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TOXICOLOGICAL PROFILE FOR 

1,1-DICHLOROETHANE 

PUBLIC COMMENT PERIOD ENDS 

September 30, 2013 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES 

Public Health Service 

Agency for Toxic Substances and Disease Registry 

April 2013 
 

 

 

 

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. 

This information is distributed solely for the purpose of pre dissemination public comment under 

applicable information quality guidelines. It has not been formally disseminated by the Agency for Toxic 

Substances and Disease Registry. It does not represent and should not be construed to represent any 

agency determination or policy. 

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1,1-DICHLOROETHANE iii 

UPDATE STATEMENT 

A Toxicological Profile for 1,1-Dichloroethane was released in 1990. This present 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 30333 

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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 and EPA. 

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. We plan 

to revise these documents in response to public comments and as additional data become available. 

Therefore, we encourage comments that will make the toxicological profile series of the greatest use. 

Electronic comments may be submitted via: www.regulations.gov. 

Follow the on-line instructions for submitting comments. 

Written comments may also be sent to: 

Agency for Toxic Substances and Disease Registry 

Division of Toxicology and Human Health Sciences 

Environmental Toxicology Branch 

Regular Mailing Address: Physical Mailing Address: 

1600 Clifton Road, N.E. 4770 Buford Highway 

Mail Stop F-57 Building 106, 3rd floor, MS F-57 

Atlanta, Georgia 30333 Chamblee, Georgia 30341 

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1,1-DICHLOROETHANE vi 

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. 

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 is being made available for public review. Final responsibility for the 

contents and views expressed in this toxicological profile resides with ATSDR. 

Robin M. Ikeda, MD, MPH 

Acting Assistant Administrator 

Agency for Toxic Substances and 

Disease Registry 

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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: 

Section 1.6 How Can (Chemical X) Affect Children? 

Section 1.7 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) Fax: (770) 488-4178 

E-mail: cdcinfo@cdc.gov Internet: http://www.atsdr.cdc.gov 

The following additional material can be ordered through the ATSDR Information Center: 

Case Studies in Environmental Medicine: Taking an Exposure History—The importance of taking an 

exposure history and how to conduct one are described, and an example of a thorough exposure 

history is provided. Other case studies of interest include Reproductive and Developmental 

Hazards; Skin Lesions and Environmental Exposures; Cholinesterase-Inhibiting Pesticide 

Toxicity; and numerous chemical-specific case studies. 

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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 (ToxFAQs) 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, 200 Independence Avenue, 

SW, Washington, DC 20201 • Phone: 800-356-4674 or NIOSH Technical Information Branch, 

Robert A. Taft Laboratory, Mailstop C-19, 4676 Columbia Parkway, Cincinnati, OH 45226-1998 

• Phone: 800-35-NIOSH. 

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. 

Referrals 

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. 

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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. 

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. 

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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. 

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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 ................................................................................................... 9 

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

THE UNITED STATES................................................................................................................. 9 

2.2 SUMMARY OF HEALTH EFFECTS ........................................................................................... 9 

2.3 MINIMAL RISK LEVELS (MRLs) ............................................................................................ 13 

3. HEALTH EFFECTS .............................................................................................................................. 15 

3.1 INTRODUCTION ........................................................................................................................ 15 

3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE ..................................... 15 

3.2.1 Inhalation Exposure .............................................................................................................. 16 

3.2.1.1 Death .............................................................................................................................. 16 

3.2.1.2 Systemic Effects............................................................................................................. 21 

3.2.1.3 Immunological and Lymphoreticular Effects ................................................................ 22 

3.2.1.4 Neurological Effects ...................................................................................................... 22 

3.2.1.5 Reproductive Effects...................................................................................................... 22 

3.2.1.6 Developmental Effects ................................................................................................... 22 

3.2.1.7 Cancer ............................................................................................................................ 23 

3.2.2 Oral Exposure........................................................................................................................ 23 

3.2.2.1 Death .............................................................................................................................. 23 

3.2.2.2 Systemic Effects............................................................................................................. 28 

3.2.2.3 Immunological and Lymphoreticular Effects ................................................................ 29 

3.2.2.4 Neurological Effects ...................................................................................................... 29 

3.2.2.5 Reproductive Effects...................................................................................................... 29 

3.2.2.6 Developmental Effects ................................................................................................... 29 

3.2.2.7 Cancer ............................................................................................................................ 30 

3.2.3 Dermal Exposure................................................................................................................... 31 

3.2.3.1 Death .............................................................................................................................. 31 

3.2.3.2 Systemic Effects............................................................................................................. 31 

3.2.3.3 Immunological and Lymphoreticular Effects ................................................................ 31 

3.2.3.4 Neurological Effects ...................................................................................................... 31 

3.2.3.5 Reproductive Effects...................................................................................................... 31 

3.2.3.6 Developmental Effects ................................................................................................... 31 

3.2.3.7 Cancer ............................................................................................................................ 31 

3.3 GENOTOXICITY ........................................................................................................................ 32 

3.4 TOXICOKINETICS ..................................................................................................................... 34 

3.4.1 Absorption............................................................................................................................. 34 

3.4.1.1 Inhalation Exposure ....................................................................................................... 34 

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3.4.1.2 Oral Exposure ................................................................................................................ 34 

3.4.1.3 Dermal Exposure ........................................................................................................... 35 

3.4.2 Distribution ........................................................................................................................... 35 

3.4.2.1 Inhalation Exposure ....................................................................................................... 35 

3.4.2.2 Oral Exposure ................................................................................................................ 35 

3.4.2.3 Dermal Exposure ........................................................................................................... 35 

3.4.2.4 Other Routes of Exposure .............................................................................................. 36 

3.4.3 Metabolism............................................................................................................................ 36 

3.4.4 Elimination and Excretion..................................................................................................... 40 

3.4.4.1 Inhalation Exposure ....................................................................................................... 40 

3.4.4.2 Oral Exposure ................................................................................................................ 40 

3.4.4.3 Dermal Exposure ........................................................................................................... 40 

3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models ............. 40 

3.5 MECHANISMS OF ACTION ..................................................................................................... 43 

3.5.1 Pharmacokinetic Mechanisms ............................................................................................... 43 

3.5.2 Mechanisms of Toxicity........................................................................................................ 43 

3.5.3 Animal-to-Human Extrapolations ......................................................................................... 43 

3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS ............................. 43 

3.7 CHILDREN’S SUSCEPTIBILITY .............................................................................................. 44 

