethane there were no reporting releases to TRI via a TRI
Form A (which is allowed for use by those facilities releasing less than 500 lbs of the chemical
reported). Furthermore, EPA conducted a multi-year analysis using 6 years of TRI and 2 years of NEI
data.
AERMOD uses the latitude/longitude information reported by each facility to TRI as the location for the
point of release. While this may generally be a close approximation of the release point for a small
facility (e.g., a single building), it may not represent the release point within a much larger facility.
Therefore, there is some uncertainty associated with the modeled distances from each release point and
the associated exposure concentrations to which fenceline communities may be exposed. The TRI
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reported data used for AERMOD do not include source-specific stack parameters that can affect plume
characteristics and associated dispersion of the plume. Therefore, EPA used pre-defined stack
parameters within IIOAC to represent stack parameters of all facilities modeled using each of these
methodologies. Those stack parameters include a stack height 10 m above ground with a 2-meter inside
diameter, an exit gas temperature of 300° Kelvin, and an exit gas velocity of 5 m/s (see Table 6 of the
IIOAC User Guide). These parameters were selected since they represent a slow-moving, low-to-the-
ground plume with limited dispersion that results in a more conservative estimate of exposure
concentrations at the distances evaluated. As such, these parameters may result in some overestimation
of emissions for certain facilities modeled. Additionally, the assumption of a 10x10 m area source for
fugitive releases may impact the exposure estimates very near a releasing facility (i.e., 10 m from a
fugitive release). This assumption places the 10-meter exposure point just off the release point that may
result in either an over or underestimation of exposure depending on other factors like meteorological
data, release heights, and plume characteristics. Contrary to the TRI reported data, the NEI reported data
used for AERMOD include source-specific stack parameters. Therefore, specific parameter values were
used in modeling, when available. When parameters were not available, and/or values were reported
outside of normal bounds, reported values were replaced using procedures outlined in Appendix D.3.
AERMOD modeled concentrations of releases from TRI reporting facilities ranged from 0 to 232 |ig/m3
(Table 3-9) with the maximum modeled concentration being one order of magnitude higher than the
maximum monitored concentration of 26 |ig/m3 from AMTIC (Table 3-8) and approximately four orders
of magnitude higher than the maximum concentration of 4.0 x 10~2 |ig/m3 measured in literature (Logue
et al.. 2010). Because the ranges of the ambient air modeled concentrations from AERMOD, reported
measured concentrations for ambient air found in the peer-reviewed and gray literature from the
systematic review (Logue et al.. 2010). and monitored concentrations from AMTIC displayed overlap,
EPA has high confidence in the modeled results.
As an example, Figure 3-20 shows the location of a 1,1-dichloroethane releasing facility as reported in
TRI and six AMTIC ambient air monitoring sites located within 10 km of the facility. AERMOD TRI
modeled concentrations of 1,1-dichloroethane and the corresponding years of monitoring data are listed
in Table 3-22. As shown in Table 3-22, modeled concentrations are within an order of magnitude with
the monitored 1,1-dichloroethane concentrations.
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211390004
211570021
211570016
211570020
42029WSTLK2468I
211570014
211570018
42029WSTLK2468I
Figure 3-20. Location of TRI Facility (TRI ID 42029WSTLK2468I, Yellow Dot) and AMTIC
Monitoring Sites within 10 km of the TRI Facility (Green Dots)
Table 3-22. Comparison of 1,1 -Dichloroethane AERMOD Modeled Concentrations for a TRI
Facility with 1,1 -Dichloroethane Ambient Air Monitoring Data from Six AMTIC Monitoring Sites
within 10 km of the Facility from 2015 to 2020
Facility TRI ID
Year
Lowest P95
Modeled
Concentration
(ppb)
Max 1 Day
Monitoring
Concentration
(ppb)
Distance from TRI
Facility to
Monitoring Site
(m)
Modeled -
Monitoring
Concentration
Difference
42029WSTLK2468I
2015
0.212
0.097
2,268
0.115
42029WSTLK2468I
2015
0.212
0.063
719
0.149
42029WSTLK2468I
2015
0.212
0.013
2,049
0.199
42029WSTLK2468I
2016
0.221
0.109
2,268
0.112
42029WSTLK2468I
2016
0.221
0.274
719
-0.053
42029WSTLK2468I
2016
0.221
0.228
2,049
-0.007
42029WSTLK2468I
2017
0.228
0.091
2,268
0.137
42029WSTLK2468I
2017
0.228
0.183
719
0.045
42029WSTLK2468I
2018
0.291
0.268
2,268
0.023
42029WSTLK2468I
2018
0.291
0.206
719
0.085
42029WSTLK2468I
2019
0.132
0.028
2,268
0.104
42029WSTLK2468I
2019
0.132
0.123
719
0.009
42029WSTLK2468I
2020
0.157
0.013
2,813
0.144
42029WSTLK2468I
2020
0.157
0.054
1,919
0.103
42029WSTLK2468I
2020
0.157
0.361
513
-0.204
AERMOD was used to model daily (g/m2/day) and annual (g/m2/year) deposition rates from air to land
and water from each TRI and NEI releasing facility. Based on physical and chemical properties of 1,1-
dichloroethane (Section 2.1), EPA considered only gaseous deposition. The Agency used chemical-
specific parameters as input values for AERMOD deposition modeling. Thus, EPA has high confidence
in the deposition rates estimated from TRI and NEI release data using AERMOD.
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Surface and Drinking Water Monitored and Modeled Concentrations
Unlike the example given above correlating ambient air modeling/monitoring, the available measured
surface water concentration data are poorly co-located with 1,1-dichloroethane facility release sites.
EPA relied primarily on modeling to estimate aqueous concentrations resulting from releases to surface
waters as reported in the EPA Pollutant Loading Tool. The tool compiles and makes public discharges
as reported in DMRs required in NPDES permits and provides data on the amount of 1,1-dichloroethane
in discharged effluent and the receiving waterbody. The evaluation of general population drinking water
exposure scenarios are impacted by uncertainties and assumptions surrounding inputs and the
approaches used for modeling surface water concentrations and estimation of the drinking water doses.
In Section 3.2.2, EPA assesses the overall confidence of estimated releases for various OESs. For those
OESs releasing to surface water, confidence is rated as moderate to robust depending on the individual
OES.
The modeling used, and the associated default and user-selected inputs can affect the overall strength in
evaluating exposures to the general population. The facility-specific releases methodology described in
Section 3.2.1, and the results in 3.3.3.2.2 rely on a modeling framework that does not consider
downstream fate. Drinking water estimates do account for downstream transport and treatment removal
processes, while concentration estimates to evaluate exposure to ecological species account for key
source/sink fate processes at the facility release site. To reduce uncertainties, EPA incorporated an
updated hydrologic flow network and flow data into this assessment that allowed a more site-specific
consideration of release location and associated receiving water body flows. However, these releases are
evaluated on a per facility basis that do not account for additional sources of 1,1-dichloroethane that
may be present in the evaluated waterways. Finally, drinking water exposures are not likely to occur
from the receiving water body at the point of facility-specific releases. Specifically, the direct receiving
water bodies may or may not be used as drinking water sources. To address this limitation, EPA
evaluated the proximity of known 1,1-dichloroethane releases to known drinking water sources as well
as known drinking water intakes as described in Section 3.3.3.6.
The measured data encompassed both ambient surface water monitoring as well as drinking water
system monitoring data. For ambient surface water, data is limited geographically and temporally, with
many states having no reported data, and even those areas reporting measured values having limited
samples over time. Monitored concentrations near modeled releases were rare, often making direct
comparisons of modeled results unavailable. In most cases, monitoring data represented waterbodies
without identified releases of 1,1-dichloroethane nearby. To an extent, monitoring data in finished
drinking water data provided a comparison for the low-range of modeled concentrations at individual
PWS, although it is important to recognize that even this comparison is weak given the poor temporal
alignment between modeled and measured concentrations of 1,1-dichloroethane in drinking water.
At the higher end, the modeled surface water concentrations of 1,1-dichloroethane from facility releases
are several orders of magnitude greater than those observed in the 1,1-dichloroethane monitoring data
(Figure 3-8). All measured concentrations in surface waters acquired from the WQP fall below 2 (J,g/L,
with 95 percent of the concentrations below 0.5 (J,g/L. In comparison, the median of 1,1-dichloroethane
concentrations in surface waters (based on 30Q5 hydrologic values) was approximately 50 (J,g/L.
Validation of facility-specific 1,1-dichloroethane surface water concentration estimates is not available
as EPA did not identify monitoring data associated spatially and temporally to facility-specific releases.
There are a few reasons that can help explain why higher aqueous concentrations of 1,1-dichloroethane
were modeled in comparison to those that have been observed from measured samples. The locations
where measurements were taken could have been collected further downstream or on-stream segments
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not impaired by facility releases of 1,1-dichloroethane. In addition, many of the facilities release into
very small streams or industrial canals, which can elevate modeled concentration at the point of release
when release amounts are high. As this water travels downstream, it is expected to eventually join with
larger waterbodies, where some decrease in concentration due to dilution would be expected to occur.
Measured concentrations of 1,1-dichloroethane in finished drinking water from the UCMR3 and state
database were compared to 30Q5-based model estimates for individual PWSs where co-located data
were available. It is important to note, however, both the timing and location of release and sample
collection must align to make a true comparison of the modeled versus measured results. Thus, the
comparison described herein provides a broader sense of agreement. For the low range of modeled
drinking water estimates (<1 to 5 (J,g/L), there was a strong agreement with measured data from UCMR3
data, provided these results were all less than 1 (J,g/L.
To further refine the possible distribution and concentrations of 1,1-dichloroethane between water
column, benthic pore water and sediment, EPA used the PSC to estimate 1,1-dichloroethane
concentrations in the corresponding media resulting from TSCA releases. PSC is a thoroughly reviewed
modeling tool developed and maintained by the EPA, and so the confidence in the tool's ability to
estimate accurate concentrations is robust. In addition, estimates of water column concentrations and
surface water concentrations are closely aligned, demonstrating that PSC is an appropriate tool for 1,1-
dichloroethane concentration estimates in aqueous environments. Benthic pore water and sediment
concentrations of 1,1-dichloroethane were estimated using physical chemical properties such as log Koc,
a measure of chemical adsorption to organic materials such as sediment or soils. EPA has robust
confidence in estimates of 1,1-dichloroethane concentrations in benthic pore water and sediments.
Land Pathway (Soils, Groundwater, and Biosolids)
As 1,1-dichloroethane is a chlorinated solvent with decades of use in U.S. chemical manufacturing, there
is evidence that previous releases or disposal resulted in concentrations of 1,1-dichloroethane in
groundwater. However, current reported releases to landfills are not anticipated to result in any
measurable 1,1-dichloroethane groundwater concentrations. Uncertainties and limitations are inherent in
the modeling of groundwater concentrations from disposing chemical substances into poorly managed
RCRA Subtitle D landfills as well as those that are not regulated as closely. These uncertainties include,
but are not limited to, (1) determining the total and leachable concentrations of waste constituents, (2)
estimating the release of pollutants from the waste management units to the environment, and (3)
estimating and transport of pollutants in a range of variable environments by process that often are not
completely understood or are too complex to quantify accurately. To address some of these uncertainties
and add strength to the assessment, EPA considered multiple loading rates and multiple leachate
concentrations. These considerations add value to estimate exposure that falls at an unknown percentile
of the full distribution of exposures. The DRAS model is based on a survey of drinking water wells
located downgradient from a waste management unit (U.S. EPA. 1988). Due to the age of the survey, it
is unclear how the survey represents current conditions and proximity of drinking water wells to
disposal units. Similarly, it is not clear if the surveyed waste management units are representative of
current waste management practices.
Based on NEI data, 1,1-dichloroethane is reported to be emitted from several landfills, which also report
methane as an indicator of anaerobic activity and degradation. Those landfills reporting measured
anaerobic activity presumably emit 1,1-dichloroethane as an anaerobic degradant of 1,1,1-
trichloroethane - containing materials disposed in landfills. EPA therefore has moderate confidence in
estimates of 1,1-dichloroethane in groundwater from TSCA releases.
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EPA did estimate additional possible media for 1,1-dichloroethane exposures, specifically, via air
deposition from air releases and releases from POTWs via land application of biosolids. These media
concentrations are further used for ecological species exposure estimates (Section 4.1.4) and for limited
general population exposures (Appendix G). Given the lack of soil and biosolids monitoring data, and
the reliance on estimates based on reported releases and assumptions of POTW biosolids use in land
application, EPA has a moderate confidence conclusion in the presence of 1,1-dichloroethane in
biosolids/soils.
Table 3-23 presents a summary of the weight of scientific evidence conclusions for each of the media
concentrations considered in environmental and human exposures to 1,1-dichloroethane. Evidence for
1,1-dichloroethane presence in each media is most dependent on the releases reported in TRI and NEI
for ambient air, TRI and DMR for surface water, and TRI for releases to land. The confidence in these
releases is reported in Table 3-7 and presented in Table 3-23.
Table 3-23. Confidence and Weight of Scientific Evidence per OES for 1,1-Dichlorethane
Concentration in Media
OES
Media
Confidence
for Releases
Measured/
Monitoring
Confidence
Level
Modeling/
Estimation
Confidence
Level
Measured/
Modeling
Comparison
Overall
Confidence
Manufacturing
Ambient air
Moderate to
robust
++
+++
++
Robust
Indoor air
Moderate to
robust
+
++
+
Moderate
Surface water
Moderate to
Robust
++
+++
++
Robust
Land
Moderate to
Robust
+
++
N/A
Moderate
Processing as a
reactive
intermediate
Ambient air
Moderate to
Robust
++
+++
++
Robust
Indoor air
Moderate to
robust
+
++
+
Moderate
Surface water
Moderate to
Robust
++
+++
++
Robust
Land
Moderate to
Robust
+
++
N/A
Moderate
Processing -
repackaging
Ambient air
Moderate to
Robust
++
+++
++
Robust
Surface water
Moderate to
Robust
++
+++
++
Robust
Land
Moderate to
Robust
+
++
N/A
Moderate
Commercial use
as a lab chemical
Ambient air
Moderate
-
++
N/A
Moderate
Surface water
Moderate
-
++
N/A
Moderate
Land
Moderate
-
++
N/A
Moderate
General waste
handling,
treatment, and
disposal
Ambient air
Moderate to
Robust
++
+++
++
Robust
Indoor air
Moderate to
robust
+
++
+
Moderate
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OES
Media
Confidence
for Releases
Measured/
Monitoring
Confidence
Level
Modeling/
Estimation
Confidence
Level
Measured/
Modeling
Comparison
Overall
Confidence
Surface water
Moderate to
Robust
+++
Robust
Land
Moderate to
Robust
N/A
Moderate
Waste handling,
treatment, and
disposal (POTW)
Surface water
Moderate to
Robust
+++
Robust
Land
Moderate to
Robust
N/A
Moderate
Waste handling,
treatment, and
disposal
(remediation)
Surface water
Moderate to
Robust
+++
Robust
Land
Moderate to
Robust
N/A
Moderate
+ + + Robust confidence suggests the supporting weight of scientific evidence outweighs the uncertainties to the point
where it is unlikely that the uncertainties could have a significant effect on the media concentration estimate.
+ + Moderate confidence suggests the supporting scientific evidence weighed against the uncertainties is reasonably
adequate to characterize the media concentration estimates.
+ Slight confidence is assigned when the weight of scientific evidence may not be adequate to characterize the
scenario, and when the assessor is making the best scientific assessment possible in the absence of complete
information. There are additional uncertainties that may need to be considered.
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4.1.1 Approach and Methodology
The major environmental compartments for 1,1-dichloroethane exposures to ecological receptors are
surface water and air (see Section 2.2.2). EPA assessed 1,1-dichloroethane exposures via surface water,
sediment, soil, and air, which were used to determine risks to aquatic and terrestrial species (see Section
4.3). Ambient air is assessed for its contribution via deposition to soil.
Environmental Exposures (Section 4.1):
Key Points
EPA evaluated the reasonably available information for environmental exposures of 1,1-
dichloroethane to aquatic and terrestrial species. The key points of the environmental exposure
assessment are summarized below:
• EPA expects the main environmental exposure pathways for 1,1-dichloroethane to be
surface water and air. The ambient air exposure pathway was assessed for its contribution
via deposition to soil.
• 1,1-Dichloroethane exposure to aquatic species through surface water and sediment were
modeled to estimate concentrations near industrial and commercial uses.
o Modeled data based on number of operating days per year estimate surface water
concentrations range from 0.7 to 85 |ig/L, benthic pore water concentrations range
from 0.55 to 78 |ig/L, and sediment concentrations range from 0.85 to 124 |ig/kg
from facility releases to surface waters.
o EPA also estimated fish tissue and crayfish tissue concentrations by COU using the
modeled water releases from industrial uses.
• 1,1-Dichloroethane exposure to terrestrial species through soil, surface water, and sediment
was also assessed using modeled data.
o Exposure through diet was assessed through a trophic transfer analysis, which
estimated the transfer of 1,1-dichloroethane from soil through the terrestrial food web
and from surface water and sediment through the aquatic food web using
representative species.
o 1,1-Dichloroethane exposure to terrestrial organisms occurs primarily through diet
via the surface water pathway for semi-aquatic terrestrial mammals, with release of
1,1-dichloroethane to surface water as a source and via the soil pathway for terrestrial
mammals. Deposition from air to soil and land-applied biosolids are also sources of
1,1-dichloroethane.
o For terrestrial mammals and birds, relative contribution to total exposure associated
with inhalation is generally secondary in comparison to exposures by diet and
indirect ingestion. Therefore, direct inhalation exposure of 1,1-dichloroethane to
terrestrial receptors via air was not assessed quantitatively.
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EPA used two models, PSC and AERMOD, to assess the environmental concentrations resulting from
the industrial and commercial release estimates (Section 3.2). Additional information on these models is
available in Section 3.3. EPA modeled 1,1-dichloroethane surface water, benthic pore water, and
sediment concentrations using PSC as described in Section 3.3. EPA modeled 1,1-dichloroethane
concentrations in soil via air deposition near facility (10 m from the source) as described in Section
3.3.4.1. The distance of 10 m from source was selected as the most conservative scenario, as the highest
concentrations occurred at this distance. Modeled surface water, sediment, and benthic pore water
concentrations were used to assess 1,1-dichloroethane exposures to aquatic species.
EPA used calculated soil concentrations to assess risk to terrestrial species via trophic transfer (see
Section 4.1.4). Specifically, EPA based trophic transfer of 1,1-dichloroethane and potential risk to
terrestrial animals on modeled air deposition to soil from AERMOD as well as estimated biosolids land
application. Potential risk to aquatic dependent wildlife used surface water and benthic pore water
concentrations modeled via PSC for each COU in combination with 1,1-dichloroethane fish and crayfish
concentrations, respectively, using the estimated BCFs shown in Table 2-2. Exposure factors for
terrestrial organisms used within the trophic transfer analyses are presented in Section 4.1.4. Application
of exposure factors and hazard values for organisms at different trophic levels is detailed within Section
4.3 and used equations described in the U.S. EPA Guidance for Developing Ecological Soil Screening
Levels (U.S. EPA. 2005a).
4.1.2 Exposures to Aquatic Species
4.1.2.1 Measured Concentrations in Aquatic Species
There are very limited data available on 1,1-dichloroethane concentrations in fish or other aquatic biota.
Only one study was identified where 1,1-dichloroethane was detected, in oysters in Lake Pontchartrain
(33 ng/g) (Ferrario et al.. 1985). Other similar chlorinated solvents, including 1,1,1-trichloroethane, 1,2-
dichloroethane, and trichloroethylene reported concentrations in bivalves between 0.6 and 310 ng/g.
(Gotoh et al.. 1992; Ferrario et al.. 1985). No reasonably available data on 1,1-dichloroethane
concentrations in fish tissue were identified; however, data in fish muscle and liver tissue for other
chlorinated solvents range from 0.51 to 4.89 ng/g for 1,1,1-trichloroethane and 0.36 to 29.3 ng/g
trichloroethylene (Roose and Brinkman. 1998). Therefore, 1,1-dichloroethane concentrations in fish and
crayfish were calculated as described below to estimate exposure.
4.1.2.2 Calculated Concentrations in Aquatic Species
EPA used PSC to estimate maximum daily average 1,1-dichloroethane surface water, benthic pore water
and sediment concentrations as described in Section 3.3.3.2 and Section 3.3.3.4. The days of exceedance
modeled in PSC are not necessarily consecutive and could occur throughout a year at different times.
Days of exceedance is calculated as the probability of exceedance multiplied by the total modeled days
of release as described in Appendix 11.
EPA calculated 1,1-dichloroethane concentrations in fish and crayfish for each industrial and
commercial release scenario (TableApx 1-5 and TableApx 1-6). The highest calculated concentrations
of 1,1-dichloroethane in fish and crayfish were 590 ng/g and 550 ng/g, respectively, for the
manufacturing OES with the lowest calculated concentrations as 4.5 ng/g and 3.8 ng/g for fish and
crayfish, respectively for the OES commercial use as a laboratory chemical. These calculated
concentrations are similar to the 1,1-dichloroethane concentration reported in oysters (Ferrario et al..
1985) and the highest reported concentrations of other chlorinated solvents in fish tissues (Roose and
Brinkman. 1998). Concentrations of 1,1-dichloroethane in fish were calculated by multiplying the
maximum PSC modeled surface water concentrations based on the number of operating days per year
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for each industrial and commercial release scenario (Table 3-3) by the EPI Suite™-generated BCF of 7
(Table 2-2). Similarly, concentrations of 1,1-dichloroethane in crayfish were calculated by multiplying
the maximum PSC modeled benthic pore water concentrations based on the number of operating days
per year for each industrial and commercial release scenario (Table 3-3) by the estimated BCF. These
whole fish and crayfish 1,1-dichloroethane concentrations were utilized within the screening level
assessment for trophic transfer described in Section 4.1.4.
4.1.3 Exposures to Terrestrial Species
4.1.3.1 Measured Concentrations in the Terrestrial Environment
No reasonably available data on 1,1-dichloroethane concentrations in terrestrial biota were identified.
One study of urban rats in Oslo, Norway tested for but did not detect any related chlorinated solvents
such as 1,2-dichloroethane in the livers of rats (detection limit of 20 ng/g dry weight) (COWI AS. 2018).
4.1.3.2 Modeled Concentrations in the Terrestrial Environment
In general, for terrestrial mammals and birds, relative contribution to total exposure associated with
inhalation is secondary in comparison to exposures by diet and indirect ingestion. EPA has
quantitatively evaluated the relative contribution of inhalation exposures for terrestrial mammals and
birds in previous peer-reviewed Guidance for Developing Ecological Soil Screening Levels (Eco-SSLs)
(U.S. EPA. 2003a. b). For 1,1-dichloroethane, other factors that guided EPA's decision to qualitatively
assess 1,1-dichloroethane inhalation exposure to terrestrial receptors at a population level were: limited
facility releases and the lack of 1,1-dichloroethane inhalation hazard data in terrestrial mammals for
ecologically relevant endpoints. Air deposition to soil modeling is described in Section 3.3.4.1. EPA
determined the primary exposure pathway for terrestrial organisms is through soil via dietary uptake and
incidental ingestion. As described in Section 3.3.4.1, IIOAC and subsequently AERMOD were used to
assess the estimated release of 1,1-dichloroethane to soil via air deposition 10 m from the facility (Table
3-17) from fugitive emissions reported to TRI. Air deposition of 1,1-dichloroethane to soil based on
fugitive and/or stack emissions reported to NEI or modeled in generic scenarios was assessed
qualitatively for exposure to terrestrial receptors since the modeled annual maximum 95th percentile
(NEI) or high-end (generic scenario) air concentrations of 1,1-dichloroethane at 10 m from these sources
were less than or approximately equal to that of the modeled 1,1-dichloroethane annual maximum 95th
percentile air concentrations resulting from TRI-reported fugitive emissions at 10 m from releasing
facilities (Table 3-8, Table 3-12 , Table 3-13). Annual application of biosolids were also considered as a
potential source of 1,1-dichloroethane in soil as described in Section 3.3.4.6.1 (Table 3-18). Resulting
soil pore water concentrations from daily air deposition or annual biosolids land application were
calculated as described in Section 3.3.4.6.2.
Terrestrial plants were assessed for exposure to 1,1-dichloroethane soil pore water concentrations as
described in Section 4.3.3, and 1,1-dichloroethane soil and soil pore water concentrations were used for
estimating dietary exposure through trophic transfer as described in Section 4.3.4. For trophic transfer,
EPA assumed 1,1-dichloroethane concentrations in dietary species Trifolium sp. as equal to the 1,1-
dichloroethane maximum soil pore water concentrations for daily air deposition to soil (TableApx 1-7)
or biosolids land application of 1,1-dichloroethane (Table Apx 1-10) and in earthworms as equal to the
aggregate of maximum soil and soil pore water concentrations from daily air deposition of 1,1-
dichloroethane (Table Apx 1-7) or biosolids land application of 1,1-dichloroethane (Table Apx 1-10).
The highest concentrations of 1,1-dichloroethane resulting from air deposition to soil in Trifolium sp.
and earthworms were 0.15 mg/kg and 0.38 mg/kg, respectively, for the manufacturing OES. The highest
concentrations of 1,1-dichloroethane resulting from biosolids application to pastureland in Trifolium sp.
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and earthworms were 3.7x10 2 mg/kg and 9.5x10 2 mg/kg, respectively, for the waste handling,
treatment and disposal (POTW) OES, which was the only OES with this environmental release pathway.
4.1.4 Trophic Transfer Exposure
4.1.4.1 Trophic Transfer (Wildlife)
Trophic Transfer is the process by which chemical contaminants can be taken up by organisms through
dietary and media exposures and be transferred from one trophic level to another. EPA has assessed the
available studies collected in accordance with the Draft Systematic Review Protocol Supporting TSCA
Risk Evaluations for Chemical Substances (U.S. EPA. 2021b) and Draft Risk Evaluation for 1,1-
Dichloroethane - Systematic Review Protocol (U.S. EPA. 2024t) relating to the biomonitoring of 1,1-
dichloroethane.
1,1-Dichloroethane is released to the environment by multiple exposure pathways (see Figure 2-1). The
primary exposure pathway for terrestrial mammals and birds is through diet. On land, deposition of 1,1-
dichloroethane from air to soil and application of biosolids are the primary exposure pathways for
dietary exposure to terrestrial mammals, whereas the primary exposure pathway for water is releases
from facilities. Benthic pore water 1,1-dichloroethane concentrations determined by VVMW-PSC
modeling based on the COU/OES-specific number of operating days per year (Table 3-3) are
approximately equal to surface water concentrations across all COUs (see Section 3.3.3.4.2), indicating
that the exposure to 1,1-dichloroethane through the aquatic dietary exposure pathway for higher trophic
levels will occur from consumption of organisms in the water column or in the sediment.
Representative mammal species are chosen to connect the 1,1-dichloroethane transport exposure
pathway via terrestrial trophic transfer. Uptake of contaminated soil pore water is connected by the
representative plant Trifolium sp. to the representative herbivorous mammal meadow vole (Microtus
pennsylvanicas). The meadow vole was selected to represent herbivores as the majority of its diet
consists of plant matter, it is a native North American species, and it is a similar size to the small
mammals used to derive the TRV. Trifolium sp. was selected as the representative plant because plants
of this genus comprise a significant portion of the meadow vole diet (Lindroth and Batzli. 1984). Uptake
of aggregated contaminated soil and soil pore water is connected by the representative soil invertebrate
earthworm (Eisenia fetida) to the representative insectivorous mammal, short-tailed shrew {Blarina
brevicauda). The short-tailed shrew was selected to represent insectivores as it is highly insectivorous, it
is a native North American species, and it is a similar size to the small mammals used to derive the
TRV. The earthworm was selected as the representative soil invertebrate because earthworms and other
annelids comprise a significant portion of the short-tailed shrew diet (U.S. EPA. 1993b).
Meadow voles primarily feed on plant shoots with a preference for dicot shoots in the summer and fall.
When green vegetation is not available, meadow voles will feed on other foods such as seeds and roots
and are therefore representative herbivorous terrestrial mammals for use in trophic transfer. Depending
on the location and season, dicot shoots may comprise 12 to 66 percent of the meadow vole's diet (U.S.
EPA. 1993b). Short-tailed shrews primarily feed on invertebrates with earthworms comprising
approximately 31 percent (stomach volume) to 42 percent (frequency of occurrence) of their diet and are
therefore representative insectivorous terrestrial mammals for use in trophic transfer. The calculations
for assessing 1,1-dichloroethane exposure from soil uptake by plants and earthworms and the transfer of
1,1-dichloroethane through diet to higher trophic levels are presented in Section 4.3.1.1 as well as and
biota concentrations shown in TableApx 1-7 and TableApx 1-10. Because surface water sources for
wildlife water ingestion are typically ephemeral, the trophic transfer analysis for terrestrial organisms
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assumed 1,1-dichloroethane exposure concentration for wildlife water intake are equal to soil
concentrations for each corresponding exposure scenario.
The representative semi-aquatic terrestrial species is the American mink (Mustela vison), which has a
highly variable diet depending on their habitat. In a riparian habitat, American mink derive 74 to 92
percent of their diet from aquatic organisms, which includes fish, crustaceans, birds, mammals, and
vegetation (Alexander. 1977). Similar to soil concentrations used for terrestrial organisms, the highest
modeled surface water and benthic pore water 1,1-dichloroethane concentration across exposure
scenarios were used as surrogates for the 1,1-dichloroethane concentration found in the American
mink's diet in the form of both water intake and a diet of either fish (bioconcentration from surface
water) or crayfish (bioconcentration from benthic pore water). For trophic transfer, fish and crayfish
concentrations shown in TableApx 1-5 and TableApx 1-6, respectively, are used in conjunction with
trophic transfer calculations provided below in Section 4.3.1.1.
4.1.4.2 Trophic Transfer (Dietary Exposure)
EPA conducted screening level approaches for aquatic and terrestrial risk estimation based on exposure
via trophic transfer using conservative assumptions for factors such as area use factor as well as 1,1-
dichloroethane absorption from diet, soil, sediment, and water. This chlorinated solvent has releases to
aquatic and terrestrial environments as shown in Figure 2-1 and Table 3-6. Due to lack of reasonably
available measured data, a BCF of 7 for 1,1-dichloroethane was estimated using EPI Suite™ (U.S. EPA.
2012c). Section 4.1.2.2 reports estimated concentrations of 1,1-dichloroethane within representative fish
and crayfish tissue based the estimated BCF. A screening level analysis was conducted for trophic
transfer, which employs a combination of conservative assumptions (i.e., conditions for several exposure
factors included within Equation 4-lbelow) and utilization of the maximum values obtained from
modeled and/or monitoring data from relevant environmental compartments.
Following the basic equations as reported in Chapter 4 of the U.S. EPA Guidance for Developing
Ecological Soil Screening Levels (U.S. EPA. 2005a). wildlife receptors may be exposed to contaminants
in soil by two main pathways: incidental ingestion of soil while feeding, and ingestion of food items that
have become contaminated due to uptake from soil. The general equation used to estimate dietary
exposure via these two pathways is provided below (Equation 4-1) and was adapted to also include
consumption of water contaminated with 1,1-dichloroethane, and for semi-aquatic mammals, incidental
ingestion of sediment instead of soil (see also Table 4-1).
Exposure factors for food intake rate (FIR) and water intake rate ( Will) were sourced from the EPA's
Wildlife Exposure Factors Handbook (U.S. EPA. 1993b). and the exposure factor for sediment intake
rate (SIR) was sourced from the EPA's Second Five Year Review Report Hudson River PCBs Superfund
Site Appendix 11 Human Health and Ecological Risks (U.S. EPA. 2017a). The proportion of total food
intake that is soil (Ps) is represented at the 90th percentile for representative taxa (short-tailed shrew and
meadow vole) and was sourced from calculations and modeling in EPA's Guidance for Developing
Ecological Soil Screening Levels (U.S. EPA. 2005a). The proportion of total food intake that is sediment
(Ps) for representative taxa (American mink) was calculated by dividing the sediment ingestion rate
(SIR) by food consumption which was derived by multiplying the FIR by the body weight of the mink
(sourced from Wildlife Exposure Factors Handbook (U.S. EPA. 1993b). The SIR for American mink
was sourced from calculations in EPA's Second Five Year Review Report Hudson River PCBs
Superfund Site Appendix 11 Human Health and Ecological Risks (U.S. EPA. 2017a).
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Equation 4-1.
IDE] J = ([.SJ * P_s * FIR * AF_sj ] + [WJ * lAF] _wj * WIR] + [£_(/
= 1 )AJV B_ij * P_i * FIR * AF Jj ]) * AUF
Where:
DEj =
Sj =
Ps =
SIR =
FIR =
AFSJ =
Wj =
AFWj =
WIR =
N
Bij =
Pt =
AFij =
AUF =
Dietary exposure for contaminant (j) (mg/kg-body weight [bw]/day)
Concentration of contaminant (j) in soil or sediment (mg/kg dry weight)
Proportion of total food intake that is soil or sediment (kg soil/kg food;
SIR/[(FIR)(bw)])
Sediment intake rate (kg of sediment [dry weight] per day)
Food intake rate (kg of food [dry weight] per kg body weight per day)
Absorbed fraction of contaminant (j) from soil or sediment (s) (for screening
purposes set equal to 1)
Concentration of contaminant (j) in water (mg/L); assumed to equal soil pore
water concentrations for the purposes of terrestrial trophic transfer
Absorbed fraction of contaminant (j) from water (w) (for screening purposes set
equal to 1)
Water intake rate (kg of water per kg body weight per day)
Number of different biota type (i) in diet
Concentration of contaminant (j) in biota type (i) (mg/kg dry weight)
Proportion of biota type (i) in diet
Absorbed fraction of contaminant (j) from biota type (i) (for screening
purposes set equal to 1)
Area use factor (for screening purposes set equal to 1)
Table 4-1. Terms and Values Used to Assess Potential Trophic Transfer of 1,1-Dichloroethane for
Term
Earthworm
{Eisenia fetida)
Short-Tailed Shrew
(Blarina brevicauda)
Trifolium sp.
Meadow Vole
{Microtus
pennsylvanicus)
American Mink
(Mustela vison)
Ps
1
0.03°
1
0.032°
5.35E-04*
FIR
1
0.555c
1
0.325c
0.22°
AF,
1
1
1
1
1
P,
1
1
1
1
1
WIR
1
0.223c
1
0.2F
0.105c
AFWJ
1
1
1
1
1
AF,,
1
1
1
1
1
SIR
N/A
N/A
N/A
N/A
1.20E-04rf
bw
N/A
N/A
N/A
N/A
1.0195 kge
N
1
1
1
1
1
AUF
1
1
1
1
1
Highest values based on air deposition
s/
0.382 mg/kgg 1,1-
dichloroethane
0.382 mg/kgg
1,1-dichloroethane
0.146 mg/kg'1
1,1-dichloroethane
0.382 mg/kgg
1,1-dichloroethane
N/A
II'
0.382 mg/kgg 1,1-
dichloroethane
0.382 mg/kgg
1,1-dichloroethane
0.146 mg/kg'1
1,1-dichloroethane
0.382 mg/kgs
1,1-dichloroethane
N/A
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Term
Earthworm
(Eisenia fetida)
Short-Tailed Shrew
(Blarina brevicauda)
Trifolium sp.
Meadow Vole
{Microtus
pennsylvanicus)
American Mink
(Mustela vison)
By
0.382 mg/kg g 1,1-
dichloroethane
(soil and soil pore
water)
0.382 mg/kg
1,1-dichloroethane
(worm)
0.146 mg/kg'1
1,1-dichloroethane
(soil pore water)
0.146 mg/kg
1,1-dichloroethane
(plant)
N/A
Highest values based on biosolid land application
s/
0.095 mg/kgg 1,1-
dichloroethane
0.095 mg/kgg
1,1-dichloroethane
0.037 mg/kg'1
1,1-dichloroethane
0.095 mg/kgg
1,1-dichloroethane
N/A
II'
0.095 mg/kgg
1,1-dichloroethane
0.095 mg/kgg
1,1-dichloroethane
0.037 mg/kg'1
1,1-dichloroethane
0.095 mg/kgg
1,1-dichloroethane
N/A
By
0.095 mg/kgs
1,1-dichloroethane
(soil and soil pore
water)
0.095 mg/kg
1,1-dichloroethane
(worm)
0.037 mg/kg'1
1,1-dichloroethane
(soil pore water)
0.037 mg/kg
1,1-dichloroethane
(plant)
N/A
Highest values based on release to surface water
s/
N/A
N/A
N/A
N/A
0.12 mg/kg'
1,1-dichloroethane
II'
N/A
N/A
N/A
N/A
0.085 mg/L'
1,1-dichloroethane
By
N/A
N/A
N/A
N/A
0.59 mg/kg4'
1,1-dichloroethane
(fish)
0.55 mg/kg'
1,1-dichloroethane
(crayfish)
" Soil ingestion as proportion of diet represented at the 90th percentile sourced from EPA's Guidance for Developing
Ecological Soil Screening Levels (U.S. EPA. 2005a)
b Sediment ingestion as proportion of diet, calculated by dividing the SIR by kg food, where kg food = FIR multiplied by
body weight (bw) of the mink
c Exposure factors (FIR and WIR) sourced from EPA's Wildlife Exposure Factors Handbook (U.S. EPA. 1993b)
d Exposure factor (SIR) sourced from EPA's Second Five Year Review Report Hudson River PCBs Superfund Site
Appendix 11 Human Health and Ecological Risks (U.S. EPA. 2017a)
e Mink bodv weieht used to calculate P„ sourced from EPA's Wildlife Exposure Factors Handbook (U.S. EPA. 1993b)
' 1,1-Dichloroethane concentration in aggregated soil and soil pore water for earthworm, short-tailed shrew, and meadow
vole; 1,1-Dichloroethane concentration in soil pore water for Trifolium sp.; 1,1-Dichloroethane concentration in sediment
for mink
g Highest modeled aggregated soil and soil pore water concentration of 1,1-dichloroethane calculated based on AERMOD
modeling (daily deposition) for fugitive air 1,1-dichloroethane releases reported to TRI for the COU/OES Manufacturing
of 1,1-dichloroethane. Concentration of contaminant in water assumed to be equal to this concentration
h Highest modeled soil pore water concentration of 1,1-dichloroethane calculated based on AERMOD modeling (daily
deposition) for fugitive air 1,1-dichloroethane releases reported to TRI for the COU/OES Manufacturing of 1,1-
dichloroethane. Concentration of contaminant in water assumed to be equal to this concentration
' Highest sediment concentration of 1,1-dichloroethane obtained using PSC modeling
'Highest surface water concentration of 1,1-dichloroethane obtained using PSC modeling
k Highest fish concentration (mg/kg) calculated from highest surface water concentration of 1,1-dichloroethane (PSC) and
estimated BCF of 7 (U.S. EPA 2012c)
'Highest crayfish concentration (mg/kg) calculated from highest benthic pore water concentration of 1,1-dichloroethane
(PSC) and estimated BCF of 7 (U.S. EPA 2012c)
3550
3551 As illustrated in Figure 4-1, representative mammal species were chosen to connect (1) the 1,1-
3552 dichloroethane transport exposure pathway via trophic transfer of 1,1-dichloroethane uptake from
3553 contaminated soil and soil pore water to earthworm followed by consumption by an insectivorous
3554 mammal (short-tailed shrew); and (2) 1,1-dichloroethane uptake from contaminated soil pore water to
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plant (Trifolium sp.) followed by consumption by an herbivorous mammal (meadow vole). For semi-
aquatic terrestrial species, a representative mammal (American mink) was chosen to connect the 1,1-
dichloroethane transport exposure pathway via trophic transfer from fish or crayfish uptake of 1,1-
dichloroethane from contaminated surface water and benthic pore water.
At the screening level, one conservative assumption is that the invertebrate diet for the short-tailed
shrew comprises 100 percent earthworms from contaminated soil. Similarly, the dietary assumption for
the meadow vole is 100 percent Trifolium sp. from contaminated soil. For mink, in one scenario 100
percent of the American mink's diet is predicted to come from fish, and in the second scenario 100
percent of the American mink's diet is predicted to come from crayfish. Additionally, the screening
level analysis uses the highest modeled 1,1-dichloroethane soil, soil pore water, surface water, or benthic
pore water contaminate levels based on daily air deposition or annual biosolids land application (soil and
soil pore water) as well as the COU/OES-specific number of operating days per year for surface water
releases (surface water, benthic pore water, and sediment) to determine whether a more detailed
assessment is required. Because surface water sources for terrestrial wildlife water ingestion are
typically ephemeral, the trophic transfer analysis for the short-tailed shrew and meadow vole assumed
1,1-dichloroethane exposure concentration for wildlife water intake are equal to aggregated soil and soil
pore water concentrations for each corresponding exposure scenario.
The highest soil and soil porewater concentrations calculated based on AERMOD daily air deposition
for the COU/OES described in TableApx 1-7 or annual biosolids land application for the COU/OES
described in Table Apx 1-10 were used to represent 1,1-dichloroethane concentrations in media for
terrestrial trophic transfer. Similarly, the highest PSC-modeled surface water and sediment
concentrations over the operating days per year for the COU/OES described in Table Apx 1-5 and
Table Apx 1-6 were used to represent 1,1-dichloroethane concentrations in media for trophic transfer to
a semi-aquatic mammal (mink). Additional assumptions for this analysis have been considered to
represent conservative screening values (U.S. EPA. 2005a). Within this model, incidental oral soil or
sediment exposure is added to the dietary exposure (including water consumption) resulting in total oral
exposure to 1,1-dichloroethane. In addition, EPA assumes that 100 percent of the contaminant is
absorbed from both the soil (AFSj), water {AFWJ) and biota representing prey (Aluj). The proportional
representation of time an animal spends occupying an exposed environment is known as the area use
factor (AUF) and has been set at 1 for all biota within this equation (Table 4-1). Values for calculated
dietary exposure by COU are shown in Table Apx 1-11 and Table Apx 1-12 for trophic transfer to
shrew and vole from air deposition of 1,1-dichloroethane to soil; Table Apx 1-13 and Table Apx 1-14
for trophic transfer to shrew and vole from biosolids land application of 1,1-dichloroethane to soil; and
Table Apx 1-7 and Table Apx 1-8 for trophic transfer to mink consuming fish and crayfish. In each
trophic transfer scenario for concentrations resulting from air deposition to soil, the manufacturing OES
results in the highest biota concentrations and dietary exposure (Appendix 1.2). The waste handling,
treatment, and disposal (POTW) OES was the only OES with releases to soil via biosolid land
application. In each trophic transfer scenario for this pathway, the pastureland pathway resulted in the
highest biota concentrations and dietary exposure (Appendix 1.2). In each trophic transfer scenario for
concentrations resulting from releases to surface water, the manufacturing OES results in the highest
biota concentrations and dietary exposure (Appendix 1.2). The highest dietary exposure across all
scenarios results from the manufacturing OES surface water releases and consumption of fish by mink
and is 0.14 mg/kg/day (Table_Apx 1-7). Earthworm and Trifolium sp. concentrations (mg/kg) were
conservatively assumed equal to aggregated soil and soil pore water concentrations (earthworm) or soil
pore water concentrations only (Trifolium sp.). Fish and crayfish concentrations (mg/kg) were calculated
using surface water and benthic pore water concentrations of 1,1-dichloroethane, respectively, from PSC
and an estimated BCF of seven (U.S. EPA. 2012c). A comparison of fish consumption in mink is also
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provided using actual measured concentrations of 1,1-dichloroethane in Lake Pontchartrain oysters
(Ferrario et a'L 1985) and the maximum measured surface water concentration of 1,1-dichloroethane as
reported in Section 3.3.3.1. The estimated exposure for mink consuming fish based on these reported
values is 7.5xl0"3 mg/kg/day as compared to the highest and lowest COU/OES-based dietary exposure
estimates of 0.14 mg/kg/day and 1,0><10"3 mg/kg/day for the manufacturing COU/'OES and use as a
laboratory chemical COU/OES, respectively.
The trophic transfer of 1,1-dichloroethane from media to biota is illustrated in Figure 4-1 with the
movement of 1,1-dichloroethane through the food web indicated by black arrows. Within the aquatic
environment, the benthic zone is bounded by dashed black lines from the bottom of the water column to
sediment surface and subsurface layers. The depth that the benthic environment extends into subsurface
sediment is site-specific. Figure 4-1 illustrates the 1,1-dichloroethane BCF for aquatic organisms and
food intake rates (FIRs) for the representative terrestrial organisms.
Surface Water
Uptake
from Water
ft*!_ _ BCF_= 7 _
Benthic Zone
Sediment/
Pore Water
Meadow Vole
FIR = 0.325
Vegetation
Short-tail Shrew
FIR = 0.555 * Land applied biosolids
Earthworm
FIR = 1
Mink
4 FIR = 0.22
Daphnia
Crayfish
| Groundwater
Figure 4-1. Trophic Transfer of 1,1-DichIoroethane jn Aquatic and Terrestrial Ecosystems
FIR = Food Ingestion Rate.
4.1.5 Weight of Scientific Evidence Conclusions for Environmental Exposures
4.1.5.1 Strengths, Limitations, Assumptions, and Key Sources of Uncertainty for the
Environmental Exposure Assessment
EPA used a combination of chemical-specific parameters and generic default parameters when
estimating surface water, sediment, soil, and fish-tissue concentrations.
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Concentrations of 1,1-dichloroethane in environmental media are expected to vary by exposure scenario.
Release from industrial facilities, either by water or air, contribute to concentrations of 1,1-
dichloroethane in the environment. Proximity to facilities and other sources is likely to lead to elevated
concentrations via air deposition compared to locations that are more remote. The ability to locate
releases by location reduces uncertainty in assumptions when selecting model input parameters that are
typically informed by location (e.g., meteorological data, land cover parameters for air modeling, flow
data for water modeling).
Measured surface water monitoring data for 1,1-dichloroethane is available but does not generally align
well either geographically or temporally with modeled releases. In most cases, comparison between
measured and modeled surface water concentrations was not possible. Environmental exposures of
aquatic invertebrates, vertebrates, and plants to 1,1-dichloroethane were assessed using modeled surface
water, benthic pore water, and sediment concentrations resulting from 1,1-dichloroethane releases to
surface water (Section 3.3.3.2) using site-specific information such as flow data for the receiving
waterbody at a release location. The confidence in the estimated surface water, benthic pore water, and
sediment concentrations resulting from surface water releases is characterized as "robust". For
additional details see Section 3.3.5.1.
Neither 1,1-dichloroethane soil monitoring data reflecting releases to air and deposition to soil or
reflecting releases to soil via land application of biosolids were found for comparison to modeled
concentration estimates. Environmental exposures of soil invertebrates, terrestrial plants, and mammals
to 1,1-dichloroethane were assessed using modeled air deposition of 1,1-dichloroethane releases to soil
(Section 3.3.4.1) and estimation of resulting bulk soil and soil porewater concentrations using
conservative assumptions regarding persistence and mobility. Exposure of these receptors via land
application of biosolids was assessed using modeled biosolids concentrations and both screening level
calculations and modeling, and similar conservative assumptions (see Section 3.3.4.6.1 for details).
Although the screening level models and methods used to estimate soil concentrations from air
deposition and land application of biosolids are scientifically sound and largely peer reviewed, some key
inputs such as the concentration of 1,1-dichloroethane in land applied biosolids and biosolids land
application practices are highly variable or unknown. Thus, the confidence in the estimated soil
concentrations resulting from land application of biosolids is characterized as "moderate."
4.1.5.2 Trophic Transfer Confidence
EPA uses several considerations when weighing the scientific evidence to determine confidence in the
dietary exposure estimates. These considerations include the quality of the database, consistency,
strength and precision, and relevance (Table Apx K-2). This approach is in agreement with the Draft
Systematic Review Protocol Supporting TSCA Risk Evaluations for Chemical Substances (U.S. EPA.
2021b) and Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Protocol (U.S. EPA.
2024t). Table 4-2 summarizes how these considerations were determined for each dietary exposure
threshold. For trophic transfer EPA considers the evidence for insectivorous terrestrial mammals
moderate, the evidence for herbivorous terrestrial mammals moderate, the evidence for fish-consuming
semi-aquatic mammals moderate, and the evidence for crayfish-consuming semi-aquatic mammals
slight (Table 4-2).
Quality of the Database; Consistency; and Strength (Effect Magnitude) and Precision
Few empirical biomonitoring data in ecological receptors were reasonably available for 1,1-
dichloroethane or related chlorinated solvents. These data include one study containing 1,1-
dichloroethane measurements in oysters (Ferrario et al.. 1985). one study containing fish tissue
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concentrations in other similar chlorinated solvents (1,1,1-trichloroethane and trichloroethylene) (Roose
and Brinkman. 1998) and a third study with non-detect of 1,2-dichlorethane in urban rats (COWI AS,
2018). Thus, the quality of the database was rated slight. For COU/OES-based dietary exposure
estimates, biota concentrations in representative species and their diet were calculated based on the
methodology described in Section 4.3.1.1. The calculated aquatic biota concentrations were of similar
range to the reported concentrations of 1,1-dichloroethane and related chlorinated solvents in aquatic
biota, which resulted in a moderate confidence for consistency of the aquatic-based dietary exposure
estimates for the trophic transfer analyses shown in Table 4-2 whereas this consideration was
determined 'NA' for terrestrial-based dietary exposure estimates. No empirical BCF or BAF data were
reasonably available, therefore concentrations in aquatic biota were calculated based on a predicted BCF
derived from bioconcentration of a training set of chemicals from water to fish. Since the training set
utilized to generate the 1,1-dichloroethane BCF value in EPI Suite™ contains other low-molecular
weight chlorinated solvents (U.S. EPA. 2012c). this results in a moderate confidence for strength and
precision for the trophic transfer based on fish consumption. Applying this predicted BCF value based
on fish to calculate whole crayfish concentrations adds uncertainty to dietary exposures estimates from
consumption of sediment-dwelling invertebrates by mink resulting in a slight confidence in the strength
and precision of the dietary exposure estimates based on crayfish consumption. For terrestrial mammal
trophic transfer, due to lack of empirical BAF values, it was conservatively assumed that whole
earthworm and whole plant concentrations were equal to soil and/or soil pore water concentrations,
respectively. However, the use of species-specific exposure factors (i.e., feed intake rate, water intake
rate, the proportion of soil or sediment within the diet) from reliable resources assisted in obtaining
dietary exposure estimates within the RQ equation (U.S. EPA. 2017a. 1993b). thereby increasing the
confidence for strength and precision, resulting in an moderate confidence for strength and precision of
the dietary exposure estimates in terrestrial trophic transfer.
Relevance (Biological, Physical and Chemical, and Environmental)
The short-tailed shrew, meadow vole, and American mink were selected as representative mammals for
the soil invertivore-, soil herbivore-, and aquatic-based trophic transfer analyses, respectively (U.S.
EPA. 1993b). based on their import in previous trophic transfer analyses conducted by the U.S. EPA
(U.S. EPA. 2003a. b). Appropriate dietary species (earthworm, plant, fish, crayfish) were selected based
on dietary information for shrew, vole, and mink provided in the Wildlife Exposure Factors Handbook
(U.S. EPA. 1993b). The selection of the relevant apex and their representative dietary species in the
trophic transfer analyses increases confidence in the biological relevance of the dietary exposure
estimates. Modeled concentrations for water and soil used to determine biota concentrations for trophic
transfer were based on 1,1-dichloroethane data and not those of an analog, therefore increasing
confidence in physical and chemical relevance of the dietary exposures in the trophic transfer analyses
(for information on analog selection see Section 4.2.1 and Appendix J.l). The current trophic transfer
analysis investigated dietary exposure resulting from 1,1-dichloroethane in biota and environmentally
relevant media such as soil, sediment, and water. The screening-level analysis for trophic transfer used
equation terms (e.g., area use factor and the proportion of 1,1-dichloroethane absorbed from diet, and
soil or sediment) all set to the most conservative values, emphasizing a cautious approach to risk to 1,1-
dichloroethane via trophic transfer.
Assumptions within the trophic transfer equation (Equation 4-3) for this analysis have been considered
to represent conservative screening values (U.S. EPA. 2005a) and those assumptions were applied
similarly for each trophic level and representative species. Applications across representative species
included assuming 100 percent 1,1-dichloroethane bioavailability from both the soil (AF*,-) and biota
representing prey (AFy). No additional dietary species other than the selected dietary species were
included as part of the dietary exposure for the respective terrestrial mammal (P, = 1). The area use
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factor (AUF), defined as the home range size relative to the contaminated area {i.e., site ^ home range =
AUF), within this screening level analysis was designated as 1 for all organisms, which assumes a
potentially longer residence within an exposed area or a large exposure area. These conservative
approaches, which likely overrepresent 1,1-dichloroethane's ability to transfer among the trophic levels,
decrease environmental relevance of the dietary exposures within the trophic transfer analyses, resulting
in an overall moderate confidence for relevance of the dietary exposure estimates.
Trophic Transfer Confidence
Due to moderate confidence in both the strength and precision and relevance for the dietary exposure
estimates to insectivorous and herbivorous terrestrial mammals, the trophic transfer confidence is
moderate in both cases. Due to moderate confidence in strength and precision and relevance in dietary
exposure estimates to mink based on fish consumption, the trophic transfer confidence is moderate. Due
to slight confidence in quality of the database and strength and precision considerations for dietary
exposure estimates to mink based on crayfish consumption, the trophic transfer confidence is assigned
slight.
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Table 4-2.1,1-Dichloroethane
Evidence Table Summarizing Overall Confidence Derived for Trophic Transfer (Dietary)
Types of Evidence
Quality of the
Database
Consistency
Strength and
Precision
Relevance"
Trophic Transfer
Confidence
Chronic Avian Assessment
N/A
N/A
N/A
N/A
Indeterminate
Chronic Mammalian Assessment
(insectivorous)
+
N/A
++
++
Moderate
Chronic Mammalian Assessment
(herbivorous)
+
N/A
++
++
Moderate
Chronic Mammalian Assessment
(fish consumption)
+
++
++
++
Moderate
Chronic Mammalian Assessment
(crayfish consumption)
+
++
+
++
Slight
11 Relevance includes biological, physical/chemical, and environmental relevance.
+ + + Robust confidence suggests thorough understanding of the scientific evidence and uncertainties. The supporting weight of scientific evidence
outweighs the uncertainties to the point where it is unlikely that the uncertainties could have a significant effect on the dietary exposure estimate.
+ + Moderate confidence suggests some understanding of the scientific evidence and uncertainties. The supporting scientific evidence weighed against
the uncertainties is reasonably adequate to characterize dietary exposure estimates.
+ Slight confidence is assigned when the weight of scientific evidence may not be adequate to characterize the scenario, and when the assessor is making
the best scientific assessment possible in the absence of complete information. There are additional uncertainties that may need to be considered.
N/A Indeterminate confidence corresponds to entries in evidence tables where information is not available within a specific evidence consideration.
3739
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4.2 Environmental Hazards
1,1-Dichloroethane _ Environmental Hazards (Section 4.2):
Key Points
EPA evaluated the reasonably available information for environmental hazard endpoints associated
with 1,1-dichloroethane exposure. The key points of the environmental hazard assessment are
summarized below:
• Aquatic species hazard:
o Few empirical data were reasonably available on aquatic species for 1,1-
dichloroethane; therefore, EPA used analog data and predictions to supplement the
data for hazard characterization,
o To estimate aquatic and benthic hazards (mortality) from acute exposures, EPA
supplemented empirical data on 1,1-dichloroethane with an identified analog, 1,2-
dichloropropane, with hazard predictions from an EPA predictive tool, Web-based
Interspecies Correlation Estimation (Web-ICE). These data were used with the
empirical aquatic invertebrate and fish data to create a Species Sensitivity
Distribution and calculate a concentration of concern (COC) for acute exposures of
aquatic species (7,898 ppb) using the lower 95th percentile of an HC05, a hazardous
concentration threshold for 5 percent of species,
o EPA also calculated a COC for chronic exposures (reproduction in Daphnia magna)
to aquatic species (93 ppb) using empirical 1,1-dichloroethane data,
o EPA calculated two COCs for chronic exposures in benthic pore water and sediment
to benthic-dwelling species (reproduction of Ophryotrocha labronica and growth and
development of Chironomus riparius, 6,800 ppb in benthic pore water and 2,900
Mg/kg in sediment, respectively) using empirical sediment-dwelling invertebrate data
on a close analog, 1,1,2-trichloroethane.
o EPA also calculated an algal COC for exposures (growth of Skeletonema costatam)
to aquatic plants (1,000 ppb) using empirical 1,2-dichloropropane data on algae.
• Terrestrial species hazard:
o Terrestrial hazard data for 1,1-dichloroethane were available for plants and
mammals.
o Based on empirical toxicity data for Canadian poplar, the chronic hazard threshold
for terrestrial plants is 802 mg/kg soil,
o Empirical toxicity data for mice and rats were used to estimate a chronic toxicity
reference value (TRY) for terrestrial mammals of 1,189 mg/kg-bw/day.
4.2.1 Approach and Methodology
During scoping, EPA reviewed potential environmental hazards associated with 1,1-dichloroethane and
identified the eight sources of environmental hazard data shown in Figure 2-9 of Final Scope of the Risk
Evaluation for 1,1 -Dichloroethane CASRN 75-34-3( U.S. EPA. 2020b).
EPA completed the review of environmental hazard data/information sources during risk evaluation
using the data quality review evaluation metrics and the rating criteria described in the Draft Systematic
Review Protocol Supporting TSCA Risk Evaluations for Chemical Substances (U.S. EPA. 2021b) and
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Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Protocol (U.S. EPA. 2024t). Studies
were assigned an overall quality of high, medium, low, or uninformative.
EPA assigned overall quality determinations of high or medium to five acceptable aquatic toxicity
studies and four acceptable terrestrial toxicity studies. There were few aquatic toxicity data for 1,1-
dichloroethane, so EPA also used environmental hazard information for the analog 1,2-dichloropropane.
1,2-Dichloropropane was selected as an analog for 1,1-dichloroethane aquatic hazard read-across due to
similar structure, physical, chemical, and environmental fate and transport, and toxicity. Because no
benthic hazard data were identified for 1,1-dichloroethane or analog 1,2-dichloropropane, benthic hazard
data from a second analog 1,1,2-trichloroethane (1,1,2-trichloroethane) were used to read-across to 1,1-
dichloroethane. Although 1,1,2-trichloroethane was not considered as robust an analog as 1,2-
dichloropropane for read-across of certain aquatic hazard (e.g., algal hazard), 1,1,2-trichloroethane was
considered a sufficient analog for a targeted read-across of benthic hazard to 1,1-dichloroethane. See
Appendix 1.2 for the analog selection rationale. EPA identified eight sources of environmental hazard
analog data, including six sources shown in Figure 2-9 of Final Scope of the Risk Evaluation for 1,2-
Dichloropropane CASRN 78-87-5 (U.S. EPA. 2020f) to assess hazard to aquatic species, and two
sources shown either in Figure 2-9 of Final Scope of the Risk Evaluation for 1,1,2-Trichloroethane
CASRN 79-00-5 (U.S. EPA. 2020d) or generated from a 1,1,2-trichloroethane section 4(a)(2) test order
(Smithers. 2023) to assess hazards to benthic species. Studies on the analogs were also reviewed and
assigned an overall quality of high, medium, low, or uninformative. In lieu of terrestrial wildlife studies,
controlled laboratory studies that used mice and rats as human health model organisms were used to
calculate a TRV which is expressed as doses in units of mg/kg-bw/day. These studies were used to
calculate a TRV for mammals, which is expressed as doses in units of mg/kg-bw/day. Although the
TRV for 1,1-dichloroethane is derived from laboratory mice and rat studies, because body weight is
normalized, the TRV can be used with ecologically relevant wildlife species to evaluate chronic dietary
exposure to 1,1-dichloroethane. Chronic hazard thresholds for representative wildlife species are
evaluated in the trophic transfer assessments using the TRV (Section 4.2.5.2).
4.2.2 Aquatic Species Hazard
Toxicity to Aquatic Organisms
EPA assigned overall quality determinations of high to five acceptable aquatic toxicity studies for 1,1-
dichloroethane, high or medium to six acceptable aquatic studies for analog 1,2-dichloropropane, and
high or medium to two acceptable aquatic study for analog 1,1,2-trichloroethane. Analog selection for
environmental hazard is discussed in Appendix J.l. EPA identified twelve aquatic toxicity studies,
displayed in Table 4-3, as the most relevant for quantitative assessment. The remaining study was
represented by a short-term exposure (1 hour) of a single low-dose of 1,1-dichloroethane, resulting in a
no-effect for ventilation frequency, ventilation amplitude, or swimming behavior in rainbow trout
(Oncorhynchus mykiss) (Kaiser K et al.. 1995). and was therefore considered less relevant for
establishing a hazard threshold. The Web-ICE application was used to predict LC50 toxicity values for
33 additional aquatic organisms (15 fish, an amphibian, and 18 aquatic invertebrate species) from the
1,1-dichloroethane Daphnia magna 48-hour effective concentration 50 (EC50) and 1,2-dichloropropane
fathead minnow and opossum shrimp 96-hour LC50 data (Raimondo. 2010). The test species (n = 3) and
predicted species (n = 33) toxicity data were then used to calculate the distribution of species sensitivity.
Due to the lack of sufficient reasonably available information on benthic species toxicity and the
uncertainties involved in using read-across and assessment factors in lieu of data regarding benthic
toxicity thresholds, EPA required data to be developed through TSCA section 4(a)(2) test orders in
January 2021 on 1,1-dichloroethane toxicity to Chironomus riparins. However, due to delays associated
with performance of the test order, including a June 2023 modification to the test protocol and receipt of
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the test order data in June 2024, EPA will consider the results of the completed test data in the final risk
evaluation.
Aquatic Vertebrates
EPA assigned overall quality determinations of high to a single study with 1,1-dichloroethane fish
hazard data and high or medium to three studies with analog 1,2-dichloropropane fish hazard data as
relevant for quantitative assessment. The 1,1-dichloroethane study and two of the 1,2-dichloropropane
studies contained fish hazard resulting from acute exposures whereas the remaining 1,2-dichloropropane
study contained fish hazard data for acute and chronic exposures to 1,2-dichloropropane (Table 4-3).
For acute toxicity studies in fish, Japanese medaka (Oryzias latipes) no greater than 6 months old
exposed to measured concentrations of 1,1-dichloroethane for 96 hours under semi-static conditions
(renewal every 24 hours) had abnormal swimming behavior with a derived EC50 value of 70.7 mg/L
(Mitsubishi Chemical Medience Corporation. 2009b). Authors noted abnormal swimming behavior if
any of the following were observed: inactivity, hyperactivity, surface swimming, loss of balance,
directionless swimming, or convulsions (Mitsubishi Chemical Medience Corporation. 2009b). Details
on EC50 derivation are described in Appendix K.2.1.3. Twenty-eight to thirty-four-day old fathead
minnow (Pimephalespromelas) exposed to measured concentrations of analog 1,2-dichloropropane for
96 hours in flow-through conditions exhibited loss of equilibrium, swimming near the surface, loss of
schooling behavior, hypoactivity, and mortality with a reported LC50 for mortality of 127 mg/L (Geiger
et al.. 1985). Similarly, 30- to 35-day old fathead minnow exposed to measured concentrations of 1,2-
dichloropropane for 96 hours under flow-through conditions had a reported mortality LC50 of 140 mg/L
(Walbridge et al.. 1983) (Table 4-3).
For chronic toxicity in fish, no data were reasonably available for 1,1-dichloroethane; therefore, the data
are represented by exposure to 1,2-dichloropropane. In the fish early life stage test, fathead minnow
exposed to measured concentrations of 1,2-dichloropropane under flow-through conditions for 32 to 33
days resulted in a no-observed-effect-concentration (NOEC) and lowest-observed-effect-concentration
(LOEC) for survival of 11 and 25 mg/L, respectively, and a NOEC and LOEC for decreased weight of 6
and 11 mg/L, respectively (Benoit et al.. 1982). EPA calculated the 32- to 33-day survival NOEC and
LOEC geometric mean of 16.58 mg/L as the chronic value (ChV) for survival and the growth NOEC
and LOEC geometric mean of 8.12 mg/L (Table 4-3).
Amphibians
No amphibian studies were reasonably available to assess potential hazards from 1,1-dichloroethane
exposure. However, modeled data from Web-ICE predicted a bullfrog (Lithobates catesbeicinus) 96-
hour LC50 of 131.59 |ig/L from the empirical data of 1,1-dichloroethane and analog 1,2-
dichloropropane (Table Apx K-l). Therefore, amphibian acute toxicity is accounted for within the Web-
ICE and SSD results (Figure Apx K-4).
Aquatic Invertebrates
EPA assigned overall quality determinations of high to two studies with 1,1-dichloroethane aquatic
invertebrate hazard data and high or medium to three studies with 1,2-dichloropropane or 1,1,2-
trichloroethane aquatic invertebrate hazard data as relevant for quantitative assessment. Three of these
studies contained hazard data for acute and/or chronic exposures of water column-dwelling invertebrates
to 1,1-dichloroethane or 1,2-dichloropropane.
For acute toxicity studies for water column-dwelling invertebrates, Daphnia magna exposed to
measured concentrations of 1,1-dichloroethane for 48-hours in semi-static conditions (renewal every 24
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hours) in covered beakers had an immobilization EC50 value of 34.3 mg/L (Mitsubishi Chemical
Medience Corporation. 2009a). In a saltwater-dwelling invertebrate study, opossum shrimp
(Americamysis bahia or Mysidopsis bahia) less than 24 hours old had a LC50 of 24.79 mg/L when
exposed to measured concentrations of analog 1,2-dichloropropane for 96-hours under flow-through
conditions (Dow Chemical 1988). In the same study, the 96-hour LC50 for 3-to 4-day old A. bahia was
greater than 26.65 mg 1,2-dichloropropane/L (also based on measured concentrations), suggesting
neonates are more sensitive to 1,2-dichloropropane than more developed shrimp. The mortality NOEC
for neonate opossum shrimp was 4.92 mg 1,2-dichloropropane/L, therefore EPA assigned the mortality
LOEC as the next highest concentration tested in the study which was 6.89 mg 1,2-dichloropropane/L
(Table 4-3).
For chronic toxicity studies for water-column dwelling invertebrates, D. magna exposed to measured
concentrations of 1,1-dichloroethane for 21 days in semi-static conditions (renewal daily) in covered
beakers had a chronic 21-day NOEC of 0.525 mg/L and LOEC of 1.64 mg/L for reproductive inhibition
(based on number of young produced), resulting in a reproductive ChV of 0.93 mg/L (Mitsubishi
Chemical Medience Corporation. 2009d). A median EC50 of 6.67 mg/L was also reported for
reproductive inhibition (Mitsubishi Chemical Medience Corporation. 2009d).
Benthic Invertebrates
No acute toxicity studies were reasonably available to assess potential hazards from 1,1-dichloroethane
exposure to sediment-dwelling organisms. However, modeled data from Web-ICE predicted 96-hour
LC50 values for thirteen benthic invertebrates from the empirical data of 1,1-dichloroethane and analog
1,2-dichloropropane (Table Apx K-l, Figure Apx K-4). Therefore, acute toxicity to sediment-dwelling
invertebrates is accounted for within the Web-ICE and SSD results.
No reasonably available data on chronic hazard of sediment-dwelling invertebrates were available for
1,1-dichloroethane or its primary analog 1,2-dichloropropane. Therefore, chronic hazard data from two
high or medium-rated studies for sediment-dwelling invertebrates on a secondary analog, 1,1,2-
trichloroethane were considered. EPA deemed 1,1,2-trichloroethane suitable for targeted read-across of
chronic benthic hazard to 1,1-dichloroethane as described in Appendix J.l. The marine polycheate worm
species Ophryotrocha labronica exposed to increasing nominal concentrations of 1,1,2-trichloroethane
in water for 15 days under semi-static renewal conditions had reduced hatching with a modeled EC 10 of
68 mg/L (Rosenberg et al.. 1975). Derivation of the EC 10 is described in Appendix K.2.1.3. Larvae of
the freshwater midge Chironomus riparius exposed over two generations to measured concentrations of
1,1,2-trichloroethane in sediment had significantly decreased emergence in second-generation (Fl)
larvae exposed to the highest tested concentration of 1,1,2-trichloroethane (measured 44 mg 1,1,2-
trichloroethane/kg sediment dry weight, nominal 1,000 mg/kg), resulting in a chronic 28-day NOEC of
19 mg/kg and LOEC of 44 mg/kg, which EPA then calculated a ChV of 29 mg/kg for growth and
development (Table 4-3). The decrease in Fl larval emergence at the LOEC was approximately half of
control value (42 ± 24 percent emergence in the 44 mg 1,1,2-trichloroethane/kg treatment group
compared to 77 ± 8 percent emergence in the control group; values presented as average ± standard
deviation) (Smithers. 2023). The NOEC and LOEC for the same endpoint within this study were also
expressed in measured pore water concentrations at 66 and 130 mg/L, which the EPA then calculated a
growth and development ChV of 93 mg/L in benthic pore water (Table 4-3).
None of the other measured endpoints for Fl midges or parent midges (F0) in the definitive study
resulted in a definitive LOEC; however, it should be noted that percent emergence was significantly
decreased in F0 larvae (44 ±16 percent compared to 81 ± 8 percent emergence in the controls) exposed
to the second highest tested 1,1,2-trichloroethane concentration (measured 10 mg/kg) but not the highest
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tested 1,1,2-trichloroethane concentration (30 mg/kg), therefore a LOEC was not established for percent
emergence in the F0 larval midges. In the preliminary 2-generation sediment screening portion of this
same study, decreased emergence was also noted in F1 larval midges exposed to the highest tested
concentration of 1,1,2-trichloroethane (14 ± 6 percent emergence of F1 larval midges exposed to
nominal 1,000 mg 1,1,2-trichloroethane/kg sediment dry weight compared to 90 ± 11 percent emergence
in the control larval midges (Smithers. 2023). Although this endpoint received an uninformative rating
due to not reporting measured concentrations of 1,1,2-trichloroethane in the sediment and nominal
concentrations not expected to be representative of actual concentrations, the results support decreased
emergence in F1 larvae in the medium-rated definitive study.
Aquatic Plants
EPA assigned overall quality determinations of high to one study with 1,1-dichloroethane aquatic plant
hazard data and high or medium to three studies with analog 1,2-dichloropropane aquatic plant hazard
data as relevant for quantitative assessment.
For studies that reported growth inhibition in the form of EC50 values, green algae species
(Clamydomonoas reinhardtii) exposed to measured concentrations of 1,2-dichloropropane for 96-hours
under flow-through conditions had an EC50 of 83 mg/L for growth rate (Schafer et al.. 1994). This study
also reported C. reinhardtii EC50 values for 7 to 10-days of exposure ranging from 50 to 62 mg/L and
NOECs ranging from 29 to 31.5 mg/L, demonstrating increasing toxicity with increasing exposure
durations. EPA used the 96-hour EC50 value from (Schafer et al.. 1994) and the 96-hour EC50 hazard
value of 15.1 mg/L for marine diatom (Skeletonema costatam) growth rate exposed to measured
concentrations of 1,2-dichloropropane in closed vessels (Dow Chemical 2010) to calculate a geometric
mean of 35.4 mg/L, representing multiple algal species.
For studies reporting growth inhibition NOECs and LOECs, the 1,2-dichloropropane data presented in
Dow Chemical (2010) are a reanalysis of S. costatum 120-hour NOEC and LOEC biomass data
originally presented in Dow Chemical (1988). In Dow Chemical (2010). the authors report data for
additional hazard values (EC 10 and EC50 in addition to NOEC and LOEC), growth endpoints (growth
rate and abundance in addition to biomass), and durations (72 hours and 96 hours in addition to 120-
hours). The authors also used the geometric means of the daily measured chemical concentrations to
establish the hazard values in the reanalysis presented in Dow Chemical (2010). From the 72-, 96-, and
120-hour EC10 values of 8.47 mg/L, 8.49 mg/L, and 6.19 mg/L 1,2-dichloropropane, respectively, EPA
calculated the geometric mean of 72- to 120-hour biomass (area under the growth curve) EC 10 as 7.64
mg/L 1,2-dichloropropane in S. costatam. From the 72-, 96-, and 120-hour NOECs of 8.50 mg/L, 7.12
mg/L, and 6.87 mg/L 1,2-dichloropropane, respectively, and 72-, 96-, and 120-hour LOECs of 16.5
mg/L, 13.2 mg/L, and 10.9 mg/L 1,2-dichloropropane, respectively, EPA also calculated geometric
means for 72- to 120-hour biomass NOEC and LOEC from Dow Chemical (2010) as 7.46 mg/L 1,2-
dichloropropane and 13.3 mg/L 1,2-dichloropropane, respectively, in S. costatum. EPA calculated the
geometric mean of this NOEC and LOEC, generating a ChV of 10.0 mg/L 1,2-dichloropropane for
growth in S. costatam. In comparison, the 96-hour NOEC for green algae species C. reinhardtii was
38.0 mg/L (Schafer et al.. 1994). Green algae species (Raphidocelis sabcapitata, previously
Pseudokirchneriella sabcapitata) exposed to measured concentrations of 1,1-dichloroethane for 72
hours in closed vessels reported no observed effects for growth at the highest tested concentration, 94.3
mg/L 1,1-dichloroethane (Mitsubishi Chemical Medience Corporation. 2009c). Similarly, green algae
species (Raphidocelis sabcapitata, previously Selenastram capricornatam) exposed to measured
concentrations of 1,2-dichloropropane for 120-hours in closed vessels (Dow Chemical. 1988) reported
no observed effects for growth at the highest tested concentration (23.33-675.93 mg/L 1,2-
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3945 dichloropropane), for which EPA calculated the geometric mean as 162 mg/L 1,2-dichloropropane
3946 (Table 4-3).
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3947 Table 4-3. Aquatic Organisms Environmental Hazard Studies for 1,1-Dichloroethane, Supplemented with 1,2-Dichloropropane
3948 and/or
Study
Type
Test
Organism
Species
Endpoint
Hazard
Values"
(mg/L)
Geometric
Mean6
(mg/L)
Effect Endpoint
Citation (Study Quality)
Fish
Japanese medaka
(Oryzias latipes)
96-hour freshwater
EC50
70.7
Behavior (abnormal
swimming)
(Mitsubishi Chemical Medience
Corporation. 2009b) (High)
Fathead minnow
(Pimephcrfes promelas)
96-hour freshwater
LC50
127c;
140c
133.34
Mortality
(Walbridae et al.. 1983) (Medium);
(Geiger et al.. 1985) (High)
Acute
Aquatic
invertebrates
Daplmia magna
4 8-hour freshwater
EC50
34.3
Immobilization
(Mitsubishi Chemical Medience
Corporation. 2009a) (High)
Mysid shrimp
(Americamysis bahia)
96-hour saltwater LC50
24.79c,
>26.65c
Mortality
(Dow Chemical. 1988) (High)
Mysid shrimp
(Americamysis bahia)
96-hour saltwater
NOEC/LOEC
4.92/6.89c
(Dow Chemical. 1988) (High)
Fish
Fathead minnow
(Pimephales promelas)
32- to 33-day freshwater
NOEC/LOEC
ll/25c
16.58
(ChV)
Mortality (survival)
(Benoit et al.. 1982) (High)
Fathead minnow
(Pimephales promelas)
32- to 33-day freshwater
NOEC/LOEC
6/1 lc
8.12 (ChV)
Growth/
development (weight)
(Benoit et al.. 1982) (High)
Aquatic
Daplmia magna
21-day freshwater EC50
6.67
Reproduction (young
produced)
(Mitsubishi Chemical Medience
Corporation. 2009d) (High)
Chronic
invertebrates
Daplmia magna
21-day freshwater
NOEC/LOEC
0.525/1.6
4
0.93 (ChV)
Reproduction (young
produced)
(Mitsubishi Chemical Medience
Corporation. 2009d) (High)
Ophryotrocha
labronica
15-day saltwater EC 10
68 d
Reproduction
(hatchability)
(Rosenberg et al.. 1975) (High)
Benthic
invertebrates
Chironomus riparitis
2-generation freshwater
NOEC/LOEC
66/13 0'#
19/44'/e
93(ChV)
29 (ChV)e
Growth/
development
(decreased
emergence)
(Smithers. 2023) (Medium)
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Study
Type
Test
Organism
Species
Endpoint
Hazard
Values"
(mg/L)
Geometric
Mean6
(mg/L)
Effect Endpoint
Citation (Study Quality)
Algae
Skeletonema costatum,
Clamydomonoas reinhctrdtii
EC50
15.4-83c
35.4
Growth/
development
(Schafer et al.. 1994) (Medium).
(Dow Chemical. 2010) (Medium)
Skeletonema costatum
NOEC
6.19-
8.49c
7.64
(Dow Chemical. 2010) (Medium)
Clamydomonoas reinhardtii
NOEC
38.0C
(Schafer et al.. 1994) (Medium)
Skeletonema costatum
NOEC/LOEC
6.87-
8.50/
10.9-
16.5C
10.0
(ChV)
(Dow Chemical. 2010) (Medium).
(Dow Chemical. 1988) (High)
Raphidocelis subcapitata
NOEC
>94.3
(Mitsubishi Chemical Medience
Corporation. 2009c) (High)
Raphidocelis subcapitata
NOEC
>29.33-
675.93c
162
(Dow Chemical. 1988) (High)
" Hazard values presented as ranges represent the range of all the definitive values in the citations and are presented with the number of significant figures reported by
the authors.
b Geometric mean of definitive values only.
c Hazard values represented by analog 1,2-dichloropropane data.
J Hazard values represented by analog 1,1,2-trichloroethane data.
e Hazard values in mg/kg sediment.
Values in bold were used to derive Concentrations of Concern (COC) as described in Section 4.2.4 of this document. All values are listed individually with study quality
in (U.S. EPA. 2024aa) and (U.S. EPA. 2024u).
3949
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^.2.3 Terrestrial Species Hazard
EPA assigned overall quality determinations of high or medium to three acceptable terrestrial toxicity
studies. These studies contained relevant 1,1-dichloroethane terrestrial toxicity data for one Norway rat
(.Rattus norvegicus) strain (Sprague-Dawley), one mouse (Mas musculus) strain (B6C3F1), and the
Canadian poplar (Populus x canadensis). EPA identified these three terrestrial toxicity studies, displayed
in Table 4-4, as the most relevant for quantitative assessment.
Terrestrial Vertebrates
Three relevant chronic toxicity studies for terrestrial vertebrates that reported no-observed-adverse-
effect-level (NOAEL) and/or lowest-observed-adverse-effect4evel (LOAEL) information for 1,1-
dichloroethane were assigned an overall quality level of high or medium with behavior (e.g., water
intake and central nervous system [CNS] depression), growth, and/or mortality endpoints for rodents
(species n = 2). No acceptable hazard studies were identified for avian species exposed to 1,1-
dichloroethane. For terrestrial mammals and birds, relative contribution to total exposure associated with
inhalation is generally minor in comparison to exposures by diet and indirect ingestion. EPA has
quantitatively evaluated the relative contribution of inhalation exposures for terrestrial mammals and
birds in previous peer-reviewed Guidance of Ecological Soil Screening Levels (Eco-SSL) (U.S. EPA.
2003a. b), therefore, EPA selected toxicity studies with oral exposure to 1,1-dichloroethane and not
inhalation exposure to represent ecological hazard to terrestrial vertebrates.
Mammals
Observed effects occurred at relatively high doses (e.g., LOAELs equal to or greater than 1,000 mg/kg-
bw/day) in rats and mice.
Behavior: EPA identified behavior data for terrestrial mammalian vertebrates from two studies
(Muralidhara et al.. 2001; Klaunig et al.. 1986). Klaunig et al. (1986) demonstrated no adverse effects on
water intake in B6C3F1 mice from ad libitum drinking water consumption for 52 weeks at the highest
1,1-dichloroethane dose tested (2,500 mg/L). This corresponded to a NOAEL reported by the authors as
3.8 mg/g-bw/week which the EPA further converted to a NOAEL of 543 mg/kg-bw/day (Table 4-4). In
Muralidhara et al. (2001). authors observed moderate central nervous system depression (e.g.,
progressive motor impairment and sedation) in Sprague-Dawley rats gavaged for 13 weeks with 2 g/kg-
bw/day 1,1-dichloroethane, which the EPA then adjusted as shown in (U.S. EPA. 2024s) for dosing
number of days per week and maximum body weight (200 g) to calculate a NOAEL and LOAEL of 714
mg/kg-bw/day and 1429 mg/kg-bw/day, respectively (Table 4-4).
Reproduction: No ecologically relevant adverse reproductive effects from 1,1-dichloroethane treatment
were identified in rats and mice.
Growth: EPA identified growth data for terrestrial mammalian vertebrates from three studies
(Muralidhara et al.. 2001; Klaunig et al.. 1986; NCI. 1978). Adverse growth effects were observed in
rats but not mice. In a 10-day study where Sprague Dawley rats were gavaged daily with 1,1-
dichloroethane, significantly decreased body weight was observed at the lowest dose administered,
which was reported as a LOAEL of 1 g/kg-bw/day (Muralidhara et al.. 2001) which the EPA then
converted to a LOAEL of 1000 mg/kg-bw/day (Table 4-4). In the same study, Sprague-Dawley rats
were gavaged 5 times weekly for 13 weeks with 1,1-dichloroethane, and a NOAEL and LOAEL were
established in the 13-week study for decreased body weight compared to the control group at 1.0 g/kg-
bw/day and 2.0 g/kg-bw/day, respectively, which the EPA adjusted as shown in (U.S. EPA. 2024s) for
dosing number of days per week to calculate a NOAEL and LOAEL of 714 mg/kg-bw/day and 1,429
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mg/kg-bw, respectively. A 52-week B6C3F1 mouse study demonstrated no adverse effects on growth
(body weight change) from ad libitum drinking water consumption at the highest 1,1-dichloroethane
dose tested in the study (2,500 mg/L) (Klaunig et al.. 1986). This corresponded to a NOAEL reported by
the authors as 3.8 mg/g-bw/week which the EPA further converted to a NOAEL of 543 mg/kg-bw/day
(Table 4-4).
A 78-week study tested for effects on several endpoints, including growth, in B6C3F1 mice gavaged
1,1-dichloroethane in corn oil 5 times weekly (NCI. 1978). No effect was observed for growth (mean
body weight) in the 1,1-dichloroethane-treated B6C3F1 mice when compared to the control, therefore a
time-weighted average NOAEL for growth was established as 2,885 mg/kg-bw/day for males and 3,331
mg/kg-bw/day for females as reported by NTP (NCI. 1978). which the EPA then adjusted for dosing
number of days per week to 2061 mg/kg-bw/day and 2,379 mg/kg-bw/day, respectively (Table 4-4).
Within the same report (NCI. 1978). no effect on body weight was observed in male and female
B6C3F1 mice gavaged five times weekly for 6 weeks with 1,1-dichloroethane in corn oil up to doses of
10,000 mg/kg/day. Therefore, a NOAEL of 10,000 mg/kg-bw/day was established by the authors, which
the EPA then adjusted as shown in (U.S. EPA. 2024s) for dosing number of days per week to 7,143
mg/kg-bw/day (Table 4-4).
Survival: EPA identified mortality data for terrestrial mammalian vertebrates from three studies
(Muralidhara et al.. 2001; Klaunig et al.. 1986; NCI. 1978). Two of the three studies demonstrated
adverse effects on survival in rat and mice, although these two studies (which utilized gavage
administration) tested higher concentrations than the third study, which did not demonstrate an adverse
effect via drinking water administration. In Muralidhara et al. (2001). a NOAEL and LOAEL for
survival was established in male Sprague-Dawley rats gavaged five times weekly for 13 weeks with 1,1-
dichloroethane. The highest tested dose group (4.0 g/kg) experienced significant mortality and were
terminated at 11 weeks into the study with a NOAEL and LOAEL of 2 g/kg-bw/day and 4 g/kg-bw/day,
respectively, which the EPA then adjusted as shown in (U.S. EPA. 2024s) for dosing number of days per
week and converted into a NOAEL of 1,429 mg/kg-bw/day and a LOAEL of 2,857 mg/kg-bw/day
(Table 4-4). A 78-week NOAEL and LOAEL for survival were established in B6C3F1 female mice
gavaged 1,1-dichloroethane in corn oil 5 times weekly (NCI. 1978). with the NOAEL and LOAEL
reported as time-weighted averages of 1,665 mg/kg-bw/day and 3,331 mg/kg-bw/day, respectively,
which the EPA then adjusted for dosing number of days per week to a NOAEL of 1,189 mg/kg-bw/day
and a LOAEL of 2,379 mg/kg/bw/day, respectively. Survival for female mice in the control, vehicle
control, low dose and high dose groups within this study was 80%, 80%, 80%, and 50%, respectively. A
52-week B6C3F1 mouse study (Klaunig et al.. 1986) demonstrated no adverse effect on survival from
ad libitum drinking water consumption at the highest 1,1-dichloroethane dose tested in the study
(reported by the authors as 3.8 mg/g-bw/week, which the EPA further converted to a NOAEL of 543
mg/kg-bw/day (Table 4-4).
Avian
No avian studies were available to assess potential hazards from 1,1-dichloroethane exposure.
Soil Invertebrates
No soil invertebrate studies were reasonably available to assess potential hazards from 1,1-
dichloroethane exposure. Available soil invertebrate hazard data for analog 1,2-dichloropropane was
determined Uninformative (Neuhauser et al.. 1986). Available soil invertebrate hazard data for analog
1,1,2-trichloroethane was assigned an overall quality determination of high (Neuhauser et al.. 1985). A
48-hour contact exposure of earthworms to 1,1,2-trichloroethane applied to filter paper reported a
mortality LC50 of 42 microgram/cm2 (Neuhauser et al.. 1985). However, because the filter paper contact
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test is not considered a relevant exposure pathway for soil invertebrates due to the absorbed amount of
chemical to earthworm via dermal contact being uncertain, EPA did not establish a hazard threshold
from the 1,1,2-trichloroethane earthworm hazard data. A 14-day LC50 toxicity prediction of 181 mg/L
1,1-dichloroethane for earthworm can be generated from the neutral organics category using U.S. EPA's
Ecological Structure Activity Relationships (ECOSAR) Prediction Model (v2.2) (U.S. EPA. 2022d).
The neutral organics category in ECOSAR includes data from several species of earthworm, including
data from Eisenicifetida (U.S. EPA. 2022d).
Terrestrial Plants
For terrestrial plant species, one medium-quality study was identified by EPA as relevant for
quantitative assessment (Table 4-4). (Dietz and Schnoor. 2001) reported zero-growth and 50 percent
transpiration reduction concentrations in Canadian poplar seedlings for a 2-week exposure to 1,1-
dichloroethane in growth medium (ECO and EC50 values of 1,059 mg/L and 802 mg/L, respectively).
Table 4-4. Terrestrial Organisms Environmental Hazard Studies Used for 1,1-Dichloroethane
Duration
Test Organism
(Species)
Endpoint
Hazard Values
(m g/kg-bw/day)fl
Effect
Citation
(Data Evaluation Rating)
Terrestrial vertebrates
52 weeks
(chronic)
B6C3F1 Mouse
{Mus musculus)
NOAEL
543
Behavior
(water intake)
(Klaunia et al.. 1986)
(High)
13 weeks
(subchronic)
Sprague-Dawley Rat
(Rattus norvegicus)
NOAEL/
LOAEL
714/1,429
Behavior (CNS
depression)
(Muralidhara et al.. 2001)
(Medium)
10 days
(short-term)
Sprague-Dawley Rat
(Rattus norvegicus)
LOAEL
1,000
Growth (body
weight)
(Muralidhara et al.. 2001)
(High)
13 weeks
(subchronic)
Sprague-Dawley Rat
(Rattus norvegicus)
NOAEL/
LOAEL
714/1,429
Growth (body
weight)
(Muralidhara et al.. 2001)
(High)
52 weeks
(chronic)
B6C3F1 Mouse
(Mus musculus)
NOAEL
543
Growth (body
weight)
(Klaunia et al.. 1986)
(High)
78 weeks
(chronic)
B6C3F1 Mouse
{Mus musculus)
NOAEL
2,061
Growth (body
weight, male)
(NCI. 1978) (Hiah)
78 weeks
(chronic)
B6C3F1 Mouse
(Mus musculus)
NOAEL
2,379
Growth (body
weight, female)
(NCI. 1978) (Hiah)
6 weeks
(subchronic)
B6C3F1 Mouse
(Mus musculus)
NOAEL
7,143
Growth (body
weight)
(NCI. 1978) (Hiah)
13 weeks
(subchronic)
Sprague-Dawley Rat
(Rattus norvegicus)
NOAEL/
LOAEL
1,429/2,857
Survival
(Muralidhara et al.. 2001)
(High)
78 weeks
(chronic)
B6C3F1 Mouse
(Mus musculus)
NOAEL/
LOAEL
1,189/2,379
Survival
(NCI. 1978) (Hiah)
52 weeks
(chronic)
B6C3F1 Mouse
(Mus musculus)
NOAEL
543
Survival
(Klaunia et al.. 1986)
(High)
Terrestrial plants
14 days
(short-term)
Canadian poplar
(Populus X
canadensis)
EC50
802 mg/L
Transpiration
(Dietz and Schnoor. 2001)
(Medium)
Values in bold were used to derive hazard thresholds for terrestrial species as described in Section 4.2.4 of this
document. All values are listed individually with study quality in (U.S. EPA. 2024ac) and (U.S. EPA. 2024u).
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4.2.4 Weight of Scientific Evidence Conclusions for Environmental Hazards
4.2.4.1 Strengths, Limitations, Assumptions, and Key Sources of Uncertainty for the
Environmental Hazard Assessment
EPA uses several considerations when weighing the scientific evidence to determine confidence in the
environmental hazard data. These considerations include the quality of the database, consistency,
strength and precision, biological gradient/dose response, and relevance (Table Apx K-2). This
approach is in agreement with the Draft Systematic Review Protocol Supporting TSCA Risk Evaluations
for Chemical Substances (U.S. EPA. 2021b) and Draft Risk Evaluation for 1,1-Dichloroethane -
Systematic Review Protocol (U.S. EPA. 2024t). Table 4-5 summarizes how these considerations were
determined for each environmental hazard threshold. Overall, EPA/OPPT considers the evidence for
acute aquatic hazard as robust, the evidence for acute benthic hazard as moderate, the evidence for
chronic aquatic hazard as robust, the evidence for chronic benthic hazard as moderate, the evidence for
algal hazard as moderate, the evidence for terrestrial mammalian hazard as moderate, and the evidence
for terrestrial plant hazard as slight. Due to lack of reasonably available hazard data, the confidence for
avian hazard and soil invertebrate hazard are described as indeterminate. A more detailed explanation of
the weight of scientific evidence, uncertainties, and overall confidence for the 1,1-dichloroethane
environmental hazard evidence is presented in Appendixes K.2.3.1 and K.2.3.2.
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Table 4-5. 1,1-Dichloroethane Evidence Table Summarizing the Overall Confidence Derived from Hazard Thresholds
Types of Evidence
Quality of the
Database
Consistency
Strength and
Precision
Biological
Gradient/Dose-Response
Relevance"
Hazard
Confidence
Aquatic
Acute aquatic assessment
+++
+++
+++
+++
++
Robust
Acute benthic assessment
++
++
++
++
++
Moderate
Chronic aquatic assessment
++
++
+++
+++
+++
Robust
Chronic benthic assessment
++
++
+++
+++
+
Moderate
Algal assessment
++
++
+++
++
++
Moderate
Terrestrial
Chronic mammalian assessment
++
++
++
+++
++
Moderate
Avian assessment
NAfe
NA
NA
NA
NA
Indeterminatec
Soil invertebrate assessment
NAfe
NA
NA
NA
NA
Indeterminatec
Terrestrial plant assessment
+
+
++
++
+
Slight
11 Relevance includes biological, physical/chemical (including use of analogs), and environmental relevance.
+++ Robust confidence suggests thorough understanding of the scientific evidence and uncertainties. The supporting weight of scientific evidence outweighs
the uncertainties to the point where it is unlikely that the uncertainties could have a significant effect on the hazard estimate.
++ Moderate confidence suggests some understanding of the scientific evidence and uncertainties. The supporting scientific evidence weighed against the
uncertainties is reasonably adequate to characterize hazard estimates.
+ Slight confidence is assigned when the weight of scientific evidence may not be adequate to characterize the scenario, and when the assessor is making
the best scientific assessment possible in the absence of complete information. There are additional uncertainties that may need to be considered.
h NA indicates that a slight, moderate, or robust confidence cannot be assigned due to the lack of reasonably available data.
c Indeterminate is noted when a hazard confidence cannot be assigned to an assessment.
4081
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^4.2.5 Environmental Hazard Thresholds
EPA calculates hazard thresholds to identify potential concerns to aquatic and terrestrial species. For
aquatic species, the hazard threshold is called a concentration of concern (COC), and for terrestrial
species, the hazard threshold is called a hazard value or toxicity reference value (TRV). These terms
(COC, TRV, and hazard value) describe how the values are derived and can encompass multiple taxa or
ecologically relevant groups of taxa as the environmental risk characterization serves populations of
organisms within a wide diversity of environments. See Section 4.2.5 and Appendix K.2.3.1 for more
details on how EPA weighed the scientific evidence. After weighing the scientific evidence, EPA selects
the appropriate toxicity value from the integrated data to use for hazard thresholds.
For aquatic species, EPA estimates hazard by calculating a COC for a hazard threshold. COCs can be
calculated using a deterministic method by dividing a hazard value by an AF according to EPA methods
as defined in Equation 4-2 (U.S. EPA. 2016c. 2013b. 2012b).
Equation 4-2.
COC = toxicity value -h AF
COCs can also be calculated using probabilistic methods. For example, a Species Sensitivity
Distribution (SSD) can be used to calculate a hazardous concentration for 5 percent of species (HC05).
The HC05 estimates the concentration of 1,1-dichloroethane that is expected to be protective for 95
percent of species. This HC05 can then be used to derive a COC, and the lower bound of the 95 percent
confidence interval (CI) of the HC05 can be used to account for uncertainty instead of applying an AF.
EPA has more confidence in the probabilistic approach when enough data are available because an
HC05 is representative of a larger portion of species in the environment. The use of the lower 95 percent
CI instead of a fixed AF of 5 also increases confidence as it is a more data-driven way of accounting for
uncertainty (EPA-HO-OPPT-2023-Q265Y
For terrestrial species, EPA estimates hazard by calculating a toxicity reference value (TRV), in the case
of terrestrial mammals and birds, or by assigning the hazard value as the hazard threshold in the case of
terrestrial plants and soil invertebrates. EPA prefers to derive the TRV by calculating the geometric
mean of the NOAELs across sensitive endpoints (growth and reproduction) rather than using a single
endpoint. The TRV method is preferred because the geometric mean of NOAELs across studies, species,
and endpoints provides greater representation of environmental hazard to terrestrial mammals and/or
birds. However, when the criteria for using the geometric mean of the NOAELs as the TRV are not met
(according to methodology described in Appendix K.2.2), the TRVs for terrestrial mammals and birds
are derived using a single endpoint.
4.2.5.1 Aquatic Species COCs
EPA derived two acute COCs, two chronic COCs, and an aquatic plant COC using a combination of
probabilistic and deterministic approaches with 1,1-dichloroethane hazard data supplemented with read-
across from 1,2-dichloropropane and 1,1,2-trichloroethane. Algae was assessed separately and not
incorporated into acute or chronic COCs, because durations normally considered acute for other species
(e.g., up to 96 hours) can encompass several generations of algae. See Appendix K for additional
information on methods used to derive COCs. Table 4-6 summarizes the aquatic hazard thresholds.
Acute Aquatic Threshold
Due to few reasonably available acute toxicity data for aquatic organisms exposed to 1,1-dichloroethane,
for the acute aquatic COC, EPA used the 48-hour 1,1-dichloroethane EC50 immobilization data from
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Daphnia magna and the 96-hour 1,2-dichloropropane LC50 toxicity data from mysid shrimp and fathead
minnow (Table 4-3) as surrogate species to predict LC50 toxicity values for 33 additional aquatic
organisms (15 fish, an amphibian, and 18 aquatic invertebrate species) using the Web-ICE application as
described in Appendix K.2.1.1 (Raimondo. 2010). The test species (n=3) and predicted species (n = 33)
toxicity data were then used to calculate the distribution of species sensitivity to 1,1-dichloroethane and
1,2-dichloropropane exposure (as read-across to 1,1-dichloroethane) through the SSD toolbox as shown
in Appendix K.2.1.2 (Etterson. 2020a). The calculated HC05 was 10,784 |ig/L (95 percent CI = 7,898 to
15,440 |ig/L) (Figure_Apx K-4). The lower 95 percent CI of the HC05, 7,898 |ig/L, was then used as the
acute aquatic COC.
Acute Benthic Threshold
Due to the lack of reasonably available acute toxicity data for benthic organisms exposed to 1,1-
dichloroethane or acute empirical data on an appropriate analog, modeled data from the Web-ICE
application (Raimondo. 2010) were considered for assessing acute hazard to sediment-dwelling
organisms. Predicted 96-hour LC50 values were generated for thirteen benthic invertebrates based on
empirical data for 1,1-dichloroethane and the analog 1,2-dichloropropane (Table Apx K-l). Because the
benthic invertebrate predicted hazard values were represented relatively equally in the low, middle, and
high portions of the species sensitivity distribution (SSD, FigureApx K-4), EPA used the lower 95
percent CI of the calculated HC05 resulting from the above SSD analysis to represent the acute COC for
sediment-dwelling organisms. This resulted in an acute benthic COC of 7,898 |ig/L or ppb to be
compared to benthic pore water exposures.
Chronic Aquatic Threshold
The chronic aquatic COC was derived from the 1,1-dichloroethane ChV of the 21-day LOEC/NOEC of
0.93 mg/L for the aquatic invertebrate Daphnia magna with the application of an AF of 10. The ChV for
Daphnia magna was the most sensitive chronic endpoint represented in Table 4-3 for aquatic vertebrates
and invertebrates representing effects of reproductive inhibition of adult Daphnia magna (Mitsubishi
Chemical Medience Corporation. 2009d).
Chronic Benthic Thresholds
Due to the lack of reasonably available chronic toxicity data for benthic organisms exposed to 1,1-
dichloroethane and the chronic benthic COCs were derived from the 1,1,2-trichloroethane 15-day EC10
of 68 mg/L for Ophryotrocha labronica with the application of an AF of 10 and from the 1,1,2-
trichloroethane ChV of the 2-generation LOEC/NOEC of 29 mg/kg for Chironomus riparius with the
application of an AF of 10. The EC 10 for O. labronica was the most sensitive hazard value for benthic
species exposed to 1,1,2-trichloroethane and represents reproductive effects on hatching (Rosenberg et
al.. 1975). and the ChV for C. riparius was the single sediment hazard value for benthic species
representing growth and development effects for second generation larvae (Smithers. 2023).
Aquatic Plant Threshold
Due to the lack of reasonably available toxicity data with definitive hazard for aquatic plants exposed to
1,1-dichloroethane, the algal COC was derived from the 1,2-dichloropropane ChV of the 72-120 hour
NOEC/LOEC of 10.0 mg/L for Skeletonema costatam with the application of an AF of 10. The ChV for
S. costatnm was carefully recalculated in Dow Chemical (2010) from data in a robust study (Dow
Chemical. 1988) and represents growth and development effects over multiple generations.
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Table 4-6. Environmental Hazart
Thresholds for Aquatic Environmental Toxicity
Environmental Aquatic Toxicity
Analog
Hazard
Value (ppb)
Assessment
Factor (AF)
coc
(ppb)
Assessment
Medium
Acute aquatic exposure:
Lower 95% CI of HC05 from SSD
1,1-
dichloroethane
and 1,2-
dichloropropane
7,898
NA17
7,898
Water
column
Acute benthic exposure: Lower 95%
CI of HC05 from SSD
1,1-
dichloroethane
and 1,2-
dichloropropane
7,898
NA17
7,898
Benthic pore
water
Chronic aquatic exposure: based on
aquatic invertebrate ChV
1,1-
dichloroethane
930
10
93
Water
column
Chronic benthic exposure: based on
benthic invertebrate EC 10
1,1,2-
trichloroethane
68,000
10
6,800
Benthic pore
water
Chronic benthic exposure: based on
benthic invertebrate ChV
1,1,2-
trichloroethane
29,000fe
10
2,900fe
Sediment
Aquatic plant exposure: based on
algae ChV
1,2-
dichloropropane
10,000
10
1,000
Water
column
17 EPA used the lower 95% CI of the HC05 to account for uncertainties rather than an AF.
h Values in mg/kg, otherwise, hazard values in mg/L.
4.2.5.2 Terrestrial Species Hazard Values
For terrestrial species exposed to 1,1-dichloroethane EPA identified hazard values (thresholds) for
terrestrial vertebrates and plants. Table 4-7 summarizes the environmental hazard thresholds for
terrestrial species.
Terrestrial Vertebrate Threshold
EPA estimated hazard for terrestrial vertebrates by calculating a toxicity reference value (TRV), for
mammals (Figure 4-2). For terrestrial mammals, the TRV is expressed as doses in units of mg/kg-
bw/day. Although the TRV for 1,1-dichloroethane is derived from laboratory mice and rat studies, body
weight is normalized, therefore the TRV can be used with ecologically relevant wildlife species to
evaluate chronic dietary exposure to 1,1-dichloroethane. Representative wildlife species chronic hazard
threshold will be evaluated in the trophic transfer assessments using the TRV. The following criteria
were used to select the data to calculate the TRV with NOAEL and/or LOAEL data (U.S. EPA. 2007).
For more details see Appendix K.2.2.
Step 1: The minimum data set required to derive either a mammalian or avian TRV consists of three
results (NOAEL or LOAEL values) for reproduction, growth, or mortality for at least two
mammalian or avian species.
• Because this condition was met, proceed to step 2.
Step 2: Calculation of a geometric mean requires at least three NOAEL results from the reproduction
and growth effect groups.
• Because this condition was met, then proceed to step 4.
Step 4: When the geometric mean of the NOAEL for reproduction and growth is higher than the
lowest bounded LOAEL for reproduction, growth, or mortality,
• Then the TRV is equal to the highest bounded NOAEL below the lowest bounded LOAEL.
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For 1,1-dichloroethane, the geometric mean of NOAELs for growth endpoints is 1,685 mg/kg-bw/day
which is higher than the lowest bounded LOAEL for reproduction, growth, or mortality (1,429 mg/kg-
bw/day, growth). Therefore, according to the decision flowchart in Appendix K.2.2, the TRV was set as
the highest bounded NOAEL below the lowest bounded LOAEL for reproduction, growth, or mortality,
resulting in a TRV of 1,189 mg/kg-bw/day (mortality in female mice) (Figure 4-2). The TRV is
representative of various exposure durations (e.g., chronic [>90 days], subchronic [>30 to 90 days],
short-term [>3 to 30 days]) with the exception of an acute exposure durati on. This is reflective of the
COUs where dietary exposure by trophic transfer is assessed from releases to surface water and daily
maximum deposition and/or annual land application of 1,1-dichloroethane to soil.
(BEH) (GRO) (SUR)
# (dosed circte) - No-Observed Adverse Effect Dose O (°Pen circle)- Lowest-Observed Adverse Effect Dose
Result number 1) 10 - Rat, MORT Effect Measure Key: ... ~
# . * ;—: . y Lowest-Observed Adverse Effect Dose
/ \ \ BDWT - body weight changes
Reference number Test Species Effect Measure GBHV - behavioral changes * Paired values from same study when
Test Species Kev: Mou - Mouse MORT - mortality joined by line
Rat - Rat WCON - water consumption — No-Observed Adverse Effect Dose
Wildlife TRV Derivation Process
1) There are at least three results available for two test species within the growth, reproduction, and survival effect groups. There are enough data to derive a
TRV.
2) There are at least three NOAEL results available in the growth effect group for calculation of a geometric mean. (There are no data m the reproduction
effect group.)
3) The geometric mean of the NOAEL values for growth effects equals 1685 mg 1,1 -dichloroethane/kg BW/day, which is greater than the lowest bounded
LOAEL of 1429 mg 1,1-dichloroethane/kg BW/day for growth or survival.
4) The Mammalian wildlife TRV for Ll-dichloroethane is equal to 1189 mg LI -dichloroethane/kg BW/day, which is the highest bounded NOAEL below the
lowest bounded LOAEL for growth or survival.
Figure 4-2. Mammalian TRV Derivation for 1,1-Dichloroethane
Terrestrial Plant Threshold
The terrestrial plant hazard threshold was derived from the 1,1-dichloroethane 2-week EC50 of 802
mg/L for Populus x canadensis (Canadian poplar). The EC50 for Populus x canadensis was the most
sensitive hazard value in the single terrestrial plant reference representing transpiration effects for
seedlings (Dietz and Schnoor, 2001).
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Table 4-7. Environmental Hazard Thresholds
'or Terrestrial Environmental Toxicity
Environmental Terrestrial
Toxicity
Analog
Hazard Value or TRV
Assessment Medium
Mammal: TRV
NA
1,189 mg/kg-bw/day
Dietary (Trophic Transfer)
Avian
NA
No data
No data
Soil invertebrate
NA
No data
No data
Terrestrial plant (Populus x
canadensis): based on EC50
NA
802 mg/L
Soil porewater
NA = Not applicable, data derived
rom 1,1 -dichloroethane.
4223
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4224 4.3 Environmental Risk Characterization
4225
1,1-Dichloroethane - Environmental Risk Characterization (Section 4.3):
Key Points
EPA evaluated the reasonably available information to support environmental risk characterization. The key
points of the environmental risk characterization are summarized below:
• For aquatic species in the water column, chronic risk quotients (RQs) based on a hazard-based 21-
day release to surface waters are above 1 and have corresponding days of exceedance equal to or
greater than 21 days for five out of seven COUs evaluated quantitatively for risk to aquatic species
from surface water releases. For algal species, an RQ based on a 21-day release to surface water is
above 1 and has corresponding days of exceedance equal to or greater than 4 days for the
manufacturing COU.
o No acute RQs exceeded 1 for aquatic species in the water column or sediment compartment
for seven COUs evaluated quantitatively for risk to aquatic species from surface water
releases. Chronic RQs based on total number of operating days are below 1 for aquatic
species in the water column or sediment compartment for all seven COUs.
o Because EPA lacked information on estimated days of release to surface waters, exposure
durations are based on a hazard-based release duration or the total number of operating days,
o Analog data were used to assess hazard in the water column (specifically, algal hazard and
partial use in acute hazard) and in the sediment compartment, and 1,1-dichloroethane data
were used to determine the exposure. The methodology demonstrating robustness of the
analog selection is described in Appendix J.l.
o Because of 1.1 -dichlorocthane's high water solubility and releases to surface water, biota in
the water column are particularly susceptible to 1,1-dichloroethane exposure. This could
have potential community-level impacts from chronic 1,1-dichloroethane exposures in the
water column.
o EPA has robust confidence in the RQ inputs for the acute and chronic aquatic assessments
and moderate confidence in the RQ inputs for the algal and benthic assessments.
• RQs were below 1 for five COUs evaluated quantitatively and expected to be below 1 for eight
COUs evaluated qualitatively for risk to terrestrial species from air deposition and biosolids land
application.
o EPA has slight confidence in the RQ inputs for the terrestrial plant assessments,
o EPA has moderate confidence in the RQ inputs for the screening level trophic transfer
assessment.
o RQs calculated for five COUs were below 1 for dietary exposure of 1,1-dichloroethane to
representative insectivorous (shrew) and herbivorous (vole) mammals via trophic transfer
using calculated soil and soil pore water concentrations resulting from air deposition or
biosolid land application,
o RQs for five COUs were below 1 for semi-aquatic terrestrial receptors (mink) via trophic
transfer from fish and crayfish using the highest modeled 1,1-dichloroethane surface water
concentrations and corresponding benthic pore water concentrations.
4226
4227 EPA considered fate, exposure, and environmental hazard to characterize the environmental risk of 1,1-
4228 dichloroethane. For environmental receptors, EPA quantitatively estimated risks to aquatic species via
4229 water and sediment (including benthic pore water and sediment), and to terrestrial species via exposure
4230 to soil and soil pore water by air deposition and biosolids land application, and diet through trophic
4231 transfer. Risk estimates to aquatic-dependent terrestrial species were conducted to include exposures to
4232 1,1-dichloroethane via diet, water, and incidental ingestion of sediment. As described in Section 2.2.2,
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when released to the environment, 1,1-dichloroethane is expected to partition primarily to air (85%) with
lesser amounts to water (15%), sediment (<1%) and soil (<1%). Based on its physical chemical
properties, 1,1-dichloroethane is not likely to accumulate in sediment, soil, wastewater biosolids or biota
and is not described as persistent and bioaccumulative. Direct exposure of 1,1-dichloroethane to
terrestrial receptors via air was not assessed quantitatively, because dietary exposure was determined to
be the driver of exposure to wildlife. In general, for terrestrial mammals and birds, relative contribution
to total exposure associated with inhalation is secondary in comparison to exposures by diet and indirect
ingestion. EPA has quantitatively evaluated the relative contribution of inhalation exposures for
terrestrial mammals and birds in previous peer-reviewed Guidance of Ecological Soil Screening Levels
(Eco-SSL) (U.S. EPA. 2003a. b).
Section 4.1.5.2 details reasonably available environmental hazard data and indicated that 1,1-
dichloroethane presents hazard to aquatic and terrestrial organisms. For acute exposures, 1,1-
dichloroethane, supplemented with analog 1,2-dichloropropane data, is a hazard to aquatic animals in
the water-column and sediment at 7,898 ppb based on the lower 95 percent CI of the HC05 resulting
from an SSD utilizing EPA's Web-ICE (Raimondo. 2010) and SSD toolbox applications (Etterson.
2020a). For chronic exposures, 1,1-dichloroethane is a hazard to aquatic organisms in the water column
with a ChV of 930 ppb for aquatic invertebrates. For exposures to algal species, 1,1-dichloroethane,
based on analog 1,2-dichloropropane, is a hazard to algae in the water column with a ChV of 10,000
ppb. For chronic exposures to sediment-dwelling organisms, 1,1-dichloroethane, based on analog 1,1,2-
trichloroethane, is a hazard with ChVs of 68,000 and 29,000 ppb in benthic pore water and sediment,
respectively for sediment-dwelling invertebrates. For terrestrial exposures, 1,1-dichloroethane is a
hazard to mammals at 1,189 mg/kg-bw/day and a hazard to terrestrial plants with a hazard value of
802,000 ppb. As detailed in Section 4.2.5, EPA considers the evidence for aquatic hazard thresholds
robust, algal thresholds as moderate, benthic/sediment thresholds as moderate, terrestrial mammalian
threshold moderate, and the evidence for terrestrial plants threshold slight.
For the draft 1,1-dichloroethane risk evaluation, facility emissions data were obtained from databases
such as TRI, DMR and the NEI. The emissions data from these sources are the facility-specific releases
of 1,1-dichloroethane to air, water and land on an annual basis (lbs/site-yr or kg/site-yr). The total
number of operating days/year for these facilities can be estimated with good confidence. For example,
manufacturing processes are typically continuous process that run year-round with maybe some brief
shut-down periods. The total number of operating days/year for these types of processes can be reliably
estimated as 350. However, the number of days/year that the site manufactures, process or uses releases
the chemical is uncertain. The number of release days/year may be less than the total number of
operating days for the facility. To address this uncertainty, EPA has modeled two distinct "what-if'
scenarios for releases to surface water to cover a range of possible release days at the facility. One
scenario assumes the number of release days is equivalent to the hazard duration from which the chronic
COCs were derived (Table 4-3). A second scenario assumes that the release is averaged out over the
total number of operating days (Table 3-3), so an equal average daily release occurs on each of the
operating days. Exposure concentrations from both scenarios were compared to the acute, algal, and
chronic COCs.
4.3.1 Risk Characterization Approach
EPA characterized the environmental risk of 1,1-dichloroethane using risk quotients (RQs) (U.S. EPA.
1998; Barnthouse et al.. 1982). The RQ is defined in Equation 4-3 as
Equation 4-3.
RQ = Predicted Environmental Concentration/Hazard Threshold
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Environmental concentrations for each compartment (i.e., wastewater, surface water, sediment, soil)
were based on modeled (i.e., surface water, benthic pore water, and sediment estimated from VVMW-
PSC) and/or calculated (i.e., soil and soil pore water concentrations estimated from AERMOD-modeled
air deposition rates) concentrations of 1,1-dichloroethane from Sections 3.3 and 4.1. EPA calculates
hazard thresholds to identify potential concerns to aquatic and terrestrial species. These terms describe
how the values are derived and can encompass multiple taxa or ecologically relevant groups of taxa as
the environmental risk characterization serves populations of organisms within a wide diversity of
environments. For hazard thresholds, EPA used the COCs calculated for aquatic organisms, and the
hazard values or TRVs calculated for terrestrial organisms as detailed within Section 4.2.5.
RQs equal to 1 indicate that environmental exposures are the same as the hazard threshold. If the RQ is
above 1, the exposure is greater than the hazard threshold. If the RQ is below 1, the exposure is less than
the hazard threshold. RQs derived from modeled data for 1,1-dichloroethane are described in Section
4.3.1.1 for aquatic organisms and Sections 4.3.3 and 4.3.4 for terrestrial organisms. Although exposure
concentrations in the water column, benthic porewater, and sediment were determined according to two
different release scenarios (e.g., the first is a hazard based-release duration and the second is based on
total number of operating days), days of exceedance information was used to determine whether the
exposure concentrations resulting from these release scenarios exceeded the COCs for a relevant length
of time. For aquatic species in the water column, acute RQ days of exceedance were determined as equal
to or greater than one day, whereas for chronic RQs days of exceedance are equal to or greater than 21
days. RQs for algal species are presented separately and neither described as acute or chronic due to the
relatively rapid replication time of most algal species. Algal RQs days of exceedance are equal to or
greater than four days. For sediment-dwelling species exposed to benthic pore water, acute RQs days of
exceedance are equal to or greater than one day, and days of exceedance for chronic RQs are equal to or
greater than 15 days. For sediment-dwelling species exposed to sediment, chronic RQs days of
exceedance are equal to or greater than 35 days. Acute RQs for exposure to 1,1-dichloroethane in
sediment (mg/kg) were not calculated due to lack of hazard data. Exposure to the benthic compartment
is represented by acute RQs calculated for exposure to 1,1-dichloroethane in benthic pore water (mg/L).
EPA used modeled (e.g., PSC, AERMOD, SimpleTreat) data to characterize environmental
concentrations for 1,1-dichloroethane and to calculate the RQ. Table 3-1 describes the COUs and OESs
which result in environmental releases of 1,1-dichloroethane.
Aquatic Risk Characterization Approach; Surface Water, Benthic Pore Water, and Sediment
Risk estimates for seven COUs were developed for releases of 1,1-dichloroethane to surface water.
Within the aquatic environment, a modeling approach was employed to predict surface water, benthic
pore water, and sediment 1,1-dichloroethane concentrations. PSC considers model inputs of physical
and chemical properties of 1,1-dichloroethane (i.e., Kow, Koc, water column half-life, photolysis half-
life, hydrolysis half-life, and benthic half-life) allowing EPA to model predicted benthic pore water and
sediment concentrations. The PSC modeled 7Q10 surface water concentrations from facility-specific
release pollutant loads. If the 7Q10 surface water concentrations corresponding to the respective
exposure durations represented by the various COCs were greater than the acute, chronic, or algal COCs
in the water column, the PSC model was then used to confirm the modeled surface water concentration
days of exceedance as determined by the respective COCs. For example, for 1,1-dichloroethane, five
COUs modeled in PSC produced aquatic chronic RQ values greater than or equal to 1 based on the
number of release days based on chronic hazard studies, prompting the days of exceedance analysis in
PSC. Similarly, if modeled benthic pore water and sediment concentrations corresponding to the
respective exposure durations exceeded the benthic COCs, the PSC model was used to confirm the
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modeled benthic pore water and sediment concentration days of exceedance as determined by those
COCs. In cases of highly effluent-dominated release sites where facility discharge flow is considerably
greater than the 7Q10 flow of the receiving water body, the facility discharge flow was substituted in
place of the receiving water body flow as an input in PSC. This scenario can occur when e.g., a facility
produces high effluent discharge into a concrete basin with intermittent stream flow. This modification
was applied only to the COU/OES Disposal/Disposal/Disposal/Waste Handling, Treatment and Disposal
(Remediation), where the highest-releasing facility discharge flow was approximately three times the
7Q10 flow of the receiving stream. The plant flow is 0.416 MLD and was taken from the discharge
permit.
Releases of 1,1-dichloroethane to surface water were assessed quantitatively whereas air deposition of
1,1-dichloroethane to surface water from releasing facilities of TRI-reported fugitive emissions was
assessed qualitatively. As described in Section 3.3.3.2.3, EPA does not expect 1,1-dichloroethane
surface water concentrations modeled from air deposition to streams 100 m from releasing facilities of
fugitive and/or stack air emissions to exceed the hazard thresholds for aquatic organisms. The analysis in
Section 3.3.3.2.3 was based on the air deposition rates from the manufacturing COU/OES which had the
highest maximum and mean deposition rates by over an order of magnitude in comparison to the
maximum and mean air deposition rates of the other COU/OESs at 100 m based on TRI fugitive
emissions. Because the nearest body of water from the manufacturing facility with the highest daily air
deposition rate was approximately 340 m from facility, EPA does not expect risk estimates greater than
or equal to 1 for aquatic receptors exposed to 1,1-dichloroethane in surface water resulting from air
deposition.
EPA considers the biological relevance of species that COCs or hazard values are based on when
integrating these values with the location of the surface water, pore water, and sediment concentration
data to produce RQs. Life-history and habitat of aquatic organisms influence the likelihood of exposure
above the hazard threshold in an aquatic environment. EPA has identified COC values associated with
aquatic hazard values and include acute aquatic COC, chronic aquatic COC, acute benthic COC, two
chronic benthic COCs, and algal COC. The acute aquatic COC and acute benthic COC are the lower 95
percent CI of the HC05 of an SSD, a modeled probability distribution of toxicity values from multiple
taxa (including but not limited to Daphnia magna, mysid shrimp, and fathead minnow) inhabiting the
water column and benthic pore water. The chronic COC is represented by a reproductive endpoint from
a 21-day exposure of Daphnia magna to 1,1-dichloroethane within the water column. The chronic
benthic COC compared to benthic pore water is represented by a reproductive endpoint from a 15-day
exposure of Ophryotrocha labronica to analog 1,1,2-trichloroethane within benthic pore water. A
second chronic benthic COC compared to sediment is represented by an emergence endpoint from a 2-
generation exposure of Chironomus riparius to analog 1,1,2-trichloroethane within sediment. The algal
COC is represented by growth and development endpoints from 72 to 120-hour exposures to analog 1,2-
dichloropropane within the water column.
Environmental RQ values by exposure scenario with 1,1-dichloroethane surface water concentrations
(|ig/L) were modeled by PSC and are presented in Table 4-8. The max daily average concentrations
produced by PSC represent the maximum concentration (|ig/L) over a 21-day (Scenario 1) or total
number of operating days (Scenario 2) average period corresponding with the acute or chronic aquatic
COC used for the RQ estimate. Max daily average surface water concentrations were also produced by
PSC over a 21-day (Scenario 1) or total number of operating days (Scenario 2, Table 3-3) average period
corresponding with the algal COC used for the RQ estimate as presented in Table 4-9. Environmental
RQ values by exposure scenario with 1,1-dichloroethane benthic pore water concentrations (ppb) were
modeled by PSC and are presented in Table 4-10. The benthic pore water concentrations produced by
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PSC represent the maximum concentration (ppb) over a 15-day (Scenario 1) or total number of
operating days (Scenario 2, Table 3-3) average period corresponding with the acute or chronic benthic
COC used for the RQ estimate. Environmental RQ values by exposure scenario with 1,1-dichloroethane
sediment concentrations (mg/kg) were modeled by PSC and are presented in Table 4-11. The sediment
concentrations produced by PSC represent the maximum concentration (mg/kg) over a 35-day (Scenario
1) or total number of operating days (Scenario 2, Table 3-3) average period corresponding with the
chronic benthic COC. Use of surface water and benthic pore water concentrations in trophic transfer is
described in Section 4.3.1.1.
Terrestrial Risk Characterization Approach; Air Deposition and Biosolids
As described in Section 3.3, IIOAC and subsequently AERMOD were used to estimate the release of
1,1-dichloroethane to soil via air deposition from specific exposure scenarios. Estimated concentrations
of 1,1-dichloroethane that could be in soil via air deposition near-facility sources (10 m from the source)
have been calculated for 1,1-dichloroethane releases reported to TRI in fugitive emissions,
encompassing five COUs. EPA selected a distance of 10 m for evaluating 1,1-dichloroethane exposure
to terrestrial organisms that could result from air deposition since this was the distance that resulted in
the highest average daily deposition rate of 1,1-dichloroethane (Table 3-10). Soil and soil pore water
concentrations were obtained using maximum 95th percentile daily air deposition rates of 1,1-
dichloroethane (Table 4-3). EPA calculated RQs for exposure of terrestrial plants to 1,1-dichloroethane
by directly comparing the 1,1-dichloroethane soil pore water concentrations to the terrestrial plant
hazard value for 1,1-dichloroethane (Table 4-12). Releases of 1,1-dichloroethane in fugitive and/or stack
emissions modeled by Monte Carlo simulation (two COUs) or reported to NEI (eight COUs) which
could result in exposure to terrestrial receptors were assessed qualitatively for air deposition to soil due
to the modeled maximum 95th percentile (NEI) or high-end (Monte-Carlo) air concentrations at 10 m
from these sources being comparable or lower than modeled maximum 95th percentile air
concentrations from fugitive emissions reported to TRI (Table 3-9, Table 3-13, Table 3-13). EPA also
estimated soil and soil pore water concentrations of 1,1-dichloroethane from annual application of
biosolids to tilled agricultural soil and pastureland (Table 4-4) as described in Sections 3.3.4.6.1 and
3.3.4.6.2 to calculate RQs for terrestrial plants (Table 4-13). Briefly, SimpleTreat was used to predict
1,1-dichloroethane concentrations in biosolids, and an EU/REACH screening method and modified
Equilibrium Partitioning methodology to estimate soil and soil pore water concentrations, respectively,
from biosolid application. Use of 1,1-dichloroethane soil and soil pore water concentrations in trophic
transfer is described in Section 4.3.1.1.
In general, for terrestrial mammals and birds, relative contribution to total exposure associated with
inhalation is secondary in comparison to exposures by diet and indirect ingestion. For 1,1-
dichloroethane, other factors that guided EPA's decision to qualitatively assess 1,1-dichloroethane
inhalation exposure to terrestrial receptors were: limited facility releases and the lack of 1,1-
dichloroethane inhalation hazard data in terrestrial mammals for ecologically relevant endpoints.
Therefore, direct exposure of 1,1-dichloroethane to terrestrial receptors via air was not assessed
quantitatively.
4.3.1.1 Risk Characterization Approach for Trophic Transfer
Trophic transfer is the process by which chemical contaminants can be taken up by organisms through
dietary and media exposures and transfer from one trophic level to another. Chemicals can be transferred
from contaminated media and diet to biological tissue and accumulate throughout an organisms' lifespan
(bioaccumulation) if they are not readily excreted or metabolized. Through dietary consumption of prey,
a chemical can subsequently be transferred from one trophic level to another. If biomagnification occurs,
higher trophic level predators will contain greater body burdens of a contaminant compared to lower
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trophic level organisms. Although 1,1-dichloroethane is not expected to be bioaccumulative, it is
continuously released to the environment. When continuous releases occur, dietary exposure to wildlife
is possible.
EPA conducted screening level approaches for aquatic and terrestrial risk estimation based on exposure
via trophic transfer using conservative assumptions for factors such as: area use factor, 1,1-
dichloroethane absorption from diet, soil, sediment, and water. A screening level analysis was conducted
for trophic transfer and formulation of RQ values for aquatic and terrestrial pathways to representative
mammalian species. If RQ values were greater than or equal to 1, further refined analysis is warranted.
If an RQ value is less than 1, no further assessment is necessary. The screening level approach employs
a combination of conservative assumptions (i.e., conditions for several exposure factors included within
Equation 4-4 below) and utilization of the maximum values obtained from modeled and/or monitoring
data from relevant environmental compartments.
Equation 4-4.
IRQ} J = IDE] J/ IHT] J
Where:
ROj = Risk quotient for contaminant (j) (unitless)
DEj = Dietary exposure for contaminant (j) (mg/kg-BW/day)
HTj = Hazard threshold (mg/kg-BW/day)
Dietary exposure estimates are presented in Section 4.1.4.2. Terrestrial hazard data are available for
mammals using hazard values detailed in Section 4.2.4. As described in Section 4.1.4.1, representative
mammal species were chosen to connect the 1,1-dichloroethane transport exposure pathway via trophic
transfer of 1,1-dichloroethane uptake from contaminated soil and soil pore water to earthworm followed
by consumption by an insectivorous mammal (short-tailed shrew), 1,1-dichloroethane uptake from
contaminated soil pore water to plant (Trifolium sp.) followed by consumption by an herbivorous
mammal (meadow vole). For semi-aquatic terrestrial species, a representative mammal (American mink)
was chosen to connect the 1,1-dichloroethane transport exposure pathway via trophic transfer from fish
or crayfish uptake of 1,1-dichloroethane from contaminated surface water and benthic pore water
modeled from 1,1-dichloroethane surface water releases. As mentioned above, trophic transfer of 1,1-
dichloroethane to semi-aquatic terrestrial species from air deposition to surface water is not anticipated
due to low maximum daily air deposition rates of 1,1-dichloroethane to streams at distances > 100 m
from releasing facilities of fugitive emissions (Section 3.3.3.2.3). Therefore, EPA does not expect that
risk estimates for trophic transfer of 1,1-dichloroethane to a semi-aquatic terrestrial mammal from air
deposition to surface water would be equal to or greater than 1.
4.3.2 Risk Characterization for Aquatic Receptors
Because of 1,1-dichloroethane's high water solubility (Table 2-1), low log Koc (Table 2-2), and known
releases to surface water (Table 3-6), biota in the water column are more likely to be exposed to 1,1-
dichloroethane than biota in the sediment. For example, surface water RQs for chronic exposures were
greater than 1 for five COUs evaluated for 1,1-dichloroethane surface water releases based on a hazard
guideline-based 21-day release scenario with days of exceedance equal to or greater than the
corresponding hazard duration (21 days) and approaching 1 (greater than 0.9) for the manufacturing
COU when the release is based on the total number of operating days (Table 3-3, Table 4-8), whereas
none of the seven COUs evaluated quantitatively for surface water release resulted in RQs greater than
or equal to 1 for chronic exposure to benthic pore water or sediment (Table 4-10, Table 4-11). No RQs
were greater than 1 for acute exposures to biota in the water column or sediment for the seven COUs
Page 150 of 664
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4483
4484
4485
4486
4487
4488
4489
4490
4491
4492
4493
4494
4495
4496
4497
4498
4499
4500
4501
4502
4503
4504
4505
4506
4507
4508
4509
4510
4511
4512
4513
4514
4515
4516
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PUBLIC RELEASE DRAFT
July 2024
evaluated for surface water releases (Table 4-8, Table 4-10). Exposures to algal species in the water
column resulted an RQ greater than 1 for only the manufacturing COU when based on a hazard
guideline-based 21-day release scenario with days of exceedance equal to or greater than the
corresponding hazard duration (4 days) and RQs less than 1 for all COUs evaluated for surface water
releases based on total number of operating days (Table 4-9). The observation of surface water RQs
greater than 1 for a hazard guideline-based release scenario (e.g., hypothetical hazard-based release
duration shorter than the number of operating days) indicate potential community-level impacts (e.g.,
decline in aquatic invertebrate and algal populations leading to impacts on fish populations which
depend on these species as food sources) for biota in the water-column from surface water releases of
1,1-dichloroethane, particularly for the COUs manufacturing of 1,1-dichloroethane and remediation of
waste handling, treatment, and disposal of 1,1-dichloroethane.
Releases of 1,1-dichloroethane to surface water were identified for seven COUs (Life cycle stage/
Category/ Sub-category with their respective OES) with three COUs (processing/as a
reactant/intermediate in all other basic organic chemical manufacture; processing/as a
reactant/intermediate in all other chemical product and preparation manufacturing; and
processing/recycling/recycling) represented by 1 OES (processing as a reactive intermediate) and 1
COU (disposal of 1,1-dichloroethane) represented by three OESs (general waste handling, POTW, and
remediation) as described below. As described in Section 3.3.3.2.1, the highest facility-specific release
data reported between 2015-2020 was utilized for individual facility modeling with the exception for the
release data of the manufacturing COU facility where the next highest release data which occurred in
2016 was used in lieu of the highest release data corresponding with a hurricane event in 2020 (U.S.
EPA. 2024dY
Manufacture/Domestic Manufacturing/Domestic Manufacturing/Manufacturing
Surface water: Surface water acute aquatic RQ values for manufacturing 1,1-dichloroethane were less
than 1. The chronic aquatic RQ value based on a hazard guideline-based release duration (21 days) for
manufacturing 1,1-dichloroethane was greater than 1 at 15.38 with 21 days of exceedance for the
chronic aquatic COC which is equal to or greater than the 21-day duration of the chronic aquatic hazard
data (Table 4-8). The surface water chronic aquatic RQ value based on total number of operating days
(350 days) for manufacturing 1,1-dichloroethane was less than 1 at 0.91 (Table 4-8). The surface water
algal RQ value based on a hazard guideline-based release duration (21 days) for manufacturing 1,1-
dichloroethane was greater than 1 for the algal COC at 1.4, with 13 days of exceedance for the algal
COC, which is greater than or equal to the 4-day duration of the algal hazard data, whereas the surface
water algal RQ value based on the total number of operating days (350 days) for manufacturing 1,1-
dichloroethane was less than 1 at 0.08 (Table 4-9).
Benthic Pore Water: The benthic pore water acute and chronic RQ values for manufacturing 1,1-
dichloroethane were less than 1 for the acute benthic and chronic benthic COCs (Table 4-10).
Sediment: The sediment chronic RQs based on a hazard guideline-based release duration (35 days) or
the total number of operating days (350 days) for manufacturing 1,1-dichloroethane were less than 1 for
the chronic benthic COC (Table 4-11).
Processing/As a Reactant/Intermediate in All Other Basic Organic Chemical
Manufacture/Processing as a Reactive Intermediate; Processing/as a Reactant/intermediate in all
Other Chemical Product and Preparation Manufacturing/Processing as a Reactive Intermediate;
Processing/Recycling/Recycling/Processing as a Reactive Intermediate
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4528
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4530
4531
4532
4533
4534
4535
4536
4537
4538
4539
4540
4541
4542
4543
4544
4545
4546
4547
4548
4549
4550
4551
4552
4553
4554
4555
4556
4557
4558
4559
4560
4561
4562
4563
4564
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Surface water: The surface water acute RQ for processing 1,1-dichloroethane as a reactive intermediate
represented by three COUs (Processing/As a reactant/ Intermediate in all other basic organic chemical
manufacture, Processing/As a reactant/Intermediate in all other chemical product and preparation
manufacturing, and Processing/Recycling/Recycling) was less than 1 for the acute aquatic COC. The
surface water chronic RQ value based on a hazard guideline-based release duration (21 days) for
processing 1,1-dichloroethane as a reactant was greater than 1 at 2.54, with 21 days of exceedance for
the chronic aquatic COC, whereas the surface water chronic RQ value based on the total number of
operating days (350 days) for processing 1,1-dichloroethane as a reactant was less than 1 at 0.14 (Table
4-8). The surface water algal RQ values for processing 1,1-dichloroethane as a reactant were less than 1
for the algal COC (Table 4-9).
Benthic Pore Water: The benthic pore water acute and chronic RQ values for processing 1,1-
dichloroethane as a reactive intermediate were less than 1 for the acute benthic COC and chronic benthic
COC (Table 4-10).
Sediment: The sediment chronic RQs for processing 1,1-dichloroethane as a reactive intermediate were
less than 1 for the chronic benthic COC (Table 4-11).
Processing/Processing - Repackaging/Processing — Repackaging/Processing — Repackaging
Surface water: The surface water acute and chronic RQ values for repackaging 1,1-dichloroethane were
less than 1 for the acute aquatic COC, chronic aquatic COC, and algal COC (Table 4-8, Table 4-9).
Benthic Pore Water: The benthic pore water acute and chronic RQ values for repackaging 1,1-
dichloroethane were less than 1 for the acute benthic COC and chronic benthic COC (Table 4-10).
Sediment: The sediment chronic RQs for repackaging 1,1-dichloroethane were less than 1 for the
chronic benthic COC (Table 4-11).
Commercial Use/Other Uses/Laboratory Chemicals/Commercial Use as a Laboratory Chemical
Surface Water: The surface water acute and chronic RQ values for commercial use of 1,1-
dichloroethane as a laboratory chemical were less than 1 for the acute aquatic COC, chronic aquatic
COC, and algal COC (Table 4-8, Table 4-9).
Benthic Pore Water: The benthic pore water acute and chronic RQ values for commercial use of 1,1-
dichloroethane as a laboratory chemical were less than 1 for the acute benthic COC and chronic benthic
COC (Table 4-10).
Sediment: The sediment chronic RQs for commercial use of 1,1-dichloroethane as a laboratory chemical
were less than 1 for the chronic benthic COC (Table 4-11).
Disposal/Disposal/Disposal/General Waste Handling, Treatment and Disposal
Surface Water: The surface water acute RQ values for general waste handling, treatment, and disposal
of 1,1-dichloroethane were less than 1 for the acute aquatic COC. The surface water chronic RQ value
based on a hazard guideline-based release duration (21 days) for waste handling, treatment, and disposal
of 1,1-dichloroethane at a non-POTW facility was greater than 1 at 2.34, with 21 days of exceedance for
the chronic aquatic COC, whereas the surface water chronic RQ value based on the total number of
operating days (250 days) for general waste handling, treatment, and disposal of 1,1-dichloroethane was
less than 1 at 0.13 (Table 4-8). The surface water algal RQ values for general waste handling, treatment,
and disposal of 1,1-dichloroethane were less than 1 (Table 4-9).
Page 152 of 664
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4574
4575
4576
4577
4578
4579
4580
4581
4582
4583
4584
4585
4586
4587
4588
4589
4590
4591
4592
4593
4594
4595
4596
4597
4598
4599
4600
4601
4602
4603
4604
4605
4606
4607
4608
4609
4610
4611
4612
4613
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Benthic Pore Water: The benthic pore water acute and chronic RQ values for general waste handling,
treatment, and disposal of 1,1-dichloroethane were less than 1 for the acute benthic COC and chronic
benthic COC (Table 4-10).
Sediment: The sediment chronic RQs for general waste handling, treatment, and disposal of 1,1-
dichloroethane were less than 1 for the chronic benthic COC (Table 4-11).
Disposal/Disposal/Disposal/Waste Handling, Treatment and Disposal (POTW)
Surface Water: The surface water acute and algal RQ values for waste handling, treatment, and disposal
of 1,1-dichloroethane at POTW facilities were less than 1 for the acute aquatic COC and the algal COC
(Table 4-8 and Table 4-9). The surface water chronic RQ value based on a hazard guideline-based
release duration (21 days) for remediation of waste handling, treatment, and disposal of 1,1-
dichloroethane was greater than 1 at 1.5 with 21 days of exceedance for the chronic aquatic COC, the
surface water chronic RQ value based on the total number of operating days (365 days) for waste
handling, treatment, and disposal of 1,1-dichloroethane at POTW facilities was less than 1 at 0.09 (Table
4-8).
Benthic Pore Water: The benthic pore water acute and chronic RQ values for waste handling, treatment,
and disposal of 1,1-dichloroethane at POTW facilities were less than 1 for the acute benthic COC and
chronic benthic COC (Table 4-10).
Sediment: The sediment chronic RQ for waste handling, treatment, and disposal of 1,1-dichloroethane at
POTW facilities was less than 1 for the chronic benthic COC (Table 4-11).
Disposal/Disposal/Disposal/Waste Handling, Treatment and Disposal (Remediation)
Surface Water: The surface water acute and algal RQ values for remediation of waste handling,
treatment, and disposal of 1,1-dichloroethane were less than 1 (Table 4-8 and Table 4-9). The surface
water chronic RQ value based on a hazard guideline-based release duration (21 days) for remediation of
waste handling, treatment, and disposal of 1,1-dichloroethane was greater than 1 at 6.2 with 35 days of
exceedance for the chronic aquatic COC, whereas the surface water chronic aquatic RQ value based on
total number of operating days (365 days) for remediation of waste handling, treatment, and disposal of
1,1-dichloroethane was less than 1 at 0.33 (Table 4-8).
Benthic Pore Water: The benthic pore water acute RQ and chronic values for remediation of waste
handling, treatment, and disposal of 1,1-dichloroethane were less than 1 for the acute benthic and
chronic benthic COCs (Table 4-10).
Sediment: The sediment chronic RQs for remediation of waste handling, treatment, and disposal of 1,1-
dichloroethane were less than 1 for the chronic benthic COC (Table 4-11).
Distribution in Commerce/Distribution in commerce/Distribution in commerce/Distribution in
Commerce
Distribution of 1,1-dichloroethane in Commerce does not result in surface water releases (Table 3-6)
therefore RQs were not generated for this COU/OES.
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Table 4-8. Environmental Risk Quotients (RQs) by COU for Aquatic Organisms with 1,1-Dichloroethane Surface Water
Concentration (^ig/L) Modeled by PSC
COU (Life Cycle
Stage/Category/Subcategory)
OES
Number of
Facilities"
Days of
Release
Pollutant
Load
(kg/day)6
Max Daily
Average
(^g/L)c
coc
Type
COC
(^g/L)rf
Days of
Exceedance
(days per
year)rf
RQ
Manufacture/Domestic
manufacturing/Domestic
manufacturing
Manufacturing
1/1
21
5.79
1,430
Acute
7,898
0
0.18
350e
0.347
84.7
Acute
7,898
0
1.1E-02
21
5.79
1,430
Chronic
93
21
15
350e
0.347
84.7
Chronic
93
0
0.91
Processing/As a reactant/
Intermediate in all other basic
organic chemical manufacture
Processing as a
reactive intermediate
2/58
21
1.06
236
Acute
7,898
0
3.0E-02
350e
6.34E-02
12.9
Acute
7,898
0
1.6E-03
Processing/As a
reactant/Intermediate in all other
chemical product and
preparation manufacturing
21
1.06
236
Chronic
93
21
2.5
Processing/Recycling/Recycling
350e
6.34E-02
12.9
Chronic
93
0
0.14
Processing/Processing -
repackaging/Processing -
repackaging
Processing -
repackaging
0/3
21
5.51E-03
8.67
Acute
7,898
0
1.1E-03
260e
4.45E-04
0.702
Acute
7,898
0
8.9E-05
21
5.51E-03
8.67
Chronic
93
0
9.3E-02
260e
4.45E-04
0.702
Chronic
93
0
7.6E-03
Commercial Use/Other
use/Laboratory chemicals
Commercial use as a
laboratory chemical
0/2
21
2.27E-03
7.78
Acute
7,898
0
9.9E-04
260e
1.83E-04
0.638
Acute
7,898
0
8.1E-05
21
2.27E-03
7.78
Chronic
93
0
8.4E-02
260e
1.83E-04
0.638
Chronic
93
0
6.9E-03
Disposal/Disposal/Disposal
General waste
handling, treatment,
and disposal
1/22
21
2.37
218
Acute
7,898
0
2.8E-02
250e
0.199
12.4
Acute
7,898
0
1.6E-03
21
2.37
218
Chronic
93
21
2.3
250e
0.199
12.4
Chronic
93
0
0.13
Disposal/Disposal/Disposal
1/125
21
3.88
143
Acute
7,898
0
1.8E-02
Page 154 of 664
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COU (Life Cycle
Stage/Category/Subcategory)
OES
Number of
Facilities"
Days of
Release
Pollutant
Load
(kg/day)6
Max Daily
Average
(^g/L)c
COC
Type
COC
(^g/L)rf
Days of
Exceedance
(days per
year)rf
RQ
Waste handling,
treatment, and
365e
0.233
8.16
Acute
7,898
0
1.0E-03
21
3.88
143
Chronic
93
21
1.5
disposal (POTW)
365e
0.223
8.16
Chronic
93
0
8.8E-02
Waste handling,
treatment, and
21
0.243
580
Acute
7,898
0
7.3E-02
Disposal/Disposal/Disposal
2/42
365e
1.40E-02
30.7
Acute
7,898
0
3.9E-03
disposal
21
0.243
580
Chronic
93
35
6.2
(Remediation)
365e
1.40E-02
30.7
Chronic
93
0
0.33
Distribution in
commerce/Distribution in
Distribution in
N/A'
commerce/Distribution in
commerce
commerce
11 Number of facilities for a given OES with RQ > 1 & DOE >21 days
h Based on facility release data.
c Max daily average represents the maximum surface water concentration over a 21-day or total number of operating day average period corresponding with the
acute aquatic or chronic aquatic COC used for the RQ estimate.
d Based on (acute) the lower 95% CI of the SSD HC05 based on empirical hazard data from Daphnia magna exposed to 1,1-dichloroethane in water and mysid
shrimp and fathead minnow (Pimephales promelas) exposed to 1,2-dichloropropane in water and Web-ICE predictions or (chronic) 21-day hazard data from
Daphnia magna exposed to 1,1-dichloroethane in water.
'' Highest days of release based on total number of operating days (Table 3-3).
'Distribution in Commerce does not result in surface water releases (Table 3-6).
4620
4621
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Table 4-9. Environmental Risk Quotients (RQs) by COU for Aquatic Non-vascular Plants with 1,1-Dichloroethane Surface Water
Concentration (^ig/L) Modeled by PSC i
COU (Life Cycle
Stage/Category/Subcategory)
OES
Number of
Facilities"
Days of
Release
Pollutant
Load
(kg/day)6
Max Daily
Average
(^g/L)c
coc
Type
COC
(^g/L)rf
Days of
Exceedance
(days per
year)rf
RQ
Manufacture/
Domestic manufacturing/
Domestic manufacturing
Manufacturing
1/1
21
5.79
1,430
Algal
1,000
13
1.4
350e
0.347
84.7
0
8.5E-02
Processing/As a reactant/
Intermediate in all other basic
organic chemical manufacture
Processing as a reactive
intermediate
0/58
21
1.06
236
Algal
1,000
0
0.24
Processing/As a
Reactant/Intermediate in all
other chemical product and
preparation manufacturing
Processing/Recycling/Recycling
350e
6.34E-02
12.9
0
1.3E-02
Processing/Processing -
repackaging/Processing -
repackaging
Processing - repackaging
0/3
21
5.51E-03
8.67
Algal
1,000
0
8.7E-03
260e
4.45E-04
0.702
0
7.0E-04
Commercial Use/Other
use/Laboratory chemicals
Commercial use as a
laboratory chemical
0/2
21
2.27E-03
7.78
Algal
1,000
0
7.8E-03
260e
1.83E-04
0.638
0
6.4E-04
Disposal/Disposal/Disposal
General waste handling,
treatment, and disposal
0/22
21
2.37
218
Algal
1,000
0
0.22
250e
0.199
12.4
0
1.2E-02
Disposal/Disposal/Disposal
Waste handling, treatment,
and disposal (POTW)
0/125
21
3.88
143
Algal
1,000
0
0.14
365e
0.223
8.16
0
8.2E-03
Disposal/Disposal/Disposal
Waste handling, treatment,
and disposal (remediation)
0/42
21
0.243
580
Algal
1,000
0
0.58
365e
1.40E-02
30.7
0
3.1E-02
Distribution in
commerce/Distribution in
commerce/Distribution in
commerce
Distribution in commerce
~N/Af
11 Number of facilities for a given OES with RQ > 1 & DOE > 4 days
h Based on facility release data.
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COU (Life Cycle
Stage/Category/Subcategory)
OES
Number of
Facilities"
Days of
Release
Pollutant
Load
(kg/day)6
Max Daily
Average
(^g/L)c
COC
Type
COC
(^g/L)rf
Days of
Exceedance
(days per
year)rf
RQ
c Max daily average represents the maximum surface water concentration over a 21-day or total number of operating day average perioc
algal COC used for the RQ estimate.
d Based on 4-day hazard data from diatom Skeletonema costatum exposed to 1,2-dichloropropane in water.
'' Highest days of release based on total number of operating days (see Table 3-3).
' Distribution in Commerce does not result in surface water releases (see Table 3-6).
corresponding with the
4624
4625
4626 Table 4-10. Environmental Risk Quotients (RQs) by COU for Aquatic Organisms with 1,1-Dichloroethane Benthic Pore Water
4627 Concentration (^ig/L) Modeled by PSC
COU (Life Cycle
Stage/Category/Subcategory)
OES
Number of
Facilities"
Days of
Release
Pollutant
Load
(kg/day)6
Benthic Pore Water
Concentration
(^g/L)c
COC
Type
COC
(^g/L)rf
Days of
Exceedance
(days per
year)rf
RQ
Manufacture/
Domestic
manufacturing/Domestic
manufacturing
Manufacturing
0/1
15
8.10
413
Acute
7,898
0
5.2E-02
350e
0.347
78
Acute
7,898
0
9.9E-03
15
8.10
413
Chronic
6,800
0
6.1E-02
350e
0.347
78
Chronic
6,800
0
1.1E-02
Processing/As a reactant/
intermediate in all other basic
organic chemical manufacture
Processing as a
reactive
intermediate
0/58
15
1.48
66.5
Acute
7,898
0
8.4E-03
350e
6.34E-02
12.4
Acute
7,898
0
1.6E-03
Processing/As a
reactant/intermediate in all other
chemical product and
preparation manufacturing
15
1.48
66.5
Chronic
6,800
0
9.8E-03
Processing/Recycling/Recycling
350e
6.34E-02
12.4
Chronic
6,800
0
1.8E-03
Processing/Processing -
repackaging/Processing -
repackaging
Processing -
repackaging
0/3
15
7.71E-03
2.51
Acute
7,898
0
3.2E-04
260e
4.45E-04
0.61
Acute
7,898
0
7.7E-05
15
7.71E-03
2.51
Chronic
6,800
0
3.7E-04
260e
4.45E-04
0.61
Chronic
6,800
0
9.0E-05
Commercial Use/Other
use/Laboratory chemicals
Commercial use
as a laboratory
chemical
0/2
15
3.18E-03
2.28
Acute
7,898
0
2.9E-04
260e
1.83E-04
0.546
Acute
7,898
0
6.9E-05
15
3.18E-03
2.28
Chronic
6,800
0
3.4E-04
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COU (Life Cycle
Stage/Category/Subcategory)
OES
Number of
Facilities"
Days of
Release
Pollutant
Load
(kg/day)6
Benthic Pore Water
Concentration
(^g/L)c
COC
Type
COC
(^g/L)rf
Days of
Exceedance
(days per
year)rf
RQ
260e
1.83E-04
0.546
Chronic
6,800
0
8.0E-05
Disposal/Disposal/Disposal
General waste
handling,
treatment, and
disposal
0/22
15
3.32
62
Acute
7,898
0
7.8E-03
250e
0.199
11.8
Acute
7,898
0
1.5E-03
15
3.32
62
Chronic
6,800
0
9.1E-03
250e
0.199
11.8
Chronic
6,800
0
1.7E-03
Disposal/Disposal/Disposal
Waste handling,
treatment, and
disposal
(POTW)
0/125
15
5.43
40.8
Acute
7,898
0
5.2E-03
365e
0.223
7.85
Acute
7,898
0
9.9E-04
15
5.43
40.8
Chronic
6,800
0
6.0E-03
365e
0.223
7.85
Chronic
6,800
0
1.2E-03
Disposal/Disposal/Disposal
Waste handling,
treatment, and
disposal
(remediation)
0/42
15
0.34
168
Acute
7,898
0
2.1E-02
365e
1.40E-02
29.3
Acute
7,898
0
3.7E-03
15
0.34
168
Chronic
6,800
0
2.5E-02
365e
1.40E-02
29.3
Chronic
6,800
0
4.3E-03
Distribution in
Commerce/Distribution in
commerce/Distribution in
commerce
Distribution in
commerce
N/A'
11 Number of facilities for a given OES with RQ > 1 & DOE >15 days
h Highest days of release based on total number of operating days (Table 3-3).
c Based on facility release data.
d Max daily average of benthic pore water concentration represents the maximum benthic pore water concentration over a 15-day or total number of operating
day average period corresponding with the acute benthic or chronic benthic COC used for the RQ estimate.
'' Based on (acute) probabilistic hazard threshold (e.g., lower bound of the 95th confidence interval of the HC05) which included hazard predictions of sediment-
dwelling organisms exposed to 1,1-dichloroethane and analog 1,2-dichloropropane or (chronic) 15-day hazard data from sediment-dwelling Ophryotrocha
labronica exposed to analog 1,1,2-trichloroethane in water.
' Distribution in Commerce does not result in surface water releases (Table 3-6).
4628
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Table 4-11. Environmental Risk Quotients (RQs) by COU for Aquatic Organisms with 1,1-Dichloroethane Sediment Concentration
COU (Life
Cycle/Stage/ Category/
Subcategory)
Occupational
Exposure Scenario
Number of
Facilities"
Days of
Release
Pollutant
Load
(kg/day)6
Sediment
Concentration
(jig/kg)c
coc
Type
COC
(|ig/kg)rf
Days of
Exceedance
(days per
year)rf
RQ
Manufacture/
Domestic
manufacturing/Domestic
manufacturing
Manufacturing
0/1
35
3.47
519
Chronic
2,900
0
0.18
350e
0.347
124
0
4.3E-02
Processing/As a reactant/
intermediate in all other basic
organic chemical manufacture
Processing as a reactive
intermediate
0/58
35
0.634
77.4
Chronic
2,900
0
2.7E-02
Processing/As a
reactant/intermediate in all other
chemical product and
preparation manufacturing
Processing/Recycling/Recycling
350e
6.34E-02
19.6
0
6.8E-03
Processing/Processing -
repackaging/Processing -
repackaging
Processing -
Repackaging
0/3
35
3.30E-03
3.13
Chronic
2,900
0
1.1E-03
260e
4.45E-04
0.962
0
3.3E-04
Commercial use/Other
use/Laboratory chemicals
Commercial use as a
laboratory chemical
0/2
35
1.36E-03
2.84
Chronic
2,900
0
9.8E-04
260e
1.83E-04
0.854
0
2.9E-04
Disposal/Disposal/Disposal
General waste
handling, treatment,
and disposal
0/22
35
1.42
76.5
Chronic
2,900
0
2.6E-02
250e
0.199
18.6
0
6.4E-03
Disposal/Disposal/Disposal
Waste handling,
treatment, and disposal
(POTW)
0/125
35
2.33
50.5
Chronic
2,900
0
1.7E-02
365e
0.223
12.4
0
4.3E-03
Disposal/Disposal/Disposal
Waste handling,
treatment, and disposal
(remediation)
0/42
35
0.146
211
Chronic
2,900
0
7.3E-02
365e
1.40E-02
46.3
0
1.6E-02
Distribution in
commerce/Distribution in
Distribution in
commerce
N/A'
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COU (Life
Cycle/Stage/ Category/
Subcategory)
Occupational
Exposure Scenario
Number of
Facilities"
Days of
Release
Pollutant
Load
(kg/day)6
Sediment
Concentration
(jig/kg)c
COC
Type
COC
(|ig/kg)rf
Days of
Exceedance
(days per
year)rf
RQ
commerce/Distribution in
commerce
11 Number of facilities for a given OES with RQ > 1 & DOE >35 days
h Based on facility release data.
c Max daily average of sediment concentration represents the maximum sediment concentration over a 35-day or total number of operating day average
period corresponding with the chronic benthic COC used for the RQ estimate.
d Based on 35-day hazard data from Chironomns riparins exposed to 1,1,2-trichloroethane in sediment.
'' Highest days of release based on total number of operating days (Table 3-3).
t Distribution in Commerce does not result in surface water releases (Table 3-6).
4632
4633
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4634
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4636
4637
4638
4639
4640
4641
4642
4643
4644
4645
4646
4647
4648
4649
4650
4651
4652
4653
4654
4655
4656
4657
4658
4659
4660
4661
4662
4663
4664
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4.3.3 Risk Characterization for Terrestrial Organisms
RQs were less than 1 for the five COUs quantitatively assessed for air deposition to soil from TRI-
reported fugitive emissions of 1,1-dichloroethane when using the highest AERMOD predictions for
daily air deposition to soil at 10 m from facility. EPA expects risk estimates for air deposition to soil
from NEI and environmental release modeled stack and/or fugitive emissions to be comparable or less
than those developed based on TRI fugitive emissions, therefore, two additional COU/OESs
(repackaging of 1,1-dichloroethane and commercial use of 1,1-dichloroethane as a laboratory chemical)
were assessed qualitatively for risk to terrestrial organisms. Table 4-12 presents soil pore water
concentrations and RQ values for daily air deposition to soil pore water, indicating RQs below 1 for
terrestrial plants. The highest 1,1-dichloroethane soil pore water concentration calculated using
AERMOD predictions at 10 m from facility is 146 |ig/L based on the COU/OES manufacturing 1,1-
dichloroethane. EPA expects that the RQs for terrestrial plants exposed to air deposition to soil from
NEI-reported fugitive and/or stack emissions of 1,1-dichloroethane (eight COUs) or environmental
release-modeled (Monte-Carlo simulated) fugitive and/or stack emissions of 1,1-dichloroethane (two
COUs) would be similar or less than the RQ values for air deposition to soil from TRI-reported fugitive
emissions of 1,1-dichloroethane (with the highest RQ value for terrestrial plants = 1.8/10 4 based on
manufacturing 1,1-dichloroethane). This is because the modeled 1,1-dichloroethane air concentrations at
10 m from releasing facilities resulting from NEI-reported or Monte-Carlo simulated fugitive and stack
emissions (Table 3-13 and Table 4-12, respectively) are less than or comparable to modeled 1,1-
dichloroethane air concentrations at 10 m from releasing facilities resulting from TRI-reported fugitive
emissions of 1,1-dichloroethane (Table 3-9). Therefore, estimates of risk associated with air deposition
to soil from NEI-reported or environmental release-modeled (Monte-Carlo simulated) fugitive and/or
stack emissions of 1,1-dichloroethane are assessed qualitatively in Table 4-12.
In the case of commercial use of 1,1-dichloroethane as a laboratory chemical, the modeled air
concentration at 10 m from releasing facility included both fugitive and stack emissions in the
environmental release-model (Monte-Carlo simulation) and could not be attributed to one emission type.
However, this modeled air concentration (1.5 mg/m3) is two orders of magnitude less than the maximum
air concentration of 230 mg/m3 modeled from TRI-reported fugitive emissions from manufacturing 1,1-
dichloroethane, the COU/OES with the highest modeled air concentration at 10 m from releasing facility
(RQ for terrestrial plants = 1.8E-04 from 1,1-dichloroethane air deposition to soil).
RQs were less than 1 for the disposal COU when using the highest predictions for biosolids land
application to tilled agricultural and pastureland soils. Table 4-13 presents soil pore water concentrations
and RQ values for waste handling, treatment, and disposal of 1,1-dichloroethane at POTWs, indicating
RQs below 1 for terrestrial plants.
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4671
Table 4-12. Calculated Risk Quotients (RQs) For Terrestrial Plants Based on Modeled Air Deposition of 1,1-Dichloroethane to Soil
COU (Life Cycle
Stage/Category/Subcategory)
OES
Source
Number of
Facilities"
Soil Pore Water
Concentration
(jig/L) at 10 m6
Hazard
Threshold
(mg/L)c
RQ
Manufacture/Domestic
manufacturing/Dome stic manufacturing
Manufacturing
TRI
0/9
1.50E02
8.00E05
1.8E-04
NEI
0/9
Assessed qualitatively due to modeled air
concentrations < those based on TRI data
Processing/As a reactant/ intermediate
in all other basic organic chemical
manufacture
Processing as a
reactive
intermediate
TRI
0/6
3.2
8.00E05
4.0E-06
Processing/As a reactant/intermediate
in all other chemical product and
preparation manufacturing
NEI
0/50
Assessed qualitatively due to modeled air
concentrations ~ those based on TRI data
Processing/Recycling/Recycling
Processing/ Processing - repackaging/
Processing - repackaging
Processing -
repackaging
Modeled d
N/A
Assessed qualitatively due to modeled air
concentrations ~ those based on TRI data
Distribution in commerce/Distribution
in commerce/Distribution in commerce
Distribution in
commerce
NEI
0/5
Assessed qualitatively due to modeled air
concentrations ~ those based on TRI data
Commercial use/Other use/Laboratory
chemicals
Commercial use
as a laboratory
chemical
NEI
0/2
Assessed qualitatively due to modeled air
concentrations ~ those based on TRI data
Modeled d e
N/A
Disposal/Disposal/Disposal
General waste
handling,
treatment, and
disposal
TRI
0/8
7.6E-02
8.02E05
9.5E-08
NEI
0/102
Assessed qualitatively due to modeled air
concentrations ~ those based on TRI data
11 Number of facilities for a given OES with RQ > 1
h Soil pore water concentrations calculated from estimated soil catchment concentrations that could be in soil via maximum daily air deposition (95th
percentile) of 1,1-dichloroethane at a distance of 10 m from facility based on releases reported to TRI.
c Based on hazard data from Canadian poplar (Populus x canadensis) exposed to 1,1-dichloroethane for 2 weeks in growth medium.
d COU/OESs for which releases were Monte-Carlo simulated (environmental release-modeled)
'' Estimates of fugitive air emissions could not be separated from stack emission estimates.
4672
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4673
4674
4675
4676
4677
4678
4679
4680
4681
4682
4683
4684
4685
4686
4687
4688
4689
4690
4691
4692
4693
4694
4695
4696
4697
4698
4699
4700
4701
4702
4703
4704
4705
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PUBLIC RELEASE DRAFT
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Table 4-13. Calculated Risk Quotients (RQs) For Terrestrial Plants Based on 1,1-Dichloroethane
Soil Pore Water Concentrations (jig/L) as Calculated Using Modeled Biosolid Land Application
Data
COU (Life Cycle
Stage/Category/Subcategory)
Occupational
Exposure
Scenario
Number
of
Facilities"
Soil Type
Soil pore water
concentration
(~g/L)6
Hazard
Threshold
(~g/L)c
RQ
Disposal/Disposal/Disposal
Waste handling,
treatment, and
disposal
(POTW)
NA
Tilled
agricultural
18.5
8.02E05
2.3E-05
Pastureland
36.6
8.02E05
4.6E-05
3 In the absence of measured data, EPA estimated the maximum amount of 1,1-dichloroethane entering wastewater
treatment from the maximum releases reported for any facility in its Discharge Monitoring Report
b Soil pore water concentration calculated from estimated concentration of 1,1-dichloroethane in soil receiving an
annual application of biosolids.
' Based on hazard data from Canadian poplar (.Populus x canadensis) exposed to 1,1-dichloroethane for 2 weeks in
growth medium.
4,3.4 Risk Characterization Based on Trophic Transfer in the Environment
Trophic transfer of 1,1-dichloroethane and risk to terrestrial species was evaluated using a screening
level approach conducted as described in the EPA's Guidance for Developing Ecological Soil Screening
Levels (U.S. EPA. 2005a). 1,1-Dichloroethane concentrations within biota and resulting RQ values for 5
relevant COUs represented by 3 OESs for air deposition to soil 10 m from releasing facilities of TRI-
reported fugitive emissions are presented in TableApx L-lfor trophic transfer to insectivorous
mammals (represented by the short-tailed shrew) and Table Apx L-2 for trophic transfer to herbivorous
mammals (represented by the meadow vole). Table 4-14 and Table 4-15 presents biota concentrations
and RQ values for the COU/OES with the highest soil and soil porewater concentrations from air
deposition 10 m from releasing facilities of TRI-reported fugitive emissions in trophic transfer to
insectivorous and herbivorous mammals, respectively (manufacturing 1,1-dichloroethane). Trophic
transfer in soil to insectivorous and herbivorous mammals from 1,1-dichloroethane air deposition 10 m
from releasing facilities of NEI-reported or environmental release-modeled (Monte-Carlo simulated)
fugitive and/or stack emissions (seven COUs and two COUs, respectively) were assessed qualitatively
for reasons described in Section 4.3.3 (briefly, based on maximum air concentrations reported in Table
3-9, Table 3-12, and Table 3-13, air deposition to soil 10 m from releasing facilities of NEI-reported
fugitive or stack emissions or environmental release-modeled fugitive and/or stack emissions was
anticipated to be comparable or lower than levels quantified for TRI-reported fugitive emissions of 1,1-
dichloroethane at the same distance from releasing facilities). Therefore, EPA expects that the RQs for
trophic transfer of 1,1-dichloroethane from air deposition to soil from NEI-reported fugitive and/or stack
emissions (seven COUs) or environmental release-modeled (Monte-Carlo simulated) fugitive and/or
stack emissions (two COUs) would be similar or less than the RQ values for trophic transfer of 1,1-
dichloroethane from air deposition to soil from TRI-reported fugitive emissions (with the highest RQ
value for trophic transfer based on air deposition to soil = 2.1E-04 for manufacturing 1,1-
dichloroethane).
1,1-dichloroethane concentrations within biota and resulting RQ values for 1 COU represented by 1
OES for biosolids land application to agricultural tilled and pastureland soils are presented in Table 4-16
and Table 4-17 for trophic transfer to insectivorous mammals (shrew) and herbivorous mammals (vole),
respectively. RQs were below 1 for all soil and soil pore water concentrations and COUs based on the
mammalian TRY, calculated using empirical toxicity data with mice and rats.
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4708
4709
4710
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4712
4713
4714
4715
4716
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1,1-dichloroethane concentrations within biota and resulting RQ values for six relevant COUs
represented by seven OESs for releases to surface water and benthic pore water are presented in
TableApx L-3 for trophic transfer to semi-aquatic mammals (mink) consuming fish and TableApx
L-4 for trophic transfer to semi-aquatic mammals consuming crayfish. Table 4-18 and Table 4-19
present biota (fish and crayfish, respectively) concentrations and RQ values for the COU/OES with the
highest surface water and benthic pore water concentrations via PSC based on total number of operating
days, which was the COU/OES manufacture/manufacturing of 1,1-dichloroethane. The chronic TRV,
calculated using empirical toxicity data with mice and rats and representing hazard in a semi-aquatic
mammal (mink), resulted in RQs less than 1 for all modeled surface water and benthic pore water
concentrations.
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4718
4719
Table 4-14. Risk Quotients (RQs) for Screening Level Trophic Transfer of 1,1-Dichloroethane fr0m Air Deposition in Insectivorous
COU (Life Cycle
Stage/Category/Subcategory)
OES
Earthworm Concentration
(mg/kg)"
TRV
(mg/kg-bw/day)b
Short-Tailed shrew
(Marina brevicauda)
1,1-Dichloroethane Dietary
Exposure (mg/kg/day)c
RQ
Manufacture/
Domestic manufacturing/
Domestic manufacturing
Manufacturing
0.38
1,189
0.25
2.1E-04
11 Estimated 1,1-dichloroethane concentration in representative soil invertebrate, earthworm, assumed equal to aggregated highest calculated soil and soil pore
water concentration via air deposition to soil 10 m from releasing facilities of TRI-reported fugitive emissions.
'' Mammal 1.1-dichloroethane TRV value calculated using several studies as per (U.S. EPA. 2007).
c Dietary exposure to 1,1-dichloroethane includes consumption of biota (earthworm), incidental ingestion of soil, and ingestion of water.
Table 4-15. Risk Quotients (RQs) for Screening Level Trophic Transfer of 1,1-Dichloroethane from Air Deposition in Herbivorous
COU (Life Cycle
Stage/Category/Subcategory)
OES
Plant Concentration
(mg/kg)
TRV
(mg/kg-bw/day)b
Meadow Vole
(Microtus pennsylvanicus)
1,1-Dichloroethane Dietary
Exposure (mg/kg/day)c
RQ
Manufacture/
Domestic manufacturing/
Domestic manufacturing
Manufacturing
0.15
1,189
8.2E-02
6.9E-05
11 Estimated 1,1-dichloroethane concentration in representative terrestrial plant Trifolium sp., assumed equal to the highest calculated soil pore water
concentration via air deposition to soil 10 m from releasing facilities of TRI-reported fugitive emissions.
'' Mammal 1.1-dichloroethane TRV value calculated using several studies as ocr (U.S. EPA. 2007).
c Dietary exposure to 1,1-dichloroethane includes consumption of biota (Trifolium sp.), incidental ingestion of soil, and ingestion of water.
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4724
4725
Table 4-16. Risk Quotients (RQs) for Screening Level Trophic Transfer of 1,1-Dichloroethane fr0m Biosolid Land Application in
COU (Life Cycle
Stage/Category/Subcategory)
OES
Soil Type
Earthworm Concentration
(mg/kg)"
TRV
(mg/kg-bw/day)b
Short-tailed shrew
(Marina brevicauda)
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day)c
RQ
Disposal/Disposal/Disposal
Waste handling,
treatment, and
disposal (POTW)
Tilled
agricultural
4.8E-02
1,189
3.1E-02
2.6E-05
Pastureland
9.5E-02
1,189
6.3E-02
5.3E-05
11 Estimated 1,1-dichloroethane concentration in representative soil invertebrate, earthworm, assumed equal to aggregatec
water concentration via biosolids land application.
