TOXICOLOGICAL PROFILE FOR 

1,2-DICHLOROETHENE 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
 

Public Health Service
 

Agency for Toxic Substances and Disease Registry
 

August 1996 
1,2-DICHLOROETHENE 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. 
1,2-DICHLOROETHENE iii 

UPDATE STATEMENT
 

A Toxicological Profile for 1,2-dichloroethene was released in December 1990. This edition 

supersedes any previously released draft or final profile. 

Toxicological profiles are revised and republished as necessary, but no less than once every three 

years. For information regarding the update status of previously released profiles, contact ATSDR at: 

Agency for Toxic Substances and Disease Registry
 

Division of Toxicology/Toxicology Information Branch
 

1600 Clifton Road NE, E-29
 

Atlanta, Georgia 30333
 












1,2-DICHLOROETHENE 1 

1. PUBLIC HEALTH STATEMENT 

This public health statement tells you about 1,2-dichloroethene and the effects of exposure. 

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

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

long-term federal cleanup activities. Cis-1,2-dichloroethene has been found in at least 146 of the 

1,430 current or former NPL sites. Trans- 1,2-dichloroethene has been found in at least 563 of 

the 1,430 current or former NPL sites. In 336 of the NPL sites, 1,2-dichloroethene was found 

but the isomer was not specified. However, it’s unknown how many NPL sites have been 

evaluated for this substance. As more sites are evaluated, the sites with 1,2-dichloroethene may 

increase. This information is important because exposure to this substance may harm you and 

because these sites may be sources of exposure. 

When a substance 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. This release does not always lead to 

exposure. You are exposed to a substance only when you come in contact with it. You may be 

exposed by breathing, eating, or drinking the substance or by skin contact. 

If you are exposed to 1,2-dichloroethene, many factors determine whether you’ll be harmed. 

These factors include the dose (how much), the duration (how long), and how you come in 

contact with it. You must also consider the other chemicals you’re exposed to and your age, sex, 

diet, family traits, lifestyle, and state of health. 
1,2-DICHLOROETHENE 2 

1. PUBLIC HEALTH STATEMENT 

1 .1 WHAT IS 1,2-DICHLOROETHENE? 

1,2-Dichloroethene is also called 1,2-dichloroethylene. It is a highly flammable, colorless 

liquid with a sharp, harsh odor. You can smell very small amounts of 1,2-dichloroethene in 

air (beginning at a level of about 17 parts per million or ppm). There are two forms of 

1,2-dichloroethene; one form is called cis-1,2-dichloroethene and the other is called 

trans- 1,2-dichloroethene. Sometimes both forms are present as a mixture. 1,2-Dichloroethene 

is used most often to produce solvents and in chemical mixtures. 

1,2-Dichloroethene enters the environment through industrial activity of people. This 

chemical has been found in air, water, and soil. 1,2-Dichloroethene is released to the 

environment from chemical factories that make or use this chemical, from landfills and 

hazardous waste sites containing this chemical, from chemical spills, from burning of objects 

made of vinyl, and from breakdown of other chlorinated chemicals. 

1.2 WHAT HAPPENS TO 1,2-DICHLOROETHENE WHEN IT ENTERS 

THE ENVIRONMENT? 

1,2-Dichloroethene evaporates rapidly. When released to moist soil surfaces or to lakes, 

rivers, and other bodies of water, most of it evaporates into the air. Once in the air, it usually 

takes about 5-12 days for half of any amount of it to break down (half-life in air). 

1,2-Dichloroethene that is below soil surfaces in landfills or hazardous waste sites may 

dissolve in water, seep deeper into the soil, and possibly contaminate groundwater. Some 

1,2-dichloroethene may escape as a vapor. Once in groundwater, it takes about 13-48 weeks 

for half of a given amount to break down (half-life in water). There is a slight chance that 

small amounts of the 1,2-dichloroethene found in landfills will eventually break down into 

vinyl chloride, which is believed to be a more hazardous chemical. 
1,2-DICHLOROETHENE 3 

1. PUBLIC HEALTH STATEMENT 

1.3 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 the tap water in your home is contaminated, you could also be 

breathing 1,2-dichloroethene vapors while cooking, bathing, or washing dishes. There are no 

known products you can buy that contain 1,2-dichloroethene. People who are most likely to 

be exposed live near landfills and hazardous waste sites that contain this chemical, work at 

factories where this chemical is made or used, work at 1,2-dichloroethene contaminated 

landfills, or work as firefighters. Job-related exposure results from breathing in 1,2-dichloroethene 

from workplace air or from touching contaminated chemicals or materials. According 

to a survey conducted between 1981 and 1983 by the National Institute for Occupational 

Safety and Health (NIOSH), an estimated 215 people in the United States may have been 

exposed to 1,2-dichloroethene while working. 

People who live in cities or suburbs are more likely to be exposed than people living in rural 

areas. Most people who are exposed to 1,2-dichloroethene through air or water are exposed 

to very low levels, in the range of parts per million (ppm) to parts per billion (ppb). 

1.4 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. 

When 1,2-dichloroethene enters the body, the blood and other tissues absorb it. It is broken 

down to other compounds in the liver. Animal studies have looked at how quickl.y the 

compound enters and leaves the body and what may happen to it in the body. These animal 

studies describe effects at levels far greater than those levels at which most people would be 

exposed. No studies show specifically how 1,2-dichloroethene enters a person’s body and 

how it is changed or removed by the body. 
1,2-DICHLOROETHENE 4 

1. PUBLIC HEALTH STATEMENT 

1.5 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 its vapor can kill you. When animals breathed high 

levels of trans-1,2-dichloroethene for short or longer periods of time, their livers and lungs 

were damaged. The effects were more severe with longer exposure times. Animals that 

breathed very high levels of trans-1,2-dichloroethene had damaged hearts. Animals given 

extremely high doses of cis- or trans-1,2-dichloroethene by mouth died. Lower oral doses of 

cis-1,2-dichloroethene caused effects on the blood, such as decreased numbers of red blood 

cells, and effects on the liver. 

The long-term human health effects after exposure to low concentrations of 1,2-dichloroethene 

are not known. Results of a recent animal study suggest that an exposed fetus may not grow 

as quickly as one that is not exposed. No studies have been done to see whether cancer in 

people or animals is caused by exposure to 1,2-dichloroethene; exposure has not been shown 

to affect fertility in people or animals. 

1.6 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN 

EXPOSED TO 1,2-DICHLOROETHENE? 

Methods are available to measure concentrations of 1,2-dichloroethene in blood, urine, and 

tissues. However, these methods are not routinely used to determine whether a person has 

been exposed to this compound, because the expected breakdown products resulting from 

exposure to 1,2-dichloroethene may also result from exposure to other chemicals. 

1.7 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH? 

The federal government has developed regulatory standards and guidelines to protect people 

from possible health effects of 1,2-dichloroethene in water and air. The EPA has established 
1,2-DICHLOROETHENE 5 

1. PUBLIC HEALTH STATEMENT 

water quality guidelines to protect both aquatic life and people who eat fish and shellfish. 

The EPA Office of Drinking Water has set a drinking water regulation that states that water 

delivered to any user of a public water system shall not exceed 0.07 milligrams per liter 

(mg/L) for cis- 1,2-dichloroethene and 0.1 mg/L for trans- 1,2-dichloroethene. For very short term 

exposures (1 day) for children, EPA advises that concentrations in drinking water should 

not be more than 4 mg/L for cis- 1,2-dichloroethene or 20 mg/L for trans-1,2-dichloroethene. 

For l0-day exposures for children, EPA advises that drinking water concentrations should not 

be more than 3 mg/L for cis-1,2-dichloroethene or 2 mg/L for trans-1,2-dichloroethene. For 

industrial or waste disposal sites, any release of 1,000 pounds or more must be reported to the 

EPA. 

The National Institute for Occupational Safety and Health (NIOSH) and the American 

Conference of Governmental Industrial Hygienists (ACGIH) have established guidelines for 

occupational exposure to cis- or trans- 1,2-dichloroethene. Average concentrations should not 

exceed 200 ppm in the air. 

1.8 WHERE CAN I GET MORE INFORMATION? 

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

environmental quality department or: 

Agency for Toxic Substances and Disease Registry
 

Division of Toxicology
 

1600 Clifton Road NE, E-29
 

Atlanta, Georgia 30333
 

Phone: 404-639-6000
 

This agency can also tell you where to find occupational and environmental health clinics. 

These clinics specialize in recognizing, evaluating, and treating illness resulting from exposure 

to hazardous substances. 

 

1,2-DICHLOROETHENE 7 

2. HEALTH EFFECTS 

2.1 INTRODUCTION 

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

other interested individuals and groups with an overall perspective of the toxicology of 1,2­

dichloroethene. It contains descriptions and evaluations of toxicological studies and epidemiological 

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

data to public health. 

There are two geometric isomers of 1,2-dichloroethene, the cis form and the trans form. Isomers of an 

organic substance are different structures with the same molecular formula. In this case, the cis and 

trans forms have the chlorine atoms in different positions around the double bond. Each of these 

geometric isomeric forms has slightly different physical, chemical, and biological properties, because 

of their different molecular structures. These properties determine how the compound may affect the 

health of exposed individuals and how 1,2 dichloroethene behaves in air, water, and soil. The trans 

isomer is the more common industrial product. 

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

2.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 

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

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

-inhalation, oral, and dermal; and then by health effect--death, systemic, immunological, 

neurological, reproductive, developmental, genotoxic, and carcinogenic effects. These data are 

discussed in terms of three exposure periods-acute (14 days or less), intermediate (15-364 days), and 

chronic (365 days or more). 

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

figures. The points in the figures showing no-observed-adverse-effect levels (NOAELs) or 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. “Serious” effects are 
1,2-DICHLOROETHENE 8 

2. HEALTH EFFECTS
 

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

respiratory distress or death). “Less serious” effects are those that are not expected to cause significant 

dysfunction or death, or those whose significance to the organism is not entirely clear. ATSDR 

acknowledges that a considerable amount of judgment may be required in establishing whether an end 

point should be classified as a NOAEL, “less serious” LOAEL, or “serious” LOAEL, and that in some 

cases, there will be insufficient data to decide whether the effect is indicative of significant dysfunction. 

However, the Agency has established guidelines and policies that are used to classify these end points. 

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

between “less serious” and “serious” effects. The distinction between “less serious” effects and “serious” 

effects is considered to be important because it helps the users of the profiles to identify levels of 

exposure at which major health effects start to appear. LOAELs or NOAELs should also help in 

determining whether or not the effects vary with dose and/or duration, and place into perspective the 

possible significance of these effects to human health. 

The significance of the exposure levels shown in the LSE tables and figures may differ depending on 

the user’s perspective. Public health officials and others concerned with appropriate actions to take at 

hazardous waste sites may want information on levels of exposure associated with more subtle effects 

in humans or animals (LOAEL) or exposure levels below which no adverse effects (NOAELs) have 

been observed. Estimates of levels posing minimal risk to humans (Minimal Risk Levels or MRLs) 

may be of interest to health professionals and citizens alike. 

Estimates of exposure levels posing minimal risk to humans (Minimal Risk Levels or MRLs) have 

been made for 1,2-dichloroethene. An MRL is defined as an estimate of daily human exposure to a 

substance that is likely to be without an appreciable risk of adverse effects (noncarcinogenic) over a 

specified duration of exposure. MRLs are derived when reliable and sufficient data exist to identify 

the target organ(s) of effect or the most sensitive health effect(s) for a specific duration within a given 

route of exposure. MRLs are based on noncancerous health effects only and do not consider 

carcinogenic effects, MRLs can be derived for acute, intermediate, and chronic durationexposures for 

inhalation and oral routes. Appropriate methodology does not exist to develop MRLs for dermal 

exposure. 

Although methods have been established to derive these levels (Barnes and Dourson 1988; EPA 

1990a), uncertainties are associated with these techniques. Furthermore, ATSDR acknowledges 
1,2-DICHLOROETHENE 9 

2. HEALTH EFFECTS
 

additional uncertainties inherent in the application of the procedures to derive less than lifetime MRLs. 

As an example, acute inhalation MRLs may not be protective for health effects that are delayed in 

development or are acquired following repeated acute insults, such as hypersensitivity reactions, asthma, 

or chronic bronchitis. As these kinds of health effects data become available and methods to assess levels 

of significant human exposure improve, these MRLs will be revised. 

A User’s Guide has been provided at the end of this profile (see Appendix B). This guide should aid in 

the interpretation of the tables and figures for Levels of Significant Exposure and the MRLs. 

2.2.1 Inhalation Exposure 

2.2.1.1 Death 

A single fatality was reported to have occurred after inhalation of 1,2dichloroethene 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 of a single exposure by inhalation of trans-1,2-dichloroethene has been determined in mice 

(Gradiski et al. 1978). The lethal concentration resulting in 50% fatalities (LC50) was 21,723 ppm trans1,2-dichloroethene, presented in Table 2-l and in Figure 2-1, and 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- 1 ,2dichloroethene in any animal species. 

2.2.1.2 Systemic Effects 

No studies were located regarding gastrointestinal, endocrine, dermal, or ocular effects in humans or 

animals after inhalation exposure to cis- or trans-1,2-dichloroethene. The highest NOAEL values and all 

LOAEL values from each reliable study for each systemic effect in each species and duration category are 

recorded in Table 2-1 and plotted in Figure 2-l. 





1,2-DICHLOROETHENE 15 

2. HEALTH EFFECTS
 

Respiratory Effects. No studies were located regarding respiratory effects in humans following 

inhalation exposure to cis- or trans-1,2-dichloroethene. 

Pathologic changes in the lung have been described in rats exposed to trans-1,2-dichloroethene (Freundt 

et al. 1977). The pathology consisted of pulmonary capillary hyperemia, and alveolar septal distention. As 

shown in Table 2-l and Figure 2-1, after repeated exposure to 200 ppm effects in the lung were more 

severe than effects that occurred after a single exposure. This is the only reported study of lung pathology 

in animals exposed to trans-1,2-dichloroethene. This study had several weaknesses: several of the control 

rats also developed pulmonary capillary hyperemia and alveolar septal distention, a small number of 

animals were examined, and the upper respiratory tract was not examined for pathology. Also, a statistical 

evaluation of the histological data was not presented. Corroborative evidence for toxicity of trans-1,2-

dichloroethene to the lung has not been reported. 

No studies were located regarding the 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 severe fibrous swelling of the myocardium and hyperemia. 

As shown in Table 2-l and Figure 2- 1, the effects were evident after an 8-hour exposure to 3,000 ppm but 

not after exposures 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 ,2dichloroethene. 

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 erythrocytes was 
1,2-DICHLOROETHENE 16 

2. HEALTH EFFECTS
 

observed after an 8-hour exposure to 1,000 ppm trans-1,2-dichloroethene. No studies were located 

regarding hematological effects in animals after inhalation exposure to cis- 1,2dichloroethene. 

Musculoskeletal Effects. No studies were located regarding musculoskeletal effects in humans 

following inhalation exposure to cis- or trans-1,2-dichloroethene. 

Histological examination of muscle tissue revealed no compound-related effects in rats exposed to 200, 

1,000 or 3,000 ppm trans-1,2dichloroethene for up to 16 weeks (Freundt et al. 1977). 

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 accumulation of liver lobules and Kupffer cells, 

have been observed in a small group of 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 in Kupffer cells. However, the incidence 

and severity of fat accumulation did increase with increasing exposure levels and duration. This study 

is the basis of an acute-duration inhalation MRL of 0.2 ppm for trans-1,2-dichloroethene, as explained 

in the footnote to Table 2-l and in Appendix A. In the same study, rats were exposed to 200 ppm 

trans-1,2-dichloroethene for 8 hours per day, 5 days per week for either 8 or 16 weeks. Fatty 

accumulation was found in hepatocytes (liver lobules). This LOAEL of 200 is the basis for the 

intermediate-duration inhalation MRL of 0.2 ppm for trans-1,2-dichloroethene, as explained in the 

footnote to Table 2-l and in Appendix A. 

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 effects due to the 

cis isomer are stronger than those of the trans isomer. These effects suggest inhibition of the mixed 

function oxidase system. 
1,2-DICHLOROETHENE 17 

2. HEALTH EFFECTS
 

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

exposure to cis- or trans- 1,2-dichloroethene. 

Histological examination of the kidney revealed no compound-related effects in rats exposed to 200, 

1,000 or 3,000 ppm trans-1,2-dichloroethene for up to 16 weeks (Freundt et al. 1977). No studies 

were located regarding renal effects in animals after inhalation exposure to cis-1,2-dichloroethene. 

Body Weight Effects. No studies were located regarding body weight effects in humans 

following inhalation of cis- or trans-1,2-dichloroethene. 

Weight gain in pregnant rats was inversely related to dose from 2,000 to 12,000 ppm 

trans-1,2-dichloroethene, and was concomitant with the reduced food consumption of dams at 

2,000 ppm on gestational days 13-15 in the developmental study of Hurtt et al. (1993). No studies 

were located regarding body weight effects in animals after inhalation exposure to cis-1,2-dichloroethene. 

Other Systemic Effects. No studies were located regarding other systemic effects in humans 

following inhalation of cis- or trans-1,2-dichloroethene. 

Several other systemic effects were found in the study of Hurtt et al. (1993). Brown-stained periocular 

hair was observed in all rats exposed to trans-1,2-dichloroethene at concentrations of 

2,000-12,000 ppm. This effect was also observed in 1 of 24 control rats. Reduced food consumption 

of dams was observed on gestational days 13-15 at a concentration of 2,000 ppm. No studies were 

located regarding other systemic effects in animals after inhalation exposure to cis-1 ,2dichloroethene. 

2.2.1.3 Immunological and Lymphoreticular Effects 

Detailed studies were not located regarding the immunological or lymphoreticular effects-in humans or 

animals after inhalation exposure to cis- or trans-1 ,2dichloroethene. 

Freundt et al. (1977), however, reported that inhalation exposure of rats to trans-1,2-dichloroethene at 

a concentration of 200 ppm or greater caused slight to severe fatty degeneration of Kupffer cells. 

Kupffer cells are highly phagocytic macrophages involved in protecting the systemic circulation from 
1,2-DICHLOROETHENE 18 

2. HEALTH EFFECTS
 

gastrointestinal bacteria. In addition, decreased leukocyte (white blood cell) counts were observed in rats 

after an 8-hour exposure to 200 and 1,000 ppm trans-1 ,2dichloroethene, and pneumonic infiltration was 

observed after 8 and 16 weeks exposure to 200 ppm, suggesting that inhalation of trans- 1,2­

dichloroethene may have adverse immunological effects. 

2.2.1.4 Neurological Effects 

Inhalation of high concentrations of vaporized trans-1,2-dichloroethene depresses the central nervous 

system in humans. Low levels of trans-1,2dichloroethene have been reported to cause neurological effects 

(Lehmann and Schmidt-Kehl 1936). Inhalation of 6.8-8.8 mg/L (1,700-2,220 ppm) of trans-1,2­

dichloroethene for 5 minutes, or of 4.8 mg/L (1,200 ppm) for 10 minutes, reportedly caused nausea, 

drowsiness, fatigue, vertigo, and intracranial pressure in two human subjects. It is uncertain whether the 

human subjects were exposed to a vapor or an aerosol; however, based on information on the volatility of 

trans-1,2-dichloroethene, it was likely a vapor (see Chapter 3). Also, the degree of purity of the trans 

isomer and the precise concentrations are unclear. 

The effects of inhaled cis- or trans-1,2-dichloroethene on the nervous system have not been extensively 

examined in animals. Hurtt et al. (1993) reported increased incidences of lethargy and salivation in 

pregnant rats exposed to 12,000 ppm trans-1,2-dichloroethene. Behavioral changes have been observed in 

mice exposed acutely (4 hours) to 1,2dichloroethene (form not specified) (De Ceaurriz et al. 1983). The 

reported changes consisted of a dose-related decrease in the duration of immobility in the “behavioral 

despair” swimming test. A 45% decrease in the total duration of immobility occurred at a concentration of 

1,720 ppm. The neurological significance of changes in the duration of swimming immobility is not 

known. Frantik et al. (1994) studied inhibition of propagation and maintenance of the electrically evoked 

seizure discharge in rats and mice. The air concentration evoking a 30% depression in the duration of 

hindlimb tonic extension in rats was 1,810 ppm and the air concentration evoking a 30% increase in the 

latency for hindlimb tonic extension in mice was 

3,400 pp. 

2.2.1.5 Reproductive Effects 

No studies were located regarding reproductive effects in humans after inhalation exposure to cis- or 

trans- 1,2-dichloroethene. 
1,2-DICHLOROETHENE 19 

2. HEALTH EFFECTS
 

Significant increases in the mean number of resorptions per litter were seen in rats exposed to 6,000 

and 12,000 ppm of trans-1,2-dichloroethene for 6 hours per day on days 7-16 of gestation (Hurtt et al. 

1993). The authors interpreted this increase as not being treatment related because resorption values 

were within the range of historical controls. No studies were located regarding reproductive effects in 

animals after inhalation exposure to cis-1,2-dichloroethene. 

2.2.1.6 Developmental Effects 

No studies were located regarding developmental effects in humans after inhalation exposure to cis- or 

trans- 1,2-dichloroethene. 

Inhalation exposure to trans-1,2-dichloroethene has been shown to affect fetal weight in animals. Hurtt 

et al. (1993) administered trans-1,2-dichloroethene to pregnant rats 6 hours daily, on days 7-16 of 

gestation, at 0, 2,000, 6,000, or 12,000 ppm. Mean fetal weights were significantly reduced in the 

litters of the dams exposed to 12,000 ppm. However, the reduced mean fetal weights probably 

resulted from reduced food consumption and reduced weight gain, which were seen in the pregnant 

rats in this study. No studies were located regarding developmental effects in animals after inhalation 

exposure to cis-1,2-dichloroethene. 

2.2.1.7 Genotoxic Effects 

No studies were located regarding in vivo genotoxic effects in humans or animals after inhalation 

exposure to cis- or trans- 1,2-dichloroethene. 

Genotoxicity studies (in vitro) are discussed in Section 2.5. 

2.2.1.8 Cancer 

No studies were located regarding cancer in humans or animals after inhalation exposure to cis- or 

trans-1,2-dichloroethene. 
1,2-DICHLOROETHENE 20 

2. HEALTH EFFECTS 

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. 

Lethal effects of orally-administered trans-1,2-dichloroethene in rats and mice have been investigated. 

Acute-duration dose levels exceeding 1,000 mg/kg are lethal in both species: 7 of 10 rats died 

following exposure to 1,130 mg/kg/day trans-1,2-dichloroethene (Freundt et al. 1977), and 2 of 6 rats 

died following exposure to 4,900 mg/kg/day cis-1,2-dichloroethene (McMillan 1986). In mice, LD50 

values ranging from 2,200 mg/kg/day (males) to 2,400 mg/kg/day (females) were reported from 

trans-1,2-dichloroethene exposure (Munson et al. 1982). The difference in these values among and 

between rats and mice could be attributable to a number of different factors, including species 

differences, strain differences, 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 rats 

(Hayes et al. 1987), and hyperemia of the mucosal surface of the stomach and small intestine in mice 

(Barnes et al. 1985). In a 16day study, increased mortality was observed in rats exposed to 

970 mg/kg/day cis-1,2-dichloroethene; 2 of 20 rats died within the first week of dosing (McCauley et 

al. 1990). 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 10 male rats treated with 290 mg/kg/day, 4 of 10 male rats treated with 870 mg/kg/day, and 1 of 10 

female rats treated with both 32 and 97 mg/kg/day died within the first week of dosing. The incidence 

of these deaths was not statistically significant when compared with controls (l/20); no other rats died 

during the 90-day treatment, and the authors could not specifically relate the death to the chemical 

exposure (McCauley et al. 1990). The LD 5O 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. 