3.8 BIOMARKERS OF EXPOSURE AND EFFECT ....................................................................... 46 

3.8.1 Biomarkers Used to Identify or Quantify Exposure to 1,1-Dichloroethane.......................... 48 

3.8.2 Biomarkers Used to Characterize Effects Caused by 1,1-Dichloroethane ............................ 48 

3.9 INTERACTIONS WITH OTHER CHEMICALS ....................................................................... 48 

3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE .................................................. 48 

3.11 METHODS FOR REDUCING TOXIC EFFECTS...................................................................... 49 

3.11.1 Reducing Peak Absorption Following Exposure............................................................... 49 

3.11.2 Reducing Body Burden ..................................................................................................... 49 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects ............................................ 49 

3.12 ADEQUACY OF THE DATABASE .......................................................................................... 50 

3.12.1 Existing Information on Health Effects of 1,1-Dichloroethane......................................... 50 

3.12.2 Identification of Data Needs .............................................................................................. 52 

3.12.3 Ongoing Studies ................................................................................................................ 57 

4. CHEMICAL AND PHYSICAL INFORMATION ................................................................................ 59 

4.1 CHEMICAL IDENTITY.............................................................................................................. 59 

4.2 PHYSICAL AND CHEMICAL PROPERTIES........................................................................... 59 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL ............................................................ 63 

5.1 PRODUCTION ............................................................................................................................ 63 

5.2 IMPORT/EXPORT ...................................................................................................................... 65 

5.3 USE .............................................................................................................................................. 65 

5.4 DISPOSAL ................................................................................................................................... 65 

6. POTENTIAL FOR HUMAN EXPOSURE ........................................................................................... 67 

6.1 OVERVIEW................................................................................................................................. 67 

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

6.2.1 Air ......................................................................................................................................... 70 

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

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

6.3 ENVIRONMENTAL FATE ........................................................................................................ 73 

6.3.1 Transport and Partitioning..................................................................................................... 73 

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6.3.2 Transformation and Degradation .......................................................................................... 75 

6.3.2.1 Air .................................................................................................................................. 75 

6.3.2.2 Water.............................................................................................................................. 75 

6.3.2.3 Sediment and Soil .......................................................................................................... 76 

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

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

6.4.2 Water ..................................................................................................................................... 78 

6.4.3 Sediment and Soil ................................................................................................................. 80 

6.4.4 Other Environmental Media .................................................................................................. 80 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE .......................................... 81 

6.6 EXPOSURES OF CHILDREN .................................................................................................... 83 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES ................................................ 83 

6.8 ADEQUACY OF THE DATABASE .......................................................................................... 83 

6.8.1 Identification of Data Needs ................................................................................................. 84 

6.8.2 Ongoing Studies .................................................................................................................... 87 

7. ANALYTICAL METHODS.................................................................................................................. 89 

7.1 BIOLOGICAL MATERIALS ...................................................................................................... 89 

7.2 ENVIRONMENTAL SAMPLES ................................................................................................ 95 

7.3 ADEQUACY OF THE DATABASE .......................................................................................... 98 

7.3.1 Identification of Data Needs ................................................................................................. 98 

7.3.2 Ongoing Studies .................................................................................................................... 99 

8. REGULATIONS, ADVISORIES, AND GUIDELINES..................................................................... 101 

9. REFERENCES .................................................................................................................................... 105 

10. GLOSSARY ...................................................................................................................................... 129 

APPENDICES 

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

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

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

D. INDEX ................................................................................................................................................ D-1 

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LIST OF FIGURES 

2-1. Health Effects for Following Inhalation Exposure to 1,1-Dichloroethane ......................................... 11 

2-2. Health Effects for Following Oral Exposure to 1,1-Dichloroethane .................................................. 12 

3-1. Levels of Significant Exposure to 1,1-Dichloroethane – Inhalation................................................... 19 

3-2. Levels of Significant Exposure to 1,1-Dichloroethane – Oral............................................................ 26 

3-3. Proposed Metabolic Scheme for 1,1-Dichloroethane ......................................................................... 39 

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

Hypothetical Chemical Substance ...................................................................................................... 42 

3-5. Existing Information on Health Effects of 1,1-Dichloroethane .......................................................... 51 

6-1. Frequency of NPL Sites with 1,1-Dichloroethane Contamination ..................................................... 68 

1,1-DICHLOROETHANE xvii 

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LIST OF TABLES 

3-1. Levels of Significant Exposure for 1,1-Dichloroethane – Inhalation ................................................. 17 

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

3-3. Genotoxicity of 1,1-Dichloroethane In Vitro...................................................................................... 33 

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

Phenobarbital-Induced Rats ............................................................................................................... 38 

4-1. Chemical Identity of 1,1-Dichloroethane ........................................................................................... 60 

4-2. Physical and Chemical Properties of 1,1-Dichloroethane .................................................................. 61 

5-1. Facilities that Produce, Process, or Use 1,1-Dichloroethane .............................................................. 64 

6-1. Releases to the Environment from Facilities that Produce, Process, or Use 1,1-Dichloroethane ...... 71 

7-1. Analytical Methods for Determining 1,1-Dichloroethane in Biological Materials ............................ 90 

7-2. Analytical Methods for Determining 1,1-Dichloroethane in Environmental Samples....................... 91 

8-1. Regulations, Advisories, and Guidelines Applicable to 1,1-Dichloroethane ................................... 102 

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1,1-DICHLOROETHANE 1 

1. PUBLIC HEALTH STATEMENT FOR 

1,1-DICHLOROETHANE 

Overview 

We define a public health statement and show how it can help you learn about 1,1-dichloroethane. 

Introduction	 A public health statement summarizes information about a hazardous 

substance. The information is taken from a toxicological profile developed by 

ATSDR’s Division of Toxicology and Human Health Sciences (DTHHS). A 

toxicological profile is a thorough review of a hazardous substance. 

This toxicological profile examines 1,1-dichloroethane. This public health 

statement summarizes the DTHHS’s findings on 1,1-diochloroethane, 

describes the effects of exposure to it, and describes what you can do to limit 

that exposure. 

1,1-Dichloroethane 

at hazardous waste 

The U.S. Environmental Protection Agency (EPA) identifies the most serious 

hazardous waste sites in the nation. U.S. EPA then includes these sites the 

sites National Priorities List (NPL) and targets them for 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. 

However, the possibility remains that as more sites are evaluated, the number 

of sites at which 1,1-dichloroethane is found may increase. This information 

is important; these future sites may be sources of exposure, and exposure to 

1,1-dichloroethane may be harmful. 

