TOXICOLOGICAL PROFILE FOR
 

1,1-DICHLOROETHANE
 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
 

Public Health Service
 

Agency for Toxic Substances and Disease Registry
 

August 2015 
 

 

 

1,1-DICHLOROETHANE ii 

DISCLAIMER 

Use of trade names is for identification only and does not imply endorsement by the Agency for Toxic 

Substances and Disease Registry, the Public Health Service, or the U.S. Department of Health and Human 

Services. 
 

 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

1,1-DICHLOROETHANE iii 

UPDATE STATEMENT
 

A Toxicological Profile for 1,1-Dichloroethane, Draft for Public Comment was released in April 2013. 

This edition supersedes any previously released draft or final profile. 

Toxicological profiles are revised and republished as necessary. For information regarding the update 

status of previously released profiles, contact ATSDR at: 

Agency for Toxic Substances and Disease Registry
 

Division of Toxicology and Human Health Sciences
 

Environmental Toxicology Branch
 

1600 Clifton Road NE
 

Mailstop F-57
 

Atlanta, Georgia 30329-4027
 
1,1-DICHLOROETHANE iv 

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1,1-DICHLOROETHANE v 

FOREWORD 

This toxicological profile is prepared in accordance with guidelines* developed by the Agency for Toxic 

Substances and Disease Registry (ATSDR) and the Environmental Protection Agency (EPA). The 

original guidelines were published in the Federal Register on April 17, 1987. Each profile will be revised 

and republished as necessary. 

The ATSDR toxicological profile succinctly characterizes the toxicologic and adverse health effects 

information for these toxic substances described therein. Each peer-reviewed profile identifies and 

reviews the key literature that describes a substance's toxicologic properties. Other pertinent literature is 

also presented, but is described in less detail than the key studies. The profile is not intended to be an 

exhaustive document; however, more comprehensive sources of specialty information are referenced. 

The focus of the profiles is on health and toxicologic information; therefore, each toxicological profile 

begins with a public health statement that describes, in nontechnical language, a substance's relevant 

toxicological properties. Following the public health statement is information concerning levels of 

significant human exposure and, where known, significant health effects. The adequacy of information to 

determine a substance's health effects is described in a health effects summary. Data needs that are of 

significance to protection of public health are identified by ATSDR. 

Each profile includes the following: 

(A) The examination, summary, and interpretation of available toxicologic information and 

epidemiologic evaluations on a toxic substance to ascertain the levels of significant human 

exposure for the substance and the associated acute, subacute, and chronic health effects; 

(B) A determination of whether adequate information on the health effects of each substance 

is available or in the process of development to determine levels of exposure that present a 

significant risk to human health of acute, subacute, and chronic health effects; and 

(C) Where appropriate, identification of toxicologic testing needed to identify the types or 

levels of exposure that may present significant risk of adverse health effects in humans. 

The principal audiences for the toxicological profiles are health professionals at the Federal, State, and 

local levels; interested private sector organizations and groups; and members of the public. 

This profile reflects ATSDR’s assessment of all relevant toxicologic testing and information that has been 

peer-reviewed. Staffs of the Centers for Disease Control and Prevention and other Federal scientists have 

also reviewed the profile. In addition, this profile has been peer-reviewed by a nongovernmental panel 

and was made available for public review. Final responsibility for the contents and views expressed in 

this toxicological profile resides with ATSDR. 

Patrick N. Breysse, Ph.D., CIH
 

Director, National Center for Environmental Health and
 

Agency for Toxic Substances and Disease Registry
 

Centers for Disease Control and Prevention
 
 

 

 

 

1,1-DICHLOROETHANE vi 

*Legislative Background 

The toxicological profiles are developed under the Comprehensive Environmental Response, 

Compensation, and Liability Act of 1980, as amended (CERCLA or Superfund). CERCLA section 

104(i)(1) directs the Administrator of ATSDR to “...effectuate and implement the health related 

authorities” of the statute. This includes the preparation of toxicological profiles for hazardous 

substances most commonly found at facilities on the CERCLA National Priorities List and that pose the 

most significant potential threat to human health, as determined by ATSDR and the EPA. Section 

104(i)(3) of CERCLA, as amended, directs the Administrator of ATSDR to prepare a toxicological profile 

for each substance on the list. In addition, ATSDR has the authority to prepare toxicological profiles for 

substances not found at sites on the National Priorities List, in an effort to “...establish and maintain 

inventory of literature, research, and studies on the health effects of toxic substances” under CERCLA 

Section 104(i)(1)(B), to respond to requests for consultation under section 104(i)(4), and as otherwise 

necessary to support the site-specific response actions conducted by ATSDR. 
 

 

 

 

 

 

 

 

 

 

 

 


 


 


 


 


 


 


 

1,1-DICHLOROETHANE vii 

QUICK REFERENCE FOR HEALTH CARE PROVIDERS 

Toxicological Profiles are a unique compilation of toxicological information on a given hazardous 

substance. Each profile reflects a comprehensive and extensive evaluation, summary, and interpretation 

of available toxicologic and epidemiologic information on a substance. Health care providers treating 

patients potentially exposed to hazardous substances will find the following information helpful for fast 

answers to often-asked questions. 

Primary Chapters/Sections of Interest 

Chapter 1: Public Health Statement: The Public Health Statement can be a useful tool for educating 

patients about possible exposure to a hazardous substance. It explains a substance’s relevant 

toxicologic properties in a nontechnical, question-and-answer format, and it includes a review of 

the general health effects observed following exposure. 

Chapter 2: Relevance to Public Health: The Relevance to Public Health Section evaluates, interprets, 

and assesses the significance of toxicity data to human health. 

Chapter 3: Health Effects: Specific health effects of a given hazardous compound are reported by type 

of health effect (death, systemic, immunologic, reproductive), by route of exposure, and by length 

of exposure (acute, intermediate, and chronic). In addition, both human and animal studies are 

reported in this section. 

NOTE: Not all health effects reported in this section are necessarily observed in the clinical 

setting. Please refer to the Public Health Statement to identify general health effects observed 

following exposure. 

Pediatrics: Four new sections have been added to each Toxicological Profile to address child health 

issues: 

Chapter 1 How Can (Chemical X) Affect Children?
 

Chapter 1 How Can Families Reduce the Risk of Exposure to (Chemical X)?
 

Section 3.7 Children’s Susceptibility
 

Section 6.6 Exposures of Children
 

Other Sections of Interest: 

Section 3.8 Biomarkers of Exposure and Effect 

Section 3.11 Methods for Reducing Toxic Effects 

ATSDR Information Center 

Phone: 1-800-CDC-INFO (800-232-4636) or 1-888-232-6348 (TTY) 

Internet: http://www.atsdr.cdc.gov 

The following additional material is available online at www.atsdr.cdc.gov: 

Case Studies in Environmental Medicine—Case Studies are self-instructional publications designed to 

increase primary care provider’s knowledge of a hazardous substance in the environment and to 

aid in the evaluation of potentially exposed patients. 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE viii 

Managing Hazardous Materials Incidents is a three-volume set of recommendations for on-scene 

(prehospital) and hospital medical management of patients exposed during a hazardous materials 

incident. Volumes I and II are planning guides to assist first responders and hospital emergency 

department personnel in planning for incidents that involve hazardous materials. Volume III— 

Medical Management Guidelines for Acute Chemical Exposures—is a guide for health care 

professionals treating patients exposed to hazardous materials. 

Fact Sheets (ToxFAQsTM) provide answers to frequently asked questions about toxic substances. 

Other Agencies and Organizations 

The National Center for Environmental Health (NCEH) focuses on preventing or controlling disease, 

injury, and disability related to the interactions between people and their environment outside the 

workplace. Contact: NCEH, Mailstop F-29, 4770 Buford Highway, NE, Atlanta, 

GA 30341-3724 • Phone: 770-488-7000 • FAX: 770-488-7015. 

The National Institute for Occupational Safety and Health (NIOSH) conducts research on occupational 

diseases and injuries, responds to requests for assistance by investigating problems of health and 

safety in the workplace, recommends standards to the Occupational Safety and Health 

Administration (OSHA) and the Mine Safety and Health Administration (MSHA), and trains 

professionals in occupational safety and health. Contact: NIOSH, 395 E Street, S.W., Suite 9200, 

Patriots Plaza Building, Washington, DC 20201 • Phone: (202) 245-0625 or 1-800-CDC-INFO 

(800-232-4636). 

The National Institute of Environmental Health Sciences (NIEHS) is the principal federal agency for 

biomedical research on the effects of chemical, physical, and biologic environmental agents on 

human health and well-being. Contact: NIEHS, PO Box 12233, 104 T.W. Alexander Drive, 

Research Triangle Park, NC 27709 • Phone: 919-541-3212. 

Clinical Resources 

The Association of Occupational and Environmental Clinics (AOEC) has developed a network of clinics 

in the United States to provide expertise in occupational and environmental issues. Contact: 

AOEC, 1010 Vermont Avenue, NW, #513, Washington, DC 20005 • Phone: 202-347-4976 

• FAX: 202-347-4950 • e-mail: AOEC@AOEC.ORG • Web Page: http://www.aoec.org/. 

The American College of Occupational and Environmental Medicine (ACOEM) is an association of 

physicians and other health care providers specializing in the field of occupational and 

environmental medicine. Contact: ACOEM, 25 Northwest Point Boulevard, Suite 700, Elk 

Grove Village, IL 60007-1030 • Phone: 847-818-1800 • FAX: 847-818-9266. 
 

 

 

 

 

 


 


 


 


 


 


 


 


 

	 

	 

	 

	 


 


 


 


 


 


 


 


 

	 

	 

	 

	 

1,1-DICHLOROETHANE ix 

CONTRIBUTORS 

CHEMICAL MANAGER(S)/AUTHOR(S): 

Malcolm Williams, DVM, Ph.D. 

Annette Ashizawa, Ph.D. 

G. Daniel Todd, Ph.D.
 

Eugene Demchuk, Ph.D.
 

ATSDR, Division of Toxicology and Human Health Sciences, Atlanta, GA
 

Lisa Ingerman, Ph.D., DABT
 

Christina Coley, B.S.
 

Mary Kawa, M.A.
 

Mario Citra, Ph.D.
 

SRC, Inc., North Syracuse, NY
 

THE PROFILE HAS UNDERGONE THE FOLLOWING ATSDR INTERNAL REVIEWS: 

1.	 Health Effects Review. The Health Effects Review Committee examines the health effects 

chapter of each profile for consistency and accuracy in interpreting health effects and classifying 

end points. 

2.	 Minimal Risk Level Review. The Minimal Risk Level Workgroup considers issues relevant to 

substance-specific Minimal Risk Levels (MRLs), reviews the health effects database of each 

profile, and makes recommendations for derivation of MRLs. 

3.	 Data Needs Review. The Environmental Toxicology Branch reviews data needs sections to 

assure consistency across profiles and adherence to instructions in the Guidance. 

4.	 Green Border Review. Green Border review assures the consistency with ATSDR policy. 
1,1-DICHLOROETHANE x 

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1,1-DICHLOROETHANE xi 

PEER REVIEW
 

A peer review panel was assembled for 1,1-dichloroethane. The panel consisted of the following 

members: 

1.	 Gary Stoner, Ph.D., Department of Medicine, Division of Hematology and Oncology, Medical 

College of Wisconsin, Milwaukee, Wisconsin; 

2.	 G.A. Shakeel Ansari, Ph.D., Department of Human Biological Chemistry & Genetics and 

Pathology, University of Texas Medical Branch, Galveston Texas; 

3.	 Hermann Bolt, Ph.D., Institut für Arbeitsphysiologie an der Universität Dortmund (IfADo), 

Leibniz Research Centre for Working Environment and Human Factors, Dortmund, Germany. 

These experts collectively have knowledge of 1,1-dichloroethane’s physical and chemical properties, 

toxicokinetics, key health end points, mechanisms of action, human and animal exposure, and 

quantification of risk to humans. All reviewers were selected in conformity with the conditions for peer 

review specified in Section 104(I)(13) of the Comprehensive Environmental Response, Compensation, 

and Liability Act, as amended. 

Scientists from the Agency for Toxic Substances and Disease Registry (ATSDR) have reviewed the peer 

reviewers' comments and determined which comments will be included in the profile. A listing of the 

peer reviewers' comments not incorporated in the profile, with a brief explanation of the rationale for their 

exclusion, exists as part of the administrative record for this compound. 

The citation of the peer review panel should not be understood to imply its approval of the profile's final 

content. The responsibility for the content of this profile lies with the ATSDR. 
1,1-DICHLOROETHANE xii 

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1,1-DICHLOROETHANE xiii 

CONTENTS
 

DISCLAIMER ..............................................................................................................................................ii
 

UPDATE STATEMENT .............................................................................................................................iii
 
 

FOREWORD ................................................................................................................................................v
 

QUICK REFERENCE FOR HEALTH CARE PROVIDERS....................................................................vii
 
 

CONTRIBUTORS.......................................................................................................................................ix
 

PEER REVIEW ...........................................................................................................................................xi
 

CONTENTS...............................................................................................................................................xiii
 

LIST OF FIGURES ..................................................................................................................................xvii
 

LIST OF TABLES.....................................................................................................................................xix
 

1. PUBLIC HEALTH STATEMENT FOR 1,1-DICHLOROETHANE.....................................................1
 

2. RELEVANCE TO PUBLIC HEALTH ...................................................................................................7
 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO 1,1-DICHLOROETHANE
 
 

IN THE UNITED STATES ...........................................................................................................7
 

2.2 SUMMARY OF HEALTH EFFECTS...........................................................................................7
 

2.3 MINIMAL RISK LEVELS (MRLs) ............................................................................................11
 

3. HEALTH EFFECTS..............................................................................................................................13
 

3.1 INTRODUCTION........................................................................................................................13
 

3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE .....................................13
 

3.2.1 Inhalation Exposure ..............................................................................................................14
 

3.2.1.1 Death..............................................................................................................................14
 

3.2.1.2 Systemic Effects.............................................................................................................15
 

3.2.1.3 Immunological and Lymphoreticular Effects................................................................20
 

3.2.1.4 Neurological Effects ......................................................................................................20
 

3.2.1.5 Reproductive Effects......................................................................................................20
 

3.2.1.6 Developmental Effects...................................................................................................20
 

3.2.1.7 Cancer............................................................................................................................21
 

3.2.2 Oral Exposure........................................................................................................................21
 

3.2.2.1 Death..............................................................................................................................21
 

3.2.2.2 Systemic Effects.............................................................................................................26
 

3.2.2.3 Immunological and Lymphoreticular Effects................................................................27
 

3.2.2.4 Neurological Effects ......................................................................................................27
 

3.2.2.5 Reproductive Effects......................................................................................................27
 

3.2.2.6 Developmental Effects...................................................................................................27
 

3.2.2.7 Cancer............................................................................................................................28
 

3.2.3 Dermal Exposure...................................................................................................................29
 

3.2.3.1 Death..............................................................................................................................29
 

3.2.3.2 Systemic Effects.............................................................................................................29
 

3.2.3.3 Immunological and Lymphoreticular Effects................................................................29
 

3.2.3.4 Neurological Effects ......................................................................................................29
 

3.2.3.5 Reproductive Effects......................................................................................................29
 

3.2.3.6 Developmental Effects...................................................................................................29
 

3.2.3.7 Cancer............................................................................................................................29
 

3.3 GENOTOXICITY........................................................................................................................31
 

3.4 TOXICOKINETICS.....................................................................................................................32
 

3.4.1 Absorption.............................................................................................................................32
 

3.4.1.1 Inhalation Exposure .......................................................................................................32
 
1,1-DICHLOROETHANE xiv 

3.4.1.2 Oral Exposure ................................................................................................................32
 

3.4.1.3 Dermal Exposure ...........................................................................................................33
 

3.4.2 Distribution ...........................................................................................................................33
 

3.4.2.1 Inhalation Exposure .......................................................................................................33
 

3.4.2.2 Oral Exposure ................................................................................................................33
 

3.4.2.3 Dermal Exposure ...........................................................................................................33
 

3.4.2.4 Other Routes of Exposure..............................................................................................34
 

3.4.3 Metabolism............................................................................................................................34
 

3.4.4 Elimination and Excretion.....................................................................................................38
 

3.4.4.1 Inhalation Exposure .......................................................................................................38
 

3.4.4.2 Oral Exposure ................................................................................................................38
 

3.4.4.3 Dermal Exposure ...........................................................................................................38
 

3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models.............38
 

3.5 MECHANISMS OF ACTION .....................................................................................................41
 

3.5.1 Pharmacokinetic Mechanisms...............................................................................................41
 

3.5.2 Mechanisms of Toxicity........................................................................................................41
 

3.5.3 Animal-to-Human Extrapolations.........................................................................................41
 

3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS.............................41
 

3.7 CHILDREN’S SUSCEPTIBILITY..............................................................................................42
 

3.8 BIOMARKERS OF EXPOSURE AND EFFECT .......................................................................44
 

3.8.1 Biomarkers Used to Identify or Quantify Exposure to 1,1-Dichloroethane..........................46
 

3.8.2 Biomarkers Used to Characterize Effects Caused by 1,1-Dichloroethane............................46
 

3.9 INTERACTIONS WITH OTHER CHEMICALS .......................................................................46
 

3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE..................................................46
 

3.11 METHODS FOR REDUCING TOXIC EFFECTS......................................................................47
 

3.11.1 Reducing Peak Absorption Following Exposure...............................................................47
 

3.11.2 Reducing Body Burden .....................................................................................................47
 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects............................................47
 

3.12 ADEQUACY OF THE DATABASE ..........................................................................................48
 

3.12.1 Existing Information on Health Effects of 1,1-Dichloroethane.........................................48
 

3.12.2 Identification of Data Needs..............................................................................................50
 

3.12.3 Ongoing Studies ................................................................................................................55
 

4. CHEMICAL AND PHYSICAL INFORMATION................................................................................57
 

4.1 CHEMICAL IDENTITY..............................................................................................................57
 

4.2 PHYSICAL AND CHEMICAL PROPERTIES...........................................................................57
 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL............................................................61
 

5.1 PRODUCTION ............................................................................................................................61
 

5.2 IMPORT/EXPORT ......................................................................................................................63
 

5.3 USE ..............................................................................................................................................63
 

5.4 DISPOSAL...................................................................................................................................63
 

6. POTENTIAL FOR HUMAN EXPOSURE...........................................................................................65
 

6.1 OVERVIEW.................................................................................................................................65
 

6.2 RELEASES TO THE ENVIRONMENT.....................................................................................67
 

6.2.1 Air .........................................................................................................................................68
 

6.2.2 Water.....................................................................................................................................72
 

6.2.3 Soil ........................................................................................................................................72
 

6.3 ENVIRONMENTAL FATE ........................................................................................................72
 

6.3.1 Transport and Partitioning.....................................................................................................72
 
6.3.2 Transformation and Degradation ..........................................................................................74
 

6.3.2.1 Air..................................................................................................................................74
 

6.3.2.2 Water..............................................................................................................................74
 

6.3.2.3 Sediment and Soil ..........................................................................................................75
 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT....................................76
 

6.4.1 Air .........................................................................................................................................76
 

6.4.2 Water.....................................................................................................................................80
 

6.4.3 Sediment and Soil .................................................................................................................83
 

6.4.4 Other Environmental Media..................................................................................................84
 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE..........................................84
 

6.6 EXPOSURES OF CHILDREN....................................................................................................87
 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES ................................................87
 

6.8 ADEQUACY OF THE DATABASE ..........................................................................................88
 

6.8.1 Identification of Data Needs .................................................................................................88
 

6.8.2 Ongoing Studies....................................................................................................................91
 

7. ANALYTICAL METHODS..................................................................................................................93
 

7.1 BIOLOGICAL MATERIALS......................................................................................................93
 

7.2 ENVIRONMENTAL SAMPLES ................................................................................................99
 

7.3 ADEQUACY OF THE DATABASE ........................................................................................102
 

7.3.1 Identification of Data Needs ...............................................................................................102
 

7.3.2 Ongoing Studies..................................................................................................................103
 

8. REGULATIONS, ADVISORIES, AND GUIDELINES.....................................................................105
 

9. REFERENCES ....................................................................................................................................109
 

10. GLOSSARY ......................................................................................................................................127
 

APPENDICES 

A. ATSDR MINIMAL RISK LEVELS AND WORKSHEETS .............................................................A-1
 

B. USER’S GUIDE.................................................................................................................................. B-1
 

C. ACRONYMS, ABBREVIATIONS, AND SYMBOLS...................................................................... C-1
 

1,1-DICHLOROETHANE xv 
1,1-DICHLOROETHANE xvi 

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LIST OF FIGURES
 

2-1. Health Effects for Following Inhalation Exposure to 1,1-Dichloroethane ...........................................9
 

2-2. Health Effects for Following Oral Exposure to 1,1-Dichloroethane ..................................................10
 

3-1. Levels of Significant Exposure to 1,1-Dichloroethane – Inhalation................................................... 18
 

3-2. Levels of Significant Exposure to 1,1-Dichloroethane – Oral............................................................ 24
 

3-3. Proposed Metabolic Scheme for 1,1-Dichloroethane.........................................................................37
 

3-4. Conceptual Representation of a Physiologically Based Pharmacokinetic (PBPK) Model for a
 

Hypothetical Chemical Substance ......................................................................................................40
 

3-5. Existing Information on Health Effects of 1,1-Dichloroethane..........................................................49
 

6-1. Frequency of NPL Sites with 1,1-Dichloroethane Contamination .....................................................66
 

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1,1-DICHLOROETHANE xix 

LIST OF TABLES
 

3-1. Levels of Significant Exposure for 1,1-Dichloroethane – Inhalation................................................. 16
 

3-2. Levels of Significant Exposure for 1,1-Dichloroethane – Oral .......................................................... 22
 

3-3. Genotoxicity of 1,1-Dichloroethane In Vitro......................................................................................30
 

3-4. Production of Metabolites from 1,1-Dichloroethane with Hepatic Microsomes from
 

Phenobarbital-Induced Rats ...............................................................................................................36
 

4-1. Chemical Identity of 1,1-Dichloroethane ...........................................................................................58
 

4-2. Physical and Chemical Properties of 1,1-Dichloroethane ..................................................................59
 

5-1. Facilities that Produce, Process, or Use 1,1-Dichloroethane..............................................................62
 

6-1. Releases to the Environment from Facilities that Produce, Process, or Use 1,1-Dichloroethane ......69
 

6-2. Estimated Yearly Emissions of 1,1-Dichloroethane (mg/m2 per Year)..............................................71
 

6-3. 2013 Air Monitoring Data from Air Toxics Data Ambient Monitoring Archive for
 
 

1,1-Dichloroethane.............................................................................................................................77
 

6-4. Geometric Mean and Selected Percentiles of Blood Concentrations of 1,1-Dichloroethane 

(in ng/L) for the U.S. Population from the National Health and Nutrition Examination 

Survey (NHANES).............................................................................................................................85
 

7-1. Analytical Methods for Determining 1,1-Dichloroethane in Biological Materials............................94
 

7-2. Analytical Methods for Determining 1,1-Dichloroethane in Environmental Samples.......................95
 

8-1. Regulations, Advisories, and Guidelines Applicable to 1,1-Dichloroethane ...................................106
 
1,1-DICHLOROETHANE xx 

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1,1-DICHLOROETHANE 1 

1. PUBLIC HEALTH STATEMENT FOR 

1,1-DICHLOROETHANE
 

This Public Health Statement summarizes the Division of Toxicology and Human Health Science’s 

findings on 1,1-dichloroethane, tells you about it, the effects of exposure, and describes what you can do 

to limit that exposure. 

The U.S. Environmental Protection Agency (EPA) identifies the most serious hazardous waste sites in the 

nation. These sites make up the National Priorities List (NPL) and are sites targeted for long-term federal 

clean-up activities. U.S. EPA has found 1,1-dichloroethane in at least 673 of the 1,699 current or former 

NPL sites. The total number of NPL sites evaluated for 1,1-dichloroethane is not known. But the 

possibility remains that as more sites are evaluated, the sites at which 1,1-dichloroethane is found may 

increase. This information is important because these future sites may be sources of exposure, and 

exposure to 1,1-dichloroethane may be harmful. 

If you are exposed to 1,1-dichloroethane, many factors determine whether you’ll be harmed. These 

include how much you are exposed to (dose), how long you are exposed (duration), and how you are 

exposed (route of exposure). You must also consider the other chemicals you are exposed to and your 

age, sex, diet, family traits, lifestyle, and state of health. 

WHAT IS 1,1-DICHLOROETHANE? 

1,1-Dichloroethane is a colorless oily liquid with a chloroform-like odor. 1,1-Dichloroethane is a 

chemical used mostly as an intermediate in the manufacture of 1,1,1-trichloroethane (1,1,1-TCE). 

1,1-Dichloroethane is also used in limited amount as a solvent for cleaning and degreasing, and in the 

manufacture of plastic wrap, adhesives, and synthetic fiber. 

More information on the chemical and physical properties as well as the production and uses of 

1,1-dichloroethane is presented in Chapters 4 and 5 of this profile. 

WHERE IS 1,1-DICHLOROETHANE FOUND? 

1,1-Dichloroethane can be released into the air, water, and soil at places where it is produced or used as a 

solvent. The majority of the monitoring data for 1,1-dichloroethane focuses on air and water, specifically 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 2 

1. PUBLIC HEALTH STATEMENT 

at hazardous waste sites. Minimal data are available for concentrations of 1,1-dichloroethane measured in 

soil. It is expected that the lack of available soil data is, in part, due to the rapid partitioning of 

1,1-dichloroethane to air and water from soil or sediment. 1,1-Dichloroethane has been detected and 

measured in air samples at concentrations ranging from parts per trillion (ppt) to parts per million (ppm). 

In the air, 1,1-dichloroethane is slow to break down and has the potential for long-range transport. 

1,1-Dichloroethane has been detected in drinking water and groundwater. 1,1-Dichloroethane does not 

degrade quickly in water, but it can evaporate from the water into the air. Minimal information was found 

on concentrations of 1,1-dichloroethane in soil, releases of 1,1-dichloroethane to land surfaces, or the 

disposal of waste products containing 1,1-dichloroethane into landfills. 1,1-Dichloroethane released to 

soil surfaces would rapidly evaporate to the air. Residual 1,1-dichloroethane remaining on soil surfaces 

would be available for transport into groundwater, since it is not expected to bind to soil particulates 

unless the organic content of the soil is high. Minimal information was found on the levels of 

1,1-dichloroethane in other media. 

In a survey of 234 table ready foods evaluated for the presence of volatile organic compounds (VOCs), 

1,1-dichloroethane was not found in any of the samples. It was detected in three peanut butter samples at 

levels of 1.1, 1.9, and 3.7 micrograms per kilogram (μg/kg); however, the compound was not found in 

several other foods that were analyzed. 

More information on levels of 1,1-dichorethane found in the environment is presented in Chapter 6 of this 

profile. 

HOW MIGHT I BE EXPOSED TO 1,1-DICHLOROETHANE? 

The use of 1,1-dichloroethane as a solvent, cleaning agent, and degreaser, and its use in manufacturing of 

other compounds, such as 1,1,1-TCE, may result in releases to the environment. 1,1-Dichloroethane has 

been detected in ambient air and water. Exposure to 1,1-dichloroethane occurs mainly by breathing air 

near contaminated areas or by drinking water contaminated with 1,1-dichloroethane. However, most 

people who are exposed to 1,1-dichloroethane through air or water are exposed to very low levels, in the 

range of ppm to ppt. People may be exposed to higher levels of 1,1-dichloroethane if they smoke 

cigarettes or are exposed to cigarette smoke. People may also be exposed to 1,1-dichloroethane by using 

consumer products that contain this compound. 
 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 3 

1. PUBLIC HEALTH STATEMENT 

Job-related exposure of 1,1-dichloroethane results from breathing in workplace air or from touching 

contaminated chemicals or materials at workplaces where 1,1-dichloroethane is used. According to a 

survey conducted between 1980 and 1983 by the National Institute for Occupational Safety and Health 

(NIOSH), an estimated 1,957 people in the United States may have been exposed to 1,1-dichloroethane 

while working. In general, people who work with 1,1-dichloroethane or live near industrial emission 

sources and hazardous waste sites containing 1,1-dichloroethane are more likely to be exposed. 

Additional information on levels in the environment and potential for human exposure is presented in 

Chapter 6 of the toxicological profile. 

HOW CAN 1,1-DICHLOROETHANE ENTER AND LEAVE MY BODY? 

If you breathe air containing 1,1-dichloroethane, it will enter your body through your lungs. 1,1-Dichloroethane in your drinking water will enter your body through the digestive tract. We do not know 

how much will be absorbed; studies with similar compounds suggested that 1,1-dichloroethane will be 

rapidly and extensively absorbed. 

1,1-Dichloroethane leaves your body in the breath or is broken down into other chemicals, which leave 

your body in the breath or in the urine. 

HOW CAN 1,1-DICHLOROETHANE AFFECT MY HEALTH? 

No information is available in humans on the health effects associated with occupational or environmental 

exposure to 1,1-dichloroethane. 1,1-Dichloroethane was used as an anesthetic; however, it is no longer 

used for this purpose because of the heart effects that also occurred at these very high concentrations. 

Kidney effects have been observed in cats exposed to 1,1-dichloroethane in air for long periods. 

However, kidney effects have not been observed in other animal species following long-term inhalation 

or oral exposure. 

The results of a study in rats and mice suggest that 1,1-dichloroethane may cause cancer. However, the 

study had several flaws and the results are not conclusive. Another long-term study of mice that drank 

water containing 1,1-dichloroethane did not find cancer. 
 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 4 

1. PUBLIC HEALTH STATEMENT 

The U.S. Department of Health and Human Services (DHHS) and The International Agency for Research 

on Cancer (IARC) have not evaluated the carcinogenic potential of 1,1-dichloroethane. The U.S. EPA 

has determined that 1,1-dichloroethane is a possible human carcinogen. 

See Chapters 2 and 3 for more information on 1,1-dichloroethane health effects. 

HOW CAN 1,1-DICHLOROETHANE AFFECT CHILDREN? 

This section discusses potential health effects of 1,1-dichloroethane exposure in humans from when 

they’re first conceived to 18 years of age, and how you might protect against such effects. 

No available studies have described the effects of exposure to 1,1-dichloroethane on children or young 

animals. Although we think that children would likely show the same health effects as adults, we don’t 

know whether children are more susceptible than are adults to 1,1-dichloroethane effects. 

We don’t know whether 1,1-dichloroethane can harm an unborn child. Minor skeletal problems were 

observed in the fetuses of rats exposed to 1,1-dichloroethane in the air; decreases in body weight were 

also observed in the mothers. 

HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO 1,1-DICHLOROETHANE? 

If your doctor finds that you have been exposed to significant amounts of 1,1-dichloroethane, ask whether 

your children might also be exposed. Your doctor might need to ask your state health department to 

investigate. 

1,1-Dichloroethane can enter your body from air, water, or consumer products containing this substance. 

Contact local drinking water authorities and follow their advice if you have any concerns about the 

presence of 1,1-dichloroethane in your tap water. 1,1-Dichloroethane has the potential to contaminate 

foods, although the levels found in food are generally low. 1,1-Dichloroethane can also be present in 

groundwater and soil underneath a building or a home, resulting in above-ground vapors through vapor 

intrusion (movement of vapors from groundwater or soil into air). To minimize risks associated with 

breathing in contaminated vapors, ensure that the area is well ventilated. If you think that you may have 

groundwater contaminated with 1,1-dichloroethane, contact your local state health department. Follow 

instructions on product labels to minimize exposure to 1,1-dichloroethane. Storing these items in a shed 

or an outside location may reduce exposure and decrease the impact on indoor air. 
 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 5 

1. PUBLIC HEALTH STATEMENT 

ARE THERE MEDICAL TESTS TO DETERMINE WHETHER I HAVE BEEN EXPOSED TO 

1,1-DICHLOROETHANE? 

1,1-Dichloroethane and its breakdown products (metabolites) can be measured in blood and urine. 

However, the detection of 1,1-dichoroethane or its metabolites cannot predict the kind of health effects 

that might develop from that exposure. Because 1,1-dichloroethane and its metabolites leave the body 

fairly rapidly, the tests need to be conducted within days after exposure. 

For more information on the different substances formed by 1,1-dichloroethane breakdown and on tests to 

detect these substances in the body, see Chapters 3 and 7. 

WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO PROTECT 

HUMAN HEALTH? 

The federal government develops regulations and recommendations to protect public health. Regulations 

can be enforced by law. Federal agencies that develop regulations for toxic substances include the 

Environmental Protection Agency (EPA), the Occupational Safety and Health Administration (OSHA), 

and the Food and Drug Administration (FDA). Recommendations provide valuable guidelines to protect 

public health but cannot be enforced by law. Federal organizations that develop recommendations for 

toxic substances include the Agency for Toxic Substances and Disease Registry (ATSDR) and the 

National Institute for Occupational Safety and Health (NIOSH). 

Regulations and recommendations can be expressed as “not-to-exceed” levels; that is, levels of a toxic 

substance in air, water, soil, or food that do not exceed a critical value usually based on levels that affect 

animals; levels are then adjusted to help protect humans. Sometimes these not-to-exceed levels differ 

among federal organizations. Different organizations use different exposure times (an 8-hour workday or 

a 24-hour day), different animal studies, or emphasize some factors over others, depending on their 

mission. 

Recommendations and regulations are also updated periodically as more information becomes available. 

For the most current information, check with the federal agency or organization that issued the regulation 

or recommendation. 
 

 

 

 

	 
 


 

	 
 


 


 


 


 


 

	 
 


 

	 
 


 


 


 


 


 

1,1-DICHLOROETHANE 6 

1. PUBLIC HEALTH STATEMENT 

OSHA set a legal limit of 100 ppm 1,1-dichloroethane in workplace air averaged over an 8-hour work 

day. NIOSH recommends a limit of 100 ppm 1,1-dichloroethane in workplace air averaged over a 

10-hour work day. 

WHERE CAN I GET MORE INFORMATION? 

If you have any questions or concerns, please contact your community or state health or environmental 

quality department, or contact ATSDR at the address and phone number below. ATSDR can also provide 

publically available information regarding medical specialists with expertise and experience recognizing, 

evaluating, treating, and managing patients exposed to hazardous substances. 

•	 Call the toll-free information and technical assistance number at
 

1-800-CDCINFO (1-800-232-4636) or
 

•	 Write to:
 

Agency for Toxic Substances and Disease Registry
 

Division of Toxicology and Human Health Sciences
 

1600 Clifton Road NE
 

Mailstop F-57
 

Atlanta, GA 30329-4027
 

Toxicological profiles and other information are available on ATSDR’s web site: 

http://www.atsdr.cdc.gov. 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 7 

2. RELEVANCE TO PUBLIC HEALTH
 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO 1,1-DICHLOROETHANE IN 

THE UNITED STATES 

The production and use of 1,1-dichloroethane as a solvent, cleaning agent, and degreaser, and in the 

manufacture of 1,1,1-trichloroethane, vinyl chloride, and high vacuum rubber may result in its release to 

the environment. Volatilization is expected to be high based on its vapor pressure and Henry’s Law 

constant. Atmospheric photooxidation occurs slowly in the environment, as does biodegradation and 

hydrolysis. 1,1-Dichloroethane has high mobility in soil and has the potential to leach from surface soils 

into groundwater. The bioaccumulation potential of 1,1-dichloroethane is low. 

Monitoring data indicate that the general population may be exposed to 1,1-dichloroethane via inhalation 

for people living near source areas, ingestion of contaminated drinking water, and use of consumer 

products such as paint removers, which may contain this compound. Ingestion of food sources 

contaminated with 1,1-dichloroethane is not an important exposure pathway. 

A National Health and Nutrition Survey of the U.S. population in 2003–2004 screened for 1,1-dichloroethane in blood from 1,367 participants (670 males and 679 females) in the age range of 20–59 years old. 

The portion of the data below the limit of detection (LOD) was too high to provide valid results. 

2.2 SUMMARY OF HEALTH EFFECTS 

Relatively little information is available on the health effects of 1,1-dichloroethane in humans or animals. 

Chlorinated aliphatics as a class are known to cause central nervous system depression and respiratory 

tract and dermal irritation when humans are exposed by inhalation to sufficiently high levels. In the past, 

1,1-dichloroethane was used as an anesthetic; however, this use was discontinued due to the risk of 

cardiac arrhythmia induction in humans at anesthetic doses (approximately 26,000 ppm). A small number 

of animal studies have examined the toxicity and carcinogenicity of 1,1-dichloroethane; these studies 

have failed to conclusively identify the critical targets of toxicity. Nonneoplastic effects are limited to 

renal toxicity in cats, maternal and fetal toxicity in rats, and alterations in body weight gain. Crystal 

precipitations and obstruction in the renal tubule lumina and increases in serum urea and creatinine were 

observed in cats exposed to 500 ppm for 13 weeks followed by a 13-week exposure to 1,000 ppm for 

13 weeks. However, these effects were not observed in rats, guinea pigs, or rabbits similarly exposed to 

1,1-dichloroethane, and renal effects have not been observed following gavage administration of 764 or 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 8 

2. RELEVANCE TO PUBLIC HEALTH 

950 mg/kg/day in rats or 2,885 or 3,331 mg/kg/day in mice 5 days/week for 78 weeks or in mice exposed 

to 465 mg/kg/day 1,1-dichloroethane in drinking water for 52 weeks. Kidney effects have also been 

observed in mice administered a lethal intraperitoneal injection of 1,1-dichloroethane; the effects included 

increased glucose and protein in the urine and tubular swelling. The toxicological significance of the 

nephrotoxicity observed in cats and the mice with regard to human health is not known given the small 

number of animals tested (cats), the lack of a nephrotoxic effect in other species and in other studies 

where 1,1-dichloroethane was administered orally. 

The liver is the only other organ that has been examined in multiple studies; no hepatic effects have been 

reported following intermediate-duration inhalation exposure of rats, guinea pigs, rabbits, or cats, 

intermediate-duration oral exposure of mice, or chronic-duration exposure of rats and mice. The potential 

reproductive toxicity, immunotoxicity, and neurotoxicity of 1,1-dichloroethane have not been examined 

following inhalation, oral, or dermal exposure. A single developmental toxicity study reported retarded 

fetal development (delayed ossification of vertebrae) in rats at 6,000 ppm (7 hours/day on gestation 

days 6–15); an 11% decrease in maternal body weight gain and a decrease in maternal food consumption 

were also reported at this concentration. There is inconclusive evidence that 1,1-dichloroethane may be 

carcinogenic in rodents. A significant positive dose-related trend was observed for the incidence of 

hemangiosarcomas and mammary adenocarcinomas in female rats, hepatocellular carcinomas in male 

mice, and endometrial stromal polyps in female mice. However, only the incidence of endometrial 

stromal polyps in female mice was significantly increased over the corresponding control animals. 

Limitations in this study, particularly the poor survival in treated and control animals, preclude the 

consideration of these results as conclusive evidence of carcinogenicity. A 52-week drinking water study, 

testing much lower doses, did not find increases in the incidence of lung, liver, or kidney tumors in mice. 