1,2-DICHLOROETHENE 29 

2. HEALTH EFFECTS 

2.2.2.2 Systemic Effects 

No studies were located regarding ocular effects in humans or animals after oral exposure to cis- or 

trans-1,2-dichloroethene. The highest NOAEL values and all LOAEL values from each reliable study 

for each systemic effect in each species and duration category are recorded in Table 2-2 and plotted in 

Figure 2-2. 

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-dichloroethene on the respiratory tract of animals have not been 

examined extensively. As shown in Table 2-2 and Figure 2-2, male mice have been shown to tolerate 

exposure to 387 mg/kg body weight per day of trans-1,2-dichloroethene administered in drinking water 

for up to 90 days without developing histopathological changes in the lung (Barnes et al. 1985). The only 

change reported in this study was a slight decrease (11%) in lung weight in female mice at 452 

mg/kg/day. No change in lung weight occurred in male rats exposed to 3,114 mg/kg/day trans1,2dichloroethene 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. It is notable that similar changes have 

been observed in rats exposed by inhalation to trans-1,2-dichloroethene (see 

Section 2.2.1.2). 

Cardiovascular Effects. No studies were located regarding cardiovascular effects in humans 

following oral exposure to cis- or trans-1,2-dichloroethene. 

Female rats exposed to 1,130-l ,400 mg/kg trans-1 ,2dichloroethene through oral gavage (single 

exposure) showed changes in cardiac muscle structure along with swelling and hyperemia (Freundt et 

al. 1977). No cardiovascular effects were noted in rats exposed to 1,900 mg/kg/day cis-1,2-dichloroethene 

for 14 days or 870 mg/kg/day cis-1,2-dichloroethene for 90 days (McCauley et al. 1990). 

Gastrointestinal Effects. No studies were located regarding gastrointestinal effects in humans 

following oral exposure to cis- or trans- 1,2-dichloroethene. 
1,2-DICHLOROETHENE 30 

2. HEALTH EFFECTS
 

Mice that received lethal doses of trans- 1,2-dichloroethene had hyperemia of the stomach and small 

intestines (Barnes et al. 1985). No gastrointestinal effects were noted in rats exposed to 

1,900 mg/kg/day cis-1,2-dichloroethene for 14 days or 870 mg/kg/day cis- 1 ,2dichloroethene for 

90 days (McCauley et al. 1990). 

Hematological Effects. No studies were located regarding hematological effects in humans 

following oral exposure to cis- or trans- 1 ,2-dichloroethene. 

McMillan (1986) reported unchanged values of electrolytes, total blood cell counts, and total leukocyte 

counts, as compared to controls, from 14-day administration of a 50% mixture of the l,2dichloroethene 

cis and trans isomers (480 mg/kg/day) in rats. In contrast, the same dose, administered over 30 

days, resulted in a significant depression of the total blood cell count, the red blood cell count, 

peripheral blood hemoglobin, and hematocrit levels. 

No significant changes in hematological parameters occurred in rats (Hayes et al. 1987) or mice 

(Barnes et al. 1985) following oral exposure to trans-1,2-dichloroethene. As shown in Table 2-2 and 

Figure 2-2, rats tolerated repeated doses of 3,114 mg/kg/day (males) and 2,809 mg/kg/day (females) of 

trans-1 ,2dichloroethene in drinking water (emulsified with emulphor, a polyethoxylated vegetable oil) 

for 90 days without exhibiting significant hematological abnormalities (Barnes et al. 1985; Hayes et al. 

1987). In contrast, dose-related hematotoxicity was the most evident effect in rats exposed orally by 

gavage to cis-1,2-dichloroethene in corn oil (McCauley et al. 1990). Decreased red blood cell count 

and hematocrit levels were observed in female rats exposed to 290 mg/kg/day for 14 days. No such 

changes were detected in female rats after exposure to 97 mg/kg/day or in male rats at all dose levels. 

Based on this value, an acute-duration oral MRL of 1 mg/kg/day was calculated for cis-1,2­

dichloroethene as described in the footnote to Table 2-2 and in Appendix A. 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 290 mg/kg/day. The NOAEL level was 32 

mg/kg/day. This. value was used for derivation of an intermediate-duration oral MRL –for cis-1,2­

dichloroethene of 0.3 mg/kg/day as described in the footnote to Table 2-2 and in Appendix A. 

Musculoskeletal Effects. No studies were located regarding musculoskeletal effects in humans 

following oral exposure to cis- or trans- 1,2-dichloroethene. 
1,2-DICHLOROETHENE 31 

2. HEALTH EFFECTS
 

Histological examination of muscle tissue revealed no compound-related effects in rats exposed to 1,900 

or 870 mg/kg/day of cis-1,2-dichloroethene for 14 or 90 days, respectively (McCauley et al. 1990), or in 

rats exposed by gavage to 1,600 mg/kg/day of trans-1,2-dichloroethene (Freundt et al. 1977). 

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. At 1,130 mg/kg/day of trans- 1,2-dichloroethene, 2 of 10 rats 

had severe fatty infiltration of the liver lobules and Kupffer cells; however, these effects were not seen 

in the rats given higher doses (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 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. However, at 

175 mg/kg/day increased serum alkaline phosphatase was seen, indicating some degree of hepatic 

damage (Barnes et al. 1985). 

McMillan (1986) examined the hepatic toxicity of cis- and trans-1,2-dichloroethene in rats after oral 

and intraperitoneal administration, respectively. At an exposure level of 4,400 mg/kg (single dose) of 

trans-1,2-dichloroethene, a significant increase in plasma alanine aminotransferase was noted, and at 

2,500 mg/kg (single dose) of cis-1,2-dichloroethene, a significant increase in plasma sorbitol 

dehydrogenase activity was noted. Intermediate exposure (30 days) did not result in any treatmentrelated 

lesions in the liver. However, significantly elevated liver weights were noted at 480 mg/kg/day 

of a mixture of the cis and trans isomers for 30 days. 

Biochemical changes in the liver have been reported in mice and rats exposed to cis- and 

trans-1,2-dichloroethene (Barnes et al. 1985; Jenkins et al. 1972). However, a connection between 

these biochemical changes and the 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 1,500 mg/kg 
1,2-DICHLOROETHENE 32 

2. HEALTH EFFECTS
 

of cis- or trans-1,2dichloroethene (Jenkins et al. 1972). Although the changes observed in 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 treatment group, and the lack of reporting of animal 

responses to dosing. A dose-related decrease in the levels of serum glutamicoxaloacetic transaminase 

(SGOT) and serum glutamic-pyruvic transaminase (SGPT) was 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. Increased serum alkaline phosphatase and increased relative 

liver weights were seen in male mice exposed to 175 mg/kg/day of trans-1,2-dichloroethene for 90 days. 

No such effects were noted in female mice. Based on a NOAEL of 17 mg/kg/day, an intermediateduration oral MRL for trans-1,2-dichloroethene of 0.2 mg/kg/day was calculated as described in the 

footnote to Table 2-2 and in Appendix A. 

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 assessed by Barnes 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 bg 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. 

A dose-related increase in relative liver weight was observed in rats exposed for 14 and 90 days to 

cis-1,2-dichloroethene (McCauley et al. 1990). In the 90-day study, effects were significant at 

97 mg/kg/day and above. Slight increases in serum cholesterol were observed in the female rats in the 

14-day study, and slight decreases in SGOT 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. 

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 laboratory 

animals. The few studies that have been reported provide evidence to suggest that the kidney is 
1,2-DICHLOROETHENE 33 

2. HEALTH EFFECTS
 

probably not a primary target for toxicity of trans-1,2-dichloroethene. As presented in Table 2-2 and 

Figure 2-2, animals tolerated repeated exposure to trans-1 ,2dichloroethene in drinking water without 

adverse effects on the kidney. A dose-related increase in absolute and relative kidney weight occurred 

in female rats treated with trans-1,2-dichloroethene for 90 days, but no histopathological lesions were 

identified (Hayes et al. 1987). No detectable chemically-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 study (Barnes et al. 1985; Hayes et al. 1987). 

A significant increase in rat kidney weight was reported from a 16-day oral exposure to a 50% mixture 

of the 1,2-dichloroethene isomers (480 mg/kg/day) (McMillan 1986). An increase in absolute and 

relative kidney weight, along with a decrease in blood urea nitrogen, was also found in female rats 

exposed for 14 days to 970 mg/kg/day of cis-1,2-dichloroethene, and in male rats orally exposed to 

1,900 mg/kg/day of cis-1,2-dichloroethene (McCauley et al. 1990). However, these changes did not 

occur in female rats exposed to 870 mg/kg/day of the cis isomer or less for 90 days. In male rats 

exposed to 870 mg/kg/day of cis-1,2-dichloroethene for 90 days, a significant increase in relative 

kidney weight and decreases in blood urea nitrogen and creatinine levels occurred. No changes 

occurred in males exposed to 1,900 mg/kg/day or less for 14 days. The toxicological significance of 

decreased blood urea nitrogen and creatinine levels is not clear since increases in these parameters are 

usually associated with renal toxicity. Furthermore, no histological evidence of kidney pathology was 

observed. In the absence of histological and clinical evidence of renal toxicity, the toxicological 

significance of the increased kidney weight is not known. 

Endocrine Effects. No studies were located regarding endocrine effects in humans following oral 

exposure to cis-or trans-1,2-dichloroethene. 

Histological examination revealed no compound-related effects in the thyroid in rats exposed to 

cis-1,2-dichloroethene at doses up to 1,900 or 870 mg/kg/day for 14 or 90 days, respectively 

(McCauley et all 1990). 

Dermal Effects. No studies were located regarding dermal effects in humans following oral 

exposure to cis- or trans- 1,2-dichloroethene. 
1,2-DICHLOROETHENE 34 

2. HEALTH EFFECTS
 

Histological examination revealed no compound-related effects on the skin of rats exposed to cis-1,2­

dichloroethene at doses up to 1,900 or 870 mg/kg/day for 14 or 90 days, respectively (McCauley et al. 

1990). 

Body Weight Effects. No studies were located regarding body weight effects in humans following oral 

exposure to cis- or trans-1 ,2dichloroethene. 

Body weight was not altered either by 21 or 210 mg/kg/day of trans-1,2-dichloroethene administered 

for 14 days to mice by gavage (Barnes et al. 1985). In rats, body weight was not altered by a 16day 

exposure to a 50% mixture of the 1,2-dichloroethene isomers (480 mg/kg/day) (McMillan 1986), nor 

by exposure to trans-1,2-dichloroethene (353-3,114 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. 1990). The changes were not 

dose-related; increased body weight gain occurred at 97 and 290 mg/kg/day and decreased body 

weight gain occurred at 970 and 1,900 mg/kg/day. The toxicological significance of these binodal 

body weight changes over a 14-day treatment period is not clear, although it could be due to decreased 

food intake at higher doses. In the 90-day study, only the male rats receiving the highest dose of 

cis-1,2-dichloroethene (870 mg/kg/day) had significantly decreased body weight gain when compared 

with control males. 

Other Systemic Effects. No studies were located regarding other systemic effects in humans 

following oral exposure to cis-or trans-1,2-dichloroethene. 

In female rats, a significant increase in water consumption was seen at 97 mg/kg/day. The authors 

stated that since cis-1,2-dichloroethene was administered by gavage, this effect must be considered to 

be compound-related and not associated with water palatability. They additionally noted that 

determining whether this effect is related to the compound’s influence on the renal, central nervous 

system, or other-organ system will require more data (McCauley et al. 1990). 

2.2.2.3 Immunological and Lymphoreticular Effects 

No studies were located regarding immunological effects in humans following oral exposure to cis- or 

trans- 1,2-dichloroethene. 
1,2-DICHLOROETHENE 35 

2. HEALTH EFFECTS
 

The effect of orally-administered trans-1,2-dichloroethene on the immune system has been investigated 

in rats and mice. No effects were seen on the spleen (Freundt et al. 1977; McCauley et al. 1990) or 

on leukocyte counts (Barnes et al. 1985; McMillan 1986; Munson et al. 1982) in rats or mice. Barnes 

et al. (1985) reported increased leukocyte count and decreased relative thymus weight in female mice 

exposed to 224 mg/kg/day of trans-1,2-dichloroethene for 90 days. Mice exposed to 

trans-1,2-dichloroethene (up to 220 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-1,2dichloroethene in drinking water for 90 days had no effect on the cell-mediated 

immune status of either sex or on 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 each of 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. 

Immunological effects were noted from exposure to 1,900 mg/kg/day of cis-1,2-dichloroethene in rats 

for 14 days, while an increase in absolute and relative thymus weights was noted in female rats 

exposed to 870 mg/kg/day for 90 days (McCauley et al. 1990). 

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, though acute exposure and stimuli/response research do provide insight. 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. 1990). Central nervous system depression (not further specified) was reported in rats treated with 

cis-1,2-dichloroethene at 1,900 mg/kg/day for 14 days (McCauley et al. 1990). The highest NOAEL 
1,2-DICHLOROETHENE 36 

2. HEALTH EFFECTS
 

value and the LOAEL values from each reliable study with neurological end points are presented in 

Table 2-2 and plotted in 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. 

2.2.2.5 Reproductive Effects 

No studies were located regarding reproductive effects in humans following oral exposure to cis- or 

trans- 1,2-dichloroethene. 

Neither acute nor intermediate exposures (14 and 90 days) have caused histological changes in 

reproductive organs of rats exposed to levels of cis-1,2-dichloroethene up to 1,900 mg/kg/day 

(McCauley et al. 1990). Rats exposed by gavage showed no treatment-related lesions in mammary 

glands, clitoral glands, ovaries, uterus, seminal vesicles, prostate, testes or preputial glands. No 

treatment-related histopathological lesions in the reproductive organs were seen in rats exposed to 

trans-1,2-dichloroethene for up to 90 days (Barnes et al. 1985; Hayes et al. 1987). 

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

to cis- or trans-1,2-dichloroethene: 

2.2.2.6 Developmental Effects 

2.2.2.7 Genotoxic Effects 

Genotoxicity studies- are discussed in Section 2.5. 

2.2.2.8 Cancer 
1,2-DICHLOROETHENE 37 

2. HEALTH EFFECTS 

2.2.3 Dermal Exposure 

2.2.3.1 Death 

No studies were located regarding lethal effects in humans following dermal exposure to cis- or 

trans- 1.2-dichloroethene. 

No deaths were reported from application of trans-1,2-dichloroethene at 5,000 mg/kg body weight on 

clipped, intact skin of 2 male and 3 female rabbits (Brock 1990). Table 2-3 summarizes the 

significant dermal exposure studies, presenting the highest NOAEL values and all LOAEL values from 

each important study. No studies were located regarding lethal effects in animals following dermal 

exposure to cis- 1,2-dichloroethene. 

2.2.3.2 Systemic Effects 

No dermal exposure studies of cis- or trans-1,2 dichloroethene were located regarding respiratory, 

cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, or endocrine effects in 

humans or animals. 

Dermal Effects. No studies were located regarding dermal effects in humans following dermal 

exposure to cis- or trans- 1,2-dichloroethene. 

Dermal effects have been shown in laboratory animals exposed dermally to trans-1,2-dichloroethene. 

Application of 170 mg/kg (0.5 mL) of trans-1,2dichloroethene for 24 hours to clipped, intact skin of 

1 female and 5 male rabbits under an occlusive wrapping produced mild or moderate erythema at all 

observation times (24, 48 and 72 hours) (Brock 1990). In a separate experiment (Brock 1990), 

5,000 mg/kg of trans-1,2-dichloroethene was applied to the clipped, intact skin of 2 male and 3 female 

rabbits. Severe dermal irritation was observed, but no clinical signs of toxicity other than body weight 

loss were found. No studies were located regarding dermal effects in animals following dermal 

exposure to cis- 1,2-dichloroethene. 

1,2-DICHLOROETHENE 39 

2. HEALTH EFFECTS
 

Ocular Effects. An early study by Lehmann and Schmidt-Kehl (1936) reported a slight burning of 

the eyes in two human subjects exposed for 30 minutes to concentrations between 830 and 2,220 ppm 

of trans-1,2-dichloroethene in air. The subjects were exposed under controlled conditions, not as an 

occupational accident. It is not certain whether the subjects were exposed to a vapor or to an aerosol 

of this chemical. The accuracy of the reported exposure levels is questionable because of the 

insensitivity of the methods used in 1936 to measure the concentration of 1,2dichloroethene in air. 

Also, the degree of purity of the trans isomer used is uncertain. No studies were located regarding 

ocular effects in humans following dermal exposure to cis-1,2-dichloroethene. 

Severe corneal opacity, moderate iritis, conjunctivitis and lacrimation have been shown in rats after 

direct eye exposure to trans-1,2-dichloroethene. Trans-1,2-dichloroethene (0.01 mL) was placed in the 

lower conjunctival sac of two female rabbits and 20 seconds later, the eyes of one rabbit were washed 

with tap water while the eyes of the other rabbit remained unwashed. Severe cornea1 opacity was 

observed in the washed eye and moderate iritis and conjunctivitis were observed in both treated eyes; 

however, all irritation was resolved by day 3 (Brock 1990). Airborne exposure to trans-1,2-dichloroethene 

caused lacrimation in rats at 2,000 ppm (Hurtt et al. 1993). No studies were located regarding 

ocular effects in animals following dermal exposure to cis-1,2-dichloroethene. 

Body Weight Effects. No studies were located regarding body weight effects in humans 

following dermal exposure to cis- or trans- 1,2-dichloroethene. 

Brock (1990) applied 5,000 mg/kg trans-1,2-dichloroethene to the clipped, intact skin of 2 male and 

3 female rabbits. Loss of body weight (amount unspecified) was observed. No studies were located 

regarding body weight effects in animals following dermal exposure to cis-1,2-dichloroethene. 
1,2-DICHLOROETHENE 40 

2. HEALTH EFFECTS
 

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

exposure to cis- or trans- 1,2-dichloroethene: 

2.2.3.3 Immunological and Lymphoreticular Effects 

2.2.3.4 Neurological Effects 

2.2.3.5 Reproductive Effects 

2.2.3.6 Developmental Effects 

2.2.3.7 Genotoxic Effects
 

Genotoxicity studies are discussed in Section 2.5.
 

2.2.3.8 Cancer
 

2.3 TOXICOKINETICS
 

1,2-Dichloroethene appears to be absorbed quickly by the lungs. One study reported that 

approximately 75% of the inhaled chemical was absorbed through the lungs in humans. 

1,2-Dichloroethene is metabolized in the liver, by hepatic microsomal cytochrome P-450, to form 

dichloroethanol and dichloroacetic acid. Animal studies have shown that metabolism of the cis isomer 

occurs faster than metabolism of the trans isomer, and the cis isomer frequently inhibits activity or 

destroys cytochrome P-450 levels, while the trans isomer frequently increases the enzyme levels. No 

information is available on the excretion of 1.2-dichloroethene in humans or animals. 

2.3.1 Absorption 

2.3.1.1 Inhalation Exposure 

In tests for partitioning between human blood and air (Gargas et al. 1989), the results show a relatively 

high affinity of 1,2-dichloroethene for blood (cis- 1,2-dichloroethene - blood:air partition coefficient = 
1,2-DICHLOROETHENE 41 

2. HEALTH EFFECTS
 

9.58 [±0.70] and trans-1,2-dichloroethene = 6.04 [±0.38]). Several other studies appear to support the 

conclusion that 1,2dichloroethene is absorbed relatively quickly by the lungs. Sato and Nakajima (1979) 

reported blood:air partition coefficients (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). Gargas et al. 

(1988, 1989) determined 1iquid:air and tissue:air partition coefficients for cis- and trans-1,2-

dichloroethene. Partition coefficients were determined with 0.9% saline; olive oil; and blood, liver, 

muscle, and fat tissues from rats. The partition coefficients for cis-1,2-dichloroethene are: blood = 21.6 

(±2.0), 0.9% saline = 3.25 (±0.12), olive oil = 278 (±6), fat = 227 (±11), liver = 15.3 (±11), and muscle = 

6.09 (±1.02). The coefficients for trans-1,2-dichloroethene are: blood = 9.58 (±0.94), 0.9% saline = 1.41 

(±0.04), olive oil = 178 (±6), fat = 148 (±11), liver = 8.96 (±0.61), and muscle = 3.52 (±0.54). Lehmann 

and Schmidt-Kehl (1936) reported that 72-75% of inhaled trans-1,2-dichloroethene is absorbed through 

the lungs in humans. Further insight is provided by Anderson et al. (1980), who reported that trans-1,2-

dichloroethene follows mixed-form uptake kinetics, with a composite of a slow first-order and a saturable 

uptake process. 

No studies were located regarding the rate and extent of cis- or trans-1,2dichloroethene absorption for 

the following: 

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 routes. 

2.3.3 Metabolism 

Metabolism of 1,2-dichloroethene is initially catalyzed by hepatic microsomal cytochrome P-450 

(Costa and Ivanetich 1982, 1984). Although there is no direct evidence, studies on the synthesis of the 

epoxides suggest that this metabolism involves epoxidation of the ethylene double bond, forming 
1,2-DICHLOROETHENE 42 

2. HEALTH EFFECTS
 

dichlorinated epoxides (Figure 2-3). Dichlorinated epoxides, in turn, can undergo a non-enzymatic 

rearrangement. Studies on the metabolism of 1,2-dichloroethene by hepatic microsomes and 

hepatocytes provide evidence to suggest that dichloroacetaldehyde is the predominant metabolite of 

microsomal cytochrome P-450 and that it, in turn, is extensively converted to dichloroethanol and 

dichloroacetate by cytosolic and/or mitochondrial aldehyde and alcohol dehydrogenases present in 

hepatocytes (Costa and Ivanetich 1982, 1984; Leibman and Ortiz 1977). This is consistent with the 

report that both the cis and trans isomers of 1,2-dichloroethene were converted to dichloroethanol and 

dichloroacetic acid by perfused rat liver (Bonse et al. 1975). 

Similarities and differences have been observed in the metabolism of cis- and trans-1,2-dichloroethene. 

Both isomers have been shown to bind to the active site of hepatic cytochrome P-450 (Costa and 

Ivanetich 1982). In addition, classic inhibitors of cytochrome P-450 have been shown to inhibit the 

production of dichloroacetaldehyde from both isomers. The binding and metabolism of 1,2-

dichloroethene do not appear to be specific for any one form of cytochrome P-450. The cis isomer had a 

4-fold greater rate of turnover in hepatic microsomes in vitro than the trans isomer. This is consistent 

with studies on isolated perfused rat livers, where metabolism of the cis isomer occurred at a greater 

rate than metabolism of the trans isomer (Bonse et al. 1975). In addition, differences between cis- and 

trans-1,2-dichloroethene in the rates of formation of dichloroethanol and dichloroacetic acid have been 

reported in rat hepatocytes (Costa and Ivanetich 1984). 