'' Mammal 1.1-dichloroethane TRV value calculated using several studies as per (U.S. EPA. 2007).
c Dietary exposure to 1,1-dichloroethane includes consumption of biota (earthworm), incidental ingestion of soil, and ing
highest calculated soil and soil pore
estion of water.
Table 4-17. Risk Quotients (RQs) for Screening Level Trophic Transfer of 1,1-Dichloroethane from Biosolid Land Application in
COU (Life Cycle
Stage/Category/Subcategory)
OES
Soil Type
Plant
Concentration
(mg/kg)
TRV
(mg/kg-
bw/day)6
Meadow Vole
(Microtus pennsylvanicus)
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day)c
RQ
Disposal/Disposal/Disposal
Waste handling,
treatment, and
disposal (POTW)
Tilled agricultural
1.9E-02
1,189
1.0E-02
8.7E-06
Pastureland
3.7E-02
1,189
2.1E-02
1.7E-05
a Estimated 1,1-dichloroethane concentration in representative terrestrial plant Trifolium sp., assumed equal to the highest calculated soil pore water
concentration via biosolids land application.
'' Mammal 1.1-dichloroethane TRV value calculated using several studies as per (U.S. EPA. 2007).
c Dietary exposure to 1,1-dichloroethane includes consumption of biota (Trifolium sp.), incidental ingestion of soil, and ingestion of water.
4730
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4731
4732
Table 4-18. Risk Quotient (RQ) Based on Potential Trophic Transfer of 1,1-Dichloroethane fr0m Fish to American Mink (Mustela
COU (Life Cycle
Stage/Category/Subcategory)
OES
SWCfl
(^g/L)
Fish
Concentration
(mg/kg)
TRV
(mg/kg-
bw/day)6
American Mink (Mustela vison)
1,1- Dichloroethane
Dietary Exposure
(mg/kg/day)c
RQ
Manufacture/Domestic
Manufacturing/Domestic Manufacturing
Manufacturing
85
0.59
1,189
0.14
1.2E-04
11 1,1-dichloroethane concentration represents the highest modeled surface water concentration via PSC modeling.
'' Mammal 1.1-dichloroethane TRV value calculated using several studies as oer (U.S. EPA. 2007).
c Dietary exposure to 1,1-dichloroethane includes consumption of biota (fish), incidental ingestion of sediment, and ingestion of water.
Table 4-19. Risk Quotient (RQ) Based on Potential Trophic Transfer of 1,1-Dichloroethane from Crayfish to American Mink
COU (Life Cycle
Stage/Category/Subcategory)
OES
Benthic Pore
Water" (jig/L)
Crayfish
Concentration
(mg/kg)
TRV
(mg/kg-
bw/day) b
American Mink (Mustela vison)
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day)c
RQ
Manufacture/Domestic
Manufacturing/Domestic
Manufacturing
Manufacturing
78
0.55
1,189
0.13
1.1E-04
11 1,1-dichloroethane concentration represents the highest modeled benthic pore water concentration via PSC modeling.
'' Mammal 1.1-dichloroethane TRV value calculated using several studies as oer (U.S. EPA. 2007).
c Dietary exposure to 1,1-dichloroethane includes consumption of biota (crayfish), incidental ingestion of sediment, and ingestion of water.
4737
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4743
4744
4745
4746
4747
4748
4749
4750
4751
4752
4753
4754
4755
4756
4757
4758
4759
4760
4761
4762
4763
4764
4765
4766
4767
4768
4769
4770
4771
4772
4773
4774
4775
4776
4777
4778
4779
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4.3,5 Overall Confidence and Remaining Uncertainties Confidence in Environmental
Risk Characterization
4.3.5.1 Risk Characterization Confidence
The overall confidence in the risk characterization combines the confidence from the environmental
exposure, hazard threshold, and trophic transfer sections. This approach aligns with the Draft Systematic
Review Protocol Supporting TSCA Risk Evaluations for Chemical Substances (U.S. EPA. 2021b) and
Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Protocol (U.S. EPA. 2024t). In the
environmental risk characterization, confidence was evaluated from environmental exposures and
environmental hazards. Hazard confidence was represented by evidence type as reported previously in
Section 4.2.5 and again in Table 4-20. Trophic transfer confidence was represented by evidence type as
reported in the Section 4.1.5.2 in Table 4-2. Exposure confidence has been synthesized from Section 3
and is further detailed within Section 4.1.5. Synthesis of confidence for exposure, hazard, and trophic
transfer (when applicable) resulted in the following confidence ranks for risk characterization RQ
inputs: robust for acute and chronic aquatic evidence, moderate for algal evidence, moderate for acute
and chronic benthic evidence, moderate for mammalian evidence, slight for terrestrial plant evidence
based on air deposition, slight for terrestrial plant evidence based on biosolid land application,
indeterminate for soil invertebrate evidence, and indeterminate for avian evidence (Table 4-20).
RQ Inputs for Aquatic, Algal, Benthic, and Senu-Aquatic Mammalian Assessments
Uncertainties and confidence in modeled exposure estimates from PSC have been described in Section
4.1.4.2. A robust confidence has been assigned to the exposure component of the RQ input for the
aquatic, algal, and benthic assessments as well as the mammalian assessments based on consumption of
fish or crayfish by a semi-aquatic terrestrial mammal (Table 4-20). Combining the robust exposure
confidence for the PSC-modeled surface water, benthic pore water, and sediment 1,1-dichloroethane
concentrations with the hazard confidences for aquatic, algal, and benthic assessments (robust,
moderate, and moderate, respectively) resulted in overall confidences of robust, moderate, and moderate
in the RQ inputs for the aquatic (acute and chronic), algal, and benthic (acute and chronic) assessments,
respectively (Table 4-20).
Combining the moderate exposure confidence for the PSC-modeled surface water and benthic pore
water 1,1-dichloroethane concentrations with the moderate hazard confidence for the mammalian
assessments and moderate trophic transfer confidence based on the consumption of fish (surface water)
or crayfish (benthic pore water) resulted in overall confidences of moderate in the RQ inputs for the
mammalian assessments represented by a semi-aquatic terrestrial mammal (Table 4-20).
RQ Inputs for Terrestrial Mammalian and Terrestrial Plant Assessments
Uncertainties and confidence in air deposition from AERMOD have been described in Section 4.1.4.2.
Calculations of soil and soil pore water concentrations from 1,1-dichloroethane daily air deposition rates
may add further uncertainty from the robust confidence in the AERMOD air deposition, therefore
resulting in a moderate confidence in the 1,1-dichloroethane soil and soil porewater concentrations from
air deposition. The uncertainties in the soil and soil pore water concentrations resulting from land
application of biosolids containing 1,1-dichloroethane have been described in Section 4.1.4.2, resulting
in moderate confidence for 1,1-dichloroethane soil and soil pore water concentrations from biosolid land
application.
Combining the moderate exposure confidence for the calculated soil and soil pore water concentrations
based on AERMOD modeling of 1,1-dichloroethane air deposition from TRI-reported fugitive emissions
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4786
4787
4788
4789
4790
4791
4792
4793
4794
4795
4796
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with the respective hazard confidences for terrestrial mammalian and terrestrial plant assessments
(moderate and slight, respectively) and trophic transfer confidence of moderate for the terrestrial
mammalian assessment resulted in overall confidences of moderate and slight in the RQ inputs for the
terrestrial mammalian and terrestrial plant assessments, respectively (Table 4-20). Although air
deposition of 1,1-dichloroethane to soil from NEI-reported or environmental release-modeled fugitive
and/or stack emissions (seven and two COUs, respectively) was assessed qualitatively, the same
confidences of moderate and slight apply for the terrestrial mammal and terrestrial plant assessments,
respectively. Combining the moderate exposure confidence for the calculated 1,1-dichloroethane soil
and soil pore water concentrations based on biosolid land application with the respective hazard
confidences for terrestrial mammalian and terrestrial plant assessments (moderate and slight,
respectively) and trophic transfer confidence of moderate for the terrestrial mammalian assessment
resulted in overall confidences of moderate and slight in the RQ inputs for the terrestrial mammalian and
terrestrial plant assessments, respectively (Table 4-20).
Table 4-20. Evidence Table Summarizing Overall Confidence for Environmental Risk
Characterization
Types of Evidence
Exposure
Hazard
Trophic
Transfer
Risk Characterization RQ
Inputs
Aquatic
Acute aquatic assessment
+++
+++
N/A
Robust
Acute benthic assessment
+++
++
N/A
Moderate
Chronic aquatic assessment
+++
+++
N/A
Robust
Chronic benthic assessment
+++
++
N/A
Moderate
Algal assessment
+++
++
N/A
Moderate
Terrestrial
Chronic avian assessment
N/A
N/A
N/A
Indeterminate
Chronic mammalian assessment
(air deposition to soil)
++
++
++
Moderate
Chronic mammalian assessment
(biosolids to soil)
++
++
++
Moderate
Chronic mammalian assessment
(surface water)
+++
++
++
Moderate
Chronic mammalian assessment
(benthic pore water)
+++
++
+
Moderate
Soil invertebrate assessment
N/A
N/A
N/A
Indeterminate
Terrestrial plant assessment, air
deposition
++
+
N/A
Slight
Terrestrial plant assessment,
biosolid deposition
++
+
N/A
Slight
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4809
4810
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4812
4813
4814
4815
4816
4817
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4819
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Types of Evidence
Exposure
Hazard
Trophic
Transfer
Risk Characterization RQ
Inputs
+ + + Robust confidence suggests thorough understanding of the scientific evidence and uncertainties. The
supporting weight of scientific evidence outweighs the uncertainties to the point where it is unlikely that the
uncertainties could have a significant effect on the risk estimate.
+ + Moderate confidence suggests some understanding of the scientific evidence and uncertainties. The
supporting scientific evidence weighed against the uncertainties is reasonably adequate to characterize risk
estimates.
+ Slight confidence is assigned when the weight of scientific evidence may not be adequate to characterize
the scenario, and when the assessor is making the best scientific assessment possible in the absence of complete
information. There are additional uncertainties that may need to be considered.
Indeterminate confidence corresponds to entries in evidence tables where information is not available within a
specific evidence consideration.
4.3.6 Summary of Environmental Risk Characterization
Exposure concentrations were modeled based on COU-related releases to the aquatic and terrestrial
environment. Table 4-21 displays RQ estimates for COU-related surface water releases to surface water,
benthic pore water, and sediment (seven COUs):
• Manufacture/Domestic Manufacturing/Domestic Manufacturing
o OES: Manufacturing
• Processing/As a Reactant/Intermediate in all Other Basic Organic Chemical Manufacture
• Processing/As a Reactant/Intermediate in all Other Chemical Product and Preparation
Manufacturing
• Processing/Recycling/Recycling
o OES: Processing as a reactive intermediate
• Processing/Processing - Repackaging/Processing - Repackaging
o OES: Processing - Repackaging
• Commercial Use/Other Use/Laboratory Chemicals
o OES: Commercial use as a laboratory chemical
• Disposal/Disposal/Disposal
o OES: General waste handling, treatment, and disposal
o OES: Waste handling, treatment, and disposal (POTW)
o OES: Waste handling, treatment, and disposal (remediation)
Table 4-22 displays RQ estimates and/or qualitative estimates of risk for COU-related releases resulting
in air deposition to soil (eight COUs) and biosolid land application to soil (one COU):
• Manufacture/Domestic Manufacturing/Domestic Manufacturing
o OES: Manufacturing
• Processing/As a Reactant/Intermediate in all Other Basic Organic Chemical Manufacture
• Processing/As a Reactant/Intermediate in all Other Chemical Product and Preparation
Manufacturing
• Processing/Recycling/Recycling
o OES: Processing as a reactive intermediate
• Processing/Processing - Repackaging/Processing - Repackaging
o OES: Processing - repackaging
• Commercial Use/Other Use/Laboratory Chemicals
o OES: Commercial use as a laboratory chemical
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4835
4836
4837
4838
4839
4840
4841
4842
4843
4844
4845
4846
4847
4848
4849
4850
4851
4852
4853
4854
4855
4856
4857
4858
4859
4860
4861
4862
4863
4864
4865
4866
4867
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• Disposal/Disposal/Disposal
o OES: General waste handling, treatment, and disposal
o OES: Waste handling, treatment, and disposal (POTW)
• Distribution in Commerce/Distribution in commerce/Distribution in commerce
o OES: Distribution in commerce
Table 4-21 displays RQ estimates for seven COUs in modeled 1,1-dichloroethane concentrations in
surface water, benthic pore water, and sediment. Within the water column, acute RQs were below 1 for
all seven COUs. Although chronic RQs based on a 21-day (hazard-based) release for aquatic receptors
are above 1 for five COUs, with days of exceedance equal to or greater than the duration of exposure,
the corresponding chronic RQs based on total number of operating days were below 1. Since EPA lacks
information on estimated days of 1,1-dichloroethane release to surface waters for each COU/OES, total
number of operating days was assumed as the maximum release duration and a chronic hazard-based
duration was assumed as a lower-end release duration. However, it's likely that actual days of release of
1,1-dichloroethane to surface waters (and thereby refined RQ values) for each COU/OES falls
somewhere in between these two durations. The manufacturing COU/OES had the highest chronic and
algal RQ values based on the hazard-based duration (RQs =15 and 1.4, respectively) and total number
of operating days (RQs = 0.91 and 0.085, respectively). The estimated exposure concentrations in water
for the manufacturing COU/OES are based on TRI data from a single facility. The confidence in the
acute and chronic aquatic RQ inputs were rated as "robust" and confidence in the algal RQ inputs rated
as moderate as described in Section 4.3.5.1. Benthic pore water and sediment RQs were below 1 for all
seven COUs. The confidence in the benthic RQ inputs were rated as "moderate" as described in Section
4.3.5.1. Because of 1,1-dichloroethane's high water solubility and relatively low log Koc, EPA expects
1,1-dichloroethane to partition more to water than to sediment.
Table 4-22 displays RQ estimates for five COUs in calculated 1,1-dichloroethane concentrations in soil
and soil pore water from air deposition of fugitive emissions (five COUs) or biosolid land application (1
COU). Risk was also qualitatively estimated for eight COUs for air deposition of 1,1-dichloroethane to
soil and soil pore water. RQs for terrestrial plants from 1,1-dichloroethane exposure in soil pore water
were below 1 for all five COUs and expected to be below 1 for the remaining three COUs from air
deposition and below 1 for the one COU from biosolids land application. The confidence in these RQ
inputs were rated as "slight" as described in Section 4.3.5.1. RQ estimates for the trophic transfer of 1,1-
dichloroethane to insectivorous (short-tailed shrew) or herbivorous (meadow vole) terrestrial mammals
were below 1 for five COUs and expected to be below 1 for eight COUs based on NEI release data for
air deposition to soil and soil pore water and below 1 for the one COU in soil and soil pore water from
biosolids land application. The confidence in these RQ inputs were rated as "moderate" as described in
Section 4.3.5.1. Additionally, Table 4-22 displays RQ estimates for seven COUs for trophic transfer of
1,1-dichloroethane from biota in surface water and sediment to semi-aquatic terrestrial mammals. RQ
estimates for trophic transfer of 1,1-dichloroethane to semi-aquatic terrestrial mammals based on fish
consumption or crayfish consumption were below 1 for all seven COUs in surface water and benthic
pore water, respectively. The confidence in these RQ inputs were rated as "moderate" as described in
Section 4.3.5.1. Avian and soil invertebrate assessments are not reflected in Table 4-22 due to lack of
reasonably available hazard evidence.
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4875 Table 4-21. COUs and Corresponding Environmental Risk for Aquatic Receptors Exposed to 1,1-Dichloroethane jn Surface Water,
4876 Benthic Pore Water, and Sediment
Aquatic Receptors ab
COU (Life Cycle
Stage/Category/
Subcategory)
OES
Surface Water
Benthic Pore Water
Sediment
Acute (Robust)e
Chronic (Robust)e
Algal (Moderate)e
Acute (Moderate)e
Chronic (Moderate)e
Chronic (Moderate)e
RQ c
DoE d
RQC
DoE d
RQ c
DoE d
RQ c
DoE d
RQ c
DoE d
RQ c
DoE d
Manufacture/
Domestic Manufacturing/
Domestic manufacturing
Manufacturing
0.011 to
0.18
0
0.91 to
15
0 to 21
0.085 to
1.4
13
9.9E-03 to
5.2E-02
0
1.1E-02 to
6.1E-02
0
0.043 to
0.18
0
Processing/As a Reactant/
Intermediate in All Other Basic
Organic Chemical Manufacture
1.6E-03 to
3.0E-02
0
0.14 to 2.5
0 to 21
0.013 to
0.24
0
1.6E-03 to
8.4E-03
0
1.8E-03 to
9.8E-03
0
6.8E-03 to
2.7E-02
0
Processing/As a
Reactant/Intermediate in all
Other Chemical Product and
Preparation Manufacturing
Processing as a
reactant
Processing/Recycling/
Recycling
Processing/Processing -
Repackaging/Processing -
Repackaging
Processing -
repackaging
9.3E-02 to
8.9E-05
0
7.6E-03 to
9.3E-02
0
7.0E-04 to
8.7-03
0
7.7E-05 to
3.2E-04
0
9.0E-05 to
3.7E-04
0
3.3E-04 to
1.1E-03
0
Commercial Use/Other
use/Laboratory chemicals
Commercial use
as a laboratory
chemical
8.1E-05 to
9.9-04
0
6.9E-03
to8.4E-02
0
6.4E-04 to
7.8E-03
0
6.9E-05 to
2.9E-04
0
8.0E-05 to
3.4E-04
0
2.9E-04 to
9.8E-04
0
Dispo sal/Dispo sal/Dispo sal
General waste
handling,
treatment, and
disposal
1.6E-03 to
2.8E-02
0
0.13 to 2.3
0 to 21
0.012 to
0.022
0
1.5E-03 to
7.8E-03
0
1.7E-03 to
9.1E-03
0
6.4E-03 to
2.6E-02
0
Dispo sal/Dispo sal/Dispo sal
Waste handling,
treatment, and
disposal (POTW)
1.0E-03 to
1.8E-02
0
0.088 to
1.5
0 to 21
0.0082 to
0.14
0
9.9E-04 to
5.2E-03
0
1.2E-03 to
6.0E-03
0
4.3E-03 to
1.7E-02
0
Dispo sal/Dispo sal/Dispo sal
Waste handling,
treatment, and
disposal
(remediation)
3.9E-03 to
7.3E-02
0
0.33 to 6.2
Oto 35
0.031 to
0.58
0
3.7E-03 to
2.1E-02
0
4.3E-03 to
2.5E-02
0
1.6E-02 to
7.3E-02
0
Distribution in
Commerce/Distribution in
commerce/Distribution in
commerce
Distribution in
commerce
N/A*
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COU (Life Cycle
Stage/Category/
Subcategory)
OES
Aquatic Receptors ab
Surface Water
Benthic Pore Water
Sediment
Acute (Robust)e
Chronic (Robust)e
Algal (Moderate)e
Acute (Moderate)e
Chronic (Moderate)e
Chronic (Moderate)e
RQ c DoE d
RQc DoE d
RQ c DoE d
RQ c DoE d
RQ c DoE d
RQ c DoE d
Modeled 1,1-dichloroethane concentrations andRQ values for all relevant COUs are available in Table 4-8, Table 4-9, Table 4-10, and Table 4-11.
" Risk assessed to aquatic receptors based on 1,1-dichloroethane releases to surface waters.
4 All exposure values and Days of Exceedance (DoE) modeled using PSC.
c Acute Risk Quotient (ARQ) derived using an acute Concentration of Concern of 7,898 ppb.
rfDays of Exceedance (DoE) modeled using PSC.
e Confidence in Acute Risk Quotient (ARQ), Chronic Risk Quotient (CRQ), or Algal Risk Quotient inputs is detailed in Section 4.3.5
^Chronic Risk Quotient (CRQ) derived using a chronic Concentration of Concern of 93 ppb and presented as a range based on 21-day release or total number of operating days (Table 3-3).
g Algal Risk Quotient derived using an algal Concentration of Concern of 1,000 ppb and presented as a range based on a 4-day release or total number of operating days (Table 3-3).
h Chronic Risk Quotient (CRQ) for sediment derived using benthic chronic Concentration of Concern of 2,900 ppb and presented as a range based on a 15-day release or total number of
operating days (Table 3-3).
' Acute Risk Quotient (ARQ) for benthic pore water derived using benthic acute Concentration of Concern of 7,898 ppb.
' Chronic Risk Quotient (CRQ) for benthic pore water derived using benthic chronic Concentration of Concern of 6,800 ppb and presented as a range based on a 35-day release or total
number of operating days (Table 3-3).
k Distribution in Commerce does not result in surface water releases (Table 3-6).
4877
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4878
4879
Table 4-22. COUs and Corresponding Environmental Risk for Terrestrial Receptors Exposed to 1,1-Dichloroethane jn Soil Pore
COU (Life Cycle
Stage/Category/
OES
Terrestrial Receptors"
Soil Pore Water
(Plants)
Trophic Transfer (Soil and Soil Pore Water)4
Trophic Transfer
(Water)c
Trophic Transfer
(Sediment)c
Plant RQ
Conf. in
RQ
Inputs''
Shrew RQ
Conf. in RQ
Inputs''
Vole RQ
Conf. in RQ
Inputs''
Mink RQ
Conf. in RQ
Inputs''
Mink RQ
Conf. in RQ
Inputs''
Manufacture/Domestic
Manufacturing/Domestic
manufacturing
Manufacturing
3.3E-06
Slight
3.9E-06
Moderate
1.3E-06
Moderate
1.2E-04f
Moderate
1.1E-04/
Moderate
Processing/As a Reactant/
Intermediate in All Other Basic
Organic Chemical Manufacture
Processing as a
reactant
1.8E-04
Slight
2.1E-04
Moderate
6.9E-05
Moderate
1.8E-05f
Moderate
i.7E-oy
Moderate
Processing/As a
Reactant/Intennediate in All
Other Chemical Product and
Preparation Manufacturing
Processing/Recycling/Recycling
Processing/Processing -
Repackaging/Processing -
Repackaging
Processing -
repackaging
Risk estimates for air deposition to soil expected to be less than those
generated based on TRI-fugitive emissions
9.7E-07
Moderate
8.5E-07
Moderate
Commercial Use/Other
Use/Laboratory Chemicals
Commercial use as a
laboratory chemical
Risk estimates for air deposition to soil expected to be less than those
generated based on TRI-fugitive emissions
8.8E-07
Moderate
7.6E-07
Moderate
Dispo sal/Dispo sal/Dispo sal
General waste
handling, treatment,
and disposal
5.0E-07
Slight
5.8E-07
Moderate
1.9E-07
Moderate
1.7E-05f
Moderate
i.6E-oy
Moderate
Waste handling,
treatment, and
disposal (POTW)
2.3E-05®
Slight
2.6E-05®
Moderate
8.7E-06®
Moderate
l.lE-05f
Moderate
i.iE-oy
Moderate
4.6E-05''
Slight
5.3E-05''
Moderate
1.7E-05''
Moderate
Waste handling,
treatment, and
disposal
(remediation)
N/A
1.2E-04f
Moderate
1.2E-04/
Moderate
Distribution in
Commerce/Distribution in
Commerce/Distribution in
Commerce
Distribution in
commerce
Risk estimates for air deposition to soil expected to be less than those
generated based on TRI-fugitive emissions
N/A'
" Exposure to terrestrial receptors based on 1,1-dichloroethane releases as fugitive air and stack air deposition to soil, biosolids land application, and trophic transfer. RQs generated for air
deposition to soil based on TRI-fugitive emissions of 1,1-dichloroethane.
4 Estimated concentrations of 1,1-dichloroethane (95tli percentile) that could be in soil via daily air deposition at a conservative (10 m from the source) exposure scenario.
c Fish and crayfish concentrations (mg/kg) were calculated using surface water and benthic pore water concentrations of 1,1-dichloroethane, respectively, from PSC assuming a BCF of 7 as
estimated bv EPI Suite™ (U.S. EPA, 2012c).
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COU (Life Cycle
Stage/Category/
OES
Terrestrial Receptors"
Soil Pore Water
(Plants)
Trophic Transfer (Soil and Soil Pore Water)4
Trophic Transfer
(Water)c
Trophic Transfer
(Sediment)c
Plant RQ
Conf. in
RQ
Inputs''
Shrew RQ
Conf. in RQ
Inputs''
Vole RQ
Conf. in RQ
Inputs''
Mink RQ
Conf. in RQ
Inputs''
Mink RQ
Conf. in RQ
Inputs''
d Conf = Confidence; Confidence in Risk Quotient (RQ) inputs are detailed in Section 4.3.5.
e Mink RQ based on fish concentrations of 1,1 -dichloroethane.
•^Mink RQ based on crayfish concentrations of 1,1-dichloroethane.
g Tilled agricultural soil type.
h Pastureland soil type.
' Distribution in Commerce does not result in surface water releases (Table 3-6).
4880
4881
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4884
4885
4886
4887
4888
4889
4890
4891
4892
4893
4894
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5 HUMAN HEALTH RISK ASSESSMENT
5.1 Human Exposures
EPA evaluated all reasonably available information for occupational and general population human
exposures, including consideration of increased exposure or susceptibility across PESS considerations
(see Section 5.3.2). Exposures for consumers are not evaluated as no consumer use of 1,1-
dichloroethane was identified in Section 1.1.3, Populations Assessed (see text box below).
5.1.1 Occupational Exposures
1,1-Dichloroethane _ Occupational Exposures (Section 5.1.1):
Key Points
EPA evaluated the reasonably available information for occupational exposures. The following
bullets summarize the key points of this section of the draft risk evaluation:
• EPA identified OESs for each condition of use of 1,1-dichloroethane.
• EPA assessed occupational exposures for each OES.
• The objective was to assess exposures to workers and also to occupational non-users (ONUs).
• EPA estimated occupational inhalation exposure (in ppm as an 8-hour TWA) and dermal
exposures (in mg/day) to 1,1-dichloroethane and provided both high-end and central
tendency exposures for occupational exposure scenarios associated with each OES.
o Monitoring data for 1,1-dichloroethane was available for the Manufacturing OES. For
the remaining OESs, exposures were estimated using the 1,1-dichloroethane
manufacturing exposure data, surrogate exposure data for 1,2-dichloroethane and
other solvents assessed in previous EPA risk evaluations and modeling,
o High-end inhalation exposures range from 2.4x 10~2 ppm to 13 ppm. High-end dermal
exposures are 6.7 mg/day for all OESs.
• EPA also evaluated the weight of scientific evidence for the exposure assessment of each
OES.
For each OES, EPA distinguishes exposures for workers and ONUs. Similar Exposure Groups (SEGs)
for 1,1-dichloroethane are provided for each OES in Table 5-2. If SEGs are not available, EPA's
practice is to assess "workers" and Occupational Non-Users (ONUs). Where possible, for each OES,
EPA identified job types and categories for workers and ONUs.
1,1-Dichloroethane has a vapor pressure of approximately 230 mmHg at 25 °C. Based on this high
volatility, EPA anticipates that workers and ONUs will be exposed to vapor via the inhalation route.
Based on the physical state, EPA does not expect particulate or mist inhalation. EPA expects worker
exposure to liquids via the dermal route. EPA does not expect dermal exposure for ONUs because they
do not directly handle 1,1-dichloroethane.
The United States has several regulatory and non-regulatory exposure limits for 1,1-dichloroethane: the
Occupational Safety and Health Administration (OSHA) permissible exposure limit (PEL) (29 CFR
1910.1000) is 100 ppm or 400 mg/m3 over an 8-hour work day, time-weighted average (TWA) (OSHA.
2019). This chemical also has a National Institute for Occupational Safety and Health (NIOSH)
recommended exposure limit (REL) of 100 ppm (400 mg/m3) TWA (NIOSH 2018). The American
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4907
4908
4909
4910
4911
4912
4913
4914
4915
4916
4917
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PUBLIC RELEASE DRAFT
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Conference of Governmental Industrial Hygienists (ACGIH) sets the threshold limit value (TLV) at 100
ppm TWA.
The following subsections briefly describe EPA's approach to assessing occupational exposures and
results for each COU assessed. For additional details on development of approaches and results refer to
Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Environmental Releases and
Occupational Exposure Assessment (U.S. EPA. 2024e).
5.1.1.1 Approach and Methodology
EPA's approach for assessing occupational exposure to 1,1-dichloroethane is illustrated in Figure 5-1:
Identify and Describe Occupational Exposure Scenarios to Assess
Section 5.1.1.1.1
V
Estimate Inhalation Exposure for OES Using
1,1-Dichloroethane Inhalation Monitoring Data
Section 5.1.1.1.2
V
Fill in Data Gaps Using Other Approaches to
Estimate Inhalation Exposure for OES
Sections 5.1.1.1.3 and 5.1.1.1.4
V
Estimate Dermal Exposure
Section 5.1.1.1.5
v
Est'mate the Number of Workers and ONUs
Potentially Exposed per OES Facility
Section 5.1.1.1.6
V
Present Exposure Estimates per OES for Workers and ONUs
Section 5.1.1.2
V
Assess the Weight-of-Scientific Evidence for
the Exposure Assessment for Each OES
Section 5.1.1.3
V
Calculate Acute, Sub-Chronic, and Chronic (Non-cancer and Cancer)
Exposure Metrics from Inhalation Exposure Estimates to Determine Risk
Section 5.3.3.1
Figure 5-1. Overview of EPA's Approach to Estimate Occupational
Exposures for 1,1-Dichloroethane
EPA follows the hierarchy established in Table 5-1 in selecting data and approaches for assessing
occupational exposures. The basis of this hierarchy is from the 1991 CEB Manual (U.S. EPA. 1991).
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4922 Table 5-1. Data and Approaches for Assessing Occupational Exposures to 1,1-Dichloroethane
Type of Approach
Description
1. Monitoring data
a) Personal and directly applicable
b) Area and directly applicable
c) Personal and potentially applicable or similar
d) Area and potentially applicable or similar
2. Modeling approaches
a) Surrogate monitoring data
b) Fundamental modeling approaches
c) Statistical regression modeling approaches
3. Occupational exposure limits
a) Company-specific occupational exposure limits (OELs) (for
site-specific exposure assessments; for example, there is only
one manufacturer who provided their internal OEL to EPA but
did not provide monitoring data)
b) OSHAPELs
c) Voluntary limits: ACGIH TLVs, NIOSH RELs, Occupational
Alliance for Risk Science (OARS) workplace environmental
exposure level (WEELs; formerly by AIHA)
4923
4924 For additional information regarding the approaches taken to estimate occupational exposures, refer to
4925 Sections 5.1.1.1.1 through 5.1.1.1.5.
4926 5.1.1.1.1 Identify and Describe Occupational Exposure Scenarios to Assess
4927 As discussed in Section 3.1.1.1, EPA has identified seven OESs from the COUs to group scenarios with
4928 similar sources of exposure at industrial and commercial workplaces within the scope of the draft risk
4929 evaluation. EPA assessed occupational exposures during the Distribution in commerce of 1,1-
4930 dichloroethane qualitatively. Under the Waste handling, treatment, and disposal COU, EPA assessed
4931 occupational exposures for the OES of General disposal and POTW (Table 5-2).
4932
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Table 5-2. Similar Exposure Groups (SEGs) for 1,1-Dichloroethane
OES
Similar Exposure Groups (SEGs) for 1,1-Dichloroethane
Manufacturing
Operators/Process technicians operate production control panels, record process parameters, conduct walk-throughs
of production areas, perform equipment checks, and collect process samples. Maintenance technicians install
equipment, troubleshoot problems, diagnose issues, repair equipment or machinery in process areas of maintenance
shops. Laboratory technicians conduct laboratory tests to assist with quality control, perform chemical
experimentation, testing and analyses. ONUs perform office work, control board operations, production area walk-
throughs.
Processing as a reactive
intermediate
SEGs expected to be similar as for Manufacture. Workers are potentially exposed to 1,1-dichloroethane when
unloading transport containers, cleaning transport containers, and cleaning reaction vessels or other equipment.
These activities are all potential sources of worker exposure via inhalation of vapor or dermal contact with liquids.
ONUs are expected to have lower inhalation exposures, lower vapor-through-skin uptake, and no dermal exposure.
EPA assumes that 1,1-dichloroethane recycling is for processing as a reactive intermediate.
Processing - repackaging
EPA assessed the general SEG categories of workers and ONUs. Workers are potentially exposed to 1,1-
dichloroethane when transferring 1,1-dichloroethane from bulk containers into smaller containers. Workers may
also be exposed via inhalation of vapor or dermal contact with liquids when cleaning transport containers following
emptying. ONUs are expected to have lower inhalation exposures, lower vapor-through-skin uptake, and no dermal
exposure.
Distribution in commerce
The activities of loading 1,1-dichloroethane product into transport containers and unloading at receiving sites as
well as repackaging into smaller containers are considered part of Distribution in Commerce and these are assessed
under those OES. Cleanup of accidents/spills that may occur during transport are not within the scope of this Risk
Evaluation.
Commercial use as a laboratory
chemical
Laboratory technicians conduct laboratory tests to assist with quality control, perform chemical experimentation,
testing and analyses. During these activities workers may be exposed via inhalation of vapor or dermal contact with
1,1-dichloroethane. EPA also assessed the general SEG of ONU. ONUs are expected to have lower inhalation
exposures, lower vapor-through-skin uptake, and no dermal exposure.
General waste handling,
treatment, and disposal
EPA assessed the general SEG categories of workers and ONUs. Workers are potentially exposed to 1,1-
dichloroethane during the unloading and cleaning of transport containers. Workers may experience inhalation of
vapor or dermal contact with liquids during the unloading process. ONUs are expected to have lower inhalation
exposures, lower vapor-through-skin uptake, and no dermal exposure.
Waste handling, treatment, and
disposal (POTW)
EPA assessed the general SEG categories of workers and ONUs. Workers are potentially exposed to 1,1-
dichloroethane during the unloading and cleaning of transport containers. Workers may experience inhalation of
vapor or dermal contact with liquids during the unloading process. ONUs are expected to have lower inhalation
exposures, lower vapor-through-skin uptake, and no dermal exposure.
Waste handling, treatment, and
disposal (remediation)
EPA did not assess occupational exposures during remediation of 1,1-dichloroethane. 1,1-dichloroethane is a
contaminant removed by a remediation process. EPA did not find evidence that 1,1-dichloroethane is used for
remediation.
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5.1.1.1.2 Estimate Inhalation Exposure for OES Using 1,1-Dichloroethane
Inhalation Monitoring Data
EPA used the evaluation strategies described in the Application of Systematic Review in TSCA Risk
Evaluations (U.S. EPA. 2018a) to collect inhalation exposure monitoring data. EPA's approach is to
collect inhalation monitoring data from literature sources and then evaluate the quality of the data. Data
having high, medium, or low quality ratings would then be used in the risk evaluation for estimating
exposures. In general, higher rankings are given preference over lower ratings; however, lower ranked
data may be used over higher ranked data when specific aspects of the data are carefully examined and
compared. For example, a lower ranked data set that precisely matches the OES of interest may be used
over a higher ranked study that does not as closely match the OES of interest.
EPA reviewed workplace inhalation monitoring data collected by government agencies such as OSHA
and NIOSH, and monitoring data found in published literature (i.e., personal exposure monitoring data
and area monitoring data). EPA considered 8-hour TWA personal breathing zone (PBZ) monitoring data
first. If full-shift PBZ samples were not available, area samples were used for exposure estimates.
Occupational inhalation data for 1,1-dichloroethane during manufacturing were provided via a Test
Order submission from the Vinyl Institute (VI), which includes manufacturers and processors of 1,1-
dichloroethane (Stantec ChemRisk. 2023). These data were used to estimate inhalation exposures for the
following OESs: Manufacturing, Processing as a reactive intermediate, and Commercial use of
laboratory chemicals.
Manufacturing
EPA identified 57 worker and 5 ONU full-shift PBZ samples from the test order data to estimate
inhalation exposures during the manufacturing process. The worker samples collected were from
operators/process technicians, maintenance technicians, and laboratory technicians. In addition, 36 task-
length samples were collected for these workers. These samples were shorter in duration, ranging from
15 to 176 minutes. For further discussion of the task length samples, refer to the Draft Risk Evaluation
for 1,1-Dichloroethane - Supplemental Information File: Environmental Releases and Occupational
Exposure Assessment (U.S. EPA. 2024e).
For comparison, EPA also collected surrogate monitoring data, which refers to data from similar
chemicals and the same OES, from other volatile liquids assessed in previous EPA Risk Evaluations.
EPA identified a total of 166 full-shift worker samples from the following chemicals: 1-bromopropane,
carbon tetrachloride, and trichloroethylene. These chemicals were selected based on their similar vapor
pressure to 1,1-dichloroethane. A summary of the inhalation exposure estimates for the manufacturing
OES using 1,1-dichloroethane test order data is presented in Table 5-3. Surrogate data from published
Risk Evaluations is also presented for comparison showing comparable high-end values and higher
central tendency values. No vapor correction factor was applied to these estimates as the data is intended
solely for comparative purposes.
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Table 5-3. Summary of Manufacturing Inhalation Exposures to 1,1-Dichloroethane
OES
Type of Data
Vapor
Pressure
(mmHg)
Similar Exposure
Group (SEG)
# of Data
Points
Worker Inhalation
Estimates (ppm)
High-End
Central
Tendency
Manufacturing
1,1 -Dichloroethane
test order data
227
Operator/process
technician
40
1.1
4.7E-03
Maintenance technician
8
0.41
7.9E-02
Laboratory technician
9
2.4E-02
1.1E-03
ONU
5
2.0E-02
3.2E-03
1-BP surrogate data
111
Worker
3
0.27
9.0E-02
Carbon tetrachloride
surrogate data
115
Worker
113
0.64
0.12
TCE surrogate data
73
Worker
50
2.5
0.12
1-BP = 1-bromopropane; TCE = trichloroethylene
For the operator/process technician SEG, EPA investigated the top five samples contributing to the wide
range in high-end and central tendency 8-hour TWA estimates. The worker activities that likely
contributed to the elevated exposure concentrations are described in Table 5-4.
Table 5-4. Worker Activities Associated with the Five Highest Sampling Results
Similar
Exposure
Group (SEG)
8-hr TWA
Worker Activities Contributing to Elevated 8-hr TWA
Operator/process
technician
7.3E-01
The collection of process samples from a slip stream into an open-
top container likely contributed to the elevated full-shift
concentration.
Operator/process
technician
7.4E-01
Routine rounds, equipment checks, and process sample collection,
as well as response to a non-routine catalyst leak. The catalyst leak
may have contributed to the elevated full-shift concentration.
Operator/process
technician
1.0E+00
Sample was collected during regular work activities, with no
specific task significantly impacting the full-shift average.
Operator/process
technician
1.8E+00
This sample was identified as an outlier in the data set. During this
full-shift sample, the operator isolated a valve due to an abnormal
plant condition. This activity was classified as emergency response,
rather than typical of the routine operator exposure profile.
Operator/process
technician
1.9E+00
This sample was identified as an outlier in the data set. During this
full-shift sample, the operator isolated a valve due to an abnormal
plant condition. This activity was classified as emergency response,
rather than typical of the routine operator exposure profile.
Processing as a Reactive Intermediate
EPA did not identify monitoring data for the processing as a reactive intermediate OES; however, EPA
assumed the exposures to be similar to manufacturing due to similar worker activities and the use of
primarily closed systems during processing. Therefore, EPA incorporated the manufacturing data into
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the processing as a reactive intermediate exposure estimates as "analogous data." EPA refers to
analogous monitoring data as monitoring data for the same chemical but and similar OES. EPA has used
this assessment approach in previous risk evaluations, including the Risk Evaluation for
Perchloroethylene (PCE) (U.S. EPA. 2020g).
Table 5-5. Summary of Processing as a Reactive Intermediate Inhalation Exposure Estimates
OES
Type of Data
Vapor
Pressure
(mmHg)
Similar Exposure
Group (SEG)
# of Data
Points
Worker Inhalation
Estimates (ppm)
High-End
Central
Tendency
Processing as
a reactive
intermediate
1,1 -dichloroethane
test order data
227
Operator/process technician
40
1.1
4.7E-03
Maintenance technician
8
0.41
7.9E-02
Laboratory technician
9
2.4E-02
1.1E-03
ONU
5
2.0E-02
3.2E-03
Commercial Use as a Laboratory Chemical
During the manufacturing process, EPA identified nine worker full-shift samples for laboratory
technicians. EPA utilized this data as analogous for the commercial use as a laboratory chemical OES.
Due to potential differences in the activities between laboratory technicians during the manufacturing
process and the commercial use as a laboratory chemical OES, there is uncertainty that this assessment
covers the full range of possible exposures.
For comparison, the Agency gathered surrogate monitoring data from a similar chemical, methylene
chloride, based on its published risk evaluation. A summary of the inhalation exposure estimates using
1,1-dichloroethane test order data is presented in Table 5-6. Surrogate data for methylene chloride is
also presented for comparison showing higher central tendency and high-end values. No vapor
correction factor was applied to these estimates as the data is intended solely for comparative purposes.
Table 5-6. Summary of Commercial Use as a Laboratory Chemical Inhalation Exposure Estimates
OES
Type of Data
Vapor
Pressure
(mmHg)
Similar Exposure
Group (SEG)
# of Data
Points
Worker Inhalation
Estimates (ppm)
High-End
Central
Tendency
Commercial
use as a
laboratory
chemical
1,1 -dichloroethane
test order data
227
Laboratory technician
9
2.4E-02
1.1E-03
Methylene chloride
surrogate data
435
Worker
76
15
0.90
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Table 5-7. Summary of Approaches for the Occupational Exposure Scenarios Using 1,1-
Dichloroethane Monitoring Data
OES
1,1-Dichloroethane Monitoring Data Approach
Manufacturing
For the purposes of this risk evaluation, EPA used 1,1-dichloroethane test order
data from the Vinyl Institute during the manufacturing of 1,1-dichloroethane as an
isolated intermediate. For comparison, EPA also collected surrogate monitoring
data from the following chemicals: 1,4-dioxane, 1-bromopropane (1-BP), carbon
tetrachloride, methylene chloride, trichloroethylene (TCE), and 1,2-dichloroethane.
Processing as a reactive
intermediate
EPA used 1,1-dichloroethane test order data from the Vinyl Institute during the
manufacturing of 1,1-dichloroethane as an isolated intermediate due to expected
similarities in exposure points. For comparison, EPA also collected surrogate
monitoring data from 1,2-dichloroethane.
Commercial use as a
laboratory chemical
EPA used 1,1-dichloroethane test order data from the Vinyl Institute for laboratory
technicians during manufacturing process. EPA expects that laboratory exposures
during manufacturing would be similar to exposures during commercial use. As a
comparison, EPA collected surrogate data from methylene chloride.
For the remaining OESs, occupational inhalation exposure monitoring data for 1,1-dichloroethane were
not available from the sources investigated. Therefore, EPA considered other assessment approaches as
described in Sections 5.1.1.1.3 and 5.1.1.1.5, respectively.
The test order report also included information on PPE use at the site where the monitoring data was
from. For details on the PPE used during the various worker activities, refer to Draft Risk Evaluation for
1,1-Dichloroethane - Supplemental Information File: Environmental Releases and Occupational
Exposure Assessment (U.S. EPA. 2024e).
5.1.1.1.3 Estimate Inhalation Exposure for OES Using Surrogate Monitoring Data
As described in Section 5.1.1.2, inhalation exposure monitoring data were not available for 1,1-
dichloroethane for several of the OES. Therefore, EPA collected monitoring data from 1,2-
dichloroethane and methylene chloride to use as surrogate monitoring data for the same OES. EPA
refers to "surrogate monitoring data" as monitoring data for a different chemical but the same (or
similar) COU. Surrogate monitoring data is used when there are similarities in chemical properties,
nature of workplace environment, and worker activities associated with the use of the chemical.
EPA determined exposure estimates using surrogate monitoring data for the following OESs: Waste
handling, treatment, and disposal (general), and Waste handling, treatment, and disposal (specifically for
POTWs). In both cases, the OESs are directly analogous; therefore, EPA expects the process and
associated exposure points to be the same or similar. EPA applied a vapor correction factor when
determining the exposure estimates for these OESs.
For General waste handling, treatment, and disposal OES, EPA identified 22 full-shift worker samples
from methylene chloride. The inhalation exposure estimates for this OES are presented in Table 5-8.
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Table 5-8. Summary of General Waste Handling, Treatment, and Disposal Inhalation Exposure
Estimates
OES
Type of Data
Vapor
Pressure
(mmHg)
Worker
Description
# of Data
Points
Worker Inhalation
Estimates (ppm)
High-End
Central
Tendency
General waste handling,
treatment, and disposal
Methylene chloride
surrogate data
435
Worker
22
10
0.3
For the Waste handling, treatment, and disposal (POTW) OES, EPA identified three full-shift worker
samples from 1,2-dichloroethane. The inhalation exposure estimates for this OES are presented in Table
5-9.
Table 5-9. Summary of Waste Handling, Treatment, and Disposal (POTW) Inhalation Exposure
Estimates
OES
Type of Data
Vapor
Pressure
(mmHg)
Worker
Description
# of Data
Points
Worker Inhalation
Estimates (ppm)
High-End
Central
Tendency
General waste handling,
treatment, and disposal
1,2-dichloroethane
surrogate data
79
Worker
3
0.68
0.25
Table 5-10. Approach for the C
Occupational Exposure Scenarios Using Surrogate Monitoring Data
OES
Surrogate Monitoring Data Approach
General waste handling,
treatment, and disposal
EPA used surrogate monitoring data from methylene chloride.
Waste handling, treatment, and
disposal (POTW)
EPA used surrogate monitoring data from 1,2-dichloroethane.
For additional details on the use of surrogate monitoring data, refer to Draft Risk Evaluation for 1,1-
Dichloroethane - Supplemental Information File: Environmental Releases and Occupational Exposure
Assessment (U.S. EPA. 2024e).
5.1.1.1.4 Approaches for Estimating Inhalation Exposure for Remaining OESs and
ONU Exposures
This section outlines the method for estimating inhalation exposures for the remaining OES lacking
chemical-specific, analogous, or surrogate monitoring data, as well as the approach for estimating ONU
exposures in the absence of data.
EPA did not identify inhalation monitoring data from 1,1-dichloroethane or surrogate data from other
chemicals to assess exposures during the Processing - repackaging of 1,1-dichloroethane OES.
Therefore, EPA estimated inhalation exposures using a Monte Carlo simulation with 100,000 iterations
and the Latin Hypercube sampling method using the models and approaches described in the Draft Risk
Evaluation for 1,1-Dichloroethane - Supplemental Information File: Environmental Releases and
Occupational Exposure Assessment (U.S. EPA. 2024e).
For this OES, EPA applied the EPA Mass Balance Inhalation Model to exposure points described in the
July 2022 Chemical Repackaging GS (U.S. EPA. 2022a)—particularly for the emptying of drums,
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filling of containers, and cleaning of drums process. The EPA Mass Balance Inhalation Model estimates
the concentration of the chemical in the breathing zone of the worker based on a vapor generation rate
(G). An 8-hour TWA is then estimated and averaged over eight hours assuming no exposure occurs
outside of those activities.
EPA used the vapor generation rate and exposure duration parameters from the 1991 CEBManual (U.S.
EPA. 1991) in addition to those used in the EPA Mass Balance Inhalation Model to determine a time-
weighted exposure for each exposure point. EPA estimated the time-weighted average inhalation
exposure for a full work-shift (EPA assumed an 8-hour work-shift) as an output of the Monte Carlo
simulation by summing the time-weighted inhalation exposures for each of the exposure points and
assuming 1,1-dichloroethane exposures were zero outside these activities. The inhalation exposure
estimates for this OES are presented in Table 5-11.
Table 5-11. Summary ol
' Processing - Repackaging Inhalation Exposure Estimates
OES
Type of Data
Worker
Description
Worker Inhalation Estimates
(ppm)
High-End
Central
Tendency
Processing - repackaging
1,1 -dichloroethane
modeled data
Worker
13
3.5
Table 5-12. Approach for the Occupational Exposure Scenarios Using Modeling
OES
Inhalation Exposure Modeling Approach
Processing - repackaging
EPA used assumptions and values from the July 2022 Chemical
Repackaging GS (U.S. EPA. 2022a) and applied the EPA Mass Balance
Inhalation Model to exposure points listed in that GS.
Where EPA was not able to estimate ONU inhalation exposure from monitoring data or models, ONU
exposure was assumed to be equivalent to the central tendency experience by workers for the
corresponding OES. This was done for the following OESs: Processing - repackaging, commercial use
as a laboratory chemical; General waste handling, treatment, and disposal; and Waste handling,
treatment, and disposal (POTW).
5.1.1.1.5 Estimate Dermal Exposure to 1,1-Dichloroethane
Dermal exposure monitoring data were not available for the OES in the assessment from systematic
review of the literature. Therefore, to assess dermal exposure, EPA used the EPA Dermal Exposure to
Volatile Liquids Model to calculate the dermal retained dose for each OES. This model determines an
acute potential dose rate (APDR) based on an assumed amount of liquid on skin during contact event per
day and the theoretical steady-state fractional absorption for 1,1-dichloroethane. The exposure
concentration is determined based on EPA's review of currently available products and formulations
containing 1,1-dichloroethane. The dose estimates assume one dermal exposure event (applied dose) per
work day and approximately 0.3 percent of the applied dose is absorbed through the skin, for 1,1-
dichloroethane in neat form and at 50 percent concentration in the 1,2-dichloroethane vehicle.
A test order for an in vitro dermal absorption study (conducted per OECD 428 guideline) for 1,1-
dichloroethane was issued and data received (Labcorp Early Development. 2024). The guideline study
utilized human skin which is typically obtained from cosmetic surgery. The testing was composed of
skin from 92 percent female and 8 percent male samples, which does not represent the workforce
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demographics or human general population. It is unknown whether the test samples represented
minorities or people with skin diseases (i.e., PESS). The dermal fractional absorption of 0.3 percent is
used to estimate dermal exposure as described above and is derived from this test order study data as
described in the following paragraphs and Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental
Information File: in vitro Dermal Absorption Study Analysis (U.S. EPA. 2024f) and Draft Risk
Evaluation for 1,1-Dichloroethane - Supplemental Information File: in vitro Dermal Absorption Study
Calculation Sheet (U.S. EPA. 2024g).
EPA's calculations addressing missing mass balance and high data variability are based on OECD
GDI56 guidance and EFSA2017 guidance. Recommendations state missing mass should be corrected
for use in risk assessments, where Corrected %Absorption = Raw % Absorption/(% mass balance/100).
If the data variability is excessive for an in vitro assay, then OECD GDI 56 recommends addressing this
deficit by either using the highest absorption value measured or the highest Kp value measured or to
calculate the 95 percent Upper Confidence Level (UCL) instead of using the mean values based on
highly variable data. The dermal absorption data coefficient of variation was 38 to 200 percent with
mass balance results of 54 to 93 percent, so the raw data was corrected according to OECD GDI56
guidance for missing mass and data variability. In general, EPA exposure assessments regularly report
the 95th percentile exposures to be human health protective and specifically to include subpopulations
that are potentially highly exposed or more susceptible to the hazards of 1,1-dichloroethane (PESS). The
test order submission report data had a sensitive LOD of 0.008 percent. The highest dermal absorption
value reported in the study was 0.27 percent at 50 percent concentration in 1,2-dichloroethane as the
vehicle with a mass balance corrected value of 0.59 percent absorption. This replicate also had the
lowest mass recovery, the guideline study indicates that there is simultaneously dermal absorption and
evaporation processes occurring.
To be human health protective, EPA did not assume that the missing mass is not absorbable, nor was it
assumed that all of the missing mass simply evaporated. Instead, it was assumed that part of the missing
mass is potentially absorbable. The mass balance corrected mean absorption for neat 1,1-dichloroethane
was 0.22 percent and the 95 percent upper confidence limit for the neat chemical was 0.29 percent
dermal absorption, or similar to the dermal absorption reported for the analog 1,2-dichloroethane at 0.21
percent. The highest 95 percent upper confidence level based on a mean value was 0.35 percent
absorption for 50 percent 1,1-dichloroethane in the 1,2-dichloroethane vehicle. In context, a "down the
glove" worker scenario limiting evaporation could have higher dermal absorption values than these in
vitro results. Five of the 50 percent 1,1-dichloroethane (in 1,2-dichloroethane vehicle) replicates had raw
absorption values over 0.05 percent indicating dermal risks. The coefficient of variation for the Kp
values were 31 to 82 percent, so the raw data was corrected for data variability according to OECD
GD156 guidance by calculating the 95 percent upper confidence level. The mean Kp value and the 95
percent upper confidence limit for neat 1,1-dichloroethane were 0.00229 and 0.00371 cm/hour,
respectively.
EPA also compared the 1,1-dichloroethane dermal absorption estimate of 0.3 percent with that of its
isomer, 1,2-dichloroethane. 1,2-dichloroethane has an identical molecular weight and a very similar log
Kow value as 1,1-dichloroethane, key parameters for EPA dermal modeling. The reported in vitro mean
Kp value for the analog 1,2-dichloroethane in peer-reviewed literature was similar at 0.00109 cm/hour
for the neat chemical (Schenk, 2018, 4940676). and the estimated fraction absorbed was also similar at
0.6 percent using default settings for the American Industrial Hygiene Association (AIHA) skin
permeation model, IHSkinPerm.
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To assess exposure, EPA used the Dermal Exposure to Volatile Liquids Model (see Equation 5-1) to
calculate the dermal retained dose. The equation modifies EPA/OPPT 2-Hand Dermal Exposure to
Liquids Model (peer-reviewed) by incorporating a "fraction absorbed (fobs)" parameter to account for the
evaporation of volatile chemicals:
Equation 5-1. EPA Dermal Exposure to Volatile Liquids Model
Dexp — 0^ ^ Qu ^ fabs ^ ^derm ^ FT) / BW
Where:
Dexp
Dermal retained dose (mg/kg-day)
s
Surface area of contact (cm2)
Qu
Quantity remaining on the skin after an exposure event (high-end: 2.1 mg/cm
-event central tendencv 1.4 m«/cm2-event (U.S. EPA, 1992))
Yderm ~
Weight fraction of the chemical of interest in the liquid (wt %)
FT
Frequency of events (default: 1)
fabs ~
Fraction of applied mass that is absorbed (%)
BW =
Body weight (kg)
The standard model considers an assumed amount of liquid on skin during one contact event per day
(On), an absorption factor (fabs), surface area of the hands (S) and the weight fraction of 1,1-
dichloroethane (Yderm) in the formulation to calculate a dermal dose. The model reduces to an assumed
amount of liquid on the skin during one contact event per day adjusted by the weight fraction of 1,1-
dichloroethane in the liquid to which the worker is exposed. EPA assumed the worker would be
handling neat 1,1-dichloroethane for all OESs; therefore, EPA assessed all exposure scenarios at a 100
percent weight fraction. Table 5-13 summarizes the model parameters and their values for estimating
dermal exposures.
Table 5-13. Summary of Dermal Model Input Values
Input Parameter
Symbol
Value(s)
Unit
Surface area
S
535 (central tendency)
1,070 (high-end)
cm2
Dermal load
Q>i
1.4 (central tendency)
2.1 (high-end)
mg/cm2-event
Weight fraction of chemical
Yderm
1
unitless
Frequency of events
FT
1
events/day
Fractional absorption
fabs
0.003 (neat 1,1-dichloroethane)
unitless
Body weight
BW
80
kg
For details on workers activities that could potentially result in dermal exposure, refer to Table 5-2. EPA
used a high-end exposed skin surface area (S) for workers of 1,070 cm2 based on the mean two-hand
surface area for adult males ages 21 or older from Chapter 7 of EPA's Exposure Factors Handbook
(U.S. EPA. 2011a). For central tendency estimates, EPA assumed the exposure surface area was
equivalent to only a single hand (or one side of two hands) and used half the mean values for two-hand
surface areas (i.e., 535 cm2 for workers). The model estimates dermal exposure to the hands and does
not account for dermal exposures to other parts of the body.
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The values of the dermal load (Qu) were based on experimental studies of non-aqueous liquids to
measure the quantity remaining on the skin after contact. In the study, an initial wipe test was performed
that consisted of the subjects wiping their hands with a cloth saturated in the liquid. The amount of
liquid retained on the hands was measured immediately after the application.
Data on dermal exposure measurements at facilities that manufacture, process, and use chemicals is
limited. Table 5-14 below includes measured data that can be used for comparison with the dermal
loading values used in the DEVL model and the 1,1-dichloroethane dermal exposure model estimates
provided in Table 5-15. The experimental dermal loading values in the DEVL model are comparable to
measured values recorded in the Pesticide Handlers Exposure Database (PHED) (per SAIC, 1996).
Table 5-14. Comparison of Dermal Exposure Values
Dermal Exposure
Value
Type of Data
Notes
Reference
1.4 mg/cm2-event
(central tendency)
2.1 mg/cm2-event
(high-end)
Experimental data
Used in EPA/OPPT Dermal
Contact with Liquids Models
OPPT Dermal
Framework
Underlying data from
(USEPA, 1992)
2.9 mg
metalworking
fluid/cm2-hr
(geometric mean)
Measured data
Study of dermal exposures to
electroplating and metalworking
fluids during metal shaping
operations
Roff, 2004 (as reported
in OECD ESD on
Metalworking Fluids)
0.5-1.8 mg/cm2
Measured data
Dermal exposure data for
workers involved in pesticide
mixing and loading. The data
included various combinations
of formulation type and
mixing/loading methods.
1992 Pesticide
Handlers Exposure
Database (PEHD), as
reported in (SAIC,
1996)
0.0081-505.4
mg/day
Measured data
PMN manufacturer study of
unprotected dermal exposures to
trichloroketone for maintenance
workers
Anonymous, 1996 (as
reported in (SAIC,
1996)
0.0071-2.457
mg/day
Measured data
PMN manufacturer study of
unprotected dermal exposures to
trichloroketone for process
operators
Anonymous, 1996 (as
reported in (SAIC,
1996)
0.0105-0.0337
mg/day
Measured data
PMN manufacturer study of
protected dermal exposures to
trichloroketone for maintenance
workers
Anonymous, 1996 (as
reported in (SAIC,
1996)
0.0098-0.2417
mg/day
Measured data
PMN manufacturer study of
protected dermal exposures to
trichloroketone for process
operators
Anonymous, 1996 (as
reported in (SAIC,
1996)
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5213
5214
5215
5216
5217
5218
5219
5220
5221
5222
5223
5224
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The dermal potential dose rate estimates are presented in Table 5-15. As previously stated, the estimates
are the same across all OES.
Table 5-15. Dermal Potential Dose Rate Estimates
Category
Potential Dose Rate
(mg/day)
High-End
Central Tendency
Worker, no gloves
6.7
2.3
For additional rationale on the dermal exposure assessment and parameters, refer to Draft Risk
Evaluation for 1,1-Dichloroethane - Supplemental Information File: Environmental Releases and
Occupational Exposure Assessment (U.S. EPA. 2024e).
5.1.1.1.6 Estimate the Number of Workers and Occupational Non-users Potentially
Exposed
An assessment objective is to estimate the number of workers and ONUs potentially exposed. Normally,
a primary difference between workers and ONUs is that workers may handle 1,1-dichloroethane and
have direct contact with the chemical, while ONUs are working in the general vicinity of workers but do
not handle 1,1-dichloroethane and do not have direct contact with 1,1-dichloroethane being handled by
the workers. The size of the area that ONUs may work can vary across each OES and across facilities
within the same OES and will depend on the facility configuration, building and room sizes, presence of
vapor barrier, and worker activity pattern. Where possible, for each COU, EPA identified job types and
categories for workers and ONUs. The Agency evaluated inhalation exposures to workers and ONUs,
and dermal exposures to workers. EPA did not assess dermal exposures to ONUs as EPA does not
expect ONUs to have routine dermal exposures in the course of their work. Depending on the condition
of use, ONUs may have incidental dermal exposures due to surface contamination. However, data (e.g.,
frequency and amount of liquid on the skin after contact) were not identified to assess this exposure.
Methodology
Where available, EPA used CDR data to provide a basis to estimate the number of workers and ONUs.
Data were available from the 2016 and 2020 CDR for manufacturing sites; however, EPA determined
this was not sufficient to determine the total number of workers for that OES. EPA supplemented the
available CDR data using available market data; NAICS and SIC code data from TRI, DMR, and NEI
sites identified for each condition of use (for number of sites estimated see Section 3.2.1.1); and
analyzing Bureau of Labor Statistics (BLS) and U.S. Census data using the methodology described in
the Environmental Releases and Occupational Exposure Assessment. Where market penetration data and
site-specific NAICS/SIC codes from TRI/DMR/NEI were not available, EPA estimated the number of
workers using data from GSs and ESDs. For additional details on development of estimates of number
of workers refer to Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File:
Environmental Releases and Occupational Exposure Assessment (U.S. EPA. 2024e).
EPA also determined the number of days per year that workers are potentially exposed to 1,1-
dichloroethane. In general, the exposure frequency is the same as the number of operating days per year
for a given OES (see Section 3.1.1.5). However, if the number of operating days is greater than 250 days
per year, EPA assumed that a single worker would not work more than 250 days per year such that the
maximum exposure days per year was still 250.
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Results
Table 5-16 provides a summary for the number of workers and ONUs potentially exposed to 1,1-
dichloroethane per facility. The estimates are provided for a facility within each OES and are specific to
1,1-dichloroethane with the exception of the Processing - repackaging OES.
Table 5-16. Total Number of Workers and ONUs Potentially Exposed to 1,1-Dichloroethane for
Each OES
Exposure
Potential
Potential
Potential
OES
Days per
Number of
Number of
Number of ONUs
Notes
Year
Sites
Workers per Site
per Site
Manufacturing
350
10
119
56
Number of workers and
ONU estimates based on
U.S. Census Bureau data,
CDR, DMR, TRI, and NEI
(U.S. Census Bureau.
2015).
Processing as
350
90
94
21
Number of workers and
a Reactive
ONU estimates based on
Intermediate
U.S. Census Bureau data,
DMR, TRI, and NEI (U.S.
Census Bureau. 2015).
Processing -
repackaging
128
2
3
1
Based on the July 2022
Chemical Repackaging GS
(U.S. EPA. 2022a).
Commercial
260
43-138
3
3
Based on the 2022 Draft GS
use as a
laboratory
chemical
on the Use of Laboratory
Chemicals (U.S. EPA.
2023c).
Waste
250
672
49
15
Number of workers and
handling,
ONU estimates based on
treatment, and
U.S. Census Bureau data,
disposal
DMR, TRI, and NEI (U.S.
Census Bureau. 2015).
Waste
250
125
24
12
Number of workers and
handling,
ONU estimates based on
treatment, and
U.S. Census Bureau data,
disposal
(POTW)
DMR, TRI, and NEI (U.S.
Census Bureau. 2015).
5.1.1.2 Estimates of Occupational Exposure (ppm) and Dermal Exposure (mg/day)
Table 5-17 provides a summary for each of the OES by indicating whether monitoring data were used,
how many data points were identified, the quality of the data, and also whether EPA used modeling to
estimate inhalation and dermal exposures for workers and ONUs.
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5258 Table 5-17. Summary of Assessment Methods for Each Occupational Exposure Scenario
Inhalation Exposure
Dermal Exposure
OES
1,1-Dichloroethane Monitoring
Surrogate Monitoring
Modeling
Monitoring
Modeling
# Data
Points
# Data
Points
Data
# Data
Points
# Data
Points
Data
Data
Worker
ONU
Quality
Ratings
Worker
ONU
Quality
Ratings
Worker
ONU
Worker
Quality
Rating
Worker
Manufacturing
ii
57
ii
5
H
ii
172
0
N/A
H
0
0
0
N/A
ii
Processing as a
ii
57
ii
5
H
ii
46
0
N/A
M
0
0
0
N/A
ii
reactive
intermediate
Processing -
0
N/A
0
N/A
N/A
0
N/A
0
N/A
N/A
ii
0
0
N/A
ii
repackaging
Commercial use as
ii
9
0
N/A
H
ii
76
0
N/A
H
0
0
0
N/A
ii
a laboratory
chemical
Distribution in
Not estimated
commerce
Waste handling.
0
N/A
0
N/A
N/A
ii
3
0
N/A
M
0
0
0
N/A
ii
treatment, and
disposal (POTW)
General waste
0
N/A
0
N/A
N/A
ii
22
0
N/A
M
0
0
0
N/A
ii
handling, treatment,
and disposal
O = no data available; ii = data available
Where EPA was not able to estimate ONU inhalation exposure from monitoring data or models, this was assumed equivalent to the central tendency experienced by
workers for the corresponding PES; dennal exposure for ONUs was not evaluated because they are not expected to be in direct contact with 1.1-dichloroelhane.
5259
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5270
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5272
5273
5274
A summary of inhalation and dermal exposure estimates for each OES is presented below in Table 5-18.
Table 5-18. Summary of Inhalation and Dermal Exposure
Estimates for Each C
)ES
OES
Worker
Description
Exposure
Days
(day/year)
Worker
Esti
(P
Inhalation
mates
)m)
ONU
Inhalation Estimates
(PPm)
Worker Dermal
Exposure Estimates
(mg/day)
High-
End
Central
Tendency
High-End
Central
Tendency
High-
End
Central
Tendency
Manufacturing
Operator/
process
technician
250
1.1
4.7E-03
2.0E-02
3.2E-03
6.7
2.3
Maintenance
technician
250
0.41
7.9E-02
Laboratory
technician
250
2.4E-02
1.1E-03
Processing as a
reactive
intermediate
Operator/
process
technician
250
1.1
4.7E-03
2.0E-02
3.2E-03
6.7
2.3
Maintenance
technician
250
0.41
7.9E-02
Laboratory
technician
250
2.4E-02
1.1E-03
Processing -
repackaging
-
250
13
3.5
3.5
6.7
2.3
Commercial use as
a laboratory
chemical
Laboratory
technician
250
2.4E-02
1.1E-03
1.1E-03
6.7
2.3
Distribution in
commerce
Not Estimated
General waste
handling,
treatment, and
disposal
250
10
0.30
0.30
6.7
2.3
Waste handling,
treatment, and
disposal (POTW)
250
0.68
0.25
0.25
6.7
2.3
Where EPA was not able to estimate ONU inhalation exposure from monitoring data or models, this was assumed
equivalent to the central tendency experienced by workers for the corresponding OES; dermal exposure for ONUs was not
evaluated because they are not expected to be in direct contact with 1,1-dichloroethane.
Using these 8-hour TWA exposure concentrations, EPA then calculated acute, subchronic, and chronic
(non-cancer and cancer) exposures. These exposure metrics are then used to determine risk, as described
in Section 5.3.3.1.
5.1.1.3 Weight of Scientific Evidence for the Estimates of Occupational Exposures
from Industrial and Commercial Sources
EPA's conclusion on the weight of scientific evidence is based on the strengths, limitations, and
uncertainties associated with the release estimates. The Agency considers factors that increase or
decrease the strength of the evidence supporting the exposure estimate—including quality of the
data/information, applicability of the exposure data to the COU (including considerations of temporal
relevance, locational relevance) and the representativeness of the estimate for the whole industry.
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5275 The best professional conclusion is summarized using the descriptors of robust, moderate, slight, or
5276 indeterminant, according to EPA's 2021 Draft Systematic Review Protocol (U.S. EPA. 2021b). For
5277 example, a conclusion of moderate weight of scientific evidence is appropriate where there is measured
5278 exposure data from a limited number of sources such that there is a limited number of data points that
5279 may not be representative of the worker activities or potential exposures. A conclusion of slight weight
5280 of scientific evidence is appropriate where there is limited information that does not sufficiently cover
5281 all potential exposures within the COU, and the assumptions and uncertainties are not fully known or
5282 documented. See EPA's 2021 Draft Systematic Review Protocol (U.S. EPA. 2021b) for additional
5283 information on weight of scientific evidence conclusions. A summary of the weight of scientific
5284 evidence conclusions for the inhalation estimates is provided below in Table 5-19.
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5285 Table 5-19. Weight of Scientific Evidence Conclusions for the Inhalation Exposure Assessment
OES
Weight of Scientific
Evidence Conclusion
Overall Confidence in Release Estimate Rationale
Manufacturing
Moderate to Robust
EPA considered the assessment approach, the quality of the data, and uncertainties in assessment results to
determine a weight of scientific evidence conclusion for the 8-hour TWA inhalation exposure estimates. EPA
used 1,1-dichloroethane test order inhalation data to assess inhalation exposures. The primary strength of these
data is the use of personal and directly applicable data, and the number of samples available for workers and
ONUs. The primary limitation is that the data is from one site and may not be representative of all
manufacturing sites. Additionally, EPA assumed 250 exposure days per year based on 1,1-dichloroethane
exposure each working day for a typical worker schedule; it is uncertain whether this captures actual worker
schedules and exposures.
Based on these strengths and limitations, EPA has concluded that the weight of scientific evidence for this
assessment is moderate to robust and provides a plausible estimate of exposures in consideration of the
strengths and limitations of reasonably available data.
Processing as a
reactive
intermediate
Moderate
1,1-Dichloroethane monitoring data for this scenario was not available. EPA used 1,1-dichloroethane test
order data from the Manufacturing OES to assess inhalation exposures. The primary strength of this data is the
use of personal and potentially applicable data. The primary limitations of these data include the uncertainty of
the representativeness of these data toward the true distribution of inhalation concentrations in this scenario
since the data was analogous from the manufacturing OES. EPA also assumed 250 exposure days per year
based on 1,1-dichloroethane exposure each working day for a typical worker schedule; it is uncertain whether
this captures actual worker schedules and exposures.
Based on these strengths and limitations, EPA has concluded that the weight of scientific evidence for this
assessment is moderate and provides a plausible estimate of exposures in consideration of the strengths and
limitations of reasonably available data.
Processing -
repackaging
Moderate
1,1-Dichloroethane monitoring data was not available for this scenario. Additionally, the Agency did not
identify relevant monitoring data from other scenarios or chemicals assessed in previous EPA Risk
Evaluations. Therefore, EPA modeled inhalation exposures. The Agency used assumptions and values from
the Julv 2022 Chemical Repackaging GS (U.S. EPA. 2022a). which the systematic review process rated high
for data aualitv. to assess inhalation exposures (OECD. 2009). The Agency used EPA/OPPT models combined
with Monte Carlo modeling to estimate inhalation exposures. A strength of the Monte Carlo modeling
approach is that variation in model input values and a range of potential exposure values is more likely than a
discrete value to capture actual exposure at sites. The primary limitation is the uncertainty in the
representativeness of values toward the true distribution of potential inhalation exposures. In addition, EPA
lacks 1,1-dichloroethane facility production volume data; and therefore, throughput estimates are based on
CDR reporting thresholds. Also, EPA could not estimate the number of exposure days per year associated with
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OES
Weight of Scientific
Evidence Conclusion
Overall Confidence in Release Estimate Rationale
repackaging operations, so the exposure days per year estimates are based on an assumed site throughput of
imported containers.
Based on these strengths and limitations, EPA has concluded that the weight of scientific evidence for this
assessment is moderate and provides a plausible estimate of exposures.
Commercial
use as a
laboratory
chemical
Moderate
1,1-Dichloroethane monitoring data for this scenario was not available. EPA used 1,1-dichloroethane test
order data for laboratory technicians from the manufacturing OES to assess inhalation exposures. EPA
considered the assessment approach, the quality of the data, and uncertainties in assessment results to
determine a weight of scientific evidence conclusion for the 8-hour TWA inhalation exposure estimates. EPA
used inhalation data to assess inhalation exposures. The primary strength of these data is the use of personal
and potentially applicable data. The primary limitation is the number of samples available for workers. Data
was not available for ONUs. Additionally, there is uncertainty in the representativeness of these data toward
the true distribution of inhalation concentrations in this scenario since the laboratory use occurred in a
manufacturing setting. EPA assumed 250 exposure days per year based on 1,1-dichloroethane exposure each
working day for a typical worker schedule; it is uncertain whether this captures actual worker schedules and
exposures.
Based on these strengths and limitations, EPA has concluded that the weight of scientific evidence for this
assessment is moderate and provides a plausible estimate of exposures in consideration of the strengths and
limitations of reasonably available data.
Waste
handling,
treatment, and
disposal
(general)
Moderate
1,1-Dichloroethane monitoring data was not available for this scenario. Additionally, EPA did not identify 1,1-
dichloroethane monitoring data from other scenarios. Therefore, the Agency used surrogate inhalation data
from methylene chloride to assess inhalation exposures. The primary limitations of these data include the
uncertainty of the representativeness of these data toward the true distribution of inhalation concentrations in
this scenario since the data were surrogate from methylene chloride, which results in a moderate confidence
rating. EPA also assumed 250 exposure days per year based on 1,1-dichloroethane exposure each working day
for a typical worker schedule; it is uncertain whether this captures actual worker schedules and exposures.
Based on these strengths and limitations, EPA has concluded that the weight of scientific evidence for this
assessment is moderate and provides a plausible estimate of exposures in consideration of the strengths and
limitations of reasonably available data.
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OES
Weight of Scientific
Evidence Conclusion
Overall Confidence in Release Estimate Rationale
Waste
handling,
treatment, and
disposal
(POTW)
Moderate
1,1-Dichoroethane monitoring data was not available for this scenario. Additionally, EPA did not identify 1,1-
dichloroethane monitoring data from other scenarios. Therefore, the Agency used surrogate inhalation data
from 1,2-dichloroethane to assess inhalation exposures. The primary limitations of these data include the
uncertainty of the representativeness of these data toward the true distribution of inhalation concentrations in
this scenario since the data were surrogate from 1,2-dichloroethane, which results in a low confidence rating.
In addition, the available surrogate data only provided 3 worker inhalation monitoring data samples for
wastewater treatment. EPA also assumed 250 exposure days per year based on 1,1-dichloroethane exposure
each working day for a typical worker schedule; it is uncertain whether this captures actual worker schedules
and exposures.
Based on these strengths and limitations, EPA has concluded that the weight of scientific evidence for this
assessment is moderate and provides a plausible estimate of exposures in consideration of the strengths and
limitations of reasonably available data.
5286
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5289
5290
5291
5292
5293
5294
5295
5296
5297
5298
5299
5300
5301
5302
5303
5304
5305
5306
5307
5308
5309
5310
EPA estimated dermal exposures using modeling methodologies, which are supported by moderate
evidence. EPA used the EPA Dermal Exposure to Volatile Liquids Model to calculate the dermal
retained dose. This model modifies the EPA/OPPT 2-Hand Dermal Exposure to Liquids Model by
incorporating a "fraction absorbed (fobs)" parameter to account for the evaporation of volatile chemicals.
These modifications improve the modeling methodology; however, the modeling approach is still
limited by the low variability for different worker activities/exposure scenarios. Therefore, the weight of
scientific evidence for the modeling methodologies is moderate. The exposure scenarios and exposure
factors underlying the dermal assessment are supported by moderate to robust evidence.
Dermal exposure scenarios were informed by moderate to robust process information and GS/ESD.
Exposure factors for occupational dermal exposure include amount of material on the skin, surface area
of skin exposed, and absorption of 1,1-dichloroethane through the skin. These exposure factors were
informed by literature sources, the ChemSTEER User Guide (U.S. EPA 2015) for standard exposure
parameters, and a European model, with ratings from moderate to robust. Based on these strengths and
limitations, EPA concluded that the weight of scientific evidence for the dermal exposure assessment is
moderate to robust for all OESs.
5.1.2 General Population Exposures
1,1-Dichloroethane _ General Population Exposures (Section 5.1.2):
Key Points
EPA evaluated the reasonably available information for the following general population exposures,
the key points of which are summarized below:
• Inhalation exposure is the major general population exposure pathway.
o For exposures through ambient air, EPA considered potential exposures for communities
within 10 km of a release site,
o EPA estimated general population inhalation exposures based on modeled air
concentrations estimated in Section 3.3.1 using equations and exposure factors described
in Appendix E.2.
• Dermal exposures from the exposure scenario of swimming in receiving water from 1,1-
dichloroethane releases were estimated to result in low exposures.
• Oral exposures to 1,1-dichloroethane from ingestion of drinking water were estimated to
result in low exposures.
• Oral exposures to 1,1-dichloroethane from ingestion of fish-containing 1,1-dichloroethane
were estimated for adults, children and for subsistence and tribal fishers. Low
bioaccumulation potential in fish results in low exposures.
• Oral exposures to 1,1-dichloroethane by children playing with and ingestion of 1,1-
dichloroethane containing biosolids as applied to land were expected to result in low
exposures.
General population exposures occur when 1,1-dichloroethane is released into the environment and the
media is then a pathway for exposure. Section 3.3 provides a summary of the monitoring, database, and
modeled data on concentrations of 1,1-dichloroethane in the environment. Figure 5-2 provides a graphic
representation of where and in which media 1,1-dichloroethane is estimated to be found and the
corresponding route of exposure.
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5312
5313
5314
5315
5316
5317
5318
5319
5320
5321
5322
5323
5324
5325
5326
5327
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Bathing
Water
Dermal,
Inhalation
Drinking
Water
Oral
tundwl
.pump.
I—-—- Ambient Air
1 I Inhalation
Soil and Dust
Oral, Inhalation
Groundwater
Aquatic and
Terrestrial Animal
rfgestion
Oral
| Sediment |
Drinking
Water
Treatment
water , ,
Recreation I Surface W.ter |
Oral, Dermal
Figure 5-2. Potential Human Exposure Pathways to 1,1-Dichloroethane for the General
Population"
11 The diagram presents the media (white text boxes) and routes of exposure (italics for oral, inhalation, or dermal)
for the general population. Sources of drinking water is depicted with grey arrows. This diagram pairs with Figure
2-1 and Figure 4-1 depicting the fate and transport of the subject chemical in the environment.
5.1.2.1 Approach and Methodology
Exposure to 1,1-dichloroethane results from direct releases to ambient air and surface water resulting
from its use in the chemical manufacturing processes. 1,1-Dichloroethane has been detected in the
indoor and outdoor environment although exposures likely vary across the general population. See
tornado plots and associated tables in the Draft Risk Evaluation for 1,1-Dichloroethane - Systematic
Review Protocol (U.S. EPA. 2024t) for a summary of the various environmental media 1,1-
dichloroethane has been detected.
Releases of 1,1-dichloroethane are likely to occur through the direct release to air, water, and soil, with
partitioning between the environmental compartments. Most 1,1-dichloroethane releases will ultimately
partition to air based on its vapor pressure; however, a smaller amount will remain in water due to its
water solubility. For a more detailed discussion about 1,1-dichloroethane environmental partitioning,
please see Section 2.2.2. and Appendix D.2.1.2.
Exposure to the general population was estimated for the industrial and commercial releases per OES.
Table 3-4 illustrates how the industrial and commercial releases to the environmental media varies by
OES.
Modeled air concentrations (Sections 3.3.1 and 3.3.2) were utilized to estimate inhalation exposures
(5.1.2.2) to the general population at various distances from a release facility. In addition, a detailed
population analysis was performed for a subset of TRI and NEI release facilities for which estimated
cancer risks exceeded the lifetime cancer benchmark of 1 in 1,000,000 (110 Cl). This analysis includes
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5339
5340
5341
5342
5343
5344
5345
5346
5347
5348
5349
5350
5351
5352
5353
5354
5355
5356
5357
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an evaluation of PESS as well as metrics associated with racial demographics and poverty status of the
population. Proximity of general population to community infrastructures was also evaluated, such as
parks, schools, places of worship, childcare centers, and hospitals (Section 5.3.4).
Modeled surface water concentrations (Sections 3.3.3.2) were utilized to estimate oral drinking water
exposures (Section 5.1.2.4.1) oral fish ingestions exposures (Section 5.1.2.4.2), incidental oral exposures
(Sections 5.1.2.4.3, 5.1.2.4.4, and 5.1.2.4.5), and incidental dermal exposures (Section 5.1.2.3.1) for the
general population. Modeled groundwater concentrations (Section 3.3.4.3), resulting from 1,1-
dichloroethane TSCA land disposal were estimated but not evaluated as a potential pathway of concern
for drinking water exposures. Although 1,1-dichloroethane has been detected in groundwater as drinking
water monitoring data, the low 1,1-dichloroethane concentrations confirmed low oral drinking water
exposures (Section 5.1.2.4.1) to the general population. Modeled (Section 3.3.4.1) soil concentrations
via deposition were used to estimate dermal exposures (Sections 5.1.2.4.5) to children who play in mud
and other activities with soil.
Exposures estimates from industrial and commercial releases of 1,1-dichloroethane were compared to
exposure estimates from non-scenario specific monitoring data to ground truth the results (e.g., ambient
air exposures). Figure 3-5 and Table 3-8 summarize the environmental media monitoring data that was
available in the United States For a description of statistical methods, methodology of data integration
and treatment of non-detects and outliers used to generate the AMTIC estimates please reference the
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Ambient Monitoring
Technology Information Center (AMTIC), 1,1-Dichloroethane Monitoring Data 2015 to 2020 (U.S.
EPA. 2024bY
Exposure to general population per conditions of use were estimated for emissions to water and air, as
depicted in Figure 5-3.
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5371
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5373
5374
5375
5376
5377
5378
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PUBLIC RELEASE DRAFT
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Uses
Summary of
Release Types
Summary of Media
or Pathways
Exposure
Scenarios
Media Estimation
Methods
Emissions to Air
Ambient air,
General
.Ambient air:
AERMOD
Dispersion
Conditions
of Use
Discharges to
Surface Water
Indoor air.
Deposition SoiL
Drinking Water,
Surface Water
Population,
Recreational
Shimming,
Fishing
Modeling
Surface water:
E-F AST1 dilution
estimates
Releases to Land
Soil:
Simpletreat 4.0
Figure 5-3. Overview of General Population Exposure Assessment for 1,1-Dichloroethane
For each exposure pathway, central tendency and high-end doses were estimated. EPA's Guidelines for
Human Exposure Assessment defined central tendency exposures as "an estimate of individuals in the
middle of the distribution." It is anticipated that these estimates apply to most individuals in the United
States. High-end exposure estimates are defined as "plausible estimate of individual exposure for those
individuals at the upper end of an exposure distribution, the intent of which is to convey an estimate of
exposure in the upper range of the distribution while avoiding estimates that are beyond the true
distribution." It is anticipated that these estimates apply to some individuals, particularly those who may
live near facilities with elevated concentrations.
5.1.2.1.1 General Population Exposure Scenarios
Figure 5-2 provides an illustration of the exposure scenarios considered for general population exposure.
Ambient Air Exposure Scenarios
The Multi-Year Methodology AERMOD using TRI or NEI release data evaluated exposures to
members of the general population at eight finite distances (10, 30, 60, 100, 1,000, 2,500, 5,000, and
10,000 m) and two area distances (30 to 60 m and 100 to 1,000 m) from each TRI and NEI releasing
facility for each OES (or generic facility for alternative release estimates). Human populations for each
of the eight finite distances were placed in a polar grid every 22.5 degrees around the respective distance
ring. This results in a total of 16 modeled exposure points around each finite distance ring for which
exposures are modeled. Figure 5-4 provides a visual depiction of the placement of exposure points
around a finite distance ring. Although the visual depiction only shows exposure point locations around
a single finite distance ring, the same placement occurred for all eight finite distance rings.
Page 200 of 664
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PUBLIC RELEASE DRAFT
July 2024
10 m
1000 m
Exposure Points around each Finite Distance Ring
2,500 m
Releasing Facility
30 m
60 m
30-60 m
100-1,000 m
100 m
10,000 m
Location of
OCJ Exposed
Individual
Figure 5-4. Modeled Exposure Points for Finite Distance Rings for Ambient Air
Modeling (AERMOD)
Modeled exposure points for the area distance 30 to 60 m evaluated were placed in a cartesian grid at
equal distances between 30 and 60 in around each releasing facility. Exposure points were placed at IO-
meter increments. This results in a total of 80 points for which exposures are modeled. Modeled
exposure points for the area distance 100 to 1,000 m evaluated were placed in a cartesian grid at equal
distances between 100 and 1,000 m around each releasing facility. Exposure points were placed at 100-
meter increments. This results in a total of 300 points for which exposures are modeled, provides a
visual depiction of the placement of exposure points (each dot) around the 100 to 1,000 m area distance
ring. All exposure points were at 1.8 m above ground, as a proximation for breathing height for ambient
air concentration estimations. A duplicate set of exposure points was at ground level (0 m) for
deposition estimations.
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5409
5410
5411
5412
5413
5414
5415
5416
5417
5418
5419
5420
5421
5422
5423
5424
5425
5426
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PUBLIC RELEASE DRAFT
July 2024
Figure 5-5. Modeled Exposure Point Locations for Area
Distance for Ambient Air Modeling (AERMOD)
The ambient air is a major pathway for 1,1-dichloroethane and the general population may be exposed to
ambient air concentrations and air deposition because of 1,1-dichloroethane releases. Relevant
exposures scenarios considered in this draft risk evaluation include ambient air inhalation for
populations living nearby releasing facilities, and ingestion exposure of soil to children resulting from
ambient air deposition from a nearby facility.
Soil Exposure Scenarios
1,1-Dichloroethane may also be present in the biosolids resulting from the 125 POTWs treating effluent
containing 1,1-dichloroethane (see Table 3-4). These 1,1-dichloroethane-containing biosolids may be
spread onto soils as a common biosolids disposal method. EPA considered exposure pathway via
children playing in soil where biosolids were spread. Given pica behavior of children where soil is
ingested, EPA used the EPA Exposure Factors Handbook (U.S. EPA. 201 la) recommended 3 to 6 year
old ingestion rate to estimate the possible ingestion of 1,1-dichloroethane in soil via the biosolids
pathway.
As mentioned above, air deposition fluxes from AERMOD were used to estimate soil concentrations at
various distances from the largest emitting facility for each OES. Oral ingestion exposure estimates of
soil were calculated for children aged 3 to 6 years using the EPA's Exposure Factors Handbook (U.S.
EPA. 2011a) recommended ingestion rate for that age group.
Water Exposure Scenarios
1,1-Dichloroethane is expected to be found in surface waters through the direct facility release of the
chemical into receiving water bodies. Section 3.3.3.2 provides modeled estimates of 1,1-dichloroethane
in surface water at the site of release and Section 3.3.3.6 presents modeled estimates in downstream
Page 202 of 664
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5441
5442
5443
5444
5445
5446
5447
5448
5449
5450
5451
5452
5453
5454
5455
5456
5457
5458
5459
5460
5461
5462
5463
5464
5465
5466
5467
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5470
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PUBLIC RELEASE DRAFT
July 2024
locations that are expected to supply public water systems (PWS) and become a source of drinking water
for the general public. Section 3.3.3.4 provides model estimates of 1,1-dichloroethane in benthic pore
waters and benthic sediment, but these scenarios are not expected to lead to general population
exposure. Likewise, surface water concentrations of 1,1-dichloroethane resulting from air deposition
were estimated for the ecological assessment but are not expected to result in any significant exposure to
the general population. Section 3.3.4.3 provides modeled estimates of 1,1-dichloroethane in groundwater
due to estimated migration from landfill leachate, although groundwater estimates are very low and so
do not expect to result in a general population exposure. The relevant surface water estimates at PWS
locations were used to calculate an exposure dose from drinking water for the general population.
Additionally, modeled surface water concentrations (see Section 3.3.3.6) were used to calculate a dermal
exposure estimate from swimming, incidental ingestion estimates from swimming, fish ingestion
exposure at the site of facility release of 1,1-dichloroethane.
5.1.2.2 Summary of Inhalation Exposure Assessment
EPA evaluated acute, chronic and lifetime general population exposures to 1,1-dichloroethane in air. For
the ambient air exposure, the analysis focuses on general population exposures that may occur within 10
km of release facilities.
5.1.2.2.1 Ambient Air Exposure
To evaluate human inhalation exposures from industrial and commercial fugitive and stack emissions,
EPA calculated ACs, ADCs, and LADCs based on IIOAC- and AERMOD-modeled air concentrations
estimated in Section 3.3.1. The LADCs presented in Table 5-20 are based on the maximum 95th
percentile air concentrations estimated for the facilities within each OES reporting to TRI. LADCs
within 10 km of release types considered here range from 0 to 232 |ig/m3. The LADCs presented in
Table 5-21 are based on the maximum 95th percentile air concentrations estimated for the facilities
within each OES reporting to NEI. LADCs within 10 km of release types considered here range from 0
to 32 |ig/m3, which is within a similar range to LDACs estimated from TRI air releases. These lifetime
exposure estimates are based on 78 years of exposure over a 78-year lifetime and are relevant to all
lifestages. These lifetime exposures were estimated from TRI air releases as shown in Figure 3-3, and
from NEI air releases as show in Figure 3-4. As mentioned in Section 3.3.1, approximately 30 percent of
the facilities reporting 1,1-dichloroethane releases to TRI (7 out of 23 facilities) are in the State of Texas
and approximately 40 percent of them (9 out of 23 facilities) are in the State of Louisiana.
Table 5-22 provides a summary of the LADCs for the Commercial use as a laboratory chemical, and
Processing - repackaging OESs where there was no site-specific data available for modeling. These
lifetime exposure estimates are presented for high-end modeled releases, high-end meteorology (Lake
Charles, Louisiana14), both rural and urban setting, and the maximum 95th percentile air concentrations
estimated for each OES. The LADCs are based on 78 years of exposure over a 78-year lifetime and are
relevant to all lifestages. LADCs within 10 km of release types presented here range from 4,7/10 4 to
1.5 |ig/m3.
The complete set of inhalation exposure estimates are presented in the Draft RiskEvaluation for 1,1-
Dichloroethane - Supplemental Information File: Supplemental Information on AERMOD TRI
Exposure and Risk Analysis (U.S. EPA. 2024n). Draft Risk Evaluation for 1,1-Dichloroethane -
Supplemental Information File: Supplemental Information on AERMOD Generic Releases Exposure and
Risk Analysis (U.S. EPA. 20241). and in the Draft Risk Evaluation for 1,1-Dichloroethane -
14 The high-end meteorological station used represents meteorological datasets that tended to provide high-end concentration
estimates relative to the other stations within IIOAC (Appendix E. 1.2.4).
Page 203 of 664
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PUBLIC RELEASE DRAFT
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5478 Supplemental Information File: Supplemental Information on AERMOD NEI Exposure and Risk
5479 Analysis (U.S. EPA. 2024m).
Page 204 of 664
-------
5480 Table 5-20. Lifetime Average Dai
y Concentrations Estimated within 10,000 in of 1,1-Dichloroethane TRI Releases to Air
OES
# Facilities
Evaluated in OES
Maximum 95th Percentile LADCs Estimated within 10-10,000 m of Facilities i
jig/m3)
10 m
30 m
30 to 60 m
60 m
100 m
100 to 1,000 m
1,000 m
2,500 m
5,000 m
10,000 m
Manufacturing
9
2.3E02
9.0E01
6.9E01
3.7E01
1.8E01
2.5
4.1E-01
9.3E-02
3.0E-02
1.0E-02
Processing as a
reactive
intermediate
6
1.5E01
6.4
4.3
2.5
1.2
1.6E-01
2.7E-02
1.3E-02
6.8E-03
2.9E-03
General waste
handling,
treatment, and
disposal
8
1.9E01
9.3
6.1
3.9
1.9
1.4E-01
4.8E-02
1.1E-02
3.4E-03
1.1E-03
Table 5-21. Lifetime Average Daily Concentrations Estimated within 10,000 m of 1,1-Dichloroethane Releases to Air Reported to NE
OES
# Releases
Maximum 95th Percentile LADCs Estimated within 10-10,000 m of Facilities (jug/m3)
Evaluated in OES
10 m
30 m
30 to 60 m
60 m
100 m
100 to 1,000 m
1,000 m
2,500 m
5,000 m
10,000 m
Commercial use
as a laboratory
chemical
2
3.7E-02
1.2E-02
7.2E-03
4.2E-03
1.9E-03
1.9E-04
3.8E-05
8.2E-06
2.6E-06
8.4E-07
Manufacturing
9
2.1E01
6.1
6.1
6.1
5.7
1.0
1.2E-01
2.6E-02
8.3E-03
2.6E-03
Processing as a
reactive
intermediate
50
3.2E01
1.2E01
8.2
4.9
2.2
2.7E-01
4.8E-02
1.7E-02
6.7E-03
2.4E-03
General waste
handling,
treatment, and
disposal
102
1.3E01
8.2
6.5
4.1
2.1
2.1E-01
5.2E-02
1.1E-02
3.4E-03
1.0E-03
Facilities not
mapped to an
OES
59
9.2
3.7
2.8
1.5
7.3E-01
1.2E-01
1.8E-02
3.9E-03
1.3E-03
4.0E-04
5484
5485
5486
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5487 Table 5-22. Lifetime Average Daily Concentrations Estimated within 10,000 m of 1,1-Dichloroethane Releases to Air for the
5488 Commercial Use as a Laboratory Chemical, and Processing - Repackaging for Laboratory Chemicals OESs, for the 95th Percentile
5489 Production Volume
OES
Meteorology
Source
Land
Maximum 95th Percentile LADCs Estimated within 10-10,000 m of Facilities (jug/m3)
10 m
30 m
30 to 60 m
60 m
100 m
100 to 1,000 m
1,000 m
2,500 m
5,000 m
10,000 m
Processing -
repackaging
for laboratory
chemicals
High
Stack and
Fugitive
Urban
9.3E-01
2.6E-01
2.1E-01
1.5E-01
1.4E-01
3.8E-02
1.3E-02
3.8E-03
1.3E-03
4.7E-04
High
Stack and
Fugitive
Rural
9.3E-01
2.6E-01
2.0E-01
1.2E-01
1.0E-01
3.4E-02
1.5E-02
4.5E-03
1.9E-03
9.8E-04
Commercial
use as a
laboratory
chemical
High
Stack and
Fugitive
Urban
1.5
4.4E-01
3.9E-01
3.1E-01
3.5E-01
1.0E-01
3.4E-02
1.0E-02
3.7E-03
1.3E-03
High
Stack and
Fugitive
Rural
1.5
4.3E-01
3.5E-01
2.5E-01
2.4E-01
9.0E-02
4.0E-02
1.3E-02
5.1E-03
2.5E—03
5490
5491
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5495
5496
5497
5498
5499
5500
5501
5502
5503
5504
5505
5506
5507
5508
5509
5510
5511
5512
5513
5514
5515
5516
5517
5518
5519
5520
5521
5522
5523
5524
5525
5526
5.1.2.2.2 Indoor Air Exposure
EPA calculated LADCs for indoor air exposure based on the IIOAC modeled indoor air concentrations
in Section 3.3.2.2. Table 5-23 shows LADCs based on the maximum 95th percentile air concentrations
estimated for the facilities within each OES reporting to TRI. LADCs from 100 to 1,000 m of release
types considered here range from 1.3/10 2 to 7.4 |ig/m3. These lifetime exposure estimates are based on
78 years of exposure over a 78-year lifetime and are relevant to all lifestages.
The complete set of inhalation exposure estimates are presented in the Draft RiskEvaluation for 1,1-
Dichloroethane - Supplemental Information File: Supplemental Information on IIOAC TRI Exposure
and Risk Analysis (U.S. EPA. 2024p).
Table 5-23. Indoor Air Lifetime Average Daily Concentrations (LADCs) Estimated within 1,000 m
of 1,1-Dichloroethane Releases to Air Reported to TRI
OES
# Facilities
Evaluated in
OES
Maximum LADCs Estimated within 100 to 1,000
m of Facilities (jig/m3)
100 m
100 to 1,000 m
1,000 m
Manufacturing
9
1.8E01
2.0
8.3E-01
Processing as a reactive intermediate
6
9.5E-01
1.1E-01
4.5E-02
General waste handling, treatment, and
disposal
8
6.4E-01
7.5E-02
3.0E-02
5.1.2.2.3 Populations in Proximity to Air Emissions
EPA reviewed the 95th percentile LADC (lifetime average daily concentration) as a basis for selecting
AERMOD TRI sites that reflect high-end exposures. Of the 23 TRI facility releases that were modeled
using AERMOD, a subset of 10 AERMOD TRI release sites with the highest LADC were the focus of
the population evaluation. The goal of this evaluation was to characterize the general population, the
population that comprises PESS groups (i.e., women of childbearing age - associated with decreases in
maternal body weight, as well as people with the aldehyde dehydrogenase-2 mutation which is more
likely in people of Asian descent, see Section 5.3.2), and the population with respect to age/lifestage,
race/ethnicity, and poverty-level that surrounds this subset of high-end exposure sites at relevant
distances. Nearby environments and community infrastructure of interest were also examined to further
understand exposure to these groups and the general public in locations outside their residence. Census
block level information that captures residential areas were used to estimate population numbers and
metrics. Distance estimates between AERMOD TRI release sites, census block centroids, and
community locations of interest were compared with modeled AERMOD distances to evaluate the
degree of exposure possible. A full description of the purpose, methods, and uncertainties of this
evaluation can be found in D.3.
Of these 10 AERMOD TRI release sites, four (three in Louisiana and one in Texas) were estimated to
have populations living within 1,000 m of the source of emissions (see Table 5-24) and the presence of
general population living within 1,000 meters was considered relevant for high-end exposure
characterization.
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5538
5539
5540
5541
5542
5543
5544
5545
5546
5547
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5549
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5551
5552
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Table 5-24. Population Density Estimates within 1,000 m of a Subset of AERMOD TRI Air
Release Sites that Reflect High-End Exposures
OES
TRIFID
Facility
Location
Highest LADC
AERMOD Modeled
Next
AERMOD
Modeled
Distance (m)
Distance to
Closest Census
Distance (m)
Block (m)
70734VLCNMASHLA
Geismar, LA
30
60
1,599
77571LPRTC2400M
La Porte, TX
100
1,000
N/A
70734BRDNCLOUIS
Geismar, LA
100
1,000
1,300
Manufacturing
70669GRGGL1600V
Westlake, LA
60
100
890
70669PPGNDCOLUM
Westlake, LA
1,000
2,500
1,391
7076WBLCBP21255
Plaquemine, LA
100
1,000
505
7754WBLCBP231NB
Freeport, TX
10
30
267
70765GRGGLHIGHW
Plaquemine, LA
30
60
2,139
Processing as a
70764LLMNXHWY40
Plaquemine, LA
100
1,000
975
reactant
Waste handling.
71836SHGRVPOBOX
Foreman, AR
100
1,000
1,371
disposal.
treatment, and
recycling
While the results from Table 5-24 provide an understanding of the size of the general population in the
areas surrounding high-end exposures, EPA also evaluated the modeled AERMOD TRI distances where
high-end exposures are expected with respect to where these populations are anticipated to live. Table
5-24 shows the greatest discrete AERMOD modeled distance from the emission source where a high-
end exposure has been identified and also includes the next discrete AERMOD modeled distance, where
high-end exposure was not identified. Both modeled distances were evaluated since in some cases the
area in between is lacking modeled results, and so it is possible a population can experience a high-end
exposure in between the "highest" and the "next" AERMOD modeled distances. The last column in
Table 5-24 includes the estimated distance between the AERMOD TRI release site and the nearest
census block with an expected population. Of the 10 subset AERMOD TRI release sites, 4 have
populations within proximity to the release sites that may experience high-end exposures. It is important
to note that there is a degree of uncertainty in distance estimates for reasons outlined in D.3. Thus, these
results should not be overinterpreted; distances that overlap within a few hundred meters may be within
the error bound surrounding the distance estimates and comparisons.
The population of targeted PESS groups, race/ethnicities, and at poverty levels were estimated based on
a weighted approach that scales census information at the block group level to individual census blocks.
The results from individual census blocks within 1,000 and 2,600 m of the AERMOD TRI release sites
were then evaluated. The PESS groups included children under 5 and 18 years old because childcare
centers and public schools were observed near several of the ARMOD TRI release sites and children
could be susceptible to lifetime exposures and potential cancer risks. Pregnant females were identified as
a potential PESS group in Section 5.3.2, however, the census information does not include pregnancy
data explicitly. In turn, the population of females of reproductive age (15 to 50 years old; per the census
data on fertility) was used as a proxy for pregnant females. The population aged over 65 was also
estimated, although this age range was not explicitly identified as a PESS group for 1,1-dichloroethane.
The populations that make up these age groups within 1,000 m of the subset of AERMOD TRI release
sites are shown in Table 5-25. It shows that there are children, females ages 15 to 50, and adults older
than 65 living within or near areas of high-end exposures to 1,1-dichloroethane. Of the 4 sites with
estimated populations living within or near high-end exposure areas, almost 500 females of reproductive
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5563
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5565
5566
5567
5568
5569
5570
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PUBLIC RELEASE DRAFT
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age were estimated to live within 1,000 m of the source of emission, or approximately 30 percent of the
total general population within 1,000 m. Although the population of females of reproductive age may be
greater than the population of pregnant women, these results indicate that the number of pregnant
females within or near areas of high-end exposures to 1,1-dichloroethane are still considerable.
Table 5-25. Population Density Estimates by Age Groups within 1,000 m of the Subset of
AERMOD TRI Air Release Sites
OES
TRIFID
Facility
Location
Total
Population
Children
Under 5
Children
Under 18
Females
15-49
Population
Over 65
70734VLCNMASHLA
Geismar, LA
0
0
0
0
0
77571LPRTC2400M
La Porte, TX
0
0
0
0
0
70734BRDNCLOUIS
Geismar, LA
0
0
0
0
0
Manufacturing
70669GRGGL1600V
Westlake, LA
135
0
8
62
17
70669PPGNDCOLUM
Westlake, LA
0
0
0
0
0
7076WBLCBP21255
Plaquemine, LA
128
9
17
33
24
7754WBLCBP231NB
Freeport, TX
1,378
60
446
392
116
70765 GRGGLHIGHW
Plaquemine, LA
0
0
0
0
0
Processing as
a reactant
70764LLMNXHWY40
Plaquemine, LA
21
1
5
5
3
Waste
handling,
disposal,
treatment and
recycling
71836SHGRVPOBOX
Foreman, AR
0
0
0
0
0
Population estimates with respect to race/ethnicity and poverty level were compared to national averages
to identify potentially overburdened communities. In addition, a known metabolite is reactive
dichloroacetaldehyde supporting that a PESS group are people with the aldehyde dehydrogenase-2
mutation that is more likely in people of Asian descent which have a higher risk for several diseases
affecting many organ systems, including a particularly high incidence relative to the general population
of esophageal cancer, myocardial infarction, and osteoporosis due to decreased reactive aldehyde
clearance (Gross et al.. 2015). Table 5-26 shows that there are populations of non-white races and
ethnicities living within 1,000 m of the subset of AERMOD TRI release sites that are greater than their
respective national averages. Of particular note for populations within 1000 m of release sites in
Westlake, Louisiana, 26 percent are of Asian descent compared to a national average of six percent. As
noted in Section 5.3.2, this racial/ethnic group is identified as PESS due to the possible identified
mutation and increased rate of cancer. Although exposures to maximum 1,1-dichloroethane
concentrations resulting in risk are not expected, the PESS populations within 1,000 m represent an
exposure to high-end ambient air concentrations to 1,1-dichloroethane.
Page 209 of 664
-------
5583
5584
5585
5586
5587
5588
5589
5590
5591
5592
5593
5594
5595
PUBLIC RELEASE DRAFT
July 2024
Table 5-26. Population Density by Race and Ethnicity Expressed as a Percentage of the Total
Population wit
iin 1,000 m of the Subset of AER
MOD n
U Release Sites
OES
TRIFID
Facility
Location
%
White
%
Black
%
Asian
%
AV
AN
%
Other
Race
Alone
%
Multi-
Racial
%
Hispanic
/Latino
Manufacturing
70734VLCNMASHLA
Geismar, LA
0
0
0
0
0
0
0
77571LPRTC2400M
La Porte, TX
0
0
0
0
0
0
0
70734BRDNCLOUIS
Geismar, LA
0
0
0
0
0
0
0
70669GRGGL1600V
Westlake, LA
63
0
26
0
0
11
7
70669PPGNDCOLUM
Westlake, LA
0
0
0
0
0
0
0
7076WBLCBP21255
Plaquemine, LA
78
0
0
0
22
0
0
7754WBLCBP231NB
Freeport, TX
53
20
0
0.2
13
13
73
70765GRGGLHIGHW
Plaquemine, LA
0
0
0
0
0
0
0
Processing as a
reactant
70764LLMNXHWY40
Plaquemine, LA
17
79
0
0
0.2
4
1
Waste handling,
disposal,
treatment, and
recycling
71836SHGRVPOBOX
Foreman, AR
0
0
0
0
0
0
0
National Average
68
13
6
0.8
6
7
18
Estimates of the population density in poverty and the median household income were evaluated to
provide an understanding of high-end exposures that may affect potential disadvantaged communities
(Table 5-27). The population density below poverty results were also summarized by their OES
designation).
Table 5-27. Median Household Income, Population Density, and Poverty Status for Populations
within 1,000 in of the Subset AERMOD TRI Release Sites
OES
TRIFID
Facility
Location
Household
Median Income"
Number of People
in Poverty6
Manufacturing
70734VLCNMASHLA
Geismar, LA
N/A
N/A
77571LPRTC2400M
La Porte, TX
N/A
N/A
70734BRDNCLOUIS
Geismar, LA
N/A
N/A
70669GRGGL1600V
Westlake, LA
65,941
37
70669PPGNDCOLUM
Westlake, LA
N/A
N/A
7076WBLCBP21255
Plaquemine, LA
85,313
13
7754WBLCBP231NB
Freeport, TX
48,870
226
70765GRGGLHIGHW
Plaquemine, LA
N/A
N/A
Processing as a reactant
70764LLMNXHWY40
Plaquemine, LA
43,421
4
Waste handling, disposal,
treatment, and recycling
71836SHGRVPOB OX
Foreman, AR
N/A
N/A
National Average
" Median income is shown as N/A if one of the block groups did not have a determined median income.
b A population is designated as being in poverty if the income to poverty level ratio in the past 12 months is below 1.
The locations of childcare centers, schools, places of worship, and healthcare facilities were also
identified within 1,000 m of the subset of AERMOD TRI release sites. No private schools, colleges or
Page 210 of 664
-------
5596
5597
5598
5599
5600
5601
5602
5603
5604
5605
5606
5607
5608
5609
5610
5611
5612
5613
5614
5615
5616
5617
5618
5619
5620
5621
5622
5623
5624
5625
5626
5627
5628
5629
5630
5631
5632
5633
5634
5635
5636
5637
5638
5639
5640
5641
PUBLIC RELEASE DRAFT
July 2024
universities, hospitals, urgent care centers, VA health facilities, or dialysis clinics were located even
out to within 2,600 m of any of the subset of AERMOD TRI release sites. One childcare center and
two places of worship were located within 1,000 m of the subset of AERMOD TRI release sites.
Collectively these results do indicate that other PESS groups that attend, work, or frequent these
community locations may be susceptible to high-end exposures from the subset of AERMOD TRI
release sites.
5.1.2.3 Summary of Dermal Exposure Assessment
5.1.2.3.1 Incidental Dermal Exposure from Swimming
The general population may swim in surface waters that are affected by 1,1-dichloroethane
contamination. Modeled surface water concentrations assuming the facility release annual load was over
the number of facility operating days. The surface water concentrations were used to estimate acute
doses and average daily doses from dermal exposure while swimming.
The following equations from the EPA Office of Pesticide Program Swimmer Exposure Assessment
Model (SWIMODEL) were used to calculate incidental dermal (swimming) doses for all COUs, for
adults, youth, and children:
Equation 5-2.
ADR = (SWC x K_p x SA x ET x CF1 x CF2) / BW
Equation 5-3.
ADD = (SWC x K_p x SA x ET x RD x ET x CF1 x CF2) / (BW x AT x CF3)
Where:
ADR =
Acute Dose Rate (mg/kg-day)
ADD =
Average Daily Dose (mg/kg-day)
SWC =
Chemical concentration in water (|ig/L)
KP =
Permeability coefficient (cm/hour)
SA
Skin surface area exposed (cm2)
ET
Exposure time (hours/day)
RD =
Release days (days/year)
ED =
Exposure duration (years)
BW =
Body weight (kg)
AT =
Averaging time (years)
CF1 =
Conversion factor (1.0/ 10 3 mg/|ig)
CF2 =
Conversion factor (1.0/ 10 3 L/cm3)
CF3 =
Conversion factor (365 days/year)
The 1,1-dichloroethane skin permeability coefficient used in the equation above was the predicted Kp
value presented in the EPA Risk Assessment Guidance for Superfund for organic contaminants in water
(Kp = 6.7x 10 3 cm/hour). This Kp was chosen above the permeability coefficient received from
submitted 1,1-dichloroethane dermal test order study data since the one from test orders measured the
1,1-dichloroethane Kp in a solvent instead of in an aqueous solution as would be appropriate to estimate
exposures from a swimming scenario (see dermal test order data description Section 5.1.1.1.5).
Page 211 of 664
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PUBLIC RELEASE DRAFT
July 2024
5642 Table 5-28 presents a summary of the estimated dermal exposures from facility releases to surface
5643 waters. The table lists the facility corresponding to the maximum 1,1-dichloroethane surface water
5644 concentrations per OES and the highest resultant dermal exposures from swimming.
Page 212 of 664
-------
5645 Table 5-28. Highest Modeled Incidental Dermal (Swimming) Doses for all CPUs, for Adults, Youth, and Children
OES
Facility
Receiving
Waterbody
Surface Water
Concentration
Adult (>21 years)
Youth (11-15 years)
Child (6-10 years)
30Q5
Cone.
(Hg/L)
Harmonic
Mean Cone.
(Hg/L)
ADRpot
(mg/kg-day)
ADD
(mg/kg-day)
ADRpot
(mg/kg-day)
ADD
(mg/kg-day)
ADRpot
(mg/kg-day)
ADD
(mg/kg-day)
Manufacturing
LA0000761
Bayou D'Indc
& Bayou
Verdine
1.7E04
9.7E03
8.4E-02
1.3E-04
6.4E-02
1.0E-04
3.9E-02
6.1E-05
Processing as a
reactant
intermediate
TXO119792
Unnamed,
San Jacinto
Bay
4.8E03
4.8E03
2.3-02
6.4E-05
1.8E-02
4.9E-05
1.1E-02
3.0E-05
Processing -
repackaging
IL0064564
Rock River
1.8E02
1.82E02
8.9E-04
2.4E-06
6.8E-04
1.9E-06
4.2E-04
1.1E-06
Commercial
use as a
laboratory
chemical
IL0034592
Sawmill
Creek
8.7E01
5.1E01
4.2E-04
6.8E-07
3.2E-04
5.2E-07
2.0E-04
3.2E-07
Waste
handling,
treatment, and
disposal (non-
POTW)
NN0021610
Little
Colorado
River
7.3E02
7.3E02
3.6E-03
9.8E-06
2.7E-03
7.5E-06
1.7E-03
4.6E-06
Waste
handling,
treatment, and
disposal
(POTW)
NE0043371
Stevens Creek
2.7E03
1.7E03
1.3E-02
2.3E-05
1.0E-02
1.7E-05
6.1E-03
1.1E-05
Waste
handling,
treatment, and
disposal
(remediation)
CA0064599
South Fork of
Arroyo
Conejo Creek
4.1E04
4.1E04
2.0E-01
5.5E-04
2.0E-01
4.2E-04
9.3E-02
2.5E-04
Unknown
OH0143880
Spring Creek
7.2E03
7.2E03
3.5E-02
9.7E-05
2.7E-02
7.4E-05
1.6E-02
4.5E-05
5646
5647
5648
Page 213 of 664
-------
5649
5650
5651
5652
5653
5654
5655
5656
5657
5658
5659
5660
5661
5662
5663
5664
5665
5666
5.1.2.4 Summary of Oral Exposure Assessment
5.1.2.4.1 Drinking Water Exposure
EPA estimated drinking water exposures for those facility effluents containing 1,1-dichloroethane
discharged to receiving water bodies upstream of drinking water intakes. The Manufacturing and
Commercial use as a laboratory chemical COUs/OES did not have downstream drinking water intakes
and were not included in the drinking water exposure estimates. The surface water exposures presented
in Table 5-29 are the maximum acute dose rate (ADR) and average daily dose (ADD) and lifetime
average daily dose (LADD) estimates for adults and infants (using drinking water for formula) at the
calculated drinking water intake after dilution from the point of release. The point of release
concentrations were based on the 30Q5 flow of each of the corresponding receiving water bodies and the
annual effluent discharges occurring over the facility operating days (see Table 3-3).
Table 5-29. Highest Drinking Water Exposures from Surface Water Releases
Surface
OES
Facility
Water
Concentration
Adult (>21 years)
Infant (birth to <1 year)
30Q5 Cone.
(Hg/L)
ADRpot
ADD
LADD
ADRpot
ADD
LADD
(mg/kg-
day)
(mg/kg-
day)
(mg/kg-
day)
(mg/kg-
day)
(mg/kg-
day)
(mg/kg-
day)
Manufacturing
-
Processing as a
IL0000141
8.7E-04
3.5E-08
1. IE—11
4.8E-12
1.2E-07
2.9E-11
3.8E-13
reactant
intermediate
Processing -
LAO 1245 83
1.3E-04
5.4E-09
1.7E-12
7.3E-13
1.9E-08
4.4E-12
5.7E-14
repackaging
Commercial
-
use as a
laboratory
chemical
Waste
MI0044130
2.5E-01
1.0E-05
7.5E-09
3.2E-09
3.5E-05
1.9E-08
2.5E-10
handling,
treatment, and
disposal (non-
POTW)
Waste
CA0048194
1.1E-06
4.4E-11
1.8E-14
7.7E-15
1.5E-10
4.7E-14
6.0E-16
handling,
treatment, and
disposal
(POTW)
Waste
MI0042994
2.6E-04
1.0E-08
3.6E-12
1.5E-12
3.7E-08
9.3E-12
1.2E-13
handling,
treatment, and
disposal
(remediation)
Unknown
MI00004057
5.2E-04
2.1E-08
6.4E-12
2.7E-12
7.3E-08
1.6E-11
2.1E-13
1,1-Dichloroethane concentrations in drinking water and population exposures have also been evaluated
through the EPA Office of Water, Office of Ground Water and Drinking Water and described in the
Final Regulatory Determination 4 Support Document (January 2021, EPA 815-R-21-001). 1,1-
dichloroethane was evaluated as a candidate for regulation under SDWA as a drinking water
Page 214 of 664
-------
5667
5668
5669
5670
5671
5672
5673
5674
5675
5676
5677
5678
5679
5680
5681
5682
5683
5684
5685
5686
5687
5688
5689
5690
5691
5692
5693
5694
5695
5696
5697
5698
5699
5700
5701
5702
5703
5704
5705
5706
5707
5708
5709
5710
PUBLIC RELEASE DRAFT
July 2024
contaminant under the fourth Contaminant Candidate List (CCL 4) Regulatory Determination process.
In 2021, 1,1-Dichloroethane was determined to not satisfy the criteria required under SDWA and did not
warrant regulation. Maximum 1,1-dichloroethane concentrations among sampled large, medium, and
small PWSs were 1.5ug/L, and none of the detections exceeded the health reference level of 1,000 ug/L.
Based on the data indicating that 1,1-dichloroethane was not occurring in drinking water at levels of
public health concern, the EPA Office of Water made a determination to not regulate 1,1-dichloroethane
under SDWA. The estimated drinking water concentrations presented Table 5-29. from TSCA releases
represent estimates of water concentrations near the discharge sites, well below those reported in the
Office of Water PWS monitoring data of finished drinking water data at public water systems.
5.1.2.4.2 Fish Ingestion Exposure
EPA calculated fish ingestion exposure using modeled surface water concentrations for 1,1-
dichloroethane per corresponding COU using the release pattern of facility discharges equal to the
facilities' operating days (see Table 3-3) and both a high-end and a central tendency ingestion rates for
adults and children and a high-end ingestion rate characterizing adult subsistence fisher ingestion rate of
142.40 g/day (see Table 5-30). To further characterize potential tribal exposures, EPA considered and
included two facilities releasing in tribal lands (Navajo Nation: NN0021610 and NN0020265). Habits
and practices of members of tribal nations may result in their higher exposures from fish consumption.
Concentrations of 1,1-dichloroethane in fish were calculated by multiplying the maximum modeled
surface water concentrations based on the number of operating days per year for each industrial and
commercial release scenario (Table 3-3) by the EPI SuiteTM-generated BCF of 7 (Table 2-2). EPA
estimated exposure from fish consumption using an adult ingestion rate, for 6 to less than 11 and 11 to
less than 16 years according to the following equation (Equation 5-4):
Equation 5-4.
Exposure Estimate = (SWC x BAF x IR x CF1 x CF2 x ED)/(AT x BW)
Where:
SWC =
Surface water (dissolved) concentration (|ig/L)
BAF =
Bioaccumulation factor (L/kg wet weight)
IR
Fish ingestion rate (g/day)
CF1 =
Conversion factor (0.001 mg/|ig)
CF2 =
Conversion factor for kg/g (0.001 kg/g)
ED =
Exposure duration (year)
AT =
Averaging time (year)
BW =
Body weight (80 kg)
The years within an age group (i.e., 33 years for adults) was used for the exposure duration and
averaging time. The lifetime exposures were assumed to be 78 years. Table 5-30 presents the summary
of the highest fish ingestion dose resulting from the corresponding highest receiving water concentration
and facility release per COU/OES.
A BCF is preferred in estimating exposure because it considers the animal's uptake of a chemical from
both diet and the water column. For 1,1-dichloroethane, the BCF value (see Table 2-2) was estimated as
7 using EPISUITE™ (U.S. EPA. 2012c). The modeled surface water concentrations were converted to
fish tissue concentrations using the estimated BCF.
Page 215 of 664
-------
5711 Table 5-30. Summary of Fish Ingestion Exposures
OES
Facility
Receiving
Waterbody
Surface
Water
Cone.
Adult (>21 years)
High-End/Subsistencefl
Small Child (1-2 years)
High-En d/90th Percentile6
7Q10
(Hg/L)
Acute
(mg/kg-day)
Chronic
(mg/kg-day)
Lifetime
Avg. Dose
(mg/kg-day)
Acute
(mg/kg-day)
Chronic
(mg/kg-day)
Lifetime
Avg. Dose
(mg/kg-day)
Manufacturing
LA0000761
Bayou D'Indc &
Bayou Verdine
85.7
1.1E-03
2.9E-06
1.2E-06
2.5E-04
6.8E-07
8.7E-09
Processing as a
reactant intermediate
TXO119792
Unnamed Ditch,
San Jacinto Bay
13.6
1.7E-04
4.6E-07
2.0E-07
3.9E-05
1.1E-07
1.4E-09
Processing -
repackaging
IL0064564
Rock River
0.7
8.7E-06
2.4E-08
1.0E-08
2.0E-06
5.5E-09
7. IE—11
Commercial use as a
laboratory chemical
IL0034592
Sawmill Creek
0.6
8.0E-06
2.2E-08
9.2E-09
1.8E-06
5.0E-09
6.5E-11
Waste handling,
treatment, and disposal
(non-POTW)
NE0043371
Steven's Creek
18.1
2.3E-04
6.2E-07
2.6E-07
5.2E-05
1.4E-07
1.8E-09
NN0021610
Little Colorado
River, AZ
2.9
3.6E-05
1.0E-07
4.2E-08
8.4E-06
2.3E-08
3.0E-10
Waste handling,
treatment, and disposal
(POTW)
KY0022039
Valley Creek
8.2
1.0E-04
2.8E-07
1.2E-07
2.4E-05
1.4E-07
1.8E-09
NN0020265
Chinle Wash,
AZ
5.0
6.2E-05
1.7E-07
7.2E-08
1.4E-05
4.0E-08
5.1E-10
Waste handling,
treatment, and disposal
(remediation)
CA0064599
South Fork of
Arroyo Conejo
Creek
30.7
1.4E-03
3.8E-06
1.6E-06
3.2E-04
8.8E-07
1.1E-08
Unknown
OH0143880
Spring Creek
20.6
2.6E-04
7.0E-07
3.0E-07
5.9E-05
1.6E-07
2.1E-09
" High-end assumes subsistence fish ingestion rate: 142.4g/day
h High-end child 90th percentile fish ingestion rate: 7.7g/day
5712
5713
5714
Page 216 of 664
-------
5715
5716
5717
5718
5719
5720
5721
5722
5723
5724
5725
5726
5727
5728
5729
5730
5731
5732
5733
5734
5735
5736
5737
5738
5739
5740
5741
5742
5743
5744
5745
5746
5747
5748
5749
5750
5.1.2.4.3 Incidental Oral Ingestion from Swimming
The general population may swim in surfaces waters (streams and lakes) that are affected by 1,1-
dichloroethane contamination. Modeled surface water concentrations where discharges occur were used
to estimate acute doses and average daily doses due to ingestion exposure while swimming. EPA
estimated the annual load from facility releases occurred over the number of facility operating days in
modeling surface water concentrations.
The following equations (Equation 5-5 and Equation 5-6) were used to calculate incidental oral
(swimming) doses for all COUs, for adults, youth, and children:
Equation 5-5.
SWC xIRx CF1
Equation 5-6.
SWC x IR x ED x RD x CF 1
ADD ~ BW x AT x CF2
Where:
ADR = Acute Dose Rate (mg/kg/day)
ADD = Average Daily Dose (mg/kg/day)
SWC = Surface water concentration (ppb or |ig/L)
IR = Daily ingestion rate (L/day)
RD = Release days (days/year)
ED = Exposure duration (years)
BW = Body weight (kg)
AT = Averaging time (years)
CF1 = Conversion factor (1,0/ 10 3 mg/|ig)
CF2 = Conversion factor (365 days/year)
Table 5-31 presents a summary of the estimated oral exposures from facility releases to surface waters.
The table lists the facility corresponding to the maximum 1,1-dichloroethane surface water
concentrations per OES and the highest resultant oral exposures from swimming. Because the acute dose
of 1,1-dichloroethane is estimated to be very low compared to oral hazard values, acute and chronic risk
estimates of oral exposures are only presented in the supplemental files and not in subsequent sections of
this draft risk evaluation.
Page 217 of 664
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PUBLIC RELEASE DRAFT
July 2024
5751 Table 5-31. Summary of Incidental Oral Exposures from Swimming
OES
Facility
Receiving
Water Body
Surface Water Concentration
Adult (>21 years)
Youth (11-15 years)
Child (6-10 years)
30Q5 Cone.
(fig/L)
Harmonic Mean
Cone. (jig/L)
ADRpot
(mg/kg-day)
ADD
(mg/kg-day)
ADRpot
(mg/kg-day)
ADD
(mg/kg-day)
ADRpot
(mg/kg-day)
ADD
(mg/kg-day)
Manufacturing
LA0000761
Bayou D'Inde &
Bayou Verdine
1.7E04
9.7E03
5.9E-02
9.2E-05
9.2E-02
1.4E-04
5.2E-02
8.1E-05
Processing as a
reactant
intermediate
TXO119792
Unnamed
Stream, San
Jacinto Bay
4.8E03
4.8E03
1.6-02
4.5E-05
2.6E-02
7.0E-05
1.4E-02
3.9E-05
Processing -
repackaging
IL0064564
Rock River
1.8E02
1.82E02
6.3E-04
1.7E-06
9.8E-04
2.7E-06
5.5E-04
1.5E-06
Commercial use
as a laboratory
chemical
IL0034592
Sawmill Creek
8.7E01
5.1E01
3.0E-04
4.8E-07
4.6E-04
7.4E-07
2.6E-04
4.2E-07
Waste handling,
treatment, and
disposal
(non-POTW)
NN0021610
Little Colorado
River
7.3E02
7.3E02
2.5E-03
6.9E-06
3.9E-03
1.1E-05
2.2E-03
6.0E-06
Waste handling,
treatment, and
disposal
(POTW)
NE0043371
Stevens Creek
2.7E03
1.7E03
9.2E-03
1.6E-05
14E-02
2.5E-05
8.1E-03
14E-05
Waste handling,
treatment, and
disposal
(remediation)
CA0064599
South Fork of
Arroyo Conejo
Creek
4.1E04
4.1E04
1.0E-01
3.9E-04
2.0E-01
6.0E-04
1.0E-01
34E-04
Unknown
OH0143880
Spring Creek
7.2E03
7.2E03
2.5E-02
6.8E-05
3.9E-02
1.1E-04
2.2E-02
6.0E-05
5752
5753
Page 218 of 664
-------
5754
5755
5756
5757
5758
5759
5760
5761
5762
5763
5764
5765
5766
5767
5768
5769
5770
5771
5772
5773
5774
5775
5776
5777
5778
5779
5780
5781
5782
5783
5784
5785
5786
5787
5788
5789
5790
5791
5792
5793
PUBLIC RELEASE DRAFT
July 2024
5.1.2.4.4 Incidental Oral Ingestion from Soil (Biosolids)
No current information on the concentration of 1,1-dichloroethane in wastewater treatment sludge or
biosolids was found. In the absence of measured data, EPA estimated the maximum amount of 1,1-
dichloroethane entering wastewater treatment from the releases reported for any facility in its DMR. The
releases were converted to daily loading rates and used as input to the SimpleTreat 4.0 wastewater
treatment plant model (RIVM 2014). It was assumed that the modeled site used activated sludge
wastewater treatment and that SimpleTreat 4.0 defaults were a reasonable representation of the activated
sludge treatment at the site. Using this loading data, the model predicted 1,1-dichloroethane
concentration in combined sludge of 20 mg/kg.
To assess soil concentrations resulting from biosolid applications, EPA relied upon modeling work
conducted in Canada (EC/HC 2011), which used Equation 60 of the European Commission Technical
Guidance Document (TGD) (ECB 2003). The equation in the TGD is provided in Equation 5-7 below:
Equation 5-7.
PECsoii — {Csiudge X ARsiudge)/(Dsoil X BDsoii)
Where:
PECsoil =
C,
sludge
AR
sludge
Dsoil
BDsoU
Predicted environmental concentration (PEC) for soil (mg/kg)
Concentration in sludge (mg/kg)
Application rate to sludge amended soils (kg/m2/year); default = 0.5 from Table A-
11 of TGD
Depth of soil tillage (m); default = 0.2 m in agricultural soil and 0.1 m in
pastureland from Table A-l 1 of TGD
Bulk density of soil (kg/m3); default = 1,700 kg/m3 from Section 2.3.4 of TGD
Using Equation 5-7, the concentration of 1,1-dichloroethane in pastureland soil receiving an annual
application of biosolids was estimated to be 58.8 (J,g/kg. See Section 3.3.4.3 for details on the estimation
of 1,1-dichloroethane biosolids concentrations.
ADDs for children ingesting soil receiving biosolids were calculated for 1,1-dichloroethane using
Equation 5-8:
Equation 5-8.
ADD = (C xIRxEF x ED x CF)/(BW x AT )
Where:
ADD =
Average Daily Dose (mg/kg/d)
C
Soil concentration (mg/kg)
IR
Intake tate of contaminated soil (mg/d)
EF
Exposure frequency (d)
CF =
Conversion factor (1,0x 10 6 kg/mg)
BW =
Body weight (kg)
AT =
Averaging time (non-cancer: ED x EF, cancer: 78 years x EF)
The recommended intake rate for children aged 3 to 6 years for soil pica (soil ingestion) is 1,000 mg/d.
(U.S. EPA. 2017d). Mean body weight (18.6 kg) for 3- to 6-year-olds was taken from EPA's Exposure
Factors Handbook (U.S. EPA. 201 la).
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Table 5-32. Modeled Exposure to 1,1-Dichloroethane jn
Land Applied Biosolids for Children
OES
Average Daily Dose
(mg/kg-day)
Disposal
3.16E-06
Thus, at the estimated 1,1-dichloroethane soil concentration of 58.8 ug/kg, the ADD for a 3- to 6-year
old child ingesting 1,000 mg/day of contaminated soil would be 3.16xl0~6 mg/kg/day (Table 5-32).
An alternate approach to estimating the concentration of 1,1-dichloroethane in soil from land applied
biosolids and subsequent childrens exposure employed the use of the Biosolids Tool (BST) (U.S. EPA.
2023a). The BST is a multimedia, multipathway, multireceptor deterministic, problem formulation, and
screening-level model that can estimate high-end human and ecological hazards based on potential
exposures associated with land application of biosolids or placement of biosolids in a surface disposal
unit. The BST was peer reviewed by the EPA Science Advisory Board in 2023 (EPA-SAB-24-001). A
default annual biosolids land application rate of 1 kg/m2/year and a 1,1-dichloroethane biosolids
concentration of 20 mg/kg, estimated using the SimpleTreat 4.0 wastewater treatment plant model, were
used as input to the BST. The model predicted a maximum soil concentration of approximately 1.6
ug/kg corresponding to an average daily dose of 8.6x 10~8 mg/kg-day using the described assumptions
above. Because this acute dose estimate of 1,1-dichloroethane exposure is very low compared to oral
hazard values, acute and chronic risk of oral exposures from ingestion of soil were not expected and
were not estimated.
5.1.2.4.5 Incidental Oral Ingestion from Soil (Air Deposition)
No information on the concentration of or exposure to 1,1-dichloroethane in soil from air deposition was
found. Estimates of 1,1-dichloroethane air deposition to soil are discussed in detail in Section 3.3.4.1.
The deposition rates and soil concentrations of 1,1-dichloroethane were calculated with Equation 5-9
and Equation 5-10 below.
Equation 5-9.
AnnDep = TotDep x Ar x CF
Where:
AjlYlDgp
TotDep
Ar
CF
Equation 5-10.
Where:
SoilConc
AnnDep
Mix
Ar
Total annual deposition to soil (|ig)
Annual deposition flux to soil (g/m2)
Area of soil (m2)
Conversion of grams to micrograms
SoilConc = AnnDep/(Ar x Mix x Dens)
Annual-average concentration in soil (|ig/kg)
Total annual deposition to soil (|ig)
Mixing depth (m); default = 0.1 m from the European Commission
Technical Guidance Document (ECB. 2003)
Area of soil (m2)
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Dens = Density of soil; default = 1,700 kg/m3 from the European
Commission Technical Guidance Document (ECB. 2003)
The above equations assume instantaneous mixing with no degradation or other means of chemical
reduction in soil over time and that 1,1-dichloroethane loading in soil is only from direct air-to-surface
deposition (i.e., no runoff).
Section 3.3.4.1 presents the range of calculated soil concentrations corresponding to the emission
scenarios considered. From Table 3-19, the highest estimated 95th percentile soil concentration amongst
all exposure scenarios was for the processing as a reactant (OES) scenario:
• 4.91 x 103 |ig/kg at "fenceline" populations (100 m from the source); and
• 6.29x 101 |ig/kg at "community" populations (1,000 m from the source).
ADDs were calculated for air deposited 1,1-dichloroethane ingestion via soil using Equation 5-11
below:
Equation 5-11.
ADD = (C x IRx EF x ED x CF)/(BW x AT )
Where:
ADD
C
IR
EF
CF
BW
AT
Average Daily Dose (mg/kg/d)
Soil concentration (mg/kg)
Intake rate of contaminated soil (mg/d)
Exposure frequency (d)
Conversion factor (10/ 10 6 kg/mg)
Body weight (kg)
Averaging time (non-cancer: ED x EF, cancer: 78 years x EF)
Modeled soil concentrations were calculated from 95th percentile air deposition (Section 3.3.1.2.2)
concentrations for 100 and 1,000 m from a facility. These calculations were conducted for the
Processing as a reactant OES (Table 5-33).
The recommended intake rate for children aged 3 to 6 years for soil pica is 1,000 mg/d (U.S. EPA.
2017d). Mean body weight (18.6 kg) for 3- to 6-year-olds was taken from the Exposure Factors
Handbook (U.S. EPA. 201 la).
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Table 5-33. Modeled Soil Ingestion Doses for the Processing as a Reactant PES, for Children
OES
Distance
(m)
95th Percentile Soil Concentration
(jug/kg)
Average Daily Dose
(mg/kg-day)
Processing as a reactant
100
4.91E3
2.64E-04
1,000
6.29E1
3.72E-06
Because this average daily dose estimate of 1,1-dichloroethane exposure is very low compared to oral
hazard values, acute and chronic risk of oral exposures from ingestion of soil were not expected and
were not estimated.
5.1.2.5 Weight of Scientific Evidence Conclusions for General Population Exposure
5.1.2.5.1 Strengths, Limitations, Assumptions, and Key Sources of
Uncertainty for the General Population Exposure Assessment
Except for two OESs, site-specific information was reasonably available when estimating releases of
1,1-dichloroethane to the environment. Thus, there is certainty in the environmental release estimates
and the resulting modeled exposure estimates. In addition, there is certainty in the relevancy of the
monitoring data to the modeled estimates presented in this evaluation.
Ambient and Indoor Air Inhalation Exposures
The weight of scientific evidence for inhalation exposure estimates is determined by several different
evidence streams, including evidence supporting the exposure scenarios (Section 5.1.2.1.1), the quality
and representativeness of available monitoring data (Sections 3.3.1.1 and 3.3.2.1), evidence supporting
modeling approaches and input data (Sections 3.3.1.2 and 3.3.2.2), evidence supporting release data
used as model input data (Section 3.2.2), and concordance between modeled and monitored ambient air
concentrations (Section 3.3.5).
Releases: 1,1-dichloroethane concentrations in air were estimated for areas around industrial and
commercial COUs/OESs reported to TRI and NEI, and for two COUs/OESs for which release estimates
are based on modeled information (Sections 3.3.1.2 and 3.3.2.2). The associated strengths and
limitations of these estimated environmental concentrations are described in Section 3.3.5. Industrial and
commercial COUs/OESs that rely on release data reported to TRI and NEI, site-specific release
estimates are supported by moderate to robust evidence. For COUs/OESs that rely primarily on generic
scenarios, release estimates are supported by moderate evidence as described in Section 3.2.2.
Modeling Methodologies and Model Input Data: As stated in Section 3.3.5, the modeling methodology
used to estimate exposure concentrations via the ambient air pathway is supported by robust evidence.
Model input data on air releases are supported by moderate to robust evidence. The ability to locate
releases by location strengthens assumptions when selecting model input parameters that are typically
informed by location (e.g., meteorological data, land cover parameters). Thus, model input data on air
releases are supported by moderate to robust evidence.
Comparison of Modeled and Monitored Data: Measured or monitored data were available for
comparison. Comparison of estimated and measured exposures provide robust evidence (Section 3.3.5).
Exposure Scenarios and Exposure Factors: The general population air exposure scenarios and exposure
factors used to estimate exposures are described in Section 5.1.2.1. The exposure factors used to build
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the exposure scenarios are directly relevant to general population exposures for communities living near
releasing facilities. While the long-term exposure scenarios are most directly relevant for individuals
who reside in fenceline communities for many years, these scenarios are expected to be within the range
of normal habits and exposure patterns expected in the general population. However, there is uncertainty
around the extent to which people actually live and work around the specific facilities where exposures
are highest, decreasing the overall strength of evidence for these exposure scenarios—particularly at the
distances nearest to facilities. For this analysis EPA minimizes that uncertainty by assuming exposed
individuals live or work nearby facilities for 78 years (and have a 78-year life span). This period is
within the range of normal habits and exposure patterns expected in the general population. Therefore,
exposure scenarios underlying these exposure estimates are supported by robust evidence.
Overall Confidence in Exposure Estimates: Overall confidence in air inhalation exposure estimates
resulting for air concentrations modeled based on industrial and commercial releases is consistent across
COUs. The AERMOD modeling methodology used for this analysis is robust and considers
contributions from both stack and fugitive emissions. The exposure scenarios considered are most
relevant to long-term residents in fenceline communities. Overall confidence varies due to variable
levels of confidence in underlying release information used to the support the analysis.
Oral Exposures: Surface Water Concentrations
Facility-specific estimates of aqueous concentration (derived from facility annual loads and receiving
water body hydrology) to the water column were estimated to evaluate human exposures via drinking
water, oral ingestion, dermal contact, and via fish ingestion. In this first step, annual load estimates were
acquired from the ECHO Pollutant Loading Tool for 6 years between 2015 to 2020. The Loading Tool
uses facility reported data from DMRs to calculate and then extrapolate loads for the entire year. There
are several hierarchically organized steps that the ECHO Loading Tool takes to prioritize reported data
for the calculation inputs in order to ensure an annual load estimate is of the best quality possible. For
example, reported measurements of the quantity (load) of a chemical in facility effluent is prioritized
over measurements of concentration from grab samples that must be paired with an effluent hydrologic
flow value. There are inherent uncertainties surrounding the annual load estimates based on the quality
of the input data from DMRs, and thus could be several reasons why annual load estimates may be
considered moderate-to-poor quality. For instance, too few periods of reported DMR data make
extrapolation across the year unreasonable; concentration measurements from grab samples may not
have been taken at the same time or location as measurements of effluent hydrologic flow; and detection
limit reporting and usage may be inconsistent. While annual load estimates from the ECHO Loading
Tool do lend themselves to more efficient national-scale evaluations, the quality of the annual loads are
strongly linked to the quality of reported DMR data, which should be viewed with moderate confidence
at best unless it can be demonstrated that high-quality input data from DMRs are being used.
The highest annual load across the 2015 to 2020 timeframe was identified and used to estimate aqueous
(water column) concentrations within the receiving water body at the site of effluent release. Thus, these
initial aqueous concentrations only account for the effect of dilution and do not include source/sink
processes that may increase or decrease the concentration in the ambient environment. This was done to
remain conservative with our methodology and assumptions: Using the highest annual load from 2015 to
2020 provides a more conservative, high-end exposure scenario, which was preferred over taking an
annual average that may underestimate realized exposure levels. As a result, is expected that annual
loads may be considerably lower in other years. It is also important to note that the Loading Tool
calculations replace non-detects with one-half the detection limit to ensure potentially non-zero
concentration estimates were considered. This is a Loading Tool option that was discussed and selected.
While using concentration estimates based on one-half the detection limit may overestimate
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concentration (and thus load) in some cases, this step was taken to likewise remain conservative with
our methodology and assumptions to avoid underestimating exposure levels.
Aqueous concentrations used for human exposure assessment were estimated using the highest 2015
to2020 annual releases and estimates of 30Q5 and harmonic mean (HM) hydrologic flow data for the
receiving water body that were derived from National Hydrography Dataset (NHD) modeled (EROM)
flow data. NHD 14-digit HUC reach codes were obtained directly from the DMRs for the facilities
(based on their NPDES codes), which was then used to obtain modeled NHD hydrologic flow values
(e.g., lowest monthly and annual means). This flow data was used to estimate 30Q5 and HM flow using
a regression-based approach that is discussed in further detail in Appendix F. The confidence in these
flow values should be considered moderate-to-robust provided modeled NHD flow data has been widely
used and thoroughly vetted. However, a regression-based calculation as opposed to a modeling approach
was used to estimate 30Q5 and HM from NHD-acquired flow data. The latter possibly yielding a more
robust confidence level. Aqueous concentrations of 1,1-dichloroethane are based on simply flow dilution
using this approach, while no other source/sink processes are included.
Aqueous concentrations for human exposure assessment were based on annual releases that occurred
within a single operation day; that is, it is assumed that the entire annual release occurs in a single day.
While facilities may be releasing 1,1-dichloroethane over longer periods of time throughout the year,
this was done to maintain a conservative exposure scenario and to avoid underestimating exposure
levels.
Additional information surrounding the methods and uncertainties for the drinking water, oral ingestion,
dermal contact, and fish ingestion can be found in Appendix F.
Oral Exposures: Fish Ingestion Estimates
To account for the variability in fish consumption across the United States, fish intake estimates were
considered for both subsistence fishing populations and the general population. In estimating fish
concentrations, diluted surface water concentrations were not considered. It is unclear what level of
dilution may occur between the surface water at the facility outfall and habitats where fish reside. A
source of uncertainty in the fish ingestion estimates was the BAF estimate. No monitoring data were
available indicating the consumption of fish containing 1,1-dichloroethane.
Oral Exposures: Soil and Swimming Ingestion Estimates
Land application of biosolids containing 1,1-dichloroethane and air deposition onto land represent two
pathways where soils containing 1,1-dichloroethane could be a source of exposure to children who play
and potentially ingest soils. EPA's Exposure Factors Handbook provided detailed information on the
child skin surface areas and event per day of the various scenarios (U.S. EPA. 2017d). It is unclear how
relevant dermal and ingestion estimates from soil exposure are as 1,1-dichloroethane is expected to
either volatilize or migrate from surface soils to groundwater. Furthermore, there are inherent
uncertainties associated with estimating exposures from the transport of chemicals through various
media (e.g., air to land and subsequent soil ingestion and dermal absorption).
Non-diluted surface water concentrations were used when estimating dermal exposures to adults and
youth swimming in streams and lakes. 1,1-Dichloroethane concentrations will dilute when released to
surface waters, but it is unclear what level of dilution will occur when the general population swims in
waters containing a number of releases of 1,1-dichloroethane over a year.
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Sections 5.1.2.2, 5.1.2.2.3, and 5.1.2.4 summarize exposure assessment approaches taken to estimate
general population exposures. The weight of scientific evidence conclusions supporting the exposure
estimate is decided based on the strengths, limitations, and uncertainties associated with the various lines
of evidence and considerations used in estimating exposures. The conclusions are summarized using the
following descriptors: robust, moderate, slight, or indeterminate.
EPA used general considerations (i.e., relevance, data quality, representativeness, consistency,
variability, uncertainties) as well as chemical-specific considerations to characterize the confidence of
each of the exposure scenarios.
EPA modeled three routes of exposure: (1) inhalation from ambient air; (2) oral ingestion from drinking
water, fish ingestion, and soil intake; and (3) dermal exposures from surface water. Within each of these
modeled pathways, EPA considered multiple variations in its analyses (to help characterize the general
population exposure estimates and to explore potential variability. The resulting exposure estimates
were a combination of central tendency and high-end inputs for the various exposure scenarios. Modeled
estimates were compared with monitoring data to evaluate overlap, magnitude, and trends.
Table 5-34 presents the weight of scientific evidence conclusions for the routes exposures and
corresponding exposure scenarios assessed for the general population exposed to 1,1-dichloroethane.
Table 5-34. Weight of Scientific Evidence (WOSE) Conclusions for General Population Exposure
Assessments
OES
Route of
Exposure
Media
Relevance
to
Exposure
Scenario
Modeling/
Estimation
Confidence
Level
Measured/
Monitoring
Confidence
Levelfl
Measured/
Modeling
Comparison
WOSE
Inhalation
Ambient Air
+++
+++
++
++
Robust
Inhalation
Indoor Air
++
++
++
+
Moderate
Oral/
Drinking
+++
+++
++
++
Robust
Ingestion
Water
Oral/Fish
Surface
+++
+++
++
++
Robust
Ingestion
Water
Oral/
Surface
++
++
++
++
Moderate
Manufacturing
Ingestion
Water/
Swimming
Oral/
Soil
++
++
-
N/A
Slight
Ingestion
(Biosolids)
Oral/
Land; Soil
++
++
-
N/A
Slight
Ingestion
(Air
Deposition)
Dermal
Swimming
++
++
++
+
Moderate
Inhalation
Ambient Air
+++
+++
++
++
Robust
Inhalation
Indoor Air
++
++
++
+
Moderate
Oral/
Drinking
+++
+++
++
++
Robust
Processing as a
Ingestion
Water
reactive
Oral/Fish
Surface
+++
+++
++
++
Robust
intermediate
Ingestion
water
Oral/
Surface
++
++
++
++
Moderate
Ingestion
Water/
Swimming
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OES
Route of
Exposure
Media
Relevance
to
Exposure
Scenario
Modeling/
Estimation
Confidence
Level
Measured/
Monitoring
Confidence
Levelfl
Measured/
Modeling
Comparison
WOSE
Oral/
Soil
++
++
-
N/A
Slight
Ingestion
(Biosolids)
Oral/
Land; Soil
++
++
-
N/A
Slight
Ingestion
(Air
Deposition)
Dermal
Swimming
++
++
++
+
Moderate
Inhalation
Ambient Air
+++
+++
++
++
Robust
Oral/
Drinking
+++
+++
++
++
Robust
Ingestion
Water
Oral/ Fish
Surface
+++
+++
++
++
Robust
Ingestion
water
Oral/
Surface
++
++
++
++
Moderate
Processing -
repackaging
Ingestion
Water/
Swimming
Oral/
Soil
++
++
-
N/A
Slight
Ingestion
(Biosolids)
Oral/
Land; Soil
++
++
-
N/A
Slight
Ingestion
(Air
Deposition)
Dermal
Swimming
++
++
++
+
Moderate
Inhalation
Ambient Air
+++
+++
++
++
Robust
Oral/
Drinking
+++
+++
++
++
Robust
Ingestion
Water
Oral/ Fish
Surface
+++
+++
++
++
Robust
Ingestion
Water
Commercial use
as a lab
chemical
Oral/
Ingestion
Surface
Water/
Swimming
++
++
++
++
Moderate
Oral/
Ingestion
Soil
(Biosolids)
++
++
-
N/A
Slight
Oral/
Land; Soil
++
++
-
N/A
Slight
Ingestion
(Air
Deposition)
Dermal
Swimming
++
++
++
+
Moderate
Inhalation
Ambient Air
+++
+++
++
++
Robust
Inhalation
Indoor Air
++
++
++
+
Moderate
Oral/
Drinking
+++
+++
++
++
Robust
Ingestion
Water
Oral/ Fish
Surface
+++
+++
++
++
Robust
General waste
Ingestion
Water
handling,
Oral/
Surface
++
++
++
++
Moderate
treatment, and
Ingestion
Water/
disposal
Swimming
Oral/
Soil
++
++
-
N/A
Slight
Ingestion
(Biosolids)
Oral/
Land; Soil
++
++
-
N/A
Slight
Ingestion
(Air
Deposition)
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OES
Route of
Exposure
Media
Relevance
to
Exposure
Scenario
Modeling/
Estimation
Confidence
Level
Measured/
Monitoring
Confidence
Levelfl
Measured/
Modeling
Comparison
WOSE
Dermal
Swimming
++
++
++
+
Moderate
General waste
handling,
treatment and
disposal
(POTW)
Oral/
Ingestion
Drinking
Water
+++
+++
++
++
Robust
Oral/ Fish
Ingestion
Surface
Water
+++
+++
++
++
Robust
Oral/
Ingestion
Surface
Water/
Swimming
++
++
++
++
Moderate
Oral/
Ingestion
Soil
(Biosolids)
++
++
-
N/A
Slight
Oral/
Ingestion
Land; Soil
(Air
Deposition)
++
++
N/A
Slight
Dermal
Swimming
++
++
++
+
Moderate
General waste
handling,
treatment and
disposal
(REMEDIATI
ON)
Oral/
Ingestion
Drinking
Water
+++
+++
++
++
Robust
Oral/ Fish
Ingestion
Surface
Water
+++
+++
++
++
Robust
Oral/
Ingestion
Surface
Water/
Swimming
++
++
++
++
Moderate
Oral/
Ingestion
Soil
(Biosolids)
++
++
—
N/A
Slight
Oral/
Ingestion
Land; Soil
(Air
Deposition)
++
++
N/A
Slight
Dermal
Swimming
++
++
++
+
Moderate
+ + + Robust confidence suggests the supporting weight of scientific evidence outweighs the uncertainties to the point
where it is unlikely that the uncertainties could have a significant effect on the media concentration estimate.
+ + Moderate confidence suggests the supporting scientific evidence weighed against the uncertainties is reasonably
adequate to characterize the media concentration estimates.
+ Slight confidence is assigned when the weight of scientific evidence may not be adequate to characterize the scenario,
and when the assessor is making the best scientific assessment possible in the absence of complete information. There
are additional uncertainties that may need to be considered.
5.1.3 Aggregate Exposure Scenarios
Section 6(b)(4)(F)(ii) of amended TSCA requires EPA, as a part of the risk evaluation, to describe
whether aggregate or sentinel exposures under the COUs were considered and the basis for their
consideration.
EPA has defined aggregate exposure as "the combined exposures from a chemical substance across
multiple routes and across multiple pathways" (89 FR 37028, May 3, 2024, to be codified at 40 CFR
702.33). The fenceline methodology, Draft Screening Level Approach for Assessing Ambient Air and
Water Exposures to Fenceline Communities Version 1.0. aggregated inhalation estimates and drinking
water estimates from co4ocated facilities. In this draft risk evaluation, EPA employed this approach for
the general population ambient air exposure scenarios and quantitatively evaluated combined exposure
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and risk across multiple TRI facilities in proximity releasing 1,1-dichlorethane to air. For inhalation, this
aggregate screening analysis did not identify locations where the proximity and risk estimates of nearby
facilities led to aggregate risk estimates greater than 1 x 10~6 and therefore did not have a substantial
impact on the overall findings. Details of the methods and results of this screening aggregate analysis
are described in Appendix E.4.
5.1.4 Sentinel Exposures
EPA defines sentinel exposure as "the exposure from a chemical substance that represents the plausible
upper bound of exposure relative to all other exposures within a broad category of similar or related
exposures" (89 FR 37028, May 3, 2024, to be codified at 40 CFR 702.33). In terms of this draft risk
evaluation, EPA considered sentinel exposures by considering risks to human populations who may
have upper bound exposures; for example, workers and ONUs who perform activities with higher
exposure potential, or certain physical factors like body weight or skin surface area exposed. EPA
characterized high-end exposures in evaluating exposure using both monitoring data and modeling
approaches. Where statistical data are available, EPA typically uses the 95th percentile value of the
available dataset to characterize high-end exposure for a given COU.
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6058 5.2 Human Health Hazard
6059
1,1-Dichloroethane - Human Health Hazards
Key Points
EPA evaluated the reasonably available information for human health hazards and identified hazard points of
departure (PODs) for adverse effects following acute, short-term/subchronic, and chronic exposures.
Differences in endpoints used in past assessments have been identified. These differences are based on OPPT
systematic review criteria. EPA is requesting the SACC to provide input on the selection of the non-cancer
and cancer PODs in the draft 1,1-dichloroethane risk evaluation. These PODs represent the potential for
greater biological susceptibility across subpopulations. The most biologically relevant and sensitive PODs for
non-cancer and cancer effects for 1,1-dichloroethane from among the human health hazards identified—along
with the corresponding Human Equivalent Dose (HED), the Human Equivalent Concentration (HEC), and the
total combined uncertainty factors (UF) for each route and exposure duration—are summarized below. For
non-cancer, the lack of adequate data by all routes and durations of exposure for 1,1-dichloroethane required
the use of data from 1,2-dichloroethane as read-across. The lack of adequate non-cancer data by the dermal
route for 1,2-dichloroethane required route-to-route extrapolation from oral PODs. Similarly for cancer, the
lack of adequate cancer data for 1,1-dichloroethane by any route required data from 1,2-dichloroethane using
read-across. The following bullets summarize the key points of this section of the risk evaluation.
Non-cancer
The POD for the acute oral/dermal exposure route is renal toxicity (BMDLh>=153); the POD for the acute
inhalation exposure route is nasal necrosis (BMCLio = 48.9 mg/m3).
• HED (worker) = 19.9 mg/kg; HED (continuous) = 19.9 mg/kg
• HEC (worker) = 10.14 ppm; HEC (continuous) = 2.42 ppm
• Total UF = 30 for oral, inhalation, and dermal
The POD for the short-term/subchronic oral/dermal exposure route is suppression of immune system
response (LOAELadj = 4.89 mg/kg); the POD for the short-term/subchronic inhalation exposure route is male
reproductive effects (BMCL5 = 21.2 mg/m3).
• HED (worker) = 0.890 mg/kg; HED (continuous) = 0.636 mg/kg
• HEC (worker) = 22 ppm; HEC (continuous) = 5.2 ppm
• Total UF = 100 for oral and dermal; 30 for inhalation
The POD for the chronic oral/dermal exposure route is suppression of immune system response (LOAELadj =
4.89 mg/kg); the POD for the chronic inhalation exposure route is male reproductive effects (BMCL5 = 21.2
mg/m3).
• HED (worker) = 0.890 mg/kg; HED (continuous) = 0.636 mg/kg
• HEC (worker) = 22 ppm; HEC (continuous) = 5.2 ppm
• Total UF = 1000 for oral and dermal; 300 for inhalation
Cancer
The POD for the oral/dermal exposure routes is hepatocellular carcinomas in male mice based on read-across
from 1,2-dichloroethane (U.S. EPA. 1987a; NTP. 1978); the IUR is hepatocellular carcinomas based on read-
across from 1,2-dichloroethane (Nagano et al.. 2006); DW is based on route-to-route extrapolation of the oral
data.
• Oral/dermal cancer slope factor (continuous/worker) = 0.062 per mg/kg/day
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5.2.1 Approach and Methodology
EPA used the general approach described in Figure 5-6 to evaluate and extract evidence for 1,1-
dichloroethane human health hazard and dose-response information. This approach is based on the
Draft Systematic Review Protocol Supporting TSCA Risk Evaluations for Chemical Substances (U.S.
EPA. 2021b) (hereafter referred to as the 2021 Draft Systematic Review Protocol), updates to the
systematic review processes presented in the Draft Risk Evaluation for 1,1-Dichloroethane - Systematic
Review Protocol (U.S. EPA. 2024t) (hereafter referred to as the 1,1-Dichloroethane Systematic Review
Protocol) and the Framework for Raman Health Risk Assessment to Inform Decision Making (U.S.
EPA. 2014c).
Data
Evaluation
Results
Supplemental
File
1 Consideration of PESS i
Describing uncertainties / j
assumptions _ J
Figure 5-6. EPA Approach to Hazard Identification, Evidence Integration, and Dose-Response
Analysis for Human Health Hazard
5.2.1.1 Identification and Evaluation of 1,1-Dichloroethane Hazard Data
For the human health hazard assessment, EPA used a systematic review (SR) approach described in the
Draft Systematic Review Protocol Supporting TSCA Risk Evaluations for Chemical Substances (U.S.
EPA. 2021b). to identify relevant studies of acceptable data quality and integrate the pertinent data while
evaluating the weight of scientific evidence. For identified hazards and endpoints with the weight of
scientific evidence supporting an adverse outcome, studies were considered for dose-response analysis.
The 2021 Draft Systematic Review Protocol (U.S. EPA. 2021b) describes the general process of
evidence evaluation and integration, with relevant updates to the process presented in the 1,1-
Dichloroethane Systematic Review Protocol (U.S. EPA. 2024t).
For data quality evaluation, EPA systematically reviewed literature studies for 1,1-dichloroethane first
by reviewing screened titles and abstracts and then full texts for relevancy using population, exposure,
comparator, and outcome (PECO) screening criteria. Studies that met the PECO criteria were evaluated
for data quality using pre-established metrics as specified in the 1,1-Dichloroethane Systematic Review
Protocol (U.S. EPA. 2024t). Studies (based on the specified metrics) received overall data quality
determinations of either Uninformative, Low, Medium, or High. The results and details of the data
quality evaluation for 1,1-dichloroethane human health hazard epidemiology studies are included in the
Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File: Data Quality
Evaluation Information for Raman Health Hazard Epidemiology (U.S. EPA. 2024ad). This
supplemental file is hereafter referred to as the 1,1-Dichloroethane Data Quality Evaluation Information
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for Human Health Hazard Epidemiology (U.S. EPA. 2024acT). The results and details of the data quality
evaluation for 1,1-dichloroethane animal toxicity studies are included in the Draft Risk Evaluation for
1,1-Dichloroethane - Systematic Review Supplemental File: Data Quality Evaluation Information for
Human Health Hazard Animal Toxicology (U.S. EPA. 2024ac). This supplemental file is hereafter
referred to as 1,1-Dichloroethane Data Quality Evaluation Information for Human Health Hazard
Animal Toxicology (U.S. EPA. 2024ac) or OPPT SR review (U.S. EPA. 2024ac).
Following data quality evaluation, EPA completed data extraction of the toxicological information from
each on topic study that met the PECO criteria. This data extraction included studies of all data quality
determinations including "uninformative". The results of data extraction for human and animal for 1,1-
dichloroethane toxicity studies are reported in the Draft Risk Evaluation for 1,1-Dichloroethane -
Systematic Review Supplemental File: Data Extraction Information for Environmental Hazard and
Human Health Hazard Animal Toxicology and Epidemiology (U.S. EPA. 2024u). This supplemental file
is hereafter referred to as the 1,1-Dichloroethane Data Extraction Information for Environmental
Hazard and Human Health Hazard Animal Toxicology and Epidemiology (U.S. EPA. 2024u).
EPA completed a hazard identification and evidence integration for 1,1-dichloroethane based on a
review and evaluation of the results of the SR process including data quality evaluation and data
extraction. The hazard identification and evidence integration completed for 1,1-dichloroethane are
provided in Section 5.2.1.5 for toxicokinetics, Section 5.2.3 for non-cancer human and animal study data
(stratified by organ system), Section 5.2.4 for genotoxicity and Section 5.2.5 for cancer. Details are
provided in Appendix M.
Based on these hazard identification and evidence integration results, EPA completed a dose-response
assessment for 1,1-dichloroethane in Section 5.2.5.3. These analyses of the 1,1-dichl or ethane data
resulted in the identification of data gaps that are summarized in Section 5.2.1.2.
5.2.1.2 1,1-Dichloroethane Data Gaps
EPA identified three community-based epidemiological studies, one occupational epidemiological study
and 16 animal toxicity studies for inclusion in the risk evaluation and thereby, candidate studies to
complete dose-response assessment and inform the identification of points of departure (PODs) for 1,1-
dichloroethane. Excluding studies rated as Uninformative in the data quality evaluation left nine 1,1-
dichloroethane animal toxicity studies and the three community-based epidemiological studies with
acceptable quality for subsequent consideration as candidates for dose-response analysis. Each of these
studies was evaluated in the dose-response assessment (Section 5.2.5.3) and none were identified as
suitable for the identification of PODs for use in the risk evaluation. In short, the available toxicity
database for 1,1-dichloroethane consists of a small number of animal studies evaluating a limited
number of measured parameters.
In summary, EPA identified data gaps for 1,1-dichloroethane for non-cancer PODs by the acute, short-
term/sub chronic, and chronic oral, dermal, and inhalation routes; and cancer PODs by the oral,
inhalation, and dermal routes (see Sections 5.2.1.2.1 and 5.2.1.2.2 for details). In support of EPA's
analyses, the ATSDR (2015) 1,1-Dichloroethane Report reached a similar conclusion that "the
uncertainties associated with identification of the most sensitive target and the associated concentration-
response relationships, precludes deriving inhalation MRLs for 1,1-dichloroethane."
A summary of the identified data gaps for 1,1-dichloroethane are provided in the following subsections
for non-cancer and cancer, respectively.
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5.2.1.2.1 Non-cancer Data Gaps
Oral
EPA evaluated and extracted the data for human health hazard identification and evidence integration
for oral exposures of 1,1-dichlorethane. In the dose-response assessment, EPA did not identify
acceptable studies to inform the identification and derivation of PODs for 1,1-dichloroethane for acute,
short-term/sub chronic, and chronic oral exposures.
There were two acute-duration oral studies of 1,1-dichloroethane that were rated acceptable and were
considered in the dose-response assessment for use in the risk evaluation. These studies included an
acute lethality study in guinea pigs by Dow Chemical (1947) and a single-dose lethality study in rats by
Muralidhara et al. (2001). The limitations of these studies that preclude their use for POD derivation are
described in Section 5.2.6.1.2.
There were three short-term (>1-30 days) and sub-chronic (>30-91 days)-duration animal toxicology
studies that were rated acceptable and were considered in the dose response assessment for use in the
risk evaluation. These studies include a 10-day exposure in rats (Muralidhara et al.. 2001). a 14-day
exposure in rats (Ghanavem et al.. 1986). and a 13-week exposure in rats (Muralidhara et al.. 2001). The
limitations of these studies that preclude their use for POD derivation are described in Section 5.2.6.1.3.
There was one chronic-duration oral study of 1,1-dichloroethane in mice that was rated acceptable and
considered in the dose-response assessment for use in the risk evaluation. This study was a 52-week
drinking water study in mice (Klaunig et al.. 1986). The limitation of this study that precludes its use for
POD derivation is described in detail in Section 5.2.6.1.4.
Inhalation
EPA evaluated and extracted the data for human health hazard identification and evidence integration
for inhalation of 1,1-dichlorethane. EPA did not identify available or acceptable data for dose-response
assessment to inform the identification of PODs for 1,1-dichloroethane for acute, short-term/sub chronic,
and chronic inhalation exposures.
There were no acute duration (<24 hours) inhalation exposure studies of 1,1-dichloroethane identified as
from the OPPT SR process. One developmental inhalation toxicity study in rats for 1,1-dichloroethane
Schwetz et al. (1974) was rated acceptable and was considered in the dose-response analyses for use in
the risk evaluation for identification of an acute and/or short-term/sub chronic inhalation POD. The
limitation of this study that precludes its use for POD derivation is described in Section 5.2.6.1.2 and
Section 5.2.6.1.3.
There were two chronic-duration inhalation studies of 1,1-dichloroethane that were rated acceptable and
were considered in the dose-response assessment for use in the risk evaluation. These studies include a
13-week exposure for rats, cats, guinea pigs, and rabbits Hofmann et al. (1971a)and a 6-month exposure
for a single mongrel dog Mellon Institute (1947). The limitations of these studies that preclude their use
for POD derivation are described in Section 5.2.6.1.4.
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Dermal
EPA did not identify any non-cancer animal toxicological data for 1,1-dichloroethane by the dermal
route.
5.2.1.2.2 Cancer Data Gaps
Oral
After data quality evaluation and data extraction as described in Section 5.2.1.1 EPA identified cancer
data on 1,1-dichloroethane from one study. This study is a National Toxicological Program (NTP) study
in rats and mice NCI (1978). The rat portion of this study was rated as uninformative by SR review
(U.S. EPA. 2024ac) based on a confounding health outcome unrelated to exposure. Specifically, "rats
from all study groups (including both sexes and controls) exhibited high incidences of pneumonia (up to
95%), indicating infections in these animals". This aspect was not discussed nor mentioned by the study
authors. It is unclear how these infections impacted study results. The mouse portion of this 1,1-
dichloroethane cancer study revealed a statistically significant increase in benign uterine endometrial
stromal polyps (4/46) in high-dose females, which were not observed in any other group. No other
statistically significant evidence of cancer was observed. Pre-cancerous endometrial polyps are not a
tissue growth amenable to calculate cancer slope factors. As a result, EPA did not use the NCI (1978)
oral cancer study on 1,1-dichloroethane in Osborne-Mendel rats and B6C3F1 mice to calculate cancer
slope factors for 1,1-dichloroethane.
Inhalation
EPA after data quality evaluation and data extraction as described in Section 5.2.1.1 did not identify a
cancer study via the inhalation exposure route for 1,1-dichloroethane.
Dermal
EPA after data quality evaluation and data extraction as described in Section 5.2.1.1 did not identify a
cancer study via the dermal exposure route for 1,1-dichloroethane.
5.2.1.3 Identification of an Analog and the Use of Read-Across from 1,2-
Dichloroethane Hazard Data
As acceptable human health hazard data were not available to assess risks for 1,1-dichloroethane, EPA
chose to use a "read-across" approach using data available for a closely related chemical or analog to
evaluate the human health hazard of 1,1-dichloroethane. An analysis of other chlorinated solvents as
potential analogs for read-across data was performed following the general principles for read-across as
outlined in Lizarraga et al. (2019). taking into consideration structural similarities, physical-chemical
properties, metabolism, and toxicological similarities. The analyses resulted in the identification of 1,2-
dichloroethane (an isomer of 1,1-dichlorethane) as the most appropriate analog to fill the identified data
gaps for 1,1-dichloroethane and a consultation with the EPA Office of Research and Development
(ORD) agreed. EPA has high confidence that the 1,2-dichloroethane data will accurately reflect the
hazards of 1,1-dichloroethane.
5.2.1.3.1 Structural Similarity
The first step in identification of possible analogs is to examine structural similarity. There are several
different methods for determining structural similarity. A fragment-based approach (e.g., as
implemented by AIM) searches for compounds with similar structural moieties or functional groups. A
structural identifier approach (e.g., the Tanimoto coefficient) calculates a similarity coefficient based on
molecular fingerprinting (Belford. 2023). Molecular fingerprinting approaches look at similarity in
atomic pathway radius between the analog and target chemical substance (e.g., Morgan fingerprint in
GenRA which calculates a Jaccard similarity index). Some fingerprints may be better suited for certain
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characteristics and chemical classes. For example, substructure fingerprints like PubChem fingerprints
perform best for small molecules such as drugs, while atom-pair fingerprints, which assigns values for
each atom within a molecule and thus computes atom pairs based on these values, are preferable for
large molecules. Some tools implement multiple methods for determining similarity. Regarding
programs which generate indices, it has been noted that because the similarity value is dependent on the
method applied, that these values should form a line of evidence rather than be utilized definitively
(Pestana et al.. 2021; Mellor et al.. 2019).