Based on the available carcinogenicity data for 1,1-dichloroethane and supporting data on 1,2-dichloroethane, the EPA has classified 1,1-dichloroethane as a possible human carcinogen (group C). Neither the 

Department of Health and Human Services nor the International Agency for Research on Cancer have 

classified the carcinogenic potential of 1,1-dichloroethane. 

An overview of these data is presented in Figures 2-1 and 2-2. 
 

1,1-DICHLOROETHANE 9 

2. RELEVANCE TO PUBLIC HEALTH 

Figure 2-1. Health Effects for Following Inhalation Exposure to 

1,1-Dichloroethane 
 

1,1-DICHLOROETHANE 10 

2. RELEVANCE TO PUBLIC HEALTH 

Figure 2-2. Health Effects for Following Oral Exposure to 1,1-Dichloroethane 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 11 

2. RELEVANCE TO PUBLIC HEALTH 

2.3 MINIMAL RISK LEVELS (MRLs) 

Inhalation MRLs 

There are limited data to derive inhalation MRLs for 1,1-dichloroethane; the database consists of two 

inhalation studies. Hofmann et al. (1971) examined the potential for 1,1-dichloroethane to induce liver 

and/or kidney effects in rats, guinea pigs, rabbits, and cats exposed to 500 ppm 6 hours/day, 5 days/week 

for 13 weeks followed by a second 13-week exposure period to 1,000 ppm. No adverse effects were 

observed in the rats, guinea pigs, or rabbits. In three of four cats, increases in serum urea and creatinine 

levels and renal tubular effects (crystalline precipitates, obstruction of lumina, and dilatation) were 

observed at the end of the 26-week period. Tubular degeneration and periglomerular fibrosis were also 

noted; however, it is not known if this was observed in all affected cats. In a developmental toxicity 

study (Schwetz et al. 1974), decreases in maternal body weight gain and decreases in maternal food 

consumption were observed in rats exposed to 3,800 or 6,000 ppm 1,1-dichloroethane on gestation 

days 6–15 (7 hours/day); the magnitude of the decrease in weight gain was 8 and 11%, respectively. 

Increases in the incidence of fetuses with delayed ossification of sternebrae were also observed at 

6,000 ppm. No other developmental effects, including alterations in fetal resorptions, fetal growth, or 

incidences of gross or soft tissue anomalies, were observed. 

These studies examined a limited number of end points and there is a great deal of uncertainty regarding 

the primary targets of toxicity following inhalation exposure. The lowest adverse effect level that has 

been identified is 750 ppm (time-weighted average) for renal effects in cats following a 26-week exposure 

(Hofmann et al. 1971). However, this effect has not been corroborated in other species following 

inhalation (Hofmann et al. 1971) or oral (Klaunig et al. 1986; NCI 1977) exposure. Additionally, it is not 

known if cats are a good model for 1,1-dichloroethane-induced crystal formation and tubular damage and 

there is uncertainty regarding the threshold concentration for these renal effects due to the exposure 

protocol, which involved increasing the exposure concentration mid-way through the study. Both 

maternal and fetal growth retardation were observed at 6,000 ppm in an acute-duration study; however, it 

is not known if systemic or neurological effects would occur at lower concentrations. 1,1-Dichloroethane 

has anesthetic properties at fairly high concentrations (approximately 26,000 ppm) (Miller et al. 1965), a 

concentration also associated with cardiac arrhythmias (Reid and Muianga 2012). It is not known if 

exposure to lower concentrations would also result in central nervous system depressive effects or 

cardiotoxic effects because these end points have not been examined. Uncertainties associated with 
 

 

 

1,1-DICHLOROETHANE 12 

2. RELEVANCE TO PUBLIC HEALTH 

identification of the most sensitive target and the associated concentration-response relationships, 

precludes deriving inhalation MRLs for 1,1-dichloroethane. 

Oral MRLs 

Two studies have examined the oral toxicity of 1,1-dichloroethane following intermediate- or chronicduration exposure. No lung, liver, or kidney effects were observed in mice exposed to doses as high as 

465 mg/kg/day 1,1-dichloroethane in drinking water for 52 weeks (Klaunig et al. 1986); no other potential 

targets were examined. Similarly, no nonneoplastic effects were noted in major tissues and organs of rats 

and mice administered 1,1-dichloroethane in corn oil 5 days/week for 78 weeks (NCI 1977). The highest 

doses tested were 764 and 950 mg/kg/day, respectively, in male and female rats and 2,885 and 

3,331 mg/kg/day, respectively, in male and female mice. A 6-week study found decreases in body weight 

gain (>16%) in male rats administered 562 mg/kg/day and female rats administered 1,780 mg/kg/day 

1,1-dichloroethane 5 days/week in corn oil (NCI 1977). No additional information was reported, and the 

cause of the decreased weight gain is not known. The chronic-duration rat study did not find significant 

alterations in body weight gain at higher concentrations in the male rats. Thus, the oral studies have not 

identified a target of toxicity, precluding the derivation of oral MRLs for 1,1-dichloroethane. 
 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 13 

3. HEALTH EFFECTS 

3.1 INTRODUCTION 

The primary purpose of this chapter is to provide public health officials, physicians, toxicologists, and 

other interested individuals and groups with an overall perspective on the toxicology of 

1,1-dichloroethane. It contains descriptions and evaluations of toxicological studies and epidemiological 

investigations and provides conclusions, where possible, on the relevance of toxicity and toxicokinetic 

data to public health. 

A glossary and list of acronyms, abbreviations, and symbols can be found at the end of this profile. 

3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 

To help public health professionals and others address the needs of persons living or working near 

hazardous waste sites, the information in this section is organized first by route of exposure (inhalation, 

oral, and dermal) and then by health effect (death, systemic, immunological, neurological, reproductive, 

developmental, genotoxic, and carcinogenic effects). These data are discussed in terms of three exposure 

periods: acute (14 days or less), intermediate (15–364 days), and chronic (365 days or more). 

Levels of significant exposure for each route and duration are presented in tables and illustrated in 

figures. The points in the figures showing no-observed-adverse-effect levels (NOAELs) or lowestobserved-adverse-effect levels (LOAELs) reflect the actual doses (levels of exposure) used in the studies. 

LOAELs have been classified into "less serious" or "serious" effects. "Serious" effects are those that 

evoke failure in a biological system and can lead to morbidity or mortality (e.g., acute respiratory distress 

or death). "Less serious" effects are those that are not expected to cause significant dysfunction or death, 

or those whose significance to the organism is not entirely clear. ATSDR acknowledges that a 

considerable amount of judgment may be required in establishing whether an end point should be 

classified as a NOAEL, "less serious" LOAEL, or "serious" LOAEL, and that in some cases, there will be 

insufficient data to decide whether the effect is indicative of significant dysfunction. However, the 

Agency has established guidelines and policies that are used to classify these end points. ATSDR 

believes that there is sufficient merit in this approach to warrant an attempt at distinguishing between 

"less serious" and "serious" effects. The distinction between "less serious" effects and "serious" effects is 

considered to be important because it helps the users of the profiles to identify levels of exposure at which 

major health effects start to appear. LOAELs or NOAELs should also help in determining whether or not 
 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 14 

3. HEALTH EFFECTS 

the effects vary with dose and/or duration, and place into perspective the possible significance of these 

effects to human health. 

The significance of the exposure levels shown in the Levels of Significant Exposure (LSE) tables and 

figures may differ depending on the user's perspective. Public health officials and others concerned with 

appropriate actions to take at hazardous waste sites may want information on levels of exposure 

associated with more subtle effects in humans or animals (LOAELs) or exposure levels below which no 

adverse effects (NOAELs) have been observed. Estimates of levels posing minimal risk to humans 

(Minimal Risk Levels or MRLs) may be of interest to health professionals and citizens alike. 

3.2.1 Inhalation Exposure 

Very little information is available regarding the health effects of 1,1-dichloroethane following inhalation 

exposure in humans or animals. 1,1-Dichloroethane was used in the past as an anesthetic at a pressure of 

0.026 atm, which is approximately equivalent to a concentration of 105,000 mg/m3 (26,000 ppm) (Miller 

et al. 1965). This use was discontinued when it was discovered that this compound induced cardiac 

arrhythmias at anesthetic doses (Reid and Muianga 2012). 

Table 3-1 and Figure 3-1 describe the health effects observed in laboratory animals associated with 

inhalation exposure levels at varying time and exposure durations. 

3.2.1.1 Death 

No studies were located regarding death in humans following inhalation exposure to 1,1-dichloroethane. 

In a review paper, Smyth (1956) reported that no deaths were observed in rats exposed to 4,000 ppm for 

8 hours, but an 8-hour exposure to 16,000 ppm was lethal. It has been reported in the early literature that 

the lethal exposure level of 1,1-dichloroethane in mice was 17,500 ppm (Reid and Muianga 2012). These 

values were reported in a secondary source and it is therefore impossible to assess their validity. 

Subchronic intermittent exposure to 500 ppm of 1,1-dichloroethane for 13 weeks followed by 1,000 ppm 

of 1,1-dichloroethane for an additional 13 weeks was not lethal to rats, rabbits, guinea pigs, or cats 

(Hofmann et al. 1971). 

The highest NOAEL values for death in each species and duration category are recorded in Table 3-1 and 

plotted in Figure 3-1. 
 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 15 

3. HEALTH EFFECTS 

3.2.1.2 Systemic Effects 

No studies were located regarding respiratory, gastrointestinal, hematological, musculoskeletal, or 

dermal/ocular effects in humans or animals following inhalation exposure to 1,1-dichloroethane. 

Cardiovascular Effects. A cardiostimulatory effect resulting in arrhythmias prompted the 

discontinuance of the use of 1,1-dichloroethane as an anesthetic in humans (Reid and Muianga 2012). 

This effect was noted at the relatively high dose used to induce anesthesia (0.026 atm, which is 

approximately equivalent to 105,000 mg/m3

, or 26,000 ppm) (Miller et al. 1965). No studies were located 

regarding cardiovascular effects in animals following inhalation exposure to 1,1-dichloroethane. 

Hepatic Effects. No studies were located regarding hepatic effects in humans following inhalation 

exposure to 1,1-dichloroethane. Rats, rabbits, guinea pigs, and cats experienced no change in serum 

alanine aminotransferase or aspartate aminotransferase activity after intermittent 6-hour inhalation 

exposure to 500 ppm 1,1-dichloroethane for 13 weeks followed by 13 weeks of exposure 6 hours/day to 

1,000 ppm 1,1-dichloroethane (Hofmann et al. 1971). Furthermore, no treatment-related histopathological lesions were noted in the livers of these animals after this 26-week exposure regimen. Six days 

after termination of a 10-day exposure to 6,000 ppm 1,1-dichloroethane (7 hours/day), a slight but 

statistically significant increase in relative liver weight (26% higher than controls) was observed in female 

Sprague-Dawley rats (Schwetz et al. 1974). However, there was no increase in aspartate aminotransferase activity over control values, and no changes in the gross appearance of the liver were noted at 

necropsy in these animals; the slight increase in liver weight was not considered adverse. 

Renal Effects. No studies were located regarding renal effects in humans following inhalation 

exposure to 1,1-dichloroethane. Renal injury was apparent in cats intermittently exposed 6 hours/day to 

1,000 ppm 1,1-dichloroethane for 13 weeks following 13 weeks of intermittent exposure to 500 ppm 

1,1-dichloroethane (Hofmann et al. 1971). Serum urea and creatinine were increased in these animals. 

One cat was so severely affected that it had to be removed from the study. Histopathological lesions in 

the kidney tubules (including crystalline precipitates and dilation) were noted in three of four cats at 

necropsy; renal tubular degenerations without preliminary lumen displacement and periglomerular 

fibrosis and tubule destruction were also observed. The ill health of these animals was also manifest by a 

progressive decrease in body weight. Rats, rabbits, and guinea pigs similarly exposed to 1,1-dichloroethane exhibited no adverse effects. 
258

6000

257

3000

6800

272

750750750

274

750750750

273

750750750

Table 3-1 Levels of Significant Exposure to 1,1-Dichloroethane - Inhalation Exposure/ LOAEL 

Duration/

a 

Key to Species Frequency NOAEL Less Serious Serious Reference (Route) Figure (Strain) System (ppm) (ppm) (ppm) Chemical Form 

ACUTE EXPOSURE Systemic 

1 Rat 

(SpragueDawley) 

7 hr/d 10 d 

Developmental 

2 Rat 

(SpragueDawley) 

7 hr/d Gd 6-15 

Hepatic 6000 F 

3000 F 6800 F (Increased incidence of 

delayed ossification) 

Schwetz et al. 1974 Schwetz et al. 1974 

INTERMEDIATE EXPOSURE Systemic 

3 Rat 6 hr/d 

5 d/wk (SpragueDawley) 26 wk Hepatic 750 Hofmann et al. 1971 1,1-DCE 

Renal 750 Bd Wt 750 

4 Gn Pig 

(FirbrightWhite) 

6 hr/d 5 d/wk 26 wk 

Hepatic 750 Hofmann et al. 1971 

1,1-DCE 

Renal 750 Bd Wt 750 

5 Rabbit 

(Brunte) 

6 hr/d 5 d/wk 26 wk 

Hepatic 750 Hofmann et al. 1971 

1,1-DCE 

Renal 750 Bd Wt 750 
275

750

750

750

Table 3-1 Levels of Significant Exposure to 1,1-Dichloroethane - Inhalation (continued) 

a 

Key to Species 

Figure (Strain) 

Exposure/ 

Duration/ 

Frequency 

(Route) System NOAEL (ppm) Less Serious (ppm) 

LOAEL 

Serious 

(ppm) 

Reference Chemical Form 

6 Cat 

(NS) 

6 hr/d 5 d/wk 26 wk 

Hepatic 750 Hofmann et al. 1971 

1,1-DCE 

Renal 750 (crystal precipitation and 

obstruction in tubule lumina) 

Bd Wt 750 

a The number corresponds to entries in Figure 3-1. Bd Wt = body weight; d = day(s); F = Female; Gd = gestational day; Gn pig = guinea pig; hr = hour(s); LOAEL = lowest-observed-adverse-effect level; NOAEL = no-observed-adverse-effect level; NS = not specified; wk = week(s) 
Hepatic 

Developmental 


	

10000 

Systemic 

ppm 

2r 

1r 

2r 

Cancer Effect Level-Animals

 LOAEL, More Serious-Animals

LOAEL, Less Serious-Animals

NOAEL - Animals

 Cancer Effect Level-Humans

 LOAEL, More Serious-Humans

LOAEL, Less Serious-Humans

NOAEL - Humans

 LD50/LC50

Minimal Risk Level

 for effects

 other than

 Cancer 

r-Rat 

1000 


	


	

Figure 3-1 Levels of Significant Exposure to 1,1-Dichloroethane - Inhalation
	

Acute (≤14 days)

1,1-DICHLOROETHANE 3. HEALTH EFFECTS 18
Hepatic 

Renal Body Weight 


 


	

Figure 3-1 Levels of Significant Exposure to 1,1-Dichloroethane - Inhalation (Continued)
 

Intermediate (15-364 days) 

Systemic 

ppm 

1,1-DICHLOROETHANE

100 

1000 

6c 4g 3r 5h 6c 4g 3r 5h 6c 4g 3r 5h 

c-Cat 

r-Rat 

h-Rabbit 

g-Guinea Pig

 Cancer Effect Level-Animals

 LOAEL, More Serious-Animals

LOAEL, Less Serious-Animals

NOAEL - Animals

 Cancer Effect Level-Humans

 LOAEL, More Serious-Humans

LOAEL, Less Serious-Humans

NOAEL - Humans

 LD50/LC50

Minimal Risk Level

 for effects

 other than

 Cancer 

3. HEALTH EFFECTS 19
 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 20 

3. HEALTH EFFECTS 

3.2.1.3 Immunological and Lymphoreticular Effects 

No studies were located regarding immunological effects in humans or animals after inhalation exposure 

to 1,1-dichloroethane. 

3.2.1.4 Neurological Effects 

Since 1,1-dichloroethane was once used as a gaseous anesthetic, it can be inferred that it causes central 

nervous system depression upon acute exposure. No information is available on the long-term neurologic 

effects of inhaled 1,1-dichloroethane in humans. 

No studies were located regarding neurologic effects in animals after inhalation exposure to 1,1-dichloroethane. 

3.2.1.5 Reproductive Effects 

No studies were located regarding developmental effects in humans or animals following inhalation 

exposure to 1,1-dichloroethane. 

3.2.1.6 Developmental Effects 

No studies were located regarding reproductive effects in humans following inhalation exposure to 

1,1-dichloroethane. 

One study examined the developmental toxic potential of 1,1-dichloroethane following inhalation 

exposure. No alterations in litter size, fetal resorptions, fetal growth, or incidences of gross or soft tissue 

anomalies were observed in the offspring of Sprague-Dawley rats exposed to 3,800 or 6,000 ppm 

7 hours/day on gestation days 6–15 (Schwetz et al. 1974). A significant increase in the incidence of 

fetuses with delayed ossification of sternebrae was observed at 6,000 ppm. Maternal food consumption 

and body weight were significantly reduced in the treated animals during the exposure period but returned 

to normal by day 21 of gestation; on gestation day 3, dams in the 3,800 and 6,000 ppm groups weighed 

8 and 11% less than controls, respectively. No other adverse effects were noted in the dams. Based on 

the observed effects, the LOAEL value for the developmental toxicity of 1,1-dichloroethane in rats was 

6,000 ppm; the NOAEL was 3,800 ppm. These values are listed in Table 3-1 and plotted in Figure 3-1. 
 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 21 

3. HEALTH EFFECTS 

3.2.1.7 Cancer 

No studies were located regarding cancer in humans or animals after inhalation exposure to 1,1-dichloroethane. 

3.2.2 Oral Exposure 

Two studies were located that investigated the health effects associated with oral exposure to 1,1-dichloroethane in rats and mice (Klaunig et al. 1986; NCI 1977). With the exception of body weight 

depression observed in one subchronic range-finding study, neither one provided any conclusive evidence 

of adverse toxic effects associated with oral exposure to 1,1-dichloroethane. 

Table 3-2 and Figure 3-2 describe the health effects observed in laboratory animals associated with oral 

exposure levels at varying time and exposure durations. No MRLs to humans for adverse effects (other 

than cancer) were calculated for the oral route of exposure because of the limited database. 

3.2.2.1 Death 

No studies were located regarding death in humans following oral exposure to 1,1-dichloroethane. 

Secondary sources report the following oral LD50 values in rats: 725 mg/kg (Lewis 2004) and 14.1 g/kg 

(Archer 1978). Since these values were obtained from secondary sources, no details were available to 

assess the quality of these data. Survival was poor in both treated and control rats and mice in the chronic 

bioassay conducted by the National Cancer Institute (NCI 1977), but a significant dose-related trend for 

mortality was noted in the male rats and mice. The deaths could not be attributed to cancer or any other 

non-neoplastic lesions, although pneumonia was observed in a large percentage of the rats, and this was 

thought to be related to the increased mortality (NCI 1977). 

The highest NOAEL values and all reliable LOAEL values for death in each species and duration 

category are recorded in Table 3-2 and plotted in Figure 3-2. 
265

3160

268

5620

264

562 1000

269

465465465465

267

2885

Table 3-2 Levels of Significant Exposure to 1,1-Dichloroethane - Oral 

a 

Key to 

Figure 

Species 

(Strain) 

Exposure/ 

Duration/ 

Frequency 

(Route) System 

NOAEL 

(mg/kg/day) 

Less Serious 

(mg/kg/day) 

LOAEL 

Serious 

(mg/kg/day) 

Reference Chemical Form 

INTERMEDIATE EXPOSURE Death 

1 Rat 

(OsborneMendel) 

5 d/wk 6 wk (GO) 

3160 F (2/5 rats died) NCI 1977 

1,1-DCE 

2 Mouse 

(B6C3F1) 

5 d/wk 6 wk (GO) 

5620 (4/10 deaths) NCI 1977 

1,1-DCE 

Systemic 

3 Rat 

(OsborneMendel) 

5 d/wk 6 wk (GO) 

Bd Wt 562 M (16% decreased body 

weight gain) 

1000 M (29% decreased body 

weight gain) 

NCI 1977 1,1-DCE 

4 Mouse 

(B6C3F1) 

daily 52 wk (W) 

Resp 

Hepatic Renal Bd Wt 

465 M 

465 M 

465 M 465 M 

Klaunig et al. 1986 1,1-DCE 

5 Mouse 

(B6C3F1) 

5 d/wk 6 wk (GO) 

Bd Wt 2885 M NCI 1977 

1,1-DCE 
259

764764764764764764764764764

261

288528852885288528852885288528852885

Table 3-2 Levels of Significant Exposure to 1,1-Dichloroethane - Oral (continued) Exposure/ 

Duration/

a Frequency Key to Species (Route) Figure (Strain) 

CHRONIC EXPOSURE Systemic 

6 Rat 5 d/wk 

78 wk (OsborneMendel) (GO)

7 Mouse 5 d/wk 

78 wk (B6C3F1) (GO) 

System 

Resp Cardio Hemato Musc/skel Hepatic Renal Endocr Dermal Bd Wt Resp Cardio Gastro Musc/skel Hepatic Renal Endocr Dermal Bd Wt 

LOAEL 

NOAEL Less Serious Serious Reference

(mg/kg/day) (mg/kg/day) (mg/kg/day) Chemical Form 

764 M NCI 1977 

1,1-DCE 

764 M 

764 M 764 M 764 M 764 M 

764 M 

764 M 764 M 

2885 M NCI 1977 

1,1-DCE 

2885 M 

2885 M 2885 M 2885 M 2885 M 

2885 M 

2885 M 2885 M 

a The number corresponds to entries in Figure 3-2. Bd Wt = body weight; Cardio = cardiovascular; d = day(s); Endocr = endocrine; F = Female; Gastro = gastrointestinal; (GO) = gavage in oil; Hemato = hematologicaLOAEL = lowest-observed-adverse-effect level; M = male; Musc/skel = musculoskeletal; NOAEL = no-observed-adverse-effect level; NS = not specified; Resp = resdrinking water; wk = week(s) 
Death 

RespiratHepatic Renal Body We 

ory 

ight 

Systemic 

mg/kg/day 

10000 

2m 

1r 

5m 

1000 3r 

3r 

4m 4m 4m 4m 

100 

r-Rat 

m-Mouse

 Cancer Effect Level-Animals

 LOAEL, More Serious-Animals

LOAEL, Less Serious-Animals

NOAEL - Animals

 Cancer Effect Level-Humans

 LOAEL, More Serious-Humans

LOAEL, Less Serious-Humans

NOAEL - Humans

 LD50/LC50

Minimal Risk Level

 for effects

 other than

 Cancer 


	


	

Figure 3-2 Levels of Significant Exposure to 1,1-Dichloroethane - Oral 

Intermediate (15-364 days) 

1,1-DICHLOROETHANE 3. HEALTH EFFECTS 24
mg/kg/day Respirator

CardiovasGastrointeHematologMusculoskHepatic Renal Endocrine Dermal Body Weig

10000 

7m 7m 7m 7m 7m 7m 7m 7m 7m 

1000 

6r 6r 6r 6r 6r 6r 6r 6r 6r 

100 

r-Rat 

m-Mouse

 Cancer Effect Level-Animals

 LOAEL, More Serious-Animals

LOAEL, Less Serious-Animals

NOAEL - Animals

 Cancer Effect Level-Humans

 LOAEL, More Serious-Humans

LOAEL, Less Serious-Humans

NOAEL - Humans

 LD50/LC50

Minimal Risk Level

 for effects

 other than

 Cancer 

y 

cul

sti

ica

ele

ht 


 

ar 

nal 

l 

tal 

Figure 3-2 Levels of Significant Exposure to 1,1-Dichloroethane - Oral (Continued)
 

Chronic (≥365 days) 

Systemic 

1,1-DICHLOROETHANE 3. HEALTH EFFECTS 25
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 26 

3. HEALTH EFFECTS 

3.2.2.2 Systemic Effects 

No studies were located regarding systemic effects in humans following oral exposure to 1,1-dichloroethane. 

There were no treatment-related histopathological changes in the liver, kidneys, or other tissues of the rats 

examined in the NCI (1977) study. Similarly, no histopathological alterations were noted in the liver, 

kidneys, or lungs of male mice that ingested relatively high levels of 1,1-dichloroethane in drinking water 

(up to 2500 mg/L) for 52 weeks (Klaunig et al. 1986). 

Respiratory Effects. No histological alterations were observed in the lungs of mice exposed to 

465 mg/kg/day 1,1-dichloroethane in drinking water for 52 weeks (Klaunig et al. 1986). Similarly, no 

significant alterations in respiratory tract lesions were observed in rats or mice chronically exposed to 

1,1-dichloroethane for 78 weeks (NCI 1977). The highest gavage doses were 764 and 950 mg/kg/day 

(5 days/week) in male and female rats, respectively, and 2,885 and 3,331 mg/kg (5 days/week) in male 

and female mice, respectively. 

Cardiovascular Effects. The NCI (1977) chronic-duration gavage study did not find significant 

alterations in the incidence of lesions in the cardiovascular system. 

Gastrointestinal Effects. No gastrointestinal effects were reported in rats or mice administered 

gavage doses of 1,1-dichloroethane for 78 weeks (NCI 1977). 

Hematological Effects. No histological alterations were observed in hematological tissues in rats or 

mice chronically exposed to 1,1-dichloroethane (NCI 1977); however, the study did not examine the 

potential for alterations in erythrocyte or leukocyte counts or hemoglobin levels. 

Musculoskeletal Effects. No musculoskeletal alterations were reported in the NCI (1977) chronic 

study of rats and mice. 

Hepatic Effects. No nonneoplastic alterations were observed in mice exposed to 465 mg/kg/day via 

drinking water for 52 weeks (Klaunig et al. 1986) or in rats or mice administered 764/950 mg/kg/day or 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 27 

3. HEALTH EFFECTS 

2,885/3,331 mg/kg/day 1,1-dichloroethane, respectively, via gavage 5 days/week for 78 weeks (NCI 

1977). 

Renal Effects. Intermediate-duration drinking exposure of mice (Klaunig et al. 1986) or chronic 

gavage administration to rats and mice (NCI 1977) did not result in significant alteration in the occurrence 

of renal lesions. 

Endocrine Effects. No histological alterations in endocrine tissues were observed in rats or mice 

chronically administered 1,1-dichloroethane (NCI 1977). 

Dermal Effects. No dermal effects were noted in rats or mice administered 1,1-dichloroethane for 

78 weeks (NCI 1977). 

Ocular Effects. No eye damage was noted in rats or mice following chronic administration of 

1,1-dichloroethane (NCI 1977). 

Body Weight Effects. Administration of doses as high as 562 mg/kg/day in male rats and 

1,780 mg/kg/day in female rats 5 days/week for 6 weeks resulted in decreases in body weight gain 

(≥16%) (NCI 1977); no alterations in body weight were observed in mice similarly exposed to doses as 

high as 10,000 mg/kg/day (NCI 1977). This study did not find significant decreases in body weight gain 

following 78 weeks of exposure (5 days/week) to 764 and 950 mg/kg/day, respectively, in male and 

female rats and 2,885 and 3,331 mg/kg/day, respectively, in male and female mice (NCI 1977). 

Similarly, no alterations in body weight gain were observed in mice exposed to 465 mg/kg/day in 

drinking water for 52 weeks (Klaunig et al. 1986). 

No studies were located regarding the following health effects in humans or animals following oral 

exposure to 1,1-dichloroethane: 

3.2.2.3 Immunological and Lymphoreticular Effects 

3.2.2.4 Neurological Effects 

3.2.2.5 Reproductive Effects 

3.2.2.6 Developmental Effects 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 28 

3. HEALTH EFFECTS 

3.2.2.7 Cancer 

No studies were located regarding carcinogenic effects in humans following oral exposure to 

1,1-dichloroethane. The results of the bioassay conducted by NCI (1977) suggest carcinogenic effects 

induced by 1,1-dichloroethane in rats and mice. A significant positive dose-related trend was observed 

for the incidence of hemangiosarcomas and mammary adenocarcinomas in female rats, hepatocellular 

carcinoma in male mice, and endometrial stromal polyps in female mice. However, only the incidence of 

endometrial stromal polyps in female mice exposed to 3,331 mg/kg/day, 5 days/week was significantly 

increased over the corresponding control animals. When only male mice surviving at least 52 weeks were 

examined, there was a significant increase in the incidence of hepatocellular carcinomas in the 

2,885 mg/kg/day group. There are several limitations to this study. Survival was poor in both treated and 

control animals, thereby limiting the validity of these results. Although survival was significantly lower 

in the exposed groups, it is not clear that the increase in mortality was treatment-related. Furthermore, 

there were no other treatment-related effects on body weight, clinical signs, or the incidence of nonneoplastic lesions. Because of the high mortality in both the treated and control animals, the authors 

concluded that not enough animals survived to be at risk for late-developing tumors. Thus, though the 

results of this bioassay suggest that 1,1-dichloroethane is carcinogenic to rats and mice, the evidence is 

not conclusive. 

The carcinogenicity of 1,1-dichloroethane was also examined in mice exposed to 155 or 465 mg/kg/day 

of the compound in the drinking water for 52 weeks (Klaunig et al. 1986). A two-stage carcinogenesis 

protocol was also employed in this study to assess the ability of 1,1-dichloroethane to act as a tumor 

promoter. Neither 1,1-dichloroethane-treated animals initiated with diethylnitrosamine (DENA) or 

animals treated with 1,1-dichloroethane without initiation showed a significant increase in the incidence 

of lung or liver tumors over their corresponding controls. However, the conclusion that 1,1-dichloroethane is not a tumor promoter may not be entirely justified since a maximal response was observed in 

terms of tumor incidence in the DENA-alone-treated mice (100% tumor incidence at 52 weeks). 

Therefore, an increase in the incidence of liver tumors due to 1,1-dichloroethane following DENA 

initiation, if it existed, could not have been detected. Furthermore, since measurement of water 

consumption and replenishment were only done once a week, there was no way to determine the extent, if 

any, evaporation contributed to loss of the test chemical and affected the reported level of exposure. 

However, precautions were taken to minimize the loss of test chemical during the 1-week period; amber 

bottles with Teflon stoppers and double sipper tubes were used. Since 1,1-dichloroethane is a volatile 
 

 

 

 

 

1,1-DICHLOROETHANE 29 

3. HEALTH EFFECTS 

chemical, this may present a limitation to the interpretation of results obtained from drinking water 

administration. 

The difference in results (e.g., induction of liver tumors) between the NCI (1977) and Klaunig et 

al. (1986) studies may be due to the method of administration, vehicle, and/or doses used. The 

pharmacokinetics of 1,1-dichloroethane may vary considerably when administered in drinking water ad 

libitum over a week as compared to bolus doses given in corn oil. Evidence obtained with carbon 

tetrachloride indicates that corn oil likely acts as a reservoir in the gut to delay and diminish the systemic 

absorption of the lipophilic chemical, while such a chemical is probably rapidly absorbed when ingested 

in water (Kim et al. 1990a, 1990b). Furthermore, the doses given to mice by gavage were approximately 

6 times higher than the drinking water concentrations. Sufficient information is not available to assess the 

contributions of these factors to the apparently disparate responses. 

Milman et al. (1988) examined the carcinogenic potential of 1,1-dichloroethane in initiation and 

promotion assays. In partially hepatectomized Osborne-Mendel rats receiving a single gavage dose of 

700 mg/kg 1,1-dichloroethane in corn oil followed by dietary exposure to phenobarbitol for 7 weeks, 

there were no alterations in gamma-glutamyltranspeptidase (GGT)-altered foci. However, in the 

promotion assay in which partially hepatecomized Osborne-Mendel rats received an intraperitoneal dose 

of diethylnitrosamine followed by gavage administration of 700 mg/kg 1,1-dichloroethane in corn oil 

5 days/week for 7 weeks, there was an increase in the total number of GGT-altered foci. 

3.2.3 Dermal Exposure 

No studies were located regarding the following health effects in humans or animals after dermal 

exposure to 1,1-dichloroethane: 

3.2.3.1 Death 

3.2.3.2 Systemic Effects 

3.2.3.3 Immunological and Lymphoreticular Effects 

3.2.3.4 Neurological Effects 

3.2.3.5 Reproductive Effects 

3.2.3.6 Developmental Effects 

3.2.3.7 Cancer 
 

 


 


 


 


 

1,1-DICHLOROETHANE 30 

3. HEALTH EFFECTS 

Table 3-3. Genotoxicity of 1,1-Dichloroethane In Vitro 

Results 

With Without 

Species (test system) End point activation activation Reference 

Prokaryotic organisms: 

Salmonella typhimuriu,m strains Gene mutation – – Nohmi et al. 1986 

TA97, TA98, TA100, and TA102 

(Ames assay) 

S. typhimurium, strains TA1535, Gene mutation – – Simmon et al. 1977 

TA1537, TA1538, TA98, and 

TA100 (Ames assay) 

S. typhimurium, strains TA1537, Gene mutation + + Riccio et al. 1983 

TA98, TA100, and TA1535 

(dessicator assay; vapor exposure) 

S. typhimurium, strains TA1535, Gene mutation + + Milman et al. 1988 

TA98, and TA100 (Ames assay; 

dessicator) 

Eukaryotic organisms: 

Saccharomyces cerevisiae D7 Gene mutation – – Bronzetti et al. 1987 

Mammalian cells 

Syrian hamster embryo (cell DNA viral No data + Hatch et al. 1983 

transformation assay; vapor transformation 

exposure) 

Osborne-Mendel rat and B6C3F1 DNA repair No data + Milman et al. 1988 

mouse hepatocytes 

BALB/C-3T3 (cell transformation Cell transformation No data – Tu et al. 1985 

assay; exposure in sealed 

chamber) 

BALB/C-3T3 (cell transformation Cell transformation No data – Milman et al. 1998 

assay; exposure in sealed 

chamber) 

Chinese hamster lung fibroblasts Chromosomal – – Matsuoka et al. 

(chromosomal aberration assay; aberrations 1998) 

exposure in sealed chamber) 

C = negative result; + = positive result; ± = weakly positive 
 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 31 

3. HEALTH EFFECTS 

3.3 GENOTOXICITY 

A limited number of studies have examined the genotoxicity of 1,1-dichloroethane. No studies were 

located regarding in vivo genotoxic effects in humans. The genotoxic potential of 1,1-dichloroethane has 

been investigated in vitro in bacteria, fungus, and mammalian systems; the results of these studies are 

summarized in Table 3-3. 1,1-Dichloroethane did not result in an increase in reverse mutations in 

Salmonella typhimurium strains with or without metabolic activation in Ames assays (Nohmi et al. 1985; 

Simmon et al. 1977). In contrast, Riccio et al. (1983, as reported in an abstract) and Milman et al. (1988) 

reported positive mutagenic alterations in S. typhimurium exposed to 1,1-dichloroethane vapor in a 

desiccator assay in the presence and absence of S9 mix. Negative findings for mutagenicity were 

observed in Saccharomyes cerevisiae exposed to 1,1-dichloroethane, with or without metabolic activation 

(Bronzetti et al. 1987). 

Similarly, negative genotoxicity results have been observed in mammalian cell assays. In vitro exposure 

to 1,1-dichloroethane did not induce increases in cell transformations in BALB/C-3T3 cells (Milman et al. 

1988; Tu et al. 1985) or chromosomal aberrations in Chinese hamster lung fibroblasts (Matsuoka et al. 

1998). However, an increase in Simian adenovirus (SA7)-induced transformations was observed in 

Syrian hamster embryo cells (Hatch et al. 1983) and an increase in DNA repair was found in hepatocytes 

from Osborne-Mendel rats and B6C3F1 mice (Milman et al. 1988). 

In an in vivo study by Colacci et al. (1985), 1,1-dichloroethane (98% purity) was found covalently bound 

to nucleic acids and proteins from liver, lung, kidney, and stomach of male rats and mice 22 hours 

following a single intraperitoneal injection of approximately 1.2 mg/kg. In vitro binding of 

1,1-dichloroethane to nucleic acids and proteins was mediated by liver P-450 dependent microsomal 

mixed function oxidase system. Glutathione-S-transferase (GSH) shifted the equilibrium of the 

enzymatic reaction and thereby decreased binding, presumably by reducing the amount of toxic 

metabolite available for binding to macromolecules. On the other hand, phenobarbitone increased 

binding by increasing cytochrome P-450 activity, thus generating more toxic metabolites available for 

binding to macromolecules. Presumably, the metabolites generated from P-450 enzymatic action on 

1,1-dichloroethane bind to cellular macromolecules. Lung microsomes were weakly effective whereas 

kidney and stomach microsomal fractions were ineffective. Therefore, the binding to macromolecules of 

various organs detected in vivo may have been due to a stable hepatic metabolite that was circulated to 

reach extrahepatic organs. Pretreatment with phenobarbitone enhanced the binding to DNA, microsomal 

RNA and proteins while addition of glutathione-s-transferase to the microsomal systems caused 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 32 

3. HEALTH EFFECTS 

suppression of binding. Because only radioactivity was measured it is difficult to determine whether the 

μmole bound represents 1,1-dichloroethane or its metabolite(s). However, the fact that binding is 

enhanced with induction of P-450 suggests that it represents the metabolite(s). Thus, GSH appears to 

play a detoxification role in the metabolism of 1,1-dichloroethane. The fact that 1,1-dichloroethane binds 

to nucleic acid suggests that it may have a potential to produce mutation in a mammalian system. 

3.4 TOXICOKINETICS 

3.4.1 Absorption 

3.4.1.1 Inhalation Exposure 

No studies were located in humans or animals regarding the absorption of inhaled 1,1-dichloroethane. 

However, its use as a gaseous anesthetic agent in humans provides evidence of its absorption. 

Furthermore, the volatile and lipophilic nature of 1,1-dichloroethane favors pulmonary absorption. 

Structurally related chlorinated aliphatics and gaseous anesthetics are known to be rapidly and extensively 

absorbed from the lung. The total amount absorbed from the lungs will be directly proportional to the 

concentration in inspired air, the duration of exposure, the blood/air partition coefficient of 

1,1-dichloroethane, its solubility in tissues, and the individual's ventilation rate and cardiac output. One 

of the most important factors controlling pulmonary absorption is the blood/air partition coefficient of the 

chemical. The concentration of the chemical and the duration of exposure are also important 

determinants of the extent of systemic absorption. 

It is known that an isomer of 1,1-dichloroethane, 1,2-dichloroethane, is well-absorbed following 

inhalation exposure. However, the blood/air partition coefficient for 1,2-dichloroethane is approximately 

4 times that of 1,1-dichloroethane. This suggests that 1,1-dichloroethane would not be absorbed into the 

blood from air as readily as 1,2-dichloroethane, but it will still be well absorbed from the lung (Sato and 

Nakajima 1987). 

3.4.1.2 Oral Exposure 

No studies were located that quantitated the absorption of ingested 1,1-dichloroethane in humans or 

animals. However, when 700 mg [14C]-1,1-dichloroethane/kg was orally administered to rats and mice, 

absorption was evidenced by the presence of radiolabel in expired air and the presence of radiolabeled 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 33 

3. HEALTH EFFECTS 

metabolites in urine, although there was no quantitative assessment made of the extent or rate of 

absorption (Mitoma et al. 1985). 