Several reports suggest that 1,2dichloroethene can alter cytochrome P-450 and mixed-function oxidase 

activities. McMillan (1986) reported depression of cytochrome P-450 dependent microsomal 

metabolism by both isomers of 1,2-dichloroethene, while Paolini et al. (1992) reported the induction of 

cytochrome P-450 enzymes by trans-1,2-dichloroethene. Freundt and Macholz (1978) demonstrated 

that each of the isomers of 1,2dichloroethene competitively inhibited the metabolism of hexobarbital 

in vivo following a single 8-hour inhalation exposure of rats to 200 ppm of these isomers. The effects 

of the cis isomer were more potent than those of the trans isomer. In addition, trans-1,2-dichloroethene 

competitively inhibited the oxidative N-demethylation of aminopyrine and the O-demethylation 

of p-nitroanisole by hepatic microsomes. Bronzetti et al. (1984) demonstrated that an intraperitoneal 

injection of the trans isomer can increase cytochrome P-450 levels (consistent with the work of Paolini 

1992) and aminopyrine N-demethylase activity in mice, while injection of the cis isomer more 

frequently tended to inhibit activity or destroy the enzyme. 

1,2-DICHLOROETHENE 44 

2. HEALTH EFFECTS
 

The metabolic elimination of 1,2-dichloroethene has been described as a saturable, dose-dependent 

process (Filser and Bolt 1979). In rats exposed to atmospheric concentrations of 1,2-dichloroethene 

that 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 1,2dichloroethene 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 

1982) and by isolated perfused liver (Bonse et al. 1975). 

2.3.4 Excretion 

No studies were located regarding the excretion of 1,2-dichloroethene in humans or animals following 

exposure by any routes. 

2.4 MECHANISMS OF ACTION 

Both cis- and trans-1,2-dichloroethene are volatile, lipophilic molecules that easily move through the 

respiratory and gastrointestinal systems. Based on their molecular size and lipophilicity, they probably 

pass through membranes by simple (passive) diffusion. Toxicokinetic evidence shows they have a 

high affinity for lipids and blood, but little accumulation in tissues. Both the cis and trans isomers of 

1,2-dichloroethene are converted to dichloroethanol and dichloroacetic acid by rat liver (Bonse et al. 

1975, with the cis isomer exhibiting a higher rate of metabolism than the trans isomer (Costa and 

Ivanetich 1982). 

1,2-Dichloroethene isomers inhibit liver enzymes involved in metabolism and may increase the “toxic” 

response to other chemicals (Bolt et al. 1980; McMillan 1986). Reactive metabolites of 1,2-dichloro 

ethene modify the heme moiety of hepatic microsomal cytochrome P-450, resulting in a loss of both 

cytochrome P-450 and heme (Costa and Ivanetich 1982). This modification could account for the 

observed in vivo and in vitro inhibition of other cytochrome P-450 substances by 1,2-dichloroethene. 

Compounds, such as carbon monoxide, that inactivate or inhibit the cytochrome P-450 system, should 
1,2-DICHLOROETHENE 45 

2. HEALTH EFFECTS
 

also inhibit the metabolism of 1,2-dichloroethene. 1,2Dichloroethene is oxidized to its epoxide, which 

is relatively stable (Bolt et al. 1980). Its lack of genotoxicity is related to this stability. 

The differences in metabolism, and possibly toxicity, between the cis and tram isomers have been 

partially explained by differences in the stereochemistry of the epoxides formed. The asymmetrical 

metabolites appear to be more electrophilic and also more mutagenic (Greim et al. 1975; Henschler 

1977). The cis isomer is more actively metabolized than the tram isomer, because the trans isomer is a 

more stable form and the proximity of the two chlorine atoms in the cis isomer increases the binding to 

other molecules with which it reacts (Henschler 1977). 

Physiologically based pharmacokinetic modeling (PBPK) has been used to explain metabolic rates for 

1,2-dichloroethene. A model that included suicide enzyme inhibition-resynthesis has been used to 

describe the metabolism of 1,2-dichloroethene in the rat (Gargas et al. 1990). In this model, metabolism 

results in the inactivation of cytochrome P-450, which could result in an increase or decrease in the 

toxicity of 1,2dichloroethene. 

2.5 RELEVANCE TO PUBLIC HEALTH 

Inhalation, oral, and dermal routes of exposure to 1,2dichloroethene are of concern to humans because 

1,2-dichloroethene has been found in air, drinking water, and soil (Shah and Singh 1988; Westrick et al. 

1984; VIAR 1987). Toxicokinetic data are very limited for both human and animal exposures. Partition 

coefficients suggest that 1,2-dichloroethene has a much stronger affinity for blood and fats than for air. 

Although the compound is relatively lipophilic, there is no good evidence for accumulation in important 

organs such as liver, brain, kidney, and adipose tissue. Tissue saturation should not be found at 

anticipated exposure levels. 1,2Dichloroethene is likely to be metabolized to more hydrophilic byproducts, and, therefore, eliminated quickly by the kidneys as metabolites. 

The most significant effects of 1,2-dichloroethene exposure are hematological and hepatic. At high levels 

of exposure, clinical symptoms that have been reported in humans exposed to 1,2dichloroethene in air 

include nausea, drowsiness, fatigue, intracranial pressure and ocular irritation. One fatality has been 

reported. No information is available on oral toxicity for 1,2dichloroethene in humans. No information is 

available on the relative toxicities of the cis and trans isomers of 1,2dichloroethene in humans. 
1,2-DICHLOROETHENE 46 

2. HEALTH EFFECTS 

Pathological lesions of the heart, liver, and lungs have been reported in rats exposed to 

trans-1,2-dichloroethene 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. 

A variety of genotoxicity tests have been performed for 1,2-dichloroethene. The predominant results 

are negative, and no carcinogenicity studies were found in the literature. Federal and international 

agencies have given 1,2dichloroethene a non-cancer rating or a “not classifiable” rating. 

Minimal Risk Levels for 1,2-Dichloroethene. 

MRLs have been derived for acute and intermediate exposure to the cis and trans isomers of 

1,2-dichloroethene; no chronic studies are available from which to derive MRLs for chronic exposure. 

The derivation of each MRL is discussed fully in Appendix A. 

Inhalation MRLs. 

• An MRL of 0.2 ppm has been derived for acute-duration exposure (14 days or less) and for 

intermediate-duration inhalation exposure (15-364 days) to trans- 1,2-dichloroethene. 

The acute MRL is based on a LOAEL of 200 ppm for trans-1,2-dichloroethene over an 8-hour period 

that caused fatty degeneration of the liver (Freundt et al. 1977). Longer periods of exposure at 

200 ppm showed increased numbers and severity of response. The intermediate MRL is based on the 

same study and effects (Freundt et al. 1977) in which rats were exposed to 200 ppm 

trans-1,2-dichloroethene for 8 hours per day, 5 days per week for 8 or 16 weeks. An uncertainty 

factor of 1,000 is used: 10 for using a LOAEL, 10 for extrapolation from animals to humans, and 10 

for human variability. 

No chronic inhalation MRL has been derived for trans-1,2-dichloroethene because no study tested 

1,2-dichloroethene for a sufficiently long period of time. No acute-, intermediate- or chronic-duration 

MRLs have been derived for cis-1,2-dichloroethene because of lack of data. 
1,2-DICHLOROETHENE 47 

2. HEALTH EFFECTS 

Oral MRLs. 

Studies of oral exposure to 1,2-dichloroethene exist to develop oral MRLs for both the cis and trans 

isomers. 

•	 An MRL of 1 mg/kg/day has been derived for acute-duration oral exposure (14 days or less) 

to cis- 1.2-dichloroethene. 

This MRL for the cis isomer is based on a NOAEL of 97 mg/kg/day for decreased red blood cell 

counts and hematocrit levels in female rats exposed to 97 mg/kg/day cis-1,2-dichloroethene for 

14 days (McCauley et al. 1990). An uncertainty factor of 100 is used: 10 for extrapolation from 

animals to humans, and 10 for human variability. Hematological effects have also been noted in other 

oral studies (Barnes et al. 1985). 

No acute oral MRL has been derived for trans- 1,2-dichloroethene. 

Separate intermediate-duration oral MRLs were derived for exposure to the cis and trans isomers. 

• An MRL of 0.3 mg/kg/day has been derived for intermediate-duration oral exposure to 
1,2-DICHLOROETHENE 48 

2. HEALTH EFFECTS
 

al. 1985). An uncertainty factor of 100 was developed for the MRL, using factors of 10 for animal-tohuman extrapolation and 10 to protect sensitive individuals. In this study, serum alkaline phosphatase 

levels were significantly increased. Though the two highest doses caused increased serum alkaline 

phosphatase levels in a non-dose-related manner, the effects are consistent with the fatty accumulation in 

hepatocytes. This hepatic intermediate end point is slightly lower than a hematological NOAEL 

(decreased hematocrit). Other organs and end points were an order of magnitude less sensitive to cis- 1,2-

dichloroethene than were hepatic and hematologic target organs. 

Death. A fatality was reported to have occurred after inhalation of 1,2-dichloroethene in a small 

enclosure (Hamilton 1934). Details regarding the exposure levels (cis and trans) in this accident and 

the cause of death are not available. No reports of lethality related to oral exposure of humans to 

1,2-dichloroethene were located. 

Terminal symptoms in animals exposed orally to cis- or trans-1,2-dichloroethene involve central nervous 

system depression (e.g., ataxia and loss of righting reflex) and respiratory depression (Barnes et al. 1985; 

Hayes et al. 1987; McCauley et al. 1990; Munson et al. 1982). Results of studies in which animals have 

inhaled or ingested trans-1,2,-dichloroethene implicate the heart, liver, and lung as potential targets for 

toxicity (Barnes et al. 1985; Freundt et al. 1977; Hayes et al. 1987; McMillan 1986). The relative lethal 

potency of the cis and trans isomers to each other is not known. 

Systemic Effects. Trans-1,2dichloroethene appears to be an ocular irritant in humans. Two human 

participants in a self-experimentation study reported mild burning of the eyes after acute exposure to 

either vapors or aerosols of trans-1,2-dichloroethene (Lehmann and Schmidt-Kehl 1936). No other 

specific systemic effects have been reported in humans. Cis- 1 ,2dichloroethene may induce a similar 

toxicological effect; however, no reports were located that specifically implicated cis- 1.2-dichloroethene 

as an ocular irritant. 

Systemic effects-involving the heart, liver, and lungs have been observed in animals exposed to 

trans-1,2-dichloroethene. Evidence for serious adverse effects in these organs consists of only one 

study (Freundt et al. 1977). Effects reported in the rat include lung lesions (hyperemia and alveolar 

septal distension), fibrous swelling of the myocardium, and fatty degeneration of the liver. All three 

effects were observed after inhalation exposures to trans- 1,2-dichloroethene at concentrations of 

200 ppm or greater for 8 hours. Liver and lung lesions were observed after gavage dosing, but only 
1,2-DICHLOROETHENE 49 

2. HEALTH EFFECTS
 

after near lethal doses were administered. The treatment groups in this study were too small to establish a 

high degree of confidence in these findings. However, one additional serious systemic effect was found in 

rats-reduced weight gain for pregnant dams exposed to airborne 1,2-dichloroethene (Hurtt et al. 1993). 

Exposure of rats (Hayes et al. 1987) or mice (Barnes et al. 1985) to trans-1,2-dichloroethene at doses up 

to 3,114 mg/kg/day, 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 with cis-1,2-dichloroethene for 

14 or 90 days, but these increased organ weights were not accompanied by any histopathological 

lesions in either organ (McCauley et al. 1990). Rats exposed to the cis isomer by gavage for 14 and 

90 days showed a dose-related decrease in red blood cell count and hematocrit levels (McCauley et al. 

1990). Hematotoxicity was not observed in mice or rats exposed to the trans isomer (Barnes et al. 

1985; Hayes et al. 1987). The different results in the rat studies could be due to differential toxicity 

between the two isomers, as well as to other factors, including initial age of the rats, vehicle 

differences, and different exposure methods. Hayes et al. (1987) exposed rats with an initial age of 

26 days to the trans isomer in a 1% emulphor drinking water suspension, while McCauley et al. 

(1990) treated rats with an initial age of 70 days with the cis isomer in corn oil by gavage. Data 

regarding toxic systemic effects of 1,2-dichloroethene in animals are too limited to draw any 

conclusions for human exposure. 

Respiratory Effects. Pulmonary effects of inhalation and oral exposure to 1,2-dichloroethene have 

been shown over a range of exposure levels and for both inhalation and oral routes. No effect levels 

are reported from 485 to 2,000 mg/kg/day; however, several studies found pronounced respiratory 

effects around 1,000 mg/kg/day or 1,000 ppm (Freundt et al. 1977; McCauley et al. 1990; McMillan 

1986). All these values are relatively high. 

Cardiovascular Effects. The likelihood of acute exposure to 1,2-dichloroethene is quite small. Only 

at high levels (3,000 ppm or 1,100 mg/kg/day) is there animal evidence of swelling of heart muscle 

and congestion of blood in and near the heart (Freundt et al. 1977). 

Hematological Effects. There are known blood effects of 1,2-dichloroethene, but these occur at 

exposure levels above those expected for the general population. Acute- and intermediate-exposure 

hematologic studies are the bases for oral MRLs for cis-1,2-dichloroethene (McCauley et al. 1990). 
1,2-DICHLOROETHENE 50 

2. HEALTH EFFECTS
 

Musculoskeletal Effects. Animal studies have not reported effects on the musculoskeletal system 

(Freundt et al. 1977; McCauley et al. 1990). Thus, it does not appear that musculoskeletal effects are 

of concern for human exposure to 1,2-dichloroethene. 

Hepatic Effects. Liver effects in animals include fatty degeneration of liver lobules; such effects are 

reasonable to anticipate among humans, though exposure levels of greater than 100 mg/kg/day are not 

anticipated. Higher exposure levels produced enzyme changes (decreased serum alkaline phosphatase, 

serum albumin and blood urea nitrogen or increased plasma enzyme activity) according to some of the 

available literature (Freundt et al. 1977; McMillan 1986). Acute- and intermediate-exposure hepatic 

studies are the bases for inhalation MRLs for trans-1,2-dichloroethene (Freundt et al. 1977) and for an 

oral MRL for tram-1,2dichloroethene (Barnes et al. 1985). 

Renal Effects. Reduced kidney function and increased kidney weight are expected with acute high 

level exposure (McCauley et al. 1990; McMillan 1986); however, the public health concern is 

relatively small because such effects are not known to occur at chronic lower level exposure. 

Dermal Effects. Acute exposure of the skin causes effects that are readily reversible. Irritation and 

mild effects on skin are the most frequent effects likely to be observed (Brock 1990). 

Ocular Effects. Acute exposure causes readily reversible effects such as a slight burning of the eyes 

(Lehman and Schmidt-Kehl 1936). 

Body Weight Effects. Acute- and intermediate-duration exposure has affected weight gain in pregnant 

and young rats (Hurtt et al. 1993; McCauley et al. 1990). In pregnant rats, reduced food consumption 

was observed along with reduced weight gain. Intermediate oral exposure caused smaller weight gains 

for growing rats. 

Immunological and Lymphoreticular 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 rats and 

mice have not shown effects on the spleen, leukocytes, or liver Kupffer cells (Barnes et al. 1985; 

Freundt et al. 1977; McMillan 1986; Munson et al. 1982). 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 
1,2-DICHLOROETHENE 51 

2. HEALTH EFFECTS
 

the humoral immune system did not constitute a 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 ,2dichloroethene 

represent an important effect in humans. Dizziness, drowsiness, vertigo, and intracranial pressure are 

some of the symptoms that 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. 1990; Munson et al. 1982). 

A study in rats and mice reported on the air concentrations evoking a depression in the duration of 

hindlimb extension (Frantik et al. 1994). A marked species dependent effect was observed in this 

study. Therefore, it is difficult to draw any conclusions regarding the significance of this type of 

neurological effect in humans. 

Reproductive Effects. There are no reports of reproductive effects in humans as a result of 

exposure to cis- or trans-1,2-dichloroethene by any route. 

It is not known whether reproductive effects may be of concern to humans. One study showed an 

increase in resorption rates in rats; however, the authors interpreted this effect as not being treatment 

related (Hurtt et al. 1993). 

Developmenta! Effects. There are no reports of developmental effects in humans as a result of 

exposure to cis- or trans-1,2dichloroethene by any route. 

It is not known whether developmental effects may be of concern to humans. Fetal weights were 

reduced significantly in a developmental rat study; however, this was probably due to reduced food 

consumption in the pregnant rats (Hurtt et al. 1993). 
1,2-DICHLOROETHENE 52 

2. HEALTH EFFECTS
 

Genotoxic Effects. Genotoxic effects of cis- and trans-1,2-dichloroethene in humans are unknown. 

Mutagenicity of 1,2dichloroethene has been examined in a variety of test systems. 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 

(Cema and Kypenova 1977). Bronzetti et al. (1984) also found that the cis isomer was mutagenic in 

Saccharomyces cerevisiae D7 in a host-mediated assay in mice, with significant increases in convertants 

at the trp locus and revertants at the ilv locus. Cantelli-Forti and Bronzetti (1988) also reported that cis1,2-dichloroethene was mutagenic in the S. cerevisiae D7 strain in mice. Dose-dependent toxicity 

increased in the presence of the mouse, S9 microsomal fraction. In addition, repeated intraperitoneal 

injection of cis- 1,2-dichloroethene produced chromosomal aberrations in mouse bone marrow cells 

(Cema and Kypenova 1977). Negative results were obtained with trans-1,2-dichloroethene in these 

assays. 

In vitro tests of genotoxicity of the cis and trans isomers are summarized in Table 2-5. Neither isomer was 

genotoxic with or without metabolic activation in Escherichia coli K12 (Greim et al. 1973, in several 

strains of S. typhimurium in spot tests (Cema and Kypenova 1977; Mortelmans et al. 1986), or in gene 

mutation and gene conversion tests in S. cerevisiue D7 (Galli et al. 1982). However, Bronzetti et al. 

(1984) found positive results for gene mutation tests of the cis isomer in S. cerevisiue D7, with metabolic 

activation. 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). 

Cancer. To date, cancer effects of cis- and trans-1,2-dichloroethene have not been studied in humans or 

animals. 

2.6 BIOMARKERS OF EXPOSURE AND EFFECT 

Biomarkers are broadly defined as indicators signaling events in biologic systems or samples. They have 

been classified as markers of exposure, markers of effect, and markers of susceptibility (NAS/NRC 

1989). 



1,2-DICHLOROETHENE 56 

2. HEALTH EFFECTS
 

Due to a nascent understanding of the use and interpretation of biomarkers, implementation of 

biomarkers as tools of exposure in the general population is very limited. A biomarker of exposure is 

a xenobiotic substance or its metabolite(s), or the product of an interaction between a xenobiotic agent 

and some target molecule(s) or cell(s) that is measured within a compartment of an organism (NRC 

1989). The preferred biomarkers of exposure are generally the substance itself or substance-specific 

metabolites in readily obtainable body fluid(s) or excreta. However, several factors can confound the 

use and interpretation of biomarkers of exposure. The body burden of a substance may be the result 

of exposures from more than one source. The substance being measured may be a metabolite of 

another xenobiotic substance (e.g., high urinary levels of phenol can result from exposure to several 

different aromatic compounds). Depending on the properties of the substance (e.g., biologic half-life) 

and environmental conditions (e.g., duration and route of exposure), the substance and all of its 

metabolites may have left the body by the time samples can be taken. It may be difficult to identify 

individuals exposed to hazardous substances that are commonly found in body tissues and fluids (e.g., 

essential mineral nutrients such as copper, zinc, and selenium). Biomarkers of exposure to 

1,2-dichloroethene are discussed in Section 2.6.1. 

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 (NAWNRC 1989). This definition encompasses biochemical or cellular signals 

of tissue dysfunction (e.g., increased liver enzyme activity or pathologic changes in female genital 

epithelial cells), as well as physiologic signs of dysfunction such as increased blood pressure or 

decreased lung capacity. Note that these markers are not often substance specific. They also may not 

be directly adverse, but can indicate potential health impairment (e.g., DNA adducts). Biomarkers of 

effects caused by 1,2-dichloroethene are discussed in Section 2.6.2. 

A biomarker of susceptibility is an indicator of an inherent or acquired limitation of an organism’s 

ability to respond to the challenge of exposure to a specific xenobiotic substance. It can be an 

intrinsic genetic pr other characteristic or a preexisting disease that results in an increase in absorbed 

dose, a decrease in the biologically effective dose, or a target tissue response. If biomarkers of 

susceptibility exist, they are discussed in Section 2.8, Populations That Are Unusually Susceptible. 
1,2-DICHLOROETHENE 57 

2. HEALTH EFFECTS 

2.6.1 Biomarkers Used to Identify or Quantify Exposure to 1,2-Dichloroethene 

There currently are no biomarkers available to quantify exposure to 1,2-dichloroethene. 

Methods exist for determining 1,2dichloroethene in blood and biological tissues (see Chapter 6), but 

specific levels of 1,2-dichloroethene have not been directly correlated with exposure via any route. 

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 is not a metabolite of 

1,2dichloroethene exposure, but rather may be caused by stimulation of cellular systems that lead to 

increased acetone production.) 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 ,2dichloroethene since acetone can 

be found in blood and exhaled air after exposure to other chemicals such as vinyl chloride, vinylidene 

fluoride, and perchloroethylene (Filser and Bolt 1980), as well as in patients with 

diabetes, hepatic insufficiency, and other metabolic disorders. 

2.6.2 Biomarkers Used to Characterize Effects Caused by 1,2-Dichloroethene 

There currently are no biomarkers available to characterize effects caused by 1,2-dichloroethene in 

humans. 

As discussed in Section 2.6.1, 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 in invoking this response. 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. This would lead to an increase in mitochondrial acetyl-coenzyme A 

and, consequently, to 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 levels in the body. 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 
1,2-DICHLOROETHENE 58 

2. HEALTH EFFECTS
 

observed in rats exposed to 1,2-dichloroethene (Freundt et al. 1977). However, acetone exhalation is 

extremely common and is associated with some disorders that do not obviously produce any liver 

degeneration. 

For more information on biomarkers for renal and hepatic effects of chemicals see ATSDRKDC 

Subcommittee Report on Biological Indicators of Organ Damage (1990) and for information on 

biomarkers for neurological effects see OTA (1990). 

2.7 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. 

As mentioned in Section 2.3.3, 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 (1982) showed that multiple forms of hepatic 

microsomal cytochrome P-450, including the forms induced by P-naphthoflavone and phenobarbital, can 

bind and metabolize 1,2-dichloroethene. Thus, 1,2-dichloroethene may potentiate the toxic actions of any 

chemical that undergoes detoxication 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. 

2.8 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE 

A susceptible population will exhibit a different or enhanced response to 1,2-dichloroethene than will 

most persons exposed to the same level of 1,2-dichloroethene in the environment. Reasons include 

genetic make-up, developmental stage, age, health and nutritional status (including dietary habits that 

may increase susceptibility, such as inconsistent diets or nutritional deficiencies), and substance 

exposure history (including smoking). These parameters result in decreased function of the 

detoxification and excretory processes (mainly hepatic, renal, and respiratory) or the pre-existing 

compromised function of target organs (including effects or clearance rates and any resulting 
1,2-DICHLOROETHENE 59 

2. HEALTH EFFECTS
 

end-product metabolites). For these reasons we expect the elderly with declining organ function and 

the youngest of the population with immature and developing organs will generally be more vulnerable 

to toxic substances than healthy adults. Populations who are at greater risk due to their unusually high 

exposure are discussed in Section 5.6, Populations With Potentially High Exposure. 

While no populations with unusual susceptibility to the health effects of 1,2-dichloroethene could be 

identified, based on the available literature, certain diabetics may be unusually susceptible because of 

impairment of glucose metabolism and increased production of acetone. In addition, individuals with 

impaired livers, such as alcoholics, and those with exposure to other halogenated hydrocarbons may be 

unusually susceptible to 1,2-dichloroethene exposure. 

