Toxicological
Profile
for
cis-l,2-DICHLORETHENE
trans-l,2-DICHLOROETHENE
1,2-DICHLORETHENE
U.S. DEPARTMENT OF HEALTH & HUMAN SERVICES
Public Health Service
Agency for Toxic Substances and Disease Registry
TP-90-13
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TOXICOLOGICAL PROFILE FOR
1,2-DICHLOROETHENES
Prepared by:
Syracuse Research Corporation
Under Subcontract to:
Clement Associates, Inc.
Under Contract No. 205-88-0608
Prepared for:
Agency for Toxic Substances and Disease Registry
U.S. Public Health Service
December 1990
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Ii
DISCLAIMER
The use of company or product name(s) is for identification only and
does not imply endorsement by the Agency for Toxic Substances and Disease
Registry.
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iii
FOREWORD
The Superfurid Amendments and Reauthorization Act (SARA) of 1986
(Public Law 99-499) extended and amended the Comprehensive Environmental
Response, Compensation, and Liability Act of 1980 (CERCLA or Superfund).
This public law directed the Agency for Toxic Substances and Disease
Registry (ATSDR) to prepare toxicological profiles for hazardous
substances which are most commonly found at facilities on the CERCLA
National Priorities List and which pose the most significant potential
threat to human health, as determined by ATSDR and the Environmental
Protection Agency (EPA). The lists of the 250 most significant hazardous
substances were published in the Federal Register on April 17, 1987, on
October 20, 1988, on October 26, 1989, and on October 17, 1990.
Section 104(i)(3) of CERCLA, as amended, directs the Administrator of
ATSDR to prepare a toxicological profile for each substance on the list.
Each profile must include the following content:
(A) An examination, summary, and interpretation of available
toxicological information and epidemiological evaluations on the
hazardous substance in order 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 which present a
significant risk to human health of acute, subacute, and chronic
health effects, and
(C) Where appropriate, an identification of toxicological testing
needed to identify the types or levels of exposure that may present
significant risk of adverse health effects in humans.
This toxicological profile is prepared in accordance with guidelines
developed by ATSDR and EPA. The original guidelines were published in the
Federal Register on April 17, 1987. Each profile will be revised and
republished as necessary, but no less often than every three years, as
required by CERCLA, as amended.
The ATSDR toxicological profile is intended to characterize succinctly
the toxicological and adverse health effects information for the hazardous
substance being described. Each profile identifies and reviews the key
literature (that has been peer-reviewed) that describes a hazardous
substance's toxicological properties. Other pertinent literature is also
presented but 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.
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iv
Foreword
Each toxicological profile begins with a public health statement,
which describes in nontechnical language a substance's relevant
toxicological properties. Following the public health statement is
information concerning significant health effects associated with exposure
to the substance. The adequacy of information to determine a substance's
health effects is described. Data needs that are of significance to
protection of public health will be identified by ATSDR, the National
Toxicology Program (NTP) of the Public Health Service, and EPA. The focus
of the profiles is on health and toxicological information; therefore, we
have included this information in the beginning of the document.
The principal audiences for the toxicological profiles are health
professionals at the federal, state, and local levels, interested private
sector organizations and groups, and members of the public.
This profile reflects our assessment of all relevant toxicological
testing and information that has been peer reviewed. It has been reviewed
by scientists from ATSDR, the Centers for Disease Control, the NTP, and
other federal agencies. It has also been reviewed by a panel of
nongovernment peer reviewers and Is being made available for public
review. Final responsibility for the contents and views expressed in this
toxicological profile resides with ATSDR.
Wi 1.
Administrator
Agency for Toxic Substances and
Disease Registry
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V
CONTENTS
FOREWORD iii
LIST OF FIGURES ix
LIST OF TABLES xi
1. PUBLIC HEALTH STATEMENT 1
1.1 WHAT IS 1, 2-DICHLOROETHENE? 1
1.2 HOW MIGHT I BE EXPOSED TO 1,2-DICHLOROETHENE? 2
1.3 HOW CAN 1,2-DICHLOROETHENE ENTER AND LEAVE MY BODY? 3
1.4 HOW CAN 1,2-DICHLOROETHENE AFFECT MY HEALTH? 3
1.5 WHAT LEVELS OF EXPOSURE HAVE RESULTED IN HARMFUL HEALTH
EFFECTS? 3
1.6 IS THERE A MEDICAL TEST TO DETERMINE IF I HAVE BEEN
EXPOSED TO 1, 2-DICHLOROETHENE? 8
1.7 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE
TO PROTECT HUMAN HEALTH? 8
1.8 WHERE CAN I GET MORE INFORMATION? 8
2. HEALTH EFFECTS 9
2.1 INTRODUCTION 9
2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 9
2.2.1 Inhalation Exposure 10
2.2.1.1 Death 10
2.2.1.2 Systemic Effects 10
2.2.1.3 Immunological Effects 14
2.2.1.4 Neurological Effects 14
2.2.1.5 Developmental Effects 15
2.2.1.6 Reproductive Effects 15
2.2.1.7 Genotoxic Effects 15
2.2.1.8 Cancer 15
2.2.2 Oral Exposure 15
2.2.2.1 Death. 15
2.2.2.2 Systemic Effects 16
2.2.2.3 Immunological Effects 22
2.2.2.4 Neurological Effects 23
2.2.2.5 Developmental Effects 23
2.2.2.6 Reproductive Effects 23
2.2.2.7 Genotoxic Effects 23
2.2.2.8 Cancer 23
2.2.3 Dermal Exposure 23
2.2.3.1 Death 23
2.2.3.2 Systemic Effects 23
2.2.3.3 Immunological Effects 23
2.2.3.4 Neurological Effects 23
2.2.3.5 Developmental Effects 23
2.2.3.6 Reproductive Effects 24
2.2.3.7 Genotoxic Effects 24
2.2.3.8 Cancer 24
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1
2.3 TOXICOKINETICS 2«
2 . 3. 1 Ahs<>rj)t ion 24
2.3.1.1 I nti.i 1 .j t i oil I-'.vjmishi i- 24
2 . j. ] . 2 o i . 11 E 11 o •; i w i ¦ 24
. 3 . 1 . 3 !)<• i in.11 Kxpnssii <• . 24
2.3.? Distribution 24
2 . 3 . 2 . 1 1 nli.i 1 .i t i oii Exj>¦ j•.u11- 24
2.3.2.? Or a 1 Exposure 24
2.3.2.3 Dermal Exposure 24
2.3.3 MeUibol ism 24
2.1.'* F.xorct ion 27
2 . 3 . 4 . 1 11ili.i J a t i on Exposure _ 2"J
2.3.4.2 Oral Exposure 27
2 . 3 . 4 . 3 !)«• nna 1 Kxposm «• . 27
2.4 RELEVANCE TO PUBLIC HEALTH 27
2.5 BIOMARKERS OF KXl'oSCI-'K AN!) EFFECT 33
2 .5.1 Bioitiarkers I'sed to idenliiv or Ou.mtiiv
Kxpo.su re to 1 , 2 -1) 5 i'M or oei hctu- 33
2.5.2 BiomaiVu-rs Used to Charart f r i :*.<• Effects Caused
by 1,2-Dichloroetbene 33
2.6 INTERACTIONS WITH OTHKK CHEMICALS 33
2.7 POPULATIONS THAT ARK UNUSUALLY SUSCEPTIBLE 34
2.8 ADEQUACY OF THE DATABANK 34
2.8.1 Existing Information cm Health Eltects of
1 , 2 -Dich 1 oroct bene 34
2.8.2 Identification of Data Needs 37
2.8.3 On-goinp, Studies 42
3. CHEMICAL AND PHYSICAL INFORMATION 43
3.1 CHEMICAL IDENTITY 43
3.2 PHYSICAL AND CHEMICAL PROPERTIES 43
4. PRODUCTION, IMPORT, USE. AND DISPOSAL
4.1 PRODUCTION 49
4.2 IMPORT 49
4.3 USE 49
4.4 DISPOSAL
5. POTENTIAL FOR HUMAN EXPOSURE 53
5.1 OVERVIEW 53
5.2 RELEASES TO THE ENVIRONMENT
5.2.1 Air 53
5.2.2 Water 55
5.2.3 Soil
5.3 ENVIRONMENTAL FATE 56
5.3.1 Transport and Partitioning ^
5.3.2 Transformation and Degradation ^
5.3.2.1 Air " ' 57
5.3.2.2 Water 57
5.3.2.3 Soil " ' 5g
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vii
5.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 59
5.4.1 Air 59
5.4.2 Water 59
5.4.3 Soil 69
5.4.4 Other Media 69
5.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE 69
5.6 POPULATIONS WITH POTENTIALLY HIGH EXPOSURE 70
5.7 ADEQUACY OF THE DATABASE 70
5.7.1 Identification of Data Needs 70
5.7.2 On-going Studies 73
6. ANALYTICAL METHODS 75
6.1 BIOLOGICAL MATERIALS 75
6.2 ENVIRONMENTAL SAMPLES 75
6.3 ADEQUACY OF THE DATABASE 79
6.3.1 Identification of Data Needs 79
6.3.2 On-going Studies 80
7. REGULATIONS AND ADVISORIES 81
8. REFERENCES 85
9. GLOSSARY 107
APPENDIX HI
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ix
LIST OF FIGURES
2-1 Levels of Significant Exposure to 1,2-Dichloroethene
Inhalation 12
2-2 Levels of Significant Exposure to 1,2-Dichloroethene - Oral .... 19
2-3 Metabolic Scheme for 1,2-Dichloroethene 25
2-4 Existing Information on Health Effects of
cis-1, 2-Dichloroethene 35
2-5 Existing Information on Health Effects of
trans-1,2-Dichloroethene 36
5-1 Frequency of Sites with 1,2-Dichloroethene Contamination 54
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xi
LIST OF TABLES
1-1 Human Health Effects from Breathing 1,2-Dichloroethenes 4
1-2 Animal Health Effects from Breathing 1,2-Dichloroethenes 5
1-3 Human Health Effects from Eating or Drinking 1,2-
Dichloroethenes 6
1-4 Animal Health Effects from Eating or Drinking 1,2-
Dichloroethenes 7
2-1 Levels of Significant Exposure to 1,2-Dichloroethene -
Inhalation 11
2-2 Levels of Significant Exposure to 1,2-Dichloroethene - Oral .... 17
2-3 Genotoxicity of cis- and trans-1,2-Dichloroethene In Vitro .... 30
2-4 Genotoxicity of cis- and trans -1,2-Dichloroethene In Vivo 31
3-1 Chemical Identity of 1,2-Dichloroethene 44
3-2 Chemical Identity of cis-1,2-Dichloroethene 45
3-3 Chemical Identity of trans -1,2-Dichloroethene 46
3-4 Physical and Chemical Properties of cis- and trans-
1,2-Dichloroethene 47
4-1 U.S. EPA TSCA Production File Data for 1,2-Dichloroethene 50
5-1 Air Monitoring Data for 1,2-Dichloroethene 60
5-2 Water Monitoring Data for 1,2-Dichloroethene 62
6-1 Analytical Methods for Determining 1,2-Dichloroethene in
Biological Samples 76
6-2 Analytical Methods for Determining 1,2-Dichloroethene in
Environmental Samples 77
7-1 Regulations and Guidelines Applicable to 1,2-Dichloroethene .... 82
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1
1. PUBLIC HEALTH STATEMENT
This Statement was prepared to give you information about 1,2-
dichloroethene and to emphasize the human health effects that may result
from exposure to it. The Environmental Protection Agency (EPA) has
identified 1177 sites on its National Priorities List (NPL).
1,2-Dichloroethene has been found in at least 275 of these sites. However,
we do not know how many of the 1177 NPL sites have been evaluated for
1,2-dichloroethene. As EPA evaluates more sites, the number of sites at
which 1,2-dichloroethene is found may change. The information is important
for you because 1,2-dichloroethene may cause harmful health effects and
because these sites are potential or actual sources of human exposure to
1,2-dichloroethene.
When a chemical 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 as a chemical emission. This emission, which is also called a
release, does not always lead to exposure. You can be exposed to a chemical
only when you come into contact with the chemical. You may be exposed to it
in the environment by breathing, eating, or drinking substances containing
the chemical or from skin contact with it.
If you are exposed to a hazardous substance such as 1,2-dichloroethene,
several factors will determine whether harmful health effects will occur and
what the type and severity of those health effects will be. These factors
include the dose (how much), the duration (how long), the route or pathway
by which you are exposed (breathing, eating, drinking, or skin contact), the
other chemicals to which you are exposed, and your individual
characteristics such as age, sex, nutritional status, family traits, life
style, and state of health.
1.1 WHAT IS 1,2-DICHLOROETHENE?
1, 2-Dichloroethene, also called 1,2-dichloroethylene or acetylene
dichloride, is a highly flammable, colorless liquid with a sharp, harsh
odor. You can begin to smell 1,2-dichloroethene in air at a level of 17
parts 1,2-dichloroethene per million parts air (17 ppm). There are two
forms of 1,2-dichloroethene; one form is called cis-1,2-dichloroethene,
while the other is called trans-1,2-dichloroethene. Sometimes both forms
are present as a mixture. It is used most often in the production of
solvents and in chemical mixtures.
Occurrence of 1,2-dichloroethene in the environment is due entirely to
human activity. This chemical has been found in air, water, and soil.
1,2-Dichloroethene is released to the environment from chemical factories
which make or use this chemical, from landfills and hazardous waste sites
containing this chemical, from chemical spills, and from the burning of
vinyl-containing objects.
1,2-Dichloroethene evaporates rapidly. When released to moist soil
surfaces or to lakes, rivers and other bodies of water, most of it will
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2
1. PUBLIC HEALTH STATEMENT
evaporate into air. Once in the air, it usually takes about 4 to 8 days for
half of any given amount of 1,2-dichloroethene to break down. When 1,2-
dichloroethene occurs below soil surfaces in landfills or hazardous waste
sites, it may dissolve in water, seep deeper into the soil, and possibly
contaminate groundwater. Some 1,2-dichloroethene may escape, as a gas. Once
in groundwater, it takes about 13 to 48 weeks for half of a given amount to
break down. There is a chance that small amounts of the 1,2-dichloroethene
found in landfills will eventually break down into vinyl chloride (a more
hazardous chemical). For more information please refer to Chapters 3, 4,
and 5.
1.2 HOW MIGHT I BE EXPOSED TO 1,2-DICHLOROETHENE?
You might be exposed to 1,2-dichloroethene by breathing contaminated
air or by drinking contaminated tap water. If you have contaminated tap
water, you could also be breathing 1,2-dichloroethene vapors while cooking,
bathing, or washing dishes. There are no known products which you can buy
which contain 1,2-dichloroethene. People who live near landfill and
hazardous waste sites that contain this chemical and people who work at
chemical factories where this chemical is made or used, and those who work
at landfills or work as firefighters are likely to be exposed to higher
levels of this chemical than other people. Job-related exposure results
from breathing in 1,2-dichloroethene or from skin contact with the chemical
or materials contaminated with it. According to a National Institute for
Occupational Safety and Health (NIOSH) survey conducted between 1981 and
1983, an estimated 215 people in the United States may have been exposed to
1,2-dichloroethene while working.
1,2-Dichloroethene has been found in the soil at 8 hazardous waste
sites in the United States at average levels of 5 to 4000 parts
1,2-dichloroethene per billion (ppb) parts of soil (0.005 to 4.0 ppm). Air
in urban and suburban areas has been found to contain an average of about 13
to 76 parts trans-1,2-dichloroethene per trillion (ppt) parts of air
(0.000013 to 0.000076 ppm). Little is known about the levels in air in
rural areas.
In a survey of tap water derived from groundwater in the United States,
16 of 466 randomly selected sites contained 1,2-dichloroethene. In this
study it was found that contaminated tap water contained as much as 0.002
ppm. Little is known about the typical level of 1,2-dichloroethene in tap
water originating from lake water or river water. It appears that people in
urban and suburban areas commonly breathe small amounts of
1,2-dichloroethene in contaminated air. People are more likely to breathe
1,2-dichloroethene from contaminated air than to swallow It in drinking
water. Exposure to 1,2-dichloroethene as the result of eating food is
unlikely, unless the food is prepared with contaminated tap water. Heating
will reduce the amount present in food. For further information refer to
Chapter 5.
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1. PUBLIC HEALTH STATEMENT
1.3 HOW CAN 1,2-DICHLOROETHENE ENTER AND LEAVE MY BODY?
1,2-Dichloroethene can enter the body through your lungs when you
breathe air contaminated with it, through your stomach and intestines when
you eat food or drink water contaminated with it, or through your skin upon
contact with the chemical.
No studies have been performed that specifically show how
1,2-dichloroethene leaves the body. Based on available data, some of the
swallowed 1,2-dichloroethene may leave the body unchanged, while some of it
may be broken down to other substances in the body. The rate of elimination
of 1,2-dichloroethene from the body is unknown. Refer to Chapter 2 for more
information.
1.4 HOW CAN 1,2-DICHLOROETHENE AFFECT MY HEALTH?
Breathing high levels of trans-1,2-dichloroethene can make you feel
nauseous, drowsy, and tired. Breathing very high levels of
1,2-dichloroethene vapor can cause death. Animals that breathed high levels
of trans-1,2-dichloroethene for short or long periods of time had damaged
livers and lungs. The effects were more severe with increased exposure
time. Animals that breathed very high levels of trans -1,2-dichloroethene
had damaged hearts. Extremely high doses of cis- or trans -
1,2-dichloroethene given by mouth caused death in animals. Lower oral doses
of cis-1,2-dichloroethene caused decreased numbers of red blood cells.
The long-term human health effects following exposure to low
concentrations of 1,2-dichloroethene are unknown. Neither birth defects nor
cancer have been reported in humans or animals exposed to
1,2-dichloroethene. 1,2-Dichloroethene is not known to affect fertility in
humans or animals. For more information on the health effects of
1,2-dichloroethene in humans and animals, see Chapter 2.
1.5 WHAT LEVELS OF EXPOSURE HAVE RESULTED IN HARMFUL HEALTH EFFECTS?
Tables 1-1 through 1-4 show the relationship between exposure to
1,2-dichloroethenes and known health effects. As shown in Table 1-1 the
exposure levels of 1,2-dichloroethenes in the air that cause adverse health
effects in humans are not known. This chemical has a sharp, slightly
unpleasant odor. You can begin to smell 1,2-dichloroethene when it is in
the air at a level of 17 ppm. Minimal Risk Levels (MRLs) for cis-1,2-
dichloroethene are included in Table 1-3. These MRLs were derived from
animal data for both short-term and long-term exposure, as described in
Chapter 2 and in Table 2-2. The MRLs provide a basis for comparison with
levels that people might encounter in food. If a person is exposed to
cis-1,2-dichloroethene at an amount below the MRL, it is not expected that
harmful (noncancer) health effects will occur. Since these levels are
based on information currently available, there is always some uncertainty
associated with them. Also, since the method for deriving MRLs does not use
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1. PUBLIC HEALTH STATEMENT
TABLE 1-1. Human Heal th Effects from BrcviLhirift 1,2-Dichloroelhenos*
Short-terra Exposure
(less than or equal to 1A clays)
levels in Air Leni^o
Description of Effects
The health el feet.s re.sul 11 ng
from short -term human
exposure t« nir containing
specific luve 1 s of 1,2-
ciehloroethene are not
known.
Long-term Exposure
(greater than 14 days)
T lr Air T h of Exposure Be a c rjiLU ° f K1" f e cts
Levels in — - The health effects resulting
from long-term human
exposure to ,i i r containing
specific levels of 1,2-
dichlorocthene are not
known.
*See Section 1.2 for a discussion of exposures encountered in daily
life.
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1. PUBLIC HEALTH STATEMENT
TABLE 1-2. Animal Health Effects from Breathing 1,2-Dichloroethenes*
Short-term Exposure
(less than or equal to 14 days)
Levels in Air
(ppm)
Length of Exposure
Description of Effects**
200
8 hours
Liver and lung damage
in rats.
1000
8 hours
Decreased numbers of red
and white blood cells
in rats.
3000
8 hours
Heart damage in rats.