3.4.1.3 Dermal Exposure 

No studies were located regarding the absorption of 1,1-dichloroethane in humans or animals following 

dermal exposure. However, Reid and Muianga (2012) reported evidence that 1,1-dichloroethane 

penetrates the skin. 1,1-Dichloroethane was applied to the shaved abdominal skin of rabbits that were 

fitted with masks to prevent inhalation of the compound. Exhaled air from the rabbits was passed into 

pure alcohol, and the presence of halogen was tested by flaming a copper wire introduced into it. The 

green color observed after 1 hour indicated that the halogen ion was absorbed into the bloodstream, 

although no quantitative assessment of the extent or rate of absorption was possible. 

3.4.2 Distribution 

3.4.2.1 Inhalation Exposure 

No studies were located in humans or animals regarding the distribution of 1,1-dichloroethane following 

inhalation exposure. However, since this chemical was once used as a gaseous anesthetic, it can be 

assumed that it is distributed to the central nervous system as well as to the other tissues of the body. 

Tissue uptake of halocarbons such as 1,1-dichloroethane is governed by the affinity of each tissue for the 

lipophilic chemical (i.e., the higher the lipid content of a tissue, the greater its uptake of 1,1-dichloroethane) (Sato and Nakajima 1987). 

3.4.2.2 Oral Exposure 

No studies were located regarding the distribution of 1,1-dichloroethane following oral exposure in 

humans or animals. 

3.4.2.3 Dermal Exposure 

No studies were located regarding the distribution of 1,1-dichloroethane following dermal exposure in 

humans or animals. 
 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 34 

3. HEALTH EFFECTS 

3.4.2.4 Other Routes of Exposure 

Rats and mice were intraperitoneally injected with 1.2 mg [14C]-1,1-dichloroethane/kg and sacrificed 

22 hours later. 1,1-Dichloroethane was covalently bound to proteins, RNA, and DNA of liver, kidney, 

lung, and stomach. The extent of binding was greatest in the tissue proteins and least in the DNA. 

Binding to rat and mouse DNA was greatest in the stomach and liver, respectively (Colacci et al. 1985). 

Although distribution of 1,1-dichloroethane very likely occurs to other tissues, the liver, kidney, lung, and 

stomach were the only tissues analyzed in this study. 

3.4.3 Metabolism 

The metabolism of 1,1-dichloroethane has not been extensively characterized. In vivo studies of the 

metabolism of 1,1-dichloroethane in humans and animals are very limited. Elucidation of 1,1-dichloroethane's metabolic scheme to date is primarily based on in vitro studies. In general, the identification of 

specific metabolites and the monitoring of enzyme activities indicate that the biotransformation of 

1,1-dichloroethane is mediated by hepatic microsomal cytochrome P-450 system. 

In rats and mice orally administered 700 or 1,800 mg/kg, respectively, 1,1-dichloroethane (5 days/week 

for 4 weeks followed by a single dose of radiolabelled 1,1-dichloroethane), most of the radiolabel was 

detected in expired air; the investigators assumed that this was parent compound (Mitoma et al. 1985). 

Forty-eight hours after oral administration, 7.4 and 29.3% of the radiolabel was detected in the urine, 

carcass, or expired carbon dioxide. The investigators assumed that this represented metabolized 

1,1-dichloroethane; however, only radiolabel was measured in the carcass. It is likely that the ingested 

radiolabeled 1,1-dichloroethane underwent first-pass extraction by the liver. It is possible that high doses 

used in this study exceeded the capacity of the animals to metabolize 1,1-dichloroethane. The 

radiolabeled compound that was not excreted unchanged in the expired air was probably largely 

metabolized in the liver, followed by subsequent redistribution of labeled metabolites to other organs 

prior to their excretion. 

An in vitro study demonstrated cytochrome P450 metabolism of 1,1-dichloroethane. McCall et al. (1983) 

demonstrated 1,1-dichloroethane binding to hepatic microsomal cytochrome P450 from rats; as compared 

to microsomes from untreated rats, cytochrome P450 binding was 2.25 times higher, per mole of 

cytochrome, in microsomes from phenobarbital-stimulated rats. Administration of β-naphthaflavone had 

no effect on the extent of 1,1-dichloroethane binding to cytochrome P450 binding. In vitro exposure of 

hepatic microsomal to 1,1-dichloroethane also stimulated NADPH oxidation. The rate and extent of 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 35 

3. HEALTH EFFECTS 

1,1-dichloroethane metabolism was increased 6.3 times in the hepatic microsomes of rats that were 

induced by chronic ethanol consumption (Sato et al. 1980). 

Metabolism of 1,1-dichloroethane by hepatic microsomes resulted in the production of acetic acid as the 

major metabolite and 2,2-dichloroethanol, mono-, and dichloroacetic acid as minor metabolites 

(Table 3-4) (McCall et al. 1983). On the basis of these results, pathways for the metabolism of 

1,1-dichloroethane were proposed (Figure 3-3). The initial steps in the metabolism of 1,1-dichloroethane 

were proposed to involve cytochrome P-450-dependent hydroxylations at either carbon. Hydroxylation at 

C-1 would result in the production of an unstable alpha-haloalcohol, which can lose HCl to yield acetyl 

chloride. An alternative, but less favorable reaction, would be a chlorine shift to yield chloroacetyl 

chloride. These acyl chlorides can react with water to generate free acids or react with cellular 

constituents. Hydroxylation at C-2 would produce 2,2-dichloroethanol, which would undergo subsequent 

oxidation to dichloroacetaldehyde and dichloroacetic acid (McCall et al. 1983). 

Chloroethanes have been shown to undergo dechlorination by an enzyme system that is similar to the 

hepatic microsomal mixed function oxidase system (Van Dyke and Wineman 1971). Dechlorination was 

inducible by phenobarbital and required oxygen and NADPH. However, dechlorination also required a 

factor from the cytosolic fraction of the liver homogenate for optimal dechlorinating activity. In terms of 

structural requirements, dechlorination was enhanced if the carbon atom containing the chlorine had only 

one hydrogen. In a microsomal incubation, 13.5% of the 36Cl of 1,1-dichloroethane was enzymatically 

removed after 30 minutes, while <0.5% of the 36Cl of 1,2-dichloroethane was removed (Van Dyke and 

Wineman 1971). 

Under hypoxic conditions, 1,1-dichloroethane gives rise to free radicals. However, its ability to develop 

free radicals is much less when compared to other chlorinated hydrocarbons like trichloroethane and 

carbon tetrachloride. It has been suggested that these free radicals possess the potential to induce toxic 

and carcinogenic effects. There is no correlation between the ease of free radical activation, covalent 

binding formation, or carcinogenic potency (Tomasi et al. 1984). 
 

 


 


 


 

1,1-DICHLOROETHANE 36 

3. HEALTH EFFECTS 

Table 3-4. Production of Metabolites from 1,1-Dichloroethane with Hepatic 

Microsomes from Phenobarbital-Induced Rats
 

Metabolic productiona
 

Metabolites (nmoles/mg microsomal protein/20 minutes)
 

Acetic acid 179 (15) 

2,2-Dichloroethane 0.12 (0.02) 

Chloroacetic acid 0.22 (0.08) 

Dichloroacetic acid 0.048 (0.005) 

Chloroacetaldehyde <0.07 (0.03) 

aValues represent means (standard deviation) for determinations in triplicate on three to five separate preparations of 

hepatic microsomes. 

Source: McCall et al. 1983 
 

 

1,1-DICHLOROETHANE 37 

3. HEALTH EFFECTS 

Figure 3-3. Proposed Metabolic Scheme for 1,1-Dichloroethane 

Cl2HCCH3 Cl2HCCH2OH 

P450 

(C-1) 

2,2-dichloroethanol 

C 

O 

Cl2HC H 

dichloroacetaldehyde 

C 

O 

Cl2HC OH

dichloroacetic acid 

[HOCl2CCH3] 

alpha-haloalcohol 

chlorine 

shift 

C 

O 

[ClCH2 Cl] 

chloroacetyl 

chloride 

-HCl 

H2O 

C 

O 

ClCH2 OH 

monochloroacetic 

acid 

-HCl 

C 

O 

[Cl CH3] 

acetyl 

chloride 

-HCl 

H2O 

CH3COOH 

acetic 

acid 

Source: McCall et al. 1983 

P450 (C-2) 
 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 38 

3. HEALTH EFFECTS 

3.4.4 Elimination and Excretion 

3.4.4.1 Inhalation Exposure 

No empirical data on the elimination of excretion of 1,1-dichloroethane in humans or animals were 

identified. Sato and Nakajima (1987) predicted that 59% of inhaled 1,1-dichloroethane would be 

metabolized and excreted in the urine and 41% would be eliminated in expired air. 

3.4.4.2 Oral Exposure 

Mitoma et al. (1985) examined excretion of 1,1-dichloroethane in rats and mice administered 

1,1-dichloroethane via gavage 700 or 1,800 mg/kg, respectively, 5 days/week for 4 weeks followed by a 

single dose of radiolabelled 1,1-dichloroethane. In the rats, 86% of the administered dose was excreted in 

expired air 5% expired as carbon dioxide and 0.9% was detected in the urine. In mice, 70% was excreted 

in expired air, 25% was expired as carbon dioxide, and 1.6% was detected in urine. Because rats and 

mice were administered different doses, a determination cannot be made as to whether the differences in 

excretion and metabolism are due to species differences or are a reflection of different doses. 

3.4.4.3 Dermal Exposure 

No studies were located in humans or animals regarding excretion of 1,1-dichloroethane following dermal 

exposure 

3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models 

Physiologically based pharmacokinetic (PBPK) models use mathematical descriptions of the uptake and 

disposition of chemical substances to quantitatively describe the relationships among critical biological 

processes (Krishnan et al. 1994). PBPK models are also called biologically based tissue dosimetry 

models. PBPK models are increasingly used in risk assessments, primarily to predict the concentration of 

potentially toxic moieties of a chemical that will be delivered to any given target tissue following various 

combinations of route, dose level, and test species (Clewell and Andersen 1985). Physiologically based 

pharmacodynamic (PBPD) models use mathematical descriptions of the dose-response function to 

quantitatively describe the relationship between target tissue dose and toxic end points. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 39 

3. HEALTH EFFECTS 

PBPK/PD models refine our understanding of complex quantitative dose behaviors by helping to 

delineate and characterize the relationships between: (1) the external/exposure concentration and target 

tissue dose of the toxic moiety, and (2) the target tissue dose and observed responses (Andersen and 

Krishnan 1994; Andersen et al. 1987). These models are biologically and mechanistically based and can 

be used to extrapolate the pharmacokinetic behavior of chemical substances from high to low dose, from 

route to route, between species, and between subpopulations within a species. The biological basis of 

PBPK models results in more meaningful extrapolations than those generated with the more conventional 

use of uncertainty factors. 

The PBPK model for a chemical substance is developed in four interconnected steps: (1) model 

representation, (2) model parameterization, (3) model simulation, and (4) model validation (Krishnan and 

Andersen 1994). In the early 1990s, validated PBPK models were developed for a number of 

toxicologically important chemical substances, both volatile and nonvolatile (Krishnan and Andersen 

1994; Leung 1993). PBPK models for a particular substance require estimates of the chemical substancespecific physicochemical parameters, and species-specific physiological and biological parameters. The 

numerical estimates of these model parameters are incorporated within a set of differential and algebraic 

equations that describe the pharmacokinetic processes. Solving these differential and algebraic equations 

provides the predictions of tissue dose. Computers then provide process simulations based on these 

solutions. 

The structure and mathematical expressions used in PBPK models significantly simplify the true 

complexities of biological systems. If the uptake and disposition of the chemical substance(s) are 

adequately described, however, this simplification is desirable because data are often unavailable for 

many biological processes. A simplified scheme reduces the magnitude of cumulative uncertainty. The 

adequacy of the model is, therefore, of great importance, and model validation is essential to the use of 

PBPK models in risk assessment. 

PBPK models improve the pharmacokinetic extrapolations used in risk assessments that identify the 

maximal (i.e., the safe) levels for human exposure to chemical substances (Andersen and Krishnan 1994). 

PBPK models provide a scientifically sound means to predict the target tissue dose of chemicals in 

humans who are exposed to environmental levels (for example, levels that might occur at hazardous waste 

sites) based on the results of studies where doses were higher or were administered in different species. 

Figure 3-4 shows a conceptualized representation of a PBPK model. 
 


 


 

1,1-DICHLOROETHANE 40 

3. HEALTH EFFECTS 

Figure 3-4. Conceptual Representation of a Physiologically Based
 

Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance
 

Inhaled chemical Exhaled chemical 

Lungs 

Liver 

Fat 

Slowly 

perfused 

tissues 

Richly 

perfused 

tissues 

Kidney 

Skin 

V 

E 

N 

O 

U 

S 

B 

L 

O 

O 

D 

A 

R 

T 

E 

R 

I 

A 

L 

B 

L 

O 

O 

D 

Vmax 

Km 

Ingestion 

GI 

Tract 

Feces 

Urine

 Chemicals 

contacting skin 

Note: This is a conceptual representation of a physiologically based pharmacokinetic (PBPK) model for a 

hypothetical chemical substance. The chemical substance is shown to be absorbed via the skin, by inhalation, or by 

ingestion, metabolized in the liver, and excreted in the urine or by exhalation. 

Source: adapted from Krishnan and Andersen 1994 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 41 

3. HEALTH EFFECTS 

If PBPK models for 1,1-dichloroethane exist, the overall results and individual models are discussed in 

this section in terms of their use in risk assessment, tissue dosimetry, and dose, route, and species 

extrapolations. 

No PBPK models were identified for 1,1-dichloroethane. 

3.5 MECHANISMS OF ACTION 

3.5.1 Pharmacokinetic Mechanisms 

No information was identified on the pharmacokinetic mechanisms of action of 1,1-dichloroethane. 

3.5.2 Mechanisms of Toxicity 

There are limited data to identify the critical targets of 1,1-dichloroethane toxicity or to elucidate the 

mode of action for the observed effects. 

3.5.3 Animal-to-Human Extrapolations 

The inhalation study by Hofmann et al. (1971) found species differences in the renal toxicity of 

1,1-dichloroethane. Crystalline precipitations and tubular obstruction were observed in cats, but not in 

rats, rabbits, or guinea pigs. There are insufficient data to determine whether this would also be a relevant 

end point in humans and whether humans would be as sensitive to this effect as cats. 

3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS 

Recently, attention has focused on the potential hazardous effects of certain chemicals on the endocrine 

system because of the ability of these chemicals to mimic or block endogenous hormones. Chemicals 

with this type of activity are most commonly referred to as endocrine disruptors. However, appropriate 

terminology to describe such effects remains controversial. The terminology endocrine disruptors, 

initially used by Thomas and Colborn (1992), was also used in 1996 when Congress mandated the EPA to 

develop a screening program for “...certain substances [which] may have an effect produced by a 

naturally occurring estrogen, or other such endocrine effect[s]...”. To meet this mandate, EPA convened a 

panel called the Endocrine Disruptors Screening and Testing Advisory Committee (EDSTAC), and in 

1998, the EDSTAC completed its deliberations and made recommendations to EPA concerning endocrine 

disruptors. In 1999, the National Academy of Sciences released a report that referred to these same types 
 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 42 

3. HEALTH EFFECTS 

of chemicals as hormonally active agents. The terminology endocrine modulators has also been used to 

convey the fact that effects caused by such chemicals may not necessarily be adverse. Many scientists 

agree that chemicals with the ability to disrupt or modulate the endocrine system are a potential threat to 

the health of humans, aquatic animals, and wildlife. However, others think that endocrine-active 

chemicals do not pose a significant health risk, particularly in view of the fact that hormone mimics exist 

in the natural environment. Examples of natural hormone mimics are the isoflavinoid phytoestrogens 

(Adlercreutz 1995; Livingston 1978; Mayr et al. 1992). These chemicals are derived from plants and are 

similar in structure and action to endogenous estrogen. Although the public health significance and 

descriptive terminology of substances capable of affecting the endocrine system remains controversial, 

scientists agree that these chemicals may affect the synthesis, secretion, transport, binding, action, or 

elimination of natural hormones in the body responsible for maintaining homeostasis, reproduction, 

development, and/or behavior (EPA 1997). Stated differently, such compounds may cause toxicities that 

are mediated through the neuroendocrine axis. As a result, these chemicals may play a role in altering, 

for example, metabolic, sexual, immune, and neurobehavioral function. Such chemicals are also thought 

to be involved in inducing breast, testicular, and prostate cancers, as well as endometriosis (Berger 1994; 

Giwercman et al. 1993; Hoel et al. 1992). 

No studies were located regarding endocrine disruption in [humans and/or animals] after exposure to 

1,1-dichloroethane. 

No in vitro studies were located regarding endocrine disruption of 1,1-dichloroethane. 

3.7 CHILDREN’S SUSCEPTIBILITY 

This section discusses potential health effects from exposures during the period from conception to 

maturity at 18 years of age in humans, when all biological systems will have fully developed. Potential 

effects on offspring resulting from exposures of parental germ cells are considered, as well as any indirect 

effects on the fetus and neonate resulting from maternal exposure during gestation and lactation. 

Relevant animal and in vitro models are also discussed. 

Children are not small adults. They differ from adults in their exposures and may differ in their 

susceptibility to hazardous chemicals. Children’s unique physiology and behavior can influence the 

extent of their exposure. Exposures of children are discussed in Section 6.6, Exposures of Children. 
 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 43 

3. HEALTH EFFECTS 

Children sometimes differ from adults in their susceptibility to hazardous chemicals, but whether there is 

a difference depends on the chemical (Guzelian et al. 1992; NRC 1993). Children may be more or less 

susceptible than adults to health effects, and the relationship may change with developmental age 

(Guzelian et al. 1992; NRC 1993). Vulnerability often depends on developmental stage. There are 

critical periods of structural and functional development during both prenatal and postnatal life, and a 

particular structure or function will be most sensitive to disruption during its critical period(s). Damage 

may not be evident until a later stage of development. There are often differences in pharmacokinetics 

and metabolism between children and adults. For example, absorption may be different in neonates 

because of the immaturity of their gastrointestinal tract and their larger skin surface area in proportion to 

body weight (Morselli et al. 1980; NRC 1993); the gastrointestinal absorption of lead is greatest in infants 

and young children (Ziegler et al. 1978). Distribution of xenobiotics may be different; for example, 

infants have a larger proportion of their bodies as extracellular water, and their brains and livers are 

proportionately larger (Altman and Dittmer 1974; Fomon 1966; Fomon et al. 1982; Owen and Brozek 

1966; Widdowson and Dickerson 1964). The fetus/infant has an immature (developing) blood-brain 

barrier that past literature has often described as being leaky and poorly intact (Costa et al. 2004). 

However, current evidence suggests that the blood-brain barrier is anatomically and physically intact at 

this stage of development, and the restrictive intracellular junctions that exist at the blood-CNS interface 

are fully formed, intact, and functionally effective (Saunders et al. 2008, 2012). 

However, during development of the blood-brain barrier, there are differences between fetuses/infants and 

adults which are toxicologically important. These differences mainly involve variations in physiological 

transport systems that form during development (Ek et al. 2012). These transport mechanisms (influx and 

efflux) play an important role in the movement of amino acids and other vital substances across the 

blood-brain barrier in the developing brain; these transport mechanisms are far more active in the 

developing brain than in the adult. Because many drugs or potential toxins may be transported into the 

brain using these same transport mechanisms—the developing brain may be rendered more vulnerable 

than the adult. Thus, concern regarding possible involvement of the blood-brain barrier with enhanced 

susceptibility of the developing brain to toxins is valid. It is important to note however, that this potential 

selective vulnerability of the developing brain is associated with essential normal physiological 

mechanisms; and not because of an absence or deficiency of anatomical/physical barrier mechanisms. 

The presence of these unique transport systems in the developing brain of the fetus/infant is intriguing; as 

it raises a very important toxicological question as to whether these mechanisms provide protection for 

the developing brain or do they render it more vulnerable to toxic injury. Each case of chemical exposure 
 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 44 

3. HEALTH EFFECTS 

should be assessed on a case-by-case basis. Research continues into the function and structure of the 

blood-brain barrier in early life (Kearns et al. 2003; Saunders et al. 2012; Scheuplein et al. 2002). 

Many xenobiotic metabolizing enzymes have distinctive developmental patterns. At various stages of 

growth and development, levels of particular enzymes may be higher or lower than those of adults, and 

sometimes unique enzymes may exist at particular developmental stages (Komori et al. 1990; Leeder and 

Kearns 1997; NRC 1993; Vieira et al. 1996). Whether differences in xenobiotic metabolism make the 

child more or less susceptible also depends on whether the relevant enzymes are involved in activation of 

the parent compound to its toxic form or in detoxification. There may also be differences in excretion, 

particularly in newborns who have a low glomerular filtration rate and have not developed efficient 

tubular secretion and resorption capacities (Altman and Dittmer 1974; NRC 1993; West et al. 1948). 

Children and adults may differ in their capacity to repair damage from chemical insults. Children also 

have a longer remaining lifetime in which to express damage from chemicals; this potential is particularly 

relevant to cancer. 

Certain characteristics of the developing human may increase exposure or susceptibility, whereas others 

may decrease susceptibility to the same chemical. For example, although infants breathe more air per 

kilogram of body weight than adults breathe, this difference might be somewhat counterbalanced by their 

alveoli being less developed, which results in a disproportionately smaller surface area for alveolar 

absorption (NRC 1993). 

Information on children’s susceptibility to the toxic effects of 1,1-dichloroethane is limited to a 

developmental toxicity study in rats (Schwetz et al. 1974) that found an increase in the incidence of 

delayed ossifications in the fetuses of dams exposed to 6,000 ppm 1,1-dichloroethane on gestation 

days 6–15. An in vitro study (Andrews et al. 2002; only available as an abstract) utilizing rat whole 

embryo cultures reported eye defects in at 17.9 mM; this concentration also reported in 35% 

embryolethality. 

3.8 BIOMARKERS OF EXPOSURE AND EFFECT 

Biomarkers are broadly defined as indicators signaling events in biologic systems or samples. They have 

been classified as markers of exposure, markers of effect, and markers of susceptibility (NAS/NRC 

1989). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 45 

3. HEALTH EFFECTS 

The National Report on Human Exposure to Environmental Chemicals provides an ongoing assessment 

of the exposure of the U.S. population to environmental chemicals using biomonitoring. This report is 

available at http://www.cdc.gov/exposurereport/. The biomonitoring data for 1,1-dichloroethane from 

this report is discussed in Section 6.5. A biomarker of exposure is a xenobiotic substance or its 

metabolite(s) or the product of an interaction between a xenobiotic agent and some target molecule(s) or 

cell(s) that is measured within a compartment of an organism (NAS/NRC 1989). The preferred 

biomarkers of exposure are generally the substance itself, substance-specific metabolites in readily 

obtainable body fluid(s), or excreta. However, several factors can confound the use and interpretation of 

biomarkers of exposure. The body burden of a substance may be the result of exposures from more than 

one source. The substance being measured may be a metabolite of another xenobiotic substance (e.g., 

high urinary levels of phenol can result from exposure to several different aromatic compounds). 

Depending on the properties of the substance (e.g., biologic half-life) and environmental conditions (e.g., 

duration and route of exposure), the substance and all of its metabolites may have left the body by the 

time samples can be taken. It may be difficult to identify individuals exposed to hazardous substances 

that are commonly found in body tissues and fluids (e.g., essential mineral nutrients such as copper, zinc, 

and selenium). Biomarkers of exposure to 1,1-dichloroethane are discussed in Section 3.8.1. 

Biomarkers of effect are defined as any measurable biochemical, physiologic, or other alteration within an 

organism that, depending on magnitude, can be recognized as an established or potential health 

impairment or disease (NAS/NRC 1989). This definition encompasses biochemical or cellular signals of 

tissue dysfunction (e.g., increased liver enzyme activity or pathologic changes in female genital epithelial 

cells), as well as physiologic signs of dysfunction such as increased blood pressure or decreased lung 

capacity. Note that these markers are not often substance specific. They also may not be directly 

adverse, but can indicate potential health impairment (e.g., DNA adducts). Biomarkers of effects caused 

by 1,1-dichloroethane are discussed in Section 3.8.2. 

A biomarker of susceptibility is an indicator of an inherent or acquired limitation of an organism's ability 

to respond to the challenge of exposure to a specific xenobiotic substance. It can be an intrinsic genetic or 

other characteristic or a preexisting disease that results in an increase in absorbed dose, a decrease in the 

biologically effective dose, or a target tissue response. If biomarkers of susceptibility exist, they are 

discussed in Section 3.10, Populations That Are Unusually Susceptible. 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 46 

3. HEALTH EFFECTS 

3.8.1 Biomarkers Used to Identify or Quantify Exposure to 1,1-Dichloroethane 

As summarized in Section 6.5, 1,1-dichloroethane was not detected in blood samples collected from the 

National Health and Nutrition Examination Survey (2003–2004). No other biomarkers that could be used 

to identify or quantify exposure to 1,1-dichloroethane were identified. 

3.8.2 Biomarkers Used to Characterize Effects Caused by 1,1-Dichloroethane 

1,1-Dichloroethane was used as an anesthetic in the early part of the 20th century (Konietzko 1984; Reid 

and Muianga 2012). No information was available on blood levels associated with anesthesia or the 

occurrence of anesthesia-induced cardiac arrhythmias. 

3.9 INTERACTIONS WITH OTHER CHEMICALS 

No information was located regarding toxic interactions of 1,1-dichloroethane with other xenobiotics. 

Evidence exists to indicate that 1,1-dichloroethane is detoxified by glutathione (Colacci et al. 1985). 

Thus, it is likely that other substances that deplete glutathione stores such as other chlorinated 

hydrocarbons (e.g., 1,1-dichloroethene and 1,2-dichloroethane), acetaminophen, and bromobenzene may 

enhance the toxicity of 1,1-dichloroethane. Substances that alter the activity of the microsomal enzymes 

that are responsible for the metabolism of 1,1-dichloroethane may also affect the toxicity of this chemical. 

For example, it has been shown that ethanol increases the metabolism of 1,1-dichloroethane in vitro (Sato 

et al. 1980). 

3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE 

A susceptible population will exhibit a different or enhanced response to 1,1-dichloroethane than will 

most persons exposed to the same level of 1,1-dichloroethane in the environment. Reasons may include 

genetic makeup, age, health and nutritional status, and exposure to other toxic substances (e.g., cigarette 

smoke). These parameters result in reduced detoxification or excretion of 1,1-dichloroethane, or 

compromised function of organs affected by 1,1-dichloroethane. Populations who are at greater risk due 

to their unusually high exposure to 1,1-dichloroethane are discussed in Section 6.7, Populations with 

Potentially High Exposures. 

No populations unusually susceptible to 1,1-dichloroethane or chlorinated ethanes in general have been 

identified. NIOSH (1978) has identified the following individuals as possibly being at increased risk 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 47 

3. HEALTH EFFECTS 

from exposure to 1,1-dichloroethane: (1) individuals with skin disease because of the purported dermal 

irritant effects induced by 1,1-dichloroethane; (2) individuals with liver disease because of the role of this 

organ in the biotransformation and detoxification of xenobiotics such as 1,1-dichloroethane; 

(3) Individuals with impaired renal function because of the limited evidence that 1,1-dichloroethane is 

nephrotoxic in animals; and (4) individuals with chronic respiratory disease because of the purported 

respiratory irritant effects induced by 1,1-dichloroethane. Although there are no data to substantiate this, 

additional populations that may be unusually susceptible to 1,1-dichloroethane include children and the 

elderly because of immature or compromised metabolic capabilities, and phenobarbital or alcohol 

consumers because of the ability of these substances to alter the activity of the cytochrome P-450 system. 

It should be noted that no reliable data were found regarding dermal or respiratory irritant effects of 

1,1-dichloroethane. 

3.11 METHODS FOR REDUCING TOXIC EFFECTS 

This section will describe clinical practice and research concerning methods for reducing toxic effects of 

exposure to 1,1-dichloroethane. However, because some of the treatments discussed may be experimental 

and unproven, this section should not be used as a guide for treatment of exposures to 1,1-dichloroethane. 

When specific exposures have occurred, poison control centers and medical toxicologists should be 

consulted for medical advice. No texts providing specific information about treatment following 

exposures to 1,1-dichloroethane were identified. 

3.11.1 Reducing Peak Absorption Following Exposure 

No information specific to 1,1-dichloroethane was identified. 

3.11.2 Reducing Body Burden 

No information specific to 1,1-dichloroethane was identified. 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects 

The mechanisms of toxicity have not been identified for 1,1-dichloroethane. 
 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 48 

3. HEALTH EFFECTS 

3.12 ADEQUACY OF THE DATABASE 

Section 104(I)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of 1,1-dichloroethane is available. Where adequate 

information is not available, ATSDR, in conjunction with the National Toxicology Program (NTP), is 

required to assure the initiation of a program of research designed to determine the health effects (and 

techniques for developing methods to determine such health effects) of 1,1-dichloroethane. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 

3.12.1 Existing Information on Health Effects of 1,1-Dichloroethane 

The existing data on health effects of inhalation, oral, and dermal exposure of humans and animals to 

1,1-dichloroethane are summarized in Figure 3-5. The purpose of this figure is to illustrate the existing 

information concerning the health effects of 1,1-dichloroethane. Each dot in the figure indicates that one 

or more studies provide information associated with that particular effect. The dot does not necessarily 

imply anything about the quality of the study or studies, nor should missing information in this figure be 

interpreted as a “data need”. A data need, as defined in ATSDR’s Decision Guide for Identifying 

Substance-Specific Data Needs Related to Toxicological Profiles (Agency for Toxic Substances and 

Disease Registry 1989), is substance-specific information necessary to conduct comprehensive public 

health assessments. Generally, ATSDR defines a data gap more broadly as any substance-specific 

information missing from the scientific literature. 

Figure 3-5 graphically depicts the information that currently exists on the health effects of 

1,1-dichloroethane. The literature reviewed concerning the health effects of 1,1-dichloroethane in 

humans consisted solely of an anecdotal report describing the occurrence of cardiac arrhythmias when 

this compound was used as a gaseous anesthetic. Chlorinated aliphatics as a class are known to cause 

central nervous system depression, and respiratory tract and dermal irritation when humans are exposed 
 

1,1-DICHLOROETHANE 49 

3. HEALTH EFFECTS 

Figure 3-5. Existing Information on Health Effects of 1,1-Dichloroethane 

Death 

Acute 

Intermediate

Chronic 

Immunologic/Lymphoretic

Neurologic

Reproductive

Developmental

Genotoxic

Cancer 

Systemic 

Human 

Inhalation 

Oral 

Dermal 

Death 

Acute 

Intermediate

Chronic 

Immunologic/Lymphoretic

Neurologic

Reproductive

Developmental

Genotoxic

Cancer 

Systemic 

Animal 

Inhalation 

Oral 

Dermal 

Existing Studies 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 50 

3. HEALTH EFFECTS 

by inhalation to sufficiently high levels. It has been inferred that 1,1-dichloroethane causes these effects, 

but no reliable data were found that verified this activity. 

The database for the health effects of 1,1-dichloroethane in experimental animals is lacking, and the 

studies reviewed consisted primarily of one subchronic inhalation study, one inhalation developmental 

toxicity study, and two oral chronic bioassays. No information is available on the effects of 

1,1-dichloroethane following dermal exposure. The limited information available in animals suggests that 

1,1-dichloroethane may be nephrotoxic, fetotoxic, and possibly carcinogenic. The data also indicate that 

1,1-dichloroethane is considerably less toxic than 1,2-dichloroethane and the tetrachlorinated aliphatics. 

3.12.2 Identification of Data Needs 

Acute-Duration Exposure. No reliable information is available on the effects of acute exposure to 

1,1-dichloroethane in humans. Information on the lethality of 1,1-dichloroethane following inhalation or 

oral exposure of animals comes from secondary sources (Archer 1978; Smyth 1956). One study 

examined the nonlethal toxicity of 1,1-dichloroethane following inhalation exposure (Schwetz et al. 

1974); this study reported decreases in maternal weight gain and delayed ossification in the fetuses. 

Because the potential systemic toxicity of 1,1-dichloroethane has not been evaluated following acute 

inhalation or dermal exposure, the database was not considered adequate for derivation of acute-duration 

inhalation or oral MRLs for 1,1-dichloroethane. 

Since the chlorinated aliphatics in general are known to cause central nervous system depression and 

irritation of respiratory and ocular mucosal epithelium following single high-level exposures, more 

information on the effects of acute-duration exposures to 1,1-dichloroethane by all routes would be useful 

to assess more fully the acute hazards of this chemical. 

Intermediate-Duration Exposure. No reliable information is available on the effects of repeated 

exposure in humans. Limited information is available on the effects of repeated inhalation and oral 

exposures to 1,1-dichloroethane in animals. The studies reviewed indicate that 1,1-dichloroethane is 

possibly nephrotoxic, but this effect has only been demonstrated at high doses in cats, but not in rats, 

guinea pigs, or rabbits (Hofmann et al. 1971). No other toxic effects have been attributed to 

1,1-dichloroethane following intermediate-duration inhalation exposures in animals. The lack of 

supporting toxicity or mechanistic data precluded using this study as the basis on an intermediate-duration 

inhalation MRL. More information on the systemic effects of repeated-dose exposures in animals, 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 51 

3. HEALTH EFFECTS 

particularly by the inhalation route since this is the most likely route of human exposure, would be useful 

to determine whether nephrotoxic effects observed in one study are an actual result of exposure to 

1,1-dichloroethane, to determine if 1,1-dichloroethane reacts like other chlorinated aliphatics (e.g., causes 

neurotoxicity and liver toxicity), and to more fully assess potential human health hazards from repeated 

exposure to 1,1-dichloroethane. Two studies have examined the intermediate-duration oral toxicity of 

1,1-dichloroethane. In a limited reported study, NCI (1977) found alterations in body weight gain in rats, 

but not mice, administered 1,1-dichloroethane for 6 weeks. In the second study, no adverse effects were 

observed in mice exposed to 1,1-dichloroethane in drinking water for 52 weeks (Klaunig et al. 1986). 

Additional oral studies are needed to identify sensitive targets of toxicity and establish dose-response 

relationships. Dermal studies are also necessary to evaluate the toxicity of this compound. 

Chronic-Duration Exposure and Cancer. No information is available on the effects of chronic 

exposure to 1,1-dichloroethane in humans. No chronic-duration inhalation or dermal exposure studies 

were identified. In chronic-duration oral exposure studies in rats and mice (NCI1977), no nonneoplastic 

alterations were observed. Without information on the targets of toxicity and dose-response relationships, 

inhalation and oral MRLs cannot be derived. Additional chronic toxicity studies particularly by the 

inhalation route would be useful to fully assess potential human health hazard from long-term exposure to 

1,1-dichloroethane. 

Two bioassays were reviewed that investigated the potential carcinogenic effect of 1,1-dichloroethane by 

the oral route of exposure in animals. One study provided suggestive evidence of carcinogenicity, but 

because there was poor survival in this study and the statistical significance of the cancer incidence is 

uncertain, the results could not be considered conclusive (NCI 1977). The other bioassay yielded 

negative results for 1,1-dichloroethane (Klaunig et al. 1986). Given the limitations (high mortality) 

present in the NCI (1977) study and the observations that 1,1-dichloroethane possibly forms DNA 

adducts and metabolizes to free radicals, more information obtained from well-conducted carcinogenicity 

studies would be useful to assess more fully the carcinogenic potential of 1,1-dichloroethane in humans 

and animals. Studies conducted by the inhalation route would be useful. 

Genotoxicity. The genotoxic potential of 1,1-dichloroethane has been investigated in in vitro assays; 

in vivo genotoxicity studies are necessary to evaluate the genotoxic potential of this chemical. In general, 

these studies provide suggestive evidence that 1,1-dichloroethane is not genotoxic. 1,1-Dichloroethane 

has been observed to enhance cell transformation in Syrian hamster embryo cells (Hatch et al. 1983) and 

results suggest that 1,1-dichloroethane or a metabolite can bind to cellular macromolecules such as DNA 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 52 

3. HEALTH EFFECTS 

(Colacci et al. 1985). More information on the genotoxic effects of 1,1-dichloroethane in animals both in 

vitro and in vivo would be useful to resolve the discrepancies in the present data and to assess the 

genotoxic hazard of this chemical in humans. 

Reproductive Toxicity. No information on the reproductive effects of 1,1-dichloroethane in humans 

or animals is available. Reproductive toxicity studies in animals would be useful particularly by the 

inhalation route since this is the most likely route of human exposure. 

Developmental Toxicity. No information on the developmental effects of 1,1-dichloroethane in 

humans is available. One study was located that investigated the developmental effects of inhaled 

1,1-dichloroethane in animals (Schwetz et al. 1974). The results from this study indicated that 

1,1-dichloroethane is fetotoxic in rats, causing retarded fetal development (i.e., delayed ossification of the 

vertebrae) in the presence of decreases in maternal food consumption and body weight gain. 

Additionally, well-conducted developmental toxicity studies on 1,1-dichloroethane, particularly by the 

inhalation route since this is the most likely route of human exposure, would be useful to verify the data 

from the single study that suggest this compound may cause adverse developmental effects. 

Immunotoxicity. No information is available on the immunotoxic effects of 1,1-dichloroethane in 

humans or animals. Immunotoxicity studies in animals, particularly by the inhalation route since this is 

the most likely route of human exposure, would be useful to assess the potential risk for 

1,1-dichloroethane-induced adverse immunologic effects in humans. 

Neurotoxicity. Chlorinated aliphatics as a class are known to cause central nervous system depression 

in humans exposed by inhalation to sufficiently high levels. 1,1-Dichloroethane can also cause this effect, 

evidenced by its former use as an anesthetic. However, no reliable data were found that indicated a 

threshold level for this effect. No data (behavioral, histopathological, neurochemical, or 

neurophysiological) are available on possible neurotoxic effects of long-term low level exposures to 

1,1-dichloroethane. More information on potential short- and long-term neurotoxic effects of inhaled 

1,1-dichloroethane would be useful to determine whether this compound can produce neurotoxic effects 

following low-level, long-term exposures, and to determine the threshold exposure level for 

1,1-dichloroethane-induced central nervous system depression. 

Epidemiological and Human Dosimetry Studies. No epidemiological studies were located on 

1,1-dichloroethane. Well-controlled epidemiological studies of people living in close proximity to areas 
 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 53 

3. HEALTH EFFECTS 

where 1,1-dichloroethane contamination of surface water and groundwater or air is known to have 

occurred, people living near hazardous waste sites, and of occupationally exposed people could add to the 

limited database and clarify health effects in humans induced by 1,1-dichloroethane. However, while this 

information would be useful, it is unlikely that it could be easily obtained from occupational studies. 

Other short-chain halogenated hydrocarbons are usually encountered in the same facilities where 

1,1-dichloroethane is manufactured or used, thus confounding the results obtained in such a study. 