Structural similarity between 1,1-dichloroethane and other chlorinated solvents was assessed using two
TSCA NAMs (the AIM program and OECD QSAR Toolbox) and two EPA Office of Research products
(GenRA) and the Search Module within the Cheminformatics Modules (Hazard Comparison Dashboard
(HCD) previously). AIM analysis was performed on the CBI-side and potential analogs were described
as 1st or 2nd pass. Tanimoto-based PubChem fingerprints were obtained in the OECD QSAR Toolbox
(v4.4.1, 2020) using the Structure Similarity option. Chemical Morgan Fingerprint scores were obtained
in GenRA (v3.1, no ToxRef filter) (limit of 100 analogs). Tanimoto scores were obtained in the ORD
Cheminformatics Search Module (Hazard Comparison Dashboard or HCD) using similarity analysis.
The top 100 analogs with indices greater than 0.5 generated from the OECD QSAR Toolbox and the
Cheminformatics Search Module and indices greater than 0.1 generated from GenRA were compiled
with AIM 1st and 2nd pass analogs. Analogs that appeared in three out of four programs were identified
as potential analog candidates. A more complete description of the structural similarity tools are
provided in Appendix J.2.
1,2-Dichloroethane was identified as a possible analog based on structural similarity as well as 1,1,2-
trichloroethane (1,1,2-TCA), and 1,2-dichloropropane (1,2-DCP). The results of the comparison of the
structural similarity of the target chemical 1,1-dichloroethane to other chlorinated solvents using the
structural similarity tools are shown in Table 5-35. The higher the similarity score, the better the
structural match, with a value of 1.00 being an exact match, whereas AIM 1st pass indicates better
structural agreement than AIM 2nd pass. 1,2-Dichloroethane was indicated as structurally similar to 1,1-
dichloroethane in AIM (2nd pass), OECD QSAR Toolbox (PubChem features = 0.79), and the
Cheminformatics Search Module (Tanimoto coefficient = 0.63). 1,2-Dichloropropane was indicated as
structurally similar to 1,1-dichloroethane in AIM (2nd pass), OECD QSAR Toolbox (PubChem features
= 0.75), and GenRA (Morgan Fingerprint = 0.45) and had a lower Tanimoto score in the
Cheminformatics Search Module (Tanimoto coefficient = 0.42). 1,1,2-Trichloroethane was indicated as
structurally similar to 1,1-dichloroethane in AIM (2nd pass), OECD QSAR Toolbox (PubChem features
= 0.79), and the Cheminformatics Search Module (Tanimoto coefficient = 0.78). 1,2-dichloroethane was
identified as the best available candidate chemical to fill the identified data gaps for 1,1-dichloroethane
hazard based on further lines of evidence and the fact that they are structurally similar as reactive di-
chlorinated ethanes and both are isomers with identical molecular formulas/molecular weight.
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Table 5-35. Structural Similarity of 1-1 Dichloroethane Compared to Other
Chlorinated Solvents
Target
Candidate
Analogs
Chlorinated
Solvent
AIM
OECD
QSAR
Toolbox
GenRA
HCD
1,1-
Dichloroethane
Exact
match
1.00
1.00
1.00
1,2-
Dichloroethane
2nd pass
0.79
-
0.63
1,1,2-
Trichloroethane
2nd pass
0.79
-
0.78
1,2-
Dichloropropane
2nd pass
0.75
0.45
0.42
T ri chl oroethy 1 ene
-
0.73
-
0.33
Dichloromethane
2nd pass
0.46
-
0.57
trans-\ ,2-
di chl oroethy 1 ene
-
0.63
-
0.30
Perchl oroethy 1 ene
-
0.47
-
0.33
Carbon
tetrachloride
2nd pass
0.29
-
0.44
5.2.1.3.2 Physical and Chemical Similarities
The comparison of key physical and chemical properties of 1,1-dichloroethane and the three top
candidate analogs identified based on structural similarities (1,2-dichloroethane, 1.1,2-trichloroethane,
and 1,2-dichloropropane) is shown in Table 5-36. Considering the common variability in physical and
chemical results across methods and laboratories over time, 1,1-dichloroethane has similar values to 1,2-
dichloroethane for water solubility, log Kow, molecular weight, physical state, Henry's Law constant
and vapor pressure, all of which can affect their ADME and target tissue levels. For example, in Table
5-36, water solubility and Kow between 1,1-dichloroethane and 1,2-dichloroethane appear to be
different. However, in general, variability in physical and chemical properties results for the same
chemical for water solubility and Kow can differ by orders of magnitude, therefore, differences in
reported physical and chemical values are not uncommon (Gigante et al.. 2021; Pontolilloand and
Eganhouse. 2001). In addition, the physical and chemical properties for 1,1,2-Trichloroethane and 1,2-
dichloropropane are also included in Table 5-36. For 1,1,2-trichloroethane, the vapor pressure is 10
times lower, the Henry's Law constant is 7 times lower, and the molecular weight is 35 percent higher
than 1,1-dichloroethane, which has ADME implications, and therefore was not considered as close of a
chemical candidate analog for read-across compared to 1,2-dichloroethane.
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Table 5-36. Comparison of 1,1-Dichloroethane an(| 1,2-Dichloroethane for Physical and Chemical
Properties Relevant to Human Health Hazard
Chlorinated Solvent
Water
Solubility
(mg/L)
Log
Kow
Molecular
Weight
Physical
State
Henry's Law
Constant
(atm-m3/mol)
Vapor
Pressure
(mm Hg)
1,1 -Dichloroethane
5,040
1.79
98.95
Liquid
0.00562
227
1,2-Dichloroethane
8,600
1.48
98.96
Liquid
0.00118
79
1,1,2-Trichloroethane
4,590
1.89
133.41
Liquid
0.00082
23
1,2-Dichloropropane
2,800
1.99
112.99
Liquid
0.00282
40
5.2.1.3.3 Metabolic Similarities
In Vitro Metabolism Studies — 1,1-Dichloroethane
The metabolic pathways for 1,1-dichloroethane have been elucidated from in vitro studies using rat
hepatic microsomes (McCall et al.. 1983; Sato et al.. 1983; Van Dyke and Wineman. 1971). As outlined
in FigureApx J-l, the primary metabolic pathway involves oxidation of the C-l carbon by cytochrome
P450 (CYP) to give an unstable alpha-haloalcohol followed by dechlorination to produce acetyl chloride
and acetic acid, which is the major metabolite. The alpha-haloalcohol may also undergo a chlorine shift
to yield chloroacetyl chloride and monochloroacetic acid, although this reaction is not favored. CYP
oxidation at the C-2 position results in the formation of 2,2-dichloroethanol, dichloroacetaldehyde, and
dichloroacetic acid as minor metabolites. Metabolism of 1,1-dichloroethane was increased by induction
with phenobarbital and ethanol, but not P-naphthoflavone (McCall et al.. 1983; Sato et al.. 1983).
Similarly, enzymatic dechlorination was inducible by phenobarbital, but not 3-methylcholanthrene ("Van
Dyke and Wineman. 1971).
In Vivo and In Vitro Metabolism Studies — 1,2-Dichloroethane
No human studies on the metabolism of 1,2-dichloroethane were located. Figure Apx J-2 outlines the
primary metabolic pathways for 1,2-dichloroethane, elucidated from in vitro studies and in vivo studies
in rats and mice, include cytochrome P450 (CYP) oxidation and glutathione (GSH) conjugation (IPCS.
1995). Metabolism by CYP results in an unstable gem-chlorohydrin that releases hydrochloric acid,
resulting in the formation of 2-chloroacetaldehyde. 2-Chloroacetaldehyde is oxidized to form
chloroacetic acid or reduced to form 2-chloroethanol, and these metabolites are conjugated with GSH
and excreted in the urine. Metabolism via glutathione-S-transferase results in formation of S-(2-
chloroethyl)-glutathione, which rearranges to form a reactive episulfonium ion. The episulfonium ion
can form adducts with protein, DNA or RNA or interact further with GSH to produce water soluble
metabolites that are excreted in the urine.
5.2.1.3.4 Toxicological Similarity - Cancer
There are no adequate non-cancer data available by the acute, short-term/sub chronic and chronic
inhalation routes, and dermal routes by any exposure duration for 1,1-dichloroethane. As a result, the
1,2-dichloroethane database was systematically reviewed and evaluated to identify non-cancer PODs to
be used as read-across from 1,2-dichloroethane to fill in those 1,1-dichloroethane data gaps and calculate
quantitative risk estimates.
Table 5-37 shows a qualitative comparison of common non-cancer findings between 1,1-dichloroethane
and 1,2-dichloroethane, highlighting an overall similarity. Table 5-37 does not, however, reflect the full
database for either chemical. The final non-cancer quantitative PODs selected for both chemicals were
based upon the strength of the evidence from data that ranked Moderate to High in our SR, was of
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reliable and sufficient quality, and was the most biologically relevant and sensitive using the best
available science.
Table 5-37. Qualitative Comparison of Cancer Findings for 1,1-Dichloroethane compared to 1,2-
Dichloroethane
Studies
1,1-Dichloroethane
1,2-Dichloroethane
NTP Oral Rat Studies
(Uninformative by SR)
Mammary gland
adenocarcinomas,
hemansiosarcoma. (NCI. 1978)
Mammary gland adenocarcinomas,
hemansiosarcoma (NTP. 1978)
NTP Oral Mouse Studies (High
SR rating)
Endometrial stromal polyps
(precursor). (NCI. 1978)
Endometrial stromal polyps (precursor),
NTP (1978b)
Hepatocarcinomas. (NTP. 1978)
Inhalation Studies
Chronic study, but not a cancer
studv. (Hofmann et al.. 1971b).
Uninformative by SR)
Mammary gland adenomas; fibroadenomas,
adenocarcinomas; subcutaneous fibromas;
bronchioalveolar adenoma & carcinoma;
endometrial stromal polyps; hepatocellular
adenoma. (Nagano et al.. 2006). High SR
rating
Dermal Study
None
Bronchioalveolar adenomas and
adenocarcinomas (mice. 1 dose). (Suauro et
al.. 2017). Hieh SR ratine)
Human Studies
Indeterminate
Indeterminate
Table 5-38 provides a comparison of the cancer study findings between 1,1-dichloroethane and 1,2-
dichloroethane.
Table 5-38. Comparison of Cancer St
udy Findings for 1,1-Dichloroethane and 1,2-Dichloroethane
Chronic Study Finding
1,1-Dichloroethane
1,2-Dichloroethane
Endometrial polyps
+
+
Hepatocellular carcinomas
+
+
Hemangiosarcomas
+
+
Mammary gland tumors
+
+
11 In general, similar tumor types or pre-cancerous lesions were observed with 1,1-dichloroethane as seen in the
bioassays of the similar isomer 1,2- dichloroethane {i.e., hepatocellular carcinomas, endometrial polyps,
h c m an e i o s arco m as. mammarv aland tumors; High SR studv in F344 rats and BDF1 mice (Nagano et al..
2006).
Table 5-39 provides the results of the predicted carcinogenicity of 1,1-dichloroethane and 1,2-
dichloroethante using the OncoLogic™ model. This model was developed by EPA to evaluate the
carcinogenic potential of chemicals following sets of knowledge rules based on studies of how
chemicals cause cancer in animals and humans. Both 1,1-dichloroethane and 1,2-dichloroethane
possessed similar results based on OncoLogic™ and similar precursor events (see Table Apx J-12).
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Table 5-39. OncoLogic Carcinogenic Potential Results for 1,1-Dichloroethane and 1,2-
Dichloroethane
Parameter
1,1-Dichloroethane
1,2-Dichloroethane
Classification for
carcinogenicity
Low-Medium Concern
Medium Concern
Chemistry
Geminal alkyl dihalide
Vicinal alkyl dihalide
Chemical reactivity
Geminal alkyl dihalide < vicinal alkyl dihalide
5.2.1.3.5 Toxicological Similarity - Non-cancer
There are no adequate non-cancer data available by the acute, short-term/sub chronic and chronic
inhalation routes, and dermal routes by any exposure duration for 1,1-dichloroethane. As a result, the
1,2-dichloroethane database was systematically reviewed and evaluated to identify non-cancer PODs to
be used as read-across from 1,2-dichloroethane to fill in those 1,1-dichloroethane data gaps and calculate
quantitative risk estimates.
Table 5-40 shows a qualitative comparison of common non-cancer findings between 1,1-dichloroethane
and 1,2-dichloroethane, highlighting an overall similarity. The final non-cancer quantitative PODs
selected for 1,1-dichloroethane (using 1,2-dichloroethane data as read across) were based upon the
strength of the evidence from data that ranked Moderate to High in the OPPT SR, was of reliable and
sufficient quality, and was the most biologically relevant and sensitive using the best available science.
Table 5-40. Qualitative Comparison of Non-cancer Findings between 1,1-Dichloroethane and 1,2-
Dichloroethane
Effects
1,1-Dichloroethane
1,2-Dichloroethane
Reproductive/
Developmental
Evidence is inadequate to assess
whether 1,1-dichloroethane exposure
may cause reproductive/ developmental
toxicity under relevant exposure
circumstances.
Evidence suggests, but is not sufficient to
conclude, that 1,2-dichloroethane may cause
effects on male reproductive structure and/or
function under relevant exposure conditions.
Evidence is inadequate to determine whether
1,2-dichloroethane may cause effects on the
developing organism. There is no evidence that
1,2-dichloroethane causes effects on female
reproductive structure and/or function.
Renal
Evidence is inadequate to assess
whether 1,1-dichloroethane exposure
may cause renal toxicity under relevant
exposure circumstances.
Evidence indicates that 1,2-dichloroethane
likely causes renal effects under relevant
exposure circumstances.
Hepatic
Evidence suggests, but is not sufficient
to conclude, that 1,1-dichloroethane
exposure causes hepatic toxicity under
relevant exposure circumstances.
Evidence suggests, but is not sufficient to
conclude, that 1,2-dichloroethane may cause
hepatic effects under relevant exposure
conditions.
Nutritional/
Metabolic
Evidence suggests, but is not sufficient
to conclude, that 1,1-dichloroethane
exposure causes body weight
decrements under relevant exposure
circumstances.
Evidence suggests that 1,2-dichloroethane may
cause body weight decrements under relevant
exposure circumstances.
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Effects
1,1-Dichloroethane
1,2-Dichloroethane
Neurological/
Behavioral
Evidence suggests, but is not sufficient
to conclude, that 1,1-dichloroethane
exposure causes neurological effects
under relevant exposure circumstances.
Evidence indicates that 1,2-dichloroethane
likely causes neurological/behavioral effects
under relevant exposure circumstances.
Immune/
Hematological
Evidence suggests, but is not sufficient
to conclude, that 1,1-dichloroethane
exposure causes immune system
suppressions (Zabrodskii et al.. 2004).
Evidence suggests, but is not sufficient to
conclude, that 1,2-dichloroethane may cause
immune system suppression under relevant
exposure conditions.
Respiratory Tract
Evidence suggests, but is not sufficient to
conclude, that 1,2-dichloroethane may cause
nasal effects under relevant exposure
conditions.
Mortality
Evidence indicates that 1,1-
dichloroethane exposure is likely to
cause death under relevant exposure
circumstances.
Evidence indicates that 1,2-dichloroethane may
cause death under relevant exposure
circumstances and lethal levels have been
identified in animal studies.
5.2.1.3.6 Read-Across Conclusions
1,2-Dichloroethane was identified as the best available candidate chemical to fill the identified data gaps
for 1,1-dichloroethane. This conclusion is based on the fact that both 1,1-dichloroethane and 1,2-
dichloroethane are structurally similar as reactive di-chlorinated ethanes, both are isomers of each other
with identical molecular weights and formulas, both have similar physical-chemical properties, both are
volatile liquids, both have similar ADME patterns and metabolic pathways, both are reactive alkyl
halides, and both possess, overall, similar non-cancer and cancer outcomes (mutagenicity, common
tumor types, many common hazard endpoints).
Table 5-41 illustrates the many qualitative non-cancer and cancer toxicity endpoints and other chemical
properties both 1,1-dichloroethane and 1,2-dichloroethane have in common. This comparison is based
on the literature studies and the ATSDR reports for both isomers (AT SDR. 2022. 2015). Many of the
identified endpoints for 1,1-dichloroethane and 1,2-dichloroethane were from studies that passed OPPT
SR were not always but were not robust enough to identify a non-cancer PODs or cancer slope factors to
use for quantitative risk estimates.
Table 5-41. Common Hazards and Properties of 1,1-Dichloroethane and 1,2-Dichloroethane
1,1-Dichloroethane and 1,2-Dichloroethane Common Hazards and Properties
Hazard-Property
1,1-Dichlorethane
1,2-Dichloroethane
Chemical Reactivity
+
+
Dichloroethane Isomers
+
+
Irritation
+
+
Narcosis
+
+
Genotoxicity without Metabolic Activation
+
+
Immunotoxicity
+
+
Endometrial Polyps
+
+
Hepatocellular Carcinoma
+
+
Hemangiosarcomas
+
+
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1,1-Dichloroethane and 1,2-Dichloroethane Common Hazards and Properties
Mammary Gland Tumors
+
+
Nephrotoxicity
+
+
Hepatoxicity
+
+
Metabolic Toxicity
+
+
Cardiotoxicity
+
+
5.2.1.4 Identification and Evaluation of 1,2-Dichloroethane Hazard Data
The same process as described for 1,1-dichloroethane in Section 5.2.1.1 applies to the identification and
evaluation of 1,2-dichloroethane hazard data. The results of the SR process (data quality evaluation and
data extraction) for 1,2-dichloroethane are recorded in the same respective supplemental files for 1,1-
dichloroethane including 1,1-Dichloroethcme Data Quality Evaluation Information for Raman Health
Hazard Epidemiology (U.S. EPA. 2024ad). 1,1-Dichloroethane Data Quality Evaluation Information
for Human Health Hazard Animal Toxicology (U.S. EPA. 2024ac). and 1,1-Dichloroethane Data
Extraction Information for Environmental Hazard and Human Health Hazard Animal Toxicology and
Epidemiology (U.S. EPA. 2024u).
After EPA completed the data evaluation and data extraction for 1,2-dichloroethane, a hazard
identification and evidence integration of the data were completed and the results are provided in
Section 5.2.1.5 for toxicokinetics, Section 5.2.3 for non-cancer data stratified by organ system, Section
5.2.4 for genotoxicity, and Section 5.2.5 for cancer. Based on these hazard identification and evidence
integration results, EPA completed a dose-response assessment for 1,2-dichloroethane in Section
5.2.5.3.
5.2.1.5 Structure of the Human Health Hazard Assessment
6.3.1Appendix M provides the details of the human health hazard assessment for 1,1-dichloroethane and
the identified analog 1,2-dichloroethane. Appendix M.l provides a summary of toxicokinetics for both
1,1-dichloroethane and 1,2-dichloroethane. Appendix M.2 provides a non-cancer dose response
assessment for both chemicals. Appendix 6.3.1M.3 provides the equations used in derivation of non-
cancer and cancer PODs for the 1,1-dichloroethane risk assessment. Appendix 6.3.1M.4 describes the
non-cancer POD derivation for acute, short/intermediate-term, and chronic durations. Appendix M.5
provides evidence integration tables for 1,1-dichloroethane. Appendix M.6 provides evidence
integration tables for 1,2-dichloroethane. Appendix M.7 describes evidence for mutagenicity and cancer
for both chemicals. Appendix M.8 provides a cancer dose-response assessment for 1,1-dichloroethane
using data for 1,2-dichloroethane as read-across.
The following subsections provide a summary of the human health hazard assessment for 1,1-
dichloroethane and the analog 1,2-dichloroethane (used to fill data gaps in a read-across approach).
5.2.2 Toxicokinetics Summary
This section provides a summary on the absorption, distribution, metabolism, and elimination (ADME)
data available for 1,1-dichloroethane and 1,2-dichloroethane. For full details on toxicokinetics see
Appendix M.l. which provides details on the toxicokinetics of 1,1-dichloroethane including absorption
(Appendix M.l. 1.1), distribution (Appendix M.l.2), metabolism (Appendix M. 1.3.1) and excretion
(Appendix M.l.4.1).
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5.2.2.1 1,1-Dichloroethane
The pulmonary absorption of 1,1-dichloroethane is likely to occur since previous use of 1,1-
dichloroethane as a gaseous anesthetic in humans provides evidence of systemic absorption and
distribution to the CNS by the inhalation route (ATSDR. 2015). Qualitative evidence of dermal
absorption was provided by a rabbit study that detected halogen ion in exhaled breath following
application of 1,1-dichloroethane to shaved abdominal skin (Reid and Muianga. 2012). Tissue:air
partition coefficients calculated using a vial equilibration method on tissues obtained from male Fischer
344 rats suggest that 1,1-dichloroethane is likely distributed to highly perfused tissues (i.e., liver,
muscle) and will accumulate in fat (Gargas and Andersen. 1989).
The metabolic pathways for 1,1-dichloroethane have been elucidated from in vitro studies using rat
hepatic microsomes (McCall et al.. 1983; Sato et al.. 1983; Van Dyke and Wineman. 1971). The primary
metabolic pathway involves oxidation by cytochrome P450 to give an unstable alpha-haloalcohol
followed by dechlorination to produce acetyl chloride and acetic acid, which is the major metabolite.
Cytochrome P450 oxidation results in the formation of 2,2-dichloroethanol, reactive
dichloroacetaldehyde, and dichloroacetic acid as minor metabolites.
Via inhalation, the metabolic rate constants for 1,1-dichloroethane were estimated for male Fischer 344
rats using a gas uptake method in rats exposed to initial concentrations of 360, 1,980, 4,500, or 8,804
mg/m3, from which concluded that the liver metabolism of 1,1-dichloroethane is saturable process at
high concentrations (Gargas et al.. 1990).
The extent of oral metabolism was evaluated in Osborne-Mendel rats and B6C3F1 mice administered
700 or 1,800 mg/kg-bw/day 1,1-dichloroethane, respectively, by gavage for 4 weeks (Mitoma et al..
1985). The total percentages of administered dose found in exhaled CO2, excreta, and body carcass 48
hours after the administration of the radiolabeled dose were 7.45 percent in rats and 29.3 percent in
mice. The 1,1-dichloroethane is highly absorbed orally. Within 48 hours in rats, 91 percent of the
administered dose was eliminated in expired air (86 percent unchanged, 5 percent as CO2). In mice, 95
percent of the administered dose was eliminated in expired air (70 percent unchanged, 25 percent as
CO2) within 48 hours.
EPA did not identify in vivo animal data that evaluated elimination following exposure to 1,1-
dichloroethane by the dermal route nor inhalation routes and PBPK models were not identified. The
highest dermal absorption value reported in the 1,1-dichloroethane OECD 428 study was 0.27 percent at
50 percent concentration in 1,2-dichloroethane as the COU vehicle. The mass balance corrected mean
dermal absorption for neat 1,1-dichloroethane was 0.22 percent and the 95 percent upper confidence
limit for the neat chemical was 0.29 percent dermal absorption, or similar to the dermal absorption
reported for the identified analog 1,2-dichloroethane at 0.21 percent. The mean Kp value and the 95
percent upper confidence limit Kp value for neat 1,1-dichloroethane were 0.00229 and 0.00371 cm/hour,
respectively. The reported in vitro mean Kp value and 95 percent upper confidence limit Kp value for the
analog 1,2-dichloroethane were similar at 0.00109 and 0.00137 cm/hour, respectively for the neat
chemical (Schenk, 2018, 4940676).
5.2.2.2 1,2-Dichloroethane
Following oral administration in rats the elimination of 1,2-dichloroethane was rapid and occurred
primarily via unchanged parent compound and carbon dioxide in the expired air and via excretion of
soluble metabolites in the urine. Women inhaling 1,2-dichloroethane present in the workplace air
eliminated the compound unchanged in the expired air with similar observations in women exposed via
dermal contact to liquid 1,2-dichloroethane. It should be noted that in female workers exposed dermally
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to 1,2-dichloroethane, the breast milk levels were considerable at 283 micromolar and that similar
concentrations caused cytotoxicity to human immune T cells in vitro at 5 and 10 percent cell death at
concentrations of 157 and 379 micromolar, respectively. Test Order data for dermal absorption for 1,2-
dichloroethane has been requested but is currently not available, however, the dermal absorption of 1,2-
dichloroethane has been reported to be 0.21 percent or very similar to its isomer 1,1-dichoroethane
(ATSDR. 2022). The 26-week 1,2-dichloroethane dermal study in mice produced lung tumors
supporting that long term dermal exposure can produce serious systemic effects despite low dermal
absorption levels (exposures 3 times/week induced 100 percent lung tumor incidence in female mice,
Suguro, 2017, 4451542).
Details on the toxicokinetics of 1,2-dichloroethane are provided in Appendix 6.3.1M.1. ADME details
are described for 1,2-dichloroethane for adsorption (Appendix M. 1.1.1), distribution (Appendix M.1.2),
metabolism (Appendix M.1.3.1) and excretion (Appendix M.l.4.1).
5.2.3 Non-cancer Hazard Identification and Evidence Integration
The sections below describe adverse outcome and mechanistic data available as well as evidence
integration conclusions for each human health hazard outcome observed in 1,1- and 1,2-dichloroethane
toxicity studies. EPA identified very few epidemiological studies relevant to non-cancer endpoints.
Therefore, evidence is primarily based on available laboratory animal toxicity studies—exclusively via
the oral and inhalation routes.
The 2021 Draft Systematic Review Protocol (U.S. EPA. 2021b) describes the general process of
evidence evaluation and integration, with relevant updates to the process presented in the 1,1-
Dichloroethane Systematic Review Protocol (U.S. EPA. 2024t). Appendix M provides a detailed
evaluation of the 1,1- and 1,2-dichloroethane hazard outcomes and evidence integration conclusions.
The analyses are presented as a series of evidence integration tables in Appendix M.5 for 1,1-
dichloroethane (non-cancer), Appendix M.6 for 1,2-dichloroethane (non-cancer), Appendix M.7 for 1,1-
dichloroethane (cancer) and Appendix M.8 for 1,2-dichloroethane (cancer).
5.2.3.1 Critical Human Health Hazard Outcomes
The sections below focus on hazard identification and evidence integration of kidney toxicity,
immunotoxicity, and neurotoxicity, which are the most sensitive critical human health hazard outcomes
associated with 1,1- and 1,2-dichloroethane. These hazard outcome categories received likely evidence
integration conclusions, and sensitive health effects were identified for these hazard outcomes. In the
risk evaluation, renal toxicity forms the basis of the POD used for acute oral exposure scenarios and
immunotoxicity is the basis of the POD used for short-term and chronic oral exposure scenarios. The
2022 ATSDR document for 1,2-dichloroethane confirmed that immunotoxicity is the most sensitive
endpoint (ATSDR. 2022). Neurotoxicity is the basis of the POD used for acute inhalation exposure and
reproductive effects is the basis for short-term/subchronic and chronic inhalation exposure scenarios.
Due to a lack of adequate dermal studies, dermal hazard was based on route-to-route extrapolation from
oral exposure, based on ADME properties (see Appendix M. 1). Additionally, hazard identification and
evidence integration of other toxicity outcomes are also outlined to emphasize the integration of the
identified health outcomes of both 1,1- and 1,2-dichloroethane.
5.2.3.1.1 Renal Toxicity
Humans
EPA did not identify epidemiological studies that evaluated any potential renal hazards for 1,1- or 1,2-
dichloroethane.
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Laboratory Animals
A review of high and medium quality acute, subchronic, and chronic studies identified studies that
indicated renal effects following 1,1-dichloroethane exposure and studies were also identified that
demonstrate renal effects following 1,2-dichloroethane exposure.
Oral
In the short-term Muralidhara et al. (2001) 10-day single oral gavage study, male Sprague-Dawley rats,
administered 1,1-dichlorethane at a dose of 0, 1,000, 2,000, 4,000 or 8,000 mg/kg-bw/day resulted in a
significantly reduced absolute kidney weights and nonprotein sulfhydryl (NPSH) content in the 2,000
and 4,000 mg/kg-bw/day dose groups on day 10. All rats at the 8,000 mg/kg-bw/day dose died within 24
hours of dosing.
In the subchronic study by Muralidhara et al. (2001). male Sprague-Dawley rats, administered 1,1-
dichlorethane via oral gavage for 5 days/week for 13 weeks at a dose of 0, 500, 1,000, 2,000, or 4,000
mg/kg-bw/day indicated elevated acid phosphatase (ACP) in the 2,000 and 4,000 mg/kg bw groups at 6
weeks, and ACP and N-acetylglucosaminidase (NAG) were elevated in the 1,000, 2,000, and 4,000
mg/kg-bw/day groups at 8 weeks. In addition, histopathological effects on the kidney showed
nephropathy, however, the incidences were high in the control group (7/10 animals). Animals also died
in the highest two groups of 2,000 and 4,000 mg/kg-bw/day (1/15 and 5/15, respectively) that resulted in
ceasing continuation of exposure at the highest dose.
B6C3F1 mice in the Storer et al. (1984) study that were administered a single oral gavage dose at 0, 100,
200, 300, 400, 500, 600 mg/kg-bw resulted in kidney weights increased at 300 mg/kg-bw doses and
greater. In support, L-iditol dehydrogenase (IDH, 9-fold increase) and blood urea nitrogen (BUN)
indicated a trend increase at 200 mg/kg-bw and greater doses but was not statistically significant due to
the low number of animals tested (N=5).
In the Morel et al. (1999) acute single exposure oral gavage study in male Swiss OF1 mice treated with
0, 1,000, or 1,500 mg/kg-bw of 1,2-dichloroethane, a significant increase in damaged renal tubules
(7.66% vs. 0.32% in controls) was seen only seen in the highest dose group with the lowest dose already
above the limit dose.
In the subchronic 90 day (7 day/week for 13 weeks) oral gavage study by Daniel et al. (1994). male and
female Sprague-Dawley rats treated with 0, 37.5, 75, or 150 mg/kg-bw/day of 1,2-dichloroethane
resulted in increased relative kidney weights in both males and females (18 and 15 percent higher than
controls, respectively) at the 75 and 150 mg/kg-bw/day.
The subchronic 90-day oral gavage study in Wistar rats by van Esch et al. (1977) dosed at 0, 10, 30 or
90 mg/kg-bw/day resulted in a significantly increase in relative kidney weight of 17 and 16 percent
higher than controls in males and females in the 90 mg/kg-bw/day, respectively.
In the subchronic study by NTP (1991). oral gavage of 1,2-dichloroethane at the dosages of 0, 30, 60,
120, 240 or 480 mg/kg-bw/day for 13 weeks in male F344 rats, resulted in significant increases in
absolute kidney weights at 30, 60, and 120 mg/kg/day ( 9, 21 and 25 percent, respectively) and
significant increases in relative kidney weights at 60 and 120 mg/kg-bw/day doses (15 and 26 percent,
respectively). Female F344 rats dosed at 0, 18, 37, 75, 150, or 300 mg/kg/day at 5 days/week via oral
gavage for 13 weeks caused significant increases in absolute kidney weights (12 and 23 percent) and
relative kidney weights (10 and 21 percent) at 75 and 150 mg/kg-bw/day, respectively.
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Inhalation
In the Hofmann et al. (1971a) 1,1-dichloroethane inhalation study, there was kidney damage in cats
exposed to 1000 ppm (4047 mg/m3) 1,1-dichloroethane for 10 weeks (6 hours/day), as indicated in
histopathology analysis but limited information regarding these effects were provided in the report.
Storer et al. (1984) identified increased serum BUN (85%) and relative kidney weight (12%) in B6C3F1
male mice as compared to controls after a 4 hour exposure to 1,2-dichloroethnae vapor of 499 ppm
(2020 mg/m3). Increased mortality at concentrations greater than 499 ppm precluded a more thorough
evaluation of these effects in this study and subsequent dose -response analysis.
Mechanistic
EPA did not identify mechanistic studies that evaluated any potential renal hazards for 1,1- or 1,2-
dichloroethane.
Evidence Integration Summary
There were no human epidemiological nor mechanistic studies available for either 1,1- or 1,2-
dichlorethane and therefore, there is indeterminate human evidence and mechanistic support to assess
whether 1,1-dichloroethane or 1,2-dichloroethane may cause renal changes in humans.
The evidence in animals is indeterminate based on studies on 1,1-dichloroethane on the magnitude and
severity of histological changes in the kidney and clinical signs of renal toxicity. Available toxicological
studies showed changes in kidney weight, clinical chemistry, urinary excretion, and/or kidney histology,
however, many of the studies that observed effects had limitations, and kidney effects were not seen
consistently across studies using different species, exposure routes, or study durations. In contrast,
evidence in animal studies for 1,2-dichloroethane is moderate based on several high- and medium-
quality studies that found associations between 1,2-dichloroethane exposure and increased kidney
weights, blood urea nitrogen (BUN), and/or renal tubular histopathology in rats (both sexes) and mice
following inhalation, oral, dermal, and intraperitoneal injection exposures.
Overall, EPA concluded that while evidence is inadequate to assess whether 1,1-dichloroethane
exposure may cause renal toxicity under relevant exposure circumstances, evidence indicates that 1,2-
dichloroethane likely causes renal effects under relevant exposure circumstances.
5.2.3.1.2 Immunological/Hematological
Humans
EPA did not identify epidemiological studies that evaluated any potential immunological/hematological
hazards for 1,1- or 1,2-dichloroethane. However, an in vitro study utilizing human Jurkat immune T cells
indicated cytotoxicity by the analog 1,2-dichloroethane and other similar chlorinated solvents such as
trichloroethylene, perchlorethylene and dichloromethane (McDermott and Heffron. 2013). Human T cell
death at 5 and 10 percent responses occurred at concentrations of 157 and 379 micromolar, respectively.
Importantly, these 1,2-dichloroethane cytotoxic concentrations are similar to milk levels in female
workers (i.e., 283 micromolar) and blood levels in rats {i.e., 1.36 mM), both via dermal exposures
(ATSDR. 2022; McDermott and Heffron. 2013). It should be noted that trichloroethylene was regulated
in its OPPT risk evaluation also based on immunosuppression, validating the results in this in vitro study
for a similar chlorinated solvent. This data supports that immunotoxicity by 1,2-dichloroethane is a
likely hazard to humans at relevant exposure conditions.
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Laboratory Animals
A review of high and medium quality acute, subchronic, and chronic studies identified studies that
indicated immunological/hematological effects following 1,1-dichloroethane exposure and studies were
also identified that demonstrate immunological/hematological effects following 1,2-dichloroethane
exposure.
Oral
Only one study by Zabrodskii et al. (2004) was identified that involved random-bred male and female
albino rats being administered inducers of the monooxygenase system (phenobarbital or benzenal) three
days prior to a single gavage dose of dichloroethane at 930 mg/kg-bw. The effects included significant
decreases in T-cell dependent (1.71-fold) and T-cell independent (1.54-fold) humoral responses 5 days
after exposure as measured by the number of antibody-producing cells in the spleen, natural cytotoxicity
(1.91-fold) evaluated 48 hours after the exposure, antibody-dependent cell cytotoxicity (1.64-fold) 5
days after immunization of the rats with 108 sheep erythrocytes and delayed hypersensitivity reactions
(1.63-fold) that was evaluated 24 hours post-exposure as compared to control. However, this study was
identified as Uninformative as the chemical identity was only identified as dichloroethane, not as either
isomer. However, in perspective since 1,2-dichloroethane data is being utilized for read-across to 1,1-
dichloroethane the study is still relevant for hazard identification.
Munson et al. (1982). a study in male CD-I mice administered 1,2-dichloroethane by oral gavage for 14
days at doses of 0, 4.9, 49 mg/kg-bw/day resulted in decreased antibody-forming cells with
immunosuppression at adverse 25 and 40 percent levels at the 4.9 and 49 mg/kg-bw/day dose groups,
respectively. Suppression of cell-mediated immune responses were also indicated at both dosages. A
decrease in leukocytes at approximately 30 percent was reported in the highest dosage group. No effects
were observed regarding the organ weights of the liver, spleen, lungs, thymus, kidney,
or brain. Additionally, hepatic clinical chemistry also remained unchanged. It is important to note that
the 2022 1,2-dichloroethane ATSDR document concluded that the immune system was the most
sensitive target, but it also considered this 14-day study in the acute duration category so it was not
utilized for the sub-chronic or chronic PODs. Human immune T cell in vitro data supports that
immunotoxicity by 1,2-dichoroethane is likely to humans at relevant exposure levels, this McDermott
study was not cited in the ATSDR document.
Inhalation
In the study by Sherwood et al. (1987). female CD-I mice exposed to 1,2 dichloroethane for 3 hours at
5.4 ppm (22 mg/m3) resulted in mortality following streptococcal challenge but it needs to be noted that
the inoculation with the bacteria was unlikely representative of a human equivalent immunological
challenge. Male SD rats in the same study did not exhibit any effects to the streptococcal immunological
challenge after exposures up to 200 ppm (801 mg/m3). In addition, in Sherwood et al. (1987). identified
no effects in female CD-I mice or male SD rats due to streptococcal challenge after 1,2-dichloroethane
inhalation exposure for 5 or 12 days in the mice or rats, respectively.
Other similar chlorinated solvents also indicated immunosuppression such as 1,1,2-trichloroethane at 44
mg/kg/day in CD-I mice (Aualiitia and Pickering. 1987) and trichloroethylene at 18 mg/kg/day in CD-I
mice (Sanders et al.. 1982).
Mechanistic
EPA did not identify mechanistic studies that evaluated any potential immunological/hematological
hazards for 1,1-dichloroethane. However, its analog 1,2-dichloroethane was cytotoxic to human Jurkat T
lymphocyte cells in vitro. Human T cell death at 5 and 10 percent levels occurred at concentrations of
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157 and 379 micromolar, respectively, or similar to milk levels in female workers and blood levels in
rats both via dermal exposures (ATSDR. 2022; McDermott and Heffron. 2013). Other similar
chlorinated solvents such as trichloroethylene, perchlorethylene and dichloromethane also caused human
T cell death. This study also reported increases in reactive oxygen species and increased cellular calcium
levels by 1,2-dichloroethane and other similar chlorinated solvents such as trichloroethylene,
perchlorethylene and dichloromethane. The human T cell death caused by 1,2-dichloroethane and the
other similar chlorinated solvents trichloroethylene, perchlorethylene and dichloromethane was inhibited
by the antioxidant N-acetylcysteine. Additionally, 1,2-dichloroethane possessing
immunological/hematological effects is demonstrated in an in vitro study that identified reduced
phagocytic activity of mouse peritoneal macrophages to 76 percent of control levels at a concentration
of 200 mM (Utsumi et al.. 1992). Immunosuppression is a recognized characteristic of carcinogens and
tumors were reported for 1,2-dichloroethane in various studies.
Evidence Integration Summary
There were no human epidemiological nor mechanistic studies available for 1,1-dichl or ethane and
therefore, there is indeterminate human evidence and mechanistic support to assess whether 1,1-
dichloroethane may cause immunological/hematological changes in humans. Additionally, there were no
human epidemiological studies available for 1,2-dichlorethane and therefore, there is indeterminate
human evidence to assess whether 1,2-dichloroethane may cause immunological/hematological changes
in humans. Limited mechanistic evidence based on in vitro data that showed reductions in macrophage
phagocytic activity and erythrocyte GST activity after exposure to 1,2-dichloroethane was also
considered to be indeterminate.
The evidence in animals is indeterminate based on only one available study on 1,1-dichloroethane on the
magnitude and severity of immunological/hematological effects in rats. Available toxicological studies
based on high-quality inhalation and gavage studies of immune function in mice indicated an association
between 1,2-dichloroethane exposure and immunosuppression was observed. A more limited inhalation
study in rats and a longer-term drinking water study in mice that was rated uninformative did not show
any effects. Evidence from other studies showed only small effects on hematology and no effects on
relevant organ weights or histopathology. Based on this information, evidence based on animal studies
for 1,2-dichloroethane, suggests the immunological/hematological effects as slight.
Overall, EPA concluded that evidence is inadequate to assess whether 1,1-dichloroethane exposure may
cause immunological/hematological toxicity under relevant exposure circumstances. 1,1-Dichloroethane
did cause immunosuppression in an acute study at 930 mg/kg, however due to the paucity of data for
1,1-dichloroethane longer term studies to indicate the progression of immunotoxicity to lower LOAEL
values were not available. However robust WOSE information indicates that its isomer 1,2-
dichloroethane likely causes immune system suppression under relevant exposure conditions to both
animals and humans. This conclusion is supported by multiple lines of evidence such as the cytotoxicity
to human immune T cells in vitro at relevant human tissue levels, the cell mediated immunosuppression
in mice at the low LOAEL value of 4.89 mg/kg/day, decreased leukocytes counts in mice and the fact of
analogy that other similar chlorinated solvents also cause immunosuppression in vivo, such as 1,1,2-
trichloroethane with a NOAEL at 3.9 mg/kg/day and the trichloroethylene LOAEL is 18 mg/kg/day
(regulated by OPPT on the immunosuppression endpoint). Human immune T cell cytotoxicity was also
caused by other similar chlorinated solvents in vitro, such as trichloroethylene, perchloroethylene and
dichloromethane. In support, the 1,2-dichloroethane ATSDR (2022) authoritative document concluded
that "the immune system was the most sensitive target for short-term exposure to 1,2-dichloroethane by
both the inhalation and oral routes in mice."
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5.2.3.1.3 Neurological/Behavioral
Humans
EPA did not identify any epidemiological studies that evaluated potential neurological hazards for 1,1-
dichloroethane. The clinical use of 1,1-dichloroethane as an anesthetic supports narcotic effects on the
human nervous system and this clinical use was discontinued due to cardiac arrythmias (Reid and
Muianga. 2012). Chlorinated aliphatic solvents are known to cause central nervous system depression,
and respiratory tract and dermal irritation in humans (ATSDR. 2015). Case reports of human exposure
to 1,2-dichloroethane by inhalation or ingestion indicated clinical signs of neurotoxicity (dizziness,
tremors, paralysis, coma) as well as histopathology changes in the brain at autopsy (ATSDR. 2022).
Workers exposed to 1,2-dichloroethane for extended periods were shown to develop cerebral edema and
toxic encephalopathy (ATSDR. 2022). A single study of Russian aircraft manufacturing workers noted
decreased visual-motor reaction and decreased upper extremity motor function, as well as increased
reaction making errors in workers exposed to 1,2-dichloroethane compared to those that were not,
however the results were only described qualitatively and no statistical analyses were conducted, and the
study was determined to be uninformative by systematic review (Kozik. 1957).
Laboratory Animals
A review of high and medium quality acute, subchronic, and chronic studies identified studies that
indicated neurological/behavioral effects following 1,1-dichloroethane exposure and studies were also
identified that demonstrate neurological/behavioral effects following 1,2-dichloroethane exposure.
Oral
In the short-term Muralidhara et al. (2001) 10-day oral gavage study, male Sprague-Dawley rats,
administered 1,1-dichlorethane at a dose of 0, 1,000, 2,000, 4,000 or 8,000 mg/kg-bw/day resulted in
rats exhibiting excitations that subsequently progressed into motor impairment and CNS depression at
dosages exceeding 2,000 mg/kg-bw/day.
In the subchronic study by Muralidhara et al. (2001). male Sprague-Dawley rats, administered 1,1-
dichlorethane via oral gavage for 5 days/week for 13 weeks at a dose of 0, 500, 1,000, 2,000, or 4,000
mg/kg-bw/day resulted in rats exhibiting excitations that subsequently progressed into motor impairment
and CNS depression at dosages greater or equal than 2,000 mg/kg-bw/day. The methodology of how
CNS depression was not defined, and results were only described qualitatively. Histopathology on the
brain was also not observed.
Inhalation
Male SD rats exposed to 1.5 hours of 1,2-dicloroethane in Zhou et al. (2016) were shown to develop
histological changes in the brain as denoted by edema at 975.9 ppm (3,950 mg/m3).
Neurotoxicity and histological changes in the brains of SD rats exposed to 1,2-dichloroethane for 12
hours was seen in a study by Qin-li et al. (2010) at a LOAEL of 5,000 mg/m3 as indicated by abnormal
behavior and edema, however, details regarding the histological severity of edema were not provided.
In the acute Dow Chemical (2006b) inhalation study, histological changes and injury were identified in
the olfactory mucosa of F344/DUCRL rats exposure for 4 or 8 hours to 1,2-dichlorethane vapor at 100
and 200 ppm, respectively. The effect on the olfactory mucosa is also considered neurological, as this
tissue is neuroepithelial in nature.
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Mechanistic
EPA did not identify mechanistic studies that evaluated any potential neurological hazards for 1,1-
dichloroethane. EPA identified mechanistic studies that suggest 1,2-dichloroethane can result in brain
edema due to a downregulation of tight junction proteins (occluding and ZO-1) and mRNA, increase of
free calcium, decreased ATP content, and decrease ATPase activity in the brains of mice after an
exposure of to 296 ppm (1200 mg/m3) for 3.5 hours/day for 3 days (Wang et al.. 2018a; Wang et al..
2014).
Evidence Integration Summary
There were no human epidemiological nor mechanistic studies available for 1,1-dichl or ethane and
therefore, there is indeterminate human evidence and mechanistic support to assess whether 1,1-
dichloroethane may cause neurological/behavioral changes in humans.
Case reports document clinical signs of neurotoxicity and brain histopathology changes in humans
exposed to 1,2-dichloroethane by inhalation or ingestion as well as the ability of 1,2-dichloroethane to
downregulate tight junction proteins and energy production while also upregulating aquaporin and
matrix metalloproteinase in the brains of exposed mice. Based on these human epidemiological and
mechanistic data available for 1,2-dichlorethane, the evidence is slight for an association between 1,2-
dichloroethane and adverse neurological effects.
Animal studies identified the capability of 1,1-dichloroethane to induce central nervous system
depression in rats exposed by gavage, and this finding is consistent with its past use as a human
anesthetic. Several high- and medium-quality studies using rats exposed to 1,2-dichloroethane by
inhalation or gavage or mice exposed by intraperitoneal injection showed the occurrence of
neurobehavioral changes, clinical signs of neurotoxicity, and/or changes in brain histopathology.
Therefore, EPA determined that the animal evidence for adverse neurological/behavioral effects based
on these data are moderate for the association between both 1,1- and 1,2-dichloroethane and adverse
neurological/behavioral effects.
Overall, EPA concluded that while evidence suggests, but is not sufficient to conclude, that
1,1-dichloroethane exposure causes neurological effects under relevant exposure circumstances. The
evidence indicates that 1,2-dichloroethane likely causes neurological/ behavioral effects under relevant
exposure circumstances.
5.2.3.1.4 Reproductive/Developmental
Humans
EPA did not locate any human epidemiology studies for 1,1-dichloroethane that could be utilized for a
non-cancer dose response analysis and the overall non-cancer 1,1-dichloroethane epidemiology
literature is considered indeterminate for non-cancer health effects. A case-control study relating birth
defects to exposure to various chlorinated solvents as estimated by maternal residential proximity to
industrial point sources of emissions found that exposure risk values greater than zero were associated
with increased odds of spina bifida and septal heart defects (Brender et al.. 2014). This study also found
that low exposure risk for 1,1-dichloroethane was associated with increased odds of septal heart defects,
but medium and high exposure risk for 1,1-dichloroethane were not (Brender et al.. 2014). This was the
only acceptable study located in the literature that evaluated the relationship between 1,1-dichloroethane
and any non-cancer health outcome in humans.
Evidence from the 1,2-dichloroethane literature is similarly indeterminate. The aforementioned Brender
et al. (2014) study found associations between any exposure to 1,2-dichloroethane and neural tube
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defects and spina bifida, however as previously mentioned exposure was estimated based on maternal
residential proximity to industrial point sources of emissions rather than using a measured level of
exposure. Additionally, two studies of 1,2-dichloroethane presence in drinking water and congenital
anomalies found a relationship between 1,2-dichloroethane detection and major cardiac defects in
newborns, but the same relationship was not significant when comparing odds of major cardiac defects
between newborns with 1,2-dichloroethane water concentrations above 1 ppb versus equal to or below 1
ppb (Bove. 1996; Bove et al.. 1995).
Laboratory Animals
A review of high and medium quality acute, subchronic, and chronic studies identified studies that
indicated reproductive/developmental effects following 1,1-dichloroethane exposure and studies were
also identified that demonstrate reproductive/developmental effects following 1,2-dichloroethane
exposure.
Oral
In the short-term Muralidhara et al. (2001) 10-day oral gavage study, male Sprague-Dawley rats,
administered 1,1-dichlorethane at a dose of 0, 1.000, 2,000, 4,000 or 8,000 mg/kg-bw/day did not
develop chemically associated lesions as examined by H&E-stained sections of the testis, or epididymis
of rats sacrificed at 1, 5, or 10 days.
Sprague-Dawley dams that were administered 1,2-dichloroethane by gavage at doses of 0, 1.2, 1.6, 2.0,
and 2.4 mmol/kg (corresponding to 0, 120, 160, 200, and 240 mg/kg-bw/day in the Pavan et al. (1995)
study during gestation day (GD) 6 to GD 21 resulted in increases in non-implantations and resorptions.
The increases in non-implants and resorptions are difficult to interpret given the significant maternal
toxicity (decreases in maternal body weight gain) observed at corresponding doses (30 and 49% at 200
and 240 mg/kg/day, respectively), and the fact that there was no effect on the number of live fetuses per
litter despite the changes in non-surviving implants/litter and resorption sites/litter.
Inhalation
The inhalation study by Schwetz et al. (1974) that exposed nonpregnant female rats for 7 hours/day for
10 days or pregnant rats on GD 6 to 15 to 1,1-dichloroethane identified increased incidence of delayed
ossification of sternabrae at 6,000 ppm (24,300 mg/m3).
Rao et al. (1980). a reproductive/developmental study in pregnant SD rats exposed to 1,2-dichloroethnae
vapor at 0, 100, or 300 ppm during GD 6 to 15 identified a significant decrease in bilobed thoracic
centra incidences, however, due to increased incidence in maternal mortality a dose-response evaluation
could not be performed on this effect. Additionally, a multi-generational evaluation by Rao et al. (1980)
also identified decreased boody weight of FIB male weanlings as a result of exposure to 150 ppm (613
mg/m3) for 6 hours/day for 7 weeks in atero.
Exposure to pregnant SD rats to 1,2-dichlorethane in Pavan et al. (1995) indicated a significant decrease
in pregnancy rate at 250 ppm (1000 mg/m3), however, this effect was not seen at the highest
concentration of 300 ppm (1200 mg/m3).
Zhang et al. (2017). a reproductive study, that evaluated the effects of 1,2-dichloroethane on male Swiss
mice due to a 4 week exposure resulted in changes is sperm morphology and concentration along with
decreased seminiferous tubules and the height of germinal epithelium at 25 ppm (102 mg/m3).
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Mechanistic
EPA did not identify mechanistic studies that evaluated any potential reproductive/developmental
hazards for 1,1-dichloroethane. Male mice treated with 86 ppm or 173 ppm (350 or 700 mg/m3,
respectively) for 4 weeks resulted in an inhibition of the cyclic adenosine monophosphate (cAMP)-
response element binding (CREB) protein and the cAMP-response element modulator (CREM),
subsequently inducing apoptosis, and resulting in reproductive toxicity in male mice as indicated by a
decrease in sperm concentration of greater than 25 percent (4.65 ± 0.52 vs. 3.30 ± 0.57 M/g), in the
control vs. 700 mg/m3 treated animals, respectively (Zhang et al.. 2017).
Evidence Integration Summary
Due to limited and inconclusive epidemiological as well as a lack of mechanistic studies, there is
indeterminate human evidence and mechanistic support to assess whether 1,1-dichloroethane may cause
reproductive/developmental changes in humans. Additionally, the available animal toxicological studies
were also limited and inconclusive and thus provided evidence that was identified as indeterminate for
reproductive/developmental effects due to 1,1-dichloroethane.
In high- and medium-quality studies, associations were observed between 1,2-dichloroethane exposure
and various birth defects (neural tube defects including spina bifida and heart defects of different types).
However, the effect sizes were small with associations that were weak and, in some cases, based on very
low group sizes. Results of the two available epidemiological studies were also not consistent (neural
tube defects/spina bifida in one study but not the other; different types of cardiac defects in the two
studies), and both studies were limited in various ways (e.g., incomplete data on neural tube defects,
potential exposure misclassification, questionable temporality, co-exposures to other chemicals that
were also associated with the same defects). Based on these evaluations, the evidence of
reproductive/developmental effects due to 1,2-dichloroethnae was considered indeterminate for these
effects.
In high-quality studies, mice exposed to 1,2-dichloroethane by inhalation or intraperitoneal injection, but
not by drinking water, exhibited effects on testicular pathology and sperm parameters. Most of the data
in rats indicated no effect on the testes (or other reproductive organs); however, sperm parameters were
not evaluated in rats. Thus, the evidence for effects on the male reproductive tract was considered
moderate. Evidence was considered moderate based on inhalation studies in rats, oral studies in rats and
mice, and a dermal study in mice that all indicated no effects of 1,2-dichloroethane on female
reproductive organ weights or histopathology. With regard to developmental effects, a high-quality
study on 1,2-dichlorethane indicated sterility in male mice exposed by intraperitoneal injection. In
addition, evidence for effects on weanling pup body weight after 1,2-dchloroethane inhalation exposure
was considered weak and inconsistent. Thus, evidence was considered slight for developmental effects
due to 1,2-dichloroethane.
Mechanistic evidence for reproductive/developmental effects based on inhibition of CREM/CREB
signaling and the occurrence of apoptosis in testes of male mice exposed to 1,2-dichloroethane in vivo to
support observed effects on testes pathology, sperm morphology, and fertility in this species was
considered moderate.
Overall, EPA concluded that the evidence is inadequate to assess whether 1,1-dichloroethane exposure
may cause reproductive/ developmental toxicity under relevant exposure circumstances; the evidence
indicates that 1,2-dichloroethane likely causes effects on male reproductive structure and/or function
under relevant exposure conditions. The nature of the effect chosen for calculating risks— changes in
sperm morphology and concentration identified by Zhang et al. (2017) - is considered adverse, and the
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fertility of human males is known to be sensitive to changes in sperm numbers and quality (U.S. EPA.
1996). The evidence is inadequate to determine whether 1,2-dichloroethane may cause effects on the
developing organism and there is no evidence that 1,2-dichloroethane causes effects on female
reproductive structure and/or function.
5.2.3.1.5 Hepatic
Humans
EPA did not identify epidemiological studies that evaluated any potential hepatic hazards for 1,1-
dichloroethane. A single study of liver damage markers in the blood of vinyl chloride workers showed
abnormal levels of aspartate aminotransferase (AST) and alanine transaminase (ALT) in the moderate
1,2-dichloroethane exposure intensity group compared with the low 1,2-dichloroethane exposure
intensity group; however, all participants were also exposed to low levels of vinyl chloride monomer,
which may also affect liver enzyme levels (Cheng et al.. 1999).
Laboratory Animals
A review of high and medium quality acute, subchronic, and chronic studies identified studies that
indicated hepatic effects following 1,1-dichloroethane exposure and studies were also identified that
demonstrate hepatic effects following 1,2-dichloroethane exposure.
Oral
In the short-term Muralidhara et al. (2001) 10 day single oral gavage study, male Sprague-Dawley rats,
administered 1,1-dichlorethane at a dose of 0, 1000, 2000, 4000 or 8000 mg/kg-bw/day resulted in liver
weight was significantly reduced in all dose groups on days 5 and 10.
In the subchronic study by Muralidhara et al. (2001). male Sprague-Dawley rats, administered 1,1-
dichlorethane via oral gavage for 5 days/week for 13 weeks at a dose of 0, 500, 1000, 2000, or 4000
mg/kg-bw/day did not show any histopathological or organ weight effects on the liver. Additionally, no
elevation in serum sorbitol dehydrogenase (SDH) or ornithine-carbamyl transferase (OCT) were
observed at any dose after 4, 8 or 12 weeks of exposure.
In Cottalasso et al. (2002). a single gavage of 628 mg/kg-bw of 1,2-dichloroethane in female Sprague-
Dawley rats after 16 hours of fasting resulted in increased alanine aminotransferase (ALT), aspartate
aminotransferase (AST), and lactate dehydrogenase at 45, 44 and 67 percent as compared to controls,
respectively. Histological examination also identified moderate steatosis.
In the 10-day oral gavage study by Daniel et al. (1994). male and female Sprague-Dawley rats
administered 0, 10, 30, 100, or 300 mg/kg-bw/day of 1,2-dichloroethane exhibited significantly
increased relative liver weights (14% relative to controls) and serum cholesterol levels in male rats alone
at 100 mg/kg-bw/day.
The short-term 10-day oral gavage study in Wistar rats by van Esch et al. (1977) dosed at 0, 3, 10, 30,
100, or 300 mg/kg-bw/day 1,2-dichloroethane resulted in death of all animals in the 300 mg/kg-bw/day
that upon subsequent histological evaluation showed extensive liver vacuolization and lipid droplets.
In the subchronic 90 day (7 day/week for 13 weeks) oral gavage study by Daniel et al. (1994). male and
female Sprague-Dawley rats treated with 0, 37.5, 75, or 150 mg/kg-bw/day of 1,2-dichloroethane
resulted in a 20 percent increase in relative liver weights in only male rats at 75 mg/kg-bw/day.
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The subchronic 90-day oral gavage study in male Wistar rats by van Esch et al. (1977) dosed at 0, 10,
30, 90 mg/kg-bw/day resulted in a significantly increase in relative liver weight of 13 percent higher
than controls in females at the highest dose. However, this change was not accompanied by any changes
in serum enzymes or liver histopathology.
Inhalation
An inhalation study that exposed nonpregnant female rats for 7 hours/day for 10 days or pregnant rats on
GD 6 to 15 to 1,1-dichloroethane evaluated serum ALT and AST, liver weights, and gross liver
pathology (Schwetz et al.. 1974). This study identified relative increase in liver weight in the
nonpregnant females at 6000 ppm (24,300 mg/m3) but did not identify any effects on liver parameters in
the pregnant rats as compared to the pooled controls.
Exposure to 1,2-dichloroethane for 4 hours at 499 ppm (2020 mg/m3) via inhalation in Storer et al.
(1984) identified increased serum ALT (2-fold) and SDH (11-fold) in B6C3F1 male mice as compared to
controls.
Absolute and relative liver weights in male Swiss mice at >10% as compared to controls was indicated
in a 6 hour/day for 28 days study by Zeng et al. (2018) at a concentration of 89.83 ppm (364 mg/m3).
IRFMN (1978). in a chronic 12 month study in both male and female SD rats, resulted in an increase of
ALT and LDH in both sexes when exposure to 50 ppm (200 mg/m3).
Mechanistic
EPA did not identify mechanistic studies that evaluated any potential hepatic hazards for 1,1-
dichloroethane. In the study by Storer et al. (1984). B6C3F1 mice were administered a single dose of
1,2-dichloroetane at 100, 200, 300, or 400 mg/kg via oral gavage in corn oil and euthanized 4 hours
later. It was identified that a statistically significant increase in DNA damage in hepatic nuclei was
present in all dose groups, as characterized by single-strand breaks, when compared to controls.
Evidence Integration Summary
There were no human epidemiological nor mechanistic studies available for either 1,1-dichlorethane and
therefore, there is indeterminate human evidence and mechanistic support to assess whether 1,1-
dichloroethane may cause hepatic changes in humans. In additon, there is indeterminate human evidence
as the only human epidemiological study was considered inadequate due to confounding associated with
co-exposure to vinyl chloride. No adequate mechanistic studies were identified as hepatic enzyme
induction was demonstrated by intraperitoneal injection in mice. Limited in vitro data indicate that 1,2-
dichloroethane may increase oxidative stress or impair glucose and/or lipid metabolism in mice and in
rat hepatocytes and liver slices, however, this information suggests that overall mechanistic evidence for
hepatic effects is indeterminate.
Due to limitation in the availability of toxicological studies on 1,1-dichlorethane that showed changes in
liver weight and/or histology in the absence of relevant clinical chemistry findings, EPA determined that
the animal evidence for adverse effects on the liver are slight for the association between 1,1-
dichloroethane and adverse hepatic effects. Several high- and medium-quality studies in rats and mice
found associations between 1,2-dichloroethane exposure and increased liver weights, serum enzymes,
and/or histopathology changes following inhalation, oral, and intraperitoneal injection exposures. Based
on these studies, EPA determined that the animal evidence for adverse effects on the liver are moderate
for the association between 1,2-dichloroethane and adverse hepatic effects.
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Overall, EPA concluded that evidence suggests, but is not sufficient to conclude, that 1,1-dichloroethane
exposure or 1,2-dichlorethane cause hepatic toxicity under relevant exposure circumstances.
5.2.3.1.6 Nutritional/Metabolic
Humans
EPA did not identify epidemiological studies that evaluated any potential nutritional/metabolic hazards
for 1,1- or 1,2-dichloroethane.
Laboratory Animals
A review of high and medium quality acute, subchronic, and chronic studies identified studies that
indicated nutritional/metabolic effects following 1,1-dichloroethane exposure and studies were also
identified that demonstrate nutritional/metabolic effects following 1,2-dichloroethane exposure.
Oral
In the short-term Muralidhara et al. (2001)10 day oral gavage study, male Sprague-Dawley rats,
administered 1,1-dichlorethane at a dose of 0, 1,000, 2,000, 4,000 or 80,00 mg/kg-bw/day resulted in a
dose-dependent decreases in body weight at doses >1000 mg/kg-bw/day with rats in the 2,000 and 4,000
mg/kg-bw/day dosage groups not gaining any weight during the 10 day exposure period. All rats in the
8000 mg/kg-bw/day exposure group died within 24 hours of dosing.
In the subchronic study by Muralidhara et al. (2001). male Sprague-Dawley rats, administered 1,1-
dichlorethane via oral gavage for 5 days/week for 13 weeks at a dose of 0, 500, 1,000, 2,000, or 4,000
mg/kg-bw/day resulted in the rats receiving 4,000 mg/kg-bw/day, the highest dose, experienced body
weight gain consistently lower than that of controls and the other treated groups. This effect was
accompanied by a progressive increase in the number of deaths, from the initial week of exposure until
week 11, when the seven surviving 4,000 mg/kg-bw/day treated rats were terminated. One death
occurred in the 2,000 mg/kg-bw/day group during the sixth week of 1,1-dichlorethane treatment with
body weight gain significantly lower than controls from the fourth week until the end of the 13-week
study. There were no fatalities in the 500 or 1,000 mg/kg-bw/day groups were observed and no
reductions in body weight gain were seen as compared to controls.
In the study by Pavan et al. (1995). pregnant SD rats exposed to 1,2-dichloroethane via oral gavage
exhibited a decrease in absolute maternal body weight during GD 6-21 relative to controls. The short-
term NTP (1978) preliminary dose-range finding study in male and female Osborne-Mendel rats
gavaged with 0, 40, 63, 100, 150 or 251 mg/kg-bw/day of 1,2-dichloroethane for 5 days/week for 6
weeks suggested body weight effects during exposure, however, due to the lack of quantitative data
provided in the study report, a thorough evaluation of the data could not be performed.
Inhalation
The inhalation study by Schwetz et al. (1974) that exposed nonpregnant female rats for 7 hours/day for
10 days or pregnant rats on GD 6 to 15 to 1,1-dichloroethane identified decreased maternal body weight
gains at 3800 ppm (15,372 mg/m3).
Mechanistic
EPA did not identify mechanistic studies that evaluated any potential nutritional/metabolic hazards for
1,1- or 1,2-dichloroethane.
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Evidence Integration Summary
There were no human epidemiological nor mechanistic studies available for either 1,1- or 1,2-
dichlorethane and therefore, there is indeterminate human evidence and mechanistic support to assess
whether 1,1-dichloroethane or 1,2-dichloroethane may cause nutritional/metabolic changes in humans.
An evaluation of 1,1-dichloroethane animal studies identified an induction of body weight decrements
in rats at high gavage exposures (>2,000 mg/kg-bw/day) and in one dog exposed by inhalation (1,067
ppm). No body weight effects were seen, however, in mice or in rats at lower exposure levels. Thus, the
evidence for nutritional/metabolic effects due to 1,1-dichloroethane is considered moderate.
The evidence is considered slight for animal studies for 1,2-dichlorethane based on decreased body
weight as reported in mice and guinea pigs exposed by inhalation and rats and mice exposed orally to
1,2-dichloroethane in high- and medium-quality studies. Several high- and medium-quality studies in a
few species via various routes of exposure also reported no effect on body weight, sometimes at lower
exposure levels and/or shorter exposure durations to 1,2-dichloroethane.
Overall, EPA concluded that evidence suggests, but is not sufficient to conclude, that
1.1-dichloroethane exposure causes body weight decrements under relevant exposure circumstances.
EPA also concluded that the evidence suggests, that 1,2-dichloroethane may cause nutritional/ metabolic
effects under relevant exposure conditions.
5.2.3.1.7 Respiratory
Humans
EPA did not identify epidemiological studies that evaluated any potential respiratory hazards for 1,1- or
1.2-dichloroethane.
Laboratory Animals
A review of high and medium quality acute, subchronic, and chronic studies did not identify studies that
indicated respiratory effects following 1,1-dichloroethane exposure and studies were identified that
demonstrate respiratory effects following 1,2-dichloroethane exposure.
Oral
In the study by Salovsky et al. (2002). a single oral dose of 136 mg/kg-bw 1,2-dichloroethane in male
Wistar rats resulted in increased total number of cells in the bronchioalveolar lavage fluid (BALF) of
male Wister rats at 30 days after dosing. Non-inflammatory histological changes such as cyanosis,
interstitial edema, vacuolar changes, desquamative changes, atelectasis and alveolar macrophage
proliferation were also seen in the lungs. Inflammatory histological such as macrophage proliferation
that was mixed with a small number of neutrophils and eosinophils) occurred in the peribronchial (mild
degree on day 5 and mild-moderate on days 15 and 30), interstitial (mild-moderate on days 5 and 30 and
moderate on day 15), and interbronchial (mild on day 1, mild-moderate on day 5) regions. These
histological data were only presented qualitatively.
Inhalation
In the acute Dow Chemical (2006b) inhalation study, histological changes and injury were identified in
the olfactory mucosa of F344/DUCRL rats exposed for 4 or 8 hours to 1,2-dichlorethane vapor at 100
and 200 ppm, respectively.
Mechanistic
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EPA did not identify mechanistic studies that evaluated any potential respiratory hazards for 1,1- or 1,2-
dichloroethane.
Evidence Integration Summary
There were no human epidemiological nor mechanistic studies available for 1,1-dichl or ethane and
therefore, there is indeterminate human evidence and mechanistic support to assess whether 1,1-
dichloroethane may cause respiratory tract changes in humans. Additionally, there were no human
epidemiological nor mechanistic studies identified for 1,2-dichlorethane and therefore, there is
indeterminate human evidence to assess whether 1,2-dichloroethane may cause respiratory tract changes
in humans.
Evidence based on animal studies was indeterminate as no studies were identified that indicated as
association between respiratory tract effects and 1,1-dichloroethane exposure.
In a high-quality study, an association between 1,2-dichloroethane inhalation exposure and nasal lesions
was observed in rats exposed to concentrations > 435 mg/m3 (>107.5 ppm). Although one medium-
quality study reported lung lesions in rats after a single gavage dose, high- and medium- quality studies
of longer duration and higher doses, as well as a high-quality study of acute inhalation exposure, did not
show effects of 1,2-dichloroethane on lower respiratory tract tissues of rats. Based on this, evidence
from animal studies was considered slight to moderate.
Overall, EPA concluded that the evidence is inadequate to assess whether 1,1-dichloroethane exposure
may cause respiratory tract toxicity under relevant exposure circumstances. EPA also concluded that the
evidence suggests, but is not sufficient to conclude, that 1,2-dichloroethane may cause lower respiratory
tract effects under relevant exposure conditions.
5.2.3.1.8 Mortality
Humans
EPA did not identify epidemiological studies that evaluated any potential mortality hazards for 1,1-
dichloroethane. EPA identified two limited retrospective cohort studies that found no increase in
mortality of workers from either petrochemical or herbicide manufacturing plants with presumed
exposure to 1,2-dichloroethane relative to the general U.S. population (BASF. 2005; Teta et al.. 1991).
Laboratory Animals
A review of high and medium quality acute, subchronic, and chronic studies identified studies that
indicated mortality following 1,1-dichloroethane exposure and studies were also identified that
demonstrate mortality following 1,2-dichloroethane exposure.
Oral
In the acute Muralidhara et al. (2001) single dose oral gavage study, male Sprague-Dawley rats were
administered a single dose of 0, 1,000, 2,000, 4,000, 8,000, 12,000, or 16,000 mg/kg bw and observed
for 2 weeks. Mortality was increased in a dose-dependent manner at concentrations >4000 mg/kg-bw.
In the short-term Muralidhara et al. (2001) 10-day oral gavage study, male Sprague-Dawley rats,
administered 1,1-dichlorethane at a dose of 0, 1,000, 2,000, 4,000 or 8,000 mg/kg-bw/day resulted in all
rats at the 8000 mg/kg-bw/day dose died within 24 hours of dosing.
In the subchronic study by Muralidhara et al. (2001). male Sprague-Dawley rats, administered 1,1-
dichlorethane via oral gavage for 5 days/week for 13 weeks at a dose of 0, 500, 1,000, 2,000, or 4,000
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mg/kg-bw/day resulted in 1/15 animals dying in the 2000 mg/kg bw dose group and 8/15 animals dying
in the 4,000 mg/kg bw dose group, which resulted in early termination of the highest dose group at 11
weeks.
The short-term 10 day oral gavage study in male Wistar rats by van Esch et al. (1977) dosed at 0, 3, 10,
30, 100, or 300 mg/kg-bw/day 1,2-dichloroethane resulted in death of all animals in the 300 mg/kg-
bw/day exposure group.
Inhalation
In the study by Francovitch et al. (1986). male CD-I mice treated with 1,2-dichloroethane for 4 hours
via inhalation resulted in a dose-related increase in mortality beginning at a concentration of 1000 ppm
(4050 mg/m3).
Male SD rats exposed via inhalation to 1,2-dichloroethane for 7 hours/day for 5 days/weeks resulted in
the occurrence of mortality starting at 304 ppm (1230 mg/m3) (Igwe et al.. 1986b).
Female SD rats exposed to 300 ppm (1210 mg/m3) 1,2-dichloroethane resulted in increased incidences
in mortality in dams when exposed for 10 days during GD 6 to 15 (Rao et al.. 1980). Additionally, in
Rao et al. (1980). New Zealand white rabbits treated with 1,2-dichloroethane for 7 hours/day during the
13 days of GD 6-18 also showed increased incidences of maternal mortality beginning at the exposure
concentration of 100 ppm (405 mg/m3).
In the study by Pavan et al. (1995). female SD rats treated with 1,2-dichlorethnae resulted in increased
incidence of maternal death at a LOAEL of 329 ppm (1330 mg/m3).
Mechanistic
EPA did not identify mechanistic studies that evaluated any potential mortality hazards for 1,1-or 1,2-
dichloroethane.
Evidence Integration Summary
There were no human epidemiological nor mechanistic studies available for 1,1-dichl or ethane and
therefore, there is indeterminate human evidence and mechanistic support to assess whether 1,1-
dichloroethane may cause mortality in humans. Limited epidemiological data show no increase in
mortality among workers with presumed exposure to 1,2-dichloroethane but are insufficient to draw any
broader conclusions. Therefore, there is indeterminate human evidence to assess whether 1,2-
dichloroethane may cause mortality in humans. There were no mechanistic studies available for 1,2-
dichlorethane and therefore, there is indeterminate mechanistic support to assess whether 1,2-
dichloroethane may cause mortality in humans.
The evidence in laboratory animals is robust based on an evaluation of studies that identified the
occurrence of mortalities in several species of animal exposed to 1,1-dichloroethane (>1000 mg/kg-bw)
via gavage in high quality studies. Evidence was also considered robust with regard to animal studies of
1,2-dichloroethane as treatment-related increases in the incidence of mortality were observed in several
animal species exposed to 1,2-dichloroethane via inhalation, oral, or dermal exposure for acute, short-
term/intermediate, or chronic durations in multiple studies.
Overall, EPA concluded that the evidence indicates that 1,1-dichloroethane exposure is likely to cause
death under relevant exposure circumstances and the evidence also indicates that 1,2-dichloroethane
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may cause death under relevant exposure circumstances and lethal levels have been identified in animal
studies.
5.2.4 Genotoxicity Hazard Identification and Evidence Integration
Genotoxicity hazard identification and evidence integration for 1,1-dichloroethane and the identified
analog 1,2-dichloroethane can be found in Appendix M.6 and M.7.2. Mutagenicity and genotoxicity data
for 1,1-dichloroethane are very limited and consist of a small number of genotoxicity experiments.
Available information shows that 1,1-dichloroethane induces DNA repair and binds to DNA in liver
cells, and that it induces chromosomal aberrations and micronuclei in bone marrow. Overall, the
available data provide limited support for the genotoxicity of 1,1-dichloroethane. For more details, see
TableApx M-40 and TableApx M-41 showing the results of in vitro and in vivo genotoxicity, and cell
transformation assays of 1,1-dichloroethane. However, the Milman et al. (1988) study with a High
systematic review rating demonstrated positive findings in the Ames assay with and without metabolic
activation.
Evidence from in vivo studies using multiple animal species and routes of exposure and in vitro studies
using multiple test systems indicates that 1,2-dichloroethane and/or its metabolites can induce mutations,
chromosomal aberrations, DNA damage, and DNA adducts in certain test systems. The available data
show that biotransformation of 1,2-dichloroethane to reactive metabolites via a major CYP450-mediated
oxidative pathway and a minor glutathione conjugation pathway contributes to the observed effects.
There are species-, sex-, tissue-, and dose-related differences in the interactions between 1,2-
dichloroethane and/or its metabolites and DNA.
For more details, see Appendix M.7.2 that provides a summary of the studies identified for in vitro and
in vivo genotoxicity, and cell transformation assays of 1,2-dichloroethane.
5.2.5 Cancer Hazard Identification, Mode of Action (MOA) Summary and Evidence
Integration
5.2.5.1 Cancer Hazard Identification and Evidence Integration
Appendix M.7 provides hazard identification and evidence integration for cancer for 1,1-dichloroethane
and the identified analog 1,2-dichloroethane.
5.2.5.1.1 Human Evidence
Human Evidence for 1,1-Dichloroethane
EPA did not locate any human epidemiology studies for 1,1-dichloroethane that could be utilized for a
cancer dose response analysis, and the overall 1,1-dichloroethane cancer epidemiology literature is
considered indeterminate. A study of ambient air concentration estimates of 1,1-dichloroethane and
breast cancer in women in the United States did not find significantly increased risk in the upper four
quintiles of exposure when compared individually to the first quintile, nor did the study find
significantly increased risk when the case definition of breast cancer only included those tumors that
were estrogen-receptor positive (Niehoff et al.. 2019). An additional study, Garcia et al. (2015)
investigated cancer risk based on female teachers in California's exposure to ambient air concentrations
of 1,1-dichloroethane broken into quintiles, and also generally did not provide adequate evidence of
carcinogenicity. The study did not find evidence of increased risk of breast cancer in the upper four
quintiles of exposure when compared individually to the first quintile in the full study population, but
did find limited increased risk for breast cancer when defining cases of breast cancer as those with
tumors that were either estrogen-receptor positive or progesterone-receptor positive (ER+/PR+), and
when defining cases of breast cancer as only those cases that were not currently using hormone therapy.
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However, this increased risk was only observed in quintiles three and four of exposure but not quintile
five for the ER+/PR+ case definition subset, and only observed in quintile three of exposure but not
quintiles four or five for the subset not currently using hormone therapy. Therefore, the evidence of 1,1-
dichloroethane carcinogenicity from the human study data is inadequate to draw definitive conclusions.
Human Evidence for 1,2-Dichloroethane
The 1,2-dichloroethane human epidemiology literature is similarly indeterminate as to whether 1,2-
dichloroethane exposure causes cancer due to a lack of published studies. A few studies showed
significant relationships between 1,2-dichloroethane and certain types of cancers, however these
relationships existed in very specific subgroups and were not consistent across exposure groups, which
limits our ability to draw conclusions from their results. For example, although Niehoff et al. (2019)
found a slight increase in the risk for ER+ invasive breast cancer in the fourth quintile of exposure as
compared with the first, this relationship was not significant in the fifth quintile of exposure as
compared with the first. This study also did not find a significant relationship between 1,2-
dichloroethane exposure and overall incidence of breast cancer, which was consistent with the only
other study investigating this relationship (Garcia et al.. 2015). Similarly, 1,2-dichloroethane exposure
was associated with a borderline significant increase in pancreatic cancer, but only among Black females
with low estimated exposure intensity (and not medium or high exposure intensity) (Kernan et al..
1999). Studies of brain cancer and kidney cancer showed no significant relationship with 1,2-
dichloroethane exposure (Dosemeci et al.. 1999; Austin and Schnatter. 1983).
Another study observed higher incidence of all-cause cancer than was expected in a cohort of workers
when compared to the general population, but the statistical significance of this result was not reported,
and the significance of all-cause cancer is not clear (BASF. 2005). This same study looked at many
specific cancer SIRs as well, but none were statistically significantly elevated except for prostate cancer,
which no other studies in the literature reported observing. Sobel et al. (1987) did not show a statistically
significant relationship between 1,2-dichloroethane exposure and soft-tissue sarcoma, but also had very
low statistical power with a sample size of seven 1,2-dichloroethane exposed participants. In general,
more studies would be needed to draw conclusions about the weight of evidence for the relationship
between 1,2-dichloroethane exposure and cancer from the epidemiologic literature, and none of the
existing studies measured exposure in a way that could be used to estimate a quantitative dose-response
relationship.
5.2.5.1.2 Animal Evidence
Animal Evidence for 1,1-Dichloroethane
The NCI (1978) cancer study on 1,1-dichloroethane in Osborne-Mendel rats provides limited evidence
of the carcinogenicity based on significant dose-related increases in the incidence of hemangiosarcomas
at various sites and mammary carcinomas in female rats, neither of which were observed in male rats.
However, the high incidence of pneumonia and deaths in all groups prevented the use of the data for
calculation of oral slope factors. Technical grade 1,1-dichloroethane in corn oil was administered by
gavage 5 days/week for 78 weeks to groups of rats/sex/dose. In male rats, survival at 111 weeks was low
at 30, 5, 4, and 8 percent (untreated control, the vehicle control, the low-dose, and the high- dose groups,
respectively). In female rat groups survival was also low at 40, 20, 16, and 18 percent (untreated control,
vehicle control, low- and high-dose groups, respectively). For hemangiosarcomas, the incidence in
female rats there was a statistically significant positive dose-related trend at 0/19 for matched vehicle
controls, 0/50 for the low-dose group, and 4/50 for the high-dose group. In female rats, the incidence of
mammary gland adenocarcinomas was 1/20 for the untreated group, 0/19 for the vehicle control group,
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1/50 for low-dose, and 5/50 for high-dose groups which showed a statistically significant dose-related
positive trend in rats surviving at least 52 weeks.
The NCI (1978) cancer study on 1,1-dichloroethane in B6C3F1 mice revealed a statistically significant
increase in benign uterine endometrial stromal polyps (4/46) in high-dose females, which were not
observed in any other group. However, pre-cancerous endometrial polyps are not a tissue growth
amenable to calculate cancer slope factors. In the study, groups of 50 B6C3F1 mice/sex/group were
administered technical grade 1,1-dichloroethane in corn oil by gavage 5 days/week for 70 weeks with 20
mice/sex/group in the control groups. In female mice, survival at termination was 80, 80, 80, and 50
percent for the untreated control group, the vehicle control group, the low-, and high-dose groups,
respectively. Survival in male mice was 35, 55, 62, and 32 percent in the untreated control group, the
vehicle control group, the low-, and high-dose groups, respectively. Liver carcinomas were reported in
only the vehicle control (1/19) and the low-dose groups (1/47) in female mice, no liver tumors were seen
in the untreated controls or in the high-dose group. The incidence of hepatocellular carcinomas in male
mice surviving at least 52 weeks was 1/19, 6/72, 8/48, and 8/32 in the matched vehicle control group
with a statistically significant trend test, a pooled vehicle control group consisting of mice from this
group and identical controls from other concurrent experiments, and the low-, and high- dose groups,
respectively. However, an increased incidence of hepatocellular carcinoma in male mice was not
statistically significant by either pair-wise or trend test at 2/17 in the untreated control group, 1/19 in the
vehicle control group, 8/49 in the low-dose, and 8/47 in the high-dose groups.
Because the cancer studies for 1,1-dichloroethane were not usable for the cancer assessment, the cancer
data for the identified analog 1,2-dichloroethane was identified and evaluated in Appendix M.7
There is no reliable cancer study via the inhalation route for 1,1-dichloroethane, so the cancer data for
1,2-dichloroethane was utilized for the inhalation route by the same read-across rationale as for the oral
route. The 1,2-dichloroethane inhalation cancer study produced some of the same tumors as observed in
the 1,2-dichloroethane oral cancer study. The highest estimated inhalation unit risk (IUR) is 7.1 x 10 6
(per |ig/m3) for combined mammary gland adenomas, fibroadenomas, and adenocarcinomas and
subcutaneous fibromas in female rats in the inhalation study by Nagano et al. (2006).
The NTP (1978) cancer study for 1,2-dichloroethane in Osborne-Mendel rats and B6C3F1 mice
provides evidence of the carcinogenicity treated by oral gavage for 78 weeks. Male rats had significantly
increased incidence of forestomach squamous-cell carcinomas and circulatory system
hemangiosarcomas. Significant increases in mammary adenocarcinoma incidence in female rats and
mice were observed. Alveolar/bronchiolar adenomas developed in mice of both sexes and females
developed endometrial stromal polyps and sarcomas, while males developed hepatocellular carcinomas.
The high incidence of death in the rat study caused it to have an uninformative rating in systematic
review so cancer slope factors were not modeled from this data set.
5.2.5.2 Mode of Action (MOA) Summary
The U.S. EPA (2005b) Guidelines for Carcinogen Risk Assessment defines mode of action as "a
sequence of key events and processes, starting with the interaction of an agent with a cell, proceeding
through operational and anatomical changes and resulting in cancer formation."
Appendix M.7 provides hazard identification and evidence integration for cancer for 1,1-dichloroethane
and the identified analog 1,2-dichloroethane. A limited number of in vitro and in vivo experiments on
1,1-dichloroethane genotoxicity are available. In vitro experiments include two bacterial mutagenicity
studies, a study of chromosomal aberrations in mammalian cells, studies of DNA repair in mouse and
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rat, hepatocytes studies of mammalian cell transformation, a test of chromosome malsegregation in
fungi, and a study of cell-free DNA binding. In vivo experiments include two DNA binding assays and a
bone marrow chromosomal aberration assay. The 1988 Milman study (1988) demonstrated positive
findings in the Ames assay with and without metabolic activation. The 2004 Zabrodskii study
demonstrated immunotoxicity as well (Zabrodskii et al.. 2004). Immunotoxicity was also demonstrated
for the identified analog 1,2-dichloroethane (Munson et al.. 1982). Both mutagenicity and
immunosuppression are accepted mechanisms for tumorigenesis.
Overall MO A Conclusions
Animal studies provide limited evidence that 1,1-dichloroethane may cause cancer in rodents. Rats and
mice exposed via gavage for 78 weeks exhibited a positive dose-related trend in the incidence of liver
tumors in male mice as well as mammary gland tumors and hemangiosarcomas in female rats. Poor
survival in both control and treated rats limits the validity of these results. The mouse cancer study
indicated that 1,1-dichloroethane produced pre-cancerous endometrial polyps. Cancer mode-of-action
data for 1,1-dichloroethane are limited and consist of a small number of genotoxicity experiments. The
Milman initiation-promotion study in rats indicated that 1,1-dichloroethane is a liver tumor promotor
when dosed at 700 mg/kg/day for 7 weeks and it was positive in the Ames assay with and without
metabolic activation (Milman et al.. 1988).
In summary, MOA information pertaining specifically to tissues susceptible to tumor formation after
exposure to 1,1-dichloroethane (e.g., liver, mammary, blood) is limited to studies showing that 1,1-
dichloroethane induces DNA repair and binds to DNA in liver cells, and that it induces chromosomal
aberrations and micronuclei in bone marrow. These data are not sufficient to determine the mode of
action for any tumor type associated with exposure to 1,1-dichloroethane. Alkyl halides such as 1,1-
dichloroethane are known to be DNA alkylating agents. Overall, the available data provide limited
support for the genotoxicity of 1,1-dichloroethane and with immunosuppression as an alternative mode
of carcinogenic action (Zabrodskii et al.. 2004).
5.2.5.3 Weight of Scientific Evidence
Weight of Scientific Evidence Conclusions
There are no human epidemiology studies that were amenable to dose-response analysis; however,
studies in rats and mice were available for 1,1-dichloroethane and its analog 1,2-dichloroethane.
Chronic cancer studies performed by NCI (1978) on 1,1-dichloroethane qualitatively resulted in the
same tumor types or pre-cancerous lesions as seen in the bioassays of the similar isomer 1,2-
dichloroethane (i.e., hepatocellular carcinomas, endometrial polyps, hemangiosarcomas, etc). However,
the rat studies for both chemicals were not utilized for cancer slope factor derivation due to the
excessive animal deaths and pre-cancerous endometrial polyps in mice for 1,1-dichloroethane are not
considered for cancer slope factor analysis.
The cancer classification of 1,1-dichloroethane is Group C, a possible human carcinogen, based on
similarities in chemical structure and target organs with the carcinogenic evidence for the identified
analog 1,2-dichloroethane with an oral slope factor of 6,2x ] 0 2 (mg/kg)/day from reliable dose response
data on hepatocellular carcinomas in male mice (U.S. EPA. 1987a). In context, the oral slope factor for
rats for 1,2-dichloroethane was a similar value of 9.1 x 10~2 (mg/kg)/day based on a common tumor of
hemangiosarcomas in rats. The Nagano et al. (2006) inhalation study for 1,2-dichloroethane provided a
reliable IUR value for risk evaluation. Considering that 1,2-dichloroethane is categorized to be a more
potent carcinogen than 1,1-dichloroethane by OncoLogic and that vicinal dihalides such as 1,2-
dichloroethane are more reactive than geminal dihalides such as 1,1-dichloroethane, utilizing the oral
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slope factor and IUR value from 1,2-dichloroethane for 1,1-dichloroethane risk evaluation is considered
to be human health protective.
5.2.6 Dose-Response Assessment
According to the Draft Systematic Review Protocol Supporting TSCA Risk Evaluations for Chemical
Substances (U.S. EPA. 202lb), hazard endpoints that receive evidence integration judgments of
demonstrates and likely are considered for dose-response analysis. Endpoints with suggestive evidence
can be considered on a case-by-case basis. Studies that received high or medium overall quality
determinations (or low-quality studies if no other data are available) with adequate quantitative
information and sufficient sensitivity can be compared.
The only hazard outcome category for which evidence demonstrates or is likely for 1,1-dichloroethane
to cause the effect in humans was for mortality. Therefore, hazard outcomes that received suggestive
judgements would then be the most robust evidence integration decisions in the case of 1,1-
dichloroethane. These evidence, however, were identified as suggestive but not conclusive or inadequate
regarding 1,1-dicholoethane. This limitation is evidence necessitated the utilization of an integration of
data from both 1,1-dichlorethane and the identified analog 1,2-dichlorethane to provide a more adequate
weight of evidence evaluation of comprehensive toxicological endpoints. As the health effect with the
most robust and sensitive POD among these suggestive outcomes were derived from 1,2-
dichloroethane, these data were used for risk characterization for each exposure scenario to be protective
of other adverse effects as described in the sections below.
Data for the dose-response assessment were selected from oral and inhalation toxicity studies in animals
specifically from 1,2-dichlorethane. Additionally, no usable PBPK models are available to extrapolate
between animal and human doses or between routes of exposure using 1,1- or 1,2-dichloroethane-
specific information. The PODs estimated based on effects in animals were converted to HEDs or CSFs
for the oral and dermal routes and HECs or IURs for the inhalation route. For this conversion, EPA used
guidance from U.S. EPA (2011b) to allometrically scale oral data between animals and humans.
Although the guidance is specific for the oral route, EPA used the same HEDs and CSFs for the dermal
route of exposure as the oral route because the extrapolation from oral to dermal routes is done using the
human oral doses, which do not need to be scaled across species. EPA accounts for dermal absorption in
the dermal exposure estimates, which can then be directly compared to the dermal HEDs.
For the inhalation route, EPA extrapolated the daily oral HEDs and CSFs to HECs and IURs using
human body weight and breathing rate relevant to a continuous exposure of an individual at rest. For
consistency, all HEDs and the CSF are expressed as daily doses and all HECs are based on daily,
continuous concentrations (24 hours per day) using a breathing rate for individuals at rest. Adjustments
to exposure durations, exposure frequencies, and breathing rates are made in the exposure estimates used
to calculate risks for individual exposure scenarios.
The endpoints of concern for 1,1-dichloroethane (based on read across from 1,2-dichloroethane includes
renal/kidney, nasal, neurological, immune system, reproductive effects and cancer. These data were used
for risk characterization for each exposure scenario to be protective of other adverse effects as described
in the sections below. The health effects identified as suggestive and evaluated for dose response were
renal, immunological, neurological, reproductive/developmental and hepatic.
5.2.6.1 Selection of Studies and Endpoints for Non-cancer Toxicity
The following subsections provide a description of the selection of critical non-cancer PODs for acute,
short-term/sub chronic and chronic exposures for 1,1-dichloroethane (using data for the analog 1,2-
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dichloroethane to fill data gaps). The sections provide a summary of the evaluation of the possible PODs
and the rationale for selection of the critical study (and POD) in a series of tables. The tables are
intended to streamline the text of this draft RE. Appendix M.2 provides the details of the non-cancer
dose response assessment for 1,1-dichloroethane and the analog 1,2-dichloroethane.
For the 1,1-dichloroethane risk evaluation, all data considered for PODs are obtained from animal
toxicity studies in rats or mice. EPA used dichotomous models to fit quantal data (e.g., incidences of
tumors) and continuous models to fit continuous data (e.g., body and organ weights), as recommended
by EPA's BMD Technical Guidance (U.S. EPA. 2012b). The BMDs/BMDLs (benchmark doses lower
95 percent confidence limit) are provided based on a daily exposure (i.e., seven days per week) for
easier comparison across all hazard endpoints and thus, doses were adjusted as needed before BMD
modeling. EPA modeled endpoints that had statistically significant pairwise comparisons between
individual doses and controls or significant dose-response trends. EPA also considered potential
biologically significant changes from controls where possible and/or that appeared to exhibit a dose-
response relationship upon visual inspection. Multiple health endpoints may have been modeled from
each study, depending on the relevance of the data to adverse health outcomes and to identify sensitive
health endpoints for each domain.
EPA relied on the BMD guidance and other information to choose benchmark responses (BMRs)
appropriate for each endpoint. Although the BMD Technical Guidance doesn't recommend default
BMRs, it describes how various BMD modeling results compare with NOAEL values, and the guidance
does recommend calculating 10 percent extra risk (ER) for quantal data and one standard deviation (SD)
for continuous data to compare modeling results across endpoints. EPA also modeled percent relative
deviations (RD) for certain continuous endpoints such as a BMR for decreased sperm concentration at
five percent, as this was considered biologically relevant. EPA's choice of BMRs for the 1,1-
dichloroethane health endpoints are described in more detail in the Draft Risk Evaluation for 1,1-
Dichloroethane - Supplemental Information File: Benchmark Dose Modeling (U.S. EPA. 2024c) that
present BMD modeling results for each health domain.
5.2.6.1.1 Uncertainty Factors Used for Non-cancer Endpoints
For the non-cancer health effects, EPA applied specific uncertainty factors (UF) to identify benchmark
MOEs for acute, short term, and chronic exposure durations for each exposure route among studies that
are used to estimate risks. U.S. EPA (1993a) and U.S. EPA (2002b) further discuss use of UFs in human
health hazard dose-response assessment. A total uncertainty factor for each POD is calculated by
multiplication of each of the five individual uncertainty factors. These uncertainty factors and their use
in risk characterization is further described in Section 5.3.1.1. In general, the higher the total uncertainty
factor applied to a POD to identify a benchmark MOE, the higher the uncertainty in the hazard value.
The following five individual UFs are considered for each of the PODs identified for use in risk
estimation. In the case of 1,1-dichloroethane, the database uncertainty factor was not used for any of the
PODs.
1. Interspecies Uncertainty Factor (UFa) of 3
EPA uses data from oral toxicity studies in animals to derive relevant HEDs, and (U.S. EPA.
2011a) recommends allometric scaling (using the 3/4 power of body weight) to account for
interspecies toxicokinetics differences for oral data. When applying allometric scaling, EPA
guidance recommends reducing the UFA from 10 to 3. The remaining uncertainty is associated
with interspecies differences in toxicodynamics. EPA also uses a UFa of 3 for the inhalation
HEC that accounts for dosimetric adjustment and dermal HED values as these values are derived
from the oral HED.
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2. Intraspecies Uncertainty Factor (UFh) of 10
EPA uses a default UFh of 10 to account for variation in sensitivity within human populations
due to limited information regarding the degree to which human variability may impact the
disposition of or response to, 1,2-dichloroethane.
3. LOAEL-to-NOAEL Uncertainty Factor (UFl) of 1 or 3
For the PODs chosen to calculate risks based on BMDL values, EPA used a UFl of 1. EPA
compared these values with other endpoints that were based on LOAELs, which used a UFl of 3
to account for the uncertainty inherent in extrapolating from the LOAEL to the NOAEL.
4. Subchronic-to-Chronic Duration Uncertainty Factor (UFs) of 10
EPA uses a default of 10 to account for extrapolating from data obtained in a study with less-
than-lifetime (subchronic) exposure to lifetime (chronic) exposure. A default value of 10 for this
UF is applied to the NOAEL/LOAEL or BMDL/BMCL from the subchronic study on the
assumption that effects from a given compound in a subchronic study occur at a 10-fold higher
concentration than in a corresponding (but absent) chronic study.
5. Database Uncertainty Factor (UFd) of 1
EPA considers the application of a database UF to account for the potential for deriving an
under-protective POD due to an incomplete characterization of the chemical's toxicity. As the
database for 1,2-dichlorethane possesses data that informs several toxicological endpoints, a UFd
of 1 was applied.
5.2.6.1.2 Non-cancer PODs for Acute Exposures
Oral
Table 5-42 shows the recommended acute oral study and POD (in consideration of both 1,1-
dichloroethane and 1,2-dichloroethane toxicity data) followed by co-critical endpoints (PODs within the
range of the recommended study) and other studies considered in support of the recommended POD.
1,1 -Dichloroethane
Only the single-dose experiment by (Muralidhara et al.. 2001) was considered as a potential study
adequate for evaluation of 1,1-dichloroethane toxicity and POD derivation following acute oral
exposures. A NOAEL of 1,000 mg/kg-bw and a LOAEL of 2,000 mg/kg-bw were identified based on
clinical signs of neurotoxicity characterized by the authors as "excitation followed by progressive motor
impairment and sedation." Although the acute-duration oral data are limited, the observation of central
nervous system or CNS effects is consistent with the past use of 1,1-dichloroethane as a human
anesthetic (ATSDR. 2015). This study, however, was not selected for the acute POD as this dose
approaches the LD50 for 1,1-dichloroethane and the effect of sedation/CNS depression not a sensitive
endpoint, thus necessitating the integration of studies within the 1,2-dichloroethane database to identify
a more sensitive endpoint.
The data available for 1,1-dichloroethane in Muralidhara et al. (2001) were near the LD50 value and
were not considered appropriate for use for POD identification. For 1,2-dichloroethane, a total of four
oral animal toxicity studies are available, with three studies having medium or high data quality for
dose-response analysis and identification of the short-term/sub-chronic oral duration POD.
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There were two acute-duration oral studies of 1,1-dichloroethane that were rated acceptable based on
systematic review evaluation (Table_Apx M-8): an acute lethality study in guinea pigs by (Dow
Chemical 1947) and a single-dose lethality study in rats bvCMuralidhara et al. 2001). The study by
(Dow Chemical 1947). however, reported no details on the animal strain, sex, age, or condition; number
of animals tested; method of administration; or duration of follow-up. These limitations in the study
preclude its use for POD derivation.
1,2-Dichloroethane
When looking within the 1,2-dichloroethane study database, a greater number of toxicological endpoints
were identified. These studies were evaluated by systematic review and only 4 studies were considered
for the acute oral non-cancer dose assessment (Table Apx M-14). In Cheever et al. (1990). it was noted
that in a preliminary study on 4 month old Osborne-Mendel rats dosed with 150 mg/kg-bw by oral
gavage of radiolabeled 1,2-dichloroethane it was identified that the 14C was almost completely
eliminated within 24 hours after administration. Elimination of the 14C was found primarily in the urine
(49.7-51.5 percent), in expired air (35.5-39.6 percent) and only a small portion in the feces as detected as
14C02. This suggested that the kidneys are a potential target due to oral exposure to 1,2-dichloroethane.
In the Morel et al. (1999) acute single exposure oral gavage study in male Swiss OF1 mice treated with
0, 1000, or 1500 mg/kg-bw of 1,2-dichloroethane, a significant increase in damaged renal tubules
(7.66% vs. 0.32% in controls) was seen only seen in the highest dose group with the lowest dose already
above the limit dose. B6C3F1 mice in the Storer et al. (1984) study that were administered a single oral
gavage dose at 0, 100, 200, 300, 400, 500, 600 mg/kg-bw resulted in absolute kidney weights increased
at 300 mg/kg-bw doses and greater. Relative kidney weights in Storer et al. (1984) were also increased
in the 300 mg/kg and higher dose groups along with serum BUN (serum BUN showed a trend increase
but the 300 mg/kg/day dose was not statistically significant to control at N = 5; however, the benchmark
dose [BMD] analysis using all data points together showed significance above 106 mg/kg/day). Thus,
based on both histological and clinical chemistry parameters, the Storer et al. (1984) study based on
mice kidney weight was identified as the recommended candidate for the acute oral POD. To calculate
risks for the acute exposure duration in the risk evaluation, EPA used a daily HED of 19.9 mg/kg-bw
(based on a BMDLio% of 153 mg/kg-bw) from Storer et al. (1984) and based on a significant (13
percent) increase in relative kidney weight in male B6C3F1 mice administered a single dose of 1,2-
dichloroetane at 100, 200, 300, or 400 mg/kg via oral gavage in corn oil. This study was given a high
overall quality determination and a UF of 30 was used for the benchmark MOE during risk
characterization (Table 5-49).
Evaluation of the 1,2-dichloroethane studies also suggest the liver and respiratory system as targets of
oral 1-2-dichloroethane exposure. In the Munson et al. (1982) study, an acute single oral gavage to 1-2-
dichloroethane in CD-I mice identified a LD50 of 413 and 489 mg/kg for female and male mice,
respectively. Upon necropsy of these animals, it was identified that the lungs and liver appeared to be
the primary target organs.
In support of liver toxicity, in the study by Storer et al. (1984). B6C3F1 mice were administered a single
dose of 1,2-dichloroetane at 100, 200, 300, or 400 mg/kg via oral gavage in corn oil and euthanized 4
hours later. It was identified that a statistically significant increase in DNA damage in hepatic nuclei was
present in all dose groups, as characterized by single-strand breaks, when compared to controls. The
study by Storer et al. (1984) also indicated increased IDH (also known as sorbitol dehydrogenase, SDH)
and AAT (alanine aminotransferase) serum levels were also increased at the 200 mg/kg and higher doses
in the B6C3F1 mice. In Cottalasso et al. (2002). a single gavage of 628 mg/kg of 1,2-dichloroethane in
female Sprague-Dawley rats resulted in increased alanine aminotransferase (ALT), aspartate
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aminotransferase (AST), and lactate dehydrogenase as compared to controls. Additionally, histological
evaluation of the liver showed moderate steatosis. Increased malondialdehyde (MDA), a marker of lipid
peroxidation, was also seen in the treated animals when compared to controls. Although clinical
chemistry for liver enzyme-implicates liver injury due to 1,2-dichloroethane exposure, gross pathology
(changes in liver weight or quantified histological changes) was not identified.
With regard to the respiratory system, only the study by Salovsky et al. (2002). a single oral dose of 136
mg/kg-bw 1,2-dichloroethane in male Wistar rats resulted in increased total number of cells in the
bronchioalveolar lavage fluid (BALF) of male Wister rats at 30 days after dosing. Histological changes
were only presented qualitatively. Thus, this study was not identified as the POD due to limited data that
was quantitative.
Inhalation
Table 5-43 shows the recommended acute inhalation study and POD for 1,1-dichloroethane (using 1,2-
dichloroethane data to read-across) followed by co-critical endpoints (PODs within the range of the
recommended study) and other studies considered in support of the recommended POD.
No acute PODs were identified from studies for inhalation exposures to 1,1-dichloroethane. The 10-day
inhalation study by Schwetz et al. (1974) was not used because the effects on developing fetuses and/or
offspring are limited and inconclusive and were considered inadequate for derivation of an acute
inhalation POD, and because the only effect reported were decreases in maternal body weight which
occurred following 10-days of exposure. Likewise, a route-to-route extrapolation from the acute Storer
et al. (1984) oral study was not conducted given the differences in absorption rates across routes, method
of dosing effects on blood levels and hazards (i.e., gavage bolus dose vs. slower inhalation dosing), the
lack of a PBPK model, and the inherent uncertainties when performing oral-to-inhalation route
extrapolations for a volatile solvent (i.e., most of the oral dose is eliminated in expired air). Therefore,
there is inadequate data to identify an inhalation POD for the acute duration scenario. An 8-hour
inhalation study in male and female rats exposed to 1,2-dichloroethane by Dow Chemical (2006b) was
used based on read-across to 1,1-dichloroethane. A BMCLio of 48.9 mg/m3 and BMD of 81.4 mg/m3
were identified based on degeneration with necrosis of the olfactory mucosa. The acute inhalation HEC
for occupational and continuous exposure of 10.14 ppm (41.1 mg/m3) and 2.42 ppm (9.78 mg/m3),
respectively, with a benchmark MOE of 30, was used for risk assessment of acute inhalation exposure
(Table 5-49). The resulting RGDR value of 0.2 is the combined value for male (0.25) and female (0.16)
F344 rats used to calculate HEC continuous (U.S. EPA. 2012a).
Dermal
No acute exposure studies on 1,1-dichloroethane via the dermal route were identified. Therefore, the
acute oral HED of 19.9 mg/kg-bw/day was extrapolated for the dermal route, with a benchmark MOE of
30, and was used for risk assessment of acute dermal exposures (Table 5-49).
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Table 5-42. Acute C
»ral Non-cancer PO
)-Endpoint Selection Table
Chemical/Endpoint
POD
(mg/kg/day)
Study Parameters
Comments
POD selected for risk evaluation of non-cancer for acute oral exposures
1,2-Dichloroethane,
Kidney Weight
BMDL= 153
BMD = 270
NOAEL = 200 mg/kg;
LOAEL = 300 mg/kg
Storer et al. (1984). Gavaae. SR High
B6C3F1 Mice - Male
Single exposure (0, 200, 300, 400,
500, or 600 mg/kg)
Single exposure study with a POD dose virtually identical to the POD
dose where resorptions were observed. This POD is protective for
other endpoints such as narcosis, BUN, IDH, resorptions, etc.
Death started at 400 mg/kg; LD50 (males) = 450 mg/kg).
Co-critical studies
1,2-Dichloroethane,
Blood Urea Nitrogen
(BUN)
NOAEL = 200
LOAEL = 300
Storer et al. (1984). Gavaae. SR High
B6C3F1 Mice - Male
Single exposure (0, 200, 300, 400,
500, or 600 mg/kg)
Adverse increase in BUN supporting kidney effects, not statistically
significant due to low N=5.
The BMD 10 for BUN was 55 which is far lower than the BUN
NOAEL value of 200 mg/kg, thus the BMD10 value is not
representative of the BUN data. Also, none of the models derived
goodness-of-fit p-values for the means.
1,2-Dichloroethane,
L-iditol
dehydrogenase (IDH)
NOAEL = 200
LOAEL = 300
Storer et al. (1984). Gavaae. SR High
B6C3F1 Mice - Male
Single exposure (0, 200, 300, 400,
500, or 600 mg/kg)
Nine-fold adverse increase in IDH marker of tissue damage (associated
mostly with kidney and liver damage), not statistically significant due
to low N = 5.
Neither the constant nor nonconstant variance models provided
adequate fit to the variance data. No model selected.
Other studies/endpoints considered
1,1 -Dichloroethane,
CNS
Depression/Sedation
NOAEL = 1,000
LOAEL = 2,000
Muralidhara et al. (2001).
Gavage, SR Medium
SD Rats - Male
Single exposure (0, 1,000, 2,000,
4,000, or 8,000 mg/kg)
1,2-Dichloroethane Oral LD50 is 725 mg/kg (PubChem), so POD too
near lethal doses. Narcosis is not a sensitive endpoint in the database.
This is the only 1,2-dichloroethane study that passed SR with an acute
oral POD.
1,2-Dichloroethane,
Kidney
Histopathology
NOAEL = 1,000
LOAEL = 1,500
Morel et al. (1999). Gavaae. SR High
Swiss OF1 Mice - Male
(0, 1,000, 1,500 mg/kg)
Significant increase in damaged renal tubules but lowest dose above
the limit dose.
1,2-Dichloroethane,
Liver Weight
LOAEL = 625
Moodv et al. (1981). Gavage. SR
Medium
Increased liver weight. Dose is not a sensitive endpoint.
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Chemical/Endpoint
POD
(mg/kg/day)
Study Parameters
Comments
SD Rats - Male
Single exposure (0, 625 mg/kg)
1,2-Dichloroethane,
Liver Clinical
Chemistry
NOAEL = 134
Kitchin et al. (1993). Gavaae. SR High
SD Rats - Female
Single exposure (0, 134 mg/kg)
No effects reported. Inadequate dosing (too low).
1,2-Dichloroethane,
Fetal Resorptions
NOAEL= 160
LOAEL = 200
(Data not amenable for
BMD modeling)
Pavan et al. (1995). Gavage
Pre-Natal Developmental, SR High
SD Rats - Female
Dosing GD6-20 (0, 120, 160, 200, or
240 mg/kg)
The increases in non-implants and resorptions are difficult to interpret
given the significant maternal toxicity at corresponding doses (30%
and 49% at 200 and 240 mg/kg/day, respectively) consisting of
decreases in maternal bw gain, and the fact that there was no effect on
the number of live fetuses per litter despite the changes in non-
surviving implants/litter and resorption sites/litter. Therefore, cannot
be used as POD.
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7599 Table 5-43. Acute Inhalation Non-cancer POD-Endpoint Selection Table
Chemical/
Endpoint
POD
(mg/m3)
Study Parameters
Comments
POD selected for non-cancer risk evaluation for acute inhalation exposures
1,2-Dichloroethane,
Neurological
BMDLio = 48.9
mg/m3 or 12.1 ppm
NOAEL: 202
LOAEL: 405
Dow Chemical (2006b). SR High
F344 Rats - Male
8 hours/day 1 days (0, 50, 100, 150, 200, 600, 2000
ppm; 0, 202, 405, 607, 809, 2428, 8095 mg/m3)
Degeneration with necrosis of the olfactory neuroepithelial
mucosa.
Co-critical endpoints
1,2-Dichloroethane,
Reproductive
Toxicity/Fetal
Development
Reproductive/
Developmental
BMDL5= 25 Pup
BW decreased at 613
BMDLio = 50 mg/m3
NOAEL: 305
LOAEL: 613
Rao et al. (1980). Vapor. SR Medium
SD Rats - Both sexes
Inhalation. Prior to mating, during gestation, and
post-natally for two F1 generations (0, 25, 75, 150
ppm; 0, 102, 305 or 613 mg/m3
Decreased body weight of selected FIB male weanlings at 150
ppm
Study used for co-critical endpoints with BMDLio very close
to that from the recommended endpoint. Considering
NOAELs/LOAELs, using the recommended endpoint will be
protective of the decreases in pup body weight. Also, portal of
entry effects can be considered more sensitive than systemic
effects.
Other studies/endpoints considered
1,2-Dichloroethane
Prenatal
Developmental
Reproductive/
Developmental
Toxicity:
NOAEL: 1,200
Maternal Toxicity:
NOAEL = 1,000
LOAEL: 1,200
Pavan et al. (1995). Van or. SR High
SD Rats - Both Sexes
Inhalation exposure for 2 weeks. GD 6-20. 6
hours/day 7 days/week, at 0, 150, 200, 250, 300
ppm; 0, 610, 820, 1,000, 1,200 mg/m3
Repro/Dev Toxicity: Pregnancy rate among females at 250
ppm was significantly lower (p<0.05). This was not observed
at the highest concentration of 300 ppm. No other significant
effects reported.
Maternal Toxicity: 2/26 dams died at 300 ppm (highest dose).
Maternal body weight gain at GD 6-21 was significantly
decreased at 300 ppm. No mention of food consumption.
NOAEL/LOAEL higher than recommended endpoint.
Not amenable to BMD modeling.
1,2-Dichloroethane
Prenatal
Developmental
Reproductive/
Developmental
LOAEL: 405
Maternal Toxicity:
NOAEL: 405
Rao et al. (1980). Vapor. SR Medium
SD Rats - Female
Inhalation exposure for 10 days. GD 6-15. 7
hours/day.0, 100, 300 ppm (0, 405, 1,214 mg/m3)
Developmental Toxicity: A significant decrease in the
incidence of bilobed thoracic centra was seen at 100 ppm
however study essentially becomes a single dose study and not
amenable to dose-response modeling due to the high maternal
toxicity at 300 ppm (10/16 maternal rats died at 300 ppm).
Therefore, this study is not acceptable for POD derivation.
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Chemical/
Endpoint
POD
(mg/m3)
Study Parameters
Comments
LOAEL: 1214
1,2-Dichloroethane
Prenatal
Developmental
Toxicity
Reproductive/
Developmental
Liver
NOAEL: 16,000
Maternal Toxicity:
LOAEL: 16,000
Schwetz et al. (1974). Vapor. SR Medium
7 hours/day 10 days
Exposed on GD 6-15 (0, 3,800, 6,000 ppm; 0,
16,000, 24,300 mg/m3)
At 6000 ppm: Increased relative liver weight (SGPT/ALT
activity was not determined); an increased incidence of
delayed ossification of stemabrae. At 3800 ppm: decrease in
maternal body weight gains observed LOAEL: 15,372 mg/m3
(3798 ppm).
Study precluded for POD derivation because of several
methodological and control issues.
1,2-Dichloroethane,
Liver
NOAEL = 2,527
LOAEL = 3,475
Brondeau et al. (1983). whole bodv inhalation
chamber, SR Medium
SD Rats - Male
0, 618, 850, 1,056, 1,304 ppm; 0, 2,527, 3,475,
4,318, 5,332 mg/m3
Significant increases in serum GLDH and SDH levels were
seen at >850 ppm (3475 mg/m3); serum ALT and AST were
significantly increased at 850 ppm (3475 mg/m3) but not at
higher concentrations. Dose-response analysis inadequate.
Histopathology and organ weight were not assessed.
1,2-Dichloroethane,
Liver, Metabolic,
Kidney,
Neurological
Liver, Metabolic &
Kidney (Organ
Weight/
Overall study
NOAEL/LOAEL:
Metabolic (Body
Weight):
NOAEL: 809
LOAEL: 2,428
Dow Chemical (2006b). Vaoor. SR High
F344 Rats- Both sexes
4 or 8 hours:
(0, 50, 100, 150, 200, 600, or 2,000 ppm; 202, 405,
607, 809, 2,428 or 8,095 mg/m3)
Organ weight changes (liver, adrenal, kidney); histological
changes (liver, kidney, olfactory mucosa); multiple FOB
changes, bw changes were observed although most effects
were inconsistent or transient but supportive of liver and
kidney effects; the neurological effect (degeneration of the
olfactory neuroepithelial mucosa) from this study was used as
the recommended POD (see first entry above).
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Chemical/
Endpoint
POD
(mg/m3)
Study Parameters
Comments
1,2-Dichloroethane,
Liver/Kidney
relative organ
weights
Liver (relative organ
weight):
NOAEL: 5,111
LOAEL: 6,134
Kidney (relative
organ weight):
NOAEL: N/A
LOAEL :4089
Francovitch et al. (1986). Vaoor. SR Medium
CD-I Mice-Male
4 hours:
(0, 1000, 1250, 1500 ppm; 0, 4,089, 5,111 or 6,134
mg/m3)
Organ weight changes and histology (liver and kidney);
however, exposure group where these changes occurred, and
negative control data were not reported. While study is
supportive of liver and kidney effects, it is not suitable for
dose-response analysis. Observed effects are occurring at
higher concentrations than the recommended POD.
1,2-Dichloroethane,
Immunological/
Streptococcal
infection challenge
CD-I (Female):
NOAEL: 9.21
LOAEL: 21.6
SD Rats (Male):
NOAEL: 801.2
Sherwood et al. (1987). Vaoor. SR High
CD-I Mice - Female:
3 hour single exposure; 0, 2.3, 5.4, 10.8 ppm; 0,
9.21, 21.6, 43.3 mg/m3
SD Rats - Male:
3 or 5 hour single exposure; 0, 10, 20, 50, 100, 200
ppm; 0, 40.1, 80.1, 200.3, 400.6 and 801.2 mg/m3
Mice: Increased mortality from streptococcal challenge;
decreased bactericidal activity; no effects in cell counts or
phagocytic activity of alveolar macrophages; increased leucine
aminopeptidase (LAP) activity.
Rats: No effects observed
1,2-Dichloroethane,
Neurological
For 12 hours/day for
1 day:
NOAEL: 2,500
LOAEL: 5,000
2, 4, or 6 hours/day
for 1 day:
LOAEL: 5,000
Oin-li et al. (2010). Vaoor. SR Medium
SD Rats: Both sexes
12 hours/day for 1 day:
0, 2,500, 5,000, 1,0000 mg/m3
2, 4, or 6 hours/day for 1 day:
0 or 5,000 mg/m3
12 hours/day for 1 day:
No mortality observed; signs of abnormal behavior; effects on
brain histology (edema corresponding with water content in
the cortex, no details on severity or dose-response).
2, 4, or 6 hours/day for 1 day:
Effects on brain histology less severe than at 12 hours (edema
corresponding with water content of cortex, perineural and
perivascular spaces).
These effects no suitable for dose-response analysis but are
supportive of neurological effects seen in the recommended
study and POD.
1,2-Dichloroethane,
Neurological
For 1.5 or 4 hours:
NOAEL: 4,000
Zhou et al. (2016). Vapor. SR Medium
SD Rats - Males
Effects on the brain lesions with edema, and a significant
decrease in the number of fiber tracts were observed compared
to control. Study not suitable for dose- response analysis.
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Chemical/
Endpoint
POD
(mg/m3)
Study Parameters
Comments
1.5 or 4 hours; 0, 4,000, or 12,000 mg/m3
Study supports neurological effects seen in the recommended
study and POD.
1,2-Dichloroethane,
Liver/Kidney
Clinical Chemistry
Liver Clinical
Chemistry:
NOAEL: 640
LOAEL: 2,020
Kidney weight/BUN:
NOAEL: 640
LOAEL: 2,020
Mortality:
NOAEL: 2,020
LOAEL: 4,339
Storer et al. (1984). Gas. SR High
B6C3F1 Mice-Males
4 hours (0, 58, 499, 1,072, and
1,946 ppm; 0, 640, 2,020, 4,339, and 7,876 mg/m3
Increased serum levels of IDH, ALT, and BUN; increased liver
and kidney weights; evidence of DNA damage; and increased
mortality (4/5 and 5/5 at > 499 ppm) essentially reducing this
study to a single dose study and unsuitable for dose-response
analysis.
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5.2.6.1.3 Non-cancer POPs for Short-Term/Subchronic Exposures
Oral Short-Term/Subchronic
Table 5-44 shows the recommended short term/sub chronic oral study and POD for 1,1-dichloroethane
(using 1,2-dichloroethane data to read-across) followed by co-critical endpoints (PODs within the range
of the recommended study) and other studies considered in support of the recommended POD.
There were 4 short-term (>1-30 days) and sub-chronic (>30-91 days)-duration animal toxicology
studies from the 1,1-dichloroethane database rated as acceptable based on data quality evaluation using
systematic review approaches (Table Apx M-8). Three other studies that met this exposure duration
were uninformative and excluded from study and endpoint selections based on quality metrics including
lack of concurrently run controls, limited methodological details and deficient data reporting. Overall,
the 1,1-dichloroethane database did not have enough information to identify NOAELs and LOAELs by
target organ/system. Identifying only overall non-cancer NOAELs and LOAELs yielded one study,
Muralidhara et al. (2001) adequate for dose-response analysis and POD selection for the short-term/sub-
chronic exposure duration. In this 13-week study following 1,1-dichloroethane exposure (Muralidhara et
al.. 2001). and further described above in Section 5.2.3, a NOAEL of 1,000 mg/kg-bw/day and a
LOAEL of 2,000 mg/kg-bw/day were identified for mortality (1/15 rats), CNS depression, and
decreased body weight. At the high dose in this study (4,000 mg/kg-bw/day), the rats exhibited
protracted narcosis, and 8/15 rats died between weeks 1 and 11, when the surviving rats in this group
were sacrificed. While this study was initially considered for short-term/sub-chronic exposure duration
POD selection, the oral LD50 was near lethal doses. Taken together with narcosis lacking sensitivity as
a critical endpoint, Muralidhara et al. (2001) from the 1,1-dichloroethane database was not useable as a
sub-chronic oral POD.
Thus, read-across from 1,2-dichloroethane was used for 1,1- dichloroethane to identify non-cancer
short-term/sub-chronic oral and dermal PODs. For 1,2- dichloroethane, a total of 4 animal toxicity
studies were available, and 3 of these studies had acceptable data quality for dose-response analysis and
identification of the short-term/sub-chronic oral duration POD. There were no dermal data for the short-
term/sub-chronic duration exposure.
Using the 1,2-dichloroethane database, the selected critical study was (Munson et al.. 1982). In this 14-
day short-term study in CD1 mice of both sexes and dosed with 1,2-dichloroethane via oral gavage at
doses of 0, 4.9, 49 mg/kg. Endpoints evaluated included body weight, hematology, gross necropsy,
organ weights (liver, spleen, lungs, thymus, kidney, and brain), humoral immunity, and cell-mediated
immunity. The treatment-related effect observed in this study was immunosuppression based on
observed suppression of a cell-mediated immune response at doses 4.9 and 49 mg/kg/day. Co-critical
endpoints identified in this same Munson et al. (1982) study included an observed 30 percent decrease in
leukocytes at 49 mg/kg/day, and a dose-dependent trend of antibody forming cells/spleen towards
immune suppression with 25 and 40 percent suppression at 4.9 and 49 mg/kg/day, respectively.
NTP (1991) provided additional support for immunotoxicity. It was a 13-week oral gavage study of
F344/N rats dosed with 30, 60, 120, 240, or 480 mg/kg for males or 18, 37, 75, 150 or 300 for females
of 1,2-dichloroethane that observed possible dose-related incidences of thymus necrosis. Female rat
absolute thymus weight was decreased. This study's quality was limited by lack of drinking water
consumption reporting that would ensure consistent dosing of test animals throughout the study and also
limited by the changes in thymus co-occuring with mortality. NTP (1991) also reported a statistically
significant absolute and relative kidney weights at 60 and 120 mg/kg/day or 75 and 150 mg/kg/day in
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male or female rats, respectively. Increased absolute kidney weight was initially seen at 30 mg/kg in
male mice.
The 1,1-dichloroethane database also had an acute oral study by Zabrodskii et al. (2004) that identified
immunotoxicity, however the study LOAEL of 930mg/kg was insensitive compared to the much lower
POD of 4.9 mg/kg/day in the 1,2-dichloroethane Munson et al. (1982) multi-dose study and compared to
other identified critical effects. Further, Zabrodskii et al. (2004) was not appropriate for POD selection
because inductors of the monooxygenase system (i.e., phenobarbital (50 mg/kg) and benzenal [70
mg/kg]), which in part can mediate the immune system and acted as sensitizers in this study for the
treatment-related effects that were observed, were orally administered prior to 1,1-dichloroethane
administration. This immunotoxicity finding in the 1,1-dichloroethane database further supports the
immunosuppression POD using 1,2-dichloroethane as the analog. Other similar chlorinated solvents
demonstrate immunotoxicity. EPA's independent convergence on Munson et al. (1982) for the non-
cancer oral, short-term POD selection is validated by the 2022 ATSDR ToxProfile for 1,2-Dichroethane
(ATSDR.. 2022). which also identified immunosuppression as the most sensitive human health
protective endpoint.
Important to underscore, immunotoxicity found in both the 1,1- and 1,2-dichloroethane databases, is
recognized as a cancer mechanism (Hanahan and Weinberg. 2011). Specifically, inflammatory cell
recruitment that can actively promote tumor formation and was observed in both the Munson et al.
(1982) and Zabrodskii et al. (2004). through cell-mediated immune responses.
Several other studies were considered from across the 1,1- and 1,2-dichloroethane databases including
sedation which was insensitive as a selected POD from 1,1-dichloroethane (Muralidhara et al.. 2001). as
discussed; changes in kidney organ weight from a drinking water study from 1,2-dichloroethane (NTP.
1991). as discussed; reproductive/developmental outcomes following exposure to 1,2-dichloroethane,
including fetal resorptions and decreases in maternal body weight (Pavan et al.. 1995) and likely
confounded results for fertility and implantation success for 1,2-dichloroethane (Lane et al.. 1982).
Inhalation
No other short/intermediate-term inhalation studies with a rating of acceptable were located for 1,1-
dichloroethane except for Schwetz et al. (1974). Among the effects reported by Schwetz et al. (1974).
only the decreased maternal body weight (LOAEL of 3,798 ppm) was considered to be a suitable
endpoint for POD derivation. Uncertainties of the data from Schwetz et al. (1974) were (1) the
evaluations of maternal endpoints did not include histopathology or effects in organs other than the liver,
(2) the disparate findings on delayed ossification in the two control groups mean that a conclusion
regarding this endpoint cannot be made with confidence, and (3) there are no supporting studies that
evaluated comprehensive endpoints. A 4-week short-term study in male mice exposed to 1,2-
dichloroethane by Zhang et al. (2017) was thus used based on read-across to 1,1-dichloroethane. A
BMCL5 and BMC5 of 6.6 ppm (26.7 mg/m3) and 5.24 ppm (21.2 mg/m3), were identified based on
decreased sperm concentration. The short-term/sub chronic inhalation HEC for occupational and
continuous exposure of 22 ppm (89 mg/m3) and 5.2 ppm (21.2 mg/m3), respectively, with a benchmark
MOE of 100, was used for risk assessment of short-term/subchronic inhalation exposure (see Table
5-50).
Dermal
No short-term/sub chronic exposure studies on 1,1-dichloroethane via the dermal route were located.
Therefore, the short-term/sub chronic oral HED for occupational and continuous exposures of 171 and
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7696 239 mg/kg-bw/day, respectively, was extrapolated for the dermal route, with a benchmark MOE of 100,
7697 and was used for risk assessment of short-term dermal exposure (see Table 5-50).
7698
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Table 5-44. Short-Term/Subchronic Oral Non-cancer POD-Endpoint Selecl
tion Table
Chemical/Endpoint
POD
(mg/kg/day)
Study Parameters
Comments
POD selected for non-cancer risk evaluation for short-tenn/subchronic oral exposures
1,2-Dichloroethane
Decreased cell based immune
response
LOAELadj =4.9
Munson et al. (1982). Gavaae. SR
High
CD1 Mice - Both sexes
14 days (0, 4.9, 49 mg/kg-day)
ATSDR (2022) Report for 1.2-Dichloroethane confirms that
immunosuppression is the most sensitive human health protective
endpoint, Other similar chlorinated solvents demonstrate
immunotoxicity.
The Munson study had a much higher adverse response of 25%
immunosuppression at only 4.89 mg/kg/day when the NTP gavage
study only had an 8.9% increase in kidney weight at 30 mg/kg/day.
Co-critical endpoints
1,2-Dichloroethane
Decreased leukocytes
LOAELadj =4.9
Munson et al. (1982). Gavaae. SR
High
CD1 Mice - Both sexes
14 days (0, 4.9, 49 mg/kg-day)
Supports cell-based immunosuppression endpoint.
Other studies/endpoints considered
1,2-Dichloroethane
Immunotoxicity
• Humoral immune response
to T-dependent and T-
independent antigens
• Antibody-dependent cell
cytotoxicity
• Delayed Hypersensitivity
(DTH) reaction
LOAEL= 930
Zabrodskii et al. (2004). Gavaae.
SR Medium
Random-Bred Albino Rat - Both
sexes
Single Dose (0, 930 mg/kg-bw)
Qualitatively supports immunosuppression. A multi-day exposure
produces more sensitive PODs for immune suppression than a
single exposure study.
However, dose is close to LD50. Single acute exposure to one dose
and monitored - various immune reactions and indices were
evaluated 48 h and 5 days after exposure.
1,2-Dichloroethane
Sedation
NOAELadj=714
Muralidhara et al. (2001).
Gavage, SR Medium
SD Rats -Male
13 weeks (0, 500, 1,000, 2,000,
4,000 mg/kg-bw/day)
1,2-Dichloroethane acute oral LD50 is 725 mg/kg (PubChem), the
POD is near lethal doses, narcosis is well-known to occur at high
doses and is not considered a sensitive endpoint in the database.
This is the only study that passed SR with a useable subchronic oral
POD.
1,2-Dichloroethane
Immune (Thymus)
NOAEL =240
mg/kg-day
(males); 150
NTP (1991). Gavaee. SR Hieh
Qualitatively supports immunosuppression. However, thymus
necrosis occurs at dosages where mortality was also occurring
therefore cannot be used as a POD.
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Chemical/Endpoint
POD
(mg/kg/day)
Study Parameters
Comments
mg/kg-day
(females)
LOAEL= 480
mg/kg-day for
thymus necrosis
in males; 300
mg/kg-day for
thymus necrosis
in females
F344 Rats - Both sexes
13 weeks (0, 30, 60, 120, 240,
480 mg/kg-day (males); 0, 18, 37,
75, 150, 300 mg/kg/day (females)
1,2-Dichloroethane
Kidney Weight
NOAEL=30
(males)
LOAEL=75
(females)
NTP (1991). Gavaee. SR Hieh
F344 Rats - Both sexes
13 weeks (0, 30, 60, 120, 240,
480 mg/kg-day (males); 0, 18, 37,
75, 150, 300 mg/kg/day (females)
Study was considered for POD selection but not selected as this is
not the most sensitive endpoint compared to immunosuppression.
1,2-Dichloroethane
Fetal Resorptions
NOAEL=160
LOAEL=200
(Data were not
amenable for
BMD modeling)
Pavan et al. (1995). Gavaee
Pre-Natal Developmental, SR
High
SD Rats - Female
Dosing GD6-20 (0, 120, 160,
200, or 240 mg/kg)
The increases in non-implants and resorptions are difficult to
interpret given the significant maternal toxicity at corresponding
doses (30% and 49% at 200 and 240 mg/kg/day, respectively)
consisting of decreases in maternal bw gain, and the fact that there
was no effect on the number of live fetuses per litter despite the
changes in non-surviving implants/litter and resorption sites/litter.
Therefore, cannot be used as POD.
1,2-Dichloroethane
Decreases in Maternal Body
Weight Gain
NOAEL=160
LOAEL=200
(BMD = 99.1;
BMDL = 41.8)
Pavan et al. (1995). Gavaee
Pre-Natal Developmental, SR
High
SD Rats - Female
Dosing GD6-20 (0, 120, 160,
200, or 240 mg/kg)
A dose-related reduction in adjusted (for gravid uterine weight)
maternal bodyweight gain during treatment occurred, with statistical
significance achieved at the two highest doses (30 and 49%
reduction compared with controls, p < 0.05). However, this POD is
not as sensitive (LOAEL = 200; BMDL = 41.8) as the
Immunotoxicity Endpoint (LOAELadj =4.9).
1,2-Dichloroethane
Multigenerational/Reproductive
LOAEL= 50
Lane et al. (1982). Drinking
Water, SR High
Drinking water not measured to confirm actual dosage, therefore not
reliable for a dose-response analysis. Also, not as sensitive
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Chemical/Endpoint
POD
(mg/kg/day)
Study Parameters
Comments
Pup weight
ICR Mice - Both Sexes
Multigenerational (0, 5, 15 or 50
mg/kg-day)
(LOAEL=50) as the Immunotoxicity Endpoint identified in the
Munson et al. (1982). LOAELarn =4.9.
Pup weight was biologically significantly (>5%) decreased at >0.09
mg/ml (50mg/kg/day) in Fl/B mice.
1,2-Dichloroethane
Chronic 26-week dermal study
Decreased body weight in
females; increased distal
tubular mild karyomegaly (both
sexes); renal karyomegaly &
tubular degeneration (females)
LOAEL= 6300
Suauro et al. (2017). Dermal. SR
High
CB6F1- Tg rasH2@Jcl (rasH2)
mice - Both sexes
3 days/week 26 weeks (0, 126
mg; 0, 6,300 mg/kg-day
Not considered acceptable for dose response assessment as the study
used a single dose using transgenic mice.
7700
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7701 Table 5-45. Short-Term/Subchronic Inhalation Non-cancer POD-Endpoint Selection Table
Chemical-Endpoint
POD
(mg/m3)
Study Parameters
Comments
POD selected for non-cancer risk evaluation for short-tenn/subchronic inhalation exposures
1,2-Dichloroethane
BMDL5 =21.2 mg/m3
NOAEL:350
LOAEL:700
Zhang et al. (2017). 4 week
morphological analysis of
sperm parameters, SR High
Swiss Mice -Male
6 hours/day, 7 days/week, 4
weeks (0, 100, 350, 700
mg/m3)
Decreases in sperm concentration.
Co-critical endpoints
1,2-Dichloroethane, Fetal
Development
Reproductive/
Developmental
BMDL5= 25 Pup BW
decreased at 613
BMDL10 = 50 mg/m3
NOAEL: 305
LOAEL: 613
Rao et al. (1980). Vapor. SR
Medium
SD Rats - Both sexes
Inhalation. Prior to mating,
during gestation, and post-
natally for two F1 generations
(0, 25,75, 150 ppm; 0, 102,
305 or 613 mg/m3
Decreased body weight of selected FIB male weanlings at 150 ppm.
Study used for co-critical endpoints with BMDL5 very close to that from
the recommended endpoint. Considering NOAELs/LOAELs, using the
recommended endpoint will be protective of the decreases in pup body
weight. Also, portal of entry effects can be considered more sensitive than
systemic effects.
Other studies/endpoints considered
1,1 -Dichloroethane
Prenatal Developmental
Toxicity
Reproductive/
Developmental
Liver
NOAEL: 16,000
Maternal Toxicity:
LOAEL: 16,000
Schwetz et al. (1974). Vaoor.
SR Medium
7 hours/day 10 days
Exposed on GD 6-15 (0, 3,800,
6,000 ppm; 0, 16,000, 24,300
mg/m3)
At 6000 ppm: Increased relative liver weight (SGPT/ALT activity was not
determined); an increased incidence of delayed ossification of stemabrae.
At 3800 ppm: decrease in maternal body weight gains observed LOAEL:
15,372 mg/m3 (3798 ppm).
Study precluded for POD derivation because of several methodological
and control issues.
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Chemical-Endpoint
POD
(mg/m3)
Study Parameters
Comments
1,2-Dichloroethane,
Liver
LOAEL: 3424
Brondeau et al. (1983). Vapor.
SR Medium
SD Rats - Males
6 hours/day for 2 or 4 days; 0
or 3424 mg/m3
6 hours/day for 2 days:
Significant increases in serum ALT, GLDH and SDH levels ; liver
histopathology and organ weight were not assessed.
6 hours/day for 4 days:
Serum SDH levels were significantly increased.
Liver histopathology and organ weight were not assessed.
1,2-Dichloroethane,
Liver
LOAEL: 619
Igwe et al. (1986c). Vapor. SR
Increased relative liver weight and 5'-NT. Absolute liver weight was not
reported. No changes in hepatic GST activity, hepatic DNA content, or
serum enzymes ALT or SDH were observed at any concentration.
High
SD Rats - Male
7 hours/day, 5 days/week, 4
weeks:
0, 153,304, 455 ppm; 619,
1,230, and 1,842 mg/m3
1,2-Dichloroethane-
Liver/
Reproductive/Metabolic/
Mortality
Immune:
NOAEL: 1842
Reproductive:
NOAEL: 1842
Liver:
LOAEL: 619
Mortality, Metabolic:
NOAEL: 619
LOAEL: 1230
Iawe et al. (1986c). Vaoor. SR
Immune, Reproductive/Developmental: No effects on organ weight or
histopathology.
Liver: Increased relative liver weight, absolute liver weight was not
reported.
Mortality: Occurred in 1/12 and 2/12 animals in 1230 and 1842 mg/m3,
respectively
Metabolic: Decreased body weight.
NOAEL/LOAEL higher than recommended endpoint.
Not amenable to BMD modeling
High
SD Rats - Male
7 hours/day, 5 days/week, 30
days:
0, 153,304, 455 ppm; 619,
1,230, and 1,842 mg/m3
1,2-Dichloroethane-
Reproductive/
Developmental/ Maternal
Toxicity
Reproductive/
Developmental
NOAEL: 1200
Maternal Toxicity:
NOAEL = 1000
LOAEL: 1200
Pavan et al. (1995). Vauor. SR
Repro/Dev Toxicity: Pregnancy rate among females at 250 ppm was
significantly lower, but not at 300 ppm; no other significant effects
reported.
Maternal Toxicity: 2/26 dams died at 300 ppm (highest dose). Maternal
body weight gain at GD 6-21 was significantly decreased at 300 ppm. No
mention of food consumption.
NOAEL/LOAEL higher than recommended endpoint.
Not amenable to BMD modeling.
High
SD Rats - Both Sexes
Inhalation exposure for 2
weeks. GD 6-20. 6 hours/day 7
days/week,
0, 150, 200, 250, 300 ppm; 0,
610, 820, 1000, 1200 mg/m3
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Chemical-Endpoint
POD
(mg/m3)
Study Parameters
Comments
1,2-Dichloroethane-
Reproductive/
Developmental; Maternal
Toxicity
Reproductive/
Developmental
LOAEL: 405
Maternal Toxicity:
NOAEL: 405
LOAEL: 1214
Rao et al. (1980). Vapor. SR
Medium
SD Rats - Female
Inhalation exposure for 10
days. GD 6-15. 7 hours/day.0,
100,300 ppm (0, 405, 1214
mg/m3)
Developmental Toxicity: A significant decrease in the incidence of
bilobed thoracic centra was seen at 100 ppm however study essentially
becomes a single dose study and not amenable to dose-response modeling
due to the high maternal toxicity at 300 ppm (10/16 maternal rats died at
300 ppm). Therefore, this study is not acceptable for POD derivation.
1,2-Dichloroethane-
Immunological/
Streptococcal infection
challenge
CD-I Mice:
NOAEL: 9.21
SD Rats:
NOAEL: 400.6
Sherwood et al. (1987). Vapor.
SR High
CD-I Mice - Female:
3 hour/day, 5 days/week, 5
days; 0, 2.3; 0, 9.21 mg/m3
SD Rats - Male:
5 hour/day, 5 days/week, 12
days; 0, 10, 20, 50, 100; 0,
40.1, 80.1, 200.3, 400.6 mg/m3
CD-I mice and SD rats showed no effects.
1,2-Dichloroethane-
Liver/Metabolic
Liver:
NOAEL: 350
Metabolic:
NOAEL: 350
LOAEL: 700
Zeng et al. (2018). Aerosol. SR
Liver: Increased absolute and relative liver weight, increased liver
concentrations of glycogen, triglycerides, and free fatty acids at all
concentrations; increased ALT (1.9-fold) at 700 mg/m3; increased serum
AST (1.3-fold-1.7-fold), triglycerides, and free fatty acids; decreased
serum glucose at both exposure concentrations.
Metabolic: Body weight was significantly reduced at 700 mg/m3.
High
Swiss Mice: Male
6 hours/day, 7 days/week, 28
days
0, 350, 700 mg/m3
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Chemical-Endpoint
POD
(mg/m3)
Study Parameters
Comments
1,2-Dichloroethane
Neurological,
Reproductive,
Immune/Hematological,
Liver, Mortality,
Metabolic, Kidney (Rat):
Respiratory:
NOAEL:809
Liver, Metabolic &
Kidney (Guinea Pig):
NOAEL: 405
Spencer et al. (1951). Vapor.
Rats: High mortality at 400 ppm starting at 2 weeks; no other effects
reported.
Guinea Pigs: High mortality at 400 ppm starting at 2 weeks; reductions in
body weight starting at 100 ppm; increases in liver weight; possible liver
histopathology and changes in kidney weight, but incidence not reported.
SR Medium
Wistar Rats - Both sexes
7 hours/day 5 days/week
212 days*, (0, 100, 200, 400
ppm; 0, 405, 809, 1619 mg/m3)
* Although all exposure
groups were intended for
chronic duration exposures,
animals at the high exposure
level died within 14 days
(females) and 56 days (males).
Guinea Pigs - Both sexes
7 hours/day 5 days/week
248 days, (0, 100, 200, 400
ppm; 0, 405, 809, 1619 mg/m3)
7702
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5.2.6.1.4 Non-cancer POPs for Chronic Exposures
Oral
Table 5-46 shows the recommended chronic oral study and POD for 1,1-dichloroethane (using 1,2-
dichloroethane data to read-across) followed by co-critical endpoints (PODs within the range of the
recommended study) and other studies considered in support of the recommended POD.
No studies of chronic oral exposure in laboratory animals were considered suitable for POD
determination (see Appendix M.2.5 for 1,1-dichloroethane and Appendix M.2.8 for 1,2-dichloroethane).
Therefore, the short-term/sub chronic POD identified in Section 5.2.6.1.2 was also used for chronic
exposure. The short-term/sub chronic continuous HED was 0.636 mg/kg-bw/day and the worker HED
was 0.890 mg/kg-bw/day (see Appendix M.2.7). The benchmark MOE for this POD is 1,000 based on 3
for interspecies extrapolation when a dosimetric adjustment is used, 10 for human variability, 3 for the
use of a LOAEL to extrapolate a NOAEL (based on the dose-response), and 10 for extrapolating from a
subchronic study duration to a chronic study duration for chronic exposures (Table 5-51).
Inhalation
Table 5-47 shows the recommended chronic inhalation study and POD for 1,1-dichloroethane (using
1,2-dichloroethane data to read-across) followed by co-critical endpoints (PODs within the range of the
recommended study) and other studies considered in support of the recommended POD.
No chronic PODs were identified from studies for inhalation exposures to 1,1-dichloroethane. A
duration extrapolation from the 10-day inhalation study by Schwetz et al. (1974) was not conducted due
to the inherent uncertainties when extrapolating from a 10-day study to a chronic duration. Likewise, a
route-to-route extrapolation from the 13-week subchronic oral study Muralidhara et al. (2001) was not
conducted given the differences in absorption rates across routes, method of dosing effects on blood
levels and hazards (i.e., gavage bolus dose vs. slower inhalation dosing), the lack of a PBPK model, and
the inherent uncertainties when performing oral-to-inhalation route extrapolations for a volatile solvent
(i.e., most of it is eliminated in expired air). Therefore, there is inadequate data to identify an inhalation
POD for the chronic duration scenario using 1,1-dichloroethane (see Table 5-51). A 4-week short-term
study in male mice exposed to 1,2-dichloroethane by Zhang et al. (2017) was thus used based on read-
across to 1,1-dichloroethane. A duration extrapolation from the 4-week short-term/sub chronic to a
chronic duration was conducted in order to account for uncertainty. A subchronic to chronic UF of 10
was thus applied for extrapolating from a subchronic to chronic study duration. A BMCL5 and BMC5 of
6.6 ppm (26.7 mg/m3) and 5.24 ppm (21.2 mg/m3), were identified based on decreased sperm
concentration. The short-term/sub chronic inhalation HEC for occupational and continuous exposure of
22 ppm (89 mg/m3) and 5.2 ppm (21.2 mg/m3), respectively, with a benchmark MOE of 300, was used
for risk assessment of chronic inhalation exposure. Although an uncertainty regarding study duration
may have been reduced while performing read-across by use of the chronic (Nagano et al.. 2006) study
that evaluated 1,2-dichloroethane, the study did not adequately evaluate non-cancer effects, preventing
the determination of a non-cancer chronic POD.
Dermal
No chronic studies on 1,1-dichloroethane or 1,2-dichloroethan via the dermal route were located.
Therefore, the chronic oral HED for occupational and continuous exposures of 0.89 and 0.636 mg/kg-
bw/day, respectively, was extrapolated for the dermal route, with a benchmark MOE of 1,000, and was
used for risk assessment of chronic dermal exposure (see Table 5-51).
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7751 Table 5-46. Chronic Oral Non-cancer POD-Endpoint Selection Table
Chemical-Endpoint
POD
(mg/kg/day)
Study Parameters
Comments
POD selected for non-cancer risk evaluation for chronic oral exposures
1,2-Dichloroethane
Decreased cell based immune
response
LOAELadj =4.9
Munson et al. (1982). Gavaae
SR High
CD1 Mice - Both sexes
14 days (0, 4.9, 49 mg/kg-day)
ATSDR (2022) Report for 1.2-dichloroethane confirms that
immunosuppression is the most sensitive human health
protective endpoint, Other similar chlorinated solvents
demonstrate immunotoxicity.
Co-critical endpoints
1,2-Dichloroethane
Decreased leukocytes
LOAELadj =4.9
Munson et al. (1982). Gavaae
SR High
CD1 Mice - Both sexes
14 days (0, 4.9, 49 mg/kg-day)
Supports cell-based immunosuppression endpoint
Other studies considered
1,1 -Dichloroethane
Immunotoxicity
• Humoral immune response
to T-dependent and T-
independent antigens
• Antibody-dependent cell
cytotoxicity
• Delayed Hypersensitivity
(DTH) reaction
LOAEL= 930
Zabrodskii et al. (2004). Gavaae.
SR Medium
Random-Bred Albino Rat - Both
sexes
Single Dose (0, 930 mg/kg-bw)
Qualitatively supports immunosuppression. A multi-day
exposure produces more sensitive PODs for immune
suppression than a single exposure study.
However, dose is close to LD50. Single acute exposure to one
dose and monitored - various immune reactions and indices
were evaluated 48 h and 5 days after exposure.
1,1-Dichloroethane Sedation
NOAELadj=714
Muralidhara et al. (2001). Gavaae.
SR Medium
SD Rats - Male
13 weeks (0, 500, 1,000, 2,000,
4,000 mg/kg-bw/day)
1,1-Dichloroethane Acute Oral LD50 is 725 mg/kg
(PubChem), the POD is near lethal doses, Narcosis is well-
known to occur at high doses and is not considered a sensitive
endpoint in the database. This is the only study that passed SR
with a useable subchronic oral POD.
Would require a UFs of 10 for duration extrapolation from
sub-chronic to chronic and a database uncertainty factor.
1,2-Dichloroethane
Immune (Thymus)
NOAEL=240 mg/kg-day
(males); 150 mg/kg-day
(females)
NTP (1991). Gavaae. SR Hiah
(NTP 1991)
F344 Rats - Both sexes
Qualitatively supports immunosuppression. However, thymus
necrosis occurs at dosages where mortality was also occurring
therefore cannot be used as a POD.
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Chemical-Endpoint
POD
(mg/kg/day)
Study Parameters
Comments
LOAEL= 480 mg/kg-day
for thymus necrosis in
males; 300 mg/kg-day for
thymus necrosis in
females
13 weeks (0, 30, 60, 120, 240, 480
mg/kg-day (males); 0, 18, 37, 75,
150, 300 mg/kg/day (females)
1,2-Dichloroethane
Kidney Weight
LOAEL=30 (males)
LOAEL=75 (females)
NTP (1991). Gavaee. SR Hieh
F344 Rats - Both sexes
13 weeks (0, 30, 60, 120, 240,
480 mg/kg-day (males); 0, 18,
37, 75, 150, 300 mg/kg/day
(females)
Study was considered for POD selection but not selected as
this is not the most sensitive endpoint compared to
immunosuppression.
1,2-Dichloroethane
Fetal Resorptions
NOAEL=160
LOAEL=200
(Data were not amenable
to modeling)
Pavan et al. (1995). Gavaee
Pre-Natal Developmental, SR
High
SD Rats - Female
Dosing GD6-20 (0, 120, 160, 200,
or 240 mg/kg)
The increases in non-implants and resorptions are difficult to
interpret given the significant maternal toxicity at
corresponding doses (30% and 49% at 200 and 240
mg/kg/day, respectively) consisting of decreases in maternal
bw gain, and the fact that there was no effect on the number of
live fetuses per litter despite the changes in non-surviving
implants/litter and resorption sites/litter. Therefore, cannot be
used as POD.
1,2-Dichloroethane
Decreases in Maternal Body
Weight Gain
NOAEL=160
LOAEL=200
(BMD = 99.1; BMDL =
41.8)
Pavan et al. (1995). Gavaee
Pre-Natal Developmental, SR
High
SD Rats - Female
Dosing GD6-20 (0, 120, 160, 200,
or 240 mg/kg)
A dose-related reduction in adjusted (for gravid uterine
weight) maternal bodyweight gain during treatment occurred,
with statistical significance achieved at the two highest doses
(30 and 49% reduction compared with controls, p < 0.05).
However, this POD is not as sensitive (LOAEL = 200; BMDL
= 41.8) as the Immunotoxicity Endpoint (LOAELadj =4.9).
1,2-Dichloroethane
Multigenerational/Reproductive
Pup weight
LOAEL= 50
Lane et al. (1982). Drinkine Water.
SR High
ICR Mice - Both Sexes
Reproductive Toxicity
(0, 5, 15 or 50 mg/kg-day)
Drinking water not measured to confirm actual dosage. Also,
not as sensitive (LOAEL=50) as the Immunotoxicity Endpoint
(LOAEL =4.9)
Pup weight was biologically significantly (>5%) decreased at
>0.09 mg/ml (50mg/kg/day) in Fl/B mice.
1,2-Dichloroethane
40-week chronic study
LOAEL = 150 (females)
Storer et al. (1995). Gavaee. SR
Medium
Minimal endpoints evaluated, only non-cancer endpoints were
body weight and lymphoma at 150.
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Chemical-Endpoint
POD
(mg/kg/day)
Study Parameters
Comments
Body weight/lymphoma
ppG64 Mice - Both sexes
7 days/week for 40 weeks (0, 150,
300 mg/kg-day (female); 0, 100,
200 mg/kg/day (males)
Doses adjusted due to substantial mortality females at 300
mg/kg/day. Clear dose-response could not be assessed.
1,2-Dichloroethane
Chronic 26-week dermal study
LOAEL= 6300
Decreased body weight in
females; increased distal
tubular mild karyomegaly
(both sexes); renal
karyomegaly &
tubular degeneration
(females)
Sumiro et al. (2017). Dermal. SR
Single dosage using transgenic mice.
High
CB6F1- Tg rasH2@Jcl (rasH2)
mice - Both sexes
3 days/week 26 weeks (0, 126 mg;
0, 6,300 mg/kg-day
7752
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7753 Table 5-47. Chronic Inhalation Non-cancer POD-Endpoint Selection Table
Chemical-Endpoint
POD
(mg/m3)
Study Parameters
Comments
POD selected for non-cancer risk evaluation for chronic inhalation exposures
1,2-Dichloroethane-
Male Reproductive
BMDL5= 21.2 mg/m3
NOAEL: 350
LOAEL: 700
Zhang et al. (2017). 4 week morphological
analysis of sperm parameters, SR High
Swiss Mice - Male
6 hours/day 7 days/week 4
weeks (0, 100, 350, 700
mg/m3)
Decreases in sperm concentration.
Co-critical endpoints
1,2-Dichloroethane,
Fetal Development
Reproductive/
Developmental
BMDLS= 25 Pup BW
decreased at 613
BMDLio = 50 mg/m3
NOAEL: 305
LOAEL: 613
Rao et al. (1980). Vapor. SR Medium
SD Rats - Both sexes
Inhalation. Prior to mating, rats were
exposed for 60 days (6 hours/day, 5
days/week). The rest of the time, exposed to
6 hours/day, 7 days/week, except from
gestational day 21-post natal day 4 maternal
exposure stopped to allow for delivery and
rearing of the young). Two F1 generations
were evaluated, 0,25,75,150 ppm; 0, 102,
305 or 613 mg/m3
Decreased body weight of selected FIB male weanlings at
150 ppm.
Study used for co-critical endpoints with BMDLio very
close to that from the recommended endpoint.
Considering NOAELs/LOAELs, using the recommended
endpoint will be protective of the decreases in pup body
weight. Also, portal of entry effects can be considered
more sensitive than systemic effects.
Other studies considered
1,2-Dichloroethane
Reproductive/
Developmental
NOAEL: 1,200
Maternal Toxicity:
NOAEL = 1,000
LOAEL: 1,200
Pavan et al. (1995). Vapor. SR High
SD Rats - Both Sexes
Inhalation exposure for 2 weeks. GD 6-20. 6
hours/day 7 days/week,
0, 150, 200, 250, 300 ppm; 0, 610, 820,
1,000, 1,200 mg/m3
Repro/Dev Toxicity: Pregnancy rate among females at
250 ppm was significantly lower; not observed at the
highest concentration of 300 ppm;no other significant
effects reported.
Maternal Toxicity: 2/26 dams died at 300 ppm (highest
dose). Maternal body weight gain at GD 6-21 was
significantly decreased at 300 ppm. No mention of food
consumption.
NOAEL/LOAEL higher than recommended endpoint.
Not amenable to BMD modeling.
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Chemical-Endpoint
POD
(mg/m3)
Study Parameters
Comments
1,2-Dichloroethane
Reproductive/Developm
ental
LOAEL: 405
Maternal Toxicity:
NOAEL: 405
LOAEL: 1214
50). Vapor. SR Medium
SD Rats - Female
Inhalation exposure for 10 days. GD 6-15. 7
hours/day.0, 100, 300 ppm (0, 405, 1214
mg/m3)
Developmental Toxicity: A significant decrease in the
incidence of bilobed thoracic centra was seen at 100 ppm
however study essentially becomes a single dose study
and not amenable to dose-response modeling due to the
high maternal toxicity at 300 ppm (10/16 maternal rats
died at 300 ppm). Therefore, this study is not acceptable
for POD derivation.
1,2-Dichloroethane
Hematological:
NOAEL: 202
LOAEL: 607
Liver:
LOAEL: 20
Kidney:
NOAEL: 202
LOAEL: 607
IRFMN (1978). Vanor. SR Medium
SD Rats - Both sexes
7 hours/day, 5 days/week for 12
months: 0, 5, 10, 50, 150 ppm; 0, 20, 40,
202, 607 mg/m3
Hemoglobin levels were significantly decreased in both
sexes at 150 ppm; changes in hematocrit (increases rather
than decreases) were of questionable biological
significance and did not show a dose-response; decreases
in cholesterol and calcium levels at >10 ppm; clinical
chemistry signs of liver toxicity but did not show a dose-
response, kidney BUN increases at 150 ppm; other kidney
changes were male rat-specific and not relevant to
humans.
1,2-Dichloroethane
Reproductive/Developm
ental, Mortality &
Metabolic:
NOAEL: 204
Liver:
LOAEL: 204
Cheever et al. (1990). Vaoor. SR High
SD Rats - Both sexes
7 hours/day 5 days/week
104 weeks (0, 50 ppm; 0, 204 mg/m3)
Gross testicular lesions were found in higher frequency in
exposed males (24%) compared to control (10%) (data
not shown and gross pathologic observations were not
evaluated statistically); mortality similar in both treatment
and control groups, survival rate in exposed rats (60 and
64%) was similar to control (58 and 54%) in males and
females, respectively; absolute and relative liver weights
were not different from controls.
1,2-Dichloroethane
Immunological/Hematol
ogical, Liver, & Kidney:
NOAEL: 809
IRFMN (1976). Vaoor. SR Medium
SD Rats - Both sexes
7 hours/day 5 days/week 24
weeks, (0, 5, 10, 50, 150, 250
ppm; 0, 20, 40, 202, 607, 1,012 mg/m3)*
*Animals in the highest exposure group were
exposed
to 250 ppm for "a few weeks" and then the
exposure concentration was reduced to 150
ppm due to acute toxicity. A reliable TWA
All observed hematological, serum chemistry, and
urinalysis changes observed either did not reach
statistical significance, showed no clear relation to
exposure concentration, and/or were not biologically
significant.
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Chemical-Endpoint
POD
(mg/m3)
Study Parameters
Comments
concentration cannot be determined based on
the information available in this report,
IRFMN (1978) suggested that the change
occurred after 12 weeks of exposure. If this
is accurate, then the TWA exposure
concentration for the high exposure group
was 200 ppm.
1,2-Dichloroethane
Immunological/Hematol
ogical, Liver, & Kidney:
NOAEL: 607
IRFMN (1987). Vaoor. SR Medium
SD Rats - Both sexes
7 hours/day 5 days/week 78
weeks, (0, 5, 10, 50, 150, 250
ppm; 0, 20, 40, 202, 607, 1,012 mg/m3)*
* Animals in the highest exposure group were
exposed
to 250 ppm for "a few weeks" and then the
exposure concentration was reduced to 150
ppm due to acute toxicity. A reliable TWA
concentration cannot be determined based on
the information available in this report,
IRFMN (1978) suggested that the change
occurred after 12 weeks of exposure. If this
is accurate, then the TWA exposure
concentration for the high exposure group
was 200 ppm.
Significant decrease in segmented neutrophils in the high
exposure group in males; no other hematological changes
were observed; serum liver and kidney chemistry changes
either did not reach statistical significance, showed no
clear relation to exposure, concentration, and/or were not
biologically significant; no urinary changes were
observed.
1,2-Dichloroethane
Mortality (Rats):
NOAEL: 654
Mortality (Mice):
NOAEL: 368
Nagano et al. (2006)
F344 Rats - Both sexes
6 hours/day 5 days/week 104 weeks total, (0,
10, 40, 160 ppm; 0, 41, 164, or 654 mg/m3)
Cij:BDFl Mice - Both sexes
6 hours/day 5 days/week 104 weeks total, 0,
10, 30, 90 ppm; 0, 41, 123, or 368 mg/m3)
Endpoints evaluated included mortality, clinical signs of
toxicity, body weight, food consumption, hematology,
blood biochemistry, urinalysis, organ weight, gross
necropsy of organs & histopathology. No significant
effects reported.
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Chemical-Endpoint
POD
(mg/m3)
Study Parameters
Comments
1,2-Dichloroethane
Immune/Hematological,
Nutritional/Metabolic,
Liver, Mortality &
Kidney
(Rats/Rabbits/Guinea
Pigs/Cats):
NOAEL: 405
Hofmann et al. (1971a). Vaoor. SR Medium
SD Rats - Both sexes
Bunte Rabbits - Both sexes
Pirbright-White Guinea Pigs- Both sexes
Cats - Both sexes
6 hours/day 5 days/week 17
weeks, (0, 100 ppm; 0, 405 mg/m3)
The endpoints evaluated included mortality, body
weights, hematological effects (blood counts, not further
specified), liver effects (serum AST and ALT, liver
weight, and liver histology), and renal effects (BUN and
serum creatinine, urinary status - not further specified,
kidney weight, and kidney histology); bromsulphthalein
test in rabbits & cats does not indicate liver effects.
Rats, cats & guinea pigs: No significant effects reported.
One of 4 rabbits showed increased BUN and kidney
histology (not further specified); the observation of these
effects in 1 rabbit was not considered adverse (or of
questionable adversity).
1,2-Dichloroethane
Neurological, Liver, &
Mortality (Rabbits):
Not determined
Hematological, Kidney,
Liver, & Mortality
(Monkeys):
NOAEL: 405
Socnccr et al. (1951). Vaoor. SR Medium
Rabbit - Both sexes
7 hours/day 5 days/week
248 days*, (0, 100, 400 ppm; 0, 405, 1,619
mg/m3)
*The exact duration of exposure is unclear.
At 400 ppm rabbits "tolerated" exposure for
232 days" and at 100 ppm, rabbits
"tolerated" exposure for 248 days without
signs of adverse effects; the time of
termination is not specified.
Monkeys - Males
7 hours/day 5 days/week
212 days*, (0, 100, 400 ppm; 0, 405, 1,619
mg/m3)
*At 400 ppm both Monkeys were killed in a
moribund state after 8 and 12 exposures,
respectively. The duration noted above
applies only to the 100 ppm group.
No significant effects reported in rabbits;
histopathological changes reported in the liver and kidney
in monkeys; mortality observed in rats and guinea pigs;
uncertain signs of body weight changes, and possible
signs of liver and kidney toxicity in guinea pigs but the
data either did not show dose-response, or quantal data for
these endpoints or incidence values and a statement
whether any control animals exhibited these changes were
not included.
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Chemical-Endpoint
POD
(mg/m3)
Study Parameters
Comments
Wistar Rats - Both sexes
7 hours/day 5 days/week
212 days*, (0, 100, 400 ppm; 0, 405, 1,619
mg/m3)
* Although all exposure groups were intended
for chronic duration exposures, animals at
the high exposure level died within 14 days
(females) and 56 days (males).
Guinea Pigs - Both sexes
7 hours/day 5 days/week
248 days, (0, 100, 200, 400 ppm; 0, 405, 809,
1,619 mg/m3)
7754
7755
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5.2.6.2 Endpoint Derivation for Carcinogenic Dose-Response Assessment
1,2-Dichloroethane IUR for Inhalation Exposures (Read-Across to 1,1-Dichloroethane)
In 1987, the IRIS program derived an IUR of 2.6x 10~5 (per |ig/m3) based on route-to-route extrapolation
from the oral CSF derived at the same time. The inhalation cancer bioassay by Nagano et al. (2006) was
not available at the time of the IRIS assessment.
IUR estimates based on the tumor data sets in Nagano et al. (2006) were calculated using the following
equation (Equation 5-12):
Equation 5-12.
IUR = BMR/HEC
Where:
BMR = benchmark response
HEC = human equivalent concentration in |ig/m3
A BMR of 10 percent extra risk was selected for all datasets. HECs were calculating using the ratio of
blood:gas partition coefficients, as shown in Appendix M.1.2. Gargas and Andersen (1989) estimated
blood:air partition coefficients for 1,2-dichloroethane of 19.5 and 30.4 in humans and rats, respectively.
Because the rat partition coefficient is greater than the human partition coefficient, the default ratio of
1 is used in the calculation in accordance with U.S. EPA (1994) guidance. A blood:air partition
coefficient for mice was not available from the literature reviewed; thus, the default ratio of 1 was used
to calculate HECs for data in mice.
Details of the BMD modeling are provided in Draft Risk Evaluation for 1,1-Dichloroethane -
Supplemental Information File: Benchmark Dose Modeling (U.S. EPA. 2024c).
and the BMCL, HEC, and IUR estimate for each dataset is shown Table 5-48.
Table 5-48. IUR Estimates for Tumor Data from Nagano et al. (2006) Study of 1,2-Dichloroethane
Using Linear Low-Dose Extrapolation Approach
Species
and Sex
Tumor Type
Selected Model
BMCL10%
(ppm)
BMCL10%
(jig/m3)
HEC
(jig/m3)
IUR
Estimate
(Ug/m3)1
Male
rats
Subcutaneous fibroma
Multistage 1-degree
7
28,332
28,332
3.5E-06
Mammary gland
fibroadenomas
Multistage 1-degree
17
68,807
68,807
1.5E-06
Mammary gland
fibroadenomas and
adenomas combined
Multistage 3-degree
15
60,712
60,712
1.6E-06
Peritoneal mesothelioma
Multistage 3-degree
19
76,901
76,901
1.3E-06
Combined mammary gland,
subcutaneous, and
peritoneum tumors
MS Combo
5
20,237
20,237
4.9E-06
Female
rats
Subcutaneous fibroma
Multistage 1-degree
17
68,807
68,807
1.5E-06
Mammary gland adenomas
Multistage 1-degree
9
36,427
36,427
2.7E-06
Mammary gland
fibroadenomas
Multistage 1-degree
8
32,380
32,380
3.1E-06
Mammary gland
fibroadenomas and
adenomas combined
Multistage 1-degree
5
20,237
20,237
4.9E-06
Mammary gland
adenocarcinoma
Multistage 3-degree
23
93,091
93,091
1.1E-06
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Species
and Sex
Tumor Type
Selected Model
BMCL10%
(ppm)
BMCL10%
(jig/m3)
HEC
(jig/m3)
IUR
Estimate
(Ug/m3)1
Mammary gland
fibroadenomas adenomas,
and adenocarcinomas
combined
Multistage 1-degree
4
16,190
16,190
6.2E-06
Combined mammary gland
and subcutaneous tumors
MS Combo
4
16,190
16,190
6.2E-06
Female
mice
Bronchiolo -alveolar
adenomas
Multistage 3-degree
9
36,427
36,427
2.7E-06
Bronchiolo -alveolar
carcinomas
Multistage 2-degree
14
56,664
56,664
1.8E-06
Bronchiolo -alveolar
adenomas and carcinomas
combined
Multistage 2-degree
7
28,332
28,332
3.5E-06
Mammary gland
adenocarcinomas
Multistage 3-degree
10
40,474
40,474
2.5E-06
Hepatocellular adenomas
Multistage 3-degree
11
44,522
44,522
2.2E-06
Hepatocellular adenomas
and carcinomas combined
Multistage 2-degree
10
40,474
40,474
2.5E-06
Combined lung, mammary
gland, and liver tumors3
MS Combo
5
20,237
20,237
4.9E-06
" In addition to the tumor types shown in the table, EPA conducted BMD modeling on the combined incidence of lung,
mammary gland, and liver tumors and endometrial stromal polyps to evaluate whether including the polyps would result in
a lower BMCL10%. The BMCL10% for combined tumors with polyps was 5 ppm (20 ng/m3), unchanged from the
BMCL10% without the polyps.
The highest estimated IUR is 6,2/ 10 6 (per (J,g/m3) for combined mammary gland adenomas,
fibroadenomas, and adenocarcinomas and subcutaneous fibromas in female rats in the inhalation study
by Nagano et al. (2006).
CSF for Oral Exposures
The IRIS program derived an oral CSF of 9.1 x 10~2 (per mg/kg-bw/day) for 1,2-dichloroethane in 1987
based on the incidence of hemangiosarcomas in male rats in the chronic bioassay by NTP (1978).
however, this study did not pass EPA systematic review. The oral CSF for male mice based on
hepatocarcinomas was 6,2/ 10 3 (per mg/kg-bw/day) in a reliable study NTP (1978). No oral cancer
bioassays of 1,2-dichloroethane have been published since the IRIS assessment. The IRIS CSF was
derived using time-to-tumor modeling to account for intercurrent mortality of the rats in the NTP (1978)
study. No updates to the time-to-tumor modeling approach have been made since the 1987 assessment.
Hemangiosarcomas in male rats were determined to be the most sensitive species, strain, and site,
however this study was deemed unacceptable by EPA systematic review. Although CSF does not
account for other tumor types induced by 1,2-dichloroethane in the male rat, there is currently no time-
to-tumor modeling approach available that accounts for multiple tumor types. Therefore, the oral CSF
for 1,2-dichloroethane from the reliable NTP mouse cancer study NTP (1978) was selected for use in
assessment of cancer risks associated with exposure to 1,1-dichloroethane.
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Dose (nig/kg/day)
Figure 5-7. Hepatocellular Carcinoma Dose Response in Mice for Oral Exposure to 1,2-
Dichloroethane NTP (1978)
CSF for Dermal Exposures
There are no reliable dermal cancer studies of 1,2-dichloroethane; thus, the CSF for 1,2-dichloroethane
was obtained from route-to-route extrapolation using oral data. There are uncertainties associated with
extrapolation from both oral and inhalation. Use of an oral POD for dermal extrapolation may not be
preferred for chemicals known to undergo extensive liver metabolism because the "first-pass effect" that
directs intestinally absorbed chemicals directly to the liver applies only to oral ingestion. In contrast, the
accuracy of extrapolation of inhalation toxicity data for dermal PODs is dependent on assumptions about
inhalation exposure factors such as breathing rate and any associated dosimetric adjustments. Whole-body
inhalation studies may also already be incorporating some level of dermal absorption. Given these competing
uncertainties, in the absence of data to support selection of either the oral CSF or inhalation IUR, the method
resulting in the most protective dermal CSF was selected. The value of the oral CSF is 6.2xl0~2 (per
mg/kg-bw/day). For comparison, a CSF of 3.3'10 2 (per mg/kg-bw/day) was obtained using route-to-
route extrapolation from the IUR of 6.0 x 10 6 per jjg/m3 (6.0x10 1 per nig/m3) as follows:
Dermal CSF (per mg/kg-bw/day) = 6,0/10 3 (per mg/m3) * (80 kg/14.7 nrVday)
= 3.3 10 2 (per mg/kg-bw/day)
The more protective value of 6.2x 10~2 per mg/kg-bw/day based on the oral CSF was selected for the
dermal CSF.