22,000
6 hours
Death in mice.
Long-term Exposure
(greater than 14 days)
Levels in Air
(ppm)
Lenpth of Exposure
i
Description of Effects**
200
16 weeks
Severe lung and liver
damage in rats.
*Data are based on studies with trans-1,2-dichloroethene.
**These effects are listed at the lowest level at which they were
first observed. They may also be seen at higher levels.
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1. PUBLIC HEALTH STATEMENT
TABLE 1-3. Hunan Health Effects from Eating or Drin|cing
1,2-Dichloroethenes*
Short-term Exposure
(less than or equal to 14 days)
rnrnl fnnni> Tntir^ of Exposure
necjrriPtiori of Effects
Levels in
35
Minimal Risk Level for cis-1,2-
dlchloroethene (based on
animal studies; see Section
1.5 for discussion).
Levels in
Water
The health effects resulting
from short-term human
exposure to water containing
specific levels of 1,2-
dichloroethene are not
known.
Long-term Exposure
(greater than 14 days)
Food (EEffil Lenp.tfa. of Exposure
Description of Effects
1 IS III
11
Minimal Risk Level for cis-1,2-
dichloroethene (based on
animal studies; see Section
1.5 for discussion).
T pa/p.Is in
Water
The health effects resulting
from long-term human
exposure to water containing
specific levels of 1,2-
dichloroethene are not
known.
*See Section 1.2 for a discussion of exposures encountered in daily
life.
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1. PUBLIC HEALTH STATEMENT
Table 1-4. Animal Health Effects from Eating or Drinking
1,2-Dichloroethenes*
Short-term Exposure
(less than or equal to 14
days)
Levels in Food
(upnO Length of Exposure
Description of Effects
5 ,800
14 days
Blood changes in rats (cis-
1,2-dichloroethene).
25,500
1 day
Death in rats (trans-1,2-
dichloroethene).
16,300
1 day
Death in mice (trans-1,2-
dichloroethene).
Levels in Water
(PPnO
The health effects resulting
from short-term animal
exposure to water
containing specific levels
of 1,2-dichloroethene are
not known.
Long-term Exposure
(greater than 14 days)
Levels in Food
Length of Exposure
Description of Effects
1,900
90 days
Blood changes in rats (cis-
1,2-dichloroethene).
Levels in Water
The health effects resulting
from long-term animal
exposure to water
containing specific levels
of 1,2-dichloroethene are
not known.
¦*These effects are listed at the lowest level at which they were
first observed. They may also be seen at higher levels.
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8
1. PUBLIC HEALTH STATEMENT
any information about cancer, an MRL does not imply anything about the
presence, absence, or levels of risk for cancer. MRLs have not been derived
for trans-1,2-dichloroethene in food or for cis- and trans - 1,2-dichloro-
ethene in water or air. The health effects resulting from skin contact with
1,2-dichloroethene in humans and animals are not presently known. For more
information on the concentrations of 1,2-dichloroethene that result in
harmful effects in humans and animals, see Chapter 2.
1.6 IS THERE A MEDICAL TEST TO DETERMINE IF I HAVE BEEN EXPOSED TO
1,2-DICHLOROETHENE?
Although methods are presently available for measuring the;
concentration of 1,2-dichloroethene in the blood and tissues, the methods
are not routinely used to determine if you have been exposed to
1,2-dichloroethene. The expected effects are not specific to
1,2-dichloroethene and may result from a number of other causes.
1.7 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO PROTECT HUMAN
HEALTH?
The Environmental Protection Agency (EPA) requires notification of the
National Response Center when 1000 pounds or more of 1,2-dichloroethone is
discharged or spilled into the environment. The Occupational Safety and
Health Administration (OSHA) limits 1,2-dichloroethene levels in the air in
the workplace to 200 ppm (790 mg/m3) for an 8-hour workday, 40-hour
workweek. For more information on federal and state recommendations, see
Chapter 7.
1.8 WHERE CAN I GET MORE INFORMATION?
If you have any more questions or concerns not covered here, please
contact your State Health or Environmental Department or:
Agency for Toxic Substances and Disease Registry
Division of Toxicology
1600 Clifton Road, E-29
Atlanta, Georgia 30333
This agency can also give you information on the location of the
nearest occupational and environmental health clinics. Such clinics
specialize in recognizing, evaluating, and treating illnesses that result
from exposure to hazardous substances.
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9
2. HEALTH EFFECTS
2.1 INTRODUCTION
This chapter contains descriptions and evaluations of studies and
interpretation of data on the health effects associated with exposure to
cis- and trans -1,2-dichloroethene. Its purpose is to present levels of
significant exposure for cis- and trans-1,2-dichloroethene based on
toxicological studies, epidemiological investigations, and environmental
exposure data. This information is presented to provide public health
officials, physicians, toxicologists, and other interested individuals and
groups with (1) an overall perspective of the toxicology of cis- and trans-
1,2-dichloroethene and (2) a depiction of significant exposure levels
associated with various adverse health effects.
2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE
To help public health professionals address the needs of persons
living or working near hazardous waste sites, the data in this section are
organized first by route of exposure -- inhalation, oral, and dermal -- and
then by health effect -- death, systemic, immunological, neurological,
developmental, reproductive, genotoxic, and carcinogenic effects. These
data are discussed in terms of three exposure periods -- acute,
intermediate, and chronic.
Levels of significant exposure for each exposure route and duration
(for which data exist) are presented in tables and illustrated in figures.
The points in the figures showing no-observed-adverse-effect levels (KOAELs)
or lowest-observed-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, These distinctions are intended to
help the users of the document identify the levels of exposure at which
adverse health effects start to appear, determine whether or not the
intensity of the effects varies 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 on the tables and graphs
may differ depending on the user's perspective. For example, physicians
concerned with the interpretation of clinical findings in exposed persons or
with the identification of persons with the potential to develop such
disease may be interested in levels of exposure associated with "serious"
effects. Public health officials and project managers concerned with
response actions at Superfund sites may want information on levels of
exposure associated with more subtle effects in humans or animals (LOAEL) or
exposure levels below which no adverse effects (NOAEL) have been observed.
Estimates of levels posing minimal risk to humans (Minimal Risk Levels,
MRLs) are of Interest to health professionals and citizens alike.
Estimates of exposure levels posing minimal risk to humans (MRLs) have
been made, where data were believed reliable, for the most sensitive
noncancer end point for each exposure duration. MRLs include adjustments to
-------
10
2. HEALTH EFFECTS
reflect human variability and, where appropriate, the uncertainty of
extrapolating from laboratory animal data to humans. Although methods hive
been established to derive these levels (Barnes et al - 1987; Ep^ 1986a)
uncertainties are associated with the techniques.
2.2.1 Inhalation Exposure
2.2.1.1 Death
One fatality occurred after inhalation of 1,2-dichloroethene vapor in a
small enclosure (Hamilton 1934) . Neither the level and duration of
exposure associated with the fatality nor the symptoms of toxicity were
reported. The isomeric composition of the vapor was not reported No
further information regarding lethal effects in humans following inhalation
of 1,2-dichloroethene could be located in the literature.
The lethality after a single exposure by inhalation of trans-
1,2-dichloroethene has been determined in mice (Gradiski et al. 1978) The
LC50 of 21,723 ppm trans -1,2-dichloroethene presented in Table 2-1 and in
Figure 2-1 was for a single 6-hour exposure. The cause of death was not
reported.
No other studies were located regarding lethality following inhalation
exposure to cis- or trans-dichloroethene in any animal species.
2.2.1.2 Systemic Effects
No studies were located regarding gastrointestinal, musculoskeletal or
renal effects in humans or animals after inhalation exposure to cis- or
trans-1,2-dichloroethene.
Respiratory Effects. No studies were located regarding respiratory
effects in humans following inhalation exposure to cis- and trans -
1,2-dichloroethene.
Pathologic changes in the lung have been described in rats exposed to
trans -1, 2-dichloroethene (Freundt ai. 1977). Xhe pathology consisted of
pulmonary capillary hyperemia, ar septal distention and pulmonary
edema. As is shown in Table 2"iosurp^gu" 2-1, more severe effects on the
lung occurred after repeated exp to 200 ppm than after a single
exposure. This is the only repo^ study 0f lung pathology in animals
exposed to trans-l,2-dichloroetn ^ ^veral of the control rats were also
observed to develop pulmonary ry hyperemia and alveolar- cental
distention. This study has s. The 3^^!^ I
number of animals and did not ® eval ne upper respiratory tract for
pathology. Also, a statistical f ^Jon of the histological data was not
presented. Corroborative evidei toxicity of trans-1,2-dichloroethene
to the lung has not been report studies were located regarding the
-------
TABLE 2-1. Levels of Si^tificait Exposure to 1,2Dichloroethene - Inhalation
Exposure
Figure Frequency/ LOAEL (Effect)
Key Species Duration Effect NOAEL Less Serious Serious Reference Isomer
(ppm) (ppm) (ppm)
ACUTE EXPOSURE
Death
1 House
Systemic
2 Rat
Rat
Rat
1 d
6 hr/d
2 wk
5 d/wk
8 hr/d
1 d
8 hr/d
1 d
8 hr/d
INTERMEDIATE EXPOSURE
Systemic
8
9
Rat
16 wk
5 d/wk
8 hr/d
Hepatic
Resp
Cardio
Hepatic
Hemato
Hepatic
Resp
Hepatic
21,723 (LC50)
200 (fatty
degeneration)
200a (hyperemia of lung)
200 (fatty
degeneration)
1000 (decreased red and
white blood cell
counts)
200 (decreased drug
metaboli sm)
1000
3000a
1000
(more severe hyperemia)
(enlargement of heart)
(more severe fatty
degenerati on)
200 (pneumonic infiltration)
200a (fatty degeneration)
Gradiski et al.
1978
Freundt et al.
1977
Freundt et al.
1977
Freundt and
Hacholz 1978
Freundt et al.
1977
trans
trans
trans
trans
cis
trans
w
>
r1
H
SC
W
W
n
H
V)
Presented in Table 1-2.
cardio = cardiovascular; d = day; Hemato = hematological; hr = hour; LCjq = lethal concentration, 50% kill; resp = respiratory; wk = week.
-------
ACUTE
(<14 Days)
INTERMEDIATE
(15-364 Days)
(ppm)
100,000 r
# /
/
4* C7
& J-
I^ ^
./ *
~ ~
¦ 1m (t)
10,000
1,000
• «r(t)
• >(t)
t-1
H
ac nj
m
•n
T!
in
n
H
oo
® >(0
100
®2r, 3r (t). It (t,c) •»r{l) •*¦<()
Key
r
Rat
¦ LC50
m
Moum
0 LOAEL tor serious effects (animals)
& LOAEL tor less serious effects (animals)
(e)
da
(»)
trana
The number next to each point corresponds to entries In Table 2-1.
FIGURE 2-1. Levels of Significant Exposure to
1,2 - Dichloroethene - Inhalation
-------
13
2. HEALTH EFFECTS
effects of cis-1,2-dichloroethene on the respiratory tract of any animal
species.
Cardiovascular Effects. No studies were located regarding
cardiovascular effects in humans following inhalation exposure to cis- or
trans-1,2-dichloroethene.
Pathological changes in the heart have been observed in rats exposed to
trans -1,2-dichloroethene (Freundt et al. 1977). The changes were described
as fibrous swelling of the myocardium and hyperemia. As is shown in Table
2-1 and Figure 2-1, the effects were evident after an 8-hour exposure to
3000 ppm but not after an exposure to lower levels. Corroborative evidence
for heart toxicity of trans-1,2-dichloroethene has not been reported. No
studies were located regarding the effects of cis-1,2-dichloroethene on the
cardiovascular system of any animal species.
Hematological Effects. No studies were located regarding
hematological effects in humans following inhalation of cis- or trans-
1,2-dichloroethene.
A variety of effects on composition of the blood and plasma have been
observed in rats exposed to trans -1,2-dichloroethene (Freundt et al. 1977),
A reduction in the number of circulating leukocytes and erythrocytes was
observed after an 8-hour exposure to 1000 ppm trans-1,2-dichloroethene
(Table 2-1, Figure 2-1). After a similar exposure to 200 ppm, a decrease in
leukocyte count was observed. No studies were located regarding
hematological effects in animals after inhalation exposure to
cis-1,2-dichloroethene.
Hepatic Effects. No studies were located regarding hepatic effects in
humans following inhalation of cis- or trans-1,2-dichloroethene.
Pathological changes in the liver consisting of fatty degeneration of
liver lobules and Kupffer cells have been observed in rats exposed to
trans-1,2-dichloroethene (Freundt et al. 1977). Five of six rats exposed to
200 ppm for 8 hours had livers that appeared normal when stained for fat
accumulation, but one rat showed evidence of fat deposition, Although fat
accumulation was not observed in the control rats for the 200 ppm exposure
group, control rats for other exposure groups also showed histopathological
evidence of fat accumulation. However, the incidence and severity of fat
accumulation did increase with increasing exposure levels and duration (see
Table 2-1 and Figure 2-1).
A single 8-hour exposure to cis- or trans-1,2-dichloroethene at 200 ppm
has been shown to increase hexobarbital sleeping time and zoxazolamine
paralysis time in rats (Freundt and Macholz 1978). These effects were more
pronounced at higher 1,2-dichloroethene concentrations; the effect of the
cis isomer being stronger than the trans isomer. These effects suggest
inhibition of the mixed function oxidase system.
-------
14
2. HEALTH EFFECTS
Dermal/Ocular Effects. No studies were located regarding dermal
effects in humans following inhalation of cis- or trans -1,2-dichloroethene.
However trans-1,2-dichloroethene is probably an ocular irritant in humans
(Lehmann and Schmidt-Kehl 1936). Two human subjects experienced mild
burning of the eyes following exposure to 3.3-6.8 mg/L (832-1715 ppm) , but
it is not certain whether the subjects were exposed to a gas or to an
aerosol of this chemical. The accuracy of the reported exposure levels is
questionable because of the insensitivity of the methods used Co measure the
concentration of 1,2-dichloroethene in the air. Also, the degree of purity
of the trans isomer used is uncertain.
2.2.1.3 Immunological Effects
Detailed studies were not located regarding the immunological effects
in humans or animals after inhalation exposure to cis- or trans-1,2-
dichloroethene. However, Freundt et al. (1977) reported that inhalation
exposure of rats to trans-1,2-dichloroethene at a concentration of 200 ppm
or greater caused a slight to severe fatty degeneration of liver Kupffer
cells. Kupffer cells are highly phagocytic macrophages involved in
protecting the systemic circulation from gastrointestinal bacteria. In
addition, the decrease in white blood cells observed in rats after an 8-hour
exposure'to 200 and 1000 ppm trans-1,2-dichloroethene and pneumonic
xltration observed after 8 hours and 16 weeks exposure suggest that
inhalation of trans -1,2-dichloroethene may have adverse immunological
effects.
2.2.1.4 Neurological Effects
Inhalation of high concentrations of vaporized 1,2-dichloroethene
depress the central nervous system in humans. Neurological effects of low
levels of trans-1,2-dichloroethene have been reported (Lehmann and Schmidt-
Kehl 1936) Inhalation of 6.8-8.8 mg/L (1715-2220 ppm) trans -1,2-dichloro-
ethene for 5 minutes, or of 4.8 mg/L (1210 ppm) for 10 minutes, reportedly
caused nausea drowsiness, fatigue, vertigo and intracranial pressure in two
human subjects, but as mentioned earlier, it is uncertain whether the human
subiects were exposed to a gas or an aerosol. However, based on volatility,
a gas is likely. Also, the degree of purity of the trans isomer and the
actual concentrations are unclear.
The effects of inhaled cis-1,2-dichloroethene or trans-1,2-dichloro-
ethene on the nervous system have not been extensively examined in animals.
Rphflvioral changes have been observed in mice exposed acutely (4 hours) to a
mixture of the cis and trans isomers (De Ceaurriz et al. 1983). The
reported changes consisted of a dose-related decrease in the duration of
immobility in tfce "behavioral despair" swimming test._ A 50% decrease in the
total duration of immobility occurred at a concentration of 1983 ppm. The
cis and trans isomers were not examined separately; consequently,
conclusions about the relative potencies of the two isomers cannot be made.
-------
15
2. HEALTH EFFECTS
The neurological significance of these changes in the duration of immobility
during swimming is not known.
No studies were located regarding the following effects in humans or
animals after inhalation exposure to cis- or trans-1,2-dichloroethene:
2.2.1.5 Developmental Effects
2.2.1.6 Reproductive Effects
2.2.1.7 Genotoxic Effects
2.2.1.8 Cancer
2.2.2 Oral Exposure
2.2.2.1 Death
No studies were located regarding lethality in humans from ingestion of
cis- or trans-1,2-dichloroethene.
The lethal effects of orally - administered trans-1,2-dichloroethene in
rats and mice have been investigated. Acute dose levels exceeding 1000
mg/kg are lethal in both species. The differences in the single exposure
LD50 values among and between rats and mice could be attributable to a
number of different factors, including species, strain, age of animals,
physiological status (e.g., fasting), experimental conditions, and vehicle
used to dissolve the chemical. Symptoms associated with lethal oral doses
included decreased activity, ataxia, suppressed or total loss of righting
reflex, and depressed respiration (Barnes et al. 1985; Hayes et al. 1987).
Necropsy revealed severe pulmonary capillary hyperemia and alveolar septal
distension, along with fibrous swelling and hyperemia of cardiac muscle in
several of the dead rats, and hyperemia of the mucosal surface of the
stomach and small intestine in mice (Barnes et al. 1985). In a 14-day
study, increased mortality was observed in rats exposed to 1939 mg/kg/day
cis-1,2-dichloroethene; 5 out of 20 rats died within the first week of
dosing (McCauley et al, n.d). Although the cause of death was not reported,
the rats displayed central nervous system depression and secretions around
the nose and mouth. In a 90-day study of cis-1,2-dichloroethene, 3 of 20
rats treated with 291 mg/kg/day and 4 of 20 rats treated with 872 mg/kg/day
died within the first week of dosing. The incidences of these deaths were
not statistically significant when compared with controls (1/20), no other
rats died during the 90-day treatment, and the authors could not relate the
death to the chemical exposure. The LD50 values, the highest NOAEL values,
and all reliable LOAEL values for death in each species in the acute
duration category are recorded in Table 2-2 and plotted in Figure 2-2.
-------
16
2 . HEALTH EFFECTS
2.2.2.2 Systemic Effects
No studies were located regarding cardiovascular, musculoskeletal, or
dermal/ocular effects in humans or animals after oral exposure to cis- or
trans-1,2-dichloroethene.
Respiratory Effects. No studies were located regarding respiratory
effects in humans following oral exposure to cis- or trans-
1,2-dichloroethene.
The effects of orally administered 1,2-dLchloroethtme on the
respiratory tract of animals has not been examined exte>i1K i Ve 1 y. As is
shown in Table 2-2 and Figure 2-2, mice have been shown to tolerate
exposure to 452 mg/kg body weight trans -1)2-dichloioethene administered in
drinking water for up to 90 days without developing hi^topathological
changes in the lung (Barnes et al. 1985). The only change reported in this
study was a slight (11%) decrease in lUng weight in female mice. No change
in lung weight occurred in male or female rats exposed to about 3000
mg/kg/day trans -1, 2-dichloroethene for 90 days (Hayes et al. 1987).
Pulmonary capillary hyperemia and alveolar septal distention have been
observed in rats given lethal doses of trans -1,2-dichloroethene (Freundt
et al. 1977). It is not clear whether this pathology represents a primary
effect of the chemical on the lung or is secondary to disruption of
cardiovascular function prior to death. js notable that", similar changes
have been observed in rats exposed t0 trans -1,2-dichloroe thene in air (see
Section 2.2.1.2).
Rats that died within 1 days during gavage treatment with cis-1,2-
dichloroethene at 1939 mg/kg/day ^ nasal discharges
and mouth secretions
that may indicate respiratory tent? (McCauley et al. n.d.). In the
90-day study, some of the ra^s 7 days during gavage dosing
with cis-1,2-dichloroethene a e^Ue °naty conges tion. Whether the pulmonary
congestion was a direct consequenc of exposure to the cis j_SOmer is not
known.