Biomarkers of Exposure and Effect. For high exposure to 1,1-dichloroethane, the levels of this 

compound in the blood, urine, and breath may be used for biomarkers of exposure. However, these 

methods should be more sensitive and quantitative. The formation of DNA adducts has been suggested, 

and if they do occur in vivo, they may serve to identify long-term exposure to 1,1-dichloroethane. The 

development of methods for detecting metabolites in the fluids and tissue of humans is needed to indicate 

1,1-dichloroethane exposure. 

Biomarkers of effect would be useful for identifying 1,1-dichloroethane-specific injury (e.g., 

hepatotoxicity, renal toxicity, neurotoxicity) for short-, intermediate-, and long-term exposure. Presently, 

no biomarkers of effect are available; however, DNA adducts may be useful for indicating 

carcinogenicity in animals or humans following chronic exposure to 1,1-dichloroethane. 

Absorption, Distribution, Metabolism, and Excretion. Studies of the toxicokinetics of 

1,1-dichloroethane are very limited. Much of the information regarding the disposition of 1,1-dichloroethane is based on indirect evidence. Toxicokinetic data are useful for providing information on 

mechanisms of toxicity and can often support findings of toxicity studies. 

Absorption of 1,1-dichloroethane occurs following exposure via all routes. The presence of a 

1,1-dichloroethane metabolite in urine and expired air and its binding to tissue macromolecules provide 

evidence of its absorption. Studies regarding the direct analysis of the extent and rate of 

1,1-dichloroethane absorption are lacking and would provide useful information on the potential health 

hazards associated with exposure to 1,1-dichloroethane via inhalation of contaminated air or ingestion of 

contaminated water. 

Studies in humans and animals regarding tissue distribution of 1,1-dichloroethane are not available. Its 

lipophilicity suggests that the compound would be well absorbed and distributed to tissues according to 

their lipid content. Binding studies conducted in rats following intraperitoneal injection indicate that 
 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 54 

3. HEALTH EFFECTS 

1,1-dichloroethane localizes in the liver, kidney, lung, and stomach. However, analysis has been limited 

to these tissues. Distribution studies using routes of administration relevant to human exposure 

(inhalation, oral) would provide useful information on potential target organs of 1,1-dichloroethaneinduced toxicity in humans. 

Characterization of 1,1-dichloroethane's metabolism relies heavily on in vitro data. These studies reveal 

that the biotransformation process is mediated by cytochrome P-450 with hepatic microsomes being the 

most effective. Identification of products in these microsomal studies allows for the prediction of 

metabolic pathways. However, exposure to 1,1-dichloroethane under in vivo conditions may alter 

substrate availability and consequently alter the metabolic scheme. In vivo studies would provide a better 

understanding of the rate and extent of 1,1-dichloroethane metabolism and a more realistic perspective of 

its metabolic fate. This information would allow more accurate prediction of the potential of 

1,1-dichloroethane to induce toxic effects, and aid in devising methods to detoxify exposed persons. 

Studies regarding the excretion of 1,1-dichloroethane by humans were not available. One study was 

located in animals regarding the extent or rate of 1,1-dichloroethane excretion. Studies monitoring levels 

in blood and excretion would be useful to estimate pharmacokinetic parameters. 

Comparative Toxicokinetics. The absorption, distribution, metabolism, and excretion data for 

1,1-dichloroethane are all derived from animal studies. It is likely that human disposition would follow a 

scheme similar to that found in animals, but this conclusion is highly speculative. However, similar 

results obtained in vivo across several animal species would provide supportive evidence for the 

assumption that 1,1-dichloroethane is handled in a similar manner in humans. 

Methods for Reducing Toxic Effects. Limited information regarding methods for reducing the 

toxic effects of 1,1-dichloroethane were identified. Additional information regarding the toxicity of 

1,1-dichloroethane is needed prior to research on mitigating the toxicity of this compound. 

Children’s Susceptibility. Data needs relating to both prenatal and childhood exposures, and 

developmental effects expressed either prenatally or during childhood, are discussed in detail in the 

Developmental Toxicity subsection above. 
 

 

 

 

1,1-DICHLOROETHANE 55 

3. HEALTH EFFECTS 

No data were identified on children’s susceptibility to the toxic effects of 1,1-dichloroethane and whether 

there are toxicokinetic differences in the metabolism of this chemical between adults and children. As 

noted previously, one developmental toxicity study (Schwetz et al. 1974) reported altered fetal growth. 

Child health data needs relating to exposure are discussed in Section 6.8.1, Identification of Data Needs: 

Exposures of Children. 

3.12.3 Ongoing Studies 

No ongoing studies sponsored by NIH, NTP, or EPA were identified for 1,1-dichloroethane. 
 

1,1-DICHLOROETHANE 56 

3. HEALTH EFFECTS 

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1,1-DICHLOROETHANE 57 

4. CHEMICAL AND PHYSICAL INFORMATION 

4.1 CHEMICAL IDENTITY 

The synonyms, and identification numbers for 1,1-dichloroethane are listed in Table 4-1. 

4.2 PHYSICAL AND CHEMICAL PROPERTIES 

Important physical and chemical properties of 1,1-dichloroethane are listed in Table 4-2. 
 

 

 

 

1,1-DICHLOROETHANE 58 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-1. Chemical Identity of 1,1-Dichloroethane 

Characteristic Informationa Reference 

Chemical name 1,1-Dichloroethaneb 

Synonym(s) Alpha,alpha-dichloroethane; asymmetrical dichloroethane; 

S-dichloroethene; Dutch oil; ethane, 1,1-dichloro-; ethylidene 

chloride; ethylidene dichloride; 1,1-ethylidene dichloridec 

Registered trade name(s) No data 

Chemical formula C2H4Cl2b 

Chemical structure Cl H 

Cl C C H 

H H 

Identification numbers: 

CAS registry 75-34-3b 

NIOSH RTECS KI0175000 

EPA hazardous waste U076 

OHM/TADS No data 

DOT/UN/NA/IMDG shipping DOT 2362; UN 2362; IMO 3.2 

HSDB 64 

NCI C04535d 

aAll information obtained from HSDB 2012, except where noted

bO’Neil et al. 2006 cArcher 1978; Weiss 1986 dChemIDPlus Lite 2012 

CAS = Chemical Abstracts Service; DOT/UN/NA/IMDG = Department of Transportation/United Nations/North 

America/International Maritime Dangerous Goods Code; EPA = Environmental Protection Agency; 

HSDB = Hazardous Substances Data Bank; NCI = National Cancer Institute; NIOSH = National Institute for 

Occupational Safety and Health; OHM/TADS = Oil and Hazardous Materials/Technical Assistance Data System; 

RTECS = Registry of Toxic Effects of Chemical Substances 
1,1-DICHLOROETHANE 59 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-2. Physical and Chemical Properties of 1,1-Dichloroethane 

Property Information Reference 

Molecular weight 98.97 HSDB 2012 

Color Colorless 

Physical state Oily liquid O’Neil et al. 2006 

Melting point -96.9 °C HSDB 2012 

Boiling point 57.3 °C O’Neil et al. 2006 

Density at 20 °C 1.175 g/cm3 HSDB 2012 

Odor Aromatic ethereal; chloroform-like 

Odor threshold: 

Water No data 

Air 120 ppm; 200 ppm Verschueren 1983 

Solubility: 

Water at 20 °C 0.55 g/100 g HSDB 2012 

Organic solvents Miscible with oxygenated and chlorinated 

solvents 

Partition coefficients: 

Log Kow 1.79 HSDB 2012 

Log Koc 1.48 HSDB 2012 

Vapor pressure at 25 °C 230 mmHg HSDB 2012 

Henry's law constant at 24 °C 5.62x10-3 atm-m3/mol HSDB 2012 

5.51x10-3 atm-m3/mol Chen et al. 2012 

Autoignition temperature 457.8 °C HSDB 2012 

Flashpoint Closed cup -12 °C; open cup 14 °C HSDB 2012 

Flammability limits Lower 5.4%; upper 11.4% HSDB 2012 

Conversion factors 1 ppm x 4.05 = 1 mg/m3 

1 mg/m3 x 0.25 = 1 ppm 

Explosive limits Lower explosive limit: 5.6%; moderate HSDB 2012 

explosion hazard when exposed to heat or 

flame 
1,1-DICHLOROETHANE 60 

4. CHEMICAL AND PHYSICAL INFORMATION 

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1,1-DICHLOROETHANE 61 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

5.1 PRODUCTION 

Table 5-1 lists the number of facilities in each state that manufacture or process 1,1-dichloroethane, the 

activities and uses, and the range of maximum amounts of 1,1-dichloroethane that are stored on site. The 

data listed in Table 5-1 are derived from the Toxics Release Inventory (TRI13 2014). Based on the TRI 

information from 2013, there are 19 facilities that produce or process 1,1-dichloroethane in the United 

States. The TRI data should be used with caution since only certain types of facilities were required to 

report. This is not an exhaustive list. 

1,1-Dichloroethane is produced commercially through the reaction of hydrogen chloride and vinyl 

chloride at 20–55 °C in the presence of an aluminum, ferric, or zinc chloride catalyst (HSDB 2012). 

Other production methods include the direct chlorination of ethane, addition of hydrogen chloride to 

acetylene, the reaction of ethylene and chlorine in the presence of calcium chloride, and the reaction of 

phosphorus chloride and acetaldehyde (HSDB 2012). 1,1-Dichloroethane can also be produced as a 

byproduct during the manufacture of chloral, as a byproduct in the production of vinyl chloride via 

ethylene oxychlorination (HSDB 2012; Marshall 2003), and as an intermediate in the production of 

1,1,1-trichloroethane by thermal or photochemical chlorination of vinyl chloride (Cowfer 2006). It has 

been reported that 1,1-dichloroethane often occurs as an unwanted byproduct in numerous chlorination 

and oxychlorination processes of C2 hydrocarbons (HSDB 2012). 

Information regarding the production volume of 1,1-dichloroethane in the United States is not reported in 

SRI Directory of Chemical Producers (SRI 2011). Additionally, no data are reported for U.S. production 

volume in the Hazardous Substance Data Bank (HSDB 2012). 

Data from the Chemical Data Reporting (CDR) information system indicates that three companies within 

the United States manufactured or imported 1,1-dichloroethane (EPA 2014a). The Dow Chemical 

Company reported 0 pounds/year for imported and exported data, confidential business information (CBI) 

for manufactured data, 0 pounds/year for volume used on site and ‘CBI’ for past production volume data. 

1,1-Dichloroethane is reported to be used as an intermediate, a substance used to form another compound 

by the Dow Chemical Company. The Shin Etsu Company reports ‘withheld’ for imported data, 

1,844,512 pounds/year for exported data, ‘withheld’ for manufactured data, 2,629,704 pounds/year for 

volume used on site data, and 2,959,696 pounds/year for past production volume data (EPA 2014a). The 
 

 

 

 

 

 

 

 


 


 


 

1,1-DICHLOROETHANE 62 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

Table 5-1. Facilities that Produce, Process, or Use 1,1-Dichloroethane 

Minimum Maximum 

Number of amount on site amount on site 

Statea facilities in poundsb in poundsb Activities and usesc 

KY 1 10,000 99,999 1, 3, 6 

LA 9 0 9,999,999 1, 2, 3, 4, 5, 6, 8, 12, 13 

NY 1 100 999 12 

OH 1 1,000 9,999 12 

SC 1 100 999 12 

TX 6 1,000 999,999 1, 2, 3, 5, 6, 8, 12, 13, 14 

aPost office state abbreviations used.
 bAmounts on site reported by facilities in each state.
 cActivities/Uses:
 

1. Produce 6. Reactant 11. Manufacturing Aid 

2. Import 7. Formulation Component 12. Ancillary/Other Uses 

3. Onsite use/processing 8. Article Component 13. Manufacturing Impurity 

4. Sale/Distribution 9. Repackaging 14. Process Impurity 

5. Byproduct 10. Chemical Processing Aid 

Source: TRI13 2014 (Data are from 2013) 
 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 63 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

Shin Etsu Company reports use of 1,1-dichloroethane as ‘not reasonably known or ascertainable.’ The 

national production volume ranged between 1,000,000 and 10,000,000 pounds/year. There are no data 

reported for consumer products or consumer uses. 

According to EPA Inventory Update Rule (IUR) records, in 2006, two companies in the United States 

produced 1,1-dichloroethane in 2006: Oxy Vinyls in La Porte, Texas and The Dow Chemical Company 

in Plaquemine, Louisiana (EPA 2010). Both of these companies manufactured 1,1-dichloroethane 

primarily to be used as an intermediate, a substance used to form another compound. Production volume 

data were not provided for each specific company. Aggregated national production volumes reported in 

2006 were in the range of 500,000–<1 million pounds (EPA 2010). 

5.2 IMPORT/EXPORT 

No information was found concerning U.S. imports and exports of 1,1-dichloroethane. 

5.3 USE 

The largest individual use of 1,1-dichloroethane is as an intermediate in the manufacture of 

1,1,1-trichloroethane (Dreher et al. 2014; HSDB 2012). 1,1-Dichloroethane also has limited use as a 

solvent for plastics, oils, and fats, and is thus employed as both a cleaning agent and a degreaser (O’Neil 

et al. 2006). In the past, 1,1-dichloroethane was used as an anesthetic (HSDB 2012; O’Neil et al. 2006). 

Other uses of 1,1-dichloroethane include fabric spreading, varnish and finish removers, organic synthesis, 

ore flotation, and as a fumigant and insecticide spray (HSDB 2012). 1,1-Dichloroethane is also used in 

the manufacture of plastic wrap, adhesives, and synthetic fiber (USGS 2006a). No information is 

available regarding the use proportions among these categories. 

5.4 DISPOSAL 

1,1-Dichloroethane may be disposed of by atomization within a combustion chamber equipped with an 

appropriate effluent gas cleaning device, by high-temperature incineration with a hydrochloric acid 

scrubber, or by placing product residues and sorbent media into 17H epoxy-lined drums and disposing of 

them at an EPA-approved site. However, the criteria for treatment or sanitary landfill disposal practices 

are currently undergoing revision. Waste water treatment technologies investigated by the EPA include 

concentration processes such as stripping, solvent extraction, activated carbon, and resin adsorption. 
1,1-DICHLOROETHANE 64 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

Consultation with environmental regulatory agencies is advised (HSDB 2012; Marshall 2003; NIOSH 

1978). 
 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 65 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.1 OVERVIEW 

1,1-Dichloroethane has been identified in at least 673 of the 1,699 hazardous waste sites that have been 

proposed for inclusion on the EPA National Priorities List (NPL) (HazDat 2007). However, the number 

of sites evaluated for 1,1-dichloroethane is not known. The frequency of these sites can be seen in 

Figure 6-1. 

1,1-Dichloroethane has been identified in at least 400 of the 1,760 proposed (51), final (1,323), and 

deleted (386) hazardous waste sites listed on the EPA Superfund NPL under the synonym 

1,1-dichloroethene (CASRN: 75-34-3) and at least 26 of the 1,760 EPA Superfund NPL sites under the 

synonym ethylidene dichloride (CASRN: 75-34-3) (EPA 2015c; NLM 2015). However, the number of 

sites evaluated for 1,1-dichloroethane is not known. 

1,1-Dichloroethane in the environment is mainly related to the production, storage, consumption, 

transport, and disposal of 1,1-dichloroethane used as a chemical intermediate, solvent, finish remover, and 

degreaser. 1,1-Dichloroethane may occur in the environment as a biodegradation product of 

1,1,1-trichloroethane. In addition, 1,1-dichlrooethane was reported as a constituent in the gaseous 

emissions of cigarette smoke. Releases from industrial processes are almost exclusively to the 

atmosphere. Releases of the compound to surface waters and soils are expected to partition rapidly to the 

atmosphere through volatilization. Hydrolysis, photolysis, and biodegradation do not appear to be 

important processes in determining the environmental fate of 1,1-dichloroethane. It has been detected at 

generally low levels in ambient air, surface water, groundwater, drinking water, and human breath. 

Concentrations in environmental media are greatest near source areas (e.g., industrial point sources, 

hazardous waste sites). 

The main route of human exposure to 1,1-dichloroethane is through inhalation of 1,1-dichloroethane in 

ambient or workplace air. Estimates of populations potentially exposed to 1,1-dichloroethane in 

workplace environments in the 1980s ranged from 715 to 1,957 workers (EPA 2001c). Ingestion of 

contaminated drinking water may also be an important route of exposure for populations living near 

industrial facilities and hazardous waste sites. Boman and Maibach (1996) concluded that exposure to 

skin results in very little absorption due to the compound’s volatility; in addition, the concentration levels 

greatly diminish in properly ventilated areas. 
1,1-DICHLOROETHANE 66

6. POTENTIAL FOR HUMAN EXPOSURE

Figure 6-1. Frequency of NPL Sites with 1,1-Dichloroethane Contamination

Frequency 

of 

NPL Sites 

Derived from HazDat 

Derived from HazDat 

2007 

1-3 

4-6 

7-9 

10-14 

17-28 

50-62 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 67 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.2 RELEASES TO THE ENVIRONMENT 

The Toxics Release Inventory (TRI) data should be used with caution because only certain types of 

facilities are required to report (EPA 2005). This is not an exhaustive list. Manufacturing and processing 

facilities are required to report information to the TRI only if they employ 10 or more full-time 

employees; if their facility is included in Standard Industrial Classification (SIC) Codes 10 (except 1011, 

1081, and 1094), 12 (except 1241), 20–39, 4911 (limited to facilities that combust coal and/or oil for the 

purpose of generating electricity for distribution in commerce), 4931 (limited to facilities that combust 

coal and/or oil for the purpose of generating electricity for distribution in commerce), 4939 (limited to 

facilities that combust coal and/or oil for the purpose of generating electricity for distribution in 

commerce), 4953 (limited to facilities regulated under RCRA Subtitle C, 42 U.S.C. section 6921 et seq.), 

5169, 5171, and 7389 (limited S.C. section 6921 et seq.), 5169, 5171, and 7389 (limited to facilities 

primarily engaged in solvents recovery services on a contract or fee basis); and if their facility produces, 

imports, or processes ≥25,000 pounds of any TRI chemical or otherwise uses >10,000 pounds of a TRI 

chemical in a calendar year (EPA 2005). 

Of the 21,526 TRI facilities reporting nationwide, 1,1-dichloroethane (CASRN: 75-34-3), has been 

reported in 0 onsite TRI releases for the reporting year 2013. Of these TRI facilities reporting 

nationwide, 1,1-dichloroethane, under the synonym ethylidene dichloride (CASRN: 75-34-3), has been 

reported in 18 onsite TRI releases for the reporting year 2013 (NLM 2015). 

Section 112 of the Clean Air Act (CAA) lists 1,1-dicloroethane as one of 188 hazardous air pollutants 

(HAPs) known to cause or suspected of causing cancer or other serious human health effects or ecosystem 

damage (EPA 2000). EPA's National Emission Inventory (NEI) database contains data regarding sources 

that emit criteria air pollutants and their precursors, and HAPs for the 50 United States, Washington DC, 

Puerto Rico, and the U.S. Virgin Islands (prior to 1999, criteria pollutant emission estimates were 

maintained in the National Emission Trends [NET] database and HAP emission estimates were 

maintained in the National Toxics Inventory [NTI] database). The NEI database derives emission data 

from multiple sources including: state and local environmental agencies; the TRI database; computer 

models for on-road and off-road emissions; databases related to EPA's Maximum Achievable Control 

Technology (MACT) programs to reduce emissions of hazardous air pollutants. Using composite data 

from the NTI database from 1990 to 1993, it was estimated that the annual emissions of 1,1-dichloroethane in the United States was approximately 274 tons per year during that time frame (EPA 2000). 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 68 

6. POTENTIAL FOR HUMAN EXPOSURE 

Data downloaded from the 2005 NEI indicated that the total emission of 1,1-dichloroethane was 

approximately 387 tons, with the biggest source arising from point source waste disposal (EPA 2012c). 

There are no known natural sources of 1,1-dichloroethane. It has been reported that 1,1,1-trichloroethane 

is rapidly biodegraded in anaerobic methanogenic environments, such as those found in landfills, to form 

1,1-dichloroethane as the major product, with slow, yet complete anaerobic degradation of 1,1-dichloroethane to carbon dioxide also indicated (deBest et al. 1997; van Eekert et al. 1999; Vogel and McCarty 

1987). 1,1,1-Trichloroethane occurs in the environment as a result of accidental spills, industrial 

manufacturing, and use processes. Laboratory studies designed to elucidate the degradation reactions of 

chloroethenes and chloroethanes have been described by Hallen et al. (1986) and Vogel and McCarty 

(1987). Hallen et al. (1986) observed that dechlorination reactions appear to be reversible, and 

chlorinated ethanes can be converted to chlorinated ethenes. Releases of 1,1-dichloroethane to the 

environment are a result of industrial manufacturing use processes and from the degradation of 

1,1,1-trichloroethane. Additional sources of environmental release are fugitive emissions from storage, 

distribution, and disposal; use as an extraction solvent and fumigant or insecticide spray and in paints, 

varnish, and paint removers; as a constituent of medicines and stone, clay, and glass products; and in ore 

floatation (EPA 2001c; Infante and Tsongas 1982). 

6.2.1 Air 

Estimated releases of 20,972 pounds (~9.51 metric tons) of 1,1-dichloroethane to the atmosphere from 

19 domestic manufacturing and processing facilities in 2013, accounted for about 90.1% of the estimated 

total environmental releases from facilities required to report to the TRI (TRI13 2014). These releases are 

summarized in Table 6-1. 

Emissions to the atmosphere comprise >98% of all releases of 1,1-dichloroethane to the environment 

(TRI10 2012). 1,1-Dichloroethane released in the production of 1,1,1-trichloroethane accounts for about 

52% of the atmospheric releases, with the production of 1,2-dichloroethane accounting for about 35%. 

Pellizzari (1982) reported the presence of low levels of 1,1-dichloroethane in ambient air of the Baton 

Rouge industrial area and at the Kin-Buc waste disposal site outside Edison, New Jersey. Eitzer (1995) 

observed low levels of 1,1-dichloroethane (≤1 μg/m3

) in at least one of eight municipal solid waste sites 

sampled in the United States. 
 

 


 
 


 


 


 


 


 


 


 


 


 


 


 


 


 


 
 


 


 


 


 


 


 


 


 


 


 


 


 


 

1,1-DICHLOROETHANE 69 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-1. Releases to the Environment from Facilities that Produce, Process, or
 

Use 1,1-Dichloroethanea
 

Reported amounts released in pounds per yearb 

Total release 

Statec RFd Aire Waterf UI

g Landh Otheri On-sitej Off-sitek On- and off-site 

KY 1 56 0 0 0 0 56 0 56 

LA 9 20,612 80 0 11 0 20,692 11 20,703 

NY 1 2 0 0 0 0 2 0 2 

OH 1 4 0 0 10 0 4 10 14 

SC 1 1 0 0 0 0 1 0 1 

TX 6 297 2 2,200 0 0 2,498 0 2,498 

Total 19 20,972 82 2,200 21 0 23,254 21 23,275 

aThe TRI data should be used with caution since only certain types of facilities are required to report. This is not an 

exhaustive list. Data are rounded to nearest whole number.
 bData in TRI are maximum amounts released by each facility.
 cPost office state abbreviations are used.
 dNumber of reporting facilities.
 eThe sum of fugitive and point source releases are included in releases to air by a given facility.
 f

Surface water discharges, waste water treatment-(metals only), and publicly owned treatment works (POTWs) (metal
 

and metal compounds).
 gClass I wells, Class II-V wells, and underground injection.
 hResource Conservation and Recovery Act (RCRA) subtitle C landfills; other onsite landfills, land treatment, surface 

impoundments, other land disposal, other landfills.
 i

Storage only, solidification/stabilization (metals only), other off-site management, transfers to waste broker for
 

disposal, unknown
 j

The sum of all releases of the chemical to air, land, water, and underground injection wells.
 kTotal amount of chemical transferred off-site, including to POTWs.
 

RF = reporting facilities; UI = underground injection 

Source: TRI13 2014 (Data are from 2013) 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 70 

6. POTENTIAL FOR HUMAN EXPOSURE 

Approximately 52,000 kg of 1,1-dichloroethane are released to the atmosphere by privately owned 

treatment work facilities (POTWs) each year (EPA 1980). 

In 2002, air emissions from point, area, and mobile sources in the Great Lakes region were calculated. 

Data from Illinois, Indiana, Michigan, Minnesota, New York, Ontario, Pennsylvania, and Wisconsin were 

evaluated. Total emissions of 1,1-dichloroethane in the Great Lakes region were calculated to be 

27,110 pounds from point sources and 1,360 pounds from area sources. All states reported only point 

source emissions for the compound with the exception of Minnesota, which reported 341 pounds from 

point sources and 1,360 pounds from area sources. Ontario and Illinois accounted for the majority of the 

emissions (41 and 33%, respectively). The other states each accounted for 1–9% of the emissions (Great 

Lakes Commission 2006). 

1,1-Dichloroethane was detected with the VOCs emanating from a low-level radioactive waste disposal 

facility at the U.S. Geological Survey (USGS) Amargosa Desert Research Site in Nevada (Baker et al. 

2012). The study quantified VOCs being emitted over an 11-year period and estimated the yearly vertical 

diffusive flux of the detected VOCs to the atmosphere. Concentrations decreased as the distance from the 

site increased. Samples taken at the site contained 29.9, 33.6, and 66 mg dichloroethane/m2 per year, 

while samples taken 100 m from the site along the north south transect contained 2.8, 3.6, and 9.7 mg 

dichloroethane/m2 per year in 2001, 2003, and 2005 respectively. At distances of 200 and 300 m, 

concentrations were reported as 0.0 mg dichloroethane/m2 for 2001, 2003, and 2005. Table 6-2 

summarizes the estimates obtained from locations along the north-south transect at distances of 0–400 m 

from the facility. 

Emissions from six commercial cigarette brands were examined in a chamber study; five cigarettes per 

brand were smoked for approximately 6 minutes (Wang et al. 2012). The amount of 1,1-dichloroethane 

emitted during smoking ranged between 51 and 110 μg/cigarette. The average concentration of 

1,1-dichloroethane during smoking ranged from 12 to 26 μg/m3 and the average concentration during the 

post-smoking period ranged from 7.9 to 17 μg/m3

. 

In 2011, 1,1-dichloroethane was detected in the gaseous emissions of a commercial poultry farm in 

Poland (Witkowska 2013). The farm consisted of five buildings that had mechanical ventilation systems. 

Measurements were taken over the turkey’s rearing period, from week 4 to 19. The average 

concentrations detected in the turkey houses at week 4, 7, 10, and 13 were 1.15±0.55, 1.08±0.82, 
 

1,1-DICHLOROETHANE 71 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-2. Estimated Yearly Emissions of 1,1-Dichloroethane (mg/m2 per Year) 

Distance from landfill (m) 2001 2003 2005 

0 29.9 33.6 66 

25 22.6 31.8 51.5 

50 18.4 17.9 Not reported 

75 Not reported 16.4 Not reported 

100 2.8 3.6 9.7 

150 Not reported 0.1 Not reported 

200 0.0 0.0 0.0 

300 0.0 0.0 0.0 

400 0.0 Not reported Not reported 

Source: Baker et al. 2012 
 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 72 

6. POTENTIAL FOR HUMAN EXPOSURE 

1.57±0.45, and 1.33±0.55 ppm, respectively. Reported concentrations for week 16 and 19 were 

0.00 ppm. 

6.2.2 Water 

Estimated releases of 82 pounds (~0.037 metric tons) of 1,1-dichloroethane to surface water from 

15 domestic manufacturing and processing facilities in 2013, accounted for <1% of the estimated total 

environmental releases from facilities required to report to the TRI (TRI13 2014). This estimation 

includes surface water discharges, waste water treatment (metal only), and POTWs (metal and metal 

compounds) (TRI13 2014). These releases are summarized in Table 6-1. 

Industrial releases of 1,1-dichloroethane to surface waters are minor in comparison to releases to the 

atmosphere. Industrial processes involving the use of 1,1-dichloroethane as a chemical intermediate or 

cleaning solvent are believed to be the largest sources of surface water releases. Young et al. (1983) 

reported 1,1-dichloroethane in the primary, secondary, and final effluents from municipal wastewater 

treatment plants. Approximately 1,000 kg of 1,1-dichloroethane are discharged in effluent from POTWs 

each year (EPA 1980). 

6.2.3 Soil 

Estimated releases of 21 pounds (~0.009 metric tons) of 1,1-dichloroethane to soils from eight domestic 

manufacturing and processing facilities in 2013, accounted for <0.01% of the estimated total 

environmental releases from facilities required to report to the TRI (TRI13 2014). An additional 2,200 

pounds (~1.0 metric tons), constituting about 9.46% of the total environmental emissions, were released 

via underground injection (TRI13 2014). These releases are summarized in Table 6-1. 

Little information was found regarding releases of 1,1-dichloroethane to soils. Approximately 4,000 kg 

of 1,1-dichloroethane from POTWs are dispersed on land each year as sludge (EPA 1980). 

6.3 ENVIRONMENTAL FATE 

6.3.1 Transport and Partitioning 

Releases of 1,1-dichloroethane to the environment as a result of industrial activity are expected to be 

primarily to the atmosphere (see Section 6.2). 1,1-Dichloroethane released to the atmosphere may be 
 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 73 

6. POTENTIAL FOR HUMAN EXPOSURE 

transported long distances before being washed out in precipitation. For example, Pearson and 

McConnell (1975) attributed the presence of chlorinated organic compounds, including 1,1-dichloroethane, in upland waters to long-range aerial transport and deposition in precipitation. EPA (1982b) 

discussed the atmospheric fate of 1,1-dichloroethane in the Gulf Coast area, where there is a high 

percentage of cloudy days. Increased atmospheric losses due to washout in frequent, heavy rains could 

occur, although much of the 1,1-dichloroethane could be revolatilized. Dichloroethanes released in this 

area could be transported north by the prevailing winds to populated areas before significant 

photochemical degradation could occur. 

Cupitt (1980), however, considered the loss of 1,2-dichloroethane from the atmosphere by dissolution 

into rain drops or adsorption onto aerosols insignificant compared with loss from chemical degradation 

based on mathematical calculations. Since 1,1-dichloroethane has higher volatility and lower aqueous 

solubility than the 1,2-isomer, physical removal of 1,1-dichloroethane from the atmosphere would be 

even less likely to be important. Pellizzari et al. (1979) measured actual concentrations of airborne 

contaminants in the vicinity of known emission sources of 1,1-dichloroethane, making aerial transport the 

logical source of downwind concentrations. 

The Henry's law constant value for 1,1-dichloroethane (5.51x10-3 atm-m3

/mol) suggests that it should 

partition rapidly to the atmosphere. The evaporation half-life depends on a number of factors; wind speed 

and mixing conditions of the receiving waters are particularly important. Dilling et al. (1975) and Dilling 

(1977) estimated a volatilization half-life of 22 minutes for 1,1-dichloroethane present at 1 ppm 

concentration in an open water column held at 25 °C and stirred at 200 rpm. Under these conditions, 90% 

of the compound was removed within 109 minutes. Volatilization half-lives determined in the laboratory 

are related to actual environmental situations by a correction factor that takes into account the oxygen reaeration rate ratio. The re-aeration rate ratio has been determined to be 0.55 for 1,1-dichloroethane 

(Cadena et al. 1984). Using the values of Mabey et al. (1982) for oxygen re-aeration rates in ponds and 

rivers (0.19 and 0.96 day-1, respectively), the evaporation half-life of 1,1-dichloroethane is estimated to be 

approximately 5 times longer for ponds than for rivers (>1 day for river water and >6 days for pond 

water). 

Little information was found regarding partitioning of 1,1-dichloroethane from the water column onto 

sediments. According to DeWulf et al. (1996), 1,1-dichloroethane does not really accumulate on marine 

sediment and it will therefore not be an important sink for this compound. Analogs of the compound (i.e., 

dichloromethane, trichloromethane, and 1,1,1-trichloroethane) have not been found to concentrate 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 74 

6. POTENTIAL FOR HUMAN EXPOSURE 

selectively onto sediments (Dilling et al. 1975; Pearson and McConnell 1975). The Koc values for these 

compounds are similar to the Koc for 1,1-dichloroethane; therefore, partitioning to sediment from the 

water column is not likely to be an important environmental fate process for 1,1-dichloroethane. 

1,1-Dichloroethane released to land surfaces in spills would rapidly volatilize to the atmosphere, but 

1,1-dichloroethane remaining on soil surfaces would be available for transport into groundwater, since the 

compound does not sorb to soil particulates unless the organic content of the soil is high. Experimentally 

derived Koc values for a silt loam soil also indicate that little sorption of 1,1-dichloroethane to low organic 

content soil is expected. Goodin and Webber (1992) conducted studies of several volatile organic 

compounds (VOCs), including 1,1-dichloroethane, to determine their fate in soils. It was determined that 

the compounds were lost from the soils mainly by volatilization, with first-order disappearance half-lives 

ranging from 1 to 949 hours. Wilson et al. (1981) found that although 50% of the applied 1,1-dichloroethane volatilized to the atmosphere, the remainder percolated rapidly through a sandy soil, suggesting 

ready availability to groundwater transport processes. 

Gossett et al. (1983) analyzed the tissues of several species of aquatic organisms for 1,1-dichloroethane 

near the discharge of the Los Angeles County waste water treatment plant. The concentration of 

1,1-dichloroethane in the effluent was 3.5 ppb; however, none was found in the animal tissues (detection 

limit of 0.3–0.5 ppb). These results may be evidence that the potential for 1,1-dichloroethane to 

bioconcentrate is low in aquatic organisms. An estimated bioconcentration factor of 5 indicates that 

bioconcentration would be low (HSDB 2012). 

6.3.2 Transformation and Degradation 

6.3.2.1 Air 

In the atmosphere, 1,1-dichloroethane is oxidized by reaction with hydroxyl radicals. The rate constant 

for the vapor-phase reaction is 2.74x10-13 cm3

/molecule-second at 25 °C (HSDB 2012). The residence 

time of the compound in the atmosphere has been estimated to be 49 days (HSDB 2012). 

6.3.2.2 Water 

1,1-Dichloroethane in surface water is expected to be lost to the atmosphere through volatilization before 

undergoing any significant chemical or biological degradation. The hydrolytic half-life of 1,1-dichloroethane at pH 7 and 25 °C has been estimated to be 60 years (Jeffers et al. 1989). 
 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 75 

6. POTENTIAL FOR HUMAN EXPOSURE 

As summarized in Klecka et al. (1990), 1,1-dichloroethane is produced by biodegradation of 

1,1,1-trichloroethane in groundwater. Further degradation could also occur. In the absence of oxygen 

and in the presence of anaerobic, methane-producing bacteria, halocarbons are transformed by reductive 

dehydrohalogenation in a step-wise manner: 1,1,1-trichloroethane → 1,1-dichloroethane → chloroethane.

van Eeker et al. (1999) reported 31.1% anaerobic degradation of 1,1-dichloroethane to mainly 

chloroethane (14.5%) in living sludge after 25 days. Under aerobic conditions, Tabak et al. (1981) 

reported about 50% degradation of 1,1-dichloroethane by unadapted microorganisms isolated from 

municipal waste water inoculum after 7 days, which was increased to 78% degradation by adapted 

organisms in the same time period. 1,1-Dichloroethane has been reported to be resistant to biological 

degradation by bacteria isolated from shallow aquifer aerobic groundwater after 8–16 weeks incubation 

(Wilson et al. 1983). 

Data from landfill sites with a documented contamination history were examined by Cline and Viste 

(1985). They observed that 1,1-dichloroethane was detected in groundwater at sites where the compound 

had not been handled or disposed of and concluded that 1,1-dichloroethane had been produced by 

anaerobic degradation of other compounds present, particularly 1,1,1-trichloroethane. Washington and 

Cameron (2001) used well monitoring data, from a landfill with a contamination history, to calculate a 

degradation rate constant for 1,1-dichloroethane. Under sulfate-reducing conditions at 10 °C, the rate 

constant was found to be 6.0x10-3 L/day with a half-life of 115 days. 

6.3.2.3 Sediment and Soil 

1,1-Dichloroethane in soils is expected to volatilize to the atmosphere or be transported to groundwater 

before undergoing significant abiotic transformation; the compound is not expected to sorb to soils of low 

organic content. As in surface waters, direct photolysis of 1,1-dichloroethane on soil surfaces is not 

expected. The rate of biodegradation of 1,1-dichloroethane in soils is unknown. In subsurface soil, the 

loss of 1,1-dichloroethane through biodegradation is expected to be insignificant (Wilson et al. 1983). 

The biodegradation half-life of 1,1,1-trichloroethane under anaerobic conditions has been reported to be 

about 16 days, whereas the half-life of 1,1-dichloroethane has been reported to be >30–60 days (Wood et 

al. 1985). 

Hamonts et al. (2012) monitored chlorinated aliphatic hydrocarbons, such as 1,1-dichloroethane, in 

groundwater that discharges into the Zenne River over a 21-month period. The Zenne River had been 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 76 

6. POTENTIAL FOR HUMAN EXPOSURE 

previously continuously contaminated with municipal sewage containing chlorinated aliphatic 

hydrocarbons. The study also evaluated microbial reductive dechlorination occurring under anaerobic 

conditions in the river sediments. Microbial degradation of 1,1-dichloroethane was evident in the 

riverbed locations in which Dehalobactor spp. was detected; however, in the absence of this 

microorganism, 1,1-dichloroethane did not appear to degrade. 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 

Reliable evaluation of the potential for human exposure to 1,1-dichloroethane depends in part on the 

reliability of supporting analytical data from environmental samples and biological specimens. 

Concentrations of 1,1-dichloroethane in unpolluted atmospheres and in pristine surface waters are often 

so low as to be near the detection limits of analytical methods. In reviewing data on 1,1-dichloroethane 

levels monitored or estimated in the environment, it should also be noted that the amount of chemical 

identified analytically is not necessarily equivalent to the amount that is bioavailable. The analytical 

methods available for monitoring 1,1-dichloroethane in a variety of environmental media are detailed in 

Chapter 7. 

1,1-Dichloroethane has been detected in ambient urban and rural air, in waste gas generated from garbage 

dumps, and in surface water, groundwater, and drinking water. Quantitative concentration information is 

presented in the following sections by environmental medium. 

6.4.1 Air 

The Air Quality System (AQS) database is EPA’s repository of criteria air pollutants and hazardous air 

pollutants (HAPs) containing monitoring data from over 2,600 monitoring sites across the United States. 