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Oral Slope Factor
An oral cancer slope factor of 6.2xl0~2 (mg/kg)/day was calculated from a well conducted 1,2-
dichloroethane mouse cancer study from data on hepatocellular carcinomas in male mice based on the
excellent dose response for 1,2-dichloroethane (U.S. EPA. 1987a). This cancer slope factor can also be
utilized for dermal exposures. Alkyl halides, such as 1,2-dichloroethane and 1,1-dichloroethane, are
considered to be direct acting alkylating agents. Thus, it is considered to be hypothetical the relevance of
metabolic saturation of liver metabolic capacity for the formation of oncogenic intermediates (OECD.
2002). OncoLogic software categorizes 1,2-dichloroethane as a moderate concern and 1,1-
dichloroethane as a low-moderate concern for carcinogenicity based on their potential as biological
alkylating agents. Geminal alkyl halides such as 1,1-dichloroethane are less chemically reactive than
vicinal alkyl halides such as 1,2-dichloroethane. Thus, the 1,2-dichloroethane mouse cancer study
provides human health protective analog data for the 1,1-dichloroethane cancer assessment.
The cancer database for 1,1-dichloroethane was inadequate for both the oral and inhalation routes. 1,1-
Dichloroethane presented data gaps for cancer slope factors so an analysis of other chlorinated solvents
as analogs for read-across data was performed. This analysis considered structural similarities, physical-
chemical properties and toxicological similarities which resulted overall that 1,2-dichloroethane was
selected as an analog based on these various parameters as described in Appendix J.
The data gap for 1,1-dichloroethane is based on the lack of a reliable cancer study. The 1,1-
dichloroethane results were compared to 1,2-dichloroethane results in the cancer studies. 1,2-
dichloroethane has several high-quality cancer studies available for data read-across. The chronic oral
cancer studies performed by NTP (1978) qualitatively resulted in the same tumor types or pre-cancerous
lesions as seen in the bioassays of its isomer 1,1-dichloroethane (i.e., hepatocellular carcinomas,
endometrial polyps, hemangiosarcomas, etc). Thus, the oral cancer slope factor for the 1,2-
dichloroethane mouse study was selected for read-across to 1,1-dichloroethane (NTP. 1978). The
Nagano 2006 inhalation study provided a reliable cancer study for 1,2-dichloroethane to derive the IUR
value for read-across to 1,1-dichloroethane and produced similar tumor types as the oral NTP study on
1,2-dichloroethane (Nagano et al.. 2006).
5.2.6.3 PODs for Non-cancer and Cancer Human Health Hazard Endpoints
Table 5-49, Table 5-50, and Table 5-51 list the non-cancer PODs and corresponding HECs, HEDs, and
UFs that EPA used in the draft 1,1-dichloroethane risk evaluation to estimate risks following acute,
short-term/sub chronic, and chronic exposure, respectively. Table 5-52 provides the cancer PODs for
evaluating lifetime exposure.
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Table 5-49. PODs and Toxicity Va
ues Used to Estimate Non-cancer Risks for Acul
te Exposure Scenarios"
Target
Organ/
System "
Species/
Gender
Duration/
Route
Study
POD/Type
Effect
Worker
HEC4
(ppm)
[mg/m3]
Continuous
HEC4
(ppm)
[mg/m3]
Worker
HED c
(mg/kg-
bw/day)
Continuous
HED c
(mg/kg-
bw/day)
Uncertainty
Factors g
Total
Uncertainty
Factors
Reference
Data
Quality
Renal
Mice
(male)
Oral
1,2-dichloroethane
data
1 -day oral gavage
BMDLio
= 153
mg/kg
BMD = 270
mg/kg
Increased
kidney weight
N/A
N/A
19.9
19.9
UFa = 3
UFh = 10
UFl = 1
UFs = 1
UFd = 1
30 d
Storer et al. (1984)
High
Neurological
Rats
(males
and
females
combinec
Inhalation
1,2-dichloroethane
data
8-hour inhalation
BMCio =
48.9 mg/m3
or 12.1 ppm
Degeneration
with necrosis
of the
olfactory
mucosa
10.14 ppm
(41.1
mg/m3)
2.42 ppm
(9.78 mg/m3)
N/A
N/A
UFa = 3
UFh = 10
UFl = 1
UFs = 1
UFd = 1
30 e
Dow Chemical
(2006b)
High
Renal
Mice
(male)
Dermal
(extrapolated from
oral)
1,2-dichloroethane
data
1 -day oral gavage
BMDLio
= 153
mg/kg
BMD=270
mg/kg
Increased
kidney weight
N/A
N/A
19.9
19.9
UFa = 3
UFh = 10
UFl = 1
UFS = 1
UFd = 1
30f
Storer et al. (1984)
High
"See Section 5.2.1.2 for details.
4 BMCL10 of 48.9 mg/m3 continuous adjusted x RGDR value (0.2) = 9.78 mg/m3 for the HEC for continuous (adjusted for 24 hours). The HEC for the worker is the HECCOnt x 4.2
(hours in a week divided by the # of working hours in a week; 168/40) = 60.1 mg/m3. Both HEC worker and continuous were converted to ppm by dividing by a factor of 4.05 (based
24.45/MW).
c BMDLio of 153 x DAF (0.13 BW3/4for mice) = 20.3 mg/kg. All oral PODs were first adjusted to 7 days/week and inhalation PODs adjusted to 24 hours/day, 7 days/week
(continuous exposure). All continuous oral PODs were then converted to HEDs using DAFs. Dermal PODs were set equal to the oral HED. It is often necessary to convert between
ppm and mg/m3 due to variation in concentration reporting in studies and the default units for different OPPT models. Therefore, EPA presents all inhalation PODs in equivalents of
both units to avoid confusion and errors. PODs converted for use in worker exposure scenarios were adjusted to 8 hours/day, 5 days/week and converted to HECs.
d No PODs were identified from acute exposure by the oral route to 1,1-dichloroethane; therefore, read-across from 1,2-dichloroethane was used to identify a POD. An acute-
duration oral HED for both worker and continuous exposure of 19.9 mg/kg-bw/day was used for risk assessment of acute oral exposure, with a total uncertainty factor of 30, based on
a combination of uncertainty factors: 3 for interspecies extrapolation when a dosimetric adjustment is used and 10 for human variability.
fNo PODs were identified from acute exposure by the inhalation route to 1,1-dichloroethane; therefore, read-across from 1,2-dichloroethane was used to identify a POD. An acute-
duration inhalation HEC of 10.14 ppm for worker and 2.42 ppm for continuous exposures was used for risk assessment of acute inhalation exposure, with a total uncertainty factor of
30, based on a combination of uncertainty factors: 3 for interspecies extrapolation when a dosimetric adjustment is used and 10 for human variability.
^No PODs were identified from acute exposure by the dermal route to 1,1-dichloroethane; therefore, route-to-route extrapolation from the oral route was used to identify a POD. An
acute-duration dermal HED for both worker and continuous exposure of 19.9 mg/kg-bw/day was used for risk assessment of acute dermal exposure, with a total uncertainty factor of
30, based on a combination of uncertainty factors: 3 for interspecies extrapolation when a dosimetric adjustment is used and 10 for human variability.
g UF = uncertainty factor; UFa = extrapolation from animal to human (interspecies); UFh = potential variation in sensitivity among members of the human population (intraspecies);
UFl = use of a LOAEL to extrapolate a NOAEL; UFs = use of a short-term study for long-term risk assessment; UFd = to account for the absence of key data (i.e., lack of a critical
study). A default value of 1 was applied for the UFd due to a complete database for 1,2-dichloroethane.
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7865 Table 5-50. POPs and Toxicity Values Used to Estimate Non-cancer Risks for Short-Term Exposure Scenarios"
Target
Organ
System
Species
Duration/
Route
Study
POD/
Type
Effect
Worker
HEC4
(ppm)
[mg/m3]
Continuous
HEC
(ppm)
[mg/m3]
Worker
HED c
(mg/kg-
bw/day)
Continuous
HED c
(mg/kg-
bw/day)
Uncertainty
Factors g
Total
Uncertainty
Factors
Reference
Data
Quality
Immune
System
Mice
(male)
Oral
1,2-
dichloroethane
data
14-days oral
gavage
LOAELadj —
4.89 mg/kg
Suppression of
immune
response
(AFCs/spleen)
N/A
N/A
0.890
0.636
LTFa = 3
UFh= 10
UFl= 3
LTFs = 1
UFd= 1
O
O
Munson et
al. (1982)
High
Reproductive
Mice
(male)
Inhalation
1,2-
dichloroethane
data
4-week
morphological
analysis of sperm
parameters/
bmcl5=
21.2 mg/m3
Decreases in
sperm
concentration
22.0
ppm
(89.0
mg/m3)
5.2 ppm
(21.2
mg/m3)
N/A
N/A
LTFa = 3
UFh= 10
LTFl = 1
LTFs = 1
LTFd = 1
30-
Zhang et al.
(2017)
High
Immune
System
Mce
(male)
Dermal
(extrapolated from
oral)
1,2-dichloroethane
data
14-days oral gavage
LOAELadj ~
4.89 mg/kg
Suppression of
immune
response
(AFCs/spleen)
N/A
N/A
0.890
0.636
LTFa = 3
UFh= 10
LTFl = 3
LTFs = 1
LTFd = 1
10 Of
Munson et
al. (1982)
High
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Target
Organ
System
Species
Duration/
Route
Study
POD/
Type
Effect
Worker
HEC4
(ppm)
[mg/m3]
Continuous
HEC
(ppm)
[mg/m3]
Worker
HF.D'
(mg/kg-
bw/day)
Continuous
HED c
(mg/kg-
bw/day)
Uncertainty
Factors g
Total
Uncertainty
Factors
Reference
Data
Quality
7866
7867
a See Section 5.2.1.2.1 for details.
b BMCL5 = 21.2 mg/m3 was adjusted to continuous adjusted (with no respiratory effects, there is no RGD; the blood:air ratio = 1, based on eq M-7 from Appendix M; therefore,
the HECcont is the same as the adjusted POD of 21.2 mg/m3. The HEC worker is the HECCOnt x 4.2 (hours in a week divided by the # of working hours in a week; 168/40) = 89.0
mg/m3. Both HEC worker and continuous converted to ppm divided by a factor of 4.05 (based 24.45/MW).
c All oral PODs were first adjusted to 7 days/week. All continuous oral PODs were then converted to HEDs using DAFs. Dermal PODs were set equal to the oral HED. It is often
necessary to convert between ppm and mg/m3 due to variation in concentration reporting in studies and the default units for different OPPT models. Therefore, EPA presents all
PODs in equivalents of both units to avoid confusion and errors. PODs converted for use in worker exposure scenarios were adjusted to 8 hours/day, 5 days/week and converted
to HECs.
d No PODs were identified from short-term/subchronic exposure by the oral route to 1,1-dichloroethane; therefore, read-across from 1,2-dichloroethane was used to identify a
POD. A short-term/subchronic-duration oral HED for worker of 0.890 mg/kg-bw/day and a HED for continuous exposure of 0.636 mg/kg-bw/day was used for risk assessment
of short-term/subchronic oral exposure, with a total uncertainty factor of 100, based on a combination of uncertainty factors: 3 for interspecies extrapolation when a dosimetric
adjustment is used, 10 for human variability, and 3 for use of a LOAEL to extrapolate a NOAEL (based on the dose-response).
e No PODs were identified from short-term/subchronic exposure by the inhalation route to 1,1-dichloroethane. Therefore, read-across from 1,2-dichloroethane was used to
identify a POD. A short-term/subchronic-duration inhalation HEC for worker exposure of 89.0 mg/m3, and a HEC for continuous exposure of 21.2 mg/m3, was used for risk
assessment of short-term/subchronic inhalation exposure, with a total uncertainty factor of 30, based on a combination of uncertainty factors: 3 for interspecies extrapolation when
a dosimetric adjustment is used and 10 for human variability.
f No PODs were identified from short-term/subchronic exposure by the dermal route to 1,1-dichloroethane; therefore, route-to-route extrapolation from the oral route was used
to identify a POD. A short-term/subchronic-duration dermal HED for worker of 0.890 mg/kg-bw/day and a HED for continuous exposure of 0.636 mg/kg-bw/day was used for
risk assessment of short-term/subchronic dermal exposure, with a total uncertainty factor of 100, based on a combination of uncertainty factors: 3 for interspecies extrapolation
when a dosimetric adjustment is used, 10 for human variability, and 3 for use of a LOAEL to extrapolate a NOAEL (based on the dose-response).
g UF = uncertainty factor; UFa= extrapolation from animal to human (interspecies); UFh = potential variation in sensitivity among members of the human population
(intraspecies); UFl = use of a LOAEL to extrapolate a NOAEL; UFs = use of a short-term study for long-term risk assessment; UFd = to account for the absence of key data (i.e.,
lack of a critical study). A default value of 1 was applied for the UFd due to a complete database for 1,2-dichloroethane.
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Table 5-51. POPs and Toxicity Values Used to Estimate Non-cancer Risks for Chronic Exposure Scenarios"
Target
Organ
System
Species
Duration/
Route
Study
POD/
Type
Effect
Worker
HEC
(ppm)
[mg/m3]
Continuous
HEC4
(ppm)
[mg/m3]
Worker
HED c
(mg/kg-
bw/day)
Continuous
HED c
(mg/kg-
bw/day)
Uncertainty
Factors g
Total
Uncertainty
Factors
Reference
Data
Quality
Immune
System
Mice
(male)
Oral
1,2-dichloroethane
data
14-days oral gavage
LOAELadj —
4.89 mg/kg
Suppression
of immune
response
(AFCs/spleen)
N/A
N/A
0.890
0.636
LTFa = 3
UFh= 10
UFl= 3
UFS= 10
UFd= 1
l,000rf
Munson et al.
(1982)
High
Reproductive
Mice
(male)
Inhalation
1,2-dichloroethane
data
4-week
morphological
analysis of sperm
parameters/
inhalation
bmcl5=
21.2 mg/m3
Decreases in
sperm
concentration
22.0 ppm
(89.0
mg/m3)
5.2 ppm
(21.2 g/m3)
N/A
N/A
LTFa = 3
UFh= 10
LTFl = 1
UFS= 10
LTFd = 1
300"
Zhang et al.
(2017)
High
Immune
System
Mce
(male)
Dermal
(extrapolated from
oral)
1,2-dichloroethane
data
14-days oral gavage
LOAELadj ~
4.89 mg/kg
Suppression
of immune
response
(AFCs/spleen)
N/A
N/A
0.890
0.636
LTFa = 3
UFh= 10
LTFl = 3
UFS= 10
LTFd = 1
l,00(y
Munson et al.
(1982)
High
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Target
Organ
System
Species
Duration/
Route
Study
POD/
Type
Effect
Worker
HEC
(ppm)
[mg/m3]
Continuous
HEC4
(ppm)
[mg/m3]
Worker
HED c
(mg/kg-
bw/day)
Continuous
HED c
(mg/kg-
bw/day)
Uncertainty
Factors g
Total
Uncertainty
Factors
Reference
Data
Quality
" See Section 5.2.1.2.1 for details.
4 BMCL5 =21.2 mg/m3 was adjusted to continuous adjusted (with no respiratory effects, there is no RGD; the blood:air ratio = 1, based on eq M-7 from Appendix M; therefore, the
HECcont is the same as the adjusted POD of 21.2 mg/m3. The HEC worker is the HECCOnt x 4.2 (hours in a week divided by the # of working hours in a week; 168/40) = 89.0 mg/m3.
Both HEC worker and continuous converted to ppm divided by a factor of 4.05 (based 24.45/MW).
c All oral PODs were first adjusted to 7 days/week. All continuous oral PODs were then converted to HEDs using DAFs. Dermal PODs were set equal to the oral HED. It is often
necessary to convert between ppm and mg/m3 due to variation in concentration reporting in studies and the default units for different OPPT models. Therefore, EPA presents all
PODs in equivalents of both units to avoid confusion and errors. PODs converted for use in worker exposure scenarios were adjusted to 8 hours/day, 5 days/week and converted to
HECs.
d No PODs were identified from chronic exposure by the oral route to 1,1-dichloroethane; therefore, read-across from 1,2-dichloroethane was used to identify a POD. A chronic-
duration oral HED for worker of 0.890 mg/kg-bw/day and a HED for continuous exposure of 0.636 mg/kg-bw/day was used for risk assessment of chronic oral exposure, with a
total uncertainty factor of 1000, based on a combination of uncertainty factors: 3 for interspecies extrapolation when a dosimetric adjustment is used, 10 for human variability, 3 for
the use of a LOAEL to extrapolate a NOAEL (based on the dose-response), and 10 for extrapolating from a subchronic study duration to a chronic study duration.
fNo PODs were identified from chronic exposure by the inhalation route to 1,1-dichloroethane. Therefore, read-across from 1,2-dichloroethane was used to identify a POD. The
chronic-duration inhalation HEC for worker exposure of 89.0 mg/m3, and a HEC for continuous exposure of 21.2 mg/m3, was used for risk assessment of chronic inhalation
exposure, with a total uncertainty factor of 300, based on a combination of uncertainty factors: 3 for interspecies extrapolation when a dosimetric adjustment is used, 10 for human
variability, and 10 for extrapolating from a subchronic study duration to a chronic study duration.
/No PODs were identified from chronic exposure by the dermal route to 1,1-dichloroethane; therefore, route-to-route extrapolation from the oral route was used to identify a
POD. A chronic-duration dermal HED for worker of 0.890 mg/kg-bw/day and a HED for continuous exposure of 0.636 mg/kg-bw/day was used for risk assessment of chronic
dermal exposure, with a total uncertainty factor of 1000, based on a combination of uncertainty factors: 3 for interspecies extrapolation when a dosimetric adjustment is used, 10
for human variability, 3 for the use of a LOAEL to extrapolate a NOAEL (based on the dose-response), and 10 for extrapolating from a subchronic study duration to a chronic
study duration.
g UF = uncertainty factor; UFa= extrapolation from animal to human (interspecies); UFh = potential variation in sensitivity among members of the human population
(intraspecies); UFl = use of a LOAEL to extrapolate a NOAEL; UFs = use of a short-term study for long-term risk assessment; UFdb = to account for the absence of key data (i.e.,
lack of a critical study). A default value of 1 was applied for the UFo due to a complete database for 1,2-dichloroethane.
7869
Page 299 of 664
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7870
7871
7872
7873
7874
7875
7876
7877
7878
7879
7880
7881
7882
7883
7884
7885
7886
7887
7888
7889
7890
7891
7892
7893
7894
7895
7896
7897
PUBLIC RELEASE DRAFT
July 2024
Table 5-52. Cancer PODs for 1,1-Dichloroethane Lifetime Exposure Scenarios - Read-Across
from 1,2-Dichloroethane Data
Exposure
Assumption "
Oral Slope
Factor b
Dermal Slope
Factor b
Inhalation Unit
Risk c
Drinking Water
Unit Risk d
Extra Cancer Risk
Benchmark
Continuous
Exposure
0.062 per
mg/kg/day
0.062 per
mg/kg/day
7.1E-06 (per
pg/m3)
2.9E-2 (per ppm)
1.8E-06 per ug/L
1E-06 (general
population)
Worker
0.062 per
mg/kg/day
0.062 per
mg/kg/day
2.4E-06 (per
pg/m3)
9.5E-3 (per ppm)
1.8E-06 per ug/L
1E-04 (occupational)
° Cancer slope factor and unit risk will be derived based on continuous exposure scenarios. Due to the exposure
averaging time adjustments incorporated into lifetime exposure estimates, separate cancer hazard values for
occupational scenarios are not required.
b The oral CSF for male mice based on hepatocarcinomas was 6.2E-02 (per mg/kg-bw/day) in a reliable study NTP
(1978). Read-across using cancer PODs from 1,2-dichloroethane based on hepatocellular carcinomas in male mice
NTP (1978). Due to scarcity of data, route-to-route extrapolation from the oral slope factor is used for the dermal
route.
c Read-across using cancer inhalation PODs from 1,2-dichloroethane based on based on combined mammary gland
adenomas, fibroadenomas, and adenocarcinomas and subcutaneous fibromas in female rats (Nagano et al.. 2006).
''Therefore, the oral CSF for 1,2-dichloroethane from the reliable NTP mouse cancer study NTP (1978) was selected
for use in assessment of cancer risks associated with exposure to 1,1-dichloroethane. This mouse CSF was used to
calculate a drinking water unit risk of 1.8 E-06 per ug/L using a drinking water intake of 2 L/day and body weight of
70 kg.
5.2.6.4 Human Health Hazard Values Used by Other Agencies
Historically, offices across EPA and other agencies (ATSDR), have developed their own assessments
for 1,1- and 1,2-dichloroethane. A comparison of these assessments is outlined in Table 5-53 for non-
cancer based on exposure duration and route.
EPA first reviewed existing assessments of 1,1-and 1,2-dichloroethane conducted by regulatory and
authoritative agencies such as ATSDR (2015) and ATSDR (20221 as well as several systematic reviews
of studies of 1,2-dichloroethane published by U.S. EPA Integrated Risk Information System (IRIS)
program (U.S. EPA. 1990. 1987b) and U.S. EPA Provisional Peer-Reviewed Toxicity Values (U.S.
EPA. 2010. 2006b).
With regard to the U.S. EPA Integrated Risk Information System (IRIS) program (U.S. EPA. 1990.
1987b) assessments for 1,1- and 1,2-dichloroethane, non-cancer exposure durations/routes were not
assessed. Upon evaluation of the (ATSDR. 2015) Toxicological Profile for 1,1-Dichloroethane and U.S.
EPA Provisional Peer-Reviewed Toxicity Values for 1,1-Dichloroethane ATSDR (2022) Toxicological
Profile for 1,2-Dichloroethane and U.S. EPA Provisional Peer-Reviewed Toxicity Values for 1,1-
Dichloroethane (U.S. EPA. 2006b) and U.S. EPA Provisional Peer-Reviewed Toxicity Values for 1,1-
Dichloroethane (U.S. EPA. 2010). the studies identified for minimal risk level (MRL) and provisional
values, respectively, by these assessment were evaluated by the Draft Systematic Review Protocol
Supporting TSCA Risk Evaluations for Chemical Substances (U.S. EPA. 2021b). While there are many
areas of agreement with these assessments, these assessments either did not derive values for exposure
durations and/or routes, used studies that were not considered as "sensitive endpoints", or used studies
that were identified as "Uninformative" based on systematic review for the subchronic duration
scenarios.
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7898
7899
7900
7901
7902
7903
7904
7905
7906
7907
7908
7909
7910
7911
7912
7913
7914
7915
7916
7917
7918
7919
7920
7921
7922
7923
7924
7925
7926
7927
7928
7929
7930
7931
7932
7933
7934
7935
7936
7937
7938
7939
7940
7941
7942
7943
7944
PUBLIC RELEASE DRAFT
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For 1,1-dichloroethane, no provisional value was derived in (U.S. EPA. 2006b) for the acute duration for
any exposure route and the study by (Muralidhara et al.. 2001). based on sedation in male rats, was
identified for the oral subchronic and chronic duration. This study was not used as the POD based on a
NOAEL of 714 mg/kg/day in male rats with limited assessment of neurotoxicity.
Furthermore, as the database for 1,1-dichloroethane contained data gaps and the use of the 1,2-
dichloroethane database was used to fill those gaps, a thorough evaluation for both ATSDR (2022) and
(U.S. EPA. 2010). that identified the 13-week study by (NTP. 1991). where male and female F344/N,
Sprague Dawley, and Osborne-Mendel rats as well as B6C3F1 mice exposed to 1,2-dichloroethane in
drinking water was used to derive their respective values. A significant dose-related increase in kidney
weight and the kidney-body-ratio of female F344 rats was identified at 58 mg/kg/day among the three
rat strains. This study was considered as a potential candidate for POD derivation, however, the daily
intake doses were estimated on a mg/kg body weight basis and not measured throughout the duration of
exposure. The means by which the dosage estimates were calculated was by dividing the mean water
consumption over the 13-week study by the initial and final body weights of ten animals. Additionally,
weight gain depression was seen in males and females in the two higher dose groups throughout the
study and was likely caused by dehydration due to poor palatability of the formulated drinking water.
The study also indicated that water consumption was substantially decreased with increasing dose.
According to the study, a decrease of as much as 60 percent in water intake was also seen in both male
and female Osborne-Mendel rats at the highest concentration of 8000 ppm (a range of 500 -725
mg/kg/day) that indicates that the dose received by all exposed animals was less than the target dose.
The authors indicate that as water intake was reduced at most exposure levels, equivalent exposure did
not, however, occur at different dose levels within a strain. Due to the uncertainty regarding the
delivered dose and the inherit volatility associated with 1,2-dichloroethane, it was not recommended
using this drinking water study for this dose-response assessment.
(NTP. 1991). however, also included a 13-week gavage study that was rated high by systematic review
and considered for a POD for subchronic exposures based on kidney weight (30 mg/kg/day LOAEL
males; 75 mg/kg/day LOAEL females), however, the study had a higher POD via oral gavage, and was
not ultimately selected as the use of the most sensitive endpoint, immunosuppression from Munson et al.
(1982) (LOAEL 4.9 mg/kg-day), was considered instead. In support, the 1,2-dichloroethane ATSDR
(2022) authoritative document also concluded that "the immune system was the most sensitive target for
short-term exposure to 1,2-dichloroethane by both the inhalation and oral routes in mice."
With regard to identification of a subchronic provisional reference concentration (p-RfC) in (U.S. EPA.
2010) for 1,-2-dichloroethane, the occupational Kozik (1957) study used identified in this assessment
was rated "Uninformative" by systematic review based on a number of limitations (poor data and test
method reporting, lack of description of the analytical methodology, limited quantitative data and
statistical analyses, unstated criteria for diagnosis of disease, limited number of study participants and no
matched control group, lack of control for potential confounding, lack of exposure duration
information). Furthermore, Kozik (1957) did not report any data that could be used for BMD modeling.
Additionally, PPRTV also commented on the confidence of the study as well as confidence in the
calculated p-RfC as being very low. This study was also used for the chronic p-RfC irrespective of this
low confidence with additional uncertainty factor of 10 for the duration adjustment.
Therefore, studies only studies that received a rating of high and medium by systematic review were
considered for PODs as outlined in Appendix M.2 with study evaluation and selection rationale.
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7945 Table 5-53. Non-Cancer Human Health Hazard Values Used by Other Agencies and EPA Offices
OPPT/ECRAD
Exposure
Solvent
Oral
Inhalation
Dermal
Comments
Acute
u-
Dichloroethane
1,1-Dichlorothane human
and animal data inadequate -
endpoints for animal data
near the limit dose. Used
read-across to 1,2-
dichlorothane animal data
for more biologically
relevant and sensitive PODs.
1,1 -Dichlorothane
human and animal data
inadequate. Used read-
across to 1,2-
dichlorothane animal
data for more
biologically relevant and
sensitive PODs.
No data by this route for
1.1-dichlorothane or 1,2-
dichlorothane. Used
route-to-route
extrapolation from oral
1.2-dichlorothane data.
1,2-
Dichloroethane
POD BMDLio
= 153 mg/kg based on
increased kidney weight via
gavage (Storer et al.. 1984).
UF = 30
POD BMCio = 48.9
mg/m3 or 12.1 ppm
based on olfactory
necrosis (Dow
Chemical. 2006b).
UF = 30
POD BMDLio
= 153 mg/kg based on
increased kidney weight
(Storer et al.. 1984).
UF = 30
Subchronic
u-
Dichloroethane
1,1-Dichloroethane human
and animal data inadequate.
Used read-across to 1,2-
dichlorothane animal data
for more biologically
relevant and sensitive PODs.
1,1 -Dichloroethane
human and animal data
inadequate. Used read-
across to 1,2-
dichlorothane animal
data for more
biologically relevant and
sensitive PODs.
No data by this route for
1.1-dichloroethane or
1.2-dichloroethane. Used
route-to-route
extrapolation from oral
1,2-dichloroethane data.
1,2-
Dichloroethane
POD = LOAELadj = 4.89
mg/kg based on
immunosuppression in a 14-
dav aavaae studv (Munson
et al.. 1982).
UF = 100
pod = bmcl5=
21.2 mg/m3 based on
decreases in sperm
concentration (Zhang et
al.. 2017).
UF = 30
POD = LOAELadj = 4.89
mg/kg based on
immunosuppression in a
14-day gavage study
(Munson et al.. 1982).
UF= 100
(ATSDR. 2022) identified immunosuroression
as the most sensitive endpoint - however,
ATSDR characterized the Munson et al. (1982)
study as an acute study and therefore it was
excluded from derivation of MRLs for
subchronic and chronic exposures.
Chronic
1,1-
Dichloroethane
1,1-Dichloroethane human
and animal data inadequate.
Used read-across to 1,2-
dichloroethane animal data
for more biologically
relevant and sensitive PODs.
1,1 -Dichloroethane
human and animal data
inadequate. Used read-
across to 1,2-
dichloroethane animal
data for more
biologically relevant and
No data by this route for
1.1-dichloroethane and
inadequate data for 1,2-
dichloroethane. Used
route-to-route
extrapolation from oral
1.2-dichlorothane data.
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OPPT/ECRAD
Exposure
Solvent
Oral
Inhalation
Dermal
Comments
sensitive PODs.
Chronic
1,2-
Dichloroethane
POD = LOAELadj = 4.89
mg/kg based on
POD = BMCLs =
21.2 mg/m3 based on
POD = LOAELadj = 4.89
mg/kg based on
A standard default of a UFS of 10 was added for
use of subchronic data for chronic duration.
immunosuppression in a 14-
day gavage
study (Munson et al.. 1982).
UF = 1,000 b
decreases in sperm
concentration (Zhang et
al.. 2017).
UF = 300
immunosuppression m a
14-day gavage study
(Munson et al.. 1982).
UF= 1,000
(ATSDR. 2022) identified immunosuppression
as the most sensitive endpoint - however,
ATSDR characterized the Munson et al. (1982)
study as an acute study and therefore it was
excluded from derivation of MRLs for
subchronic and chronic exposures.
IRIS (U.S. EPA. 1990. 1987b)
Acute
u-
Dichloroethane
Not assessed under IRIS
Not assessed under IRIS
Not assessed under IRIS
1,2-
Dichloroethane
Not assessed under IRIS
Not assessed under IRIS
Not assessed under IRIS
Subchronic
1,1-
Dichloroethane
Not assessed under IRIS
Not assessed under IRIS
Not assessed under IRIS
1,2-
Dichloroethane
Not assessed under IRIS
Not assessed under IRIS
Not assessed under IRIS
Chronic
1,1-
Dichloroethane
Not assessed under IRIS
Not assessed under IRIS
Not assessed under IRIS
1,2-
Dichloroethane
Not assessed under IRIS
Not assessed under IRIS
Not assessed under IRIS
PPRTV (U.S. EPA. 2010. 2006b)
Acute
u-
Dichloroethane
Did not derive a provisional
value
Did not derive a
provisional value
Did not derive a
provisional value
Database considered inadequate
1,2-
Dichloroethane
Did not derive a provisional
value
Did not derive a
provisional value
Did not derive a
provisional value
Database considered inadequate
1,1-
Dichloroethane
1,1-Dichlorothane animal
data was used. Data base is
Available inhalation data
in animals and humans
considered inadequate
Did not derive a
provisional value
OPPT/ECRAD did not use this study because
the endpoint/POD was based on a NOAELadj=
714 mg/kg/day, in male rats only, with limited
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OPPT/ECRAD
Exposure
Solvent
Oral
Inhalation
Dermal
Comments
Subchronic
Subchronic
lacking human data by the
oral route.
RfD = 2 mg/kg-day (by
dividing the NOAELadj of
714 mg/kg/day by the total
UF of 300) based sedation
(Muralidhara et al.. 2001) for
13 weeks.
UF = 300
for derivation of a RfC
provisional.
assessments of neurotoxicity, very close to the
limit dose of 1,000 mg/kg/day.
OPPT/ECRAD used read-across data from 1,2-
dichlorothane for this route and duration for a
more biologically relevant, sensitive, and
human health protective POD.
PPRTV commented confidence in the study is
medium (and a UFd of 3 was used in their total
UF calculation), and overall confidence in the
calculation of the provisional RfD is low.
1,2-
Dichloroethaiie
1,2-Dichlorothane animal
data was used. Database is
lacking human data by the
oral route.
RfD = 0.02 mg/kg-day based
on increased kidney weights
(NTP. 1991; Morgan et al..
1990). 90-dav drinking water
(DW)
UF = 3000
In context, the OPPT MRL
is 0.049 mg/kg/day based on
the Munson et al. (1982)
immunotoxicity POD of 4.89
mg/kg/day and a total UF of
100
1,2-Dichlorothane
animal data was not
used - human data was
selected as the only
feasible study for
subchronic durations.
RfC = 0.07 mg/m3
based on
neurobehavioral
impairment (Kozik.
1957)
UF = 300
In context, based on
decreased sperm count
in the Zhang et al.
(2017) studv with the
UF of 30, the OPPT
RfC = 0.71 mg/m3
Did not derive a
provisional value
For the oral route:
PPRTV used a UFd of 3 to account for
database inadequacies. OPPT/ECRAD did not
use the (NTP. 1991)/(Morgan et al.. 1990) DW
study as it rated "Uninfonnative" in our SR due
to a reported 59% decrease in dose at the end
of each day, as well as noted dehydration due
to decreased water consumption. Kidney
effects could be due to dehydration and not
direct result of chemical exposure. PPRTV
made no mention of the limitations of the DW
study.
PPRTV makes no mention of the gavage
portion of the (NTP. 1991)/ (Morgan et al..
1990).
Note: OPPT/ECRAD c
PPRTV commented d
For the inhalation route:
OPPT/ECRAD did not use the Kozik (1957)
study because it rated as "Uninfonnative" in
our SR based on a number of limitations (poor
data and test method reporting, lack of
description of the analytical methodology,
limited quantitative data and statistical
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OPPT/ECRAD
Exposure
Solvent
Oral
Inhalation
Dermal
Comments
analyses, unstated criteria for diagnosis of
disease, limited number of study participants
and no matched control group, lack of control
for potential confounding, lack of exposure
duration information). Kozik (1957) did not
report any data that could be used for BMD
modeling.
PPRTV commented"
Chronic
u-
Dichloroethaiie
1,1-Dichlorothane animal
was used. Data base is
lacking human data by the
oral route.
RiD = 0.2 mg/kg-day (by
dividing the NOAELadj of
714 mg/kg/day divided by
the total UF) based sedation
(Muralidhara et al.. 2001) for
13 weeks.
UF = 3,000
Available inhalation data
in animals and humans
considered inadequate
for derivation of a RfC
provisional value.
Did not derive a
provisional value
Same study and conclusions as for the
subchronic duration only added an additional
UF of 10 for use of subchronic study for
chronic duration to yield a total UF = 3,000.
1,2-
Dichloroethaiie
Did not derive a provisional
value.
RfC = 0.007 nig/in3
based on
neurobehavioral
impairment (Kozik.
1957)
UF = 3,000
In context, based on
decreased sperm count
in the Zhang et al.
(2017) studv with the
UF of 300, the OPPT
RfC = 0.071 lng/m3
Did not derive a
provisional value
For the RfD:
PPRTV commented
For the RfC:
Same study and conclusions as for the
subchronic duration only added an additional
UF of 10 for use of subchronic study for
chronic duration to yield a total UF = 3,000.
ATSDR (ATSDR. 2022. 2015)
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OPPT/ECRAD
Exposure
Solvent
Oral
Inhalation
Dermal
Comments
u-
Dichloroethane
Did not derive an MRL
Did not derive an MRL
Did not derive an MRL
Database was considered inadequate
Acute
1,2-
Dichloroethane
Did not derive an MRL
0.3 ppm based on
Degeneration, with
necrosis, olfactory
epithelium in rats
(Hotchkiss et al.. 2010;
Dow Chemical. 2006b);
BMCLm = 57
(BMCLhec = 9.2)
UF = 30
In context, OPPT
determined an MRL of
0.3 ppm
Did not derive an MRL
ATSDR did not use the Munson et al. (1982)
gavage study because of a difference in
classification of acute and subchronic between
ATSDR and EPA. ATSDR classifies a 14-day
study as "acute," and therefore it was not used
by them for subchronic or chronic POD
derivation.
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OPPT/ECRAD
Exposure
Solvent
Oral
Inhalation
Dermal
Comments
u-
Dichloroethaiie
Did not derive an MRL
Did not derive an MRL
Did not derive an MRL.
Database was considered inadequate
1,2-
Dichloroethaiie
0.2 mg/kg/day based on
kidnev weight in rats (NTP.
1991)/ (Morgan et al.. 1990).
Did not derive an MRL
Did not derive an MRL
OPPT/ECRAD did not use the drinking water
portion of either the Munson et al. (1982) or
(NTP. 1991)/(Morgan et al.. 1990) studies for
90-day drinking water (DW)
LOAEL = 58
identification of a POD. The (NTP.
1991)/(Morgan et al.. 1990) study identified
Subchronic
UF = 300
In context, the OPPT MRL
is 0.049 mg/kg/day based on
the Munson immunotoxicity
POD of 4.89 mg/kg/day and
a total UF of 100
kidney weight as a POD via DW (58 mg/kg).
The DW portion of the study rated
"Uninformative" in our SR. The rationale for
that rating is based on up to a 59% loss of
concentration at the end of each day, with a
60% decrease in water consumption which lead
to dehydration and therefore the kidney effects
could likely be artifacts of dehydration.
1,1-
Dichloroethaiie
Did not derive an MRL
Did not derive an MRL
Did not derive an MRL
Database was considered inadequate
Chronic
1,2-
Dichloroethane
Did not derive an MRL
Did not derive an MRL
Did not derive an MRL
According to AT SDR, data were insufficient to
derive an acute-duration provisional oral MRL
due to uncertainty about the validity of results
at the lowest effect level based on differences
in effect between gavage doses and drinking
water doses. Data were insufficient for the
derivation of a chronic-duration provisional
oral MRL as the most sensitive endpoint was
represented by a serious effect (such as death).
ATSDR concluded that the inhalation database
was inadequate for derivation of intermediate-
and chronic-duration inhalation MRLs.
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Exposure Solvent
Oral
Inhalation
Dermal
Comments
7946
a OPPT/ECRAD: Following an analysis, 1,2-dichlorothane (a close analog and isomer of 1,1-dichloroethane) was identified as an analog to be used for read-
across where toxicological data on 1,1-dichloroethane were inadequate or missing.
b Per EPA RfC/RfD Guidance Document (U.S. EPA. 2002b). UF's of up to 3,000 are acceptable. In the case of the RfC, the maximum UF would be 3,000,
whereas the maximum would be 10,000 for the RfD.
c OPPT/ECRAD used the gavage portion of the Munson et al. (1982) study to derive an oral POD for subchronic duration, as opposed to the gavage portion of
the (NTP. 1991)/ (Morgan et al.. 1990) study, as it represented a more biologically relevant and sensitive POD. PPRTV briefly mentions the Munson et al.
(1982) study.
d ppRXV commented confidence in the study (NTP. 1991)/ (Morgan et al.. 1990) is medium (a UFD of 3 was used in their total UF calculation), and overall
confidence in the calculation of the provisional RfD is medium.
'' PPRTV commented confidence in the study (Kozik. 1957) is very low (and a UFD of 3 was used in their total UF calculation), and overall confidence in the
calculation of the provisional RfC is low.
' PPRTV commented "In the absence of suitable chronic data, the POD from the subchronic (NTP. 1991) p-RfD could be used to derive the chronic p-RfD;
however, the composite UF would include the additional UFs of 10 for applying data from a subchronic study to assess potential effects from chronic exposure.
This would result in the large composite UF of greater than 3,000, thereby relegating this derivation of the chronic p-RfD to an appendix screening value."
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5.2.7 Weight of Scientific Evidence Conclusions for Human Health Hazard
The weight of scientific evidence supporting the human health hazard assessment is based on the
strengths, limitations, and uncertainties associated with the hazard studies identified. The weight of
scientific evidence is summarized using confidence descriptors: robust, moderate, slight, or
indeterminate. This approach is consistent with the Draft Systematic Review Protocol Supporting TSCA
Risk Evaluations for Chemical Substances (U.S. EPA. 2021b). When weighing and integrating evidence
to estimate the potential that 1,1-dichloroethane may cause a given non-cancer or cancer health hazard
endpoint (e.g., immune system, reproductive, hepatocarcinomas), EPA uses several factors adapted from
Sir Bradford Hill (1965). These elements include consistency, dose-response relationship, strength of the
association, temporal relationship, biological plausibility, and coherence among other considerations.
EPA considered evidence integration conclusions from Sections 5.2.3, 5.2.4, and 5.2.5 and additional
factors when choosing studies for dose-response modeling and for each exposure scenario (acute, short-
term/sub chronic, and chronic), as described in Section 5.2.5.3. Additional considerations pertinent to the
overall hazard confidence levels include evidence integration conclusions from Appendix M, selection
of the critical endpoint and study, relevance to the exposure scenario, dose-response considerations and
PESS sensitivity. Section 5.2.7.1 presents a summary table of confidence for each hazard endpoint and
exposure duration (see Table 5-54).
Weight of Scientific Evidence Conclusions
For reproductive/developmental toxicity, overall weight of scientific evidence conclusion based on
integration of information across evidence streams suggests evidence is inadequate to assess whether
1,1-dichloroethane exposure may cause reproductive/developmental toxicity under relevant exposure
circumstances Table_Apx M-26.
For renal toxicity, overall weight of scientific evidence conclusion based on integration of information
across evidence streams suggests evidence is inadequate to assess whether 1,1-dichloroethane exposure
may cause renal toxicity under relevant exposure circumstances TableApx M-27.
For hepatic toxicity, overall weight of scientific evidence conclusion based on integration of information
across evidence streams suggests, but is not sufficient to conclude, that 1,1-dichloroethane exposure
causes hepatic toxicity under relevant exposure circumstances Table Apx M-28.
For complete details on weight of scientific evidence conclusions for both within and across evidence
streams, see the evidence profile tables for each organ domain in Appendix M.5M. For a more detailed
description of the hazard database and weight of scientific evidence evaluation see Draft Systematic
Review Protocol Supporting TSCA Risk Evaluations for Chemical Substances (U.S. EPA. 2021b) for
details on the process of evidence evaluation and integration.
Several limitations exist for the 1,1-dichloroethane database. First, the database for studies in humans
and animals consisted of a small number of studies, with limited evaluations performed in many of these
studies, thereby precluding the identification of target organs for 1,1-dichloroethane. Second, no
acceptable toxicological data were available by the dermal or drinking water route, and PBPK/PD
models that would facilitate route-to-route extrapolation to the dermal route have not been identified for
1,1-dichloroethane. However, in oral dosing, the dose is rapidly absorbed and over 80% is exhaled
through the lungs unchanged. Dermal exposures have similar elimination through the lungs. Therefore,
oral PODs were used for extrapolation via the dermal route. Third, no adequate data were available to
identify non-cancer PODs for the inhalation route for either acute or short-term/subchronic exposure
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durations. Data for the identified analog for 1,1-dichloroethane, 1,2-dichloroethane was used to read-
across and fill identified data gaps (Section 5.2.1.2).
In the study by Hofmann et al. (1971a). a repeated 6-hour inhalation 13-week exposure to 500 ppm 1,1-
dichloroethane or 1,2-dichloroethane in rats, guinea pigs, and rabbits indicated toxicity only in animals
exposed to 1,2-dichloroethane. Although this study cannot be utilized quantitatively, qualitative
evaluation based on this comparison of equivalent concentrations for 1,1-dichloroethane and 1,2-
dichloroethane identifies 1,2-dichloroethane to possess greater toxicity among rats, guinea pigs and
rabbits. Rats, as the most sensitive species, displayed an onset of dyspnea and death within the first five
exposure sessions in contrast to the lack of any clinical or pathological changes in 1,1-dichloroethane
exposed animals through the duration of the study. Taking this in account, Hofmann et al. (1971a).
suggest that 1,2-dichloroethane is approximately 5 times more toxic than 1,1-dichloroethane via the
inhalation route based on this exposure scenario.
Due to the lack of acute, short-term/sub chronic, and chronic studies for 1,1-dichloroethane via the
inhalation route, studies assessing the toxicological effects of 1,2-dichloroethane were identified as
potential study candidates to derive PODs as read-across to 1,1-dichloroethane. As indicated previously,
the 10-day inhalation study by Schwetz et al. (1974) was not used because the effects on developing
fetuses and/or offspring were limited and inconclusive and were considered inadequate for derivation of
an acute inhalation POD, and because the only effect reported were decreases in maternal body weight
which occurred following 10-days of exposure. The 4-week study by Zhang et al. (2017) was chosen for
read-across from 1,2-dichloroethane to 1,1-dichloroethane to derive a POD for short-term/sub chronic
exposure via inhalation as other studies using 1,2-dichloroethane were deemed inadequate for this
determination due to study limitations. The study by (Pavan et al.. 1995). a 15-day study in female
Sprague-Dawley rats exposed to 1,2-dichloroethane for 6 hours/day identified no significant effects in
the body weight of dams nor pups in exposure groups up to 250 ppm. In addition, the pregnancy rate
among females at 250 ppm was significantly lower than controls; however, the effect was not seen in the
300 ppm group, so it was assumed not to be related to exposure. At the highest concentration of 300
ppm, a decrease of maternal body weight was the only effect observed, similarly to Schwetz et al.
(1974). but no significant morphological effects in pups were identified as compared to controls. In the
10-day teratogenicity study by (Rao et al.. 1980). mated Sprague-Dawley rats (16-30/group) were
exposed to 0, 100, 300 ppm of 1,2-dichloroethane for 7 hours/day on gestational day 6 to 15 via whole
body inhalation. Dams were sacrificed on gestational day 21 and implantation resorption was evaluated
for each exposure group, however, one litter was identified for the 300 ppm exposure group, as only one
surviving female was pregnant at sacrifice in the 300 ppm exposure group. The embryotoxicity
considered was thus considered secondary to the maternal toxicity.
In the reproduction study by (Rao et al.. 1980). male and female Sprague-Dawley rats were exposed to
0, 25, 75, or 150 ppm of 1,2-dichloroethane via whole body inhalation for 60 days, 6 hours/day and 5
days/week. After 60 days of exposure Fo male and females of each respective treatment group were bred
one-to-one to generate Fia generation. Seven days after Fia litter was sacrificed, Fo rats were bred again
to produce a Fib generation. No exposure related effect in body weight, organ weights (liver and
kidney), or histology (liver, kidneys, ovaries, and testes) were seen in the Fo rats. No significant
differences in fertility index, gestation days, sex ratio, neonatal body weight or growth of pups were
observed. Additionally, no exposure related change in liver or kidney weights or histology were seen in
the Fi generations. The apparent body weight decrease in selected male Fib weanlings at 150 ppm was
based on only five male weanlings per group, which was not a statistically significant difference from
controls.
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An evaluation of the 2-year (Nagano et al.. 2006) mouse study for read-across from 1,2-dichloroethane
to 1,1-dichloroethane was also considered for evaluation of the chronic non-cancer POD determination;
however, the study did not quantify non-cancer endpoints. The study was directed to identify cancer
endpoints at low doses and did not measure many non-cancer endpoints of concern. In mice, neither
growth rate nor food consumption was suppressed in any 1,2-dichloroethane exposure group of either
sex as compared with the respective control. The body weights of the 0, 10, 30 and 90 ppm 1,2-
dichloroethane exposure groups at the end of the 2-year exposure period were 50.8 ± 6.5, 51.7 ± 6.1,
48.1 ± 8.2 and 50.7 ± 6.6 g for males and 36.6 ± 5.2, 35.8 ± 4.1, 37.4 ± 4.9 and 34.1± 4.0 g for females,
respectively. No exposure related change in any hematological, blood biochemical, or urinary parameter
was found in any 1,2-dichloroethane-exposed group of either sex.
Cancer
The 1,1-dichloroethane cancer studies were unacceptable for risk evaluation by EPA systematic review.
The only available human study was confounded by co-exposure to vinyl chloride (Garcia et al.. 2015).
Animal studies included a 78-week study in rats and mice exposed by gavage that was limited by
premature mortality in both species (due to pneumonia in rats, and with no cause of death identified for
mice) (NCI. 1978); a drinking water study in which animals were sacrificed after only 52 weeks
(Klaunig et al.. 1986); and a 9-week study of GGT+ foci in partially hepatectomized rats (Milman et al..
1988). In the absence of chemical-specific data, cancer risk assessment for 1,1-dichloroethane employed
read-across to the related compound 1,2-dichloroethane. For the oral and dermal routes, the 1,2-
dichloroethane oral study in mice provided a cancer slope factor of 7.1 x 10~2 (per mg/kg-bw/day) based
on hepatocarcinomas in male mice NTP (1978). For the inhalation route, the 1,2-dichloroethane
inhalation study in rats provided an inhalation unit risk of 6.2xl0~6 (per |ig/m3) based on combined
mammary gland adenomas, fibroadenomas, and adenocarcinomas and subcutaneous fibromas in female
rats Nagano et al. (2006).
PESS
1,1-Dichloroethane: Relevant data on lifestages and target organs were evaluated to identify potentially
susceptible subpopulations exposed to 1,1-dichloroethane; however, available data in humans and test
animals on lifestages and target organs are limited. An evaluation of the limited human health hazard
database in animals for 1,1-dichloroethane found only one study Schwetz et al. (1974) with information
on lifestages following exposure to 1,1-dichloroethane. The only effect reported was a decrease in
maternal body weight (LOAEL of 3,798 ppm), which could support the pregnant female as having
greater biological susceptibility. The reported delays in fetal ossification from this same study, however,
were more difficult to interpret as this effect also occurred in the two control groups. The only other
effect considered as a POD for 1,1-dichloroethane was from a 13-week repeated-dose toxicity study by
Muralidhara et al. (2001). with a NOAELCOntinuous and LOAELCOntinuous for CNS depression of 714 and
1,429 mg/kg-bw/day, respectively. This endpoint, however, was near lethal doses (Oral LD50 is 725
mg/kg (PubChem) and was therefore not considered a sensitive endpoint for assessing potential
biological susceptibility.
Although information on other considerations potentially impacting greater biological susceptibility
(such as pre-existing disease, lifestyle activities, sociodemographic factors, nutritional status, genetic
predispositions, or other chemical co-exposures and non-chemical stressors), was sparse, there is some
information on 1,1-dichloroethane as impacting greater biological susceptibility. For example, the
ATSDR (2015) does mention some factors that could impact greater susceptibility in the general
population. These factors include, individuals with skin disease because of the purported dermal irritant
effects induced by 1,1-dichloroethane; individuals with liver disease because of the role of this organ in
the biotransformation and detoxification of xenobiotics such as 1,1-dichloroethane; individuals with
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impaired renal function based on limited evidence that 1,1-dichloroethane is nephrotoxic in animals; and
individuals with chronic respiratory disease because of the purported respiratory irritant effects induced
by 1,1-dichloroethane. Additional potential populations that may be unusually susceptible to 1,1-
dichloroethane include children and the elderly because of immature or compromised metabolic
capabilities; phenobarbital or alcohol consumers because of the ability of these substances to alter the
activity of the cytochrome P-450 system; people with compromised immune systems may be
particularly susceptible to exposure to 1,1-dichl or ethane based on the known general immunotoxicity of
various similar chlorinated solvents; and people with pre-existing heart conditions based on reports of
cardiac arrythmias from the clinical use of 1,1-dichloroethane as an anesthetic. The anesthetic use of
1.1-dichloroethane was discontinued when discovered that it induced cardiac arrhythmias at anesthetic
doses (Reid and Muianga. 2012).
1.2-Dichloroethane: As described in further detail in Section 5.2.1.2 and in Appendix J, an evaluation of
the limited human health hazard database for 1,1-dichloroethane concluded that the available
information was insufficient to derive PODs for use in quantitative risk estimates. As a result, a read-
across approach using available data from an identified analog 1,2-dichloroethane was used. Relevant
data on lifestages and target organs were evaluated to identify potentially susceptible subpopulations
exposed to 1,2-dichloroethane. An evaluation of 1,2-dichloroethane in animals identified non-cancer
effects such as (1) increased kidney weight (reported by Storer et al. (1984)); (2) degeneration with
necrosis of the olfactory mucosa (reported by Dow Chemical (2006b)); (3) suppression of immune
response (reported by Munson et al. (1982)); and (4) decreases in sperm concentrations (reported by
Zhang et al. (2017)); and cancer effects such as (5) liver cancer (based on hepatocarcinomas in male
mice (NTP. 1978); and (4) combined mammary gland adenomas, fibroadenomas, and adenocarcinomas
and subcutaneous fibromas Nagano et al. (2006). These effects were considered as representative of the
potential for greater biological susceptibility across subpopulations. In addition, significant decreases in
maternal body weight gain were observed in a prenatal developmental toxicity study by Pay an et al.
(1995). which could support the pregnant female as having greater biological susceptibility.
Although information on other considerations potentially impacting greater biological susceptibility
(such as pre-existing disease, lifestyle activities, sociodemographic factors, nutritional status, genetic
predispositions, or other chemical co-exposures and non-chemical stressors), was sparse, there is some
information on 1,2-dichloroethane as impacting greater biological susceptibility. For example,
individuals with impaired renal function based on evidence that 1,2-dichloroethane is nephrotoxic in
animals, people with compromised immune systems may be particularly susceptible to exposure to 1,1-
dichlorethane based on evidence that 1,2-dichloroethante is immunotoxic, individuals with chronic
respiratory disease because of the effects on the olfactory mucosa induced by 1,2-dichloroethane, and
finally, impacts on male reproduction based on evidence that 1,2-dichloroethane causes decreases in
sperm concentration in animals.
For PESS, specifically susceptibility, across both chemical databases for 1,1- and 1,2-dichloroethane,
uncertainty exists based on limited number of studies, and the differences in results and
comprehensiveness of endpoints assessed towards specific health outcomes across studies.
5.2.7.1 Overall Confidence - Strengths, Limitations, Assumptions, and Key Sources of
Uncertainty in the Human Health Hazard Assessment
As discussed in Section 5.2.1.2, EPA identified data gaps for 1,1-dichloroethane for non-cancer PODs
by the acute, short-term/subchronic, and chronic oral, dermal, and inhalation routes; and cancer PODs
by the oral, inhalation, and dermal routes. A read-across approach was used to identify the best chemical
analog to fill those data gaps. The analyses resulted in the identification of 1,2-dichloroethane (an
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isomer of 1,1-dichlorethane) as the most appropriate analog to fill the identified data gaps for 1,1-
dichloroethane (See Section 5.2.1.3 and Appendix J.2). EPA has high confidence in the use of this
approach based on structural similarity (1,2-dichloroethane was consistently identified as structurally
similar with high scores (>0.5) across all tools used), physical-chemical properties (both 1,1-
dichloroethane and 1,2-dichlroethane are reactive di-chloroethanes and isomers of each other with
identical molecular formulas and molecular weight), ADME (both have simila metabolic properties) and
non-cancer and cancer qualitative toxicological similarities (see Appendix J.2.4 and J.2.5). Each of these
lines of evidence were evaluated as described in Appendix J.2. Overall, based on the similarities in
chemical structure, metabolism and toxicological responses, EPA confirmed the choice of 1,2-
dichloroethane as the appropriate analog. EPA has high confidence that the 1,2-dichloroethane isomer
data accurately reflects the human health hazards of 1,1-dichloroethane where there are data gaps.
In addition, 1,2-dichloroethane lacked adequate data by the dermal route for any exposure duration.
Therefore, EPA used a route-to-route extrapolation approach from the available 1,2-dichloroethane oral
data to fill in the dermal data gap. EPA also has high confidence in this approach. Since both oral and
dermal routes are similar metabolically and by-pass first pass metabolism through the liver, and since
oral ADME studies showed that most of the 1,1-dichloroethane oral dose was eliminated unchanged in
expired air, oral PODs were used for extrapolation via the dermal route.
EPA has high confidence in the human health hazard database for 1,2-dichloroethane and in the
selection of the critical PODs. This is based on several reasons. First, all studies used to assess the
hazards for 1,2-dichloroethane were rated high to medium in SR. Second, critical non-cancer effects that
were ultimately selected as PODs for quantitative risk estimates (kidney toxicity, neurotoxicity,
immunotoxicity, and reproductive toxicity), were considered the most sensitive and biologically relevant
effects, supported by multiple lines of evidence that spanned across species, routes, and durations of
exposure (see Section 5.2.6.4 and endpoint selection tables: Table 5-42, Table 5-43, Table 5-44, Table
5-45, Table 5-46, and Table 5-47).
While EPA has high confidence in the hazard identification of PODs used for quantitative risk estimates,
there are some uncertainties in the 1,2-dichloroethane database. For example, while there were several
studies via the chronic exposure duration for both oral and inhalation exposures, none of those studies
were selected for the chronic POD for a variety of reasons including the identified NOAELs/LOAELs
were higher than the recommended endpoint, or there were limited endpoints evaluated, or other
methodological issues (see endpoint selection tables: Table 5-46 and Table 5-47). As a result,
subchronic data was used for the chronic POD and an uncertainty factor (UFS) of 10x was applied to
account for the use of a short-term study for long-term (chronic) assessment.
Table 5-54 presents a summary of confidence for each hazard endpoint and relevant exposure duration
based on critical human health hazards considered for the acute, short-term/intermediate, chronic, and
lifetime exposure scenarios used to calculate risks.
EPA considered evidence integration conclusions from Sections 5.2.3, 5.2.4, and 5.2.5 and additional
factors listed below when choosing studies for dose-response modeling and for each relevant exposure
scenario (acute, short-term/intermediate, and chronic), as described in Section 5.2.6.4. Additional
considerations pertinent to the overall hazard confidence levels that are not addressed in previous
sections are described above (see Section 5.2.7.1).
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Table 5-54. Confidence Summary for Human Health Hazard Assessment
Hazard Domain
Evidence
Integration
Conclusion
Selection of
Most Critical
Endpoint and
Study
Relevance to
Exposure
Scenario
Dose-Response
Considerations
PESS
Sensitivity
Overall
Hazard
Confidence
Acute non-cancer
Oral
Kidney
Robust
Inhalation
Neurotoxicity'7
Robust
Short-term/intermediate non-cancer
Oral
Immunotoxicity
Robust
Inhalation
Reproductive
Robust
Chronic non-cancer
Oral
Immunotoxicity
Robust
Inhalation
Reproductive
Robust
Cancer
Cancer6
Robust
+ + + Robust confidence suggests thorough understanding of the scientific evidence and uncertainties. The supporting
weight of scientific evidence outweighs the uncertainties to the point where it is unlikely that the uncertainties could have a
significant effect on the hazard estimate.
+ + Moderate confidence suggests some understanding of the scientific evidence and uncertainties. The supporting
scientific evidence weighed against the uncertainties is reasonably adequate to characterize hazard estimates.
+ Slight confidence is assigned when the weight of scientific evidence may not be adequate to characterize the scenario,
and when the assessor is making the best scientific assessment possible in the absence of complete information. There are
additional uncertainties that may need to be considered.
" Degeneration with necrosis of olfactory mucosa
b Oral based on combined mammary gland adenomas, fibroadenomas, and adenocarcinomas and subcutaneous fibromas
c Inhalation based on hepatocellular carcinomas
5.2.7.2 Hazard Considerations for Aggregate Exposure
EPA has defined aggregate exposure as "the combined exposures from a chemical substance across
multiple routes and across multiple pathways" (89 FR 37028, May 3, 2024, to be codified at 40 CFR
702.33). For use in this draft risk evaluation and assessing risks from other exposure routes, EPA
conducted route-to-route extrapolation of the toxicity values from the oral studies for use in the dermal
exposure routes and scenarios. Because the health outcomes are different for oral and inhalation studies,
EPA did not consider it possible to aggregate risks across exposure routes for all exposure durations and
endpoints for the selected PODs.
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8197 5.3 Human Health Risk Characterization
8198
1,1-Dichloroethane - Human Health Risk Characterization (Section 5.3):
Key Points
EPA evaluated all reasonably available information to support human health risk characterization.
The key points of the human health risk characterization are summarized below:
Occupational - Inhalation
• Inhalation exposures contribute to risks to workers and ONUs in occupational settings.
Occupational - Dermal
• Dermal exposures contribute to risks to workers in occupational settings.
General Population
• Inhalation exposures contribute to risks to the general population.
• A land use analysis did not identify residential communities at locations where inhalation
exposures are associated with risks greater than 1 x 1CT6.
o Inhalation acute and chronic non-cancer risks were not found beyond 30 m from a 1,1-
dichloroethane releasing facility,
o Inhalation cancer risks were not found beyond 1,000 m from a 1,1-dichloroethane
releasing facility.
8199 5.3.1 Risk Characterization Approach
8200 The exposure scenarios, populations of interest, and toxicological endpoints used for evaluating risks
8201 from acute, short-term/intermediate, and chronic/lifetime exposures are summarized in Table 5-55.
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Table 5-55. Exposure Scenarios, Populations of Interest, and Hazard Values
Populations of
Interest and
Exposure
Scenarios
Workers
Male and female adolescents and adults (>16 years old) directly working with 1,1-
dichloroethane under light activity (breathing rate of 1.25 m3/hour)
Exposure Durations
• Acute - 8 hours for a single work day (most OESs)
• Short-Term - 8 hours per work day for 22 working days
• Chronic - 8 hours per work day for 250 days per year for 31 or 40 working years
Exposure Routes - Inhalation and dermal
Occupational Non-users
Male and female adolescents and adults (>16 years old) indirectly exposed to 1,1-
dichloroethane within the same work area as workers (breathing rate of 1.25 m3/hour)
Exposure Durations
• Acute, Short-Term, and Chronic - Same as workers
Exposure Route - Inhalation
General Population
Male and female infants, children and adults exposed to 1,1-dichloroethane through drinking
water, ambient water, ambient air, soil, and fish ingestion
Exposure Durations
• Acute - Exposed to 1,1-dichloroethane continuously for a 24-hour period
• Chronic - Exposed to 1,1-dichloroethane continuously up to 33 years
Exposure Routes - Inhalation, dermal, and oral (depending on exposure scenario)
Health Effects,
Hazard Values,
and Benchmarks
Non-cancer 11
The acute oral/dermal endpoint is increased kidney weight.
• HED (occupational) = 19.9 mg/kg; HED (continuous) = 19.9 mg/kg
• Acute uncertainty factors (Benchmark MOE) = 30 for oral and dermal
(UFa= 3; UFh= 10; UFL = 1; UFS = 1; UFD= 1)c
The short-term/subchronic oral/dermalfe endpoint is suppression of immune response
(AFCs/spleen).
• HED (occupational) = 0.890 mg/kg; HED (continuous) = 0.636 mg/kg
• Short-term/subchronic uncertainty factors (benchmark MOE) = 100 for oral and
dermal
(UFa= 3; UFh= 10; UFL = 3; UFS = 1; UFD= 1)c
The chronic oral/dermal endpoint is suppression of immune response (AFCs/spleen).
• HED (occupational) = 0.890 mg/kg; HED (continuous) = 0.636 mg/kg
• Chronic uncertainty factors (benchmark MOE) = 1,000 for oral and dermal
(UFa= 3; UFh= 10; UFL = 3; UFS = 10; UFD= 1)c
The acute inhalation endpoint is neurotoxicity - degeneration with necrosis of the olfactory
mucosa.
• HEC (occupational) = 41 mg/cm3 or 10.14 ppm; HEC (continuous) = 9.78 mg/cm3
or 2.42 ppm
• Acute uncertainty factors (benchmark MOE) = 30 for inhalation
(UFa = 3; UFh = 10; UFL = 1; UFS = 1; UFD = 1)c
The short-term/subchronic inhalation endpoint is decrease in sperm concentration.
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• HEC (occupational) = 89 mg/cm3 or 22 ppm; HEC (continuous) = 21.2 mg/cm3 or
5.2 ppm
• Short-term/subchronic uncertainty factors (benchmark MOE) = 100
(UFa= 3; UFh= 10; UFL= 1; UFS = 3; UFD= 1)c
The chronic inhalation endpoint is decrease in sperm concentration.
• HEC (occupational) = 89 mg/cm3 or 22 ppm; HEC (continuous) = 21.2 mg/cm3 or
5.2 ppm
• Chronic uncertainty factors (benchmark MOE) = 300
(UFa= 3; UFh= 10; UFL= 1; UFS = 10; UFD= 1)c
Cancer 11
The cancer endpoint is based on hepatocellular carcinomas in male mice.
• Oral/dermal cancer slope factor (continuous/worker) = 0.062 per mg/kg/day
• Inhalation Unit Risk (IUR) (continuous) = 6E-06 per (.ig/rn3. IUR (worker) = 2E-06
per (ig/m3
• Drinking water (DW) unit risk (continuous/worker) = 1.8E-6 per ug/L
" All non-cancer and cancer hazard values are based on data for 1,2-dicholorethane read directly across to 1,1-dichloroethane
as an analog.
b The dennal HED and IUR are extrapolated from the oral HED or CSF and are assumed to be equal.
"Uncertainty factors in the benchmark MOE (margin of exposure): UFA= interspecies (animal to human); UFH=intraspecies
(human variability); UFL = LOAEC(L) to NOAEC(L), for PODs that rely on a LOAEC(L); UFS = subchronic to chronic;
UFD = database uncertainty factor
5.3.1.1 Estimation of Non-cancer Risks
EPA used a margin of exposure (MOE) approach to estimate non-cancer risks. The MOE is the ratio of
the non-cancer hazard value divided by a human exposure dose. Acute and chronic MOEs for non-
cancer inhalation and dermal risks were calculated using Equation 5-13:
Equation 5-13.
MOE = (Noncancer Hazard Value (POD))/(Human Exposure)
Where:
MOE = Margin of exposure for acute, short-term, or chronic
risk comparison (unitless)
Noncancer Hazard Value (POD) = HEC (mg/m3) or HED (mg/kg-day)
Human Exposure = Exposure estimate (mg/m3 or mg/kg-day)
MOE risk estimates may be interpreted in relation to benchmark MOEs. Benchmark MOEs are typically
the total UF for each non-cancer hazard value. The MOE estimate is interpreted as a human health risk
of concern if the MOE estimate is less than the benchmark MOE (i.e., the total UF). On the other hand,
if the MOE estimate is equal to or exceeds the benchmark MOE, risk is not considered to be of concern
and mitigation is not needed. Typically, the larger the MOE, the more unlikely it is that a non-cancer
adverse effect occurs relative to the benchmark. When determining if a chemical substance presents
unreasonable risk to human health or the environment, calculated risk estimates are not "bright-line"
indicators of unreasonable risk, and EPA has discretion to consider other risk-related factors in addition
to risks identified in risk characterization.
5.3.1.2 Estimation of Cancer Risks
Extra cancer risks for repeated exposures to a chemical were estimated using Equation 5-14 or Equation
5-15:
Health Effects,
Hazard Values,
and Benchmarks
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Equation 5-14.
Inhalation Cancer Risk = Human Exposure x IUR
Or
Equation 5-15.
Dermal or Oral Cancer Risk = Human Exposure x CSF
Where:
Risk
Raman Exposure
Extra cancer risk (unitless)
Exposure estimate (LADC in ppm)
Inhalation unit risk (risk per mg/m3)
Cancer slope factor (risk per mg/kg-day)
IUR
CSF
Estimates of extra cancer risks are interpreted as the incremental probability of an individual developing
cancer over a lifetime following exposure (i.e., incremental or extra individual lifetime cancer risk).
5.3.2 Risk Characterization for Potentially Exposed or Susceptible Subpopulations
EPA considered PESS throughout the exposure assessment and throughout the hazard identification and
dose-response analysis. EPA has identified several factors that may contribute to a group having
increased exposure or biological susceptibility. Examples of these factors include lifestage, preexisting
disease, occupational and certain consumer exposures, nutrition, and lifestyle activities.
For the 1,1-dichloroethane draft risk evaluation, EPA accounted for the following PESS groups: infants
exposed to drinking water during formula bottle feeding, subsistence and Tribal fishers, pregnant
women and people of reproductive age, individuals with compromised immune systems or neurological
disorders, workers, people with the aldehyde dehydrogenase-2 mutation which is more likely in people
of Asian descent, lifestyle factors such as smoking cigarettes or secondhand smoke, and communities
who live near facilities that emit 1,1-dichloroethane.
Table 5-56 summarizes how PESS were incorporated into the risk evaluation and the remaining sources
of uncertainty related to consideration of PESS.
Additional information on other factors that could possibly impact greater biological susceptibility
following exposure to 1,1-dichloroethane—such as more comprehensive information on pre-existing
diseases in humans, lifestyle activities, nutritional status, or other chemical co-exposures and non-
chemical stressors—was completely lacking.
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Table 5-56. Summary of PESS Categories in the Draft Ris
i. Evaluation and Remaining Sources of Uncertainty
PESS
Categories
Potential Increased Exposures Incorporated
into Exposure Assessment
Potential Sources of Biological Susceptibility Incorporated into Hazard
Assessment
Lifestage
Lifestage-specific exposure scenarios included
infants exposed to drinking water during formula
bottle feeding.
Exposure factors by age group were applied to
calculate exposure.
Other scenarios of children swimming or playing
in soil may be considered for dermal and oral
exposure. It is unclear how relevant dermal and
ingestion estimates from soil exposure are as 1,1-
dichloroethane is expected to either volatilize or
migrate from surface soils to groundwater. Other
factors by age may be relevant.
Direct evidence of a reproductive/developmental effect was the basis for the chronic
inhalation POD used for risk estimation. Other reproductive/developmental data was
difficult to interpret across the chemical databases, including delayed fetal ossification
(1,1-dichloroethane) and fetal resorptions (1,2-dichloroethane). However, the chronic
inhalation POD selected was considered to be protective. The analog 1,2-
dichloroethane partitions in the milk of women exposed dermallv (ATSDR. 2022;
Urusova. 1953). The analog 1.2-dichloroethane partitions in the milk of women
exposed dermallv (ATSDR. 2022; Urusova. 1953).
Children in households that smoke cigarettes, receiving secondhand smoke, may be
exposed to higher levels of 1.1-dichloroethane (ATSDR. 2022; Wans et al.. 2012).
The increase in susceptibility due to secondhand smoke is not known and is a source
of uncertainty in part reliant on proximity to the smoker, space ventilation, and
frequency of smoking/number of cigarettes smoked.
Evidence in mice revealed a statistically significant increase in benign uterine
endometrial stromal polyps in high-dose analog 1,2-dichloroethane females which
may have implications for women of childbearing age, or fertility challenges.
Evidence also from mice showed changes in sperm parameters in decreases in sperm
count following short-term exposures to the analog 1,2-dichloroethane.
Potential susceptibility of older adults due to toxicokinetic differences was addressed
through a 10/ UF for human variability.
Pre-existing
Disease
EPA did not identify pre-existing disease factors
influencing exposure
Indirect evidence suggesting chronic liver disease may delay detoxification was
addressed qualitatively and through the 10/ UF for human variability. The 1,1-
dichloroethane 2015 ATSDR Report (ATSDR. 2015) cited concerns for individuals
with skin disease, impaired kidney function, chronic respiratory disease, cancer, the
young and elderly with altered metabolic capacity and interactions with
phenobarbital/ethanol consumption. Its use as an anesthetic support potential
susceptibility for individuals with cardiac and neurological disease. ATSDR indicates
concern for individuals with compromised immune systems exposed to 1,2-
dichloroethane.
Observed impaired motor activity and CNS depression, from evidence in rats
following 1,1-dichloroethane exposure, have potential implications for greater
susceptibility in people with Parkinson's Disease, other neurological disorders.
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PESS
Categories
Potential Increased Exposures Incorporated
into Exposure Assessment
Potential Sources of Biological Susceptibility Incorporated into Hazard
Assessment
The increase in susceptibility due to pre-existing disease is not known and is a source
of uncertainty.
Lifestyle
Activities
EPA evaluated exposures resulting for subsistence
and Tribal fishers and considered increased intake
of fish in these populations.
People that smoke cigarettes may be exposed to higher levels of 1,1-dichloroethane.
Emissions from smoking cigarettes can contain between 51 and 110 |ug 1,1-
dichlorocthanc/ciearcttc (ATSDR. 2022; Wane et al.. 2012).
Occupational
Exposures
EPA considered increased exposure specific to
worker activities.
EPA did not identify occupational exposures that influence susceptibility.
Sociodemogr
aphic
EPA evaluated exposure differences between
racial/ethnic groups and women of reproductive
age based on location of exposures to 1,1-
dichloroethane in ambient air.
EPA did not identify sociodemographic factors that influence susceptibility.
Geography
and site-
specific
Potential for increased exposures included
children under 5 and 18 years old because
childcare centers and public schools were
observed near several of the AERMOD TRI
release sites. See Section 5.3.4.
There is some uncertainty associated with the
modeled distances from each release point and the
associated exposure concentrations to which
residential communities proximal to releasing
facilities may be exposed.
EPA did not specifically identify geography and/or site-specific factors that influence
susceptibility.
Nutrition
EPA did not identify nutritional factors
influencing exposure.
EPA did not identify nutritional factors that influence susceptibility.
Genetics/
Epigenetics
EPA did not identify genetic factors influencing
exposure.
Indirect evidence that genetic variants may increase susceptibility of the target organ
was addressed through a 10* UF for human variability. However, a known metabolite
of 1,1-dichloroethane is the reactive dichloroacetaldehyde supporting that a PESS
group are people with the aldehyde dehydrogenase-2 mutation which is more
likely in people of Asian descent which have a higher risk for several diseases
affecting many organ systems, including a particularly high incidence relative to the
general population of esophageal cancer, myocardial infarction, and osteoporosis due
to decreased reactive aldehvde clearance Gross et al. (2015). which is not addressed
by the UFH (-28-54% incidence in Asians, ~7 million in the U.S.). Cancer studies in
animals with the aldehyde dehydrogenase-2 clearance enzyme mutation are not
available to quantitatively assess this PESS group.
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PESS
Categories
Potential Increased Exposures Incorporated
into Exposure Assessment
Potential Sources of Biological Susceptibility Incorporated into Hazard
Assessment
Other Unique
Activities
EPA did not identify unique activities that
influence exposure.
EPA did not identify unique activities that influence susceptibility.
Aggregate
Exposures
EPA assessed aggregate exposures to the general
populations to the combined ambient air
concentrations from several adjacent facility air
releases.
EPA did not aggregate routes of exposure as the
endpoints are different and dependent on the
corresponding route of exposure.
Not relevant to susceptibility.
Other
Chemical and
Nonchemical
Stressors
EPA did not identify other chemical and non-
chemical factors influencing exposure.
EPA did not identify other chemical and nonchemical stressors that influence
susceptibility.
8268
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5.3.3 Human Health Risk Characterization
5.3.3.1 Risk Estimates for Workers and ONUs
For each condition of use, EPA assessed 1,1-dichloroethane inhalation exposures to workers and ONUs
in occupational settings, presented as 8-hour (i.e., full-shift) TWA described in Section 5.1.1. These
estimated exposures were then used to calculate acute, short-term/sub chronic, and chronic (non-cancer
and cancer) inhalation exposures and dermal doses. These calculations require additional parameter
inputs such as years of exposure, exposure duration and frequency, and lifetime years. EPA used
combinations of point estimates of each parameter to estimate a central tendency and high-end for each
final exposure metric result. EPA documented the method and rationale for selecting parametric
combinations to be representative of central tendency and high-end.
EPA also assessed 1,1-dichloroethane dermal exposures to workers in occupational settings, presented
as a dermal APDR. The APDRs are then used to calculate acute retained doses (ARD), subchronic
average daily doses (SCDD), chronic retained dose (CRD) for chronic non-cancer risks, and lifetime
average daily doses (LADD) for chronic cancer risks.
The input parameter values in Table 5-57 are used to calculate each of the above acute, subchronic, and
chronic exposure estimates. For additional details on the parameters, refer to Draft Risk Evaluation for
1,1-Dichloroethane - Supplemental Information File: Environmental Releases and Occupational
Exposure Assessment (U.S. EPA. 2024e).
Table 5-57. Parameter Values for Calculating Ex
posure Estimates
Parameter Name
Symbol
Value
Unit
Exposure Duration
ED
h/day
Breathing Rate Ratio
BR
2.041
unitless
Exposure Frequency
EF
125-250'
days/year
Exposure Frequency, subchronic
22
days
Days for Subchronic Duration
SCD
30
days
Working years
WY
31 (50th percentile)
40 (95th percentile)
years
Lifetime Years, Cancer
LT
78
years
Averaging Time, Subchronic
AT*
720
hours
Averaging Time, Non-cancer
AT
271,560 (central tendency)
350,400 (high-end) d
hours
Averaging Time, Cancer
ATC
683.280
hours
Body Weight
BW
80 (average adult worker)
72.4 (female of reproductive age)
kg
" EPA uses a breathing rate ratio, which is the ratio between the worker breathing rate and resting breathing rate, to
account for the amount of air a worker breathes during exposure. The typical worker breathes about 10 m3 of air in !
hours, or 1.25 m3/hr (U.S. EPA. 1991) while the resting breathing rate is 0.6125 m3/hr (U.S. EPA. 1991). The ratio
of these two values is equivalent to 2.04.
h Depending on OES; maximum number of exposure days was assumed to be 250 days per year.
c Calculated using the 95th percentile value for working years (WY).
h Calculated using the 50th percentile value for WY.
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5.3.3.1.1 Acute Risk
Acute non-cancer (AC) is used to estimate workplace inhalation exposures for acute risks {i.e., risks
occurring as a result of exposure for less than one day), per Equation 5-16:
Equation 5-16.
Where:
AC = (C X ED X BR)/(ATacute)
AC = Acute exposure concentration
C = Contaminant concentration in air (TWA)
ED = Exposure duration (hr/day)
BR = Breathing rate ratio (unitless)
ATacute = Acute averaging time (hr)
A sample calculation for the high-end acute inhalation exposure concentration (AChe) for the
Manufacturing OES is demonstrated in Equation 5-17 below:
Equation 5-17.
AChe = (CHE x ED x BR)/(Aacute)
AChe = (1.1 ppm x 8 hr/day x 2.04)/(24 hr/day) = 0.72 ppm
Acute Retained Dose (ARD) is used to estimate workplace dermal exposures for acute risks and are
calculated using Equation 5-18:
Equation 5-18.
ARD = APDR/BW
Where:
ARD = Acute retained dose (mg/kg-day)
APDR = Acute potential dose rate (mg/day)
BW = Body weight (kg)
A sample calculation for the high-end acute retained dose for the Manufacturing OES is demonstrated in
Equation 5-19 below:
Equation 5-19.
ARD HE = APDRhe/BW
ARDhe = (6.7 mg/day)/(80 kg) = 0.08 mg / (kg — day)
5.3.3.1.2 Short-Term Subchronic Risk
Short-term, subchronic non-cancer (SADC) is used to estimate workplace inhalation exposures for
subchronic risks and is estimated in Equation 5-20 and Equation 5-21, as follows:
Equation 5-20.
SADC = (C X ED X EFSC X BR)/ATSC
Equation 5-21.
ATSC = SCD x 24 hr/day
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Where:
SADC = Subchronic average daily concentration
EFSC = Subchronic exposure frequency
ATSC = Averaging time (hr) for subchronic exposure
SCD = Days for subchronic duration (day)
A sample calculation for the high-end, short-term, subchronic exposure concentration {SADChe) for the
Manufacturing OES is demonstrated in Equation 5-22 below:
Equation 5-22.
SADC = (CHE XED X EFSC X BR)/ATSC
SADChe = (1.1 ppm x 8 "hr"/day x 22 "days"/year x 2.04)/(24 "hr"/day x 30 "days"/year)
= 0.53 ppm
Sub-chronic average daily dose (SCDD) is used to estimate workplace dermal exposures for subchronic
risks, and is estimated using Equation 5-23:
Equation 5-23.
SCDD = (AD X EFSC X WY)/ATSC
Where:
SCDD = Sub-chronic average daily dose (mg/kg-day)
A sample calculation for the high-end subchronic average daily dose for the Manufacturing OES is
demonstrated in Equation 5-24 below:
Equation 5-24.
SCDDhe = (ARDhe X EFSC X WYhe)/ATsc
SCDDhe = (0.08 mg/(kg — day) x 22 "day"/yr x 40 "yr")/(30 "day") = 0.06 mg / (kg—) day
5.3.3.1.3 Chronic Non-cancer Risk
The Average daily concentration (ADC) is used to estimate workplace inhalation exposures for non-
cancer risk. This exposure is estimated as follows in Equation 5-25 and Equation 5-26:
Equation 5-25.
Equation 5-26.
Where:
ADC = (C x ED x EF xWY x BR)/AT
AT = WY x 365 "day" /"yr" x 24 "hr" /"day"
ADC = Average daily concentration used for chronic non-cancer risk calculations
ED = Exposure duration (hr/day)
EF = Exposure frequency (day/year)
WY = Working years per lifetime (yr)
AT = Averaging time (hr) for chronic, non-cancer risk
Page 324 of 664
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8381
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8386
8387
8388
8389
8390
8391
8392
8393
8394
8395
8396
8397
8398
8399
8400
8401
8402
8403
8404
8405
8406
8407
8408
8409
8410
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8412
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PUBLIC RELEASE DRAFT
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A sample calculation for the high-end chronic non-cancer exposure concentration (ADChe) for the
Manufacturing OES is demonstrated in Equation 5-27 below:
Equation 5-27.
ADCHE = (CHE x ED x EF x WY x BR)/AT
ADChe = (1.1 ppm x 8 hr/day x 250 days/year x 40 years x 2.04)/(40 years x 365 days/yr
x 24 hr/day) = 0.49 ppm
The chronic retained dose (CRD) is used to estimate workplace dermal exposures for non-cancer risk
and is calculated using Equation 5-28:
Equation 5-28.
CRD = (.ARD X EF X WY)/(ATchronic )
A sample calculation for the high-end chronic retained dose for the Manufacturing OES is demonstrated
in Equation 5-29 below:
Equation 5-29.
CRDhe = (ARDHe x EF X WY)/(ATchroniC )
CRDhe = (0.08 mg/(kg — day) x 250 day/yr x 40 yr)/(14,600 day) = 0.06 ( mg) / (kg—) day
5.3.3.1.4 Cancer Risk
Lifetime average daily concentration (LADC) is used to estimate workplace inhalation exposures for
cancer risk. This exposure is estimated as follows in Equation 5-30 and Equation 5-31:
Equation 5-30.
LADC = (C x ED x EF x WY x BR)/ATC
Equation 5-31.
ATC = LT x 365 "day" /"yr" x 24 "hr" /"day"
Where:
LADC =
Lifetime average daily concentration used for chronic cancer risk calculations
ED
Exposure duration (hr/day)
EF
Exposure frequency (day/year)
WY =
Working years per lifetime (yr)
ATC =
Averaging time (hr) for cancer risk
LT
Lifetime years (yr) for cancer risk
A sample calculation for the high-end chronic cancer exposure concentration (LADChe) for the
Manufacturing OES is demonstrated in Equation 5-32 below:
Equation 5-32.
LADChe = (CHE x ED x EF x WY x BR)/(ATC )
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PUBLIC RELEASE DRAFT
July 2024
LADChe = (1.1 ppm x Bhr/day x 250 days/year x 40 years x 2.04)/(78 years x 365 days
/year x 24 hr/day) = 0.25 ppm
Lifetime chronic retained dose (LCRD) is used to estimate workplace dermal exposures for cancer risk
and is estimated using Equation 5-33:
Equation 5-33.
LCRD = (ARD XEFX WY)/ATC
LCRD = (0.08 mg/(kg — day) x 250 day/yr x 40 yr)/(28,470 day) = 0.03 mg / (kg—) day
5.3.3.1.5 Occupational Exposure Summary by OES
The occupational inhalation exposure metrics described in 5.3.3.1.1 through 5.3.3.1.4 are presented in
Table 5-58, and the occupational dermal exposure metrics are presented in Table 5-59. EPA used the
exposure metrics presented in Table 5-58 and Table 5-59 and the approach described in Sections 5.3.1.1
and 5.3.1.2 to develop risk estimates for each 1,1-dichloroethane exposure scenario. The risk estimates
are presented below in Table 5-60. For additional details on the risk estimates, refer to Risk Evaluation
for 1,1-Dichloroethane - Supplemental Information File: Risk Calculator for Occupational Exposure.
Page 326 of 664
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8444 Table 5-58. Summary of Occupational Inhalation
Exposure Metrics
8-Hour TWA
Acute, Non-cancer
Short
T erm/Subchronic,
Non-cancer
Chronic, Non-cancer
Chronic, Cancer
Exposures
Exposures
Exposures
Exposures
OES
Category
8-hr TWA (ppm)
ACs-hr TWA (ppm)
ADCs-hr TWA (ppm)
ADCs-hr TWA (ppm)
LADCshr TWA (ppm)
High-
Central
High-
Central
High-
Central
High-
Central
High-
Central
End
Tendency
End
Tendency
End
Tendency
End
Tendency
End
Tendency
Manufacturing
Worker
1.1
4.7E-03
0.72
3.2E-03
0.53
2.3E-03
0.49
2.2E-03
0.25
8.7E-04
(operator/process
technician)
Manufacturing
Worker
0.41
7.9E-02
0.28
5.4E-02
0.21
4.0E-02
0.19
3.7E-02
9.9E-02
1.5E-02
(maintenance
technician)
Manufacturing
Worker
2.4E-02
1.1E-03
1.6E-02
7.7E-04
1.2E-02
5.7E-04
1.1E-02
5.3E-04
5.6E-03
2.1E-04
(laboratory
technician)
Manufacturing
ONU
2.0E-02
3.2E-03
1.4E-02
2.2E-03
1.0E-02
1.6E-03
9.4E-03
1.5E-03
4.8E-03
5.9E-04
Processing as a
reactive
intermediate
Worker
1.1
7.9E-02
0.72
5.4E-02
0.53
4.0E-02
0.49
3.7E-02
0.25
1.5E-02
ONU
2.0E-02
3.2E-03
1.4E-02
2.2E-03
1.0E-02
1.6E-03
9.4E-03
1.5E-03
4.8E-03
5.9E-04
Processing -
Worker
13
3.5
8.8
2.4
6.4
1.8
3.1
0.17
1.6
6.8E-02
repackaging
ONU
3.5
3.5
2.4
2.4
1.8
1.8
0.84
0.17
0.43
6.8E-02
Commercial use as a
Worker
2.4E-02
1.1E-03
1.6E-02
7.7E-04
1.2E-02
5.7E-04
1.1E-02
3.7E-04
5.6E-03
1.5E-04
laboratory chemical
ONU
1.1E-03
1.1E-03
1.1E-03
1.1E093
7.7E-04
7.7E-04
5.3E-04
3.7E-04
2.7E-04
1.5E-04
General waste
Worker
10
0.30
7.1
0.20
5.2
0.15
4.9
0.14
2.5
5.5E-02
handling, treatment,
and disposal
ONU
0.30
0.30
0.20
0.20
0.15
0.15
0.14
0.14
7.1E-02
5.5E-02
Waste handling,
Worker
0.68
0.25
0.46
0.17
0.34
0.13
0.32
0.12
0.16
4.7E-02
treatment, and
ONU
0.25
0.25
0.17
0.17
0.13
0.13
0.12
0.12
6.1E-02
4.7E-02
disposal (POTW)
8445
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8446 Table 5-59. Summary of Occupational Dermal Exposure Metrics
OES
Category
Acute Retained
Dose
Short Term/Subchronic
Retained Dose, Non-cancer
Chronic Retained
Dose, Non-cancer
Chronic Retained
Dose, Cancer
ARD (mg/kg-day)
SCRD (mg/kg-day)
CRD (mg/kg-day)
LCRD (mg/kg-day)
High-
End
Central
Tendency
High-End
Central
Tendency
High-
End
Central
Tendency
High-
End
Central
Tendency
Manufacturing
(operator/process technician)
Worker
0.08
0.03
0.06
0.02
0.06
0.02
0.03
0.01
Manufacturing (maintenance
technician)
Worker
0.08
0.03
0.06
0.02
0.06
0.02
0.03
0.01
Manufacturing (laboratory
technician)
Worker
0.08
0.03
0.06
0.02
0.06
0.02
0.03
0.01
Processing as a reactive
intermediate
Worker
0.08
0.03
0.06
0.02
0.06
0.02
0.03
0.01
Processing - repackaging
Worker
0.08
0.03
0.06
0.02
0.06
0.02
0.03
0.01
Commercial use as a
laboratory chemical
Worker
0.08
0.03
0.06
0.02
0.06
0.02
0.03
0.01
General waste handling,
treatment, and disposal
Worker
0.08
0.03
0.06
0.02
0.06
0.02
0.03
0.01
Waste handling, treatment,
and disposal (POTW)
Worker
0.08
0.03
0.06
0.02
0.06
0.02
0.03
0.01
8447
8448
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8449 Table 5-60. Occupational Risk Summary Table
Life Cycle
Stage/
Category
Subcategory
OES
Scenario
Population
Exposure
Route and
Duration
Exposure
Level
Risk Estimates for Each Exposure Scenario
Acute Non-
cancer
(Benchmark
MOE:
Dermal = 30;
Inhalation = 30)
Short-
Term/Subchronic,
Non-cancer
(Benchmark MOE:
Dermal = 100
Inhalation = 30)
Chronic, Non-
cancer (Benchmarl
MOE:
Dermal = 1,000;
Inhalation=300)
Cancer
(Benchmark =
10E-4)
Manufacture/
Domestic
Manufacturing
Domestic
manufacture
Manufacturing
Operator /
Process
Technician
Inhalation
Central
Tendency
3,175
9,394
1.0E04
8.3E-06
High-
End
14
42
45
2.4E-03
Maintenance
Technician
Inhalation
Central
Tendency
188
555
595
1.4E-04
High-
End
36
107
114
9.4E-04
Laboratory
Technician
Inhalation
Central
Tendency
1.3E04
3.9E04
4.2E04
2.0E-06
High-
End
631
1,866
1,998
5.4E-05
Worker
Dermal
Central
Tendency
709
43
46
4.7E-04
High-
End
236
14
15
1.8E-03
ONU
Inhalation
Central
Tendency
4,643
1.4E04
1.5E04
5.6E-06
High-
End
741
2,192
2,346
4.6E-05
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Risk Estimates for Each Exposure Scenario
Life Cycle
Stage/
Category
Subcategory
OES
Scenario
Population
Exposure
Route and
Duration
Exposure
Level
Acute Non-
cancer
(Benchmark
MOE:
Dermal = 30;
Inhalation = 30)
Short-
Term/Subchronic,
Non-cancer
(Benchmark MOE:
Dermal = 100
Inhalation = 30)
Chronic, Non-
cancer (Benchmarl
MOE:
Dermal = 1,000;
Inhalation=300)
Cancer
(Benchmark =
10E-4)
Intermediate
Central
188
555
595
1.4E-04
in all other
Tendency
basic organic
chemical
Inhalation
High-
End
14
42
45
2.4E-03
manufacturing
Intermediate
in all other
Processing as a
reactive
intermediate
Worker
Central
Tendency
709
43
46
4.7E-04
chemical
product and
Dermal
High-
End
236
14
15
1.8E-03
preparation
manufacturing
Recycling
Central
4,643
1.4E04
1.5E04
5.6E-06
ONU
Inhalation
Tendency
Processing
High-
End
741
2,192
2,346
4.6E-05
Central
4.2
13
129
6.4E-04
Inhalation
Tendency
High-
1.2
3.4
7.1
1.5E-02
Worker
End
Central
709
43
445
4.9E-05
Processing -
Processing -
Dermal
Tendency
Repackaging
repackaging
High-
End
236
14
30
9.4E-04
Central
4.2
13
129
6.4E-04
ONU
Inhalation
Tendency
High-
End
4.2
13
26
4.1E-03
Page 330 of 664
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Life Cycle
Stage/
Category
Subcategory
OES
Scenario
Population
Exposure
Route and
Duration
Exposure
Level
Risk Estimates for Each Exposure Scenario
Acute Non-
cancer
(Benchmark
MOE:
Dermal = 30;
Inhalation = 30)
Short-
Term/Subchronic,
Non-cancer
(Benchmark MOE:
Dermal = 100
Inhalation = 30)
Chronic, Non-
cancer (Benchmarl
MOE:
Dermal = 1,000;
Inhalation=300)
Cancer
(Benchmark =
10E-4)
Commercial
Use/
Laboratory
Chemicals
Laboratory
Chemicals
Reference
Material
Commercial us
as a laboratory
chemical
Worker
Inhalation
Central
Tendency
1.3E04
3.9E04
6.0E04
1.4E-06
High-
End
631
1,866
1,998
5.4E-05
Dermal
Central
Tendency
709
43
66
3.3E-04
High-
End
236
14
15
1.8E-03
ONU
Inhalation
Central
Tendency
1.3E04
3.9E04
6.0E04
1.4E-06
High-
End
1.3E04
3.9E04
4.2E04
2.6E-06
Disposal/
Disposal
Disposal
General waste
handling,
treatment, and
disposal
Worker
Inhalation
Central
Tendency
50
149
159
5.2E-04
High-
End
1.4
4.2
4.5
2.4E-02
Dermal
Central
Tendency
709
43
46
4.7E-04
High-
End
236
14
15
1.8E-03
ONU
Inhalation
Central
Tendency
50
149
159
5.2E-04
High-
End
50
149
159
6.7E-04
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Life Cycle
Stage/
Category
Subcategory
OES
Scenario
Population
Exposure
Route and
Duration
Exposure
Level
Risk Estimates for Each Exposure Scenario
Acute Non-
cancer
(Benchmark
MOE:
Dermal = 30;
Inhalation = 30
Short-
Term/Subchronic,
Non-cancer
(Benchmark MOE:
Dermal = 100
Inhalation = 30)
Chronic, Non-
cancer (Benchmarl
MOE:
Dermal = 1,000;
Inhalation=300)
Cancer
(Benchmark =
10E-4)
Disposal/
Disposal
Disposal
Waste
handling,
treatment, and
disposal
(POTW)
Worker
Inhalation
Central
Tendency
58
173
185
4.5E-04
High-
End
22
65
69
1.5E-03
Dermal
Central
Tendency
709
43
46
4.7E-04
High-
End
236
14
15
1.8E-03
ONU
Inhalation
Central
Tendency
58
173
185
4.5E-04
High-
End
58
173
185
5.8E-04
8450
Page 332 of 664
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8451
8452
8453
8454
8455
8456
8457
8458
8459
8460
8461
8462
8463
8464
8465
8466
8467
8468
8469
8470
8471
8472
8473
8474
8475
8476
8477
8478
8479
8480
8481
8482
8483
8484
8485
8486
8487
8488
8489
8490
8491
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PUBLIC RELEASE DRAFT
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5.3.3.2 Risk Estimates for the General Population
The following sections summarize the risk estimates and conclusions for inhalation, dermal and oral
exposures for all general population exposure scenarios. Risk estimates that exceed the benchmark (i.e.,
MOEs less than the benchmark MOE or cancer risks greater than the cancer risk benchmark) are
highlighted by holding the number. The general population exposure assessment is described in Section
5.1.2.
5.3.3.2.1 Inhalation Exposure Risk
EPA estimated risks of general population exposures to 1,1-dichloroethane released to air, with a focus
on exposures in general populations residing near 1,1-dichloroethane emitting facilities. Risks were
evaluated for air releases from industrial and commercial COUs based on exposure estimates in Section
5.1.2.2 and human health hazard values (selected PODs) for chronic inhalation exposures in Section
5.2.6.3.
Ambient Air
Cancer and non-cancer risk estimates for general population exposures to ambient air within 10,000 m
of industrial and commercial releases were calculated for the 10th, 50th, and 95th percentiles of modeled
air concentrations estimated in Section 3.3.1.2. Risk estimates were highest within 1,000 m of the
releasing facilities and lower at distances beyond 1,000 m. Risks were not indicated for any OESs/COUs
beyond 1,000 m from a facility.
EPA found inhalation cancer risks greater than the benchmark for the 50th percentile air concentrations
for manufacturing, processing, and disposal OESs/COUs at distances as far as 1,000 m from the
releasing facility. EPA also found inhalation cancer risks greater than the benchmark for the 95th
percentile air concentrations for manufacturing, processing, and disposal OESs/COUs at distances as far
as 1,000 m from the releasing facility. No inhalation cancer risks were found for commercial use as a
laboratory chemical OESs/COUs.
Table 5-61 and Table 5-62 summarize the cancer risks estimates for 95th percentile (high-end) exposure
concentrations within 1,000 m of the facilities with the greatest risk in each OES, ranging from 3,4/ 10 7
to 1.6xl0~3 and 2.7xlO~10 to 2.3xl0~4 based on TRI and NEI modeled exposure data, respectively. Table
5-41 and Table 5-42 summarize the cancer risks estimates for 50th percentile (central tendency)
exposure concentrations within 1,000 m of the facilities with the greatest risk in each OES, ranging from
4.6><10~8 to 1.2xl0~3 and 1.0xl0~10to 1.8xl0~4, based on TRI and NEI modeled exposure data,
respectively. Cancer risk estimates ranges for the TRI modeled exposure concentrations are within three
orders of magnitudes higher than the NEI cancer risk estimates. However, the maximum cancer risk
estimates for both TRI and NEI modeled exposure concentrations are withing one order of magnitude
higher for high-end exposures, and within the same order of magnitude for central tendency exposures.
Table 5-63 and Table 5-64 summarize the cancer risks estimates per release type based on TRI and NEI
modeled exposure data, respectively. As shown in Table 5-65., fugitive releases are driving exposures
and associated risks at each distance evaluated for TRI releases. As discussed in Section 3.3.2.2,
exposure estimates very near facilities (10 m) may be impacted by assumptions made for modeling
around an area source (the assumption places the 10-meter modeled exposure point just off the release
point). This, in combination with other factors like meteorological data, release heights, and plume
characteristics can result in lower or higher exposures. Air concentrations from fugitive emissions tend
to peak within 10 m of release sites while contributions from stack releases generally peak around 100
Page 333 of 664
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8497
8498
8499
8500
8501
8502
8503
8504
8505
8506
8507
8508
8509
8510
8511
8512
8513
8514
8515
8516
8517
8518
8519
8520
8521
8522
8523
8524
8525
8526
8527
8528
8529
8530
8531
8532
8533
8534
8535
8536
8537
8538
8539
8540
8541
8542
8543
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PUBLIC RELEASE DRAFT
July 2024
m, meaning that risks nearest to release sites are often driven by fugitive releases, as shown in Table
5-65. and Table 5-66.
Table 5-67 summarizes the cancer risks estimates for 95th percentile (high-end) exposure concentrations
within 1,000 m of the release facility for the Commercial use as a laboratory chemical, and Processing -
repackaging for laboratory chemicals OESs where there was no site-specific data available for modeling.
Risk estimates are presented for high-end modeled releases, high-end meteorology (Lake Charles,
Louisiana), and both rural and urban settings. Cancer risks estimates for 95th percentile exposure
concentrations ranged from 2.8x 10~7 to 1.1 x ] o 5 for the Commercial use as a laboratory chemical OES,
and from 8.9x 10~8 to 6.6/ 10 6 for the Processing - repackaging for laboratory chemicals OES. As
shown in Table 5-67, fugitive releases are driving exposures and associated risks at each distance
evaluated for the Commercial use as a laboratory chemical OES. No inhalation acute and chronic non-
cancer risks were found based on the 50th percentile air concentrations for either OES.
No inhalation acute and chronic non-cancer risks (not shown) were found based on the 50th percentile
air concentrations—except for one TRI facility within the manufacturing OES/COU that shows chronic
non-cancer risk at 10 m from the releasing facility. Acute non-cancer risk estimates (not shown) indicate
risk relative to benchmark MOE based on the 95th percentile air concentrations for manufacturing
OES/COU at 10 m from the releasing facility (for one TRI facility within the OES/COU). Chronic non-
cancer risk estimates (not shown) indicate risk relative to benchmark MOE based on the 95th percentile
air concentrations for manufacturing OES/COU at distances as far as 30 m from the releasing facility
(for one TRI facility within the OES/COU).
Complete cancer and non-cancer risk results are provided in the Draft Risk Evaluation for 1,1-
Dichloroethane - Supplemental Information File: Supplemental Information on AERMOD TRI
Exposure and Risk Analysis (U.S. EPA. 2024n). Draft Risk Evaluation for 1,1-Dichloroethane -
Supplemental Information File: Supplemental Information on AERMOD Generic Releases Exposure and
Risk Analysis (U.S. EPA. 20241). and in the Draft Risk Evaluation for 1,1-Dichloroethane -
Supplemental Information File: Supplemental Information on AERMOD NEI Exposure and Risk
Analysis (U.S. EPA. 2024m).
Aggregate Risk
Within the ambient air pathway, EPA also evaluated cancer and non-cancer risks from aggregate
exposures from multiple neighboring facilities using a conservative screening methodology. The
methodology for this analysis is consistent with what was previously described in the Draft Supplement
to the Risk Evaluation for 14-Dioxane (U.S. EPA. 2023b). EPA identified four groups of two to six
facilities reporting 1,1-dichloroethane releases in proximity to each other (i.e., within 10 km).
Aggregating risks estimated for these groups of facilities were generally dominated by the facility with
the greatest risk. This aggregate analysis did not identify locations with cancer risk greater than 1 x 10~6
that did not already have cancer risk above that level from an individual facility. Details of the methods
and results of this aggregate analysis are described in Appendix E.4.
Indoor Air
Risks were evaluated for air releases from industrial and commercial COUs based on LADC exposure
estimates in Section 5.1.2.2.2. Cancer and non-cancer risk estimates for general population exposures to
indoor air within 1,000 m of industrial and commercial releases were calculated for the mean and high-
end of modeled exposure concentrations estimated in Section 3.3.2.2. Table 5-68 and Table 5-69
summarizes the lifetime cancer risks estimates for the high-end and central tendency exposure
concentrations within 1,000 m of the facilities within each OES category, respectively. The lifetime
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8546 cancer estimates ranged from 9.1x10 8 to 5.3x10 5 and 5.0x10 8 to 3.1x10 5 based on TRI modeled
8547 exposure data for high-end and central tendency, respectively.
8548
8549 Complete cancer and non-cancer risk results are provided in the Draft Risk Evaluation for 1,1-
8550 Dichloroethane - Supplemental Information File: Supplemental Information on IIOAC TRI Exposure
8551 and Risk Analysis (U.S. EPA. 2024p).
Page 335 of 664
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8552 Table 5-61. Inhalation Lifetime Cancer Risks" within 1 km of TRI Air Releases Based on 95th Percentile Modeled Ambient Air
8553 Exposure Concentrations
OES
Corresponding COUs
# Facilities
Maximum 95th Percentile Cancer Risks Estimated within 10-1,000 m of
Facilities* c
Overall
Confidence
Life Cycle
Stage/Category
Subcategory
Total
Risk
>lE-06
10 m
30 m
30-60 m
60 m
100 m
100-1,000 m
1,000 m
Manufacturing
Manufacturing/
domestic
manufacturing
Domestic
manufacturing
9
7
1.6E-03
6.4E-04
4.9E-04
2.6E-04
1.2E-04
1.7E-05
2.9E-06
High
Processing as a
reactive
intermediate
Processing/
as a reactant,
recycling
Intermediate in all
other basic organic
chemical
manufacturing;
Intermediate in all
other chemical
product and
preparation
manufacturing;
Recycling
6
2
1.1E-04
4.5E-05
3.1E-05
1.8E-05
8.4E-06
1.2E-06
1.9E-07
High
General waste
handling,
treatment, and
disposal
Disposal/
Disposal
Disposal
8
1
1.4E-04
6.6E-05
4.3E-05
2.8E-05
1.4E-05
1.0E-06
3.4E-07
High
"Lifetime cancer risks based on 78 years of continuous inhalation exposure averaged over a 78-year lifetime.
h Cancer risks were also calculated at 2,500, 5,000, and 10,000 m from all facilities.
c Cancer risk estimates that exceed the benchmark (i.e., cancer risks greater than the cancer risk benchmark) are bolded.
8554
8555
8556
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8557 Table 5-62. Inhalation Lifetime Cancer Risks" within 1 km of NEI Air Releases Based on 95th Percentile Modeled Ambient Air
8558 Exposure Concentrations
OES
Corresponding COUs
# Facilities
Maximum 95th Percentile Cancer Risks Estimated within 1,000 m of
Releases 4'
Overall
Confidence
Life Cycle
Stage/Category
Subcategory
Total
Risk
>lE-06
10 m
30 m
30 to
60 m
60 m
100 m
100 to
1,000 m
1,000 m
Commercial use
as a laboratory
chemical
Commercial use/
Other use
Laboratory
chemicals
2
0
2.6E-07
8.2E-08
5.1E-08
3.0E-08
1.3E-08
1.4E-09
2.7E-10
Moderate
Manufacturing
Manufacturing/
Domestic manufacturing
Domestic
manufacturing
9
4
1.5E-04
4.3E-05
4.3E-05
4.3E-05
4.1E-05
7.2E-06
8.6E-07
High
Processing as a
reactive
intermediate
Processing/
As a reactant;
Recycling
Intermediate in all
other basic organic
chemical
manufacturing;
Intermediate in all
other chemical
product and
preparation
manufacturing;
Recycling
50
14
2.3E-04
8.7E-05
5.9E-05
3.5E-05
1.6E-05
1.9E-06
3.4E-07
High
General waste
handling,
treatment, and
disposal
Disposal/
Disposal
Disposal
102
48
8.9E-05
5.9E-05
4.6E-05
2.9E-05
1.5E-05
1.5E-06
3.7E-07
High
Facilities not
mapped to an
OES
59
12
6.5E-05
2.6E-05
2.0E-05
1.1E-05
5.2E-06
8.4E-07
1.2E-07
N/A
"Lifetime cancer risks based on 78 years of continuous inhalation exposure averaged over a 78-year lifetime.
4 Cancer risks were also calculated at 2,500, 5,000 and 10,000 m from all facilities.
c Cancer risk estimates that exceed the benchmark (i.e., cancer risks greater than the cancer risk benchmark) are bolded.
8559
8560
8561
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8562 Table 5-63. Inhalation Lifetime Cancer Risks" within 1 km of TRI Air Releases Based on 50th Percentile Modeled Ambient Air
8563 Exposure Concentrations
OES
Corresponding COUs
# Facilities
Maximum 50th Percentile Cancer Risks Estimated within 10-1,000 m of
Facilitiesb c
Overall
Confidence
Life Cycle
Stage/Category
Subcategory
Total
Risk
>lE-06
10 m
30 m
30-60 m
60 m
100 m
100-1,000 m
1,000 m
Manufacturing
Manufacturing/
domestic
manufacturing
Domestic
manufacturing
9
7
1.2E-03
4.7E-04
2.5E-04
1.9E-04
8.6E-05
3.2E-06
1.7E-06
High
Processing as a
reactive
intermediate
Processing/
as a reactant,
recycling
Intermediate in
all other basic
organic chemical
manufacturing;
Intermediate in
all other
chemical product
and preparation
manufacturing;
Recycling
6
2
6.0E-05
2.4E-05
1.5E-05
9.8E-06
4.6E-06
2.1E-07
1.0E-07
High
General waste
handling,
treatment, and
disposal
Disposal/
disposal
Disposal
8
1
3.7E-05
1.2E-05
7.5E-06
4.3E-06
2.0E-06
1.1E-07
4.6E-08
High
"Lifetime cancer risks based on 78 years of continuous inhalation exposure averaged over a 78-year lifetime.
b Cancer risks were also calculated at 2,500, 5,000 and 10,000 m from all facilities.
c Cancer risk estimates that exceed the benchmark (i.e., cancer risks greater than the cancer risk benchmark) are bolded.
8564
8565
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8566
8567
Table 5-64. Inhalation Lifetime Cancer Risks" within 1 km of NEI Air Releases Based on 50th Percentile Modeled Ambient Air
OES
Corresponding COUs
# Releases
Maximum 50th Percentile Cancer Risks Estimated within 1,000 m of
Releases 4'
Overall
Confidence
Life Cycle
Stage/Category
Subcategory
Total
Risk
>lE-06
10 m
30 m
30 to
60 m
60 m
100 m
100 to
1,000 m
1,000 m
Commercial use as a
laboratory chemical
Commercial use/
Other use
Laboratory chemicals
2
0
1.3E-07
3.6E-08
1.9E-08
1.3E-08
5.5E-09
2.0E-10
1.0E-10
High
Manufacturing
Manufacturing/
Domestic
manufacturing
Domestic manufacturing
9
3
9.2E-05
4.2E-05
4.1E-05
4.0E-05
3.4E-05
8.9E-07
3.9E-07
High
Processing as a reactive
intermediate
Processing/
As a reactant;
Recycling
Intermediate in all other
basic organic chemical
manufacturing;
Intermediate in all other
chemical product and
preparation
manufacturing;
Recycling
50
14
1.8E-04
5.7E-05
3.2E-05
2.2E-05
9.7E-06
3.7E-07
2.0E-07
High
General waste handling,
treatment, and disposal
Disposal/
Disposal
Disposal
102
39
4.8E-05
2.4E-05
1.3E-05
8.3E-06
3.6E-06
1.9E-07
7.4E-08
High
Facilities not mapped to an
OES
59
9
5.1E-05
2.1E-05
1.2E-05
8.4E-06
4.0E-06
1.6E-07
8.5E-08
N/A
"Lifetime cancer risks based on 78 years of continuous inhalation exposure averaged over a 78-year lifetime.
4 Cancer risks were also calculated at 2,500, 5,000 and 10,000 m from all facilities.
c Cancer risk estimates that exceed the benchmark (i.e., cancer risks greater than the cancer risk benchmark) are bolded.
8568
8569
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8570 Table 5-65. Inhalation Lifetime Cancer Risks" within 1 km of TRI Air Releases
OES
Cancer Risks above Benchmarks
Release TypE-Risk
Driver
Maximum Risk
Estimate b c
Further
Distance
(m)
Release Scenario
50th
95th
Fugitive
Stack
Both
Manufacturing
Y
Y
X
1.6E-03
1,000
Processing as a reactive intermediate
Y
Y
X
1.1E-04
100-1,000
General waste handling, treatment, and disposal
Y
Y
X
1.4E-04
100-1,000
11 Lifetime cancer risks based on 78 years of continuous inhalation exposure averaged over a 78-year lifetime. Estimated cancer risks calculated using maximum
concentration across facilities within OES by distance from the release point.
h Cancer risk estimates that exceed the benchmark (i.e., cancer risks greater than the cancer risk benchmark) are highlighted by holding the number.
c Risk estimates based on 95th percentile modeled ambient air exposure concentrations.
Table 5-66. Inhalation Lifetime Cancer Risks" within 1 km of NEI Air Releases
OES
Cancer Risks above Benchmarks
Release Type-Risk Driver
Maximum Risk
Estimatebc
Further
Distance
(m)
Release Scenario
50th
95th
Fugitive
Stack
Both
Commercial use as a laboratory chemical
N
N
X
2.6E-07
N/A
Manufacturing
Y
Y
X
1.5E-04
100-1,000
Processing as a reactive intermediate
Y
Y
X
2.3E-04
100-1,000
General waste handling, treatment, and disposal
Y
Y
X
8.9E-05
100-1,000
Facilities not mapped to an OES
Y
Y
X
6.5E-05
100
"Lifetime cancer risks based on 78 years of continuous inhalation exposure averaged over a 78-year lifetime. Estimated cancer risks calculated using maximum
concentration across facilities within OES by distance from the release point.
h Cancer risk estimates that exceed the benchmark (i.e., cancer risks greater than the cancer risk benchmark) are highlighted by holding the number.
0 Risk estimates based on 95th percentile modeled ambient air exposure concentrations.
8574
8575
8576
8577
8578
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8579 Table 5-67. Inhalation Lifetime Cancer Risks" within 1 km of Air Releases Based on 95th Percentile Modeled Exposure
8580 Concentrations for the Commercial Use as a Laboratory Chemical, and Processing - Repackaging for Laboratory Chemicals OESs
OES
Meteorology
Source
Land
Maximum 95th Percentile Cancer Risks Estimated within 1,000 m of Releases6 c
10 m
30 m
30 to 60 m
60 m
100 m
100 to 1,000 m
1,000 m
Processing -
repackaging
High
Stack and
Fugitive
Urban
6.6E-06
1.9E-06
1.4E-06
8.7E-07
7.1E-07
2.4E-07
1.0E-07
High
Stack and
Fugitive
Rural
6.6E-06
1.9E-06
1.5E-06
1.1E-06
1.0E-06
2.7E-07
8.9E-08
Commercial use as a
laboratory chemical
High
Stack and
Fugitive
Urban
1.1E-05
3.1E-06
2.5E-06
1.8E-06
1.7E-06
6.4E-07
2.8E-07
High
Stack and
Fugitive
Rural
1.1E-05
3.1E-06
2.8E-06
2.2E-06
2.5E-06
7.2E-07
2.4E-07
"Lifetime cancer risks based on 78 years of continuous inhalation exposure averaged over a 78-year lifetime. Estimated cancer risks calculated using maximum
concentration by distance from the release point.
b Cancer risk estimates that exceed the benchmark (i.e., cancer risks greater than the cancer risk benchmark) are highlighted by holding the number.
0 Risk estimates based on 95th percentile modeled ambient air exposure concentrations.
8581
8582
8583 Table 5-68. IIOAC Indoor Air Inhalation Lifetime Cancer Risks" within 1 km of TRI Air Releases Based on 95th Percentile Modeled
8584 Exposure Concentrations
OES
Corresponding COUs
# Facilities
Distance from Facility with (m)bc
Overall
Confidence
Life Cycle
Stage/Category
Subcategory
Total
Risk
>lE-06
100 m
100 to 1,000 m
1,000 m
Manufacturing
Manufacturing/Domestic
Manufacturing
Domestic manufacturing
9
3
1.2E-04
1.5E-05
5.3E-06
Medium
Processing as a
reactive intermediate
Processing/As a Reactant,
Recycling
Intermediate in all other basic
organic chemical
manufacturing;
Intermediate in all other
chemical product and
preparation manufacturing;
Recycling
6
2
6.7E-06
7.3E-07
3.2E-07
Medium
General waste
handling, treatment,
and disposal
Disposal/Disposal
Disposal
8
1
4.6E-06
5.3E-07
2.1E-07
Medium
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OES
Corresponding COUs
# Facilities
Distance from Facility with (m)bc
Overall
Confidence
Life Cycle c , ,
Stage/Category Subcategory
rr , . Risk
Total >lE-06
100 m 100 to 1,000 m 1,000 m
"Lifetime cancer risks based on 78 years of continuous inhalation exposure averaged over a 78-year lifetime. Estimated cancer risks calculated using maximum concentration across
facilities within OES by distance from the release point.
4 Cancer risk estimates that exceed the benchmark (i.e., cancer risks greater than the cancer risk benchmark) are highlighted by bolding the number.
c Risk estimates based on 95th percentile modeled ambient air exposure concentration.
8585
8586
8587
8588
Table 5-69. IIOAC Indoor Air Inhalation Lifetime Cancer Risks" within 1 km of TRI Air Releases Based on 50th Percentile Modeled
OES
Corresponding COUs
# Facilities
Distance from Facility with (m) bc
Overall
Confidence
Life Cycle
Stage/Category
Subcategory
Total
Risk
>lE-06
100
100 to 1,000
1,000
Manufacturing
Manufacturing/
Domestic Manufacturing
Domestic manufacturing
9
3
7.4E-05
8.4E-06
3.2E-06
Medium
Processing as a reactive
intermediate
Processing/As a
Reactant, Recycling
Intermediate in all other basic
organic chemical manufacturing;
Intermediate in all other chemical
product and preparation
manufacturing; Recycling
6
2
4.0E-06
4.5E-07
1.7E-07
Medium
General waste handling,
treatment, and disposal
Disposal/Disposal
Disposal
8
1
2.7E-06
3.1E-07
1.2E-07
Medium
"Lifetime cancer risks based on 78 years of continuous inhalation exposure averaged over a 78-year lifetime. Estimated cancer risks calculated using maximum
concentration across facilities within OES by distance from the release point.
h Cancer risk estimates that exceed the benchmark (i.e., cancer risks greater than the cancer risk benchmark) are highlighted by bolding the number.
0 Risk estimates based on 95th percentile modeled ambient air exposure concentration.
8589
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8590
8591
8592
8593
8594
8595
8596
8597
8598
8599
8600
8601
8602
8603
8604
8605
8606
8607
8608
8609
8610
8611
8612
8613
8614
8615
8616
8617
8618
8619
8620
8621
8622
8623
8624
8625
8626
8627
8628
8629
8630
8631
8632
8633
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5.3.3.2.2 Land Use Analysis
For locations where lifetime cancer risk would exceed 1 x 10~6 (10 of the 23 GIS-mapped TRI facilities),
EPA evaluated land use patterns to determine residential or industrial/commercial businesses or other
public spaces relative to facilities emitting 1,1-dichloroethane and whether general population
community risks may be reasonably anticipated. A detailed discussion of the methodology used, and the
results of this analysis are provided in Appendix E.3. In summary, EPA determined whether residential,
industrial/ commercial businesses, or other public spaces are present within the radial distances where
cancer risk would exceed 1 x 10~6 from each releasing facility based on exposures to the 95th percentile
modeled air concentrations. As shown in Table Apx E-8, EPA's land use analysis did not identify any
residential, industrial/commercial businesses, or other public spaces within those 1,000 m where risk
would exceed 1 x 10 6, Based on this characterization of land use patterns and expected risk estimates,
EPA does not expect exposure and therefore does not expect a risk to the general population resulting
from 1,1-dichloroethane releases via the ambient air pathway. As stated in Appendix E.4, additional land
use analysis was not warranted for aggregate analysis. Also, EPA did not consider possible future
residential use of areas.
5.3.3.2.3 Dermal Exposures
No acute, chronic, nor cancer dermal risks were identified from the various exposure scenarios outlined
in Section 5.1.2.2.3. Detailed calculations and results are presented in the supplemental file,
Supplemental Information File: Surface Water Concentration and Fish Ingestion and Swimming High-
End Exposure Estimates (U.S. EPA. 2024r).
5.3.3.2.4 Oral Exposures
EPA estimated the possibility of risks associated with oral exposures from drinking water consumption.
Facilities were identified with releases of 1,1-dichloroethane resulting in either the median (central
tendency) or maximum exposures (see Section 5.1.2.4.1). None of the drinking water general population
oral exposures were estimated to result in either acute, chronic or cancer risks (see Table 5-70).
Oral exposures from fish ingestion did not result in acute or chronic risks but there were several
conditions of use/OES exposures that resulted in cancer risks (Table 5-70). Specifically, the adult high-
end/subsistence fisher exposures for Manufacturing, Processing as a reactant intermediate, Waste
handling (POTW), Waste Handling/Remediation and unknown COU/OES. This Remediation COU/OES
also had estimates of oral cancer risk resulting from 50th percentile fish ingestion rate exposures.
EPA assumed that subsistence fishing is a likely scenario in receiving waters associated with the above
listed COUs/OES. That is, it is common to fish in the bayous of Louisiana where the manufacturing
facility releases occur and likely in the Navajo Nation in Arizona where the POTW releases occur. The
high-end surface water concentrations are estimated in Arizona because the receiving waterbody, the
Chinle Wash, may be intermittent, so that the effluent would in essence be the dominant source of
surface water. Additional areas of exposure resulting in fish ingestion risk include a small tributary to
San Jacinto Bay in Texas (associated with Processing as a reactant COU), Spring Creek in Ohio
(Unknown COU) and South Fork of Arroyo Conejo Creek in California (Waste handling/remediation
COU).
As presented in Sections 5.1.2.4.3, 5.1.2.4.4 and 5.1.2.4.5, the estimated oral exposures of 1,1-
dichloroethane from incidental ingestion of surface water during swimming, ingestion of soil from
biosolids land application or ingestion of soil containing 1,1-dichloroethane from air deposition are low
Page 343 of 664
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8635
8636
8637
8638
8639
8640
8641
8642
8643
8644
8645
8646
8647
8648
8649
8650
8651
8652
PUBLIC RELEASE DRAFT
July 2024
compared to oral hazard values. Non-cancer risks below the benchmark MOE from these acute/chronic
oral exposures are not expected.
5.3.3.2.5 Summary of Risk Estimates for General Population
Table 5-70 below presents a summary of the risk estimates for the three main exposure scenarios
associated with facility releases: ambient air inhalation, indoor air inhalation, drinking water ingestion
(surface water), and fish ingestion.
Ambient air inhalation risk values in Table 5-70 are presented and correlated to the distance from the
emitting facility. For example, for the manufacturing COU, the highest chronic risk is found at
exposures at 10m from the facility releasing 1,1-dichloroethane. Exposures beyond 10 m will not result
in chronic inhalation risk. Likewise, cancer risk for the manufacturing COU is estimated to be greater
than lxl0~6 only for locations within 1,000 m of the emitting facility. However, as stated in Section
5.3.3.2.2, no general population residential communities were identified within the 1,000 m distance.
Therefore, no general population non-cancer nor cancer inhalation risks are anticipated. Since indoor air
inhalation risks are directly correlated and calculated from ambient air concentrations, no general
population risks are anticipated for indoor air since, again, there are no residential populations within
1,000 m. Lastly, no general population risks were identified for drinking water ingestion or fish
ingestion.
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8653 Table 5-70. General Population Risk Summary
Life Cycle
Stage/
Category
Subcategory
OES
Exposure Route
and Duration
Exposure Level
Risk Estimates for Each Exposure Scenario'
Acute Non-cancer
(Benchmark MOE:
Oral = 100;
Inhalation = 30)
Chronic Non-cancer
(Benchmark MOE:
Oral = 1,000;
Inhalation = 300)
Cancer
(Benchmark
1.111 1 (I h)
Manufacture/
Domestic
Manufacturing
Domestic
manufacture
Manufacturing
Ambient Air
Inhalation
Central Tendency
1.4E02
1.2E02
(Risk at 10 m)
5.3E-04
(Risk at 10-1,000 m)
High-End
1.7E01
(Risk at 10 m)
9.1E1
(Risk at 30 m)
7.0E-04
(Risk at 10-1,000 m)
Indoor Air
Inhalation
Central Tendency
5.2E06
1.1E07
3.1E-05
(Risk at 100-1,000 m)
High-End
3.1E06
6.7E06
5.3E-05
(Risk at 100-1,000 m)
Drinking Water
Ingestion"
Central Tendency
N/A
N/A
N/A
High-End
N/A
N/A
N/A
Fish Ingestion
Central Tendency
6.3E06
1.7E09
2.7E-09
High-End
2.2E05
5.8E07
7.7E-08
Processing/As a
Reactant
Intermediate in
all other basic
organic chemical
manufacturing /
Intermediate in
all other chemical
product and
preparation
manufacturing /
Recycling
Processing as £
reactive
intermediate
Ambient Air
Inhalation
Central Tendency
2.2E03
2.5E03
2.5E-05
(Risk at 10-
100 m)
High-End
2.8E02
14E03
4.6E-05
(Risk at 10-
100 m)
Indoor Air
Inhalation
Central Tendency
7.3E07
1.6E08
1.7E-06
(Risk at 100 m)
High-End
4.1E07
9.0E07
2.9E-06
(Risk at 100 m)
Drinking Water
Ingestion
Central Tendency
5.7E08
7.8E10
3.0E-13
High-End
6.5E06
7.7E08
2.2E-11
Fish Ingestion
Central Tendency
4.0E07
1.0E10
4.3E-10
High-End
1.4E06
3.7E08
1.2E-08
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Life Cycle
Stage/
Category
Subcategory
OES
Exposure Route
and Duration
Exposure Level
Risk Estimates for Each Exposure Scenario'
Acute Non-cancer
(Benchmark MOE:
Oral = 100;
Inhalation = 30)
Chronic Non-cancer
(Benchmark MOE:
Oral = 1,000;
Inhalation = 300)
Cancer
(Benchmark
1.111 1 (I h)
Processing/
Processing
Repackaging
Processing -
Repackaging
Processing -
repackaging
Ambient Air
Inhalation
Central Tendency
N/A
242E+08
1.4E-06
(Risk at 10 m)
High-End
3.43E+06
1.60E+08
2.8E-06
(Risk at 10 m)
Indoor Air
Inhalation''
Central Tendency
N/A
N/A
N/A
High-End
N/A
N/A
N/A
Drinking Water
Ingestion
Central Tendency
3.7E09
3.7E11
4.5E-14
High-End
2.6E07
2.3E09
7.3E-12
Fish Ingestion
Central Tendency
7.8E08
2.0E11
2.2E-11
High-End
2.7E07
7.1E09
6.3E-10
Commercial
Use/Other use
Laboratory
Chemicals
Commercial
use as a
laboratory
Chemical
Ambient
Air Inhalation
Central Tendency
2.79E+14
8.68E+07
2.6E-06
(Risk at 10-
30 m)
High-End
1.48E+06
5.87E+07
4.6E-06
(Risk at 10-
100 m)
Indoor Air
Inhalation''
Central Tendency
N/A
N/A
N/A
High-End
N/A
N/A
N/A
Drinking Water
Ingestion"
Central Tendency
N/A
N/A
N/A
High-End
N/A
N/A
N/A
Fish Ingestion
Central Tendency
8.5E08
2.2E11
2.0E-11
High-End
3.0E07
7.8E09
5.7E-10
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Life Cycle
Stage/
Category
Subcategory
OES
Exposure Route
and Duration
Exposure Level
Risk Estimates for Each Exposure Scenario'
Acute Non-cancer
(Benchmark MOE:
Oral = 100;
Inhalation = 30)
Chronic Non-cancer
(Benchmark MOE:
Oral = 1,000;
Inhalation = 300)
Cancer
(Benchmark
1.111 1 (I h)
Disposal/
Disposal
Disposal
General waste
handling,
treatment, and
disposal
Ambient
Air Inhalation
Central Tendency
5.8E03
4.1E03
1.6E-05
(Risk at 1-60 m)
High-End
3.1E02
3.1E03
5.8E-05
(Risk at 1-100 m)
Indoor
Air Inhalation
Central Tendency
2.9E10
6.3E10
1.1E-06
(Risk at 100 m)
High-End
1.7E10
3.6E10
1.9E-06
(Risk at 100 m)
Drinking Water
Ingestion
Central Tendency
1.1E08
1.0E10
1.6E-12
High-End
2.0E06
84E07
2.0E-10
Fish
Ingestion
Central Tendency
3.0E07
7.8E09
5.7E-10
High-End
1.1E06
2.8E08
1.6E-08
Disposal/
Disposal
Disposal
Waste
handling,
treatment, and
disposal
(POTW)
Drinking Water
Ingestion
Central Tendency
2.5E09
1.6E11
1. IE—13
High- End
4.1E06
1.7E08
9.6E-11
Fish
Ingestion
Central Tendency
6.7E07
1.7E10
2.6E-10
High- End
2.4E06
6.1E08
7.3E-09
Disposal/
Disposal
Disposal
Waste
handling,
treatment, and
disposal
(remediation)
Drinking Water
Ingestion
Central Tendency
1.9E09
1.7E11
9.6E-14
High-End
4.0E07
3.7E09
4.5E-12
Fish
Ingestion
Central Tendency
4.9E06
1.3E09
3.5E-09
High-End
1.7E05
4.5E07
1.0E-07
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Life Cycle
Stage/
Category
Subcategory
OES
Exposure Route
and Duration
Exposure Level
Risk Estimates for Each Exposure Scenario'
Acute Non-cancer
(Benchmark MOE:
Oral = 100;
Inhalation = 30)
Chronic Non-cancer
(Benchmark MOE:
Oral = 1,000;
Inhalation = 300)
Cancer
(Benchmark
1.111 1 (I h)
Facilities not
mapped to an
OES/Facilities not
mapped to an OES
Facilities not
mapped to an
OES
Facilities not
mapped to an
OES
Ambient Air
Inhalation
Central Tendency
7.5E09
7.7E07
2.1E-05
(Risk at 10-
100 m)
High-End
5.6E06
5.2E07
2.8E-05
(Risk at 10-
100 m)
Drinking Water
Ingestion
Central Tendency
9.6E08
1.0E11
1.7E-13
High-End
1.4E07
6.0E08
2.8E-11
Fish
Ingestion
Central Tendency
2.6E07
6.9E09
6.5E-10
High-End
9.4E05
2.4E08
1.8E-08
" Drinking water risks were not assessed for this COU. Drinking water intakes were not identified downstream of the largest releasing facility within the COU.
h Indoor air inhalation risks were not assessed for this COU. Indoor air inhalation risks were assessed only for TRI facilities using EPA's IIOAC model.
c Ambient and indoor air inhalation risk shown is the maximum risk value estimated from TRI and NEI air releases at any distance between 10 and 10,000 meters.
Distance range shown corresponds to distances where risk is exceeding benchmark.
N/A - not applicable - modeled concentrations were zero and resulted in indeterminate (invalid) risk.
N/A - not applicable - not assessed.
8654
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5.3.4 Risk Characterization of Aggregate and Sentinel Exposures
As stated in Section 5.1.4, EPA considered sentinel exposures by considering risks to populations who
may have upper bound exposures; for example, workers and ONUs who perform activities with higher
exposure potential, or certain physical factors like body weight or skin surface area exposed. EPA
characterized high-end exposures in evaluating exposure using both monitoring data and modeling
approaches. Where statistical data are reasonably available, EPA typically uses the 95th percentile value
of the reasonably available dataset to characterize high-end exposure for a given condition of use. In
cases where sentinel exposures result in MOEs greater than the benchmark or cancer risk lower than the
benchmark (i.e., risks were not identified), EPA did no further analysis because sentinel exposures
represent the worst-case scenario.
EPA aggregated ambient air concentrations to estimate inhalation risks from co-located facilities (see
Section 5.1.3). EPA aggregated oral and dermal risks for the swimming scenario (U.S. EPA. 2024r)
since endpoints for the selected PODs are the same. However, EPA did not aggregate risks across
exposure routes for all exposure durations as the health outcomes (endpoints for the selected PODs)
were different for oral/dermal and inhalation studies. EPA did not aggregate inhalation risks for workers
and general population because there is no general population at risk residing near facilities (see Section
5.3.3.2.2).
5.3.5 Overall Confidence and Remaining Uncertainties in Human Health Risk
Characterization
EPA took fate, exposure (occupational, and general population), and human health hazard
considerations into account when characterizing the human health risks of 1,1-dichloroethane. Human
health risk characterization evaluated confidence from occupational and general population exposures
and human health hazards. Hazard confidence and uncertainty is represented by health outcome and
exposure duration as reported in Section 5.2.7, which presents the confidence, uncertainties, and
limitations of the human health hazards for 1,1-dichloroethane using 1,2-dichloroethane toxicity data as
an analog for read-across. Confidence in the exposure assessment has been synthesized in the respective
weight of scientific evidence conclusion sections for occupational exposures (see Section 5.3.5.1) and
general population exposures (see Section 5.3.5.2). Table 5-71 provides a summary of confidence for
exposures and hazards for non-cancer endpoints for the COUs that resulted in any non-cancer risks;
Table 5-72 provides a confidence summary for cancer for the COUs that resulted in cancer risks.
5.3.5.1 Occupational Risk Estimates
Uncertainties associated with the occupational exposure assessment are assessed in consideration of the
following:
1. Release data for 1,1-dichloroethane are reported from databases such as TRI, NEI, DMR, and
more recently, CDR.
2. Breathing zone monitoring data are available for 1,1-dichloroethane for several COUs from a
completed test order and represent measurements of exposures during manufacturing and are
representative of industries and workplace practices.
3. Dermal absorption measurements for 1,1-dichloroethane are available from a completed test
order and are representative of exposures for workers in the manufacturing and processing of
1,1-dichloroethane in the workplace.
5.3.5.2 General Population Risk Estimates
Section 5.3.5.2 illustrates the confidence in the assessment of the general population exposure scenarios.
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Air Pathway
Overall confidence in risk estimates is high for OESs/COUs that rely primarily on release data reported
to TRI and NEI (based on high levels of confidence in underlying release information used to estimate
exposures). Overall confidence in risk estimates is medium for OESs/COUs for which release estimates
are based on modeled information.
As described in Section 3.3.5.1, EPA has high confidence in the air concentrations estimated from TRI
and NEI release data using AERMOD. As described in Section 5.1.2.5.1 the overall confidence in
exposure estimates varies due to variable levels of confidence in underlying release information used to
the support the analysis (high levels of confidence for release data reported to TRI and NEI and medium
levels of confidence for modeled release estimates).
EPA identified cancer risks relative to the benchmark for 10 of the 23 TRI facilities representing three of
the five COUs. Based on characterization of land use patterns, fenceline community exposures are not
anticipated for any of the GIS located facilities with risk for all three of the COUs that rely on release
data reported to TRI.
EPA identified cancer risks relative to the benchmark for two of the COUs for which release estimates
are based on modeled information. Due to the lack of site-specific information, the exposures
assessment relied on assumptions for location specific model inputs. This lack of data results in
uncertainties surrounding these location specific parameters (e.g., flow parameters and meteorological
data). Additionally, as discussed in Appendix E.3, EPA review of land use patterns was limited to those
facilities with GIS locations that showed risk. Because estimated releases do not have a physical location
associated with a facility, EPA was unable to visually examine land use patterns around the theoretical
facility. Therefore, EPA was unable to conduct such analysis for alternative release estimates showing
risk.
Distance Where Risk Identified
IIOAC and AERMOD provided exposure concentrations at discrete distances from air releases. EPA
calculated risk at modeled discrete distances. Therefore, there is uncertainty of risk between the two
distances modeled. For example, if risk was found risk at 1,000 m and not at 2,500 m, EPA is uncertain
if there is risk at 1,001 to 2,499 m. To not underestimate risk beyond the risk showing distance (e.g., at
1,001 meters), or overestimate risk closer to the distance where risk was not found (e.g., at 2,499
meters), remodeling may be required to determine exposure concentrations, and thus calculating risk
between the two discrete distances previously modeled. Additionally, reported TRI facility's location
data (latitude/longitude) may not represent the actual location of the releasing source (e.g., a processes
stack).
However, for 1,1-dichloroethane, fenceline community exposures are not at levels of 1,1-dichloroethane
concentrations that present risk. That is, the fenceline community locations are beyond the location of
non-cancer or cancer risk relative to the benchmark. EPA has high confidence in the estimate of general
population exposures as a basis for confidence in the absence of risk to the general population. General
population risk is therefore not included in either Table 5-71 or Table 5-72.
Uncertainties associated with the general population exposures assessment included the lack of site-
specific information, the incongruence between the modeled concentrations and doses with the
monitoring data, and the complexity of the assessed exposure scenarios.
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5.3.5.3 Hazard Values
Based on the similarities in chemical structure, metabolism and toxicological responses, EPA confirmed
the choice of 1,2-dichloroethane as the appropriate analog. EPA has high confidence that the 1,2-
dichloroethane isomer data accurately reflects the human health hazards of 1,1-dichloroethane where
there are data gaps. In addition, 1,2-dichloroethane lacked adequate data by the dermal route for any
exposure duration. Therefore, EPA used a route-to-route extrapolation approach from the available 1,2-
dichloroethane oral data to fill in the dermal data gap. EPA also has high confidence in this approach.
However, in oral dosing, the dose is rapidly absorbed and over 80 percent is exhaled through the lungs
unchanged. Dermal exposures have similar elimination through the lungs. Therefore, oral PODs were
used for extrapolation via the dermal route.
EPA has high confidence in the human health hazard database for 1,2-dichloroethane and in the
selection of the critical PODs. This is based on several reasons. First, all studies used to assess the
hazards for 1,2-dichloroethane were rated high to medium in SR. Second, critical non-cancer effects that
were ultimately selected as PODs for quantitative risk estimates (kidney toxicity, neurotoxicity,
immunotoxicity, and reproductive toxicity), were considered the most sensitive and biologically relevant
effects, supported by multiple lines of evidence that spanned across species, routes, and durations of
exposure (see Section 5.2.6.4 and endpoint selection tables: Table 5-42, Table 5-43, Table 5-44, Table
5-45, Table 5-46, and Table 5-47.
While EPA has high confidence in the hazard identification of PODs used for quantitative risk estimates,
there are some uncertainties in the 1,2-dichloroethane database. For example, while there were several
studies via the chronic exposure duration for both oral and inhalation exposures, none of those studies
were selected for the chronic POD for a variety of reasons including the identified NOAELs/LOAELs
were higher than the recommended endpoint, or there were limited endpoints evaluated, or other
methodological issues (see endpoint selection tables: Table 5-46 and Table 5-47). As a result,
subchronic data was used for the chronic POD and an uncertainty factor (UFS) of 10x was applied to
account for the use of a short-term study for long-term (chronic) assessment.
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8777 Table 5-71. Overall Confidence for Acute, Short-Term, and Chronic Human Health Non-cancer Risk Characterization for COUs
8778 Resulting in Risks"h
cou
Exposure
Route/Exposed Group
Exposure
Confidence
Hazard
Confidence
Risk
Characterization
Confidence
Life Cycle Stage
Category
Subcategory
Occupational
Manufacturing/
Domestic
Manufacturing
Domestic manufacturing
Manufacturing
Inhalation/Worker
(operator/process
technician)
+++
+++
+++
Inhalation/Worker
(maintenance technician)
+++
+++
+++
Dermal/Worker
+++
+++
+++
Processing/
As a Reactant
Intermediate in all other basic
organic chemical
manufacturing/intermediate
in all other chemical product
and preparation
manufacturing/recycling
Processing as reactive
intermediate
Inhalation/Worker
++
+++
+++
Dermal/Worker
++
++
+++
Processing/
Processing -
Repackaging
Processing - repackaging
Processing -
repackaging
Inhalation/Worker
++
+++
+++
Inhalation/ONU
++
+++
+++
Dermal/Worker
++
++
+++
Commercial
Use/Laboratory
Chemicals
Laboratory chemicals
reference material
Commercial use as a
laboratory chemical
Dermal/Worker
++
++
+++
Disposal
Disposal
General waste
handling, treatment,
and disposal
Inhalation/Worker
++
+++
+++
Dermal/Worker
++
++
+++
Disposal
Disposal
Waste handling,
treatment, and disposal
(WWT)
Inhalation/Worker
++
+++
+++
Dermal/Worker
++
++
+++
11 This table identifies COUs that have any non-cancer risk (acute, short-term, or chronic) and the route associated with the risk.
h Short-term risks were evaluated for workers only and not the general population.
8779
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8780 Table 5-72. Overall Confidence for Lifetime Human Health Cancer Risk Characterization for CPUs Resulting in Risks
COUs
Life Cycle Stage
Category
Subcategory
Exposure Route/Exposed
Group
Exposure
Confidence
Hazard
Confidence
Risk
Characterization
Confidence
Occupational
Manufacturing/
Domestic
Manufacturing
Domestic Manufacturing
Manufacturing
Inhalation/Worker
(operator/process
technician)
Inhalation/Worker
(maintenance technician)
Dermal/Worker
+++
+++
+++
Processing/
As a Reactant
Intermediate in all other
basic organic chemical
manufacturing/intermediate
in all other chemical product
and preparation
manufacturing/recycling
Inhalation/Worker
Processing as
reactive intermediate
Dermal/Worker
Processing/
Processing -
Repackaging
Processing - repackaging
Processing -
repackaging
Inhalation/Worker
Inhalation/ONU
Dermal/Worker
Commercial
Use/Laboratory
Chemicals
Laboratory chemicals
reference material
Commercial use as a
laboratory chemical
Dermal/Worker
Disposal
Disposal
General waste
handling, treatment,
and disposal
Inhalation/Worker
Dermal/Worker
8781
Disposal
Disposal
Waste handling,
treatment, and
disposal (WWT)
Inhalation/Worker
Dermal/Worker
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6 UNREASONABLE RISK DETERMINATION
TSCA section 6(b)(4) requires EPA to conduct a risk evaluation to determine whether a chemical
substance presents an unreasonable risk of injury to health or the environment, without consideration of
costs or other non-risk factors, including an unreasonable risk to a potentially exposed or susceptible
subpopulation identified by EPA as relevant to the risk evaluation, under the conditions of use (COUs).
EPA has preliminarily determined that 1,1-dichloroethane presents an unreasonable risk of injury to
health and the environment under the COUs. 1,1-Dichloroethane is a highly volatile organic compound
mainly used as an industrial processing chemical to manufacture 1,1,1-trichloroethane (CASRN 71-55-
6) and other chlorinated solvents, including 1,2-dichloroethane currently undergoing risk evaluation as
well. There are no commercial or consumer applications besides laboratory research. Exposure is
generally isolated to a few regions with no risks of injury to fenceline communities that would
contribute to the unreasonable risk determination for 1,1-dichloroethane. This draft unreasonable risk
determination is based on the information in previous sections of this draft risk evaluation and the
appendices and supporting documents in accordance with TSCA section 6(b), as well as TSCA's best
available science (TSCA section 26(h)) and weight of scientific evidence standards (TSCA section
26(i)), and relevant implementing regulations in 40 CFR part 702.
Eight COUs were evaluated for 1,1-dichloroethane and are listed in Table 1-1. In this preliminary
determination EPA is concluding that the following COUs contribute to the unreasonable risk:
• Manufacture (domestic manufacture);
• Processing as a reactant as an intermediate in all other basic organic chemical manufacturing;
• Processing as a reactant as an intermediate in all other chemical product and preparation;
manufacturing
• Processing: repackaging;
• Processing: recycling;
• Commercial use in laboratory chemicals; and
• Disposal.
EPA has preliminarily determined that the following COU does not contribute to the unreasonable risk:
Distribution in commerce.
Whether EPA makes a determination of unreasonable risk for a particular chemical substance under
amended TSCA depends upon risk-related factors beyond exceedance of benchmarks, such as the
endpoint under consideration, the reversibility of effect, exposure-related considerations (e.g., duration,
magnitude, or frequency of exposure, or population exposed), and the confidence in the information
used to inform the hazard and exposure values. In this draft risk evaluation, the Agency describes the
strength of the scientific evidence supporting the exposure assessment as robust, moderate, slight, or
indeterminate. The Agency generally has a moderate or robust degree of confidence in its
characterization of risk where the scientific evidence weighed against the uncertainties is robust enough
to characterize hazards, exposures, and risk estimates, as well as where the uncertainties inherent in all
risk estimates do not undermine EPA's confidence in its risk characterization. This draft risk evaluation
discusses important assumptions and key sources of uncertainty in the risk characterization, and these
are described in more detail in the respective weight of scientific evidence conclusions sections for fate
and transport (Section 2.2.3), environmental release (Section 3.2.2), environmental exposures (Section
4.1.5), environmental hazards (Section 4.2.4), and human health hazards (Section 5.2.6.4). It also
includes overall confidence and remaining uncertainties sections for human health (Section 5.3.5) and
environmental risk characterizations (Section 4.3.5).
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In the 1,1-dichloroethane draft unreasonable risk determination, EPA considered risk estimates with an
overall confidence rating of slight, moderate, robust, or indeterminate. In general, the Agency makes an
unreasonable risk determination based on risk estimates that have an overall confidence rating of
moderate or robust, since those confidence ratings indicate the scientific evidence is adequate to
characterize risk estimates despite uncertainties or is such that it is unlikely the uncertainties could have
a significant effect on the risk estimates (see Appendix K.2.3.1 and Appendix M).
If in the final risk evaluation for 1,1-dichloroethane EPA determines that 1,1-dichloroethane presents an
unreasonable risk of injury to health or the environment under the COUs, EPA will initiate risk
management rulemaking for 1,1-dichloroethane by applying one or more of the requirements under
TSCA section 6(a) to the extent necessary so that 1,1-dichloroethane no longer presents an unreasonable
risk. Under TSCA section 6(a), EPA is not limited to regulating the specific activities found to
contribute to unreasonable risk and may select from among a suite of risk management options related to
manufacture, processing, distribution in commerce, commercial use, and disposal to address the
unreasonable risk. For instance, EPA may regulate upstream activities (e.g., processing, distribution in
commerce) to address downstream activities that contribute to unreasonable risk (e.g., use)—even if the
upstream activities do not contribute to unreasonable risk. EPA would also consider whether such risk
may be prevented or reduced to a sufficient extent by action taken under another Federal law, such that
referral to another agency under TSCA section 9(a) or use of another EPA-administered authority to
protect against such risk pursuant to TSCA section 9(b) may be appropriate.
6.1 Unreasonable Risk to Human Health
Calculated risk estimates (MOEs or cancer risk estimates) can provide a risk profile of 1,1-
dichloroethane by presenting a range of estimates for different health effects for different COUs. When
characterizing the risk to human health from occupational exposures during risk evaluation under TSCA,
EPA conducts baseline assessments of risk and makes its determination of unreasonable risk from a
baseline scenario that does not assume use of respiratory protection or other PPE.15 Making
unreasonable risk determinations based on the baseline scenario should not be viewed as an indication
that EPA believes there are no occupational safety protections in place at any location, or that there is
widespread noncompliance with existing regulations that may be applicable to 1,1-dichloroethane. A
calculated MOE that is less than the benchmark MOE is a starting point for supporting a determination
of unreasonable risk of injury to health, based on non-cancer effects. Similarly, a calculated cancer risk
estimate that is greater than the cancer benchmark is a starting point for supporting a determination of
unreasonable risk of injury to health from cancer. It is important to emphasize that these calculated risk
estimates alone are not "bright-line" indicators of unreasonable risk, and factors must be considered
other than whether a risk estimate exceeds a benchmark.
6.1.1 Populations and Exposures EPA Assessed to Determine Unreasonable Risk to
Human Health
EPA evaluated exposures to workers, including ONUs, and the general population using reasonably
available monitoring and modeling data for inhalation and dermal exposures, as applicable. EPA
evaluated risk from inhalation and dermal exposure of 1,1-dichloroethane to workers as well as
inhalation exposures to ONUs. Because the Agency did not identify any consumer uses for 1,1-
dichloroethane, exposures to consumers were not evaluated. For the general population, EPA evaluated
risk from (1) inhalation exposure; (2) dermal exposures to swimmers; and (3) oral exposures via
15 It should be noted that in some cases, baseline conditions may reflect certain mitigation measures, such as engineering
controls, in instances where exposure estimates are based on monitoring data at facilities that have engineering controls in
place.
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drinking water, fish ingestion, and incidental oral ingestions from swimming and activities with soil.
Descriptions of the data used for human health exposure and human health hazards are provided in
Sections 5.1 and 5.2 of this draft risk evaluation. Uncertainties for overall exposures and hazards are
presented in Section 5.3.5 and are summarized in Table 5-19 in Section 5.1.1.3 for occupational
exposures, Table 5-34 in Section 5.1.2.5 for general population exposures, and Appendix M—all are
considered in the preliminary unreasonable risk determination. Note that Table 5-47 of this draft risk
evaluation presents 1,1-dichloroethane exposure durations by population.
6.1.2 Summary of Unreasonable Risks to Human Health
EPA is preliminarily determining that the unreasonable risks to human health presented by 1,1-
dichloroethane are due to
• Risk of non-cancer effects and cancer in workers from dermal and inhalation exposures; and
• Risk of non-cancer effects and cancer in ONUs from inhalation exposures.
With respect to health endpoints upon which EPA is basing this unreasonable risk determination, the
Agency has moderate to robust overall confidence in the following PODs for: (1) increased kidney
weight from acute oral/dermal exposure and degeneration with necrosis of the olfactory mucosa from
acute inhalation exposure; (2) immune response suppression (antibody-forming cells [AFCs] and spleen)
from short-term oral/dermal exposure and decrease in sperm concentration from short-term inhalation
exposure; (3) non-cancer immune response suppression (AFCs and spleen) from chronic oral/dermal
exposure and a non-cancer effect of decrease in sperm concentration from chronic inhalation exposure;
and (4) hepatocellular carcinomas from chronic oral/dermal exposure and combined carcinogenic
mammary gland adenomas, fibroadenomas, and adenocarcinomas and subcutaneous fibromas from
inhalation exposure. EPA's exposure and overall risk characterization confidence levels again varied
from moderate to high and are summarized in Table 5-19 in Section 5.1.1.3, Sections 5.2.6.4, 5.3.5, and
Appendix M.
For general population exposures, risk estimates are provided in Section 5.3.3.2 of this draft risk
evaluation only when margins of exposure (MOEs) were smaller than benchmark MOEs for non-cancer
effects or when cancer risks exceeded benchmark risk levels. A complete list of health risk estimates for
the general population is in the following supplemental files of the draft risk evaluation (see also
Appendix C): Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File:
Data Quality Evaluation Information for General Population, Consumer, and Environmental Exposure
and Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File: Data
Extraction Information for General Population, Consumer, and Environmental Exposure.
6.1.3 Basis for EPA's Determination of Unreasonable Risk to Human Health
In developing the exposure and hazard assessments for 1,1-dichloroethane, EPA analyzed reasonably
available information to ascertain whether some human populations may have greater exposure and/or
susceptibility than the general population to the hazard posed by 1,1-dichloroethane. For the 1,1-
dichloroethane draft risk evaluation, EPA accounted for the following PESS groups: infants exposed to
drinking water during formula bottle feeding, subsistence and Tribal fishers, pregnant women and
people of reproductive age, individuals with compromised immune systems or neurological disorders,
workers, people with the aldehyde dehydrogenase-2 mutation that is more likely in people of Asian
descent, lifestyle factors such as smoking cigarettes or secondhand smoke, and fenceline communities
who live near facilities that emit 1,1-dichloroethane (see Section 5.3.2, Table 5-48)
Risk estimates based on high-end exposure levels (e.g., 95th percentile) are generally intended to cover
individuals with sentinel exposure levels whereas risk estimates at the central tendency exposure are
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generally estimates of average or typical exposure. EPA applied various uncertainty factors (UFs) for
each route (oral, inhalation, and dermal) and exposure duration (acute, short-term/sub chronic, chronic)
to account for human variability, deficiencies, and the overall lack of comprehensive toxicological
information in the 1,1-dichloroethane database, as described in Section 5.2.5.3. Additionally, 1,2-
dichloroethane studies were utilized for read-across to 1,1-dichloroethane for all non-cancer PODs and
cancer slope factors to account for data gaps for 1,1-dichloroethane as described in Section 5.2.5.3. In
general, 1,2-dichloroethane is more toxic compared to 1,1-dichloroethane so the read-across approach is
human health protective. EPA also generally relies on high-end exposure levels to make an unreasonable
risk determination to capture populations that are expected to have higher exposures. The non-cancer
PODs represent the potential for greater biological susceptibility across subpopulations.
For cancer, although there is likely to be variability in susceptibility across the human population, EPA
did not identify specific human groups that are expected to be more susceptible to cancer following 1,1-
dichloroethane exposure. More information on how EPA characterized sentinel and aggregate risks is
provided in Section 5.3.4. Cancer risk estimates represent 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. 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., 1 x 10 6 to 1 x 10 4) depending on the subpopulation exposed. EPA considers the range of
1 x 10~6 to 1 x ] 0 4 as the appropriate benchmark for increased cancer risk for the general population,
including fenceline communities. These benchmarks are not bright lines and EPA has discretion to
consider other factors in making an unreasonable risk determination for the chemical substance.
Additional information regarding the cancer benchmark is provided in Section 5.3.1.2.
6.1.4 Unreasonable Risk in Occupational Settings
Based on the occupational risk estimates and related risk factors, EPA is preliminarily determining
cancer and non-cancer inhalation risks from acute, short-term/sub chronic, and chronic worker exposure
to 1,1-dichloroethane from the manufacturing, processing, and disposal COUs at many of the central
tendency and high-end exposures, as depicted in Table 6-1 contribute to the unreasonable risk. EPA is
preliminarily determining cancer and non-cancer risks from ONU inhalation exposure to 1,1-
dichloroethane in two COUs, processing - repackaging and disposal, contribute to the unreasonable risk
based on central tendency. However, considering the many conservative considerations in the risk
characterization resulting in the extreme range in MOEs between the high-end (e.g., 45) and the central
tendency (e.g., 10,000), EPA may determine in the final risk determination that it is more appropriate to
determine whether inhalation exposure for workers contributes to unreasonable risk based on the central
tendency rather than based on the high-end.
EPA has a high level of certainty in the contribution of inhalation exposures to the unreasonable risk for
workers; however, EPA has less confidence in dermal exposure for short-term/sub chronic and chronic
cancer and non-cancer risk contributing to the unreasonable risk for workers due to the number of
uncertainties particularly for short-term/sub chronic and chronic cancer and non-cancer where the
composite factor is nearing excessive uncertainty as well as an expected low dermal absorption. EPA is
preliminarily determining that cancer and non-cancer dermal risks from short-term/subchronic and
chronic worker exposure to 1,1-dichloroethane in occupational settings for all COUs except distribution
in commerce contribute to unreasonable risk from 1,1-dichloroethane. Due to the uncertainties identified
in this Draft Risk Evaluation for 1,1-dichloroethane for short-term/subchronic and chronic cancer and
non-cancer dermal risk, EPA may determine in the final risk determination that it is not plausible for that
risk to contribute to the unreasonable risk. Cancer and non-cancer inhalation risks from the commercial
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use of 1,1-dichloroethane as a laboratory chemical do not contribute to unreasonable risk. More
information on occupational risk estimates is in Section 5.3.3.1 of this draft risk evaluation.
The Agency used accepted approaches to estimate inhalation exposures in occupational settings as
explained in Section 5.1.1. EPA's inhalation exposure scenarios for 1,1-dichloroethane are based on
robust reasonably available information. These include specific inhalation monitoring data from test
orders and other inhalation monitoring, both from 1,1-dichloroethane and from the surrogate
chemicals—including 1,2-dichloroethane as well as other volatile liquids assessed in previous EPA risk
evaluations. For the Repackaging COU EPA did not identify any inhalation exposure monitoring data
for 1,1-dichloroethane or surrogate data from other chemicals and estimated inhalation exposures using
a Monte Carlo simulation and applied the EPA Mass Balance Inhalation Model. EPA estimated the
time-weighted average inhalation exposure for a full 8-hour work-shift. Where EPA was not able to
estimate ONU inhalation exposure from monitoring data or models, the ONU exposure was assumed to
be equivalent to the central tendency experience by workers for the corresponding COU.
EPA is using the EPA Dermal Exposure to Volatile Liquids Model to calculate dermal exposure to 1,1-
dichloroethane in occupational settings. This model assumes one dermal exposure event per work day of
a fraction of neat 1,1-dichloroethane; however, the model does not address variability in exposure
duration and frequency. Even with these uncertainties and limitations, EPA still considers the weight of
scientific evidence for dermal risk estimates generated by the model to be sufficient for determining
whether a COU contributes to unreasonable risk.
More information on EPA's confidence in these risk estimates and the uncertainties associated with
them can be found in Section 5.1.1.3 of this draft risk evaluation.
6.1.5 Unreasonable Risk to the General Population
Based on the risk estimates calculated using releases from manufacturing, processing, and commercial
uses of 1,1-dichloroethane, and related risk factors, EPA is preliminarily determining that exposures to
the general population from cancer and non-cancer risks do not contribute to the unreasonable risk of
1,1-dichloroethane from any routes of exposure. EPA identified the following exposure routes for 1,1-
dichloroethane that are described in the sections that follow.
Ambient Air Inhalation
EPA estimated risks from fenceline exposures that could occur in communities immediately neighboring
releases from COUs by modeling facility-specific chemical releases reported to TRI and NEI. Cancer
and non-cancer risk estimates for fenceline exposures within 10,000 m of industrial releases were
calculated for the modeled exposure concentrations. Overall confidence is high for the facility specific
industrial releases and AERMOD modeling methodology for non-cancer and cancer risk estimates.
Descriptions of the ambient air inhalation risk estimates are in Table 5-61 to Table 5-64, and these data
are summarized in Table 5-70, and supplemental files listed in Section 5.3.3.2.1 . Non-cancer risk
estimates did not exceed the benchmark MOE for any COUs as close as 100m. Cancer risk estimates for
all but one COU did not exceed lxl0~6 at 1,000 m, and risk estimates for one COU, domestic
manufacturing, fell within the 1 x 10~6 to 1 /10 4 risk range at 1,000 m. EPA considers risk estimates at
various distances from the facility to determine whether fenceline exposures are anticipated. In general,
non-cancer risk estimates did not indicate risk for any COUs at 100m and cancer risk estimates fell
within 1x10-6 and 1x10-4 for all COUs at 100 m. A review of land use patterns (D.3) around few
facilities where cancer risk exceeded 1 x 10~6 was conducted to determine residential locations relative to
facilities emitting 1,1-dichlroethane and, therefore, whether fenceline community exposures are
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9021
9022
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9027
9028
9029
9030
9031
9032
9033
9034
9035
9036
9037
9038
9039
9040
9041
9042
9043
9044
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reasonably anticipated. Based on the land use analysis no fenceline communities are reasonably
anticipated within that distance. EPA determined that ambient air inhalation does not contribute to
unreasonable risk to the general population.
Additionally, EPA notes that concentrations from fugitive emissions tend to peak within 10 m of release
sites while contributions from stack releases generally peak around 100 m, meaning that risks nearest to
release sites are often driven by fugitive releases and therefore EPA does not expect risks to be higher at
greater distances. Cancer inhalation risks are presented in Table 5-67.
Indoor Air Inhalation
EPA estimates that cancer risk estimates exceed 1 x 10~6 up to 1,000 m for one COU—Domestic
manufacturing. EPA conducted a review of land use patterns (D.3) around the facilities where cancer
risk estimates exceeded 1 x 10 6 to determine if EPA can reasonably expect an exposure to fenceline
communities, including to general population. These facilities did not have fenceline communities
surrounding them. EPA preliminarily determined that indoor air inhalation does not contribute to
unreasonable risk to the general population. EPA's confidence in inhalation risk estimates is high. A
summary of indoor air lifetime risk estimates is presented in Table 5-68 and Table 5-69 of this draft risk
evaluation, and supplemental files listed in Section 5.3.3.2.1.
Incidental Dermal from Swimming
Incidental dermal exposure from swimming in surface waters affected by 1,1-dichloroethane
contamination were estimated to be very low compared to the dermal hazard values and preliminarily do
not contribute to unreasonable risk to the general population. Acute and average daily doses from dermal
exposure while swimming were modeled for a worst-case scenario in which the annual release occurred
in one day. Exposure estimates for swimming for adults (adults >21), youth (11-15 years), and children
(6-10 years) are provided in Table 5-28 of this draft risk evaluation.
Drinking Water Exposure
Ingestion of drinking water (diluted) or drinking water from groundwater contaminated with 1,1-
dichloroethane leaching from landfills risk estimates are in Table 5-62, and do not exceed the non-
cancer or cancer benchmarks and preliminarily do not contribute to unreasonable risk to the general
population. Oral acute and chronic non-cancer and cancer risk exposures for drinking water for adults
(adults >21) and infants (birth to <1 year) are presented in Table 5-29 of this draft risk evaluation.
Fish Ingestion
Oral exposure from consumption of fish contaminated with 1,1-dichloroethane among the general
population and subsistence fishers and fishers who are members of tribes whose habits and practices
may result in higher exposures to 1,1-dichloroethane from fish consumption. EPA preliminarily
determined that fish consumption does not contribute to unreasonable risk to the general population.
Oral acute and chronic non-cancer and cancer risk exposures for fish consumption for adults (>21 years,
including subsistence fish ingestion) and small children (1-2 years, including high-end 90th percentile
ingestion rate) are presented in Table 5-28, and risk estimates to the general population in Table 5-62 of
this draft risk evaluation.
Incidental Oral Ingestion from Swimming
Incidental oral ingestion exposure during swimming in surface waters affected by 1,1-dichloroethane
contamination was estimated to be very low compared to the oral hazard values and preliminarily do not
contribute to unreasonable risk to the general population. Incidental oral ingestion from swimming acute
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and chronic non-cancer and cancer exposure estimates for adults (adults >21), youth (11-15 years), and
children (6-10 years) are presented in Table 5-31 5-29 of this draft risk evaluation.
Soil Ingestion
Incidental oral ingestion from soil (biosolids) was estimated to be very low compared to the oral hazard
values and preliminarily do not contribute to unreasonable risk to the general population. Average
exposures for children (3-6 years) playing with and ingesting soil (receiving biosolids with 1,1-
dichloroethane contamination) were calculated in Table 5-30. Incidental oral ingestion from soil (air
deposition) of 1,1-dichloroethane was estimated to result in low exposure to 1,1-dichloroethane for any
COU. Average exposures for children (3-6 years) were calculated in Table 5-31.
6.2 Unreasonable Risk to the Environment
Calculated risk quotients (RQs) can provide a risk profile by presenting a range of estimates for different
environmental hazard effects for different COUs. An RQ equal to 1 indicates that the exposures are the
same as the concentration that causes effects. An RQ less than 1, when the exposure is less than the
effect concentration, generally indicates that there is not risk of injury to the environment that would
support a determination of unreasonable risk for the chemical substance. An RQ greater than 1, when the
exposure is greater than the effect concentration, generally indicates that there is risk of injury to the
environment that would support a determination of unreasonable risk for the chemical substance.
Additionally, if an RQ is 1 or greater, the Agency evaluates whether the RQ is 1 or greater for the days
of exceedance before making a determination of unreasonable risk. EPA evaluated days of exceedance
in two scenarios, at or above the total number of operating days, or at or above a range of days as
described in Section 4.3.1. These are 21 or more days in surface water, 4 or more days in surface water
algal, 15 or more days in benthic pore water, and 35 or more days in sediment.
6.2.1 Populations and Exposures EPA Assessed to Determine Unreasonable Risk to the
Environment
For aquatic organisms, EPA evaluated exposures via surface water and sediment (including benthic pore
water). For terrestrial organisms, EPA evaluated exposures via soil, air, surface water, and sediment.
The Agency did not directly assess terrestrial organism exposures from air due to soil and terrestrial
food web being the driver of exposures to terrestrial organisms; however, EPA assessed terrestrial
organism exposures from air deposition of 1,1-dichloroethane to soil. Additionally, EPA estimated
terrestrial organism exposures from trophic transfer of 1,1-dichloroethane from soil and surface water.
6.2.2 Summary of Unreasonable Risks to the Environment
EPA quantitatively and qualitatively assessed risk for 1,1-dichloroethane and determined that five COUs
contribute to the unreasonable risk to the environment presented by 1,1-dichloroethane in surface water
due to
• Risk of chronic reproductive effects to Daphnia magna aquatic invertebrates; and
• Risk of growth and developmental effects to algae.
EPA is preliminarily determining that risks to terrestrial organisms and risks from soil pore water and
trophic transfer (soil and soil pore water, water, sediment) do not contribute to the unreasonable risk to
the environment presented by 1,1-dichloroethane.
6.2.3 Basis for EPA's Determination of Unreasonable Risk of Injury to the Environment
Consistent with EPA's approach to benchmarks associated with human health risks, the RQ is not
treated as a bright-line for environmental risks and other risk-based factors may be considered (e.g.,
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9121
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9127
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9130
9131
9132
9133
9134
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confidence in the hazard and exposure characterization, duration, magnitude, uncertainty) for purposes
of making an unreasonable risk determination. 1,1-Dichloroethane is a volatile liquid that evaporates
readily at ambient temperature and environmental releases of the chlorinated solvent are expected to
partition primarily to air with lesser amounts to water, sediment and soil. 1,1-Dichloroethane does not
meet the criteria to be classified as persistent and bioaccumulative.
EPA has moderate and robust confidence in the chronic aquatic hazards and exposures contributing to
unreasonable risk. Additionally, the Agency has slight and moderate confidence in the terrestrial hazards
and exposures, which do not support EPA's determining that this pathway contributes to unreasonable
risk. Due to chemical and physical properties, and the low amounts of 1,1-dichloroethane undergoing
wastewater treatment, land application of biosolids from 1,1-dichloroethane wastewater treatment is not
expected to be a significant exposure pathway, and EPA does not expect exposure to 1,1-dichloroethane
from wastewater treatment to contribute to unreasonable risk to terrestrial organisms. Similarly, EPA
does not expect exposure to 1,1-dichloroethane via biosolids to contribute to unreasonable risk to the
environment. The Agency's overall environmental risk characterization confidence levels were varied
and are summarized in Table 4-20 through Table 4-22.
EPA had limited data available and was not able to quantify risks to the environment for distribution in
commerce.
6.3 Additional Information Regarding the Basis for the Unreasonable Risk
Determination
Table 6-1 and Table 6-2 summarize the basis for this draft unreasonable risk determination of injury to
human health and the environment presented in this draft 1,1-dichloroethane risk evaluation. In these
tables, a checkmark (ii) indicates how the COU contributes to the unreasonable risk by identifying the
type of effect (e.g., non-cancer and cancer for human health; acute or chronic environmental effects) and
the exposure route to the population or receptor that results in such contribution. Not all COUs, exposure
routes, or populations or receptors evaluated are included in the tables. The tables only include the
relevant exposure route, or the population or receptor that supports the conclusion that the COU
contributes to the 1,1-dichloroethane unreasonable risk determination. As explained in Section 1, for this
draft unreasonable risk determination, EPA considered the effects of 1,1-dichloroethane to human health
at the central tendency and high-end, as well as effects of 1,1-dichloroethane to human health and the
environment from the exposures associated from the condition of use, risk estimates, and uncertainties in
the analysis. See Section 5.3.3 of this draft risk evaluation for a summary of risk estimates.