Gastrointestinal Effects ftuc^ies were located regarding
¦i i n humans toll-., ¦ , .
gastrointestinal effects J-1 ^ owing oral exposure to cis- or trans-
1 2-dichloroethene. Necropsy e tVia^ received lethal doses of trans-
, _H. nypereniiq o-p , ,
1,2-dichloroethene reveal® J t the stomach and small intestines
(Barnes et al. 1985).
No studjeq
Hematological Effects • ^ e*Po Were located regarding hematological
effects in humans following sute to ci s- or trans-
1,2-dichloroethene.
hematoic
No remarkable chang®s (Barnes al parameters occurred in rats
(Hayes et al. 1987) or mice^ is sl>°wn following oral exposure to
trans-1,2-dichloroethene. doses 0f 3j5n Table 2-2 and Figure 2-2, rats
and mice tolerated repeate 14 mg/kg/day arid 452 mg/kg/day,
-------
TABLE 2-2. Levels of Significant Exposure to 1,2-Dichloroethene - Oral
Figure
Key Species Route
Exposure
Frequency/
Duration
Effect
NOAEL
(mg/kg/d)
Less Serious
(mg/kg/d)
LOAEL (Effect)
Serious
(mg/kg/d)
Reference
Isomer
ACUTE EXPOSURE
Death
Rat
Rat
Rat
4 House
5 House
6 Mouse
Systemic
7 Rat
B
9
10 Mouse
11
12
Immunological
13 Mouse
Neurological
14 Rat
(G)
(G)
(G)
r1
¦x
TI
pj
o
H
GO
1939 (CNS McCauley et al. cis
depression) n.d.
-------
TABLE 2-2. (Continued)
Exposure
Figure Frequency/
Key Species Route Duration
Effect
NOAEL
(mg/kg/d)
Less Serious
(mg/kg/d)
LOAEL (Effect)
Seri ous
(mg/kg/d)
Reference Isomer
INTERMEDIATE EXPOSURE
Systemic
15 Rat (G)
\1
18
19
20
21
22
23
24
Rat
House
Immunological
25 Mouse
(W)
(W)
(U)
90 d
1x/d
90 d
90 d
90 d
Hemato
Hepatic
Renal
Other
Hemato
Renal
Other
Resp
Hemato
Hepat ic
Inmuno
32
872
872
291
3114
3114
3114
452
452
452
452
97
(decreased
hematocrit in
males)
872 (decreased body
ueight gain
in male mice
McCauley et al. cis
n.d.
Hayes et al.
1987
Barnes et. al.
1985
Shopp et al.
1985
trans
trans
5C
>
s
x
m
M
O
H
in
^Converted to an equivalent concentration of 25,500 ppm in food for presentation in Table 1-4.
Converted to an equivalent concentration of 16,300 ppm in food for presentation in Table 1-4.
Sjsed to derive an acute oral Minimal Risk Level (MRL) of 1 mg/kg/day; dose adjusted for intermittent exposure and divided by an
uncertainty factor of 100 (10 for extrapolation from animals to hunans, and 10 for human variability). This MRL has been converted to
an equivalent concentration in food (35 ppm) for presentation in Table 1-3.
Converted to an equivalent concentration of 5800 ppm in food for presentation in Table 1-4.
^sed to derive an intermediate-duration oral Minimal Risk Level (MRL) of 0.3 mg/kg/day; dose adjusted for intermittent exposure and
divided by an uncertainty factor of 100 (10 for extrapolation from animals to hunans, and 10 for human variability). This MRL has been
converted to an equivalent concentration in food (11 ppm) for presentation in Table 1-3.
Converted to an equivalent concentration of 1900 ppm in food for presentation in Table 1-4.
d = day; (G) = gavage; hemato = hematological; iirmuno = immunological; LD^g = lethal dose, 50% kill; resp = respiratory; (w) = water.
-------
ACUTE
(<14 Days)
(mg/kg/day)
£
J*
&
//
$ $ $ ^ ^ A
10,000 r
Hr(t)
1,000
100
4m (t) *¦ W
¦ B •*(«)
-•Bm(B) tig $
O Br(e) 09r(c)
10
®7r(e)
Ol0m(t)
97r(e)
• l4r(e)
Ol4r(c)
12m (t) 13m (t)
Ol1m(t) O O
INTERMEDIATE
(15 - 364 Days)
^ /
P
/
/
20r(t) 21 r (t)
019r(t) O O
16r(c) 17r (e) 1#r(c)
o o a
22m (t) 23m (t)
o o
O 24m (t)
»1Sr(e)
Q1Sr(c)
025m(t)
01«r(e)
33
M
>
r
H
a:
w
•n
m
o
H
on
0.1
Kev
f ¦ LC50
m Moum 0 LOAEL tor serious effects (animals)
9 LOAEL for less serious effects (animals)
O NOAEL (animals) ^
(e) da
(1) trans
(B) mix of both The number next to each point corresponds to enfries In Table 2-2.
Minimal risk level for
effects other than cancer
FIGURE 2-2. Levels of Significant Exposure to
1,2 - Dichloroethene - Oral
-------
20
2. HEALTH EFFECTS
respectively, trans -1,2-dichloroethene in drinking water (emulsified with
emulphor, a polyethoxylated vegetable oil) for 90 days without exhibiting
hematological abnormalities. In contrast, dose-related hematotoxicity was
the most evident effect in rats exposed orally by gavago to cis-1,2-
dichloroethene in corn oil (McCauley et al. n.d.). Decreased red blood
cell count and hematocrit levels were observed in female rats exposed to 291
mg/kg/day for 14 days. No such changes were detected after exposure to 97
mg/kg/day. Based on this value, an acute oral MRL of 1 mg/kg/day was
calculated as described in the footnote in Table 2-2. Similarly, decreased
hematocrit levels were found in male rats exposed to 97 mg/kg/day cis-1,2-
dichloroethene for 90 days and decreased hemoglobin levels were reported in
both sexes at 291 mg/kg/day. The NOAEL level was 32 mg/kg/day. This value
was used for derivation of intermediate-duration oral MRL of 0.3 mg/kg/day
as described in the footnote in Table 2-2.
Hepatic Effects. No studies were located regarding hepatic effects in
humans following oral exposure to cis- or trans -1,2-dichloroethene.
Liver pathology has been demonstrated in rats exposed orally to lethal
or near lethal doses (e.g., 70% lethal dose) of trans -1,2-dichloroethene
(Freundt et al. 1977). The pathology is similar to that observed in rats
exposed by the inhalation route (i.e., fatty degeneration of the Kupffer
cells and liver lobules) (Freundt et al. 1977). However, for oral
exposure, the effects occurred only after exposure to lethal dose levels.
As is shown in Table 2-2 and Figure 2-2, repeated exposure to lower levels
of trans-1,2-dichloroethene in drinking water for 90 days was tolerated by
mice and did not result in liver pathology (Barnes et al. 1985).
Biochemical changes in the liver have been reported in mice and rats
exposed to cis- and trans -1,2-dichloroethene (Jenkins et al. 1972; Barnes
et al. 1985). However, a connection between these changes and pathology or
impaired liver function has not been established. As such, the effects can
not be classified as adverse or as being indicative of liver toxicity.
Changes in hepatic alkaline phosphatase, tyrosine transaminase, glucose-6-
phosphatase and plasma alanine transaminase activities have been observed in
rats exposed to single oral doses of 400 or 1500 mg/kg of cis- or trans-
1,2-dichloroethene (Jenkins et al. 1972). Although the changes observed in
the these enzyme activities were significant, the validity of the study is
limited by the lack of dose-related patterns of the changes, the use of
only three or four rats per group, and the lack of reporting of animal
responses to dosing. A dose-related decrease in the levels of serum
glutamic-oxaloacetic transaminase and serum glutamic-pyruvic transaminase
were observed in female mice exposed to 23-452 mg/kg/day of trans-1,2-
dichloroethene in the drinking water for 90 days (Barnes et al. 1985).
Increased serum levels of these hepatic enzymes are usually indicative of
liver damage; the toxicological significance of decreased levels is unknown.
The effect of 90-day exposure to trans-1,2-dichloroethene (17-452
mg/kg/day in drinking water) on hepatic microsomal drug metabolism was
-------
21
2. HEALTH EFFECTS
assessed by Barries et al. (1985). In contrast to findings with inhalation
exposure studies, oral exposure to trans-1,2-dichloroethene had no effect on
the duration of hexobarbital-induced narcosis. In addition, no significant
changes were found in hepatic microsomal cytochrome P-450 or cytochrome b5
specific content. However, a decrease in microsomal aniline hydroxylase
activity was reported in all exposed groups. A significant decrease in
hepatic glutathione levels occurred in males after 90 days of exposure to
387 mg/kg/day. The mixed function oxidase system and glutathione are
important in the metabolic transformation and management of endogenous
compounds and xenobiotics; therefore, alterations in levels and activities
are of interest in assessing the metabolic fate of compounds.
A dose-related increase in absolute and relative liver weight was
observed in rats exposed for 14 and 90 days to cis-1,2-dichloroethene
(McCauley et al. n.d.). Effects were significant at 97 mg/kg/day and above.
Slight increases in serum cholesterol were observed in the 14-day study, and
slight decreases in serum glutamic-oxaloacetic transaminase were observed in
the 90-day study. The increased liver weight and biochemical changes cannot
be considered adverse because they were not associated with
histopathological liver lesions.
The NOAEL values for hepatic effects in each species and duration
category are recorded in Table 2-2 and plotted in Figure 2-2.
Renal Effects. No studies were located regarding renal effects in
humans following oral exposure to cis- or trans -1,2-dichloroethene.
The effects of 1,2-dichloroethene on the kidney have not been examined
extensively in animals. The few studies that have been reported provide
evidence to suggest that the kidney is probably not a primary target for
toxicity of trans -1,2-dichloroethene. As is shown in Table 2-2 and
Figure 2-2, animals tolerated repeated exposure to trans-1,2-dichloroethene
in drinking water without adverse effects on the kidney. A dose-related
increase in absolute and relative kidney weight occurred in treated female
rats, but no histopathological lesions were identified (Hayes et al. 1987).
No detectable chemical - induced changes in blood urea nitrogen or serum
creatinine levels were found in animals exposed to trans-1,2-dichloroethene
in either the 14-day or 90-day exposure studies (Barnes et al. 1985; Hayes
et al. 1987). These endpoints, however, would detect only a severe
impairment of kidney function.
An increase in absolute and relative kidney weight, along with a
decrease in blood urea nitrogen, was found in female rats exposed for
14 days to 969 mg/kg/day cis-1,2-dichloroethene (McCauley et al. n.d.).
However, these changes did not occur in female rats exposed to 872 mg/kg/day
or less for 90 days. In male rats exposed to 872 mg/kg/day cis-1,2-
dichloroethene for 90 days, a significant increase in the relative kidney
weight and decreases in blood urea nitrogen and creatinine levels occurred.
No changes occurred in males exposed to 1939 mg/kg/day or less for 14 days.
-------
22
2. HEALTH EFFECTS
The toxicological significance of decreased blood urea nitrogen and
creatinine levels is not clear; increases in these parameters are usually
associated with renal toxicity. Furthermore, no histological evidence of
kidney pathology was observed. In the absence of histological ancj clinj_ca}
evidence of renal toxicity, the toxicological significance of the increased
kidney weight is not known.
Other Systemic Effects. Body weight was not altered by 21 and 210
mg/kg/day trans -1,2-dichloroethene administered for 14 days to mice by
gavage (Barnes et al. 1985). Body weight was not altered in rats exposed
to trans-1,2-dichloroethene (353-3114 mg/kg/day) in drinking water for 90
days (Hayes et al. 1987). Significant changes in body weight gain were
observed in both male and female rats treated with cis - 1,2-dichloroethene
for 14 days (McCauley et al. n.d.). The changes were not dose-related,
however, with increased body weight gain occurring at 97 and 291 mg/kg/day
and decreased body weight gain occurring at 969 and 1939 mg/kg/day. The
toxicological significance of these sporadic body weight changes over a
14-day treatment period is not clear. In the 90-day study, only the male
rats receiving the highest dose of cis-1,2-dic.hloroethene (872 mg/kg/day)
had significantly decreased body weight gain when compared with control
males. Appropriate NOAEL and LOAEL values are presented in Table 2-2 and
Figure 2-2.
2.2.2.3 Immunological Effects
No studies were located regarding immunological effects in humans
following oral exposure to cis- or trans-1,2-dichloroethene.
The effect of orally-administered trans-1,2-dichloroethene on the
immune system in mice has been investigated. Mice exposed to trans-1,2-
dichloroethene (up to 221 mg/kg/day by gavage) for 14 days showed no
significant changes in cell-mediated or humoral immunity (Munson et al.
1982; Shopp et al. 1985). Repeated exposure of mice to trans-1,2-
dichloroethene in drinking water for 90 days had no effect on cell-mediated
immune status of either sex or in the humoral immune status of females
(Shopp et al. 1985). A suppression in humoral immune status, as measured by
spleen cell antibody production directed against sheep erythrocytes, was
observed in male mice treated with all three doses (17, 175, and 387
mg/kg/day) of trans-1,2-dichloroethene. Although the suppression was
significant, it was not severe enough to depress the functional ability of
the humoral immune system, as indicated by a normal spleen cell response to
B cell mitogen lipopolysaccharide and normal hemagglutination titers. The
highest NOAEL values for immunological effects in mice in each duration
category are recorded in Table 2-2 and plotted in Figure 2-2.
No studies were located regarding immunological effects of cis-
1,2-dichloroethene in animals.
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23
2. HEALTH EFFECTS
2.2.2.4 Neurological Effects
No studies were located regarding neurological effects in humans
following oral exposure to cis- or trans-1,2-dichloroethene.
The neurological effects of cis- and trans -1,2-dichloroethene in
animals have not been extensively examined. Signs of central nervous system
depression have been observed in rats and mice at the terminal stages after
receiving lethal doses of cis- and trans -1,2-dichloroethene (Barnes et al,
1985; Hayes et al. 1987; McCauley et al. n.d.). These signs include ataxia,
suppressed or total loss of righting reflex, depressed respiration, and
ruffled fur. No signs of neurotoxicity were observed in rats treated with
cis-1,2-dichloroethene at 969 mg/kg/day for 14 days (see Table 2-2 and
Figure 2 - 2).
Dose-related conditioned taste aversion to saccharin was produced in
mice exposed to a mixture of cis- and trans-1,2-dichloroethene (Kallman
et al. 1983). This neurobehavioral test will detect both neurological and
non-neurological effects that are perceived by the test animal to be
adverse. The nature of the adverse stimuli that results in taste aversion
has not been identified.
No studies were located regarding the following effects in humans or
animals upon oral exposure to 1,2-dichloroethene:
2.2.2.5 Developmental Effects
2.2.2.6 Reproductive Effects
2.2.2.7 Genotoxic Effects
2.2.2.8 Cancer
2.2.3 Dermal Exposure
No studies were located regarding the following effects in humans or
animals upon dermal exposure to cis- or trans-1,2-dichloroethene:
2.2.3.1
Death
2.2.3.2
Systemic Effects
2.2.3.3
Immunological Effects
2.2.3.4
Neurological Effects
2.2.3.5
Developmental Effects
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24
2. HEALTH EFFECTS
2.2.3.6 Reproductive Effects
2.2.3.7 Genotoxic Effects
2.2.3.8 Gancer
2.3 TOXICOKINETICS
2.3.1 Absorption
2.3.1.1 Inhalation Exposure
Sato and Nakajiraa (1979) reported a blood/air partition coefficient
(ratio concentrations in blood and air at 37°C) of 9.2 and 5.8 for cis and
trans isomers of 1,2-dichloroethene, respectively. Both isomers of
1,2-dichloroethene in inspired air achieve an equilibrium with the whole
animal within 1.5-2 hours (Filser and Bolt 1979). The partition
coefficients of both isomers in the various body tissues of an animal have
not been determined. Lehmann and Schmidt-Kehl (1936) reported that 72-75%
of inhaled trans -1,2-dichloroethene is absorbed through the lungs in humans
No studies were located regarding the rate and extent of cis- or trans
1,2-dichloroethene absorption following either of the exposures listed
below:
2.3.1.2 Oral Exposure
2.3.1.3 Dermal Exposure
2.3.2 Distribution
No studies were located regarding the distribution of cis- and trans-
1,2-dichloroethene following exposure by any of these routes:
2.3.2.1 Inhalation Exposure
2.3.2.2 Oral Exposure
2.3.2.3 Dermal Exposure
2,3.3 Metabolism
o£ 1 2-dichloroethene is catalyzed by
The first step in met^b° ^^Ronse et al. Costa and Ivanetich
hepatic microsomal cytochrome _ this step twelves epoxidaticm of
1982a, 198^; Leibman ^ichlorinated epoxides (Flgnie 1-3) or possibly
ethylene double bond to - TjlcVi\orinated epoxides t tutu, cav»
enzyme-bound analog tV^teot.
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25
2. HEALTH EFFECTS
CICH = CHCI
1,2 - dichloroethen©
CICH CHCI
CI 2 CH - CHO
dichloroacetaldehyde
O
Epoxide
CI j CH-CHOH CI 2 CH-COOH
dichloroethanol dichloroacetlc acid
Source: Costa and Ivanetich 1982a, 1984
FIGURE 2-3. Metabolic Scheme for 1,2-Dichloroethene
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26
2. HEALTH EFFECTS
undergo a non-enzymic "®^^S^^sora"UfndShepatocytes',proii3e°fvidence to
kggesfthirdichloroacetaldehyde is the predominant metabolite of
microsomal cytochrome P-^450 and that it in turn^ ,sj t0
dichloroethano^^ dichloroacetat^ ^y^ ^ (Costa and
aldehyde an consistent with the report that both the
Ivanetich 1984 1982a) ini hpne were converted to
di^roe^orrd^i^^^rtic acid by perked rat H.r (Bon„ et al
1975) .
,.ff nces have been observed in the metabolism of
• Both isomers have bee,, .hoim to bind to
CIS- and tra , cytochrome P-450 (Cost and Ivanetich, 1982a). In
the active s e ,?hitors Df cytochrome P-450 have been shown to inhibit
addition, c assic oroacetaldehyde from both isomers. The binding and
the ^^"^ne doL not appear to be specific for any one
metabolism , isomer had a 4-fold greater rate of
for. of cytochrome I^frosomes in vitro than the trans isomer. This is
turnover in ®Pa isolated perfused rat livers, where metabolism of
consistent with studies on r * than the „ans Uoi while the cis isomer more frequently tended
demethylasejic^iv ^ destroy the enzyme. Costa and Ivanetich (1982a)
to mniD , . „f cis and trans isomers with hepatic microsomes
reported a nc system resulted in loss of microsomal cytochrome
TlsT Further tests strongly suggested that the reactive species that are
It hv t-hp biotransformation of either isomer via hepatic cytochrome
generated y h moiety at the active site of cytochrome P-450.
P'450 coufd account for the observed in vivo and jn vitro
^h^bition of other cytochrome P-450 substrates, mentioned previously, by
1,2-dichloroethene.
ThA metabolic elimination of 1,2-dichloroethene has been described as a
saturable, dose-dependent process (Filser and Bolt 1979). In rats exposed
-------
27
2. HEALTH EFFECTS
to atmospheric concentrations of 1,2-dichloroethene which exceed a "point of
saturation," elimination proceeds by zero-order kinetics (rate independent
of the concentration of the compound); below saturation, first-order
kinetics apply (Filser and Bolt 1979). Pharmacokinetic studies on
1,2-dichloroethene elimination in the gas phase of a closed inhalation
exposure system show that cis-1,2-dichloroethene has a higher rate of
first-order clearance than the trans isomer. The cis isomer also exhibits
a higher rate of metabolic elimination under saturation conditions, in
comparison to the trans isomer. This observation is consistent with the
higher rate of metabolism of the cis isomer relative to the trans isomer by
rat liver microsomes (Costa and Ivanetich 1982a) and by isolated perfused
liver (Bonse et al. 1985).
2.3.4 Excretion
No studies were located regarding the excretion of 1,2-dichloroethene
following inhalation, oral, and dermal exposure.