Detailed AQS ambient air monitoring data from 2013 for 1,1-dichloroethane are summarized in Table 6-3 

(http://www.epa.gov/ttnamti1/toxdat.html#data*). Data for other years are available as zipped Microsoft 

Access database files that may be accessed directly from the EPA website. In general, the average 

concentration of the samples for 1,1-dichloroethane in outdoor air was approximately 0.02 μg/m3

. The 

highest reported concentration (4.4 μg/m3

) occurred in one sample from Kentucky. The second highest 

reported concentration (0.83 μg/m3

) also occurred in one sample from Kentucky. The third highest 

reported concentration (0.81 μg/m3

) was detected in 173 samples from Ohio. Rhode Island had the 

largest number of samples with detectable concentrations, 836 samples, that ranged in concentration from 

0.004 to 0.12 μg/m3

. The 24-hour average concentration of 1,1-dichloroethane in outdoor air ranged from 

 

1,1-DICHLOROETHANE 77 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-3. 2013 Air Monitoring Data from Air Toxics Data Ambient Monitoring 

Archive for 1,1-Dichloroethane
 

Statea Number of samples Concentration range (μg/m3) 

AK 61 0 

AZ 104 0 

CO 61 0 

FL 32 0.0081–0.18 

FL 376 0 

GA 237 0 

IA 87 0 

IL 180 0 

IN 28 0.04 

IN 442 0 

KY 33 0.044–4.4 

KY 467 0 

MA 141 0.004–0.0081 

MA 25 0 

ME 36 0.016–0.4 

ME 244 0 

MI 2 0.34–0.35 

MI 329 0 

MN 1 0.004 

MN 1,008 0 

MO 61 0 

MS 121 0 

NC 437 0 

NJ 1 0.045 

NJ 239 0 

NY 238 0.004–0.47 

NY 483 0 

OH 173 0.81 

OH 243 0 

OK 303 0 

PA 27 0.04–0.12 

PA 274 0 

RI 836 0.004–0.012 

RI 42 0 

SC 118 0 

TX 6 0.04–0.2 

TX 2,355 0 

UT 52 0 

VA 89 0 

 

1,1-DICHLOROETHANE 78 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-3. 2013 Air Monitoring Data from Air Toxics Data Ambient Monitoring 

Archive for 1,1-Dichloroethane
 

Statea Number of samples Concentration range (μg/m3) 

VT 140 0 

WA 57 0 

WI 95 0 

aPost office state abbreviations used. 

Source: EPA 2015b 
 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 79 

6. POTENTIAL FOR HUMAN EXPOSURE 

approximately 0.008 to 3.5.4 μg/m3 (0.001–1.09 ppb). The analytical methods had detection limits that 

ranged between 0.0081 and 3.4 μg/m3 (EPA, 2015b). 

1,1-Dichloroethane was not seen at a detection limit of 5 ppt in ambient rural air samples taken in 

southeastern Washington state (Grimsrud and Rasmussen 1975). It has been found at higher 

concentrations in ambient air samples from urban areas of the United States. EPA (1983b) tabulated 

atmospheric levels at urban, rural, and industrial sites across the United States and reported a median 

concentration of 55 ppt. Pellizzari (1982) reported the detection of low levels (unspecified 

concentrations) of the compound in the vicinity of the Baton Rouge industrial area. EPA (1983a) 

reported that the average concentration of the compound in the air of seven urban locations in 1980–1981 

ranged from 0.1 to 1.5 ppb. It has also been detected in samples of ambient air collected in the vicinity of 

hazardous waste disposal sites, such as the Kin-Buc site near Edison, New Jersey, at a level of 23 μg/m3 

(5.68 ppm) (Pellizzari 1982). EPA (1978) tabulated analytical results for 1,1-dichloroethane in the 

ambient air of various locations generally in close proximity to industrial plants, including Magna, Utah 

(0.082 ppb); Iberville, Louisiana (0.12 ppm); Deer Park, Texas (0.14 ppb); and Baton Rouge (0.058 ppb) 

and Geismar, Louisiana (0.14 ppb). 

Barkley et al. (1980) found no 1,1-dichloroethane in the ambient air surrounding nine houses bordering 

the old Love Canal. Gupta et al. (1984) found 1,1-dichloroethane at higher levels indoors (mean 

concentration of 3.2 ppb) than outdoors (not detected) in residences in suburban Knoxville, Tennessee, 

and concluded that there must be a source of the compound inside the home. Possible sources were not 

identified except to suggest building materials or chlorinated water. 

Air monitoring data from 22 tire fire incidents across the United States were evaluated. 1,1-Dichloroethane was detected at low levels in the vicinity of several of the fires. It was noted that the source may 

be from something other than the burning tires (EPA 1993). 

Air was monitored over a 3-week period at the Fresh Kills Landfill of Staten Island, New York. The 

overall air emission rate for 1,1-dichloroethane was 0.216 g/second (EPA1996a). 

In 1994, 1,1-dichloroethane was not detected in six spatial sites around the Columbus metro area. 

Detection limits of the analysis were 0.05 ppb (Spicer 1996). 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 80 

6. POTENTIAL FOR HUMAN EXPOSURE 

In 1996, Mohamed et al. (2002) monitored VOCs in air at 13 urban locations in the United States for 

1 year. Monitoring sites were located in Louisiana, Texas, Vermont, and New Jersey. TRI reporting 

facilities near the monitoring sites ranged from 0 to 38 facilities. 1,1-Dichloroethane was detected at all 

13 of the monitoring stations at levels <1 ppb by volume (ppbv). The detection limit of the analytical 

method was <0.5 ppbv. 

1,1-Dichloroethane was detected in the headspace of five out of eight household bleach products at levels 

ranging from 0.7 to 176 μg/m3

. It was concluded that the compound was formed by the reaction of 

hypochlorite and the organic matter of the product’s additives. In addition, 1,1-dichloroethane levels of 

indoor air increased during the use of bleach products, from 0.004–0.01 μg/m3 before use, to 0.01– 

0.62 μg/m3 during use, and then to 0.01–0.29 μg/m3 after use (Odabasi 2008). 

From February to December 2009, 1,1-dichloroethane was detected in ambient air samples from four sites 

in Seoul, Korea (Jong Ro, Yang Jae, Gwang Jin, and Gang Seo) at concentrations of 0.04–0.18, 0.03– 

0.08, 0.04–0.15, and 0.04–0.32 ppb, respectively (Kim et al. 2012). 

6.4.2 Water 

. The compound has been found in samples of urban runoff from Long Island, New York, and Eugene, 

Oregon, at concentrations of 1.5 and 3 ppb, respectively (Cole et al. 1984). Coniglio et al. (1980) 

summarized groundwater monitoring data obtained by numerous state agencies and reported that 

1,1-dichloroethane was found in 18% of the wells tested, with a maximum concentration of 11,330 ppb. 

They cautioned that the state data may have been biased since the monitoring was generally conducted by 

the states in areas where contamination was suspected. However, 1,1-dichloroethane has been detected in 

groundwater sampled during random testing of water supplies (see further discussion). 

Finished water supplies obtained from groundwater sources were tested by EPA for contaminants. It was 

reported that up to 10.8% of 158 nonrandom sample sites from across the United States contained 

detectable levels of 1,1-dichloroethane. The maximum concentration was 4.2 ppb (Westrick et al. 1984). 

Drinking water samples from a number of urban and rural locations in the United States have been 

reported to be contaminated with 1,1-dichloroethane. Unspecified levels of the compound have been 

detected in drinking water samples taken from Philadelphia (Suffet et al. 1980). Private drinking water 

wells in Wisconsin were found to contain unspecified levels of 1,1-dichloroethane in 11 of 617 wells 
 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 81 

6. POTENTIAL FOR HUMAN EXPOSURE 

surveyed (Krill and Sonzogni 1986). Concentrations of 1–3 ppb were reported in four public well water 

supplies in Iowa (EPA 1985). 

Groundwater samples taken from 178 hazardous waste disposal sites were found to contain 1,1-dichloroethane at 18% frequency (Plumb 1987), with an average concentration of 0.31 ppm and a maximum 

concentration of 56.1 ppm (Yang and Rauckman 1987). Using the STORET database, Staples et al. 

(1985) reported median concentrations of <0.1 ppb in 8,716 samples of ambient water (3% detectable 

values), <1.0 ppb in 1,375 effluent samples (5% detectable values), <5.0 ppb in 354 sediment samples 

(0.6% detectable values), and <0.05 ppb in 94 biota samples (no detectable values). 

Nine shallow groundwater samples contained 1,1-dichloroethane with a maximum concentration of 

2.2 μg/L, in 5.3% of 208 urban wells sampled in the United States (Kolpin et al. 1997).

1,1-Dichloroethane was detected above background levels in groundwater beneath Savannah River Site’s 

Interim Sanitary Landfill. Several wells at the site were sampled twice each in 2005. The site was in 

operation from 1992 to 1998 (DOE2005). 

The Aerojet-General Corporation reports that 1,1-dichloroethane is present as a groundwater contaminant 

just outside Sacramento, California, in varying concentrations in several separate domestic and industrial 

well water samples and test borings. Additionally, a 1996 study indicated the presence of the compound 

in groundwater from the Glassboro region of Southern New Jersey at a detection frequency of 5% and a 

concentration of >0.1 μg/L (HSDB 2012).

The Solid Waste Management Unit 12 in South Carolina was in use from the 1970s until 1981. In 

September 1999, water sampled from an excavation hole that contained a leaking underground storage 

tank (UST) contained 1,1-dichloroethane at a concentration of 84,300 μg/L. Monitoring efforts of wells

surrounding the site from August 2000 to November 2007 detected 1,1-dichloroethane as a consistent 

contaminant in the groundwater. Groundwater samples from August 2001 indicated that the highest 

concentrations of contaminants in groundwater were near the UST, indicating that it was the source area. 

Maximum measured concentrations of 1,1-dichloroethane of 155,000 μg/L were found at that time. 

Natural and engineered remediation efforts have contributed to the irregular decline of contaminants. On 

the northern side of the facility, concentrations of 1,1-dichloroethane in groundwater at one of the wells 

declined from >100 μg/L in 2000 to approximately 20–30 μg/L in 2003, remained relatively unchanged in 

2003–2005, and declined in 2006–2007 (USGS 2006b). 
 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 82 

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The National Water Quality Assessment Program (NAWQA) evaluated 3,496 wells nationwide for the 

presence of VOCs from 1985 to 2001. 1,1-Dichloroethane had an overall detection frequency of 0.86% at 

an assessment level of 0.2 μg/L; a detection frequency of 0.17% at an assessment level of 1 μg/L; and a 

detection frequency of 0.029% at an assessment level of 5 μg/L. The compound was also detected as a 

mixture with 1,1,1-trichloroethane in 0.71% of the samples (USGS 2006a). According to the report, there 

were 30 detections of 1,1-dichloroethane in 3,496 aquifer samples. More specifically, 7 detections 

occurred in 2,400 domestic well samples, 22 detections occurred in 1,096 public well samples, 

20 detections occurred in 847 urban area shallow groundwater samples, and 1 detection occurred in 

723 agricultural area shallow groundwater samples. Reported concentrations ranged from approximately 

0.007 to 9 μg/L, with the bulk of the samples falling in the range of 0.02–0.2 μg/L (USGS 2006a). 

1,1-Dichloroethane was detected in 2.3% of 130 groundwater well samples at a maximum concentration 

of 0.6 μg/L (Bi et al. 2012). Samples were collected during 2008 and 2009 from five alluvial plains in 

East China considered to be susceptible to contamination from human activities. 

From May 3, 1999 through October 23, 2000, random samples from 954 water sources across the United 

States were collected. The sources included 579 groundwater and 375 surface water samples. 

1,1-Dichloroethane was detected in 11 groundwater samples at levels between 0.1 and 10 μg/L (USGS 

2003a). 

Shallow groundwaters underlying areas of residential and commercial use in Salt Lake Valley, Utah were 

analyzed for VOCs such as 1,1-dichloroethane using monitoring wells at 30 separate sites (USGS 2003b). 

1,1-Dichloroethane was detected in one of the samples, at an estimated concentration of 0.03 μg/L (below 

the laboratory reporting level of 0.07μg/L). 

1,1-Dicholorethane was one of the primary VOCs detected in several water quality studies from the Snake 

River Plain aquifer conducted between 1987 and 2005 (USGS 2010a). In April 2007, the USGS National 

Water Quality Laboratory analyzed perched groundwater samples from well USGS 92 at the Radioactive 

Waste Management Complex in the Snake River Plain aquifer and 1,1-dichloroethane was detected at a 

concentration of 0.8 μg/L (USGS 2010a). 
 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 83 

6. POTENTIAL FOR HUMAN EXPOSURE 

The CALEPA (2003) analysis of 13,347 California groundwater sources of drinking water found 

1,1-dichloroethane in 68 samples, ranging from 0.51 to 30 ppb. 1,1-Dichloroethane was not found in any 

of the 754 surface water sources of drinking water sampled. 

Samples from 2,948 wells across the United States were sampled between 1985 and 1995. The sources 

consisted of both drinking water and non-drinking water in 406 urban wells and 2,542 rural wells. The 

detection frequency of 1,1-dichloroethane was 6.4% in urban wells and 0.7% in rural wells. Reported 

concentrations were approximately 0.2–60 μg/L with a median of approximately 0.45 μg/L, and 

approximately 0.2–8 μg/L with a median of about 0.7 μg/L, respectively (Squillace et al. 1999). 

VOCs were examined in 30 public water supply wells in the Columbia aquifer in Delaware (USGS 

2010c). In 2000, 1,1-dichloroethane was detected 6 times at concentrations ranging from 0.015 to 

0.149 μg/L and in 2008, the chemical was detected 4 times at concentrations of <0.04–0.135 μg/L. 

Active wells were resampled in a study by the Source Water Assessment and Protection Program from 

August through November 2008. Twenty-two of the original wells and 8 similar wells were sampled. 

The range of detected concentrations remained the same; however, the number of detections decreased by 

1 for both years. 

The USGS assessed the quality of source water from public supply wells in the United States from 1993 

to 2007 (USGS 2010d). 1,1-Dichloroethane was detected in 7.7% of 832 samples, and 1.4% of the 

samples contained ≥0.2 μg/L (USGS 2010b). The maximum concentration of 1,1-dichloroethane 

detected was 4.878 μg/L. 

6.4.3 Sediment and Soil 

Very little information was found on the ambient concentrations of 1,1-dichloroethane in soil, or on the 

current disposal of waste products containing the compound in landfills. 1,1-Dichloroethane was 

detected, yet not quantified, in soil samples of Love Canal, New York. At a detection limit of 0.5 ppb, 

1,1-dichloroethane was not detected in sediment of the submarine outfall region of the Los Angeles 

County (Joint Water Pollution Control Plant [JWPCP]) municipal waste water treatment plant (HSDB 

2012). The compound has more commonly been detected in ambient air and groundwater samples taken 

at hazardous waste sites, and it is expected that the lack of available soil monitoring data is at least in part 

due to rapid partitioning of 1,1-dichloroethane released to soils to these other media. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 84 

6. POTENTIAL FOR HUMAN EXPOSURE 

Soil gas was monitored for the U.S. Army from October 2010 until September 2011 in Fort Gordon, 

Georgia (USGS 2012). Soil-gas samplers were installed at three former fuel-dispensing stations in order 

to assess organic soil-gas contaminants for the Resource Conservation and Recovery Act Part B 

Hazardous Waste Permit process. There were 55 samplers at one site, 30 samplers at a second site, and 

39 samplers at a third site. 1,1-Dichloroethane was reported as not detected in all samples and the method 

detection limit was 0.02 μg (USGS 2012). 

6.4.4 Other Environmental Media 

Little information was found on the levels of 1,1-dichloroethane in other media. Ferrario et al. (1985) 

measured 33 ppb wet weight of 1,1-dichloroethane in oysters from Lake Pontchartrain near New Orleans, 

Louisiana; however, 1,1-dichloroethane was not detected in two types of clams. Kallonen et al. (1985) 

detected 1,1-dichloroethane in the effluent gases of burning polyester fiber fill. Data on concentrations in 

human breath are presented in Section 6.5. 1,1-Dichloroethane was not found in any samples in a survey 

of 234 table-ready foods evaluated for the presence of VOCs (Heikes et al. 1995). Page and Lacroix 

(1995) found 1,1-dichloroethane in three peanut butter samples at levels of 1.1, 1.9, and 3.7 μg/kg; 

however, the compound was not found in several other foods that were analyzed. 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE 

The greatest source of exposure to 1,1-dichloroethane for most of the U.S. population is inhalation of the 

compound in contaminated air, especially near source areas. Another potential route of human exposure 

is ingestion of the compound in contaminated drinking water, and use of consumer products that may 

contain 1,1-dichloroethane. The general population may also be exposed through inhalation of cigarette 

smoke (Wang et al. 2012). Occupational exposure to 1,1-dichloroethane may occur via inhalation or 

dermal contact at workplaces where it is produced or used (HSDB 2012). 

The Fourth National Report on Human Exposures to Environmental Chemicals, published and updated by 

the Centers for Disease Control and Prevention (CDC 2015), reported data for 1,1-dichlorethane from the 

National Health and Nutrition Examination Survey (NHANES) for the survey years 2003–2004 and 

2005–2006. These data are summarized in Table 6-4. Blood concentrations of 1,1-dichloroethane for 

male and female participants of ages 12–>60 years and various ethnicities were reported. Concentrations 

of 1,1-dichloroethane in all categories for all NHANES survey years were below the detection limit of the 

method (0.01 μg/L) (CDC 2015). 
 

 

 

 

1,1-DICHLOROETHANE 85 

6. POTENTIAL FOR HUMAN EXPOSURE 

Table 6-4. Geometric Mean and Selected Percentiles of Blood Concentrations of 

1,1-Dichloroethane (in ng/L) for the U.S. Population from the National Health and 

Nutrition Examination Survey (NHANES) 

Geometric Selected percentiles (95% CI) 

Survey 

years 

mean 

(95% CI) 50th 75th 90th 95th 

Sample 

size 

Total 2003–2004 *a <LODb <LOD <LOD <LOD 1,367 

2005–2006 * <LOD <LOD <LOD <LOD 3,193 

Age group 

12–19 years 2005–2006 * <LOD <LOD <LOD <LOD 941 

20–59 years 2003–2004 * <LOD <LOD <LOD <LOD 1,367 

2005–2006 * <LOD <LOD <LOD <LOD 1,569 

≥60 years 2005–2006 * <LOD <LOD <LOD <LOD 683 

Gender 

Males 2003–2004 * <LOD <LOD <LOD <LOD 670 

2005–2006 * <LOD <LOD <LOD <LOD 1,510 

Females 2003–2004 * <LOD <LOD <LOD <LOD 697 

2005–2006 * <LOD <LOD <LOD <LOD 1,683 

Race/ethnicity 

Mexican 2003–2004 * <LOD <LOD <LOD <LOD 267 

Americans 2005–2006 * <LOD <LOD <LOD <LOD 778 

Non-Hispanic 2003–2004 * <LOD <LOD <LOD <LOD 300 

blacks 2005–2006 * <LOD <LOD <LOD <LOD 832 

Non-Hispanic 2003–2004 * <LOD <LOD <LOD <LOD 695 

whites 2005–2006 * <LOD <LOD <LOD <LOD 1,347 

aNot calculated; the proportion of results below limit of detection (LOD) was too high to provide a valid result. The b<LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. 

LODs for survey years 2003–2004 and 2005–2006 were 0.01 and 0.01 μg/L, respectively. 

CI = confidence interval 

Source: CDC 2015 
 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 86 

6. POTENTIAL FOR HUMAN EXPOSURE 

The National Occupational Exposure Survey (NOES), conducted by NIOSH from 1981 to 1983, indicated 

that 1,957 workers, including 272 women, were potentially exposed to 1,1-dichloroethane in the 

workplace (NOES 1990). The exposed workers were employed in the chemical and allied products and 

business service industries, as chemical technicians; plumbers, pipefitters, and steamfitters; supervisors in 

production occupations; electricians; machinists; chemical engineers; and welders and cutters. The 

estimates were based on direct observation by the surveyor of the actual use of the compound. 

NIOSH (1978) noted that there was a large potential for exposure to 1,1-dichloroethane in the workplace 

during its use as a dewaxer of mineral oils, extractant for heat-sensitive substances, or fumigant, and in 

the manufacture of vinyl chloride and high-vacuum rubber and silicon grease. 

The EPA (1982a) and Wallace et al. (1982) conducted a study of the levels of 1,1-dichloroethane in the 

inhaled and exhaled air and drinking water of college students in Texas and North Carolina. Low levels 

(<0.49 ppb) of 1,1-dichloroethane were found in the personal air quality monitors of the Texas students, 

whose campus bounded a petrochemical manufacturing area, but none was detected in the exhaled breath 

samples. 1,1-Dichloroethane was not detected in the breathing zone air of the North Carolina students. 

Barkley et al. (1980) found a trace of 1,1-dichloroethane in the expired breath of one resident whose 

home bordered the old Love Canal, but none was detected in ambient air. Wallace et al. (1984) found a 

trace of 1,1-dichloroethane in the expired breath and drinking water of one resident of New Jersey). 

Assuming a median ambient air level of 55 pptv reported by EPA (1983b) and a theoretical average 

inhalation of 20 m3 air/day, the average inhalation exposure to 1,1-dichloroethane for an individual in the 

United States is estimated at 4 μg/day.

Buckley et al. (1997) reported the detection of 1,1-dichlorethane in 1 of 16 blood samples at a 

concentration of 0.01 μg/L. 1,1-Dichloroethane was detected in <10% of blood samples from 

1,000 people between the years 1988 and 1994 (Needham et al. 1995). In October 2001, Edelman et al. 

(2003) analyzed blood and urine samples from World Trade Center firefighters for VOCs, including 

1,1-dichloroethane; detection of the compound was insignificant. A National Health and Nutrition 

Survey of the U.S. population in 2003–2004 screened for 1,1-dichloroethane in blood samples at a limit 

of detection (LOD) concentration of 0.01 ng/mL (CDC 2015). The samples were taken from 

1,367 participants in the age range of 20–59 years old, about half females (n=679) and half males 

(n=670). The survey included Mexican Americans (n=267), non-Hispanic blacks (n=300), and non­
 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 87 

6. POTENTIAL FOR HUMAN EXPOSURE 

Hispanic whites (n=695). The portion of the data below the LOD for 1,1-dichloroethane was too high to 

provide valid results (CDC 2015). 

6.6 EXPOSURES OF CHILDREN 

This section focuses on exposures from conception to maturity at 18 years in humans. Differences from 

adults in susceptibility to hazardous substances are discussed in Section 3.7, Children’s Susceptibility. 

Children are not small adults. A child’s exposure may differ from an adult’s exposure in many ways. 

Children drink more fluids, eat more food, breathe more air per kilogram of body weight, and have a 

larger skin surface in proportion to their body volume. A child’s diet often differs from that of adults. 

The developing human’s source of nutrition changes with age: from placental nourishment to breast milk 

or formula to the diet of older children who eat more of certain types of foods than adults. A child’s 

behavior and lifestyle also influence exposure. Children crawl on the floor, put things in their mouths, 

sometimes eat inappropriate things (such as dirt or paint chips), and spend more time outdoors. Children 

also are closer to the ground, and they do not use the judgment of adults to avoid hazards (NRC 1993). 

There are no exposure studies or body burden measurements of 1,1-dichloroethane in children. 

1,1-Dichloroethane has been detected in air, as discussed in Section 6.4.1, and inhalation of contaminated 

air likely represents the greatest route of potential exposure for children. 1,1-Dichloroethane has also 

been detected in drinking water, and therefore, ingestion of contaminated water is a possible source of 

exposure. Dichloroethane (isomer not specified) has been detected in human milk (Urusova 1953); 

however, these data are not current. 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 

Human exposure to 1,1-dichloroethane is expected to be highest among certain occupational groups (e.g., 

chemical and allied products industry workers) and members of the general population living in the 

vicinity of industrial point emission sources (EPA 2001c) and hazardous waste sites. The compound has 

been detected in both ambient air and water in low concentrations, with substantially higher 

concentrations in localized areas around industrial and disposal sites. No information was found 

regarding the number of people potentially exposed around hazardous waste sites. 

Smokers are exposed to higher concentrations of 1,1-dichloroethane than nonsmokers. Emissions from 

cigarette smoke can contain between 51 and 110 μg 1,1-dichloroethane/cigarette (Wang et al. 2012). The 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 88 

6. POTENTIAL FOR HUMAN EXPOSURE 

average concentration of 1,1-dichloroethane at the onset of smoking and 60 minutes after smoking ranges 

from 7.9 to 26 μg/m3

. In addition, nonsmokers who are in close proximity to cigarette smoke are 

susceptible to higher exposure concentrations. 

6.8 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of 1,1-dichloroethane is available. Where adequate 

information is not available, ATSDR, in conjunction with NTP, is required to assure the initiation of a 

program of research designed to determine the health effects (and techniques for developing methods to 

determine such health effects) of 1,1-dichloroethane. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 

6.8.1 Identification of Data Needs 

Physical and Chemical Properties. The physical/chemical properties of 1,1-dichloroethane are 

sufficiently well characterized to enable assessment of the environmental fate of this compound. 

Production, Import/Export, Use, Release, and Disposal. According to the Emergency 

Planning and Community Right-to-Know Act of 1986, 42 U.S.C. Section 11023, industries are required 

to submit substance release and off-site transfer information to the EPA. The TRI, which contains this 

information for 2013, became available in October of 2014. This database is updated yearly and should 

provide a list of industrial production facilities and emissions. 

Based on its industrial use, 1,1-dichloroethane is primarily released to the atmosphere, and humans are 

potentially exposed to this chemical through the inhalation or ingestion of contaminated air or water. 

However, because the data available on production, import, export, use, and disposal are limited, it is 

difficult to estimate whether or not the potential for human exposure to 1,1-dichloroethane may be 

substantial. Data concerning the production and use of 1,1-dichloroethane both within the United States 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 89 

6. POTENTIAL FOR HUMAN EXPOSURE 

and worldwide are extremely limited. Information regarding possible disposal methods, criteria, and 

regulations are available; however, the present criteria may undergo revision in the near future. 

Information on current production levels, quantities imported and exported, proportions allocated to 

various uses, and proportions and efficiencies associated with differing modes of disposal is limited. This 

information would be useful in identifying potential sources and levels of exposure, thus enabling 

identification of exposed populations. 

Environmental Fate. Releases from industrial processes are almost exclusively to the atmosphere, 

and releases of the compound to surface waters and soils are expected to partition rapidly to the 

atmosphere through volatilization. 1,1-Dichloroethane released to the atmosphere may be transported 

long distances before being washed out in precipitation. Although 1,1-dichloroethane released to land 

surfaces in spills would rapidly volatilize to the atmosphere, the 1,1-dichloroethane remaining on soil 

surfaces would be available for transport into groundwater. The atmospheric residence time of 

1,1-dichloroethane is about 44 days. The dominant removal mechanism is reaction with hydroxyl free 

radicals. Hydrolysis and biodegradation do not appear to be important processes in the environmental 

fate of this compound. Data are lacking on the partitioning of 1,1-dichloroethane from the water column 

onto sediments. Additional information on the atmospheric transformation and on the rate of 

biodegradation of 1,1-dichloroethane in soils would be useful in the determination of its environmental 

fate. 

Bioavailability from Environmental Media. Data are incomplete on the bioavailability of 

1,1-dichloroethane from environmental media. Animal data on 1,1-dichloroethane exposure via 

inhalation and oral administration in drinking water suggest that the compound is bioavailable following 

inhalation of ambient air and ingestion of drinking water. Additional information on the bioavailability of 

1,1-dichloroethane from air, water, soil, and sediment would be useful in determining actual risks 

associated with exposure to environmental levels of 1,1-dichloroethane. 

Food Chain Bioaccumulation. The information located on the potential for bioconcentration of 

1,1-dichloroethane in plants, aquatic organisms, or animals is limited. An analysis of animal tissues from 

several species of aquatic organisms near the discharge of a waste water treatment plant did not detect 

1,1-dichloroethane in the animal tissues, although the compound was found in the effluent. However, 

1,1-dichloroethane has been detected in oysters (33 ppb wet weight). An estimated bioconcentration 

potential of <1 from the Kow suggests that bioconcentration would not be expected. Very little 

information was found regarding the biomagnification of 1,1-dichloroethane among food chain trophic 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 90 

6. POTENTIAL FOR HUMAN EXPOSURE 

levels. Additional information on bioconcentration and biomagnification would be useful in determining 

whether food chain bioaccumulation is an important source of human exposure. 

Exposure Levels in Environmental Media. Reliable monitoring data for the levels of 

1,1-dichloroethane in contaminated media at hazardous waste sites are needed so that the information 

obtained on levels of 1,1-dichloroethane in the environment can be used in combination with the known 

body burden of 1,1-dichloroethane to assess the potential risk of adverse health effects in populations 

living in the vicinity of hazardous waste sites. 

Limited information is available regarding ambient concentrations of 1,1-dichloroethane in soils. Based 

on a median ambient air level reported in 1982, the average inhalation exposure to 1,1-dichloroethane for 

an individual in the United States has been estimated to be 4 μg/day. The information on foodstuffs is

limited to the detection of 1,1-dichloroethane in oysters (33 ppb wet weight). Additional site-specific 

concentration data for ambient air, drinking water, soil, and biota would be helpful in estimating potential 

exposure of the general population as well as populations in the vicinity of hazardous waste sites. 

Exposure Levels in Humans. Although relatively recent estimates of the size of the population 

occupationally exposed to 1,1-dichloroethane are available from NIOSH, monitoring data on workplace 

exposures are generally limited, with a few observations about 1,1-dichloroethane included in detailed 

studies of 1,2-dichloroethane. A study of the levels of 1,1-dichloroethane in the inhaled and exhaled air 

and drinking water of college students in Texas and North Carolina found low levels (<0.49 ppb) of 

1,1-dichloroethane in the personal air quality monitors of the Texas students, whose campus bounded a 

petrochemical manufacturing area, but none in samples of their exhaled breath. Additional information 

on the availability of biomarkers that could be used to indicate human exposure to 1,1-dichloroethane 

would be helpful. 

This information is necessary for assessing the need to conduct health studies on these populations. 

Exposures of Children. A data need has been identified to conduct body burden studies of 

1,1-dichloroethane in children. Measurements of 1,1-dichloroethane in blood samples for a population of 

adults was conducted in 2003–2004 as part of the National Health and Nutrition Examination Survey 

(CDC 2015). Most of the samples were below the detection limit of 0.01 ng/mL. Similar results among a 

group of children would demonstrate that exposure to 1,1-dichloroethane is low for both children and 

adults. 
 

 

 

 

 

1,1-DICHLOROETHANE 91 

6. POTENTIAL FOR HUMAN EXPOSURE 

Child health data needs relating to susceptibility are discussed in Section 3.12.2, Identification of Data 

Needs: Children’s Susceptibility. 

Exposure Registries. No exposure registries for 1,1-dichloroethane were located. This substance is 

not currently one of the compounds for which a sub-registry has been established in the National 

Exposure Registry. The substance will be considered in the future when chemical selection is made for 

sub-registries to be established. The information that is amassed in the National Exposure Registry 

facilitates the epidemiological research needed to assess adverse health outcomes that may be related to 

exposure to this substance. 

6.8.2 Ongoing Studies 

No ongoing studies regarding sponsored by NIH or EPA were identified for 1,1-dichloroethane. 
1,1-DICHLOROETHANE 92 

6. POTENTIAL FOR HUMAN EXPOSURE 

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1,1-DICHLOROETHANE 93 

7. ANALYTICAL METHODS 

The purpose of this chapter is to describe the analytical methods that are available for detecting, 

measuring, and/or monitoring 1,1-dichloroethane, its metabolites, and other biomarkers of exposure and 

effect to 1,1-dichloroethane. The intent is not to provide an exhaustive list of analytical methods. Rather, 

the intention is to identify well-established methods that are used as the standard methods of analysis. 

Many of the analytical methods used for environmental samples are the methods approved by federal 

agencies and organizations such as EPA and the National Institute for Occupational Safety and Health 

(NIOSH). Other methods presented in this chapter are those that are approved by groups such as the 

Association of Official Analytical Chemists (AOAC) and the American Public Health Association 

(APHA). Additionally, analytical methods are included that modify previously used methods to obtain 

lower detection limits and/or to improve accuracy and precision. 

The analytical methods used to quantify 1,1-dichloroethane in biological and environmental samples are 

summarized below. Table 7-1 lists the applicable analytical methods used for determining 1,1-dichloroethane in biological fluids and tissues, and Table 7-2 lists the methods used for determining 1,1-dichloroethane in environmental samples. 

7.1 BIOLOGICAL MATERIALS 

The determination of trace levels of 1,1-dichloroethane in biological tissues and fluids has been restricted 

to gas chromatography (GC) equipped with mass spectrometry (MS) or flame ionization detection (FID). 

Work conducted by Cramer and co-workers (1988) showed that 1,1-dichloroethane can be detected at 

nanogram per liter (ppt) levels in whole human blood using a dynamic headspace analyzer and GC/MS 

technique. A disadvantage of the GC/MS technique is that only limited mass scanning can be employed 

to obtain better sensitivity of target VOCs at ppt levels. This is because of the inherent differences in 

sensitivity between the full-scan MS and the limited mass scanning MS techniques (Cramer et al. 1988). 

Uehori et al. (1987) developed a retention index in GC to screen and quantify VOCs in blood. A dynamic 

headspace analyzer and GC/FID with retention indices were employed for the detection of 1,1-dichloroethane at nanogram levels. Uehori et al. (1987) noted that this method is simple and reliable, and requires 

little or no sample preparation. 
 

 

 

 


 


 

1,1-DICHLOROETHANE 94 

7. ANALYTICAL METHODS 

Table 7-1. Analytical Methods for Determining 1,1-Dichloroethane in Biological
 

Materials
 

Sample matrix Preparation method 

Analytical 

method 

Sample 

detection limit 

Percent 

recovery Reference 

Blood Vaporize blood sample in a 

headspace vial and inject into 

GC column 

GC/FID ng range No data Uehori et al. 

1987 

Whole blood Purge-and-trap on Tenax 

adsorbent 

GC/MS 100 ng/L 76–110 Cramer et 

al. 1988 

Blood and urine Heat biological sample; 

purge-and-trap volatile 

compounds on Tenax GC 

adsorbent 

GC/MS No data No data Barkley et 

al. 1980 

Whole blood Collect by venipuncture, store 

cold; inject sample into purgeand-trap apparatus 

GC/MS 0.013 ppb 102–118 Ashley et al. 

1992 

Breath Collect human breath sample 

by means of a spirometer and 

analyze 

GC/MS Not detected No data Barkley et 

al. 1980 

Breath Collect human breath sample 

by means of a spirometer and 

analyze 

GC/MS Not reported No data Raymer et 

al. 1990 

FID = flame ionization detector; GC = gas chromatography; MS = mass spectrometry 
 

 

 

 

 

 


 
 

1,1-DICHLOROETHANE 95 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining 1,1-Dichloroethane in 

Environmental Samples
 

Sample Analytical Sample Percent 

matrix Preparation method method detection limit recovery Reference 

Groundwater, Purge-and-trap (EPA GC/MS 4.7 μg/L 59–155% EPA 1994a (Method 

aqueous method 624) or direct (groundwater; 8240B), 2015a 

sludges, injection (EPA Method 5 μg/kg 

caustic 5030) (soil/sediment) 

liquors, soils, 

sediments 

Groundwater, Purge-and-trap (EPA GC with 0.002 μg/L 47–132 EPA 1994b (Method 

surface water, method 624) or direct HECD 8010B) 

waste water injection (EPA Method 

5030) 

Groundwater Purge-and-trap on GC/MS 0.0001– <±5 Lopez-Avila et al. 

absorbent 0.02 μg/sample relative 1987a 

standard 

deviation 

Groundwater Purge-and-trap on GC/FID-FID No data No data Driscoll et al. 1987 

absorbent 

Groundwater Purge-and-trap on GC/EICD-FID Water=0.1– 83–102 Lopez-Avila 1987b 

and soil absorbent 0.9 μg/L; 

soil=1–5 μg/L

Drinking water Heat water sample; GC/MS Not detected No data Barkley et al. 1980 

purge-and-trap volatile 

compounds on Tenax 

GC absorbent 

Drinking water Pass sample through GC/MS <1 μg/L No data Suffet et al. 1986 

XAD-2 macroreticular 

resin and extract 

continuously with ether 

Drinking water Purge-and-trap water GC/MS 0.2 μg/L 94 Otson and Chan 

sample 1987 

Drinking water Extract sample in GC-EICD <1 μg/L No data Otson and Chan 

hexane and analyze 

Drinking water Purge-and-trap on GC-EICD-FID <1 μg/L >75 Otson and Williams 

Tenax absorbent 1982 

Drinking water Purge-and-trap water GC/EICD 80 μg/L 84 Comba and Kaiser 

sample 1983 

Drinking water Purge-and-trap water GC/EICD-FID 0.1–0.5 μg/L No data Kingsley et al. 1983 

sample 

Water (river; Inject 1 mL into flow MIMS/ITD 0.2 ppb No data Bauer and Solyom 

sea) injection analysis 1994 

system 

Waste water Collect water sample GC/FID μg/L (ppb) <6 relative Blanchard and 

through a permeation range standard Hardy 1986 

cell membrane and deviation 

direct into GC 
 

 

 

 

 

 


 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 


 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

1,1-DICHLOROETHANE 96 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining 1,1-Dichloroethane in 

Environmental Samples
 

Sample Analytical Sample Percent 

matrix Preparation method method detection limit recovery Reference 

Waste water	 Collect sample through 

a permeation cell 

membrane; adsorb onto 

charcoal; extract with 

carbon disulfide 

Waste water	 Purge-and-trap (EPA 

(municipal method 601) with direct 

and industrial	 aqueous injection; the 

discharges)	 trap is backflushed and 

heated to desorb 

compounds onto column 

Waste water	 Purge-and-trap (EPA 

(municipal method 624); the trap is 

and industrial	 backflushed and heated 

discharges)	 to desorb compounds 

onto column 

Waste water	 Purge-and-trap with 

isotopic dilution (EPA 

method 1624); stable 

isotopes are added; the 

trap is backflushed and 

heated to desorb 

compounds onto column 

Waste water	 Purge-and-trap on 

and sludge	 adsorbent 

Drinking,	 Purge and trap water 

ground, and sample 

surface water 

Air (ambient)	 Purge-and-trap on 

charcoal absorbent; 

extract with carbon 

disulfide 

Air (ambient)	 Collect air sample on 

Tenax adsorbent; 

vaporize thermally and 

analyze 

Air (ambient)	 Collect air particulates 

on a glass fiber filter and 

Tenax GC adsorbent; 

extract with MeOH 

pentane 

Air (ambient)	 Adsorb air sample onto 

charcoal tube; extract 

with carbon disulfide 

GC/FID	 74– 

16,800 μg/L

GC/MS	 0.07 μg/L

GC/MS	 4.7 μ/L

GC/MS	 10 μg/L

GC/MS	 No data 

GC/AED	 0.17 μg/L

GC/ECD	 0.001 ppm 

range 

GC/MS	 23 μg/m3 

GC/MS	 Not detected 

GC/FID	 ppm range 

No data	 Blanchard and 

Hardy 1985 

47–132	 EPA 2001a 

59–155	 EPA 1999, 2015a 

Labeled EPA 2001b 

compound 

recovery: 

23–191 

No data	 Giabbaie et al. 1983 

No data	 Silgoner et al. 1997 

No data	 Bruner et al. 1978 

No data	 Pellizari 1982 

No data	 Barkley et al. 1980 

No data	 NIOSH 2003 

(method 1003) 
 

 


 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 


 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

1,1-DICHLOROETHANE 97 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining 1,1-Dichloroethane in 

Environmental Samples
 

Sample Analytical Sample Percent 

matrix Preparation method method detection limit recovery Reference 

Air (space Dehydrohalogenate air 

cabin) sample with lithium 

hydroxide and analyze 

Air (high Collect vapor sample in 

humidity a Tedlar gas bag 

atmosphere) 

Air Air collected in cooled 

trap; heated upon 

injection 

Air (ambient) Collection on 

multiadsorbent traps; 

automated 

preconcentration 

Air Sample collected on 

Tenax GC/carboxene 

1000 trap, separated by 

capillary column 

Various food Food containing >70% 

(e.g., dairy fat: dissolve sample in 

products, isooctane and shake; 

meat, cleanup on florisil 

vegetables, column 

and soda) 

Various food Cold liquid (4 °C) and 

(e.g., fruit aqueous flour-based 

juices, soda, samples injected; 

coffees, plunge sampling tube or 

cream, peanut needle into dry/viscous 

butter, and foods for injection; 

butter) steam distillation; purge 

and trap 

Compound Prepare dilute solution 

formulation of sample in MeOH; 

introduce into 

headspace trap 

Fish tissue Add water to fish 

sample; homogenize 

and extract 

ultrasonically; purgeand-trap on adsorbent 

Fish tissue Freeze fish sample; 

homogenize in liquid 

nitrogen; distill in 

vacuum 

GC/MS	 0.5–4.0 ppm 

Portable 25 ppm 

organic vapor 

analyzer with 

PID 

GC/IMS	 No data 

Capillary 0.71 ppbv 

GC/MS 

GC/PID/EICD	 0.1 ppb 

GC/ECD- ng/g range 

EICD 

SD/PT/GC	 0.003 μg/kg 

GC/PID	 20 pg 

GC/MS	 0.01 μg/g

GC/MS No data 

equipped with 

fused-silica 

capillary 

column 

No data	 Spain et al. 1985 

0.998 Barsky et al. 1985 

correlation 

coefficient 

No data	 Simpson et al. 1996 

Oliver et al. 1996 

Maeda et al. 1998 

~70	 Daft 1988 

95.2	 Page and Lacroix 

1995 

No data	 Jerpe and Davis 

1987 

77	 Easley et al. 1981 

No data	 Hiatt 1983 
 

 

 

 

 

 


 

1,1-DICHLOROETHANE 98 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining 1,1-Dichloroethane in 

Environmental Samples
 

Sample Analytical Sample Percent 

matrix Preparation method method detection limit recovery Reference 

Fish tissue Warm sample; purge- GC/FID No data ~32 Reinert et al. 1983 

and-trap volatiles on 

activated carbon 

adsorbent; extract with 

carbon disulfide 

Fish tissue Edible tissue and liver GC/EICD 5 pg/g 115±25 Roose and 

homogenized in blender; Brinkman 1998 

organic-free water and 

standard added; vial 

sealed and placed in 

ultrasonic bath; purge 

and trap 

Whole fish Freeze fish sample and GC/MS 7.5x10-4 μg/g 6.2 relative Dreisch and 

homogenize; add MeOH equipped with standard Munson 1983 

and extract fused-silica deviation 

ultrasonically; purge- capillary 

and-trap on adsorbent column 

Fish and Add water containing GC/MS 0.025 μg/g Sediment Hiatt 1981 

sediment acrolein and acrylonitrile matrix 101; 

to sample; freeze fish matrix 

sample; extract in 90 

vacuum 

AED = atomic emission detection; ECD = electron captive detector; EICD = electrolytic conductivity detector; 

FID = flame ionization detector; GC = gas chromatography; HECD = Hall electrolytic conductivity detector; IMS = ion 

mobility spectrometry; ITD = ion trap detector; MIMS = membrane introduction mass spectrometry; MS = mass 

spectrometry; PID = photoionization detector; PT = purge-and-trap; SD = steam distillation 
 

 

 

 

 

 

1,1-DICHLOROETHANE 99 

7. ANALYTICAL METHODS 

Gas purging-and-trapping on a Tenax GC adsorbent and GC/MS technique has been employed by 

Barkley et al. (1980) and Ashley et al. (1992) for the determination of trace levels of volatile halogenated 

compounds (including 1,1-dichloroethane) in water, human blood, and urine. 