2.9 METHODS FOR REDUCING TOXIC EFFECTS 

This section will describe clinical practice and research concerning methods for reducing toxic effects 

of exposure to 1,2-dichloroethene. However, because some of the treatments discussed may be 

experimental and unproven, this section should not be used as a guide for treatment of exposures to 

1,2dichloroethene. When specific exposures have occurred, poison control centers and medical 

toxicologists should be consulted for medical advice. 

2.9.1 Reducing Peak Absorption Following Exposure 

1,2-Dichloroethene is available commercially as the cis or trans isomer or as a mixture. Human 

exposure to 1,2dichloroethene may occur by inhalation, ingestion, or by dermal contact. There are 

conflicting data regarding the relative toxicity of the two isomers. Vapors are extremely irritating to 

the eyes and upper respiratory tract, and once absorbed can cause central nervous system and 

respiratory depression. 1,2-Dichloroethene was used as a general anesthetic in humans, and central 

nervous system depression is one of its toxic effects (ACGIH 1991). It is recommended that exposed 

individuals be moved to fresh air and administered 100% humidified supplemental oxygen. The 

potential risk of aspiration, especially for infants, leading to airway and pulmonary damage, usually 

outweighs the potential benefit of administering syrup of ipecac to induce emesis (TOMES 1994). 

Once in the care of a health professional, gastric lavage can be useful if administered within 1 hour of 

the exposure to reduce the amount of absorbed solvent. 
1,2-DICHLOROETHENE 60 

2. HEALTH EFFECTS
 

Following ocular contamination, the eyes should be irrigated with copious amounts of room temperature 

water or normal (0.9%, w/v, isotonic) saline, for at least 15 minutes. Reversible, corneal opacification has 

been described after exposure to 1,2-dichloroethene vapor, and ophthalmologic consultation should 

generally be sought after ocular contamination to evaluate the potential ocular damage (Gosselin 1984). 

Following acute exposure to many chlorinated solvents, hypotension and cardiac arrhythmias due to 

myocardial sensitization have led to ventricular fibrillation and death (TOMES 1994). Unfortunately there 

is no specific treatment for 1,2dichloroethene exposure except for supportive measures to combat the 

effects of central nervous system, respiratory depression, and cardiac irritability. 

2.9.2 Reducing Body Burden 

The body does not retain significant amounts of 1,2-dichloroethene. It is largely excreted through the 

lungs; thus, prompt and adequate ventilation is the only known way to reduce body burden (ACGIH 

1991). There is no currently recognized treatment to enhance elimination, and orthodox treatment for 

ingestion is entirely supportive. 

2.9.3 Interfering with the Mechanism of Action for Toxic Effects 

Clinical effects caused by acute exposure to 1,2-dichloroethene include central nervous system and 

respiratory depression, eye and upper respiratory irritation, nausea, vomiting, weakness, tremors, and 

epigastric cramps, all of which may resolve rapidly after the exposure ceases. There is one reported 

industrial fatality caused by inhalation of vapor in a small enclosure, but the level of exposure, symptoms 

of toxicity, and isomeric composition are unknown (ACGIH 1991). Muscular cramping and vomiting 

have been relieved by intravenous administration of calcium gluconate (Gosselin 1984). The mechanism 

of action for the central nervous system effects of 1,2-dichloroethene has not been clearly established, but 

may be related to solvent effects on cellular membranes. Neurotransmitter effects have also been 

demonstrated for some solvents, and it is reasonable to speculate that these effects on neurotransmitters 

might be mitigated by pharmacologic intervention. However, no such interventions are currently available 

for clinical use. 

Fatty degeneration of the liver has been reported in animal studies, but 1,2-dichloroethene appears to 

have less hepatic and renal toxicity than many other chlorinated hydrocarbons (ACGIH 1991). 
1,2-DICHLOROETHENE 61 

2. HEALTH EFFECTS
 

However, ethanol in alcoholic beverages may compete with or enhance the metabolic activation of 

solvents and can increase the severity of health effects, particularly liver toxicity. Alcoholic beverages 

should be avoided following exposure to 1,2dichloroethene and other solvents. 

2.10 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with 

the Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of 1,2-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 the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will 

be evaluated and prioritized, and a substance-specific research agenda will be proposed. 

2.10.1 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 

1,2-dichloroethene are summarized in Figures 2-4 and 2-5. The purpose of these figures is to illustrate 

the existing information concerning the health effects of 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 necessarily imply anything about the quality of the study or studies, nor should missing 

information in this figure be interpreted as a “data need.” A data need, as defined in ATSDR’s 

Decision Guide for Identifying Substance-Specific Data Needs Related to Toxicological Profiles 

(ATSDR 1989),-is substance-specific information necessary to conduct comprehensive public health 

assessments. Generally, ATSDR defines a data gap more broadly as any substance-specific 

information missing from the scientific literature. 


1,2-DICHLOROETHENE 64 

2. HEALTH EFFECTS
 

There are very few studies or case reports of human exposure to 1,2-dichloroethene by any route of 

exposure. One report describes neurologic symptoms in humans following acute inhalation of 

trans-1,2-dichloroethene. This property of depressing the central nervous system is an important effect 

of 1,2-dichloroethene exposure. Another study reported an industrial fatality related to accidental 

inhalation exposure to 1,2-dichloroethene (isomeric composition unknown). 

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. For inhalation and 

oral exposure routes, toxicity to the heart, liver, blood, 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. Several studies examined the effects of either cis- or trans-1,2-dichloroethene on the immune 

systems of mice exposed by inhalation or oral routes. 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. In addition to central nervous 

system effects, inhalation exposure to trans- 1,2-dichloroethene appears to affect development of the fetus 

and development of the newborn and young. When inhaled, there also may be effects on reproduction 

because of reduced maternal weight gain and reduced litter size. As shown in Figures 2-4 and 2-5, no 

information on carcinogenic effects in animals by inhalation, oral, or dermal exposure is available for 

either cis- or trans-1,2-dichloroethene. 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 may be genotoxic; the trans isomer has shown no indication 

of being genotoxic. 

2.10.2 Identification of Data Needs 

Acute-Duration Exposure. Reliable health effects data for human exposure by any route to 1,2-

dichloroethene were not located. One human fatality was reported, but the cause of death, the length of 

exposure, and the concentration and isomeric identity of 1,2-dichloroethene in the air were not described 

(Hamilton 1934). Two human volunteers reported mild burning of the eyes after acute dermal exposure to 

trans-1,2-dichloroethene (Lehmann and Schmidt-Kehl 1936). However, the methods used in 1936 to 

generate and test for exposure levels were relatively insensitive, and it is unclear whether the 1,2-

dichloroethene was in an aerosol or gaseous state. No information was located for systemic toxicity in 

humans after oral exposure or for the relative toxicities of the cis and trans 
1,2-DICHLOROETHENE 65 

2. HEALTH EFFECTS
 

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 (Barnes et al. 1985; 

Freundt et al. 1977; Gradiski et al. 1978; Hayes et al. 1987; Kallman et al. 1983; McMillan 1986; Munson 

et al. 1982). An acute-duration inhalation MRL was derived from the Freundt et al. (1977) study, based 

on the hepatic effect of fatty degeneration of the liver seen at 200 ppm in rats. A wide range of LD50 

values for the trans isomer, 1,300-10,000 mg/kg/day, exists in the present literature. Inhalation LC50 and 

oral LD50 values for cis-1,2-dichloroethene are not well defined. One study suggests an LD50 around 

5,000 mg/kg/day for the cis isomer (McMillan 1986). 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 (Freundt et al. 1977). Neurological problems, such as narcosis, lethargy, and 

behavioral changes, have been shown with acute inhalation of both cis and trans isomers (De Ceaurriz et 

al. 1983; Hurtt et al. 1993). Oral exposure to 1,2-dichloroethene is also associated with central nervous 

system depression and other neurological effects (Barnes et al. 1985; Hayes et al. 1987). The finding of 

acetone in the air exhaled by 1,2-dichloroethene-exposed rats indicates possible alterations in lipid and 

fatty acid metabolism at high exposure levels (Filser and Bolt 1980). This may support the observation of 

fatty infiltration of liver in the rat inhalation study. Evidence of target effects for oral acute exposure 

exists for both the cis and trans isomers. Hematotoxicity after acute oral exposure to cis- and trans-1,2-

dichloroethene was reported in rats and mice and included adverse effects of decreases in fibrinogen 

levels, hematocrit, and erythrocyte counts (Barnes et al. 1985; McCauley et al. 1990). The NOAEL value 

for decreased hematocrit in female rats was used for the derivation of an acute oral MRL for 

cis-1,2-dichloroethene. Serious respiratory, cardiovascular, and hepatic effects were also noted in rats 

exposed orally. Along with the serious responses of pulmonary and fibrous hyperemia, alveolar 

distention, cardiac muscle changes, and decreases in blood urea nitrogen, milder hepatic changes were 

recorded (Barnes et al. 1985; Freundt et al. 1977; McCauley et al. 1990; McMillan 1986). Limited 

data were located for dermal exposure to trans-1,2-dichloroethene indicating mild to moderate, 

reversible, dermal and ocular effects (Brock 1990; Hurtt et al. 1993; Lehmann and Schmidt-Kehl 

1936). The available toxicity data do not allow a definitive conclusion regarding the relative toxicity 

of the cis and tram isomers. However, in vivo and in vitro studies suggest differences in the 

metabolism of the two isomers (Filser et al. 1978, 1979, 1982; Gargas et al. 1988, 1989, 1990; Sato 

and Nakajima 1979). Furthermore, pharmacokinetic data are insufficient to identify target organs for 

either isomer across routes of exposure. Further studies to identify target organs of cis- and 

trans-1,2-dichloroethene toxicity and to assess dose-response relationships would be particularly useful 
1,2-DICHLOROETHENE 66 

2. HEALTH EFFECTS
 

for inhalation and dermal exposure routes. Additional oral exposure studies would increase the 

possibilities of assessing dose-response relationships and target organs. 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 in rats, similar to that found with acute exposure, was observed after 

intermediate-duration inhalation exposure (Freundt et al. 1977). The exposure level that was 

associated with capillary hyperemia, alveolar distention and pneumonic infiltration, and fatty 

accumulation in liver lobules and Kupffer cells was the same as that tested with acute exposure; 

therefore, an intermediate inhalation MRL at the same level as the acute inhalation MRL was derived. 

Studies in rats and mice exposed orally to trans-1,2-dichloroethene at doses ranging from 17 to 

3,100 mg/kg/day (Barnes et al. 1985; Hayes et al. 1987; McCauley et al. 1990; McMillan 1986; Shopp 

et al. 1985) have examined many target organs including the blood, liver, kidneys, lungs, heart and 

immune system. Respiratory (lung weight), hematological (blood cell counts), and body weight effects 

were reported at doses of 100 to 400 mg/kg/day (Barnes et al. 1985; McCauley et al. 1990; McMillan 

1986). Hepatic effects in male mice at 175 mg/kg/day and a NOAEL at 17 mg/kg/day are the basis 

for an intermediate-duration oral MRL for trans-1,2-dichloroethene (Barnes et al. 1985). Hematologic 

effects at 97 mg/kg/day and a NOAEL at 32 mg/kg/day are the basis of an intermediate-duration oral 

MRL for cis-1,2-dichloroethene. A 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 2.10.3). The full 

published report may provide dose-response data when it becomes available. The differences in the 

observed effects of cis- and trans-1,2-dichloroethene that were seen in rats in the oral 90-day studies 

may be due to differences in toxicity of these isomers as discussed above (see acute-duration exposure) 

(Barnes et al. 1985; Hayes et al. 1987; McCauley et al. 1990; McMillan 1986; Shopp et al. 1985). No 

studies were located regarding 1,2-dichloroethene toxicity in animals after dermal exposure. 

Additional studies regarding 1,2-dichloroethene toxicity after inhalation exposure are necessary, with a 

specific need for inhalation studies using the cis isomer. 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. The target organs-liver, blood, and lungs-should be 

emphasized. 
1,2-DICHLOROETHENE 67 

2. HEALTH EFFECTS
 

Chronic-Duration Exposure and Cancer. No human or animal data were located regarding 

health effects of long-term (chronic) exposure to 1,2-dichloroethene by inhalation, oral, or dermal 

routes. Therefore, no chronic MRLs could be derived. There is a need to conduct chronic animal 

studies with the isomers of 1,2-dichloroethene by inhalation, oral and dermal routes. These studies 

could provide information on subtle toxicological changes in organs/systems and on dose-response 

relationships associated with 1,2-dichloroethene toxicity. Furthermore, there are communities around 

hazardous sites that may be exposed to low levels of 1,2-dichloroethene for long periods of time. 

No studies were located regarding the carcinogenic potential of 1,2-dichloroethene in humans and 

animals following inhalation, oral, or dermal exposure. However, genotoxicity studies revealed 

mutagenic activity of the cis isomer in the host-mediated assay (Cantelli-Forti and Bronzetti 1988; 

Cema and Kypenova 1977; Galli et al. 1982; Greim et al. 1975; Sawada et al. 1987). Furthermore, a 

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 2.10.3). Although this study has not yet 

been published, it raises a concern about the carcinogenicity of 1,2-dichloroethene, which should be 

further investigated in long-term oral and inhalation studies of both isomers. In humans, dermal 

exposure is less likely than oral or inhalation exposure; however, dermal studies could add valuable 

insights about 1 ,2dichloroethene toxicity. 

Genotoxicity. No study was located regarding 1,2-dichloroethene genotoxicity in humans. Neither 

isomer of 1,2-dichloroethene was mutagenic in in vitro experiments with E. coli, S. typhimurium, and 

S. cerevisiae (Cantelli-Forti and Bronzetti 1988; Cema and Kypenova 1977; Galli et al. 1982; Greim et 

al. 1975). Neither isomer produced chromosomal aberrations or sister chromatid exchanges in Chinese 

hamster cells (Sawada et al. 1987). Reductions in numbers of convertants and revertants (positive 

results) were obtained with the cis isomer, but not the trans isomer, in host-mediated assays in mice 

(Cantelli-Forti and Bronzetti 1988). Furthermore, repeated intraperitoneal injections of the cis isomer 

induced chromosomal aberrations in mouse bone marrow cells (Cema and Kypenova 1977); thus, 

cis-1,2-dichloroethene may be a potential mutagen in animals. The weight of evidence ef genotoxicity 

is still small; additional studies would help to confirm the existing information or uncover unknown 

genetic effects. Chronic animal studies might elucidate the potential for, or isomeric differences in, 

cancer development. If an appropriate group of exposed workers could be identified, cytogenetic 

testing might help determine 1 ,2dichloroethene’s genotoxic potential in humans. 
1,2-DICHLOROETHENE 68 

2. HEALTH EFFECTS
 

Reproductive Toxicity. No studies were located regarding reproductive toxicity of 1,2-dichloroethene 

in humans by inhalation, oral, or dermal exposure. No studies were located regarding 

reproductive toxicity of 1,2-dichloroethene in animals following dermal exposure. An inhalation study 

published in 1993 (Hurtt et al. 1993) is the sole report to address the reproductive effects of 

1,2-dichloroethene. In this study, maternal weight gain was reduced, proportional to dose, and 

possible increases in resorption were reported. In other studies, histopathological examination of the 

reproductive organs of animals exposed orally for 90 days to 1,2-dichloroethene has not shown effects 

on reproductive organs (Hayes et al. 1987; McCauley et al. 1990). Further investigation of 

reproductive effects, including results of dermal exposure, are necessary for understanding possible 

effects suggested by the existing evidence on the reproductive system. 

Developmental Toxicity. No studies were located regarding developmental effects in humans 

after inhalation, oral, or dermal exposure to cis- or trans-1,2-dichloroethene. No data are available on 

developmental effects in animals after oral or dermal exposure to 1,2-dichloroethene. Fetal weights 

appear to be reduced after exposure to 1,2-dichloroethene, as shown in an inhalation study (Hurtt et al. 

1993). During critical developmental stages (days 7-16 in rats), trans-1,2-dichloroethene exposure was 

associated with reduced weight gain in rat pups at a level of 12,000 ppm. Additional developmental 

toxicity studies in animals by inhalation, oral, and dermal exposure may provide relevant information 

for humans exposed near hazardous waste sites. 

Immunotoxicity. No information about 1,2-dichloroethene toxicity to the human immune system 

was located. Findings of fatty degeneration of Kupffer cells, decreased numbers of white blood cells, 

and pneumonic infiltration in rats after inhalation exposure to trans-1,2-dichloroethene (Freundt et al. 

1977), and of suppressed humoral immune status in male mice exposed to trans.-1,2-dichloroethene in 

drinking water for 90 days, as measured by mouse spleen cell antibody production (Shopp et al. 1985), 

suggest that 1,2-dichloroethene may be immunotoxic. Immunological studies of cis- 1 ,2dichloroethene 

and additional studies of trans-1,2-dichloroethene would help determine more definitely the 

immunotoxic potential and possible differences between the isomers. No immunotoxicity-data in 

animals were located for the dermal route of exposure. New dermal studies would be valuable, both 

because no such studies have been reported and because of the potential immuno-dermal effects of 

dermal exposure. 
1,2-DICHLOROETHENE 69 

2. HEALTH EFFECTS
 

Neurotoxicity. Symptoms of central nervous system depression (vertigo, drowsiness, intracranial 

pressure, nausea) were observed in two human volunteers during a 30-minute inhalation exposure to 

1,2-dichloroethene. The symptoms disappeared after discontinuation of exposure (Lehmann and 

Schmidt-Kehl 1936). No information was located regarding neurotoxicity after exposure by other 

routes of exposure in humans. In animals, inhalation exposure to 1,2dichloroethene was associated 

with behavioral changes, narcosis, and lethargy at levels ranging from 1,700 to 12,000 ppm (De 

Caurriz et al. 1983; Hurtt et al. 1993). Similarly, symptoms of central nervous system depression were 

observed in rodents after acute oral exposure to 1,2-dichloroethene (Barnes et al. 1985; Hayes et al. 

1987; McCauley et al. 1990; Munson et al. 1982). The observations were restricted to behavioral 

tests. Further information regarding 1 ,2dichloroethene neurotoxicity in animals after exposure by 

inhalation, oral, and dermal routes would be valuable. Animal 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 of 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, or possibly by dermal 

contact. The occupationally exposed population is relatively small (285 individuals) (NIOSH 1988). The 

confounding exposure to other related compounds makes it difficult to perform an epidemiological study 

for 1,2-dichloroethene. Animal studies suggest that hematological, hepatic, neurological and reproductive 

effects would be the end points of concern (Barnes et al. 1985; Freundt et al. 1977; Hurtt et al. 1993; 

McCauley et al. 1990; McMillan 1986). Therefore, if a worker or a population with appropriate exposure 

can be identified, epidemiological studies could be designed to study the possibility that similar effects 

may be 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 a dose-effect relationship 

would be useful for monitoring individuals near hazardous 

waste sites for preventive purposes. 

Biomarkers of Exposure and Effect. 

Exposure. Methods exist for determining 1,2-dichloroethene in blood and biological tissues (Ashley et 

al. 1992; Hara et al. 1980; Lin et al. 1982; Raymer et al. 1990; Streete et al. 1992; Uehori et al. 1987), 

but specific levels of 1,2-dichloroethene have not been correlated with exposure. Exhalation of 
1,2-DICHLOROETHENE 70 

2. HEALTH EFFECTS
 

acetone and the presence of acetone in blood have been noted in rats after inhalation exposure to cis and 

trans-1,2-dichloroethene, but the amounts exhaled or the levels in blood have not been correlated with 

exposure levels (Freundt et al. 1977). Furthermore, acetonemia is not specific for 1,2-dichloroethene; 

increased acetone levels were found after exposure to other chemicals (e.g., vinyl chloride and 

perchlorethylene) and in patients with diseases such as diabetes (Filser and Bolt 1980). 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. 

Effect. 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 (Filser et al. 1978, 1980; Freundt et al. 1977). Based on these studies, a possible 

mechanism for the production of acetone was suggested, whereby a metabolite (dichloroacetate 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, to an alteration in lipid and fatty acid metabolism to 

form ketone bodies (Filser et al. 1982). 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, and Excretion. The absorption, distribution, 

metabolism and excretion of a chemical can influence its toxicity. Several inhalation studies have 

examined the absorption of l,2dichloroethene, and they indicate that 1,2-dichloroethene vapors can be 

absorbed through the lung (Filser and Bolt 1979; Gargas et al. 1988, 1989; Lehmann and SchmidtKehl 1936). Studies by Gargas et al. (1988, 1989) and Sato and Nakajima (1979) determined 

1,2-dichloroethene partition coefficients between a number of body tissues and show differences 

between the cis and trans isomers. The cis isomer has higher partition coefficients (tissue:air) and, 

therefore, greater affinity or absorption in biological tissue. These are important properties that 

influence toxicological effects. Absorption by the dermal route has not been investigated, although the 

lipophilic properties of this chemical make it likely. According to an ongoing study, 

trans-1,2-dichloroethene was quickly absorbed from the gastrointestinal tract of rats after oral exposure 

(see Section 2.10.3). No other studies on the absorption of 1,2-dichloroethene following oral exposure 

were located. The few oral toxicity studies support this conclusion (McCauley et al. 1990; McMillan 
1,2-DICHLOROETHENE 71 

2. HEALTH EFFECTS
 

1986). No studies were located regarding the distribution and excretion of 1,2dichloroethene 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 (Costa and Ivanetich 1982, 1984). Differences in the 

metabolism rate and the metabolite profile have been reported for the cis and trans isomers, for 

example, the cis isomer had a 4-fold greater turnover rate in hepatic microsomes in vitro than the trans 

isomer (Bonse et al. 1975; Costa and Ivanetich 1982, 1984). The metabolism of 1,2-dichloroethene 

has not been extensively studied in tissues other than the liver. Distribution studies of cis- and 

trans-1,2-dichloroethene and metabolites would help identify those tissues, if any, that accumulate 

them. Excretion studies of 1,2-dichloroethene and its breakdown products would be useful for 

understanding the metabolic fate of this chemical and determining major routes and rates of excretion. 

One important question to be addressed is the difference in metabolism and excretion at low and high 

exposure levels. 

Comparative Toxicokinetics. Although there are relatively few existing studies for comparative purposes, 

some general conclusions can be drawn. The human exposure studies consist of two

 inhalation studies from the 1930s, one of which is too sketchy to use in making any comparisons 

(Hamilton 1934; Lehmann and Schmidt-Kehl 1936). When two volunteers were exposed for

 30 minutes to an unknown ratio of cis:trans 1,2-dichloroethene (Lehmann and Schmidt-Kehl 1936), 

their neurological responses were consistent with animal studies that show lethargy and drowsiness. 

No human toxicokinetic or dosimetry data were located. Among the animal species there is general 

consistency for both inhalation and oral exposure routes in the end points identified. Hepatic, 

hematological, and neurological end points are found in both rats and mice (Barnes et al. 1985; De 

Ceaurriz et al. 1983; McCauley et al. 1990; McMillan 1986). Investigation of 1,2-dichloroethene 

toxicokinetics in different animal species and comparison of detected metabolites with those detected

 in occupationally exposed individuals would be useful for determining an appropriate animal model for 

studying the toxicokinetics of 1,2-dichloroethene. 