2.3.4.1 Inhalation Exposure
2.3.4.2 Oral Exposure
2.3.4.3 Dermal Exposure
2.4 RELEVANCE TO PUBLIC HEALTH
The inhalation, oral, and dermal routes of exposure to
1,2-dichloroethene are of concern to humans because 1,2-dichloroethene has
been found in air, drinking water, and soil (see Chapter 5). Clinical
symptoms that have been reported in humans exposed to 1,2-dichloroethene in
air include nausea, drowsiness, fatigue, intracranial pressure and ocular
irritation. One fatality has been reported. No information is available on
toxicity upon ingestion or dermal contact with 1,2-dichloroethene in humans.
No information is available on the relative toxicities of the cis and trans
isomers of 1,2-dichloroethene in humans. Pathological lesions of the heart,
liver, and lung have been reported in rats exposed to trans-1,2-dichloro-
ethene in air. Ataxia and respiratory depression occur in the terminal
stages prior to death in animals. Since these conditions have not been
observed in humans, their relevance to public health is not known.
Death. Exposure of humans to high levels of 1,2-dichloroethene in air
has resulted in death on at least one occasion (Hamilton 1934) . Details
regarding the exposure levels and duration in this accident and the cause of
death are not available. The concentration of cis- and trans-
1,2-dichloroethene in air that is lethal to humans is not known. No
reports of lethality related to oral exposure of humans to
1,2-dichloroethene were located.
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28
2. HEALTH EFFECTS
¦l. . „ death in the accident described previously is
Although t e ca s tem toxicity may have, been involved. Terminal
unknown, central nervous y or crans. l 2-dichloroethene orally
symptoms in ~ ®**°system depression (e.g., ataxia and loss of righting
involve central nervous V ^ (Barnes et al. 1985; Hayes et al. 1987;
reflex) and respi y lt£. of studles in which animals have inhaled or
McCauley et al. n^ hene impUcate the heart, liver, and lung as
ingested trans-1,2 dichl (Barnes et ai. 1985; Freundt et al. 1977;
. The relative lethal potency of the ds and trans
isomers is not known.
Systemic effects. It appears that crans-1,2-dichl°r„e thene U an
i • ,'tanr in humans Two human participants in ^ .If
ocular ir""n reported mild burning of the eyes after acute exposure
experimentation study rep _ -dichloroethen* (Lehmann and
Totier specific systemic effect, have been reported
in humans.
C effects involving the heart, liver, and lungs have been
a animals exposed to trans -1.2-dichloroethene . However, evidence
observed m effects in these organs consists of only one study
for serious ad Effects reported in the rat include lung lesions
(Freundt et al 1 7 distension), fibrous swelling of the
(hyperemia and *£eol Peration of the liver. All three lesions were
myocardium and y^^g expQsures t£J trans_! >2.dichloroethene at
observed af or raQre for g hours. Liver and lung lesions were
concentratio s dosing, tut only after near lethal doses were
observe a ter g. ^ of clie treatment groups in this study were tco
adainistfite . " deeree of confidence in these findings. Exposure of
small to establish high deg ^ ^ ^ ^ ^ trana.1>2.
dichloroethene in'the drinking water for 90 days did not reSult in adverse
systemic effects.
increased liver and kidney weights were observed in rats treated orally
. ^ lT? r?-dichloroethene for 14 or 90 days, but these increased organ
with cis , nmnanied by any histopathological lesions (McCauley et
weights were not «co»pan«
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29
2. HEALTH EFFECTS
Imnunological Effects. There are no reports of immunological effects
in humans as a result of exposure to cis- or trans-1,2-dichloroethene by any
route. Studies in mice have demonstrated perturbations of the humoral
immune system (suppressed spleen cell antibody production against sheep
erythrocytes) after exposure to trans-1,2-dichloroethene (Shopp et al.
1985). The observed changes in the humoral immune system did not result in
functional impairment of the humoral immune response and therefore are not
considered to be adverse. The data regarding immunological effects of
1,2-dichloroethene in animals are too limited to draw any conclusion about
potential immunological effects in humans.
Neurological Effects. The central nervous system depressant
properties of 1,2-dichloroethene represent an important effect in humans.
Dizziness, drowsiness, vertigo and intracranial pressure are some of the
symptoms which have been reported in humans after inhalation of trans-
1,2-dichloroethene (Lehmann and Schmidt-Kehl 1936). These symptoms
disappeared quickly after exposure was terminated. The pharmacological
basis for the 1,2-dichloroethene-mediated narcosis has not been studied.
Central nervous system depression (e.g., ataxia, loss of righting
reflex) has been observed in some animal studies as well, but only at the
terminal stages after the administration of lethal doses of both cis- and
trans -1,2-dichloroethene (Hayes et al. 1987; McCauley et al. n.d.; Munson
et al. 1982) .
Genotoxic Effects. Genotoxic effects of cis- and trans-1,2-dichloro-
ethene in humans are unknown. Mutagenicity of 1,2-dichloroethene has been
examined in a variety of test systems. In vitro tests of genotoxicity of
the cis and trans isomers are summarized in Table 2-3. Neither isomer was
genotoxic with or without metabolic activation in Escherichia coli K12
(Greim et al. 1975), in several strains of Salmonella tvphimurium in spot
tests (Cerna and Kypenova 1977; Mortelmans et al. 1986), or in gene
mutation and gene conversion tests in Saccharomvces cerevisiae D7 (Bronzetti
et al. 1984; Galli et al. 1982). Neither isomer produced chromosomal
aberrations or sister chromatid exchanges in Chinese hamster cells (Sawada
et al. 1987). The cis isomer, but not the trans isomer, induced
unscheduled DNA synthesis in rat hepatocytes (Costa and Ivanetich 1984).
In vivo tests (Table 2-4) indicate that cis-1,2-dichloroethene, but
not trans-1,2-dichloroethene, is genotoxic. The cis isomer was found to be
mutagenic in the host-mediated assay using a series of Salmonella tester
strains in mice (Cerna and Kypenova 1977). Bronzetti et al. (1984) also
found that the cis isomer was mutagenic in S. cerevisiae D7 in a host-
mediated assay in mice, with significant increases in convertants at the trp
locus and revertants at the ilv locus. In addition, repeated
intraperitoneal injection of cis-1,2-dichloroethene produced chromosomal
aberrations in mouse bone marrow cells (Cerna and Kypenova 1977). Negative
results were obtained with trans-1,2-dichloroethene in these assays.
-------
TABLE 2-3. Genotoxicity of cis- and trans-1,2-Dichloroethene In Vitro
Result
End Point
Species (test system)
With
Activation
Without
Activation
Reference
cis-1.2-Dichloroethene
Prokaryotic organisms:
Gene mutation
Escherichia coli K12
Salmonella tvphimuriun
NO
Greim et al. 1975
Cerna and Kypenova 1977
Hortelmans et al. 1986
Eukaryotic organisms:
Fungi:
Gene mutation
Gene conversion
Mammalian cells:
Chromosomal aberrations
Saccharoiwces cerevisiae D7
S. cerevisiae D7
Chinese hamster CHL cells
Sister chromatid exchange Chinese hamster CHL cells
Unscheduled DNA synthesis Rat hepatocytes
trans-1.2-Dichloroethene
NA
Prokaryotic organisms:
Gene mutation
Eukaryotic organisms:
Fungi:
Gene mutation
Gene conversion
Marnnalian eel Is:
Chromosomal aberrations
Sister chromatid exchange
Unscheduled DNA synthesis
E. coli K12
S. typhimuriLTi
S. cerevisiae D7
S. cerevisiae D7
Chinese hamster CHL cells
Chinese hamster CHL cells
Rat hepatocytes
ND
NA
Bronzetti et al. 1984
Galli et al. 1982
Bronzetti et al. 1984
Galli et al. 1982
Sawada et al. 1987
Sauada et al. 1987
Costa and Ivanetich 1984
Greim et al. 1975
Cerna and ICypenova 1977
Hortelmans et al. 1986
Bronzetti et al. 1984
Galli et at. 1982
Bronzetti et al. 1984
Gal Ii et al. 1982
Sawada et al. 1987
Sawada et al. 1987
Costa and Ivanetich 1984
m
>
s
EC
m
m
n
H
w
U>
o
NA = not applicable; NO = no data; - = negative results; + = positive results.
-------
TABLE 2-4. Genotoxicity of cis- and trans-1,2-Dicfiloroethene In Vivo
End Point
Species (Test System)
Results
Reference
cis-1.2-Dichloroethene
Manual ian systems:
Chromosomal aberrations
Mouse bone
+
Cerna and Kypenova 1977
Host-mediated assays:
Gene mutation
Gene conversion
Salmonella tvDhimurium
(mouse host-mediated assay)
Saccharomvces cerevisiae D7
(mouse host-mediated assay)
S. cerevisiae 07
(mouse host-mediated assay)
+
+
+
Cerna and Kypenova 1977
Bronzetti et al. 1984
Bronzetti et al. 1984
trans-1.2-0 i chloroethene
EC
m
>
Mammalian systems:
Chromosomal aberrations
Mouse bone marrow
-
Cerna and Kypenova 1977
EC
M
Tl
*J
M
Cl
H
W
Host-mediated assays:
Gene mutation
Gene conversion
S. tvchimurium
(mouse host-mediated assay)
S. cerevisiae D7
(mouse host-mediated assay)
S. cerevisiae 07
(mouse host-mediated assay)
-
Cerna and Kypenova 1977
Bronzetti et al. 1984
Bronzetti et al. 1984
+ = Positive result; - = negative result.
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32
2. HEALTH EFFECTS
Cancer. To date, cancer effects of cis- and trans -1,2-dichloroethene
have not been studied in humans or animals.
2.5 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).
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 or cell that is measured within a compartment of an organism
(NAS/NRC 1989). The preferred biomarkers of exposure are generally the
substance itself or substance-specific metabolites in readily obtainable
body fluid 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 (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 biologic 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 1,2-dichloroethene are discussed
in Section 2.5.1.
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 often not substance
specific. They also may not be directly adverse, but can indicate potential
health impairment (e.g., DNA adducts). Biomarkers of effects caused by 1,2-
dichloroethene are discussed in Section 2.5.2.
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. It can be an intrinsic genetic or other
characteristic or a preexisting disease that results in an increase in
absorbed dose, biologically effective dose, or target tissue response. If
biomarkers of susceptibility ex«t, they are discussed in Section 2.7,
"POPULATIONS THAT ARE UNUSUALL SUSCEPTIBLE."
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33
2. HEALTH EFFECTS
2.5.1 Biomarkers Used to Identify or Quantify Exposure to
1,2-Dichloroethene
No studies were located regarding tissue, fluid, or excreta levels of
1,2-dichloroethene in humans. The post-exposure levels of 1,2-dichloro-
ethene or its metabolites in various body tissues of animals were not
determined. Methods exist for determining 1,2-dichloroethene in blood and
biological tissues (see Chapter 6), but specific levels of
1,2-dichloroethene have not been correlated with exposure. Acetonemia and
acetone exhalation were observed in rats after inhalation exposure to
halogenated ethylenes, including cis- and trans-1,2-dichloroethene (Filser
et al. 1978). Acetone exhalation occurred during exposure of rats to a
concentration of trans-1,2-dichloroethene as low as 50 ppm. This finding
cannot, however, be used as a biomarker of exposure because the amount of
acetone exhaled was not correlated with different exposure concentrations.
Furthermore, acetone exhalation is not specific for 1,2-dichloroethene
since acetone can be found in blood and exhaled air after exposure to other
chemicals such as vinyl chloride, vinyltdene fluoride, and perchlorethylene
(Filser and Bolt 1980), as well as in patients with diabetes, hepatic
insufficiency, and other metabolic disorders.
2.5.2 Biomarkers Used to Characterize Effects Caused by 1,2-Dichloroethene
No known biomarkers are currently used to characterize effects caused
by 1,2-dichloro-ethene in humans. As discussed in Section 2.5.1,
acetonemia and acetone exhalation were observed in rats after inhalation
exposure to halogenated ethylenes, including the two isomers of
1,2-dichloroethene (Filser et al. 1978). Based on results of experiments
with vinylidene fluoride, Filser and Bolt (1980) concluded that metabolites,
rather than the parent compounds, were involved. Based on results of
studies with the monohaloacetate metabolites of vinylidene fluoride and
vinylidene chloride, which are known to inhibit enzymes of the citric acid
cycle, Filser et al. (1982) suggested that the production of acetone by the
halogenated ethylenes might also result from the inhibition of the enzymes
of the citric acid cycle, which would lead to an increase in mitochondrial
acetyl-coenzyme A and, consequently, in an alteration in lipid and fatty
acid metabolism and ketosis. A similar mechanism was suggested for 1,2-
dichloroethene because the primary metabolite, dichloroacetate, can also
increase ketone body levels. If such a mechanism operated, acetone
exhalation could conceivably serve as a biomarker for such effects as fatty
degeneration of the liver, which has been observed in rats exposed to
1,2-dichloroethene (Freundt et al. 1977).
2.6 INTERACTIONS WITH OTHER CHEMICALS
No studies were located regarding the health effects in humans or
animals exposed to 1,2-dichloroethene in combination with other chemicals
that are likely to be found with 1,2-dichloroethene in the environment,
workplace, or at hazardous waste sites.
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34
2. HEALTH EFFECTS
As mentioned previously, both isomers of 1,2-dichloroethene can inhibit
the cytochrome P-450-dependent metabolism of hexobarbital (Freundt and
Macholz 1978). Such inhibition has also been shown to increase hexobarbital
sleeping time. Costa and Ivanetich (1982b) showed that multiple forms of
hepatic microsomal cytochrome P-450, including the forms induced by
/3-naphthoflavone and phenobarbital, can bind and metabolize the
1,2-dichloroethenes. Thus, 1,2-dichloroethene may potentiate the toxic
actions of any chemical which undergoes detoxification by cytochrome P-450-
dependent metabolism by competing for binding to the active site of
cytochrome P-450. Conversely, 1,2-dichloroethene may antagonize the toxic
actions of any chemical that undergoes toxic activation by cytochrome-P-450-
dependent metabolism.
2.7 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE
Human populations that have experienced health effects from exposure to
1,2-dichloroethene have not been identified; thus, populations that are
likely to be unusually susceptible are unknown. However, based on the
limited data available on toxicity in animals, it can be inferred that such
groups might include individuals with disease of the liver, heart, or
respiratory tract. In addition, individuals with kidney disorders, and
infants and the elderly who have much slower rates of clearance and
metabolism, may be considered as potentially susceptible individuals.
2.8 ADEQUACY OF THE DATABASE
Section 104(i)(5) of CERCLA, 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 1,2-dichloroethene 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 1,2-dichloroethene.
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 or
eliminate the uncertainties of human health assessment. In the future, the
identified data needs will be evaluated and prioritiEed, and a substance-
specific research agenda will be proposed.
2.8.1 Existing Information on Health Effects of 1,2-Dichloroethene
The existing data on health effects of inhalation, oral and dermal
exposure of humans and animals to cis- and trans-1,2-dichloroethene are
summarized in Figures 2-4 ai*d 2-5. The purpose of this figure is to
illustrate the existing information concerning the health effects of
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35
2. HEALTH EFFECTS
SYSTEMIC
Inhalation
Oral
Dermal
HUMAN
SYSTEMIC
o®
Inhalation
Oral
Dermal
ANIMAL
Existing Studies
FIGURE 2-4. Existing Information on Health Effects
of cis-l,2-Dichloroethene
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36
2. HEALTH EFFECTS
Inhalation
Oral
Dermal
HUMAN
Inhalation
Oral
Dermal
ANIMAL
# Existing Studtes
FIGURE 2-5. Existing Information on Health Effects
of trans-l,2-Dichloroethene
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37
2. HEALTH EFFECTS
1,2 -dichloroethene. Each dot in the figure indicates that one or more
studies provide information associated with that particular effect. The dot
does not imply anything about the quality of the study or studies. Gaps in
this figure should not be interpreted as "data needs" information.
One report describes neurologic symptoms in humans following acute
inhalation of trans -1,2-dichloroethene. The central nervous system
depressant property of 1,2-dichloroethene is recognized as an important
effect of this chemical. Other than one reported industrial fatality upon
accidental inhalation exposure to 1,2-dichloroethene (isomeric composition
unknown), no other human health effects have been reported.
Information has been reported regarding the lethality and toxic
effects of trans -1,2 -dichloroethene in animals exposed by the inhalation and
oral routes for acute and intermediate durations. Toxicity to the heart,
liver, and lung has been reported. Central nervous system depression has
been reported in animals given lethal doses of trans-1,2-dichloroethene by
the oral route. One study has examined the effects of trans -
1,2-dichloroethene on the immune system of mice, A 14-day and a 90-day
gavage study of cis-1,2-dichloroethene found hematological effects in rats.
No information is available on the toxic effects of chronic exposure to
either cis- or trans-1,2-dichloroethene by any route. As is shown in
Figures 2-b and 2-5, no information is available on developmental,
reproductive, or carcinogenic effects of either cis- or trans-
1,2-dichloroethene in animals. No studies were located regarding genotoxic
effects in humans or animals after inhalation, oral, or dermal exposure to
1,2-dichloroethene, but studies in mice injected intraperitoneally indicate
that the cis isomer is genotoxic; the trans isomer is not genotoxic.
2.8.2 Identification of Data Needs
Acute-Duration Exposure. Reliable data regarding health effects in
humans after exposure to 1,2-dichloroethene were not located. One human
fatality was reported, but the cause of death, the length of exposure, and
the concentration of 1,2-dichloroethene in the air were not described. Two
human volunteers reported mild burning of the eyes after acute inhalation
exposure to trans-1,2-dichloroethene. No information was located regarding
systemic toxicity in humans after oral or dermal exposure or on the relative
toxicities of the cis and trans isomers of 1,2-dichloroethene in humans.
The acute lethal levels of trans-1,2-dichloroethene were established after
inhalation exposure in mice and after oral exposure in mice and rats.
Inhalation LC50 and oral LD50 values cis-1,2-dichloroethene are not known.
This information is important to compare the relative toxicities of the two
isomers. Pathological lesions in the heart, liver, and lungs were reported
in rats after acute inhalation exposure to trans -1,2-dichloroethene;
however, the study was limited in size and scope. The finding of acetone in
the exhaled air of 1,2-dichloroethene-exposed rats indicates possible
alterations in lipid and fatty acid metabolism. This may support the
observation of fatty infiltration of liver in the rat inhalation study.
-------
38
2. HEALTH EFFECTS
Because the levels of exposure that cause effects were not sufficiently
identified in the available literature, the MRL for acute inhalation
exposure to trans - 1,2-dichloroethene was not derived. No data were located
for inhalation exposure to cis-1,2-dichloroethene. No target organs were
identified in animals after acute oral exposure to trans-1,2-dichloroethene
Hematotoxicity after an acute oral exposure to cis-1,2-dichloroethene was
reported in rats. The NOAEL value for this effect was used for the
derivation of an acute oral MRL for cis-1,2-dichloroethene. The results of
oral animal studies suggest differences in toxicity of trans and cis
isomer, since no hematological effects were found in rats exposed to similar
doses of trans-1,2-dichloroethene for 14 days. In addition, in vivo and in
vitro studies suggest differences in the metabolism of the two isomers
data were located for cis- or trans -1,2-dichloroethene for the dermal route
of exposure. Pharmacokinetic data, however, are not sufficient to identify
target organs for either isomer. Further studies for identification of
target organs of cis- and trans-1,2-dichloroethene toxicity and their
correlation with concentration levels would be useful for all routes of
exposure. The information is important for populations living near
hazardous waste sites that might be exposed to 1,2-dichloroethene for brief
periods of time.
Intermediate-Duration Exposure. No studies were located regarding
intermediate-duration exposure to 1,2-dichloroethene in humans by any route
of exposure. Liver and lung toxicity of trans -1,2 -dichloroethene was
observed in rats after intermediate-duration inhalation exposure. However
the study was limited in size and scope. Pharmacokinetic, data were
insufficient to identify target organs. Additional studies regarding
1,2-dichloroethene toxicity after inhalation exposure would be useful to
support the results. The available data were insufficient to derive an
inhalation MRL. Studies in rats and mice exposed orally to trans-1,2-
dichloroethene have been conducted, but they did not establish adverse
effect levels. A recently conducted 60-day oral study of trans-1,2-
dichloroethene in rats, available as an abstract, indicated that the lungs
spleen, and kidney are targets (see Section 2.8.3). The full published
report may provide dose-response data when it becomes available.