7.2 ENVIRONMENTAL SAMPLES 

A GC equipped with an appropriate detector is the most frequently used analytical technique for 

determining the concentrations of 1,1-dichloroethane in air, water, soil, fish, dairy products, and various 

foods. Volatile organic compounds in environmental samples may exist as complex mixtures or at very 

low concentrations (ppt to ppb range). Subsequently, the GC technique must be supplemented by some 

method of sample preconcentration. The EPA updated Method 624 with revised quality control 

frequencies and improved internal standards and surrogates (EPA 2015a). GC columns were changed 

from packed columns to open tubular capillary columns in order to increase resolution and decrease 

losses due to adsorption. 

Gas purging-and-trapping is the generally accepted method for the isolation, concentration, and 

determination of VOCs in water and various environmental samples (Bellar et al. 1979; EPA 1994a, 

1994b, 1996b, 1999, 2001a, 2001b; Lopez-Avila et al. 1987a, 1987b; Page and Lacroix 1995; Reding 

1987; Wylie 1988). This method appears to be most adaptable for use with almost any GC detector— 

MS, FID, electron capture detector (ECD), and electrolytic conductivity detector (EICD). In addition, the 

method offers an important preliminary separation of highly volatile compounds from often highly 

complex samples prior to GC analysis. Detection limits at <1 μg 1,1-dichloroethane/L of sample have 

been achieved by this method (Dreisch and Munson 1983; Kingsley et al. 1983; Lopez-Avila et al. 1987a, 

1987b; Otson and Williams 1982). Page and Lacroix (1995) successfully coupled purge-and-trap 

procedures with steam distillation collection methods to yield an analytical method, for various foods, 

with a detection limit of 0.003 μg/kg for 1,1-dichloroethane. Bruner et al. (1978) employed purge-andtrap technique on charcoal adsorbent and GC/ECD for determination at ppt levels of volatile halo organic 

compounds in air. A major problem is that some of the halocarbons in the atmosphere are present as 

ultra-trace impurities in highly pure commercial inert gases. Subsequently, these impurities may interfere 

with the quantitative and qualitative analysis of 1,1-dichloroethane in environmental samples. 

A purge-and-trap method with cryogenic trapping (cryofocusing) for concentrating VOCs from water 

samples into the headspace, for analysis by capillary GC, was described by Pankow and Rosen (1988). 

The purge-and-trap technique offers advantages over other techniques in that it allows easy isolation and 
 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 100 

7. ANALYTICAL METHODS 

concentration of target compounds, which reduces interference, thereby improving overall limits of 

detection and recovery of sample (Otson and Chan 1987). Among the other advantages of the purge-andtrap technique with cryofocusing are its simplicity and therefore its reliability; the low background 

contamination since no sorbent traps are needed; and the relatively short time of sample analysis (Pankow 

and Rosen 1988). Roose and Brinkman (1998) capitalized on these techniques to analyze fish samples in 

a rapid, selective, and sensitive manner. An automated GC system with dual multi-adsorbent traps was 

successfully operated in a mobile laboratory to collect and analyze ambient air samples. The system 

continuously collects air samples, uses a pre-concentration approach (cryofocusing), and recovers 

analytes using thermal desorption. The detection limit for 1,1-dichloroethane was reported as 0.71 ppbv 

(Oliver et al. 1996). 

Purge-and-trap techniques have been successfully coupled with atomic emission detection (AED) for the 

analysis of water (Silgoner et al. 1997). Solutes eluting from the GC are atomized in a microwaveinduced plasma, and individual wavelengths are measured using a photodiode array. The detection limit 

of this method for 1,1-dichloroethane is 0.17 μg/L. While some improvement is still needed, the purgeand-trap technique coupled with AED offers some advantages over other methods. Dynamic headspace 

analyzer GC has been used for the analysis and identification of 1,1-dichloroethane in water and fish 

tissue (Comba and Kaiser 1983; Mehran et al. 1986; Otson and Williams 1982; Reinert et al. 1983;). The 

analytic sample is placed in a sealed flask connected to the headspace analyzer, which is directly 

interfaced with the injection port of the GC system. This arrangement allows for a greater proportion of 

compound contained in a sample to be analyzed. Detection limits of <1 μg 1,1-dichloroethane/L water 

and <1 μg 1,1-dichloroethane/g fish tissue were achieved (Mehran et al. 1986; Otson and Williams 1982; 

Reinert et al. 1983; Trussel et al. 1983). A disadvantage of this technique is that the inherent volatility of 

the halo organic compounds gives rise to an excessive foaming in the headspace system, thereby forming 

low yields and causing interference with the GC quantification. The typical yield of 1,1-dichloroethane 

was approximately 32% (Reinart et al. 1983). The authors indicated that use of an antifoaming agent 

such as silicone surfaces greatly reduced the foam, but extraneous chromatographic components and peak 

masking problems were encountered. 

Bauer and Solyom (1994) and Wong et al. (1995) reported that membrane introduction mass spectrometry 

(MIMS) offers measurements of trace-level organics in environmental media, including polluted 

seawater, without sample preparation, using a non-porous silicon membrane. A detection limit of 0.2 ppb 

was reported for 1,1-dichloroethane (Bauer and Solyom 1994). 
 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 101 

7. ANALYTICAL METHODS 

Pellizzari (1982) initiated the development and evaluation of trace levels of VOCs in industrial and 

chemical waste disposal sites. Ambient air samples were collected by a sampler equipped with Tenax GC 

adsorbent cartridges. Compounds were thermally removed from the adsorbent and analyzed by capillary 

GC/MS. The detection limit was at the μg/m3 level (Pellizzari 1982). 

Simpson et al. (1996) developed a method that has potential for on-site monitoring of vapor-phase 

organics in air. GC is coupled with ion mobility spectrometry to offer high sensitivity and the ability to 

operate at ambient pressure. While a detection limit for 1,1-dichloroethane was not reported, detection 

limits for several other EPA priority pollutants ranged from 0.05 to 140 pg/second. Maeda et al. (1998) 

also investigated analytical methods that may be applied to on-site monitoring techniques of HAPs. The 

analytical methods that they employed included a Tenax GC and Carboxene 1000 trap, followed by 

capillary separation and either photo ionization detector (PID) or EICD detection methods. The detection 

limit of the system was reported as 0.1 ppb. Another method for sampling and analyzing VOCs in air is 

proposed to have some advantages for use in field situations and may provide satisfactory results. The 

method uses teraglyme as a sample enrichment tool and employs purge-and-trap methods along with 

GC/MS (Huybrechts et al. 2001). 

Blanchard and Hardy (1985, 1986) developed a method that allows for continuous monitoring or 

intermittent analysis of volatile organic priority pollutants in environmental media. The method is based 

on permeation of VOCs through a silicone polycarbonate membrane from wastewater sample matrix, into 

an inert gas stream and directed into a capillary GC/FID via a sampling loop (Blanchard and Hardy 1986). 

Advantages of this procedure are that it is simple, it does not require time-consuming preconcentration 

steps, and it can be used either in the field or in the laboratory. 

The liquid-liquid extraction procedure provides a simple, rapid, screening method for semiquantitative 

determination of 1,1-dichloroethane in aqueous samples containing limited number of VOCs. It is less 

effective for aqueous samples containing large numbers of VOCs. Furthermore, interference from the 

organic (hexane) extraction solvent makes it more difficult to identify completely all compounds (Otson 

and Williams 1981). GC/EICD was employed by Otson and Williams (1981) for the detection of trace 

amounts (<1 μg/L of sample) of 1,1-dichloroethane in drinking water. 

Daft (1988) employed a photoionization detector and an electrolytic conductivity detector connected in 

series to a capillary GC to detect 1,1-dichloroethane at ng/g levels in fumigants and industrial chemical 

residues of various foods (e.g., dairy products, meat, vegetables, and soda). Typically, foods were 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 102 

7. ANALYTICAL METHODS 

extracted with isooctane and injected in GC column for analysis. However, foods containing lipid and fat 

were subjected to further clean-up on micro-florisil column prior to GC analysis. 

A procedure was developed by Hiatt (1983) and Dreisch and Munson (1983) to identify and quantify 

1,1-dichloroethane in fish tissue samples by GC/MS, employing a fused-silica capillary column (FSCC) 

and vacuum distillation (extraction). An advantage of the vacuum extraction is that the system does not 

require elevated temperatures or the addition of reagents, which could produce unwanted degradation 

products (Hiatt 1981). The FSCC provides a more attractive approach than packed column for 

chromatographic analysis of VOCs, because FSCC can be heated to a higher-temperature (350 °C) than 

that recommended for packed column thereby improving the resolution (at the ng/g level) of compounds 

at a lesser retention time. A physical limitation for compounds that can be detected, however, is that the 

vapor pressure of the compounds must be >0.78 torr (approximately 50 °C) in the sample chamber (Hiatt 

1983). 

7.3 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of 1,1-dichloroethane is available. Where adequate 

information is not available, ATSDR, in conjunction with NTP, is required to assure the initiation of a 

program of research designed to determine the health effects (and techniques for developing methods to 

determine such health effects) of 1,1-dichloroethane. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 

7.3.1 Identification of Data Needs 

Methods for Determining Biomarkers of Exposure and Effect. Reliable methods are available 

for detecting and quantifying 1,1-dichloroethane in the tissues and body fluids of humans. GC/MS or 

GC/FID has been employed to detect 1,1-dichloroethane at nanogram to picogram levels in blood and 

tissue samples of humans. No additional analytical methods for determining trace levels of 1,1-dichloro­
 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 103 

7. ANALYTICAL METHODS 

ethane in the blood of humans are needed. Also, no detection limits for detecting 1,1-dichloroethane in 

urine samples by GC/MS were indicated by Barkley et al. (1980). Therefore, additional research and 

development of sensitive and selective methods for detecting and quantifying the levels of 

1,1-dichloroethane and its metabolites in the tissues and urine of humans would be useful. If methods 

were available, it would assist investigators in determining whether specific levels of 1,1-dichloroethane 

found in the tissues/fluids of exposed persons correlate with any adverse health effects. 

Methods for Determining Parent Compounds and Degradation Products in Environmental 

Media. Analytical methods are available to detect 1,1-dichloroethane in environmental samples. 

Purge-and-trap or direct injection followed by analysis with GC/ECD and GC/MS have been used to 

detect and quantify 1,1-dichloroethane in water samples at ppt and ppb levels (methods 5030, 8240, 

8010B [EPA 1994a, 1994b, 1996b]; method 601, 624, 1624 [EPA 1999, 2001a, 2001b]). GC equipped 

with FID, PID, or EICD has also been used to detect and quantify 1,1-dichloroethane in air, water, milk, 

vegetables, and fish at ppb levels NIOSH (method 1003 [NIOSH 2003]). No additional analytical 

methods for determining trace levels of 1,1-dichloroethane in environmental media are needed. 

7.3.2 Ongoing Studies 

No ongoing studies regarding sponsored by NIH or EPA were identified for 1,1-dichloroethane. 
 

 

1,1-DICHLOROETHANE 104 

7. ANALYTICAL METHODS 

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1,1-DICHLOROETHANE 105 

8. REGULATIONS, ADVISORIES, AND GUIDELINES
 

MRLs are substance specific estimates, which are intended to serve as screening levels, are used by 

ATSDR health assessors and other responders to identify contaminants and potential health effects that 

may be of concern at hazardous waste sites. 

No inhalation or oral MRLs were derived for 1,1-dichloroethane. 

The EPA (IRIS 2002) has not derived an oral reference dose (RfD) or an inhalation reference 

concentration (RfC) for 1,1-dichloroethane. 

1,1-Dichloroethane appears on the list of chemicals in “The Emergency Planning and Community Rightto-Know Act of 1986” and has been assigned a reportable quantity (RQ) limit of 1,000 pounds (EPA 

2014e). The RQ represents the amount of a designated hazardous substance which, when released to any 

environmental media, must be reported to the appropriate authority. 

The international and national regulations, advisories, and guidelines regarding 1,1-dichloroethane in air, 

water, and other media are summarized in Table 8-1. 
 

 

1,1-DICHLOROETHANE 106 

8. REGULATIONS, ADVISORIES, AND GUIDELINES 

Table 8-1. Regulations, Advisories, and Guidelines Applicable to 

1,1-Dichloroethane 

Agency Description Information Reference 

INTERNATIONAL 

Guidelines: 

IARC Carcinogenicity classification No data IARC 2015 

WHO Air quality guidelines No data WHO 2010 

Drinking water quality guidelines No dataa WHO 2011 

NATIONAL 

Regulations and 

Guidelines: 

a. Air 

ACGIH TLV (8-hour TWA) 100 ppm ACGIH 2014 

AIHA ERPGs No data AIHA 2014 

DOE PAC-1 and PAC-2b 160 ppm DOE 2012a 

PAC-3b 4,000 ppm 

EPA AEGLs No data EPA 2014b 

NAAQS No data EPA 2012b 

NIOSH REL (10-hour TWA) 100 ppm (400 mg/m3)c NIOSH 2015 

IDLH 3,000 ppm 

OSHA PEL (8-hour TWA) for general industry 100 ppm (400 mg/m3) OSHA 2013 

29 CFR 1910.1000, 

Table Z-1 

PEL (8-hour TWA) for construction 100 ppm (400 mg/m3) OSHA 2014a 

29 CFR 1926.55, 

Appendix A 

PEL (8-hour TWA) for shipyards 100 ppm (400 mg/m3) OSHA 2014b 

29 CFR 1915.1000 

b. Water 

EPA Designated as hazardous substances in No data EPA 2013a 

accordance with Section 311(b)(2)(A) of 40 CFR 116.4 

the Clean Water Act 

Drinking water standards and health No data EPA 2012a 

advisories 

Master Testing List Yesd EPA 2014c 

National primary drinking water No data EPA 2009 

standards 

National recommended water quality No data EPA 2013b 

criteria: human health for the 

consumption of 

Reportable quantities of hazardous No data EPA 2013c 

substances designated pursuant to 40 CFR 117.3 

Section 311 of the Clean Water Act 
 

1,1-DICHLOROETHANE 107 

8. REGULATIONS, ADVISORIES, AND GUIDELINES 

Table 8-1. Regulations, Advisories, and Guidelines Applicable to 

1,1-Dichloroethane 

Agency Description Information Reference 

NATIONAL (cont.) 

c. Food 

FDA EAFUSe No data FDA 2013 

d. Other 

ACGIH Carcinogenicity classification A4f ACGIH 2014 

EPA Carcinogenicity classification Cg IRIS 2002 

RfC No data 

RfD No data 

Identification and listing of hazardous 

waster 

U076 EPA 2013e 

40 CFR 261, 

Appendix VIII 

Inert pesticide ingredients in pesticide 

products 

No data EPA 2014d 

Superfund, emergency planning, and 

community right-to-know 

Designated CERCLA hazardous 

substance and reportable quantity 

1,000 poundsh EPA 2014e 

40 CFR 302.4 

Effective date of toxic chemical 

release reporting 

01/01/1994 EPA 2014f 

40 CFR 372.65 

Extremely hazardous substances 

and its threshold planning quantity 

No data EPA 2013d 

40 CFR 355, 

Appendix A 

TSCA chemical lists and reporting 

periods 

EPA 2014g 

40 CFR 712.30 

Effective date 03/11/1994 

Reporting date 05/10/1994 

TSCA health and safety data reporting 

Effective date 06/01/1987 

EPA 2014h 

40 CFR 716.120 

Reporting date 06/01/1997 

NTP Carcinogenicity classification No data NTP 2014 

aIn view of the very limited database on toxicity and carcinogenicity, the Guidelines concluded that no guideline value 

for 1,1-dichloroethane should be proposed. bDefinitions of PAC terminology are available from U.S. Department of Energy (DOE 2012b). 

cNIOSH recommends that 1,1-dichloroethane be treated in the workplace with caution because of its structural 

similarity to the four chloroethanes (ethylene dichloride, hexachloroethane, 1,1,2,2-tetrachloroethane, and 

1,1,2-trichloroethane) shown to be carcinogenic in animals. d1,-Dichloroethane was recommended to the MTL by the EPA’s Office of Water and Office of Drinking Water in 1990 

and was later removed in 1995. The initial chemical testing program was for prechronic toxicity (14–28 day) and 

subchronic toxicity (90 day) health effects. eThe EAFUS list of substances contains ingredients added directly to food that FDA has either approved as food 

additives or listed or affirmed as GRAS. 

f

A4: not classifiable as a human carcinogen 

gC: possible human carcinogen

hDesignated CERCLA hazardous substance pursuant to Section 307(a)of the Clean Water Act, Section 112 of the 

Clean Air Act, and Section 3001 of RCRA. 
 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 108 

8. REGULATIONS, ADVISORIES, AND GUIDELINES 

Table 8-1. Regulations, Advisories, and Guidelines Applicable to 

1,1-Dichloroethane 

Agency Description Information Reference 

ACGIH = American Conference of Governmental Industrial Hygienists; AEGL = acute exposure guideline levels; 

AIHA = American Industrial Hygiene Association; CERCLA = Comprehensive Environmental Response, 

Compensation, and Liability Act; CFR = Code of Federal Regulations; DOE = Department of Energy; 

EAFUS = Everything Added to Food in the United States; EPA = Environmental Protection Agency; 

ERPG = emergency response planning guidelines; FDA = Food and Drug Administration; GRAS = Generally 

Recognized As Safe; IARC = International Agency for Research on Cancer; IDLH = immediately dangerous to life or 

health; IRIS = Integrated Risk Information System; MTL = Master Testing List; NAAQS = National Ambient Air Quality 

Standards; NIOSH = National Institute for Occupational Safety and Health; NTP = National Toxicology Program; 

OSHA = Occupational Safety and Health Administration; PAC = Protective Action Criteria; PEL = permissible 

exposure limit; RCRA = Resource Conservation and Recovery Act; REL = recommended exposure limit; 

RfC = inhalation reference concentration; RfD = oral reference dose; TLV = threshold limit values; TSCA = Toxic 

Substances Control Act; TSD = treatment, storage, and disposal; TWA = time-weighted average; WHO = World 

Health Organization 
 

 

 

 

 

 

 

 

 

 


 

1,1-DICHLOROETHANE 109 

9. REFERENCES
 

ACGIH. 2014. 1,1-Dichloroethane. In: TLVs and BEIs based on the documentation of the threshold 

limit values for chemical substances and physical agents and biological exposure indices. Cincinnati, 

OH: American Conference of Governmental Industrial Hygienists, 24. 

Adlercreutz H. 1995. Phytoestrogens: Epidemiology and a possible role in cancer protection. Environ 

Health Perspect Suppl 103(7):103-112. 

Agency for Toxic Substances and Disease Registry. 1989. Decision guide for identifying substancespecific data needs related to toxicological profiles; Notice. Agency for Toxic Substances and Disease 

Registry, Division of Toxicology. Fed Regist 54(174):37618-37634. 

AIHA. 2014. Current ERPG Values (2014). Fairfax, VA: American Industrial Hygiene Association. 

https://www.aiha.org/getinvolved/AIHAGuidelineFoundation/EmergencyResponsePlanningGuidelines/Documents/2014%20ERP 

G%20Values.pdf. March 4, 2015. 

Altman PL, Dittmer DS. 1974. Biological handbooks: Biology data book. Vol. III. 2nd ed. Bethesda, 

MD: Federation of American Societies for Experimental Biology, 1987-2008, 2041. 

Andersen ME, Krishnan K. 1994. Relating in vitro to in vivo exposures with physiologically based tissue 

dosimetry and tissue response models. In: Salem H, ed. Animal test alternatives: Refinement, 

reduction, replacement. New York, NY: Marcel Dekker, Inc., 9-25. 

Andersen ME, Clewell HJ, Gargas ML, et al. 1987. Physiologically based pharmacokinetics and the risk 

assessment process for methylene chloride. Toxicol Appl Pharmacol 87(2):185-205. 

Andrews JE, Nichols H, Hunter ES. 2002. Developmental toxicity of di- and tetrachloroethane and 

dichloropropane in the rat whole embryo culture system [Abstract]. Toxicologist 66(1-S):23. 

Archer, WL. 1978. Other chloroethanes. In: Kirk-Othmer encyclopedia of chemistry and technology. 

Vol. 5, 3rd ed. New York, NY: John Wiley and Sons, Inc., 722-742. 

Ashley DL, Bonin MA, Cardinali FL, et al. 1992. Determining volatile organic compounds in human 

blood from a large sample population by using purge and trap gas chromatography/mass spectrometry. 

Anal Chem 64:1021-1029. 

Baker RJ, Andraski BJ, Stonestrom DA, et al. 2012. Volatile organic compounds in the unsaturated zone 

from radioactive wastes. J Environ Qual 41(4):1324-1336. I 10.2134/jeq2011.0480. 

Barkley J, Bunch J, Bursey JT, et al. 1980. Gas chromatography mass spectrometry computer analysis of 

volatile halogenated hydrocarbons in man and his environment - a multimedia environmental study. 

Biomed Mass Spectrom 7:139-147. 

Barsky JB, Hee SSQ, Clark CS. 1985. An evaluation of the response of some portable, direct-reading 

10.2 electron volt and 11.8 electron volt photoionization detectors and a flame ionization gas 

chromatograph for organic vapors in high humidity atmospheres. Am Ind Hyg Assoc J 46:9-14. 
 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 110 

9. REFERENCES 

Bauer S, Solyom D. 1994. Determination of volatile organic compounds at the parts per trillion level in 

complex aqueous matrices using membrane introduction mass spectrometry. Anal Chem 66(24):4422­

4431. 

Bellar TA, Budde WL, Eichelberger JW. 1979. The identification and measurement of volatile organic 

compounds in aqueous environmental samples. In: Schuetzle D, ed. Monitoring toxic substances. 

American Chemical Society Symposium Series No. 94. Washington, DC: American Chemical Society, 

49-62. 

Berger GS, ed. 1994. Epidemiology of endometriosis. In: Endometriosis: Advanced management and 

surgical techniques. New York, NY: Springer-Verlag, 3-7. 

Bi E, Liu Y, He J, et al. 2012. Screening of emerging volatile organic contaminants in shallow 

groundwater in east China. Ground Water Monit Remed 32(1):53-58. I 10.1111/j.1745­

6592.2011.01362.x. 

Blanchard RD, Hardy JK. 1985. Use of a permeation sampler in the collection of 23 volatile organic 

priority pollutants. Anal Chem 57:2349-2351. 

Blanchard RD, Hardy JK. 1986. Continuous monitoring device for the collection of 23 volatile organic 

priority pollutants. Anal Chem 58:1529-1532. 

Boman A, Maibach H. 1996. Influence of evaporation and repeated exposure on the percutaneous 

absorption of organic solvents. In: Elsner P, Lachapelle JM, Wahlberg JE, et al., eds. Current problems 

in dermatology (Basel), Vol. 25. Prevention of Contact Dermatitis; International Conference on the 

Prevention of Contact Dermatitis, Zurich, Switzerland, October 4-7, 1995, 47-56. 

Bronzetti G, Galli A, Vellosi R, et al. 1987. Genetic activity of chlorinated ethanes [Abstract]. Eur J 

Cancer Clin Oncol 23:1737-1738. 

Bruner F, Bertoni G, Crescentini G. 1978. Critical evaluation of sampling and gas chromatographic 

analysis of halocarbons and other organic air pollutants. J Chromatogr 167:399-407. 

Buckley TJ, Liddie J, Ashley DL, et al. 1997. Environmental and biomarker measurements in nine 

homes in the lower Rio Grande Valley: Multimedia results for pesticides, metals, PAHs, and VOCs. 

Environ Int 23(5):705-732. 

Cadena F, Eiceman GA, Vandiver VJ. 1984. Removal of volatile organic pollutants from rapid streams. 

J Water Pollut Control Fed 56:391-490. 

Cal EPA. 2003. Public health goal for 1,1-dichloroethane in drinking water. California Environmental 

Protection Agency, Office of Environmental Health Hazard Assessment. 

CDC. 2015. Fourth national report on human exposure to environmental chemicals. Centers for 

Disease Control and Prevention. 

http://www.cdc.gov/biomonitoring/pdf/FourthReport_UpdatedTables_Feb2015.pdf. March 10, 2015. 

ChemIDplus Lite. 2012. 1,1-Dichloroethane. 

http://chem.sis.nlm.nih.gov/chemidplus/ProxyServlet?objectHandle=Search&actionHandle. February 13, 

2012. 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 111 

9. REFERENCES 

Clewell HJ, Andersen ME. 1985. Risk assessment extrapolations and physiological modeling. Toxicol 

Ind Health 1(4):111-131. 

Cline PV, Viste DR. 1985. Migration and degradation patterns of volatile organic compounds. Waste 

Manag Res 3:351-360. 

Colacci A, Arfellini G, Mazzullo M, et al. 1985. Genotoxicity of 1,1-dichloroethane. Res Commun 

Chem Pathol Pharmacol 49:243-254. 

Cole RH, Frederick RE, Healy RP, et al. 1984. Preliminary findings of the priority pollutant monitoring 

project of the Nationwide Urban Runoff Program. J Water Pollut Control Fed 56:898-908. 

Comba ME, Kaiser KLE. 1983. Determination of volatile contaminants at the ng/l level in water by 

capillary gas chromatography with electron capture detection. Int J Environ Anal Chem 16:17-31. 

Coniglio WA, Miller K, MacKeever D. 1980. The occurrence of volatile organics in drinking water. 

Briefing for the Deputy Assistant Administrator for Drinking Water, March 1980. 

Costa LG, Aschner M, Vitalone A, et al. 2004. Developmental neuropathology of environmental agents. 

Annu Rev Pharmacol Toxicol 44:87-110. 10.1146/annurev.pharmtox.44.101802.121424. 

Cowfer JA, Gorenser MB, Company TG. 2006. Vinyl chloride. In: Kirk-Othmer encyclopedia of 

chemical technology. New York, NY: John Wiley & Sons, Inc., 1-31. 

Cramer PH, Boggess K, Hosenfeld JM, et al. 1988. Determination of organic chemicals in human whole 

blood: Preliminary method development for volatile organics. Bull Environ Contam Toxicol 40:612­

618. 

Cupitt LT. 1980. Fate of toxic and hazardous materials in the air environment. Research Triangle Park, 

NC: U.S. Environmental Protection Agency. EPA600S380084. 

Daft JL. 1988. Rapid determination of fumigant and industrial chemical residues in food. J Assoc Off 

Anal Chem 71:748-760. 

de Best JH, Jongema H, Weijling A, et al. 1997. Transformation of 1,1,1-trichloroethane in an anaerobic 

packed-bed reactor at various concentrations of 1,1,1-trichloroethane, acetate and sulfate. Appl Microbiol 

Biotechnol 48(3):417-423. 

Dewulf J, Dewettinck T, De Visscher A, et al. 1996. Sorption of chlorinated C1- and C2-hydrocarbons 

and monocyclic aromatic hydrocarbons on sea sediment. Water Res 30(12):3130-3138. 

Dilling WL. 1977. Interphase transfer processes. II. Evaporation rates of chloromethanes, ethanes, 

ethylenes, propanes, and propylenes from dilute aqueous solutions. Comparisons with theoretical 

predictions. Environ Sci Technol 11:405-409. 

Dilling WL, Tefertiller NB, Kallos GJ. 1975. Evaporation rates and reactivities of methylene chloride, 

chloroform, 1,1,1-trichloroethane, trichloroethylene, tetrachloroethylene, and other chlorinated 

compounds in dilute aqueous solutions. Environ Sci Technol 9:833-837. 

DOE. 2005. Interim sanitary landfill 2005 annual groundwater report. U.S. Department of Energy. 

WSRC-TR-2005-00548. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 112 

9. REFERENCES 

DOE. 2012a. Table 3: PACs by CASRN (pdf). PAC Rev 27 Tables - PAC data and chemical properties 

presented in pdf and excel tables. Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: 

Rev. 27 for Chemicals of Concern - March 2012. Oak Ridge, TN: U.S. Department of Energy. 

http://energy.gov/ehss/protective-action-criteria-pac-aegls-erpgs-teels-rev-27-chemicals-concern-march2012. March 4, 2015. 

DOE. 2012b. Protective action criteria (PAC): Chemicals with AEGLs, ERPGs, & TEELs. Definition 

of PACs (AEGLs, ERPGs or TEELs). Protective Action Criteria (PAC) with AEGLs, ERPGs, & TEELs: 

Rev. 27 for Chemicals of Concern - March 2012. Oak Ridge, TN: U.S. Department of Energy. 

http://energy.gov/ehss/protective-action-criteria-pac-aegls-erpgs-teels-rev-27-chemicals-concern-march2012. March 24, 2015. 

Dreher EL, Beutel KK, Myers JD, et al. 2014. Chloroethanes and chloroethylenes. In: Ullmann's 

encyclopedia of industrial chemistry. Vol. 10.1002/14356007.o06_o01.pub2. 

Dreisch FA, Munson TO. 1983. Purge-and-trap analysis using fused silica capillary column gas 

chromatography-mass spectrometry. J Chromatogr Sci 21:111-118. 

Driscoll JN, Duffy M, Pappas S, et al. 1987. Analysis for purgeable organics in water by capillary 

GC/PID-EICD. J Chromatogr Sci 25:369-375. 

Easley DM, Kleopfer RD, Carasea AM. 1981. Gas chromatographic-mass spectrometric determination 

of volatile organic compounds in fish. J Assoc Off Anal Chem 64:653-656. 

Eitzer BD. 1995. Emissions of volatile organic chemicals from municipal solid waste composting 

facilities. Environ Sci Technol 29:896-902. 

Ek CJ, Dziegielewska KM, Habgood MD, et al. 2012. Barriers in the developing brain and 

neurotoxicology. Neurotoxicology 33(3):586-604. 10.1016/j.neuro.2011.12.009. 

EPA. 1978. Quantification of chlorinated hydrocarbons in previously collected air samples. Research 

Triangle Park, NC: U.S. Environmental Protection Agency. EPA450378112. 

EPA. 1980. Ambient water quality criteria for chlorinated ethanes. Washington, DC: U.S. 

Environmental Protection Agency, Office of Water Regulations and Standards, Criteria and Standards 

Division. EPA440580029. 

EPA. 1982a. An exposure and risk assessment for dichloroethanes. U.S. Environmental Protection 

Agency. EPA440485009. http://nepis.epa.gov/Exe/ZyPURL.cgi?Dockey=40001LDV.txt. June 4, 2015. 

EPA. 1982b. Direct measurement of volatile organic compounds in breathing-zone air, drinking water, 

breath, blood and urine. Research Triangle Park, NC: U.S. Environmental Protection Agency. 

EPA600482015. PB82186545. 

EPA. 1983a. Measurements of hazardous organic chemicals in the ambient atmosphere. Research 

Triangle Park, NC: U.S. Environmental Protection Agency, Office of Research and Development. 

EPA600383002. PB83156935. 

EPA. 1983b. Volatile organic chemicals in the atmosphere: An assessment of available data. Menlo 

Park, CA: U.S. Environmental Protection Agency. EPA600S83027. 
 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 113 

9. REFERENCES 

EPA. 1985. Synthetic organic compound sampling survey of public water supplies. Washington, DC: 

U.S. Environmental Protection Agency. PB85214427. 

EPA. 1993. Analyis of ambient monitoring data in the vicinity of open tire fires. Research Triangle 

Park, NC: U.S. Environmental Protection Agency, Office of Air Quality. 

EPA. 1994b. Method 8010B. Halogenated volatile organics by gas chromatography. Test methods for 

evaluating solid waste. U.S. Environmental Protection Agency. 

EPA. 1994a. Method 8240B. Volatile organic compounds by gas chromatography/mass spectrometry 

(GC/MS). Test methods for evaluating solid wastes physical/chemical methods. Washington, DC: U.S. 

Environmental Protection Agency. 

EPA. 1996a. Determination of landfill gas composition and pollutant emission rates at fresh kills 

landfill. Volume 1. New York, NY: U.S. Environmental Protection Agency. 

EPA. 1996b. Method 5030B. Purge-and-trap for aqueous samples. Test methods for evaluating solid 

wastes physical/chemical methods. U.S. Environmental Protection Agency. 

http://www.epa.gov/epawaste/hazard/testmethods/sw846/pdfs/5030b.pdf. June 28, 2012. 

EPA. 1997. Special report on environmental endocrine disruption: An effects assessment and analysis. 

Washington, DC: U.S. Environmental Protection Agency, Risk Assessment Forum. EPA630R96012. 

EPA. 1999. Appendix A to part 136-methods for organic chemical analysis of municipal and industrial 

waste-water. Method 624-purgeables. U.S. Environmental Protection Agency. Code of Federal 

Regulations 40 CFR 136 Appendix A, Method 624. 

https://www.nemi.gov/apex/f?p=237:38:2361622513108808::::P38_METHOD_ID:5249. June 28, 2012. 

EPA. 2000. National air pollutant emission trends, 1900-1998. Research Triangle Park, NC: U.S. 

Environmental Protection Agency, Office of Air Quality Planning and Standards. EPA450R00002. 

EPA. 2001a. Appendix A to part 136-methods for organic chemical analysis of municipal and industrial 

waste-water. Method 601-purgeable halocarbons. U.S. Environmental Protection Agency. Code of 

Federal Regulations 40 CFR 136 Appendix A, Method 601. 

https://www.nemi.gov/pls/nemi_pdf/nemi_data.download_pdf?p_file=3091. June 28, 2012. 

EPA. 2001b. Appendix A to part 136-method 1624 revision B-volatile organic compounds by isotope 

dilution GC/MS. U.S. Environmental Protection Agency. Code of Federal Regulations 40 CFR 136 

Appendix A, Method 1624. https://www.nemi.gov/pls/nemi_pdf/nemi_data.download_pdf?p_file=3051. 

June 28, 2012. 

EPA. 2001c. Sources, emission and exposure for trichloroethylene(TCE) and related chemicals. 

Washington, DC: U.S. Environmental Protection Agency, National Center for Environmental 

Assessment, Office of Research and Development. 
 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 114 

9. REFERENCES 

EPA. 2005. Toxic chemical release inventory reporting forms and instructions: Revised 2004 version. 

Section 313 of the Emergency Planning and Community Right-to-Know Act (Title III of the Superfund 

Amendments and Reauthorization Act of 1986). U.S. Environmental Protection Agency. Office of 

Environmental Information. EPA260B05001. 

EPA. 2009. National primary drinking water regulations. Washington, DC: U.S. Environmental 

Protection Agency, Office of Ground Water and Drinking Water. EPA816F090004. 

http://water.epa.gov/drink/contaminants/upload/mcl-2.pdf. March 4, 2015. 

EPA. 2010. CAS 75-34-3. Non-confidential 2006 IUR records by chemical, including manufacturing, 

processing and use information. U.S. Environmental Protection Agency. 

http://cfpub.epa.gov/iursearch/index.cfm?err=t#chemical. May 16, 2012. 

EPA. 2012a. 2012 Edition of the drinking water standards and health advisories. Washington, DC: U.S. 