6.3.1 Additional Information about COUs Characterized Qualitatively
As explained earlier in this section, EPA did not have enough data to calculate risk estimates for all
COUs, and EPA characterized the risk by integrating limited amounts of reasonably available
information in a qualitative characterization. While the Agency is concluding that 1,1-dichloroethane, as
a whole chemical, presents unreasonable risk to human health and the environment, at this time, (1) EPA
does not have enough information to quantify with enough weight of scientific evidence how much of
the unreasonable risk of 1,1-dichloroethane may be contributed by some COUs, or (2) EPA does not
expect some COUs to contribute to the unreasonable risk of 1,1-dichloroethane due to negligible
environmental releases or negligible human exposures. EPA has summarized the basis for its conclusion
about these COUs below.
EPA characterized distribution in commerce qualitatively since the Agency had limited data about
exposures from this COU besides those exposures from other COUs already quantified with release
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9150 estimates. Although EPA cannot calculate risk estimates for distribution in commerce separately from
9151 the risk related to loading and unloading from transport vehicles already estimated for other relevant
9152 COUs, the Agency has preliminarily concluded that distribution in commerce does not contribute to 1,1-
9153 dichloroethane's unreasonable risk.
9154
9155 For Processing - repackaging, and the Commercial use - laboratory chemicals, EPA does not expect
9156 significant releases to the environment for terrestrial receptors from air deposition to soil to occur and
9157 does not expect these COUs to preliminarily contribute to the unreasonable risk of 1,1-dichloroethane to
9158 the environment (see Section 4.3.4).
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9159 Table 6-1. Supporting Basis for the Draft Unreasonable Risk Determination for Human Health
cou
Population
Exposure
Route
Human Health Effects
Life Cycle
Stage
Category
Subcategory
Acute
Non-cancer
Short-
Term/subchronic
Non-cancer
Chronic
Non-cancer
Lifetime
Cancer
Manufacturing
Domestic
manufacture
Domestic manufacture
Worker
Dermal
ii"
u"
ii"
Worker - Operator/
Process Technician
Inhalation
ii*
ii*
u*
Worker - Maintenance
Technician
Inhalation
ii*
ii"
Worker - Laboratory
Technician
Inhalation
ONU
Inhalation
Processing
Processing as a
reactant
Intermediate in all other
basic organic chemical
manufacturing
Worker
Dermal
ii"
u"
ii"
Worker
Inhalation
ii*
ii*
ii"
ONU
Inhalation
Processing as a
reactant
Intermediate in all other
chemical product and
preparation manufacturing
Worker
Dermal
ii"
u"
ii"
Worker
Inhalation
ii*
ii*
u"
ONU
Inhalation
Repackaging
Repackaging
Worker
Dermal
ii"
ii"
u"
Worker
Inhalation
u"
ii"
u"
u"
ONU
Inhalation
u"
ii"
u"
u"
Recycling
Recyling
Worker
Dermal
ii"
u"
u"
Worker
Inhalation
ii*
ii*
u"
ONU
Inhalation
Commercial
Use
Other uses
Laboratory chemicals
Worker
Dermal
ii"
u"
u"
Worker
Inhalation
ONU
Inhalation
Disposal
Disposal
General Waste Handling,
Treatment, and Disposal
Worker
Dermal
ii"
u"
u"
Worker
Inhalation
ii*
ii*
u"
u"
ONU
Inhalation
u"
u"
Disposal
Disposal
Waste handling, treatment,
and disposal (POTW)
Worker
Dermal
ii"
u"
u"
Worker
Inhalation
ii*
u"
u"
ONU
Inhalation
u"
u"
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cou
Population
Exposure
Route
Human Health Effects
Life Cycle
Stage
Category
Subcategory
Acute
Non-cancer
Short-
Term/subchronic
Non-cancer
Chronic
Non-cancer
Lifetime
Cancer
" The risk estimate exceeded the benchmark for both the central tendency and the high-end.
b The risk estimate exceeded the benchmark for the high-end only.
9160
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9161 Table 6-2. Supporting Basis for the Draft Unreasonable Risk Determination for the Environment
cou
Population/
Receptor
Compartment
Environmental Effects
Life Cycle
Stage
Category
Subcategory
Acute
Chronic
Algal
Manufacturing
Domestic
manufacturing
Domestic manufacturing
Aquatic
Surface water
ii
ii
Processing
Processing as a
reactant
Intermediate in all other
basic organic chemical
manufacture
Aquatic
Surface water
ii
Processing
Processing as a
reactant
Intermediate in all other
chemical product and
preparation manufacturing
Aquatic
Surface water
ii
Processing
Recycling
Recycling
Aquatic
Surface water
ii
Disposal
Disposal
Disposal (general waste
handling, treatment, and
disposal)
Aquatic
Surface water
ii
Disposal (waste handling,
treatment, and disposal
[POTW])
Aquatic
Surface water
ii
Disposal (waste handling,
treatment, and disposal
[remediation])
Aquatic
Surface water
ii
9162
9163
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9173
9174
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9176
9177
9178
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9180
9181
9182
9183
9184
9185
9186
9187
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9189
9190
9191
9192
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9196
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APPENDICES
Appendix A ABBREVIATIONS, ACRONYMS, AND GLOSSARY OF
SELECT TERMS
A.l Key Abbreviations and Acronyms
7Q10
Lowest 7-day average flow occuring in a 10-year period
30Q5
Lowest 30-day average flow occuring in a 5-year period
ACGM
American Conference of Governmental Industrial Hygienists
ACS
American Community Survey
ADME
Absorption, distribution, metabolism, and elimination
AF
Assessment factor
AIM
Analog Identification Methodology
AMTIC
Ambient Monitoring Technology Information Center
AT SDR
Agency for Toxic Substances and Disease Registry
BAF
Bioaccumulation factor
BCF
Bioconcentration factor
BMC
Benchmark concentration
BMD
Benchmark dose
BMR
Benchmark response
CAA
Clean Air Act
CAP
Criteria Air Pollutants
CASRN
Chemical Abstracts Service Registry Number
CBI
Confidential Business Information
CDR
Chemical Data Reporting
CERCLA
Comprehensive Environmental Response, Compensation, and Liability Act
CFR
Code of Federal Regulations
CHRIP
Chemical Risk Information Platform
ChV
Chronic Value
coc
Concentration(s) of concern
CR
Cancer risk
CRD
Chronic retained dose
CSATAM
Community-Scale Air Toxics Ambient Monitoring
CSCL
Chemical Substances Control Law
CWA
Clean Water Act
CWS
Community water systems
CYP
Cytochrome P450
DMR
Discharge Monitoring Report
DOT
Department of Transportation
ECEL
Existing chemical exposure limit
ECHA
European Chemicals Agency
ECHO
Enforcement and Compliance History Online
ECx
Effect concentration at which x percent of test organisms exhibit an effect
EPA
Environmental Protection Agency
EPCRA
Emergency Planning and Community Right-to-Know Act
ERS
Environmental release scenario(s)
ESD
Emission Scenario Document
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10552
10553
10554
10555
10556
10557
10558
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10563
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EU
GD
GS
GSH
HAP
HC05
HEC
HED
HERO
HM
HMTA
HSDB
ICIS
IMAP
IRIS
ISHA
IUR
Koc
Kow
LADC
LADD
LCRD
LCx
LDx
LOD
LOAEL
LOEC
MACT
MCL
MSW
NAAQS
NAC
NAICS
NATA
NCR
ND
NEI
NESHAP
NHD
NICNAS
NIH
NIOSH
NITE
NOAEL
NOEC
NPDES
NPDWR
NRC
NSSS
European Union
Gestation day
Generic Scenario(s)
Glutathione
Hazardous Air Pollutant
Hazardous concentration for 5 percent of species
Human Equivalent Concentration
Human Equivalent Dose
Health and Environmental Research Online (Database)
Harmonic Mean
Hazardous Materials Transportation Act
Hazardous Substances Data Bank
Integrated Compliance Information System
Inventory Multi-Tiered Assessment and Prioritisation
Integrated Risk Information System
Industrial Safety and Health Act
Inhalation Unit Risk
Organic carbon: water partition coefficient
Octanol: water partition coefficient
Lifetime average daily concentration
Lifetime average daily dose
Lifetime chronic retained dose
Lethal concentration at which x percent of test organisms die
Lethal dose at which x percent of test organisms die
Limit of detection
Lowest-observed-adverse-effect4evel (LOAEL
Lowest-observed-effect-concentration
Maximum Achievable Control Technology
Maximum Contaminant Level
Municipal solid waste
National Ambient Air Quality Standard
National Advisory Committee
North American Industry Classification System
National Scale Air-Toxics Assessment
Non-cancer risk
Non-detect
National Emissions Inventory
National Emission Standards for Hazardous Air Pollutants
National Hydrography Dataset
National Industrial Chemicals Notification and Assessment Scheme
National Institutes of Health
National Institute for Occupational Safety and Health
National Institute of Technology and Evaluation
No-observed-adverse-effect-level
No-observed-effect-concentration
National Pollutant Discharge Elimination System
National Primary Drinking Water Regulation
National Response Center
National Sewage Sludge Survey
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10598
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10600
10601
10602
10603
10604
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NTP
National Toxicology Program
OCSPP
Office of Chemical Safety and Pollution Prevention
OECD
Organisation for Economic Co-operation and Development
OEHHA
Office of Environmental Health Hazard Assessment
OEL
Occupational exposure limit
OES
Occupational exposure scenario
ONU
Occupational non-user
OPPT
Office of Pollution Prevention and Toxics
ORD
Office of Research and Development
OSHA
Occupational Safety and Health Administration
PBPD
Physiologically based pharmacodynamic
PBPK
Physiologically based pharmacokinetic
PBZ
Personal breathing zone
PECO
Population, exposure, comparator, and outcome
PEL
Permissible exposure limit
POD
Point of departure
POTW
Publicly owned treatment works
PPE
Personal protective equipment
PSC
Point Source Calculator
PV
Production volume
PWS
Public Water Systems
RCRA
Resource Conservation and Recovery Act
REACH
Registration, Evaluation, Authorisation and Restriction of Chemicals (European Union)
REL
Recommended exposure limit
RfD
Reference Dose
RQ
Reportable Quantity OR Risk Quotient
RTR
Risk and technology review
SADC
Subchronic average daily concentration
SCDD
Subchronic average daily dose
SDS
Safety data sheet
SDWA
Safe Drinking Water Act
SR
Systematic review
SSD
Species Sensitivity Distribution
STEL
Short-Term Exposure Limit
TGD
European Commission Technical Guidance Document
TLV
Threshold Limit Value
TRI
Toxics Release Inventory
TRV
Toxicity reference value
TSCA
Toxic Substances Control Act
TWA
Time-weighted average
UCMR3
Third Unregulated Contaminant Monitoring Rule
UF
Uncertainty factor
U.S.
United States
USGS
United States Geological Survey
VOC
Volatile organic compound
WHO
World Health Organization
WQP
Water Quality Portal
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A.2 Glossary of Select Terms
Aggregate exposure (40 CFR 702.33): "means the combined exposures from a chemical substance
across multiple routes and across multiple pathways."
Aggregate risk (U.S. EPA. 2003): "The risk resulting from aggregate exposure to a single agent or
stressor."
Biomonitoring (U.S. EPA. 2019): "measures the amount of a stressor in biological matrices."
Chemical substance (15 U.S.C. § 2602(2)): "means any organic or inorganic substance of a particular
molecular identity, including—(i) any combination of such substances occurring in whole or in part as a
result of a chemical reaction or occurring in nature, and (ii) any element or uncombined radical. Such
term does not include—(i) any mixture, (ii) any pesticide (as defined in the Federal Insecticide,
Fungicide, and Rodenticide Act [7 U.S.C. 136 et seq.]) when manufactured, processed, or distributed in
commerce for use as a pesticide, (iii) tobacco or any tobacco product, (iv) any source material, special
nuclear material, or byproduct material (as such terms are defined in the Atomic Energy Act of 1954 [42
U.S.C. 2011 et seq.] and regulations issued under such Act), (v) any article the sale of which is subject
to the tax imposed by section 4181 of the Internal Revenue Code of 1986 [26 U.S.C. 4181] (determined
without regard to any exemptions from such tax provided by section 4182 or 4221 or any other
provision of such Code) and any component of such an article (limited to shot shells, cartridges, and
components of shot shells and cartridges), and (vi) any food, food additive, drug, cosmetic, or device (as
such terms are defined in section 201 of the Federal Food, Drug, and Cosmetic Act [21 U.S.C. 321])
when manufactured, processed, or distributed in commerce for use as a food, food additive, drug,
cosmetic, or device."
Conditions of use (COUs) (15 U.S.C. § 2602(4)): "means 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."
Consumer exposure (40 CFR § 711.3): Human exposure resulting from consumer use. This exposure
includes passive exposure to consumer bystanders.
Consumer use (40 CFR § 711.3): "means the use of a chemical substance or a mixture containing a
chemical substance (including as part of an article) when sold to or made available to consumers for
their use."
Fenceline exposure: General population exposures occuring in communities near facilities that emit or
release chemicals to air, water, or land with which they may come into contact.
General population: The human population potentially exposed to chemicals released into the
environment.
Margin of exposure (MOE) (U.S. EPA. 2002a): "a numerical value that characterizes the amount of
safety to a toxic chemical-a ratio of a toxicological endpoint (usually a NOAEL [no observed adverse
effect level]) to exposure. The MOE is a measure of how closely the exposure comes to the NOAEL."
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Mode of action (MOA) (U.S. EPA. 2000b): "a series of key events and processes starting with
interaction of an agent with a cell, and proceeding through operational and anatomical changes causing
disease formation."
Non-chemical stressors (U.S. EPA. 2022b): "Non-chemical stressors are factors found in the built,
natural, and social environments including physical factors such as noise, temperature, and humidity and
psychosocial factors (e.g., poor diet, smoking, and illicit drug use)."
Occupational exposure: Exposure to a chemical substance by industrial or commercial workers.
Occupational non-users (ONU): Employed persons who do not directly handle the chemical substance
but may be indirectly exposed to it as part of their employment due to their proximity to the substance.
Pathways (40 CFR § 702.33): "means the physical course a chemical substance takes from the source to
the organism exposed."
Point of departure (POD) (U.S. EPA. 2002a): "dose that can be considered to be in the range of
observed responses, without significant extrapolation. A POD can be a data point or an estimated point
that is derived from observed dose-response data. A POD is used to mark the beginning of extrapolation
to determine risk associated with lower environmentally relevant human exposures."
Potentially exposed or susceptible subpopulation (PESS) (15 U.S.C. § 2602(12)): "means a group of
individuals within the general population identified by the Agency 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."
Reasonably available information (40 CFR 702.33): "means information that EPA possesses or can
reasonably generate, obtain, and synthesize for use in risk evaluations, considering the deadlines
specified in TSC A section 6(b)(4)(G) for completing such evaluation. Information that meets the terms
of the preceding sentence is reasonably available information whether or not the information is
confidential business information (CBI), that is protected from public disclosure under TSCA section
14."
Routes (40 CFR 702.33): "means the ways a chemical substance enters an organism after contact, e.g.,
by ingestion, inhalation, or dermal absorption."
Sentinel exposure (40 CFR 702.33): "means the exposure from a chemical substance that represents the
plausible upper bound of exposure relative to all other exposures within a broad category of similar or
related exposures."
Stressor (U.S. EPA. 2019b): "Any chemical, physical or biological entity that induces an adverse
response."
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10721 Appendix B REGULATORY AND ASSESSMENT HISTORY
10722 B.l Federal Laws and Regulations
10723
10724 Table Apx B-l. Federal Laws and Regulations
Statutes/Regulations
Description of Authority/Regulation
Description of Regulation
EPA statutes/regulations
Toxic Substances
Control Act (TSCA) -
Section 6(b)
EPA is directed to identify high-priority
chemical substances for risk evaluation; and
conduct risk evaluations on at least 20 high
priority substances no later than
three and one-half years after the date of
enactment of the Frank R. Lautenberg
Chemical Safety for the 21st Century Act.
1,1-dichloroethane is one of the 20
chemicals EPA designated as a High-
Priority Substance for risk evaluation
under TSCA (84 FR 71924. December
30, 2019).
Designation of 1,1-dichloroethane as a
high-priority substance constitutes the
initiation of the risk evaluation on the
chemical.
Toxic Substances
Control Act (TSCA) -
Section 8(a)
The TSCA section 8(a) CDR Rule requires
manufacturers (including importers) to give
EPA basic exposure-related information on the
types, quantities, and uses of chemical
substances produced domestically and
imported into the United States.
1,1 -dichloroethane manufacturing
(including importing), processing and
use information is reported under the
CDR rule (85 FR 20122. Aoril 2. 2020).
Toxic Substances
Control Act (TSCA) -
Section 8(e)
Manufacturers (including importers),
processors, and distributors must immediately
notify EPA if they obtain information that
supports the conclusion that a chemical
substance or mixture presents a substantial risk
of injury to health or the environment.
One substantial risk report received for
1,1-dichloroethane (1993: 2991004)
(U.S. EPA. ChemView. Accessed April
3,2019.)
Toxic Substances
Control Act (TSCA) -
Section 4
Provides EPA with authority to issue rules and
orders requiring manufacturers (including
importers) and processors to test chemical
substances and mixtures.
Eight chemical data submissions from
test rules and enforceable consent
agreements were received for 1,1-
dichloroethane: Persistence (3), Physical
and chemical properties (5). (U.S. EPA,
ChemView. Accessed April 11. 2019).
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Statutes/Regulations
Description of Authority/Regulation
Description of Regulation
Emergency Planning
and Community
Right-to-Know Act
(EPCRA) - Section
313
Requires annual reporting from facilities in
specific industry sectors that employ 10 or
more full-time equivalent employees and that
manufacture, process or otherwise use a TRI-
listed chemical in quantities above threshold
levels. A facility that meets reporting
requirements must submit a reporting form for
each chemical for which it triggered reporting,
providing data across a variety of categories,
including activities and uses of the chemical,
releases and other waste management (e.g.,
quantities recycled, treated, combusted) and
pollution prevention activities (under section
6607 of the Pollution Prevention Act). These
data include on- and off-site data as well as
multimedia data (i.e.. air, land, and water).
1,1 -dichloroethane (Ethylidene
Dichloride) is a listed substance subject
to reporting requirements under 40 CFR
372.65 effective as of January 1. 1994.
Clean Air Act (CAA)
- Section 112(b)
Defines the original list of 189 HAPs. Under
112(c) of the CAA, EPA must identify and list
source categories that emit HAP and then set
emission standards for those listed source
categories under CAA section 112(d). CAA
section 112(b)(3)(A) specifies that any person
may petition the Administrator to modify the
list of HAP by adding or deleting a substance.
Since 1990, EPA has removed two pollutants
from the original list leaving 187 at present.
1,1-dichloroethane is listed as a HAP (42
U.S. Code Section 7412).
Clean Air Act (CAA)
- Section 112(d)
Directs EPA to establish, by rule, NESHAPs
for each category or subcategory of listed
major sources and area sources of HAPs (listed
pursuant to section 112(c)). The standards must
require the maximum degree of emission
reduction that EPA determines is achievable by
each particular source category. This is
generally referred to as maximum achievable
control technology (MACT).
EPA has established NESHAP for a
number of source categories that emit
1,1-dichloroethane to air.
Clean Air Act (CAA)
- Sections 112(d) and
112(f)
Risk and technology review (RTR) of section
112(d) national emission standards for
hazardous air pollutants (NESHAP). Section
112(f)(2) requires EPA to conduct risk
assessments for each source category subject to
section 112(d) NESHAP that require maximum
achievable control technology (MACT), and to
determine if additional standards are needed to
reduce remaining risks. Section 112(d)(6)
requires EPA to review and revise the emission
standards, as necessary, taking into account
developments in practices, processes, and
control technologies.
EPA has promulgated a number of RTR
NESHAP and will do so. as reauired. for
the remaining source categories with
NESHAP.
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Statutes/Regulations
Description of Authority/Regulation
Description of Regulation
Clean Water Act
(CWA) - Sections
301, 304, 306, 307 and
402
Clean Water Act Section 307(a) establishes a
list of toxic pollutants or combination of
pollutants under the CWA. The statute
specifies a list of families of toxic pollutants
also listed in the Code of Federal Regulations
at 40 CFR Part 401.15. The "priority
pollutants" specified by those families are
listed in 40 CFR Part 423 Appendix A. These
are pollutants for which best available
technology effluent limitations
must be established on either a national basis
through rules (Sections 301(b), 304(b), 307(b),
306) or on a case-by-case best professional
judgement basis in NPDES permits, see
Section 402(a)(1)(B). EPA identifies the best
available technology that is economically
achievable for that industry after considering
statutorily prescribed factors and sets
regulatory requirements based
on the performance of that technology.
1,1-Dichloroethane is designated as a
priority pollutant under Section 307(a)(1)
of the CWA and as such is subject to
effluent limitations.
Under CWA Section 304, 1,1-
dichloroethane is included in the list of
total toxic organics (TTO) (40 CFR
413.02(i)V
Safe Drinking Water
Act (SDWA) -
Section 1412(b)
Every 5 years, EPA must publish a list of
contaminants that: (1) are not subject to any
proposed or promulgated national primary
drinking water regulations, (2) are known or
anticipated to occur in public water systems
(PWSs) and (3) may require regulation under
SDWA. EPA must make determinations of
whether or not to regulate at least five
contaminants from the list every 5 years.
Contaminant Candidate List (CCL) 63 FR
10274, March 2, 1998; 70 FR 9071, February
24, 2005; 74 FR51850, October 8, 2009; 81
FR 81099, November 17, 2016; 87 FR 68060,
November 11, 2022 Final Regulatory
Determination 4 (RD4) 86 FR 12272, March 3,
2021.
1,1-Dichloroethane was identified on
CCL1 (1998), CCL2 (2005), CCL3
(2016), and CCL4 (2016). Contaminant
Candidate List (CCL) 63 FR 10274.
March 2. 1998; 70 FR 9071. February
24.2005; 74 FR51850. October 8. 2009;
81 FR 81099. November 17. 2016.
Safe Drinking Water
Act (SDWA) -
Section 1445(a)
Every 5 years, EPA must issue a new list of no
more than 30 unregulated contaminants to be
monitored by PWSs. The data obtained must
be entered into the National Drinking Water
Contaminant Occurrence Database.
1,1-Dichloroethane was identified in the
third Unregulated Contaminant
Monitoring Rule (UCMR3), issued in
2012 (77 FR 26071. Mav 2. 2012).
Resource
Conservation and
Recovery Act (RCRA)
- Section 3001
Directs EPA to develop and promulgate criteria
for identifying the characteristics of hazardous
waste, and for listing hazardous
waste, taking into account toxicity, persistence,
and degradability in nature, potential for
accumulation in tissue and other related factors
such as flammability, corrosiveness, and other
hazardous characteristics.
1,1-Dichloroethane is included on the list
of hazardous wastes pursuant to RCRA
3001.
RCRA Hazardous Waste Code: U076
(40 CFR 261.33).
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Statutes/Regulations
Description of Authority/Regulation
Description of Regulation
Comprehensive
Environmental
Response,
Compensation and
Liability Act
(CERCLA) - Sections
102(a) and 103
Authorizes EPA to promulgate regulations
designating as hazardous substances those
substances which, when released into the
environment, may present substantial danger to
the public health or welfare or the environment.
EPA must also promulgate regulations
establishing the quantity of any hazardous
substance the release of which must be
reported under section 103.
Section 103 requires persons in charge of
vessels or facilities to report to the National
Response Center if they have knowledge of a
release of a hazardous substance above the
reportable quantity threshold.
1,1-Dichloroethane is a hazardous
substance under CERCLA. Releases of
1,1-dichloroethane in excess of 1,000 lbs
must be reported (40 CFR 302.4).
Superfund
Amendments and
Reauthorization
Act (SARA)
Requires the Agency to revise the hazardous
ranking system and update the National
Priorities List of hazardous waste sites,
increases state and citizen
involvement in the superfund program and
provides new enforcement
authorities and settlement tools.
1.1-Dichloroethane is listed on SARA,
an amendment to CERCLA and the
CERCLA Priority List of Hazardous
Substances. This list includes substances
most commonly found at facilities on the
CERCLA National Priorities List
(NPL) that have been deemed to pose the
greatest threat to public health.
Other federal statutes/regulations
Occupational Safety
and Health Act
(OSHA)
Requires employers to provide their workers
with a place of employment free from
recognized hazards to safety and health, such
as exposure to toxic chemicals, excessive noise
levels, mechanical dangers, heat or cold stress
or unsanitary conditions (29 U.S.C section 651
et seq.). Under the Act, OSHA can issue
occupational safety and health standards
including such provisions as PEL, exposure
monitoring, engineering and administrative
control measures, and respiratory protection.
In 1993, OSHA issued occupational
safety and health standards for 1,1-
dichloroethane that included a PEL of
100 ppm TWA, exposure monitoring,
control measures and respiratory
protection (29 CFR 1910.1000).
OSHA Annotated Table Z-l, Accessed
April 16, 2019.
Hazardous Materials
Transportation Act
(HMTA)
Section 5103 of the Act directs the Secretary of
Transportation to:
• Designate material (including an
explosive, radioactive material, infectious
substance, flammable or combustible
liquid, solid or gas, toxic, oxidizing or
corrosive material, and compressed gas)
as hazardous when the Secretary
determines that transporting the material
in commerce may pose an unreasonable
risk to health and safety or property.
• Issue regulations for the safe
transportation, including security, of
hazardous material in intrastate, interstate,
and foreign commerce.
1,1-Dichloroethane is listed as a
hazardous material with regard to
transportation and is subject to
regulations prescribing
requirements applicable to the shipment
and transportation of listed hazardous
materials (70 FR 34381. June 14. 2005).
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Statutes/Regulations
Description of Authority/Regulation
Description of Regulation
Department of Energy
Protective Action Criteria
PAC listed for 1.1-dichloroethane.
10725 B.2 State Laws and Regulations
10726
10727 Table Apx B-2. State Laws and Regulations
State Actions
Description of Action
State Air Regulations
Allowable Ambient Levels: New Hampshire 2037 24-hour AAL (|ig/m3) 1358 Annual
AALB (ua/m3) (Env-A 1400: Regulated Toxic Air Pollutants). Rhode Island 0.6 Annual
(fj,a/m3) (Air Pollution Reaulation No. 22).
State Drinking Water
Standards and
Guidelines
California (Cal Code Reas. Title 26. § 22-64444). Connecticut - **A MCL has not been
established for this chemical (Conn. Agencies Reas. § 19-13-B102). Florida (Fla.
Admin. Code R. Chap. 62-550). Massachusetts (310 Code Mass. Reas. § 22.00).
Michiaan (Mich. Admin. Code r.299.44 and r.299.49. 2017). Minnesota (Minn R. Chap.
4720). New Jersev (7:10 N.J Admin. Code § 5.2).
State Water Pollution
Discharge Programs
Illinois has adopted water pollution discharge programs which categorize 1,1-
dichloroethane as an "halogenated organic chemical," as applicable to the process
wastewater discharaes resultina from the manufacture of bulk oraanic chemicals (35 111.
Adm. Code 307-2406).
State PELs
California (PEL of 110 ppm (Cal Code Reas. Title 8. § 5155)
Hawaii PEL: 100 ppm (Hawaii Administrative Rules Section 12-60-50).
State Right-to-Know
Acts
Massachusetts (105 Code Mass. Reas. § 670.000 Appendix A). New Jersev (N.J.A.C.
7:1G) and Pennsylvania (P.L. 734. No. 159 and 34 Pa. Code § 323).
Chemicals of High
Concern to Children
Several states have adopted reporting laws for chemicals in children's products
containing 1,1-dichloroethane, including Maine's list of Chemical of Concern (38
MRSA Chapter 16-D). Minnesota (Toxic Free Kids Act Minn. Stat. 116.9401 to
116.9407).
Other
California listed 1,1-dichloroethane on Proposition 65 in 1990 due to cancer risk (Cal
Code Reas. Title 27. § 27001).
1,1-Dichloroethane is listed as a Candidate Chemical under California's Safer
Consumer Products Program established under Health and Safety Code § 25252 and
25253 (California. Candidate Chemicals List. Accessed April 18. 2019) (CDTSC.
2017).
California lists 1,1-dichloroethane as a designated priority chemical for biomonitoring
under criteria established bv California SB 1379 (CDPH. 2015) (Accessed February
2019).
1,1-Dichloroethane is on the MA Toxic Use Reduction Act (TURA) list of 1994 (301
Code Mass. Reas. § 41.03).
10728
10729
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10730 B.3 International Laws and Regulations
10731
10732 Table Apx B-3. International Laws and Regulations
Country/ Organization
Requirements and Restrictions
Canada
Canada requires notification for 1,1-dichloroethane under the New Substances
Notification Regulations (Chemicals and Polymers) so that health and ecological
risks can be assessed before the substance is manufactured or imported into Canada
above threshold quantities, however they are subject to fewer information
requirements. Canada Gazette Part I. Vol. 142. No. 25. June 21. 2008.
European Union
1,1-Dichloroethane is registered for use in the EU. (European Chemicals Agency
(ECHA) database. Accessed April 17. 2019.)
Australia
1,1-Dichloroethane can be manufactured or imported into Australia for commercial
purposes without notifying the Australian government, provided that the Australian
importer/manufacturer is currently registered with the Australian government.
1,1-Dichloroethane was assessed under Human Health Tier II of the Inventory
Multi-Tiered Assessment and Prioritisation (IMAP). No specific Australian use,
import, or manufacturing information has been identified. (NICNAS. Ethane. 1.1-
dichloro-: Human health tier II assessment, Accessed April 17, 2019/
Japan
1,1-Dichloroethane is regulated in Japan under the following legislation:
Act on the Evaluation of Chemical Substances and Regulation of Their Manufacture,
etc. (Chemical Substances Control Law; CSCL)
Industrial Safety and Health Act (ISHA) (National Institute of Technology and
Evaluation [NITE1 Chemical Risk Information Platform ICHRIPI. Accessed April
17, 2019).
Australia, Austria,
Belgium, Canada,
Denmark, European
Union, Finland, France,
Germany, Hungary,
Ireland, Italy, Japan,
Latvia New Zealand,
Poland, Romania,
Singapore, South Korea,
Spain, Sweden,
Switzerland, The
Netherlands, Turkey,
United Kingdom
Occupational exposure limits for 1.1-dichloroethane (GESTIS International limit
values for chemical agents (Occupational exposure limits, OELs) database, Accessed
April 18,2019).
10733 B.4 Assessment History
10734
10735 Table Apx B-4. Assessment History of 1,1-Dichloroethane
Authoring Organization
Publication
EPA publications
U.S. EPA, Integrated Risk
Information System (IRIS)
IRIS Summary. 1.1-Dichloroethane; CASRN 75-34-3
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Authoring Organization
Publication
U.S. EPA, National Service Center
for Environmental Publications
(NSCEP)
Exposure and Risk Assessment (fori Dichloroethanes 1.1-dichloroethane.
1,2-dichloroethane
U.S. EPA, Office of Chemical
Safety and Pollution Prevention
(OCSPP)
Final Scope of the Risk Evaluation for 1,1-Dichloroethane CASRN 75-34-3
(2020)
U.S. EPA, Office of Pollution
Prevention and Toxics (OPPT)
Chemview (TSCA submissions - chemical test rule data and substantial
risk reports)
U.S.EPA, Superfund Health Risk
Technical Support Center, National
Center for Environmental
Assessment, Office of Research and
Development
Provisional Peer Reviewed Toxicitv Values for 1.1-Dichloroethane
(CASRN 75-34-3)
Other U.S.-based organizations
Agency for Toxic Substances and
Disease Registry (ATSDR)
Toxicoloaical Profile for 1.1-Dichloroethane CAS#: 75-34-3. Auaust 2015
Centers for Disease Control (CDC)
2015. Fourth National Report on Human Exposure to Environmental
Chemicals
National Cancer Institute (NCI)
National Cancer Institute (NCI) 1978. Bioassay of 1,1-Dichloroethane for
Possible Carcinogenicity (CAS No. 75-34-3). Technical Report Series No.
66 (NCI-CG-TR-66). U.S. Department of Health. Education. And Welfare.
National Cancer Institute (NCI)
National Cancer Institute (NCI) 1977. Bioassay of 1,1-dichloroethane for
possible carcinogenicity. Bethesda, MD: National Cancer Institute. NIH
publication No. 78-1316
National Institute for Occupational
Safety and Health (NIOSH)
Current Intelligence Bulletin 27: Chloroethanes Review of Toxicitv
National Institute for Occupational
Safety and Health (NIOSH)
Occupational health guidelines for 1,1-dichloroethane. Occupational health
guidelines for chemical hazards. Washington, DC: US Department of
Labor, National Institute for Occupational Safety and Health, 1-4. 1978.
National Institute for Occupational
Safety and Health (NIOSH)
1.1-Dichloroethane. NIOSH Pocket Guide to Chemical Hazards. Atlanta.
GA: National Institute for Occupational Safety and Health, Centers for
Disease Control and Prevention. 2015.
National Toxicology Program
(NTP), National Institute of
Environmental Health Sciences
(NIEHS), National Institutes of
Health (NIH)
1.1-Dichloroethane: Target Organs and Levels of Evidence for TR-066
Occupational Safety and Health
Administration (OSHA)
Occupational Exposure to Methylene Chloride (OSHA, 1997)
International
ECHA European Union Risk
Assessment Report
https://echa.europa.eu/information-on-chemicals/information-from-
cxistine-substanccs-rceulation
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Authoring Organization
Publication
Government of Canada,
Environment Canada, Health
Canada
Chemicals at a Glance (fact sheets) International Resources Assessment or
Related Document
10736
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10751
10752
10753
10754
10755
10756
10757
10758
10759
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10762
10763
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Appendix C LIST OF SUPPLEMENTAL DOCUMENTS
This appendix includes a list and citations for all supplemental documents included in the Draft Risk
Evaluation for 1,1-Dichloroethane. See Docket https://www.regulations.gov/docket/EPA-HQ-OPPT-
2024-0114 for all publicly released files associated with this draft risk evaluation package and peer
review and public comments.
Associated Systematic Review Protocol and Data Quality Evaluation and Data Extraction
Documents - Provide additional detail and information on systematic review methodologies used as
well as the data quality evaluations and extractions criteria and results.
Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Protocol (U.S. EPA. 2024t) -
In lieu of an update to the Draft Systematic Review Protocol Supporting TSCA Risk Evaluations
for Chemical Substances, also referred to as the "2021 Draft Systematic Review Protocol" (U.S.
EPA. 202lb), this systematic review protocol for the Draft Risk Evaluation for 1,1-
Dichloroethane describes some clarifications and different approaches that were implemented
than those described in the 2021 Draft Systematic Review Protocol in response to (1) SACC
comments, (2) public comments, or (3) to reflect chemical-specific risk evaluation needs. This
supplemental file may also be referred to as the "1,1-Dichloroethane Systematic Review
Protocol."
Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File: Data
Quality Evaluation and Data Extraction Information for Physical and Chemical Properties (U.S.
EPA. 2024z) - Provides a compilation of tables for the data extraction and data quality
evaluation information for 1,1-dichloroethane. Each table shows the data point, set, or
information element that was extracted and evaluated from a data source that has information
relevant for the evaluation of physical and chemical properties. This supplemental file may also
be referred to as the "1,1-Dichloroethane Data Quality Evaluation and Data Extraction
Information for Physical and Chemical Properties."
Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File: Data
Quality Evaluation and Data Extraction Information for Environmental Fate and Transport
(U.S. EPA. 2024x) - Provides a compilation of tables for the data extraction and data quality
evaluation information for 1,1-dichloroethane. Each table shows the data point, set, or
information element that was extracted and evaluated from a data source that has information
relevant for the evaluation for Environmental Fate and Transport. This supplemental file may
also be referred to as the "1,1-Dichloroethane Data Quality Evaluation and Data Extraction
Information for Environmental Fate and Transport."
Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File: Data
Quality Evaluation and Data Extraction Information for Environmental Release and
Occupational Exposure (U.S. EPA. 2024y) - Provides a compilation of tables for the data
extraction and data quality evaluation information for 1,1-dichloroethane. Each table shows the
data point, set, or information element that was extracted and evaluated from a data source that
has information relevant for the evaluation of environmental release and occupational exposure.
This supplemental file may also be referred to as the "1,1-Dichloroethane Data Quality
Evaluation and Data Extraction Information for Environmental Release and Occupational
Exposure."
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Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File: Data
Quality Evaluation and Data Extraction Information for Dermal Absorption (U.S. EPA.
2024w) Provides a compilation of tables for the data extraction and data quality evaluation
information for 1,1-dichloroethane. Each table shows the data point, set, or information element
that was extracted and evaluated from a data source that has information relevant for the
evaluation for Dermal Absorption. This supplemental file may also be referred to as the "1,1 -
Dichloroethane Data Quality Evaluation and Data Extraction Information for Dermal
Absorption."
Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File: Data
Quality Evaluation Information for General Population, Consumer, and Environmental
Exposure. (U.S. EPA. 2024ab) - Provides a compilation of tables for the data quality evaluation
information for 1,1-dichloroethane. Each table shows the data point, set, or information element
that was evaluated from a data source that has information relevant for the evaluation of general
population, consumer and environmental exposure. This supplemental file may also be referred
to as the "1,1 -Dichloroethane Data Quality Evaluation Information for General Population,
Consumer, and Environmental Exposure."
Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File: Data
Extraction Information for General Population, Consumer, and Environmental Exposure (U.S.
EPA. 2024v) - Provides a compilation of tables for the data extraction for 1,1-dichloroethane.
Each table shows the data point, set, or information element that was extracted from a data
source that has information relevant for the evaluation of general population, consumer, and
environmental exposure. This supplemental file may also be referred to as the "1,1-
Dichloroethane Data Extraction Information for General Population, Consumer, and
Environmental Exposure."
Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File: Data
Quality Evaluation Information for Human Health Hazard Epidemiology (U.S. EPA. 2024ad) -
Provides a compilation of tables for the data quality evaluation information for 1,1-
dichloroethane. Each table shows the data point, set, or information element that was evaluated
from a data source that has information relevant for the evaluation of epidemiological
information. This supplemental file may also be referred to as the "1,1 -Dichloroethane Data
Quality Evaluation Information for Human Health Hazard Epidemiology."
Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File: Data
Quality Evaluation Information for Human Health Hazard Animal Toxicology (U.S. EPA.
2024ac) - Provides a compilation of tables for the data quality evaluation information for 1,1-
dichloroethane. Each table shows the data point, set, or information element that was evaluated
from a data source that has information relevant for the evaluation of human health hazard
animal toxicity information. This supplemental file may also be referred to as the "1,1-
Dichloroethane Data Quality Evaluation Information for Human Health Hazard Animal
Toxicology."
Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File: Data
Quality Evaluation Information for Environmental Hazard (U.S. EPA. 2024aa) - Provides a
compilation of tables for the data quality evaluation information for 1,1-dichloroethane. Each
table shows the data point, set, or information element that was evaluated from a data source that
has information relevant for the evaluation of environmental hazard toxicity information. This
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10850
10851
10852
10853
10854
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10856
10857
10858
10859
10860
10861
10862
10863
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supplemental file may also be referred to as the "1,1-Dichloroethane Data Quality Evaluation
Information for Environmental Hazard."
Draft Risk Evaluation for 1,1-Dichloroethane - Systematic Review Supplemental File: Data
Extraction Information for Environmental Hazard and Human Health Hazard Animal
Toxicology and Epidemiology (U.S. EPA. 2024u) - Provides a compilation of tables for the data
extraction for 1,1-dichloroethane. Each table shows the data point, set, or information element
that was extracted from a data source that has information relevant for the evaluation of
environmental hazard and human health hazard animal toxicology and epidemiology
information. This supplemental file may also be referred to as the "1,1-Dichloroethane Data
Extraction Information for Environmental Hazard and Human Health Hazard Animal Toxicology
and Epidemiology."
Associated Supplemental Information Documents - Provide additional details and information on
fate, exposure, hazard, and risk assessments.
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Environmental
Releases and Occupational Exposure Assessment (U.S. EPA. 2024e).
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Risk Calculator
for Occupational Exposure (U.S. EPA. 2024k).
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Laboratory
Chemical Occupational Exposure and Environmental Release Modeling Results (U.S. EPA.
202410.
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Repackaging
Occupational Exposure and Environmental Release Modeling Results (U.S. EPA. 2024\).
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Occupational
Exposure Scenario Mapping Results (U.S. EPA. 2024i).
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Supplemental
Information on AERMOD TRI Exposure and Risk Analysis (U.S. EPA. 2024n).
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Supplemental
Information on AERMOD Generic Releases Exposure and Risk Analysis (U.S. EPA. 20241).
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Supplemental
Information on AERMOD NEI Exposure and Risk Analysis (U.S. EPA. 2024m).
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Supplemental
Information on Ambient Monitoring Technology Information Center (AMTIC'), 1,1-
Dichloroethane Monitoring Data 2015 to 2020 (U.S. EPA. 2024b).
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Supplemental
Information on IIOAC TRI Exposure and Risk Analysis (U.S. EPA. 2024p).
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10893
10894
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Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: AERMOD Input
Specifications (U.S. EPA. 2024a).
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Surface Water
Concentration and Fish Ingestion and Swimming Central Tendency Exposure Estimates (U.S.
EPA. 2024a)
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Surface Water
Concentration and Fish Ingestion and Swimming High-End Exposure Estimates (U.S. EPA.
2024r)
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Drinking Water
Exposure Estimates (U.S. EPA. 2024cT)
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: TRV Calculator
(U.S. EPA. 2024s).
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Benchmark
Dose Modeling (U.S. EPA. 2024c).
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: Supplemental
Information on EPI Suite Modeling Results in the Fate Assessment (U.S. EPA. 2024o).
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: in vitro Dermal
Absorption Study Analysis (U.S. EPA. 2024f)
Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File: in vitro Dermal
Absorption Study Calculation Sheet (U.S. EPA. 2024g)
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Appendix D PHYSICAL AND CHEMICAL PROPERTIES AND
FATE AND TRANSPORT DETAILS
D.l Physical and Chemical Properties
Selection of a Physical-Chemical Property Value from Multiple High-Quality Sources
The systematic review process identified multiple data with the same quality rating for many physical-
chemical properties discussed in this document. Some of these data were duplicates that were initially
extracted more than once (e.g., when multiple databases cite the same study), but were later removed
during data curation before any further analysis. Much of the remaining data were collected under
standard environmental conditions (i.e., 20-25 °C and 760 mm Hg). These data are presented in box and
whisker plots (Figure Apx D-l), which also include descriptive statistics such as the mean and median.
Data that were collected under non-standard conditions are also presented in scatter plots, where
appropriate, to provide a clear visualization of the temperature- or pressure-dependence of the physical-
chemical parameters. It is important to visualize this dependence to illustrate that high data variance may
be due to measurements across different experimental conditions, and not necessarily high uncertainty in
the data. Such visualizations may also allow for the identification of trends that can approximate the
parameter under other environmental conditions. Finally, a data point measured under non-standard
conditions could better simulate a given scenario for fate assessments or other modeling purposes (e.g.,
when a temperature other than approximately 25 °C would be more relevant for a particular chemical
and assessment scenario).
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. -97.00 -
O
§ -97.50-
I-
59.00-
O
220-
E
E^
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10949
10950
10951
10952
10953
10954
10955
10956
10957
10958
10959
10960
10961
10962
10963
10964
10965
10966
10967
10968
10969
10970
10971
10972
10973
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which are conducted according to scientific principles with sufficient documentation. Finally, estimated,
or calculated data are only presented in the instance that no measured data is available.
Key Sources of Uncertainty of Physical-Chemical Property Values
The physical-chemical property data discussed in this document were the product of a systematic review
of reasonably available information. The data analyses, therefore, consider only a subset of all physical-
chemical data, not an exhaustive acquisition of all potential data. Due to cross-referencing between
many of the databases identified and assessed through the systematic review process, there is potential
for data from one primary source to be collected multiple times resulting in duplication within the
dataset. This duplication should be considered as a potential source of uncertainty in the data analyses;
however, data-collection procedures and expert judgement were used to minimize this possibility
whenever possible.
Overall, there is little uncertainty in the physical-chemical data and analyses presented. The analyses
below present the average and standard deviation of all data collected through the systematic review
process for each physical-chemical parameter. The standard deviation is reported as uncertainty in the
form of tolerance limits (± range) on the average value. Data extracted as a range of values were
excluded from the calculations unless expert judgement could identify precise data points within the
range. These statistical analyses may be indicative of the amount of uncertainty related to different
instrumental techniques or other experimental differences between the studies used to generate the data.
Additional sources of uncertainty in these reported physical-chemical values may be inherent to the
measurement of the data point itself (e.g., sources of uncertainty or measurement error related to the
instrumental method, precision with which a data point is measured and reported in the data source).
Finally, all data were assumed to be collected under standard environmental conditions (i.e., 20 to 25 °C
and 760 mm Hg) unless otherwise specified. Additional discussions of uncertainty are included within
the appropriate subsections below, when necessary.
Molecular Formula: By definition, the molecular formula of 1,1-dichloroethane is C2H4CI2. This
parameter was not obtained by systematic review and there is no uncertainty in this value.
Molecular Weight: By definition, the molecular weight of 1,1-dichloroethane is 98.95 g/mol. This value
was not obtained by systematic review, but rather is calculated from the known molecular formula. The
uncertainty in this value inherent to molecular weight determination from atomic masses is negligible
for the purpose of this risk evaluation.
Physical Form: 1,1-Dichloroethane is a liquid under ambient conditions (i.e., at approximately 20 °C
and 760 mm Hg) (Government of Canada. 2021). It is qualitatively described as being colorless, oily,
and having a chloroform- or ether-like odor (NLM. 2018; NIOSH. 2007). These descriptions agree with
the qualitative descriptions identified in the Final Scope of the Risk Evaluation for 1,1-Dichloroethane
CASRN 75-34-3 (U.S. EPA. 2020b).
Melting Point: Systematic review identified 13 melting point data that cover the range -98 to -96.6°C.
The average melting point of the 13 data was -97.1 ± 0.4 °C. The value -96.93 °C (NLM. 2018) was
selected as the melting point of 1,1-dichloroethane for this risk evaluation because it is in close
agreement with the average of all data identified, has a high level of precision, was independently
reported in multiple high-quality experimental studies, and aligns with the value reported in the final
scope. The standard deviation of the collected data is relatively low, indicating that the value of this
parameter is well-defined.
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Boiling Point: Systematic review identified 34 boiling point data, including 29 data collected at 760 mm
Hg. The data collected under standard conditions cover the range 56.3 to 83.6 °C. Excluding statistical
outliers, the range condenses to 28 data covering 56.3 to 59.2 °C. The average boiling point of the 28
data was 57.3 ± 0.5 °C. The variation of boiling point as a function of pressure is visualized in
Figure_Apx D-2. The value 57.3°C (O'Neil. 2013) was selected as the boiling point of 1,1-
dichloroethane for this risk evaluation because it is in close agreement with the average of all the data
identified and it was independently reported in multiple high-quality studies. The selected value differs
minimally from the value reported in the Final Scope of the Risk Evaluation for 1,1-Dichlor ethane
CASRN 75-34-3 (U.S. EPA. 2020b). The standard deviation of the collected data is relatively low,
indicating that the value of this parameter is well-defined.
1,1-DCA
Boiling Point
59.00
5- 58.00
-------
11011
11012
11013
11014
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(U.S. EPA. 2020b). The standard deviation of the collected data is relatively low, indicating that the
value of this parameter is well-defined.
1,1-DCA
Density
1.11
o 20 40
Temperature (°C)
FigureApx D-3. Density of 1,1-Dichloroethane as a Function of Temperature
Vapor Pressure: Systematic review identified 108 vapor pressure data, including 10 data collected at 25
°C. The data collected under standard conditions cover the range 194.49-228 mm Hg at 25 °C. The
average vapor pressure of the 10 data was 223 ± 10.3 mm Hg at 25 °C. The variation of vapor pressure
as a function of temperature, which is governed by the Clausius-Clapeyron relationship, is visualized in
Figure_Apx D-4. The value 228 mm Hg at 25 °C (Rumble. 2018b) was selected as the vapor pressure of
1,1-dichloroethane for this risk evaluation because it is in close agreement with this analysis, and it was
independently reported in multiple high-quality studies. The selected value differs minimally from the
value reported in the Final Scope of the Risk Evaluation for 1,1 -Dichlor ethane CASRN 75-34-3 (U.S.
EPA. 2020b). The standard deviation of the collected data is relatively low, indicating that the value of
this parameter is well-defined. Additionally, the vapor pressure at non-standard temperatures can be
determined using the results of the systematic review and Figure_Apx D-4, although there is increasing
uncertainty at high temperatures and data should not be extrapolated outside of -50 to 250 °C.
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1,1-DCA
Vapor Pressure
j •—Datu m
Selected
value
Leaend
•V
y = -3638 x + 18, ^ = 0.999
•
0.0020 0.0025 0.0030 0.0035 0.0040
1/T (K-1)
FigureApx D-4. Vapor Pressure of 1,1-Dichloroethane as a Function of Temperature
Vapor Density: Systematic review identified four vapor density data that cover the range 3.4-3.44
(relative to air = 1 g/cm3). The average vapor density of the four data was 3.43 ± 0.02. The value 3.44
(NCBL 2020b) was selected as the vapor density of 1,1-dichloroethane for this risk evaluation because it
is in close agreement with the average of all the data identified, it has a high level of precision, it was
independently reported in multiple high-quality studies, and it aligns with the value reported in the Filial
Scope of the Risk Evaluation of 1,1-Dichloroethane CASRN 75-34-3 (IS EPA, 2020b). The standard
deviation of the collected data is relatively low, indicating that the value of this parameter is well-
defined.
Water Solubility: Systematic review identified 32 water solubility data, including 12 data collected at 25
°C. The data collected under standard conditions cover the range 4,842 to 5,555 mg/L at 25 °C. The
average water solubility of the 12 data was 5,126 ± 202 mg/L at 25 °C. The variation of water solubility
as a functi on of temperature is visualized in Figure_Apx D-5. The value 5,040 mg/L at 25 °C (NLM.
2018) was selected as the water solubility of 1,1-dichloroethane for this risk evaluation because it is in
rough agreement with the mean and median of all the date identified, it has a high level of precision, it
was independently reported in multiple high-quality studies and it aligns with the value reported in the
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11049
11050
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Final Scope of the Risk Evaluation of 1,1-Dichloroe thane CASRN 75-34-3 (U.S. EPA. 2020b).
However, due to the spread of the data identified and the inconsistencies between data reported at the
same temperature, there is non-negligible uncertainty in this selected value. Alternative water solubility
values could be appropriate at environmentally relevant conditions.
1,1-DCA
Water Solubility
6,500
g • —Datum
A- Selected
value
Legend
§ 5,500
I
5,000 # •
0 20 40 60
Temperature (°C)
FigureApx D-5. Water Solubility of 1,1-Dichloroethane as a Function of Temperature
Octanol Water Partition Coefficient (log Kow): Systematic review identified 16 log Kow data, including
10 data collected at 25 °C. The data collected under standard conditions cover the range of 1.68-1.92 at
25 °C. The average log Kow of the 10 data was 1.80 ± 0.07 at 25 °C. The variation of low Kow as a
function of temperature is visualized in Figure Apx D-6. The value 1.79 at 25 °C (Elsevier. 2019) was
selected as the log Kow of 1,1-dichloroethane for this risk evaluation because it is in close agreement
with the data identified, it was independently reported in multiple high-quality studies, and it aligns with
the value reported in the Final Scope of the Risk Evaluation of 1,1-Dichloroethane CASRN 75-34-3
(U.S. EPA. 2020b). The standard deviation of the collected data is relatively low, indicating this
parameter is well-defined.
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1,1-DCA
log Kow
| • — Datum
•
Selected
value
1 pnpnri
•
•
•
w
•
•
•
5 10 15 20 25
Temperature (°C)
FigureApx D-6. Octanol/Water Partition Coefficient (log Kow) of 1,1-Dichloroethane as a
Function of Temperature
Henry's Law Constant: Systematic review identified 25 Henry's law constant data, including seven data
collected at 24 to 25 °C. The data collected under standard conditions cover the range 0.005 to 0.0058 at
24 to 25 °C. The average Henry's law constant of the seven data was 0.00542 ± 0.00026 at 24-25 °C.
The variation of Henry's law constant as a function of temperature is visualized in FigureApx D-7. The
value 0.00562 atm m3/mol at 24 °C (NLM. 2018) was selected as the Henry's law constant of 1,1-
dichloroethane for this risk evaluation because it is in close agreement with this analysis, it was
independently reported in multiple high-quality studies, and it aligns with the value reported in the Final
Scope for the Risk Evaluation of 1,1-Dichloroethane CASRN 75-34-3 (U.S. EPA. 2020b). The standard
deviation of the collected data is relatively low, indicating that the value of this parameter is well-
defined. Additionally, the Henry's law constant at non-standard temperatures can be determined using
the results of the systematic review and Figure Apx D-7, although there is increasing uncertainty at high
temperatures and data should not be extrapolated outside of 0 to 100 °C.
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1,1 -DCA
Henry's Law Constant
E 0.0300
£
e
ra 0 0200
0)
X
0.0100
•i '
25
50
Temperature (°C)
75
FigureApx D-7. Henry's Law Constant of 1,1-Dichloroethane as a Function of
Temperature
Flash Point: Systematic review identified seven flash point data that cover the range -17 to 14 °C. The
flash point data collected include values measured using both closed cup and open cup techniques, with
some sources reporting values for both techniques, and some sources not indicating the technique used.
Closed and open cup measurement techniques generally result in a different value for flash point, and so
for each reported value it is important to note the measurement technique used. The average flash point
of the seven data was -8.2 ± 10.6 °C. The value -12 °C (Dreher et al.. 2014) was selected as the flash
point of 1,1-dichloroethane for this risk evaluation because it is in rough agreement with the data
identified and was independently reported in multiple high-quality studies. Due to the multiple
experimental methods for quantifying flash point (e.g., open cup and closed cup), there is considerable
variance in the data collected.
Autoflammability: Systematic review identified four autoflammability data. All four data were equal at
458 °C. The value 458 °C (Rumble. 2018b) was selected as the autoflammability of 1,1-dichloroethane
for this risk evaluation because it is in absolute agreement with all identified data, it is reported in
multiple high-quality studies, and it aligns with the value reported in the Final Scope of the Risk
Evaluation for 1,1 -Dichloroethane CASRN 75-34-3 (U.S. EPA. 2020b).
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Viscosity: Systematic review identified nine viscosity data, including four data collected at 25°C. The
data collected under standard conditions cover the range 0.464-0.47 cP at 25 °C. The average viscosity
of the four data was 0.467 ± 0.003 cP at 25 °C. The variation of viscosity as a function of temperature is
visualized in FigureApx D-8. The value 0.464 cP at 25 °C (Rumble. 2018c) was selected as the
viscosity of 1,1-dichloroethane for this risk evaluation because it is in close agreement with the
identified data, it is reported in multiple high-quality studies, and it aligns with the value reported in the
Final Scope of the Risk Evaluation for 1,1-Dichloroethane CASRN 75-34-3 (U.S. EPA. 2020b). The
standard deviation of the collected data is relatively low, indicating that this parameter is well-defined.
1,1-DCA
Viscosity
0.500
0.400
20 30 40 50
Temperature (°C)
Figure Apx D-8. Viscosity of 1,1-Dichloroethane as a Function of Temperature
Refi'active Index: Systematic review identified 14 refractive index data that cover the range 1.416-
1.4171. The average refractive index of the 14 data was 1.4166 ± 0.0003. The value 1.4164 (Rumble.
2018a) was selected as the refractive index of 1,1-dichloroethane for this risk evaluation because it is in
close agreement with the average of all data identified, it was independently reported in multiple high-
quality experimental studies, and it aligns with the value reported in the Final Scope for the Risk
Evaluation of 1,1-Dichloroethane CASRN 75-34-3 (U.S. EPA. 2020b). The standard deviation of the
collected data is relatively low, indicating that the value of this parameter is well-defined.
Other Physical-Chemical Properties: Systematic review identified other physical-chemical properties
for 1,1-dichloroethane of relevance for this risk evaluation. The following values were selected for the
-Datum
Selected
value
Legend
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indicated physical-chemical property of 1,1-dichloroethane for this risk evaluation; however, there is
potential uncertainty for these selected values because systematic review did not identify a significant
amount of data for these properties:
• Dielectric constant: 10.9 at 20 °C (NLM. 2018: Dreher et al.. 2014) (N = 2); and
• Heat of evaporation: 30.8 kJ/mol at 25 °C (Dreher et al.. 2014) (N = 1)
D.2 Fate and Transport
D.2.1 Approach and Methodology
EPA conducted a Tier I assessment to identify the environmental compartments (i.e., surface water,
sediment, biosolids, soil, groundwater, air) of major and minor relevance to the fate and transport of 1,1-
dichloroethane. EPA then conducted a Tier II assessment to identify the fate pathways and media most
likely to cause exposure as a result of environmental releases. Media-specific fate analyses were
performed as described in Section 2.2.
D.2.1.1 EPI Suite™ Model Inputs
Measured values for bioconcentration and bioaccumulation factors for 1,1-dichloroethane were not
found in the literature. As an alternative, these values were estimated using the BCF/BAF model in
EPISuiteTM™. To set up EPI Suite™ for estimating these properties, the "Search CAS" function was
used. The octanol-water partition coefficient (Kow) used to estimate BCF and BAF was the
recommended value in Table 2-1 in the physical and chemical properties section of the Risk Evaluation
to conduct Level III fugacity modeling discussed in Appendix D.2.1.2 below, EPI Suite™ was run using
default settings (i.e., no other parameters were changed or input), with the following exceptions:
measured Koc, half-lives estimated from literature values, and emission rates from the Toxics Release
Inventory reporting year 2020.
D.2.1.2 Fugacity Modeling
To inform how environmental releases of 1,1-dichloroethane partition between environmental
compartments (air, water, sediment, and soil) the approach described by (Mackav et al.. 1996) using the
Level III fugacity model in EPISuiteTM was employed. The model predicts the partitioning of a
substance released to an evaluative environment between air, water, soil, and sediment and identifies
important intermedia transfer processes. The Level III Fugacity model is described as a steady-state,
non-equilibrium model that includes the processes of degradation, advection (flow out of the evaluative
environment) and intermedia transfer. The Level III Fugacity model requires fate assessor input for 1,1-
dichloroethane physical-chemical properties, releases to each compartment of the evaluative
environment, and half-lives in each compartment. Physical and chemical properties were taken directly
from Table 2-1. Environmental degradation half-lives were taken from acceptable studies identified
through systematic review as well as additional studies identified after the completion of systematic
review. Where environmental degradation half-lives could not be found, they were estimated using EPI
Suite™. All other input variables were left at their default settings. Release information was collected
from the Toxics Release Inventory (TRI) and the National Emissions Inventory (NEI) for the year 2020.
Table Apx D-l below lists release and half-life inputs for the Level III Fugacity model runs.
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Table Apx D-l. Inputs and Results or Level III Fugacity Modeling for 1,1-Dichloroethane
Environmental
Releases
(kg/yr TRI 2020)
Compartment
Half-Lives
(hours)
Data Source
Level III Results
Percent Mass
Distribution
Air
15,813
936
(U.S. EPA. 2012c)
85
Water
961
2J60a
(Washington and Cameron, 2001)
15
Soil
1
2,760
(Washington and Cameron, 2001)
<1
Sediment
N/A
2,760
(Washington and Cameron, 2001)
<1
11V acquired through modeling of a mixed contaminant plume under sulfate reducing conditions at a landfill.
The results of the Level III Fugacity model using the reported releases indicate that emissions of 1,1-
dichloroethane will primarily partition to air (85 percent) and water (15 percent) with less than 1 percent
partitioning to soil and sediment. Thus, air and to a lesser extent water are expected to be important
environmental compartments for 1,1-dichloroethane released to the environment.
D.2.1.3 Evidence Integration
The Draft Systematic Review Protocol Supporting TSCA Risk Evaluations for Chemical Substances
(U.S. EPA. 2021b) states that during evidence integration, a determination of confidence in the range of
fate endpoint(s) are made based on the study quality of contributing data point. The evaluations of the
available studies of fate endpoints inform interpretations about the extent to which the data support a
conclusion as interpreted from relevant fate and transport parameters determined from systematic
review. Interpretations of the strength of a study, model, or data point that contributes to a fate endpoint
for a chemical are judged and considered together. This culminates in a final conclusion about the extent
to which the available evidence supports the environmental fate endpoint. The following summarizes the
data availability, data quality, and data gap filling methods used to address environmental fate endpoints
for evidence integration.
Fate in Air
No measured data on 1,1-dichloroethane atmospheric OH radical oxidation rates, overall environmental
persistence, long range transport or partitioning between environmental compartments were found in the
literature search conducted as part of Systematic Review. Because no high quality measured data were
available for these endpoints, EPA relied on high quality physical-chemical properties data described in
Section 2.1 of the draft risk evaluation (HLC, VP, WS), EPISuite™, and the OECD LRTP Pov models
to estimate key fate parameters used to assess the fate of 1,1-dichloroethane in air. EPISuite™ has
undergone peer review by the EPA Science Advisory Board (SAB. 2007).
Fate in Aquatic Environments (Surface Water, Sediments)
No data directly applicable to the fate of 1,1-dichloroethane in surface water were found in the literature
search conducted as part of Systematic Review for the chemical. Because no high quality measured data
were available, EPA relied on high quality physical-chemical properties data described in Sections 2.1
and 0 of this draft risk evaluation (e.g., HLC, VP, WS, Kow, Koc), EPISuite™ and the PSC models
(discussed further in the Section 3.3.3.2.3.) to inform 1,1-dichloroethane partitioning to sediments and
volatilization from water. EPISuite™ has undergone peer review by the EPA Science Advisory Board
(SAB. 2007). Conclusions on the biodegradation rates of 1,1-dichloroethane in aquatic environments
(aerobic surface water and anaerobic sediments) were informed by the results of OECD Ready
Biodegradability tests conducted on analogous chlorinated ethanes, propanes and butanes as well as
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aerobic groundwater biodegradation studies, the majority of which demonstrated slow biodegradation of
1,1-dichloroethane in aerobic aquatic environments. A single high quality aerobic biodegradation study
(Tabak et al.. 1981) showing rapid biodegradation in the presence of added amendments was considered
an outlier and not directly used in the assessment. Two microcosm studies of 1,1-dichloroethane
biodegradation in anaerobic sediments collected from contaminated sites were identified after
Systematic Review was completed and informed conclusions on aquatic sediment half4ives for 1,1-
dichloroethane.
Fate in Terrestrial Environments
Limited data directly applicable to the fate of 1,1-dichloroethane in soil were found in the literature
search conducted as part of Systematic Review. High and medium quality studies on the sorption of 1,1-
dichloroethane to soil and sediment were used in combination with high quality physical-chemical
properties data described in Sections 2.1 and 0 of this draft risk evaluation (e.g., HLC, VP, WS, Kow),
EPISuiteTMTM, and the Hazardous Waste Delisting Risk Assessment Software (DRAS) to inform the
fate assessment of 1,1-dichloroethane in soil. EPISuiteTMTM has undergone peer review by the EPA
Science Advisory Board (SAB. 2007).
Conclusions on the biodegradation rates of 1,1-dichloroethane in aerobic and anaerobic soils were
informed by studies identified after Systematic Review. Because data on the biodegradation of 1,1-
dichloroethane in surface soils were not found, studies on the biodegradation of 1,1-dichloroethane
conducted in laboratory groundwater systems and sediments were used to inform the potential rates of
biodegradation in soils. The majority of the studies demonstrated slow biodegradation of 1,1-
dichloroethane in anaerobic groundwater and sediment environments. Assumptions were therefore made
that the rates of 1,1-dichloroethane biodegradation in soil will be similar. The groundwater and sediment
biodegradation studies are discussed further in Appendices D.2.4.2 and D.2.3.2.
Conclusions on the fate of 1,1-dichloroethane drew from multiple studies identified after the completion
of the Systematic Review literature search. These consisted of studies that determined biodegradation
rates in groundwater from field studies, laboratory microcosm studies, and groundwater monitoring
studies. The majority of the studies demonstrated slow biodegradation of 1,1-dichloroethane in
groundwater. The groundwater biodegradation studies are discussed further in Appendix D.2.4.2 of the
Risk Evaluation.
Limited data directly applicable to the fate of 1,1-dichloroethane in landfills and landfill leachate plumes
were found in the literature search conducted as part of Systematic Review. High and medium quality
studies on the sorption of 1,1-dichloroethane to soil and sediment were used in combination with high
quality physical-chemical properties data described in Sections 2.1 and 0 of the risk evaluation (e.g.,
HLC, VP, WS, Kow, Koc), and the Hazardous Waste Delisting Risk Assessment Software (DRAS) to
inform the fate assessment of 1,1-dichloroethane in landfills, landfill leachate plumes and potential
impacts on groundwater. Conclusions on the biodegradation rates of 1,1-dichloroethane in landfills and
landfill leachate plumes were further informed by studies identified after Systematic Review. Because
data on the biodegradation of 1,1-dichloroethane in landfills and landfill leachate plumes were not
found, studies on the biodegradation of 1,1-dichloroethane conducted in sediments and laboratory
groundwater systems were used to inform the potential rates of biodegradation. The studies are
discussed further in Appendices D.2.4.1, D.2.4.2, and D.2.4.3 below. The majority of the studies
demonstrated slow biodegradation of 1,1-dichloroethane. Assumptions were therefore made that the
rates of 1,1-dichloroethane biodegradation in landfills and landfill leachate plumes will be similar.
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No data directly applicable to the fate of 1,1-dichloroethane in biosolids were found in the literature
search conducted as part of Systematic Review for the chemical. Because no high quality measured data
were available, EPA relied on high quality physical-chemical properties data described in Sections 2.1
and 0 of the draft risk evaluation (e.g., HLC, VP, WS, Kow, Koc), and the Office of Water Biosolids
Tool to inform the fate and transport of 1,1-dichloroethane in land applied biosolids and potential
impacts on groundwater. The use of the Biosolids Tool is discussed further in Section 3.3.4.5.
Environmental Persistence
EPA integrated the results of studies identified and evaluated during and after the Systematic Review to
assess the environmental persistence of 1,1-dichloroethane. The studies are discussed in Appendix D
2.2, 2.3, and 2.4.
Removal in Wastewater Treatment
A high-quality study was used to inform the fate of 1,1-dichloroethane in Publicly Owned Treatment
Works (POTWs). The study was conducted by EPA and monitored the fate of Priority Pollutants in 40
representative wastewater treatment plants across the US. The results from 11 POTWs with data showed
a wide range of removal of 1,1-dichloroethane but most values indicated greater than 50 percent
removal. The evidence was supplemented with wastewater treatment plant monitoring studies for 1,1-
dichloroethane identified after completion of Systematic Review that showed higher values and
estimated removal rates from the Sewage Treatment Plant (STP) model in EPISuiteTMTM.
EPISuiteTMTM has undergone peer review by the EPA Science Advisory Board (SAB. 2007). This
information further informed conclusions regarding a range of removal of 1,1-dichloroethane in
POTWs. The studies are discussed further in Appendix D.2.5.2.
Bioconcentration/Bioaccumulation
No data were found on the bioaccumulation/bioconcentration potential of 1,1-dichloroethane. In the
absence of data, EPA relied on high quality physical-chemical properties data described in Section 2.1
of the draft risk evaluation (Kow), EPISuiteTMTM, and the Office of Water BCF/BAF estimation
methodology described in Ambient Water Quality for the Protection of Raman Health (U.S. EPA.
2003c) to estimate the values. Estimated BCF/BAF values were compared to available measured values
for similar halogenated ethanes and propanes to inform the reliability of the estimated values for 1,1-
dichloroethane. EPISuiteTMTM has undergone peer review by the EPA Science Advisory Board (SAB.
2007). The selection of BCF and BAF values for 1,1-dichloroethane is discussed in Appendix D.2.6.
D.2.2 Air and Atmosphere
1,1-dichloroethane is not expected to undergo significant direct photolysis because it does not absorb
radiation in the environmentally available region of the electromagnetic spectrum that has the potential
to cause molecular degradation (HSDB. 2008). 1,1-Dichloroethane in the vapor phase will be degraded
by reaction with photochemically produced hydroxyl radicals in the atmosphere. A half-life of 39 days
was calculated from an estimated rate constant of 2,74/10 13 cmVmolecules-second at 25 °C, assuming
an atmospheric hydroxyl radical concentration of 1.5><106 molecules/cm3 and a 12-hour day (U.S. EPA.
2012c). Based on an estimated octanol air partition coefficient (Koa) of 269, 1,1-dichloroethane is not
expected to associate strongly with airborne particulates. The results of the Level III Fugacity Model in
EPISuite™ using environmental releases of 1,1-dichloroethane reported in the 2020 Toxics Release
Inventory discussed in Appendix D.2.1.2 indicate that at steady state, greater than 75 percent of the mass
of 1,1-dichloroethane released to the environment will partition to the air compartment.
With an expected atmospheric half-life of 39 days, significant vapor pressure (227 mm Hg at 25C, and
reported releases to air, the potential for long range transport was assessed using the OECD Pov and
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LRTP Screening Tool. The tool includes features that are recommended by the OECD expert group on
multimedia modeling. It incorporates a fugacity based steady state multimedia mass balance model of a
global evaluative environment representing soil, water and the troposphere. In addition to calculating
overall environmental persistence (Pov) the model provides two other indicators of long range transport
potential, characteristic travel distance (CTD) and transfer efficiency (TE). CTD is the distance from the
point of release of the chemical to the point at which the concentration of the chemical has dropped to
He or about 37 percent of its initial value. CTDs are calculated for emissions to air and water and only
transport in the medium that receives the release is considered. Because soil is not considered mobile, no
CTD is calculated for emissions to soil. The tool considers multiple emission modes to air, water and
soil and reports maximum values for Pov, CTD (with the exception of soil) and TE. Transfer efficiency
(TE) is the ratio of the mass flux of a substance into an environmental compartment and the emissions
mass flux. TE is calculated for emissions to air, water, and soil. The TE is an indicator of how much of
an emission reaches a distant target.
The 1,1-dichloroethane chemical properties required as input for the model were taken from Table 2-1,
and media specific half-lives were derived after consideration of the range of half-life values reported in
the respective environmental fate discussions for the medium. The tool estimated an overall
environmental persistence of 129 days, a characteristic travel distance of 19,031 km and a transfer
efficiency of 1.9 percent. These results suggest 1,1-dichloroethane may travel long distances, but a low
percentage of the release will reach a distant target. Relative to the Pov and LRTP of 10 reference POP
chemicals in the tool's database, 1,1-dichloroethane has lower overall environmental persistence and
characteristic travel distance.
D.2.2.1 Key Sources of Uncertainty in the Fate Assessment for Air and the Atmosphere
The assessment of the fate of 1,1-dichloroethane in air relied on estimated OH radical oxidation half
lives from the AOP model and the Level III Fugacity model in EPISuite™. The assumptions,
applicability domain and accuracy of the AOP model are discussed in the EPISuite™ help menus.
Accurate inputs are critical for fugacity modeling. Inputs to the level III fugacity model include half
lives in various media, physical chemical properties, and emissions to air, water and soil. Model results
are significantly impacted by emissions assumptions. Thus, for optimal use of the model, accurate
emissions data and, if possible, complete emissions inventories should be used.
D.2.3 Aquatic Environments
1,1-dichloroethane has a hydrolysis half-life of approximately 61 years (Jeffers et al.. 1989). therefore
hydrolysis is not expected to be an important fate process for 1,1-dichloroethane in aquatic
environments. Based on a measured Koc of 31 (Poole and Poole. 1999). partitioning from the water
column to suspended and benthic sediments is not expected to be an important process for 1,1-
dichloroethane. A Henry's Law constant of 0.00562 atmm3/mol at 25 °C, calculated based on a vapor
pressure of 227 mm Hg at 25 °C and a water solubility of 5040 mg/L, indicates that 1,1-dichloroethane
may volatilize from water surfaces. Biodegradation in water is not expected to be an important loss
process for 1,1-dichloroethane. based on aerobic aquatic biodegradation studies on 1,1-dichloroethane
and other chlorinated ethanes, propanes and butanes. Overall evidence suggests that biodegradation of
1,1-dichloroethane in the water column may be possible, but rates are expected to be slow and
volatilization from water will occur more rapidly than biodegradation.
D.2.3.1 Surface Water
1,1-Dichloroethane released to surface water will be subject to loss primarily via volatilization to air.
Biodegradation and sorption to suspended and benthic sediments will be minor removal processes. A
half-life for the volatilization from a model river was estimated using the WVol Model in EPI Suite™
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(U.S. EPA. 2012c) which follows a two-film concept for estimating the flux of volatiles across the air-
water interface (Liss and Slater. 1974). For a model river 1 m deep with a current velocity of 1 meter per
second and wind velocity of 5 m per second, a volatilization half-life of approximately 1 hour was
calculated. Although volatilization is expected to be rapid, some of the substance will remain in water
due to its water solubility (5,040 mg/L) and depending on where its continuous releases to water are
occurring. Biodegradation in water is not expected to be an important loss process for 1,1-
dichloroethane based on a single aerobic aquatic biodegradation study on 1,1-dichloroethane as well as
Ready Biodegradability studies on other chlorinated ethanes and chlorinated propanes and chlorinated
butanes. A study using multiple inoculum subculture transfers promoting acclimation resulted in up to
91 percent biodegradation with loss by volatilization also observed (Tabak et al.. 1981). However, these
results appear to be an outlier. The Japanese National Institute of Technology and Evaluation (NITE)
collected OECD method 301C Ready Biodegradability data for several chlorinated ethanes
(chloroethane (NITE. 2023 g). 1,2-dichloroethane (NITE. 2023b) chloropropanes (2-chloropropane
(NITE. 2023f). 1,2-dichloropropane (NITE. 2023 c). 1,2,3-trichloropropane (NITE. 2023 d)) and
chlorobutanes (1-chlorobutane (NITE. 2023a). 1,4-dichlorobutane (NITE. 2023e)). The study results
indicated that 0 to 8 percent biodegradation occurred in up to four weeks. Overall, these studies suggest
that aerobic biodegradation of 1,1-dichloroethane in the water column may be possible, but rates are
expected to be slow and volatilization from water will occur more rapidly than biodegradation.
Based on a measured Koc value of 31 (Poole and Poole. 1999). 1,1-dichloroethane is not expected to
bind strongly to sediment or suspended organic matter in the water column.
D.2.3.2 Sediments
1,1-Dichloroethane released to water is not expected to significantly partition to organic matter in
suspended and benthic sediments based on its measured Koc of 31 (Poole and Poole. 1999). Koc
represents the ratio of the concentration of 1,1-dichloroethane sorbed to organic carbon in sediment or
soil to the concentration of 1,1-dichloroethane in the overlying water at equilibrium. For comparison,
highly hydrophobic chemicals known to partition to and accumulate in sediments such as PCBs have
measured Koc values of in the range of 10,000 to 100,000 or greater. Biodegradation of 1,1-
dichloroethane has been shown to occur in freshwater sediment microcosms isolated from contaminated
sites. (Hamonts et al.. 2009) constructed anaerobic microcosms from sediments collected from Zenne
River near Brussels, Belgium with a history of chlorinated aliphatic hydrocarbon exposure. The source
of exposure was the infiltration of contaminated groundwater into the river. Reduction of 1,1-
dichloroethane within 13 to 46 days was observed for 9 of the 12 sampling sites with conversion from
1,1-dichloroethane to chloroethane and ethane. High organic matter content of the sediments was
associated with the most rapid biodegradation with the organic matter perhaps serving as an electron
donor for the dechlorination of 1,1-dichloroethane. (Simsir et al.. 2017) observed biodegradation of 1,1-
dichloroethane in microcosms using contaminated anaerobic sediment samples collected from the
interface of contaminated groundwater from a fractured bedrock aquifer and surface water in Third
Creek, a Tennessee River tributary in Knoxville, Tennessee. 1,1-Dichloroethane and lactate were added
to the microcosms which were then incubated. After 20 months, 75 to 100 percent of the added 1,1-
dichloroethane had been converted to chloroethane. Analysis of the microbial populations present
showed a relatively uniform distribution over the 300m site. It was noted that at some sites, members of
the bacteria family Methylococcaceae were found in low abundance, suggesting the possibility of
aerobic cometabolic biodegradation of 1,1-dichloroethane at the aerobic-anaerobic transition zone. The
distribution of microorganisms capable of aerobic cometabolism of 1,1-dichloroethane is uncertain.
(Kuhn et al.. 2009) used compound stable isotope analysis for c/.s-dichloroethy 1 ene and vinyl chloride to
confirm the occurrence and determine the extent of biodegradation of the compounds in the
contaminated aquifer and river sediments of the Zenne River in Belgium also studied by (Hamonts et al..
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2009). The study identified some zones where indigenous microorganisms biodegraded the substances
and other zones where significant biodegradation did not occur. This suggests that even at a relatively
small scale, biodegradation of chlorinated alkanes and alkenes may not be uniformly distributed and
may or may not occur.
D.2.3.3 Key Sources of Uncertainty in the Fate Assessment for Aquatic Environments
Uncertainty in rates of biodegradation and volatilization are key sources of uncertainty in the fate
assessment for aquatic environments. There is limited evidence on the aerobic and anaerobic
biodegradation of 1,1-dichloroethane in uncontaminated aquatic environments under environmental
conditions. The majority of the studies consist of laboratory microcosm studies or field studies with
microbial populations which have developed and acclimated to biodegrade 1,1-dichloroethane through
addition of electron donors and/or acceptors over extended periods of exposure. As such, extrapolating
rates of biodegradation observed in the laboratory study to environmental biodegradation rates
introduces uncertainty. The Volatilization from Water (WVol) Model in EPISuite™ is a screening level
model that estimates the rate of volatilization of a chemical from a model river and lake. The program's
default parameters for a model river were selected to yield a half-life that may be indicative of relatively
fast volatilization from environmental waters due to default current velocity, river depth, and wind
velocity. The default parameters for the lake yield a much slower volatilization rate. The low wind
velocity and current speed are indicative of a pond (or very shallow lake) under relatively calm
conditions. These default parameters were selected to specifically model a body of water under calm
conditions. Although physical chemical properties of the modeled substance and wind speed, water flow
velocity and water depth can be modified by the user, the model does not employ all site specific
environmental parameters that effect the rates of volatilization. Therefore, rates of volatilization at a
specific location under specific environmental conditions could be over or underestimated by the model.
D.2.4 Terrestrial Environments
The measured organic carbon partition coefficient of 31 (Poole and Poole. 1999) for 1,1-dichloroethane
indicates it will have a low affinity for organic matter in terrestrial environments and thus be subject to
transport processes including migration with water through surface soil and unlined landfills to
groundwater. 1,1-Dichloroethane releases to soil surfaces may also be subject to volatilization based on
its vapor pressure (229 mm Hg at 25 C) and Henry's Law constant (0.00526 atm-m3/mol). 1,1-
Dichloroethane is expected to be bioavailable in soil porewater and groundwater due to its water
solubility of 5040 mg/L. 1,1-Dichloroethane has been detected in groundwater and landfill leachate,
however because 1,1-dichloroethane can be formed from the anaerobic biodegradation of 1,1,1-
trichloroethane (1,1,1-trichloroethane), there is uncertainty whether its presence results from the release
and anaerobic biodegradation of 1,1,1- trichloroethane or the release of 1,1-dichloroethane itself.
D.2.4.1 Soil
When released to land, 1,1-dichloroethane may migrate from the surface downward due to its density
and relatively low affinity for soil organic matter. Volatilization from soil surfaces may also occur. Once
below the soil surface. The zone between land surface and the water table within which the moisture
content is less than saturation contains soil pore space which typically contains air or other gases. 1,1-
Dichloroethane will partition between four phases in the unsaturated (vadose) zone, soil solids, soil
water, interstitial air, and if present at sufficiently high concentrations, nonaqueous phase liquid.
If released to land in sufficient quantities, 1,1-dichloroethane could be present and persist as a non-
aqueous phase liquid (NAPL) and more specifically as a dense non-aqueous phase liquid (DNAPL) due
to its greater density relative to water. 1,1-Dichloroethane as DNAPL may migrate through the vadose
zone under the influence of gravity and then vertically downward through groundwater until it reaches
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an impermeable layer where it subsequently becomes a continuous source of contamination in the
aquifer (Poulsen and Kueper. 1992). However, at the concentrations expected to result from releases to
soil from the COUs under consideration, 1,1-dichloroethane is not expected to be present as DNAPL but
rather in the dissolved phase only. Dissolved 1,1-dichloroethane moves with soil water; however, the
rate at which it moves may be slower than soil water due to its sorptive interaction with soil and other
factors. Although 1,1-dichloroethane has a relatively low organic carbon: water partition coefficient
(Koc = 31), some will be partitioned into organic matter on soil particle surfaces in the vadose zone and
in groundwater. Particulate-bound 1,1-dichloroethane generally has a lower potential to migrate to
groundwater because particles may be retained in soil due to a physical filtering effect. 1,1-
Dichloroethane has a relatively high vapor pressure (227 mmHg at 25 °C) and may exist as a vapor in
subsurface voids. This vapor is mobile and can spread through diffusion. Vapor phase transport can also
result in releases from the subsurface to the atmosphere.
Biotic and abiotic processes have been shown to degrade 1,1-dichloroethane in soil; however, a number
of environmental conditions appear to be necessary for degradation to occur. For biotic degradation
(biodegradation) to occur, the presence of microorganisms with the capability of degrading the
compound is required as well as favorable environmental conditions that impact biodegradation
including temperature, pH, salinity and water content, redox potential, and availability of nutrients.
Where high concentrations of 1,1-dichloroethane or other contaminants exhibit toxicity to
microorganisms, or 1,1-dichloroethane is present at concentrations too low to induce degradative
enzymes, biodegradation may not occur.
1,1-Dichloroethane has been shown to biodegrade slowly in soil under both aerobic and anaerobic
conditions but by different microbial populations and different mechanisms. 1,1-Dichloroethane can be
biodegraded under aerobic conditions by means of co-metabolic transformation reactions. These are
reactions that are catalyzed by microbial oxygenase enzymes, molecular oxygen, and a source of
reducing equivalents and that yield no carbon or energy benefits to the biodegrading microorganisms
(Alvarez-Cohen and Speitel. 2001; Horvath. 1972). The chlorinated solvent oxidation products of the
oxygenase reaction may react and be further degraded to CO2 by microorganisms. These reactions can
be carried out by a wide range of oxygenase-expressing microorganisms including those that utilize a
range of nonchlorinated aliphatics and some aromatics, as energy and/or carbon source. (Alvarez-Cohen
and Speitel 2001).
Soils may become anaerobic as microorganisms consume oxygen as a terminal electron acceptor to
biodegrade soil organic matter and when soil is saturated or flooded. Whether anaerobic biodegradation
occurs, and the rate and extent of anaerobic biodegradation, are influenced primarily by the
microorganisms present and the oxidation-reduction (redox) reactions that occur. As oxygen in soils
becomes depleted and the soil becomes anaerobic, microbial processes shift generally in a sequence
from aerobic respiration to nitrate reduction (denitrification), manganese reduction, iron (III) reduction,
sulfate reduction, and finally methanogenesis. Several of these processes may occur at the same time in
close proximity, or one process may be relatively dominant. The anaerobic biodegradation of 1,1-
dichloroethane is carried out by microorganisms mediating oxidation-reduction reactions where soil
organic matter or organic contaminants act as electron donors and 1,1-dichloroethane acts as an electron
acceptor. This process is known as reductive dechlorination and is an important biodegradation pathway
for 1,1-dichloroethane. Generally, the reduction involves the replacement of a chlorine substituents by
hydrogen (hydrogenolysis).
No studies were found on the anaerobic biodegradation of 1,1-dichloroethane in surface soils (upper soil
horizons). However, anaerobic biodegradation pathways may be similar for anaerobic soil, aquifers and
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sediments, as well as anaerobic digestion waste treatment where similar microbial populations and
conditions are present. Studies on the anaerobic biodegradation on 1,1,1-trichloroethane are useful in
informing the pathway for 1,1-dichloroethane anaerobic biodegradation as it is known is known to
undergo reductive dehalogenation to 1,1-dichloroethane where degradation pathways converge.
A critical review of anaerobic degradation of 1,1,1-trichloroethane and its degradation products
identified several studies demonstrating the microbially mediated sequential reductive dechlorination of
1,1,1-trichloroethane to 1,1-dichloroethane and chloroethane (Scheutz et al.. 2011). The process has
been observed in laboratory experiments with marine sediments, methanogenic biofilm reactors, pure
cultures, in batch reactors, and aquifer microcosms. In some of these studies, 1,1-dichloroethane was the
primary product of trichloroethane dechlorination, while in other studies chloroethane was the observed
terminal dechlorination product presumably forming as a result of sequential dechlorination from 1,1,1-
trichloroethane to 1,1-dichloroethane to chloroethane.
Overall, the results of these studies show that (1) biological reductive dechlorination of tri chloroethane
to chloroethane occurs in anaerobic systems; (2) dechlorination of 1,1-dichloroethane occurs more
slowly than dechlorination of tri chloroethane; and (3) 1,1-dichloroethane or chloroethane may form as
terminal products of the dechlorination reaction, depending on the microbiology and/or redox chemistry
of the system.
Vogel and McCartv (1987) studied the biotic and abiotic transformations 14C 1,1,1-trichloroethane and
related compounds including 14C 1,1-dichloroethane under methanogenic conditions. 14C 1,1-
dichloroethane was incubated with a mixed methanogenic culture and the addition of acetate as a
primary substrate (electron donor) in a small, fixed film reactor with a liquid detention time of 4 days.
The reactor had been previously dosed with 14C 1,1,1-trichloroethane. 14C 1,1-dichloroethane was also
added to anaerobic batch fermenters containing an inoculum from an anaerobic column and sampled for
14C02 over time. 1,1-Dichloroethane fed to the small, fixed film reactors was partially mineralized to
14C02. About 20 percent mineralization of 1,1-dichloroethane also occurred in the batch fermenters over
84 days.
Sun et al. (2002) observed the reductive dechlorination of 1,1-dichloroethane by a microorganism
isolated from a sediment microcosm capable of dechlorinating tri chloroethane. Sequential
dechlorination from tri chloroethane to 1,1-dichloroethane was observed, with some accumulation,
followed by conversion to chloroethane. Acetate, tri chloroethane and hydrogen or formate were required
for growth. When the microorganism was added to anoxic aquifer sediments from sites contaminated
with PCE, tri chloroethane, and di chloroethane, tri chloroethane was completely converted to
chloroethane within 2 months, presumably via sequential dechlorination involving transient 1,1-
dichloroethane.
Grostern and Edwards (2006) followed the biodegradation of 1,1,1-trichloroethane, and 1,1-
dichloroethane by a mixed anaerobic microbial culture derived from the groundwater and solids of a
1,1,1-trichloroethane contaminated site. In part of the experiment, anaerobic microcosms were
established with the cultures. Methanol, ethanol, acetate, and lactate were added as the electron donors
and 1,1-dichloroethane as the electron acceptor. Dechlorination in the 1,1-dichloroethane treatment
bottles started with no lag and was complete in 12 days. Methanogenesis occurred throughout 1,1-
dichloroethane degradation.
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U.S. EPA (2013a) compiled first order biodegradation rate constants for 1,1-dichloroethane from the
literature. Most of the data were collected from contaminated sites. The type of study, biogeochemical
conditions, rate constant statistics for multiple values were reported.
Table Apx D-2. First Order Biodegradation Rate Constants for 1,1-Dichloroethane
Type
of
Study
Biogeochemical
Conditions
First Order Rate Constants (day1)
Number
of
Studies
Reference
Min
25th
Median
75th
Max
Mean
Field
Reductive
dechlorination
0.0005
0.0005
0.0008
0.0019
0.0033
0.0014
3
(Aziz et al..
2000)
Lab
Not Specified
0.0044
0.0096
(Aziz et al..
2000)
Lab
and
Field
All studies
0
0
0.001
0.014
0.131
0.017
25
(Suarez and
Rifai. 1999)
Lab
Aerobic
cometabolism
0.014
0.019
0.047
0.123
0.131
0.067
5
(Suarez and
Rifai. 1999)
Field
Reductive
dechlorination
0
0.011
0.002
16
(Suarez and
Rifai. 1999)
Lab
Reductive
dechlorination
0.028
0.044
0.036
2
(Suarez and
Rifai. 1999)
Field
Reductive
dechlorination:
sulfate-reducing
0
0
0
0.001
0.028
0.003
13
(Suarez and
Rifai. 1999)
Field
Reductive
dechlorination:
methanogenesis
0.006
3
(Suarez and
Rifai. 1999)
When converted to 1,1-dichloroethane, biodegradation half4ives assuming first order kinetics with the
reported rate constants spannin from 72 days to 3.8 years.
D.2.4.2 Groundwater
Releases of 1,1-dichloroethane to land (e.g., landfills without adequate leachate controls or land
application of contaminated biosolids) may migrate through soil and reach groundwater. The measured
organic carbon partition coefficient of 31 for 1,1-dichloroethane indicates it will have a low affinity for
organic matter and will not significantly sorb to suspended solids in groundwater. At the groundwater
concentrations expected to result from releases of 1,1-dichloroethane COUs, 1,1-dichloroethane will
likely behave as a freely soluble substance. 1,1-Dichloroethane has a hydrolysis half-life of
approximately 61 years (Jeffers et al.. 1989). Therefore, losses of 1,1-dichloroethane from groundwater
are most likely due to biodegradation, which is expected to be slow. A single study was found on the
rates of biodegradation of 1,1-dichloroethane in groundwater. (Washington and Cameron. 2001)
developed an analytical solution for first-order degradation coupled with advective losses and adsorption
to solve for degradation constants for perchloroethene, trichloroethene, 1,1,1-trichloroethane, 1,1-
dichloroethane, and chloroethane under sulfate reducing conditions at a landfill field site in southeastern
Pennsylvania. Samples were collected 4 times yearly from 13 monitoring wells that were spaced to
include water from the upper watershed boundary to the most down-gradient discharge location. A
degradation half-life of 115 days was calculated for 1,1-dichloroethane. It is important to note that
conditions at the site modeled were much more conducive to biodegradation of 1,1-dichloroethane
relative to other more aerobic and less contaminated sites. At less contaminated sites, where reducing
conditions may not exist or where organic electron donors may not be adequately present, 1,1-
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dichloroethane biodegradation half4ives may be on the order of years. (Huff et al.. 2000) calculated
first-order decay constants using the BIOCHLOR model and changes in 1,1-dichloroethane
concentrations up gradient and down gradient from monitoring wells along an apparent groundwater
path at a contaminated petrochemical reclamation site in Texas. Redox conditions ranged from sulfate
reducing to methanogenic as indicated by the presence of methane in ground water and the range of
molecular hydrogen concentrations. An increased ratio of 1,2-dichloroethane to 1,1,2-trichloroethane
downgradient from the assumed contaminant source area supported the conclusion that reductive
dechlorination was occuring. Reductive dechlorination of chlorinated ethanes apparently occurred to a
lesser extent than chlorinated ethenes, indicating relatively less potential for natural attenuation of
chlorinated ethanes. Apparent first-order decay constants, which gave simulated concentrations in best
agreement with observed changes in concentrations along the segments of the approximate groundwater
flowpath were slightly greater than literature values and gave half-lives ranging from 1.5 to 6.9 years.
The possible groundwater concentrations resulting from releases of 1,1-dichloroethane to land under the
COUs are discussed in detail in Section 3.3.4.1.
D.2.4.3 Landfills
Releases of 1,1-dichloroethane to land via disposal to landfills (TRI2015-2020 average 1 kg/year, EPA
estimated <22,682 kg/year to RCRA Subtitle C Hazardous Waste Landfills) may occur across as many
as 138 sites under the TSCA COUs. The required design and operating procedures of Subtitle C landfills
minimize the movement of leachate from the landfill. The combination of the expected waste
management practices and the relatively low and disperse quantity of 1,1-dichloroethane disposed of in
landfill suggests that the contamination of groundwater by 1,1-dichloroethane released to Subtitle C
landfill will not be an important pathway. However, releases of 1,1-dichloroethane to landfills without
adequate leachate controls may migrate through soil and reach groundwater.
Two studies which measured the concentration of 1,1-dichloroethane in landfill leachate in the United
States were found through systematic review. Concentrations ranged from not detected to 46,000 ng/L
from 11 samples collected between 1984 and 1993. 1,1-Dichloroethane is a dense liquid with a low
affinity for soil organic carbon and water solubility of approximately 5,040 mg/L. Landfill leachate is
generated by excess rainwater percolating through the waste layers of a landfill. Pollutants such as 1,1-
dichloroethane can be transferred from the landfilled waste material to the percolating leachate through
combined physical, chemical, and microbial processes (Christensen et al.. 2001). Compounds in leachate
entering an aquifer will be subject to dilution as the leachate mixes with the groundwater. 1,1-
Dichloroethane does not appreciably bind to aquifer suspended solids and biodegradation may be slow;
thus, dilution may be the only attenuating factor. Due in part to slow groundwater flow rates and
complex (tortuous) flow paths, contaminants such as 1,1-dichloroethane may form plumes.
Concentrations in a plume may vary but are generally highest in the center of the plume and closest to
the source and decrease with distance from the source.
When a landfill leachate plume reaches groundwater, its dissolved organic carbon can significantly
impact the native groundwater microbial communities and may lead to an increase in microbial
populations and activity. Microorganisms capable of carrying out a variety of processes, mostly
reductive (denitrification, Mn, Fe, and sulfate reduction, methanogenesis) have been found in leachate
plumes (L et al.. 1999; Beeman and Suflita. 1990. 1987) and under some conditions may be able to
partially biodegrade 1,1-dichloroethane to chloroethane. However, the rates of biodegradation are
expected to be slow.
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Migration of 1,1-dichloroethane disposed of in landfills under the COUs to groundwater is not expected
to be a significant exposure pathway. To support this conclusion, range-finding estimates were made
using the Hazardous Waste Delisting Risk Assessment Software (DRAS) (U.S. EPA. 2020h). DRAS
performs a multi-pathway and multi-chemical risk assessment to evaluate the acceptability of a
petitioned waste to be disposed in a Subtitle D landfill or surface impoundment instead of under RCRA
Subtitle C requirements. For landfills, DRAS models a mismanagement scenario at an unlined Subtitle
D landfill where releases to groundwater are not controlled and 30 days of waste is always left
uncovered at the surface and subject to air emission and runoff. DRAS uses leachate analysis of the
waste to model exposure of nearby residents to impacted groundwater via ingestion, shower-inhalation,
and dermal exposure. Using totals analysis of the waste, DRAS models exposure of nearby residents to
surface water and fish ingestion impacted by runoff, inhalation of particulate and volatile emissions
from the uncovered waste, and incidental ingestion of residential soil contaminated by settled particulate
emissions from the waste.
For the assessment of 1,1-dichloroethane, EPA used the estimated 1,1-dichloroethane groundwater
concentrations resulting from leachate contamination to make an initial determination of the importance
of the landfill leachate groundwater exposure pathway. Further discussion and details of the modeling
are provided in Section 3.3.4.3.
D.2.4.4 Biosolids
Chemical substances in wastewater undergoing biological wastewater treatment may be removed from
the wastewater by processes including biodegradation, sorption to wastewater solids, and volatilization.
As discussed in Section D.2.5.2, 1,1-dichloroethane is expected to be removed in wastewater treatment
primarily by volatilization with little removal by biodegradation or sorption to solids. Chemicals
removed by sorption to sewage sludge may enter the environment when sewage sludge is land applied
following treatment to meet standards. The treated solids are known as biosolids.
The removal of a nonbiodegradable neutral organic chemical present in WWTP influent via sorption to
sludge is evaluated by considering its partitioning to the organic carbon in suspended solids. Because
organic substances predominantly partition to organic carbon, the measured sorption coefficient is
normalized to the fraction of organic carbon (foe) present in the solid to yield the chemical's organic-
carbon:water partition coefficient (Koc).
The organic carbon:water partition coefficient is the expressed as :
Koc = Kd/foc
Where:
Kd = solids:water partition coefficient
foc = fraction of organic carbon
As the organic-carbon:water partition coefficient (Koc) increases, more of the chemical will be found
associated with the suspended solids.
Based on its Koc value of 31, 1,1-dichloroethane is not expected to significantly partition to sewage
sludge. Based on the amounts of 1,1-dichloroethane undergoing wastewater treatment (insert value) land
application of biosolids from 1,1-dichloroethane wastewater treatment is not expected to be a significant
exposure pathway.
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Section 405(d) of the Clean Water Act requires EPA to promulgate regulations for pollutants that may
be present in sewage sludge to protect public health and the environment. In 1996 EPA published
Technical Support for the Round Two Sewage Sludge Pollutants. This report provides information on
how both the candidate list and the final list of pollutants for the Round Two sewage sludge regulation
were derived. Candidates for Round Two were chosen that were frequently detected in sewage sludge in
the 1988 National Sewage Sludge Survey. TheNSSS sampled 208 representative POTWs. The survey
pollutants with a frequency of detection of less than 10 percent were dropped from further consideration.
1,1-Dichloroethane had a zero percent detection frequency in the National Sludge Survey and not
considered further.
To assess soil concentrations resulting from biosolid applications, EPA relied upon modeling work
conducted in Canada (EC/HC. 2011). which used Equation 60 of the European Commission Technical
Guidance Document (TGD) (ECBi_2003). The equation in the TGD is as follows:
EquationApx D-l.
PECson — (CsiUdge x ARgindgg)/{Dson x BDsoii)
Where:
PECsoil =
C,
AR
sludge
sludge
Dsoil
BDsoU =
Predicted environmental concentration (PEC) for soil (mg/kg)
Concentration in sludge (mg/kg)
Application rate to sludge amended soils (kg/m2/year); default = 0.5 from Table
A-11 of TGD
Depth of soil tillage (m); default = 0.2 m in agricultural soil and 0.1 m in
pastureland from Table A-l 1 of TGD
Bulk density of soil (kg/m3); default = 1,700 kg/m3 from Section 2.3.4 of TGD
The concentration in sludge was set to 20 mg/kg dry weight based on the combined sludge concentration
estimated by SimpleTreat 4.0. Using these assumptions, the estimated 1,1-dichloroethane soil
concentrations after the first year of biosolids application were 29.4 ug/kg in tilled agricultural soil and
58.8 ug/kg in pastureland. See Section 3.3.4.5 for discussion of the estimation of biosolids
concentrations.
The method assumes complete mixing of the chemical in the volume of soil it is applied to as well as no
losses from transformation, degradation, volatilization, erosion, or leaching to lower soil layers.
Additionally, it is assumed there is no input of 1,1-dichloroethane from atmospheric deposition and there
are no background 1,1-dichloroethane accumulations in the soil.
To estimate soil pore water concentrations for 1,1-dichloroethane in soil receiving biosolids for
ecological species' exposures, EPA used a modified version of the equilibrium partitioning (EqP)
equation developed for weakly adsorbing chemicals such as 1,1-dichloroethane and other VOCs. The
modified equation accounts for the contribution of dissolved chemical to the total chemical
concentration in soil or sediment (Fuchsman, 2002). The equation assumes that the adsorption of
chemical to the mineral components of sediment particles is negligible:
Equation Apx D-2.
Qotai = Cdissolved x (foe x KOC) ^ 7
J solids
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Where:
Total chemical concentration in soil [(J-g/kg]
Chemical concentration dissolved in pore water [jag/L]
Fraction of sediment present as organic carbon
Organic carbon-water partition coefficient
Fraction of soil solids
Using EquationApx D-l and estimating Cdissoived from the Kocfor 1,1-dichloroethane assuming a soil
organic carbon fraction (foe) of 0.02, and a soil solids fraction of 0.5, the estimated pore water
concentrations are 18.2 [j,g/L in tilled agricultural soil and 36.6 [j,g/L in pastureland.
Uncertainty in rates of biodegradation and volatilization are key sources of uncertainty in the fate
assessment for terrestrial environments. The majority of the studies consist of laboratory microcosm
studies or field studies with microbial populations that have acclimated to biodegrade 1,1-dichloroethane
during long periods of exposure. Therefore, extrapolating biodegradation rates observed in laboratory
studies to environmental biodegradation rates introduces uncertainty. Volatilization of 1,1-
dichloroethane from soil, landfills, and land applied biosolids is a complex process. Although the
importance of the process is qualitatively addressed, quantitative estimates were not made. As a result,
there is uncertainty regarding the estimated concentrations of 1,1-dichloroethane in terrestrial
environments; values may have been overestimated because volatilization was not quantitatively
addressed.
D.2.5 Persistence Potential
Based on the studies described in Appendix D.2.2, 1,1-dichloroethane is expected to be persistent in air
based on its atmospheric oxidation half-life of 39 days. It is likely to be persistent in soil, surface water
and groundwater, where biodegradation half-lives of months to years are expected depending on
environmental conditions.
Disposal of 1,1-dichloroethane may include incineration of up to 1,200 kg/year. Environmental Release
Scenarios include Processing - repackaging for laboratory chemicals and Commercial Use as a
laboratory chemical (see Section 3.2.1.2 for details). Incineration of 1,1-dichloroethane from these
activities is expected to occur at hazardous waste incinerators at a Destruction and Removal Efficiency
(DRE) of greater or equal to 99.99 percent.
The Clean Air Act 40CFR Part 63, Subpart EEE—National Emission Standards for Hazardous Air
Pollutants from Hazardous Waste Combustors requires all hazardous waste combustors—hazardous
waste incinerators, hazardous waste cement kilns, hazardous waste lightweight aggregate kilns,
hazardous waste solid fuel boilers, hazardous waste liquid fuel boilers, and hazardous waste
hydrochloric acid production furnaces—to achieve a destruction and removal efficiency (DRE) of 99.99
percent for each principle organic hazardous constituent (POHC). Organic constituents which represent
the greatest degree of difficulty of incineration will be those most likely to be designated as POHCs. If
the dioxin-listed hazardous wastes F020, F021, F022, F023, F026, or F027 are burned 99.9999 percent
DRE is required.
D.2.4.5 Key Sources of Uncertainty in the Fate Assessment for Terrestrial
Environments
D.2.5.1 Destruction and Removal Efficiency
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D.2.5.2 Removal in Wastewater Treatment
1,1-Dichloroethane is a volatile liquid with a vapor pressure of 227 mm Hg at 25 °C, water solubility of
5040 mg/L, log octanol/water partition coefficient of 1.79, and a Henry's law constant of 0.00562
atmm3/mol. 1,1-Dichloroethane is not readily biodegradable and biodegrades slowly in most aerobic
biodegradation studies identified through systematic review.
Based on these properties the removal of 1,1-dichloroethane in activated sludge wastewater treatment is
expected to be by volatilization due to its high vapor pressure and Henry's law constant. However, 1,1-
dichloroethane also has appreciable water solubility. Therefore, although volatilization from wastewater
will occur, a portion of 1,1-dichloroethane may remain in the wastewater and be discharged with the
effluent.
The removal of 1,1-dichloroethane from wastewater was measured in eleven wastewater treatment
plants using activated sludge treatment in the EPA 40 POTW study (U.S. EPA. 1982). The minimum
observed removal was 33 percent, maximum 100 percent and the median was 64 percent. (Hannah et al..
1986) compared the removal of 1,1-dichloroethane across four pilot scale biological treatment system
types acclimated for 30 days prior to measurement of removal of the chemical. Activated sludge
wastewater treatment, commonly used to treat wastewater in the United States, achieved 94 percent
removal of 1,1-dichloroethane.
For comparison, the Sewage Treatment Plant (STP) model in EPI Suite (U.S. EPA. 2012c) was run
using the physical and chemical properties reported in Section 2.1 of this risk evaluation and assuming
no biodegradation of the chemical during treatment. The model predicted 69 percent overall removal
with 68 percent attributable to volatilization and less than one percent by sorption to activated sludge
and biodegradation.
Based on its Koc value of 31, 1,1-dichloroethane is not expected to significantly partition to sewage
sludge. Releases of 1,1-dichloroethane to wastewater treatment are expected to be low and disperse
across many sites, therefore, land application of biosolids containing 1,1-dichloroethane is not expected
to be a significant exposure pathway. To support this conclusion, range-finding estimates were made to
evaluate the concentrations of 1,1-dichloroethane in biosolids, in soil receiving biosolids, and soil pore
water concentrations resulting from biosolids application.
D.2.5.3 Key Sources of Uncertainty in the Persistence Assessment
A high quality study indicated 1,1-dichloroethane has a long hydrolysis half-life of approximately 60
years under environmental conditions. 1,1-Dichloroethane biodegradation has been shown to occur
slowly in under most environmental conditions with reported half-lives on the order of months or
greater. Although other degradation processes may occur, they are not considered to be important in the
overall environmental degradation of 1,1-dichloroethane. Thus, uncertainty regarding the environmental
persistence of 1,1-dichloroethane is considered to be low.
D.2.6 Bioaccumulation Potential
No data were found on the bioaccumulation/bioconcentration potential of 1,1-dichloroethane. In the
absence of data, the EPISuite™ BCF/BAF model (Version 4.1) (U.S. EPA. 2012c) was used to estimate
bioaccumulation and bioconcentration factors. A full discussion of the performance of the BCF/BAF
estimation methods used in EPISuite™ is available in the help files. Based on estimated BCF and BAF
values of 7 and 6.8, respectively, bioaccumulation and bioconcentration in aquatic and terrestrial
organisms are not expected to be major environmental processes for 1,1-dichloroethane.
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An alternative to estimating BCF and BAF values with EPISuite™ is the use of the Office of Water
methodology for deriving bioaccumulation factors intended to develop BAFs for setting national water
quality criteria (U.S. EPA. 2003c). Procedure #3 for chemicals classified in the Office of Water
methodology as nonionic organic chemicals with low hydrophobicity (log Kow <4) and low metabolism
was used to calculate BAF values for upper trophic level fish of 2.6 L/kg tissue. This value is in general
agreement with the EPISuite™ predicted BAF value of 6.8 and suggests low concern for
bioaccumulation of 1,1-dichloroethane. The differences are due, in part, to consideration of particulate
and dissolved organic carbon levels in water (which impact the bioavailability), and the octanol water
partition coefficient (Kow) used in the Office of Water methodology to derive the upper trophic level
(TL 4) BAF.
D.2.6.1 Key Sources of Uncertainty in the Bioaccumulation Assessment
There is uncertainty associated with the EPISuite™ BCF/BAF model estimates of BCF and BAF values
for 1,1-dichloroethane. To address the uncertainty in the estimated BCF values, EPA compared
measured BCF values for a series of halogenated ethanes and propanes and EPI Suite estimated BCF
values. Log BCFs for the chemicals ranged from 0.7 to 1.1 The BCF/BAF model overestimated all BCF
values and the largest observed error for BCF estimation was 1.5 log units. Thus, even if the log BCF
estimate for 1,1-dichloroethane of 0.85 was subject to the maximum observed error, its log BCF would
not be expected to exceed 2.3, indicating low bioconcentration potential (BCF <1,000).
D.3 Measured Data in Literature for Environmental Media
A literature search was conducted to identify peer-reviewed or gray sources of 1,1-dichloroethane
measured and reported modeled data. A summary of the measured and reported modeled data for the
various environmental media is provided below. Detail information can also be found in the Draft Risk
Evaluation for 1,1-Dichloroethane - Systematic Review Protocol (U.S. EPA. 2024t).
D.3.1 Example Tornado Plot
EPA used tornado plots to display exposure data from studies identified during EPA's systematic
review. An example is provided in Figure Apx D-9 below. The plots provide the range of media
concentrations in monitoring various studies. The plots show U.S. and non-U.S. data, fraction (e.g.,
vapor, gas, particle, and the studies are ordered from top to bottom from newer to older data. The plots
are colored to indicate general population, remote, near facility, and unknown population information.
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Estimated arithmetic moan
based on lognormal
distribution
Estimated 90'" percentile
based on lognormal
distribution
r"
V
Lowest reported
central tendency
(Mean, median. GM)
hggjmgg|
EHHHEBI
SUM34 timnmd. »l* A# H* 11 WV
)MM24- HmcnttU »ll MHOlUiaiOLMX
MMU Mnail.Xn IT
MIMl> • VUrm <1 4 M20 ES
. %<•( >
Figure Apx D-9. Example Tornado Plot
Exposure data is classified into a variety of location type as follows:
Near Facility
Near facility samples are not strictly contaminated sites and may be site-specific or not site-specific.
General Population
General population exposures are ambient measurements taken in areas near residential populations with
no known near facility sources nearby. The data often represents widely distributed releases to the
environment.
Remote
Remote exposures are measurements taken in areas away from residential and industrial activity and
have no known sources of contamination beyond long-range transport. Examples of remote exposures
include samples collected from polar regions, samples from oceans (not including ports), and sample
locations specifically described as remote.
Indoor Media
Indoor air and dust samples will have indications in the legend based on sampling location such as
commercial buildings, residential homes, public buildings, and vehicles. If studies report more than one
of these micro-environments, then they are classified as mixed use.
Wastewater
Wastewater samples will indicate their sampling location at the wastewater processing facility.
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There is one tornado plot for every media type where chemical concentrations are plotted on a
logarithmic scale. The y-axis of the tornado plot is a list of each study representing a media sampled in a
similar micro-environment and location and reported on the same unit/weight basis. A study may have
more than one representation. For example, if a study reports exposure data collected at two different
locations, the data would be plotted as two separate entries.
Each study on the y-axis is reported with its HERO ID, a short citation, and the country abbreviation of
data collection. Additional details on tissue type or metabolite might also be reported. The studies are
grouped by US, combined with US, or non-US data by unit/weight basis, and sorted in descending order
by latest data collection year. Every study has a colored bar stretching across the x-axis. The color of the
bar corresponds to the location type of the exposure data. The lighter bar represents the range of the
reported concentrations, and the darker bar represents the range of reported central tendencies. A study
with only dark bars indicates that the only data reported was a measure of central tendency.
Using the reported exposure data, EPA represent the arithmetic mean and 90th percentile. If sufficient
central tendency and variance data were reported, the mean and 90th percentile were calculated directly
from the study values assuming data were normally or lognormally distributed. When at least a central
tendency and percentile value were provided, they were estimated by fitting the data to a lognormal
distribution to all available data within the study aggregate. When fitting a lognormal distribution was
not possible, a normal distribution was fit. The central tendency and 90th percentile of each distribution
are plotted as triangles. Lognormal values are shown as upside-down triangles, while normal values are
shown as right-side up. A study with no triangles indicates that there was insufficient data to fit a
distribution. A study may not have reported concentrations because all data is below the limit of
detection. In these circumstances, the plot will show a circle with an X at half the reported limit of
detection. The color of the symbol will correspond to the color of the data's location type such as near
facility, general population, wastewater.
D.3.2 Ambient Air
Measured concentrations of 1,1-dichloroethane in ambient air extracted from four studies are
summarized in FigureApx D-10 and supplemental information is provided in Table Apx D-3. Overall,
concentrations ranged from not detected to 0.34 |ig/m3 from 472 samples collected between 2005 and
2017 in three countries (Canada, Spain, and United States). Location types were categorized as "General
Population" and "Near Facility". Detection frequencies ranged from 0 to not reported.
General Population
Near Facility
A Normal Distribution (CT and 90th percentile)
US Vapor/Gas
1255270 - Logue et al., 2010 - US
gj Non-Detect
4 A
1255270 - Logue et al., 2010 - US
1
NonUS Vapor/Gas
5431563 - Huang et al., 2019 - CN
4
A
2517712 - Marti et al., 2014 - ES
4 A
2443817 - Ras-Mallorqui et al., 2007 - ES
•
10A-4
0.001
0.01 0.1
i
Concentration (ug/m3)
Figure Apx D-10. Concentrations of 1,1-Dichloroethane (jig/m3) in the Vapor/Gas Fraction of
Ambient Air from U.S.-Based and International Studies, 2005-2017
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TableApx D-3. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (^g/m3)
Levels in the Vapor/Gas Fraction of Ambient Air from U.S.-Based and International Studies,
2005-2017
Citation
Country
Location
Type
Sampling
Year(s)
Sample Size
(Frequency
of Detection)
Detection
Limit
(jig/m3)
Overall
Quality
Level
Losue et al.
(2010)
US
General
Population
2006-2008
244 (N/R)
N/R
High
Losue et al.
US
Near Facility
2006-2008
122 (N/R)
N/R
High
(2010)
Huans et al.
CN
General
2016-2017
37 (N/R)
N/R
High
(2019)
Population
Marti et al.
ES
Near Facility
2014
36 (N/R)
N/R
Medium
(2014)
Ras-Mallorciui et
ES
General
2005-2006
33 (0)
30
High
al. (2007)
Population
(Background)
CN = Canada; ES = Spain; US = United States
D.3.3 Drinking Water
Measured concentrations of 1,1-dichloroethane in drinking water extracted from two studies are
summarized in FigureApx D-l 1 and supplemental information is provided in Table Apx D-4). Overall,
concentrations ranged from not detected to 367 |ig/L from 170 samples collected between 2002 and
2012 in United States. Location types were categorized as "General Population." Reported detection
frequency ranged from 0 to 0.17.
US Not Specified
General Population
V Lognormal Distribution (CT and 90th percentile)
gi Non-Detect
5639273 - Landmeyer and Campbell, 2014 - US
3364193 - Kingsbury et al., 2008 - US
•
0.001
0.01
0.1 1 10 100
Concentration (ug/L)
1000
Figure Apx D-ll. Concentrations of 1,1-Dichloroethane (ji/L) in Drinking Water from a U.S.-
Based Study, 2002-2012
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TableApx D-4. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (jig/L)
Levels in Drinking Water from a U.S.-Based Study, 2002-2012
Citation
Country
Location
Type
Sampling
Years
Sample Size
(Frequency
of Detection)
Detection
Limit
(^g/L)
Overall
Quality
Level
Landmever and
US
General
Population
2010-2012
23 (0.17)
44
High
Campbell (2014)
Kinssburv et al.
US
General
Population
2002-2004
147(0)
35
High
(2008)
D.3.4 Groundwater
Measured concentrations of 1,1-dichloroethane in groundwater extracted from nine studies are
summarized in FigureApx D-12 and supplemental information is provided in Table Apx D-5. Overall,
concentrations ranged from not detected to 10,800 |ig/L from 497 samples collected between 1984 and
2005 in Taiwan and United States. Location types were categorized as "General Population" and "Near
Facility." Reported detection frequency ranged from 0 to 0.86.
| General Population
H Near Facility
V Lognormal Distribution (CT and 90th percentile)
US Not Specified
3975066 - Hopple et al., 2009 - US
4912133 - Buszka et al., 2009 - US
1740826 - Westinghouse Savannah River, 1997 - US
1 v V
659873 - Chen et al., 1995 - US
5438509 - Heck et al., 1992 - US
KZ2
5449639 - Bigsby and Myers, 1989 - US
•
724484 - Sabel and Clark, 1984 - US
1335577 - Enwright, 1985 - US
5436115-Roy, 1986-US
si
NonUS Not Specified
631540 - Fan et at., 2009 - TW
•
10**6 10*-4 0.01 1 100 10A4
Concentration (ug/L)
Figure Apx D-12. Concentrations of 1,1-Dichloroethane (ji/L) in Groundwater from U.S.-Based
and International Studies, 1984-2005
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TableApx D-5. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (jig/L)
Levels in Groundwater from U.S.-Based and International Studies, 1984-2005
Citation
Country
Location Type
Sampling
Year(s)
Sample Size
(Frequency of
Detection)
Detection
Limit (jig/L)
Overall Quality
Level
Hopple et
al. (2009)
US
General
Population
2002-2005
292 (0.07)
24
High
Buszka et
al. (2009)
US
Near Facility
2000-2002
7 (0.86)
N/R
Medium
Wcstingho
use
Savannah
River
Com nan v
(1997)
us
Near Facility
1995-1996
136 (0.19)
20,000
Medium
Chen and
Zoltek
(1995)
us
Near Facility
1989-1993
8 (0.62)
N/R
Medium
Heck et al.
(1992)
us
Near Facility
1990
13 (0.23)
200
Medium
Bigsbv and
Mvers
(1989)
us
Near Facility
1988
7(0)
500
Medium
Sabel and
Clark
(1984)
us
General
Population
1984
20 (0.35)
N/R
Medium
Rov F.
Weston Inc
(1986)
us
Near Facility
1984
8 (0.25)
5000
Medium
Fan et al.
(2009)
TW
Near Facility
2005
6 (0.83)
640
Medium
TW = Taiwan; US = United States
D.3.5 Indoor Air
Measured concentrations of 1,1-dichloroethane in indoor air extracted from three studies are
summarized in Figure Apx D-13 and supplemental information is provided in Table Apx D-6. Overall,
concentrations ranged from not detected to 1.700 from 3,602 |ig/m3 samples collected between 1992 and
2017 in three countries (Canada, China, and United States). Location types were categorized as
"Residential". Reported detection frequency was 0.
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US Vapor/Gas
NonUS Vapor/Gas
78782 - Lindstrom et al., 1995 - US
5431563 - Huang et al., 2019 - CN
5736601 - Li et al., 2019 - CA
0.001
0.01
Residential
gj Non-Detect
A Normal Distribution (CT and 90th percentile)
K
4 A
0.1
Concentration (ug/m3)
FigureApx D-13. Concentrations of 1,1-Dichloroethane (^g/m3) in the Vapor/Gas Fraction in
Indoor Air, from U.S.-Based and International Studies, 1992-2017
TableApx D-6. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (jig/m3)
Levels in the Vapor/Gas Fraction in Indoor Air, from U.S.-Based and International Studies, 1992-
2017
Citation
Country
Location
Type
Sampling
Years
Sample Size
(Frequency of
Detection)
Detection
Limit
(Ug/m3)
Overall
Quality Level
Lindstrom et
al. 0995)
US
Residential
1992-1993
34 (0)
1,210
Medium
Huans et al.
(2019)
CN
Residential
2016-2017
44 (N/R)
N/R
High
Li et al.
(2019)
CA
Residential
2012-2013
3,524 (0)
53
High
CA = China; CN = Canada; US = United States
D.3.6 Soil and Soil-Water Leachate
Measured concentrations of 1,1-dichloroethane in soil extracted from one study are summarized in
Figure Apx D-14 and supplemental information is provided in Table Apx D-7. Overall, concentrations
ranged from 0.050 to 0.060 |ig/m3 from seven samples collected between 2012 and 2014 in Spain.
Location types were categorized as "Near Facility." Reported detection frequency was not reported.
NonUS Vapor/Gas
2517712 - Marti et al., 2014 - ES
Bl Near Facility
A Normal Distribution (CT and 90th percentile)
10A-6
10*-5
10A-4
0.001 0.01 0.1 1
Concentration (ug/m3)
10
Figure Apx D-14. Concentrations of 1,1-Dichloroethane (jig/m3) in the Vapor/Gas Fraction of
Soil, from International Studies, 2012-2014
Table Apx D-7. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (jig/m3)
Levels in the Vapor/Gas Fraction of Soil, from International Studies, 2012-2014
Citation
Country
Location
Type
Sampling
Years
Sample
Size
(Frequency
of
Detection)
Detection
Limit
(lug/m3)
Overall
Quality Level
Marti et al. (2014)
ES
Near
Facility
2012-2014
7 (N/R)
0.0011
Medium
ES = Spain
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Measured concentrations of 1,1-dichloroethane in soil-water leachate extracted from two sources are
summarized in FigureApx D-15 and supplemental information is provided in TableApx D-8. Overall,
concentrations ranged from not detected to 46 |ig/L from 11 samples collected between 1984 and 1993
in the United States. Location types were categorized as Near Facility. Reported detection frequency
ranged from 0.2 to 0.83.
US Wet
Near Facility
A Normal Distribution (CT and 90th percentile)
661846 - Schrab ct al., 1993 - US
724484 - Sabel and Clark, 1984 - US
10A-6
0.001 0.01 0.1
Concentration (ug/L)
Figure Apx D-15. Concentrations of 1,1-Dichloroethane (jig/L) in the Soil-Water Leachate from
U.S.-Based Studies for Locations near Facility Releases, 1984-1993
Table Apx D-8. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (jig/L)
Levels in the Soil-Water Leachate from U.S.-Based Studies for Locations near Facility Releases,
1984-1993
Citation
Country
Location
Type
Sampling
Year
Sample Size
(Frequency
of Detection)
Detection
Limit
0ig/L)
Overall
Quality Level
Schrab et al.
(1993)
US
Near Facility
1993
5 (0.20)
N/R
Medium
Sabel and
Clark 0984)
US
Near Facility
1984
6 (0.83)
N/R
Medium
D.3.7 Surface Water
Measured concentrations of 1,1-dichloroethane in surface water extracted from six studies are
summarized in Figure Apx D-16 and supplemental information is provided in Table Apx D-9. Overall,
concentrations ranged from not detected to 48.7 |ig/L from 155 samples collected between 1984 and
2005 in three countries (Australia, Great Britain, and United States). Location types were categorized as
"General Population" and "Near Facility". Reported detection frequency ranged from 0 to 0.5.
US Not Specified
659873 - Chen et al., 1995 - US
5449639 - Bigsby and Myers, 1989 - US
1335577 - Enwright, 1985 - US
5436115-Roy, 1986-US
NonUS Not Specified
5438705 - Hunt el al., 2007 - AU
3544475 . Ellis and Rivelt, 2007 - GB
0.001
| Near Facility
General Population
Non-Detect
*
0.1 1
Concentration (ug/L)
Figure Apx D-16. Concentrations of 1,1-Dichloroethane (ji/L) in Surface Water from U.S.-Based
and International Studies, 1984-2005
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TableApx D-9. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (jig/L)
Levels in Surface Water from U.S.-Based and International Studies, 1984-2005
Citation
Country
Location
Type
Sampling
Year(s)
Sample Size
(Frequency
of Detection)
Detection
Limit
(Ug/L)
Overall Quality
Level
Chen and
US
Near Facility
1989-1993
12 (0.50)
N/R
Medium
Zoltek (1995)
Bissbv and
US
General
1988
3(0)
500
Medium
Mvers (1989)
Population
Enwrisht
us
Near Facility
1984
6(0)
4,500
Medium
Associates
(1985)
Rov F. Weston
us
Near Facility
1984
6(0)
5,000
Medium
Inc 0986)
Hunt et al.
AU
General
2004-2005
93 (N/R)
N/R
High
(2007)
Population
Ellis and Rivett
GB
Near Facility
2001
35 (0.37)
100
Medium
(2007)
AU = Australia; GB
= Great Britain; US = United States
D.3.8 Wastewater
Measured concentrations of 1,1-dichloroethane in wastewater untreated effluent extracted from two
sources are summarized in FigureApx D-17 and supplemental information is provided in Table Apx
D-10. Overall, concentrations ranged from not detected to 594 |ig/L from 29 samples collected between
1981 and 1984 in U.S. Location types were categorized as "Untreated Effluent" at "Discharge Origin".
Reported detection frequency ranged from 0 to 0.25.
US Not Specified
| Untreated Effluent at Discharge Origin
Non-Detect
1335577 - Enwright, 1985 - US - wastewater
1358515 - Ghassemi et al., 1984 - US - sludge
10A-6 10A-5
0.01 0.1
Concentration (ug/L)
Figure Apx D-17. Concentrations of 1,1-Dichloroethane (ji/L) in Wastewater Untreated Effluent
from U.S.-Based Studies, 1981-1984
Table Apx D-10. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane (jig/L)
Levels in Wastewater Untreated Effluent from U.S.-Based Studies, 1981-1984
Citation
Country
Location Type
Sampling
Year(s)
Sample Size
(Frequency
of Detection)
Detection
Limit
(Ug/L)
Overall
Quality Level
Enwright
Associates
(1985)
US
Untreated
Effluent at
Discharge Origin
1984
21(0)
4,500
Medium
Ghassemi et al.
(1984)
US
Untreated
Effluent at
Discharge Origin
1981-1983
8 (0.25)
N/R
Low
Measured concentrations of 1,1-dichloroethane in wastewater row influent extracted from one source are
summarized in Figure Apx D-18 and supplemental information is provided in Table Apx D-l 1.
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11980 Overall, concentrations were not detected from eight samples collected in 1993 in California (CA), U.S.
11981 Location types were categorized as "Raw Influent." Reported detection frequency was not reported.
11982
NonUS Not Specified
&aw Influent
658661 - Bell et al., 1993 - CA - off gas
10A-6
10A-5
10**4
0.001
0.01 0.1 1
10
100
1000
Concentration (ug/m3)
11984 FigureApx D-18. Concentrations of 1,1-Dichloroethane (^g/m3) in Wastewater in Raw Influent
11985 U.S.-Based Study in 1993
11986
11987 Table Apx D-ll. Summary of Peer-Reviewed Literature that Measured 1,1-Dichloroethane
jig/m3) Levels in Wastewater in Raw Inf
uent U.S.-Based Study in 1993
Citation
Country
Location
Type
Sampling
Year
Sample Size
(Frequency
of Detection)
Detection
Limit
(jig/m3)
Overall
Quality Level
Bell et al.
(1993)
US/CA
Raw Influent
1993
8 (N/R)
1,000
Medium
US/CA = United States, Cali:
ornia
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Appendix E AIR EXPOSURE PATHWAY
E.l Modeling Approach for Estimating Concentrations of 1,1-
Dichloroethane in Air and Deposition to Land and Water
EPA applied a tiered approach to estimate ambient air concentrations and exposures for members of the
general population that are in proximity (between 10 to 10,000 m) to emissions sources, emitting the
chemical being evaluated to the ambient air (Figure Apx E-l.). All exposures were assessed for the
inhalation route only.
Figure Apx E-l. Brief Description of Methodologies and Analyses Used to Estimate Air
Concentrations and Exposures
E.l.l Multi-year Analysis Methodology IIOAC
The Multi-year Analysis Methodology IIOAC identifies, at a high level, if there are inhalation exposures
to select populations from a chemical undergoing risk evaluation which indicates a potential risk. This
methodology inherently includes both estimates of exposures as well as estimates of risks to inform the
need, or potential need, for further analysis. If findings from the Multi-year Analysis Methodology
IIOAC indicate any potential risk (acute non-cancer, chronic non-cancer, or cancer) for a given chemical
above (or below as applicable) typical Agency benchmarks, EPA generally will conduct a higher tier
analysis of exposures and associated risks for that chemical. If findings from the Multi-year Analysis
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Methodology IIOAC do not indicate any potential risks for a given chemical above (or below as
applicable) typical agency benchmarks, EPA would not expect a risk would be identified with higher tier
analyses, but may still conduct a limited higher tier analysis at select distances to ensure potential risks
are not missed (for example at distances less than 100 m to ensure risks don't appear very near a facility
where human populations may be exposed).
E.1.1.1 Model
The Multi-year Analysis Methodology IIOAC utilizes EPA's Integrated Indoor/Outdoor Air Calculator
(IIOAC) model16 to estimate high-end and central tendency (mean) exposures for members of the
general population at three pre-defined distances from a facility releasing a chemical to the ambient air
(100, 100 to 1,000, and 1,000 m). IIOAC is an Excel-based tool that estimates indoor and outdoor air
concentrations using pre-run results from a suite of dispersion scenarios run in a variety of
meteorological and land-use settings within EPA's American Meteorological Society/Environmental
Protection Agency Regulatory Model (AERMOD). As such, IIOAC is limited by the parameterizations
utilized for the pre-run scenarios within AERMOD (meteorologic data, stack heights, distances, etc.)
and any additional or new parameterization would require revisions to the model itself. Readers can
learn more about the IIOAC model, equations within the model, detailed input and output parameters,
pre-defined scenarios, default values used, and supporting documentation by reviewing the IIOAC users
guide (U.S. EPA. 2019d).
E.1.1.2 Releases
EPA modeled exposures using the release data developed as described in Section 3.2. Release data was
provided (and modeled) on a facility-by-facility basis using facility-specific chemical releases (fugitive
and stack releases) as reported to the TRI.
E.1.1.3 Exposure Scenarios
EPA evaluated the most "conservative exposure scenario" of the 16 scenarios evaluated in the Draft
TSCA Screening Level Approach for Assessing Ambient Air and Water Exposures to Fenceline
Communities referred to here as the 2022 Fenceline Report.17. This most conservative exposure scenario
consists of a facility that operates year-round (365 days per year, 24 hours per day, 7 days per week), a
South Coastal meteorologic region, and a rural topography setting.
EPA selected 1 of the 14 climate regions to represent a high-end (South [Coastal]) climate region. This
climate regions selected represents the meteorological data set that tended to provide high-end
concentration estimates relative to the other stations within IIOAC. The meteorological data within the
IIOAC model are from years 2011 to 2015 as that is the meteorological data utilized in the suite of pre-
run AERMOD exposure scenarios during development of the IIOAC model (see IIOAC users guide
(U.S. EPA. 2019dV). While this is older meteorological data, sensitivity analyses related to different
years of meteorological data found that although the data does vary, the variation is minimal across
years so the impacts to the model outcomes remain relatively unaffected.
For complete input parameters, including release scenarios, refer to the Draft Risk Evaluation for 1,1-
Dichloroethane - Supplemental Information File: Supplemental Information on IIOAC TRI Exposure
and Risk Analysis (U.S. EPA. 2024p).
16 The IIOAC website is available at https://www.epa.gov/tsca-screening-tools/iioac-integrated-indoor-outdoor-air-calculator.
17 The 2022 Fenceline Report is available at https://www.epa.gov/assessing-and-managing-chemicals-under-tsca/tsca-
screening-level-approach-assessing-ambient-air-and.
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E.1.2 Multi-year Analysis Methodology AERMOD (TRI or NEI)
The Multi-year Methodology AERMOD (TRI or NEI) was developed to allow EPA to conduct a higher-
tier analysis of releases, exposures, and associated risks to members of the general population around
releasing facilities at multiple finite distances and area distances when EPA has site-specific data like
reported releases, facility locations (for local meteorological data), and source attribution. This
methodology can incorporate additional process level, site- and scenario-specific information like stack
parameters (stack height, stack temperature, plume velocity, etc.), building characteristics, release
patterns, different terrains, and other parameters when reasonably available. The Multi-year
Methodology AERMOD can be performed independent of the Multi-year Analysis Methodology IIOAC
described above, can include wet and dry deposition estimates, and with process level-, site-, and
scenario-specific information, provides a more refined analysis that allows EPA to fully characterize
risks for chemicals undergoing risk evaluation.
E.1.2.1 Model
The Multi-year Methodology AERMOD (TRI or NEI) utilizes EPA's AERMOD to estimate exposures
to members of the general population at multiple finite distances and area distances from a facility
releasing a chemical to the ambient air. AERMOD is a steady-state Gaussian plume dispersion model
that incorporates air dispersion based on planetary boundary layer turbulence structure and scaling
concepts, including treatment of both surface and elevated sources and both simple and complex terrain.
AERMOD can incorporate a variety of emission source characteristics, chemical deposition properties,
complex terrain, and site-specific hourly meteorology to estimate air concentrations and deposition
amounts at user-specified receptor distances and at a variety of averaging times. Readers can learn more
about AERMOD, equations within the model, detailed input and output parameters, and supporting
documentation by reviewing the AERMOD users guide (U.S. EPA. 2018b).
E.1.2.2 Releases
EPA modeled exposures using the release data developed as described in Section 3.2 and summarized
below. Release data was provided (and modeled) on a facility-by-facility basis:
1. Facility-specific chemical releases (fugitive and stack releases) as reported to the TRI or NEI,
where available.
2. Alternative release estimates where facility specific data were not available.
E.1.2.3 Exposure Scenarios
The Multi-year Methodology AERMOD (TRI or NEI) evaluated exposures to members of the general
population at eight finite distances (10, 30, 60, 100, 1,000, 2,500, 5,000, and 10,000 m) and two area
distances (30 to 60 m and 100 to 1,000 m) from each TRI or NEI releasing facility for each OES (or
generic facility for alternative release estimates). Human populations for each of the eight finite
distances were placed in a polar grid every 22.5 degrees around the respective distance ring. This results
in a total of 16 modeled exposure points around each finite distance ring for which exposures are
modeled. Figure Apx E-2 provides a visual depiction of the placement of exposure points around a
finite distance ring. Although the visual depiction only shows exposure point locations around a single
finite distance ring, the same placement occurred for all eight finite distance rings.
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10 m
1000 m
Exposure Points around each Finite Distance Ring
2,500 m
Releasing Facility
30 m
60 m
30-60 m
100-1,000 m
100 m
10,000 m
Location of
OCJ Exposed
Individual
FigureApx E-2. Modeled Exposure Points for Finite Distance Rings for Ambient Air Modeling
(AERMOD)
Modeled exposure points for the area distance 30 to 60 m evaluated were placed in a cartesian grid at
equal distances between 30 and 60 in around each releasing facility. Exposure points were placed at IO-
meter increments. This results in a total of 80 points for which exposures are modeled. Modeled
exposure points for the area distance 100 to 1,000 m evaluated were placed in a cartesian grid at equal
distances between 100 and 1,000 m around each releasing facility. Exposure points were placed at 100-
meter increments. This results in a total of 300 points for which exposures are modeled.
Figure Apx E-3 provides a visual depiction of the placement of exposure points (each dot) around the
100 to 1,000 m area distance ring. All exposure points were at 1.8 m above ground, as a proximation for
breathing height for ambient air concentration estimations. A duplicate set of exposure points was at
ground level (0 m) for deposition estimations.
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Ambient Air Modeling (AERMOD)
E.1.2.4 Meteorological Data
Meteorological data for TRI reporting facilities was obtained using the same AERMOD-ready
meteorological data that EPA's Risk and Technology Review (RTR) program uses for multimedia,
multipathway-risk modeling in review of National Emission Standards for Hazardous Air Pollutants
(NESHAP). The 2019 meteorological data18 that the RTR program currently uses, includes 838 hourly
stations with data mostly from the year 2019. For 47 stations (mainly in Alaska and West Virginia),
EPA utilized data from 2016, 2017, or 2018 to fill notable spatial gaps. The 2016 meteorological data
(no longer available for download from the EPA website) covers 824 hourly stations in the 50 states,
District of Columbia, and Puerto Rico. The 2019 meteorological data was used to model 2018, 2019,
and 2020 air emission releases. The 2016 meteorological data was used to model air emission releases
reported from 2014 through 2017. The 2016 meteorologic data was processed with version 16216 of
AERMOD's meteorological preprocessor (AERMET) and the 2019 meteorologic data was processed
with version 19191 of AERMET. Following EPA guidance, all processing utilized sub-hourly wind
measurements (to calculate hourly-averaged wind speed and wind direction; see Section 8.4.2 of that
guidance). The processing for the 2016 and 2019 data also used the "ADJ U*" option for mitigating
modeling issues during light-wind, stable conditions. Facility coordinates, in the form of
latitude/longitude coordinates, were used to match the facility to the closest available meteorological
station. All processing also used automatic substitutions for small gaps in data for cloud cover and
temperature. Each facility was matched to its closest surface meteorological station.
For NEI facilities, where the latitude/longitude can vary by individual source, EPA consolidated each
facility around a single latitude/longitude by averaging the individual source latitudes and longitudes.
The average latitude/longitude was used to determine the meteorological station closest to the NEI
facility, the urban/rural designation, and surrounding land cover setting for the deposition modeling.
18 2019 meteorological data: https://www.epa.gov/fera/download-human-exposure-model-hem.
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Meteorological data for the EPA estimated releases (two OESs where there was no site-specific data
available for modeling; Commercial use as a laboratory chemical, and Processing - repackaging for
laboratory chemicals) were modeled with two meteorological stations, Sioux Falls, South Dakota, for
central-tendency meteorology, and Lake Charles, Louisiana, for higher-end meteorology. These two
meteorological stations represent meteorological datasets that tended to provide high-end and central
tendency concentration estimates relative to the other stations within IIOAC based on a sensitivity
analysis of the average concentration and deposition predictions conducted in support of IIOAC
development. These two meteorological stations are based on five years of data (2011 to 2015) and
provide high-end and central tendency exposure concentrations utilized for risk calculation purposes to
identify potential risks. All processing used sub-hourly wind measurements to calculate hourly-averaged
wind speed and wind direction. The "ADJ U*" option was not used for the 2011 to 2015 data as this
could lead to model overpredictions of ambient concentrations during those conditions. All processing
also used automatic substitutions for small gaps in data for cloud cover and temperature.
E.1.2.5 Urban/Rural Designations
Urban/rural designations of the area around a facility are relevant when considering possible boundary
layer effects on concentrations. Air emissions taking place in an urbanized area are subject to the effects
of urban heat islands, particularly at night. When sources are set as urban in AERMOD, the model will
modify the boundary layer to enhance nighttime turbulence, often leading to higher nighttime air
concentrations. AERMOD uses urban-area population as a proxy for the intensity of this effect.
EPA utilized a population density analysis to identify facilities warranting an urban designation for the
AERMOD runs. Specifically, EPA considered a facility to be in an urban area if it had a population
density greater than 750 people per square kilometer (km2) within a 3-kilometer radius of the facility
(see Section 7.2.1.1 of the guidance referenced in footnote 19) and set the relevant inputs to urban within
AERMOD. For facilities set for urban modeling, AERMOD requires an estimate of the urban population
count. EPA estimated the urban-area population by identifying a proxy for the area of urbanization. The
urban-area proxy was the largest radius around the facility (out to a limit of 15 km) having a population
density greater than 750 people per km2. EPA identified the population within that radius and applied it
for modeling purposes. EPA used U.S. Census data at the level of block groups for these analyses (with
geographies from the 2019 census TIGER/Line shapefiles19 and population counts from the American
Community Survey20 2015 to 2019 5-year estimates-detailed tables [table B01003]). For the NEI facility
mentioned earlier (EIS Facility ID 16206511) that did not have latitude/longitude, EPA assumed its
locations were not urban.
For the EPA estimated releases where TRI or city data were not available for a facility requiring
modeling (Commercial use as a laboratory chemical, and Processing - repackaging for laboratory
chemicals) EPA modeled each such facility once as urban and once as not urban.21 There is no
recommended default urban population for AERMOD modeling, so for these facilities EPA assumed an
urban population of 1 million people, which is consistent with the estimated populations used with
IIOAC. Although slightly higher, the assumed urban population is close to the average of all the urban
populations used for the TRI reporting facilities (which was 847,906 people).
19 2019 census TIGER/Line shapefiles page: https://www.census.gov/geographies/mapping-files/timE-series/geo/tiger-
linE-file.2019.html.
211 American Community Survey page: https://www.census.gov/programs-survevs/acs.
21 Although this may be viewed as a potential double counting of these releases, EPA only utilized the highest estimated
releases from a single exposure scenario from the suite of exposure scenarios modeled for surrogate/estimated facility
releases as exposure estimates and for associated risk calculations.
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E.1.2.6 Physical Source Specifications for TRI Release Facilities and Alternative
Release Estimates
Source-specific physical characteristics like actual release location, stack height, exit gas temperature,
etc. are generally not reported as part of the TRI dataset but can affect the plume characteristics and
associated dispersion of the plume. TRI release facilities and EPA estimated releases (where TRI or city
data were not available) were modeled centering all emissions on one location and using IIOAC default
physical parameters. Stack emissions were modeled from a point source at 10 m above ground from a 2-
meter inside diameter, with an exit gas temperature of 300 Kelvin and an exit gas velocity of 5 m/sec
(Table 6 of the IIOAC User Guide). Fugitive emissions were modeled at 3.05 m above ground from a
square area source of 10 m on a side (Table 7 of the IIOAC User Guide).
E.1.2.7 Temporal Emission Patterns
TRI and NEI Release Facilities
Temporal emission patterns are another factor that can affect the overall modeled concentration
estimates. The release assessments for this work included information on temporal emission patterns—
release duration (across the hours of a day, or intraday) and release pattern (across the days of a year, or
inter-day)—stratified by OES. When release duration was "unknown," EPA assumed releases occurred
each hour of the day. EPA's assumptions for intraday release duration are provided in TableApx E-l.
The hours shown conform to AERMOD's notation scheme of using hours 1 to 24, where hour 1 is the
hour ending at 1 a.m. and hour 24 is the final hour of the same day ending at midnight.
Table Apx E-l. Assumptions for Intraday Emission-Release Duration
Hours per Day
of Emissions
Assumed Hours of the Day Emitting (Inclusive)
Unknown
All (hours 1-24)
1
Hour 13 (hour ending at 1 p.m.; i.e., 12 to 1 p.m.)
2
Hours 13-14 (hour ending at 1 p.m. through hour ending at 2 p.m.; i.e., 12 to 2 p.m.)
3
Hours 13-15 (hour ending at 1 p.m. through hour ending at 3 p.m.; i.e., 12 to 3 p.m.)
4
Hours 13-16 (hour ending at 1 p.m. through hour ending at 4 p.m.; i.e., 12 to 4 p.m.)
5
Hours 13-17 (hour ending at 1 p.m. through hour ending at 5 p.m.; i.e., 12 to 5 p.m.)
8
Hours 9-16 (hour ending at 9 a.m. through hour ending at 4 p.m.; i.e., 8 a.m. to 4 p.m.)
12
Hours 9-20 (hour ending at 9 a.m. through hour ending at 8 p.m.; i.e., 8 a.m. to 8 p.m.)
14
Hours 7-20 (hour ending at 7 a.m. through hour ending at 8 p.m.; i.e., 6 a.m. to 8 p.m.)
EPA's assumptions for inter-day release pattern are provided in Table Apx E-2. EPA started with the
assumption that emissions took place every day of the year. Next, EPA turned emissions off for certain
days of the year as needed to achieve the desired number of emission days: assumptions such as no
emissions on Saturday and Sunday, no emissions on the days around New Year's Day, no emissions at
regular patterns like the first Monday of every month, and so on.
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Table Apx E-2. Assumptions for Inter-day
Emission-Release Pattern
Provided Language for Release Pattern
Implemented Release Pattern:
Days When Emissions Are on
(Format of Month Number/Day Number)
Release pattern: 365 davs/vear assumes vear-
round operations
All days
Release pattern: 350 davs/vear assumes emitting
operations 7 days/week and 50 weeks/year
All days except 1/1-1/4 and 12/21-12/31 (and 1/5 for years
2016 and 2020)
Release pattern: 260 davs/vear
All Monday through Friday, except 1/1 in years 2015, 2016,
2018, 2019, and 2020, and except 12/25 in year 2020
Release pattern: 258 davs/vear
All Monday through Friday, except 12/24-12/26, and except
12/27 in years 2011, 2014, 2015, 2016, and 2020, and except
12/28 in 2015, 2016, and 2020, and except 12/29 in 2020
Release pattern: 250 davs/vear assumes emitting
operations 5 days/week and 50 weeks/year
All Monday through Friday, except 1/1-1/4 and 12/21-12/31
(and 1/5 for years 2016 and 2020)
Release pattern: 235 davs/vear
All Monday through Friday, except 1/1-1/8, 4/1-4/7, 7/1—
7/7, 10/1-10/7, and 12/25-12/31, and except 12/24 in 2012
and 2020
Release pattern: 129 davs/vear
The first 10 days of each month, plus the 11th of January
through September
Release pattern: 26 davs/vear
The first and 15th of each month, plus the 25th of June and
December
Note: Some of the "Provided Language for Release Pattern" is specific to an OES.
Alternative Release Estimates
EPA's assumptions for intraday release duration for the EPA estimated releases (Commercial use as a
laboratory chemical, and Processing - repackaging for laboratory chemicals) are provided in TableApx
E-3. The hours shown conform to AERMOD's notation scheme of using hours 1 to 24, where hour 1 is
the hour ending at 1 a.m. and hour 24 is the final hour of the same day ending at midnight.
Table Apx E-3. Assumptions for Intraday Emission-Release Duration
Hours per Day
of Emissions
Assumed Hours of the Day Emitting (Inclusive)
1
Hour 13 (hour ending at 1 p.m.; i.e., 12 to 1 p.m.)
2
Hours 13-14 (hour ending at 1 p.m. through hour ending at 2 p.m.; i.e., 12 to 2 p.m.)
4
Hours 13-16 (hour ending at 1 p.m. through hour ending at 4 p.m.; i.e., 12 to 4 p.m.)
5
Hours 13-17 (hour ending at 1 p.m. through hour ending at 5 p.m.; i.e., 12 to 5 p.m.)
8
Hours 9-16 (hour ending at 9 a.m. through hour ending at 4 p.m.; i.e., 8 a.m.to 4 p.m.)
24
All hours
EPA's assumptions for inter-day release frequency are provided in Table Apx E-4.
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Table Apx E-4. Assumptions for Inter-day Emission-Release Pattern
Days of Emissions per Year
Implemented Release Pattern: Days When Emissions Are on
(Format of Month Number/Day Number)
28
All Monday through Friday, except 12/24-12/26, and except 12/27 in years
2011, 2014, and 2015, and except 12/28 in 2015
235
All Monday through Friday, except 1/1-1/8, and except 4/1-4/7, and 7/1-7/7,
and 10/1-10/7, and 12/25-12/31, and 12/24 in 2012
129
The first 10 days of each month, plus the 11th of January through September
26
The first and 15th of each month, plus the 25th of June and December
E.1.2.8 Emission Rates
The release assessments included emission rates for each facility in pounds per year for TRI reporting
facilities, tons per year for NEI reporting facilities, and kilograms per year for each scenario for the EPA
estimated releases (Commercial use as a laboratory chemical, and Processing - repackaging for
laboratory chemicals), for fugitive and stack sources as appropriate. Emission rates included in the
release assessments were converted to units needed by AERMOD (g/s for stack sources; g/s/m2 for
fugitive sources). The conversion from per-hour to per-second utilized the number of emitting hours per
year based on the assumed temporal release patterns (see Section E.l.2.7). The conversion to per m2 for
fugitive sources utilized length and width values outlined in Section E. 1.2.6.
E.1.2.9 Deposition Parameters
AERMOD was used to model daily (g/m2/day) and annual (g/m2/year) deposition rates from air to land
and water at eight finite distances (10, 30, 60, 100, 1,000, 2,500, 5,000, and 10,000 m) and two area
distances (30 to 60 m, and 100 to 1,000 m) from each releasing facility. Concentrations of 1,1-
dichloroethane in soil from total (wet and dry) air deposition was estimated to assess exposures of 1,1-
dichloroethane to terrestrial species. AERMOD can model both gaseous and particle deposition. Based
on physical and chemical properties of 1,1-dichloroethane (see Section 2.1), EPA considered only
gaseous deposition. Input parameter values for AERMOD deposition modeling are shown in Table Apx
E-5.
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Table Apx E-5. Settings for Gaseous Deposition
Parameter
Value
Source(s)
Diffusivity in air
8.36E-02 cm2/s
Diffusivity in water
1.06E-05 cm2/s
Henry's Law constant
569.4 Pa m3/mol
Table 2-1
rci: Cuticular resistance
to uptake by lipids for
individual leaves
1.82E05 s/cm
Based on Method 1: Approximation
of Rci Value as a Function of Vapor
Pressure (Welke et al.. 1998; Kerler
and Schoenherr. 1988) (see below)
Seasons
DJF = winter with no snow; MAM = transitional
spring with partial green coverage or short
annuals; JJA = midsummer with lush vegetation;
SON = autumn with unharvested cropland
Assumption
Land cover
Site-specific in 36 directions around the source,
utilizing the 2019 version of the National Land
Cover Database (supplemented with the 2011
version for Hawaii and 2001 version for Puerto
Rico)
National Land Cover Database
Pa = Pascal; mol = mole; log = logarithm base 10; jim = micrometer; DJF = December-February; MAM = March-
May; JJA = June-August; SON = September-November
Cuticular Resistance
The cuticular resistance (rci) value represents the resistance of a chemical to uptake by individual leaves
in a vegetative canopy. For chemicals, for which the rci value is not readily available in literature, EPA
developed three methods to estimate the rci value. For 1,1-dichloroethane, EPA used rci value estimated
using Method 1, as described below. After additional review of information, EPA did identify a reported
rci value of 1.16x 105 (Wesely et al.. 2002). Due to the similarity between the two values, EPA is
presenting results using the calculated rci value.
Method 1: Approximation of Rci Value as a Function of Vapor Pressure: Data from the literature
indicate that rci value varies as a function of the vapor pressure (FT5, units of Pa) of a chemical (Welke et
al.. 1998; Kerler and Schoenherr. 1988). A high VP indicates that chemical has a high propensity for the
vapor phase relative to the condensed phase, and therefore, would have high resistance to uptake from
the atmosphere into leaves (i.e., high rci). Furthermore, Wesely et al. (2002) provides a large database of
VP and rci values.
Analysis of the Wesley et al. data reveals that there is a linear correlation between log({ 7J) and log(rci),
as illustrated in Figure Apx E-4 and EquationApx E-l below. Linear regression yields rci as a function
of VP (R2 = 0.606):
Equation Apx E-l.
log(r_cl ) = 0.489 log (VP) + 3.068
r_cl = 1170 [VP] A0.498
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16
14
12
10
8
o
4
2
0
-2
-4
-12 -10 -8 -6 -4 -2 0 2 4 6 8
log (VP)
FigureApx E-4 Cuticular Resistance as a Function of Vapor Pressure
Method 2: Empirical Calculation of Cuticular Resistance: Method 2 estimates rci value using various
empirical equations found in literature. This method assumes the vapor pressure of the chemical at 20 to
25 °C is equal to the saturation vapor pressure. For VOCs, using the equations collectively provided
under equation below (Welke et al.,) the polymer matrix-air partition coefficient (Kmxo.) can be
calculated as follows:
log (KMXa ) = 6.290 - 0.892 log [(VP) /
Next, Khixa can be converted to the cuticular membrane-air partition coefficient, Kcma:
KjCMa = 0.77 KMXa
Welke, et al. also provide an empirical relationship between the polymer matric-water partition
coefficient and the air-water partition coefficient, K\/xw. Recognizing the air-water partition coefficient is
the Henry's law constant, HLC (unitless), yields:
K_MXw = KMXa HLC
This relationship can be generalized from the polymer matrix to the cuticular membrane:
K_CMw = KCMa HLC
In a separate study, Kerler and Schoenherr (1988) have developed an empirical relationship that equates
Kcmw to the permeance coefficient for cuticular membranes, Pcm. However, this relationship was
developed using data for non-volatile chemicals. Consequently, applying it to volatile organic chemicals
introduces a large amount of uncertainty to the analysis and may not be scientifically justifiable.
log (PCM ) = 238 ((log 0K_CMw))/MV) - 12.48
y = 0.4892x +3.0682
R2 = 0.6058
•
• •
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In the above equation, MV'is the molecular volume of the chemical in question, which can be calculated
from the molar mass, m (units of g/mol), and density, d (units of g/cm3):
MV = m/d
Finally, rci is understood to be the inverse of Pcm. The above relationships can be put together and
simplified to yield a single equation for rci as a function of vapor pressure, molar mass, and density:
r_cl = ((HLC x 1.51 x 10A6)/ iVP] A0.892 )A((-238 d)/m) x 10A12.48
Method 3: Read-Across of Cuticular Resistance from an Analog: This method assumes that chemicals
that have structural similarity, physical and chemical similarity, and exhibit similar vapor pressures will
also exhibit similar rci values. Available data in literature (Wesely et al.. 2002) can be used as a
crosswalk for read-across determination of rci. The unknown rci value is then assumed to be equal to the
rci of the analog.
E.1.2.10 Other Model Settings
EPA assumed flat terrain for all modeling scenarios.
E.1.2.11 Ambient Air Exposure Concentration Outputs
Hourly-average air concentration and total (wet and dry) deposition rate outputs were provided from
AERMOD for each exposure point around each distance ring (i.e., each of 16 exposure points around a
finite distance ring or each exposure point within the area distance ring). Daily and period averages were
then calculated from the modeled hourly data. Daily averages for the finite distance rings were
calculated as arithmetic averages of all hourly data for each day modeled for each exposure point around
each ring. Daily averages for the area distance ring were calculated as the arithmetic average of the
hourly data for each day modeled across all exposure points within the area distance ring. This results in
the following number of daily average concentrations at each distance modeled.
1. Daily averages for TRI and NEI reporting facilities (using 2016 calendar year meteorological
data): One daily average concentration for each of 366 days for each of 16 exposure points
around each finite distance ring. This results in a total of 5,856 daily average concentration
values for each finite distance modeled (366 x 16 = 5,856).
2. Daily averages for TRI reporting facilities (using 2019 calendar year meteorological data): One
daily average concentration for each of 365 days for each of 16 exposure points around each
finite distance ring. This results in a total of 5,840 daily average concentration values for each
finite distance modeled (365 x 16 = 5,840).
Period averages were calculated by averaging all the hourly values at each exposure points for each
distance ring over 1 year. This results in a total of 16 period average concentration values for each finite
distance ring. Additionally, period averages across all years were calculated by averaging all hourly
values at each exposure points for each distance ring across all multiple years.
Daily and period average outputs were stratified by different source scenarios, such as urban/not urban
setting or emission-strengths where needed. Outputs from AERMOD are provided in units of
micrograms per cubic meter (|ig/m3) for ambient air concentrations and grams per square meter (g/m2)
for deposition rates.
Post-processing scripts were used to extract and summarize the output concentrations for each facility,
release, and exposure scenario. The following statistics for daily- and period-average concentrations
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were extracted or calculated from the results for each of the modeled distances (i.e., each ring or grid of
exposure points) and scenarios (also see Table Apx E-6):
• minimum;
• maximum;
• average;
• standard deviation; and
• 10th, 25th, 50th, 75th, and 95th percentiles.
The above equations assume instantaneous mixing with no degradation or other means of chemical
reduction in soil over time and that 1,1-dichloroethane loading in soil is only from direct air-to-surface
deposition (i.e., no runoff).
Table Apx E-6. Description of Daily or Period Average and Air Concentration Statistics
Statistic
Description
Minimum
The minimum daily or period average concentration estimated across all exposure points at the
modeled distance.
Maximum
The maximum daily or period average concentration estimated across all exposure points at the
modeled distance.
Average
Arithmetic mean of all daily or period average concentrations estimated across all exposure points
at the modeled distance. This incorporates lower values (from days when the receptor location
largely was upwind from the facility) and higher values (from days when the receptor location
largely was downwind from the facility).
Percentiles
The daily or period average concentration estimate representing the numerical percentile value
across the entire distribution of all concentrations across all exposure points at the modeled
distance. The 50th percentile represents the median of the daily or period average concentration
across all concentration values for all receptor locations on any day at the modeled distance.
Using the modeled 95th percentile maximum daily deposition rates described in Table 3-10, the
concentration of 1,1-dichloroethane in soil was calculated using the following equations:
EquationApx E-2.
Where:
AjlYlDgp
TotDep
Ar
CF
Equation Apx E-3.
Where:
Soil cone
AjlYlDgp
Mix
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DailyDep = TotDep x Ar x CF
Total daily deposition to soil (pg)
Daily deposition flux to soil (g/m2)
Area of soil (m2)
Conversion of grams to micrograms
SoilConc = DailyDep/(Ar x Mix x Dens)
Daily-average concentration in soil (pg/kg)
Total daily deposition to soil (pg)
Mixing depth (m); default = 0.1 m from the European Commission
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Technical Guidance Document (ECB. 2003)
Ar = Area of soil (m2)
Dens = Density of soil; default = 1,700 kg/m3 from the European Commission
Technical Guidance Document (ECB. 2003)
The above equations assume instantaneous mixing with no degradation or other means of chemical
reduction in soil over time and that 1,1-dichloroethane loading in soil is only from direct air-to-surface
deposition (i.e., no runoff).
E.1.2.12 Physical Source Specifications: NEI Release Facilities
EPA modeled each NEI emission source in its own model run, even for facilities with multiple sources.
Site-specific parameter values were used in modeling, when available. When parameters were not
available and/or values were reported outside of normal bounds, reported values were replaced using
procedures that EPA uses in its AirToxScreen (see Section 2.1.3 of the AirToxScreen Technical Support
Document22 and Section E.l.2.6 herein). For some stack parameters, a default values based on the
source classification code (SCC) of the emission source (as reported in the NEI) was used. If there was
no default value for the source's SCC, a global default value was used.
EPA used replacement values for release height, length, and width for most fugitive sources. For 2,453
NEI fugitive sources which had release heights, length, and width values that were missing or reported
as zero, EPA set their release heights to 3.048 m. For 62 NEI fugitive sources which had values above
zero for length and width, but the release heights value that were missing or reported as zero, EPA set
their release heights to 0 m. Values were missing or reported as 0 m for length for 2,641 sources and for
width for 2,630 sources. EPA replaced these values with a value of 10 m. For any missing values of
angle (1,584 sources), EPA replaced them with zero degrees. There were 6,889 regular vertical sources
(modeled as "POINT" sources in AERMOD), while 129 were vertical sources with rain caps (modeled
as "POINtrichloroethaneP"), 95 were horizontal sources (modeled as "POINTHOR"), and 9 were
downward-facing vents (also modeled as "POINTHOR"). These source-type designations in AERMOD
engage distinct algorithms regarding how the releases initially disperse when leaving the sources. SCCs
were provided for each point source.
EPA used the NEI-provided values for most point sources, but replacement values were needed for exit
gas temperature and/or exit gas velocity for over 1,000 point sources. For 17 sources that had reported
exit gas temperature of 0 °F, EPA replaced the value with the default values by SCC. One of the sources
that was not in the SCC default file. EPA used a global default value of 295.4 K for the exit gas
temperature. All point sources had in-bounds values for release heights and inside stack diameters, so no
replacements were required for those parameters. Three sources that had exit gas velocity values slightly
above the maximum bounding value of 1,000 feet per second (ft/s), were replaced with the maximum in-
bounds value of 1,000 ft/s (304.8 m/s). For sources that had values for exit gas velocity that were
missing or 0 (1,344 sources) the values of inside stack diameter and exit gas flow rate was used to
calculate exit gas velocity as shown in Table Apx E-7. Minimum or maximum in-bounds values were
used for those calculated exit gas velocity values that were out of bounds (15 sources).
22 Technical Support Document: EPA 'sAir Toxics Screening Assessment 2018 AirToxScreen TSD.
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TableApx E-7. Procedures for Replacing Values Missing, Equal to Zero, or Out of Normal
Bounds for
'hysical Source Parameters for NEI Sources
Parameter
Bounds
Condition
Value Missing or 0
Value Out of Normal
Bounds
First Pass
Second Pass
(First Pass
Unsuccessful)
Third Pass (First
Two Passes
Unsuccessful)
Stack height
1-1,300 ft
(0.3048-396
m)
Use default value by
SCC (pstk file)
Use global
default: 3 m
N/A
Use the minimum or
maximum in-bound value
if below or above
bounds, respectively
Stack inside
diameter
0.001-300 ft
(0.0003048-
91.4 m)
Use default value by
SCC (pstk file)
Use global
default: 0.2 m
N/A
Use the minimum or
maximum in-bound value
if below or above
bounds, respectively
Stack exit
gas
temperature 11
>0-4,000 °F
(>255.4-
2,477.6 K)
Use default value by
SCC (pstk file)
Use global
default: 295.4 K
N/A
Use the minimum or
maximum in-bound value
if below or above
bounds, respectively
Stack exit
gas velocity
0.001-1,000
ft/s
(0.0003048-
304.8 m/s)
Calculate from
existing exit gas flow
rate and inside
diameter: (4*flow) /
(pi*diameter2)
Use default
value by SCC
(pstk file)
Use global
default: 4 m/s
Use the minimum or
maximum in-bound value
if below or above
bounds, respectively
Fugitive
height
N/A
0 m if length and
width are not missing
and are above 0;
3.048 m if length or
width are missing or 0
N/A
N/A
N/A
Fugitive
length
N/A
10m
N/A
N/A
N/A
Fugitive
width
N/A
10m
N/A
N/A
N/A
Fugitive
angle
N/A
0 deg
N/A
N/A
N/A
" For exit gas temperatures, AirToxScreen's bounds were set so that values must exceed 0 °F.
Notes: pstk file = file of default stack parameters by source classification code (SCC) from EPA's SMOKE emissions
kernel: ostk 13nov2018 vl.txt. retrieved on 28 September 2022 from httos://cmascenter.ore/smoke/.
K = Kelvin; SCC = source classification code
E.2 Inhalation Exposure Estimates for Fenceline Communities
Acute and chronic inhalation exposures were estimated based on air concentrations estimated in Section
3.3.1 using the methodologies described above. Acute and chronic inhalation exposures used to evaluate
non-cancer risks are estimated as an Acute Concentration (AC) or Average Daily Concentration (ADC),
respectively. Lifetime exposures used to evaluate cancer risks are estimated as a Lifetime Average Daily
Concentration (LADC).
The equations used to calculate each of the exposure values provided below:
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EquationApx E-4.
AC = (DACxET)/AT
ADC = (AACXET X EF X ED)/AT
LADC = (AAC X ET X EF X ED)/AT
Where:
EF
ED
AT
AC
DAC
ET
AAC
Acute concentration (|ig/m3)
Daily Average Air Concentration, model output reflecting average concentrations
over a 24-hour period (|ig/m3)
Exposure time (24 hours/day)
Annual Average Air Concentration, model output reflecting average
concentrations over a year (|ig/m3)
Exposure frequency (365 days/year)
Exposure duration (1 year for non-cancer ADC; 78 years for cancer LADC)
Averaging time; averaging time for AC = 24 hours; averaging time for ADC = 24
hours/day x 365 days/year x 1 year; averaging time for LADC = 24 hours/day x
365 days/year x 78 years
For fenceline communities, all exposure estimates assume continuous exposure (24 hours/day)
throughout the duration of exposure. The exposure duration used to calculate the LADC is based on the
95th percentile of the expected duration at a single residence, 78 years and the averaging time is based
on a 78-year lifetime.
Detailed reporting of modeled air concentrations and corresponding AC, ADC, and LADC estimates are
provided in the Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File:
Supplemental Information on AERMOD TRI Exposure and Risk Analysis (U.S. EPA. 2024n). Draft Risk
Evaluation for 1,1-Dichloroethane - Supplemental Information File: Supplemental Information on
AERMOD Generic Releases Exposure and Risk Analysis (U.S. EPA. 20241). and in the Draft Risk
Evaluation for 1,1-Dichloroethane - Supplemental Information File: Supplemental Information on
AERMOD NEI Exposure and Risk Analysis (U.S. EPA. 2024m).
E.3 Land Use Analysis
EPA conducted a review of land use patterns around TRI facilities where cancer risk would exceed
1 xl0~6. The methodology for this analysis is consistent with what was previously described in the Draft
TSCA Screening Level Approach for Assessment Ambient Air and Water Exposures to Fenceline
Communities Version 1.0.23 This review was limited to those facilities with real Global Information
System (GIS) locations. The land use analysis does not include generic facilities where alternative
release estimates were modeled to estimate exposures since there is no real location around which to
conduct the land use analysis. The purpose of this review was to determine if EPA can reasonably
expect exposures to the general population within the modeled distances where cancer risk would
exceed 1 x 10 6, This detailed review consisted of visual analysis using aerial imagery and interpreting
land use/zoning practices around the facility. More specifically, EPA used ESRI ArcGIS (Version 10.8)
and Google maps to characterize land use patterns within the radial distances evaluated where cancer
risk would exceed 1 x 10~6 for each facility based on the 95th percentile modeled air concentrations. For
23 https://www.epa.gov/assessing-and-managing-chemicals-under-tsca/tsca-screening-level-approach-assessing-ambient-air-
and.
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locations where residential or industrial/commercial businesses or other public spaces are present within
those radial distances indicating risk, EPA reasonably expects exposures and therefore associated
potential risks to the general population. Where the radial distances showing an indication of risk occur
within the boundaries of the facility or is limited to uninhabited areas, EPA does not reasonably expect
exposures to the general population and therefore does not expect associated risks. EPA did not consider
possible future residential use of areas. Also, as stated in Appendix E.4, additional land use analysis was
not warranted for aggregate analysis.
As show in TableApx E-8, EPA's land use analysis did not identify any residential, industrial/
commercial businesses, or other public spaces within those 1,000 m where risk estimates would exceed
1 xl0~6. Based on this characterization of land use patterns and identified risk estimates, EPA does not
expect exposures to the general population for any of the TRI facilities and aggregate groups (Appendix
E.4) where cancer risk would exceed 1 x 10~6 for the 95th percentile modeled air concentrations.
Therefore, EPA does not expect a risk to the general population resulting from 1,1-dichloroethane
releases via the ambient air pathway.
Table Apx E-8. Summary of the General Population Exposures Expected near Facilities Where
TRI Modeled Air Concentrations Indicated Risk for 1,1-Dichloroethane
OES
cou
Total Number
of Facilities
Evaluated
Number of
Facilities with
Risk Indicated
Number of Facilities with Risk
Indicated and General Population
Exposures Expected
Manufacturing
Manufacturing
9
7
0
Processing as a
reactive intermediate
Processing as a
reactant
6
2
0
General waste
handling, treatment,
and disposal
Waste handling,
disposal, and
treatment
8
1
0
Individual facility summaries are available in the Draft Risk Evaluation for 1,1-Dichloroethane -
Supplemental Information File: Supplemental Information on AERMOD TRI Exposure and Risk
Analysis (U.S. EPA. 2024n).