Why a 

1,1-dichloroethane 

When a contaminant is released from a large area such as an industrial plant or 

from a container such as a drum or bottle, it enters the environment. 

release can be 

harmful 

However, such a release doesn’t always lead to exposure. You can only be 

exposed to a contaminant when you come in contact with it. That contact— 

and therefore that exposure—can occur when you breathe, eat, or drink the 

contaminant, or when it touches your skin. 

Even if you’re exposed to 1,1-dichloroethane, you might not be harmed. 

Whether you are harmed will depend on such factors as the dose (how 

much), the duration (how long), and how you happen to contact it. Harm 

might also depend on whether you’ve been exposed to any other chemicals, 

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

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1,1-DICHLOROETHANE 2 

1. PUBLIC HEALTH STATEMENT 

A Closer Look at 1,1-Dichloroethane 

Overview 

This section describes 1,1-dichloroethane in detail and how you can be exposed to it. 

What is 1,1-Dichloroethane is a colorless oily liquid with a chloroform1,1-dichloroethane? like odor. 

How is 1,1-Dichloroethane is a chemical used mostly as an intermediate in the 

1,1-dichloroethane manufacture of 1,1,1-trichloroethane, and to a lesser extent, vinyl chloride and 

used? high vacuum rubber. 

Where is 1,1-di- 1,1-Dichloroethane can be released into the air, water, and soil at 

chloroethane places where it is produced or used as a solvent. 

found? 

Possible Sources Outcome 

Air: Levels of 1,1-dichloroethane in 

air samples have been measured at 

concentrations ranging from parts 

per trillion to parts per million, 

depending upon the location. 

In the air, 1,1-dichloroethane is slow 

to break down and has the potential for 

long-range transport. 

Water: 1,1-Dichloroethane is 

infrequently detected in drinking 

water. Analyses of 

13,347 California groundwater 

sources of drinking water found 

1,1-dichloroethane in 68 samples, 

ranging from 0.51 to 30 parts per 

billion (ppb). 

1,1-Dichloroethane is not expected to 

rapidly break down in water. It can 

evaporate from the water into the air. 

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 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 bind to soil 

particulates unless the organic content 

of the soil is high. 

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1,1-DICHLOROETHANE 3 

1. PUBLIC HEALTH STATEMENT 

Other Media: Little 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. 

How 1,1-Dichloroethane Can Affect Your Health 

Overview 

This section looks at how 1,1-dichloroethane enters your body and potential 1,1-dichloroethane health 

effects found in human and animal studies. 

How 1,1-dichloro- 1,1-Dichloroethane can enter your body from the air, water or consumer 

ethane products. 

Possible Sources Possible Exposure Pathway 

Air If you breathe air containing 

1,1-dichloroethane, it will enter your 

body through your lungs. 

Water 1,1-Dichloroethane in your drinking 

water will enter your body through the 

digestive tract. 

How 1,1-dichloro- 1,1-Dichloroethane leaves your body in the breath or is broken down into other 

ethane leaves your chemicals and these chemicals leave your body in the breath or in the urine. 

body 

Introduction to 

1,1-dichloroethane 

health effects 

The health effects of 1,1-dichloroethane depends on how much 1,1-dichloroethane you are exposed to and the length of that exposure. Environmental 

monitoring data are limited. However, they do suggest that any 1,1-dichloroethane levels the public might encounter through contact, through air, water, or 

soil are generally much lower than animal-study levels. 

Effects in humans No information is available in humans on the health effects 

associated with exposure to 1,1-dichloroethane. 

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1,1-DICHLOROETHANE 4 

1. PUBLIC HEALTH STATEMENT 

Long-term 

exposure effects 

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. 

1,1-Dichloroethane 

and cancer 

A study in rats and mice found suggestive evidence that 1,1-dichloroethane may 

cause cancer. However, the study had several flaws and the results are not 

conclusive. Another long-term study in mice drinking water containing 

1,1-dichloroethane did not find cancer. 

Some cancer 

findings by 

government and 

other agencies 

•	 The U.S. Department of Health and Human Services (HHS) 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. 

Children and 1,1-Dichloroethane 

Overview 

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. 

Exposure effects in No data describe the effects of exposure to 1,1-dichloroethane on children or 

children	 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. 

What about birth We don’t know whether 1,1-dichloroethane can harm an unborn child. Minor 

defects? skeletal problems were observed in the fetuses of rats breathing 1,1-dichloroethane; decreases in body weight were also observed in the mothers. 

Medical Tests to Determine 1,1-Dichloroethane Exposure 

Overview 

We identify medical tests that can detect whether 1,1-dichloroethane is in your body, and we recommend 

safe toxic-substance practices. 

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1,1-DICHLOROETHANE 5 

1. PUBLIC HEALTH STATEMENT 

1,1-Dichloroethane 

can be measured in 

1,1-Dichloroethane and its breakdown products (metabolites) can be measured 

in blood and urine. However, the detection of 1,1-dichoroethane or its 

blood and urine 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. 

Federal Government Recommendations to Protect Human 

Health 

Overview 

One way the federal government promotes public health is by regulating toxic substances or 

recommending ways to handle or to avoid toxic substances. 

The federal 

government 

regulates toxic 

substances 

Regulations are enforceable by law. The U.S. EPA, the Occupational Safety and 

Health Administration (OSHA), and the Food and Drug Administration (FDA) 

are some federal agencies that have adopted toxic substances regulations. 

The federal 

government 

recommends safe 

toxic substance 

practices 

The Agency for Toxic Substances and Disease Registry (ATSDR) and the 

National Institute for Occupational Safety and Health (NIOSH) have made 

recommendations about toxic substances. Unlike enforceable regulations, these 

recommendations are advisory only. 

Toxic substance 

regulations 

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. 

Check for Recommendations and regulations are also updated periodically as more 

regulation updates information becomes available. For the most current information, check with the 

federal agency or organization that issued the regulation or recommendation. 

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1,1-DICHLOROETHANE 6 

1. PUBLIC HEALTH STATEMENT 

Some regulations and recommendations for 1,1-dichloroethane include: 

Federal Organization Regulation or Recommendation 

U.S. EPA The U.S. EPA has included 

1,1-dichloroethane as a priority 

contaminant in the drinking water 

program. 

Occupational Safety and Health 

Administration (OSHA) 

OSHA set a legal limit of 100 ppm 

1,1-dichloroethane in air averaged over 

an 8-hour work day. 