Hematotoxic effects of oral exposure to cis-1,2-dichloroethene were observed
in rats in a 90-day study. Based upon a NOAEL value for this effect, an
intermediate-duration oral MRL was established. The differences in observed
effects between cis- and trans-1,2-dichloroethene that were seen in rats in
the 90 day studies may be due to different toxicity of these isomers as
discussed above (see acute-duration exposure). No studies were located
regarding 1,2-dichloroethene toxicity in animals after dermal exposure.
Because people living near hazardous waste sites may be exposed for longer
periods of time, more dose-response data for intermediate-duration exposures
by all routes are important.
Chronic-Duration Exposure and Cancer. No data were located regarding
health effects in humans or animals following chronic exposure to
1,2-dichloroethene by any route. Therefore, no chronic inhalation or oral
-------
39
2. HEALTH EFFECTS
MRLs could be derived. Pharmacokinetic data were insufficient to identify
target organs of 1,2-dichloroethene toxicity. Chronic toxicity studies in
animals would be useful for all routes of exposure. These studies could
provide information on subtle toxicological changes in organs associated
with long-term exposure to low-levels of 1,2-dichloroethene. Furthermore,
studies in drinking water are particularly relevant to humans, since low
levels of 1,2-dichloroethene have been detected in this medium. Information
regarding the toxic effect of chronic exposure to 1,2-dichloroethene is also
important for populations living near waste sites, because they might be
exposed for a long period of time.
No chronic studies were located regarding carcinogenicity of
1,2-dichloroethene in humans or animals by any route of exposure.
Genotoxicity studies revealed mutagenic activity of the cis isomer in the
host-mediated assay. Furthermore, a recently conducted 60-day oral study
of trans-1,2-dichloroethene in rats, which was available in abstract form,
indicated a high incidence of lymphosarcoma in the lungs (see Section
2.8.3). Although this study has not yet been published, it raises a concern
for carcinogenicity, which should be further investigated in long-term oral
and inhalation studies of both isomers.
Genotoxicity. No studies were located regarding 1,2-dichloroethene
genotoxicity in humans. Neither isomer of 1,2-dichloroethene was mutagenic
in in vitro experiments with E. coli. S. tvphimurium. and S. cerevisiae.
Furthermore, neither isomer produced chromosomal aberrations or sister
chromatid exchanges in Chinese hamster cells. The cis isomer, but not the
trans isomer induced unscheduled DNA synthesis in rat hepatocytes.
Positive results were obtained with the cis isomer but not the trans isomer
in host-mediated assays in mice. Furthermore, repeated intraperitoneal
application induced chromosomal aberrations in mouse bone marrow cells, thus
indicating that cis-1,2-dichloroethene may be a potential mutagen in
animals. Further studies in animals would be useful to support this result.
Further studies regarding the differences in genotoxic potential between
cis and trans isomer would be helpful. Reliable cytogenetic studies among
exposed workers would be useful to determine possible genotoxic effect in
humans.
Reproductive Toxicity. No studies were located regarding reproductive
effects of 1,2-dichloroethene in humans or animals after exposure by any
route. Pharmacokinetic data are insufficient to draw any conclusion
regarding possible reproductive toxicity of 1,2-dichloroethene.
Histopathological examination of the reproductive organs of animals exposed
to 1,2-dichloroethene either orally or by inhalation for 90 days would
provide useful information on possible effect on reproductive system.
Developmental Toxicity. No studies were located regarding
developmental toxicity of 1,2-dichloroethene in humans or animals by any
route of exposure. Pharmacokinetic data are insufficient to predict
developmental effects; however, there is no reason to suspect that the
-------
40
2. HEALTH EFFECTS
isomers could not cross the placenta. The results of an on-going study
indicate that trans-1,2-dichloroethene induced fetotoxicity in rats after
inhalation exposure of the dams (see Section 2.8.3). This study, when
published, and further studies in animals regarding developmental toxicity
of cis- and trans-1,2-dichloroethene after inhalation, oral, and dermal
exposure would be useful to determine its fetotoxic and teratogenic
potential. The information would be useful for possible extrapolation of
animal data to humans.
Immunotoxicity. No information about 1,2-dichloroethene toxicity to
human immune system was located. The findings of fatty degeneration of
Kupffer cell, decreased number of white blood cells, and pneumonic
infiltration observed in rats after inhalation exposure to trans-1,2-
dichloroethene and of suppression in humoral immune status of male mice
exposed to trans-1,2-dichloroethene in drinking water for 90 days suggest
that 1,2-dichloroethene may be immunotoxic. Immunological studies of the
cis-1,2-dichloroethene and additional studies of trans -1,2-dichloroethene
would help determine more definitively the immunotoxic potential and
possible differences between the isomers. No immunotoxicity data in animals
were located for the dermal route of exposure.
Neurotoxicity. Symptoms of central nervous system depression were
observed in human volunteers during inhalation exposure to 1,2-dichloro-
ethene. The symptoms disappeared after discontinuation of exposure. No
information was located regarding neurotoxicity after other routes of
exposure in humans. Similarly, symptoms of CNS depression were observed in
rodents after oral exposure to 1,2-dichloroethene, but only after lethal
concentrations. The observations were restricted to behavioral tests.
Further information regarding 1,2-dichloroethene neurotoxicity in animals
after all routes of exposure would be useful. Studies of the effects of
1,2-dichloroethene on the morphology of neurons, glial and myelinated cells
and on the synthesis and degradation of neurotransmitters would permit more'
accurate assessment of neurotoxic potential of this chemical.
Epidemiological and Human Dosimetry Studies. No epidemiologic studies
in populations exposed to 1,2-dichloroethene were located. The general
population might be exposed to low levels of 1,2-dichloroethene in
contaminated urban air, or in contaminated drinking water. The
occupationally exposed group is relatively small (for further information
see Section 5). Should specific toxic effects in animals be identified
epidemiology studies could be designed to study the possibility that similar
effects are observed in humans. Studies that correlate exposure with blood
or urine levels of biomarkers and/or with effects would be useful in
establishing causality. The knowledge of dose/effect relationship would be
useful for monitoring individuals near hazardous waste sites for preventive
purposes,
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41
2, HEALTH EFFECTS
Biomarkers of Exposure and Effect. Methods exist for determining
1,2-dichloroethene in blood and biological tissues (see Chapter 6), but
specific levels of 1,2-dichloroethene have not been correlated with
exposure. Exhalation of acetone and the presence of acetone in blood have
been noted in rats after inhalation exposure to cis- and trans-1,2-dichloro-
ethene, but the amounts exhaled or the levels in blood have not been
correlated with exposure levels. Furthermore, acetonemia is not specific
for 1,2-dichloroethene; increased acetone levels were found after exposure
to other chemicals and in patients with certain disease states. Studies
focusing on correlating blood or urine levels of 1,2-dichloroethene or its
metabolites with exposure levels would be useful to facilitate future
medical surveillance that can lead to early detection.
No known biomarkers are currently used to characterize effects caused
by 1,2-dichloroethene. Rats exposed by inhalation to halogenated ethylenes,
including cis- and trans -1,2 -dichloroethene, were shown to exhale acetone.
Based on these studies, a possible mechanism for the production of acetone
was suggested, whereby a metabolite (dichloroethene for 1,2-dichloroethene)
inhibits the enzymes of the citric acid cycle, which would lead to an
increase in mitochondrial acetyl-coenzyme A and, consequently, in an
alteration in lipid and fatty acid metabolism to form ketone bodies.
Further studies that support this hypothesis might determine whether acetone
exhalation could serve as a biomarker for such effects as fatty degeneration
of the liver, which was observed in rats exposed by inhalation to trans-1,2-
dichloroethene (Freundt et al. 1977).
Absorption, Distribution, Metabolism, Excretion. The absorption,
distribution, metabolism and excretion of a chemical can influence its
toxicity. Only a few studies have examined the absorption of
1,2-dichloroethene. These indicate that 1,2-dichloroethene vapors can be
absorbed through the lung. Absorption by dermal route has not been
investigated, although the lipophilic properties of this chemical make it
likely. According to an on-going study, trans-1,2-dichloroethene was
quickly absorbed from the gastrointestinal tract of rats after oral exposure
(see Section 2.8.3). The few oral toxicity studies support this conclusion.
No studies were located regarding the excretion of 1,2-dichloroethene after
inhalation, oral, or dermal exposure.
Cytochrome P-450 has been implicated in the initial step of metabolism
of 1,2-dichloroethene in the liver. Subsequent steps are believed to be
catalyzed by cytosolic and/or mitochondrial aldehyde and alcohol
dehydrogenases or related enzymes. Differences in the metabolism rate and
the metabolite profile have been reported for the cis and trans isomers.
The extrahepatic metabolism of 1,2-dichloroethene has not been extensively
studied. No studies were located regarding the excretion of
1,2-dichloroethene after inhalation, oral, or dermal exposure. Studies of
the distribution of cis- and trans-1,2-dichloroethene and their metabolites
following oral, inhalation, and dermal exposure would identify the tissues,
if any, that can accumulate these chemicals. They can also provide
-------
42
2. HEALTH EFFECTS
information on target organ toxicity. Studies on the excretion of
1,2-dichloroethene can reveal the metabolic fate of this chemical. For
example, they can show the percentage of 1,2-dichloroethene excreted
unchanged or as metabolites. These studies can also determine the major
route and rate of excretion and indicate if the excretion of low
1,2-dichloroethene levels differs from that of high levels, in which
metabolism might be saturated.
Comparative Toxicokinetics. The database for 1,2-dichloroethene is
weak. Existing human and animal data do not sufficiently identify target
organs of 1,2-dichloroethene toxicity. No human toxicokinetic or dosimetry
data were located. Toxicokinetic studies in animals were performed only in
rats. Therefore, no comparison of toxicokinetic data could be made.
Further investigation of 1,2-dichloroethene toxicokinetics in different
animal models and the comparison of detected metabolites with those detected
in humans would be useful.
2.8.3 On-going Studies
Both cis- and trans-1,2-dichloroethene, including the mixture of the
two isomers, have been approved for subchronic toxicity studies by the
National Toxicology Program. Microencapsulation procedures for the cis
trans, and cis/trans isomer mixture have been developed, and the material
is being tested for stability by the National Toxicology Program.
Several abstracts of studies in progress were located. A high
incidence of lymphosarcoma in the lungs and histopathological lesions in the
spleen and kidneys were reported in rats after 60 days of oral treatment
with 1/2, 1/20, and 1/200 of the reported LD50 for trans -1,2-dichloroethene
(Witmer et al. 1990). An increase in mean resorptions per litter was
observed in rats after inhalation exposure to 6000 and 12,000 ppm trans -
1,2-dichloroethene during gestation days 7-16 (Alvarez et al. 1990).
Fetotoxicity expressed as weight reduction was observed after 12,000 ppm
exposure. Absorption of trans-1,2-dichloroethene has been studied in rats
after intravenous and oral applications (Manning et al. 1990). In these
studies, trans-1,2-dichloroethene was quickly absorbed from the
gastrointestinal tract reaching peak blood concentrations in 2 to 6 minutes
after exposure.
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A3
3. CHEMICAL AND PHYSICAL INFORMATION
3.1 CHEMICAL IDENTITY
Data on the chemical identities of 1,2-dichloroethene, cis-
1,2-dichloroethene, and trans -1,2-dichloroethene are listed in Tables 3-1,
3-2, and 3-3, respectively.
3.2 PHYSICAL AND CHEMICAL PROPERTIES
The physical and chemical properties of cis- and trans -1,2-dichloro-
ethene are presented in Table 3-4. 1,2-Dichloroethene is a mixture of two
geometric isomers, cis- and trans-1,2-dichloroethene. The proportion of the
cis isomer to the trans isomer in the mixture depends upon the
manufacturer's specifications. The properties of the mixture are expected
to be similar to those of the Individual isomers.
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44
3. CHEMICAL AND PHYSICAL INFORMATION
TABLE 3-1. Chemical Identity of 1,2-Dichloroethene
Value
Reference
Chemical name
Synonyms
Trade name
Chemical formula
Chemical structure
Identification numbers:
CAS Registry
NIOSH RTECS
EPA Hazardous Waste
OHM-TADS
DOT/UN/NA/IMCO Shipping
HSBD
NCI
1,2-Dichloroethene
Acetylene dichloride;
1,2-dichloroethene;
1,2-dichloroethylene;
sym-1,2-dichloroethylene
Dioform
c2h2ci2
CHC1=CHC1
540-59-0
KV9360000
U079a
8300194
UN 1150; dichloroethylene
IMC0 3.2; dichloroethylene
149
C56031
CAS 1988
SANSS 1988;
CHEMLINE 1988
Bennett 1981
CAS 1988
SANSS 1988
CAS 1988
RTECS 1988
HSDB 1988
OHM-TADS 1988
HSDB 1988
HSDB 1988
HSDB 1988
CHEMLINE 1988
aThis number for trans -1,2-dichloroethene (U079) applies to 1,2-dichloro
ethene, since 1,2-dichloroethene is a mixture containing trans-1 2-
dichloroethene (HSDB 1988).
CAS — Chemical Abstract Service
EPA — Environmental Protection Agency
DOT/UN/NA/IMCO - Department of Transportation/United Nations/North
America/International Maritime Consultive Organization
HSDB - Hazardous Substance 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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45
3. CHEMICAL AND PHYSICAL INFORMATION
TABLE 3-2. Chemical Identity of cis-1,2-Dichloroethene
Value
Reference
Chemical name
Synonyms
Trade names
Chemical formula
Chemical structure
cis-1,2-Dichloroethene
(Z)-1,2-Dichloroethene;
(Z)-1,2-dichloroethylene;
cis-acetylene dichloride;
cis-1,2-dichloroethylene;
cis-dichloroethylene
Not available
C2H2C12
CI
c = c
H
H
CI
SANSS 1988
SANSS 1988;
CHEMLINE 1988
CAS 1988
SANSS 1988
Identification Numbers:
CAS Registry
NIOSH RTECS
EPA Hazardous Waste
OHM-TADS
DOT/UN/NA/IMCO Shipping
HSBD
NCI
156-59-2
KV9420000
Not available
8300194
Not available
5656
Not available
CAS 1988
RTECS 1988
OHM-TADS 1988
HSDB 1988
CAS - Chemical Abstract Service
EPA - Environmental Protection Agency
DOT/UN/NA/IMCO - Department of Transportation/United Nations/North
America/International Maritime Consultive Organization
HSDB - Hazardous Substance 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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46
3. CHEMICAL AND PHYSICAL INFORMATION
TABLE 3-3. Chemical Identity of trans-1,2-Dichloroethene
Value
Reference
Chemical name
Synonyms
Trade nantes
Chemical formula
Chemical structure
trans -1,2-Dichloroethene
(E)-1,2-Dichloroethene;
(E)-1,2-dichloroethylene;
trans - acetylene dichloride;
trans -1,2-dichloroethylene;
trans-dichloroethylene
Not available
C2H2CI2
c 1 C 1
\ . c'
h' \
SANSS 1988
SANSS 1988;
CHEMLINE 1988
CAS 1988
SANSS 1988
Identification numbers:
CAS Registry
NIOSH RTECS
EPA Hazardous Waste
OHM-TADS
DOT/UN/NA/IMCO Shipping
HSBD
NCI
156-60-5
KV9400000
U079
8300194
UN 1150; 1,2-dichloroethylene
IMCO 3.2; 1,2-dichloroethylene
6361
Not available
CAS 1988
RTECS 1988
HSDB 1988
OHM-TADS 1988
HSDB 1988
HSDB 1988
HSDB 1988
CAS - Chemical Abstract Service
EPA - Environmental Protection Agency
DOT/UN/NA/IMCO - Department of Transportation/United Nations/North
America/International Maritime Consultive Organization
HSDB - Hazardous Substance 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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47
3. CHEMICAL AND PHYSICAL INFORMATION
TABLE 3-4. Physical and Chemical Properties of cis- and
trans-1,2-Dichloroethene
Value
Property
cis-
trans -
Reference
Molecular weight
96.94
96 .94
Weast 1983
Color
Colorless
Colorless
Hawley 1981
Physical state
Liquid
Liquid
Hawley 1981
Melting point
- 80.5°C
-50° C
Weast 1983
Boiling point
60.3°C
47.5°C
Weast 1983
Specific gravity at 20/4°C
1.2837
1.2565
Weast 1983
Odor
Ethereal,
Ethereal,
Windholz 1983
slightly
slightly
acrid
acrid
Odor threshold:
Water
No data
0.26 ppm
Amoore and
Air
No data
17 ppm
Hautala 1983
Solubility:
Water at 25°C
3,500 mg/L
6,260 mg/L
Horvath 1982
Organic solvents
Soluble in
Soluble in
Weast 1983
ether,
ether,
alcohol,
alcohol,
benzene,
benzene,
acetone,
acetone,
chloroform
chloroform
Partition coefficients:
Log octanol/water
1.86
2.09
Hansch and Leo
1985
Log Koc
1.51-1.69
1.51-1.69
Lyman 1982;
Vapor pressure at 25°C
(estimated)
(estimated)
Sabljic 1984
215 mmHg
336 mmHg
Stevens 1979
Henry's law constant
at 24.8°C:
4.08x10"3
9.38xl0"3
Gossett 1987
atm-nr/mol
atm-m3/mol
Autoignition temperature
460° C
460°C
Sax 1979
Flashpoint
6°C
4°C
Stevens 1979
Flammability limits
in air
9.7-12.8
9.7-12.8
Stevens 1979
volume %
volume %
Conversion factors:
ppm (v/v) to mg/m3
in air at 25°C
1 ppm (v/v)=
1 ppm (v/v)=
3.96 mg/m3
3.96 mg/m3
mg/m to ppm (v/v)
in air at 25°C
1 mg/m3=
1 mg/m3=
0.25 ppm(v/v)
0,25 ppm(v/v)
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49
4. PRODUCTION, IMPORT, USE, AND DISPOSAL
4.1 PRODUCTION
1,2-Dichloroethene is often a by-product in the manufacture of
chlorinated compounds. It is recycled as an intermediate for the synthesis
of commercially important chloroethenes (Stevens 1979). Direct chlorination
of acetylene at about 40°C can also produce 1,2-dichloroethene (Stevens
1979) .
1,2-Dichloroethene (cis-, trans-, and mixture) production data for 1977
from the U.S. EPA Toxic Substances Control Act (TSCA) Production File appear
in Table 4-1. Apparently, industrial-scale quantities of
1,2-dichloroethylene are produced for on-site use to form other chlorinated
compounds, which are the final commercial product. Columbia Organics of
Columbia, SC, and Aldrich Chemical, of Milwaukee, WI, sell research
quantities of 1,2-dichloroethene (cis-, trans-, and mixture); Columbia
Organics also sells cis-1,2-dichloroethene in 55-gallon drums (Kuney 1988;
Van 1988). Data about the volume and trends of 1,2-dichloroethene
production in the United States are not available.
4.2 IMPORT
No data were found on United States import or export of
1,2-dichloroethene.
4.3 USE
1,2-Dichloroethene is used primarily as a chemical intermediate in the
synthesis of chlorinated solvents and compounds; it has also been used as a
low-temperature extraction solvent for organic materials such as dyes,
perfumes, lacquers, and thermoplastics (Stevens 1979). No information is
available as to how much, if any, 1,2-dichloroethene is currently used for
solvent purposes.
4.4 DISPOSAL
1,2-Dichloroethene may be released from industries in wastewater
streams; however, these compounds can be removed from wastewater by air
stripping (Dilling 1977; Gossett 1987; Shen 1982a). Product residues and
sorbent media containing 1,2-dichloroethene may be packaged in epoxy-lined
drums and disposed of at an EPA-approved landfill (OHM-TADS 1988).