Methods for Reducing Toxic Effects. General recommendations for reducing the absorption 

and metabolic responses to 1,2-dichloroethene are based on limited mitigation studies and reports 

found in the primary and review/consensus literature. Few individuals have received intense exposure 
1,2-DICHLOROETHENE 72 

2. HEALTH EFFECTS
 

to 1 ,2-dichloroethene, whether accidental, clinical or occupational. Its neurological, hepatic, hematic, 

and respiratory effects are similar to those of other solvents, and therefore, generalized interventions 

have been drawn from experience with these other solvents. Supportive measures to combat the 

effects of central nervous system, respiratory depression, and cardiac irritability are the clinical 

recommendations (TOMES 1994). There is no specific treatment for 1 ,2dichloroethene exposure, 

partly because its mechanisms of action are not well defined and the numbers of exposed individuals 

needing treatment are small. 

2.10.3 Ongoing Studies 

Several abstracts of studies in progress were located. A high incidence of lymphosarcoma in the lungs 

and histopathological lesions in the spleen and kidneys was reported in rats after 60 days of oral 

treatment with l/2, l/20, and l/200 of the reported LD50 for trans-1 ,2dichloroethene (Witmer et al. 

1990). 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 2-6 minutes after exposure. 
1,2-DICHLOROETHENE 73 

3. CHEMICAL AND PHYSICAL INFORMATION 

3.1 CHEMICAL IDENTITY 

Information regarding the chemical identity of 1,2-dichloroethene is located in Table 3-l. 

3.2 PHYSICAL AND CHEMICAL PROPERTIES 

Information regarding the physical and chemical properties of 1,2dichloroethene is located in 

Table 3-2. There are two isomers of 1,2-dichloroethene, the cis form and the trans form. Some 

important characteristics of the two forms are that they possess a high vapor pressure and the vapor is 

heavier than air (HSDB 1995). The trans form is sufficiently volatile that 50% evaporates from water 

in 22 minutes when stirred at 25 °C; the cis form is similarly volatile (HSDB 1995). Experiments 

have shown that the degradation of the trans form is relatively slow due to ultraviolet irradiation, 

unless lamps of approximately 15-20 watts are used (Guertler et al. 1994) to allow greater relative 

stability of the vapor form in the environment. 



1,2-DICHLOROETHENE 77 

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

4.1 PRODUCTION 

1,2-Dichloroethene has been produced as a commercial end product by the direct chlorination of 

acetylene at about 40 °C or by a technique involving the dehydrochlorination of l,l,2trichloroethane 

at 500 °C (HSDB 1995). Such commercial preparations are mixtures of cis- and trans-l,2dichloroethene. 

The trans isomer is preferred in most industrial applications, which has tended to limit sales of 

the commercially available mixtures (HSDB 1995). 1,2-Dichloroethene is highly flammable and 

extremely corrosive, and yields the explosive compound chloroacetylene in the presence of copper or 

heated alkaline solutions (HSDB 1995). 

Industrial quantities of 1,2-dichloroethene are produced for on-site use in the production of other 

chlorinated compounds, which are the final commercial product. Columbia Organics of South 

Carolina, and Aldrich Chemical of Milwaukee, Wisconsin, 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). Complete data about the volume and trends of 1,2-dichloroethene 

production in the United States are not available (HSDB 1995). As with many chemicals, especially 

those whose production or use involves proprietary information, quantitative estimates of production 

are virtually impossible to obtain (Bason and Colbom 1992). Table 4-l lists the facilities in each state 

that manufacture or process 1,2-dichloroethene, the intended use, and the range of maximum amount 

of 1,2-dichloroethene that is stored at the site. The data listed in Table 4-l are derived from the 

Toxics Release Inventory (TR193 1995). Only certain types of facilities were required to report and 

therefore this is not an exhaustive list. Twelve facilities were identified as producers or processors of 

1,2-dichloroethene, with most of the producers located in Gulf Coast states (Louisiana and Texas). 

4.2 IMPORT/EXPORT 

No data were found on U.S. imports or exports of 1,2-dichloroethene (HSDB 1995). 

1,2-DICHLOROETHENE 79 

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

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 solvent for waxes, resins, acetylcellulose, perfumes, dyes, 

lacquers, thermoplastics, fats, and phenols. It is used in the extraction of rubber, as a refrigerant, in 

the manufacture of pharmaceuticals and artificial pearls, and in the extraction of oils and fats from fish 

and meat (HSDB 1995). It has also been used as a low-temperature extraction solvent for organic 

materials such as decaffeinated coffee (HSDB 1995). No information is available about how much, if 

any, 1,2-dichloroethene is currently used for solvent purposes. The trans isomer is more widely used 

in industry than either the cis isomer or the commercial mixture (Gosselin et a1.1984). 

4.4 DISPOSAL 

1,2-Dichloroethene may be released from industries in waste water streams; however, these compounds 

can be removed from waste water by air stripping (Dilling 1977; Gossett 1987; Shen 1982a). 

Improved waste water treatment methods at publicly owned treatment works (POTWs) now use air 

stripping processes to remove most 1,2-dichloroethene and other volatile organic compounds (VOCs) 

from final effluents and deposit them in sludges or release them in air emissions (Bennett 1989). 

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). 1,2-Dichloroethene is a 

potential candidate for rotary kiln incineration at 820-1,600 °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 

650-1,600 °C with residence times of 0.1-2 seconds (HSDB 1995). Care must be exercised to assure 

complete combustion to prevent the formation of phosgene. Acid scrubbers are required to control air 

emissions. Information regarding the amount disposed of by each method is not available. 

Experiments using a vacuum-ultraviolet excimer flow-through reactor to degrade chloro-organic 

compounds in water have had promising results (Baum and Oppenlander 1995). After 60 minutes of 

irradiation at 172 nm, the level of 1,2-dichloroethene in contaminated groundwater was reduced from 

25 mg/L to below the detection limit of 0.1 mg/L. After 180 minutes of irradiation, more than 93% of 

the originally organic- bound chlorine atoms were converted to inorganic chloride ions. 
1,2-DICHLOROETHENE 80 

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

The EPA has identified trans- 1,2dichloroethene as a hazardous waste; its disposal is regulated under 

the Resource Conservation and Recovery Act (RCRA). Cis-1,2-dichloroethene has not been identified 

as a hazardous waste by the EPA. 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 waste water 

is regulated under the Clean Water Act by the National Pollutant Discharge Elimination System 

(NPDES). Information regarding effluent guidelines and standards for trans-1 ,2dichloroethene 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 

(EPA 1988b). It may be disposed on land only if prior treatment standards have been met, or if 

disposal occurs in units that satisfy the statutory no-migration standard (EPA 1988b). Proper 

guidelines and standards are outlined in the Code of Federal Regulations (EPA 1988b). Current 

criteria for land treatment or burial are subject to significant revision; prior to implementing land 

disposal of waste residue (including waste sludge) environmental regulatory agencies should be 

consulted for guidance on acceptable disposal practices (HSDB 1995; OHM/TADS 1988). 

Rules and regulations regarding disposal practices are discussed in Chapter 7. 
1,2-DICHLOROETHENE 81 

5. POTENTIAL FOR HUMAN EXPOSURE 

5.1 OVERVIEW 

1,2-Dichloroethene is a compound produced by human industrial activities. Sources of environmental 

exposure to 1,2-dichloroethene include: process and fugitive emissions from its production and use as 

a chemical intermediate; evaporation from waste water 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 l,2dichloroethene 

released in the environment will eventually enter the atmosphere or groundwater, where it may 

be subject to further biotic or abiotic degradation processes. 

1 ,2-Dichloroethene is removed from the atmosphere chiefly through reaction with photochemicallygenerated oxygenated species (e.g., hydroxyl radicals). The estimated atmospheric lifetimes for cisand trans-1,2-dichloroethene due to this removal process are 12 and 5 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, with an estimated half-life of about 3-6 hours in a model 

river (Thomas 1982). 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). Aerobic or facultative biodegradation processes have also been documented (Vannelli et 

al. 1990). Since 1,2-dichloroethene will often be found in mixtures with other chlorinated solvents, 

half-lives for degradation processes can be estimated only approximately. 

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 (EPA 1983a). These exposure levels correspond to an 

average daily intake of l-6 μg/day assuming an average daily intake of 20 m3 of air. Additional 

exposure may occur from contaminated tap water, through consumption, inhalation during showering, 

and dermal contact. Occupational exposure may occur by inhalation and/or dermal contact. 

According to a 1981-1983 NIOSH survey, an estimated 215 workers in the United States are 
1,2-DICHLOROETHENE 82 

5. POTENTIAL FOR HUMAN EXPOSURE
 

potentially exposed to 1,2-dichloroethene in the workplace (NIOSH 1988). This figure does not 

include firefighters and landfill workers. 

Cis-1,2-dichloroethene has been identified in at least 146 of the 1,430 current or former EPA National 

Priorities List (NPL) hazardous waste sites and trans-1,2-dichloroethene has been identified in at least 

563 of the current or former NPL sites. In 336 of the NPL sites, 1,2-dichloroethene was identified but 

the isomer was not specified (HazDat 1996). However, the number of sites evaluated for 1,2-dichloroethene is not known. The frequency of these sites can be seen in Figures 5-1, 5-2, and 5-3, for cis, 

trans, and unspecified, respectively. Two of the sites where trans-1,2-dichloroethene was found are 

located in the Commonwealth of Puerto Rico (not shown) and all other sites are located in the United 

States. 

5.2 RELEASES TO THE ENVIRONMENT 

5.2.1 Air 

1,2Dichloroethene may be released to the atmosphere in emissions from production facilities, 

contaminated waste waters, contaminated waste disposal sites, and the pyrolysis and combustion of 

polyvinyl chloride and some vinyl copolymers. It may also be released during its use as a solvent and 

extractant, in organic synthesis, and in the manufacture of perfumes, lacquers, and thermoplastics. 

(HSDB 1995; Michal 1976; Shen 1982b). Not enough data are currently available to estimate the total 

amount of 1,2-dichloroethene released to the atmosphere. 

According to the Toxics Release Inventory (TRI), an estimated total of 29,478 pounds of 1,2-dichloroethene representing >99.9% of the total environmental release was discharged to air from

 manufacturing and processing facilities in the United States in 1993 (TR193 1995). Table 5-l lists the 

amounts released from each of these identified facilities. The TRI data should be used with caution 

since only certain types of facilities are required to report. Therefore, this is not an exhaustive list. 

There is a potential for atmospheric release of 1,2-dichloroethene from hazardous waste sites. 

Cis-1,2-dichloroethene has been detected in air samples from 3 of the 146 NPL sites where 

cis-1,2-dichloroethene has been identified in some medium (HazDat 1996). Tram+1,2-dichloroethene 




1,2-DICHLOROETHENE 87 

5. POTENTIAL FOR HUMAN EXPOSURE
 

has been detected in air samples from 17 of the 563 NPL sites where trans-1,2-dichloroethene has 

been identified in some medium (HazDat 1996). 1,2-Dichloroethene (isomer unspecified) has been 

detected in air samples from 15 of the 336 NPL sites where 1,2-dichloroethene has been identified, 

without specifying the isomer, in some medium (HazDat 1996). 

While there is disagreement in the literature on the persistence of 1,2-dichloroethene released to the 

atmosphere, the half-lives would likely be measured in days, allowing for transport over large regional 

or even continental areas (Hall et al. 1989; Winer and Atkinson 1987). However, areas like southern 

California, where 1,2-dichloroethene is not commonly used as an end product or a chemical 

intermediate, have not shown detectable levels of 1,2dichloroethene in ambient air. 

5.2.2 Water 

1,2-Dichloroethene may be released to surface waters via surface runoff from contaminated waste 

disposal sites, waste water from a variety of industrial sources, and from some publicly owned 

treatment works (POTWs). 1,2-Dichloroethene may be found in effluents from manufacturing and 

processing sites and from industries involved in its use as a solvent and extractant, in its use in organic 

synthesis, and in its use in the manufacture of perfumes, lacquers, and thermoplastics (Hawley 1981). 

As part of a comprehensive EPA survey of industrial facilities and POTWs, 4,000 samples of waste 

water were analyzed. The findings indicate that cis- or trans.-1,2-dichloroethene is sometimes found in 

waste water from: petroleum refining; coal mining; foundries; nonferrous metal manufacture; POTWs; 

paint and ink formulation; rubber processing; steam electricity generation; leather tanning; iron and 

steel manufacture; textile mills; auto and other laundries; explosives factories; and production of 

inorganic chemicals, mechanical products, plastics and synthetics, electrical components and 

electronics, pharmaceuticals, organic chemicals and plastics, and transportation equipment (EPA 

1980b; Shackelford et al. 1983). Effluents from iron, steel, and nonferrous metal manufacturing; and 

organics, plastics, and rubber processing exceeded 100 ppb of cis-1,2-dichloroethene. Effluents of iron 

and steel manufacturing, electronics, and POTWs also contained trans- 1,2-dichloroethene (see Section 

5.4.2) (Shackelford et al. 1983). It has been estimated that between 1982 and 1984, trans-l,2dichloroethene 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 88 

5. POTENTIAL FOR HUMAN EXPOSURE
 

During the 1980s as steady progress was made in negotiating final discharge permits for POTWs 

under EPA’s National Pollutant Discharge Elimination System (NPDES) permitting program, the 

incidence of 1,2-dichloroethene inputs to surface waters from point source discharges may have 

substantially decreased. Improved levels of waste treatment have the potential to remove virtually all 

VOCs from final effluents. These materials will become air emissions or become immobilized in 

sludges (Bennett 1989). 

According to TRI93 (TRI93 1995), an estimated total of only 28 pounds of 1,2-dichloroethene, 

Representing <0.1% of the total environmental release, was discharged to water from manufacturing 

and processing facilities in the United States in 1993. Table 5-l lists the amounts released to water 

from each of the identified facilities. The TRI data should be used with caution since only certain 

types of facilities are required to report; therefore, this is not an exhaustive list. 

1,2-Dichloroethene may be released to groundwater as a result of leaching from contaminated waste 

disposal sites, and by anaerobic degradation of other more highly chlorinated ethenes and ethanes 

present in groundwater (Cline and Viste 1985; HSDB 1995; Parsons et al. 1984; Smith and Dragun 

1984). Barber et al. (1988) reported 280 ppb of 1,2-dichloroethene (isomer unspecified) in 

groundwater under a sandy rapid infiltration site that had received secondary sewage effluent since 

1936. 

1,2-Dichloroethene in drinking water may result from raw water source contamination (Otson et al. 

1982). There is very little documentation of direct 1,2dichloroethene contamination of groundwater. 

Research suggests that most 1,2-dichloroethene detections in groundwater involve biodegradation 

processes related to primary pollution from trichloroethylene (TCE) or tetrachloroethylene (PCE) (see 

Section 5.3). 

In addition to spills or leachates from waste disposal sites, groundwater may be contaminated by 

cracked sewer interceptors carrying industrial wastes. Especially after rains, substantial loadings may 

leave the interceptor system through infiltration and inflow (I&I) processes and enter groundwater 

supplies. Such phenomena have been documented in Europe (Milde et al. 1988) and similar I&I 

problems are common in most older U.S. cities. 
1,2-DICHLOROETHENE 89 

5. POTENTIAL FOR HUMAN EXPOSURE
 

There is also a potential for release of 1,2-dichloroethene to water from hazardous waste sites. 

Cis-1,2-dichloroethene has been detected in groundwater samples collected at 130 of the 146 NPL 

sites, in surface water samples collected at 14 of the 146 NPL sites, and in leachate samples collected 

at 8 of the 146 NPL sites where cis-1,2-dichloroethene has been identified in some medium (HazDat 

1996). Trans-1,2-dichloroethene has been detected in groundwater samples collected at 487 of the 563 

NPL sites, in surface water samples collected at 137 of the 563 NPL sites, and in leachate samples 

collected at 48 of the 563 NPL sites where trans-1,2-dichloroethene has been identified in some 

medium (HazDat 1996). 1,2-dichloroethene (isomer unspecified) has been detected in groundwater 

samples collected at 263 of the 336 NPL sites, in surface water samples collected at 57 of the 336 

NPL sites, and in leachate samples collected at 29 of the 336 NPL sites where 1,2-dichloroethene 

(isomer unspecified) has been identified in some medium (HazDat 1996). 

5.2.3 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, aquifers, or 

sediments as anaerobic biodegradation products of tetrachloroethene, trichloroethene, 1,l ,l -

trichloroethane, and 1,1,2,2-tetrachloroethane, solvents commonly found in municipal and industrial 

landfills (Parsons et al. 1984; Smith and Dragun 1984). In muck and sediment microcosms, 

tetrachloroethylene is converted to 1,2-dichloroethene with a preponderance of the cis isomer (Parsons et 

al. 1984). Cis-1,2-dichloroethene apparently is the more common isomer found, although it may be 

mistakenly reported as the trans isomer. Because it is a priority pollutant, the trans isomer is more 

commonly analyzed for, and the analytical procedures used generally do not distinguish between isomers 

(Cline and Viste 1995). Insufficient data are available to estimate the amount of 1,2-dichloroethene 

released to soil. 

According to TRI93 (TRI93 1995), no 1,2-dichloroethene was released to land from manufacturing 

and processing facilities in the United States in 1993. Table 5-l lists the amounts released from these 

facilities. The TRI data should be used with caution since only certain types of facilities are required 

to report; therefore, this is not a comprehensive list. 

Available information for aquatic sediments is also very limited. Some researchers feel that the 

subsurface behavior of 1,2-dichloroethene would be similar in groundwater, soils, and sediments (Yeh 
 

1,2-DICHLOROETHENE 90 

5. POTENTIAL FOR HUMAN EXPOSURE
 

and Kastenberg 1991). Most empirical information, however, derives from groundwater remediation 

studies, usually involving controlled laboratory microcosm studies. For some highly polluted 

waterbodies, for instance the Delaware and Raritan Canal, 1,2-dichloroethene detections in the water 

column probably reflect extensive contamination with chlorinated toxics in the sediments (Granstrom 

et al. 1984). Analyzing cause-source pathways in such complicated systems can be extremely difficult. 

There is also a potential for release of 1,2-dichloroethene to soils and sediments from hazardous waste 

sites. Cis-1,2-dichloroethene has been detected in soil samples collected at 12 of the 146 NPL sites, in 

sediment samples collected at 1 of the 146 NPL sites where cis-1,2-dichloroethene has been identified 

in some medium (HazDat 1996). Trans-1,2-dichloroethene has been detected in soil samples collected 

at 179 of the 563 NPL sites, in sediment samples collected at 61 of the 563 NPL sites, in sludge 

samples collected at 14 of the 563 NPL sites where trans-1,2-dichloroethene has been identified in 

some medium (HazDat 1996). 1,2-Dichloroethene (isomer unspecified) has been detected in soil 

samples collected at 76 of the 336 NPL sites, in sediment samples collected at 30 of the 336 NPL sites 

where 1,2-dichloroethene (isomer unspecified) has been identified in some medium (HazDat 1996). 

5.3 ENVIRONMENTAL FATE 

5.3.1 Transport and Partitioning 

Occurrence of 1,2-dichloroethene in rainwater samples (Kawamura and Kaplan 1983) indicates thatthis 

compound may be removed from the atmosphere by precipitation; however, most of the1,2dichloroethene 

so removed is likely to reenter the atmosphere by volatilization. Organics with avapor pressure of >10-4 

mmHg 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 and 336 mmHg at 25 °C, 

respectively (Stevens 1979), are not expected to partition from the vapor phase to particulates in the 

atmosphere. Because it is relatively long-lived in the atmosphere, significant transport from source areas 

should occur (HSDB 1995). 

The dominant removal mechanism for 1,2-dichloroethene in surface waters is volatilization (EPA 

1979). Henry’s Law constants are 4.08x10-3 atm-m3

/mol at 24.8 °C for cis-1,2-dichloroethene and 

9.38x10-3 atm-m3

/mol at 24.8 °C for trans-1,2-dichloroethene (Gossett 1987). Based on these values, 

the volatilization half-life from a model river 1 m deep, flowing 1 m/second with a wind speed of 
1,2-DICHLOROETHENE 91 

5. POTENTIAL FOR HUMAN EXPOSURE 

3 m/second 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 minutes for the 

cis isomer and 24 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. 

In fish, bioconcentration factors (BCFs) 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 (Bysshe 1982; Hansch and Leo 1985; Horvath 1982; Lyman et al. 1982). A BCF value of 6 for 

the fathead minnow (Pimephales promelas) was estimated in ASTER (1994) using the method of 

Veith and Kosian (1983). These estimated BCFs suggest that 1,2-dichloroethene does not 

bioconcentrate significantly in aquatic organisms. Based on this information, there is little potential 

for biomagnification within aquatic food chains. 

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, 1,2-dichloroethene can leach into groundwater where 

very slow biodegradation should occur (HSDB 1995). 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 oxygenated species (e.g., hydroxyl radicals) in the troposphere. The 

estimated atmospheric lifetimes for cis- and trans-1,2-dichloroethene due to this removal process are 

12 and 5 days, respectively (Goodman et al. 1986). These estimates are based on experimentally 

determined hydroxyl reaction rate constants of 2.0x10-l2 cm3

/molecules-sec at 25 °C for the cis 
1,2-DICHLOROETHENE 92 

5. POTENTIAL FOR HUMAN EXPOSURE
 

isomer and 4.5x10-12 cm3

/molecules-sec at 25 °C for the trans isomer. Formyl chloride has been 

positively identified as a product of this reaction. 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; Sanhueza and Heicklen 1975a, 

1975b). The half-life resulting from ozone attack of the double bond is 44 days for the trans isomer 

and 129 days for the cis isomer (Tuazon et al. 1984). There also is evidence that cis-1 ,2-dichloroethene 

will be scavenged by rain (HSDB 1995) 

The primary ultraviolet (UV) absorption band for cis-1,2-dichloroethene is at 190 nm, which extends 

to about 240 nm (Ausbel and Wijnen 1975). The primary UV absorption band for the trans isomer 

also extends to about 240 nm (Dahlberg 1969). A minute amount of light is absorbed in the 

environmentally significant range (wavelengths greater than 290-380 nm). However, such absorption 

is insufficient for direct photolysis to be a significant fate process in the atmosphere. 

Gtirtler et al. (1994) investigated the photochemical decomposition and oxidation of the chloroethenes 

in the gas phase by irradiation with a low-pressure mercury lamp in an oxygen atmosphere. 

Trans-1,2-dichloroethene slowly disappears after several hours of irradiation at 254 nm. After a period 

of restrained degradation, sudden decomposition is observed, probably resulting from the start of a 

chain mechanism. Trans-1,2-dichloroethene decomposes more slowly at low concentrations than at 

high ones. The primary photooxidation products are formyl chloride and, in small amounts, 

monochloro-acetyl chloride and dichloroacetaldehyde. Further photooxidation leads to the formation 

of phosgene, additional formyl chloride, formaldehyde, carbon monoxide, carbon dioxide, and 

hydrochloric acid. 

In polluted urban airsheds, photolytic processes are a major factor in generating free radicals. Several 

studies summarized in Hall et al. (1989) emphasize that 1,2-dichloroethene degradation will proceed 

2-4 times faster in polluted urban air exposed to UV radiation than with “pure air” contained no free 

radical precursors. Tuazon et al. (1988) and Jeffers et al. (1989) provide other convenient summaries 

of the reaction chemistry of chloroethenes and OH radicals. 
1,2-DICHLOROETHENE 93 

5. POTENTIAL FOR HUMAN EXPOSURE 

5.3.2.2 Water 

There is relatively little literature dealing with 1,2dichloroethene fate and transport in surface waters. 

Since 1,2-dichloroethene is appreciably volatile, the usual assumption is that 1 ,2dichloroethene 

introduced into surface waters will rapidly be transferred to the atmosphere (see Section 5.3.1). 