NIOSH NIOSH recommends a limit of 100 ppm 

1,1-dichloroethane in air averaged over 

a 10-hour work day. 

Additional Information 

Overview 

Where to find more information about 1,1-dichloroethane. 

Whom to If you have any more questions or concerns, please contact your community or state 

contact first health or environmental quality department, or contact ATSDR at the address and 

phone number below. 

Additional ATSDR can also tell you the location of occupational and environmental health 

information clinics. These clinics specialize in recognizing, evaluating, and treating illnesses 

from ATSDR that result from exposure to hazardous substances. 

Where to 

obtain 

toxicological 

profile copies 

Toxicological profiles are also available online at www.atsdr.cdc.gov and on 

CD-ROM. Request a copy of the ATSDR ToxProfilesTM CD-ROM by 

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

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

•	 E-mailing cdcinfo@cdc.gov, or 

•	 Writing to 

Agency for Toxic Substances and Disease Registry 

Division of Toxicology and Human Health Sciences 

1600 Clifton Road NE 

Mailstop F-57 

Atlanta, GA 30333 

Fax: 1-770-488-4178 

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1,1-DICHLOROETHANE 7 

1. PUBLIC HEALTH STATEMENT 

For-profit organizations should request final toxicological profile copies from 

National Technical Information Service (NTIS) 

5285 Port Royal Road 

Springfield, VA 22161 

Phone: 1-800-553-6847 or 1-703-605-6000 

Web site: http://www.ntis.gov/ 

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1,1-DICHLOROETHANE 8 

1. PUBLIC HEALTH STATEMENT 

This page is intentionally blank. 

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1,1-DICHLOROETHANE 9 

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 in the age range of 20–59 years old, about half females (n=679) 

and half males (n=670). 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 

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1,1-DICHLOROETHANE 10 

2. RELEVANCE TO PUBLIC HEALTH 

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

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 

reproductive, immunotoxicity, and neurotoxicity of 1,1-dichloroethane has 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 both 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. 

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

1,1-Dichloroethane 

Dose (ppm) Effects in Animals 

6,000 

750 (TWA) 

Maternal and developm ental effectsa 

Renal effects in catsb; no liver or kidney 

effects in rats, guinea pigs, or rabbits 

1,1-DICHLOROETHANE 11 

2. RELEVANCE TO PUBLIC HEALTH 

a

11% decrease in maternal body weight gain and increased incidence of fetuses with delayed 

ossification 

b

Increased serum urea and creatinine levels, crystal precipitations and obstruction in tubule 

lum ina and dilatation of proximal section of renal tubules 

TWA = tim e-weighted average 

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

Dose (mg/kg/day)a Effects in Animals 

2,061 (males); 

2,379 (f emales) 

546 (males); 

679 (f emales) 

401 (males) 

Highest no-effect level in mice following 

chronic exposure 

Highest no-effect level in rats following 

chronic exposure 

Decreases in body weight gain following 

5 week exposure 

a

Doses adjusted for intermittent exposure (5 days/week) 

1,1-DICHLOROETHANE 12 

2. RELEVANCE TO PUBLIC HEALTH 

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1,1-DICHLOROETHANE 13 

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 

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1,1-DICHLOROETHANE 14 

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. 

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1,1-DICHLOROETHANE 15 

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 

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1,1-DICHLOROETHANE 16 

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. 

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258

6000

257

3000

6800

272

750750750

274

750750750

273

750750750

Table 3-1 Levels of Significant Exposure to 1,1-dichloroethane - Inhalation 

a 

Key to 

Figure 

Species 

(Strain) 

Exposure/ 

Duration/ 

Frequency 

(Route) 

ACUTE EXPOSURE Systemic 

1 Rat 

(SpragueDawley) 

7 hr/d 10 d 

Developmental 

2 Rat 

(SpragueDawley) 

7 hr/d Gd 6-15 

System 

Hepatic 

NOAEL 

(ppm) 

6000 F 

3000 F 

LOAEL 

Less Serious 

(ppm) 

Serious 

(ppm) 

6800 F (Increased incidence of 

delayed ossification) 

Reference Chemical Form 

Schwetz et al. 1974Schwetz et al. 1974

INTERMEDIATE EXPOSURE Systemic 

3 Rat 

(SpragueDawley) 

6 hr/d 5 d/wk 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 

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275

750

750

750

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

a 

Key to 

Figure 

Species 

(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 

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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 

1,1-DICHLOROETHANE 19 ***DRAFT FOR PUBLIC COMMENT*** 3. HEALTH EFFECTS

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

Acute (≤14 days)

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 
Hepatic 

Renal Body Weight 

1,1-DICHLOROETHANE 20 ***DRAFT FOR PUBLIC COMMENT*** 3. HEALTH EFFECTS

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

Intermediate (15-364 days)
	

Systemic 

ppm 

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 
 

 

 

 

 

 

 

 

 

 

 

 

1,1-DICHLOROETHANE 21 

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. 

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1,1-DICHLOROETHANE 22 

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. 

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1,1-DICHLOROETHANE 23 

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. 

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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) 

INTERMEDIATE EXPOSURE Death 

1 Rat 

(OsborneMendel) 

5 d/wk 6 wk (GO) 

System 

NOAEL 

(mg/kg/day) 

Less Serious 

(mg/kg/day) 

LOAEL 

Serious 

(mg/kg/day) 

3160 F (2/5 rats died) 

Reference Chemical Form 

NCI 1977 1,1-DCE 

2 Mouse 

(B6C3F1) 

Systemic 

3 Rat 

(OsborneMendel) 

5 d/wk 6 wk (GO) 5 d/wk 6 wk (GO) 

Bd Wt 562 M (16% decreased body 

weight gain) 

5620 (4/10 deaths) 

1000 M (29% decreased body 

weight gain) 

NCI 1977 1,1-DCE NCI 1977 1,1-DCE 

4 Mouse 

(B6C3F1) 

daily 52 wk (W) 

Resp 465 M Klaunig et al. 1986 

1,1-DCE 

Hepatic Renal 

465 M 465 M 

Bd Wt 465 M 

5 Mouse 

(B6C3F1) 

5 d/wk 6 wk (GO) 

Bd Wt 2885 M NCI 1977 

1,1-DCE 

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259

764764764764764764764764764

261

288528852885288528852885288528852885

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

Exposure/ 

Duration/

a 

Key to Species Frequency 

Figure (Strain) (Route) 

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 

(mg/kg/day) 

Less Serious 

(mg/kg/day) 