I,2-Dichloroethene may be destroyed in high-temperature incinerators
equipped with acid scrubbers (HSDB 1988). This compound is a candidate for
disposal by: rotary kiln incineration at 820-1600°C with residence times of
seconds for liquids and gases, and longer for solids; fluidized bed
incineration at 450-980°C with residence times of seconds for liquids and
gases, and longer for solids; and liquid injection incineration at
650-1600°C with residence times of 0.1-2 seconds (HSDB 1988). Environmental
regulatory agencies should be consulted to confirm acceptable disposal
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50
4. PRODUCTION, IMPORT, USE, AND DISPOSAL
TABLE 4-1. U.S. EPA TSCA Production File Data
for l,2-Dichloroethenea
Compound
Company/Location
1977 Production Volume
1,2-Dichloroethene
(mixture)
1,2-Dichloroethene
(cis-isomer)
Dow Chemical,
Freeport, TX
PPG Industries,
Lake Charles, LA
PPG Industries,
Ponce, Puerto Rico
Columbia Organics
Columbia, SC
Continental Oil Co.
Westlake, LA
PPG Industries
Lake Charles, LA
PPG Industries
Ponce, Puerto Rico
10-50 million pounds
(site limited use)
1-10 million pounds
(site limited use)
0.1-1 million pounds
<1000 pounds
0.1-1 million pounds
1-10 million pounds
0.1-1 million pounds
1,2-Dichloroethene
(trans - isomer)
No data
aSource: EPA 1977
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51
4. PRODUCTION, IMPORT, USE, AND DISPOSAL
procedures (HSDB 1988; OHM-TADS 1988). Information regarding the amount
disposed of by each method is not available.
The EPA identified trans -1,2-dichloroethene as a hazardous waste; its
disposal is regulated under the Resource Conservation and Recovery Act
(RCRA). Specific information on federal regulations concerning hazardous
waste disposal by land treatment, landfilling, incineration, thermal
treatment, chemical/physical/biological treatment, underground injection and
deep sea injection appears in the Code of Federal Regulations (40 CFR 190 to
399). Release of trans-1,2-dichloroethene in wastewater is regulated under
the Clean Water Act by the National Pollutant Discharge Elimination System
(NPDES). Information regarding effluent guidelines and standards for trans-
1,2-dichloroethene can be found in 40 CFR 122, 40 CFR 125, 40 CFR 413.02(i),
40 CFR 414, and 40 CFR 433.11(e).
Pursuant to RCRA Section 3004(g)(5), EPA has restricted the land
disposal of trans-1,2-dichloroethene (Federal Register 1989). It may be
land disposed only if prior treatment standards have been met, or if
disposal occurs in units that satisfy the statutory no migration standard
(Federal Register 1989). Proper guidelines and standards are outlined in
the Federal Register 1989.
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53
5. POTENTIAL FOR HUMAN EXPOSURE
5.1 OVERVIEW
1,2-Dichloroethenes are man-made compounds. Sources of environmental
exposure to 1,2-dichloroethene include: process and fugitive emissions from
its production and use as a chemical intermediate; evaporation from
wastewater streams, landfills, and solvents; emissions from combustion or
heating of polyvinyl chloride and some vinyl copolymers; formation via
anaerobic biodegradation of some chlorinated solvents; and leaching from
landfills. Most of the 1,2-dichloroethene released in the environment will
eventually enter the atmosphere or groundwater, where it is broken down
further.
1,2-Dichloroethene in the atmosphere is removed chiefly through
reaction with photochemically-generated hydroxyl radicals. The estimated
atmospheric half-lives for cis- and trans -1,2-dichloroethene are 8.3 and 3.6
days, respectively (Goodman et al. 1986). Precipitation may also remove it;
however, most 1,2-dichloroethene thus removed will probably reenter the
atmosphere by volatilization. When released to surface water,
volatilization is expected to be the primary fate process (half-life =3-6
hours in a model river). When released to soil, 1,2-dichloroethene
volatilizes rapidly from moist soil surfaces and leaches through subsurface
soil, where it could become a groundwater contaminant. In groundwater,
1,2-dichloroethene is susceptible to anaerobic biodegradation. Experimental
data indicate that the anaerobic biodegradation half-life of
1,2-dichloroethene is about 13-48 weeks (Barrio-Lage et al. 1986).
The general population may be exposed to low levels (0.013-0.076 ppb)
of 1,2-dichloroethene through inhalation of contaminated air in urban areas
(Singh et al. 1983). These exposure levels correspond to an average daily
intake of 1-6 /zg/day assuming an average daily intake of 20 of air.
Additional exposure may occur through consumption of, inhalation while
showering with, and dermal contact with contaminated tap water.
Occupational exposure may occur by inhalation and/or dermal contact.
According to a 1981-83 NI0SH survey, an estimated 215 workers in the United
States are potentially exposed to 1,2-dichloroethene in the workplace. This
figure does not include fire fighters and workers at landfills.
The VIEW Database (1989) indicates that trans-1,2-dichloroethene, cis-
1,2-dichloroethene, and dichloroethene (isomer not specified) have been
identified at 227, 31, and 48 sites, respectively, out of 1177 National
Priorities List (NPL) sites. The frequency of these sites within the United
States can be seen in Figure 5-1.
5.2 RELEASES TO THE ENVIRONMENT
5.2.1 Air
1,2-Dichloroethene may be released to the atmosphere in emissions from
its production and use facilities, contaminated wastewaters, contaminated
-------
5
54
POTENTIAL FOR HUMAN EXPOSURE
TJWM J TO 8 SITES
¦¦¦ oven 10 sites
FIGURE 5-1. Frequency of Sites with 1,2-Dichloroethene Contamination
-------
55
5. POTENTIAL FOR HUMAN EXPOSURE
waste disposal sites, and from the pyrolysis and combustion of poly-(vinyl
chloride) and some vinyl copolymers (HSDB 1988; Michal 1976; Shen 1982b).
Not enough data are available to estimate the amount of 1,2-dichloroethene
released to the atmosphere.
5.2.2 Water
It has been estimated that between 1982 and 1984, trans-1,2-dichloro-
ethene was loaded into the Niagara River at an average of 13.6 pounds per
day (Spagnoli 1986). Insufficient data are available to estimate the amount
of 1,2-dichloroethene released to other surface waters in the United
States. 1,2-Dichloroethene may be released to surface waters via surface
runoff from contaminated waste disposal sites. Wastewater from a variety of
industrial sources and from some publicly owned treatment works may also
release this substance. 1,2-Dichloroethene may be found in effluents from
its manufacturing sites and from industries involved in its use as a solvent
and extractant, in organic synthesis, and in the manufacture of perfumes,
lacquers, and thermoplastics. As part of a comprehensive EPA survey of
industrial facilities and publicly-owned treatment works, 4000 samples of
wastewater were analyzed. The findings indicate that cis- or trans-
1,2-dichloroethene is sometimes found in wastewater from: petroleum
refining, coal mining, electrical component and electronics, foundries,
nonferrous metal manufacture, inorganic chemicals, mechanical products,
transportation equipment, publicly-owned treatment works, pharmaceuticals,
organic chemical and plastics manufacture, paint and ink formulation, rubber
processing, steam electricity generation, leather tanning, iron and steel
manufacture, textile mills, plastics and synthetics, auto and other
laundries, and explosives (EPA 1980b; Shackelford et al. 1983). Similarly,
effluents from iron, steel, and nonferrous metal manufacturing, organics,
plastics, and rubber processing exceeded 100 ppb of cis-1,2-dichloroethene.
Effluents of iron and steel manufacturing, electronics, and publicly-owned
treatment works also contained trans-1,2-dichloroethene (see Section 5.4.2)
(Shackelford et al. 1983).
1,2-Dichloroethene occurs in groundwater because of leaching from
contaminated waste disposal sites, and anaerobic degradation of more highly
chlorinated ethenes and ethanes in groundwater (Cline and Viste 1985; HSDB
1988; Parson et al. 1984; Smith and Dragun 1984). Barber et al. (1988)
reported 280 ppb of dichloroethene (isomer unspecified) in groundwater under
a sandy rapid infiltration site that had received secondary sewage effluent
since 1936. However, only extremely low concentrations of
1,2-dichloroethene or its precursors were found in the present-day effluent,
and the aerobic conditions in the shallow aquifer make its formation by
reductive dehalogenation unlikely. Either 1,2-dichloroethene was disposed
of at higher concentrations in the past, or it has accumulated over the
years.
1,2-Dichloroethene in drinking water may result from raw water source
contamination. Otson et al. (1982) monitored 1,2-dichloroethene levels at
-------
56
5. POTENTIAL FOR HUMAN EXPOSURE
30 potable water treatment plants in Canada and found a higher frequency of
occurrence and concentration in treated water than in raw water. The reason
for these results is unclear. One possible explanation is that the
1,2-dichloroethene concentration varied In the raw water supplies, and since
collection of the finished water samples was not delayed to take into
account retention time in the plant, frequency of occurrence and
concentration differed. Other possible explanations are that the water was
contaminated during treatment, chlorination of organics occurred during
water treatment,or that the supplies contained some compounds which were
converted into 1,2-dichloroethene in the biologically active raw water.
5.2.3 Soil
Insufficient data are available to estimate the amount of
1,2-dichloroethene released to soil, cis- and trans -1,2-Dichloroethene are
released to soil from the disposal of waste materials containing these
compounds (Barber et al. 1988; Fain et al. 1987). They also may be formed
in landfills as anaerobic biodegradation products of tetrachloroethene,
trichloroethene, 1,1,1-trichloroethane, and 1,1,2,2 -tetrachloroethane,
solvents commonly found in municipal and industrial landfills (Parson et al
1984; Smith and Dragun 1984).
5.3 ENVIRONMENTAL FATE
5.3.1 Transport and Partitioning
Occurrence of 1,2-dichloroethene in rainwater samples (Kawamura and
Kaplan 1983) indicates that this compound may be removed from the
atmosphere by precipitation; however, most of the 1,2-dichloroethene so
removed is likely to reenter the atmosphere by volatilization. Organics
with a vapor pressure of >10"^ mniHg should exist almost entirely in the
vapor phase in the atmosphere (Eisenreich et al. 1981). Thus, cis- and
trans-1,2-dichloroethene, which have vapor pressures of 215-336 mmHg at 25°C
(Stevens 1979), are not expected to partition from the vapor phase to
particulates in the atmosphere.
The dominant removal mechanism for the dichloroethenes in surface
waters is volatilization. Henry's Law constants are 4.08xl0~3 atm-m3/mol at
24.8°C for cis-1,2-dichloroethene and 9.38x10"^ atm-m^/mol at 24.8°C for
trans-1,2-dichloroethene (Gossett 1987); based on this, the volatilization
half-lives from a model river 1 m deep, flowing 1 m/sec with a wind speed of
3 m/sec is estimated to be 3 hours, using the method of Thomas (1982).
Dilling (1977) experimentally determined that the volatilization half-life
in an open beaker containing 1 ppm of test compound at a solution depth of
6.5 cm under continuous stirring (200 rpm) was 19.4 minutes for the cis-
isomer and 24.0 minutes for the trans- isomer. These values correspond to
volatilization half-lives of 5.0 and 6.2 hours, respectively, from a body of
water 1 m deep.
-------
57
5. POTENTIAL FOR HUMAN EXPOSURE
Bioconcentration factors (BCFs) in fish ranging between 5 and 23 have
been estimated for the 1,2-dichloroethene isomers using linear regression
equations based on log Kow and water solubility data provided in Table 3-4
(Bysshe 1982; Hansch and Leo 1985; Horvath 1982). These BCFs suggest that
these compounds do not bioconcentrate significantly in aquatic organisms.
Based on this information, there is little potential for biomagnification
within the food chain.
Soil adsorption coefficients (Koc) of 32-49 were estimated for the
1,2-dichloroethene isomers using a linear regression equation based on
water solubility data (Lyman 1982) and the structure-activity relationship
developed by Sabljic (1984). These Koc values suggest that adsorption of
the 1,2-dichloroethene isomers to soil, sediment, and suspended solids in
water is not a significant fate process. Without significant adsorption to
soil, leaching into groundwater is a strong possibility. The presence of
1,2-dichloroethene in groundwater, especially under sandy soil (Barber
et al. 1988) substantiates its leachability. The relatively low Koc and
high vapor pressure of 1,2-dichloroethene indicate that this compound should
also readily volatilize from moist soil surfaces (Swann et al. 1983).
5.3.2 Transformation and Degradation
5.3.2.1 Air
The dominant atmospheric removal process for 1,2-dichloroethene is
predicted to be reaction with photochemically generated hydroxyl radicals in
the troposphere. The estimated atmospheric half-lives for cis- and trans-
1,2-dichloroethene are 12 and 5 days, respectively; these estimates are
based on experimentally determined hydroxyl reaction rate constants of
2.0x10"-'-^ cm^/molecules-sec at 25°C for the cis- isomer and 4.5x10"-'-^
cm^/molecules-sec at 25°C for the trans- isomer. Formyl chloride has been
positively identified as a product of this reaction (Goodman et al. 1986).
Experimental data indicate that the reaction of cis- and trans-
1,2-dichloroethene with ozone, nitrate radicals, or singlet oxygen in the
troposphere is too slow to be environmentally significant (Atkinson and
Carter 1984; Atkinson et al. 1987; Sanhueza and Heicklen 197 5a,b).
The primary UV absorption band for cis-1,2-dichloroethene is at 190 nm,
which extends to about 240 nm (Ausubel and Wijnen 1975). A minute amount of
light is absorbed in the environmentally significant range (wavelengths
greater than 290 nm to 380 nm). However, such absorption is insufficient
for direct photolysis to be a significant fate process in the atmosphere.
5.3.2.2 Water
Chemical hydrolysis and oxidation are probably not environmentally
important fate processes for 1,2-dichloroethene (Callahan et al. 1979; Jaber
et al. 1984; Mabey et al. 1981). Kinetic data pertaining specifically to
the abiotic degradation of the 1,2-dichloroethene isomers in the environment
-------
58
5. POTENTIAL FOR HUMAN EXPOSURE
were not located; however, data were available for two closely related
structural analogues, trichloroethene and tetrachloroethene. The combined
hydrolytic-oxidative half-lives for these compounds in a closed-aqueous
system are 8.8 and 10.7 months, respectively (Dilling et al. 1975). Direct
photolysis of 1,2-dichloroethene is also not likely to be important in
sunlit natural waters (see Section 5.3.2.1).
Generally, 1,2-dichloroethene and other chlorinated ethenes resist
biodegradation under aerobic conditions (Fogel et al. 1986; Mudder 1981;
Mudder and Musterman 1982). However, in one study, the 1,2-dichloroethene
isomers were susceptible to aerobic biodegradation. Settled domestic
wastewater was used as the inoculum in this study (Tabak et al. 1981). The
inoculum may have contained a facultative methanotroph capable of degrading
the dichloroethenes (Fogel et al. 1986). No information was found
regarding biodegradation in biological waste treatment plants.
1,2-Dichloroethenes undergo slow reductive dechlorination under
anaerobic conditions (Barrio-Lage et al. 1986; Fogel et al. 1986) . In one
study, anoxic microcosms containing uncontaminated organic sediment and
water to simulate the groundwater environment were spiked with 5 mg/L of
test compound. First-order rate constants were obtained that correspond to
half-lives of 88-339 and 132-147 days for the cis and trans isomers,
respectively. No degradation occurred in sterile microcosms; thus, loss of
the compounds was assumed to be due entirely to anaerobic biodegradation.
The cis isomer degraded to chloroethane and vinyl chloride, a human
carcinogen, while the trans isomer degraded to vinyl chloride only (Barrio-
Lage et al. 1986). When cis- and trans-1,2-dichloroethene were incubated
with methanogenic aquifer material from a site near a landfill, at least 16
weeks passed before trans isomer degradation began (Wilson et al. 1986).
During the same time, the cis isomer was reduced to <2% of the
concentration in the autoclaved control, and vinyl chloride appeared after
only 1-2 weeks incubation. After 40 weeks, the trans isomer concentration
fell to 18% of that in the autoclaved control containing the trans isomer.
Trace amounts of the cis isomer remained in the unsterilized microcosm
beyond 40 weeks.
5.3.2.3 Soil
Studies showing that cis- and trans-1,2-dichloroethene degrade in
nonsterile groundwater microcosms (Barrio-Lage et al. 1986; Wilson et al.
1986) suggest that these compounds undergo anaerobic biodegradation in
soil. Also, this process may be the sole mechanism by which
1,2-dichloroethenes degrade in soil- Hallen et al. (1986) found that when
cis- and trans-1,2-dichloroethene were incubated in a system inoculated with
anaerobic sludge from a municipal digester to simulate anaerobic conditions
in a landfill, vinyl chloride appeared within 6 weeks.
-------
59
5. POTENTIAL FOR HUMAN EXPOSURE
5.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT
5.4.1 Air
1,2-Dichloroethene has been frequently detected in air samples of urban
locations throughout the United States and in landfill gas. Data in
Table 5-1 represent available air monitoring data for 1,2-dichloroethene.
Only one rural air monitoring study was located in the literature.
5.4.2 Water
1,2-Dichloroethene has been detected in surface, ground, and drinking
waters, as well as in industrial and municipal effluents, urban runoff and
leachate from landfills throughout the United States. Data in Table 5-2
represent the available monitoring data for 1,2-dichloroethene in these
media. In some of the studies, only one of the 1,2-dichloroethene isomers
was monitored. Some of the studies did not mention the specific isomer
monitored. 1,2-Dichloroethene has been detected in groundwater in Nebraska,
Wisconsin, and New Jersey. A maximum concentration of 818.6 ppb was found
in the New Jersey study, and a maximum of 2.9 ppb was found in the Nebraska
study (Goodenkauf and Atkinson 1986; Page 1981). Quantitative data were not
discussed in the Wisconsin study (Krill and Sonzogni 1986). Groundwater
contamination has been reported at numerous waste disposal sites in the
United States. In a detailed study, the Wisconsin Department of Natural
Resources sampled groundwater at 20 municipal and 6 industrial landfills in
Wisconsin. 1,2-Dichloroethene was detected in samples from 5 of 26
landfills at a maximum concentration of 3900 ppb, and in leachate from 8 of
26 landfills at a maximum concentration of 310 ppb (Friedman 1988) . The
contract laboratory statistical data base reports that trans-
1,2-dichloroethene has been detected in water at 34 of 357 hazardous waste
sites in the United States (VIAR 1987). The mean concentrations at these
sites ranged from 6.6 to 34,000 ppb. The contract laboratory statistical
data base has one major shortcoming: no distinction is made between
groundwater and surface water monitoring data. In a comprehensive survey of
United States drinking water derived from groundwater, 16 of 466 randomly
selected sites and 38 of 479 purposely selected sites contained
1,2-dichloroethene. The maximum concentration was 2 ppb at random sites and
120 ppb at the nonrandon sites (Westrick et al. 1984).
Industrial effluent monitoring data from Shackelford et al. (1983) was
obtained from a data base of a comprehensive EPA survey of 4000 effluent
samples from Industries and publicly-owned treatment works (POTW). This
survey was conducted in response to the consent decree between the National
Resources Defense Council and the EPA on June 7, 1976.
-------
TABLE 5-1. Air Monitoring Data for 1,2-Dichloroethene
Media Location Sanpling Date Isomer Concentration Comments Reference
(ppb)
Ambient air
Houston, TX
St. Louis, MO
Denver, CO
Riverside, CA
Staten Island, NY
Pittsburgh, PA
Chicago, IL
Edison, NJ
Tulsa, OK
Kanawha Valley, UV
Front Royal, VA
So. Charleston, WV
Birmingham, AL
Baton Rouge, LA
Upland, CA
Magna, VT
Grand Canyon, AZ
Geismar, LA
Niagara Palls, NY
c\s
May 1980
May-June 1980
June 1980
July 19B0
March-April 1981
April-May 1981
NS
NS
General urban atmosphere
NS
NS
1978
NS
0.071 (mean)
0.039 (mean)
0.076 (mean)
0.060 (mean)
0.018 (mean)
0.013 (mean)
0.019 (mean)
1.3 (max.) Kin-Buc disposal site
<0.1
0.08
0.1
<0.08
<0.1
<0.1
<0.1
0.08
0.065
2.6 (max.)