E.4 Aggregate Analysis across TRI Facilities
A conservative screening method for aggregated risk within the air pathway is included to address
whether the combined general population exposures to emissions from nearby facilities present any
additional risk not represented by the individual facility analysis. By taking a conservative approach, this
methodology can effectively screen out aggregate concerns where no additional air risk is identified, and
flag groups of facilities that demonstrate the potential for additional aggregate air risk. The methodology
for this analysis is consistent with what was previously described in the Draft Supplement to the Risk
Evaluation for 1,4-Dioxane (U.S. EPA. 2023b).
The aggregate air approach utilized the existing modeling results for individual facilities, which modeled
releases out to 10 km from the point of release. Facilities with releases to air were mapped using
location coordinates from the TRI database. A 10 km buffer was drawn around each facility, and groups
of facilities were identified by any overlap between these buffers (i.e., any facilities within 20 km of
another facility, even if not all of the facilities have overlapping buffers) (Figure Apx E-5).
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aBMHi
M6WBITSB»2-Sa
KOiffiSGgSBIlfflGM
BlHiM
PjlGmu pT41
[((6IRgcilities))]
Kilometers
^ 1,1-DCA Air Facilities
Air Facility Groups (10km buffer)
FigureApx E-5. Example of Group of Air Releasing Facilities with
Overlapping 10 km Buffers for Aggregate Air Risk Screening
EPA combined modeled air concentrations from each facility in the group to generate hypothetical
"worst-case scenario" aggregate air concentrations for the facility group. Due to the modeling
methodology for individual facilities producing resulting air concentrations at discrete distances from
each facility, the aggregate screening analysis also assesses concentrations and risk at discrete distances.
For this analysis, the facilities are treated as if they are all releasing from the same point. This is a
conservative approach, since the facilities within each group all have some distance between them, and
the air concentrations tend to decrease with greater distance from the source facility. Within each facility
group, the 95th percentile total (stack and fugitive) air concentrations for each facility were summed for
each modeled distance interval. Cancer risk levels were similarly added together for each modeled
distance interval, due to their proportional relationship to concentration, and non-cancer MOE values
were combined using Equation_Apx E-5 below for each distance interval.
EquationApx E-5.
MOEtotal = l/CL/(MOEx ) + 1 /{MOE2 ) + 1 /(MOE3 ) + •••)
Where:
MOEtotai = The aggregated MOE value for the group
MOE1i2i3 ... = The individual MOE values for each facility in the group
Aggregated risk values were then compared against cancer and non-cancer benchmarks to identify
values indicating risk relative to benchmarks. For each facility included in an aggregated group, it was
noted whether the individual risk calculation results indicated risk relative to cancer or non-cancer
benchmarks before aggregating. Additionally, for each facility group the relative contribution of each
facility to the 95th percentile cancer risk was calculated, by dividing the individual facility risk by the
aggregated group risk, to determine whether the resulting numbers may be disproportionately due to
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only one or more facilities. The resulting aggregate risk calculations were reviewed to determine where
the numerical results suggested a concern for aggregate air risk that had not been represented by the
individual facility risk analysis. Where this additional risk was flagged, the mapped locations of the
facilities were then inspected to confirm that the distances between the facilities supported aggregating
releases from the facilities at the flagged distance interval. The review of the aggregated results and
facility locations was applied to characterize whether aggregate air risk relative to benchmarks is
expected for each group. For example, if the aggregate risk calculations for a group of two facilities
indicated cancer risk greater than 1 in 1 million (1 x 10~6) at the 100 m distance, and the individual
facilities only showed that level of risk up to 60 m, the map would be inspected. If the facilities were
found to be located 1,000 m apart, the group would be characterized as not showing risk relative to a 1
in 1 million benchmark beyond what was captured by the individual analysis. However, if the facilities
were located within 200 m of one another, such that their 100 m distance intervals would intersect, the
group would be characterized as showing potential for aggregated air risk beyond what was captured by
the individual analysis. If aggregate air risk relative to benchmarks is identified, then an additional land
use check is performed to confirm the potential for a general population exposure at the new distance.
The grouping analysis for 1,1-dichloroethane resulted in four groups of nearby facilities, ranging from
two to six facilities per group (Table Apx E-9). No additional aggregate air risk relative to benchmarks
was identified for each of the four groups. For one of the groups (Group 2) there is an additional
distance interval (100 m) showing risk from the aggregate calculation greater than 1 x 10~6, but not from
the individual facilities. However, the inspection of the mapped locations of the facilities within Group 2
shows that the contributing facilities are greater than 1 km apart, so this aggregate scenario would not
occur. Therefore, further inspection and additional land use analysis were not warranted for Group 2.
While Groups 3 and 4 each contained one or more facilities showing risk out to some distance, there was
no additional distance interval showing risk from the aggregate calculation greater than 1 x 10~6.
Although the proximity of the facilities may indicate a reality of greater localized air concentrations than
are represented in the individual facility analysis, the aggregated concentrations did not result in
noticeable increased risk estimates (i.e., aggregation did not increase cancer risk levels beyond
individual facility risk levels), so any determinations of risk are already accounted for by the individual
facility analysis. No cancer risk estimates in Group 1 exceeded 1 in 1 million benchmark.
Table Apx E-9. Summary of Aggregate Analysis for TRI Facilities
Total Air Facilities
with TRI Release
Data
Number of Facilities
in Groups
Number of Groups
Number of Groups
with Additional
Aggregate Risk
23
13
4
0
Maps of the four facility groups with the 10 km buffers used to define them are provided below in
FigureApx E-6 through FigureApx E-9. Results of the aggregate analysis are presented in the Draft
Risk Evaluation for 1,1-Dichloroethane — Supplemental Information File: Supplemental Information
on AERMOD TRI Exposure and Risk Analysis (U.S. EPA. 2024n).
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12572 FigureApx E-6. Map of Aggregated Air Facilities, Group 1
12573
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12576 Figure Apx E-7. Map of Aggregated Air Facilities, Group 2
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1,1-DCA Air Facilities
Air Facility Groups (10km buffer)
B3m37B
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lft2IF^ilities))1
Kilometers
f 1,1-DCA Air Facilities
Air Facility Groups (10km buffer)
w 4
—^BeRTgaaooisii
r7/7,536g61j)[
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12578
12579 FigureApx E-8. Map of Aggregated Air Facilities, Group 3
12580
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12582
12583 Figure Apx E-9. Map of Aggregated Air Facilities, Group 4
12584 E.5 Ambient Air Exposure to Population Evaluation
12585 TRIPopulation Evaluation
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Air Facility Groups (10km buffer)
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I Kilometers
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This evaluation aimed to quantify population exposure around a subset of AERMOD TRI release sites
where estimates of non-cancer risk or cancer risk exceed minimum benchmarks for human health, and
thus reflect high-end exposures of 1,1-dichloroethane. The 95th percentile (p95) of AERMOD average
daily modeled results were used in order to remain conservative with the scenario modeled. Average
daily p95 air concentrations (ADC) and life-time average daily p95 concentrations (LADC) of 1,1-
dichloroethane were estimated prior to this evaluation. Cancer risk (CR) values were then estimated
from LADC values. Of the 23 TRI facility releases modeled using AERMOD, 10 resulted in CR values
that exceeded the minimum CR value of 1 x 10~6 while none resulted in modeled air concentrations that
exceeded the minimum non-cancer risk (NCR), which would include a margin of exposure (MOE)
calculation below the benchmark of 300. These 10 AERMOD TRI release sites thus became the focus of
the population evaluation because of the ability to capture high-end exposures of 1,1-dichloroethane in
ambient air.
The goal of population evaluation was to quantify population density and percentages associated with
the general population, identified PESS groups, the race/ethnicity makeup of the general population, and
the poverty level of the general population. Nearby environments and community infrastructure of
interest were identified, and distances between the subset of ARMOD TRI air release sites and
population census blocks and community locations were estimated to understand the likelihood that
these populations experience high-end exposures of 1,1-dichloroethane.
Analysis Assumptions and Uncertainties
There is an inherent uncertainty associated with the TRI coordinates that are meant to represent sites of
1,1-dichloroethane release to ambient air. For instance, in some cases the TRI coordinates may be
located at the edge of the facility complex, such as at an entrance to the facility, a mailbox address, or a
road leading up to the facility, which may not capture the actual site of emission. The accuracy of the
facility's release site coordinates is thus strictly tied to the accuracy of the AERMOD results at the
various distances modeled, and which were considered in this evaluation. This degree of uncertainty
should be considered when interpreting the population results.
The population metrics and distances estimated as a part of the analysis also relies on computed centroid
coordinates from the boundaries of U.S. census (polygon shapefile) blocks. Since the size of census
blocks is determined by population, rural areas tend to have larger census block polygons compared to
densely populated urban or suburban areas. This "centroid effect" is also a factor that affects the
distances estimated between facility release sites and the surrounding census blocks, and thus as with the
modeled AERMOD distances, the distances relative to census blocks and community infrastructure that
are being calculated should not be overinterpreted.
In some cases, CR values greater than or equal to 1 x 10~6 are found at 1,000 m, but not 2,500 m, so it
cannot be ruled out that CR does not exceed 1 x 10~6 between 1,000 and 2,500 m away from the
AERMOD TRI release site. Since it is unlikely that populations beyond 2,500 m are exposed to CR
values > 1 x 10"6, only census block centroids within 2,600 m were considered for this evaluation. It is
important to note, however, that there is a possibility that census block areas exist within 2,600 m, but
are not included in this evaluation because their centroids are positioned just beyond 2,600 m.
Methods
Overview of Approach: After identifying which AERMOD TRI release sites to focus on for this
evaluation (i.e., those with CR values > 1 x 10 6 that reflect a high-end exposure), the next step involved a
visualization of the surrounding landscape and community infrastructure using Google Earth/Maps to
inform which kinds of population, household, and community location data to obtain and analyze. The
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methodology for this analysis is consistent with what was previously described in the Draft TSCA
Screening Level Approach for Assessment Ambient Air and Water Exposures to Fenceline Communities
Version 1.0.24 However, radial distance measurements were not made in Google Earth since these
measurements were made a later step with more precision. An internal decision framework document to
aid in identifying PESS groups was used to help identify which environments and community
infrastructure to examine. Specific population densities, environment and community locations of
interest, and distances between the TRI release sites and census blocks and spatial boundaries of these
environments/infrastructure were quantitated using GIS and R computing software. Input data was
obtained from external sources and imported into R. New results generated as a part of this evaluation
were compared with AERMOD results and their associated modeled distances to identify the likelihood
that these populations experience high-end exposures to 1,1-dichloroethane. FigureApx E-10 provides
an overview of the conceptual design and approach taken as a part of this evaluation.
Figure Apx E-10. Flowchart Illustrating the Conceptual Design and Approach
Taken for this Evaluation
Site Selection and Visualization: LADC results from all 23 AERMOD TRI release sites were used to
estimate cancer risk values at the following discrete or areal modeled distances: 10, 30, 30 to 60, 60,
100, 100 to 1,000, 1,000, 2,500, 5,000, and 10,000 m. Ten TRI facilities with LADC levels and
calculated cancer risk values greater than 1 x 10~6 were identified. Site characteristics of these 10 TRI
facilities are included in Table Apx E-10.
24 https://www.epa.gov/assessing-and-managing-chemicals-under-tsca/tsca-screening-level-approach-assessing-ambient-air-
and.
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TableApx E-10. Facilities Reporting TRI Emission Included in General Population
Characterization
OES
Facility Name
City
State
TRI ID
Manufacturing
Occidental Chemical Holding Corp - Geismar
Plant
Geismar
LA
70734VLCNMASHLA
Oxy Vinyls LP La Porte VCM Plant
La Porte
TX
77571LPRTC2400M
Processing as a
reactant
Westlake Vinyls Inc
Calvert City
KY
42029WSTLK2468I
Westlake Lake Charles North
Westlake
LA
70669GRGGL1600V
Eagle US 2 LLC
Westlake
LA
70669PPGNDCOLUM
Shintech Plaquemine Plant
Plaquemine
LA
70764LLMNXHWY40
Blue Cube Operations LLC - Plaquemine Site
Plaquemine
LA
7076WBLCBP21255
FreeportOlin BC
Freeport
TX
7754WBLCBP231NB
Waste handling,
disposal, treatment,
and recycling
Axiall LLC
Plaquemine
LA
70765 GRGGLHIGHW
Ash Grove Cement
Foreman
AR
71836SHGRVPOBOX
Google Earth/Google Maps was used to conduct a preliminary (visual) analysis of the areas surrounding
these 10 TRI facilities to identify residential neighborhoods and environments or community
infrastructure of interest that may include a PESS group. For example, homes, parks, childcare centers,
schools, places of worship, hospitals and clinics were among the types of environments and community
infrastructure being considered and that were visually inspected.
Population and Household Data Selection
Population data associated with census block groups was gathered from the American Community
Survey (ACS) 2017 to 2021, which includes 5-year estimates for age, race, ethnicity, and household
income. This data and the 2021 census block polygon (shapefile) dataset were obtained from
data.census.gov and TIGER/Line Shapefile. respectively. Data for the locations of childcare centers,
public schools, private schools, colleges and universities, places of worship, and healthcare facilities
(hospitals, urgent cares, VA health facilities, and dialysis centers) were obtained from the Department of
Homeland Security's Homeland Infrastructure Foundation-Level Data Geoportal.
ACS Data Selection and Justification
The following bullets for population data related to age, race, ethnicity, and household income provide a
brief justification for the selection of the various metrics evaluated herein. This also includes the
environments and community infrastructures identified in the visual inspection of the TRI release sites:
Population Age:
• Children under 5 years old: childcare centers and public schools were observed near several of
the facilities
• Children under 18 years old: public schools were observed near several of the facilities
• Females of reproductive age (15-49 years): pregnant females were indicated as a potential PESS
group, so females of reproductive age were used as a proxy for pregnant females since the census
does not explicitly provide data on pregnancy
• Population over 65 years old: indicated as a group of interest in the PESS framework document
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Population Race:
• White alone
• Black alone
• Asian alone
• American Indian/Alaska Native (AI/AN) alone
• Native Hawaiian/Pacific Islander (NH/PI) alone
• Other race alone
• Multiracial (2+ races)
Ethnicity Data:
• Total population identifying as Hispanic/Latino
Income Data:
• Population with income to poverty ratio under 1 (for population whose poverty status is
determined)
o Total population whose poverty status is determined (for finding percentage of
population in poverty)
• Median household income
• Households in each of the income brackets used by the census
Environments and Community Infrastructure
• Childcare Centers: seen nearby several of the facilities during Google Earth analysis
• Schools: observed nearby several of the facilities during Google Earth analysis
o Separate datasets for public schools, private schools, and colleges/universities were used
• Places of Worship: observed nearby several of the facilities during Google Earth analysis
• Healthcare centers: draft RE identified people with liver cancer as a potential PESS group, and
these subpopulations may visit/be admitted to healthcare centers more often
o Separate datasets for hospitals, urgent care centers, VA Health facilities, and dialysis
clinics were used
Data Pre-processing
Much of the data analysis in this evaluation was performed using R computing software. The census
block dataset contains over 8 million rows, which is an impractical size to perform complex geospatial
operations with. To make the dataset more manageable to work with in R, the census block dataset was
clipped to 2,600 m of the subset of AERMOD TRI release sites. The 2,600 m distance was chosen
because 1,000 m is the furthest distance in which a CR great or equal to lxl0~6 was observed, but it
cannot be ruled out that CR does not exceed lxl0~6between 1,000 and 2,500 m in those instances. The
clipping area was extended an additional 100 m to account for small changes in the geospatial area that
can result when transforming spatial data from one projection system to another. Only census block
centroids within 2,600 m of the subset of AERMOD TRI release sites were included for the next steps in
the analysis.
The ACS database containing population and household-level information is available at the census
block group level, which may contain one of more individual census blocks. Our goal was to estimate
population and household metrics for each individual census block and then evaluate block4evel results
at relevant distances to the subset of AERMOD TRI release sites. Thus, it was necessary to downscale
the ACS population and household data from the census block group level to the level of individual
blocks. To do this, the proportion of individual blocks within a block group was used with population
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and household data at the block group level to estimate the expected results scaled down to individual
blocks.
Identifying Sites with a General Population
Prior to performing any weighted statistics, individual census blocks without a population based on the
population column of the census block group centroid dataset were removed. This column describes the
2020 Census population count for the census block. However, to protect the privacy of survey
respondents, these population counts were subjected to random noise, which means that a small amount
may have been added or subtracted to the population count to slightly obscure the original population
value. Although this pre-processing step may be less conservative than assuming every census block has
a population, it likely removes census blocks in non-residential areas and so was the preferred step to
take. All census block centroids within 1,000 and 2,600 m of each facility were first grouped by their
census block group ID. Then, the number of populated census blocks per block group located within
1,000 or 2,600 m of the facility was calculated. The block group's population was then multiplied by the
number of populated census blocks within 1,000 or 2,600 m of the facility and then divided by the total
number of census blocks in the block group. The weighted populations for each of the census block
groups were then summed together to provide the estimated weighted population size around each
facility.
When adding population metrics together for a given OES, it is important to identify where potential
overlap between facilities and populations exist to avoid double counting. None of the census blocks
within 1,000 m of the facilities overlapped with each other, so all the facility populations were simply
added to find the population by OES. Some census blocks were within 2,600 m of multiple facilities.
One census block was within 2,600 m of the Shintech Plaquemine Plant site (OES: Processing as a
reactant), Blue Cube Operations LLC Plaquemine Site (OES: Processing as a reactant), and the Axiall
LLC site (OES: Waste handling, disposal, treatment, and recyling). Additionally, two more census
blocks were located within 2,600 m of both the Westlake Lake Charles North site and the Eagle US 2
LLC site (both of which have an OES of Processing as a reactant).
To account for these population overlaps and avoid double counting populations when summing
population totals by OES, the census blocks associated with more than one TRI facility were first
identified. The maximum weighted population of these block groups was then calculated. When adding
the populations for each OES together, the non-maximum weighted population(s) for the same census
blocks were then subtracted. This avoids double counting populations, while still allowing for a
conservative estimate of the total population by OES.
Characterizing Exposure
AERMOD models air concentrations at eight discrete distances ranging from 10 to 10,000 m and two
areal-averaged distances at 30 to 60 m and 100 to 1,000 m. This means if high levels of 1,1-
dichloroethane in ambient air are modeled at 1,000 m, EPA cannot rule out that distances between 1,000
to 2,500 m do not also experience high levels of 1,1-dichloroethane in air. Comparing estimated
distances of the general population to both the maximum AERMOD modeled distance that reflect high-
end exposure, as well as the next modeled distance, allows us to evaluate the possibility of exposure at
and in between these two distances. However, given that air concentrations decrease linearly with
distance, a possible exposure may not be a likely exposure if the general population lives well beyond
the AERMOD modeled distance that CR was found. Unreasonable risk determinations based on high-
end exposures should consider these relevant distances between modeled concentrations and where
populations are expected as well as the magnitude of distances being evaluated. This is important given
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the uncertainty surrounding distance estimates is greater at shorter distances than longer distances since
TRI coordinates may not necessarily reflect the true air release sites of 1,1-dichloroethane.
NEI Population Evaluation
The methods taken for the NEI population evaluation were very similar to those taken for the TRI
population evaluation, and so much of the goals, assumptions and uncertainties, methods, site/data
selection, and exposure characterization applies equally. There were a few notable differences in how
the AERMOD NEI results were analyzed, which are outlined below.
The NEI data include releases from multiple emission units for a given facility. These units may be
fugitive and/or stack type emissions, each of which may be assigned a different OES designation. This
data was obtained for 2014 and 2017. It is important to note that the facility release sites, number of
emission units per site, their type of emissions, and their subsequent OES designation can change
between 2014 and 2017. Since concentrations from multiple emission units were modeled using
AERMOD, it was desirable to account for their aggregate release and exposure. This was done by
adding calculated CR values for each AERMOD modeled distance across emission units of a given
facility. This step was taken separately for 2014 and 2017. These facility total CR values were then used
to identify a subset of AERMOD NEI release sites to focus on for the population evaluation by selecting
on those facility CR totals that exceed the minimum CR value of 1 x 10~6.
The population and household data were collected using the same approach for the TRI population
evaluation with one notable exception. While the TRI evaluation considered only a single site
(coordinate) for the geospatial analysis, our NEI evaluation accounted for all emissions units within a
facility. In other words, census blocks and their associated ACS data were geospatially analyzed relative
to each emission unit with a given facility complex. The population metrics were obtained for a given
emission unit, and then summed across all units for a given distance threshold (e.g., 1,000 m from the
emission units). This was done for facility release sites in both the 2014 and 2017 datasets; however, the
list of facilities and number of emission units were largely the same between the two years.
With respect to exposure characterization, it is important to note using an aggregate approach it is
assumed that each population surrounding an individual emission unit is equally exposed to the facility
total 1,1-dichloroethane levels and CR values. Although this may overestimate exposure and CR values
for a given population around a emission unit, this conservation step was preferred over underestimating
exposure that may result by assuming that emission units are not aggregating with one another.
EPA determined that 517 facility release sites have estimated CR values that exceed the minimum CR
value of lxlO"6. In an effort to refine the focus on those sites that pose a likely exposure to these CR
values, the Agency evaluated the population for only those AERMOD NEI release sites that have a
populated census block that overlaps or is within 100 m of the furthered modeled distances where CR
greater than or equal to 1 x 10~6 is expected. For example, if a facility total CR value for the AERMOD
modeled 100 to 1,000 m area exceeds lxl0~6, then this site was only considered with a populated census
block was measured within 1,100m of any individual emission unit. This subset of AERMOD NEI
release sites were evaluated specifically to interpret population results that have a greater confidence of
true exposure to the estimated CR values. It should not preclude, however, that there are additional
AERMOD release sites that have a likely exposure to estimated CR values if a populated census block
was measured beyond the 100-m threshold. That is, EPA cannot rule out that exposure is not occuring a
distances from 100 m to a few hundred meters or greater from the emission units because of the
uncertainties in where populations may be living that come with performing a proximity analysis based
on census block centroids.
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12831 Another notable different between the NEI and TRI population evaluations is that (at present), only
12832 populations within 1,000 m of the emission units were considered for the NEI evaluation. In addition,
12833 proximity to community locations and infrastructure of interest have not yet been evaluated.
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12846
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12849
12850
12851
12852
12853
12854
12855
12856
12857
12858
12859
12860
12861
12862
12863
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12868
12869
12870
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Appendix F SURFACE WATER CONCENTRATIONS
F.l Surface Water Monitoring Data
F.l.l Monitoring Data Retrieval and Processing
The complete set of 1,1-dichloroethane monitoring results stored in the Water Quality Portal (WQP) was
downloaded in March 2023 (NWQMC. 2022) using the datciRetrieval package in R (R Core Team.
2022) and imported directly into the R computing platform console. Specifically, the readWOPdata and
whatWOPsites functions were used to acquire all WQP sample results and site data with a "1,1-
Dichloroethane" characteristic name. No additional arguments were used with both functions. The
downloaded dataset is large and comprehensive, where only certain data fields were desired for EPA's
intended use in the 1,1-dichloroethane risk evaluation. The WQP dataset was subsequently filtered for
only surface water sample types with the following "MonitoringLocationTypeName:"
• Spring
• Stream
• Wetland
• Lake
• Great Lake
• Reservoir
• Impoundment
• Stream: Canal
• Stream: Ditch
• Facility Other
• Floodwater Urban
• River/Stream
• River/Stream Ephemeral,
• River/Stream Intermittent
• River/Stream Perennial
Sample results identified as below the detection limit or non-detects (i.e., "ResultMeasureValue"
indicated with an N/A) were replaced with values at one-half the quantitation limit
("DetectionQuantitationLimitMeasure.MeasureValue'72). All rows without a sample result value or
reported detection quantitation limit were subsequently removed. The sample result values of any
replicate samples collected on the same day at the same time were averaged. Rows with an
"ActivityYear" between 2015 and 2020 were kept, representative samples collected during this time
period. Samples flagged as QC blanks in the "ActivityTypeCode" column were removed. Only
dissolved aqueous samples were kept as indicated by a "|ig L b' or "mg L b' unit identifier in the
"ResultMeasure.MeasureUnitCode" column. Sample units were adjusted to |ig L 1 if needed. All sample
results less than zero were forced to equal zero. Since V2 the detection quantitation limit was used to
replace below detection or non-detection sample result values, an appropriate detection quantitation
limit cutoff was determined. The 95th quantile, 99th quantile, and max detection quantitation limits were
examined to identify that <5 |igL 1 is a reasonable detection quantitation limit. Any adjusted sample
result values greater than 5 |igL 1 was removed.
Monitoring data from drinking water systems were acquired from the Third Unregulated Contaminant
Monitoring Rule (UCMR3) database (U.S. EPA. 2017c). The UCMR3 dataset includes public water
systems (PWS) serving more than 10,000 people and 800 of the nation's PWSs that serve 10,000 or
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12883
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12888
12889
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12891
12892
12893
12894
12895
12896
12897
12898
12899
12900
12901
12902
12903
12904
12905
12906
12907
12908
12909
12910
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fewer people. The complete history of 1,1-dichloroethane measurements in the UCMR3 finished
drinking water dataset was acquired. Sample result values below the Minimum Reporting Limit (MRL)
as indicated by a "<" sign in the "AnalyticalResultsSign" column were replaced with the MRL. In this
case, the highest reported MRL for all 1,1-dichloroethane drinking water measurements is 0.03 |igL ',
which is low enough where the full MRL as opposed to V2 the MRL can be used. Sample details were
reviewed and screened to remove those indicating that they were collected from groundwater (i.e., those
including "Well" in the "SamplePointName" column) and select for those only including surface water
source types (i.e., those including "SW" in the "FacilityWaterType").
F.2 Surface Water Concentration Modeling
F.2.1 Hydrologic Flow Data Assimilation
The joint U.S. Geological Survey (USGS) and EPA National Hydrography Dataset (NHDPlus V2.1)
national seamless flowline network database was used to obtain modeled stream or river (hereby
referred to as stream) hydrologic flow data. The NHD dataset is one of the largest national hydrologic
datasets, containing geospatially delineated flowline stream networks, information on the sequential
linkages between flowline reach segments (i.e., to-node and from-node identifiers), and modeled flow
values for greater than 2.7 million stream segments nationwide (U.S. EPA and U.S.G.S.. 2016). The
NHD dataset is comprehensive at the nation scale and has been used for numerous regional and national
hydrologic modeling studies since its creation. The NHD dataset contains mean annual and monthly
stream flows for nearly all individual stream segments in the national flow network. Stream flows were
determined by the Enhanced Runoff Method (EROM) Flow Estimate model, which determines flow
values through from multi-step estimation and calibration process with each step designed to
incrementally improve the stream flow estimate. The first step involves accumulating runoff based on
flow balance grids from a 30-year period from 1971 to 2000. The last step involves correcting flows at a
distance upstream and downstream of an observed gage flow. The modeled EROM flow data fields are
labeled with a leading "QE_". The dataset is incorporated into recordkeeping and modeling across EPA
programs that require knowledge of a national stream network, providing consistency and compatibility
with projects across the EPA. Pertaining to our efforts in this risk evaluation, the EPA's Enforcement
and Compliance History Online (ECHO) database uses facility-linkages to the 14-digit Hydrologic Unit
Classification (HUC) reach codes associated with the NHD flowline network.
A list of facilities releasing 1,1-dichloroethane to surface waters were obtained from the ECHO
Pollutant Load Tool "Custom Search" tab as outlined in Draft Risk Evaluation for 1,1-Dichloroethane -
Supplemental Information File: Environmental Releases and Occupational Exposure Assessment. These
facilities include those that directly discharge into surface waters, compiled from their parent TRI and
Discharge Monitoring Reports (DMR) database. None of the facilities indirectly discharge to a surface
water body; for example, which may arise from the transfer of 1,1-dichloroethane to a disposal facility.
For each facility, the National Pollutant Discharge Elimination System (NPDES) identifier was used to
retrieve a corresponding 14-digit NHDPlusV2 reach code using the ECHO DMR API wrapper
("dmr_rest_services.get_facility_report"). This step was repeated for each year between 2015 to 2020 to
obtain reach codes that correspond to the year that wastewater discharge data was collected. Note, all
NPDES pulled from TRI are also represented in the DMR database.
Values of modeled EROM mean annual stream flow (QE MA) and monthly annual stream flow (e.g.,
QE 01, QE 02, QE 03, etc.) were retrieved from the seamless NHDPlusV2 flowline network database
for all acquired reach codes. Since individual reach codes may include one or more flowline segments
(i.e., a unique COMID identifier) and thus multiple modeled flow values, the lowest flow value for a
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12941
12942
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12947
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12949
12950
12951
12952
12953
12954
12955
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given reach code was kept. Although most NHD flowlines represent streams, some may represent
coastal water bodies, where the mean annual stream flow values are reported as an N/A or as zero. Flow
values reported as N/A or zero were subsequently flagged as possible coastlines. In some cases, a reach
code was not returned through the ECHO DMR API wrapper. When this occurs, a calculated facility
effluent flow was used instead of a NHD modeled flow value, thus reflecting the effluent flow at the
facility outfall instead of the receiving water body. Facility effluent flow was also used when a reach
code was returned, but the value was reported as an N/A or zero. EPA decided this was a more
conservative and efficient approach than to identify where the true outfall and receiving water body is
for a given facility NPDES that did not return a reach code. Because DMR reach codes were assigned
using the NHD flowline database, instances when a reach code is not returned could reflect a reporting
error or an instance where the receiving water body was a lentic system such as a lake or pond. Thus,
through this approach, a calculated facility effluent flow was also used in the event the receiving water
body is a lake, pond, or reservoir, which would require detailed information of the lentic water body's
volume to estimate the aqueous concentration. An average annual facility effluent flow (in millions of
liters) was calculated by dividing the annual pollutant load (kg yr ') by the average concentration (mg
L '), derived from the Pollutant Load Tool estimation function. This value was then divided by 365 to
obtain an average facility effluent flow in units of millions of liters per day (MLD).
To estimate an aqueous concentration of 1,1-dichloroethane in a receiving stream, the annual pollutant
load (kg yr-1) was divided by a hydrologic flow value (in MLD) originating from the NHD EROM
dataset and the units adjusted accordingly. Several different hydrologic flow metrics were estimated,
which detailed in the next section. For each of the metrics, stream flow was compared to the calculated
facility effluent flow, and the lower of the two flow values was kept. When NHD-based flow could not
be estimated, the calculated facility effluent flow was chosen. The Pollutant Loading Tool returns a
continuous dataset of annual pollutant load and average concentrations, so a calculated facility effluent
flow value can always be used, allowing for a continuous record of flow metrics to choose from to
estimate an aqueous concentration of 1,1-dichloroethane.
F.2.2 Facility-Specific Release Modeling
In previous TSCA risk evaluations, EPA applied the E-FAST 2014 tool (U.S. EPA. 2014a) to estimate
aqueous chemical concentrations and exposure resulting from individual facility discharges to surface
waters. To make the calculations more flexibility, efficient, and repeatable, many of the underlying
calculations that EPA uses were translated to an excel workbook format. Without the need to use the E-
FAST software directly which can be cumbersome and time consuming, facility pollutant loads,
associated flow data, and facility release schedules can be used with the nimbler E-FAST-style excel
workbook. This refinement in methodology allows an assessor to manual enter and adjust inputs
parameters as needed, but more importantly, provides an opportunity to enter newer and more relevant
hydrologic flow information than what was included in the older, underlying, E-FAST software (the
EPA original Reach File 1 dating back to 1984). With this improved approach, facility-specific
modeling can be conducted using similar methodology and logic of the E-FAST 2014 tool but with
update hydrologic flow data and an overall improved confidence in the accuracy of the estimated
aqueous concentrations and linkages between the facility releases and their true receiving water body.
This updated approach was first employed in EPA's risk evaluation of 1,4-dioxane. This draft risk
evaluation of 1,1-dichloroethane has adopted a similar approach herein.
Several different types of metrics were estimated using either the annual or monthly mean modeled
EROM flow values: arithmetic mean flow, harmonic mean flow, the lowest 30-day average flow
occuring in a 5-year period (30Q5), and the lowest 7-day average flow occuring in a 10-year period
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(7Q10). The harmonic mean and 30Q5 flow metrics have been used in previous risk evaluations for
exposures from drinking water consumption, dermal contact, and fish ingestion that affect human health.
The 7Q10 flow metric has previously been used to evaluate exposures to aquatic ecological species. Of
these flow metrics, only the arithmetic mean can be acquired from the NHDPlusV2 EROM dataset. The
other flow metrics (harmonic mean, 30Q5, and 7Q10) have historically required an extensive, costly,
and generally inefficient modeling procedure, which is impractical to do in a timely manner for a large
list of new sites until the procedure is made more efficient. Thus, an alternative approach to estimating
these flow metrics was taken, consistent with how they are calculated in the underlying E-FAST
Probabilistic Dilution Model (PDM). Regression equations from the E-FAST user manual ("Versar.
2014) were applied as detailed below. NHD EROM mean annual and lowest monthly flow values serve
as the foundation for these calculations, where the mean annual flow served as the arithmetic mean and
the lowest monthly average flow (i.e., lowest of the monthly series: QE_1, QE_2, QE_3, etc.) was used
as a proxy for 30Q5 flow. Since the modeled EROM flow metrics represent averages across a 30-year
timeframe, the lowest of the monthly means for a given reach is a close representation of the lowest 30-
day average flow occuring in a 30-year time period (i.e., 30Q30), and thus reflects a longer term average
in comparison to 30Q5 flow. The arithmetic mean and "30Q30" were entered into the regression
equations below to solve for the harmonic mean and 7Q10 flow metrics:
EquationApx F-l.
7Q10 = (0.409 cfs/MLD * 30Q5/1.782 ) A1.0352/(0.409 cfs/MLD)
Where:
7Q10 = the modeled 7Q10 flow, in MLD
30(^5 = the lowest monthly average flow from NHD, in MLD
HM = 1.194 * ((0.409 cfs/MLD * AM)A0A73 * (0.409 cfs/MLD
* 7Q10 )A0.552)/(0.409 cfs/MLD)
Where:
HM = the modeled harmonic mean flow, in MLD
AM = the annual average flow from NHD, in MLD
7Q10 = the modeled 7Q10 flow from the previous equation, in MLD
These different calculated stream flow metrics were then compared to the calculated facility effluent
flow. When facility effluent flow exceeded a given stream flow metric (i.e., facility flow > HM, 3005,
or 7O10), then facility effluent flow replaced the stream flow metric value. When a stream flow metric
could not be estimated for the reasons outlined above, then the facility effluent flow value was also used.
For each facility, the highest annual load during the 2015 to 2020 time period was used to estimate
aqueous 1,1-dichloroethane concentration. Average daily loadings are calculated by dividing the annual
loading by the number of days of operation per year. Three different scenarios for operating days were
evaluated: 1 day, 30 days, and the maximum expected days of operation listed in Table 3-3. The 1- and
30-day scenarios provide more conservative approaches to evaluating resulting stream concentrations
and allow more confidence in screening out risk from facilities (that is, identifying which facilities have
releases that do not exceed any thresholds for risk). Conversely, the maximum number of days of
operation provides more confidence for identifying risk that exceeds a threshold.
For each scenario, the aqueous concentration was calculated using Equation Apx F-2:
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EquationApx F-2.
Concentration (\igfL) = (Daily Load (kg/day) * 109 (jj.g/kg))/(Flow (MLD) * 106 (L/ML) )
F.2.3 Modeling at Drinking Water Intakes
To estimate aqueous 1,1-dichloroethane concentrations in drinking water, surface water intake locations
downstream of the facilities releasing 1,1-dichloroethane (in Section 2) were identified. The coordinates
of surface water intake locations for public water systems (PWS) were obtained from the Safe Drinking
Water Information (SDWIS) Federal Data Warehouse. The site coordinates and associated NHDPlusV2
reach codes associated with facilities releasing 1,1-dichloroethane to surface waters were already
obtained in the steps outlined in Section F.2.1. To obtain the reach codes associated with drinking water
intake locations, the nearest neighboring flowline or waterbody from the NHDPlusV2 dataset was
identified using the "Near" tool in ArcGIS Pro software. In addition, flowlines and their reach codes that
intersect with standing water bodies were identified. This can occur when reservoirs are constructed
from dammed rivers, which may have intake locations at the bank of the reservoir as opposed to the
center link of the river (FigureApx F-l).
An R script was developed to search for and identify reach codes with intake locations that exist
downstream of each reach code with a facility release site by using the "to-node" and "from-node" reach
code sequence identifiers as a part of the NHDPlusV2 database. For each facility, the script functions by
starting with the facility-linked reach code and incrementally stepping downstream to the next reach
code, recording the length of the stream segment (in km) and whether the reach has a drinking water
intake. When a reach with a drinking water intake is identified, the PWS details and the total distance
traveled is recorded in a separate data file. The script then continues to search downstream until hitting a
terminal reach code (i.e., where no subsequent reach codes can be search, such as is the case with a
coastline) or when the maximum search distance is realized. For this assessment, a maximum search
stream length of 250 km was applied.
Figure Apx F-l. Generic Schematic of Hypothetical Release Point with Surface
Water Intakes for Drinking Water Systems Located Downstream
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The search function creates a separate data file that includes all possible combinations of PWS intakes
downstream of the facility release sites. Thus, a given facility release site may encounter multiple PWSs,
which each may have multiple intake locations during the search 250 km downstream. For each intake,
the accompanying reach code was used to acquire modeled EROM flow data from the NHD flowline
database using the approach outlined in Section 3.3.3.6.1. Since a PWS may have multiple intakes, the
most upstream intake location was kept while all others removed for the next step. Aqueous
concentrations of 1,1-dichloroethane were then estimated at each intake location using a dilution factor
that was calculated by dividing the stream flow of the reach or the facility effluent plant flow at the
facility release site (i.e., start flow) by the stream flow of the reach at the drinking water intake location
(i.e., end flow). If the end flow was greater than the start flow, the dilution factor was made equal to 1.
The concentration estimated at the site of facility discharge was multiplied by the dilution factor to
estimate an aqueous concentration of 1,1-dichloroethane at the site of the drinking water intake. For
each PWS, additional information was obtained from the Safe Drinking Water Information System
(SDWIS) Federal Reporting System (U.S. EPA. 2022e). The "PWS TYPE CODE" column was used to
select only sites representing Community Water Systems (CWS) and Non-Transient Non-Community
Water Systems (NTNCWS) for exposure analysis. In some cases, PWSs draw water from sources other
than surface water, including groundwater or purchased water from another location. In a prior step, site
information from SDWIS was used to select for only those PWSs that draw from surface waters as the
primary source (i.e., those with identified as "SW" for surface water in the "PrimarySourceCode"
Column).
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Appendix G GROUNDWATER CONCENTRATIONS
G.l Groundwater Monitoring Data
G.l.l Monitoring Data Retrieval and Processing
The complete set of 1,1-dichloroethane monitoring results stored in the Water Quality Portal (WQP) was
downloaded in March 2023 (NWOMC. 2022) using the datciRetrieval package in R (R Core Team.
2022) and imported directly into the R computing platform console. Specifically, the readWOPdata and
whatWOPsites functions were used to acquire all WQP sample results and site data with a "1,1-
Dichloroethane" characteristic name. No additional arguments were used with both functions. The
downloaded dataset is large and comprehensive, where only certain data fields were desired for EPA's
intended use in the 1,1-dichloroethane risk evaluation. The WQP dataset was subsequently filtered for
only groundwater sample types with the following "MonitoringLocationTypeName:"
• Well;
• Subsurface;
• Subsurface: Groundwater drain; and
• Well: Multiple wells.
Sample results identified as below the detection limit or non-detects (i.e., "ResultMeasureValue"
indicated with an N/A) were replaced with values at one-half the quantitation limit
("DetectionQuantitationLimitMeasure.MeasureValue" ^ 2). All rows without a sample result value or
reported detection quantitation limit were subsequently removed. The sample result values of any
replicate samples collected on the same day at the same time were averaged. Rows with an
"ActivityYear" between 2015 and 2020 were kept, representative of samples collected during this time
period. Samples flagged as QC blanks in the "ActivityTypeCode" column were removed. Only
dissolved aqueous samples were kept as indicated by a "|ig L b' or "mg L b' unit identifier in the
"ResultMeasure.MeasureUnitCode" column. Sample units were adjusted to |ig L 1 if needed. All sample
results less than zero were forced to equal zero. Since V2 the detection quantitation limit was used to
replace below detection or non-detection sample result values, an appropriate detection quantitation
limit cutoff was determined. The 95th quantile, 99th quantile, and max detection quantitation limits were
examined to identify that less than or equal to 20 |ig L 1 is a reasonable detection quantitation limit. Any
adjusted sample result values exceeding 20 |ig L 1 were removed.
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Appendix H DRINKING WATER EXPOSURE ESTIMATES
Levels of acute and chronic exposure from the consumption of 1,1-dichloroethane in drinking water
were estimated using the surface water concentrations estimated in Sections 3.3.3.2.2 and groundwater
concentrations estimated in Section 3.3.4.3.2. Additional information on these drinking source-waters
are described in Sections H. 1 and H.2 below.
Acute and chronic drinking water exposures used to evaluate non-cancer risks were estimated as an
Acute Dose Rate (ADR) or Average Daily Dose (ADD), respectively. Lifetime exposures used to
evaluate cancer risks were estimated as a Lifetime Average Daily Dose (LADD). The following
equations were used to calculate each of these exposure values:
EquationApx H-l.
ADR = (SWC x (1 - DWT/100) x IRdw x RD x CF1)/(BW x AT)
Equation Apx H-2.
ADD = (SWC x (1 - DWT/100) x IRdw x ED x RD x CF1)/(BW x AT x CF2)
Equation Apx H-3.
LADD = (SWC x (1 - DWT/100) x IRdw x ED x RD x CF1)/(BW x AT x CF2)
Where:
SWC = Surface water concentration (ppb or |ig/L)
DWT = Removal during drinking water treatment (%)
lRdw= Drinking water intake rate (L/day)
RD = Release days (days/year for ADD, LADD and LADC; 1 day for ADR)
ED = Exposure duration (years for ADD, LADD and LADC; 1 day for ADR)
BW = Body weight (kg)
AT = Exposure duration (years for ADD, LADD and LADC; 1 day for ADR)
CF 1 = Conversion factor (1.0xl0~3 mg/|ig)
CF2 = Conversion factor (365 days/year)
The same inputs for body weight, averaging time (AT), and exposure duration were applied across the
evaluations of drinking water, incidental oral exposure, and incidental dermal exposure. For all
calculations, mean body weight data were derived from Chapter 8, Table 8-1 in EPA's Exposure
Factors Handbook (EFH) (U.S. EPA. 2011a). To align with the age groups of interest, weight averages
were calculated for the infant age group (birth to <1 year) and toddlers (1 to 5 years). The ranges given
in the EFH were weighted by their fraction of the age group of interest. For example, the EFH provides
body weight for 0 to 1 month, 1 to 3 months, 3 to 6 months, and 6 to 12 months. Each of those body
weights were weighted by their number of months out of 12 to determine the weighted average for an
infant 0 to 1 year old. For all ADR calculations, the AT is 1 day, and the days of 1,1-dichloroethane
release are assumed to be 1 according to the methodology used in E-FAST 2014 (U.S. EPA. 2014a).
Thus, exposure levels are derived from aqueous concentration estimates that assume the entire annual
load of 1,1-dichloroethane is released from the facility at single time. For all ADD calculations, the AT
and the ED are both equal to the number of years in the relevant age group up to the 95th percentile of
the expected duration at a single residence, 33 years (U.S. EPA. 2011a). For example, estimates for a
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13185
13186
13187
13188
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13190
13191
13192
PUBLIC RELEASE DRAFT
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child between 6 and 10 years old would be based on an AT and ED of 5 years. For all LADD and LADC
calculations, the AT is based on a lifetime of 78 years, and the ED is the number of years of exposure in
the relevant age group, up to 33 years.
Drinking water exposure levels were estimated for the following age groups: Adult (21+ years), Youth
(16 to 20 years), Youth (10 to 15 years), Child (6 to 10 years), Toddler (1 to 5 years), and infant (birth to
<1 year). Drinking water intake rates are provided in the 2019 update of Chapter 3 of the EFH (U.S.
EPA. 2019a). Weighted averages were calculated for acute and chronic drinking water intakes for adults
21 years or older and toddlers aged 1 to 5 years. From Table 3-17 in the EFH, 95th percentile consumer
data were used for acute drinking water intake rates. From Table 3-9 in the EFH, mean per capita data
were used for chronic drinking water intake rates.
H.l Surface Water Sources of Drinking Water
Exposure levels resulting from the contamination of 1,1-dichloroethane in drinking water sourced from
surface waters was estimated from aqueous concentrations generated at individual PWS intake locations
as described in Section F.2.3. It is important to note that aqueous concentrations of 1,1-dichloroethane
were not estimated in still water bodies, such as lakes, ponds, or reservoirs, even if PWS draws from
these surface water bodies. Rather, in these cases, modeled EROM stream flow values or the facility
effluent plant flow (e.g., when upstream flow > downstream flow) served as the basis for estimate
aqueous concentrations at the PWS intake location. Given the difficulty of determining lake volume for
many sites and the uncertainty around applying generic dilution factors was avoided.
The aqueous concentrations derived from a modeled 30Q5 stream flow, or from the facility effluent
flow, were used to estimate an ADR or acute exposure level. The aqueous concentrations derived from
the modeled harmonic mean stream flow, or from the facility effluent flow, were used to estimate an
ADD, LADD, and LADC or chronic exposure levels. Prior to estimating exposure levels, information on
the treatment processes for each PWS was obtained from SDWIS. For PWSs that treat raw source water
using packed tower aeration, aqueous concentration estimates at those drinking water intakes were
adjusted to account for 80 percent drinking water treatment removal. For all other sites and their
corresponding treatment processes, drinking water treatment removal was set to 0 percent to represent a
conservative estimate of possible drinking water exposures.
It is important to note that water treatment systems may vary widely across the country based on
available and utilized water treatment processes that depend on whether source water is groundwater or
surface water. These processes typically include disinfection, coagulation/flocculation, sedimentation,
and filtration (U.S. EPA. 2006a). In assessing drinking water exposures, the ability to treat and remove
or transform chemicals in possible drinking water supplies should be considered. Because of the wide
range of treatment processes that inconsistently remove 1,1-dichloroethane from ambient surface water
and groundwater prior to possible general population consumption as drinking water, EPA assumes zero
removal except for PWSs that utilize packed tower aeration processes to provide a conservative estimate
of general population drinking water exposures (further details are described in Section D.2.3.1).
H.2 Groundwater Sources of Drinking Water
Exposure levels resulting from the contamination of 1,1-dichloroethane in drinking water sourced from
groundwater was estimated from aqueous concentrations generated from the DRAS model as described
in Section 3.3.4.1.
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13193
13194
13195
13196
13197
13198
13199
13200
13201
13202
13203
13204
13205
13206
13207
13208
13209
13210
13211
13212
13213
13214
PUBLIC RELEASE DRAFT
July 2024
Chronic and lifetime exposures (ADD and LADD) were calculated based on groundwater concentrations
estimated using the DRAS Model. Acute exposures to groundwater were not calculated because the
available models EPA used for estimating groundwater concentrations are designed to predict long-term
trends rather than short peaks in exposure. Drinking water treatment removal (DWT) was set to 0
percent for groundwater under the assumption that home wells are unlikely to remove 1,1-
dichloroethane.
H.3 Removal through Drinking Water Treatment
Removal of 1,1-dichloroethane in drinking water treatment is expected to be primarily due to its
volatility and potential to be adsorbed to activated carbon where activated carbon treatment is in place.
The effectiveness of treatment such as air stripping for the removal of volatile chemicals can be
predicted by physical and chemical properties such as the Henry's Law constant (HLC). Removal of
chemicals in granular activated carbon (GAC) treatment systems are more difficult to predict from
physical and chemical properties, but information on the adsorption capacity of GAC for chemicals
helps inform the effectiveness and feasibility of GAC treatment for the removal of the chemical from
water.
1,1-Dichloroethane can be removed by GAC (U.S. EPA. 2021a). To achieve high removal of 1,1-
dichloroethane a GAC system would have to incorporate design and operating parameters that account
for the 1,1-dichloroethane sorptive capacity of GAC. In conclusion, a GAC treatment system could be
designed and operated to achieve high removal of 1,1-dichloroethane, but without performance data
there is high uncertainty estimating its treatment efficiency.
Page 483 of 664
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13215
13216
13217
13218
13219
13220
13221
13222
13223
13224
13225
13226
13227
13228
13229
13230
13231
13232
13233
13234
13235
13236
13237
13238
13239
13240
13241
13242
13243
13244
13245
13246
13247
13248
13249
13250
13251
13252
13253
13254
13255
13256
13257
13258
13259
PUBLIC RELEASE DRAFT
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Appendix I ECOLOGICAL EXPOSURE ESTIMATES
Estimated aqueous concentrations at the facility release sites were compared to their respective acute
and chronic concentration of concern (CoC). Initial surface water (water column) concentrations were
estimated by dividing the annual load for a given facility by the number of ecological exposure days that
correspond to the acute or chronic scenario for the water column and benthic pore water. Details on how
the CoCs for aquatic ecological species were determined can be found in Section 4. Concentrations that
exceeded their respective acute and chronic water column and benthic pore water CoCs were kept for a
second modeling step using the Point Source Calculator (PSC).
1.1 The Point Source Calculator
1.1.1 Description of the Point Source Calculator
The PSC is a tool designed to estimate acute and chronic concentrations of chemicals directly released to
surface water bodies. It is a proposed potential refinement to E-FAST for estimating exposures from
wastewater discharges to surface waters. In addition to calculating aqueous concentrations (in the water
column) based on the chemical loading release rate and receiving water body streamflow as E-FAST
does, the PSC accounts for several key physicochemical processes that can affect levels of a released
chemical during transport. More specifically, the PSC allows for chemical removal through sorption to
sorption to sediment, volatilization, and transformation processes (i.e., aerobic and anaerobic
metabolism, hydrolysis, and photolysis), thus providing a higher tiered model that produces a potentially
less conservative estimates of concentration and exposure compared to E-FAST. In addition, the PSC
provides estimates of the chemical concentration in the benthic pore water and bulk sediment of a
receiving water body. Because of these additional processes, PSC requires a number of chemical-
specific input parameters, including chemical partitioning (sediment, air, water) and degradation rates.
PSC also requires specific release site parameters, such as waterbody dimensions, baseflow, and
meteorological data as well as a group of water column and benthic porewater/sediment biogeochemical
parameters. A description of the PSC input parameters can be found in Section 4 of the Point Source
Calculator: A model for Estimating Chemical Concentration in Water Bodies document (U.S. EPA.
2019c).
The PSC is particularly useful for estimating benthic pore water concentrations for assessing benthic
organism exposures, but was designed for use on a site-specific basis, thus requiring a number of
assumptions about release site parameters before applying to national-scale exposure assessments. Since
the PSC has more input parameters and requires default assumptions for national-scale assessments,
EPA's Office of Pesticides Program (OPP) performed a thorough sensitivity analysis to identify a
standard set of assumptions for PSC runs that can be applied nationally. This sensitivity analysis
informed our use of the PSC model and choice of input parameters, which are detailed below. Of the
additional parameters considered to effect chemical concentration in the water column, benthic
porewater, and benthic bulk sediment, the most are the user's selection of the meteorological file, water
body dimensions, and waterbody baseflow. While the baseflow should be included for each individual
site, without sufficient information on the meteorology or receiving water body dimensions, it is
recommended to use the following standard input parameters: the 90th percentile meteorological file
(i.e., w24027) and water body dimensions of5mxlmx40m (wi dth x depth x length).
1.1.2 Point Source Calculator Input Parameters
TableApx 1-1 to TableApx 1-4 include the standard set of input parameters used with the PSC,
excluding the mass release and constant flow rate parameters, which changed for each site and scenario
(acute or chronic). A new list of facility release sites were created from those releases that resulted in an
Page 484 of 664
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13260
13261
13262
13263
13264
13265
13266
13267
13268
13269
13270
13271
13272
13273
13274
13275
13276
13277
13278
13279
13280
13281
13282
13283
13284
13285
13286
PUBLIC RELEASE DRAFT
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estimated aqueous (water column) concentration of 1,1-dichlorethane exceeding a water column and
benthic pore water acute CoC (7,898 [j,g/L and 7,898 (J,g/L, respectively) or water column and benthic
pore water chronic CoC (93 [j,g/L and 6,800 (J,g/L, respectively). For either scenario, the constant flow
rate remained the same. Here the estimated 7Q10 flow value created in Section F.2 was used. For those
facility release sites with estimated concentrations exceeding the respective acute CoC, the mass release
parameter equaled the annual load, thus reflecting a 1-day maximum release scenario. For those facility
release sites with estimated concentrations exceeding the respective chronic CoC, the mass release
parameters equaled the annual load divided by 21 (water column chronic) or 15 (benthic pore water
chronic), thus reflecting a 21- or 15-day release schedule where the annual load was released in equal
amounts over 21 or 15 consecutive days. The default Water Column and Benthic compartment PSC
input parameters were used as well as the default Mass Transfer Coefficient.
The respective water column and benthic acute and chronic CoCs were used for each of the water
column and benthic pore water toxicity options. For example, for the chronic water column scenario, a
user defined "21-Day Avg" scenario was included. For those sites that exceeded the benthic pore water
chronic CoC with initial (water column) concentrations, they were then modeled with PSC to estimate
their benthic chronic sediment concentration and compared to the respective CoC (2,900 (J,g/L). It is
important to note that initial estimates of aqueous concentration in the water column were used to create
a new list of facilities to model in PSC for benthic water pore and sediment concentrations. Thus, it is
assumed that if an initial water column concentration did not exceed the benthic pore water CoC than it
would not exceed the benthic pore water CoC post-PSC modeling. This is expected to be the case for
1,1-dichloroethane because benthic pore water concentrations are not expected to exceed the water
column concentrations from which they were derived using the PSC Model.
Table Apx 1-1.1,1-Dichloroethane Chemical-Specific PSC Input Parameters
Physiochemical PSC Input Parameters
Sorption Coefficient Koc (ml/g)
30.20
Water Column Half-life (days)
365 at 25 °C
Photolysis Half-life (days)
365 at 0 °Lat.
Hydrolysis Half-life (days)
365 at 25 °C
Benthic Half-life (Days)
365 at 25 °C
Volatilization (yes/no)
Yes - Use Henry's constant
Molecular Weight
98.95
Henry's Constant (atm m3/mol)
0.00562
Heat of Henry (J/mol)
0
Reference Temp (deg C)
24
Page 485 of 664
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13287
13288
13289
13290
13291
13292
13293
13294
13295
13296
13297
13298
13299
13300
13301
13302
13303
13304
13305
13306
13307
13308
13309
13310
13311
13312
13313
13314
13315
PUBLIC RELEASE DRAFT
July 2024
TableApx 1-2.1,1-Dichloroethane psc Mass Release Schedule for an Acute
Exposure Scenario
Mass Release Schedule
Offset (# of lead days before release begins)
0
Days on (# of consecutive release days)
1
Days off (# of consecutive days without release)
364
Mass release (kg/day)
Site annual load
Table Apx 1-3.1,1-Dichloroethane PSC Mass Release Schedule for a Chronic
Exposure Scenario
Mass Release Schedule
Offset (# of lead days before release begins)
0
Days on (# of consecutive release days)
21, 15, or 35
Days off (# of consecutive days without release)
344, 350, or 330
Mass release (kg/day)
Site annual load ^ # of days off
Table Apx 1-4. Meteorologic and Hydrologic PSC Input Parameters
Meteorologic and Hydrologic Input Parameters
Meteorologic Data File
w24027
Water Body Dimensions (Width x Depth x Length)
5 m x 1 m x 40 m
Constant Flow Rate (m3/day)
Site 7Q10 flow
1.1.3 Water Column, Pore Water, and Benthic Sediment Results
The PSC estimates daily concentrations of the chemical in the water column, benthic pore water, and
bulk benthic sediment for a given year, and repeats the simulation for 30 consecutive years. The main
Results tab of the PSC software includes a time series graph of these daily simulations repeated for 30
years. The Results tab also provides concentration estimates on a daily sliding average (i.e., "1-Day
Avg", "7-Day Avg", "28-Day Avg"). These averages reflect the maximum of the entire times series for
the period of days indicated, meaning a "1-Day Avg" is the maximum estimated daily concentration for
the entire time series and a "21-Day Avg" is the maximum average of 21 consecutive daily estimated
concentrations. However, these average metrics do not necessarily correspond to the first group of that
might be indicates by the metric. For example, the "35-Day Average" may not include the first 35 days
of each year's simulation. Concentration results for the water column ((J,g/L), benthic pore water (jag/L),
and total benthic sediment ([j,g/kg) were retrieved from either the "1-Day Avg", "21-Day Avg", "15-Day
Avg", or "35-Day Avg" to coincide with the acute and chronic release toxicity scenarios.
The PSC also estimates the number of days that the chemical concentration exceeds a user-defined
concentration of concern for each of the water column, pore water, and benthic bulk sediment
compartments. Since a sediment toxicity CoC was not applied, this data was not included. The days of
exceedance was estimated by multiplying the "1-Day Avg" "Days > CoC" fraction by 10,957 (the total
number of days in the time series) and then divided by 30 (the total number of years in the simulation).
This metric aligns with the daily concentration output file. Note, through this approach the user's mass
release schedule bounds the days of exceedance metric in the water column primarily because of
washout (i.e., replacement of "clean water" from downstream water transport) that occurs immediately
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July 2024
13316 following the last day of chemical mass release in the model. The days of exceedance metric should be
13317 interpreting with caution for this reason.
13318 1.2 Concentrations in Biota and Associated Dietary Exposure Estimates
13319
13320 TableApx 1-5.1,1-Dichloroethane pish Concentrations Calculated from PSC-Modeled Industrial
13321 and Commercial 1,1-Dichloroethane Releases
COU (Life
Cycle/Category/Subcategory)
OES
Facility
Receiving
Waterbody
SWC
(Hg/L)
Fish
Concentration
(ng/g)
Manufacture/
Domestic manufacturing/
Domestic manufacturing
Manufacturing
LA0000761
Bayou D'Indc
& Bayou
Verdine
85
590
Processing/As a reactant/
Intermediate in all other basic
organic chemical manufacture
Processing/As a reactant/
Intermediate in all other
chemical product and
preparation manufacturing
Processing/Recycling/Recycling
Processing as a reactive
intermediate
TXO119792
Unnamed ditch,
San Jacinto Bay
13
90
Processing/Processing -
repackaging/Processing -
repackaging
Processing -
repackaging
IL0064564
Rock River
7.0E-01
4.9
Commercial use/Other
use/Laboratory chemicals
Commercial use as a
laboratory chemical
IL0034592
Sawmill Creek
6.4E-01
4.5
Disposal/Disposal/Disposal
General waste handling,
treatment, and disposal
NE0043371
Stevens Creek
12
87
Disposal/Disposal/Disposal
Waste handling,
treatment, and disposal
(POTW)
KY0022039
Valley Creek
8.2
57
Disposal/Disposal/Disposal
Waste handling,
treatment, and disposal
(remediation)
CA0064599
South Fork of
Arroyo Conejo
Creek
31
210
Distribution in
commerce/Distribution in
commerce/Distribution in
commerce
Distribution in
commerce
N/Afe
" Max daily average represents the maximum surface water concentration (SWC) over the COU/OES-specific operating
days per year (Table 3-3).
h Distribution in commerce does not result in surface water releases (Table 3-6).
13322
13323
Page 487 of 664
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13324 TableApx 1-6.1,1-Dichloroethane Crayfish Concentrations Calculated from PSC-Modeled
13325 Industrial and Commercial 1,1-Dichloroethane Releases
COU (Life
Cycle/Category/Subcategory)
Scenario Name
Facility
Receiving
Waterbody
PWC
(ng/L r
Crayfish
Concentration
(ng/g)
Manufacture/domestic
manufacturing/domestic
manufacturing
Manufacturing
LA0000761
Bayou DTnde &
Bayou Verdine
78
550
Processing/as a reactant/
intermediate in all other basic
organic chemical manufacture
Processing as a
Reactive
Intermediate
TXO119792
Unnamed ditch,
San Jacinto Bay
12
87
Processing/as a reactant/
intermediate in all other
chemical product and
preparation manufacturing
Processing/recycling/recycling
Processing/processing -
repackaging/processing -
repackaging
Processing -
Repackaging
IL0064564
Rock River
6.1E-01
4.3
Commercial use/other
use/laboratory chemicals
Commercial Use as a
Laboratory Chemical
IL0034592
Sawmill Creek
5.5E-01
3.8
Disposal/disposal/disposal
General Waste
Handling, Treatment
and Disposal
NE0043371
Stevens Creek
12
83
Disposal/disposal/disposal
Waste Handling,
Treatment and
Disposal (POTW)
KY0022039
Valley Creek
7.9
55
Disposal/disposal/disposal
Waste Handling,
Treatment, and
Disposal
(Remediation)
CA0064599
South Fork of
Arroyo Conejo
Creek
29
210
Distribution in commerce/
distribution in commerce/
distribution in commerce
Distribution in
Commerce
N/Afe
" Max daily average represents the maximum benthic pore water concentration (PWC) over the COU/OES-specific
operating days per year (Table 3-3).
h Distribution in Commerce does not result in surface water releases (Table 3-6).
13326
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TableApx 1-7. Dietary Exposure Estimates Using EPAs Wildlife Risk Model for Eco-SSLs for
Screening Level Trophic Transfer of 1,1-Dichloroethane to the American Mink from
COU (Life Cycle
Stage/Category/Subcategory)
OES
Fish Concentration
(mg/kg)"
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day)h
Manufacture/domestic
manufacturing/domestic manufacturing
Manufacturing
5.9E-01
1.4E-01
Processing/as a reactant/intermediate in all
other basic organic chemical manufacture
Processing as a reactive
intermediate
9.0E-02
2.1E-02
Processing/as a reactant/intermediate in all
other chemical product and preparation
manufacturing
Processing/recycling/recycling
Processing/processing -
repackaging/processing - repackaging
Processing - repackaging
4.9E-03
1.2E-03
Commercial use/other use/laboratory
chemicals
Commercial use as a
laboratory chemical
4.5E-03
1.0E-03
Disposal/disposal/disposal
General waste handling,
treatment, and disposal
8.7E-02
2.0E-02
Disposal/disposal/disposal
Waste handling,
treatment, and disposal
(POTW)
5.7E-02
1.3E-02
Disposal/disposal/disposal
Waste handling,
treatment, and disposal
(remediation)
2.1E-01
5.1E-02
Distribution in commerce/distribution in
commerce/distribution in commerce
Distribution in commerce
N/Ac
Published data
Lake Pontchartrain ovsters (Ferrario et al.. 1985)
3.3E-02
7.5E-03
11 Whole fish concentrations were calculated using the highest modeled max daily average surface water concentrations
for 1,1-dichloroethane (via PSC modeling based on total number of operating days) and a BCF of 7.
h Dietary exposure to 1,1-dichloroethane includes consumption of biota (fish), incidental ingestion of sediment, and
ingestion of water.
c Distribution in Commerce does not result in surface water releases (Table 3-6).
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TableApx 1-8. Dietary Exposure Estimates Using EPAs Wildlife Risk Model for Eco-SSLs for
Screening Level Trophic Transfer of 1,1-Dichloroethane to the American Mink from
Consumption of Crayfish
COU (Life Cycle
Stage/Category/Subcategory)
OES
Crayfish
Concentration
(mg/kg)"
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day)6
Manufacture/domestic
manufacturing/domestic manufacturing
Manufacturing
5.5E-01
1.3E-01
Processing/as a reactant/intermediate in all
other basic organic chemical manufacture
Processing/as a reactant/intermediate in all
other chemical product and preparation
manufacturing
Processing as a reactive
intermediate
8.7E-02
Processing/recycling/recycling
2.0E-02
Processing/processing -
repackaging/processing - repackaging
Processing - repackaging
4.3E-03
1.0E-03
Commercial use/other use/laboratory
chemicals
Commercial use as a
laboratory chemical
3.8E-03
9.1E-04
Disposal/disposal/disposal
General waste handling,
treatment, and disposal
8.3E-02
1.9E-02
Disposal/disposal/disposal
Waste handling, treatment,
and disposal (POTW)
5.5E-02
1.3E-02
Disposal/disposal/disposal
Waste handling, treatment,
and disposal (remediation)
2.1E-01
4.8E-02
Dstribution in commerce/distribution in
commerce/distribution in commerce
Distribution in commerce
N/Ac
11 Whole crayfish concentrations were calculated using the highest modeled max daily average benthic pore water
concentrations for 1,1-dichloroethane (via PSC modeling based on total number of operating days) and a BCF of 7.
h Dietary exposure to 1,1-dichloroethane includes consumption of biota (crayfish), incidental ingestion of sediment,
and ingestion of water.
c Distribution in Commerce does not result in surface water releases (Table 3-6).
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TableApx 1-9. 1,1-Dichloroethane Trifolium sp. and Earthworm Concentrations Calculated from
AERMOD Modeled Industrial and Commercial Releases Reported t
o TRI
COU (Life Cycle
Stage/Category/Subcategory)
OES
Soil
(mg/kg)"
Soil Pore
Water
Concentration
(mg/L)
Plant
Concentration
(mg/kg)
Earthworm
Concentration
(mg/kg)
Manufacture/domestic
manufacturing/ domestic
manufacturing
Manufacturing
2.4E-01
1.5E-01
1.5E-01
3.8E-01
Processing/as a reactant/
intermediate in all other basic
organic chemical manufacture
Processing as a
reactive
Intermediate
5.2E-03
3.2E-03
3.2E-03
8.4E-03
Processing/as a reactant/
intermediate in all other
chemical product and
preparation manufacturing
Processing/recycling/recycling
Disposal/disposal/disposal
General waste
handling,
treatment, and
disposal
1.2E-04
7.6E-05
7.6E-05
2.0E-04
11 Soil catchment and soil catchment pore water concentrations estimated from 95th percentile maximum daily air
deposition rates 10 m from facility for fugitive air 1,1-dichloroethane releases reported to TRI.
TableApx 1-10. 1,1-Dichloroe
from Land Application of 1,1-
thane Trifolium sp. and Earthworm Concentrations Calculated
Jichloroethane in Biosolids
COU (Life Cycle
Stage/Category/
Subcategory)
OES
Pathway
Soil
(mg/kg)
Soil Pore Water
Concentration
(mg/Lr
Plant
Concentration
(mg/kg)
Earthworm
Concentration
(mg/kg)
Disposal/disposal/
disposal
Waste
handling,
treatment,
and disposal
(POTW)
Tilled
Agricultural
2.9E-02
1.9E-02
1.9E-02
4.8E-02
Pastureland
3.7E-02
5.9E-02
3.7E-02
9.5E-02
11 Soil and soil pore water concentrations estimated from annual application of
)iosolids.
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13344 TableApx 1-11. Dietary Exposure Estimates Using EPAs Wildlife Risk Model for Eco-SSLs for
13345 Screening Level Trophic Transfer of 1,1-Dichloroethane to the Short-Tailed Shrew that Could
13346 Result from Air Deposition to Soil for 1,1-Dichloroethane Releases Reported to TRI
COU (Life Cycle
Stage/Category/Subcategory)
OES
Earthworm
Concentration
(mg/kgr
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day) b
Manufacture/Domestic manufacturing/
Domestic manufacturing
Manufacturing
3.8E-01
2.5E-01
Processing/As a reactant/Intermediate in all
other basic organic chemical manufacture
Processing as a reactive
intermediate
8.5E-03
5.6E-03
Processing/As a reactant/intermediate in all
other chemical product and preparation
manufacturing
Processing/Recycling/Recycling
Disposal/Disposal/Disposal
General waste handling,
treatment, and disposal
2.0E-04
1.3E-04
11 Estimated 1,1-dichloroethane concentration in representative soil inverte
aggregated highest calculated soil and soil pore water concentration via aii
fugitive air releases reported to TRI to soil.
h Dietary exposure to 1,1-dichloroethane includes consumption of biota (e
ingestion of water.
3rate, earthworm, assumed equal to
deposition of 1,1-dichloroethane in
arthworm), incidental ingestion of soil, and
13347
13348
13349 Table Apx 1-12. Dietary Exposure Estimates Using EPAs Wildlife Risk Model for Eco-SSLs for
13350 Screening Level Trophic Transfer of 1,1-Dichloroethane to the Meadow Vole that Could Result
from Air Deposition to Soil for 1,1-Dic
lloroethane Releases Reported to TRI
COU (Life Cycle
Stage/Category/Subcategory)
OES
Plant
Concentration
(mg/kgr
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day)6
Manufacture/domestic manufacturing/
domestic manufacturing
Manufacturing
1.5E-01
8.2E-02
Processing/as a reactant/intermediate in all
other basic organic chemical manufacture
Processing as a reactive
intermediate
3.2E-03
1.8E-03
Processing/as a reactant/intermediate in all
other chemical product and preparation
manufacturing
Processing/recycling/recycling
Disposal/disposal/disposal
General waste handling,
treatment, and disposal
7.6E-05
4.3E-05
11 Estimated 1,1-dichloroethane concentration in representative terrestrial plant Trifolium sp., assumed equal to the
highest calculated soil pore water concentration via air deposition of 1,1-dichloroethane in fugitive air releases
reported to TRI to soil.
h Dietary exposure to 1,1-dichloroethane includes consumption of biota (Trifolium sp.), incidental ingestion of soil,
and ingestion of water.
13352
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TableApx 1-13. Dietary Exposure Estimates Using EPAs Wildlife Risk Model for Eco-SSLs for
Screening Level Trophic Transfer of 1,1-Dichloroethane to the Short-Tailed Shrew that Could
Result from Land Application of Biosolids
COU (Life Cycle
Stage/Category/Subcategory)
OES
Pathway
Earthworm
Concentration
(mg/kg)"
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day)6
Disposal/disposal/disposal
Waste handling,
treatment, and
disposal (POTW)
Tilled
agricultural
4.8E-02
3.1E-02
Pastureland
9.5E-02
6.3E-02
11 Estimated 1,1-dichloroethane concentration in representative soil invertebrate, earthworm, assumed equal to
aggregated highest calculated soil and soil pore water concentration via land application of biosolids to soil.
h Dietary exposure to 1,1-dichloroethane includes consumption of biota (earthworm), incidental ingestion of soil, and
ingestion of water.
Table Apx 1-14. Dietary Exposure Estimates Using EPAs Wildlife Risk Model for Eco-SSLs for
Screening Level Trophic Transfer of 1,1-Dichloroethane to the Meadow Vole that Could Result
from Land Application of Biosolids
COU (Life Cycle
Stage/Category/Subcategory)
OES
Pathway
Plant
Concentration
(mg/kg)
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day)h
Disposal/Disposal/Disposal
Waste handling,
treatment, and
disposal (POTW)
Tilled
agricultural
1.9E-02
1.0E-02
Pastureland
3.7E-02
2.1E-02
11 Estimated 1,1-dichloroethane concentration in representative terrestrial p
highest calculated soil pore water concentration via land application of bio
h Dietary exposure to 1,1-dichloroethane includes consumption of biota (T
ingestion of water.
ant Trifolium sp., assumed equal to the
solids to soil.
ifolium sp.), incidental ingestion of soil, and
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Appendix J ANALOG SELECTION FOR READ-ACROSS
J.l Analog Selection for Environmental Hazard
Few data were identified for 1,1-dichloroethane for aquatic invertebrates, fish, and algae and no chronic
benthic hazard data. Analog selection was performed to identify an appropriate analog to read-across to
1.1-dichloroethane. 1,2-Dichloropropane was selected as an analog for read-across of aquatic
environmental hazard data to supplement the 1,1-dichloroethane aquatic environmental hazard based on
structural similarity, physical and chemical similarity, toxicological similarity and availability of 1,2-
dichloropropane aquatic hazard data from data sources that received ratings of either high or medium.
No chronic benthic hazard data were reasonably available for 1,1-dichloroethane or its primary analog,
1.2-dichloropropane, therefore, 1,1,2-trichloroethane was selected as an analog for read-across of
chronic benthic environmental hazard to 1,1-dichloroethane based on structural similarity, physical and
chemical similarity, toxicological similarity and availability of 1,1,2-trichloroethane chronic benthic
hazard data from data sources receiving a high or medium rating. The similarities between 1,1-
dichloroethane and analogs 1,2-dichloropropane and 1,1,2-trichloroethane are described in detail below.
J. 1.1 Structural Similarity
Structural similarity between 1,1-dichloroethane and candidate analogs was assessed using two TSCA
NAMs (the Analog Identification Methodology (AIM) program and the Organisation of Economic
Cooperative Development Quantitative Structure Activity Relationship [OECD QSAR] Toolbox) and
two EPA Office of Research products (Generalized Read-Across [GenRA]) and the Search Module
within the Cheminformatics Modules) as shown in Table Apx J-l. These four programs provide
complementary methods of assessing structural similarity. There are several different methods for
determining structural similarity. A fragment-based approach (e.g., as implemented by AIM) searches
for compounds with similar structural moieties or functional groups. A structural identifier approach
(e.g., the Tanimoto coefficient) calculates a similarity coefficient based on molecular fingerprinting
(Belford. 2023). Molecular fingerprinting approaches look at similarity in atomic pathway radius
between the analog and target chemical substance (e.g., Morgan fingerprint in GenRA which calculates
a Jaccard similarity index). Some fingerprints may be better suited for certain characteristics and
chemical classes. For example, substructure fingerprints like PubChem fingerprints perform best for
small molecules such as drugs, while atom-pair fingerprints, which assigns values for each atom within
a molecule and thus computes atom pairs based on these values, are preferable for large molecules.
Some tools implement multiple methods for determining similarity. Regarding programs which generate
indices, it has been noted that because the similarity value is dependent on the method applied, that these
values should form a line of evidence rather than be utilized definitively (Pestana et al.. 2021; Mellor et
al.. 2019V
AIM analysis was performed on CBI-side and analogs were described as 1st or 2nd pass. Tanimoto-
based PubChem fingerprints were obtained in the OECD QSAR Toolbox (v4.4.1, 2020) using the
Structure Similarity option. Chemical Morgan Fingerprint scores were obtained in GenRA (v3.1) (limit
of 100 analogs, no ToxRef filter). Tanimoto scores were obtained in the Cheminformatics Search
Module using Similar analysis. AIM 1st and 2nd pass analogs were compiled with the top 100 analogs
with indices greater than 0.5 generated from the OECD QSAR Toolbox and the Cheminformatics
Search Module and indices greater than 0.1 generated from GenRA. Analogs that appeared in three out
of four programs were identified as potential analog candidates. Using these parameters, 17 analogs
were identified as potentially suitable analog candidates for 1,1-dichloroethane based on structural
similarity. Only the results for structural comparison of 1,2-dichloropropane, 1,1,2-trichloroethane, and
1,2-dichloroethane to 1,1-dichloroethane are shown below due to having completed data evaluation and
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extraction. 1,2-Dichloropropane and 1,1,2-trichloroethane were ultimately selected for read-across of
aquatic and benthic hazard to 1,1-dichloroethane based on the additional lines of evidence (physical,
chemical, and environmental fate and transport similarity and toxicological similarity).
1,2-Dichloropropane was indicated as structurally similar to 1,1-dichloroethane in AIM (2nd pass),
OECD QSAR Toolbox (PubChem features = 0.75), and GenRA (Morgan Fingerprint = 0.45) and had a
lower Tanimoto score in the Cheminformatics Search Module (Tanimoto coefficient = 0.42). 1,1,2-
Trichloroethane was indicated as structurally similar to 1,1-dichloroethane in AIM (2nd pass), OECD
QSAR Toolbox (PubChem features = 0.79), and the Cheminformatics Search Module (Tanimoto
coefficient = 0.78). 1,2-Dichloroethane was indicated as structurally similar to 1,1-dichloroethane in
AIM (2nd pass), OECD QSAR Toolbox (PubChem features = 0.79), and the Cheminformatics Search
Module (Tanimoto coefficient = 0.63). The structural similarity of 1,1-dichloroethane to its analogs
indicated in these tools supported the selection of 1,2-dichloropropane and 1,1,2-trichloroethane in the
read-across to 1,1-dichloroethane aquatic and benthic environmental hazard.
TableApx J-l. Structural Similarity between 1,1-Dichloroethane an(| Analog Candidates 1,2-
Dichloropropane, 1,1,2-Tric
lloroethane, and 1,2-Dichloroethane
Chlorinated Solvent
AIM
OECD QSAR
Toolbox
GenRA
Cheminformatics
1,1-Dichloroethane (target)
Exact Match
1.00
1.00
1.00
1,2-Dichloropropane
2nd pass
0.75
0.45
0.42
1,1,2-Trichloroethane
2nd pass
0.79
—
0.78
1,2-Dichloroethane
2nd pass
0.79
-
0.63
J.1.2 Physical, Chemical, and Environmental Fate and Transport Similarity
1,1-Dichloroethane analog candidates from the structural similarity analysis were preliminarily screened
based on similarity in log octanol-water partition coefficient (log Kow) and vapor pressure obtained
using EPI Suite™. Measured values were used when available for screening. For this screening step,
1.1-dichloroethane, 1,2-dichloropropane, 1,1,2-trichloroethane, and 1,2-dichloroethane values were
obtained from Table 2-1, the Final Scope of the Risk Evaluation for 1,2-Dichloropropane, the Final
Scope of the Risk Evaluation for 1,1,2-Trichloroethane, and the Final Scope of the Risk Evaluation for
1.2-Dichloroethane (U.S. EPA. 2020c. e, f). Analog candidates with log Kow and vapor pressure within
one log unit relative to 1,1-dichloroethane were considered potentially suitable analog candidates for
1,1-dichloroethane. This preliminary screening analysis narrowed the analog candidate list from 17
candidate analogs to 11 candidate analogs. Three of the 11 candidate analogs represented 1,2-
dichloropropane, 1,1,2-trichloroethane, and 1,2-dichloroethane. Because these three solvents had
completed data evaluation and extraction, a more expansive analysis of physical, chemical,
environmental fate and transport similarities between 1,1-dichloroethane and candidate analogs 1,2-
dichloropropane, 1,1,2-trichloroethane, and 1,2-dichloroethane was conducted. 1,2-Dichloropropane and
1,1,2-trichloroethane were ultimately selected for read-across of aquatic and benthic hazard to 1,1-
dichloroethane based on the additional line of evidence (toxicological similarity).
Physical, chemical, and environmental fate and transport similarities between 1,1-dichloroethane and its
analog candidates 1,2-dichloropropane, 1,1,2-trichloroethane, and 1,2-dichloroethane were assessed
based on properties relevant to the aquatic, benthic, and soil compartments (Table Apx J-2). These
properties were selected based on their general importance in determining similar exposure potential in
the aquatic, benthic, and soil compartments. Physical, chemical, and environmental fate and transport
values for 1,1-dichloroethane, 1,2-dichloropropane, 1,1,2-trichloroethane, and 1,2-dichloroethane are
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specified in Appendix D, the Final Scope of the Risk Evaluation for 1,2-Dichloropropane (U.S. EPA.
2020f) and the Final Scope of the Risk Evaluation for 1,1,2-Trichloroethane (U.S. EPA. 2020c).
respectively. Similar values are observed for 1,1-dichloroethane, 1,2-dichloropropane, 1,1,2-
trichloroethane, and 1,2-dichloroethane water solubilities (2,800-8,600 mg/L), log Kow (1.48-1.99), and
log Koc (1.28-2.32) indicating all four solvents as highly water soluble with low affinity for sediment
and soil (TableApx J-2). 1,1-Dichloroethane, 1,2-dichloropropane, 1,1,2-trichloroethane, and 1,2-
dichloroethane had relatively low bioconcentration factors (BCF, 0.5-7) and bioaccumulation factors
(3.8-7.1), indicating low bioaccumulation potential in aquatic and terrestrial environments. Although
hydrolysis half-lives are relatively long for all four solvents—particularly for 1,1-dichloroethane, 1,2-
dichloropropane, and 1,2-dichloroethane—other properties of 1,1-dichloroethane, 1,2-dichloropropane,
1,1,2-trichloroethane, and 1,2-dichloroethane indicate that the chemicals will likely volatilize well
before hydrolyzing in aqueous environments.
All four chlorinated solvents are highly volatile (Henry's Law constants 8.24><104 to 5,62/ 10 3 atm-
m3/mol and vapor pressures 23-227 mm Hg), indicating volatilization from both water and soil will
occur. The vapor pressures indicate some difference in volatility between the four chlorinated solvents;
that is, 40, 23, and 78 mm Hg for 1,2-dichloropropane, 1,1,2-trichloroethane, and 1,2-dichloroethane,
respectively, compared to 227 mm Hg for 1,1-dichloroethane. However, potential impacts of volatility
differences on read-across to 1,1-dichloroethane for environmental hazard can be addressed by factoring
in experimental design considerations in the 1,2-dichloropropane and 1,1,2-trichloroethane hazard
dataset such as chemical measurement of the substance in the test medium, regular renewal with
chemical solution, capping of test vessels, and/or use of flow-through/dilutor systems. All four solvents
exist as colorless liquids at room temperature and have similar low molecular weights (Table Apx J-2).
The similarity of the physical, chemical, fate, and environmental transport behavior of these three
chlorinated solvents in aquatic, benthic, and terrestrial environments support the ability to read-across to
1,1-dichloroethane from 1,2-dichloropropane and 1,1,2-trichloroethane environmental hazard data.
Table Apx J-2. Comparison of 1,1-Dichloroethane and Analog Candidates 1,2-Dichloropropane,
1,1,2-Trichloroethane, and 1,2-Dichloroethane for Several Physical and Chemical and
Environmental Fate Properties Relevant
to Water, Sediment, and Soil
Property
1,1-Dichloroethane
(Target)
1,2-
Dichloropropane
1,1,2-
Trichloroethane
1,2-Dichloroethane
Water solubility
5,040 mg/L
2,800 mg/L
4,590 mg/L
8,600 mg/L
Log Kow
1.79
1.99
1.89
1.48
Log Koc
1.48
1.67
1.9-2.05,2.2-
2.32
1.28-1.62
BCF
7
0.5-6.9
0.7-6.7
2
BAF
6.8
7.1
6.9
3.8
Hydrolysis t'A
61.3 years
15.8 years
85 days
65 years, 72 years
Henry's Law
constant (atm-
m3/mol)
5.62E-03
2.82E-03
8.24E-04
1.18E-03
Vapor pressure
(mmHg)
227
40
23
79
Molecular weight
98.95 g/mol
112.99 g/mol
133.41 g/mol
98.96 g/mol
Physical state of
the chemical
Colorless liquid
Colorless liquid
Colorless liquid
Colorless liquid
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J.1.3 Toxicological Similarity
Two lines of ecotoxicological evidence, predicted and empirical hazard, factored into the comparison of
toxicological similarity between 1,1-dichloroethane and its analogs 1,2-dichloropropane and 1,1,2-
trichloroethane. 1,2-Dichloroethane was considered as an analog candidate but was ultimately not
selected for read-across of environmental hazard to 1,1-dichloroethane due to predictions of aquatic
toxicity that were less conservative than 1,1-dichloroethane or its two analogs 1,2-dichloropropane and
1,1,2-trichloroethane.
Similarity in Predicted Hazard
ECOSAR-predicted acute and chronic toxicity values for freshwater and saltwater aquatic receptors and
earthworms were obtained (neutral organics category, v2.2) using inputs CASRNs of target and analogs
and measured log Kow values (TableApx J-2) (U.S. EPA. 2022d). Predicted toxicity values for aquatic
taxa (fish, aquatic invertebrates, algae) were very similar between 1,1-dichloropropane, 1,2-
dichloropropane and 1,1,2-trichloroethane (Table Apx J-2). The average ratio of analog/target predicted
hazard was almost 1:1 at 0.77 ± 0.02 (standard error) for 1,2-dichloropropane and 1.10 ± 0.02 for 1,1,2-
trichloroethane, supporting the ability to read-across 1,2-dichloropropane and/or 1,1,2-trichloroethane
aquatic hazard to 1,1-dichloroethane. For analog candidate 1,2-dichloroethane, the average ratio of
analog/target predicted hazard was 1.88 ± 0.11, suggesting this analog candidate was less toxic to
aquatic taxa than 1,1-dichloroethane. Therefore, 1,2-dichloroethane was not selected for read-across of
aquatic hazard to 1,1-dichloroethane. Predicted chronic hazard for aquatic invertebrates (daphnid and
mysid) exposed to 1,1,2-trichloroethane was in almost perfect agreement to those of 1,1-dichloroethane,
supporting the ability to read-across to 1,1-dichloroethane from 1,1,2-trichloroethane chronic benthic
invertebrate hazard. ECOSAR hazard predictions for earthworm were also compared between 1,1-
dichloroethane and its analogs (Table Apx J-3). Predicted 14-day LC50 values for earthworm showed
good agreement between the three chlorinated solvents (180.9-238.1 mg/L), supporting the ability to
read-across 1,2-dichloropropane and/or 1,1,2-trichloroethane earthworm hazard data to 1,1-
dichloroethane. The neutral organics class in ECOSAR v2.2 has a robust dataset for predicting
environmental hazard which increases the confidence in the predicted toxicological similarity observed
between 1,1-dichloroethane and its analogs.
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13509 TableApx J-3. ECOSAR Acute (LC50, EC50) and Chronic (ChV) Toxicity Predictions for 1,1-Dichloroethane an(| Analog
13510 Candidates 1,2-Dichloropropane, 1,1,2-Trichloroethane, and 1,2-Dichloroethane for Aquatic and Terrestrial Taxa
Taxa
Endpoint
1,1-Dichloroethane
(Target)
1,2-Dichloropropane
(Analog)
1,1,2-Trichloroethane
(Analog)
1,2-Dichloroethane
(Analog)
Predicted Toxicity
(mg/L)
Predicted Toxicity
(mg/L)
Ratio to 1,1-
Dichloroethane
Predicted
Toxicity
(mg/L)
Ratio to 1,1-
Dichloroethane
Predicted
Toxicity
(mg/L)
Ratio to 1,1-
Dichloroethane
Fish
LC50
125.5
94.8
0.76
137.6
1.10
238.3
1.90
Daphnid
69.9
53.8
0.77
77.3
1.11
128.9
1.84
Fish (SW)17
157.8
119.3
0.76
173.1
1.11
299.0
1.89
Mysid
135.2
89.3
0.66
138.6
1.03
316.1
2.34
Green algae
EC50
48.1
39.9
0.83
55.2
1.15
78.6
1.63
Fish
ChV
12.0
9.3
0.78
13.3
1.11
22.0
1.83
Daphnid
6.5
5.2
0.80
7.3
1.12
11.0
1.69
Fish (SW)17
15.1
12.9
0.85
17.6
1.17
23.6
1.56
Mysid (SW)17
12.4
7.7
0.62
12.4
1.00
31.9
2.57
Green algae
12.1
10.4
0.86
14.1
1.17
18.5
1.53
Earthworm
LC50
180.9
196.9
1.09
238.1
1.32
194.8
1.08
17 SW = saltwater. All other aquatic taxa are considered freshwater taxa.
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Similarity in Empirical Hazard
The reasonably available empirical environmental hazard dataset also indicated toxicological similarity
between 1,1-dichloroethane and analogs 1,2-dichloropropane and 1,1,2-trichloroethane. To compare
toxicological similarity between these three chlorinated solvents, definitive hazard data were compared
for various taxa exposed to 1,1-dichloroethane or its analogs. These were 48-hour immobilization data
for Daphnia magna (Mitsubishi Chemical Medience Corporation. 2009a; NITE. 1995a; 3M
Environmental Lab. 1984; Richter et al.. 1983; LeBlanc. 1980). 21-day reproductive inhibition data for
Daphnia magna (Mitsubishi Chemical Medience Corporation. 2009d; NITE. 1995b; 3M Environmental
Lab. 1984). 7-day mortality data in guppies (Poecila reticulata) (Konemann. 1981). and 48-hour growth
inhibition data in green algae (Pseudokirchneriella subcapitata) (Tsai and Chen. 2007). Closer
agreement in empirical hazard across aquatic taxa were noted between 1,1-dichloroethane and 1,2-
dichloropropane (ratio to 1,1-dichloroethane empirical hazard = 0.94 ± 0.24) than 1,1-dichloroethane
and 1,1,2-trichloroethane (ratio to 1,1-dichloroethane empirical hazard = 2.10 ± 0.62), which indicates
that 1,1,2-trichloroethane analog data is generally less conservative than 1,1-dichloroethane data,
therefore 1,2-dichloropropane was considered a preferential analog for read-across of aquatic hazard to
1.1-dichloroethane (TableApx J-4).
To confirm consistency of empirical analog data to its ECOSAR predictions, these definitive empirical
hazard data were also compared to their respective ECOSAR-predicted hazard values. Close agreement
of empirical-to-predicted hazard were noted for both 1,2-dichloropropane and 1,1,2-trichloroethane
(0.73 ± 0.20-fold and 1.02 ± 0.32-fold, respectively) as well as for 1,1-dichloroethane (0.82 ± 0.32-fold)
[Table Apx J-5]). This agreement between empirical and predicted hazard increased confidence that the
predicted hazard, also used to compare toxicological similarity between target and analog when the
target lacks empirical hazard, is reflective of the empirical hazard data. The strong agreement in
toxicological similarity between 1,1-dichloroethane and analog predicted hazard values, empirical
hazard values, and concordance between predicted and empirical hazard supports the use of primarily
1.2-dichloropropane aquatic hazard data with targeted application of 1,1,2-trichloroethane analog data to
supplement the 1,1-dichloroethane aquatic and benthic hazard data.
Table Apx J-4. Empirical Acute (EC50, LC50) and Chronic (ChV) Hazard Comparison for
Various Aquatic Species Exposed to 1,1-Dichloroethane or Analogs 1,2-Dichloropropane and
l,l;2-Trichloroethane
Species
Endpoint
1,1-
Dichloroethane
(Target)
1,2-Dichloropropane
(Analog)
1,1,2-Trichloropropane
(Analog)
Empirical
Toxicity
(mg/L)
Empirical
Toxicity
(mg/L)
Ratio to 1,1-
Dichloroethane
Empirical
Toxicity
(mg/L)
Ratio to 1,1-
Dichloroethane
Poecila reticulata
(guppyr
LC50
202
116
0.57
94.4
0.47
Daphnia magna
EC50
34 c
29.5 e
0.87
81.6 gh
2.40
Pseudokirchneriell
a subcapitata b'
EC50
49.92
34.42
0.69
105.42
2.11
Daphnia magna
ChV
0.93'#
1.5/
1.63
3.2h
3.44
a Data are from (1981).
h Data are from (2007).
c Data are from (2009a).
d Data are from (2009d).
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Species
Endpoint
1,1-
Dichloroethane
(Target)
1,2-Dichloropropane
(Analog)
1,1,2-Trichloropropane
(Analog)
Empirical
Toxicity
(mg/L)
Empirical
Toxicity
(mg/L)
Ratio to 1,1-
Dichloroethane
Empirical
Toxicity
(mg/L)
Ratio to 1,1-
Dichloroethane
'' Data are from (1995a).
' Data are from (1995b).
g Data are from (1983; 1980).
h Data are from (3M Environmental Lab. 1984).
' These studies were rated uninformative for not stating the doses and/or number of doses utilized in the dose-response
(Tsai and Chen. 2007; Konemann. 1981) and not stating inclusion of a control group (Konemann. 1981); however.
EPA finds other aspects of both studies otherwise useful for comparing the relative toxicity of 1,1-dichloroethane and
1,2-dichloropropane or 1,1,2-trichloroethane.
TableApx J-5. Comparison of Predicted and Empirical Toxicities for Various Aquatic Taxa
Exposed to 1,1-Dichloroet
lane, 1,2-Dichloropropane, and 1,1,2-Trichloroethane
Taxa
Endpoint
1,1-Dichloroethane
(Target)
1,2-Dichloropropane
(Analog)
1,1,2-Trichloropropane
(Analog)
Empirical'VPredicted"
Empirical'VPredicted"
Empirical'VPredicted"
Fish
LC50
1.61
1.22
0.69
Daphnid
EC50
0.49
0.55
1.06
Green algae
EC50
1.04
0.86
1.22
Daphnid
ChV
0.14
0.29
0.44
11 Predictions are from ECOSAR v2.2, neutral organics category.
b Empirical data are from (2009a. d; 2007; 1995a. b; 1984; 1983; 1981; 1980).
J. 1.4 Analog Data Availability
The 1,2-dichloropropane aquatic hazard data set and 1,1,2-trichloroethane benthic hazard data are
described in Section 4.2.2 and (U.S. EPA. 2024t). Briefly, for 1,2-dichloropropane, high-rated and/or
medium-rated aquatic invertebrate hazard data are available for acute (Dow Chemical 1988) and
chronic (Dow Chemical 1988) exposure to 1,2-dichloropropane, and high-rated and/or medium-rated
aquatic vertebrate hazard data are available for acute (Geiger et al. 1985; Walbridge et al. 1983; Benoit
et al. 1982) and chronic (Benoit et al. 1982) exposure to 1,2-dichloropropane. High-rated and/or
medium-rated aquatic plant hazard data are also available for 1,2-dichloropropane (Dow Chemical.
2010; Schafer et al. 1994; Dow Chemical. 1988). Two high-rated and/or medium-rated benthic
invertebrate hazard studies are available for 1,1,2-trichloroethane (Smithers. 2023; Rosenberg et al.
1975).
J.2 Analog Selection for Human Health Hazard
EPA identified data gaps for 1,1-dichloroethane for non-cancer PODs for acute, subchronic and chronic
inhalation, dermal routes by all exposure durations, and for cancer PODs for oral, inhalation, and dermal
routes. Therefore, an analysis of other chlorinated solvents as potential analogs for read-across data was
performed following the general principles for read-across as outlined in Lizarraga et al. (2019). taking
into consideration structural similarities, physical-chemical properties, metabolism, and toxicological
similarities. Overall, 1,2-dichloroethane was identified as the best available candidate chemical isomer
to fill the identified data gaps for 1,1-dichloroethane, and a consultation with the EPA Office of
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Research and Development (ORD) agreed. Based on the numerous similarities in hazards (see
TableApx J-8. TableApx J-9, TableApx J-10, TableApx J-11, TableApx J-12, TableApx J-13,
and Table Apx J-14), EPA has high confidence that the 1,2-dichloroethane data will accurately reflect
the hazards of 1,1-dichloroethane where there are data gaps.
J.2.1 Structural Similarity
The first step in identification of possible analogs is to examine structural similarity. There are several
different methods for determining structural similarity. A fragment-based approach (e.g., as
implemented by AIM) searches for compounds with similar structural moieties or functional groups. A
structural identifier approach (e.g., the Tanimoto coefficient) calculates a similarity coefficient based on
molecular fingerprinting (Belford. 2023). Molecular fingerprinting approaches look at similarity in
atomic pathway radius between the analog and target chemical substance (e.g., Morgan fingerprint in
GenRA which calculates a Jaccard similarity index). Some fingerprints may be better suited for certain
characteristics and chemical classes. For example, substructure fingerprints like PubChem fingerprints
perform best for small molecules such as drugs, while atom-pair fingerprints, which assigns values for
each atom within a molecule and thus computes atom pairs based on these values, are preferable for
large molecules. Some tools implement multiple methods for determining similarity. Regarding
programs which generate indices, it has been noted that because the similarity value is dependent on the
method applied, that these values should form a line of evidence rather than be utilized definitively
(Pestana et al.. 2021; Mellor et al.. 2019).
Structural similarity between 1,1-dichloroethane and other chlorinated solvents was assessed using two
TSCA NAMs (the AIM program and OECD QSAR Toolbox) and two EPA Office of Research products
(GenRA) and the Search Module within the Cheminformatics Modules (Hazard Comparison Dashboard
(HCD) previously). AIM analysis was performed on the CBI-side and potential analogs were described
as 1st or 2nd pass. Tanimoto-based PubChem fingerprints were obtained in the OECD QSAR Toolbox
(v4.4.1, 2020) using the Structure Similarity option. Chemical Morgan Fingerprint scores were obtained
in GenRA (v3.1, no ToxRef filter) (limit of 100 analogs). Tanimoto scores were obtained in the ORD
Cheminformatics Search Module (Hazard Comparison Dashboard or HCD) using similarity analysis.
AIM 1st and 2nd pass analogs were compiled with the top 100 analogs with indices greater than 0.5
generated from the OECD QSAR Toolbox and the Cheminformatics Search Module and indices greater
than 0.1 generated from GenRA. Analogs that appeared in three out of four programs were identified as
potential analog candidates.
The results of the comparison of the structural similarity of the target chemical 1,1-dichloroethane to
other chlorinated solvents using the QSAR tools AIM, the OECD QSAR Toolbox, GenRA, and HCD
can be seen in Table Apx J-6. The higher the similarity score, the better the structural match, with a
value of 1.00 being an exact match, whereas AIM 1st pass indicates better structural agreement than
AIM 2nd pass. 1,2-Dichloroethane was indicated as structurally similar to 1,1-dichloroethane in AIM
(2nd pass), OECD QSAR Toolbox (PubChem features = 0.79), and the Cheminformatics Search Module
(Tanimoto coefficient = 0.63). 1,2-Dichloropropane was indicated as structurally similar to 1,1-
dichloroethane in AIM (2nd pass), OECD QSAR Toolbox (PubChem features = 0.75), and GenRA
(Morgan Fingerprint = 0.45) and had a lower Tanimoto score in the Cheminformatics Search Module
(Tanimoto coefficient = 0.42). 1,1,2-Trichloroethane was indicated as structurally similar to 1,1-
dichloroethane in AIM (2nd pass), OECD QSAR Toolbox (PubChem features = 0.79), and the
Cheminformatics Search Module (Tanimoto coefficient = 0.78). 1,2-dichloroethane was identified as the
best available candidate chemical to fill the identified data gaps for 1,1-dichloroethane based on
additional lines of evidence and the fact that they are structurally similar as reactive di-chlorinated
ethanes and both are isomers with identical molecular formulas/molecular weight. 1,1-Dichloroethane
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has an identical MW and same number of reactive chlorines as 1,2-dichloroethane. 1,1,2-trichloroethane
has one more reactive vicinal chlorine than 1,1-dichloroethane. 1,2-dichloropropane has one more
carbon than 1,1-dichloroethane. Trans-1,2-dichloroethylene contains a double bond, thus it has cis and
trans isomers complicating the analysis.
TableApx J-6. Structural Similarity between 1,1-Dichloroethane
and Other Chlorinated Solvents
Target
Candidate
Analogs
Chlorinated
Solvent
AIM
OECD
QSAR
Toolbox
GenRA
HCD
1,1-
Dichloroethane
Exact
match
1.00
1.00
1.00
1,2-
Dichloroethane
2nd pass
0.79
-
0.63
1,1,2-
Trichloroethane
2nd pass
0.79
-
0.78
1,2-
Dichloropropane
2nd pass
0.75
0.45
0.42
T ri chl oroethy 1 ene
-
0.73
-
0.33
Dichloromethane
2nd pass
0.46
-
0.57
trans-\ ,2-
di chl oroethy 1 ene
-
0.63
-
0.30
Perchl oroethy 1 ene
-
0.47
-
0.33
Carbon
tetrachloride
2nd pass
0.29
-
0.44
J.2.2 Physical and Chemical Similarity
The comparison of 1,1-dichloroethane and its close structural isomer 1,2-dichloroethane, for key
physical and chemical properties is shown below in Table Apx J-7. Considering the common variability
in physical and chemical results across methods and laboratories over time, 1,1-dichloroethane has
similar values to 1,2-dichloroethane for water solubility, log Kow, molecular weight, physical state,
Henry's Law constant and vapor pressure, all of which can affect their ADME and target tissue levels.
For example, in Table Apx J-7, water solubility and Kow between 1,1-dichloroethane and 1,2-
dichloroethane appear to be different. However, in general, variability in physical and chemical
properties results for the same chemical for water solubility and Kow can differ by orders of magnitude,
therefore, differences in reported physical and chemical values are not uncommon (Gigante et al.. 2021;
Pontolilloand and Eganhouse. 2001). In addition, the physical and chemical properties for 1,1,2-
Trichloroethane and 1,2-dichloropropane are also included in Table Apx J-7. For 1,1,2-trichloroethane,
the vapor pressure is 10x lower, the Henry's Law constant is 7 times lower, and the molecular weight is
35 percent higher than 1,1-dichloroethane, which has ADME implications, and therefore was not
considered as close of a chemical candidate analog for read-across compared to 1,2-dichloroethane.
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TableApx J-7. Comparison of 1,1-Dichloroethane an(| 1,2-Dichloroethane for Several Physical
and Chemical Properties Relevant to Human Health Hazard
Chlorinated Solvent
Water
Solubility
(mg/L)
Log
Kow
Molecular
Weight
Physical
State
Henry's Law
Constant
(atm-m3/mol)
Vapor
Pressure
(mm Hg)
1,1 -Dichloroethane
5,040
1.79
98.95
Liquid
0.00562
227
1,2-Dichloroethane
8,600
1.48
98.96
Liquid
0.00118
79
1,1,2-Trichloroethane
4,590
1.89
133.41
Liquid
0.00082
23
1,2-Dichloropropane
2,800
1.99
112.99
Liquid
0.00282
40
J.2.3 Metabolic Similarities
In Vitro Metabolism Studies — 1,1-Dichloroethane
The metabolic pathways for 1,1-dichloroethane have been elucidated from in vitro studies using rat
hepatic microsomes (McCall et al.. 1983; Sato et al.. 1983; Van Dyke and Wineman. 1971). As outlined
in FigureApx J-l, the primary metabolic pathway involves oxidation of the C-l carbon by cytochrome
P450 (CYP) to give an unstable alpha-haloalcohol followed by dechlorination to produce acetyl chloride
and acetic acid, which is the major metabolite. The alpha-haloalcohol may also undergo a chlorine shift
to yield chloroacetyl chloride and monochloroacetic acid, although this reaction is not favored. CYP
oxidation at the C-2 position results in the formation of 2,2-dichloroethanol, dichloroacetaldehyde, and
dichloroacetic acid as minor metabolites. Metabolism of 1,1-dichloroethane was increased by induction
with phenobarbital and ethanol, but not P-naphthoflavone (McCall et al.. 1983; Sato et al.. 1983).
Similarly, enzymatic dechlorination was inducible by phenobarbital, but not 3-methylcholanthrene ("Van
Dyke and Wineman. 1971).
ci2hcch3
P450 (C-2)
P450
(C-1)
[HOCI2CCH3]
alpha-haloalcohol
CI2HCCH2OH
2,2-dichloroethanol
chlorine
shift
[CICH2CCI]
O
chloroacetyl
chloride
-HCI
CI2HCCH
dichloroacetaldehyde
- CI2HCC-OH
O
dichloroacetic acid
H,Q
-HCI
[CICCHj]
O
acetyl
chloride
O
CICH2COH
monochloroacetic
acid
-HCI
CH3COOH
acetic
acid
Figure Apx J-l. Proposed Metabolic Scheme for 1,1-Dichloroethane (McCall et al.,
1983)
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In Vivo and In Vitro Metabolism Studies - 1,2-Dichloroethane
No human studies on the metabolism of 1,2-dichloroethane were located. FigureApx J-2 outlines the
primary metabolic pathways for 1,2-dichloroethane, elucidated from in vitro studies and in vivo studies
in rats and mice, include cytochrome P450 (CYP) oxidation and glutathione (GSH) conjugation (IPCS,
1995). Metabolism by CYP results in an unstable gem-chlorohydrin that releases hydrochloric acid,
resulting in the formation of 2-chloroacetaldehyde. 2-Chloroacetaldehyde is oxidized to form
chloroacetic acid or reduced to form 2-chloroethanol, and these metabolites are conjugated with GSH
and excreted in the urine. Metabolism via glutathione-S-transferase results in formation of S-(2-
chloroethyl)-glutathione, which rearranges to form a reactive episulfonium ion. The episulfonium ion
can form adducts with protein, DNA or RNA or interact further with GSH to produce water soluble
metabolites that are excreted in the urine.
/\ &
a A/
S-{2 -Chkxoethyl >-glutathiooe
(Hart-Mustard) ^ GSH
Celular
macrtxnotecular
adducts
/\,P NADH. . 01
2 -ChJoroacetaldehyde 2 -Chkxoethanol
GS' V °S
S-<2-Formytmethyl)-9lutathone S-(2-Hydroxyettiyl>-glutathione
Cellular
macromolecular
adducts
o H NHj o
S-Carboxymethyi-L-cystenylglycne
S-Caftx)xymethy1 glutathione
OH
csA/50
S S' -Ett>ene bisglutathione
I
I
S.S'-Ethene bis-L-cystetne
\
I Urine metabolites 1
NHj O
S-CarboxymeViyl-L-cysteine
HN CH3 O
V
0
N-Acetyl-S-carboxymcthyl-L-cysteirw
Thsodiacetic acid
(thiodiglycolic aod)
OH
Figure Apx J-2. Proposed Metabolic Scheme for 1,2-Dichloroethane ( PCS, 1995)
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As depicted in FigureApx J-l and FigureApx J-2, in terms of metabolic similarities between 1,1-
dichloroethane and 1,2-dichloroethane, both are directly reactive and both form chloroaldehydes, which
can form persistent DNA crosslinks (OECD. 2015).
J.2.4 Toxicological Similarity - Non-cancer
There are no adequate non-cancer data available by the acute, short-term/sub chronic and chronic
inhalation routes, and dermal routes by any exposure duration for 1,1-dichloroethane. As a result, the
1,2-dichloroethane database was systematically reviewed and evaluated to identify non-cancer PODs to
be used as read-across from 1,2-dichloroethane to fill in those 1,1-dichloroethane data gaps and calculate
quantitative risk estimates.
TableApx J-8 shows a qualitative comparison of common non-cancer findings between 1,1-
dichloroethane and 1,2-dichloroethane, highlighting an overall similarity. Table Apx J-9 does not,
however, reflect the full database for either chemical. The final non-cancer quantitative PODs selected
for both chemicals were based upon the strength of the evidence from data that ranked Moderate to High
in our SR, was of reliable and sufficient quality, and was the most biologically relevant and sensitive
using the best available science. These are shown in Table 5-49, Table 5-50, Table 5-51.
Table Apx J-8. Qualitative Comparison of Common Non-cancer Findings between
1,1-Dichloroethane and 1,2-Dichloroethane
Effects
1,1-Dichloroethane
1,2-Dichloroethane
Reproductive/
Developmental
Evidence is inadequate to assess
whether 1,1-dichloroethane exposure
may cause reproductive/
developmental toxicity under relevant
exposure circumstances.
Evidence suggests, but is not sufficient to
conclude, that 1,2-dichloroethane may cause
effects on male reproductive structure and/or
function under relevant exposure conditions.
Evidence is inadequate to determine whether
1,2-dichloroethane may cause effects on the
developing organism. There is no evidence that
1,2-dichloroethane causes effects on female
reproductive structure and/or function.
Renal
Evidence is inadequate to assess
whether 1,1-dichloroethane exposure
may cause renal toxicity under relevant
exposure circumstances.
Evidence indicates that 1,2-dichloroethane
likely causes renal effects under relevant
exposure circumstances.
Hepatic
Evidence suggests, but is not sufficient
to conclude, that 1,1-dichloroethane
exposure causes hepatic toxicity under
relevant exposure circumstances.
Evidence suggests, but is not sufficient to
conclude, that 1,2-dichloroethane may cause
hepatic effects under relevant exposure
conditions.
Nutritional/
Metabolic
Evidence suggests, but is not sufficient
to conclude, that 1,1-dichloroethane
exposure causes body weight
decrements under relevant exposure
circumstances.
Evidence suggests that 1,2-dichloroethane may
cause body weight decrements under relevant
exposure circumstances.
Neurological/
Behavioral
Evidence suggests, but is not sufficient
to conclude, that 1,1-dichloroethane
exposure causes neurological effects
under relevant exposure circumstances.
Evidence indicates that 1,2-dichloroethane
likely causes neurological/behavioral effects
under relevant exposure circumstances.
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Effects
1,1-Dichloroethane
1,2-Dichloroethane
Immune/
Hematological
Evidence suggests, but is not sufficient
to conclude, that 1,1-dichloroethane
exposure causes immune system
suppressions (Zabrodskii et al.. 2004).
Evidence suggests, but is not sufficient to
conclude, that 1,2-dichloroethane may cause
immune system suppression under relevant
exposure conditions.
Respiratory Tract
Evidence suggests, but is not sufficient to
conclude, that 1,2-dichloroethane may cause
nasal effects under relevant exposure
conditions.
Mortality
Evidence indicates that 1,1-
dichloroethane exposure is likely to
cause death under relevant exposure
circumstances.
Evidence indicates that 1,2-dichloroethane may
cause death under relevant exposure
circumstances and lethal levels have been
identified in animal studies.
J.2.5 Toxicological Similarity - Cancer
Due to the data gap for a reliable 1,1-dichloroethane cancer study by the oral, inhalation and dermal
routes, the 1,1-dichloroethane cancer database was compared to the 1,2-dichloroethane cancer database.
Systematic review identified three high-quality 1,2-dichloroethane cancer studies available. TableApx
J-9 and Table Apx J-10 show a qualitative comparison of common cancer findings between 1,1-
dichloroethane and 1,2-dichloroethane, highlighting an overall similarity. In general, the oral cancer
studies in mice performed by NTP (1978) on 1,2-dichloroethane resulted in similar tumor types or pre-
cancerous lesions as seen in the bioassays of its close structural analog and isomer, 1,1-dichloroethane
{i.e., hepatocellular carcinomas, endometrial polyps, hemangiosarcomas, and mammary gland tumors,
among others) even for studies that were not used quantitatively. The NTP (1978) oral study in 1.2-
dichloroethane_also showed an excellent dose response for hepatocellular carcinomas as shown below in
Table Apx J-9. Additionally, the 1,2-dichloroethane inhalation cancer study by Nagano et al. (2006)
produced similar tumors as observed in the 1,2-dichloroethane oral cancer study. As a result, the cancer
slope factor for 1,2-dichloroethane was selected from the NTP (1978) study in mice, which had a High
OPPT SR rating for read-across to 1,1-dichloroethane (see Table 5-52).
Table Apx J-9. Qualitative Comparison of Common Cancer Findings between 1,1-Dichloroethane
and 1,2-Dichloroethane
Studies
1,1-Dichloroethane
1,2-Dichloroethane
NTP Oral Rat Studies
(Uninformative by SR)
Mammary gland
adenocarcinomas,
hemaneiosarcoma. (NCI. 1978)
Mammary gland adenocarcinomas,
hemansiosarcoma.(NTP. 1978)
NTP Oral Mouse Studies (High
SR rating)
Endometrial stromal polyps
(precursor). (NCI. 1978)
Endometrial stromal polyps (precursor),
NTP (1978b)
Hepatocarcinomas. (NTP. 1978)
Inhalation Studies
Chronic study, but not a cancer
studv. (Hofmann et al.. 1971b).
Uninformative by SR)
Mammary gland adenomas;
fibroadenomas, adenocarcinomas;
subcutaneous fibromas; bronchioalveolar
adenoma & carcinoma; endometrial
stromal polyps; hepatocellular adenoma,
(Nagano et al.. 2006). High SR rating
Dermal Study
None
Bronchioalveolar adenomas and
adenocarcinomas (mice. 1 dose). (Suauro
et al.. 2017). High SR ratine)
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Studies
1,1-Dichloroethane
1,2-Dichloroethane
Human Studies
Indeterminate
Indeterminate
Table Apx J-10. 1,1-Dichloroethane and 1,2-Dichloroethane Common Chronic Study Findings"
Chronic Study Finding
1,1-Dichloroethane
1,2-Dichloroethane
Endometrial polyps
+
+
Hepatocellular carcinomas
+
+
Hemangiosarcomas
+
+
Mammary gland tumors
+
+
11 In general, similar tumor types or pre-cancerous lesions were observed with 1,1-dichloroethane as seen in the
bioassays of the similar isomer 1,2- dichloroethane (i.e., hepatocellular carcinomas, endometrial polyps,
hemansiosarcomas. mammarv aland tumors; Hish SR studv in F344 rats and BDF1 micciNaeano et al..
2006).
Dose (mg/kg/day)
FigureApx J-3. Hepatocellular Carcinomas Dose Response in Mice for 1,2-Dichloroethane
NTP (1978)
The OncoLogic™ model developed by the EPA evaluates the carcinogenic potential of chemicals
following sets of knowledge rules based on studies of how chemicals cause cancer in animals and
humans. Both 1,1-dichloroethane and 1,2-dichloroethane were compared by the OncoLogic™ software
in TableApx J-l 1. Both 1,1-dichloroethane and 1,2-dichloroethane possessed similar results based on
OncoLogic™ and similar precursor events (see Table Apx J-12).
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Table Apx J-ll. 1,1-Dichloroethane and 1,2-Dichloroethane Oncologic Results
Parameter
1,1-Dichloroethane
1,2-Dichloroethane
Classification for
carcinogenicity
Low-Medium Concern
Medium Concern
Chemistry
Geminal alkyl dihalide
Vicinal alkyl dihalide
Chemical reactivity
Geminal alkyl dihalide < vicinal alkyl dihalide
Table Apx J-12.1,1-Dichloroethane and 1,2-Dichloroethane Precursor Events"
Parameter
1,1-Dichloroethane
1,2-Dichloroethane
Ames assay
+
+
DNA repair test rats
+
+
DNA repair test mice
+
+
Endometrial polyps
+
+
11 Ames Assay positive with and without metabolic activation, Alkyl halides are directly reactive
J.2.6 Read-Across Utilized in Other Program Offices
Historically, offices across EPA and other agencies (OW, OLEM, CalEPA), 1,2-dichloroethane cancer
studies have routinely been utilized to assess the cancer risk for 1,1-dichloroethane. The IRIS
assessment of carcinogenic potential of 1,2-dichloroethane was considered to be 'supportive' of 1,1-
dichloroethane carcinogenic potential . .Because of similarities in structure and target organs...." A
comparison of the cancer slope factors across other program offices for 1,1-dichloroethane can be seen
in TableApx J-13; those for 1,2-dichloroethane can be seen in TableApx J-14.
Table Apx J-13.1,1-Dichloroethane Cancer Slope Factors across EPA Offices/Programs
1,1-Dichloroethane Cancer Slope Factors and Cancer Classifications
EPA Program
Oral Slope Factor
Inhalation Unit Risk
Assess for Cancer
OPPT RE
Continuous Exposure
• 0.062 per mg/kg/day
• Read-across from
mouse 1,2-
dichloroethane
hepatocellular
carcinoma data (NTP,
1978)
• High OPPT SR rating
• 7.1E-06 (per (ig/m3)
• Read-across from
inhalation rat 1,2-
dichloroethane (Nasano
et al.. 2006)
• Combined tumors in
females
• High OPPT SR rating
• Yes
IRIS
1987. U.S. EPA
0987a); IRIS 1990
U.S. EPA (1990)
• Not evaluated
• Not evaluated
• Possible human
carcinogen partially based
on 1,2-dichloroethane
data
OW
• 0.0057 per mg/kg/day
• Same as CAL EPA
(OEHHA)
• Read-across using oral
rat 1,2-dichloroethane
data (NTP, 1978)
• Failed OPPT SR
• Not reported
• Yes
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1,1-Dichloroethane Cancer Slope Factors and Cancer Classifications
OAR
• Not reported
• 1.6E-06 (per (ig/m3)
• Same as CAL EPA
(OEHHA)
• Read-across from oral
1,2-dichloroethane
• Yes
OLEM
• 0.0057 per mg/kg/day
• Same as CAL EPA
(OEHHA)
• Read-across using rat
1,2-dichloroethane
• Failed OPPTSR
• 1.6E-06 (per (ig/m3)
• Same as CAL EPA
(OEHHA)
• Read-across from oral
1,2-dichloroethane
(NTP. 1978)
• Yes
Cal EPA
1992
• 0.0057 per mg/kg/day
• Read-across using oral
rat 1,2-dichloroethane
data (NTP, 1978)
• Failed OPPTSR
• 1.6E-06 (per (ig/m3)
• Read-across using oral
rat 1,2-dichloroethane
data (NTP, 1978)
• Failed OPPTSR
• Yes
13740
13741
13742 Table Apx J-14.1,2-Dichloroethane Cancer Slope Factors across EPA Offices/Programs
1,2-Dichloroethane Cancer Slope Factors
EPA Program
Oral Slope Factor
Inhalation Unit Risk
OPPT RE
Continuous
Exposure
• 0.062 per mg/kg/day
• Mouse (NTP, 1978)
• Hepatocellular carcinoma data
• High OPPT SR rating
• 7.1E-06 per ug/m3
• Rat inhalation (Nasano et al., 2006)
• Combined tumors in females
• High OPPT SR rating
IRIS 1987
Assessment
U.S. EPA
(1987a)
• 0.091 per mg/kg/day
• Rat hemangiosarcoma data (using a time to
death analysis) (NTP, 1978)
• Rat study rated Uninformative OPPT SR
• 2.6E-05 per ug/m3
• Rat oral hemangiosarcoma data (using a
time to death analysis) (NTP, 1978)
• Rat study rated Uninformative OPPT SR
OW
• 0.091 per mg/kg/day based on (U.S. EPA,
1987a)
• Rat hemangiosarcoma data (using a time to
death analysis) (NTP, 1978)
• Rat study rated Uninformative OPPT SR
• Not reported
OAR
• Not reported
• 2.6E-5 per ug/m3 based on (U.S. EPA,
1987a)
• Rat oral hemangiosarcoma data (using a
time to death analysis) (NTP, 1978)
• Rat study rated Uninformative OPPT SR
OLEM
• 0.091 per mg/kg/day based on (U.S. EPA,
1987a)
• Rat oral hemangiosarcoma data (using a time
to death analysis) (NTP, 1978)
• Rat study rated Uninformative OPPT SR
• 2.6E-05 per ug/m3 based on (U.S. EPA,
1987a)
• Rat oral hemangiosarcoma data (using a
time to death analysis) (NTP, 1978)
• Rat study rated Uninformative OPPT SR
Cal EPA
• 0.072 per mg/kg/day
• Rat oral hemangiosarcoma data (using a
Weibull model) (NTP, 1978)
• Rat study rated Uninformative OPPT SR
• 2.1E-05 per (ig/m3
• Derived from oral rat data
• Rat study rated Uninformative OPPT SR
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J.2.7 Read-Across Conclusions
1,2-Dichloroethane was identified as the best available candidate chemical to fill the identified data gaps
for 1,1-dichloroethane. This conclusion is based on the fact that both 1,1-dichloroethane and 1,2-
dichloroethane are structurally similar as reactive di-chlorinated ethanes, both are isomers of each other
with identical molecular weights and formulas, both have similar physical-chemical properties, both are
volatile liquids, both have similar ADME patterns and metabolic pathways, both are reactive alkyl
halides, and both possess, overall, similar non-cancer and cancer outcomes (mutagenicity, common
tumor types, many common hazard endpoints).
TableApx J-15 illustrates the many qualitative non-cancer and cancer toxicity endpoints and other
chemical properties both 1,1-dichloroethane and 1,2-dichloroethane have in common. This comparison
is based on the literature studies and the ATSDR reports for both isomers (ATSDR. 2022. 2015). Many
of the identified endpoints for 1,1-dichloroethane and 1,2-dichloroethane were from studies that passed
OPPT SR were not always but were not robust enough to identify a non-cancer PODs or cancer slope
factors to use for quantitative risk estimates.
Table Apx J-15. Summary of Hazards and Chemical Properties for 1,1-Dichloroethane and 1,2-
Dichloroethane
1,1-Dichloroethane and 1,2-Dichloroethane Common Hazards and Properties
Hazard-Property
1,1-Dichlorethane
1,2-Dichloroethane
Chemical Reactivity
+
+
Dichloroethane Isomers
+
+
Irritation
+
+
Narcosis
+
+
Genotoxicity without Metabolic Activation
+
+
Immunotoxicity
+
+
Endometrial Polyps
+
+
Hepatocellular Carcinoma
+
+
Hemangiosarcomas
+
+
Mammary Gland Tumors
+
+
Nephrotoxicity
+
+
Hepatoxicity
+
+
Metabolic Toxicity
+
+
Cardiotoxicity
+
+
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Appendix K ENVIRONMENTAL HAZARD DETAILS
K.1 Approach and Methodology
For aquatic species, EPA estimates hazard by calculating a concentration of concern (CoC) for a hazard
threshold. COCs can be calculated using a deterministic method by dividing a hazard value by an
assessment factor (AF) according to EPA methods (Suter. 2016; U.S. EPA. 2013b. 2012b).
EquationApx K-l.
COC = toxicity value/AF
CoCs can also be calculated using probabilistic methods. For example, an SSD can be used to calculate
a hazardous concentration for 5 percent of species (HC05). The HC05 estimates the concentration of a
chemical that is expected to protect 95 percent of aquatic species. This HC05 can then be used to
calculate a CoC. For 1,1-dichloroethane, Web-based Interspecies Correlation Estimation (Web-ICE)
(Appendix K.2.1.1) followed by the Species Sensitivity Distribution (SSD) probabilistic method
(Appendix K.2.1.2) was used to calculate the HC05 on which the acute COC is based. The deterministic
method was used to calculate a chronic COC.
Terrestrial receptor groups are simplified to terrestrial plants, soil dwelling invertebrates, mammals, and
birds. For terrestrial plants and soil dwelling organisms, EPA estimates hazard by using a hazard value
based on hazard information relating soil or soil pore water concentrations to a hazard value. For avian
and mammalian toxicity reference values (TRVs) in units of an oral dose in mg/kg/bw-day are identified
using a peer reviewed approach used to establish soil screening levels for the Superfund Program. The
TRV is expressed as doses in units of mg/kg-bw/day. Although the TRV for 1,1-dichloroethane is
derived from mammalian laboratory studies, body weight is normalized, therefore the TRV can be used
with ecologically relevant wildlife species to evaluate chronic dietary exposure to 1,1-dichloroethane
(U.S. EPA. 2007).
K.2 Hazard Identification
K.2.1 Aquatic Hazard Data
K.2.1.1 Web-Based Interspecies Correlation Estimation (Web-ICE)
Results from the systematic review process assigned an overall quality level of high to five acceptable
aquatic toxicity studies for 1,1-dichloroethane, high or medium to six acceptable aquatic studies for
analog 1,2-dichloropropane, and high or medium to two acceptable aquatic study for analog 1,1,2-
trichloroethane, with one 1,1-dichloroethane and two 1,2-dichloropropane studies producing LC50
endpoint data (Table 4-3). To supplement the empirical data, EPA used a modeling approach, Web-ICE.
Web-ICE predicts toxicity values for environmental species that are absent from a dataset and can
provide a more robust dataset to estimate toxicity thresholds. Specifically, EPA used Web-ICE to
quantitatively supplement empirical data for aquatic organisms for acute exposure durations.
The Web-ICE application was developed by EPA and collaborators to provide interspecies extrapolation
models for acute toxicity (Raimondo. 2010). Web-ICE models estimate the acute toxicity (LC50/LD50)
of a chemical to a species, genus, or family with no test data (the predicted taxon) from the known
toxicity of the chemical to a species with test data (the commonly tested surrogate species).
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13815
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13822
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Web-ICE models are log4inear least square regressions of the relationship between surrogate and
predicted taxon based on a database of acute toxicity values. It returns median effect or lethal water
concentrations for aquatic species (EC50/LC50). Separate acute toxicity databases are maintained for
aquatic animals (vertebrates and invertebrates), aquatic plants (algae), and wildlife (birds and
mammals), with 1,440 models for aquatic taxa and 852 models for wildlife taxa in Web-ICE version 3.3
(Willming et al.. 2016). Open-ended toxicity values (i.e., >100 mg/kg or <100 mg/kg) and duplicate
records among multiple sources are not included in any of the databases.
The aquatic animal database within Web-ICE is composed of 48- or 96-hour EC50/LC50 values based
on death or immobility. This database is described in detail in the Aquatic Database Documentation
found on the Download Model Data page of Web-ICE and describes the data sources, normalization,
and quality and standardization criteria (e.g., data filters) for data used in the models. Data used in
model development adhered to standard acute toxicity test condition requirements of the ASTM
International (ASTM. 2014) and OCSPP (U.S. EPA. 2016a).
EPA used the 1,1-dichloroethane 48-hour LC50 data for Daphnia magna and the 1,2-dichloropropane
96-hour LC50 toxicity data for fathead minnow and opossum shrimp (Table 4-3) as surrogate species to
predict LC50 toxicity values using the Web-ICE application (Raimondo. 2010). The Web-ICE model
estimated toxicity values for 149 species. For model validation, the model results are then screened by
the following quality standards to ensure confidence in the model predictions. If a predicted species did
not meet all the quality criteria below, the species was eliminated from the data set (Willming et al..
2016):
• High R2 (>0.6)
o The proportion of the data variance that is explained by the model. The closer the R2
value is to one, the more robust the model is in describing the relationship between the
predicted and surrogate taxa.
• Low mean square error (MSE; <0.95)
o An unbiased estimator of the variance of the regression line.
• High slope (>0.6)
o The regression coefficient represents the change in loglO value of the predicted taxon
toxicity for every change in loglO value of the surrogate species toxicity.
Previously published guidance on ICE model did not include quantitative guidance on confidence
intervals, so the following criterium was also applied for inclusion in the 1,1-dichloroethane analysis.
• Narrow 95 percent confidence intervals
o One order of magnitude between lower and upper limit
After screening, the acute toxicity values for 33 additional aquatic organisms (15 fish, 1 amphibian, and
18 aquatic invertebrate species) were added to the fathead minnow 96-hour LC50, daphnia 48-hour
LC50, and opossum shrimp 96-hour LC50 data (Table Apx K-l). The toxicity data were then used to
calculate the distribution of species sensitivity through the SSD toolbox (Etterson. 2020a) as shown in
Table 4-15 and described in Appendix K.2.1.2.
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Table Apx K-l. Empirical and Web-ICE Predicted Species that Met Model Selection Criteria
Common Name
Genus
Species
Surrogate
Estimated
Toxicity
(ug/L)
95% CI
R2
MSE
Slope
Fathead minnow
Pimpephcdes
promelas
133,34017
Daphnid
Daphnia
magna
34,30017
Opossum shrimp
Americctmysis
bahia
24,79017
Amphipod
Gammctrus
fasciatus
Daphnid
26,138.12
9,188.01 to 74,357.92
0.75
0.77
0.86
Beaver-tail fairy shrimp
Thamnocephcdu
s
platyurus
Daphnid
23,443.61
15,609.91 to 35,208.57
0.98
0.05
0.91
Bluegill
Lepomis
macrochirus
Daphnid
23,537.05
16,647.25 to 33,278.34
0.62
0.8
0.66
Bluegill
Lepomis
macrochirus
Opossum shrimp
24,166.74
14,072.18 to 41,502.53
0.66
0.61
0.64
Bluegill
Lepomis
macrochirus
Fathead minnow
54,533.98
31,794.44 to 93,536.97
0.75
0.57
0.92
Bullfrog
Lithobates
catesbeianus
Fathead minnow
131,593.83
505,06.37 to 342,866.35
0.97
0.19
0.93
Channel catfish
Ictcdurus
punctatus
Fathead minnow
107,915.57
56,215.24 to 207,163.92
0.84
0.4
0.96
Coho salmon
Oncorhvnchus
kisutch
Fathead minnow
12,947.96
2,255.81 to 74,318.92
0.75
0.47
0.81
Common carp
Cyprinus
carpio
Fathead minnow
97,468.41
24,777.04 to 383,423.16
0.91
0.19
1.04
Cutthroat trout
Oncorhvnchus
clarkii
Fathead minnow
25,904.49
8,199.8 to 81,836.44
0.79
0.39
0.94
Daphnid
Ceriodctphnict
dubia
Daphnid
24,082.48
14,906.4 to 38,907.18
0.95
0.26
1
Daphnid
Daphnia
pulex
Daphnid
30,090.04
15,748.11 to 57,493.29
0.97
0.12
1.01
Fatmucket
Lampsilis
siliquoidea
Daphnid
17,504.7
7,080.4 to 43,276.44
0.86
0.47
0.74
Goldfish
Carassins
auratus
Fathead minnow
119,554.18
75,704.99 to 188,801.3
0.96
0.1
0.97
Guppy
Poe cilia
reticulata
Fathead minnow
485,55.94
26,934.99 to 87,532.22
0.83
0.27
0.85
Isopod
Asellus
aquaticus
Opossum shrimp
897,057.16
585,834.85 to 1,373,615.02
0.99
0
0.89
Isopod
Caecidotea
intermedia
Fathead minnow
60,699.62
10,645.13 to 346,115.21
0.71
0.27
0.63
Leon springs pupfish
Cyprinodon
bovinus
Fathead minnow
13,566.15
3,483.21 to 52,836.41
0.99
0
0.67
Medaka
Orvzias
latipes
Fathead minnow
160,480.59
57,645.49 to 446,765.59
0.92
0.23
0.91
Midge
Paratanytarsus
parthenogen
eticus
Daphnid
99,504.41
60,585.81 to 163,423.21
0.98
0.04
0.93
Midge
Paratanytarsus
parthenogen
eticus
Fathead minnow
42,2617.57
127,830.56 to 1,397,205.84
0.97
0.13
1.05
Mosquitofish
Gambusia
affinis
Fathead minnow
71,334.5
10,685.43 to 476,219.55
0.98
0.12
0.96
Mozambique tilapia
Oreochromis
mossambicu
s
Fathead minnow
65,745.19
11,024.05 to 392,090.8
0.78
0.28
0.91
Oligochaete
Lumbri cuius
variegatus
Fathead minnow
150,551.07
55,625.4 to 407,468.95
0.86
0.3
1.1
Paper pondshell
Utterbackia
imbecillis
Daphnid
17,897.25
10,686.93 to 29,972.28
0.96
0.11
0.9
Rainbow trout
Oncorhvnchus
mvkiss
Fathead minnow
48,513.34
32,978.52 to 71,365.97
0.83
0.36
0.96
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Common Name
Genus
Species
Surrogate
Estimated
Toxicity
(Hg/L)
95% CI
R2
MSE
Slope
Sheepshead minnow
Cyprinodon
variegcttiis
Fathead minnow
37,098.68
12,893.35 to 106,745.85
0.74
0.43
0.69
Swamp lymnaea
Lvmnaect
stagnalis
Daphnid
38,279.48
17,260.02 to 84,896.69
0.96
0.19
1.01
Tadpole physa
Phvsct
gyrina
Daphnid
29,787.34
14,824.65 to 59,852.07
0.96
0.14
0.99
Threeridge
Amblema
plicata
Daphnid
7,800.16
3,716.62 to 16,370.36
0.94
0.18
0.87
Threeridge
Amblema
plicata
Fathead minnow
11,893.55
1,598.8 to 88,476.7
0.83
0.59
1.15
Washboard
Megalonaias
nervosa
Daphnid
14,692.06
7,781.98 to 27,738.01
0.96
0.16
0.92
Western pearlshell
Mcirgciritifera
fcdcata
Daphnid
20,647.3
10,708.95 to 39,808.88
0.95
0.14
0.86
White heelsplitter
Lasmigona
complcmata
Daphnid
12,661.92
5,387.58 to 29,758.15
0.98
0.1
0.92
Rohu
Lctbeo
rohita
Opossum shrimp
2,945,839.1
5
937,110.05 to 9,260,351.28
0.99
0
0.91
Water flea
Pseudosida
ramosa
Daphnid
9,707.03
1,238.21 to 76,098.54
0.87
0.57
0.93
Vernal pool fairy
shrimp
Brcmchinecta
lvnchi
Daphnid
24,921.96
11,928.2 to 52,070.23
0.98
0.09
0.9
11 Empirical value
13849
13850
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K.2.1.2 Species Sensitivity Distribution (SSD)
The SSD Toolbox is a resource created by EPA's Office of Research and Development (ORD) that can
fit SSDs to environmental hazard data (Etterson. 2020a). The SSD Toolbox runs on Matlab 2018b (9.5)
for Windows 64 bit. For the 1,1-dichloroethane Risk Evaluation, EPA calculated an SSD with the SSD
Toolbox using acute LC50 hazard data for 1,1-dichloroethane and 1,2-dichloropropane from systematic
review, and estimated data from the Web-ICE application (Appendix K.2.1.1) that included 15 fish, one
amphibian, and 18 invertebrate species. The SSD is used to calculate, a hazardous concentration for 5
percent of species (HC05). In other words, HC05 estimates the concentration that is expected to be
protective for 95 percent of species.
The SSD toolbox contains functions for fitting up to six distributions (normal, logistic, triangular,
Gumbel, Weibull, and Burr) across four model estimation methods (maximum likelihood, moment
estimators, graphical methods, and Bayesian methods, in this case the Metropolis-Hastings algorithm).
Maximum likelihood was used to model the data for 1,1-dichloroethane due to its general acceptance for
fitting SSDs (Etterson. 2020b). its low sampling variance, and the fact that models can also be compared
a posteriori using information theoretic methods, in this case Akaike's Information Criterion corrected
for sample size (AICc). AICc was used along with a comparison of p-values and a visual assessment of
Q-Q plots, which are methods available to all model estimation methods, to select the distribution used
to calculate the HC05 for this analysis.
SSD Toolbox uses a parametric bootstrap method to calculate a p-value to compare goodness-of-fit
across distributions. In this type of test, the larger the deviation of the p-value from 0.5, the greater the
indication of lack of fit. Thus, p-values closest to 0.5 are preferred (Etterson. 2020b). The Gumbel and
Burr distributions (p = 0.57 and 0.6, respectively) had the best goodness-of-fit using using p-values
(Figure Apx K-l). The sample-size corrected AICc was lowest for the Gumbel distribution
(Figure Apx K-2). Because numerical methods may lack statistical power for small sample sizes, a
visual inspection of the data was also used to assess goodness-of-fit, in this case a comparison of Q-Q
plots between the two distributions. In a Q-Q plot, the horizontal axis gives the empirical quantiles, and
the vertical axis gives the predicted quantiles (from the fitted distribution). A good model fit shows the
data points in close proximity to the diagonal line across the data distribution. Comparison of Q-Q plots
between the Gumbel and Burr distributions did not identify a significantly better fit between them. Thus,
the Gumbel distribution was selected on the basis of its lowest AICc and its p-value being slightly closer
to 0.5. This distribution was then plotted along with data points for both measured and modeled species.
Life history information was attached to each species, indicating an even distribution of various life
history strategies along the curve (Figure_Apx K-4). The calculated HC05 was 10,784 |ig/L (95 percent
CI = 7,898 to 15,440 |ig/L). The lower 95 percent CI of the HC05, 7,898 |ig/L, was then used as the
acute aquatic CoC.
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*• SSD Toolbox
File Plot
~
C:\Users\LHOUSLEY\OneDrive - Environmental Protection Agency (EPA)\Desktop\1,1 DCA WeblCE ugL.csv
Fit Distribution
Distribution:
burr
Fitting method
maximum likelihood
Goodness of Fit:
Iterations: I 1000
Scaling parameters
~ Scale to Body Weight
Scaling factor: 1.15
Target weight: 10O
13889
13890
13891
13892
13893
Toolbox
Status:
Ready
Results:
Distribution
Method
HC05
p
1
normal
ML
6.4040e+03
0.0390
2
logistic
ML
6.1886e+03
0.0909
3
triangular
ML
4.9739e+03
9.9900e-04
4
gumbel
ML
1.0784e+04
0.5714
5
weibull
ML
2.9743e-75
0.3517
6
burr
ML
1.0781e+04
0.60541
FigureApx K-t. SSD Toolbox Interface Showing HC05s and P Values for Each Distribution
Using Maximum Likelihood Fitting Method Using 1,2-Dichloropropane's Acute Aquatic Hazard
Data (Etterson, 2020a)
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* ModelSelection
Percentile of interest:
Model-averaaed HCd:
Model-averaaed SE of HCd:
X
CV of HCd:
13894
13895
13896
13897
AlCc Table
Distribution
gumbel
burr
logistic
normal
triangular
weibull
AlCc
delta AlCc
Wt
HCp
SE HCp
883.3612
885.7542
891.0004
894.2221
904 4075
1 1446e+03
0 0.7527 1.0784e+04 1.7779e+03
2.3930 0.2275 1.0781e+04 1.7796e+03
7.6392 0.0165 6.1886e+03 1 9098e+03
10.8609 0.0033 6.4040e+03 1.9777e+03
21.0463 2.0252e-05 4.9739e+03 545.0990
261.2456 1 4055e-57 2.9743e-75 0.0000e+...
FigureApx K-2. AlCc for the Six Distribution Options in the SSD Toolbox for 1,2-
Dichloropropane Acute Aquatic Hazard Data (Etterson, 2020a)
13898
13899
13900
0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1
Predicted Quantiles
Figure Apx K-3. Q-Q plot of 1,2-Dichloropropane Acute Aquatic Hazard Data with the Gumbel
Distribution (Etterson, 2020a)
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1
0.9
0.8
0.7
>>
to 0.6
.Q
2
CL
a) 0.5
0
3.5
~ HC05
95% CL HC05
— LXtteoTohita •
Organism Habitat
Freshwater Benthic Invertebrate
Saltwater Benthic Invertebrate
Freshwater Water Column Invertebrate
Saltwater Water Column Invertebrate
Freshwater Water Column Vertebrate
Saltwater Water Column Vertebrate
Amphibian
5.5
Log10 Toxicity Value (|jg/L)
6.5
FigureApx K-4. SSD Distribution for 1,2-Dichloropropane Acute Hazard Data (Etterson, 2020a)
K.2.1.3 Dose-Response Curve Fit Methods
Swimming behavior data for Oryzicts Icitipes exposed to 1,1-dichloroethane were further analyzed to
derive an EC so value by fitting a dose-response curve. The authors of the original dose-response study
(Mitsubishi Chemical Medience Corporation. 2009b) recorded number of fish out of 10 fish per
treatment concentration with abnormal swimming behavior at 96-hour. For this EC50 derivation, data
were first censored for mortalities, then the response was expressed as percent abnormal at each
concentration. The control group had zero abnormal swimmers, so there was no need to standardize the
response as a percent of control. Preliminary analyses indicated this relationship was well characterized
using a log-logistic curve in R v.4.2.1 (R Core Team. 2022; Ritz et al.. 2015) with slope and inflection
point as the estimated parameters. The lower asymptote was fixed to 0 percent and the upper asymptote
to 100 percent to constrain the predicted y value to a realistic range. The inflection point estimated by
the curve fit (i.e., the point along the curve halfway between the upper and lower asymptotes) was used
to estimate the EC50. Figure Apx K-5 shows the log-logistic curve for the 96h time point, with a
vertical dotted line indicating the EC50.
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FigureApx K-5. Log-Logistic Curve Fit to 96-Hour Abnormal Swimming Behavior Data from
(Mitsubishi Chemical Medience Corporation, 2009b) for Oryzias latipes Exposed to 1,1-
Dichloroethane
The hatching rate endpoint for Ophryotrocha labronica exposed to 1,1,2-trichloroethane was further
analyzed to derive EC50 and EC 10 values by fitting a dose-response curve. The authors of the original
dose-response study (Rosenberg et al.. 1975) reported for each concentration of 1,1,2-trichloroethane the
hatching percent of O. labronica eggs. The hatching rate endpoint is expressed as percent relative to
control response. Hormetic observations (i.e., treatments having a response exceeding that of the
control) were not censored. Characterizing EC50 and EC10 values required defining the 0 percent effect
and 100 percent effect. Estimated between these two thresholds are the EC50, or the 50 percent
inhibition of egg hatching, and EC 10, 10 percent inhibition of egg hatching. Responses plateaued as
concentration increased. Since zero was the minimum possible realistic value, the 100 percent effect
(i.e., lower asymptote) was set at zero. The 0 percent effect was defined as the control response;
therefore, the upper asymptote was fixed at 100 percent of the control response. Hatching percent
followed a decreasing logistic shape. Several functions were tested using R v. 4.2.1, with and without
upper and lower asymptotes (R Core Team. 2022; Ritz et al.. 2015). A log-logistic curve was ultimately
fit to the data with slope and inflection point as the estimated parameters. The EC50 was calculated as
the concentration along the curve halfway between 0 and 100 percent control response and the EC 10 as
the concentration a tenth of the way along the curve. Figure Apx K-6 shows the log-logistic curve, with
vertical dotted lines indicating the EC50 and EC 10.
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1,1,2-TCA percent hatching
100 -
Q
'
o \ I
80 -
i \cf
jo\i
60 -
40 -
| \
20 -
EC50= 104.562 , icio\ 67.618
o -
! ! o
0 10 100 1000 10000
Dose
FigureApx K-6. Log-logistic Curve Fit to Hatching Percent Data from Ophryotrocha labronica
Exposed to 1,1,2-Trichloroethane (Rosenberg et al., 1975).
K.2.2 Terrestrial Hazard Data
For mammalian species, EPA estimates hazard by calculating a TRV. The TRV is expressed as doses in
units of mg/kg-bw/day. Data from laboratory rat and mouse studies can be used to evaluate chronic
dietary exposure in ecologically relevant wildlife species because of this normalization to body weight.
For calculation of the mammal TRV, an a priori framework for selection of the TRV value based on the
results of the NOAEL and LOAEL data (Figure Apx K-7) is used. The minimum data set required to
calculate a TRV consists of three results with NOAEL or LOAEL values for reproduction, growth, or
mortality for at least two species. If these minimum results are not available, then a TRV is not
calculated.
For mammalian species, EPA estimates hazard by calculating a TRV. The TRV is expressed as doses in
units of mg/kg-bw/day. Although the TRV for 1,1-dichloroethane is derived from laboratory mice and
rat studies, body weight is normalized, therefore the TRV can be used with ecologically relevant wildlife
species to evaluate chronic dietary exposure to 1,1-dichloroethane. Representative wildlife species
chronic hazard threshold will be evaluated in the trophic transfer assessments using the TRV. The flow
chart in Figure Apx K-7 was used to select the data to calculate the TRV with NOAEL and/or LOAEL
data (U.S. EPA. 2007). The movement through the flowchart used to calculate the TRV for 1,1-
dichloroethane is described below and illustrated in Figure 4-2.
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Step 1: At least three results and two species tested for reproduction, growth, or mortality general
end points.
Yes, 15 results across 2 species (rats and mice) were identified as suitable for use. Endpoints
included 10-day, 6-week, 13-week, 52-week, and 78-week NOAEL/LOAELs in both male and
female organisms. These results are summarized in Table 4-4.
Step 2: Are there three or more NOAELs in reproduction or growth effect groups?
Yes, nine of the above-referenced results report a NOAEL in the reproduction or growth effect
groups.
Move from Step 2 to Step 4: Calculate a geometric mean of the NOAELs for Reproduction and
Growth. Is this number lower than the lowest bounded LOAEL for reproduction, growth, and
mortality?
The geometric mean of the NOAELs for reproduction and growth is 1,935 mg/kg-bw/day. This
is greater than 1,429 mg/kg-bw/day, which is the lowest bounded LOAEL for reproduction,
growth, and mortality.
TRV = Highest bounded NOAEL below lowest bounded LOAEL for reproduction, growth, and
mortality.
The mammalian wildlife TRV for 1,1-dichloroethane is 1,189 mg/kg-bw/day.
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FigureApx K-7. TRY Flow Chart
K.2.3 Evidence 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 scientific evidence. As stated in the Draft
Systematic Review Protocol Supporting TSCA Risk Evaluations for Chemical Substances (U.S. EPA,
2021b), data integration 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.
The general analytical approaches for integrating evidence for environmental hazard is discussed in
Section 7.4 of the Draft Systematic Review Protocol Supporting TSCA Risk Evaluations for Chemical
Substances (U.S. EPA, 2021b).
The organization and approach to integrating hazard evidence is determined by the reasonably available
evidence regarding routes of exposure, exposure media, duration of exposure, taxa, metabolism and
distribution, effects evaluated, the number of studies pertaining to each effect, as well as the results of
the data quality evaluation.
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The environmental hazard integration is organized around effects to aquatic and terrestrial organisms as
well as the respective environmental compartments (e.g., pelagic, benthic, soil). Environmental hazard
assessment may be complex based on the considerations of the quantity, relevance, and quality of the
available evidence.
For 1,1-dichloroethane, environmental hazard data from toxicology studies identified during systematic
review have used evidence that characterizes apical endpoints, i.e., endpoints that could have population
level effects such as reproduction, growth, and/or mortality. Additionally, mechanistic data that can be
linked to apical endpoints will add to the weight of scientific evidence supporting hazard thresholds.
EPA also considered predictions from Web-ICE to supplement the empirical data found during
systematic review.
K.2.3.1 Weight of Scientific Evidence
After calculating the hazard thresholds that were carried forward to characterize risk, a narrative
describing the weight of scientific evidence and uncertainties was completed to support EPA's
decisions. The weight of scientific evidence fundamentally means that the evidence is weighed (i.e.,
ranked), and weighted (i.e., a piece or set of evidence or uncertainty may have more importance or
influence in the result than another). Based on the weight of scientific evidence and uncertainties, a
confidence statement was developed that qualitatively ranks (i.e., Robust, Moderate, Slight, or
Indeterminate) the confidence in the hazard threshold. The qualitative confidence levels are described
below and illustrated in Table Apx K-2.
The evidence considerations and criteria detailed within (U.S. EPA. 2021b) will guide the application of
strength-of-evidence judgments for environmental hazard effect within a given evidence stream and
were adapted from Table 7-10 of the Draft Systematic Review Protocol Supporting TSCA Risk
Evaluations for Chemical Substances (U.S. EPA. 2021b).
EPA used the strength-of-evidence and uncertainties from (U.S. EPA. 2021b) for the hazard assessment
to qualitatively rank the overall confidence using evidence for environmental hazard. Confidence levels
of Robust (+ + +), Moderate (+ +), Slight (+), or Indeterminant are assigned for each evidence property
that corresponds to the evidence considerations (U.S. EPA. 2021b). The rank of the Quality of the
Database consideration is based on the systematic review data quality rank (High, Medium, or Low) for
studies used to calculate the hazard threshold, and whether there are data gaps in the toxicity dataset.
Another consideration in the Quality of the Database is the risk of bias (i.e., how representative is the
study to ecologically relevant endpoints). Additionally, because of the importance of the studies used for
deriving hazard thresholds, the Quality of the Database consideration may have greater weight than the
other individual considerations. The High, Medium, and Low systematic review ranks correspond to the
evidence table ranks of Robust (+ + +), Moderate (+ +), or Slight (+), respectively. The evidence
considerations are weighted based on professional judgement to obtain the Overall Confidence for each
hazard threshold. In other words, the weights of each evidence property relative to the other properties
are dependent on the specifics of the weight of scientific evidence and uncertainties that are described in
the narrative and may or may not be equal. Therefore, the overall score is not necessarily a mean or
defaulted to the lowest score. The confidence levels and uncertainty type examples are described below.
Confidence Levels
• Robust (+ + +) confidence suggests thorough understanding of the scientific evidence and
uncertainties. The supporting weight of scientific evidence outweighs the uncertainties to the
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point where it is unlikely that the uncertainties could have a significant effect on the exposure or
hazard estimate.
• Moderate (+ +) confidence suggests some understanding of the scientific evidence and
uncertainties. The supporting scientific evidence weighed against the uncertainties is reasonably
adequate to characterize exposure or hazard estimates.
• Slight (+) confidence is assigned when the weight of scientific evidence may not be adequate to
characterize the scenario, and when the assessor is making the best scientific assessment possible
in the absence of complete information. There are additional uncertainties that may need to be
considered.
• Indeterminant (N/A) corresponds to entries in evidence tables where information is not available
within a specific evidence consideration.
Types of Uncertainties
The following uncertainties may be relevant to one or more of the weight of scientific evidence
considerations listed above and will be integrated into that property's rank in the evidence table
(TableApx K-2).
• Scenario uncertainty: Uncertainty regarding missing or incomplete information needed to fully
define the exposure and dose.
o The sources of scenario uncertainty include descriptive errors, aggregation errors, errors
in professional judgment, and incomplete analysis.
• Parameter uncertainty: Uncertainty regarding some parameter.
o Sources of parameter uncertainty include measurement errors, sampling errors,
variability, and use of generic or surrogate data.
• Model uncertainty: Uncertainty regarding gaps in scientific theory required to make predictions
on the basis of causal inferences.
o Modeling assumptions may be simplified representations of reality.
Table Apx K-2 summarizes the weight of scientific evidence and uncertainties, while increasing
transparency on how EPA arrived at the overall confidence level for each exposure hazard threshold.
Symbols are used to provide a visual overview of the confidence in the body of evidence, while de-
emphasizing an individual ranking that may give the impression that ranks are cumulative (e.g., ranks of
different categories may have different weights).
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14082 TableApx K-2. Considerations that Inform Evaluations of the Strength of the Evidence within an Evidence Stream Apical
14083 Endpoints, Mechanistic, or Field Studies)
Consideration
Increased Evidence Strength (of the Apical Endpoints,
Mechanistic, or Field Studies Evidence)
Decreased Evidence Strength (of the Apical Endpoints,
Mechanistic, or Field Studies Evidence)
The evidence considerations and criteria laid out here guide the application of strength-of-evidence judgments for an outcome or environmental hazard effect
within a given evidence stream. Evidence integration or synthesis results that do not warrant an increase or decrease in evidence strength for a given
consideration are considered "neutral" and are not described in this table (and, in general, are captured in the assessment-specific evidence profile tables).
Quality of the
Database* (risk of bias)
• A large evidence base of high- or medium-quality studies
increases strength.
• Strength increases if relevant species are represented in a
database.
• An evidence base of mostly /ow-quality studies decreases strength.
• Strength also decreases if the database has data gaps for relevant
species, i.e., a trophic level that is not represented.
• Decisions to increase strength for other considerations in this table
should generally not be made if there are serious concerns for risk
of bias; in other words, all the other considerations in this table are
dependent upon the quality of the database.'1
Consistency
Similarity of findings for a given outcome (e.g., of a similar
magnitude, direction) across independent studies or
experiments increases strength, particularly when consistency
is observed across species, life stage, sex, wildlife populations,
and across or within aquatic and terrestrial exposure pathways.
• Unexplained inconsistency (i.e., conflicting evidence; see (U.S.
EPA. 2005b) decreases strength.
• Strength should not be decreased if discrepant findings can be
reasonably explained by study confidence conclusions; variation in
population or species, sex, or life stage; frequency of exposure (e.g.,
intermittent or continuous); exposure levels (low or high); or
exposure duration.
Strength (effect
magnitude) and
precision
• Evidence of a large magnitude effect (considered either within
or across studies) can increase strength.
• Effects of a concerning rarity or severity can also increase
strength, even if they are of a small magnitude.
• Precise results from individual studies or across the set of
studies increases strength, noting that biological significance is
prioritized over statistical significance.
• Use of probabilistic model (e.g., Web-ICE, SSD) may
increase strength.
Strength may be decreased if effect sizes that are small in
magnitude are concluded not to be biologically significant, or if
there are only a few studies with imprecise results.
Biological
gradient/dose-response
• Evidence of dose-response increases strength.
• Dose-response may be demonstrated across studies or within
studies and it can be dose- or duration-dependent.
• Dose response may not be a monotonic dose-response
(monotonicity should not necessarily be expected, e.g.,
different outcomes may be expected at low vs. high doses due
• A lack of dose-response when expected based on biological
understanding and having a wide range of doses/exposures
evaluated in the evidence base can decrease strength.
• In experimental studies, strength may be decreased when effects
resolve under certain experimental conditions (e.g., rapid
reversibility after removal of exposure).
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Consideration
Increased Evidence Strength (of the Apical Endpoints,
Mechanistic, or Field Studies Evidence)
Decreased Evidence Strength (of the Apical Endpoints,
Mechanistic, or Field Studies Evidence)
to activation of different mechanistic pathways or induction of
systemic toxicity at very high doses).
• Decreases in a response after cessation of exposure (e.g.,
return to baseline fecundity) also may increase strength by
increasing certainty in a relationship between exposure and
outcome (this particularly applicable to field studies).
• However, many reversible effects are of high concern. Deciding
between these situations is informed by factors such as the
toxicokinetics of the chemical and the conditions of exposure, see
(U.S. EPA. 1998). cndooint severity, iudaments regarding the
potential for delayed or secondary effects, as well as the exposure
context focus of the assessment (e.g., addressing intermittent or
short-term exposures).
• In rare cases, and typically only in toxicology studies, the
magnitude of effects at a given exposure level might decrease with
longer exposures (e.g., due to tolerance or acclimation).
• Like the discussion of reversibility above, a decision about
whether this decreases evidence strength depends on the exposure
context focus of the assessment and other factors.
• If the data are not adequate to evaluate a dose-response pattern,
then strength is neither increased nor decreased.
Biological relevance
Effects observed in different populations or representative
species suggesting that the effect is likely relevant to the
population or representative species of interest (e.g.,
correspondence among the taxa, life stages, and processes
measured or observed and the assessment endpoint).
An effect observed only in a specific population or species without
a clear analogy to the population or representative species of
interest decreases strength.
Physical/chemical
relevance
Correspondence between the substance tested and the substance
constituting the stressor of concern.
The substance tested is an analog of the chemical of interest or a
mixture of chemicals which include other chemicals besides the
chemical of interest.
Environmental
relevance
Correspondence between test conditions and conditions in the
region of concern.
The test is conducted using conditions that would not occur in the
environment.
" Database refers to the entire dataset of studies integrated in the environmental hazard assessment and used to inform the strength of the evidence. In this context,
database does not refer to a computer database that stores aggregations of data records such as the ECOTOX Knowledgebase.
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K.2.3.2 Data Integration Considerations Applied to Aquatic and Terrestrial Hazard
Representing the 1,1,-Dichloroethane Environmental Hazard Database
Quality of the Database; Consistency; and Strength (Effect Magnitude) and Precision
For the acute aquatic assessment, the database consisted of four studies with overall quality
determinations of high with both aquatic invertebrates and vertebrates represented. Data from three of
these studies were supplemented using Web-ICE to generate a subsequent SSD output, therefore a
robust confidence was assigned to quality of the database. Outcomes in the empirical and predicted data
were generally consistent with the majority of toxicity values falling within a log scale of each other
(Figure Apx K-4). For example, the ECOSAR acute toxicity daphnid prediction for 1,1-dichloroethane
was in good agreement with the 1,1-dichloroethane empirical hazard value for Daphnia magna (69.9 vs.
34.3 mg/L, respectively) as was the analog 1,2-dichloropropane fish acute toxicity prediction in close
agreement with the respective 1,2-dichloropropane empirical hazard value (94.8 vs. 133.34 mg/L,
respectively). Although the ECOSAR 1,1-dichloroethane and 1,2-dichloropropane predictions for mysid
shrimp were in less agreement with the 1,2-dichloropropane empirical toxicity value for mysid shrimp,
the predictions were still within three to four-fold of the empirical datapoint (TableApx J-5) Therefore,
a robust confidence was assigned to consistency of the acute aquatic assessment. The effects observed in
the 1,1-dichloroethane and 1,2-dichloropropane empirical dataset for acute aquatic assessment were
immobilization, abnormal swimming, and mortality, and EC50 {Daphnia magna) and LC50 (fathead
minnow and mysid shrimp) values were reported in the three species utilized in the SSD analysis with
additional predicted LC50 values reported from Web-ICE, therefore a robust confidence was assigned to
the strength and precision consideration (Table 4-17).
For the acute benthic assessment, the database consisted of 96-hour LC50 toxicity predictions for
thirteen benthic invertebrates based on empirical fish and aquatic invertebrate data for 1,1-
dichloroethane and analog 1,2-dichloropropane (Table Apx K-l). EPA determined this to be a sufficient
number of benthic invertebrate predictions but acknowledging the fact that there were no reasonably
available empirical acute toxicity data for sediment-dwelling organisms for 1,1-dichloroethane or its
analogs, a moderate confidence was assigned to quality of the database. Moderate confidence was
assigned to the consistency consideration for the acute benthic assessment since the data, although
indicating toxicity, were sourced from Web-ICE predictions of benthic invertebrate hazard. Similarly,
moderate confidence was assigned to the strength and precision consideration as the predicted data
indicate mortality in thirteen benthic species; however, there are a lack of reasonably available empirical
data to confirm acute hazard in sediment-dwelling organisms.
For the chronic aquatic assessment, the database consisted of two studies with overall quality
determinations of high (one study containing 1,1-dichloroethane hazard data obtained according to
OECD Guideline for the Testing of Chemicals, 211 and the other study containing analog 1,2-
dichloropropane hazard data), resulting in moderate confidence for quality of the database. Outcomes
differed by taxa with mortality and growth effects observed in fathead minnow based on analog hazard
data and reproductive effects observed in Daphnia magna based on 1,1-dichloroethane hazard data. 1,1-
Dichloroethane and 1,2-dichloropropane ECOSAR chronic toxicity predictions were consistent with the
1,2-dichloropropane chronic fish toxicity hazard value (e.g., ChV predictions of 12.0 mg/L 1,1-
dichloroethane and 9.3 mg/L 1,2-dichloropropane compared to the empirical ChV 8.12 mg/L 1,2-
dichloropropane), whereas the 1,1-dichloroethane chronic hazard prediction for daphnid was in less
agreement but still within 10-fold of the 1,1-dichloroethane empirical hazard value for Daphnia magna
utilized in setting the hazard threshold (6.5 mg/L vs. 0.93 mg/L, respectively) (Table Apx J-3).
Therefore, a moderate confidence was assigned to the consistency consideration. In the two chronic
studies, reproductive and growth effects were considered the most sensitive endpoints with high doses
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resulting in approximately 25 percent of control values for those endpoints. Therefore, a robust
confidence was assigned to the strength and precision consideration for the chronic aquatic assessment
(Table 4-17).
For the chronic benthic assessment, the database consisted of two studies with overall quality
determinations of high or medium based on analog hazard data. One of the studies is a TSCA section
4(a)(2) test order report conducted according to OECD Guideline for the Testing of Chemicals,
Guideline 233 ("Sediment-Water Chironomid Life-Cycle Toxicity Test Using Spiked Water or Spiked
Sediment"), and the second study was a high-rated exposure of Ophryotrocha labronica in water,
resulting in moderate confidence for quality of the database. Outcomes occurred in offspring of both
studies (percent emerged or hatched), therefore a moderate confidence was assigned for consistency in
chronic benthic assessment. Percent of O. labronica eggs hatched decreased to 0 percent at higher 1,1,2-
trichloroethane concentrations, and emergence in the second-generation (Fl) larvae in the 1,1,2-
trichloroethane test order report was approximately 50 percent of the control treatment emergence.
Additionally, the definitive chironomid emergence result is qualitatively supported by similar findings in
the preliminary 2-generation screening study in the same study report where percent emergence at the
high dose was less than 20 percent that of the control treatment, therefore the strength and precision
consideration was assigned robust confidence (Table 4-17).
For the algal assessment, the database consisted of one study with an overall quality determination of
high containing 1,1-dichloroethane hazard data and three high or medium-rated studies based on analog
(1,2-dichloropropane) data resulting in a moderate confidence for quality of the database. Outcomes
were consistent for two of the three algal species (e.g., showing growth inhibition effects at comparable
concentrations) whereas the third species showed no effect on growth to the highest concentrations
tested across two studies, therefore a moderate confidence was assigned to the consistency
consideration. The endpoints were based on growth reduction in algae, with 1,2-dichloropropane EC50
values achieved in two of the studies. Additionally, ECOSAR ChV predictions for 1,1-dichloroethane
and 1,2-dichloropropane (12.1 and 10.4 mg/L, respectively) were closely aligned with the ChV utilized
for the algal hazard threshold (10.0 mg/L); therefore, a robust confidence was assigned to the strength
and precision consideration for the algal assessment (Table 4-17).
For terrestrial mammal assessment, no wildlife studies were available from systematic review; however,
three studies with overall quality determinations of high representing two species (mice and rats), were
used from human health animal model studies. A TRV derived from the mammal studies was used to
calculate the hazard threshold in mg/kg-bw. The terrestrial mammal data suggest potential trends (e.g.,
species-specific growth effects, potential route of administration-specific effects on survival); however,
the ability to fully assess these trends for consistency is limited by the low number of studies. Regarding
strength of the effect, mortality was substantial in the datum representing the TRV (approximately 40
percent reduction in survival) whereas reduction in growth, although significant, was smaller in
magnitude. Moderate confidence was assigned to quality of the database, consistency, and strength and
precision for the terrestrial mammalian assessment (Table 4-17).
For the terrestrial plant assessment, a single study with an overall quality determination of medium was
available for the Canadian poplar resulting in slight confidence for the quality of the database. The
terrestrial plant study measured growth inhibition and transpiration reduction effects. The single
terrestrial plant study was insufficient to characterize consistency in the outcome resulting in slight
confidence for consistency. For strength of effect in the terrestrial plant assessment, reduction in
transpiration was substantial (50 percent reduction achieved), therefore moderate confidence was
assigned to this consideration.
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Biological Gradient/Dose-Response
All studies used for calculating hazard thresholds contained multiple doses. For the acute aquatic
assessment, effects were noted at increased doses and particularly for the fish data, effects increased as
duration increased, therefore a robust confidence was assigned to this consideration. For the acute
benthic assessment, LC50 predictions were generated using the Web-ICE predictive tool, however,
dose-specific responses outside the predicted LC50 are not presented. Nevertheless, species-specific
sensitivity in benthic invertebrates was indicated as the 13 predicted LC50 values for benthic
invertebrates are distributed relatively evenly along the SSD (Figure Apx K-4); therefore, moderate
confidence was assigned to this consideration. For the chronic acute assessment, increase in effect was
observed as chemical concentration increased, therefore a robust confidence was assigned to this
consideration. For the chronic benthic assessment, decrease in percent eggs hatched and second-
generation larval emergence was observed as chemical concentration increased, therefore a robust
confidence was assigned to this consideration. For the algal assessment, when effects were noted, the
effects increased as chemical dose and duration increased but was not demonstrated across species,
therefore a moderate confidence was assigned to this consideration.
For terrestrial mammalian assessment, effects were generally noted at higher 1,1-dichloroethane
concentrations and increased over duration, therefore robust confidence was assigned to this
consideration. For the terrestrial plant assessment, there is evidence of dose-response with both reported
endpoints (zero-growth and transpiration reduction); however, the zero-growth concentration was
extrapolated outside the tested concentrations of 1,1-dichloroethane, therefore moderate confidence was
assigned to this consideration (Table 4-17).
Relevance (Biological; Physical/Chemical; Environmental)
For the acute aquatic assessment, immobilization and mortality were noted in the empirical data for
freshwater and saltwater aquatic invertebrates and a freshwater fish, all three of which are considered
representative test species for aquatic assessments, and mortality was predicted in additional species.
Although, modeled approaches such as Web-ICE can have more uncertainty than empirical data when
determining the hazard or risk, the use of the probabilistic approach within this risk evaluation increases
confidence compared to a deterministic approach and the use of the lower 95 percent CI instead of a
fixed AF also increases confidence, as it is a more data-driven way of accounting for uncertainty. Two
of the three species with empirical hazard data were exposed to 1,2-dichloropropane rather than 1,1-
dichloroethane. Although EPA concludes that 1,2-dichloropropane is a robust analog for the
environmental hazard read-across to 1,1-dichloroethane, the use of an analog still affects the physical
and chemical relevance of the hazard confidence; therefore, a moderate confidence was assigned to the
relevance consideration for the acute aquatic assessment (Table 4-17).
For the acute benthic assessment, mortality predictions were observed in thirteen benthic invertebrates,
including representative test species such as Lumbriculus variegatus and Gammarus fasciatus. As stated
above, the use of the lower 95 percent CI of a probabilistically-derived hazard value instead of a fixed
AF is a more data-driven way of accounting for uncertainty and increases confidence. The predictions
were based in part on empirical analog data (1,2-dichloropropane), therefore a moderate confidence was
assigned to the relevance consideration for the acute benthic assessment (Table 4-17).
For the chronic aquatic assessment, ecologically relevant population level effects (reproductive, growth,
mortality) were observed in two different species (Daphnia magna and fathead minnow), both of which
are considered representative test species for aquatic toxicity tests. Although the Daphnia magna study
utilized semi-static renewal, chemical measurements were obtained, and the fathead minnow study
utilized flow-through conditions which is environmentally relevant for chronic exposure. In the case of
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14242
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14247
14248
14249
14250
14251
14252
14253
14254
14255
14256
14257
14258
14259
14260
14261
14262
14263
14264
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the study on which the chronic aquatic threshold was based, the exposure was to 1,1-dichloroethane.
Therefore, robust confidence was assigned to the relevance consideration for the chronic aquatic
assessment.
For the chronic benthic assessment, an ecologically relevant population level effect (emergence) was
observed in a representative species (Chironomus riparius) for benthic toxicity tests whereas
Ophryotrocha labronica, a marine annelid, is less represented in the literature as a test species.
Regarding physical and chemical relevance, the exposure was to 1,1,2-trichloroethane rather than 1,1-
dichloroethane even though EPA concludes that 1,1,2-trichloroethane is an appropriate analog for
environmental hazard read-across to 1,1-dichloroethane. Regarding environmental relevance, in the
study exposing C. riparius, the test was conducted with sediment present in the system which is
environmentally relevant for benthic exposure; however, the chemical exposure was administered at the
beginning of each sediment exposure phase with 1,1,2-trichloroethane concentrations in sediment and
benthic pore water significantly decreasing over the duration of the exposure phase (therefore not truly
representative of chronic exposure in the benthic environment). The second study exposed O. labronica
to 1,1,2-trichloroethane in aqueous conditions without sediment present in the system. Therefore, slight
confidence is assigned to relevance.