Serious 

(mg/kg/day) 

Reference 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 = hematologica

LOAEL = 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) 

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Death 

Respiratory Hepatic Renal Body Weight 

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

Intermediate (15-364 days) 

Systemic 

mg/kg/day 

100 

1000 

10000 

2m 

1r 

4m 4m 4m 4m 

5m 

3r 

3r 

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 

1,1-DICHLOROETHANE 26 ***DRAFT FOR PUBLIC COMMENT*** 3. HEALTH EFFECTS
Respiratory 

Cardiovascular Gastrointestinal Hematological Musculoskeletal Hepatic Renal Endocrine Dermal Body Weight 

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

Chronic (≥365 days)
	

Systemic 

mg/kg/day 

100 

1000 

10000 

7m 

6r 

7m 

6r 

7m 

6r 

7m 

6r 

7m 

6r 

7m

6r 

7m 

6r 

7m 

6r 

7m 

6r 

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 

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1,1-DICHLOROETHANE 28 

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 

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1,1-DICHLOROETHANE 29 

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 

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1,1-DICHLOROETHANE 30 

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 

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1,1-DICHLOROETHANE 31 

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 

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1,1-DICHLOROETHANE 32 

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 

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Results 

With Without 

Species (test system) End point activation activation Reference 

Prokaryotic organisms: 

Salmonella typhimuriu,m strains 

TA97, TA98, TA100, and TA102 

(Ames assay) 

S. typhimurium, strains TA1535, 

TA1537, TA1538, TA98, and 

TA100 (Ames assay) 

S. typhimurium, strains TA1537, 

TA98, TA100, and TA1535 

(dessicator assay; vapor exposure) 

S. typhimurium, strains TA1535, 

TA98, and TA100 (Ames assay; 

dessicator) 

Eukaryotic organisms: 

Saccharomyces cerevisiae D7 

Mammalian cells 

Syrian hamster embryo (cell 

transformation assay; vapor 

exposure) 

Osborne-Mendel rat and B6C3F1 

mouse hepatocytes 

BALB/C-3T3 (cell transformation 

assay; exposure in sealed 

chamber) 

BALB/C-3T3 (cell transformation 

assay; exposure in sealed 

chamber) 

Chinese hamster lung fibroblasts 

(chromosomal aberration assay; 

exposure in sealed chamber) 

Gene mutation 

Gene mutation 

Gene mutation 

Gene mutation 

Gene mutation 

DNA viral 

transformation 

DNA repair 

Cell transformation 

Cell transformation 

Chromosomal 

aberrations 

– – Nohmi et al. 1986 

– – Simmon et al. 1977 

+ + Riccio et al. 1983 

+ + Milman et al. 1988 

– – Bronzetti et al. 1987 

No data + Hatch et al. 1983 

No data + Milman et al. 1988 

No data – Tu et al. 1985 

No data – Milman et al. 1998 

– – Matsuoka et al. 

1998) 

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

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

1,1-DICHLOROETHANE 33 

3. HEALTH EFFECTS 

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1,1-DICHLOROETHANE 34 

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 

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1,1-DICHLOROETHANE 35 

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. 

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1,1-DICHLOROETHANE 36 

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 

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1,1-DICHLOROETHANE 37 

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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). 

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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) 

a

Values 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 38 

3. HEALTH EFFECTS 

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1,1-DICHLOROETHANE 39 

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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 

Cl OH 2HC 

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) 

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1,1-DICHLOROETHANE 40 

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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. 

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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. 

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al Exhaled chemical 

1,1-DICHLOROETHANE 42 

3. HEALTH EFFECTS 

Figure 3-4. Conceptual Representation of a Physiologically Based 

Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance 

Inhaled chemic

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 

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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. Crystaline 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 

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disruptors. In 1999, the National Academy of Sciences released a report that referred to these same types 

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. 

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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 

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1,1-DICHLOROETHANE 46 

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the developing brain or do they render it more vulnerable to toxic injury. Each case of chemical exposure 

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). 

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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. 

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1,1-DICHLOROETHANE 48 

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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 

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1,1-DICHLOROETHANE 49 

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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. 

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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 

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. 

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1, 1 -DI CHL O RO E T HA N E 51 

3 . H E A L TH E FFE C TS 

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

Inhalation 

Oral 

Dermal 

Death 

Acute 

Intermediate

Chronic 

Immunologic/Lymphoretic

Neurologic

Reproductive

Developmental

Genotoxic

Cancer 

Systemic 

Human 

Animal 

Existing Studies 

Inhalation 

Oral 

Dermal 

Death 

Acute 

Intermediate

Chronic 

Immunologic/Lymphoretic

Neurologic

Reproductive

Developmental

Genotoxic

Cancer 

Systemic 

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1,1-DICHLOROETHANE 52 

3. HEALTH EFFECTS 

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 exposure, the database was not considered adequate for derivation of an acute-duration 

inhalation MRL. The lack of oral data precluded derivation of an oral MRL 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, 

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 

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1,1-DICHLOROETHANE 53 

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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 

(Colacci et al. 1985). More information on the genotoxic effects of 1,1-dichloroethane in animals both in 

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1,1-DICHLOROETHANE 54 

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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 

where 1,1-dichloroethane contamination of surface water and groundwater or air is known to have 

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1,1-DICHLOROETHANE 55 

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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 localizes in the liver, kidney, lung, and stomach. However, analysis has been limited 

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1,1-DICHLOROETHANE 56 

3. HEALTH EFFECTS 

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. 

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. 

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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. 

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1,1-DICHLOROETHANE 59 

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. 

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1,1-DICHLOROETHANE 60 

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 

a

All information obtained from HSDB 2012, except where noted

b

O’Neil et al. 2006 c

Archer 1978; Weiss 1986 d

ChemIDPlus 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 

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1,1-DICHLOROETHANE 61 

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 

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1,1-DICHLOROETHANE 63 

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 (TRI10 2012). Based on the TRI 

information from 2010, there are 204 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). 

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 2010a). Both of these companies manufactured 1,1-dichloroethane 

primarily to be used as an intermediate. 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 2010a). 