Singh et al. 19&3
trace
Detected in air outside 3
of homes in Old Love
Canal hazardous waste
site (detection limit
not stated)
Pellizzari 1978
Pellizzari 1978
Barkley et at. 1986
*0
O
H
m
2
H
M
>
r1
•n
o
pa o
s
c
m
X
TJ
O
C/}
c
m
New Jersey
Pullman, WA
(rural area)
NS
NS
December 1974 to NS
February 1975
NS 4 NPL sites and 1 municipal
landfill; detected in air
samples collected at 3 of 5
sites; occurred in 75-100%
of samples collected at
these sites (detection
limit >0.1 ppb)
ND Detection limit 5 ppt
LaRegina et al. 1986
Grimsrud and Rasmussen 1975
-------
TABLE 5-1 (continued)
Media
Location
Sampling Date Isomer
Concentration
(ppb)a
Comments
Reference
Indoor air Niagara Falls, NY 1978
Knoxville, TN Winter 1982
Landfill gas Selected United NS
States landfills
NS
NS
NS
0.015
Air in a basement of a
home in Old Love Canal
Barkley et al. 1980
8.1 (mean) Detected in 16 of 16 samples Gupta et al. 1984
(detection limit not stated)
Municipal landfill
simulator
February 1983 to NS
February 1984
70 (mean) Secondary source
3600 (max.)
210 (mean) Simulation
3260 (max.)
Vogt and Walsh 1985
Vogt and Walsh 1985
Long Island, NY NS
California NS
trans- 75,600 (max.) Air samples collected from Lipsky and Jacot 1985
methane vents at 2 sanitary
landfiI Is
trans- 59,000 (max.) 20 class II landfills
Uood and Porter 1987
"13
O
H
m
23
H
M
>
t-1
O
73
EC
G
PJ
X
T3
O
C
w
aUnless otherwise specified.
NS = Not stated; ND - not detected.
-------
TABLE 5-2. Water Monitoring Data for 1,2-Dichloroethene
Media
Location
Sampling Date
Isomer
Concentration
(ppb)
Comments
Reference
Surface water
Hylebos Waterway 1979
in the Puget
Sound
NS
0.8-2.4
Ri ley et al.
1980
Potomac River in Spring 1986
Quantico, VA
trans- <2
12 sites in the
Delaware and
Raritan Canal in
New Jersey
August 1979 to
January 1980
Indian River in May 1981 to May
Vero Beach, FL 1982
Drainage canal
discharging into
the Indian River
in Vero Beach, FL
New Jersey
Quinipiac River
in Southington,
CT
May 1981 to May
1982
1977-1979
1980
NS
NS
NS
ND
ND
4.0-48.1
15.7 (mean)
trans- 1307.5 (max.)
trans- 0.43 (mean)
1 sample analyzed (detection
limit not reported)
Detection limit not reported
13 samples (detection limit
4.0 /ig/L)
Canal receiving contaminated
groundwater; detected in 23
of 39 sarnies (detection
limit 4.0 ug/L)
Hall et al. 1987
Granstron et al.
1984
Wang et al. 1985b
Wang et al.
1985b
Detected in 172 of 273 Page 1981
samples (detection limit not
reported)
Detected in A of 5 samples Hall 1984
(detection limit not
reported)
o
H
pn
z
H
t—(
>
r1
o
•po
•x,
c;
M
X
id
O
C
fo
CT>
CO
UiI son Creek
(adjacent to
hazardous waste
site in Bui lit
County, KY
February 1979
NS
75 (max.)
Stonebraker and
Smith 1980
Groundwater
178 CERCLA sites
(Comprehensive
Envi ronmental
Response, Compen-
sation, and
LiabiIity Act)
1981-1984
trans- NS
Fequency of detection =29.1% Plunt) 1987
-------
TABLE 5-2 (continued)
Media Location Sampling Date Isomer Concentration Comments Reference
n
o
pa
X
a
pi
HQ
O
3
CT\
w
-------
TABLE 5-2 (continued)
Media Location Sampling Date Isomer Concentration Comments Reference
(ppb>
Groundwater
Biscayne aquifer
in the vicinity
of the Miami
Drunsite
1983
NS
19 (mean)
Detected in 2 of 3 samples
(detection limit not
reported)
Myers 1983
Vero Beach, FL
Piper Aircraft
Corp. in Vero
Beach, FL
Lakewood, UA
Western
Processing, Kings
County, WA
April 1981 to
December 1983
April 1981 to
December 1983
Decent>er 1983
Noventoer 19S2
NS
NS
trans-
trans-
40-1800
1000-4000
250-435
330 (mean)
Qualitatively
i dent i f i ed
Near a leaking subsurface
trichloroethylene storge
tank
At site of a leaking subsur-
face trichloro- ethylene
storage tank
Detected in 11 of 11
samples; in the vicinity of
an NPL site
Hazardous waste site
Wang et al. 1985a
Wang et al.
1985a
Wolf and Gorelik
1984
Aldis et al.
1983
T3
O
H
M
S3
H
M
>
r
0
70
1
C
cr\
Marshall landfill NS
in Boulder
County, Co
Forest Waste NS
Disposal site in
Otisville, MI
trans-
trans-
530 (on site)
66 (off site)
100 (max.)
NPL site
NPL site
EPA 1986a
EPA 1986b
H
X
h3
O
C/}
C2
?a
M
Lang Property
site in Pemberton
Township, NJ
NS
trans- 942 (mean)
2500 (max.)
NPL Site
EPA 1987a
Vega Alta Public
Supply Wells in
Puerto Rico
NS
NS
74 (max.)
NPL site; detected in 89 of
168 samples (detection limit
not reported)
EPA 1988a
Ponders Corner in 1984-1985
Pierce County, UA
trans- 85 (max.)
NPL site EPA 1986c
Hoi Iinsworth
Solderless Term-
inal Co. in Fort
Lauderdale, FL
1983
NS 2160 (max.) NPL site; level of dichloro- EPA 1986d
ethene (there was no indica-
tion whether this was 1,1- or
1,2-dichlproethene)
-------
TABLE 5-2 (continued)
Media Location Sampling Date Isomer Concentration Comments Reference
(ppb)
Drinking water
(using groundwater
sources)
United States
NS
NS 2.0 (max.) Detected in samples
collected from 16 of 466
randomly selected sites
using groundwater as a raw
water source (detection
limit 0.2 fig/L)
Westrick et a I.
1984
United States
NS
NS
120 (max.)
Drinking water
Raw and treated
drinking water
Philadelphia, PA
5 United States
cities
10 potable water
treatment plants
in Canada
February 1975 to
January 1977
1975
NS
July 1982 to July
1983
NS
NS
cis- and NS
trans-
trace
Detected in samples
collected from 38 of 479
non-randomly selected sites
using groundwater as a raw
water source (detection
limit 0.2 /ig/L)
Detected in 1 of 17 samples
(detection limit not
reported)
U.S. EPA National Organics
Reconnaissance Survey; cis
isomer positively identified
in samples from Miami, FL,
Philadelphia, PA, and
Cincinnati, OH; trans isomer
positively identified in
samples from Miami, FL
Positively identified in 3
raw and 3 treated water
sanples (detection limit not
reported)
Uestrick et al.
1984
Suffet et al.
1980
EPA 1975
Otson 1987
*0
o
H
tn
z
H
t-H
>
§
§
M
X
I-S
O
w
e
fo
n
as
30 potable water
treatment plants
in Canada
August 1979 to
December 1979
NS
raw water -
23 (max.)
treated water
32 (max.)
Positively identified in 2 Otson et al.
raw and 11 treated water 1982
samples
Leachate
NS (landfill
containing mixed
industrial waste)
NS
trans- 0.045-0.799
average
concentration of
leachates
Detected in 2 of 8 leachates
(detection limit not
reported)
Ghassemi et al.
1984
-------
TABLE 5-2 (continued)
Media
Location
Sampling Date
Isomer
Concentration
(ppb)
Ccmnents
Reference
Leachate
Aqueous lagoon
Urban stormwater
runoff
Minnesota
Minnesota
NS
NS
Lyon, MN, munici- NS
pal landfill
Meeker, MN,
municipal land-
fill
Meeker, MN,
municipal land-
fill
Rochester, MN,
municipal land-
fill
Rochester, MN,
municipal land-
fill
Wisconsin, 20
municipal and
industrial
laridf i I Is
Forest Waste
Disposal site in
Otisville, MI
15 United States
cities
NS
NS
NS
NS
1985-1987
NS
as of July 1982
cis- 20,000 (max.) Detected in leachate from 7
of 13 sites (detection limit
not reported)
trans-
trans-
cis-
trans-
cis-
trans-
NS
88 (max.)
3.8 (mean)
190 (mean)
170 (mean)
470 (mean)
88 (mean)
310
trans- 50
trans- 1-3 (in positive
samples)
Detected in leachate from 3
of 6 sites (detection limit
not reported)
Detected in leachate from 8
of 26 sites
NPl site; estimate level
(compound detected below the
quantification limit)
Detected in runoff from
Little Rock, AR, and
Eugene, OR
Sabel and Clark
1984
Sabel and Clark
1984
Brown and
Donnelly 1988
Brown and
Donnelly 1988
Brown and
Donnelly 1988
Brown and
Donnelly 1988
Brown and
Donnelly 1988
Friednan 1988
EPA 1986b
Cole et al. 1984
TJ
O
H
m
2;
H
I—I
>
r1
O
7°
K
d
X
*0
O
to
C
pa
w
On
a-*
-------
TABLE 5-2 (continued)
Media Location Sampling Date Isomer Concentration Conments Reference
(ppb)
Wastewater
Los Angeles, CA NS
NS 5.2 (mean) Effluent from a county Gossett et al.
sewage treatment plant 1983
NS
1980/1981
trans-
untreated: 52-60
effluent: 31-37
Municipal sewage treatment
plant; detected in 5 of 5
samples
Lao et al. 1982
Chicago, IL
NS
NS
NS
Owensboro, KY August 1975
Calvert City, KY October 1975
United States NS
trans-
trans-
cis-
trans-
trans-
trans-
trans-
trans-
trans-
trans-
trans-
trans-
<50
20 (max.)
NS
NS
10 (max.)
46 (max.)
10 (max.)
10 (max.)
75 (max.)
12 (mean)
190 (max.)
<10 (max.)
290 (max.)
Effluent from a municipal
sewage treatment plant
Treated effluent from a
petroleun refinery
Chemical plant effluent
Chemical plant effluent
Industry:
coal mining
electrical electronic
components
foundri es
pharmaceutical manufac-
turing
nonferrous metals manufac-
turing
organic chemicals and
plastics manufacturing
paint and ink formulation
petroleum refining
rubber processing
Lue-Hing et al.
1981
Snider and
Manning 1982
Shackelford and
Keith 1976
Shackelford and
Keith 1976
EPA 1980
o
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w
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OS
-------
TABLE 5-2 (continued)
Media Location Sampling Date Isomer Concentration Comments Reference
(ppb)
Wastewater
United States
NS
United States
NS
Industry: Shackelford
cis- 1.6 steam electric (detected in et al. 1983
one sample)
cis- 3.3 leather tanning (detected
in one sample)
cis- 1400.8 (median) iron and steel manufac-
trans- 2265.9 (median) turing (detected in 2
samples)
cis- 314.6 nonferrous metal (detected
in 1 sample)
cis- 121.5 (median) organics and plastics
trans- 14.6 (median) [(detected in 2 samples)
(cis) and 3 samples (trans)]
trans- 3.9 inorganic chemicals
(detected in 2 samples)
cis- 8.3 textile mill (detected in 1
sample)
cis- 20.1 (median) plastics and synthetics
(detected in 3 samples)
cis- 712.0 rubber processing
trans- 19.0 (median) [detected in 1 sample
(cis) and 2 samples
(trans)]
trans- 60.6 auto and other laundries
(detected in 1 sample)
cis- 1.5 explosives (detected in 1
trans- 3.9 sample)
Industry: Shackelford
trans- 140.7 (median) electronics (detected in 7 et al. 1983
samples)
trans- 13.7 (median) mechanical products
(detected in 2 samples)
trans- 29.3 transportation equipment
(detected in 1 sample)
trans- 16.3 (median) publicly owned treatment
works (POTW) (detected in
63 samples)
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m
ON
CO
Rainwater
UCLA campus 3/26/82
Los Angeles, CA
NS
0.230
1 sample
Kawamura and
Kaplan 1983
NS = not stated.
ND = not detected.
-------
69
5. POTENTIAL FOR HUMAN EXPOSURE
5.4.3 Soil
Available data on 1,2-dichloroethene in soil are limited to those
obtained through hazardous waste site monitoring (Aldis et al. 1983; EPA
1986c, 1987a; Pennington 1983; VIAR 1987). Soil gas pollutants in a
shallow, unconfined aquifer receiving wastewater from metal-plating
operations at Picattinny Arsenal in Morris County, NJ, were found to have a
maximum cis-1,2-dichloroethene concentration of 33 ppb in the vadose zone
(Smith 1988). The EPA Contract Laboratory Program Statistical Database
reports that 1,2-dichloroethene occurs in soil at 8 of 357 hazardous waste
sites in the United States. In all cases, the isomer was reported as trans.
The mean concentrations at these sites ranged from 5-4000 ppb (VIAR 1987).
5.4.4 Other Media
trans -1,2-Dichloroethene concentrations ranging from 22-54,993 yxg/L
have been detected in municipal sludge from various treatment plants
throughout the United States (Feiler et al. 1980; Naylor and Loehr 1982).
Few reports exist of 1,2-dichloroethene in biota from United States
waters. This is because 1,2-dichloroethene is not a typical biota
contaminant (Staples et al. 1985). Nicola et al. (1987) reported mean and
maximum 1,2-dichloroethene levels of 0.04 and 0.05 ppm, respectively, in
fish tissue from Commencement Bay, Tacoma, WA. No fish obtained at the 95
stations in EPA's ST0RET data base contained detectable levels of
1,2-dichloroethene (Staples et al. 1985).
In the early 1980s, 1,2-dichloroethene was found at a concentration of
>5 ppb (wet weight) in sediment at 4% of 361 stations reported in EPA's
STORET data base (Staples et al. 1985). No further information was located
on the occurrence of 1,2-dichloroethene in sediments.
5.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE
The general population is exposed to 1,2-dichloroethene in urban air
and drinking water. Contaminated tap water can cause exposure via
ingestion, inhalation and dermal exposure while showering and bathing.
Inhalation is the most probable route of exposure. 1,2-Dichloroethene has
been detected in urban air at average concentrations of 0.013-0.076 ppb
(0.052-0.30 /ig/m^) (Singh et al. 1983). These exposure levels correspond to
an average daily intake of 1-6 /ng 1,2-dichloroethene, assuming an average
daily intake of 20 m^ of air. Data are insufficient for estimating
1,2-dichloroethene intake via other routes of exposure.
According to a National Occupational Exposure Survey (NOES) conducted
by NI0SH between 1981 and 1983, an estimated 215 workers in the United
States are potentially exposed to 1,2-dichloroethene (mixture of cis and
trans isomers); an estimated 61 workers in the United States are
potentially exposed to cis-1,2-dichloroethene (NIOSH 1988). These tentative
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70
5. POTENTIAL FOR HUMAN EXPOSURE
estimates will be updated as additional information on trade name compounds
containing 1,2-dichloroethene becomes available. There was no NOES estimate
for the trans isomer. Common operations in which there is potential
industrial exposure to 1,2-dichloroethene include: use as a low-temperature
solvent for heat-sensitive substances in extraction of caffeine, perfume
oils, and fats from animal flesh; in rubber and dye industries in extraction
and application; use as a direct solvent in gums, waxes, etc.; use in
solvent mixtures for ester and ether derivatives, lacquers, resins,
thermoplastics, and artificial fibers; in organic synthesis for polymers and
telomeres; and in miscellaneous applications as a liquid dry cleaning agent,
cleaning agent for printed circuit boards, food packaging adhesives, and
germicidal fumigants (NIOSH/OSHA 1978). Continued use of 1,2-dichloroethene
in these operations is unknown. Fire fighters and workers at landfill sites
may also be exposed to 1,2-dichloroethene (Michal 1976; NIOSH/OSHA 1978;
Vogt and Walsh 1985) . No information was located on exposure levels in
other occupational settings.
5.6 POPULATIONS WITH POTENTIALLY HIGH EXPOSURE
Populations with potentially high exposure include those living near
hazardous waste sites and municipal landfills, and those occupationally
exposed. Near certain hazardous waste sites and municipal landfills,
potential exists for exposure to elevated levels of dichloroethene in air
downwind of the sites and in contaminated drinking water from groundwater
downgradient of the sites. Potential exposure levels cannot be estimated
with the data available.
5.7 ADEQUACY OF THE DATABASE
Section 104(i)(5) of CERCLA, 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 1,2-dichloroethene 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 1,2 dichloroethene.
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 or
eliminate the uncertainties of human health assessment. In the future, the
identified data needs will be evaluated and prioritized, and a substance-
specific research agenda will be proposed.
5.7.1 Identification of Data Needs
Physical and Chemical Properties. The physical and chemical
properties of both cis- and trans-1,2-dichloroethene have been described and
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71
5. POTENTIAL FOR HUMAN EXPOSURE
are readily available in the literature. Some of these physical properties
were required for assessing the fate and transport of 1,2-dichloroethene in
the environment because experimental data were not available. The
literature values were sufficient for performing the necessary estimates.
Production, Import/Export, Use, and Disposal. Production methods for
1,2-dichloroethene are described and no further information is required.
Current production and import/export volumes and usage data are presently
unavailable in the literature. Much of the information regarding
1,2-dichloroethene may be difficult to obtain because many manufacturing
companies maintain confidentiality. Historical production volumes have
been documented, whereas information regarding future domestic production,
and past, present and future imports and exports are lacking in the
literature. Furthermore, determining the percentage of 1,2-dichloroethene
that is used as a captive intermediate (i.e., the 1,2-dichloroethene
consumed in closed processes in which the compound is not isolated), as
opposed to its use as a solvent, is critical to estimating the amount
released to the environment. Differences in toxicity and environmental fate
also suggest that isomer-specific information on use and consumption is
important. Determination of the levels of 1,2-dichloroethene in consumer
products is essential for estimating the exposure to the general population.
With up-to-date and accurate production, import/export, and use data,
the extent of release into the environment and the subsequent potential for
human exposure could be more realistically determined. According to the
Emergency Planning and Community Right-to-Know Act of 1986, 42 U. S. C.
Section 11023, industries are required to submit chemical release and off-
site transfer information to the EPA. The Toxics Release Inventory (TRI),
which contains this information for 1987, became available in May of 1989.
This database will be updated yearly and should provide a list of industrial
production facilities and emissions.
Disposal methods have been described and appear to be satisfactory.
Even if information on the production, use and disposal of
1,2-dichloroethene were available, estimating its total release to the
environment would be difficult because substantial amounts of 1,2-dichloro-
ethene may be formed in the environment as an anaerobic biodegradation
product of other various chlorinated solvents.
Environmental Fate. Information concerning the partitioning of
1,2-dichloroethene in the environment is available; 1,2-dichloroethene
occurs in all environmental media. Information on the transport of
1,2-dichloroethene in environmental media is also available; however,
precise and accurate prediction of the behavior of 1,2-dichloroethene in the
environment is difficult because of the influence of site specific
environmental characteristics and the effects of competing fate processes,
such as volatilization and adsorption. Volatilization is expected to be an
important fate process; however, data on the rate of volatilization from
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72
5. POTENTIAL FOR HUMAN EXPOSURE
soil were not located in the available literature. Likewise, we do not know
if 1,2-dichloroethene is transported long distances from its point of
release in air, or if rapid oxidation prevents dispersal. A better
understanding in these areas will enable scientists to more accurately
assess the extent of human exposure to 1,2-dichloroethene, especially among
populations living near points of release to the environment.