For the algal assessment, similar effects were observed in two different species (a marine diatom and a
green algae species), both of which are considered representative test species for algal toxicity tests, and
the testing likely encompassed several generations of algae; however, a definitive approach was utilized
with an AF of 10 to account for uncertainty when applying results from these two species to all algal
species. The algal testing took place in aqueous growth medium which is considered environmentally
relevant but was conducted with 1,2-dichloropropane rather than 1,1-dichloroethane. Therefore, a
moderate confidence was assigned to the relevance consideration for the algal assessment (Table 4-17).
Regarding biological relevance and physical/chemical relevance for the terrestrial mammalian
assessment, ecologically relevant population-level effects include behavior, growth, and mortality, and
these data were on 1,1-dichloroethane. The TRV was established using a mortality endpoint in female
mice; which is considered an ecologically relevant apical effect in mammalian receptors. It should be
noted that two of the studies utilized gavage administration which could be considered less
environmentally relevant than other methods of administration such as via drinking water or feed.
Nevertheless, moderate confidence was assigned to the relevance consideration for the terrestrial
mammal assessment (Table 4-17).
The ecologically relevant population level effects in the terrestrial plant assessment include lack of
growth (zero-growth) and reduced transpiration (which would be a proxy for reduced
growth/development even though the endpoint is reported as respiratory) and the testing was performed
with 1,1-dichloroethane. However, testing was performed in a single species in growth medium which
could be considered less environmentally relevant than tests conducted in soil. Therefore, a slight
confidence was assigned to the relevance consideration for the terrestrial plant assessment (Table 4-17).
Hazard Confidence
Due to the robust confidence in quality of the database, consistency, strength and precision, and
biological response, an overall hazard confidence rating of robust was assigned to the acute aquatic
assessment (Table 4-17). As a result of moderate confidence in all considerations, an overall hazard
confidence rating of moderate was assigned to the acute benthic assessment. Due to the robustness in
strength and precision, observed dose-response, and relevance, a robust confidence was assigned to the
chronic aquatic assessment. Because of the moderate confidence in quality of the database and
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14280 consistency, a moderate confidence was assigned to the chronic benthic assessment. Due to the moderate
14281 confidence in the number of studies, consistency, and relevance, an overall hazard confidence rating of
14282 moderate was assigned to the algal assessment (Table 4-17). Owing to the moderate confidence in
14283 number of studies, consistency, and strength and magnitude of effect, an overall hazard confidence of
14284 moderate was assigned to the terrestrial mammalian assessment. Due to the slight confidence in number
14285 of studies, consistency, and relevance, an overall hazard confidence of slight was assigned to the
14286 terrestrial plant assessment (Table 4-17). Indeterminate ratings were assigned to the confidence for the
14287 avian and soil invertebrate assessments due to lack of reasonably available data.
14288
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14289 Appendix L ENVIRONMENTAL RISK DETAILS
14290 L.l Risk Estimation for Aquatic Receptors
14291 Details described in Section 4.3.1.
14292 L.2 Risk Estimation for Terrestrial Receptors
14293 Details described in Section 4.3.1.
14294
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14295 L.3 Trophic Transfer Analysis Results
14296 TableApx L-l. Risk Quotients for Screening Level Trophic Transfer of 1,1-Dichloroethane ^at Could Result from Air Deposition
14297 (1,1-Dichloroethane Releases Reported to TRI) in Insectivorous Terrestrial Ecosystems Using EPA's Wildlife Risk Model for Eco-
14298 SSLs
COU (Life Cycle
Stage/Category/Subcategory)
OES
Earthworm
Concentration
(mg/kgr
TRV
(mg/kg-bw/day)b
Short-tailed shrew
(Marina brevicaucla)
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day)c
RQ
Manufacture/Domestic
Manufacturing/Domestic manufacturing
Manufacturing
7.0E-03
1,189
4.6E-03
3.9E-06
Processing/As a reactant/Intermediate in all
other basic organic chemical manufacture
Processing as a reactive
Intermediate
0.38
1,189
0.25
2.1E-04
Processing/As a Reactant/Intermediate in
all other chemical product and preparation
manufacturing
Disposal/Disposal/Disposal
General waste handling,
treatment, and disposal
1.1E-03
1,189
6.9E-04
5.8E-07
11 Estimated 1,1-dichloroethane concentration in representative soil invertebrate, earthworm, assumed equal to aggregated highest calculated soil and soil pore
water concentration via air deposition to soil for fugitive air releases of 1,1-dichloroethane reported to TRI.
'' Mammal 1,1-dichloroethane TRV value calculated using several studies as per (U.S. EPA. 2007).
c Dietary exposure to 1,1-dichloroethane includes consumption of biota (earthworm), incidental ingestion of soil, and ingestion of water.
14299
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14300 TableApx L-2. Risk Quotients for Screening Level Trophic Transfer of 1,1-Dichloroethane Which Could Result from Air Deposition
14301 (1,1-Dichloroethane Releases Reported to TRI) in Herbivorous Terrestrial Ecosystems Using EPA's Wildlife Risk Model for Eco-
14302 SSLs
COU (Life Cycle
Stage/Category/Subcategory)
OES
Plant
Concentration
(mg/kg)"
TRV
(mg/kg-bw/day)b
Meadow Vole
(Microtus pennsylvanicus)
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day)c
RQ
Manufacture/Domestic
Manufacturing/Domestic manufacturing
Manufacturing
2.7E-03
1,189
1.5E-03
1.3E-06
Processing/As a reactant/Intermediate in all
other basic organic chemical manufacture
Processing as a reactive
intermediate
0.15
1,189
8.2E-02
6.9E-05
Processing/As a Reactant/Intermediate in
all other chemical product and preparation
manufacturing
Disposal/Disposal/Disposal
General waste handling,
treatment, and disposal
4.0E-04
1,189
2.3E-04
1.9E-07
11 Estimated 1,1-dichloroethane concentration in representative terrestrial plant Trifolium sp., assumed equal to the highest calculated soil pore water
concentration via air deposition to soil for fugitive air releases of 1,1-dichloroethane reported to TRI.
'' Mammal 1,1-dichloroethane TRV value calculated using several studies as per (U.S. EPA. 2007).
c Dietary exposure to 1,1-dichloroethane includes consumption of biota (Trifolium sp.), incidental ingestion of soil, and ingestion of water.
14303
14304
14305
14306
14307
14308
14309
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TableApx L-3. Risk Quotients Based on Potential Trophic Transfer of 1,1-Dichloroethane from Fish to American Mink (Mustela
vison) as a Model Aquatic Predator Using EPA's Wildlife Risk JV
odel for Eco-SSLs
COU (Life Cycle
Stage/Category/Subcategory)
OES
SWC
(^g/L)"
Fish
Concentration
(mg/kg)
TRV
(mg/kg-
bw/day)6
American Mink
(Mustela vison)
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day)c
RQ
Manufacture/Domestic
Manufacturing/Domestic manufacturing
Manufacturing
85
0.59
1,189
0.14
1.2E-04
Processing/As a reactant/ Intermediate in
all other basic organic chemical
manufacture
Processing as a reactive
intermediate
13
9.0E-02
1,189
2.1E-02
1.8E-05
Processing/As a Reactant/Intermediate in
all other chemical product and preparation
manufacturing
Processing/Processing -
repackaging/Processing - repackaging
Processing - repackaging
0.7
4.9E-03
1,189
1.2E-03
9.7E-07
Commercial Use/Other use/Laboratory
chemicals
Commercial use as a
laboratory chemical
0.64
4.5E-03
1,189
1.0E-03
8.8E-07
Disposal/Disposal/Disposal
General waste handling,
treatment, and disposal
12
8.7E-02
1,189
2.0E-02
1.7E-05
Disposal/Disposal/Disposal
Waste handling, treatment,
and disposal (POTW)
8.2
5.7E-02
1,189
1.3E-02
1.1E-05
Disposal/Disposal/Disposal
Waste handling, treatment,
and disposal (Remediation)
31
0.21
1,189
5.0E-02
4.2E-05
11 1,1-Dichloroethane concentration represents the highest modeled surface water concentration via PSC modeling.
'' Mammal 1.1-dichloroethane TRV value calculated using several studies as per (U.S. EPA. 2007).
c Dietary exposure to 1,1-dichloroethane includes consumption of biota (fish), incidental ingestion of sediment, and ingestion of water.
d Distribution in Commerce does not result in surface water releases (Table 3-6).
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14313 TableApx L-4. Highest Risk Quotients Based on Potential Trophic Transfer of 1,1-Dichloroethane from Crayfish to American Mink
Mustela vison) as a Model Aquatic Predator Using EPA's Wildlife Risk
Model for Eco-SSLs
COU (Life Cycle
Stage/Category/Subcategory)
OES
Benthic
Pore
Water
(^g/L)"
Crayfish
Concentration
(mg/kg)
TRV
(mg/kg-bw/day) b
American Mink
(Mustela vison)
1,1-Dichloroethane
Dietary Exposure
(mg/kg/day)c
RQ
Manufacture/Domestic
Manufacturing/Domestic manufacturing
Manufacturing
78
0.55
1,189
0.13
1.1E-04
Processing/As a reactant/ Intermediate in
all other basic organic chemical
manufacture
Processing as a reactive
intermediate
12
8.7E-02
1,189
2.0E-02
1.7E-05
Processing/As a Reactant/Intermediate in
all other chemical product and
preparation manufacturing
Processing/Processing -
repackaging/Processing - repackaging
Processing - repackaging
6.1E-01
4.3E-03
1,189
1.0E-03
8.5E-07
Commercial Use/Other use/Laboratory
chemicals
Commercial use as a
laboratory chemical
5.5E-01
3.8E-03
1,189
9.1E-04
7.6E-07
Disposal/Disposal/Disposal
General waste handling,
treatment, and disposal
12
8.3E-02
1,189
1.9E-02
1.6E-05
Disposal/Disposal/Disposal
Waste handling, treatment,
and disposal (POTW)
7.9
5.5E-02
1,189
1.3E-02
1.1E-05
Disposal/Disposal/Disposal
Waste handling, treatment,
and disposal (remediation)
29
0.21
1,189
4.8E-02
4.1E-05
Distribution in Commerce/Distribution in
commerce/Distribution in commerce
Distribution in commerce
N/A'#
11 1,1-Dichloroethane concentration represents the highest modeled benthic pore water concentration via PSC modeling.
'' Mammal 1.1-dichloroethane TRV value calculated using several studies as ocr (U.S. EPA. 2007).
c Dietary exposure to 1,1-dichloroethane includes consumption of biota (crayfish), incidental ingestion of sediment, and ingestion of water.
d Distribution in Commerce does not result in surface water releases (Table 3-6).
14315
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14325
14326
14327
14328
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14333
14334
14335
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14341
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Appendix M HUMAN HEALTH HAZARD DETAILS
This appendix provides details on the human health hazard assessment for 1,1-dichloroethane and the
identified analog 1,2-dichloroethane. Human health hazard data for 1,2-dichloroethane were used to fill
data gaps for 1,1-dichloroethane. Appendix M.l provides a summary of toxicokinetics for both 1,1-
dichloroethane and 1,2-dichloroethane. Appendix M.2 provides a non-cancer dose response assessment
for both chemicals. Appendix M.3 provides the equations used in derivation of non-cancer and cancer
PODs for the 1,1-dichloroethane risk assessment. Appendix M.4 describes the non-cancer POD
derivation for acute, short/intermediate-term, and chronic durations. Appendix M.5 provides evidence
integration tables for 1,1-dichloroethane. Appendix M.6 provides evidence integration tables for 1,2-
dichloroethane. Appendix M.7 describes evidence for mutagenicity and cancer for both chemicals.
Lastly, Appendix M.8 provides a cancer dose-response assessment for 1,1-dichloroethane using data for
1,2-dichloroethane as read-across.
M.l Toxicokinetics
M.1.1 Absorption
M.l.1.1 1,1-Dichloroethane
Oral
Oral absorption of 1,1-dichloroethane was demonstrated by the detection of radiolabel in expired air,
excreta, and body carcass following gavage administration of 700 mg/kg-bw/day 1,1-dichloroethane
(unlabeled) via gavage 5 days/week for 4 weeks followed by a single dose of 700 mg/kg 14C-1,1-
dichloroethane in rats or 1,800 mg/kg-bw/day 1,1-dichloroethane (unlabeled) via gavage 5 days/week
for 4 weeks followed by a single dose of 1,800 mg/kg 14C-1,1-dichloroethane in mice (Mitoma et al..
1985). Within 48 hours in rats, 91 percent of the administered dose was eliminated in expired air (86
percent unchanged, 5 percent as CO2). Less than 1 percent of the radiolabel was detected in urine and
feces of rats and 1 percent was detected in carcass. In mice, 95 percent of the administered dose was
eliminated in expired air (70 percent unchanged, 25 percent as CO2) within 48 hours. Less than 2
percent of the radiolabel was detected in urine and feces of mice, and 2 percent was detected in carcass
(Mitoma et al.. 1985).
Inhalation
Previous use of 1,1-dichloroethane as a gaseous anesthetic in humans provides evidence of systemic
absorption by the inhalation route (ATSDR. 2015). EPA did not identify any in vivo animal data
evaluating the absorption of 1,1-dichloroethane by the inhalation route of exposure. The blood:air
coefficient for 1,1-dichloroethane (4.94 ± 0.24 in humans and 11.2 ± 0.1 in rats) suggests that
pulmonary absorption is likely to occur (Gargas and Andersen. 1989).
Dermal
Qualitative evidence of dermal absorption was provided by a rabbit study that detected halogen ion in
exhaled breath following application of 1,1-dichloroethane to shaved abdominal skin (ATSDR. 2015).
No data were located on the rate and extent of 1,1-dichloroethane absorption through the skin.
M.l.1.2 1,2-Dichloroethane
Oral
Oral absorption of 1,2-dichloroethane in humans is suggested by case reports of intentional or accidental
ingestion resulting in systemic health effects including death (ATSDR. 2022). Experimental animal
studies indicate that oral absorption is rapid and complete (Reitz et al 1982. 1980. Spreafico et al. 1980
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14366
14367
14368
14369
14370
14371
14372
14373
14374
14375
14376
14377
14378
14379
14380
14381
14382
14383
14384
14385
14386
14387
14388
14389
14390
14391
14392
14393
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14395
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as cited in Reitz et al 1982. 1980. Spreafico et al. 1980 as cited in ATSDR. 2022). In rats given a single
gavage dose of 150 mg/kg in corn oil, peak blood concentrations were reached within 15 minutes and
approximately 94 percent of the administered dose was absorbed within 48 hours (Reitz et al. 1982.
1980 as cited in Reitz et al. 1982. 1980 as cited in ATSDR. 2022). Spreafico et al. (1980 as cited in 1980
as cited in AT SDR. 2022) also demonstrated rapid oral absorption, with peak blood levels occurring
between 30 and 60 minutes in rats given gavage doses of 25, 50, or 100 mg/kg in corn oil. Examination
of the peak blood level curves at the different doses shows a linear curve up to 50 mg/kg 1,2-
dichloroethane and a decrease in steepness of the curve at 100 mg/kg, suggesting a relative saturation of
oral absorption at doses exceeding 100 mg/kg. In rats given a single gavage dose of 100 mg/kg 1,2-
dichloroethane in corn oil or water, peak blood concentrations (Cmax) were approximately 4-fold higher
and the time to reach Cmax was 3-fold faster following administration in water compared to corn oil
(Withev et al. 1983 as cited in Withev et al. 1983 as cited in ATSDR. 2022). Similar findings regarding
the rate of absorption were observed in rats given gavage doses of 43 mg/kg/day in water or 150
mg/kg/day in corn oil (Cmaxvalues of 15 or 30 minutes, respectively) (Dow Chemical. 2006a).
Inhalation
1,2-dichloroethane was detected in the breast milk of nursing women exposed to 16 ppm in workplace
air (with concurrent dermal exposure) (Ursova 1953 as cited in Ursova 1953 as cited in ATSDR. 2022).
A fatal case report of exposure to 1,2-dichloroethane in an enclosed space for 30 minutes provides
further support for absorption through the lungs (Nouchi et al. 1984 as cited in Nouchi et al. 1984 as
cited in ATSDR. 2022). Absorption by inhalation was rapid, with steady-state Cmax concentrations
measured 1-3 hours after the onset of exposure to 150-250 ppm in rats (Reitz et al. 1982, 1980,
Spreafico et al. 1980 as cited in Reitz et al. 1982, 1980, Spreafico et al. 1980 as cited in ATSDR. 2022;
Dow Chemical. 2006a) or 25 to 185 ppm in mice (Zhong et al.. 2022). In rats exposed to 150 ppm 14C-
1,2-dichloroethane for 6 hours, approximately 93 percent absorption occurred, based on recovery of
radiolabel in urine and feces and as CO2 in expired air by 48 hours (Reitz et al. 1982 as cited in Reitz et
al. 1982 as cited in ATSDR. 2022). The blood:air coefficients for 1,2-dichloroethane (19.5 ± 0.7 in
humans and 30.4 ± 1.2 in rats) also suggest that pulmonary absorption is likely to occur (Gargas et al.
1989 as cited in Gargas et al. 1989 as cited in ATSDR. 2022).
Dermal
In vivo animal studies have demonstrated that 1,2-dichloroethane is readily absorbed through the skin
(Jakobson et al. 1982, Tsuruta et al. 1982 as cited in Jakobson et al. 1982, Tsuruta et al. 1982 as cited in
ATSDR. 2022; Morgan et al.. 1991). Application of neat 1,2-dichloroethane to the shaved and abraded
skin of rats using covered dermal cells resulted in approximately 50 percent absorption of the applied
dose with the peak blood level measured at 24 hours (Morgan et al.. 1991). Dermal absorption was faster
and more complete for aqueous solutions of 1,2-dichloroethane, with peak blood levels measured within
1 to 2 hours and greater than 99 percent of the applied dose absorbed within the 24-hour exposure period
(Morgan et al.. 1991). In guinea pigs dermally exposed to neat 1,2-dichloroethane, using a covered
dermal cell on clipped intact skin, blood concentrations rose rapidly during the first 30 minutes and
continued to increase over a 12-hour period (Jakobson et al. 1982 as cited in Jakobson et al. 1982 as
cited in ATSDR. 2022). Tsuruta (1975 as cited in 1975 as cited in ATSDR. 2022) estimated a
percutaneous absorption rate of 480 nmol/minute/cm2 for 1,2-dichloroethane through the clipped, intact
abdominal skin of mice following a 15-minute exposure using a closed dermal cell.
In Vitro
In vitro studies using skin from humans, pigs, and guinea pigs have reported apparent partition
coefficients (Kp), steady-state flux (Jss) values, and lag time estimates {i.e., the time to achieve a steady-
state concentration) (see TableApx M-l). In human skin, 0.1 to 0.2 percent of the applied dose was
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14411
14412
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14414
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14417
14418
14419
14420
14421
14422
14423
14424
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absorbed over 24 hours, with the maximum flux occurring within 10 minutes of exposure (Gaiiar and
Kasting. 2014). Evaporation from the skin surface accounted for the majority of applied dose in this
study. The Kp and lag time values for 1,2-dichloroethane were similar for human and guinea pig skin
(Frasch and Barbero. 2009); however, the dermal permeability rate was lower in pig skin (decreased Kp
value; longer lag time) (Schenk et al.. 2018). In guinea pig skin, the flux was lower in saturated aqueous
solution compared to the undiluted test substance (Frasch et al.. 2007). This result appears to differ from
the in vivo study using abraded skin of rats, which showed a higher percent absorption for an aqueous
solution of 1,2-dichloroethane compared to a neat application (Morgan et al.. 1991).
Table Apx M-l. 1,2-Dichloroethane Partition Coefficients Steady State Estimates
Partition Coefficients (Kp) Steady-State Flux (Jss) Estimates from In Vitro Dermal Absorption Studies
Species
Test
Material(s)
KP
(cm/hour)
Jss
(jig/cm2-hour)
Lag Time
(minutes)
Reference
Human
Neat
ND
37-193'1
ND
Gaiiar and Kastina (2014)
Human
Guinea pig
Neat
Neat
0.259
0.259
ND
ND
6
6
Frasch and Barbero (2009)
Pig
Neat
1.9E-03
1,360
30.7
Schenk et al. (2018)
Guinea pig
Neat
Aqueous
ND
ND
6,280fe
1,076
ND
ND
Frasch et al. (2007)
"Range of Jss values for applied doses of 7.9, 15.8, 31.5, or 63.1 mg/cm2.
h Also reported a Jss value of 3,842 ng/cm2-hour from a different laboratory.
ND = not derived
M.1.2 Distribution
M.l.2.1 1,1-Dichloroethane
Oral, Inhalation, and Dermal
Distribution to the CNS is suggested by the previous use of 1,1-dichloroethane as a gaseous anesthetic in
humans (ATSDR. 2015). No experimental studies were located regarding distribution following oral,
inhalation, or dermal exposure to 1,1-dichloroethane.
Other Routes (Intraperitoneal Injection)
Radiolabeled 1,1-dichloroethane was detected as protein, DNA, and RNA adducts in the liver, kidney,
lung, and stomach, 22 hours after a single intraperitoneal injection of 1.2 mg/kg 14C-1,1-dichloroethane
in Wistar rats and BALB/c mice (Colacci et al.. 1985). No additional tissues were examined in this
study.
In Vitro
Tissue:air partition coefficients calculated using a vial equilibration method on tissues obtained from
male Fischer 344 rats suggest that 1,1-dichloroethane is likely distributed to highly perfused tissues (i.e.,
liver, muscle) and will accumulate in fat (Table Apx M-2) (Gargas and Andersen. 1989).
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Table Apx M-2.1,1-Dichloroethane Partition Coefficients
Species
Strain
Sex
Partition Coefficient
Blood/Air
Liver/Air
Muscle/Air
F at/Air
Rat
F344
Male
11.2 ±0.1
10.8 ±0.5
5.12 ±0.48
164 ±4
Source: Garaas and Andersen (1989)
M.l.2.2 1,2-Dichloroethane
Oral
Distribution was rapid following gavage dosing, with concentrations peaking first in the liver at 6-7
minutes, followed by lung at 10 to 20 minutes and adipose tissue at 20 to 60 minutes (MCA. 1979).
Tissue levels were dose-dependent and the highest peak tissue concentration at any dose was detected in
fat. Similar mean peak tissue levels in liver and lung were seen following 11 daily doses of 50 mg/kg,
indicating that bioaccumulation does not occur in these tissues with multiple doses. Bioaccumulation in
adipose tissue is suggested by higher peak adipose tissue levels after 11 gavage doses, compared to a
single gavage dose (Table_Apx M-3).
Table Apx M-3. Tissue Levels and Time to Peak Tissue Level in Rats Exposed to 1,2-
Dichloroethane by Gavage in Corn Oil
Organ/Peak Concentration/Time
to Peak Concentration
Dose (mg/kg)
25 (Single)
50 (Single)
50 (11 Oral Doses)
150 Single)
Liver
l-Lg/g
30.02 ±3.29
55.00 ±4.12
53.12 ± 3.87
92.10 ±7.58
Minutes
6
6
6
7.5
Lung
l-Lg/g
2.92 ±0.38
7.20 ±0.39
7.19 ±0.59
8.31 ± 1.27
Minutes
10
20
15
20
Adipose
l-Lg/g
110.67 ±6.98
148.92 ±20.75
161.69 ±9.93
259.88 ±25.03
Minutes
20
60
40
40
Source: (MCA. 1979)
In pregnant rats exposed to a single dose of 160 mg/kg 14C-l,2-dichloroethane on GD 12, the highest
tissue concentrations were found in the liver and intestine after 48 hours (radiolabel was also detected in
the stomach, kidney, and ovary) Pavan et al. (1995) as cited in ATSDR (2022). Distribution across the
placenta was demonstrated by detection of radiolabel in the developing fetus within 1 hour; the
maximum concentration was detected 4 hours after exposure Pavan et al. (1995) as cited in ATSDR
(2022). Administration of 160 mg/kg 14C-l,2-dichloroethane on GD 18 showed a greater degree of
accumulation in the developing fetuses and the placenta Pavan et al. (1995) as cited in ATSDR (2022).
Inhalation
1,2-dichloroethane was detected in breath (14.3 ppm) and breast milk (0.54-0.64 mg % [per 100 mL]) of
nursing mothers 1 hour after leaving an occupational facility with exposure concentrations of 15.6 ppm
1,2-dichloroethane Urusova (1953) as cited in ATSDR (2022). 1,2-Dichloroethane was readily
distributed in rats following a 6-hour inhalation exposure and tissue levels were concentration dependent
Spreafico et al. (1980) as cited in ATSDR (2022). Peak tissue levels in liver and lung were lower than
concentrations in blood, but adipose tissue levels were 8 to 9 times higher than blood levels Spreafico et
al. (1980) as cited in ATSDR (2022) (see Table_Apx M-4).
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TableApx M-4. Tissue Levels and Time to Peak Tissue Level in
Rats Exposed by Inhalation to 1,2-Dichloroethane for 6 Hours
Organ/Peak Concentration/
Time to Peak Concentration
Concentration
(ppm)
50
250
Blood
w?/g
1.37 ± 0.11
31.29 ± 1.19
Hours
6
6
Liver
w?/g
1.14 ± 0.17
22.49 ± 1.12
Hours
4
6
Lung
0.42 ±0.05
14.47 ± 1.12
Hours
4
3
Adipose
11.08 ±0.77
273.32 ± 12.46
Hours
4
6
Source: Soreafico et al. (1980) as cited in ATSDR (2022)
A similar study in male rats exposed to 160 ppm 1,2-dichloroethane for 6 hours showed the highest
tissue levels of 1,2-dichloroethane in abdominal fat Take et al. (2013) as cited in ATSDR (2022). In
pregnant rats exposed to 150 to 2,000 ppm 1,2-dichloroethane for 5 hours on GD 17, concentrations of
1,2-dichloroethane in maternal blood and fetal tissue increased linearly with exposure concentration,
indicating distribution across the placenta Withev and Karpinski (1985) as cited in ATSDR (2022).
Dermal
No studies were located regarding distribution following dermal exposure to 1,2-dichloroethane.
In Vitro
Tissue:air partition coefficients calculated using a vial equilibration method and tissues obtained from
male Fischer 344 rats suggest that 1,2-dichloroethane is preferentially distributed to highly perfused
tissues and will accumulate in fat (see following table) (Dow Chemical 2006a; Gargas and Andersen.
1989).
Table Apx M-5.1,2-Dichloroethane Tissue:Air Partition Coefficients
Partition Coefficient
Blood/Air
Liver/Air
Muscle/Air
Fat/Air
Brain/Air
Kidney/Air
Testis/Air
Ovary/Air
30.4 ± 1.2"
35.7 ± 1.6'1
23.4 ± 1.4"
344 ± 511
39.5 ±2.89fe
44.89 ±6.77fe
31.14 ± 7.98fe
74.59 ±9.82fe
11 Gar a as and Andersen (1989).
b Dow Chemical (2006a).
M.1.3 Metabolism
M.l.3.1 1,1-Dichloroethane
In Vitro
The metabolic pathways for 1,1-dichloroethane have been elucidated from in vitro studies using rat
hepatic microsomes (McCall et al.. 1983; Sato et al.. 1983; Van Dyke and Wineman. 1971) (see
FigureApx M-l). The primary metabolic pathway involves oxidation of the C-l carbon by CYP to give
an unstable alpha-haloalcohol followed by dechlorination to produce acetyl chloride and acetic acid,
which is the major metabolite. The alpha-haloalcohol may also undergo a chlorine shift to yield
chloroacetyl chloride and monochloroacetic acid, although this reaction is not favored. CYP oxidation at
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the C-2 position results in the formation of 2,2-dichloroethanol, dichloroacetaldehyde, and
dichloroacetic acid as minor metabolites. Metabolism of 1,1-dichloroethane was increased by induction
with phenobarbital and ethanol, but not P-naphthoflavone (McCall et al.. 1983; Sato et al.. 1983).
Similarly, enzymatic dechlorination was inducible by phenobarbital, but not 3-methylcholanthrene ("Van
Dyke and Wineman. 1971).
CI2HCCH3
P450 (C-2)
ci2hcch2oh
2,2-dichloroethanol
P450
(C-1)
[HOC^CCHJ
alpha-haloalcohol
chlorine
shift
[CICI-LCCI]
chloroacetyl
chloride
CI2HCCH
dichloroacetaldehyde
ci2hcc-oh
dichloroacetic acid
H20
-HCI
cich2coh
monochloroacetic
acid
-HCI H20
[CICCH3] ^ CH3COOH
I -HCI
O acetic
acetyl acid
chloride
FigureApx M-l. Proposed Metabolic Scheme for 1,1-Dichloroethane (McCall et al., 1983)
Oral
The extent of metabolism was evaluated in Osborne-Mendel rats and B6C3F1 mice administered 700 or
1,800 mg/kg-bw/day 1,1-dichloroethane, respectively, by gavage in corn oil 5 day/week for 4 weeks,
followed by a single dose of 14C-1,1-dichloroethane (Mitoma et al.. 1985). The total percentages of
administered dose found in exhaled CO2, excreta, and body carcass 48 hours after the administration of
the radiolabeled dose were 7.45 percent in rats and 29.3 percent in mice. It is possible that a portion of
the radioactivity detected in the urine, feces, and body carcass is present as parent 1,1-dichloroethane
and not downstream metabolites.
Inhalation
The metabolic rate constants for 1,1-dichloroethane were estimated for male Fischer 344 rats using a gas
uptake method (Gargas etal.. 1990) (Table Apx M-6). The rats were exposed to an initial concentration
of 90, 490, 1,100, or 2,175 ppm (360, 1,980, 4,500, or 8,804 mg/m3) and the disappearance of the gas
was studied for about 5 hours. A kinetic model that assumed metabolism occurred exclusively in the
liver was used to analyze the data. The metabolism of 1,1-dichloroethane was best described as a
saturable process.
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TableApx M-6. Estimates of Metabolic Parameters for 1,1-Dichloroethane Obtained from Gas
Uptake Experiments in Male F344 Rats
Y
maxc
Km
mg/hour*kg
jimol/hour
mg/L
HM
7.5
75.8
0.2
2.02
Vmaxc = maximum reaction velocity (scaled to 1 kg animal); Km = concentration at 'A Vmax (Michaelis
constant)
Source: Gareas et al. (1990)
Dermal
EPA did not identify in vivo animal data that evaluated metabolism of 1,1-dichloroethane by the dermal
route of exposure.
M.l.3.2 1,2-Dichloroethane
Oral Metabolism
In male rats exposed to a single oral dose of 150 mg/kg [14C]-l,2-dichloroethane, 60 percent of the
administered dose was detected as urinary metabolites and 29 percent was released unchanged in
expired air, suggesting that metabolic saturation occurred at this dose (Reitz et al. 1982 as cited in Reitz
et al. 1982 as cited in ATSDR. 2022). Although urinary metabolites were not characterized in this study,
a decrease in hepatic nonprotein sulfhydryl content suggests that the GSH conjugation pathway was
involved.
Inhalation Metabolism
Metabolism was near complete in rats exposed to 150 ppm of [14C]-l,2-dichloroethane for 6 hours, with
84 percent of radiolabel excreted as urinary metabolites and 2 percent released as unchanged compound
in expired air (Reitz et al. 1982 as cited in Reitz et al. 1982 as cited in ATSDR. 2022). Urinary
metabolites were not characterized; however, a decrease in the hepatic nonprotein sulfhydryl content
suggest involvement of the GSH conjugation pathway. In a rat inhalation study comparing blood
concentrations resulting from exposure to 50 or 250 ppm, peak blood levels of 1,2-dichloroethane were
22-fold higher at the higher concentration (Spreafico et al. 1980 as cited in Spreafico et al. 1980 as cited
in ATSDR. 2022). Taken together, these results suggest that metabolic saturation occurs at a
concentration between 150 and 250 ppm 1,2-dichloroethane, corresponding to blood levels of 5 to 10
|ig/mL (Reitz et al. 1988. Spreafico et al. 1980 as cited in Reitz et al. 1988. Spreafico et al. 1980 as cited
in AT SDR. 2022V
Dermal Metabolism
EPA did not identify in vivo animal data that evaluated metabolism of 1,2-dichloroethane following
exposure by the dermal route.
In Vivo and In Vitro Metabolism Studies
No human studies on the metabolism of 1,2-dichloroethane were located. The primary metabolic
pathways for 1,2-dichloroethane, elucidated from in vitro studies and in vivo studies in rats and mice,
include CYP oxidation and GSH conjugation (Figure Apx M-2) (NTP 1991 as cited inNTP 1991 as
cited in AT SDR. 2022). Metabolism by CYP results in an unstable gem-chlorohydrin that releases
hydrochloric acid, resulting in the formation of 2-chloroacetaldehyde. 2-Chloroacetaldehyde is oxidized
to form chloroacetic acid or reduced to form 2-chloroethanol, and these metabolites are conjugated with
GSH and excreted in the urine (Figure Apx M-l) (NTP 1991 as cited in NTP 1991 as cited in AT SDR.
2022). Metabolism via glutathione-S-transferase results in formation of S-(2-chloroethyl)-glutathione,
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which rearranges to form a reactive episulfonium ion. The episulfonium ion can form adducts with
protein, DNA or RNA or interact further with GSH to produce water soluble metabolites that are
excreted in the urine (Figure_Apx M-2) ( TP 1991 as cited in NTP 1991 as cited in ATSDR. 2022).
a A/"
O s.S' -Ethene bisgtuiathione
S-Cartjoxymethyl glutathione .
Figure Apx M-2. Proposed Metabolic Scheme for 1,2-Dichloroethane ( IPCS, 1995)
In Vitro Metabolism Studies
In vitro studies using rat and human liver microsomes have demonstrated that oxidative metabolism via
CYP2E1 results in the formation of 2-chloroacetaldehyde by dechlorination of an unstable chlorohydrin
molecule (Casciola and Ivaneticb 1984 as cited in Casciola and Ivanetich 1984 as cited in ATSDR,
2022; Guengerich et al.. 1991; McCall et al.. 1983; Guengerich et al.. 1980). GSH conjugation of 1,2-
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dichloroethane was demonstrated in primary rat hepatocytes resulting in the formation of
S-(2-hydroxyethyl) glutathione, S-(carboxymethyl) glutathione, and S,S'-(l,2-ethanediyl)bis-
(glutathione), and GSH depletion was observed (Jean and Reed. 1992). The S-(carboxymethyl)
glutathione metabolite likely results from conjugation of 2-chloroacetic acid with GSH (Johnson 1967 as
cited in Johnson 1967 as cited in ATSDR. 2022). This metabolite can be degraded to form glycine,
glutamic acid, and S-carboxymethylcysteine, which may be oxidized to yield thiodiglycolic acid (see
Figure_Apx M-2) (NTP 1991 as cited in NTP 1991 as cited in ATSDR. 2022). Metabolic rate constants
were determined using rat liver microsomes and substrate concentrations between 50 |iM and 1 mM
(V max — 0.24 nmol/minute per mg protein; Km = 0.14 mM) (Salmon et al.. 1981).
M.1.4 Elimination
M.l.4.1 1,1-Dichloroethane
Oral
The elimination pattern in rats exposed to 700 mg/kg-bw/day 1,1-dichloroethane (unlabeled) via gavage
5 days/week for 4 weeks followed by a single dose of 14C-1,1-dichloroethane was as follows: 86 percent
eliminated unchanged in expired air, 5 percent eliminated as CO2, and 0.9 percent in excreta (feces and
urine) at 48 hours (Mitoma et al.. 1985). The total recovery was 93 percent in rats, with 1.4 percent of
the administered dose remaining in the carcass. In mice exposed to 1800 mg/kg-bw/day 1,1-
dichloroethane (unlabeled) via gavage 5 days/week for 4 weeks followed by a single dose of 14C-1,1-
dichloroethane, 70 percent of the administered dose was eliminated unchanged in expired air, 25 percent
was eliminated as CO2 in expired air, and 1.6 percent was recovered in excreta (feces and urine) at 48
hours (Mitoma et al.. 1985). Total recovery in mice was 99 percent, with 2 percent remaining in the
carcass.
Oral Metabolism
In male rats exposed to a single oral dose of 150 mg/kg [14C]-l,2-dichloroethane, 60 percent of the
administered dose was detected as urinary metabolites and 29 percent was released unchanged in
expired air, suggesting that metabolic saturation occurred at this dose (Reitz et al. 1982 as cited in Reitz
et al. 1982 as cited in ATSDR. 2022). Although urinary metabolites were not characterized in this study,
a decrease in hepatic nonprotein sulfhydryl content suggests that the GSH conjugation pathway was
involved.
Inhalation
No in vivo animal data on elimination following exposure to 1,1-dichloroethane by the inhalation route
were identified.
Dermal
EPA did not identify in vivo animal data that evaluated elimination following exposure to 1,1-
dichloroethane by the dermal route.
EPA did not identify any PBPK models for 1,1-dichloroethane.
M.l.4.2 1,2-Dichloroethane
Oral
1,2-dichloroethane was rapidly eliminated following oral exposure, primarily via urinary excretion of
water-soluble metabolites and exhalation of unchanged compound or CO2 (Payan et al. 1993. Mitoma et
al. 1985. Reitz et al. 1982 as cited in Pavan et al. 1993. Mitoma et al. 1985. Reitz et al. 1982 as cited in
ATSDR. 2022). In rats given a single gavage dose of 150 mg/kg [14C]-l,2-dichloroethane, elimination
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was 96 percent complete within 48 hours, with 60 percent of the radiolabel excreted as urinary
metabolites (70 percent thiodiacetic acid, 26-28 percent thiodiacetic acid sulfoxide), 29 percent exhaled
as unchanged 1,2-dichloroethane, 5 percent exhaled as CO2, and the remaining 6 percent recovered in
feces, carcass, and cage washes (Reitz et al. 1982 as cited in Reitz et al. 1982 as cited in ATSDR. 2022).
The elimination kinetics were described as biphasic with an initial elimination half4ife (t1^) of
90 minutes, followed by a W2 of approximately 20 to 30 minutes when blood levels were 5 to 10 |ag/m L
(Reitz et al. 1982 as cited in Reitz et al. 1982 as cited in ATSDR. 2022).
In rats and mice given gavage doses of 100 and 150 mg/kg [14C]-1,2-dichloroethane, respectively,
following pretreatment with unlabeled 1,2-dichloroethane 5 days/week for 4 weeks, recovery of
radiolabel in excreta (urine and feces) was 69.5 percent in rats and 81.9 percent in mice after 48 hours
(Mitoma et al. 1985 as cited in Mitoma et al. 1985 as cited in ATSDR. 2022). Exhalation of volatile
compounds and CO2 accounted for 11.5 and 8.2 percent, respectively, in rats and 7.7 and 18.2 percent,
respectively, in mice. The recovery of radiolabel in the carcass was 7 percent of the administered dose in
rats and 2.4 percent of administered dose in mice (Mitoma et al. 1985 as cited in Mitoma et al. 1985 as
cited in AT SDR. 2022).
The excretion of thioglycolic acid and other thioether metabolites was measured in rat urine 24 hours
after gavage administration of 0.25, 0.5, 2.02, 4.04, or 8.08 mmol/kg (25, 50, 200, 400, or 800 mg/kg)
[14C]-l,2-dichloroethane (Pavan et al. 1993 as cited in Pavan et al. 1993 as cited in ATSDR. 2022). The
total concentration of urinary metabolites increased linearly with administered doses between 25 and
400 mg/kg; however, the percentage of the administered dose excreted in the urine decreased with
increasing dose level, likely due to metabolic saturation (ranging from 63 to 7.4%) (Pavan et al. 1993 as
cited in Pavan et al. 1993 as cited in ATSDR. 2022).
Inhalation
1,2-dichloroethane was detected in expired air of women occupationally exposed to 15.6 ppm by
inhalation (Ursova 1953 as cited in Ursova 1953 as cited in ATSDR. 2022). Similar findings were noted
in women exposed by dermal contact only (Ursova 1953 as cited in Ursova 1953 as cited in ATSDR.
2022). In rats exposed via inhalation, elimination occurred by excretion of metabolites in urine and
exhalation of unchanged compound or CO2 (Reitz et al. 1982. Spreafico et al. 1980 as cited in Reitz et
al. 1982. Spreafico et al. 1980 as cited in ATSDR. 2022). Following inhalation of 150 ppm [14C]-1,2-
dichloroethane for 6 hours, elimination from the blood was near complete by 48 hours, with 84 percent
of the dose detected as urinary metabolites (70% thiodiacetic acid, 26-28% thiodiacetic acid sulfoxide),
2 percent excreted unchanged in feces, and 7% exhaled as CO2 (Reitz et al. 1982 as cited in Reitz et al.
1982 as cited in ATSDR. 2022). The elimination kinetics of 1,2-dichloroethane in rats were described as
monophasic with XV2 values of 12.7 and 22 minutes at inhalation concentrations of 25 and 250 ppm 1,2-
dichloroethane, respectively (Spreafico et al. 1980 as cited in Spreafico et al. 1980 as cited in ATSDR.
2022). Excretion was dose-dependent, with the percentage exhaled as unchanged 1,2-dichloroethane
increased at the highest concentration; elimination from adipose tissue was slower than elimination from
blood, liver, or lung (Spreafico et al. 1980 as cited in Spreafico et al. 1980 as cited in ATSDR. 2022).
In mice exposed to 25, 87, or 185 ppm 1,2-dichloroethane for 6 hours, elimination was rapid, with
clearance of parent compound from the blood near complete within 1 hour after exposure (Zhong et al..
2022; Liang et al.. 2021). In a 28-day study using the same concentrations for 6 hours/day, 5 days/week,
2-chloroacetic acid was detected as the primary metabolite in urine at concentrations of 300, 1,000, and
1,300 |ig/L, respectively (Zhong et al.. 2022; Liang et al.. 2021).
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Dermal
1,2-dichloroethane was detected in expired air of women occupationally exposed by dermal contact only
(gas masks were worn to prevent inhalation) (TJrsova 1953 as cited in Ursova 1953 as cited in ATSDR.
2022).
Physiologically-Based Pharmacokinetic (PBPK) Modeling Approach
Two PBPK models were developed to describe the disposition of 1,2-dichloroethane. The D'Souza et al.
(1988. 1987 as cited in 1988. 1987 as cited in ATSDR. 2022) model used five compartments (lung,
liver, richly perfused tissues, slowly perfused tissues, and fat) and assumed that metabolism occurs only
in the liver and lung. Metabolic pathways included a saturable oxidation pathway and GSH conjugation.
This PBPK model, which was validated in rats and mice, predicted that inhalation produces less GSH-
conjugate metabolites (measured as GSH depletion in the liver) than gavage exposure.
Sweeney et al. (2008 as cited in 2008 as cited in ATSDR. 2022) extended and updated the D'Souza et al.
(1988. 1987 as cited in 1988. 1987 as cited in ATSDR. 2022) model by adding two gastrointestinal
compartments, a compartment for the kidney, and an additional metabolism pathway for extrahepatic
enzymes. Model parameter values that were revised included the oral absorption rate, time delay
constant for GSH synthesis following depletion, and GSH levels in liver and lung. Model predictions
were compared to experimental rat data for intravenous, oral, and inhalation routes, and the model
performed well for single and repeated exposure. Because the model has not been validated in humans,
it is unclear whether this model would be useful for extrapolating between rats and humans (ATSDR.
2022).
M.2 Non-cancer Dose-Response Assessment
Sections M.2.1 and M.2.2 describe dose-response assessment for 1,1-dichloroethane and 1,2-
dichloroethane, respectively. Sections M.2.3, M.2.4, and M.2.5 describe the non-cancer POD derivation
for acute, short/intermediate-term, and chronic durations for 1,1-dichloroethane. Sections M.2.6, M.2.7,
and M.2.8 describe the non-cancer POD derivation for acute, short-term/intermediate-term, and chronic
durations for 1,2-dichloroethane. Section M.3 provides the equations used in derivation of non-cancer
and cancer PODs for the Draft 1,1-Dichloroethane Risk Assessment. Finally, Section M.4 provides a
summary of the non-cancer PODs selected for use in the draft risk assessment for 1,1-dichloroethane
based on read-across from 1,2-dichloroethane, including PODs for both continuous and occupational
exposure scenarios.
M.2.1 Non-cancer Dose-Response Assessment for 1,1-Dichloroethane
EPA evaluated data from studies with adequate quantitative information and sufficient sensitivity as
described in Sections 5.2.3.1.2 and 5.2.7.1. In order to characterize the dose-response relationships of
1,1-dichloroethane. The database for 1,1-dichloroethane toxicity in animals is very limited and many of
the available studies were rated Unacceptable/Uninformative. Table Apx M-7 shows the studies that
were excluded from consideration for dose-response assessment along with the reason for excluding
each.
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14709
14710
14711
14712
14713
14714
14715
14716
14717
14718
14719
14720
14721
14722
14723
14724
14725
14726
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Table Apx M-7. Studies Not Considered Suitable for POPs for 1,1-Dichloroethane
Reference
Study Rating
Reason Not Suitable for POD
Dow Chemical (1947)
Unacceptable
Rating
Plaa and Larson (1965)
Unacceptable
Rating
Mellon Institute (1947)
Unacceptable
Rating
Hofmann et al. (1971a)
Unacceptable
Rating
Vozovaia (1977)
Unacceptable
Rating
NCI (1978): Rat
Unacceptable
Rating
Weisbureer (1977)
Unacceptable
Ratine; reports same data as NCI (1978)
Storv et al. (1986)
Medium
Reports same data as Milman et al. (1988)
Zabrodskii et al. (2004)
Medium
Tested chemical is uncertain (reported only as
dichloroethane)
Natsvuk and Chekman (1975)
Low
Tested chemical is uncertain (reported only as
dichloroethane)
Natsvuk and Fedurov (1974)
Unacceptable
Rating; tested chemical is uncertain (reported only as
dichloroethane)
In addition to the studies above, the study by Milman et al. (1988) was excluded from consideration.
Milman et al. (1988) examined GGT+ foci in the liver in rats exposed to 1,1-dichloroethane in four
separate experiments. In the initiation experiments, the rats were exposed once to 1,1-dichloroethane 1
day after a 2/3 partial hepatectomy, and then were either treated with phenobarbital or no phenobarbital
for 7 weeks. 1,1-Dichloroethane did not increase the number of GGT+ foci under either condition. In the
promotion experiments, the rats were pretreated (intraperitoneal) with diethylnitrosamine or water 1 day
after 2/3 partial hepatectomy; 6 days later, the rats were given 1,1-dichloroethane by gavage 5
days/week for 7 weeks. In animals pretreated with diethylnitrosamine, there was a significantly
increased number of GGT+ liver foci. In animals pretreated with water followed by 1,1-dichloroethane,
the number of foci was higher than in controls, but the number was not statistically significantly
different from control. Other non-cancer endpoints examined in the study were body weight and liver
weight; no statistically significant effects were observed in any of the experiments with 1,1-
dichloroethane. Milman et al. (1988) was not considered suitable for POD identification for 1,1-
dichloroethane because (1) all animals in all experiments were partially hepatectomized prior to
treatment, and (2) the only statistically significant effect (increased GGT+ foci) was seen in animals that
were pretreated with diethylnitrosamine.
Excluding the study by Milman et al. (1988). as well and those provided in TableApx M-7, leaves the
studies shown in Table Apx M-8 for potential use in POD derivation.
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14729
14730
14731
14732
14733
14734
14735
14736
14737
14738
14739
14740
14741
14742
14743
14744
14745
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TableApx M-8. Summary of Studies Considered for Non-cancer Dose-Response Assessment of
1,1-Dichloroethane
Reference
Duration Category
(Duration)
Species, Strain, and Sex
Study Rating for
Non-cancer Endpoints
Oral
Dow Chemical (1947)
Acute (once)
Guinea pig
Low
Muralidhara et al.
(2001)
Acute (once)
Rat (Sprague-Dawley, male)
Medium
Muralidhara et al.
(2001)
Short/intermediate -
term (10 days)
Rat (Sprague-Dawley, male)
High
Ghanavem et al. (1986)
Short/intermediate -
term (2 weeks)
Rat (F344, male)
Medium
Muralidhara et al.
(2001)
Short/intermediate -
term (13 weeks)
Rat (Sprague-Dawley, male)
High
Klaunie et al. (1986)
Chronic (52 weeks)
Mouse (B6C3F1, male)
High
NCI (1978)
Chronic (78 weeks)
Mouse (B6C3F1, male and
female)
High
Inhalation
Schwetz et al. (1974)
Short/intermediate -
term (10 days)
Rat (Sprague-Dawley,
female)
Medium-High
Mellon Institute (1947)
Chronic (26 weeks)
Dog, mongrel
Medium
Hofmann et al. (1971a)
Chronic (26 weeks)
Rat, guinea pig, rabbit
Medium
Dermal
No data
No dermal exposure studies received acceptable ratings. Due to the extremely small number of available
studies, limited evaluations performed in many studies, and paucity of information available to identify
target organs for 1,1-dichloroethane, overall NOAELs and LOAELs were identified for each study,
rather than identifying NOAELs and LOAELs by organ/system. Table Apx M-9 and Table Apx M-10
summarize the NOAELs and LOAELs identified from the oral and inhalation studies, respectively. Each
NOAEL and LOAEL was converted to reflect continuous exposure (NOAELCOntinuous and
LOAELcontinuous) using EquationApx M-4 and EquationApx M-5. After adjustment for continuous
exposure, each oral NOAEL and LOAEL was converted to a HED using Equation Apx M-6 and each
inhalation NOAEL and LOAEL was converted to a HEC using Equation Apx M-8. Dose-response
considerations for these studies are briefly described below. Benchmark dose (BMD) modeling results
are provided in Draft Risk Evaluation for 1,1-Dichloroethane - Supplemental Information File:
Benchmark Dose Modeling (U.S. EPA. 2024c).
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Table Apx M-9. Summary of Candidate Non-cancer Oral POPs for 1,1-Dichloroethane
Species (Strain,
Sex, n/Group)
Exposure
NOAEL
(mg/kg-bw/day)
LOAEL
(mg/kg-bw/day)
Effect(s)
Candidate POD
(mg/kg-bw/day)
(POD type)
Reference
Study Rating for Non-
cancer (Significant
Limitations)
Acute
Guinea pig
(strain, sex, and
number/group not
specified)
Once ("fed")
NOAEL: 300
NOAELcontmuous: 300
NOAELhed: 81
LOAEL: 1,000
LOAELcontinuous. 1,000
LOAEL hed: 271
100% mortality
81
(NOAELhed)
Dow
Chemical
(1947)
Low (no control; strain,
sex, number/group,
method of
administration, and
duration of follow-up
not reported)
Rat (Sprague-
Dawley,
8 males/group)
Once
(gavage)
NOAEL: 1000
NOAELcontmuous: 1000
NOAELhed: 240
LOAEL: 2000
LOAELcontinuous: 2,000
LOAELhed: 480
Sedation
240
(NOAELhed)
Muralidhara
et al. ("20011
Medium (evaluated
only clinical signs and
mortality)
Short/intermediate-term
Rat (Sprague-
Dawley,
24 males/group)
10 days
(gavage)
NOAEL: 1,000
NOAELcontmuous: 1,000
NOAELhed: 240
LOAEL: ,2000
LOAELcontinuous: 2,000
LOAEL hed: 480
>10% decrease in
body weight
1167
(BMDLio'o for body
weight)
280
(BMDLio%hed for
body weight)
Muralidhara
et al. (2001)
High
Rat (F344,
8 males/group)
2 weeks
5 days/week
(gavage)
NOAEL: 700
NOAELcontmuous. 500
NOAELhed: 120
ND
None
120
(NOAELhed)
Ghanavem et
al. (1986)
Medium (evaluated
only forestomach
histopathology)
Rat (Sprague-
Dawley,
15 males/group)
13 weeks,
5 days/week
(gavage)
NOAEL: 1,000
NOAELcontmuous. 714
NOAELhed: 171
LOAEL: 2,000
LOAELcontinuous: 1,429
LOAELhed: 343
Mortality
(1/15 rats); CNS
depression; >10%
decrease in body
weight
171
(NOAELhed)
1,248
(BMDLio'o for body
weight)
300
(BMDLio%hed for
body weight)
Muralidhara
et al. (2001)
High
Chronic
Mouse
(B6C3F1,
35 males/group)
52 weeks,
7 days/week
NOAELcontmuous. 543
NOAELhed: 71
ND
None
71
(NOAELhed)
Klaunie et al.
(1986)
High (evaluated only
body weight and liver.
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Species (Strain,
Sex, n/Group)
Exposure
NOAEL
(mg/kg-bw/day)
LOAEL
(mg/kg-bw/day)
Effect(s)
Candidate POD
(mg/kg-bw/day)
(POD type)
Reference
Study Rating for Non-
cancer (Significant
Limitations)
(drinking
water)
kidney, and lung weight
and histopathology)
Mouse
(B6C3F1, 50 males
and
50 females/group)
15-78 weeks,
5 days/week
(gavage)
NOAEL (time-weighted
across weeks as
reported by NCI):
1,665 (F) '
NOAELcontinuous
(adjusted for
5/7 days/week)
1,189 (F)
NOAELhed:
155 (F)
LOAEL (time-
weighted across weeks
as reported by NCI):
,3331 (F)
L 0 AEL continuous
(adjusted for
5/7 days/week):
2.379 (F)
LOAELhed:
309 (F)
Decreased
survival
155 (F)
(NOAELhed)
NCI (1978)
High
14747
14748
Table Apx M-10. Summary of Candidate Non-cancer Inhalation
'ODs for 1,1-Dichloroethane
Species (Strain, Sex,
n/Group)
Exposure
NOAEL
LOAEL
Effect
Candidate
POD (POD
Type)
Reference
Study Rating
for Non-cancer
(Significant
Limitations)
Acute
No data
Short/intermediate-term
Rat (Sprague-
10 days
ND
LOAEL: 15,372
Decreased maternal body
4,525 mg/m3
Schwetz et al.
High for body
Dawley,
GD 6-15,
mg/m3
weight (9-11% less than
or 1,118 ppm
(1974)
weight; medium
20 females/group)
7 hours/day
(3,798 ppm)
LOAELcontinuous
LOAELhec:
4,485 mg/m3
(1,108 ppm)
controls) on GD 13
(BMCLhec)
for other
endpoints
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Species (Strain, Sex,
n/Group)
Exposure
NOAEL
LOAEL
Effect
Candidate
POD (POD
Type)
Reference
Study Rating
for Non-cancer
(Significant
Limitations)
Chronic
Rat (Sprague-
Dawley,
5/sex/group), guinea
pig (Pirbright-Wliite,
5/sex/group), and
rabbit (strain not
specified,
2/sex/group)
26 weeks
5 days/week
6 hours/day
NOAEL:
3,036 mg/m3
(750 ppm)
NOAELconhi,nous
NOAELhec:
542 mg/m3
(134 ppm)
ND
No effect on any species
542 mg/m3
or 134 ppm
(NOAELhec)
(Hofmann et al..
1971a)
Medium
(histopathology
evaluations
limited to liver
and kidney)
Dog (mongrel,
1 male/group)
6 months,
3.5 days/week,
7 hours/day
ND
LOAEL:
4,319 mg/m3
(1,067 ppm)
LOAELadj =
LOAELhec:
630 mg/m3
(156 ppm)
Decreased body weight
(magnitude unknown);
lung congestion
630 mg/m3
or 156 ppm
(LOAELhec)
Mellon Institute
(1947)
Medium (one
dog, body weight
reported as
percentage of
starting weight)
14750
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14752
14753
14754
14755
14756
14757
14758
14759
14760
14761
14762
14763
14764
14765
14766
14767
14768
14769
14770
14771
14772
14773
14774
14775
14776
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M.2.2 Non-cancer Dose-Response Assessment for 1,2-Dichloroethane
According to U.S. EPA (2021b) Draft Systematic Review Protocol, hazard endpoints that receive
evidence integration judgments of demonstrates and likely would generally be considered for dose-
response analysis. Endpoints with suggestive evidence can be considered on a case-by-case basis.
Studies that received high or medium overall quality determinations (or low-quality studies if no other
data are available) with adequate quantitative information and sufficient sensitivity can be compared.
The only hazard outcome for which evidence demonstrates that 1,2-dichloroethane causes the effect was
mortality. For neurological/behavioral effects, EPA's evidence integration judgment was likely. For
nutritional/metabolic, renal/kidney, hepatic/liver, lung/respiratory, immune/hematological, and
reproductive effects, EPA's evidence integration conclusion was that the evidence was suggestive.
Finally, EPA concluded that the available evidence was inadequate to determine whether 1,2-
dichloroethane induces developmental effects.
No human studies provided adequate information for POD determination. Animal studies of oral,
inhalation, or dermal exposure that received high or medium quality determinations for one or more of
these health outcomes were considered for dose-response information, with some exceptions. Studies
that identified a NOAEL at the highest dose/concentration tested were not considered for dose-response
assessment but were considered as part of evidence integration for the relevant health outcomes. In
addition, acute lethality studies that did not include untreated or vehicle-treated controls, or other studies
that did not present sufficient information to determine a NOAEL or LOAEL were not considered.
Finally, only studies in intact, wild-type laboratory animal strains were considered for dose-response
assessment. A small number of studies using partially-hepatectomized animals or transgenic models
were excluded from consideration, as shown in the tables.
Table_Apx M-l 1, Table_Apx M-12, and
Table Apx M-l3 show the animal studies of oral, inhalation, and dermal exposure (respectively) that
were excluded from consideration for dose-response assessment along with the reason for excluding
each.
Table Apx M-ll. Oral Studies Not Considered Suitable for POPs for 1,2-Dichloroethane
Duration
Category
Reference
HERO ID
Species
Specific
Route
Rationale
Acute
Cottalasso et al. (1995)
200280
Rat
Gavage
Not suitable for POD due to dosing
uncertainties
Acute
Dow Chemical (2006a)
625286
Rat
Gavage
Freestanding NOAEL'1
Acute
Kettering Laboratory
(1943)
4528351
Rabbit
Gavage
Uninfonnative
Acute
Kitchin et al. (1993)
6118
Rat
Gavage
Freestanding NOAEL'1
Acute
Mellon Institute (1948)
5447301
Rat
Gavage
Uninfonnative
Acute
Mellon Institute (1948)
5447301
Mouse
Gavage
Uninfonnative
Acute
Mellon Institute (1948)
5447301
Rabbit
Gavage
Uninfonnative
Acute
Moodv et al. (1981)
18954
Rat
Gavage
Not suitable for POD; evaluation
limited to liver weight and data not
shown
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Duration
Category
Reference
HERO ID
Species
Specific
Route
Rationale
Acute
Munson et al. (1982)
62637
Mouse
Gavage
Low
Acute
Stauffer Chern Co (1973)
6569955
Rat
Gavage
Not suitable for POD; no control
group
Acute
Miltnan et al. (1988)
200479
Rat
Gavage
Study of partially hepatectomized
animals
Short-term
Dow Chemical (2006a)
625286
Rat
Gavage
Freestanding NOAEL'1
Short-term
NTP (1978)
5441108
Mouse
Gavage
Freestanding NOAEL'1
Subchronic
Miltnan et al. (1988)
200479
Rat
Gavage
Study of partially hepatectomized
animals
Subchronic
Alumot et al. (1976)
194588
Rat
Diet
Freestanding NOAEL'1 (for 5-week
female and 13-week male growth
studies); not suitable for POD due
to dosing uncertainties (for 5- to 7-
week preliminary study)
Subchronic
NTP (1991)
1772371
Rat
Drinking
water
Uninfonnative
Subchronic
NTP (1991)
1772371
Mouse
Drinking
water
Uninfonnative
Subchronic
Munson et al. (1982)
62637
Mouse
Drinking
water
Uninfonnative
Chronic
Alumot et al. (1976)
194588
Rat
Diet
Uninfonnative
Chronic
Klaunig et al. (1986)
200427
Mouse
Drinking
water
Not suitable for POD due to
reporting limitations
Chronic
Storer et al. (1995)
200612
Mouse
Gavage
Study of transgenic mice
predisposed to cancer
Chronic
NTP (1978)
5441108
Mouse
Gavage
Not suitable for POD due to
confounding by tumors
Chronic
NTP (1978)
5441108
Rat
Gavage
Uninfonnative
Reproduction/
Developmental
Lane et al. (1982)
62609
Mouse
Drinking
water
Freestanding NOAEL'1
Reproduction/
Developmental
WIL Research (2015)
7310776
Rat
Drinking
water
Uninfonnative
Reproduction/
Developmental
Alumot et al. (1976)
194588
Rat
Diet
Uninfonnative
11 No effects observed at highest dose tested for all apical health outcomes rated Low or higher.
14782
14783
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14784 Table Apx M-12. Inhalation Studies Not Considered Suitable for POPs for 1,2-Dichloroethane
Duration
Category
Reference
HERO ID
Species
Rationale
Acute
Brondeau et al. (1983)
200247
Rat
Not suitable for POD due to limited
evaluations
Acute
Dow Chemical (2005)
10699112
Rat
Not suitable for POD determination; no
control group
Acute
Dow Chemical (2017)
10699356
Rat
Not suitable for POD determination; no
control group
Acute
Sherwood et al. (1987)
200590
Rat
Freestanding NOAEL'1
Acute
Guo and Niu (2003)
200352
Rat
Uninformative
Acute
Jin et al. (2018a); Jin et al.
(2018b)
5431556,
5557200
Mouse
Uninformative
Acute
Mellon Institute (1948)
5447301
Rat
Uninformative
Acute
Mellon Institute (1948)
5447301
Rabbit
Uninformative
Acute
Mellon Institute (1948)
5447301
Mouse
Uninformative
Acute
Spencer et al. (1951)
62617
Rat
Not suitable for POD determination; no
control group
Acute
Zhang et al. (2011)
734177
Rat
Uninformative
Short-term
Brondeau et al. (1983)
200247
Rat
Not suitable for POD due to limited
evaluations
Short-term
Dow Chemical (2014)
10609985
Rat
Freestanding NOAEL'1
Short-term
Jin et al. (2018a); Jin et al.
(2018b)
5431556,
5557200
Mouse
Uninformative
Short-term
Li et al. (2015b)
4492694
Rat
Uninformative
Short-term
Pang et al. (2018)
4697150
Rat
Uninformative
Short-term
Sherwood et al. (1987)
200590
Rat
Freestanding NOAEL3
Short-term
Sherwood et al. (1987)
200590
Mouse
Freestanding NOAEL'1
Short-term
Spencer et al. (1951)
62617
Rat
Uninformative
Short-term
Spencer et al. (1951)
62617
Guinea
Pig
Uninformative
Short-term
Sun et al. (2016c)
4451633
Mouse
Uninformative
Short-term
Wang et al. (2013)
1522109
Mouse
Uninformative
Short-term
Wang et al. (2014)
4453007
Mouse
Uninformative
Short-term
Zhang and Jin (2019)
5556105
Mouse
Uninformative
Subchronic
Hofmann et al. (1971a)
1937626
Rat
Uninformative
Subchronic
Hofmann et al. (1971a)
1937626
Guinea
Pig
Uninformative
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Duration
Category
Reference
HERO ID
Species
Rationale
Subchronic
Hofmann et al. (1971a)
1937626
Cat
Not suitable for POD due to reporting
limitations and small group size6
Subchronic
Hofmann et al. (1971a)
1937626
Rabbit
Uninfonnative
Subchronic
Kettering Laboratory (1943)
4528351
Rabbit
Uninfonnative
Chronic
Cheever et al. (1990)
12097
Rat
Freestanding NOAEL'1
Chronic
Hofmann et al. (1971a)
1937626
Rat
Freestanding NOAEL'1 (17- and 26-
week experiments)
Chronic
Hofmann et al. (1971a)
1937626
Rabbit
Freestanding NOAEL'1 (17- and 26-
week experiments)
Chronic
Hofmann et al. (1971a)
1937626
Guinea
Pig
Freestanding NOAEL3 (17- and 26-
week experiments)
Chronic
Hofmann et al. (1971a)
1937626
Cat
Freestanding NOAEL'1 (17-week
experiment); Uninfonnative (26-week
experiment)
Chronic
IRFMN (1976)
5447359
Rat
Freestanding NOAEL'1
Chronic
IRFMN (1987)
94773
Rat
Freestanding NOAEL'1
Chronic
IRFMN (1987)
94773
Mouse
Freestanding NOAEL'1
Chronic
IRFMN (1987)
5447260
Rat
Freestanding NOAEL'1
Chronic
Mellon Institute (1947)
1973131
Rat
Uninfonnative
Chronic
Mellon Institute (1947)
1973131
Dog
Not suitable for POD due to reporting
limitations and small group size6
Chronic
Naaano et al. (2006)
200497
Rat
Freestanding NOAEL'1
Chronic
Nagano et al. (2006)
200497
Mouse
Not suitable for POD due to
confounding by tumors
Chronic
Spencer et al. (1951)
62617
Rat
Not suitable for POD due to variable
exposure durations and reporting
limitations
Chronic
Spencer et al. (1951)
62617
Guinea
Pig
Not suitable for POD due to variable
exposure durations and reporting
limitations
Chronic
Spencer et al. (1951)
62617
Rabbit
Not suitable for POD due to variable
exposure durations, reporting
limitations, and small group size6
Chronic
Spencer et al. (1951)
62617
Monkey
Not suitable for POD due to variable
exposure durations, reporting
limitations, and small group size6
Reproduction/
Developmental
Rao et al. (1980)
5453539
Rat
Freestanding NOAEL'1 (one-generation
reproduction study)
Reproduction/
Developmental
Zhao et al. (1997)
77864
Rat
Uninfonnative
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Duration
Category
Reference
HERO ID
Species
Rationale
Reproduction/
Developmental
Zhao et al. (1989)
200708
Rat
Uninformative
Reproduction/
Developmental
Zhao et al. (1989)
200708
Mouse
Uninformative
"No effects observed at highest dose tested for all apical health outcomes rated Low or higher.
b Group size of 1-2 per exposure level.
14785
14786
14787 Table Apx M-13. Dermal Studies Not Considered Suitable for POPs for 1,2-Dichloroethane
Duration
Category
Reference
HERO ID
Species
Rationale
Acute
Kronevi et al. (1981)
58151
Guinea pig
Uninformative
Acute
Van Duuren et al. (1979)
94473
Mouse
Uninformative
Acute
Dow Chemical (1956)
725343
Rabbit
Low (no control; LD50 study)
Acute
Kettering Laboratory (1943)
4528351
Rabbit
Uninformative
Acute
Dow Chemical (1962)
5447286
Cattle
Low (no sex, strain or n/group reported)
Acute
Mellon Institute (1948)
5447301
Rabbit
Uninformative
Acute
Stauffer Chem Co (1973)
6569955
Rabbit
Negative for skin and eye irritation
Chronic
Van Duuren et al. (1979)
94473
Mouse
Uninformative
Chronic
Suauro et al. (2017)
4451542
Mouse
Study of transgenic mice predisposed to
cancer
14788
14789 TableApx M-14 shows the studies considered for potential use in POD derivation.
14790
14791 Table Apx M-14. Summary of Studies Considered for Non-cancer, Dose-Response Assessment of
14792 1,2-Dichloroethane
Reference
Duration Category
(Duration)
Species, Strain, and Sex
Study Rating for
Non-cancer
Endpoints
Oral
Storer et al. (1984)
Acute (once by gavage)
Mouse (B6C3F1, male)
High
Morel et al. (1999)
Acute (once by gavage)
Mouse (Swiss OF1, male)
High
Cottalasso et al. (2002)
Acute (once by gavage)
Rat (Sprague-Dawley,
female)
Medium
Salovsky et al. (2002)
Acute (once by gavage)
Rat (Wistar, male)
Medium
Daniel et al. (1994)
Short-term (10 days by
daily gavage)
Rat (Sprague-Dawley, male
and female)
High
Munson et al. (1982)
Short-term (14 days by
daily gavage)
Mouse (CD-I, male)
High
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Reference
Duration Category
(Duration)
Species, Strain, and Sex
Study Rating for
Non-cancer
Endpoints
van Esch et al. (1977)
Short-term (2 weeks by
gavage 5 days/week)
Rat (Wistar, male)
High
NTP (1978)
Short-term (6 weeks by
gavage 5 days/week)
Rat (Osbome-Mendel, male
and female)
Medium
Daniel et al. (1994)
Subchronic (90 days by
daily gavage)
Rat (Sprague-Dawley, male
and female)
High
van Esch et al. (1977)
Subchronic (90 days by
gavage 5 days/week)
Rat (Wistar, male and female)
High
NTP (1991)
Subchronic (13 weeks by
gavage, 5 days/week)
Rat (F344, males and female)
High
Pavan et al. (1995)
Repro/Dev (15 days, GD
6-20 by daily gavage)
Rat (Sprague-Dawley,
female)
High
Inhalation
Francovitch et al. (1986)
Acute (4 hours)
Mouse (CD, male)
Medium
Storer et al. (1984)
Acute (4 hours)
Mouse (B6C3F1, male)
High
Dow Chemical (2006b)
Acute (4 or 8 hours)
Rat (F344/ DUCRL, male and
female)
High
Sherwood et al. (1987)
Acute (3 hours)
Mouse (CD-I, female)
High
Zhou et al. (2016)
Acute (1.5 or 4 hours)
Rat (Sprague-Dawley, male)
Medium
Oin-li et al. (2010)
Acute (12 hours)
Rat (Sprague-Dawley, male
and female)
Medium
Iawe et al. (1986b)
Short-term (30 days;
5 days/week; 7 hours/day)
Rat (Sprague-Dawley, male)
High
Zhana et al. (2017)
Short-term (1 or 4 weeks;
6 hours/day)
Mouse (Swiss, male)
High
Zena et al. (2018)
Short-term (28 days;
6 hours/day)
Mouse (Swiss, male)
High
IRFMN (1978)
Chronic (12 months;
5 days/week; 7 hours/day)
Rat (Sprague-Dawley, male
and female)
Medium
Rao et al. (1980)
Repro/Dev (10 days;
7 hours/day; GD 6-15)
Rat (Sprague-Dawley,
female)
Medium
Rao et al. (1980)
Repro/Dev (13 days; 7
hours/day; GD 6-18)
Rabbit (New Zealand White,
female)
Medium
Pavan et al. (1995)
Repro/Dev (15 days; 6
hours/day; GD 6-20)
Rat (Sprague-Dawley,
female)
High
Dermal
No data
14793
14794 No dermal exposure studies of 1,2-dichloroethane were considered suitable for use in determining a
14795 POD. TableApx M-15 through TableApx M-19 summarize the NOAELs and LOAELs identified
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14796 from the oral (acute and short-term/sub chronic) and inhalation (acute, short-term/sub chronic, and
14797 chronic) studies, respectively. Only the endpoint with the lowest LOAEL for a given study was included
14798 in the table (if the lowest LOAEL was for multiple endpoints, all were included in the table). Each
14799 NOAEL and LOAEL was converted to reflect continuous exposure (NOAELCOntinuous and
14800 LOAELcontinuous) using EquationApx M-4 and EquationApx M-5. After adjustment for continuous
14801 exposure, each oral NOAEL and LOAEL was converted to a HED using Equation Apx M-6 and each
14802 inhalation NOAEL and LOAEL was converted to a HEC using Equation Apx M-7 (for extrarespiratory
14803 effects) or Equation Apx M-8 (for nasal effects).
14804
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Table Apx M-15. Summary of Candidate Acute, Non-cancer, Oral POPs for 1,2-Dichloroethane
Target
Organ/
System
Species (Strain,
Sex, n/Group)
Exposure
NOAEL
(mg/kg-bw)
LOAEL
(mg/kg-bw)
Basis for
NOAEL/LOAEL
Candidate POD*
(mg/kg-bw)
(POD Type)
Reference
Study Rating
for Target
Organ/System
Renal/Kidney
{evidence
suggests)
Mouse (B6C3F1,
5 males/group)
Once
(gavage)
NOAEL:
200
NOAELhed:
26.0
LOAEL:
300
LOAELhed:
39.0
Significantly increased
relative kidney weight
(13% higher than controls)
19.9
(BMDLio% hed for
kidney weight)
Storer et al.
(1984)
High
Mouse
(Swiss OF1, 10
males/group)
Once
(gavage)
NOAEL:
1,000
NOAELhed:
130
LOAEL:
1,500
LOAELhed:
195
Increased percentage of
damaged proximal tubules
130
(NOAELhed)
Morel et al.
(1999)
High
Hepatic/Liver
{evidence
suggests)
Rat (Sprague-
Dawley; 10
females/group)
Once
(gavage)
ND
LOAEL:
628
LOAELhed:
151
Significantly increased
ALT, AST, and LDH (45,
44, and 67% higher than
controls, respectively) and
liver steatosis
151
(LOAELhed)
Cottalasso et
al. (2002)
Medium
Respiratory
{evidence
suggests)
Rat (Wistar, 4-6
males/group)
Once
(gavage)
ND
LOAEL:
136
LOAELhed:
32.6
Significantly increased
total number of cells in
BALF; inflammatory and
noninflammatory
histological changes in lung
(data reported qualitatively)
32.6
(LOAELhed)
Salovskv et
al. (2002)
Medium
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Table Apx M-16. Summary of Candidate Short-Term/Intermediate, Non-cancer, Oral POPs for 1,2-Dichloroethane"
Target Organ/
System
Species (Strain,
Sex, n/Group)
Exposure
NOAEL
(mg/kg-bw/day)
LOAEL
(mg/kg-bw/day)
Basis for
NOAEL/LOAEL
Candidate POD b
(mg/kg-bw/day)
(POD Type)
Reference
Study Rating
for Target
Organ/System
Mortality
(evidence
demonstrates)
Rat (SPF Wistar,
6 males/group)
2 weeks
(gavage, 5
days/week)
NOAEL: 100
NOAELcontmuous •
71.4
NOAELhed: 7.1
LOAEL: 300
LOAELcontmuous •
214
LOAELhed: 51.4
Mortality in all animals
(6/6 animals by day 5)
17.1
(NOAELhed)
van Esch et al.
(1977)
High
Nutritional/
Metabolic
(evidence
suggests)
Rat (Sprague-
Dawley; 25-26
females/group)
15 days
GD 6-20
(daily
gavage)
NOAELcontmuous •
158
NOAELhed: 37.9
LOAELcontmuous •
198
LOAELhed: 47.5
Decreased absolute
maternal body weight gainc
on GD 6-21 (reduced
>30% relative to controls)
10.0
(BMDLio'o hed for
maternal body
weight)
Pavan et al.
(1995)
High
Rat (Osborne-
Mendel,
5/sex/group)
6 weeks
(gavage, 5
days/week)
ND
LOAEL: 40
LOAELcontmuous •
29
LOAELhed: 7.0
Decreased body weights
(10%) in females
7.0
(LOAELhed)
NTP (1978)
Medium
Hepatic/Liver
(evidence
suggests)
Rat (Sprague-
Dawley;
10/sex/group)
10 days
(gavage,
daily)
NOAELcontmuous •
30
NOAELhed: 7.2
LOAELcontmuous •
100
LOAELhed: 24
Significantly increased
relative liver weights (14%
relative to controls) and
serum cholesterol levels
(data not shown) in males
7.2
(NOAELhed)
Daniel et al.
(1994)
High
Rat (Sprague-
Dawley;
10/sex/group)
90 days
(gavage,
daily)
NOAELcontmuous •
37.5
NOAELhed: 9.00
LOAELcontmuous •
75
LOAELhed: 18
Significantly increased
relative liver weight (20%
higher than controls) and
serum ALP (data not
shown) in males
9.00
(NOAELhed)
Daniel et al.
(1994)
High
Rat (SPF Wistar,
10/sex/group)
90 days
(gavage, 5
days/week)
NOAEL: 30
NOAELcontmuous •
21
NOAELhed: 5.0
LOAEL: 90
LOAELcontmuous •
64
LOAELhed: 15
Significantly increased
relative liver weight (13%
higher than controls) in
females
5.0
(NOAELhed)
van Esch et al.
(1977)
Medium
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Target Organ/
System
Species (Strain,
Sex, n/Group)
Exposure
NOAEL
(mg/kg-bw/day)
LOAEL
(mg/kg-bw/day)
Basis for
NOAEL/LOAEL
Candidate POD b
(mg/kg-bw/day)
(POD Type)
Reference
Study Rating
for Target
Organ/System
Rat (Sprague-
Dawley;
10/sex/group)
90 days
(gavage,
daily)
NOAELconhi,nous •
37.5
NOAELhed: 9.00
LO AELcoiitinuous •
75
LOAELhed: 18
Significantly increased
relative kidney weights in
males and females (18 and
15% higher than controls,
respectively)
9.00
(NOAELhed)
Daniel et al.
(1994)
High
Renal/
Kidney
(evidence
suggests)
Rat (SPF Wistar,
10/sex/group)
90 days
(gavage, 5
days/week)
NOAEL: 30
NOAELcontmuous •
21
NOAELhed: 5.0
LOAEL: 90
LO AELcoiitinuous •
64
LOAELhed: 15
Significantly increased
relative kidney weight (17
and 16% higher than
controls in males and
females, respectively)
5.0
(NOAELhed)
van Esch et al.
(1977)
Medium
Rat (F344;
10/sex/group)
13 weeks
(gavage, 5
days/week)
ND
LOAEL: 30
LO AELcoiitinuous •
21
LOAELhed: 5
Significantly increased
absolute kidney weights in
males (9% higher than
controls)
3.4
(BMDLio'o hed for
absolute kidney
weight)
NOAEL: 37
NOAELcontmuous •
26
NOAELhed: 6.2
LOAEL: 75
LO AELcoiitinuous •
54
LOAELhed: 13
Increased absolute and
relative kidney weights in
females (12 and 10%
higher than controls,
respectively)
6.2 (NOAELhed,
NTP (1991)
High
Immune/
Hematological
(evidence
suggests)
Mouse (CD-I;
10-12
males/group)
14 days
(daily
gavage)
ND
LO AELcoiitinuous •
4.89
LOAELhed: 0.636
Suppression of humoral and
cell-mediated immune
responses
0.636 (LOAELhedi
Munson et al.
(1982)
High
14809
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Table Apx M-17. Summary of Candidate Acute, Non-cancer, Inhalation POPs for 1,2-Dic
lloroethane
Target Organ/
System
Species
(Strain, Sex,
n/Group)
Exposure
NOAEL
LOAEL
Basis for
NOAEL/LOAEL
Candidate
POD"
(POD Type)
Reference
Study Rating
for Target
Organ/System
Mortality
(evidence
demonstrates)
Mouse (CD-
1, 10-15
males/group)
4 hours
ND
LOAEL:
4,050 mg/m3
(1,000 ppm)
LOAELcontmuous •
LOAELhec:
675 mg/m3
(167 ppm)
Dose-related
increase in mortality
compared with
controls
(quantitative data
not reported)
675 mg/m3
or 167 ppm
(LOAELhec)
Francovitch
etal. (1986)
Medium
Renal/Kidney
(evidence
suggests)
Mouse
(B6C3F1, 5
males/group)
4 hours
NOAEL:
639 mg/m3
(158 ppm)
NOAELcontmuous •
NOAELhec:
107 mg/m3
(26.3 ppm)
LOAEL:
2,020 mg/m3
(499 ppm)
LOAELcontmuous •
LOAELhec:
337 mg/m3
(83.2 ppm)
Significantly
increased serum
BUN and relative
kidney weight (85
and 12% higher than
controls,
respectively)
207 mg/m3 or
51.1 ppm
(BMCLiwoHec
for relative
kidney weight)
Storer et al.
(1984)
High
Hepatic/Liver
(evidence
suggests)
Mouse
(B6C3F1, 5
males/group)
4 hours
NOAEL:
639 mg/m3
(158 ppm)
NOAELcontmuous •
NOAELhec:
107 mg/m3
(26.3 ppm)
LOAEL:
2020 mg/m3
(499 ppm)
LOAELcontmuous •
LOAELhec:
337 mg/m3
(83.2 ppm)
Increased serum
ALT (2-fold higher
than controls [ns])
and SDH (11-fold
higher than controls;
p < 0.05)
107 mg/m3 or
26.3 ppm
(NOAELhec)
Storer et al.
(1984)
High
Lung/
Respiratory
(evidence
suggests)
Rat (F344/
DUCRL,
5/sex/group)
4 hours
NOAEL:
212 mg/m3
(52.4 ppm)
NOAELcontmuous •
35.3 mg/m3
(8.73 ppm)
NOAELhec:
7.06 mg/m3
(1.74 ppm)
LOAEL:
794.9 mg/m3
(196.4 ppm)
LOAELcontmuous •
132.5 mg/m3
(32.73 ppm)
LOAELhec:
26.50 mg/m3
(6.547 ppm)
Histological changes
to the olfactory
mucosa in males and
females
1.75 mg/m3 or
0.432 ppm
(BMCLi ohec for
degeneration
with necrosis in
males and
females)
Dow
Chemical
(2006b)
High
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Target Organ/
System
Species
(Strain, Sex,
n/Group)
Exposure
NOAEL
LOAEL
Basis for
NOAEL/LOAEL
Candidate
POD"
(POD Type)
Reference
Study Rating
for Target
Organ/System
Rat (F344/
DUCRL,
10/sex/group)
4 hours
ND
LOAEL:
794.9 mg/m3
(196.4 ppm)
LO AELcontinuous •
132.5 mg/m3
(32.73 ppm)
Histological changes
to the olfactory
mucosa in males and
females
4.636 mg/m3 or
1.145 ppm
(BMCLi ohec for
regeneration in
males and
females)
Dow
Chemical
(2006b)
High
Lung/
Respiratory
LOAELhec:
26.50 mg/m3
(6.547 ppm)
(evidence
suggests)
Rat (F344/
DUCRL,
5/sex/group)
8 hours
NOAEL
214 mg/m3
(52.8 ppm)
NOAELcontmuous •
71.3 mg/m3
(17.6 ppm)
NOAELhec :
14.3 mg/m3
(3.52 ppm)
LOAEL=
435.1 mg/m3
(107.5 ppm)
LO AELcontinuous •
145.0 mg/m3
(35.83 ppm)
LOAELhec:
29.01 mg/m3
(7.166 ppm)
Histological changes
to the olfactory
mucosa in males and
females
9.78 mg/m3 or
2.42 ppm
(BMCLi ohec for
degeneration
with necrosis in
males and
females)
Dow
Chemical
(2006b)
High
Immune/
Hematological
(evidence
suggests)
Mouse (CD-
1, 140
females/
group)
3 hours
NOAEL:
9.3 mg/m3
(2.3 ppm)
NOAELcontmuous •
NOAELhec:
1.2 mg/m3
(0.29 ppm)
LOAEL:
22 mg/m3
(5.4 ppm)
LO AELcontinuous •
LOAELhec:
2.8 mg/m3
(0.68 ppm)
Mortality following
streptococcal
challenge
1.2 mg/m3 or
0.29 ppm
(NOAELhec)
Sherwood et
al. (1987)
High
(Note: Mice
inhaled -2E04
aerosolized
streptococci
1 hour after
exposure. This
is unlikely to
represent
typical
immunological
challenges in
humans).
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Target Organ/
System
Species
(Strain, Sex,
n/Group)
Exposure
NOAEL
LOAEL
Basis for
NOAEL/LOAEL
Candidate
POD"
(POD Type)
Reference
Study Rating
for Target
Organ/System
Rat (Sprague-
Dawley, 6
males/group)
1.5 hours
ND
LOAEL:
3,950 mg/m3
(975.9 ppm)
Changes in brain
histopathology
246.9 mg/m3 or
61.00 ppm
(LOAELhec)
Zhou et al.
(2016)
Medium
Neurological/
Behavioral
LO AELcontinuous •
LOAELhec:
246.9 mg/m3
(61.00 ppm)
(evidence
likely)
Rat (Sprague-
Dawley,
12/sex/group)
12 hours
NOAEL:
2,500 mg/m3
(617.7 ppm)
NO AELcontinuous •
NOAELhec:
1,250 mg/m3
(308.9 ppm)
LOAEL:
5,000 mg/m3
(1,240 ppm)
LO AELcontinuous •
LOAELhec:
2,500 mg/m3
(620 ppm)
Clinical signs of
neurotoxicity and
changes in brain
histology
1250 mg/m3 or
308.9 ppm
(NOAELhec)
Oin-li et al.
(2010)
Medium
" BMCLs are presented as HECs for comparison with other candidate PODs. BMCL1SD = BMCL for benchmark response of 1 standard deviation change from control
mean. BMCL10% = BMCL for benclunark response of 10% relative deviation from control mean. BMCL10 = BMCL for benclunark response of 10% extra risk.
14811
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Table Apx M-18. Summary of Candidate Short-Term/Intermediate, Non-cancer, Inhalation
PODs for 1,2-E
tichloroethane
Target Organ/
System
Species
(Strain, Sex,
n/Group)
Exposure
NOAEL
LOAEL
Basis for
NOAEL/LOAEL
Candidate
PODa
(POD Type)
Reference
Study Rating
for Target
Organ/System
Mortality
(evidence
demonstrates)
Rat (Sprague-
Dawley, 12
males/group)
30 days
5 days/week
7 hours/day
NOAEL:
619 mg/m3
(153 ppm)
NOAELconhi,nous
NOAELhec:
129 mg/m3
(31.9 ppm)
LOAEL:
1230 mg/m3
(304 ppm)
LOAELcontinuous
LOAELhec:
256 mg/m3
(63.3 ppm)
Mortality
(1/12 animals)
154 mg/m3 or
38.0 ppm
(BMCLiohec
for mortality)
Iewe et al.
(1986b)
Iewe et al.
(1986c)
High
Rat (Sprague-
Dawley, 16-30
females/group)
10 days
7 hours/day
GD 6-15
NOAEL:
405 mg/m3
(100 ppm)
NOAELcontinuous
NOAELhec:
118 mg/m3
(29.2 ppm)
LOAEL:
1210 mg/m3
(300 ppm)
LOAELcontinuous
LOAELhec:
353 mg/m3
(87.5 ppm)
Mortality
(10/16 animals)
118 mg/m3 or
29.2 ppm
(NOAELhec)
Rao et al.
(1980)
Medium
Rat (Sprague-
Dawley, 26
females/
group)
15 days
6 hours/day
GD 6-20
NOAEL:
1,030 mg/m3
(254 ppm)
NOAELcontinuous
NOAELhec:
258 mg/m3
(63.5 ppm)
LOAEL:
1,330 mg/m3
(329 ppm)
LOAELcontinuous
LOAELhec:
333 mg/m3
(82.3 ppm)
Mortality
(2/26 dams)
258 mg/m3 or
63.5 ppm
(NOAELhec)
Pavan et
al. (1995)
High
Rabbit (New
Zealand White,
19-21 females/
group)
13 days
7 hours/day
GD 6-18
ND
LOAEL:
405 mg/m3
(100 ppm)
LOAELcontinuous
LOAELhec:
118 mg/m3
(29.2 ppm)
Mortality
(4/21 animals)
59.4 mg/m3 or
14.7 ppm
(BMCLiohec
for mortality)
Rao et al.
(1980)
Medium
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Target Organ/
System
Species
(Strain, Sex,
n/Group)
Exposure
NOAEL
LOAEL
Basis for
NOAEL/LOAEL
Candidate
PODa
(POD Type)
Reference
Study Rating
for Target
Organ/System
Hepatic/Liver
(evidence
suggests)
Mouse (Swiss,
10 males/
group)
28 days
6 hours/day
ND
LOAEL:
363.58 mg/m3
(89.830 ppm)
LOAELcontinuous
LOAELhec:
90.895 mg/m3
(22.457 ppm)
Increased absolute
and relative liver
weights (>10%
higher than
controls)
51.720 mg/m3
or 12.778 ppm
(BMCLio%hec
for relative
liver weight)
Zens et al.
(2018)
High
Reproductive/
Developmental
(evidence
suggests)
Mouse (Swiss,
5-15 males/
group)
4 weeks
6 hours/day
ND
LOAEL:
102.70 mg/m3
(25.374 ppm)
LOAELcontinuous
LOAELhec:
25.675 mg/m3
(6.3435 ppm)
Changes in sperm
parameters
(increased total,
sperm head, body,
and tail
abnormalities;
decreased sperm
concentration;
decreased height of
seminiferous
tubules and height
of germinal
epithelium)
21.240 mg/m3
or 5.2500 ppm
(BMCL5o0hec
for sperm
concentration)
18.815 mg/m3
or 4.6486 ppm
(BMCLisdhec
for
seminiferous
tubule height)
8.6304 mg/m3
or 2.1323 ppm
(BMCLisdhec
for germinal
epithelium
height)
Zhane et
al. ("20171
High
" BMCLs are presented as HECs for comparison with other candidate PODs. BMCLisd = BMCL for benchmark response of 1 standard deviation change from control
mean. BMCLi0% = BMCL for benclunark response of 10% relative deviation from control mean. BMCL5%hec = BMCL for benclunark response of 5% relative
deviation from control mean. BMCLio = BMCL for benclunark response of 10% extra risk
14813
14814
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14815 Table Apx M-19. Summary of Candidate Chronic, Non-cancer, Inhalation POPs for 1,2-Dichloroethane
Target Organ/
System
Species
(Strain, Sex,
n/Group)
Exposure
NOAEL
LOAEL
Basis for
NOAEL/LOAEL
Candidate
POD"
(POD Type)
Reference
Study Rating
for Target
Organ/System
Hepatic/Liver
(evidence
suggests)
Rat (Sprague-
Dawley, 8-
10/sex/group)
12 months
5 days/week
NOAF.L:
40 mg/m3
(10 ppm)
N O AEL continuous
= NOAELhec:
8.3 mg/m3
(2.1 ppm)
LOAF.L:
200 mg/m3
(50 ppm)
LOAELcontinuous
LOAELhec:
42 mg/m3
(10 ppm)
Increased ALT
(>2-fold higher than
controls) and LDH
(18% higher than
controls) in males
8.3 mg/m3 or
2.1 ppm
(NOAELhec)
IRFMN
(1978)
Medium
7 hours/day
NOAF.L:
40 mg/m3
(10 ppm)
N O -AEL continuous
= NOAELhec:
8.3 mg/m3
(2.1 ppm)
LOAF.L:
200 mg/m3
(50 ppm)
LOAELcontinuous
LOAELhec:
42 mg/m3
(10 ppm)
Increased ALT
(>2-fold higher than
controls) and LDH
(25% higher than
controls) in females
1.7 mg/m3
or 0.42 ppm
(BMCLl SDHEC
for LDH in
females)
a BMCLs are presented as HECs for comparison with other candidate PODs. BMCL1SD = BMCL for benchmark response of 1 standard deviation change from control
mean. BMCL10% = BMCL for benchmark response of 10% relative deviation from control mean. BMCL10 = BMCL for benchmark response of 10% extra risk.
14816
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M.2.3 Non-cancer PODs for Acute Exposures for 1,1-Dichloroethane
Oral
There were two acute-duration oral studies of 1,1-dichloroethane that were rated acceptable: an acute
lethality study in guinea pigs by Dow Chemical (1947) and a single-dose lethality study in rats by
Muralidhara et al. (2001) (see Table Apx M-10). The acute lethality study by Dow Chemical (1947)
reported no details on the animal strain, sex, age, or condition; number of animals tested; method of
administration; or duration of follow-up. The study authors reported only that all guinea pigs survived
being fed a dose of 300 mg/kg, while 1,000 mg/kg-bw was lethal for all the animals given this dose. The
limitations in the study preclude its use for POD derivation.
Likewise, a single-dose experiment by Muralidhara et al. (2001). with a NOAEL of 1,000 mg/kg-bw and
a LOAEL of 2,000 mg/kg-bw was also not considered suitable for POD derivation due to the selection
of doses near those exhibiting mortality and the lack of sensitive endpoints other than death. Effects
identified included clinical signs of neurotoxicity characterized by the authors as "excitation followed by
progressive motor impairment and sedation." The only endpoints evaluated in the experiment were death
within the 14 days after dosing and clinical signs. Deaths occurred at doses >8,000 mg/kg-bw (within 24
hours of dosing) and the LD50 was 8,200 mg/kg-bw. Although the acute-duration oral data are limited,
the observation of CNS effects is consistent with the past use of 1,1-dichloroethane as a human
anesthetic (ATSDR. 2015).
Inhalation
No adequate acute-duration (< 24 hours) inhalation studies of 1,1-dichloroethane were identified.
Dermal
No adequate acute-duration (<24 hours) dermal studies of 1,1-dichloroethane were identified.
M.2.4 Non-cancer PODs for Short/Intermediate-Term Exposures for 1,1-Dichloroethane
Oral
Three short/intermediate-term gavage studies of 1,1-dichloroethane in rats provided sufficient
information to identify candidate non-cancer PODs: a 10-day experiment (Muralidhara et al.. 2001). a
14-day experiment (Ghanavem et al.. 1986). and a 13-week experiment (Muralidhara et al.. 2001).
In the 14-day experiment, Ghanavem et al. (1986) identified a freestanding NOAEL of 700 mg/kg-
bw/day; the only endpoint evaluated in this study was forestomach histopathology. This study was not
considered further for the short/intermediate-term oral POD for 1,2-dichloroethane due to the limited
evaluations.
In the 10-day experiment (Muralidhara et al.. 2001). a NOAEL and LOAEL of 1,000 and 2,000 mg/kg-
bw/day, respectively, were identified for decreased body weight. Other endpoints evaluated in this
experiment were liver and kidney weights; serum and urinary clinical chemistry markers of liver and
kidney effects; and histopathology of the liver, kidney, lung, brain, adrenal, spleen, testis, and
epididymis. Dosing was daily, so no adjustment for continuous exposure was necessary. BMD modeling
of the data on decreased body weight yielded a BMDLio% of 1,167 mg/kg-bw/day. This study was not
considered further due to a NOAEL near the limit dose of 1,000 mg/kg-bw/day.
In the 13-week experiment (Muralidhara et al.. 2001). evaluations were the same as in the 10-day
experiment described above. In this experiment, a NOAEL of 1,000 mg/kg-bw/day and a LOAEL of
2000 mg/kg-bw/day were identified for mortality (1/15 rats), CNS depression, and decreased body
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weight. At the high dose in this study (4,000 mg/kg-bw/day), the rats exhibited protracted narcosis, and
8/15 rats died between weeks 1 and 11, when the surviving rats in this group were sacrificed.
Mortality was not considered to be a suitable endpoint for BMD modeling. Quantitative data on CNS
depression were not reported, precluding BMD modeling of this endpoint. BMD modeling of the data on
decreased body weight yielded a BMDLio% of 1,248 mg/kg-bw/day; however, it is not clear that a POD
based on body weight would be adequately protective for mortality and neurotoxicity.
Inhalation
One short/intermediate-term inhalation study provided adequate information to identify a LOAEL. In
the inhalation developmental toxicity study of rats by Schwetz et al. (1974). the following maternal
endpoints were evaluated: maternal body weight and liver weight, serum ALT, and gross necropsy.
Developmental endpoints were also assessed, including gross, skeletal, and visceral anomalies. Effects
observed in the study were as follows:
• Decreased maternal body weight on GD 13 (~9 and 11 percent compared with controls at low
and high exposure levels, respectively).
• An uncertain effect on the incidence of litters with delayed ossification of the sternebrae at the
high exposure level. In this study, each of the two exposure groups had its own control group,
and the incidence of this effect differed between the two control groups (61 percent in the control
for low exposure and 11 percent in the control for the high exposure). Incidences in low and high
exposure groups were 44 and 42 percent, respectively, intermediate between the two control
groups.
• Increased relative liver weight (15 percent compared with controls) 6 days after the end of
exposure in nonpregnant rats in the high exposure group. However, no difference in absolute or
relative liver weight was seen at the end of the exposure period.
No other short/intermediate-term inhalation studies with a rating of acceptable were located. The data
from Schwetz et al. (1974) were not considered adequate for derivation of a short/intermediate-term
inhalation POD for the following reasons: (1) the evaluations of maternal endpoints did not include
histopathology or effects in organs other than the liver, (2) the disparate findings on delayed ossification
in the two control groups mean that a conclusion regarding this endpoint cannot be made with
confidence, and (3) there are no supporting studies that evaluated comprehensive endpoints.
Dermal
No adequate short/intermediate-term dermal studies of 1,1-dichloroethane were identified.
M.2.5 Non-cancer PODs for Chronic Exposures for 1,1-Dichloroethane
Oral
Two chronic-duration oral studies of 1,1-dichloroethane in mice provided sufficient information to
identify NOAELs and/or LOAELs: a 52-week drinking water experiment (Klaunig et al.. 1986) and a
78-week gavage experiment (NCI. 1978). In the 52-week experiment (Klaunig et al.. 1986) (study rating
of High for non-cancer endpoints), a freestanding NOAEL of 543 mg/kg-bw/day was identified based
on the absence of effects on body weight and liver, kidney, and lung weight and histology. No other
endpoints were evaluated. Because this study did not conduct comprehensive toxicological evaluations,
it is possible that effects on other organs or systems could have occurred at the NOAEL. Therefore, the
freestanding NOAEL from this study was not considered suitable for use as the chronic oral non-cancer
POD for 1,1-dichloroethane.
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In the 78-week experiment (NCI 1978) (study rating of High for mice), male and female mice were
exposed to increasing doses over time for 78 weeks followed by a 13-week recovery period prior to
sacrifice (see Table_Apx M-20).
Table Apx M-20. Dosing Regimen in (NCI, 1978) Chronic Mouse Study
Group
Dose
(mg/kg-bw/day Administered 5 Days/Week)
Number of Weeks
at this Dose
Time-Weighted Average
across 78 Dosing Weeks
Males
900
6
Low dose
1,200
3
1,442
1,500
69
0
13
1,800
6
High dose
2,400
3
2,885
3,000
69
0
13
Females
900
6
1,200
3
Low dose
1,500
11
1,665
1,800
58
0
13
1,800
6
2,400
3
High dose
3,000
11
3,331
3,600
58
0
13
(NCI. 1978) averaged the doses across the 78 exposure weeks and reported time-weighted average doses
of 0, 1,442, or 2,885 mg/kg-bw/day (males) and 0, 1,665, or 3,331 mg/kg-bw/day (females) (these doses
were administered 5 days/week). Decreased survival was observed in both males and females in the high
dose group, but the findings in males were confounded by reduced survival in untreated control males
(beginning around week 35). (NCI. 1978) did not report cause of death or any explanation for the
control male deaths. In females of the high dose group, there was a statistically significant reduction in
survival. Based on survival data presented graphically, there were no deaths among female mice
exposed for 9 weeks at doses up to 2,400 mg/kg-bw/day. The first high dose female death occurred at
around week 15 when the females were receiving 3,000 mg/kg-bw/day, but additional deaths did not
occur until around week 30, after the dose had been increased to 3,600 mg/kg-bw/day. Because of the
variable dosing regimen, there is significant uncertainty regarding the dose that resulted in decreased
survival in females. In addition, the reduced survival of untreated male mice calls into question the
reliability of the study findings.
Inhalation
Two chronic-duration inhalation studies of 1,1-dichloroethane were rated acceptable; however, neither
provided sufficient information to determine a POD. In the study by Hofmann et al. (1971a) (rated
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Medium), rats, guinea pigs, and rabbits were exposed 6 hours/day, 5 days/week for 13 weeks to
500 ppm followed by 13 weeks at 1,000 ppm 1,1-dichloroethane. Evaluations included clinical signs,
body weight, hematology, urinalysis, blood chemistry, and liver function (in rabbits) after 13 weeks, and
liver and kidney weight and histopathology at the end of the exposure period (26 weeks). No effects
were observed in rats, guinea pigs, or rabbits, so the only exposure level tested is a NOAEL. These data
are not sufficient to determine a POD due to the limited evaluations (lack of organ weights and
histopathology for organs/systems other than liver and kidney).
The study of dogs by Mellon Institute (1947) received a Medium study rating. In this study, a single
mongrel dog was exposed to 1,067 ppm 1,1-dichloroethane 7 hours/day, every other day for 6 months.
Reporting for this study is very limited, but it appears that there was a significant decrease in the
exposed dog's weight compared to the control(s) and marked lung congestion at necropsy. While these
results suggest a freestanding LOAEL of 1,067 ppm or 4,319 mg/m3 (156 ppm or 630 mg/m3 after
adjustment for continuous exposure), the data are not sufficient for use as a POD due to (1) use of a
single animal and single exposure concentration; (2) lack of data on the magnitude of body weight
change; and (3) failure to identify a NOAEL.
Dermal
No adequate chronic dermal studies of 1,1-dichloroethane were identified.
M.2.6 Non-cancer PODs for Acute Exposures for 1,2-Dichloroethane
Oral
The acute-duration oral POD for 1,2-dichloroethane was based on increased relative kidney weight in
male mice given a single gavage dose of 1,2-dichloroethane (Storer et al.. 1984). For this study, a
NOAEL of 200 mg/kg-bw/day and a LOAEL of 300 mg/kg-bw/day were identified for kidney weight
effects. To obtain a POD, BMD modeling was conducted on the relative kidney weight data using U.S.
EPA's Benchmark Dose Software (BMDS; v. 3.3). TableApx M-21 shows the relative kidney weights
corresponding to each dose. BMD modeling was conducted using a benchmark response (BMR) of 10
percent% relative deviation from the control mean (U.S. EPA. 2012b).
Table Apx M-21. Relative Kidney Weights in Male Mice Exposed to 1,2-
Dichloroethane Once by Gavage
Dose
Number of
Mean
Standard
(mg/kg-day)
Mice
(g/100 g body weight)
Deviation
0
5
1.50
0.09
200
5
1.58
0.19
300
5
1.69
0.09
400
3
1.75
0.08
500
ja
1.82
N/A
600
ja
1.61
N/A
Source: Storer etal. (1984)
11 4/5 mice died in this group.
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Following (U.S. EPA. 2012b) guidance, the polynomial 2-degree model with constant variance was
selected for these data. The BMDio% and BMDLio% values for this model were 270 and 153 mg/kg-
bw/day, respectively. The BMDLio% of 153 mg/kg-bw/day was selected as the POD.
The BMDLio% of 153 mg/kg-bw/day was converted to a HED of 19.9 mg/kg-bw/day using the DAF of
0.13 for mice (see Appendix M.3.1.3) and Equation_Apx M-l, as shown below:
EquationApx M-l.
HED = 153 mg/kg x 0.13 = 19.9 mg/kg
The HED of 19.9 mg/kg-bw/day does not need to be adjusted for occupational exposure. The benchmark
MOE for this POD is 30 (3 for interspecies extrapolation when a dosimetric adjustment is used and 10
for human variability).
Inhalation
The acute-duration inhalation POD for 1,2-dichloroethane was based on nasal lesions in rats exposed
once by inhalation for 8 hours (Dow Chemical 2006b). For this study, a NOAEL of 71.3 mg/m3 and
LOAEL of 145 mg/m3 were identified for increased incidences of degeneration with necrosis in the
olfactory mucosa of the nasal passages in male and female rats. To obtain a POD, BMD modeling was
conducted using EPA's BMDS (v. 3.3.2) on the incidence of these nasal lesions in male and female rats
(combined). The male and female data were combined for modeling because incidences were similar in
both sexes and the combined data set provided increased statistical power relative to the sex-specific
data sets. Prior to modeling, the exposure concentrations in the (Dow Chemical 2006b) rat 8-hour study
were adjusted from the exposure scenario of the original study to continuous (24 hours/day) exposure
using Equation Apx M-5. TableApx M-22 shows the nasal lesion incidences corresponding to each
exposure concentration. BMD modeling was conducted on the incidences using the continuous
equivalent concentrations and the default BMR for quantal data of 10 percent extra risk (U.S. EPA.
2012b).
Table Apx M-22. Incidence of Nasal Lesions in Male and Female Rats (Combined) Exposed to
1,2-Dichloroethane for 8 Hours
Unadjusted Exposure
Concentration (mg/m3)
Adjusted (Continuous) Exposure
Concentration (mg/m3)
Incidence of Degeneration with
Necrosis of the Olfactory Mucosa
0
0
0/10
214
71.3
0/10
435.1
145.0
4/10
630.6
210.2
9/10
Source: Dow Chemical (2006b)
Following U.S. EPA (2012b) guidance, the multistage 3-degree model was selected for these data. The
BMCio and BMCLio for this model were 81.4 and 48.9 mg/m3, respectively. The BMCLio of 48.9
mg/m3 was selected as the POD.
U.S. EPA (1994) guidance was used to convert the BMCLio of 48.9 mg/m3 to a HEC. For nasal lesions,
the RGDRetin rats is used. The RGDRet of 0.2 was calculated using Equation Apx M-9 (U.S. EPA.
1994).
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The BMCLio (48.9 mg/m3) was multiplied by the RGDRet (0.2) to calculate the HEC, as shown in the
EquationApx M-10.
The resulting HEC is 9.78 mg/m3 for continuous exposure. The continuous HEC of 9.78 mg/m3 is
converted to an equivalent worker HEC using Equation Apx M-13. The resulting POD for workers is
41.1 mg/m3. The benchmark MOE for this POD is 30 (3 for interspecies extrapolation when a dosimetric
adjustment is used and 10 for human variability).
EPA presents all inhalation PODs in equivalents of both mg/m3 and ppm to avoid confusion and errors.
Equation Apx M-3 was used with the molecular weight of 1,2-dichloroethane (98.96 mg/mmol) to
convert the continuous and worker PODs (9.78 and 41.1 mg/m3, respectively) to 2.42 and 10.2 ppm,
respectively.
Dermal
No PODs were identified from acute studies of dermal exposure to 1,2-dichloroethane. Therefore, the
acute oral HED of 19.9 mg/kg-bw/day with benchmark MOE of 30 was used for risk assessment of
acute dermal exposure for both continuous and worker exposure scenarios. As noted in Section M.3.1.4,
when extrapolating from oral data that incorporated BW3 4 scaling to obtain the oral HED, EPA uses the
same HED for the dermal route of exposure. The same uncertainty factors are used in the benchmark
MOE for both oral and dermal scenarios.
M.2.7 Non-cancer PODs for Short/Intermediate-Term Exposures for 1,2-Dichloroethane
Oral
The short-term/subchronic-duration oral POD for 1,2-dichloroethane was based on decreased immune
response in mice exposed to 1,2-dichloroethane by gavage for 14 days (Munson et al.. 1982). In this
study, a dose-related significant decrease in the number of antibody-forming cells per spleen
(AFC/spleen) was observed at all doses; the LOAEL was 4.89 mg/kg-bw/day. Using EPA's BMDS (v.
3.3), BMD modeling was conducted on the AFC/spleen data. The mice in the study by Munson et al.
(1982) were exposed 7 days/week, so no adjustment for continuous exposure was needed. TableApx
M-23 shows the AFC/spleen corresponding to each dose.
Table Apx M-23. Antibody-Forming Cells per Spleen in Male Mice Exposed to 1,2-
Dichloroethane by Daily Gavage for 14 Days i
Dose
(mg/kg-bw/day)
Number of Mice
Mean Number AFC/Spleen
(xlO5)
Standard Error
0
12
3.00
0.3
4.89
10
2.20
0.2
48.9
10
1.80
0.1
Source: Munson et al. (1982)
None of the models provided adequate fits to the means either assuming constant or non-constant
variance. Therefore, the LOAEL (lowest dose tested) was used as the POD.
The LOAEL of 4.89 mg/kg-bw/day was converted to a HED of 0.636 mg/kg-bw/day using the DAF of
0.13 for mice (see Section M.3.1.3) and Equation Apx M-6.
The continuous HED of 0.636 mg/kg-bw/day was converted to a worker HED of 0.890 mg/kg-bw/day
using Equation Apx M-12. The benchmark MOE for this POD is 100 based on a combination of
uncertainty factors: 3 for interspecies extrapolation when a dosimetric adjustment is used, 10 for human
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variability, and 3 for use of a LOAEL to extrapolate a NOAEL (based on the dose-response) for short-
term and subchronic exposures.
Inhalation
The short-term/subchronic-duration inhalation POD for 1,2-dichloroethane was based on decreased
sperm concentration in mice exposed to 1,2-dichloroethane by inhalation for 4 weeks (Zhang et al..
2017). In this study, a concentration-related decrease in sperm concentration was observed, reaching
statistical significance (relative to controls) at 707.01 mg/m3. Using EPA's BMDS (v. 3.3.2), BMD
modeling was conducted on the sperm concentrations using mouse exposure concentrations. The mice in
the study by Zhang et al. (2017) were exposed for 6 hours/day, 7 days/week. Prior to BMD modeling,
the exposure concentrations in the Zhang et al. (2017) study were adjusted from the exposure scenario of
the original study to equivalent continuous (24 hours/day) exposure concentrations using EquationApx
M-5. Table Apx M-24 shows the sperm concentrations corresponding to each exposure concentration.
BMD modeling was conducted on these data using a BMR of 5 percent relative deviation from controls.
Table Apx M-24. Sperm Concentration in Male Mice Exposed to 1,2-Dichloroethane for 4 Weeks
Unadjusted Exposure
Concentration
(mg/m3)
Adjusted (Continuous)
Exposure Concentration
(mg/m3)
Number of
Animals
Mean Sperm
Concentration
(M/g)
SD
(M/g)
0.30
0.075
10
4.65
0.52
102.70
25.675
10
4.36
0.40
356.04
89.010
10
3.89
0.47
707.01
176.75
10
3.30
0.57
Source: Zhang et al. (2017)
Following U.S. EPA (2012b) guidance, the exponential 3 model with constant variance was selected for
these data. The BMCs°o and BMCLs%for this model were 26.735 and 21.240 mg/m3, respectively. The
BMCL5% of 21.240 mg/m3 was selected as the POD.
U.S. EPA (1994) guidance was used to convert animal inhalation PODs to HECs. For systemic
(extrarespiratory) effects, the HEC is calculated by multiplying the animal POD by the ratio of the
blood:gas partition coefficients in animals and humans, as shown in Equation Apx M-8.
A human blood:air partition coefficient of 19.5 ± 0.7 has been reported for 1,2-dichloroethane (Gargas et
al.. 1989). No blood:air partition coefficient for mice was identified in the literature reviewed. In the
absence of a blood:air partition coefficient for mice, the default ratio of 1 is used in the calculation, in
accordance with U.S. EPA (1994) guidance. Therefore, the POD of 21.240 mg/m3 is multiplied by 1 to
give the HEC.
The resulting POD is 21.240 mg/m3 for continuous exposure. The continuous POD of 21.240 mg/m3 is
converted to an equivalent worker POD using Equation Apx M-14. The resulting POD for workers is
89.208 mg/m3. The benchmark MOE for this POD is 30 based on a combination of uncertainty factors: 3
for interspecies extrapolation when a dosimetric adjustment is used and 10 for human variability for
short-term and subchronic exposures.
Dermal
No PODs were identified from short-term or subchronic studies of dermal exposure to 1,2-
dichloroethane. Therefore, the short-term/subchronic oral HED of 0.636 mg/kg-bw/day and worker
HED of 0.890 mg/kg-bw/day with benchmark MOE of 100 were used for risk assessment of
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short/intermediate-term dermal exposure. As noted in Appendix M.3.1.4, when extrapolating from oral
data that incorporated BW3 4 scaling to obtain the oral HED, EPA uses the same HED for the dermal
route of exposure. The same uncertainty factors are used in the benchmark MOE for both oral and
dermal scenarios.
M.2.8 Non-cancer PODs for Chronic Exposures for 1,2-Dichloroethane
Oral
No studies of chronic oral exposure in laboratory animals were considered suitable for POD
determination (see TableApx M-l 1). Therefore, the short-term/sub chronic POD was also used for
chronic exposure. The short-term/subchronic continuous HED was 0.636 mg/kg-bw/day and the worker
HED was 0.890 mg/kg-bw/day (see Appendix M.2.7). The benchmark MOE for this POD is 1,000 based
on 3 for interspecies extrapolation when a dosimetric adjustment is used, 10 for human variability, 3 for
the use of a LOAEL to extrapolate a NOAEL (based on the dose-response), and 10 for extrapolating
from a subchronic study duration to a chronic study duration for chronic exposures.
Inhalation.
Only one study of chronic inhalation exposure in laboratory animals (IRFMN. 1978) was considered
suitable for POD determination (see Table Apx M-14). However, the 12-month study by IRFMN
(1978) evaluated limited endpoints (serum chemistry changes only) and identified a higher LOAEL than
the study of sperm parameters by Zhang et al. (2017) that was used as the basis for the short-
term/subchronic POD. Therefore, the POD from Zhang et al. (2017) was also used for chronic exposure.
The resulting POD is 21.240 mg/m3 for continuous exposure. The continuous POD of 21.240 mg/m3 is
converted to an equivalent worker POD using EquationApx M-l3. EquationApx M-3 was used with
the molecular weight of 1,2-dichloroethane (98.96 mg/mmol) to convert the continuous and worker
short-term/subchronic/chronic PODs (21.240 and 89.208 mg/m3, respectively) to 5.2478 and 22.041
ppm, respectively. The resulting POD for workers is 89.208 mg/m3. (see Table_Apx M-25). The
benchmark MOE for this POD is 300 based on 3 for interspecies extrapolation when a dosimetric
adjustment is used, 10 for human variability, and 10 for extrapolation from a 4-week study to chronic
exposure duration for chronic exposures.
Dermal
No PODs were identified from chronic-duration studies of dermal exposure to 1,2-dichloroethane (see
Table Apx M-13). Therefore, the oral HEDs of 0.636 mg/kg-bw/day (continuous) and 0.890 mg/kg-
bw/day (for workers) with benchmark MOE of 1,000 were used for risk assessment of chronic-duration
dermal exposure. As noted in Section M.3.1.3, when extrapolating from oral data that incorporated
BW3 4 scaling to obtain the oral HED, EPA uses the same HED for the dermal route of exposure. The
same uncertainty factors are used in the benchmark MOE for both oral and dermal scenarios.
M.3 Equations
Section M.3 provides the equations used in derivation of non-cancer and cancer PODs for 1,2-
dichloroethane risk assessment. Section M.4 describes the non-cancer POD derivation for acute,
short/intermediate-term, and chronic durations.
M.3.1 Equations
This section provides equations used in calculating non-cancer PODs, including air concentration
conversions (ppm to mg/m3 and the converse), adjustments for continuous exposure, calculation of
human equivalent concentrations (HECs) and human equivalent doses (HEDs), and route-to-route
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extrapolation calculations. All PODs were initially derived for continuous exposure scenarios
(7 days/week, and 24 hours/day for inhalation). See Appendix M.3.1.5 for the calculated continuous
exposure PODs as well as PODs converted for use in occupational exposure scenarios (8 hours/day,
5 days/week).
M.3.1.1 Air Concentration Unit Conversion
It is often necessary to convert between ppm and mg/m3 due to variation in concentration reporting in
studies and the default units for different OPPT models. Therefore, EPA presents all PODs in
equivalents of both units to avoid confusion and errors. EquationApx M-2 presents the conversion of
the HEC from ppm to mg/m3 and Equation Apx M-3 shows the reverse conversion.
Equation Apx M-2. Converting ppm to mg/m3
HECcontinuous(mg/m3) = HECcontinuous (ppm) * (molecular weight/24.45)
Equation Apx M-3. Converting mg/m3 to ppm
HECcontinuous (ppm) = HECcontinuous (mg/m3 ) * (2AAS/molecular weight)
For 1,1-dichloroethane, the molecular weight used in the equations is 98.96 mg/mmol.
M.3.1.2 Adjustment for Continuous Exposure
Non-cancer PODs for oral studies are adjusted from the exposure scenario of the original study to
continuous exposure following Equation Apx M-4.
Equation Apx M-4. Adjusting Non-cancer Oral POD for Continuous Exposure
P0Dcontinuous PO^study ^ (days Weeks^uciy/days weekcontinous)
Where:
days week.continuous ~ 7 days
Non-cancer PODs for inhalation studies are adjusted from the exposure scenario of the original study to
continuous exposure following Equation Apx M-5.
Equation Apx M-5. Adjusting Non-cancer Inhalation POD for Continuous Exposure
P 0 D continuous D study ^ (hoUTS d.Q.ystudy /hoUT S day continous) ^ (dciyS W66hstuciy / days W6 6k continous*)
Where:
hours daycontinous — 24 hours
days w£-£"^contt7ious — 7 days
M.3.1.3 Calculation of HEDs and HECs from Animal PODs
Consistent with U.S. EPA (2011c) guidance, oral PODs from animal studies are scaled to HEDs using
EquationApx M-6.
Equation Apx M-6. Calculation of Continuous HED from Continuous Animal Oral POD
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Where:
DAF
Human equivalent dose for continuous exposure (mg/kg-day)
Oral POD assuming daily doses (mg/kg-day)
Dosimetric adjustment factor (unitless)
DAFs for scaling oral animal PODs to HEDs are calculated using EquationApx M-7.
EquationApx M-7. Calculating DAF for Oral HED Calculation
l
Where:
DAF = dosimetric adjustment factor (unitless)
BW.4 = body weight of species used in toxicity study (kg)
BWff = body weight of adult human (kg)
U.S. EPA (2011c) presents DAFs for extrapolation to humans from several species. However, because
those DAFs used a human body weight of 70 kg, EPA has updated the DAFs using a human body
weight of 80 kg from the EPA Exposure Factors Handbook (U.S. EPA. 201 la). EPA used the body
weights of 0.025 and 0.25 kg for mice and rats, respectively, as presented in U.S. EPA (2011c). The
resulting DAFs for mice and rats are 0.13 and 0.24, respectively. For guinea pigs, EPA used a body
weight of 0.43 kg, resulting in a DAF of 0.27.
U.S. EPA (1994) guidance was used to convert animal inhalation PODs to HECs. Effects in animals
exposed to 1,1-dichloroethane by inhalation consisted of systemic (extrarespiratory) effects. Therefore,
consistent with U.S. EPA (1994) guidance, the HEC for extrarespiratory effects is calculated by
multiplying the animal POD by the ratio of the blood:gas partition coefficients in animals and humans.
Equation Apx M-8 shows the HEC calculation for extrarespiratory effects.
Equation Apx M-8. Calculation of HEC from Animal Inhalation POD
Blood:air coefficients for 1,2-dichloroethane were 19.5 in humans and 30 in rats (Gargas et al.. 1989).
Blood:air partition coefficients for other species were not located. When the animal blood:air partition
coefficient is greater than the human blood:air partition coefficient, the default ratio of 1 is used in the
calculation in accordance with U.S. EPA (1994) guidance.
HEC = POD,
1continuous ^
Where:
= blood:air partition coefficient for animals (A) to humans (H)
t)h
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Nasal effects were observed in one study of F344 rats exposed by inhalation to 1,2-dichloroethane (Dow
Chemical 2006b). For nasal effects, in accordance with U.S. EPA (1994) guidance, the HEC was
calculated using the regional gas dose ratio for extrathoracic effects (RGDRet) using EquationApx
M-9.
Equation Apx M-9. Calculating HEC Using Animal Inhalation POD and RGDRet
HEC continuous — POD continuous X RGDRgj*
Where:
HECcontinuous = Human equivalent concentration for continuous exposure (mg/m3)
PODcontinuous = Animal POD for continuous exposure (mg/m3)
RGDRet = Regional gas dose ratio for extrathoracic effects (unitless)
The RGDRet for nasal effects in F344 rats was calculated as shown in Equation Apx M-10.
Equation Apx M-10. Calculating RGDRet in Rats
RGDRet —
VEa /VEh
SAa / SAfr
Where:
RGDRet = Regional gas dose ratio for extrathoracic effects (unitless)
VE = Ventilation rate for male and female F344 rats = 0.211 L/minute
(U.S. EPA. 1994)
SAa = Surface area of the extrathoracic region in rats =15 cm2
U.S. EPA, 1994, 6488}
VEfi = Ventilation rate for humans = 13.8 L/minute (U.S. EPA. 1994)
SAh = Surface area of the extrathoracic region in humans = 200 cm2
(U.S. EPA. 1994)
The RGDRet for nasal effects in F344 rats calculated using the equation above is 0.2.
M.3.1.4 Cancer Inhalation Unit Risk
For cancer risk assessment, an Inhalation Unit Risk (IUR) can be converted to a Cancer Slope Factor
(CSF) using the exposure parameters described above for non-cancer conversions, as in Equation Apx
M-ll.
Equation Apx M-ll. Calculating CSF from IUR
CSF =IUR
BWh
x1r7
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Where:
CSF = Oral cancer slope factor based on daily exposure (per mg/kg-day)
IUR = Inhalation unit risk based on continuous daily exposure (per mg/m3)
BWh = Body weight of adult humans (kg) = 80
IRr = Inhalation rate for an individual at rest (m3/day) = 14.7
M.3.1.5 Conversion of Continuous POPs to Worker POPs
All PODs were initially derived for continuous exposure, and then converted to an equivalent POD for
occupational exposure for convenience in risk calculations. EquationApx M-12 and EquationApx
M-13 were used to convert from continuous to occupational exposure scenarios for oral and inhalation
non-cancer PODs, respectively.
Equation Apx M-12. Adjusting Non-cancer Oral POP from Continuous to Occupational
Exposure
PODoccupational PODcontinuous ^ days/WBBk*)
Equation Apx M-13. Adjusting Non-cancer Inhalation POP from Continuous to Occupational
Exposure
PODoccupational P^^continuous ^ (24/8 hoUTS / day^ X (7/5 days/W66k^
To adjust a continuous IUR for occupational scenarios, Equation Apx M-14 was used (days per week
adjustment is not required because it is already accounted for in the Lifetime Average Daily
Concentration).
Equation Apx M-14. Adjusting Continuous IUR For Occupational Scenarios
IU ^occupational ~ W ^continuous ^ (hoUTS — day occupational/hoUTS — day continuous^
M.4 Summary of Continuous and Worker Non-cancer PODs
Each of the continuous non-cancer PODs described in the preceding sections was converted to an
equivalent POD for occupational exposure for convenience in risk calculations. Equations used to
convert from continuous to occupational exposure scenarios for oral and inhalation exposure,
respectively are provided in Appendix M.3. Table Apx M-25 provides a summary of the non-cancer
PODs for both continuous and occupational exposure scenarios for 1,1-dichloroethane using read-across
from 1,2-dichloroethane.
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15295 TableApx M-25. Summary of Non-cancer PODs for 1,1-Dichloroethane (Read-Across from
15296 1,2-Dichloroethane)
Route
Duration
Continuous POD
Worker POD
Benchmark
MOE
Reference
Oral
Acute
19.9 mg/kg-bw/day
19.9 mg/kg-bw/day
30
Storer et al. (1984)
Short/
Intermediate-term
0.636 mg/kg-bw/day
0.890 mg/kg-bw/day
100
Munson et al. (1982)
Chronic
0.636 mg/kg-bw/day
0.890 mg/kg-bw/day
1,000
Munson et al. (1982)
Inhalation
Acute
9.78 mg/m3
41 mg/m3
30
Dow Chemical (2006b)
Short/
Intermediate-term
21.2 mg/m3
89 mg/m3
30
Zhang et al. (2017)
Chronic
21.2 mg/m3
89 mg/m3
300
Zhang et al. (2017)
Dermal
(Route-to-
Route
Extrapolation
from Oral)
Acute
19.9 mg/kg-bw/day
19.9 mg/kg-bw/day
30
Storer et al. (1984)
Short/
Intermediate-term
0.636 mg/kg-bw/day
0.890 mg/kg-bw/day
100
Munson et al. (1982)
Chronic
0.636 mg/kg-bw/day
0.890 mg/kg-bw/day
1,000
Munson et al. (1982)
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M.5 Evidence Integration Tables for Non-cancer for 1,1-Dichloroethane
Table Apx M-26. Evidence Integration Table for Reproductive/Developmental Effects
Database Summary
Factors that Increase Strength
Factors that Decrease
Strength
Summary of Key
Findings and within-
Stream Strength of the
Evidence Judgment
Inferences across Evidence
Streams and Overall Weight
of Scientific Evidence
Judgement
Evidence Integration Summary Judgement on Reproductive/Developmental Effects
Evidence from human studies
• A retrospective case-control
study of mother-infant pairs
evaluated exposure based on
maternal residential proximity
to industrial air releases and
its association with birth
defects (neural tube, oral
cleft, and heart defects; limb
deficiencies; and
anencephaly) (Brender et al..
2014). Study quality: High
Biological gradient/dose-response:
• Spina bifida and septal heart
defects were associated with
maternal residential exposures
(any vs. none) to 1,1-
dichloroethane.
Magnitude and precision:
• The study was large and
accounted for multiple facilities
and their chemical releases,
allowing for evaluations of
associations between exposure to
individual chlorinated solvents
and specific birth defects.
Quality of the database:
• Associations between birth
defects and exposure were
observed in a high-quality study.
Biological gradient/dose-
response:
• Analyses based on quartiles
of exposure intensity did
not show a dose-response
relationship with spina
bifida or septal heart
defects.
Magnitude and precision:
• Exposure was based on
maternal address at
delivery and industry
releases reported to TRI;
changes in address between
conception and delivery
and failure to account for
prevailing wind directions
may have contributed to
exposure misclassification.
• Effect estimates were not
adjusted for concurrent
exposure to other
chemicals.
Key findings'.
Available
epidemiological data are
limited and inconclusive.
Overall WOSE
judgement for
reproductive/developme
ntal toxicity effects
based on human
evidence:
• Indeterminate
Evidence from apical endpoints in in vivo mammalian animal studies
Overall WOSE judgement for
reproductive/developmental
effects based on integration of
information across evidence
streams:
Evidence is inadequate to
assess whether 1,1-
dichloroethane exposure may
cause reproductive/
developmental toxicity under
relevant exposure
circumstances.
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Database Summary
Factors that Increase Strength
Factors that Decrease
Strength
Summary of Key
Findings and within-
Stream Strength of the
Evidence Judgment
Inferences across Evidence
Streams and Overall Weight
of Scientific Evidence
Judgement
Oral:
• Short-term, subchronic, and
chronic gavage studies in
male rats and male and
female mice examined
histology of the testes,
epididymis, prostate,
mammary gland, ovary,
and/or uterus (Muralidhara et
al.. 2001: NCI. 1978). Studv
quality: High
Inhalation:
• A subchronic inhalation
toxicity study in male dogs
evaluated testis
histooatholoev (Mellon
Institute. 1947). Studv
quality: Medium
• An inhalation study that
exposed female rats during
GD 6-15 evaluated numbers
of litters, corpora lutea,
implantations, resorptions,
and live fetuses; fetal sex,
length, and body weights; and
gross, soft tissue, and skeletal
anomalies (Schwetz et al..
1974). Studv aualitv: Medium
Studv aualitv ranked as
Uninfonnative:
• Chronic gavage studies in
male and female rats "
examined histology of the
testes, epididymis, prostate,
mammary gland, ovary,
and/or uterus (NCI. 1978).
Biolosical eradient/dose-resoonse:
• A significantly increased litter
incidence of delayed ossification
of sternebrae was observed in the
offspring of rats exposed via
inhalation at the higher of two
tested concentrations.
• In a study ranked as
Uninfonnative because
methodological details were not
fully reported, lengthening of the
estrus phase was reported in
female rats exposed via inhalation
for 2-3 months prior to mating,
and embryolethality was
increased in female rats exposed
prior to and throughout gestation
(but not in those exposed only
prior to gestation).
Consistencv:
• In the study reporting
delayed sternebral
ossification associated with
exposure, separate control
groups used for each
exposure level showed
significantly different
incidences of this outcome.
The incidence in the higher
exposed group was
statistically significant only
compared with the
concurrent control, which
had a much lower incidence
than the other control group.
Biolosical olausibilitv:
• Maternal weight gain and
food intake were decreased
at the same exposure level
that resulted in increased
incidence of delayed
ossification in rat offspring.
Magnitude and precision:
• Only one concentration was
tested in the Uninfonnative
study that identified effects
on embryonic mortality.
Oualitv of the database:
• The database lacks a 1- or
2-generation reproduction
toxicity study of acceptable
quality, and only one
developmental toxicity
study is available.
• Data pertaining to effects
on estrous cyclicity and
Key findings'.
Available animal
toxicological studies are
limited and inconclusive.
Overall WOSE
judgement for
reproductive/develop-
mental effects based on
animal evidence:
• Indetenninate
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Database Summary
Factors that Increase Strength
Factors that Decrease
Strength
Summary of Key
Findings and within-
Stream Strength of the
Evidence Judgment
Inferences across Evidence
Streams and Overall Weight
of Scientific Evidence
Judgement
• A subchronic inhalation
toxicity study in male rats h
evaluated testis
histooatholoev (Mellon
Institute. 1947).
• An inhalation study c that
exposed female rats during
premating, mating, and/or
gestation evaluated mating,
fertility, fetal development,
estrous cyclicity, and
histology of the ovaries
(Vozovaia. 1977).
preimplantation viability
are limited to a single study
rated Uninfonnative.
• The subchronic inhalation
toxicity study in dogs,
which did not identify
effects on testis histology,
used only one mixed-breed
animal and lacked
methodological details.
• Several of the available
studies were rated
Uninfonnative based on
reporting limitations, high
incidences of pathological
findings in negative
controls, and/or mortality
unrelated to exposure.
Evidence from mechanistic studies - indeterminate (no studies)
" The 78-week studv in male and female rats (NCI. 1978) was considered Uninfonnative owins to high mortality related to Diicumonia.
b The subchronic inhalation studv in male and female rats (Mellon Institute. 1947) was considered Uninfonnative owins to high incidences of oatholoeical findings in
controls and high mortality due to virus or infection.
"The rcDrodiictivc/dcYcloDmcntal inhalation studv in female rats (Vozovaia. 1977) was considered Uninfonnative because methodological details regarding exposure
(type of inhalation exposure, description of air chamber, number of air changes, etc.) were not reported.
15301
15302
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Table Apx M-27. Evidence Int
egration Table for Renal Effects
Database Summary
Factors that Increase Strength
Factors that Decrease
Strength
Summary of Key
Findings and within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
Evidence Integration Summary Judgement on Renal Effects
Evidence from human studies (none)
• Indetenninate
Overall WOSE
judgement for renal
effects based on
integration of
information across
evidence streams:
Evidence indicates
that 1,2-
dichloroethane likely
causes renal effects
under relevant
exposure
circumstances.
Evidence from apical endpoints in in vivo mammalian animal studies
Oral:
• Short-term and subchronic
gavage studies in male rats
evaluated blood urea nitrogen
(BUN), urinalysis parameters,
kidney weights, and/or gross and
microscopic pathology of the
kidnev (Muralidhara et al..
2001). Studv aualitv: Hieh
• A chronic gavage study in male
and female mice evaluated gross
and microscopic pathology of the
kidney and urinary bladder (NCI,
1978). Studv aualitv: Hieh
Inhalation:
• A subchronic inhalation study in
dogs evaluated BUN and kidney
histoloev (Mellon Institute.
1947). Studv aualitv: Medium
• Subchronic inhalation studies in
male and female rats, guinea
pigs, and rabbits evaluated BUN,
serum creatinine, urinalysis
parameters, kidney weights,
and/or kidney histology
(Hofmannet al.. 1971a). Studv
quality: Medium
Studv aualitv ranked as
Uninfonnative:
• A chronic gavage study in male
and female rats " evaluated gross
and microscopic pathology of the
Biolosical eradient/dose-resoonse:
• Absolute kidney weight was
significantly decreased at the two
highest doses in male rats evaluated
after 10 days of gavage exposure.
• Urinary excretion of acid
phosphatase (ACP) and
N-acetylglucosaminidase (NAG)
were significantly increased at the
three highest doses tested in male
rats after 8 weeks of gavage
exposure.
• In a study ranked as Uninfonnative,
increased BUN and serum creatinine
were observed in cats after 26 weeks
of exposure via inhalation. Three of
four treated cats also showed renal
tubular dilatation.
• In acute and short-term
intraperitoneal studies ranked as
Uninfonnative (due to limited
reporting on negative controls and
lack of histological examinations in
controls, respectively); male mice
showed dose-related increases in
percentages of animals with
"significant" urinary protein and
glucose d levels; swelling of >50% of
the renal proximal tubules was
reported in 3/5 mice at the mid-dose.
Oualitv of the database:
Biolosical eradient/dose-
rcsDonsc:
• Urinary excretion of ACP
was significantly decreased
at all doses after 12 weeks of
gavage exposure in male
rats. Urinary NAG in treated
rats was not different from
the control at this time point.
Consistency:
• The changes in kidney
weights and urinary
parameters in the gavage
studies did not conespond to
adverse histopathology
changes in rats, and no renal
histopathology changes were
seen in mice exposed
chronically by gavage or in
dogs, rats, guinea pigs, or
rabbits exposed
subchronically by inhalation.
Magnitude and precision:
• Changes in BUN and serum
creatinine in cats were
influenced by values for one
cat that was sacrificed after
23 weeks due to poor general
condition. In addition, only
four cats/group were tested.
• In a study ranked as
Uninfonnative due to the
lack of histological
examinations in controls, a
Key findings'.
Available toxicological
studies showed changes
in kidney weight, clinical
chemistry, urinary
excretion, and/or kidney
histology. However,
many of the studies that
observed effects had
limitations, and kidney
effects were not seen
consistently across
studies using different
species, exposure routes,
or study durations.
Overall WOSE
judgement for renal
effects based on animal
evidence:
• Indetenninate
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Database Summary
Factors that Increase Strength
Factors that Decrease
Strength
Summary of Key
Findings and within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
kidney and urinary bladder (NCI,
1978).
• A subchronic inhalation study in
male and female rats b evaluated
kidney weights and histology
(Mellon Institute. 1947).
• Subchronic inhalation studies in
cats evaluated BUN, serum
creatinine, urinalysis parameters,
kidney weights, and kidney
histoloev (Hofmann et al..
1971a).
• Acute and short-term
intraperitoneal studies in male
mice c evaluated urinary glucose
and protein and kidney histology
(Plaa and Larson 1965).
• Kidney effects were observed in one
high-quality study and in two studies
ranked as Uninfonnative.
cut-off value was used to
quantify effects on kidney
histology in mice (>50%, or
<50% of the proximal tubule
area affected) and
histological results were only
reported for mid-dose
animals.
Oualitv of the database:
• The subchronic inhalation
toxicity study in dogs, which
did not identify effects on
BUN or kidney histology,
used only one mixed-breed
animal and lacked
methodological details.
Biolosical olausibilitv:
• In the 10-day gavage study
in male rats, decreased
absolute kidney weights
occuned in conjunction with
decreased body weight; there
were no significant changes
in relative kidney weight.
Evidence from mechanistic studies (none)
• Indetenninate
" The study in male and female rats was ranked as Uninfonnative owing to high mortality related to pneumonia.
b The 6-month study in male and female rats was ranked as Uninfonnative because negative controls had a high incidence of pathological lesions and there was high
mortality related to virus or infection.
c The acute and short-term intraperitoneal studies in male mice were ranked as Uninfonnative because details regarding negative controls were not reported and
histology was not perfonned in controls, respectively.
d "Significant" urinary protein and glucose was quantified as 100 and 250 mg%, respectively.
15304
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Table Apx M-28. Evidence Integration Table for Hepatic Effects
Database Summary
Factors that Increase
Strength
Factors that Decrease Strength
Summary of Key
Findings and within-
Stream Strength of
the Evidence
Judgement
Inferences across
Evidence Streams and
Overall WOSE
Judgement
Evidence Integration Summary Judgement on Hepatic Effects
Evidence from human studies (none)
• Indeterminate
Evidence from apical endpoints in in vivo mammalian animal studies
Oral:
• Short-term and subchronic gavage
studies in male rats evaluated serum liver
enzymes (ALT, SDH, and OCT), liver
weights, and gross and microscopic
pathology of the liver (Muralidhara et
al„ 2001). Study quality: High
• A chronic gavage study in male and
female mice evaluated gross and
microscopic pathology of the liver (NCI.
1978). Study quality: High
• Nine-week studies in male rats
determined the potential for tumor
initiation or promotion based on
numbers of GGT-positive foci in the
liver (Milman et al„ 1988: Story et al„
1986). Study quality: High
Inhalation:
• A subchronic inhalation study in dogs
evaluated liver function
(bromsulphthalein excretion and thymol-
barbital turbidity) and histology (Mellon
Institute. 1947). Study quality: Medium
• Subchronic inhalation toxicity studies in
male and female rats, guinea pigs, and
rabbits evaluated serum ALT and AST
and liver function (bromsulphthalein
test), weights, and histology (Hofmann
et al.. 1971a). Study quality: Medium
• An inhalation study that exposed
nonpregnant female rats for 10 days or
pregnant rats on GD 6-15 evaluated
Biological gradient/dose-
response:
• Absolute and relative liver
weights were significantly
decreased in treated male
rats after 5 and 10 days of
gavage exposure.
• Slight changes in
hepatocyte histology (mild
condensation and changes
in cytoplasmic staining
consistent with glycogen
mobilization) were
reported in male rats
treated via gavage for 11
weeks.
• Exposure resulted in
increased numbers of
GGT-positive foci in the
livers of male rats
pretreated with a tumor
initiator.
• Nonpregnant female rats
exposed for 10 days via
inhalation showed
increased relative liver
weight.
Quality of the database:
• Liver effects were
observed in high- and
medium-quality studies.
Biological gradient/dose-response:
• Changes in hepatocyte
histology were observed only
at a dose that caused significant
mortality (8/15 rats) and in the
absence of liver weight or
clinical chemistry changes.
Consistency:
• Changes in liver weight
(increased in female rats
exposed via inhalation and
decreased in male rats treated
by gavage) were observed in
10-day toxicity studies but not
in longer-duration studies in
rats, guinea pigs, rabbits, or
cats.
• Increased liver weight was
observed after a 10-day
exposure of nonpregnant rats
but there were no liver effects
in females exposed to the same
concentration during GD 6-15.
• Chronic oral exposure of mice
did not result in liver
pathology.
Magnitude and precision:
• Only one dose was used in the
9-week tumor initiation and
promotion protocols.
Quality of the database:
Key findings:
Available
toxicological studies
showed changes in
liver weight and/or
histology in the
absence of relevant
clinical chemistry
findings.
Overall WOSE
judgement for hepatic
effects based on
animal evidence:
• Slight
Overall WOSE
judgement for hepatic
effects based on
integration of
information across
evidence streams:
Evidence suggests, but is
not sufficient to
conclude, that 1,1-
dichloroethane exposure
causes hepatic toxicity
under relevant exposure
circumstances.
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Factors that Increase
Strength
Factors that Decrease Strength
Summary of Key
Findings and within-
Stream Strength of
the Evidence
Judgement
Inferences across
Evidence Streams and
Overall WOSE
Judgement
serum ALT and AST, liver weights, and
sross liver oatholoev (Schwetz et al..
1974). Studv aualitv: Medium
Studv aualitv ranked as Uninfonnative:
• A chronic gavage study in male and
female rats " evaluated gross and
microscopic natholoev of the liver (NCI.
1978).
• A subchronic inhalation study in male
and female rats b evaluated icterus index,
liver weights, fat content, and histology
(Mellon Institute. 1947).
• Subchronic inhalation toxicity studies in
cats evaluated serum ALT and AST and
liver function (bromsulphthalein test),
weiehts. and histoloev (Hofmann et al..
1971a).
• An inhalation study c that exposed
female rats during premating, mating,
and/or gestation evaluated liver function
(Quick-Pytel test) and/or liver weights
(Vozovaia. 1977).
• The subchronic inhalation
toxicity study in dogs, which
did not identify effects on liver
functional tests or liver
histology, used only one
mixed-breed animal and
lacked methodological details.
• Several of the available
studies, which did not identify
liver effects, were ranked as
Uninfonnative based on
reporting limitations, high
incidences of pathological
findings in negative controls,
and/or mortality unrelated to
exposure.
Biolosical olausibilitv and human
relevance:
• The toxicological significance
of decreased liver weight in the
10-day gavage study in male
rats is unclear and may be
partly attributable to decreased
body weights.
Evidence from mechanistic studies (none)
• Indetenninate
" The chronic study in male and female rats was ranked as Uninfonnative owing to high mortality related to pneumonia.
b The 6-month study in male and female rats was ranked as Uninfonnative because negative controls had a high incidence of pathological lesions and there was high
mortality related to virus or infection.
c The reproductive/developmental inhalation study in female rats was considered Uninfonnative because methodological details regarding exposure (type of inhalation
exposure, description of air chamber, number of air changes per hour, etc.) were not reported.
15307
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Table Apx M-29. Evidence Integration Table for Nutritional/Metabolic Effects
Database Summary
Factors that Increase Strength
Factors that Decrease
Strength
Summary of Key
Findings and within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams and
Overall WOSE
Judgement
Evidence Integration Summary Judgement on Nutritional/Metabolic Effects
Evidence from human studies (none)
• Indeterminate
Overall WOSE
judgement for
nutritional/metabolic
effects based on
integration of
information across
evidence streams:
Evidence suggests, but
is not sufficient to
conclude, that
1,1-dichloroethane
exposure
causes body weight
decrements under
relevant exposure
circumstances.
Evidence from apical endpoints in in vivo mammalian animal studies
Oral:
• Short-term and subchronic gavage
studies in male rats evaluated body
weieht (Muralidhara et al.. 2001).
Study quality for endpoint: High
• Six-week and 2-year gavage studies in
male and female mice evaluated body
weieht (NCI. 1978). Studv aualitv for
endpoint: High
• A cancer bioassay and a tumor
promotion assay in male mice
evaluated body weights during a 52-
week drinking water exposure
(Klaunie et al.. 1986). Studv aualitv
for endpoint: High
• Single dose initiation and 7-week
promotion studies (gavage) in partially
hepatectomized rats evaluated body
weieht (Milmanet al.. 1988). Studv
quality for endpoint: Medium
Inhalation:
• An inhalation study that exposed
female rats during GD 6-15 evaluated
maternal bodv weiehts (Schwetz et al..
1974). Studv aualitv for endooint:
High
• A 6-month inhalation study in one dog
evaluated bodv weieht (Mellon
Institute. 1947). Studv aualitv for
endpoint: Medium
• 26-week inhalation studies in male and
female rats, guinea pigs, and rabbits
Bioloeical eradicnt/dosc-rcsDonsc:
• In the short-term and
subchronic gavage studies in
rats, significantly decreased
body weights (>10% relative to
controls) were seen at >2,000
mg/kg-bw/day.
• Maternal body weight was
significantly decreased (>0%
relative to controls) at >3,798
ppm in rats exposed by
inhalation during gestation.
• One dog exposed to 1,067 ppm
by inhalation for 6 months
exhibited lower body weight
than the control.
Oualitv of the database:
• Decreased body weight was
observed in two high quality
studies and one medium
quality study.
Bioloeical eradient/dose-
rcsDonsc and Consistencv:
• No treatment-related
change in body weight was
observed in mice exposed
to doses up to 2,885-3,331
mg/kg-bw/day by gavage
for up to 78 weeks.
• No treatment-related
change in body weight was
observed in rats exposed to
doses up to 543 mg/kg-
bw/day in drinking water
for 52 weeks.
• No treatment-related
change in body weight was
observed in initiation or
promotion studies in
partially hepatectomized
rats exposed by gavage to
doses up to 700 mg/kg-
bw/day.
• No treatment-related
change in body weight was
observed in male and
female rats, guinea pigs,
and rabbits exposed to 750
ppm by inhalation for 26
weeks.
Maenitude and precision:
• The magnitude of the body
weight decrease (-10%) in
the gestational exposure
Key findings'.
1,1-dichloroethane
induced body weight
decrements in rats at
high gavage exposures
(>2,000 mg/kg-bw/day)
and in one dog exposed
by inhalation (1,067
ppm). No body weight
effects were seen in mice
or in rats at lower
exposure levels.
Overall WOSE
judgement for
nutritional/metabolic
effects based on animal
evidence:
• Moderate
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Factors that Decrease
Strength
Summary of Key
Findings and within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams and
Overall WOSE
Judgement
evaluated bodv weisht (Hofmann et
al.. 1971a). Studv aualitv for endooint:
Medium
Studv aualitv ranked as Uninformative
for this endDoint:
• Six-week and clironic gavage studies
in male and female rats " evaluated
bodv weisht (NCI. 1978).
• A 6-month inhalation study in male
and female rats b evaluated body
weisht (Mellon Institute. 1947).
• A 26-week inhalation study in cats c
evaluated bodv weisht (Hofmann et
al.. 1971a).
study was small and the
decrease lacked a dose-
response relationship.
Oualitv of the database:
• No treatment-related effects
on body weight were
observed in two high
quality studies and two
medium quality studies.
Evidence from mechanistic studies (none)
• Indeterminate
" The 6-week gavage study in rats was ranked Uninformative due to inadequate data reporting, and the clironic gavage study in rats was ranked as Uninformative owing
to high mortality related to pneumonia.
b The 6-month inhalation study in male and female rats was ranked as Uninformative because a significant number of animals died due to apparent lung infections
unrelated to exposure.
c The 26-week inhalation study in cats was ranked as Uninformative due to an intercurrent "catarrhal" infection that rendered it impossible to differentiate effects of
infection from effects of exposure
15310
15311
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Table Apx M-30. Evidence Integration Table for Mortality
Database Summary
Factors that Increase Strength
Factors that Decrease
Strength
Summary of Key
Findings and within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams and
Overall WOSE
Judgement
Evidence Integration Summary Judgement on Mortality
Evidence from human studies (none)
• Indeterminate
Overall WOSE
judgement for mortality
based on integration of
information across
evidence streams:
Evidence indicates that
1,1-dichloroethane
exposure is likely to
cause death under
relevant exposure
circumstances.
Evidence from apical endpoints in in vivo mammalian animal studies
Oral:
• An acute gavage study in guinea pigs
evaluated mortality (Dow Chemical.
1947). Studv aualitv for endooint: Low
• Acute, short-term, and subchronic
gavage studies in male rats evaluated
mortality (Muralidhara et al.. 2001).
Study quality for endpoint: High
• A chronic gavage study in male and
female mice evaluated mortality (NCI.
1978). Studv duality for endooint: Hieh
• A cancer bioassay and a tumor
promotion assay in male mice evaluated
mortality during a 52-week drinking
water exposure (Klaunie et al.. 1986).
Study quality for endpoint: High
Inhalation:
• A 6-month inhalation study in one dog
evaluated mortality (Mellon Institute.
1947). Studv duality for endooint: Low
• 26-week inhalation studies in male and
female rats, guinea pigs, and rabbits
evaluated mortality (Hofmann et al..
1971a). Studv duality for endooint:
Medium
Studv duality ranked as Uninfonnative for
this endDoint:
• Six-week gavage studies in male and
female mice and rats " evaluated
mortality (NCI. 1978).
Biolosical eradient/dose-resoonse:
• In an acute gavage study, all
guinea pigs (sample size not
reported) died at 1,000 mg/kg-
bw.
• In an acute gavage study in
rats, deaths occurred at doses
>8,000 mg/kg-bw within 24
hours of dosing; the LD50 was
8200 mg/kg-bw.
• In a short-term gavage study in
rats, 3/8 rats died at 8,000
mg/kg-bw/day.
• In a subchronic gavage study in
rats, 1/15 rats died at 2,000
mg/kg-bw/day and 8/15 died at
4000 mg/kg-bw/day.
• In 6-week gavage studies
ranked Uninfonnative due to
the lack of mortality data at
doses other than the highest
dose, 2/5 female rats died at
3,160 mg/kg-bw/day, and 2/5
male mice and 3/5 female mice
died at 5,620 mg/kg-bw/day.
• In a chronic gavage study in
mice, significantly reduced
survival was observed at
2,885-3,331 mg/kg-bw/day.
Oualitv of the database:
• Mortalities were reported in
high- and low-quality studies.
Biolosical eradient/dose-
rcsDonsc and Consistency:
• In the 52-week drinking
water study, no effect on
survival was observed at
doses up to 543 mg/kg-
bw/day.
• No treatment-related
effects on survival were
seen in animals exposed
by inhalation.
Key findings'.
Mortalities occurred in
several species of animal
exposed to 1,1-
dichloroethane (>1000
mg/kg-bw) via gavage in
high quality studies.
Overall WOSE
judgement for mortality
based on animal
evidence:
• Robust
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Factors that Decrease
Strength
Summary of Key
Findings and within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams and
Overall WOSE
Judgement
• A chronic gavage study in male and
female rats b evaluated mortality (NCI.
1978).
• An inhalation study c that exposed
female rats during premating, mating,
and/or gestation evaluated mortality
(Vozovaia. 1977).
• A 6-month inhalation study in male and
female rats d evaluated mortality
(Mellon Institute. 1947).
• A 26-week inhalation study in cats e
evaluated mortality (Hofmann et al..
1971a).
• An acute intraperitoneal study in male
mice ^evaluated mortality (Plaa and
Larson. 1965).
Evidence from mechanistic studies (none)
• Indetenninate
" The 6-week gavage studies in mice and rats were ranked as Uninfonnative because mortality data were reported only for the high dose group, and statistical analysis
was not performed on mortality data.
b The chronic gavage study in male and female rats was ranked as Uninfonnative owing to high mortality related to pneumonia.
c The reproductive/developmental inhalation study in female rats was considered Uninfonnative because methodological details regarding exposure (type of inhalation
exposure, description of air chamber, number of air changes per hour, etc.) were not reported
J The 6-month inhalation study in male and female rats was ranked as Uninfonnative because a significant number of animals died due to apparent lung infections
unrelated to exposure.
e The 26-week inhalation study in cats was ranked as Uninfonnative due to an intercunent "catanhal" infection that rendered it impossible to differentiate effects of
infection from effects of exposure.
' The acute intraperitoneal study in male mice was ranked as Uninfonnative because details regarding negative controls were not reported.
15313
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Table Apx M-31. Evidence Integration Table for Neurological Effects
Database Summary
Factors that Increase Strength
Factors that Decrease
Strength
Summary of Key
Findings and within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
Evidence Integration Summary Judgement on Neurological Effects
Evidence from human studies (none)
• Indeterminate
Evidence from apical endpoints in in vivo mammalian animal studies
Oral:
• An acute gavage study in male rats
evaluated clinical signs (Muralidhara et
al.. 2001). Study quality for endpoint:
Medium
• Short-term and subchronic gavage
studies in male rats evaluated clinical
signs, brain weight, and brain
histopathology (Muralidhara et al..
2001). Study quality for endpoint:
Medium
Study quality ranked as Uninfonnative for
this endpoint:
• A chronic gavage study in male and
female rats " evaluated clinical signs,
brain histopathology, and gross
pathology (NCI. 1978).
Biological gradient/dose-response:
• Clinical signs of neurotoxicity
(excitation followed motor
impairment and sedation) were
observed in rats given a single
gavage dose of >2,000 mg/kg-
bw.
• Central nervous system
depression (not further
described) was observed in rats
exposed to 2,000 mg/kg-
bw/day for 13 weeks, and the
rats exhibited protracted
narcosis at 4,000 mg/kg-
bw/day.
Biological plausibility:
• 1,1 -dichloroethane was used as
an anesthetic for humans
(administered via inhalation) in
the past (ATSDR. 2015).
Quality of the database:
• Clinical signs of central
nervous system effects were
seen in medium quality studies.
Consistency:
• 1,1-dichloroethane
exposure did not affect
brain weight or
histopathology after short-
term or subchronic gavage
exposure in rats.
• 1,1-dichloroethane
exposure did not induce
clinical signs or changes in
brain histopathology in
mice exposed by gavage to
doses up to 2,885-3,331
mg/kg-bw/day for 78
weeks.
Quality of the database:
• There are no studies of
sensitive neurobehavioral
endpoints.
Evidence from mechanistic studies (none)
Key findings:
1,1-dichloroethane
induced central nervous
system depression in rats
exposed by gavage, and
this finding is consistent
with its past use as a
human anesthetic.
Overall WOSE
judgement for
neurological effects
based on animal
evidence:
• Moderate
• Indeterminate
Overall WOSE
judgement for
neurological effects
based on integration
of information across
evidence streams:
Evidence suggests, but
is not sufficient to
conclude, that
1,1-dichloroethane
exposure
causes neurological
effects under relevant
exposure
circumstances.
' The study in male and female rats was ranked as Uninfonnative owing to high mortality related to pneumonia.
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M.6 Evidence Integration Tables for Non-cancer for 1,2-Dichloroethane
Table Apx M-32.1,2-Dichloroethane Evidence Integration Table for Reproductive/Developmental Effects
Database Summary
Factors that Increase
Strength
Factors that Decrease
Strength
Summary of Key Findings
and within-Stream
Strength of the Evidence
Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
Evidence Integration Summary Judgement on Reproductive/Developmental Effects
Evidence from human studies
A case-control study examined the association
between proximity to point sources of
chlorinated solvents and birth defects.
Exposure was assessed based on metrics that
combined residential distances to industrial
sources and annual amounts of chemicals
released (using EPA's Toxic Release
Inventory), and birth defects were assessed
using Texas birth registries. The geocoded
address of mothers on day of delivery and the
amount of solvent was used in the Emission
Weighted Probability model to assign each
mother an exposure risk value (Brender et al..
2014). Study quality: High
A retrospective cohort study examined the
association between chlorinated solvents in
drinking water and birth outcomes in 75 New
Jersey towns. Exposure was based on
measurements of chlorinated solvents in public
water supplies in the maternal town of
residence at the time of birth. Birth outcomes
and some covariate data were obtained from
birth certificates, fetal death certificates, and
the NJ Birth Defects Registry (Bove. 1996:
Bove et al.. 1995). Study quality: Medium
Biological gradient/dose-
response:
• In women of all ages, any
exposure to 1,2-
dichloroethane (based on
residential proximity to air
emissions) was positively
associated with neural tube
defects OR =1.28 (CI 1.01,
1.62) and in particular spina
bifida OR =1.64 (CI 1.24,
2.16). In analyses by
intensity of exposure,
significant trends were
observed for spina bifida
and also for septal heart
defects.
• Exposure to 1,2-
dichloroethane in drinking
water (detected vs. not
detected) was positively
associated with major
cardiac defects (OR = 2.81,
95% CI 1.11,6.65). This
category of heart defects did
not include septal defects,
which were evaluated
separately.
Quality of the database:
• Positive associations were
found in high and medium
quality studies.
Magnitude and precision:
• Effect sizes were small and
associations weak for all
1,2 -dichloroethane
outcomes in both studies
(ORs< 2.81, lower 95% CI
< 1.24). The association
between 1,2-dichloroethane
in drinking water and major
cardiac defects was based
on a very small number of
cases (6 with detectable 1,2-
dichloroethane).
• In the Texas study, elective
terminations lacked a vital
record, so 31% of mothers
with neural tube defects
were not geocoded.
• In both studies, there was
the potential for exposure
misclassification for
mothers that changed
residences between the first
trimester (period relevant to
morphogenesis of birth
defects) and delivery,
because exposure was based
on residence at delivery.
Consistency:
• No significant associations
were observed between 1,2-
dichloroethane exposure in
public water supplies and
neural tube defects, septal
Key findings:
In high and medium quality
studies, associations were
observed between 1,2-
dichloroethane exposure and
various birth defects (neural
tube defects including spina
bifida and heart defects of
different types). However,
the effect sizes were small,
the associations were weak
and in some cases based on
very low group sizes, results
of the studies were not
consistent (neural tube
defects/spina bifida in one
study but not the other;
different types of cardiac
defects in the two studies),
and both studies were
limited in various ways (e.g.,
incomplete data on neural
tube defects, potential
exposure misclassification,
questionable temporality,
co-exposures to other
chemicals that were also
associated with the same
defects).
Overall WOSE judgement
for reproductive/
developmental effects based
on human evidence:
• Indeterminate
Overall WOSE
judgement for
reproductive/developm
ental effects based on
integration of
information across
evidence streams:
Evidence indicates that
1,2 -dichloroethane
likely causes effects
on male reproductive
structure and/or
function under
relevant exposure
conditions. Evidence
is inadequate to
determine whether
1,2 -dichloroethane
may cause effects on
the developing
organism. There is no
evidence that 1,2-
dichloroethane causes
effects on female
reproductive structure
and/or function.
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Database Summary
Factors that Increase
Strength
Factors that Decrease
Strength
Summary of Key Findings
and within-Stream
Strength of the Evidence
Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
heart defects, or total
cardiac defects.
Biological plausibility and
human relevance:
• There was limited evidence
of temporality (exposure
prior to outcome) in either
study.
• In both studies, subjects had
multiple overlapping
exposures, and positive
associations with spina
bifida or neural tube
defects, heart defects, and
other defects were found for
many of the other chemicals
considered in the analyses.
Evidence from apical endpoints in in vivo mammalian animal studies
Effects on male reproductive organs
• An inhalation study in rats evaluated testis
weight and gross and microscopic pathology
of the testes after 30 davs exposure (Igwe et
al., 1986b) Studv quality: High
• An inhalation study in a single dog evaluated
testis histopathology after 6 months exposure
(Mellon Institute, 1947) Studv qualitv:
Medium
• An inhalation study in mice evaluated testis
and epididymis weight, sperm parameters and
morphology, histology of the testis,
seminiferous tubules, and caput epididymis,
and plasma and testis hormone levels after 1 -
or 4-week exposure (Zhang et al., 2017) Studv
quality: High
• An inhalation study in rats and guinea pigs
evaluated weight and gross and microscopic
pathology of the testes after up to 212 and 246
davs of exposure, respectivelv ( Spencer et al..
1951) Studv qualitv: Medium
Biological gradient/dose-
response:
• In mice exposed by
inhalation for one week,
decreased sperm
concentration and motility,
increased sperm
abnormalities, and
occasional testicular and
epididymal histopathology
changes) were seen at 700
mg/m3. After 4 weeks,
effects seen at > 350
mg/m3 included more
pronounced sperm changes,
more extensive/severe
histological effects, and
increases in plasma and
testicular testosterone and
LH and testicular GnRH.
Consistencv:
Oualitv of the database:
• No studies of sperm
parameters in any species
other than mice were
available.
Consistencv:
• No testicular
histopathology changes
were observed in mice
exposed by drinking water
for subchronic duration.
• No testicular
histopathology changes
were observed in rats,
guinea pigs, or a single dog
exposed by inhalation for
durations between 30 and
246 days.
• No testicular
histopathology changes
were observed in rats
Key findings:
In high-quality studies, mice
exposed to 1,2-
dichloroethane by inhalation
or intraperitoneal injection,
but not by drinking water,
exhibited effects on
testicular pathology and
sperm parameters. Most of
the data in rats indicated no
effect on the testes (or other
reproductive organs);
however, sperm parameters
were not evaluated in rats.
Overall WOSE judgement
for male reproductive tract
effects based on animal
evidence:
• Moderate
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Database Summary
Factors that Increase
Strength
Factors that Decrease
Strength
Summary of Key Findings
and within-Stream
Strength of the Evidence
Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
• A one-generation reproduction study in rats
exposed by inhalation evaluated
histopathology of F0 testes after 176 days of
exposure (Rao et al., 1980) Studv quality:
Medium
• An inhalation cancer bioassay in rats evaluated
gross pathology of the accessory sex organs,
testes, and seminal vesicles and histopathology
of the prostate and testes after 2 years
exposure (Cheever et al.. 1990) Studv quality:
High
• Gavage studies in rats evaluated testes
weights, gross pathology of the testes, and
histopathology (testes, seminal vesicles,
prostate, and preputial gland) after 10- or 90-
dav exposures (Daniel et al., 1994) Studv
quality: High
• A gavage study in rats evaluated testes weights
and histopathology of the testes, epididymis,
seminal vesicles, and prostate after 13 weeks
exposure (NTP, 1991) Studv qualitv: High
• A gavage cancer bioassay in mice evaluated
comprehensive histopathology after 78 weeks
exposure (NTP, 1978) Studv qualitv: High
• A drinking water study in mice evaluated
testes weights and histopathology of the testes,
epididymis, seminal vesicles, and prostate
after 13 weeks exposure (NTP, 1991) Studv
quality: High
• A dermal cancer bioassay in transgenic mice
susceptible to cancer evaluated testes weights
and histopathology of the prostate, seminal
vesicle, and epididymis after 26 weeks
exposure (Suguro et al., 2017) Studv qualitv:
High
• An intraperitoneal injection study in mice
evaluated histopathology of the testes 8 to 46
days after a 5-day exposure and
histopathology and fertility for up to 9 months
after a 5-day exposure plus 45 days recovery
• Mice exposed to >5
mg/kg/day by daily
intraperitoneal injection for
5 days exhibited reduced
spermatogenesis, loss of
spermatogonia,
histopathology changes in
the testes, and sterility.
exposed by intraperitoneal
injection for 30 days or by
gavage for subchronic
durations.
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for spermatogenesis turnover (Daigle et al.,
2009) Studv quality: High
• An intraperitoneal injection study in rats
evaluated testis weight and gross and
microscopic pathology of the testes after 30
davs exposure (Igwe et al.. 1986b) Studv
quality: Medium
Effects on female reproductive organs
• An inhalation study in female rats evaluated
serum prolactin levels and morphometry and
histopathology of mammary tissue after at
least 28 davs exposure (Dow Chemical. 2014)
Study quality: High
• A one-generation reproduction study in female
rats exposed by inhalation evaluated
histopathology of F0 ovaries and uterus after
176 davs of exposure (Rao et al.. 1980) Studv
quality: Medium
• An inhalation cancer bioassay in female rats
evaluated gross and microscopic pathology of
the mammary tissue, ovaries, and uterus after
2 vears exposure (Cheever et al., 1990) Studv
quality: High
• Gavage studies in rats evaluated ovary
weights, gross pathology of the ovaries, and
histopathology (ovaries, uterus, clitoral gland,
and mammary gland) after 10- or 90-day
exposures (Daniel et al., 1994) Studv qualitv:
High
• A gavage cancer bioassay in mice evaluated
comprehensive histopathology after 78 weeks
exposure (NTP. 1978) Studv qualitv: High
• A drinking water study in mice and a gavage
study in rats evaluated histopathology of the
uterus, mammary gland, clitoral gland, and
ovaries after 13 weeks exposure (NTP, 1991)
Study quality: High
• A dermal cancer bioassay in transgenic mice
susceptible to cancer evaluated ovary weights
and histopathology of the uterus, mammary
Consistencv:
• Several high- and medium-
quality studies of rats and
mice exposed by inhalation,
gavage, drinking water,
and/or dermal contact
reported no treatment-
related changes in
reproductive organ weights
or histopathology.
Key findings:
Inhalation studies in rats,
oral studies in rats and mice,
and a dermal study in mice
observed no effects of 1,2-
dichloroethane on female
reproductive organ weights
or histopathology.
Overall WOSE judgement
for female reproductive tract
effects based on animal
evidence:
• Moderate evidence of no
effect.
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Judgement
gland, and vagina after 26 weeks exposure
(Suguro et al., 2017) Studv quality: High
Effects on reproduction or offspring
• An inhalation study in male and female rats
evaluated numbers of live and dead pups; and
pup weight, sex, gross pathology, liver and
kidney weights, and liver and kidney
histopathology after one generation exposure
(Rao et al.. 1980) Studv qualitv: Medium
• Inhalation studies in female rats and rabbits
evaluated numbers of corpora lutea; numbers
of live, dead, and resorbed fetuses; fetal
weight, length, and sex; external and skeletal
alterations; and cleft palate after gestational
exposure (Rao et al.. 1980) Studv qualitv:
Medium
• Inhalation and gavage studies in female rats
evaluated pregnancy outcomes and fetal
external, skeletal, and visceral examinations
after gestational exposure (Pavan et al.. 1995)
Study quality: High
• A drinking water study in male and female
mice evaluated fertility and gestation indices,
numbers of implantations and resorptions,
viability and lactation indices, litter size, pup
weight, and teratology after multigenerational
exposure (Lane et al., 1982) Studv qualitv:
High
• An intraperitoneal injection study in male
mice evaluated male fertility for up to 9
months after a 5-day exposure plus 45 days
recovery for spermatogenesis turnover (Daigle
et al.. 2009) Studv qualitv: High
Biological gradient/dose-
response:
• An apparent decrease in
necropsy body weight was
observed at the high
concentration of 150 ppm
in a small subset of male
FIB weanling rats exposed
by inhalation in a one-
generation study.
• Male mice exposed by
daily intraperitoneal
injection at > 10 mg/kg-d
for 5 days exhibited
permanent sterility (defined
as sterility for 6 months or
longer).
Magnitude and precision:
• The apparent body weight
decrease in selected male
FIB weanlings at 150 ppm
was based on only 5 male
weanlings per group, was
not statistically
significantly different from
controls, was not seen in
female weanlings, and is
not supported by the study
authors' analysis of the full
data set, which showed no
effect on neonatal body
weight or growth of pups to
weaning in either F1A or
FIB litters.
Key findings:
In a high-quality study,
sterility was observed in
male mice exposed by
intraperitoneal injection.
Evidence for effects on
weanling pup body weight
after inhalation exposure is
weak and inconsistent.
Overall WOSE judgement
for developmental effects
based on animal evidence:
• Slight
Evidence from mechanistic studies
• An in vivo inhalation study in male rats
evaluated elemental content in the testes after
30 davs exposure (Oue et al.. 1988).