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1,1-DICHLOROETHANE 64 

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 

AL 1 1,000 9,999 12 

AR 8 1,000 99,999 12 

CA 2 100 999 12 

FL 1 10,000 99,999 12 

KS 1 10,000 99,999 1, 4 

KY 6 10,000 99,999 1, 3, 6 

LA 102 0 9,999,999 1, 2, 3, 4, 5, 6, 10, 12, 13 

MI 1 10,000 99,999 7, 12 

MO 2 1,000 999,999 9, 12 

MS 3 1,000 99,999 12 

OH 12 100 9,999 12 

PA 2 100 9,999 12 

SC 1 100 999 12 

TX 62 0 9,999,999 1, 2, 3, 4, 5, 6, 12, 13, 14 

a

Post office state abbreviations used. b

Amounts on site reported by facilities in each state. c

Activities/Uses: 

1. Produce 6. Impurity 11. Chemical Processing Aid 

2. Import 7. Reactant 12. Manufacturing Aid 

3. Onsite use/processing 8. Formulation Component 13. Ancillary/Other Uses 

4. Sale/Distribution 9. Article Component 14. Process Impurity 

5. Byproduct 10. Repackaging 

Source: TRI10 2012 (Data are from 2010) 

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1,1-DICHLOROETHANE 65 

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

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, and to a lesser extent, vinyl chloride and high vacuum rubber (Cowfer 2006; HSDB 

2012; Marshall 2003). 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. 

Consultation with environmental regulatory agencies is advised (HSDB 2012; Marshall 2003; NIOSH 

1978). 

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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 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. In addition, 1,1-dichloroethane may occur in the environment as a biodegradation product of 

1,1,1-trichloroethane. 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). 

Inhalation of 1,1-dichloroethane in ambient or workplace air is generally the main route of human 

exposure to the compound. 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 levels greatly 

diminish in properly ventilated areas. 

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 

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1,1-DICHLOROETHANE 68 

6. POTENTIAL FOR HUMAN EXPOSURE 

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

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1,1-DICHLOROETHANE 69 

6. POTENTIAL FOR HUMAN EXPOSURE 

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). 

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). 

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 2012d). 

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 

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6. POTENTIAL FOR HUMAN EXPOSURE 

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 8,470 pounds (~3.84 metric tons) of 1,1-dichloroethane to the atmosphere from 

14 domestic manufacturing and processing facilities in 2010, accounted for about 98.8% of the estimated 

total environmental releases from facilities required to report to the TRI (TRI10 2012). 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. 

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 in air samples at two current or former NPL hazardous waste sites where 

it was detected in some environmental media (HazDat 2007). 

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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 UIg Landh Otheri On-sitej Off-sitek On- and off-site 

KY 1 56 0 0 0 0 56 0 56 

LA 7 8,186 72 0 9 0 8,258 9 8,267 

OH 1 4 0 0 22 0 4 22 26 

TX 4 223 3 0 0 0 226 0 226 

Total 14 8,470 75 0 31 0 8,544 31 8,575 

a

The 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. b

Data in TRI are maximum amounts released by each facility. c

Post office state abbreviations are used. d

Number of reporting facilities. e

The 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). g

Class I wells, Class II-V wells, and underground injection. h

Resource 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.

k

Total amount of chemical transferred off-site, including to POTWs. 

RF = reporting facilities; UI = underground injection 

Source: TRI10 2012 (Data are from 2010) 

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6.2.2 Water 

Estimated releases of 75 pounds (~0.034 metric tons) of 1,1-dichloroethane to surface water from 

11 domestic manufacturing and processing facilities in 2010, accounted for <1% of the estimated total 

environmental releases from facilities required to report to the TRI (TRI10 2012). This estimation 

includes surface water discharges, waste water treatment (metal only), and POTWs (metal and metal 

compounds) (TRI10 2012). 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. Releases from solvent use and POTWs account for only 2,000 kg annually (EPA 1982b). 

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). 

1,1-Dichloroethane was detected in groundwater samples at 106 current or former NPL hazardous waste 

sites where it was detected in some environmental media (HazDat 2007). It was detected in surface water 

at 27 current or former NPL hazardous waste sites where it was detected in some environmental media 

(HazDat 2007). 

6.2.3 Soil 

Estimated releases of 31 pounds (~0.014 metric tons) of 1,1-dichloroethane to soils from eight domestic 

manufacturing and processing facilities in 2010, accounted for <0.5% of the estimated total 

environmental releases from facilities required to report to the TRI (TRI10 2012). These releases are 

summarized in Table 6-1. 

Little information was found regarding releases of 1,1-dichloroethane to soils. Solvent use and POTWs 

are the only identified sources of 1,1-dichloroethane releases to the land, with 6,000 kg released in 1978 

(EPA 1982b). Approximately 4,000 kg of 1,1-dichloroethane from POTWs are dispersed on land each 

year as sludge (EPA 1980). 

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1,1-Dichloroethane was detected in soil samples at 170 current or former NPL hazardous waste sites 

where it was detected in some environmental media (HazDat 2007). It was detected in sediment at 

37 current or former NPL hazardous waste sites where it was detected in some environmental media 

(HazDat 2007). 

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 

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 re-

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aeration 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. (1981) 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 

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). 

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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). 

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. 

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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). 

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 

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 

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6. POTENTIAL FOR HUMAN EXPOSURE 

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). 

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). 

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6.4.2 Water 

EPA (1982b) summarized data from EPA's STORET database, where reported concentrations of 

1,1-dichloroethane range from undetected (<10 ppb) to 1,900 ppb, with the highest reading in the Upper 

Mississippi River basin at Alton, Illinois. However, they observed that monitoring results reported for 

1,1-dichloroethane in surface waters are almost always below the detection limit (generally 10 ppb). The 

compound has also 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 

surveyed (Krill and Sonzogni 1986). Concentrations of 1–3 ppb were reported in four public well water 

supplies in Iowa (EPA 1985b). 

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). Also using the 

STORET database, EPA (1982b) reported that 1,1-dichloroethane was not found in the sediment of the 

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lower Mississippi or the western Gulf of Mexico; however, a maximum concentration of 5 ppb was 

detected in sediment samples from the Pacific Northwest. 

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). 

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 

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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). 

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 

2003). 

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). 

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. 

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, 

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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. Occupational exposure to 1,1-dichloroethane may occur via inhalation or 

dermal contact at workplaces where it is produced or used (HSDB 2012). 

The National Occupational Hazard Survey (NOHS), conducted by NIOSH from 1972 to 1974, estimated 

that 715 workers in 143 plants were potentially exposed to 1,1-dichloroethane in the workplace in 1970 

(NIOSH 1976). These estimates were derived from observations of the actual use of 1,1-dichloroethane 

(90% of total estimate) and the use of trade name products known to contain 1,1-dichloroethane (10%). 