Bioavailability from Environmental Media. No information is available
regarding inhalation, oral, or dermal absorption of 1,2-dichloroethene from
air, water, food, or soil. Exposure via contaminated drinking water is
particularly relevant to humans. Since 1,2-dichloroethene is a neutral
lipophilic chemical with a low molecular weight, it probably is readily
absorbed. The few available toxicity studies of animals exposed to
1,2-dichloroethene support this contention. Information pertaining to human
exposure to 1,2-dichloroethene in the environment and Che resultant
concentrations in human tissue was not located in the available literature
Studies of absorption of 1,2-dichloroethene from air, water, food, and soil
would allow for determination of the rate and extent of absorption from
each of these media and for comparison of the potential hazards posed by
1,2-dichloroethene within these media.
Food Chain Bioaccumulation. Few data are available describing the food
chain bioaccumulation of 1,2-dichloroethene. Experimental data are
unavailable; therefore, it is not known if the bioconcentration potential is
consistent with estimated values obtained from regression equations.
Estimates suggest the potential for 1,2-dichloroethene to bioconcentrate is
low. Biomagnification studies would enable scientists to assess the dangers
of human exposure to 1,2-dichloroethene from fish and seafood.
Exposure Levels in Environmental Media. Data describing exposure
levels in air, surface water, drinking water, groundwater, and soil are
limited. 1,2-Dichloroethene has been detected in urban and rural air, air
near hazardous waste sites, and indoor air. Where it is used as a dry
cleaning agent and in the manufacture of other chemicals, indoor air
concentrations of 1,2-dichloroethene are likely to be greater than
concentrations in outdoor air. Information concerning the number of persons
potentially exposed to 1,2-dichloroethene near waste sites, manufacturing
and production facilities, and use facilities, however, is not available.
In these areas and in areas of widespread use, the potential for human
exposure is high. Monitoring data that showed the existence of
1,2-dichloroethene in food other than fish could not be located.
1,2-Dichloroethene has been detected infrequently in drinking water
supplies. Estimates of human intake of 1,2-dichloroethene via air, water
and food are not available.
Exposure Levels in Humans. 1,2-Dichloroethene is not a naturally
occurring substance. Monitoring data pertaining to the presence of
1,2-dichloroethene in human urine, breast milk, blood or adipose tissue were
not located in the available literature.
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73
5. POTENTIAL FOR HUMAN EXPOSURE
Exposure Registries. No exposure registries for 1,2-dichloroetherie
were located. This compound is not currently one of the compounds for which
a subregistry has been established in the National Exposure Registry. The
compound will be considered in the future when chemical selections are made
for subregistries 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 certain
compounds.
5.7.2 On-going Studies
As part of the Third National Health and Nutrition Evaluation Survey
(NHANES III), the Environmental Health Laboratory Sciences Division of the
Center for Environmental Health and Injury Control, Centers for Disease
Control, will be analyzing human blood samples for 1,2-dichloroethene and
other volatile organic compounds. These data will give an indication of the
frequency of occurrence and background levels of these compounds in the
general population.
No studies on the environmental fate of 1,2-dichloroethene are in
progress. NIOSH is now updating its occupational exposure estimates with
additional information about exposure to trade name compounds. No other
information about on-going studies that would meet data needs on general
population and worker exposure to 1,2-dichloroethene were found.
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75
6. ANALYTICAL METHODS
The purpose of this chapter is to describe the analytical methods that
are available for detecting and/or measuring and monitoring
1,2 -dichloroethene in environmental media and in biological samples. The
intent is not to provide an exhaustive list of analytical methods that
could be used to detect and quantify 1,2-dichloroethene. Rather, the
intention is to identify well-established methods that are used as the
standard methods of analysis. Many of the analytical methods used to
detect 1,2-dichloroethene in environmental samples are the methods
approved by federal agencies 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 a trade association such as the
Association of Official Analytical Chemists (AOAC) and the American Public
Health Association (APHA). Additionally, analytical methods are included
that refine previously used methods to obtain lower detection limits, and/or
to improve accuracy and precision.
6.1 BIOLOGICAL MATERIALS
Methods of analysis for 1,2-dichloroethene in biological materials are
presented in Table 6-1. The purge and trap method of Lin et al. (1982) is a
suitable method for extraction and measurement of cis- and trans -
1,2-dichloroethene in body tissues. Recovery of trans-1,2-dichloroethene
varied with the type of body tissue; however, this finding generally agrees
with those of other investigators who have attempted to measure levels of
volatile halocarbons in body tissues. The headspace analysis methods of
Hara et al. (1980) and Uehori et al. (1987) allow qualitative identification
of 1,2-dichloroethene in biological materials. The methods most sensitive
for determining 1,2-dichloroethene levels in environmental samples, and the
advantages and disadvantages of the commonly used methods, are discussed in
Section 6.2. These also apply to biological samples.
6.2 ENVIRONMENTAL SAMPLES
Analytical methods for determining cis- and trans-1,2-dichloroethene in
environmental samples are presented in Table 6-2. Analysis of
1,2-dichloroethene in air samples can be determined by NIOSH method 1003
(NIOSH 1987).
Methodologies appearing in the literature for sampling
1,2-dichloroethene in air are essentially the same technique, with minor
changes. Capillary columns are more versatile in terms of separating the
contaminate of interest, and usually offer superior resolution. Different
detectors can be used, such as flame ionization detectors (FID), electron
capture detectors (ECD), Hall electroconductivity detectors (HECD), and mass
spectrometers (MS). The FID detector is the least sensitive of the four
listed to halogenated hydrocarbons, yet it is sensitive enough for
environmental samples. Solid sorbents other than charcoal have appeared in
some analytical methods, the most popular being the resin, TenaxN GC. In
the analysis of air samples for 1,2-dichloroethene, the weakest link in the
-------
TABLE 6-1. Analytical Methods for Determining 1,2-Dichloroethene in Biological Samples
Sample
Sample Matrix Sample Preparation Analytical Method Detection Accuracy8 Reference
Limit
Adipose, kidney,
and brain tissue
Blood
Blood
Body tissue
Mince and purge tissue at 60*C;
trap in TenaxTM; thermal desorption
Heat in a closed vial at 55"C
Mix with water; heat in a closed
vial at 40*C; headspace analysis
Homogenize and mix tissue with
water; heat in a closed vial at
40*C; headspace analysis
GC/HECD
GC/FID
GC/MS
GC/MS
50 pg 93.3±12.4% (adipose)
53.4t2.4%~ (kidney)
62.6t2.6X (brain)
No data No data
10-20 pg No data
10-20 pg No data
a,
Lin et al. 1982
Uehori et al. 1987
Hara et al. 1980
Kara et al. 1980
'Defined as the average percent recovery of a blank sample.
°trans isaner.
FID = flame ionization detectors; GC = gas chromatography; HECD = Hall electrolytic conductivity detector; MS = mass spectrometry.
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TABLE 6-2. Analytical Methods for Determining 1,2-Dichloroethene in Environmental Saaples
Sample Matrix
Sample Preparation
Analytical Method
Sample
Detection
Limit
Accuracy
Reference
Air
Uastewater
Charcoal tube collection
and CS2 desorption
Purge and trap onto
adsorbent; backflush to
cryogenically cooled trap
GC/FID
GC/HECD
(EPA 601)
16 ppm
0.10 iig/L
No data
91+19%
NIOSH 1987
EPA 1982
Uastewater
Soi I
Drinking water
Purge and trap onto
adsorbent; backflush to
cryogenically cooled trap
Purge and trap onto
adsorbent; rapid heating
desorption
Purge and trap onto
adsorbent; backflush to
cryogenically cooled trap
GC/MS
(EPA 601)
GC/MS
GC/HECD
1.6 ng/L
5 M9/kg
0.002 iig/l
99+12%
No data
8+7%
EPA 1982
EPA 1987b
EPA 1986e
Defined as the average percent recovery of a blank sample.
FID = flame ionization detectors; GC = gas chromatography; HECD = Hall electrolytic conductivity detector; MS = mass
spectrometry.
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-------
78
6. ANALYTICAL METHODS
process is adsorption to the solid sorbent. As a result, complete removal
of highly volatile compounds such as 1,2-dichloroethene from the air stream
may not occur.
EPA method 601 - purgeable halocarbons and EPA method 624 - purgeables
describe analysis of 1,2-dichloroethene in municipal and industrial
wastewater (EPA 1982). In both these methods, a 5 mL grab sample of water
is connected to an apparatus called a purging chamber. This chamber allows
an inert gas to bubble through the water sample; the gas flow is directed
through an adsorbent tube.
In EPA method 601, nitrogen or helium is the purging gas, and the
adsorbent column consists of two different adsorbents and a drying agent.
In EPA method 624, helium is the purging gas, and the adsorbent column is
made up of one adsorbent and a drying agent. The collected organics are
liberated from the sorbent by heating the sorbent column while backflushing
with an inert gas; these organics are then introduced into the GC.
EPA methods 601 and 624 were developed to analyze volatile priority
pollutants. In EPA method 601, analysis by GC uses a carbopack B column, a
poracil C column, and a HECD detector. In EPA method 624, analysis by GC
uses a carbopack B column and a mass spectrometer (MS), Since trans-
1,2-dichloroethene is a priority pollutant and cis-1,2-dichloroethene is
not, only the trans isomer is mentioned in this method.
Purge and trap methodology sometimes involves direct trapping of the
bubbled compound cryogenically. Water contamination can become a problem in
this method. The cryogenic trap described in EPA methods 601 and 624 is a
specialized item and may not be adaptable to all GCs. The considerations
discussed above regarding use of different columns and detectors also apply
here .
EPA method 502.1 is used to analyze 1,2-dichloroethene in finished or
raw source water (EPA 1986e). This method is similar to EPA method 601.
However, once the compound has been purged from the water sample to the
adsorbent tube, the compound is introduced to the GC by rapidly heating the
adsorbent tube, with no intermediate cryogenic trapping.
The EPA guidelines for contract laboratories include methodology for
water and soil sample analysis (EPA 1987b). The method listed in Table 6-2
is identical to EPA method 502.1 for the purposes of this discussion (except
for the use of a mass spectrometer as the detector). The procedure for
analyzing low-level contamination in soil is also similar to EPA method
502.1, except that the purging gas passes through a soil sample rather than
a water sample. For higher-level soil contamination, the soil sample is
first extracted with methanol. An aliquot of the extract is diluted with
water; then, the purge and trap methodology is followed.
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79
6. ANALYTICAL METHODS
6.3 ADEQUACY OF THE DATABASE
Section 104(i)(5) of CERCLA, 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 1,2-dichloroethene 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 1,2-dichloroethene.
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 or
eliminate the uncertainties of human health assessment, In the future,
these data needs will be evaluated and prioritized, and a substance - specific
research agenda will be proposed.
6.3.1 Identification of Data Needs
Methods for Determining Biomarkers of Exposure and Effect. The
available data base provides one analytical method adequate for the
measurement of cis- and trans-1,2-dichloroethene in body tissue; however,
there are no proven, reliable methods for quantifying levels in biological
fluids. There are no known biomarkers of exposure which are unique to 1,2-
dichloroethene. Therefore, standardized analytical methods for their
determination are not warranted.
There are no known biomarkers of effect which are unique to
1,2-dichloroethene. Therefore, standardized analytical methods for their
determination are not warranted.
Methods for Parent Compounds and Degradation Products in Environmental
Media. Numerous analytical methods exist for analysis of cis- and trans -
1,2-dichloroethene in environmental matrices, in addition to those
summarized above. These procedures may be used to identify areas of 1,2-
dichloroethene contamination, and to determine the potential threat to human
health of 1,2-dichloroethene in the environment. Standardized methods exist
for the analysis of drinking water, wastewater, soil and air. Standardized
methods for analyzing other media such as sediments and surface water will
aid in establishing levels of human exposure to 1,2-dichloroethene.
Inhalation is the most probable route of exposure, and atmospheric exposure
is likely to be of greatest concern to humans. However, the standardized
methods for detecting 1,2-dichloroethene in air appear to be weak. The
detection limit of 16 ppm, outlined by the NIOSH 1987 technique, is
relatively high. Information regarding the recovery efficiency of the NIOSH
1987 procedure for detecting 1,2-dichloroethene in air was lacking.
Therefore, the NIOSH 1987 procedure is not sufficiently sensitive or
accurate to assess background levels of 1,2-dichloroethene in air.
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6. ANALYTICAL METHODS
6.3.2 On-going Studies
On-going studies for developing new analytical methods for 1,2-
dichloroethene in environmental matrices could not be located. The
Environmental Health Laboratory Sciences Division of the Center for
Environmental Health and Injury Control, Centers for Disease Control, is
currently developing methods for the analysis of both cis- and trans-
1,2-dichloroethene in blood. These methods use purge and trap methodology
and magnetic sector mass spectrometry and provide detection limits in the
low parts per trillion range.
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81
7. REGULATIONS AND ADVISORIES
Table 7-1 summarizes national and state regulations and guidelines on
human exposure to 1,2-dichloroethene.
The Clean Water Effluent Guidelines regulate trans-1,2-dichloroethene
for the following industrial point sources: electroplating, organic
chemicals, steam electric, asbestos, timber products processing, metal
finishing, paving and roofing, paint formulating, gum and wood, and carbon
black (EPA 1988c).
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82
7. REGULATIONS AND ADVISORIES
TABLE 7-1. Regulations and Guidelines Applicable to 1,2-Dichloroethene
Agency
Description
Value
Reference
Regulations:
a. Air:
OSHA
b. Uater
EPA
c. Non-specific media:
EPA/OERR
Guidelines:
a. Air:
ACGIH
b. Other:
EPA
national
PEL (8-hour TUA) 200 ppm
1-Day health advisory for cis-1,2-
dichloroethene
chiId 4.0 mg/l
10-Day health advisory for cis-1,2-
dichloroethene
chiId 1.0 mg/L
adult 3.5 mg/L
Longer-term health advisory for cis-1,2-
dichloroethene
chi td 1.0 mg/L
adult 3.5 mg/L
1-Day health advisory for trans-1,2-
dichloroethene
chi Id 20.0 mg/L
10-Day health advisory for trans-1,2-
dichloroethene
chiId 1.43 mg/L
adult 5.0 mg/L
Longer-term health advisory for trans-1,2-
dichloroethene
chiId 1.43 mg/L
adult 5.0 mg/L
Reportable quantity for trans-1,2- 1000 lbs
dichloroethane
TUA for occupational exposure for 200 ppm
cis-, trans-1,2-dichloroethane
Reference dose for chronic oral exposure 20 iig/kg/d
for trans-1,2-dichloroethane
State
OSHA 1985
29 CFR 1910.1000
EPA 1987c
EPA 1987c
EPA 1987c
EPA 1987c
EPA 1987c
EPA 1987d
EPA 1987d
EPA 1987d
EPA 1987d
EPA 1987d
50 FR 13456
(04/04/85)
40 CFR 117, 302
ACGIH 1989
EPA 1988d
Regulations:
a. Air:
Connecticut
Massachusetts
Nevada
Virginia
Acceptable ambient limits of toxic air
pollutants (cis-, trans-1,2-
dichloroethane)
15.8 mg/m3 (8 hr) NAT ICH 1988
0.1 mg/m3 (24 hr)
18.8 mginr (8 hr)
13 mg/nr (24 hr)
-------
83
7. REGULATIONS AND ADVISORIES
TABLE 7-1 (Continued)
Agency
Description
Value
Reference
b. Water: Drinking water guidelines
cis-1,2-Dichloroethene
Cat ifornia
Kansas
Maine
Minnesota
Wisconsin
trans-1,2-Dichloroethene
California
Kansas
Minnesota
Wisconsin
1,2-Dichloroethenes
Ari zona
New Jersey (Proposed standard)
Vermont
16 |ig/L
70 /ig/L
400 fig/L
70 M9/L
100 /ig/L
16 /ig/L
70 /ig/L
70 ng/i
100 /ig/L
70 H9/1
10 (tg/L
70 fig/1
FSTRAC 1988
ACGIH = American Council of Governmental Industrial Hygienists
EPA = Environmental Protection Agency
0ERR = Office of Emergency and Remedial Response
0SHA = Occupational Safety and Health Adninistration
PEL = Permissible Exposure Limit
TWA = Time-Weighted Average.
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9. CIjOSSARY
Acute Exposure -- Exposure to a chemical for a duration of 14 days or less,
as specified in the Toxicological Profiles.
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 a 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.
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.
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.
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.
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.
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
occurred. The terms, as used here, include malformations and variations,
altered growth, and in utero death.
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.
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9. GLOSSARY
Immediately Dangerous to Life or Health (IDLH) -- The maximum environmental
concentration of a contaminant from which one could escape within 30 min
without any escape-impairing symptoms or irreversible health effects.
Intermediate Exposure -- Exposure to a chemical for a duration of 15-364
days as specified in the Toxicological Profiles.
Immunologic Toxicity -- The occurrence of adverse effects on the immune
system that may result from exposure to environmental agents such as
chemicals.
In Vitro -- Isolated from the living organism and artificially maintained,
as in a test tube.
In Vivo -- Occurring within the living organism.
Lethal Concentration^) (LClO) -- The lowest concentration of a chemical in
air which 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(LQ) (LDlq) "" The l°west dose of a chemical introduced by a
route other than inhalation that is expected to have caused death in humans
or animals.
Lethal Dose(50) (LD50) "" T^e dose a chemical which has been calculated
to cause death in 50% of a defined experimental animal population.
Lethal Time(5Q) (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 dose 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.
Malformations -- Permanent structural changes that may adversely affect
survival, development, or function.
Minimal Risk Level --An estimate of daily human exposure to a chemical that
is likely to be without an appreciable risk of deleterious effects
(noncancerous) over a specified duration of exposure.
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9. GLOSSARY
Mutagen -- A substance that causes mutations. A mutation is a change in the
genetic material in a body cell. Mutations can lead to birth defects,
miscarriages, or cancer.
Neurotoxicity -- The occurrence of adverse effects on the nervous system
following exposure to chemical.
No-Observed-Adverse-Effect Level (NOAEL) -- The dose of 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.
Permissible Exposure Limit (PEL) --An allowable exposure level in
workplace air averaged over an 8-hour shift.
q-j* -- The upper-bound estimate of the low-dose slope of the dose - response
curve as determined by the multistage procedure. The q^* can be used to
calculate an estimate of carcinogenic potency, the incremental excess cancer
risk per unit of exposure (usually g/L for water, mg/kg/day for food, and
g/m^ for air).
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 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 CERCLA. Reportable quantities are (1) 1 lb or
greater or (2) for selected substances, an amount established by regulation
either under CERCLA or under Sect. 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.
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9. GLOSSARY
Short-Term Exposure Limit (STEL) -- The maximum concentration to which
workers can be exposed for up to 15 min continually. No more than four
excursions are allowed per day, and there must be at least 60 mm between
exposure periods. The daily TLV-TWA may not be exceeded.
Tareet OrRan Toxicity -- This term covers a broad range of adverse effects
Qvstems ( e . f7 . , renal, cardiovascular)
on target organs or physiological systems
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) -- A concentration of a substance to which most
workers can be exposed without adverse effect. The TLV may be expressed as
a TWA, as a STEL, or as a CL.
Time-Weighted Average (TWA) -- An allowable exposure concentration averaged
over a normal 8-hour workday or 40-hour workweek.
Toxic Dose (TD50) -- A calculated dose of a chemical, introduced by a route
other than inhalation, which is expected to cause a specific toxic effect m
50% of a defined experimental animal population.
Uncertainty Factor (UF) -- A factor used in operationally deriving the RfD
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 m using LOAEL data rather
than NOAEL data. Usually each of these factors is set equal to 10.
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APPENDIX: PEER REVIEW
A peer review panel was assembled for 1,2-dichloroethene. The panel
consisted of the following members: Dr. Kirk Brown, Texas A&M University;
Dr. Carson Conuway, Research Scientist, American Health Foundation;
Dr. Curtis Klaassen, Associate Director, Environmental Health Science
Division; and Dr. Theodore Torkelson, Private Consultant. These experts
collectively have knowledge of 1,2-dichloroethenes' 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 brief explanation of the
rationale for their exclusion, exists as part of the administrative record
for this compound. A list of databases reviewed and a list of unpublished
documents cited are also included in the administrative record.
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 Agency for Toxic Substances and
Disease Registry.
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