Environmental Protection Agency, Office of Water. EPA822S12001. 

http://water.epa.gov/action/advisories/drinking/upload/dwstandards2012.pdf. March 4, 2015. 

EPA. 2012b. National ambient air quality standards (NAAQS). Washington, DC: U.S. Environmental 

Protection Agency, Office of Air and Radiation. http://www.epa.gov/air/criteria.html. January 08, 2014. 

EPA. 2012c. 2005 National emissions inventory data and documentation. U.S. Environmental 

Protection Agency. http://www.epa.gov/ttn/chief/net/2005inventory.html#inventorydata. May 18, 2012. 

EPA. 2013a. Designation of hazardous substances. U.S. Environmental Protection Agency. Code of 

Federal Regulations 40 CFR 116.4. http://www.gpo.gov/fdsys/pkg/CFR-2014-title40-vol22/pdf/CFR2014-title40-vol22-sec116-4.pdf. March 4, 2015. 

EPA. 2013b. National recommended water quality criteria. Washington, DC: U.S. Environmental 

Protection Agency, Office of Water, Office of Science and Technology. 

http://water.epa.gov/scitech/swguidance/standards/criteria/current/index.cfm. March 4, 2015. 

EPA. 2013c. Determination of reportable quantities for hazardous substances. Subpart A - General 

provisions. U.S. Environmental Protection Agency. Code of Federal Regulations 40 CFR 117.3. 

http://www.gpo.gov/fdsys/pkg/CFR-2014-title40-vol22/pdf/CFR-2014-title40-vol22-sec117-3.pdf. 

March 4, 2015. 

EPA. 2013d. Appendix A to Part 355—The list of extremely hazardous substances and their threshold 

planning quantities. U.S. Environmental Protection Agency. Code of Federal Regulations 40 CFR 355. 

http://www.gpo.gov/fdsys/pkg/CFR-2013-title40-vol29/pdf/CFR-2013-title40-vol29-part355-appA.pdf. 

September 10, 2014. 

EPA. 2013e. Appendix VIII to Part 261-Hazardous constituents. U.S. Environmental Protection 

Agency. Code of Federal Regulations 40 CFR 261, Appendix VIII. http://www.gpo.gov/fdsys/pkg/CFR2013-title40-vol27/pdf/CFR-2013-title40-vol27-part261-appVIII.pdf. September 10, 2014. 

EPA. 2014a. CAS 75-34-3. Pollution prevention and toxics. Chemical Data Access Tool (CDAT). 

U.S. Environmental Protection Agency. http://java.epa.gov/oppt_chemical_search/. February 26, 2015. 

EPA. 2014b. Final AEGLs (162). Washington, DC: U.S. Environmental Protection Agency, Office of 

Pollution Prevention and Toxics. 

http://www.epa.gov/oppt/aegl/pubs/compiled_aegls_update_03oct2014.pdf. March 4, 2015. 
 

 

 

 

 

 

 

1,1-DICHLOROETHANE 115 

9. REFERENCES 

EPA. 2014c. Master testing list. Washington, DC: U.S. Environmental Protection Agency, Office of 

Pollution Prevention and Toxics. http://www.epa.gov/opptintr/chemtest/pubs/index1.pdf. September 10, 

2014. 

EPA. 2014d. InertFinder. U.S. Environmental Protection Agency. 

http://iaspub.epa.gov/apex/pesticides/f?p=101:1:. March 31, 2015. 

EPA. 2014e. Designation of hazardous substances. U.S. Environmental Protection Agency. Code of 

Federal Regulations 40 CFR 302.4. http://www.gpo.gov/fdsys/pkg/CFR-2014-title40-vol28/pdf/CFR2014-title40-vol28-sec302-4.pdf. March 4, 2015. 

EPA. 2014f. Chemicals and chemical categories to which this part applies. Subpart D - Specific toxic 

chemical listings. U.S. Environmental Protection Agency. Code of Federal Regulations 40 CFR 372.65. 

http://www.gpo.gov/fdsys/pkg/CFR-2014-title40-vol28/pdf/CFR-2014-title40-vol28-sec372-65.pdf. 

March 4, 2015. 

EPA. 2014g. Chemical lists and reporting periods. Subpart B - Manufacturers reporting - Preliminary 

assessment information. Code of Federal Regulations 40 CFR 712.30. 

http://www.gpo.gov/fdsys/pkg/CFR-2014-title40-vol31/pdf/CFR-2014-title40-vol31-sec712-30.pdf. 

April 6, 2015. 

EPA. 2014h. Substances and listed mixtures to which this subpart applies. Subpart B - Specific 

chemical listings. Code of Federal Regulations 40 CFR 716.120. http://www.gpo.gov/fdsys/pkg/CFR2014-title40-vol31/pdf/CFR-2014-title40-vol31-sec716-120.pdf. April 6, 2015. 

EPA. 2015a. Clean water act methods update rule For the analysis of effluent. U.S. Environmental 

Protection Agency. Fed Regist 80(33):8956-9075. 

EPA. 2015b. 1,1-Dichloroethane. Ambient monitoring technology information center. Air toxics data. 

Air toxics-data analysis. U.S. Environmental Protection Agency. 

http://www.epa.gov/ttnamti1/toxdat.html#data. April 2, 2015. 

EPA. 2015c. National Priorities List (NPL). U.S. Environmental Protection Agency. 

http://www.epa.gov/superfund/sites/npl/. April 2, 2015. 

FDA. 2013. Everything added to food in the United States (EAFUS). Washington, DC: U.S. Food and 

Drug Administration. http://www.accessdata.fda.gov/scripts/fcn/fcnnavigation.cfm?rpt=eafuslisting. 

January 08, 2014. 

Ferrario JB, Lawler GC, DeLeon IR, et al. 1985. Volatile organic pollutants in biota and sediments of 

Lake Pontchatrain. Bull Environ Contam Toxicol 34:246-255. 

Fomon SJ. 1966. Body composition of the infant: Part I: The male reference infant. In: Falkner F, ed. 

Human development. Philadelphia, PA: WB Saunders, 239-246. 

Fomon SJ, Haschke F, Ziegler EE, et al. 1982. Body composition of reference children from birth to age 

10 years. Am J Clin Nutr 35(Suppl 5):1169-1175. 
 

 

 

 

 

 

1,1-DICHLOROETHANE 116 

9. REFERENCES 

Giabbai M, Roland L, Chian ESK. 1983. Trace analysis of organic priority pollutants by high-resolution 

gas chromatography and selective detectors (FID, ECD, NPD, and MS-DS): Application to municipal 

wastewater and sludge samples. Chromatogr Biochem Med Environ Res 13:41-52. 

Giwercman A, Carlsen E, Keiding N, et al. 1993. Evidence for increasing incidence of abnormalities of 

the human testis: A review. Environ Health Perspect Suppl 101(2):65-71. 

Goodin JD, Webber MD. 1992. The persistence and fate of industrial organics in sludge-treated soil. 

Can J Soil Sci 72:310-311. 

Gossett RW, Brown DA, Young DR. 1983. Predicting the bioaccumulation of organic compounds in 

marine organisms using octanol/water partition coefficients. Mar Pollut Bull 14:387-392. 

Great Lakes Commission. 2006. 2002 Inventory of toxic air emissions for the Great Lakes Region. Ann 

Arbor, MI: Great Lakes Commission. 

Grimsrud EP, Rasmussen RA. 1975. Survey and analysis of halocarbons in the atmosphere by gas 

chromatography- mass spectrometry. Atmos Environ 9:1014-1017. 

Gupta KC, Ulsamer AG, Gammage R. 1984. Volatile organic compounds in residential air: Levels, 

sources and toxicity. Proceedings of the 77th Air Pollution Control Association Annual Meeting 1:9. 

Guzelian PS, Henry CJ, Olin SS, eds. 1992. Similarities and differences between children and adults: 

Implications for risk assessment. Washington, DC: International Life Sciences Institute Press. 

Hallen RT, Pyne JR Jr., Molton PM. 1986. Transformation of chlorinated ethenes and ethanes by 

anaerobic microorganisms. In: Proceedings of 192nd national meeting: ACS Division of Environmental 

Chemistry, Vol. 26, 344-346. 

Hamonts K, Kuhn T, Vos J, et al. 2012. Temporal variations in natural attenuation of chlorinated 

aliphatic hydrocarbons in eutrophic river sediments impacted by a contaminated groundwater plume. 

Water Res 46(6):1873-1888. I 10.1016/j.watres.2012.01.001. 

Hatch GG, Mamay PD, Ayer ML, et al. 1983. Chemical enhancement of viral transformation in Syrian 

hamster embryo cells. Cancer Res 43:1945-1950. 

HazDat. 2007. 1,1-Dichloroethane. HazDat Database: ATSDR’s Hazardous Substance Release and 

Health Effects Database. Atlanta, GA: Agency for Toxic Substances and Disease Registry. 

Heikes DL, Jensen SR, Fleming-Jones ME. 1995. Purge and trap extraction and GC-MS determination 

of volatile organic compounds in table-ready food. J Agric Food Chem 43:2869-2875. 

Herren-Freund SL, Pereira MA. 1986. Carcinogenicity of by-products of disinfection in mouse and rat 

liver. Environ Health Perspect 69:59-65. 

Hiatt MH. 1981. Analysis of fish and sediment for volatile priority pollutants. Anal Chem 53:1541­

1543. 

Hiatt MH. 1983. Determination of volatile organic compounds in fish samples by vacuum distillation 

and fused silica capillary gas chromatography/mass spectrometry. Anal Chem 55:506-516. 
 

 

 

 

 

 

1,1-DICHLOROETHANE 117 

9. REFERENCES 

Hoel DG, Davis DL, Miller AB, et al. 1992. Trends in cancer mortality in 15 industrialized countries, 

1969-1986. J Natl Cancer Inst 84(5):313-320. 

Hofmann HT, Birnstiel H, Jobst P. 1971. [Inhalation toxicity of 1,1- and 1,2-dichloroethane]. Arch 

Toxikol 27:248-265. (German). 

Howard CJ, Evenson KM. 1976. Rate constants for the reactions of OH with ethane and some halogen 

substituted ethanes at 296 K. J Chem Phys 64:4303-4306. 

HSDB. 2012. 1.1-Dichloroethane. Hazardous Substances Data Bank. National Library of Medicine. 

http://toxnet.nlm.nih.gov. May 14, 2012. 

Huybrechts T, Dewulf J, Van Craeynest K, et al. 2001. Evaluation of tetraglyme for the enrichment and 

analysis of volatile organic compounds in air. J Chromatogr A 922(1-2):207-218. 

IARC. 2012. Agents classified by the IARC Monographs. Volumes 1–104. Lyon, France: International 

Agency for Research on Cancer. 

http://monographs.iarc.fr/ENG/Classification/ClassificationsCASOrder.pdf. April 25, 2012. 

IARC. 2015. Lyon, France: International Agency for Research on Cancer. 

http://monographs.iarc.fr/ENG/Classification/ClassificationsCASOrder.pdf. March 31, 2015. 

Infante PF, Tsongas TA. 1982. Mutagenic and oncogenic effects of chloromethanes. Chloromethanes 

and halogenated analogues of vinyl chloride. Environ Sci Res 25:301-327. 

IRIS. 2002. 1,1-Dichloroethane (CASRN 75-34-3). Integrated Risk Information System. Washington, 

DC: U.S. Environmental Protection Agency. http://www.epa.gov/iris/subst/0409.htm. April 6, 2015. 

Jeffers PM, Ward LM, Woytowitch LM, Wolfe NL. 1989. Homogeneous hydrolysis rate constants for 

selected chlorinated methanes, ethanes, ethenes, and propanes. Environ Sci Technol 23:965-969. 

Jerpe J, Davis A. 1987. Ambient capillary chromatography of volatile organics with a portable gas 

chromatograph. J Chromatogr Sci 25:154-157. 

Kallonen R, von Wright A, Tikkanen L, et al. 1985. The toxicity of fire effluents from textiles and 

upholstery materials. J Fire Sci 3:145-160. 

Kearns GL, Abdel-Rahman SM, Alander SW, et al. 2003. Developmental pharmacology-drug 

disposition, action, and therapy in infants and children. N Engl J Med 349(12):1157-1167. 

10.1056/NEJMra035092. 

Kim HF, Bruckner JV, Dallas CE, et al. 1990b. Effect of dosing vehicles on the pharmacokinetics of 

orally administered carbon tetrachloride in rats. Toxicol Appl Pharmacol 102:5060. 

Kim HJ, Odend'hal S, Bruckner JV. 1990a. Effect of oral dosing vehicles on the acute hepatotoxicity of 

carbon tetrachloride in rats. Toxicol Appl Pharmacol 102:34-49. 

Kim KH, Ho DX, Park CG, et al. 2012. Volatile organic compounds in ambient air at four residential 

locations in Seoul, Korea. Environ Eng Sci 29(9):875-889. I 10.1089/ees.2011.0280. 
 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 118 

9. REFERENCES 

Kingsley BA, Gin C, Coulson DM, et al. 1983. Gas chromatographic analysis of purgeable halocarbon 

and aromatic compounds. Water Chlorination: Environmental Impact and Health Effects 4:593-608. 

Klaunig JE, Ruch RJ, Pereira MA. 1986. Carcinogenicity of chlorinated methane and ethane compounds 

administered in drinking water to mice. Environ Health Perspect 69:89-95. 

Klecka GM, Gonsior SJ, Markham DA. 1990. Biological transformations of 1,1,1-trichloroethane in 

subsurface soils and ground water. Environ Toxicol Chem 9(12):1437-1452. 

Kolpin DW, Squillace PJ, Zogorski JS. 1997. Pesticides and volatile organic compounds in shallow 

urban groundwater of the United States. In: Groundwater in the urban environment: Problems, 

processes and management. Rotterdam: Balkema, 469-474. 

Komori M, Nishio K, Kitada M, et al. 1990. Fetus-specific expression of a form of cytochrome P-450 in 

human livers. Biochemistry 29(18):4430-4433. 

Konietzko H. 1984. Chlorinated ethanes: Sources, distribution, environmental impact, and health 

effects. In: Saxena J, ed. Hazard assessment of chemicals: Current developments. Orlando, FL: 

Academic Press, 3:401-448. 

Krill RM, Sonzogni WC. 1986. Chemical monitoring of Wisconsin's groundwater. J Am Water Works 

Assoc 78:70-75. 

Krishnan K, Andersen ME. 1994. Physiologically based pharmacokinetic modeling in toxicology. In: 

Hayes AW, ed. Principles and methods of toxicology. 3rd ed. New York, NY: Raven Press, Ltd., 149­

188. 

Krishnan K, Andersen ME, Clewell HJ, et al. 1994. Physiologically based pharmacokinetic modeling of 

chemical mixtures. In: Yang RSH, ed. Toxicology of chemical mixtures: Case studies, mechanisms, 

and novel approaches. San Diego, CA: Academic Press, 399-437. 

Leeder JS, Kearns GL. 1997. Pharmacogenetics in pediatrics: Implications for practice. Pediatr Clin 

North Am 44(1):55-77. 

Leung HW. 1993. Physiologically-based pharmacokinetic modelling. In: Ballentyne B, Marrs T, 

Turner P, eds. General and applied toxicology. Vol. 1. New York, NY: Stockton Press, 153-164. 

Lewis RJ. 2004. 1,1-Dichloroethane. In: Sax's dangerous properties of industrial materials. 11th ed. 

Hoboken, NJ: John Wiley & Sons, 1189. 

Livingston AL. 1978. Forage plant estrogens. J Toxicol Environ Health 4(2-3):301-324. 

Lopez-Avila V, Heath N, Hu A. 1987b. Determination of purgeable halocarbons and aromatics by 

photoionization and hall electrolytic conductivity detectors connected in series. J Chromatogr Sci 25:356­

363. 

Lopez-Avila V, Wood R, Flanagan M, et al. 1987a. Determination of volatile priority pollutants in water 

by purge and trap and capillary column gas chromatography/mass spectrometry. J Chromatogr Sci 

25:286-291. 
 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 119 

9. REFERENCES 

Mabey WR, Smith JH, Podoll TT, et al. 1982. Aquatic fate process data for organic priority pollutants. 

Washington, DC: U.S. Environmental Protection Agency, Office of Water Regulations and Standards. 

EPA440481014. 

Maeda T, Funaki K, Yanaguchi Y, et al. 1998. On-site monitoring system for hazardous air pollutants 

using an adsorption-thermal desorption-capillary GC system equipped with a photoionization detector and 

an electrolytic conductivity detector. J High Resolut Chromatogr 21(8):471-474. 

Marshall KA. 2003. Chlorocarbons and chlorohydrocarbons, survey. In: Kirk-Othmer encyclopedia of 

chemical technology. New York, NY: John Wiley & Sons, Inc., 226-253. 

Matsuoka A, Hayashi M, Sofuni T. 1998. In vitro clastogenicity of 19 organic chemicals found in 

contaminated water and 7 structurally related chemicals. Kenkyo Hen'igen Kenkyu 20(3):159-165. 

Mayr U, Butsch A, Schneider S. 1992. Validation of two in vitro test systems for estrogenic activities 

with zearalenone, phytoestrogens and cereal extracts. Toxicology 74(2-3):135-149. 

McCall SN, Jurgens P, Ivanetich KM. 1983. Hepatic microsomal metabolism of the dichloroethanes. 

Biochem Pharmacol 32:207-213. 

Mehran M, Cooper WJ, Mehran M, et al. 1986. Comparison of direct headspace and aqueous injection 

techniques for halogenated hydrocarbons in water. J Chromatogr Sci 24:142-146. 

Miller KW, Paton WDM, Smith EB. 1965. Site of action of general anaesthetics GA. Nature 206:574­

577. 

Milman HA, Story DL, Riccio ES, et al. 1988. Rat liver foci and in vitro assays to detect initiating and 

promoting effects of chlorinated ethanes and ethylenes. Ann N Y Acad Sci 534:521-530. 

Mitoma C, Steeger T, Jackson SE, et al. 1985. Metabolic disposition study of chlorinated hydrocarbons 

in rats and mice. Drug Chem Toxicol 8:183-194. 

Mohamed MF, Kang D, Aneja VP. 2002. Volatile organic compounds in some urban locations in United 

States. Chemosphere 47:863-882. 

Morselli PL, Franco-Morselli R, Bossi L. 1980. Clinical pharmacokinetics in newborns and infants: 

Age-related differences and therapeutic implications. Clin Pharmacokin 5(6):485-527. 

NAS/NRC. 1989. Report of the oversight committee. In: Biologic markers in reproductive toxicology. 

Washington, DC: National Academy of Sciences, National Research Council, National Academy Press, 

15-35. 

NCI. 1977. Bioassay of 1,1-dichloroethane for possible carcinogenicity. Bethesda, MD: National 

Cancer Institute. NIH publication No. 78-1316. 

Needham LL, Ashley DL, Hill RH, et al. 1995. Human levels of selected non-persistent chlorinated 

compounds. Organohalogen Comp 26:35-38. 

NIOSH. 1978. 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. 
 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 120 

9. REFERENCES 

NIOSH. 2003. Method 1003. Hydrocarbons, halogenated. NIOSH manual of analytical methods. 

National Institute for Occupational Safety and Health http://www.cdc.gov/niosh/docs/2003­

154/pdfs/1003.pdf. June 28, 2012. 

NIOSH. 2011. 1,1-Dichloroethane. NIOSH pocket guide to chemical hazards. Atlanta, GA: National 

Institute for Occupational Safety and Health, Centers for Disease Control and Prevention. 

http://www.cdc.gov/niosh/npg/. April 25, 2012. 

NIOSH. 2015. 1,1-Dichloroethane. NIOSH pocket guide to chemical hazards. Atlanta, GA: National 

Institute for Occupational Safety and Health, Centers for Disease Control and Prevention. 

http://www.cdc.gov/niosh/npg/npgd0194.html. April 6, 2015. 

NLM. 2015. TOXMAP:® Environmental Health Maps. Superfund NPL. 1,1 Dichloroethene and 

ethylidene dichloride. U.S. National Library of Medicine, National Institutes of Health. http://toxmapclassic.nlm.nih.gov/toxmap/search/select.do#. April 2, 2015. 

NOES. 1990. Estimated numbers of employees potentially exposed to specific agents by occupation. 

CAS #: 75-34-3. National Occupational Exposure Survey conducted from 1981 to 1983. National 

Occupational Exposure Survey. National Institute for Occupational Safety and Health. 

http://www.cdc.gov/noes/. May 11, 2015. 

Nohmi T, Miyata R, Yoshikawa K, et al. 1985. [Mutagenicity tests on organic chemical contaminants in 

city water and related compounds: I. Bacterial mutagenicity tests]. Bulletin of National Hygiene Science 

103:60-64. (Japanese). 

NRC. 1993. National Research Council. Pesticides in the diets of infants and children. Washington, 

DC: National Academy Press. 

NTP. 2011. Report on carcinogens. 11th ed. Research Triangle Park, NC: National Toxicology 

Program. U.S. Department of Health and Human Services, Public Health Service. 

http://ntp-server.niehs.nih.gov/ntp/roc/twelfth/roc12.pdf. April 25, 2012. 

NTP. 2014. Report on carcinogens, thirteenth edition. Research Triangle Park, NC: U.S. Department of 

Health and Human Services, Public Health Service, National Toxicology Program. 

http://ntp.niehs.nih.gov/pubhealth/roc/roc13/. March 31, 2015. 

Oliver KD, Adams JR, Daughtrey EHJ, et al. 1996. Technique for monitoring toxic VOCs in air: 

Sorbent preconcentration, closed-cycle cooler cryofocusing, and GC analysis. Environ Sci Technol 

30(6):1939-1945. 

O'Neil MJ, Heckelman PE, Koch CB, et al., eds 2006. Ethylidene chloride. In: The Merck index. 

Whitehouse Station, NJ: Merck & Co., Inc., 653. 

OSHA. 2013. Subpart Z - Toxic and hazardous substances. Air contaminants. Occupational Safety and 

Health Standards. Code of Federal Regulations 29 CFR 1910.1000. http://www.gpo.gov/fdsys/pkg/CFR2014-title29-vol6/pdf/CFR-2014-title29-vol6-sec1910-1000.pdf. March 4, 2015. 
 

 

 

 

 

 

1,1-DICHLOROETHANE 121 

9. REFERENCES 

OSHA. 2014a. Gases, vapors, fumes, dusts, and mists. Appendix A to 1926.55-1970. American 

Conference of Governmental Industrial Hygienists’ threshold limit values of airborne contaminants for 

construction. Subpart D-Occupational health and environmental controls. Occupational Safety and 

Health Standards. Code of Federal Regulations 29 CFR 1926.55. http://www.gpo.gov/fdsys/pkg/CFR2014-title29-vol8/pdf/CFR-2014-title29-vol8-sec1926-55.pdf. March 4, 2015. 

OSHA. 2014b. Subpart Z - Toxic and hazardous substances. Air contaminants. Table Z - Shipyards. 

Occupational Safety and Health Standards. Code of Federal Regulations 29 CFR 1915.1000. 

http://www.gpo.gov/fdsys/pkg/CFR-2013-title29-vol7/pdf/CFR-2013-title29-vol7-sec1915-1000.pdf. 

March 4, 2015. 

Otson R, Chan C. 1987. Sample handling and analysis for 51 volatile organics by an adapted purge and 

trap GC-MS technique. Int J Environ Anal Chem 30:275-287. 

Otson R, Williams DT. 1981. Evaluation of a liquid-liquid extraction technique for water pollutants. J 

Chromatogr 212:187-198. 

Otson R, Williams DT. 1982. Headspace chromatographic determination of water pollutants. Anal 

Chem 54:942-946. 

Owen GM, Brozek J. 1966. Influence of age, sex and nutrition on body composition during childhood 

and adolescence. In: Falkner F, ed. Human development. Philadelphia, PA: WB Saunders, 222-238. 

Page BD, LaCroix GM. 1995. On-line steam distillation/purge and trap analysis of halogenated, 

nonpolar, volatile contaminants in foods. J AOAC Int 78(6):1416-1428. 

Pankow JF, Rosen ME. 1988. Determination of volatile compounds in water by purging directly to a 

capillary column with whole column cryotrapping. Environ Sci Technol 22:398-405. 

Parker JC, Casey GE, Bahlman LJ, et al. 1979. Chloroethanes: Review of toxicity. Am Ind Hyg Assoc 

J 40:A46-A57. 

Pearson CR, Mcconnell G. 1975. Chlorinated C1 and C2 hydrocarbons in the marine environment. Proc 

R Soc London 189:305-332. 

Pellizzari ED. 1982. Analysis for organic vapor emissions near industrial and chemical waste disposal 

sites. Environ Sci Technol 16:781-785. 

Pellizzari ED, Erickson MC, Zweidinger RA. 1979. Formulation of preliminary assessment of 

halogenated organic compounds in man and environmental media. Washington, DC: U.S. 

Environmental Protection Agency. PB80112170 

Perwak J, Byrne M, Goyer M, et al. 1982. Exposure and risk assessment for dichloroethanes. 

1,1-Dichloroethane, 1,2-dichloroethane. Washington, DC: U.S. Environmental Protection Agency, 

Office of Water Regulations and Standards. EPA440485009. PB85220564. 

Plaa GL, Larson RE. 1965. Relative nephrotoxic properties of chlorinated methane, ethane, and ethylene 

derivatives in mice. Toxicol Appl Pharmacol 7:37-44. 

Plumb RH. 1987. A comparison of groundwater monitoring data from CERCLA and RCRA sites. 

Ground Water Monit Rev 7:94-100. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 122 

9. REFERENCES 

Raymer JH, Thomas KW, Cooper SD, et al. 1990. A device for sampling of human alveolar breath for 

the measurement of expired volatile organic compounds. J Anal Toxicol 14(6):337-344. 

Reding R. 1987. Chromatographic monitoring methods for organic contaminants under the Safe 

Drinking Water Act. J Chromatogr Sci 25:338-344. 

Reid JB, Muianga CV. 2012. Saturated halogenated aliphatic hydrocarbons two to four carbons. In: 

Bingham E, Cohrssen B, eds. Patty's industrial hygiene and toxicology. 6th ed. 61-127. 

http://onlinelibrary.wiley.com/doi/10.1002/0471435139.tox063.pub2/abstract. October 4, 2012. 

Reinert KH, Hunter JV, Sabatino T. 1983. Dynamic heated headspace analyses of volatile organic 

compounds present in fish tissue samples. J Agric Food Chem 31:1057-1060. 

Riccio E, Griffin A, Mortelmans K, et al. 1983. A comparative mutagenicity study of volatile 

halogenated hydrocarbons using different metabolic activation systems. Environ Mutagen 5:472. 

Roose P, Brinkman UA. 1998. Determination of volatile organic compounds in marine biota. J 

Chromatogr A 799(1-2):233-248. 

Sato A, Nakajima T. 1987. Pharmacokinetics of organic solvent vapors in relation to their toxicity. 

Scand J Work Environ Health 13:81-93. 

Sato A, Nakajima T, Koyama Y. 1980. Effects of chronic ethanol consumption on hepatic metabolism of 

aromatic and chlorinated hydrocarbons in rats. Br J Ind Med 37:382-386. 

Saunders NR, Ek CJ, Habgood MD, et al. 2008. Barriers in the brain: A renaissance? Trends Neurosci 

31(6):279-286. 10.1016/j.tins.2008.03.003. 

Saunders NR, Liddelow SA, Dziegielewska KM. 2012. Barrier mechanisms in the developing brain. 

Front Pharmacol 3:Article 46. 10.3389/fphar.2012.00046. 

Scheuplein R, Charnley G, Dourson M. 2002. Differential sensitivity of children and adults to chemical 

toxicity. I. Biological basis. Regul Toxicol Pharmacol 35(3):429-447. 

Schwetz BA, Leong BKJ, Gehring PJ. 1974. Embryo-and fetotoxicity of inhaled carbon tetrachloride, 

1,1-dichloroethane and methyl ethyl ketone in rats. Toxicol Appl Pharmacol 28:452-464. 

Silgoner I, Rosenberg E, Grasserbauer M. 1997. Determination of volatile organic compounds in water 

by purge-and-trap gas chromatography coupled to atomic emission detection. J Chromatogr A 68(2):259­

270. 

Simmon VF, Kauhanen K, Tardiff RG. 1977. Mutagenic activity of chemicals identified in drinking 

water. Dev Toxicol Environ Sci 2:249-258. 

Simpson G, Klasmeier M, Hill H, et al. 1996. Evaluation of gas chromatography coupled with ion 

mobility spectrometry for monitoring vinyl chloride and other chlorinated and aromatic compounds in air 

samples. J High Resolut Chromatogr 19(6):301-312. 

Singh HB, Salas LJ, Smith AJ, et al. 1981. Measurements of some potentially hazardous organic 

chemicals in urban environments. Atmos Environ 15:601-612. 
 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 123 

9. REFERENCES 

Smyth HF. 1956. Improved communication: Hygienic standards for daily inhalation. Am Ind Hyg 

Assoc Q 17:129-195. 

Spain MA, Middleditch BS, Bafus DA, et al. 1985. Dehydrohalogenation of atmospheric contaminants 

in the space cabin. Aviat Space Environ Med 56:262-264. 

Spicer CW, Buxton B, Holdren MW, et al. 1996. Variability of hazardous air pollutants in an urban area. 

Atmos Environ 30(20):3443-3456. 

Squillace PJ, Moran MJ, Lapham WW, et al. 1999. Volatile organic compounds in untreated ambient 

groundwater of the United States, 1985-1995. Environ Sci Technol 33(23):4176-4187. 

SRI. 2011. 2011 Directory of chemical producers United States. SRI Consulting. 

Staples CA, Werner AF, Hoogheem TJ. 1985. Assessment of priority pollutant concentrations in the 

United States using STORET database. Environ Toxicol Chem 4:131-142. 

Suffet IH, Brenner L, Cairo PR. 1980. Gas chromatography-mass spectrometry identification of trace 

organics in Philadelphia, Pennsylvania, USA, drinking waters during a 2-year period. Water Res 14:853­

867. 

Tabak HH, Quave SA, Mashni CI, et al. 1981. Biodegradability studies with organic priority pollutant 

compounds. J Water Pollut Control Fed 53:1503-1518. 

Thomas K, Colborn T. 1992. Organochlorine endocrine disruptors in human tissue. In: Colborn T, 

Clement C, eds. Chemically induced alterations in sexual and functional development: The 

wildlife/human connection. Princeton, NJ: Princeton Scientific Publishing, 365-394. 

Tomasi A, Albano E, Bini A, et al. 1984. Free radical intermediates under hypoxic conditions in the 

metabolism of halogenated carcinogens. Toxicol Pathol 12:240-246. 

TRI13. 2014. TRI explorer: Providing access to EPA’s toxics release inventory data. Washington, DC: 

Office of Information Analysis and Access. Office of Environmental Information. U.S. Environmental 

Protection Agency. Toxics Release Inventory. http://www.epa.gov/triexplorer/. November 12, 2014. 

Tu AS, Murray TA, Hatch KM, et al. 1985. In vitro transformation of BALB/c-3T3 cells by chlorinated 

ethanes and ethylenes. Cancer Lett 28:85-92. 

Uehori R, Nagata T, Kimura K, et al. 1987. Screening of volatile compounds present in human blood 

using retention indices in gas chromatography. J Chromatogr 411:251-257. 

Ursova TP. 1953. [The possible presence of dichloroethane in human milk with exposure to industrial 

conditions]. Gig Sanit 18:36-37. (Russian) 

USGS. 2003a. A national survey of methyl tert-butyl ether and other volatile organic compounds in 

drinking-water sources: Results of the random survey. U.S. Geological Survey. U.S. Department of the 

Interior. 
 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 124 

9. REFERENCES 

USGS. 2003b. Quality and sources of shallow ground water in areas of recent residential development in 

Salt Lake Valley, Salt Lake Country, Utah. U.S. Geological Survery. Water-Resources Investigations 

Report 03-4028. http://pubs.usgs.gov/wri/wri034028/PDF/WRI034028.pdf. April 1, 2015. 

USGS. 2006a. Volatile organic compounds in the nation's ground water and drinking-water supply 

wells. U.S. Geological Survey. U.S. Department of the Interior, National Water Quality Assessment 

Program. 

USGS. 2006b. Investigation of contaminated ground-water at solid waste management Unit 12, Naval 

Weapons Station Charleston, North Charleston, South Carolina, 2006-2007. U.S. Geological Survey. 

U.S. Department of the Interior. 

USGS. 2010a. An update of hydrologic conditions and distribution of selected constituents in water, 

Snake River Plain aquifer and perched groundwater zones, Idaho National Laboratory, Idaho, emphasis 

2006-08. U.S. Geological Survey. U.S. Department of Energy. Scientific Investigations Report 2010­

5197. http://pubs.er.usgs.gov/publication/sir20105197. April 1, 2015. 

USGS. 2010b. Appendixes to quality of source water from public-supply wells in the United States, 

1993-2007. Scientific Investigations Report 2010–5024. U.S. Geological Survey. Scientific 

Investigations Report 2010–5024. http://pubs.usgs.gov/sir/2010/5024/pdf/sir20105024_appendixes.pdf. 

April 1, 2015. 

USGS. 2010c. Occurrence and distribution of organic chemicals and nutrients and comparison of waterquality data from public drinking-water supplies in the Columbia aquifer in Delaware, 2000-08. U.S. 

Geological Survey. Scientific Investigations Report 2010–5206. http://pubs.usgs.gov/sir/2010/5206/. 

April 1, 2015. 

USGS. 2010d. Quality of source water from public-supply wells in the United States, 1993-2007. U.S. 

Geological Survey. Scientific Investigations Report 2010–5024. http://pubs.usgs.gov/sir/2010/5024/. 

April 1, 2015. 

USGS. 2012. Assessment of soil-gas contamination at three former fuel-dispensing sites, Fort Gordon, 

Georgia, 2010-2011. U.S. Geological Survey. Open-File Report 2012–1082. 

http://pubs.usgs.gov/of/2012/1082/. April 1, 2015. 

Van Dyke RA, Wineman CG. 1971. Enzymatic dechlorination: Dechlorination of chloroethanes and 

propanes in vitro. Biochem Pharmacol 20:463-470. 

van Eekert MH, Stams AJ, Field JA. 1999. Gratuitous dechlorination of chloroethanes by methanogenic 

granular sludge. Appl Microbiol Biotechnol 51(1):46-52. 

Verschueren K. 1983. Handbook of environmental data on organic chemicals. 2nd ed. New York, NY: 

Van Nostrand Reinhold Co., 486. 

Vieira I, Sonnier M, Cresteil T. 1996. Developmental expression of CYP2E1 in the human liver: 

Hypermethylation control of gene expression during the neonatal period. Eur J Biochem 238(2):476-483. 

Vogel TM, McCarty PL. 1987. Abiotic and biotic transformations of 1,1,1-trichloroethane under 

methanogenic conditions. Environ Sci Technol 21:1208-1213. 
 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 125 

9. REFERENCES 

Wallace L, Zweidinger R, Erickson M, et al. 1982. Monitoring individual exposure. Measurements of 

volatile organic compounds in breathing air, drinking water, and exhaled breath. Environ Int 8:269-282. 

Wallace LA, Pellizzari E, Harwell T, et al. 1984. Personal exposure to volatile organic compounds. I. 

Direct measurements. Environ Res 35:293-319. 

Wang B, Ho SSH, Ho KF, et al. 2012. An environmental chamber study of the characteristics of air 

pollutants released from environmental tobacco smoke. Aerosol Air Qual Res 12(6):1269-1281. 

I 10.4209/aaqr.2011.11.0221. 

Weiss G. 1986. Hazardous chemicals databook. 2nd ed. Park Ridge, NJ: Noyes Data Corporation, 359. 

West JR, Smith HW, Chasis H. 1948. Glomerular filtration rate, effective renal blood flow, and maximal 

tubular excretory capacity in infancy. J Pediatr 32:10-18. 

Westrick JJ, Mello JW, Thomas RF. 1984. The groundwater supply survey. J Am Water Works Assoc 

76:52-59. 

WHO. 2010. Guidelines for indoor air quality: Selected pollutants. Geneva, Switzerland: World Health 

Organization. http://www.euro.who.int/__data/assets/pdf_file/0009/128169/e94535.pdf. September 9, 

2014. 

WHO. 2011. Guidelines for drinking-water quality. Geneva, Switzerland: World Health Organization. 

http://whqlibdoc.who.int/publications/2011/9789241548151_eng.pdf?ua=1. September 9, 2014. 

Widdowson EM, Dickerson JWT. 1964. Chemical composition of the body. In: Comar CL, Bronner F, 

eds. Mineral metabolism: An advanced treatise. Volume II: The elements Part A. New York, NY: 

Academic Press, 1-247. 

Wilson JT, McNabb JF, Wilson BH, et al. 1983. Biotransformation of selected organic pollutants in 

groundwater. Dev Ind Microbiol 24:225-233. 

Wilson JT, Enfield CG, Dunlap WJ, et al. 1981. Transport and fate of selected organic pollutants in a 

sandy soil. J Environ Qual 10(4):501-506. 

Witkowska D. 2013. Volatile gas concentrations in indoor turkey farms. Br Poult Sci 54(3):289-297. 

I 10.1080/00071668.2013.781264. 

Wong PS, Cooks RG, Cisper ME, et al. 1995. On-line in situ analysis with membrane introduction MS. 

A new analytical technique promises rapid environmental analyses for volatile organics in air and water. 

Environ Sci Technol 29(5):215A-218A. 

Wood PR, Lang RF, Payan IL. 1985. Anaerobic transformation, transport, and removal of volatile 

chlorinated organics in ground water. In: Ward CH, Giger W, eds. Ground water quality. New York, 

NY: John Wiley and Sons, 493-511. 

Wylie PL. 1988. Comparing headspace with purge and trap for analysis of volatile priority pollutants. J 

Am Water Works Assoc 80:65-72. 

Yang RSH, Rauckman EJ. 1987. Toxicological studies of chemical mixtures of environmental concern 

at the National Toxicology Program: health effects of groundwater contaminants. Toxicology 47:15-34. 
1,1-DICHLOROETHANE 126 

9. REFERENCES 

Young DR, Gossett RW, Baird RB, et al. 1983. Wastewater inputs and marine bioaccumulation of 

priority pollutant organics off Southern California. Water Chlorination: Environmental Impact and 

Health Effects 4:871-884. 

Ziegler EE, Edwards BB, Jensen RL, et al. 1978. Absorption and retention of lead by infants. Pediatr 

Res 12(1):29-34. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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Absorption—The taking up of liquids by solids, or of gases by solids or liquids. 

Acute Exposure—Exposure to a chemical for a duration of 14 days or less, as specified in the 

Toxicological Profiles. 

Adsorption—The adhesion in an extremely thin layer of molecules (as of gases, solutes, or liquids) to the 

surfaces of solid bodies or liquids with which they are in contact. 

Adsorption Coefficient (Koc)—The ratio of the amount of a chemical adsorbed per unit weight of 

organic carbon in the soil or sediment to the concentration of the chemical in solution at equilibrium. 