Chemical hydrolysis and oxidation are probably not environmentally important fate processes for 

1,2-dichloroethene (EPA 1979, 1981a, 1984). Kinetic data pertaining specifically to the abiotic 

degradation of the 1,2-dichloroethene isomers in the environment were not located. Direct photolysis 

of 1,2dichloroethene is also not likely to be important in sunlit natural waters (EPA 1979) (see 

Section 5.3.2.1). 

When dealing with surface waters, 1,2-dichloroethene and other chlorinated ethenes generally 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. In this study (Tabak et al. 1981), settled domestic waste water was used as the 

inoculum with 5 ppm each of the cis and trans isomers. Losses in 7 days were 54% of the cis isomer 

and 67% of the trans isomer. Losses due to volatilization over a lo-day period were 34 and 33% for 

the cis and tram isomers, respectively. 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. 

There is a growing body of literature dealing with fate and transport processes in groundwater. These 

studies are related to programs under the EPA Safe Drinking Water Act that address health risks from 

VOC contaminants in community drinking water systems, and to efforts to mitigate pollution at older 

waste disposal sites and remediate areas showing smaller-scale spills. While work through the early 

1980s focussed on the biodegradation of 1,2-dichloroethene itself, it quickly became apparent that 

1,2dichloroethene contamination at many sites was part of a complicated series of biotransformations 

where such solvents- as trichloroethylene or tetrachloroethylene were the principle driving-forces 

(Vogel et al. 1987). 

1,2-Dichloroethene undergoes 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 
1,2-DICHLOROETHENE 94 

5. POTENTIAL FOR HUMAN EXPOSURE
 

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 tram 

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 l-2 weeks incubation; therefore, the cis isomer degrades more rapidly. After 40 weeks, the 

tram 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. Tandoi et 

al. (1994) found that an anaerobic enrichment culture, using methanol as an electron donor, rapidly 

metabolized cis-1 ,2dichloroethene to vinyl chloride with near zero-order kinetics and apparent 

inhibition of subsequent vinyl chloride dechlorination. Trans- 1 ,2dichloroethene was converted to 

vinyl chloride more slowly with first order kinetics and an estimated half-life of 9.5 hours and did not 

inhibit vinyl chloride dechlorination. 

Hopkins and McCarty (1995) performed an evaluation of the aerobic cometabolism of dichloroethene 

isomers, using phenol and toluene as the primary substrates, in a shallow aquifer at a pilot test facility. 

In an earlier study, a methane substrate was highly successful at transforming trans-1,2-dichloroethene 

in groundwater, but removal efficiency was rather low for cis-1,2-dichloroethene. Phenol was found to 

be superior to methane for in situ degradation of cis-1,2-dichloroethene, providing up to 90% removal 

in one pass at concentrations up to 1 mg/L. Removal of trans-1,2-dichloroethene was 74% when 

phenol was used. Semprini (1995) also demonstrated in pilot scale field studies of aerobic 

cometabolic transformations that indigenous microbes grown on phenol are more effective at degrading 

cis- 1,2-dichloroethene than are microbes grown on methane. 

A study was performed on a sand aquifer at an industrial site near the town of St. Joseph; Michigan, 

to improve the understanding of the distribution of chlorinated aliphatic hydrocarbons (CAHs) years 

after contamination occurred (Semprini 1995). Groundwater concentrations varied significantly with 

depth. Relatively high concentrations of CAHs existed at all locations within 20 m of the center of 

the plume. The dominant dichloroethene isomer present was the cis isomer, with maximum 
1,2-DICHLOROETHENE 95 

5. POTENTIAL FOR HUMAN EXPOSURE
 

concentrations of the cis and trans isomers of 133 and 3.9 mg/L, respectively. Cis-1,2-dichloroethene 

was observed in a transition zone between high and decreasing trichloroethene concentrations. 

Anaerobic biotransformation by methanogenic bacteria was the earliest documented research on the 

biodegradation of 1,2-dichloroethene. In addition to studies in the United States (Barrio-Lage at al. 

1986; Ehlke et al. 1992; Parsons et al. 1984; Silka and Wallen 1988), there has been good 

documentation of similar phenomena in sandy aquifers near Berlin, Germany (Kastner 1991; Leschber 

et al. 1990) and in groundwater supplies near a landfill in Ottawa, Canada (Lesage et al. 1990). In 

addition to anaerobic pathways, laboratory studies suggest that ammonia-oxidizing aerobic bacteria 

(Vannelli et al. 1990) and facultative sulfur-bacteria (Bagley and Gossett 1990) can biodegrade 

chlorinated aliphatic hydrocarbons. Burback and Perry (1993) demonstrated that 1,2-dichloroethene, 

when added singly to groundwater, is catabolized by Mycobacterium vaccae. At 100 ppm, 

1,2dichloroethene was catabolized <50%. A wide range of estimates for reaction rates and pollutant 

half-lives have been reported. The biodegradation processes appear to be highly site specific, and 

influenced by the types of bacteria present, the presence of aerobic or anaerobic conditions, the 

presence of other substrates such as methane or sulfide, and the toxicity impacts from the various 

metabolites (Janssen et al. 1988). 

5.3.2.3 Sediment and 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 and that this process may be the sole mechanism by which 1,2-dichloroethene 

degrades 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. Biodegradation of 

trans- 1,2-dichloroethene was studied in microcosms containing uncontaminated organic sediment from 

the Everglades and allowed to stand to ensure oxygen depletion. Under these anoxic conditions, 50% 

of the chemical was lost within 6 months (Barrio-Lage et al. 1986). The fact that ethyl chloride as 

well as vinyl chloride are produced indicates that there are different pathways in the sequential 

dechlorination of cis- 1,2-dichloroethene. 
1,2-DICHLOROETHENE 96 

5. POTENTIAL FOR HUMAN EXPOSURE
 

There are no transformation and degradation studies dealing with sediments. 1,2-Dichloroethene does 

not show significant bioconcentration or bioaccumulation tendencies, and outside groundwater would 

tend to volatilize and move to the atmosphere. Some researchers feel that the behavior of 

1,2dichloroethene in sediments would be similar to patterns documented for soils or groundwater 

(Yeh and Kastenberg 1991). 

5.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 

5.4.1 Air 

1,2Dichloroethene has been frequently detected in air samples from urban locations throughout the 

United States and in landfill gas. Data in Table 5-2 represent available air monitoring data for 

1,2-dichloroethene. Only one rural air monitoring study was located (Grimsrud and Rasmussen 1975). 

Maximum 1,2-dichloroethene concentrations detected in landfill gas ranged from 3,260 ppb (Vogt and 

Walsh 1985) in a municipal landfill simulator to 75,600 ppb at two Long Island landfills (Lipsky and 

Jacot 1985). 

In 1986, EPA carried out an update to its National Ambient Database, with a focus on updating the 

coverage for VOCs (Shah and Singh 1988). Based on information from 161 data points, outdoor 

1,2-dichloroethene daily ambient air concentrations averaged 0.326 ppb, with a median of 0.037 ppb 

and with 75% of the values falling below a concentration of 0.113 ppb. 

With steady improvements in the efficiency of waste water treatment plants, the loadings of various 

toxics to receiving waters has substantially decreased over the last decade (Bennett 1989). However, 

reductions to surface water loadings have often resulted in increased emission to the atmosphere as 

volatile constituents of the waste influents are removed through techniques such as air stripping. 

Wastes, including organics like 1,2-dichloroethene, will also be transferred to sludges generated from 

biotic digestion processes or the use of chemical coagulants. Where sludge drying beds are located. 

close to waste water plants, volatile constituents in the residuals will be vented to the air. These 

phenomena can present toxic exposure risks to workers at the treatment plants and to populations 

living close to these facilities. 


1,2-DICHLOROETHENE 99 

5. POTENTIAL FOR HUMAN EXPOSURE 

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. 

Table 5-3 shows the available monitoring data for 1,2dichloroethene in these media. In some of the 

studies, only one of the 1,2-dichloroethene isomers was monitored; while in several of the studies the 

authors did not mention the specific isomer monitored. Concentrations of 1,2-dichloroethene detected 

in surface water ranged from 0.43 ppb in the Quinipiac River in Connecticut (Hall 1984) to 

1,307.5 ppb in New Jersey (Table 5-3). 

1,2-Dichloroethene has been detected in groundwater in several states and U.S. territories including 

Colorado, Connecticut, Florida, Maryland, Michigan, Nebraska, New Jersey, Pennsylvania, Puerto 

Rico, Washington, and Wisconsin (Table 5-3). Concentrations of 1,2dichloroethene isomers detected 

in groundwater ranged from 0.25 to 0.28 ppb (range of average concentrations) from 6 areas near 

Miami, Florida (Singh and Orban 1987) to a maximum of 500,000 ppb in Southington, Connecticut 

(Hall 1984). 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. 1,2Dichloroethene was detected 

in samples from 5 of 26 landfills at a maximum concentration of 3,900 ppb, and in leachate from 8 of 

26 landfills at a maximum concentration of 310 ppb (Friedman 1988). 

Since 1,2-dichloroethene can be produced from biodegradation of a variety of VOCs, screening tests 

for VOCs or tests for such widely used solvents as TCE or PCE can provide useful screening tools for 

follow-up testing for 1,2-dichloroethene. For instance, a study of 19 landfill sites in Wisconsin 

showed that while the incidence of 1,2-dichloroethene in all test wells was 19%, approximately 

two-thirds of the wells showing detectable VOCs also showed detectable 1,2dichloroethene (Battista 

and Connelly 1989). In a study of a western Connecticut manufacturing plant that used large 

quantities of high quality trichloroethylene for degreasing, it was found that 7 of 9 monitoring wells 

contained 1.2-320.9 ppb of trans-1,2-dichloroethene (Stuart 1983). More localized problems from 

leaking underground storage tanks or chemical spills may also show up in screens for VOCs (Stenzel 

and Gupta 1985). Where pollution levels are not excessive, remediation or permanent treatment 

technologies involving combinations of granular activated carbon or air stripping can remove over 







1,2-DICHLOROETHENE 107 

5. POTENTIAL FOR HUMAN EXPOSURE
 

96% of VOCs such as cis-1,2-dichloroethene (Clark et al. 1988; Lee et al. 1988; Stenzel and Gupta 1985). 

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 nonrandom sites (Westrick 

et al. 1984). Trans-1,2-dichloroethene was found in Miami, Florida, drinking water at 1 ppb. 

Cis-1,2-dichloroethene was found in Miami drinking water at 16 ppb; and in Cincinnati, Ohio, and 

Philadelphia, Pennsylvania, drinking water at 0.1 ppb; but was not detected in 7 other drinking waters 

surveyed (EPA 1980d). 

In a four-city study (Cincinnati, Ohio; St. Louis, Missouri; Atlanta, Georgia; Hartford, Connecticut) to 

determine the major source type of priority pollutants in tap water and POTW influents, it was found 

that 43, 38, and 28% of commercial sources, industrial sources, and POTW influents, respectively, 

contained trans- 1 ,2dichloroethene (EPA 198 lc). The average concentrations from the industrial 

sources were between 10 and 100 ppb while the others were <10 ppb. Industrial effluent monitoring 

data from Shackelford et al. (1983) was obtained from a database of a comprehensive EPA survey of 

4,000 effluent samples from industries and POTWs. This survey was conducted in response to the 

consent decree between the National Resources Defense Council and the EPA on June 7, 1976. Data 

from this study are presented in Table 5-3. 

Over the last decade, the Safe Drinking Water Act has focussed attention on improved controls over 

VOC contamination (including 1,2-dichloroethene) of community drinking water systems. Based on 

available national statistics, 1,2-dichloroethene has been found in detectable concentrations at less than 

5% of the community systems using surface water sources. The figures jumped to 21%, however, for 

community systems relying on groundwater (Coniglio et al. 1980). No comparable figures are 

available for noncommunity systems, such as truck stops or highway convenience stores in rural areas, 

or for domestic groundwater wells. 

5.4.3 Sediment and 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 
1,2-DICHLOROETHENE 108 

5. POTENTIAL FOR HUMAN EXPOSURE
 

in a shallow, unconfined aquifer receiving waste water from metal-plating operations at Picattinny 

Arsenal in Morris County, New Jersey, were found to have a maximum cis-1,2-dichloroethene 

concentration of 33 ppb in the vadose zone (Smith 1988). 1,2-Dichloroethene has been detected, but 

not quantified, in sediment samples at Love Canal, New York (HSDB 1995). 

Recent summaries related to data on 1,2dichloroethene in sediments have not been located. 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 database (Staples et al. 1985). No further summary 

information was located on the occurrence of 1,2-dichloroethene in sediments. EPA is in the process 

of consolidating all available information on toxics in sediments to comply with provisions of the 

Water Resources Development Act of 1992. This will lead to the creation of a National Sediment 

Inventory, which should eventually facilitate custom data retrievals and encourage research studies to 

analyze available sediment monitoring results (EPA 1993). 

5.4.4 Other Environmental Media 

Trans-1,2dichloroethene concentrations ranging from 22 to 55 g/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 U.S. 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 1,2dichloroethene levels of 0.04 and 0.05 ppm, respectively, in fish tissue from 

Commencement Bay in Tacoma, Washington. No fish obtained at the 95 stations in EPA’s STORET 

database contained detectable levels of 1,2-dichloroethene (Staples et al. 1985). A BCF of 6 was 

estimated for fathead minnows (ASTER 1995) using the method of Veith and Kosian (1983). Using a 

log octanol/water partition coefficient of 2.06 for trans-1,2-dichloroethene and a recommended 

regression equation (Lyman et al. 1982), a BCF of 22 has been estimated (HSDB 1995). Based on 

these estimated BCFs, 1,2-dichloroethene is not expected to bioaccumulate to any appreciable extent. 
1,2-DICHLOROETHENE 109 

5. POTENTIAL FOR HUMAN EXPOSURE
 

The general population is exposed to 1,2-dichloroethene in urban air and drinking water, with higher 

possibilities of exposure in community systems relying on groundwater supplies. Contaminated tap 

water can cause exposure via ingestion, inhalation, and dermal contact during 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 μg/m3

) (EPA 1983a). These exposure 

levels correspond to an average daily intake of l-6 μg 1,2-dichloroethene, assuming an average daily 

intake of 20 m3

 of air. Risks from inhalation exposures may be of more concern to populations in 

regions such as Gulf Coast states that have substantial production facilities for chlorinated polymers 

(Hall et al. 1989). An average daily intake of 0.5-5.4 μg from water is calculated assuming a 

concentration of 0.23-2.7 ppb (HSDB 1995). Data are insufficient for estimating 1,2-dichloroethene 

intake via other routes of exposure. 

Ashley et a1.(1994) determined the internal dose of 32 volatile organic compounds in 600 or more 

people in the United States who participated in the Third National Health and Nutrition Survey 

(NHANES III). Detectable concentrations of cis- and tram-1,2-dichloroethene were found in fewer 

than 10% of the samples examined. Their detection limits were 0.013 and 0.014 ppb, respectively. 

According to a National Occupational Exposure Survey (NOES) conducted by NIOSH 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 estimates will be updated as 

additional information on trade name compounds containing 1 ,2dichloroethene becomes available. 

There was no NOES estimate for the trans isomer. Occupational exposure is by dermal contact with 

the vapor and liquid or by inhalation (HSDB 1995). 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; as a direct solvent in gums, waxes, etc.; 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 adhesive, and germicidal fumigant (NIOSWOSHA 

1978). The extent of continuing use of 1,2-dichloroethene in these operations is unknown. 
1,2-DICHLOROETHENE 110 

5. POTENTIAL FOR HUMAN EXPOSURE
 

Firefighters and workers at landfill sites may also be exposed to 1,2dichloroethene (Michal 1976; 

NIOSWOSHA 1978; Vogt and Walsh 1985). No information was located on exposure levels in other 

occupational settings. 

5.6 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 

Other than individuals who are occupationally exposed, populations with potentially high exposure 

include those living near production and processing facilities, hazardous waste sites, municipal waste 

water treatment plants, and municipal landfills. Near production and processing facilities, 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, as amended, directs the Administrator of ATSDR (in consultation with 

the Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of 1,2-dichloroethene is available. Where adequate 

information is not available, ATSDR, in conjunction with the 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 the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will 

be evaluated and prioritized, and a substance-specific research agenda will be proposed. 

5.7.1 Identification of Data Needs 

Physical and Chemical Properties. The physical and chemical properties of both cis- and 

trans-1,2-dichloroethene are well characterized (see Table 3-2) and allow prediction of the transport 
1,2-DICHLOROETHENE 111 

5. POTENTIAL FOR HUMAN EXPOSURE
 

and transformation of the chemicals in the environment. Therefore, no data needs have been identified 

at this time. 

Current production and import/export volumes and usage data are presently unavailable in the literature. 

Much of the information regarding 1,2dichloroethene may be difficult to obtain because many 

manufacturing companies maintain confidentiality. In 1977, the estimated production of cis-1,2­

dichloroethene was 500 metric tons. No information was available for the trans isomer or for the mixture 

(HSDB 1995). Also, information about future domestic production, and past, present and future imports 

and exports is lacking. Furthermore, determining the percentage of 1,2dichloroethene that is used as a 

captive intermediate (i.e., the 1,2dichloroethene 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 of the general population. 

With up-to-date and accurate production, import/export, and use data, the extent of release into the 

environment and the potential for human exposure could be more realistically determined. Disposal 

methods have been described and appear to be satisfactory. 

Because 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 ,2dichloroethene 

in waste water 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 CFR433.1l(e). 

Environmental Fate. 1,2Dichloroethene released to the environment partitions mainly to the 

atmosphere (Eisenreich et al. 1981; Swann et al. 1983; Thomas 1982). It is primarily found in the 

atmosphere and groundwater (HSDB 1995; TR193 1995). Important sources of 1,2dichloroethene 

include industrial releases and degradation products from other solvents such as trichloroethene, 
1,2-DICHLOROETHENE 112 

5. POTENTIAL FOR HUMAN EXPOSURE
 

tetrachlorethene, and vinyl chloride (Parsons et al. 1984; Shen 1982b; Smith and Dragun 1984; Vogel et 

al. 1987). 1,2Dichloroethene isomers have predicted atmospheric half-lives of 12 days (cis) and 5 days 

(trans) (Goodman et al. 1986). Both isomers react with hydroxyl radicals in the atmosphere, forming formy1 chloride, but atmospheric ozone, nitrate radicals and singlet oxygen have little environmental effect 

(Atkinson and Carter 1984). In surface waters, the isomers of 1,2dichloroethene are rapidly volatized; 

half-lives of 5-6.2 hours are estimated for water 1 m deep (Dilling 1977). The compound is not 

significantly bound to soils or sediments (Barber et al. 1988). Soil-groundwater degradation processes are 

anaerobic and may involve multiple pathways. Additional information about the long-term atmospheric 

fate would be useful, because of the importance of this pathway and the uncertainty of atmospheric 

degradation processes. 

Bioavailability from Environmental Media. No specific information is available regarding 

human 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 through 

the lungs and gastrointestinal tract. The few available toxicity studies of animals exposed to 

1,2-dichloroethene support this contention (Filser and Bolt 1979; Gargas et al. 1988, 1989). No 

information about human exposure to 1,2-dichloroethene in the environment and the resulting 

concentrations in human tissue was located. Studies of absorption of 1,2dichloroethene from air, 

water, food, and soil in contaminated environments near hazardous waste sites 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 1,2dichloroethene. Experimental data are unavailable; therefore, it is not known if the 

bioconcentration potential is consistent with estimated values obtained from regression equations. The 

estimated BCF of 6 for fathead minnows (ASTER 1995; Veith and Kosian 1983) suggests that the 

potential for 1,2dichloroethene to bioconcentrate is low for aquatic organisms. Therefore, further 

studies on bioaccumulation are not recommended. However, biomagnification studies would enable 

scientists to assess the dangers of human exposure to 1,2dichloroethene from fish and seafood. 

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 
1,2-DICHLOROETHENE 113 

5. POTENTIAL FOR HUMAN EXPOSURE
 

air (Grimsrud and Rasmussen 1975; Lipsky and Jacot 1985; Shah and Singh 1988; Vogt and Walsh 

1985). 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 could not be located. 1,2-Dichloroethene has been detected 

infrequently in drinking water supplies. Reliable estimates of human intake of 1,2-dichloroethene via air, 

water, and food are not available. Therefore, it is recommended that further studies on human intake of 

1,2-dichloroethene from air, water, and food, particularly around hazardous waste sites, be undertaken. 

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. Information on biological media monitoring 

of the general populations, particularly populations near waste sites, is necessary for assessing the need 

to conduct health studies on these populations. 

Exposure Registries. No exposure registries for 1,2-dichloroethene were located. This substance 

is not currently one of the compounds for which a subregistry has been established in the National 

Exposure Registry. The substance will be considered in the future when chemical selection is 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 this substance. 

Production, Import/Export, Use, Release, and Disposal. According to the Emergency 

Planning and Community Right-to-Know Act of 1986, 42 U.S.C. Section 11023, industries are 

required to submit substance release and off-site transfer information to the EPA. The Toxics Release 

Inventory (TRI), which contains this information for 1993, became available in 1995. This database 

will be updated yearly and should provide a list of industrial production facilities and emissions. 

Exposure Levels in Environmental Media. Reliable monitoring data for the levels of 

1,2dichloroethene in contaminated media at hazardous waste sites are needed so that the information 
1,2-DICHLOROETHENE 114 

5. POTENTIAL FOR HUMAN EXPOSURE
 

obtained on levels of 1,2-dichloroethene in the environment can be used in combination with the 

known body burden of 1,2-dichloroethene to assess the potential risk of adverse health effects in 

populations living in the vicinity of hazardous waste sites. 

5.7.2 Ongoing Studies 

As part of the Third National Health and Nutrition Evaluation Survey (NHANES III), the 

Environmental Health Laboratory Sciences Division of the National Center for Environmental Health, 

Centers for Disease Control and Prevention, 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 1,2dichloroethene are in progress. NIOSH is now updating 

its occupational exposure estimates with additional information about exposure to trade name 

compounds. No other ongoing studies that would address data needs on general population and 

worker exposure to 1,2-dichloroethene were found. 
1,2-DICHLOROETHENE 115 

6. ANALYTICAL METHODS
 

The purpose of this chapter is to describe the analytical methods that are available for detecting, and/or 

measuring, and/or monitoring 1,2-dichloroethene, its metabolites, and other biomarkers of 1,2-dichloroethene exposure and effect. The intent is not to provide an exhaustive list of analytical methods. 

Rather, the intention is to identify well-established methods that are used as the standard methods of 

analysis. Many of the analytical methods used for environmental samples are the methods approved 

by federal agencies and organizations such as EPA and the National Institute for Occupational Safety 

and Health (NIOSH). Other methods presented in this chapter are those that are approved by groups 

such as the Association of Official Analytical Chemists (AOAC) and the American Public Health 

Association (APHA). Additionally, analytical methods are included that modify previously used 

methods to obtain lower detection limits, and/or to improve accuracy and precision. 

To determine dichloroethenes in various matrixes, most approaches involve purge procedures. Since 

these analytes are volatile (bp: 60.3 °C cis; 48.0-48.5 °C trans), removing them from an often complex 

matrix has very distinct advantages, particularly for biological and environmental samples. Virtually 

all standard methods use purge and trap procedures, in which the compounds are volatilized by passing 

an inert gas through a sample solution or suspension and the purged components are trapped on a solid 

sorbent for subsequent removal and analysis by gas chromatography (GC). Because of the presence of 

halogens, dichloroethenes can be selectively detected using devices such as electron capture, Hall 

electrolytic conductivity, or photoionization detectors. The most common detection technique 

specified by the standard methods is mass spectrometry (MS), which can readily achieve a high degree 

of selectivity and sensitivity. 