The exposed workers were in the rubber and plastic, chemical and allied products, electrical equipment 

and supply, medical and other health services, miscellaneous business services, and oil and gas extraction 

industries. The occupational groups with exposed workers were assemblers, agricultural and biological 

technicians, chemists, electrical and electronic engineering technicians, therapists, geologists, and 

machine operators. 

Preliminary data from a second workplace survey, the National Occupational Exposure Survey (NOES), 

conducted by NIOSH from 1980 to 1983, indicated that 1,957 workers, including 272 women, were 

potentially exposed to 1,1-dichloroethane in the workplace in 1980 (NIOSH 1984). 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 (100%). 

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Neither the NOHS nor the NOES databases contain information on the frequency, level, or duration of 

exposure of workers to any of the chemicals listed therein. They provide only estimates of workers 

potentially exposed to the chemicals. 

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 (1982) 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 2009). 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 nonHispanic whites (n=695). The portion of the data below the LOD for 1,1-dichloroethane was too high to 

provide valid results (CDC 2009). 

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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. 

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 

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1,1-DICHLOROETHANE 84 

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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 2010, became available in February of 2012. 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 

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. 

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1,1-DICHLOROETHANE 85 

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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 

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 

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1,1-DICHLOROETHANE 86 

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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 2009). 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. 

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 

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1,1-DICHLOROETHANE 87 

6. POTENTIAL FOR HUMAN EXPOSURE 

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. 

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1,1-DICHLOROETHANE 88 

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1,1-DICHLOROETHANE 89 

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. 

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1,1-DICHLOROETHANE 90 

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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 

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1,1-DICHLOROETHANE 91 

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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 5 μg/L 59–155% EPA 1994a Method 

aqueous method 624) or direct (groundwater; 8240B 

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 W illiams 

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 

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Table 7-2. Analytical Methods for Determining 1,1-Dichloroethane in 

Environmental Samples 

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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 

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 93 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining 1,1-Dichloroethane in 

Environmental Samples 

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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 94 

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 

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1,1-DICHLOROETHANE 95 

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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. 

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 1994, 

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 

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 

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1,1-DICHLOROETHANE 96 

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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). 

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 

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1,1-DICHLOROETHANE 97 

7. ANALYTICAL METHODS 

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 

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. 

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1,1-DICHLOROETHANE 98 

7. ANALYTICAL METHODS 

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-dichloroethane 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 

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1,1-DICHLOROETHANE 99 

7. ANALYTICAL METHODS 

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. 

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1,1-DICHLOROETHANE 100 

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1,1-DICHLOROETHANE 101 

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 2012) 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 

2011g). The RQ represents the amount of a designated hazardous substance which, when released to any 

environmental media, must be reported to the appropriate authority. 1,1-Dichloroethane also appears on 

the EPA’s list as a priority candidate for the drinking water contaminant list (EPA 1998a). 

The international and national regulations, advisories, and guidelines regarding 1,1-dichloroethane in air, 

water, and other media are summarized in Table 8-1. 

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1,1-DICHLOROETHANE 102 

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 2012 

WHO Air quality guidelines 

Drinking water quality guidelines 

No data 

No dataa 

WHO 2010 

WHO 2008 

NATIONAL 

Regulations and 

Guidelines: 

a. Air 

ACGIH TLV (8-hour TWA) 100 ppm ACGIH 2011 

AIHA ERPGs No data AIHA 2011 

DOE PAC-1 and PAC-2b 

PAC-3b 

160 ppm 

4,000 ppm 

DOE 2012 

EPA AEGLs No data EPA 2011a 

Second AEGL chemical priority list Yes EPA 2012a 

Hazardous air pollutant Yes EPA 2012b 

42 USC 7412 

NIOSH 

NAAQS 

REL (10-hour TWA) 

No data 

100 ppmc 

EPA 2010b 

NIOSH 2011 

IDLH 3,000 ppm 

OSHA PEL (8-hour TWA) for general industry 100 ppm OSHA 2012 

29 CFR 1910.1000, 

Table Z-1 

b. W ater 

EPA Designated as hazardous substances in 

accordance with Section 311(b)(2)(A) of 

the Clean Water Act 

No data EPA 2011b 

40 CFR 116.4 

Drinking water contaminant candidate 

list 

Yes EPA 1998a 

63 FR 10274 

Drinking water standards and health 

advisories 

No data EPA 2011c 

Master Testing List Yesd EPA 2012c 

National primary drinking water 

standards 

No data EPA 2009a 

National recommended water quality 

criteria: human health for the 

consumption of 

No data EPA 2009b 

Reportable quantities of hazardous 

substances designated pursuant to 

Section 311 of the Clean Water Act 

No data EPA 2011f 

40 CFR 117.3 

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1,1-DICHLOROETHANE 103 

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 2012 

d. Other 

ACGIH Carcinogenicity classification A4f ACGIH 2011 

EPA Carcinogenicity classification Cg IRIS 2012 

RfC No data 

RfD No data 

Identification and listing of hazardous 

waster 

U076 EPA 2011d 

40 CFR 261, 

Appendix VIII 

Inert pesticide ingredients in pesticide 

products 

No data EPA 2011e 

RCRA waste minimization PBT priority 

chemical list 

Yes EPA 1998b 

63 FR 60332 

Standards for owners and operators of 

hazardous waste TSD facilities; 

groundwater monitoring list 

Yes EPA 2011j 

40 CFR 264, 

Appendix IX 

Superfund, emergency planning, and 

community right-to-know 

Designated CERCLA hazardous 

substance and reportable quantity 

1,000 poundsh EPA 2011g 

40 CFR 302.4 

Effective date of toxic chemical 

release reporting 

01/01/1994 EPA 2011h 

40 CFR 372.65 

Extremely hazardous substances 

and its threshold planning quantity 

No data EPA 2011i 

40 CFR 355, 

Appendix A 

TSCA chemical lists and reporting 

periods 

EPA 2011k 

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 2011l 

40 CFR 716.120 

Reporting date 06/01/1997 

NTP Carcinogenicity classification No data NTP 2011 

a

In view of the very limited database on toxicity and carcinogenicity, the Guidelines concluded that no guideline value 

for 1,1-dichloroethane should be proposed. b

PAC-1: mild, transient health effects. PAC-2: irreversible or other serious health effects that could impair the ability 

to take protective action. PAC-3: life-threatening health effects. c

NIOSH recommends that 1,1-dichloroethane be treated in the workplace with caution because of their 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. d

1,-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. 