• An in vivo inhalation study in male mice
evaluated mRNA expression in the testis and
Biological gradient/dose-
response:
• Inhalation exposure to 1,2-
dichloroethane did not alter
zinc concentration in the
testes. Statistically
Biological plausibility and
human relevance:
• The biological relevance of
the altered element content
in the testes is uncertain.
Key findings:
Evidence for inhibition of
CREM/ CREB signaling and
apoptosis in testes of male
mice exposed to 1,2-
dichloroethane in vivo
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genetic damage in spermatozoa after 1- or 4-
week exposure (Zhang et al.. 2017)
• An in vivo study in mice exposed by
intratesticular injection evaluated testicular
DNA synthesis (Borzelleca and Carchman.
1982).
significant changes in other
element concentrations
included decreased Al, Hg,
and S and increased Ca and
P at the highest tested
concentration (1,840 mg/m3
or 455 ppm)
• Expression consistent with
inhibition of CREM/ CREB
signaling and the induction
of apoptosis was observed
in the testis of mice.
• Intratesticular injection of
1,2-dichloroethane resulted
in a 53% decrease in
testicular DNA synthesis in
mice at the highest dose
tested (250 mg/kg) but not
at doses <100 mg/kg.
• The human relevance of
intratesticular injection
exposure is uncertain.
support observed effects on
testes pathology, sperm
morphology, and fertility in
this species.
Overall WOSE judgement
for reproductive/
developmental effects based
on mechanistic evidence:
• Moderate
15319
15320
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Table Apx M-33.1,2-Dichloroethane Evidence Integration Table
'or Renal Effects
Database Summary
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Factors that Decrease
Strength
Summary of Key
Findings and within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
Evidence Integration Summary Judgement on Renal Effects
Evidence from human studies
Indeterminate
Overall WOSE
judgement for renal
effects based on
integration of
information across
evidence streams:
Evidence indicates
that 1,2-
dichloroethane
likely causes renal
effects under
relevant exposure
circumstances.
Evidence from apical endpoints in in vivo mammalian animal studies
Studies evaluating histooatholoev in
coniunction with other renal endooints:
• Acute inhalation studies in male and
female rats and male mice evaluated
kidney histopathology and weight after a
sinsle 4-hour exposure (Dow Chemical.
2006b): Studv quality: Hieh. (Francovitch
et al.. 1986); Studv aualitv: Medium.
• A short-term inhalation study in male rats
evaluated kidney histopathology and
weieht and after 30 davs of exposure (Iaw e
et al.. 1986b): Studv aualitv: Hieh.
• A chronic inhalation study in F0 male and
female rats evaluated kidney
histopathology and weight after exposure
in a reproduction study from pre-breeding
throueh the generation of 2 litters (Rao et
al.. 1980). Studv aualitv: Medium.
• Chronic inhalation studies in male and
female rats evaluated kidney
histopathology, kidney weight, and/or
clinical chemistry after 212 days or 17-
weeks of exposure (Hofmann et al.. 1971a:
Spencer et al.. 1951): Studv aualitv:
Medium.
• Chronic inhalation studies in a single dog,
guinea pigs, and rabbits evaluated kidney
histopathology, kidney weight, and/or
clinical chemistry after 6 months, 212
davs. or 17 weeks of exposure (Hofmann et
al.. 1971a: Spencer et al.. 1951: Mellon
Institute. 1947): Studv aualitv: Medium.
Biolosical eradient/dose-
rcsDonsc:
• In acute inhalation studies:
o Rats exhibited
significantly increased
incidences of basophilia
of the renal tubular
epithelium (males) or
degeneration/ necrosis
(females) in addition to
significantly increased
absolute and relative
kidney weights (>10%,
both sexes) at 8,212
mg/m3 (2,029 ppm).
o Male mice exhibited
significantly increased
kidney weights (>10%)
and BUN (86%) at >2,020
mg/m3 (>499 ppm).
o In a chronic inhalation
study in rats, a statistically
significant increase in
BUN (-50%) was
reported at 607 mg/m3
(150 ppm).
o In acute gavage studies,
male mice exhibited
significant increases in
relative kidney weight
(>10%) at >300 mg/kg
and significantly
increased percentage of
Biolosical sradient/dose
response:
• High-quality short-term and
chronic inhalation studies
found no treatment-related
effects on kidney weight or
histopathology in rats
exposed up to 647 mg/m3
(159.7 ppm) or mice exposed
up to 368 mg/m3 (89.8 ppm)
• High-quality short-term
gavage studies found no
treatment-related effects on
kidney histopathology,
kidney weight, or BUN in
rats (both sexes) exposed up
to 300 mg/kg-day or on
kidney weight or gross
pathology in mice (both
sexes) exposed up to 49
mg/kg-day.
• High-quality subchronic
gavage studies in male and
female rats found no
treatment-related
histopathology changes at
doses up to 150 mg/kg-day.
• A high-quality chronic
gavage cancer bioassay in
mice found no treatment-
related effects on kidney
histopathology at doses up to
299 mg/kg-day.
Key findings'.
Several high- and
medium-quality studies
found associations
between 1,2-
dichloroethane exposure
and increased kidney
weights, BUN, and/or
renal tubular
histopathology in rats
(both sexes) and mice
following inhalation,
oral, dermal, and
intraperitoneal injection
exposures.
Overall WOSE
judgement for renal
effects based on animal
evidence:
• Moderate
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» Short-term and subchronic gavage studies
in male and female rats evaluated kidney
and bladder histopathology, kidney weight,
and/or clinical chemistry, and/or urinary
chemistry after 10 or 13 weeks of exposure
(Daniel et al.. 1994: NTP. 1991): Study
quality: High.
» A subchronic drinking water study in male
and female mice evaluated kidney
histopathology, weight of kidney and
urinary bladder, and BUN after 13 weeks
of exposure (NTP. 1991): Study quality:
High.
» A dermal cancer bioassay in male and
female transgenic mice susceptible to
cancer evaluated kidney histopathology
and weight after 26 weeks exposure
(Suguro et al.. 2017): Study quality: High.
» A short-term intraperitoneal injection study
in male rats evaluated kidney
histopathology, kidney weight, and/or
clinical chemistry after 30 days of
exposure (Igwe et al.. 1986b): Study
quality: Medium.
Studies evaluating histopathology only:
» An acute inhalation study in rats, mice,
rabbits and guinea pigs evaluated
microscopic kidney pathology after 1.5- to
7-hour exposures (Heppel et al„ 1945):
Study quality: Medium.
» Subchronic and chronic inhalation studies
in rats, rabbits, guinea pigs, and dogs
evaluated kidney histopathology after 13 to
35 weeks of exposure (Heppel et al„ 1946):
Study quality: Low or Medium.
» Inhalation cancer bioassays in male and
female rats and mice evaluated
damaged renal proximal
tubules at 1,500 mg/kg.
o In subchronic gavage
studies, rats exhibited
significantly increased
kidney weights (>10%,
both sexes) at >30 mg/kg-
day and increased BUN
(20%, males) at 120
mg/kg-day.
o In a subchronic drinking
water study, mice
exhibited significantly
increased incidences of
tubular regeneration
(males) at >781 mg/kg-
day and significantly
increased kidney weights
(>10%, both sexes) at
244 448 mg/kg-day.
o In an acute intraperitoneal
injection study in male
mice, a statistically
significant increase in
relative kidney weight
was observed at >400
mg/kg reaching >10% at
500 mg/kg.
Consistency:
• Renal histopathology
changes were also reported
in studies that were limited
by lack of reporting on
control findings. These
included:
o Degeneration of renal
tubular epithelium in rats
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and Overall WOSE
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histopathology of the kidney and urinary
bladder after 2 vears c\ do sure (Naeano et
al.. 2006; Cheeveret al.. 1990); Studv
quality: High.
• An acute gavage study in male mice
evaluated kidney immunohistochemistry
after a sinsle exposure (Morel et al.. 1999).
Study quality: High.
• A gavage cancer bioassay in male and
female mice evaluated kidney
histopathology after 78 weeks of exposure
(NTP. 1978); Studv aualitv: Hieh.
Studies evaluating kidnev weieht. sross
oatholoev. and/or clinical chemistry:
• An acute inhalation study in mice
evaluated kidney weight and BUN levels
after a 4-hour c\ do sure (Storcr et al..
1984); Studv aualitv: Hieh.
• Chronic inhalation studies in male and
female rats evaluated serum chemistry and
urinalysis parameters after 6, 12, or 18
months of exposure (IRFMN. 1987. 1978.
1976); Studv aualitv: Medium.
• An acute gavage study in male mice
evaluated kidney weight and BUN after a
sinsle exposure (Storcr et al.. 1984); Studv
quality: High.
• A short-term gavage study in male and
female mice evaluated kidney weight and
gross pathology after 14 days exposure
(Munsonet al.. 1982); Studv aualitv: Hieh.
• Acute intraperitoneal injection studies in
male rats and mice evaluated kidney
weight and serum chemistry parameters
after a sinsle exposure (Storer and Conollv.
1985; Storer et al.. 1984; Livesev. 1982);
and rabbits after acute
inhalation exposure,
o Increased severity of
renal tubular damage in
mice after acute
inhalation exposure,
o Moderate fatty
degeneration of the
kidney in guinea pigs
after chronic inhalation
exposure,
o Mild karyomegaly of
distal tubules and tubular
degeneration in
transgenic mice after
chronic dermal exposure.
Biolosical plausibility and
human relevance:
• Metabolism of 1,2-
dichloroethane via
glutathione-S-transferase is
believed to yield a reactive
episulfonium ion which can
form the potent nephrotoxic
conjugate S-(2-chloroethyl)-
DL-cysteine.
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and Overall WOSE
Judgement
Studv aualitv: Hieh; (Storcr and Conollv.
1983); Studv aualitv: Medium.
• A short-term intraperitoneal injection study
in male mice evaluated kidney gross
oatholoev after 5 davs of exposure (NTP.
1978); Studv quality: High.
Evidence from mechanistic studies (none)
• Indeterminate
15322
15323
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Table Apx M-34. 1,2-Dichloroet
iane Evidence Integration Table
'or Hepatic Effects
Database Summary
Factors that Increase Strength
Factors that Decrease
Strength
Summary of Key Findings
and within-Stream
Strength of the Evidence
Judgement
Inferences across
Evidence Streams
and Overall
WOSE Judgement
Evidence Integration Summary Judgement on Hepatic Effects
Evidence from human studies
Overall WOSE
judgement for
hepatic effects
based on
integration of
information across
evidence streams:
Evidence suggests,
but is not sufficient
to conclude, that
1,2-dichloroethane
may cause hepatic
effects under
relevant exposure
conditions.
• A cohort study of 251 male workers
from 4 vinyl chloride monomer
(VCM) manufacturing plants
evaluated associations between
exposure to airborne 1,2-
dichloroethane (in conjunction with
low exposure to VCM) and serum
AST, ALT, and GGT. Personal and
area air sampling were used to
determine VCM and 1,2-
dichloroethane exposures and group
participants by job category into low
1,2-dichloroethane (job medians of
0.26-0.44 ppm) or moderate 1,2-
dichloroethane (job medians of 0.77-
1.31 ppm) plus low VCM (job
medians of 0.18-0.39 DDin). (Chens
et al.. 1999). Studv quality: Medium
Bioloeical eradient/dose-resoonse:
• Increased odds of abnormal serum
AST (>37 IU/L) and ALT (>41IU/L)
were observed when comparing the
moderate-1,2-dichloroethane/low-
VCM group with the low-1,2-
dichloroethane/low-VCM group (OR
= 2.2, 95% CI = 1.0-5.4 for abnormal
AST; OR = 2.1, 95% CI = 1.1-4.2 for
abnormal ALT).
Maenitude/orecision:
• Exposure concentrations in
the low- and moderate-1,2-
dichloroethane groups were
overlapping.
Bioloeical olausibilitv/human
relevance:
• All subjects were also
exposed to vinyl chloride
monomer, a known liver
toxicant.
Key findings'.
In a medium-
quality study, increased
odds of abnormal serum
liver enzyme levels were
observed among workers
with higher exposure to
1,2-dichloroethane, in a
cohort with co-exposure to
vinyl chloride.
Overall WOSEjudgement
for hepatic effects based on
human evidence:
Indeterminate
Evidence from apical endpoints in in vivo mammalian animal studies
Studies evaluatine histooatholoev in
Bioloeical aradicnt/dosc-rcsdonsc:
Consistency:
Key findings'.
Several high- and medium-
quality studies in rats and
mice found associations
between 1,2-dichloroethane
exposure and increased
liver weights, serum
enzymes, and/or
histopathology changes
following inhalation, oral,
and intraperitoneal
injection exposures.
Overall WOSE judgement
for hepatic effects based on
animal evidence:
coniunction with other liver
endDoint(s):
• Acute inhalation studies in male and
female rats and male mice evaluated
liver weight and histopathology after
single 4- and/or 8- hour exposures
(Dow Chemical. 2006b): Studv
aualitv: Hieh. (Francovitch et al..
1986); Studv aualitv: Medium
• A short-term inhalation study in male
rats evaluated serum chemistry
(ALP, SDH, and 5'NT), liver weight,
and histopathology after 30 days
• In an acute inhalation study, rats
exhibited minimal histological
changes in the liver at 8212.3 mg/m3
(2029.0 ppm). Liver weight changes
were small (<10%) and inconsistent.
• In an acute inhalation study, male
mice exhibited a significant increase
in relative liver weight (>10%) at
6071 mg/m3 (1,500 ppm).
Histological observations in the liver
included hepatocyte swelling, swollen
nuclei, fat accumulation, and
occasional small areas of necrosis
• In a high-quality short-term
inhalation study in rats, no
treatment-related effects on
liver weight, serum chemistry
or histopathology were
observed in rats at
concentrations up to 1840
mg/m3 (455 ppm).
• In high-quality chronic
inhalation cancer bioassays
in rats and mice, no
significant effects on liver
weight or histology were
observed at concentrations up
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and Overall
WOSE Judgement
exposure (Iawe et al.. 1986b. c)
Study quality: High
• Subchronic and chronic inhalation
studies in male and female rats,
rabbits, cats, and guinea pigs
evaluated serum chemistry (ALT and
AST), bromsulphthalein retention,
liver weight and/or histopathology
after up to 17 weeks exposure
(Hofmann et al.. 1971a) Studv
quality: Medium.
• Chronic inhalation studies in male
and female rats and guinea pigs,
male monkeys, and a single dog
evaluated hepatic lipids/cholesterol,
liver function, liver weight, and/or
histopathology after 170-248 days
exposure (Socnccr et al.. 1951) Studv
aualitv: Medium. (Mellon Institute.
1947) Studv aualitv: Medium.
• Chronic inhalation cancer bioassays
in male and female rats and mice
evaluated liver weight and
histopathology after 2 years exposure
(Nasano et al.. 2006; Cheever et al..
1990) Studv duality: Hieh.
• A one-generation inhalation
reproduction study in rats evaluated
parental liver weight and
histopathology after up to 176 days
exposure (Rao et al.. 1980) Studv
quality: Medium.
• An acute gavage study in female rats
evaluated serum chemistry (ALT,
AST, and LDH) and histopathology
after a sinsle dose (Cottalasso et al..
2002) Studv duality: Medium.
(incidence and severity were not
reported)
• In a chronic inhalation cancer
bioassay, male (but not female) rats
exhibited increased absolute (but not
relative) liver weight (>10%) at 204
mg/m3 (50 ppm)
• In a short-term gavage study, male
(but not female) rats had significantly
increased relative liver weight (>10%)
and serum cholesterol at 100 mg/kg-
day in the absence of histopathology
changes.
• In subchronic gavage studies, male
and female rats exhibited significantly
increased relative liver weights
(>10%) at >75 mg/kg-day in the
absence of biologically significant
serum chemistry changes or
treatment-related histopathology
changes.
• In a subchronic drinking water study,
male and female mice exhibited
significantly increased (>10%)
absolute and relative liver weights at
> 2,478 mg/kg-day in the absence of
treatment-related histopathology
changes.
Consistency:
to 646.4 mg/m3 (159.7 ppm
and 363 mg/m3 (89.8 ppm),
respectively.
• Moderate
• Hepatic histopathology changes and
liver weight increases were also
reported in low- and medium-quality
studies that were limited by lack of
quantitative data reporting and
variable exposure regimens. The
lesions included:
o Congestion, fatty degeneration
and/or necrosis in rats, mice.
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and within-Stream
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Inferences across
Evidence Streams
and Overall
WOSE Judgement
• Short-term and subchronic gavage
studies in male and female rats
evaluated serum chemistry, liver
weight, and liver histopathology after
10-day and 13-week exposures
(Daniel et al.. 1994; NTP. 1991);
Study quality: High.
• A subchronic drinking water study in
male and female mice evaluated liver
weight and histopathology after 13
weeks exposure (NTP. 1991) Studv
quality: High.
• A chronic dermal cancer bioassay in
male and female transgenic mice
evaluated liver weights and
histopathology after 26 weeks
exposure (Sueuro et al.. 2017) Study
quality: High.
Studies evaluating liver histooatholoev
rabbits, and guinea pigs after acute
to short-term inhalation exposures
that were sometimes lethal,
o Cloudy swelling, fatty
degeneration, necrosis, and/or
occasional fat vacuoles in rats and
guinea pigs after subchronic to
chronic inhalation exposure,
o Moderate steatosis in rats without
biologically significant changes in
AST or ALT after a single gavage
dose.
• In studies that did not evaluate
histopathology, findings included:
o Biologically and/or statistically
significant increases in serum SDH
and ALT in mice exposed for 4
hours by inhalation,
o Increased serum ALT, SDH and/or
glutamate dehydrogenase in rats
after single or repeated inhalation
exposures,
o Increased liver weight in mice
exposed by inhalation for 28 days,
o Increased ALT and AST in rats
after single gavage dose,
o Increased relative liver weight and
biologically significant increases
in serum SDH and ALT in mice
after a single gavage or
intraperitoneal dose.
onlv:
• Acute inhalation studies in rats,
mice, rabbits, and guinea pigs
evaluated gross and microscopic
liver pathology after 1.5- to 7-hour
exposures (HcddcI et al.. 1945).
Study quality: Medium
• Subchronic- and chronic inhalation
studies in male and/or female rats,
rabbits, guinea pigs, dogs, and cats
evaluated liver histopathology after 5
to 35 weeks of c\do sure (HcddcI et
al.. 1946); Study aualitv: Medium or
Low.
• A chronic gavage cancer bioassay in
male and female mice evaluated liver
histopathology after 78 weeks of
exDosure (NTP. 1978) Studv aualitv:
High.
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Studies evaluating onlv liver weieht.
sross oatholoev and/or clinical
chemistry:
• An acute inhalation study in male
mice evaluated liver weight and
serum chemistry (Storcr et al.. 1984)
Study quality: High.
• Acute- and short-term inhalation
studies in male rats evaluated serum
chemistry (Brondeau et al.. 1983)
Study quality: Medium.
• A short-term inhalation study in male
mice evaluated liver weight and
serum chemistry (Zens et al.. 2018)
Study quality: High.
• Chronic inhalation studies in male
and female rats evaluated serum
chemistry (IRFMN. 1987. 1978.
1976) Study duality: Medium.
• Acute gavage studies in male and
female rats evaluated serum
chemistry and/or liver weight
(Kitchin et al.. 1993): Study duality:
Hieh. (Cottalasso et al.. 1995) Study
quality: Medium.
• An acute gavage study in male mice
evaluated liver weight and serum
chemistry (Storcr et al.. 1984) Study
quality: High.
• A short-term gavage study in male
and female mice evaluated liver
weieht and sross oatholoev (Munson
et al.. 1982) Study duality: Hieh.
• A subchronic dietary study in rats
evaluated serum chemistry (Alumot
et al.. 1976). Study duality: Medium
• Acute, short-term, and subchronic
intraperitoneal injection studies in
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male rats and male mice evaluated
liver weight, serum chemistry, and/or
eross uatholosv (Storer and Conollv.
1985; Storer et al.. 1984; Livesev.
1982); Studv quality: Hieh. (Daiele
et al.. 2009; Iewe et al.. 1986b;
Storer and Conollv. 1983) Studv
quality: Medium.
Evidence from mechanistic studies
• An in vivo inhalation study in male
rats evaluated elemental content in
the liver after 30 days exposure (Que
et al.. 1988).
• An in vivo inhalation study in male
mice evaluated hepatic micro-RNA
(miR) expression and
sluconeosenesis (Zens et al.. 2018).
• In vivo genotoxicity tests were
conducted in the liver of male mice
after single inhalation oral, and
intraperitoneal exposures (Storer et
al.. 1984).
o An in vivo intraperitoneal
injection study in male mice
evaluated hepatic enzyme
induction (Paolini et al.. 1994).
o A series of studies in vivo in rats
and in vitro in rat hepatocytes
evaluated effects on
glycolipoprotein metabolism
(Cottalasso et al.. 2002;
Cottalasso et al.. 1995;
Cottalasso et al.. 1994).
o In vitro studies in rat
hepatocytes or rat liver slices
evaluated oxidative stress
parameters (Cottalasso et al..
Bioloeical aradicnt/dosc-rcsdonsc:
Bioloeical eradient/dose-
Key findings'.
Available data on liver
toxicity mechanisms are
limited and nonspecific.
Hepatic enzyme induction
was demonstrated in mice
exposed by intraperitoneal
injection. Limited in vitro
data indicate that 1,2-
dichloroethane may
increase oxidative stress or
impair glucose and/or lipid
metabolism in mice and in
rat hepatocytes and liver
slices.
Overall WOSEjudgement
for hepatic effects based on
mechanistic evidence:
• Indeterminate
• 1,2-Dichloroethane induced DNA
damage after oral and intraperitoneal
(but not inhalation) exposure.
• 1,2-Dichloroethane induced a dose-
related increase in PROD activity (a
probe for CYP450 2B1) in mice.
Oxidative stress:
• Incubation of rat liver slices with 1,2-
dichloroethane (up to 10 inM for up to
30 minutes) resulted in dose-and time-
dependent increases in MDA
production.
• Levels of GSH were significantly
decreased in rat hepatocytes cultured
with 4.4 to 6.5 mM 1,2-dichloroethane
for up to 1 hour.
• Free radicals were detected in rat
hepatocytes cultured with 1,2-
dichloroethane under anaerobic (but
not aerobic) conditions.
• The cysteine S conjugate of 1,2-
dichloroethane was cytotoxic and
depleted GSH in hepatocytes; co-
treatment with antioxidants and GSH
precursors mitigated these effects.
rcsDonsc:
• Rat hepatocytes exposed to
1,2-dichloroethane for 1
hour at 1.2 mM did not
show significantly
decreased GSH.
Consistencv:
• Rat hepatocytes cultured
with 10 mM 1,2-
dichloroethane for 2 hours
did not show evidence of
lipid peroxidation (i.e.,
increased PCOOH or
PEOOH levels).
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1994; Suzuki et al.. 1994; Jean
and Reed. 1992; Thomas et al..
1989; Tomasi et al.. 1984).
o An in vitro study in rat
hepatocytes incubated with the
cysteine S conjugate of 1,2-
dichloroethane, S-(2-
chloroethyl)-DL-cysteine
(CEC), evaluated cytotoxicity
related to oxidative stress (Webb
et al.. 1987).
Effects on gluconeogenesis and
glycolipoprotein metabolism:
• Inhalation exposure increased miR-
451a expression and decreased
glycerol gluconeogenesis in the liver
of exposed mice.
• Rats treated with 1,2-dichloroethane
via gavage showed impairment of
glycoprotein biosynthesis.
• 1,2-dichloroethane treatment
increased retention and decreased
secretion of glycolipoproteins in rat
hepatocytes.
" Based on a density for 1,2-dichloroethane of 1.25 g/cm3.
5'-NT = 5'-nucleotidase; ALP = alkaline phosphatase; ALT - alanine aminotransferase; AST = aspartate aminotransferase; F = female; GGT = gamma-glutamyl
transferase; GLDH = glutamate dehydrogenase; GSH = glutathione; LDH = lactate dehydrogenase; M = male; MDA = malondialdehyde; ODC = orinithine
decarboxylase activity; PCOOH = phosphatidylcholine hydroperoxide; PEOOH = phosphatidylethanolamine hydroperoxide; PROD = pentoxyresorufin dealkylation;
SDH = sorbitol dehydrogenase.
15325
15326
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Table Apx M-35.1,2-Dichloroethane Evidence Integration Table
'or Immune/Hematological Effects
Database Summary
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and Overall WOSE
Judgement
Evidence Integration Summary Judgement on Immune/Hematological Effects
Evidence from human studies (none)
Indeterminate
Overall WOSE
judgement for
immune/hematologi
cal effects based on
integration of
information across
evidence streams:
Evidence indicates
that 1,2-
dichloroethane
likely causes
immune system
suppression under
relevant exposure
conditions.
Evidence from apical endpoints in in vivo mammalian animal studies
Studies of immune function:
• An inhalation study evaluated mortality
from Streptococcus zooepidemicus aerosol
challenge in female mice and lymphocyte
stimulation, alveolar macrophage inhibition,
and pulmonary bactericidal activity against
Klebsiella pneumoniae in female mice and
male rats after exposure once or for 5 (mice)
or 12 (rats) davs (Sherwood et al.. 1987)
Study quality: High
• An oral gavage study in male mice
evaluated hematology (including
coagulation), humoral immunity (spleen cell
antibody response), cell-mediated immunity
(delayed hypersensitivity response), spleen
and thymus weight, and gross necropsy after
14 davs (Munson et al.. 1982) Studv aualitv:
High
Studies of hematoloev. orsan weiehts. and
histooatholoev:
• Inhalation studies in rats, mice, rabbits, and
guinea pigs (sex not specified) evaluated
gross pathology and histopathology of the
sdIcch after acute exposures (HcddcI et al..
1945). Studv aualitv: Medium
• An inhalation study in male rats evaluated
spleen weight, gross pathology, and
historatholoev after 30 davs exposure (Iswe
et al.. 1986b) Studv aualitv: Hieh
• Inhalation studies in rats, rabbits, guinea
pigs, monkeys, cats and a single dog
evaluated hematology (and/or clotting
parameters or IgM) and/or spleen
Biolosical eradient/dose-
rcsDonsc:
• Female mice exposed by
inhalation for 3 hours
exhibited a concentration-
related increase in mortality
due to S. zooepidemicus
infection at concentrations
>22 mg/m3 (5.4 ppm).
Mortality incidences were
1.5 and 2.1-fold higher than
controls at 22 and 43.7
mg/m3, respectively.
Female mice also exhibited
a small decrease in
bactericidal activity against
K. pneumoniae at 43.7
mg/m3 (10.8 ppm).
• In a gavage study,
decreased humoral and
cell-mediated immune
responses were observed in
male mice after 14 days
exposure to >4.89 mg/kg-
day; decreased leukocyte
counts were observed at
48.9 mg/kg-day.
• In a gavage study in rats,
small decreases in
erythrocyte count,
hemoglobin and
hematocrit were observed
in both sexes along with
increased platelets (both
Consistencv:
• Male rats exhibited no effects
in the K. pneumoniae
challenge assays after
exposures up to 810 mg/m3
for 5 hours or up to 405
mg/m3 for 12 days.
• In a study rated
uninfonnative due to
decreased drinking water
intake at the high dose of
189 mg/kg-day, no effect on
humoral or cell-mediated
immune responses or
leukocyte counts were
observed in mice exposed to
doses of 3, 24, or 189 mg/kg-
day via drinking water for 90
days.
• No treatment-related
changes in hematology were
observed in a gavage study
of male rats exposed to
doses up to 120 mg/kg-day
for 13 weeks, or in studies of
several species exposed by
inhalation for durations from
5 weeks to 2 years.
• Multiple studies of several
species exposed by
inhalation or oral
administration for acute,
subchronic, or chronic
durations showed no effects
Key findings'.
In high-quality
inhalation and gavage
studies of immune
function in mice, an
association between 1,2-
dichloroethane exposure
and immunosuppression
was observed; a more
limited inhalation study
in rats and a longer-term
drinking water study in
mice rated
Uninfonnative did not
show any effects.
Evidence from other
studies showed only
small effects on
hematology and no
effects on relevant organ
weights or
histopathology.
Overall WOSE
judgement for
immune/hematological
effects based on animal
evidence:
• Moderate
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histopathology after 5 to 35 weeks of
exposure (HcddcI et al.. 1946) (IRFMN.
1987. 1978. 1976; Hofmann et al.. 1971a:
Soencer et al.. 1951; Mellon Institute. 1947)
Study quality: Low to Medium
• Inhalation cancer bioassays in male and
female rats and mice evaluated hematology
and/or comprehensive histopathology after 2
vears exposure (Naeano et al.. 2006;
Cheever et al.. 1990) Studv aualitv: Hieh
• A drinking water study in male and female
mice evaluated comprehensive
histopathology after 13 weeks exposure
(NTP. 1991) Studv aualitv: Hieh
• Gavage studies in male and female rats
evaluated hematology, spleen and/or thymus
weights, and comprehensive histopathology
after 10- and/or 90-dav exposures (Daniel et
al.. 1994; NTP. 1991) Studv aualitv: Hieh
• A gavage cancer bioassay in male and
female mice evaluated comprehensive
histopathology after 78 weeks exposure
(NTP. 1978) Studv aualitv: Hieh
• A gavage cancer bioassay in male and
female transgenic mice susceptible to cancer
evaluated hematology and histopathology of
the thymus, spleen, lymph nodes, and bone
marrow after 40 weeks exposure (Storer et
al.. 1995) Studv aualitv: Medium
• A dermal cancer bioassay in male and
female transgenic mice susceptible to cancer
evaluated thymus and spleen weights and
histopathology of the lymph nodes, thymus,
and bone marrow after 26 weeks exposure
(Sueuro et al.. 2017) Studv aualitv: Hieh
Studies Rated Uninfonnative:
• An oral study in male mice evaluated
hematology, humoral immunity (spleen cell
sexes) and leukocytes
(females only) after 90
days at 150 mg/kg-day.
• In a subchronic gavage
study, increased incidences
of thymus necrosis were
observed in male and
female rats that died
prematurely (>240 mg/kg-
day in males and at 300
mg/kg-day in females).
on relevant organ weights or
histopathology.
Bioloeical olausibilitv and
human relevance:
• In the mouse inhalation
study, mice were exposed for
30 minutes to aerosols of
streptococcal bacteria (-2E04
inhaled viable streptococci).
The relevance of this
immune challenge to typical
human bacterial exposures is
uncertain.
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antibody response), cell-mediated immunity
(delayed hypersensitivity response), spleen
cell response to mitogens, function of the
reticuloendothelial system, spleen and
thymus weight, and gross necropsy after 90
davs drinkine water exposure. (Munson et
al.. 1982)
Evidence from mechanistic studies
• An in vitro study investigated phagocytic
activity of mouse peritoneal macrophages
incubated with 1.2-dichloroethane (Utsumi
et al.. 1992).
• Cell-free and in vitro studies investigated
1,2-dichloroethane effects on erythrocyte
elutathione-S-transferase (GST) (Ansariet
al.. 1987)
• An inhalation study in rats evaluated
elemental content in the spleen after 30 days
exposure to 1.2-dichloroethane (Oue et al..
1988).
Biolosical eradient/dose-
rcsDonsc:
• 1,2-dichloroethane induced
dose-related reductions in
erythrocyte GST activity in
both the cell-free
experiment and in human
erythrocytes in vitro.
• 1,2-dichloroethane reduced
macrophage phagocytic
activity to 76% of control
levels at a concentration of
200 mM.
Key findings'.
Limited in vitro data
showed reductions in
macrophage phagocytic
activity and erythrocyte
GST activity after
exposure to 1,2-
dichloroethane.
Overall WOSE
judgement for
immune/hematological
effects based on
mechanistic evidence:
• Indeterminate
15328
15329
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Table Apx M-36.1,2-Dichloroethane Evidence Integration Table for Neurological/Behavioral Effects
Database Summary
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Factors that Decrease
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Judgement
Evidence Integration Summary Judgement on Neurological/Behavioral Effects
Evidence from human studies
Overall WOSE
judgement for
neurological/behav
ioral effects based
on integration of
information across
evidence streams:
Evidence indicates
that 1,2-
dichloroethane
likely causes
neurological/
behavioral effects
under relevant
exposure
circumstances.
• Case reports of human exposure to 1,2-
dichloroethane by inhalation or ingestion
indicated clinical signs of neurotoxicity
(dizziness, tremors, paralysis, coma) as
well as histopathology changes in the
brain at autODSv (ATSDR. 2022).
• Workers exposed to 1,2-dichloroethane
for extended periods have developed
cerebral edema and toxic encephalopathy
(ATSDR. 2022).
Key findings'.
Case reports document
clinical signs of
neurotoxicity and brain
histopathology changes
in humans exposed to
1,2-dichloroethane by
inhalation or ingestion.
Overall WOSE
judgement for
neurological/behavioral
effects based on human
evidence:
• Slight
Evidence from apical endpoints in in vivo mammalian animal studies
Studies evaluating neurobehavioral
endDoints:
• An inhalation study in male and female
rats evaluated clinical signs, functional
observational battery (FOB), grip
performance, landing foot splay, rectal
temperature, motor activity, brain
weight, and gross and microscopic
pathology of nervous system tissues after
4 hours exposure (Hotchkiss et al.. 2010;
Dow Chemical. 2006b) Studv aualitv:
High
• A range-finding inhalation study in male
and female rats evaluated detailed
clinical observations (cage-side, hand-
held, and open-field; recorded
systematically) and gross pathology
(tissues not specified) after 4 hours
Biolosical eradient/dose-resoonse:
• In rats exposed by inhalation
once for four hours,
neurobehavioral changes
including incoordination,
palpebral closure, decreased
sensory responses, and decreased
motor activity were seen at >
7,706 mg/m3 (1904 ppm) one
hour after exposure but not at
subsequent times up to 15 days
later.
• In rats exposed by inhalation for
> 1.5 hr to > 4000 mg/m3 brain
edema was seen, and
microstructural alterations were
detected by diffusion MRI 3 days
after exposure.
Consistencv:
• No treatment-related brain
weight or histopathology
changes were seen in
nervous system tissues 15
days after single 4-hour
exposure up to 8,212.3
mg/m3 (2,029.0 ppm).
• No histopathology changes
were observed in the brain,
sciatic nerve, or spinal cord
of rats exposed by
inhalation for 204 mg/m3
(50.4 ppm) for 2 years in a
cancer bioassay.
• No clinical signs of toxicity
or histopathology changes
in the brain or sciatic nerve
were observed in rats
Key findings'.
Several high- and
medium-quality studies
using rats exposed to
1,2-dichloroethane by
inhalation or gavage or
mice exposed by
intraperitoneal injection
showed the occurrence
of neurobehavioral
changes, clinical signs of
neurotoxicity, and/or
changes in brain
histopathology.
Overall WOSE
judgement for
neurological/behavioral
effects based on animal
evidence:
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exposure (Dow Chemical. 2005) Study
quality: High
• An intraperitoneal injection study in
male mice evaluated righting reflex,
bridge test, and operant tests after single
exposure (Umezu and Shibata. 2014)
Study quality: High
Studies evaluating neuropathology:
• An inhalation study in male rats
evaluated clinical signs and brain MRI
and histopathology after 1.5- or 4-hour
exposures (Zhou et al.. 2016) Study
quality: Medium
• An inhalation study in male and female
rats evaluated clinical signs, histology
and electron microscopy, and water
content of the brain after 2-, 4-, 6-, or
12-hour exposures (Oin-li et al.. 2010)
Study quality: Medium
• An inhalation cancer bioassay in male
and female rats evaluated brain, sciatic
nerve, and spinal cord gross and/or
microscopic pathology after 2 years
exposure (Cheever et al.. 1990) Study
quality: High
• A gavage study in male and female rats
evaluated clinical signs, brain weight,
and gross and/or microscopic pathology
of the brain and sciatic nerve after 10-
or 90-day exposure (Daniel et al.. 1994)
Study quality: High
• A gavage study in male and female rats
evaluated clinical signs, brain weight,
and histopathology of the brain, sciatic
nerve, and spinal cord after 13 weeks
exposure (NTP. 1991) Study quality:
High
• In rats exposed by inhalation to >
5,000 mg/m3, increased water
content in the cortex was
observed after >2-hour exposure
and edema and histopathological
changes in the brain were
observed by light and
transmission electron
microscopy at the end of > 6-
hour exposure.
• In animals of several species
exposed by inhalation for up to
12 hours, clinical signs including
hyperactivity, weakness,
sedation, dysphoria, and/or
trembling were reported.
• In rats exposed by gavage for 13
weeks, clinical signs of
neurotoxicity (including tremors
and abnormal posture) and
necrosis in the cerebellum were
observed at >240 mg/kg-day.
Consistency:
• Mice exposed by intraperitoneal
injection showed a dose-related
decrease in response rate in lever-
pressing operant behavior test at >
62.5 mg/kg but no effects on
other tests.
exposed by gavage to up to
300 mg/kg-d for 10 days or
150 mg/kg-d for 90 days.
• No histopathology changes
were observed in the brain,
sciatic nerve, or spinal cord
of mice exposed via
drinking water for 13
weeks, by gavage for 78
weeks in a cancer bioassay,
or in transgenic mice
exposed by dermal
application for 40 weeks in
a cancer bioassay.
• Exposure to 1,2-
dichloroethane did not alter
brain weights of rats
exposed by gavage for up to
90 days or in mice exposed
by gavage for 14 days or
drinking water for 90 days.
• Moderate
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• A drinking water study in male and
female mice evaluated clinical signs,
brain weight, and histopathology of the
brain, sciatic nerve, and spinal cord
after 13 weeks exposure (NTP. 1991)
Study quality: High
• A gavage cancer bioassay in male and
female mice evaluated clinical signs
and histopathology of the
brain/meninges after 78 weeks exposure
(NTP. 1978) Studv aualitv: Medium
• A dermal cancer bioassay in male and
female transgenic mice evaluated
clinical signs, brain weights, and brain,
spinal cord, and sciatic nerve
histopathology after 26 weeks exposure
(Sueuro et al.. 2017) Studv aualitv:
High
Studies evaluating clinical sisns. brain
weieht. and/or sross oatholoev:
• Inhalation studies in rats, mice, rabbits,
and guinea pigs evaluated clinical signs
of neurotoxicity after 1.5- to 7-hour
exposures (HcddcI et al.. 1945) Studv
quality: Medium
• An inhalation study in male and female
rats and guinea pigs and male monkeys
evaluated clinical signs and/or brain
histology after up to 35 weeks exposure
(Sdcneer et al.. 1951) Studv aualitv:
High
• A gavage study in male rats evaluated
clinical signs and gross pathology after
a sinsle exposure (S Unifier Chem Co.
1973) Studv aualitv: Medium
• A gavage study in male and female
mice evaluated brain weight and gross
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pathology after 14-day exposure
(Munson et al.. 1982) Studv aualitv:
High
• An intraperitoneal (intraperitoneal)
injection study of fertility in male mice
evaluated gross pathology of the brain
after 5-dav exposure (Daisle et al..
2009) Studv quality: Medium
Evidence from mechanistic studies
• In vivo inhalation studies in mice aimed
at identifying mechanisms of brain
edema induced by 1,2-dichloroethane
evaluated aquaporin and matrix
metalloproteinases protein expression or
ATP generation and tight junction
protein expression after 1-, 2-, or 3-day
exposure (Wans et al.. 2018a: Wans et
al.. 2014).
• An in vivo oral study in rats evaluated
neurotransmitter levels in the brain after
a sinsle exposure (Kanada et al.. 1994).
• In vitro studies in rat astrocytes exposed
to 2-chloroethanol (metabolite of 1,2-
dichloroethane) evaluated the roles of
mitochondrial function, glutamate
metabolism, matrix metalloproteinases,
and MAPK cell signaling in cerebral
edema induced by 1,2-dichloroethane
(Wans et al.. 2018b: Wans et al.. 2017;
Sun et al.. 2016a: Sun et al.. 2016b).
Biolosical sradicnt/dosc-rcsDonsc:
• Exposure to 1,2-dichloroethane
upregulated the mRNA and/or
protein expression of aquaporin
and a matrix metalloproteinase
(MMP9).
• Exposure to 1,2-dichloroethane
resulted in decreased expression
of tight junction proteins
(occludin and ZO-1) and mRNA,
increased free calcium, decreased
ATP content, and decreased
ATPase activity in the brains of
mice.
Consistency:
• Exposure to 2-chloroethanol in
vitro resulted in decreased
ATPase activity, mitochondrial
function (membrane potential),
and glutamate metabolism
(expression of enzymes involved
in glutamate metabolism) in rat
astrocytes. Exposure also
upregulated matrix
metalloproteinases (MMP2 and
MMP9) via increased p38 MAPK
signaling. Pretreatment with the
antioxidant N-acetyl-l-cysteine
Key findings'.
1,2-dichloroethane may
downregulate tight
junction proteins and
energy production and
upregulate aquaporin and
a matrix
metalloproteinase in the
brains of exposed mice.
Overall WOSE
judgement for
neurological/behavioral
effects based on
mechanistic evidence:
• Slight
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mitigated effects on p38 and
MMP levels, suggesting a role for
oxidative stress.
Table Apx M-37.1,2-Dichloroethane Evidence Integration Table for Respiratory Tract Effects
Database Summary
Factors that Increase
Strength
Factors that Decrease
Strength
Summary of Key
Findings and Within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
Evidence Integration Summary Judgement on Respiratory Tract Effects
Evidence from human studies (none)
• Indeterminate
Evidence from apical endpoints in in vivo mammalian animal studies
Studies examining upper and lower respiratory
tract:
• An acute inhalation study in male and
female rats evaluated BAL, lung weight, and
histopathology of the respiratory tract
including nasal cavity 24 hours after 4- or 8-
hour exposures (Hotchkiss et al.. 2010: Dow
Chemical. 2006b). Study quality: High
• An inhalation cancer bioassay in male and
female rats evaluated histopathology of the
respiratory tract including nasal cavity after
104 weeks of exposure (Cheever et al..
1990). Study quality: High
• Two gavage studies in rats evaluated lung
weight and histopathology of the lungs and
nasal cavity and turbinates after 10 and 90
days of exposure (Daniel et al.. 1994). Study
quality: High
• A gavage study in male and female rats
evaluated histopathology of the respiratory
tract including nasal cavity and turbinates,
after 13 weeks of exposure (NTP. 1991).
Study quality: High
Biological gradient/dose-
response:
• In a high-quality study,
dose-related increased
incidences and/or severity
of degeneration/ necrosis of
the nasal olfactory mucosa
occurred in male and
female rats after inhalation
exposures >795 mg/m3
(>196.4 ppm) for 4 hours or
> 435 mg/m3 (>107.5 ppm)
for 8 hours. Regeneration of
the olfactory epithelium
was seen in groups
sacrificed 15 days after a 4-
hour exposure to 795
mg/m3 (196.4 ppm).
• Lung effects including a
transient decrease in ALP in
BALF and histopathology
changes (edema, vacuolar
changes, desquamation.
Biological gradient/dose-
response:
• No treatment-related nasal
lesions were observed in
cancer bioassays of rats
exposed by inhalation up to
654 mg/m3 (160 ppm) for 2
years.
• High-quality studies in rats
did not show effects of 1,2-
dichloroethane on the lung
after gavage exposure up to
150 mg/kg/day for 90 days.
Magnitude and precision:
• Group sizes were small
(5/sex) in the acute
inhalation study that
observed nasal lesions.
Consistency:
• High- and medium-quality
studies in rats did not show
effects of 1,2-dichloroethane
on the lung after chronic
Key findings:
In a high-quality study,
an association between
1,2-dichloroethane
inhalation exposure and
nasal lesions was
observed in rats exposed
to concentrations >435
mg/m3 (>107.5 ppm).
Although one medium-
quality study reported
lung lesions in rats after
a single gavage dose,
high- and medium-
quality studies of longer
duration and higher
doses, as well as a high-
quality study of acute
inhalation exposure, did
not show effects of 1,2-
dichloroethane on lower
respiratory tract tissues
of rats.
Overall WOSE
judgement for
respiratory tract
effects based on
integration of
information across
evidence streams:
Evidence suggests,
but is not sufficient
to conclude, that
1,2-dichloroethane
may cause nasal
effects under
relevant exposure
conditions.
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Factors that Decrease
Strength
Summary of Key
Findings and Within-
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Evidence Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
• A drinking water study in male and female
mice evaluated histopathology of the
respiratory tract including nasal cavity and
turbinates, after 13 weeks of exposure (NTP.
1991). Study quality: High
• A dermal cancer bioassay in male and female
transgenic mice susceptible to cancer
evaluated lung weight and histopathology of
the nasal cavity, trachea, and lungs after 26
weeks of exposure (Suguro et al.. 2017).
Study quality: High
Studies examining only lower respiratory tract:
• An inhalation cancer bioassay in male and
female rats and mice evaluated lung weight
and histopathology after 104 weeks of
exposure (Nagano et al„ 2006). Study
quality: High
• An inhalation study in male and female rats
and guinea pigs evaluated lung weight and
histopathology after -170 - 246 days
(Spencer et al„ 1951). Study quality:
Medium
• A gavage study in male rats evaluated
BALF, lung weight, and lung histopathology
1 to 30 days after a single dose (Salovskv et
al.. 2002). Study quality: Medium
• A gavage study in mice evaluated lung
weight and gross pathology after 14 days of
exposure (Munson et al„ 1982). Study
quality: High
• A gavage study in male and female mice
evaluated the lungs, bronchi, and trachea for
histopathology after 78 weeks of exposure
(NTP. 1978). Study quality: High
• An intraperitoneal injection study in male
rats evaluated lung weight and
histopathology (Igwe et al„ 1986b). Study
quality: Medium
atelectasis, macrophage
proliferation, and
inflammation) were
reported in rats after a
single gavage dose of 136
mg/kg.
inhalation exposure up to
810 mg/m3 (200 ppm) for
212 days or up to 654 mg/m3
(160 ppm) for 2 years.
• High-quality studies in mice
did not show effects of 1,2-
dichloroethane on the lungs
after 14 days of gavage
exposure up to 49 mg/kg/day
or 13 weeks of drinking
water exposure up to 4,926
mg/kg/day.
• A medium-quality study in
guinea pigs did not show
effects of 1,2-dichloroethane
on the lungs after exposure
up to 1,620 mg/m3 (400
ppm) for 246 days.
• BAL parameters, lung
weight, and lung
histopathology were not
affected in rats exposed by
inhalation up to 8,212.26
mg/m3 (2029.0 ppm) for 4
hours.
Quality of the database:
• Lung histopathology data in
the acute gavage study that
reported lung effects were
presented qualitatively.
Biological plausibility and
human relevance:
• Lung tumors are associated
with chronic inhalation or
gavage exposure in mice and
with subchronic dermal
exposure in susceptible
transgenic mice. Increases in
Overall WOSE
judgement for
respiratory effects based
on animal evidence:
• Slight to moderate
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Factors that Increase
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Factors that Decrease
Strength
Summary of Key
Findings and Within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
• An intratracheal injection lethality study in
rats (sex NS) evaluated gross pathology of
the lungs at death or 3 days after a single
dose (Dow Chemical. 1989). Studv aualitv:
Medium
lung weight and
preneoplastic lesions, such as
hyperplasia, in some of these
studies are related to tumor
development and not
indicative of a separate
nonneoplastic effect on the
lung.
Evidence from mechanistic studies (none)
• Indeterminate
Table Apx M-38.1,2-Dichloroethane Evidence Integration Table for Nutritional/Metabolic Effects
Database Summary
Factors that Increase Strength
Factors that Decrease Strength
Summary of Key
Findings and Within-
Stream Strength of
the Evidence
Judgement
Inferences
across Evidence
Streams and
Overall WOSE
Judgement
Evidence Integration Summary Judgement on Nutritional/Metabolic Effects
Evidence from human studies (none)
• Indeterminate
Body weight was evaluated in the
following studies:
• Acute inhalation studies in male
and female rats (Dow Chemical.
2006b): Study quality: High.
• Short-term inhalation studies in
male mice (Zeng et al.. 2018:
Zhang et al.. 2017): Study quality:
High.
• A short-term inhalation study in
female rats (Dow Chemical.
2014): Study quality: High.
• Short-term, subchronic, and
chronic inhalation studies in male
and/or female rats, mice, rabbits,
dogs, guinea pigs, monkeys, and
cats (Spencer et al.. 1951: Heppel
Evidence from apical endpoints in in vivo mammalian animal studies
Biological gradient/dose-response:
Treatment-related adverse " effects on
body weight occurred in high or
medium quality studies of (species,
route, exposure level and duration):
• Mouse inhalation:
o >707 mg/m3 (175 ppm), males,
4 wks
• Guinea pig inhalation:
o 405 mg/m3 (100 ppm) in
females and 809 mg/m3 (200
ppm) in males, up to 246 d
• Rat gavage:
o >40 mg/kg-day, females, 6
wks
o 150 mg/kg-day, males, 13 wks
Biological gradient/dose-response:
No treatment-related adverse effects on
body weight occurred in high or
medium quality studies of (species,
route, exposure level, and duration):
• Rat inhalation:
o <8,212 mg/m3 (2,029 ppm),
males and females, 4 hours
o 832 mg/m3 (205 ppm), females,
4 wks
o <809 mg/m3 (200 ppm), males
and females, up to 212 d
o <648 mg/m3 (160 ppm), males
and females, 2 yrs
• Monkey inhalation:
o 405 mg/m3 (100 ppm), males,
up to 212 days
Key findings:
Decreased body
weight was reported in
mice and guinea pigs
exposed by inhalation
and rats and mice
exposed orally to 1,2-
dichloroethane in
high- and medium-
quality studies.
Several high- and
medium-quality
studies in a few
species via various
routes of exposure
reported no effect on
body weight.
Overall WOSE
judgement for
nutritional/
metabolic effects
based on
integration of
information
across evidence
streams:
Evidence
suggests that 1,2-
dichloroethane
may cause
nutritional/
metabolic effects
under relevant
exposure
conditions.
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Factors that Decrease Strength
Summary of Key
Findings and Within-
Stream Strength of
the Evidence
Judgement
Inferences
across Evidence
Streams and
Overall WOSE
Judgement
et al.. 1946); Studv aualitv:
Medium or Low.
• A one-generation inhalation
reproduction studv in rats (Rao et
al.. 1980); Studv aualitv: Medium.
• Chronic inhalation cancer
bioassays in male and female rats
(Naeano et al.. 2006; Cheever et
al.. 1990); Studv aualitv: Hieh.
• An acute oral gavage study in
male rats (Moody et al.. 1981);
Study quality: Medium.
• A gavage study in female rats
cxooscd durine eestation (Pavan
et al.. 1995); Studv aualitv: Hieh.
• A short-term gavage study in male
and female mice (Munson et al..
1982); Studv aualitv: Hieh.
• Short-term and subchronic gavage
studies in male and female rats
(Daniel et al.. 1994; NTP. 1991;
vanEsch et al.. 1977); Studv
aualitv: Hieh. (NTP. 1978); Studv
quality Medium.
• A subchronic drinking water
study in male and female mice
(NTP. 1991); Studv aualitv: Hieh.
• A subchronic dietary study in rats
(Alumot et al.. 1976); Studv
quality: Medium.
• A multigenerational drinking
water studv in mice (Lane et al..
1982); Studv aualitv: Hieh.
• Chronic gavage and dermal
studies in transgenic mice
susceptible to cancer (Sueuro et
o 198 mg/kg-day, maternal
weight gain, GD 6-20
• Mouse drinking water:
o 4,207 mg/kg-day in males and
>647 mg/kg-day in females, 13
wks
Consistencv:
• Decreased body weight was
observed in male transgenic mice
exposed to 200 mg/kg-day by
gavage for 40 wks.
• Rat gavage:
o 625 mg/kg-day, males, single
dose
o <300 mg/kg-day, males, and
females, 10 d
o <100 mg/kg-day, males, 2 wks
o <90 mg/kg-day, males, and
females, 13 wks
o <120 mg/kg-day in males and
<150 mg/kg-day in females, 13
wks
Consistencv:
• Body weight was not affected in low
quality inhalation studies of female
dogs exposed to 1,540 mg/m3 (380.5
ppm) for 34-35 weeks or male
rabbits exposed to 730 mg/m3 (180
ppm) for 13-25 wks.
• Body weight was not affected in rats
given feed fumigated with 1,2-
dichloroethane in a 13-week study
with dose uncertainties.
• Body weight was not affected in
male transgenic mice exposed to
dermal doses up to 6,300 mg/kg-day
for 26 wks.
• Body weight was not affected after
intraperitoneal administration in
male rats given 150 mg/kg-day for
30 days or in male mice given 40
mg/kg-day for 5 days.
sometimes at lower
exposure levels and/or
shorter exposure
durations.
Overall WOSE
judgement for
nutritional/metabolic
effects based on
animal evidence:
• Slight
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Inferences
across Evidence
Streams and
Overall WOSE
Judgement
al.. 2017; Storer et al.. 1995);
Study quality: High.
• Short-term intraperitoneal
injection studies in male rats and
male mice (Daiele et al.. 2009);
Studv aualitv: Hieh: (Iawe et al..
1986b): Studv quality: Medium.
Evidence from mechanistic studies (none)
• Indeterminate
" In adult animals, decreases in body weight of at least 10% change from control are considered adverse unless the changes are attributable to food or drinking water
intake decreases due to palatability. Statistically significant decreases (relative to controls) in maternal body weight gain during gestation are considered adverse.
Effects on body weight of offspring at ages up to sexual maturity are considered developmental effects.
15337
15338
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Table Apx M-39. 1,2-Dichloroethane Evidence Integration Table for Mortality
Database Summary
Factors that Increase Strength
Factors that Decrease
Strength
Summary of Key Findings
and within-Stream
Strength of the Evidence
Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
Evidence Integration Summary Judgement on Mortality
Evidence from human studies
Overall WOSE
judgement for
mortality effects
based on integration
of information
across evidence
streams:
Evidence indicates
that 1,2-
dichloroethane may
cause death under
relevant exposure
circumstances and
lethal levels have
been identified in
animal studies.
• A retrospective cohort mortality study
evaluated all-cause mortality in 7849
white male petrochemical plant workers
followed from 1950 to 1983. SMRs
were calculated using age-, race-, and
calendar year-specific mortality rates of
males in the United States (Teta et al..
1991). Studv aualitv: Medium
• A retrospective cohort mortality study
evaluated all-cause mortality in
251 employees of an herbicide
manufacturing facility between 1979
and 1987, followed until 2003. SMRs
were calculated using age- and gender-
specific mortality rates in the United
States. (BASF. 2005). Studv aualitv:
Medium
Biolosical olausibi 1 it\ and
human relevance:
• Two limited retrospective
cohort studies found no
increase in mortality of
workers with presumed
exposure to 1,2-
dichloroethane (and other
chemicals) relative to the
general U.S. population.
Key findings'.
Limited epidemiological
data show no increase in
mortality among workers
with presumed exposure to
1,2-dichloroethane but are
insufficient to draw any
broader conclusions.
Overall WOSEjudgement
for mortality effects based
on human evidence:
• Indeterminate
Evidence from apical endpoints in in vivo mammalian animal studies
• Acute-duration inhalation studies
evaluated mortality in rats, mice, and
suinea Diss (Dow Chemical. 2017.
2006b: Storeretal.. 1984; Soenceret
al.. 1951). Studv aualitv: Hish.(Oin-li
et al.. 2010; Francovitch et al.. 1986;
Hetroel et al.. 1945). Studv aualitv:
Medium
• Short-term- and subclironic-duration
inhalation studies evaluated mortality in
rats, guinea pigs, mice, rabbits, dogs,
and cats (Dow Chemical. 2014; Pavan
et al.. 1995; Iswe et al.. 1986b). Studv
aualitv: Hish. (Rao et al.. 1980; HcddcI
et al.. 1946). Studv aualitv: Medium
• Clironic-duration inhalation studies
evaluated mortality in rats, mice.
Biolosical sradient/dose-
rcsDonsc:
Treatment-related deaths" or
effects on survival occurred in
studies of (species, route,
exposure, and intended
duration):
• Rat inhalation:
o 10,200 mg/m3 (2,520 ppm),
4 lirs
o 4,050 mg/m3 (1,000 ppm),
7 lirs
o 1,230 mg/m3 (455 ppm),
30 d
o >730 mg/m3 (0.73 mg/L),
6 wks
Biolosical sradient/dose-
rcsDonsc:
No treatment-related1
deaths/effects on survival were
seen in studies of (species,
route, exposure, duration):
• Rat inhalation:
o <8,212 mg/m3 (2,029
ppm), 4 lirs
o 5,000 mg/m3, 2-6 lirs
o 630.6 mg/m3 (155.8
ppm), 8 lirs
o 10,000 mg/m3, 12 lirs
o 404 mg/m3, 17 wks
o <646.4 mg/m3 (158
ppm), 2 yrs
• Mouse inhalation:
Key findings'.
Treatment-related increases
in the incidence of mortality
were observed in several
animal species exposed to
1,2-dichloroethane via
inhalation, oral, or dermal
exposure for acute, short-
term/intermediate, or
clironic durations in
multiple studies.
Overall WOSE judgement
for mortality effects based
on animal evidence:
• Robust
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Summary of Key Findings
Inferences across
Database Summary
Factors that Increase Strength
Factors that Decrease
and within-Stream
Evidence Streams
Strength
Strength of the Evidence
and Overall WOSE
Judgement
Judgement
rabbits, guinea pigs, dogs, monkeys.
o 1,214 mg/m3 (300 ppm).
o <700 mg/m3, 1 wk
and cats (Naeano et al.. 2006; Cheever
gestational exposure
o 420 mg/m3, 4 wks
et al.. 1990). Studv aualitv: Hieh.
• Mouse inhalation:
o <363 mg/m3 (89.8 ppm).
(Hofmann et al.. 1971a: Soencer et al..
o >4,339 mg/m3 (1,072 ppm).
2 yrs
1951). Studv quality: Medium; (Hcppcl
4 lirs
• Rabbit, guinea pig, and cat
et al.. 1946). Studv aualitv: Low or
o 6,071 mg/m3 (1,500 ppm).
inhalation:
Medium; (Mellon Institute. 1947).
7 lirs
o 404 mg/m3, 17 wks
Study quality: Low
• Rabbit inhalation:
• Rat gavage:
• Acute-duration gavage studies
o 12,100 mg/m3 (3,000 ppm).
o 625 mg/kg, once
evaluated mortality in rats and mice
7 lirs
o 150 mg/kg-day, 90 d
(Kitchin et al.. 1993; Storeretal.. 1984;
o 6,071 mg/m3 (1,500 ppm).
o 240 mg/kg-day.
Moodv et al.. 1981). Studv aualitv:
5 d
gestational exposure
Hieh: (Stauffer Chem Co. 1973). Studv
o 1,980 mg/m3 (490 ppm).
• Mouse drinking water:
quality: Medium
6 wks
o 2,710 mg/kg-day, 90 d
• Short-term- and subclironic-duration
o 1,540 mg/m3 (1.54 mg/L),
(male)
gavage studies evaluated mortality in
20 wks
• Mouse intraperitoneal:
rats (Daniel et al.. 1994; NTP. 1991).
o >405 mg/m3 (100 ppm).
o 600 mg/kg, once
Study quality: High
gestational exposure
• Clironic-duration gavage studies
• Guinea pig inhalation:
evaluated mortality in wild type and
o 6,071 mg/m3 (1,500 ppm).
transgenic mice (Storeret al.. 1995;
7 lir
NTP. 1978). Studv aualitv: Hieh
o 3,900 mg/m3 (3.9 mg/L), 4
• A subclironic drinking water study
d
evaluated mortalitv in mice (NTP.
o 730 mg/m3 (0.73 mg/L),
1991). Studv aualitv: Hieh
25 wks
• Clironic-duration drinking water studies
• Dog inhalation:
evaluated mortalitv in mice (Klaunie et
o 3,900 mg/m3 (3.9 mg/L),
al.. 1986; Lane et al.. 1982). Studv
5 wks
quality: High
• Cat inhalation:
• An acute-duration dermal exposure
o 3,900 mg/m3 (3.9 mg/L),
study evaluated mortality in rabbits
11 wks
(Dow Chemical. 1956). Studv aualitv:
• Rat gavage:
Medium
o >1,000 mg/kg, once
• A clironic-duration dermal exposure
o >240 mg/kg-day, 90 d
study evaluated mortality in transgenic
• Mouse gavage:
mice (Sueuro et al.. 2017). Studv
o >400 mg/kg, once
quality: High
o 150 mg/kg-day, 40 wks
(female transgenic)
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Database Summary
Factors that Increase Strength
Factors that Decrease
Strength
Summary of Key Findings
and within-Stream
Strength of the Evidence
Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
• A single dose intratracheal exposure
study evaluated mortality in rats (Dow
Chemical. 1989). Studv aualitv:
Medium
• Single dose intraperitoneal injection
studies evaluated mortality mice
(Umezu and Shibata. 2014; Storer et al..
1984). Studv quality: Hieh; (Storer and
Conollv. 1983). Studv aualitv: Medium;
(Crebelli et al.. 1999). Studv aualitv:
Low
• Mouse drinking water:
o 4,926 mg/kg-day, 90 d
(female)
• Rabbit dermal:
o 2,800 mg/kg (LD50), 24 lirs
• Rat intratracheal:
o 120 mg/kg, once
• Mouse intraperitoneal:
o 486 mg/kg (LD50), once
Evidence from mechanistic studies (none)
• Indeterminate
"Apart from chronic bioassays, most studies did not report statistical significance of mortality incidences. For the purpose of hazard identification, deaths were
considered to be related to treatment if they occurred at a higher incidence than in controls, occurred at the highest dose tested or with a relationship to dose, and were
not attributed to factors unrelated to treatment (accident or disease). For clironic-duration studies, only statistically-significant, treatment-related effects on survival were
included.
15340
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M.7 Mutagenicity and Cancer
M.7.1 1,1-Dichloroethane
Animal studies provide limited evidence that 1,1-dichloroethane may cause cancer in rodents. Rats and
mice exposed via gavage for 78 weeks exhibited a positive dose-related trend in the incidence of liver
tumors in male mice and mammary gland tumors and hemangiosarcomas in female rats. Poor survival in
both control and treated animals limits the validity of these results. Cancer mode-of-action data for 1,1-
dichloroethane are very limited and consist of a small number of genotoxicity experiments. TableApx
M-40 and Table Apx M-41 show the results of in vitro and in vivo genotoxicity, respectively, and cell
transformation assays of 1,1-dichloroethane.
Table Apx M-40. In Vitro Genotoxicity Tests of 1,1-Dichloroethane
Reference
Test System
Doses and
Exposure
Conditions
Endpoint
Results
Comment
Simmon et al. (1977)
Salmonella
tvphimurium
TA1535,
TA1537,
TA1538, TA98,
TA100
Up to 5 mg/plate
or cytotoxic dose
Mutation
Negative
Efforts to mitigate
volatility were not
reported.
Zeiseret al. (1992)
S. tvphimurium
TA1535,
TA1537, TA97,
TA98, TA100
Up to 1 mg/plate;
capped tubes to
prevent
evaporation
Mutation
Negative
(+/- S9)
Milman et al. (1988)
S. tvphimurium
TA1535,
TA1537, TA98,
TA100
Not reported;
plates enclosed in
9 L desiccator
Mutation
Positive
(+/- S9)
Positive inTA1535 and
TA100 with and without
S9 from rats and mice of
both sexes; positive in
TA98 (metabolic
activation conditions not
reported).
Crebelli et al. (1995)
Crebelli et al. (1988)
Aspergillus
nidulans diploid
strain PI
0.2, 0.3, 0.4%
(v:v)
Chromosome
malsegregation
Equivocal
1,1-dichloroethane
induced significant
increase in mitotic
segregation (measured as
numbers of abnormal
colonies) at 0.2% but not
at 0.3 or 0.4%.
Matsuoka et al. (1998)
Chinese hamster
lung fibroblasts
Up to cytotoxic
dose or
preparation limit;
6 hours in glass
culture bottle with
rubber stopper
Chromosomal
aberrations
Negative
(+/- S9)
Milman et al. (1988)
B6C3F1 mouse
hepatocytes
Not reported
DNA repair
Positive
Assay modified to
mitigate volatility. No
further details provided.
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Reference
Test System
Doses and
Exposure
Conditions
Endpoint
Results
Comment
Milman et al. (1988)
Williams et al. (1989)
Osborne-
Mendel rat
hepatocytes
Not reported, 18-
20 hours
DNA repair
Positive
Lowest positive
concentration was
1.3E-02 M. Assay
modified to mitigate
volatility. No further
details provided.
Hatch etal. (1983)
Syrian hamster
embryo cells
0,0.062,0.125,
0.25,0.50,
1.0 mL/chamber
(vapor) for
20 hours in sealed
test system
Cell (viral)
transformation
Positive
No cells survived at the
highest dose. 1,1-
Dichloroethane enhanced
transformation of cells by
SA7 (simian) adenovirus
at doses between 0.062
and 0.5 mL/chamber (1.4-
to 2.2-fold).
Arthur D. Little Inc
(1983)
Milman et al. (1988)
Tu et al. (1985)
BALB/c mouse
3T3 cell line
0, 4, 20, 100,
250 |ig/mL for 24
hours in sealed
glass incubation
chamber
Cell
transformation
Negative
(-S9)
No metabolic activation.
Preliminary cytotoxicity
assay showed no effect on
survival except at 100 and
250 ng/mL (41-53 and 46-
67% survival,
respectively).
Colacci et al. (1985)
Calf thymus
DNA (cell-free)
2.5 nCi for
90 minutes, with
or without
microsomes from
phenobarbital-
induced rat or
mouse liver,
kidney, lung,
stomach
DNA binding
DNA binding
observed under
all conditions
Significantly higher
binding in presence (vs.
absence) of liver and lung
microsomes from rats or
mice. No significant
difference with kidney or
stomach microsomes of
either species. No
information provided on
methods to mitigate
volatilization.
Table Apx M-41. In Vivo Genotoxicil
ty Studies of 1,1-1
lichloroethane
Reference
Species
Tissue/Cell
Type
Dose, Frequency,
and Route
Endpoint
Result
Patlolla et al.
(2005)
Male
Swiss-
Webster
mouse
Bone marrow
0, 100, 200, 300,
400, 500 mg/kg
(single dose,
intraperitoneal)
Chromosomal
aberrations and
micronuclei
24 hours after
dosing
Significant, dose-related increases in
percent chromosomal aberrations
and percent micronucleated cells at
>200 mg/kg. Mitotic index was
significantly decreased at
>300 mg/kg.
Tanineher et al.
(1991)
Male
BALB/c
mouse
Hepatic nuclei
900 mg/kg (single
dose intraperitoneal)
DNA unwinding
4 hours after
dosing
No significant effect on percent
double-stranded DNA.
Colacci et al.
(1985)
Male
BALB/c
mouse
Liver, kidney,
lung, stomach
127 |iCi/kg (single
dose,
intraperitoneal)
DNA binding 22
hours after
dosing
Binding highest in liver, followed by
stomach, lung, and kidney.
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Reference
Species
Tissue/Cell
Type
Dose, Frequency,
and Route
Endpoint
Result
Colacci et al.
(1985)
Male
Wistar rat
Liver, kidney,
lung, stomach
127 |iCi/kg (single
dose,
intraperitoneal)
DNA binding 22
hours after
dosing
Binding highest in stomach,
followed by liver, lung, and kidney.
In vitro experiments on 1,1-dichloroethane genotoxicity include two bacterial mutagenicity studies, a
study of chromosomal aberrations in mammalian cells, studies of DNA repair in mouse and rat,
hepatocytes studies of mammalian cell transformation, a test of chromosome malsegregation in fungi,
and a study of cell-free DNA binding. In vitro genotoxicity testing of 1,1-dichloroethane is hampered by
this chemical's volatility, which requires the use of methods to mitigate chemical loss from the test
system. 1,1-Dichloroethane was mutagenic both with and without exogenous activation in an experiment
conducted in a desiccator to mitigate volatilization (Milman et al.. 1988); however, negative results were
obtained in a preincubation assay using capped tubes to limit volatilization (Zeiger et al.. 1992). Another
Ames assay yielded negative results, but there was no indication of whether chemical volatility was
controlled (Simmon et al.. 1977). In mammalian cells tested under conditions controlling for volatility,
1,1-dichloroethane did not increase the frequency of chromosomal aberrations in Chinese hamster lung
fibroblasts (Matsuoka et al.. 1998) but increased DNA repair in hepatocytes from B6C3F1 mice and
Osborne Mendel rats (Williams et al.. 1989; Milman et al.. 1988).
Assays for cell transformation showed that 1,1-dichloroethane enhanced simian adenovirus
transformation of Syrian hamster embryo cells (Hatch et al.. 1983) but did not induce morphological
transformation of BALB/c mouse 3T3 cells at concentrations associated with approximately 50 percent
survival (Milman et al.. 1988; Tu et al.. 1985; Arthur D. Little Inc. 1983). In tests for chromosome
malsegregation in Aspergillus nidulans diploid strain PI (conducted in capped tubes), 1,1-
dichloroethane induced a significant increase in mitotic segregation (measured as numbers of abnormal
colonies) at a concentration of 0.2 percent (v:v), but not at higher concentrations (0.3 and 0.4 percent)
(Crebelli et al.. 1995; Crebelli et al.. 1988).
Colacci et al. (1985) evaluated the binding of 1,1-dichloroethane to cell-free calf thymus DNA in the
presence or absence of liver, kidney, lung, and stomach microsomes from phenobarbital-pretreated rats
and mice. 1,1-Dichloroethane binding to DNA was enhanced when co-cultured with liver and lung
microsomes from either rats or mice but not in the presence of kidney or stomach microsomes (Colacci
et al.. 1985). suggesting that metabolism of 1,1-dichloroethane in the liver and lung results in
metabolites capable of binding DNA. In another experiment by these study authors, addition of
glutathione to the incubation system resulted in lower DNA binding (reported to be 26 percent lower
than control without further detail), suggesting that glutathione conjugation is detoxifying for 1,1-
dichloroethane. These study authors also measured DNA binding of 14C-l,l-dichloroethane in the liver,
kidney, lung, and stomach of male BALB/c mice and Wistar rats 22 hours after an intraperitoneal
injection of 14C-1,1-dichloroethane (127 |iCi/kg) (Colacci et al.. 1985). Table_Apx M-42 shows the
results, which indicate the highest binding in the stomach of rats and liver of mice. These results differ
from the in vitro findings, possibly due to the fact that the animals in the in vivo study were not
pretreated with phenobarbital to induce liver enzymes.
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TableApx M-42. Binding of 14C-l,l-Dichloroethane to DNA (pmol/mg) after
Intraperitoneal Exposure
Tissue"
Rat
Mouse
Stomach
4.78
2.33
Liver
3.10
2.54
Lung
2.24
1.51
Kidney
1.81
0.65
11 Pooled organs from 4 rats and 12 mice
Source: Colacci et al. (1985)
In another in vivo study, 1,1-dichloroethane induced significant, dose-related increases in chromosomal
aberrations and micronucleated cells in the bone marrow of male Swiss Webster mice given single
intraperitoneal doses of 200 to 500 mg/kg-bw (Patlolla et al.. 2005). No increase in DNA unwinding was
seen in the livers of mice when sacrificed 4 hours after intraperitoneal injection of 900 mg/kg-bw 1,1-
dichloroethane (Taningher et al.. 1991).
In summary, mode-of-action information pertaining specifically to tissues susceptible to tumor
formation after exposure to 1,1-dichloroethane (e.g., liver, mammary, blood) is limited to studies
showing that 1,1-dichloroethane induces DNA repair and binds to DNA in liver cells, and that it induces
chromosomal aberrations and micronuclei in bone marrow. These data are not sufficient to determine
the mode of action for any tumor type associated with exposure to 1,1-dichloroethane. Overall, the
available data provide limited support for the genotoxicity of 1,1-dichloroethane, and no information on
alternative modes of carcinogenic action.
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15411 M.7.1.1 Evidence Integration Table for Cancer for 1,1-Dichloroethane
15412
15413 Table Apx M-43. Evidence Integration Table for Cancer
Database Summary
Factors that Increase Strength
Factors that Decrease Strength
Summary of Key
Findings and Within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams and
Overall WOSE
Judgement
Evidence Integration Summary on Cancer
Evidence from human studies
Overall WOSE
judgement for cancer
effects based on
integration of
information across
evidence streams:
Evidence suggests, but
is not sufficient to
conclude, that 1,1-
dichloroethane causes
cancer in humans under
relevant exposure
circumstances.
• A prospective study of
women from the California
Teacher Study Cohort, for
which the EPA's National-
Scale Air Toxics
Assessment (NATA) was
used to estimate exposure,
evaluated the association
between 1,1-dichloroethane
exposure and the incidence
of invasive breast cancer
(Garcia et al.. 2015). Studv
quality: High
Bioloeical eradient/dose-resoonse:
• Exposure to 1,1 -dichloroethane
was associated with estrogen
receptor/progesterone receptor-
positive (ER+/PR+) tumors and
tumors among women who were
past or never users of hormone
therapy.
Magnitude and precision:
• The study used quantitative
exposure estimates and accounted
for covariate information on
individual breast cancer risk
factors.
Oualitv of the database:
• Associations between breast cancer
and exposure were observed in a
high-quality study.
Bioloeical eradicnt/dosc-rcsDonsc:
• The overall risk for invasive
breast cancer was not
significantly increased in 1,1-
dichloroethane-exposed women
relative to unexposed controls.
• Analyses based on quintiles of
exposure did not show a dose-
response relationship with
ER+/PR+ tumors.
Maenitude and precision:
• The effect estimates were small
(hazard ratios <1.35).
• Exposure estimates based on
modeling of emissions data may
have contributed to exposure
misclassification; confidence in
the exposure assessment was
rated "medium" by US EPA.
• Concentrations of 1,1-
dichloroethane and vinyl
chloride were highly correlated
in this study and this co-
exposure may have confounded
the results.
Key findings'.
In a high-quality study, an
association between 1,1-
dichloroethane exposure in
humans and certain breast
tumors was observed. This
association was seen in the
absence of a significant
increase in overall risk for
invasive breast cancer in
1,1 -dichloroethane-
exposed women.
Overall WOSEjudgement
for cancer effects based on
human evidence:
• Indeterminate
Evidence from apical endpoints in in vivo mammalian animal studies
Breast cancer
• A gavage study in male and
female mice examined the
mammary gland for
neoplasms after 78 weeks
Bioloeical eradient/dose-resnonse:
• In a study ranked as Uninfonnative
due to high mortality related to
pneumonia, a significant dose-
Maenitude and precision:
• The incidence of mammary
gland tumors in treated female
rats was not statistically
Key findings'.
Increased breast cancer
incidence was observed in
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Database Summary
Factors that Increase Strength
Factors that Decrease Strength
Summary of Key
Findings and Within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams and
Overall WOSE
Judgement
of exposure (NCI. 1978).
Study quality: High
Studv aualitv ranked as
Uninformative:
• A gavage study in male and
female rats " examined the
mammary gland for
neoplasms after 78 weeks
of exposure (NCI. 1978).
related trend for increased
incidence of mammary gland
adenocarcinomas was observed in
female rats using matched vehicle
controls (based on analyses of all
females and females surviving at
least 52 weeks), despite poor
survival limiting the ability to
detect late-developing tumors.
significantly increased based on
pairwise comparison to pooled
or matched vehicle controls or
based on a trend test using
pooled vehicle controls.b
Oualitv of the database:
• Increased incidence of
mammary tumors was observed
only in a study ranked as
Uninformative.
female rats in a study
ranked as Uninformative.
Overall WOSEjudgement
for breast cancer effects
based on animal evidence:
• Indeterminate
Liver cancer
• A gavage study in male and
female mice examined the
liver for neoplasms after
78 weeks of exposure
(NCI. 1978). Studv aualitv:
High
• Nine-week studies in male
rats, which were
administered 1,1-
dichloroethane via gavage,
determined the potential for
tumor initiation or
promotion based on
numbers of GGT-positive
foci in the liver (Milman et
al.. 1988; Storv et al..
1986). Studv aualitv: Hieh
Studv aualitv ranked as
Uninformative:
• A gavage study in male and
female rats d examined the
liver for neoplasms after
78 weeks of exposure
(NCI. 1978).
• A cancer bioassay and a
tumor promotion assay in
male mice e assessed the
Biolosical aradicnt/dosc-rcsdorise:
• A significant dose-related trend for
increased incidence of
hepatocellular carcinomas was
observed in male mice surviving at
least 52 weeks in the 78-week
study using pooled vehicle
controls,c and the pairwise
comparison showed a significant
increase at the high dose. These
effects were observed despite poor
survival in high-dose male mice
limiting the ability to detect late-
developing tumors.
• Exposure resulted in increased
numbers of GGT-positive foci in
the livers of male rats pretreated
with a tumor initiator.
Oualitv of the database:
• Evidence of increased liver tumor
incidence was observed in a high-
quality study.
Magnitude and precision:
• The incidence of liver tumors in
male mice was not statistically
significantly increased in
pairwise comparison and trend
test using matched vehicle
controls.
• Only one dose was used in the
9-week tumor initiation and
promotion protocols.
Oualitv of the database:
• Increased incidence of liver
tumors was observed in only
one study in one sex (males)
followed only for 78 weeks.
Key findings:
In high-quality studies,
increased liver tumor
incidence was observed in
male mice and evidence
supporting tumor
promotion was observed in
male rats. Overall WOSE
judgement for liver cancer
effects based on animal
evidence:
• Slight
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Database Summary
Factors that Increase Strength
Factors that Decrease Strength
Summary of Key
Findings and Within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams and
Overall WOSE
Judgement
incidence of liver
adenomas and/or
carcinomas after a 52-week
drinking water exposure
(Klaunis et al.. 1986).
Endometrial stromal polyps
• A gavage study in female
mice conducted
histopathological
examination of the uterus
after 78 weeks of exposure
(NCI. 1978). Studv aualitv:
High
Studv aualitv ranked as
Uninfonnative:
• A gavage study in female
rats ^conducted
histopathological
examination of the uterus
after 78 weeks of exposure
(NCI. 1978).
Biolosical eradient/dose-resoonse:
• The incidence of endometrial
stromal polyps in female mice
showed a significant dose-related
trend using either pooled or
matched vehicle controls and a
significant increase at the high dose
in pairwise comparison to the
pooled vehicle controls. g
Oualitv of the database:
• Evidence of increased endometrial
stromal polyp incidence was
observed in a high-quality study.
Biolosical eradient/dose-resoonse:
• The incidence of endometrial
stromal polyps in female mice
was not significantly increased
in pairwise comparison to
matched vehicle controls.
Oualitv of the database:
• Increased incidence of
endometrial stromal polyps was
observed in only one study in
mice followed for only
78 weeks.
Biolosical olausibilitv and human
relevance:
• The relevance to humans of
endometrial stromal polyps in
rodents is uncertain due to
differences in etiology and
honnone sensitivitv (Davis.
2012).
Key findings'.
In a high-quality study,
increased endometrial
stromal polyp incidence
was observed in female
mice. The relevance of
these findings to humans is
uncertain due to
differences in etiology and
honnone sensitivity among
rodents and humans. In
addition, there is
uncertainty within the
scientific community
whether endometrial
stromal polyps should be
considered benign tumors
or nonneoplastic lesions.
Overall WOSEjudgement
for uterine cancer effects
based on animal evidence:
• Indetenninate
Circulatory system cancer
• A gavage study in male and
female mice subjected
animals to comprehensive
histological examinations
for neoplasms after 78
weeks of c\ do sure (NCI.
1978). Studv aualitv: Hish
Studv aualitv ranked as
Uninfonnative:
Biolosical eradient/dose-resoonse:
• In a study ranked as Uninfonnative
due to high mortality related to
pneumonia, a significant dose-related
trend for increased incidence of
hemangiosarcomas was observed in
female rats using either pooled or
matched vehicle controls, despite
Consistencv:
• The incidence of
hemangiosarcomas was not
increased in male rats.
Masnitude and precision:
• The incidence of
hemangiosarcomas in treated
female rats was not statistically
significantly increased based on
Key findings'.
Increased incidence of
hemangiosarcomas was
observed in female rats in a
study ranked as
Uninfonnative.
Overall WOSE judgement
for circulatory system
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Database Summary
Factors that Increase Strength
Factors that Decrease Strength
Summary of Key
Findings and Within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams and
Overall WOSE
Judgement
• A gavage study in male and
female rats h subjected
animals to comprehensive
histological examinations
for neoplasms after 78
weeks of c\ do sure (NCI.
1978).
poor survival limiting the ability to
detect late-developing tumors.
pairwise comparison to pooled
or matched vehicle controls.
Oualitv of the database:
• Increased incidence of
hemangiosarcomas was
observed in a study ranked as
Uninfonnative.
cancer effects based on
animal evidence:
• Indeterminate
Evidence from mechanistic studies
Genotoxicitv:
• Three in vitro experiments
evaluated reverse mutation
in Salmonella typhimurium
(Zeieer et al.. 1992;
Milmanetal.. 1988;
Simmon et al.. 1977)
• Three in vitro experiments
evaluated chromosomal
aberrations or DNA repair
in mammalian cells
(Matsuoka et al.. 1998;
Williams et al.. 1989;
Milmanetal.. 1988)
• Two in vitro experiments
evaluated cell
transformation (Milman et
al.. 1988; Tu et al.. 1985;
Arthur D. Little Inc. 1983;
Hatch et al.. 1983). one
evaluated DNA binding in
a cell-free svstem (Colacci
et al.. 1985). and one
evaluated chromosome
malsegregation in fungi
(Crebelli et al.. 1995;
Crebelli et al.. 1988).
• Four in vivo experiments
evaluated chromosomal
aberrations, micronuclei.
Biolosical eradient/dose-resoonse:
• There were significant, dose-
related increases in chromosomal
aberrations and micronuclei in the
bone marrow of treated mice.
• 1,1 -dichloroethane treatment
resulted in dose-related
enhancement of Syrian hamster
embryo cell transformation by S A7
(simian) adenovirus.
Consistency:
• Treatment induced DNA repair in
cultured hepatocytes from rats and
mice.
• DNA adducts were induced by
treatment in vivo and in a cell-free
system.
Biolosical eradient/dose-resoonse:
• Increased chromosomal
malsegregation mAspergillus
nidulans induced by treatment
was not strictly concentration-
related.
Consistency:
• 1,1 -dichloroethane did not
increase the percent double-
stranded DNA in hepatic nuclei
of mice exposed in vivo
• Tests of reverse mutations in S.
typhimurium yielded
inconsistent results.
• Some tests of reverse mutation
in S. typhimurium yielded
negative results.
• No chromosomal aberrations
were observed in Chinese
hamster lung fibroblasts tested
in vitro.
• Results were negative for cell
transformation in BALB/c-3T3
cells
Oualitv of the database:
• The available studies did not
evaluate mutagenicity in
mammalian cells in vitro or in
vivo.
Key findings'. Available
data are limited but suggest
that 1,1 -dichloroethane
may be genotoxic based on
evidence of chromosomal
abnormalities and
micronuclei in mice in
vivo. Bacterial
mutagenicity findings were
not consistent.
Overall WOSEjudgement
for cancer effects based on
mechanistic evidence:
• Slight
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Database Summary
Factors that Increase Strength
Factors that Decrease Strength
Summary of Key
Findings and Within-
Stream Strength of the
Evidence Judgement
Inferences across
Evidence Streams and
Overall WOSE
Judgement
DNA binding, or DNA
unwinding in rodents
(Patlolla et al.. 2005;
Tanineher et al.. 1991;
Colacci et al.. 1985).
" The study in male and female rats was considered Uninfonnative due to high mortality related to pneumonia.
h Pooled controls from several bioassays were used based on data for the same strain, tested by the same laboratory no more than 6 months apart, and diagnosed by the
same pathologist.
c Pooled controls from several bioassays were used based on data for the same strain, tested by the same laboratory no more than 6 months apart, and diagnosed by the
same pathologist.
d The study in male and female rats was considered Uninfonnative due to high mortality related to pneumonia.
e The 52-week study in male mice was considered Uninfonnative because the duration of the study was not adequate to detennine tumorigenicity (cancer bioassay) and
because the negative control response was too strong, precluding the ability to detennine if 1,1 -dichloroethane increased tumor incidence (tumor promotion assay).
' The study in female rats was considered Uninfonnative due to high mortality related to pneumonia.
g Pooled controls from several bioassays were used based on data for the same strain, tested by the same laboratory no more than 6 months apart, and diagnosed by the
same pathologist.
h The study in male and female rats was considered Uninfonnative due to high mortality related to pneumonia.
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M.7.2 1,2-Dichloroethane
1,2-Dichloroethane is considered a "probable human carcinogen" (U.S. EPA. 1987b) based on evidence
of tumorigenicity in animal studies, including significant increases in tumors of the mammary gland
(robust evidence), lung (moderate evidence), liver (slight-to-moderate evidence), circulatory system
(slight evidence) and other tissues (indeterminate evidence) in male and/or female rats and/or mice by
oral, inhalation, and/or dermal exposure (see Section M.8.1). The occurrence of tumors in multiple
tissues and treated groups is suggestive of a genotoxic mode of action, and most data relating to mode of
action for 1,2-dichloroethane carcinogenicity are assays for genetic toxicity. Recent comprehensive
reviews (ATSDR. 2022; Gwinn et al.. 2011) were used to develop an overview of genotoxicity data for
1,2-dichloroethane and the role of metabolism, which is presented below. Potential nongenotoxic modes
of action for rat mammary tumors were investigated in one study (Lebaron et al.. 2021). Brief
discussions of the information (both genotoxic and non-genotoxic mechanisms) that pertain to specific
tumor sites associated with 1,2-dichloroethane exposure (mammary gland, lung, liver, and circulatory
system) follow the general genotoxicity discussion.
Genotoxicity Overview
Evidence from in vivo studies using multiple animal species and routes of exposure and in vitro studies
using multiple test systems indicates that 1,2-dichloroethane and/or its metabolites can induce mutations,
chromosomal aberrations, DNA damage, and DNA adducts in certain test systems. The available data
show that biotransformation of 1,2-dichloroethane to reactive metabolites via a major CYP450-mediated
oxidative pathway and a minor glutathione conjugation pathway contributes to the observed effects.
There are species-, sex-, tissue-, and dose-related differences in the interactions between 1,2-
dichloroethane and/or its metabolites and DNA.
Evidence that 1,2-dichloroethane induces gene mutation is based largely on in vitro studies. Reverse
mutation studies in Salmonella typhimurium were predominantly positive, especially with metabolic
activation (as reviewed by as reviewed by ATSDR. 2022; Gwinn et al.. 2011). Mutagenicity was seen
more consistently in Salmonella strains that detect base-pair substitutions (e.g., TA1535) than those that
detect frameshift mutations (e.g., TA97) (as reviewed by as reviewed by ATSDR. 2022; Gwinn et al..
2011). Mutations at the HGPRT locus were increased in Chinese hamster ovary (CHO) cells in the
presence of metabolic activation, both when 1,2-dichloroethane was incorporated in media (Tan and
Hsie. 1981) and when cells were exposed to 1,2-dichloroethane as a vapor in a closed system (Zamoraet
al.. 1983). There are limited gene mutation data from in vivo studies. Oral and inhalation studies
assessing various types of mutations in Drosophila were generally positive, but many of the studies were
limited by lack of methodological details and/or the use of a single exposure level (as reviewed by as
reviewed by ATSDR. 2022; Gwinn et al.. 2011). A single study of lacZ mutations in the liver and testis
of Muta™ mice showed no increase in the mutation frequency after exposure to 1,2-dichloroethane by
oral or intraperitoneal administration at doses up to 150 or 280 mg/kg-bw, respectively (Hachiya and
Motohashi. 2000).
In vivo rodent studies showing clastogenic effects, DNA damage, and DNA adducts in the mammary
gland, lung, liver, and circulatory system tissues are discussed in the subsections below on potential
mechanisms for carcinogenicity in these tissues. A small number of in vivo studies of genotoxicity
endpoints in other tissue types showed evidence of DNA damage (Comet assay) in mouse kidney,
bladder, and brain (Sasaki et al.. 1998); and DNA binding or DNA adducts in mouse and rat stomach,
forestomach, and kidney (Watanabe et al.. 2007; Hellman and Brandt. 1986; Inskeep et al.. 1986; Prodi
et al.. 1986; Arfellini et al.. 1984) after exposure by intraperitoneal injection.
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Role of Metabolism
Available data are not sufficient to determine whether metabolism of 1,2-dichloroethane is a necessary
first step in its genotoxic action. In vitro studies in bacteria have shown that exogenous metabolic
activation is either required for, or increases the mutagenic activity of, 1,2-dichloroethane (as reviewed
by as reviewed by ATSDR. 2022; Gwinn et al.. 2011). In contrast, experiments in human lymphocytes
cultured in vitro with 1,2-dichloroethane showed increased micronucleus formation in the absence of S9,
but not in the presence of S9 (Tafazoli et al.. 1998).
Evidence suggests that metabolism of 1,2-dichloroethane, especially via the glutathione pathway, does
lead to increased genotoxicity. Crespi et al. (1985) compared the genotoxicity of 1,2-dichloroethane in
human cell lines with differing metabolic capacities. Crespi et al. (1985) observed 25-fold higher
HGPRT mutation frequencies in AHH-1 compared with TK6 human lymphoblastoid cells. The study
authors measured 5-fold greater glutathione-S-transferase activity in the AHH-1 cells than the TK6 cells,
suggesting that the glutathione metabolic pathway increased the frequency of mutations induced by 1,2-
dichloroethane.
Several studies have inhibited or stimulated enzymes to elucidate the relative importance of the CYP450
and glutathione pathways in 1,2-dichloroethane genotoxicity. In Ames assays, supplementation of the
media with glutathione or glutathione-S-transferase increases the mutagenicity of 1,2-dichloroethane (as
reviewed by as reviewed by ATSDR. 2022; Gwinn et al.. 2011). Drosophila melanogaster pretreated
with buthionine sulfoximine (BSO, an inhibitor of glutathione synthesis) before inhalation exposure to
1,2-dichloroethane exhibited reduced mutations (measured using somatic mutation and recombination
tests [SMARTs]) compared with those that were not pretreated (Romert et al.. 1990). Pretreatment of
fruit flies with an inducer of glutathione-S-transferase (phenobarbital) significantly increased mutation
frequency (Romert et al.. 1990). In support of these findings, Chroust et al. (2001) observed increased
mutagenicity in transgenic fruit flies expressing human glutathione-S-transferase (Al subunit), an effect
that was mitigated by pretreatment with BSO.
Inhibition of CYP450 metabolism has been shown to potentiate DNA damage and increase DNA
binding from exposure to 1,2-dichloroethane. In rats exposed to piperonyl butoxide in addition to 1,2-
dichloroethane (via intraperitoneal injection), increased levels of hepatic DNA damage (measured with
alkaline DNA unwinding assay) were seen in comparison to the levels in rats treated with 1,2-
dichloroethane alone (Storer and Conolly. 1985). Similarly, increased DNA binding in the liver, kidney,
spleen, and testes was observed in rats exposed to 1,2-dichloroethane by inhalation with concurrent
dietary exposure to the CYP450 inhibitor disulfiram (relative to 1,2-dichloroethane exposure alone)
(Igwe et al.. 1986a).
Mammary Gland Cancer Mechanisms
Lebaron et al. (2021) conducted in vivo experiments to assess potential mechanisms of rodent mammary
tumors induced by 1,2-dichloroethane. The study authors exposed female F344 rats by inhalation to 0 or
200 ppm 1,2-dichloroethane for 6 hours/day on at least 28 consecutive days. At sacrifice, blood samples
were obtained for assessment of serum prolactin, and mammary tissues were collected for
histopathology and assays of epithelial cell proliferation (Ki-67 immunohistochemistry), DNA damage
(Comet assay), and levels of glutathione, reduced glutathione, and oxidized glutathione. There was no
difference between exposed and control groups for any of these endpoints, nor was there an effect of
exposure on 8-oxo-2'-deoxyguanosine (8-OHdG) adduct levels, a marker of oxidative DNA damage.
Exposure to 1,2-dichloroethane did, however, induce a significant increase in S-(2-N7-guanylethyl)
glutathione DNA adducts, as also found in the liver in this and other studies (see below). In vitro studies
have shown these adducts to be mutagenic (Gwinn et al.. 2011). Lebaron et al. (2021). however, argue
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that in vivo evidence does not support this conclusion and that these adducts should be considered
biomarkers of exposure, rather than mutagenic adducts.
No other data on potential mechanisms were located. The DNA adducts in mammary tissue resulting
from 1,2-dichloroethane exposure in vivo could plausibly be related to subsequent formation of
mammary tumors, although the role of these adducts in carcinogenicity of 1,2-dichloroethane has not
been conclusively demonstrated.
Lung Cancer Mechanisms
Studies relevant to carcinogenic mechanisms of 1,2-dichloroethane-induced lung cancers are limited to
measurements of DNA damage in the lung of mice exposed by intraperitoneal injection (Sasaki et al..
1998) and quantification of DNA adducts in the lungs of rats and mice also exposed by intraperitoneal
injection (Baertsch et al.. 1991; Prodi et al.. 1988). Increased DNA damage (measured by alkaline single
cell gel [SCG] assay and compared with measurement at time 0) was observed in the lungs of mice
when measured 3 or 24 hours after dosing with 200 mg/kg 1,2-dichloroethane (Sasaki et al.. 1998).
DNA binding in the lungs of female rats was observed after 12 hours of inhalation exposure to 14C-1,2-
dichloroethane (Baertsch et al.. 1991). Prodi et al. (1988) observed higher binding of 14C-1,2-
dichloroethane to DNA in the lungs of mice compared with rats, consistent with the susceptibility of
mice, but not rats, to 1,2-dichloroethane-induced lung tumors (Nagano et al.. 2006). Experiments on
binding of radiolabeled 1,2-dichloroethane to calf thymus DNA in the presence of microsomes and/or or
cytosol from mouse and rat lung indicated binding in the presence of lung-derived microsomes
(containing CYP450), but not cytosol (containing glutathione-S-transferase) (Prodi et al.. 1988).
In an in vitro experiment, Matsuoka et al. (1998) observed dose-related increases in chromosomal
aberrations in Chinese hamster lung fibroblast (CHL) cells when incubated with 1,2-dichloroethane in
the presence of S9. In the absence of S9, the results were judged to be equivocal (Matsuoka et al.. 1998).
No other data on potential mechanisms were located. The observed genotoxic effects and DNA
binding/adduct formation in lung tissue following 1,2-dichloroethane exposure in vitro and in vivo could
plausibly be related to subsequent formation of lung tumors, although a direct connection between these
events and 1,2-dichloroethane-induced lung carcinogenesis has not been conclusively demonstrated.
Liver Cancer Mechanisms
One study evaluated potential mutations in the livers of animals exposed to 1,2-dichloroethane. Hachiya
and Motohashi (2000) measured the frequency of hepatic tissue lacZ mutations in the Muta™ Mouse
model 14 and 28 days after single gavage doses up to 150 mg/kg-bw or after repeated intraperitoneal
injections resulting in cumulative doses up to 280 mg/kg-bw. No increase in mutation frequency was
observed in the liver in any of the experiments.
When measured 3 and 24 hours after mice were exposed to 1,2-dichloroethane by intraperitoneal
injection, an increase in DNA damage in the liver was detected by alkaline SGC assay (when compared
to levels seen at time 0) (Sasaki et al.. 1998). Significant decreases in the percentage of double-stranded
DNA were observed in mice given single intraperitoneal doses of 300 mg/kg (Taningher et al.. 1991) or
2 and 3 mmol/kg (200 and 300 mg/kg) (Storer and Conolly. 1983). Storer et al. (1984) assessed route
differences in DNA damage in the livers of mice exposed by gavage (100-400 mg/kg), intraperitoneal
injection (100-300 mg/kg), and inhalation (4 hours at 150-2,000 ppm). The fraction of double stranded
DNA was significantly decreased in a dose-related fashion at all doses (>100 mg/kg) after gavage
administration, at doses greater than or equal to 150 mg/kg after intraperitoneal injection, and at
concentrations greater than or equal to 1,000 ppm after inhalation exposure. While the lower doses
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producing DNA damage by oral and intraperitoneal exposure did not produce systemic effects in parallel
groups of similarly-treated mice, all concentrations producing DNA damage by inhalation exposure
were lethal to the similarly exposed mice (Storer et al.. 1984). In a study comparing alkylation of hepatic
DNA in rats and mice exposed to 1,2-dichloroethane by intraperitoneal injection, higher levels of
alkylation were observed in mice compared with rats (at least 40-fold higher in the first 30 minutes after
dosing) (Baneriee. 1988).
Binding of 1,2-dichloroethane or its metabolites to hepatic DNA of rats and mice exposed in vivo has
been demonstrated in a number of studies (Lebaron et al.. 2021; Watanabe et al.. 2007; Baertsch et al..
1991; Prodi et al.. 1988; Inskeep et al.. 1986). Available data show sex-, species-, and dose-related
differences in adduct levels. For example, an early study that compared DNA adduct levels in the livers
of male rats and mice exposed to 1,2-dichloroethane by intraperitoneal injection (127 |iCi/kg) showed
higher binding in mouse compared to rat (Prodi et al.. 1988). In contrast, in hepatic tissue from male and
female mice and male rats exposed by intraperitoneal administration of a much lower dose of 1,2-
dichloroethane (21 |iCi/kg, corresponding to 5 mg/kg), the highest levels of adducts were in female mice
(57 fmol/mg DNA), followed by male rats (46 fmol/mg DNA) and male mice (29 fmol/mg DNA)
(Watanabe et al.. 2007). In rats exposed by inhalation (50 ppm) for 2 years and then given a single oral
dose of radiolabeled 1,2-dichloroethane, no exposure-related difference in DNA adduct levels was
detected (Cheever et al.. 1990). Notably, this exposure level also failed to induce an increase in tumors
at any site.
DNA adducts from the glutathione metabolic pathway have been demonstrated to occur in the livers of
laboratory rodents exposed in vivo. In mice and rats administered 5 mg/kg 1,2-dichloroethane by
intraperitoneal injection, the primary adduct was S-(2-N7-guanylethyl) glutathione (Watanabe et al..
2007). Similarly, in rats given 150 mg/kg 14C-l,2DCAby intraperitoneal injection and sacrificed 8 hours
later, prominent adducts in the liver were identified by high-performance liquid chromatography
(HPLC) as S-[2-(N7-guanyl)ethyl]glutathione and S-[2-(N7-guanyl)ethyl]cysteinylglycine (Inskeep et
al.. 1986). Also, after 28 days of inhalation exposure to 200 ppm 1,2-dichloroethane, a significant
increase in S-(2-N7-guanylethyl) glutathione DNA adducts was detected in the livers of female rats
(Lebaron et al.. 2021). As discussed above for mammary tumors, there is some uncertainty as to the
toxicological significance of these adducts. While in vitro studies have shown these adducts to be
mutagenic (Gwinn et al.. 2011). Lebaron et al. (2021) argue that in vivo evidence does not support this
conclusion and that these adducts should be considered biomarkers of exposure, rather than mutagenic
adducts.
One study was located presenting in vitro data pertaining to the genotoxicity of 1,2-dichloroethane in the
liver. In this study, 1,2-dichloroethane induced DNA repair in both rat and mouse primary hepatocytes
(Milman et al.. 1988).
No other data on potential mechanisms were located. The observed DNA damage and DNA
binding/adduct formation in liver tissue following exposure to 1,2-dichloroethane in vitro and in vivo
could plausibly be related to subsequent formation of liver tumors, although a direct connection between
these events and 1,2-dichloroethane-induced liver carcinogenesis has not been conclusively
demonstrated.
Circulatory System Cancer Mechanisms
Data pertaining to mechanisms of circulatory system cancers induced by 1,2-dichloroethane consist of
genotoxicity studies, including one in vivo study in rats (Lone et al.. 2016). three in vivo studies in mice
(Witt et al.. 2000; Sasaki et al.. 1998; Giri and Que Hee. 1988). and three in vitro experiments in human
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lymphoblastoid cells or lymphocytes (Tafazoli et al.. 1998; Dohertv et al.. 1996; Crespi et al.. 1985).
Rats exposed by intraperitoneal injection to doses of 80.7, 161.4, or 242.1 mg/kg-bw exhibited
statistically significant, dose-related increases in the incidences of chromosomal aberrations and
micronuclei in bone marrow, as well as DNA damage (measured by alkaline comet assay) in blood cells
(Lone et al.. 2016). In mice exposed by intraperitoneal injection, significant increases in sister chromatid
exchange frequencies (Giri and Que Hee. 1988) and DNA damage (Sasaki et al.. 1998) were observed in
bone marrow. However, 90 days of drinking water exposure to 1,2-dichloroethane (up to 8000 mg/L)
did not increase the frequency of micronuclei in mice (Witt et al.. 2000). A study of workers exposed to
1,2-dichloroethane and vinyl chloride showed increased sister chromatid exchanges in the blood of those
exposed to moderate levels of 1,2-dichloroethane with low levels of vinyl chloride exposure (Cheng et
al.. 2000).
Several in vitro genotoxicity experiments were conducted in cells of the circulatory system. Increases in
mutations (measured using the hypoxanthine-guanine phosphoribosyltransferase [HGPRT] assay) and
micronuclei were observed in human lymphoblastoid cells cultured with 1,2-dichloroethane (Dohertv et
al.. 1996; Crespi et al.. 1985). Incubation with 1,2-dichloroethane resulted in increased micronuclei and
DNA damage (by Comet assay) in human peripheral lymphocytes in the absence of exogenous
metabolic activation (Tafazoli et al.. 1998).
No other data on potential mechanisms were located. The observed genotoxic effects of 1,2-
dichloroethane in hematopoietic cells and tissues in vitro and in vivo could plausibly be related to
subsequent formation of tumors, although a direct connection between these events and 1,2-
dichloroethane-induced circulatory system cancers has not been conclusively demonstrated.
Summary
1,2-dichloroethane is likely to be carcinogenic to humans, based on evidence of tumorigenicity in animal
studies, including multiple tumor sites in male and/or female rats and/or mice by oral, inhalation, and/or
dermal exposure. The occurrence of tumors in multiple tissues and treated groups is suggestive of a
genotoxic mode of action, and most data relating to mode of action for 1,2-dichloroethane
carcinogenicity are assays for genetic toxicity. Evidence from in vivo studies using multiple animal
species and routes of exposure and in vitro studies using multiple test systems indicates that 1,2-
dichloroethane and/or its metabolites can induce mutations, chromosomal aberrations, DNA damage,
and DNA binding/adduct formation in certain test systems. The available data also show that
biotransformation of 1,2-dichloroethane to reactive metabolites via a major CYP450-mediated oxidative
pathway and a minor glutathione conjugation pathway contributes to the observed effects. In vivo and in
vitro data showing genotoxicity and DNA binding/adduct formation in tissues where tumors associated
with 1,2-dichloroethane exposure have been observed (mammary gland, lung, liver, and circulatory
system) support that these effects could plausibly be related to formation of tumors in these tissues,
although a direct connection between these events and 1,2-dichloroethane-induced carcinogenesis has
not been conclusively demonstrated. Potential nongenotoxic modes of action were explored only in one
study of rat mammary tissue, and no supporting results were obtained.
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M.7.2.1 Evidence Integration Tables for Cancer for 1,2-Dichloroethane
Table Apx M-44.1,1-Dichloroethane Cancer Evidence Integration Table Based on Read-Across from 1,2-Dichloroethane
Database Summary
Factors that Increase Strength
Factors that Decrease Strength
Summary of Key Findings
and within-Stream
Strength of the Evidence
Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
Evidence Integration Summary Judgement on Cancer Effects
Evidence from human studies
Breast cancer
• A prospective study of women from
the California Teacher Study Cohort,
for which the U.S. EPA's National-
Scale Air Toxics Assessment (NATA)
was used to estimate exposure,
evaluated the association between 1,2-
dichloroethane exposure and the
incidence of invasive breast cancer
(Garcia et al„ 2015). Study quality:
High
• A prospective study of women from
the Sister Study Cohort, for which the
U.S. EPA's NATA was used to
estimate exposure, evaluated the
association between 1,2-
dichloroethane and the incidence of
invasive breast cancer and/or ductal
carcinoma in situ (Niehoff et al„
2019). Study quality: Medium
Biological gradient/dose-response:
• The risk for ER+ invasive breast
cancer was slightly, but
significantly, increased in
quintile 4 (but not quintile 5) of
exposure relative to quintile 1 in
the medium-quality study.
Magnitude and precision:
• The study used quantitative
exposure estimates and
accounted for covariate
information on individual breast
cancer risk factors.
Biological gradient/dose-response:
• The overall risk for breast cancer
(both studies) and ER- invasive
breast cancer (medium-quality
study) was not significantly
increased in 1,2-dichloroethane-
exposed women.
• Analyses based on quintiles of
exposure did not show an
exposure-response relationship
between 1,2-dichloroethane
exposure and ER+ invasive breast
cancer.
Magnitude and precision:
• The significant effect estimate for
ER+ invasive breast cancer was
small (hazard ratio = 1.17).
• Exposure estimates based on
modeling of emissions data
and/or at the census tract level
may have contributed to exposure
misclassification.
Key findings'.
In a medium-quality study,
an association between 1,2-
dichloroethane exposure and
ER+ invasive breast cancer
was observed, but it was
small and did not show a
clear exposure-response
relationship.
Overall WOSE judgement
for cancer effects based on
human evidence:
• Indeterminate
Circulatory system cancer
• A nested case-control study of male
workers from three Union Carbide
facilities, for which job assigmnent
and history of departmental use were
taken to estimate exposure
Biological gradient/dose-response:
• In the medium-quality study,
there was a nonsignificant
increase in the OR for
nonlymphocytic leukemia
Biological gradient/dose-response:
• In the medium-quality study,
exposure levels of 1,2-
dichloroethane were not
provided.
Key findings'.
Significant limitations in the
available studies preclude
conclusions regarding
associations between 1,2-
Overall WOSE
judgement for cancer
effects based on
integration of
information across
evidence streams:
Evidence indicates
that 1,2-
dichloroethane likely
causes cancer under
relevant exposure
circumstances.
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Database Summary
Factors that Increase Strength
Factors that Decrease Strength
Summary of Key Findings
and within-Stream
Strength of the Evidence
Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
(ever/never), evaluated the association
between 1,2-dichloroethane exposure
and the incidence of hematopoietic
tissue cancer (Ott et al.. 1989; Union
Carbide. 1989). Studv aualitv:
Medium
Studv aualitv ranked as Uninfonnative:
• A retrospective cohort study of male
workers " from one Union Carbide
facility (one of the three evaluated by
(Ott et al.. 1989; Union Carbide.
1989)). for which exposure
(ever/never) was based on the history
and/or duration of work in the
chlorohydrin unit (which produced
1,2-dichloroethane as a byproduct),
evaluated the association between
chemical exposure and the risk of
mortality due to lymphopoietic
cancers (Benson and Teta. 1993).
(NLL) in 1,2-dichloroethane-
exposed workers, which was
higher in those working more
than 5 years.
• In a study ranked as
Uninfonnative owing to lack of
an appropriate comparison
group and lack of 1,2-
dichloroethane exposure levels,
work in the chlorohydrin unit
was significantly associated
with mortality from lymphatic
and hematopoietic cancers.
Magnitude and precision:
• In the medium-quality study,
there was potential for
confounding because covariates
were not considered (race,
smoking status, concunent
exposure to other chemicals).
• In the medium-quality study,
statistical power was limited
because cancer case numbers
were low (n = 5 for NLL).
• In the medium-quality study,
statistical methods were not
specified and ORs were provided
without CIs.
Consistencv:
• In the Uninfonnative study,
analysis was conducted based on
work department rather than
specific chemicals.
dichloroethane exposure in
humans and circulatory
system cancers.
Overall WOSEjudgement
for cancer effects based on
human evidence:
• Indetenninate
Pancreatic cancer
• A case-control study of men and
women from 24 states, which
estimated intensity and probability of
1,2-dichloroethane exposure (low,
medium, high) based on listed
occupation and industry (from death
certificates) and a job exposure matrix
(JEM), evaluated the association
between 1,2-Dichloroethane exposure
and the risk of pancreatic cancer
(Kernanet al.. 1999). Studv aualitv:
High
Studv aualitv ranked as Uninfonnative:
• A retrospective cohort study of male
workers b from a Union Carbide
facility, for which exposure
Biolosical aradicnt/dosc-rcsDonsc:
• In the high-quality study, 1,2-
dichloroethane exposure was
associated with a slight, but
borderline significant, increased
OR for pancreatic cancer among
Black females with low
estimated exposure intensity.
• In a study ranked as
Uninfonnative owing to lack of
an appropriate comparison
group and lack of 1,2-
dichloroethane exposure levels,
work in the chlorohydrin unit
was significantly associated
Biolosical eradient/dose-resoonse:
• In the high-quality study, the risk
for pancreatic cancer in Black
females was not increased in
groups with medium or high
intensity exposure.
Consistencv:
• In the high-quality study, 1,2-
dichloroethane exposure was not
associated with an increased risk
of pancreatic cancer in Black
males. White females, or White
males.
• In the Uninfonnative study,
analysis was conducted based on
Key findings:
In a high-quality study, a
slight, but significant,
association between low
intensity 1,2-dichloroethane
exposure and pancreatic
cancer was observed in
Black females, but the
association did not show an
exposure-response
relationship, and no
association was observed in
Black males or White males
or females.
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Database Summary
Factors that Increase Strength
Factors that Decrease Strength
Summary of Key Findings
and within-Stream
Strength of the Evidence
Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
(ever/never) was based on the history
and/or duration of work in the
chlorohydrin unit (which produced
1,2-dichloroethane as a byproduct),
evaluated the association between
chemical exposure and the risk of
mortality due to pancreatic cancer
(Benson and Teta. 1993).
with mortality from pancreatic
cancer.
work department rather than
specific chemicals.
Magnitude and precision:
• In the high-quality study, the
effect estimate in Black females
was small (OR = 1.2, 95% CI
1.0-1.4).
• In the high-quality study, there
was the potential for exposure
misclassification based on the
occupation and industry data
captured on death certificates.
Overall WOSEjudgement
for cancer effects based on
human evidence:
• Indeterminate
Kidney cancer
• A population-based, case-control
study of men and women from the
Minnesota Cancer Surveillance
System (cases) and the general
population of Minnesota or the Health
Care Financing administration
(controls), for which exposure was
estimated based on occupational
history and JEMs, evaluated the
association between 1,2-
dichloroethane exposure and the risk
for renal cell carcinoma (Dosemeci et
al.. 1999). Studv aualitv: Medium
Biological eradient/dose-resoonse:
Biolosical eradient/dose-resoonse:
Key findings:
In a medium-quality study,
no significant association
between 1,2-dichloroethane
exposure in humans and
renal cell carcinoma was
observed; however, the
number of exposed subjects
in the study population was
small.
Overall WOSE judgement
for cancer effects based on
human evidence:
• Indeterminate
• The risk of renal cell carcinoma
was significantly increased in
women exposed to all organic
solvents combined and all
chlorinated aliphatic
hydrocarbons combined.
Magnitude and precision:
• The use of a priori assessment of
exposure to solvents (including
1,2-dichloroethane) using JEMs
reduced recall bias among men
and women and cases and
controls.
• No significant increase in the risk
of renal cell carcinoma was
observed based on exposure to
1,2-dichloroethane among men,
women, or all participants.
Magnitude and precision:
• The number of participants
exposed to 1,2-dichloroethane
(40 cases and 48 controls) may
have been too low to detect
effects associated with 1,2-
dichloroethane exposure.
Oualitv of the database:
• Only one medium-quality study
was available to assess risk of
renal cancer due to 1,2-
dichloroethane exposure.
Prostate cancer
• A retrospective cohort study
evaluated cancer incidence in
251 employees of an herbicide
manufacturing facility (bentazon unit)
between 1979 and 1987, followed
Biolosical aradicnt/dosc-rcsDonsc:
Magnitude and precision:
Key findings'.
In a medium-quality study,
an association between work
in bentazon production and
prostate cancer was
• A statistically significant
association was observed
between employment in the
bentazon unit and prostate
• The study did not directly assess
the association between exposure
to 1,2-dichloroethane and
prostate cancer. Other chemicals
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Database Summary
Factors that Increase Strength
Factors that Decrease Strength
Summary of Key Findings
and within-Stream
Strength of the Evidence
Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
until 2003. SMRs were calculated
using age-, gender-, and race-specific
cancer incidence rates in South
Louisiana. (BASF. 2005). Studv
quality: Medium
cancer incidence (SIR = 2.2,
95% CI = 1.1-3.9)
were also used in the bentazon
unit.
observed; however, the
association with 1,2-
dichloroethane was not
directly assessed.
Overall WOSEjudgement
for cancer effects based on
human evidence:
Indeterminate
Evidence from apical endpoints in in vivo mammalian animal studies
Breast cancer
• A gavage study in male and female
mice examined the mammary gland
for neoplasms after 78 weeks of
exposure (NTP. 1978). Studv aualitv:
High
• Two inhalation studies in male and
female rats (Naeano et al.. 2006;
Cheever et al.. 1990) and one
inhalation study in male and female
mice (Naeano et al.. 2006) examined
the mammary gland for neoplasms
after 104 weeks of exposure. Study
quality: High
• A dermal study in male and female
transgenic mice susceptible to cancer
examined the mammary gland for
neoplasms after 26 weeks of exposure
(Sueuro et al.. 2017). Studv aualitv:
High
Studv aualitv ranked as Uninfonnative:
• A gavage study in male and female
rats J examined the mammary gland
for neoplasms after 78 weeks of
exposure (NTP. 1978).
• An inhalation study in male and
female rats and mice e examined the
mammary gland for neoplasms at
Biolosical aradicnt/dosc-rcsDonsc:
Consistencv:
Key findings:
Mammary gland tumors
were observed in male and
female rats and in female
mice exposed to 1,2-
dichloroethane orally or via
inhalation in high-quality
studies.
Overall WOSE judgement
for breast cancer effects
based on animal evidence:
• Robust
• A significant dose-related trend
for increased incidence of
mammary gland
adenocarcinomas was observed
in female mice in the 78-week
gavage study using pooled
vehicle controls c; pairwise
comparisons showed significant
increases at both doses.
• Significant dose-related trends
for increased mammary gland
adenomas, fibroadenomas,
and/or adenocarcinomas were
observed in male and female rats
after 104 weeks of inhalation
exposure; pairwise comparisons
showed significant increases at
the highest exposure.
• A significant dose-related trend
for increased incidence of
mammary gland
adenocarcinoma was observed
in female mice after 104 weeks
of inhalation exposure.
• In a study ranked as
Uninfonnative due to high
• The incidence of mammary gland
tumors was not increased in a 26-
week dermal study in transgenic
mice.
Magnitude and precision:
• Pairwise comparisons were not
significant for increased
incidence of mammary gland
adenocarcinoma in female mice
after 104 weeks of inhalation
exposure.
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Database Summary
Factors that Increase Strength
Factors that Decrease Strength
Summary of Key Findings
and within-Stream
Strength of the Evidence
Judgement
Inferences across
Evidence Streams
and Overall WOSE
Judgement
natural death after 78 weeks of
exposure (Maltoni et al.. 1980).
mortality from pneumonia,
significant dose-related trends
for increased mammary gland
adenocarcinomas or
adenocarcinomas and
fibroadenomas were observed in
female rats in the 78-week
study; pairwise comparisons
showed a significant increase at
the high dose for
adenocarcinomas and at both
doses for combined tumors.
• In a study ranked uninfonnative
due to lack of inhalation
exposure details, the incidence
of mammary gland fibromas and
fibroadenomas was significantly
increased in rats after 78 weeks
of inhalation exposure.
Oualitv of the database:
• Evidence of mammary gland
tumors in rats and mice was
observed in high-quality studies.
Liver cancer
• A gavage study in male and female
mice examined the liver for
neoplasms after 78 weeks of exposure
(NTP. 1978). Studv aualitv: Hieh
• Two inhalation studies in male and
female rats (Naeano et al.. 2006;
Cheever et al.. 1990) and one
inhalation study in male and female
mice (Naeano et al.. 2006) examined
the liver for neoplasms after
104 weeks of exposure. Study quality:
High
Biolosical eradient/dose-resoonse:
• A significant dose-related trend
for increased incidence of
hepatocellular carcinomas was
observed in male (but not
female) mice in the 78-week
gavage study using pooled and
matched vehicle controls ^, and
the pairwise comparison to
pooled vehicle controls showed
a significant increase at the high
dose.
Consistency:
• The incidence of liver tumors was
not increased in transgenic mice
following 26 weeks of dermal
exposure.
Magnitude and precision:
• In female mice, incidences of
hepatocellular adenomas and
adenomas or carcinomas in the
104-week inhalation study were
not significantly increased based
Key findings'.
In high-quality studies,
increased liver tumor
incidence was observed in
male or female mice
following exposure via
gavage or inhalation,
respectively.
Overall WOSEjudgement
for liver cancer effects
based on animal evidence:
• Slight to Moderate
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• A dermal exposure study in male and
female transgenic mice susceptible to
cancer examined the liver for
neoplasms after 26 weeks of exposure
(Sueuro et al.. 2017). Studv aualitv:
High
• Nine-week gavage studies in male rats
evaluated the potential for tumor
initiation and/or promotion in the liver
based on numbers of gamma-
glutamyltranspeptidase (GGT)-
Dositive foci (Milman et al.. 1988;
Storv et al.. 1986). Studv aualitv:
High
Studv aualitv ranked as Uninfonnative:
• A gavage study in male and female
rats g examined the liver for
neoplasms after 78 weeks of exposure
(NTP. 1978).
• A significant dose-related trend
for increased incidence of
hepatocellular adenomas and
adenomas or carcinomas was
observed in female (but not
male) mice following 104 weeks
of inhalation exposure.
Oualitv of the database:
• Evidence of increased liver
tumor incidence was observed in
high-quality studies.
on pairwise comparisons to
controls.
• A cancer bioassay and a tumor
promotion assay in male mice h
assessed the incidence of liver
adenomas and/or carcinomas after 52
weeks drinking water exposure
(Klaunie et al.. 1986). An inhalation
study in male and female rats and
mice ' examined the liver for
neoplasms at natural death after 78
weeks of exposure (Maltoni et al..
1980).
• A dermal exposure study in female
mice ¦' examined the liver for
neoplasms after up to 85 weeks of
exposure (Van Duuren et al.. 1979).
Lung cancer
• A gavage study in male and female
mice examined the lung for
Biolosical eradient/dose-resoonse:
Magnitude and precision:
Key findings'.
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neoplasms after 78 weeks of exposure
(NTP. 1978). Studv aualitv: Hieh
• Two inhalation studies in male and
female rats (Naeano et al.. 2006;
Cheever et al.. 1990) and one
inhalation study in male and female
mice (Naeano et al.. 2006) examined
the lung for neoplasms after
104 weeks of exposure. Study quality:
High
• A dermal exposure study in male and
female transgenic mice susceptible to
cancer examined the lung for
neoplasms after 26 weeks of exposure
(Sueuro et al.. 2017). Studv aualitv:
High
Studv aualitv ranked as Uninfonnative:
• A gavage study in male and female
rats k examined the lung for
neoplasms after 78 weeks of exposure
(NTP. 1978).
• Significant trends and pairwise
comparisons for increased
incidence of
alveolar/bronchiolar adenomas
were observed in male and
female mice in the 78-week
gavage study.
• Significant trends for increased
incidence of bronchiolo-alveolar
carcinomas and carcinomas or
adenomas were observed in
female mice following 104
weeks of inhalation exposure.
• Significant increases in the
incidence and multiplicity of
bronchiolo-alveolar adenomas
and adenocarcinomas were
observed in both sexes in the
dermal study using transgenic
mice.
Consistencv:
• Pairwise comparisons did not
show a significant increase in the
incidence of lung tumors in
female mice in the 104-week
study.
In high-quality studies,
increased lung tumor
incidence was observed in
male and/or female mice
following gavage,
inhalation, or dermal
exposure.
Overall WOSEjudgement
for lung cancer effects based
on animal evidence:
• Moderate
• A cancer bioassay and a tumor
promotion assay in male mice '
assessed the incidence of lung
adenomas and/or carcinomas after 52
weeks of drinking water exposure
(Klaunie et al.. 1986).
• An inhalation study in male and
female rats and miceexamined the
lungs for neoplasms at natural death
after 78 weeks of c\do sure (Maltoni
et al.. 1980).
• A dermal exposure study in female
mice " reported neoplasms in the lung
(not routinely examined) after up to
82 weeks of exposure (Van Duuren et
al.. 1979).
• In the dermal study ranked as
Uninfonnative due to the use of
methods that did not account for
the volatility of 1,2-
dichloroethane, a significantly
increased incidence of benign
lung papillomas was observed
in female mice.
Oualitv of the database:
• Evidence of lung tumors was
observed in three high-quality
studies.
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and Overall WOSE
Judgement
Mesothelioma of the peritoneum
• A gavage study in male and female
mice conducted comprehensive
histopathological examination after
78 weeks of exposure (NTP. 1978).
Study quality: High
• Two inhalation studies in male and
female rats (Naeano et al.. 2006;
Cheever et al.. 1990) and one
inhalation study in male and female
mice (Naeano et al.. 2006) conducted
comprehensive histopathological
examination after 104 weeks of
exposure. Study quality: High
• A dermal exposure study in male and
female transgenic mice susceptible to
cancer conducted comprehensive
histopathological examination after
26 weeks of exposure (Sueuro et al..
2017). Studv aualitv: Hieh
Studv aualitv ranked as Uninfonnative:
• A gavage study in male and female
rats ° conducted comprehensive
histopathological examination after
78 weeks of exposure (NTP. 1978).
• An inhalation study in male and
female rats and mice p conducted
comprehensive histopathological
examination at natural death after 78
weeks of exposure (Maltoni et al..
1980).
Biolosical eradient/dose-response:
• A significant trend for increased
incidence of mesothelioma of
the peritoneum was observed in
male rats following 104 weeks
of inhalation exposure.
Oualitv of the database:
• Evidence of mesothelioma of the
peritoneum was observed in a
high-quality study.
Magnitude and precision:
• Pairwise comparisons did not
show a significant increase in the
incidence of mesothelioma of the
peritoneum in male rats in the
104-week inhalation study.
Consistencv:
• There was no significant increase
in incidence of mesothelioma of
the peritoneum in female rats
following 104 weeks of
inhalation exposure.
• The incidence of mesothelioma
of the peritoneum was not
increased in transgenic mice
following 26 weeks of dermal
exposure.
Key findings'.
In a high-quality study, a
trend for increased
incidence of mesothelioma
of the peritoneum was
observed in male mice
following inhalation
exposure; no significant
increase was noted in
pairwise comparison, and no
increase was seen in female
mice.
Overall WOSEjudgement
for mesothelioma of the
peritoneum based on animal
evidence:
• Indeterminate
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and Overall WOSE
Judgement
Endometrial stromal polyps
• A gavage study in female mice
conducted histopathological
examination of the uterus after 78
weeks of exposure (NTP. 1978).
Study quality: High
• Two inhalation studies in female rats
(Nasano et al.. 2006; Cheever et al..
1990) and one inhalation studv in
female mice (Naeano et al.. 2006)
conducted histopathological
examination of the uterus after 104
weeks of exposure. Study quality:
High
• A dermal exposure study in female
transgenic mice susceptible to cancer
conducted histopathological
examination of the uterus after 26
weeks of exposure (Susuro et al..
2017). Studv aualitv: Hish
Studv aualitv ranked as Uninfonnative:
• A gavage study in female rats q
examined the uterus for neoplasms
after 78 weeks of c\do sure (NTP.
1978).
Biolosical eradient/dose-resoonse:
• A significant trend for increased
incidence of endometrial stromal
polyps or sarcomas was
observed in female mice in the
78-week gavage study using
pooled vehicle controls and
the pairwise comparison showed
a significant increase at both
doses.
• A significant trend for increased
incidence of endometrial stromal
polyps was observed in female
mice following 104 weeks of
inhalation exposure.
Oualitv of the database:
• Evidence of endometrial stromal
polyps in mice was observed in
high-quality oral and inhalation
studies.
Biolosical eradient/dose-resoonse:
• The incidence of endometrial
stromal polyps in female mice
was not significantly increased in
a 26-week dermal exposure study
in transgenic mice.
Magnitude and precision:
• Pairwise comparisons using
matched controls did not show a
significant increase in the
incidence of stromal polyps or
sarcomas, and the incidence of
sarcomas (alone) was not
significantly increased in female
mice in the 78-week gavage
study.
• Pairwise comparisons did not
show a significantly increased
incidence in stromal polyps in
female mice in the 104-week
inhalation study.
Biolosical plausibility and human
relevance:
The relevance to humans of
endometrial stromal polyps in mice
is uncertain due to differences in
etiology and hormone sensitivity
(Davis." 2012)
Key findings'.
In high-quality oral and
inhalation studies, the
incidence of endometrial
stromal polyps was
increased in female mice.
The relevance of these
findings to humans is
uncertain due to differences
in etiology and hormone
sensitivity among rodents
and humans. In addition,
there is uncertainty within
the scientific community
whether endometrial stromal
polyps should be considered
benign tumors or
nonneoplastic lesions.
Overall WOSEjudgement
for uterine cancer effects
based on animal evidence:
• Indeterminate
Circulatory System Cancer
• A gavage study in male and female
mice subjected animals to
comprehensive histological
examinations for neoplasms after 78
weeks of exposure (NTP. 1978).
Study quality: High
Biolosical eradient/dose-resoonse:
• Significant pairwise increases in
the incidence of
hemangiosarcoma in the liver
were observed in male mice at
the two highest exposure
Biolosical sradicnt/dosc-rcsDonsc:
• There was not a significant dose-
related trend for increased
hemangiosarcomas of the liver in
male mice following 104 weeks
of inhalation exposure.
Key findings'.
In medium- and high-quality
studies, the incidence of
circulatory system tumors
(e.g., hemangiosarcomas)
was increased in mice
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• A gavage study in female transgenic
mice susceptible to cancer subjected
animals to histological examinations
after 40 weeks of c\do sure (Storcr et
al.. 1995). Studv aualitv: Medium
• Two inhalation studies in male and
female rats (Naeano et al.. 2006;
Cheever et al.. 1990) and one
inhalation study in male and female
mice (Naeano et al.. 2006) subiected
animals to comprehensive histological
examinations for neoplasms after 104
weeks of exposure. Study quality:
High
• A dermal study in transgenic mice
susceptible to cancer subjected
animals to comprehensive histological
examinations for neoplasms after 26
weeks of exposure (Sueuro et al..
2017). Studv aualitv: Hieh
Studv aualitv ranked as Uninfonnative:
• A gavage study in male and female
rats v subjected animals to
comprehensive histological
examinations for neoplasms after 78
weeks of exposure (NTP. 1978).
concentrations following 104
weeks of inhalation exposure.
• A significantly increased
incidence of malignant
lymphoma was observed in
female transgenic mice in a 40-
week gavage study.
• In a study ranked as
Uninfonnative due to high
mortality from pneumonia, there
was a significant trend for
increased hemangiosarcomas in
male and female rats in a
78-week gavage study using
pooled vehicle controls and the
pairwise comparison showed a
significant increase at both
doses.
Oualitv of the database:
• Increased incidences of
circulatory system cancers were
observed in medium- and high-
quality studies.
• The incidence of circulatory
system cancers was not increased
in mice in a 78-week gavage
study. There was a significant
trend for decreased malignant
lymphomas of the hematopoietic
system in females using matched
vehicle controls.
• No hemangiomas or
hemangiosarcomas were observed
in male or female transgenic mice
in a 26-week dermal study.
Magnitude and precision:
• In the 78-week gavage study
ranked Uninfonnative, the trends
for increased hemangiosarcomas
in male and female rats were not
significant using matched
controls.
following inhalation and
dennal exposure.
Overall WOSEjudgement
for circulatory system
cancer effects based on
animal evidence:
• Slight
• A gavage study in male transgenic
mice " susceptible to cancer examined
the incidence of malignant
lymphomas after 40 weeks of
exposure (Storcr et al.. 1995).
• An inhalation study in male and
female rats and mice v examined
animals for neoplasms at natural death
after 78 weeks of exposure (Maltoni
et al.. 1980).
Gastrointestinal tract cancer
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and Overall WOSE
Judgement
• A gavage study in male and female
mice examined the gastrointestinal
tract for neoplasms after 78 weeks of
exposure (NTP. 1978). Studv aualitv:
High
• Two inhalation studies in male and
female rats (Nasano et al.. 2006;
Cheever et al.. 1990) and one
inhalation study in male and female
mice (Naeano et al.. 2006) examined
the gastrointestinal tract for
neoplasms after 104 weeks of
exposure. Study quality: High
• A dermal exposure study in male and
female transgenic mice susceptible to
cancer examined the gastrointestinal
tract for neoplasms after 26 weeks of
exposure (Susuro et al.. 2017). Studv
quality: High
Studv aualitv ranked as Uninfonnative:
• A gavage study in male and female
rats r examined the gastrointestinal
tract for neoplasms after 78 weeks of
exposure (NTP. 1978).
• An inhalation study in male and
female rats and mice y examined the
stomach and intestines for neoplasms
at natural death after 78 weeks of
exposure (Maltoni et al.. 1980).
• A dermal exposure study in female
mice : examined the stomach for
neoplasms after up to 85 weeks of
exposure (Van Duuren et al.. 1979).
Biolosical sradient/dose-resnonse:
Biolosical sradicnt/dosc-rcsDonsc:
Key findings'.
In high-quality and
Uninfonnative gavage
studies, increased incidences
of gastrointestinal tract
tumors were observed in
female mice and male rats.
The effect appears to be
route-specific because
several high-quality studies
did not identify
gastrointestinal tumors
following inhalation or
dennal exposure.
Overall WOSEjudgement
for gastrointestinal cancer
effects based on animal
evidence:
• Indetenninate
• A significant trend for increased
incidence of squamous-cell
carcinomas in the stomach was
observed in female mice in the
78-week gavage study using
pooled vehicle controls.
• In a study ranked as
Uninfonnative owing to high
mortality from pneumonia, a
significant trend for increased
incidence of squamous-cell
carcinomas in the stomach was
observed in male rats in the 78-
week gavage study using pooled
and matched vehicle controls " :
the pairwise comparisons
showed a significant increase at
the highest dose.
• The incidence of gastrointestinal
tumors (forestomach tumors) was
not increased in rats or mice
following 104 weeks of inhalation
exposure.
• The incidence of gastrointestinal
tumors was not increased in two
dermal studies, including a study
in transgenic male and female
mice treated for 26 weeks, and an
85-week study in female mice
ranked as Uninfonnative due to
the use of methods that did not
account for the volatility of 1,2-
dichloroethane.
Masnitude and precision:
• The trend for increased incidence
of squamous-cell carcinomas in
female mice in the 78-week
gavage study was not significant
using matched controls, and the
pairwise comparisons using
pooled and matched controls
were not significant.
Subcutaneous fibromas
• A gavage study in male and female
mice conducted comprehensive
histopathological examination after 78
Biolosical sradicnt/dosc-resDonse:
• A significant trend for increased
incidence subcutaneous fibroma
Masnitude and precision:
• A significant dose-related trend
for increased incidence of
Key findings'.
In a high-quality study, an
increased incidence of
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weeks of exposure (NTP. 1978).
Study quality: High
• Two inhalation studies in male and
female rats (Naeano et al.. 2006;
Cheever et al.. 1990) and one
inhalation study in male and female
mice (Naeano et al.. 2006) conducted
comprehensive histopathological
examination after 104 weeks of
exposure. Study quality: High
• A dermal exposure study in male and
female transgenic mice susceptible to
cancer conducted comprehensive
histopathological examination after 26
weeks of exposure (Sueuro et al..
2017). Studv aualitv: Hieh
Studv aualitv ranked as Uninfonnative:
• A gavage study in male and female
rats aa conducted comprehensive
histopathological examination after 78
weeks of exposure (NTP. 1978).
• An inhalation study in male and
female rats and mice hh conducted
comprehensive histopathological
examination at natural death after 78
weeks of exposure (Maltoni et al..
1980).
was observed in male and
female rats following 104 weeks
of inhalation exposure; pairwise
comparisons showed a
significant increase at the high
dose in female rats only.
• In a study ranked as
Uninfonnative due to high
mortality from pneumonia, a
significant dose-related trend for
increased incidence of
subcutaneous fibromas was
observed in male rats in the 78-
week gavage study using pooled
vehicle controls clcl: pairwise
comparisons showed significant
increases at both doses.
Oualitv of the database:
• Evidence of subcutaneous
fibroma was observed in a high-
quality study.
subcutaneous fibromas was not
observed in male rats in the 78-
week gavage study using
matched vehicle controls.
Consistencv:
• The incidence of subcutaneous
tumors was not increased in
transgenic mice following 26
weeks of dermal exposure.
subcutaneous fibromas in
male and female rats was
seen following inhalation
exposure.
Overall WOSEjudgement
for subcutaneous fibromas
based on animal evidence:
• Indeterminate
Evidence from mechanistic studies
Genotoxicitv:cc
• Two recent authoritative reviews
(ATSDR. 2022; Gwinn et al.. 2011)
were the primary sources used to
provide an overview of the database
of genotoxicity studies available for
11,2 dichloroethane, including
numerous studies of gene mutation in
Salmonella tvphimurium', gene
Consistencv:
• In most of the available studies,
1,2 dichloroethane induced
mutations in S. tvphimurium in
the presence of metabolic
activation. Many of these
studies also reported positive
results without metabolic
activation.
Oualitv of the database:
• Alternative modes of action were
investigated only for mammary
gland tumors and not for other
tumor types induced by 1,2-
dichloroethane.
Key findings:
1,2-dichloroethane has
induced mutations,
clastogenic effects, DNA
damage, and DNA
binding/adduct formation in
vitro and in vivo. The
preponderance of the
substantial database consists
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mutation in fruit flies; gene mutation,
micronucleus formation, DNA
damage, and DNA binding/adduct
formation in mammalian cells/tissue
isolates in vitro; and clastogenicity,
DNA damage, and DNA
binding/adduct formation in mammals
in vivo.
Other mechanisms:
• A 28-day inhalation exposure
experiment in female rats evaluated
cell proliferation in mammary tissue
and serum Drolactin levels (Lcbaron et
al.. 2021).
• 1,2 dichloroethane induced gene
mutations in multiple studies of
fruit flies.
• 1,2 dichloroethane yielded
positive results in gene mutation
assays in Chinese hamster ovary
cells and human lymphoblastoid
cells in vitro.
• 1,2 dichloroethane produced
clastogenic effects including
micronuclei in human
lymphocytes in vitro and
micronuclei, chromosomal
aberrations, and sister chromatid
exchanges in rat and mouse
bone marrow in vivo.
• DNA damage was observed in
human lymphocytes and rat and
mouse hepatocytes exposed to
1,2 dichloroethane in vitro and
in multiple tissues from rats and
mice exposed in vivo.
• DNA binding/adduct formation
after 1,2 dichloroethane
exposure was observed in vitro
and in multiple tissues from rats
and mice in vivo.
Biolosical olausibilitv and human
relevance:
• Several metabolites of
1,2-dichloroethane, particularly
those from the glutathione
conjugation pathway, have been
shown to bind DNA and induce
DNA damage in vivo, and to
induce mutations in S.
typhimurium in vitro.
Oualitv of the database:
of positive results. While
these effects could plausibly
be related to formation of
tumors, a direct connection
between these events and
1,2 dichloroethane induced
carcinogenesis has not been
conclusively demonstrated.
Few mechanistic data
examining alternative modes
of carcinogenic action are
available.
Overall WOSEjudgement
for cancer effects based on
mechanistic evidence:
• Moderate
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The genotoxicity database
includes numerous in vitro and
in vivo studies evaluating a wide
variety of genotoxic endpoints
in multiple test systems.
° The study was ranked as Uninfonnative because SMRs were calculated based on expected deaths from a reference population matched on sex, but not age, and exposure
was assessed based on duration of work in the facility; no information was provided on levels of exposure to 1,2-dichlororethane.
b The study was ranked as Uninfonnative because SMRs were calculated based on expected deaths from a reference population matched on sex and exposure was
assessed based on duration of work in the facility; no information was provided on levels of exposure to 1,2-dichloroethane.
c Pooled controls from several bioassays were used based on data for the same strain, tested by the same laboratory no more than 6 months apart, and diagnosed by the
same pathologist.
d The study in male and female rats was considered Uninfonnative due to high mortality from pneumonia in all groups (including controls).
e Pending evaluation.
' Pooled controls from several bioassays were used based on data for the same strain, tested by the same laboratory no more than 6 months apart, and diagnosed by the
same pathologist
g The study in male and female rats was considered Uninfonnative due to high mortality from pneumonia in all groups (including controls).
h The study in male mice was considered Uninfonnative due to inadequate study duration (52-week cancer bioassay) and a high tumor response rate in the initiation-only
control group (tumor promotion assay).
' This chronic inhalation study was ranked Uninfonnative due to lack of infonnation on the inhalation exposure methodology.
¦' The study in female mice was considered Uninfonnative because methods used to conduct the study did not account for volatility of the test substance.
k The study in male and female rats was considered Uninfonnative due to high mortality from pneumonia in all groups (including controls).
' The study in male mice was considered Uninfonnative due to inadequate study duration (52-week cancer bioassay) or a high tumor response rate in the initiation-only
control group (tumor promotion assay).
in This chronic inhalation study was ranked Uninfonnative due to lack of infonnation on the inhalation exposure methodology.
n The study in female mice was considered Uninfonnative because methods used to conduct the study did not account for volatility of the test substance.
° The study in male and female rats was considered Uninfonnative due to high mortality from pneumonia in all groups (including controls).
p This chronic inhalation study was ranked Uninfonnative due to lack of infonnation on the inhalation exposure methodology.
q The study in female rats was considered Uninfonnative due to high mortality from pneumonia in all groups (including controls).
' Pooled controls from several bioassays were used based on data for the same strain, tested by the same laboratory no more than 6 months apart, and diagnosed by the
same pathologist.
v The study in male and female rats was considered Uninfonnative due to high mortality from pneumonia in all groups (including controls).
' Pooled controls from several bioassays were used based on data for the same strain, tested by the same laboratory no more than 6 months apart, and diagnosed by the
same pathologist.
" The study in male transgenic mice was considered Uninfonnative because the duration of the study was potentially inadequate for tumor development and no tumors
were observed (the same study in female transgenic mice was considered Infonnative because tumors were observed).
v This chronic inhalation study was ranked Uninfonnative due to lack of infonnation on the inhalation exposure methodology.
" Pooled controls from several bioassays were used based on data for the same strain, tested by the same laboratory no more than 6 months apart, and diagnosed by the
same pathologist.
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and Overall WOSE
Judgement
r The study in male and female rats was considered Uninfonnative due to high mortality from pneumonia in all groups (including controls).
-v Pending evaluation.
: The study in female mice was considered Uninfonnative due to the use of methods that did not account for the volatility of 1,2-dichloroethane.
aa The study in male and female rats was considered Uninfonnative due to high mortality from pneumonia in all groups (including controls).
bb This chronic inhalation study was ranked Uninfonnative due to lack of infonnation on the inhalation exposure methodology.
cc Including experiments reviewed by Gwinnet al. (2011). and/or ATSDR (2022) that were not flagged as inconsistent with OECD guidance on genotoxicity testing, as
well as the one study published subsequently (Lone et al.. 2016).
dd Pooled controls from several bioassays were used based on data for the same strain, tested by the same laboratory no more than 6 months apart, and diagnosed by the
same pathologist.
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15672
15673
15674
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M.8 Cancer Dose-Response Assessment (Read-Across from 1,2-
Dichloroethane)
The available cancer dose-response data for 1,1-dichloroethane are not adequate for use in deriving
cancer PODs. The only available human study was confounded by co-exposure to vinyl chloride (Garcia
et al.. 2015). Animal studies included a 78-week study in rats and mice exposed by gavage that was
limited by premature mortality in both species (due to pneumonia in rats, and with no cause of death
identified for mice) (NCI. 1978); a drinking water study in which animals were sacrificed after only 52
weeks (Klaunig et al.. 1986); and a 9-week study of GGT+ foci in partially hepatectomized rats (Milman
et al.. 1988). In the absence of chemical-specific data, as described in Section 5.2.1.3, the cancer risk
assessment for 1,1-dichloroethane uses read-across from data for the identified analog 1,2-
dichloroethane.
1,2-Dichloroethane IUR for Inhalation Exposures
In 1987, the IRIS program derived an IUR of 2.6x 10~5 (per |ig/m3) based on route-to-route extrapolation
from the oral CSF derived at the same time. The inhalation cancer bioassay by Nagano et al. (2006) was
not available at the time of the IRIS assessment.
IUR estimates based on the tumor data sets in Nagano et al. (2006) were calculated using the following
equation: IUR = BMR ^ HEC, where BMR is the benchmark response and HEC is the human equivalent
concentration in |ig/m3,
A BMR of 10 percent extra risk was selected for all datasets. HECs were calculating using the ratio of
blood:gas partition coefficients, as shown in Appendix M.1.2. Gargas and Andersen (1989) estimated
blood:air partition coefficients for 1,2-dichloroethane of 19.5 and 30.4 in humans and rats, respectively.
Because the rat partition coefficient is greater than the human partition coefficient, the default ratio of 1
is used in the calculation in accordance with U.S. EPA (1994) guidance. A blood:air partition coefficient
for mice was not available from the literature reviewed; thus, the default ratio of 1 was used to calculate
HECs for data in mice.
Details of the BMD modeling are provided in a Supplemental File and the BMCL, HEC, and IUR
estimate for each dataset is shown in Table Apx M-45.
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15688
15689
TableApx M-45. IUR Estimates for Tumor Data from Nagano et al. (2006) Study of 1,2-
Species
and Sex
Tumor Type
Selected Model
BMCL10%
(PPm)
BMCL10%
(fig/m3)
HEC
(fig/m3)
IUR
Estimate
(Ug/m3)1
Male
rats
Subcutaneous fibroma
Multistage 1-degree
7
28,332
28,332
3.5E-06
Mammary gland
fibroadenomas
Multistage 1-degree
17
68,807
68,807
1.5E-06
Mammary gland
fibroadenomas and
adenomas combined
Multistage 3-degree
15
60,712
60,712
1.6E-06
Peritoneal mesothelioma
Multistage 3-degree
19
76,901
76,901
1.3E-06
Combined mammary
gland, subcutaneous, and
peritoneum tumors
MS Combo
5
20,237
20,237
4.9E-06
Female
rats
Subcutaneous fibroma
Multistage 1-degree
17
68,807
68,807
1.5E-06
Mammary gland
adenomas
Multistage 1-degree
9
36,427
36,427
2.7E-06
Mammary gland
fibroadenomas
Multistage 1-degree
8
32,380
32,380
3.1E-06
Mammary gland
fibroadenomas and
adenomas combined
Multistage 1-degree
5
20,237
20,237
4.9E-06
Mammary gland
adenocarcinoma
Multistage 3-degree
23
93,091
93,091
1.1E-06
Mammary gland
fibroadenomas
adenomas, and
adenocarcinomas
combined
Multistage 1-degree
4
16,190
16,190
6.2E-06
Combined mammary
gland and subcutaneous
tumors
MS Combo
4
16,190
16,190
6.2E-06
Female
mice
Bronchiolo-alveolar
adenomas
Multistage 3-degree
9
36,427
36,427
2.7E-06
Bronchiolo-alveolar
carcinomas
Multistage 2-degree
14
56,664
56,664
1.8E-06
Bronchiolo-alveolar
adenomas and
carcinomas combined
Multistage 2-degree
7
28,332
28,332
3.5E-06
Mammary gland
adenocarcinomas
Multistage 3-degree
10
40,474
40,474
2.5E-06
Hepatocellular adenomas
Multistage 3-degree
11
44,522
44,522
2.2E-06
Hepatocellular adenomas
and carcinomas
combined
Multistage 2-degree
10
40,474
40,474
2.5E-06
Combined lung,
mammary gland, and
liver tumors3
MS Combo
5
20,237
20,237
4.9E-06
15690
15691 The highest estimated IUR is 6.2x 1CT6 (per (J,g/m3) for combined mammary gland adenomas,
15692 fibroadenomas, and adenocarcinomas and subcutaneous fibromas in female rats in the inhalation study
15693 by Nagano et al. (2006).
15694
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15700
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15704
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15706
15707
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15709
15710
15711
15712
15713
15714
15715
15716
15717
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15720
15721
15722
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CSF for Oral Exposures
The IRIS program derived an oral CSF of 9.1 x 10~2 (per mg/kg-bw/day) for 1,2-dichloroethane in 1987
based on the incidence of hemangiosarcomas in male rats in the chronic bioassay by NTP (1978).
however, this study did not pass EPA systematic review. The oral CSF for male mice based on
hepatocarcinomas of 6,2/ 10 2 (per mg/kg-bw/day) in a reliable study NTP (1978). No oral cancer
bioassays of 1,2-dichloroethane have been published since the IRIS assessment. The IRIS CSF was
derived using time-to-tumor modeling to account for intercurrent mortality of the rats in the NTP (1978)
study. No updates to the time-to-tumor modeling approach have been made since the 1987 assessment.
Hemangiosarcomas in male rats were determined to be the most sensitive species, strain, and site,
however this study was deemed unacceptable by EPA systematic review. Although CSF does not
account for other tumor types induced by 1,2-dichloroethane in the male rat, there is currently no time-
to-tumor modeling approach available that accounts for multiple tumor types. Therefore, the oral CSF
for 1,2-dichloroethane from the reliable NTP mouse cancer study NTP (1978) was selected for use in
assessment of cancer risks associated with exposure to 1,1-dichloroethane. This mouse CSF was used to
calculate a drinking water unit risk of 1.8 E-6 per ug/L using a drinking water intake of 2 L/day and
body weight of 70 kg.
CSF for Dermal Exposures
There are no reliable dermal cancer studies of 1,2-dichloroethane; thus, the CSF for 1,2-dichloroethane
was obtained from route-to-route extrapolation using oral data. There are uncertainties associated with
extrapolation from both oral and inhalation. Use of an oral POD for dermal extrapolation may not be
preferred for chemicals known to undergo extensive liver metabolism because the "first-pass effect" that
directs intestinally absorbed chemicals directly to the liver applies only to oral ingestion. In contrast, the
accuracy of extrapolation of inhalation toxicity data for dermal PODs is dependent on assumptions about
inhalation exposure factors such as breathing rate and any associated dosimetric adjustments. Whole-body
inhalation studies may also already be incorporating some level of dermal absorption. Given these competing
uncertainties, in the absence of data to support selection of either the oral CSF or inhalation IUR, the method
resulting in the most protective dermal CSF was selected. The value of the oral CSF is 6.2x 10~2 (per
mg/kg-bw/day). For comparison, a CSF of 3.3xl0~2 (per mg/kg-bw/day) was obtained using route-to-
route extrapolation from the IUR of 6.Ox 10~6 per [jg/m3 (6.Ox 10 3 per mg/m3) per Equation_Apx M-15
as follows:
EquationApx M-15.
Dermal CSF (per mg/kg-bw/day) = 6.Ox 10-03 (per mg/m3) * (80 kg/14.7 m3/day)
= 3.3x 10-02 (per mg/kg-bw/day)
The more protective value of 6.2x 10~2 per mg/kg-bw/day based on the oral CSF was selected for the
dermal CSF.
M.8.1 Summary of Continuous and Worker PODs
The continuous IUR was adjusted for occupational scenarios using equations provided in Appendix M.3
Table Apx M-46 provides a summary of the cancer PODs for both continuous and occupational
exposure scenarios.
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15739 TableApx M-46. Summary of Cancer PODs for 1,1-Dichloroethane (Read-Across from 1,2-
15740 Dichloroethane)
Route
Continuous POD
Worker POD
Reference
Inhalation
6.0E-06 (per (ig/m3)
2.1E-06 (per (ig/m3)
Naaano et al. (2006)
Oral
6.2E-02 (per mg/kg-bw/day)
Same as continuous
NTP (1978)
Dermal
6.2E-02 (per mg/kg-bw/day)
Same as continuous
Route-to-route extrapolation from oral
15741
15742
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15771
15772
15773
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Appendix N DRAFT OCCUPATIONAL EXPOSURE VALUE
DERIVATION
EPA has calculated a draft 8-hour existing chemical occupational exposure value to summarize the
occupational exposure scenario and sensitive health endpoints into a single value. This calculated draft
value may be used to support risk management efforts for 1,1-dichloroethane under TSCA section 6(a),
15 U.S.C. §2605. EPA calculated the draft value rounded to 0.044 ppm (0.178 mg/m3) for inhalation
exposures to 1,1-dichloroethane as an 8-hour time-weighted average (TWA) and for consideration in
workplace settings (see Section N.l below) based on the lifetime cancer inhalation unit risk (IUR) for a
combined cancer model.
TSCA requires risk evaluations to be conducted without consideration of cost and other non-risk factors,
and thus this draft occupational exposure value represents a risk-only number. If risk management for
1,1-dichloroethane follows the final risk evaluation, EPA may consider cost and other non-risk factors,
such as technological feasibility, the availability of alternatives, and the potential for critical or essential
uses. Any existing chemical exposure limit (ECEL) used for occupational safety risk management
purposes could differ from the draft occupational exposure value presented in this appendix based on
additional consideration of exposures and non-risk factors consistent with TSCA section 6(c).
This calculated draft value for 1,1-dichloroethane represents the exposure concentration below which
workers and occupational non-users are not expected to exhibit any appreciable risk of adverse
toxicological outcomes, accounting for potentially exposed and susceptible populations (PESS). It is
derived based on the most sensitive human health effect (i.e., cancer) relative to benchmarks and
standard occupational scenario assumptions of 8 hours per day, 5 days per week exposures for a total of
250 days exposure per year, and a 40-year working life.
All hazard values used in these calculations are based on non-cancer HECs and associated uncertainty
factor derivations and the IUR from this draft Risk Evaluation for 1,1-Dichloroethane (Section 5.2.6.3).
EPA expects that at the lifetime cancer occupational exposure value of 0.044 ppm (0.178 mg/m3), a
worker or an occupational non-user also would be protected against degeneration with necrosis of the
olfactory mucosa and deceases in sperm concentration resulting from acute and intermediate
occupational exposures. This calculated lifetime cancer occupational exposure value would protect
against excess risk of cancer above the 1 x 10~4 benchmark value resulting from lifetime exposure if
ambient exposures are kept below this draft occupational exposure value. EPA has also separately
calculated a short-term occupational exposure value or ceiling limit for 1,1-dichloroethane.
Of the identified occupational monitoring data for 1,1-dichloroethane, there have been measured
workplace air concentrations below the calculated draft exposure value. A summary table of available
monitoring methods from the Occupational Safety and Health Administration (OSHA), the National
Institute for Occupational Safety and Health (NIOSH), and EPA is included in Section N.2. The table
covers validated methods from governmental agencies and is not intended to be a comprehensive list of
available air monitoring methods for 1,1-dichloroethane. The calculated draft exposure value is above
the limit of detection (LOD) and limit of quantification (LOQ) using at least one of the monitoring
methods identified.
The Occupational Safety and Health Administration (OSHA) has set a permissible exposure limit (PEL)
as an 8-hour TWA for 1,1-dichloroetane of 100 ppm. However, as noted on OSHA's website, "OSHA
recognizes that many of its permissible exposure limits (PELs) are outdated and inadequate for ensuring
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15799
15800
15801
15802
15803
15804
15805
15806
15807
15808
15809
15810
15811
15812
15813
15814
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protection of worker health. Most of OSHA's PELs were issued shortly after adoption of the
Occupational Safety and Health (OSH) Act in 1970 and have not been updated since that time." In
addition, OSHA's PEL must undergo both risk assessment and feasibility assessment analyses before
selecting a level that will substantially reduce risk under the OSH Act. EPA's calculated draft calculated
exposure value is a lower value and is based on newer information and analysis from this draft risk
evaluation.
Other governmental agencies and independent groups have also set recommended exposure limits
established for 1,1-dichloroethane. The American Conference of Governmental Industrial Hygienists
(ACGIH) has set a Threshold Limit Value (TLV) at 100 ppm TWA and 100 ppm STEL. This chemical
also has a NIOSH Recommended Exposure Limit (REL) of 100 ppm TWA (400 mg/m3).
NIOSH considers the chloroethanes: ethylene dichloride (1,2-dichloroethane); hexachloroethane;
1,1,2,2-tetrachloroethane; and 1,1,2-trichloroethane; to be potential occupational carcinogens.
Additionally, NIOSH recommends that the other five chloroethane compounds—1,1-dichloroethane,
ethyl chloride, methyl chloroform, pentachloroethane, and 1,1,1,2-tetrachloroethane—be treated in the
workplace with caution because of their structural similarity to the four chloroethanes shown to be
carcinogenic in animals.
N.l Draft Occupational Exposure Value Calculations
This section presents the calculations used to estimate the draft occupational exposure values using
inputs derived in this draft risk evaluation. Multiple values are presented below for hazard endpoints
based on different exposure durations. For 1,1-dichloroethane, the most sensitive occupational exposure
value is based on cancer and the resulting 8-hour TWA is rounded to 0.044 ppm. The human health
hazard values (HECs, IUR) used in the equations are derived in the risk evaluation for 1,1-
dichloroethane.
Draft Lifetime Cancer Occupational Exposure Value
The EVcancer is the concentration at which the extra cancer risk is equivalent to the benchmark cancer
risk of 1 x 10 4:
BeflchmCLTk(2ajiCer ATjur Unresting
cancer ~ lUR X ED XEFX WY IRworkers
h 365 d
1X10~4 24dx^Tx78y 0.6125 m3 /hr
— x± x '
9.5x10~3 per ppm 2S0rf .Q 1.25 m3/hr
d y y
= 0.044 ppm = 0.179 mg/m3
, . 3. EVppmxMW 0.044 ppm x 98.96-£-
EVranrpr (ma m) = = ? = 0.179 ma m
cancer v m J MoiarVoiume 24.45 —
mol
Where:
Molar Volume = 24.45 L/mol, the volume of a mole of gas at 1 atm and 25 °C
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15839
15840
15841
15842
15843
15844
15845
15846
15847
15848
15849
15850
15851
15852
15853
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MW = Molecular weight of 1,1-dichloroethane (98.96 g/mole)
Draft Chronic Non-cancer Occupational Exposure Value
The draft chronic occupational exposure value (EVchronic) was calculated as the concentration at which
the chronic margin of exposure (MOE) would equal the benchmark MOE for 8-hour chronic
occupational exposures with the following equation:
_ HECchroniCi ^ -^TheC ehronic: w ^resting
^ ''chronic — ~ ' ' ...... X „ „ 777: 77777 X
Benchmark MOEchronic ED * EF * WY IRWorkers
24 h 365 d An n^rm3
99 ^ ^ ^ 0.6125 .
zzppm d y J hr
x ¦
, X x40yxl.25-r—
d y J hr
300 8h 250d _ _ _ m3
= 0.157 ppm
EV,
chronic
/m|\ = EVppmxMW = 0.157 ppm x 98.96 ^ = q ^ mg/m3
Vm3/ Molar Volume 24 45
mo l
Draft Intermediate Non-cancer Occupational Exposure Value
The draft intermediate occupational exposure value (EVintermediate) was calculated as the concentration at
which the intermediate MOE would equal the benchmark MOE for intermediate occupational exposure
using the following equation:
gy. HECjnterme(jjate ^ AThec intermediate ^ ^resting
Benchmark MOE intermediate EDXEF IRworkers
22 ppm 0.6125^
= x -4; x -¥¦ = 1.47 ppm
30 2^X22 d 1.2-ai
d hr
FV. /mg\ _ EV ppm x MW _ 1.47 ppm x 98.96 ^ _
^intermediate ym3) ~ Moiar volume ~ 2445^- VSmg/m
mol
Draft Acute Non-cancer Occupational Exposure Value
The draft acute occupational exposure limit (EVaCute) was calculated as the concentration at which the
acute MOE would equal the benchmark MOE for acute occupational exposures using the following
equation:
HECacute wATHECacute Unresting
EVapntp — X X y r-.
Benchmark MOEamtr ED IR,
acute c u 1 ^workers
24/i c m3
10.14 ppm ~T~ 0.6125 -j—
x -St- * ¥- = °-497 PPm = 2.011 mg/m
30 Oh m3 5/
d i"Zb hr
3
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15866
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15868
15869
15870
15871
15872
15873
15874
15875
15876
15877
15878
15879
15880
15881
15882
15883
15884
15885
15886
15887
15888
15889
15890
15891
15892
15893
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9
EV;
acute
EV ppm x MW 0-497 ppm x 98.96
~) = = =
vm
Molar Volume
24.45
2.011 mg/rrr
Where:
AThEC chronic
AT HECintermediate
ATHECacute
ATlUR
Benchmark MOEchronic =
Benchmark MOEintermediate =
Benchmark MOEaCute =
Benchmarkcancer =
E V acute
IV intermediate —
E V chronic —
E V cancer —
ED
EF
HECacute, intermediate, or chronic —
IUR
IR
WY
mol
Averaging time for the POD/HEC used for evaluating non-cancer,
chronic occupational risk, based on study conditions and/or HEC
adjustments (24 hours/day for 365 days/yr) and assuming the number
of years matches the high-end working years (WY, 40 yrs) for a
worker
Averaging time for the POD/HEC used for evaluating non-cancer,
intermediate occupational risk, based on study conditions and/or any
HEC adjustments (24 hours/day for 30 days)
Averaging time for the POD/HEC used for evaluating non-cancer,
acute occupational risk, based on study conditions and/or any HEC
adjustments (24 hours/day)
Averaging time for the cancer IUR, based on study conditions and any
adjustments (24 hours/day for 365 days/year) and averaged over a
lifetime (78 years)
Chronic non-cancer benchmark margin of exposure, based on the total
uncertainty factor of 300 (Table 5-51)
Intermediate non-cancer benchmark margin of exposure, based on the
total uncertainty factor of 30 (Table 5-50)
Acute non-cancer benchmark margin of exposure, based on the total
uncertainty factor of 30 (Table 5-49)
Benchmark for excess lifetime cancer risk
Draft occupational exposure value based on degeneration with necrosis
of the olfactory mucosa
Draft occupational exposure value based on decrease in sperm
concentration
Draft occupational exposure value based on decrease in sperm
concentration
Draft occupational exposure value based on excess cancer risk
Exposure duration (8 hours/day)
Exposure frequency (250 days/year)
Human equivalent concentration for acute, intermediate, or chronic
occupational exposure scenarios (Table 5-49, Table 5-50, and Table
5-51)
Inhalation unit risk (per ppm) (Table 5-52)
Inhalation rate (default is 1.25 m3/hr for workers and 0.6125 m3/hr for
the general population at rest)
Working years per lifetime at the 95th percentile (40 years)
Unit conversion:
1 ppm = 4.05 mg/m3 (based on the molecular weight of 98.96 g/mol for 1,1-dichlorethane)
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N.2 Summary of Air Sampling Analytical Methods Identified
EPA conducted a search to identify relevant NIOSH, OSHA, and EPA analytical methods used to
monitor for the presence of 1,1-dichloroethane in air (see TableApx N-l). This table covers validated
methods from governmental agencies and is not intended to be a comprehensive list of available air
monitoring methods for 1,1-dichloroethane. The sources used for the search included the following:
1. NIOSH Manual of Analytical Methods (NMAM); 5th Edition
2. NIOSH NMAM 4th Edition
3. OSHA Index of Sampling and Analytical Methods
4. EPA Environmental Test Method and Monitoring Information
Table Apx N-l. Limit of LOD and LOQ Summary for Air Sampling Analytical Methods
Identified
Air Sampling
Analytical Methods
Year
Published
LODfl
LOQ
Notes
Source
NIOSH Method 1003
2003
2.0 jig/
sample
5.1 jig/
sample
The working range is 4
to 250 ppm at 15 L.
NIOSH NMAM. 4th
Edition
OSHA Method 07fe
1979 (last
update:
2000)
N/A
N/A
The estimated detection
limit is based on the
lowest mass per sample
injected as a standard.
OSHA Index of Sampling
and Analytical Methods
ppm = parts per million; ppb = parts per billion; ppt = parts per trillion
" These sources cover a range of LOD including both below and above the ECEL value.
h This method has been withdrawn and is provided for historical record only.
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Appendix O 1,1-DICHLOROETHANE CONDITIONS OF USE
O.l Additions and Name Changes to Conditions of Use Based on Updated
2020 CDR Reported Data and Stakeholder Engagement
After the final scope (U.S. EPA. 2020b). EPA received updated submissions under the 2020 CDR
reported data. In addition to new submissions received under the 2020 CDR, the reporting name codes
did not change for the 2020 CDR reporting cycle.
Q.2 Consolidation and Other Changes to Conditions of Use Table
When developing this draft risk evaluation, EPA concluded that an additional subcategory of the
conditions of use listed in the final scope (U.S. EPA. 2020b) was needed. EPA added the COU
processing - repackaging to account for the repackaging for distribution of 1,1-dichloroethane for use as
a laboratory chemical. Table Apx O-l summarizes the change to the COU subcategory descriptions.
Table Apx O-l. Subcate
gory Editing from the Final Scope Document to t
ie Draft Risk Evaluation
Life Cycle Stage and
Category
Original Subcategory in
the Final Scope
Document
Occurred Change
Revised Subcategory in
the 2024 Draft Risk
Evaluation
Processing
N/A
Added "Processing:
Repackaging"
subcategory
Processing: Repackaging
Q.3 Descriptions of 1,1-Dichloroethane Conditions of Use
0.3.1 Manufacturing
Manufacturing means to manufacture or produce 1,1-dichloroethane within the Unites States. For
purposes of the 1,1-dichloroethane risk evaluation, this included the production of 1,1-dichloroethane.
This risk evaluation does not include the manufacture of 1,1-dichloroethane as a byproduct during the
manufacture of 1,2-dichloroethane (that exposure will be assessed in the risk evaluation for 1,2-
dichloroethane).
0.3.1.1 Domestic Manufacturing
1,1-Dichloroethane can be manufactured by chlorination of ethane or chloroethane, via thermal
chlorination, photochlorination, or oxychlorination. Alternatively, 1,1-dichloroethane can be produced
by adding hydrogen chloride to acetylene.
0.3.2 Processing - As a Reactant
Processing as a reactant or intermediate is the use of 1,1-dichloroethane as a feedstock in the production
of another chemical via a chemical reaction in which 1,1-dichloroethane is consumed to form the
product.
0.3.2.1 Intermediate in All Other Basic Organic Chemical Manufacture
Processing as an intermediate in all other basic organic chemical manufacture includes the use of 1,1-
dichloroethane as an intermediate for the manufacture of chlorinated solvents, mainly 1,1,1-
tri chloroethane, 1,2-dichloroethane, and vinyl chloride.
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0.3.2.2 Intermediate in All Other Chemical Product and Preparation Manufacturing
Processing as an intermediate in all other chemical product and preparation manufacturing includes the
use of 1,1-dichloroethane as chlorinated solvent intermediate.
0.3.2.3 Repackaging
Repackaging refers to preparation of 1,1-dichloroethane for distribution into commerce in a different
form, state, or quantity than originally received or stored. Such activities include transferring 1,1-
dicloroethane from a bulk storage container into smaller containers.
Q.3.2.4 Recycling
This COU refers to the process of treating generated waste streams (i.e., which would otherwise be
disposed of as waste) that are collected, either on-site or transported to a third-party site, for commercial
purpose.
0.3.3 Distribution in Commerce
For purposes of assessment in this risk evaluation, distribution in commerce consists of the
transportation associated with the moving of 1,1-dichloroethane. 1,1-Dichloroethane is expected to be
distributed in commerce for processing as a reactive intermediate and commercial laboratory use. EPA
expects 1,1-dichloroethane to be transported from manufacturing sites to downstream processing and
repackaging sites, or for final disposal of 1,1-dichloroethane. More broadly under TSCA, "distribution
in commerce" and "distribute in commerce" are defined under TSCA section 3(5).
0.3.4 Commercial Use in Laboratory Chemicals
This COU refers to the use of 1,1-dichloroethane as laboratory chemical, such as a chemical standard or
reference material during analysis. A commenter (EPA-HQ-OPPT-2018-0426-0026) provided
descriptions of their use of 1,1- dichloroethane in analytical standard, research, equipment calibration
and sample preparation applications, including reference sample for analysis of terrestrial and
extraterrestrial material samples.
Q.3.5 Disposal
Each of the conditions of use of 1,1-dichloroethane may generate waste streams of the chemical that are
collected and transported to third-party sites for disposal, treatment, or recycling. Wastes of 1,1-
dichloroethane that are generated during a condition of use and sent to a third-party site for treatment
and disposal include wastewater and solid waste. 1,1-Dichloroethane may be contained in wastewater
discharged to POTW or other, non-public treatment works for treatment. Industrial wastewater
containing 1,1-dichloroethane discharged to a POTW may be subject to EPA or authorized NPDES state
pretreatment programs. Solid wastes are defined under RCRA as any material that is discarded by being:
abandoned; inherently waste-like; a discarded military munition; or recycled in certain ways (certain
instances of the generation and legitimate reclamation of secondary materials are exempted as solid
wastes under RCRA). The presence of 1,1-dichloroethane in the reuse of produced water is included in
the disposal condition of use.
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