6.1 BIOLOGICAL SAMPLES 

Methods of analysis for 1 ,2dichloroethene 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 cisand 

trans- 1,2-dichloroethene in body tissues. However, recovery of trans- 1,2-dichloroethene varies 

with the type of body tissue. This finding generally agrees with those of the investigators who have 

attempted to measure levels of volatile halocarbons in body tissues. In addition to purge and trap, the 

headspace analysis methods of Hara et al. (1980) and Uehori et al. (1987) allow qualitative 

1,2-DICHLOROETHENE 117 

6. ANALYTICAL METHODS
 

identification of 1,2-dichloroethene in biological materials. A combination of detectors enabled Streete 

et al. (1992) to determine dichloroethenes in the headspace of blood, urine, and solid tissues. 

Dichloroethenes in breath can be determined by GUMS after collection with a portable spirometer 

(Raymer et al. 1990). In this approach, recoveries exceeded 90% for the dichloroethene isomers. The 

detection limit for dichloroethenes in human blood has been extended to part-per-trillion levels by 

Ashley et al. (1992), using an automated purge and trap technique that suppresses sample foaming 

with an antifoaming agent. High resolution GUMS can be used to enhance the contaminant 

separation abilities of gas chromatography on blood samples (Ashley et al. 1992; Bonin et al. 1992). 

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 workplace 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 

with minor variations. Capillary columns are versatile in separating contaminants of interest, and usually 

offer superior resolution and limits of detection (Oxenford et al. 1989). Various detectors are used, such 

as flame ionization detectors (FID), electron capture detectors (ECD), Hall electroconductivity detectors 

(HECD), and mass spectrometers. Multiple detectors are often employed in series or in parallel to 

increase the number and types of compounds detectable by purge and trap methods (Ho 1989; Kessels et 

al. 1992). Of the four listed, the FID is the least sensitive to halogenated hydrocarbons, yet it is sensitive 

enough for environmental samples. 

For 1,2-dichloroethene, adsorption to the solid sorbent is a significant analytical concern because of its 

volatility. It may be difficult to completely remove highly volatile compounds such as 1,2-dichloroethene 

from the air stream. Solid sorbents other than charcoal appear in some analytical methods; the 

most popular is the resin, Tenax GC. In addition to Tenax, Mehran et al. (1990) usedCarbosieve

with capillary chromatography to decrease the analysis time for EPA method 502.2. Pollack and 

coworkers (1991) provide for automating the collection and analysis of cis-1,2-dichloroethene by 

focusing the sample on a trap consisting of Carbopack-B and Carbosieve S-III instead of on glass 

beads. Substituting spray and trap for purge and trap enhances extraction efficiencies by a factor of 

2-5 and eliminates difficulties associated with sample foaming (Matz and Kesners 1993). 


1,2-DICHLOROETHENE 120 

6. ANALYTICAL METHODS
 

EPA method 601 (purgeable halocarbons) and EPA method 524 (purgeables) describe analysis of 

1,2-dichloroethene in municipal and industrial waste water (EPA 1982). In both methods, a 5 mL grab 

sample of water is connected to 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 gas chromatograph. 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. 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. 

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 gas chromatograph by rapidly 

heating the adsorbent tube, with no intermediate cryogenic trapping. 

Numerous researchers have applied modifications of the EPA methods to environmental samples. 

EPA’s Master Analytical Scheme (Michael et al. 1991) incorporates automated purge and trap and 

capillary chromatography into method 624 to achieve sensitivity of 1 ppb. Method 624 was compared 

to purgeable organic chloride analysis by Barber et al. (1992) and found to be superior by virtue of its 

contaminant identification capabilities. Eichelberger et al. (1990) modified method 524 by using a 

capillary column and an ion trap detector (ITD) to achieve detection levels below 200 ppt. Headspace 

sampling coupled with capillary GUMS offers a promising screening tool since it requires minimal 

sample preparation (Gryder-Boutet and Kennish 1988). Headspace GUMS can also been used for 

determining dichloroethenes in landfill leachate (Forst et al. 1989). 

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 gas 
1,2-DICHLOROETHENE 121 

6. ANALYTICAL METHODS
 

chromatographs. The considerations discussed above regarding use of different columns and detectors 

also apply here. 

The EPA guidelines for contract laboratories include methodology for water and soil sample analysis 

(EPA 1987c). The method listed in Table 6-2 is identical to EPA method 502.1 for the purpose of this 

discussion (except for the use of a mass spectrometer as the detector). The procedure for analyzing lowlevel 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. With respect to dichloroethene recoveries, Hewitt et al. (1991) found a 

headspace technique that is comparable to EPA SW-846 method 8240 for soil. It is practical for sample 

screening where contaminant identities were not required. The various SW-846 methods for 1,2-

dichloroethene presented in Table 6-2 are similar except for detection method. 

EPA method TO-14 uses an evacuated stainless steel canister to collect ambient air samples. Sample 

aliquots are analyzed by GUMS. McClenny et al. (1991) report a method detection limit of 0.3 ppb for 

this method. A method which represents a significant departure from more traditional methods for 

environmental samples is solid-phase microextraction (SPME). Solid phase microextraction uses a coated 

fused-silica fiber to collect contaminants from air and water samples. Chai et al. (1993) describe a simple 

non-purge and trap technique for determining dichloroethenes in air and water using this approach. The 

contaminants on the coated fused-silica fiber can then be thermally desorbed directly into the gas 

chromatograph for analysis. Page and Lacroix (1993) show the utility of headspace sampling coupled 

with fused-silica fiber adsorption in determining dichloroethenes at the 100 ppt level in foods. Their 

method satisfies the detection limit requirements of EPA method 524.2 for chloroethenes. Bauer and 

Solyom (1994) have developed a method to directly analyze waters in an ion trap mass spectrometer and 

have achieved a limit of detection for trans-1,2-dichloroethene of 0.5 ppt using single ion monitoring of 

m/z 96 (Soni et al. 1995). 

6.3 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with 

the Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of 1,2-dichloroethene is available. Where adequate 
1,2-DICHLOROETHENE 122 

6. ANALYTICAL METHODS
 

information is not available, ATSDR, in conjunction with the 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 the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will 

be evaluated and prioritized, and a substance-specific research agenda will be proposed. 

6.3.1 Identification of Data Needs 

Methods for Determining Biomarkers of Exposure and Effect. The available database 

provides several analytical methods adequate for the measurement of cis- and trans- 1,2dichloroethene 

in body tissue (see Section 6.1). Accuracy measurements for 1,2dichloroethene by Lin et al. (1982) 

show excellent recovery from adipose tissue but marginal recoveries from kidney and brain tissues. 

1,2Dichloroethene was recovered at 88-150% from blood (Ashley et al. 1992). Limits of detection 

for all biological matrices ranged from 10 to 50 pg. Additional recovery data in all condensed 

biological media are needed. Other than the parent compounds, there are no known biomarkers of 

exposure or the effects of exposure that are unique to 1,2-dichloroethene. Consequently, biomarkers of 

exposure or the effect of exposure should be identified; standardized analytical methods for their 

determination should be identified or developed in response. These biomarkers could allow an easier 

route for identification of exposure, especially for some tissues where bioconcentration of 

1,2-dichloroethene does not occur. 

Methods for Determining Parent Compounds and Degradation Products in 

Environmental Media. Numerous analytical methods exist for analysis of cis- and 

trans-1,2-dichloroethene in environmental matrices (see Section 6.2). These analytical methods 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, waste water, soil and air (APHA 1992; EPA 1986, 1987b; NIOSH 1987). 

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 
1,2-DICHLOROETHENE 123 

6. ANALYTICAL METHODS
 

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. For example, its detection 

limit of 16 ppm, outlined by the NIOSH technique (NIOSH 1987), is relatively high. Conversely, the 

stainless steel canister method of McClenny et al. (1991) purports to have a detection limit of 0.3 ppb and 

although not rigorously standardized, shows promise in detecting ambient background levels of 1,2-

dichloroethene. Information regarding the recovery efficiencies of the NIOSH (1987), McClenny (1991), 

and Ke et al. (1992b) procedures for detecting 1,2-dichloroethene in air were lacking. Additional data is 

needed to assess both accuracy and precision in the analysis of 1,2-dichloroethene in air. 

Contamination of surface water, groundwater, and foods in the vicinity of waste sites poses a threat to 

humans through oral exposure to 1,2-dichloroethene. Near quantitative recoveries and <.02 ppb 

detection limits were reported by Eichelberger et al. (1990). Low part-per-trillion detection limits were 

reported by Kessels et al. (1992) and an 0.5 ppt detection limit was reported by Soni et al. (1995). 

These recoveries and detection limits for 1,2-dichloroethene in water, coupled with the specificity 

offered by capillary gas chromatography and selective detection used by these researchers provide a 

means for determining 1,2-dichloroethene at very low levels in water. 

Currently, no viable method exists for determining 1,2-dichloroethene in food. The detection limit of 

100 μg/kg reported by Page and Lacroix (1993) is at least two orders of magnitude higher than what is 

required to be comparable to existing air and water methods for 1,2-dichloroethene. Appreciable 

additional work is needed in this area. 

6.3.2 Ongoing Studies 

The Environmental Health Laboratory Sciences Division of the National Center for Environmental 

Health, Centers for Disease Control and Prevention, is developing methods for the analysis of both cisand 

trans-1,2-dichloroethene and other volatile organic compounds in blood. These methods use purge 

and trap methodology, high resolution gas chromatography, and magnetic sector mass spectrometry 

which gives detection limits in the low parts per trillion (ppt) range. 

Ongoing studies for developing new analytical methods for 1,2-dichloroethene in environmental 

matrices could not be located. 

1,2-DICHLOROETHENE 125 

7. REGULATIONS AND ADVISORIES
 

The international, national, and state regulations and guidelines regarding 1,2-dichloroethene in air, 

water, and other media are summarized in Table 7-l. 

ATSDR has derived an MRL of 0.2 ppm for both acute-duration inhalation exposure (14 days or less) 

and intermediate-duration inhalation exposure (15-365 days) to trans- 1,2-dichloroethene based on a 

study by Freundt et al. (1977) that found fatty degeneration of the liver. The acute MRL is based on 

an LOAEL of 200 ppm over an 8-hour period, and the intermediate MRL is based on an LOAEL of 

200 ppm for 8 hours per day, 5 days per week for 8 or 16 weeks. 

ATSDR has derived oral MRLs for both acute- and intermediate-duration exposure. For acute oral 

exposure, data supported the derivation of an MRL for cis-1,2-dichloroethene of 1 mg/kg/day; 

however, no acute-duration MRL was derived for trans-1,2-dichloroethene. The acute oral MRL for 

cis-1,2-dichloroethene is based on a study by McCauley et al. (1990) that found hematological effects 

at 290 mg/kg/day and reported a NOAEL of 97 mg/kg/day. 

Intermediate-duration oral exposure MRLs were derived for both the cis and trans isomers. The 

intermediate duration oral MRL for cis-1,2-dichloroethene is 0.3 mg/kg/day based on a hematological 

study (McCauley et al. 1990). For trans-1,2-dichloroethene, the intermediate oral MRL is 

0.2 mg/kg/day, based on hepatic effects (Barnes et al. 1985). 

EPA has given cis-1,2-dichloroethene a non-cancer rating or a “not classifiable” rating (D) (IRIS 

1995). No National Toxicology Program (NTP) or IARC classifications exists. 

OSHA requires employers of workers who are occupationally exposed to a mixture of trans- and 

cis-1,2-dichloroethene (CAS No. 540-59-0) to institute engineering controls and work practices to 

reduce exposure-to and maintain employee exposure at or below permissible exposure limits (PEL). 

The employer must use engineering and work practice controls, if feasible, to reduce exposure to or 

below an g-hour time-weighted average (TWA) of 200 ppm (790 mg/m3

). Respirators must be 

provided during the time period necessary to install or implement feasible engineering and work 

practice controls (OSHA 1989). 
1,2-DICHLOROETHENE 126 

7. REGULATIONS AND ADVISORIES 

1,2-Dichloroethene is regulated by the Clean Water Effluent Guidelines as stated in Title 40, Section 

400-475, of the Code of Federal Regulations. The point source category for which 1,2-dichloroethene 

is controlled as a Total Toxic Organic is electroplating (EPA 1981). 

The Resource Conservation and Recovery Act (RCRA) identifies 1,2-dichloroethene as a hazardous 

waste when it is discarded as a commercial chemical product, off-spec species, container residue, or 

spill residue (EPA 1980a). 








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*Sawada M, Sofuni T, Ishidate M, Jr. 1987. Cytogenetic studies on l,l-dichloroethylene and its two 

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*Smith LR, Dragun J. 1984. Degradation of volatile chlorinated aliphatic priority pollutants in 

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1,2-DICHLOROETHENE 157 

9. GLOSSARY
 

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. 

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. 
1,2-DICHLOROETHENE 158 

9. GLOSSARY
 

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 IO) 

Lethal Concentration (LO) (LCLO) -- The lowest concentration of a chemical in air which has been 

reported to have cause death in humans or animals. 

Lethal Concentration(50) (LC50) -- A calculated concentration of a chemical in air to which exposure 

for a specific length of time is expected to cause death in 50% of a defined experimental animal 

population. 

Lethal Dose(LO) (LDLO) -- The lowest dose of a chemical introduced by a route other than inhalation 

that is expected to have caused death in humans or animals. 

Lethal Dose(50) (LT50) -- The dose of a chemical which has been calculated to cause death in 50% of 

a defined experimental animal population. 

Lethal Time(50) (LT50) -- A calculated period of time within which a specific concentration of a 

chemical is expected to cause death in 50% of a defined experimental animal population. 

Lowest-Observed-Adverse-Effect Level (LOAEL) -- The lowest 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 dose of a chemical that is likely to 

be without an appreciable risk of adverse noncancerous effects over a specified duration of exposure. 

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. 
1,2-DICHLOROETHENE 159 

9. GLOSSARY
 

q1* -- The upper-bound estimate of the low-dose slope of the dose-response curve as determined by 

the multistage procedure. The q1* can be used to calculate an estimate of carcinogenic potency, the 

incremental excess cancer risk per unit of exposure (usually μg/L for water, mg/kg/day for food, and 

μg/m3

 for air). 

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 pound 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. 

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 min between exposure periods. The daily TLV-TWA may not be exceeded. 

Target Organ Toxicity -- This term covers a broad range of adverse effects on target organs or 

physiological systems (e.g., renal, cardiovascular) extending from those arising through a single limited 

exposure to those assumed over a lifetime of exposure to a chemical. 

Teratogen -- A chemical that causes structural defects that affect the development of an organism. 

Threshold Limit Value (TLV) -- 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 

S-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 in 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 in using 

LOAEL data rather than NOAEL data. Usually each of these factors is set equal to 10. 

1,2-DICHLOROETHENE A-1 

APPENDIX A
 

ATSDR MINIMAL RISK LEVEL
 

The Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) [42 U.S.C. 

9601 et seq.], as amended by the Superfund Amendments and Reauthorization Act (SARA) [Pub. L. 

99-4991, requires that the Agency for Toxic Substances and Disease Registry (ATSDR) develop jointly 

with the U.S. Environmental Protection Agency (EPA), in order of priority, a list of hazardous substances 

most commonly found at facilities on the CERCLA National Priorities List (NPL); prepare toxicological 

profiles for each substance included on the priority list of hazardous substances; and assure the initiation 

of a research program to fill identified data needs associated with the substances. 

The toxicological profiles include an examination, summary, and interpretation of available toxicological 

information and epidemiologic evaluations of a hazardous substance. During the development of 

toxicological profiles, Minimal Risk Levels (MRLs) are derived when reliable and sufficient data exist to 

identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration for a 

given route of exposure. An MRL is an estimate of the daily human exposure to a hazardous substance 

that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration 

of exposure. MRLs are based on noncancer health effects only and are not based on a consideration of 

cancer effects. These substance-specific estimates, which are intended to serve as screening levels, are 

used by ATSDR health assessors to identify contaminants and potential health effects that may be of 

concern at hazardous waste sites. It is important to note that MRLs are not intended to define clean-up or 

action levels. 

MRLs are derived for hazardous substances using the no-observed-adverse-effect level/uncertainty factor 

approach. They are below levels that might cause adverse health effects in the people most sensitive to 

such chemical-induced effects. MRLs are derived for acute (1-14 days), intermediate (15-364 days), and 

chronic (365 days and longer) durations and for the oral and inhalation routes of exposure. Currently, 

MRLs for the demal route of exposure are not derived because ATSDR has not yet identified a method 

suitable for this route of exposure. MRLs are generally based on the most sensitive chemical-induced end 

point considered to be of relevance to humans. Serious health effects (such as irreparable damage to the 

liver or kidneys, or birth defects) are not used as a basis for establishing MRLs. Exposure to a level above 

the MRL does not mean that adverse health effects will occur. 
1,2-DICHLOROETHENE A-2 

APPENDIX A
 

ATSDR MINIMAL RISK LEVEL
 

MRLs are intended only to serve as a screening tool to help public health professionals decide where to 

look more closely. They may also be viewed as a mechanism to identify those hazardous waste sites that 

are not expected to cause adverse health effects. Most MRLs contain a degree of uncertainty because of 

the lack of precise toxicological information on the people who might be most sensitive (e.g., infants, 

elderly, nutritionally or immunologically compromised) to the effects of hazardous substances. ATSDR 

uses a conservative (i.e., protective) approach to address this uncertainty consistent with the public health 

principle of prevention. Although human data are preferred, MRLs often must be based on animal studies 

because relevant human studies are lacking. In the absence of evidence to the contrary, ATSDR assumes 

that humans are more sensitive to the effects of hazardous substance than animals and that certain persons 

may be particularly sensitive. Thus, the resulting MRL may be as much as a hundredfold below levels 

that have been shown to be nontoxic in laboratory animals. 

Proposed MRLs undergo a rigorous review process: Health Effects/MRL Workgroup reviews within the 

Division of Toxicology, expert panel peer reviews, and agencywide MRL Workgroup reviews, with 

participation from other federal agencies and comments from the public. They are subject to change as 

new information becomes available concomitant with updating the toxicological profiles. Thus, MRLs in 

the most recent toxicological profiles supersede previously published levels. For additional information 

regarding MRLs, please contact the Division of Toxicology, Agency for Toxic Substances and Disease 

Registry, 1600 Clifton Road, Mailstop E-29, Atlanta, Georgia 30333. 
1,2-DICHLOROETHENE A-3 

MINIMAL RISK LEVEL (MRL) WORKSHEET 

Chemical name: trans- 1,2-dichloroethene 

CAS number: 156-60-5 

Date: August 1996 

Profile status: Final 

Route: [x] Inhalation [ ] Oral 

Duration: [x] Acute [ IIntermediate [ ] Chronic 

Key to figure: 2 

Species: Rat 

MRL: 0.2 [ ] mg/kg/day [x] ppm [ ] mg/m3 

Reference: Freundt, KJ, Liebaldt, GP, and Lieberwirth, E. 1977. Toxicity Studies on 

Trans-1,2-Dichloroethylene. Toxicology, 7, pp. 141-153. 

Experimental design 

•	 l Female, mature SPF Wistar Rats; 180-200 g. 

•	 l Exposure for 8 hours; 0, 200, 1,000, and 3,000 ppm of trans-1,2-dichloroethene by inhalation. 

•	 6 rats/group. 

•	 Animals were sacrificed immediately following exposure and examined for gross pathology including 

lung, heart, liver, kidney, spleen, brain, quadriceps muscle and sciatic nerve. Standard hematological 

tests, clinical chemistry tests, and tests of clearance of bromosulphthalein in bile were carried out. 

Effects noted in study and corresponding doses: 

•	 Slight to severe fatty degeneration of the hepatic lobules and Kupffer cells was seen in all dosing 

groups (except controls). At 200 ppm fatty degeneration and fatty accumulation in Kupffer cells was 

seen in l/6 rats; at 1,000 and 3,000 ppm 1 or 2/6 rats showed similar liver and Kupffer cell changes. 

•	 Slight increases in capillary hyperaemia and alveolar septum distention were noted. 

•	 Fibrous swelling, hyperemia and modified muscular striation were found in the cardiac muscles at 

3,000 ppm in 2/6 rats. 

•	 No pathological changes were seen in the kidneys, spleen, brain, or peripheral nerves. No central 

nervous system depression was seen. 

Dose endpoint used for MRL derivation: 

Fatty degeneration of liver cells: LOAEL = 200 ppm 

[ ] NOAEL [x] LOAEL 
 

1,2-DICHLOROETHENE A-4 

APPENDIX A 

Uncertainty factors used in MRL derivation: 

[ ] 1 [ ] 3 [x] 10 (for use of a LOAEL)
 

[ ] 1 [ ] 3 [xl 10 (for extrapolation from animals to humans)
 

[ ] 1 [ ] 3 [x] 10 (for human variability)
 

Was a conversion factor used from ppm in food or water to a mg/body weight dose? No.
 

If so, explain:
 

If an inhalation study in animals, list conversion factors used in determining human eauivalent dose: The
 

NOAEL (HEC) was calculated for a gas:extrarespiratory effect in rats assuming periodicity was attained,
 

using the following equation: NOAEL (HEC) = NOAEL (adj.) x λA/λH, where: NOAEL (HEC) = the NOAEL
 

human equivalent concentration; NOAEL (adj) = the NOAEL adjusted for continuous exposure (e.g.,
 

adjusted for exposure regimen by h hours/24 hours and d days/7 days); λA/λH, = the ratio of the blood to
 

air partition coefficient of the chemical for the animal species to the human value, used only if λA/λH .
 

For the situation in which λA>λH, and in the case where I values are unknown, the default value of λA/λH,
 

= 1 is recommended. For 1,2-dichloroethene, λA = 9.58 and λH = 6.04, therefore λA>λH, and a default
 

value of 1 was used.
 

Was a conversion used from intermittent to continuous exposure? No.
 

If so, explain:
 

Other additional studies or pertinent information that lend support to this MRL:
 

McCauley et al. (1990), Barnes et al. (1985), and McMillan (1986) also reported hepatic effects, from oral
 

exposure to cis- or trans-1,2-dichloroethene.
 

Agency Contact (Chemical Manager): Carolyn Harper
 
 

 

 

1,2-DICHLOROETHENE A-5 

APPENDIX A 

MINIMAL RISK LEVEL WORKSHEET 

Chemical name:trans-1,2-dichloroethene 

CAS number: 156-60-5 

Date: August 1996 

Profile status: Final 

Route: [x] Inhalation [ ] Oral 

Duration: [ ] Acute [x] Intermediate [ ] Chronic 

Key to figure: 11 

Species: Rat 

MRL: 0.2 [ ] mg/kg/day [xl ppm [ ] mg/m3 

Reference: Freundt, KI, Liebaldt, GP, and Lieberwirth, E. 1977. Toxicity Studies on 

Trans-1,2-Dichloroethylene. Toxicology, 7, pp. 141-153. 

Experimental design 

•	 Female, mature SPF Wistar Rats; 180-200 g. 

•	 Exposure for g-hour periods, 5 days per week, for either 8 or 16 weeks, at or 200 ppm of 

trans-1,2-dichloroethene by inhalation. 

•	 6 rats/group. 

•	 Animals were sacrificed immediately following exposure and examined for gross pathology including 

lung, heart, liver, kidney, spleen, brain, quadriceps muscle and sciatic nerve. 