Adsorption Ratio (Kd)—The amount of a chemical adsorbed by sediment or soil (i.e., the solid phase) 

divided by the amount of chemical in the solution phase, which is in equilibrium with the solid phase, at a 

fixed solid/solution ratio. It is generally expressed in micrograms of chemical sorbed per gram of soil or 

sediment. 

Benchmark Dose (BMD)—Usually defined as the lower confidence limit on the dose that produces a 

specified magnitude of changes in a specified adverse response. For example, a BMD10 would be the 

dose at the 95% lower confidence limit on a 10% response, and the benchmark response (BMR) would be 

10%. The BMD is determined by modeling the dose response curve in the region of the dose response 

relationship where biologically observable data are feasible. 

Benchmark Dose Model—A statistical dose-response model applied to either experimental toxicological 

or epidemiological data to calculate a BMD. 

Bioconcentration Factor (BCF)—The quotient of the concentration of a chemical in aquatic organisms 

at a specific time or during a discrete time period of exposure divided by the concentration in the 

surrounding water at the same time or during the same period. 

Biomarkers—Broadly defined as indicators signaling events in biologic systems or samples. They have 

been classified as markers of exposure, markers of effect, and markers of susceptibility. 

Cancer Effect Level (CEL)—The lowest dose of chemical in a study, or group of studies, that produces 

significant increases in the incidence of cancer (or tumors) between the exposed population and its 

appropriate control. 

Carcinogen—A chemical capable of inducing cancer. 

Case-Control Study—A type of epidemiological study that examines the relationship between a 

particular outcome (disease or condition) and a variety of potential causative agents (such as toxic 

chemicals). In a case-controlled study, a group of people with a specified and well-defined outcome is 

identified and compared to a similar group of people without outcome. 

Case Report—Describes a single individual with a particular disease or exposure. These may suggest 

some potential topics for scientific research, but are not actual research studies. 

Case Series—Describes the experience of a small number of individuals with the same disease or 

exposure. These may suggest potential topics for scientific research, but are not actual research studies. 
 

 

 

 

 

 

 

 

 

 

 

 

 

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Ceiling Value—A concentration of a substance that should not be exceeded, even instantaneously. 

Chronic Exposure—Exposure to a chemical for 365 days or more, as specified in the Toxicological 

Profiles. 

Cohort Study—A type of epidemiological study of a specific group or groups of people who have had a 

common insult (e.g., exposure to an agent suspected of causing disease or a common disease) and are 

followed forward from exposure to outcome. At least one exposed group is compared to one unexposed 

group. 

Cross-sectional Study—A type of epidemiological study of a group or groups of people that examines 

the relationship between exposure and outcome to a chemical or to chemicals at one point in time. 

Data Needs—Substance-specific informational needs that if met would reduce the uncertainties of human 

health assessment. 

Developmental Toxicity—The occurrence of adverse effects on the developing organism that may result 

from exposure to a chemical prior to conception (either parent), during prenatal development, or 

postnatally to the time of sexual maturation. Adverse developmental effects may be detected at any point 

in the life span of the organism. 

Dose-Response Relationship—The quantitative relationship between the amount of exposure to a 

toxicant and the incidence of the adverse effects. 

Embryotoxicity and Fetotoxicity—Any toxic effect on the conceptus as a result of prenatal exposure to 

a chemical; the distinguishing feature between the two terms is the stage of development during which the 

insult occurs. The terms, as used here, include malformations and variations, altered growth, and in utero 

death. 

Environmental Protection Agency (EPA) Health Advisory—An estimate of acceptable drinking water 

levels for a chemical substance based on health effects information. A health advisory is not a legally 

enforceable federal standard, but serves as technical guidance to assist federal, state, and local officials. 

Epidemiology—Refers to the investigation of factors that determine the frequency and distribution of 

disease or other health-related conditions within a defined human population during a specified period. 

Genotoxicity—A specific adverse effect on the genome of living cells that, upon the duplication of 

affected cells, can be expressed as a mutagenic, clastogenic, or carcinogenic event because of specific 

alteration of the molecular structure of the genome. 

Half-life—A measure of rate for the time required to eliminate one half of a quantity of a chemical from 

the body or environmental media. 

Immediately Dangerous to Life or Health (IDLH)—The maximum environmental concentration of a 

contaminant from which one could escape within 30 minutes without any escape-impairing symptoms or 

irreversible health effects. 

Immunologic Toxicity—The occurrence of adverse effects on the immune system that may result from 

exposure to environmental agents such as chemicals. 
 

 

 

 

 

 

 

 

 

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10. GLOSSARY 

Immunological Effects—Functional changes in the immune response. 

Incidence—The ratio of individuals in a population who develop a specified condition to the total 

number of individuals in that population who could have developed that condition in a specified time 

period. 

Intermediate Exposure—Exposure to a chemical for a duration of 15–364 days, as specified in the 

Toxicological Profiles. 

In Vitro—Isolated from the living organism and artificially maintained, as in a test tube. 

In Vivo—Occurring within the living organism. 

Lethal Concentration(LO) (LCLO)—The lowest concentration of a chemical in air that has been reported 

to have caused death in humans or animals. 

Lethal Concentration(50) (LC50)—A calculated concentration of a chemical in air to which exposure for 

a specific length of time is expected to cause death in 50% of a defined experimental animal population. 

Lethal Dose(LO) (LDLo)—The lowest dose of a chemical introduced by a route other than inhalation that 

has been reported to have caused death in humans or animals. 

Lethal Dose(50) (LD50)—The dose of a chemical that has been calculated to cause death in 50% of a 

defined experimental animal population. 

Lethal Time(50) (LT50)—A calculated period of time within which a specific concentration of a chemical 

is expected to cause death in 50% of a defined experimental animal population. 

Lowest-Observed-Adverse-Effect Level (LOAEL)—The lowest exposure level of chemical in a study, 

or group of studies, that produces statistically or biologically significant increases in frequency or severity 

of adverse effects between the exposed population and its appropriate control. 

Lymphoreticular Effects—Represent morphological effects involving lymphatic tissues such as the 

lymph nodes, spleen, and thymus. 

Malformations—Permanent structural changes that may adversely affect survival, development, or 

function. 

Minimal Risk Level (MRL)—An estimate of daily human exposure to a hazardous substance that is 

likely to be without an appreciable risk of adverse noncancer health effects over a specified route and 

duration of exposure. 

Modifying Factor (MF)—A value (greater than zero) that is applied to the derivation of a Minimal Risk 

Level (MRL) to reflect additional concerns about the database that are not covered by the uncertainty 

factors. The default value for a MF is 1. 

Morbidity—State of being diseased; morbidity rate is the incidence or prevalence of disease in a specific 

population. 

Mortality—Death; mortality rate is a measure of the number of deaths in a population during a specified 

interval of time. 
 

 

 

 

 

 

 

 

 

 

 

 

 

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Mutagen—A substance that causes mutations. A mutation is a change in the DNA sequence of a cell’s 

DNA. Mutations can lead to birth defects, miscarriages, or cancer. 

Necropsy—The gross examination of the organs and tissues of a dead body to determine the cause of 

death or pathological conditions. 

Neurotoxicity—The occurrence of adverse effects on the nervous system following exposure to a 

chemical. 

No-Observed-Adverse-Effect Level (NOAEL)—The dose of a chemical at which there were no 

statistically or biologically significant increases in frequency or severity of adverse effects seen between 

the exposed population and its appropriate control. Effects may be produced at this dose, but they are not 

considered to be adverse. 

Octanol-Water Partition Coefficient (Kow)—The equilibrium ratio of the concentrations of a chemical 

in n-octanol and water, in dilute solution. 

Odds Ratio (OR)—A means of measuring the association between an exposure (such as toxic substances 

and a disease or condition) that represents the best estimate of relative risk (risk as a ratio of the incidence 

among subjects exposed to a particular risk factor divided by the incidence among subjects who were not 

exposed to the risk factor). An OR of greater than 1 is considered to indicate greater risk of disease in the 

exposed group compared to the unexposed group. 

Organophosphate or Organophosphorus Compound—A phosphorus-containing organic compound 

and especially a pesticide that acts by inhibiting cholinesterase. 

Permissible Exposure Limit (PEL)—An Occupational Safety and Health Administration (OSHA) 

allowable exposure level in workplace air averaged over an 8-hour shift of a 40-hour workweek. 

Pesticide—General classification of chemicals specifically developed and produced for use in the control 

of agricultural and public health pests. 

Pharmacokinetics—The dynamic behavior of a material in the body, used to predict the fate 

(disposition) of an exogenous substance in an organism. Utilizing computational techniques, it provides 

the means of studying the absorption, distribution, metabolism, and excretion of chemicals by the body. 

Pharmacokinetic Model—A set of equations that can be used to describe the time course of a parent 

chemical or metabolite in an animal system. There are two types of pharmacokinetic models: data-based 

and physiologically-based. A data-based model divides the animal system into a series of compartments, 

which, in general, do not represent real, identifiable anatomic regions of the body, whereas the 

physiologically-based model compartments represent real anatomic regions of the body. 

Physiologically Based Pharmacodynamic (PBPD) Model—A type of physiologically based doseresponse model that quantitatively describes the relationship between target tissue dose and toxic end 

points. These models advance the importance of physiologically based models in that they clearly 

describe the biological effect (response) produced by the system following exposure to an exogenous 

substance. 

Physiologically Based Pharmacokinetic (PBPK) Model—Comprised of a series of compartments 

representing organs or tissue groups with realistic weights and blood flows. These models require a 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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10. GLOSSARY 

variety of physiological information: tissue volumes, blood flow rates to tissues, cardiac output, alveolar 

ventilation rates, and possibly membrane permeabilities. The models also utilize biochemical 

information, such as air/blood partition coefficients, and metabolic parameters. PBPK models are also 

called biologically based tissue dosimetry models. 

Prevalence—The number of cases of a disease or condition in a population at one point in time. 

Prospective Study—A type of cohort study in which the pertinent observations are made on events 

occurring after the start of the study. A group is followed over time. 

q1*—The upper-bound estimate of the low-dose slope of the dose-response curve as determined by the 

multistage procedure. The q1* can be used to calculate an estimate of carcinogenic potency, the 

incremental excess cancer risk per unit of exposure (usually μg/L for water, mg/kg/day for food, and 

μg/m3 for air). 

Recommended Exposure Limit (REL)—A National Institute for Occupational Safety and Health 

(NIOSH) time-weighted average (TWA) concentration for up to a 10-hour workday during a 40-hour 

workweek. 

Reference Concentration (RfC)—An estimate (with uncertainty spanning perhaps an order of 

magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) 

that is likely to be without an appreciable risk of deleterious noncancer health effects during a lifetime. 

The inhalation reference concentration is for continuous inhalation exposures and is appropriately 

expressed in units of mg/m3 or ppm. 

Reference Dose (RfD)—An estimate (with uncertainty spanning perhaps an order of magnitude) of the 

daily exposure of the human population to a potential hazard that is likely to be without risk of deleterious 

effects during a lifetime. The RfD is operationally derived from the no-observed-adverse-effect level 

(NOAEL, from animal and human studies) by a consistent application of uncertainty factors that reflect 

various types of data used to estimate RfDs and an additional modifying factor, which is based on a 

professional judgment of the entire database on the chemical. The RfDs are not applicable to 

nonthreshold effects such as cancer. 

Reportable Quantity (RQ)—The quantity of a hazardous substance that is considered reportable under 

the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA). Reportable 

quantities are (1) 1 pound or greater or (2) for selected substances, an amount established by regulation 

either under CERCLA or under Section 311 of the Clean Water Act. Quantities are measured over a 

24-hour period. 

Reproductive Toxicity—The occurrence of adverse effects on the reproductive system that may result 

from exposure to a chemical. The toxicity may be directed to the reproductive organs and/or the related 

endocrine system. The manifestation of such toxicity may be noted as alterations in sexual behavior, 

fertility, pregnancy outcomes, or modifications in other functions that are dependent on the integrity of 

this system. 

Retrospective Study—A type of cohort study based on a group of persons known to have been exposed 

at some time in the past. Data are collected from routinely recorded events, up to the time the study is 

undertaken. Retrospective studies are limited to causal factors that can be ascertained from existing 

records and/or examining survivors of the cohort. 

Risk—The possibility or chance that some adverse effect will result from a given exposure to a chemical. 
 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 132 

10. GLOSSARY 

Risk Factor—An aspect of personal behavior or lifestyle, an environmental exposure, or an inborn or 

inherited characteristic that is associated with an increased occurrence of disease or other health-related 

event or condition. 

Risk Ratio—The ratio of the risk among persons with specific risk factors compared to the risk among 

persons without risk factors. A risk ratio greater than 1 indicates greater risk of disease in the exposed 

group compared to the unexposed group. 

Short-Term Exposure Limit (STEL)—The American Conference of Governmental Industrial 

Hygienists (ACGIH) maximum concentration to which workers can be exposed for up to 15 minutes 

continually. No more than four excursions are allowed per day, and there must be at least 60 minutes 

between exposure periods. The daily Threshold Limit Value-Time Weighted Average (TLV-TWA) may 

not be exceeded. 

Standardized Mortality Ratio (SMR)—A ratio of the observed number of deaths and the expected 

number of deaths in a specific standard population. 

Target Organ Toxicity—This term covers a broad range of adverse effects on target organs or 

physiological systems (e.g., renal, cardiovascular) extending from those arising through a single limited 

exposure to those assumed over a lifetime of exposure to a chemical. 

Teratogen—A chemical that causes structural defects that affect the development of an organism. 

Threshold Limit Value (TLV)—An American Conference of Governmental Industrial Hygienists 

(ACGIH) concentration of a substance to which most workers can be exposed without adverse effect. 

The TLV may be expressed as a Time Weighted Average (TWA), as a Short-Term Exposure Limit 

(STEL), or as a ceiling limit (CL). 

Time-Weighted Average (TWA)—An allowable exposure concentration averaged over a normal 8-hour 

workday or 40-hour workweek. 

Toxic Dose(50) (TD50)—A calculated dose of a chemical, introduced by a route other than inhalation, 

which is expected to cause a specific toxic effect in 50% of a defined experimental animal population. 

Toxicokinetic—The absorption, distribution, and elimination of toxic compounds in the living organism. 

Uncertainty Factor (UF)—A factor used in operationally deriving the Minimal Risk Level (MRL) or 

Reference Dose (RfD) or Reference Concentration (RfC) from experimental data. UFs are intended to 

account for (1) the variation in sensitivity among the members of the human population, (2) the 

uncertainty in extrapolating animal data to the case of human, (3) the uncertainty in extrapolating from 

data obtained in a study that is of less than lifetime exposure, and (4) the uncertainty in using lowestobserved-adverse-effect level (LOAEL) data rather than no-observed-adverse-effect level (NOAEL) data. 

A default for each individual UF is 10; if complete certainty in data exists, a value of 1 can be used; 

however, a reduced UF of 3 may be used on a case-by-case basis, 3 being the approximate logarithmic 

average of 10 and 1. 

Xenobiotic—Any chemical that is foreign to the biological system. 
 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE A-1 

APPENDIX A. ATSDR MINIMAL RISK LEVELS AND WORKSHEETS 

The Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) [42 U.S.C. 

9601 et seq.], as amended by the Superfund Amendments and Reauthorization Act (SARA) [Pub. L. 99– 

499], requires that the Agency for Toxic Substances and Disease Registry (ATSDR) develop jointly with 

the U.S. Environmental Protection Agency (EPA), in order of priority, a list of hazardous substances most 

commonly found at facilities on the CERCLA National Priorities List (NPL); prepare toxicological 

profiles for each substance included on the priority list of hazardous substances; and assure the initiation 

of a research program to fill identified data needs associated with the substances. 

The toxicological profiles include an examination, summary, and interpretation of available toxicological 

information and epidemiologic evaluations of a hazardous substance. During the development of 

toxicological profiles, Minimal Risk Levels (MRLs) are derived when reliable and sufficient data exist to 

identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration for a 

given route of exposure. An MRL is an estimate of the daily human exposure to a hazardous substance 

that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration 

of exposure. MRLs are based on noncancer health effects only and are not based on a consideration of 

cancer effects. These substance-specific estimates, which are intended to serve as screening levels, are 

used by ATSDR health assessors to identify contaminants and potential health effects that may be of 

concern at hazardous waste sites. It is important to note that MRLs are not intended to define clean-up or 

action levels. 

MRLs are derived for hazardous substances using the no-observed-adverse-effect level/uncertainty factor 

approach. They are below levels that might cause adverse health effects in the people most sensitive to 

such chemical-induced effects. MRLs are derived for acute (1–14 days), intermediate (15–364 days), and 

chronic (365 days and longer) durations and for the oral and inhalation routes of exposure. Currently, 

MRLs for the dermal route of exposure are not derived because ATSDR has not yet identified a method 

suitable for this route of exposure. MRLs are generally based on the most sensitive chemical-induced end 

point considered to be of relevance to humans. Serious health effects (such as irreparable damage to the 

liver or kidneys, or birth defects) are not used as a basis for establishing MRLs. Exposure to a level 

above the MRL does not mean that adverse health effects will occur. 

MRLs are intended only to serve as a screening tool to help public health professionals decide where to 

look more closely. They may also be viewed as a mechanism to identify those hazardous waste sites that 
 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE A-2 

APPENDIX A 

are not expected to cause adverse health effects. Most MRLs contain a degree of uncertainty because of 

the lack of precise toxicological information on the people who might be most sensitive (e.g., infants, 

elderly, nutritionally or immunologically compromised) to the effects of hazardous substances. ATSDR 

uses a conservative (i.e., protective) approach to address this uncertainty consistent with the public health 

principle of prevention. Although human data are preferred, MRLs often must be based on animal studies 

because relevant human studies are lacking. In the absence of evidence to the contrary, ATSDR assumes 

that humans are more sensitive to the effects of hazardous substance than animals and that certain persons 

may be particularly sensitive. Thus, the resulting MRL may be as much as 100-fold below levels that 

have been shown to be nontoxic in laboratory animals. 

Proposed MRLs undergo a rigorous review process: Health Effects/MRL Workgroup reviews within the 

Division of Toxicology and Human Health Sciences, expert panel peer reviews, and agency-wide MRL 

Workgroup reviews, with participation from other federal agencies and comments from the public. They 

are subject to change as new information becomes available concomitant with updating the toxicological 

profiles. Thus, MRLs in the most recent toxicological profiles supersede previously published levels. 

For additional information regarding MRLs, please contact the Division of Toxicology and Human 

Health Sciences, Agency for Toxic Substances and Disease Registry, 1600 Clifton Road NE, Mailstop 

F-57, Atlanta, Georgia 30329-4027. 

MRLs were not derived for 1,1-dichloroethane, as discussed in Section 2.3. 
 

 

 

 

 

 

 

 

 

 

 

 

 

	 

	 

	 

1,1-DICHLOROETHANE B-1 

APPENDIX B. USER'S GUIDE 

Chapter 1 

Public Health Statement 

This chapter of the profile is a health effects summary written in non-technical language. Its intended 

audience is the general public, especially people living in the vicinity of a hazardous waste site or 

chemical release. If the Public Health Statement were removed from the rest of the document, it would 

still communicate to the lay public essential information about the chemical. 

The major headings in the Public Health Statement are useful to find specific topics of concern. The 

topics are written in a question and answer format. The answer to each question includes a sentence that 

will direct the reader to chapters in the profile that will provide more information on the given topic. 

Chapter 2 

Relevance to Public Health 

This chapter provides a health effects summary based on evaluations of existing toxicologic, 

epidemiologic, and toxicokinetic information. This summary is designed to present interpretive, weightof-evidence discussions for human health end points by addressing the following questions: 

1.	 What effects are known to occur in humans? 

2.	 What effects observed in animals are likely to be of concern to humans? 

3.	 What exposure conditions are likely to be of concern to humans, especially around hazardous 

waste sites? 

The chapter covers end points in the same order that they appear within the Discussion of Health Effects 

by Route of Exposure section, by route (inhalation, oral, and dermal) and within route by effect. Human 

data are presented first, then animal data. Both are organized by duration (acute, intermediate, chronic). 

In vitro data and data from parenteral routes (intramuscular, intravenous, subcutaneous, etc.) are also 

considered in this chapter. 

The carcinogenic potential of the profiled substance is qualitatively evaluated, when appropriate, using 

existing toxicokinetic, genotoxic, and carcinogenic data. ATSDR does not currently assess cancer 

potency or perform cancer risk assessments. Minimal Risk Levels (MRLs) for noncancer end points (if 

derived) and the end points from which they were derived are indicated and discussed. 

Limitations to existing scientific literature that prevent a satisfactory evaluation of the relevance to public 

health are identified in the Chapter 3 Data Needs section. 

Interpretation of Minimal Risk Levels 

Where sufficient toxicologic information is available, ATSDR has derived MRLs for inhalation and oral 

routes of entry at each duration of exposure (acute, intermediate, and chronic). These MRLs are not 

meant to support regulatory action, but to acquaint health professionals with exposure levels at which 

adverse health effects are not expected to occur in humans. 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE B-2 

APPENDIX B 

MRLs should help physicians and public health officials determine the safety of a community living near 

a chemical emission, given the concentration of a contaminant in air or the estimated daily dose in water. 

MRLs are based largely on toxicological studies in animals and on reports of human occupational 

exposure. 

MRL users should be familiar with the toxicologic information on which the number is based. Chapter 2, 

"Relevance to Public Health," contains basic information known about the substance. Other sections such 

as Chapter 3 Section 3.9, "Interactions with Other Substances,” and Section 3.10, "Populations that are 

Unusually Susceptible" provide important supplemental information. 

MRL users should also understand the MRL derivation methodology. MRLs are derived using a 

modified version of the risk assessment methodology that the Environmental Protection Agency (EPA) 

provides (Barnes and Dourson 1988) to determine reference doses (RfDs) for lifetime exposure. 

To derive an MRL, ATSDR generally selects the most sensitive end point which, in its best judgement, 

represents the most sensitive human health effect for a given exposure route and duration. ATSDR 

cannot make this judgement or derive an MRL unless information (quantitative or qualitative) is available 

for all potential systemic, neurological, and developmental effects. If this information and reliable 

quantitative data on the chosen end point are available, ATSDR derives an MRL using the most sensitive 

species (when information from multiple species is available) with the highest no-observed-adverse-effect 

level (NOAEL) that does not exceed any adverse effect levels. When a NOAEL is not available, a 

lowest-observed-adverse-effect level (LOAEL) can be used to derive an MRL, and an uncertainty factor 

(UF) of 10 must be employed. Additional uncertainty factors of 10 must be used both for human 

variability to protect sensitive subpopulations (people who are most susceptible to the health effects 

caused by the substance) and for interspecies variability (extrapolation from animals to humans). In 

deriving an MRL, these individual uncertainty factors are multiplied together. The product is then 

divided into the inhalation concentration or oral dosage selected from the study. Uncertainty factors used 

in developing a substance-specific MRL are provided in the footnotes of the levels of significant exposure 

(LSE) tables. 

Chapter 3 

Health Effects 

Tables and Figures for Levels of Significant Exposure (LSE) 

Tables and figures are used to summarize health effects and illustrate graphically levels of exposure 

associated with those effects. These levels cover health effects observed at increasing dose 

concentrations and durations, differences in response by species, MRLs to humans for noncancer end 

points, and EPA's estimated range associated with an upper- bound individual lifetime cancer risk of 1 in 

10,000 to 1 in 10,000,000. Use the LSE tables and figures for a quick review of the health effects and to 

locate data for a specific exposure scenario. The LSE tables and figures should always be used in 

conjunction with the text. All entries in these tables and figures represent studies that provide reliable, 

quantitative estimates of NOAELs, LOAELs, or Cancer Effect Levels (CELs). 

The legends presented below demonstrate the application of these tables and figures. Representative 

examples of LSE Table 3-1 and Figure 3-1 are shown. The numbers in the left column of the legends 

correspond to the numbers in the example table and figure. 
 

 

 

 

 

 

 

 

 

 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

1,1-DICHLOROETHANE B-3 

APPENDIX B 

LEGEND 

See Sample LSE Table 3-1 (page B-6) 

(1)	 Route of Exposure. One of the first considerations when reviewing the toxicity of a substance 

using these tables and figures should be the relevant and appropriate route of exposure. Typically 

when sufficient data exist, three LSE tables and two LSE figures are presented in the document. 

The three LSE tables present data on the three principal routes of exposure, i.e., inhalation, oral, 

and dermal (LSE Tables 3-1, 3-2, and 3-3, respectively). LSE figures are limited to the inhalation 

(LSE Figure 3-1) and oral (LSE Figure 3-2) routes. Not all substances will have data on each 

route of exposure and will not, therefore, have all five of the tables and figures. 

(2)	 Exposure Period. Three exposure periods—acute (less than 15 days), intermediate (15– 

364 days), and chronic (365 days or more)—are presented within each relevant route of exposure. 

In this example, an inhalation study of intermediate exposure duration is reported. For quick 

reference to health effects occurring from a known length of exposure, locate the applicable 

exposure period within the LSE table and figure. 

(3)	 Health Effect. The major categories of health effects included in LSE tables and figures are 

death, systemic, immunological, neurological, developmental, reproductive, and cancer. 

NOAELs and LOAELs can be reported in the tables and figures for all effects but cancer. 

Systemic effects are further defined in the "System" column of the LSE table (see key number 

18). 

(4)	 Key to Figure. Each key number in the LSE table links study information to one or more data 

points using the same key number in the corresponding LSE figure. In this example, the study 

represented by key number 18 has been used to derive a NOAEL and a Less Serious LOAEL 

(also see the two "18r" data points in sample Figure 3-1). 

(5)	 Species. The test species, whether animal or human, are identified in this column. Chapter 2, 

"Relevance to Public Health," covers the relevance of animal data to human toxicity and 

Section 3.4, "Toxicokinetics," contains any available information on comparative toxicokinetics. 

Although NOAELs and LOAELs are species specific, the levels are extrapolated to equivalent 

human doses to derive an MRL. 

(6)	 Exposure Frequency/Duration. The duration of the study and the weekly and daily exposure 

regimens are provided in this column. This permits comparison of NOAELs and LOAELs from 

different studies. In this case (key number 18), rats were exposed to “Chemical x” via inhalation 

for 6 hours/day, 5 days/week, for 13 weeks. For a more complete review of the dosing regimen, 

refer to the appropriate sections of the text or the original reference paper (i.e., Nitschke et al. 

1981). 

(7)	 System. This column further defines the systemic effects. These systems include respiratory, 

cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, and 

dermal/ocular. "Other" refers to any systemic effect (e.g., a decrease in body weight) not covered 

in these systems. In the example of key number 18, one systemic effect (respiratory) was 

investigated. 

(8)	 NOAEL. A NOAEL is the highest exposure level at which no harmful effects were seen in the 

organ system studied. Key number 18 reports a NOAEL of 3 ppm for the respiratory system, 

which was used to derive an intermediate exposure, inhalation MRL of 0.005 ppm (see 

footnote "b"). 
 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

	 

1,1-DICHLOROETHANE B-4 

APPENDIX B 

(9)	 LOAEL. A LOAEL is the lowest dose used in the study that caused a harmful health effect. 

LOAELs have been classified into "Less Serious" and "Serious" effects. These distinctions help 

readers identify the levels of exposure at which adverse health effects first appear and the 

gradation of effects with increasing dose. A brief description of the specific end point used to 

quantify the adverse effect accompanies the LOAEL. The respiratory effect reported in key 

number 18 (hyperplasia) is a Less Serious LOAEL of 10 ppm. MRLs are not derived from 

Serious LOAELs. 

(10)	 Reference. The complete reference citation is given in Chapter 9 of the profile. 

(11)	 CEL. A CEL is the lowest exposure level associated with the onset of carcinogenesis in 

experimental or epidemiologic studies. CELs are always considered serious effects. The LSE 

tables and figures do not contain NOAELs for cancer, but the text may report doses not causing 

measurable cancer increases. 

(12)	 Footnotes. Explanations of abbreviations or reference notes for data in the LSE tables are found 

in the footnotes. Footnote "b" indicates that the NOAEL of 3 ppm in key number 18 was used to 

derive an MRL of 0.005 ppm. 

LEGEND 

See Sample Figure 3-1 (page B-7) 

LSE figures graphically illustrate the data presented in the corresponding LSE tables. Figures help the 

reader quickly compare health effects according to exposure concentrations for particular exposure 

periods. 

(13)	 Exposure Period. The same exposure periods appear as in the LSE table. In this example, health 

effects observed within the acute and intermediate exposure periods are illustrated. 

(14)	 Health Effect. These are the categories of health effects for which reliable quantitative data 

exists. The same health effects appear in the LSE table. 

(15)	 Levels of Exposure. Concentrations or doses for each health effect in the LSE tables are 

graphically displayed in the LSE figures. Exposure concentration or dose is measured on the log 

scale "y" axis. Inhalation exposure is reported in mg/m3 or ppm and oral exposure is reported in 

mg/kg/day. 

(16)	 NOAEL. In this example, the open circle designated 18r identifies a NOAEL critical end point in 

the rat upon which an intermediate inhalation exposure MRL is based. The key number 18 

corresponds to the entry in the LSE table. The dashed descending arrow indicates the 

extrapolation from the exposure level of 3 ppm (see entry 18 in the table) to the MRL of 

0.005 ppm (see footnote "b" in the LSE table). 

(17)	 CEL. Key number 38m is one of three studies for which CELs were derived. The diamond 

symbol refers to a CEL for the test species-mouse. The number 38 corresponds to the entry in the 

LSE table. 
 

 

 

	 

	 

1,1-DICHLOROETHANE B-5 

APPENDIX B 

(18)	 Estimated Upper-Bound Human Cancer Risk Levels. This is the range associated with the upperbound for lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. These risk levels are derived 

from the EPA's Human Health Assessment Group's upper-bound estimates of the slope of the 

cancer dose response curve at low dose levels (q1*). 

(19)	 Key to LSE Figure. The Key explains the abbreviations and symbols used in the figure. 
 1

SAMPLE

1 → Table 3-1. Levels of Significant Exposure to [Chemical x] – Inhalation 

LOAEL (effect) Exposure 

Key to Less serious Serious (ppm) frequency/ NOAEL (ppm) figurea Species duration System (ppm) Re

2 3 4 

→ INTERMEDIATE EXPOSURE 

5 

→ Systemic ↓

18 Rat 

→

CHRONIC EXPOSURE Cancer 38 Rat 39 Rat 40 Mouse 

6 ↓13 wk 5 d/wk 6 hr/d 18 mo 5 d/wk 7 hr/d 89–104 wk 5 d/wk 6 hr/d 79–103 wk 5 d/wk 6 hr/d 

7 ↓

8 ↓

9 

↓

Resp 3b 10 (hyperplasia) 

11 ↓20 (CEL, multiple 

organs) 

10 (CEL, lung tumors, 

nasal tumors) 

10 (CEL, lung tumors, 

hemangiosarcomas) 

10 

↓

NitWoNTNT

12 → a The number corresponds to entries in Figure 3-1. 

b Used to derive an intermediate inhalation Minimal Risk Level (MRL) of 5x10-3 ppm; dose adjusted for intermittent exby an uncertainty factor of 100 (10 for extrapolation from animal to humans, 10 for human variability). 

1,1-DICHLOROETHANE B-8 

APPENDIX B 

This page is intentionally blank. 
1,1-DICHLOROETHANE C-1 

APPENDIX C. ACRONYMS, ABBREVIATIONS, AND SYMBOLS 

ACGIH American Conference of Governmental Industrial Hygienists 

ACOEM American College of Occupational and Environmental Medicine 

ADI acceptable daily intake 

ADME absorption, distribution, metabolism, and excretion 

AED atomic emission detection 

AFID alkali flame ionization detector 

AFOSH Air Force Office of Safety and Health 

ALT alanine aminotransferase 

AML acute myeloid leukemia 

AOAC Association of Official Analytical Chemists 

AOEC Association of Occupational and Environmental Clinics 

AP alkaline phosphatase 

APHA American Public Health Association 

AST aspartate aminotransferase 

atm atmosphere 

ATSDR Agency for Toxic Substances and Disease Registry 

AWQC Ambient Water Quality Criteria 

BAT best available technology 

BCF bioconcentration factor 

BEI Biological Exposure Index 

BMD/C benchmark dose or benchmark concentration 

BMDX dose that produces a X% change in response rate of an adverse effect 

BMDLX 95% lower confidence limit on the BMDX 

BMDS Benchmark Dose Software 

BMR benchmark response 

BSC Board of Scientific Counselors 

C centigrade 

CAA Clean Air Act 

CAG Cancer Assessment Group of the U.S. Environmental Protection Agency 

CAS Chemical Abstract Services 

CDC Centers for Disease Control and Prevention 

CEL cancer effect level 

CELDS Computer-Environmental Legislative Data System 

CERCLA Comprehensive Environmental Response, Compensation, and Liability Act 

CFR Code of Federal Regulations 

Ci curie 

CI confidence interval 

CL ceiling limit value 

CLP Contract Laboratory Program 

cm centimeter 

CML chronic myeloid leukemia 

CPSC Consumer Products Safety Commission 

CWA Clean Water Act 

DHEW Department of Health, Education, and Welfare 

DHHS Department of Health and Human Services 

DNA deoxyribonucleic acid 

DOD Department of Defense 

DOE Department of Energy 

DOL Department of Labor 
 

 

1,1-DICHLOROETHANE C-2 

APPENDIX C 

DOT Department of Transportation 

DOT/UN/ Department of Transportation/United Nations/ 

NA/IMDG North America/Intergovernmental Maritime Dangerous Goods Code 

DWEL drinking water exposure level 

ECD electron capture detection 

ECG/EKG electrocardiogram 

EEG electroencephalogram 

EEGL Emergency Exposure Guidance Level 

EPA Environmental Protection Agency 

F Fahrenheit 

F1 first-filial generation 

FAO Food and Agricultural Organization of the United Nations 

FDA Food and Drug Administration 

FEMA Federal Emergency Management Agency 

FIFRA Federal Insecticide, Fungicide, and Rodenticide Act 

FPD flame photometric detection 

fpm feet per minute 

FR Federal Register 

FSH follicle stimulating hormone 

g gram 

GC gas chromatography 

gd gestational day 

GLC gas liquid chromatography 

GPC gel permeation chromatography 

HPLC high-performance liquid chromatography 

HRGC high resolution gas chromatography 

HSDB Hazardous Substance Data Bank 

IARC International Agency for Research on Cancer 

IDLH immediately dangerous to life and health 

ILO International Labor Organization 

IRIS Integrated Risk Information System 

Kd adsorption ratio 

kg kilogram 

kkg metric ton 

Koc organic carbon partition coefficient 

Kow octanol-water partition coefficient 

L liter 

LC liquid chromatography 

LC50 lethal concentration, 50% kill 

LCLo lethal concentration, low 

LD50 lethal dose, 50% kill 

LDLo lethal dose, low 

LDH lactic dehydrogenase 

LH luteinizing hormone 

LOAEL lowest-observed-adverse-effect level 

LSE Levels of Significant Exposure 

LT50 lethal time, 50% kill 

m meter 

MA trans,trans-muconic acid 

MAL maximum allowable level 

mCi millicurie 
 

 

 

1,1-DICHLOROETHANE C-3 

APPENDIX C 

MCL maximum contaminant level 

MCLG maximum contaminant level goal 

MF modifying factor 

MFO mixed function oxidase 

mg milligram 

mL milliliter 

mm millimeter 

mmHg millimeters of mercury 

mmol millimole 

mppcf millions of particles per cubic foot 

MRL Minimal Risk Level 

MS mass spectrometry 

NAAQS National Ambient Air Quality Standard 

NAS National Academy of Science 

National Air Toxics Information Clearinghouse 

NATO North Atlantic Treaty Organization 

NCE normochromatic erythrocytes 

NCEH National Center for Environmental Health 

NCI National Cancer Institute 

ND not detected 

NFPA National Fire Protection Association 

ng nanogram 

NHANES National Health and Nutrition Examination Survey 

NIEHS National Institute of Environmental Health Sciences 

NIOSH National Institute for Occupational Safety and Health 

NIOSHTIC NIOSH's Computerized Information Retrieval System 

NLM National Library of Medicine 

nm nanometer 

nmol nanomole 

NOAEL no-observed-adverse-effect level 

NOES National Occupational Exposure Survey 

NOHS National Occupational Hazard Survey 

NPD nitrogen phosphorus detection 

NPDES National Pollutant Discharge Elimination System 

NPL National Priorities List 

NR not reported 

NRC National Research Council 

NS not specified 

NSPS New Source Performance Standards 

NTIS National Technical Information Service 

NTP National Toxicology Program 

ODW Office of Drinking Water, EPA 

OERR Office of Emergency and Remedial Response, EPA 

OHM/TADS Oil and Hazardous Materials/Technical Assistance Data System 

OPP Office of Pesticide Programs, EPA 

OPPT Office of Pollution Prevention and Toxics, EPA 

OPPTS Office of Prevention, Pesticides and Toxic Substances, EPA 

OR odds ratio 

OSHA Occupational Safety and Health Administration 

OSW Office of Solid Waste, EPA 

OTS Office of Toxic Substances 
 

 

1,1-DICHLOROETHANE C-4 

APPENDIX C 

OW Office of Water 

OWRS Office of Water Regulations and Standards, EPA 

PAH polycyclic aromatic hydrocarbon 

PBPD physiologically based pharmacodynamic 

PBPK physiologically based pharmacokinetic 

PCE polychromatic erythrocytes 

PEL permissible exposure limit 

pg picogram 

PHS Public Health Service 

PID photo ionization detector 

pmol picomole 

PMR proportionate mortality ratio 

ppb parts per billion 

ppm parts per million 

ppt parts per trillion 

PSNS pretreatment standards for new sources 

RBC red blood cell 

REL recommended exposure level/limit 

RfC reference concentration 

RfD reference dose 

RNA ribonucleic acid 

RQ reportable quantity 

RTECS Registry of Toxic Effects of Chemical Substances 

SARA Superfund Amendments and Reauthorization Act 

SCE sister chromatid exchange 

SGOT serum glutamic oxaloacetic transaminase 

SGPT serum glutamic pyruvic transaminase 

SIC standard industrial classification 

SIM selected ion monitoring 

SMCL secondary maximum contaminant level 

SMR standardized mortality ratio 

SNARL suggested no adverse response level 

SPEGL Short-Term Public Emergency Guidance Level 

STEL short term exposure limit 

STORET Storage and Retrieval 

TD50 toxic dose, 50% specific toxic effect 

TLV threshold limit value 

TOC total organic carbon 

TPQ threshold planning quantity 

TRI Toxics Release Inventory 

TSCA Toxic Substances Control Act 

TWA time-weighted average 

UF uncertainty factor 

U.S. United States 

USDA United States Department of Agriculture 

USGS United States Geological Survey 

VOC volatile organic compound 

WBC white blood cell 

WHO World Health Organization 
 

1,1-DICHLOROETHANE C-5 

APPENDIX C 

> greater than ≥ greater than or equal to 

= equal to 

< less than ≤ less than or equal to 

% percent α alpha β beta γ gamma δ delta 

μm micrometer 

μg microgram q1

* cancer slope factor 

– negative 

+ positive 

(+) weakly positive result 

(–) weakly negative result