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1,1-DICHLOROETHANE 104 

8. REGULATIONS, ADVISORIES, AND GUIDELINES 

Table 8-1. Regulations, Advisories, and Guidelines Applicable to 

1,1-Dichloroethane 

Agency Description Information Reference e

The 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 g

C: possible human carcinogen

h

Designated 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. 

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; FR = Federal Register; 

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; 

PBT = Persistent, Bioaccumulative, and Toxic; 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; USC = United States Code; WHO = World Health Organization 

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10. GLOSSARY 

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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10. GLOSSARY 

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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1,1-DICHLOROETHANE 131 

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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1,1-DICHLOROETHANE 132 

10. GLOSSARY 

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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1,1-DICHLOROETHANE 133 

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. 

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1,1-DICHLOROETHANE 134 

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. 

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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 

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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 30333. 

MRLs were not derived for 1,1-dichloroethane, as discussed in Section 2.3. 

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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. 

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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. 

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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"). 

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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. 

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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. 

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1 

2 3 4 

→

SAMPLE 

Table 3-1. Levels of Significant Exposure to [Chemical x] – Inhalation 

→→

Exposure frequency/ 

Species duration 

Key to figurea 

INTERMEDIATE EXPOSURE 

↓6 

↓

5 

Systemic 

System ↓7 

NOAEL (ppm) ↓8 

LOAEL (effect) Less serious (ppm) 

↓

9 

Serious (ppm) 

Re

↓

10 

→→

Nit

CHRONIC EXPOSURE 

WoNTNT

(CEL, multiple organs) (CEL, lung tumors, nasal tumors) (CEL, lung tumors, hemangiosarcomas) 

10 (hyperplasia) 

11 ↓20 10 10 

3b 13 wk Resp 

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 

Rat Rat Rat Mouse 

18 Cancer 38 39 40 

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 ex

by an uncertainty factor of 100 (10 for extrapolation from animal to humans, 10 for human variability). 

12 

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1,1-DICHLOROETHANE B-8 

APPENDIX B 

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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 

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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 

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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 

NATICH 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 

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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 

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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 

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1,1-DICHLOROETHANE C-6 

APPENDIX C 

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1,1-DICHLOROETHANE D-1 

APPENDIX D. INDEX 

absorbed dose.............................................................................................................................................. 47 

adenocarcinomas ................................................................................................................................... 10, 30 

adsorption.............................................................................................................................................. 65, 73 

aerobic......................................................................................................................................................... 75 

alanine aminotransferase............................................................................................................................. 21 

ambient air ............................................................................................ 67, 70, 76, 77, 80, 82, 83, 85, 86, 96 

anaerobic ......................................................................................................................................... 69, 75, 76 

aspartate aminotransferase .......................................................................................................................... 21 

bioaccumulation ...................................................................................................................................... 9, 85 

bioavailability ............................................................................................................................................. 85 

bioconcentration factor ............................................................................................................................... 74 

biodegradation....................................................................................................................... 9, 67, 75, 76, 85 

biomarker ............................................................................................................................ 47, 48, 55, 86, 89 

body weight effects ..................................................................................................................................... 29 

breast milk................................................................................................................................................... 83 

cancer .................................................................................................................................... 4, 23, 46, 53, 69 

carcinogen ....................................................................................................................................... 4, 10, 103 

carcinogenic ................................................................................................ 4, 10, 15, 30, 31, 37, 52, 53, 103 

carcinogenicity .............................................................................................................. 9, 10, 30, 53, 55, 103 

carcinoma .............................................................................................................................................. 10, 30 

cardiac arrhythmia ................................................................................................................ 9, 13, 16, 48, 50 

cardiovascular ....................................................................................................................................... 21, 28 

cardiovascular effects............................................................................................................................ 21, 28 

chromosomal aberrations ............................................................................................................................ 32 

death................................................................................................................................................ 15, 16, 23 

dermal effects.............................................................................................................................................. 29 

developmental effects ................................................................................................... 13, 22, 29, 31, 54, 56 

endocrine......................................................................................................................................... 29, 43, 44 

endocrine effects ......................................................................................................................................... 29 

fetus....................................................................................................................................................... 44, 45 

gastrointestinal effects ................................................................................................................................ 28 

general population............................................................................................................................. 9, 83, 86 

genotoxic......................................................................................................................................... 15, 32, 53 

genotoxicity........................................................................................................................................... 32, 53 

groundwater .................................................................... 2, 9, 54, 67, 72, 74, 75, 76, 78, 79, 80, 85, 91, 103 

growth retardation ....................................................................................................................................... 13 

half-life...................................................................................................................................... 47, 73, 75, 76

hematological effects .................................................................................................................................. 28 

hepatic effects ................................................................................................................................. 10, 21, 28 

hydrolysis ...................................................................................................................................................... 9 

hydroxyl radical .......................................................................................................................................... 75 

immunological ...................................................................................................................................... 15, 22 

immunological effects................................................................................................................................. 22 

Kow ........................................................................................................................................................ 61, 85 

LD50............................................................................................................................................................. 23 

milk ....................................................................................................................................................... 83, 99 

musculoskeletal effects ............................................................................................................................... 28 

neoplastic .............................................................................................................................................. 23, 30 

neurobehavioral........................................................................................................................................... 44 

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1,1-DICHLOROETHANE D-2 

APPENDIX D 

neurochemical ............................................................................................................................................. 54 

neurological effects ................................................................................................................... 13, 22, 29, 31 

neurophysiological ...................................................................................................................................... 54 

ocular effects ......................................................................................................................................... 21, 29 

pharmacodynamic ....................................................................................................................................... 40 

pharmacokinetic ...................................................................................................... 31, 40, 41, 42, 43, 45, 56 

photolysis .............................................................................................................................................. 67, 76 

rate constant ................................................................................................................................................ 75 

renal effects ............................................................................................................................... 10, 13, 21, 29 

reproductive effects................................................................................................................... 22, 29, 31, 54 

respiratory effects........................................................................................................................................ 28 

retention ................................................................................................................................................ 89, 98 

solubility ............................................................................................................................................... 34, 73 

systemic effects ......................................................................................................................... 21, 28, 31, 52 

T3 .......................................................................................................................................................... 17, 24 

toxicokinetic.................................................................................................................................... 15, 55, 56 

tumors ............................................................................................................................................. 10, 30, 31 

vapor pressure ......................................................................................................................................... 9, 98 

volatility .......................................................................................................................................... 67, 73, 96 

volatilization ....................................................................................................................... 67, 73, 74, 75, 85 

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