Effects noted in study and corresuonding doses: 

•	 In the 8-week experiment, slight fatty degeneration of the hepatic lobules was observed in 316 

exposed rats and severe fatty accumulation in the Kupffer cells was seen in 3/6 exposed rats (200 

ppm). In the16-week experiment, slight (2/6 exposed) and severe (3/6 exposed) fatty accumulation in 

the liver lobule was seen and slight fatty accumulation in the Kupffer cells was seen in 5/6 exposed 

rats (200 PPm). 

•	 Slight increases in capillary hyperaemia and alveolar septum distention were seen. 

•	 No pathological changes were seen in the kidneys, spleen, brain, striated muscle, or peripheral nerves. 

No central nervous system depression was seen. 

Dose endpoint used for MRL derivation: 

Fatty degeneration of liver cells: LOAEL = 200 ppm 

[ ] NOAEL [x] LOAEL 

Uncertainty factors used in MRL derivation: 

[] 1 [] 3 [x] lO(foruseofaLOAEL)
 

[ ] 1 [ ] 3 [x] 10 (for extrapolation from animals to humans)
 

[ ] 1 [ ] 3 [x] 10 (for human variability)
 
1,2-DICHLOROETHENE A-6 

APPENDIX A
 

If an inhalation study in animals. list conversion factors used in determining. human equivalent dose: The 

NOAEL (HEC) was calculated for a gas:extrarespiratory effect in rats assuming periodicity was attained, 

using the following equation: NOAEL (HEC) = NOAEL (adj.) x λA/λH, where: NOAEL (HEC) = the NOAEL 

human equivalent concentration; NOAEL (adj) = the NOAEL adjusted for continuous exposure (e.g., 

adjusted for exposure regimen by h hours/24 hours and d days/7 days); λA/λH, = the ratio of the blood to 

air partition coefficient of the chemical for the animal species to the human value, used only if λA/λH . 

For the situation in which λA>λH, and in the case where I values are unknown, the default value of λA/λH, 

= 1 is recommended. For 1,2-dichloroethene, λA = 9.58 and λH = 6.04, therefore λA>λH, and a default 

value of 1 was used. 

Was a conversion used from intermittent to continuous exposure? No. 

If so, explain: 

Other additional studies or pertinent information that lend support to this MRL:
 

McCauley et al. (1990), Barnes et al. (1985), and McMillan (1986) also reported hepatic effects, from oral
 

exposure to cis- or trans-1,2-dichloroethene.
 

Agency Contact (Chemical Manager): Carolyn Harper
 
 

1,2-DICHLOROETHENE A-7 

APPENDIX A 

MINIMAL RISK LEVEL WORKSHEET 

Chemical name:cis- 1,2-dichloroethene 

CAS number: 156-60-5 

Date: August 28, 1996 

Profile status: Final 

Route: [ ] Inhalation [x ]Oral 

Duration: [x ] Acute [ ]Intermediate [ ] Chronic 

Key to figure: 8 

Species: rat 

MRL: 1 [x] mg/kg/day [ ] ppm [ ] mg/m3 

Reference: McCauley et al. 1990. The effects of subacute and subchronic oral exposure to 

cis- 1,2-dichloroethylene in rats. Health Effects Research Laboratory, U.S. EPA, Cincinnati, OH and Air 

Force Aerospace Medical Research Laboratory, Wright-Patterson AFB, OH. 

Experimental design : 

•	 Male and female Sprague-Dawley-derived Charles River rats. 

•	 Doses: 1.0, 3.0, 10.0,20.0 n-M/kg/day (97, 290,970, 1,900 mg/kg/day) 

•	 Administration was in corn oil via gavage for 14 days. 

•	 10 rats/sex/group. 

•	 Food and water were available ad libitum, body weights were taken weekly. At the end of the 

exposure 

period, all animals were sacrificed and specimens were collected for clinical chemistry, hematology, 

and histopathology studies. 

Effects noted in studv and corresnonding doses: 

•	 Mortality was observed in rats treated with 970 mg/kg/day (2/20) and 1,900 mg/kg/day (5/20). 

•	 CNS depression was observed at 1,900 mg/kg/day. 

•	 Increased absolute and relative liver weights in treated males and female rats at 97 mg/kg/day. 

•	 Increased absolute and relative kidney weights in females at doses greater than or equal to 

970 mglkglday. 

•	 Decreased blood urea nitrogen at 290 mg/kg/day and increased serum cholesterol in females at 1,900 

mg/kg/day. 

•	 Decreased hematocrit levels and erythrocyte counts in females at doses greater than or equal to 

290 mg/kg/day. 

•	 Increased serum calcium levels in males at doses greater or equal to 970 mg/kg/day. 

Dose endnoint used for MRL derivation: 

Decreased hematocrit in females NOAEL = 97 mg/kg/day. 

[x ] NOAEL [ ]LOAEL 
 

 

1,2-DICHLOROETHENE A-8 

APPENDIX A 

Uncertainty factors used in MRL derivation:
 

[] 1 []3 [] l0(for use of a LOAEL)
 

[ ] 1 [ ] 3 [x ] 10 (for extrapolation from animals to humans)
 

[ ] 1 [ ] 3 [x ] 10 (for human variability)
 

Was a conversion factor used from ppm in food or water to a mg/body weight dose? 

If so, explain: No 

If an inhalation study in animals, list conversion factors used in determining human equivalent dose: 

Was a conversion used from intermittent to continuous exposure? 

If so, explain: No 

Other additional studies or pertinent information that lend support to this MRL:
 

Hematological effects have also been noted in other oral studies. Barnes et al. (1985) reported a 12%
 

decrease in fibrinogen levels and a 7% decrease in prothrombin time in mice exposed to 210 mg/kg/day
 

trans- 1,2-dichloroethene.
 

Agency Contact (Chemical Manager): Carolyn Harper 
1,2-DICHLOROETHENE A-9 

APPENDIX A 

MINIMAL RISK LEVEL WORKSHEET 

Chemical name:cis- 1,2-dichloroethene 

CAS number: 156-60-5 

Date: August 28, 1996 

Profile status: Final 

Route: [ ] Inhalation [x ]Oral 

Duration: [ ] Acute [x ]Intermediate [ ] Chronic 

Key to figure: 15 

Species: rat 

MRL: 0.3 [x ] mg/kg/day [ I ppm [ I mg/m3 

Reference: McCauley et al. 1990. The effects of subacute and subchronic oral exposure to 

cis-1,2-dichloroethylene in rats. Health Effects Research Laboratory, U.S. EPA, Cincinnati, OH and Air 

Force Aerospace Medical Research Laboratory, Wright-Patterson AFB, OH. 

Experimental design: 

•	 Male and female Sprague-Dawley-derived Charles River rats. 

•	 Doses: 0.33, 1.0, 3.0, and 9.0 mM/kg/day (32, 97, 290, 870 mg/kg/day) 

•	 Administration was in corn oil via gavage for 90 days. 

•	 10 rats/sex/group. 

•	 Food and water were available ad libitum, body weights were taken weekly. At the end of the 

exposure 

period, all animals were sacrificed and specimens were collected for clinical chemistry, hematology, 

and histopathology studies. 

Effects noted in study and corresponding doses: 

•	 Mortality was observed in the control group and all four treatment groups within the first week: l/20, 

l/20, l/20, 3/20,4/20 respectively. 

•	 Increased relative kidney weight in male rats at 870 mg/kg/day and increased relative liver weights in 

male and female rats given greater than or equal to 97 mg/kg/day were observed. 

•	 Increased relative thymus weights were observed in females treated at 870 mg/kg/day. 

•	 A dose related decrease in blood urea nitrogen and serum creatinine was observed at 870 mg/kg/day. 

•	 Decreased hematocrit levels in males at doses greater than or equal to 97 mg/kg/day and in females at 

doses greater than or equal to 290 mg/kg/day was observed. 

•	 Decreased hemoglobin levels in males at doses greater than or equal to 290 mg/kg/day and in females 

at 290 mg/kg/day was noted. 

•	 A 27% decrease in body weight was observed in males at 290 mg/kg/day and a 10% decrease in body 

weight was observed in males at 97 mg/kg/day. 
 

 

1,2-DICHLOROETHENE A-10 

APPENDIX A 

Dose endpoint used for MRL derivation:
 

Decreased hematocrit and hemoglobin: NOAEL = 32 mg/kg/day.
 

[x ] NOAEL [ ]LOAEL 

Uncertainty factors used in MRL derivation: 

[] 1 []3 [] l0(for use of a LOAEL)
 

[ ] 1 [ ] 3 [x ] 10 (for extrapolation from animals to humans)
 

[ ] 1 [ ] 3 [x ] 10 (for human variability)
 

Was a conversion factor used from ppm in food or water to a mg/body weight dose?
 

If so, explain: No
 

If an inhalation study in animals. list conversion factors used in determining human equivalent dose:
 

Was a conversion used from intermittent to continuous exposure?
 

If so, explain: No
 

Other additional studies or pertinent information that lend support to this MRL:
 

Hematological effects have also been noted in other oral studies. Barnes et al. (1985) reported a 12%
 

decrease in fibrinogen levels and a 7% decrease in prothrombin time in mice exposed to 210 mg/kg/day
 

trans- 1,2-dichloroethene.
 

Agency Contact (Chemical Manager): Carolyn Harper 
 

1,2-DICHLOROETHENE A-11 

APPENDIX A 

MINIMAL RISK LEVEL WORKSHEET 

Chemical name:trans- 1,2-dichloroethene 

CAS number: 156-60-5 

Date: August 28, 1996 

Profile status: Final 

Route: [ ] Inhalation [x] Oral 

Duration: [ ] Acute [x] Intermediate [ ] Chronic 

Key to figure: 17 

Species: Mouse 

MRL: 0.2 [x] mg/kg/day [ ] ppm [ ] mg/m3 

Reference: 

Barnes DW, Sanders VM, White KL Jr, Shopp GM, and Munson AE. 1985. Toxicology of 

trans-1,2-Dichloroethylene in the Mouse. Drug and Chemical Toxicology 8(5):373-392. 

Experimental design: 

•	 90-day study with 260 male and 260 female mice in the control group and 140 mice of each sex in 

groups exposed to drinking water with 0.1, 1.0, or 2.0 mg trans-1,2-dichlorethene/mL (males: 0, 

17, 175, 387 mg/kg/day; females: 0,23, 224,452 mg/kg/day). 

•	 Exposure was averaged over the 90 days. 

•	 Trans-1,2-dichloroethene was maintained in solution using a 1% emulphor (vegetable oil) and 

deionized water. 

Effects noted in study and corresponding doses: 

•	 No trans-1,2-dichloroethene-induced changes in terminal body weight or gross pathology. 

•	 Male mice showed an increase in relative liver weights (8%) and increased serum alkaline 

phosphatase at 175 mg/kg/day. 

•	 Glucose levels were elevated in all exposure groups for both sexes and males showed decreased 

glutathione levels at 387 mg/kg/day. 

•	 An 11% decrease in relative lung weight was seen in female mice at 452 mg/kg/day. 

•	 No effects were noted on hematocrit, hemoglobin, or erythrocyte and platelet counts. 

Dose endpoint used for MRL derivation: 

Increased serum alkaline phosphatase NOAEL = 17 mg/kg/day 

[x] NOAEL [ ]LOAEL 
 

 

1,2-DICHLOROETHENE A-12 

APPENDIX A 

Uncertainty factors used in MRL derivation: 

[] 1 [] 3 [] l0(for use of a LOAEL)
 

[ ] 1 [ ] 3 [x] 10 (for extrapolation from animals to humans)
 

[ ] 1 [ ] 3 [x] 10 (for human variability)
 

Was a conversion factor used from ppm in food or water to a mg/body weight dose? Author provided.
 

If so, explain:
 

If an inhalation study in animals, list conversion factors used in determining human equivalent dose:
 

Was a conversion used from intermittent to continuous exposure? No.
 

If so, explain:
 

Other additional studies or pertinent information that lend support to this MRL:
 

McCauley et al. (1990) and McMillan (1986) also reported hepatic effects from oral exposure to
 

trans- 1,2-dichloroethene.
 

Agency Contact (Chemical Manager): Carolyn Harper 
1,2-DICHLOROETHENE B-1 

APPENDIX B 

USER’S GUIDE 

Chapter 1 

Public Health Statement 

This chapter of the profile is a health effects summary written in non-technical language. Its intended 

audience is the general public especially people living in the vicinity of a hazardous waste site or 

chemical release. If the Public Health Statement were removed from the rest of the document, it 

would still communicate to the lay public essential information about the chemical. 

The major headings in the Public Health Statement are useful to find specific topics of concern. The 

topics are written in a question and answer format. The answer to each question includes a sentence 

that will direct the reader to chapters in the profile that will provide more information on the given 

topic. 

Chapter 2 

Tables and Figures for Levels of Significant Exposure (LSE) 

Tables (2-1, 2-2, and 2-3) and figures (2-l and 2-2) are used to summarize health effects and illustrate 

graphically levels of exposure associated with those effects. These levels cover health effects observed 

at increasing dose concentrations and durations, differences in response by species, minimal risk levels 

(MRLs) to humans for noncancer endpoints, and EPA’s estimated range associated with an upperbound 

individual lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. Use the LSE tables and 

figures for a quick review of the health effects and to locate data for a specific exposure scenario. The 

LSE tables and figures should always be used in conjunction with the text. All entries in these tables 

and figures represent studies that provide reliable, quantitative estimates of No-Observed-AdverseEffect Levels (NOAELs), Lowest-Observed-Adverse-Effect Levels (LOAELs), or Cancer Effect Levels 

(CELs). 

The legends presented below demonstrate the application of these tables and figures. Representative 

examples of LSE Table 2- 1 and Figure 2-l are shown. The numbers in the left column of the legends 

correspond to the numbers in the example table and figure. 

LEGEND 

See LSE Table 2-l 

(1)	 Route of Exposure One of the first considerations when reviewing the toxicity of a substance 

using these tables and figures should be the relevant and appropriate route of exposure. When 

sufficient data exists, three LSE tables and two LSE figures are presented in the document. The 

three LSE tables present data on the three principal routes of exposure, i.e., inhalation, oral, and 

dermal (LSE Table 2-1, 2-2, and 2-3, respectively). LSE figures are limited to the inhalation 

(LSE Figure 2-l) and oral (LSE Figure 2-2) routes. Not all substances will have data on each 

route of exposure and will not therefore have all five of the tables and figures. 
1,2-DICHLOROETHENE B-2 

APPENDIX B
 

(2)	 Exposure Period Three exposure periods - acute (less than 15 days), intermediate (15-364 days), 

and chronic (365 days or more) are presented within each relevant route of exposure. In this 

example, an inhalation study of intermediate exposure duration is reported. For quick reference 

to health effects occurring from a known length of exposure, locate the applicable exposure 

period within the LSE table and figure. 

(3)	 Health Effect The major categories of health effects included in LSE tables and figures are 

death, systemic, immunological, neurological, developmental, reproductive, and cancer. 

NOAELs and LOAELs can be reported in the tables and figures for all effects but cancer. 

Systemic effects are further defined in the “System” column of the LSE table (see key number 

18). 

(4)	 Key to Figure Each key number in the LSE table links study information to one or more data 

points using the same key number in the corresponding LSE figure. In this example, the study 

represented by key number 18 has been used to derive a NOAEL and a Less Serious LOAEL 

(also see the 2 “18r” data points in Figure 2-l). 

(5)	 Species The test species, whether animal or human, are identified in this column. Section 2.5, 

“Relevance to Public Health,” covers the relevance of animal data to human toxicity and Section 

2.3, “Toxicokinetics,” contains any available information on comparative toxicokinetics. 

Although NOAELs and LOAELs are species specific, the levels are extrapolated to equivalent 

human doses to derive an MRL. 

(6)	 Exposure Frequency/Duration The duration of the study and the weekly and daily exposure 

regimen are provided in this column. This permits comparison of NOAELs and LOAELs from 

different studies. In this case (key number 18), rats were exposed to toxaphene via inhalation for 

6 hours per day, 5 days per week, for 3 weeks. For a more complete review of the dosing 

regimen refer to the appropriate sections of the text or the original reference paper, i.e., Nitschke 

et al. 1981. 

(7)	 System This column further defines the systemic effects. These systems include: respiratory, 

cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, and 

dermal/ocular. “Other” refers to any systemic effect (e.g., a decrease in body weight) not covered 

in these systems. In the example of key number 18, 1 systemic effect (respiratory) was 

investigated. 

(8)	 NOAEL A No-Observed-Adverse-Effect Level (NOAEL) is the highest exposure level at which 

no harmful effects were seen in the organ system studied. Key number 18 reports a NOAEL of 

3 ppm for the respiratory system which was used to derive an intermediate exposure, inhalation 

MRL of 0.005 ppm (see footnote “b”). 

(9)	 LOAEL A Lowest-Observed-Adverse-Effect Level (LOAEL) is the lowest dose used in the 

study that caused a harmful health effect. LOAELs have been classified into “Less- Serious” and 

“Serious” effects. These distinctions help readers identify the levels of exposure at which 

adverse health effects first appear and the gradation of effects with increasing dose. A brief 

description of the specific endpoint used to quantify the adverse effect accompanies the LOAEL. 

The respiratory effect reported in key number 18 (hyperplasia) is a Less serious LOAEL of 10 

ppm. MRLs are not derived from Serious LOAELs. 

(10)	 Reference The complete reference citation is given in chapter 8 of the profile. 
1,2-DICHLOROETHENE B-3 

APPENDIX B
 

(11) CEL A Cancer Effect Level (CEL) is the lowest exposure level associated with the onset of 

carcinogenesis in experimental or epidemiologic studies. CELs are always considered serious 

effects. The LSE tables and figures do not contain NOAELs for cancer, but the text may report 

doses not causing measurable cancer increases. 

(12) Footnotes Explanations of abbreviations or reference notes for data in the LSE tables are found 

in the footnotes. Footnote “b” indicates the NOAEL of 3 ppm in key number 18 was used to 

derive an MRL of 0.005 ppm. 

LEGEND 

See Figure 2-l 

LSE figures graphically illustrate the data presented in the corresponding LSE tables. Figures help the 

reader quickly compare health effects according to exposure concentrations for particular exposure 

periods. 

(13)	 Exposure Period The same exposure periods appear as in the LSE table. In this example, health 

effects observed within the intermediate and chronic exposure periods are illustrated. 

(14)	 Health Effect These are the categories of health effects for which reliable quantitative data 

exists. The same health effects appear in the LSE table. 

(15)	 Levels of Exposure concentrations or doses for each health effect in the LSE tables are 

graphically displayed in the LSE figures. Exposure concentration or dose is measured on the log 

scale “y” axis. Inhalation exposure is reported in mg/m3

 or ppm and oral exposure is reported in 

mg/kg/day . 

(16)	 NOAEL In this example, 18r NOAEL is the critical endpoint for which an intermediate 

inhalation exposure MRL is based. As you can see from the LSE figure key, the open-circle 

symbol indicates to a NOAEL for the test species-rat. The key number 18 corresponds to the 

entry in the LSE table. The dashed descending arrow indicates the extrapolation from the 

exposure level of 3 ppm (see entry 18 in the Table) to the MRL of 0.005 ppm (see footnote “b” 

in the LSE table). 

(17)	 CEJ Key number 38r is 1 of 3 studies for which Cancer Effect Levels were derived. The 

diamond symbol refers to a Cancer Effect Level for the test species-mouse. The number 38 

corresponds to the entry in the LSE table. 

(18)	 Estimated Upper-Bound Human Cancer Risk Levels This is the range associated with the 

upper-bound for lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. These risk levels are 

derived from the EPA’s Human Health Assessment Group’s upper-bound estimates-of the slope 

of the cancer dose response curve at low dose levels (ql*). 

(19) Key to LSE Figure The Key explains the abbreviations and symbols used in the figure. 


1,2-DICHLOROETHENE B-6 

APPENDIX B 

Chapter 2 (Section 2.5) 

Relevance to Public Health 

The Relevance to Public Health section provides a health effects summary based on evaluations of 

existing toxicologic, epidemiologic, and toxicokinetic information. This summary is designed to 

present interpretive, weight-of-evidence discussions for human health endpoints by addressing the 

following questions. 

1.	 What effects are known to occur in humans? 

2.	 What effects observed in animals are likely to be of concern to humans? 

3.	 What exposure conditions are likely to be of concern to humans, especially around 

hazardous waste sites? 

The section covers endpoints in the same order they appear within the Discussion of Health Effects by 

Route of Exposure section, by route (inhalation, oral, dermal) and within route by effect. Human data 

are presented first, then animal data. Both are organized by duration (acute, intermediate, chronic). In 

vitro data and data from parenteral routes (intramuscular, intravenous, subcutaneous, etc.) are also 

considered in this section. If data are located in the scientific literature, a table of genotoxicity 

information is included. 

The carcinogenic potential of the profiled substance is qualitatively evaluated, when appropriate, using 

existing toxicokinetic, genotoxic, and carcinogenic data. ATSDR does not currently assess cancer 

potency or perform cancer risk assessments. Minimal risk levels (MRLs) for noncancer endpoints (if 

derived) and the endpoints from which they were derived are indicated and discussed. 

Limitations to existing scientific literature that prevent a satisfactory evaluation of the relevance to 

public health are identified in the Data Needs section. 

Interpretation of Minimal Risk Levels 

Where sufficient toxicologic information is available, we have derived minimal risk levels (MRLs) for 

inhalation and oral routes of entry at each duration of exposure (acute, intermediate, and chronic). 

These MRLs are not meant to support regulatory action; but to acquaint health professionals with 

exposure levels at which adverse health effects are not expected to occur in humans. They should 

help physicians and public health officials determine the safety of a community living near a chemical 

emission, given the concentration of a contaminant in air or the estimated daily dose in water. MRLs 

are based largely on toxicological studies in animals and on reports of human occupational exposure. 

MRL users should be familiar with the toxicologic information on which the number is based. 

Chapter 2.5, “Relevance to Public Health,” contains basic information known about the substance. 

Other sections such as 2.7, “Interactions with Other Substances,” and 2.8, “Populations that are 

Unusually Susceptible” provide important supplemental information. 

MRL users should also understand the MRL derivation methodology. MRLs are derived using a 

modified version of the risk assessment methodology the Environmental Protection Agency (EPA) 

provides (Barnes and Dourson 1988) to determine reference doses for lifetime exposure (RfDs). 
1,2-DICHLOROETHENE B-7 

APPENDIX B
 

To derive an MRL, ATSDR generally selects the most sensitive endpoint which, in its best judgement, 

represents the most sensitive human health effect for a given exposure route and duration. ATSDR 

cannot make this judgement or derive an MRL unless information (quantitative or qualitative) is 

available for all potential systemic, neurological, and developmental effects. If this information and 

reliable quantitative data on the chosen endpoint are available, ATSDR derives an MRL using the 

most sensitive species (when information from multiple species is available) with the highest NOAEL 

that does not exceed any adverse effect levels. When a NOAEL is not available, a lowest-observedadverse-effect level (LOAEL) can be used to derive an MRL, and an uncertainty factor (UF) of 10 

must be employed. Additional uncertainty factors of 10 must be used both for human variability to 

protect sensitive subpopulations (people who are most susceptible to the health effects caused by the 

substance) and for interspecies variability (extrapolation from animals to humans). In deriving an 

MRL, these individual uncertainty factors are multiplied together. The product is then divided into the 

inhalation concentration or oral dosage selected from the study. Uncertainty factors used in 

developing a substance-specific MRL are provided in the footnotes of the LSE Tables.